bortezomib profile

ID Source	ID
PubMed CID	387447
CHEMBL ID	325041
CHEBI ID	52717
SCHEMBL ID	192129
MeSH ID	M0350110

Synonym
peptide boronate
c19h25bn4o4
AB01273951-02
AB01273951-01
nsc681239
NCI60_029010
velcade
dpba
mln-341
ldp-341
velcade (tn)
bortezomib (jan/usan/inn)
D03150
n-((1s)-1-benzyl-2-(((1r)-1-(dihydroxyboranyl)-3-methylbutyl)amino)2-oxoethylpyrazinecarboxamide
ps 341 (pharmaceutical)
nsc 681239
ldp 341
boronic acid, (3-methyl-1-((1-oxo-3-phenyl-2-((pyrazinylcarbonyl)amino)propyl)amino)butyl)-, (s-(r,s))-
mg 341
n-((1s)-1-benzyl-2-(((1r)-1-(dihydroxyboranyl)-3-methylbutyl)amino)-2-oxoethyl)pyrazinecarboxamide
((1r)-3-methyl-1-(((2s)-3-phenyl-2-((pyrazinylcarbonyl)amino)propanoyl)amino)butyl)boronic acid
boronic acid, ((1r)-3-methyl-1-(((2s)-1-oxo-3-phenyl-2-((pyrazinylcarbonyl)amino)propyl)amino)butyl)-
n-[(1r)-1-(dihydroxyboryl)-3-methylbutyl]-n-(pyrazin-2-ylcarbonyl)-l-phenylalaninamide
bortezomib ,
ps-341
ps 341
179324-69-7
lpd-341
boronic acid, [(1(r)-3-methyl-1-[[(2s)-1-oxo-3-phenyl-2-[(pyrazinylcarbonyl)amino]propyl]amino]butyl]-
pyz-phe-boroleu
[(1r)-3-methyl-1-[[(2s)-3-phenyl-2-(pyrazine-2-carbonylamino)propanoyl]amino]butyl]boronic acid
lpd 341
DB00188
[(1r)-3-methyl-1-({(2s)-3-phenyl-2-[(pyrazin-2-ylcarbonyl)amino]propanoyl}amino)butyl]boronic acid
velcade (millenium)
nsc-681239
S1013 ,
proscript boronic acid
n-[(1r)-1-(dihydroxyboranyl)-3-methylbutyl]-nalpha-(pyrazin-2-ylcarbonyl)-l-phenylalaninamide
n-[(1r)-1-(dihydroxyboranyl)-3-methylbutyl]-n(alpha)-(pyrazin-2-ylcarbonyl)-l-phenylalaninamide
CHEBI:52717 ,
bortezomib accord
bortezomib hydrate
CHEMBL325041 ,
bdbm50069989
(r)-3-methyl-1-((s)-3-phenyl-2-(pyrazine-2-carboxamido)propanamido)butylboronic acid
(r)-3-methyl-1-((s)-3-phenyl-2-(pyrazine-6-carboxamido)propanamido)butylboronic acid
A18332
((r)-3-methyl-1-((s)-3-phenyl-2-(pyrazine-2-carboxamido)propanamido)butyl)boronic acid
NCGC00242506-01
mg-341
dtxcid1020980
tox21_112672
cas-179324-69-7
dtxsid3040980 ,
tox21_112630
MLS004774142
smr003500787
boronic acid, b-[(1r)-3-methyl-1-[[(2s)-1-oxo-3-phenyl-2-[(2-pyrazinylcarbonyl)amino]propyl]amino]butyl]-
[(1r)-3-methyl-1-[[(2s)-1-oxo-3-phenyl-2-[(pyrazinylcarbonyl)amino]propyl]amino]butyl]boronic acid
69g8bd63pp ,
unii-69g8bd63pp
hsdb 7666
bortezomib [usan:inn:ban]
HY-10227
CS-1039
bortezomib,velcade
bortezomib (ps-341)
[(1r)-3-methyl-1-[[(2s)-3-phenyl-2-[(pyrazinylcarbonyl)amino]propanoyl]amino]butyl]boronic acid
bortezomib [vandf]
bortezomib [hsdb]
bortezomib [inn]
bortezomib [mi]
bortezomib hydrate [jan]
bortezomib [jan]
bortezomib [orange book]
bortezomib [who-dd]
bortezomib [mart.]
bortezomib [ema epar]
1610526-91-4
bortezomib [usan]
AKOS015909706
gtpl6391
GXJABQQUPOEUTA-RDJZCZTQSA-N
AM81235
SCHEMBL192129
tox21_112672_1
3MG0
NCGC00242506-02
[(1r)-3-methyl-1-[[(2s)-1-oxo-3-phenyl-2-[(pyrazinylcarbonyl)amino]propyl]amino]-butyl]boronic acid
(r)-3-methyl-1-((s)-3-phenyl-2-(pyrazine-2-carboxamido)propanamido)butan-2-ylboronic acid
HB4036
ps-341 [bortezomib]
AB01273951_03
mfcd09056737
bortezomib (velcade) ,
B5741
brotezamide
radiciol
sr-01000939863
SR-01000939863-2
(1r)-3-methyl-1-({(2s)-3-phenyl-2-[(2-pyrazinylcarbonyl)amino]propanoyl}amino)butylboronic acid, aldrichcpr
NCGC00242506-07
SW208077-3
bortezomib (velcade,mg-341,ps-341)
Q419319
AS-15721
BRD-K88510285-001-02-0
CCG-268449
NCGC00242506-06
nsc756655
nsc-756655
((r)-3-methyl-1-((s)-3-phenyl-2-(pyrazine-2-carboxamido)propanamido)butyl)boronicacid
EN300-657180
[(1r)-3-methyl-1-[(2s)-3-phenyl-2-[(pyrazin-2-yl)formamido]propanamido]butyl]boronic acid
BB164258
bortezomib- bio-x
bortexomib
n-((1r)-1-(dihydroxyboranyl)-3-methylbutyl)-n(alpha)-(pyrazin-2-ylcarbonyl)-l-phenylalaninamide
bortezomibum
l01xx32
bortezomib for injection
n-((1r)-1-(dihydroxyboryl)-3-methylbutyl)-n-(pyrazin-2-ylcarbonyl)-l-phenylalaninamide
bortezomib (mart.)
Z2213886907

Excerpt	Reference	Relevance
"Bortezomib is a proteasome inhibitor with anticancer effects."	( Proteasome inhibition by bortezomib parallels a reduction in head and neck cancer cells growth, and an increase in tumor-infiltrating immune cells. Barillari, G; Bei, R; Benvenuto, M; Bonanno, E; Ciuffa, S; Coletta, M; Fazi, S; Focaccetti, C; Manzari, V; Masuelli, L; Modesti, A; Sbardella, D; Scimeca, M; Segni, M; Tundo, GR, 2021)	1.65
"Bortezomib (BTZ) is a well-characterized anticancer agent that inhibits proteasome, and its effect is associated with the function of miRs."	( miR-466 Contributes to the Enhanced Antitumor Effect of Bortezomib on Non-Small-Cell Lung Cancer by Inhibiting CCND1. Jiang, DW; Liu, WY; Tang, YL; Wang, WH; Zhan, JM; Zhou, N, 2022)	1.69
"Bortezomib is a neurotoxic drug used in multiple myeloma and responsible for chemotherapy-induced peripheral neuropathy (CIPN). "	( Relation between auditory difficulties and bortezomib-induced peripheral neuropathy in multiple myeloma: a single-center cross-sectional study. Balayssac, D; Barreau, F; Bay, JO; Busserolles, J; Cabrespine, A; Chaleteix, C; Giraudet, F; Kerckhove, N; Lemal, R; Nguyen, D; Pereira, B; Selvy, M; Soubrier, M, 2022)	2.43
"Bortezomib (BTZ) is a traditional medicine for MM treatment, but there are limitations for current treatment methods."	( Trifluoperazine Synergistically Potentiates Bortezomib-Induced Anti-Cancer Effect in Multiple Myeloma via Inhibiting P38 MAPK/NUPR1. Chen, J; Chen, X; Chen, Y; Jing, Z; Li, A; Yu, W, 2022)	1.7
"Bortezomib is a frequently used chemotherapeutic agent in patients with multiple myeloma and care should be taken in terms of the risk of developing phrenic nerve palsy in patients. "	( Asymptomatic unilateral phrenic nerve palsy after bortezomib treatment in a newly diagnosed multiple myeloma patient. Coşkunpınar, M; Erdoğdu, B; Goker, H, 2023)	2.61
"Bortezomib (BTZ) is a promising drug used in CRC treatment; however, its main limitation result from drug resistance."	( TRIM59 guards ER proteostasis and prevents Bortezomib-mediated colorectal cancer (CRC) cells' killing. Chen, L; Feng, X; Shim, JS; Tao, S; Wu, Q; Yang, G; Zhang, L, 2022)	1.71
"Bortezomib (BTZ) is a proteasome inhibitor and may be explored for treating breast cancer."	( Chaurasiya, A; Gupta, U; Jain, S; Katke, S; Kuche, K; Kulkarni, O; Kumar, V; Mahale, A; Nakhate, KT; Rani, S; Sahoo, RK; Yadav, V, 2023)	1.63
"Bortezomib (BTZ) is a first-generation proteasome inhibitor with anti-tumor properties for multiple myeloma and mantle cell lymphoma. "	( Bortezomib induces cellular senescence in A549 lung cancer cells by stimulating telomere shortening. Huang, C; Huang, S; Liu, H; Wang, L; Yin, H; Zhang, Z, )	3.02
"Bortezomib (BTZ) is a proteasome inhibitor widely used in MM therapy whose potent activity is often hampered by the development of resistance."	( The Evidence That 25(OH)D3 and VK2 MK-7 Vitamins Influence the Proliferative Potential and Gene Expression Profiles of Multiple Myeloma Cells and the Development of Resistance to Bortezomib. Baumert, B; Kulig, P; Machaliński, B; Łuczkowska, K, 2022)	1.64
"Bortezomib (BTZ) is a selective and reversible proteasome inhibitor and first line treatment for multiple myeloma (MM). "	( Neurofilament light chain levels indicate acute axonal damage under bortezomib treatment. Cebulla, N; Einsele, H; Flamm, L; Gommersbach, S; Kortüm, KM; Reinhold, AK; Rittner, H; Rogalla von Bieberstein, B; Runau, E; Schirmer, D; Sommer, C; Stengel, H; Zeller, D; Zhou, X, 2023)	2.59
"Bortezomib (BTZ) is a proteasome inhibitor serves as a first-line drug for multiple myeloma treatment. "	( Lysosomal dysfunction in Schwann cells is involved in bortezomib-induced peripheral neurotoxicity. Li, X; Wang, H; Wang, K; Wu, J; Wu, Z; Xu, G; Yan, W; Yang, M; Zhang, X; Zhu, D, 2023)	2.6
"Bortezomib is an inhibitor of proteasomes and an anti-cancer drug. "	( In situ Electrochemical Evaluation of the Interaction of dsDNA with the Proteasome Inhibitor Anticancer Drug Bortezomib. Bunea, MC; Diculescu, VC; Enache, TA, 2023)	2.57
"Bortezomib (Bor) is a specific and reversible inhibitor of the chymotrypsin-like activity of the 20S core of the proteasome, currently approved for the treatment of multiple myeloma and mantle cell lymphoma."	( Antitumoral effects of Bortezomib in malignant mesothelioma: evidence of mild endoplasmic reticulum stress in vitro and activation of T cell response in vivo. Angiolini, V; Barillari, G; Bei, R; Benvenuto, M; Carrano, R; Cirone, M; Ferretti, E; Focaccetti, C; Mancini, P; Masuelli, L; Miele, MT; Mutti, L; Nardozi, D; Palumbo, C; Rufini, A; Tundo, GR, 2023)	1.94
"Bortezomib (bort) is an effective therapeutic agent for patients with multiple myeloma (MM); however, most patients develop drug resistance. "	( TRIM21 enhances bortezomib sensitivity in multiple myeloma by halting prosurvival autophagy. Cai, Z; Cao, W; Chen, J; Chen, Q; Guo, X; He, J; Huang, X; Li, A; Liu, Y; Qu, J; Yang, L; Yao, S; Ye, S; Zhang, E, 2023)	2.7
"Bortezomib is a proteasome inhibitor that acts synergistically and additively with standard chemotherapy for ALL."	( Phase 2 study of combination chemotherapy with bortezomib in children with relapsed and refractory acute lymphoblastic leukemia. Goto, H; Hara, J; Hiramatsu, H; Iijima-Yamashita, Y; Kikuta, A; Kosaka, Y; Miyagawa, N; Mochizuki, S; Nakayama, H; Ogawa, A; Ogawa, C; Sanada, M; Sekimizu, M; Tomizawa, D; Toyoda, H; Yoshimura, K, 2023)	1.89
"Bortezomib is a cornerstone in the management of multiple myeloma. "	( Resource implications of bortezomib therapy in a large UK cohort: An evaluation study. Djebbari, F; Kothari, J; Panitsas, F; Peniket, A; Ramasamy, K; Sultanova, M; Tatarczuch, M; Vallance, G, 2019)	2.26
"Bortezomib is a first proteasome inhibitor drug, widely used in MM treatment."	( XPO1 is a critical player for bortezomib resistance in multiple myeloma: A quantitative proteomic approach. Chanukuppa, V; Chatterjee, T; Kumar, S; Paul, D; Rapole, S; Santra, MK; Sharma, S; Taunk, K, 2019)	1.52
"Bortezomib (BTZ) is a proteasome inhibitor used for multiple myeloma and mantle cell lymphoma treatment. "	( Glycine-Poly-L-Lactic Acid Copolymeric Nanoparticles for the Efficient Delivery of Bortezomib. Chaudhari, D; Gupta, U; Jain, S; Rajoria, S; Rani, S, 2019)	2.18
"Bortezomib is a standard therapy in light-chain amyloidosis (AL), but little is known about response duration. "	( A prospective observational study of 915 patients with systemic AL amyloidosis treated with upfront bortezomib. Cohen, O; Foard, D; Fontana, M; Gillmore, JD; Hawkins, PN; Lachmann, HJ; Mahmood, S; Manwani, R; Quarta, C; Sachchithanantham, S; Sharpley, F; Wechalekar, AD; Whelan, C, 2019)	2.17
"Bortezomib (Btz) is a proteasome inhibitor approved by the FDA to treat multiple myeloma. "	( Targeting Bortezomib to Bone Increases Its Bone Anabolic Activity and Reduces Systemic Adverse Effects in Mice. Boeckman, RK; Boyce, BF; Ebetino, FH; Lin, X; Srinivasan, V; Sun, W; Tao, J; Wang, H; Wu, T; Xing, L; Zhang, H, 2020)	2.4
"Bortezomib (VELCADE®) is a boronate peptide and first-in-class proteasome inhibitor serving an important role in degenerating several intracellular proteins. "	( Enhancing the Therapeutic Efficacy of Bortezomib in Cancer Therapy Using Polymeric Nanostructures. Jaafari, MR; Johnston, TP; Korani, M; Korani, S; Nikpoor, AR; Orafai, HM; Sahebkar, A; Zendehdel, E, 2019)	2.23
"Bortezomib is a proteasome inhibitor with activity in pediatric acute lymphoblastic leukemia."	( Treatment of children with relapsed and refractory acute lymphoblastic leukemia with mitoxantrone, vincristine, pegaspargase, dexamethasone, and bortezomib. August, KJ; Gamis, AS; Guest, EM; Hays, JA; Lewing, K, 2020)	1.48
"Bortezomib is a selective and reversible inhibitor of the 26S proteasome, which is used to treat oncologic and rare autoimmune disorders in pediatric patients. "	( Bortezomib-Responsive Refractory Anti-N-Methyl-d-Aspartate Receptor Encephalitis. Buratti, S; Castagnola, E; Cordani, R; Fioredda, F; Franciotta, D; Gastaldi, M; Giacomini, T; Lanteri, P; Mancardi, MM; Micalizzi, C; Morana, G; Pirlo, D; Renna, S; Risso, M; Vari, MS, 2020)	3.44
"Bortezomib is a highly efficacious proteasome inhibitor widely used to treat multiple myeloma and light chain (AL) amyloidosis patients."	( Cytomegalovirus reactivation after bortezomib treatment for multiple myeloma and light chain amyloidosis. De-Silva, D; Garcia Mingo, A; Griffiths, PD; Hughes, D; Kyriakou, C; Mahmood, S; Mehta, A; Ramsay, I; Sachchithanantham, S; Sharpley, FA; Wechalekar, AD; Worthington, S, 2020)	1.56
"Bortezomib (BTZ) is an FDA approved proteasome inhibitor for the treatment of mantle cell lymphoma and multiple myeloma. "	( The Effect of Phase Transition Temperature on Therapeutic Efficacy of Liposomal Bortezomib. Attar, H; Ghaffari, S; Jaafari, MR; Korani, M; Mashreghi, M; Nikoofal-Sahlabadi, S; Nikpoor, AR, 2020)	2.23
"Bortezomib (Velcade®) is a reversible proteasome inhibitor that shows potent antineoplastic activity, by inhibiting the constitutively increased proteasome activity in myeloma cells, and is approved as a first-line therapy for multiple myeloma (MM). "	( Population-based meta-analysis of bortezomib exposure-response relationships in multiple myeloma patients. Mager, DE; Zhang, L, 2020)	2.28
"Bortezomib is an anti-tumor agent, which inhibits 26S proteasome degrading ubiquitinated proteins. "	( Molecular Mechanisms of Bortezomib Action: Novel Evidence for the miRNA-mRNA Interaction Involvement. Machaliński, B; Paczkowska, E; Rogińska, D; Schmidt, CA; Ulańczyk, Z; Łuczkowska, K, 2020)	2.31
"Bortezomib (BTZ) is a Proteasome Inhibitor (PI) that is used for the treatment of a variety of cancers."	( Utilization of Lipid-based Nanoparticles to Improve the Therapeutic Benefits of Bortezomib. Jaafari, MR; Korani, M; Korani, S; Sahebkar, A; Sathyapalan, T; Zendehdel, E, 2020)	1.51
"Bortezomib is a proteasome inhibitor used in the treatment of multiple myeloma, Waldenström's macroglobulinemia, mantle cell lymphoma. "	( Bortezomib-induced motor neuropathy: A case report. Mulay, S; Singh, M; Thomas, VM, 2020)	3.44
"Bortezomib (BTZ) is a proteasome inhibitor as approved by US FDA for the treatment of multiple myeloma. "	( Biotinylated HPMA centered polymeric nanoparticles for Bortezomib delivery. Gupta, U; Nakhate, KT; Rani, S; Sahoo, RK, 2020)	2.25
"Bortezomib is a boronic acid-based potent proteasome inhibitor that has been actively studied for its anti-tumour effects through inhibition of the proteasome."	( Inhibition of PLK4 might enhance the anti-tumour effect of bortezomib on glioblastoma via PTEN/PI3K/AKT/mTOR signalling pathway. Cheng, R; Ji, H; Jia, G; Ma, J; Ren, D; Ren, J; Sun, Y; Tu, Y; Wang, C; Wang, J; Wang, L; Xu, C, 2020)	1.52
"Bortezomib is a reversible proteasome inhibitor affects the ubiquitin-proteasome mechanism to kill cancer cells, and inhibition of the proteasome modulates the expression of multiple target genes at the transcriptional level. "	( Regulation of Fas in response to bortezomib and epirubicin in colorectal cancer cells. Cacan, E; Ozmen, ZC, 2020)	2.28
"Bortezomib is a reversible inhibitor of proteasome proteins in mammalian cells. "	( Bortezomib - First Therapeutic Proteasome Inhibitor for Cancer Therapy: A Review of Patent Literature. Dharamsi, A; Patel, R; Vora, PA, 2020)	3.44
"Bortezomib is a potent 20S proteasome inhibitor approved for the treatment of multiple myeloma and mantle cell lymphoma. "	( A Translational Physiologically Based Pharmacokinetics/Pharmacodynamics Framework of Target-Mediated Disposition, Target Inhibition and Drug-Drug Interactions of Bortezomib. Hanley, M; Iwasaki, S; Venkatakrishnan, K; Xia, C; Zhu, A, 2020)	2.2
"Bortezomib (BOZ) is a proteasome inhibitor chemotherapeutic agent utilized to treat multiple myeloma and recently offered to cure melanoma. "	( Alpha-lipoic acid alters the antitumor effect of bortezomib in melanoma cells in vitro. Istenes, I; Kőhidai, L; Lajkó, E; Láng, O; Takács, A, 2020)	2.26
"Bortezomib (BTZ) is a proteasome inhibitor approved for the treatment of multiple myeloma and mantle cell lymphoma."	( Bortezomib-loaded lipidic-nano drug delivery systems; formulation, therapeutic efficacy, and pharmacokinetics. Löbenberg, R; Mahmoudian, M; Valizadeh, H; Zakeri-Milani, P, 2021)	2.79
"Bortezomib is a common multiple myeloma therapy that can cause treatment-related peripheral neuropathy, a risk factor for falls. "	( Bortezomib in first-line therapy is associated with falls in older adults with multiple myeloma. Fiala, MA; Schoenbeck, KL; Wildes, TM, 2021)	3.51
"Bortezomib (BT) is a reversible inhibitor of proteasome which is used in the treatment of hematological cancers. "	( Separation, identification and characterization of stress degradation products of bortezomib using HPLC and LC-MS. Narayana Rao, K; Purushotham Reddy, C; Ramakrishna, K, 2021)	2.29
"Bortezomib is a classical proteasome inhibitor and previous researches have reported its roles of anti-oxidation and anti-inflammatory functions in various diseases. "	( Bortezomib alleviates myocardial ischemia reperfusion injury via enhancing of Nrf2/HO-1 signaling pathway. He, S; Li, D; Lin, J; Liu, C; Liu, S; Wang, B; Yang, W; Zheng, Y; Zhou, J, 2021)	3.51
"Bortezomib is a proteasome inhibitor that has a promising role in autoimmune conditions."	( Bortezomib in anti-N-Methyl-d-Aspartate-Receptor (NMDA-R) encephalitis: A systematic review. Bratina, A; Cheli, M; Dinoto, A; Manganotti, P; Sartori, A, 2021)	2.79
"Bortezomib is a first-line chemotherapeutic drug widely used for multiple myeloma and other nonsolid malignancies. "	( Activation of RAGE/STAT3 pathway by methylglyoxal contributes to spinal central sensitization and persistent pain induced by bortezomib. Ding, HH; Lei, WL; Liu, CC; Liu, M; Ma, C; Ouyang, HD; Wei, JY; Wu, SL; Xie, MX; Xin, WJ, 2017)	2.1
"Bortezomib (Bz) is a proteasome inhibitor that directly targets antibody-producing plasma cells. "	( Bortezomib treatment induces a higher mortality rate in lupus model mice with a higher disease activity. Fujii, H; Harigae, H; Ikeda, T; Ishii, T; Kamogawa, Y; Nose, M; Shirai, T; Shirota, Y, 2017)	3.34
"Bortezomib (BZM) is a proteasome inhibitor used for the treatment of multiple myeloma (MM)."	( The proteasome inhibitor bortezomib attenuates renal fibrosis in mice via the suppression of TGF-β1. Chiga, M; Isobe, K; Mandai, S; Mori, T; Nomura, N; Rai, T; Sohara, E; Uchida, S; Yui, N; Zeniya, M, 2017)	1.48
"Bortezomib is a landmark drug in the therapeutic history of multiple myeloma as the first-generation proteasome inhibitor. "	( Bortezomib-induced syndrome of inappropriate antidiuresis in a patient with multiple myeloma: A case report and literature review . Chen, H; Lou, X; Peng, B, 2017)	3.34
"Bortezomib is a chemotherapeutic agent used to treat several cancers; however, it exhibits severe side effects in testicular tissue. "	( Protective effects of agomelatine on testicular damage caused by bortezomib. Akaras, N; Atilay, H; Bal, T; Halici, MB; Selli, J, 2017)	2.14
"Bortezomib, which is a potent proteasome inhibitor, has been used as a first-line drugs to treat multiple myeloma for a few decades, and radiotherapy has frequently been applied to manage acute bone lesions in the patients. "	( The combination of ionizing radiation and proteasomal inhibition by bortezomib enhances the expression of NKG2D ligands in multiple myeloma cells. Bae, J; Heo, W; Jeung, YH; Lee, YS; Nam, J, 2018)	2.16
"Bortezomib (Btz) is an active agent used to treat multiple myeloma (MM). "	( Low expression of neural cell adhesion molecule, CD56, is associated with low efficacy of bortezomib plus dexamethasone therapy in multiple myeloma. Ashour, R; Iida, S; Ishida, T; Ito, A; Kinoshita, S; Komatsu, H; Kusumoto, S; Narita, T; Ri, M; Totani, H; Yoshida, T, 2018)	2.14
"Bortezomib is a first-in-class proteasome inhibitor approved for the treatment of multiple myeloma and mantle cell lymphoma after one prior therapy."	( Clinical Pharmacokinetics and Pharmacodynamics of Bortezomib. Abdul-Majeed, S; Barta, SK; Cael, B; Tan, CRC, 2019)	1.49
"Bortezomib (BORT) is an anti-tumour agent that inhibits proteasome, which is responsible for the degradation of many intracellular proteins. "	( The protective effect of the proteasome inhibitor bortezomib on the uterus of ovariectomized rats. Bozkurt, M; Buyuk, B; Can, I; Can, S; Inaloz, SS; Karakas, B; Karamese, SA, )	1.83
"Bortezomib is a mainstay of therapy for multiple myeloma, frequently complicated by painful neuropathy. "	( Clinical, electrophysiological, and cutaneous innervation changes in patients with bortezomib-induced peripheral neuropathy reveal insight into mechanisms of neuropathic pain. Bechakra, M; de Zeeuw, CI; Groeneveld, GJ; Jongen, JL; Nieuwenhoff, MD; Scheltens-de Boer, M; Sonneveld, P; van Doorn, PA; van Rosmalen, J, )	1.8
"Bortezomib is a relatively new drug and there are only a few reports with respect to its psychiatric side effects."	( [Mania Associated with the Use of Bortezomib and Dexamethasone]. Coşar, B; Geniş, B, 2018)	1.48
"Bortezomib (BTZ) is an approved anticancer drug, classified as a selective reversible inhibitor of the ubiquitin-dependent proteasome system, that leads to cancer cell cycle arrest and apoptosis reducing the invasion ability of Osteosarcoma cells in vitro."	( Bortezomib and endocannabinoid/endovanilloid system: a synergism in osteosarcoma. Argenziano, M; Casale, F; Di Paola, A; Di Pinto, D; Pota, E; Punzo, F; Rossi, F; Tortora, C, 2018)	2.64
"Bortezomib is a frequently used chemotherapeutic drug for the treatment of multiple myeloma and other nonsolid malignancies. "	( Reduction of SIRT1 epigenetically upregulates NALP1 expression and contributes to neuropathic pain induced by chemotherapeutic drug bortezomib. Chen, K; Fan, J; Liu, CC; Luo, ZF; Xin, WJ; Yang, Y, 2018)	2.13
"Bortezomib is a boronate proteasome inhibitor widely used as an efficient anticancer drug; however, the clinical use of bortezomib is hampered by its adverse effects such as hematotoxicity and peripheral neuropathy, and low efficacy on solid tumors due to unfavorable pharmacokinetics and poor penetration in the solid tumors. "	( A Targeted and pH-Responsive Bortezomib Nanomedicine in the Treatment of Metastatic Bone Tumors. Cai, X; Li, L; Tong, L; Wang, C; Wang, M; Xiao, J; Yang, J, 2018)	2.21
"Bortezomib is a proteasome inhibitor that shows both anticancer and bone anabolic properties and is being evaluated for its positive effects in MM patients with skeletal complications."	( Systems Modeling of Bortezomib and Dexamethasone Combinatorial Effects on Bone Homeostasis in Multiple Myeloma Patients. Mager, DE; Zhang, L, 2019)	1.56
"Bortezomib is a dipeptidyl boronic acid that selectively inhibits the ubiquitin proteasome pathway, which plays a role in the degradation of many intracellular proteins. "	( Bortezomib for the Treatment of Hematologic Malignancies: 15 Years Later. Robak, P; Robak, T, 2019)	3.4
"Bortezomib is a selective and reversible proteasome inhibitor used for the treatment of patients with multiple myeloma (MM)."	( Acute pancreatitis caused by bortezomib. Akin, E; Akyol, P; Atalay, R; Buyukasik, NS; Demirezer Bolat, A; Dilek, I; Ersoy, O; Guney, T; Koseoglu, H; Solakoglu, T, )	1.14
"Bortezomib is an important agent in multiple myeloma treatment, but resistance in cell lines and patients has been described. "	( The interaction of bortezomib with multidrug transporters: implications for therapeutic applications in advanced multiple myeloma and other neoplasias. Anderson, K; Clynes, M; Delmore, J; Jakubikova, J; Klippel, S; Meiller, J; Mitsiades, CS; O'Connor, R; O'Gorman, P; Ooi, MG; Richardson, P, 2013)	2.16
"Bortezomib is a proteasome inhibitor active in classical Hodgkin lymphoma (cHL) cell lines, but poorly active in the clinic when used as a single agent, suggesting that the microenvironment could protect from drug efficacy. "	( Bortezomib down-modulates the survival factor interferon regulatory factor 4 in Hodgkin lymphoma cell lines and decreases the protective activity of Hodgkin lymphoma-associated fibroblasts. Aldinucci, D; Borghese, C; Carbone, A; Casagrande, N; Celegato, M; Colombatti, A, 2014)	3.29
"Bortezomib is a highly selective and reversible inhibitor of the 26S proteasome. "	( Effect of bortezomib in combination with cisplatin and 5‑fluorouracil on 4T1 breast cancer cells. Altıkat, S; Boyaci, I; Cavga, FZ; Irmak, R; Kocacan, SA; Yerlikaya, A, 2013)	2.23
"Bortezomib is a proteasome inhibitor commonly indicated for the treatment of multiple myeloma and non Hodgkin lymphoma. "	( Bortezomib and heart failure: case-report and review of the French Pharmacovigilance database. Carrie, D; Despas, F; Dumonteil, N; Galinier, M; Honton, B; Montastruc, JL; Pathak, A; Roussel, M; Rouvellat, C, 2014)	3.29
"Bortezomib is a proteasome inhibitor with high efficacy for multiple myeloma but with severe peripheral neurotoxicity, leading to dose modification and severe neurological disability. "	( Bortezomib-induced neuropathy: axonal membrane depolarization precedes development of neuropathy. Beppu, M; Fujimaki, Y; Isose, S; Iwai, Y; Kuwabara, S; Misawa, S; Mitsuma, S; Nakaseko, C; Nasu, S; Ohmori, S; Ohwada, C; Sekiguchi, Y; Shibuya, K; Shimizu, N; Takeda, Y, 2014)	3.29
"Bortezomib is a reversible proteasome inhibitor used as an anticancer drug. "	( Proteasome inhibition induces DNA damage and reorganizes nuclear architecture and protein synthesis machinery in sensory ganglion neurons. Berciano, MT; Casafont, I; Lafarga, M; Palanca, A, 2014)	1.85
"Bortezomib is a first-in-class proteasome inhibitor approved by the US Food and Drug Administration for the treatment of all phases of multiple myeloma (MM) and it is also used for the treatment of [corrected] light-chain amyloidosis (AL). "	( Bortezomib subcutaneous injection in combination regimens for myeloma or systemic light-chain amyloidosis: a retrospective chart review of response rates and toxicity in newly diagnosed patients. Comenzo, R; Cossor, F; Fallo, S; Kaul, E; Klein, A; Miller, K; Shah, G; Smith, H; Sprague, K, 2013)	3.28
"Bortezomib is a proteasome inhibitor used for the treatment of relapsed/refractory multiple myeloma (MM). "	( Combination treatment with 2-methoxyestradiol overcomes bortezomib resistance of multiple myeloma cells. Han, J; Heo, HJ; Jeong, SH; Jeong, YJ; Kim, HK; Kim, N; Ko, KS; Ko, TH; Lee, SR; Rhee, BD; Song, IS; Youm, JB, 2013)	2.08
"Bortezomib is an important agent for the treatment of patients with multiple myeloma and has recently been reported as efficacious in the treatment of patients with POEMS syndrome."	( Successful treatment of POEMS syndrome with bortezomib and dexamethasone, combined with radiotherapy, and followed by autologous stem cell transplantation. Hagihara, M; Hattori, Y; Ishigatsubo, Y; Ishii, Y; Ishiyama, Y; Tomita, N; Yamamoto, E; Yamazaki, E, 2013)	1.37
"Bortezomib is a proteasome inhibitor used as an antineoplastic drug, although its neurotoxicity frequently causes a severe sensory peripheral neuropathy."	( Reactive nucleolar and Cajal body responses to proteasome inhibition in sensory ganglion neurons. Berciano, MT; Casafont, I; Lafarga, M; Palanca, A, 2014)	1.12
"Bortezomib is an anti-neoplastic drug acting against multiple myeloma but its use is associated with the onset of painful peripheral neuropathy. "	( Antibody against tumor necrosis factor-α reduces bortezomib-induced allodynia in a rat model. Canta, A; Carozzi, V; Cavaletti, G; Chiorazzi, A; Meregalli, C; Monbaliu, J; Oggioni, N; Sala, B; VAN DE Velde, H, 2013)	2.09
"Bortezomib is a proteasome inhibitor with remarkable clinical antitumor activity in multiple myeloma (MM) and is under evaluation in clinical trials in various types of cancer including breast cancer. "	( IKKβ inhibitor in combination with bortezomib induces cytotoxicity in breast cancer cells. Anderson, KC; Hide, M; Hideshima, H; Hideshima, T; Ikeda, H; Iwasaki, A; Yoshida, Y, 2014)	2.12
"Bortezomib (BTZ) is a frequently used chemotherapeutic drug for the treatment of refractory multiple myeloma and hematological neoplasms. "	( TNF-α-mediated JNK activation in the dorsal root ganglion neurons contributes to Bortezomib-induced peripheral neuropathy. Cui, Y; Huang, ZZ; Li, D; Liu, XG; Pang, RP; Su, YM; Wei, JY; Xin, WJ; Xue, Z; Zhang, J, 2014)	2.07
"Bortezomib is a novel proteasome inhibitor that has promising antitumor activity against various cancer cells. "	( Inhibition of autophagy by autophagic inhibitors enhances apoptosis induced by bortezomib in non-small cell lung cancer cells. Ji, Z; Jiang, X; Lei, Y; Li, H; Sun, M; Wu, G, 2014)	2.07
"Bortezomib is a proteasome inhibitor currently studied in clinical trials of childhood cancers. "	( Protective role of humanin on bortezomib-induced bone growth impairment in anticancer treatment. Eksborg, S; Eriksson, E; Johnsen, JI; Kogner, P; Perup, LS; Sävendahl, L; Wickström, M, 2014)	2.13
"Bortezomib (BZB) is a chemotherapeutic agent approved for treating multiple myeloma (MM) patients. "	( Bortezomib enhances the osteogenic differentiation capacity of human mesenchymal stromal cells derived from bone marrow and placental tissues. Issaragrisil, S; Kheolamai, P; Klincumhom, N; Manochantr, S; Sanvoranart, T; Supokawej, A; U-Pratya, Y; Wattanapanitch, M, 2014)	3.29
"Bortezomib is a potent proteasome inhibitor that has been extensively used to treat multiple myeloma. "	( Bortezomib induces thrombocytopenia by the inhibition of proplatelet formation of megakaryocytes. Fujishima, Y; Ishida, Y; Ito, S; Kowata, S; Murai, K; Shimoyama, T; Yashima-Abo, A, 2014)	3.29
"Bortezomib is an FDA-approved proteasome inhibitor, and oncolytic herpes simplex virus-1 (oHSV) is a promising therapeutic approach for cancer. "	( Bortezomib-induced unfolded protein response increases oncolytic HSV-1 replication resulting in synergistic antitumor effects. Bailey, Z; Bolyard, C; Caligiuri, MA; Cripe, TP; Eaves, D; He, S; Hurwitz, BS; Kaur, B; Old, M; Parris, DS; Rath, KS; Selvendiran, K; Yoo, JY; Yu, J; Yu, JG; Zhang, J, 2014)	3.29
"Bortezomib is an active agent in AL amyloidosis and responses to this drug in combination with cyclophosphamide and dexamethasone are both rapid and deep. "	( Efficacy of bortezomib, cyclophosphamide and dexamethasone in treatment-naïve patients with high-risk cardiac AL amyloidosis (Mayo Clinic stage III). Bridoux, F; Comenzo, RL; Decaux, O; Gillmore, J; Hari, P; Hawkins, PN; Jaccard, A; Lavergne, D; Lazaro, E; Macro, M; Mercie, P; Mohty, D; Morel, P; Pellegrin, JL; Roussel, M; Venner, CP; Wechalekar, AD, 2014)	2.22
"Bortezomib is a chemotherapeutic agent that acts via proteasome inhibition resulting in cellular apoptosis and inhibition of angiogenesis. "	( Posterior reversible encephalopathy syndrome resulting from repeat bortezomib usage. Nixon, NA; Parhar, K, 2014)	2.08
"Bortezomib is a proteasome inhibitor that has shown important clinical efficacy either as a single agent or in combination in patients with multiple myeloma (MM). "	( Bendamustine and prednisone in combination with bortezomib (BPV) in the treatment of patients with newly diagnosed/untreated multiple myeloma. Andrea, M; Becker, C; Behre, G; Bourgeois, M; Edelmann, T; Gutsche, K; Hammerschmidt, D; Hennig, E; Heyn, S; Hoffmann, FA; Holzvogt, B; Kaiser, T; Krahl, R; Kreibich, U; Lindner, T; Niederwieser, D; Plötze, M; Pönisch, W; Reifenrath, K; Remane, Y; Schliwa, T; Schwarz, M; Schwarzer, A; Vucinic, V; Winkelmann, C; Zehrfeld, T, 2014)	2.1
"Bortezomib is a first generation proteasome inhibitor that is the frontline chemotherapy for multiple myeloma with the chief dose-limiting side effect of painful peripheral neuropathy. "	( Altered discharges of spinal neurons parallel the behavioral phenotype shown by rats with bortezomib related chemotherapy induced peripheral neuropathy. Dougherty, PM; Robinson, CR; Zhang, H, 2014)	2.07
"Bortezomib is a potent inhibitor of proteasomes currently used to eliminate malignant plasma cells in multiple myeloma patients. "	( Proteasome inhibition with bortezomib depletes plasma cells and specific autoantibody production in primary thymic cell cultures from early-onset myasthenia gravis patients. Buurman, WA; De Baets, MH; Duimel, H; Gomez, AM; Hummel, J; Losen, M; Martinez-Martinez, P; Molenaar, PC; Nogales-Gadea, G; Saxena, A; Verheyen, F; Vrolix, K; Willcox, N, 2014)	2.14
"Bortezomib is a proteasome inhibitor approved by the FDA for treatment of multiple myeloma and mantel cell lymphoma."	( Bortezomib prevents the expression of MMP-13 and the degradation of collagen type 2 in human chondrocytes. Chen, A; Guo, F; Hu, W; Li, F; Zhang, W, 2014)	2.57
"Bortezomib (Velcade) is a potent and reversible PI that has been used successfully in the treatment of patients with MM."	( Current advances in novel proteasome inhibitor-based approaches to the treatment of relapsed/refractory multiple myeloma. Boise, LH; Lonial, S, 2011)	1.09
"Bortezomib is an U.S."	( Bortezomib reduces pre-existing antibodies to recombinant immunotoxins in mice. Manning, ML; Mason-Osann, E; Onda, M; Pastan, I, 2015)	2.58
"Bortezomib is a proteasome inhibitor used for hematologic cancer treatment. "	( Proteasome inhibitor bortezomib suppresses nuclear factor-kappa B activation and ameliorates eye inflammation in experimental autoimmune uveitis. Chen, SH; Hsu, SM; Lin, CJ; Shen, FH; Shieh, CC; Yang, CH, 2015)	2.18
"Bortezomib is a proteasome inhibitor which has demonstrated activity against recurrent or newly diagnosed multiple myeloma (MM) and mantle cell lymphoma. "	( Meta-analysis of incidence and risk of peripheral neuropathy associated with intravenous bortezomib. Peng, L; Ye, X; Zhang, J; Zhao, Q; Zhou, Y, 2015)	2.08
"Bortezomib is a selective inhibitor of the proteosoma that is used in multiple myeloma. "	( [Retrospective study comparing low-dose versus standard dose of bortezomib in patients with multiple myeloma]. Befferman Cordova, N; Espinoza Zelada, M; Galleguillos M, M; Ocqueteau Tachini, M; Ramírez Villanueva, P; Sarmiento Maldonado, M, 2015)	2.1
"Bortezomib is a proteasome inhibitor that is largely employed as a first-line treatment for multiple myeloma."	( Bortezomib in type I cryoglobulinemic vasculitis: are we acting too late? Campochiaro, C; D'Aliberti, T; Marcatti, M; Pagliula, G; Praderio, L; Ramirez, GA; Salmaggi, C; Tresoldi, M, 2015)	2.58
"Bortezomib is a proteasome inhibitor that is frequently used for multiple myeloma and lymphoma. "	( Bortezomib-associated demyelinating neuropathy--clinical and pathologic features. Brannagan, TH; De Sousa, EA; Tanji, K; Thawani, SP; Weimer, LH, 2015)	3.3
"Bortezomib (Velcade(®)) is a proteasome inhibitor that is approved for the treatment of multiple myeloma and mantle cell lymphoma (MCL). "	( Bortezomib: A Review in Mantle Cell Lymphoma in Previously Untreated Patients Unsuitable for Stem-Cell Transplantation. McCormack, PL, 2015)	3.3
"Bortezomib is a commonly used first-line agent in MM treatment; however, knowledge of the signal transduction pathways regulating bortezomib-mediated cell cytotoxicity is incomplete."	( Logic-Based and Cellular Pharmacodynamic Modeling of Bortezomib Responses in U266 Human Myeloma Cells. Abernethy, DR; Chudasama, VL; Mager, DE; Ovacik, MA, 2015)	1.39
"Bortezomib is an inhibitor of the ubiquitin-proteasome proteolytic pathway responsible for intracellular protein turnover. "	( Modulatory effects of bortezomib on host immune cell functions. Dudimah, DF; Pellom, ST; Sayers, TJ; Shanker, A; Thounaojam, MC, 2015)	2.17
"Bortezomib is a reversible proteasome inhibitor with potent antineoplastic activity that exhibits dose- and time-dependent pharmacokinetics (PK). "	( Physiologically-based pharmacokinetic modeling of target-mediated drug disposition of bortezomib in mice. Mager, DE; Zhang, L, 2015)	2.08
"Bortezomib is a proteasome inhibitor that can eliminate plasma cells and has demonstrated utility in the treatment of ABMR."	( Bortezomib for refractory acute antibody-mediated rejection in kidney transplant recipients: A single-centre case series. Campistol, JM; Cid, J; Cofan, F; De Sousa-Amorim, E; Diekmann, F; Lozano, M; Oppenheimer, F; Palou, E; Revuelta, I; Sole, M, 2016)	2.6
"Bortezomib appears to be a promising early desensitizing agent in the world of kidney transplantation and high short-term success rates have been observed. "	( Bortezomib in kidney transplantation. Meouchy, J; Qazi, Y; Shah, N, 2015)	3.3
"Bortezomib (BTZ) is a frequently used chemotherapeutic drug for the treatment of refractory multiple myeloma and hematological neoplasms. "	( Upregulation of CCL2 via ATF3/c-Jun interaction mediated the Bortezomib-induced peripheral neuropathy. Huang, Z; Liu, C; Luan, S; Ma, C; OuYang, H; Wei, J; Wu, S; Xin, W, 2016)	2.12
"Bortezomib is a novel proteasome inhibitor in myeloma. "	( Bortezomib in newly diagnosed patients with multiple myeloma: A retrospective analysis from a tertiary care center in India. Digumarti, R; Gundeti, S; Linga, VG; Pragnya, C; Thota, NK, )	3.02
"Bortezomib is a selective reversible proteasome inhibitor with proapoptotic effects. "	( A phase II, open-label trial of bortezomib (VELCADE(®)) in combination with gemcitabine and cisplatin in patients with locally advanced or metastatic non-small cell lung cancer. Agelaki, S; Filippa, G; Georgoulias, V; Kentepozidis, N; Kontopodis, E; Kotsakis, A; Mala, A; Mavroudis, D; Moutsos, M; Syrigos, K; Vamvakas, L; Ziras, N, 2016)	2.16
"Bortezomib is an anti-cancer agent that induces ER stress by inhibiting proteasomal degradation. "	( Bortezomib attenuates palmitic acid-induced ER stress, inflammation and insulin resistance in myotubes via AMPK dependent mechanism. Bae, YA; Cheon, HG; Choi, HE; Jang, J; Kwak, HJ; Park, SK, 2016)	3.32
"Bortezomib is a safe and well-tolerated therapy for patients with AL amyloidosis with a rapid hematologic response and cardiac response, as assessed by the NT-proBNP level."	( Bortezomib-Containing Regimens for the Treatment of Newly Diagnosed and Relapsed Amyloid Light Chain Amyloidosis: A Single-Center Experience. Bahlis, NJ; Duggan, P; Jimenez-Zepeda, VH; Neri, P, 2016)	3.32
"Bortezomib is a proteasome inhibitor with a remarkable antitumor activity, used in the clinic as first line treatment for multiple myeloma. "	( Inhibition of the neuronal NFκB pathway attenuates bortezomib-induced neuropathy in a mouse model. Alé, A; Bruna, J; Calls, A; Haralambous, S; Karamita, M; Navarro, X; Probert, L; Udina, E, 2016)	2.13
"Bortezomib is a powerful proteasome inhibitor used in the treatment of hematological malignancies."	( The combined effects of proteasome inhibitor bortezomib with topoisomerase I and II inhibitors on topoisomerase enzymes. Kerimoğlu, B; Öksüzoğlu, E; Tırınoğlu, Ç, 2016)	1.42
"Bortezomib is a modified dipeptidyl boronic acid that disrupts essential intracellular pathways by inhibiting proteasomes. "	( Bortezomib: a novel chemotherapeutic agent for hematologic malignancies. Kolesar, J; Utecht, KN, 2008)	3.23
"Bortezomib is a boron-containing molecule, which reversibly inhibits the proteasome, an intracellular organelle, which is central to the breakdown of ubiquitinated proteins and consequently crucial for normal cellular homeostasis."	( Acute severe cardiac failure in a myeloma patient due to proteasome inhibitor bortezomib. Gonullu, E; Hacihanefioglu, A; Tarkun, P, 2008)	1.3
"Bortezomib is a first-in-class proteasome inhibitor with remarkable antitumor activity that is approved for the treatment of patients with multiple myeloma. "	( Features and risk factors of peripheral neuropathy during treatment with bortezomib for advanced multiple myeloma. Auran-Schleinitz, T; Blaise, D; Bouabdallah, R; Coso, D; de Collela, JM; de Lavallade, H; El-Cheikh, J; Gastaut, JA; Mohty, M; Stoppa, AM, 2008)	2.02
"Bortezomib is a proteasome inhibitor whose anticancer action is partly mediated through inhibition of NF-kappaB."	( Dynamic effect of bortezomib on nuclear factor-kappaB activity and gene expression in tumor cells. Bagain, L; Chen, Z; Hager, GL; Karpova, T; McNally, JG; Silvin, C; Sung, MH; Van Waes, C; Voss, TC; Yang, X, 2008)	1.4
"Bortezomib proved to be a more potent inductor of apoptosis than gefitinib and alkylating agents."	( Cytotoxic and apoptotic effects of bortezomib and gefitinib compared to alkylating agents on human glioblastoma cells. Cambar, J; De Giorgi, F; Ichas, F; L'Azou, B; Passagne, I; Pédeboscq, S; Pometan, JP, 2008)	1.34
"Bortezomib is an inhibitor of proteasome, a multicatalytic enzyme complex that degrades several intracellular proteins."	( An EORTC phase I study of Bortezomib in combination with oxaliplatin, leucovorin and 5-fluorouracil in patients with advanced colorectal cancer. Anthoney, A; Bauer, J; Caponigro, F; Govaerts, AS; Lacombe, D; Marréaud, S; Milano, A; Twelves, C, 2009)	1.37
"Bortezomib is a new chemotherapeutic drug available for the treatment of lymphoid disorders, including multiple myeloma. "	( Immune-mediated neuropathies in myeloma patients treated with bortezomib. Alfonsi, E; Corso, A; Costa, A; Lazzarino, M; Lozza, A; Mangiacavalli, S; Moglia, A; Piccolo, G; Ravaglia, S; Varettoni, M; Zappasodi, P, 2008)	2.03
"Bortezomib is a proteasome inhibitor that has shown activity in vitro and in vivo in prostate cancer. "	( Bortezomib-mediated inhibition of steroid receptor coactivator-3 degradation leads to activated Akt. Ayala, G; Ding, Y; Frolov, A; Harper, JW; Hayes, TG; Ittmann, MM; Kadmon, D; Li, R; Lynch, RG; MacDonnell, V; Miles, BJ; Mims, MP; Thompson, TC; Tsai, MJ; Wheeler, TM; Yan, J, 2008)	3.23
"Bortezomib is a small-molecule proteasome inhibitor with single-agent activity in patients with non-small cell lung carcinoma (NSCLC) and synergy with gemcitabine in preclinical studies. "	( Bortezomib plus gemcitabine/carboplatin as first-line treatment of advanced non-small cell lung cancer: a phase II Southwest Oncology Group Study (S0339). Albain, KS; Chansky, K; Crowley, J; Davies, AM; Gandara, DR; Gumerlock, PH; Lara, PN; Vogel, SJ, 2009)	3.24
"Bortezomib is a first in class proteosomal inhibitor, that is Food and Drug Administration approved, for the treatment of plasma cell-derived tumors that is multiple myeloma."	( Bortezomib provides effective therapy for antibody- and cell-mediated acute rejection. Alloway, RR; Arend, LJ; Brailey, P; Cardi, M; Everly, JJ; Everly, MJ; Govil, A; Mogilishetty, G; Rike, AH; Roy-Chaudhury, P; Susskind, B; Tevar, A; Wadih, G; Woodle, ES, 2008)	2.51
"Bortezomib (BZM) is a proteasome inhibitor in clinical use for multiple myeloma."	( Green tea polyphenols block the anticancer effects of bortezomib and other boronic acid-based proteasome inhibitors. Cadenas, E; Chen, TC; Gaffney, KJ; Golden, EB; Kardosh, A; Lam, PY; Louie, SG; Petasis, NA; Schönthal, AH, 2009)	1.32
"Bortezomib is a selective and potent inhibitor of the proteasome and has prominent effects in vitro and in vivo against tumors. "	( Proteasome inhibition induces apoptosis in primary human natural killer cells and suppresses NKp46-mediated cytotoxicity. Fadeel, B; Feng, X; Henter, JI; Ji, C; Nordenskjöld, M; Ottosson, A; Wang, X; Zheng, C, 2009)	1.8
"Bortezomib is a new and effective agent for refractory/relapsed multiple myeloma."	( [Development of an extramedullary plasmacytoma despite disappearing M protein in multiple myeloma by bortezomib treatment]. Handa, H; Karasawa, M; Koiso, H; Mawatari, M; Murakami, H; Nojima, Y; Osaki, Y; Saitoh, T; Sekigami, T; Tahara, K; Tsukamoto, N; Uchiumi, H; Yokohama, A, 2009)	1.29
"Bortezomib proved to be a rapid (<24 hour) and potent inhibitor of the release of several NFkappaB-inducible cytokines (including TNF-alpha, IL-1Beta, IL-6 and IL-10) by activated T-cells from healthy volunteers and RA patients, regardless of their clinical responsiveness to methotrexate. "	( The proteasome inhibitor bortezomib inhibits the release of NFkappaB-inducible cytokines and induces apoptosis of activated T cells from rheumatoid arthritis patients. Dijkmans, BA; Jansen, G; Lems, WF; Oerlemans, R; Scheper, RJ; van der Heijden, JW, )	1.88
"Bortezomib is a proteasome inhibitor that induces apoptosis in primary Waldenström's macroglobulinemia (WM) cells and WM cell lines. "	( Bortezomib in relapsed or refractory Waldenström's macroglobulinemia. Chen, C; Eisenhauer, E; Kouroukis, CT; Powers, J; Stadtmauer, E; Stewart, AK; Voralia, M; Walsh, W; White, D; Wright, JJ, 2009)	3.24
"Bortezomib is a proteasome inhibitor that can synergize with interferon-alpha (IFN-alpha) to induce apoptosis in melanoma cells in vitro and inhibit tumor growth in vivo. "	( Bortezomib pre-treatment prolongs interferon-alpha-induced STAT1 phosphorylation in melanoma cells. Benninger, K; Carson, WE; Kreiner, M; Lesinski, GB; Quimper, M; Young, G, 2009)	3.24
"Bortezomib is a selective and potent inhibitor of the 26S proteasome and is approved for the treatment of multiple myeloma."	( The role of ATF4 stabilization and autophagy in resistance of breast cancer cells treated with Bortezomib. Bottini, A; Generali, D; Harris, AL; Mellor, HR; Milani, M; Pike, L; Rzymski, T, 2009)	1.29
"Bortezomib is a proteasome inhibitor with remarkable preclinical and clinical antitumor activity in multiple myeloma (MM) patients. "	( Bortezomib induces canonical nuclear factor-kappaB activation in multiple myeloma cells. Anderson, KC; Carrasco, RD; Chauhan, D; Hideshima, T; Ikeda, H; Mitsiades, C; Munshi, NC; Okawa, Y; Podar, K; Raje, N; Richardson, PG, 2009)	3.24
"Bortezomib (VELCADE) is a proteasome inhibitor that not only targets the myeloma cell, but also acts in the bone marrow micro-environment, inhibiting the binding of myeloma cells to bone marrow stromal cells, as well as demonstrating anabolic effects on bone. "	( Bortezomib: a review of its use in patients with multiple myeloma. Curran, MP; McKeage, K, 2009)	3.24
"Bortezomib (Velcade) is a proteasome inhibitor used in the treatment of myeloma and other blood dyscrasias. "	( [Bortezomib-induced eruption: Sweet syndrome? Two case reports]. Billet, A; Chaby, G; Chatelain, D; Christophe, O; Dadban, A; Damaj, G; Lenglet, A; Lok, C; Marolleau, JP; Royer, R; Thuillier, D; Vaida, I; Viseux, V, 2009)	2.71
"Bortezomib (Velcade) is a proteasome used in the treatment of myeloma. "	( [Bortezomib-induced neutrophilic dermatosis with CD30+ lymphocytic infiltration]. Andreoli, A; Briere, J; Cavelier Balloy, B; Petit, A; Thomas, M, 2009)	2.71
"Bortezomib is a well-established treatment option for patients with multiple myeloma (MM). "	( The proteasome inhibitor bortezomib aggravates renal ischemia-reperfusion injury. Eller, K; Heininger, D; Huber, JM; Mayer, G; Rosenkranz, AR; Tagwerker, A, 2009)	2.1
"Bortezomib is a therapeutic proteasome inhibitor with antimyeloma activity and polyphenols are well known compounds that exert antiproliferative effects against tumuors. "	( Natural polyphenols antagonize the antimyeloma activity of proteasome inhibitor bortezomib by direct chemical interaction. Cheong, JW; Jeong, TS; Kim, HJ; Kim, TY; Lee, DS; Lee, JH; Min, HJ; Oh, B; Park, J; Park, SB; Suh, C; Yoon, SS, 2009)	2.02
"Bortezomib is a proteasome inhibitor and enhances TNF-alpha-induced cell death."	( Combination effect between bortezomib and tumor necrosis factor alpha on gefitinib-resistant non-small cell lung cancer cell lines. Adachii, M; Ando, K; Hirose, T; Hosaka, T; Inoue, F; Ishida, H; Kadofuku, T; Kanome, T; Kusumoto, S; Ohmori, T; Ohnishi, T; Okuda, K; Saijo, N; Shirai, T; Sugiyama, T; Yamaoka, T, 2009)	1.37
"Bortezomib is a potent, selective proteasome inhibitor. "	( Bortezomib-induced perivascular dermatitis in a patient with multiple myeloma. Aki, SZ; Erdem, O; Ozkurt, ZN; Sucak, GT; Yağci, M, 2009)	3.24
"Bortezomib is a first in a class proteasome inhibitor that has been shown to effectively treat antibody-mediated rejection in kidney transplant recipients."	( Proteasome inhibition for antibody-mediated rejection. Alloway, RR; Everly, JJ; Walsh, RC; Woodle, ES, 2009)	1.07
"Bortezomib is a proteasome inhibitor showing strong antitumor activity against many tumors, primarily multiple myeloma. "	( Bortezomib-induced painful neuropathy in rats: a behavioral, neurophysiological and pathological study in rats. Avezza, F; Canta, A; Carozzi, VA; Cavaletti, G; Ceresa, C; Chiorazzi, A; Crippa, L; Gilardini, A; Marmiroli, P; Meregalli, C; Oggioni, N, 2010)	3.25
"Bortezomib is a viable therapy to treat donor-specific HLA antibody in allograft recipients."	( Elimination of post-transplant donor-specific HLA antibodies with bortezomib. Dave, SD; Everly, MJ; Feroz, A; Idica, A; Kaneku, H; Khemchandani, SI; Modi, PR; Shankar, V; Terasaki, PI; Trivedi, HL; Trivedi, VB; Vanikar, AV, 2008)	1.3
"Bortezomib is a promising novel immunomodulatory agent in allogeneic transplantation."	( Bortezomib, tacrolimus, and methotrexate for prophylaxis of graft-versus-host disease after reduced-intensity conditioning allogeneic stem cell transplantation from HLA-mismatched unrelated donors. Alyea, EP; Antin, JH; Armand, P; Cutler, C; Garcia, M; Ho, VT; Kim, HT; Koreth, J; Ritz, J; Soiffer, RJ; Stevenson, KE, 2009)	2.52
"Bortezomib is a new agent for the treatment of patients with myeloma, with high response rates and controllable side effects."	( Bortezomib and dexamethasone therapy for newly diagnosed patients with multiple myeloma complicated by renal impairment. Duan, MH; Jiao, L; Li, J; Shen, T; Zhang, W; Zhao, YQ; Zhou, DB, 2009)	2.52
"Bortezomib is a first-in-class proteasome inhibitor whose pharmacokinetic/pharmacodynamic parameters are poorly understood in terms of their relationship with efficacy."	( The relationship among tumor architecture, pharmacokinetics, pharmacodynamics, and efficacy of bortezomib in mouse xenograft models. Babcock, T; Bannerman, B; Cao, Y; Hatsis, P; Kupperman, E; Robertson, R; Silva, MD; Terkelsen, J; Williamson, MJ; Xia, C; Yu, L, 2009)	1.29
"Bortezomib is a potent proteasome inhibitor currently used to treat various malignancies with promising results. "	( Bortezomib suppresses focal adhesion kinase expression via interrupting nuclear factor-kappa B. Chang, CC; Chang, TC; Chen, CH; Golubovskaya, VM; Hsu, C; Ko, BS; Kuo, CC; Liou, JY; Liu, CC; Shen, TL; Shen, YC; Shyue, SK, 2010)	3.25
"Bortezomib is a new addition to drugs used in MM and has shown good efficacy and safety profiles."	( Rapid improvement in renal function in patients with multiple myeloma and renal failure treated with bortezomib. Al Diab, AR; Al Momen, AK; Aleem, A; Niaz, F; Qayum, A, 2010)	1.3
"Bortezomib is a proteasome inhibitor. "	( Bortezomib: a new pro-apoptotic agent in cancer treatment. Adamo, V; Bronte, G; Cicero, G; Fulfaro, F; Gebbia, N; Rizzo, S; Russo, A, 2010)	3.25
"Bortezomib (Velcade) is a proteasome inhibitor that has been approved for patients with multiple myeloma."	( Optimized combination therapy using bortezomib, TRAIL and TLR agonists in established breast tumors. Celis, E; Lee, S; Sayers, TJ; Yagita, H, 2010)	1.36
"Bortezomib is a proteasome inhibitor that has shown impressive efficacy for the treatment of multiple myeloma."	( The proteasome inhibitor bortezomib inhibits T cell-dependent inflammatory responses. Hara, T; Muroi, E; Ogawa, F; Sato, S; Shimizu, K; Yanaba, K; Yoshizaki, A, 2010)	1.39
"Bortezomib (BTZ) is a proteasome inhibitor approved in the treatment of multiple myeloma (MM). "	( Neurological monitoring reduces the incidence of bortezomib-induced peripheral neuropathy in multiple myeloma patients. Bruna, J; Clapés, V; Navarro, X; Petit, J; Velasco, R; Verdú, E, 2010)	2.06
"Bortezomib is a proteasome inhibitor approved for anticancer therapy. "	( G(alpha)12/13 inhibition enhances the anticancer effect of bortezomib through PSMB5 downregulation. Dhanasekaran, DN; Ha, JH; Jayaraman, M; Kim, SG; Kwak, MK; Lee, CH; Lee, S; Nam, CW; Yang, YM, 2010)	2.05
"Bortezomib is a proteasome inhibitor that has shown some activity in patients with T-cell lymphoma."	( Pralatrexate is synergistic with the proteasome inhibitor bortezomib in in vitro and in vivo models of T-cell lymphoid malignancies. Marchi, E; O'Connor, OA; Paoluzzi, L; Scotto, L; Seshan, VE; Zain, JM; Zinzani, PL, 2010)	1.33
"Bortezomib is a potent inducer of apoptosis in malignant as well as non-malignant human plasma cells. "	( Bortezomib affects the function of human B cells: possible implications for desensitization protocols. Claas, FH; Doxiadis, II; Heidt, S; Mulder, A; Roelen, DL; Vergunst, M, 2009)	3.24
"Bortezomib is an effective agent for treating multiple myeloma (MM). "	( Bortezomib-resistant myeloma cell lines: a role for mutated PSMB5 in preventing the accumulation of unfolded proteins and fatal ER stress. Iida, S; Inagaki, A; Ishida, T; Ito, A; Komatsu, H; Kusumoto, S; Miyazaki, H; Mori, F; Nakashima, T; Ri, M; Shiotsu, Y; Ueda, R, 2010)	3.25
"Bortezomib is a proteasome inhibitor with in vitro synergy with corticosteroids and clinical activity in human lymphoid malignancies."	( Phase I study of bortezomib combined with chemotherapy in children with relapsed childhood acute lymphoblastic leukemia (ALL): a report from the therapeutic advances in childhood leukemia (TACL) consortium. Bostrom, BC; Dubois, S; Eckroth, E; Gaynon, P; Glade-Bender, J; Hutchinson, R; Messinger, Y; Raetz, E; Sposto, R; van der Giessen, J, 2010)	1.42
"Bortezomib is a novel proteasome inhibitor, which has shown high antimyeloma activity. "	( Bortezomib and dexamethasone for Japanese patients with relapsed and refractory multiple myeloma: a single center experience. Chou, T; Hirose, T; Igarashi, N; Imai, Y; Ishiguro, T, 2010)	3.25
"Bortezomib is a modified dipeptidyl boronic acid analogue used to treat multiple myeloma, mantle cell lymphoma, and, more recently, renal transplantation graft rejection."	( Stability of unused reconstituted bortezomib in original manufacturer vials. Kolesar, JM; Pomplun, ML; Vanderloo, JP; Vermeulen, LC, 2011)	1.37
"Bortezomib is an inhibitor of 26S proteasome, which is an effective treatment for multiple myeloma. "	( Complete atrioventricular block secondary to bortezomib use in multiple myeloma. Jeon, SH; Kim, DH; Kwan, J; Lee, WS; Park, KS; Park, SD; Shin, SH; Woo, SI; Yi, HG, 2011)	2.07
"Bortezomib is a potent agent for multiple myeloma (MM); however, severe treatment-related toxicities such as peripheral neuropathy have been observed in conjunction with its use. "	( Successful treatment with a modified bortezomib schedule of weekly and longer intervals for patients with refractory/resistance multiple myeloma. Hanzawa, K; Kizaki, M; Mori, S; Nemoto, T; Sagawa, M; Tokuhira, M; Tomikawa, T; Watanabe, R, 2011)	2.08
"Bortezomib is a new chemotherapeutic agent approved for the treatment of relapsed/refractory and newly diagnosed multiple myeloma. "	( Somatic and autonomic small fiber neuropathy induced by bortezomib therapy: an immunofluorescence study. Borsini, W; Di Stasi, V; Donadio, V; Giannoccaro, MP; Gomis Pèrez, C; Liguori, R, 2011)	2.06
"Bortezomib (Velcade®) is a first-in-class proteasome inhibitor and has been approved for first-line treatment of multiple myeloma and second-line treatment of mantle cell lymphoma."	( The ubiquitin-proteasome system (UPS) and the mechanism of action of bortezomib. Cvek, B; Dvorak, Z, 2011)	1.33
"Bortezomib is a proteasome inhibitor demonstrating substantial activity in multiple myeloma. "	( Inflammatory autoimmune neuropathy, presumably induced by bortezomib, in a patient suffering from multiple myeloma. Fingerle-Rowson, G; Goldschmidt, H; Ho, AD; Neben, K; Pham, M; Schmitt, S; Storch-Hagenlocher, B, 2011)	2.06
"Bortezomib (Velcade) is a proteasome inhibitor approved by the FDA for the treatment of multiple myeloma."	( Bortezomib as an adjuvant to conventional therapy in the treatment of antibody mediated rejection (AMR): the full spectrum. Al Meshari, K; Altalhi, M; Alzayer, F; Elgamal, H; Pall, A, 2010)	2.52
"Bortezomib is a first-in-class proteasome inhibitor that was originally Food and Drug Administration approved for the treatment of multiple myeloma. "	( Proteasome inhibitor treatment of antibody-mediated allograft rejection. Alloway, RR; Girnita, A; Woodle, ES, 2011)	1.81
"Bortezomib is a potential novel molecular targeting drug for the treatment of unresectable advanced gastric cancer."	( Anti-tumor activity of the proteasome inhibitor bortezomib in gastric cancer. Hayakawa, Y; Hirata, Y; Kinoshita, H; Koike, K; Maeda, S; Nakagawa, H; Nakata, W; Sakamoto, K; Takahashi, R, 2011)	1.35
"Bortezomib is a proteasome inhibitor that is currently approved for use in multiple myeloma (MM) and mantle-cell lymphoma."	( Pilot study of bortezomib for patients with imatinib-refractory chronic myeloid leukemia in chronic or accelerated phase. Borthakur, G; Cortes, J; Faderl, S; Ferrajoli, A; Kantarjian, H; McConkey, D; O'Brien, S; Santos, FP; Wright, J, 2011)	1.44
"Bortezomib (Velcade®) is a proteasome inhibitor that has been approved for the treatment of multiple myeloma and mantle cell lymphoma. "	( Anti-inflammatory and immunomodulatory effects of bortezomib in various in vivo models. Cheung, PH; Foreman, O; Hain, HS; Kaur, P; Kavirayani, A; Saha, S; Tung, D, 2011)	2.07
"Bortezomib is a proteasome inhibitor important to the therapy of multiple myeloma (MM), though a number of patients show resistance to this drug. "	( Bortezomib resistance in a myeloma cell line is associated to PSMβ5 overexpression and polyploidy. Balsas, P; Galán-Malo, P; Marzo, I; Naval, J, 2012)	3.26
"Bortezomib is a proteasome inhibitor that induces apoptosis in various cancer cells and has been shown to be effective as a salvage therapy for relapsed/refractory multiple myeloma."	( Cyclin kinase subunit 1B nuclear expression predicts an adverse outcome for patients with relapsed/refractory multiple myeloma treated with bortezomib. Chang, H; Chen, MH; Qi, C; Reece, D, 2012)	1.3
"Bortezomib, is a highly selective proteasome inhibitor with anti-NHL activity; it is currently FDA approved for second-line treatment of mantle cell lymphoma (MCL)."	( The HB22.7 Anti-CD22 monoclonal antibody enhances bortezomib-mediated lymphomacidal activity in a sequence dependent manner. Churchill, E; Ma, Y; Mahaffey, CM; Martin, SM; McKnight, H; O'Donnell, RT; Tuscano, JM, 2011)	1.34
"Bortezomib is a proteasome inhibitor that blocks the NF-κB pathway."	( A phase II study of the combination of endocrine treatment and bortezomib in patients with endocrine-resistant metastatic breast cancer. De Mesmaeker, P; Deleu, I; Dirix, LY; Prové, A; Rasschaert, M; Sas, L; Tjalma, WA; Trinh, XB; Van Dam, PA; Van de Velde, H; Van Laere, SJ; Vermeulen, PB; Vinken, P; Wojtasik, A, 2012)	1.34
"Bortezomib is a promising potential therapy for acute leukemia, especially mdr1 drug-resistant leukemia."	( Proteasome inhibitor bortezomib overcomes P-gp-mediated multidrug resistance in resistant leukemic cell lines. Gong, Y; Shan, Q; Yang, X; Zheng, B; Zhou, R, 2012)	2.14
"Bortezomib is a proteasome inhibitor with minimal clinical activity as a monotherapy in solid tumours, but its combination with other targeted therapies is being actively investigated as a way to increase its anticarcinogenic properties. "	( Indole-3-carbinol synergistically sensitises ovarian cancer cells to bortezomib treatment. Agadjanian, H; Guo, X; Karlan, BY; Kwon, S; Miller, C; Nassanian, H; Orsulic, S; Taylor-Harding, B; Walsh, CS, 2012)	2.06
"Bortezomib is a potent inhibitor of plasma cell production and it appears to be useful for the treatment of antibody-mediated graft dysfunction."	( Lung transplantation across donor-specific anti-human leukocyte antigen antibodies: utility of bortezomib therapy in early graft dysfunction. Chan, KM; Kamoun, M; Stuckey, LJ, 2012)	1.32
"Bortezomib (Velcade™) is a reversible proteasome inhibitor that is approved for the treatment of multiple myeloma (MM). "	( Molecular mechanisms of bortezomib resistant adenocarcinoma cells. Arastu-Kapur, S; Bennett, MK; Bergsagel, PL; Demo, S; Deu, E; Keats, J; Kirk, CJ; Suzuki, E, 2011)	2.12
"Bortezomib is a proteasome inhibitor with excellent antimyeloma activity. "	( Bortezomib-associated fatal liver failure in a haemodialysis patient with multiple myeloma. Beckers, EA; Cornelis, T; Driessen, AL; Koek, GH; van der Sande, FM, 2012)	3.26
"Bortezomib is a proteasome inhibitor that has shown impressive efficacy in the treatment of multiple myeloma. "	( Proteasome inhibitor bortezomib ameliorates intestinal injury in mice. Asano, Y; Kadono, T; Sato, S; Sugaya, M; Tada, Y; Yanaba, K, 2012)	2.14
"Bortezomib is a novel proteasome inhibitor initially approved for use in multiple myeloma and currently under continued investigation as a treatment for numerous subtypes of non-Hodgkin's lymphoma. "	( Bortezomib: a proteasome inhibitor with an evolving role in select subtypes of B-cell non-Hodgkin's lymphoma. Cheson, BD; Koprivnikar, JL, 2012)	3.26
"Bortezomib is a proteasome inhibitor that has proven to be a very effective treatment for multiple myeloma. "	( Bortezomib and bilateral herpes zoster. Bergamo, S; di Meo, N; Dondas, A; Trevisan, G, 2012)	3.26
"Bortezomib is a proteasome inhibitor and is active against multiple myeloma. "	( Bortezomib-induced pneumonitis during bortezomib retreatment in multiple myeloma. Itoh, K; Sasaki, M; Yamaguchi, T, 2012)	3.26
"Bortezomib is a selective and reversible inhibitor of the proteasome."	( Cytotoxic effects of bortezomib in myelodysplastic syndrome/acute myeloid leukemia depend on autophagy-mediated lysosomal degradation of TRAF6 and repression of PSMA1. Bolanos, L; Cloos, J; Cortelezzi, A; Cuzzola, M; Fang, J; Goyama, S; Jansen, G; Mulloy, JC; Oliva, EN; Rasch, C; Rhyasen, G; Rigolino, C; Starczynowski, DT; Varney, M; Wunderlich, M, 2012)	1.42
"Bortezomib is a proteasome inhibitor that inactivates NF-κB."	( Phase II 2-arm trial of the proteasome inhibitor, PS-341 (bortezomib) in combination with irinotecan or PS-341 alone followed by the addition of irinotecan at time of progression in patients with locally recurrent or metastatic squamous cell carcinoma of Argiris, A; Arun, P; Feldman, LE; Forastiere, AA; Gilbert, J; Haigentz, M; Jang, M; Lee, JW; Van Waes, C, 2013)	1.36
"Bortezomib is a proteasome inhibitor with efficacy in relapsed/refractory multiple myeloma that inhibits tumor angiogenesis, a process that has been implicated in multiple myeloma pathogenesis."	( Results from AMBER, a randomized phase 2 study of bevacizumab and bortezomib versus bortezomib in relapsed or refractory multiple myeloma. Bhaskar, B; Kassim, A; Paton, VE; Wamstad, K; White, D; Yi, J, 2013)	1.35
"Bortezomib (BZ) is a proteasome inhibitor and interferes with degradation of misfolded proteins."	( Synergistic effects of nelfinavir and bortezomib on proteotoxic death of NSCLC and multiple myeloma cells. Dennis, PA; Gills, JJ; Hollander, MC; Kawabata, S; Lopiccolo, J; Mercado-Matos, JR; Wilson, W, 2012)	1.37
"Bortezomib is a novel, first-in-class peptide which reversibly inhibits the proteasome and is Food and Drug Administration approved for the treatment of multiple myeloma, non-Hodgkin lymphoma, Waldenström's macroglobulinemia, and systemic light chain amyloidosis, among others."	( Severe heart failure after bortezomib treatment in a patient with multiple myeloma: a case report and review of the literature. Bockorny, B; Bockorny, M; Bona, R; Chakravarty, S; Schulman, P, 2012)	2.12
"Bortezomib appears to be an ideal target drug for HCC with LC."	( Bortezomib induces tumor-specific cell death and growth inhibition in hepatocellular carcinoma and improves liver fibrosis. Fujisawa, K; Hirose, Y; Matsumoto, T; Murata, Y; Saeki, I; Sakaida, I; Takami, T; Terai, S; Yamamoto, N; Yamasaki, T, 2013)	3.28
"Bortezomib is a highly selective inhibitor of the 26S proteasome and has been approved for clinical use in the treatment of relapsing and refractory multiple myeloma and mantle cell lymphoma. "	( Requirement of apoptotic protease-activating factor-1 for bortezomib-induced apoptosis but not for Fas-mediated apoptosis in human leukemic cells. Ceder, R; Fadeel, B; Grafström, RC; Grandér, D; Hedenfalk, I; Heyman, M; Ottosson-Wadlund, A; Pokrovskaja, K; Preta, G; Robertson, JD; Söderhäll, S, 2013)	2.08
"Bortezomib is an important component of the chemotherapy regimen associated with multiple myeloma, and has been previously applied to POEMS syndrome."	( Effective induction therapy with subcutaneous administration of bortezomib for newly diagnosed POEMS syndrome: a case report and a review of the literature. Li, J; Liu, T; Niu, T; Wei, Q; Yang, JR; Yang, YM; Zeng, K, 2013)	1.35
"Bortezomib (BOR) is an effective drug for the treatment of multiple myeloma and BOR-induced peripheral neuropathy (BIPN) is a major adverse event. "	( Itraconazole may increase the risk of early-onset bortezomib-induced peripheral neuropathy. Hashimoto, N; Okamoto, S; Sadahira, K; Tsukada, Y; Ueda, T; Yokoyama, K, 2012)	2.07
"Bortezomib (Velcade) is a proteasome inhibitor that has shown important clinical efficacy either as a single agent or in combination with other cytostatic agents in multiple myeloma (MM). "	( Combined bendamustine, prednisone and bortezomib (BPV) in patients with relapsed or refractory multiple myeloma. Ali, HA; Aßmann, M; Becker, C; Bourgeois, M; Edelmann, T; Hensel, G; Heyn, S; Hoffmann, FA; Hurtz, HJ; Jäkel, N; Krahl, R; Löschcke, K; Mohren, M; Moll, B; Niederwieser, D; Pönisch, W; Rohrberg, R; Schmalfeld, M; Schönfelder, U; Schwarzer, A; Wagner, I; Zehrfeld, T, 2013)	2.1
"Bortezomib is a proteasome inhibitor approved for treating patients with multiple myeloma, a plasma cell malignancy."	( Targeting plasma cells with proteasome inhibitors: possible roles in treating myasthenia gravis? Buurman, W; De Baets, MH; Gomez, AM; Losen, M; Martinez-Martinez, P; Molenaar, PC; Willcox, N, 2012)	1.1
"Bortezomib is an effective antimyeloma therapy, but clinical benefits can be limited by neurotoxicity. "	( Weekly intravenous bortezomib is effective and well tolerated in relapsed/refractory myeloma. Atwal, S; D'Sa, S; Johnston, R; Khan, I; Moore, S; Narat, S; Percy, L; Rabin, N; Sachchithanantham, S; Schey, S; Streetly, M; Yong, K, 2013)	2.16
"Bortezomib is an antitumor drug that competitively inhibits proteasome beta-1 and beta-5 subunits. "	( Alterations of the intracellular peptidome in response to the proteasome inhibitor bortezomib. Berezniuk, I; Castro, LM; Dasgupta, S; Ferro, ES; Fricker, LD; Gelman, JS; Gozzo, FC; Sironi, J, 2013)	2.06
"Bortezomib is a proteasome inhibitor and a drug used for molecular-targeted therapy (targets NF-κB)."	( Bortezomib-enhanced radiosensitization through the suppression of radiation-induced nuclear factor-κB activity in human oral cancer cells. Fujisawa, K; Hara, K; Kinouchi, M; Kuribayashi, N; Miyamoto, Y; Nagai, H; Ohe, G; Takamaru, N; Tamatani, T; Uchida, D, 2013)	2.55
"Bortezomib is a proteasome inhibitor with potent antimyeloma activity in relapsed/refractory multiple myeloma (MM) patients. "	( Lymphocytopenia is associated with an increased risk of severe infections in patients with multiple myeloma treated with bortezomib-based regimens. Ahn, JS; Bae, SY; Jung, SH; Kang, SJ; Kim, HJ; Kim, YK; Lee, JJ; Yang, DH, 2013)	2.04
"Bortezomib is a dipeptidyl boronic acid proteasome inhibitor that effectively and specifically inhibits proteasome activity."	( Proteasome inhibitors in the treatment of B-cell malignancies. Schenkein, D, 2002)	1.04
"Bortezomib is a peptide boronic acid inhibitor of the proteasome developed for cancer therapy. "	( Effects of the proteasome inhibitor, bortezomib, on apoptosis in isolated lymphocytes obtained from patients with chronic lymphocytic leukemia. Andreeff, M; Calvert, LR; Faderl, S; Keating, M; McConkey, DJ; Niemer, I; Pahler, JC; Ruiz, S, 2003)	2.03
"Bortezomib is a novel anticancer agent with significant activity in relapsed and refractory MM."	( Bortezomib treatment for multiple myeloma. Stanford, BL; Zondor, SD, 2003)	2.48
"Bortezomib is a specific and potent proteasome inhibitor."	( Simultaneous inhibition of hsp 90 and the proteasome promotes protein ubiquitination, causes endoplasmic reticulum-derived cytosolic vacuolization, and enhances antitumor activity. Bisht, KS; Gius, D; Isaacs, JS; Mimnaugh, EG; Neckers, L; Vos, M; Xu, W; Yuan, X, 2004)	1.04
"Bortezomib is a proteasome inhibitor that was recently approved for treatment of myeloma."	( Inhibition of acute graft-versus-host disease with retention of graft-versus-tumor effects by the proteasome inhibitor bortezomib. Barao, I; Blazar, BR; Liu, H; Murphy, WJ; O'Shaughnessy, MJ; Panoskaltsis-Mortari, A; Riordan, W; Sayers, TJ; Serody, JS; Sitcheran, R; Sun, K; Welniak, LA; Wysocki, C, 2004)	1.25
"Bortezomib (PS-341) is an inhibitor of the S26 proteasome. "	( The bortezomib-induced mitochondrial damage is mediated by accumulation of active protein kinase C-delta. Durrant, D; Lee, RM; Liu, J; Yang, HS, 2004)	2.32
"Bortezomib (VELCADE) is a proteasome inhibitor, which has been recently used for the treatment of relapsed/refractory multiple myeloma (MM) with encouraging results. "	( Tumour lysis syndrome in multiple myeloma after bortezomib (VELCADE) administration. Politou, M; Rahemtulla, A; Terpos, E, 2004)	2.02
"Bortezomib is a potent, reversible proteasome inhibitor that has been approved for the treatment of recurrent and/or refractory multiple myeloma, but its activity in patients with renal impairment has not been studied to date."	( Bortezomib in recurrent and/or refractory multiple myeloma. Initial clinical experience in patients with impared renal function. Alexanian, R; Anderson, J; Anderson, KC; Barlogie, B; Berenson, JR; Esseltine, DL; Jagannath, S; Nix, D; Orlowski, RZ; Richardson, PG; Singhal, S; Srkalovic, G, 2005)	3.21
"Bortezomib is a novel proteasome inhibitor with significant antimyeloma activity. "	( Bortezomib-induced severe hepatitis in multiple myeloma: a case report. Bladé, J; Cibeira, MT; Montoto, S; Rosiñol, L, 2005)	3.21
"Bortezomib is a proteasome inhibitor with manageable clinical toxicity and laboratory evidence of anti-melanoma activity. "	( A phase II study of bortezomib in the treatment of metastatic malignant melanoma. Adjei, AA; Albertini, M; Dawkins, F; Erlichman, C; Fitch, T; Fracasso, PM; Geyer, SM; Lorusso, P; Maples, W; Markovic, SN; Sharfman, W, 2005)	2.09
"Bortezomib is an extremely potent and selective proteasome inhibitor that shows strong activity in in vitro and in vivo laboratory studies against many solid and hematologic tumor types."	( Preclinical and clinical development of the proteasome inhibitor bortezomib in cancer treatment. Albanell, J; Gascon, P; Mellado, B; Montagut, C; Ross, JS; Rovira, A, 2005)	1.29
"Bortezomib (PS-341) is a novel antineoplastic agent that is well tolerated at doses not exceeding 3.0 mg (equivalent to 1.75 mg/m2), repeated on D1 and D4 every other week. "	( Proteasome inhibition with bortezomib (PS-341): a phase I study with pharmacodynamic end points using a day 1 and day 4 schedule in a 14-day cycle. Adams, J; Boyden, J; Chachoua, A; Clark, JW; Eder, JP; Elliott, P; Farrell, K; Garcia-Carbonero, R; Hamilton, AL; Kinchla, N; Liebes, L; Muggia, FM; Pavlick, AC; Ryan, DP; Soma, V; Wright, J; Yee, H; Zeleniuch-Jacquotte, A, 2005)	2.07
"Bortezomib is a novel, reversible, and highly specific proteasome inhibitor that appears as a new hope for MCL treatment."	( The proteasome inhibitor bortezomib induces apoptosis in mantle-cell lymphoma through generation of ROS and Noxa activation independent of p53 status. Campo, E; Colomer, D; Montserrat, E; Pérez-Galán, P; Roué, G; Villamor, N, 2006)	1.36
"Bortezomib is a novel proteasome inhibitor approved for therapy of multiple myeloma."	( Sequencing bortezomib with chemotherapy and targeted agents. Adjei, AA, 2005)	1.44
"Bortezomib is a selective 26S proteasome inhibitor that has been approved for the treatment of multiple myeloma."	( The potential role of bortezomib in combination with chemotherapy and radiation in non-small-cell lung cancer. Edelman, MJ, 2005)	1.36
"Bortezomib is a proteasome inhibitor that can decrease Bcl-2 expression through diminished IkappaB degradation."	( Proteasome inhibition in small-cell lung cancer: preclinical rationale and clinical applications. Bold, RJ; Davies, AM; Gandara, DR; Gumerlock, PH; Lara, PN; Mack, PC, 2005)	1.05
"Bortezomib is a selective proteasome inhibitor which has shown significant activity in a variety of hematologic malignancies including multiple myeloma, mantle cell lymphoma and marginal zone lymphoma. "	( Treatment of relapsed or refractory Waldenström's macroglobulinemia with bortezomib. Anagnostopoulos, A; Bitsaktsis, A; Castritis, E; Dimopoulos, MA; Kyrtsonis, MC; Pangalis, GA, 2005)	2
"Bortezomib (VELCADE) is a potent inhibitor of the 26S proteasome with broad antitumor activity. "	( Bortezomib (VELCADE) in metastatic breast cancer: pharmacodynamics, biological effects, and prediction of clinical benefits. Booser, DJ; Broglio, KR; Cristofanilli, M; Esseltine, D; Gonzalez-Angulo, AM; Hortobagyi, GN; Islam, R; Krishnamurthy, S; Pusztai, L; Reuben, JM; Stec, J; Yang, CH, 2006)	3.22
"Bortezomib is a novel proteasome inhibitor with significant antimyeloma activity. "	( Severe pulmonary complications in Japanese patients after bortezomib treatment for refractory multiple myeloma. Fujii, T; Kami, M; Kawabata, M; Matsumura, T; Miyakoshi, S; Narimatsu, H; Oshimi, K; Ozawa, K; Sasaki, M; Takatoku, M; Taniguchi, S; Yuji, K, 2006)	2.02
"Bortezomib is a potent and selective proteasome inhibitor recently introduced in the treatment of multiple myeloma (MM). "	( Bortezomib: an effective agent in extramedullary disease in multiple myeloma. Bladé, J; Cibeira, MT; Laura, R; Montserrat, E; Salamero, O; Uriburu, C; Yantorno, S, 2006)	3.22
"Bortezomib (VELCADE) is a first-in-class proteasome inhibitor developed specifically for use as an antineoplastic agent."	( Bortezomib: proteasome inhibition as an effective anticancer therapy. Mitsiades, C; Richardson, PG, 2005)	2.49
"Bortezomib (1) is a potent first-in-class dipeptidyl boronic acid proteasome inhibitor employed in the treatment of patients with relapsed multiple myeloma where the disease is refractory to conventional lines of therapy. "	( Oxidative deboronation of the peptide boronic acid proteasome inhibitor bortezomib: contributions from reactive oxygen species in this novel cytochrome P450 reaction. Daniels, JS; Gan, LS; Huang, R; Labutti, J; Miwa, G; Parsons, I, 2006)	2.01
"Bortezomib, which is a proteasome inhibitor and inhibits NF-kappaB activity, has also excellent efficacy like thalidomide."	( [New treatment strategy of multiple myeloma for cure]. Handa, H; Murakami, H, 2006)	1.06
"Bortezomib is a proteasome inhibitor which seems to be effective in MDS."	( Bortezomib is an effective agent for MDS/MPD syndrome with 5q- anomaly and thrombocytosis. Banti, A; Kaloutsi, V; Lazaridou, A; Terpos, E; Verrou, E; Zervas, K, 2007)	2.5
"Bortezomib is a biologically active agent, producing predictable, dose-related and reversible proteasome inhibition; it has shown antitumor activity in various malignancies and is the first proteasome inhibitor to be used in clinical practice."	( Bortezomib: efficacy comparisons in solid tumors and hematologic malignancies. Amadori, S; Boccadoro, M; Caravita, T; de Fabritiis, P; Palumbo, A, 2006)	2.5
"Bortezomib is a selective and reversible inhibitor of the 26S proteasome that shows potent antitumor activity in vitro and in vivo against several human cancers of adulthood. "	( Effect of bortezomib on human neuroblastoma cell growth, apoptosis, and angiogenesis. Brignole, C; Cilli, M; Cioni, M; Corrias, MV; Di Paolo, D; Marimpietri, D; Nico, B; Pagnan, G; Pastorino, F; Pezzolo, A; Piccardi, F; Pistoia, V; Ponzoni, M; Ribatti, D, 2006)	2.18
"Bortezomib is an effective inhibitor of neuroblastoma cell growth and angiogenesis. "	( Effect of bortezomib on human neuroblastoma cell growth, apoptosis, and angiogenesis. Brignole, C; Cilli, M; Cioni, M; Corrias, MV; Di Paolo, D; Marimpietri, D; Nico, B; Pagnan, G; Pastorino, F; Pezzolo, A; Piccardi, F; Pistoia, V; Ponzoni, M; Ribatti, D, 2006)	2.18
"Bortezomib is a first-in-class proteasome inhibitor developed as an antineoplastic agent with marked activity in relapsed/refractory MM."	( Response to bortezomib and activation of osteoblasts in multiple myeloma. Cavallo, F; Esseltine, D; Tricot, G; Yaccoby, S; Zangari, M, 2006)	1.43
"Bortezomib (Velcade) is a proteasome inhibitor, which is used as a novel anticancer drug in the treatment of multiple myeloma."	( Pleomorphic presentation of cutaneous lesions associated with the proteasome inhibitor bortezomib in patients with multiple myeloma. Heule, F; Lam, K; Sonneveld, P; Wu, KL, 2006)	1.28
"Bortezomib is a proteosome inhibitor with good clinical activity in multiple myeloma. "	( Severe pulmonary complications in African-American patient after bortezomib therapy. Arena, FP; Ohri, A, )	1.81
"Bortezomib (Btz), is a proteasome inhibitor, currently undergoing clinical trials whose function, at least in part, by stabilizing the IkappaBalpha protein and inhibiting NFkappaB activation."	( Bortezomib induces different apoptotic rates in B-CLL cells according to IgVH and BCL-6 mutations. Benet, I; García-Conde, J; Jantus-Lewintre, E; Sarsotti, E; Terol, MJ, 2006)	2.5
"Bortezomib is a reversible proteasome inhibitor with significant activity in MM."	( Activity and safety of bortezomib in multiple myeloma patients with advanced renal failure: a multicenter retrospective study. Chanan-Khan, AA; Kaufman, JL; Lonial, S; Mehta, J; Miller, KC; Munshi, NC; Richardson, PG; Schlossman, R; Singhal, S; Tariman, J, 2007)	1.37
"Bortezomib (PS-341) is a newly developed proteosome inhibitor that shows extremely promising antineoplastic effects against a variety of neoplasias. "	( Quantitative sensory findings in patients with bortezomib-induced pain. Burton, AW; Cata, JP; Dougherty, PM; Giralt, S; Villareal, H; Weng, HR, 2007)	2.04
"Bortezomib is a proteasome inhibitor that can be effective in the treatment of refractory and relapsed multiple myeloma. "	( Lung injury associated with bortezomib therapy in relapsed/refractory multiple myeloma in Japan: a questionnaire-based report from the "lung injury by bortezomib" joint committee of the Japanese society of hematology and the Japanese society of clinical h Dan, K; Gotoh, A; Hotta, T; Ikeda, Y; Ohyashiki, K; Oshimi, K; Usui, N, 2006)	2.07
"Bortezomib is a proteasome inhibitor which target mainly is NF-kappaB."	( [Salvage therapy with proteasome inhibitor bortezomib for relapsed and refractory multiple myeloma]. Bo, J; Da, WM; Gao, CJ; Huang, WR; Jing, Y; Li, R; Wang, QS; Wu, XX; Yu, L; Zhang, YZ, 2006)	1.32
"Bortezomib is a new proteasome inhibitor with a high antitumor activity, but also with a potentially severe peripheral neurotoxicity. "	( Bortezomib-induced peripheral neurotoxicity: a neurophysiological and pathological study in the rat. Bossi, M; Canta, A; Cavaletti, G; Ceresa, C; D'Incalci, M; De Coster, R; Gilardini, A; Marmiroli, P; Oggioni, N; Rigamonti, L; Rodriguez-Menendez, V, 2007)	3.23
"Bortezomib is a novel agent that inhibits proteasome and has shown activity against multiple myeloma."	( Bortezomib-induced tumor lysis syndrome in multiple myeloma. Boral, AL; Esseltine, DL; Jakob, C; Mehta, J; Richardson, P; Sezer, O; Singhal, S; Stadtmauer, E; Vesole, DH, 2006)	2.5
"Bortezomib is a proteasome inhibitor that can be effective in the treatment of refractory and relapsed multiple myeloma. "	( [Lung injury associated with bortezomib therapy in relapsed/refractory multiple myeloma in Japan: a questionnaire-based report from the "Lung Injury by Bortezomib" Joint Committee of the Japanese Society of Hematology and the Japanese Society of Clinical Dan, K; Gotoh, A; Hotta, T; Ikeda, Y; Ohyashiki, K; Oshimi, K; Usui, N, 2006)	2.07
"Bortezomib is a proteasome inhibitor with proven efficacy in multiple myeloma and non-Hodgkin's lymphoma. "	( The proteasome inhibitor bortezomib acts independently of p53 and induces cell death via apoptosis and mitotic catastrophe in B-cell lymphoma cell lines. Allen, P; Higginbottom, K; Joel, SP; Jüliger, S; Lister, TA; Maharaj, L; Schenkein, D; Strauss, SJ, 2007)	2.09
"Bortezomib is a proteasome inhibitor that has been approved by FDA for the treatment of multiple myeloma and that has completed phase 1 testing in children. "	( Initial testing (stage 1) of the proteasome inhibitor bortezomib by the pediatric preclinical testing program. Carol, H; Houghton, PJ; Keir, ST; Keshelava, N; Kolb, EA; Lock, R; Maris, JM; Morton, CL; Reynolds, CP; Smith, MA; Wu, J, 2008)	2.04
"Bortezomib appears to be an effective drug for PCL that could significantly improve the usually adverse clinical outcome of these patients."	( Efficacy and safety of bortezomib in patients with plasma cell leukemia. D'Arena, G; Ferrara, F; Filardi, N; Gay, F; Guariglia, R; Guglielmelli, T; Musto, P; Palumbo, A; Pitini, V; Rossini, F, 2007)	2.09
"Bortezomib is a potent drug for the treatment of multiple myeloma. "	( Bortezomib significantly impairs the immunostimulatory capacity of human myeloid blood dendritic cells. Bachmann, M; Bornhäuser, M; Rieber, EP; Schmitz, M; Straube, C; Wehner, R; Wendisch, M, 2007)	3.23
"Bortezomib is an FDA-approved proteasome inhibitor that is currently under clinical investigation in multiple neoplasms but has not been studied extensively in MPM."	( Preclinical studies of the proteasome inhibitor bortezomib in malignant pleural mesothelioma. Bueno, R; Gordon, GJ; Kindler, HL; Mani, M; Maulik, G; Mukhopadhyay, L; Salgia, R; Sugarbaker, DJ; Yeap, BY, 2008)	1.32
"Bortezomib is a proteasome inhibitor for the treatment of relapsed/refractory multiple myeloma (MM). "	( A pivotal role for Mcl-1 in Bortezomib-induced apoptosis. Amiot, M; Anderson, KC; Chauhan, D; Gouill, SL; Harousseau, JL; Hideshima, T; Opferman, JT; Podar, K; Tai, YT; Zhang, J; Zorn, E, 2008)	2.08
"Bortezomib is a proteasome inhibitor with pleiotropic antitumor activity. "	( Bortezomib inhibits angiogenesis and reduces tumor burden in a murine model of neuroblastoma. Davidoff, AM; Dickson, PV; Hamner, JB; Ng, CY; Sims, TL; Spence, Y; Zhou, J, 2007)	3.23
"Bortezomib is a novel proteasome inhibitor that has shown marked antitumor effects in patients with multiple myeloma (MM). "	( Therapy with bortezomib plus dexamethasone induces osteoblast activation in responsive patients with multiple myeloma. Abe, M; Asano, J; Choraku, M; Fujii, S; Hashimoto, T; Kagawa, K; Kitazoe, K; Matsumoto, T; Miki, H; Ozaki, S; Shigekiyo, Y; Takeuchi, K; Tanaka, O, 2007)	2.15
"Bortezomib is a novel molecular targeting agent which was designed to exhibit an antitumor effect by selectively inhibiting the 20S proteasome."	( Proteasome inhibitor, bortezomib, for myeloma and lymphoma. Tobinai, K, 2007)	1.38
"Bortezomib is a novel anti-cancer agent which has shown promising activity in non-small lung cancer (NSCLC) patients. "	( The proteasomal and apoptotic phenotype determine bortezomib sensitivity of non-small cell lung cancer cells. Checińska, A; Giaccone, G; Voortman, J, 2007)	2.04
"Bortezomib is a proteasome inhibitor with proven activity in multiple myeloma, and the addition of dexamethasone results in superior outcome."	( Treatment of light chain (AL) amyloidosis with the combination of bortezomib and dexamethasone. Anagnostopoulos, A; Delibasi, S; Dimopoulos, MA; Kastritis, E; Mellou, S; Migkou, M; Nanas, J; Pamboukas, C; Psimenou, E; Roussou, M; Tassidou, A; Terpos, E; Toumanidis, S; Xilouri, I, 2007)	1.3
"Bortezomib is a proteasome inhibitor that has direct antitumor effects. "	( Sensitization of tumor cells to NK cell-mediated killing by proteasome inhibition. Ames, E; Barao, I; Hallett, WH; Hudig, D; Motarjemi, M; Murphy, WJ; Sayers, TJ; Shanker, A; Tamang, DL, 2008)	1.79
"Bortezomib is a small-molecule proteasome inhibitor with single-agent activity in patients with non-small cell lung carcinoma (NSCLC) and synergy with gemcitabine in preclinical studies. "	( The proteasome inhibitor bortezomib in combination with gemcitabine and carboplatin in advanced non-small cell lung cancer: a California Cancer Consortium Phase I study. Bold, R; Davies, AM; Gandara, DR; Gumerlock, PH; Lara, PN; Lau, DH; Lenz, HJ; Ruel, C; Schenkein, DP; Shibata, S, 2008)	2.09
"Bortezomib (Velcade) is a boron containing molecule which reversibly inhibits the proteasome, an intracellular organelle which is central to the breakdown of ubiquinated proteins and consequently crucial for normal cellular homeostasis. "	( Position statement on the use of bortezomib in multiple myeloma. Cavenagh, JD; Davies, FE; Jackson, GH; Morgan, GJ, 2008)	2.07
"Bortezomib (Velcad) is a proteasome inhibitor recently developed and mainly used for the treatment of multiple myeloma. "	( Bortezomib-induced skin eruption. Dietrich, PY; Favet, L; Kerl, K; Piguet, V; Sanchez-Politta, S, 2008)	3.23
"Bortezomib (Bzb) is a clinically available proteasome inhibitor used in the treatment of multiple myeloma."	( Pharmacologic targeting of a stem/progenitor population in vivo is associated with enhanced bone regeneration in mice. Anderson, KC; Aronson, JP; Bouxsein, ML; Chhetri, S; Fulciniti, M; Glimcher, LH; Hideshima, T; Jones, DC; Lian, JB; Liu, JC; Mukherjee, S; Patel, C; Pozzi, S; Purton, LE; Raje, N; Scadden, DT; Schoonmaker, JA; Seo, YD; Stein, G; Vallet, S; Wein, MN, 2008)	1.07
"Bortezomib is an inhibitor of proteasome and NF-kappaB, with activity in various solid tumors and hematological malignancies."	( Activity of bortezomib in adult de novo and relapsed acute myeloid leukemia. Debski, R; Dytfeld, D; Gil, L; Kazmierczak, M; Kolodziej, B; Komarnicki, M; Kubicka, M; Nowicki, A; Rafinska, B; Styczynski, J; Wysocki, M, )	1.95
"Bortezomib is a proteasome inhibitor with preclinical activity against UC."	( Phase II study of bortezomib in patients with previously treated advanced urothelial tract transitional cell carcinoma: CALGB 90207. Atkins, JN; Bajorin, DF; Halabi, S; Himelstein, AL; Hohl, RJ; Millard, F; Rosenberg, JE; Sanford, BL; Small, EJ, 2008)	1.4
"Bortezomib is a boronic acid dipeptide derivative, which is a selective and potent inhibitor of the proteasome and has prominent effects in vitro and in vivo against several solid tumors."	( Effects of the proteasome inhibitor bortezomib alone and in combination with chemotherapeutic agents in gastric cancer cell lines. Bae, SH; Hyun, MS; Kim, MK; Lee, KH; Ryoo, HM; Sin, JI, 2008)	1.34
"Bortezomib is an efficacy drug for the second line treatment of MM."	( [Efficiency of bortezomib and dexamethasone in relapsed multiple myeloma treatment: retrospective study in consecutive cases]. Encinas García, S; Izarzugaza Perón, Y; Khosravi Shahi, P; Pérez Manga, G; Sabin Domínguez, P, 2008)	1.42
"Bortezomib is a novel, first-in-class proteasome inhibitor that has improved outcomes in multiple myeloma, with manageable toxicities."	( Bortezomib in multiple myeloma. Dimopoulos, MA; Roussou, M; Terpos, E, 2008)	3.23

Excerpt	Reference	Relevance
"Bortezomib has a potential risk to cause drug-induced GMA without systemic thrombotic microangiopathy, in which vascular endothelial growth factor-nuclear factor-κ B pathway could be involved."	( Bortezomib-induced glomerular microangiopathy complicated with monoclonal immunoglobulin deposition disease. Kitayama, C; Mizuno, S; Sanada, S; Sato, T, 2021)	2.79
"Bortezomib has a 33% response rate in relapsed/refractory MCL and has shown additive and/or synergistic effects in preclinical trials with known effective agents."	( Phase 2 trial of bortezomib in combination with rituximab plus hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone alternating with bortezomib, rituximab, methotrexate, and cytarabine for untreated mantle cell lymphoma. Fanale, M; Fayad, LE; Feng, L; Ford, P; Fowler, N; Goy, A; Hagemeister, F; Hartig, K; Kantarjian, HM; Kwak, LW; McLaughlin, P; Medeiros, LJ; Naig, A; Neelapu, S; Oki, Y; Orlowski, R; Pro, B; Rodriguez, MA; Romaguera, JE; Samaniego, F; Smith, J; Valentinetti, M; Wang, M; Younes, A, 2018)	1.54
"Bortezomib has been used as a first-line for treating MM for decades."	( Bortezomib Rescues Ovariectomy-Induced Bone Loss via SMURF-Mediated Ubiquitination Pathway. Fang, Y; He, F; Hou, M; Liu, Y; Lu, Y; Shen, X; Shi, Q; Yang, H; Zhang, Y; Zhao, Z; Zhu, T; Zhu, X, 2021)	2.79
"Bortezomib has shown clinical success in the treatment of multiple myeloma."	( Treatment with bortezomib for recurrent proliferative glomerulonephritis with monoclonal IgG deposits in kidney allograft. Case report and review of the literature. Ishida, H; Oki, R; Takagi, T; Taneda, S; Unagami, K, 2022)	1.8
"Bortezomib has become the primary drug in the treatment of patients with MM."	( Baseline peripheral neuropathy was associated with age and a prognostic factor in newly diagnosed multiple myeloma patients. Cai, Z; Dong, M; Han, X; He, J; Zhang, J; Zheng, G, 2022)	1.44
"Bortezomib has many side effects, mainly hematological, neurological, and gastrointestinal."	( Pneumonitis associated with bortezomib in a patient with multiple myeloma. Çeneli, Ö; Kars, TU; Yaşkıran, O, 2023)	1.93
"Bortezomib and ixazomib have been found to reduce tumor weight briefly, but once the dose is reduced, the tumor begins to grow again. "	( Pharmacokinetics-Pharmacodynamics Modeling and Evaluation of Tumor Response to Bortezomib Proteasome Inhibitor in Waldenstrom Macroglobulinemia. Bhatti, AI; Fazal, S; Munir, A; Sajjad, B, 2023)	2.58
"Bortezomib has putative activity against Kaposi's."	( Iatrogenic Kaposi's sarcoma from induction therapy for myeloma: to transplant or not to transplant? Babic, D; Farrugia, D; Grech, M; Sultana, E, 2023)	1.63
"Bortezomib has been successful for treatment of multiple myeloma, but not against solid tumors, and toxicities of neuropathy, thrombocytopenia and the emergence of resistance have triggered efforts to find alternative proteasome inhibitors. "	( Development and anticancer properties of Up284, a spirocyclic candidate ADRM1/RPN13 inhibitor. Anchoori, RK; Anchoori, V; Chang, YN; Das, S; Karanam, B; Lam, B; Patnam, R; Poddatoori, D; Roden, RBS; Rudek, MA; Tseng, SH; Velasquez, FC, 2023)	2.35
"Bortezomib, which has been FDA-approved for multiple myeloma and mantle cell lymphoma, was further investigated in downstream studies."	( Bortezomib inhibits chikungunya virus replication by interfering with viral protein synthesis. Chu, JJH; Dutta, SK; Kaur, P; Lello, LS; Merits, A; Utt, A, 2020)	2.72
"Bortezomib has been reported to prevent the progression of fibrosis in organs."	( Bortezomib limits renal allograft interstitial fibrosis by inhibiting NF-κB/TNF-α/Akt/mTOR/P70S6K/Smurf2 pathway via IκBα protein stabilization. Chen, H; Fei, S; Gu, M; Gui, Z; Suo, C; Tan, R; Wang, Z; Zheng, M; Zhou, J, 2021)	2.79
"Bortezomib has a potential risk to cause drug-induced GMA without systemic thrombotic microangiopathy, in which vascular endothelial growth factor-nuclear factor-κ B pathway could be involved."	( Bortezomib-induced glomerular microangiopathy complicated with monoclonal immunoglobulin deposition disease. Kitayama, C; Mizuno, S; Sanada, S; Sato, T, 2021)	2.79
"Bortezomib (BTZ) has demonstrated its efficacy in several hematological disorders and has been associated with thrombocytopenia. "	( The Proteasome Inhibitor Bortezomib Induces Apoptosis and Activation in Gel-Filtered Human Platelets. Debreceni, IB; Fejes, Z; Ghansah, H; Kappelmayer, J; Nagy, B, 2021)	2.37
"Bortezomib has been extensively studied for the maintenance treatment of MM."	( Efficacy and safety of bortezomib maintenance in patients with newly diagnosed multiple myeloma: a meta-analysis. Chen, L; Chu, ZB; Hu, Y; Li, JY; Sun, CY; Zhang, L, 2017)	1.49
"Bortezomib has a 33% response rate in relapsed/refractory MCL and has shown additive and/or synergistic effects in preclinical trials with known effective agents."	( Phase 2 trial of bortezomib in combination with rituximab plus hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone alternating with bortezomib, rituximab, methotrexate, and cytarabine for untreated mantle cell lymphoma. Fanale, M; Fayad, LE; Feng, L; Ford, P; Fowler, N; Goy, A; Hagemeister, F; Hartig, K; Kantarjian, HM; Kwak, LW; McLaughlin, P; Medeiros, LJ; Naig, A; Neelapu, S; Oki, Y; Orlowski, R; Pro, B; Rodriguez, MA; Romaguera, JE; Samaniego, F; Smith, J; Valentinetti, M; Wang, M; Younes, A, 2018)	1.54
"Bortezomib has been widely used to treat multiple myeloma and other hematological malignancies. "	( Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells. Ao, N; Chen, Q; Dai, Y; Feng, Y; Li, M; Liu, F; Liu, G; Wang, C; Yu, J, 2019)	2.22
"Bortezomib has also demonstrated clinical efficacy both as a single drug and in combination with other agents in light chain amyloidosis, lymphoplasmacytic lymphoma/Waldenstrom macroglobulinemia, and peripheral T-cell lymphomas."	( Bortezomib for the Treatment of Hematologic Malignancies: 15 Years Later. Robak, P; Robak, T, 2019)	2.68
"Bortezomib has remarkably improved MM patient outcome, but dose-limiting toxicities and development of resistance limit its long-term utility."	( Intracellular NAD⁺ depletion enhances bortezomib-induced anti-myeloma activity. Acharya, C; Anderson, KC; Cagnetta, A; Calimeri, T; Cea, M; Chauhan, D; Fulciniti, M; Gobbi, M; Hideshima, T; Munshi, N; Nencioni, A; Patrone, F; Richardson, P; Tai, YT; Zhong, MY, 2013)	1.38
"Bortezomib has appeared recently as a potential active treatment for acute AMR for few years. "	( Failure of bortezomib to cure acute antibody-mediated rejection in a non-compliant renal transplant patient. Allain-Launay, E; Blancho, G; Blin, N; Cesbron, A; Moreau, A; Roussey, G; Ryckewaert, A, 2013)	2.22
"Bortezomib (Btz) has emerged as a standard of care in the treatment of patients with multiple myeloma (MM), but Btz-induced peripheral neuropathy (PNP) has a particularly negative impact on patients' quality of life. "	( Bortezomib administered subcutaneously is well tolerated in bortezomib-based combination regimens used in patients with multiple myeloma. Drach, J; Drach-Schauer, B; Eder, S; Lamm, W, 2013)	3.28
"Bortezomib has demonstrated substantial activity in the treatment of patients with multiple myeloma and is widely incorporated into treatment strategies across the different settings. "	( The effects of bortezomib on bone disease in patients with multiple myeloma. Malard, F; Mohty, B; Mohty, M; Moreau, P; Savani, B; Terpos, E, 2014)	2.2
"Bortezomib has been known as the most promising anti-cancer drug for multiple myeloma (MM). "	( Establishment and characterization of bortezomib-resistant U266 cell line: constitutive activation of NF-κB-mediated cell signals and/or alterations of ubiquitylation-related genes reduce bortezomib-induced apoptosis. Ahn, KS; Bae, EK; Choi, JH; Jung, WJ; Lee, C; Park, J; Yoon, SS, 2014)	2.12
"Bortezomib therapy has shown promising clinical activity in mantle cell lymphoma (MCL), but the development of resistance to proteasome inhibition may limit its efficacy. "	( Synergistic antitumor activity of lenalidomide with the BET bromodomain inhibitor CPI203 in bortezomib-resistant mantle cell lymphoma. Balsas, P; Campo, E; Colomer, D; Martínez, A; Montraveta, A; Moros, A; Normant, E; Pérez-Galán, P; Rodríguez, V; Roué, G; Saborit-Villarroya, I; Sandy, P; Wiestner, A, 2014)	2.07
"Bortezomib therapy has been proven successful for the treatment of relapsed and/or refractory multiple myeloma (MM). "	( Down-regulation of CD9 by methylation decreased bortezomib sensitivity in multiple myeloma. Du, H; Hu, X; Huang, J; Jiang, H; Xuan, H, 2014)	2.1
"Bortezomib has been used to reduce HLA antibody in patients either before transplantation or as treatment for antibody-mediated rejection (AMR). "	( Differential effect of bortezomib on HLA class I and class II antibody. Leffell, MS; Montgomery, RA; Philogene, MC; Sikorski, P; Zachary, AA, 2014)	2.16
"Bortezomib has significantly improved multiple myeloma (MM) response rates, but strategies for choosing bortezomib-based regimens for initial MM therapy are not standardized. "	( The choice of regimens based on bortezomib for patients with newly diagnosed multiple myeloma. Cai, Z; Fu, J; Han, X; He, J; Huang, H; Huang, W; Li, L; Shi, J; Wei, G; Wu, W; Xie, W; Yang, L; Ye, X; Zhang, J; Zhang, X; Zhao, Y; Zheng, G; Zheng, W, 2014)	2.13
"Bortezomib has been proposed to stimulate autophagy, but scientific observations did not always support this."	( Bortezomib enhances cancer cell death by blocking the autophagic flux through stimulating ERK phosphorylation. Chao, A; Chen, GC; Chuang, WC; Huang, WP; Kao, C; Lai, CH; Lin, CY; Tsai, CL; Wang, HS; Wang, TH, 2014)	2.57
"Bortezomib has been widely used for the treatment of MM with encouraging results, but TLS seems to occur more frequently in patients with MM receiving bortezomib than in patients receiving other conventional agents."	( Management of tumor lysis syndrome in patients with multiple myeloma during bortezomib treatment. Gao, W; Jian, Y; Wang, L; Wu, Y; Yang, G; Zuo, L, 2015)	1.37
"Bortezomib has antitumor activity on a variety of hematological malignancies and exhibits a number of favorable immunomodulatory effects that include inhibition of dendritic cells."	( Short Course of Post-Transplantation Cyclophosphamide and Bortezomib for Graft-versus-Host Disease Prevention after Allogeneic Peripheral Blood Stem Cell Transplantation Is Feasible and Yields Favorable Results: A Phase I Study. Al-Homsi, AS; Bogema, M; Cole, K; Duffner, U; Mageed, A; Williams, S, 2015)	1.38
"Bortezomib has become a cornerstone in the treatment of AL amyloidosis. "	( Translocation t(11;14) is associated with adverse outcome in patients with newly diagnosed AL amyloidosis when treated with bortezomib-based regimens. Benner, A; Bochtler, T; Goldschmidt, H; Granzow, M; Hegenbart, U; Ho, AD; Hose, D; Jauch, A; Kimmich, C; Kunz, C; Schönland, SO; Seckinger, A, 2015)	2.07
"Bortezomib treatment has shown upregulated DIABLO and NF-κBIB (a NF-κB inhibitor) and downregulated NF-κB1, NF-κB2, and BIRC1 gene expressions. "	( Bortezomib and Arsenic Trioxide Activity on a Myelodysplastic Cell Line (P39): A Gene Expression Study. Canesastraro, M; Di Raimondo, F; Galimberti, S; Nagy, B; Palumbo, G; Petrini, M; Savlı, H; Sünnetçi, D, 2015)	3.3
"Bortezomib has been increasingly used especially in renal related indications such as multiple myeloma and monoclonal gammopathy of renal significance."	( Bortezomib-induced acute interstitial nephritis. Angioi, A; Cheungpasitporn, W; Cornell, LD; Fervenza, FC; Leung, N; Rajkumar, SV; Sethi, S, 2015)	2.58
"Bortezomib (bort) has improved overall survival in patients with multiple myeloma (MM), but the majority of them develop drug resistance. "	( Halting pro-survival autophagy by TGFβ inhibition in bone marrow fibroblasts overcomes bortezomib resistance in multiple myeloma patients. Angelucci, E; Annese, T; Catacchio, I; Dammacco, F; De Veirman, K; Derudas, D; Desantis, V; Di Marzo, L; Frassanito, MA; Fumarulo, R; Maffia, M; Menu, E; Nico, B; Racanelli, V; Ria, R; Ribatti, D; Ruggieri, S; Vacca, A; Vanderkerken, K; Vergara, D, 2016)	2.1
"Bortezomib has been shown to induce apoptosis and inhibit cell growth of many cancer cells."	( Bortezomib-mediated downregulation of S-phase kinase protein-2 (SKP2) causes apoptotic cell death in chronic myelogenous leukemia cells. Bhat, AA; Iskandarani, A; Khan, MA; Krishnankutty, R; Kulinski, M; Kuttikrishnan, S; Mohammad, RM; Nasr, RR; Prabhu, KS; Siveen, KS; Uddin, S, 2016)	2.6
"Bortezomib has been used in adults for the reversal of antibody-mediated rejection; however, pediatric data are limited."	( Bortezomib in the treatment of antibody-mediated rejection in pediatric kidney transplant recipients: A multicenter Midwest Pediatric Nephrology Consortium study. Ashoor, I; Chen, A; Claes, D; Jandeska, S; Kizilbash, S; Matar, RB; Misurac, J; Sherbotie, J; Twombley, K; Verghese, P, 2017)	2.62
"Bortezomib has demonstrated significant activity in clinical trials, mainly against recurrent or newly diagnosed multiple myeloma (MM). "	( Bortezomib-induced peripheral neuropathy in multiple myeloma: a comprehensive review of the literature. Argyriou, AA; Iconomou, G; Kalofonos, HP, 2008)	3.23
"Bortezomib has been used in multiple myeloma and other lymphoid malignancies because of its antitumor activity."	( Antitumor activity of bortezomib alone and in combination with TRAIL in human acute myeloid leukemia. Adamo, L; Anastasi, G; Caruso, L; Conticello, C; Cupri, A; De Maria, R; Di Raimondo, F; Giuffrida, R; Giustolisi, R; Gulisano, M; Iannolo, G; Moschetti, G; Palumbo, GA; Vicari, L, 2008)	1.38
"Bortezomib has significantly advanced the treatment of patients with multiple myeloma (MM). "	( Bortezomib and the increased incidence of herpes zoster in patients with multiple myeloma. Do, YR; Joo, YD; Kim, BS; Kim, H; Kim, HJ; Kim, I; Kim, K; Kim, SJ; Kwon, JH; Lee, HJ; Lee, JH; Lee, NR; Lee, WS; Nam, SH; Shin, HJ; Sohn, SK; Suh, C; Won, JH; Yoon, SS, 2008)	3.23
"Bortezomib has been introduced recently in the therapy of multiple myeloma (MM), a disease that is frequently associated with progressive renal failure. "	( Bortezomib-induced survival signals and genes in human proximal tubular cells. Eder, S; Enrich, J; Hochegger, K; Mayer, B; Mayer, G; Perco, P; Pirklbauer, M; Rosenkranz, AR; Rudnicki, M; Sarközi, R; Schramek, H; Wiesinger, M, 2008)	3.23
"Bortezomib has recently become the new treatment standard for relapsed or refractory multiple myeloma. "	( Effects of combination treatment of bortezomib and dexamethasone in SCCHN cell lines depend on tumor cell specificity. Arnoldner, C; Baghi, M; Bisdas, S; Gstöttner, W; Hambek, M; Knecht, R; May, A; Wagenblast, J, 2008)	2.06
"Bortezomib therapy has become an important part of the standard of care for patients with relapsed multiple myeloma, and preliminary clinical evidence suggests that bortezomib retreatment in patients previously treated with the drug may prolong disease control. "	( Utility of bortezomib retreatment in relapsed or refractory multiple myeloma patients: a multicenter case series. Battleman, DS; LeBlanc, A; Richardson, PG; Schuster, M; Walters, IB; Wolf, J, 2008)	2.18
"Bortezomib has offered some patients with relapsed and refractory disease an opportunity for prolonged survival."	( Clinical and immunohistochemical features associated with a response to bortezomib in patients with multiple myeloma. Dawson, MA; Donovan, M; Hertzberg, M; Horvath, N; McLean, CA; Monaghan, K; Opat, SS; Prince, HM; Roberts, AW; Spencer, A; Taouk, Y; Zammit, M, 2009)	1.31
"Bortezomib has been shown to induce synergistic activity when combined with other antineoplastic agents."	( The combined therapeutic effects of bortezomib and fenretinide on neuroblastoma cells involve endoplasmic reticulum stress response. Brignole, C; Carosio, R; Cilli, M; Di Paolo, D; Galietta, LJ; Loi, M; Marimpietri, D; Nico, B; Pagnan, G; Pastorino, F; Pezzolo, A; Piccardi, F; Pistoia, V; Ponzoni, M; Ribatti, D, 2009)	1.35
"Bortezomib has been shown to be a safe and efficacious for the treatment of relapsed and refractory multiple myeloma (MM). "	( Safety and efficacy results from an international expanded access programme to bortezomib for patients with relapsed and/or refractory multiple myeloma: a subset analysis of the Australian and New Zealand data of 111 patients. Butcher, BE; Cannell, P; Horvath, N; Mikhael, JR; Prince, HM; Quach, H, 2009)	2.02
"Bortezomib has anticancer effects on neuroblastoma cells in vitro and in a metastatic xenograft model. "	( Effects of bortezomib on human neuroblastoma cells in vitro and in a metastatic xenograft model. Haane, C; Nehmann, N; Schumacher, U; Valentiner, U, 2009)	2.19
"Bortezomib has proven to be effective as single agent in myeloma patients. "	( Bortezomib plus dexamethasone is highly effective in relapsed and refractory myeloma patients but responses are short-lived. Algarotti, A; Corso, A; Lazzarino, M; Mangiacavalli, S; Pascutto, C; Pica, GM; Varettoni, M; Zappasodi, P, 2009)	3.24
"Bortezomib has shown significant efficacy in the treatment of patients with relapsed multiple myeloma (MM) and is generally well tolerated. "	( Multiple significant bortezomib-related toxicities in one patient: case report and literature review. Knopf, KB; Moretto, JC; Waller, JM, 2009)	2.11
"Bortezomib has minimal activity as a single-agent in the treatment of recurrent platinum-sensitive EOC/PPC. "	( A phase II evaluation of bortezomib in the treatment of recurrent platinum-sensitive ovarian or primary peritoneal cancer: a Gynecologic Oncology Group study. Aghajanian, C; Blessing, JA; Darcy, KM; DeGeest, K; Mannel, RS; Reid, G; Riordan, W; Rotmensch, J; Rubin, SC; Schilder, RJ, 2009)	2.1
"Bortezomib has shown synergistic effects with melphalan and no prolonged hematologic toxicity."	( Bortezomib and high-dose melphalan as conditioning regimen before autologous stem cell transplantation in patients with de novo multiple myeloma: a phase 2 study of the Intergroupe Francophone du Myelome (IFM). Araujo, C; Attal, M; Avet-Loiseau, H; Caillot, D; Danho, C; Dib, M; Dorvaux, V; Fruchart, C; Garderet, L; Harousseau, JL; Hulin, C; Huynh, A; Kolb, B; Lenain, P; Marit, G; Mary, JY; Mathiot, C; Moreau, P; Pégourié, B; Randriamalala, E; Roussel, M; Royer, B; Stoppa, AM, 2010)	2.52
"Bortezomib has been shown to be highly active in MM patients with RI."	( Safety and efficacy of bortezomib-based regimens for multiple myeloma patients with renal impairment: a retrospective study of Italian Myeloma Network GIMEMA. Baldini, L; Boccadoro, M; Bringhen, S; Callea, V; Casulli, AF; Catalano, L; Cavo, M; Ciolli, S; Di Raimondo, F; Galimberti, S; Gentile, M; Mannina, D; Mele, G; Morabito, F; Musto, P; Offidani, M; Palmieri, S; Palumbo, A; Petrucci, MT; Pinotti, G; Piro, E; Tosi, P, 2010)	1.39
"Bortezomib has been shown to affect multiple cellular pathways and levels of numerous intracellular proteins, including targets of importance in hematologic malignancies. "	( Enhancing activity and overcoming chemoresistance in hematologic malignancies with bortezomib: preclinical mechanistic studies. Czuczman, MS; Reddy, N, 2010)	2.03
"Bortezomib has been shown to strongly induce osteoblast differentiation and elevate the levels of osteoblast-related differentiation markers in the serum of patients with myeloma."	( The proteasome inhibitor bortezomib inhibits FGF-2-induced reduction of TAZ levels in osteoblast-like cells. Aoki, K; Eda, H; Kato, S; Marumo, K; Ohkawa, K; Okawa, Y; Takada, K; Tanaka, T, 2010)	1.39
"Bortezomib has no adverse effect on stem cell harvesting and engraftment, making it a feasible treatment option in transplantation-eligible patients."	( Bortezomib as a treatment option in patients with Waldenström macroglobulinemia. Chen, C; Dimopoulos, MA; Gavriatopoulou, M; Kastritis, E; Treon, SP, 2010)	2.52
"Bortezomib has been successfully used in the treatment of multiple myeloma and has been proposed as a potential treatment for chronic lymphocytic leukemia. "	( Role of NOXA and its ubiquitination in proteasome inhibitor-induced apoptosis in chronic lymphocytic leukemia cells. Baou, M; Butterworth, M; Cohen, GM; Dinsdale, D; Dyer, MJ; Eldering, E; Kohlhaas, SL; Majid, A; Vogler, M; Walewska, R, 2010)	1.8
"Bortezomib has proven to be successful in the treatment of multiple myeloma, and its mechanism indicates that it may have merit in autoimmune or other plasmacytic disorders."	( Treatment with bortezomib of a patient having hyper IgG4 disease. Colby, TV; Fonseca, R; Khan, ML; Viggiano, RW, 2010)	1.43
"Bortezomib has been well tolerated."	( The fate of anti-HLA antibody among renal transplantation recipients treated with bortezomib. Dagher, NN; Lonze, BE; Montgomery, RA; Segev, DL; Simpkins, CE; Singer, AL; Zachary, AA, 2009)	1.3
"Bortezomib has proven to be active in patients with multiple myeloma (MM), including elderly patients. "	( Bortezomib plus intermediate-dose dexamethasone and thalidomide in elderly untreated patients with multiple myeloma: a Chinese experience. Chen, F; Chen, H; Guo, H; Jiang, Y; Lu, M; Mao, J; Qian, X; Shen, Y; Sun, C; Sun, H; Xia, J; Yang, G; Zhou, X; Zhuang, Y, 2010)	3.25
"Bortezomib has preclinical and clinical in B-cell lymphomas, both alone and in combination with other agents. "	( Phase 1 trial of bortezomib plus R-CHOP in previously untreated patients with aggressive non-Hodgkin lymphoma. Cheung, YK; Coleman, M; Elstrom, R; Furman, RR; LaCasce, AS; Leonard, JP; Martin, P; Ruan, J; Vose, JM, 2010)	2.14
"Bortezomib has shown single agent activity of 33% in relapsed MCL and has an additive/synergistic effect in vitro when combined with drugs currently used to treat MCL."	( Phase I trial of bortezomib in combination with rituximab-HyperCVAD alternating with rituximab, methotrexate and cytarabine for untreated aggressive mantle cell lymphoma. Fayad, LE; Feldman, T; Ford, P; Goldberg, S; Goy, A; Hartig, K; Kwak, LW; McLaughlin, P; Pecora, A; Pro, B; Rodriguez, A; Romaguera, JE; Smith, J; Wang, M; Weaver, P, 2010)	1.42
"Bortezomib has also been successfully used several times in heavily pre-treated patients with myeloma relapse or progression after allogeneic stem cell transplantation."	( [Bortezomib in multiple myeloma patients after allogeneic stem cell transplantation]. Vokurka, S, 2010)	1.99
"Bortezomib has shown a positive clinical benefit either alone or as a part of combination therapy to induce chemo-/radio-sensitization or overcome drug resistance."	( Bortezomib as the first proteasome inhibitor anticancer drug: current status and future perspectives. Chen, D; Dou, QP; Frezza, M; Kanwar, J; Schmitt, S, 2011)	2.53
"Bortezomib has received US Federal Drug Administration approval for the treatment of the hematologic malignancies such as multiple myeloma and mantle cell lymphoma."	( Targeting the proteasome with bortezomib in multiple myeloma: update on therapeutic benefit as an upfront single agent, induction regimen for stem-cell transplantation and as maintenance therapy. Annunziata, CM; Burris, J; Driscoll, JJ, 2012)	1.39
"Bortezomib has shown antihemostatic effects in patients with relapsed or refractory MM, which supports that it exerts antithrombotic actions and thus potentially provides a protective effect in combination with regimens with an elevated VTE risk."	( Low venous thromboembolic risk with bortezomib in multiple myeloma and potential protective effect with thalidomide/lenalidomide-based therapy: review of data from phase 3 trials and studies of novel combination regimens. Fink, L; Tricot, G; Zangari, M; Zhan, F, 2011)	1.37
"Bortezomib has demonstrated promising activity in patients with follicular lymphoma (FL). "	( Bortezomib ADDED to R-CVP is safe and effective for previously untreated advanced-stage follicular lymphoma: a phase II study by the National Cancer Institute of Canada Clinical Trials Group. Basi, S; Cantin, G; Chen, BE; Couban, S; Crump, M; Djurfeldt, M; Gascoyne, RD; Imrie, K; Lemieux, B; MacDonald, D; Rubin, S; Rubinger, M; Sehn, LH; Shepherd, L; Sussman, J, 2011)	3.25
"Bortezomib has been reported to impair tumor growth by also inhibiting HIF-1α."	( Bortezomib represses HIF-1α protein expression and nuclear accumulation by inhibiting both PI3K/Akt/TOR and MAPK pathways in prostate cancer cells. Befani, CD; Bonanou, S; Hatzidaki, E; Liakos, P; Papandreou, CN; Patrikidou, A; Simos, G; Vlachostergios, PJ, 2012)	2.54
"Bortezomib has become an important backbone of frontline myeloma treatment. "	( Bortezomib for previously untreated multiple myeloma. Delforge, M, 2011)	3.25
"Bortezomib has potent chemo-/radio-sensitizing effects and can overcome traditional drug resistance in tumors when used in combination with potential chemotherapies."	( Advances in the understanding of mechanisms and therapeutic use of bortezomib. Dou, QP; Mujtaba, T, 2011)	1.33
"Bortezomib has shown great promise in the treatment of amyloid light-chain (AL) amyloidosis. "	( Cyclophosphamide, bortezomib, and dexamethasone therapy in AL amyloidosis is associated with high clonal response rates and prolonged progression-free survival. Foard, D; Gibbs, SD; Gillmore, JD; Hawkins, PN; Lachmann, HJ; Lane, T; Pinney, JH; Rannigan, L; Venner, CP; Wechalekar, AD; Whelan, CJ, 2012)	2.16
"Both bortezomib and metformin have been proposed as potential therapeutics in TSC."	( Therapeutic trial of metformin and bortezomib in a mouse model of tuberous sclerosis complex (TSC). Auricchio, N; Kwiatkowski, DJ; Malinowska, I; Manning, BD; Shaw, R, 2012)	1.11
"Bortezomib has demonstrated efficacy in patients with relapsed B-cell non-Hodgkin lymphoma (NHL) both alone and in combination with other agents; however, limited data exist regarding its toxicity in combination with common frontline therapies for indolent NHL. "	( A phase 1 dose escalation study of bortezomib combined with rituximab, cyclophosphamide, doxorubicin, modified vincristine, and prednisone for untreated follicular lymphoma and other low-grade B-cell lymphomas. Bumpers, K; Flowers, CR; Heffner, LT; Hutchison-Rzepka, A; Kaufman, JL; Khoury, HJ; King, N; Lechowicz, MJ; Lewis, C; Lonial, S; Shenoy, PJ; Sinha, R; Tighiouart, M, 2012)	2.1
"Bortezomib has also been incorporated into conditioning regimens before autologous stem cell transplantation, as well as into post-ASCT consolidation therapy, and in the maintenance setting."	( Proteasome inhibitors in multiple myeloma: 10 years later. Cavo, M; Harousseau, JL; Moreau, P; Orlowski, RZ; Palumbo, A; Richardson, PG; San Miguel, JF, 2012)	1.1
"Bortezomib has subsequently been approved for multiple myeloma as a second-line treatment on its own and as a first-line therapy in combination with an alkylating agent and a corticosteroid."	( Proteasome inhibitors. Cvek, B, 2012)	1.1
"Bortezomib has been used without much success in desensitization regimens, but we hypothesized that its use during induction may be helpful in targeting antibody production by long-lived plasma cells."	( High immunologic risk living donor kidney transplant using bortezomib in a novel induction regimen without acute antibody mediated rejection. Borja-Cacho, D; Chinnakotla, S; Dunn, TB; Finger, E; Kandaswamy, R; Kim, Y; Krefting, P; Manivel, C; Matas, A; Maurer, D; Noreen, H; Pruett, T; Tamayo, G; Verghese, P, 2011)	1.33
"Bortezomib therapy has proven successful for the treatment of relapsed/refractory, relapsed, and newly diagnosed multiple myeloma (MM); however, dose-limiting toxicities and the development of resistance limit its long-term utility. "	( A small molecule inhibitor of ubiquitin-specific protease-7 induces apoptosis in multiple myeloma cells and overcomes bortezomib resistance. Altun, M; Anderson, KC; Carrasco, R; Chauhan, D; Fulcinniti, M; Hideshima, T; Kessler, BM; Kingsbury, WD; Kodrasov, MP; Kumar, KG; Leach, CA; McDermott, JL; Minvielle, S; Munshi, N; Nicholson, B; Orlowski, R; Richardson, P; Shah, PK; Tian, Z; Weinstock, J; Zhou, B, 2012)	2.03
"Bortezomib has been widely used in the treatment of various cancers; however, its exact mechanisms of action are not fully understood, particularly in acute T lymphoblast leukemia (T-ALL). "	( Bortezomib suppresses the growth of leukemia cells with Notch1 overexpression in vivo and in vitro. Cheng, H; Hu, X; Huang, C; Lü, S; Song, X; Wang, J; Wang, L; Yang, J, 2012)	3.26
"Bortezomib has previously demonstrated activity in indolent lymphomas including follicular lymphoma with response rate ranging from 13% to 56%. "	( Efficacy and toxicity of two schedules of bortezomib in patients with recurrent or refractory follicular lymphoma: a randomised phase II trial from the Groupe d'Etude des Lymphomes de l'Adulte (GELA). Bosly, A; Bouabdallah, R; Boue, F; Bron, D; Casasnovas, O; Coiffier, B; Delarue, R; Feugier, P; Haioun, C; Offner, F; Ribrag, V; Tilly, H, 2013)	2.1
"Bortezomib has demonstrated activity with manageable toxicity in a variety of hematologic malignancies in addition to MM, including leukemia and non-Hodgkin's lymphoma."	( Proteasome inhibition in hematologic malignancies. Anderson, K; Hideshima, T; Mitsiades, C; Richardson, PG, 2004)	1.04
"Bortezomib has been studied extensively in vitro and in vivo, and anticancer activity has been seen in cell and animal models for several solid tumor types, including prostate cancer."	( Bortezomib as a potential treatment for prostate cancer. Logothetis, CJ; Papandreou, CN, 2004)	2.49
"Bortezomib has recently shown significant preclinical and clinical activity in several cancers, confirming the therapeutic value of proteasome inhibition in human malignancy."	( Proteasome inhibition as a novel therapeutic target in human cancer. Anderson, KC; Hideshima, T; Rajkumar, SV; Richardson, PG, 2005)	1.05
"Bortezomib has been shown to be a substrate of several cytochrome P450 isoenzymes using in vitro systems."	( Pharmacology, pharmacokinetics, and practical applications of bortezomib. Davidson, T; Schwartz, R, 2004)	1.29
"Bortezomib has minimal activity in soft tissue sarcoma as a single agent. "	( A multicenter Phase II study of bortezomib in recurrent or metastatic sarcomas. Antonescu, CR; Kraft, AS; Maki, RG; Scheu, K; Schwartz, GK; Wadler, S; Wright, JJ; Yamada, J, 2005)	2.05
"Bortezomib therapy has set an outstanding example of translational research in the field of oncology."	( Proteasome inhibitor therapy in multiple myeloma. Anderson, KC; Chauhan, D; Hideshima, T; Mitsiades, C; Richardson, P, 2005)	1.05
"Bortezomib has been investigated in combination with taxanes, gemcitabine, carboplatin, histone deactylase inhibitors, and other molecularly targeted agents in various NSCLC cell lines."	( Preclinical data with bortezomib in lung cancer. Schenkein, DP, 2005)	1.36
"Bortezomib has demonstrated in vitro chemotherapy- and RT-sensitizing properties as well as single-agent activity in lung cancer."	( The potential role of bortezomib in combination with chemotherapy and radiation in non-small-cell lung cancer. Edelman, MJ, 2005)	1.36
"Bortezomib therapy has proven successful for the treatment of relapsed and/or refractory multiple myeloma (MM); however, prolonged treatment is associated with toxicity and development of drug resistance. "	( A novel orally active proteasome inhibitor induces apoptosis in multiple myeloma cells with mechanisms distinct from Bortezomib. Anderson, KC; Berkers, C; Catley, L; Chao, TH; Chauhan, D; Hideshima, T; Letai, A; Li, G; Mitsiades, C; Mitsiades, N; Neuteboom, ST; Nicholson, B; Ovaa, H; Palladino, MA; Podar, K; Richardson, P; Velankar, M; Yasui, H, 2005)	1.98
"Bortezomib has been found to inhibit AML blast survival."	( Acute myelogenous leukemia--microenvironment interactions: role of endothelial cells and proteasome inhibition. Abboud, CN; Bechelli, J; Lancet, JE; Liesveld, JL; Lu, C; Phillips, G; Rosell, KE, 2005)	1.05
"Bortezomib has been approved by the United States Food and Drug Administration for the treatment of relapsed or refractory multiple myeloma."	( Marked clinical activity of the proteasome inhibitor bortezomib in patients with follicular and mantle-cell lymphoma. O'Connor, OA, 2005)	1.3
"Bortezomib has demonstrated significant antitumor activity as a single agent in refractory and/or relapsed MM, with a significantly longer survival than with dexamethasone (1-year overall survival rate of 80% vs."	( A practical update on the use of bortezomib in the management of multiple myeloma. Bladé, J; Boccadoro, M; Cavenagh, J; Glasmacher, A; Jagannath, S; Lonial, S; Ludwig, H; Orlowski, RZ; San Miguel, J; Sonneveld, P, 2006)	1.34
"Bortezomib has shown synergy with melphalan in preclinical models. "	( Phase I/II trial assessing bortezomib and melphalan combination therapy for the treatment of patients with relapsed or refractory multiple myeloma. Adams, J; Berenson, JR; Jarutirasarn, SG; Lee, SP; Mapes, R; Morrison, B; Purner, M; Sadler, K; Schenkein, D; Swift, R; Vescio, RA; Wilson, J; Yang, HH, 2006)	2.07
"Bortezomib has the potential to play a significant role throughout the NHL treatment algorithm in the future."	( Proteasome inhibition with bortezomib: a new therapeutic strategy for non-Hodgkin's lymphoma. Coleman, M; Furman, RR; Leonard, JP, 2006)	1.35
"Bortezomib has been licensed to be used in relapsed and refractory multiple myeloma. "	( Life-threatening motor neurotoxicity in association with bortezomib. Devereux, S; Gupta, S; Mufti, GJ; Pagliuca, A; Schey, S, 2006)	2.02
"Bortezomib has been reported to down-regulate cytokine-induced expression of VCAM-1, a major ligand on bone marrow stromal cells for VLA-4; it inhibits the heterotypic adherence between the myeloma cells and stromal cells and blocks the signalling pathways of resistance to apoptosis."	( Bortezomib (Velcade)--a new therapeutic strategy for patients with refractory multiple myeloma. Goranov, SE; Goranova-Marinova, VS, 2005)	2.49
"Bortezomib has recently gained European Commission approval for the treatment of relapsed multiple myeloma on the basis of clinical trials demonstrating its efficacy, tolerability and superiority to high-dose dexamethasone."	( Bortezomib for multiple myeloma. Cavenagh, J; Joel, S; Oakervee, H; Popat, R, 2006)	2.5
"Bortezomib has shown significant activity in trials of patients with relapsed or refractory multiple myeloma; approximately one third of patients have shown significant improvement with bortezomib monotherapy in phase II and III clinical trials."	( Optimizing the efficacy and safety of bortezomib in relapsed multiple myeloma. Colson, K; Jagannath, S; Richardson, P, 2006)	1.33
"Bortezomib has modest single-agent activity in patients with relapsed or refractory advanced NSCLC using this schedule, with minor enhancement in combination with docetaxel. "	( Randomized phase II study of bortezomib alone and bortezomib in combination with docetaxel in previously treated advanced non-small-cell lung cancer. Akerley, W; Axelrod, R; Belt, R; Carbone, DP; Crawford, J; Fanucchi, MP; Fidias, P; Fossella, FV; Govindan, R; Kashala, O; Kelly, K; Limentani, SA; Natale, R; Raez, LE; Reimers, HJ; Ribeiro, M; Robert, F; Schiller, JH; Sheng, S, 2006)	2.07
"Bortezomib has the boronic acid moiety which improves the specificity of proteasome inhibition and can be used as non-beta-lactam-based beta-lactamase inhibitors."	( Pseudomembranous colitis following bortezomib therapy in a myeloma patient. Kim, CC; Kim, M; Kim, Y; Lee, DG; Lee, JW; Lee, S; Min, CK; Min, WS; Moon, SJ; Park, G, 2007)	1.34
"Bortezomib has efficacy in WM, but neurotoxicity can be dose limiting. "	( Bortezomib is active in patients with untreated or relapsed Waldenstrom's macroglobulinemia: a phase II study of the National Cancer Institute of Canada Clinical Trials Group. Chen, CI; Eisenhauer, E; Kouroukis, CT; Powers, J; Stadtmauer, E; Stewart, AK; Voralia, M; Walsh, W; White, D; Wright, JJ, 2007)	3.23
"Bortezomib has many cutaneous side effects including erythematous plaques or nodules, a generalized morbilliform erythema with ulcerations and fever, purpuric eruptions, leukocytoclastic vasculitis, Sweet's syndrome, and folliculitis."	( A review of deferasirox, bortezomib, dasatinib, and cyclosporine eye drops: possible uses and known side effects in cutaneous medicine. Scheinfeld, N, 2007)	1.36
"Bortezomib has minimal activity in patients with HRPC and is unlikely to make any impact on treatment efficacy."	( Weekly docetaxel and bortezomib as first-line treatment for patients with hormone-refractory prostate cancer: a Minnie Pearl Cancer Research Network phase II trial. Barton, J; Gould, B; Greco, FA; Hainsworth, JD; Meluch, AA; Meng, C; Simons, L; Spigel, DR, 2007)	1.38
"Bortezomib has no detectable effect on expression of TRAIL receptor DR4/DR5 in these two cell lines."	( Bortezomib induces caspase-dependent apoptosis in Hodgkin lymphoma cell lines and is associated with reduced c-FLIP expression: a gene expression profiling study with implications for potential combination therapies. Hsi, ED; Kung, J; Peng, X; Qiu, W; Yegappan, M; Yen-Lieberman, B; Zhao, X, 2008)	2.51
"Bortezomib has been found to possess remarkable activity, especially in combination with other chemotherapeutic agents, in relapsed/refractory and newly diagnosed MM, as well as in patients presenting adverse prognostic factors."	( New therapies in multiple myeloma. Dammacco, F; Merchionne, F; Perosa, F, 2007)	1.06
"Bortezomib has demonstrated significant anti-myeloma activity as a single agent in refractory/relapsed MM."	( Bortezomib in multiple myeloma. Mateos, MV; San Miguel, JF, 2007)	2.5
"Bortezomib has been shown to exert inhibitory effects on NFkappaB activity."	( Alkylating agents induce activation of NFkappaB in multiple myeloma cells. Baumann, P; Mandl-Weber, S; Oduncu, F; Schmidmaier, R, 2008)	1.07
"Bortezomib has been approved for the treatment of multiple myeloma and mantle cell lymphoma."	( Proteasome inhibitor Bortezomib induces cell cycle arrest and apoptosis in cell lines derived from Ewing's sarcoma family of tumors and synergizes with TRAIL. Chaudhary, PM; Lu, G; Punj, V, 2008)	1.39
"Bortezomib has shown significant activity in myeloma. "	( Bortezomib, doxorubicin and dexamethasone in advanced multiple myeloma. Avonto, I; Boccadoro, M; Bringhen, S; Bruno, B; Callea, V; Caravita, T; Cascavilla, N; Falcone, A; Gay, F; Magarotto, V; Morabito, F; Musto, P; Palumbo, A; Pescosta, N; Ruggeri, M, 2008)	3.23
"Bortezomib has profound effects on tumor cell growth inhibition and induction of apoptosis in human gastric cancer cells, suggesting that bortezomib may be an effective therapeutic drug for patients with gastric cancer."	( Effects of the proteasome inhibitor bortezomib alone and in combination with chemotherapeutic agents in gastric cancer cell lines. Bae, SH; Hyun, MS; Kim, MK; Lee, KH; Ryoo, HM; Sin, JI, 2008)	1.34
"Bortezomib has presently become a significant rescue treatment in multiple myeloma (MM) due to its observed effectiveness and safety in multicenter trials. "	( [Bortezomib in relapsed or refractory multiple myeloma: results in a cohort of 39 patients]. Aguirre Errasti, C; Alonso Alonso, JJ; Barreiro García, JG; Cánovas Fernández, A, 2008)	2.7
"Bortezomib has improved response rates, overall survival, and time to progression in relapsed or refractory disease, both as a single agent and as part of combination regimens. "	( Bortezomib in multiple myeloma. Dimopoulos, MA; Roussou, M; Terpos, E, 2008)	3.23

Excerpt	Reference	Relevance
"Bortezomib plays an important role in the treatment of MM."	( Clinical Observation and Pharmacoeconomic Evaluations of Original Research Drug and Generic Drug Bortezomib in the Treatment of Multiple Myeloma. Chen, Z; Li, B; Liang, Y; Liu, A; Liu, L; Zhang, Y; Zhu, Y, 2022)	1.66
"Bortezomib was found to inhibit glioma growth and improved TMZ chemotherapy efficacy, probably via down-regulating the FOXM1-Survivin axis. "	( Bortezomib inhibits growth and sensitizes glioma to temozolomide (TMZ) via down-regulating the FOXM1-Survivin axis. Chen, JX; Du, L; Huang, GH; Li, QR; Lv, SQ; Tang, JH; Xiang, Y; Xu, QF; Yang, L; Zhang, ZX; Zhou, Z; Zhu, LR, 2019)	3.4
"Bortezomib could increase the apoptosis of U266 and RPMI8226 cells."	( ANXA7 promotes the cell cycle, proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells by up-regulating CDC5L. Guo, D; Hong, L; Huang, H; Jiang, Y; Liu, H; Lu, L; Sha, Y; Zhang, C; Zhang, J, 2020)	1.28
"Bortezomib exhibited a lower inhibitory capacity on the caspase- and trypsin-like activity of proteasomes from G/G individuals."	( Proteasome Subunit Beta Type 1 P11A Polymorphism Is a New Prognostic Marker in Multiple Myeloma. Andrikovics, H; Balassa, K; Homolya, L; Kiss, KP; Kosóczki, É; Kövy, P; Masszi, T; Meggyesi, N; Mikala, G; Szabó, E; Szombath, G; Tegze, B; Tordai, A; Varga, G, 2017)	1.18
"A bortezomib-induced increase in density of TRPV1- and CGRP-immunoreactive innervation in the dorsal horn was also observed."	( Bortezomib treatment produces nocifensive behavior and changes in the expression of TRPV1, CGRP, and substance P in the rat DRG, spinal cord, and sciatic nerve. Boi, M; Carozzi, VA; Cavaletti, G; Chiorazzi, A; Del Fiacco, M; Dorsey, SG; Marmiroli, P; Melis, T; Meregalli, C; Picci, C; Poddighe, L; Quartu, M; Renn, CL; Serra, MP, 2014)	2.4
"Bortezomib did not inhibit tripeptidyl peptidase 2 and only weakly inhibited cellular aminopeptidase activity, as did some of the other proteasome inhibitors."	( Proteasome inhibitors alter levels of intracellular peptides in HEK293T and SH-SY5Y cells. Castro, LM; Dasgupta, S; Dulman, R; Ferro, ES; Fricker, LD; Schmidt, M; Yang, C, 2014)	1.12
"At a bortezomib dose lower than that in other combination therapy studies, antitumor activity was observed (phase 1)."	( Phase 1/2 study of cyclin-dependent kinase (CDK)4/6 inhibitor palbociclib (PD-0332991) with bortezomib and dexamethasone in relapsed/refractory multiple myeloma. Badros, AZ; Chanan-Khan, AA; Chen-Kiang, S; Costa, LJ; Di Liberto, M; Ely, SA; Haideri, NA; Hess, G; Huang, X; Jayabalan, D; Jiang, Y; Kim, ST; Lentzsch, S; Niesvizky, R; Raab, MS; Randolph, S; Singhal, SB; Spicka, I; Stadtmauer, EA; Tarantolo, S; Vij, R; Yacoub, A; Zonder, JA, 2015)	1.09
"Bortezomib can inhibit the proliferation of DCs in a dose- and time-dependent manner."	( Bortezomib inhibits bone marrow-derived dendritic cells. Liang, Y; Liu, H; Wang, Y; Wu, D; Zhang, Y, 2015)	2.58
"Bortezomib could inhibit the proliferation of Jurkat and Raji cells and induce their apoptosis with time-and dose-dependent manner. "	( [Effect of Bortezomib on Proliferation, Apoptosis and SHP-2 Gene Expression of Lymphoma Cells]. Jiang, LC; Luo, JM, 2015)	2.25
"Bortezomib can inhibit the proliferation and induc the apoptosis of Jurkat and Raji cells obviously, upregulate the expression of SHP-2 mRNA, suggesting that the SHP-2 may participate in regulation of bortezomib induced apoptosis of Jurkat cells and Raji cells."	( [Effect of Bortezomib on Proliferation, Apoptosis and SHP-2 Gene Expression of Lymphoma Cells]. Jiang, LC; Luo, JM, 2015)	2.25
"Bortezomib-treated cells activate the cytoprotective heat shock response (HSR), including upregulation of heat shock proteins (HSPs)."	( Bortezomib-induced heat shock response protects multiple myeloma cells and is activated by heat shock factor 1 serine 326 phosphorylation. Bahlis, NJ; Boise, LH; Jaye, DL; Lonial, S; Nooka, AK; Shah, SP, 2016)	2.6
"Bortezomib can increase the incidence of herpes zoster regardless of disease duration, previous treatments, and concomitantly administered drugs. "	( Bortezomib and the increased incidence of herpes zoster in patients with multiple myeloma. Do, YR; Joo, YD; Kim, BS; Kim, H; Kim, HJ; Kim, I; Kim, K; Kim, SJ; Kwon, JH; Lee, HJ; Lee, JH; Lee, NR; Lee, WS; Nam, SH; Shin, HJ; Sohn, SK; Suh, C; Won, JH; Yoon, SS, 2008)	3.23
"Bortezomib can inhibit proliferation and induce apoptosis of HL-60/ADM cells and fresh refractory/relapse acute leukemia cells, especially combined with HT or As2O3."	( [In vitro effect of bortezomib alone or in combination with harringtonine or arsenic trioxide on proliferation and apoptosis of multidrug resistant leukemia cells]. Cai, YX; Fu, YB; Li, L; Meng, FY; Sun, QX, 2008)	2.11
"Bortezomib might inhibit HL-60 cells adhension function by down-regulation of Pyk2 expression."	( [The influence of bortezomib on HL-60 cell function induced by all-trans retinoic acid plus bufalin and its mechanism]. Liu, YP; Ma, YJ; Qu, XJ, 2008)	1.4
"Bortezomib did not increase hematologic toxicity."	( Bortezomib and high-dose melphalan as conditioning regimen before autologous stem cell transplantation in patients with de novo multiple myeloma: a phase 2 study of the Intergroupe Francophone du Myelome (IFM). Araujo, C; Attal, M; Avet-Loiseau, H; Caillot, D; Danho, C; Dib, M; Dorvaux, V; Fruchart, C; Garderet, L; Harousseau, JL; Hulin, C; Huynh, A; Kolb, B; Lenain, P; Marit, G; Mary, JY; Mathiot, C; Moreau, P; Pégourié, B; Randriamalala, E; Roussel, M; Royer, B; Stoppa, AM, 2010)	2.52
"Bortezomib can inhibit migration of endothelial cell HMEC-1 by downregulating the expression of VEGF and Annexin A2, displaying a new mechanism of bortezomib for inhibition of tumor proliferation."	( [The effect of bortezomib on migration of endothelial cells and angiogenesis]. Jiang, M; Ruan, CG; Xie, LQ; Xue, LX, 2010)	2.16
"Bortezomib can inhibit the proliferation of K562 cells, and induce apoptosis by down-regulating the expression of XIAP, providing the laboratory evidence for the targeted therapy in acute leukemia."	( [Effect of proteasome inhibitor bortezomib on proliferation, apoptosis and XIAP expression in K562 cells]. Chen, SM; Cui, XY; Han, XF; Ling, Z; Shao, M; Sun, L; Wang, F; Zhang, H, 2011)	2.1
"Bortezomib caused an increase in intracellular reactive oxygen species (ROS) and treatment with the ROS scavenger NAC inhibited phosphorylation of ATM leading to a decrease in the number of cells in G2-M phase."	( Bortezomib induces G2-M arrest in human colon cancer cells through ROS-inducible phosphorylation of ATM-CHK1. Heo, DS; Hong, SW; Hong, YS; Jin, DH; Kim, KP; Kim, SM; Kim, TW; Lee, JL; Lee, JS; Shin, JS; Yoon, DH, 2012)	2.54
"Bortezomib can inhibit the proliferation of HL-60 cells and reverse multidrug-resistance in the cells. "	( [Proliferation-inhibiting and multidrug-resistant reversing effect of bortezomib on human HL-60 cells]. Chen, WM; Chen, ZZ; Shang, J; Wei, TN; Wu, WB, 2012)	2.06
"Bortezomib could inhibit the degradation of IkappaBalpha in ATL cells, resulting in suppression of NF-kappaB and induction of cell death in ATL cells in vitro."	( Proteasome inhibitor, bortezomib, potently inhibits the growth of adult T-cell leukemia cells both in vivo and in vitro. Koya, Y; Matsuoka, M; Nosaka, K; Satou, Y; Toyokuni, S; Yasunaga, JI, 2004)	1.36
"Bortezomib can cause a predominately sensory axonal polyneuropathy. "	( An electrodiagnostic evaluation of the effect of pre-existing peripheral nervous system disorders in patients treated with the novel proteasome inhibitor bortezomib. Esseltine, D; MacGregor-Cortelli, B; Muzzy, J; O'Connor, OA; Schenkein, D; Scher, H; Slovin, S; Stubblefield, MD; Wright, J, 2006)	1.97
"Bortezomib did not inhibit expression of several other antiapoptotic proteins, including Bcl-2 and Bcl-XL."	( Bortezomib induces apoptosis of Epstein-Barr virus (EBV)-transformed B cells and prolongs survival of mice inoculated with EBV-transformed B cells. Cohen, JI; Kawada, J; Pesnicak, L; Zou, P, 2007)	2.5

Excerpt	Reference	Relevance
"Bortezomib, used for the treatment of multiple myeloma, has been reported to induce potent neurotoxicity. "	( Inhibition of Neurotoxicity/Anticancer Activity of Bortezomib by Caffeic Acid and Chlorogenic Acid. Amano, S; Iijima, Y; Matsuda, R; Oishi, Y; Sakagami, H; Sano, M; Takeshima, H; Tamura, N; Uesawa, Y, 2022)	2.42
"Bortezomib-based treatment might benefit the PFS for patients with 3 copies but could not improve the adverse effect of ≥ 4 copies. 1q21+ was an independent risk factor for inferior PFS and OS in multivariate analysis (P < .001 and P = .028)."	( The Importance of FISH Signal Cut-off Value and Copy Number Variation for 1q21 in Newly Diagnosed Multiple Myeloma: Is it Underestimated? Feng, L; Gao, L; Huang, X; Lai, Y; Li, Y; Liu, Y; Lu, J; Wang, F; Wang, Z; Wen, L, 2022)	1.44
"Bortezomib treatment may adversely affect ovarian function by accelerating ovarian reserve depletion and changing ERα and PR hormone levels that can cause fertility problems in the long term."	( Bortezomib-Induced Ovarian Toxicity in Mice. Monsef, YA; Mutluay, D; Tenekeci, GY, 2022)	2.89
"Bortezomib treatment resulted in significantly higher reporting odds ratios (RORs) for cardiac failure, cardiac failure congestive, and atrial fibrillation. "	( Cardiac Adverse Events Associated with Multiple Myeloma Patients Treated with Proteasome Inhibitors. Endo, M; Fujiwara, M; Goto, M; Shimizu, T; Uchida, M, 2023)	2.35
"Bortezomib-containing treatment regimens were more frequently associated with TLS events than were other multiple myeloma treatment regimens (cytotoxic chemotherapy, lenalidomide, and thalidomide)."	( Tumor lysis syndrome associated with bortezomib: A post-hoc analysis after signal detection using the US Food and Drug Administration Adverse Event Reporting System. Hotta, Y; Kimura, K; Kondo, M; Nishikawa, R; Sanagawa, A; Tohkin, M, 2020)	1.55
"In bortezomib retreatment, overall response rate was 34.5%, median progression-free survival was 7.8 months (95% CI: 6.7-8.9), median duration of response was 10.5 months (95% CI: 8.0-13.0) and median overall survival was 20.3 months (95% CI: 17.9-22.7)."	( Bortezomib retreatment is effective in relapsed multiple myeloma patients - real-life clinical practice data. Brozova, L; Gregora, E; Hajek, R; Jelinek, T; Jungova, A; Maisnar, V; Minarik, J; Pour, L; Sevcikova, S; Spicka, I; Stork, M; Velichova, R, 2020)	2.51
"Bortezomib-based treatment in the real world setting still carries a high risk of toxicity in the elderly population."	( Bortezomib use and outcomes for the treatment of multiple myeloma. Hollingworth, S; Loke, C; McPherson, I; Mollee, P; Mutsando, H; Tomlinson, R; Walpole, E; Weston, H; Wong, P; Yue, M, 2020)	2.72
"2509 bortezomib-treated patients and 1445 patients in non-bortezomib-based control arms were included."	( A retrospective analysis of 3954 patients in phase 2/3 trials of bortezomib for the treatment of multiple myeloma: towards providing a benchmark for the cardiac safety profile of proteasome inhibition in multiple myeloma. Anderson, KC; Desai, A; Dow, E; Elliott, J; Esseltine, DL; Faber, EA; Feng, H; Francis, SA; Jobanputra, N; Laubach, JP; Lonial, S; Marquez, L; Mateos, MV; Moreau, P; Moslehi, JJ; Niculescu, L; Orlowski, RZ; Richardson, PG; Rosiñol, L; San Miguel, JF; Shi, H; Sonneveld, P; van de Velde, H; Voorhees, P, 2017)	1.15
"Bortezomib treatment markedly increased the baseline frequency of miniature excitatory postsynaptic currents (EPSCs), which was completely normalized by the NMDAR antagonist 2-amino-5-phosphonopentanoic acid (AP5)."	( Bortezomib induces neuropathic pain through protein kinase C-mediated activation of presynaptic NMDA receptors in the spinal cord. Chen, H; Chen, SR; Pan, HL; Xie, JD, 2017)	2.62
"BV6/Bortezomib co-treatment primarily triggers necroptosis or, alternatively, engages both apoptotic and necroptotic cell death."	( Identification of a synergistic combination of Smac mimetic and Bortezomib to trigger cell death in B-cell non-Hodgkin lymphoma cells. Abhari, BA; Bhatti, IA; Fulda, S, 2017)	1.17
"Bortezomib treatment is effective in MM, but can be complicated with neurological side effects."	( Bortezomib-Induced Muscle Toxicity in Multiple Myeloma. Guglielmi, V; Malatesta, M; Manganotti, P; Marini, M; Meneghini, V; Nowis, D; Paoli, L; Sadowski, R; Tinelli, M; Tomelleri, G; Vattemi, G; Wilczynski, GM, 2017)	2.62
"The bortezomib-treated group showed a complete dentin bridge with very few irregular tubules after 42 days."	( Bortezomib Facilitates Reparative Dentin Formation after Pulp Access Cavity Preparation in Mouse Molar. An, CH; An, SY; Gwon, GJ; Ha, JH; Jung, JK; Kim, JY; Kim, KR; Kwon, TY; Lee, Y; Neupane, S; Sohn, WJ, 2017)	2.38
"Bortezomib-based treatment can not improve the poor survival in patients with 1q21 amplification."	( [Prognostic Impact of 1q21 Amplification in Newly Diagnosed Multiple Myeloma Patients Receiving Bortezomib-Based First-Line Treatment]. Deng, P; Li, F; Li, P; Wei, YL; Zhou, YL, 2017)	1.39
"Bortezomib treatment significantly lowered the percentage of bone marrow plasma cells in SLE mice."	( Plasma Cell Depletion Attenuates Hypertension in an Experimental Model of Autoimmune Disease. Barati, MT; Powell, DW; Ryan, MJ; Taylor, EB; Turbeville, HR, 2018)	1.2
"Bortezomib-based treatment was successful in reverting plasma cell-rich acute rejection and stabilizing graft function, with graft survival of 90% at 2 years. "	( Management of Plasma Cell-Rich Acute Rejection in Living-Related Kidney Transplant: Role of Proteasome Inhibitor. Abbas, K; Aziz, T; Imam, M; Mubarak, M; Musharraf, W; Rizvi, AH; Zafar, MN, 2019)	1.96
"BD: bortezomib/doxorubicin treatment; CDK: cyclin-dependent kinases; CHCA: α-cyanohydroxycinnamic acid; IDP: intrinsically disordered proteins; IDR: intrinsically disordered regions; IPG: immobilized pI gradient; MALDI TOF/TOF: matrix-assisted laser desorption/ionization time-of-flight tandem mass-spectrometry; MM: multiple myeloma; ODC: ornithine decarboxylase; PI: proteasomal inhibitors; PSMA: alpha-type 20S proteasome subunits; PTMs: post-translational modifications; SDS-PAGE: sodium dodecylsulphate polyacrylamide gel electrophoresis; UIP: ubiquitin-independent proteasomal proteolysis."	( Combined treatment of human multiple myeloma cells with bortezomib and doxorubicin alters the interactome of 20S proteasomes. Barlev, NA; Fedorova, OA; Gorbach, DP; Kuzyk, VO; Mittenberg, AG; Shabelnikov, SV; Shatrova, AN, 2018)	1.29
"Bortezomib is standard treatment in AL amyloidosis (AL), but is contraindicated in patients with significant neuropathy. "	( Carfilzomib is an effective upfront treatment in AL amyloidosis patients with peripheral and autonomic neuropathy. Cheesman, S; Gillmore, JD; Hawkins, PN; Kyriakou, C; Lachmann, HJ; Mahmood, S; Manwani, R; Popat, R; Rabin, N; Sachchithanantham, S; Shah, R; Sharpley, F; Smith, M; Wechalekar, AD; Worthington, S; Yong, K, 2019)	1.96
"ST80/Bortezomib cotreatment upregulates BAG3 mRNA and protein levels in surviving cells in addition to triggering the accumulation of insoluble protein aggregates."	( BAG3 induction is required to mitigate proteotoxicity via selective autophagy following inhibition of constitutive protein degradation pathways. Fulda, S; Jung, M; Rapino, F, 2014)	0.86
"Bortezomib based treatment is a highly effective and safe option in MM patients with impaired renal function."	( [Clinical feature and efficacy of patients with multiple myeloma and renal impairment treated with bortezomib based chemotherapy]. An, G; Deng, SH; Feng, XY; Hao, M; Li, F; Qiu, LG; Sui, WW; Wang, YF; Xu, Y, 2013)	1.33
"Bortezomib retreatment regimen is demonstrated a higher response rate in patients who achieved deeper response in initial treatment, with no more adverse events."	( [The efficacy and safety analysis of bortezomib retreatment in 76 patients with relapsed/refractory multiple myeloma]. Du, J; Fan, JL; Fu, WJ; Hou, J; Jiang, H; Jin, LN; Lan, HF; Lu, J; Yuan, ZG; Zeng, TM; Zhang, CY; Zhou, F; Zhou, LL, 2013)	2.11
"Bortezomib-treated D307H mice had lower CPVT prevalence and less premature ventricular beats during peak exercise."	( The role of mutant protein level in autosomal recessive catecholamine dependent polymorphic ventricular tachycardia (CPVT2). Afek, A; Arad, M; Aravot, D; El-Ani, D; Eldar, M; Hochhauser, E; Issac, A; Katz, G; Kurtzwald-Josefson, E; Seidman, CE; Seidman, JG; Shainberg, A, 2013)	1.11
"Bortezomib treatment was repeated, and no pulmonary adverse reactions occurred."	( Development of acute pulmonary hypertension after bortezomib treatment in a patient with multiple myeloma: a case report and the review of the literature. Akosman, C; Eroglu, E; Ordu, C; Oyan, B, )	1.11
"Bortezomib treatment requires four visits to a chemotherapy unit in each 21-day cycle. "	( Authorising bortezomib treatment prior to reviewing haematology results: a step toward home administration. Cain, R; Waight, CC, 2014)	2.22
"Bortezomib plus 2ME treatment induces a higher level of cell death compared with treatment with bortezomib alone and increases mitochondrial ROS and Ca(2+) levels in KMS20 cells."	( Combination treatment with 2-methoxyestradiol overcomes bortezomib resistance of multiple myeloma cells. Han, J; Heo, HJ; Jeong, SH; Jeong, YJ; Kim, HK; Kim, N; Ko, KS; Ko, TH; Lee, SR; Rhee, BD; Song, IS; Youm, JB, 2013)	1.36
"Bortezomib treatment also resulted in decreased histone H3 and H4 acetylation and decreased occupancy of histone acetyltransferase, p300."	( The proteasome inhibitor bortezomib induces an inhibitory chromatin environment at a distal enhancer of the estrogen receptor-α gene. Alarid, ET; Bickford, B; Powers, GL; Rajbhandari, P; Solodin, NM, 2013)	1.41
"Bortezomib treatment after dendritic cell (DC) activation resulted in drastically elevated IL-1β production, whereas bortezomib treatment before DC activation inhibited IL-1β production, suggesting that the timing of bortezomib administration significantly affected IL-1β production by DCs."	( IL-1β and TLR4 signaling are involved in the aggravated murine acute graft-versus-host disease caused by delayed bortezomib administration. Cheng, Q; Jin, Y; Liang, Y; Liu, H; Ma, S; Wang, Y; Wu, D; Wu, Y; Zhang, Y; Zheng, D, 2014)	1.33
"Bortezomib treatment reduced the expression of YKL-40 and MMP to basal levels."	( Protective role of bortezomib in steatotic liver ischemia/reperfusion injury through abrogation of MMP activation and YKL-40 expression. Anderson, CD; Busch, RA; Chapman, WC; Dines, JN; Gunter, KL; Jia, J; Knolhoff, BL; Mohanakumar, T; Ramachandran, S; Sarma, NJ; Tiriveedhi, V; Upadhya, GA, 2014)	1.45
"Bortezomib, a current treatment option, inhibits angiogenesis by proteasome inhibition and is known to be effective in the treatment of MM."	( Acupuncture for neuropathic pain due to bortezomib in a patient with multiple myeloma. Aylı, M; Cevik, C; Mandıroğlu, S, 2014)	1.39
"Bortezomib treatment induced ER stress, evident by strong induction of Grp78, CHOP, PERK, and IRE1α (Western blot analysis) and the UPR (induction of hsp40, 70, and 90)."	( Bortezomib-induced unfolded protein response increases oncolytic HSV-1 replication resulting in synergistic antitumor effects. Bailey, Z; Bolyard, C; Caligiuri, MA; Cripe, TP; Eaves, D; He, S; Hurwitz, BS; Kaur, B; Old, M; Parris, DS; Rath, KS; Selvendiran, K; Yoo, JY; Yu, J; Yu, JG; Zhang, J, 2014)	2.57
"Bortezomib treatment causes long-term gonadal dysfunction in male mice. "	( Bortezomib treatment causes long-term testicular dysfunction in young male mice. Eriksson, E; Hou, M; Jahnukainen, K; Meinhardt, A; Sävendahl, L; Söder, O; Svechnikov, K, 2014)	3.29
"Bortezomib treatment, chemotherapy, International Staging System (ISS) stage I, and better performance status significantly correlated with survival benefit."	( The treatment outcome of multiple myeloma patients ineligible for hematopoietic transplantation--a single institutional experience in Taiwan. Chang, PY; Chao, TY; Chen, JH; Chen, YC; Dai, MS; Ho, CL; Huang, TC; Kao, WY; Wu, YY, 2015)	1.14
"Bortezomib treatment induced a progressively increasing hyperalgesia in rat which was accompanied by a significant reduction in sensory nerve conduction velocity (SNCV)."	( Spinal administration of mGluR5 antagonist prevents the onset of bortezomib induced neuropathic pain in rat. Bianchi, E; Cerretani, D; Ghelardini, C; Menicacci, C, 2014)	1.36
"Bortezomib pretreatment induced NOXA expression and downregulated c-FLIP, neither of which caused the TRAIL-sensitizing effect."	( Bortezomib sensitizes primary meningioma cells to TRAIL-induced apoptosis by enhancing formation of the death-inducing signaling complex. Bauer, M; Boehm, C; Ganten, TM; Haas, TL; Holland, H; Keller, M; Koschny, R; Koschny, T; Krupp, W; Meixensberger, J; Mueller, WC; Sinn, P; Sprick, MR; Walczak, H; Xu, LX, 2014)	2.57
"Bortezomib treatment of myeloma cells lead to ATG5 cleavage through a calpain-dependent manner while calpain inhibition or a calpain-insensitive Atg5 mutant promoted bortezomib-resistance."	( Bortezomib induces AMPK-dependent autophagosome formation uncoupled from apoptosis in drug resistant cells. Driscoll, JJ; Jaganathan, S; Malek, E; Vallabhapurapu, S, 2014)	2.57
"Bortezomib retreatment provided a similar depth and time to response as first-line therapy; however, as could be expected, the duration of response was shorter with retreatment. "	( Efficacy and safety of bortezomib-based retreatment at the first relapse in multiple myeloma patients: A retrospective study. Angermund, R; Corso, A; Couturier, C; Giraldo, P; Kotsianidis, I; Olie, R; Oriol, A, 2015)	2.17
"Bortezomib treatment did not cause any increase in nuclear foci containing phosphorylated histone H2AX, and knockdown of BRCA2 did not entail sensitivity to bortezomib, suggesting that the DNA repair function of BRCA1 may not be directly involved."	( Suppression of BRCA1 sensitizes cells to proteasome inhibitors. Bouwman, P; Greco, D; Gu, Y; Jonkers, J; Kuznetsov, SG; Saarela, J; Yadav, B, 2014)	1.12
"Bortezomib treatment led to GRP78 co-localization with proteotoxic protein aggregates, known as aggresomes."	( Molecular chaperone GRP78 enhances aggresome delivery to autophagosomes to promote drug resistance in multiple myeloma. Abd El-Azeem, HG; Abdel Malek, MA; Driscoll, JJ; Elgammal, SA; Jagannathan, S; Malek, E; Sayed, DM; Thabet, NM, 2015)	1.14
"ST80/Bortezomib cotreatment upregulates mRNA and protein expression of NIK, which is accompanied by an initial increase in histone H3 acetylation."	( NIK is required for NF-κB-mediated induction of BAG3 upon inhibition of constitutive protein degradation pathways. Abhari, BA; Fulda, S; Jung, M; Rapino, F, 2015)	0.87
"Bortezomib treatment has shown upregulated DIABLO and NF-κBIB (a NF-κB inhibitor) and downregulated NF-κB1, NF-κB2, and BIRC1 gene expressions. "	( Bortezomib and Arsenic Trioxide Activity on a Myelodysplastic Cell Line (P39): A Gene Expression Study. Canesastraro, M; Di Raimondo, F; Galimberti, S; Nagy, B; Palumbo, G; Petrini, M; Savlı, H; Sünnetçi, D, 2015)	3.3
"Bortezomib treatment did not affect the nuclear/cytoplasmic distribution of the non-structural S-segment protein (NSs); however, the ability of NSs to form nuclear filaments was abolished as a result of Bortezomib treatment."	( Characterizing the effect of Bortezomib on Rift Valley Fever Virus multiplication. Amaya, M; Bailey, C; Keck, F; Kehn-Hall, K; Narayanan, A; Roberts, B, 2015)	1.43
"Bortezomib rescue treatment was administered after a 42-year-old woman failed to respond to steroid pulse and plasmapheresis with intravenous immunoglobulin (IVIG)."	( Treatment of acute antibody-mediated rejection using bortezomib: a case report. Kim, JK; Kim, SM; Kim, YJ; Lee, JH; Oh, JS; Sin, YH, 2015)	1.39
"Bortezomib-based treatment resulted in a strong decrease of renal deposits."	( A mouse model recapitulating human monoclonal heavy chain deposition disease evidences the relevance of proteasome inhibitor therapy. Bender, S; Bonaud, A; Bridoux, F; Cogné, M; Delpy, L; Druilhe, A; Javaugue, V; Lacombe, C; Oblet, C; Quellard, N; Sirac, C; Srour, N; Touchard, G, 2015)	1.14
"Bortezomib treatment inhibited proteasome activities and increased ubiquitin-protein conjugates after sham and burn injury."	( Proteasome Inhibition After Burn Injury. Gamelli, RL; Kennedy, RH; LaPorte, HM; Majetschak, M; Vana, PG; Wong, YM, )	0.85
"Bortezomib treatment activated apoptosis, evidenced by increased expression of cleaved caspase-3 and cleaved PARP in both HeLa cells and CaSki cells. "	( Endoplasmic reticulum stress and autophagy participate in apoptosis induced by bortezomib in cervical cancer cells. Bai, C; Gao, L; Lu, D; Wu, X; Zhang, W; Zhang, Y, 2016)	2.1
"The bortezomib treatment of leukemic (HEL) and gastric cancer cells (BGC-823) led to significant inhibition of hTERT and telomerase expression, widespread dysregulation of shelterin protein expression, and telomere shortening, thereby triggering telomere dysfunction and DNA damage."	( Bortezomib-mediated down-regulation of telomerase and disruption of telomere homeostasis contributes to apoptosis of malignant cells. Björkholm, M; Ci, X; Jia, J; Kong, F; Li, B; Ma, X; Xu, D; Zheng, C, 2015)	2.34
"Bortezomib treatment significantly reduced VZV-specific CMI, and high baseline SFC counts in patients receiving this treatment without acyclovir prophylaxis were associated with a significantly increased risk for herpes zoster."	( Varicella-zoster virus-specific cell-mediated immunity and herpes zoster development in multiple myeloma patients receiving bortezomib- or thalidomide-based chemotherapy. Choe, PG; Kim, BS; Kim, I; Kim, JW; Koh, Y; Kwon, JH; Min, CK; Mun, YC; Nam, SH; Park, WB; Park, Y, 2015)	2.07
"Bortezomib/CX-4945 treatment inhibited NF-κB signaling in T-ALL cell lines and primary cells from T-ALL patients, but, intriguingly, in B-ALL cells the drug combination activated NF-κB p65 pro-apoptotic functions."	( Synergistic cytotoxic effects of bortezomib and CK2 inhibitor CX-4945 in acute lymphoblastic leukemia: turning off the prosurvival ER chaperone BIP/Grp78 and turning on the pro-apoptotic NF-κB. Bertacchini, J; Bertaina, A; Buontempo, F; Cappellini, A; Chiarini, F; Evangelisti, C; Locatelli, F; Lonetti, A; Martelli, AM; McCubrey, JA; Melchionda, F; Neri, LM; Orsini, E; Pession, A, 2016)	1.44
"Bortezomib effectively treated antibody-mediated renal transplantation rejection in this case study, but clinical trials with large sample sizes are still needed to explore clinical safety and tolerability."	( Bortezomib-based treatment of acute antibody-mediated rejection: a case report. Cai, M; Chen, CQ; Han, Y; Li, XL; Li, ZL; Shi, BY; Wang, Q; Xu, XG; Zhang, X; Zhang, ZM; Zhou, WQ, 2015)	2.58
"Bortezomib-treated patients were identified from consecutive cases managed at two UK referral centres."	( Bortezomib in the treatment of refractory thrombotic thrombocytopenic purpura. Blombery, PA; Cranfield, T; Dutt, T; McGuckin, S; Patriquin, CJ; Scully, M; Thomas, MR; Westwood, JP, 2016)	2.6
"Bortezomib-treated cells activate the cytoprotective heat shock response (HSR), including upregulation of heat shock proteins (HSPs)."	( Bortezomib-induced heat shock response protects multiple myeloma cells and is activated by heat shock factor 1 serine 326 phosphorylation. Bahlis, NJ; Boise, LH; Jaye, DL; Lonial, S; Nooka, AK; Shah, SP, 2016)	2.6
"Bortezomib treatment of HMECS induced dose- and time-dependent expression of HO-1 and COX-2 mRNA and protein, and triggered nuclear translocation of nuclear factor erythroid 2-related transcription factor (Nrf2)."	( Bortezomib Effects on Human Microvascular Endothelium in vitro. Sahni, A; Sahni, SK; Shah, R; Thomasson, ED, 2016)	2.6
"Bortezomib treatment showed clinical improvement or disease remission, which was accompanied by a partial NMDAR antibody titer decline in 4 of 5 patients. "	( Bortezomib for treatment of therapy-refractory anti-NMDA receptor encephalitis. Alexander, T; Hiepe, F; Kohler, S; Köhnlein, M; Meisel, A; Mengel, AM; Nümann, A; Prüss, H; Ruprecht, K; Scheibe, F, 2017)	3.34
"In bortezomib-treated 4T1HA tumor-bearing mice, CD4+T-cells showed increased IL-2 production, CD11c+ dendritic cells showed increased IL-12 and IL-15 production, and HA-specific activated CD8+T-cells showed enhanced expression of IFNγ, granzyme-B and transcription factor eomesodermin."	( Bortezomib augments lymphocyte stimulatory cytokine signaling in the tumor microenvironment to sustain CD8+T cell antitumor function. Dudimah, DF; Pellom, ST; Richmond, A; Shanker, A; Singhal, A; Thounaojam, MC; Uzhachenko, RV, 2017)	2.41
"Bortezomib treatment given intravenously twice weekly for 1 month (1.3 mg/m"	( Humoral Compensation after Bortezomib Treatment of Allosensitized Recipients. Burghuber, C; Gibby, A; Hong, JJ; Iwakoshi, N; Knechtle, S; Kwun, J; Manook, M, 2017)	1.47
"Bortezomib treatment inhibited hepatoma cell growth with IC(50) values between 2.4 and 7.7 nmol/L. "	( Direct and natural killer cell-mediated antitumor effects of low-dose bortezomib in hepatocellular carcinoma. Armeanu, S; Baltz, KM; Bitzer, M; Krusch, M; Lauer, UM; Salih, HR; Smirnow, I; Steinle, A; Weiss, TS, 2008)	2.02
"Bortezomib treatment significantly enhanced apoptosis with inhibition of nuclear RELA in three of four tumors, but other NF-kappaB subunits, ERK1/2, and STAT3 were variably or not affected, and tumor progression was observed within 3 months."	( Bortezomib-induced apoptosis with limited clinical response is accompanied by inhibition of canonical but not alternative nuclear factor-{kappa}B subunits in head and neck cancer. Allen, C; Arun, P; Chen, Z; Nottingham, L; Saigal, K; Van Waes, C, 2008)	2.51
"Bortezomib-treated animals showed significantly higher tumor burden compared with gemcitabine-treated and control animals, although bortezomib was locally active and induced a decrease of proteasome activity, which was most pronounced following the simultaneous administration of gemcitabine."	( Bortezomib is ineffective in an orthotopic mouse model of pancreatic adenocarcinoma. Märten, A; Mehrle, S; Schmidt, J; Serba, S; von Lilienfeld-Toal, M; Zeiss, N, 2008)	2.51
"Bortezomib treatment did not significantly alter plasma membrane amount of DR4 and DR5 but increased Apo2L/TRAIL-induced caspase-8 and caspase-3 activation."	( Cooperation between Apo2L/TRAIL and bortezomib in multiple myeloma apoptosis. Anel, A; Balsas, P; Galán-Malo, P; López-Royuela, N; Marzo, I; Naval, J, 2009)	1.35
"Bortezomib treatment increases the intracellular levels of several important apoptosis regulators that may mediate enhanced sensitivity to mapatumumab and lexatumumab."	( Mapatumumab and lexatumumab induce apoptosis in TRAIL-R1 and TRAIL-R2 antibody-resistant NSCLC cell lines when treated in combination with bortezomib. Carrell, JA; Humphreys, R; Luster, TA; McCormick, K; Sun, D, 2009)	1.28
"In bortezomib-treated HL-60/ADM cells, the proliferation inhibition rate and apoptotic cells increased in a time- and dose-dependent manner. "	( [In vitro effect of bortezomib alone or in combination with harringtonine or arsenic trioxide on proliferation and apoptosis of multidrug resistant leukemia cells]. Cai, YX; Fu, YB; Li, L; Meng, FY; Sun, QX, 2008)	1.29
"Bortezomib treatment induced an earlier improvement in sciatic functional index and a more rapid restoration of contractile force and wet weight of extensor digitorum longus muscle. "	( Proteasome inhibition promotes functional recovery after peripheral nerve reperfusion injury. Jang, HS; Kim, KM; Oh, KJ; Park, JW; Rhyu, IJ, 2009)	1.8
"Bortezomib treatment elicited substantial reduction in both donor-specific antibody (DSA) and non-DSA levels. "	( Abrogation of anti-HLA antibodies via proteasome inhibition. Dave, SD; Everly, MJ; Feroz, A; Idica, AK; Kaneku, H; Khemchandani, SI; Modi, PR; Shankar, V; Terasaki, PI; Trivedi, HL; Trivedi, VB; Vanikar, AV, 2009)	1.8
"Bortezomib pre-treatment significantly reduced the pancreatic weight/body weight ratio, and improved the histology by decreasing the extent of vacuolization and infiltration."	( Simultaneous proteosome inhibition and heat shock protein induction by bortezomib is beneficial in experimental pancreatitis. Biczó, G; Halm, G; Rakonczay, Z; Szabolcs, A; Takács, T; Tiszlavicz, L; Wittmann, T, 2009)	1.31
"Bortezomib treatment was generally well tolerated."	( Single-agent bortezomib in previously untreated multiple myeloma: efficacy, characterization of peripheral neuropathy, and molecular correlations with response and neuropathy. Amato, AA; Anderson, KC; Avigan, DE; Briemberg, HR; Chanan-Khan, AA; Doss, D; Esseltine, DL; Hassoun, H; Heffner, LT; Kesari, S; Kuter, DJ; Lonial, S; Mitsiades, C; Munshi, NC; Oaklander, AL; Richardson, PG; Schlossman, RL; Weller, E; Wen, PY; Xie, W, 2009)	1.44
"Bortezomib treatment of EOC cells causes apoptosis by involving mitochondrial pathway, activation of caspases and downregulation of XIAP, and survivin."	( Bortezomib-mediated expression of p27Kip1 through S-phase kinase protein 2 degradation in epithelial ovarian cancer. Ahmed, M; Al-Dayel, F; Al-Kuraya, KS; Bavi, P; Hussain, AR; Jehan, Z; Munkarah, A; Uddin, S, 2009)	2.52
"Bortezomib treatment led to inhibition of BCR-ABL-induced suppression of FoxO proteins and their proapoptotic targets, tumor necrosis factor-related apoptosis-inducing ligand and BIM, thereby providing novel insights into the molecular effects of proteasome inhibitor therapy."	( Proteasome inhibition causes regression of leukemia and abrogates BCR-ABL-induced evasion of apoptosis in part through regulation of forkhead tumor suppressors. Dewar, MR; Ghaffari, S; Grassian, A; Jagani, Z; Khosravi-Far, R; Kutok, JL; Melet, A; Miller, K; Ren, R; Rodin, HY; Santos, T; Song, K; Wu, C; Yeckes-Rodin, H, 2009)	1.07
"Bortezomib treatment caused a reduced expansion of CD8(+) T lymphocytes and increased viral titers in LCMV-infected mice."	( The proteasome inhibitor bortezomib enhances the susceptibility to viral infection. Basler, M; Beck, U; Groettrup, M; Lauer, C, 2009)	1.38
"Bortezomib treatment resulted in promoter-specific changes in estrogen-induced gene transcription that related with occupancy of ERalpha and RNA polymerase II (PolII) on endogenous promoters."	( Proteasome inhibition represses ERalpha gene expression in ER+ cells: a new link between proteasome activity and estrogen signaling in breast cancer. Alarid, ET; Casa, AJ; Ellison-Zelski, SJ; Lee, AV; Powers, GL, 2010)	1.08
"Bortezomib treatment was administered during this period and therapeutic response was assessed using cerebellar volumes at the end of treatment."	( Functional evaluation of therapeutic response for a mouse model of medulloblastoma. Duong, TQ; Jung, I; Keller, C; Kilcoyne, A; Lin, AL; Morgan, WW; Nelon, LD; Nowak, BM; Ohshima-Hosoyama, S; Prajapati, SI; Rubin, BP; Samano, AK; Taniguchi, E; Togao, O; Whitney, TG, 2010)	1.08
"Bortezomib treatment did not significantly decrease DSA MFI within the 150-day posttreatment period in any patient."	( Bortezomib as the sole post-renal transplantation desensitization agent does not decrease donor-specific anti-HLA antibodies. Anglicheau, D; Candon, S; Hermine, O; Legendre, C; Leruez, M; Loupy, A; Martinez, F; Nochy, D; Pallet, N; Rabant, M; Sberro-Soussan, R; Snanoudj, R; Suberbielle-Boissel, C; Thervet, E; Zuber, J, 2010)	2.52
"Bortezomib treatment of immunocompetent C57BL/6 mice bearing LLC-induced subcutaneous tumors and MPEs significantly blocked tumor-specific NF-kappaB activation."	( Specific effects of bortezomib against experimental malignant pleural effusion: a preclinical study. Blackwell, TS; Kalomenidis, I; Karabela, SP; Kollintza, A; Magkouta, S; Moschos, C; Psallidas, I; Roussos, C; Sherrill, TP; Stathopoulos, GT; Theodoropoulou, P, 2010)	1.41
"Bortezomib treatment exhibited greater sensitivities in Huh7 and SNU886 cells (epithelial type) than SK-Hep1 and SNU449 cells (mesenchymal type) that exhibited higher levels of G(alpha)(12/13)."	( G(alpha)12/13 inhibition enhances the anticancer effect of bortezomib through PSMB5 downregulation. Dhanasekaran, DN; Ha, JH; Jayaraman, M; Kim, SG; Kwak, MK; Lee, CH; Lee, S; Nam, CW; Yang, YM, 2010)	1.33
"Bortezomib treatment did not significantly decrease DSA MFI within the 270-day post-treatment period in any patient."	( Bortezomib alone fails to decrease donor specific anti-HLA antibodies: 4 case reports. Legendre, C; Sberro-Soussan, R; Suberbielle-Boissel, C; Zuber, J, 2009)	2.52
"Bortezomib treatment activated endoplasmic reticulum (ER) stress-mediated apoptosis, as demonstrated by the induction of GADD153, an ER stress-inducible transcription factor, and of the death receptor DR5, in EGFR inhibitor-resistant cells, but not in parental cells."	( Antitumor activity of bortezomib in human cancer cells with acquired resistance to anti-epidermal growth factor receptor tyrosine kinase inhibitors. Cascone, T; Ciardiello, F; D'Aiuto, E; De Palma, R; De Vita, F; Martinelli, E; Morgillo, F; Orditura, M; Troiani, T, 2011)	1.41
"Bortezomib treatment initiated following inoculation of tumor cells strikingly reduced tumor growth, restricted tumor cells mainly to the marrow cavity, and almost completely inhibited osteolysis in the bone microenvironment over a 3- to 4-week period as shown by [(18)F]fluorodeoxyglucose positron emission tomography, micro-computed tomography scanning, radiography, and histology."	( A proteasome inhibitor, bortezomib, inhibits breast cancer growth and reduces osteolysis by downregulating metastatic genes. Ayers, DC; Barthel, TK; Bouxsein, ML; Cheng, D; Hussain, S; Jones, MD; Lian, JB; Liu, JC; Lovria, E; Mukherjee, S; Mulay, S; Schoonmaker, JA; Stein, GS, 2010)	1.39
"Bortezomib treatment strongly reduced T-dependent Ab titers mainly due to depletion of plasma cells."	( The early marginal zone B cell-initiated T-independent type 2 response resists the proteasome inhibitor bortezomib. Böhm, C; Jäck, HM; Lang, VR; Meister, S; Mielenz, D; Neubert, K; Schett, G; Voll, RE, 2010)	1.3
"Bortezomib treatment markedly enhanced bone metabolic activity and increased alkaline phosphatase levels, and decreased monoclonal protein levels."	( Bone scan images reveal increased osteoblastic function after bortezomib treatment in patients with multiple myeloma. Cho, BS; Cho, SG; Eom, KS; Kim, DW; Kim, HJ; Kim, YJ; Lee, JW; Lee, S; Lee, SE; Min, CK; Min, WS; Park, CW; Yahng, SA, 2011)	1.33
"Bortezomib-treated MM patients whose tumours had high baseline expression of genes suppressed by LCQ195 had significantly shorter progression-free and overall survival than those with low levels of these transcripts in their MM cells."	( Molecular and cellular effects of multi-targeted cyclin-dependent kinase inhibition in myeloma: biological and clinical implications. Anderson, KC; Buon, L; Delmore, J; Hayden, P; Jacobs, HM; Jakubikova, J; Laubach, J; Lengauer, C; McMillin, DW; Mitsiades, CS; Munshi, NC; Negri, J; Ooi, M; Richardson, PG; Schlossman, R, 2011)	1.09
"Bortezomib-treated hTNF-transgenic mice showed moderately increased inflammatory activity and dramatically enhanced bone erosions associated with a significant increase in the number of synovial osteoclasts. "	( Proteasome inhibition aggravates tumor necrosis factor-mediated bone resorption in a mouse model of inflammatory arthritis. Baum, W; Distler, JH; Frey, B; Gückel, E; Meister, S; Neubert, K; Polzer, K; Schett, G; Voll, RE; Zwerina, J, 2011)	1.81
"Bortezomib treatment leads to increased binding of C/EBP to previously recognized binding sites in the ZTA promoter."	( Bortezomib induction of C/EBPβ mediates Epstein-Barr virus lytic activation in Burkitt lymphoma. Ambinder, RF; Chen, J; Hayward, SD; Li, H; Shamay, M; Shirley, CM; Zahnow, CA, 2011)	2.53
"Bortezomib treatment reduced proteasome activity in the diaphragm of emphysematous and normal hamsters."	( Proteasome inhibition improves diaphragm function in an animal model for COPD. Dekhuijzen, R; Ennen, L; Heunks, L; Linkels, M; Ottenheijm, C; van Hees, H, 2011)	1.09
"Bortezomib treatment is able to overcome the survival disadvantage in patients with MYC activation."	( Clinical and biological implications of MYC activation: a common difference between MGUS and newly diagnosed multiple myeloma. Bergsagel, PL; Chesi, M; Chng, WJ; Chung, TH; Fonseca, R; Gonzalez-Paz, N; Huang, GF; Mulligan, G; Ng, SB; Troska-Price, T, 2011)	1.09
"Bortezomib treatment did not significantly decrease DSA MFI within the 270-day posttreatment period in any patient."	( Bortezomib alone fails to decrease donor specific anti-HLA antibodies: even after one year post-treatment. Legendre, C; Sberro-Soussan, R; Suberbielle-Boissel, C; Zuberl, J, 2010)	2.52
"Bortezomib treatment led to phosphorylation/activation of jun N-terminal kinase (JNK) enzymes and JNK-dependent phosphorylation of Bcl-2 on serine 70."	( Bortezomib induces autophagy in head and neck squamous cell carcinoma cells via JNK activation. Johnson, DE; Li, C, 2012)	2.54
"Bortezomib treatment was supplied for patients before autoPBSCT and in the conditioning of transplantation, it was also used in maintaining treatment."	( [Bortezomib combined with autologous peripheral blood hematopoietic stem cell transplantation for therapy of patients with multiple myeloma]. Bai, H; Ling, YQ; Wang, CB; Wang, ML; Wu, B; Zhang, Q, 2011)	2
"Bortezomib maintenance treatment upgraded post-ASCT CR responses with no severe grade 3/4 peripheral neuropathy."	( Sequential bortezomib, dexamethasone, and thalidomide maintenance therapy after single autologous peripheral stem cell transplantation in patients with multiple myeloma. Cai, JL; Duarte, L; Farol, L; Forman, SJ; Frankel, PH; Htut, M; Karanes, C; Kogut, NM; Krishnan, AY; Murata-Collins, JL; Parker, PM; Popplewell, LL; Reburiano, E; Ruel, C; Sahebi, F; Somlo, G; Spielberger, RT; Thomas, SH, 2012)	1.49
"Bortezomib treatment also reduced expression of pro-inflammatory cytokines MIP-2 compared with control treated steatotic and lean liver transplants respectively (106±17.5 vs."	( Ischemia-reperfusion injury in rat steatotic liver is dependent on NFκB P65 activation. Chapman, WC; Csontos, K; Glasgow, SC; Jia, J; Liaw, JM; Liu, W; Mohanakumar, T; Ramachandran, S; Upadhya, GA, 2012)	1.1
"Bortezomib-treated mast cells lost the ability to induce neovasculization and fibrosis, and did not promote the growth of Hodgkin tumor in vivo."	( Mast cells promote the growth of Hodgkin's lymphoma cell tumor by modifying the tumor microenvironment that can be perturbed by bortezomib. Miyata, Y; Mizuno, H; Nakao, N; Nakayama, T; Naoe, T; Nishiwaki, S; Saito, S; Takeshita, K, 2012)	1.31
"Bortezomib treatment was shown to potently inhibit murine DSS-induced colitis. "	( Proteasome inhibitor bortezomib ameliorates intestinal injury in mice. Asano, Y; Kadono, T; Sato, S; Sugaya, M; Tada, Y; Yanaba, K, 2012)	2.14
"Bortezomib treatment is likely to induce T cell death, thereby suppressing DSS-induced colitis by reducing IFN-γ production."	( Proteasome inhibitor bortezomib ameliorates intestinal injury in mice. Asano, Y; Kadono, T; Sato, S; Sugaya, M; Tada, Y; Yanaba, K, 2012)	2.14
"Bortezomib treatment resulted in a significant reduction of superoxide content, lipid peroxidation and protein oxidation products, serum levels of monocyte chemoattractant protein-1, and interleukin-6."	( Attenuation of early atherogenesis in low-density lipoprotein receptor-deficient mice by proteasome inhibition. Arias, A; Baumann, G; Dreger, H; Fechner, M; Hewing, B; Ludwig, A; Meiners, S; Stangl, K; Stangl, V; Wilck, N, 2012)	1.1
"Bortezomib as retreatment was well tolerated, and the safety profile was consistent with previous studies of bortezomib in relapsed MM."	( Effective response with bortezomib retreatment in relapsed multiple myeloma--a multicentre retrospective survey in Switzerland. Olie, RA; Taverna, C; Trojan, A; Voegeli, J; von Rohr, A, 2012)	1.41
"Bortezomib pre-treatment reduced cellular packing density, improved penetration, and enhanced cytotoxcity of several anticancer drugs in MCC derived from epithelioid cell lines."	( Penetration of anticancer drugs through tumour tissue as a function of cellular packing density and interstitial fluid pressure and its modification by bortezomib. Grantab, RH; Tannock, IF, 2012)	1.3
"Bortezomib-treated HLA-mismatched patients experienced rates of NRM, acute and chronic GVHD, and survival similar to those of contemporaneous HLA-matched RIC HSCT at our institution."	( Bortezomib-based graft-versus-host disease prophylaxis in HLA-mismatched unrelated donor transplantation. Alyea, EP; Antin, JH; Armand, P; Bindra, B; Blazar, BR; Cutler, C; Ho, VT; Kim, HT; Koreth, J; McDonough, SM; Ritz, J; Soiffer, RJ; Stevenson, KE, 2012)	2.54
"Bortezomib treatment significantly enhanced p21(WAF1) protein levels in all cell lines but with different mechanisms according to ERα status."	( Roles of estrogen receptor and p21(Waf1) in bortezomib-induced growth inhibition in human breast cancer cells. Basile, I; Cathiard, AM; Garcia, M; Gary-Bobo, M; Gleizes, M; Maynadier, M; Sheikh, MS; Shi, J; Vaillant, O; Wah, JL, 2012)	1.36
"Bortezomib rescue treatment was administered after the patients failed to respond to plasmapheresis/intravenous immunoglobulin and splenectomy."	( The use of bortezomib as a rescue treatment for acute antibody-mediated rejection: report of three cases and review of literature. Benedetti, E; Jeon, H; Joseph, J; Oberholzer, J; Spaggiari, M; Thielke, J; Tzvetanov, I, 2012)	1.49
"Bortezomib (BRZ) treatment at non-toxic doses of rats fed alcohol chronically has shown protective effects by increasing liver antioxidant enzymes."	( Proteasome inhibitors protect the steatotic and non-steatotic liver graft against cold ischemia reperfusion injury. Bardag-Gorce, F; Bejaoui, M; Ben Abdennebi, H; Carbonell, T; Oliva, J; Pantazi, E; Rimola, A; Roselló-Catafau, J; Zaouali, MA, 2013)	1.11
"Bortezomib treatment did not affect tissue cytokine levels."	( Proteasome inhibition prolongs survival during lethal hemorrhagic shock in rats. Bach, HH; Gamelli, RL; Laporte, HM; Majetschak, M; Wong, YM, 2013)	1.11
"Bortezomib treatment led to accumulation of p21(WAF1/CIP1) and p27(KIP1) and decreased BCL-2; gemcitabine decreased p27(KIP1), induced BCL-2 and had no effect on p21(WAF1/CIP1)."	( Schedule-dependent molecular effects of the proteasome inhibitor bortezomib and gemcitabine in pancreatic cancer. Bold, RJ; Fahy, BN; Schlieman, MG; Virudachalam, S, 2003)	1.28
"Bortezomib/HA14-1 treatment triggered an increase in reactive oxygen species (ROS), which, along with apoptosis, was blocked by the free radical scavenger N-acetyl-L-cysteine (L-NAC)."	( The proteasome inhibitor bortezomib promotes mitochondrial injury and apoptosis induced by the small molecule Bcl-2 inhibitor HA14-1 in multiple myeloma cells. Dai, Y; Grant, S; Pei, XY, 2003)	1.34
"Bortezomib-treated LNCaP-Pro5 tumors displayed reduced microvessel densities and vascular endothelial cell growth factor secretion and high levels of endothelial cell apoptosis consistent with angiogenesis inhibition."	( Differential effects of the proteasome inhibitor bortezomib on apoptosis and angiogenesis in human prostate tumor xenografts. Logothetis, C; McConkey, DJ; Papandreou, C; Pettaway, C; Song, R; Williams, S, 2003)	1.29
"Bortezomib treatment did not affect stem cell mobilization in eight or transplantation in six patients."	( Bortezomib therapy alone and in combination with dexamethasone for previously untreated symptomatic multiple myeloma. Camacho, E; Crowley, J; Durie, BG; Gabayan, E; Irwin, D; Jagannath, S; Lutzky, J; Mazumder, A; McKinley, M; Schenkein, D; Wolf, J, 2005)	2.49
"Bortezomib treatment did not alter CYP3A activity and docetaxel clearance."	( Phase I trial of bortezomib in combination with docetaxel in patients with advanced solid tumors. Almuete, VI; Armstrong, DK; Baker, SD; Carducci, MA; Dinh, K; Donehower, RC; Lassiter, L; Messersmith, WA; Sullivan, RA; Wright, JJ, 2006)	1.39
"Bortezomib-treated neuroblastoma cells were arrested at G2/M and underwent apoptosis (mean percentage of apoptotic cells in four neuroblastoma cell lines treated with 20 nM bortezomib for 24 hours ranged from 20% to 35%, and caspases were activated by two- to fivefold with respect to untreated cells)."	( Effect of bortezomib on human neuroblastoma cell growth, apoptosis, and angiogenesis. Brignole, C; Cilli, M; Cioni, M; Corrias, MV; Di Paolo, D; Marimpietri, D; Nico, B; Pagnan, G; Pastorino, F; Pezzolo, A; Piccardi, F; Pistoia, V; Ponzoni, M; Ribatti, D, 2006)	1.46
"Bortezomib/TRAIL cotreatment bears the risk of severe hepatotoxicity at high but clinically relevant concentrations of bortezomib. "	( TRAIL/bortezomib cotreatment is potentially hepatotoxic but induces cancer-specific apoptosis within a therapeutic window. Ganten, TM; Haas, TL; Kolb, A; Koschny, R; Sprick, MR; Stremmel, W; Sykora, J; Walczak, H, 2007)	2.26
"Bortezomib treatment resulted in dose and time-dependent decreases in cell proliferation and resulted in cell cycle arrest. "	( Bortezomib inhibits angiogenesis and reduces tumor burden in a murine model of neuroblastoma. Davidoff, AM; Dickson, PV; Hamner, JB; Ng, CY; Sims, TL; Spence, Y; Zhou, J, 2007)	3.23
"Bortezomib/PXD101 treatment markedly triggered reactive oxygen species (ROS) generation that was accompanied by p53, H2A.X and p38-mitogen-activated protein kinase phosphorylation."	( The histone deacetylase inhibitor, PXD101, potentiates bortezomib-induced anti-multiple myeloma effect by induction of oxidative stress and DNA damage. Anderson, G; Belani, C; Feng, R; Lentzsch, S; Mapara, MY; Oton, A, 2007)	1.31
"Bortezomib treatment decreases intracellular glutathione both in MM cell lines and in malignant plasma cells obtained from MM patients."	( Redox homeostasis modulates the sensitivity of myeloma cells to bortezomib. Caligaris-Cappio, F; Cozza, S; Ferrarini, M; Nerini-Molteni, S; Sitia, R, 2008)	1.31
"Bortezomib treatment increased the Bax protein expression."	( Effects of the proteasome inhibitor bortezomib alone and in combination with chemotherapeutic agents in gastric cancer cell lines. Bae, SH; Hyun, MS; Kim, MK; Lee, KH; Ryoo, HM; Sin, JI, 2008)	1.34
"Bortezomib treatment significantly improved diaphragm single fiber force generating capacity (approximately 30-40%) and cross-bridge cycling kinetics (approximately 20%) in CHF."	( Proteasome inhibition improves diaphragm function in congestive heart failure rats. Dekhuijzen, PN; Heunks, LM; Jin, B; Li, YP; Linkels, M; Ottenheijm, CA; Pigmans, CJ; van Hees, HW, 2008)	1.07
"In bortezomib-treated mice, autophagy was activated in hepatocytes as determined by EM and biochemical analysis."	( Autophagy activation by rapamycin eliminates mouse Mallory-Denk bodies and blocks their proteasome inhibitor-mediated formation. Ghori, N; Hanada, S; Harada, M; Omary, MB; Toivola, DM, 2008)	0.86
"AMR treatment with bortezomib was effective, showing stable renal function at 24 months. "	( Antibody-Mediated Rejection Treatment With Bortezomib in Renal Transplant Recipients: A Single-Center 24-Month Follow-up Case Report. Baca Córdova, A; Bahena Méndez, J; Carmona-Escamilla, MA; Galindo-Lopéz, R; López Y López, LR; Sebastián Díaz, MA; Trejo Curiel, I; Vázquez Dávila, RA; Wasung de Lay, M; Zarate Rodríguez, PA, 2020)	1.15
"If treatment with bortezomib is beneficial in these cases, this will be the basis for implementation in the current guidelines."	( Generate-Boost: study protocol for a prospective, multicenter, randomized controlled, double-blinded phase II trial to evaluate efficacy and safety of bortezomib in patients with severe autoimmune encephalitis. Chung, HY; Geis, C; Günther, A; Lehmann, T; Leypoldt, F; Platzer, S; Prüss, H; Scherag, A; Wickel, J, 2020)	1.08
"Treatment with Bortezomib (a proteasome inhibitor) and Daratumumab (DARA, a monoclonal anti CD38 antibody) are effective in patients with multiple myeloma (MM). "	( Effect of Bortezomib Regimens and Daratumumab Monotherapy on Cellular Immunity in Multiple Myeloma Patients. Al-Attar, M; Kakoo, A; Rasheed, T, 2021)	1.38
"Treatment with bortezomib and dexamethasone significantly improved the patient's symptoms."	( The Coexistence of Multiple Myeloma-associated Amyloid Light-chain Amyloidosis and Fabry Disease in a Hemodialysis Patient. Fukami, K; Kodama, G; Moriyama, A; Nakayama, Y; Taguchi, K, 2017)	0.79
"Treatment with bortezomib followed by daunorubicin treatment was more effective, compared with treatment with daunorubicin followed by bortezomib."	( Combination of bortezomib and daunorubicin in the induction of apoptosis in T-cell acute lymphoblastic leukemia. Du, S; Du, X; He, C; Jia, P; Li, J; Lu, H; Shen, Z; Tong, J; Wu, Y; Xu, H; Zhao, W; Zhou, L, 2017)	1.15
"Pretreatment with bortezomib (50-250 nM, 2-7 h) significantly decreased transport of [3H]CCK-8, a specific OATP1B3 substrate, in HEK293-OATP1B3 and human sandwich-cultured hepatocytes (SCH)."	( Treatment with proteasome inhibitor bortezomib decreases organic anion transporting polypeptide (OATP) 1B3-mediated transport in a substrate-dependent manner. Alam, K; Crowe, A; Ding, K; Farasyn, T; Yue, W, 2017)	1.05
"Treatment with bortezomib completely overcame the negative prognosis of high-risk CA in patients without subclones, but not in patients with additional subclonal CA."	( Prognostic significance of cytogenetic heterogeneity in patients with newly diagnosed multiple myeloma. Bertsch, U; Blau, IW; Bochtler, T; Goldschmidt, H; Haenel, M; Hielscher, T; Hillengass, J; Hose, D; Jauch, A; Lindemann, HW; Merz, M; Neben, K; Raab, MS; Salwender, H; Scheid, C; Schmidt-Wolf, IGH; Schönland, SO; Seckinger, A; Weisel, KC, 2018)	0.82
"Treatment with bortezomib decreased RPE viability in a dose-dependent manner, and flow cytometry revealed that these effects were due to arrest of the G2/M phase cell-cycle. "	( Bortezomib inhibits proliferation, migration, and TGF-β1-induced epithelial-mesenchymal transition of RPE cells. Baek, WK; Joo, CK; Jun, JH; Kim, JY; Kim, KS; Lee, HG; Lee, Y; Moon, K, 2017)	2.25
"Treatment with bortezomib and dexamethasone was initiated; due to side effects, the treatment was later switched to lenalidomide, which was better tolerated."	( Primary systemic amyloidosis with skin and cardiac involvement: a case report Jurčić, V; Marko, PB; Trajber Horvat, A; Trčko, K, 2018)	0.82
"Co-treatment with bortezomib and either doxorubicin or carboplatin was more toxic to canine osteosarcoma cells than each agent alone."	( Pre-clinical evaluation of proteasome inhibitors for canine and human osteosarcoma. Hawkins, CJ; Patatsos, K; Shekhar, TM, 2018)	0.8
"Treatment with bortezomib did not improve the melena or the underlying disease."	( Therapeutic effects of lenalidomide on hemorrhagic intestinal myeloma-associated AL amyloidosis. Aoki, K; Arima, H; Imai, H; Ishikawa, T; Kato, A; Matsushita, A; Mori, M; Nagano, S; Ono, Y; Tabata, S; Takahashi, T; Takiuchi, Y; Yanagita, S, 2013)	0.73
"Treatment with bortezomib or mycophenolic acid induced B-cell apoptosis and inhibited secretion of antibodies."	( Effect of mycophenolic acid and bortezomib on purified human B cells: an in vitro study of long-term functionally stable MICA-sensitized renal recipients. Li, Zw; Luo, M; Qiu, Jx; Wang, Y; Wen, Xf, 2013)	1.01
"Treatment with bortezomib induced dose-dependent dissociation of protein synthesis machinery (chromatolysis) and nuclear retention of poly(A) RNA granules resulting in neuronal dysfunction."	( Reactive nucleolar and Cajal body responses to proteasome inhibition in sensory ganglion neurons. Berciano, MT; Casafont, I; Lafarga, M; Palanca, A, 2014)	0.74
"Treatment with bortezomib, almost in the second- or third-line setting, was associated with longer median OS (35.5 months) and the median time to progression (TTP) (6.0 months)."	( The treatment outcome of multiple myeloma patients ineligible for hematopoietic transplantation--a single institutional experience in Taiwan. Chang, PY; Chao, TY; Chen, JH; Chen, YC; Dai, MS; Ho, CL; Huang, TC; Kao, WY; Wu, YY, 2015)	0.76
"Treatment with bortezomib, a protease inhibitor, eliminated residual host-type plasma cells secreting anti-A and restored normal donor-derived erythropoiesis."	( Successful treatment of severe immune hemolytic anemia after allogeneic stem cell transplantation with bortezomib: report of a case and review of literature. Cohen, C; Hosoba, S; Jaye, DL; Roback, JD; Waller, EK, 2015)	0.97
"Retreatment with bortezomib (B) is often considered for patients with relapsed multiple myeloma (MM), but this strategy is hindered by uncertainty of response and emergence of B-induced peripheral neuropathy (PN). "	( Acetyl-L-carnitine (ALCAR) for the prevention of chemotherapy-induced peripheral neuropathy in patients with relapsed or refractory multiple myeloma treated with bortezomib, doxorubicin and low-dose dexamethasone: a study from the Wisconsin Oncology Netwo Asimakopoulos, F; Callander, N; Campbell, T; Eickhoff, J; Go, R; Hegeman, R; Hematti, P; Hutson, P; Longo, W; Markovina, S; Miyamoto, S; Williams, E, 2014)	0.94
"Treatment with bortezomib and dexamethasone alone was sufficient to clear the bilateral cystoid macular edema and subretinal fluid."	( Resolution of bilateral cystoid macular edema and subfoveal serous retinal detachments after treatment with bortezomib in a patient with "smoldering" multiple myeloma. Dewan, VN; Grannis, CH; Wang, RC, 2014)	0.95
"Co-treatment with bortezomib and DT97 reduced the growth of myeloma xenotransplants in murine models and prolonged host survival."	( High throughput chemical library screening identifies a novel p110-δ inhibitor that potentiates the anti-myeloma effect of bortezomib. Driscoll, JJ; Malek, E, 2016)	0.96
"Treatment was bortezomib 1.7 mg/m(2) IV on days 1, 4 and 8 and then surgery on day 8 or 9."	( A phase II trial evaluating the effects and intra-tumoral penetration of bortezomib in patients with recurrent malignant gliomas. Bredel, M; Chandler, JP; Ferrarese, R; Grimm, SA; Helenowski, I; Levy, RM; Muro, K; Paton, M; Rademaker, A; Raizer, JJ; Rosenow, J, 2016)	1.01
"Treatment with bortezomib alone increased the phosphorylation of AKT (P-AKT), whereas the addition of BKM120 markedly downregulated P-AKT in both bortezomib-sensitive and bortezomib-resistant cells."	( Novel phosphatidylinositol 3-kinase inhibitor BKM120 enhances the sensitivity of multiple myeloma to bortezomib and overcomes resistance. Chen, Y; Tong, J; Wang, Y; Wu, Y; Xiang, R; Xu, W; Yan, H; Yu, W; Zhang, N, 2017)	1.01
"Mice treated with bortezomib before the transfusion of KEL RBCs became alloimmunized in three of three experiments, although their serum anti-KEL IgG levels were 2.6-fold lower than those in untreated mice."	( Bortezomib decreases the magnitude of a primary humoral immune response to transfused red blood cells in a murine model. Gibb, DR; Hendrickson, JE; Liu, J; Natarajan, P; Santhanakrishnan, M; Slater, LM, 2017)	2.22
"Co-treatment with bortezomib and doxorubicin prolonged the survival of BCP-ALL xenograft mice, with a significant reduction of leukemia cells in BM."	( Bortezomib interferes with adhesion of B cell precursor acute lymphoblastic leukemia cells through SPARC up-regulation in human bone marrow mesenchymal stromal/stem cells. Andoh, A; Fujii, S; Fujishiro, A; Hirai, H; Hishita, T; Ichinohe, T; Iwasa, M; Maekawa, T; Miura, Y; Sugino, N; Yokota, A; Yoshioka, S, 2017)	2.22
"Treatment with bortezomib depleted plasma cells producing antibodies to double-stranded DNA, eliminated autoantibody production, ameliorated glomerulonephritis and prolonged survival of two mouse strains with lupus-like disease, NZB/W F1 and MRL/lpr mice."	( The proteasome inhibitor bortezomib depletes plasma cells and protects mice with lupus-like disease from nephritis. Amann, K; Kalden, JR; Manz, RA; Maseda, D; Meister, S; Moser, K; Neubert, K; Voll, RE; Weisel, F; Wiethe, C; Winkler, TH, 2008)	0.99
"Retreatment with bortezomib-based therapy is feasible, with predictable toxicities. "	( An observational, retrospective analysis of retreatment with bortezomib for multiple myeloma. Beveridge, RA; Conner, TM; Doan, QD; LeBlanc, AL; Walters, IB, 2008)	0.93
"Pretreatment with bortezomib was able to ameliorate CAM-DR of myeloma cells to vincristine and dexamethasone."	( Bortezomib overcomes cell-adhesion-mediated drug resistance through downregulation of VLA-4 expression in multiple myeloma. Furukawa, Y; Kano, Y; Kikuchi, J; Mori, M; Muroi, K; Nagai, T; Noborio-Hatano, K; Nobuyoshi, M; Oh, I; Ozaki, K; Ozawa, K; Sato, K; Shimizu, R; Suzuki, T; Takatoku, M; Ueda, M; Wada, T, 2009)	2.12
"Treatment with bortezomib and dexamethasome was subsequently started and a complete hematological response was achieved."	( Generalized cutis laxa and fibrillar glomerulopathy resulting from IgG Deposition in IgG-lambda Monoclonal Gammopathy: pulmonary hemorrhage during stem cell mobilization and complete hematological response with bortezomib and dexamethasone therapy. Bladé, J; Cibeira, MT; Fernández de Larrea, C; Lloreta, J; Mascaró, JM; Rovira, M; Serra, N; Solé, M; Torras, A, 2009)	0.88
"Treatment with bortezomib produced a significant reduction of cystatin-C, mainly in responders."	( Cystatin-C is an independent prognostic factor for survival in multiple myeloma and is reduced by bortezomib administration. Anargyrou, K; Christoulas, D; Dimopoulos, MA; Kastritis, E; Katodritou, E; Michalis, E; Pouli, A; Terpos, E; Tsiftsakis, E; Tsionos, K; Verrou, E; Zervas, K, 2009)	0.91
"Pretreatment with bortezomib does not improve the intracellular anthracycline concentration in K562/A02 cells."	( The effects of proteasome inhibitor bortezomib on a P-gp positive leukemia cell line K562/A02. Chen, L; Chen, Z; Han, F; Li, J; Lü, S; Wang, J; Xu, X; Yang, J; Zhou, H, 2010)	0.96
"Treatment with bortezomib at 1.5 mg/m(2)/dose was not feasible in this patient population due to excess toxicity."	( A phase II evaluation of bortezomib in the treatment of recurrent platinum-sensitive ovarian or primary peritoneal cancer: a Gynecologic Oncology Group study. Aghajanian, C; Blessing, JA; Darcy, KM; DeGeest, K; Mannel, RS; Reid, G; Riordan, W; Rotmensch, J; Rubin, SC; Schilder, RJ, 2009)	1
"Retreatment with bortezomib alone or in combination is effective and well tolerated in patients with MM who have responded to their initial bortezomib treatment."	( Retreatment with bortezomib alone or in combination for patients with multiple myeloma following an initial response to bortezomib. Carloss, H; Druck, M; Kerr, R; Lee, M; Lopez, J; Noga, SJ; Sood, R; Walters, IB, 2009)	1.02
"Pretreatment with bortezomib effectively overcomes APO2L/TRAIL apoptosis resistance in myeloma cell lines and in CD138+ cells while directly adhered or in transwell assay. "	( Bortezomib restores stroma-mediated APO2L/TRAIL apoptosis resistance in multiple myeloma. Anasetti, C; Dalton, W; Meads, M; Parquet, N; Perez, LE, 2010)	2.14
"Retreatment with bortezomib provided prompt, complete, and durable DSA elimination."	( Proteasome inhibitor-based primary therapy for antibody-mediated renal allograft rejection. Alloway, RR; Arend, LJ; Brailey, P; Everly, JJ; Govil, A; Mogilishetty, G; Rike, AH; Roy-Chaudhury, P; Walsh, RC; Woodle, ES, 2010)	0.69
"Treatment with bortezomib caused a significant increase in bone-specific alkaline phosphatase and pro-collagen type I N-terminal propeptide, a novel bone formation marker. "	( First-line treatment with bortezomib rapidly stimulates both osteoblast activity and bone matrix deposition in patients with multiple myeloma, and stimulates osteoblast proliferation and differentiation in vitro. Abildgaard, N; Delaissé, JM; Garnero, P; Lund, T; Ormstrup, T; Pedersen, PT; Plesner, T; Søe, K, 2010)	1.01
"Cotreatment with bortezomib (5 μM) and TGF-β (10 μM) increased the proportion of apoptotic cells in HTFs on FACS analysis, whereas either bortezomib or TGF-β treatment alone did not. "	( Potentiation of bortezomib-induced apoptosis by TGF-beta in cultured human Tenon's fibroblasts: contribution of the PI3K/Akt signaling pathway. Cho, YJ; Chung, EJ; Jung, SA; Kim, SW; Lee, JH; Moon, SW, 2010)	1.05
"Pretreatment with bortezomib for 3 weeks before inoculation of tumor cells was also effective in reducing osteolysis."	( A proteasome inhibitor, bortezomib, inhibits breast cancer growth and reduces osteolysis by downregulating metastatic genes. Ayers, DC; Barthel, TK; Bouxsein, ML; Cheng, D; Hussain, S; Jones, MD; Lian, JB; Liu, JC; Lovria, E; Mukherjee, S; Mulay, S; Schoonmaker, JA; Stein, GS, 2010)	0.99
"Cotreatment of bortezomib with eeyarestatin markedly enhanced cell death in cervical cancer cells, allowing reduction of the bortezomib concentration necessary for efficient cell death to as low as 5 ng/ml. "	( Eeyarestatin causes cervical cancer cell sensitization to bortezomib treatment by augmenting ER stress and CHOP expression. Brem, GJ; Brüning, A; Mylonas, I, 2013)	0.99
"Treatment with bortezomib, a therapeutic proteasome inhibitor induced apoptosis and repressed the proliferation of RPMI8226 and U266 cells through inhibition of NF-κB p65 and IκBα."	( BlyS: a potential hallmark of multiple myeloma. Chen, X; Hu, C; Huang, Q; Liu, B; Ma, Y; Miao, P; Qian, L; Shen, L; Wang, L; Wang, P; Yu, Q; Yuan, X; Zhang, D; Zhang, J, 2013)	0.73
"Treatment with bortezomib led to a moderate increase in osteoblastic differentiation markers in hMSCs and hOBs."	( The proteasome inhibitor bortezomib stimulates osteoblastic differentiation of human osteoblast precursors via upregulation of vitamin D receptor signalling. Heider, U; Kaiser, MF; Mieth, M; Sezer, O; von Metzler, I; Zang, C, 2013)	1.03
"Co-treatment of bortezomib and calyculin A, a PP2A inhibitor, reduced the effect of bortezomib on P-Akt, P-4EBP1, and autophagy."	( Cancerous inhibitor of protein phosphatase 2A mediates bortezomib-induced autophagy in hepatocellular carcinoma independent of proteasome. Chen, KF; Cheng, AL; Hou, DR; Lin, CS; Liu, CY; Shiau, CW; Yu, HC, 2013)	0.97
"Treatment with bortezomib reduced butyrate-induced activation of nuclear factor kappa B to baseline levels."	( Combined proteasome and histone deacetylase inhibition in non-small cell lung cancer. Broad, RM; Denlinger, CE; Jones, DR; Keller, MD; Mayo, MW, 2004)	0.66
"Treatment with Bortezomib induced procaspase-3 and poly(ADP-ribose) polymerase cleavage and decreased the amount of extracellular signal regulated kinase (Erk1/2) and phospho-Erk1/2."	( Bortezomib is an efficient agent in plasma cell leukemias. Aguado, B; Alegre, A; Bladé, J; Esparís-Ogando, A; Gutiérrez, N; Mateo, G; Pandiella, A; San Miguel, JF; Schenkein, D, 2005)	2.11
"Treatment with bortezomib resulted in decreased transcription of the BCL-2 promoter, decreased BCL-2 levels, and induced apoptosis."	( Reduction in BCL-2 levels by 26S proteasome inhibition with bortezomib is associated with induction of apoptosis in small cell lung cancer. Bold, RJ; Davies, AM; Gandara, DG; Lara, PN; Mortenson, MM; Schlieman, MG; Virudachalam, S, 2005)	0.91
"DCs treated with bortezomib show skewed phenotypic maturation in response to stimuli of bacterial (lipopolysaccharide [LPS]) and endogenous sources (including TNF-alpha and CD40L), as well as reduced cytokine production and immunostimulatory capacity."	( Proteasome inhibitor bortezomib modulates TLR4-induced dendritic cell activation. Ballestrero, A; Brauer, KM; Brossart, P; Grünebach, F; Nencioni, A; Schmidt, SM; Schwarzenberg, K, 2006)	0.98
"Treatment with bortezomib reduces adverse cerebrovascular events including secondary thrombosis, inflammatory responses, and blood brain barrier (BBB) disruption, and hence reduces infarct volume and neurological functional deficit when administrated within 4 h after stroke onset."	( Treatment of embolic stroke in rats with bortezomib and recombinant human tissue plasminogen activator. Chopp, M; Hozeska, A; Liu, X; Lu, M; Riordan, W; Stagliano, N; Zhang, L; Zhang, ZG, 2006)	0.94
"Treatment with bortezomib at 4 to 8 hours post-gemcitabine significantly induced cell death in KBwt cell lines."	( SUMOylation plays a role in gemcitabine- and bortezomib-induced cytotoxicity in human oropharyngeal carcinoma KB gemcitabine-resistant clone. Ann, DK; Boo, LM; Chen, Y; Chung, V; Liu, X; Nguyen, HV; Song, J; Yen, Y; Zhou, B; Zhu, L, 2006)	0.93
"Treatment with bortezomib and MD5-1 reduced lung metastases in mice carrying Renca and 4T1 tumors (mean number of metastases, bortezomib + MD5-1 vs MD5-1: Renca-FLAG, 1 vs 8, difference = 7, 95% CI = 5 to 9, P < .001; 4T1, 1 vs 12, difference = 11, 95% CI = 9 to 12, P < .001) and increased median survival of mice bearing Renca-FLAG tumors (bortezomib + MD5-1 vs bortezomib + control isotype antibody: 22 of 30 [73%] were still alive at day 180 vs median survival of 42 days [95% CI = 41 to 44 days, P < .001]) in the absence of obvious toxicity."	( Treating metastatic solid tumors with bortezomib and a tumor necrosis factor-related apoptosis-inducing ligand receptor agonist antibody. Brooks, AD; Elliott, PJ; Murphy, WJ; Sayers, TJ; Shanker, A; Smyth, MJ; Takeda, K; Tristan, CA; Wine, JW; Yagita, H, 2008)	0.96

Excerpt	Reference	Relevance
" Their toxic profile is favorable, but during the drug development process some severe (sometimes lethal) toxicities have been observed, such as interstitial lung disease in patients treated with drugs targeting the epidermal growth factor receptor."	( Side effects of anti-cancer molecular-targeted therapies (not monoclonal antibodies). Awada, A; de Castro, G, 2006)	0.33
" Adverse events, including thrombocytopenia and peripheral neuropathy, have affected 30% to 60% of patients overall, and interrupted therapy in 10% to 20%."	( A multicenter retrospective analysis of adverse events in Korean patients using bortezomib for multiple myeloma. Bang, SM; Cho, KS; Jo, DY; Kim, CC; Kim, CS; Kim, K; Lee, JH; Lee, JJ; Lee, KH; Lee, NR; Min, CK; Min, YH; Park, S; Seong, CM; Sohn, SK; Suh, C; Yoon, HJ; Yoon, SS, 2006)	0.56
" This article speculates that cyclosporine eye drops would also be useful for any disease causing ectropion or eclabion of the eye as well as toxic epidermal necrolysis-related eye pathology (in particular corneal scarring)."	( A review of deferasirox, bortezomib, dasatinib, and cyclosporine eye drops: possible uses and known side effects in cutaneous medicine. Scheinfeld, N, 2007)	0.64
" As in the total APEX population, rates of grade 3/4 adverse events were higher in bortezomib- versus dexamethasone-treated patients aged > or =65 years and with >1 prior line, while rates of serious adverse events were similar; toxicities generally proved manageable."	( Safety and efficacy of bortezomib in high-risk and elderly patients with relapsed multiple myeloma. Anderson, KC; Ben-Yehuda, D; Cavenagh, JD; Facon, T; Harousseau, JL; Irwin, D; Lonial, S; Richardson, PG; San Miguel, JF; Schuster, MW; Sonneveld, P; Stadtmauer, EA, 2007)	0.88
" Grade 3/4 hematologic or neurologic toxicities (graded according to the Common Terminology Criteria for Adverse Events [CTCAE; version 3]) were reported to occur in 9 patients and 1 patient, respectively, whereas 6 patients experienced possible or documented infections."	( Efficacy and safety of bortezomib in patients with plasma cell leukemia. D'Arena, G; Ferrara, F; Filardi, N; Gay, F; Guariglia, R; Guglielmelli, T; Musto, P; Palumbo, A; Pitini, V; Rossini, F, 2007)	0.65
"Bortezomib appears to be an effective drug for PCL that could significantly improve the usually adverse clinical outcome of these patients."	( Efficacy and safety of bortezomib in patients with plasma cell leukemia. D'Arena, G; Ferrara, F; Filardi, N; Gay, F; Guariglia, R; Guglielmelli, T; Musto, P; Palumbo, A; Pitini, V; Rossini, F, 2007)	2.09
" Awareness of the various potential gastrointestinal toxic effects of bortezomib is of relevance given the growing number of patients undergoing treatment with this important and effective new cancer drug."	( Bortezomib-induced paralytic ileus is a potential gastrointestinal side effect of this first-in-class anticancer proteasome inhibitor. Brugnatelli, S; Brunetti, L; Corazza, GR; Gobbi, PG; Palladini, G; Perfetti, V; Sgarella, A, 2007)	2.02
" The most frequently reported adverse events were thrombocytopenia (34%), peripheral neuropathy (31%), diarrhoea (20%) and fatigue (19%)."	( Daily practice use of Bortezomib in relapsed/refractory multiple myeloma. Safety/efficacy results of a compassionate use program in Switzerland. Calderoni, A; Cornu, P; Freimann, H; Olie, R, 2007)	0.65
"Our results in daily oncology practice confirm findings from clinical trials, demonstrating high response rates and predictable adverse events in patients with relapsed/refractory multiple myeloma treated with bortezomib."	( Daily practice use of Bortezomib in relapsed/refractory multiple myeloma. Safety/efficacy results of a compassionate use program in Switzerland. Calderoni, A; Cornu, P; Freimann, H; Olie, R, 2007)	0.84
" With dexamethasone, grade 3/4 adverse events (AEs), serious AEs and discontinuations for AEs were significantly elevated in patients with CrCl < or =50 vs >50 ml min(-1)."	( Efficacy and safety of bortezomib in patients with renal impairment: results from the APEX phase 3 study. Anderson, KC; Ben-Yehuda, D; Bladé, J; Boccadoro, M; Boral, AL; Cavenagh, JD; Esseltine, DL; Facon, T; Goldschmidt, H; Harousseau, JL; Irwin, D; Lonial, S; Neuwirth, R; Reece, D; Richardson, PG; San-Miguel, JF; Schuster, MW; Sonneveld, P; Stadtmauer, EA, 2008)	0.66
" Coexposure of LBH589 and bortezomib at minimally toxic doses of either drug alone resulted in a striking induction of apoptosis in established U251, U87, and D37 GBM cell lines, as well as in GBM8, GBM10, GBM12, GBM14, and GBM56 short-term cultured cell lines."	( Mitochondrial Bax translocation partially mediates synergistic cytotoxicity between histone deacetylase inhibitors and proteasome inhibitors in glioma cells. Adjei, AA; Atadja, P; Friday, BB; Sarkaria, J; Wigle, D; Yang, L; Yu, C, 2008)	0.65
" The most common grade 3/4 hematologic adverse events (AEs) were neutropenia (31%/0%), thrombocytopenia (25%/2%), and anemia (13%/0%)."	( Safety and efficacy of bortezomib and melphalan combination in patients with relapsed or refractory multiple myeloma: updated results of a phase 1/2 study after longer follow-up. Berenson, JR; Hilger, J; Lee, SP; Mapes, R; Morrison, B; Nassir, Y; Swift, R; Vescio, RA; Wilson, J; Yang, HH; Yellin, O, 2008)	0.66
" However, patients with impaired renal function were at a slightly increased risk of a drug-related serious adverse event (28% vs."	( Pegylated liposomal doxorubicin plus bortezomib in relapsed or refractory multiple myeloma: efficacy and safety in patients with renal function impairment. Bladé, J; Cibeira, MT; Hajek, R; Harousseau, JL; Nagler, A; Orlowski, RZ; Robak, T; San Miguel, JF; Sonneveld, P; Spencer, A; Sutherland, HJ; Zhuang, SH, 2008)	0.62
"Bortezomib has been shown to be a safe and efficacious for the treatment of relapsed and refractory multiple myeloma (MM)."	( Safety and efficacy results from an international expanded access programme to bortezomib for patients with relapsed and/or refractory multiple myeloma: a subset analysis of the Australian and New Zealand data of 111 patients. Butcher, BE; Cannell, P; Horvath, N; Mikhael, JR; Prince, HM; Quach, H, 2009)	2.02
" Grade 3-4 treatment-related adverse events were reported in 57 patients (52%); the most common were thrombocytopenia (25."	( Safety and efficacy results from an international expanded access programme to bortezomib for patients with relapsed and/or refractory multiple myeloma: a subset analysis of the Australian and New Zealand data of 111 patients. Butcher, BE; Cannell, P; Horvath, N; Mikhael, JR; Prince, HM; Quach, H, 2009)	0.58
"Our analysis confirms that bortezomib is safe and effective in relapsed and refractory MM in a real-life clinical setting."	( Safety and efficacy results from an international expanded access programme to bortezomib for patients with relapsed and/or refractory multiple myeloma: a subset analysis of the Australian and New Zealand data of 111 patients. Butcher, BE; Cannell, P; Horvath, N; Mikhael, JR; Prince, HM; Quach, H, 2009)	0.88
" In conclusion, bortezomib-based regimens are safe and effective and should be considered as appropriate treatment options for MM patients with any degree of RI."	( Safety and efficacy of bortezomib-based regimens for multiple myeloma patients with renal impairment: a retrospective study of Italian Myeloma Network GIMEMA. Baldini, L; Boccadoro, M; Bringhen, S; Callea, V; Casulli, AF; Catalano, L; Cavo, M; Ciolli, S; Di Raimondo, F; Galimberti, S; Gentile, M; Mannina, D; Mele, G; Morabito, F; Musto, P; Offidani, M; Palmieri, S; Palumbo, A; Petrucci, MT; Pinotti, G; Piro, E; Tosi, P, 2010)	1.02
"VD regimen might be an efficient, rapid effective and safe regimen in the treatment of AL amyloidosis."	( [The effects and safety of bortezomib combined with dexamethasone in the treatment of primary systemic amyloidosis]. Li, J; Su, C; Wang, HH; Zeng, LJ; Zhao, Y, 2009)	0.65
"Bortezomib/ PLD/dexamethasone combination is safe and effective in elderly patients with resistant-relapsing MM."	( Weekly bortezomib, pegylated liposomal doxorubicin, and dexamethasone is a safe and effective therapy for elderly patients with relapsed/refractory multiple myeloma. Bocchia, M; Defina, M; Fabbri, A; Gozzetti, A; Lauria, F; Marchini, E; Oliva, S, 2010)	2.26
" Most adverse events were of mild degree and manageable."	( Bortezomib, doxorubicin, and dexamethasone combination therapy followed by thalidomide and dexamethasone consolidation as a salvage treatment for relapsed or refractory multiple myeloma: analysis of efficacy and safety. Bang, SM; Chung, J; Do, YR; Jin, JY; Joo, YD; Kang, HJ; Kim, BS; Kim, HY; Kim, K; Lee, DS; Lee, GW; Lee, JH; Lee, JJ; Lee, MH; Lee, SS; Park, J; Ryoo, HM; Shim, H; Suh, C; Yoon, SS, 2010)	1.8
" The major adverse events associated with these treatments are somnolence (thalidomide), venous thromboembolism (thalidomide and lenalidomide), myelosuppression (lenalidomide and bortezomib), gastrointestinal disturbance, and peripheral neuropathy (thalidomide and bortezomib)."	( Management of treatment-related adverse events in patients with multiple myeloma. Mateos, MV, 2010)	0.55
"The study was aimed to evaluate the adverse effects of PAD (bortezomib + adriamycin + dexamethasone) and VAD (vincristine + adriamycin + dexamethasone) as chemotherapy regimens in multiple myeloma patients."	( [Adverse effects of PAD and VAD regimens in multiple myeloma patients]. Bo, J; Dou, LP; Gao, CJ; Han, XP; Huang, WR; Jing, Y; Li, F; Li, HH; Wang, FF; Wang, QS; Wang, SH; Yu, L; Zhao, Y; Zhu, HY, 2010)	0.6
" Nonhematologic grade 3/4 adverse events were reported in 35% of once-weekly patients and 51% of twice-weekly patients (P = ."	( Efficacy and safety of once-weekly bortezomib in multiple myeloma patients. Benevolo, G; Boccadoro, M; Bringhen, S; Callea, V; Cangialosi, C; Cavalli, M; Cavo, M; De Rosa, L; Evangelista, A; Falcone, AP; Gaidano, G; Gentili, S; Genuardi, M; Grasso, M; Guglielmelli, T; Larocca, A; Levi, A; Liberati, AM; Musto, P; Nozzoli, C; Palumbo, A; Patriarca, F; Ria, R; Rizzo, V; Rossi, D, 2010)	0.64
"To compare the efficacy and adverse effects of bortezomib + adriamycin + dexamethasone (PAD) and vincristine + adriamycin + dexamethasone (VAD) regimens in untreated multiple myeloma (MM)."	( [The efficacy and safety of PAD and VAD regimens for untreated multiple myeloma]. Bo, J; Dou, LP; Gao, CJ; Han, XP; Huang, WR; Jing, Y; Li, HH; Wang, QS; Wang, SH; Yu, L; Zhao, Y; Zhu, HY, 2010)	0.62
" Both clinical effects and adverse effects were observed."	( [The efficacy and safety of PAD and VAD regimens for untreated multiple myeloma]. Bo, J; Dou, LP; Gao, CJ; Han, XP; Huang, WR; Jing, Y; Li, HH; Wang, QS; Wang, SH; Yu, L; Zhao, Y; Zhu, HY, 2010)	0.36
" However, these benefits are accompanied by increases in treatment-related adverse events (AEs), which may be particularly pronounced in older individuals."	( Practical management of adverse events in multiple myeloma: can therapy be attenuated in older patients? Bringhen, S; Mateos, MV; Palumbo, A; San Miguel, JF, 2011)	0.37
"Toxicity data from cancer trials are summarized into a single outcome, dose-limiting toxicity (DLT), which does not account for multiple lower grade toxic effects nor differentiates between toxicity types and gradations within DLT."	( Toxicity burden score: a novel approach to summarize multiple toxic effects. Cheung, YK; Hershman, DL; Lee, SM; Leonard, JP; Martin, P, 2012)	0.38
"17 for each grade 3 or higher nonhematologic toxic effects unrelated to treatment."	( Toxicity burden score: a novel approach to summarize multiple toxic effects. Cheung, YK; Hershman, DL; Lee, SM; Leonard, JP; Martin, P, 2012)	0.38
" It includes information from the grades and types of multiple toxic effects and can be applied in all phases of drug development."	( Toxicity burden score: a novel approach to summarize multiple toxic effects. Cheung, YK; Hershman, DL; Lee, SM; Leonard, JP; Martin, P, 2012)	0.38
" The most common adverse events were mild to moderate (grades 1, 2)."	( [The efficacy and safety of bortezomib plus thalidomide in treatment of newly diagnosed multiple myeloma]. Chen, SL; Gao, W; Jiang, B; Qiu, LG; Yu, L; Zhong, YP, 2011)	0.66
"To establish the clinical use of bortezomib with fewer adverse events, we retrospectively analyzed the efficacy and safety of bortezomib plus dexamethasone (BD) therapy for relapsed or refractory multiple myeloma."	( Efficacy and safety of bortezomib plus dexamethasone therapy for refractory or relapsed multiple myeloma: once-weekly administration of bortezomib may reduce the incidence of gastrointestinal adverse events. Fujita, Y; Fukushima, T; Iwao, H; Masaki, Y; Miki, M; Motoo, Y; Nakajima, A; Nakajima, H; Nakamura, T; Sakai, T; Sato, T; Sawaki, T; Tanaka, M; Umehara, H, 2011)	0.96
" Initially, bortezomib was administered twice-weekly, but some severe adverse events developed; therefore, from January 2008, bortezomib was administered twice-weekly for the first two courses, followed by once-weekly for the subsequent courses."	( Efficacy and safety of bortezomib plus dexamethasone therapy for refractory or relapsed multiple myeloma: once-weekly administration of bortezomib may reduce the incidence of gastrointestinal adverse events. Fujita, Y; Fukushima, T; Iwao, H; Masaki, Y; Miki, M; Motoo, Y; Nakajima, A; Nakajima, H; Nakamura, T; Sakai, T; Sato, T; Sawaki, T; Tanaka, M; Umehara, H, 2011)	1.06
"Once-weekly administration of bortezomib in BD therapy may reduce the incidence of gastrointestinal adverse events without reducing the clinical efficacy of this therapy for refractory or relapsed multiple myeloma."	( Efficacy and safety of bortezomib plus dexamethasone therapy for refractory or relapsed multiple myeloma: once-weekly administration of bortezomib may reduce the incidence of gastrointestinal adverse events. Fujita, Y; Fukushima, T; Iwao, H; Masaki, Y; Miki, M; Motoo, Y; Nakajima, A; Nakajima, H; Nakamura, T; Sakai, T; Sato, T; Sawaki, T; Tanaka, M; Umehara, H, 2011)	0.97
" In both arms, greater rates of severe hematologic adverse events were associated with RI (eGFR < 50 mL/min), however, therapy discontinuation rates were unaffected."	( Safety and efficacy of bortezomib-melphalan-prednisone-thalidomide followed by bortezomib-thalidomide maintenance (VMPT-VT) versus bortezomib-melphalan-prednisone (VMP) in untreated multiple myeloma patients with renal impairment. Baldini, L; Benevolo, G; Boccadoro, M; Bringhen, S; Cascavilla, N; Cavo, M; Di Raimondo, F; Gentile, M; Grasso, M; Guglielmelli, T; Majolino, I; Marasca, R; Mazzone, C; Montefusco, V; Morabito, F; Musolino, C; Musto, P; Nozzoli, C; Offidani, M; Palumbo, A; Patriarca, F; Petrucci, MT; Ria, R; Rossi, D; Vincelli, I, 2011)	0.68
" Adverse reactions to bortezomib or a treatment regimen that included it occurred in 32 (54%) patients, highlighting neurotoxicity in 19 patients (32%) and gastrointestinal toxicity in 12 (20%)."	( [Observational retrospective study to evaluate the effectiveness and safety of treatment schemes with bortezomib for multiple myeloma in our hospital]. de Arriba de la Fuente, F; Iranzo Fernández, MD; León-Villar, J; Moreno Belmonte, MJ; Titos-Arcos, JC, )	0.66
"A 74-year-old female with relapsed multiple myeloma was treated with twice-weekly bortezomib plus dexamethasone (BD)therapy, but severe gastrointestinal adverse events(grade 3 paralytic ileus and constipation)developed."	( [Once-weekly bortezomib plus dexamethasone therapy induced complete response, reducing severe gastrointestinal adverse events for a patient with relapsed multiple myeloma - a case report]. Fujita, Y; Fukushima, T; Iwao, H; Masaki, Y; Miki, M; Nakajima, A; Nakamura, T; Sakai, T; Sato, T; Sawaki, T; Tanaka, M; Umehara, H, 2012)	0.97
"Combined curcumin and PS-341 treatment has been reported to enhance cytotoxicity and minimize adverse effects through ERK and p38MAPK mechanisms in human multiple myeloma cells."	( Curcumin enhances cytotoxic effects of bortezomib in human multiple myeloma H929 cells: potential roles of NF-κB/JNK. Bai, QX; Zhang, XY, 2012)	0.65
"Patients were graded for bortezomib-related toxicities: hematologic and gastrointestinal toxicities by Common Terminology Criteria for Adverse Events and peripheral neuropathy by modified Functional Assessment of Cancer Therapy questionnaire and Common Terminology Criteria for Adverse Events."	( Prospective evaluation of the toxicity profile of proteasome inhibitor-based therapy in renal transplant candidates and recipients. Alloway, RR; Girnita, AL; Hanseman, DJ; Sadaka, B; Schmidt, N; Shields, AR; Walsh, RC; Woodle, ES, 2012)	0.68
" Evidence from animal models of chemotherapy-induced painful peripheral neuropathy produced by the taxane agent, paclitaxel, and the platinum-complex agent, oxaliplatin, indicate that they produce neuropathy via a common mechanism-a toxic effect on the mitochondria in primary afferent sensory neurons."	( Mitotoxicity and bortezomib-induced chronic painful peripheral neuropathy. Bennett, GJ; Xiao, WH; Zheng, H, 2012)	0.72
" However, adverse effects and drug resistance have been observed in patients, which is now emerging as a great challenge for the extended application of bortezomib."	( Dissecting bortezomib: development, application, adverse effects and future direction. Cao, B; Li, J; Mao, X, 2013)	0.98
" These agents have specific adverse event (AE) profiles, and it is especially important to consider severe AEs that may lead to premature discontinuation, negatively affecting outcomes."	( How to maintain patients on long-term therapy: understanding the profile and kinetics of adverse events. Mateos, MV, 2012)	0.38
" Most drug-related adverse events (AEs) (all grades, all cycles) were mild."	( Efficacy and toxicity of two schedules of bortezomib in patients with recurrent or refractory follicular lymphoma: a randomised phase II trial from the Groupe d'Etude des Lymphomes de l'Adulte (GELA). Bosly, A; Bouabdallah, R; Boue, F; Bron, D; Casasnovas, O; Coiffier, B; Delarue, R; Feugier, P; Haioun, C; Offner, F; Ribrag, V; Tilly, H, 2013)	0.65
"Cutaneous toxicity is a frequent side effect of new anticancer targeted therapies."	( Cutaneous adverse reactions linked to targeted anticancer therapies bortezomib and lenalidomide for multiple myeloma: new drugs, old side effects. Brandi, G; Dika, E; Maibach, H; Patrizi, A; Tacchetti, P; Venturi, M, 2014)	0.64
"This study evaluates the impact of cutaneous adverse drug reactions (cADR) of the new therapies bortezomib and lenalidomide and presents a review of their skin side effects."	( Cutaneous adverse reactions linked to targeted anticancer therapies bortezomib and lenalidomide for multiple myeloma: new drugs, old side effects. Brandi, G; Dika, E; Maibach, H; Patrizi, A; Tacchetti, P; Venturi, M, 2014)	0.86
" Three adverse events linked to bortezomib and 4 to lenalidomide forced to a complete withdrawal of the drug, while 3 reactions due to bortezomib mandated a dose reduction."	( Cutaneous adverse reactions linked to targeted anticancer therapies bortezomib and lenalidomide for multiple myeloma: new drugs, old side effects. Brandi, G; Dika, E; Maibach, H; Patrizi, A; Tacchetti, P; Venturi, M, 2014)	0.92
" Our study suggests that cutaneous toxicities, when researched by Dermatologists, are a side effect even more frequent than the reported data."	( Cutaneous adverse reactions linked to targeted anticancer therapies bortezomib and lenalidomide for multiple myeloma: new drugs, old side effects. Brandi, G; Dika, E; Maibach, H; Patrizi, A; Tacchetti, P; Venturi, M, 2014)	0.64
"Bortezomib retreatment regimen is demonstrated a higher response rate in patients who achieved deeper response in initial treatment, with no more adverse events."	( [The efficacy and safety analysis of bortezomib retreatment in 76 patients with relapsed/refractory multiple myeloma]. Du, J; Fan, JL; Fu, WJ; Hou, J; Jiang, H; Jin, LN; Lan, HF; Lu, J; Yuan, ZG; Zeng, TM; Zhang, CY; Zhou, F; Zhou, LL, 2013)	2.11
" Low-dose lenalidomide therapy was effective and safe against MM with a bortezomib-associated lung disorder."	( Safety and effectiveness of low-dose lenalidomide therapy for multiple myeloma complicated with bortezomib-associated interstitial pneumonia. Ihara, K; Inomata, H; Kato, J; Kikuchi, S; Koyama, R; Muramatsu, H; Nagamachi, Y; Nishisato, T; Nozawa, E; Okamoto, T; Ono, K; Tanaka, S; Yamada, H; Yamauchi, N; Yano, T, 2013)	0.84
"4%) experienced grade 3 or higher adverse events, while only one (5."	( [Efficacy and safety study of subcutaneous injection of bortezomib in the treatment of de novo patients with multiple myeloma]. Fu, CC; Gu, B; Jin, S; Li, WY; Liu, H; Ma, L; Sun, AN; Wu, DP; Wu, Q; Xin, X; Xue, SL; Zhao, SF; Zhu, XM, 2013)	0.64
"The improved PAD regimen by changing bortezomib from intravenous administration to subcutaneous injection significantly reduced adverse events, improved the safety of clinical application of bortezomib without affecting curative effect, and had great progress."	( [Efficacy and safety study of subcutaneous injection of bortezomib in the treatment of de novo patients with multiple myeloma]. Fu, CC; Gu, B; Jin, S; Li, WY; Liu, H; Ma, L; Sun, AN; Wu, DP; Wu, Q; Xin, X; Xue, SL; Zhao, SF; Zhu, XM, 2013)	0.91
" Peripheral neuropathy is likely to be a class side effect of these drugs, although its severity is largely variable, and it deserves to be further investigated, since the mechanisms of BTZ-induced peripheral neurotoxicity (BiPN) are still unknown."	( Evaluation of tubulin polymerization and chronic inhibition of proteasome as citotoxicity mechanisms in bortezomib-induced peripheral neuropathy. Bennett, DL; Canta, A; Carozzi, VA; Cavaletti, G; Ceresa, C; Chiorazzi, A; Colombo, M; Foudah, D; La Russa, F; Marmiroli, P; Meregalli, C; Miloso, M; Nicolini, G; Oggioni, N; Sala, B, 2014)	0.62
" The outcomes and adverse effects of two groups were retrospectively evaluated and compared."	( [Safety and efficacy of subcutaneous administration of bortezomib in the treatment of multiple myeloma]. Ding, SH; Wang, QS; Wang, YS; Wang, ZT; Wu, F, 2014)	0.65
" No significant differences of other adverse events between the two groups were observed."	( [Safety and efficacy of subcutaneous administration of bortezomib in the treatment of multiple myeloma]. Ding, SH; Wang, QS; Wang, YS; Wang, ZT; Wu, F, 2014)	0.65
" Because a safe Bu exposure was unknown in patients receiving this combination, Bu was initially targeted to a total area under the concentration-time curve (AUC) of 20,000 μM × minute."	( Safety and efficacy of targeted-dose busulfan and bortezomib as a conditioning regimen for patients with relapsed multiple myeloma undergoing a second autologous blood progenitor cell transplantation. Akpek, G; Armstrong, E; Elekes, A; Freytes, CO; Kato, K; Patil, S; Ratanatharathorn, V; Reece, DE; Rodriguez, TE; Sahovic, E; Shaughnessy, PJ; Smith, A; Solomon, SR; Stadtmauer, EA; Toro, JJ; Tricot, GJ; White, DJ; Yeh, RF; Yu, LH; Zhao, C, 2014)	0.66
" Salvage therapy must be tailored according to an individual patient's clinical profile, with the risks and potential effects of treatment-related adverse events being major determinants of the choice of therapy."	( Treatment-related adverse events in patients with relapsed/refractory multiple myeloma. Vij, R, 2011)	0.37
" One of the most significant adverse events is peripheral neuropathy, mainly involving sensory nerve fibers that can lead to withdrawal of treatment."	( Toxic effects of bortezomib on primary sensory neurons and Schwann cells of adult mice. Alé, A; Bruna, J; Herrando, M; Navarro, X; Udina, E, 2015)	0.76
"To explore the biomarker for predicting the occurrence of adverse events in myeloma patients treated by intravenous bortezomib, we measured proteasome activity in peripheral blood mononuclear cells."	( Measurement of Proteasome Activity in Peripheral Blood Mononuclear Cells as an Indicator of Susceptibility to Bortezomib-Induced Severe Neurological Adverse Events in Patients with Multiple Myeloma. Cho, Y; Fujisawa, F; Hori, M; Kamoshita, M; Katsura, Y; Kojima, H; Komeno, T; Kudo, D; Mukai, HY; Okoshi, Y; Ota, I; Sasaki, K; Shimizu, S; Shinagawa, A; Tanaka, K; Yoshida, C, 2015)	0.84
" BTZ loaded liposomes showed a significant reduction of drug systemic adverse effects with respect to free drug, even at the highest dose tested."	( Tumor vascular targeted liposomal-bortezomib minimizes side effects and increases therapeutic activity in human neuroblastoma. Brignole, C; Cilli, M; Di Paolo, D; Emionite, L; Loi, M; Marchetti, C; Milelli, A; Minarini, A; Pagnan, G; Parise, A; Pastorino, F; Perri, P; Petretto, A; Piaggio, F; Pistoia, V; Ponzoni, M; Tumiatti, V; Zuccari, G, 2015)	0.7
" Our data suggest that single-dose gemcitabine together with G-CSF is an effective mobilization regimen in myeloma patients and a safe alternative non-myelosuppressive mobilization chemotherapy for myeloma patients with bortezomib-induced polyneuropathy."	( Stem cell mobilization chemotherapy with gemcitabine is effective and safe in myeloma patients with bortezomib-induced neurotoxicity. Betticher, D; Egger, T; Keller, S; Mansouri Taleghani, B; Mueller, BU; Pabst, T; Rauch, D; Seipel, K, 2016)	0.84
"Pomalidomide and dexamethasone favored prolonged and safe exposure to treatment in 40% of heavily treated and end-stage RRMM, a paradigm shift in the natural history of RRMM characterized with a succession of shorter disease-free intervals and ultimately shorter survival."	( Safe and prolonged survival with long-term exposure to pomalidomide in relapsed/refractory myeloma. Arnulf, B; Attal, M; Avet-Loiseau, H; Banos, A; Benbouker, L; Brechiniac, S; Caillot, D; Decaux, O; Escoffre-Barbe, M; Facon, T; Fermand, JP; Fouquet, G; Garderet, L; Hulin, C; Karlin, L; Kolb, B; Leleu, X; Macro, M; Marit, G; Mathiot, C; Moreau, P; Pegourie, B; Petillon, MO; Richez, V; Rodon, P; Roussel, M; Royer, B; Stoppa, AM; Wetterwald, M, 2016)	0.43
"Chemotherapy-induced peripheral neuropathy (CIPN) is a major dose limiting side effect that can lead to long-term morbidity."	( Neurotoxicity to DRG neurons varies between rodent strains treated with cisplatin and bortezomib. Beutler, AS; Kanwar, R; Kulkarni, A; Pleticha, J; Podratz, JL; Staff, NP; Windebank, AJ, 2016)	0.66
" Complete response (CR), progression-free survival (PFS), overall survival (OS), and adverse events (AE) were combined."	( Efficacy and Safety of Novel Agent-Based Therapies for Multiple Myeloma: A Meta-Analysis. Li, Y; Wang, X; Yan, X, 2016)	0.43
" Response rates, overall survival, progression-free survival, and adverse effects were retrospectively analyzed."	( [A cohort study comparing the efficacy and safety of bortezomib plus dexamethasone versus bortezomib, epirubicin and dexamethasone in patients with multiple myeloma]. Chen, H; Hao, QY; Huang, XJ; Liu, KY; Lu, J; Wen, L, 2016)	0.68
" (4) Grade 3 and 4 adverse events were recorded with a higher number of patients in the PAD group than those in the BD group."	( [A cohort study comparing the efficacy and safety of bortezomib plus dexamethasone versus bortezomib, epirubicin and dexamethasone in patients with multiple myeloma]. Chen, H; Hao, QY; Huang, XJ; Liu, KY; Lu, J; Wen, L, 2016)	0.68
" Areas covered: This review focuses on the safety data from clinical trials for the three approved PIs and how to manage adverse effects."	( Safety of proteasome inhibitors for treatment of multiple myeloma. Lonial, S; Panjic, EH; Schlafer, D; Shah, KS, 2017)	0.46
" We comprehensively compared the overall response rate (ORR) and the incidence of adverse events between subcutaneous and intravenous bortezomib."	( Efficacy and safety of subcutaneous versus intravenous bortezomib in multiple myeloma: a meta-analysis . Cao, J; Hu, B; Wang, J; Wu, T; Yang, X; Yi, L; Zhou, Q; Zhuang, L, 2017)	0.91
" The RCTs subgroup did not find statistical differences in these two adverse events."	( Efficacy and safety of subcutaneous versus intravenous bortezomib in multiple myeloma: a meta-analysis . Cao, J; Hu, B; Wang, J; Wu, T; Yang, X; Yi, L; Zhou, Q; Zhuang, L, 2017)	0.7
" We demonstrated that CK1α inactivation, while toxic for myeloma cells, is dispensable for the survival of healthy B lymphocytes and stromal cells."	( Inactivation of CK1α in multiple myeloma empowers drug cytotoxicity by affecting AKT and β-catenin survival signaling pathways. Barilà, G; Bonaldi, L; Cabrelle, A; Carrino, M; Costacurta, M; Gianesin, K; Macaccaro, P; Manni, S; Manzoni, M; Martines, A; Neri, A; Nunes, SC; Piazza, F; Semenzato, G; Taiana, E; Trentin, L; Tubi, LQ; Zambello, R, 2017)	0.46
" The common adverse events (AEs) were in line with the well-known toxicity profiles associated with VMP."	( A prospective, open-label, multicenter, observational study to evaluate the efficacy and safety of bortezomib-melphalan-prednisone as initial treatment for autologous stem cell transplantation-ineligible patients with multiple myeloma. Bae, SB; Bae, SH; Cho, DY; Choi, CW; Do, YR; Hyun, MS; Jeong, SH; Jo, DY; Joo, YD; Kim, BS; Kim, H; Kim, HG; Kim, HJ; Kim, JA; Kim, JS; Kim, K; Kim, KH; Kim, MK; Kim, SH; Kim, SJ; Kim, SY; Kim, YS; Kwak, JY; Lee, HS; Lee, JH; Lee, JJ; Lee, JO; Lee, MH; Lee, SM; Lee, WS; Lim, SN; Min, CK; Moon, JH; Mun, YC; Nam, SH; Park, JS; Park, KW; Park, MR; Park, SK; Shin, HJ; Song, MK; Yi, HG; Yoon, SS, 2017)	0.67
" The main concerns on adverse events were thrombosis/embolism events, peripheral neuropathy, and second primary malignancies."	( Efficacy and safety of bortezomib, thalidomide, and lenalidomide in multiple myeloma: An overview of systematic reviews with meta-analyses. Aguiar, PM; Colleoni, GWB; de Mendonça Lima, T; Storpirtis, S, 2017)	0.77
"Neurotoxicity is a relevant side effect of bortezomib treatment."	( Kinesin-5 Blocker Monastrol Protects Against Bortezomib-Induced Peripheral Neurotoxicity. Barham, M; Bobylev, I; Klein, I; Lehmann, HC; Neiss, WF; Peters, D; von Strandmann, EP; Vyas, M, 2017)	0.98
" Despite this benefit, patients in the panobinostat arm experienced higher rates of adverse events (AEs) and higher rates of discontinuation due to AEs."	( Panobinostat plus bortezomib and dexamethasone: impact of dose intensity and administration frequency on safety in the PANORAMA 1 trial. Beksac, M; Corrado, C; Dimopoulos, MA; Einsele, H; Elghandour, A; Guenther, A; Hou, J; Hungria, VTM; Jedrzejczak, WW; Lee, JH; Lonial, S; Moreau, P; Na Nakorn, T; Paul, S; Redhu, S; Richardson, PG; Salwender, H; San-Miguel, JF; Schlossman, RL; Siritanaratkul, N; Sopala, M; Yoon, SS, 2017)	0.79
"Fibroblast growth factor receptor 1 oncogene partner N-terminal like gene (FOPNL) rs72773978 polymorphism was identified as an adverse prognostic factor in multiple myeloma (MM)."	( The adverse effect of FOPNL genomic variant is reversed by bortezomib-based treatment protocols in multiple myeloma. Andrikovics, H; Balassa, K; Bors, A; Csacsovszki, O; Kiss, KP; Kovy, P; Kozma, A; Masszi, T; Meggyesi, N; Mikala, G; Remenyi, P; Tordai, A; Valyi-Nagy, I; Varga, G, 2018)	0.72
" Interestingly, we found that metformin could be used to potentiate the bortezomib-mediated cytotoxicity against PEL cells and to inhibit the activation of KSHV lytic cycle, a side effect of this treatment that resulted in a block of autophagy in these cells."	( Metformin triggers apoptosis in PEL cells and alters bortezomib-induced Unfolded Protein Response increasing its cytotoxicity and inhibiting KSHV lytic cycle activation. Cirone, M; D'Orazi, G; Faggioni, A; Gilardini Montani, MS; Gonnella, R; Granato, M; Romeo, MA; Santarelli, R, 2017)	0.94
" The most common study drug-related adverse events (all grades) were thrombocytopenia (72%), fatigue (56%), neuropathy (50%), anorexia (44%) and rash (39%)."	( Phase I trial of bortezomib daily dose: safety, pharmacokinetic profile, biological effects and early clinical evaluation in patients with advanced solid tumors. Angevin, E; Bahleda, R; Bernard, A; Chaturvedi, S; Deutsch, E; Gazzah, A; Hanley, M; Hollebecque, A; Le Deley, MC; Massard, C; Poterie, A; Ribrag, V; Ricard, D; Sallansonnet-Froment, M; Soria, JC; Taillia, H; Touat, M; Van De Velde, H; Varga, A, 2018)	0.82
" Interestingly, several adverse effects are less common, compared to BTZ, in patients treated with CFZ."	( Milder degenerative effects of Carfilzomib vs. Bortezomib in the Drosophila model: a link to clinical adverse events. Bagratuni, T; Brieudes, V; Dimopoulos, MA; Florea, BI; Halabalaki, M; Kastritis, E; Overkleeft, HS; Papanagnou, ED; Scorrano, L; Skaltsounis, AL; Terpos, E; Trougakos, IP; Tsakiri, EN, 2017)	0.71
" All patients (n = 8) experienced Grade ≥ 3 treatment-emergent adverse events (TEAE), with thrombocytopenia (n = 6, 75%) being the most frequent."	( Safety and efficacy of daratumumab in combination with bortezomib and dexamethasone in Japanese patients with relapsed or refractory multiple myeloma. Aoki, M; Ichinohe, T; Iida, S; Shinagawa, A; Suzuki, K; Takezako, N, 2018)	0.73
" Adverse events included neutropenia (92/76%), thrombocytopenia (70/10%) and leukopenia (65/50%)."	( Efficacy and safety of frontline rituximab, cyclophosphamide, doxorubicin and prednisone plus bortezomib (VR-CAP) or vincristine (R-CHOP) in a subset of newly diagnosed mantle cell lymphoma patients medically eligible for transplantation in the randomized Belch, A; Bosly, A; Bunworasate, U; Cavalli, F; Dascalescu, A; Drach, J; Farber, C; Huang, H; Masliak, Z; Novak, J; Pei, L; Robak, T; Rooney, B; Samoilova, O; van de Velde, H; Vilchevskaya, K; Zaucha, J, 2018)	0.7
"In the bortezomib group, four out of eight patients discontinued the trial; three others failed to complete the minimum protocol treatment due to adverse reactions."	( Multicenter double-blind randomized controlled trial to evaluate the effectiveness and safety of bortezomib as a treatment for refractory systemic lupus erythematosus. Chiu, SW; Fujii, H; Fujita, Y; Harigae, H; Ichinose, K; Ishii, T; Kawakami, A; Saito, K; Shirai, T; Shirota, Y; Tanaka, Y; Watanabe, R; Yamaguchi, T, 2018)	1.15
"As bortezomib therapy for SLE is associated with many adverse reactions, treatment indications should be selected carefully, and protocols should aim to prevent these occurrences."	( Multicenter double-blind randomized controlled trial to evaluate the effectiveness and safety of bortezomib as a treatment for refractory systemic lupus erythematosus. Chiu, SW; Fujii, H; Fujita, Y; Harigae, H; Ichinose, K; Ishii, T; Kawakami, A; Saito, K; Shirai, T; Shirota, Y; Tanaka, Y; Watanabe, R; Yamaguchi, T, 2018)	1.32
" One hundred thirty-seven multiple myeloma patients on maintenance lenalidomide or bortezomib post-auto-HCT who received either MMR or herpes zoster vaccine were analyzed and any adverse events documented in the medical record in the 42 days following vaccination were recorded."	( Safety of live-attenuated measles-mumps-rubella and herpes zoster vaccination in multiple myeloma patients on maintenance lenalidomide or bortezomib after autologous hematopoietic cell transplantation. Baden, LR; Hammond, SP; Issa, NC; Laubach, JP; Leblebjian, H; Marty, FM; Pandit, A; Richardson, PG, 2018)	0.91
" The primary endpoint was adverse events."	( Bortezomib is safe in and stabilizes pulmonary function in patients with allo-HSCT-associated pulmonary CGVHD. Budinger, G; Dematte, J; Duffey, S; Jain, M; Jovanovic, B; Mehta, J, 2018)	1.92
" We confirmed that overall incidence of adverse events, including peripheral neuropathy, was low, and in no case required admission to emergency service, contributing to reduce the rate of therapy discontinuation."	( Safety and comfort of domestic bortezomib injection in real-life experience. Catalano, L; Cerchione, C; Di Perna, M; Nappi, D; Pane, F; Pareto, AE; Picardi, M; Zacheo, I, 2018)	0.77
" Carfilzomib (CFZ) has high selectivity and minimal off-target adverse effects including lower rates of PNP."	( Efficacy and toxicity profile of carfilzomib based regimens for treatment of multiple myeloma: A systematic review. Abraham, I; Anwer, F; Iftikhar, A; Kapoor, V; Latif, A; McBride, A; Mushtaq, A; Riaz, IB; Zahid, U, 2018)	0.48
"The therapeutic efficacy of different doses of dexamethasone combined with bortezomib and thalidomide for patients with multiple myeloma is similar, can obviously enhance remission rate, prolong the survival time, promote life quality, but the incidence of adverse reactions in low dose dexamethason rigemen is significantly reduced, and the safety is better."	( [Clinical Efficacy and Safety of Different Doses of Dexamethasone Combined with Bortezomib and Thalidomide for Treating Patients with Multiple Myeloma]. Fu, LP; Ji, Y; Li, CS; Zhang, WP, 2018)	0.94
" While the addition of panobinostat to bortezomib and dexamethasone has demonstrated response and progression-free survival benefits, the incidence and severity of adverse events associated with it can create a challenge for clinicians and patients."	( Incidence and management of adverse events associated with panobinostat in the treatment of relapsed/refractory multiple myeloma. Arnall, JR; Harvey, RD; Moore, DC, 2019)	0.78
" Although gastrointestinal disturbances and fatigue are the most common adverse effects, peripheral neuropathy and thrombocytopenia are the key dose-limiting toxicities of bortezomib-based combination regimens."	( The safety of bortezomib for the treatment of multiple myeloma. Beksac, M; Cengiz Seval, G, 2018)	1.04
"Chemotherapy-induced peripheral neurotoxicity (CIPN) is a severe adverse effect in patients receiving antitumor agents, and no effective treatment is available."	( High-dose intravenous immunoglobulins reduce nerve macrophage infiltration and the severity of bortezomib-induced peripheral neurotoxicity in rats. Alberti, P; Ballarini, E; Briani, C; Brivio, R; Canta, A; Carozzi, VA; Cavaletti, G; Chiorazzi, A; Fumagalli, G; Galliani, C; Marjanovic, I; Marmiroli, P; Meregalli, C; Monza, L; Oggioni, N; Pozzi, E; Quartu, M; Rodriguez-Menendez, V; Scali, C; Spinoni, N, 2018)	0.7
"Our results suggest a prominent role of neuroinflammation in BIPN and that IVIg might be considered as a possible safe and effective therapeutic option preventing M1 macrophage infiltration."	( High-dose intravenous immunoglobulins reduce nerve macrophage infiltration and the severity of bortezomib-induced peripheral neurotoxicity in rats. Alberti, P; Ballarini, E; Briani, C; Brivio, R; Canta, A; Carozzi, VA; Cavaletti, G; Chiorazzi, A; Fumagalli, G; Galliani, C; Marjanovic, I; Marmiroli, P; Meregalli, C; Monza, L; Oggioni, N; Pozzi, E; Quartu, M; Rodriguez-Menendez, V; Scali, C; Spinoni, N, 2018)	0.7
" Neither cumulative nor transient alterations were found in our metrics, suggesting that bortezomib is safe from a cardiovascular standpoint for patients free of cardiovascular disease."	( Bortezomib-based Chemotherapy for Multiple Myeloma Patients Without Comorbid Cardiovascular Disease Shows No Cardiotoxicity. Broberg, C; Ferencik, M; Heitner, SB; Medvedova, E; Minnier, J; Naher, A; Ritts, A; Scott, EC; Silbermann, R; Van Woerkom, RC, 2018)	2.15
" We observed minimal adverse effects, mainly hematological toxicity."	( A Bortezomib-Based Protocol Induces a High Rate of Complete Remission with Minor Toxicity in Adult Patients with Relapsed/Refractory Acute Lymphoblastic Leukemia. Gatt, ME; Gural, A; Nachmias, B; Shapira, M; Shaulov, A, 2018)	1.2
" A grade 4 hematological adverse event (AE) was observed in 1 patient."	( Efficacy and Safety of a Weekly Cyclophosphamide-Bortezomib-Dexamethasone Regimen as Induction Therapy Prior to Autologous Stem Cell Transplantation in Japanese Patients with Newly Diagnosed Multiple Myeloma: A Phase 2 Multicenter Trial. Akiyama, M; Doki, N; Fujio, T; Hori, M; Igarashi, A; Kakihana, K; Kobayashi, T; Kojima, H; Komeno, T; Kudo, D; Kumagai, T; Mukae, J; Najima, Y; Nakamura, Y; Ohashi, K; Okoshi, Y; Saito, T; Shinagawa, A; Takano, H; Tanaka, K; Toyota, S; Tsutsumi, I; Wakimoto, N; Yamamoto, K; Yamamoto, M; Yoshida, C, 2019)	0.77
" The aggresome pathway has been described as an escape mechanism from proteotoxicity by sequestering toxic cellular aggregates."	( Proteasome inhibitor b-AP15 induces enhanced proteotoxicity by inhibiting cytoprotective aggresome formation. Brnjic, S; D'Arcy, P; Hillert, EK; Linder, S; Mazurkiewicz, M; Mofers, A; Saei, AA; Selvaraju, K; Zhang, X; Zubarev, R, 2019)	0.51
" Common adverse events included hematological toxicities including neutropenia and lymphopenia; however, the rate of febrile neutropenia was low (3."	( Evaluation of the safety and efficacy of daratumumab outside of clinical trials. Abe, Y; Kitadate, A; Kobayashi, H; Matsue, K; Miura, D; Narita, K; Takeuchi, M; Terao, T; Tsushima, T, 2019)	0.51
" Exposure-adjusted incidences per 100 patient-years of adverse events (AEs) were 1352."	( Carfilzomib-Dexamethasone Versus Bortezomib-Dexamethasone in Relapsed or Refractory Multiple Myeloma: Updated Overall Survival, Safety, and Subgroups. Chng, WJ; Dimopoulos, M; Goldschmidt, H; Kimball, AS; Ludwig, H; Moreau, P; Niesvizky, R; Oriol, A; Orlowski, RZ; Yang, Z, 2019)	0.8
" Twenty-six (65%) patients experimented adverse events: 8 patients (20%) underwent 12 serious AE (≥grade 3)."	( Efficacy and safety of autologous stem cell transplantation after induction therapy with lenalidomide, bortezomib, and dexamethasone. Arcani, R; Azouza, W; Brunet, C; Colle, J; Costello, R; Fanciullino, R; Farnault, L; Ivanov, V; Lafage, M; Mercier, C; Pourroy, B; Roche, P; Suchon, P; Venton, G, 2019)	0.73
"Administration of 1 dose of BTZ at peak G-CSF mobilization was safe and well tolerated, enhanced stem cell mobilization, and did not affect graft viability."	( A Phase I Study of the Safety and Feasibility of Bortezomib in Combination With G-CSF for Stem Cell Mobilization in Patients With Multiple Myeloma. DiPersio, JF; Fiala, MA; Ghobadi, A; Rettig, M; Schroeder, M; Stockerl-Goldstein, K; Uy, GL; Vij, R; Westervelt, P, 2019)	0.77
" There were 10 fatal infections, and the most frequent adverse events were mild infusion-associated reactions and hematologic toxicities."	( Real-world data on the efficacy and safety of daratumumab treatment in Hungarian relapsed/refractory multiple myeloma patients. Adamkovich, N; Alizadeh, H; Bereczki, Á; Borbényi, Z; Csacsovszki, O; Csukly, Z; Egyed, M; Farkas, P; Illés, Á; Lovas, S; Masszi, T; Mikala, G; Nagy, Z; Plander, M; Rajnics, P; Rejtő, L; Schneider, T; Szaleczky, E; Szendrei, T; Szomor, Á; Varga, G; Váróczy, L; Wohner, N; Wolf, K, 2019)	0.51
" Peripheral neuropathy was the most widely reported adverse event."	( The efficacy and safety of bortezomib-based chemotherapy for immunoglobulin light chain amyloidosis: A systematic review and meta-analysis. Bai, M; Dong, R; Li, L; Liu, B; Sun, S; Wang, D; Wang, Y; Zhao, J, 2019)	0.81
"Current evidence indicates that bortezomib-based regimens might be effective and safe therapies for patients with AL amyloidosis."	( The efficacy and safety of bortezomib-based chemotherapy for immunoglobulin light chain amyloidosis: A systematic review and meta-analysis. Bai, M; Dong, R; Li, L; Liu, B; Sun, S; Wang, D; Wang, Y; Zhao, J, 2019)	1.09
" However, Btz has severe systemic adverse effects, which would limit its use as a bone anabolic agent."	( Targeting Bortezomib to Bone Increases Its Bone Anabolic Activity and Reduces Systemic Adverse Effects in Mice. Boeckman, RK; Boyce, BF; Ebetino, FH; Lin, X; Srinivasan, V; Sun, W; Tao, J; Wang, H; Wu, T; Xing, L; Zhang, H, 2020)	0.96
" The most common adverse events included diarrhea, fatigue and nausea."	( Pilot Trial AMC-063: Safety and Efficacy of Bortezomib in AIDS-associated Kaposi Sarcoma. Aboulafia, D; Ambinder, RF; Dickson, MA; Dittmer, DP; Gorelick, RJ; Lensing, SY; Maldarelli, F; Mitsuyasu, R; Reid, EG; Suazo, A; Wachsman, W, 2020)	0.82
" Outcomes assessed included overall response rate (ORR), complete response (CR) rate, overall survival (OS), progression-free survival (PFS), and adverse events."	( Matching-adjusted Indirect Comparisons of the Efficacy and Safety of Acalabrutinib Versus Other Targeted Therapies in Relapsed/Refractory Mantle Cell Lymphoma. Abhyankar, S; Kabadi, SM; Signorovitch, J; Song, J; Telford, C; Yao, Z; Zhao, J, 2019)	0.51
" However, some patients discontinue VRd because of severe adverse events, despite its high efficacy."	( The efficacy and safety of modified bortezomib-lenalidomide-dexamethasone in transplant-eligible patients with newly diagnosed multiple myeloma. Abe, Y; Ishida, T; Miyazaki, K; Nashimoto, J; Ogura, M; Okazuka, K; Sato, K; Suzuki, K; Tsukada, N; Uto, Y; Yoshiki, Y, 2020)	0.83
" In this study, we aimed to identify anticancer agents that increase TLS risk, as classified by a TLS panel consensus, using the US Food and Drug Administration Adverse Event Reporting System (FAERS) database."	( Tumor lysis syndrome associated with bortezomib: A post-hoc analysis after signal detection using the US Food and Drug Administration Adverse Event Reporting System. Hotta, Y; Kimura, K; Kondo, M; Nishikawa, R; Sanagawa, A; Tohkin, M, 2020)	0.83
" PRACTICAL APPLICATIONS: The testis damage caused by the treatment with bortezomib was not eliminated by (1 → 3)-β-D-glucan and as a result, β-1,3-(D)-glucan enhanced the toxicity by leading a decrease in the levels of GSH, SOD, and CAT, thus caused an elevation in the immunoreactivity of NF-κB and altered the histopathological changes by enhancing the toxic effects of bortezomib."	( (1 → 3)-β-d-glucan enhances the toxicity induced by Bortezomib in rat testis. Abuc, OO; Akaras, N; Atilay, H; Bal, T; Erol, HS; Geyikoglu, F; Gul, M; Koc, K; Yigit, S, 2020)	1.04
" In this systematic review, associations of the efficacy of each approved regimen with adverse events (AEs) and the total cost per cycle were compared with a Bayesian network meta-analysis (NMA) of phase 3 randomized controlled trials (RCTs)."	( Association of adverse events and associated cost with efficacy for approved relapsed and/or refractory multiple myeloma regimens: A Bayesian network meta-analysis of phase 3 randomized controlled trials. Aryal, M; Chhabra, S; D'Souza, A; Dhakal, B; Ghose, S; Giri, S; Hamadani, M; Hari, PN; Janz, S; Narra, RK; Pathak, LK; Smunt, TL; Szabo, A, 2020)	0.56
" Treatment-emergent adverse events were consistent with DARA SC in MM and CyBorD."	( Daratumumab plus CyBorD for patients with newly diagnosed AL amyloidosis: safety run-in results of ANDROMEDA. Bumma, N; Comenzo, RL; Jaccard, A; Kastritis, E; Kaufman, JL; Kovacsovics, T; Lee, HC; Maurer, MS; Medvedova, E; Merlini, G; Minnema, MC; Palladini, G; Qin, X; Rosenzweig, M; Sanchorawala, V; Vasey, SY; Vermeulen, J; Wechalekar, AD; Weiss, BM; Zonder, J, 2020)	0.56
" General and bortezomib-specific adverse events are monitored continuously."	( Generate-Boost: study protocol for a prospective, multicenter, randomized controlled, double-blinded phase II trial to evaluate efficacy and safety of bortezomib in patients with severe autoimmune encephalitis. Chung, HY; Geis, C; Günther, A; Lehmann, T; Leypoldt, F; Platzer, S; Prüss, H; Scherag, A; Wickel, J, 2020)	1.13
"Neurotoxicity is a common side effect of chemotherapeutics that often leads to the development of chemotherapy-induced peripheral neuropathy (CIPN)."	( Prokineticin Receptor Inhibition With PC1 Protects Mouse Primary Sensory Neurons From Neurotoxic Effects of Chemotherapeutic Drugs Amodeo, G; Franchi, S; Kalpachidou, T; Kress, M; Lattanzi, R; Moschetti, G; Sacerdote, P, 2020)	0.56
" All patients experienced adverse events (AEs), with diarrhea (80."	( Phase II, Multicenter, Single-Arm, Open-Label Study to Evaluate the Efficacy and Safety of Panobinostat in Combination with Bortezomib and Dexamethasone in Japanese Patients with Relapsed or Relapsed-and-Refractory Multiple Myeloma. Maki, A; Matsumoto, M; Shimada, F; Shimizu, K; Sunami, K; Suzuki, K, 2021)	0.83
" Grade 3-4 adverse events occurred in 71 (91%) of 78 patients in the 20 mg three times weekly group, 69 (83%) of 83 patients in the 20 mg twice weekly group, and 60 (75%) of 80 patients in the 10 mg three times weekly group; the most common (≥20% patients in any group) grade 3-4 adverse events were thrombocytopenia (33 [42%] of 78, 26 [31%] of 83, and 19 [24%] of 83 patients) and neutropenia (18 [23%], 13 [16%], and six [8%])."	( Efficacy and safety of oral panobinostat plus subcutaneous bortezomib and oral dexamethasone in patients with relapsed or relapsed and refractory multiple myeloma (PANORAMA 3): an open-label, randomised, phase 2 study. Abdo, A; Beksac, M; Bladé, J; Chari, A; Dimopoulos, MA; Gonçalves, IZ; Hájek, R; Hungria, VTM; Illés, Á; Jacobasch, L; Laubach, JP; Lech-Maranda, E; Lonial, S; Maison-Blanche, P; Mariz, M; Moreau, P; Polprasert, C; Rajkumar, SV; Richardson, PG; San-Miguel, JF; Schjesvold, F; Shelekhova, T; Spencer, A; Spicka, I; Sureda, A; Wróbel, T, 2021)	0.86
"6% adverse cytogenetics and 25."	( Real-world effectiveness and safety of daratumumab, bortezomib and dexamethasone in relapsed/refractory multiple myeloma in Slovakia. Bátorová, A; Chudej, J; Drgoňa, Ľ; Flochová, E; Guman, T; Harvanová, Ľ; Hlebašková, M; Kubala, J; Ladická, M; Mistrík, M; Simančíková, I; Šimek, M; Štecová, N; Štulajterová, V; Vranovský, A; Wild, A, 2021)	0.87
" Most common (≥2 patients) grade 3 or 4 adverse events were neutropenia (12 patients [27%]), rash (4 patients [9%]), lung infection (3 patients [7%]), and increased alanine aminotransferase level (2 patients [4%])."	( Safety and Effectiveness of Weekly Carfilzomib, Lenalidomide, Dexamethasone, and Daratumumab Combination Therapy for Patients With Newly Diagnosed Multiple Myeloma: The MANHATTAN Nonrandomized Clinical Trial. Arcila, ME; Caple, J; Chansakul, A; Chung, DJ; Ciardello, A; Concepcion, I; Derkach, A; Diamond, B; Dogan, A; Giralt, SA; Harrison, A; Hassoun, H; Ho, C; Hultcrantz, M; Jones, K; Korde, N; Lahoud, OB; Landau, HJ; Landgren, O; Lesokhin, AM; Lu, SX; Maclaughlan, K; Mailankody, S; Maura, F; Murata, K; Piacentini, C; Ramanathan, L; Rispoli, J; Roshal, M; Rustad, EH; Salcedo, M; Sams, A; Schlossman, J; Scordo, M; Shah, G; Shah, UA; Shekarkhand, T; Tan, C; Tavitian, E; Thoren, K; Verducci, D; Werner, K; Yellapantula, V, 2021)	0.62
" This study evaluated reports of PN encountered with all three PIs using the Food and Drug Administration Adverse Event (AE) Reporting System (FAERS)."	( Post-Marketing Analysis of Peripheral Neuropathy Burden with New-Generation Proteasome Inhibitors Using the FDA Adverse Event Reporting System Burns, EA; Hashmi, SK; Mina, SA; Muhsen, IN; Pingali, SR; Sarfraz, H; Xu, J, 2021)	0.62
" Observational studies based on the FDA Adverse Event Reporting System database analysis and systematic reviews indicate that the incidence of peripheral neuropathy (PN) and tumor lysis syndrome (TLS) tends to be higher with bortezomib than that of other drugs."	( Comprehensive Analysis of Bortezomib-Induced Adverse Events Using the Japanese Real-World Database. Fujiwara, M; Satoki, A; Shimizu, T; Uchida, M; Uesawa, Y, 2022)	1.21
"The purpose of this study was to determine the frequency of bortezomib AEs in Japanese patients and to determine the incidence, time to onset, and post hoc outcomes of unique AEs using the Japanese Adverse Drug Event Report database."	( Comprehensive Analysis of Bortezomib-Induced Adverse Events Using the Japanese Real-World Database. Fujiwara, M; Satoki, A; Shimizu, T; Uchida, M; Uesawa, Y, 2022)	1.26
"To investigate the association between bortezomib and AEs, we analyzed the Japanese Adverse Drug Event Report database, which contains spontaneous AE reports submitted to the Pharmaceuticals and Medical Devices Agency from April 2004 to December 2020."	( Comprehensive Analysis of Bortezomib-Induced Adverse Events Using the Japanese Real-World Database. Fujiwara, M; Satoki, A; Shimizu, T; Uchida, M; Uesawa, Y, 2022)	1.29
"The clinical data of elderly patients with MM were retrospectively analyzed, including age, treatment regimen, efficacy, adverse reactions, and the Frailty score included in the activity of daily living score, the instrumental activity of daily living scale and the Charlson comorbidity index."	( [Evaluation of the Efficacy and Safety of Chemotherapy in Elderly Patients with Multiple Myeloma under Different Frailty Scores]. Cheng, L; Ma, YP; Song, LM; Xue, R, 2022)	0.72
" During the induction of bortezomib, the incidence of adverse reactions for the patients in the triple group (78."	( [Evaluation of the Efficacy and Safety of Chemotherapy in Elderly Patients with Multiple Myeloma under Different Frailty Scores]. Cheng, L; Ma, YP; Song, LM; Xue, R, 2022)	1.02
"Cancer survivors may experience long-term adverse effects of cancer treatments such as premature ovarian failure and infertility."	( Bortezomib-Induced Ovarian Toxicity in Mice. Monsef, YA; Mutluay, D; Tenekeci, GY, 2022)	2.16
"For transplant-ineligible newly diagnosed multiple myeloma, DARA SC (monotherapy/with Rd) was safe and preferred over DARA IV."	( Switching to daratumumab SC from IV is safe and preferred by patients with multiple myeloma. Basu, S; Beksac, M; Carson, R; Cook, G; Delioukina, M; Gries, KS; Kudva, A; Mateos, MV; Pei, H; Rigaudeau, S; Schots, R; Spicka, I; Tromp, B; Van Rampelbergh, R; White, D; Wrobel, T; Wroblewski, S, 2023)	0.91
"1% had grade 3-4 or higher drug-related adverse reactions, mainly hematological toxicity, and no patients died of adverse reactions."	( Efficacy and safety analysis of bortezomib-based triplet regimens sequential lenalidomide in newly diagnosed multiple myeloma patients. Liu, Y; Su, J; Wen, J; Xu, F; Yue, J; Zhang, Y; Zhou, Q, 2023)	1.19
" Adverse events of grade 3 or worse that occurred with a higher incidence in the carfilzomib-based regimens group compared with the bortezomib-based regimens group were dyspnea, hypertension, acute kidney injury, and heart failure."	( Efficacy and toxicity of carfilzomib- or bortezomib-based regimens for treatment of transplant-ineligible patients with newly diagnosed multiple myeloma: A meta-analysis. Huang, J; Liu, Q; Wei, M; Wu, F; Xie, C; Yang, F, 2022)	1.19
" Selinexor combination therapy is both safe and effective for patients with pretreated RRMM."	( Efficacy and safety of selinexor-based regimens for relapsed/refractory multiple myeloma: a systematic review of literature. Davis, JA; Ehsan, H; Hansen, DK; Hashmi, H; Iqbal, Q; Masood, A, 2022)	0.72
" Altogether, these findings indicate that arginase inhibitors could be further tested as a complementary strategy in multiple myeloma to mitigate adverse cardiac events without compromising antitumor efficacy of proteasome inhibitors."	( Targeting arginase-1 exerts antitumor effects in multiple myeloma and mitigates bortezomib-induced cardiotoxicity. Bany-Laszewicz, U; Barankiewicz, J; Borg, K; Ciepiela, O; Garbicz, F; Golab, J; Grzywa, TM; Juszczynski, P; Kedzierska, H; Lech-Maranda, E; Mackiewicz, U; Maczewski, M; Nowis, D; Okninska, M; Papiernik, D; Paterek, A; Pilch, Z; Pyrzynska, B; Ramji, K; Rodziewicz-Lurzynska, A; Sadowski, R; Sklepkiewicz, P; Sosnowska, A; Staruch, A; Zerrouqi, A, 2022)	0.95
" BTZ-induced peripheral neuropathy (BIPN) is the most common adverse effect of BTZ with an incidence as high as 40-60%."	( Lysosomal dysfunction in Schwann cells is involved in bortezomib-induced peripheral neurotoxicity. Li, X; Wang, H; Wang, K; Wu, J; Wu, Z; Xu, G; Yan, W; Yang, M; Zhang, X; Zhu, D, 2023)	1.16
" The risk of cardiac adverse events (CAEs) with PIs has been documented with bortezomib and carfilzomib; however, only a few studies have been reported on ixazomib."	( Cardiac Adverse Events Associated with Multiple Myeloma Patients Treated with Proteasome Inhibitors. Endo, M; Fujiwara, M; Goto, M; Shimizu, T; Uchida, M, 2023)	1.14
"This study aimed to determine the safety signals of adverse events related to CAEs, the effect of concomitant medications, the time to the occurrence of CAEs, and the incidence of fatal clinical outcomes after the occurrence of CAEs for three PIs using the US Pharmacovigilance database."	( Cardiac Adverse Events Associated with Multiple Myeloma Patients Treated with Proteasome Inhibitors. Endo, M; Fujiwara, M; Goto, M; Shimizu, T; Uchida, M, 2023)	0.91
"We examined 1,567,240 cases of 231 drugs registered as anticancer drugs in the US Food and Drug Administration Adverse Event Reporting System (FAERS) database from January 1997 to March 2021."	( Cardiac Adverse Events Associated with Multiple Myeloma Patients Treated with Proteasome Inhibitors. Endo, M; Fujiwara, M; Goto, M; Shimizu, T; Uchida, M, 2023)	0.91
" However, no adverse event CAE signals were observed with ixazomib treatment."	( Cardiac Adverse Events Associated with Multiple Myeloma Patients Treated with Proteasome Inhibitors. Endo, M; Fujiwara, M; Goto, M; Shimizu, T; Uchida, M, 2023)	0.91
" Our study showed VPd induction is safe and efficacious in NDMM."	( Efficacy and safety of pomalidomide, bortezomib, and dexamethasone combination chemotherapy for newly diagnosed multiple myeloma: POMACE Phase II Study. Dubashi, B; Ganesan, P; Halanaik, D; Kar, R; Kayal, S; Nisha, Y; Saj, F, 2023)	1.18
" The primary outcomes were Overall Survival (OS) and Progression Free Survival (PFS, measured as time to next treatment), and the secondary outcomes were Adverse Events (AE)."	( Real-world effectiveness and safety of multiple myeloma treatments based on thalidomide and bortezomib: A retrospective cohort study from 2009 to 2020 in a Brazilian metropolis. Costa, IHFD; Drummond, PLM; Malta, JS; Menezes de Pádua, CA; Reis, AMM; Santos, RMMD; Silveira, LP, 2023)	1.13

Excerpt	Reference	Relevance
" Bortezomib is rapidly distributed into tissues after administration of a single dose, with an initial plasma distribution half-life of less than 10 minutes, followed by a terminal elimination half-life of more than 40 hours."	( Pharmacology, pharmacokinetics, and practical applications of bortezomib. Davidson, T; Schwartz, R, 2004)	1.47
" Pharmacokinetic evaluation showed a biexponential decline, characterized by a rapid distribution followed by a longer elimination, after dose administration, whereas the area under the concentration-time curve increased proportionately with the dose."	( Phase I and II pharmacokinetic and pharmacodynamic study of the proteasome inhibitor bortezomib in Japanese patients with relapsed or refractory multiple myeloma. Ando, K; Hotta, T; Itoh, K; Kagami, Y; Kobayashi, Y; Maruyama, D; Minami, H; Morishima, Y; Nakata, M; Ogawa, Y; Ogura, M; Taji, H; Tobinai, K; Tsuchiya, T; Watanabe, T, 2008)	0.57
" Pharmacodynamic studies performed included assessment of levels of 20S proteasome activity and ubiquitin-protein conjugates."	( A phase I pharmacodynamic trial of bortezomib in combination with doxorubicin in patients with advanced cancer. Alberti, D; Binger, K; Eickhoff, J; Geiger, P; Heideman, J; Kolesar, J; LoConte, NK; Marnocha, R; Thomas, JP; Utecht, K; Wilding, G, 2008)	0.62
" pharmacokinetic data on 670 drugs representing, to our knowledge, the largest publicly available set of human clinical pharmacokinetic data."	( Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds. Lombardo, F; Obach, RS; Waters, NJ, 2008)	0.35
"This open-label, crossover, pharmacokinetic drug-drug interaction study was conducted at seven institutions in the US and Europe between January 2005 and August 2006."	( Effect of the cytochrome P450 2C19 inhibitor omeprazole on the pharmacokinetics and safety profile of bortezomib in patients with advanced solid tumours, non-Hodgkin's lymphoma or multiple myeloma. Acharya, M; Britten, CD; Chan, K; Cohen, N; Dudov, A; Fuloria, J; Gabrail, N; Nemunaitis, J; Quinn, DI; Yee, L, 2009)	0.57
" Bortezomib pharmacokinetic parameters were similar when bortezomib was administered alone or with omeprazole (maximum plasma concentration 120 vs 123 ng/mL; area under the plasma concentration-time curve from 0 to 72 hours 129 vs 135 ng ."	( Effect of the cytochrome P450 2C19 inhibitor omeprazole on the pharmacokinetics and safety profile of bortezomib in patients with advanced solid tumours, non-Hodgkin's lymphoma or multiple myeloma. Acharya, M; Britten, CD; Chan, K; Cohen, N; Dudov, A; Fuloria, J; Gabrail, N; Nemunaitis, J; Quinn, DI; Yee, L, 2009)	1.48
" Using 20S proteasome inhibition as a pharmacodynamic marker and analyzing bortezomib tumor exposures, we show that efficacy was achieved only when suitable drug exposures drove proteasome inhibition that was sustained over time."	( The relationship among tumor architecture, pharmacokinetics, pharmacodynamics, and efficacy of bortezomib in mouse xenograft models. Babcock, T; Bannerman, B; Cao, Y; Hatsis, P; Kupperman, E; Robertson, R; Silva, MD; Terkelsen, J; Williamson, MJ; Xia, C; Yu, L, 2009)	0.8
" Systemic exposures of bortezomib were similar between dose groups considering the relatively narrow dose range and the observed pharmacokinetic variability, although there was no readily apparent deviation from dose-proportionality."	( Pharmacokinetic and pharmacodynamic study of two doses of bortezomib in patients with relapsed multiple myeloma. Acharya, M; Burris, H; Chatta, G; Karol, M; Keith Stewart, A; Lonial, S; Mohrbacher, AF; Neuwirth, R; Reece, DE; Riordan, WJ; Shustik, C; Sullivan, D; Venkatakrishnan, K; von Moltke, LL; Zannikos, P, 2011)	0.92
" This study evaluated the effects of co-administration of a potent CYP3A4 inducer (rifampicin [rifampin]) and a weak CYP3A4 inducer (dexamethasone) on the pharmacokinetic, pharmacodynamic and safety profiles of bortezomib."	( Effect of cytochrome P450 3A4 inducers on the pharmacokinetic, pharmacodynamic and safety profiles of bortezomib in patients with multiple myeloma or non-Hodgkin's lymphoma. Feng, H; Girgis, S; Hellmann, A; Louw, VJ; Patel, H; Rule, S; Shpilberg, O; Skee, DM; van de Velde, H; Walewski, J, 2011)	0.77
" Blood samples were collected on days 11 through 14 of cycles 2 and 3 before and after bortezomib administration, at prespecified time points, for pharmacokinetic and pharmacodynamic (proteasome inhibition) assessments."	( Effect of cytochrome P450 3A4 inducers on the pharmacokinetic, pharmacodynamic and safety profiles of bortezomib in patients with multiple myeloma or non-Hodgkin's lymphoma. Feng, H; Girgis, S; Hellmann, A; Louw, VJ; Patel, H; Rule, S; Shpilberg, O; Skee, DM; van de Velde, H; Walewski, J, 2011)	0.81
" Pharmacokinetic data showed peak plasma levels of ACY-1215 at 4 hours after treatment coincident with an increase in acetylated α-tubulin, a marker of HDAC6 inhibition, by immunohistochemistry and Western blot analysis."	( Preclinical activity, pharmacodynamic, and pharmacokinetic properties of a selective HDAC6 inhibitor, ACY-1215, in combination with bortezomib in multiple myeloma. Anderson, KC; Bradner, J; Canavese, M; Cirstea, D; Eda, H; Hideshima, T; Jarpe, M; Jones, SS; Kung, AL; Mazitschek, R; Ogier, WC; Raje, N; Rodig, S; Santo, L; Scullen, T; Tamang, D; Tseng, JC; van Duzer, JH; Yang, M, 2012)	0.58
"The mechanism, preclinical testing, and clinical activity of perifosine in CRC and MM are discussed, with supportive pharmacokinetic information presented."	( Perifosine , an oral, anti-cancer agent and inhibitor of the Akt pathway: mechanistic actions, pharmacodynamics, pharmacokinetics, and clinical activity. Anderson, KC; Eng, C; Hideshima, T; Kolesar, J; Richardson, PG, 2012)	0.38
" Pharmacodynamic analysis showed FLT3 down-regulation on day 26 of cycle 1 (P = ."	( Clinical and pharmacodynamic activity of bortezomib and decitabine in acute myeloid leukemia. Bloomfield, CD; Blum, W; Byrd, JC; Caligiuri, MA; Chan, KK; Curfman, JP; Devine, SM; Eisfeld, AK; Garr, C; Garzon, R; Geyer, S; Grever, MR; Jacob, S; Kefauver, C; Klisovic, R; Marcucci, G; Perrotti, D; Santhanam, R; Schwind, S; Tarighat, SS; Walker, A; Wang, H; Whitman, S, 2012)	0.64
"Data were analysed from the pharmacokinetic substudy of the randomized phase III MMY-3021 study and the phase I CAN-1004 study of subcutaneous versus intravenous bortezomib in patients aged ≥18 (MMY-3021) or ≤75 (CAN-1004) years with symptomatic relapsed or refractory MM after 1-3 (MMY-3021) or ≥1 (CAN-1004) prior therapies."	( Pharmacokinetic, pharmacodynamic and covariate analysis of subcutaneous versus intravenous administration of bortezomib in patients with relapsed multiple myeloma. Cakana, A; Deraedt, W; Domnikova, N; Doronin, VA; Esseltine, DL; Facon, T; Feng, H; Girgis, S; Hulin, C; Karamanesht, II; Kyselyova, MY; Leleu, X; Moreau, P; Schmidt, A; Skee, D; van de Velde, H; Venkatakrishnan, K; Vilchevska, KV, 2012)	0.79
" Blood 20S proteasome inhibition pharmacodynamic parameters were also similar with subcutaneous versus intravenous bortezomib: mean maximum effect (E(max)) was 63."	( Pharmacokinetic, pharmacodynamic and covariate analysis of subcutaneous versus intravenous administration of bortezomib in patients with relapsed multiple myeloma. Cakana, A; Deraedt, W; Domnikova, N; Doronin, VA; Esseltine, DL; Facon, T; Feng, H; Girgis, S; Hulin, C; Karamanesht, II; Kyselyova, MY; Leleu, X; Moreau, P; Schmidt, A; Skee, D; van de Velde, H; Venkatakrishnan, K; Vilchevska, KV, 2012)	0.8
"Subcutaneous administration results in equivalent bortezomib plasma exposure to intravenous administration, together with comparable blood 20S proteasome inhibition pharmacodynamic effects."	( Pharmacokinetic, pharmacodynamic and covariate analysis of subcutaneous versus intravenous administration of bortezomib in patients with relapsed multiple myeloma. Cakana, A; Deraedt, W; Domnikova, N; Doronin, VA; Esseltine, DL; Facon, T; Feng, H; Girgis, S; Hulin, C; Karamanesht, II; Kyselyova, MY; Leleu, X; Moreau, P; Schmidt, A; Skee, D; van de Velde, H; Venkatakrishnan, K; Vilchevska, KV, 2012)	0.84
"Abstract This phase I study was conducted to determine the maximum tolerated dose (MTD) and dose limiting toxicities (DLTs) of the heat shock protein 90 (HSP90) inhibitor 17-allyamino-17-demethoxygeldanamycin (17-AAG) in combination with bortezomib, and to provide pharmacokinetic data in relapsed or refractory acute myeloid leukemia (AML)."	( Pharmacokinetics and dose escalation of the heat shock protein inhibitor 17-allyamino-17-demethoxygeldanamycin in combination with bortezomib in relapsed or refractory acute myeloid leukemia. Binkley, P; Blum, KA; Blum, W; Byrd, JC; Garzon, R; Geyer, S; Grever, MR; Jiang, Y; Johnston, JS; Kefauver, C; Klisovic, R; Marcucci, G; Phelps, MA; Walker, AR, 2013)	0.78
" A pharmacodynamic model was developed that included three critical proteins (phospho-NFκB, BclxL, and cleaved poly (ADP ribose) polymerase)."	( Logic-Based and Cellular Pharmacodynamic Modeling of Bortezomib Responses in U266 Human Myeloma Cells. Abernethy, DR; Chudasama, VL; Mager, DE; Ovacik, MA, 2015)	0.67
" A physiologically based pharmacokinetic (PBPK) model incorporating tissue drug-target binding was developed to test the hypothesis of proteasome-mediated bortezomib disposition."	( Physiologically-based pharmacokinetic modeling of target-mediated drug disposition of bortezomib in mice. Mager, DE; Zhang, L, 2015)	0.84
" In addition, Cmax was associated with a progression-free survival advantage."	( Bortezomib pharmacokinetics in tumor response and peripheral neuropathy in multiple myeloma patients receiving bortezomib-containing therapy. Choi, K; Han, S; Hong, T; Lee, J; Lee, SE; Min, CK; Park, GJ; Yim, DS, 2017)	1.9
" We aimed at exploring if daily low dose administration of bortezomib may allow a greater and tolerable pharmacokinetic exposure which might be required for antitumor activity in solid tumors."	( Phase I trial of bortezomib daily dose: safety, pharmacokinetic profile, biological effects and early clinical evaluation in patients with advanced solid tumors. Angevin, E; Bahleda, R; Bernard, A; Chaturvedi, S; Deutsch, E; Gazzah, A; Hanley, M; Hollebecque, A; Le Deley, MC; Massard, C; Poterie, A; Ribrag, V; Ricard, D; Sallansonnet-Froment, M; Soria, JC; Taillia, H; Touat, M; Van De Velde, H; Varga, A, 2018)	1.06
" The pharmacokinetic profile of intravenous bortezomib is characterized by a two-compartment model with a rapid initial distribution phase followed by a longer elimination phase and a large volume of distribution."	( Clinical Pharmacokinetics and Pharmacodynamics of Bortezomib. Abdul-Majeed, S; Barta, SK; Cael, B; Tan, CRC, 2019)	1.03
" Population pharmacokinetic analyses were conducted to determine the pharmacokinetics of intravenous daratumumab in combination therapy versus monotherapy, evaluate the effect of patient- and disease-related covariates on drug disposition, and examine the relationships between daratumumab exposure and efficacy/safety outcomes."	( Pharmacokinetics and Exposure-Response Analyses of Daratumumab in Combination Therapy Regimens for Patients with Multiple Myeloma. Belch, A; Capra, M; Clemens, PL; Dimopoulos, MA; Gomez, D; Ho, PJ; Iida, S; Jansson, R; Leiba, M; Medvedova, E; Min, CK; Schecter, J; Sonneveld, P; Sun, YN; Xu, XS; Zhang, L, 2018)	0.48
" In this study, a pharmacodynamic systems modeling approach was used to link in vitro bortezomib exposure and myeloma cell death."	( Pharmacodynamic Models of Differential Bortezomib Signaling Across Several Cell Lines of Multiple Myeloma. Mager, DE; Ramakrishnan, V, 2019)	1.01
" This study illustrates the importance of incorporating target biology, drug-target interactions and in vitro clearance parameters into mechanistic PBPK/PD models and the utility of such models for pharmacokinetic, pharmacodynamic and DDI predictions."	( A Translational Physiologically Based Pharmacokinetics/Pharmacodynamics Framework of Target-Mediated Disposition, Target Inhibition and Drug-Drug Interactions of Bortezomib. Hanley, M; Iwasaki, S; Venkatakrishnan, K; Xia, C; Zhu, A, 2020)	0.75
" Simulations revealed that the greatest magnitude of pharmacodynamic drug interactions between bortezomib and vorinostat occurred at caspase-9, AKT, and Bcl-2."	( Cluster Gauss-Newton and CellNOpt Parameter Estimation in a Small Protein Signaling Network of Vorinostat and Bortezomib Pharmacodynamics. Chen, T; Ghasemi, M; Mager, DE; Nguyen, VA; Niu, J, 2021)	1.05
" The popPK analysis included pharmacokinetic and immunogenicity data from patients receiving daratumumab SC in combination with bortezomib, cyclophosphamide, and dexamethasone in the ANDROMEDA study (AMY3001; safety run-in, n = 28; randomized phase, n = 183)."	( Population Pharmacokinetics and Exposure-Response Modeling of Daratumumab Subcutaneous Administration in Patients With Light-Chain Amyloidosis. Comenzo, RL; Kastritis, E; Luo, MM; Merlini, G; Nnane, I; Qin, X; Sharma, A; Sun, YN; Tran, N; Vermeulen, J; Wechalekar, AD; Weiss, BM; Xiong, Y; Zhou, H; Zhu, PP, 2022)	0.93
" Pharmacokinetic profiles and pharmacodynamic analysis were performed to determine the change in tumor weight associated with the use of proteasome inhibitors."	( Pharmacokinetics-Pharmacodynamics Modeling and Evaluation of Tumor Response to Bortezomib Proteasome Inhibitor in Waldenstrom Macroglobulinemia. Bhatti, AI; Fazal, S; Munir, A; Sajjad, B, 2023)	1.14

Excerpt	Reference	Relevance
"Bortezomib and TRAIL represent a synergistic drug combination that warrants further evaluation in in vivo models of prostate cancer."	( Drug interactions between the proteasome inhibitor bortezomib and cytotoxic chemotherapy, tumor necrosis factor (TNF) alpha, and TNF-related apoptosis-inducing ligand in prostate cancer. Adams, J; An, J; Belldegrun, A; Fisher, M; Rettig, MB; Sun, YP, 2003)	2.01
"Bortezomib improves efficacy in combination with gemcitabine and carboplatin in NSCLC, but sequential effects are important and must be considered when developing therapeutic regimens."	( Effects of the proteasome inhibitor bortezomib alone and in combination with chemotherapy in the A549 non-small-cell lung cancer cell line. Bold, RJ; Mortenson, MM; Schlieman, MG; Virudachalam, S, 2004)	2.04
"3 mg/m2 IV days 1, 4, 8, and 11 every 3 weeks for eight cycles in combination with dexamethasone."	( Bortezomib in combination with dexamethasone for relapsed multiple myeloma. Berdel, WE; Bisping, G; Kienast, J; Kropff, MH; Tchinda, J; Volpert, S; Wenning, D, 2005)	1.77
"The anti-tumour in vitro activity of proteasome inhibitor bortezomib (PS-341, VELCADE) in combination with purine nucleoside analogues, cladribine (2-CdA) and fludarabine (FA) was tested in lymphocytes derived from 26 patients with B-cell chronic lymphocytic leukaemia (B-CLL)."	( In vitro cytotoxic effect of proteasome inhibitor bortezomib in combination with purine nucleoside analogues on chronic lymphocytic leukaemia cells. Cebula, B; Duechler, M; Linke, A; Robak, T; Schwarzmeier, JD; Shehata, M; Smolewski, P, 2005)	0.83
" The observed increase was especially evident when 5 nm of bortezomib were combined with suboptimal doses of 2-CdA or FA."	( In vitro cytotoxic effect of proteasome inhibitor bortezomib in combination with purine nucleoside analogues on chronic lymphocytic leukaemia cells. Cebula, B; Duechler, M; Linke, A; Robak, T; Schwarzmeier, JD; Shehata, M; Smolewski, P, 2005)	0.82
"Bortezomib, as a single agent and in combination with dexamethasone, was examined as first-line treatment in 32 consecutive patients with untreated symptomatic multiple myeloma."	( Bortezomib therapy alone and in combination with dexamethasone for previously untreated symptomatic multiple myeloma. Camacho, E; Crowley, J; Durie, BG; Gabayan, E; Irwin, D; Jagannath, S; Lutzky, J; Mazumder, A; McKinley, M; Schenkein, D; Wolf, J, 2005)	3.21
" To address the likelihood of clinical drug-drug interactions, the P450 inhibition potential of bortezomib and its major deboronated metabolites M1 and M2 and their dealkylated metabolites M3 and M4 was evaluated in human liver microsomes for the major P450 isoforms 1A2, 2C9, 2C19, 2D6, and 3A4/5."	( Investigation of drug-drug interaction potential of bortezomib in vivo in female Sprague-Dawley rats and in vitro in human liver microsomes. Gallegos, R; Gan, LS; Li, P; Lu, C; Miwa, GT; Nix, D; Pusalkar, S; Uttamsingh, V; Xia, CQ, 2006)	0.8
" We studied the in vitro cytotoxic effects of BOR in combination with anti-CD20 (rituximab, RIT) or anti-CD52 (campath, CAM) monoclonal antibodies on B-CLL cells."	( Additive cytotoxic effect of bortezomib in combination with anti-CD20 or anti-CD52 monoclonal antibodies on chronic lymphocytic leukemia cells. Cebula, B; Duechler, M; Grzybowska-Izydorczyk, O; Linke, A; Robak, T; Shehata, M; Smolewski, P, 2006)	0.63
"We present here a case of severe, but reversible, congestive cardiac failure in a lung cancer patient who had no prior cardiac history, after receiving an experimental treatment of bortezomib combined with chemotherapy."	( Severe reversible cardiac failure after bortezomib treatment combined with chemotherapy in a non-small cell lung cancer patient: a case report. Giaccone, G; Voortman, J, 2006)	0.79
" Two different treatment schedules of bortezomib in combination with paclitaxel and carboplatin were tested in this phase I study to evaluate the effects of scheduling on toxicities, pharmacodynamics and clinical activity."	( A phase I and pharmacologic study of sequences of the proteasome inhibitor, bortezomib (PS-341, Velcade), in combination with paclitaxel and carboplatin in patients with advanced malignancies. Adjei, AA; Alberts, SR; Bruzek, L; Croghan, GA; Erlichman, C; Hanson, LJ; Jatoi, A; Ma, C; Mandrekar, SJ; Pitot, HC; Reid, JM; Tan, AD; Wright, JJ, 2007)	0.84
" Findings from preclinical studies prompted a Phase I trial to determine the maximum tolerated dose (MTD) and dose-limiting toxicities (DLTs) of bortezomib in combination with gemcitabine in patients with recurring/refractory advanced solid tumors."	( Phase I clinical trial of bortezomib in combination with gemcitabine in patients with advanced solid tumors. Appleman, LJ; Clark, JW; Cusack, J; Eder, JP; Enzinger, PC; Fidias, P; Fishman, M; Kashala, O; Lynch, T; Ryan, DP; Supko, JG; Zhu, AX, 2006)	0.83
"Bortezomib has modest single-agent activity in patients with relapsed or refractory advanced NSCLC using this schedule, with minor enhancement in combination with docetaxel."	( Randomized phase II study of bortezomib alone and bortezomib in combination with docetaxel in previously treated advanced non-small-cell lung cancer. Akerley, W; Axelrod, R; Belt, R; Carbone, DP; Crawford, J; Fanucchi, MP; Fidias, P; Fossella, FV; Govindan, R; Kashala, O; Kelly, K; Limentani, SA; Natale, R; Raez, LE; Reimers, HJ; Ribeiro, M; Robert, F; Schiller, JH; Sheng, S, 2006)	2.07
"To investigate the efficacy and toxicity of bortezomib in combination with dexamethasone for the treatment of patients with relapsed or refractory multiple myeloma(MM)."	( [Bortezomib in combination with dexamethasone for the treatment of relapsed or refractory multiple myeloma]. Chen, YB; Fu, WJ; Hou, J; Xi, H; Yang, SL; Yuan, ZG; Zhou, F, 2006)	1.51
"Bortezomib in combination with dexamethasone is an effective therapy with a high response rate and manageable toxicities for patients with relapsed or refractory myeloma."	( [Bortezomib in combination with dexamethasone for the treatment of relapsed or refractory multiple myeloma]. Chen, YB; Fu, WJ; Hou, J; Xi, H; Yang, SL; Yuan, ZG; Zhou, F, 2006)	2.69
"The proteasome inhibitor PS-341 (Bortezomib, Velcade) is currently being combined with taxanes in several clinical trials for treatment of patients with various solid tumors including lung cancers."	( Assessment of apoptosis-inducing effects of docetaxel combined with the proteasome inhibitor PS-341 in human lung cancer cells. Jung, CS; Khuri, FR; Sun, SY; Zhou, Z, 2007)	0.62
"The aim of this study was to investigate the effect of bortezomib alone and in combination with harringtonine on apoptosis of HL-60 cells."	( [Induction of apoptosis in HL-60 cells by bortezomib alone or in combination with harringtonine in vitro]. Fu, YB; Li, L; Meng, FY; Sun, QX, 2007)	0.85
" Furthermore, early phase I/II clinical trials have shown impressive activity of pegylated liposomal doxorubicin and conventional doxorubicin in combination with bortezomib in patients with newly diagnosed and relapsed/refractory myeloma."	( Emerging data on the use of anthracyclines in combination with bortezomib in multiple myeloma. Orlowski, RZ; Voorhees, PM, 2007)	0.78
"To establish maximum tolerated dose (MTD) and tolerability of two schedules of bortezomib in combination with cisplatin and gemcitabine as first-line treatment of patients with advanced solid tumors."	( A parallel dose-escalation study of weekly and twice-weekly bortezomib in combination with gemcitabine and cisplatin in the first-line treatment of patients with advanced solid tumors. Giaccone, G; Honeywell, R; Kuenen, BC; Peters, GJ; Smit, EF; van de Velde, H; Voortman, J, 2007)	0.81
" Bortezomib combined with DEX and CY is a highly effective treatment for relapsed MM at an acceptable rate of grade 3/4 AE."	( Bortezomib in combination with intermediate-dose dexamethasone and continuous low-dose oral cyclophosphamide for relapsed multiple myeloma. Berdel, WE; Bisping, G; Dechow, T; Einsele, H; Engelhardt, M; Heinecke, A; Hentrich, M; Kienast, J; Kröger, N; Kropff, M; Lang, N; Liebisch, P; Metzner, B; Salwender, H; Schuck, E; Sezer, O; Volpert, S; Wolf, HH, 2007)	2.69
"To investigate the effect of bortezomib alone and in combination with arsenic trioxide on apoptosis of HL-60 cells."	( [HL-60 cell apoptosis induced by bortezomib alone or in combination with arsenic trioxide in vitro]. Fu, YB; Li, L; Meng, FY; Sun, QX; Tian, S, 2007)	0.91
"HL-60 cells were treated with bortezomib alone or in combination with arsenic trioxide for 12 to 48 h and the cell proliferation was analyzed with MTT assay, and cell apoptosis detected by DNA gel electrophoresis, fluorescence microscopy and flow cytometry."	( [HL-60 cell apoptosis induced by bortezomib alone or in combination with arsenic trioxide in vitro]. Fu, YB; Li, L; Meng, FY; Sun, QX; Tian, S, 2007)	0.91
"Dose escalation studies were performed with eight squamous cell carcinoma cell lines using bortezomib alone or in combination with TAX or CDDP."	( Antiproliferative activity of bortezomib alone and in combination with cisplatin or docetaxel in head and neck squamous cell carcinoma cell lines. Ackermann, H; Baghi, M; Gstöttner, W; Hambek, M; Knecht, R; Strebhardt, K; Wagenblast, J, 2008)	0.86
"To investigate the antiproliferative effect of the histone deacetylase (HDAC) inhibitor MS-275 on cholangiocarcinoma cells alone and in combination with conventional cytostatic drugs (gemcitabine or doxorubicin) or the novel anticancer agents sorafenib or bortezomib."	( Histone deacetylase inhibitor MS-275 alone or combined with bortezomib or sorafenib exhibits strong antiproliferative action in human cholangiocarcinoma cells. Baradari, V; Höpfner, M; Huether, A; Scherübl, H; Schuppan, D, 2007)	0.76
" Furthermore, additive anti-neoplastic effects were observed when MS-275 treatment was combined with gemcitabine or doxorubicin, while combination with the multi-kinase inhibitor sorafenib or the proteasome inhibitor bortezomib resulted in overadditive anti-neoplastic effects."	( Histone deacetylase inhibitor MS-275 alone or combined with bortezomib or sorafenib exhibits strong antiproliferative action in human cholangiocarcinoma cells. Baradari, V; Höpfner, M; Huether, A; Scherübl, H; Schuppan, D, 2007)	0.77
"The growth of human cholangiocarcinoma cells can be potently inhibited by MS-275 alone or in combination with conventional cytostatic drugs or new, targeted anticancer agents."	( Histone deacetylase inhibitor MS-275 alone or combined with bortezomib or sorafenib exhibits strong antiproliferative action in human cholangiocarcinoma cells. Baradari, V; Höpfner, M; Huether, A; Scherübl, H; Schuppan, D, 2007)	0.58
" Here, we demonstrate its efficacy, both alone and in combination with other cytotoxic agents, in gastric cancer cell lines."	( Antitumor effects and drug interactions of the proteasome inhibitor bortezomib (PS341) in gastric cancer cells. Doihara, H; Fujita, T; Ino, H; Murakami, M; Naito, M; Shimizu, N; Washio, K, 2007)	0.58
"This phase I trial evaluated the dose-limiting toxicities (DLTs) and maximum tolerated dose (MTD) of the proteasome inhibitor bortezomib when combined with carboplatin in ovarian cancer patients with recurrent and platinum- and taxane-resistant disease."	( Phase I trial of the proteasome inhibitor bortezomib in combination with carboplatin in patients with platinum- and taxane-resistant ovarian cancer. Coleman, RL; Gershenson, DM; Johnston, TA; Landen, CN; Levenback, C; Milam, MR; Ramirez, PT, 2008)	0.82
"To assess the antitumor efficacy and adverse effects of bortezomib either used alone or in combination with arsenic trioxide for transplanted tumor in nude mice."	( [Effect of bortezomib used alone or in combination with arsenic trioxide on HL-60 cell xenograft in nude mice]. Cai, YX; Fu, YB; Li, L; Meng, FY; Sun, QX, 2007)	0.98
"Bortezomib alone and in combination with arsenic trioxide could both inhibit the growth of the transplanted tumors, prolong the survival of the nude mice, and induce cell apoptosis and growth inhibition of the HL-60 cells in vivo, and the combined administration exhibited even better effects."	( [Effect of bortezomib used alone or in combination with arsenic trioxide on HL-60 cell xenograft in nude mice]. Cai, YX; Fu, YB; Li, L; Meng, FY; Sun, QX, 2007)	2.17
"Bortezomib in combination with arsenic trioxide has significant antitumor effect in nude mice bearing HL-60 cell xenografts possibly by inducing HL-60 cell apoptosis and growth inhibition without producing no significant adverse effects."	( [Effect of bortezomib used alone or in combination with arsenic trioxide on HL-60 cell xenograft in nude mice]. Cai, YX; Fu, YB; Li, L; Meng, FY; Sun, QX, 2007)	2.17
" The objective of this study was to determine the maximum tolerated dose and dose-limiting toxicities of bortezomib in combination with celecoxib in patients with advanced solid tumors."	( Bortezomib in combination with celecoxib in patients with advanced solid tumors: a phase I trial. Chaudhary, U; Dunder, S; Green, M; Hayslip, J; Kraft, A; Meyer, M; Montero, AJ; Salzer, S; Sherman, C, 2007)	2
"Patients received escalating doses of bortezomib either on a weekly schedule (days 1, 8, 15, 22, and 29 repeated every 42 days) or on a twice-weekly administration schedule (days 1, 4, 8, and 11 repeated every 21 days), in combination with escalating doses of celecoxib twice daily throughout the study period from 200 mg to 400 mg twice daily."	( Bortezomib in combination with celecoxib in patients with advanced solid tumors: a phase I trial. Chaudhary, U; Dunder, S; Green, M; Hayslip, J; Kraft, A; Meyer, M; Montero, AJ; Salzer, S; Sherman, C, 2007)	2.05
"On May 17, 2007, doxorubicin HCl liposome injection (Doxil) in combination with bortezomib (Velcade) received approval from the US Food and Drug Administration (FDA) for the treatment of relapsed or refractory multiple myeloma after at least one prior therapy that has not included bortezomib."	( Liposomal doxorubicin in combination with bortezomib for relapsed or refractory multiple myeloma. Dagher, R; Farrell, AT; He, K; Justice, R; Ning, YM; Pazdur, R; Sridhara, R, 2007)	0.83
"Liposomal doxorubicin received FDA approval for use in combination with bortezomib in patients with multiple myeloma who have not previously received bortezomib and have received at least one prior therapy."	( Liposomal doxorubicin in combination with bortezomib for relapsed or refractory multiple myeloma. Dagher, R; Farrell, AT; He, K; Justice, R; Ning, YM; Pazdur, R; Sridhara, R, 2007)	0.84
" Thirty-two patients were treated with bortezomib alone and 25 were treated with chemotherapeutic agents that were given in combination with bortezomib."	( Bortezomib in combination with conventional chemotherapeutic agents for multiple myeloma compared with bortezomib alone. Eom, KS; Han, K; Kim, CC; Kim, M; Kim, Y; Lee, JW; Lee, MJ; Lee, S; Lim, J; Min, CK; Min, WS, 2007)	2.05
" In patients who received bortezomib combined with chemotherapeutic agents, 19 out of 25 patients (76%) showed an EOR, whereas 12 out of 32 patients (37."	( Bortezomib in combination with conventional chemotherapeutic agents for multiple myeloma compared with bortezomib alone. Eom, KS; Han, K; Kim, CC; Kim, M; Kim, Y; Lee, JW; Lee, MJ; Lee, S; Lim, J; Min, CK; Min, WS, 2007)	2.08
"Bortezomib in combination with common chemotherapeutic agents is more active in the treatment of relapsed, refractory MM than with bortezomib alone."	( Bortezomib in combination with conventional chemotherapeutic agents for multiple myeloma compared with bortezomib alone. Eom, KS; Han, K; Kim, CC; Kim, M; Kim, Y; Lee, JW; Lee, MJ; Lee, S; Lim, J; Min, CK; Min, WS, 2007)	3.23
" We conducted a phase I study of gemcitabine and carboplatin in combination with bortezomib."	( The proteasome inhibitor bortezomib in combination with gemcitabine and carboplatin in advanced non-small cell lung cancer: a California Cancer Consortium Phase I study. Bold, R; Davies, AM; Gandara, DR; Gumerlock, PH; Lara, PN; Lau, DH; Lenz, HJ; Ruel, C; Schenkein, DP; Shibata, S, 2008)	0.88
" We propose that this novel drug combination should receive further evaluation as a potentially effective anticancer therapy."	( Aggravated endoplasmic reticulum stress as a basis for enhanced glioblastoma cell killing by bortezomib in combination with celecoxib or its non-coxib analogue, 2,5-dimethyl-celecoxib. Chen, TC; Golden, EB; Hofman, FM; Kardosh, A; Louie, SG; Petasis, NA; Pyrko, P; Schönthal, AH; Uddin, J, 2008)	0.57
"The aim of this study was to investigate the effect of arsenic trioxide (As(2)O(3)) combined with bortezomib on the proliferation, apoptosis and beta-catenin level in myeloma cell lines."	( [Effect of arsenic trioxide combined with bortezomib on proliferation, apoptosis and beta-catenin level in myeloma cell lines]. Fu, WJ; Hou, J; Wang, DX; Yuan, ZG; Zhou, LL, 2008)	0.83
" No dose-limiting toxicities were noted at all bortezomib dose levels when administered with full dose capecitabine and oxaliplatin."	( Phase I study of capecitabine and oxaliplatin in combination with the proteasome inhibitor bortezomib in patients with advanced solid tumors. Beard, M; Cohen, SJ; Engstrom, PF; Langer, CJ; Lewis, NL; McLaughlin, S; Meropol, NJ; Weiner, LM, 2008)	0.82
"Weekly bortezomib can be safely combined with full doses of capecitabine and oxaliplatin."	( Phase I study of capecitabine and oxaliplatin in combination with the proteasome inhibitor bortezomib in patients with advanced solid tumors. Beard, M; Cohen, SJ; Engstrom, PF; Langer, CJ; Lewis, NL; McLaughlin, S; Meropol, NJ; Weiner, LM, 2008)	1.02
" Here we examined the sensitivity of bone marrow cells from AML patients (34 patients: 25 newly diagnosed, 4 relapsed, 5 refractory) to bortezomib alone or in combination with TRAIL, a member of the TNF family that induces apoptosis in tumor cells while sparing normal cells."	( Antitumor activity of bortezomib alone and in combination with TRAIL in human acute myeloid leukemia. Adamo, L; Anastasi, G; Caruso, L; Conticello, C; Cupri, A; De Maria, R; Di Raimondo, F; Giuffrida, R; Giustolisi, R; Gulisano, M; Iannolo, G; Moschetti, G; Palumbo, GA; Vicari, L, 2008)	0.86
" Bortezomib in combination with dexamethasone was administered as first-line treatment in all 7 newly diagnosed patients with multiple myeloma."	( [Clinical study of bortezomib in combination with dexamethasone for the treatment of multiple myeloma]. Li, JY; Lu, H; Qian, SX; Qiu, HX; Shen, WY; Wang, LX; Wu, HX; Wu, YJ; Zhang, JF, 2008)	1.58
" In this study, escalating doses of Bortezomib were administered along with the standard FOLFOX-4 doses, in order to evaluate the dose-limiting toxicity (DLT), toxicity profile and activity of the combination."	( An EORTC phase I study of Bortezomib in combination with oxaliplatin, leucovorin and 5-fluorouracil in patients with advanced colorectal cancer. Anthoney, A; Bauer, J; Caponigro, F; Govaerts, AS; Lacombe, D; Marréaud, S; Milano, A; Twelves, C, 2009)	0.93
"To investigate the efficacy and toxicity of bortezomib of different doses in combination with dexamethasone for the treatment of relapsed or refractory multiple myeloma (MM)."	( [Effects of bortezomib at different doses in combination with dexamethasone in treatment of relapsed or refractory multiple myeloma: a comparative study]. Bao, L; Huang, XJ; Lu, XJ; Zhang, XH, 2008)	0.99
"The aim of the present study was to evaluate the effectiveness of bortezomib combined with epirubicin, dexamethasone, and thalidomide (BADT) for the treatment of multiple myeloma (MM)."	( Bortezomib in combination with epirubicin, dexamethasone and thalidomide is a highly effective regimen in the treatment of multiple myeloma: a single-center experience. Hu, X; Huang, C; Lü, S; Ni, X; Qiu, H; Wang, J; Xu, X; Yang, J, 2009)	2.03
" Importantly, tumor cells that are partially or completely resistant to mapatumumab or lexatumumab can often be sensitized when treated in combination with chemotherapeutic drugs."	( Mapatumumab and lexatumumab induce apoptosis in TRAIL-R1 and TRAIL-R2 antibody-resistant NSCLC cell lines when treated in combination with bortezomib. Carrell, JA; Humphreys, R; Luster, TA; McCormick, K; Sun, D, 2009)	0.56
"To investigate the effect of bortezomib alone or combined with harringtonine (HT) or arsenic trioxide (As2O3) on the proliferation capacity and apoptosis of HL-60/ADM cell line and fresh cells from refractory/relapse acute leukemia patients."	( [In vitro effect of bortezomib alone or in combination with harringtonine or arsenic trioxide on proliferation and apoptosis of multidrug resistant leukemia cells]. Cai, YX; Fu, YB; Li, L; Meng, FY; Sun, QX, 2008)	0.96
"HL-60/ADM cells or refractory/relapse leukemia cells were incubated with bortezomib at different doses alone and in combination with HT or As2O3."	( [In vitro effect of bortezomib alone or in combination with harringtonine or arsenic trioxide on proliferation and apoptosis of multidrug resistant leukemia cells]. Cai, YX; Fu, YB; Li, L; Meng, FY; Sun, QX, 2008)	0.9
" 15 micromol/L As2O3 or 752 nmol/L HT combined with different doses of bortezomib could inhibit proliferation and induce apoptosis of HL-60/ADM cells."	( [In vitro effect of bortezomib alone or in combination with harringtonine or arsenic trioxide on proliferation and apoptosis of multidrug resistant leukemia cells]. Cai, YX; Fu, YB; Li, L; Meng, FY; Sun, QX, 2008)	0.9
"Bortezomib can inhibit proliferation and induce apoptosis of HL-60/ADM cells and fresh refractory/relapse acute leukemia cells, especially combined with HT or As2O3."	( [In vitro effect of bortezomib alone or in combination with harringtonine or arsenic trioxide on proliferation and apoptosis of multidrug resistant leukemia cells]. Cai, YX; Fu, YB; Li, L; Meng, FY; Sun, QX, 2008)	2.11
" 60 MM patients including 19 de novo patients, out of them 14 patients received the treatment using regimen of bortezomib in combination with thalidomide (BT), 5 patients received bortezomib-methylprednisolone regimen (BMP)."	( [Bortezomib combined with other drugs for treating 60 cases of multiple myeloma]. Chen, SL; Hu, Y; Li, X; Zhang, JJ; Zhong, YP, 2009)	1.47
"A clinical trial was initiated to evaluate the recommended dose of cyclophosphamide in combination with bortezomib and dexamethasone as induction treatment before stem cell transplantation for younger patients with newly diagnosed multiple myeloma (MM)."	( DSMM XI study: dose definition for intravenous cyclophosphamide in combination with bortezomib/dexamethasone for remission induction in patients with newly diagnosed myeloma. Berdel, WE; Einsele, H; Gann, CN; Knop, S; Kropff, M; Liebisch, P; Wand, H; Weisel, K, 2009)	0.79
" Other research groups showed that histone deacetylase inhibitors (valproic acid or benzamide derivative MS-275) in combination with NPI-0052 or PR-171 induced greater levels of acute leukemia cell death than in combination with bortezomib."	( Antiproliferative and proapoptotic effects of proteasome inhibitors and their combination with histone deacetylase inhibitors on leukemia cells. Fuchs, O; Kuzelova, K; Marinov, I; Provaznikova, D; Spicka, I, 2009)	0.54
"Novel agents have demonstrated enhanced efficacy when combined with other antimyeloma agents especially dexamethasone."	( Bortezomib in combination with pegylated liposomal doxorubicin and thalidomide is an effective steroid independent salvage regimen for patients with relapsed or refractory multiple myeloma: results of a phase II clinical trial. Ailawadhi, S; Barcos, M; Bernstein, ZP; Chanan-Khan, A; Czuczman, MS; Iancu, D; Lee, K; Miller, KC; Mohr, A; Musial, L; Padmanabhan, S; Patel, M; Sher, T; Yu, J, 2009)	1.8
" The present study investigated the effect of bortezomib alone or in combination with a hydroxamate-based histone deacetylase inhibitor, JNJ-26481585 on tumor burden, and MM bone disease in the 5T2MM model."	( Bortezomib alone or in combination with the histone deacetylase inhibitor JNJ-26481585: effect on myeloma bone disease in the 5T2MM murine model of myeloma. Arts, J; Coulton, L; Croucher, P; De Raeve, H; Deleu, S; Lemaire, M; Menu, E; Van Camp, B; Van Valckenborgh, E; Vande Broek, I; Vanderkerken, K, 2009)	2.05
" We report on the extended follow-up of a phase II study in frontline MM of bortezomib alone and in combination with dexamethasone."	( Extended follow-up of a phase 2 trial of bortezomib alone and in combination with dexamethasone for the frontline treatment of multiple myeloma. Camacho, ES; Crowley, J; Durie, BG; Gabayan, AE; Irwin, D; Jagannath, S; Lutzky, J; Mazumder, A; McKinley, M; Potts, P; Vescio, R; Wolf, JL, 2009)	0.85
"A phase I study to determine the maximum tolerated dose (MTD) of bortezomib (B) when combined with weekly paclitaxel in patients with advanced solid tumors."	( A dose-finding and pharmacodynamic study of bortezomib in combination with weekly paclitaxel in patients with advanced solid tumors. Bekaii-Saab, T; Byrd, JC; Culler, K; Grever, MR; Lesinski, GB; Lucas, DM; Ramaswamy, B; Ruppert, AS; Schaaf, LJ; Shapiro, CL; Wilkins, D; Wright, JJ; Young, DC, 2010)	0.86
" Preliminary reports from phase I trials using bortezomib in combination with some of these standard cytotoxics have not found any pharmacologic interactions, and toxicities were not significantly increased with these regimens."	( Bortezomib in combination with other therapies for the treatment of multiple myeloma. Orlowski, RZ, 2004)	2.02
"To evaluate the effects and safety of the regimen of bortezomib combined with dexamethasone (VD) in the treatment of primary systemic (AL) amyloidosis."	( [The effects and safety of bortezomib combined with dexamethasone in the treatment of primary systemic amyloidosis]. Li, J; Su, C; Wang, HH; Zeng, LJ; Zhao, Y, 2009)	0.9
"82 ng/ml, but the IC(50) of Jurkat cells treated with bortezomib combined with adriamycin (125 ng/ml) for 24 h was significantly decreased to 20."	( [Apoptosis in Jurkat cells induced by bortezomib combined with adriamycin]. Chen, JF; Jin, J, 2009)	0.87
" The purpose of this study was to determine the maximum tolerated dose (MTD) of bortezomib in combination with chemotherapy and radiation."	( A phase I study of bortezomib in combination with standard 5-fluorouracil and external-beam radiation therapy for the treatment of locally advanced or metastatic rectal cancer. Bernard, SA; Calvo, BF; Caskey, LS; Chakravarthy, AB; Chan, E; Goldberg, RM; Ivanova, A; Kim, HJ; Myers, MO; O'Neil, BH; Raftery, L; Sanoff, HK; Tepper, JE; Wise, PE, 2010)	0.92
"The MTD of bortezomib in combination with chemotherapy and radiation may be below a clinically relevant dose, limiting the clinical applicability of this combination."	( A phase I study of bortezomib in combination with standard 5-fluorouracil and external-beam radiation therapy for the treatment of locally advanced or metastatic rectal cancer. Bernard, SA; Calvo, BF; Caskey, LS; Chakravarthy, AB; Chan, E; Goldberg, RM; Ivanova, A; Kim, HJ; Myers, MO; O'Neil, BH; Raftery, L; Sanoff, HK; Tepper, JE; Wise, PE, 2010)	1.08
" The apoptotic activity of these molecules, alone or in combination with tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) and/or Bortezomib, was tested in melanoma cell lines by MTT viability assays and western blot analysis of activated caspases."	( Novel SMAC-mimetics synergistically stimulate melanoma cell death in combination with TRAIL and Bortezomib. Anichini, A; Bolognesi, M; Delia, D; Drago, C; Kashkar, H; Lecis, D; Manzoni, L; Mastrangelo, E; Scolastico, C; Seneci, P; Walczak, H, 2010)	0.78
" With the purpose of evaluating whether the combination of ATO and bortezomib would be an option for patients with acute leukemia, we incubated HL60 leukemic cells with ATO alone and in combination with bortezomib."	( Synergistic antiproliferative effect of arsenic trioxide combined with bortezomib in HL60 cell line and primary blasts from patients affected by myeloproliferative disorders. Canestraro, M; Cine, N; Galimberti, S; Guerrini, F; Metelli, MR; Nagy, B; Palumbo, GA; Petrini, M; Piaggi, S; Savli, H; Tibullo, D, 2010)	0.83
" Bortezomib has shown single agent activity of 33% in relapsed MCL and has an additive/synergistic effect in vitro when combined with drugs currently used to treat MCL."	( Phase I trial of bortezomib in combination with rituximab-HyperCVAD alternating with rituximab, methotrexate and cytarabine for untreated aggressive mantle cell lymphoma. Fayad, LE; Feldman, T; Ford, P; Goldberg, S; Goy, A; Hartig, K; Kwak, LW; McLaughlin, P; Pecora, A; Pro, B; Rodriguez, A; Romaguera, JE; Smith, J; Wang, M; Weaver, P, 2010)	1.61
"Velcade combined with dexamethasone is a safe and effective regiment for multiple myeloma with good safety and endurance."	( [Effect of Velcade combined with Dexamethasone on multiple myeloma]. He, Q; He, Y; Tan, D; Zhao, X, 2010)	0.36
" We underwent a dose finding study of bortezomib in combination with a fixed dose of doxorubicin and intermediate-dose dexamethasone (iPAD therapy) in patients with relapsed or refractory myeloma."	( A phase I study of bortezomib in combination with doxorubicin and intermediate-dose dexamethasone (iPAD therapy) for relapsed or refractory multiple myeloma. Choi, I; Hata, H; Higuchi, M; Masaki, Y; Nagafuji, K; Sunami, K; Takamatsu, Y; Tamura, K; Uozumi, K, 2010)	0.96
" Finally, we show an additive effect of arsenic trioxide on apoptosis when used in combination with ZOL."	( The proapoptotic effect of zoledronic acid is independent of either the bone microenvironment or the intrinsic resistance to bortezomib of myeloma cells and is enhanced by the combination with arsenic trioxide. Abeltino, M; Agnelli, L; Bolzoni, M; Bonomini, S; Colla, S; Giuliani, N; Neri, A; Rizzoli, V; Storti, P; Todoerti, K, 2011)	0.58
"Our in vitro data suggest that the use of ZOL at appropriate doses could be explored clinically in bortezomib-resistant MM patients and combined with arsenic trioxide to increase its proapoptotic effect."	( The proapoptotic effect of zoledronic acid is independent of either the bone microenvironment or the intrinsic resistance to bortezomib of myeloma cells and is enhanced by the combination with arsenic trioxide. Abeltino, M; Agnelli, L; Bolzoni, M; Bonomini, S; Colla, S; Giuliani, N; Neri, A; Rizzoli, V; Storti, P; Todoerti, K, 2011)	0.79
"To determine the safety, target inhibition, and signals of clinical activity of tipifarnib in combination with bortezomib in patients with advanced acute leukemias."	( A phase I clinical-pharmacodynamic study of the farnesyltransferase inhibitor tipifarnib in combination with the proteasome inhibitor bortezomib in advanced acute leukemias. Blaskovich, MA; Burton, M; Cubitt, C; Duong, VH; Lancet, JE; Sebti, S; Stuart, RK; Sullivan, DM; Winton, EF; Wright, JJ; Zhang, S, 2011)	0.78
"To assess effects of proteasome inhibitor Bortezomib (Bor) in combination with Daunorubicin (DNR) on proliferation, apoptosis and the expression of Bcl-2 mRNA in primary leukemia cells in vitro."	( [Effects of bortezomib combined with daunorubicin on proliferation and apoptosis in primary adult acute leukemia]. Gong, YP; Yang, X; Zheng, BH; Zhou, RQ, 2010)	1
" Combined with Bor (5, 10 nmol/L),the IC50 of DNR decreased from (102 +/- 27) nmol/L to (73 +/- 26), (55 +/- 22) nmol/L respectively."	( [Effects of bortezomib combined with daunorubicin on proliferation and apoptosis in primary adult acute leukemia]. Gong, YP; Yang, X; Zheng, BH; Zhou, RQ, 2010)	0.74
"Bor combined with DNR shows synergetic effect in promoting the apoptosis of adult acute leukemia primary cells as well as inhibitory effect on the proliferation of leukemia cells."	( [Effects of bortezomib combined with daunorubicin on proliferation and apoptosis in primary adult acute leukemia]. Gong, YP; Yang, X; Zheng, BH; Zhou, RQ, 2010)	0.74
" The MTD was determined to be 1·6 mg/m(2) bortezomib on days 1, 8, 15, and 22 in combination with 25 mg temsirolimus on days 1, 8, 15, 22, and 29, for a cycle of 35 days."	( Weekly bortezomib in combination with temsirolimus in relapsed or relapsed and refractory multiple myeloma: a multicentre, phase 1/2, open-label, dose-escalation study. Anderson, KC; Armand, P; Bagshaw, M; Banwait, R; Chuma, S; Dollard, A; Ghobrial, IM; Harris, B; Jakubowiak, AJ; Kunsman, J; Laubach, J; Leduc, R; Maiso, P; Munshi, NC; Poon, T; Richardson, PG; Roccaro, A; Rodig, S; Sam, A; Schlossman, R; Vij, R; Warren, D; Weller, E, 2011)	1.09
"mTOR inhibitors could have a role in combination with weekly bortezomib for the treatment of patients with relapsed and refractory multiple myeloma without the addition of steroids."	( Weekly bortezomib in combination with temsirolimus in relapsed or relapsed and refractory multiple myeloma: a multicentre, phase 1/2, open-label, dose-escalation study. Anderson, KC; Armand, P; Bagshaw, M; Banwait, R; Chuma, S; Dollard, A; Ghobrial, IM; Harris, B; Jakubowiak, AJ; Kunsman, J; Laubach, J; Leduc, R; Maiso, P; Munshi, NC; Poon, T; Richardson, PG; Roccaro, A; Rodig, S; Sam, A; Schlossman, R; Vij, R; Warren, D; Weller, E, 2011)	1.07
" Antitumor activity of bortezomib in combination with EGCG or ascorbic acid was determined using several dosing regimens to evaluate different target plasma concentrations of EGCG and ascorbic acid."	( Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. Bannerman, B; Berger, A; Bolen, J; Claiborne, C; Dick, L; Fleming, P; Hales, P; Jones, M; Kupperman, E; Manfredi, M; Monbaliu, J; Tsu, C; Xu, L; Yu, J, 2011)	0.93
" However, when combined with EGCG such that the plasma concentrations of EGCG were >200 μM at the time of bortezomib dosing, all antitumor activity was abrogated (TGI = -17."	( Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. Bannerman, B; Berger, A; Bolen, J; Claiborne, C; Dick, L; Fleming, P; Hales, P; Jones, M; Kupperman, E; Manfredi, M; Monbaliu, J; Tsu, C; Xu, L; Yu, J, 2011)	0.83
" Our findings provide new insights for the treatment of high-risk MDS, using either Bortezomib alone, or in combination with conventional antineoplastic agents."	( Antitumor activity and drug interactions of proteasome inhibitor Bortezomib in human high-risk myelodysplastic syndrome cells. Ding, T; Huang, J; Jin, J; Liu, H; Sun, X; Yang, M, 2011)	0.83
"The activity and safety of bortezomib in combination with rituximab and dexamethasone were investigated in patients with relapsed or chemotherapy-refractory mantle cell lymphoma."	( Bortezomib combined with rituximab and dexamethasone is an active regimen for patients with relapsed and chemotherapy-refractory mantle cell lymphoma. Chott, A; Drach, J; Hoffmann, M; Kaufmann, H; Lamm, W; Raderer, M; Zielinski, C, 2011)	2.11
"Bortezomib combined with rituximab and dexamethasone has promising activity and manageable toxicity in patients with heavily pretreated mantle cell lymphoma."	( Bortezomib combined with rituximab and dexamethasone is an active regimen for patients with relapsed and chemotherapy-refractory mantle cell lymphoma. Chott, A; Drach, J; Hoffmann, M; Kaufmann, H; Lamm, W; Raderer, M; Zielinski, C, 2011)	3.25
"This study was aimed to investigate the apoptosis induced by bortezomib combined with As(2)O(3) in APL cell line NB4 and its mechanism."	( [NB4 cell apoptosis induced by bortezomib combined with As(2)O(3) and its mechanism]. Chen, XW; Xia, HL; Xia, RX, 2011)	0.9
"This study was aimed to investigate the effect of curcumin in combination with bortezomib on the proliferation and apoptosis of human MM cell line H929 in vitro, and to explore its mechanisms."	( [Effect of curcumin in combination with bortezomib on proliferation and apoptosis of human multiple myeloma cell line H929 and its mechanism]. Bai, QX; Chen, JJ; Huang, GS; Yang, LJ; Zhang, XY; Zhao, H, 2011)	0.86
"This study was aimed to investigate the effect of bortezomib alone or combined with arsenic trioxide on the apoptosis of Jurkat cells and expression of livin mRNA."	( [Effects of bortezomib alone or combined with arsenic trioxide on the apoptosis of Jurkat cells and expression of livin mRNA]. Sun, ZQ; Tan, DW, 2011)	1
"The aim of this study was to explore the clinical effect and toxicity of bortezomib combined with methylprednisolone in treatment of relapsed or refractory multiple myeloma (MM)."	( [Effects of bortezomib combined with methylprednisolone in treatment of 33 cases of relapsed or refractory multiple myeloma]. An, N; Chen, SL; Hu, Y; Li, X; Zhang, JJ; Zhong, YP, 2011)	0.98
" Increased platinum accumulation may result in increased platinum-DNA binding so that CS in combination with Bort may produce pronounced cell kill."	( Modulation of cisplatin cytotoxicity due to its combination with bortezomib and the nature of its administration. Al-Eisawi, Z; Beale, P; Chan, C; Huq, F; Yu, JQ, 2011)	0.61
" Mechanistically, SAHA combined with bortezomib enhanced protein ubiquitination synergistically and enhanced histone acetylation by inhibiting the expression of HDACs."	( Suberoylanilide hydroxamic acid (SAHA) combined with bortezomib inhibits renal cancer growth by enhancing histone acetylation and protein ubiquitination synergistically. Asano, T; Ito, K; Sato, A; Sumitomo, M, 2012)	0.9
"SAHA combined with bortezomib inhibits the proliferation of renal cancer cells in vitro and in vivo, and the effectiveness of the combination is due to its synergistic enhancement of histone acetylation and protein ubiquitination."	( Suberoylanilide hydroxamic acid (SAHA) combined with bortezomib inhibits renal cancer growth by enhancing histone acetylation and protein ubiquitination synergistically. Asano, T; Ito, K; Sato, A; Sumitomo, M, 2012)	0.96
"This study was aimed to evaluate the therapeutic efficacy of bortezomib combined with autologous peripheral blood hematopoietic stem cell transplantation (autoPBSCT) for patients with multiple myeloma (MM)."	( [Bortezomib combined with autologous peripheral blood hematopoietic stem cell transplantation for therapy of patients with multiple myeloma]. Bai, H; Ling, YQ; Wang, CB; Wang, ML; Wu, B; Zhang, Q, 2011)	1.52
" We therefore conducted a phase II trial to evaluate the efficacy of vorinostat in combination with the proteasome inhibitor bortezomib in patients with recurrent GBM."	( Phase II trial of vorinostat in combination with bortezomib in recurrent glioblastoma: a north central cancer treatment group study. Anderson, SK; Buckner, J; Friday, BB; Galanis, E; Geoffroy, F; Giannini, C; Gross, H; Jaeckle, K; Mazurczak, M; Pajon, E; Schwerkoske, J; Yu, C, 2012)	0.84
" In the present study, we investigated the preclinical activity of ACY-1215, an HDAC6-selective inhibitor, alone and in combination with bortezomib in MM."	( Preclinical activity, pharmacodynamic, and pharmacokinetic properties of a selective HDAC6 inhibitor, ACY-1215, in combination with bortezomib in multiple myeloma. Anderson, KC; Bradner, J; Canavese, M; Cirstea, D; Eda, H; Hideshima, T; Jarpe, M; Jones, SS; Kung, AL; Mazitschek, R; Ogier, WC; Raje, N; Rodig, S; Santo, L; Scullen, T; Tamang, D; Tseng, JC; van Duzer, JH; Yang, M, 2012)	0.79
"To evaluate the maximum-tolerated dose (MTD), safety, and efficacy of elotuzumab in combination with bortezomib in patients with relapsed or relapsed and refractory multiple myeloma (MM)."	( Phase I trial of anti-CS1 monoclonal antibody elotuzumab in combination with bortezomib in the treatment of relapsed/refractory multiple myeloma. Afar, DE; Anderson, KC; Bensinger, W; Benson, DM; Jakubowiak, AJ; Mohrbacher, A; Richardson, PG; Siegel, DS; Singhal, AK; Zimmerman, TM, 2012)	0.82
"To investigate reversal effect of histone deacetylase inhibitor LBH589 alone or in combination with proteasome inhibitor bortezomib on drug resistance in acute myeloid leukemia (AML) and its mechanism."	( [Reversal effect of LBH589 alone or in combination with bortezomib on drug-resistance in myeloid leukemia and its mechanism]. Chen, WW; Huang, KK; Huang, M; Jiang, XJ; Meng, FY; Wang, Q; Wang, ZX; Wu, FQ; Zhou, HS, 2011)	0.82
" These data suggest that this drug combination may be useful as a therapy for solid tumors."	( Combination with bortezomib enhances the antitumor effects of nanoparticle-encapsulated thiostrepton. Gartel, AL; Wang, M, 2012)	0.72
"This study aimed to establish the maximum tolerated dose (MTD) of weekly bortezomib in combination with fixed standard doses of carboplatin and bevacizumab, and to estimate the efficacy (response rate and progression free survival [PFS]) and safety of combination therapy with carboplatin, bortezomib, and bevacizumab as first-line therapy in patients with advanced non-small-cell lung cancer (NSCLC)."	( Phase-I/II study of bortezomib in combination with carboplatin and bevacizumab as first-line therapy in patients with advanced non-small-cell lung cancer. Bathini, V; Bradley, K; Hanrahan-Boshes, M; Hutchinson, L; Perez-Soler, R; Piperdi, B; Walsh, WV; Zhou, Z, 2012)	0.93
"8 mg/m weekly on day 1 and day 8 in combination with carboplatin AUC 6 and bevacizumab 15 mg/kg on every 21-day cycle."	( Phase-I/II study of bortezomib in combination with carboplatin and bevacizumab as first-line therapy in patients with advanced non-small-cell lung cancer. Bathini, V; Bradley, K; Hanrahan-Boshes, M; Hutchinson, L; Perez-Soler, R; Piperdi, B; Walsh, WV; Zhou, Z, 2012)	0.7
"Bortezomib has demonstrated efficacy in patients with relapsed B-cell non-Hodgkin lymphoma (NHL) both alone and in combination with other agents; however, limited data exist regarding its toxicity in combination with common frontline therapies for indolent NHL."	( A phase 1 dose escalation study of bortezomib combined with rituximab, cyclophosphamide, doxorubicin, modified vincristine, and prednisone for untreated follicular lymphoma and other low-grade B-cell lymphomas. Bumpers, K; Flowers, CR; Heffner, LT; Hutchison-Rzepka, A; Kaufman, JL; Khoury, HJ; King, N; Lechowicz, MJ; Lewis, C; Lonial, S; Shenoy, PJ; Sinha, R; Tighiouart, M, 2012)	2.1
"Bortezomib combined with modified R-CHOP produced high response rates without substantial increases in toxicity."	( A phase 1 dose escalation study of bortezomib combined with rituximab, cyclophosphamide, doxorubicin, modified vincristine, and prednisone for untreated follicular lymphoma and other low-grade B-cell lymphomas. Bumpers, K; Flowers, CR; Heffner, LT; Hutchison-Rzepka, A; Kaufman, JL; Khoury, HJ; King, N; Lechowicz, MJ; Lewis, C; Lonial, S; Shenoy, PJ; Sinha, R; Tighiouart, M, 2012)	2.1
"We performed a phase II study to evaluate the efficacy of bortezomib in combination with CHOP (cyclophosphamide, doxorubicin, vincristine and prednisone) as first-line treatment for patients with stage III/IV peripheral T-cell lymphomas (PTCLs) based on our phase I study results."	( Bortezomib in combination with CHOP as first-line treatment for patients with stage III/IV peripheral T-cell lymphomas: a multicentre, single-arm, phase 2 trial. Do, IG; Huh, J; Kang, HJ; Kim, HJ; Kim, HK; Kim, JS; Kim, SJ; Kim, WS; Ko, YH; Lee, J; Lee, SS; Min, SK; Park, SK; Ryoo, BY; Suh, C; Yang, WI; Yoon, DH, 2012)	2.07
"To study the influence of Secoisolariciresinol Diglucoside (SDG) combined with Bortezomib on induction of apoptosis in lung cancer cell line A549 and its relative mechanisms."	( [Effects of secoisolariciresinol diglucoside combined with bortezomib on induction of apoptosis in lung cancer cell line A549]. Li, XW; Yang, JR, 2012)	0.85
"The results demonstrate that SDG combined with Bortezomib can significantly induce apoptosis of A549 cells, its mechanisms may be involved in activation of the JNK pathway."	( [Effects of secoisolariciresinol diglucoside combined with bortezomib on induction of apoptosis in lung cancer cell line A549]. Li, XW; Yang, JR, 2012)	0.88
" This phase I trial was designed to determine the maximum tolerated dose (MTD) of weekly bortezomib induction combined with Y-90-ibritumomab tiuxetan followed at the time of count recovery by weekly bortezomib consolidation in patients with relapsed/refractory follicular or transformed non-Hodgkin lymphoma."	( Bortezomib may be safely combined with Y-90-ibritumomab tiuxetan in patients with relapsed/refractory follicular non-Hodgkin lymphoma: a phase I trial of combined induction therapy and bortezomib consolidation. Cilley, J; Evens, AM; Gallot, L; Gordon, LI; Larson, A; Patton, D; Rademaker, A; Roy, R; Spies, S; Variakojis, D; Winter, JN, 2013)	2.05
" We analyzed the proapoptotic effects of both TRAIL versions in combination with the proteasome inhibitor bortezomib (BZB) in hepatoma cells and primary human hepatocytes as well as in intact explants from HCC and healthy liver tissue."	( Increased apoptosis induction in hepatocellular carcinoma by a novel tumor-targeted TRAIL fusion protein combined with bortezomib. Bantel, H; Kontermann, R; Krech, T; Länger, F; Lehner, F; Manns, MP; Nüssler, A; Pfizenmaier, K; Schulze-Osthoff, K; Siegemund, M; Vondran, F; Wahl, K, 2013)	0.81
" We examined this drug combination in advanced relapsing and/or refractory MM patients (n = 34)."	( Phase I trial of vorinostat combined with bortezomib for the treatment of relapsing and/or refractory multiple myeloma. Graef, T; Hardwick, JS; Hussein, M; Jagannath, S; Lupinacci, L; Schiller, GJ; Sobecks, RM; Weber, DM, 2012)	0.64
" Vorinostat combined with bortezomib has demonstrated synergistic antiproliferative and proapoptotic activity in preclinical models of MM."	( Phase I trial of vorinostat combined with bortezomib for the treatment of relapsing and/or refractory multiple myeloma. Graef, T; Hardwick, JS; Hussein, M; Jagannath, S; Lupinacci, L; Schiller, GJ; Sobecks, RM; Weber, DM, 2012)	0.94
"Abstract This phase I study was conducted to determine the maximum tolerated dose (MTD) and dose limiting toxicities (DLTs) of the heat shock protein 90 (HSP90) inhibitor 17-allyamino-17-demethoxygeldanamycin (17-AAG) in combination with bortezomib, and to provide pharmacokinetic data in relapsed or refractory acute myeloid leukemia (AML)."	( Pharmacokinetics and dose escalation of the heat shock protein inhibitor 17-allyamino-17-demethoxygeldanamycin in combination with bortezomib in relapsed or refractory acute myeloid leukemia. Binkley, P; Blum, KA; Blum, W; Byrd, JC; Garzon, R; Geyer, S; Grever, MR; Jiang, Y; Johnston, JS; Kefauver, C; Klisovic, R; Marcucci, G; Phelps, MA; Walker, AR, 2013)	0.78
"This study was aimed to further explore the apoptosis-inducing effect of bortezomib combined with cytarabine (Ara-C) on U937 cell line."	( [Mechanism of apoptosis synergistically induced by bortezomib combined with cytarabine in U937 cell line]. DU, SH; DU, X; He, C; Jia, PM; Tong, JH; Zhou, L, 2012)	0.86
"This study was aimed to investigate the effect of arsenic trioxide (As(2)O(3)) alone and in combination with bortezomib (Bor) on proliferation and apoptosis of leukemia cell line K562, and to analyze the potential mechanism."	( [Effects of arsenic trioxide combined with bortezomib on proliferation and apoptosis of K562 cells and their mechanism]. Hao, LM; Huang, JQ; Li, XM; Wang, SM; Wei, LY; Wu, HY, 2012)	0.85
"To determine the maximum tolerated dose (MTD) and characterize the dose-limiting toxicities (DLT) of tanespimycin when given in combination with bortezomib."	( Phase I study of tanespimycin in combination with bortezomib in patients with advanced solid malignancies. Ames, MM; Erlichman, C; Hendrickson, AE; Menefee, M; Northfelt, D; Qin, R; Satele, D; Schenk, E; Toft, DO, 2013)	0.84
" A number of studies have been conducted to evaluate the activity and safety of bortezomib either alone or in combination with several cytotoxic agents and radiation."	( Effect of bortezomib in combination with cisplatin and 5‑fluorouracil on 4T1 breast cancer cells. Altıkat, S; Boyaci, I; Cavga, FZ; Irmak, R; Kocacan, SA; Yerlikaya, A, 2013)	1.02
"The protease inhibitor bortezomib attenuates the action of NF-κB and has shown preclinical activity alone and in combination with chemotherapy."	( A phase I trial of bortezomib in combination with epirubicin, carboplatin and capecitabine (ECarboX) in advanced oesophagogastric adenocarcinoma. Eatock, MM; Gallagher, R; James, CR; Law, D; Millar, J; Morris, M; Napier, E; Purcell, C; Turkington, RC; Wilson, RH, 2014)	1.04
"6 mg m(-2) on days 1 and 8 from cycle 2 onwards) in combination with Epirubicin 50 mg m(-2) intravenously on day 1, Carboplatin AUC 5 day 1 and Capecitabine 625 mg m(-2) BD days 1-21 every 21 days (VECarboX regimen), in patients with advanced oesophagogastric adenocarcinoma."	( A phase I trial of bortezomib in combination with epirubicin, carboplatin and capecitabine (ECarboX) in advanced oesophagogastric adenocarcinoma. Eatock, MM; Gallagher, R; James, CR; Law, D; Millar, J; Morris, M; Napier, E; Purcell, C; Turkington, RC; Wilson, RH, 2014)	0.73
"Thalidomide, the first clinically available immunomodulatory drug, reaches monotherapy treatment response in about 1/ 3 of significantly pretreated patients with multiple myeloma, and in combination with glucocorticoids approximately 50% response rate."	( [Thalidomide in the treatment of multiple myeloma: focus on combination with bortezomib]. Gumulec, J; Hájek, R; Plonková, H, 2013)	0.62
"We conducted a phase I dose escalation study to determine the maximal tolerated dose of bortezomib that could be combined with standard dose lenalidomide in patients with MDS or AML."	( Phase I dose escalation study of bortezomib in combination with lenalidomide in patients with myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). Amrein, PC; Attar, EC; Ballen, KK; Deangelo, DJ; Fathi, AT; Foster, J; Fraser, JW; McAfee, S; Neuberg, D; Steensma, DP; Stone, RM; Wadleigh, M, 2013)	0.89
"To compare the efficacy and safety of standard or reduced doses of bortezomib combined with adriamycin and dexamethasone (PAD) in patients with multiple myeloma (MM)."	( [Efficacy comparison between standard and reduced doses of bortezomib combined with adriamycin and dexamethasone in the treatment of patients with multiple myeloma]. Bai, QX; Chen, XQ; Dong, BX; Gao, GX; Gu, HT; Liang, R; Shu, MM; Yang, L; Zhang, T; Zhang, YQ, 2013)	0.87
" PANORAMA 2 is a phase 2 trial of panobinostat in combination with bortezomib and dexamethasone to treat patients with relapsed and bortezomib-refractory multiple myeloma (with ≥2 prior lines of therapy, including an immunomodulatory drug, and patients who had progressed on or within 60 days of the last bortezomib-based therapy)."	( PANORAMA 2: panobinostat in combination with bortezomib and dexamethasone in patients with relapsed and bortezomib-refractory myeloma. Alsina, M; Coutre, SE; Gasparetto, C; Khan, M; Lonial, S; Mukhopadhyay, S; Ondovik, MS; Paley, CS; Richardson, PG; Schlossman, RL; Weber, DM, 2013)	0.89
"We aimed to assess efficacy and tolerability of vorinostat in combination with bortezomib for treatment of patients with relapsed or refractory multiple myeloma."	( Vorinostat or placebo in combination with bortezomib in patients with multiple myeloma (VANTAGE 088): a multicentre, randomised, double-blind study. Anderson, KC; Blacklock, H; Dimopoulos, M; Eid, JE; Facon, T; Goldschmidt, H; Graef, T; Hajek, R; Houp, J; Hungria, V; Lonial, S; Palumbo, A; Qi, J; Rosinol, L; Siegel, DS; Spencer, A; Sun, L; Vuocolo, S; Williams, C, 2013)	0.88
" We randomly allocated patients (1:1) using an interactive voice response system to receive 21 day cycles of bortezomib (1·3 mg/m(2) intravenously on days 1, 4, 8, and 11) in combination with oral vorinostat (400 mg) or matching placebo once-daily on days 1-14."	( Vorinostat or placebo in combination with bortezomib in patients with multiple myeloma (VANTAGE 088): a multicentre, randomised, double-blind study. Anderson, KC; Blacklock, H; Dimopoulos, M; Eid, JE; Facon, T; Goldschmidt, H; Graef, T; Hajek, R; Houp, J; Hungria, V; Lonial, S; Palumbo, A; Qi, J; Rosinol, L; Siegel, DS; Spencer, A; Sun, L; Vuocolo, S; Williams, C, 2013)	0.87
"A phase I study to assess the maximum-tolerated dose (MTD), dose-limiting toxicity (DLT), pharmacokinetics (PK) and antitumor activity of vorinostat in combination with bortezomib in patients with advanced solid tumors."	( A phase I study of vorinostat in combination with bortezomib in patients with advanced malignancies. Alberti, D; Ames, MM; Attia, S; Bailey, HH; Eickhoff, J; Espinoza-Delgado, I; Hoang, T; Holen, KD; Jiang, Z; Kolesar, JM; Marnocha, R; McGovern, RM; Reid, JM; Schelman, WR; Traynor, AM; Wilding, G; Wright, JJ, 2013)	0.84
" We previously examined a once-daily continuous dosing schedule of vorinostat in combination with bortezomib which was well tolerated in cycles 1 and 2; however, there was concern regarding the tolerability through multiple cycles."	( A Phase I study of intermittently dosed vorinostat in combination with bortezomib in patients with advanced solid tumors. Alberti, D; Ames, MM; Bailey, HH; Deming, DA; Eickhoff, J; Espinoza-Delgado, I; Kolesar, JM; Marnocha, R; McGovern, RM; Ninan, J; Reid, JM; Schelman, WR; Wilding, G; Wright, J, 2014)	0.85
" We present a case of POEMS syndrome in a 33-year-old woman, who was successfully treated with BorDex (bortezomib and dexamethasone) combined with radiotherapy, and followed by ASCT."	( Successful treatment of POEMS syndrome with bortezomib and dexamethasone, combined with radiotherapy, and followed by autologous stem cell transplantation. Hagihara, M; Hattori, Y; Ishigatsubo, Y; Ishii, Y; Ishiyama, Y; Tomita, N; Yamamoto, E; Yamazaki, E, 2013)	0.87
"This study was aimed to investigate the effect of bortezomib combined with bisphosphonates on serum levels of DKK-1 and RANKL in multiple myeloma patients, and to evaluate its role in the therapy of osteolytic lesion."	( [Effect of bortezomib combined with bisphosphonates on bone metabolism index in multiple myeloma]. Chen, BY; Chen, WM; Liao, LS; Lin, Y; Qu, S; Wei, TN, 2013)	1.03
" RPMI 8266 cells were treated with ATO alone and in combination with bortezomib for 24 hours, and cell viability was assessed by modified MTT."	( Effects of arsenic trioxide alone and in combination with bortezomib in multiple myeloma RPMI 8266 cells. Cui, JW; Elmahi, AY; Hao, SS; Li, D; Li, W; Niu, C; Wang, GJ, 2013)	0.87
" We also investigated the effects of bortezomib, a proteasome inhibitor, alone and in combination with PU-H71 in Ewing sarcoma."	( Pre-clinical efficacy of PU-H71, a novel HSP90 inhibitor, alone and in combination with bortezomib in Ewing sarcoma. Ambati, SR; Chiosis, G; Kosugi, K; Lopes, EC; Meyers, PA; Mony, U; Moore, MA; Moreira, AL; Shah, SK; Taldone, T; Zehir, A, 2014)	0.9
"We conclude that bortezomib is not effective for the treatment of advanced adenocarcinoma of the GEJ or stomach, whether used alone or in combination with irinotecan, in an unselected patient population."	( Phase II trial of bortezomib alone or in combination with irinotecan in patients with adenocarcinoma of the gastroesophageal junction or stomach. Besanceney-Webler, C; Chen, EX; Cheng, J; Christos, P; Dilts, KT; Holloway, S; Keresztes, R; Lane, ME; Lin, J; Matulich, D; Ocean, AJ; Papetti, M; Schnoll-Sussman, F; Shah, MA; Sparano, JA; Ward, M; Wright, JJ; Xiang, J; Yantiss, RK, 2014)	1.08
"3 mg/m2/dose, 2 doses/week for 2 weeks) in combination with vincristine, doxorubicin, dexamethasone, and L-asparaginase (L-ASP)."	( [Efficacy of chemotherapy combined with bortezomib for two cases of relapsed/refractory acute lymphoblastic leukemia]. Ashikaga, T; Keino, D; Kinoshita, A; Kondoh, K; Morimoto, M; Ohyama, R; Yamashita, A, 2014)	0.67
"Several clinical trials have demonstrated the effectiveness of bortezomib in combination with various anti-myeloma agents; however, no definitive information is available regarding drugs best suited for use in combination with bortezomib."	( Suitable drug combination with bortezomib for multiple myeloma under stroma-free conditions and in contact with fibronectin or bone marrow stromal cells. Furukawa, Y; Kikuchi, J; Koyama, D; Mukai, HY, 2014)	0.93
" In the present protocol, bortezomib was combined with bendamustine and prednisone, in order to assess the efficacy and safety of this combination therapy in patients with newly diagnosed/untreated MM."	( Bendamustine and prednisone in combination with bortezomib (BPV) in the treatment of patients with newly diagnosed/untreated multiple myeloma. Andrea, M; Becker, C; Behre, G; Bourgeois, M; Edelmann, T; Gutsche, K; Hammerschmidt, D; Hennig, E; Heyn, S; Hoffmann, FA; Holzvogt, B; Kaiser, T; Krahl, R; Kreibich, U; Lindner, T; Niederwieser, D; Plötze, M; Pönisch, W; Reifenrath, K; Remane, Y; Schliwa, T; Schwarz, M; Schwarzer, A; Vucinic, V; Winkelmann, C; Zehrfeld, T, 2014)	0.96
"This Phase 2 study tested the tolerability and efficacy of bortezomib combined with reinduction chemotherapy for pediatric patients with relapsed, refractory or secondary acute myeloid leukemia (AML)."	( A Phase 2 study of bortezomib combined with either idarubicin/cytarabine or cytarabine/etoposide in children with relapsed, refractory or secondary acute myeloid leukemia: a report from the Children's Oncology Group. Adlard, K; Alonzo, TA; Ballard, J; Gamis, AS; Gerbing, RB; Horton, TM; Howard, DS; Jenkins, G; Kelder, A; Moscow, JA; Perentesis, JP; Schuurhuis, GJ; Smith, FO, 2014)	0.97
"Patients with <400 mg/m(2) prior anthracycline received bortezomib combined with idarubicin (12 mg/m(2) days 1-3) and low-dose cytarabine (100 mg/m(2) days 1-7) (Arm A)."	( A Phase 2 study of bortezomib combined with either idarubicin/cytarabine or cytarabine/etoposide in children with relapsed, refractory or secondary acute myeloid leukemia: a report from the Children's Oncology Group. Adlard, K; Alonzo, TA; Ballard, J; Gamis, AS; Gerbing, RB; Horton, TM; Howard, DS; Jenkins, G; Kelder, A; Moscow, JA; Perentesis, JP; Schuurhuis, GJ; Smith, FO, 2014)	0.98
" In conclusion, our results suggest that sTRAIL-SL might be an efficient vehicle for sTRAIL delivery and that its use in clinic, in combination with BTZ, might represent an adjuvant strategy for the treatment of stage IV, sTRAIL-resistant, NB patients."	( sTRAIL coupled to liposomes improves its pharmacokinetic profile and overcomes neuroblastoma tumour resistance in combination with Bortezomib. Becherini, P; Brignole, C; Cilli, M; Cossu, I; Destefanis, E; Di Paolo, D; Emionite, L; Giacomini, A; Loi, M; Pastorino, F; Perri, P; Piaggio, F; Ponzoni, M, 2014)	0.61
"This study was aimed to investigate the effects of bortezomib combined with 5-azacytidine on the apoptosis of K562 cells and expressiom of SHIP mRNA."	( [Effects of bortezomib combined with 5-azacytidine on the apoptosis of K562 cells and expression of SHIP mRNA]. Jia, ZQ; Rong, HQ; Su, W; Tao, J; Wei, YL; Wei, YT; Yu, CX, 2014)	1.03
" Bendamustine was administered with a cumulative dose of up to 200 mg/m(2)."	( Bendamustine in combination with thalidomide and dexamethasone is a viable salvage option in myeloma relapsed and/or refractory to bortezomib and lenalidomide. Aitchison, R; Blesing, N; Lau, IJ; Peniket, A; Rabin, N; Ramasamy, K; Roberts, P; Smith, D; Yong, K, 2015)	0.62
"We hypothesized that bortezomib, an agent that suppresses HIF-1α transcriptional activity, when combined with bevacizumab, would obviate the HIF-1α resistance pathway."	( Targeting hypoxia-inducible factor-1α (HIF-1α) in combination with antiangiogenic therapy: a phase I trial of bortezomib plus bevacizumab. Amin, HM; Angelo, LS; Falchook, GS; Hess, K; Hong, D; Howard, AN; Huang, M; Jackson, EF; Janku, F; Kurzrock, R; Lawhorn, KN; Naing, A; Ng, CS; Parkhurst, KL; Tannir, NM; Vishwamitra, D; Wheler, JJ, 2014)	0.93
"On August 5, 2013, a marketing authorization valid throughout the European Union (EU) was issued for pomalidomide in combination with dexamethasone for the treatment of adult patients with relapsed and refractory multiple myeloma (MM) who have received at least two prior treatment regimens, including both lenalidomide and bortezomib, and have demonstrated disease progression on the last therapy."	( The European medicines agency review of pomalidomide in combination with low-dose dexamethasone for the treatment of adult patients with multiple myeloma: summary of the scientific assessment of the committee for medicinal products for human use. Camarero, J; Flores, B; Gisselbrecht, C; Hanaizi, Z; Hemmings, R; Laane, E; Pignatti, F; Salmonson, T; Sancho-Lopez, A, 2015)	0.59
" We prospectively evaluated 21 newly diagnosed MM patients with severe renal impairment secondary to tubular-interstitial damage, most of them due to myeloma kidney, who were primarily treated with bortezomib-based therapy combined with high cut-off hemodialysis (HCOD)."	( Bortezomib-based therapy combined with high cut-off hemodialysis is highly effective in newly diagnosed multiple myeloma patients with severe renal impairment. Borsi, E; Brioli, A; Cavo, M; De Sanctis, LB; Mancini, E; Mancuso, K; Marzocchi, G; Pantani, L; Pezzi, A; Rizzo, R; Rocchi, S; Santoro, A; Santostefano, M; Tacchetti, P; Terragna, C; Zamagni, E; Zannetti, BA, 2015)	2.05
"The purpose of this study was to determine the potential benefits of combination therapy using dimercaptosuccinic acid modified iron oxide (DMSA-Fe3O4) magnetic nanoparticles (MNPs) combined with nontoxic concentration of bortezomib (BTZ) and gambogic acid (GA) on multiple myeloma (MM) RPMI-8226 cells and possible underlying mechanisms."	( Inducing cell cycle arrest and apoptosis by dimercaptosuccinic acid modified Fe3O4 magnetic nanoparticles combined with nontoxic concentration of bortezomib and gambogic acid in RPMI-8226 cells. Chen, B; Qiao, L; Senthilkumar, R; Wang, F; Wang, X; Zhang, W, 2015)	0.8
" We here compare bortezomib with carfilzomib and LU-102 in MM and MCL in vitro with regard to their effects on pIκB/NF-κB signaling and their cytotoxic activity in combination with ibrutinib."	( The novel β2-selective proteasome inhibitor LU-102 decreases phosphorylation of I kappa B and induces highly synergistic cytotoxicity in combination with ibrutinib in multiple myeloma cells. Bader, J; Besse, L; de Bruin, G; Driessen, C; Geurink, PP; Kisselev, AF; Kraus, J; Kraus, M; Liu, N; Overkleeft, H, 2015)	0.76
"Treatment with dose-adjusted Len combined with low-dose Dex is an effective and safe therapy for older RRMM patients exhibiting renal impairment after receiving Bor-based therapies."	( Dose-adjusted Lenalidomide Combined with Low-dose Dexamethasone Rescues Older Patients with Bortezomib-resistant Multiple Myeloma. Kadowaki, M; Kohno, K; Okamura, S; Takase, K; Yamasaki, S, 2015)	0.64
"To investigate the effect of CAL-101, a selective inhibitor of PI3Kδ, in combination with bortezomib on the proliferation and apoptosis in human mantle cell lymphoma cell lines Z138, HBL-2 and Jeko-1 in vitro, to explore its mechanisms and provide the foundation for effective treatment strategies against mantle cell lymphoma."	( [Effects of the phosphoinostitide-3'-kinase delta inhibitor, CAL-101, in combination with Bortezomib on mantle lymophma cells and exploration of its related mechanism]. Guo, S; Li, X; Qu, F; Tian, C; Xia, B; Yu, Y; Zhang, L; Zhang, Y, 2015)	0.86
"Panobinostat, a potent pan-deacetylase inhibitor, improved progression-free survival (PFS) in patients with relapsed and refractory multiple myeloma when combined with bortezomib and dexamethasone in a phase 3 trial, PANORAMA-1."	( Panobinostat PK/PD profile in combination with bortezomib and dexamethasone in patients with relapsed and relapsed/refractory multiple myeloma. Binlich, F; Corrado, C; Hino, M; Kuroda, Y; Lin, R; Mu, S; Shibayama, H; Suzuki, K; Tajima, T; Waldron, E, 2016)	0.89
"Apparent panobinostat exposure-AE and exposure-ORR relationships were observed when combined with bortezomib and dexamethasone in the treatment of patients with relapsed and refractory multiple myeloma."	( Panobinostat PK/PD profile in combination with bortezomib and dexamethasone in patients with relapsed and relapsed/refractory multiple myeloma. Binlich, F; Corrado, C; Hino, M; Kuroda, Y; Lin, R; Mu, S; Shibayama, H; Suzuki, K; Tajima, T; Waldron, E, 2016)	0.91
"3 (dose level 2) mg/m(2) in combination with melphalan 8 mg/m(2) on days 1-4 and dexamethasone 20 mg on days 1, 2, 4, 5, 8, 9, 11, and 12."	( Phase 1 study of bortezomib in combination with melphalan and dexamethasone in Japanese patients with relapsed AL amyloidosis. Abe, M; Ando, Y; Fuchida, S; Hata, H; Imai, H; Ishida, T; Miyamoto, T; Sawamura, M; Shimazaki, C; Suzuki, K; Takamatsu, H; Yamada, M, 2016)	0.77
" We determined dose-limiting toxicity and recommended dose for phase II of nelfinavir in combination with the proteasome inhibitor bortezomib."	( Treatment with the HIV protease inhibitor nelfinavir triggers the unfolded protein response and may overcome proteasome inhibitor resistance of multiple myeloma in combination with bortezomib: a phase I trial (SAKK 65/08). Bader, J; Berset, C; Berthod, G; Driessen, C; Hawle, H; Hess, D; Hitz, F; Huitema, A; Joerger, M; Kraus, M; Mey, UJ; Overkleeft, HS; Pabst, T; Rosing, H; Sessa, C; von Moos, R; Xyrafas, A, 2016)	0.83
" Findings of many preclinical studies have shown synergistic antilymphoma activity when panobinostat is combined with the proteasome inhibitor bortezomib."	( Panobinostat in combination with bortezomib in patients with relapsed or refractory peripheral T-cell lymphoma: an open-label, multicentre phase 2 trial. Chan, YH; Fadilah, S; Goh, YT; Hwang, WY; Kim, WS; Kumar, SG; Lee, YS; Lim, ST; Ng, SC; Phipps, C; Tan, D; Tan, SY; Tay, K; Yeap, CH, 2015)	0.9
"Proteasome inhibitors (PIs) in combination with immunomodulatory drugs (IMiDs) have been shown to be effective against relapsed/refractory multiple myeloma (RRMM)."	( Phase I study of once weekly treatment with bortezomib in combination with lenalidomide and dexamethasone for relapsed or refractory multiple myeloma. Hagiwara, S; Iida, S; Ishida, T; Ito, A; Kanamori, T; Kato, C; Kinoshita, S; Komatsu, H; Kusumoto, S; Masuda, A; Murakami, S; Nakashima, T; Narita, T; Ri, M; Suzuki, N; Totani, H; Yoshida, T, 2016)	0.7
"To investigate the clinical efficacy of adoptive immunotherapy using dendritic cells (DC) and cytokine-induced killer (CIK) cells combined with chemotherapy in multiple myeloma."	( Immunomodulatory effect of DC/CIK combined with chemotherapy in multiple myeloma and the clinical efficacy. Ding, HF; Ji, CY; Liu, GQ; Ma, DX; Xing, J; Xu, M; Zhao, X, 2015)	0.42
"To explore the efficacy and prognostic factors of induction therapy combined with autogenetic peripheral blood stem cells transplantation (APBSCT)in patients with multiple myeloma (MM)."	( [Efficacy and prognostic factors of induction therapy combined with autologous stem cell transplantation in 201 patients with multiple myeloma]. Chang, H; Du, J; Fan, J; Fu, W; He, H; Hou, J; Jiang, H; Jin, L; Xi, H; Zeng, T; Zhang, C; Zhou, L, 2016)	0.43
" Preclinical and phase I clinical data suggest activity of bortezomib in NSCLC, either as monotherapy or in combination with chemotherapeutic agents including gemcitabine and cisplatin."	( A phase II, open-label trial of bortezomib (VELCADE(®)) in combination with gemcitabine and cisplatin in patients with locally advanced or metastatic non-small cell lung cancer. Agelaki, S; Filippa, G; Georgoulias, V; Kentepozidis, N; Kontopodis, E; Kotsakis, A; Mala, A; Mavroudis, D; Moutsos, M; Syrigos, K; Vamvakas, L; Ziras, N, 2016)	0.96
" on days 1 and 8, and starting on day 21 (cycle 2), bortezomib (days 1 and 8) in combination with gemcitabine 1000 mg/m(2), (days 1 and 8), and cisplatin 70 mg/m(2) (day 1) in cycles of 21 days."	( A phase II, open-label trial of bortezomib (VELCADE(®)) in combination with gemcitabine and cisplatin in patients with locally advanced or metastatic non-small cell lung cancer. Agelaki, S; Filippa, G; Georgoulias, V; Kentepozidis, N; Kontopodis, E; Kotsakis, A; Mala, A; Mavroudis, D; Moutsos, M; Syrigos, K; Vamvakas, L; Ziras, N, 2016)	0.97
"The present global, open-label, single-arm, multicenter, phase IIb study was designed to determine the efficacy and tolerability of oral vorinostat combined with standard doses of bortezomib in patients with multiple myeloma considered refractory to novel myeloma agents."	( VANTAGE 095: An International, Multicenter, Open-Label Study of Vorinostat (MK-0683) in Combination With Bortezomib in Patients With Relapsed and Refractory Multiple Myeloma. Anderson, KC; Dimopoulos, M; Durrant, S; Eid, JE; Gause, C; Goldschmidt, H; Graef, T; Houp, J; Jagannath, S; Kaufman, JL; Leleu, X; Nagler, A; Offner, F; Siegel, DS; Vuocolo, S, 2016)	0.84
" This phase 1 study investigated the safety and efficacy of pralatrexate in combination with bortezomib in adults with relapsed or refractory multiple myeloma."	( A phase 1, open-label, dose-escalation study of pralatrexate in combination with bortezomib in patients with relapsed/refractory multiple myeloma. Berube, C; Coutré, SE; Dinner, S; Dunn, TJ; Gotlib, J; Hao, Y; Liedtke, M; Medeiros, BC; Price, E, 2016)	0.88
"Various cytotoxic agents were evaluated in combination with (131) I-MIP-1095 for their capacity to delay the growth of LNCaP cells cultured as multicellular tumour spheroids."	( Preliminary evaluation of prostate-targeted radiotherapy using (131) I-MIP-1095 in combination with radiosensitising chemotherapeutic drugs. Babich, JW; Mairs, RJ; Nixon, C; Rae, C; Tesson, M, 2016)	0.43
"To evaluate the clinical characteristics of multiple myeloma (MM) combined with renal amyloidosis and its curative efficacy and prognosis."	( [Clinical Characteristics and Therapeutic Efficacy of Multiple Myeloma Combined with Renal Amyloidosis]. Chen, SQ; Chen, YD; Gan, SL; Jiang, ZX; Liu, LX; Liu, YF; Ma, J; Meng, XL; Sun, H; Sun, L; Wan, DM; Wang, F; Wen, HY; Xie, XS, 2016)	0.43
"The clinical data of 22 cases of newly diagnosed multiple myeloma combined with renal amyloidosis treated in our hospital from November 2011 to July 2015 were analyzed retrospectively."	( [Clinical Characteristics and Therapeutic Efficacy of Multiple Myeloma Combined with Renal Amyloidosis]. Chen, SQ; Chen, YD; Gan, SL; Jiang, ZX; Liu, LX; Liu, YF; Ma, J; Meng, XL; Sun, H; Sun, L; Wan, DM; Wang, F; Wen, HY; Xie, XS, 2016)	0.43
" A recent study disclosed that pralatrexate has a synergistic effect in combination with bortezomib."	( Pralatrexate in Combination with Bortezomib for Relapsed or Refractory Peripheral T Cell Lymphoma in 5 Elderly Patients. Ahn, JS; Cho, MS; Jung, SH; Jung, SY; Kim, HJ; Kim, YK; Lee, JJ; Lee, SS; Yang, DH, 2016)	0.94
" Bortezomib is the first product to be approved for the treatment of patients with previously untreated MCL, for whom haematopoietic stem cell transplantation is unsuitable, and is used in combination with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (VR-CAP)."	( Cost-effectiveness analysis of bortezomib in combination with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (VR-CAP) in patients with previously untreated mantle cell lymphoma. Gairy, K; Lee, D; Seshagiri, D; Thilakarathne, P; van Keep, M, 2016)	1.63
" The aim of this study was to investigate the efficacy and safety of bortezomib combined with glucocorticoids in refractory lupus patients."	( The short-term efficacy of bortezomib combined with glucocorticoids for the treatment of refractory lupus nephritis. Hou, J; Hu, W; Huang, L; Huang, X; Liu, Z; Zhang, H; Zhou, M, 2017)	0.99
"To study the clinical efficacy of cellular immunotherapy combined with bortezomib for treatment of patients with multiple myeloma."	( [Clinical Efficacy of Cellular Immuotherapy Combined with Bortezomib for the Treatment of Patients with Multiple Myeloma]. Long, H; Shao, JH; Wang, YM; Yang, D, 2017)	0.93
"A total of 76 patients with multiple myeloma in our hospital from October 2012 to October 2013 were selected and randomly divided into 2 groups: the patients in 1 group (38 cases) were treated with cellular immunotherapy combined with chemotherapy including bortezomib (combined therapy group), the patients in other group(38 cases) were treated with only chemotherapy including bortezomib(single chemotherapy as control group)."	( [Clinical Efficacy of Cellular Immuotherapy Combined with Bortezomib for the Treatment of Patients with Multiple Myeloma]. Long, H; Shao, JH; Wang, YM; Yang, D, 2017)	0.88
"Cellular immunotherapy combined with bortezomib can significantly improve the remission rate, prolong survival, and significantly decrease adverse event rate of multiple myeloma patients."	( [Clinical Efficacy of Cellular Immuotherapy Combined with Bortezomib for the Treatment of Patients with Multiple Myeloma]. Long, H; Shao, JH; Wang, YM; Yang, D, 2017)	0.97
" This study determined the safety, preliminary clinical activity, and pharmacokinetics of KW-2478, an Hsp90 inhibitor, in combination with BTZ in patients with relapsed/refractory multiple myeloma (MM)."	( A phase I/II study of KW-2478, an Hsp90 inhibitor, in combination with bortezomib in patients with relapsed/refractory multiple myeloma. Akinaga, S; Baetiong-Caguioa, P; Cavenagh, J; Davies, F; Gharibo, M; Kurman, M; Nakashima, D; Novak, B; Oakervee, H; Rabin, N; Shiraishi, N; Yong, K, 2017)	0.69
" The antimyeloma activity of KW-2478 in combination with BTZ as scheduled in this trial appeared relatively modest; however, the good tolerability of the combination would support further exploration of alternate dosing schedules and combinations."	( A phase I/II study of KW-2478, an Hsp90 inhibitor, in combination with bortezomib in patients with relapsed/refractory multiple myeloma. Akinaga, S; Baetiong-Caguioa, P; Cavenagh, J; Davies, F; Gharibo, M; Kurman, M; Nakashima, D; Novak, B; Oakervee, H; Rabin, N; Shiraishi, N; Yong, K, 2017)	0.69
" They are administered individually or in combination with other regimens, to prevent severe side effects and resistance development."	( Bortezomib Alone and in Combination With Salinosporamid A Induces Apoptosis and Promotes Pheochromocytoma Cell Death In Vitro and in Female Nude Mice. Bullova, P; Cougnoux, A; Kopacek, J; Marzouca, G; Pacak, K, 2017)	1.9
"Daratumumab in combination with bortezomib and dexamethasone (DVd) has demonstrated longer progression-free survival than combination of bortezomib and dexamethasone in patients with relapsed or refractory multiple myeloma (RRMM)."	( Safety and efficacy of daratumumab in combination with bortezomib and dexamethasone in Japanese patients with relapsed or refractory multiple myeloma. Aoki, M; Ichinohe, T; Iida, S; Shinagawa, A; Suzuki, K; Takezako, N, 2018)	1.01
" Case reports and small reviews have evaluated the addition of agents directed against plasma cell disorders in combination with traditional lymphoma-directed regimens."	( Bortezomib in combination with dose-adjusted EPOCH (etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin) induces long-term survival in patients with plasmablastic lymphoma: a retrospective analysis. Dittus, C; Ellsworth, S; Grover, N; Park, SI; Tan, X, 2018)	1.92
"To investigate the effects of bortezomib alone and in combination with 5-fluorouracil (5-FU) on proliferation and apoptosis in the human choriocarcinoma cell line JEG-3."	( The effects of bortezomib alone or in combination with 5-fluorouracil on proliferation and apoptosis of choriocarcinoma cells. Li, CD; Liu, HP; Liu, L; Liu, QR; Tong, Y; Wang, HF, )	0.77
"Bortezomib alone or in combination with 5-FU inhibited JEG-3 cell proliferation and induced apoptosis by increasing NF-kB expression."	( The effects of bortezomib alone or in combination with 5-fluorouracil on proliferation and apoptosis of choriocarcinoma cells. Li, CD; Liu, HP; Liu, L; Liu, QR; Tong, Y; Wang, HF, )	1.93
"To study the clinical efficacy and safety of dexamethasone of different doses combined with bortezomib and thalidomide for treatment of primary multiple myeloma."	( [Clinical Efficacy and Safety of Different Doses of Dexamethasone Combined with Bortezomib and Thalidomide for Treating Patients with Multiple Myeloma]. Fu, LP; Ji, Y; Li, CS; Zhang, WP, 2018)	0.93
"The therapeutic efficacy of different doses of dexamethasone combined with bortezomib and thalidomide for patients with multiple myeloma is similar, can obviously enhance remission rate, prolong the survival time, promote life quality, but the incidence of adverse reactions in low dose dexamethason rigemen is significantly reduced, and the safety is better."	( [Clinical Efficacy and Safety of Different Doses of Dexamethasone Combined with Bortezomib and Thalidomide for Treating Patients with Multiple Myeloma]. Fu, LP; Ji, Y; Li, CS; Zhang, WP, 2018)	0.94
"To evaluate the cost-effectiveness of lenalidomide in combination with dexamethasone compared to bortezomib in combination with dexamethasone in patients with multiple myeloma previously treated with bortezomib, from the perspective of the Chilean National Health Service."	( Cost-effectiveness of lenalidomide in combination with dexamethasone compared to bortezomib in combination with dexamethasone for the second-line treatment of multiple myeloma in Chile. Aceituno, S; Appierto, M; Gozalbo, I; Lizán, L, 2018)	0.92
"Lenalidomide in combination with dexamethasone represents a potentially cost-effective alternative for the second-line treatment of patients with multiple myeloma who are not eligible for transplantation, from the perspective of the Chilean National Health Service."	( Cost-effectiveness of lenalidomide in combination with dexamethasone compared to bortezomib in combination with dexamethasone for the second-line treatment of multiple myeloma in Chile. Aceituno, S; Appierto, M; Gozalbo, I; Lizán, L, 2018)	0.71
" The treatment outcomes of MAbs versus HDACi in combination with bortezomib or lenalidomide plus dexamethasone remain unknown."	( Monoclonal Antibodies versus Histone Deacetylase Inhibitors in Combination with Bortezomib or Lenalidomide plus Dexamethasone for the Treatment of Relapsed or Refractory Multiple Myeloma: An Indirect-Comparison Meta-Analysis of Randomized Controlled Trial Chen, X; Feng, J; Gao, G; Shen, H; Tang, H; Xu, L; Zhang, N; Zheng, Y, 2018)	0.95
" In a preclinical study TNBC cells were treated with the first-generation proteasome inhibitor bortezomib in combination with cisplatin and synergistic efficacy was demonstrated."	( Ixazomib in combination with carboplatin in pretreated women with advanced triple-negative breast cancer, a phase I/II trial of the AGMT (AGMT MBC-10 trial). Balic, M; Bartsch, R; Burgstaller, S; Egle, D; Fuchs, D; Gampenrieder, SP; Greil, R; Melchardt, T; Mlineritsch, B; Petru, E; Petzer, A; Rinnerthaler, G; Rossmann, D; Rumpold, H; Singer, CF; Ulmer, H, 2018)	0.7
" Patients will receive ixazomib in combination with carboplatin on days 1, 8, and 15 in a 28-day cycle."	( Ixazomib in combination with carboplatin in pretreated women with advanced triple-negative breast cancer, a phase I/II trial of the AGMT (AGMT MBC-10 trial). Balic, M; Bartsch, R; Burgstaller, S; Egle, D; Fuchs, D; Gampenrieder, SP; Greil, R; Melchardt, T; Mlineritsch, B; Petru, E; Petzer, A; Rinnerthaler, G; Rossmann, D; Rumpold, H; Singer, CF; Ulmer, H, 2018)	0.48
" Bortezomib in combination with cyclosporine A and plasma exchange was introduced."	( Relapsing Evans syndrome and systemic lupus erythematosus with antiphospholipid syndrome treated with Bortezomib in combination with plasma exchange. Gilburd, B; Lapin, S; Maslyansky, A; Mikhailova, L; Myachikova, V; Tkachenko, O, 2019)	1.64
" To investigate the effects of these compounds on bortezomib's anti-proliferative potency and its intracellular accumulation and potency to inhibit the chymotrypsin-like proteasomal subunit, seven myeloma cell lines were investigated after exposure to bortezomib alone or either combined with adriamycin plus dexamethasone (PAD regimen) or melphalan plus prednisolone (VMP regimen), respectively."	( Elucidating the beneficial effects of melphalan, adriamycin, and corticoids in combination with bortezomib against multiple myeloma in vitro. Burhenne, J; Schäfer, J; Theile, D; Weiss, J, 2019)	0.99
" In this study, we report the effects of single reagent DAC therapy and DAC combined with BZM on β-catenin accumulation, myeloma cell survival, apoptosis, and treatment sensitivity."	( Synergistic Efficacy of the Demethylation Agent Decitabine in Combination With the Protease Inhibitor Bortezomib for Treating Multiple Myeloma Through the Wnt/β-Catenin Pathway. Chen, X; Dong, B; Feng, J; Gao, G; Gu, H; Jin, Y; Shu, M; Wu, X; Xu, L; Zhang, J, 2019)	0.73
"This phase Ib/II study aimed to determine the safety and tolerability of ulocuplumab alone and in combination with lenalidomide and dexamethasone (Arm A), or bortezomib and dexamethasone (Arm B), in patients with relapsed/refractory multiple myeloma."	( A Phase Ib/II Trial of the First-in-Class Anti-CXCR4 Antibody Ulocuplumab in Combination with Lenalidomide or Bortezomib Plus Dexamethasone in Relapsed Multiple Myeloma. Anderson, KC; Baz, R; Becker, PS; Chuma, S; Ghobrial, IM; Henrick, P; Hornburg, K; Laubach, J; Liu, CJ; Perez, RP; Redd, RA; Reyes, K; Richardson, PG; Robbins, MD; Sabbatini, P; Savell, A; Sklavenitis-Pistofidis, R; Zavidij, O, 2020)	0.97
"This study showed that blockade of the CXCR4-CXCL12 axis by ulocuplumab is safe with acceptable AEs and leads to a high response rate in combination with lenalidomide and dexamethasone in patients with relapsed/refractory myeloma, making CXCR4 inhibitors a promising class of antimyeloma drugs that should be further explored in clinical trials."	( A Phase Ib/II Trial of the First-in-Class Anti-CXCR4 Antibody Ulocuplumab in Combination with Lenalidomide or Bortezomib Plus Dexamethasone in Relapsed Multiple Myeloma. Anderson, KC; Baz, R; Becker, PS; Chuma, S; Ghobrial, IM; Henrick, P; Hornburg, K; Laubach, J; Liu, CJ; Perez, RP; Redd, RA; Reyes, K; Richardson, PG; Robbins, MD; Sabbatini, P; Savell, A; Sklavenitis-Pistofidis, R; Zavidij, O, 2020)	0.77
"We evaluated ibrutinib, a once-daily inhibitor of Bruton's tyrosine kinase, combined with bortezomib and dexamethasone in patients with relapsed or relapsed/refractory multiple myeloma who had received 1-3 prior therapies."	( A phase 2 study of ibrutinib in combination with bortezomib and dexamethasone in patients with relapsed/refractory multiple myeloma. Anagnostopoulos, A; Briso, EM; Cascavilla, N; Dobkowska, E; García Sanz, R; Hajek, R; Hauns, B; Lee, Y; Martin Sánchez, J; Oriol, A; Ozcan, M; Pour, L; Špička, I; Terjung, A, 2020)	1.03
"Ibrutinib combined with bortezomib and dexamethasone elicited clinical responses."	( A phase 2 study of ibrutinib in combination with bortezomib and dexamethasone in patients with relapsed/refractory multiple myeloma. Anagnostopoulos, A; Briso, EM; Cascavilla, N; Dobkowska, E; García Sanz, R; Hajek, R; Hauns, B; Lee, Y; Martin Sánchez, J; Oriol, A; Ozcan, M; Pour, L; Špička, I; Terjung, A, 2020)	1.12
" The patient underwent autologous transplantation and is still in remission, demonstrating the benefits of a bortezomib-based regimen in combination with PE for IgD MM with AKD."	( Plasma exchange combined with bortezomib-based chemotherapy is effective for early renal recovery in a patient with IgD-λ type multiple myeloma. Dobashi, N; Kato, J; Katsuma, A; Kawamura, T; Kimura, A; Kuno, H; Miyazaki, Y; Momoki, M; Nakashima, A; Ohba, R; Takahashi, D; Ueda, H; Yamamoto, I; Yokoo, T, 2020)	1.06
" Together, our results indicate that DCZ0847, alone or in combination with bortezomib, may represent a potential new therapy for patients with MM."	( A novel phosphoramide compound, DCZ0847, displays in vitro and in vivo anti-myeloma activity, alone or in combination with bortezomib. Chen, G; Cheng, Y; Feng, Q; Gao, L; Hu, K; Hu, L; Li, B; Lu, K; Lu, Y; Shi, J; Song, D; Sun, H; Wang, Y; Wu, X; Xu, Z; Zhang, H; Zhou, J; Zhu, W, 2020)	1
" Despite the extensive clinical use of bortezomib, the mechanism of the complex time-dependent pharmacokinetics of bortezomib has not been fully investigated in context of its pharmacodynamics (PD) and drug-drug interaction (DDI) profiles."	( A Translational Physiologically Based Pharmacokinetics/Pharmacodynamics Framework of Target-Mediated Disposition, Target Inhibition and Drug-Drug Interactions of Bortezomib. Hanley, M; Iwasaki, S; Venkatakrishnan, K; Xia, C; Zhu, A, 2020)	1.02
" We report a case of acute renal failure caused by TAFRO syndrome, successfully managed by long-term corticosteroids combined with bortezomib and cyclophosphamide."	( Acute Kidney Injury Caused by TAFRO Syndrome in a Chinese Patient: Efficacy of Long-Term Corticosteroids Combined with Bortezomib and Cyclophosphamide. Chen, L; Li, J; Li, R; Li, X; Qin, Y; Shi, X; Wang, J; Xia, P; Zhang, L; Zhang, T; Zou, M, 2020)	0.97
" A weekly dosing regimen of bortezomib, cyclophosphamide, and dexamethasone combined with medium dose prednisone in between were deployed."	( Acute Kidney Injury Caused by TAFRO Syndrome in a Chinese Patient: Efficacy of Long-Term Corticosteroids Combined with Bortezomib and Cyclophosphamide. Chen, L; Li, J; Li, R; Li, X; Qin, Y; Shi, X; Wang, J; Xia, P; Zhang, L; Zhang, T; Zou, M, 2020)	1.06
" Randomized controlled trials that assessed the effectiveness and safety of bortezomib in combination with chemotherapy for patients with mantle cell lymphoma will be included."	( The effectiveness and harms of bortezomib in combination with chemotherapy for mantle cell lymphoma: A protocol for systematic review and meta-analysis. Feng, C; Li, J; Li, W; Li, Y; Liu, X; Wang, X, 2020)	1.07
"This study will provide a detailed summary of latest evidence related to the effectiveness and safety of bortezomib in combination with chemotherapy in overall survival, progression-free survival, overall response rate, quality of life, and serious adverse events for patients with mantle cell lymphoma CONCLUSION:: The findings of this study may provide possible guidance for bortezomib in combination with chemotherapy for patients with mantle cell lymphoma."	( The effectiveness and harms of bortezomib in combination with chemotherapy for mantle cell lymphoma: A protocol for systematic review and meta-analysis. Feng, C; Li, J; Li, W; Li, Y; Liu, X; Wang, X, 2020)	1.06
"To investigate the effects of decitabine combined with bortezomib on the proliferation of mantle cell lymphoma cell lines (Jeko-1 and Grante519) in vitro and explore the underlying mechanisms."	( [Effects of Decitabine Combined with Bortezomib on the Proliferation of Mantle Cell Lymphoma Cell Lines and Its Underling Mechanisms]. Chen, D; Guo, XN; Li, Y; Qiao, SK; Xing, LN; Zhang, JN, 2020)	1.08
" Compared with single-drug treatment group, DAC combined with BTZ significantly increased the inhibitory rate and apoptotic rate of Jeko-1 and Grante519 cells; PCDH8, Caspase 3 and BAX expression levels significantly increased, and the expression levels of NF-κB, BCL-2 and CCND1 significantly decreased in Jeko-1 and Grante519 cells."	( [Effects of Decitabine Combined with Bortezomib on the Proliferation of Mantle Cell Lymphoma Cell Lines and Its Underling Mechanisms]. Chen, D; Guo, XN; Li, Y; Qiao, SK; Xing, LN; Zhang, JN, 2020)	0.83
"To investigate the influence of influence of combination with 1q21 amplification or-no in patients with newly diagnosed MM on the clinical effecacy of bortezomib-based induction chemotherapy and long-term prognosis of patients."	( [Influence of Combination with 1q21 Amplification or-No in Patients with Newly Diagnosed MM on the Clinical Effecacy of Bortezomib-based induction chemotherapy and Long-Term Prognosis of Patients]. Gu, WW; Mu, K; Ren, G; Wang, JS, 2020)	0.97
" However, concomitant use of bortezomib in combination with either of DHA or EPA decreased the cell death induced by bortezomib, indicating that timing of coincubation is important for the effects on chemosensitivity."	( The efficacy of bortezomib in human multiple myeloma cells is enhanced by combination with omega-3 fatty acids DHA and EPA: Timing is essential. Chen, J; Garssen, J; Redegeld, F, 2021)	1.26
"The present study provides novel evidence for the anticancer effects of DHA and EPA, and highlights their rational utilization in combination with bortezomib to achieve improved therapeutic outcome for MM."	( The efficacy of bortezomib in human multiple myeloma cells is enhanced by combination with omega-3 fatty acids DHA and EPA: Timing is essential. Chen, J; Garssen, J; Redegeld, F, 2021)	1.17
"A 55-year-old MM patient with a family history of MM, who was also a chronic HBV carrier, achieved HBV clearance after treatment with a bortezomib-based regimen in combination with anti-HBV drugs."	( Clearance of HBsAg in a patient with familial multiple myeloma after a bortezomib-based regimen combined with anti-HBV drug: A case report. Li, X; Liang, Y; Tong, J; Wang, W; Xu, Y; Zhang, X, 2020)	0.99
"This is the first case of MM with HBV clearance after receiving a bortezomib-based regimen combined with anti-HBV drug."	( Clearance of HBsAg in a patient with familial multiple myeloma after a bortezomib-based regimen combined with anti-HBV drug: A case report. Li, X; Liang, Y; Tong, J; Wang, W; Xu, Y; Zhang, X, 2020)	1.03
"We report results of a phase-1 study evaluating the safety and anti-cancer activity of the small molecule insulin-like growth factor-1 receptor (IGF-1R) inhibitor, linsitinib combined with bortezomib, and dexamethasone in relapsed/refractory multiple myeloma."	( A phase-1 trial of linsitinib (OSI-906) in combination with bortezomib and dexamethasone for the treatment of relapsed/refractory multiple myeloma. Gul, E; Gyger, M; Jazubowiak, A; Kaufman, J; Khan, S; Lau, A; Le, LW; LeBlanc, R; Li, Z; Paul, H; Trudel, S; White, D, 2021)	1.05
" We compared the activity of these proteasome inhibitors in combination with cyclophosphamide and dexamethasone (KCd vs."	( Carfilzomib or bortezomib in combination with cyclophosphamide and dexamethasone followed by carfilzomib maintenance for patients with multiple myeloma after one prior therapy: results from a multicenter, phase II, randomized, controlled trial (MUK Auner, HW; Brown, SR; Bygrave, C; Cavenagh, J; Croft, J; Davies, F; De Tute, RM; Flanagan, L; Garg, M; Hawkins, S; Hinsley, S; Kaiser, MF; Morgan, G; Owen, RG; Rabin, NK; Ramasamy, K; Sherratt, D; Williams, C; Yong, KL, 2021)	0.97
"To determine the safety of tipifarnib in combination with escalating doses of bortezomib and to determine the maximum tolerated dose in patients with untreated high-risk MDS and oligoblastic acute myeloid leukemia, who were not eligible for intensive therapy."	( A phase I clinical trial to study the safety of treatment with tipifarnib combined with bortezomib in patients with advanced stages of myelodysplastic syndrome and oligoblastic acute myeloid leukemia. Blijlevens, N; de Witte, T; Langemeijer, S; Muus, P; van Bijnen, S, 2021)	1.07
"This study aimed to identify the maximum-tolerated dose (MTD) of cyclophosphamide when combined with bortezomib and fludarabine (B-FC) in a phase 1b trial, and to assess the efficacy and safety of this combination in a phase 2 trial in patients with relapsed or refractory MCL (rrMCL)."	( Bortezomib in combination with fludarabine plus cyclophosphamide for patients with relapsed or refractory mantle-cell lymphoma: results of the LYM-4003 study. Cai, QQ; Cao, JN; Feng, JF; Gao, Y; Huang, HQ; Jiang, WQ; Jin, J; Li, ZM; Wang, HQ; Wang, XX; Zhang, HL, 2021)	2.28
"To investigate the effects of chidamide combined with anti-myeloma drugs on the proliferation and apoptosis of myeloma cells."	( [The Effects of Chidamide Combined with Anti-myeloma Drugs on the Proliferation and Apoptosis of Myeloma Cells]. Chen, GH; Fu, CC; Liu, W; Liu, Y; Wu, DP; Xie, Y; Xu, Y; Yan, LZ; Yan, S; Yao, WQ, 2021)	0.62
" In NCI-H929 cell line, chidamide combined with low-dose bortezomib and lenalidomide showed synergistic effect, while combined with dexamethasone and pomalidomide showed additive effect."	( [The Effects of Chidamide Combined with Anti-myeloma Drugs on the Proliferation and Apoptosis of Myeloma Cells]. Chen, GH; Fu, CC; Liu, W; Liu, Y; Wu, DP; Xie, Y; Xu, Y; Yan, LZ; Yan, S; Yao, WQ, 2021)	0.87
"Many clinical trials have assessed the effect and safety of monoclonal antibodies (MAbs) in combination with proteasome inhibitors or immunomodulators plus dexamethasone/prednisone for the treatment of multiple myeloma (MM)."	( Comparison of monoclonal antibodies targeting CD38, SLAMF7 and PD-1/PD-L1 in combination with Bortezomib/Immunomodulators plus dexamethasone/prednisone for the treatment of multiple myeloma: an indirect-comparison Meta-analysis of randomised controlled tr Deng, J; Gong, Y; Liu, X; Wu, X; Ye, W; Zheng, X, 2021)	0.84
" In conclusion, MAbs targeting CD38 are the best, followed by those targeting SLAMF7; MAbs targeting PD-1/PD-L1 are the worst when in combination with bortezomib/immunomodulators plus dexamethasone/prednisone for the treatment of MM."	( Comparison of monoclonal antibodies targeting CD38, SLAMF7 and PD-1/PD-L1 in combination with Bortezomib/Immunomodulators plus dexamethasone/prednisone for the treatment of multiple myeloma: an indirect-comparison Meta-analysis of randomised controlled tr Deng, J; Gong, Y; Liu, X; Wu, X; Ye, W; Zheng, X, 2021)	1.04
" Therefore, we prospectively compared the efficacy of bortezomib-cyclophosphamide-dexamethasone (CyBorD) and CyBorD combined with doxycycline for cardiac light chain amyloidosis."	( Doxycycline Combined With Bortezomib-Cyclophosphamide-Dexamethasone Chemotherapy for Newly Diagnosed Cardiac Light-Chain Amyloidosis: A Multicenter Randomized Controlled Trial. Cao, XX; Chen, Y; Dong, YJ; Fu, WJ; Huang, ZX; Li, CR; Li, J; Miao, HL; Shen, KN; Sun, CY; Wei, YQ; Wu, Y; Zhang, YL; Zhou, DB, 2022)	1.27
"Our trial demonstrated that doxycycline combined with CyBorD failed to prolong PFS or cardiac PFS compared with CyBorD alone in cardiac light chain amyloidosis."	( Doxycycline Combined With Bortezomib-Cyclophosphamide-Dexamethasone Chemotherapy for Newly Diagnosed Cardiac Light-Chain Amyloidosis: A Multicenter Randomized Controlled Trial. Cao, XX; Chen, Y; Dong, YJ; Fu, WJ; Huang, ZX; Li, CR; Li, J; Miao, HL; Shen, KN; Sun, CY; Wei, YQ; Wu, Y; Zhang, YL; Zhou, DB, 2022)	1.02
"2" to hypoxia stress by using bortezomib, and combined with transcriptome analysis, accurately captured the genes related to hypoxia tolerance advantage."	( The transcriptomic responses of blunt snout bream (Megalobrama amblycephala) to acute hypoxia stress alone, and in combination with bortezomib. Lu, LQ; Pan, RJ; Su, XL; Zhao, SS; Zheng, GD; Zou, SM, 2022)	1.21
" Aggressive immunotherapy combined with bortezomib and rituximab was then initiated."	( Aggressive immunotherapy combined with bortezomib and rituximab for membranous nephropathy associated with enzyme replacement therapy in Pompe disease. Hanakawa, J; Inaba, A; Ito, S; Otani, M; Sasaki, K; Uchimura, T, 2023)	1.45
" Here, we propose that rational drug combination design and validation in patient-derived HCC avatar models such as patient-derived xenografts (PDXs) and organoids can improve proteasome inhibitor-based therapeutic efficacy and clinical potential."	( Rational drug combination design in patient-derived avatars reveals effective inhibition of hepatocellular carcinoma with proteasome and CDK inhibitors. Bonney, GK; Chee, CE; Chow, EK; Chow, PK; Dan, YY; Hooi, L; Lim, JJ; Toh, TB; Zhou, L, 2022)	0.72
"Rational drug combination design in patient-derived avatars highlights the therapeutic potential of proteasome and CDK inhibitors and represents a feasible approach towards developing more clinically relevant treatment strategies for HCC."	( Rational drug combination design in patient-derived avatars reveals effective inhibition of hepatocellular carcinoma with proteasome and CDK inhibitors. Bonney, GK; Chee, CE; Chow, EK; Chow, PK; Dan, YY; Hooi, L; Lim, JJ; Toh, TB; Zhou, L, 2022)	0.72
" We present a case of HIV-negative primary testicular PBL with long-term complete remission (CR) and successful treatment with bortezomib in combination with EPOCH (V-EPOCH)."	( [Long-term complete remission of HIV-negative primary testicular plasmablastic lymphoma treated with bortezomib in combination with EPOCH]. Fujishima, T; Kawabata, Y; Kitabayashi, A; Michishita, Y; Takahashi, N, 2022)	1.14
" Therefore, this study aimed to investigate the role of p53 knockdown or overexpression in multiple myeloma and the therapeutic effect of recombinant adenovirus-p53 (rAd-p53) in combination with Bortezomib."	( Recombinant human p53 adenovirus injection combined with Bortezomib inhibits proliferation and promotes apoptosis in multiple myeloma. Chen, Y; Shen, L; Shi, Q; Wang, G; Wang, Q, 2023)	1.34
" We report the first case of primary PCL successfully treated with upfront novel agents consisting of Venetoclax and daratumumab in combination with intensive chemotherapy and allogeneic transplantation."	( Plasma Cell Leukemia with Successful Upfront Venetoclax in Combination with Allogeneic Transplantation. Ahmad Asnawi, AW; Chong, SL; Koh, AZY; Lau, NS; Liew, PK; Md Fauzi, A; Selvaratnam, V; Tan, SM; Tang, ASO, 2023)	0.91

Excerpt	Reference	Relevance
" Peptidomimetics have been developed to circumvent problems inherent in peptides such as poor bioavailability and protease-mediated degradation, while retaining biological activity."	( Retro hydrazino-azapeptoids as peptidomimetics of proteasome inhibitors. Arlot-Bonnemains, Y; Aubin, S; Baudy-Floc'h, M; Delcros, JG; Martin, B, 2005)	0.33
" Herein, the potent, selective, and orally bioavailable threonine-derived 20S human proteasome inhibitor that has been advanced to preclinical development, [(1R)-1-[[(2 S,3 R)-3-hydroxy-2-[(6-phenylpyridine-2-carbonyl)amino]-1-oxobutyl]amino]-3-methylbutyl]boronic acid 20 (CEP-18770), is disclosed."	( Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer. Allievi, C; Ator, MA; Bernardini, R; Bernareggi, A; Cassarà, PG; Chatterjee, S; D'Arasmo, G; De Munari, S; Dorsey, BD; Ferretti, E; Iqbal, M; Mallamo, JP; Menta, E; Oliva, A; Pezzoni, G; Ruggeri, B; Strepponi, I; Williams, M, 2008)	0.35
" A chemistry effort was initiated to discover orally bioavailable analogues of carfilzomib, which would have potential for improved dosing flexibility and patient convenience over intravenously administered agents."	( Design and synthesis of an orally bioavailable and selective peptide epoxyketone proteasome inhibitor (PR-047). Aujay, MA; Bennett, MK; Dajee, M; Demo, SD; Fang, Y; Ho, MN; Jiang, J; Kirk, CJ; Laidig, GJ; Lewis, ER; Lu, Y; Muchamuel, T; Parlati, F; Ring, E; Shenk, KD; Shields, J; Shwonek, PJ; Stanton, T; Sun, CM; Sylvain, C; Woo, TM; Yang, J; Zhou, HJ, 2009)	0.35
" INCB16562 was developed as a novel, selective, and orally bioavailable small-molecule inhibitor of JAK1 and JAK2 markedly selective over JAK3."	( INCB16562, a JAK1/2 selective inhibitor, is efficacious against multiple myeloma cells and reverses the protective effects of cytokine and stromal cell support. Arvanitis, A; Caulder, E; Combs, AP; Favata, M; Fridman, JS; Kelley, JA; Li, J; Newton, R; Rogers, JD; Scherle, PA; Solomon, KA; Sparks, RB; Thomas, B; Vaddi, K; Wen, X, 2010)	0.36
"One of the main functions of A Disintegrin and Metalloproteinase 10 (ADAM10) is to regulate the bioavailability of adhesion molecules and ligands to various cellular-signaling receptors."	( Constitutive activation of metalloproteinase ADAM10 in mantle cell lymphoma promotes cell growth and activates the TNFα/NFκB pathway. Anand, M; Armanious, H; Belch, A; Gelebart, P; Lai, R, 2011)	0.37
" CYT387 is a novel, orally bioavailable JAK1/2 inhibitor, which has recently been described."	( The novel JAK inhibitor CYT387 suppresses multiple signalling pathways, prevents proliferation and induces apoptosis in phenotypically diverse myeloma cells. Burns, CJ; Khong, T; Monaghan, KA; Spencer, A, 2011)	0.37
" The dietary polyphenol curcumin has been shown to exert anti-cancer activity in several cancer cell lines, but the effects of curcumin in solid tumors have been modest primarily due to poor water solubility and poor bioavailability in tissues remote from the gastrointestinal tract."	( Sensitizing human multiple myeloma cells to the proteasome inhibitor bortezomib by novel curcumin analogs. Chan, TH; Dou, QP; Kanwar, J; Mujtaba, T; Wan, SB, 2012)	0.61
" Carfilzomib and its orally bioavailable analog oprozomib, effectively decreased MM cell viability following continual or transient treatment mimicking in vivo pharmacokinetics."	( The epoxyketone-based proteasome inhibitors carfilzomib and orally bioavailable oprozomib have anti-resorptive and bone-anabolic activity in addition to anti-myeloma effects. Blanco, JF; Collins, L; Garayoa, M; Garcia-Gomez, A; Hornick, MC; Hurchla, MA; Kirk, CJ; Li, A; Ocio, EM; Pandiella, A; Piwnica-Worms, D; San Miguel, JF; Tomasson, MH; Vij, R; Weilbaecher, KN, 2013)	0.39
" To resolve these problems, we attempted to develop orally bioavailable proteasome inhibitors with distinct mechanisms of action and identified homopiperazine derivatives (HPDs) as promising candidates."	( Homopiperazine derivatives as a novel class of proteasome inhibitors with a unique mode of proteasome binding. Akutsu, M; Furukawa, Y; Izumi, T; Kano, Y; Kikuchi, J; Nobuyoshi, M; Ohki, M; Park, SY; Shibayama, N; Sugiyama, K; Wada, T; Yamada, S, 2013)	0.39
" Carfilzomib and its orally bioavailable structural analog oprozomib are second-generation, highly-selective, proteasome inhibitors."	( Carfilzomib and oprozomib synergize with histone deacetylase inhibitors in head and neck squamous cell carcinoma models of acquired resistance to proteasome inhibitors. Johnson, DE; Kirk, CJ; Zang, Y, 2014)	0.4
" However, due to its too fast elimination and to the undesired related side effects, the improvement of sTRAIL in vivo bioavailability and the specific delivery to the tumour is mandatory for increasing its therapeutic efficacy."	( sTRAIL coupled to liposomes improves its pharmacokinetic profile and overcomes neuroblastoma tumour resistance in combination with Bortezomib. Becherini, P; Brignole, C; Cilli, M; Cossu, I; Destefanis, E; Di Paolo, D; Emionite, L; Giacomini, A; Loi, M; Pastorino, F; Perri, P; Piaggio, F; Ponzoni, M, 2014)	0.61
" Entinostat is an orally bioavailable class I HDAC inhibitor with a long half-life, which is under evaluation in haematological and solid tumour malignancies."	( Entinostat, a novel histone deacetylase inhibitor is active in B-cell lymphoma and enhances the anti-tumour activity of rituximab and chemotherapy agents. Barth, MJ; Czuczman, MS; Frys, S; Gu, JJ; Hernandez-Ilizaliturri, FJ; Hu, Q; Mavis, C; Simons, Z; Skitzki, J; Song, L, 2015)	0.42
" Herein we describe our lead optimization efforts focused on in vitro potency, ADME, and pharmaceutical properties that led to the discovery of a potent, ATP-competitive, D2-selective, and orally bioavailable p97 inhibitor 71, CB-5083."	( Discovery of a First-in-Class, Potent, Selective, and Orally Bioavailable Inhibitor of the p97 AAA ATPase (CB-5083). Anderson, DJ; Djakovic, S; Kiss von Soly, S; Kumar, A; Kumar, B; Le Moigne, R; Madriaga, A; Menon, MK; Parlati, F; Rice, J; Rolfe, M; Shawver, L; Soriano, F; Valle, E; Wang, J; Wong, S; Wustrow, D; Yakes, FM; Yao, B; Zhou, HJ, 2015)	0.42
" In a pharmacokinetics study using rats, the bortezomib microemulsion failed to improve the bioavailability of the drug."	( Formulation and Evaluation of a Self-microemulsifying Drug Delivery System Containing Bortezomib. Hong, EP; Hwang, KM; Jeong, SY; Kim, DW; Kim, JY; Kim, SH; Lee, HJ; Park, CW; Park, ES; Weon, KY, 2016)	0.92
" Many recent studies have investigated the safety of orally bioavailable proteasome inhibitors, such as ixazomib and oprozomib."	( Proteasome inhibitor-induced gastrointestinal toxicity. Gibson, RJ; Stansborough, RL, 2017)	0.46
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."	( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019)	0.51

Excerpt	Relevance	Reference
" These studies provided the rationale for a twice-weekly dosing schedule employed in ongoing clinical studies."	( Development of the proteasome inhibitor PS-341. Adams, J, 2002)	0.31
" Additional studies are indicated to determine whether incorporation of dose/body surface area yields a superior PD model to dosing without normalization."	( Phase I trial of the proteasome inhibitor PS-341 in patients with refractory hematologic malignancies. Adams, J; Anderson, JK; Baldwin, AS; Bhagat, R; Depcik-Smith, ND; Elliott, PJ; Esseltine, DL; Guerciolini, R; Lehman, MJ; Mitchell, BS; Novick, SC; O'Connor, OA; Orlowski, RZ; Pien, CS; Shea, TC; Soignet, SL; Stahl, S; Stinchcombe, TE, 2002)	0.31
" Phase I trials provided evidence of manageable toxicities and support a twice-weekly dosing regimen now being examined in a Phase III study."	( Potential for proteasome inhibition in the treatment of cancer. Adams, J, 2003)	0.32
" dosing for the first 2 weeks of each 3-week cycle."	( Velcade: U.S. FDA approval for the treatment of multiple myeloma progressing on prior therapy. Bross, PF; Farrell, AT; Kane, RC; Pazdur, R, 2003)	0.32
" These results were compared to analysis using the median-dose effect method, which generated complex drug interactions due to differences in dose-response curve sigmoidicities."	( Bortezomib interactions with chemotherapy agents in acute leukemia in vitro. Berg, SL; Blaney, SM; D'Argenio, DZ; Gannavarapu, A; Horton, TM; Plon, SE, 2006)	1.78
" Phase I clinical trials established an optimal dosing strategy and demonstrated a manageable toxicity profile."	( Bortezomib, a novel proteasome inhibitor, in the treatment of hematologic malignancies. Einsele, H; Jackson, G; Miguel, JS; Moreau, P, 2005)	1.77
" Studies are underway to explore different dosing strategies as well as ways to maximize patient benefit while reducing toxicity."	( Optimizing the efficacy and safety of bortezomib in relapsed multiple myeloma. Colson, K; Jagannath, S; Richardson, P, 2006)	0.6
") The proteasome inhibitor bortezomib, which induces strong apoptosis in cancer cells, abrogated proliferation and angiogenesis of HUVECs when used at a high concentration (100 nM), yet promoted both functions at a low dosage (10 nM)."	( Hypoxia-inducible transcription factor-1 alpha determines sensitivity of endothelial cells to the proteosome inhibitor bortezomib. Belloni, D; Caligaris-Cappio, F; Cangi, MG; Ferrarini, M; Ferrero, E; Foglieni, C; Veschini, L, 2007)	0.85
"Bortezomib was dosed on days 1, 4, 8, and 11 (i."	( Tissue distribution and depletion kinetics of bortezomib and bortezomib-related radioactivity in male rats after single and repeated intravenous injection of 14 C-bortezomib. De Coster, R; Diels, L; Geerts, R; Hassler, S; Hemeryck, A; Janssen, C; Mamidi, RN; Monbaliu, J; van Beijsterveldt, L; Verhaeghe, T; Verluyten, W, 2007)	2.04
"No undue tissue accumulation of TR and of bortezomib was observed in rats following a full clinical dosing cycle of bortezomib."	( Tissue distribution and depletion kinetics of bortezomib and bortezomib-related radioactivity in male rats after single and repeated intravenous injection of 14 C-bortezomib. De Coster, R; Diels, L; Geerts, R; Hassler, S; Hemeryck, A; Janssen, C; Mamidi, RN; Monbaliu, J; van Beijsterveldt, L; Verhaeghe, T; Verluyten, W, 2007)	0.86
" The slower response in nodal disease may require prolonged therapy, perhaps with a less intensive dosing schedule to avoid early discontinuation because of toxicity."	( Bortezomib is active in patients with untreated or relapsed Waldenstrom's macroglobulinemia: a phase II study of the National Cancer Institute of Canada Clinical Trials Group. Chen, CI; Eisenhauer, E; Kouroukis, CT; Powers, J; Stadtmauer, E; Stewart, AK; Voralia, M; Walsh, W; White, D; Wright, JJ, 2007)	1.78
" In this gene expression profiling study, we show that H-MM is defined by a protein biosynthesis signature that is primarily driven by a gene dosage mechanism as a result of trisomic chromosomes."	( Molecular dissection of hyperdiploid multiple myeloma by gene expression profiling. Ahmann, G; Bergsagel, PL; Bryant, B; Carpten, J; Chng, WJ; Chung, TH; Dispenzieri, A; Fonseca, R; Gertz, M; Greipp, P; Henderson, K; Kim, S; Kumar, S; Kyle, R; Lacy, M; Mulligan, G; Price-Troska, T; Rajkumar, SV; Vanwier, S, 2007)	0.34
"Bortezomib was uniformly active against the PPTP's in vitro panel, with a median IC(50) of 23 nM and with a steep dose-response curve."	( Initial testing (stage 1) of the proteasome inhibitor bortezomib by the pediatric preclinical testing program. Carol, H; Houghton, PJ; Keir, ST; Keshelava, N; Kolb, EA; Lock, R; Maris, JM; Morton, CL; Reynolds, CP; Smith, MA; Wu, J, 2008)	2.04
" The antitumor efficacy of PR-171 delivered on 2 consecutive days is stronger than that of bortezomib administered on its clinical dosing schedule."	( Antitumor activity of PR-171, a novel irreversible inhibitor of the proteasome. Aujay, MA; Bennett, MK; Buchholz, TJ; Dajee, M; Demo, SD; Ho, MN; Jiang, J; Kirk, CJ; Laidig, GJ; Lewis, ER; Molineaux, CJ; Parlati, F; Shenk, KD; Smyth, MS; Sun, CM; Vallone, MK; Woo, TM, 2007)	0.56
"The combination of bortezomib and celecoxib was well tolerated, without dose limiting toxicities observed throughout the dosing ranges tested, and will be studied further at the highest dose levels investigated."	( Bortezomib in combination with celecoxib in patients with advanced solid tumors: a phase I trial. Chaudhary, U; Dunder, S; Green, M; Hayslip, J; Kraft, A; Meyer, M; Montero, AJ; Salzer, S; Sherman, C, 2007)	2.11
"The pharmacology, pharmacokinetics, clinical efficacy, safety, dosage and administration, place in therapy, and cost of bortezomib in the treatment of multiple myeloma and mantle cell lymphoma are reviewed."	( Bortezomib: a novel chemotherapeutic agent for hematologic malignancies. Kolesar, J; Utecht, KN, 2008)	2
" At the RD, microarray analysis of transcriptional profiles was carried out before and after the first dosing in peripheral blood mononuclear cells (PBMC)."	( Phase I study of bortezomib with weekly paclitaxel in patients with advanced solid tumours. Bertoni, F; Capri, G; Catapano, CV; Cresta, S; Gallerani, E; Gianni, L; Maccioni, E; Maur, M; Passalacqua, D; Rinaldi, A; Sessa, C; Tosi, D; Viganò, L, 2008)	0.69
"To investigate the efficacy and toxicity of bortezomib based combination therapy for Chinese patients with relapsed or refractory multiple myeloma (MM), and to determine the combination regimen, dosage and cycles in application of bortezomib for MM therapy."	( [Bortezomib-based combination therapy for relapsed or refractory multiple myeloma]. Chen, YB; Fu, WJ; Hou, J; Wang, DX; Xi, H; Yuan, ZG, 2008)	1.52
" With these drug therapies has come a more targeted approach to treatment enabling not only improved antimyeloma efficacy but also the use of decreased dosing enhancing the safety and tolerability of these regimens."	( New drugs in multiple myeloma. Berenson, JR; Yellin, O, 2008)	0.35
" Bortezomib generally showed dose-response curves with a steep slope."	( In vitro activity of bortezomib in cultures of patient tumour cells--potential utility in haematological malignancies. Aleskog, A; Carlson, K; Larsson, R; Lindhagen, E; Nygren, P; Wiberg, K, 2009)	1.58
" These events were predictable and often managed by dosage modifications and supportive therapy."	( Pegylated liposomal Doxorubicin: a review of its use in the treatment of relapsed or refractory multiple myeloma. Plosker, GL, 2008)	0.35
" 4) The most common adverse events were 1-2 grade and tolerable 3 patients had to reduce the bortezomib dosage because of peripheral neuropathy or sinus bradycardia."	( [Outcome of bortezomib plus chemotherapy with or without stem cell transplantation for treatment of multiple myeloma]. Deng, SH; Qiu, LG; Wang, Y; Wang, YF; Wu, T; Xu, Y; Zhao, YZ; Zou, DH, 2008)	0.94
" The plasma LC/MS biomolecular/biochemical profiles, comprised of thousands of endogenous small molecules, peptides and proteins, were determined for 10 multiple myeloma patients at predose and 24 h after initial dosing with bortezomib."	( Elucidation of potential bortezomib response markers in mutliple myeloma patients. Guerciolini, R; Hsieh, FY; Miwa, G; Pekol, TM; Tengstrand, E, 2009)	0.84
" However, while bortezomib was highly cytotoxic to NK-92 cells in vitro, bortezomib treatment in vivo did not decrease NK-92 function, suggesting that through alternative dosing or timing of bortezomib, greater efficacy may occur from combined therapy."	( Sensitization of human breast cancer cells to natural killer cell-mediated cytotoxicity by proteasome inhibition. Ames, E; Hallett, WH; Murphy, WJ, 2009)	0.7
" A chemistry effort was initiated to discover orally bioavailable analogues of carfilzomib, which would have potential for improved dosing flexibility and patient convenience over intravenously administered agents."	( Design and synthesis of an orally bioavailable and selective peptide epoxyketone proteasome inhibitor (PR-047). Aujay, MA; Bennett, MK; Dajee, M; Demo, SD; Fang, Y; Ho, MN; Jiang, J; Kirk, CJ; Laidig, GJ; Lewis, ER; Lu, Y; Muchamuel, T; Parlati, F; Ring, E; Shenk, KD; Shields, J; Shwonek, PJ; Stanton, T; Sun, CM; Sylvain, C; Woo, TM; Yang, J; Zhou, HJ, 2009)	0.35
" Bortezomib-based combination therapies, with consideration for attenuated or intermittent dosing of bortezomib to minimize neuropathy, are under investigation."	( Bortezomib in relapsed or refractory Waldenström's macroglobulinemia. Chen, C; Eisenhauer, E; Kouroukis, CT; Powers, J; Stadtmauer, E; Stewart, AK; Voralia, M; Walsh, W; White, D; Wright, JJ, 2009)	2.71
" Exploration of alternative schedules for bortezomib administration that includes weekly dosing should be pursued."	( Primary therapy of Waldenström macroglobulinemia with bortezomib, dexamethasone, and rituximab: WMCTG clinical trial 05-180. Birner, A; Boral, A; Diener, JG; Esseltine, DL; Ghobrial, IM; Ioakimidis, L; Keogh, GP; Matous, J; Mattern, J; Myers, TJ; Nelson, M; Patterson, CJ; Sheehy, P; Soumerai, JD; Treon, SP; Willen, M, 2009)	0.87
" Serial blood samples were collected over the day-8 dosing interval (immediately prior to bortezomib administration, and from 5 minutes to 72 hours after administration) in cycles 1 and 2 for measurement of plasma bortezomib concentrations for noncompartmental PK analysis and blood 20S proteasome inhibition for PD analysis."	( Effect of the CYP3A inhibitor ketoconazole on the pharmacokinetics and pharmacodynamics of bortezomib in patients with advanced solid tumors: a prospective, multicenter, open-label, randomized, two-way crossover drug-drug interaction study. Chatta, G; Chen, E; Cooper, M; Egorin, M; Karol, M; Neuwirth, R; Rader, M; Ramalingam, S; Ramanathan, RK; Riordan, W; Trepicchio, W; Venkatakrishnan, K; von Moltke, L, 2009)	0.79
" Moreover, antitumor activity was shown via multiple dosing routes, including oral gavage."	( Evaluation of the proteasome inhibitor MLN9708 in preclinical models of human cancer. Bannerman, B; Berger, A; Blank, J; Bolen, J; Bruzzese, F; Cao, Y; Dick, L; Fitzgerald, M; Fleming, P; Garcia, K; Hales, P; Kupperman, E; Lee, EC; Liu, J; Manfredi, M; Rolfe, M; Tsu, C; Yang, Y; Yu, J; Yu, L, 2010)	0.36
" Tests were performed during treatment and for 4weeks post dosing to evaluate electrophysiological, autonomic, pain sensibility and sensory-motor function changes."	( Neurophysiological, histological and immunohistochemical characterization of bortezomib-induced neuropathy in mice. Alé, A; Bruna, J; Monbaliu, J; Navarro, X; Silverman, L; Udina, E; Vilches, JJ; Vynckier, A, 2010)	0.59
" Plasma clearance decreased with repeat dosing (102-112 L/h for first dose; 15-32 L/h following repeat dosing), with associated increases in systemic exposure and terminal half-life."	( Pharmacokinetic and pharmacodynamic study of two doses of bortezomib in patients with relapsed multiple myeloma. Acharya, M; Burris, H; Chatta, G; Karol, M; Keith Stewart, A; Lonial, S; Mohrbacher, AF; Neuwirth, R; Reece, DE; Riordan, WJ; Shustik, C; Sullivan, D; Venkatakrishnan, K; von Moltke, LL; Zannikos, P, 2011)	0.61
"3 mg/m(2) doses, with recovery toward baseline blood proteasome activity over the dosing interval following repeat dose administration, supporting the current clinical dosing regimen."	( Pharmacokinetic and pharmacodynamic study of two doses of bortezomib in patients with relapsed multiple myeloma. Acharya, M; Burris, H; Chatta, G; Karol, M; Keith Stewart, A; Lonial, S; Mohrbacher, AF; Neuwirth, R; Reece, DE; Riordan, WJ; Shustik, C; Sullivan, D; Venkatakrishnan, K; von Moltke, LL; Zannikos, P, 2011)	0.61
"The impact of cumulative dosing and premature drug discontinuation (PMDD) of bortezomib (V), thalidomide (T), and dexamethasone (D) on overall survival (OS), event-free survival (EFS), time to next therapy, and post-relapse survival in Total Therapy 3 were examined, using time-dependent methodology, relevant to induction, peritransplantation, consolidation, and maintenance phases."	( Total Therapy 3 for multiple myeloma: prognostic implications of cumulative dosing and premature discontinuation of VTD maintenance components, bortezomib, thalidomide, and dexamethasone, relevant to all phases of therapy. Alsayed, Y; Anaissie, E; Barlogie, B; Crowley, J; Hoering, A; Nair, B; Petty, N; Shaughnessy, JD; Szymonifka, J; van Rhee, F; Waheed, S, 2010)	0.79
" In addition, both an earlier disease stage and Dex dosage had a significant impact on OS, while the attainment of VGPR within 2 cycles had a significantly longer PFS."	( Bortezomib plus dexamethasone for relapsed or treatment refractory multiple myeloma: the collaborative study at six institutes in Kyoto and Osaka. Akaogi, T; Hatsuse, M; Horiike, S; Iwai, T; Kamitsuji, Y; Kaneko, H; Kawata, E; Kiyota, M; Kobayashi, T; Kobayashi, Y; Koshida, M; Kuroda, J; Matsumoto, Y; Murakami, S; Okano, A; Shimazaki, C; Shimura, K; Tanaka, T; Taniwaki, M; Uchiyama, H; Ueda, S; Ueda, Y; Uoshima, N, 2010)	1.8
"Human T-cell lymphoma cell lines Hut-78 and Jurkat were treated with increasing doses of everolimus, alone or in combination with doxorubicin, etoposide, vincristine, or bortezomib, using different dosing schedules."	( Schedule-dependent inhibition of T-cell lymphoma cells by cotreatment with the mTOR inhibitor everolimus and anticancer drugs. He, XX; Huang, JJ; Huang, Y; Li, ZM; Lin, TY; Tian, Y; Xiao, J, 2012)	0.57
" With certain dosing schedules, everolimus showed synergism with doxorubicin, etoposide, and bortezomib, but antagonism with vincristine."	( Schedule-dependent inhibition of T-cell lymphoma cells by cotreatment with the mTOR inhibitor everolimus and anticancer drugs. He, XX; Huang, JJ; Huang, Y; Li, ZM; Lin, TY; Tian, Y; Xiao, J, 2012)	0.6
" The best use of bortezomib to treat AMR should be evaluated in controlled trials using dosing strategies that include longer courses or retreatment schedules."	( The role of proteasome inhibition with bortezomib in the treatment of antibody-mediated rejection after kidney-only or kidney-combined organ transplantation. Askar, M; Banning, S; Chiesa-Vottero, A; Fatica, R; Flechner, SM; Koo, A; Poggio, E; Srinivas, T; Stephany, BR, 2010)	0.97
" Toxicities were mainly diarrhea, thrombocytopenia, peripheral neuropathy, fatigue and herpes zoster, and 7 evaluable patients who had toxicities were adjusted dosage and 2 of them interrupted therapy."	( [Treatment of primary systemic amyloidosis with the combination of bortezomib and dexamethasone]. Li, F; Liu, HN; Song, P; Wang, XW; Yu, YP; Zhai, YP; Zhou, XG, 2010)	0.6
" A randomized phase II study is under way to further compare toxicity and efficacy of the 2 dosing schedules."	( Phase I trial of weekly and twice-weekly bortezomib with rituximab, cyclophosphamide, and prednisone in relapsed or refractory non-Hodgkin lymphoma. Dumitrescu, O; Gerecitano, J; Hamlin, P; Horanlli, E; Iasonos, A; Mo, Q; Moskowitz, CH; Noy, A; O'Connor, OA; Pappanicholaou, J; Portlock, C; Rojas, CN; Sarasohn, D; Schulman, P; Straus, D; Zelenetz, AD; Zhang, Z, 2011)	0.64
" Antitumor activity of bortezomib in combination with EGCG or ascorbic acid was determined using several dosing regimens to evaluate different target plasma concentrations of EGCG and ascorbic acid."	( Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. Bannerman, B; Berger, A; Bolen, J; Claiborne, C; Dick, L; Fleming, P; Hales, P; Jones, M; Kupperman, E; Manfredi, M; Monbaliu, J; Tsu, C; Xu, L; Yu, J, 2011)	0.93
" Clinical data demonstrate that patients exposed to higher than recommended doses of bortezomib on the standard twice-weekly dosing schedule are likely to have an increased risk of major toxicities."	( Analysis of two commercially available bortezomib products: differences in assay of active agent and impurity profile. Byrn, SR; Milton, MJ; Tishmack, PA; van de Velde, H, 2011)	0.86
"To determine the toxicities, pharmacokinetics, pharmacodynamics, and maximum tolerated dose of bortezomib in patients with renal impairment and to develop dosing guidelines for such a patient population."	( Dose-escalating and pharmacological study of bortezomib in adult cancer patients with impaired renal function: a National Cancer Institute Organ Dysfunction Working Group Study. Davies, A; Egorin, MJ; Hamilton, A; Ivy, SP; Leal, TB; Lenz, HJ; LoRusso, PA; Mani, S; Mier, J; Mulkerin, D; Neuwirth, R; Ramanathan, RK; Remick, SC; Sarantopoulos, J; Shibata, S; Takimoto, CH; Venkatakrishnan, K; von Moltke, L; Wright, JJ, 2011)	0.85
" Of note, once-weekly bortezomib dosing (in combination with MP±T) was shown to reduce the incidence of peripheral neuropathy and gastrointestinal events compared with twice-weekly dosing, while maintaining efficacy."	( Practical management of adverse events in multiple myeloma: can therapy be attenuated in older patients? Bringhen, S; Mateos, MV; Palumbo, A; San Miguel, JF, 2011)	0.68
" Additional trials are needed to better define the optimal dosing in such patients."	( A phase I study of bortezomib and temozolomide in patients with advanced solid tumors. Chow, W; Chung, V; Cristea, M; Frankel, P; Koehler, S; Leong, L; Lim, D; Martel, C; Morgan, R; Portnow, J; Reckamp, K; Shibata, S; Synold, TW; Twardowski, P, 2012)	0.71
" Finally, the prevention and management of bortezomib-induced side effects, including the latest data on weekly dosing for untreated elderly patients, is focused on."	( Bortezomib for previously untreated multiple myeloma. Delforge, M, 2011)	2.07
" Nevertheless, continued efforts to implement newer dosing regimens and to identify new partner drugs for bortezomib remain an important challenge."	( Bortezomib for previously untreated multiple myeloma. Delforge, M, 2011)	2.03
" Our modified schedule and dosing regimen achieved a high overall response rate of 86%, while showing a marked decrease in the incidence and severity of peripheral neuropathy, palmar-plantar erythrodysesthesia and myelosuppression compared to the standard dosing on a 3-week cycle using these drugs."	( A modified regimen of pegylated liposomal doxorubicin, bortezomib and dexamethasone (DVD) is effective and well tolerated for previously untreated multiple myeloma patients. Berenson, JR; Bessudo, A; Boccia, RV; Chen, CS; Eades, B; Hilger, J; Hilger, JD; Mapes, R; Nassir, Y; Patel, R; Swift, RA; Vescio, R; Wirtschafter, E; Yang, HH; Yellin, O; Yung, E, 2011)	0.62
" SKP2 gene dosage was determined in 82 independent tumors for clinical correlates."	( Characterization of gene amplification-driven SKP2 overexpression in myxofibrosarcoma: potential implications in tumor progression and therapeutics. Fang, FM; Huang, CK; Huang, HY; Kang, HY; Lan, J; Lee, JC; Li, CF; Li, SH; Shiue, YL; Wang, JM; Wang, JW; Wang, YH; Wu, LC; Wu, WR; Yu, SC, 2012)	0.38
" This study (NCI-6432; NCT00091117) was conducted to evaluate bortezomib pharmacokinetics and safety in patients with varying degrees of hepatic impairment, to inform dosing recommendations in these special populations."	( Pharmacokinetics and safety of bortezomib in patients with advanced malignancies and varying degrees of liver dysfunction: phase I NCI Organ Dysfunction Working Group Study NCI-6432. Dowlati, A; Esseltine, DL; Hamilton, A; Ivy, P; LoRusso, PM; Mani, S; Mulkerin, D; Neuwirth, R; Ramanathan, RK; Rudek, MA; Sarantopoulos, J; Shibata, SI; Takimoto, CH; Venkatakrishnan, K, 2012)	0.91
" In MM, Phase I/II clinical trials have established the optimal dosing schedule for perifosine and bortezomib in combination, and demonstrated that perifosine can sensitize to, or overcome resistance to, bortezomib, associated with prolonged responses and a favorable side effect profile."	( Perifosine , an oral, anti-cancer agent and inhibitor of the Akt pathway: mechanistic actions, pharmacodynamics, pharmacokinetics, and clinical activity. Anderson, KC; Eng, C; Hideshima, T; Kolesar, J; Richardson, PG, 2012)	0.6
" The primary objective was to determine the safest and best tolerated maintenance dosing (MD) of bortezomib (B)."	( Phase I trial of bortezomib during maintenance phase after high dose melphalan and autologous stem cell transplantation in patients with multiple myeloma. Abidi, MH; Abrams, J; Al-Kadhimi, Z; Ayash, L; Deol, A; Gul, Z; Lum, L; Mellon-Reppen, S; Ratanatharathorn, V; Uberti, J; Ventimiglia, M; Zonder, J, 2012)	0.94
" In this phase 2, open-label, multicentre clinical trial, 35 patients with relapsed and/or refractory MM following 1-3 prior therapies, including at least one bortezomib-based regimen, received carfilzomib 20 mg/m(2) in a twice-weekly, consecutive-day dosing schedule for ≤12 monthly cycles."	( An open-label, single-arm, phase 2 study of single-agent carfilzomib in patients with relapsed and/or refractory multiple myeloma who have been previously treated with bortezomib. Bahlis, N; Belch, A; Jagannath, S; Jakubowiak, AJ; Kunkel, LA; McDonagh, K; Siegel, DS; Stewart, AK; Vij, R; Wang, M; Wear, S; Wong, AF, 2012)	0.77
" Concomitant inhibition of both pathways markedly enhances the efficacy of bortezomib against cervical cancer cells and thus may be applied to reduce the bortezomib dosage required for efficient cervical cancer treatment."	( Eeyarestatin causes cervical cancer cell sensitization to bortezomib treatment by augmenting ER stress and CHOP expression. Brem, GJ; Brüning, A; Mylonas, I, 2013)	0.86
" Increasing gene dosage of more than half of the missense alleles fully restored function."	( Proteasome inhibition rescues clinically significant unstable variants of the mismatch repair protein Msh2. Arlow, T; Gammie, A; Scott, K; Wagenseller, A, 2013)	0.39
" In newly diagnosed, older patients, modification of the biweekly dosing schedule to weekly regimens improves tolerability whilst maintaining efficacy."	( Weekly intravenous bortezomib is effective and well tolerated in relapsed/refractory myeloma. Atwal, S; D'Sa, S; Johnston, R; Khan, I; Moore, S; Narat, S; Percy, L; Rabin, N; Sachchithanantham, S; Schey, S; Streetly, M; Yong, K, 2013)	0.72
" Dose-response of different concentrations of bortezomib and SAHA on inhibition of cell proliferation of NPC was determined."	( Bortezomib and SAHA synergistically induce ROS-driven caspase-dependent apoptosis of nasopharyngeal carcinoma and block replication of Epstein-Barr virus. Chiang, AK; Ho, DN; Hui, KF; Lam, BH; Tsao, SW, 2013)	2.09
" The optimum dosing combination of these two agents has yet to be determined however, and in many patients it is likely that greater overall survival will be achieved by using them in successive lines rather than in combination."	( New oxaliplatin-based combinations in the treatment of colorectal cancer. Cassidy, J; Hochster, H, 2003)	0.32
" Therefore, dosing schedules for proteasome inhibitors warrant further study to maximize anabolic actions without compromising anti-MM activity in patients with multiple myeloma (MM)."	( Activating transcription factor 4, an ER stress mediator, is required for, but excessive ER stress suppresses osteoblastogenesis by bortezomib. Abe, M; Amou, H; Fujii, S; Harada, T; Hiasa, M; Kagawa, K; Kido, S; Matsumoto, T; Miki, H; Nakamura, S; Nakano, A; Oda, A; Ozaki, S; Takeuchi, K; Watanabe, K, 2013)	0.59
" Cyclophosphamide (CY) plus granulocyte colony-stimulating factor (G-CSF) has been the conventional preparation for hematopoietic progenitor cell (HPC) mobilization, although the optimal dosage of CY in this setting has not yet been clearly defined."	( Hematopoietic progenitor cell mobilization using low-dose cyclophosphamide and granulocyte colony-stimulating factor for multiple myeloma. Horiike, S; Kaneko, H; Kawata-Iida, E; Kobayashi, T; Kobayashi, Y; Kuroda, J; Matsumoto, Y; Mizutani, S; Nagoshi, H; Shimazaki, C; Shimura, Y; Taniwaki, M; Tsutsumi, Y; Uchiyama, H; Yamamoto-Sugitani, M, 2013)	0.39
" Blood samples were obtained on days 1 and 9 of cycle 1 prior to dosing and 2 and 6 h post-dosing in all 60 subjects."	( Vorinostat in combination with bortezomib in patients with advanced malignancies directly alters transcription of target genes. Alberti, D; Bailey, HH; Espinoza-Delgado, I; Hoang, T; Holen, KD; Kim, K; Kolesar, JM; Schelman, WR; Seo, S; Traynor, AM; Wilding, G; Wright, JJ, 2013)	0.68
" PK studies at dose levels 1 and 2 showed greater mean ultrafiltrable platinum when oxaliplatin was dosed after bortezomib."	( A phase I and pharmacokinetic study of oxaliplatin and bortezomib: activity, but dose-limiting neurotoxicity. Beric, A; Hochster, H; Ivy, P; Joseph, SO; Kobrinsky, B; Liebes, L; Malankar, A; Muggia, F, 2013)	0.85
" Bortezomib dosing was increased using a standard phase I dose-escalation schema."	( A phase I study of vorinostat in combination with bortezomib in patients with advanced malignancies. Alberti, D; Ames, MM; Attia, S; Bailey, HH; Eickhoff, J; Espinoza-Delgado, I; Hoang, T; Holen, KD; Jiang, Z; Kolesar, JM; Marnocha, R; McGovern, RM; Reid, JM; Schelman, WR; Traynor, AM; Wilding, G; Wright, JJ, 2013)	1.55
" We previously examined a once-daily continuous dosing schedule of vorinostat in combination with bortezomib which was well tolerated in cycles 1 and 2; however, there was concern regarding the tolerability through multiple cycles."	( A Phase I study of intermittently dosed vorinostat in combination with bortezomib in patients with advanced solid tumors. Alberti, D; Ames, MM; Bailey, HH; Deming, DA; Eickhoff, J; Espinoza-Delgado, I; Kolesar, JM; Marnocha, R; McGovern, RM; Ninan, J; Reid, JM; Schelman, WR; Wilding, G; Wright, J, 2014)	0.85
" DLTs in the intermittent dosing scheduled included thrombocytopenia and fatigue."	( A Phase I study of intermittently dosed vorinostat in combination with bortezomib in patients with advanced solid tumors. Alberti, D; Ames, MM; Bailey, HH; Deming, DA; Eickhoff, J; Espinoza-Delgado, I; Kolesar, JM; Marnocha, R; McGovern, RM; Ninan, J; Reid, JM; Schelman, WR; Wilding, G; Wright, J, 2014)	0.64
" Tolerability was not improved with the intermittent dosing schedule of vorinostat when compared to continuous dosing."	( A Phase I study of intermittently dosed vorinostat in combination with bortezomib in patients with advanced solid tumors. Alberti, D; Ames, MM; Bailey, HH; Deming, DA; Eickhoff, J; Espinoza-Delgado, I; Kolesar, JM; Marnocha, R; McGovern, RM; Ninan, J; Reid, JM; Schelman, WR; Wilding, G; Wright, J, 2014)	0.64
" Qualifying statements by the HDSG address alternative dosing options, the management of cytopenias and the prevention of toxicities, including herpes zoster reactivation."	( Bortezomib in multiple myeloma: a practice guideline. Baldassarre, FG; Cheung, MC; Haynes, AE; Imrie, K; Kouroukis, CT; Reece, DE, 2014)	1.85
" After oral or intraperitoneal dosing of mice, RA190 distributed to plasma and major organs except the brain and inhibited proteasome function in skin and muscle."	( A bis-benzylidine piperidone targeting proteasome ubiquitin receptor RPN13/ADRM1 as a therapy for cancer. Anchoori, RK; Chen, X; Hung, CF; Jiang, R; Karanam, B; Matsui, W; Orlowski, RZ; Peng, S; Roden, RB; Rudek, MA; Tanno, T; Walters, KJ; Wang, JW; Zhao, M, 2013)	0.39
" Drugs for multiple myeloma therapy are significantly removed with both HCO and PFX, with important implications for the dosing and timing of administration, particularly in patients with cast nephropathy receiving extended dialysis."	( Clearance of drugs for multiple myeloma therapy during in vitro high-cutoff hemodialysis. Devine, E; Krause, B; Krieter, DH; Lemke, HD; Storr, M; Wanner, C, 2014)	0.4
" We illustrate the implementation of the technique in the context of phase I trials that consider multiple toxicities and phase I/II trials where dosing decisions are based on both toxicity and efficacy, and apply the benchmark to several clinical examples considered in the literature."	( Simple benchmark for complex dose finding studies. Cheung, YK, 2014)	0.4
"Substantial efficacy has been demonstrated with bortezomib-melphalan-prednisone in phase III studies in transplant-ineligible myeloma patients using various twice-weekly and once-weekly bortezomib dosing schedules."	( Bortezomib cumulative dose, efficacy, and tolerability with three different bortezomib-melphalan-prednisone regimens in previously untreated myeloma patients ineligible for high-dose therapy. Boccadoro, M; Bringhen, S; Desai, A; Di Raimondo, F; Esseltine, DL; García-Sanz, R; Lahuerta, JJ; Larocca, A; Londhe, A; Mateos, MV; Oriol, A; Palumbo, A; Richardson, PG; San Miguel, JF; van de Velde, H, 2014)	2.1
" Peripheral neuropathy was assessed using neurotoxicity subscale of the FACT/GOG-Ntx at daily clinical practice; physicians modified the dosage and schedule of bortezomib treatment."	( Impact of dose modification on intravenous bortezomib-induced peripheral neuropathy in multiple myeloma patients. Cho, J; Kang, D; Kim, K; Kim, SJ; Lee, JY, 2014)	0.86
" Using 2 mL as the maximum volume for injection would mean that many patients receiving bortezomib will receive two injections during each visit with common dosing parameters."	( Tolerability of Velcade (Bortezomib) subcutaneous administration using a maximum volume of 3 mL per injection site. Brandle, I; Chen, C; Dara, C; Incekol, D; Kaufman, M; Kukreti, V; Lee, R; Ng, P; Paisley, E; Reece, D; Tiedemann, R; Trudel, S, 2015)	0.94
" Prednisone was dosed at ."	( A phase II study of bortezomib plus prednisone for initial therapy of chronic graft-versus-host disease. Alyea, EP; Antin, JH; Armand, P; Bindra, B; Blazar, BR; Cutler, CS; Herrera, AF; Ho, VT; Jones, KT; Kim, HT; Koreth, J; Nikiforow, S; Ritz, J; Soiffer, RJ, 2014)	0.73
" Pharmacokinetic findings with the current dosing regimen were consistent with the comparable literature and the hybrid dosing regimen."	( Phase I trial of bortezomib (PS-341; NSC 681239) and "nonhybrid" (bolus) infusion schedule of alvocidib (flavopiridol; NSC 649890) in patients with recurrent or refractory indolent B-cell neoplasms. Baz, RC; Bose, P; Colevas, AD; Coppola, D; Dawson, J; Doyle, LA; Figg, WD; Grant, S; Hogan, KT; Holkova, B; Honeycutt, C; Kang, L; Kmieciak, M; Peer, CJ; Perkins, EB; Ramakrishnan, V; Roberts, JD; Roodman, GD; Sankala, H; Shrader, E; Stuart, RK; Sullivan, D; Tombes, MB; Wan, W; Weir-Wiggins, C; Wellons, M, 2014)	0.74
" As the nonhybrid regimen is less cumbersome than the previous hybrid dosing schedule regimen, the current schedule is recommended for successor studies."	( Phase I trial of bortezomib (PS-341; NSC 681239) and "nonhybrid" (bolus) infusion schedule of alvocidib (flavopiridol; NSC 649890) in patients with recurrent or refractory indolent B-cell neoplasms. Baz, RC; Bose, P; Colevas, AD; Coppola, D; Dawson, J; Doyle, LA; Figg, WD; Grant, S; Hogan, KT; Holkova, B; Honeycutt, C; Kang, L; Kmieciak, M; Peer, CJ; Perkins, EB; Ramakrishnan, V; Roberts, JD; Roodman, GD; Sankala, H; Shrader, E; Stuart, RK; Sullivan, D; Tombes, MB; Wan, W; Weir-Wiggins, C; Wellons, M, 2014)	0.74
"A prospective iterative trial of proteasome inhibitor (PI)-based therapy for reducing HLA antibody (Ab) levels was conducted in five phases differing in bortezomib dosing density and plasmapheresis timing."	( Prospective iterative trial of proteasome inhibitor-based desensitization. Abu Jawdeh, BG; Alloway, RR; Brailey, P; Cardi, MA; Ejaz, NS; Girnita, A; Govil, A; Mogilishetty, G; Roy-Chaudhury, P; Sadaka, B; Shields, AR; Walsh, RC; Woodle, ES, 2015)	0.62
" We hypothesized that bortezomib may abrogate neutralizing Ab levels, making dosing of RIT possible in mice already immune to RIT."	( Bortezomib reduces pre-existing antibodies to recombinant immunotoxins in mice. Manning, ML; Mason-Osann, E; Onda, M; Pastan, I, 2015)	2.17
" We report a phase II trial of alternate dosing and schedule of bortezomib and dexamethasone in newly diagnosed multiple myeloma patients who are not eligible for or refused autologous stem cell transplantation."	( A Phase II trial of weekly bortezomib and dexamethasone in veterans with newly diagnosed multiple myeloma not eligible for or who deferred autologous stem cell transplantation. Behler, C; Efebera, YA; Girnius, SK; Grady, T; Han, A; Hayes, TG; Houranieh, A; Kambhampati, S; Klein, CE; Lee, S; Lichtenstein, A; Mehta, P; Mohiuddin, A; Munshi, NC; Prabhala, RH; Roodman, GD; Rose, MG; Yellapragada, SV; Zimelman, A, 2015)	0.95
" Treatment-specific tools and clinical assessments can be useful for optimizing dosing and schedule adjustments to increase therapy duration, and implementing supportive care strategies (e."	( Treatment-related symptom management in patients with multiple myeloma: a review. Colson, K, 2015)	0.42
" In addition to appropriate drug dosing and administration, effective supportive care and health maintenance are crucial for maximizing quality of life and disease control."	( Treatment-related symptom management in patients with multiple myeloma: a review. Colson, K, 2015)	0.42
" Our results indicate that to have the most synergistic anticancer effect, the drugs in the optimized regimen should be dosage specific and ratio specific."	( Optimized combinations of bortezomib, camptothecin, and doxorubicin show increased efficacy and reduced toxicity in treating oral cancer. Ding, X; Matsuo, K; Xu, L; Yang, J; Zheng, L, 2015)	0.72
" The dosage and time of therapy need to be explored in the future; additional studies of large samples are needed."	( BK Virus-Associated Nephropathy with Plasma Cell-Rich Infiltrates Treated by Bortezomib-Based Regimen. Chen, JS; Cheng, DR; Ji, SM; Li, X; Liu, ZH; Wen, JQ; Wu, D; Xie, KN; Zhang, MC, 2015)	0.65
" Dosage and treatment decisions were at the discretion of the physicians."	( Bortezomib-containing regimens are effective in multiple myeloma--results of a non-interventional phase IV study. Alkemper, B; Gaede, B; Knauf, W; Reschke, D; Schlag, R; Schmits, R; Schütz, S; Schwarzer, A; Tapprich, C, 2015)	1.86
"The authors conducted a single-arm, phase 2 trial of combined temsirolimus and bortezomib in patients with relapsed and refractory B-cell non-Hodgkin lymphoma (NHL) using a dosing scheme that was previously tested in multiple myeloma."	( A phase 2 study of weekly temsirolimus and bortezomib for relapsed or refractory B-cell non-Hodgkin lymphoma: A Wisconsin Oncology Network study. Ahuja, H; Baim, AE; Blank, JH; Farnen, JP; Fenske, TS; Kahl, BS; Kim, KM; Mansky, P; Mattison, RJ; Onitilo, AA; Qamar, R; Saha, S; Shah, NM; Traynor, AM; Wassenaar, T; Zhang, C, 2015)	0.91
" We used these screening methods to evaluate the dependencies of seven patient-derived cell models: three grown on laminin and four grown as neurospheres, against 56 agents in 17-point dose-response curves in 384-well format in triplicate."	( High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma. deCarvalho, AC; Mikkelsen, T; Quartararo, CE; Reznik, E; Stockwell, BR, 2015)	0.42
" Human plasma bortezomib PK profiles following multiple IV dosing (1."	( Physiologically-based pharmacokinetic modeling of target-mediated drug disposition of bortezomib in mice. Mager, DE; Zhang, L, 2015)	1
" An in silico pharmacodynamic model using established effects of each of these agents on the cell cycle was used to validate the regimen and to guide the dosing regimen."	( Novel phase I study combining G1 phase, S phase, and G2/M phase cell cycle inhibitors in patients with advanced malignancies. Gad, Y; Helgason, T; Hong, DS; Jain, RK; Kurzrock, R; Naing, A; Shi, NY; Wheler, J, 2015)	0.42
" Conversely, the MG132 dose-response curve was unaffected by co-administration of EGCG."	( EGCG antagonizes Bortezomib cytotoxicity in prostate cancer cells by an autophagic mechanism. Bettuzzi, S; Bonacini, M; Giovanna Troglio, M; Modernelli, A; Naponelli, V; Ramazzina, I; Rizzi, F, 2015)	0.76
" To determine the optimal dosing schedule of once weekly bortezomib (BTZ) combined with lenalidomide (LEN) and dexamethasone (DEX), especially in the outpatient setting, we conducted a phase I dose escalation study."	( Phase I study of once weekly treatment with bortezomib in combination with lenalidomide and dexamethasone for relapsed or refractory multiple myeloma. Hagiwara, S; Iida, S; Ishida, T; Ito, A; Kanamori, T; Kato, C; Kinoshita, S; Komatsu, H; Kusumoto, S; Masuda, A; Murakami, S; Nakashima, T; Narita, T; Ri, M; Suzuki, N; Totani, H; Yoshida, T, 2016)	0.94
" This prompted us to explore the concept of less intense drug dosing with shorter intervals between courses with the aim of preventing inter-course relapse."	( Dose-dense and less dose-intense Total Therapy 5 for gene expression profiling-defined high-risk multiple myeloma. Alapat, D; Avery, D; Bailey, C; Barlogie, B; Crowley, J; Epstein, J; Heuck, CJ; Hoering, A; Jethava, Y; Khan, R; Mitchell, A; Morgan, G; Petty, N; Sawyer, J; Schinke, C; Smith, R; Stein, C; Steward, D; Thanendrarajan, S; Tian, E; van Rhee, F; Waheed, S; Yaccoby, S; Zangari, M, 2016)	0.43
"Stem cell transplantation (SCT), an effective therapy for amyloid light chain (AL) amyloidosis patients, is associated with low treatment-related mortality (TRM) with appropriate patient selection and risk-adapted dosing of melphalan (RA-SCT)."	( Long-term event-free and overall survival after risk-adapted melphalan and SCT for systemic light chain amyloidosis. Bello, C; Chou, JF; Comenzo, RL; Devlin, SM; Giralt, S; Hassoun, H; Landau, H; Landry, C; Smith, M, 2017)	0.46
" Increased p21 and cleaved PARP expression can potentially explain mechanisms of their enhanced effects, which require further PK/PD systems analysis to suggest an optimal dosing regimen."	( Sequential Exposure of Bortezomib and Vorinostat is Synergistic in Multiple Myeloma Cells. Mager, DE; Nanavati, C, 2017)	0.77
" Logistic regression models were utilized to determine relationships, identify subpopulations with different responses, and optimize the venetoclax dosage that balanced both efficacy and safety."	( Moving Beyond Maximum Tolerated Dose for Targeted Oncology Drugs: Use of Clinical Utility Index to Optimize Venetoclax Dosage in Multiple Myeloma Patients. Freise, KJ; Jones, AK; Maciag, PC; Menon, RM; Salem, AH; Verdugo, ME, 2017)	0.46
" On day 1 of cycle 1, seven whole-blood samples were collected for 3 h after dosing completion to obtain the maximum plasma concentration and area under the time-concentration curve during 3 h postdose (AUC0-3) in each patient."	( Bortezomib pharmacokinetics in tumor response and peripheral neuropathy in multiple myeloma patients receiving bortezomib-containing therapy. Choi, K; Han, S; Hong, T; Lee, J; Lee, SE; Min, CK; Park, GJ; Yim, DS, 2017)	1.9
" We retrospectively analysed PN rates from 32 studies (2697 patients with previously untreated multiple myeloma) incorporating bortezomib and differing dexamethasone schedules: partnered dosing (days of and after bortezomib), weekly dosing, and other dosing schedules (e."	( Impact of concomitant dexamethasone dosing schedule on bortezomib-induced peripheral neuropathy in multiple myeloma. Giove, TJ; Kumar, SK; Laubach, JP; Neuwirth, R; Quick, M; Rajkumar, SV; Richardson, PG; Yung, G, 2017)	0.91
" The incidences of several key AEs were lower in both arms following the planned reduction of bortezomib dosing frequency in TP2."	( Panobinostat plus bortezomib and dexamethasone: impact of dose intensity and administration frequency on safety in the PANORAMA 1 trial. Beksac, M; Corrado, C; Dimopoulos, MA; Einsele, H; Elghandour, A; Guenther, A; Hou, J; Hungria, VTM; Jedrzejczak, WW; Lee, JH; Lonial, S; Moreau, P; Na Nakorn, T; Paul, S; Redhu, S; Richardson, PG; Salwender, H; San-Miguel, JF; Schlossman, RL; Siritanaratkul, N; Sopala, M; Yoon, SS, 2017)	1.01
" The antimyeloma activity of KW-2478 in combination with BTZ as scheduled in this trial appeared relatively modest; however, the good tolerability of the combination would support further exploration of alternate dosing schedules and combinations."	( A phase I/II study of KW-2478, an Hsp90 inhibitor, in combination with bortezomib in patients with relapsed/refractory multiple myeloma. Akinaga, S; Baetiong-Caguioa, P; Cavenagh, J; Davies, F; Gharibo, M; Kurman, M; Nakashima, D; Novak, B; Oakervee, H; Rabin, N; Shiraishi, N; Yong, K, 2017)	0.69
" Results A total of eighteen patients were dosed in 3 bortezomib cohorts (0."	( Phase I trial of bortezomib daily dose: safety, pharmacokinetic profile, biological effects and early clinical evaluation in patients with advanced solid tumors. Angevin, E; Bahleda, R; Bernard, A; Chaturvedi, S; Deutsch, E; Gazzah, A; Hanley, M; Hollebecque, A; Le Deley, MC; Massard, C; Poterie, A; Ribrag, V; Ricard, D; Sallansonnet-Froment, M; Soria, JC; Taillia, H; Touat, M; Van De Velde, H; Varga, A, 2018)	1.07
" This article critically reviews and summarizes the clinical pharmacokinetics and pharmacodynamics of bortezomib at various dosing levels and routes of administration as well as in specific patient subsets."	( Clinical Pharmacokinetics and Pharmacodynamics of Bortezomib. Abdul-Majeed, S; Barta, SK; Cael, B; Tan, CRC, 2019)	0.98
" Using various dosing schedules, the majority of patients (684/694) received daratumumab at a dose of 16 mg/kg."	( Pharmacokinetics and Exposure-Response Analyses of Daratumumab in Combination Therapy Regimens for Patients with Multiple Myeloma. Belch, A; Capra, M; Clemens, PL; Dimopoulos, MA; Gomez, D; Ho, PJ; Iida, S; Jansson, R; Leiba, M; Medvedova, E; Min, CK; Schecter, J; Sonneveld, P; Sun, YN; Xu, XS; Zhang, L, 2018)	0.48
"These data support the recommended 16 mg/kg dose of daratumumab and the respective dosing schedules in the POLLUX and CASTOR pivotal studies."	( Pharmacokinetics and Exposure-Response Analyses of Daratumumab in Combination Therapy Regimens for Patients with Multiple Myeloma. Belch, A; Capra, M; Clemens, PL; Dimopoulos, MA; Gomez, D; Ho, PJ; Iida, S; Jansson, R; Leiba, M; Medvedova, E; Min, CK; Schecter, J; Sonneveld, P; Sun, YN; Xu, XS; Zhang, L, 2018)	0.48
" The interaction model is based on codifying multiple regulatory mechanisms of drug action and provides a platform for probing optimized bortezomib and dexamethasone combination dosing regimens to minimize skeletal side effects during myeloma therapy."	( Systems Modeling of Bortezomib and Dexamethasone Combinatorial Effects on Bone Homeostasis in Multiple Myeloma Patients. Mager, DE; Zhang, L, 2019)	1.04
" Mice dosed with INCB (30 mg/kg) showed significant reductions in tumor volume on days 28, 35, 42, 49, 56, and 63."	( The anti-myeloma effects of the selective JAK1 inhibitor (INCB052793) alone and in combination in vitro and in vivo. Berenson, JR; Chen, H; Hekmati, T; Li, M; Nosrati, JD; Patil, S; Sanchez, E; Schlossberg, RE; Soof, CM; Tanenbaum, EJ; Tang, G; Vidisheva, A; Wang, C; Zahab, B, 2019)	0.51
" This model can be used to further optimize dosing of bortezomib."	( A Semi-Mechanistic Population Pharmacokinetic/Pharmacodynamic Model of Bortezomib in Pediatric Patients with Relapsed/Refractory Acute Lymphoblastic Leukemia. Attarbaschi, A; Baruchel, A; Beijnen, JH; De Moerloose, B; Dorlo, TPC; Fagioli, F; Huitema, ADR; Janssen, JM; Kaspers, GJL; Klingebiel, T; Niewerth, D; Palumbo, G; von Stackelberg, A; Wilhelm, AJ; Zwaan, CM, 2020)	1.04
" The management of CIPN is a significant challenge, as it is not possible to predict which patients will develop symptoms, the timing for the appearance of symptoms can develop anytime during the chemotherapy course, there are no early indications that warrant a reduction in the dosage to halt CIPN progression, and there are no drugs approved to prevent or alleviate CIPN."	( Prevention of chemotherapy-induced peripheral neuropathy: A review of recent findings. Ehrlich, BE; Ibrahim, EY, 2020)	0.56
" Bortezomib was administered at the standard dosing and in combined therapy with corticosteroids, chemotherapy or thalidomide."	( Bortezomib retreatment is effective in relapsed multiple myeloma patients - real-life clinical practice data. Brozova, L; Gregora, E; Hajek, R; Jelinek, T; Jungova, A; Maisnar, V; Minarik, J; Pour, L; Sevcikova, S; Spicka, I; Stork, M; Velichova, R, 2020)	2.91
" Increased cumulative dosing levels, intravenous compared with subcutaneous administration and combination therapy with thalidomide were associated with higher rates of BIPN."	( Characteristics and risk factors of bortezomib induced peripheral neuropathy: A systematic review of phase III trials. Goldstein, D; Kiernan, MC; King, T; Li, T; Park, SB; Timmins, HC, 2020)	0.83
" In addition, model simulations confirm that a once-weekly dosing schedule represents an optimal therapeutic regimen with comparable antineoplastic activity but significantly reduced risk of thrombocytopenia."	( Population-based meta-analysis of bortezomib exposure-response relationships in multiple myeloma patients. Mager, DE; Zhang, L, 2020)	0.84
" Furthermore, careful consideration should be given to different methods of storing diluted pharmaceutical drugs and use of DMSO controls due to the potential risk of evaporation and the subsequent effect on dose-response curves."	( Optimization of cell viability assays to improve replicability and reproducibility of cancer drug sensitivity screens. Biermann, J; Engqvist, H; Forssell-Aronsson, E; Helou, K; Karlsson, P; Kovács, A; Larsson, P; Parris, TZ; Werner Rönnerman, E, 2020)	0.56
" The phase III VISTA trial established the bortezomib dosing schedule for VMP."	( Comparative Efficacy of Bortezomib, Melphalan, and Prednisone (VMP) With or Without Daratumumab Versus VMP Alone in the Treatment of Newly Diagnosed Multiple Myeloma: Propensity Score Matching of ALCYONE and VISTA Phase III Studies. Cavo, M; Deraedt, W; Dimopoulos, MA; He, J; Jakubowiak, A; Kampfenkel, T; Lam, A; Mateos, MV; Qi, M; San-Miguel, J, 2020)	1.13
" A weekly dosing regimen of bortezomib, cyclophosphamide, and dexamethasone combined with medium dose prednisone in between were deployed."	( Acute Kidney Injury Caused by TAFRO Syndrome in a Chinese Patient: Efficacy of Long-Term Corticosteroids Combined with Bortezomib and Cyclophosphamide. Chen, L; Li, J; Li, R; Li, X; Qin, Y; Shi, X; Wang, J; Xia, P; Zhang, L; Zhang, T; Zou, M, 2020)	1.06
" The most appropriate delivery and dosing regimens of these therapies for patients at advanced age and frailty status is also unclear."	( Optimising the value of immunomodulatory drugs during induction and maintenance in transplant ineligible patients with newly diagnosed multiple myeloma: results from Myeloma XI, a multicentre, open-label, randomised, Phase III trial. Cairns, DA; Collett, C; Cook, G; Davies, FE; Drayson, MT; Garg, M; Gregory, WM; Jackson, GH; Jenner, MW; Jones, JR; Kaiser, MF; Karunanithi, K; Kishore, B; Lindsay, J; Morgan, GJ; Owen, RG; Pawlyn, C; Russell, NH; Striha, A; Taylor, C; Waterhouse, A; Williams, CD; Wilson, J, 2021)	0.62
" We investigated the activity and safety of three different dosing regimens of oral panobinostat in combination with subcutaneous bortezomib and oral dexamethasone for this indication."	( Efficacy and safety of oral panobinostat plus subcutaneous bortezomib and oral dexamethasone in patients with relapsed or relapsed and refractory multiple myeloma (PANORAMA 3): an open-label, randomised, phase 2 study. Abdo, A; Beksac, M; Bladé, J; Chari, A; Dimopoulos, MA; Gonçalves, IZ; Hájek, R; Hungria, VTM; Illés, Á; Jacobasch, L; Laubach, JP; Lech-Maranda, E; Lonial, S; Maison-Blanche, P; Mariz, M; Moreau, P; Polprasert, C; Rajkumar, SV; Richardson, PG; San-Miguel, JF; Schjesvold, F; Shelekhova, T; Spencer, A; Spicka, I; Sureda, A; Wróbel, T, 2021)	1.07
" Though peripheral sensory neuropathy was more frequent with twice weekly dosing (P = ."	( Outcomes with different administration schedules of bortezomib in bortezomib, lenalidomide and dexamethasone (VRd) as first-line therapy in multiple myeloma. Buadi, F; Cook, J; Dingli, D; Dispenzieri, A; Fonder, A; Gertz, MA; Go, R; Gonsalves, W; Hayman, S; Higgins, A; Hobbs, M; Hwa, YL; Johnson, I; Kapoor, P; Kourelis, T; Kumar, S; Kyle, R; Lacy, M; Leung, N; Rajkumar, VS; Sidana, S; Warsame, R, 2021)	0.87
" Severe neutropenia during her 1st cycle prompted a dosage reduction of lenalidomide and bortezomib."	( [Cooccurrence of classic Hodgkin lymphoma and multiple myeloma]. Andoh, S; Imai, Y; Kawamata, T; Makiyama, J; Ota, Y; Tojo, A; Uchida, S; Yasui, H; Yokoyama, K, 2021)	0.84
" The model can be potentially applied to evaluate their combination regimens and explore in vivo dosing regimens."	( Network-Based Systems Analysis Explains Sequence-Dependent Synergism of Bortezomib and Vorinostat in Multiple Myeloma. Mager, DE; Nanavati, C, 2021)	0.85
" Thus, it is important to consider the dosage and timing of dexamethasone introduction on a patient-severity basis."	( Dexamethasone is associated with early deaths in light chain amyloidosis patients with severe cardiac involvement. Agbulut, O; Audard, V; Bézard, M; Damy, T; Galat, A; Gilles, F; Guendouz, S; Hamon, D; Kharoubi, M; Kordeli, E; Le Bras, F; Lemonnier, F; Molinier-Frenkel, V; Oghina, S; Poullot, E; Shourick, J; Teiger, E; Vitiello, D; Zaroui, A, 2021)	0.62
"GBM cells proliferation speed is inversely proportional to the irradiation dose and recedes when the dosage is increased, as expected."	( Effectiveness of bortezomib and temozolomide for eradication of recurrent human glioblastoma cells, resistant to radiation. Bryukhovetskiy, I; Pak, O; Sharma, A; Sharma, HS; Shevchenko, V; Zaitsev, S, 2021)	0.96
" Therefore, we investigated whether LEN-induced skin rash is affected by the duration of BOR administration and the dosing interval between BOR and LEN administration."	( Preceding bortezomib administration for a certain period reduces the risk of lenalidomide-induced skin rash. Hagihara, M; Hanai, H; Inoue, M; Kubo, K; Kushi, R; Mita, M; Ohara, S; Sugi, T; Uchida, T; Yasu, T, 2022)	1.12
" In routine clinical care, PanBorDex is used primarily in later relapses and is commonly administered in attenuated dosing schedules to mitigate the treatment-related toxicity."	( Panobinostat in combination with bortezomib and dexamethasone in multiply relapsed and refractory myeloma; UK routine care cohort. Basu, S; Bhatti, Z; Collings, F; Karim, F; Kishore, B; Kothari, J; Leary, H; Maouche, N; Ramasamy, K; Reddy, U; Ryman, N; Sundararaman, S; Tseu, B; Vallance, GD, 2022)	1
"DARA SC 1800 mg was administered every 4 weeks, per approved dosing schedules."	( Switching to daratumumab SC from IV is safe and preferred by patients with multiple myeloma. Basu, S; Beksac, M; Carson, R; Cook, G; Delioukina, M; Gries, KS; Kudva, A; Mateos, MV; Pei, H; Rigaudeau, S; Schots, R; Spicka, I; Tromp, B; Van Rampelbergh, R; White, D; Wrobel, T; Wroblewski, S, 2023)	0.91
" Further studies need to be conducted to understand the impact of dosing strategies of anti-MM agents in the real world."	( Real-world data on lenalidomide dosing and outcomes in patients newly diagnosed with multiple myeloma: Results from the Canadian Myeloma Research Group Database. Aslam, M; Gul, E; Jimenez-Zepeda, VH; Kardjadj, M; Kotb, R; LeBlanc, R; Louzada, M; Masih-Khan, E; McCurdy, A; Mian, H; Reece, D; Reiman, A; Sebag, M; Song, K; Stakiw, J; Venner, CP; White, D, 2023)	0.91
" This exposure system allows the possibility of creating dose-response curves resulting in the generation of more reliable cell-based assay data for many types of applications, such as safety analysis."	( Development and Characterization of a 96-Well Exposure System for Safety Assessment of Nanomaterials. Arz, MI; Briesen, H; Dähnhardt-Pfeiffer, S; Drexel, R; Fink, M; Fürtauer, S; Herrmann, C; Hornberger, R; Kohl, Y; Krebs, T; Mamier, M; Meier, F; Metzger, C; Müller, M; Sängerlaub, S; Wagner, S, 2023)	0.91
" Variability in patient baseline characteristics, such as the number of prior lines of treatment, refractoriness to prior treatments, prior stem cell transplant, and timing and dosing of prior lenalidomide, makes it difficult to select the best options for patients with RRMM for whom first-line treatments have failed."	( Clinical evidence for immune-based strategies in early-line multiple myeloma: current challenges in decision-making for subsequent therapy. Iida, S; Mateos, MV; Raje, N; Reece, D, 2023)	0.91

Role	Description
antineoplastic agent	A substance that inhibits or prevents the proliferation of neoplasms.
proteasome inhibitor	A drug that blocks the action of proteasomes, cellular complexes that break down proteins.
protease inhibitor	A compound which inhibits or antagonizes the biosynthesis or actions of proteases (endopeptidases).
antiprotozoal drug	Any antimicrobial drug which is used to treat or prevent protozoal infections.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Class	Description
amino acid amide	An amide of an amino acid formed formally by conversion of the carboxy group to a carboxamido group.
pyrazines
L-phenylalanine derivative	A proteinogenic amino acid derivative resulting from reaction of L-phenylalanine at the amino group or the carboxy group, or from the replacement of any hydrogen of L-phenylalanine by a heteroatom.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
RAR-related orphan receptor gamma	Mus musculus (house mouse)	Potency	0.0386	0.0060	38.0041	19,952.5996	AID1159521; AID1159523
Fumarate hydratase	Homo sapiens (human)	Potency	0.0332	0.0030	8.7949	48.0869	AID1347053
PPM1D protein	Homo sapiens (human)	Potency	0.0415	0.0052	9.4661	32.9993	AID1347411
TDP1 protein	Homo sapiens (human)	Potency	0.0092	0.0008	11.3822	44.6684	AID686978; AID686979
AR protein	Homo sapiens (human)	Potency	0.8203	0.0002	21.2231	8,912.5098	AID1259243; AID1259247; AID743035; AID743036; AID743042; AID743054; AID743063
caspase 7, apoptosis-related cysteine protease	Homo sapiens (human)	Potency	0.2113	0.0133	26.9810	70.7614	AID1346978
estrogen receptor 2 (ER beta)	Homo sapiens (human)	Potency	1.5092	0.0006	57.9133	22,387.1992	AID1259377; AID1259378
nuclear receptor subfamily 1, group I, member 3	Homo sapiens (human)	Potency	0.1111	0.0010	22.6508	76.6163	AID1224838; AID1224839; AID1224893
progesterone receptor	Homo sapiens (human)	Potency	0.9439	0.0004	17.9460	75.1148	AID1346795
cytochrome P450 family 3 subfamily A polypeptide 4	Homo sapiens (human)	Potency	3.8849	0.0123	7.9835	43.2770	AID1346984; AID1645841
EWS/FLI fusion protein	Homo sapiens (human)	Potency	0.0322	0.0013	10.1577	42.8575	AID1259252; AID1259253; AID1259255; AID1259256
glucocorticoid receptor [Homo sapiens]	Homo sapiens (human)	Potency	0.0127	0.0002	14.3764	60.0339	AID720691; AID720692
retinoic acid nuclear receptor alpha variant 1	Homo sapiens (human)	Potency	0.0094	0.0030	41.6115	22,387.1992	AID1159553
retinoid X nuclear receptor alpha	Homo sapiens (human)	Potency	0.0668	0.0008	17.5051	59.3239	AID1159527; AID1159531
estrogen-related nuclear receptor alpha	Homo sapiens (human)	Potency	0.0194	0.0015	30.6073	15,848.9004	AID1224841; AID1224842; AID1224848; AID1224849; AID1259401; AID1259403
farnesoid X nuclear receptor	Homo sapiens (human)	Potency	6.0493	0.3758	27.4851	61.6524	AID743217; AID743220
pregnane X nuclear receptor	Homo sapiens (human)	Potency	0.0084	0.0054	28.0263	1,258.9301	AID1346982
estrogen nuclear receptor alpha	Homo sapiens (human)	Potency	0.1326	0.0002	29.3054	16,493.5996	AID1259244; AID1259248; AID743069; AID743075; AID743077; AID743078; AID743079; AID743080; AID743091
polyprotein	Zika virus	Potency	0.0332	0.0030	8.7949	48.0869	AID1347053
peroxisome proliferator-activated receptor delta	Homo sapiens (human)	Potency	0.2684	0.0010	24.5048	61.6448	AID743212; AID743215; AID743227
peroxisome proliferator activated receptor gamma	Homo sapiens (human)	Potency	0.0472	0.0010	19.4141	70.9645	AID743094; AID743140; AID743191
vitamin D (1,25- dihydroxyvitamin D3) receptor	Homo sapiens (human)	Potency	1.8738	0.0237	23.2282	63.5986	AID743222; AID743223; AID743241
caspase-3	Homo sapiens (human)	Potency	0.2113	0.0133	26.9810	70.7614	AID1346978
cytochrome P450, family 19, subfamily A, polypeptide 1, isoform CRA_a	Homo sapiens (human)	Potency	0.0180	0.0017	23.8393	78.1014	AID743083
nuclear receptor subfamily 1, group I, member 2	Rattus norvegicus (Norway rat)	Potency	0.0106	0.1000	9.1916	31.6228	AID1346983
Histone H2A.x	Cricetulus griseus (Chinese hamster)	Potency	15.5565	0.0391	47.5451	146.8240	AID1224845
Caspase-7	Cricetulus griseus (Chinese hamster)	Potency	0.0067	0.0067	23.4960	68.5896	AID1346980
caspase-3	Cricetulus griseus (Chinese hamster)	Potency	0.0067	0.0067	23.4960	68.5896	AID1346980
thyroid hormone receptor beta isoform 2	Rattus norvegicus (Norway rat)	Potency	0.0250	0.0003	23.4451	159.6830	AID743065; AID743066; AID743067
heat shock protein beta-1	Homo sapiens (human)	Potency	0.2881	0.0420	27.3789	61.6448	AID743210; AID743228
nuclear factor erythroid 2-related factor 2 isoform 1	Homo sapiens (human)	Potency	0.0216	0.0006	27.2152	1,122.0200	AID743202; AID743219
Voltage-dependent calcium channel gamma-2 subunit	Mus musculus (house mouse)	Potency	0.0596	0.0015	57.7890	15,848.9004	AID1259244
Interferon beta	Homo sapiens (human)	Potency	0.0497	0.0033	9.1582	39.8107	AID1347407; AID1347411
Cellular tumor antigen p53	Homo sapiens (human)	Potency	0.0125	0.0023	19.5956	74.0614	AID651631; AID720552
Glutamate receptor 2	Rattus norvegicus (Norway rat)	Potency	0.0596	0.0015	51.7393	15,848.9004	AID1259244
ATPase family AAA domain-containing protein 5	Homo sapiens (human)	Potency	0.0204	0.0119	17.9420	71.5630	AID651632; AID720516
Ataxin-2	Homo sapiens (human)	Potency	0.0199	0.0119	12.2221	68.7989	AID651632
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Chain H, Proteasome component PUP1	Saccharomyces cerevisiae (brewer's yeast)	Ki	0.0006	0.0006	0.0006	0.0006	AID977610
Chain I, Proteasome component PUP3	Saccharomyces cerevisiae (brewer's yeast)	Ki	0.0006	0.0006	0.0006	0.0006	AID977610
Chain K, Proteasome component PRE2	Saccharomyces cerevisiae (brewer's yeast)	Ki	0.0006	0.0006	0.0006	0.0006	AID977610
Chain L, Proteasome component C5	Saccharomyces cerevisiae (brewer's yeast)	Ki	0.0006	0.0006	0.0006	0.0006	AID977610
Chain K, Proteasome component PRE2	Saccharomyces cerevisiae (brewer's yeast)	Ki	0.0006	0.0006	0.0006	0.0006	AID977610
Chain L, Proteasome component C5	Saccharomyces cerevisiae (brewer's yeast)	Ki	0.0006	0.0006	0.0006	0.0006	AID977610
Proteasome subunit beta type-11	Homo sapiens (human)	IC50 (µMol)	0.3213	0.0013	0.7099	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1903224
26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	1.0981	2.5000	AID1128229; AID1128230; AID1128231; AID1141825
Proteasome subunit alpha type-7	Homo sapiens (human)	IC50 (µMol)	0.3213	0.0013	0.7099	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1903224
Histone deacetylase 3	Homo sapiens (human)	IC50 (µMol)	1.1800	0.0004	0.6196	10.0000	AID1689693
ATP-binding cassette sub-family C member 3	Homo sapiens (human)	IC50 (µMol)	133.0000	0.6315	4.4531	9.3000	AID1473740
Multidrug resistance-associated protein 4	Homo sapiens (human)	IC50 (µMol)	133.0000	0.2000	5.6774	10.0000	AID1473741
26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
Carbonic anhydrase 12	Homo sapiens (human)	Ki	5.8700	0.0002	1.1043	9.9000	AID1460773
Bile salt export pump	Homo sapiens (human)	IC50 (µMol)	133.0000	0.1100	7.1903	10.0000	AID1473738
Prothrombin	Homo sapiens (human)	Ki	13.0000	0.0000	0.7846	9.0000	AID211777
Chymotrypsinogen A	Bos taurus (cattle)	Ki	2.4000	0.9000	4.0000	8.7000	AID1156346
Carbonic anhydrase 1	Homo sapiens (human)	Ki	1.2900	0.0000	1.3726	10.0000	AID1312152; AID1460764
Carbonic anhydrase 2	Homo sapiens (human)	Ki	1.1600	0.0000	0.7236	9.9200	AID1312153; AID1460765
Carbonic anhydrase 3	Homo sapiens (human)	Ki	4.5700	0.0002	2.0102	10.0000	AID1460766
Cathepsin B	Homo sapiens (human)	IC50 (µMol)	30.0000	0.0002	1.8453	10.0000	AID1128237
Neutrophil elastase	Homo sapiens (human)	Ki	2.3000	0.0020	1.2866	9.5499	AID66813
Cathepsin G	Homo sapiens (human)	IC50 (µMol)	1.8100	0.0137	2.4224	7.4130	AID1128238; AID316535
Cathepsin G	Homo sapiens (human)	Ki	0.6300	0.6300	0.6300	0.6300	AID48219
Lysosomal protective protein	Homo sapiens (human)	IC50 (µMol)	9.2000	0.6000	6.6000	10.0000	AID1128236
Chymotrypsinogen B	Homo sapiens (human)	Ki	0.3200	0.3200	4.4100	8.5000	AID52603
26S proteasome regulatory subunit 6A	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)	IC50 (µMol)	0.0850	0.0001	1.9731	8.0000	AID1762748
Proteasome subunit beta type-1	Homo sapiens (human)	IC50 (µMol)	0.2149	0.0006	0.7376	6.3700	AID1128229; AID1128230; AID1128231; AID1141825; AID1382145; AID1382148; AID1396602; AID1459657; AID1486824; AID1604182; AID1613999; AID1624025; AID1687105; AID1764783; AID1864398; AID1903224; AID706736; AID734753
Carbonic anhydrase 4	Homo sapiens (human)	Ki	6.5100	0.0002	1.9720	9.9200	AID1460767
Carbonic anhydrase 6	Homo sapiens (human)	Ki	4.3800	0.0001	1.4710	9.9200	AID1460770
Chymase	Homo sapiens (human)	IC50 (µMol)	1.1900	0.0260	2.6397	10.0000	AID316541
Proteasome subunit alpha type-1	Homo sapiens (human)	IC50 (µMol)	0.3213	0.0013	0.7099	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1903224
Proteasome subunit alpha type-2	Homo sapiens (human)	IC50 (µMol)	0.3213	0.0013	0.7099	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1903224
Proteasome subunit alpha type-3	Homo sapiens (human)	IC50 (µMol)	0.3213	0.0013	0.7099	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1903224
Proteasome subunit alpha type-4	Homo sapiens (human)	IC50 (µMol)	0.3213	0.0013	0.7099	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1903224
Proteasome subunit beta type-8	Homo sapiens (human)	IC50 (µMol)	0.1681	0.0013	0.3698	5.0000	AID1128229; AID1128230; AID1128231; AID1128235; AID1141825; AID1604187; AID1614003; AID1624025; AID1624027; AID1687110; AID1764783; AID1895437; AID1903224; AID354000
Proteasome subunit beta type-8	Mus musculus (house mouse)	IC50 (µMol)	0.0168	0.0168	0.0574	0.0980	AID1325773
Proteasome subunit beta type-9	Homo sapiens (human)	IC50 (µMol)	0.2059	0.0010	0.7611	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1604183; AID1614001; AID1624025; AID1687108; AID1764783; AID1895435; AID1903224
Proteasome subunit alpha type-5	Homo sapiens (human)	IC50 (µMol)	0.3213	0.0013	0.7099	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1903224
Proteasome subunit beta type-4	Homo sapiens (human)	IC50 (µMol)	0.3213	0.0013	0.7099	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1903224
Proteasome subunit beta type-6	Homo sapiens (human)	IC50 (µMol)	0.2842	0.0013	0.6912	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1895438; AID1903224
Proteasome subunit beta type-5	Homo sapiens (human)	IC50 (µMol)	15,084.2836	0.0005	0.9394	10.0000	AID1128229; AID1128230; AID1128231; AID1128234; AID1141825; AID1291318; AID1291322; AID1295429; AID1301231; AID1363797; AID1363798; AID1363799; AID1382147; AID1382150; AID1396601; AID1439183; AID1459637; AID1484607; AID1486822; AID1496304; AID1604186; AID1613994; AID1624025; AID1624026; AID1687107; AID1764783; AID1800498; AID1864383; AID1895440; AID1903224; AID706738; AID734754
Proteasome subunit beta type-5	Homo sapiens (human)	Ki	0.0067	0.0006	0.0104	0.0700	AID1128512; AID1156343; AID750162
Carbonic anhydrase 5A, mitochondrial	Homo sapiens (human)	Ki	6.9200	0.0000	1.2725	9.9000	AID1460768
26S proteasome regulatory subunit 7	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
Lon protease homolog, mitochondrial	Homo sapiens (human)	IC50 (µMol)	0.1830	0.1830	0.1830	0.1830	AID1764782
Proteasome subunit beta type-10	Homo sapiens (human)	IC50 (µMol)	0.5359	0.0013	0.8151	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1604185; AID1624025; AID1687109; AID1764783; AID1895436; AID1903224
Carbonic anhydrase 7	Homo sapiens (human)	Ki	6.9400	0.0002	1.3737	9.9000	AID1460771
26S proteasome regulatory subunit 6B	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
26S proteasome non-ATPase regulatory subunit 8	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
Proteasome subunit beta type-3	Homo sapiens (human)	IC50 (µMol)	0.3213	0.0013	0.7099	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1903224
Proteasome subunit beta type-2	Homo sapiens (human)	IC50 (µMol)	2.9860	0.0013	1.3906	7.9540	AID1128229; AID1128230; AID1128231; AID1141825; AID1382146; AID1382149; AID1396603; AID1459656; AID1486823; AID1604184; AID1614000; AID1624025; AID1624028; AID1687106; AID1764783; AID1864397; AID1903224; AID706737; AID734752
26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
26S proteasome complex subunit SEM1	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
Proteasome subunit alpha type-6	Homo sapiens (human)	IC50 (µMol)	0.3213	0.0013	0.7099	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1903224
26S proteasome regulatory subunit 4	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
26S proteasome regulatory subunit 8	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
26S proteasome regulatory subunit 10B	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
Beta-carbonic anhydrase 1	Mycobacterium tuberculosis H37Rv	Ki	7.3000	0.0048	3.3841	9.8400	AID1312159
Nuclear factor NF-kappa-B p100 subunit	Homo sapiens (human)	IC50 (µMol)	0.0850	0.0001	1.8088	8.0000	AID1762748
Transcription factor p65	Homo sapiens (human)	IC50 (µMol)	0.0850	0.0001	1.8981	8.8000	AID1762748
26S proteasome non-ATPase regulatory subunit 2	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
Histone deacetylase 1	Homo sapiens (human)	IC50 (µMol)	0.6200	0.0001	0.5543	9.9000	AID1689691
26S proteasome non-ATPase regulatory subunit 6	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
Proteasomal ubiquitin receptor ADRM1	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
Carbonic anhydrase 9	Homo sapiens (human)	Ki	3.3800	0.0001	0.7874	9.9000	AID1460772
ATP-dependent Clp protease proteolytic subunit	Staphylococcus aureus subsp. aureus NCTC 8325	IC50 (µMol)	5.3000	5.3000	5.3000	5.3000	AID1605096
Carbonic anhydrase 13	Homo sapiens (human)	Ki	8.4500	0.0003	1.2309	9.8000	AID1460774
NACHT, LRR and PYD domains-containing protein 3	Mus musculus (house mouse)	IC50 (µMol)	0.0407	0.0004	1.4419	10.0000	AID1864382
Proteasome subunit alpha-type 8	Homo sapiens (human)	IC50 (µMol)	0.3213	0.0013	0.7099	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1903224
Histone deacetylase 2	Homo sapiens (human)	IC50 (µMol)	0.8000	0.0001	0.7221	9.9700	AID1689692
Canalicular multispecific organic anion transporter 1	Homo sapiens (human)	IC50 (µMol)	133.0000	2.4100	6.3433	10.0000	AID1473739
Proteasome subunit beta type-7	Homo sapiens (human)	IC50 (µMol)	1.8772	0.0013	0.6843	5.0000	AID1128229; AID1128230; AID1128231; AID1141825; AID1624025; AID1764783; AID1895439; AID1903224
26S proteasome non-ATPase regulatory subunit 1	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
Carbonic anhydrase 15	Mus musculus (house mouse)	Ki	2.6800	0.0009	1.8846	10.0000	AID1460776
Histone deacetylase 8	Homo sapiens (human)	IC50 (µMol)	0.0720	0.0007	0.9947	9.9000	AID1689694
Histone deacetylase 6	Homo sapiens (human)	IC50 (µMol)	69.4400	0.0000	0.5376	9.9000	AID1689695
Carbonic anhydrase 14	Homo sapiens (human)	Ki	3.2800	0.0002	1.5099	9.9000	AID1460775
26S proteasome non-ATPase regulatory subunit 13	Homo sapiens (human)	IC50 (µMol)	0.5335	0.0070	0.7118	2.0000	AID1128229; AID1128230; AID1128231; AID1141825
Carbonic anhydrase 5B, mitochondrial	Homo sapiens (human)	Ki	6.8300	0.0000	1.3412	9.9700	AID1460769
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
ATP-dependent Clp protease proteolytic subunit	Staphylococcus aureus subsp. aureus NCTC 8325	EC50 (µMol)	23.5000	3.6000	3.6000	3.6000	AID1605098
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Proteasome subunit beta type-1	Homo sapiens (human)	Ki50	0.0250	0.0200	0.8600	2.0700	AID1372745; AID1372748
Proteasome subunit beta type-5	Homo sapiens (human)	Ki50	0.0100	0.0100	0.1725	0.5600	AID1372744; AID1372747
Proteasome subunit beta type-2	Homo sapiens (human)	Ki50	1.0750	0.7800	1.1500	1.3700	AID1372746; AID1372749
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
proteolysis	Proteasome subunit beta type-11	Homo sapiens (human)
T cell differentiation in thymus	Proteasome subunit beta type-11	Homo sapiens (human)
CD8-positive, alpha-beta T cell differentiation	Proteasome subunit beta type-11	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit beta type-11	Homo sapiens (human)
ubiquitin-dependent protein catabolic process	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
proteasome assembly	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
stem cell differentiation	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
double-strand break repair via homologous recombination	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
double-strand break repair via nonhomologous end joining	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
ubiquitin-dependent protein catabolic process	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
response to ethanol	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
regulation of proteasomal protein catabolic process	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
protein K63-linked deubiquitination	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
protein deubiquitination	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit alpha type-7	Homo sapiens (human)
negative regulation of myotube differentiation	Histone deacetylase 3	Homo sapiens (human)
negative regulation of transcription by RNA polymerase II	Histone deacetylase 3	Homo sapiens (human)
establishment of mitotic spindle orientation	Histone deacetylase 3	Homo sapiens (human)
in utero embryonic development	Histone deacetylase 3	Homo sapiens (human)
positive regulation of protein phosphorylation	Histone deacetylase 3	Homo sapiens (human)
chromatin organization	Histone deacetylase 3	Homo sapiens (human)
transcription by RNA polymerase II	Histone deacetylase 3	Homo sapiens (human)
protein deacetylation	Histone deacetylase 3	Homo sapiens (human)
regulation of mitotic cell cycle	Histone deacetylase 3	Homo sapiens (human)
positive regulation of protein ubiquitination	Histone deacetylase 3	Homo sapiens (human)
regulation of protein stability	Histone deacetylase 3	Homo sapiens (human)
positive regulation of TOR signaling	Histone deacetylase 3	Homo sapiens (human)
circadian regulation of gene expression	Histone deacetylase 3	Homo sapiens (human)
regulation of multicellular organism growth	Histone deacetylase 3	Homo sapiens (human)
positive regulation of protein import into nucleus	Histone deacetylase 3	Homo sapiens (human)
regulation of circadian rhythm	Histone deacetylase 3	Homo sapiens (human)
negative regulation of apoptotic process	Histone deacetylase 3	Homo sapiens (human)
negative regulation of DNA-templated transcription	Histone deacetylase 3	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Histone deacetylase 3	Homo sapiens (human)
negative regulation of JNK cascade	Histone deacetylase 3	Homo sapiens (human)
spindle assembly	Histone deacetylase 3	Homo sapiens (human)
establishment of skin barrier	Histone deacetylase 3	Homo sapiens (human)
cellular response to fluid shear stress	Histone deacetylase 3	Homo sapiens (human)
positive regulation of cold-induced thermogenesis	Histone deacetylase 3	Homo sapiens (human)
DNA repair-dependent chromatin remodeling	Histone deacetylase 3	Homo sapiens (human)
cornified envelope assembly	Histone deacetylase 3	Homo sapiens (human)
negative regulation of cardiac muscle cell differentiation	Histone deacetylase 3	Homo sapiens (human)
epigenetic regulation of gene expression	Histone deacetylase 3	Homo sapiens (human)
xenobiotic metabolic process	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
xenobiotic transmembrane transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
bile acid and bile salt transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
glucuronoside transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
xenobiotic transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
transmembrane transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
leukotriene transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
monoatomic anion transmembrane transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
transport across blood-brain barrier	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
prostaglandin secretion	Multidrug resistance-associated protein 4	Homo sapiens (human)
cilium assembly	Multidrug resistance-associated protein 4	Homo sapiens (human)
platelet degranulation	Multidrug resistance-associated protein 4	Homo sapiens (human)
xenobiotic metabolic process	Multidrug resistance-associated protein 4	Homo sapiens (human)
xenobiotic transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
bile acid and bile salt transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
prostaglandin transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
urate transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
glutathione transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
cAMP transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
leukotriene transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
monoatomic anion transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
export across plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
transport across blood-brain barrier	Multidrug resistance-associated protein 4	Homo sapiens (human)
guanine nucleotide transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
regulation of protein catabolic process	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
ubiquitin-dependent protein catabolic process	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
estrous cycle	Carbonic anhydrase 12	Homo sapiens (human)
chloride ion homeostasis	Carbonic anhydrase 12	Homo sapiens (human)
one-carbon metabolic process	Carbonic anhydrase 12	Homo sapiens (human)
fatty acid metabolic process	Bile salt export pump	Homo sapiens (human)
bile acid biosynthetic process	Bile salt export pump	Homo sapiens (human)
xenobiotic metabolic process	Bile salt export pump	Homo sapiens (human)
xenobiotic transmembrane transport	Bile salt export pump	Homo sapiens (human)
response to oxidative stress	Bile salt export pump	Homo sapiens (human)
bile acid metabolic process	Bile salt export pump	Homo sapiens (human)
response to organic cyclic compound	Bile salt export pump	Homo sapiens (human)
bile acid and bile salt transport	Bile salt export pump	Homo sapiens (human)
canalicular bile acid transport	Bile salt export pump	Homo sapiens (human)
protein ubiquitination	Bile salt export pump	Homo sapiens (human)
regulation of fatty acid beta-oxidation	Bile salt export pump	Homo sapiens (human)
carbohydrate transmembrane transport	Bile salt export pump	Homo sapiens (human)
bile acid signaling pathway	Bile salt export pump	Homo sapiens (human)
cholesterol homeostasis	Bile salt export pump	Homo sapiens (human)
response to estrogen	Bile salt export pump	Homo sapiens (human)
response to ethanol	Bile salt export pump	Homo sapiens (human)
xenobiotic export from cell	Bile salt export pump	Homo sapiens (human)
lipid homeostasis	Bile salt export pump	Homo sapiens (human)
phospholipid homeostasis	Bile salt export pump	Homo sapiens (human)
positive regulation of bile acid secretion	Bile salt export pump	Homo sapiens (human)
regulation of bile acid metabolic process	Bile salt export pump	Homo sapiens (human)
transmembrane transport	Bile salt export pump	Homo sapiens (human)
positive regulation of protein phosphorylation	Prothrombin	Homo sapiens (human)
proteolysis	Prothrombin	Homo sapiens (human)
acute-phase response	Prothrombin	Homo sapiens (human)
cell surface receptor signaling pathway	Prothrombin	Homo sapiens (human)
G protein-coupled receptor signaling pathway	Prothrombin	Homo sapiens (human)
blood coagulation	Prothrombin	Homo sapiens (human)
positive regulation of cell population proliferation	Prothrombin	Homo sapiens (human)
regulation of cell shape	Prothrombin	Homo sapiens (human)
response to wounding	Prothrombin	Homo sapiens (human)
negative regulation of platelet activation	Prothrombin	Homo sapiens (human)
platelet activation	Prothrombin	Homo sapiens (human)
regulation of blood coagulation	Prothrombin	Homo sapiens (human)
positive regulation of blood coagulation	Prothrombin	Homo sapiens (human)
positive regulation of cell growth	Prothrombin	Homo sapiens (human)
positive regulation of insulin secretion	Prothrombin	Homo sapiens (human)
positive regulation of collagen biosynthetic process	Prothrombin	Homo sapiens (human)
fibrinolysis	Prothrombin	Homo sapiens (human)
negative regulation of proteolysis	Prothrombin	Homo sapiens (human)
positive regulation of receptor signaling pathway via JAK-STAT	Prothrombin	Homo sapiens (human)
negative regulation of astrocyte differentiation	Prothrombin	Homo sapiens (human)
positive regulation of release of sequestered calcium ion into cytosol	Prothrombin	Homo sapiens (human)
regulation of cytosolic calcium ion concentration	Prothrombin	Homo sapiens (human)
cytolysis by host of symbiont cells	Prothrombin	Homo sapiens (human)
positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction	Prothrombin	Homo sapiens (human)
negative regulation of fibrinolysis	Prothrombin	Homo sapiens (human)
antimicrobial humoral immune response mediated by antimicrobial peptide	Prothrombin	Homo sapiens (human)
neutrophil-mediated killing of gram-negative bacterium	Prothrombin	Homo sapiens (human)
positive regulation of lipid kinase activity	Prothrombin	Homo sapiens (human)
negative regulation of cytokine production involved in inflammatory response	Prothrombin	Homo sapiens (human)
positive regulation of protein localization to nucleus	Prothrombin	Homo sapiens (human)
positive regulation of phospholipase C-activating G protein-coupled receptor signaling pathway	Prothrombin	Homo sapiens (human)
ligand-gated ion channel signaling pathway	Prothrombin	Homo sapiens (human)
positive regulation of reactive oxygen species metabolic process	Prothrombin	Homo sapiens (human)
digestion	Chymotrypsinogen A	Bos taurus (cattle)
one-carbon metabolic process	Carbonic anhydrase 1	Homo sapiens (human)
morphogenesis of an epithelium	Carbonic anhydrase 2	Homo sapiens (human)
positive regulation of synaptic transmission, GABAergic	Carbonic anhydrase 2	Homo sapiens (human)
positive regulation of cellular pH reduction	Carbonic anhydrase 2	Homo sapiens (human)
angiotensin-activated signaling pathway	Carbonic anhydrase 2	Homo sapiens (human)
regulation of monoatomic anion transport	Carbonic anhydrase 2	Homo sapiens (human)
secretion	Carbonic anhydrase 2	Homo sapiens (human)
regulation of intracellular pH	Carbonic anhydrase 2	Homo sapiens (human)
neuron cellular homeostasis	Carbonic anhydrase 2	Homo sapiens (human)
positive regulation of dipeptide transmembrane transport	Carbonic anhydrase 2	Homo sapiens (human)
regulation of chloride transport	Carbonic anhydrase 2	Homo sapiens (human)
carbon dioxide transport	Carbonic anhydrase 2	Homo sapiens (human)
one-carbon metabolic process	Carbonic anhydrase 2	Homo sapiens (human)
cell surface receptor signaling pathway via JAK-STAT	Interferon beta	Homo sapiens (human)
response to exogenous dsRNA	Interferon beta	Homo sapiens (human)
B cell activation involved in immune response	Interferon beta	Homo sapiens (human)
cell surface receptor signaling pathway	Interferon beta	Homo sapiens (human)
cell surface receptor signaling pathway via JAK-STAT	Interferon beta	Homo sapiens (human)
response to virus	Interferon beta	Homo sapiens (human)
positive regulation of autophagy	Interferon beta	Homo sapiens (human)
cytokine-mediated signaling pathway	Interferon beta	Homo sapiens (human)
natural killer cell activation	Interferon beta	Homo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT protein	Interferon beta	Homo sapiens (human)
cellular response to interferon-beta	Interferon beta	Homo sapiens (human)
B cell proliferation	Interferon beta	Homo sapiens (human)
negative regulation of viral genome replication	Interferon beta	Homo sapiens (human)
innate immune response	Interferon beta	Homo sapiens (human)
positive regulation of innate immune response	Interferon beta	Homo sapiens (human)
regulation of MHC class I biosynthetic process	Interferon beta	Homo sapiens (human)
negative regulation of T cell differentiation	Interferon beta	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Interferon beta	Homo sapiens (human)
defense response to virus	Interferon beta	Homo sapiens (human)
type I interferon-mediated signaling pathway	Interferon beta	Homo sapiens (human)
neuron cellular homeostasis	Interferon beta	Homo sapiens (human)
cellular response to exogenous dsRNA	Interferon beta	Homo sapiens (human)
cellular response to virus	Interferon beta	Homo sapiens (human)
negative regulation of Lewy body formation	Interferon beta	Homo sapiens (human)
negative regulation of T-helper 2 cell cytokine production	Interferon beta	Homo sapiens (human)
positive regulation of apoptotic signaling pathway	Interferon beta	Homo sapiens (human)
response to exogenous dsRNA	Interferon beta	Homo sapiens (human)
B cell differentiation	Interferon beta	Homo sapiens (human)
natural killer cell activation involved in immune response	Interferon beta	Homo sapiens (human)
adaptive immune response	Interferon beta	Homo sapiens (human)
T cell activation involved in immune response	Interferon beta	Homo sapiens (human)
humoral immune response	Interferon beta	Homo sapiens (human)
negative regulation of cell population proliferation	Cellular tumor antigen p53	Homo sapiens (human)
regulation of cell cycle	Cellular tumor antigen p53	Homo sapiens (human)
regulation of cell cycle G2/M phase transition	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response	Cellular tumor antigen p53	Homo sapiens (human)
ER overload response	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to glucose starvation	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
regulation of apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of miRNA transcription	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of transcription by RNA polymerase II	Cellular tumor antigen p53	Homo sapiens (human)
mitophagy	Cellular tumor antigen p53	Homo sapiens (human)
in utero embryonic development	Cellular tumor antigen p53	Homo sapiens (human)
somitogenesis	Cellular tumor antigen p53	Homo sapiens (human)
release of cytochrome c from mitochondria	Cellular tumor antigen p53	Homo sapiens (human)
hematopoietic progenitor cell differentiation	Cellular tumor antigen p53	Homo sapiens (human)
T cell proliferation involved in immune response	Cellular tumor antigen p53	Homo sapiens (human)
B cell lineage commitment	Cellular tumor antigen p53	Homo sapiens (human)
T cell lineage commitment	Cellular tumor antigen p53	Homo sapiens (human)
response to ischemia	Cellular tumor antigen p53	Homo sapiens (human)
nucleotide-excision repair	Cellular tumor antigen p53	Homo sapiens (human)
double-strand break repair	Cellular tumor antigen p53	Homo sapiens (human)
regulation of DNA-templated transcription	Cellular tumor antigen p53	Homo sapiens (human)
regulation of transcription by RNA polymerase II	Cellular tumor antigen p53	Homo sapiens (human)
protein import into nucleus	Cellular tumor antigen p53	Homo sapiens (human)
autophagy	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
transforming growth factor beta receptor signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
Ras protein signal transduction	Cellular tumor antigen p53	Homo sapiens (human)
gastrulation	Cellular tumor antigen p53	Homo sapiens (human)
neuroblast proliferation	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of neuroblast proliferation	Cellular tumor antigen p53	Homo sapiens (human)
protein localization	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of DNA replication	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of cell population proliferation	Cellular tumor antigen p53	Homo sapiens (human)
determination of adult lifespan	Cellular tumor antigen p53	Homo sapiens (human)
mRNA transcription	Cellular tumor antigen p53	Homo sapiens (human)
rRNA transcription	Cellular tumor antigen p53	Homo sapiens (human)
response to salt stress	Cellular tumor antigen p53	Homo sapiens (human)
response to inorganic substance	Cellular tumor antigen p53	Homo sapiens (human)
response to X-ray	Cellular tumor antigen p53	Homo sapiens (human)
response to gamma radiation	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of gene expression	Cellular tumor antigen p53	Homo sapiens (human)
cardiac muscle cell apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of cardiac muscle cell apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
glial cell proliferation	Cellular tumor antigen p53	Homo sapiens (human)
viral process	Cellular tumor antigen p53	Homo sapiens (human)
glucose catabolic process to lactate via pyruvate	Cellular tumor antigen p53	Homo sapiens (human)
cerebellum development	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of cell growth	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
mitotic G1 DNA damage checkpoint signaling	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of telomere maintenance via telomerase	Cellular tumor antigen p53	Homo sapiens (human)
T cell differentiation in thymus	Cellular tumor antigen p53	Homo sapiens (human)
tumor necrosis factor-mediated signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
regulation of tissue remodeling	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to UV	Cellular tumor antigen p53	Homo sapiens (human)
multicellular organism growth	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of mitochondrial membrane permeability	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to glucose starvation	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
entrainment of circadian clock by photoperiod	Cellular tumor antigen p53	Homo sapiens (human)
mitochondrial DNA repair	Cellular tumor antigen p53	Homo sapiens (human)
regulation of DNA damage response, signal transduction by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of neuron apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
transcription initiation-coupled chromatin remodeling	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of proteolysis	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of DNA-templated transcription	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of DNA-templated transcription	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of RNA polymerase II transcription preinitiation complex assembly	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Cellular tumor antigen p53	Homo sapiens (human)
response to antibiotic	Cellular tumor antigen p53	Homo sapiens (human)
fibroblast proliferation	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of fibroblast proliferation	Cellular tumor antigen p53	Homo sapiens (human)
circadian behavior	Cellular tumor antigen p53	Homo sapiens (human)
bone marrow development	Cellular tumor antigen p53	Homo sapiens (human)
embryonic organ development	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylation	Cellular tumor antigen p53	Homo sapiens (human)
protein stabilization	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of helicase activity	Cellular tumor antigen p53	Homo sapiens (human)
protein tetramerization	Cellular tumor antigen p53	Homo sapiens (human)
chromosome organization	Cellular tumor antigen p53	Homo sapiens (human)
neuron apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
regulation of cell cycle	Cellular tumor antigen p53	Homo sapiens (human)
hematopoietic stem cell differentiation	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of glial cell proliferation	Cellular tumor antigen p53	Homo sapiens (human)
type II interferon-mediated signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
cardiac septum morphogenesis	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of programmed necrotic cell death	Cellular tumor antigen p53	Homo sapiens (human)
protein-containing complex assembly	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stress	Cellular tumor antigen p53	Homo sapiens (human)
thymocyte apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of thymocyte apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
necroptotic process	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to hypoxia	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to xenobiotic stimulus	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to ionizing radiation	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to gamma radiation	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to UV-C	Cellular tumor antigen p53	Homo sapiens (human)
stem cell proliferation	Cellular tumor antigen p53	Homo sapiens (human)
signal transduction by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
reactive oxygen species metabolic process	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to actinomycin D	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondria	Cellular tumor antigen p53	Homo sapiens (human)
cellular senescence	Cellular tumor antigen p53	Homo sapiens (human)
replicative senescence	Cellular tumor antigen p53	Homo sapiens (human)
oxidative stress-induced premature senescence	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
oligodendrocyte apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of execution phase of apoptosis	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of mitophagy	Cellular tumor antigen p53	Homo sapiens (human)
regulation of mitochondrial membrane permeability involved in apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
regulation of intrinsic apoptotic signaling pathway by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of miRNA transcription	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of G1 to G0 transition	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of miRNA processing	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of glucose catabolic process to lactate via pyruvate	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of pentose-phosphate shunt	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to hypoxia	Cellular tumor antigen p53	Homo sapiens (human)
regulation of fibroblast apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of reactive oxygen species metabolic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of reactive oxygen species metabolic process	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of stem cell proliferation	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of cellular senescence	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
response to bacterium	Carbonic anhydrase 3	Homo sapiens (human)
one-carbon metabolic process	Carbonic anhydrase 3	Homo sapiens (human)
proteolysis	Cathepsin B	Homo sapiens (human)
thyroid hormone generation	Cathepsin B	Homo sapiens (human)
collagen catabolic process	Cathepsin B	Homo sapiens (human)
epithelial cell differentiation	Cathepsin B	Homo sapiens (human)
regulation of apoptotic process	Cathepsin B	Homo sapiens (human)
decidualization	Cathepsin B	Homo sapiens (human)
symbiont entry into host cell	Cathepsin B	Homo sapiens (human)
proteolysis involved in protein catabolic process	Cathepsin B	Homo sapiens (human)
cellular response to thyroid hormone stimulus	Cathepsin B	Homo sapiens (human)
proteolysis	Neutrophil elastase	Homo sapiens (human)
negative regulation of transcription by RNA polymerase II	Neutrophil elastase	Homo sapiens (human)
response to yeast	Neutrophil elastase	Homo sapiens (human)
leukocyte migration involved in inflammatory response	Neutrophil elastase	Homo sapiens (human)
biosynthetic process of antibacterial peptides active against Gram-negative bacteria	Neutrophil elastase	Homo sapiens (human)
proteolysis	Neutrophil elastase	Homo sapiens (human)
intracellular calcium ion homeostasis	Neutrophil elastase	Homo sapiens (human)
response to UV	Neutrophil elastase	Homo sapiens (human)
extracellular matrix disassembly	Neutrophil elastase	Homo sapiens (human)
protein catabolic process	Neutrophil elastase	Homo sapiens (human)
response to lipopolysaccharide	Neutrophil elastase	Homo sapiens (human)
negative regulation of chemokine production	Neutrophil elastase	Homo sapiens (human)
negative regulation of interleukin-8 production	Neutrophil elastase	Homo sapiens (human)
positive regulation of interleukin-8 production	Neutrophil elastase	Homo sapiens (human)
defense response to bacterium	Neutrophil elastase	Homo sapiens (human)
positive regulation of MAP kinase activity	Neutrophil elastase	Homo sapiens (human)
positive regulation of smooth muscle cell proliferation	Neutrophil elastase	Homo sapiens (human)
negative regulation of inflammatory response	Neutrophil elastase	Homo sapiens (human)
positive regulation of immune response	Neutrophil elastase	Homo sapiens (human)
negative regulation of chemotaxis	Neutrophil elastase	Homo sapiens (human)
pyroptosis	Neutrophil elastase	Homo sapiens (human)
neutrophil-mediated killing of gram-negative bacterium	Neutrophil elastase	Homo sapiens (human)
neutrophil-mediated killing of fungus	Neutrophil elastase	Homo sapiens (human)
positive regulation of leukocyte tethering or rolling	Neutrophil elastase	Homo sapiens (human)
phagocytosis	Neutrophil elastase	Homo sapiens (human)
acute inflammatory response to antigenic stimulus	Neutrophil elastase	Homo sapiens (human)
proteolysis	Cathepsin G	Homo sapiens (human)
angiotensin maturation	Cathepsin G	Homo sapiens (human)
monocyte chemotaxis	Cathepsin G	Homo sapiens (human)
protein phosphorylation	Cathepsin G	Homo sapiens (human)
proteolysis	Cathepsin G	Homo sapiens (human)
immune response	Cathepsin G	Homo sapiens (human)
protein processing	Cathepsin G	Homo sapiens (human)
cytokine-mediated signaling pathway	Cathepsin G	Homo sapiens (human)
protein metabolic process	Cathepsin G	Homo sapiens (human)
antibacterial humoral response	Cathepsin G	Homo sapiens (human)
extracellular matrix disassembly	Cathepsin G	Homo sapiens (human)
platelet activation	Cathepsin G	Homo sapiens (human)
purinergic nucleotide receptor signaling pathway	Cathepsin G	Homo sapiens (human)
neutrophil activation	Cathepsin G	Homo sapiens (human)
positive regulation of immune response	Cathepsin G	Homo sapiens (human)
defense response to Gram-negative bacterium	Cathepsin G	Homo sapiens (human)
defense response to Gram-positive bacterium	Cathepsin G	Homo sapiens (human)
defense response to fungus	Cathepsin G	Homo sapiens (human)
negative regulation of T cell activation	Cathepsin G	Homo sapiens (human)
neutrophil-mediated killing of gram-positive bacterium	Cathepsin G	Homo sapiens (human)
cellular response to lipopolysaccharide	Cathepsin G	Homo sapiens (human)
biofilm matrix disassembly	Cathepsin G	Homo sapiens (human)
positive regulation of platelet aggregation	Cathepsin G	Homo sapiens (human)
proteolysis	Lysosomal protective protein	Homo sapiens (human)
intracellular protein transport	Lysosomal protective protein	Homo sapiens (human)
regulation of protein stability	Lysosomal protective protein	Homo sapiens (human)
regulation of chaperone-mediated autophagy	Lysosomal protective protein	Homo sapiens (human)
negative regulation of chaperone-mediated autophagy	Lysosomal protective protein	Homo sapiens (human)
digestion	Chymotrypsinogen B	Homo sapiens (human)
proteolysis	Chymotrypsinogen B	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	26S proteasome regulatory subunit 6A	Homo sapiens (human)
modulation by host of viral transcription	26S proteasome regulatory subunit 6A	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	26S proteasome regulatory subunit 6A	Homo sapiens (human)
positive regulation of proteasomal protein catabolic process	26S proteasome regulatory subunit 6A	Homo sapiens (human)
negative regulation of transcription by RNA polymerase II	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cellular response to lipopolysaccharide	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
negative regulation of transcription by RNA polymerase II	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
regulation of transcription by RNA polymerase II	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
transcription by RNA polymerase II	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
apoptotic process	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
inflammatory response	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
canonical NF-kappaB signal transduction	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
JNK cascade	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
negative regulation of gene expression	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
positive regulation of macrophage derived foam cell differentiation	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
positive regulation of lipid storage	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
negative regulation of calcidiol 1-monooxygenase activity	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
negative regulation of vitamin D biosynthetic process	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
negative regulation of cholesterol transport	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
negative regulation of interleukin-12 production	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
response to muscle stretch	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
non-canonical NF-kappaB signal transduction	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
negative regulation of apoptotic process	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
positive regulation of DNA-templated transcription	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
negative regulation of inflammatory response	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
B cell receptor signaling pathway	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
negative regulation of protein metabolic process	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
mammary gland involution	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
positive regulation of transcription initiation by RNA polymerase II	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cellular response to mechanical stimulus	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cellular response to nicotine	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cellular response to interleukin-1	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cellular response to interleukin-6	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cellular response to tumor necrosis factor	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cellular response to dsRNA	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
positive regulation of canonical Wnt signaling pathway	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cellular response to interleukin-17	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cellular response to virus	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
antibacterial innate immune response	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
positive regulation of hyaluronan biosynthetic process	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cellular response to angiotensin	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
positive regulation of miRNA metabolic process	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cellular response to stress	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
innate immune response	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
response to cytokine	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit beta type-1	Homo sapiens (human)
proteolysis involved in protein catabolic process	Proteasome subunit beta type-1	Homo sapiens (human)
bicarbonate transport	Carbonic anhydrase 4	Homo sapiens (human)
one-carbon metabolic process	Carbonic anhydrase 4	Homo sapiens (human)
detection of chemical stimulus involved in sensory perception of bitter taste	Carbonic anhydrase 6	Homo sapiens (human)
one-carbon metabolic process	Carbonic anhydrase 6	Homo sapiens (human)
angiotensin maturation	Chymase	Homo sapiens (human)
peptide metabolic process	Chymase	Homo sapiens (human)
extracellular matrix disassembly	Chymase	Homo sapiens (human)
protein catabolic process	Chymase	Homo sapiens (human)
midbrain development	Chymase	Homo sapiens (human)
basement membrane disassembly	Chymase	Homo sapiens (human)
positive regulation of angiogenesis	Chymase	Homo sapiens (human)
regulation of inflammatory response	Chymase	Homo sapiens (human)
cellular response to glucose stimulus	Chymase	Homo sapiens (human)
cytokine precursor processing	Chymase	Homo sapiens (human)
immune system process	Proteasome subunit alpha type-1	Homo sapiens (human)
negative regulation of inflammatory response to antigenic stimulus	Proteasome subunit alpha type-1	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit alpha type-1	Homo sapiens (human)
response to virus	Proteasome subunit alpha type-2	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit alpha type-2	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit alpha type-3	Homo sapiens (human)
regulation of endopeptidase activity	Proteasome subunit alpha type-3	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit alpha type-4	Homo sapiens (human)
antigen processing and presentation	Proteasome subunit beta type-8	Homo sapiens (human)
fat cell differentiation	Proteasome subunit beta type-8	Homo sapiens (human)
regulation of endopeptidase activity	Proteasome subunit beta type-8	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit beta type-8	Homo sapiens (human)
immune system process	Proteasome subunit beta type-9	Homo sapiens (human)
regulation of cysteine-type endopeptidase activity	Proteasome subunit beta type-9	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit beta type-9	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit alpha type-5	Homo sapiens (human)
negative regulation of inflammatory response to antigenic stimulus	Proteasome subunit beta type-4	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit beta type-4	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit beta type-6	Homo sapiens (human)
proteolysis	Proteasome subunit beta type-5	Homo sapiens (human)
response to oxidative stress	Proteasome subunit beta type-5	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit beta type-5	Homo sapiens (human)
one-carbon metabolic process	Carbonic anhydrase 5A, mitochondrial	Homo sapiens (human)
osteoblast differentiation	26S proteasome regulatory subunit 7	Homo sapiens (human)
ubiquitin-dependent protein catabolic process	26S proteasome regulatory subunit 7	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	26S proteasome regulatory subunit 7	Homo sapiens (human)
positive regulation of proteasomal protein catabolic process	26S proteasome regulatory subunit 7	Homo sapiens (human)
mitochondrial genome maintenance	Lon protease homolog, mitochondrial	Homo sapiens (human)
response to hypoxia	Lon protease homolog, mitochondrial	Homo sapiens (human)
mitochondrion organization	Lon protease homolog, mitochondrial	Homo sapiens (human)
protein catabolic process	Lon protease homolog, mitochondrial	Homo sapiens (human)
mitochondrial DNA metabolic process	Lon protease homolog, mitochondrial	Homo sapiens (human)
cellular response to oxidative stress	Lon protease homolog, mitochondrial	Homo sapiens (human)
mitochondrial protein catabolic process	Lon protease homolog, mitochondrial	Homo sapiens (human)
negative regulation of insulin receptor signaling pathway	Lon protease homolog, mitochondrial	Homo sapiens (human)
regulation of peptidyl-tyrosine phosphorylation	Lon protease homolog, mitochondrial	Homo sapiens (human)
proteolysis involved in protein catabolic process	Lon protease homolog, mitochondrial	Homo sapiens (human)
oxidation-dependent protein catabolic process	Lon protease homolog, mitochondrial	Homo sapiens (human)
protein quality control for misfolded or incompletely synthesized proteins	Lon protease homolog, mitochondrial	Homo sapiens (human)
chaperone-mediated protein complex assembly	Lon protease homolog, mitochondrial	Homo sapiens (human)
cell morphogenesis	Proteasome subunit beta type-10	Homo sapiens (human)
humoral immune response	Proteasome subunit beta type-10	Homo sapiens (human)
T cell proliferation	Proteasome subunit beta type-10	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit beta type-10	Homo sapiens (human)
positive regulation of synaptic transmission, GABAergic	Carbonic anhydrase 7	Homo sapiens (human)
positive regulation of cellular pH reduction	Carbonic anhydrase 7	Homo sapiens (human)
neuron cellular homeostasis	Carbonic anhydrase 7	Homo sapiens (human)
regulation of chloride transport	Carbonic anhydrase 7	Homo sapiens (human)
regulation of intracellular pH	Carbonic anhydrase 7	Homo sapiens (human)
one-carbon metabolic process	Carbonic anhydrase 7	Homo sapiens (human)
blastocyst development	26S proteasome regulatory subunit 6B	Homo sapiens (human)
proteolysis	26S proteasome regulatory subunit 6B	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	26S proteasome regulatory subunit 6B	Homo sapiens (human)
positive regulation of proteasomal protein catabolic process	26S proteasome regulatory subunit 6B	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	26S proteasome non-ATPase regulatory subunit 8	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit beta type-3	Homo sapiens (human)
response to organonitrogen compound	Proteasome subunit beta type-2	Homo sapiens (human)
response to organic cyclic compound	Proteasome subunit beta type-2	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Proteasome subunit beta type-2	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)

Process	via Protein(s)	Taxonomy
threonine-type endopeptidase activity	Proteasome subunit beta type-11	Homo sapiens (human)
protein binding	Proteasome subunit beta type-11	Homo sapiens (human)
peptidase activity	Proteasome subunit beta type-11	Homo sapiens (human)
endopeptidase activity	Proteasome subunit beta type-11	Homo sapiens (human)
protein binding	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
structural molecule activity	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
protein binding	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
protein binding	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
metallopeptidase activity	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
metal ion binding	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
endopeptidase activator activity	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
K63-linked deubiquitinase activity	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
proteasome binding	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
metal-dependent deubiquitinase activity	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
protein binding	Proteasome subunit alpha type-7	Homo sapiens (human)
identical protein binding	Proteasome subunit alpha type-7	Homo sapiens (human)
transcription corepressor binding	Histone deacetylase 3	Homo sapiens (human)
chromatin binding	Histone deacetylase 3	Homo sapiens (human)
transcription corepressor activity	Histone deacetylase 3	Homo sapiens (human)
histone deacetylase activity	Histone deacetylase 3	Homo sapiens (human)
protein binding	Histone deacetylase 3	Homo sapiens (human)
enzyme binding	Histone deacetylase 3	Homo sapiens (human)
cyclin binding	Histone deacetylase 3	Homo sapiens (human)
chromatin DNA binding	Histone deacetylase 3	Homo sapiens (human)
protein lysine deacetylase activity	Histone deacetylase 3	Homo sapiens (human)
histone deacetylase binding	Histone deacetylase 3	Homo sapiens (human)
NF-kappaB binding	Histone deacetylase 3	Homo sapiens (human)
DNA-binding transcription factor binding	Histone deacetylase 3	Homo sapiens (human)
protein decrotonylase activity	Histone deacetylase 3	Homo sapiens (human)
histone decrotonylase activity	Histone deacetylase 3	Homo sapiens (human)
protein de-2-hydroxyisobutyrylase activity	Histone deacetylase 3	Homo sapiens (human)
ATP binding	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ABC-type xenobiotic transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
glucuronoside transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ABC-type bile acid transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ATP hydrolysis activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ATPase-coupled transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
xenobiotic transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
icosanoid transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ABC-type transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
guanine nucleotide transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
protein binding	Multidrug resistance-associated protein 4	Homo sapiens (human)
ATP binding	Multidrug resistance-associated protein 4	Homo sapiens (human)
ABC-type xenobiotic transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
prostaglandin transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
urate transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
purine nucleotide transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ABC-type bile acid transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
efflux transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
15-hydroxyprostaglandin dehydrogenase (NAD+) activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ATP hydrolysis activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
glutathione transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ATPase-coupled transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
xenobiotic transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ABC-type transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
protein binding	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
enzyme regulator activity	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
zinc ion binding	Carbonic anhydrase 12	Homo sapiens (human)
carbonate dehydratase activity	Carbonic anhydrase 12	Homo sapiens (human)
protein binding	Bile salt export pump	Homo sapiens (human)
ATP binding	Bile salt export pump	Homo sapiens (human)
ABC-type xenobiotic transporter activity	Bile salt export pump	Homo sapiens (human)
bile acid transmembrane transporter activity	Bile salt export pump	Homo sapiens (human)
canalicular bile acid transmembrane transporter activity	Bile salt export pump	Homo sapiens (human)
carbohydrate transmembrane transporter activity	Bile salt export pump	Homo sapiens (human)
ABC-type bile acid transporter activity	Bile salt export pump	Homo sapiens (human)
ATP hydrolysis activity	Bile salt export pump	Homo sapiens (human)
lipopolysaccharide binding	Prothrombin	Homo sapiens (human)
serine-type endopeptidase activity	Prothrombin	Homo sapiens (human)
signaling receptor binding	Prothrombin	Homo sapiens (human)
calcium ion binding	Prothrombin	Homo sapiens (human)
protein binding	Prothrombin	Homo sapiens (human)
growth factor activity	Prothrombin	Homo sapiens (human)
heparin binding	Prothrombin	Homo sapiens (human)
thrombospondin receptor activity	Prothrombin	Homo sapiens (human)
protein binding	Chymotrypsinogen A	Bos taurus (cattle)
serpin family protein binding	Chymotrypsinogen A	Bos taurus (cattle)
arylesterase activity	Carbonic anhydrase 1	Homo sapiens (human)
carbonate dehydratase activity	Carbonic anhydrase 1	Homo sapiens (human)
protein binding	Carbonic anhydrase 1	Homo sapiens (human)
zinc ion binding	Carbonic anhydrase 1	Homo sapiens (human)
hydro-lyase activity	Carbonic anhydrase 1	Homo sapiens (human)
cyanamide hydratase activity	Carbonic anhydrase 1	Homo sapiens (human)
arylesterase activity	Carbonic anhydrase 2	Homo sapiens (human)
carbonate dehydratase activity	Carbonic anhydrase 2	Homo sapiens (human)
protein binding	Carbonic anhydrase 2	Homo sapiens (human)
zinc ion binding	Carbonic anhydrase 2	Homo sapiens (human)
cyanamide hydratase activity	Carbonic anhydrase 2	Homo sapiens (human)
cytokine activity	Interferon beta	Homo sapiens (human)
cytokine receptor binding	Interferon beta	Homo sapiens (human)
type I interferon receptor binding	Interferon beta	Homo sapiens (human)
protein binding	Interferon beta	Homo sapiens (human)
chloramphenicol O-acetyltransferase activity	Interferon beta	Homo sapiens (human)
transcription cis-regulatory region binding	Cellular tumor antigen p53	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specific	Cellular tumor antigen p53	Homo sapiens (human)
cis-regulatory region sequence-specific DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
core promoter sequence-specific DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
TFIID-class transcription factor complex binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specific	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specific	Cellular tumor antigen p53	Homo sapiens (human)
protease binding	Cellular tumor antigen p53	Homo sapiens (human)
p53 binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
chromatin binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription factor activity	Cellular tumor antigen p53	Homo sapiens (human)
mRNA 3'-UTR binding	Cellular tumor antigen p53	Homo sapiens (human)
copper ion binding	Cellular tumor antigen p53	Homo sapiens (human)
protein binding	Cellular tumor antigen p53	Homo sapiens (human)
zinc ion binding	Cellular tumor antigen p53	Homo sapiens (human)
enzyme binding	Cellular tumor antigen p53	Homo sapiens (human)
receptor tyrosine kinase binding	Cellular tumor antigen p53	Homo sapiens (human)
ubiquitin protein ligase binding	Cellular tumor antigen p53	Homo sapiens (human)
histone deacetylase regulator activity	Cellular tumor antigen p53	Homo sapiens (human)
ATP-dependent DNA/DNA annealing activity	Cellular tumor antigen p53	Homo sapiens (human)
identical protein binding	Cellular tumor antigen p53	Homo sapiens (human)
histone deacetylase binding	Cellular tumor antigen p53	Homo sapiens (human)
protein heterodimerization activity	Cellular tumor antigen p53	Homo sapiens (human)
protein-folding chaperone binding	Cellular tumor antigen p53	Homo sapiens (human)
protein phosphatase 2A binding	Cellular tumor antigen p53	Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor binding	Cellular tumor antigen p53	Homo sapiens (human)
14-3-3 protein binding	Cellular tumor antigen p53	Homo sapiens (human)
MDM2/MDM4 family protein binding	Cellular tumor antigen p53	Homo sapiens (human)
disordered domain specific binding	Cellular tumor antigen p53	Homo sapiens (human)
general transcription initiation factor binding	Cellular tumor antigen p53	Homo sapiens (human)
molecular function activator activity	Cellular tumor antigen p53	Homo sapiens (human)
promoter-specific chromatin binding	Cellular tumor antigen p53	Homo sapiens (human)
carbonate dehydratase activity	Carbonic anhydrase 3	Homo sapiens (human)
protein binding	Carbonic anhydrase 3	Homo sapiens (human)
zinc ion binding	Carbonic anhydrase 3	Homo sapiens (human)
nickel cation binding	Carbonic anhydrase 3	Homo sapiens (human)
cysteine-type endopeptidase activity	Cathepsin B	Homo sapiens (human)
protein binding	Cathepsin B	Homo sapiens (human)
collagen binding	Cathepsin B	Homo sapiens (human)
peptidase activity	Cathepsin B	Homo sapiens (human)
cysteine-type peptidase activity	Cathepsin B	Homo sapiens (human)
proteoglycan binding	Cathepsin B	Homo sapiens (human)
protease binding	Neutrophil elastase	Homo sapiens (human)
transcription corepressor activity	Neutrophil elastase	Homo sapiens (human)
endopeptidase activity	Neutrophil elastase	Homo sapiens (human)
serine-type endopeptidase activity	Neutrophil elastase	Homo sapiens (human)
protein binding	Neutrophil elastase	Homo sapiens (human)
heparin binding	Neutrophil elastase	Homo sapiens (human)
peptidase activity	Neutrophil elastase	Homo sapiens (human)
cytokine binding	Neutrophil elastase	Homo sapiens (human)
serine-type endopeptidase activity	Cathepsin G	Homo sapiens (human)
protein binding	Cathepsin G	Homo sapiens (human)
heparin binding	Cathepsin G	Homo sapiens (human)
peptidase activity	Cathepsin G	Homo sapiens (human)
serine-type peptidase activity	Cathepsin G	Homo sapiens (human)
receptor ligand activity	Cathepsin G	Homo sapiens (human)
caspase binding	Cathepsin G	Homo sapiens (human)
carboxypeptidase activity	Lysosomal protective protein	Homo sapiens (human)
serine-type carboxypeptidase activity	Lysosomal protective protein	Homo sapiens (human)
enzyme activator activity	Lysosomal protective protein	Homo sapiens (human)
serine-type endopeptidase activity	Chymotrypsinogen B	Homo sapiens (human)
protein binding	26S proteasome regulatory subunit 6A	Homo sapiens (human)
ATP binding	26S proteasome regulatory subunit 6A	Homo sapiens (human)
ATP hydrolysis activity	26S proteasome regulatory subunit 6A	Homo sapiens (human)
proteasome-activating activity	26S proteasome regulatory subunit 6A	Homo sapiens (human)
identical protein binding	26S proteasome regulatory subunit 6A	Homo sapiens (human)
transcription cis-regulatory region binding	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
RNA polymerase II transcription regulatory region sequence-specific DNA binding	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specific	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specific	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specific	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
chromatin binding	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
DNA-binding transcription factor activity	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
transcription coregulator activity	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
protein binding	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
identical protein binding	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
actinin binding	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
protein binding	Proteasome subunit beta type-1	Homo sapiens (human)
protein binding	Carbonic anhydrase 4	Homo sapiens (human)
zinc ion binding	Carbonic anhydrase 4	Homo sapiens (human)
carbonate dehydratase activity	Carbonic anhydrase 4	Homo sapiens (human)
zinc ion binding	Carbonic anhydrase 6	Homo sapiens (human)
carbonate dehydratase activity	Carbonic anhydrase 6	Homo sapiens (human)
endopeptidase activity	Chymase	Homo sapiens (human)
serine-type endopeptidase activity	Chymase	Homo sapiens (human)
serine-type peptidase activity	Chymase	Homo sapiens (human)
peptide binding	Chymase	Homo sapiens (human)
lipopolysaccharide binding	Proteasome subunit alpha type-1	Homo sapiens (human)
protein binding	Proteasome subunit alpha type-1	Homo sapiens (human)
protein binding	Proteasome subunit alpha type-2	Homo sapiens (human)
protein binding	Proteasome subunit alpha type-3	Homo sapiens (human)
ubiquitin protein ligase binding	Proteasome subunit alpha type-3	Homo sapiens (human)
protein binding	Proteasome subunit alpha type-4	Homo sapiens (human)
threonine-type endopeptidase activity	Proteasome subunit beta type-8	Homo sapiens (human)
protein binding	Proteasome subunit beta type-8	Homo sapiens (human)
endopeptidase activity	Proteasome subunit beta type-8	Homo sapiens (human)
threonine-type endopeptidase activity	Proteasome subunit beta type-9	Homo sapiens (human)
protein binding	Proteasome subunit beta type-9	Homo sapiens (human)
endopeptidase activity	Proteasome subunit beta type-9	Homo sapiens (human)
protein binding	Proteasome subunit alpha type-5	Homo sapiens (human)
lipopolysaccharide binding	Proteasome subunit beta type-4	Homo sapiens (human)
protein binding	Proteasome subunit beta type-4	Homo sapiens (human)
endopeptidase activity	Proteasome subunit beta type-6	Homo sapiens (human)
threonine-type endopeptidase activity	Proteasome subunit beta type-6	Homo sapiens (human)
protein binding	Proteasome subunit beta type-6	Homo sapiens (human)
cadherin binding	Proteasome subunit beta type-6	Homo sapiens (human)
threonine-type endopeptidase activity	Proteasome subunit beta type-5	Homo sapiens (human)
protein binding	Proteasome subunit beta type-5	Homo sapiens (human)
peptidase activity	Proteasome subunit beta type-5	Homo sapiens (human)
endopeptidase activity	Proteasome subunit beta type-5	Homo sapiens (human)
carbonate dehydratase activity	Carbonic anhydrase 5A, mitochondrial	Homo sapiens (human)
zinc ion binding	Carbonic anhydrase 5A, mitochondrial	Homo sapiens (human)
protein binding	26S proteasome regulatory subunit 7	Homo sapiens (human)
ATP binding	26S proteasome regulatory subunit 7	Homo sapiens (human)
ATP hydrolysis activity	26S proteasome regulatory subunit 7	Homo sapiens (human)
proteasome-activating activity	26S proteasome regulatory subunit 7	Homo sapiens (human)
mitochondrial promoter sequence-specific DNA binding	Lon protease homolog, mitochondrial	Homo sapiens (human)
single-stranded RNA binding	Lon protease homolog, mitochondrial	Homo sapiens (human)
ATP-dependent peptidase activity	Lon protease homolog, mitochondrial	Homo sapiens (human)
serine-type endopeptidase activity	Lon protease homolog, mitochondrial	Homo sapiens (human)
protein binding	Lon protease homolog, mitochondrial	Homo sapiens (human)
ATP binding	Lon protease homolog, mitochondrial	Homo sapiens (human)
ATP hydrolysis activity	Lon protease homolog, mitochondrial	Homo sapiens (human)
PH domain binding	Lon protease homolog, mitochondrial	Homo sapiens (human)
identical protein binding	Lon protease homolog, mitochondrial	Homo sapiens (human)
ADP binding	Lon protease homolog, mitochondrial	Homo sapiens (human)
insulin receptor substrate binding	Lon protease homolog, mitochondrial	Homo sapiens (human)
sequence-specific DNA binding	Lon protease homolog, mitochondrial	Homo sapiens (human)
G-quadruplex DNA binding	Lon protease homolog, mitochondrial	Homo sapiens (human)
DNA polymerase binding	Lon protease homolog, mitochondrial	Homo sapiens (human)
single-stranded DNA binding	Lon protease homolog, mitochondrial	Homo sapiens (human)
threonine-type endopeptidase activity	Proteasome subunit beta type-10	Homo sapiens (human)
protein binding	Proteasome subunit beta type-10	Homo sapiens (human)
endopeptidase activity	Proteasome subunit beta type-10	Homo sapiens (human)
zinc ion binding	Carbonic anhydrase 7	Homo sapiens (human)
carbonate dehydratase activity	Carbonic anhydrase 7	Homo sapiens (human)
protein binding	26S proteasome regulatory subunit 6B	Homo sapiens (human)
ATP binding	26S proteasome regulatory subunit 6B	Homo sapiens (human)
ATP hydrolysis activity	26S proteasome regulatory subunit 6B	Homo sapiens (human)
proteasome-activating activity	26S proteasome regulatory subunit 6B	Homo sapiens (human)
protein binding	26S proteasome non-ATPase regulatory subunit 8	Homo sapiens (human)
protein binding	Proteasome subunit beta type-3	Homo sapiens (human)
protein binding	Proteasome subunit beta type-2	Homo sapiens (human)
peptidase activity	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
metal-dependent deubiquitinase activity	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
protein binding	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
protein homodimerization activity	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
RNA binding	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)
protein binding	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)
identical protein binding	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)
molecular adaptor activity	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)
polyubiquitin modification-dependent protein binding	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)
RNA binding	Proteasome subunit alpha type-6	Homo sapiens (human)
endopeptidase activity	Proteasome subunit alpha type-6	Homo sapiens (human)
protein binding	Proteasome subunit alpha type-6	Homo sapiens (human)
purine ribonucleoside triphosphate binding	Proteasome subunit alpha type-6	Homo sapiens (human)
NF-kappaB binding	Proteasome subunit alpha type-6	Homo sapiens (human)
RNA binding	26S proteasome regulatory subunit 4	Homo sapiens (human)
protein binding	26S proteasome regulatory subunit 4	Homo sapiens (human)
ATP binding	26S proteasome regulatory subunit 4	Homo sapiens (human)
ATP hydrolysis activity	26S proteasome regulatory subunit 4	Homo sapiens (human)
proteasome-activating activity	26S proteasome regulatory subunit 4	Homo sapiens (human)
protein binding	26S proteasome regulatory subunit 8	Homo sapiens (human)
ATP binding	26S proteasome regulatory subunit 8	Homo sapiens (human)
transcription factor binding	26S proteasome regulatory subunit 8	Homo sapiens (human)
ATP hydrolysis activity	26S proteasome regulatory subunit 8	Homo sapiens (human)
thyrotropin-releasing hormone receptor binding	26S proteasome regulatory subunit 8	Homo sapiens (human)
proteasome-activating activity	26S proteasome regulatory subunit 8	Homo sapiens (human)
general transcription initiation factor binding	26S proteasome regulatory subunit 8	Homo sapiens (human)
DNA-binding transcription factor binding	26S proteasome regulatory subunit 8	Homo sapiens (human)
protein binding	26S proteasome regulatory subunit 10B	Homo sapiens (human)
ATP binding	26S proteasome regulatory subunit 10B	Homo sapiens (human)
ATP hydrolysis activity	26S proteasome regulatory subunit 10B	Homo sapiens (human)
protein-macromolecule adaptor activity	26S proteasome regulatory subunit 10B	Homo sapiens (human)
proteasome-activating activity	26S proteasome regulatory subunit 10B	Homo sapiens (human)
identical protein binding	26S proteasome regulatory subunit 10B	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	Nuclear factor NF-kappa-B p100 subunit	Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specific	Nuclear factor NF-kappa-B p100 subunit	Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specific	Nuclear factor NF-kappa-B p100 subunit	Homo sapiens (human)
DNA-binding transcription factor activity	Nuclear factor NF-kappa-B p100 subunit	Homo sapiens (human)
protein binding	Nuclear factor NF-kappa-B p100 subunit	Homo sapiens (human)
sequence-specific double-stranded DNA binding	Nuclear factor NF-kappa-B p100 subunit	Homo sapiens (human)
transcription cis-regulatory region binding	Transcription factor p65	Homo sapiens (human)
RNA polymerase II transcription regulatory region sequence-specific DNA binding	Transcription factor p65	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	Transcription factor p65	Homo sapiens (human)
RNA polymerase II core promoter sequence-specific DNA binding	Transcription factor p65	Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specific	Transcription factor p65	Homo sapiens (human)
transcription coactivator binding	Transcription factor p65	Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specific	Transcription factor p65	Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specific	Transcription factor p65	Homo sapiens (human)
DNA binding	Transcription factor p65	Homo sapiens (human)
chromatin binding	Transcription factor p65	Homo sapiens (human)
DNA-binding transcription factor activity	Transcription factor p65	Homo sapiens (human)
protein binding	Transcription factor p65	Homo sapiens (human)
enzyme binding	Transcription factor p65	Homo sapiens (human)
protein kinase binding	Transcription factor p65	Homo sapiens (human)
chromatin DNA binding	Transcription factor p65	Homo sapiens (human)
ubiquitin protein ligase binding	Transcription factor p65	Homo sapiens (human)
peptide binding	Transcription factor p65	Homo sapiens (human)
phosphate ion binding	Transcription factor p65	Homo sapiens (human)
identical protein binding	Transcription factor p65	Homo sapiens (human)
protein homodimerization activity	Transcription factor p65	Homo sapiens (human)
actinin binding	Transcription factor p65	Homo sapiens (human)
histone deacetylase binding	Transcription factor p65	Homo sapiens (human)
NF-kappaB binding	Transcription factor p65	Homo sapiens (human)
ankyrin repeat binding	Transcription factor p65	Homo sapiens (human)
general transcription initiation factor binding	Transcription factor p65	Homo sapiens (human)
DNA-binding transcription factor binding	Transcription factor p65	Homo sapiens (human)
protein binding	26S proteasome non-ATPase regulatory subunit 2	Homo sapiens (human)
enzyme regulator activity	26S proteasome non-ATPase regulatory subunit 2	Homo sapiens (human)
nucleosomal DNA binding	Histone deacetylase 1	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	Histone deacetylase 1	Homo sapiens (human)
RNA polymerase II core promoter sequence-specific DNA binding	Histone deacetylase 1	Homo sapiens (human)
core promoter sequence-specific DNA binding	Histone deacetylase 1	Homo sapiens (human)
transcription corepressor binding	Histone deacetylase 1	Homo sapiens (human)
p53 binding	Histone deacetylase 1	Homo sapiens (human)
transcription corepressor activity	Histone deacetylase 1	Homo sapiens (human)
histone deacetylase activity	Histone deacetylase 1	Homo sapiens (human)
protein binding	Histone deacetylase 1	Homo sapiens (human)
enzyme binding	Histone deacetylase 1	Homo sapiens (human)
protein lysine deacetylase activity	Histone deacetylase 1	Homo sapiens (human)
Krueppel-associated box domain binding	Histone deacetylase 1	Homo sapiens (human)
histone deacetylase binding	Histone deacetylase 1	Homo sapiens (human)
NF-kappaB binding	Histone deacetylase 1	Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor binding	Histone deacetylase 1	Homo sapiens (human)
E-box binding	Histone deacetylase 1	Homo sapiens (human)
DNA-binding transcription factor binding	Histone deacetylase 1	Homo sapiens (human)
histone decrotonylase activity	Histone deacetylase 1	Homo sapiens (human)
promoter-specific chromatin binding	Histone deacetylase 1	Homo sapiens (human)
protein binding	26S proteasome non-ATPase regulatory subunit 6	Homo sapiens (human)
protease binding	Proteasomal ubiquitin receptor ADRM1	Homo sapiens (human)
protein binding	Proteasomal ubiquitin receptor ADRM1	Homo sapiens (human)
endopeptidase activator activity	Proteasomal ubiquitin receptor ADRM1	Homo sapiens (human)
proteasome binding	Proteasomal ubiquitin receptor ADRM1	Homo sapiens (human)
molecular function inhibitor activity	Proteasomal ubiquitin receptor ADRM1	Homo sapiens (human)
carbonate dehydratase activity	Carbonic anhydrase 9	Homo sapiens (human)
protein binding	Carbonic anhydrase 9	Homo sapiens (human)
zinc ion binding	Carbonic anhydrase 9	Homo sapiens (human)
molecular function activator activity	Carbonic anhydrase 9	Homo sapiens (human)
protein binding	Carbonic anhydrase 13	Homo sapiens (human)
zinc ion binding	Carbonic anhydrase 13	Homo sapiens (human)
carbonate dehydratase activity	Carbonic anhydrase 13	Homo sapiens (human)
nucleosomal DNA binding	Histone deacetylase 2	Homo sapiens (human)
chromatin binding	Histone deacetylase 2	Homo sapiens (human)
RNA binding	Histone deacetylase 2	Homo sapiens (human)
histone deacetylase activity	Histone deacetylase 2	Homo sapiens (human)
protein binding	Histone deacetylase 2	Homo sapiens (human)
enzyme binding	Histone deacetylase 2	Homo sapiens (human)
heat shock protein binding	Histone deacetylase 2	Homo sapiens (human)
protein lysine deacetylase activity	Histone deacetylase 2	Homo sapiens (human)
histone binding	Histone deacetylase 2	Homo sapiens (human)
histone deacetylase binding	Histone deacetylase 2	Homo sapiens (human)
NF-kappaB binding	Histone deacetylase 2	Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor binding	Histone deacetylase 2	Homo sapiens (human)
histone decrotonylase activity	Histone deacetylase 2	Homo sapiens (human)
protein de-2-hydroxyisobutyrylase activity	Histone deacetylase 2	Homo sapiens (human)
promoter-specific chromatin binding	Histone deacetylase 2	Homo sapiens (human)
protein binding	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ATP binding	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
organic anion transmembrane transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ABC-type xenobiotic transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
bilirubin transmembrane transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ATP hydrolysis activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ATPase-coupled transmembrane transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
xenobiotic transmembrane transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ABC-type transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
protein binding	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
ATP binding	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
ATP hydrolysis activity	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
DNA clamp unloader activity	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
DNA binding	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
threonine-type endopeptidase activity	Proteasome subunit beta type-7	Homo sapiens (human)
protein binding	Proteasome subunit beta type-7	Homo sapiens (human)
endopeptidase activity	Proteasome subunit beta type-7	Homo sapiens (human)
protein binding	26S proteasome non-ATPase regulatory subunit 1	Homo sapiens (human)
enzyme regulator activity	26S proteasome non-ATPase regulatory subunit 1	Homo sapiens (human)
ubiquitin protein ligase binding	26S proteasome non-ATPase regulatory subunit 1	Homo sapiens (human)
RNA binding	Ataxin-2	Homo sapiens (human)
epidermal growth factor receptor binding	Ataxin-2	Homo sapiens (human)
protein binding	Ataxin-2	Homo sapiens (human)
mRNA binding	Ataxin-2	Homo sapiens (human)
histone deacetylase activity	Histone deacetylase 8	Homo sapiens (human)
protein binding	Histone deacetylase 8	Homo sapiens (human)
Hsp70 protein binding	Histone deacetylase 8	Homo sapiens (human)
protein lysine deacetylase activity	Histone deacetylase 8	Homo sapiens (human)
metal ion binding	Histone deacetylase 8	Homo sapiens (human)
Hsp90 protein binding	Histone deacetylase 8	Homo sapiens (human)
DNA-binding transcription factor binding	Histone deacetylase 8	Homo sapiens (human)
histone decrotonylase activity	Histone deacetylase 8	Homo sapiens (human)
acetylspermidine deacetylase activity	Histone deacetylase 6	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	Histone deacetylase 6	Homo sapiens (human)
transcription corepressor binding	Histone deacetylase 6	Homo sapiens (human)
actin binding	Histone deacetylase 6	Homo sapiens (human)
histone deacetylase activity	Histone deacetylase 6	Homo sapiens (human)
protein binding	Histone deacetylase 6	Homo sapiens (human)
beta-catenin binding	Histone deacetylase 6	Homo sapiens (human)
microtubule binding	Histone deacetylase 6	Homo sapiens (human)
zinc ion binding	Histone deacetylase 6	Homo sapiens (human)
enzyme binding	Histone deacetylase 6	Homo sapiens (human)
polyubiquitin modification-dependent protein binding	Histone deacetylase 6	Homo sapiens (human)
ubiquitin protein ligase binding	Histone deacetylase 6	Homo sapiens (human)
protein lysine deacetylase activity	Histone deacetylase 6	Homo sapiens (human)
histone deacetylase binding	Histone deacetylase 6	Homo sapiens (human)
tubulin deacetylase activity	Histone deacetylase 6	Homo sapiens (human)
alpha-tubulin binding	Histone deacetylase 6	Homo sapiens (human)
ubiquitin binding	Histone deacetylase 6	Homo sapiens (human)
tau protein binding	Histone deacetylase 6	Homo sapiens (human)
beta-tubulin binding	Histone deacetylase 6	Homo sapiens (human)
misfolded protein binding	Histone deacetylase 6	Homo sapiens (human)
Hsp90 protein binding	Histone deacetylase 6	Homo sapiens (human)
dynein complex binding	Histone deacetylase 6	Homo sapiens (human)
transcription factor binding	Histone deacetylase 6	Homo sapiens (human)
zinc ion binding	Carbonic anhydrase 14	Homo sapiens (human)
carbonate dehydratase activity	Carbonic anhydrase 14	Homo sapiens (human)
structural molecule activity	26S proteasome non-ATPase regulatory subunit 13	Homo sapiens (human)
carbonate dehydratase activity	Carbonic anhydrase 5B, mitochondrial	Homo sapiens (human)
zinc ion binding	Carbonic anhydrase 5B, mitochondrial	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
cytosol	Proteasome subunit beta type-11	Homo sapiens (human)
proteasome core complex, beta-subunit complex	Proteasome subunit beta type-11	Homo sapiens (human)
nucleus	Proteasome subunit beta type-11	Homo sapiens (human)
cytosol	Proteasome subunit beta type-11	Homo sapiens (human)
proteasome complex	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
extracellular region	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
nucleus	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
nucleoplasm	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
cytosol	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
membrane	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
secretory granule lumen	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
ficolin-1-rich granule lumen	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
proteasome accessory complex	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
proteasome regulatory particle, lid subcomplex	26S proteasome non-ATPase regulatory subunit 11	Homo sapiens (human)
proteasome complex	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
extracellular region	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
nucleoplasm	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
cytosol	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
membrane	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
secretory granule lumen	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
extracellular exosome	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
ficolin-1-rich granule lumen	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
proteasome regulatory particle	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
proteasome accessory complex	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
proteasome regulatory particle, lid subcomplex	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
cytoplasm	26S proteasome non-ATPase regulatory subunit 12	Homo sapiens (human)
proteasome complex	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
extracellular region	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
nucleus	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
nucleoplasm	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
cytosol	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
secretory granule lumen	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
ficolin-1-rich granule lumen	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
proteasome regulatory particle, lid subcomplex	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
proteasome accessory complex	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
cytosolic proteasome complex	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
nucleus	26S proteasome non-ATPase regulatory subunit 14	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-7	Homo sapiens (human)
cytoplasm	Proteasome subunit alpha type-7	Homo sapiens (human)
proteasome complex	Proteasome subunit alpha type-7	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-7	Homo sapiens (human)
nucleoplasm	Proteasome subunit alpha type-7	Homo sapiens (human)
cytosol	Proteasome subunit alpha type-7	Homo sapiens (human)
extracellular exosome	Proteasome subunit alpha type-7	Homo sapiens (human)
postsynapse	Proteasome subunit alpha type-7	Homo sapiens (human)
proteasome core complex	Proteasome subunit alpha type-7	Homo sapiens (human)
proteasome core complex, alpha-subunit complex	Proteasome subunit alpha type-7	Homo sapiens (human)
nucleus	Histone deacetylase 3	Homo sapiens (human)
nucleoplasm	Histone deacetylase 3	Homo sapiens (human)
cytoplasm	Histone deacetylase 3	Homo sapiens (human)
Golgi apparatus	Histone deacetylase 3	Homo sapiens (human)
cytosol	Histone deacetylase 3	Homo sapiens (human)
plasma membrane	Histone deacetylase 3	Homo sapiens (human)
mitotic spindle	Histone deacetylase 3	Homo sapiens (human)
histone deacetylase complex	Histone deacetylase 3	Homo sapiens (human)
transcription repressor complex	Histone deacetylase 3	Homo sapiens (human)
nucleus	Histone deacetylase 3	Homo sapiens (human)
plasma membrane	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
basal plasma membrane	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
basolateral plasma membrane	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
membrane	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
nucleolus	Multidrug resistance-associated protein 4	Homo sapiens (human)
Golgi apparatus	Multidrug resistance-associated protein 4	Homo sapiens (human)
plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
basolateral plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
apical plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
platelet dense granule membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
external side of apical plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
proteasome complex	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
extracellular region	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
nucleus	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
nucleoplasm	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
cytosol	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
membrane	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
secretory granule lumen	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
extracellular exosome	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
ficolin-1-rich granule lumen	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
proteasome accessory complex	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
proteasome regulatory particle, lid subcomplex	26S proteasome non-ATPase regulatory subunit 3	Homo sapiens (human)
plasma membrane	Carbonic anhydrase 12	Homo sapiens (human)
membrane	Carbonic anhydrase 12	Homo sapiens (human)
basolateral plasma membrane	Carbonic anhydrase 12	Homo sapiens (human)
apical plasma membrane	Carbonic anhydrase 12	Homo sapiens (human)
plasma membrane	Carbonic anhydrase 12	Homo sapiens (human)
basolateral plasma membrane	Bile salt export pump	Homo sapiens (human)
Golgi membrane	Bile salt export pump	Homo sapiens (human)
endosome	Bile salt export pump	Homo sapiens (human)
plasma membrane	Bile salt export pump	Homo sapiens (human)
cell surface	Bile salt export pump	Homo sapiens (human)
apical plasma membrane	Bile salt export pump	Homo sapiens (human)
intercellular canaliculus	Bile salt export pump	Homo sapiens (human)
intracellular canaliculus	Bile salt export pump	Homo sapiens (human)
recycling endosome	Bile salt export pump	Homo sapiens (human)
recycling endosome membrane	Bile salt export pump	Homo sapiens (human)
extracellular exosome	Bile salt export pump	Homo sapiens (human)
membrane	Bile salt export pump	Homo sapiens (human)
external side of plasma membrane	Prothrombin	Homo sapiens (human)
collagen-containing extracellular matrix	Prothrombin	Homo sapiens (human)
extracellular region	Prothrombin	Homo sapiens (human)
extracellular space	Prothrombin	Homo sapiens (human)
endoplasmic reticulum lumen	Prothrombin	Homo sapiens (human)
Golgi lumen	Prothrombin	Homo sapiens (human)
plasma membrane	Prothrombin	Homo sapiens (human)
extracellular exosome	Prothrombin	Homo sapiens (human)
blood microparticle	Prothrombin	Homo sapiens (human)
collagen-containing extracellular matrix	Prothrombin	Homo sapiens (human)
extracellular space	Prothrombin	Homo sapiens (human)
extracellular region	Chymotrypsinogen A	Bos taurus (cattle)
serine protease inhibitor complex	Chymotrypsinogen A	Bos taurus (cattle)
cytosol	Carbonic anhydrase 1	Homo sapiens (human)
extracellular exosome	Carbonic anhydrase 1	Homo sapiens (human)
cytoplasm	Carbonic anhydrase 2	Homo sapiens (human)
cytosol	Carbonic anhydrase 2	Homo sapiens (human)
plasma membrane	Carbonic anhydrase 2	Homo sapiens (human)
myelin sheath	Carbonic anhydrase 2	Homo sapiens (human)
apical part of cell	Carbonic anhydrase 2	Homo sapiens (human)
extracellular exosome	Carbonic anhydrase 2	Homo sapiens (human)
cytoplasm	Carbonic anhydrase 2	Homo sapiens (human)
plasma membrane	Carbonic anhydrase 2	Homo sapiens (human)
apical part of cell	Carbonic anhydrase 2	Homo sapiens (human)
extracellular space	Interferon beta	Homo sapiens (human)
extracellular region	Interferon beta	Homo sapiens (human)
nuclear body	Cellular tumor antigen p53	Homo sapiens (human)
nucleus	Cellular tumor antigen p53	Homo sapiens (human)
nucleoplasm	Cellular tumor antigen p53	Homo sapiens (human)
replication fork	Cellular tumor antigen p53	Homo sapiens (human)
nucleolus	Cellular tumor antigen p53	Homo sapiens (human)
cytoplasm	Cellular tumor antigen p53	Homo sapiens (human)
mitochondrion	Cellular tumor antigen p53	Homo sapiens (human)
mitochondrial matrix	Cellular tumor antigen p53	Homo sapiens (human)
endoplasmic reticulum	Cellular tumor antigen p53	Homo sapiens (human)
centrosome	Cellular tumor antigen p53	Homo sapiens (human)
cytosol	Cellular tumor antigen p53	Homo sapiens (human)
nuclear matrix	Cellular tumor antigen p53	Homo sapiens (human)
PML body	Cellular tumor antigen p53	Homo sapiens (human)
transcription repressor complex	Cellular tumor antigen p53	Homo sapiens (human)
site of double-strand break	Cellular tumor antigen p53	Homo sapiens (human)
germ cell nucleus	Cellular tumor antigen p53	Homo sapiens (human)
chromatin	Cellular tumor antigen p53	Homo sapiens (human)
transcription regulator complex	Cellular tumor antigen p53	Homo sapiens (human)
protein-containing complex	Cellular tumor antigen p53	Homo sapiens (human)
cytosol	Carbonic anhydrase 3	Homo sapiens (human)
cytosol	Carbonic anhydrase 3	Homo sapiens (human)
cytoplasm	Carbonic anhydrase 3	Homo sapiens (human)
collagen-containing extracellular matrix	Cathepsin B	Homo sapiens (human)
extracellular region	Cathepsin B	Homo sapiens (human)
extracellular space	Cathepsin B	Homo sapiens (human)
lysosome	Cathepsin B	Homo sapiens (human)
external side of plasma membrane	Cathepsin B	Homo sapiens (human)
apical plasma membrane	Cathepsin B	Homo sapiens (human)
endolysosome lumen	Cathepsin B	Homo sapiens (human)
melanosome	Cathepsin B	Homo sapiens (human)
perinuclear region of cytoplasm	Cathepsin B	Homo sapiens (human)
collagen-containing extracellular matrix	Cathepsin B	Homo sapiens (human)
extracellular exosome	Cathepsin B	Homo sapiens (human)
peptidase inhibitor complex	Cathepsin B	Homo sapiens (human)
ficolin-1-rich granule lumen	Cathepsin B	Homo sapiens (human)
extracellular space	Cathepsin B	Homo sapiens (human)
lysosome	Cathepsin B	Homo sapiens (human)
extracellular region	Neutrophil elastase	Homo sapiens (human)
extracellular space	Neutrophil elastase	Homo sapiens (human)
cytoplasm	Neutrophil elastase	Homo sapiens (human)
cytosol	Neutrophil elastase	Homo sapiens (human)
cell surface	Neutrophil elastase	Homo sapiens (human)
secretory granule	Neutrophil elastase	Homo sapiens (human)
azurophil granule lumen	Neutrophil elastase	Homo sapiens (human)
specific granule lumen	Neutrophil elastase	Homo sapiens (human)
phagocytic vesicle	Neutrophil elastase	Homo sapiens (human)
collagen-containing extracellular matrix	Neutrophil elastase	Homo sapiens (human)
extracellular exosome	Neutrophil elastase	Homo sapiens (human)
transcription repressor complex	Neutrophil elastase	Homo sapiens (human)
extracellular space	Neutrophil elastase	Homo sapiens (human)
collagen-containing extracellular matrix	Cathepsin G	Homo sapiens (human)
extracellular region	Cathepsin G	Homo sapiens (human)
extracellular space	Cathepsin G	Homo sapiens (human)
nucleus	Cathepsin G	Homo sapiens (human)
lysosome	Cathepsin G	Homo sapiens (human)
cytosol	Cathepsin G	Homo sapiens (human)
plasma membrane	Cathepsin G	Homo sapiens (human)
cytoplasmic stress granule	Cathepsin G	Homo sapiens (human)
membrane	Cathepsin G	Homo sapiens (human)
secretory granule	Cathepsin G	Homo sapiens (human)
azurophil granule lumen	Cathepsin G	Homo sapiens (human)
collagen-containing extracellular matrix	Cathepsin G	Homo sapiens (human)
extracellular exosome	Cathepsin G	Homo sapiens (human)
cytoplasm	Cathepsin G	Homo sapiens (human)
intracellular membrane-bounded organelle	Cathepsin G	Homo sapiens (human)
lumenal side of lysosomal membrane	Lysosomal protective protein	Homo sapiens (human)
extracellular region	Lysosomal protective protein	Homo sapiens (human)
lysosome	Lysosomal protective protein	Homo sapiens (human)
endoplasmic reticulum	Lysosomal protective protein	Homo sapiens (human)
membrane	Lysosomal protective protein	Homo sapiens (human)
azurophil granule lumen	Lysosomal protective protein	Homo sapiens (human)
lysosomal lumen	Lysosomal protective protein	Homo sapiens (human)
intracellular membrane-bounded organelle	Lysosomal protective protein	Homo sapiens (human)
extracellular exosome	Lysosomal protective protein	Homo sapiens (human)
extracellular region	Chymotrypsinogen B	Homo sapiens (human)
proteasome complex	26S proteasome regulatory subunit 6A	Homo sapiens (human)
P-body	26S proteasome regulatory subunit 6A	Homo sapiens (human)
extracellular region	26S proteasome regulatory subunit 6A	Homo sapiens (human)
nucleus	26S proteasome regulatory subunit 6A	Homo sapiens (human)
nucleoplasm	26S proteasome regulatory subunit 6A	Homo sapiens (human)
cytosol	26S proteasome regulatory subunit 6A	Homo sapiens (human)
membrane	26S proteasome regulatory subunit 6A	Homo sapiens (human)
secretory granule lumen	26S proteasome regulatory subunit 6A	Homo sapiens (human)
ficolin-1-rich granule lumen	26S proteasome regulatory subunit 6A	Homo sapiens (human)
proteasome accessory complex	26S proteasome regulatory subunit 6A	Homo sapiens (human)
proteasome regulatory particle, base subcomplex	26S proteasome regulatory subunit 6A	Homo sapiens (human)
plasma membrane	Glutamate receptor 2	Rattus norvegicus (Norway rat)
extracellular region	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
nucleus	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
nucleoplasm	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cytoplasm	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
mitochondrion	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cytosol	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
secretory granule lumen	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
specific granule lumen	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
chromatin	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
transcription regulator complex	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
I-kappaB/NF-kappaB complex	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
nucleus	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
cytoplasm	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
NF-kappaB p50/p65 complex	Nuclear factor NF-kappa-B p105 subunit	Homo sapiens (human)
nucleus	Proteasome subunit beta type-1	Homo sapiens (human)
cytoplasm	Proteasome subunit beta type-1	Homo sapiens (human)
proteasome complex	Proteasome subunit beta type-1	Homo sapiens (human)
extracellular region	Proteasome subunit beta type-1	Homo sapiens (human)
nucleus	Proteasome subunit beta type-1	Homo sapiens (human)
nucleoplasm	Proteasome subunit beta type-1	Homo sapiens (human)
cytosol	Proteasome subunit beta type-1	Homo sapiens (human)
secretory granule lumen	Proteasome subunit beta type-1	Homo sapiens (human)
extracellular exosome	Proteasome subunit beta type-1	Homo sapiens (human)
ficolin-1-rich granule lumen	Proteasome subunit beta type-1	Homo sapiens (human)
proteasome core complex	Proteasome subunit beta type-1	Homo sapiens (human)
proteasome core complex, beta-subunit complex	Proteasome subunit beta type-1	Homo sapiens (human)
basolateral plasma membrane	Carbonic anhydrase 4	Homo sapiens (human)
rough endoplasmic reticulum	Carbonic anhydrase 4	Homo sapiens (human)
endoplasmic reticulum-Golgi intermediate compartment	Carbonic anhydrase 4	Homo sapiens (human)
Golgi apparatus	Carbonic anhydrase 4	Homo sapiens (human)
trans-Golgi network	Carbonic anhydrase 4	Homo sapiens (human)
plasma membrane	Carbonic anhydrase 4	Homo sapiens (human)
external side of plasma membrane	Carbonic anhydrase 4	Homo sapiens (human)
cell surface	Carbonic anhydrase 4	Homo sapiens (human)
membrane	Carbonic anhydrase 4	Homo sapiens (human)
apical plasma membrane	Carbonic anhydrase 4	Homo sapiens (human)
transport vesicle membrane	Carbonic anhydrase 4	Homo sapiens (human)
secretory granule membrane	Carbonic anhydrase 4	Homo sapiens (human)
brush border membrane	Carbonic anhydrase 4	Homo sapiens (human)
perinuclear region of cytoplasm	Carbonic anhydrase 4	Homo sapiens (human)
extracellular exosome	Carbonic anhydrase 4	Homo sapiens (human)
plasma membrane	Carbonic anhydrase 4	Homo sapiens (human)
extracellular region	Carbonic anhydrase 6	Homo sapiens (human)
extracellular space	Carbonic anhydrase 6	Homo sapiens (human)
cytosol	Carbonic anhydrase 6	Homo sapiens (human)
extracellular exosome	Carbonic anhydrase 6	Homo sapiens (human)
extracellular space	Carbonic anhydrase 6	Homo sapiens (human)
collagen-containing extracellular matrix	Chymase	Homo sapiens (human)
extracellular region	Chymase	Homo sapiens (human)
cytosol	Chymase	Homo sapiens (human)
secretory granule	Chymase	Homo sapiens (human)
cytoplasmic ribonucleoprotein granule	Chymase	Homo sapiens (human)
collagen-containing extracellular matrix	Chymase	Homo sapiens (human)
extracellular space	Chymase	Homo sapiens (human)
intracellular membrane-bounded organelle	Chymase	Homo sapiens (human)
cytoplasm	Chymase	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-1	Homo sapiens (human)
cytoplasm	Proteasome subunit alpha type-1	Homo sapiens (human)
proteasome complex	Proteasome subunit alpha type-1	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-1	Homo sapiens (human)
nucleoplasm	Proteasome subunit alpha type-1	Homo sapiens (human)
centrosome	Proteasome subunit alpha type-1	Homo sapiens (human)
cytosol	Proteasome subunit alpha type-1	Homo sapiens (human)
extracellular exosome	Proteasome subunit alpha type-1	Homo sapiens (human)
proteasome core complex	Proteasome subunit alpha type-1	Homo sapiens (human)
proteasome core complex, alpha-subunit complex	Proteasome subunit alpha type-1	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-2	Homo sapiens (human)
cytoplasm	Proteasome subunit alpha type-2	Homo sapiens (human)
proteasome complex	Proteasome subunit alpha type-2	Homo sapiens (human)
P-body	Proteasome subunit alpha type-2	Homo sapiens (human)
extracellular region	Proteasome subunit alpha type-2	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-2	Homo sapiens (human)
nucleoplasm	Proteasome subunit alpha type-2	Homo sapiens (human)
cytosol	Proteasome subunit alpha type-2	Homo sapiens (human)
secretory granule lumen	Proteasome subunit alpha type-2	Homo sapiens (human)
extracellular exosome	Proteasome subunit alpha type-2	Homo sapiens (human)
ficolin-1-rich granule lumen	Proteasome subunit alpha type-2	Homo sapiens (human)
proteasome core complex	Proteasome subunit alpha type-2	Homo sapiens (human)
proteasome core complex, alpha-subunit complex	Proteasome subunit alpha type-2	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-3	Homo sapiens (human)
cytoplasm	Proteasome subunit alpha type-3	Homo sapiens (human)
proteasome complex	Proteasome subunit alpha type-3	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-3	Homo sapiens (human)
nucleoplasm	Proteasome subunit alpha type-3	Homo sapiens (human)
cytoplasm	Proteasome subunit alpha type-3	Homo sapiens (human)
cytosol	Proteasome subunit alpha type-3	Homo sapiens (human)
extracellular exosome	Proteasome subunit alpha type-3	Homo sapiens (human)
proteasome core complex	Proteasome subunit alpha type-3	Homo sapiens (human)
proteasome core complex, alpha-subunit complex	Proteasome subunit alpha type-3	Homo sapiens (human)
synapse	Proteasome subunit alpha type-3	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-4	Homo sapiens (human)
cytoplasm	Proteasome subunit alpha type-4	Homo sapiens (human)
proteasome complex	Proteasome subunit alpha type-4	Homo sapiens (human)
P-body	Proteasome subunit alpha type-4	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-4	Homo sapiens (human)
nucleoplasm	Proteasome subunit alpha type-4	Homo sapiens (human)
cytosol	Proteasome subunit alpha type-4	Homo sapiens (human)
intracellular membrane-bounded organelle	Proteasome subunit alpha type-4	Homo sapiens (human)
extracellular exosome	Proteasome subunit alpha type-4	Homo sapiens (human)
proteasome core complex	Proteasome subunit alpha type-4	Homo sapiens (human)
proteasome core complex, alpha-subunit complex	Proteasome subunit alpha type-4	Homo sapiens (human)
cytosol	Proteasome subunit alpha type-4	Homo sapiens (human)
nucleoplasm	Proteasome subunit beta type-8	Homo sapiens (human)
cytosol	Proteasome subunit beta type-8	Homo sapiens (human)
extracellular exosome	Proteasome subunit beta type-8	Homo sapiens (human)
proteasome complex	Proteasome subunit beta type-8	Homo sapiens (human)
proteasome core complex	Proteasome subunit beta type-8	Homo sapiens (human)
proteasome core complex, beta-subunit complex	Proteasome subunit beta type-8	Homo sapiens (human)
spermatoproteasome complex	Proteasome subunit beta type-8	Homo sapiens (human)
nucleus	Proteasome subunit beta type-8	Homo sapiens (human)
cytosol	Proteasome subunit beta type-8	Homo sapiens (human)
nucleoplasm	Proteasome subunit beta type-8	Mus musculus (house mouse)
cytosol	Proteasome subunit beta type-8	Mus musculus (house mouse)
nucleoplasm	Proteasome subunit beta type-9	Homo sapiens (human)
cytosol	Proteasome subunit beta type-9	Homo sapiens (human)
extracellular exosome	Proteasome subunit beta type-9	Homo sapiens (human)
proteasome complex	Proteasome subunit beta type-9	Homo sapiens (human)
proteasome core complex	Proteasome subunit beta type-9	Homo sapiens (human)
proteasome core complex, beta-subunit complex	Proteasome subunit beta type-9	Homo sapiens (human)
spermatoproteasome complex	Proteasome subunit beta type-9	Homo sapiens (human)
cytosol	Proteasome subunit beta type-9	Homo sapiens (human)
nucleus	Proteasome subunit beta type-9	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-5	Homo sapiens (human)
cytoplasm	Proteasome subunit alpha type-5	Homo sapiens (human)
proteasome complex	Proteasome subunit alpha type-5	Homo sapiens (human)
extracellular region	Proteasome subunit alpha type-5	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-5	Homo sapiens (human)
nucleoplasm	Proteasome subunit alpha type-5	Homo sapiens (human)
cytosol	Proteasome subunit alpha type-5	Homo sapiens (human)
secretory granule lumen	Proteasome subunit alpha type-5	Homo sapiens (human)
extracellular exosome	Proteasome subunit alpha type-5	Homo sapiens (human)
ficolin-1-rich granule lumen	Proteasome subunit alpha type-5	Homo sapiens (human)
proteasome core complex	Proteasome subunit alpha type-5	Homo sapiens (human)
proteasome core complex, alpha-subunit complex	Proteasome subunit alpha type-5	Homo sapiens (human)
nucleus	Proteasome subunit beta type-4	Homo sapiens (human)
cytoplasm	Proteasome subunit beta type-4	Homo sapiens (human)
proteasome complex	Proteasome subunit beta type-4	Homo sapiens (human)
nucleus	Proteasome subunit beta type-4	Homo sapiens (human)
nucleoplasm	Proteasome subunit beta type-4	Homo sapiens (human)
mitochondrion	Proteasome subunit beta type-4	Homo sapiens (human)
cytosol	Proteasome subunit beta type-4	Homo sapiens (human)
ciliary basal body	Proteasome subunit beta type-4	Homo sapiens (human)
extracellular exosome	Proteasome subunit beta type-4	Homo sapiens (human)
proteasome core complex	Proteasome subunit beta type-4	Homo sapiens (human)
proteasome core complex, beta-subunit complex	Proteasome subunit beta type-4	Homo sapiens (human)
cytosol	Proteasome subunit beta type-4	Homo sapiens (human)
nucleus	Proteasome subunit beta type-6	Homo sapiens (human)
cytoplasm	Proteasome subunit beta type-6	Homo sapiens (human)
proteasome complex	Proteasome subunit beta type-6	Homo sapiens (human)
nucleus	Proteasome subunit beta type-6	Homo sapiens (human)
nucleoplasm	Proteasome subunit beta type-6	Homo sapiens (human)
mitochondrion	Proteasome subunit beta type-6	Homo sapiens (human)
cytosol	Proteasome subunit beta type-6	Homo sapiens (human)
extracellular exosome	Proteasome subunit beta type-6	Homo sapiens (human)
proteasome core complex	Proteasome subunit beta type-6	Homo sapiens (human)
proteasome core complex, beta-subunit complex	Proteasome subunit beta type-6	Homo sapiens (human)
cytosol	Proteasome subunit beta type-6	Homo sapiens (human)
nucleus	Proteasome subunit beta type-5	Homo sapiens (human)
cytoplasm	Proteasome subunit beta type-5	Homo sapiens (human)
proteasome complex	Proteasome subunit beta type-5	Homo sapiens (human)
nucleus	Proteasome subunit beta type-5	Homo sapiens (human)
nucleoplasm	Proteasome subunit beta type-5	Homo sapiens (human)
centrosome	Proteasome subunit beta type-5	Homo sapiens (human)
cytosol	Proteasome subunit beta type-5	Homo sapiens (human)
extracellular exosome	Proteasome subunit beta type-5	Homo sapiens (human)
proteasome core complex	Proteasome subunit beta type-5	Homo sapiens (human)
proteasome core complex, beta-subunit complex	Proteasome subunit beta type-5	Homo sapiens (human)
cytosol	Proteasome subunit beta type-5	Homo sapiens (human)
mitochondrial matrix	Carbonic anhydrase 5A, mitochondrial	Homo sapiens (human)
mitochondrion	Carbonic anhydrase 5A, mitochondrial	Homo sapiens (human)
cytoplasm	Carbonic anhydrase 5A, mitochondrial	Homo sapiens (human)
mitochondrion	Carbonic anhydrase 5A, mitochondrial	Homo sapiens (human)
proteasome complex	26S proteasome regulatory subunit 7	Homo sapiens (human)
P-body	26S proteasome regulatory subunit 7	Homo sapiens (human)
extracellular region	26S proteasome regulatory subunit 7	Homo sapiens (human)
nucleus	26S proteasome regulatory subunit 7	Homo sapiens (human)
nucleoplasm	26S proteasome regulatory subunit 7	Homo sapiens (human)
cytoplasm	26S proteasome regulatory subunit 7	Homo sapiens (human)
cytosol	26S proteasome regulatory subunit 7	Homo sapiens (human)
membrane	26S proteasome regulatory subunit 7	Homo sapiens (human)
secretory granule lumen	26S proteasome regulatory subunit 7	Homo sapiens (human)
cytoplasmic ribonucleoprotein granule	26S proteasome regulatory subunit 7	Homo sapiens (human)
ficolin-1-rich granule lumen	26S proteasome regulatory subunit 7	Homo sapiens (human)
proteasome accessory complex	26S proteasome regulatory subunit 7	Homo sapiens (human)
proteasome regulatory particle, base subcomplex	26S proteasome regulatory subunit 7	Homo sapiens (human)
mitochondrion	Lon protease homolog, mitochondrial	Homo sapiens (human)
nucleoplasm	Lon protease homolog, mitochondrial	Homo sapiens (human)
mitochondrion	Lon protease homolog, mitochondrial	Homo sapiens (human)
mitochondrial matrix	Lon protease homolog, mitochondrial	Homo sapiens (human)
cytosol	Lon protease homolog, mitochondrial	Homo sapiens (human)
membrane	Lon protease homolog, mitochondrial	Homo sapiens (human)
mitochondrial nucleoid	Lon protease homolog, mitochondrial	Homo sapiens (human)
mitochondrial matrix	Lon protease homolog, mitochondrial	Homo sapiens (human)
nucleoplasm	Proteasome subunit beta type-10	Homo sapiens (human)
cytosol	Proteasome subunit beta type-10	Homo sapiens (human)
proteasome complex	Proteasome subunit beta type-10	Homo sapiens (human)
proteasome core complex	Proteasome subunit beta type-10	Homo sapiens (human)
proteasome core complex, beta-subunit complex	Proteasome subunit beta type-10	Homo sapiens (human)
spermatoproteasome complex	Proteasome subunit beta type-10	Homo sapiens (human)
cytosol	Proteasome subunit beta type-10	Homo sapiens (human)
nucleus	Proteasome subunit beta type-10	Homo sapiens (human)
cytosol	Carbonic anhydrase 7	Homo sapiens (human)
cytoplasm	Carbonic anhydrase 7	Homo sapiens (human)
proteasome complex	26S proteasome regulatory subunit 6B	Homo sapiens (human)
nucleus	26S proteasome regulatory subunit 6B	Homo sapiens (human)
nucleoplasm	26S proteasome regulatory subunit 6B	Homo sapiens (human)
cytosol	26S proteasome regulatory subunit 6B	Homo sapiens (human)
membrane	26S proteasome regulatory subunit 6B	Homo sapiens (human)
inclusion body	26S proteasome regulatory subunit 6B	Homo sapiens (human)
synapse	26S proteasome regulatory subunit 6B	Homo sapiens (human)
proteasome accessory complex	26S proteasome regulatory subunit 6B	Homo sapiens (human)
cytosolic proteasome complex	26S proteasome regulatory subunit 6B	Homo sapiens (human)
proteasome regulatory particle, base subcomplex	26S proteasome regulatory subunit 6B	Homo sapiens (human)
proteasome complex	26S proteasome non-ATPase regulatory subunit 8	Homo sapiens (human)
nucleus	26S proteasome non-ATPase regulatory subunit 8	Homo sapiens (human)
nucleoplasm	26S proteasome non-ATPase regulatory subunit 8	Homo sapiens (human)
cytosol	26S proteasome non-ATPase regulatory subunit 8	Homo sapiens (human)
proteasome regulatory particle	26S proteasome non-ATPase regulatory subunit 8	Homo sapiens (human)
proteasome regulatory particle, lid subcomplex	26S proteasome non-ATPase regulatory subunit 8	Homo sapiens (human)
proteasome accessory complex	26S proteasome non-ATPase regulatory subunit 8	Homo sapiens (human)
nucleus	26S proteasome non-ATPase regulatory subunit 8	Homo sapiens (human)
nucleus	Proteasome subunit beta type-3	Homo sapiens (human)
cytoplasm	Proteasome subunit beta type-3	Homo sapiens (human)
proteasome complex	Proteasome subunit beta type-3	Homo sapiens (human)
nucleus	Proteasome subunit beta type-3	Homo sapiens (human)
nucleoplasm	Proteasome subunit beta type-3	Homo sapiens (human)
cytosol	Proteasome subunit beta type-3	Homo sapiens (human)
extracellular exosome	Proteasome subunit beta type-3	Homo sapiens (human)
proteasome core complex	Proteasome subunit beta type-3	Homo sapiens (human)
proteasome core complex, beta-subunit complex	Proteasome subunit beta type-3	Homo sapiens (human)
cytosol	Proteasome subunit beta type-3	Homo sapiens (human)
nucleus	Proteasome subunit beta type-2	Homo sapiens (human)
cytoplasm	Proteasome subunit beta type-2	Homo sapiens (human)
proteasome complex	Proteasome subunit beta type-2	Homo sapiens (human)
nucleus	Proteasome subunit beta type-2	Homo sapiens (human)
nucleoplasm	Proteasome subunit beta type-2	Homo sapiens (human)
cytosol	Proteasome subunit beta type-2	Homo sapiens (human)
membrane	Proteasome subunit beta type-2	Homo sapiens (human)
extracellular exosome	Proteasome subunit beta type-2	Homo sapiens (human)
proteasome core complex	Proteasome subunit beta type-2	Homo sapiens (human)
proteasome core complex, beta-subunit complex	Proteasome subunit beta type-2	Homo sapiens (human)
cytosol	Proteasome subunit beta type-2	Homo sapiens (human)
proteasome complex	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
extracellular region	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
nucleus	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
nucleoplasm	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
cytosol	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
membrane	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
secretory granule lumen	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
extracellular exosome	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
ficolin-1-rich granule lumen	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
proteasome regulatory particle	26S proteasome non-ATPase regulatory subunit 7	Homo sapiens (human)
proteasome complex	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)
nucleoplasm	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)
cytosol	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)
proteasome accessory complex	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)
proteasome regulatory particle, base subcomplex	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)
nucleus	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)
cytosol	26S proteasome non-ATPase regulatory subunit 4	Homo sapiens (human)
nucleoplasm	26S proteasome complex subunit SEM1	Homo sapiens (human)
cytosol	26S proteasome complex subunit SEM1	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-6	Homo sapiens (human)
cytoplasm	Proteasome subunit alpha type-6	Homo sapiens (human)
proteasome complex	Proteasome subunit alpha type-6	Homo sapiens (human)
P-body	Proteasome subunit alpha type-6	Homo sapiens (human)
nucleus	Proteasome subunit alpha type-6	Homo sapiens (human)
nucleoplasm	Proteasome subunit alpha type-6	Homo sapiens (human)
cytosol	Proteasome subunit alpha type-6	Homo sapiens (human)
ribosome	Proteasome subunit alpha type-6	Homo sapiens (human)
nuclear matrix	Proteasome subunit alpha type-6	Homo sapiens (human)
myofibril	Proteasome subunit alpha type-6	Homo sapiens (human)
sarcomere	Proteasome subunit alpha type-6	Homo sapiens (human)
extracellular exosome	Proteasome subunit alpha type-6	Homo sapiens (human)
proteasome core complex	Proteasome subunit alpha type-6	Homo sapiens (human)
proteasome core complex, alpha-subunit complex	Proteasome subunit alpha type-6	Homo sapiens (human)
proteasome complex	26S proteasome regulatory subunit 4	Homo sapiens (human)
nucleus	26S proteasome regulatory subunit 4	Homo sapiens (human)
nucleoplasm	26S proteasome regulatory subunit 4	Homo sapiens (human)
cytosol	26S proteasome regulatory subunit 4	Homo sapiens (human)
membrane	26S proteasome regulatory subunit 4	Homo sapiens (human)
proteasome accessory complex	26S proteasome regulatory subunit 4	Homo sapiens (human)
proteasome regulatory particle, base subcomplex	26S proteasome regulatory subunit 4	Homo sapiens (human)
proteasome complex	26S proteasome regulatory subunit 8	Homo sapiens (human)
nucleus	26S proteasome regulatory subunit 8	Homo sapiens (human)
nucleoplasm	26S proteasome regulatory subunit 8	Homo sapiens (human)
cytoplasm	26S proteasome regulatory subunit 8	Homo sapiens (human)
cytosol	26S proteasome regulatory subunit 8	Homo sapiens (human)
membrane	26S proteasome regulatory subunit 8	Homo sapiens (human)
cytoplasmic vesicle	26S proteasome regulatory subunit 8	Homo sapiens (human)

Bioassays (979)

Assay ID	Title	Year	Journal	Article
AID1347139	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D viability screen for TC32 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1296008	Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening	2020	SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1	Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347141	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D viability screen for RD cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346986	P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347136	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D viability screen for SJ-GBM2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347159	Primary screen GU Rhodamine qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347137	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D viability screen for Daoy cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346987	P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347138	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D caspase screen for TC32 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347140	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D viability screen for MG 63 (6-TG R) cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347135	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D viability screen for SK-N-SH cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347160	Primary screen NINDS Rhodamine qHTS for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID686947	qHTS for small molecule inhibitors of Yes1 kinase: Primary Screen	2013	Bioorganic & medicinal chemistry letters, Aug-01, Volume: 23, Issue:15	Identification of potent Yes1 kinase inhibitors using a library screening approach.
AID706484	Effect on 20S proteasome subunit beta5 chymotrypsin-like activity in human THP1 cells at 30 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID316573	Inhibition of human TACE at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1396603	Inhibition of trypsin-like activity of human 20S proteasome	2018	Bioorganic & medicinal chemistry, 08-07, Volume: 26, Issue:14	Design, synthesis, in vitro and in vivo evaluation, and structure-activity relationship (SAR) discussion of novel dipeptidyl boronic acid proteasome inhibitors as orally available anti-cancer agents for the treatment of multiple myeloma and mechanism stud
AID1156396	Growth inhibition of human OVCAR5 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID661296	Inhibition of rabbit 20S proteasome activity at 10 uM after 30 mins	2012	Journal of medicinal chemistry, Mar-08, Volume: 55, Issue:5	Discovery and synthesis of hydronaphthoquinones as novel proteasome inhibitors.
AID1604187	Inhibition of 20S proteasome beta 5i (unknown origin) after 1 hr by fluorescence based assay	2019	European journal of medicinal chemistry, Nov-15, Volume: 182	Immunoproteasome-selective inhibitors: An overview of recent developments as potential drugs for hematologic malignancies and autoimmune diseases.
AID1197979	Inhibition of USP18 (unknown origin) expressed in human A549 cells coexpressing ISG15-GFP assessed as reduction in free GFP at 25 to 100 uM after 24 hrs by immunoblot assay	2015	Journal of medicinal chemistry, Feb-26, Volume: 58, Issue:4	Synthesis, characterization, and optimization for in vivo delivery of a nonselective isopeptidase inhibitor as new antineoplastic agent.
AID706487	Effect on 20S proteasome subunit beta5 expression in human SW1573 cells at 30 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1687103	Inhibition of Plasmodium falciparum 20S proteasome beta 5 subunit chymotrypsin-like activity using fluorogenic peptide Ac-WLA-AMC as substrate in presence of PA28alpha incubated for 1 to 2 hrs by fluorescence microplate reader assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1312156	Inhibition of Cryptococcus neoformans beta-carbonic anhydrase preincubated for 15 mins by stopped-flow CO2 hydration assay	2016	Bioorganic & medicinal chemistry, 09-15, Volume: 24, Issue:18	Bortezomib inhibits bacterial and fungal β-carbonic anhydrases.
AID1506374	Antiproliferative activity against human multiple myeloma cancer stem cells after 72 hrs by MTT assay	2017	MedChemComm, Jan-01, Volume: 8, Issue:1	Withaferin A induces cell death and differentiation in multiple myeloma cancer stem cells.
AID497570	Inhibition of trypsin like proteolytic activity of rabbit 26S proteasome	2010	Bioorganic & medicinal chemistry, Aug-01, Volume: 18, Issue:15	Synthesis and biological evaluation of naphthoquinone analogs as a novel class of proteasome inhibitors.
AID397960	Cytotoxicity against human U266 cells after 72 hrs by MTT assay	2009	Journal of medicinal chemistry, Jul-23, Volume: 52, Issue:14	Design, synthesis, biological evaluation, and structure-activity relationship (SAR) discussion of dipeptidyl boronate proteasome inhibitors, part I: comprehensive understanding of the SAR of alpha-amino acid boronates.
AID496353	Induction of IL-5 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 1day by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1156370	Growth inhibition of human NCI-H522 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID625282	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID316538	Inhibition of human cathepsin S at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1687104	Inhibition of Plasmodium falciparum 20S proteasome beta 1 subunit caspase-like activity using fluorogenic peptide Ac-nLPnLD-AMC as substrate in presence of PA28alpha incubated for 1 to 2 hrs by fluorescence microplate reader assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1667214	Inhibition of human SET7 overexpressed in Escherichia coli BL21 (DE3) cells at 25 uM preincubated for 15 mins followed by addition of SAM as substrate and biotinylated Histone H3 (1-50) peptide measured after 30 mins by AlphaLISA assay relative to control	2020	Bioorganic & medicinal chemistry, 04-01, Volume: 28, Issue:7	Computational discovery and biological evaluation of novel inhibitors targeting histone-lysine N-methyltransferase SET7.
AID1459659	Apparent volume of distribution in Sprague-Dawley rat at 0.8 mg/kg, iv administered as bolus	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1576794	Cytotoxicity against anti-CD3/CD28-stimulated human CD4-positive T cells with CRISP/CAS9 20S proteasome beta 5c knockout assessed as reduction in cell viability measured on day 8 by CellTiter Glo assay relative to control	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID211777	Inhibitory activity against thrombin	1998	Bioorganic & medicinal chemistry letters, Feb-17, Volume: 8, Issue:4	Potent and selective inhibitors of the proteasome: dipeptidyl boronic acids.
AID1128235	Inhibition of beta5i subunit of immunoproteasome (unknown origin) by active-site ELISA	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID1624028	Inhibition of human 20s proteasome subunit beta2 caspase-like activity using Z-LLE-AMC as substrate preincubated for 15 mins followed by substrate addition	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Covalent docking modelling-based discovery of tripeptidyl epoxyketone proteasome inhibitors composed of aliphatic-heterocycles.
AID1674999	Antiinflammatory activity against mouse RAW264.7 cells assessed as inhibition of TNFalpha-stimulated NF-kappaB activation by luciferase assay	2020	Bioorganic & medicinal chemistry letters, 09-01, Volume: 30, Issue:17	Synthesis and evaluation of 1,2,4-oxadiazole derivatives as potential anti-inflammatory agents by inhibiting NF-κB signaling pathway in LPS-stimulated RAW 264.7 cells.
AID1459655	Toxicity in human Bel7404 cells xenografted BALB/c mouse assessed as mortality at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 20 and 24 during compound dosing	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID496363	Induction of IFN-gamma gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 3 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID706501	Effect on PSMB5 mRNA expression in human Jurkat-B cells expressing PSMB5 C323T mutant at 1000 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID316516	Half life in CD1 mouse at 0.8 mg/kg, iv	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1156384	Growth inhibition of human LOXIMVI cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1295429	Inhibition of chymotrypsin like activity of human 20S proteasome using Suc-Leu-Leu-Val-Tyr-AMC as substrate preincubated for 10 mins followed by substrate addition measured after 1 hr by spectrofluorimetric analysis	2016	Bioorganic & medicinal chemistry, 06-01, Volume: 24, Issue:11	3D-QSAR-aided design, synthesis, in vitro and in vivo evaluation of dipeptidyl boronic acid proteasome inhibitors and mechanism studies.
AID516392	Inhibition of trypsin like activity of partially purified human proteasome	2010	Bioorganic & medicinal chemistry letters, Oct-01, Volume: 20, Issue:19	Structure-activity relationship of boronic acid derivatives of tyropeptin: proteasome inhibitors.
AID1252357	Antiproliferative activity against human CCRF-CEM cells after 72 hrs by oxyluciferin luminescence assay	2015	Bioorganic & medicinal chemistry letters, Nov-01, Volume: 25, Issue:21	Structure-activity relationship study of syringolin A as a potential anticancer agent.
AID548702	Cytotoxicity against human SKOV3 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID397956	Cytotoxicity against human KB cells after 72 hrs by MTT assay	2009	Journal of medicinal chemistry, Jul-23, Volume: 52, Issue:14	Design, synthesis, biological evaluation, and structure-activity relationship (SAR) discussion of dipeptidyl boronate proteasome inhibitors, part I: comprehensive understanding of the SAR of alpha-amino acid boronates.
AID516389	Cytotoxicity against human RPMI8226 cells	2010	Bioorganic & medicinal chemistry letters, Oct-01, Volume: 20, Issue:19	Structure-activity relationship of boronic acid derivatives of tyropeptin: proteasome inhibitors.
AID706506	Effect on PSMB5 mRNA expression in human THP1 cells at 30 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1674412	Inhibition of chymotrypsin-like activity of Leishmania tarentolae proteasome beta 5 Y113F mutant	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery and Characterization of Clinical Candidate LXE408 as a Kinetoplastid-Selective Proteasome Inhibitor for the Treatment of Leishmaniases.
AID1918919	Antiproliferative activity against human RPMI-8226 cells assessed as inhibition of cell proliferation incubated for 72 hrs by XTT assay	2022	Journal of natural products, 12-23, Volume: 85, Issue:12	Isolation and Structure Elucidation of Compounds from
AID316553	Inhibition of human MMP12 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID496347	Induction of TNFbeta gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 3 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID496367	Induction of IL-2 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 3 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID640522	Cytotoxicity against human WM266.4 cells after 72 hrs by ATPlite assay	2012	Bioorganic & medicinal chemistry, Jan-15, Volume: 20, Issue:2	Semisynthetic neoboutomellerone derivatives as ubiquitin-proteasome pathway inhibitors.
AID625292	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625279	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1604185	Inhibition of 20S proteasome beta 2i (unknown origin) after 1 hr by fluorescence based assay	2019	European journal of medicinal chemistry, Nov-15, Volume: 182	Immunoproteasome-selective inhibitors: An overview of recent developments as potential drugs for hematologic malignancies and autoimmune diseases.
AID1325790	Inhibition of 26S proteasome in human MDA-MB-468 cells assessed as accumulation of high molecular weight polyubiquitin-conjugated proteins at 35 nM after 4 hrs by Western blot analysis
AID316567	Inhibition of human thrombin at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1548290	Induction of apoptosis in bortezomib resistant human KM3/BTZ cells assessed as late apoptotic cells level at 200 nM incubated for 24 hrs by Annexin V-FITC/PI staining based FCAS analysis (Rvb = 0.38%)
AID316574	Metabolic stability in mouse liver microsomes	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1473739	Inhibition of human MRP2 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay	2013	Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1	A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID316540	Inhibition of human chymase at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID611896	Cytotoxicity against human HEK293 cells after 24 hrs by MTT assay	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Chemical and biological evaluation of dipeptidyl boronic acid proteasome inhibitors for use in prodrugs and pro-soft drugs targeting solid tumors.
AID1623367	Cell cycle arrest in human RPMI8226 cells assessed as accumulation at S phase at 3 nM after 48 hrs by propidium iodide/RNase staining based flow cytometric method	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID1473738	Inhibition of human BSEP overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-taurocholate in presence of ATP measured after 15 to 20 mins by membrane vesicle transport assay	2013	Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1	A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID761482	Cytotoxicity against wild type human THP1 cells assessed as cell viability at 0.5 uM after 72 hrs by MTS assay relative to vehicle-treated control	2013	Journal of medicinal chemistry, Jul-25, Volume: 56, Issue:14	Inhibition of the human proteasome by imidazoline scaffolds.
AID734744	Induction of apoptosis in human HCT116 cells assessed as induction of PARP cleavage by Western blotting analysis	2013	Journal of medicinal chemistry, May-09, Volume: 56, Issue:9	Potent proteasome inhibitors derived from the unnatural cis-cyclopropane isomer of Belactosin A: synthesis, biological activity, and mode of action.
AID1299914	Inhibition of chymotrypsin (unknown origin) using Suc-LLVY-AMC as substrate at 100 uM by fluorometric assay	2016	ACS medicinal chemistry letters, Mar-10, Volume: 7, Issue:3	Synthesis and Evaluation of Macrocyclic Peptide Aldehydes as Potent and Selective Inhibitors of the 20S Proteasome.
AID658060	Inhibition of chymotrypsin-like activity of human liver 26S proteasome using Suc-LLVY-AMC substrate	2012	Bioorganic & medicinal chemistry letters, May-15, Volume: 22, Issue:10	Serendipity in discovery of proteasome inhibitors.
AID1623366	Cell cycle arrest in human RPMI8226 cells assessed as accumulation at G0/G1 phase at 3 nM after 48 hrs by propidium iodide/RNase staining based flow cytometric method	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID1128241	Cell cycle arrest in human HCT116 cells assessed as accumulation at G2/M phase at 100 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 19.1%)	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID1548243	Inhibition of human proteasome pre-incubated for 30 mins before Suc-LLVY-AMC substrate addition and measured after 120 mins by fluorescence based assay
AID599472	Cell cycle arrest in human HeLa cells assessed as accumulation at S phase at 0.1 uM after 24 hrs by flow cytometry (Rvb = 30 +/- 0.46%)	2009	Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12	Synthesis and biological evaluation of boron peptide analogues of Belactosin C as proteasome inhibitors.
AID496324	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as serum HBeAg level at 5 mg/kg, iv single dose after 24 hrs by ELISA	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID516390	Inhibition of chymotrypsin like activity of partially purified human proteasome	2010	Bioorganic & medicinal chemistry letters, Oct-01, Volume: 20, Issue:19	Structure-activity relationship of boronic acid derivatives of tyropeptin: proteasome inhibitors.
AID548705	Cytotoxicity against human RPMI18226 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1325787	Cytotoxicity against human LCL cells harboring wild type p53 assessed as reduction in cell viability after 48 hrs by 7AAD-staining based FACS analysis
AID1382150	Inhibition of chymotrypsin-like activity of human 26S proteasome using Suc-LLVY-MCA as substrate measured for 1 hr by fluorescence assay	2018	European journal of medicinal chemistry, Feb-25, Volume: 146	Ridaifen-F conjugated with cell-penetrating peptides inhibits intracellular proteasome activities and induces drug-resistant cell death.
AID1459698	Toxicity in human Bel7404 cells xenografted BALB/c mouse assessed as effect on body weight at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 17 of compound dosing (Rvb = 26.29 +/- 1.03 g)	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1687134	Inhibition of human 20S constitutive proteasome beta 5 subunit assessed as inhibition of BMV037 probe labeling at 1 to 10 uM incubated for 1 hr by SDS-PAGE analysis	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1459638	Antiproliferative activity against human HepG2 cells after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID459676	Tmax in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID496335	Induction of TGTP gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 24 hrs by RT- PCR	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID452104	Cytotoxicity against human BxPC3 cells after 72 hrs by MTT assay	2009	Bioorganic & medicinal chemistry, Oct-01, Volume: 17, Issue:19	Design, synthesis and biological evaluation of tripeptide boronic acid proteasome inhibitors.
AID459681	Volume of distribution in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1623397	Induction of apoptosis in human RPMI8226 cells assessed as late apoptotic cells at 3 nM after 48 hrs by Annexin-V/propidium iodide staining based flow cytometric method (Rvb = 0.21%)	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID548707	Cmax in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1604183	Inhibition of 20S proteasome beta 1i (unknown origin) after 1 hr by fluorescence based assay	2019	European journal of medicinal chemistry, Nov-15, Volume: 182	Immunoproteasome-selective inhibitors: An overview of recent developments as potential drugs for hematologic malignancies and autoimmune diseases.
AID1548267	Induction of cell cycle arrest in human KM3 cells assessed as reduction in cell cycle progression in S phase at 100 nM incubated for 24 hrs by propidium iodide staining based flow cytometry
AID526653	Inhibition of proteasome	2010	Journal of medicinal chemistry, Oct-14, Volume: 53, Issue:19	Toward the development of innovative bifunctional agents to induce differentiation and to promote apoptosis in leukemia: clinical candidates and perspectives.
AID496366	Induction of IL-2 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 2 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID661298	Irreversible inhibition of rabbit 20S proteasome activity at 10 uM after 30 mins measured after 4 hrs of dialysis	2012	Journal of medicinal chemistry, Mar-08, Volume: 55, Issue:5	Discovery and synthesis of hydronaphthoquinones as novel proteasome inhibitors.
AID625285	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1459677	Antitumor activity against human Bel7404 cells xenografted in BALB/c nude mouse assessed as effect on tumor volume at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 20 of compound dosing relative to control	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1548286	Induction of apoptosis in bortezomib resistant human KM3/BTZ cells assessed as late apoptotic cells level at 50 nM incubated for 24 hrs by Annexin V-FITC/PI staining based FCAS analysis (Rvb = 0.38%)
AID588211	Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans	2010	Chemical research in toxicology, Jan, Volume: 23, Issue:1	Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1250152	Cytotoxicity against human Glioma cells (HF2885) after 72 hrs by CelltiterGlo assay	2015	ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8	High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1156393	Growth inhibition of human IGROV1 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID588212	Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents	2010	Chemical research in toxicology, Jan, Volume: 23, Issue:1	Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1312155	Inhibition of Candida glabrata beta-carbonic anhydrase preincubated for 15 mins by stopped-flow CO2 hydration assay	2016	Bioorganic & medicinal chemistry, 09-15, Volume: 24, Issue:18	Bortezomib inhibits bacterial and fungal β-carbonic anhydrases.
AID1576778	Selectivity ratio, ratio of IC50 for 20S proteasome beta 5c (unknown origin) to IC50 for human 20S proteasome beta 1i	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID1128515	Inhibition of bovine pancreatic alpha-chymotrypsin activity assessed as Suc-Leu-Leu-Val-Tyr-AMC substrate hydrolysis after 10 mins	2014	European journal of medicinal chemistry, Apr-09, Volume: 76	Identification of a new series of amides as non-covalent proteasome inhibitors.
AID496355	Induction of IL-5 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 3 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID548700	Cytotoxicity against human A549 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1404704	Cytotoxicity against human HepG2 cells after 48 hrs by CellTiter-Glo assay	2018	European journal of medicinal chemistry, Jun-25, Volume: 154	Enhanced antimalarial activity of plasmepsin V inhibitors by modification of the P
AID1439188	Antiproliferative activity against human A2780 cells after 72 hrs by SRB assay	2017	European journal of medicinal chemistry, Mar-10, Volume: 128	Design, synthesis and biological evaluation of novel non-peptide boronic acid derivatives as proteasome inhibitors.
AID1363818	Cytotoxicity against human PBMC after 72 hrs by CellTiter-Glo luminescent cell viability assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Discovery of the First-in-Class Dual Histone Deacetylase-Proteasome Inhibitor.
AID1156394	Growth inhibition of human OVCAR3 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1156383	Growth inhibition of human U251 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID734753	Inhibition of caspase-like activity of human 20S proteasome beta 1 subunit using Ac-nLPnLD-AMC as substrate after 60 mins by fluorescence assay	2013	Journal of medicinal chemistry, May-09, Volume: 56, Issue:9	Potent proteasome inhibitors derived from the unnatural cis-cyclopropane isomer of Belactosin A: synthesis, biological activity, and mode of action.
AID496317	Toxicity in 1.3.32 transgenic mouse assessed as serum alanine aminotransferase level liver at 1 mg/kg, iv after 6 days by Northern blot analysis	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1128236	Inhibition of recombinant cathepsin A (unknown origin) using Mca-Arg-Pro-Pro-Gly-Phe-Ser-Ala-Phe-Lys(Dnp)-OH as substrate incubated with enzyme for 5 mins prior to substrate challenge for 2 hrs by spectrofluorometer analysis	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID1687106	Inhibition of human 20S constitutive proteasome beta 2 subunit trypsin-like activity using fluorogenic peptide Ac-WLR-AMC as substrate in presence of PA28alpha incubated for 1 to 2 hrs by fluorescence microplate reader assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID459673	Toxicity against zebrafish embryo assessed as embryo death at 10 umol after 24 hrs	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID706488	Effect on 20S proteasome subunit beta5 expression in human A549 cells at 100 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID459690	Oral bioavailability in Sprague-Dawley rat	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1576786	Cytotoxicity against human plasmablasts assessed as reduction in cell viability by CellTiter Glo assay	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID316530	Inhibition of human cathepsin B at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1459640	Antiproliferative activity against human A549 cells after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1548271	Induction of cell cycle arrest in human RPMI8226 cells assessed as accumulation at G1 phase at 100 nM incubated for 24 hrs by propidium iodide staining based flow cytometry (Rvb = 48.6%)
AID1689695	Inhibition of HDAC6 in human RPMI-8226 cells incubated for 2 hrs by ELISA	2020	European journal of medicinal chemistry, Mar-01, Volume: 189	1,2,3-Triazole-Chalcone hybrids: Synthesis, in vitro cytotoxic activity and mechanistic investigation of apoptosis induction in multiple myeloma RPMI-8226.
AID316552	Inhibition of human MMP8 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID316517	AUC (0 to infinity) in CD1 mouse at 0.8 mg/kg, iv	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID640520	Inhibition of peptide-glutamyl-peptide-hydrolyzing activity of 20S proteasome in human DLD1 cells transfected with 4Ub-Luc gene using Z-Leu-Leu-Glu-AMC as substrate after 6 hrs by spectrofluorometric analysis	2012	Bioorganic & medicinal chemistry, Jan-15, Volume: 20, Issue:2	Semisynthetic neoboutomellerone derivatives as ubiquitin-proteasome pathway inhibitors.
AID526555	Inhibition of human calpain 1 at 100 uM	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID1460776	Inhibition of mouse CA15 by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID459670	Cytotoxicity against human HL60 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1548264	Antiproliferative activity against human HET-1A cells incubated for 48 hrs by MTT assay
AID316580	Protein binding in dog plasma	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1459644	Antiproliferative activity against human Bel7404 cells after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID496341	Induction of TNFalpha gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 1day by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID316545	Inhibition of human factor 10a at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID316563	Inhibition of pig pepsin at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1439187	Antiproliferative activity against human MDA-MB-231 cells after 72 hrs by SRB assay	2017	European journal of medicinal chemistry, Mar-10, Volume: 128	Design, synthesis and biological evaluation of novel non-peptide boronic acid derivatives as proteasome inhibitors.
AID496343	Induction of TNFalpha gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 3 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1266947	Antitumor activity against human A549 cells xenografted in nude SCID beige mouse assessed as tumor growth inhibition at 1 mg/kg, iv administered twice per week	2015	Journal of medicinal chemistry, Dec-24, Volume: 58, Issue:24	Discovery of a First-in-Class, Potent, Selective, and Orally Bioavailable Inhibitor of the p97 AAA ATPase (CB-5083).
AID316568	Inhibition of human TPA at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID658061	Inhibition of chymotrypsin-like activity of 26S proteasome in human Molt4 cells using MeOSuc-Phe-Leu-Phe-AFC substrate	2012	Bioorganic & medicinal chemistry letters, May-15, Volume: 22, Issue:10	Serendipity in discovery of proteasome inhibitors.
AID1325772	Inhibition of caspase like activity of rabbit 20S proteasome using Ac-nLPnLD-AMC as substrate preincubated for 15 mins followed by substrate addition measured after 2 hrs by fluorescence-based assay
AID1548288	Induction of apoptosis in bortezomib resistant human KM3/BTZ cells assessed as viable cells level at 200 nM incubated for 24 hrs by Annexin V-FITC/PI staining based FCAS analysis (Rvb = 98.1%)
AID1623360	Cell cycle arrest in human NCI-H929 cells assessed as accumulation at S phase at 2 nM after 48 hrs by propidium iodide/RNase staining based flow cytometric method relative to control	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID1473266	Toxicity in nude mouse xenografted with human RPMI8226 cells assessed as death at 1 mg/kg, iv or ip administered once in week for 35 days	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID496319	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as inhibition of HBV DNA replication at 5 mg/kg, iv single dose after 24 hrs by Southern blot analysis	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1252355	Antiproliferative activity against human RKO cells after 72 hrs by oxyluciferin luminescence assay	2015	Bioorganic & medicinal chemistry letters, Nov-01, Volume: 25, Issue:21	Structure-activity relationship study of syringolin A as a potential anticancer agent.
AID459683	Tmax in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1372748	Inhibition of immunoproteasome caspase-like activity in human erythrocytes using Z-LRR-Glo as substrate pretreated for 2 hrs followed by substrate addition measured after 10 mins by luminescence assay	2018	Bioorganic & medicinal chemistry, 01-15, Volume: 26, Issue:2	Immunoproteasome inhibition and bioactivity of thiasyrbactins.
AID706725	Resistance factor, ratio of IC50 for human Jurkat B cells harboring proteosome subunit beta5 A49V mutant to IC50 for wild type human Jurkat cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1252353	Antiproliferative activity against human A431 cells after 72 hrs by oxyluciferin luminescence assay	2015	Bioorganic & medicinal chemistry letters, Nov-01, Volume: 25, Issue:21	Structure-activity relationship study of syringolin A as a potential anticancer agent.
AID625281	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID548714	Cmax in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1325784	Cytotoxicity against human MCF10A cells harboring wild type p53 assessed as reduction in cell viability after 48 hrs by 7AAD-staining based FACS analysis
AID1325786	Cytotoxicity against HNDF cells harboring wild type p53 assessed as reduction in cell viability after 48 hrs by 7AAD-staining based FACS analysis
AID496340	Toxicity in HBV infected 1.3.32 transgenic mouse liver assessed as hepatitis at 5 mg/kg, iv single dose after 24 hrs by rotine immunohistochemistry method	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1156388	Growth inhibition of human SK-MEL-2 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1548272	Induction of cell cycle arrest in human RPMI8226 cells assessed as accumulation at S phase at 100 nM incubated for 24 hrs by propidium iodide staining based flow cytometry (Rvb = 27.6%)
AID1374298	Inhibition of chymotrypsin-like activity of human 20S proteasome at 10 nM using Suc-Leu-Leu-Val-Tyr-AMC as substrate by fluorescence assay relative to control	2018	Bioorganic & medicinal chemistry, 03-01, Volume: 26, Issue:5	Novel aromatic sulfonyl naphthalene-based boronates as 20S proteasome inhibitors.
AID1623399	Induction of apoptosis in human RPMI8226 cells assessed as viable cells at 3 nM after 48 hrs by Annexin-V/propidium iodide staining based flow cytometric method (Rvb = 98.7%)	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID1459967	Toxicity in human RPMI8226 cells xenografted in athymic mouse assessed as mortality at 1 mg/kg, ip administered once in a week	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	3-Aroylindoles display antitumor activity in vitro and in vivo: Effects of N1-substituents on biological activity.
AID734745	Inhibition of proteasome in human HCT116 cells assessed as accumulation of p53 by Western blotting analysis	2013	Journal of medicinal chemistry, May-09, Volume: 56, Issue:9	Potent proteasome inhibitors derived from the unnatural cis-cyclopropane isomer of Belactosin A: synthesis, biological activity, and mode of action.
AID1459656	Inhibition of trypsin-like activity of 20S proteasome in human HL60 cells using Z-LRRaminoluciferin as substrate after 2 hrs by fluorescence analysis	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID526553	Inhibition of tissue plasminogen activator at 100 uM	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID316559	Inhibition of human caspase 9 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID452100	Inhibition of peptidylglutamyl peptide-hydrolyzing activity of mouse liver 20S proteasome	2009	Bioorganic & medicinal chemistry, Oct-01, Volume: 17, Issue:19	Design, synthesis and biological evaluation of tripeptide boronic acid proteasome inhibitors.
AID1605100	Cytotoxicity in human HeLa cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay	2020	Journal of medicinal chemistry, 03-26, Volume: 63, Issue:6	Discovery of Novel Peptidomimetic Boronate ClpP Inhibitors with Noncanonical Enzyme Mechanism as Potent Virulence Blockers
AID1141827	Cytotoxic activity against human NCI-H929 cells after 72 hrs by MTS assay	2014	Bioorganic & medicinal chemistry, Jun-01, Volume: 22, Issue:11	Design, synthesis and biological evaluation of novel tripeptidyl epoxyketone derivatives constructed from β-amino acid as proteasome inhibitors.
AID497569	Inhibition of chymotrypsin like proteolytic activity of rabbit 26S proteasome	2010	Bioorganic & medicinal chemistry, Aug-01, Volume: 18, Issue:15	Synthesis and biological evaluation of naphthoquinone analogs as a novel class of proteasome inhibitors.
AID1687110	Inhibition of human 20S immunoproteasome beta 5 subunit chymotrypsin-like activity using fluorogenic peptide Ac-WLA-AMC as substrate in presence of PA28alpha incubated for 1 to 2 hrs by fluorescence microplate reader assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1396602	Inhibition of caspase-like activity of human 20S proteasome	2018	Bioorganic & medicinal chemistry, 08-07, Volume: 26, Issue:14	Design, synthesis, in vitro and in vivo evaluation, and structure-activity relationship (SAR) discussion of novel dipeptidyl boronic acid proteasome inhibitors as orally available anti-cancer agents for the treatment of multiple myeloma and mechanism stud
AID316572	Inhibition of pig pancreatic elastase 1 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1156364	Growth inhibition of human HOP62 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1443490	Inhibition of caspase like activity of 26S proteasome derived from human MDA-MB-231 cells at 1 uM	2017	Journal of medicinal chemistry, 04-13, Volume: 60, Issue:7	First Bispecific Inhibitors of the Epidermal Growth Factor Receptor Kinase and the NF-κB Activity As Novel Anticancer Agents.
AID1439185	Antiproliferative activity against human HL60 cells after 72 hrs by SRB assay	2017	European journal of medicinal chemistry, Mar-10, Volume: 128	Design, synthesis and biological evaluation of novel non-peptide boronic acid derivatives as proteasome inhibitors.
AID1128238	Inhibition of recombinant cathepsin G (unknown origin) using Suc-Ala-Ala-Pro-Phe-AMC as substrate by spectrofluorometer analysis	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID1197985	Induction of cell death in human A549 cells assessed as accumulation of poly-ubiquitinated proteins at 0.025 to 0.5 uM after 24 hrs by immunoblot assay	2015	Journal of medicinal chemistry, Feb-26, Volume: 58, Issue:4	Synthesis, characterization, and optimization for in vivo delivery of a nonselective isopeptidase inhibitor as new antineoplastic agent.
AID48219	Inhibitory activity against human cathepsin G	1998	Bioorganic & medicinal chemistry letters, Feb-17, Volume: 8, Issue:4	Potent and selective inhibitors of the proteasome: dipeptidyl boronic acids.
AID496368	Induction of IL-2 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 6 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1613999	Inhibition of human hepatic cell derived 20s constitutive proteasome beta1 caspase-like activity using Suc-LLE-AMC as substrate preincubated for 15 mins followed by substrate addition and measured after 60 mins by fluorescence assay	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Exploration of novel macrocyclic dipeptide N-benzyl amides as proteasome inhibitors.
AID700313	Resistance ratio of IC50 for human bortezomib-resistant GUMBUS cells to IC50 for human GUMBUS cells	2012	Bioorganic & medicinal chemistry letters, Nov-01, Volume: 22, Issue:21	Identification of a glutathione peroxidase inhibitor that reverses resistance to anticancer drugs in human B-cell lymphoma cell lines.
AID1506375	Antiproliferative activity against human RPMI18226 cells after 72 hrs by XTT assay	2017	MedChemComm, Jan-01, Volume: 8, Issue:1	Withaferin A induces cell death and differentiation in multiple myeloma cancer stem cells.
AID1895435	Inhibition of human 20S immunoproteasome beta-1i subunit using (Ac-PAL)2R110 as substrate preincubated for 2 hrs followed by substrate addition and measured after 1 hr by fluorescence intensity assay	2021	Journal of medicinal chemistry, 07-22, Volume: 64, Issue:14	Structure-Based Optimization and Discovery of M3258, a Specific Inhibitor of the Immunoproteasome Subunit LMP7 (β5i).
AID459665	Cytotoxicity against human SW480 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID526417	Inhibition of human cathepsin B at 100uM	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID316577	Metabolic stability in human liver microsomes	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1459671	Antitumor activity against human Bel7404 cells xenografted in BALB/c nude mouse assessed as effect on tumor volume at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 13 of compound dosing relative to control	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1460773	Inhibition of human CA12 by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID316561	Inhibition of human ECE1 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID496312	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as expression of 3.5 and 2.1 kb HBV mRNA at 1 mg/kg, iv single dose after 1 day by Northern blot analysis	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1548274	Antiproliferative activity against bortezomib resistant human KM3/BTZ cells incubated for 48 hrs by MTT assay
AID611897	Cytotoxicity against human FSCLL cells after 24 hrs by MTT assay	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Chemical and biological evaluation of dipeptidyl boronic acid proteasome inhibitors for use in prodrugs and pro-soft drugs targeting solid tumors.
AID1548289	Induction of apoptosis in bortezomib resistant human KM3/BTZ cells assessed as early apoptotic cells level at 200 nM incubated for 24 hrs by Annexin V-FITC/PI staining based FCAS analysis (Rvb = 1.39%)
AID459666	Cytotoxicity against human A549 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID625286	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID640446	Inhibition of 20S proteasome in human DLD1 cells transfected with 4Ub-Luc gene assessed as bioluminescence induction factor at 1 uM after 8 hrs by luciferase reporter gene assay relative to epoxomicin	2012	Bioorganic & medicinal chemistry, Jan-15, Volume: 20, Issue:2	Semisynthetic neoboutomellerone derivatives as ubiquitin-proteasome pathway inhibitors.
AID1459646	Antiproliferative activity against human SKOV3 cells after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID473008	Inhibition of 20S proteasome from human erythrocyte	2010	Journal of medicinal chemistry, Feb-25, Volume: 53, Issue:4	Studies of the synthesis of all stereoisomers of MG-132 proteasome inhibitors in the tumor targeting approach.
AID1382145	Inhibition of PGPH activity of human 20S proteasome using Z-LLE-MCA as substrate measured for 1 hr by fluorescence assay	2018	European journal of medicinal chemistry, Feb-25, Volume: 146	Ridaifen-F conjugated with cell-penetrating peptides inhibits intracellular proteasome activities and induces drug-resistant cell death.
AID1687131	Inhibition of 20S proteasome beta 1 subunit from bortezomib resistant Plasmodium falciparum 3D7 trophozoite infected erythrocytes assessed as inhibition of BMV037 probe labeling at 1 to 10 uM incubated for 1 hr by SDS-PAGE analysis	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1484605	Antiproliferative activity against human CEM cells after 72 hrs by calcein AM staining based fluorescence assay	2017	European journal of medicinal chemistry, Jul-28, Volume: 135	Synthesis and antiproteasomal activity of novel O-benzyl salicylamide-based inhibitors built from leucine and phenylalanine.
AID611894	Inhibition of intracellular chymotrypsin-like activity of 20S proteasome in human HEK293 cells after 24 hrs by fluorescence plate reader	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Chemical and biological evaluation of dipeptidyl boronic acid proteasome inhibitors for use in prodrugs and pro-soft drugs targeting solid tumors.
AID566539	Inhibition of proteasome activity in human HeLa cells assessed as induction of ubiquitinG76V-FL reporter level at 5 nM after 8 hrs by luciferase assay	2011	Journal of medicinal chemistry, Jan-27, Volume: 54, Issue:2	α,β-Unsaturated carbonyl system of chalcone-based derivatives is responsible for broad inhibition of proteasomal activity and preferential killing of human papilloma virus (HPV) positive cervical cancer cells.
AID1382149	Inhibition of trypsin-like activity of human 26S proteasome using Boc-LRR-MCA as substrate measured for 1 hr by fluorescence assay	2018	European journal of medicinal chemistry, Feb-25, Volume: 146	Ridaifen-F conjugated with cell-penetrating peptides inhibits intracellular proteasome activities and induces drug-resistant cell death.
AID1459645	Antiproliferative activity against human MKN45 cells after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID397957	Cytotoxicity against human HepG2 cells after 72 hrs by MTT assay	2009	Journal of medicinal chemistry, Jul-23, Volume: 52, Issue:14	Design, synthesis, biological evaluation, and structure-activity relationship (SAR) discussion of dipeptidyl boronate proteasome inhibitors, part I: comprehensive understanding of the SAR of alpha-amino acid boronates.
AID599461	Inhibition of chymotrypsin-like activity of human erythrocyte 20S proteasome using Suc-LLVY-AMC substrate incubated at 37 degC for 1 hr by fluorometric assay	2009	Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12	Synthesis and biological evaluation of boron peptide analogues of Belactosin C as proteasome inhibitors.
AID1180860	Inhibition of human 26S proteasomal catalytic subunit trypsin-like activity using Z-LRR-aminoluciferin as substrate after 4 hrs by luminescence assay	2014	Journal of medicinal chemistry, Jul-24, Volume: 57, Issue:14	Synthesis and evaluation of bisbenzylidenedioxotetrahydrothiopranones as activators of endoplasmic reticulum (ER) stress signaling pathways and apoptotic cell death in acute promyelocytic leukemic cells.
AID1291319	Cytotoxicity against human U266 cells after 72 hrs by MTS assay	2016	Bioorganic & medicinal chemistry letters, Apr-15, Volume: 26, Issue:8	Design, synthesis and docking studies of novel dipeptidyl boronic acid proteasome inhibitors constructed from αα- and αβ-amino acids.
AID1474166	Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index	2016	Drug discovery today, Apr, Volume: 21, Issue:4	DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1180857	Inhibition of human 26S proteasomal catalytic subunit trypsin-like activity using Z-LRR-aminoluciferin as substrate after 2 hrs by luminescence assay	2014	Journal of medicinal chemistry, Jul-24, Volume: 57, Issue:14	Synthesis and evaluation of bisbenzylidenedioxotetrahydrothiopranones as activators of endoplasmic reticulum (ER) stress signaling pathways and apoptotic cell death in acute promyelocytic leukemic cells.
AID1496304	Inhibition of chymotrypsin-like activity of human 20S proteasome using Suc-Leu-Leu-Val-Tyr-AMC as substrate after 1 hr by fluorescence analysis	2018	Bioorganic & medicinal chemistry letters, 07-01, Volume: 28, Issue:12	Discovery of novel 20S proteasome inhibitors by rational topology-based scaffold hopping of bortezomib.
AID1396604	Cytotoxicity against human RPMI8226 cells assessed as reduction in cell viability after 72 hrs by CellTiter 96 aqueous one solution assay	2018	Bioorganic & medicinal chemistry, 08-07, Volume: 26, Issue:14	Design, synthesis, in vitro and in vivo evaluation, and structure-activity relationship (SAR) discussion of novel dipeptidyl boronic acid proteasome inhibitors as orally available anti-cancer agents for the treatment of multiple myeloma and mechanism stud
AID316518	Volume of distribution at steady state in CD1 mouse at 0.8 mg/kg, iv	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID316548	Inhibition of human MMP1 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID548701	Cytotoxicity against human PC3 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID397959	Cytotoxicity against human HL60 cells after 72 hrs by MTT assay	2009	Journal of medicinal chemistry, Jul-23, Volume: 52, Issue:14	Design, synthesis, biological evaluation, and structure-activity relationship (SAR) discussion of dipeptidyl boronate proteasome inhibitors, part I: comprehensive understanding of the SAR of alpha-amino acid boronates.
AID316542	Inhibition of human chymotrypsin at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1312161	Inhibition of Drosophila melanogaster beta-carbonic anhydrase preincubated for 15 mins by stopped-flow CO2 hydration assay	2016	Bioorganic & medicinal chemistry, 09-15, Volume: 24, Issue:18	Bortezomib inhibits bacterial and fungal β-carbonic anhydrases.
AID640519	Inhibition of 20S proteasome in human DLD1 cells transfected with 4Ub-Luc gene assessed as bioluminescence induction factor at 0.1 uM after 8 hrs by luciferase reporter gene assay relative to epoxomicin	2012	Bioorganic & medicinal chemistry, Jan-15, Volume: 20, Issue:2	Semisynthetic neoboutomellerone derivatives as ubiquitin-proteasome pathway inhibitors.
AID1439191	Antiproliferative activity against human A549 cells after 72 hrs by SRB assay	2017	European journal of medicinal chemistry, Mar-10, Volume: 128	Design, synthesis and biological evaluation of novel non-peptide boronic acid derivatives as proteasome inhibitors.
AID459685	Mean residence time in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1605098	Inhibition of ClpP in methicillin-resistant Staphylococcus aureus ATCC 33591 assessed as reduction in bacteria-induced hemolysis of sheep erythrocytes by measuring hemoglobin release incubated for 15 mins	2020	Journal of medicinal chemistry, 03-26, Volume: 63, Issue:6	Discovery of Novel Peptidomimetic Boronate ClpP Inhibitors with Noncanonical Enzyme Mechanism as Potent Virulence Blockers
AID1312152	Inhibition of human carbonic anhydrase-1 preincubated for 15 mins by stopped-flow CO2 hydration assay	2016	Bioorganic & medicinal chemistry, 09-15, Volume: 24, Issue:18	Bortezomib inhibits bacterial and fungal β-carbonic anhydrases.
AID1459665	Antitumor activity against human Bel7404 cells xenografted in BALB/c nude mouse assessed as effect on tumor volume at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 6 of compound dosing relative to control	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1605110	Inhibition of Staphylococcus aureus ClpXP expressed in Escherichia coli BL2 (DE3) at 1 to 100 uM using FITC-casein substrate in presence of ATP-regenerating system incubated for 50 mins by fluorescence based assay	2020	Journal of medicinal chemistry, 03-26, Volume: 63, Issue:6	Discovery of Novel Peptidomimetic Boronate ClpP Inhibitors with Noncanonical Enzyme Mechanism as Potent Virulence Blockers
AID397953	Cytotoxicity against human SKOV3 cells after 72 hrs by MTT assay	2009	Journal of medicinal chemistry, Jul-23, Volume: 52, Issue:14	Design, synthesis, biological evaluation, and structure-activity relationship (SAR) discussion of dipeptidyl boronate proteasome inhibitors, part I: comprehensive understanding of the SAR of alpha-amino acid boronates.
AID1895439	Inhibition of human 20S proteasome beta2 subunit using Ac-RLR-AMC as substrate preincubated for 2 hrs followed by substrate addition and measured after 1 hr by fluorescence intensity assay	2021	Journal of medicinal chemistry, 07-22, Volume: 64, Issue:14	Structure-Based Optimization and Discovery of M3258, a Specific Inhibitor of the Immunoproteasome Subunit LMP7 (β5i).
AID516391	Inhibition of caspase like activity of partially purified human proteasome	2010	Bioorganic & medicinal chemistry letters, Oct-01, Volume: 20, Issue:19	Structure-activity relationship of boronic acid derivatives of tyropeptin: proteasome inhibitors.
AID1574454	Inhibition of deubiquitinase in HEK293T cells expressing N-terminal HA-tagged ubiquitin assessed as stabilization of HMW-Ub proteins at 1 uM after 2 hrs by Western blot analysis	2019	Bioorganic & medicinal chemistry letters, 01-15, Volume: 29, Issue:2	Diarylcarbonates are a new class of deubiquitinating enzyme inhibitor.
AID1576791	Inhibition of 20S proteasome beta 5i in human PBMC cells assessed as induction of PSMB6 expression at 100 nM after 3 to 72 hrs by RT-PCR analysis	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID1918921	Antiproliferative activity against human MM1.R cells assessed as inhibition of cell proliferation incubated for 72 hrs by XTT assay	2022	Journal of natural products, 12-23, Volume: 85, Issue:12	Isolation and Structure Elucidation of Compounds from
AID1180862	Inhibition of human 26S proteasomal catalytic subunit chymotrypsin-like activity using Suc-LLVYaminoluciferin as substrate after 4 hrs by luminescence assay	2014	Journal of medicinal chemistry, Jul-24, Volume: 57, Issue:14	Synthesis and evaluation of bisbenzylidenedioxotetrahydrothiopranones as activators of endoplasmic reticulum (ER) stress signaling pathways and apoptotic cell death in acute promyelocytic leukemic cells.
AID1548258	Antiproliferative activity against human RPMI8226 cells incubated for 48 hrs by MTT assay
AID1689694	Inhibition of HDAC8 in human RPMI-8226 cells incubated for 2 hrs by ELISA	2020	European journal of medicinal chemistry, Mar-01, Volume: 189	1,2,3-Triazole-Chalcone hybrids: Synthesis, in vitro cytotoxic activity and mechanistic investigation of apoptosis induction in multiple myeloma RPMI-8226.
AID1730988	Induction of human 20S proteosome mediated human alpha-synuclein degradation at 10 uM	2021	Bioorganic & medicinal chemistry letters, 03-15, Volume: 36	Dihydroquinazolines enhance 20S proteasome activity and induce degradation of α-synuclein, an intrinsically disordered protein associated with neurodegeneration.
AID459686	AUC (0 to t) in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID599473	Cell cycle arrest in human HeLa cells assessed as accumulation at G2/M phase at 0.1 uM after 24 hrs by flow cytometry (Rvb = 13.7 +/- 0.87%)	2009	Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12	Synthesis and biological evaluation of boron peptide analogues of Belactosin C as proteasome inhibitors.
AID611895	Ratio of IC50 for intracellular chymotrypsin-like activity of 20S proteasome in human HEK293 cells to IC50 for in vitro chymotrypsin-like activity of 20S proteasome	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Chemical and biological evaluation of dipeptidyl boronic acid proteasome inhibitors for use in prodrugs and pro-soft drugs targeting solid tumors.
AID1882258	Inhibition of proteasome (unknown origin)	2022	European journal of medicinal chemistry, Feb-05, Volume: 229	A review on the treatment of multiple myeloma with small molecular agents in the past five years.
AID496331	Induction of Usp18 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv by RT- PCR	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID496356	Induction of IL-5 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 6 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID548708	AUC (0-t) in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID496320	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as expression of 3.5 and 2.1 kb HBV mRNA at 0.2 mg/kg, iv single dose after 24 hrs	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID353999	Inhibition of chymotrypsin-like activity of human 20S proteasome beta 5 subunit by proteasome active site ELISA	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Design and synthesis of an orally bioavailable and selective peptide epoxyketone proteasome inhibitor (PR-047).
AID316549	Inhibition of human MMP2 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1576790	Inhibition of 20S proteasome beta 5i in human PBMC cells assessed as induction of PSMB5 expression at 100 nM after 3 to 72 hrs by RT-PCR analysis	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID1156390	Growth inhibition of human SK-MEL-5 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID353300	Inhibition of chymotrypsin-like activity of human 20S proteasome	2009	Bioorganic & medicinal chemistry letters, Apr-15, Volume: 19, Issue:8	Synthesis of boronic acid derivatives of tyropeptin: proteasome inhibitors.
AID1459692	Toxicity in human Bel7404 cells xenografted BALB/c mouse assessed as effect on body weight at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 10 of compound dosing (Rvb = 26.30 +/- 0.78 g)	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1225670	Inhibition of proteasome (unknown origin)	2015	Journal of natural products, Apr-24, Volume: 78, Issue:4	Cystargolides, 20S Proteasome Inhibitors Isolated from Kitasatospora cystarginea.
AID1459695	Toxicity in human Bel7404 cells xenografted BALB/c mouse assessed as effect on body weight at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 13 of compound dosing (Rvb = 26.10 +/- 1.08 g)	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1687123	Antiplasmodial activity against DHA-resistant and sorbitol synchronized ring stage forms of Plasmodium falciparum Cam3.II^R539T expressing K13 mutant assessed as reduction in parasitemia incubated for 3 hrs by pulse exposure based Syto-61 staining dye bas	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1325776	Cytotoxicity against human WE68 cells harboring wild type p53 assessed as reduction in cell viability after 48 hrs by 7AAD-staining based FACS analysis
AID1250150	Cytotoxicity against human Glioma cells (HF2790) after 72 hrs by CelltiterGlo assay	2015	ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8	High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID700323	Cytotoxicity against human GUMBUS cells after 72 hrs by MTT assay	2012	Bioorganic & medicinal chemistry letters, Nov-01, Volume: 22, Issue:21	Identification of a glutathione peroxidase inhibitor that reverses resistance to anticancer drugs in human B-cell lymphoma cell lines.
AID1460768	Inhibition of human CA5A by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID1604188	Selectivity index, ratio of IC50 for 20S proteasome beta 1c (unknown origin) to IC50 for 20S proteasome beta 1i (unknown origin)	2019	European journal of medicinal chemistry, Nov-15, Volume: 182	Immunoproteasome-selective inhibitors: An overview of recent developments as potential drugs for hematologic malignancies and autoimmune diseases.
AID1156356	Growth inhibition of human CCRF-CEM cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1460766	Inhibition of human CA3 by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID1291321	Cytotoxicity against human ARH77 cells after 72 hrs by MTS assay	2016	Bioorganic & medicinal chemistry letters, Apr-15, Volume: 26, Issue:8	Design, synthesis and docking studies of novel dipeptidyl boronic acid proteasome inhibitors constructed from αα- and αβ-amino acids.
AID1443452	Inhibition of IL-1beta-stimulated nuclear translocation of GFP-tagged NF-kappaB-p65 (unknown origin) expressed in CHO cells preincubated with IL-1beta for 30 mins followed by compound addition by fluorescence assay	2017	Journal of medicinal chemistry, 04-13, Volume: 60, Issue:7	First Bispecific Inhibitors of the Epidermal Growth Factor Receptor Kinase and the NF-κB Activity As Novel Anticancer Agents.
AID316558	Inhibition of human caspase 8 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID706727	Resistance factor, ratio of IC50 for 1000 nM bortezonib-resistant human Jurkat B2 cells harboring proteosome subunit beta5 A49T homozygous mutant to IC50 for wild type human Jurkat cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID706729	Resistance factor, ratio of IC50 for 100 nM bortezonib-resistant human THP1 cells harboring proteosome subunit beta5 A49T mutant to IC50 for wild type human THP1 cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1822759	Inhibition of wild type Candida albicans Fructose-1,6-Bisphosphate Aldolase transfected in Escherichia coli BL21 (DE3) at 50 uM incubated for 3 mins in presence of NADH by spectrophotometric analysis relative to control	2022	Journal of medicinal chemistry, 02-10, Volume: 65, Issue:3	Structure-Guided Discovery of the Novel Covalent Allosteric Site and Covalent Inhibitors of Fructose-1,6-Bisphosphate Aldolase to Overcome the Azole Resistance of
AID1624029	Inhibition of thrombin (unknown origin) at 10 ug/mL using substrate 3 relative to control	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Covalent docking modelling-based discovery of tripeptidyl epoxyketone proteasome inhibitors composed of aliphatic-heterocycles.
AID1459680	Antitumor activity against human Bel7404 cells xenografted in BALB/c nude mouse assessed as effect on tumor volume at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 24 of compound dosing relative to control	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1687107	Inhibition of human 20S constitutive proteasome beta 5 subunit chymotrypsin-like activity using fluorogenic peptide Ac-WLA-AMC as substrate in presence of PA28alpha incubated for 1 to 2 hrs by fluorescence microplate reader assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1375829	Inhibition of proteasome in human SKOV3/TR cells assessed as decrease in cell viability after 4 days by CellTiter-Glo assay	2018	Journal of medicinal chemistry, 06-14, Volume: 61, Issue:11	Discovery of Orally Bioavailable, Quinoline-Based Aldehyde Dehydrogenase 1A1 (ALDH1A1) Inhibitors with Potent Cellular Activity.
AID1374302	Metabolic stability in Sprague-Dawley rat liver microsomes assessed as parent compound remaining at 20 mM preincubated for 5 mins followed by NADPH addition measured after 40 mins by HPLC analysis	2018	Bioorganic & medicinal chemistry, 03-01, Volume: 26, Issue:5	Novel aromatic sulfonyl naphthalene-based boronates as 20S proteasome inhibitors.
AID496344	Induction of TNFalpha gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 6 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID459669	Cytotoxicity against human HepG2 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID459671	Cytotoxicity against human U266 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID452099	Inhibition of trypsin-like activity of mouse liver 20S proteasome	2009	Bioorganic & medicinal chemistry, Oct-01, Volume: 17, Issue:19	Design, synthesis and biological evaluation of tripeptide boronic acid proteasome inhibitors.
AID700319	Cytotoxicity against human DOGUM cells after 72 hrs by MTT assay	2012	Bioorganic & medicinal chemistry letters, Nov-01, Volume: 22, Issue:21	Identification of a glutathione peroxidase inhibitor that reverses resistance to anticancer drugs in human B-cell lymphoma cell lines.
AID496376	Induction of IL1-beta gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 6 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1473236	Cell cycle arrest in human NCI-H929 cells assessed as accumulation at S phase at 2.5 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 13.5%)	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID1128240	Cell cycle arrest in human HCT116 cells assessed as accumulation at S phase at 100 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 45.3%)	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID1156386	Growth inhibition of human M14 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1576782	Selectivity ratio, ratio of IC50 for 20S proteasome beta 1c (unknown origin) to IC50 for human 20S proteasome beta 5i	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID1548261	Antiproliferative activity against HUVEC cells incubated for 48 hrs by MTT assay
AID496377	Induction of IL-3 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 1day by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1156365	Growth inhibition of human HOP92 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID316566	Inhibition of human renin at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1156407	Growth inhibition of human UO31 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1624051	Antitumor activity against human RPMI8226 cells xenografted in CB17 NOD/SCID mouse assessed as tumor growth inhibition at 1 mg/kg, iv administered for 18 days through regimen of twice weekly for three weeks on days 1 and 4	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Covalent docking modelling-based discovery of tripeptidyl epoxyketone proteasome inhibitors composed of aliphatic-heterocycles.
AID1576784	Cytotoxicity against human PBMC cells assessed as reduction in cell viability by CellTiter Glo assay	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID625288	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1895459	Cytotoxicity against human primary hepatocytes assessed as depletion of ATP content up to 500 uM incubated for 48 to 72 hrs by CellTiter-Glo luminescent assay	2021	Journal of medicinal chemistry, 07-22, Volume: 64, Issue:14	Structure-Based Optimization and Discovery of M3258, a Specific Inhibitor of the Immunoproteasome Subunit LMP7 (β5i).
AID1250148	Cytotoxicity against human Glioma cells (HF2381) after 72 hrs by CelltiterGlo assay	2015	ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8	High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1156404	Growth inhibition of human RXF393 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1623396	Induction of apoptosis in human RPMI8226 cells assessed as early apoptotic cells at 3 nM after 48 hrs by Annexin-V/propidium iodide staining based flow cytometric method (Rvb = 1.05%)	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID496354	Induction of IL-5 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 2 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1312162	Inhibition of Flaveria bidentis beta-carbonic anhydrase preincubated for 15 mins by stopped-flow CO2 hydration assay	2016	Bioorganic & medicinal chemistry, 09-15, Volume: 24, Issue:18	Bortezomib inhibits bacterial and fungal β-carbonic anhydrases.
AID1464416	Inhibition of TNFalpha-stimulated NF-kappaB (unknown origin) activation expressed in HEK293 cells incubated for 6 hrs with TNFalpha followed by incubation in dark for 30 mins by luciferase reporter gene assay	2017	Bioorganic & medicinal chemistry letters, 10-15, Volume: 27, Issue:20	Design and synthesis of pregnenolone/2-cyanoacryloyl conjugates with dual NF-κB inhibitory and anti-proliferative activities.
AID548718	Apparent volume of distribution in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID452102	Cytotoxicity against human U266 cells after 72 hrs by MTT assay	2009	Bioorganic & medicinal chemistry, Oct-01, Volume: 17, Issue:19	Design, synthesis and biological evaluation of tripeptide boronic acid proteasome inhibitors.
AID1299911	Inhibition of PGPH-like activity of rabbit 20S proteasome using Cbz-LLE-AMC substrate incubated at 37 degC by fluorometric assay	2016	ACS medicinal chemistry letters, Mar-10, Volume: 7, Issue:3	Synthesis and Evaluation of Macrocyclic Peptide Aldehydes as Potent and Selective Inhibitors of the 20S Proteasome.
AID566538	Inhibition of proteasome activity in human HeLa cells assessed as induction of ubiquitinG76V-FL reporter level at 1 uM after 8 hrs by luciferase assay	2011	Journal of medicinal chemistry, Jan-27, Volume: 54, Issue:2	α,β-Unsaturated carbonyl system of chalcone-based derivatives is responsible for broad inhibition of proteasomal activity and preferential killing of human papilloma virus (HPV) positive cervical cancer cells.
AID316522	Oral bioavailability in CD1 mouse at 4 mg/kg	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1864398	Inhibition of 20S proteasome beta1 subunit (unknown origin) using Z-LLE-AMC as flurogenic substrate measured after 1 hr by fluorescence based analysis	2022	Journal of medicinal chemistry, 09-22, Volume: 65, Issue:18	Discovery of a Novel Oral Proteasome Inhibitor to Block NLRP3 Inflammasome Activation with Anti-inflammation Activity.
AID496322	Toxicity in HBV infected 1.3.32 transgenic mouse assessed as stress, ruffled fur at 5 mg/kg, iv after 24 hrs	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1439186	Antiproliferative activity against human RPMI8226 cells after 72 hrs by SRB assay	2017	European journal of medicinal chemistry, Mar-10, Volume: 128	Design, synthesis and biological evaluation of novel non-peptide boronic acid derivatives as proteasome inhibitors.
AID706724	Resistance factor, ratio of IC50 for human Jurkat B cells harboring proteosome subunit beta5 A49T/A50V double mutant to IC50 for wild type human Jurkat cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID548709	Mean residence time (0-t) in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1460767	Inhibition of human CA4 by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID1762748	Inhibition of TNFalpha-induced NFkappaB activation in HEK293 cells assessed as luciferase expression by luciferase reporter activity assay	2021	Bioorganic & medicinal chemistry letters, 06-15, Volume: 42	Synthesis of pyranochalcone derivatives and their inhibitory effect on NF-κB activation.
AID459662	Cytotoxicity against human BCG823 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID496318	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as inhibition of HBV DNA replication at 0.2 mg/kg, iv single dose after 24 hrs by Southern blot analysis	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID459687	Terminal half life in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID617479	Inhibition of HIF1alpha expression in human LN229 cells assessed as reduction of HIF-1alpha accumulation at 100 nM preincubated for 1 hr under normoxia condition followed by 24 hrs incubation under hypoxia condition by Western blotting	2011	Bioorganic & medicinal chemistry letters, Sep-15, Volume: 21, Issue:18	Sulfonamides as a new scaffold for hypoxia inducible factor pathway inhibitors.
AID1895458	Cytotoxicity against Wistar Han rat hepatocytes assessed as depletion of ATP content up to 500 uM incubated for 48 to 72 hrs by CellTiter-Glo luminescent assay	2021	Journal of medicinal chemistry, 07-22, Volume: 64, Issue:14	Structure-Based Optimization and Discovery of M3258, a Specific Inhibitor of the Immunoproteasome Subunit LMP7 (β5i).
AID459675	Toxicity against zebrafish embryo assessed as cell death in embryo at 1 umol after 24 hrs	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1325791	Inhibition of 26S proteasome in human MCF7 cells assessed as accumulation of high molecular weight polyubiquitin-conjugated proteins at 35 nM after 4 hrs by Western blot analysis
AID1156403	Growth inhibition of human CAKI-1 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1687109	Inhibition of human 20S immunoproteasome beta 2 subunit trypsin-like activity using fluorogenic peptide Ac-WLR-AMC as substrate in presence of PA28alpha incubated for 1 to 2 hrs by fluorescence microplate reader assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID706492	Effect on 20S proteasome subunit beta5 expression in human HT-29 cells at 200 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID496358	Induction of IL-1alpha gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 2 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID623567	Inhibition of chymotrypsin-like activity of purified human 20S proteasome in HL60 cells using N-succinyl-Leu-Leu-Val-Tyr-AMC as substrate pre-incubated for 10 mins by fluorimetric assay	2011	Journal of natural products, Oct-28, Volume: 74, Issue:10	Bioassay-guided isolation of constituents of Piper sarmentosum using a mitochondrial transmembrane potential assay.
AID496360	Induction of IL-1alpha gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 6 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1141826	Cytotoxic activity against human RPMI8226 cells after 72 hrs by MTS assay	2014	Bioorganic & medicinal chemistry, Jun-01, Volume: 22, Issue:11	Design, synthesis and biological evaluation of novel tripeptidyl epoxyketone derivatives constructed from β-amino acid as proteasome inhibitors.
AID706508	Resistance factor, ratio of IC50 for 100 nM bortezonib-resistant human A549 cells harboring proteosome subunit beta5 M45V/A49T double mutant to IC50 for wild type human A549 cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID641892	Inhibition of hypoxia-induced HIF1alpha accumulation in human LN229 cells at 20 uM after 1 hr preincubation measured after 24 hrs by Western blot analysis	2011	Journal of medicinal chemistry, Dec-22, Volume: 54, Issue:24	Design and synthesis of novel small-molecule inhibitors of the hypoxia inducible factor pathway.
AID1689693	Inhibition of HDAC3 in human RPMI-8226 cells incubated for 2 hrs by ELISA	2020	European journal of medicinal chemistry, Mar-01, Volume: 189	1,2,3-Triazole-Chalcone hybrids: Synthesis, in vitro cytotoxic activity and mechanistic investigation of apoptosis induction in multiple myeloma RPMI-8226.
AID1687108	Inhibition of human 20S immunoproteasome beta 1 subunit caspase-like activity using fluorogenic peptide Ac-nLPnLD-AMC as substrate in presence of PA28alpha incubated for 1 to 2 hrs by fluorescence microplate reader assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1548266	Induction of apoptosis in human RPMI8226 cells assessed as induction of caspase-3/7 activation incubated for 24 hrs by fluorometric assay
AID1312159	Inhibition of Mycobacterium tuberculosis beta-carbonic anhydrase Rv1284 preincubated for 15 mins by stopped-flow CO2 hydration assay	2016	Bioorganic & medicinal chemistry, 09-15, Volume: 24, Issue:18	Bortezomib inhibits bacterial and fungal β-carbonic anhydrases.
AID1128246	Binding affinity to beta5 subunit of 20S proteasome (unknown origin) assessed as dissociation half-life	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID734746	Cell cycle arrest in human HCT116 cells assessed as accumulation at G2/M phase after 24 hrs by propidium iodide staining-based flow cytometric analysis	2013	Journal of medicinal chemistry, May-09, Volume: 56, Issue:9	Potent proteasome inhibitors derived from the unnatural cis-cyclopropane isomer of Belactosin A: synthesis, biological activity, and mode of action.
AID1459632	Inhibition of trypsin-like activity of 20S proteasome in human HL60 cells using Z-LRRaminoluciferin as substrate at 0.2 uM after 2 hrs by fluorescence analysis	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID496307	Antiviral activity against HBV infected in 1.3.32 transgenic mouse liver assessed as inhibition of proteosome activity at 1 mg/kg, iv single dose after 6 hrs	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1404726	Antiproliferative activity against HUVEC after 48 hrs by CCK8 assay	2018	European journal of medicinal chemistry, Jun-25, Volume: 154	A novel NAE/UAE dual inhibitor LP0040 blocks neddylation and ubiquitination leading to growth inhibition and apoptosis of cancer cells.
AID733002	Inhibition of gamma-secretase-mediated betaAPP K670N/M671L mutant cleavage in HEK293 cells assessed as inhibition of amyloid beta40/42 production at 60 uM after 8 hrs by chemiluminescence assay relative to control	2013	Bioorganic & medicinal chemistry, Feb-15, Volume: 21, Issue:4	Further characterization of a putative serine protease contributing to the γ-secretase cleavage of β-amyloid precursor protein.
AID316570	Inhibition of human tryptase at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1156377	Growth inhibition of human SW620 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID496323	Toxicity in HBV infected 1.3.32 transgenic mouse liver assessed as serum alanine aminotransferase level at 5 mg/kg, iv after 24 hrs	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID548713	Tmax in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID734742	Reversible inhibition of chymotrypsin-like activity of human 20S proteasome beta 5 subunit using Suc-LLVY-AMC as substrate incubated for 12 hrs prior to substrate addition followed by compound wash out measured after 1 hr by dialysis method	2013	Journal of medicinal chemistry, May-09, Volume: 56, Issue:9	Potent proteasome inhibitors derived from the unnatural cis-cyclopropane isomer of Belactosin A: synthesis, biological activity, and mode of action.
AID397954	Cytotoxicity against human A549 cells after 72 hrs by MTT assay	2009	Journal of medicinal chemistry, Jul-23, Volume: 52, Issue:14	Design, synthesis, biological evaluation, and structure-activity relationship (SAR) discussion of dipeptidyl boronate proteasome inhibitors, part I: comprehensive understanding of the SAR of alpha-amino acid boronates.
AID316571	Inhibition of human neutrophil elastase 2 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1459689	Toxicity in human Bel7404 cells xenografted BALB/c mouse assessed as effect on body weight at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 6 of compound dosing (Rvb = 25.65 +/- 0.70 g)	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1815776	Cytotoxicity against oleic acid-induced human HeLa cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay	2022	ACS medicinal chemistry letters, Jan-13, Volume: 13, Issue:1	The BASHY Platform Enables the Assembly of a Fluorescent Bortezomib-GV1001 Conjugate.
AID1486819	Cytotoxicity against human HCT116 cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Synthesis and biological activity of peptide proline-boronic acids as proteasome inhibitors.
AID1895437	Inhibition of human 20S immunoproteasome beta-5i subunit using Suc-LLVY-AMC as substrate preincubated for 2 hrs followed by substrate addition and measured after 1 hr by fluorescence intensity assay	2021	Journal of medicinal chemistry, 07-22, Volume: 64, Issue:14	Structure-Based Optimization and Discovery of M3258, a Specific Inhibitor of the Immunoproteasome Subunit LMP7 (β5i).
AID1459657	Inhibition of caspase-like activity of 20S proteasome in human HL60 cells using Z-nLPnLDaminoluciferin as substrate after 2 hrs by fluorescence analysis	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1156395	Growth inhibition of human OVCAR4 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1624025	Inhibition of human 20S proteasome preincubated for 15 mins followed by substrate addition	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Covalent docking modelling-based discovery of tripeptidyl epoxyketone proteasome inhibitors composed of aliphatic-heterocycles.
AID1864397	Inhibition of 20S proteasome beta2 subunit (unknown origin) using Boc-LRR-AMC as flurogenic substrate measured after 1 hr by fluorescence based analysis	2022	Journal of medicinal chemistry, 09-22, Volume: 65, Issue:18	Discovery of a Novel Oral Proteasome Inhibitor to Block NLRP3 Inflammasome Activation with Anti-inflammation Activity.
AID1605108	Inhibition of N-terminal His6-sumo-tagged full length Staphylococcus aureus ClpP expressed in Escherichia coli BL2 (DE3) assessed as enzyme activity recovery level at 20-fold molar excess pre-incubated for 10 mins before Suc-LY-AMC addition and measured a	2020	Journal of medicinal chemistry, 03-26, Volume: 63, Issue:6	Discovery of Novel Peptidomimetic Boronate ClpP Inhibitors with Noncanonical Enzyme Mechanism as Potent Virulence Blockers
AID526551	Inhibition of human plasmin at 100 uM	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID706500	Effect on PSMB5 mRNA expression in human Jurkat-B cells expressing PSMB5 G322A/C323T mutant at 1000 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1291320	Cytotoxicity against human RPMI8226 cells after 72 hrs by MTS assay	2016	Bioorganic & medicinal chemistry letters, Apr-15, Volume: 26, Issue:8	Design, synthesis and docking studies of novel dipeptidyl boronic acid proteasome inhibitors constructed from αα- and αβ-amino acids.
AID526549	Inhibition of human chymotrypsin at 100 uM	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID1473237	Cell cycle arrest in human NCI-H929 cells assessed as accumulation at G2/M phase at 2.5 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 31.63%)	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID706737	Reversible inhibition of human erythrocyte derived 20S proteasome subunit beta2 after 30 mins by fluorogenic assay	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID459663	Cytotoxicity against human H460 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1180859	Inhibition of human 26S proteasomal catalytic subunit chymotrypsin-like activity using Suc-LLVYaminoluciferin as substrate after 2 hrs by luminescence assay	2014	Journal of medicinal chemistry, Jul-24, Volume: 57, Issue:14	Synthesis and evaluation of bisbenzylidenedioxotetrahydrothiopranones as activators of endoplasmic reticulum (ER) stress signaling pathways and apoptotic cell death in acute promyelocytic leukemic cells.
AID1461482	Inhibition of chymotrypsin-like activity of 20S proteasome in rabbit 20S proteasome pre-incubated for 10 mins before Suc-Leu-Leu-Val-Tyr-AMC substrate addition and measured after 2 hrs by fluorescence assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Azobenzene-containing photoswitchable proteasome inhibitors with selective activity and cellular toxicity.
AID496325	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as increase in serum HBsAg level at 1 mg/kg, iv single dose after 24 hrs by ELISA	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID459680	Terminal half life in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID496308	Antiviral activity against HBV infected in 1.3.32 transgenic mouse liver assessed as inhibition of HBV DNA replication at 1 mg/kg, iv single dose after 24 hrs by Southern blot analysis	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID373868	Inhibition of SDS-activated 20S proteasome activity in rabbit muscle	2009	European journal of medicinal chemistry, Apr, Volume: 44, Issue:4	3D-QSAR studies of boron-containing dipeptides as proteasome inhibitors with CoMFA and CoMSIA methods.
AID706502	Effect on PSMB5 mRNA expression in human Jurkat-B cells expressing PSMB5 G322A mutant at 1000 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID496371	Induction of OAS gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 3 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1576777	Selectivity ratio, ratio of IC50 for 20S proteasome beta 5c (unknown origin) to IC50 for human 20S proteasome beta 5i	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID496362	Induction of IFN-gamma gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 2 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID588213	Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents	2010	Chemical research in toxicology, Jan, Volume: 23, Issue:1	Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1459683	Toxicity in human Bel7404 cells xenografted BALB/c mouse assessed as effect on body weight at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 1 of compound dosing (Rvb = 25.36 +/- 0.97 g)	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1674998	Antiinflammatory activity against mouse RAW264.7 cells assessed as inhibition of LPS-stimulated NO production	2020	Bioorganic & medicinal chemistry letters, 09-01, Volume: 30, Issue:17	Synthesis and evaluation of 1,2,4-oxadiazole derivatives as potential anti-inflammatory agents by inhibiting NF-κB signaling pathway in LPS-stimulated RAW 264.7 cells.
AID496352	Induction of IL-4 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 6 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID496374	Induction of IL1-beta gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 2 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1363791	Inhibition of proteasome in human HL60 cells assessed as increase in cleaved PARP expression at 1 to 100 nM after 24 hrs by immunoblot assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Discovery of the First-in-Class Dual Histone Deacetylase-Proteasome Inhibitor.
AID706738	Reversible inhibition of human erythrocyte derived 20S proteasome subunit beta5 after 30 mins by fluorogenic assay	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1687121	Cytotoxicity against human HepG2 cells assessed as reduction in cell viability incubated for 72 hrs by cell-titer glo assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1548300	Induction of cell cycle arrest in bortezomib resistant human KM3/BTZ cells assessed as accumulation at G1 phase at 100 nM incubated for 24 hrs by propidium iodide staining based flow cytometry (Rvb = 42%)
AID1363793	Inhibition of proteasome in imatinib-resistant human SUP-B15 cells assessed as increase in cleaved PARP expression at 1 to 100 nM after 24 hrs by immunoblot assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Discovery of the First-in-Class Dual Histone Deacetylase-Proteasome Inhibitor.
AID1301231	Inhibition of human 20S proteasome chymotryptic-like activity using Suc-LLVY-AMC as substrate measured for 30 mins by fluorescence assay	2016	Bioorganic & medicinal chemistry, 06-01, Volume: 24, Issue:11	Substituted quinolines as noncovalent proteasome inhibitors.
AID1459668	Antitumor activity against human Bel7404 cells xenografted in BALB/c nude mouse assessed as effect on tumor volume at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 10 of compound dosing relative to control	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID238893	Inhibitory activity against 20S proteasome chymotrypsin-like activity	2005	Journal of medicinal chemistry, Jan-13, Volume: 48, Issue:1	Retro hydrazino-azapeptoids as peptidomimetics of proteasome inhibitors.
AID1156366	Growth inhibition of human NCI-H226 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID316498	Inhibition of chymotrypsin-like activity of human erythrocyte 20S proteasome	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1473229	Cell cycle arrest in human U266 cells assessed as accumulation at G2/M phase at 2.5 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 35.13%)	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID1404725	Antiproliferative activity against HEK293T cells after 48 hrs by CCK8 assay	2018	European journal of medicinal chemistry, Jun-25, Volume: 154	A novel NAE/UAE dual inhibitor LP0040 blocks neddylation and ubiquitination leading to growth inhibition and apoptosis of cancer cells.
AID1623349	Cytotoxicity against human RPMI8226 cells assessed as reduction in cell viability at 3 nM after 48 hrs by CCK8 assay relative to control	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID1363840	Inhibition of proteasome in human SEM cells assessed as increase in aggresome accumulation at 10 nM after 18 hrs by fluorescence microscopic method	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Discovery of the First-in-Class Dual Histone Deacetylase-Proteasome Inhibitor.
AID706730	Resistance factor, ratio of IC50 for 7 nM bortezonib-resistant human RPMI8226 cells harboring proteosome subunit beta5 T21A mutant to IC50 for wild type human RPMI8226 cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1137839	Inhibition of immunoproteasome 20S subunit beta5i in human Karpas 1106p cell extract at 10 to 100 nM	2014	ACS medicinal chemistry letters, Apr-10, Volume: 5, Issue:4	Oxathiazolones Selectively Inhibit the Human Immunoproteasome over the Constitutive Proteasome.
AID1299918	Inhibition of m-calpain (unknown origin) using Suc-LY-AMC as substrate at 100 uM by fluorometric assay	2016	ACS medicinal chemistry letters, Mar-10, Volume: 7, Issue:3	Synthesis and Evaluation of Macrocyclic Peptide Aldehydes as Potent and Selective Inhibitors of the 20S Proteasome.
AID1156367	Growth inhibition of human NCI-H23 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1918920	Antiproliferative activity against human MM1.S cells assessed as inhibition of cell proliferation incubated for 72 hrs by XTT assay	2022	Journal of natural products, 12-23, Volume: 85, Issue:12	Isolation and Structure Elucidation of Compounds from
AID706479	Effect on 20S proteasome subunit beta1/beta5 chymotrypsin-like activity in human AMO-1a cells at 20 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1372745	Inhibition of 20s constitutive proteasome caspase-like activity in human erythrocytes using Z-LRR-Glo as substrate pretreated for 2 hrs followed by substrate addition measured after 10 mins by luminescence assay	2018	Bioorganic & medicinal chemistry, 01-15, Volume: 26, Issue:2	Immunoproteasome inhibition and bioactivity of thiasyrbactins.
AID1566918	Antimalarial activity against erythrocytic stage of Plasmodium falciparum Dd2 harboring 20S beta5 proteasome A49S mutant measured after 72 hrs by SYBR green dye based fluorescence assay	2019	Journal of medicinal chemistry, 07-11, Volume: 62, Issue:13	Improvement of Asparagine Ethylenediamines as Anti-malarial
AID496333	Induction of ISG15 gene expression in HBV infected 1.3.32 transgenic mouse liver at 0.2-5 mg/kg, iv after 24 hrs by RT- PCR	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1690793	Reversible inhibition of human 20S proteasome beta5 subunit assessed as residual enzyme activity using Suc-LLVY-Glo as substrate preincubated for 2 hrs followed by compound washout and further incubated for 4 hrs followed by substrate addition and measure
AID1156412	Growth inhibition of human Hs 578T cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1156378	Growth inhibition of human SF268 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1128229	Inhibition of chymotrypsin-like activity of human 20S proteasome using Suc-LLVY-AMC as substrate	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID1548265	Induction of apoptosis in human RPMI8226 cells incubated for 24 hrs by Annexin V-FITC/PI staining based flow cytometry
AID706515	Resistance factor, ratio of IC50 for 200 nM bortezonib-resistant human CEM cells harboring proteosome subunit beta5 A49V /C52F double mutant to IC50 for wild type human CEM cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1484606	Antiproliferative activity against human U266 cells after 72 hrs by calcein AM staining based fluorescence assay	2017	European journal of medicinal chemistry, Jul-28, Volume: 135	Synthesis and antiproteasomal activity of novel O-benzyl salicylamide-based inhibitors built from leucine and phenylalanine.
AID1486817	Cytotoxicity against human MGC803 cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Synthesis and biological activity of peptide proline-boronic acids as proteasome inhibitors.
AID625280	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1459674	Antitumor activity against human Bel7404 cells xenografted in BALB/c nude mouse assessed as effect on tumor volume at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 17 of compound dosing relative to control	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID750163	Inhibition of human 20S proteasome chymotrypsin like activity using Suc-Leu-Leu-Val-Tyr-AMC as substrate at 20 uM measured over 10 mins by fluorescence assay relative to control	2013	European journal of medicinal chemistry, Jun, Volume: 64	Development of peptidomimetic boronates as proteasome inhibitors.
AID1382148	Inhibition of PGPH activity of human 26S proteasome using Z-LLE-MCA as substrate measured for 1 hr by fluorescence assay	2018	European journal of medicinal chemistry, Feb-25, Volume: 146	Ridaifen-F conjugated with cell-penetrating peptides inhibits intracellular proteasome activities and induces drug-resistant cell death.
AID1312158	Inhibition of Mycobacterium tuberculosis beta-carbonic anhydrase Rv3273 preincubated for 15 mins by stopped-flow CO2 hydration assay	2016	Bioorganic & medicinal chemistry, 09-15, Volume: 24, Issue:18	Bortezomib inhibits bacterial and fungal β-carbonic anhydrases.
AID1548287	Induction of apoptosis in bortezomib resistant human KM3/BTZ cells assessed as necrotic cells level at 50 nM incubated for 24 hrs by Annexin V-FITC/PI staining based FCAS analysis (Rvb = 0.11%)
AID1460774	Inhibition of human CA13 by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID1864384	Cytotoxicity against HEK293 cells incubated for 24 hrs	2022	Journal of medicinal chemistry, 09-22, Volume: 65, Issue:18	Discovery of a Novel Oral Proteasome Inhibitor to Block NLRP3 Inflammasome Activation with Anti-inflammation Activity.
AID1473259	Induction of apoptosis in human NCI-H929 cells at 2.5 nM after 24 hrs by Annexin V/propidium iodide staining based flow cytometry	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID1156368	Growth inhibition of human NCI-H322M cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1548291	Induction of apoptosis in bortezomib resistant human KM3/BTZ cells assessed as necrotic cells level at 200 nM incubated for 24 hrs by Annexin V-FITC/PI staining based FCAS analysis (Rvb = 0.11%)
AID625289	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1460771	Inhibition of human CA7 by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID164126	Inhibitory activity against 20S Proteasome	1998	Bioorganic & medicinal chemistry letters, Feb-17, Volume: 8, Issue:4	Potent and selective inhibitors of the proteasome: dipeptidyl boronic acids.
AID496364	Induction of IFN-gamma gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 6 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID706513	Resistance factor, ratio of IC50 for 150 nM bortezonib-resistant human SW1573 cells harboring proteosome subunit beta5 C52F mutant to IC50 for wild type human SW1573 cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID526552	Inhibition of human thrombin at 100 uM	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID706489	Effect on 20S proteasome subunit beta5 expression in human A549 cells at 40 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID526418	Inhibition of human cathepsin L at 100uM	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID316562	Inhibition of human NEP at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1295431	Cytotoxicity against human ARH77 cells assessed as cell viability after 72 hrs by CellTiter 96 aqueous one solution cell proliferation assay	2016	Bioorganic & medicinal chemistry, 06-01, Volume: 24, Issue:11	3D-QSAR-aided design, synthesis, in vitro and in vivo evaluation of dipeptidyl boronic acid proteasome inhibitors and mechanism studies.
AID496349	Induction of IL-4 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 1day by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1548279	Induction of apoptosis in bortezomib resistant human KM3 cells at 100 nM incubated for 24 hrs by TUNEL assay
AID706517	Resistance factor, ratio of IC50 for 100 nM bortezonib-resistant human RPMI8226 cells harboring proteosome subunit beta5 A49T mutant to IC50 for wild type human RPMI8226 cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1299910	Inhibition of trypsin-like activity of rabbit 20S proteasome using Cbz-ARR-AMC substrate incubated at 37 degC by fluorometric assay	2016	ACS medicinal chemistry letters, Mar-10, Volume: 7, Issue:3	Synthesis and Evaluation of Macrocyclic Peptide Aldehydes as Potent and Selective Inhibitors of the 20S Proteasome.
AID1605097	Inhibition of N-terminal His6-sumo-tagged full length Staphylococcus aureus ClpP expressed in Escherichia coli BL2 (DE3) assessed as Kinact/Ki ratio pre-incubated for 10 mins before Suc-LY-AMC addition and measured after 1 hr by fluorescence based assay	2020	Journal of medicinal chemistry, 03-26, Volume: 63, Issue:6	Discovery of Novel Peptidomimetic Boronate ClpP Inhibitors with Noncanonical Enzyme Mechanism as Potent Virulence Blockers
AID1291322	Inhibition of chymotrypsin like activity of human 20S proteasome using ZGlyGlyLeuAMC/SucLeuLeuValTyrAMC as substrate measured every minute for 25 mins by fluorescence assay	2016	Bioorganic & medicinal chemistry letters, Apr-15, Volume: 26, Issue:8	Design, synthesis and docking studies of novel dipeptidyl boronic acid proteasome inhibitors constructed from αα- and αβ-amino acids.
AID316536	Inhibition of human cathepsin H at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID706486	Effect on 20S proteasome subunit beta5 expression in human SW1573 cells at 150 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1180861	Inhibition of human 26S proteasomal catalytic subunit caspase-like activity using Z-nLPnLD-aminoluciferin as substrate after 4 hrs by luminescence assay	2014	Journal of medicinal chemistry, Jul-24, Volume: 57, Issue:14	Synthesis and evaluation of bisbenzylidenedioxotetrahydrothiopranones as activators of endoplasmic reticulum (ER) stress signaling pathways and apoptotic cell death in acute promyelocytic leukemic cells.
AID736675	Cytotoxicity against human HEK293 cells expressing murine FAP at 0.0001 uM to 100 uM after 48 hrs by CellTiter-Blue assay	2013	Journal of medicinal chemistry, May-09, Volume: 56, Issue:9	Identification of selective and potent inhibitors of fibroblast activation protein and prolyl oligopeptidase.
AID706736	Reversible inhibition of human erythrocyte derived 20S proteasome subunit beta1 after 30 mins by fluorogenic assay	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID496316	Toxicity in 1.3.32 transgenic mouse liver assessed as serum alanine aminotransferase level at 1 mg/kg, iv after 2 days	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1825582	Cytotoxicity in human bone marrow mononuclear cell assessed as viable cells at 50 nM measured after 72 hrs by Annexin V staining based flow cytometric analysis (Rvb = 77.9%)	2022	Journal of medicinal chemistry, 02-10, Volume: 65, Issue:3	Synthesis and Evaluation of Structurally Diverse C-2-Substituted Thienopyrimidine-Based Inhibitors of the Human Geranylgeranyl Pyrophosphate Synthase.
AID526554	Inhibition of human trypsin at 100 uM	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID1605106	Binding affinity to N-terminal His6-sumo-tagged full length Staphylococcus aureus ClpP expressed in Escherichia coli BL2 (DE3) assessed as change in melting temperature at 100 uM by differential scanning calorimetry analysis	2020	Journal of medicinal chemistry, 03-26, Volume: 63, Issue:6	Discovery of Novel Peptidomimetic Boronate ClpP Inhibitors with Noncanonical Enzyme Mechanism as Potent Virulence Blockers
AID1404727	Antiproliferative activity against human LO2 cells after 48 hrs by CCK8 assay	2018	European journal of medicinal chemistry, Jun-25, Volume: 154	A novel NAE/UAE dual inhibitor LP0040 blocks neddylation and ubiquitination leading to growth inhibition and apoptosis of cancer cells.
AID1604184	Inhibition of 20S proteasome beta 2c (unknown origin) after 1 hr by fluorescence based assay	2019	European journal of medicinal chemistry, Nov-15, Volume: 182	Immunoproteasome-selective inhibitors: An overview of recent developments as potential drugs for hematologic malignancies and autoimmune diseases.
AID1375844	Induction of mitotic arrest in human SKOV3/TR cells at 1 uM after overnight incubation by Hoechst 33342 staining-based assay (Rvb = 11.6 +/- 1.2%)	2018	Journal of medicinal chemistry, 06-14, Volume: 61, Issue:11	Discovery of Orally Bioavailable, Quinoline-Based Aldehyde Dehydrogenase 1A1 (ALDH1A1) Inhibitors with Potent Cellular Activity.
AID1687135	Inhibition of human 20S immunoproteasome beta 1 subunit assessed as inhibition of BMV037 probe labeling at 1 to 10 uM incubated for 1 hr by SDS-PAGE analysis	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1613994	Inhibition of human hepatic cell derived 20s constitutive proteasome beta5 chymotrypsin-like activity using Suc-WLA-AMC as substrate preincubated for 15 mins followed by substrate addition and measured after 60 mins by fluorescence assay	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Exploration of novel macrocyclic dipeptide N-benzyl amides as proteasome inhibitors.
AID497571	Inhibition of PGPH activity of rabbit 26S proteasome	2010	Bioorganic & medicinal chemistry, Aug-01, Volume: 18, Issue:15	Synthesis and biological evaluation of naphthoquinone analogs as a novel class of proteasome inhibitors.
AID1595605	Cytotoxicity against human NCI-H727 cells after 72 hrs by CellTiter 96 AQueous one solution cell proliferation assay	2019	Journal of medicinal chemistry, 05-09, Volume: 62, Issue:9	Development of Novel Epoxyketone-Based Proteasome Inhibitors as a Strategy To Overcome Cancer Resistance to Carfilzomib and Bortezomib.
AID1156387	Growth inhibition of human MDA-MB-435 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID496361	Induction of IFN-gamma gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 1day by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID706723	Resistance factor, ratio of IC50 for bortezonib-resistant human KMS11 cells harboring proteosome subunit beta5 A49T mutant to IC50 for wild type human KMS11 cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1156346	Inhibition of bovine pancreatic alpha-chymotrypsin using Suc-Leu-Leu-Val-Tyr-AMC as substrate by fluorescence assay	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1325780	Cytotoxicity against human MCF7 cells harboring wild type p53 assessed as reduction in cell viability after 48 hrs by 7AAD-staining based FACS analysis
AID1548268	Induction of cell cycle arrest in human KM3 cells assessed as reduction in cell cycle progression in G2/M phase at 100 nM incubated for 24 hrs by propidium iodide staining based flow cytometry
AID1291318	Inhibition of chymotrypsin like activity of human erythrocyte-derived 20S proteasome preincubated for 10 mins using Suc-LLVY-AMC as substrate after 60 mins by fluorescence assay	2016	Bioorganic & medicinal chemistry letters, Apr-15, Volume: 26, Issue:8	Design, synthesis and docking studies of novel dipeptidyl boronic acid proteasome inhibitors constructed from αα- and αβ-amino acids.
AID750162	Inhibition of human 20S proteasome chymotrypsin like activity using Suc-Leu-Leu-Val-Tyr-AMC as substrate measured over 10 mins by fluorescence assay	2013	European journal of medicinal chemistry, Jun, Volume: 64	Development of peptidomimetic boronates as proteasome inhibitors.
AID1363792	Inhibition of proteasome in human SEM cells assessed as increase in cleaved PARP expression at 1 to 100 nM after 24 hrs by immunoblot assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Discovery of the First-in-Class Dual Histone Deacetylase-Proteasome Inhibitor.
AID1156357	Growth inhibition of human HL-60(TB) cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1614002	Inhibition of human peripheral blood derived 20s immunoproteasome beta2 trypsin-like activity using Suc-PAL-AMC as substrate preincubated for 15 mins followed by substrate addition and measured after 60 mins by fluorescence assay	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Exploration of novel macrocyclic dipeptide N-benzyl amides as proteasome inhibitors.
AID496329	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as serum HBeAg and HBsAg level at 1 mg/kg, iv single dose after 6 days	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1548259	Antiproliferative activity against human U266 cells incubated for 48 hrs by MTT assay
AID1156402	Growth inhibition of human ACHN cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1363797	Inhibition of chymotrypsin-like activity of 20S proteasome in human HL60 cells using Suc-LLVY aminoluciferin as substrate after 2 hrs by proteasome-Glo assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Discovery of the First-in-Class Dual Histone Deacetylase-Proteasome Inhibitor.
AID1374299	Antiproliferative activity against human A549 cells after 72 hrs by SRB assay	2018	Bioorganic & medicinal chemistry, 03-01, Volume: 26, Issue:5	Novel aromatic sulfonyl naphthalene-based boronates as 20S proteasome inhibitors.
AID1180858	Inhibition of human 26S proteasomal catalytic subunit caspase-like activity using Z-nLPnLD-aminoluciferin as substrate after 2 hrs by luminescence assay	2014	Journal of medicinal chemistry, Jul-24, Volume: 57, Issue:14	Synthesis and evaluation of bisbenzylidenedioxotetrahydrothiopranones as activators of endoplasmic reticulum (ER) stress signaling pathways and apoptotic cell death in acute promyelocytic leukemic cells.
AID1576781	Selectivity ratio, ratio of IC50 for human 20S proteasome beta 1i to IC50 for 20S proteasome beta 5i (unknown origin)	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID1460772	Inhibition of human CA9 by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID706511	Resistance factor, ratio of IC50 for 80 nM bortezonib-resistant human H460 cells harboring proteosome subunit beta5 A49T mutant to IC50 for wild type human H460 cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID459667	Cytotoxicity against human PC3 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1566916	Antimalarial activity against erythrocytic stage of Plasmodium falciparum Dd2 measured after 72 hrs by SYBR green dye based fluorescence assay	2019	Journal of medicinal chemistry, 07-11, Volume: 62, Issue:13	Improvement of Asparagine Ethylenediamines as Anti-malarial
AID1198171	Metabolic stability in human liver microsomes	2015	Journal of medicinal chemistry, Feb-26, Volume: 58, Issue:4	Proteasome inhibitors with pyrazole scaffolds from structure-based virtual screening.
AID1156382	Growth inhibition of human SNB75 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1605101	Cytotoxicity in human HepG2 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay	2020	Journal of medicinal chemistry, 03-26, Volume: 63, Issue:6	Discovery of Novel Peptidomimetic Boronate ClpP Inhibitors with Noncanonical Enzyme Mechanism as Potent Virulence Blockers
AID1486818	Cytotoxicity against human 95-D cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Synthesis and biological activity of peptide proline-boronic acids as proteasome inhibitors.
AID496449	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as serum HBeAg and HBsAg level at 1 mg/kg, iv single dose after 2 days	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1156415	Growth inhibition of human MDA-MB-468 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID548720	Toxicity in Sprague-Dawley rat assessed as incidence of mortality at 1 mg/kg, iv after 10 hrs	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1325771	Inhibition of trypsin like activity of rabbit 20S proteasome using Bz-Val-Gly-Arg-AMC as substrate preincubated for 15 mins followed by substrate addition measured after 2 hrs by fluorescence-based assay
AID1584466	Induction of apoptosis in human RPMI8226 cells assessed as early apoptotic cells at 10 nM after 72 hrs by APC Annexin V/eFluor-780-viability double staining-based FACS analysis (Rvb = 3.31%)	2018	Journal of medicinal chemistry, Aug-09, Volume: 61, Issue:15	Unraveling the Prenylation-Cancer Paradox in Multiple Myeloma with Novel Geranylgeranyl Pyrophosphate Synthase (GGPPS) Inhibitors.
AID599464	Growth inhibition of human HeLa cells after 72 hrs by MTT assay	2009	Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12	Synthesis and biological evaluation of boron peptide analogues of Belactosin C as proteasome inhibitors.
AID316543	Inhibition of human chymotrypsin	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1674464	Inhibition of chymotrypsin-like activity of Leishmania tarentolae proteasome beta 4	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery and Characterization of Clinical Candidate LXE408 as a Kinetoplastid-Selective Proteasome Inhibitor for the Treatment of Leishmaniases.
AID1486826	Selectivity ratio of IC50 for PGPH-like activity of 20S proteasome in human HL60 cells to IC50 for chymotrypsin-like activity of 20S proteasome in human HL60 cells	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Synthesis and biological activity of peptide proline-boronic acids as proteasome inhibitors.
AID1396601	Inhibition of chymotrypsin-like activity of human 20S proteasome using Suc-Leu-Leu-Val-Tyr-AMC as substrate incubated for 10 mins followed by substrate addition measured after 1 hr by spectrofluorimetric method	2018	Bioorganic & medicinal chemistry, 08-07, Volume: 26, Issue:14	Design, synthesis, in vitro and in vivo evaluation, and structure-activity relationship (SAR) discussion of novel dipeptidyl boronic acid proteasome inhibitors as orally available anti-cancer agents for the treatment of multiple myeloma and mechanism stud
AID1864383	Inhibition of 20S proteasome beta5 subunit (unknown origin) using Suc-LLVY-AMC as flurogenic substrate measured after 1 hr by fluorescence based analysis	2022	Journal of medicinal chemistry, 09-22, Volume: 65, Issue:18	Discovery of a Novel Oral Proteasome Inhibitor to Block NLRP3 Inflammasome Activation with Anti-inflammation Activity.
AID706493	Effect on 20S proteasome subunit beta5 expression in human HT-29 cells at 100 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID706491	Effect on 20S proteasome subunit beta5 expression in human H460 cells at 80 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID316565	Inhibition of human plasmin at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1624033	Inhibition of trypsin (unknown origin) at 10 ug/mL relative to control	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Covalent docking modelling-based discovery of tripeptidyl epoxyketone proteasome inhibitors composed of aliphatic-heterocycles.
AID1312160	Inhibition of Mycobacterium tuberculosis beta-carbonic anhydrase Rv3588 preincubated for 15 mins by stopped-flow CO2 hydration assay	2016	Bioorganic & medicinal chemistry, 09-15, Volume: 24, Issue:18	Bortezomib inhibits bacterial and fungal β-carbonic anhydrases.
AID1486820	Cytotoxicity against human MDA-MB-231 cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Synthesis and biological activity of peptide proline-boronic acids as proteasome inhibitors.
AID706476	Effect on 20S proteasome subunit beta5 chymotrypsin-like activity in human HT-29 cells at 100 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID734747	Cytotoxicity against human HCT116 cells after 72 hrs by CCK-8 assay	2013	Journal of medicinal chemistry, May-09, Volume: 56, Issue:9	Potent proteasome inhibitors derived from the unnatural cis-cyclopropane isomer of Belactosin A: synthesis, biological activity, and mode of action.
AID1595604	Cytotoxicity against human NCI-H23 cells after 72 hrs by CellTiter 96 AQueous one solution cell proliferation assay	2019	Journal of medicinal chemistry, 05-09, Volume: 62, Issue:9	Development of Novel Epoxyketone-Based Proteasome Inhibitors as a Strategy To Overcome Cancer Resistance to Carfilzomib and Bortezomib.
AID1687102	Inhibition of Plasmodium falciparum 20S proteasome beta 2 subunit trypsin-like activity using fluorogenic peptide Ac-WLR-AMC as substrate in presence of PA28alpha incubated for 1 to 2 hrs by fluorescence microplate reader assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1687120	Cytotoxicity against human HCT116 cells assessed as reduction in cell viability incubated for 72 hrs by cell-titer glo assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID548721	Toxicity in Sprague-Dawley rat assessed as incidence of mortality at 1 mg/kg, ig after 10 hrs	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1156380	Growth inhibition of human SF539 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1198170	Metabolic stability in Balb/c mouse liver microsomes	2015	Journal of medicinal chemistry, Feb-26, Volume: 58, Issue:4	Proteasome inhibitors with pyrazole scaffolds from structure-based virtual screening.
AID761479	Inhibition of 20S proteasome (unknown origin)	2013	Journal of medicinal chemistry, Jul-25, Volume: 56, Issue:14	Inhibition of the human proteasome by imidazoline scaffolds.
AID526415	Inhibition of chymotrypsin-like activity of human 20s proteasome beta-1 subunit in human erythrocyte assessed as hydrolysis of Ac-WLA-AMC fluorogenic substrate	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID706483	Effect on 20S proteasome subunit beta5 chymotrypsin-like activity in human THP1 cells at 50 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID316554	Inhibition of human caspase 1 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1156385	Growth inhibition of human MALME-3M cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1576780	Inhibition of 20S proteasome beta 1c derived from human erythrocytes preincubated for 1 hr using Z-nLPnLD-Glo peptide as substrate by proteasome-glo caspase-like assay	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID1382147	Inhibition of chymotrypsin-like activity of human 20S proteasome using Suc-LLVY-MCA as substrate measured for 1 hr by fluorescence assay	2018	European journal of medicinal chemistry, Feb-25, Volume: 146	Ridaifen-F conjugated with cell-penetrating peptides inhibits intracellular proteasome activities and induces drug-resistant cell death.
AID1566919	Resistance index, ratio of EC50 for erythrocytic stage of Plasmodium falciparum Dd2 harboring 20S beta2 proteasome A117D mutant to EC50 erythrocytic stage of Plasmodium falciparum Dd2	2019	Journal of medicinal chemistry, 07-11, Volume: 62, Issue:13	Improvement of Asparagine Ethylenediamines as Anti-malarial
AID354000	Inhibition of chymotrypsin-like activity of LMP7 immunoproteasome by proteasome active site ELISA	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Design and synthesis of an orally bioavailable and selective peptide epoxyketone proteasome inhibitor (PR-047).
AID496369	Induction of OAS gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 1day by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1473218	Cell cycle arrest in human RPMI8226 cells assessed as accumulation at sub-G1 phase at 2.5 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 12.25%)	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID599463	Inhibition of trypsin-like activity of human erythrocyte 20S proteasome using Boc-LLR-AMC substrate incubated at 37 degC for 1 hr by fluorometric assay	2009	Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12	Synthesis and biological evaluation of boron peptide analogues of Belactosin C as proteasome inhibitors.
AID1604182	Inhibition of 20S proteasome beta 1c (unknown origin) after 1 hr by fluorescence based assay	2019	European journal of medicinal chemistry, Nov-15, Volume: 182	Immunoproteasome-selective inhibitors: An overview of recent developments as potential drugs for hematologic malignancies and autoimmune diseases.
AID1363844	Inhibition of proteasome in human SEM cells assessed as increase in aggresome accumulation at 10 nM after 18 hrs by by FACS analysis	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Discovery of the First-in-Class Dual Histone Deacetylase-Proteasome Inhibitor.
AID625284	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID452098	Inhibition of chymotrypsin-like activity of mouse liver 20S proteasome	2009	Bioorganic & medicinal chemistry, Oct-01, Volume: 17, Issue:19	Design, synthesis and biological evaluation of tripeptide boronic acid proteasome inhibitors.
AID1687105	Inhibition of human 20S constitutive proteasome beta 1 subunit caspase-like activity using fluorogenic peptide Ac-nLPnLD-AMC as substrate in presence of PA28alpha incubated for 1 to 2 hrs by fluorescence microplate reader assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID496321	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as expression of 3.5 and 2.1 kb HBV mRNA at 5 mg/kg, iv single dose after 24 hrs	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1372755	Cytotoxicity against human MYCN2 cells assessed as reduction in cell viability at 0.1 to 1 uM after 24 hrs by MTT assay	2018	Bioorganic & medicinal chemistry, 01-15, Volume: 26, Issue:2	Immunoproteasome inhibition and bioactivity of thiasyrbactins.
AID496310	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as inhibition of HBV DNA replication at 1 mg/kg, iv single dose after 3 days by Southern blot analysis	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID496381	Toxicity in HBV infected 1.3.32 transgenic mouse assessed as labored breathing, hunched posture at 5 mg/kg, iv after 24 hrs	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1771375	Antiproliferative activity against human MM1.S cells assessed as reduction in cell viability incubated for 72 hrs by XTT assay	2021	Journal of natural products, 08-27, Volume: 84, Issue:8	Structure-Activity Relationships of Withanolides as Antiproliferative Agents for Multiple Myeloma: Comparison of Activity in 2D Models and a 3D Coculture Model.
AID496332	Induction of TGTP gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv by RT- PCR	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1156408	Growth inhibition of human PC3 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID316529	Inhibition of human calpain 1 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID330780	Cytotoxicity against mouse B16-F1 cells transfected with luciferase siRNA assessed as assessed as annexin 5 uptake at 100 nM after 24 hrs by flow cytometry	2007	Proceedings of the National Academy of Sciences of the United States of America, Dec-04, Volume: 104, Issue:49	Small molecule obatoclax (GX15-070) antagonizes MCL-1 and overcomes MCL-1-mediated resistance to apoptosis.
AID1484607	Inhibition of chymotrypsin-like activity of 26S proteasome beta 5 subunit in human U266 cells using Suc-LLVY-aminoluciferin as substrate after 1 hr by Proteosome-Glo luminescence assay	2017	European journal of medicinal chemistry, Jul-28, Volume: 135	Synthesis and antiproteasomal activity of novel O-benzyl salicylamide-based inhibitors built from leucine and phenylalanine.
AID459689	Systemic clearance in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1443492	Inhibition of chymotrypsin like activity of 26S proteasome derived from human MDA-MB-231 cells at 1 uM	2017	Journal of medicinal chemistry, 04-13, Volume: 60, Issue:7	First Bispecific Inhibitors of the Epidermal Growth Factor Receptor Kinase and the NF-κB Activity As Novel Anticancer Agents.
AID1566917	Antimalarial activity against erythrocytic stage of Plasmodium falciparum Dd2 harboring 20S beta2 proteasome A117D mutant measured after 72 hrs by SYBR green dye based fluorescence assay	2019	Journal of medicinal chemistry, 07-11, Volume: 62, Issue:13	Improvement of Asparagine Ethylenediamines as Anti-malarial
AID1576776	Inhibition of human 20S proteasome beta 5i preincubated for 1 hr followed by fluorescence based assay	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID1486825	Selectivity ratio of IC50 for trypsin-like activity of 20S proteasome in human HL60 cells to IC50 for chymotrypsin-like activity of 20S proteasome in human HL60 cells	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Synthesis and biological activity of peptide proline-boronic acids as proteasome inhibitors.
AID1459641	Antiproliferative activity against human 95-D cells after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID316537	Inhibition of human cathepsin L at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1818939	Antiproliferative activity against human RPMI 8226 cells assessed as reduction in cell viability measured after 72 hrs by XTT assay	2022	Journal of natural products, 01-28, Volume: 85, Issue:1	Phytochemical Investigation of the Roots of
AID1141825	Inhibition of chymotrypsin-like enzyme activity of purified human 20S proteasome using Suc-Leu-Leu-Val-Tyr-AMC as substrate by fluorescence method	2014	Bioorganic & medicinal chemistry, Jun-01, Volume: 22, Issue:11	Design, synthesis and biological evaluation of novel tripeptidyl epoxyketone derivatives constructed from β-amino acid as proteasome inhibitors.
AID1473741	Inhibition of human MRP4 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay	2013	Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1	A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID706512	Resistance factor, ratio of IC50 for 200 nM bortezonib-resistant human HT-29 cells harboring R24C prosequence mutation and proteosome subunit beta5 C63F mutant to IC50 for wild type human HT-29 cells measured after 3 days in absence of compound	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID316550	Inhibition of human MMP3 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1825581	Cytotoxicity in human bone marrow mononuclear cell assessed as total number of mononuclear cells at 50 nM measured after 72 hrs by Annexin V staining based flow cytometric analysis (Rvb =78.2%)	2022	Journal of medicinal chemistry, 02-10, Volume: 65, Issue:3	Synthesis and Evaluation of Structurally Diverse C-2-Substituted Thienopyrimidine-Based Inhibitors of the Human Geranylgeranyl Pyrophosphate Synthase.
AID1584475	Induction of apoptosis in human RPMI8226 cells at 10 nM after 72 hrs in presence of GGOH by APC Annexin V/eFluor-780-viability double staining-based FACS analysis	2018	Journal of medicinal chemistry, Aug-09, Volume: 61, Issue:15	Unraveling the Prenylation-Cancer Paradox in Multiple Myeloma with Novel Geranylgeranyl Pyrophosphate Synthase (GGPPS) Inhibitors.
AID1486821	Cytotoxicity against human HL60 cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Synthesis and biological activity of peptide proline-boronic acids as proteasome inhibitors.
AID1459643	Antiproliferative activity against human HL60 cells after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1312157	Inhibition of Malassezia globosa beta-carbonic anhydrase preincubated for 15 mins by stopped-flow CO2 hydration assay	2016	Bioorganic & medicinal chemistry, 09-15, Volume: 24, Issue:18	Bortezomib inhibits bacterial and fungal β-carbonic anhydrases.
AID640521	Inhibition of chymotrypsin-like activity of 20S proteasome in human DLD1 cells transfected with 4Ub-Luc gene using Succinyl-Leu-Leu-Val-Tyr-AMC as substrate after 6 hrs by spectrofluorometric analysis	2012	Bioorganic & medicinal chemistry, Jan-15, Volume: 20, Issue:2	Semisynthetic neoboutomellerone derivatives as ubiquitin-proteasome pathway inhibitors.
AID459688	Volume of distribution in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1128232	Inhibition of human HCT116 cell growth	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID316546	Inhibition of HIV1 protease at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1584468	Induction of apoptosis in human RPMI8226 cells assessed as necrotic cells at 10 nM after 72 hrs by APC Annexin V/eFluor-780-viability double staining-based FACS analysis (Rvb = 3.60%)	2018	Journal of medicinal chemistry, Aug-09, Volume: 61, Issue:15	Unraveling the Prenylation-Cancer Paradox in Multiple Myeloma with Novel Geranylgeranyl Pyrophosphate Synthase (GGPPS) Inhibitors.
AID1439183	Inhibition of chymotrypsin-like activity of human 20S proteasome using Suc-Leu-Leu-Val-Tyr-AMC as substrate by fluorescence assay	2017	European journal of medicinal chemistry, Mar-10, Volume: 128	Design, synthesis and biological evaluation of novel non-peptide boronic acid derivatives as proteasome inhibitors.
AID1484608	Inhibition of trypsin like activity of 26S proteasome beta 2 subunit in human U266 cells assessed as residual activity using Z-LLE-AMC as substrate at 10 uM preincubated for 1 hr followed by substrate addition and measured after 4 hrs by fluorescence assa	2017	European journal of medicinal chemistry, Jul-28, Volume: 135	Synthesis and antiproteasomal activity of novel O-benzyl salicylamide-based inhibitors built from leucine and phenylalanine.
AID1460769	Inhibition of human CA5B by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID1548262	Antiproliferative activity against human GES-1 cells incubated for 48 hrs by MTT assay
AID1486822	Inhibition of chymotrypsin-like activity of 20S proteasome in human HL60 cells using Suc-LLVYaminoluciferin as substrate pretreated for 2 hrs followed by substrate addition by fluorescence assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Synthesis and biological activity of peptide proline-boronic acids as proteasome inhibitors.
AID1396606	Cytotoxicity against human ARH77 cells assessed as reduction in cell viability after 72 hrs by CellTiter 96 aqueous one solution assay	2018	Bioorganic & medicinal chemistry, 08-07, Volume: 26, Issue:14	Design, synthesis, in vitro and in vivo evaluation, and structure-activity relationship (SAR) discussion of novel dipeptidyl boronic acid proteasome inhibitors as orally available anti-cancer agents for the treatment of multiple myeloma and mechanism stud
AID548704	Cytotoxicity against human HL60 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1473234	Cell cycle arrest in human NCI-H929 cells assessed as accumulation at sub-G1 phase at 2.5 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 5.59%)	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID1604186	Inhibition of 20S proteasome beta 5c (unknown origin) after 1 hr by fluorescence based assay	2019	European journal of medicinal chemistry, Nov-15, Volume: 182	Immunoproteasome-selective inhibitors: An overview of recent developments as potential drugs for hematologic malignancies and autoimmune diseases.
AID496359	Induction of IL-1alpha gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 3 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1156373	Growth inhibition of human HCT116 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1372744	Inhibition of 20s constitutive proteasome chymotrypsin-like activity in human erythrocytes using Suc-LLVY-Glo as substrate pretreated for 2 hrs followed by substrate addition measured after 10 mins by luminescence assay	2018	Bioorganic & medicinal chemistry, 01-15, Volume: 26, Issue:2	Immunoproteasome inhibition and bioactivity of thiasyrbactins.
AID540212	Mean residence time in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID548699	Cytotoxicity against human SW480 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID496378	Induction of IL-3 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 2 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1156389	Growth inhibition of human SK-MEL-28 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID496330	Induction of ISG15 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv by RT- PCR	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1473258	Induction of apoptosis in human U266 cells at 2.5 nM after 24 hrs by Annexin V/propidium iodide staining based flow cytometry	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID1687133	Inhibition of human 20S constitutive proteasome beta 1 subunit assessed as inhibition of BMV037 probe labeling at 1 to 10 uM incubated for 1 hr by SDS-PAGE analysis	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID526548	Inhibition of human coagulation factor beta 12a at 100 uM	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID1156371	Growth inhibition of human COLO205 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID706482	Effect on 20S proteasome subunit beta5 chymotrypsin-like activity in human THP1 cells at 100 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1624032	Inhibition of Caspase-3 (unknown origin) at 10 ug/mL using AC-DEVD-AMC as substrate by fluorescence assay relative to control	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Covalent docking modelling-based discovery of tripeptidyl epoxyketone proteasome inhibitors composed of aliphatic-heterocycles.
AID706739	Resistance factor, ratio of IC50 for 30 nM bortezonib-resistant human SW1573 cells harboring proteosome subunit beta5 C52F mutant to IC50 for wild type human SW1573 cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID496311	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as inhibition of HBV DNA replication at 1 mg/kg, iv single dose after 6 days by Southern blot analysis	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1623361	Cell cycle arrest in human NCI-H929 cells assessed as accumulation at G0/G1 phase at 2 nM after 48 hrs by propidium iodide/RNase staining based flow cytometric method relative to control	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID1156392	Growth inhibition of human UACC62 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID316557	Inhibition of human caspase 7 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID353301	Inhibition of peptidylglutamyl-peptide hydrolyzing activity of human 20S proteasome	2009	Bioorganic & medicinal chemistry letters, Apr-15, Volume: 19, Issue:8	Synthesis of boronic acid derivatives of tyropeptin: proteasome inhibitors.
AID1903224	Inhibition of chymotrypsin-like activity of human 20S proteasome using Suc-Leu Leu-Val-Tyr-AMC as substrate preincubated for 15 mins followed by substrate addition measured by fluorescence assay	2022	European journal of medicinal chemistry, Apr-05, Volume: 233	Metabolism guided optimization of peptidomimetics as non-covalent proteasome inhibitors for cancer treatment.
AID316551	Inhibition of human MMP7 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1448881	Antiproliferative activity against human MCF7 cells after 3 days by SRB assay	2017	Journal of medicinal chemistry, 06-22, Volume: 60, Issue:12	Identification of a Water-Soluble Indirubin Derivative as Potent Inhibitor of Insulin-like Growth Factor 1 Receptor through Structural Modification of the Parent Natural Molecule.
AID1156399	Growth inhibition of human SKOV3 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1486823	Inhibition of trypsin-like activity of 20S proteasome in human HL60 cells using Z-LRRaminoluciferin as substrate pretreated for 2 hrs followed by substrate addition by fluorescence assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Synthesis and biological activity of peptide proline-boronic acids as proteasome inhibitors.
AID316534	Inhibition of human cathepsin G at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID316547	Inhibition of human plasma kallikrein at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID781077	Cytotoxicity against human RPMI8226 cells after 48 to 72 hrs by SRB assay	2013	Bioorganic & medicinal chemistry letters, Dec-01, Volume: 23, Issue:23	Design, synthesis, and biological evaluation of bone-targeted proteasome inhibitors for multiple myeloma.
AID1156362	Growth inhibition of human A549/ATCC cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID548698	Cytotoxicity against human BxPC3 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1484603	Inhibition of chymotrypsin like activity of 26S proteasome beta 5 subunit in human U266 cells assessed as residual activity using N-Suc-LLVY-AMC as substrate at 10 uM preincubated for 1 hr followed by substrate addition and measured after 4 hrs by fluores	2017	European journal of medicinal chemistry, Jul-28, Volume: 135	Synthesis and antiproteasomal activity of novel O-benzyl salicylamide-based inhibitors built from leucine and phenylalanine.
AID1895436	Inhibition of human 20S immunoproteasome beta-2i subunit using Ac-RLR-AMC as substrate preincubated for 2 hrs followed by substrate addition and measured after 1 hr by fluorescence intensity assay	2021	Journal of medicinal chemistry, 07-22, Volume: 64, Issue:14	Structure-Based Optimization and Discovery of M3258, a Specific Inhibitor of the Immunoproteasome Subunit LMP7 (β5i).
AID1576793	Cytotoxicity against anti-CD3/CD28-stimulated human CD4-positive T cells with CRISP/CAS9 20S proteasome beta 5i knockout assessed as reduction in cell viability measured on day 8 by CellTiter Glo assay relative to control	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID1252358	Antiproliferative activity against human RPMI8266 cells after 72 hrs by oxyluciferin luminescence assay	2015	Bioorganic & medicinal chemistry letters, Nov-01, Volume: 25, Issue:21	Structure-activity relationship study of syringolin A as a potential anticancer agent.
AID452101	Cytotoxicity against human HL60 cells after 72 hrs by MTT assay	2009	Bioorganic & medicinal chemistry, Oct-01, Volume: 17, Issue:19	Design, synthesis and biological evaluation of tripeptide boronic acid proteasome inhibitors.
AID1372747	Inhibition of immunoproteasome chymotrypsin-like activity in human erythrocytes using Suc-LLVY-Glo as substrate pretreated for 2 hrs followed by substrate addition measured after 10 mins by luminescence assay	2018	Bioorganic & medicinal chemistry, 01-15, Volume: 26, Issue:2	Immunoproteasome inhibition and bioactivity of thiasyrbactins.
AID1576779	Inhibition of human 20S proteasome beta 1i	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID706497	Effect on 20S proteasome subunit beta5 expression in human THP1 cells at 30 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1295430	Cytotoxicity against human RPMI8226 cells assessed as cell viability after 72 hrs by CellTiter 96 aqueous one solution cell proliferation assay	2016	Bioorganic & medicinal chemistry, 06-01, Volume: 24, Issue:11	3D-QSAR-aided design, synthesis, in vitro and in vivo evaluation of dipeptidyl boronic acid proteasome inhibitors and mechanism studies.
AID548710	Terminal half life in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1864385	Cytotoxicity against HEK293 cells at less than 20 uM incubated for 24 hrs	2022	Journal of medicinal chemistry, 09-22, Volume: 65, Issue:18	Discovery of a Novel Oral Proteasome Inhibitor to Block NLRP3 Inflammasome Activation with Anti-inflammation Activity.
AID526414	Cytotoxicity against human Calu6 cells assessed as cellular ATP level after 72 hrs by luminescence-based ATPlite assay	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID1480597	Antiproliferative activity against human A549 cells after 72 hrs by Cell Titer-Glo assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Discovery of an Inhibitor of the Proteasome Subunit Rpn11.
AID1459639	Antiproliferative activity against human MGC803 cells after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1486824	Inhibition of PGPH-like activity of 20S proteasome in human HL60 cells using Z-nLPnLDaminoluciferin as substrate pretreated for 2 hrs followed by substrate addition by fluorescence assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Synthesis and biological activity of peptide proline-boronic acids as proteasome inhibitors.
AID1543662	Antiproliferative activity against human PC3 cells incubated for 72 hrs by CellTiter-Glo luminescence assay	2019	European journal of medicinal chemistry, Apr-15, Volume: 168	Discovery of novel triazolo[4,3-b]pyridazin-3-yl-quinoline derivatives as PIM inhibitors.
AID496346	Induction of TNFbeta gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 2 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID611892	Inhibition of chymotrypsin-like activity of 20S proteasome using suc-LLVY-AMC as substrate preincubated for 10 mins before substrate addition at pH 2.0 by fluorescence assay	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Chemical and biological evaluation of dipeptidyl boronic acid proteasome inhibitors for use in prodrugs and pro-soft drugs targeting solid tumors.
AID1372749	Inhibition of immunoproteasome trypsin-like activity in human erythrocytes using Z-nLPnLD-Glo as substrate pretreated for 2 hrs followed by substrate addition measured after 10 mins by luminescence assay	2018	Bioorganic & medicinal chemistry, 01-15, Volume: 26, Issue:2	Immunoproteasome inhibition and bioactivity of thiasyrbactins.
AID625291	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID706477	Effect on 20S proteasome subunit beta5 chymotrypsin-like activity in human HBL2-BR cells at 100 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID706485	Effect on 20S proteasome subunit beta5 chymotrypsin-like activity in human NAMALWA cells at 12.5 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1156406	Growth inhibition of human TK10 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID706514	Resistance factor, ratio of IC50 for 100 nM bortezonib-resistant human HT-29 cells harboring R24C prosequence mutation and proteosome subunit beta5 C63F mutant to IC50 for wild type human HT-29 cells measured after 3 days in absence of compound	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID706505	Effect on PSMB5 mRNA expression in human THP1 cells at 50 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1156398	Growth inhibition of human NCI-ADR-RES cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1156391	Growth inhibition of human UACC257 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1764783	Inhibition of human erythrocytes 20S proteasome using QXL520-YRGITCSGRQK(5-FAM)-NH2 fluorogenic peptide as substrate preincubated for 10 mins followed by substrate addition and measured after 60 mins by HTRF assay	2021	Journal of medicinal chemistry, 04-22, Volume: 64, Issue:8	Structure-Based Design of Selective LONP1 Inhibitors for Probing
AID761481	Cytotoxicity against bortezomib-resistant human THP1 cells assessed as cell viability at 0.5 uM after 72 hrs by MTS assay relative to vehicle-treated control	2013	Journal of medicinal chemistry, Jul-25, Volume: 56, Issue:14	Inhibition of the human proteasome by imidazoline scaffolds.
AID1459662	Antitumor activity against human Bel7404 cells xenografted in BALB/c nude mouse assessed as effect on tumor volume at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 3 of compound dosing relative to control	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID496348	Induction of TNFbeta gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 6 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1614000	Inhibition of human hepatic cell derived 20s constitutive proteasome beta2 trypsin-like activity using Suc-LLE-AMC as substrate preincubated for 15 mins followed by substrate addition and measured after 60 mins by fluorescence assay	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Exploration of novel macrocyclic dipeptide N-benzyl amides as proteasome inhibitors.
AID496379	Induction of IL-3 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 3 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1459701	Toxicity in human Bel7404 cells xenografted BALB/c mouse assessed as effect on body weight at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 20 of compound dosing (Rvb = 26.43 +/- 0.94 g)	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1566920	Resistance index, ratio of EC50 for erythrocytic stage of Plasmodium falciparum Dd2 harboring 20S beta5 proteasome A49S mutant to EC50 erythrocytic stage of Plasmodium falciparum Dd2	2019	Journal of medicinal chemistry, 07-11, Volume: 62, Issue:13	Improvement of Asparagine Ethylenediamines as Anti-malarial
AID1604190	Selectivity index, ratio of IC50 for 20S proteasome beta 5c (unknown origin) to IC50 for 20S proteasome beta 5i (unknown origin)	2019	European journal of medicinal chemistry, Nov-15, Volume: 182	Immunoproteasome-selective inhibitors: An overview of recent developments as potential drugs for hematologic malignancies and autoimmune diseases.
AID1459686	Toxicity in human Bel7404 cells xenografted BALB/c mouse assessed as effect on body weight at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 3 of compound dosing (Rvb = 25.39 +/- 1 g)	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1771373	Antiproliferative activity against human MM1.R cells assessed as reduction in cell viability incubated for 72 hrs by XTT assay	2021	Journal of natural products, 08-27, Volume: 84, Issue:8	Structure-Activity Relationships of Withanolides as Antiproliferative Agents for Multiple Myeloma: Comparison of Activity in 2D Models and a 3D Coculture Model.
AID1584467	Induction of apoptosis in human RPMI8226 cells assessed as late apoptotic cells at 10 nM after 72 hrs by APC Annexin V/eFluor-780-viability double staining-based FACS analysis (Rvb = 5.80%)	2018	Journal of medicinal chemistry, Aug-09, Volume: 61, Issue:15	Unraveling the Prenylation-Cancer Paradox in Multiple Myeloma with Novel Geranylgeranyl Pyrophosphate Synthase (GGPPS) Inhibitors.
AID1156381	Growth inhibition of human SNB19 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID706722	Resistance factor, ratio of IC50 for bortezonib-resistant human OPM2 cells harboring proteosome subunit beta5 A49T mutant to IC50 for wild type human OPM2 cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID353302	Inhibition of trypsin-like activity of human 20S proteasome	2009	Bioorganic & medicinal chemistry letters, Apr-15, Volume: 19, Issue:8	Synthesis of boronic acid derivatives of tyropeptin: proteasome inhibitors.
AID540209	Volume of distribution at steady state in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1871278	Cytotoxicity against human HEK293 cells assessed as cell growth inhibition	2021	European journal of medicinal chemistry, Jan-15, Volume: 210	Renieramycin-type alkaloids from marine-derived organisms: Synthetic chemistry, biological activity and structural modification.
AID1895457	Cytotoxicity against human HepG2 cells assessed as depletion of ATP content up to 500 uM incubated for 48 to 72 hrs by CellTiter-Glo luminescent assay	2021	Journal of medicinal chemistry, 07-22, Volume: 64, Issue:14	Structure-Based Optimization and Discovery of M3258, a Specific Inhibitor of the Immunoproteasome Subunit LMP7 (β5i).
AID732585	Inhibition of presenilin-dependent gamma secretase complex in HEK293 solubilized membranes using Flag-C100 as substrate assessed as inhibition of amyloid beta40/42 production at 60 uM after 16 hrs by Western blotting analysis	2013	Bioorganic & medicinal chemistry, Feb-15, Volume: 21, Issue:4	Further characterization of a putative serine protease contributing to the γ-secretase cleavage of β-amyloid precursor protein.
AID1363798	Inhibition of chymotrypsin-like activity of 20S proteasome in human SEM cells using Suc-LLVY aminoluciferin as substrate after 2 hrs by proteasome-Glo assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Discovery of the First-in-Class Dual Histone Deacetylase-Proteasome Inhibitor.
AID1156414	Growth inhibition of human T47D cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID459661	Inhibition of chymotrypsin-like activity of human 20S proteosome assessed as hydrolysis of fluorogenic Suc-Leu-Leu-Val-Tyr-AMC substrate	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1460765	Inhibition of human CA2 by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID1825585	Cytotoxicity in human bone marrow mononuclear cell assessed as apoptotic cells at 50 nM measured after 72 hrs by Annexin V staining based flow cytometric analysis (Rvb = 21.7%)	2022	Journal of medicinal chemistry, 02-10, Volume: 65, Issue:3	Synthesis and Evaluation of Structurally Diverse C-2-Substituted Thienopyrimidine-Based Inhibitors of the Human Geranylgeranyl Pyrophosphate Synthase.
AID316578	Protein binding in mouse plasma	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1473227	Cell cycle arrest in human U266 cells assessed as accumulation at G0/G1 phase at 2.5 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 40.29%)	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID1771372	Antiproliferative activity against human RPMI-8226 cells cultured as 3D-spheroids assessed as reduction in cell viability after 48 hrs by Celltiter-Glo assay	2021	Journal of natural products, 08-27, Volume: 84, Issue:8	Structure-Activity Relationships of Withanolides as Antiproliferative Agents for Multiple Myeloma: Comparison of Activity in 2D Models and a 3D Coculture Model.
AID706478	Effect on 20S proteasome subunit beta5 chymotrypsin-like activity in human JEKO-BR cells at 100 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1548302	Induction of cell cycle arrest in bortezomib resistant human KM3/BTZ cells assessed as accumulation at G2/M phase at 100 nM incubated for 24 hrs by propidium iodide staining based flow cytometry (Rvb = 9.1%)
AID1484624	Inhibition of proteasome in human U266 cells assessed as increase in accumulation of polyubiquitinated proteins by Western blot analysis	2017	European journal of medicinal chemistry, Jul-28, Volume: 135	Synthesis and antiproteasomal activity of novel O-benzyl salicylamide-based inhibitors built from leucine and phenylalanine.
AID1624030	Inhibition of MMP12 (unknown origin) at 10 ug/mL using Ac-Pro-Leu-Gly-[(S)-2-mercapto-4-methyl-pentanoyl]-Leu-Gly-Oet as substrate relative to control	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Covalent docking modelling-based discovery of tripeptidyl epoxyketone proteasome inhibitors composed of aliphatic-heterocycles.
AID706490	Effect on 20S proteasome subunit beta5 expression in human H460 cells at 200 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1156411	Growth inhibition of human MDA-MB-231 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1128516	Inhibition of cathepsin B (unknown origin) assessed as Cbz-Phe-Arg-AMC substrate hydrolysis	2014	European journal of medicinal chemistry, Apr-09, Volume: 76	Identification of a new series of amides as non-covalent proteasome inhibitors.
AID1623369	Induction of apoptosis in human NCI-H929 cells assessed as late apoptotic cells at 2 nM after 48 hrs by Annexin-V/propidium iodide staining based flow cytometric method (Rvb = 0.23%)	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID548703	Cytotoxicity against human HepG2 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1325773	Inhibition of chymotrypsin like activity of mouse spleen 20S proteasome beta5i subunit using Suc-Leu-Leu-Val-Tyr-AMC as substrate preincubated for 15 mins followed by substrate addition measured after 2 hrs by fluorescence-based assay
AID539018	Inhibition of NF-kappaB activity in TNF-alpha-induced human HEK293 cells after 30 mins by luciferase assay	2010	Bioorganic & medicinal chemistry, Dec-01, Volume: 18, Issue:23	Rubiyunnanins C-H, cytotoxic cyclic hexapeptides from Rubia yunnanensis inhibiting nitric oxide production and NF-κB activation.
AID316576	Metabolic stability in dog liver microsomes	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1623368	Induction of apoptosis in human NCI-H929 cells assessed as early apoptotic cells at 2 nM after 48 hrs by Annexin-V/propidium iodide staining based flow cytometric method (Rvb = 17.1%)	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID548716	Mean residence time (0-t) in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID734754	Inhibition of chymotrypsin-like activity of human 20S proteasome beta 5 subunit using Suc-LLVY-AMC as substrate after 60 mins by fluorescence assay	2013	Journal of medicinal chemistry, May-09, Volume: 56, Issue:9	Potent proteasome inhibitors derived from the unnatural cis-cyclopropane isomer of Belactosin A: synthesis, biological activity, and mode of action.
AID1895441	Selectivity ratio of IC50 for inhibition of human 20S proteasome beta5 subunit to IC50 for inhibition of human 20S immunoproteasome beta-5i subunit	2021	Journal of medicinal chemistry, 07-22, Volume: 64, Issue:14	Structure-Based Optimization and Discovery of M3258, a Specific Inhibitor of the Immunoproteasome Subunit LMP7 (β5i).
AID1156361	Growth inhibition of human SR cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID526416	Inhibition of chymotrypsin-like activity of human 20s proteasome beta2 subunit in human erythrocyte assessed as hydrolysis of Ac-WLA-AMC fluorogenic substrate	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID1605096	Inhibition of N-terminal His6-sumo-tagged full length Staphylococcus aureus ClpP expressed in Escherichia coli BL2 (DE3) pre-incubated for 10 mins before Suc-LY-AMC addition and measured after 1 hr by fluorescence based assay	2020	Journal of medicinal chemistry, 03-26, Volume: 63, Issue:6	Discovery of Novel Peptidomimetic Boronate ClpP Inhibitors with Noncanonical Enzyme Mechanism as Potent Virulence Blockers
AID1156376	Growth inhibition of human KM12 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1473228	Cell cycle arrest in human U266 cells assessed as accumulation at S phase at 2.5 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 14.05%)	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID496380	Induction of IL-3 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 6 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID459691	Toxicity in Sprague-Dawley rat assessed as mortality at 1 mg/kg, iv after 10 hrs	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1623412	Cytotoxicity against human RPMI8226 cells assessed as reduction in cell viability at 2 nM after 48 hrs by CCK8 assay relative to control	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID496350	Induction of IL-4 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 2 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID548706	Tmax in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1460775	Inhibition of human CA14 by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID459682	Systemic clearance in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID625283	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1764782	Inhibition of LONP1 (unknown origin) using QXL520-YRGITCSGRQK(5-FAM)-NH2 peptide as substrate incubated for 50 mins in presence of ATP by HTRF assay	2021	Journal of medicinal chemistry, 04-22, Volume: 64, Issue:8	Structure-Based Design of Selective LONP1 Inhibitors for Probing
AID1459658	Half life in Sprague-Dawley rat at 0.8 mg/kg, iv administered as bolus	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1473740	Inhibition of human MRP3 overexpressed in Sf9 insect cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 10 mins by membrane vesicle transport assay	2013	Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1	A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID706494	Effect on 20S proteasome subunit beta5 expression in human THP1 cells at 200 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1156410	Growth inhibition of human MCF7 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID316520	Half life in CD1 mouse at 4 mg/kg, po	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1252356	Antiproliferative activity against human TOV21G cells after 72 hrs by oxyluciferin luminescence assay	2015	Bioorganic & medicinal chemistry letters, Nov-01, Volume: 25, Issue:21	Structure-activity relationship study of syringolin A as a potential anticancer agent.
AID1480598	Antiproliferative activity against human 293T cells after 72 hrs by Cell Titer-Glo assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Discovery of an Inhibitor of the Proteasome Subunit Rpn11.
AID611891	Inhibition of proteasome in mouse tumor cells relative to inhibition in blood cells	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Chemical and biological evaluation of dipeptidyl boronic acid proteasome inhibitors for use in prodrugs and pro-soft drugs targeting solid tumors.
AID1453444	Inhibition of recombinant human C-MYC/DDK-tagged ENGase expressed in HEK293T cells at 100 uM using heat inactivated bovine ribonuclease B as substrate pretreated for 15 mins followed by substrate addition after 90 mins by SDS-PAGE analysis	2017	Bioorganic & medicinal chemistry letters, 07-01, Volume: 27, Issue:13	Repurposing of Proton Pump Inhibitors as first identified small molecule inhibitors of endo-β-N-acetylglucosaminidase (ENGase) for the treatment of NGLY1 deficiency, a rare genetic disease.
AID1687128	Antiplasmodial activity against sorbitol synchronized ring stage bortezomib-resistant Plasmodium falciparum 3D7 clone B2a assessed as reduction in parasitemia incubated for 72 hrs by Syto-61 staining dye based flow cytometry analysis	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1312154	Inhibition of Candida albicans beta-carbonic anhydrase preincubated for 15 mins by stopped-flow CO2 hydration assay	2016	Bioorganic & medicinal chemistry, 09-15, Volume: 24, Issue:18	Bortezomib inhibits bacterial and fungal β-carbonic anhydrases.
AID526413	Inhibition of TNF-alpha-induced NF-kappaB activation in human HEK293 cells after 3 hrs by luciferase reporter gene assay	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID1112954	Inhibition of NF-kappaB-mediated viral replication in Homo sapiens (human) U1 cells infected with X4 tropic HIV1 NL4-3 at 10 uM after 24 hr by RT-PCR analysis in presence of TNF-alpha	2013	Bioorganic & medicinal chemistry letters, Feb-01, Volume: 23, Issue:3	Inhibition of HIV-1 replication by a tricyclic coumarin GUT-70 in acutely and chronically infected cells.
AID1687122	Selectivity index, ratio of LD50 for cytotoxicity against human HepG2 cells to LD50 for antiplasmodial activity against Plasmodium falciparum 3D7 sorbitol-treated ring stage	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID706475	Effect on 20S proteasome subunit beta5 chymotrypsin-like activity in human HT-29 cells at 200 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1128231	Inhibition of trypsin-like activity of human 20S proteasome using Ac-RLR-AMC as substrate	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID316544	Inhibition of human factor 7a at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1443491	Inhibition of trypsin like activity of 26S proteasome derived from human MDA-MB-231 cells at 1 uM	2017	Journal of medicinal chemistry, 04-13, Volume: 60, Issue:7	First Bispecific Inhibitors of the Epidermal Growth Factor Receptor Kinase and the NF-κB Activity As Novel Anticancer Agents.
AID706728	Resistance factor, ratio of IC50 for human Jurkat B2 cells harboring silent mutation and proteosome subunit beta5 A49T heterozygous mutant to IC50 for wild type human Jurkat cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1325770	Inhibition of chymotrypsin like activity of rabbit 20S proteasome using Suc-Leu-Leu-Val-Tyr-AMC as substrate preincubated for 15 mins followed by substrate addition measured after 2 hrs by fluorescence-based assay
AID1548270	Inhibition of proteasome in human RPMI8226 cells assessed as increase in polyubiquitinated proteins accumulation at 10 to 1000 nM incubated for 24 hrs Western blotting analysis
AID496351	Induction of IL-4 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 3 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID316541	Inhibition of human chymase	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1197986	Induction of cell death in human A549 cells assessed as stabilization of p53 at 0.025 to 0.5 uM after 24 hrs by immunoblot assay	2015	Journal of medicinal chemistry, Feb-26, Volume: 58, Issue:4	Synthesis, characterization, and optimization for in vivo delivery of a nonselective isopeptidase inhibitor as new antineoplastic agent.
AID1818944	Antiproliferative activity against dexamethasone-resistant human MM.1R cells assessed as reduction in cell viability at 10 uM measured after 72 hrs by XTT assay	2022	Journal of natural products, 01-28, Volume: 85, Issue:1	Phytochemical Investigation of the Roots of
AID1623350	Cytotoxicity against human RPMI8226 cells assessed as reduction in cell viability at 2 nM after 48 hrs by CCK8 assay	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID1128513	Inhibition of chymotrypsin-like activity of human 20S proteasome beta 5 subunit assessed as Suc-Leu-Leu-Val-Tyr-AMC substrate hydrolysis at 20 uM after 10 mins by fluorometric analysis	2014	European journal of medicinal chemistry, Apr-09, Volume: 76	Identification of a new series of amides as non-covalent proteasome inhibitors.
AID548697	Inhibition of human 20S proteasome chymotrypsin-like activity by fluorimetric assay	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID459678	Mean residence time in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID459679	AUC (0 to t) in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1156400	Growth inhibition of human 786-0 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID548715	AUC (0-t) in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID548719	Systemic clearance in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1128244	Reversible inhibition of chymotrypsin-like activity of human 20S proteasome using Suc-LLVY-AMC as substrate measured after drug wash-out	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID316556	Inhibition of human caspase 3 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID316579	Protein binding in rat plasma	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1375834	Cytotoxicity against human SKOV3 cells assessed as decrease in cell viability after 4 days by CellTiter-Glo assay	2018	Journal of medicinal chemistry, 06-14, Volume: 61, Issue:11	Discovery of Orally Bioavailable, Quinoline-Based Aldehyde Dehydrogenase 1A1 (ALDH1A1) Inhibitors with Potent Cellular Activity.
AID1382146	Inhibition of trypsin-like activity of human 20S proteasome using Boc-LRR-MCA as substrate measured for 1 hr by fluorescence assay	2018	European journal of medicinal chemistry, Feb-25, Volume: 146	Ridaifen-F conjugated with cell-penetrating peptides inhibits intracellular proteasome activities and induces drug-resistant cell death.
AID1548273	Induction of cell cycle arrest in human RPMI8226 cells assessed as accumulation at S phase at 100 nM incubated for 24 hrs by propidium iodide staining based flow cytometry (Rvb = 23.5%)
AID1864382	Inhibition of NLRP3 inflammasome activation in LPS-primed mouse J774.A1 cells assessed as reduction in IL-1beta secretion preincubated for 1 hr followed by nigericin stimulation and measured after 1 hr by ELISA	2022	Journal of medicinal chemistry, 09-22, Volume: 65, Issue:18	Discovery of a Novel Oral Proteasome Inhibitor to Block NLRP3 Inflammasome Activation with Anti-inflammation Activity.
AID1614003	Inhibition of human peripheral blood derived 20s immunoproteasome beta5 chymotrypsin-like activity using Suc-PAL-AMC as substrate preincubated for 15 mins followed by substrate addition and measured after 60 mins by fluorescence assay	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Exploration of novel macrocyclic dipeptide N-benzyl amides as proteasome inhibitors.
AID1687124	Antiplasmodial activity against DHA-sensitive and sorbitol synchronized ring stage forms of Plasmodium falciparum Cam3.II^rev expressing K13 wild-type genotype assessed as reduction in parasitemia incubated for 3 hrs by pulse exposure based Syto-61 staini	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID526412	Binding affinity to chymotrypsin-like activity of 20S proteasome	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID1548263	Antiproliferative activity against human HL7702 cells incubated for 48 hrs by MTT assay
AID1459653	Antitumor activity against human Bel7404 cells xenografted in BALB/c nude mouse assessed as effect on tumor volume at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 1 of compound dosing relative to control	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID611899	Ratio of CC50 for human follicular small-cell lymphocytic leukemia cells to IC50 for intracellular chymotrypsin-like activity of 20S proteasome in human HEK293 cells	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Chemical and biological evaluation of dipeptidyl boronic acid proteasome inhibitors for use in prodrugs and pro-soft drugs targeting solid tumors.
AID599471	Cell cycle arrest in human HeLa cells assessed as accumulation at G1 phase at 0.1 uM after 24 hrs by flow cytometry (Rvb = 56.4 +/- 0.39%)	2009	Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12	Synthesis and biological evaluation of boron peptide analogues of Belactosin C as proteasome inhibitors.
AID1895440	Inhibition of human 20S proteasome beta5 subunit using Suc-LLVY-AMC as substrate preincubated for 2 hrs followed by substrate addition and measured after 1 hr by fluorescence intensity assay	2021	Journal of medicinal chemistry, 07-22, Volume: 64, Issue:14	Structure-Based Optimization and Discovery of M3258, a Specific Inhibitor of the Immunoproteasome Subunit LMP7 (β5i).
AID1484612	Inhibition of caspase like activity of 26S proteasome beta 1 subunit in human U266 cells assessed as residual activity using Bz-VGR-AMC as substrate at 10 uM preincubated for 1 hr followed by substrate addition and measured after 4 hrs by fluorescence ass	2017	European journal of medicinal chemistry, Jul-28, Volume: 135	Synthesis and antiproteasomal activity of novel O-benzyl salicylamide-based inhibitors built from leucine and phenylalanine.
AID1325774	Inhibition of bovine alpha chymotrypsin using Ala-Ala-Phe-7-AMC as substrate measured for 10 mins by spectrophotometric analysis
AID1473219	Cell cycle arrest in human RPMI8226 cells assessed as accumulation at G0/G1 phase at 2.5 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 44.67%)	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID316519	Clearance in CD1 mouse at 0.8 mg/kg, iv	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID599462	Inhibition of caspase-like activity of human erythrocyte 20S proteasome using Z-LLE-AMC substrate incubated at 37 degC for 1 hr by fluorometric assay	2009	Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12	Synthesis and biological evaluation of boron peptide analogues of Belactosin C as proteasome inhibitors.
AID611893	Inhibition of chymotrypsin-like activity of 20S proteasome using suc-LLVY-AMC as substrate preincubated for 10 mins before substrate addition at pH 7.6 by fluorescence assay	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Chemical and biological evaluation of dipeptidyl boronic acid proteasome inhibitors for use in prodrugs and pro-soft drugs targeting solid tumors.
AID781078	Cytotoxicity against mouse 5TGM1 cells after 48 to 72 hrs by SRB assay	2013	Bioorganic & medicinal chemistry letters, Dec-01, Volume: 23, Issue:23	Design, synthesis, and biological evaluation of bone-targeted proteasome inhibitors for multiple myeloma.
AID1689691	Inhibition of HDAC1 in human RPMI-8226 cells incubated for 2 hrs by ELISA	2020	European journal of medicinal chemistry, Mar-01, Volume: 189	1,2,3-Triazole-Chalcone hybrids: Synthesis, in vitro cytotoxic activity and mechanistic investigation of apoptosis induction in multiple myeloma RPMI-8226.
AID1687125	Inhibition of proteasome in Plasmodium falciparum trophozoite stage transfected with GFP-DD assessed as reduction in GFP-DD fusion protein degradation at 0.02 to 0.5 uM incubated for 3 hrs in absence of Shield-1 by Western blot analysis	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1473221	Cell cycle arrest in human RPMI8226 cells assessed as accumulation at G2/M phase at 2.5 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 23.94%)	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID1584465	Induction of apoptosis in human RPMI8226 cells assessed as viable cells at 10 nM after 72 hrs by APC Annexin V/eFluor-780-viability double staining-based FACS analysis (Rvb = 87.3%)	2018	Journal of medicinal chemistry, Aug-09, Volume: 61, Issue:15	Unraveling the Prenylation-Cancer Paradox in Multiple Myeloma with Novel Geranylgeranyl Pyrophosphate Synthase (GGPPS) Inhibitors.
AID706503	Effect on PSMB5 mRNA expression in human THP1 cells at 200 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID496313	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as expression of 3.5 and 2.1 kb HBV mRNA at 1 mg/kg, iv single dose after 2 days by Northern blot analysis	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1325783	Cytotoxicity against human U266 cells harboring mutant p53 assessed as reduction in cell viability after 48 hrs by 7AAD-staining based FACS analysis
AID1459633	Inhibition of caspase-like activity of 20S proteasome in human HL60 cells using Z-nLPnLDaminoluciferin as substrate at 0.2 uM after 2 hrs by fluorescence analysis	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID706498	Effect on PSMB5 mRNA expression in human RPMI8226 cells at 7 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1156397	Growth inhibition of human OVCAR8 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1459637	Inhibition of chymotrypsin-like activity of 20S proteasome in human HL60 cells using Suc-LLVYaminoluciferin as substrate after 2 hrs by fluorescence analysis	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1818941	Antiproliferative activity against dexamethasone-resistant human MM.1R cells assessed as reduction in cell viability measured after 72 hrs by XTT assay	2022	Journal of natural products, 01-28, Volume: 85, Issue:1	Phytochemical Investigation of the Roots of
AID1156372	Growth inhibition of human HCC2998 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1614001	Inhibition of human peripheral blood derived 20s immunoproteasome beta1 caspase-like activity using Suc-PAL-AMC as substrate preincubated for 15 mins followed by substrate addition and measured after 60 mins by fluorescence assay	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Exploration of novel macrocyclic dipeptide N-benzyl amides as proteasome inhibitors.
AID330775	Cytotoxicity against mouse B16-F1 cells transfected with MCL1 siRNA assessed as assessed as annexin 5 uptake at 100 nM after 24 hrs by flow cytometry	2007	Proceedings of the National Academy of Sciences of the United States of America, Dec-04, Volume: 104, Issue:49	Small molecule obatoclax (GX15-070) antagonizes MCL-1 and overcomes MCL-1-mediated resistance to apoptosis.
AID1137838	Inhibition of immunoproteasome 20S subunit beta5i in human Karpas 1106p cell extract at 1 nM	2014	ACS medicinal chemistry letters, Apr-10, Volume: 5, Issue:4	Oxathiazolones Selectively Inhibit the Human Immunoproteasome over the Constitutive Proteasome.
AID1250153	Cytotoxicity against human Glioma cells (HF3013) after 72 hrs by CelltiterGlo assay	2015	ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8	High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID526654	Selectivity ratio of IC50 for cathepsin to IC50 for proteasome	2010	Journal of medicinal chemistry, Oct-14, Volume: 53, Issue:19	Toward the development of innovative bifunctional agents to induce differentiation and to promote apoptosis in leukemia: clinical candidates and perspectives.
AID1156369	Growth inhibition of human NCI-H460 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1486816	Cytotoxicity against human A549 cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Synthesis and biological activity of peptide proline-boronic acids as proteasome inhibitors.
AID706496	Effect on 20S proteasome subunit beta5 expression in human THP1 cells at 50 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID316564	Inhibition of bacterial prolyl oligopeptidase at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1459648	Antiproliferative activity against human SW1990 cells after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1576785	Cytotoxicity against human pDC assessed as reduction in cell viability by CellTiter Glo assay	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID316569	Inhibition of human trypsin at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1473257	Induction of apoptosis in human RPMI8226 cells at 2.5 nM after 24 hrs by Annexin V/propidium iodide staining based flow cytometry	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID1156405	Growth inhibition of human SN12C cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1325779	Cytotoxicity against p53 deficient human SKOV3 cells assessed as reduction in cell viability after 48 hrs by 7AAD-staining based FACS analysis
AID316500	Inhibition of chymotrypsin-like activity of human 20S proteasome in Molt4 cells	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1548260	Antiproliferative activity against human KM3 cells incubated for 48 hrs by MTT assay
AID1252354	Antiproliferative activity against human HCT116 cells after 72 hrs by oxyluciferin luminescence assay	2015	Bioorganic & medicinal chemistry letters, Nov-01, Volume: 25, Issue:21	Structure-activity relationship study of syringolin A as a potential anticancer agent.
AID1299917	Inhibition of human liver cathepsin B using Cbz-RR-AMC as substrate at 100 uM by fluorometric assay	2016	ACS medicinal chemistry letters, Mar-10, Volume: 7, Issue:3	Synthesis and Evaluation of Macrocyclic Peptide Aldehydes as Potent and Selective Inhibitors of the 20S Proteasome.
AID1439190	Metabolic stability in Sprague-Dawley rat liver microsomes assessed as compound remaining at 20 uM preincubated for 5 mins followed by NADPH addition measured after 20 mins by HPLC analysis	2017	European journal of medicinal chemistry, Mar-10, Volume: 128	Design, synthesis and biological evaluation of novel non-peptide boronic acid derivatives as proteasome inhibitors.
AID459684	Cmax in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1473264	Antitumor activity against human RPMI8226 cells xenografted in nude mouse assessed as tumor growth inhibition at 1 mg/kg, iv or ip administered once in week for 35 days relative to control	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID1689692	Inhibition of HDAC2 in human RPMI-8226 cells incubated for 2 hrs by ELISA	2020	European journal of medicinal chemistry, Mar-01, Volume: 189	1,2,3-Triazole-Chalcone hybrids: Synthesis, in vitro cytotoxic activity and mechanistic investigation of apoptosis induction in multiple myeloma RPMI-8226.
AID496338	Toxicity in HBV infected 1.3.32 transgenic mouse liver assessed as hepatitis at 1 mg/kg, iv single dose after 6 days by rotine immunohistochemistry method	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID496315	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as expression of 3.5 and 2.1 kb HBV mRNA at 1 mg/kg, iv single dose after 6 days by Northern blot analysis	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1605099	Induction of hemolysis in sheep erythrocytes by measuring hemoglobin release incubated for 15 mins	2020	Journal of medicinal chemistry, 03-26, Volume: 63, Issue:6	Discovery of Novel Peptidomimetic Boronate ClpP Inhibitors with Noncanonical Enzyme Mechanism as Potent Virulence Blockers
AID1295432	Cytotoxicity against human U266B1 cells assessed as cell viability after 72 hrs by CellTiter 96 aqueous one solution cell proliferation assay	2016	Bioorganic & medicinal chemistry, 06-01, Volume: 24, Issue:11	3D-QSAR-aided design, synthesis, in vitro and in vivo evaluation of dipeptidyl boronic acid proteasome inhibitors and mechanism studies.
AID397951	Cytotoxicity against human H460 cells after 72 hrs by MTT assay	2009	Journal of medicinal chemistry, Jul-23, Volume: 52, Issue:14	Design, synthesis, biological evaluation, and structure-activity relationship (SAR) discussion of dipeptidyl boronate proteasome inhibitors, part I: comprehensive understanding of the SAR of alpha-amino acid boronates.
AID1325778	Cytotoxicity against human KGN cells harboring wild type p53 assessed as reduction in cell viability after 48 hrs by 7AAD-staining based FACS analysis
AID1250147	Cytotoxicity against human Glioma cells (HF2303) after 72 hrs by CelltiterGlo assay	2015	ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8	High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1895438	Inhibition of human 20S immunoproteasome beta1 subunit using Ac-nLPnLD-AMC as substrate preincubated for 2 hrs followed by substrate addition and measured after 1 hr by fluorescence intensity assay	2021	Journal of medicinal chemistry, 07-22, Volume: 64, Issue:14	Structure-Based Optimization and Discovery of M3258, a Specific Inhibitor of the Immunoproteasome Subunit LMP7 (β5i).
AID459692	Toxicity in Sprague-Dawley rat assessed as mortality at 1 mg/kg, ig after 10 hrs	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1372746	Inhibition of 20s constitutive proteasome trypsin-like activity in human erythrocytes using Z-nLPnLD-Glo as substrate pretreated for 2 hrs followed by substrate addition measured after 10 mins by luminescence assay	2018	Bioorganic & medicinal chemistry, 01-15, Volume: 26, Issue:2	Immunoproteasome inhibition and bioactivity of thiasyrbactins.
AID316533	Inhibition of human cathepsin E at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1396605	Cytotoxicity against human U266B1 cells assessed as reduction in cell viability after 72 hrs by CellTiter 96 aqueous one solution assay	2018	Bioorganic & medicinal chemistry, 08-07, Volume: 26, Issue:14	Design, synthesis, in vitro and in vivo evaluation, and structure-activity relationship (SAR) discussion of novel dipeptidyl boronic acid proteasome inhibitors as orally available anti-cancer agents for the treatment of multiple myeloma and mechanism stud
AID625287	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID761488	Inhibition of chymotryptic-like activity of human 20S proteasome using Suc-LLVY-AMC as substrate measured every min over 30 mins by fluorescence assay	2013	Journal of medicinal chemistry, Jul-25, Volume: 56, Issue:14	Inhibition of the human proteasome by imidazoline scaffolds.
AID599476	Induction of apoptosis in human HeLa cells at 0.1 uM incubated for 12 hrs using annexin V-FITC and propidiun iodide staining based flow cytometry (Rvb = 2.6 +/- 0.14%)	2009	Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12	Synthesis and biological evaluation of boron peptide analogues of Belactosin C as proteasome inhibitors.
AID1250151	Cytotoxicity against human Glioma cells (HF2876) after 72 hrs by CelltiterGlo assay	2015	ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8	High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1815775	Cytotoxicity against human HeLa cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay	2022	ACS medicinal chemistry letters, Jan-13, Volume: 13, Issue:1	The BASHY Platform Enables the Assembly of a Fluorescent Bortezomib-GV1001 Conjugate.
AID611898	Ratio of CC50 for human follicular small-cell lymphocytic leukemia cells to IC50 for chymotrypsin-like activity of 20S proteasome at pH 2.0	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Chemical and biological evaluation of dipeptidyl boronic acid proteasome inhibitors for use in prodrugs and pro-soft drugs targeting solid tumors.
AID1156379	Growth inhibition of human SF295 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1604189	Selectivity index, ratio of IC50 for 20S proteasome beta 2c (unknown origin) to IC50 for 20S proteasome beta 2i (unknown origin)	2019	European journal of medicinal chemistry, Nov-15, Volume: 182	Immunoproteasome-selective inhibitors: An overview of recent developments as potential drugs for hematologic malignancies and autoimmune diseases.
AID430821	Inhibition of chymotrypsin-like activity of proteasome in human HL60 cells at 100 nM	2009	Journal of medicinal chemistry, Aug-27, Volume: 52, Issue:16	Synthetic analogue of rocaglaol displays a potent and selective cytotoxicity in cancer cells: involvement of apoptosis inducing factor and caspase-12.
AID496339	Toxicity in HBV infected 1.3.32 transgenic mouse liver assessed as hepatitis at 0.2 mg/kg, iv single dose after 24 hrs by rotine immunohistochemistry method	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID548711	Apparent volume of distribution in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID734752	Inhibition of trypsin-like activity of human 20S proteasome beta 2 subunit using Ac-RLR-AMC as substrate after 60 mins by fluorescence assay	2013	Journal of medicinal chemistry, May-09, Volume: 56, Issue:9	Potent proteasome inhibitors derived from the unnatural cis-cyclopropane isomer of Belactosin A: synthesis, biological activity, and mode of action.
AID459664	Cytotoxicity against human BxPC3 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID316521	AUC (0 to infinity) in CD1 mouse at 4 mg/kg, po	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1460764	Inhibition of human CA1 by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID1624026	Inhibition of human 20s constitutive proteasome beta5 chymotrypsin-like activity using Suc-LLVY-AMC as substrate preincubated for 15 mins followed by substrate addition	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Covalent docking modelling-based discovery of tripeptidyl epoxyketone proteasome inhibitors composed of aliphatic-heterocycles.
AID496372	Induction of OAS gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 6 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID496365	Induction of IL-2 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 1day by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID706510	Resistance factor, ratio of IC50 for 200 nM bortezonib-resistant human H460 cells harboring proteosome subunit beta5 A49T mutant to IC50 for wild type human H460 cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1623398	Induction of apoptosis in human RPMI8226 cells assessed as necrotic cells at 3 nM after 48 hrs by Annexin-V/propidium iodide staining based flow cytometric method (Rvb = 0.090%)	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID1156360	Growth inhibition of human RPMI8226 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID540210	Clearance in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1548285	Induction of apoptosis in bortezomib resistant human KM3/BTZ cells assessed as early apoptotic cells level at 50 nM incubated for 24 hrs by Annexin V-FITC/PI staining based FCAS analysis (Rvb = 1.39%)
AID496337	Toxicity in HBV infected 1.3.32 transgenic mouse liver assessed as hepatitis at 1 mg/kg, iv single dose after 2 days by rotine immunohistochemistry method	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1128237	Inhibition of recombinant cathepsin B (unknown origin) using Z-Leu-Arg-AMC as substrate by spectrofluorometer analysis	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID706726	Resistance factor, ratio of IC50 for human Jurkat B cells harboring proteosome subunit beta5 A49T mutant to IC50 for wild type human Jurkat cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1459647	Antiproliferative activity against human MDA-MB-231 cells after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1128517	Cytotoxicity against human NCI60 cells at 10'-5 M	2014	European journal of medicinal chemistry, Apr-09, Volume: 76	Identification of a new series of amides as non-covalent proteasome inhibitors.
AID1266946	Antitumor activity against human AMO1 cells xenografted in nude SCID beige mouse assessed as tumor growth inhibition at 1 mg/kg, iv administered twice per week	2015	Journal of medicinal chemistry, Dec-24, Volume: 58, Issue:24	Discovery of a First-in-Class, Potent, Selective, and Orally Bioavailable Inhibitor of the p97 AAA ATPase (CB-5083).
AID1374301	Antiproliferative activity against human MCF7 cells after 72 hrs by SRB assay	2018	Bioorganic & medicinal chemistry, 03-01, Volume: 26, Issue:5	Novel aromatic sulfonyl naphthalene-based boronates as 20S proteasome inhibitors.
AID459668	Cytotoxicity against human SKOV3 cells after 72 hrs by MTT assay	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1312153	Inhibition of human carbonic anhydrase-2 preincubated for 15 mins by stopped-flow CO2 hydration assay	2016	Bioorganic & medicinal chemistry, 09-15, Volume: 24, Issue:18	Bortezomib inhibits bacterial and fungal β-carbonic anhydrases.
AID623565	Cytotoxicity against human HT-29 cells after 3 days by sulforhodamine B assay	2011	Journal of natural products, Oct-28, Volume: 74, Issue:10	Bioassay-guided isolation of constituents of Piper sarmentosum using a mitochondrial transmembrane potential assay.
AID1439182	Inhibition of chymotrypsin-like activity of human 20S proteasome at 100 nM using Suc-Leu-Leu-Val-Tyr-AMC as substrate by fluorescence assay relative to control	2017	European journal of medicinal chemistry, Mar-10, Volume: 128	Design, synthesis and biological evaluation of novel non-peptide boronic acid derivatives as proteasome inhibitors.
AID397955	Cytotoxicity against human HeLa cells after 72 hrs by MTT assay	2009	Journal of medicinal chemistry, Jul-23, Volume: 52, Issue:14	Design, synthesis, biological evaluation, and structure-activity relationship (SAR) discussion of dipeptidyl boronate proteasome inhibitors, part I: comprehensive understanding of the SAR of alpha-amino acid boronates.
AID496314	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as expression of 3.5 and 2.1 kb HBV mRNA at 1 mg/kg, iv single dose after 3 days by Northern blot analysis	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID52603	Inhibitory activity against human Chymotrypsinogen	1998	Bioorganic & medicinal chemistry letters, Feb-17, Volume: 8, Issue:4	Potent and selective inhibitors of the proteasome: dipeptidyl boronic acids.
AID1818943	Antiproliferative activity against dexamethasone-sensitive human MM.1S cells assessed as reduction in cell viability at 10 uM measured after 72 hrs by XTT assay	2022	Journal of natural products, 01-28, Volume: 85, Issue:1	Phytochemical Investigation of the Roots of
AID1548284	Induction of apoptosis in bortezomib resistant human KM3/BTZ cells assessed as viable cells level at 50 nM incubated for 24 hrs by Annexin V-FITC/PI staining based FCAS analysis (Rvb = 98.1%)
AID1576775	Inhibition of 20S proteasome beta 5c (unknown origin) preincubated for 1 hr followed by fluorescence based assay	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID316531	Inhibition of bovine cathepsin C at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID504303	Inhibition of 20S proteasome	2010	Journal of natural products, Sep-24, Volume: 73, Issue:9	Cylindrocyclophanes with proteasome inhibitory activity from the Cyanobacterium Nostoc sp.
AID496357	Induction of IL-1alpha gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 1day by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID496336	Toxicity in HBV infected 1.3.32 transgenic mouse liver assessed as hepatitis at 1 mg/kg, iv single dose after 1 day by rotine immunohistochemistry method	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID459677	Cmax in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID316523	Inhibition of 20S proteasome beta5beta1 subunit binding in human RPMI 8226 cells xenografted mouse	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1325782	Cytotoxicity against human NCI-H929 cells harboring wild type p53 assessed as reduction in cell viability after 48 hrs by 7AAD-staining based FACS analysis
AID700311	Resistance ratio of IC50 for human bortezomib-resistant DOGUM cells to IC50 for human DOGUM cells	2012	Bioorganic & medicinal chemistry letters, Nov-01, Volume: 22, Issue:21	Identification of a glutathione peroxidase inhibitor that reverses resistance to anticancer drugs in human B-cell lymphoma cell lines.
AID1460770	Inhibition of human CA6 by stopped-flow CO2 hydrase assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Bortezomib inhibits mammalian carbonic anhydrases.
AID316555	Inhibition of human caspase 2 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID526550	Inhibition of human elastase at 100 uM	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID1459642	Antiproliferative activity against human HCT116 cells after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1687115	Binding affinity to human 20S constitutive proteasome beta 5 subunit assessed as half-life using fluorogenic peptide Ac-WLA-AMC as substrate in presence of PA28alpha by fluorescence based microplate reader assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1623371	Induction of apoptosis in human NCI-H929 cells assessed as viable cells at 2 nM after 48 hrs by Annexin-V/propidium iodide staining based flow cytometric method (Rvb = 82.6%)	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID1687119	Antiplasmodial activity against sorbitol synchronized ring stage Plasmodium falciparum 3D7 assessed as reduction in parasitemia incubated for 72 hrs by Syto-61 staining dye based flow cytometry analysis	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1623370	Induction of apoptosis in human NCI-H929 cells assessed as necrotic cells at 2 nM after 48 hrs by Annexin-V/propidium iodide staining based flow cytometric method (Rvb = 0.0034%)	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Translational impact of novel widely pharmacological characterized mofezolac-derived COX-1 inhibitors combined with bortezomib on human multiple myeloma cell lines viability.
AID496309	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as inhibition of HBV DNA replication at 1 mg/kg, iv single dose after 2 days by Southern blot analysis	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1299909	Inhibition of chymotrypsin-like activity of rabbit 20S proteasome using Suc-LLVY-AMC substrate incubated at 37 degC by fluorometric assay	2016	ACS medicinal chemistry letters, Mar-10, Volume: 7, Issue:3	Synthesis and Evaluation of Macrocyclic Peptide Aldehydes as Potent and Selective Inhibitors of the 20S Proteasome.
AID1156413	Growth inhibition of human BT549 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID496370	Induction of OAS gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 2 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID397952	Cytotoxicity against human SW480 cells after 72 hrs by MTT assay	2009	Journal of medicinal chemistry, Jul-23, Volume: 52, Issue:14	Design, synthesis, biological evaluation, and structure-activity relationship (SAR) discussion of dipeptidyl boronate proteasome inhibitors, part I: comprehensive understanding of the SAR of alpha-amino acid boronates.
AID1459704	Toxicity in human Bel7404 cells xenografted BALB/c mouse assessed as effect on body weight at 0.5 mg/kg, iv administered once in two days for 24 consecutive days measured on day 24 of compound dosing (Rvb = 26.29 +/- 1.36 g)	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID1325781	Cytotoxicity against human MDA-MB-468 cells harboring mutant p53 assessed as reduction in cell viability after 48 hrs by 7AAD-staining based FACS analysis
AID1156374	Growth inhibition of human HCT15 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID496373	Induction of IL1-beta gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 1day by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID526411	Inhibition of chymotrypsin-like activity of human 20s proteasome beta5 subunit in human erythrocyte assessed as hydrolysis of Ac-WLA-AMC fluorogenic substrate	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Optimization of a series of dipeptides with a P3 threonine residue as non-covalent inhibitors of the chymotrypsin-like activity of the human 20S proteasome.
AID1548301	Induction of cell cycle arrest in bortezomib resistant human KM3/BTZ cells assessed as accumulation at S phase at 100 nM incubated for 24 hrs by propidium iodide staining based flow cytometry (Rvb = 46%)
AID540211	Fraction unbound in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1687136	Inhibition of human 20S immunoproteasome beta 5 subunit assessed as inhibition of BMV037 probe labeling at 1 to 10 uM incubated for 1 hr by SDS-PAGE analysis	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID316575	Metabolic stability in rat liver microsomes	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1667215	Inhibition of human SET7 overexpressed in Escherichia coli BL21 (DE3) cells at 12.5 uM preincubated for 15 mins followed by addition of SAM as substrate and biotinylated Histone H3 (1-50) peptide measured after 30 mins by AlphaLISA assay relative to contr	2020	Bioorganic & medicinal chemistry, 04-01, Volume: 28, Issue:7	Computational discovery and biological evaluation of novel inhibitors targeting histone-lysine N-methyltransferase SET7.
AID1667213	Inhibition of human SET7 overexpressed in Escherichia coli BL21 (DE3) cells at 50 uM preincubated for 15 mins followed by addition of SAM as substrate and biotinylated Histone H3 (1-50) peptide measured after 30 mins by AlphaLISA assay relative to control	2020	Bioorganic & medicinal chemistry, 04-01, Volume: 28, Issue:7	Computational discovery and biological evaluation of novel inhibitors targeting histone-lysine N-methyltransferase SET7.
AID1156409	Growth inhibition of human DU145 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1728101	Antiproliferative activity against human MDA-MB-231 cells assessed as cell viability after 24 hrs	2021	European journal of medicinal chemistry, Jan-15, Volume: 210	Potent antiproliferative activity of bradykinin B2 receptor selective agonist FR-190997 and analogue structures thereof: A paradox resolved?
AID706504	Effect on PSMB5 mRNA expression in human THP1 cells at 100 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID496334	Induction of Usp18 gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 24 hrs by RT- PCR	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID316499	Inhibition of bovine alpha chymotrypsin	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID706495	Effect on 20S proteasome subunit beta5 expression in human THP1 cells at 100 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1374300	Antiproliferative activity against human MDA-MB-231 cells after 72 hrs by SRB assay	2018	Bioorganic & medicinal chemistry, 03-01, Volume: 26, Issue:5	Novel aromatic sulfonyl naphthalene-based boronates as 20S proteasome inhibitors.
AID397950	Inhibition of chymotrypsin-like activity of human 20s proteasome beta 5 subunit assessed as hydrolysis of fluorogenic substrate	2009	Journal of medicinal chemistry, Jul-23, Volume: 52, Issue:14	Design, synthesis, biological evaluation, and structure-activity relationship (SAR) discussion of dipeptidyl boronate proteasome inhibitors, part I: comprehensive understanding of the SAR of alpha-amino acid boronates.
AID1474167	Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status	2016	Drug discovery today, Apr, Volume: 21, Issue:4	DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1197991	Induction of cell death in human A549 cells assessed as accumulation of Noxa at 0.025 to 0.1 uM after 24 hrs by immunoblot assay	2015	Journal of medicinal chemistry, Feb-26, Volume: 58, Issue:4	Synthesis, characterization, and optimization for in vivo delivery of a nonselective isopeptidase inhibitor as new antineoplastic agent.
AID496328	Antiviral activity against HBV infected in 1.3.32 transgenic mouse assessed as serum HBeAg and HBsAg level at 1 mg/kg, iv single dose after 3 days	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1605095	Inhibition of N-terminal His6-sumo-tagged full length Staphylococcus aureus ClpP expressed in Escherichia coli BL2 (DE3) at 10 uM pre-incubated for 10 mins before Suc-LY-AMC addition and measured after 1 hr by fluorescence based assay relative to control	2020	Journal of medicinal chemistry, 03-26, Volume: 63, Issue:6	Discovery of Novel Peptidomimetic Boronate ClpP Inhibitors with Noncanonical Enzyme Mechanism as Potent Virulence Blockers
AID1815774	Cytotoxicity against human HT-29 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay	2022	ACS medicinal chemistry letters, Jan-13, Volume: 13, Issue:1	The BASHY Platform Enables the Assembly of a Fluorescent Bortezomib-GV1001 Conjugate.
AID1128239	Cell cycle arrest in human HCT116 cells assessed as accumulation at G1 phase at 100 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 35.6%)	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID1595606	Selectivity ratio of IC50 for human NCI-H727 cells to IC50 for human NCI-H23 cells	2019	Journal of medicinal chemistry, 05-09, Volume: 62, Issue:9	Development of Novel Epoxyketone-Based Proteasome Inhibitors as a Strategy To Overcome Cancer Resistance to Carfilzomib and Bortezomib.
AID1771374	Antiproliferative activity against human RPMI 8226 cells assessed as reduction in cell viability incubated for 72 hrs by XTT assay	2021	Journal of natural products, 08-27, Volume: 84, Issue:8	Structure-Activity Relationships of Withanolides as Antiproliferative Agents for Multiple Myeloma: Comparison of Activity in 2D Models and a 3D Coculture Model.
AID548717	Terminal half life in Sprague-Dawley rat at 1 mg/kg, iv	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1624027	Inhibition of human 20s immunoproteasome beta5i activity using Suc-LLVY-AMC as substrate preincubated for 15 mins followed by substrate addition	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Covalent docking modelling-based discovery of tripeptidyl epoxyketone proteasome inhibitors composed of aliphatic-heterocycles.
AID316501	Cytotoxicity against human A2780 cells	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID706499	Effect on PSMB5 mRNA expression in human RPMI8226 cells at 100 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1461483	Inhibition of caspase-like activity of 20S proteasome in rabbit 20S proteasome pre-incubated for 10 mins before Suc-Leu-Leu-Val-Tyr-AMC substrate addition and measured after 2 hrs by fluorescence assay	2017	Bioorganic & medicinal chemistry, 10-01, Volume: 25, Issue:19	Azobenzene-containing photoswitchable proteasome inhibitors with selective activity and cellular toxicity.
AID1473235	Cell cycle arrest in human NCI-H929 cells assessed as accumulation at G0/G1 phase at 2.5 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 49.39%)	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID1250149	Cytotoxicity against human Glioma cells (HF2476) after 72 hrs by CelltiterGlo assay	2015	ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8	High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1674413	Inhibition of chymotrypsin-like activity of Leishmania tarentolae proteasome beta 4 F24L mutant	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery and Characterization of Clinical Candidate LXE408 as a Kinetoplastid-Selective Proteasome Inhibitor for the Treatment of Leishmaniases.
AID452103	Cytotoxicity against human BGC823 cells after 72 hrs by MTT assay	2009	Bioorganic & medicinal chemistry, Oct-01, Volume: 17, Issue:19	Design, synthesis and biological evaluation of tripeptide boronic acid proteasome inhibitors.
AID1156343	Inhibition of chymotrypsin-like activity of 20S proteasome in human erythrocytes using Suc-Leu-Leu-Val-Tyr-AMC as substrate by fluorescence assay	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1576792	Inhibition of 20S proteasome beta 5i in human PBMC cells assessed as induction of PSMB7 expression at 100 nM after 3 to 72 hrs by RT-PCR method	2019	Journal of medicinal chemistry, 08-08, Volume: 62, Issue:15	Design and Evaluation of Highly Selective Human Immunoproteasome Inhibitors Reveal a Compensatory Process That Preserves Immune Cell Viability.
AID1687127	Antiplasmodial activity against sorbitol synchronized ring stage bortezomib-resistant Plasmodium falciparum 3D7 clone B1a assessed as reduction in parasitemia incubated for 72 hrs by Syto-61 staining dye based flow cytometry analysis	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1484604	Antiproliferative activity against human K562 cells after 72 hrs by calcein AM staining based fluorescence assay	2017	European journal of medicinal chemistry, Jul-28, Volume: 135	Synthesis and antiproteasomal activity of novel O-benzyl salicylamide-based inhibitors built from leucine and phenylalanine.
AID1459660	Plasma clearance in Sprague-Dawley rat at 0.8 mg/kg, iv administered as bolus	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID471918	Inhibition of chymotrypsin-like activity of proteasome in human HL60 cells assessed as free AMC level after 10 mins	2009	Journal of natural products, Jun, Volume: 72, Issue:6	Bioactive 5,6-dihydro-alpha-pyrone derivatives from Hyptis brevipes.
AID548712	Systemic clearance in Sprague-Dawley rat at 1 mg/kg, ig	2010	Journal of medicinal chemistry, Dec-23, Volume: 53, Issue:24	Synthesis, in vitro and in vivo biological evaluation, and comprehensive understanding of structure-activity relationships of dipeptidyl boronic acid proteasome inhibitors constructed from β-amino acids.
AID1473226	Cell cycle arrest in human U266 cells assessed as accumulation at sub-G1 phase at 2.5 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 10.76%)	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID459674	Toxicity against zebrafish embryo assessed as cell death in tail at 1 umol after 24 hrs	2010	Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5	Synthesis, in vitro and in vivo biological evaluation, docking studies, and structure--activity relationship (SAR) discussion of dipeptidyl boronic acid proteasome inhibitors composed of beta-amino acids.
AID1128230	Inhibition of caspase-like activity of human 20S proteasome using Ac-nLPnLD-AMC as substrate	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID1687130	Inhibition of 20S proteasome beta 5 subunit from bortezomib resistant Plasmodium falciparum 3D7 trophozoite infected erythrocytes assessed as inhibition of BMV037 probe labeling at 1 to 10 uM incubated for 1 hr by SDS-PAGE analysis	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Target Validation and Identification of Novel Boronate Inhibitors of the Plasmodium falciparum Proteasome.
AID1128234	Inhibition of beta5 subunit of immunoproteasome (unknown origin) by active-site ELISA	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Structurally novel highly potent proteasome inhibitors created by the structure-based hybridization of nonpeptidic belactosin derivatives and peptide boronates.
AID316532	Inhibition of human cathepsin D at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID496375	Induction of IL1-beta gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 3 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID316535	Inhibition of human cathepsin G	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1156401	Growth inhibition of human A498 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1156359	Growth inhibition of human MOLT4 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID316539	Inhibition of human cathepsin Z at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID728731	Inhibition of His-tagged Frataxin (unknown origin)/Ubiquitin interaction expressed in human Calu6 cells assessed as increase in frataxin (1-210) precursor level at 10 uM after 18 hrs by Western blotting analysis	2013	Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7	Discovery of a novel small molecule inhibitor targeting the frataxin/ubiquitin interaction via structure-based virtual screening and bioassays.
AID496345	Induction of TNF beta gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 1day by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1325785	Cytotoxicity against human IMR90 cells harboring wild type p53 assessed as reduction in cell viability after 48 hrs by 7AAD-staining based FACS analysis
AID397958	Cytotoxicity against human BGC823 cells after 72 hrs by MTT assay	2009	Journal of medicinal chemistry, Jul-23, Volume: 52, Issue:14	Design, synthesis, biological evaluation, and structure-activity relationship (SAR) discussion of dipeptidyl boronate proteasome inhibitors, part I: comprehensive understanding of the SAR of alpha-amino acid boronates.
AID1473220	Cell cycle arrest in human RPMI8226 cells assessed as accumulation at S phase at 2.5 nM after 24 hrs by propidium iodide staining based flow cytometry (Rvb = 19.53%)	2018	Journal of medicinal chemistry, 02-08, Volume: 61, Issue:3	(N-Hydroxycarbonylbenylamino)quinolines as Selective Histone Deacetylase 6 Inhibitors Suppress Growth of Multiple Myeloma in Vitro and in Vivo.
AID316560	Inhibition of human DPP4 at 10 uM	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID1363799	Inhibition of chymotrypsin-like activity of 20S proteasome in imatinib-resistant human SUP-B15 cells using Suc-LLVY aminoluciferin as substrate after 2 hrs by proteasome-Glo assay	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Discovery of the First-in-Class Dual Histone Deacetylase-Proteasome Inhibitor.
AID1325777	Cytotoxicity against human RD-ES cells harboring p53 mutant assessed as reduction in cell viability after 48 hrs by 7AAD-staining based FACS analysis
AID540213	Half life in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1459631	Inhibition of chymotrypsin-like activity of 20S proteasome in human HL60 cells using Suc-LLVYaminoluciferin as substrate at 0.2 uM after 2 hrs by fluorescence analysis	2017	European journal of medicinal chemistry, Jan-05, Volume: 125	Urea-containing peptide boronic acids as potent proteasome inhibitors.
AID316581	Protein binding in human plasma	2008	Journal of medicinal chemistry, Feb-28, Volume: 51, Issue:4	Discovery of a potent, selective, and orally active proteasome inhibitor for the treatment of cancer.
AID700310	Cytotoxicity against human bortezomib-resistant DOGUM cells after 72 hrs by MTT assay	2012	Bioorganic & medicinal chemistry letters, Nov-01, Volume: 22, Issue:21	Identification of a glutathione peroxidase inhibitor that reverses resistance to anticancer drugs in human B-cell lymphoma cell lines.
AID66813	Inhibitory activity against human leukocyte elastase	1998	Bioorganic & medicinal chemistry letters, Feb-17, Volume: 8, Issue:4	Potent and selective inhibitors of the proteasome: dipeptidyl boronic acids.
AID706480	Effect on 20S proteasome subunit beta1/beta5 chymotrypsin-like activity in human HL60a cells at 40 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1156358	Growth inhibition of human K562 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID706481	Effect on 20S proteasome subunit beta5 chymotrypsin-like activity in human THP1 cells at 200 nM relative to control	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID700312	Cytotoxicity against human bortezomib-resistant GUMBUS cells after 72 hrs by MTT assay	2012	Bioorganic & medicinal chemistry letters, Nov-01, Volume: 22, Issue:21	Identification of a glutathione peroxidase inhibitor that reverses resistance to anticancer drugs in human B-cell lymphoma cell lines.
AID706516	Resistance factor, ratio of IC50 for 7 nM bortezonib-resistant human CEM cells harboring proteosome subunit beta5 C52F mutant to IC50 for wild type human CEM cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID1156363	Growth inhibition of human EKVX cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1818940	Antiproliferative activity against dexamethasone-sensitive human MM.1S cells assessed as reduction in cell viability measured after 72 hrs by XTT assay	2022	Journal of natural products, 01-28, Volume: 85, Issue:1	Phytochemical Investigation of the Roots of
AID1156375	Growth inhibition of human HT-29 cells	2014	European journal of medicinal chemistry, Aug-18, Volume: 83	Optimization of peptidomimetic boronates bearing a P3 bicyclic scaffold as proteasome inhibitors.
AID1624031	Inhibition of DPP4 (unknown origin) at 10 ug/mL using Ala-Pro-AMC as substrate by fluorometric analysis relative to control	2019	European journal of medicinal chemistry, Feb-15, Volume: 164	Covalent docking modelling-based discovery of tripeptidyl epoxyketone proteasome inhibitors composed of aliphatic-heterocycles.
AID1372754	Cytotoxicity against human SK-N-SH cells assessed as reduction in cell viability at 0.1 to 1 uM after 24 hrs by MTT assay	2018	Bioorganic & medicinal chemistry, 01-15, Volume: 26, Issue:2	Immunoproteasome inhibition and bioactivity of thiasyrbactins.
AID1128512	Inhibition of chymotrypsin-like activity of human 20S proteasome beta 5 subunit assessed as Suc-Leu-Leu-Val-Tyr-AMC substrate hydrolysis after 10 mins by fluorometric analysis	2014	European journal of medicinal chemistry, Apr-09, Volume: 76	Identification of a new series of amides as non-covalent proteasome inhibitors.
AID625290	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID706509	Resistance factor, ratio of IC50 for 40 nM bortezonib-resistant human A549 cells harboring proteosome subunit beta5 M45V mutant to IC50 for wild type human A549 cells	2012	Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23	Molecular mechanisms of acquired proteasome inhibitor resistance.
AID496342	Induction of TNFalpha gene expression in HBV infected 1.3.32 transgenic mouse liver at 1 mg/kg, iv after 2 days by Rnase protection assay	2010	Antimicrobial agents and chemotherapy, Feb, Volume: 54, Issue:2	Bortezomib inhibits hepatitis B virus replication in transgenic mice.
AID1347097	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347127	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Saos-2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347150	Optimization screen NINDS AMC qHTS for Zika virus inhibitors: Linked NS2B-NS3 protease assay	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347111	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-MC cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347124	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for RD cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347424	RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)	2019	The Journal of biological chemistry, 11-15, Volume: 294, Issue:46	Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347129	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-SH cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID651635	Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1347107	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347113	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for LAN-5 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347126	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh30 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347155	Optimization screen NINDS Rhodamine qHTS for Zika virus inhibitors: Linked NS2B-NS3 protease assay	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347169	Tertiary RLuc qRT-PCR qHTS assay for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347110	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for A673 cells)	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845	Primary qHTS for Inhibitors of ATXN expression
AID1347119	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for MG 63 (6-TG R) cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347114	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for DAOY cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347118	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for TC32 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508630	Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay	2021	Cell reports, 04-27, Volume: 35, Issue:4	A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347101	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425	Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)	2019	The Journal of biological chemistry, 11-15, Volume: 294, Issue:46	Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347116	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SJ-GBM2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347117	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-37 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347168	HepG2 cells viability qHTS for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347082	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347090	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347407	qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection	2020	ACS chemical biology, 07-17, Volume: 15, Issue:7	High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347109	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB1643 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347112	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-12 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347115	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB-EBc1 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154	Primary screen GU AMC qHTS for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347122	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for U-2 OS cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347125	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh18 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347167	Vero cells viability qHTS for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347102	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347151	Optimization of GU AMC qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347098	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347149	Furin counterscreen qHTS for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347123	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh41 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347121	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for control Hh wild type fibroblast cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347128	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for OHS-50 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745854	NCATS anti-infectives library activity on HEK293 viability as a counter-qHTS vs the C. elegans viability qHTS	2023	Disease models & mechanisms, 03-01, Volume: 16, Issue:3	In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
AID1347415	qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: tertiary screen by RT-qPCR	2020	ACS chemical biology, 07-17, Volume: 15, Issue:7	High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1745855	NCATS anti-infectives library activity on the primary C. elegans qHTS viability assay	2023	Disease models & mechanisms, 03-01, Volume: 16, Issue:3	In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
AID1347412	qHTS assay to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: Counter screen cell viability and HiBit confirmation	2020	ACS chemical biology, 07-17, Volume: 15, Issue:7	High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347414	qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: Secondary screen by immunofluorescence	2020	ACS chemical biology, 07-17, Volume: 15, Issue:7	High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347411	qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary	2020	ACS chemical biology, 07-17, Volume: 15, Issue:7	High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1800498	20S proteasome chymotrypsin-like inhibition assay from Article 10.1111/cbdd.12342: \\Design, Synthesis and Biological Evaluation of Peptidyl Epoxyketone Proteasome Inhibitors Composed of ??????-amino Acids.\\	2014	Chemical biology & drug design, Nov, Volume: 84, Issue:5	Design, synthesis and biological evaluation of peptidyl epoxyketone proteasome inhibitors composed of β-amino acids.
AID977610	Experimentally measured binding affinity data (Ki) for protein-ligand complexes derived from PDB	2010	The Biochemical journal, Sep-15, Volume: 430, Issue:3	Characterization of a new series of non-covalent proteasome inhibitors with exquisite potency and selectivity for the 20S beta5-subunit.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	0 (0.00)	18.7374
1990's	2 (0.03)	18.2507
2000's	1549 (23.02)	29.6817
2010's	3972 (59.04)	24.3611
2020's	1205 (17.91)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	860 (12.52%)	5.53%
Reviews	970 (14.12%)	6.00%
Case Studies	848 (12.35%)	4.05%
Observational	43 (0.63%)	0.25%
Other	4,147 (60.38%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (890)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
A Phase 2, Randomized, Double-blind, Placebo-controlled Study Comparing the Combination of CNTO 328 (Anti-IL-6 Monoclonal Antibody) and Velcade Versus Velcade Alone in Subjects With Relapsed or Refractory Multiple Myeloma [NCT00401843]	Phase 2	307 participants (Actual)	Interventional	2006-11-28	Completed
An Open Label, Multicenter, Phase 2, Pilot Study, Evaluating Early Treatment With Bispecific T-cell Redirectors (Teclistamab and Talquetamab) in the Frontline Therapy of Newly Diagnosed High-risk Multiple Myeloma [NCT05849610]	Phase 2	30 participants (Anticipated)	Interventional	2023-11-30	Recruiting
A Phase II Trial of Combination Bortezomib and Rituximab as Front-line Therapy for Low-grade Non-Hodgkin's Lymphoma [NCT00369707]	Phase 2	42 participants (Actual)	Interventional	2006-08-09	Completed
A Randomized, Open-Label, Multicenter Study of VELCADE With Rituximab or Rituximab Alone in Subjects With Relapsed or Refractory, Rituximab Naive or Sensitive Follicular B-cell Non-Hodgkin's Lymphoma [NCT00312845]	Phase 3	676 participants (Actual)	Interventional	2006-03-31	Completed
A Phase II Study of PS-341 Alone or in Combination With Irinotecan in Patients With Adenocarcinoma of the Gastroesophageal Junction (GEJ) or Stomach [NCT00061932]	Phase 2	41 participants (Actual)	Interventional	2003-04-30	Completed
A Randomized Phase II Trial of Maintenance vs Consolidation Bortezomib Therapy Following Aggressive Chemo-Immunotherapy and Autologous Stem Cell Transplant for Previously Untreated Mantle Cell Lymphoma [NCT00310037]	Phase 2	151 participants (Actual)	Interventional	2006-06-30	Active, not recruiting
HLA-Haploidentical Peripheral Blood Stem Cell Transplantation With Post-transplant Cyclophosphamide and Bortezomib Following Fludarbine/Melphalan/Total Body Irradiation Conditioning Regimen [NCT03850366]	Phase 2	15 participants (Anticipated)	Interventional	2016-03-08	Recruiting
Phase II Trial of Low Toxicity GVHD Prevention and Enhanced Immune Recovery With Tacrolimus, Bortezomib and Thymoglobulin® TBT [NCT02877082]	Phase 2	5 participants (Actual)	Interventional	2016-09-30	Terminated
A Phase II Evaluation of Bortezomib (Velcade™, PS-341, NSC #681239, IND #58443) in the Treatment of Persistent or Recurrent Platinum-Sensitive Epithelial Ovarian or Primary Peritoneal Cancer [NCT00023712]	Phase 2	58 participants (Actual)	Interventional	2001-11-05	Completed
A Phase 3 Randomized Study Comparing Teclistamab Monotherapy Versus Pomalidomide, Bortezomib, Dexamethasone (PVd) or Carfilzomib, Dexamethasone (Kd) in Participants With Relapsed or Refractory Multiple Myeloma Who Have Received 1 to 3 Prior Lines of Thera [NCT05572515]	Phase 3	590 participants (Anticipated)	Interventional	2023-03-29	Recruiting
A Randomized, Controlled, Open-label, Multicenter, Inferentially Seamless Phase 2/3 Study of Ibrutinib in Combination With Rituximab Versus Physician's Choice of Lenalidomide Plus Rituximab or Bortezomib Plus Rituximab in Participants With Relapsed or Ref [NCT05564052]	Phase 2	36 participants (Actual)	Interventional	2022-12-06	Active, not recruiting
A Phase 2, Multicohort Study of Daratumumab-Based Therapies in Participants With Amyloid Light Chain (AL) Amyloidosis [NCT05250973]	Phase 2	150 participants (Anticipated)	Interventional	2022-03-01	Recruiting
Phase 1b Study of REGN5458 (Anti-BCMA x Anti-CD3 Bispecific Antibody) Plus Other Cancer Treatments for Patients With Relapsed/Refractory Multiple Myeloma [NCT05137054]	Phase 1	317 participants (Anticipated)	Interventional	2022-08-17	Recruiting
A Phase 3 Randomized Study Comparing Teclistamab in Combination With Daratumumab SC (Tec-Dara) Versus Daratumumab SC, Pomalidomide, and Dexamethasone (DPd) or Daratumumab SC, Bortezomib, and Dexamethasone (DVd) in Participants With Relapsed or Refractory [NCT05083169]	Phase 3	587 participants (Actual)	Interventional	2021-10-14	Active, not recruiting
A Phase 3 Randomized Study Comparing Bortezomib, Lenalidomide and Dexamethasone (VRd) Followed by Ciltacabtagene Autoleucel, a Chimeric Antigen Receptor T Cell (CAR-T) Therapy Directed Against BCMA Versus Bortezomib, Lenalidomide, and Dexamethasone (VRd) [NCT04923893]	Phase 3	650 participants (Anticipated)	Interventional	2021-08-19	Recruiting
A Multi-arm Phase 1b Study of Teclistamab With Other Anticancer Therapies in Participants With Multiple Myeloma [NCT04722146]	Phase 1	140 participants (Actual)	Interventional	2021-03-12	Active, not recruiting
A Phase 3 Randomized Study Comparing JNJ-68284528, a Chimeric Antigen Receptor T Cell (CAR-T) Therapy Directed Against BCMA, Versus Pomalidomide, Bortezomib and Dexamethasone (PVd) or Daratumumab, Pomalidomide and Dexamethasone (DPd) in Subjects With Rela [NCT04181827]	Phase 3	419 participants (Actual)	Interventional	2020-06-12	Active, not recruiting
A Phase 2, Multicohort Open-Label Study of JNJ-68284528, a Chimeric Antigen Receptor T Cell (CAR-T) Therapy Directed Against BCMA in Subjects With Multiple Myeloma [NCT04133636]	Phase 2	169 participants (Actual)	Interventional	2019-11-07	Active, not recruiting
A Phase II Study of High-Dose Post-Transplant Cyclophosphamide and Bortezomib (CyBor) for the Prevention of Graft-versus-Host Disease Following Allogeneic Hematopoietic Stem Cell Transplantation (HSCT) [NCT03945591]	Phase 2	23 participants (Actual)	Interventional	2019-06-20	Active, not recruiting
A Phase 3 Study Comparing Daratumumab, VELCADE (Bortezomib), Lenalidomide, and Dexamethasone (D-VRd) With VELCADE, Lenalidomide, and Dexamethasone (VRd) in Subjects With Untreated Multiple Myeloma and for Whom Hematopoietic Stem Cell Transplant is Not Pla [NCT03652064]	Phase 3	395 participants (Actual)	Interventional	2018-11-06	Active, not recruiting
A Randomized, Multicenter, Open-label, Phase 3 Study to Compare Daratumumab, Bortezomib, and Dexamethasone (DVd) vs Bortezomib and Dexamethasone (Vd) in Chinese Subjects With Relapsed or Refractory Multiple Myeloma [NCT03234972]	Phase 3	211 participants (Actual)	Interventional	2017-11-30	Active, not recruiting
A Phase 3, Multicenter, Randomized, Controlled, Open-label Study of VELCADE (Bortezomib) Melphalan-Prednisone (VMP) Compared to Daratumumab in Combination With VMP (D-VMP), in Subjects With Previously Untreated Multiple Myeloma Who Are Ineligible for High [NCT03217812]	Phase 3	220 participants (Actual)	Interventional	2017-11-23	Active, not recruiting
An Open-Label, Single Arm, Phase 2a Study of Bortezomib, Lenalidomide, Dexamethasone and Elotuzumab in Newly Diagnosed Multiple Myeloma [NCT02375555]	Phase 2	40 participants (Actual)	Interventional	2015-05-07	Active, not recruiting
Efficacy of First Line Dexamethasone, Rituximab and Cyclophosphamide (DRC) +/- Bortezomib for Patients With Waldenström's Macroglobulinemia [NCT01788020]	Phase 3	202 participants (Actual)	Interventional	2013-11-30	Active, not recruiting
Efficacy of Daratumumab Combined With Bortezomib and Dexamethasone in Patients With Mayo 04 Stage III Light Chain Amyloidosis: a Prospective Phase II Clinical Trial [NCT04474938]	Phase 2	40 participants (Anticipated)	Interventional	2021-05-24	Active, not recruiting
Phase I Trial of PD 0332991 Plus Bortezomib in Patients With Relapsed Mantle Cell Lymphoma [NCT01111188]	Phase 1	20 participants (Actual)	Interventional	2010-08-23	Terminated
A Randomized Phase II Study of DaRatumumab, Ixazomib, and Dexamethasone vs Daratumumab, Bortezomib (VElcade) and Dexamethasone Followed by Daratumumab-Ixazomib-Dexamethasone in Newly Diagnosed Multiple Myeloma (DeRIVE Study) [NCT03942224]	Phase 2	49 participants (Actual)	Interventional	2019-07-03	Active, not recruiting
(PRO#11307) Phase III Randomized Study of Autologous Stem Cell Transplantation With High-dose Melphalan Versus High-dose Melphalan and Bortezomib in Patients With Multiple Myeloma 65 Year or Older [NCT01453088]	Phase 2	63 participants (Actual)	Interventional	2010-06-24	Terminated(stopped due to Lack of Accrual)
[NCT01250808]		0 participants	Expanded Access		Available
Assessment of Bortezomib (Alvocade ®) Efficacy and Safety in Newly Diagnosed Multiple Myeloma Patients [NCT04348006]	Phase 4	0 participants (Actual)	Interventional	2020-03-01	Withdrawn(stopped due to No patients were enrolled in the study)
A Randomized, Open-label Phase 3 Study of Carfilzomib, Lenalidomide, and Dexamethasone Versus Bortezomib, Lenalidomide and Dexamethasone (KRd vs. VRd) in Patients With Newly Diagnosed Multiple Myeloma (COBRA) [NCT03729804]	Phase 3	250 participants (Anticipated)	Interventional	2019-05-07	Recruiting
A Pilot Trial to Assess Mobilization of Hematopoietic Progenitor Cells With a Combination of Bortezomib and G-CSF in Patients Undergoing Autologous Transplant for Myeloma and Lymphoma [NCT01171092]	Early Phase 1	21 participants (Actual)	Interventional	2010-09-30	Completed
Immune Modulation Therapy for ERT-naïve or ERT-treated Pompe Disease Patients [NCT02525172]	Phase 4	8 participants (Anticipated)	Interventional	2015-08-31	Recruiting
Randomized Study Comparing Conventional Dose Treatment Using a Combination of Lenalidomide, Bortezomib and Dexamethasone to High-Dose Treatment With ASCT in the Initial Management of Myeloma in Patients up to 65 Years of Age [NCT01191060]	Phase 3	700 participants (Actual)	Interventional	2010-10-31	Completed
A Phase Ⅰ Clinical Study of Mitoxantrone Hydrochloride Liposome Injection in Combination With Bortezomib and Dexamethasone in Patients With Relapsed or Refractory Multiple Myeloma [NCT05052970]	Phase 1	60 participants (Anticipated)	Interventional	2021-10-20	Recruiting
A Phase I Study of Vorinostat and Bortezomib in Children With Refractory of Recurrent Solid Tumors, Including CNS Tumors and Lymphomas [NCT01132911]	Phase 1	5 participants (Anticipated)	Interventional	2010-05-10	Completed
An Evaluation of Bortezomib (VelcadeR ) Followed by High-Dose Melphalan and Bortezomib (VelcadeR) as Conditioning Regimen for Tandem Peripheral Blood Stem Cell Transplants in Patients With Primary Refractory Multiple Myeloma and Plasma Cell Leukemia [NCT00307086]	Phase 2	30 participants (Actual)	Interventional	2005-06-30	Completed
Phase 2 Study of Bortezomib (Velcade) for the Treatment of Steroid Refractory Chronic Graft-vs-Host Disease [NCT01158105]	Phase 2	25 participants (Anticipated)	Interventional	2010-06-30	Active, not recruiting
Efficacy of the Use of Bortezomib for the Treatment of Relapsed Leukemia or Positive Minimal Residual Disease [NCT05137860]	Phase 4	56 participants (Anticipated)	Interventional	2021-12-12	Recruiting
A Phase 1b, Open-label, Multicenter Study of (BMS-936564) in Combination With Lenalidomide (Revlimid) Plus Low-dose Dexamethasone, or With Bortezomib (Velcade) Plus Dexamethasone in Subjects With Relapsed or Refractory Multiple Myeloma [NCT01359657]	Phase 1	46 participants (Actual)	Interventional	2011-09-30	Completed
University of Arkansas (UARK# 2017-03): A Single-Arm, Open-label Study of Anti-SLAMF7 mAb Therapy After Autologous Stem Cell Transplant in Patients With Multiple Myeloma (Total Therapy 8) [NCT03168100]	Phase 2	0 participants (Actual)	Interventional	2017-10-01	Withdrawn(stopped due to No study population. No subjects enrolled.)
Phase IB Dose Escalation Study of Bortezomib (VELCADE) Administered Weekly for 4 Weeks and Sunitinib (SU-011248) Administered Daily for 4 Weeks Followed by a 14 Day Rest in Patients With Refractory Solid Tumors [NCT00720148]	Phase 1	30 participants (Actual)	Interventional	2008-02-29	Completed
Study of Cyclophosphamide，Liposome Doxorubicin Dexamethasone（CDD) Plus Bortezomib Compared With CDD in the Relapsed or Refractory Multiple Myeloma Combined With Extramedullary Plasmacytoma Patients [NCT02336386]	Phase 3	100 participants (Anticipated)	Interventional	2014-12-31	Recruiting
Daratumumab Plus Cyclophosphamide, Bortezomib and Dexamethasone (Dara-CyBorD) in Previously Untreated and Relapsed Subjects With Multiple Myeloma [NCT02951819]	Phase 2	101 participants (Actual)	Interventional	2016-11-09	Completed
Randomized, Multicenter Study of Tolerability and Efficacy of Modified Combinations of Bortezomib, Dexamethasone and Cyclophosphamide in Previously Untreated Multiple Myeloma. [NCT02086942]	Phase 2	94 participants (Anticipated)	Interventional	2013-08-31	Recruiting
A Phase 2 Study to Evaluate Safety and Efficacy of Teclistamab in Combination With Daratumumab, Lenalidomide, and Dexamethasone With or Without Bortezomib as Induction Therapy and Teclistamab in Combination With Daratumumab and Lenalidomide as Maintenance [NCT05695508]	Phase 2	70 participants (Anticipated)	Interventional	2022-12-01	Recruiting
Phase II Trial for Newly Diagnosed Low-risk Multiple Myeloma Patients Comparing 6 Cycles of Isatuximab With Lenalidomide/Bortezomib/Dexamethasone (I-VRD) Compared to 3 Cycles of I-VRD Followed by One Cycle of High-dose Therapy and Both Arms Followed by Ma [NCT05665140]	Phase 2/Phase 3	100 participants (Anticipated)	Interventional	2023-02-03	Recruiting
Phase II Study of Simvastatin, Zoledronic Acid, Bortezomib, Bendamustine and Methylprednisolone for Relapsed/Refractory Myeloma [NCT01332617]	Phase 2	0 participants (Actual)	Interventional	2011-04-30	Withdrawn(stopped due to Investigators no longer interested in activating study)
Phase II Study Evaluating the Effect of Adding Bortezomib to Ibrutinib in Ibrutinib Relapsed Mantle Cell Lymphoma [NCT03617484]	Phase 2	0 participants (Actual)	Interventional	2020-07-31	Withdrawn(stopped due to Enrollment and/or interactions/interventions temporarily paused due to COVID-19 and expected to resume in the future. This is not a suspension of IRB approval.)
Multicenter Phase II, Double-blind Placebo Controlled Trial of Maintenance Ixazomib After Allogeneic Hematopoietic Stem Cell Transplantation for High Risk Multiple Myeloma (BMT CTN 1302) [NCT02440464]	Phase 2	57 participants (Actual)	Interventional	2015-08-31	Completed
Therapy of Antibody-mediated Autoimmune Diseases by Bortezomib (TAVAB) [NCT02102594]	Phase 2	11 participants (Actual)	Interventional	2014-10-31	Terminated(stopped due to recruitment difficulties)
Phase II Trial of Plitidepsin (Aplidin®) in Combination With Bortezomib and Dexamethasone in Multiple Myeloma Patients Double Refractory to Bortezomib and Lenalidomide [NCT03117361]	Phase 2	10 participants (Actual)	Interventional	2017-05-08	Terminated(stopped due to PharmaMar has decided to end this study due to the slow recruitment rate of the trial)
[NCT01376401]	Phase 2	60 participants (Anticipated)	Interventional	2011-07-31	Completed
A Phase 1b/2 Trial to Evaluate the Safety and Efficacy of Radium-223 Dichloride (BAY88-8223) in Combination With Bortezomib and Dexamethasone in Early Relapsed Multiple Myeloma [NCT02928029]	Phase 1/Phase 2	7 participants (Actual)	Interventional	2017-02-10	Terminated(stopped due to Due to the changes of standard of care and the slow recruitment of participants.)
Bendamustine Plus Bortezomib Plus Dexamethasone in the Treatment of Stage II/III Relapsed or Refractory Multiple Myeloma [NCT01168804]	Phase 2	79 participants (Actual)	Interventional	2010-06-30	Completed
An Open-Label Study of Bendamustine Combined With Bortezomib for Patients With Relapsed/Refractory Multiple Myeloma [NCT00920855]	Phase 1/Phase 2	40 participants (Actual)	Interventional	2009-06-30	Completed
Phase I Study of the Combination of Midostaurin, Bortezomib, and Chemotherapy in Relapsed/Refractory Acute Myeloid Leukemia [NCT01174888]	Phase 1	34 participants (Actual)	Interventional	2010-08-31	Completed
Randomized Phase II Study of Dose-Adjusted EPOCH-Rituximab-Bortezomib (EPOCH-R-B) Induction Followed by Bortezomib Maintenance Versus Observation in Untreated Mantle Cell Lymphoma With Microarray Profiling and Proteomics [NCT00114738]	Phase 2	53 participants (Actual)	Interventional	2005-06-15	Completed
Dose Individualization of Antineoplastic Drugs and Anti-Infective Drug in Children With Hematoplastic Disease [NCT03844360]	Phase 4	1,500 participants (Anticipated)	Interventional	2016-01-31	Recruiting
A Phase II Study of Bevacizumab and Bortezomib in Patients With Relapsed Refractory Multiple Myeloma [NCT00464178]	Phase 2	7 participants (Actual)	Interventional	2007-04-30	Terminated(stopped due to The study was closed early due to poor accrual)
Phase 1 and 2 Study of Combination Treatment of Bortezomib, Fludarabine and Cyclophosphamide in Patients With Recurrent Mantle Cell Lymphoma [NCT01322776]	Phase 1/Phase 2	40 participants (Anticipated)	Interventional	2011-03-31	Recruiting
A Phase I/II Trial of Combined Weekly Bortezomib (VELCADE®) and Y-90-Ibritumomab Tiuxetan (Zevalin) in Patients With Relapsed or Refractory Follicular Lymphoma and Transformed Non-Hodgkin's Lymphoma [NCT00372905]	Phase 1/Phase 2	18 participants (Actual)	Interventional	2007-07-24	Terminated(stopped due to Study was closed permanently before the accrual goal was met due to slow accrual)
Phase I Clinical Trial of Vorinostat (MK-0683) in Combination With Bortezomib in Patients With Advanced Multiple Myeloma [NCT00111813]	Phase 1	34 participants (Actual)	Interventional	2005-09-30	Completed
A Phase II Trial of Tamoxifen and Bortezomib in Patients With Recurrent High-Grade Gliomas [NCT00108069]	Phase 2	43 participants (Actual)	Interventional	2005-04-30	Completed
Am Open-Label Phase II Study of the Safety and Efficacy of Bortezomib, Lenalidomide, and Dexamethasone Combination Therapy for Patients With Relapsed or Relapsed and Refractory Multiple Myeloma [NCT00378209]	Phase 2	65 participants (Actual)	Interventional	2006-08-31	Completed
A Phase II Study of Combination Rituximab-CHOP and Bortezomib (Velcade®) (R-CHOP-V) Induction Therapy Followed by Bortezomib Maintenance (VM) Therapy for Patients With Newly Diagnosed Mantle Cell Lymphoma [NCT00376961]	Phase 2	68 participants (Actual)	Interventional	2006-08-31	Completed
Phase 2 Study With Minimal Residual Disease (MRD) Driven Adaptive Strategy in Treatment for Newly Diagnosed Multiple Myeloma (MM) With Upfront Daratumumab-based Therapy [NCT04140162]	Phase 2	57 participants (Actual)	Interventional	2020-10-05	Active, not recruiting
Bortezomib-based Regimen for Refractory or Relapsed Acute Lymphoblastic Leukemia in Adults [NCT06034561]	Phase 2	50 participants (Anticipated)	Interventional	2023-09-30	Not yet recruiting
TINI 2: Total Therapy for Infants With Acute Lymphoblastic Leukemia II [NCT05848687]	Phase 1/Phase 2	90 participants (Anticipated)	Interventional	2023-11-01	Not yet recruiting
A Phase 1/2, Open-label, Prospective, Multicenter Study to Evaluate the Efficacy and Safety of the Lower Dose of Bortezomib Plus Busulfan and Melphalan as a Conditioning Regimen in Patients With Multiple Myeloma Undergoing Autologous Peripheral Blood Stem [NCT01255527]	Phase 1/Phase 2	53 participants (Anticipated)	Interventional	2010-10-31	Recruiting
A Trial of Single Autologous Transplant With or Without Consolidation Therapy Versus Tandem Autologous Transplant With Lenalidomide Maintenance for Patients With Multiple Myeloma (BMT CTN 0702) [NCT01109004]	Phase 3	758 participants (Actual)	Interventional	2010-05-31	Completed
Bortezomib in Combination With Continuous Low-dose Oral Cyclophosphamide and Dexamethason Followed by Maintenance in Primary Refractory or Relapsed Bortezomib naïve Multiple Myeloma Patients. A Prospective Phase II Study. [NCT02467010]	Phase 2	73 participants (Actual)	Interventional	2008-09-30	Completed
A Randomized, Phase II Trial Evaluating the Efficacy and Safety of Lenalidomide, Bortezomib and Dexamethasone (RVD) With or Without Panobinostat in Transplant Eligible, Newly Diagnosed Multiple Myeloma [NCT02720510]	Phase 2	6 participants (Actual)	Interventional	2016-06-14	Terminated(stopped due to A study was terminated due to low enrollment.)
A Study of Thalidomide, Bendamustine and Dexamethasone (BTD) Versus Bortezomib, Bendamustine and Dexamethasone (BBD) in Patients With Renal Failure Defined as a GFR Below 30 Mls/Min [NCT02424851]	Phase 2	31 participants (Actual)	Interventional	2014-11-30	Completed
Phase 2/3 Randomized, Open-Label Clinical Trial of Tanespimycin (KOS-953) Plus Bortezomib Comparing Three Doses of Tanespimycin in Patients With Relapsed-Refractory Multiple Myeloma [NCT00514371]	Phase 2/Phase 3	22 participants (Actual)	Interventional	2007-08-31	Completed
A Phase II, Multi-center, Single Arm, Open Label Study to Evaluate the Efficacy and Safety of Panobinostat in Combination With Bortezomib and Dexamethasone in Japanese Patients With Relapsed/Refractory Multiple Myeloma [NCT02290431]	Phase 2	31 participants (Actual)	Interventional	2014-12-16	Completed
A Phase II, Multicenter, Open-Label Study of the Combination of Pomalidomide, Bortezomib, Low-Dose Dexamethasone, and Daratumumab in Patients With Relapsed or Refractory Multiple Myeloma [NCT05408026]	Phase 1/Phase 2	0 participants (Actual)	Interventional	2022-10-01	Withdrawn(stopped due to Study withdrawn, trial therapy deemed no longer novel and there was a lack of site interest.)
A Phase Ib Study of Isatuximab, Velcade, and Dexamethasone in Patients With Multiple Myeloma and Severe KIDNEY Disease [NCT04912427]	Phase 1	1 participants (Actual)	Interventional	2022-04-01	Active, not recruiting
An Open-label Phase II Study to Determine the Efficacy and Safety of Rituximab and Bortezomib in Patients With Newly Diagnosed Acquired Hemophilia A [NCT03700229]	Phase 2	22 participants (Anticipated)	Interventional	2018-10-10	Recruiting
A Phase 1b, Open-Label Study of Eftozanermin Alfa (ABBV-621) in Combination With Bortezomib and Dexamethasone in Subjects With Relapsed or Refractory Multiple Myeloma [NCT04570631]	Phase 1	40 participants (Anticipated)	Interventional	2020-11-05	Active, not recruiting
Fase II Study With Bortezomib, Rituximab and Bendamustin-BRB- for Non-Hodgkin Lymphoplasmocytic Lymphoma/Waldenstrom Macroglobulinemia's Patients at First Relapse [NCT02371148]	Phase 2	38 participants (Actual)	Interventional	2014-06-30	Completed
Bortezomib Sensitization of Recurrent Glioblastoma With Unmethylated MGMT Promoter to Temozolomide Phase 1B/II Study [NCT03643549]	Phase 1/Phase 2	63 participants (Anticipated)	Interventional	2018-08-30	Recruiting
Phase 1 Clinical Trial to Evaluate Security and Dose of Expanded and Activated Autologous NK Cells Infusions in Consolidation of Multiple Myeloma Patients Treatment on Second or Later Relapse. [NCT02481934]	Phase 1	5 participants (Actual)	Interventional	2013-03-31	Completed
Phase III Trial of High-dose Melphalan and Stem Cell Transplantation Versus High-dose Melphalan and Bortezomib and Stem Cell Transplantation in Patients With AL Amyloidosis [NCT02489500]	Phase 3	3 participants (Actual)	Interventional	2015-06-30	Terminated(stopped due to Enrollment held for toxicity evaluation; then closed due to competing trial)
Moscow-Berlin 2015 Multicenter Randomized Study for Treatment of Acute Lymphoblastic Leukemia in Children, Adolescents and Young Adults [NCT03390387]		4,000 participants (Anticipated)	Interventional	2015-11-30	Recruiting
Bendamustine, Prednisone and Velcade® for First-line Treatment of Patients With Symptomatic Multiple Myeloma Not Eligible for High-dose Chemotherapy Followed by Autologous Stem Cell Transplantation (BPV). [NCT02237261]	Phase 2	46 participants (Actual)	Interventional	2014-11-30	Completed
An Open, One-arm, Prospective Study of a Single Dose Anti-CD20 Monoclonal Antibody Combined With Bortezomib for Treatment of Relapsed Refractory Autoimmune Hemolytic Anemia [NCT04083014]	Phase 2	43 participants (Anticipated)	Interventional	2019-08-20	Recruiting
Randomized Double-Blind, Placebo-Controlled Parallel Multi-Center Study to Assess the Efficacy of Cannabidiol (BRCX014) Combined With Standard-Of-Care Treatment in Subjects With Multiple Myeloma, Glioblastoma Multiforme, and GI Malignancies [NCT03607643]	Phase 1/Phase 2	160 participants (Anticipated)	Interventional	2019-01-15	Not yet recruiting
An Open-Label, Multicenter Phase 1b Study Investigating the Safety of TAK-079 in Combination With Backbone Regimens for the Treatment of Patients With Newly Diagnosed Multiple Myeloma and for Whom Stem Cell Transplantation Is Not Planned as Initial Therap [NCT03984097]	Phase 1	50 participants (Actual)	Interventional	2019-07-29	Active, not recruiting
Phase I Exploratory Study of Panobinostat IV in Combination With Bortezomib in Relapsed/Refractory Multiple Myeloma Patients [NCT00891033]	Phase 1	12 participants (Actual)	Interventional	2009-04-30	Terminated(stopped due to This study was terminated because the drug company stopped making the study drug)
Treatment of Chronic Active Antibody-mediated Rejection With Bortezomib in Kidney Transplantation [NCT02201576]	Phase 2	60 participants (Actual)	Interventional	2015-02-11	Completed
A Phase I Study of the Safety and Feasibility of Bortezomib in Combination With G-CSF for Stem Cell Mobilization in Patients With Multiple Myeloma [NCT02220608]	Phase 1	10 participants (Actual)	Interventional	2015-02-20	Completed
Pharmacokinetic Study of Bortezomib (VELCADE) Administered Intravenously in Taiwanese Patients With Multiple Myeloma - A Post Approval Commitment Study [NCT02268890]	Phase 4	18 participants (Actual)	Interventional	2014-12-31	Completed
An Open-label, Single-Arm, Multicenter Study to Evaluate the Efficacy and Safety of Ixazomib in Combination With Lenalidomide and Dexamethasone in Patients With Relapsed and/or Refractory Multiple Myeloma Initially Treated With an Injection of Proteasome [NCT03416374]	Phase 4	45 participants (Actual)	Interventional	2018-02-18	Completed
A Phase II, Open-label Study of Bortezomib Following Nonmyeloablative Allogeneic Stem Cell Transplant in Patients With High-risk Multiple Myeloma [NCT02308280]	Phase 2	40 participants (Actual)	Interventional	2014-11-30	Completed
Phase II Trial of Velcade (Bortezomib) in Patients With Previously Untreated Multiple Myeloma [NCT00153920]	Phase 2	66 participants (Actual)	Interventional	2003-12-31	Completed
Phase 2 Study of Concurrent Monosialotetrahexosylganglioside in the Prophylactic Treatment of Bortezomib-induced Peripheral Neuropathy in Patients of Multiple Myeloma [NCT02093910]	Phase 2	100 participants (Anticipated)	Interventional	2014-04-30	Recruiting
A Phase III Randomized Study to Assess the Efficacy and Safety of Perifosine Added to the Combination of Bortezomib and Dexamethasone in Multiple Myeloma Patients [NCT01002248]	Phase 3	135 participants (Actual)	Interventional	2009-12-31	Terminated
A Phase 1/2, Multicenter, Dose-Escalation and Expansion Study of Combination Therapy With Venetoclax, Daratumumab and Dexamethasone (With and Without Bortezomib) in Subjects With Relapsed or Refractory Multiple Myeloma [NCT03314181]	Phase 2	156 participants (Actual)	Interventional	2018-04-02	Active, not recruiting
An Open-label Study of Ibrutinib in Combination With Bortezomib and Dexamethasone in Subjects With Relapsed or Relapsed and Refractory Multiple Myeloma [NCT02902965]	Phase 2	74 participants (Actual)	Interventional	2016-09-20	Completed
Isa-RVD Study: Phase II, Multi-centre, Single-Arm, Open-Label Study to Evaluate the Efficacy and Safety of the Combination Regimen Isatuximab, Lenalidomide, Bortezomib, and Dexamethasone in Patients With Newly Diagnosed Multiple Myeloma [NCT05123131]	Phase 2	43 participants (Anticipated)	Interventional	2022-04-01	Recruiting
A Phase 3, Multicenter, Randomized, Open-Label Study to Compare the Efficacy and Safety of Pomalidomide, Bortezomib and Low-Dose Dexamethasone Versus Bortezomib and Low-Dose Dexamethasone in Subjects With Relapsed or Refractory Multiple Myeloma [NCT01734928]	Phase 3	559 participants (Actual)	Interventional	2013-01-07	Completed
A Phase II Trial to Evaluate the Efficacy of Bortezomib and Pegylated Liposomal Doxorubicin in Patients With BRCA Wild-type Platinum-resistant Recurrent Ovarian Cancer [NCT03509246]	Phase 2	44 participants (Anticipated)	Interventional	2018-05-15	Recruiting
Phase I Dose Escalation Study of Velcade in Combination With Lenalidomide in Patients With Relapsed Acute Myeloid Leukemia (AML) and Myelodysplastic Syndrome (MDS) After Allogeneic Stem Cell Transplantation [NCT02312102]	Phase 1	22 participants (Actual)	Interventional	2015-02-28	Active, not recruiting
A Randomized Controlled Study of DOXIL/CAELYX (Doxorubicin HCL Liposome Injection) and VELCADE (Bortezomib) or VELCADE Monotherapy for the Treatment of Relapsed Multiple Myeloma [NCT00103506]	Phase 3	646 participants (Actual)	Interventional	2004-12-31	Completed
A Phase I/II Study of Escalating Doses of Thalidomide in Conjunction With Bortezomib and HIgh Dose Melphalan as a Conditioning Regimen for Autologous Peripheral Blood Stem Cell Transplantation in Patients With Advanced Multiple Myeloma [NCT01242267]	Phase 1/Phase 2	29 participants (Actual)	Interventional	2010-05-11	Completed
A Multicenter Phase 2 Study to Evaluate Subcutaneous Daratumumab in Combination With Standard Multiple Myeloma Treatment Regimens [NCT03412565]	Phase 2	265 participants (Actual)	Interventional	2018-04-26	Active, not recruiting
A Randomized Phase 3 Study to Evaluate the Efficacy and Safety of Daratumumab in Combination With Cyclophosphamide, Bortezomib and Dexamethasone (CyBorD) Compared to CyBorD Alone in Newly Diagnosed Systemic AL Amyloidosis [NCT03201965]	Phase 3	416 participants (Actual)	Interventional	2017-10-05	Active, not recruiting
A Phase 3, Randomized, Controlled, Open-label Study of VELCADE (Bortezomib) Melphalan-Prednisone (VMP) Compared to Daratumumab in Combination With VMP (D-VMP), in Subjects With Previously Untreated Multiple Myeloma Who Are Ineligible for High-dose Therapy [NCT02195479]	Phase 3	706 participants (Actual)	Interventional	2014-12-09	Active, not recruiting
An Open-Label, Multicenter, Phase 1b Study of JNJ-54767414 (HuMax CD38) (Anti-CD38 Monoclonal Antibody) in Combination With Backbone Regimens for the Treatment of Subjects With Multiple Myeloma [NCT01998971]	Phase 1	242 participants (Actual)	Interventional	2014-02-18	Active, not recruiting
A Randomized Phase 2 Study of Daratumumab-Selinexor-Velcade-Dexamethasone (Dara-SVD) for High-Risk Newly Diagnosed Multiple Myeloma [NCT06169215]	Phase 2	82 participants (Anticipated)	Interventional	2024-02-20	Not yet recruiting
A Phase 1/2, Multicenter, Open-label, Study to Determine the Recommended Dose and Regimen, and Evaluate the Safety and Preliminary Efficacy of CC-92480 in Combination With Standard Treatments in Subjects With Relapsed or Refractory Multiple Myeloma (RRMM) [NCT03989414]	Phase 1/Phase 2	424 participants (Anticipated)	Interventional	2019-09-30	Recruiting
A Phase I/II Trial of DFMO in Combination With Bortezomib in Patients With Relapsed or Refractory Neuroblastoma [NCT02139397]	Phase 1/Phase 2	16 participants (Actual)	Interventional	2014-05-31	Active, not recruiting
Phase I/II Study of VELCADE®-BEAM and Autologous Hematopoietic Stem Cell Transplantation for Relapsed Indolent Non-Hodgkin's Lymphoma, Transformed or Mantle Cell Lymphoma [NCT00571493]	Phase 1/Phase 2	42 participants (Actual)	Interventional	2006-04-14	Completed
Phase I Two-Dimensional Dose-Finding Study of Bortezomib in Combination With Gemcitabine/Doxorubicin in Metastatic Surgically Unresectable Urothelial Cancer or Other Solid Tumors [NCT00479128]	Phase 1	80 participants (Actual)	Interventional	2006-09-28	Active, not recruiting
A Phase I/II Trial of Hydroxychloroquine Added to Bortezomib for Relapsed/Refractory Myeloma [NCT00568880]	Phase 1	25 participants (Actual)	Interventional	2010-09-08	Completed
Serial Measurements of Molecular and Architectural Responses to Therapy (SMMART) Trial: PRIME [NCT03878524]	Phase 1	2 participants (Actual)	Interventional	2020-04-01	Active, not recruiting
International Collaborative Treatment Protocol for Children and Adolescents With Acute Lymphoblastic Leukemia - AIEOP-BFM ALL 2017 [NCT03643276]	Phase 3	5,000 participants (Anticipated)	Interventional	2018-07-15	Recruiting
Intergroup Randomized Phase 2 Four Arm Study In Patients ≥ 60 With Previously Untreated Mantle Cell Lymphoma Of Therapy With: Arm A = Rituximab+ Bendamustine Followed By Rituximab Consolidation (RB → R); Arm B = Rituximab + Bendamustine + Bortezomib Follo [NCT01415752]	Phase 2	373 participants (Actual)	Interventional	2012-08-09	Active, not recruiting
A Multicenter Prospective Randomized Study of Rituximab Combined With Bortezomib Versus Rituximab in the Treatment of Newly Diagnosed Primary Immune Thrombocytopenia (ITP) [NCT03443570]	Phase 3	200 participants (Anticipated)	Interventional	2018-03-01	Not yet recruiting
Phase 3 Randomized, Open-Label Clinical Trial of Tanespimycin (KOS-953) Plus Bortezomib Compared to Bortezomib Alone in Patients With Multiple Myeloma in First Relapse [NCT00546780]	Phase 3	31 participants (Actual)	Interventional	2008-02-29	Completed
A Phase II Trial of Weekly Bortezomib and Dexamethasone With Oral Metronomic Cyclophosphamide in Elderly Patients With Plasma Cell Myeloma [NCT02082405]	Phase 2	0 participants (Actual)	Interventional	2015-04-30	Withdrawn(stopped due to Funding unavailable)
Phase 0 Microdose Study to Evaluate the Effect of Melphalan, Bortezomib and Dexamethasone on Cellular Gene-expression in Patients With Multiple Myeloma [NCT02109861]	Early Phase 1	6 participants (Actual)	Interventional	2014-01-31	Active, not recruiting
A Phase II Study of Bortezomib in Metastatic Papillary Thyroid Carcinoma or Follicular Thyroid Carcinoma [NCT00104871]	Phase 2	24 participants (Actual)	Interventional	2004-12-31	Completed
Treatment of Renal Failure Due to Myeloma Cast Nephropathy: Comparison of Two Different Chemotherapy Regimens and Evaluation of Optimized Removal of Monoclonal Immunoglobulin Light Chains Using a High Permeability Hemodialysis Membrane. [NCT01208818]	Phase 3	284 participants (Anticipated)	Interventional	2011-06-30	Completed
A Phase I Study of Bortezomib (VELCADE) in Combination With Pralatrexate in Relapsed/Refractory Multiple Myeloma [NCT01114282]	Phase 1	11 participants (Actual)	Interventional	2010-08-31	Completed
Bortezomib in Combination With Liposomal Doxorubicin and Dexamethasone to Treat Plasma Cell Leukemia [NCT01328236]	Phase 2	20 participants (Anticipated)	Interventional	2010-09-30	Recruiting
Early Response-adapted Intensification of Induction Chemotherapy in Patients With Newly Diagnosed Multiple Myeloma (MM) Who Are Eligible for Autologous Stem Cell Transplantation: Multicenter Phase 2 Study [NCT01114048]	Phase 2	78 participants (Anticipated)	Interventional	2010-03-31	Recruiting
Phase I Dose-Escalation Study of Azacitidine (Vidaza) and Bortezomib (Velcade) in T-Cell Lymphoma [NCT01129180]	Phase 1	8 participants (Actual)	Interventional	2010-05-31	Completed
A Phase 3, Prospective, Randomized Clinical Study of VELCADE-Thalidomide-Dexamethasone (VTD) Versus Thalidomide-Dexamethasone (TD) for Previously Untreated Multiple Myeloma (MM) Patients Who Are Candidates to Receive Double Autologous Transplantation [NCT01134484]	Phase 3	480 participants (Actual)	Interventional	2006-05-31	Active, not recruiting
A Phase 2a Study of Once Daily Intravenous Busulfan With Bortezomib, Followed by an Autologous Hematopoietic Stem Cell Transplant (HSCT) in Subjects With Relapsed Multiple Myeloma After Prior Autologous HSCT [NCT01009840]	Phase 2	30 participants (Actual)	Interventional	2010-05-31	Completed
A Double-blind, Placebo-controlled, Randomized Phase 2 Study of BHQ880, an Anti-Dickkopf1 (DKK1) Monoclonal Antibody (mAb), in Patients With Untreated Multiple Myeloma and Renal Insufficiency [NCT01337752]	Phase 2	9 participants (Actual)	Interventional	2012-01-31	Completed
A Multicenter Randomized, Controlled, Double-blinded Trial to Evaluate Efficacy and Safety of Bortezomib in Patients With Severe Autoimmune Encephalitis [NCT03993262]	Phase 2	50 participants (Anticipated)	Interventional	2020-05-13	Recruiting
Phase II Study of PS-341 for Patients With High-Risk, Newly Diagnosed Multiple Myeloma [NCT00075881]	Phase 2	44 participants (Actual)	Interventional	2004-01-31	Completed
An Open-label, Multi-center, Phase I-Ib/II Study of AUY922 Administered as Single Agent and in Combination With Bortezomib With or Without Dexamethasone in Adult Patients in Relapse or Refractory Multiple Myeloma. [NCT00708292]	Phase 1/Phase 2	29 participants (Actual)	Interventional	2008-07-31	Completed
A Phase III Randomized Trial Investigating Bortezomib (NSC# 681239) on a Modified Augmented BFM (ABFM) Backbone in Newly Diagnosed T-Lymphoblastic Leukemia (T-ALL) and T-Lymphoblastic Lymphoma (T-LLy) [NCT02112916]	Phase 3	847 participants (Actual)	Interventional	2014-10-04	Active, not recruiting
Phase II Study of SOM230 LAR in Combination With Bortezomib and Dexamethasone in Patients With Refractory or Relapsed Multiple Myeloma [NCT01329289]	Phase 2	0 participants (Actual)	Interventional	2011-12-31	Withdrawn(stopped due to Clinical trial being transferred to Columbia University with the Investigator.)
Clinical Study to Evaluate the Safety and Efficacy of Daratumumab and Carfilzomib-based Induction/Consolidation/Maintenance Therapy in Transplant-eligible, Ultra High-risk, Newly Diagnosed Multiple Myeloma [NCT06140966]	Phase 2	54 participants (Anticipated)	Interventional	2023-10-20	Recruiting
Multicenter Non-interventional Study to Investigate Drug Utilization of Pomalidomide in Clinical Practice for the Treatment of Relapsed/Refractory Multiple Myeloma (rrMM) [NCT02555839]		150 participants (Anticipated)	Observational	2015-02-20	Active, not recruiting
A Randomized Phase III Trial of CC-5013 (Lenalidomide, NSC-703813) and Low Dose Dexamethasone (LLD) Versus Bortezomib (PS-341, NSC-681239), Lenalidomide and Low Dose Dexamethasone (BLLD) for Induction, in Patients With Previously Untreated Multiple Myelom [NCT00644228]	Phase 3	525 participants (Actual)	Interventional	2008-04-01	Active, not recruiting
A Phase I Study of Palbociclib in Combination With Chemotherapy in Pediatric Patients With Relapsed or Refractory Acute Lymphoblastic Leukemia [NCT03515200]	Phase 1	12 participants (Actual)	Interventional	2018-04-20	Terminated(stopped due to Due to departure of PI from St. Jude)
Open Label Study of the Anti Insulin-like Growth Factor 1 Receptor (IGF-1R) Monoclonal Antibody, AVE1642, as Single Agent (Dose Escalation, Part 1) and in Combination With Velcade® (Combination, Part 2) in Patients With Recurrent, Refractory Multiple Myel [NCT01233895]	Phase 1	26 participants (Actual)	Interventional	2006-09-30	Completed
A Phase II Study of the Efficacy and Safety of Lenalidomide, Subcutaneous Bortezomib and Dexamethasone Combination Therapy for Patients With Newly Diagnosed Multiple Myeloma [NCT02441686]	Phase 2	45 participants (Anticipated)	Interventional	2015-12-31	Active, not recruiting
An Open Label, Multicenter, Phase II Study of Belantamab Mafodotin in Combination With VRd for the Treatment of Newly Diagnosed Transplant Eligible Multiple Myeloma Patients [NCT04802356]	Phase 2	50 participants (Anticipated)	Interventional	2021-04-07	Recruiting
A National, Open-label, Multicenter, Randomized, Comparative Phase IIb Study of Treatment for Newly Diagnosed Multiple Myeloma Patients Older Than 65 Years With Sequential Melphalan/Prednisone/Velcade (MPV) Followed by Revlimid/Low Dose Dexamethasone (Rd) [NCT01237249]	Phase 2	250 participants (Actual)	Interventional	2011-02-28	Completed
A Phase 3, Randomized, Double-blind Study of Siltuximab (Anti-IL-6 Monoclonal Antibody) or Placebo in Combination With VELCADE and Dexamethasone for the Treatment of Subjects With Relapsed or Refractory Multiple Myeloma [NCT01266811]	Phase 3	0 participants (Actual)	Interventional	2011-07-31	Withdrawn(stopped due to Study canceled based on results of different study with similar hypothesis, investigational agent, & patient)
Phase I Trial of Nelfinavir and Bortezomib in Advanced Hematologic Malignancies [NCT01164709]	Phase 1	18 participants (Actual)	Interventional	2010-07-31	Completed
Velcade for Proliferative Lupus Nephritis [NCT01169857]	Phase 4	0 participants (Actual)	Interventional	2010-08-31	Withdrawn(stopped due to No participants were enrolled.)
Phase I Study of The Combination of Bortezomib and Sorafenib Followed by Decitabine in Patients With Acute Myeloid Leukemia [NCT01861314]	Phase 1	15 participants (Actual)	Interventional	2013-07-03	Active, not recruiting
IFM2008: Frontline Therapy in de Novo Multiple Myeloma Patients Under 65, (a Phase 2 Multicenter Trial) [NCT01206205]	Phase 2	31 participants (Actual)	Interventional	2009-08-31	Completed
A Phase I Study of Bortezomib in Combination With MEC (Mitoxantrone, Etoposide, and Intermediate-Dose Cytarabine) for Relapsed/ Refractory Acute Myelogenous Leukemia (AML) [NCT01127009]	Phase 1	3 participants (Actual)	Interventional	2010-07-31	Completed
An Open-Label, Pilot Study To Investigate Feasibility and Safety Of Using Bortezomib, Rituximab, Ifosfamide, Carboplatin, Etoposide As Salvage Regime In Previously Treated Patients With Diffuse Large B-Cell Lymphoma [NCT01226849]	Phase 1	6 participants (Actual)	Interventional	2010-11-30	Completed
Phase I Dose Escalation Study to Determine the Maximum Tolerated Dose of the Combination of Ruxolitinib and Bortezomib in Patients With Relapsed or Refractory Lymphoma [NCT02613598]	Phase 1	15 participants (Actual)	Interventional	2016-05-12	Completed
Phase II Study of Ibrutinib With or Without Bortezomib and Dexamethasone for the Treatment of Patients With Relapsed/Refractory Immunoglobulin Light Chain Amyloidosis [NCT03130348]	Phase 2	0 participants (Actual)	Interventional	2018-03-15	Withdrawn(stopped due to Study was dropped at site before participation)
Quantitating the Impact of Plerixafor Alone or in Combination With Bortezomib on Plasma Cell Mobilization and the Subsequent Impact on HLA Antibody Levels [NCT02522572]	Phase 1/Phase 2	12 participants (Anticipated)	Interventional	2015-08-31	Recruiting
A Phase 3 Randomized, Open-label, Multicenter Study Assessing the Clinical Benefit of Isatuximab (SAR650984) in Combination With Bortezomib (Velcade®), Lenalidomide and Dexamethasone Versus Bortezomib, Lenalidomide and Dexamethasone in Patients With Newly [NCT03319667]	Phase 3	475 participants (Actual)	Interventional	2017-12-07	Active, not recruiting
Combination of Ibrutinib and Bortezomib Followed by Ibrutinib Maintenance to Treat Patients With Relapsed and Refractory Mantle Cell Lymphoma; a Multicenter Phase I/II Trial. [NCT02356458]	Phase 1/Phase 2	58 participants (Actual)	Interventional	2015-08-31	Terminated(stopped due to SAKK Board decision of 14th November 2020 due to financial reasons.)
Phase II Study of Bortezomib (VELCADE) for the Treatment of Relapsed or Refractory T-cell Prolymphocytic Leukemia [NCT01162031]	Phase 2	0 participants (Actual)	Interventional	2010-06-30	Withdrawn(stopped due to no accrual)
A Randomized Phase III Trial of Melphalan and Dexamethasone (MDex) Versus Bortezomib, Melphalan and Dexamethasone (BMDex) for Untreated Patients With Systemic Light-Chain (AL) Amyloidosis Ineligible for Autologous Stem-Cell Transplantation [NCT01078454]	Phase 3	11 participants (Actual)	Interventional	2010-11-30	Completed
(RICE) Plus Bortezomib (Velcade) in a Dose-Escalating Fashion for Patients With Relapsed or Primary Refractory Aggressive B-Cell NHL [NCT01300793]	Phase 1	6 participants (Actual)	Interventional	2007-05-31	Terminated(stopped due to closed for low accrual and no data is available.)
A Phase 2 Study to Evaluate the Efficacy of Bortezomib in Patients With De-novo Waldenstrom's Macroglobulinemia and Lymphoplasmacytic Lymphoma [NCT03335098]	Phase 2	15 participants (Anticipated)	Interventional	2016-11-21	Recruiting
A Single Arm, Multi-center, Phase II Clinical Trial of VR-CAP in the First-line Treatment for Patients With Marginal Zone Lymphoma [NCT04433156]	Phase 2	60 participants (Anticipated)	Interventional	2020-04-22	Recruiting
Pomalidomide, Bortezomib and Dexamethasone (PVd) Versus Bortezomib and Dexamethasone (Vd) in NDMM Patients With Renal Injury (RI)：A Multicenter, Randomized Controlled, Open-label Trial. [NCT05432414]	Phase 2	79 participants (Anticipated)	Interventional	2022-12-08	Recruiting
Phase II Study of Bortezomib (PS-341) and Pegylated Liposomal Doxorubicin as Initial Therapy for Adult Patients With Symptomatic Multiple Myeloma [NCT00088855]	Phase 2	55 participants (Actual)	Interventional	2004-06-15	Completed
A Phase 1b Study of JNJ-54767414 (Daratumumab) in Combination With Bortezomib and Dexamethasone (D-Vd) in Japanese Patients With Relapsed or Refractory Multiple Myeloma (MM) [NCT02497378]	Phase 1	8 participants (Actual)	Interventional	2015-07-10	Completed
Safety and Efficacy Pilot Trial of the Anti-Viral and Anti-Tumor Activity of Velcade Combined With (R)ICE in Subjects With EBV and/or HHV-8 Positive Relapsed/Refractory AIDS-Associated Non-Hodgkin's Lymphoma [NCT00598169]	Phase 1	23 participants (Actual)	Interventional	2007-11-30	Completed
Phase 1/2 Study of Daratumumab, Bortezomib, Dexamethasone With or Without Venetoclax in Relapsed/Refractory Multiple Myeloma With Assessment for t(11;14) Status [NCT03701321]	Phase 1/Phase 2	0 participants (Actual)	Interventional	2019-01-25	Withdrawn(stopped due to Drug supply issues)
Response Adapted Therapy With Bortezomib/Dexamethasone Followed by Addition of Lenalidomide in Non Responders as Initial Treatment for Patients With Multiple Myeloma [NCT01919086]	Phase 2	30 participants (Actual)	Interventional	2013-08-31	Active, not recruiting
Phase I Study of Bortezomib and Gemcitabine in Elderly Patients With Solid Tumors (X05227) [NCT00620295]	Phase 1	17 participants (Actual)	Interventional	2007-03-31	Completed
A Phase I Study of Panobinostat in Combination With Daratumumab, Bortezomib, and Dexamethasone in Patients With Relapsed/Refractory Multiple Myeloma [NCT04956302]	Phase 1	1 participants (Actual)	Interventional	2021-09-27	Terminated(stopped due to PI Decision)
Phase 1/2 Trial of Iberdomide in Combination With Daratumumab, BortEzomib and DexamethAsone in Patients With Newly Diagnosed Multiple MyeLoma (IDEAL) [NCT05392946]	Phase 1/Phase 2	18 participants (Anticipated)	Interventional	2022-08-11	Recruiting
Thalidomide-Cyclophosphamide-Dexamethasone in Patients < 75 Years or Velcade-Melfalan-Prednisone (V-MP)/Thalidomide-Cyclophosphamide-Dexamethasone in Patients >75 Years, in Refractary or Relapsed Multiple Myeloma [NCT00652041]	Phase 4	40 participants (Anticipated)	Interventional	2007-01-31	Completed
A Phase 2 Study of Rituximab, Venetoclax (ABT 199) and Bortezomib in Relapsed or Refractory Diffuse Large B-Cell Lymphoma (DLBCL) [NCT04285268]	Phase 2	0 participants (Actual)	Interventional	2020-05-06	Withdrawn(stopped due to funding available)
Phase II Study of Bortezomib in Combination With Cyclophosphamide and Rituximab for Relapsed/Refractory Mantle Cell Lymphoma [NCT00958256]	Phase 2	22 participants (Actual)	Interventional	2009-08-31	Completed
A Randomized Phase III Trial Assessing the Benefit of the Addition of Isatuximab to Lenalidomide / Bortezomib / Dexamethasone (RVd) Induction and Lenalidomide Maintenance in Patients With Newly Diagnosed Multiple Myeloma [NCT03617731]	Phase 3	662 participants (Actual)	Interventional	2018-10-18	Active, not recruiting
A Phase II Study Incorporating Bone Marrow Microenvironment (ME) - Co-Targeting Bortezomib Into Tandem Melphalan-Based Autotransplants With DTPACE for Induction/Consolidation and Thalidomide + Dexamethasone for Maintenance [NCT00572169]	Phase 3	177 participants (Actual)	Interventional	2006-11-30	Active, not recruiting
A Phase I Study of Temsirolimus, Topotecan, and Bortezomib in Patients With Advanced Malignancy [NCT00770731]	Phase 1	80 participants (Actual)	Interventional	2008-09-30	Completed
A Phase 1b Study to Evaluate the Safety and Tolerability of AMG 655 in Combination With Bortezomib or Vorinostat in Subjects With Relapsed or Refractory Lymphoma [NCT00791011]	Phase 1	33 participants (Actual)	Interventional	2008-02-29	Completed
Lenalidomide, Adriamycin, Dexamethasone (RAD) Versus Lenalidomide, Bortezomib, Dexamethasone (VRD) for Induction in Newly Diagnosed Multiple Myeloma Followed by Response-adapted Consolidation and Lenalidomide Maintenance - A Randomized Multicenter Phase I [NCT01685814]	Phase 3	406 participants (Anticipated)	Interventional	2012-05-31	Active, not recruiting
Preemptive Strike With Bortezomib (VELCADE) in Participants With Multiple Myeloma Still Event-free on Total Therapy 2 (UARK 98-026) [NCT00657553]	Phase 3	10 participants (Actual)	Interventional	2008-02-29	Terminated(stopped due to Due to poor accrual)
Phase I/II Trial of Combination Plerixafor (AMD3100) and Bortezomib in Relapsed or Relapsed/Refractory Multiple Myeloma [NCT00903968]	Phase 1/Phase 2	58 participants (Actual)	Interventional	2009-06-01	Completed
Phase II Trial of Velcade Plus Vorinostat in the Treatment of High Risk MDS and Relapsed/Refractory AML [NCT00818649]	Phase 2	16 participants (Actual)	Interventional	2009-01-31	Terminated(stopped due to Met protocol stop rule [i.e., extreme toxicity])
A Phase 3, Randomized, Open-label Study of Subcutaneous and Intravenous VELCADE in Combination With Dexamethasone in Chinese Subjects With Relapsed or Refractory Multiple Myeloma [NCT02811978]	Phase 3	81 participants (Actual)	Interventional	2016-09-27	Completed
A Phase II Trial of Bortezomib (Velcade) Plus Prednisone for Initial Therapy of Chronic Graft Versus Host Disease [NCT00815919]	Phase 2	22 participants (Actual)	Interventional	2008-12-31	Completed
A Phase III Study for Patients Relapsing or Progressing After Autologous Transplantation on Total Therapy 2 (TT2, UARK 98-026): Bortezomib, Thalidomide and Dexamethasone Versus Bortezomib, Melphalan, and Dexamethasone [NCT00573391]	Phase 3	5 participants (Actual)	Interventional	2006-08-31	Terminated(stopped due to low accrual)
A Multi-Centre Phase II Trial Investigating the Efficacy and Tolerability of Bortezomib Added to Cyclophosphamide, Vincristine, Prednisone, and Rituximab (BCVP-R) for Patients With Advanced Stage Follicular Non-Hodgkin's Lymphoma Requiring Systemic First- [NCT00428142]	Phase 2	95 participants (Actual)	Interventional	2007-05-01	Completed
A Phase II Study of Bortezomib and Gemcitabine in Patients With Relapsed Mantle Cell Lymphoma [NCT00377052]	Phase 2	29 participants (Actual)	Interventional	2007-01-16	Completed
A Phase II Study Of PS-341 (NSC 681239) In Patients With Untreated Or Relapsed Mantle Cell Lymphoma [NCT00030875]	Phase 2	30 participants (Actual)	Interventional	2002-11-19	Completed
Phase I Dose Escalation of Velcade (Bortezomib) Daily Dose in Patients With Advances or Metastatic Solid Tumors [NCT02220049]	Phase 1	18 participants (Actual)	Interventional	2010-12-31	Completed
Phase II Two Arm Trial of the Proteasome Inhibitor, PS-341 (Velcade TM) in Combination With Irinotecan or PS-341 Alone Followed by the Addition of Irinotecan at Time of Progression in Patients With Locally Recurrent or Metastatic Squamous Cell Carcinoma o [NCT00103259]	Phase 2	71 participants (Actual)	Interventional	2005-07-31	Completed
An Open-Label Phase I/II Study of the Safety and Efficacy of Perifosine and Bortezomib With or Without Dexamethasone for Patients With Relapsed or Refractory Multiple Myeloma Previously Treated With Bortezomib [NCT00401011]	Phase 1/Phase 2	84 participants (Actual)	Interventional	2006-08-31	Completed
A Phase 2, Multi-Center, Open-Label, Randomized Study of Mapatumumab (TRM-1 [HGS1012], a Fully Human Monoclonal Antibody to TRAIL-R1) in Combination With Bortezomib (Velcade) and Bortezomib Alone in Subjects With Relapsed or Refractory Multiple Myeloma [NCT00315757]	Phase 2	105 participants (Actual)	Interventional	2006-05-31	Completed
A Phase II Study of the Proteasome Inhibitor PS-341 (NSC 681 239) in Patients With Metastatic Breast Cancer [NCT00028639]	Phase 2	0 participants	Interventional	2001-08-31	Completed
Phase I Study of Pomalidomide, Bortezomib, and Dexamethasone (PVD) as First-Line Treatment of AL Amyloidosis or Light Chain Deposition Disease [NCT01728259]	Phase 1	18 participants (Actual)	Interventional	2013-03-31	Terminated(stopped due to FDA placed the study on a clinical hold, due to the concerns by the FDA and Health Canada, Celgene decided to permanently close the study.)
Induction Therapy With Bortezomib and Dexamethasone Followed by Autologous Stem Cell Transplantation Versus Autologous Stem Cell Transplantation Alone in the Treatment of AL Amyloidosis [NCT01998503]	Phase 3	56 participants (Actual)	Interventional	2007-12-31	Completed
Bortezomib in Treating Patients With Intrahepatic Cholangiocellular Carcinoma Featuring PTEN Deficiency [NCT03345303]	Phase 3	50 participants (Anticipated)	Interventional	2017-01-31	Recruiting
Belimumab-Based Plasma Cell Targeted Therapy to Impact Transplant Eligibility [NCT02500251]	Phase 1/Phase 2	11 participants (Actual)	Interventional	2015-06-30	Completed
A Prospective, Single-center, Phase II Study of Venetoclax/Selinexor Plus VRD Combined With CART-ASCT-CART2 Treatment in Patients With Newly Diagosed Primary Plasma Cell Leukemia [NCT05870917]	Phase 2	20 participants (Anticipated)	Interventional	2023-04-25	Recruiting
A Phase I/II, Open-label, Dose Escalation and Expansion Study to Evaluate Safety, Tolerability, and Clinical Activity of the Antibody-Drug Conjugate GSK2857916 Administered in Combination With Lenalidomide Plus Dexamethasone (Arm A), or Bortezomib Plus De [NCT03544281]	Phase 1/Phase 2	152 participants (Actual)	Interventional	2018-09-20	Active, not recruiting
A Randomized Phase I/II Study of Optimal Induction Therapy of Bortezomib, Dexamethasone and Lenalidomide With or Without Elotuzumab (NSC-764479) for Newly Diagnosed High Risk Multiple Myeloma (HRMM) [NCT01668719]	Phase 1/Phase 2	142 participants (Actual)	Interventional	2012-11-30	Active, not recruiting
A Phase I Open-Label, Dose Escalation Study to Investigate the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics, Immunogenicity and Clinical Activity of the Antibody Drug Conjugate GSK2857916 in Japanese Participants With Relapsed/Refractory Multi [NCT03828292]	Phase 1	15 participants (Actual)	Interventional	2019-03-14	Active, not recruiting
A Phase Ib Clinical Study of BBI608 for Adult Patients With Advanced, Refractory Hematologic Malignancies [NCT02352558]	Phase 1	15 participants (Actual)	Interventional	2015-05-31	Completed
A Phase1 Study at Stanford of Palbociclib in Combination With Chemotherapy in Pediatric Patients With Relapsed or Refractory Acute Lymphoblastic Leukemia (RELPALL2) [NCT04996160]	Phase 1	22 participants (Anticipated)	Interventional	2021-07-09	Recruiting
A Phase 1/2 Trial of ASP7487 OSI-906)in Combination With Bortezomib and Dexamethasone for the Treatment of Relapsed or Relapsed/Refractory Multiple Myeloma [NCT01672736]	Phase 1/Phase 2	19 participants (Actual)	Interventional	2012-09-30	Terminated(stopped due to The Sponsor decided to stop further manufacture the study drug 'Linsitinib' in Nov 2015.)
A Phase I/IIa Trial of VTD-panobinostat Treatment and Panobinostat Maintenance in Relapsed and Relapsed/Refractory Multiple Myeloma Patients [NCT02145715]	Phase 1/Phase 2	54 participants (Anticipated)	Interventional	2013-01-31	Active, not recruiting
"A Phase III Randomized Trial for Newly Diagnosed Multiple Myeloma (NDMM) Patients Considered Frail or in a Subset of Intermediate Fit Comparing Upfront Three-Drug Induction Regimens Followed by Double or Single-Agent Maintenance" [NCT05561387]	Phase 3	510 participants (Anticipated)	Interventional	2023-10-12	Recruiting
A Phase III Randomized Trial for Patients With De Novo AML Using Bortezomib and Sorafenib (NSC# 681239, NSC# 724772) for Patients With High Allelic Ratio FLT3/ITD [NCT01371981]	Phase 3	1,645 participants (Actual)	Interventional	2011-06-20	Active, not recruiting
A Phase 1, Randomized, Dose and Schedule Evaluation Study to Investigate the Safety, Pharmacokinetics, Pharmacodynamics and Clinical Activity of Belantamab Mafodotin Administered in Combination With Standard of Care in Participants With Newly Diagnosed Mu [NCT04091126]	Phase 1	144 participants (Anticipated)	Interventional	2019-12-18	Recruiting
Nelfinavir as Bortezomib-sensitizing Drug in Patients With Proteasome Inhibitor-nonresponsive Myeloma. A Multicenter Phase II Trial [NCT02188537]	Phase 2	34 participants (Actual)	Interventional	2014-12-02	Completed
A Phase I Study of Dasatinib With Bortezomib (Velcade®) and Dexamethasone in Subjects With Relapsed or Refractory Multiple Myeloma [NCT00560352]	Phase 1	16 participants (Actual)	Interventional	2008-02-29	Terminated
A Protocol to Assess the Safety, Efficacy, and Pharmacokinetics of Continuous Subcutaneous Administration of Low-dose Lenalidomide (STAR-LLD) for the Treatment of Multiple Myeloma (MM) [NCT06087653]	Phase 1/Phase 2	6 participants (Anticipated)	Interventional	2023-10-02	Recruiting
A Phase II Study of CyBorD (Cyclophosphamide, Bortezomib, Dexamethasone) Plus Daratumumab for Patients With Monoclonal Gammopathy of Renal Significance (MGRS) [NCT06083922]	Phase 2	53 participants (Anticipated)	Interventional	2023-10-16	Recruiting
A Multicenter Phase II Trial of Bortezomib (Velcade), Melphalan, and Dexamethasone (V-MD) in Patients With Symptomatic AL-Amyloidosis or Light Chain Deposition Disease [NCT00520767]	Phase 2	35 participants (Actual)	Interventional	2007-09-30	Completed
A Multicenter, Open Label, Randomized Phase II Study Comparing Daratumumab Combined With Bortezomib-Cyclophosphamide-dexamethasone (Dara-VCd) Versus the Association of Bortezomib-Thalidomide-dexamethasone (VTd) as Pre Transplant Induction and Post Transpl [NCT03896737]	Phase 2	401 participants (Actual)	Interventional	2019-04-16	Active, not recruiting
Phase 1/2 Open-label Study Of The Safety And Efficacy Of Pd 0332991 In Combination With Bortezomib And Dexamethasone In Patients With Refractory Multiple Myeloma [NCT00555906]	Phase 2	53 participants (Actual)	Interventional	2008-01-31	Completed
A Phase 1b/2 Study of Standard Doses of Bortezomib and Pembrolizumab ± Reovirus (Pelareorep) Combination Therapy in Patients With Relapsed Multiple Myeloma (AMBUSH Study) [NCT05514990]	Phase 1/Phase 2	42 participants (Anticipated)	Interventional	2022-10-07	Recruiting
A Phase 2 Multi-Arm Study of Magrolimab Combinations in Patients With Relapsed/Refractory Multiple Myeloma [NCT04892446]	Phase 2	153 participants (Anticipated)	Interventional	2021-11-09	Active, not recruiting
B- PRISM (Precision Intervention Smoldering Myeloma): A Phase II Trial of Combination of Daratumumab, Bortezomib, Lenalidomide and Dexamethasone in High- Risk Smoldering Multiple Myeloma [NCT04775550]	Phase 2	60 participants (Anticipated)	Interventional	2021-03-08	Recruiting
A National, Multicentric, Open-label Study of Induction Treatment With VELCADE and Dexamethasone for Previously Untreated Patients With Multiple Myeloma and Renal Failure [NCT01084837]	Phase 2	60 participants (Actual)	Interventional	2010-03-31	Completed
A Randomized Study of 4 vs. 8 Cycles of Velcade-based Regimen With Autologous Stem Cell Transplantation in Newly-diagnosed Myeloma Patients [NCT00984828]	Phase 2/Phase 3	23 participants (Actual)	Interventional	2009-08-31	Terminated(stopped due to Very slow recruitment)
Phase 2, Multi-Center, Single-Arm, Open-Label Study to Evaluate the Efficacy and Safety of the Combination Regimen Isatuximab, Lenalidomide, Bortezomib, and Dexamethasone in Patients With Newly Diagnosed Multiple Myeloma [NCT04653246]	Phase 2	43 participants (Anticipated)	Interventional	2021-07-13	Recruiting
A Phase I Trial Evaluating the Safety and Efficacy of Vorinostat (Zolinza ®) + RVD (Lenalidomide {Revlimid ®} + Bortezomib {Velcade ®} + Dexamethasone) for Patients With Newly Diagnosed Multiple Myeloma [NCT01038388]	Phase 1	30 participants (Actual)	Interventional	2010-01-15	Completed
Phase II Trial of VELCADE® (Bortezomib) for Steroid Refractory Acute GVHD [NCT00408928]	Phase 2	11 participants (Actual)	Interventional	2005-11-30	Completed
Phase II Study to Assess the Safety, Efficacy, and Tolerability of Combination Therapy With Velcade (Bortezomib), Doxorubicin, and Dexamethasone (PAD) as Therapy for Patients With Relapsed or Refractory Multiple Myeloma [NCT00814541]	Phase 2	53 participants (Actual)	Interventional	2005-12-31	Completed
A Phase II Study of Bortezomib (Velcade, PS-341) in Combination With Ifosfamide/Vinorelbine in Pediatric Patients and Young Adults With Refractory/Recurrent Hodgkin Disease [NCT00381940]	Phase 2	26 participants (Actual)	Interventional	2007-01-31	Completed
Phase I/II Study of the Combination of Bortezomib With Arsenic Trioxide, Ascorbic Acid and High-Dose Melphalan for Patients With Multiple Myeloma [NCT00469209]	Phase 1/Phase 2	60 participants (Actual)	Interventional	2006-06-30	Completed
A Phase I Study of Vorinostat and Bortezomib in Children With Refractory or Recurrent Solid Tumors, Including CNS Tumors and Lymphomas [NCT00994500]	Phase 1	20 participants (Actual)	Interventional	2009-08-31	Completed
Active Immunization of Sibling Stem Cell Transplant Donors Against Purified Myeloma Protein of the Stem Cell Recipient With Multiple Myeloma in the Setting of Non-Myeloablative, HLA-Matched Allogeneic Peripheral Blood Stem Cell Transplantation [NCT00006184]	Phase 2	20 participants (Actual)	Interventional	2001-02-08	Completed
Phase II Study of PS-341 in Low Grade Lymphoproliferative Disorders [NCT00023764]	Phase 2	103 participants (Actual)	Interventional	2001-06-30	Completed
A Phase II Study of the Efficacy and Safety of Bortezomib Plus GDP in the Treatment of Refractory and Relapsed Non-GCB Diffuse Large B-cell Lymphoma [NCT02542111]	Phase 2	30 participants (Anticipated)	Interventional	2015-05-31	Recruiting
A Phase I Dose-Escalation Study of Erlotinib in Combination With Bortezomib in Subjects With Advanced Cancer. Companion Study to Umbrella Protocol 2007-0638. [NCT00895687]	Phase 1	24 participants (Actual)	Interventional	2009-04-30	Completed
An Open-label Phase 2 Study of Intravenous Bortezomib and Oral Panobinostat (LBH589) in Adult Patients With Relapsed/Refractory Peripheral T-cell Lymphoma or NK/T-cell Lymphoma After Failure of Conventional Chemotherapy [NCT00901147]	Phase 2	25 participants (Actual)	Interventional	2009-11-30	Completed
Phase II Trial of High-dose Melphalan and Bortezomib and Stem Cell Transplantation in Patients With AL Amyloidosis [NCT00790647]	Phase 2	10 participants (Actual)	Interventional	2008-06-30	Completed
A Phase 2 Evaluation of Daratumumab-Based Treatment in Newly Diagnosed Multiple Myeloma Patients With Renal Insufficiency [NCT04352205]	Phase 2	25 participants (Anticipated)	Interventional	2020-05-07	Recruiting
A Phase 2 Study of Subcutaneous Daratumumab in Combination With Dose-Attenuated Bortezomib, Lenalidomide, and Dexamethasone in Elderly Newly Diagnosed Multiple Myeloma Patients [NCT04052880]	Phase 2	38 participants (Anticipated)	Interventional	2019-10-24	Recruiting
Phase I/II Bortezomib, Melphalan and Low Dose TBI Conditioning for Patients Undergoing Autologous Stem Cell Transplantation for Multiple Myeloma [NCT01936090]	Phase 1	11 participants (Actual)	Interventional	2013-08-31	Completed
A Phase 3, Multicenter, Randomized, Double Blind Study of Bortezomib and Dexamethasone in Combination With Either Venetoclax or Placebo in Subjects With Relapsed or Refractory Multiple Myeloma Who Are Sensitive or Naïve to Proteasome Inhibitors [NCT02755597]	Phase 3	291 participants (Actual)	Interventional	2016-07-11	Completed
Tandem Autologous Hematopoietic Stem Cell Transplant With Melphalan Followed by Melphalan and Bortezomib in Patients With Multiple Myeloma [NCT01241708]	Phase 3	146 participants (Actual)	Interventional	2010-04-08	Completed
A Randomized Phase III Study to Compare Bortezomib, Melphalan, Prednisone (VMP) With High Dose Melphalan Followed by Bortezomib, Lenalidomide, Dexamethasone (VRD) Consolidation and Lenalidomide Maintenance in Patients With Newly Diagnosed Multiple Myeloma [NCT01208766]	Phase 3	1,503 participants (Actual)	Interventional	2011-01-31	Active, not recruiting
A Phase II Study of Bortezomib (Velcade ) Administered as a Single Agent in Metastatic Non-Clear Cell Renal Cell Carcinoma (RCC) Patients [NCT00276614]	Phase 2	4 participants (Actual)	Interventional	2006-04-30	Completed
Clinical, Multicenter, Single-arm, Treatment With a Scheme With Low Doses of Bortezomib / Melphalan / Prednisone (MPV) in Patients With Multiple Myeloma (MM) Newly Diagnosed Symptomatic ≥75 Years [NCT02773550]	Phase 4	24 participants (Actual)	Interventional	2014-01-31	Terminated(stopped due to Low recruiment.)
Daratumumab Combined With Bortezomib, Cyclophosphamide and Dexamethasone for the Treatment of Multiple Myeloma Patients Presenting With Extramedullary Disease. The ANTARES Study [NCT04166565]	Phase 2	41 participants (Actual)	Interventional	2019-10-31	Active, not recruiting
Phase I Study of Paclitaxel (Taxol) and Bortezomib (Velcade) in Patients With Refractory Solid Tumor Malignancies Involving an Activated MAPK Pathway [NCT00667641]	Phase 1	16 participants (Actual)	Interventional	2007-03-31	Completed
An Open-Label Phase 1/2a Study of the Safety and Efficacy of Melflufen and Dexamethasone in Combination With Either Bortezomib or Daratumumab in Patients With Relapsed or Relapsed-Refractory Multiple Myeloma [NCT03481556]	Phase 1/Phase 2	56 participants (Actual)	Interventional	2018-04-12	Terminated(stopped due to The sponsor decided to terminate the study following an FDA request of a partial clinical hold.)
Selinexor With Alternating Bortezomib or Lenalidomide Plus Dexamethasone in Transplant Ineligible Newly Diagnosed Multiple Myeloma Patients (SABLe): An Investigator Sponsored Trial [NCT04717700]	Phase 2	50 participants (Anticipated)	Interventional	2021-08-18	Recruiting
Phase I Study of Bortezomib (Velcade) and Cetuximab (Erbitux) for Patients With Solid Tumors Expressing EGFR [NCT00622674]	Phase 1	37 participants (Actual)	Interventional	2005-11-30	Completed
A Phase I Trial of the MUC1 Inhibitor, GO-203-2c, in Combination With Bortezomib in Patients With Relapsed or Refractory Multiple Myeloma [NCT02658396]	Phase 1	0 participants (Actual)	Interventional		Withdrawn(stopped due to Study was never open due to lack of funding)
A Dose Escalation, Safety, Pharmacokinetic, Pharmacodynamic and Preliminary Efficacy Study of SAR650984 (Isatuximab) Administered Intravenously in Combination With Bortezomib - Based Regimens in Adult Patients With Newly Diagnosed Multiple Myeloma Non Eli [NCT02513186]	Phase 1	90 participants (Actual)	Interventional	2015-09-30	Active, not recruiting
A Phase One Study of Intravenous Irinotecan and Bortezomib in Children With Recurrent/Refractory High-Risk Neuroblastoma [NCT00644696]	Phase 1	18 participants (Actual)	Interventional	2008-04-30	Completed
A Phase II Pilot Trial of Bortezomib (PS-341, Velcade) in Combination With Intensive Re-Induction Therapy for Children With Relapsed Acute Lymphoblastic Leukemia (ALL) and Lymphoblastic Lymphoma (LL) [NCT00873093]	Phase 2	148 participants (Actual)	Interventional	2009-03-31	Completed
Phase II Study of VcR-CVAD With Rituximab Consolidation and Maintenance for Untreated Mantle Cell Lymphoma [NCT00581776]	Phase 2	30 participants (Actual)	Interventional	2005-05-31	Completed
A Phase 1 Trial of the Combination of Everolimus (RAD001) and Bortezomib (VELCADE) for Relapsed or Refractory Lymphoma [NCT00671112]	Phase 1	30 participants (Actual)	Interventional	2008-06-30	Terminated(stopped due to Treatment ineffective)
IGEV +/- Bortezomib (Velcade) as Induction Before High Dose Consolidation in Relapsed/Refractory Hodgkin's Lymphoma After First Line Treatment: a Randomized Phase II Trial. On Behalf of Intergruppo Italiano Linfomi [NCT00636311]	Phase 2	13 participants (Actual)	Interventional	2008-02-29	Completed
Phase II Study of Combination Bortezomib (Velcade PS-341) and Rituximab in Patients With Previously Untreated and Relapsed/Refractory Waldenstrom's Macroglobulinemia [NCT00422799]	Phase 2	63 participants (Actual)	Interventional	2006-08-30	Completed
Phase II Study of VDT (VELCADE, Doxil® and Thalidomide) as Frontline Therapy for Patients With Previously Untreated Multiple Myeloma (MM) [NCT00523848]	Phase 2	46 participants (Actual)	Interventional	2006-06-30	Completed
Study of Daratumumab in Combination With Bortezomib (VELCADE), Thalidomide, and Dexamethasone (VTD) in the First Line Treatment of Transplant Eligible Subjects With Newly Diagnosed Multiple Myeloma [NCT02541383]	Phase 3	1,085 participants (Actual)	Interventional	2015-09-30	Active, not recruiting
A Phase 3, Multicenter, Randomized, Open Label Study of ABBV-383 Compared With Standard Available Therapies in Subjects With Relapsed or Refractory Multiple Myeloma (3L+ RRMM Monotherapy Study) [NCT06158841]	Phase 3	380 participants (Anticipated)	Interventional	2024-04-26	Not yet recruiting
Phase II Trial of PS341 (NSC 681239) in Patients With Advanced Renal Cell Carcinoma [NCT00017329]	Phase 2	0 participants	Interventional	2001-04-30	Completed
A Multicenter, Randomized, Open-label Phase 2 Study Evaluating the Safety and Efficacy of Three Different Regimens of Oral Panobinostat in Combination With Subcutaneous Bortezomib and Oral Dexamethasone in Patients With Relapsed or Relapsed/Refractory Mul [NCT02654990]	Phase 2	249 participants (Actual)	Interventional	2016-04-27	Completed
A Phase II Study of Modified VR-CAP and Acalabrutinib as First Line Therapy for Transplant-Eligible Patients With Mantle Cell Lymphoma [NCT04626791]	Phase 2	45 participants (Anticipated)	Interventional	2021-08-03	Recruiting
A Multicentre, Non-Blinded Study Exploring Self-Administration of Chemotherapy in the Home Environment [NCT04268199]	Phase 2	100 participants (Anticipated)	Interventional	2020-05-29	Recruiting
A Phase II Trial of Cyclophosphamide, Bortezomib and Dexamethasone (CYBOR-D) in Patients With Newly Diagnosed Active Multiple Myeloma [NCT00609167]	Phase 2	63 participants (Actual)	Interventional	2006-12-31	Completed
(Inhibition of NF-kB Signaling in Melanoma Therapy) A Phase I/II Clinical Trial of PS-341, a Proteasome Inhibitor, in Combination With an Extended Continuous Oral Schedule of Temozolomide in Patients With Advanced Refractory Solid Tumors With the Phase II [NCT00512798]	Phase 1/Phase 2	47 participants (Actual)	Interventional	2003-06-30	Terminated(stopped due to This study was terminated due to lack of efficacy)
Randomized Phase III Trial of Consolidation Therapy With Bortezomib (Velcade®)-Lenalidomide (Revlimid®) -Dexamethasone (VRD) Versus Bortezomib (Velcade®)-Dexamethasone (VD) for Patients With Multiple Myeloma Who Have Completed a Dexamethasone Based Induct [NCT00522392]	Phase 3	48 participants (Actual)	Interventional	2007-09-30	Terminated(stopped due to Slow accrual)
Single-Arm, Dose-Finding Pilot Trial of Single-Agent Bortezomib in Patients With Relapsed/Refractory AIDS-Associated Kaposi Sarcoma With Correlative Assessments of KSHV and HIV [NCT01016730]	Phase 1	24 participants (Actual)	Interventional	2010-01-22	Completed
Randomized Phase 3b Study of Three Treatment Regimens in Subjects With Previously Untreated Multiple Myeloma Who Are Not Considered Candidates for High-Dose Chemotherapy and Autologous Stem Cell Transplantation: VELCADE, Thalidomide, and Dexamethasone Ver [NCT00507416]	Phase 3	502 participants (Actual)	Interventional	2007-06-30	Completed
Sirolimus, Mycophenolate Mofetil and Bortezomib as Graft-Versus-Host Disease Prophylaxis After Non-Myeloablative Allogeneic Peripheral Blood Stem Cell Transplantation [NCT00548717]	Phase 2	15 participants (Actual)	Interventional	2007-10-31	Terminated(stopped due to First two patients enrolled after trial reopened, developed grade III-IV acute GVHD and subsequently passed away.)
A Phase 2, Multicentre, Randomised, Open-Label, Parallel Group Study to Evaluate the Safety and Efficacy of Velcade When Added to Adriamycin-Dexamethasone Treatment Versus Vincristine-Adriamycin-Dexamethasone Standard Treatment in Subjects With Multiple M [NCT00441168]	Phase 2	30 participants (Actual)	Interventional	2006-12-31	Terminated(stopped due to TRIAL STOPPED due to a change in standard of care and the required patient numbers could no longer be achieved)
An Observational, Prospective Analysis of Retreatment With Bortezomib for Multiple Myeloma [NCT01030302]		56 participants (Actual)	Observational	2008-11-30	Completed
A Phase I Expanded Cohort Trial of Bortezomib and Sorafenib in Advanced Malignant Melanoma [NCT01078961]	Phase 1	11 participants (Actual)	Interventional	2010-09-30	Completed
A Phase 3, Double-Blind, Multicenter Study to Evaluate the Efficacy and Safety of CAEL-101 and Plasma Cell Dyscrasia Treatment Versus Placebo and Plasma Cell Dyscrasia Treatment in Plasma Cell Dyscrasia Treatment Naïve Patients With Mayo Stage IIIa AL Amy [NCT04512235]	Phase 3	267 participants (Actual)	Interventional	2020-11-12	Active, not recruiting
Phase II Study of Combination Bortezomib, Dexamethasone, and Rituximab in Previously Untreated Patients With Waldenstroms Macroglobulinemia: A Multicenter Trial of the European Myeloma Network [NCT00832234]	Phase 2	59 participants (Actual)	Interventional	2006-09-30	Completed
An International, Multicenter, Open-Label Study of Vorinostat (MK0683) in Combination With Bortezomib in Patients With Relapsed or Refractory Multiple Myeloma [NCT00773838]	Phase 2	143 participants (Actual)	Interventional	2008-12-01	Completed
Pilot Study of RCVELP as First Line Therapy for Follicular Lymphoma (FL) and Marginal Zone Lymphoma (MZL) [NCT00772668]		3 participants (Actual)	Interventional	2009-09-25	Terminated(stopped due to Funding)
A Multicenter, Open-Label, Phase I Study of MK-0683 in Combination With Bortezomib in Patients With Relapsed and/or Refractory Multiple Myeloma [NCT00858234]	Phase 1	9 participants (Actual)	Interventional	2009-02-13	Completed
A Randomized, Open-Label, Multicenter Phase 2 Study of VELCADE With Fludarabine in Comparison to Rituximab With Fludarabine in Follicular Lymphoma Patients Previously Treated With Rituximab [NCT00850499]	Phase 2	12 participants (Actual)	Interventional	2009-09-30	Terminated
Phase II Study of Bortezomib (VELCADE) With Cisplatin as First Line Treatment of Malignant Mesothelioma [NCT00458913]	Phase 2	82 participants (Actual)	Interventional	2007-02-28	Completed
Velcade®-Melphalan Association as Conditioning Regimen Before Autologous Stem-cell Transplantation in Multiple Myeloma Patients Under 65 Years [NCT00642395]	Phase 2	61 participants (Actual)	Interventional	2007-07-31	Completed
A Phase II Trial of Romidepsin and Bortezomib for Multiple Myeloma Patients With Relapsed or Refractory Disease [NCT00765102]	Phase 2	32 participants (Actual)	Interventional	2008-09-01	Terminated(stopped due to There was a change in the Sponsor's research strategy; safety concerns were not a factor.)
A Phase I/II Study of JNJ-26866138 (Bortezomib) in Japanese Patients With Relapsed or Refractory Multiple Myeloma [NCT00752518]	Phase 1/Phase 2	35 participants (Actual)	Interventional	2004-05-31	Completed
A Phase III Randomized, Controlled, Multicenter, Open-label Study of ATG-010, Bortezomib, and Dexamethasone (SVd) Versus Bortezomib and Dexamethasone (Vd) in Patients With Relapsed or Refractory Multiple Myeloma (RRMM) [NCT04939142]	Phase 3	150 participants (Anticipated)	Interventional	2021-07-12	Active, not recruiting
An Open-Label Phase IV Study of the Efficacy of Bortezomib-based Combination Therapy the Treatment of Subjects With Multiple Myeloma [NCT02559154]	Phase 4	80 participants (Actual)	Interventional	2010-07-31	Active, not recruiting
A Phase I/II Trial of Obatoclax Mesylate (GX15-070MS) in Combination With Bortezomib for the Treatment of Relapsed Multiple Myeloma [NCT00719901]	Phase 1/Phase 2	11 participants (Actual)	Interventional	2008-07-31	Terminated(stopped due to This trial was terminated due to slow accrual and the drug supply of Obatoclax during the phase I; therefore, the phase II portion will never open.)
A Phase II Trial of Combined Weekly Bortezomib and Tositumomab I-131 in Patients With Relapsed or Refractory Follicular Non-Hodg [NCT00479167]	Phase 2	1 participants (Actual)	Interventional	2007-05-31	Terminated(stopped due to Lack of accrual and interest in study)
A Phase II Study of VDR (VELCADE™, DOXIL® and RITUXAN™) in Relapsed/Refractory Diffuse Large B-cell Lymphoma [NCT00851552]	Phase 2	9 participants (Actual)	Interventional	2009-01-31	Terminated(stopped due to Lack of sponsor support)
A Phase 2, Multicentre, Randomised, Open-Label, Parallel Group Study to Evaluate the Effect of VELCADE on Myeloma Related Bone Disease [NCT01286077]	Phase 2	106 participants (Actual)	Interventional	2009-09-30	Completed
Randomized Phase III Study on Bortezomib and Low-Dose Dexamethasone With or Without Continuous Low-Dose Oral Cyclophosphamide for Primary Refractory or Relapsed Multiple Myeloma [NCT00813150]	Phase 3	96 participants (Actual)	Interventional	2009-01-31	Completed
A Phase 2 Study to Investigate Efficacy and Safety Evaluation of Bortezomib in Patients With Relapsed/Refractory Immune Thrombocytopenia [NCT05599880]	Phase 2	29 participants (Anticipated)	Interventional	2023-07-07	Recruiting
First-line Treatment of Mantle Cell Lymphoma of Old Patients . Evaluate the Efficacy, Toxicity, and Molecular Prognostic Factors of Velcade®) in Association With Chemotherapy and Immunotherapy With Rituximab [NCT00740415]	Phase 2	39 participants (Actual)	Interventional	2007-06-30	Completed
A Phase 1b/2 Trial to Evaluate the Safety and Efficacy of Radium-223 Dichloride (BAY88-8223) in Combination With Bortezomib and Dexamethasone in Early Relapsed Multiple Myeloma [NCT02605356]	Phase 1/Phase 2	0 participants (Actual)	Interventional	2016-10-31	Withdrawn(stopped due to Study restarted under new study number 18987)
Phase I/II Study of Liposomal Doxorubicin (Doxil®)/ Melphalan/Bortezomib (Velcade®) in Relapsed/Refractory Multiple Myeloma [NCT00334932]	Phase 1/Phase 2	32 participants (Anticipated)	Interventional	2006-02-28	Recruiting
Safety and Efficacy of Velcade in Relapsed and/or Refractory Multiple Myeloma Patients With Impaired Renal Function [NCT00718640]	Phase 2	10 participants (Actual)	Interventional	2007-10-31	Terminated(stopped due to Study stopped due to lagging enrolment.)
A Two-Arm, Non-Randomized, Multicenter, Phase 2 Study of VELCADE (Bortezomib) in Combination With Rituximab, Cyclophosphamide, and Prednisone With or Without Doxorubicin Followed by Rituximab Maintenance in Patients With Relapsed Follicular Lymphoma. [NCT00715208]	Phase 2	55 participants (Actual)	Interventional	2008-09-30	Completed
An International, Multicenter, Randomized, Double-Blind Study of Vorinostat (MK-0683) or Placebo in Combination With Bortezomib in Patients With Multiple Myeloma [NCT00773747]	Phase 3	637 participants (Actual)	Interventional	2008-12-01	Completed
A Phase II Study of VcR-CVAD With Rituximab Maintenance for Untreated Mantle Cell Lymphoma [NCT00433537]	Phase 2	77 participants (Actual)	Interventional	2007-05-31	Completed
An Open-Label, Randomized, Phase 2 Study to Assess the Effectiveness of RCHOP With or Without VELCADE in Previously Untreated Non-Germinal Center B-Cell-like Diffuse Large B-Cell Lymphoma Patients [NCT00931918]	Phase 2	206 participants (Actual)	Interventional	2009-10-31	Completed
An Open Label, Phase 2 Study of Biweekly VELCADE and Intermittent CAELYX in Patients With Ovarian Cancer Failing Platinum Containing Regimens [NCT00610792]	Phase 2	91 participants (Anticipated)	Interventional	2006-07-31	Withdrawn(stopped due to Study never submitted to IND. Study is being sponsored by Johnson and Johnson in the EU only.)
H-11047: A Study of PS-341 Followed by Radical Prostatectomy for Patients With Adenocarcinoma of the Prostate (Spore #: 11-01-30-13) [NCT00425503]	Phase 2	40 participants (Actual)	Interventional	2001-12-31	Completed
Early Patient Access Single Named Patient Program for the Use of Ulocuplumab for the Treatment of Multiple Myeloma [NCT02666209]		0 participants	Expanded Access		No longer available
Phase II Trial of Doxorubicin and Bortezomib in Patients With Incurable Head and Neck Adenoid Cystic Carcinoma [NCT00581360]	Phase 2	10 participants (Actual)	Interventional	2007-11-30	Completed
A Phase I/II National, Open-label, Multicenter Study of Bortezomib (Velcade) in Combination With FLAG-IDA (VFLAG- IDA) in Patients With Relapsed or Refractory Acute Myeloid Leukemia (AML). [NCT00651781]	Phase 1/Phase 2	40 participants (Actual)	Interventional	2008-04-30	Completed
Phase I/II Study of Bortezomib (PS-341) in Combination With Carboplatin and Docetaxel for Patients With Advanced Non-Small Cell Lung Cancer [NCT00714246]	Phase 1	6 participants (Actual)	Interventional	2008-10-31	Terminated(stopped due to Low accrual)
A Randomized Phase II Trial of Ofatumumab and Bendamustine vs. Ofatumumab, Bortezomib (NSC # 681239) and Bendamustine in Patients With Untreated Follicular Lymphoma [NCT01286272]	Phase 2	135 participants (Actual)	Interventional	2011-04-08	Active, not recruiting
A Randomized Phase II Study of Fulvestrant vs. Fulvestrant in Combination With Bortezomib in Women With ER Positive Metastatic Breast Cancer [NCT01142401]	Phase 2	118 participants (Actual)	Interventional	2010-05-26	Completed
Targeted Oncolytic Virotherapy and Natural History Study of KSHV-Associated Multicentric Castleman's Disease With Laboratory and Clinical Correlates of Disease Activity [NCT00092222]	Phase 2	75 participants (Actual)	Interventional	2004-10-28	Active, not recruiting
A Randomized Phase 2 Study of SCH 727965 in Subjects With Relapsed or Refractory Mantle Cell Lymphoma (MCL) or B-Cell Chronic Lymphocytic Leukemia (B-CLL) [NCT00871546]	Phase 2	8 participants (Actual)	Interventional	2009-03-31	Terminated
Thalidomide Versus Bortezomib in Melphalan Refractory Myeloma [NCT00602511]	Phase 3	300 participants (Anticipated)	Interventional	2007-10-31	Completed
A Prospective Study of Bortezomib Combined With CHEP Regimen in the Treatment of Primary Peripheral T Cell Lymphoma [NCT04061772]	Phase 2	54 participants (Anticipated)	Interventional	2019-08-12	Recruiting
An International, Multi-Center, Randomized, Open-Label Study of PS-341 (VELCADE™) Versus High-Dose Dexamethasone in Patients With Relapsed or Refractory Multiple Myeloma [NCT00048230]	Phase 3	620 participants (Actual)	Interventional	2002-06-30	Completed
Phase I/II Study of Combination Everolimus (RAD001), and Rituximab (Rituxan), OR Everolimus, Bortezomib (Velcade, PS-341), and Rituximab in Patients With Relapsed and/or Relapsed/Refractory Waldenstrom's Macroglobulinemia [NCT01125293]	Phase 1/Phase 2	46 participants (Actual)	Interventional	2010-04-30	Terminated(stopped due to Per protocol, Phase II is to be terminated early if a less than 5% of the Phase II participants observe a Very Good Partial Response or Better in the first 23 participants enrolled to Phase II.)
A Phase 1 Dose Escalation Study of Bortezomib (Velcade®), Pegylated Liposomal Doxorubicin (Doxil®), and Vorinostat (Suberoylanilide Hydromaxic Acid, Saha, Zolinzatm) in Patients With Relapse/Refractory Multiple Myeloma [NCT00744354]	Phase 1	32 participants (Actual)	Interventional	2008-10-31	Terminated(stopped due to Drugs unavailable- study terminated 1/2/18)
A Phase II Study of Pegylated Liposomal Doxorubicin, Bortezomib and Dexamethasone (DVD) for Patients With Newly Diagnosed Multiple Myeloma (MM) [NCT00742404]	Phase 2	35 participants (Anticipated)	Interventional	2008-07-31	Active, not recruiting
Pilot Study of Bortezomib, Bendamustine and Rituximab for Patients With Relapsed or Refractory, Indolent or Mantle Cell Non-Hodgkin's Lymphoma [NCT00547534]	Phase 2	31 participants (Actual)	Interventional	2007-10-31	Completed
Progression Free Survival (PFS) Comparison Between Suberoylanilide Hydroxamic Acid (SAHA, Vorinostat TM) in Combination With Bortezomib (Velcade TM) and SAHA Alone in Refractory or Recurrent Advanced CTCL. A Randomized Study. [NCT01386398]	Phase 3	0 participants (Actual)	Interventional		Withdrawn(stopped due to Company withdrew interest)
A Phase 3, Open-Label Study of Elranatamab Monotherapy Versus Elotuzumab, Pomalidomide, Dexamethasone (EPd) Or Pomalidomide, Bortezomib, Dexamethasone (PVd) Or Carfilzomib, Dexamethasone (Kd) In Participants With Relapsed/Refractory Multiple Myeloma Who R [NCT06152575]	Phase 3	492 participants (Anticipated)	Interventional	2023-12-18	Not yet recruiting
Safety of Vorinostat in Combination With Bortezomib, Doxorubicin and Dexamethasone (VBDD) in Patients With Refractory or Relapsed Multiple Myeloma, A Phase I/II Study, Short Title: VBDD [NCT01394354]	Phase 1/Phase 2	34 participants (Actual)	Interventional	2011-08-31	Completed
Phase I Study of Bortezomib and Romidepsin in Patients With Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma, Indolent B-Cell Lymphoma, Peripheral T-Cell Lymphoma or Cutaneous T-Cell Lymphoma [NCT00963274]	Phase 1	18 participants (Actual)	Interventional	2010-04-26	Completed
Phase I/II Trial of High-Dose Post-Transplant Cyclophosphamide, Bortezomib, and Sitagliptin for the Prevention of Graft-versus-Host Disease Following Allogeneic Hematopoietic Stem Cell Transplantation [NCT05895201]	Phase 1/Phase 2	72 participants (Anticipated)	Interventional	2023-09-30	Not yet recruiting
A Prospective, Open-Label, Pilot Study of Clonal Deletion on Living-Relative Donor Kidney Transplantation [NCT01408797]	Phase 1/Phase 2	15 participants (Anticipated)	Interventional	2011-03-31	Recruiting
Phase 1/2 Study of VELCADE® (Bortezomib), Dexamethasone, and Revlimid® (Lenalidomide) Versus VELCADE, Dexamethasone, Cyclophosphamide, and Revlimid Versus VELCADE, Dexamethasone and Cyclophosphamide in Subjects With Previously Untreated Multiple Myeloma [NCT00507442]	Phase 1/Phase 2	158 participants (Actual)	Interventional	2007-08-31	Completed
A Phase II Study of Bendamustine, Velcade and Dexamethasone (BVD) in the Treatment of Elderly Patients (>= 65 Years) With Multiple Myeloma in 1st Relapse or Refractory to 1st Line Therapy [NCT01045681]	Phase 2	75 participants (Actual)	Interventional	2010-03-03	Completed
An Open-Label Study to Assess the Effect of CYP3A4 Induction on the Pharmacokinetics of VELCADE (Bortezomib) [NCT00608907]	Phase 1	61 participants (Actual)	Interventional	2007-09-30	Completed
A Phase I Protocol of the Combination Bortezomib and Tipifarnib for Relapsed or Refractory Multiple Myeloma [NCT00972712]	Phase 1	12 participants (Actual)	Interventional	2006-12-31	Completed
A Phase Ib Multiple Ascending Dose Study of BMS-833923 Alone or in Combination With Lenalidomide (Revlimid) Plus Dexamethasone or in Combination With Bortezomib (Velcade) in Subjects With Relapsed or Refractory Multiple Myeloma [NCT00884546]	Phase 1	27 participants (Actual)	Interventional	2009-07-31	Completed
Phase 1 Study of Radiosensitization Using Bortezomib in Relapsed Non-Hodgkin's Lymphoma Patients Receiving Radioimmunotherapy [NCT00777114]	Phase 1	31 participants (Actual)	Interventional	2007-04-01	Completed
A Phase II Pilot Study of Bortezomib (PS-341, Velcade) Combined With Reinduction Chemotherapy in Children and Young Adults With Recurrent, Refractory or Secondary Acute Myeloid Leukemia [NCT00666588]	Phase 2	52 participants (Actual)	Interventional	2008-04-30	Completed
A Phase IIA Trial Testing the Efficacy of Bortezomib (Velcade(R)) in Patients With Advanced Waldenström Macroglobulinemia [NCT00777738]	Phase 2	34 participants (Actual)	Interventional	2008-10-31	Completed
Efficacy and Safety of Bone Marrow-derived Mesenchymal Stem Cells (BM-MSCs) on Chronic Antibody-mediated Rejection (cAMR) After Kidney Transplantation: A Multi-center Perspective Study [NCT02563340]	Phase 1/Phase 2	60 participants (Anticipated)	Interventional	2015-11-30	Not yet recruiting
A Phase II, Open-Label, Clinical Study to Assess the Safety and Activity of SRT501 Alone or in Combination With Bortezomib in Patients With Multiple Myeloma [NCT00920556]	Phase 2	24 participants (Actual)	Interventional	2009-03-30	Terminated(stopped due to Study terminated.24 subjects enrolled;provided adequate data for decision making.)
Clinical Study on Induction of Remission Using Bortezomib (Vel), Cyclophosphamide (C), and Dexamethasone (D) in Patients Until 60 Years of Age With Untreated Multiple Myeloma and Planned for a High Dose Chemotherapy: (VelCD; Deutsche Studiengruppe Multipl [NCT00833560]	Phase 2	401 participants (Actual)	Interventional	2006-03-31	Completed
Efficacy and Safety of Velcade Plus Dexamethasone (VD), VD+Cyclophosphamide or VD Plus Lenalidomide in MMY Patients Who Are Refractory or Have Relapsed After Their Primary Therapy for MMY and Have Achieved Stable Disease After 4 Cycles of VD [NCT00908232]	Phase 2	163 participants (Actual)	Interventional	2008-05-31	Completed
REal Life, Retrospective Study of BOrtezomib Use as secoND Treatment for Myeloma Patients Previously Exposed to Bortezomib-based Therapies as First Line [NCT02797041]		100 participants (Anticipated)	Observational	2015-08-31	Active, not recruiting
Bortezomib and Vorinostat as Maintenance Therapy After Autologous Stem Cell Transplant for Multiple Myeloma [NCT00839956]	Phase 2	31 participants (Actual)	Interventional	2009-02-28	Completed
A Multicenter, Randomized, Double Blind, Placebo Controlled Phase III Study of Panobinostat in Combination With Bortezomib and Dexamethasone in Patients With Relapsed Multiple Myeloma [NCT01023308]	Phase 3	767 participants (Actual)	Interventional	2009-12-21	Completed
Bortezomib, Cyclophosphamide and Dexamethasone (BCD) in Newly Diagnosed Idiopathic Multicentric Castleman's Disease (iMCD) : a Prospective, Single-center, Single-arm, Phase-II Pilot Trial [NCT03982771]	Phase 2	30 participants (Anticipated)	Interventional	2019-01-01	Recruiting
Phase II Study of Vorinostat (SAHA) in Combination With Bortezomib (PS-341) in Patients With Recurrent Glioblastoma Multiforme [NCT00641706]	Phase 2	44 participants (Actual)	Interventional	2008-07-31	Completed
Velcade - Regulatory Post Marketing Surveillance (PMS) [NCT01005628]		1,121 participants (Actual)	Observational	2006-06-30	Completed
A Randomized, Open-Label, Multicenter Phase 3 Study of the Combination of Rituximab, Cyclophosphamide, Doxorubicin, VELCADE, and Prednisone (VcR-CAP) or Rituximab, Cyclophosphamide, Doxorubicin, Vincristine, and Prednisone (R-CHOP) in Patients With Newly [NCT00722137]	Phase 3	487 participants (Actual)	Interventional	2008-05-01	Completed
Phase I/II Study Evaluating Rituximab, Lenalidomide, and Bortezomib in the First-Line or Second-Line Treatment of Patients With Mantle Cell Lymphoma [NCT00633594]	Phase 1/Phase 2	39 participants (Actual)	Interventional	2008-06-30	Completed
Multicenter Randomized Phase II Study of Treatment With R-CHOP vs Bortezomib-R-CAP for Young Patients With Diffuse Large B-cell Lymphoma With Poor IPI. [NCT01848132]	Phase 2	121 participants (Actual)	Interventional	2013-10-03	Completed
Bortezomib in Late Antibody-mediated Kidney Transplant Rejection (BORTEJECT Study) [NCT01873157]	Phase 2	44 participants (Actual)	Interventional	2013-12-31	Completed
Impact of Proteasome Inhibition on Anti-Donor HLA Antibody Production After Kidney Transplantation [NCT01349595]	Phase 2	4 participants (Actual)	Interventional	2011-12-31	Terminated(stopped due to Study halted due to lack of funding)
Phase II Study of Combination Vorinostat and Bortezomib in Patients With Relapsed and/or Refractory Non-Hodgkin Lymphoma [NCT00837174]	Phase 2	0 participants (Actual)	Interventional	2010-06-30	Withdrawn(stopped due to Study never activated/opened as funding source and other support not available.)
Evaluating Study of Clinical Treatment of Multiple Myeloma Based on Analytical Omics [NCT04678089]		350 participants (Anticipated)	Observational	2019-05-16	Enrolling by invitation
UARK 2006-15: A Phase III Randomized Study of Tandem Transplants With or Without Bortezomib (Velcade) and Thalidomide (Thalomid) to Evaluate Its Effect on Response Rate and Durability of Response in Multiple Myeloma Patients [NCT00574080]	Phase 3	20 participants (Actual)	Interventional	2006-07-31	Terminated(stopped due to low accrual)
A Therapeutic Trial of Bortezomib (Velcade), Vorinostat (SAHA) and Dexamethasone for Relapsed/Refractory Acute Lymphoblastic Leukemia (ALL) [NCT01312818]	Phase 2	2 participants (Actual)	Interventional	2011-06-30	Terminated(stopped due to Slow accrual)
A National, Multi-Center, Open-Label Study of Velcade in Combination With Melphalan and Prednisone (V-MP) in Older Untreated Multiple Myeloma Patients. [NCT00388635]	Phase 1/Phase 2	60 participants (Actual)	Interventional	2004-04-30	Completed
A Phase II Pilot Study of VELCADE in Patients With MDS [NCT00262873]	Phase 2	8 participants (Actual)	Interventional	2005-05-31	Completed
A Phase 2 Study of Isatuximab in Combination With Bortezomib, Cyclophosphamide and Dexamethasone Followed by Isatuximab and Lenalidomide Maintenance in Newly Diagnosed Patients With Multiple Myeloma and Severe Renal Impairment (EAE116) [NCT05147493]	Phase 2	51 participants (Anticipated)	Interventional	2022-04-30	Not yet recruiting
Phase II Trial of Twice Weekly Induction Followed by Once Weekly IV Velcade (Bortezomib) With Dexamethasone in Patients With Relapsed and/or Refractory Multiple Myeloma Following at Least 1 Prior Therapy [NCT00389701]	Phase 2	30 participants (Anticipated)	Interventional	2006-03-31	Recruiting
Dose Escalation and Phase II Study of Bortezomib (IND #58443) Added to Standard Daunorubicin and Cytarabine Therapy for Patients With Previously Untreated Acute Myeloid Leukemia Age 60-75 Years [NCT00742625]	Phase 1/Phase 2	95 participants (Actual)	Interventional	2008-09-30	Completed
An Open-Label Phase 1 Study of Metformin and Nelfinavir in Combination With Bortezomib in Patients With Relapsed and/or Refractory Multiple Myeloma [NCT03829020]	Phase 1	9 participants (Actual)	Interventional	2019-04-17	Active, not recruiting
TEAM-Trial: Targeting Epigenetic Therapy Resistance in AML With Bortezomib: A Multi-centre Matched Threshold Crossing Phase II Approach [NCT04173585]	Phase 2	50 participants (Actual)	Interventional	2019-10-22	Completed
A Phase I/II Study of Escalating Doses of Bortezomib in Conjunction With High Dose Melphalan as a Conditioning Regimen for Autologous Peripheral Blood Stem Cell Transplantation in Patients With Multiple Myeloma [NCT00784823]	Phase 1/Phase 2	32 participants (Actual)	Interventional	2007-01-31	Completed
S0833, Modified Total Therapy 3 (TT3) for Newly Diagnosed Patients With Multiple Myeloma (MM): A Phase II SWOG Trial for Patients Aged ≤ 65 Years [NCT01055301]	Phase 2	0 participants (Actual)	Interventional	2011-07-31	Withdrawn(stopped due to lack of accrual)
Evaluation of Improvement of Quality of Life in Multiple Myeloma Patients Treated With Velcade (Bortezomib) IV: Prospective, Multicenter, Observational Study [NCT01021592]		140 participants (Actual)	Observational	2007-03-31	Completed
A Study of Bortezomib With Chemotherapy for Relapsed/Refractory Acute Lymphoblastic Leukemia [NCT00440726]	Phase 1/Phase 2	31 participants (Actual)	Interventional	2006-08-04	Completed
Bortezomib (Velcade®) and Reduced-Intensity Allogeneic Stem Cell Transplantation for Patients With Lymphoid Malignancies [NCT00439556]	Phase 2	40 participants (Actual)	Interventional	2007-02-13	Completed
Phase II Trial of Combination Weekly Bortezomib (VELCADE) and Docetaxel (TAXOTERE) in Patients With Recurrent and/ or Metastatic Head and Neck Squamous Cell Carcinoma (HNSCC) [NCT00425750]	Phase 2	25 participants (Actual)	Interventional	2005-08-31	Completed
A Randomised Evaluation of Molecular Guided Therapy for Diffuse Large B-cell Lymphoma With Bortezomib [NCT01324596]	Phase 3	1,132 participants (Actual)	Interventional	2011-04-30	Completed
Phase II Study of Combination Bortezomib, Dexamethasone, and Rituximab in Previously Untreated Patients With Waldenstrom's Macroglobulinemia: A Multicenter Trial of the European Myeloma Network [NCT01046006]	Phase 2	59 participants (Actual)	Interventional	2007-03-31	Completed
A Phase I Pharmacokinetic Study of Intraperitoneal CTEP-Supplied Agent Bortezomib (PS-341, NSC 681239) and Carboplatin (NSC# 241240) in Patients With Persistent or Recurrent Ovarian, Fallopian Tube, or Primary Peritoneal Cancer [NCT01074411]	Phase 1	33 participants (Actual)	Interventional	2010-04-05	Completed
Pilot Study of Daratumumab in Combination With Bortezomib, Cyclophosphamide, and Dexamethasone (Dara-CyBorD) in Newly Diagnosed Multiple Myeloma Patients With Renal Failure [NCT06142396]	Early Phase 1	30 participants (Anticipated)	Interventional	2024-01-01	Not yet recruiting
DREAMM 7: A Multicenter, Open-Label, Randomized Phase III Study to Evaluate the Efficacy and Safety of the Combination of Belantamab Mafodotin, Bortezomib, and Dexamethasone (B-Vd) Compared With the Combination of Daratumumab, Bortezomib and Dexamethasone [NCT04246047]	Phase 3	571 participants (Actual)	Interventional	2020-05-07	Active, not recruiting
A PHASE II MULTI-CENTRE, RANDOMIZED, OPEN LABEL STUDY OF PROLONGED THERAPY WITH SC BORTEZOMIB TWICE MONTHLY ASSOCIATED WITH DEXAMETHASONE, IN RELAPSED AND REFRACTORY MULTIPLE MYELOMA PATIENTS AFTER SALVAGE WITH BORTEZOMIB-BASED THERAPY. [NCT01913730]	Phase 2	63 participants (Actual)	Interventional	2013-11-30	Completed
A Phase II Study of Bortezomib (VELCADE®) in Patients With Relapsed or Refractory Cutaneous T-Cell Lymphoma (CTCL) [NCT00182637]	Phase 2	5 participants (Actual)	Interventional	2004-07-31	Completed
A Phase II Study of Bortezomib in Combination With Rituximab, Fludarabine, Mitoxantrone, and Dexamethasone (VR-FND) for Relapsed or Refractory Follicular Lymphoma [NCT00510887]	Phase 2	14 participants (Actual)	Interventional	2007-01-31	Terminated(stopped due to Low accrual.)
Phase I Study of Belinostat (PXD-101) and Velcade (Bortezomib) in Relapsed or Refractory Acute Leukemia/ Myelodysplastic Syndrome [NCT01075425]	Phase 1	41 participants (Actual)	Interventional	2010-05-31	Completed
A Sequential Phase II Trial of the Combination of Bortezomib (VELCADE), Dexamethasone (DECADRON) and Pegylated Liposomal Doxorubicin (DOXIL) Followed by High Dose Cyclophosphamide in Multiple Myeloma Patients [NCT00148317]	Phase 2	38 participants (Actual)	Interventional	2005-06-30	Completed
A Phase II Study of the Novel Proteasome Inhibitor Bortezomib in Combination With Rituximab, Cyclophosphamide and Prednisone in Patients With Relapsed/Refractory Indolent B-Cell Lymphoproliferative Disorders and Mantle Cell Lymphoma (MCL) [NCT00295932]	Phase 1/Phase 2	79 participants (Actual)	Interventional	2005-12-13	Completed
A Phase I/II Trial of Combination Bortezomib (VELCADE) and Gemcitabine Therapy for Patients With Relapsed or Refractory Aggressive B- and T-cell Non-Hodgkin's Lymphoma [NCT00290706]	Phase 1/Phase 2	32 participants (Actual)	Interventional	2006-04-07	Terminated(stopped due to Closed per Data Monitoring Committee due to lack of efficacy)
An Open-Label Phase 1/2 Study of VELCADE for Injection in Subjects With Light-Chain (AL)-Amyloidosis [NCT00298766]	Phase 1/Phase 2	70 participants (Actual)	Interventional	2005-06-30	Completed
Phase II Pilot Study of Bortezomib (VELCADE®) and Gemcitabine for Patients With Relapsed or Refractory Hodgkin's Lymphoma [NCT00262860]	Phase 2	18 participants (Actual)	Interventional	2005-04-30	Completed
Effect of Low Dose Bortezomib on Bone Formation in Smoldering Myeloma Patients [NCT00983346]	Phase 2	17 participants (Actual)	Interventional	2009-10-31	Terminated(stopped due to Lab Staff that was required left the institution, therefore accrual closed prematurely)
Observational Study of Osteoblast Activity in Velcade�(Bortezomib) IV Treated Multiple Myeloma Patients. [NCT01026701]		104 participants (Actual)	Observational	2008-03-31	Completed
Bortezomib + Pegylated Liposomal Doxorubicin (Doxil) + Dexamethasone Followed by Thalidomide + Dexamethasone or Bortezomib + Thalidomide + Dexamethasone for Patients With Symptomatic Untreated High-Risk or Primary Resistant Multiple Myeloma [NCT00458705]	Phase 2	45 participants (Actual)	Interventional	2006-11-30	Completed
A Phase II Trial of Weekly Docetaxel and Bortezomib (Velcade; PS-341) in the Treatment of Patients With Advanced Hormone-Refractory Prostate Cancer [NCT00193232]	Phase 2	50 participants	Interventional	2004-05-31	Completed
Pilot Study With Bortezomib in Combination With Rituximab Standard Therapy in Patients With Relapsed or Refractory Follicular Lymphoma and at Least 2 Previous Therapies [NCT01902862]	Phase 2	7 participants (Actual)	Interventional	2006-02-28	Terminated(stopped due to Recruitment too slow)
A Randomized, Controlled Phase 3 Study to Evaluate Optimized Retreatment and Prolonged Therapy With Bortezomib (Velcade) in Patients With Multiple Myeloma in First or Second Relapse. [NCT01910987]	Phase 3	80 participants (Actual)	Interventional	2013-04-30	Completed
A Randomized, National, Open-label, Multicenter, Phase III Trial Studying Induction Therapy With Bortezomib/Lenalidomide/Dexamethasone (VRD-GEM), Followed by High-dose Chemotherapy With Melphalan-200 (MEL-200) Versus Busulfan-melphalan (BUMEL), and Consol [NCT01916252]	Phase 3	460 participants (Anticipated)	Interventional	2013-09-30	Completed
A Phase I Study of Bortezomib During Maintenance Phase After High Dose Melphalan and Autologous Stem Cell Transplantation in Patients With Multiple Myeloma [NCT00288028]	Phase 1	15 participants (Actual)	Interventional	2005-07-31	Completed
A Phase I/II Trial of Bendamustine in Combination With Bortezomib and Pegylated Liposomal Doxorubicin in Patients With Relapsed or Refractory Multiple Myeloma: Hoosier Cancer Research Network MM08-141 [NCT01177683]	Phase 1/Phase 2	32 participants (Actual)	Interventional	2010-07-31	Terminated(stopped due to Lack of accrual)
Phase I/II Study of Bortezomib (VELCADE) Plus Rituximab-HyperCVAD Alternating With Bortezomib Plus Rituximab-High Dose Methotrexate/Cytarabine in Patients With Untreated Aggressive Mantle Cell Lymphoma [NCT00477412]	Phase 1/Phase 2	107 participants (Actual)	Interventional	2007-04-03	Completed
A Phase I Evaluation of the Combination of Pegylated Liposomal Doxorubicin (Doxil®) With PS-341 in Patients With Refractory Hematologic and Solid Malignancies [NCT00237627]	Phase 1/Phase 2	107 participants (Actual)	Interventional	2001-05-31	Completed
Phase II Study of VELCADE in Patients With Extranodal Marginal Zone B-Cell Lymphoma of MALT-Type Pretreated With More Than One Prior Systemic Therapy Regimen (X05142) [NCT00210392]	Phase 2	12 participants (Actual)	Interventional	2005-07-31	Terminated(stopped due to After IELSG25A study amendment, patients subject of the present study were eligible for inclusion in the IELSG25A study)
Phase I/II Study of Bortezomib and Low Dose Cytarabine in the Treatment of High-Risk Myelodysplastic Syndromes [NCT00411905]	Phase 1/Phase 2	39 participants	Interventional	2006-06-30	Recruiting
Phase II Study to Evaluate the Role of Bortezomib in the Management of Relapsed Acute Promyelocytic Leukemia [NCT01950611]	Phase 2	30 participants (Anticipated)	Interventional	2013-05-31	Recruiting
A Study of Low-dose Lenalidomide After Non-myeloablative Allogeneic Stem Cell Transplant With Bortezomib as GVHD Prophylaxis in High Risk Multiple Myeloma [NCT01954784]	Phase 1	8 participants (Actual)	Interventional	2013-10-07	Terminated(stopped due to Funding unavailable)
An Interventional, Prospective Open-Label Study of Immunosuppressive Therapies to Mitigate Immune-Mediated Loss of Therapeutic Response to Asfotase Alfa (STRENSIQ®) for Hypophosphatasia (RESTORE) [NCT06015750]	Phase 4	8 participants (Anticipated)	Interventional	2024-02-20	Not yet recruiting
A Phase I Open Label Study Of Panobinostat In Combination With Lenalidomide, Bortezomib, And Dexamethasone In Patients With Relapsed And Relapsed/Refractory Multiple Myeloma [NCT01965353]	Phase 1	21 participants (Actual)	Interventional	2013-10-31	Completed
Open-label, Multicenter Phase II Study of Bortezomib for Maintenance Therapy in Patients With High Risk Diffuse Large B Cell Lymphoma [NCT01965977]	Phase 2	59 participants (Actual)	Interventional	2015-04-08	Active, not recruiting
A Phase 3, Two-Stage, Randomized, Multicenter, Open-Label Study Comparing Mezigdomide (CC-92480), Bortezomib and Dexamethasone (MEZIVd) Versus Pomalidomide, Bortezomib and Dexamethasone (PVd) in Subjects With Relapsed or Refractory Multiple Myeloma (RRMM) [NCT05519085]	Phase 3	810 participants (Anticipated)	Interventional	2022-09-20	Recruiting
"A PHASE III STUDY OF VELCADE (BORTEZOMIB) THALIDOMIDE DEXAMETHASONE (VTD) VERSUS VELCADE (BORTEZOMIB) CYCLOPHOSPHAMIDE DEXAMETHASONE (VCD) AS AN INDUCTION TREATMENT PRIOR TO AUTOLOGOUS STEM CELL TRANSPLANTATION IN PATIENTS WITH NEWLY DIAGNOSED MULTIPLE M [NCT01971658]	Phase 3	358 participants (Actual)	Interventional	2013-10-31	Completed
Phase II Study of Daratumumab Based Response Adapted Therapy for Older Adults With Newly Diagnosed Multiple Myeloma [NCT04151667]	Phase 2	33 participants (Actual)	Interventional	2019-11-22	Active, not recruiting
A Comparative Study of Bortezomib-Thalidomide-Dexamethason and Bortezomib-Cyclophosphamide-Dexamethason in the Treatment of Monoclonal Immunoglobulin Light Chain Amyloidosis: A Prospective Randomized Controlled Trial（BTD-CHINA-TRIAL） [NCT04612582]	Phase 4	70 participants (Anticipated)	Interventional	2020-01-01	Recruiting
A Phase I Trial of Duvelisib in Combination With Either Romidepsin or Bortezomib in Relapsed/Refractory T-cell Lymphomas [NCT02783625]	Phase 1	114 participants (Actual)	Interventional	2016-05-31	Active, not recruiting
Phase I Study of Bortezomib With or Without Total Marrow Irradiation (TMI) Using Intensity Modulated Radiation Therapy (IMRT) in Combination With Fludarabine (FLU) and Melphalan (MEL) as a Preparative Regimen for Allogeneic Hematopoietic Stem Cell (HSC) T [NCT01163357]	Phase 1	18 participants (Actual)	Interventional	2011-01-28	Active, not recruiting
A Phase I/II Study of VELCADE in Combination With Gemcitabine in Relapsed B-Cell Non-Hodgkin's Lymphoma [NCT00863369]	Phase 1/Phase 2	33 participants (Actual)	Interventional	2005-06-29	Active, not recruiting
A Phase II Study of Suberoylanilide Hydroxamic Acid and Bortezomib in Advanced Soft Tissue Sarcomas [NCT00937495]	Phase 2	16 participants (Actual)	Interventional	2009-06-30	Completed
Prospective Assessment of the Cardiac Effects the Proteasome Inhibitor Bortezomib in Patients Undergoing Therapy for Multiple Myeloma [NCT02026505]		11 participants (Actual)	Observational	2014-03-01	Completed
Phase Ⅱ Study of G-CSF, Bortezomib, Cyclophosphamide and Dexamethasone in Patients With Multiple Myeloma [NCT02027220]	Phase 2	60 participants (Anticipated)	Interventional	2013-12-31	Recruiting
Phase 2, Open-Label Randomized Study of Daratumumab, Carfilzomib, Lenalidomide, and Dexamethasone vs Carfilzomib, Lenalidomide, and Dexamethasone in Patients With Newly Diagnosed Multiple Myeloma [NCT04268498]	Phase 2	306 participants (Anticipated)	Interventional	2020-02-11	Recruiting
Phase I Study of Weekly Bortezomib (VELCADE, PS-341) and Weekly Topotecan (HYCAMTIN) in Solid Tumor Patients With an Emphasis on Small Cell Lung Cancer (SCLC) [NCT00388089]	Phase 1	24 participants (Actual)	Interventional	2004-12-31	Completed
A Phase I Study of PS-341 in Combination With 5-FU/LV in Solid Tumors [NCT00007878]	Phase 1	30 participants (Actual)	Interventional	2000-09-30	Completed
An Open-label Phase II Study of the Efficacy of Combination Bortezomib-containing Regimens in the Treatment of Newly Diagnosed Patients With t (4; 14) Positive Multiple Myeloma [NCT00570180]	Phase 2	36 participants (Actual)	Interventional	2008-08-25	Completed
UARK 2007-01, A Phase II Pilot Study of the Combination of Melphalan, Bortezomib, Thalidomide and Dexamethasone (MEL-VTD) and Autologous Transplantation for Patients Relapsing or Progressing After Tandem Transplantation [NCT00577668]	Phase 2	0 participants (Actual)	Interventional	2007-04-30	Withdrawn(stopped due to Poor accrual)
A Phase I Dose Escalating Study of Bortezomib and Lenalidomide in Patients With Untreated or Previously Treated, Primary and Secondary Non 5q- Del Myelodysplasia [NCT00580242]	Phase 1	23 participants (Actual)	Interventional	2007-11-30	Completed
Phase I Trial of Dacarbazine and Bortezomib in Melanoma and Soft Tissue Sarcoma [NCT00580320]	Phase 1	17 participants (Actual)	Interventional	2004-09-30	Completed
MINIALO-VELCADE2005: A Phase II National, Open-label, Multicenter, no Controlled Study of Treated With Bortezomib (Velcade) Multiple Myeloma Patients Pre and Post Allogeneic Haematopoietic Progenitor Cell Transplant With no Myeloablative Conditioning [NCT00564200]	Phase 2	30 participants (Anticipated)	Interventional	2007-11-30	Completed
Phase I/II Study of Arsenic Trioxide (Trisenox), Ascorbic Acid and Bortezomib Combination Therapy in Patients With Relapsed/Refractory Multiple Myeloma [NCT00590603]	Phase 1	25 participants (Actual)	Interventional	2008-07-31	Terminated(stopped due to Poor accrual - terminated during Phase I; Phase II never started.)
A Phase I Study to Investigate the Safety and Clinical Activity of Idelalisib in Combination With Chemotherapeutic Agents, Immunomodulatory Agents and Anti-CD20 mAb in Subjects With Relapsed or Refractory Indolent B-cell Non-Hodgkin Lymphoma, Mantle Cell [NCT01088048]	Phase 1	241 participants (Actual)	Interventional	2010-03-25	Completed
A Phase II, Multi-center, Single Arm, Open Label Study of Panobinostat in Combination With Bortezomib and Dexamethasone in Patients With Relapsed and Bortezomib-refractory Multiple Myeloma [NCT01083602]	Phase 2	55 participants (Actual)	Interventional	2010-06-30	Completed
A Phase II Study of the Efficacy and Safety of Lenalidomide, Subcutaneous Bortezomib, and Dexamethasone Combination Therapy for Patients With Newly Diagnosed Multiple Myeloma [NCT02219178]	Phase 2	42 participants (Actual)	Interventional	2014-11-30	Completed
Phase II Study of Subcutaneous (SC) Bortezomib, Lenalidomide and Dexamethasone for Relapsed and/or Refractory Multiple Myeloma; Followed by SC Bortezomib Maintenance [NCT01647165]	Phase 2	0 participants (Actual)	Interventional	2012-07-11	Withdrawn
Pharmacologic Pretransplant Immunosuppression (PTIS) + Reduced Toxicity Conditioning (RTC) Allogeneic Stem Cell Transplantation in Inherited Hematologic Disorders [NCT05293509]	Phase 2	0 participants (Actual)	Interventional	2022-03-02	Withdrawn(stopped due to 0 accrual)
Lead-In and Phase II Study of Clofarabine, Etoposide, Cyclophosphamide [CEC], Liposomal Vincristine (VCR), Dexamethasone and Bortezomib in Relapsed/Refractory Acute Lymphoblastic Leukemia (ALL) and Lymphoblastic Lymphoma (LL) [NCT03136146]	Phase 2	42 participants (Anticipated)	Interventional	2017-08-09	Recruiting
Ibrutinib (Imbruvica®), Bortezomib (Velcade®) s.c., Rituximab, CHOP for the Treatment of Elderly Patients (Age 61-80 Years) With CD20+ Diffuse Large B-cell Lymphoma, IPI ≥ 2 [NCT03129828]	Phase 1/Phase 2	34 participants (Anticipated)	Interventional	2017-03-17	Active, not recruiting
Phase 3 Study Comparing Daratumumab, Bortezomib and Dexamethasone (DVd) vs Bortezomib and Dexamethasone (Vd) in Subjects With Relapsed or Refractory Multiple Myeloma [NCT02136134]	Phase 3	499 participants (Actual)	Interventional	2014-08-15	Active, not recruiting
A Phase II Study of Bortezomib in Patients With Metastatic Castration-Resistant Prostate Cancer With PTEN Deletion [NCT06029998]	Phase 2	22 participants (Anticipated)	Interventional	2023-12-31	Not yet recruiting
Bortezomib-based Graft-Versus-Host-Disease Prophylaxis After Myeloablative Allogeneic Stem Cell Transplantation for Patients Lacking HLA-matched Related Donors: A Phase 2 Study [NCT01323920]	Phase 2	35 participants (Actual)	Interventional	2011-05-31	Completed
A Phase II Study of Bortezomib, Liposomal Doxorubicin, Dexamethasone, and Cyclophosphamide in Patients With Multiple Myeloma Relapsing Within 12 Months of Autologous Stem Cell Transplant [NCT01078441]	Phase 2	2 participants (Actual)	Interventional	2010-09-30	Terminated(stopped due to The study was closed early due to weak accrual on June 26, 2012.)
Phase II Study of Proteasome Inhibitor PS-341 For Patients With Relapsed or Refractory B Cell Lymphomas Previously Treated With Chemotherapy [NCT00038571]	Phase 2	60 participants (Actual)	Interventional	2002-05-31	Completed
A Phase II, Open-Label Trial Using Velcade for ReTreatment of Multiple Myeloma Subjects Following an Initial Response to Velcade [NCT00431769]	Phase 2	130 participants (Actual)	Interventional	2006-06-30	Completed
Assessment of Molecular Remission by ASO-RQ-PCR Technique After Induction Treatment With Bortezomib-dexamethasone (Vel/Dex) Followed by HDT With ASCT [NCT00861250]	Phase 2/Phase 3	47 participants (Actual)	Interventional	2009-03-31	Completed
An International Single-Arm Study to Provide Further Safety and Efficacy Data on the Bortezomib(Velcade)/Melphalan/Prednisone Regimen in Previously Untreated Transplant Ineligible Multiple Myeloma Patients [NCT00799539]		0 participants	Expanded Access		No longer available
Phase I Study of Induction Therapy With VELCADE and Vorinostat in Patients With Surgically Resectable Non-Small Cell Lung Cancer [NCT00731952]	Phase 1	21 participants (Actual)	Interventional	2006-06-30	Completed
Phase II Study Investigating the Efficacy of VELCADE®, Rituximab, Cyclophosphamide and Decadron (VRCD Regimen) in Front-line Therapy of Patients With Low-grade Non-Hodgkin's Lymphoma [NCT00413959]	Phase 2	12 participants (Actual)	Interventional	2006-08-31	Terminated
Lenalidomide and Low Dose Dexamethasone Induction Therapy Followed by Low Dose Melphalan, Prednisone, Lenalidomide and Bortezomib Sequential Maintenance Therapy for Newly Diagnosed High-risk Multiple Myeloma [NCT00691704]	Phase 2	18 participants (Actual)	Interventional	2008-08-31	Completed
A Targeted Ph I/II Trial of ZD6474 (Vandetanib; CAPRELSA) Plus the Proteasome Inhibitor, Bortezomib (Velcade ), in Adults With Solid Tumors With a Focus on Hereditary or Sporadic, Locally Advanced or Metastatic Medullary Thyroid Ca (MTC) [NCT00923247]	Phase 1/Phase 2	22 participants (Actual)	Interventional	2009-02-19	Terminated(stopped due to Terminated due to slow accrual,primary endpoint reached & investigator left NIH.)
Phase I/II Trial of Sorafenib and Weekly Bortezomib in the Treatment of Patients With Relapsed or Refractory Multiple Myeloma [NCT00536575]	Phase 1/Phase 2	13 participants (Actual)	Interventional	2007-11-30	Completed
S0629, Observational Study of Asymptomatic Waldenstrom's Macroglobulinemia and Phase II Study of Tandem Autologous Transplant and Maintenance Treatment for Patients With Symptomatic Disease [NCT00723658]	Phase 2	0 participants (Actual)	Interventional	2008-09-30	Withdrawn(stopped due to lack of accrual)
A Two Stage, Open Label, Phase II Study of VELCADE Plus ELOXATIN in Previously Treated Patients With Malignant Pleural or Peritoneal Mesothelioma [NCT00996385]	Phase 2	29 participants (Anticipated)	Interventional	2009-09-30	Recruiting
A Phase II Single Arm Study of VELCADE and DOXIL (PLD) in Patients With Relapsed Multiple Myeloma Previously Treated With VELCADE [NCT00706953]	Phase 2	0 participants (Actual)	Interventional	2008-07-31	Withdrawn
A Phase II Study of Fludarabine, Velcade and Rituximab for Relapsed or Refractory Follicular Non-Hodgkin Lymphoma: Hoosier Oncology Group LYM08-134 [NCT01186458]	Phase 2	4 participants (Actual)	Interventional	2010-10-31	Terminated(stopped due to Slow accrual)
A Phase II Study of Pegylated Liposomal Doxorubicin, Bortezomib, Dexamethasone and Lenalidomide (DVD-R) for Patients With Relapsed/Refractory Multiple Myeloma [NCT01160484]	Phase 2	40 participants (Actual)	Interventional	2009-09-30	Completed
A Phase II Trial Evaluating the Effects of Bortezomib in Patients With Recurrent Malignant Gliomas Treated Prior to Surgery and Then Bortezomib and Temozolomide Post-operatively [NCT00990652]	Phase 2	10 participants (Actual)	Interventional	2009-05-31	Completed
Phase I Study of Vidaza and Velcade (Bortezomib) in Acute Myeloid Leukemia [NCT00624936]	Phase 1	23 participants (Actual)	Interventional	2008-04-30	Completed
Lenalidomide, Bortezomib, and Dexamethasone Combination Therapy as Induction Followed by Bortezomib and Lenalidomide Maintenance in Patients With Newly Diagnosed High Risk Multiple Myeloma [NCT03641456]	Phase 2	50 participants (Anticipated)	Interventional	2020-09-25	Recruiting
A Phase 3 Study of Velcade (Bortezomib) Dexamethasone (VD) Versus Velcade (Bortezomib) Thalidomide Dexamethasone (VTD) as an Induction Treatment Prior to Autologous Stem Cell Transplantation in Patients With Newly Diagnosed Multiple Myeloma [NCT00910897]	Phase 3	205 participants (Actual)	Interventional	2008-03-31	Active, not recruiting
The Efficacy of Cyclophosphamide Plus Dexamethasone Combinated With Rituximab or Bortezomib for the Newly Diagnosed Waldenström Macroglobulinemia - a Prospective Multicentre Randomized Control Trial From China [NCT02844322]	Phase 4	110 participants (Anticipated)	Interventional	2016-05-31	Recruiting
A Phase I Study Using Tacrolimus, Sirolimus and Bortezomib as Acute Graft Versus Host Disease Prophylaxis in Allogeneic Peripheral Blood Stem Cell (PBSC) Transplantation [NCT00670423]	Phase 1	27 participants (Actual)	Interventional	2008-05-16	Completed
Velcade Therapy for Severe IgA Nephropathy [NCT01103778]	Phase 4	11 participants (Actual)	Interventional	2010-07-31	Completed
Effect of Ketoconazole Administration on the Pharmacokinetics and Pharmacodynamics of Bortezomib in Patients With Advanced Solid Tumors [NCT00129207]	Phase 1	0 participants	Interventional		Completed
Phase II Trial of Bortezomib and Rituximab for Patients With Post Transplant Lymphoproliferative Disorders (PTLD) [NCT00869323]	Phase 2	3 participants (Actual)	Interventional	2009-03-31	Terminated(stopped due to Funding unavailable)
A Pilot Study Of Weekly Subcutaneous Bortezomib In Patients With Steroid-Refractory Or -Dependent Chronic Graft Versus Host Disease [NCT01672229]	Phase 1	16 participants (Actual)	Interventional	2012-07-31	Completed
A Phase I Pharmacokinetic Study of PS341 in Patients With Advanced Malignancies and Varying Degrees of Renal Dysfunction for the CTEP-Sponsored Organ Dysfunction Working Group [NCT00054483]	Phase 1	69 participants (Actual)	Interventional	2003-01-31	Completed
A Phase 1/2 Open-label Study to Assess the Safety, Tolerability and Preliminary Efficacy of TH-302, A Hypoxia-Activated Prodrug, and Dexamethasone With or Without Bortezomib or Pomalidomide in Subjects With Relapsed/Refractory Multiple Myeloma [NCT01522872]	Phase 1/Phase 2	98 participants (Anticipated)	Interventional	2012-02-29	Active, not recruiting
A Phase 2 Proposal to Test the Efficacy and Tolerability of Bortezomib in Pulmonary Chronic GVHD [NCT01163786]	Phase 2	17 participants (Actual)	Interventional	2010-10-07	Terminated(stopped due to Study was closed due to low accrual before the accrual goal was reached)
Phase I Study of Bortezomib and Cetuximab Without or With Cisplatin in Combination With Radiation Therapy for Advanced Head and Neck Cancer [NCT00629226]	Phase 1	46 participants (Anticipated)	Interventional	2007-10-31	Completed
Bortezomib* and Vorinostat as Maintenance Therapy After Autologous Transplant for Non-Hodgkin Lymphoma Using R-BEAM or BEAM Conditioning Transplant Regimen [NCT00992446]	Phase 2	27 participants (Actual)	Interventional	2010-09-02	Completed
A Randomized, Open-Label, Phase 2 Study of CNTO 328 (Anti-IL-6 Monoclonal Antibody) and VELCADE-Melphalan-Prednisone Compared With VELCADE-Melphalan-Prednisone for the Treatment of Previously Untreated Multiple Myeloma [NCT00911859]	Phase 2	118 participants (Actual)	Interventional	2009-06-30	Completed
Desensitization for Preformed Anti-HLA Antibodies in Kidney Transplantation [NCT00908583]	Phase 4	44 participants (Actual)	Interventional	2009-05-31	Completed
Evaluation of Melphalan+Bortezomib as a Conditioning Regimen for Autologous and Allogeneic Stem Cell Transplants in Multiple Myeloma After Cytoreductive Therapy [NCT00948922]	Phase 2	124 participants (Actual)	Interventional	2009-06-18	Completed
Phase I Study of GX15-070 (NSC # 729280) and Bortezomib in Aggressive Relapsed/Recurrent Non-Hodgkin's Lymphoma [NCT00538187]	Phase 1	18 participants (Actual)	Interventional	2007-12-31	Terminated
Phase II Trial of Bortezomib With Combination of Gemcitabine, Ifosfamide and Oxaliplatin (GIFOX-B)in Untreated NK/T Cell Lymphoma [NCT02808091]	Phase 2	7 participants (Actual)	Interventional	2011-03-31	Terminated(stopped due to Slow recruitment)
Phase 2 Study of Daratumumab Monotherapy in Previously Untreated Patients With Stage 3B Light Chain (AL) Amyloidosis [NCT04131309]	Phase 2	40 participants (Actual)	Interventional	2019-09-23	Active, not recruiting
A Phase II Study of PS-341 in Advanced or Metastatic Urothelial Cancer (Transitional Cell Cancer of the Bladder, Ureter, and Renal Pelvis) [NCT00066352]	Phase 2	0 participants	Interventional	2003-09-30	Completed
IFM 2014-02 Study: A Randomized Phase III Study of Bortezomib-Melphalan 200 Conditioning Regimen Versus Melphalan 200 for Frontline Transplant Eligible Patients With Multiple Myeloma [NCT02197221]	Phase 3	300 participants (Actual)	Interventional	2015-01-31	Completed
A Phase Ib Study to Evaluate Safety, Tolerability, Pharmacokinetics, Pharmacodynamics and Clinical Activity of the Oral AKT Inhibitor GSK2110183 Administered in Combination With Bortezomib and Dexamethasone in Subjects With Relapsed/Refractory Multiple My [NCT01428492]	Phase 1	90 participants (Actual)	Interventional	2011-12-31	Completed
A Prospective Open-Label Pilot Trial of PS-341 (Bortezomib; VELCADE) for the Therapy of Symptomatic Advanced Myeloproliferative Disorders [NCT00437086]	Early Phase 1	30 participants (Anticipated)	Interventional	2005-09-30	Completed
Retrospective Evaluation of Re-Treatment With Bortezomib in Subjects With First Relapse After Bortezomib First-Line Therapy [NCT01524445]		35 participants (Actual)	Observational	2011-03-31	Completed
Phase I Trial of Weekly Bortezomib (Velcade) in the Treatment of Patients With Refractory Multiple Myeloma [NCT00193557]	Phase 2	40 participants	Interventional	2004-05-31	Completed
A Phase 2 Study of VELCADE® (Bortezomib) With Rituximab in Subjects With Relapsed or Refractory Indolent B-Cell Lymphoma [NCT00085696]	Phase 2	66 participants	Interventional	2004-05-31	Completed
A Phase I Study of PS-341 in Patients With Hematologic Malignancies [NCT00006098]	Phase 1	0 participants	Interventional	2000-04-30	Completed
A Phase I Pharmacokinetic Study of PS-341 in Patients With Advanced Malignancies and Varying Degrees of Liver Dysfunction for the CTEPSponsored Organ Dysfunction Working Group [NCT00091117]	Phase 1	80 participants (Actual)	Interventional	2004-07-31	Completed
UARK 2003-35, A Phase III Study of Bortezomib Versus Bortezomib in Two Doses in Combination With Revlimid™ for Patients Relapsing or Progressing on Total Therapy II (UARK 98-026) [NCT00093028]	Phase 3	315 participants (Actual)	Interventional	2004-01-31	Completed
A Phase II Study of VELCADE With Rituximab in Subjects With Relapsed or Refractory Indolent B-Cell Lymphoma [NCT00093769]	Phase 2	15 participants (Actual)	Interventional	2004-08-31	Completed
Phase 2 Study of Desensitization Protocol for Highly Sensitized Wait Listed Patients [NCT01502267]	Phase 2	2 participants (Anticipated)	Interventional	2010-01-31	Enrolling by invitation
A 24-week, Open-label Extension Study of the Efficacy, Safety, and Tolerability of Oral SCIO-469 in Treatment of Relapsed Refractory Patients With Multiple Myeloma [NCT00095680]	Phase 2	30 participants (Actual)	Interventional	2004-11-30	Completed
A Phase II Open-label Rollover Study for Subjects That Have Participated in an Astellas Sponsored Linsitinib Trial [NCT02057380]	Phase 2	13 participants (Actual)	Interventional	2014-04-16	Completed
Phase I Study of Decitabine (Dacogen) and Bortezomib (Velcade) in Acute Myeloid Leukemia [NCT00703300]	Phase 1	19 participants (Actual)	Interventional	2008-06-30	Completed
A Phase I, Open Label, Dose-escalating Study of the Proteasome Inhibitor PS-341 in Combination With Two Schedules of Herceptin, in Patients With Advanced Breast Cancer That Overexpresses HER-2 [NCT00199212]	Phase 1	19 participants (Actual)	Interventional	2003-10-31	Completed
Phase II Study to Evaluate the Efficacy and Safety of Therapy With PS 341 in Patients With Advanced Stage Non Small Cell Lung Cancer [NCT00200382]	Phase 2	27 participants (Anticipated)	Interventional	2004-05-31	Terminated(stopped due to The study did not achieve the statistical success to continue.)
Phase I Trial of the Combination of Bortezomib and Clofarabine in Adults With Refractory Solid Tumors, Lymphomas, or Myelodysplastic Syndromes [NCT02211755]	Phase 1	75 participants (Anticipated)	Interventional	2014-10-06	Recruiting
A Phase II Study of Velcade (Bortezomib - PS341) in the Treatment of Patients Over 18 Years With Ph+ Leukemia [NCT00511069]	Phase 2	3 participants (Actual)	Interventional	2006-07-31	Completed
Phase II Study of VELCADE in Patients With Extranodal Marginal Zone B-cell Lymphoma of MALT-type Pretreated With Prior Systemic Therapy Regimen (X05142) [NCT00210327]	Phase 2	33 participants (Anticipated)	Interventional	2005-07-31	Completed
Primary Effusion Lymphoma: A Pilot Trial of Bevacizumab and Modified Dose-Adjusted Infusional CDE Chemotherapy Preceded by a Brief Pre-Phase Assessment of Targeted Oncolytic Virotherapy With Bortezomib, Zidovudine and Valganciclovir [NCT00217503]	Phase 2	15 participants (Anticipated)	Interventional	2005-07-31	Completed
An Open Label Phase II Multicentre Clinical Trial of Single Agent Bortezomib in Patients With Malignant Pleural Mesothelioma [NCT00513877]	Phase 2	33 participants (Actual)	Interventional	2006-05-31	Completed
A Parallel Randomised Phase II Trial of CHOP Chemotherapy With or Without Bortezomib in Relapsed Mantle Cell Lymphoma [NCT00513955]	Phase 2	50 participants (Actual)	Interventional	2006-06-30	Completed
Phase I/II Clinical Trial of Bortezomib (Velcade) + Pemetrexed (Alimta) in Previously Treated Patients With Advanced Non-Small Cell Lung Cancer [NCT00516100]	Phase 1/Phase 2	62 participants (Anticipated)	Interventional	2006-01-31	Active, not recruiting
A Phase 2 Study of Pomalidomide as a Replacement for Lenalidomide for Multiple Myeloma Patients Relapsed or Refractory to a Lenalidomide-Containing Combination Regimen [NCT02188368]	Phase 2	45 participants (Actual)	Interventional	2014-07-07	Terminated(stopped due to Lack of enrollment)
Proteasomal Inhibition for Patients With Mis-sense Mutated Dysferlin [NCT01863004]	Phase 1	3 participants (Actual)	Interventional	2012-12-31	Terminated(stopped due to insufficient enrollment rate)
Primary Treatment of Waldenstrom's Macroglobulinemia With Bortezomib (Velcade) and Rituximab (Rituxan) Followed by Autologous Stem Cell Collection [NCT00492050]	Phase 2	46 participants (Actual)	Interventional	2006-08-02	Active, not recruiting
The Efficacy and Safety of Bortezomib as First-line Treatment for Acquired Thrombotic Thrombocytopenic Purpura [NCT05135442]	Phase 4	30 participants (Anticipated)	Interventional	2021-12-01	Not yet recruiting
A Phase 2, Randomized Study of Bortezomib/Dexamethasone With or Without Elotuzumab in Subjects With Relapsed/Refractory Multiple Myeloma [NCT01478048]	Phase 2	185 participants (Actual)	Interventional	2011-11-30	Completed
A Phase II Trial of Combination Treatment With Vorinostat, Bortezomib and Dexamethasone in Patients With Relapsed and Relapsed Refractory Multiple Myeloma [NCT01720875]	Phase 2	16 participants (Actual)	Interventional	2013-08-09	Completed
Phase II Study of Bortezomib, Cyclophosphamide and Dexamethasone in Patients With Primary Systemic Light Chain Amyloidosis [NCT01072773]	Phase 2	2 participants (Actual)	Interventional	2010-03-31	Completed
UARK 2005-05, Coagulation-Related Effects of Velcade Treatment in Patients With Relapsed or Refractory Multiple Myeloma [NCT00569868]		11 participants (Actual)	Interventional	2005-08-31	Completed
Phase I Trial of PS-341 in Advanced Cancers [NCT00004002]	Phase 1	0 participants	Interventional	1999-07-31	Completed
Ofatumumab in Combination With Bortesomib in Patients With Relapsed or Refractory Low-Grade Non-Hodgkins Lymphoma [NCT01119794]	Phase 2	10 participants (Actual)	Interventional	2010-07-31	Terminated(stopped due to lack of accrual)
A Phase I Study of Ganetespib +/- Bortezomib in Patients With Relapsed and/or Refractory Multiple Myeloma [NCT01485835]	Phase 1	8 participants (Actual)	Interventional	2012-01-31	Completed
A Multi-Center, Single-Arm, Phase II Study of Vorinostat (V) in Combination With Pegylated Liposomal Doxorubicin (PLD) and Bortezomib (B) Followed by VB Maintenance in Patients With Relapsed and Relapsed/Refractory Multiple Myeloma [NCT01492881]	Phase 2	0 participants (Actual)	Interventional	2012-04-30	Withdrawn(stopped due to Doxil is currently unavailable)
A Phase I/II Trial of Romidepsin (Depsipeptide) and Bortezomib in Patients With Relapsed Myeloma [NCT00431990]	Phase 1/Phase 2	40 participants (Anticipated)	Interventional	2006-11-30	Recruiting
A Post Authorization Study, Designed to Learn More About the Safety and Efficacy of the Use of VELCADE (Bortezomib) in the Netherlands [NCT00440765]		331 participants (Actual)	Observational	2004-11-30	Completed
Phase II Study of PS341 (VELCADE) in Myelodysplastic Syndromes (MDS). EudraCT Number 2004-002935-23 [NCT00440076]	Phase 2	28 participants (Actual)	Interventional	2006-08-31	Terminated(stopped due to Low accrual)
A National, Open-Label, Multicenter, Randomized, Comparative Phase III Study of Induction Treatment With VBMCP-VBAD/Velcade Versus Thalidomide / Dexamethasone Versus Velcade / Thalidomide / Dexamethasone Followed by High Dose Intensive Therapy With Autolo [NCT00461747]	Phase 3	390 participants (Anticipated)	Interventional	2006-03-31	Completed
Single-center, Open Label Trial of Bortezomib as add-on Treatment in Relapsing Neuromyelitis Optica Spectrum Disorder [NCT02893111]	Phase 2	5 participants (Actual)	Interventional	2015-12-31	Completed
"Phase Ib Study of Weekly Cyclophosphamide-Bortezomib-Dexamethasone (CyBorD) With Daratumumab (DARA) in Transplant Eligible Patients With Newly Diagnosed Multiple Myeloma (MM): The CyBorD-DARA Study" [NCT02955810]	Phase 1	18 participants (Anticipated)	Interventional	2016-11-30	Active, not recruiting
Phase II Study of Bortezomib Dexamethasone and High-dose Melphalan in Patients With Relapse After High-dose Melphalan With Autologous Stem Cell Support [NCT00508209]	Phase 2	50 participants (Anticipated)	Interventional	2007-07-31	Active, not recruiting
A Phase II Multicenter Non-randomized Study to Assess Safety, Toxicity and Clinical Activity of the Association of Bortezomib(VELCADE)With Rituximab in Relapsed/Refractory Indolent Non Follicular and Mantle-cell Non-Hodgkin Lymphoma [NCT00509379]	Phase 2	48 participants (Actual)	Interventional	2006-09-30	Completed
Phase II, Open-Label, Multi-centre, 2-part Study to Assess the Safety, Tolerability, and Efficacy of Tipifarnib Plus Bortezomib in the Treatment of Newly Diagnosed Acute Myeloid Leukemia (AML) Unfit for Conventional Chemotherapy ( >18 Years) or in Patient [NCT00510939]	Phase 2	72 participants (Anticipated)	Interventional	2007-03-31	Recruiting
Phase I Clinical Trial of Dose Escalated Bortezomib + ATO (Arsenic Trioxide) + Melphalan as a Conditioning Regimen for Multiple Myeloma [NCT00504101]	Phase 1	0 participants (Actual)	Interventional	2007-06-30	Withdrawn(stopped due to Temporarily closed to accrual pending availablity of drug.)
Phase I Dose Escalating Trial of VELCADE (PS-341) in Combination With Idarubicin and Cytosine Arabinoside in Patients With Acute Myelogenous Leukemia [NCT00505700]	Phase 1	36 participants (Anticipated)	Interventional	2003-07-31	Completed
A Phase II Study Of PS-341 (NSC 681239) In Patients With Untreated Or Relapsed Waldenstrom's Macroglobulinemia [NCT00045695]	Phase 2	27 participants (Actual)	Interventional	2002-08-31	Completed
A Pilot Study of Standard-Dose Rituximab, Ifosfamide, Carboplatin and Etoposide (RICE) Plus Bortezomib (Velcade) in a Dose-Escalating Fashion for Patients With Relapsed or Primary Refractory Aggressive B-Cell Non-Hodgkin's Lymphoma Who Are Candidates for [NCT00515138]	Early Phase 1	7 participants (Actual)	Interventional	2007-05-31	Terminated(stopped due to Investigator left institution. 7 patients accrued and there is insufficient data to analyze.)
A Phase I/II Study of Liposomal Doxorubicin (Doxil)/Melphalan/Bortezomib (Velcade) in Relapsed/Refractory Multiple Myeloma [NCT00516191]	Phase 1/Phase 2	0 participants (Actual)	Interventional	2004-10-31	Withdrawn(stopped due to low accrual)
A Phase III, Randomized Study of Daratumumab, Cyclophosphamide, Bortezomib and Dexamethasone (Dara-VCD) Induction Followed by Autologous Stem Cell Transplant or Dara-VCD Consolidation and Daratumumab Maintenance in Patients With Newly Diagnosed AL Amyloid [NCT06022939]	Phase 3	338 participants (Anticipated)	Interventional	2023-10-31	Not yet recruiting
Phenotypic Personalized Medicine: Systematically Optimized Combination Therapy in Multiple Myeloma Using CURATE.AI [NCT03759093]	Phase 2/Phase 3	20 participants (Anticipated)	Interventional	2023-09-10	Recruiting
A Phase I Study of Samarium Sm-153 Lexidronam Combined With Bortezomib for Patients With Relapsed or Refractory Multiple Myeloma [NCT00316940]	Phase 1	36 participants (Anticipated)	Interventional	2005-12-31	Completed
A Phase 1 Study of PXD101 in Combination With Bortezomib (PS-341) in Patients With Advanced Solid Tumors and Lymphoma [NCT00348985]	Phase 1	55 participants (Actual)	Interventional	2006-03-31	Completed
A Phase I Trial of PS-341 in Combination With Topotecan in Advanced Solid Tumor Malignancies [NCT00541359]	Phase 1	54 participants (Actual)	Interventional	2004-01-31	Completed
A Phase I Study of Bortezomib and Temozolomide in Patients With Refractory Solid Tumors [NCT00544284]	Phase 1	25 participants (Actual)	Interventional	2005-01-31	Completed
An Open Label, Phase 2 Study to Evaluate Activity and Safety of Daratumumab in Combination With Bortezomib and Dexamethasone in Patients With Relapsed or Refractory Plasmablastic Lymphoma (DALYA Trial) [NCT04915248]	Phase 2	28 participants (Anticipated)	Interventional	2022-07-11	Recruiting
A Phase 1b/2a Multicenter, Open-label, Dose-escalation Study to Determine the Maximum Tolerated Dose, Assess the Safety, Tolerability, Pharmacokinetics and Efficacy of CC-220 as Monotherapy and in Combination With Other Treatments in Subjects With Multipl [NCT02773030]	Phase 1/Phase 2	532 participants (Anticipated)	Interventional	2016-10-14	Active, not recruiting
Phase II Study of VELCADE in Combination With Rituximab in Patients With Relapsed or Progressed Non Hodgkin's Follicular Lymphoma [NCT01830465]	Phase 2	45 participants (Actual)	Interventional	2006-08-31	Completed
Bortezomib-lenalidomide-dexamethasone Combined With Radiotherapy for Newly Diagnosed Solitary Plasmacytoma [NCT05248633]	Phase 2	220 participants (Anticipated)	Interventional	2022-04-21	Recruiting
A Randomized, Open-Label, Multicenter Phase 2 Study of the Combination of VELCADE, Rituximab, Cyclophosphamide, Doxorubicin, and Prednisone or Rituximab, Cyclophosphamide, Doxorubicin, Vincristine, and Prednisone in Patients With Newly Diagnosed Non-Germi [NCT01040871]	Phase 2	164 participants (Actual)	Interventional	2010-01-31	Completed
A Phase 3 Study Comparing Daratumumab, VELCADE (Bortezomib), Lenalidomide, and Dexamethasone (D-VRd) vs VELCADE, Lenalidomide, and Dexamethasone (VRd) in Subjects With Previously Untreated Multiple Myeloma Who Are Eligible for High-dose Therapy [NCT03710603]	Phase 3	690 participants (Actual)	Interventional	2018-12-14	Active, not recruiting
Phase I Study of PS-341 in Acute Myeloid Leukemias, Myelodysplastic Syndromes and Chronic Myeloid Leukemia in Blast Phase [NCT00005064]	Phase 1	30 participants (Actual)	Interventional	2000-02-29	Completed
A Phase II, Multi-Center, Open Label Study Of Melphalan, Prednisone, Thalidomide And Bortezomib In Advanced And Refractory Multiple Myeloma Patients [NCT00358020]	Phase 2	30 participants	Interventional	2004-11-30	Completed
A Phase II Trial of Bortezomib (NSC #681239) + Lenalidomide (Revlimid™, CC-5013) (NSC #703813) for Relapsed/Refractory Mantle Cell Lymphoma [NCT00553644]	Phase 2	53 participants (Actual)	Interventional	2007-11-15	Completed
An Open-Label Phase II Study of the Safety and Efficacy of Doxorubicin and Cyclophosphamide in Combination With Bortezomib, Lenalidomide, and Dexamethasone for Treatment of Patients With Newly Diagnosed Multiple Myeloma [NCT01481194]	Phase 2	35 participants (Actual)	Interventional	2011-11-30	Completed
A Phase 2 Study of VELCADE in Subjects With Relapsed or Refractory Mantle Cell Lymphoma [NCT00063713]	Phase 2	152 participants	Interventional	2003-06-30	Completed
An Open-Labeled, Randomized Study to Assess Two Different Strategies of Combining Dexamethasone and VELCADE in Patients With Relapsed Multiple Myeloma Who Have Failed Four or More Lines of Therapy [NCT00063791]		0 participants	Expanded Access		No longer available
A Phase I/II, Open Label, Dose Escalation Study to Determine the Tolerance and Preliminary Activity of PS-341 Plus Docetaxel in Patients With Advanced Androgen-Independent Prostate Cancer Requiring Chemotherapy [NCT00064610]	Phase 1/Phase 2	102 participants	Interventional	2002-12-31	Completed
Phase I Study of PS-341 (VELCADE) in Combination With 5FU/LV Plus Oxaliplatin in Patients With Advanced Colorectal Cancer [NCT00098982]	Phase 1	16 participants (Actual)	Interventional	2004-09-30	Completed
A Phase I Study of PS-341 (Velcade, Bortezomib) in Combination With 17-allylamino-17-demethoxygeldanamycin (17-AAG) in Patients With Relapsed or Refractory Hematologic Malignancies [NCT00103272]	Phase 1	74 participants (Actual)	Interventional	2005-04-30	Terminated
A Phase I Trial of PS-341 and Fludarabine for Relapsed and Refractory Indolent Non-Hodgkin's Lymphoma and Chronic Lymphocytic Leukemia [NCT00068315]	Phase 1	18 participants (Actual)	Interventional	2003-07-31	Completed
A Multicenter, Open-Label, Two-Stage, Phase II Study Of PS-341 (LDP-341, NSC # 681239) In Patients With Unresectable Or Metastatic Gastric Adenocarcinoma [NCT00074009]	Phase 2	0 participants	Interventional	2003-10-31	Completed
Phase I Dose Escalation Trial of Bortezomib in Combination With Thalidomide in Patients With Myelodysplasia [NCT00271804]	Phase 1	28 participants	Interventional	2005-06-30	Terminated(stopped due to New study with lenalidomide pending)
Phase II Trial of PS-341 in Patients With Hepatocellular Carcinoma [NCT00077441]	Phase 2	55 participants (Actual)	Interventional	2005-04-30	Completed
Phase I Trial of Bortezomib (VELCADE™) and Celecoxib in Patients With Advanced Solid Tumors [NCT00290680]	Phase 1	36 participants (Anticipated)	Interventional	2005-03-31	Completed
Comparison of Pharmacokinetics and Pharmacodynamics of Subcutaneous Versus Intravenous Administration of Bortezomib in Patients With Multiple Myeloma [NCT00291538]	Phase 1	20 participants (Anticipated)	Interventional	2006-02-28	Completed
Repeat-Dose Pharmacokinetics and Pharmacodynamics of Bortezomib in Patients With Relapsed Multiple Myeloma [NCT00080405]	Phase 1	40 participants	Interventional	2004-03-31	Completed
Phase II Trial of PS-341 (Bortezomib, NSC-681239) Followed by the Addition of Gemcitabine at Progression in Recurrent or Metastatic Nasopharyngeal Carcinoma [NCT00305734]	Phase 2	50 participants (Actual)	Interventional	2006-08-31	Completed
An Open-label Study of the Efficacy, Safety, and Tolerability of Oral SCIO-469 in Treatment of Relapsed, Refractory Patients With Multiple Myeloma [NCT00087867]	Phase 2	62 participants (Actual)	Interventional	2004-06-30	Completed
Phase I Trial of Bortezomib (PS-341; NSC 681239) and Alvocidib (Flavopiridol NSC 649890) in Patients With Recurrent or Refractory Indolent B-Cell Neoplasms [NCT00082784]	Phase 1	93 participants (Actual)	Interventional	2004-03-31	Completed
A Phase I Study of SAHA in Combination With Bortezomib in Relapsed and Refractory Multiple Myeloma [NCT00310024]	Phase 1	40 participants (Actual)	Interventional	2005-11-30	Completed
UARK 2008-03 Phase II Trial for Patients Not Qualifying for TT4 and TT5 Protocols Because of Prior Therapy (No Prior Transplant) [NCT00871013]	Phase 2	160 participants (Anticipated)	Interventional	2009-03-31	Active, not recruiting
Efficacy of First Line Bortezomib, Rituximab, Ibrutinib (B-RI) for Patients With Treatment Naive Waldenström's Macroglobulinemia [NCT03620903]	Phase 2	53 participants (Actual)	Interventional	2019-09-11	Active, not recruiting
Phase I/II Study of Neoadjuvant Bortezomib in Combination With Docetaxel and Cisplatin Followed by Surgery in Early Stage Non-Small Cell Lung Cancer. [NCT00313690]	Phase 1/Phase 2	0 participants (Actual)	Interventional	2006-04-30	Withdrawn(stopped due to Recruitment difficulties)
Velcade®, Thalidomide, Dexamethasone (VTD) Induction Therapy Followed By Melphalan, Prednisone, Thalidomide (MPT) Maintenance As a First Line Treatment For The Patients With Multiple Myeloma Who Are Non-Transplant Candidates [NCT00320476]	Phase 2	35 participants (Actual)	Interventional	2006-04-30	Completed
A Phase I Study Evaluating Combined Zevalin (Ibritumomab Tiuxetan) and Valcade (Bortezomib) in Relapsed/Refractory Low-Grade or Follicular B-Cell and Mantle Cell Lymphoma [NCT00334438]	Phase 1	12 participants (Actual)	Interventional	2006-07-31	Completed
A Randomized, Open-Label, Multicenter Study of Alimta® (Pemetrexed) Plus VELCADE® (Bortezomib) or Alimta Alone or VELCADE Alone in Subjects With Locally Advanced or Metastatic Non-Small Cell Lung Cancer Who Have Failed Prior Antineoplastic Therapy [NCT00343720]	Phase 2	0 participants	Interventional		Completed
A Phase II Study of Velcade® (Bortezomib) in Patients Stage IIIB OR IV Non-Small Cell Lung Cancer (NSCLC) Who Have Not Received Prior Chemotherapy [NCT00346645]	Phase 2	46 participants (Anticipated)	Interventional	2006-06-30	Terminated(stopped due to stopped after planned interim analysis for lack of efficacy)
A Phase I Trial of Bevacizumab and Bortezomib in Patients With Advanced Malignancy [NCT00428545]	Phase 1	104 participants (Actual)	Interventional	2007-01-31	Completed
Efficacy and Safety of Daratumumab in Combination With Bortezomib, Thalidomide, and Dexamethasone Regimens in Newly Diagnosed Multiple Myeloma With Renal Dysfunction in Real-World: A Non-interventional Prospective Multicenter Observational Study [NCT05561049]		120 participants (Anticipated)	Observational	2022-10-01	Not yet recruiting
EBV as Therapeutic Target: A Pilot Study of Inducing and Targeting EBV-TK in EBV-Positive Lymphomas by Combination of Bortezomib and Ganciclovir [NCT00093704]	Phase 1	1 participants (Actual)	Interventional	2005-03-31	Terminated(stopped due to study could not recruit any more patients)
A Phase I Trial Of 17-Allylaminogeldanamycin (17-AAG) And PS341 In Advanced Malignancies [NCT00096005]	Phase 1	36 participants (Actual)	Interventional	2004-11-30	Terminated
A Phase II Combination Trial of PS-341 and 5-FU/LV in Gastric and/or GE Junction Adenocarcinoma [NCT00103103]	Phase 2	0 participants	Interventional	2005-03-31	Terminated
A Phase II Study of VELCADE TM(PS-341) and Irinotecan in the Treatment of Progressive, Recurrent or Metastatic Cervical, Vulvar, or Vaginal Cancer [NCT00106262]	Phase 2	38 participants	Interventional	2005-03-31	Terminated(stopped due to Lack of accrual)
A Phase II Trial With VELCADE® (PS-341), Cytoxan (Cyclophosphamide), Dexamethasone and Thalomid® (VEL-CTD) in Previously Untreated Multiple Myeloma Patients [NCT00438841]	Phase 2	43 participants (Anticipated)	Interventional	2006-08-31	Active, not recruiting
An Observational Study To Determine Velcade (Bortezomib) Safety and Effectiveness at First Relapse After Participation In First Line HOVON-49/50 Clinical Studies (ADVANCE) [NCT00440479]		11 participants (Actual)	Observational	2006-09-30	Completed
International Single-Arm Protocol to Provide Expanded Access to Bortezomib for Patients With Multiple Myeloma Who Have Received at Least 2 Previous Lines of Therapy and Are Refractory to or Have Relapsed After Their Last Therapy for Multiple Myeloma [NCT00440635]		641 participants (Actual)	Observational	2004-01-31	Completed
Bortezomib-Doxorubicin-Dexamethasone as Treatment for Patients With Multiple Myeloma Presenting With Acute Renal Failure [NCT00401804]	Phase 2	72 participants (Actual)	Interventional	2006-02-28	Completed
A Phase II Study of Combination of Velcade, Doxil, and Dexamethasone (VDd) as First Line Therapy for Multiple Myeloma [NCT00116961]	Phase 2	40 participants (Actual)	Interventional	2005-06-30	Completed
A Multicenter, Open-Label, Phase 2 Study of VELCADE (Bortezomib) for Injection in Previously Treated Patients With Stage IIIB and IV Bronchioloalveolar Carcinoma and Adenocarcinoma With Bronchioloalveolar Features [NCT00117351]	Phase 2	0 participants	Interventional	2005-04-30	Terminated(stopped due to insufficient efficacy)
A Phase I/II Study of 153 Sm EDTMP (Quadramet™) and PS-341 (Velcade®) in Patients With Relapsed or Refractory Multiple Myeloma [NCT00478075]	Phase 1/Phase 2	50 participants (Anticipated)	Interventional	2005-09-30	Completed
A Phase 1b Open-label Study to Evaluate the Safety and Tolerability of Intravenous Modakafusp Alfa as Part of Combination Therapy in Adult Patients With Multiple Myeloma [NCT05556616]	Phase 1	120 participants (Anticipated)	Interventional	2022-10-27	Active, not recruiting
Phase I Study of a Combination of Doxil, Velcade, and Gemcitabine in Advanced Cancer [NCT00500422]	Phase 1	134 participants (Actual)	Interventional	2005-01-31	Completed
Study of Efficacy of PAD-regimen(Bortezomib,Pirarubicin and Dexamethasone) and TAD-regimen(Thalidomide,Pirarubicin and Dexamethasone) in Newly Diagnosed Multiple Myeloma,Influence in Concentration of Bone Metabolites,and the Relations With Different Cytog [NCT01249690]	Phase 4	100 participants (Anticipated)	Interventional	2010-06-30	Recruiting
A Phase II Study Evaluating the Efficacy and Safety of Bortezomib (Velcade™) Combined With ACVBP Regimen in Patients With Previously Untreated Peripheral T-cell Lymphoma [NCT00136565]	Phase 2	60 participants (Actual)	Interventional	2006-01-08	Completed
An Open-Label Phase I Study of the Safety and Efficacy of Bortezomib in Combination With CC-5013 in the Treatment of Subjects With Relapsed and Relapsed/Refractory Multiple Myeloma [NCT00153933]	Phase 1	58 participants (Actual)	Interventional	2004-08-31	Completed
A Phase II Trial of Bortezomib (Velcade) After Allogenic Peripheral Blood Stem Cell or Bone Marrow Transplantation for Patients With Multiple Myeloma [NCT00504634]	Phase 2	8 participants (Actual)	Interventional	2004-01-31	Completed
Sequential VAD (Vincristine, Adriamycin, Dexamethasone) and VTD (Velcade, Thalidomide, Dexamethasone) Induction Followed by HDT With ASCT and Maintenance Treatment With Velcade for Newly Diagnosed MM [NCT00378755]	Phase 2	62 participants	Interventional	2006-03-31	Recruiting
A Phase I Study of PS-341 (Bortezomib, Velcade) and Interferon-alpha-2b in Malignant Melanoma. [NCT01462773]	Phase 1	16 participants (Actual)	Interventional	2006-01-31	Completed
Comparison Between Rituximab + PLX + IVIG With and Without Bortezomib in the Treatment of Antibody Mediated Kidney Transplanted Rejection [NCT03737136]		20 participants (Anticipated)	Interventional	2019-11-01	Recruiting
A Phase 2 Clinical Trial of Rituximab, Cyclophosphamide, Bortezomib (VELCADE), and Dexamethasone (R-CYBOR-D) in Relapsed Low Grade and Mantle Cell Lymphoma [NCT00711828]	Phase 2	21 participants (Actual)	Interventional	2008-08-31	Completed
Tandem Autologous HCT/Nonmyeloablative Allogeneic HCT From HLA-Matched Related and Unrelated Donors Followed by Bortezomib Maintenance Therapy for Patients With High-Risk Multiple Myeloma [NCT00793572]	Phase 2	32 participants (Actual)	Interventional	2008-10-31	Completed
Combination High Dose Melphalan and Autologous PBSC Transplant With Bortezomib for Multiple Myeloma: A Dose and Schedule Finding Study [NCT00793650]	Phase 1/Phase 2	39 participants (Actual)	Interventional	2005-05-31	Terminated
Phase II Study of Vorinostat (SAHA, Zolinza) and Bortezomib (PS341, Velcade) as Third-Line Treatment in Patients With Advanced Non-Small Cell Lung Cancer [NCT00798720]	Phase 2	18 participants (Actual)	Interventional	2008-12-31	Completed
A Phase II Study To Determine The Safety and Efficacy Of The Combination of Vorinostat and Bortezomib In Patients With Relapsed Or Refractory T-Cell Non-Hodgkin's Lymphoma [NCT00810576]	Phase 2	1 participants (Actual)	Interventional	2009-01-31	Terminated(stopped due to Terminated due to slow accrual.)
Phase II Trial of Velcade (Bortezomib) in Combination With Temozolomide and Regional Radiation Therapy for Upfront Treatment of Patients With Newly-diagnosed Glioblastoma Multiforme [NCT00998010]	Phase 2	24 participants (Actual)	Interventional	2011-10-03	Completed
A Multicenter Prospective Phase II Study of Rituximab Combined, Lenalidomide, Dexamethasone Followed by Lenalidomide Maintenance in Patients With Newly Diagnosed Waldenström's Macroglobulinemia [NCT03697356]	Phase 2	54 participants (Anticipated)	Interventional	2019-03-06	Recruiting
A Prospective Randomized Trial Comparing Three Different Peripheral Stem Cell Mobilization Regimens in Patients With Symptomatic Multiple Myeloma or Lymphoma [NCT01146834]	Phase 3	47 participants (Actual)	Interventional	2011-03-31	Completed
A Phase III, Multicenter, Open-Label, Randomized Study to Evaluate the Efficacy and Safety of Belantamab Mafodotin in Combination With Pomalidomide and Dexamethasone (B-Pd) Versus Pomalidomide Plus Bortezomib and Dexamethasone (PVd) in Participants With R [NCT04484623]	Phase 3	357 participants (Anticipated)	Interventional	2020-10-01	Recruiting
Pilot Study of Bortezomib/Dexamethasone (BD), Followed By Autologous Stem Cell Transplantation and Maintenance Bortezomib/Dexamethasone For the Initial Treatment of Monoclonal Immunoglobulin Deposition Disease (MIDD) Associated With Multiple Myeloma and A [NCT01383759]		20 participants (Actual)	Interventional	2011-06-24	Completed
A Randomized, Blinded, Placebo-Controlled, Multicenter, Phase II Study of Bevacizumab in Combination With Bortezomib in Patients With Relapsed or Refractory Multiple Myeloma [NCT00473590]	Phase 2	102 participants (Actual)	Interventional	2007-06-30	Completed
Phase II Trial of Induction Therapy With Bortezomib and Dexamethasone Followed by High-Dose Melphalan and Stem Cell Transplantation in Patients With AL Amyloidosis [NCT01083316]	Phase 2	35 participants (Actual)	Interventional	2009-09-30	Completed
Phase I-II Study of Avastin®+ Bortezomib for Patients With Recurrent or Refractory Non-Squamous NSCLC [NCT00411593]	Phase 1/Phase 2	0 participants (Actual)	Interventional	2006-11-30	Withdrawn(stopped due to Lack of Patient Accrual)
AMN006 - Phase 2 Study of Daratumumab in Combination With Bortezomib and Dexamethasone in Newly Diagnosed Transplant Ineligible Multiple Myeloma Patients [NCT03695744]	Phase 2	27 participants (Actual)	Interventional	2019-10-02	Active, not recruiting
An Open-Label Phase 1/2 Study of the Safety and Efficacy of GCS-100 in Subjects With Relapsed or Relapsed/Refractory Multiple Myeloma [NCT00609817]	Phase 1	9 participants (Actual)	Interventional	2008-05-31	Terminated(stopped due to Lack of funding)
A Phase II Study of Velcade and Temsirolimus for Relapsed or Refractory B-cell Non-Hodgkin Lymphoma [NCT01281917]	Phase 2	40 participants (Actual)	Interventional	2011-02-28	Completed
The Efficacy of Velcade on Bone Tissue During Myelomatosis (Bone Marrow Cancer) [NCT00436059]	Phase 2	20 participants (Anticipated)	Interventional	2007-02-28	Completed
Bortezomib and Dexamethasone as Treatment and Maintenance for Multiple Myeloma Relapse An Australian Myeloma Forum Multi-Centre Phase II Trial [NCT00335348]	Phase 2	101 participants (Actual)	Interventional	2006-06-30	Completed
A Phase I/II Study of ATN-224 and Bortezomib in Patients With Multiple Myeloma Relapsed From or Refractory to Bortezomib [NCT00352742]	Phase 1/Phase 2	46 participants (Anticipated)	Interventional	2006-06-30	Terminated
Phase-I Study of Bortezomib (VELCADE) Plus ICE (Ifosfamide, Carboplatin, Etoposide) for Patients With Relapsed Classical Hodgkin Lymphoma [NCT00439361]	Phase 1	14 participants (Actual)	Interventional	2007-02-28	Completed
A National, Open-Label, Multicenter, Randomized, Comparative Phase III Study of Induction Treatment With Melphalan/Prednisone/Velcade Versus Thalidomide / Prednisone / Velcade and Maintenance Treatment With Thalidomide / Velcade Versus Prednisone / Velcad [NCT00443235]	Phase 3	260 participants (Anticipated)	Interventional	2005-03-31	Completed
[NCT01248923]	Phase 1	55 participants (Actual)	Interventional	2010-12-31	Completed
Phase II Study of Bortezomib Consolidation After High Dose Therapy and Autologous Stem Cell Transplantation for Multiple Myeloma [NCT01517724]	Phase 2	40 participants (Actual)	Interventional	2009-12-31	Completed
Lenalidomide and Low Dose Dexamethasone Versus Bortezomib, Lenalidomide and Low Dose Dexamethasone for Induction, in Patients With Previously Untreated Multiple Myeloma [NCT01530594]	Phase 3	440 participants (Actual)	Interventional	2009-01-31	Completed
A Pilot Study of G-CSF to Disrupt the Bone Marrow Microenvironment in Bortezomib-, Carfilzomib-, or IMID-Refractory Multiple Myeloma [NCT01537861]	Early Phase 1	7 participants (Actual)	Interventional	2012-06-30	Terminated(stopped due to Unexpected toxicity (2 early deaths))
Phase II Trial of Bortezomib and Bendamustine in the Treatment of Relapsed/Refractory Myeloma [NCT01315873]	Phase 2	24 participants (Actual)	Interventional	2011-09-30	Terminated(stopped due to PI left the institution before all data analysis was completed)
Randomised Comparisons, in Myeloma Patients of All Ages, of Thalidomide, Lenalidomide, Carfilzomib and Bortezomib Induction Combinations, and of Lenalidomide and Combination Lenalidomide Vorinostat as Maintenance (Myeloma XI) [NCT01554852]	Phase 3	4,420 participants (Actual)	Interventional	2010-05-31	Active, not recruiting
A Phase I and Pharmacologic Study of the Proteasome Inhibitor PS-341 in Patients With Advanced Solid Tumors and B-cell Lymphoproliferative Disorders [NCT00006362]	Phase 1	0 participants	Interventional	1999-11-30	Completed
A Phase II Trial of PS-341 in Combination With Paclitaxel and Carboplatin for Metastatic Adenocarcinoma of the Lower Esophagus, Gastroesophageal Junction, and Gastric Cardia [NCT00107341]	Phase 2	37 participants (Actual)	Interventional	2005-08-31	Completed
Phase I Evaluation of the Safety of PS 341 in the Treatment of Recurrent Gliomas [NCT00006773]	Phase 1	42 participants (Actual)	Interventional	2001-05-31	Terminated(stopped due to Administratively complete.)
An Open-Label, Randomized Study of VELCADE/Melphalan/Prednisone Versus Melphalan/Prednisone in Subjects With Previously Untreated Multiple Myeloma [NCT00111319]	Phase 3	0 participants	Interventional	2004-12-31	Completed
UARK 2005-01, A Phase III Study of Velcade, Thalidomide, and Dexamethasone (VTD) With or Without Adriamycin® in Relapsed/Refractory Patients [NCT00111748]	Phase 3	180 participants (Anticipated)	Interventional	2005-02-28	Completed
A Phase II Trial of Docetaxel Plus Cetuximab and Docetaxel Plus Bortezomib (NSC #681239, IND #58443) in Advanced Non-Small Cell Lung Cancer Patients With Performance Status (PS) 2 [NCT00118183]	Phase 2	62 participants (Actual)	Interventional	2005-07-31	Completed
A 3-Arm Randomized Phase II Study of Standard-of-Care vs. Bortezomib Based Graft-Versus-Host Disease Regimen for Reduced-Intensity Conditioning Hematopoietic Stem Cell Transplantation Patients Lacking HLA-matched Related Donors [NCT01754389]	Phase 2	138 participants (Actual)	Interventional	2013-01-31	Completed
A Phase II Study of Subcutaneous Bortezomib in Combination With Chemotherapy (VXLD) for Relapsed/Refractory Adult Acute Lymphoblastic Leukemia [NCT01769209]	Phase 2	18 participants (Actual)	Interventional	2013-03-31	Completed
Phase II Study of a Proteasome Inhibitor, PS-341 (NSC 681239) in Chronic Myelogenous Leukemia (CML) in Chronic or Accelerated Phase [NCT00023881]	Phase 2	7 participants (Actual)	Interventional	2001-07-02	Terminated(stopped due to Lack of efficacy)
A Phase I Study of Concomitant Therapy With Proteasome Inhibitor PS-341 and Radiation in Patients With Recurrent or Metastatic Squamous Cell Carcinoma of the Head and Neck [NCT00011778]	Phase 1	25 participants (Actual)	Interventional	2001-02-22	Completed
A Phase I Study of PS-341 (NSC 681239), Carboplatin, and Etoposide in Patients With Advanced Solid Tumors Refractory to Standard Therapy [NCT00027898]	Phase 1	27 participants (Actual)	Interventional	2002-01-31	Completed
Phase I Trial of Bortezomib (NSC 681239, IND#58443) and Carboplatin in Recurrent or Progressive Epithelial Ovarian Cancer or Primary Peritoneal Cancer [NCT00028912]	Phase 1	0 participants	Interventional	2001-11-30	Completed
Phase II Study of PS-341 in Metastatic Neuroendocrine Tumors [NCT00017199]	Phase 2	0 participants	Interventional	2001-04-30	Completed
A Phase II Study Of PS-341 In Metastatic Non-Small Cell Lung Cancer [NCT00040768]	Phase 2	35 participants (Actual)	Interventional	2002-04-30	Terminated(stopped due to Administratively complete.)
A Phase II Study Of PS-341 In Patients With Metastatic Colorectal Cancer [NCT00052507]	Phase 2	0 participants	Interventional	2003-01-31	Completed
A Randomized, Multicenter, Open-Label, Phase II Study Of VELCADE Alone Or VELCADE Plus Docetaxel In Previously Treated Patients With Advanced Non-Small Cell Lung Cancer [NCT00064012]	Phase 2	4 participants (Actual)	Interventional	2003-05-31	Completed
A Phase I, Open Label, Dose Escalation Study of PS-341 Plus Docetaxel in Treatment-Naive or Previously Treated Patients With Advanced Non-Small Cell Lung Cancer or Other Solid Tumors [NCT00064636]	Phase 1	46 participants	Interventional	2002-12-31	Terminated
A Phase II Study Of PS-341 (VELCADE) In Chemotherapy-Refractory Diffuse Large B-Cell Lymphoma (DLBCL) [NCT00066508]	Phase 2	7 participants (Actual)	Interventional	2003-05-31	Completed
A Phase I and Pharmacokinetic Study of Oxaliplatin (Eloxatin™) in Combination With Bortezomib (PS-341, Velcade™) in Patients With Advanced Malignancy [NCT00066625]	Phase 1	30 participants (Actual)	Interventional	2003-07-31	Terminated(stopped due to Administratively complete.)
A Phase II Trial of Gemcitabine, Carboplatin and PS-341 (NSC-681239) in the First-Line Treatment of Advanced Non-Small Cell Lung Cancer (NSCLC) [NCT00075751]	Phase 2	99 participants (Actual)	Interventional	2004-01-31	Completed
Phase II Trial of PS-341 (NSC 681239) Followed by the Addition of Doxorubicin at Progression in Advanced Adenoid Cystic Carcinoma of the Head and Neck [NCT00077428]	Phase 2	37 participants (Actual)	Interventional	2004-06-30	Completed
A Phase I Study of PS-341 (Velcade, Bortezomib) in Pediatric Patients With Refractory/Recurrent Leukemias [NCT00077467]	Phase 1	36 participants (Actual)	Interventional	2004-01-31	Completed
Safety and Efficacy of Bortezomib Plus Dexamethasone for Acquired Pure Red Cell Aplasia Failure or Relapse After First-line Treatment: A Prospective Phase II Trial [NCT04423367]	Phase 2	17 participants (Anticipated)	Interventional	2020-09-13	Recruiting
A Phase II Study of PS-341 (Bortezomib) in Patients With Relapsed or Refractory Hodgkin's Lymphoma [NCT00082966]	Phase 2	43 participants (Actual)	Interventional	2004-03-31	Completed
A Phase 2 Study of Velcade™ in Subjects With Relapsed or Refractory Follicular B-Cell Lymphoma [NCT00136591]	Phase 2	87 participants (Actual)	Interventional	2005-09-30	Terminated(stopped due to An arm closed due to lack of efficacy)
Phase II Study of Velcade in Waldenstrom's Macroglobulinemia [NCT00142129]	Phase 2	27 participants	Interventional	2003-12-31	Completed
VELCADEXA: A National, Multi-Center, Open-Label Study of Pretransplant Induction With Alternating VELCADE and Dexamethasone (VEL/Dex) in Younger (< 65 Yrs) Untreated Multiple Myeloma Patients. [NCT00391157]	Phase 2	40 participants (Actual)	Interventional	2005-08-31	Completed
A Phase I Study Of PS-341 In Pediatric Patients With Refractory Solid Tumors [NCT00021216]	Phase 1	36 participants (Actual)	Interventional	2001-11-30	Completed
Velcade/Dexamethasone/Cyclophosphamide(PCD) Versus Rituximab /Dexamethasone/Cyclophosphamide(RCD) for the Treatment of Patients With Waldenstrom's Macroglobulinemia [NCT02971982]	Phase 1/Phase 2	40 participants (Anticipated)	Interventional	2016-10-31	Recruiting
Phase II Trial Of PS-341 In Metastatic Breast Cancer [NCT00025584]	Phase 2	35 participants (Actual)	Interventional	2001-08-31	Completed
A Phase I and Pharmacologic Study of the Proteasome Inhibitor PS-341 in Combination With Paclitaxel and Carboplatin in Patients With Advanced Malignancies [NCT00028587]	Phase 1	96 participants (Actual)	Interventional	2001-12-31	Completed
A Phase II Dose-Response Study of Velcade® and Bone Formation in Patients With Relapsed/Refractory Multiple Myeloma [NCT00128921]	Phase 2	18 participants (Actual)	Interventional	2006-04-30	Terminated(stopped due to study terminated due to low accrual)
Pilot Study to Evaluate the Tolerability of Velcade (Bortezomib) and Pravastatin for the Treatment of Relapsed Leukemia Following Allogeneic Hematopoietic Stem Cell Transplantation in Children [NCT02484261]	Phase 1	10 participants (Actual)	Interventional	2015-05-31	Terminated(stopped due to Contractual/Funding/Accrual)
A Phase I and Pharmacodynamic Study of Proteasome Inhibitor, PS-341, in Combination With Doxorubicin in Patients With Advanced Solid Tumors [NCT00023855]	Phase 1	0 participants	Interventional	2001-06-30	Completed
A Phase II Study of PS-341 in the Treatment of Metastatic Malignant Melanoma [NCT00024011]	Phase 2	50 participants (Actual)	Interventional	2001-07-31	Completed
A Randomized, Multicenter, Open-Label, Phase 2b Study of VELCADE Alone and VELCADE Plus Irinotecan in Patients With Relapsed or Refractory Colorectal Carcinoma [NCT00051987]	Phase 2	175 participants	Interventional	2002-12-31	Completed
A Phase I Study Of PS-341 In Combination With Gemcitabine And Carbloplatin In Selected Stage IIIB Or IV Non-Small Cell Lung Cancer [NCT00052338]	Phase 1	34 participants (Actual)	Interventional	2002-09-30	Completed
A Randomized Phase II Trial of PS-341 and Gemcitabine in Patients With Metastatic Pancreatic Adenocarcinoma [NCT00052689]	Phase 2	88 participants (Anticipated)	Interventional	2002-12-31	Completed
Impact of First Autologous Transplant on Minimal Residual Disease Markers in Previously Untreated Myeloma Undergoing Initial Treatment With Velcade Based Therapy [NCT01215344]	Phase 2	36 participants (Actual)	Interventional	2010-11-30	Completed
A Phase II Trial of PS-341 in Patients With Renal Cell Cancer [NCT00025376]	Phase 2	23 participants (Actual)	Interventional	2001-10-31	Completed
A Phase II Randomized Study of Three Subcutaneous Bortezomib-based Consolidation Treatments for Patients Completing Induction Therapy and Stem Cell Transplantation for Newly Diagnosed Multiple Myeloma [NCT01706666]	Phase 2	3 participants (Actual)	Interventional	2012-12-07	Completed
A Multi-Institutional, Open-Label, Two-Group, Phase II Study of PS-341 (LDP-341, NSC #681239) in Patients With Advanced or Metastatic Sarcoma [NCT00027716]	Phase 2	0 participants	Interventional	2001-10-31	Completed
A Phase I Study of PS-341 in Combination With Paclitaxel in Metastatic Solid Tumors [NCT00030368]	Phase 1	45 participants (Actual)	Interventional	2001-11-30	Completed
Phase I Study of Weekly Intravenous PS-341 (Bortezomib) Plus Mitoxantrone in Patients With Advanced Androgen-Independent Prostate Cancer (AI-PCa) [NCT00059631]	Phase 1	42 participants (Actual)	Interventional	2003-03-20	Completed
An International, Non-Comparative, Open-Label Study of PS-341 Administered to Patients With Multiple Myeloma Who Experienced Relapsed or Progressive Disease After Receiving at Least Four Previous Treatment Regimens or Experienced Progressive Disease After [NCT00063726]	Phase 3	600 participants	Interventional	2002-04-30	Completed
Phase II Trial of PS-341 (Bortezomib) in Patients With Previously Treated Advanced Urothelial Tract Transitional Cell Carcinoma [NCT00072150]	Phase 2	40 participants (Actual)	Interventional	2003-10-31	Completed
A Phase II Trial of PS-341 (NSC-681239) in Patients With Platinum-Treated Extensive Stage Small Cell Lung Cancer [NCT00068289]	Phase 2	0 participants	Interventional	2003-09-30	Completed
A Phase 1b Study Evaluating the Safety and Pharmacokinetics of ABT-199 in Relapsed or Refractory Multiple Myeloma Subjects Who Are Receiving Bortezomib and Dexamethasone as Their Standard Therapy [NCT01794507]	Phase 1	66 participants (Actual)	Interventional	2012-11-19	Completed
A Dose Finding Phase I Trial of the Combination of Topotecan and PS-341, a Novel Proteasome Inhibitor, in Advanced Malignancies [NCT00068484]	Phase 1	25 participants (Actual)	Interventional	2003-07-31	Completed
An Extension or Re-Treatment Study of Bortezomib to Patients With Relapsed or Refractory Multiple Myeloma [NCT00216697]	Phase 2	13 participants (Actual)	Interventional	2005-03-31	Completed
A Pilot Study of Combination Therapy With VELCADE, Doxil, and Dexamethasone (VDd) in Multiple Myeloma [NCT00135187]		30 participants (Actual)	Interventional	2004-07-31	Completed
A Phase II Study of Bortezomib in Combination With Dexamethasone in Patients With Relapsed Hodgkin's Lymphoma [NCT00148018]	Phase 2	37 participants	Interventional	2005-03-31	Terminated
A Randomized, Multicenter, Open-Label, Phase 2 Study of VELCADE Alone or VELCADE Plus Docetaxel in Previously Treated Patients With Advanced Non-Small Cell Lung Cancer [NCT00051974]	Phase 2	155 participants	Interventional	2002-12-31	Completed
Phase II Study of the Association of Velcade to R-CHOP in the Treatment of B Cell Lymphoma [NCT00169468]	Phase 2	48 participants (Actual)	Interventional	2005-01-31	Completed
A Phase II Study of Bortezomib (Velcade®, PS-341) and Docetaxel for Patients With Hormone Refractory Prostate Cancer [NCT00183937]	Phase 2	15 participants (Actual)	Interventional	2005-04-30	Completed
[NCT00184015]	Phase 1/Phase 2	50 participants (Actual)	Interventional	2005-08-18	Active, not recruiting
A Phase I Study Evaluating the Safety and Tolerability of PS-341(Bortezomib)and Carboplatin in Patients With Platinum- and Taxane-Resistant Recurrent Ovarian Cancer, Primary Peritoneal Cancer, and Fallopian Tube Cancer [NCT00059618]	Phase 1	21 participants (Actual)	Interventional	2003-04-30	Completed
Phase I/II Trial of VELCADE® (Bortezomib) in Combination With Mitoxantrone and Etoposide for Relapsed or Refractory Acute Leukemias [NCT00410423]	Phase 1/Phase 2	55 participants (Actual)	Interventional	2006-01-31	Completed
"Phase II Trial of VIPER Chemotherapy in Relapsed and Refractory Diffuse Large B-cell Lymphoma (NHL)" [NCT00504751]	Phase 2	15 participants (Actual)	Interventional	2007-05-31	Completed
A Prospective, Multi-center, Open-label, Single-arm, Phase II Study of Bortezomib/Dexamethasone Therapy in Patients With Relapsed and/or Refractory Cutaneous T-cell Lymphoma [NCT03487133]	Phase 2	32 participants (Actual)	Interventional	2017-09-19	Completed
Targeted Therapy for High Immunologic Risk Renal Transplant Recipients: A Prospective, Randomized, Open-Label Pilot Study of B-Cell Depleting Therapy in Combination With Anti-Thymocyte Globulin [Rabbit] (Thymoglobulin®, Genzyme), Tacrolimus (Prograf®, Ast [NCT00782821]	Phase 4	40 participants (Actual)	Interventional	2008-09-30	Completed
An Open Label Phase I/II Study of the Safety and Efficacy of Cyclophosphamide, Bortezomib (VELCADE), Pegylated Liposomal Doxorubicin (DOXIL), and Dexamethasone, (CVDD) in Newly Diagnosed Patients With Multiple Myeloma [NCT00750815]	Phase 1/Phase 2	58 participants (Actual)	Interventional	2008-09-30	Completed
Comparing and Combining Bortezomib and Mycophenolate in SSc Pulmonary Fibrosis Grant Number: R34HL122558 [NCT02370693]	Phase 2	9 participants (Actual)	Interventional	2016-03-31	Completed
B-Cell Targeted Therapy for Acute Renal Allograft Rejection With an Antibody Mediated Component: A Prospective, Randomized, Open-Label Study [NCT00771875]	Phase 2	30 participants (Actual)	Interventional	2008-09-30	Completed
Risk-Adapted Intravenous Melphalan With Stem Cell Transplant and Adjuvant Bortezomib and Dexamethasone for Recently Diagnosed Untreated Patients With Systemic Light-Chain (AL) Amyloidosis [NCT00458822]	Phase 2	40 participants (Actual)	Interventional	2007-02-28	Completed
Combination Pegylated Liposomal Doxorubicin, Bortezomib, Cyclophosphamide, and Dexamethasone for Multiple Myeloma (PLD-BCD) [NCT00849251]	Phase 1/Phase 2	31 participants (Actual)	Interventional	2008-11-30	Terminated(stopped due to One of the study drugs is not available.)
A Phase II Study of Subcutaneous (SC) Bortezomib-Regimens for Patients With Relapsed/Refractory Multiple Myeloma (MM) Failing Prior Intravenous (IV) Bortezomib-Containing Regimens [NCT01695330]	Phase 2	5 participants (Actual)	Interventional	2012-05-31	Terminated(stopped due to Terminated by Sponsor of this study.)
Phase II Subcutaneous VELCADE and Oral Cyclophosphamide-based Induction + Sequential VELCADE and Revlimid Maintenance for Newly Diagnosed Multiple Myeloma in Non-transplant Candidates: An Entirely Non-intravenous Regimen [NCT01729338]	Phase 2	17 participants (Actual)	Interventional	2012-12-19	Terminated
A Phase 1b/2 Study of Selinexor (KPT-330) in Combination With Backbone Treatments for Relapsed/Refractory Multiple Myeloma and Newly Diagnosed Multiple Myeloma [NCT02343042]	Phase 1/Phase 2	518 participants (Actual)	Interventional	2015-10-31	Active, not recruiting
A Randomized Phase II Trial of Decitabine-Based Induction Strategies for Patients >/= 60 Years Old With Acute Myeloid Leukemia (AML) [NCT01420926]	Phase 2	165 participants (Actual)	Interventional	2011-11-16	Completed
Phase II Study of Subcutaneous Bortezomib for Patients With Low or Intermediate-1 Risk Myelodysplastic Syndrome [NCT01891968]	Phase 2	15 participants (Actual)	Interventional	2013-08-07	Completed
A Phase I Study of Suberoylanilide Hydroxamic Acid (SAHA) in Combination With Bortezomib in Patients With Advanced Malignancies [NCT00227513]	Phase 1	66 participants (Actual)	Interventional	2005-07-31	Completed
Etude Multicentrique Ouverte Randomisée de Phase III Comparant l'Association de VELCADE®-Dexaméthasone à la Chimiothérapie de Type VAD Pour le Traitement Des Patients Porteurs de Myélome Multiple de Novo Jusqu'à l'âge de 65 Ans [NCT00200681]	Phase 3	493 participants (Actual)	Interventional	2005-06-30	Completed
[NCT00261612]	Phase 2	16 participants	Interventional	2005-01-31	Active, not recruiting
Consolidation Therapy With Bortezomib in Patients With Multiple Myeloma Aged 61 to 75 [NCT00416208]	Phase 3	154 participants (Actual)	Interventional	2006-10-31	Completed
A Dose Escalation Study of R115777 (Zarnestra) Combined With Velcade® (PS-341) in Patients With Relapsed Multiple Myeloma. [NCT00243035]	Phase 1/Phase 2	64 participants (Anticipated)	Interventional	2005-08-31	Terminated
Phase I Study of PS-341 in Combination With 5-Fluorouracil and External Beam Radiotherapy For The Treatment Of Locally Advanced And Metastatic Rectal Cancer [NCT00280176]	Phase 1	11 participants (Actual)	Interventional	2003-04-30	Completed
Phase I, Open Label, Clinical Study to Determine the Maximum Tolerated Dose (MTD) of Oral Dovitinib (TKI258) When Given in Combination With Bortezomib and Dexamethasone for the Treatment of Relapsed/Refractory Multiple Myeloma Patients [NCT01680796]	Phase 1	0 participants (Actual)	Interventional	2013-02-28	Withdrawn(stopped due to The target drug, dovitinib, failed as a single agent in prior studies in patients with heavily treated multiple myeloma.)
Evaluation of VELCADE (Botezomib) for Injection Employed as Re-Treatment for Efficacy, Safety, and Tolerability [NCT00257114]	Phase 4	0 participants	Interventional		Completed
A Phase I Study of Arsenic Trioxide and Ascorbic Acid (ATO/AA) in Combination With Low Dose Velcade-Thalidomide-Dexamethasone (VTD) in Relapsed/Refractory Multiple Myeloma (MM) [NCT00258245]	Phase 1	5 participants (Actual)	Interventional	2005-05-31	Completed
An Open-Label Study to Assess the Effect of Omeprazole Administration on the Pharmacokinetics of VELCADE in Subjects With Either Advanced Solid Tumors or Non-Hodgkin's Lymphoma [NCT00298779]	Phase 1	20 participants (Anticipated)	Interventional		Completed
A Phase II Trial of VELCADE in Patients With Metastatic or Locally Recurrent Nasopharyngeal Carcinoma [NCT00367718]	Phase 2	0 participants (Actual)	Interventional		Withdrawn(stopped due to PI left JHU and is not able to be reached for updates)
VELCADE (Bortezomib) for Injection - Phase II Study of Bortezomib and Rituximab in Relapsed or Refractory Non-Hodgkin's Lymphoma [NCT00265928]	Phase 2	46 participants (Anticipated)	Interventional		Terminated(stopped due to Withdrawn for poor accrual)
Consolidation Therapy With Bortezomib <= 60 Year Old Patients With Multiple Myeloma [NCT00416273]	Phase 3	217 participants (Actual)	Interventional	2006-12-31	Completed
An Open-Label Randomized Study of Subcutaneous and Intravenous VELCADE in Subjects With Previously Treated Multiple Myeloma [NCT00722566]	Phase 3	222 participants (Actual)	Interventional	2008-07-31	Completed
Evaluation of Safety and Efficacy of VELCADE as Maintenance Treatment in Patients With Multiple Myeloma Following High-Dose Melphalan Treatment and Autologous PBSCT (Minimal Residual Disease, Partial Remission or Stable Disease) [NCT00311337]	Phase 2	61 participants	Interventional	2005-10-31	Recruiting
A Phase II Trial of Bortezomib + Ascorbic Acid + Melphalan (BAM) Combination Therapy for Patients With Newly Diagnosed Multiple Myeloma [NCT00317811]	Phase 2	35 participants (Anticipated)	Interventional	2005-11-30	Completed
A Randomized, Non-comparative, Multicenter, Open-Label, Phase 2 Study of Tarceva™ (Erlotinib) Alone and of Tarceva Plus VELCADE* (Bortezomib) for Injection in Patients With Relapsed or Refractory, Locally Advanced or Metastatic Non-Small Cell Lung Cancer [NCT00283634]	Phase 2	0 participants	Interventional	2005-08-31	Terminated(stopped due to insufficient efficacy)
A Phase II Trial of PS-341 in Combination With Paclitaxel and Carboplatin for the Treatment of Metastatic Melanoma [NCT00288041]	Phase 2	36 participants (Anticipated)	Interventional	2005-10-31	Completed
Phase II Trial of Bendamustine, Bortezomib, and Rituximab in Patients With Previously Untreated Low Grade Lymphoma [NCT01029730]	Phase 2	55 participants (Actual)	Interventional	2010-03-31	Completed
2015-12: A Phase II Study Exploring the Use of Early and Late Consolidation/Maintenance With Anti-CD38 (Protein) Monoclonal Antibody to Improve Progression Free Survival in Patients With Newly Diagnosed Multiple Myeloma [NCT03004287]	Phase 2	50 participants (Anticipated)	Interventional	2017-07-01	Active, not recruiting
Randomized Phase III Trial of Bortezomib, Lenalidomide, and Dexamethasone (VRd) Versus Carfilzomib, Lenalidomide, and Dexamethasone (CRd) Followed by Limited or Indefinite Duration Lenalidomide Maintenance in Patients With Newly Diagnosed Symptomatic Mult [NCT01863550]	Phase 3	1,087 participants (Actual)	Interventional	2013-12-06	Active, not recruiting
Clinical Protocol Bortezomib Consolidation in Patients With Myeloma Following Treatment With High-dose Melphalan and Autologous Stem Cell Support. A Randomised NMSG Trial (15/05) [NCT00417911]	Phase 3	400 participants (Anticipated)	Interventional	2005-12-31	Completed
A Phase I Study of the Raf Kinase/VEGFR Inhibitor BAY 43-9006 in Combination With the Proteasome Inhibitor PS-341 in Patients With Advanced Malignancies [NCT00303797]	Phase 1	50 participants (Actual)	Interventional	2005-12-31	Completed
A Phase I Open-labeled, Dose-escalation, Safety Study of the Combination of Velcade and Chemoradiation for the Treatment of Cancer Patients [NCT00329589]	Phase 1	54 participants (Actual)	Interventional	2005-09-30	Completed
A Multicenter Open-Label Phase II Study of Velcade Combined With High-Dose Dexamethasone in Patients With Newly Diagnosed Multiple Myeloma [NCT00337506]	Phase 2	50 participants	Interventional	2003-08-31	Terminated
Phase I Study of ABT-888 in Combination With Bortezomib and Dexamethasone in Patients With Relapsed Refractory Myeloma [NCT01495351]	Phase 1	19 participants (Actual)	Interventional	2011-10-31	Completed
A Phase 1, Multicenter, Open Label, Dose-escalation Study to Determine the Maximum Tolerated Dose for the Combination of Pomalidomide (POM), Bortezomib (BTZ) and Low-Dose Dexamethasone (LDDEX) in Subjects With Relapsed or Refractory Multiple Myeloma (MM) [NCT01497093]	Phase 1	34 participants (Actual)	Interventional	2012-02-15	Completed
A Phase I Study of the HER1, HER2 Dual Kinase Inhibitor, Lapatinib Plus the Proteosomal Inhibitor Bortezomib in Patients With Advanced Malignancies [NCT01497626]	Phase 1	15 participants (Actual)	Interventional	2011-09-30	Terminated(stopped due to Drug support withdrawn)
A Phase I Study of Panobinostat in Combination With Bortezomib in the Treatment of Relapsed and/or Refractory Mantle Cell Lymphoma [NCT01504776]	Phase 1	3 participants (Actual)	Interventional	2011-04-30	Completed
Daratumumab in Combination With Bortezomib and Dexamethasone in Subjects With Relapsed or Relapsed and Refractory Multiple Myeloma and Severe Renal Impairment Including Subjects Undergoing Hemodialysis: A Phase 2, Open-label, Multicenter Trial [NCT02977494]	Phase 2	22 participants (Actual)	Interventional	2016-06-30	Completed
A Phase II, Open-Label Trial of Bortezomib (VELCADE®) in Combination With Gemcitabine and Cisplatin in Patients With Locally Advanced or Metastatic Non-Small Cell Lung Cancer [NCT01633645]	Phase 2	53 participants (Actual)	Interventional	2009-06-30	Completed
UARK 2010-35, A Phase II Study of Expanded Natural Killer Cell Therapy for Multiple Myeloma [NCT01313897]	Phase 2	10 participants (Actual)	Interventional	2011-01-31	Completed
Short Course of Bortezomib in Anemic Patients With Refractory Cold Agglutinin Disease [NCT01696474]	Phase 2	21 participants (Actual)	Interventional	2012-12-31	Completed
Phase 1 Clinical Trial of a Novel CDK Inhibitor Dinaciclib (SCH 727965) in Combination With Bortezomib and Dexamethasone in Relapsed Multiple Myeloma [NCT01711528]	Phase 1	41 participants (Actual)	Interventional	2012-12-19	Completed
A Phase 3 Randomized Study Comparing Daratumumab, Bortezomib, Lenalidomide and Dexamethasone (DVRd) Followed by Ciltacabtagene Autoleucel Versus Daratumumab, Bortezomib, Lenalidomide and Dexamethasone (DVRd) Followed by Autologous Stem Cell Transplant (AS [NCT05257083]	Phase 3	750 participants (Anticipated)	Interventional	2023-10-10	Recruiting
MRD-Guided Sequential Therapy For Deep Response in Newly Diagnosed Multiple Myeloma - MASTER-2 Trial [NCT05231629]	Phase 2	300 participants (Anticipated)	Interventional	2023-12-13	Recruiting
A Phase 3, Two-Stage, Randomized, Multicenter, Open-label Study Comparing Iberdomide, Daratumumab and Dexamethasone (IberDd) Versus Daratumumab, Bortezomib, and Dexamethasone (DVd) in Subjects With Relapsed or Refractory Multiple Myeloma (RRMM) [NCT04975997]	Phase 3	864 participants (Anticipated)	Interventional	2022-06-23	Recruiting
UARK 2008-02, A Phase II Trial for High-risk Myeloma Evaluation Accelerating and Sustaining Complete Remission (AS-CR) by Applying Non-host-exhausting and Timely Dose-reduced MEL-80-VRD-PACE Tandem Transplants [NCT00869232]	Phase 2	90 participants (Actual)	Interventional	2008-10-31	Active, not recruiting
Prospective Comparison the Pharmacokinetics of Subcutaneous Versus Intravenous Administration of Bortezomib in Newly Diagnosed Patients of Multiple Myeloma in China. [NCT01812096]	Phase 1/Phase 2	20 participants (Anticipated)	Interventional	2014-05-31	Active, not recruiting
Desensitization With Bortezomib Before a Living Kidney Donation [NCT01842074]	Phase 4	10 participants (Anticipated)	Interventional	2013-03-31	Recruiting
A Randomized Controlled Study of Velcade (Bortezomib) Plus Thalidomide Plus Dexamethasone Compared to Thalidomide Plus Dexamethasone for the Treatment of Myeloma Patients Progressing or Relapsing After Autologous Transplantation [NCT00256776]	Phase 3	269 participants (Actual)	Interventional	2005-07-31	Terminated
Phase II Study Assessing the Efficacy and Toxicity of PK--directed Intravenous Busulfan in Combination With High--Dose Melphalan and Bortezomib as Conditioning Regimen for First--Line Autologous Hematopoietic Stem Cell Transplantation in Patients With Mul [NCT01605032]	Phase 2	19 participants (Actual)	Interventional	2012-02-29	Completed
A Phase I-II Study of Infusional Melphalan + Bortezomib for Myeloablative Therapy Prior to Autologous Transplant for Patients With Multiple Myeloma [NCT02353572]	Phase 1/Phase 2	3 participants (Actual)	Interventional	2009-11-30	Terminated(stopped due to Principle investigator left the institution)
Phase I/II Study of Combination of Sorafenib, Vorinostat, and Bortezomib for the Treatment of Acute Myeloid Leukemia With Complex- or Poor-risk (Monosomy 5/7) Cytogenetics or FLT3-ITD Positive Genotype [NCT01534260]	Phase 1/Phase 2	37 participants (Actual)	Interventional	2012-02-10	Completed
A Phase IV, Post Marketing, Prospective, Observational Cohort Study to Investigate Safety and Effectiveness of Alvocade® in Iranian Patients With Multiple Myeloma [NCT06012383]		57 participants (Actual)	Observational	2016-07-31	Completed
A Pilot Study Using High Dose Busulfan and Bortezomib as Part of Allogeneic Transplant Conditioning Regimen for High Risk Multiple Myeloma Patients. [NCT01534143]	Phase 2	1 participants (Actual)	Interventional	2012-02-29	Terminated(stopped due to Data was not collected, because funding was unavailable to continue study.)
A Phase I/II Study of Bortezomib + CHOP in Patients With Advanced Stage Aggressive T Cell or NK/T Cell Lymphomas [NCT00374699]	Phase 1/Phase 2	55 participants (Anticipated)	Interventional	2006-04-30	Completed
Phase II Study of Bendamustine, Bortezomib, and Dexamethasone (BBD) for Newly Diagnosed Patients With Multiple Myeloma [NCT02224729]	Phase 2	24 participants (Actual)	Interventional	2014-08-25	Completed
A Phase I/II Study of a Novel Reduced Intensity Conditioning Regimen for Allogeneic Stem Cell Transplantation in Patients With Multiple Myeloma [NCT00995059]	Phase 1/Phase 2	0 participants (Actual)	Interventional		Withdrawn
International Study for Treatment of High Risk Childhood Relapsed ALL 2010 A Randomized Phase II Study Conducted by the Resistant Disease Committee of the International Berlin, Frankfurt, Münster (BFM) Study Group [NCT03590171]	Phase 2	250 participants (Anticipated)	Interventional	2017-09-01	Recruiting
Phase I Trial of Temozolomide, Bevacizumab Plus Bortezomib for Patients With Recurrent Glioblastoma Multiforme [NCT01435395]	Phase 1	12 participants (Actual)	Interventional	2011-12-31	Completed
Bortezomib (VELCADE), Cladribine and Rituximab (VCR) in Mantle Cell Lymphoma: A Phase I/II Study (PSHCI 10-011) [NCT01439750]	Phase 1	13 participants (Actual)	Interventional	2012-05-31	Active, not recruiting
Phase I/Ib Trial of the Efficacy and Safety of Combination Therapy of Lenalidomide/Bortezomib/Dexamethasone and Panobinostat in Transplant Eligible Patients With Newly Diagnosed Multiple Myeloma (MM) [NCT01440582]	Phase 1	77 participants (Actual)	Interventional	2013-02-18	Completed
Assessment of Sensory Disorders Associated With Peripheral Neuropathy Induced by Bortezomib: Prospective Comparative Study [NCT02976272]		60 participants (Anticipated)	Observational	2016-06-07	Recruiting
Phase I Study of Bortezomib and Cetuximab Without or With Cisplatin in Combination With Radiation Therapy for Advanced Head and Neck Cancer [NCT01445405]	Phase 1	3 participants (Actual)	Interventional	2008-02-05	Completed
An Open-Label, Single Arm, Phase Ib/II Study of GSK2110183 in Subjects With Proteasome Inhibitor Refractory Multiple Myeloma [NCT01445587]	Phase 2	0 participants (Actual)	Interventional	2011-11-30	Withdrawn(stopped due to Based on the clinical activity, not safety data, of the AKT inhibitor, GSK has decided at this time to suspend further development of GSK2110183 as monotherapy.)
Efficacy and Safety of Rituximab, High-dose Ara-C and Dexamethasone (R-HAD) Alone or in Combination With Bortezomib in Patients With Relapsed or Refractory Mantle Cell Lymphoma [NCT01449344]	Phase 3	128 participants (Actual)	Interventional	2009-05-09	Active, not recruiting
Continuing Treatment for Subjects Who Have Participated in a Prior Protocol Investigating Elotuzumab [NCT02719613]	Phase 2	67 participants (Actual)	Interventional	2016-07-15	Active, not recruiting
Phase 2, Randomized, Open-Label Study Comparing Daratumumab, Lenalidomide, Bortezomib, and Dexamethasone (D-RVd) Versus Lenalidomide, Bortezomib, and Dexamethasone (RVd) in Subjects With Newly Diagnosed Multiple Myeloma Eligible for High-Dose Chemotherapy [NCT02874742]	Phase 2	224 participants (Actual)	Interventional	2016-08-29	Completed
A Phase II Study of Weekly Maintenance Bortezomib and Rituximab in Mantle Cell Lymphoma Post Autologous Hematopoietic Cell Transplantation [NCT01267812]	Phase 2	23 participants (Actual)	Interventional	2011-10-03	Completed
European Myeloma Network Sequential Phase I / Phase II Trial on RIC Allogeneic Transplantation: an Optimized Program for High Risk Relapsed Patients [NCT01460420]	Phase 1/Phase 2	49 participants (Actual)	Interventional	2011-11-30	Completed
Phase 1/2 Study of VELCADE (Bortezomib), Nipent (Pentostatin), and Rituxan (Rituximab) (VNR) in Subjects With Relapsed Follicular, Marginal Zone, and Mantle Cell Lymphoma [NCT01460602]	Phase 1/Phase 2	0 participants (Actual)	Interventional	2010-05-31	Withdrawn(stopped due to Investigator has relocated to MD Anderson)
A Phase 1b Dose Escalation Study of the Histone Deacetylase Inhibitor (HDACi) JNJ-26481585 in Combination With VELCADE (Bortezomib) and Dexamethasone for Subjects With Relapsed Multiple Myeloma [NCT01464112]	Phase 1	18 participants (Actual)	Interventional	2011-09-16	Completed
A Randomized Phase II Study of Bortezomib Plus ICE (BICE) Versus Standard ICE for Patients With Relapsed/Refractory Classical Hodgkin Lymphoma [NCT00967369]	Phase 2	20 participants (Actual)	Interventional	2009-08-24	Completed
A Phase II, Open-Label Study of Bortezomib (Velcade), Cladribine and Rituximab (VCR) in Advanced, Newly Diagnosed and Relapsed/Refractory Mantle Cell and Indolent Lymphomas [NCT00980395]	Phase 2	24 participants (Actual)	Interventional	2009-07-07	Completed
Phase I/II Trial of Dose-Adjusted EPOCH Chemotherapy With Bortezomib Combined With Integrase Inhibitor Therapy for HTLV-1 Associated T-Cell Leukemia Lymphoma [NCT01000285]	Phase 1/Phase 2	18 participants (Actual)	Interventional	2010-09-30	Completed
Phase II Study of Panobinostat (LBH589) Given in Combination With Bortezomib (Velcade) in Patients With Pancreatic Cancer Progressing on Gemcitabine Therapy Alone or Gemcitabine in Combination [NCT01056601]	Phase 2	7 participants (Actual)	Interventional	2010-09-30	Terminated(stopped due to Funding not available)
Bortezomib Plus Rituximab for EBV + Post Transplant Lymphoproliferative Disease (PTLD) [NCT01058239]	Phase 2	7 participants (Actual)	Interventional	2011-11-30	Completed
Phase II Study to Evaluate Efficacy and Safety of Single Weekly Administration of Bortezomib in Newly Diagnosed Multiple Myeloma [NCT01090921]	Phase 2	50 participants (Actual)	Interventional	2007-05-31	Completed
A Phase 2 Study of Daratumumab, Bortezomib, and Dexamethasone (DVd), Followed by Daratumumab, Ixazomib, and Dexamethasone (DId) for Relapsed and/or Refractory Myeloma [NCT03763162]	Phase 2	60 participants (Anticipated)	Interventional	2019-01-17	Recruiting
A Prospective, Multicenter, Non-comparative, Open-label, Phase II Study to Evaluate the Effects of the Combination of Bortezomib/Dexamethasone/Zoledronic Acid on Bone Mineral Density, Bone Metabolism, Radiographically-detected Osteolytic Bone Lesions, Ske [NCT00972959]	Phase 2	17 participants (Actual)	Interventional	2009-07-31	Completed
A Phase I/II Open-label Multicenter Study of AT7519M Alone and in Combination With Bortezomib in Patients With Previously Treated Multiple Myeloma [NCT01183949]	Phase 1/Phase 2	18 participants (Actual)	Interventional	2010-11-30	Completed
Bone Effect of Bortezomib in Patients With Relapsed/Refractory Multiple Myeloma [NCT01062230]	Phase 2	6 participants (Actual)	Interventional	2010-01-31	Terminated(stopped due to Slow accrual; PI left primary institution)
Reduced Intensity Allogeneic Hematopoietic Stem Cell Transplantation for Sickle Cell Anemia From HLA Matched or Partially-Matched Related Donors [NCT01350232]		2 participants (Actual)	Interventional	2009-09-30	Terminated(stopped due to Poor accrual)
A Phase II Study Incorporating Panobinostat, Bortezomib and Liposomal Vincristine Into Re-Induction Therapy for Relapsed Pediatric T-Cell Acute Lymphoblastic Leukemia or Lymphoma [NCT02518750]	Phase 2	3 participants (Actual)	Interventional	2016-11-23	Terminated(stopped due to Due to slow accrual)
A Phase 3 Trial Comparing Cyclophosphamide,Bortezomib,and Dexamethasone (CyBorD) and Bortezomib,Doxorubicin,and Dexamethasone (PAD) in the Treatment of Newly Diagnosed Multiple Myeloma [NCT02362165]	Phase 3	236 participants (Anticipated)	Interventional	2015-04-30	Recruiting
A Phase 3 Randomized, Controlled, Open-label Study of Selinexor, Bortezomib, and Dexamethasone (SVd) Versus Bortezomib and Dexamethasone (Vd) in Patients With Relapsed or Refractory Multiple Myeloma (RRMM) [NCT03110562]	Phase 3	402 participants (Actual)	Interventional	2017-05-24	Active, not recruiting
Phase I/II Study of Liposomal Doxorubicin (Doxil®)/Melphalan/Bortezomib (Velcade®) in Relapsed/Refractory Multiple Myeloma [NCT00985907]	Phase 1/Phase 2	13 participants (Actual)	Interventional	2004-10-28	Terminated(stopped due to Low Accrual)
A Phase I Study Using Bortezomib (Velcade, Formerly Known as PS-341) With Weekly Idarubicin for the Treatment of Elderly (>/= 60 Years) and Relapsed Patients With Acute Myelogenous Leukemia [NCT00382954]	Phase 1	55 participants (Anticipated)	Interventional	2004-02-29	Completed
Probiotic Supplementation Reduces Gastrointestinal Symptoms During the Therapy and Improves Therapeutic Response in AL Amyloidosis: A Randomized Controlled Trial [NCT05776940]	Phase 3	116 participants (Anticipated)	Interventional	2023-03-31	Not yet recruiting
A Phase 2 Trial to Evaluate the Efficacy of Bortezomib, Cytarabine, and Dexamethasone in Patients With Relapsed or Refractory Mantle Cell Lymphoma [NCT02840539]	Phase 2	19 participants (Actual)	Interventional	2016-10-11	Completed
An Open Label, Dose Escalation, Multicenter Phase 1/2 Study of KW-2478 in Combination With Bortezomib in Subjects With Relapsed and/or Refractory Multiple Myeloma [NCT01063907]	Phase 1/Phase 2	95 participants (Actual)	Interventional	2010-03-31	Completed
Induction Therapy With Bortezomib-melphalan and Prednisone (VMP) Followed by Lenalidomide and Dexamethasone (Rd) Versus Carfilzomib, Lenalidomide and Dexamethasone (KRd) Plus/Minus Daratumumab, 18 Cycles, Followed by Consolidation and Maintenance Therapy [NCT03742297]	Phase 3	462 participants (Actual)	Interventional	2018-10-22	Active, not recruiting
Phase I/II Study of Combination of Aurora Kinase Inhibitor MLN8237 and Bortezomib in Relapsed or Refractory Multiple Myeloma [NCT01034553]	Phase 1/Phase 2	26 participants (Actual)	Interventional	2010-02-28	Completed
A Multicenter Phase I Study Evaluating the Addition of Bortezomib to an Established Acute Graft Versus Host Disease (aGVHD) Prophylaxis Regimen in Pediatric Allogeneic Hematopoietic Stem Cell Transplant (Allo HSCT) Patients [NCT01926899]	Phase 1	15 participants (Actual)	Interventional	2013-08-01	Completed
Weekly Bendamustine and Bortezomib Combination Therapy in Relapsed or Refractory Indolent Non-Hodgkin's Lymphoma or B-CLL: A Single-Center Phase 2 Study [NCT00426855]	Phase 1/Phase 2	12 participants (Actual)	Interventional	2007-01-31	Completed
A Phase II Study of Velcade (Bortezomib, PS-341) and Rituximab in Relapsed/Refractory Mantle Cell and Follicular Non-Hodgkin's Lymphoma [NCT00201877]	Phase 2	25 participants (Actual)	Interventional	2004-12-31	Completed
PS-341 and PS-341 + Epoch Chemotherapy and Molecular Profiling in Relapsed or Refractory Diffuse Large B-Cell Lymphomas [NCT00054665]	Phase 2	50 participants (Actual)	Interventional	2003-02-28	Completed
S0417 A Phase II Study of Bortezomib (Velcade™, PS-341), Thalidomide, and Dexamethasone in Patients With Refractory Multiple Myeloma [NCT00124579]	Phase 2	7 participants (Actual)	Interventional	2005-08-31	Terminated(stopped due to poor accrual)
Phase II Trial of the Combination of Subcutaneous (SQ) Bortezomib and Pegylated Liposomal Doxorubicin (PLD or Doxil or LipoDox) for the Treatment of Patients With Relapsed/Refractory Acute Myelogenous Leukemia (AML) [NCT01736943]	Phase 2	25 participants (Actual)	Interventional	2012-12-19	Completed
A Phase II Study of Modified Lenalidomide, Bortezomib and Dexamethasone for Transplant-Ineligible Patients With Newly Diagnosed Multiple Myeloma [NCT01782963]	Phase 2	50 participants (Actual)	Interventional	2013-03-31	Completed
Feasibility of Assessing Drug Response to Precise Local Injection of Anti-cancer Drugs Using Presage's CIVO Device in Soft Tissue Sarcoma Patients Undergoing Surgery. [NCT03056599]	Phase 1	23 participants (Actual)	Interventional	2016-12-15	Completed
A Phase I, Open-Label, Multi-Center Study of CKD-581 in Combination With Bortezomib and Dexamethasone in Patients With Previously Treated Multiple Myeloma [NCT03051841]	Phase 1	18 participants (Anticipated)	Interventional	2017-01-31	Recruiting
Randomized Phase II Study of Bortezomib, Lenalidomide and Dexamethasone Versus Lenalidomide and Dexamethasone in Elderly Patients With Newly Diagnosed Multiple Myeloma [NCT04277845]	Phase 2	49 participants (Actual)	Interventional	2020-08-06	Active, not recruiting
Superiority of the Triple Combinations of Bortezomib, Cyclophosphamide and Dexamethasone (VCD) Versus Cyclophosphamide, Thalidomide and Dexamethasone (CTD) in Patients With Newly Diagnose Multiple Myeloma, Eligible for Transplantation [NCT03402295]	Phase 3	311 participants (Actual)	Interventional	2009-06-15	Completed
Phase II Trial pf Bortezomib in Patients With Advanced or Relapsed Lymphoma of the Mucosa Associated Lymphoid Tissue (MALT) Type [NCT00373906]	Phase 2	16 participants (Anticipated)	Interventional		Completed
Phase II Trial of Ofatumumab and Bortezomib in Subjects With Relapsed Cluster of Differentiation Antigen 20 (CD20)+ Diffuse Large B Cell Lymphoma, Follicular Lymphoma, or Mantle Cell Lymphoma [NCT01397591]	Phase 2	3 participants (Actual)	Interventional	2011-10-31	Terminated(stopped due to Study closed by PI due to lower than expected accrual.)
A Phase I/II Trial of VR-CHOP for Patients With Untreated Follicular Lymphoma and Other Low Grade B-Cell Lymphomas [NCT00634179]	Phase 1/Phase 2	37 participants (Actual)	Interventional	2008-02-29	Completed
Subcutaneous Bortezomib, Cyclophosphamide and Rituximab (BCR) Versus Fludarabine, Cyclophosphamide and Rituximab (FCR) for Initial Therapy of Waldenstrőm's Macroglobulinaemia (WM): a Randomized Phase II Trial [NCT01592981]	Phase 2	60 participants (Actual)	Interventional	2013-01-31	Completed
A Phase 0 Study of Autophagy Induction After Bortezomib For Myeloma [NCT01594242]	Early Phase 1	11 participants (Actual)	Interventional	2012-07-10	Completed
VELCADE® (Bortezomib) for Injection Therapy for Early Relapsed Prostate Cancer [NCT00103376]	Phase 2	23 participants (Actual)	Interventional	2004-10-31	Terminated(stopped due to Low Accrual)
MUK Nine b: OPTIMUM. A Phase II Study Evaluating Optimised Combination of Biological Therapy in Newly Diagnosed High Risk Multiple Myeloma and Plasma Cell Leukaemia. [NCT03188172]	Phase 2	95 participants (Anticipated)	Interventional	2017-09-28	Active, not recruiting
A Phase II Study of VELCADE (Bortezomib) in Combination With Bendamustine and Rituximab in Subjects With Relapsed or Refractory Follicular Lymphoma [NCT00636792]	Phase 2	73 participants (Actual)	Interventional	2008-02-29	Completed
A Phase 1 Open-label Study to Evaluate the Safety, Tolerability and Efficacy of Intravenous TAK-573 as Part of Combination Therapy in Patients With Relapsed or Refractory Multiple Myeloma [NCT04392648]	Phase 1	0 participants (Actual)	Interventional	2020-06-24	Withdrawn(stopped due to Business Decision (no enrollment))
Phase II and Pharmacodynamic Study of PS-341 in Patients With Unresectable or Metastatic Adenocarcinoma of the Bile Duct or Gallbladder [NCT00085410]	Phase 2	20 participants (Actual)	Interventional	2004-01-31	Terminated(stopped due to The trial was discontinued early due to no confirmed partial responses.)
Phase I/II Study of PS-341 in Combination With Paclitaxel, Carboplatin, and Concurrent Thoracic Radiation Therapy for Non-small Cell Lung Cancer (NSCLC) [NCT00093756]	Phase 1/Phase 2	52 participants (Actual)	Interventional	2004-09-30	Completed
A Phase II Study of the Combination Bortezomib (Velcade, PS-341), Dexamethasone, and Rituximab in Patients With Waldenstroms Macroglobulinemia [NCT00250926]	Phase 2	23 participants (Actual)	Interventional	2005-10-31	Completed
Phase I/II Trial of VELCADE+ CHOP-Rituximab in Patients With Previously Untreated Diffuse Large B Cell or Mantle Cell Non-Hodgkin's Lymphoma [NCT00151320]	Phase 1/Phase 2	76 participants (Actual)	Interventional	2004-01-31	Completed
Velcade (Bortezomib) and Sorafenib in Unresected or Metastatic Renal Cell Carcinoma [NCT01100242]	Phase 2	17 participants (Actual)	Interventional	2010-04-30	Terminated(stopped due to Low accrual)
MC1082: A Phase I/II Trial of Pomalidomide (CC-4047), Bortezomib, and Dexamethasone in Patients With Relapsed or Refractory Multiple Myeloma [NCT01212952]	Phase 1/Phase 2	50 participants (Actual)	Interventional	2011-09-30	Completed
PS-341 (Bortezomib, Velcade®), Adriamycin and Dexamethasone (PAD) Combination Therapy Followed by Thalidomide With Dexamethasone (Thal/Dex) for Relapsed or Refractory Multiple Myeloma [NCT00319865]	Phase 2	47 participants	Interventional	2005-11-30	Recruiting
Phase II Study for the Evaluation of Bendamustine, Bortezomib and Dexamethasone (BBD) in the First-Line Treatment of Patients With Multiple Myeloma Who Are Not Candidates for High Dose Chemotherapy [NCT01056276]	Phase 2	59 participants (Actual)	Interventional	2010-05-31	Completed
A Phase 2 Trial of Bortezomib in KRAS-Mutant Non-Small Cell Lung Cancer in Never Smokers or Those With KRAS G12D [NCT01833143]	Phase 2	17 participants (Actual)	Interventional	2013-04-11	Completed
Isatuximab in Combination With Bortezomib and Lenalidomide With Minimal Dexamethasone in Transplant-ineligible Multiple Myeloma [NCT04939844]	Phase 2	51 participants (Actual)	Interventional	2021-06-29	Active, not recruiting
A Phase I Dose-Escalation Study of R115777 (Tipifarnib) Plus PS-341 (Bortezomib) in Relapsed or Refractory Acute Leukemias [NCT00383474]	Phase 1	35 participants (Actual)	Interventional	2006-08-31	Completed
Prospective Observation of Bortezomib in the Treatment of Glomerular Diseases [NCT05383547]		20 participants (Anticipated)	Interventional	2022-08-02	Recruiting
A Phase I-II Study of High-Dose Post-Transplant Cyclophosphamide, Bortezomib and Abatacept for the Prevention of Graft-versus-Host-Disease (GvHD) Following Allogenic Hematopoietic Stem Cell Transplantation (HSCT) [NCT05289167]	Phase 1/Phase 2	74 participants (Anticipated)	Interventional	2022-03-13	Recruiting
An Exploratory Trial to Estimate the Proportion of Patients With Tumor Cell Contaminated, Flow Positive Leukapheresis Products Collected With and Without Bortezomib as In-vivo Purging Prior to Autologous Stem Cell Harvest for Multiple Myeloma [NCT02703779]	Phase 2	101 participants (Actual)	Interventional	2016-03-31	Completed
An Open Label, Single Arm, Multi-Center Exploratory Study to Evaluate the Efficacy and Safety of SVRd for the Treatment of Newly Diagnosed Multiple Myeloma Patients Presenting With Extramedullary Disease. [NCT05900882]	Phase 2	35 participants (Anticipated)	Interventional	2022-07-15	Recruiting
A Phase 2b, Open-label Study of Selinexor Plus Low-dose Dexamethasone (Sd) in Patients With Penta-refractory Multiple Myeloma (MM), Selinexor and Bortezomib Plus Low-dose Dexamethasone (SVd) in Patients With Triple-class Refractory MM, and Selinexor and P [NCT04414475]	Phase 2	141 participants (Anticipated)	Interventional	2020-07-01	Recruiting
A Phase 1b Study of REOLYSIN® (Reovirus Serotype 3 - Dearing Strain) Combined With Standard Doses of Bortezomib and Dexamethasone in Patients With Relapsed/Refractory Multiple Myeloma [NCT02514382]	Phase 1	14 participants (Actual)	Interventional	2015-08-21	Completed
A Phase 1/2, Open-Label, Dose-Escalation, Safety and Tolerability Study of INCB052793 in Subjects With Advanced Malignancies [NCT02265510]	Phase 1/Phase 2	83 participants (Actual)	Interventional	2014-09-10	Terminated
A RANDOMIZED, MULTICENTER, OPEN LABEL STUDY COMPARING TWO STANDARD TREATMENTS, BORTEZOMIB-MELPHALAN-PREDNISONE (VMP) WITH OR WITHOUT DARATUMUMAB (Dara-VMP) VS LENALIDOMIDE-DEXAMETHASONE (Rd) WITH OR WITHOUT DARATUMUMAB (Dara-Rd) IN AUTOLOGOUS STEM CELL TR [NCT03829371]	Phase 4	450 participants (Anticipated)	Interventional	2019-01-03	Recruiting
A 3-Arm Randomized Phase II Trial of Bendamustine-Rituximab (BR) Followed by Rituximab vs Bortezomib-BR (BVR) Followed by Rituximab vs BR Followed by Lenalidomide/Rituximab in High Risk Follicular Lymphoma [NCT01216683]	Phase 2	289 participants (Actual)	Interventional	2011-02-09	Completed
A PHASE III, MULTI-CENTER, RANDOMIZED OPEN LABEL STUDY OF VELCADE, MELPHALAN, PREDNISONE AND THALIDOMIDE (V-MPT) Versus VELCADE, MELPHALAN, PREDNISONE (V-MP) IN ELDERLY UNTREATED MULTIPLE MYELOMA PATIENTS [NCT01063179]	Phase 3	511 participants (Actual)	Interventional	2006-05-31	Completed
A Dose Escalation of Zarnestra (R115777) Combined With Velcade® (PS-341) in Patients With Relapsed Multiple Myeloma [NCT00361088]	Phase 1/Phase 2	42 participants (Actual)	Interventional	2005-08-31	Terminated(stopped due to Initial Principal Investigator left Moffitt)
Phase II Study of CHOP/Rituxan Plus VELCADE in Mediastinal Large B-cell Lymphoma [NCT00361621]	Phase 2	3 participants (Actual)	Interventional	2006-07-31	Terminated(stopped due to Closed due to slow accrual)
A Pilot Study of Mitoxantrone-Based Four Drug Reinduction in Combination With Bortezomib for Relapsed or Refractory Acute Lymphoblastic Leukemia or Lymphoblastic Lymphoma in Children and Young Adults [NCT02535806]	Phase 2	2 participants (Actual)	Interventional	2015-07-31	Terminated(stopped due to Funding source discontinued)
Allogeneic Stem Cell Transplantation vs. Conventional Therapy as Salvage Therapy for Relapsed / Progressive Patients With Multiple Myeloma After First-line Therapy [NCT05675319]	Phase 3	482 participants (Anticipated)	Interventional	2023-03-03	Recruiting
A Prospective, Randomized, Multicenter, Two-Parallel Arm Study Evaluating the Overall Efficacy and Safety of Desensitization Therapy on Selected Patients Awaiting Heart Transplantation [NCT01769443]	Phase 2	2 participants (Actual)	Interventional	2013-06-30	Terminated(stopped due to Inability to enroll within funding period)
A Multicenter Phase II Study of Ofatumumab and Bortezomib (OB) in Previously Untreated Patients With Waldenstrom Macroglobulinemia [NCT01536067]	Phase 2	3 participants (Actual)	Interventional	2012-04-30	Terminated(stopped due to funding was withdrawn)
An Open-label, Randomised Trial of Bortezomib Consolidation (With Thalidomide and Prednisolone) Vs Thalidomide and Prednisolone Alone in Previously Untreated Subjects With Multiple Myeloma After Receiving Bortezomib, Cyclophosphamide, Dexamethasone (VCD) [NCT01539083]	Phase 3	256 participants (Actual)	Interventional	2012-01-13	Completed
A Phase II Study of Bortezomib and Vorinostat in Patients With Refractory or Relapsed MLL Rearranged Hematologic Malignancies [NCT02419755]	Phase 2	12 participants (Actual)	Interventional	2015-04-14	Terminated(stopped due to Accrual goals were no longer feasible based on restrictions imposed by the DSMB.)
A Phase II Study Evaluating Combined Zevalin(Ibritumomab Tiuxetan)and Velcade(Bortezomib)in Relapsed/Refractory Mantle Cell Lymphoma [NCT01497275]	Phase 2	5 participants (Actual)	Interventional	2012-02-29	Terminated(stopped due to Low accrual due to the approval of new drugs for use in Mantle cell lymphoma.)
A Phase I Study of MLN8237 in Combination With Bortezomib and Rituximab in Relapsed and Refractory Mantle Cell and Low Grade Non-Hodgkin Lymphoma [NCT01695941]	Phase 1	24 participants (Actual)	Interventional	2012-08-31	Active, not recruiting
A Phase II Study of Bortezomib in Combination With Carboplatin in Patients With Metastatic Pancreatic Cancer [NCT00416793]	Phase 2	9 participants (Actual)	Interventional	2006-12-31	Terminated(stopped due to Study was terminated due to poor accrual)
Phase I/II Study of Two Different Schedules of Bortezomib (VELCADE, PS-341) and Pemetrexed (ALIMTA) in Advanced Solid Tumors, With Emphasis on Non-Small Cell Lung Cancer (NSCLC) [NCT00389805]	Phase 1/Phase 2	27 participants (Actual)	Interventional	2005-03-31	Completed
A Phase 2, Randomized Study of VELCADE® (Bortezomib), Dexamethasone, and Thalidomide Versus VELCADE® (Bortezomib), Dexamethasone, Thalidomide, and Cyclophosphamide in Subjects With Previously Untreated Multiple Myeloma Who Are Candidates for Autologous Tr [NCT00531453]	Phase 2	98 participants (Actual)	Interventional	2007-10-31	Completed
GEM21menos65. A Phase III Trial for NDMM Patients Who Are Candidates for ASCT Comparing Extended VRD Plus Early Rescue Intervention vs Isatuximab-VRD vs Isatuximab-V-Iberdomide-D [NCT05558319]	Phase 3	480 participants (Anticipated)	Interventional	2022-10-31	Not yet recruiting
A Phase I/II Clinical Study of JNJ-26866138 (Bortezomib) in Untreated Multiple Myeloma Patients Who Are Not Candidates for Hematopoietic Stem Cell Transplant (HSCT) [NCT00985959]	Phase 1	101 participants (Actual)	Interventional	2008-07-31	Completed
A Pilot Study of Peripheral Blood Hematopoietic Stem Cell Mobilization With the Combination of Bortezomib and G-CSF in Multiple Myeloma and Non-Hodgkin's Lymphoma Patients [NCT02037256]		23 participants (Actual)	Interventional	2011-07-31	Completed
A Phase II Study of Elotuzumab in Combination With Pomalidomide, Bortezomib, and Dexamethasone in Relapsed and Refractory Multiple Myeloma [NCT02718833]	Phase 2	52 participants (Actual)	Interventional	2016-06-30	Active, not recruiting
Selinexor(ATG-010) Plus Bortezomib, Lenalidomide and Dexamethasone (XVRd) in High Risk Newly Diagnosed Multiple Myeloma [NCT05422027]	Phase 1/Phase 2	42 participants (Anticipated)	Interventional	2022-07-25	Recruiting
A Phase 1 Study of Tabalumab (LY2127399) in Combination With Bortezomib and Dexamethasone in Japanese Patients With Relapsed or Refractory Multiple Myeloma [NCT01556438]	Phase 1	16 participants (Actual)	Interventional	2012-07-31	Completed
Effective Quadruplet Utilization After Treatment Evaluation (EQUATE): A Randomized Phase 3 Trial for Newly Diagnosed Multiple Myeloma Not Intended for Early Autologous Transplantation [NCT04566328]	Phase 3	1,450 participants (Anticipated)	Interventional	2021-02-24	Recruiting
A Multisite, Phase II Study of Bortezomib, Isatuximab, Cyclophosphamide and Dexamethasone (VICD) Induction in Transplant-Eligible Multiple Myeloma Patients [NCT04240054]	Phase 2	41 participants (Anticipated)	Interventional	2021-11-02	Recruiting
Phase II Trial of Avastin Plus Bortezomib for Patients With Recurrent Malignant Glioma [NCT00611325]	Phase 2	56 participants (Actual)	Interventional	2008-05-31	Completed
A Phase II, Trial of Chloroquine in Combination With VELCADE and Cyclophosphamide in Patients With Relapsed and Refractory Myeloma [NCT01438177]	Phase 2	11 participants (Actual)	Interventional	2011-10-31	Terminated(stopped due to PI left institution.)
Randomized Phase II Trial of Sequential Versus Concurrent Docetaxel and PS-341 (NSC 681239) in Previously Treated Non-Small Cell Lung Cancer (NSCLC) [NCT00362882]	Phase 2	81 participants (Actual)	Interventional	2006-07-31	Completed
Comparison of Bortezomib-Cyclophosphamide-Dexamethasone Chemotherapy With or Without Doxycycline in Newly Diagnosed Mayo Stage II-III Light Chain Amyloidosis Patients: A Multi-center Randomized Controlled Trial [NCT03401372]		140 participants (Actual)	Interventional	2018-04-21	Completed
Bortezomib Combined With Fludarabine and Cytarabine for Mantle Cell Lymphoma Patients：a Single Arm, Open-labelled, Phase 2 Study [NCT03016988]	Phase 2	50 participants (Anticipated)	Interventional	2017-01-31	Not yet recruiting
Slow-Go Strategy for High Risk AL Amyloidosis: Isatuximab for Upfront Therapy [NCT04754945]	Phase 1	25 participants (Anticipated)	Interventional	2021-04-28	Recruiting
Total Therapy for Infants With Acute Lymphoblastic Leukemia (ALL) I [NCT02553460]	Phase 1/Phase 2	50 participants (Actual)	Interventional	2016-01-29	Active, not recruiting
An Open-label, Multicenter, Phase 2 Trial of Selinexor (KPT-330), Bortezomib and Low-dose Dexamethasone Plus Daratumumab (SELIBORDARA) for the Treatment of Patients With Refractory or Relapsed and Refractory Multiple Myeloma [NCT03589222]	Phase 2	62 participants (Anticipated)	Interventional	2018-07-15	Recruiting
A Randomized, Open-label Phase 3 Study of Carfilzomib, Melphalan, and Prednisone Versus Bortezomib, Melphalan, and Prednisone in Transplant-ineligible Patients With Newly Diagnosed Multiple Myeloma [NCT01818752]	Phase 3	955 participants (Actual)	Interventional	2013-07-08	Completed
A Post Approval Commitment Study for Pharmacokinetic Analysis and Providing Expanded Access to Bortezomib (Velcade) for Patients With Multiple Myeloma Who Have Received at Least Two Previous Lines of Therapy and Are Refractory to or Have Relapsed After Th [NCT01801436]	Phase 3	14 participants (Actual)	Interventional	2006-12-31	Completed
Tandem Autotransplantation for Multiple Myeloma in Participants With Less Than 12 Months of Preceding Therapy, Incorporating Velcade (Bortezomib) With the Transplant Chemotherapy and During Maintenance [NCT01548573]	Phase 2	19 participants (Actual)	Interventional	2012-05-31	Terminated(stopped due to Met study stopping rules)
Phase II Study of Bortezomib (PS-341) for Patients With Advanced Bronchiolo-Alveolar Carcinoma (BAC) or Adenocarcinoma With BAC Features [NCT00118144]	Phase 2	42 participants (Actual)	Interventional	2005-06-30	Completed
An Exploratory Clinical Study on Bortezomib for the Treatment of Refractory Rheumatoid Arthritis [NCT05805891]		20 participants (Anticipated)	Interventional	2023-12-31	Recruiting
Chinese Children Cancer Group Relapsed Acute Lymphoblastic Leukemia 2017 Study [NCT04224571]	Phase 2	208 participants (Actual)	Interventional	2018-09-14	Completed
An Open-Label Phase I/II Study of the Safety and Efficacy of Bortezomib, Lenalidomide and Dexamethasone Combination Therapy for Patients With Newly Diagnosed Multiple Myeloma [NCT00378105]	Phase 1/Phase 2	68 participants (Actual)	Interventional	2006-09-30	Active, not recruiting
VELCADE (Bortezomib) and Thalidomide in Newly Diagnosed Patients With Multiple Myeloma [NCT00287872]	Phase 2	30 participants (Actual)	Interventional	2004-09-30	Completed
A Phase II, Open Label Study Evaluating an Alternative Schedule of Velcade/Dexamethasone Plus Doxil in the Treatment of Multiple Myeloma [NCT00366106]	Phase 2	32 participants (Actual)	Interventional	2006-07-31	Terminated(stopped due to Study was closed to enrollment when it became clear that enrollment was too slow to complete full enrollment target within time frame allowed.)
Phase I/II Trial of Bortezomib (Velcade) in Addition to Tacrolimus and Methotrexate to Prevent Graft Versus Host Disease (GVHD) After Mismatched Allogeneic Non-Myeloablative Peripheral Blood Stem Cell Transplantation [NCT00369226]	Phase 1/Phase 2	45 participants (Actual)	Interventional	2006-08-31	Completed
Phase I/II Study to Evaluate the Efficacy and Safety of Combination Chemotherapy With Carboplatin, Bortezomib and Bevacizumab as First Line Therapy in Patients With Advanced Non-small Cell Lung Cancer [NCT00424840]	Phase 1	12 participants (Actual)	Interventional	2006-06-30	Terminated(stopped due to Poor accrual)
Phase I/II Trial of Combination CCI-779 (Temsirolimus) and Bortezomib (Velcade) in Relapsed and/or Relapsed/Refractory Multiple Myeloma [NCT00483262]	Phase 1/Phase 2	63 participants (Actual)	Interventional	2007-05-31	Completed
Total Therapy XVII for Newly Diagnosed Patients With Acute Lymphoblastic Leukemia and Lymphoma [NCT03117751]	Phase 2/Phase 3	790 participants (Actual)	Interventional	2017-03-29	Active, not recruiting
Single Autologous Transplant Followed by Consolidation and Maintenance for Participants ≥ 65 Years of Age Diagnosed With Multiple Myeloma or a Related Plasma Cell Malignancy [NCT01849783]	Phase 2	41 participants (Actual)	Interventional	2013-04-04	Completed
A Phase II Study of V-BEAM (Bortezomib, Carmustine, Etoposide, Cytarabine, and Melphalan) as Conditioning Regimen Prior to Second Autologous Stem Cell Transplantation for Multiple Myeloma [NCT01653418]	Phase 2	10 participants (Actual)	Interventional	2012-09-30	Terminated(stopped due to Due to the high rate of morbidity and mortality)
Evaluation of the Prevalence, Intensity and Consequences of Bortezomib-induced Neuropathic Disorders: Monocentric Observational and Cross-sectional Study. [NCT03344328]		67 participants (Actual)	Observational	2019-01-15	Completed
The Impact of Velcade(TM)on Antibody Secreting Cells in Sensitized Renal Allograft Candidates [NCT00722722]	Phase 2	18 participants (Actual)	Interventional	2008-06-30	Completed
A Pilot Study of Low Dose Melphalan and Bortezomib for Treatment of Acute Myelogenous Leukemia and High-Risk Myelodysplastic Syndromes [NCT00789256]		26 participants (Actual)	Interventional	2004-09-30	Completed
A Phase II Study of Maintenance Treatment With Sequential Bortezomib, Thalidomide and Dexamethasone Following Autologous Peripheral Blood Stem Cell Transplant in Patients With Multiple Myeloma [NCT00792142]	Phase 2	45 participants (Actual)	Interventional	2008-01-16	Completed
Phase I/II Trial of Autologous Peripheral Blood Progenitor Cell Transplantation With VELCADE Maintenance as Treatment for Intermediate- and Advanced-Stage Multiple Myeloma [NCT00084747]	Phase 1/Phase 2	30 participants (Actual)	Interventional	2004-06-30	Completed
A Single-center Clinical Trial of Bortezomib in Management of Immune Thrombocytopenia (ITP) With High Anti-platelet Antibodies Level [NCT03013114]	Phase 2	20 participants (Anticipated)	Interventional	2017-01-31	Not yet recruiting
A Phase II Trial of Bortezomib Plus Doxorubicin in Hepatocellular Carcinoma [NCT00083226]	Phase 2	42 participants (Actual)	Interventional	2004-03-31	Completed
Treatment of Anti-Interferon-Gamma Autoantibody Associated Acquired Immunodeficiency Syndrome With Bortezomib: Pilot Study [NCT03103555]	Phase 2	5 participants (Anticipated)	Interventional	2017-02-27	Recruiting
Safety and the Anti- Tumor Effects of Escalating Doses of Adoptively Infused Ex Vivo Expanded Autologous Natural Killer (NK) Cells Against Metastatic Cancers or Hematological Malignancies Sensitized to NK-TRAIL Cytotoxicity With Bortezomib [NCT00720785]	Phase 1	35 participants (Actual)	Interventional	2008-08-01	Completed
A Phase I/II Study of Bortezomib Plus CHOP Every 2 Weeks in Patients With Advanced Stage Diffuse Large B-cell Lymphomas [NCT00379574]	Phase 1/Phase 2	49 participants (Actual)	Interventional	2006-09-30	Completed
A Multi-center Phase II Trial Randomizing Novel Approaches for Graft-versus-Host Disease Prevention Compared to Contemporary Controls (BMT CTN #1203; Progress I) [NCT02208037]	Phase 2	279 participants (Actual)	Interventional	2014-08-31	Completed
Phase 1 Study of Daratumumab When Given in Combination With Bortezomib, Dexamethasone, Doxil, and Lenalidomide in Patients With Plasma Cell Leukemia [NCT03591744]	Phase 1	0 participants (Actual)	Interventional	2018-10-25	Withdrawn(stopped due to Budgetary constraints)
A Phase I/II Clinical Trial of the Anti-EGFR Monoclonal Antibody, Panitumumab, and the Proteosomal Inhibitor, Bortezomib, in Patients With Advanced, Refractory KRAS Wild-Type Colorectal Cancer [NCT01504477]	Phase 1/Phase 2	6 participants (Actual)	Interventional	2011-12-31	Terminated(stopped due to Low accrual--unable to meet accrual goals)
Multi-Drug Desensitization Protocol for Heart Transplant Candidates [NCT01556347]	Phase 2	2 participants (Actual)	Interventional	2012-07-31	Terminated(stopped due to Lack of efficacy)
Phase II Trial of Bortezomib and Vorinostat in Mantle Cell and Diffuse Large B-Cell Lymphomas [NCT00703664]	Phase 2	65 participants (Actual)	Interventional	2008-07-09	Completed
Study of the Combination of Bortezomib and Dexamethasone Followed by HSCT in AL [NCT01273844]		21 participants (Actual)	Interventional	2011-03-01	Completed
A Multi-Institutional Phase I/II Study of Revlimid® (Lenalidomide), Velcade® (Bortezomib), Dexamethasone, and Doxil®, (RVDD) Combination Therapy for Patients With Newly Diagnosed Multiple Myeloma [NCT00724568]	Phase 1/Phase 2	74 participants (Actual)	Interventional	2008-05-31	Completed
Use of Bortezomib to Treat Refractory Autoimmune Cytopenia(s) in Allogeneic Stem Cell Transplantation [NCT01929980]	Phase 2	4 participants (Actual)	Interventional	2012-07-31	Completed
2015-09: A Phase II Randomized, Open-label Study of Anti-SLAMF7 mAb During Maintenance Therapy Versus Standard Maintenance Therapy in Gene Expression Profiling (GEP)- Defined Low Risk Multiple Myeloma Patients With High Risk Cytogenetic Abnormalities [NCT03000634]	Phase 2	0 participants (Actual)	Interventional	2017-05-31	Withdrawn(stopped due to Study was not and will not be initiated due to lack of funding.)
A Randomized Phase III Trial on the Effect of Elotuzumab in VRD Induction /Consolidation and Lenalidomide Maintenance in Patients With Newly Diagnosed Myeloma [NCT02495922]	Phase 3	564 participants (Actual)	Interventional	2015-06-30	Completed
A Phase II Study of Allogeneic Hematopoietic Stem Cell Transplantation for Multiple Myeloma Using a Conditioning Regimen of Fludarabine, Melphalan, and Bortezomib [NCT01453101]	Phase 2	54 participants (Actual)	Interventional	2010-06-09	Completed
Pre-Transplant Immunosuppression and Related Haploidentical Hematopoietic Cell Transplantation for Patients With Severe Hemoglobinopathies [NCT04776850]	Early Phase 1	0 participants (Actual)	Interventional	2020-12-29	Withdrawn(stopped due to Competing protocol opened in Adult SCT that will include pediatric patients and is now multi-center. No patients enrolled on study.)
An Open Label, Single-Arm, Phase 1b/2 Study of the Safety and Efficacy of Combination Treatment With Lenalidomide, Bortezomib, Dexamethasone and Siltuximab (CNTO 328) in Subjects With Newly Diagnosed, Previously Untreated Multiple Myeloma Requiring System [NCT01531998]	Phase 1/Phase 2	14 participants (Actual)	Interventional	2012-05-31	Completed
A Randomized, Phase III Study Comparing Conventional Dose Treatment Using a Combination of Lenalidomide, Bortezomib, and Dexamethasone (RVD) to High-Dose Treatment With Peripheral Stem Cell Transplant in the Initial Management of Myeloma in Patients Up to [NCT01208662]	Phase 3	729 participants (Actual)	Interventional	2010-10-31	Active, not recruiting
A Phase II Study of Subcutaneous Bortezomib as Maintenance Therapy for Patients With High-risk Acute Myeloid Leukemia in Remission [NCT01465386]	Phase 2	6 participants (Actual)	Interventional	2011-11-30	Terminated(stopped due to Closed early due to slow enrollment)
A Randomized Phase I/II Study of Bortezomib, Rituximab, Dexamethasone and Temsirolimus in Patients With Relapsed Waldenstrom Macroglobulinemia and Relapsed/Refractory Mantle Cell, Follicular, Marginal Zone or Small Lymphocytic Lymphomas (Phase I), and Unt [NCT01381692]	Phase 1/Phase 2	9 participants (Actual)	Interventional	2011-07-20	Completed
Bortezomib With Steroid Pulse Therapy for Acute Cellular Rejection in Kidney [NCT02351427]	Phase 3	30 participants (Anticipated)	Interventional	2015-02-28	Recruiting
A Prospective, Multicenter, Randomized, Double-blind, Placebo-controlled, 2-parallel Group, Phase 3 Study to Compare Efficacy and Safety of Masitinib 6 mg/kg/Day in Combination With Bortezomib and Dexamethasone to Placebo in Combination With Bortezomib an [NCT01470131]	Phase 3	147 participants (Actual)	Interventional	2011-05-31	Terminated(stopped due to Sponsor decision based on portfolio prioritization)
A Prospective Randomized Controlled Clinical Study of Bortezomib Combined With DAG Regimen in the Treatment of Refractory/Relapsed AML [NCT05982756]	Phase 1	40 participants (Anticipated)	Interventional	2020-01-01	Recruiting
Pre-Transplant Immune Suppression With Hematopoietic Cell Transplantation From Haploidentical Donors for Adults and Children With Sickle Cell Disease or ß-Thalassemia (Haplo PTCy) [NCT05736419]	Phase 2	24 participants (Anticipated)	Interventional	2023-02-09	Recruiting
UARK 2013-13, Total Therapy 4B - Formerly 2008-01 - A Phase III Trial for Low Risk Myeloma Ages 65 and Under: A Trial Enrolling Subjects to Standard Total Therapy 3 (S-TT3) [NCT00734877]	Phase 3	382 participants (Actual)	Interventional	2008-07-31	Active, not recruiting
Phase II Study: Therapy With Bortezomib + Lenalidomide + Dexamethasone With Lenalidomide + Dexamethasone as Post Transplant Consolidation and Maintenance for Patients With Symptomatic Multiple Myeloma Following Autologous Transplantation [NCT02353468]	Phase 2	3 participants (Actual)	Interventional	2009-12-31	Terminated(stopped due to Principle investigator left the institution)
A Phase II Study to Assess the Safety and Efficacy of DBd Combination Therapy (DOXIL/CAELYX) [Doxorubicin HCL Liposome Injection], VELCADE [Bortezomib] and Dexamethasone) for Previously Untreated Multiple Myeloma Patients [NCT00561743]	Phase 2	50 participants (Actual)	Interventional	2005-11-30	Completed
A Phase I/II Study of Obatoclax Mesylate (GX15-070MS) Administered in Combination With Bortezomib to Patients With Relapsed or Refractory Mantle Cell Lymphoma (MCL) [NCT00407303]	Phase 1/Phase 2	24 participants (Actual)	Interventional	2006-10-31	Completed
A Multicenter Phase II Study of Subcutaneous Velcade Plus Oral Melphalan and Prdnisone or Plus Cycloposphamide and Prednisone or Plus Prednisone in Newly Diagnosed Elderly Multiple Myeloma Patients [NCT01190787]	Phase 2	150 participants (Anticipated)	Interventional	2010-07-31	Active, not recruiting
A Multicenter, Randomized, Double-Blind, Placebo-Controlled Phase 2 Study of Tabalumab in Combination With Bortezomib and Dexamethasone in Patients With Previously Treated Multiple Myeloma [NCT01602224]	Phase 2	220 participants (Actual)	Interventional	2012-07-31	Completed
A Randomized Phase III Non-inferiority Trial Assessing Lenalidomide, Bortezomib and Dexamethasone Induction Therapy With Either Intravenous or Subcutaneous Isatuximab in Transplant-eligible Patients With Newly Diagnosed Multiple Myeloma. [NCT05804032]	Phase 3	514 participants (Anticipated)	Interventional	2023-04-14	Recruiting
A Single Arm, Multicentre, Open Label Study of Iberdomide, Weekly Bortezomib and Dexamethasone for Transplant-ineligible, Newly Diagnosed Multiple Myeloma Patients: the BOREALIS Trial [NCT05272826]	Phase 2	75 participants (Anticipated)	Interventional	2024-02-29	Not yet recruiting
A Prospective Study of Bortezomib in Combination With Melphalan and Prednisone for Patients With Previously Untreated Multiple Myeloma [NCT00734149]	Phase 2	45 participants (Actual)	Interventional	2004-07-31	Completed
A Phase I Trial of Post-Transplant Bortezomib and High Dose Cyclophosphamide as Graft-Versus-Host Disease (GVHD) Prophylaxis After Reduced-Intensity Allogeneic Hematopoietic Stem Cell Transplantation (AHSCT) [NCT01860170]	Phase 1/Phase 2	28 participants (Actual)	Interventional	2012-04-30	Completed
Phase II Trial of LDE225 (Sonidegib) Plus Bortezomib in Patients With Relapsed or Relapsed/Refractory Multiple Myeloma With a Dose-Finding Lead-In [NCT02254551]	Phase 2	7 participants (Actual)	Interventional	2015-01-31	Terminated(stopped due to Safety lead-in data did not support continuation of study.)
Minimal Residual Disease Response-adapted Deferral of Transplant in Dysproteinemia - MILESTONE Trial [NCT04991103]	Phase 2	20 participants (Anticipated)	Interventional	2021-09-22	Recruiting
Perspectives of Subcutaneous Velcade at Home of Patients With Myeloma. [NCT05163405]		10 participants (Actual)	Observational	2019-12-01	Completed
A Phase 3, Double-Blind, Multicenter Study to Evaluate the Efficacy and Safety of CAEL-101 and Plasma Cell Dyscrasia Treatment Versus Placebo and Plasma Cell Dyscrasia Treatment in Plasma Cell Dyscrasia Treatment Naïve Patients With Mayo Stage IIIb AL Amy [NCT04504825]	Phase 3	124 participants (Anticipated)	Interventional	2021-02-02	Active, not recruiting
CAEL101-203: A Phase 2, Open-label, Multicenter Dose Selection Study to Evaluate the Safety and Tolerability of CAEL-101 in Patients With AL Amyloidosis [NCT04304144]	Phase 2	25 participants (Actual)	Interventional	2020-03-18	Completed
Pilot Clinical Trial of Treatment With Bortezomib to Inhibit Homologous Recombination (HR) Followed by Pembrolizumab and Cisplatin in Patients With Chemotherapy-Pretreated Metastatic Triple Negative Breast Cancer [NCT04265872]	Early Phase 1	20 participants (Anticipated)	Interventional	2020-10-15	Recruiting
Multicenter Open Label Phase 3 Study of Isatuximab Plus Lenalidomide and Dexamethasone With/Without Bortezomib in the Treatment of Newly Diagnosed Non Frail Transplant Ineligible Multiple Myeloma Elderly Patients (≥ 65; < 80 Years). [NCT04751877]	Phase 3	270 participants (Actual)	Interventional	2021-07-17	Active, not recruiting
A Prospective, Open-label, Multicenter, Observational Study to Evaluate the Efficacy and Safety of Bortezomib, Melphalan, Prednisone(VMP) for Initial Treatment in Patients With Multiple Myeloma Who do Not Undergo Autologous Stem Cell Transplantation [NCT02474563]		171 participants (Actual)	Observational	2011-05-31	Completed
Phase I Study of Plitidepsin (Aplidin®) in Combination With Bortezomib and Dexamethasone in Patients With Relapsed and/or Refractory Multiple Myeloma [NCT02100657]	Phase 1	39 participants (Actual)	Interventional	2014-06-30	Completed
Hemostatic Effects of VELCADE®* Treatment in Multiple Myeloma Patients [NCT01720043]	Phase 2	8 participants (Actual)	Interventional	2013-07-31	Terminated(stopped due to Slow Accrual)
A Phase 2 Study Incorporating Bone Marrow Microenvironment (ME) Co-Targeting Bortezomib Into Tandem Melphalan-Based Autotransplants With DT PACE for Induction/Consolidation and Thalidomide + Dexamethasone for Maintenance [NCT00081939]	Phase 2	303 participants (Actual)	Interventional	2004-01-31	Completed
A Randomized Trial Using a Modified COG ABFM Regimen Backbone to Investigate Capizzi Escalating Methotrexate Versus High Dose Methotrexate in Children With Newly Diagnosed T-cell Lymphoblastic Lymphoma (T-LBL) [NCT05681260]	Phase 3	200 participants (Anticipated)	Interventional	2023-02-06	Recruiting
A Prospective, Observational Study, to Evaluate the Maintenance With Bortezomib Plus Daratumumab (V-Dara) After Induction With Bortezomib, Melphalan, Prednisone Plus Daratumumab (VMP-Dara) in Newly Diagnosed Multiple Myeloma (MM) Patients Non-eligible for [NCT05218603]		100 participants (Anticipated)	Observational	2021-11-30	Recruiting
A Phase 3, Multicenter, Randomized, Open-label Study to Compare the Efficacy and Safety of bb2121 Versus Standard Regimens in Subjects With Relapsed and Refractory Multiple Myeloma (RRMM) (KarMMa-3) [NCT03651128]	Phase 3	381 participants (Actual)	Interventional	2019-04-16	Active, not recruiting
An Open-Label, Phase Ib, Dose-Escalation Study of the Safety and Pharmacology of the Anti-CD40 Monoclonal Antibody SGN-40 Administered in Combination With Bortezomib (Velcade®, PS-341) in Patients With Relapsed or Refractory Multiple Myeloma [NCT00664898]	Phase 1	18 participants (Actual)	Interventional	2008-05-31	Completed
A Randomized, Open-label, Phase 3 Study of Carfilzomib Plus Dexamethasone vs. Bortezomib Plus Dexamethasone in Patients With Relapsed Multiple Myeloma [NCT01568866]	Phase 3	929 participants (Actual)	Interventional	2012-06-20	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT00006184 (2) [back to overview]	Number of Participants With Adverse Events
NCT00006184 (2) [back to overview]	Immune Response
NCT00023712 (5) [back to overview]	Overall Survival
NCT00023712 (5) [back to overview]	Progression-Free Survival
NCT00023712 (5) [back to overview]	Tumor Response Duration
NCT00023712 (5) [back to overview]	Frequency and Severity of Observed Adverse Events
NCT00023712 (5) [back to overview]	Objective Partial/Complete Tumor Response Based on the Gynecologic Oncology Group (GOG) Response Evaluation Criteria in Solid Tumors (RECIST) Criteria
NCT00023764 (1) [back to overview]	Response Rate
NCT00054665 (2) [back to overview]	Number of Participants With Adverse Events
NCT00054665 (2) [back to overview]	Clinical Response Rate
NCT00061932 (2) [back to overview]	Change in Patterns of Gene Expression Pre- and Post-treatment Performed by GeneChip Analysis
NCT00061932 (2) [back to overview]	True Response Rate Evaluated for the Combination of Irinotecan and PS341 by Response Evaluation Criteria in Solid Tumors (RECIST)
NCT00075881 (4) [back to overview]	1-year Progression Free Survival Probability
NCT00075881 (4) [back to overview]	Response Rate on Reinduction
NCT00075881 (4) [back to overview]	Response Rate on Maintenance
NCT00075881 (4) [back to overview]	Response Rate on Induction
NCT00081939 (1) [back to overview]	Percentage of Participants With Progression-Free Survival (PFS) at 3 Years From Initiation of Study Treatment
NCT00083226 (3) [back to overview]	Overall Survival
NCT00083226 (3) [back to overview]	Progression Free Survival
NCT00083226 (3) [back to overview]	Objective Response Rate Measured by Response Evaluation Criteria In Solid Tumors (RECIST)
NCT00084747 (2) [back to overview]	Overall Survival
NCT00084747 (2) [back to overview]	Progression-free Survival
NCT00085410 (8) [back to overview]	Time to Disease Progression
NCT00085410 (8) [back to overview]	Objective Response Rate
NCT00085410 (8) [back to overview]	Clinical Benefit Rate
NCT00085410 (8) [back to overview]	1-year Survival
NCT00085410 (8) [back to overview]	6-Month Survival
NCT00085410 (8) [back to overview]	Overall Survival
NCT00085410 (8) [back to overview]	6-Month and 1-Year Survival: Patients Who Did Not Derive Clinical Benefit From Study Treatment
NCT00085410 (8) [back to overview]	6-Month and 1-Year Survival for Patients Who Derived Clinical Benefit From Study Treatment
NCT00093756 (5) [back to overview]	The Primary Endpoint of This Trial is the Proportion of Patients Alive at 1 Year. Phase II Patients Only.
NCT00093756 (5) [back to overview]	Progression-free Survival
NCT00093756 (5) [back to overview]	Frequency and Severity of Observed Toxicity, Graded by Common Terminology Criteria for Adverse Events (CTCAE)
NCT00093756 (5) [back to overview]	Overall Survival
NCT00093756 (5) [back to overview]	Confirmed Tumor Response
NCT00103259 (4) [back to overview]	Response Rate on Step 1
NCT00103259 (4) [back to overview]	Progression-free Survival on Step 1
NCT00103259 (4) [back to overview]	Overall Survival on Step 1
NCT00103259 (4) [back to overview]	Response Rate on Step 2
NCT00103376 (3) [back to overview]	Prostate-specific Antigen (PSA) Response
NCT00103376 (3) [back to overview]	Number of Patients Who Experienced an Adverse Event by CTCAE v. 2.0
NCT00103376 (3) [back to overview]	Time to PSA Progression
NCT00103506 (3) [back to overview]	Time to Progression (TTP)
NCT00103506 (3) [back to overview]	Overall Survival
NCT00103506 (3) [back to overview]	Number of Participants With Serious Adverse Events (SAEs)
NCT00104871 (3) [back to overview]	Participant Tumor Response Assessed by RECIST
NCT00104871 (3) [back to overview]	Progression-free Survival Assessed by RECIST
NCT00104871 (3) [back to overview]	Objective Tumor Response Rate Assessed by RECIST
NCT00108069 (3) [back to overview]	Number of Participants With Adverse Events
NCT00108069 (3) [back to overview]	Adverse Event Grades
NCT00108069 (3) [back to overview]	Response, Defined as Stable Disease or Objective (Partial or Complete) Response.
NCT00111813 (5) [back to overview]	Laboratory AE Summary
NCT00111813 (5) [back to overview]	Clinical AE Summary
NCT00111813 (5) [back to overview]	Mean Time to First AE Resulting in a Dose Modification in Either Vorinostat or Bortezomib
NCT00111813 (5) [back to overview]	Number of Participants With Dose Modifications of Either Vorinostat or Bortezomib Due to Adverse Experiences (AEs) After Treatment With Study Drug
NCT00111813 (5) [back to overview]	Mean Duration of Treatment With Vorinostat
NCT00114738 (6) [back to overview]	Overall Progression Free Survival
NCT00114738 (6) [back to overview]	Overall Survival
NCT00114738 (6) [back to overview]	Progression Free Survival (PFS)
NCT00114738 (6) [back to overview]	Clinical Response
NCT00114738 (6) [back to overview]	Count of Participants With Serious and Non-Serious Adverse Events
NCT00114738 (6) [back to overview]	Median Overall Survival (OS)
NCT00118144 (3) [back to overview]	Objective Response Rate With Bortezomib Evaluated by Both RECIST Criteria and Computer-assisted Image Analysis.
NCT00118144 (3) [back to overview]	Overall Survival
NCT00118144 (3) [back to overview]	Progression-free Survival
NCT00124579 (3) [back to overview]	Overall Response Rate Complete Remission (CR), Remission (R), and Partial Remission (PR).
NCT00124579 (3) [back to overview]	Progression-Free Survival
NCT00124579 (3) [back to overview]	Toxicity Evaluation
NCT00128921 (6) [back to overview]	Number of Participants With a Positive Response to Bortezomib Measured by Bone Marker Osteocalcin
NCT00128921 (6) [back to overview]	Number of Participants With a Positive Response to Bortezomib Measured by Bone Markers Like Phosphate.
NCT00128921 (6) [back to overview]	Number of Participants With a Positive Response to Bortezomib Measured by the Bone Marker Parathyroid Hormone
NCT00128921 (6) [back to overview]	Number of Participants With a Positive Response to Bortezomib Measured by Bone Markers Like Magnesium
NCT00128921 (6) [back to overview]	Number of Participants With a Positive Response to Bortezomib Measured by Bone Markers Like Calcium
NCT00128921 (6) [back to overview]	Number of Participants With a Positive Response to Bortezomib Measured by Bone Marker Alkaline Phosphatase
NCT00148317 (3) [back to overview]	Efficacy of Drug Combination as Therapy for Myeloma (Overall Response Rate)
NCT00148317 (3) [back to overview]	Progression Free Survival
NCT00148317 (3) [back to overview]	Yield of CD34+ Stem Cells
NCT00151320 (1) [back to overview]	ORR
NCT00153920 (6) [back to overview]	Progression-Free Survival (PFS)
NCT00153920 (6) [back to overview]	Objective Response (OR) Rate
NCT00153920 (6) [back to overview]	Number of Participants With Treatment-Emergent Neuropathic Pain
NCT00153920 (6) [back to overview]	Time to Progression (TTP)
NCT00153920 (6) [back to overview]	Very Good Partial Response (VGPR) Rate
NCT00153920 (6) [back to overview]	Number of Participants With Treatment-Emergent Sensory Neuropathy
NCT00201877 (3) [back to overview]	Assess the Toxicity of Combination Rituximab and Velcade™ in Patients With Previously Treated Mantle Cell and Follicular Lymphoma.
NCT00201877 (3) [back to overview]	Overall Response Rate
NCT00201877 (3) [back to overview]	Progression-free Survival(PFS)
NCT00250926 (4) [back to overview]	Time to Progression
NCT00250926 (4) [back to overview]	Response Rate
NCT00250926 (4) [back to overview]	Number of Participants With Adverse Events
NCT00250926 (4) [back to overview]	Time to Best Response
NCT00256776 (2) [back to overview]	Progression Free Survival
NCT00256776 (2) [back to overview]	Median Time to Progression (TTP)
NCT00262860 (3) [back to overview]	Response Rate After 2 Courses of Therapy
NCT00262860 (3) [back to overview]	Change in Proteasome Activity Compared to Baseline (Cycle 1)
NCT00262860 (3) [back to overview]	Change in Proteasome Activity Compared to Baseline (Cycle 2)
NCT00262873 (7) [back to overview]	Average Number of Erthroid Burst Forming Units in Bone Marrow
NCT00262873 (7) [back to overview]	Average Number of Leukemia Forming Units in Bone Marrow
NCT00262873 (7) [back to overview]	Average Percentage of Light Density Cells in Apoptosis
NCT00262873 (7) [back to overview]	Interleukin 6 Levels in Serum
NCT00262873 (7) [back to overview]	Vascular Endothelial Growth Factor (VEGF) Levels in Serum
NCT00262873 (7) [back to overview]	Average Number of Colony Forming Unit-granulocyte-macrophages in Bone Marrow
NCT00262873 (7) [back to overview]	Number of Participants Who Experienced an Adverse Event
NCT00276614 (1) [back to overview]	Objective Response Rate as Measured by RECIST Criteria After Every 2 Courses of Treatment for up to 6 Courses
NCT00287872 (3) [back to overview]	Clinical Response to Treatment
NCT00287872 (3) [back to overview]	Peripheral Motor and Sensory Neuropathy (Grade 2 and Higher)
NCT00287872 (3) [back to overview]	The Time to Response
NCT00290706 (1) [back to overview]	Response Rate in Patients With Relapsed or Refractory B- and T-cell NHL With Gemcitabine and Bortezomib Combination Treatment.
NCT00295932 (2) [back to overview]	Toxicity of Participants Receiving Bortezomib, Rituximab, Cyclophosphamide, and Prednisone for Treatment of Non-Hodgkin's Lymphoma
NCT00295932 (2) [back to overview]	Maximum Tolerated Dose
NCT00298766 (6) [back to overview]	Subjects With Treatment Emergent Adverse Events Leading to Treatment Termination
NCT00298766 (6) [back to overview]	Best Confirmed Hematologic Responders
NCT00298766 (6) [back to overview]	Maximum Tolerated Dose
NCT00298766 (6) [back to overview]	Subjects Grade 3/4/5 Treatment Emergent Adverse Events
NCT00298766 (6) [back to overview]	Subjects With Serious Treatment Emergent Adverse Events
NCT00298766 (6) [back to overview]	Subjects With Treatment Emergent Adverse Events
NCT00307086 (1) [back to overview]	Overall Survival (OS)
NCT00310037 (4) [back to overview]	Number of Participants With Complete Response Intensive Chemo-immunotherapy Plus Maintenance or Consolidation Bortezomib
NCT00310037 (4) [back to overview]	Number of Participants With Grade 3, 4 or 5 Adverse Event at Least Possibly Related to Treatment.
NCT00310037 (4) [back to overview]	Overall Survival
NCT00310037 (4) [back to overview]	Progression-free Survival Rate at 18 Months
NCT00312845 (2) [back to overview]	Progression Free Survival
NCT00312845 (2) [back to overview]	Overall Response Rate
NCT00362882 (4) [back to overview]	Disease Control Rate
NCT00362882 (4) [back to overview]	Overall Response Rate
NCT00362882 (4) [back to overview]	Overall Survival
NCT00362882 (4) [back to overview]	Progression-free Survival @ 6 Months
NCT00366106 (4) [back to overview]	Relative Dose Intensity of Bortezomib
NCT00366106 (4) [back to overview]	Time to Progression (TTP)
NCT00366106 (4) [back to overview]	Number of Participants With Treatment Response
NCT00366106 (4) [back to overview]	Incidence of Treatment-emergent Peripheral Neuropathy
NCT00369226 (6) [back to overview]	Incidence of Grade II-IV Acute Graft Versus Host Disease (GVHD) by Day 100.
NCT00369226 (6) [back to overview]	Incidence of Chronic Graft Versus Host Disease (Chronic GVHD).
NCT00369226 (6) [back to overview]	Successful Initial Engraftment by Day 45 Post Peripheral Blood Stem Cell (PBSC) Infusion and Administration of Bortezomib (Velcade), Tacrolimus and Methotrexate
NCT00369226 (6) [back to overview]	Sustained Engraftment Following Transplant.
NCT00369226 (6) [back to overview]	The Maximally Tolerated Dose (MTD) of Bortezomib (Velcade) That Can be Administered With Tacrolimus and Methotrexate After Mismatched Allogeneic Non-myeloablative Peripheral Blood Stem Cell (PBSC) Transplantation
NCT00369226 (6) [back to overview]	Overall Survival and Progression-free Survival.
NCT00369707 (8) [back to overview]	Overall Survival Rate
NCT00369707 (8) [back to overview]	Number of Patients That Experience Adverse Events With Bortezomib/Rituximab Combination Treatment
NCT00369707 (8) [back to overview]	Correlation of Tumor Burden
NCT00369707 (8) [back to overview]	Progression Free Survival (PFS) Rate
NCT00369707 (8) [back to overview]	Percentage of Patients With Treatment Failure
NCT00369707 (8) [back to overview]	Overall Response Rate After Completion of Maintenance Therapy
NCT00369707 (8) [back to overview]	Overall Response Rate After 1 Course of Induction Therapy
NCT00369707 (8) [back to overview]	Overall Response Rate (Complete Response and Partial Response) After Three Inductions Cycles of Treatment.
NCT00372905 (4) [back to overview]	Maximum Tolerated Dose (MTD) and Tolerability of Bortezomib Combined With Y-90-Ibritumomab Tiuxetan Determined by Number of Dose Limiting Toxicities in a Cohort.
NCT00372905 (4) [back to overview]	Median Progression Free Survival
NCT00372905 (4) [back to overview]	Overall Response Rate
NCT00372905 (4) [back to overview]	Number of Patients With Adverse Events Related to Treatment of Bortezomib Combined With Y-90-ibritumomab Tiuxetan
NCT00376961 (4) [back to overview]	Response Rate in Patients Treated With Rituximab-CHOPbortezomib Induction Therapy (R-CHOP-V) Followed by Bortezomib Maintenance Therapy(VM).
NCT00376961 (4) [back to overview]	2-year Progression-free Survival in Patients Treated With Rituximab-CHOP-bortezomib Induction Therapy (RCHOP-V) Followed by Bortezomib Maintenance Therapy (VM)
NCT00376961 (4) [back to overview]	Number of Patients With Grade 3 Through Grade 5 Adverse Events That Are Related to Study Drug
NCT00376961 (4) [back to overview]	2-year Overall Survival in Patients Treated With Rituximab-CHOP-bortezomib Induction Therapy (RCHOP-V) Followed by Bortezomib Maintenance Therapy (VM)
NCT00378105 (4) [back to overview]	Objective Response Rate of the Drug Combination in This Patient Populations.
NCT00378105 (4) [back to overview]	Estimated 18-month Progression Free Survival (PFS) Rate
NCT00378105 (4) [back to overview]	Estimated 18-month Overall Survival Rate
NCT00378105 (4) [back to overview]	Percentage of Patients Who Remained in Response for More Than 18 Months
NCT00378209 (5) [back to overview]	Duration of Response
NCT00378209 (5) [back to overview]	Objective Response Rate
NCT00378209 (5) [back to overview]	Overall Survival
NCT00378209 (5) [back to overview]	Progression Free Survival
NCT00378209 (5) [back to overview]	The Proportion of Patients Alive and Without Progressive Disease (PD) for ≥6 Months
NCT00379574 (2) [back to overview]	Number of Patients Who Experienced Adverse Events
NCT00379574 (2) [back to overview]	Number of Patients Who Achieved Complete Response
NCT00381940 (5) [back to overview]	Complete Response (CR)
NCT00381940 (5) [back to overview]	Induction Success Rate
NCT00381940 (5) [back to overview]	Overall Response Rate
NCT00381940 (5) [back to overview]	Number of Participants With Grade 3 or 4 Toxicity
NCT00381940 (5) [back to overview]	Rate of Successful PBSC Harvest
NCT00389805 (5) [back to overview]	Maximum Tolerated Dose of Bortezomib in Combination With Pemetrexel (Phase I)
NCT00389805 (5) [back to overview]	Number of Patients With Grade ≥ 3 Toxicity (Phase I)
NCT00389805 (5) [back to overview]	Number of Patients Experiencing a Dose-limiting Toxicity (Phase I)
NCT00389805 (5) [back to overview]	Number of Participants Who Experience Adverse Events (Phase I)
NCT00389805 (5) [back to overview]	Number of Patients With Toxicity by NCI CTC v3.0 (Phase I)
NCT00401843 (5) [back to overview]	Number of Participants With Adverse Events (AEs) or Serious Adverse Events (SAEs)
NCT00401843 (5) [back to overview]	Progression-free Survival
NCT00401843 (5) [back to overview]	Percentage of Participants With Confirmed Complete Response (CR Rate)
NCT00401843 (5) [back to overview]	Percentage of Participants With Best Confirmed Response of Complete Response (CR) or Partial Response (PR) (Overall Response Rate)
NCT00401843 (5) [back to overview]	Overall Survival
NCT00408928 (2) [back to overview]	Response to Bortezomib (VELCADE®)
NCT00408928 (2) [back to overview]	Number of Toxicities Related to Bortezomib (VELCADE®)
NCT00410423 (2) [back to overview]	Complete Response Rate to 1.3mg/m^2 of Bortezomib With Mitoxantrone and Etoposide in Phase II
NCT00410423 (2) [back to overview]	Number of Participants With Dose Limiting Toxicity in Phase I
NCT00413959 (2) [back to overview]	Overall Survival
NCT00413959 (2) [back to overview]	Overall Response Rate Using This Regimen in Patients With Low-grade B-Cell Non-Hodgkin's Lymphoma.
NCT00416793 (2) [back to overview]	Overall Survival Rate at 6 Months
NCT00416793 (2) [back to overview]	Overall Response Rate
NCT00422799 (4) [back to overview]	Duration of Response in Patients With WM
NCT00422799 (4) [back to overview]	Time to Progression in Patients With WM
NCT00422799 (4) [back to overview]	Overall Response Rate of Bortezomib and Rituximab (VR) in Patients With Relapsed or Refractory Waldenstrom's Macroglobulinemia (WM)
NCT00422799 (4) [back to overview]	Overall Response Rate of Bortezomib and Rituximab (VR) in Patients With Previously Untreated Waldenstrom's Macroglobulinemia (WM)
NCT00424840 (1) [back to overview]	Number of Subjects Who Require Dose Delay/Reduction in Dose of Bortezomibin the First Cycle
NCT00425503 (1) [back to overview]	The Purpose of the Present Study is to Assess the Safety of PS-341 as a Pretreatment in Patients Who Are to Undergo a Radical Prostatectomy. Poor Wound Healing and Excessive Bleeding, With Historical Rates of <1% and 10% Respectively Will be Measured.
NCT00425750 (3) [back to overview]	Patient Response to Treatment
NCT00425750 (3) [back to overview]	Progression-free Survival
NCT00425750 (3) [back to overview]	Overall Survival
NCT00426855 (1) [back to overview]	Optimal Bendamustine Dosage for Further Studies
NCT00433537 (3) [back to overview]	3-year Overall Survival (OS)
NCT00433537 (3) [back to overview]	2-year Progression-free Survival (PFS)
NCT00433537 (3) [back to overview]	Complete Response (CR) Rate
NCT00439556 (2) [back to overview]	Number of Participants With Dose Limiting Toxicity (DLT)
NCT00439556 (2) [back to overview]	Disease-free Survival
NCT00441168 (3) [back to overview]	Duration of Response (DOR)
NCT00441168 (3) [back to overview]	Best Confirmed Disease Response
NCT00441168 (3) [back to overview]	Best Reported Disease Response
NCT00458705 (1) [back to overview]	Disease Response
NCT00458822 (1) [back to overview]	Hematologic and Organ Response
NCT00464178 (2) [back to overview]	Overall Survival (OS) - Number of Participants Alive at Study Completion
NCT00464178 (2) [back to overview]	Median Number of Cycles to Tumor Progression (TTP)
NCT00469209 (1) [back to overview]	Number of Patients Reaching Complete Response (CR)
NCT00473590 (6) [back to overview]	Number of Participants With Selected Adverse Events (AEs)
NCT00473590 (6) [back to overview]	Progression-free Survival (PFS)
NCT00473590 (6) [back to overview]	Percentage of Participants With an Overall Response
NCT00473590 (6) [back to overview]	Overall Survival (OS)
NCT00473590 (6) [back to overview]	Number of Participants With an Overall Response
NCT00473590 (6) [back to overview]	Duration of Response
NCT00477412 (4) [back to overview]	Time to Failure (Phase II)
NCT00477412 (4) [back to overview]	Overall Survival
NCT00477412 (4) [back to overview]	Number of Participants With Overall Response Rate
NCT00477412 (4) [back to overview]	Maximum Tolerated Dose of Bortezomib (Phase I)
NCT00483262 (3) [back to overview]	Progression-Free Survival
NCT00483262 (3) [back to overview]	Toxicity. Number of Patients With Specific Toxicities Are Reported.
NCT00483262 (3) [back to overview]	Best Response to Combination Treatment
NCT00492050 (3) [back to overview]	Response Rate After 2 Cycles of Treatment With Bortezomib and Rituximab
NCT00492050 (3) [back to overview]	Response Rate After 3 Cycles of Treatment With Bortezomib and Rituximab
NCT00492050 (3) [back to overview]	Participants Ability to Collect Stem Cells After Treatment With Bortezomib and Rituximab
NCT00504751 (1) [back to overview]	Complete Response
NCT00507416 (8) [back to overview]	Percentage of Participants With a Complete Response
NCT00507416 (8) [back to overview]	Time to Alternative Therapy
NCT00507416 (8) [back to overview]	Percentage of Participants With an Overall Response
NCT00507416 (8) [back to overview]	Overall Survival
NCT00507416 (8) [back to overview]	Progression Free Survival (PFS)
NCT00507416 (8) [back to overview]	Duration of Response
NCT00507416 (8) [back to overview]	Percentage of Participants With a Complete Response or a Very Good Partial Response
NCT00507416 (8) [back to overview]	Change From Baseline in EORTC QLQ-C30 - Global Health Status
NCT00507442 (11) [back to overview]	Overall Survival
NCT00507442 (11) [back to overview]	Number of Patients With Stringent Complete Response Rate
NCT00507442 (11) [back to overview]	Number of Patients With Overall Response
NCT00507442 (11) [back to overview]	Number of Patients With Combined Complete Response and Very Good Partial Response
NCT00507442 (11) [back to overview]	Number of Patients With Adverse Events (AEs)
NCT00507442 (11) [back to overview]	Duration of Response
NCT00507442 (11) [back to overview]	Number of Patients With Complete Response Rate + Near Complete Response Rate
NCT00507442 (11) [back to overview]	Time to Response
NCT00507442 (11) [back to overview]	Time to Disease Progression
NCT00507442 (11) [back to overview]	Progression-free Survival
NCT00507442 (11) [back to overview]	Probability of 1-year Survival
NCT00510887 (6) [back to overview]	Complete and Partial Response
NCT00510887 (6) [back to overview]	Duration of Response
NCT00510887 (6) [back to overview]	Number of Participants With Neuropathy, Any Grade
NCT00510887 (6) [back to overview]	Number of Participants With a Grade 3-4 Hematologic Toxicity.
NCT00510887 (6) [back to overview]	Percentage of Subjects Experiencing Overall Survival
NCT00510887 (6) [back to overview]	Percentage of Subjects Experiencing Progression Free Survival
NCT00512798 (5) [back to overview]	Patients With Inhibition in NF-kB Activation (Phase I)
NCT00512798 (5) [back to overview]	Patients With Inhibition of NF-kB (Phase II)
NCT00512798 (5) [back to overview]	Number of Patients With Clinical Anti-tumor Activity Phase II)
NCT00512798 (5) [back to overview]	Optimal Doses of Temozolomide and Bortezomib (Phase I)
NCT00512798 (5) [back to overview]	Patients With Clinical Anti-tumor Activity (Phase I)
NCT00520767 (3) [back to overview]	Overall Survival
NCT00520767 (3) [back to overview]	Time to Treatment Failure (TTF)
NCT00520767 (3) [back to overview]	Complete Hematologic Response
NCT00522392 (4) [back to overview]	Progression-free Survival (PFS)
NCT00522392 (4) [back to overview]	Response Rates (Complete Response [CR] or Very Good Partial Response [VGPR])
NCT00522392 (4) [back to overview]	Change in Quality of Life (QOL) From Baseline to 6 Months Post Consolidation as Assessed by the Functional Assessment of Cancer Therapy-Neurotoxicity Trial Outcome Index (FACT-Ntx TOI)
NCT00522392 (4) [back to overview]	Overall Survival (OS)
NCT00523848 (3) [back to overview]	Time to Disease Progression
NCT00523848 (3) [back to overview]	Overall Response Rate (Complete and Partial)
NCT00523848 (3) [back to overview]	Complete Response Rate
NCT00531453 (2) [back to overview]	Percent of Participants Achieving Overall Combined Complete Response (CR) Following High-dose Chemotherapy (HDT)/Stem Cell Transplantation (SCT)
NCT00531453 (2) [back to overview]	Percent of Particpants Achieving Overall Combined Complete Response (CR) Following Induction
NCT00536575 (1) [back to overview]	Objective Response Rate (ORR), the Percentage of Patients Who Experience an Objective Benefit From Treatment
NCT00547534 (3) [back to overview]	Toxicity of Drug Combination in the Subjects
NCT00547534 (3) [back to overview]	Overall Response Rate (ORR)
NCT00547534 (3) [back to overview]	Number of Participants With Progression Free Survival at 2 Years
NCT00548717 (7) [back to overview]	Overall Survival
NCT00548717 (7) [back to overview]	Incidence of 100 Day Mortality
NCT00548717 (7) [back to overview]	To Determine the Rate of Grade II-IV Acute GVHD When Sirolimus and Mycophenolate Mofetil or Sirolimus, Mycophenolate Mofetil and Bortezomib is Used for GVHD Prophylaxis After Allogeneic Stem Cell Transplantation in Patients With Hematologic Malignancies
NCT00548717 (7) [back to overview]	The Rate of Renal Insufficiency
NCT00548717 (7) [back to overview]	Incidence of Chronic GVHD
NCT00548717 (7) [back to overview]	Donor Stem Cell Engraftment, Including Donor-host Hematopoietic Chimerism Studies Post Transplant
NCT00548717 (7) [back to overview]	To Correlate the Serum Concentrations of Mycophenolate Mofetil and Its Metabolites With Acute GVHD Incidence
NCT00553644 (4) [back to overview]	Number of Participants With an Overall Response Defined as Complete Response and Partial Response
NCT00553644 (4) [back to overview]	Overall Survival
NCT00553644 (4) [back to overview]	Incidence of Adverse Events
NCT00553644 (4) [back to overview]	Time to Progression
NCT00555906 (14) [back to overview]	Recommended Phase II Dose (RP2D) of PD-0332991: Phase 1
NCT00555906 (14) [back to overview]	Progression-free Survival (PFS): Phase 2
NCT00555906 (14) [back to overview]	Percentage of Participants With Objective Response (OR): Phase 2
NCT00555906 (14) [back to overview]	Overall Survival (OS): Phase 2
NCT00555906 (14) [back to overview]	Number of Participants With Laboratory Abnormalities: Phase 2
NCT00555906 (14) [back to overview]	Maximum Tolerated Dose (MTD) of PD-0332991: Phase 1
NCT00555906 (14) [back to overview]	Duration of Objective Response (DR): Phase 2
NCT00555906 (14) [back to overview]	Quality of Life Questionnaire Multiple Myeloma Module (QLQ-MY20): Phase 2
NCT00555906 (14) [back to overview]	Modified Version of Brief Pain Inventory - Short Form (m-BPI-sf) Questionnaire: Phase 2
NCT00555906 (14) [back to overview]	Number of Participants With Adverse Events (AEs) by Severity: Phase 2
NCT00555906 (14) [back to overview]	Number of Participants With Treatment-Emergent Adverse Events (TEAEs) by Relationship to Study Medication: Phase 2
NCT00555906 (14) [back to overview]	European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (EORTC QLQ-C30): Phase 2
NCT00555906 (14) [back to overview]	Best Overall Response: Phase 1
NCT00555906 (14) [back to overview]	Time to Tumor Progression (TTP): Phase 2
NCT00560352 (6) [back to overview]	Maximum Tolerated Dose (MTD) and Recommended MTD of Dasatinib in Combination With Bortezomib and Dexamethasone
NCT00560352 (6) [back to overview]	MTD and Recommended MTD of Bortezomib in Combination With Dasatinib and Dexamethasone
NCT00560352 (6) [back to overview]	Progression-free Survival
NCT00560352 (6) [back to overview]	Best Overall Tumor Response Rate (RR) As Assessed Using International Uniform Response Criteria for Multiple Myeloma and Criteria of the European Bone Marrow Transplant Registry
NCT00560352 (6) [back to overview]	Duration of Response
NCT00560352 (6) [back to overview]	Number of Participants With Death As Outcome, Serious Adverse Events (SAEs), Drug-related SAEs, Drug-related Adverse Events (AEs) Leading to Discontinuation, AEs Leading to Discontinuation, AEs, and Drug-related AEs by Grade
NCT00571493 (3) [back to overview]	Progression-free Survival (PFS), and Overall Survival (OS)
NCT00571493 (3) [back to overview]	Preliminary Estimate of Overall Response Rate (ORR)
NCT00571493 (3) [back to overview]	Maximum Tolerated Dose (MTD) of Bortezomib
NCT00581360 (5) [back to overview]	Median Duration of Stable Disease Response
NCT00581360 (5) [back to overview]	Objective Response Rate (ORR)
NCT00581360 (5) [back to overview]	Stable Disease Rate
NCT00581360 (5) [back to overview]	Number of Months of Progression-free Survival (PFS)
NCT00581360 (5) [back to overview]	Number of Months of Survival
NCT00581776 (4) [back to overview]	3 Year Progression Free Survival
NCT00581776 (4) [back to overview]	3 Year Overall Survival (OS)
NCT00581776 (4) [back to overview]	Overall Response Rate (ORR) at the Completion of Induction Chemotherapy, Which is the Percent of Complete Responses (CR) Plus Percent of Partial Responses (PR).
NCT00581776 (4) [back to overview]	Complete Response Rate (CR) at the End of Induction Chemotherapy
NCT00608907 (1) [back to overview]	Area Under the Plasma Concentration-time Curve (AUC) 0-72 Hours
NCT00609167 (8) [back to overview]	Duration of Response
NCT00609167 (8) [back to overview]	Number of Participants Who Achieved a Confirmed Responses Defined as a Complete Response (CR), Near CR or Very Good Partial Response (VGPR) After the First 4 Months of Treatment
NCT00609167 (8) [back to overview]	Number of Participants Who Responded to Treatment (Complete Response,CR; Near Complete Response, nCR; Very Good Partial Response, VGPR; or Partial Response, PR) After 4 Cycles
NCT00609167 (8) [back to overview]	Number of Participants Who Responded to Treatment (CR, nCR, VGPR or PR) After 8 Cycles
NCT00609167 (8) [back to overview]	Number of Participants With Severe Adverse Events
NCT00609167 (8) [back to overview]	Overall Survival (OS)
NCT00609167 (8) [back to overview]	Participants Who Successfully Completed Collection of Peripheral Blood Stem Cells for Transplant
NCT00609167 (8) [back to overview]	Progression Free Survival (PFS)
NCT00611325 (5) [back to overview]	Median Overall Survival (OS)
NCT00611325 (5) [back to overview]	Median Progression Free Survival (PFS)
NCT00611325 (5) [back to overview]	Number of Patients With Grade 3 or Greater, Treatment-related, Non-hematologic Toxicities
NCT00611325 (5) [back to overview]	Radiographic Response Rate
NCT00611325 (5) [back to overview]	6-month Progression-free Survival (PFS)
NCT00633594 (12) [back to overview]	Time to Best Response of Previously Treated and Previously Untreated Participants
NCT00633594 (12) [back to overview]	Time to Best Response of Phase I and Phase II Participants
NCT00633594 (12) [back to overview]	Progression Free Survival (PFS) of Previously Treated and Previously Untreated Participants
NCT00633594 (12) [back to overview]	Progression Free Survival (PFS) of Phase I and Phase II Participants
NCT00633594 (12) [back to overview]	Overall Survival of Previously Treated and Previously Untreated Participants
NCT00633594 (12) [back to overview]	Overall Survival of Phase I and Phase II Participants
NCT00633594 (12) [back to overview]	Overall Response Rate (ORR) of Previously Treated and Previously Untreated Participants
NCT00633594 (12) [back to overview]	Incidence of Non-Serious Adverse Events as a Measure of Safety and Tolerability, Phase II
NCT00633594 (12) [back to overview]	Duration of Response (DoR) of Previously Treated and Previously Untreated Participants
NCT00633594 (12) [back to overview]	Maximum Tolerated Dose of Lenalidomide Combined With Bortezomib and Rituximab in Phase I Participants
NCT00633594 (12) [back to overview]	Duration of Response (DoR) of Phase I and Phase II Participants
NCT00633594 (12) [back to overview]	Overall Response Rate (ORR) of Phase I and Phase II Participants
NCT00634179 (2) [back to overview]	Maximal Tolerated Doses of Bortezomib and Vincristine When Used in Combination of Bortezomib, Rituximab and the CHOP Chemotherapy Regimen (Phase I)
NCT00634179 (2) [back to overview]	An Estimate of the Overall Response Rate (ORR)(Complete Response [CR] + CR Unconfirmed [CRu] + Partial Response [PR]) to Bortezomib and Rituximab (VR)-CHOP According to International Workshop to Standardize Response Criteria (IWRC) Criteria
NCT00636792 (2) [back to overview]	Number of Participants With Complete Response
NCT00636792 (2) [back to overview]	Number of Participants With Overall Response (Complete and Partial Response)
NCT00641706 (4) [back to overview]	Proportion of Confirmed Tumor Response Defined as an Objective Status of Confirmed Response (CR), Partial Response (PR), or Regression (REGR) on Two Consecutive Evaluations
NCT00641706 (4) [back to overview]	Time to Progression
NCT00641706 (4) [back to overview]	Progression-free Survival at 6 Months
NCT00641706 (4) [back to overview]	Overall Survival
NCT00644228 (3) [back to overview]	Response Rates ()
NCT00644228 (3) [back to overview]	Progression-free Survival
NCT00644228 (3) [back to overview]	Overall Survival
NCT00666588 (5) [back to overview]	Dose Limiting Toxicity
NCT00666588 (5) [back to overview]	NF-kB Activity by Enzyme-linked Immunosorbent Assay (ELISA)
NCT00666588 (5) [back to overview]	Feasibility of Stem Cell Quantitation: Percentage of Leukemia Initiation Cells (LIC) Depletion
NCT00666588 (5) [back to overview]	Overall Response (Complete Remission [CR] and CR With Partial Recovery [CRp]) During Course 1
NCT00666588 (5) [back to overview]	Proteasome Inhibition Activity
NCT00691704 (5) [back to overview]	Duration of Response
NCT00691704 (5) [back to overview]	Progression Free Survival
NCT00691704 (5) [back to overview]	Time to Response
NCT00691704 (5) [back to overview]	Time to Progression
NCT00691704 (5) [back to overview]	Overall Survival
NCT00703664 (5) [back to overview]	Best Response
NCT00703664 (5) [back to overview]	Progression-free Survival (PFS)
NCT00703664 (5) [back to overview]	Overall Response Rate (ORR)
NCT00703664 (5) [back to overview]	Duration of Stable Disease
NCT00703664 (5) [back to overview]	Duration of Partial Response
NCT00711828 (6) [back to overview]	Duration of Response
NCT00711828 (6) [back to overview]	Overall Survival
NCT00711828 (6) [back to overview]	Progression-free Survival
NCT00711828 (6) [back to overview]	Time to Treatment Failure
NCT00711828 (6) [back to overview]	Adverse Events
NCT00711828 (6) [back to overview]	Proportion of Responses (Complete Response or Partial Response)
NCT00715208 (5) [back to overview]	Number of Patients Who Experienced at Least One Serious Adverse Event
NCT00715208 (5) [back to overview]	Percentage of Participants With Progression-free Survival (PFS) at 1 Year
NCT00715208 (5) [back to overview]	Number of Patients With Complete Response (CR)
NCT00715208 (5) [back to overview]	Duration of Response
NCT00715208 (5) [back to overview]	Number of Participants With Overall Response (OR)
NCT00719901 (2) [back to overview]	Number of Dose-limiting Toxicity (DLT) Incidents (Phase I)
NCT00719901 (2) [back to overview]	Number of Patients Who Have at Least a Partial Response (Phase I)
NCT00722137 (11) [back to overview]	Number of Participants Experiencing an Adverse Event (AE)
NCT00722137 (11) [back to overview]	Time to Next Anti-lymphoma Treatment (TTNT)
NCT00722137 (11) [back to overview]	Time to Progression (TTP)
NCT00722137 (11) [back to overview]	Treatment-free Interval (TFI)
NCT00722137 (11) [back to overview]	Duration of Response
NCT00722137 (11) [back to overview]	Progression Free Survival (PFS)
NCT00722137 (11) [back to overview]	Overall Complete Response (CR + CRu)
NCT00722137 (11) [back to overview]	Overall Survival (OS) in Long Term Follow-up Period
NCT00722137 (11) [back to overview]	Overall Survival (OS)
NCT00722137 (11) [back to overview]	Overall Response Rate (ORR)
NCT00722137 (11) [back to overview]	18-Month Survival
NCT00722566 (2) [back to overview]	Number of Patients With Overall Response (Complete Response + Partial Response)
NCT00722566 (2) [back to overview]	Number of Patients With Complete Response
NCT00722722 (1) [back to overview]	Response to Bortezomib Monotherapy
NCT00724568 (2) [back to overview]	The Percentage of Patients That Achieved Partial or Complete Response to Treatment.
NCT00724568 (2) [back to overview]	Maximum Tolerated Dose (MTD) of Combination Therapy With VELCADE, Dexamethasone, and Doxil, (RVDD)
NCT00734149 (3) [back to overview]	Response
NCT00734149 (3) [back to overview]	Number of Patients With Any Grade or Severe Adverse Event
NCT00734149 (3) [back to overview]	Median Duration of Response
NCT00742625 (4) [back to overview]	Disease-free Survival
NCT00742625 (4) [back to overview]	Participants Experiencing a Dose-limiting Toxicity (DLT) of Bortezomib When Administered in Combination With Intermediate-dose Cytarabine
NCT00742625 (4) [back to overview]	Remission Induction Response
NCT00742625 (4) [back to overview]	Overall Survival
NCT00750815 (4) [back to overview]	Phase II: Two Year Overall Survival (OS)
NCT00750815 (4) [back to overview]	Phase II: Progression-Free Survival (PFS)
NCT00750815 (4) [back to overview]	Phase I - Maximum Planned Dose (MPD) Level
NCT00750815 (4) [back to overview]	Phase II: Overall Response Rate (ORR)
NCT00765102 (7) [back to overview]	Participants With Treatment-emergent Adverse Events (TEAEs)
NCT00765102 (7) [back to overview]	Area Under the Concentration-time Curve From Time 0 Extrapolated to Infinity (AUC0-∞)
NCT00765102 (7) [back to overview]	Maximum Observed Concentration (Cmax)
NCT00765102 (7) [back to overview]	Terminal Half-life (t1/2)
NCT00765102 (7) [back to overview]	Time to Maximum Observed Concentration (Tmax)
NCT00765102 (7) [back to overview]	Total Clearance (CL)
NCT00765102 (7) [back to overview]	Total Volume of Distribution (Vz)
NCT00771875 (7) [back to overview]	Number of Patients in Each Group With Any of the Following: Rejection Reversal or Recurrent Rejection
NCT00771875 (7) [back to overview]	Mean Serum Creatinine
NCT00771875 (7) [back to overview]	Renal Allograft Survival
NCT00771875 (7) [back to overview]	Number of Patients With Allografts With C4d Focal Positive Pretreatment Biopsy
NCT00771875 (7) [back to overview]	Incidence of Post Transplant Lymphoproliferative Disorder (PTLD)
NCT00771875 (7) [back to overview]	Incidence of Death
NCT00771875 (7) [back to overview]	Number of Patients With Allografts With C4d Diffuse Positive Pretreatment Biopsy
NCT00772668 (3) [back to overview]	Overall Survival (OS)
NCT00772668 (3) [back to overview]	Progression-free Survival (PFS)
NCT00772668 (3) [back to overview]	Rate of Toxicity in Study Participants
NCT00773747 (5) [back to overview]	Overall Survival
NCT00773747 (5) [back to overview]	Objective Response Rate
NCT00773747 (5) [back to overview]	Progression-Free Survival (PFS)
NCT00773747 (5) [back to overview]	Time to Progression
NCT00773747 (5) [back to overview]	Number of Participants With Grade 3-5 Clinical or Laboratory Adverse Events (AEs)
NCT00773838 (8) [back to overview]	Objective Response Rate (RR)
NCT00773838 (8) [back to overview]	TTP as Assessed by Investigator Per EBMT Criteria
NCT00773838 (8) [back to overview]	Number of Participants Who Discontinued Study Treatment Due to an AE
NCT00773838 (8) [back to overview]	Number of Participants Who Experienced an Adverse Event (AE)
NCT00773838 (8) [back to overview]	Progression-Free Survival (PFS) as Determined by IAC Per EBMT Criteria
NCT00773838 (8) [back to overview]	PFS as Assessed by Investigator Per EBMT Criteria
NCT00773838 (8) [back to overview]	Overall Survival (OS)
NCT00773838 (8) [back to overview]	Time To Disease Progression (TTP) as Determined by IAC Per EBMT Criteria
NCT00782821 (5) [back to overview]	Antibody-mediated Rejection by Banff '97 Criteria (Updated 2005)
NCT00782821 (5) [back to overview]	Acute Cellular Rejection by Banff '97 Criteria (Updated 2005)
NCT00782821 (5) [back to overview]	Patient Allograft Survival at 12 Months
NCT00782821 (5) [back to overview]	Incidence of Acute Rejection (Banff '97) or Antibody Mediated Rejection
NCT00782821 (5) [back to overview]	Patient Survival at 12 Months
NCT00784823 (1) [back to overview]	The Maximum Tolerated Dose of Bortezomib (MTD)
NCT00789256 (1) [back to overview]	Response Rate of the Combination of Bortezomib and Melphalan in Patients With AML and High-risk MDS.
NCT00790647 (4) [back to overview]	Number of Participants Surviving at 1 Year
NCT00790647 (4) [back to overview]	Number of Participants Surviving at 100 Days From Transplant
NCT00790647 (4) [back to overview]	Number of Participants With Hematologic Response
NCT00790647 (4) [back to overview]	Number of Participants Surviving at 2 Years
NCT00792142 (3) [back to overview]	One Year Overall Survival
NCT00792142 (3) [back to overview]	One Year Progression-free Survival (PFS)
NCT00792142 (3) [back to overview]	Number of Participants With Adverse Events
NCT00793572 (6) [back to overview]	Number of Patients Surviving Overall
NCT00793572 (6) [back to overview]	Number of Patients Surviving Progression-free
NCT00793572 (6) [back to overview]	Number of Patients With Chronic GVHD
NCT00793572 (6) [back to overview]	Number of Patients With Toxicities Related to Bortezomib Maintenance Therapy
NCT00793572 (6) [back to overview]	Number of Patients With Non-relapse Mortality
NCT00793572 (6) [back to overview]	Number of Patients With Grade II-IV Acute GVHD
NCT00793650 (2) [back to overview]	Safety and Engraftment
NCT00793650 (2) [back to overview]	Response Rate Using EBMT(European Group for Blood and Bone Marrow Transplan) Criteria at Day +100 After Transplant.
NCT00798720 (4) [back to overview]	Three-month Progression-free Survival
NCT00798720 (4) [back to overview]	Median Overall Survival
NCT00798720 (4) [back to overview]	Response Rate
NCT00798720 (4) [back to overview]	Toxicity
NCT00810576 (1) [back to overview]	Number of Patients With Response
NCT00813150 (4) [back to overview]	Time to Progression of Disease
NCT00813150 (4) [back to overview]	Overall Survival (OS)
NCT00813150 (4) [back to overview]	Progression-Free Survival (PFS)
NCT00813150 (4) [back to overview]	Overall Response Rate (ORR) - International Myeloma Working Group (IMWG) Response Criteria
NCT00815919 (5) [back to overview]	Proportion of Patients Tolerating >50% Steroid Dose Reduction After a 15 Week Course of Bortezomib Plus Prednisone in Patients With cGVHD
NCT00815919 (5) [back to overview]	Overall Response Rate After a 15 Week Course of Bortezomib Plus Prednisone in Patients With cGVHD
NCT00815919 (5) [back to overview]	Proportion of cGVHD Patients Requiring Prednisone by 1 Year After Therapy
NCT00815919 (5) [back to overview]	Overall and cGVHD Progression-free Survival by 1 Year After Therapy
NCT00815919 (5) [back to overview]	The Toxicity of a 15 Week Course of Bortezomib Plus Prednisone in Patients With cGVHD
NCT00818649 (1) [back to overview]	Number of Patients by Best Clinical Response
NCT00833560 (4) [back to overview]	Percentage of Participants With Complete Response + Partial Response in Relation to Cytogenetic Subgroups (Per-protocol Set)
NCT00833560 (4) [back to overview]	Participants With Complete Response (CR) + Partial Response (PR) (Per-protocol Analysis Set)
NCT00833560 (4) [back to overview]	Percentage of Participants With Complete Response + Partial Response in Relation to Cytogenetic Subgroups (Efficacy Set)
NCT00833560 (4) [back to overview]	Participants With Complete Response (CR) + Partial Response (PR) (Efficacy Set)
NCT00839956 (4) [back to overview]	Time to Disease Progression in Patients Who Progressed
NCT00839956 (4) [back to overview]	Median Follow-up Survival for All Patients
NCT00839956 (4) [back to overview]	Survival for All Patients
NCT00839956 (4) [back to overview]	Toxicity as Assessed by National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) v3.0
NCT00849251 (2) [back to overview]	Maximum Tolerated Dose of This Combination of Drugs as Assessed by the NCI Common Terminology Criteria for Adverse Events (CTCAE) Version 3.0 (Cohort 1) [MTD Cyclophosphamide, MTD Bortezmib, MTD Docxorubicin]
NCT00849251 (2) [back to overview]	Maximum Tolerated Dose of This Combination of Drugs as Assessed by the NCI Common Terminology Criteria for Adverse Events (CTCAE) Version 3.0 (Cohort 1). [Dexamethasone MTD]
NCT00850499 (2) [back to overview]	Complete Response Rate
NCT00850499 (2) [back to overview]	Overall Response Rate
NCT00858234 (3) [back to overview]	Number of Participants With an Adverse Event (AE)
NCT00858234 (3) [back to overview]	Area Under the Plasma Concentration-Time Curve From 0 to 24 Hours Postdose (AUC0-24hr) of Vorinostat Administered With Bortezomib on Days 1 and 11
NCT00858234 (3) [back to overview]	Number of Participants With Dose-Limiting Toxicity (DLT) During Cycle 1
NCT00863369 (3) [back to overview]	Number of Subject With Complete Response
NCT00863369 (3) [back to overview]	Recommended Phase II Dose
NCT00863369 (3) [back to overview]	Number of Participants With at Least One Dose Limiting Toxicity (DLT)
NCT00869323 (5) [back to overview]	Remission Duration Among Patients Who Respond to Treatment
NCT00869323 (5) [back to overview]	Relapse-free Survival
NCT00869323 (5) [back to overview]	Overall Survival
NCT00869323 (5) [back to overview]	Number of Patients With Overall (Complete and Partial) Response Rates
NCT00869323 (5) [back to overview]	Time to Treatment Failure
NCT00873093 (7) [back to overview]	Toxic Death Rate
NCT00873093 (7) [back to overview]	Rate of Minimal Residual Disease (MRD) < 0.01% at End Block 1
NCT00873093 (7) [back to overview]	Rate of Minimal Residual Disease (MRD) < 0.01% at End Block 2
NCT00873093 (7) [back to overview]	Rate of Minimal Residual Disease (MRD) < 0.01% at End Block 3
NCT00873093 (7) [back to overview]	Severe Adverse Events (SAE) Rate.
NCT00873093 (7) [back to overview]	Event Free Survival
NCT00873093 (7) [back to overview]	Second Complete Remission Rate at the End of Block 1 Reinduction Chemotherapy
NCT00903968 (6) [back to overview]	Response Rate of Plerixafor, Bortezomib, and Dexamethasone in Relapsed or Relapsed/ Refractory Multiple Myeloma (ORR) [Phase I and Phase II]
NCT00903968 (6) [back to overview]	Time to Progression (TTP) [Phase II]
NCT00903968 (6) [back to overview]	Plerixafor Maximum Tolerated Dose (MTD) [Phase I]
NCT00903968 (6) [back to overview]	Number of Participants With Dose Limiting Toxicity (DLT) [Phase I]
NCT00903968 (6) [back to overview]	Duration of Response (DOR) [Phase II]
NCT00903968 (6) [back to overview]	Bortezomib Maximum Tolerated Dose (MTD) [Phase I]
NCT00908232 (6) [back to overview]	Time to Progression
NCT00908232 (6) [back to overview]	Progression Free Survival
NCT00908232 (6) [back to overview]	Overall Best Confirmed Response
NCT00908232 (6) [back to overview]	One Year Survival
NCT00908232 (6) [back to overview]	Median Time to First Confirmed Response
NCT00908232 (6) [back to overview]	Overall Survival
NCT00908583 (4) [back to overview]	Number of Living Donor Transplant Candidates That Are Transplanted
NCT00908583 (4) [back to overview]	Overall Safety of Bortezomib
NCT00908583 (4) [back to overview]	Acute Rejection Rate
NCT00908583 (4) [back to overview]	Number of Patients Whose Cytotoxic Panel Reactive Antibody (PRA) is Decreased by 50%
NCT00911859 (9) [back to overview]	1-year Survival Rate
NCT00911859 (9) [back to overview]	1-year Progression-Free Survival (PFS) Rate
NCT00911859 (9) [back to overview]	Percentage of Participants Who Achieved Stringent Complete Response (sCR) - International Myeloma Working Group (IMWG) Criteria
NCT00911859 (9) [back to overview]	Percentage of Participants Who Achieved Overall Response ie, Complete Response (CR) or Partial Response (PR) - European Group for Blood and Marrow Transplantation (EBMT) Criteria
NCT00911859 (9) [back to overview]	Percentage of Participants Who Achieved Complete Response (CR) - European Group for Blood and Marrow Transplantation (EBMT) Criteria
NCT00911859 (9) [back to overview]	Overall Survival
NCT00911859 (9) [back to overview]	Duration of Response (DOR)
NCT00911859 (9) [back to overview]	Progression-Free Survival (PFS)
NCT00911859 (9) [back to overview]	Change From Baseline to Cycle 9 in Global Health Status/Quality of Life Subscale of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Core 30 (EORTC QLQ C30)
NCT00920556 (17) [back to overview]	Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)
NCT00920556 (17) [back to overview]	Change From in Baseline Biochemistry: Serum Creatinine, Total Bilirubin
NCT00920556 (17) [back to overview]	Change From Baseline in Hematology: White Blood Cell (WBC) Count, Neutrophils, Lymphocytes, Platelets
NCT00920556 (17) [back to overview]	Change From Baseline in Biochemistry -Urea, Bicarbonate
NCT00920556 (17) [back to overview]	Time to Disease Progression
NCT00920556 (17) [back to overview]	Change From Baseline in Biochemistry: Prothrombin Time (PT)/ International Normalized Ratio (INR)
NCT00920556 (17) [back to overview]	Change From Baseline in Hematology: Hematocrit
NCT00920556 (17) [back to overview]	Change From Baseline in Hematology: Hemoglobin
NCT00920556 (17) [back to overview]	Change From Baseline in Hematology: Red Blood Cell (RBC)
NCT00920556 (17) [back to overview]	Number of Participants With Minor Response (MR) as Best Response (BR)
NCT00920556 (17) [back to overview]	Number of Participants With Overall Response Rate
NCT00920556 (17) [back to overview]	Number of Participants With Partial Response (PR) as Best Response (BR)
NCT00920556 (17) [back to overview]	Number of Participants With Partial Response (PR) as Last Observed Response (LOR)
NCT00920556 (17) [back to overview]	Number of Participants With Progressive Disease (PD) PD as Best Response (BR)
NCT00920556 (17) [back to overview]	Number of Participants With Progressive Disease (PD) PD as Last Observed Response (LOR)
NCT00920556 (17) [back to overview]	Number of Participants With Stable Disease (SD) as Best Response (BR)
NCT00920556 (17) [back to overview]	Number of Participants With Stable Disease (SD) as Last Observed Response (LOR)
NCT00920855 (9) [back to overview]	Kaplan-Meier Estimate for Duration of Response
NCT00920855 (9) [back to overview]	Kaplan-Meier Estimate for Progression-Free Survival
NCT00920855 (9) [back to overview]	Summary of Participants With Adverse Events (AEs)
NCT00920855 (9) [back to overview]	Participants' Best Tumor Response as Assessed by the Investigator
NCT00920855 (9) [back to overview]	Time to the First Response
NCT00920855 (9) [back to overview]	Percentage of Participants With An Overall Tumor Response As Assessed By the Investigator
NCT00920855 (9) [back to overview]	Participants With Dose Limiting Toxicity (DLT)
NCT00920855 (9) [back to overview]	Kaplan-Meier Estimate for Time to Progression (TTP)
NCT00920855 (9) [back to overview]	Kaplan-Meier Estimate for Overall Survival (OS)
NCT00923247 (12) [back to overview]	Terminal Half-Life (T1/2) of Bortezomib
NCT00923247 (12) [back to overview]	Phase I: Maximum Tolerated Dose (MTD) of Daily Oral Bortezomib
NCT00923247 (12) [back to overview]	Phase I: Maximum Tolerated Dose (MTD) of Daily Oral Vandetanib
NCT00923247 (12) [back to overview]	Progression Free Survival (PFS)
NCT00923247 (12) [back to overview]	Area Under the Bortezomib Plasma Concentration Versus Time Curve From Time Zero to Infinity/Dose (AUCinf/D)
NCT00923247 (12) [back to overview]	Bortezomib Volume of Distribution (Vss)
NCT00923247 (12) [back to overview]	Comparison of Steady State Vandetanib Exposure With Relevant Literature Values
NCT00923247 (12) [back to overview]	Maximum Bortezomib Plasma Concentration Normalized to Dose (Cmax/D)
NCT00923247 (12) [back to overview]	Response Rate (Complete Response (CR) + Partial Response (PR) of Adults With a Diagnosis of MTC Treated With Either of Two Regimens: (1) Daily Oral Vandetanib and Bortezomib or (2) Daily Oral Vandetanib
NCT00923247 (12) [back to overview]	Phase 2: Progression Free Survival in Adults With a Diagnosis of Medullary Thyroid Cancer (MTC) Treated With Daily Oral Vandetanib and Bortezomib
NCT00923247 (12) [back to overview]	Total Systemic Clearance (CL) of Bortezomib
NCT00923247 (12) [back to overview]	Number of Participants With Adverse Events
NCT00931918 (10) [back to overview]	Duration of Response
NCT00931918 (10) [back to overview]	Overall Survival
NCT00931918 (10) [back to overview]	Progression-Free Survival (PFS) in Patients With Non-germinal Center B-cell-like (Non-GCB) Diffuse Large B-cell Lymphoma (DLBCL)
NCT00931918 (10) [back to overview]	Progression-Free Survival Rate
NCT00931918 (10) [back to overview]	Time to Progression (TTP)
NCT00931918 (10) [back to overview]	Complete Response Rate
NCT00931918 (10) [back to overview]	Fluorodeoxyglucose Positron Emission Tomography (FDG-PET) Negative Rate
NCT00931918 (10) [back to overview]	Overall Response Rate (ORR)
NCT00931918 (10) [back to overview]	Percentage of Participants With Chemistry and Hematology Laboratory Values Grade 3 or Higher
NCT00931918 (10) [back to overview]	Percentage of Participants With Treatment Emergent Adverse Events (TEAEs) by Category
NCT00937495 (3) [back to overview]	Overall Survival
NCT00937495 (3) [back to overview]	Confirmed Tumor Responses
NCT00937495 (3) [back to overview]	Progression Free Survival
NCT00948922 (3) [back to overview]	Overall Survival (OS) Rate
NCT00948922 (3) [back to overview]	Progression Free Survival (PFS)
NCT00948922 (3) [back to overview]	Percentage of Participants With Acute or Chronic Graft-versus-host Disease (GVHD) Following Transplant
NCT00958256 (1) [back to overview]	Response Rate
NCT00967369 (4) [back to overview]	Overall Response After 3 Cycles of Botezomib Plus ICE (BICE) Versus Ifosfamide, Carboplatin, Etoposide (ICE) in Patients With Relapsed/Refractory Classical Hodgkin Lymphoma
NCT00967369 (4) [back to overview]	PET Scan Response After 3 Cycles of BICE Versus ICE Chemotherapy.
NCT00967369 (4) [back to overview]	Progression Free Survival (PFS) Rate at 12 Months
NCT00967369 (4) [back to overview]	Overall Survival (OS) Rate at 24 Months
NCT00972959 (12) [back to overview]	Skeletal Survey for New Osteolytic Lesions/Fractures
NCT00972959 (12) [back to overview]	Bone Remodelling
NCT00972959 (12) [back to overview]	Bone Pain
NCT00972959 (12) [back to overview]	Bone Remodelling
NCT00972959 (12) [back to overview]	Bone Pain
NCT00972959 (12) [back to overview]	Skeletal Survey for New Osteolytic Lesions/Fractures
NCT00972959 (12) [back to overview]	Bone Mineral Density (BMD)
NCT00972959 (12) [back to overview]	New Skeletal-related Events (SRE: Pathologic Fractures, Need for Bone Radiation Therapy or Surgery)
NCT00972959 (12) [back to overview]	New Skeletal-related Events (SRE: Pathologic Fractures, Need for Bone Radiation Therapy or Surgery)
NCT00972959 (12) [back to overview]	Bone Mineral Density (BMD)
NCT00972959 (12) [back to overview]	Bone Remodelling
NCT00972959 (12) [back to overview]	Bone Remodelling
NCT00980395 (4) [back to overview]	Complete Response Rate
NCT00980395 (4) [back to overview]	Progression-free Survival at 2 Years
NCT00980395 (4) [back to overview]	Overall Survival at 2 Years
NCT00980395 (4) [back to overview]	Partial Response
NCT00983346 (1) [back to overview]	Bone Anabolic Effect of Bortezomib in Patients With Smoldering Myeloma.
NCT00985907 (1) [back to overview]	Number of Participants With Dose Limiting Toxicities (DLT) (Phase 1)
NCT00985959 (7) [back to overview]	Maximum Observed Plasma Concentration (Cmax) of Bortezomib (JNJ-26866138 Alone) - Phase I
NCT00985959 (7) [back to overview]	Maximum Observed Plasma Concentration (Cmax) of Bortezomib (JNJ-26866138 in Combination With Melphalan and Prednisolone) - Phase I
NCT00985959 (7) [back to overview]	Maximum Observed Plasma Concentration (Cmax) of Melphalan - Phase I
NCT00985959 (7) [back to overview]	Maximum Observed Plasma Concentration (Cmax) of Prednisolone - Phase I
NCT00985959 (7) [back to overview]	Median Time to First Response - Phase II
NCT00985959 (7) [back to overview]	Number of Participants With Dose Limiting Toxicity During the Phase I (Cycle 1)
NCT00985959 (7) [back to overview]	Number of Participants With Overall Response (Complete Response [CR] + Partial Response [PR]) - Phase I and II
NCT00990652 (5) [back to overview]	Overall Survival (in Days)
NCT00990652 (5) [back to overview]	Number of Grade 1, 2, 3, 4, and 5 Adverse Events Observed During Study Treatment (Defined by CTCAE v 3.0)
NCT00990652 (5) [back to overview]	Overall Survival Rate at 6 Months
NCT00990652 (5) [back to overview]	Number of Patients Surviving Without Disease Progression After 6 Months
NCT00990652 (5) [back to overview]	Number of Participants Achieving a Response to Treatment (Either Complete or Partial Response) as Defined by MacDonald Criteria
NCT00992446 (4) [back to overview]	Overall Survival
NCT00992446 (4) [back to overview]	Event-free Survival
NCT00992446 (4) [back to overview]	Toxicity of Vorinostat Bortezomib Maintenance Therapy After Autologous Transplant
NCT00992446 (4) [back to overview]	Median Time to Disease Progression
NCT00998010 (5) [back to overview]	Survival at 1 Year
NCT00998010 (5) [back to overview]	Overall Survival
NCT00998010 (5) [back to overview]	Toxicity Assessed According to the NCI Common Terminology Criteria for Adverse Events (CTCAE) Version 3.
NCT00998010 (5) [back to overview]	Tumor Progression as Assessed by Magnetic Resonance Imaging (MRI) and Neurologic Exam
NCT00998010 (5) [back to overview]	Time to Progression
NCT01000285 (8) [back to overview]	Efficacy of Treatment as Measured by Best Overall Response
NCT01000285 (8) [back to overview]	Effects of on HTLV-1 DNA After Treatment as Measured by Proviral Loads
NCT01000285 (8) [back to overview]	Effects of HTLV-1 RNA Load After Treatment as Measured by Hbz Messenger RNA
NCT01000285 (8) [back to overview]	Effects of HTLV-1 Integration Sites After Treatment
NCT01000285 (8) [back to overview]	Effects of HTLV-1 Integrase Gene Sequence After Treatment as Measured by Nucleotide Divergence
NCT01000285 (8) [back to overview]	Time to Progression
NCT01000285 (8) [back to overview]	Tolerability of Treatment as Measured by Number of Participants With Grade 3 or Higher Adverse Events
NCT01000285 (8) [back to overview]	Relation of NFκB Gene Expression Profile on Response
NCT01009840 (10) [back to overview]	Percent Difference Between Area Under Curve (AUC) and Target AUC
NCT01009840 (10) [back to overview]	Overall Survival
NCT01009840 (10) [back to overview]	Percent Change in IV Busulfan Dose
NCT01009840 (10) [back to overview]	Percentage of Participants With Hepatic Veno-Occlusive Disease Based on Baltimore Criteria
NCT01009840 (10) [back to overview]	Percentage of Participants With Overall Disease Response at Month 6
NCT01009840 (10) [back to overview]	Ratio Area Under Curve (AUC)/Target AUC
NCT01009840 (10) [back to overview]	Progression-free Survival
NCT01009840 (10) [back to overview]	Percentage of Participants With Transplant-Related Mortality
NCT01009840 (10) [back to overview]	Percentage of Participants With Progression-free Survival Events
NCT01009840 (10) [back to overview]	Percentage of Participants With Overall Survival Events
NCT01023308 (11) [back to overview]	Functional Assessment of Chronic Illness Therapy (FACIT) Measurement System : FACT/GOG-NTX-Change From Baseline by Treatment Group
NCT01023308 (11) [back to overview]	European Organization for Research and Treatment of Cancer Multiple Myeloma Module (EORTC) QLQ-MY20-Change From Baseline by Treatment Group
NCT01023308 (11) [back to overview]	Time to Response Per Investigator Assessment (mEBMT Criteria) of Response Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone.
NCT01023308 (11) [back to overview]	European Organization for Research and Treatment of Cancer Multiple Myeloma Module (EORTC ) QLQ-C30 - Summary Statistics by Treatment Group
NCT01023308 (11) [back to overview]	Overall Response Rate in Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone.
NCT01023308 (11) [back to overview]	Duration of Response Per Investigator Assessment (mEBMT Criteria) Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone.
NCT01023308 (11) [back to overview]	Overall Survival in Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone
NCT01023308 (11) [back to overview]	Overall Survival in Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone
NCT01023308 (11) [back to overview]	Progression Free Survival in Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone.
NCT01023308 (11) [back to overview]	Time to Progression/Relapse Per Investigator Assessment (mEBMT Criteria) Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone.
NCT01023308 (11) [back to overview]	Progression-free Survival Events in Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone.
NCT01029730 (4) [back to overview]	Median Progression-free Survival
NCT01029730 (4) [back to overview]	Complete Response Rate
NCT01029730 (4) [back to overview]	Number of Participants With Adverse Events as a Measure of Safety.
NCT01029730 (4) [back to overview]	Overall Response Rate
NCT01034553 (4) [back to overview]	Overall Response Rate to the Combination of MLN8237 and Bortezomib in Patients With Relapsed or Refractory Multiple Myeloma.
NCT01034553 (4) [back to overview]	Dose-limiting Toxicity (DLT) (Phase I)
NCT01034553 (4) [back to overview]	Overall Survival
NCT01034553 (4) [back to overview]	Progression-free Survival
NCT01040871 (7) [back to overview]	Rate of Durable Complete Response
NCT01040871 (7) [back to overview]	Rate of Durable Response
NCT01040871 (7) [back to overview]	Subsequent Anti-lymphoma Therapy Rate at 1-year
NCT01040871 (7) [back to overview]	Overall Survival Rate at 1-year
NCT01040871 (7) [back to overview]	Overall Response Rate
NCT01040871 (7) [back to overview]	Complete Response (CR) Rate
NCT01040871 (7) [back to overview]	Progression-free Survival (PFS)Rate at 1-year
NCT01056276 (5) [back to overview]	Complete Response Rate
NCT01056276 (5) [back to overview]	Overall Survival
NCT01056276 (5) [back to overview]	Number of Patients Who Experienced Serious and Non-serious Adverse Events
NCT01056276 (5) [back to overview]	Overall Response Rate
NCT01056276 (5) [back to overview]	Progression Free Survival
NCT01056601 (3) [back to overview]	Progression-Free Survival
NCT01056601 (3) [back to overview]	Number of Participants by Tumor Response
NCT01056601 (3) [back to overview]	Duration of Response
NCT01058239 (6) [back to overview]	Treatment Related Toxicities
NCT01058239 (6) [back to overview]	Overall Survival
NCT01058239 (6) [back to overview]	Effects of Bortezomib/Rituximab on EBV Quantitative Viral Load
NCT01058239 (6) [back to overview]	Six-Month Progression Free Survival
NCT01058239 (6) [back to overview]	Overall Response Rate
NCT01058239 (6) [back to overview]	Complete Response Rate
NCT01062230 (1) [back to overview]	Maximum Percent Change From Baseline in Intact Parathyroid Hormone Levels on Day 1
NCT01063907 (5) [back to overview]	To Establish the Safety, Tolerability, and RP2D (Phase 1); To Assess the Overall Response Rate in Subjects With Advanced Multiple Myeloma (Phase 2).
NCT01063907 (5) [back to overview]	Phase 1: PK Exposure Cmax ng/mL Day 11
NCT01063907 (5) [back to overview]	Phase 1: PK Elimination t½ hr Day 11
NCT01063907 (5) [back to overview]	Phase 1: PK Absorption Tmax hr Day 11
NCT01063907 (5) [back to overview]	Phase 1: PK Exposure AUC0-t hr*ng/mL Day 11
NCT01072773 (5) [back to overview]	Number of Participants With a Confirmed Hematologic Response
NCT01072773 (5) [back to overview]	Number of Participants With Treatment Related Adverse Events.
NCT01072773 (5) [back to overview]	Overall Survival
NCT01072773 (5) [back to overview]	Time to Disease Progression
NCT01072773 (5) [back to overview]	Number of Participants With an Organ Response.
NCT01078441 (1) [back to overview]	One-year Survival in Patients Treated With This Regimen.
NCT01078454 (1) [back to overview]	Proportion of Patients With Hematologic Overall Response (Partial Response [PR]+ Very Good PR [VGPR]+ Amyloid Complete Response [ACR]+ Stringent Complete Response [sCR]) After 3 Months (3 Cycles) of Therapy
NCT01083316 (4) [back to overview]	Number of Participants Surviving at 5 Years
NCT01083316 (4) [back to overview]	Number of Participants Proceeding to Transplant Following Induction
NCT01083316 (4) [back to overview]	Number of Participants Surviving at 100 Days Post Transplant
NCT01083316 (4) [back to overview]	Number of Participants With Disease Response
NCT01083602 (6) [back to overview]	Over All Survival
NCT01083602 (6) [back to overview]	Responders to Treatment
NCT01083602 (6) [back to overview]	Progression-free Survival
NCT01083602 (6) [back to overview]	Time to Progression
NCT01083602 (6) [back to overview]	Time to Response (Greater Than or Equal to PR) Based on Investigator Assessment
NCT01083602 (6) [back to overview]	Overall Response Rate (PR+nCR+CR)
NCT01088048 (15) [back to overview]	Time to Response
NCT01088048 (15) [back to overview]	Duration of Response
NCT01088048 (15) [back to overview]	Plasma Concentration of Everolimus
NCT01088048 (15) [back to overview]	Plasma Concentration of Bendamustine
NCT01088048 (15) [back to overview]	Plasma Concentration of IDELA (Cohort 7)
NCT01088048 (15) [back to overview]	Plasma Concentration of IDELA (Cohort 6)
NCT01088048 (15) [back to overview]	Toxicity of Administration of IDELA
NCT01088048 (15) [back to overview]	Plasma Concentration of IDELA (Cohort 1, Cohorts 2 and 3, Cohort 5)
NCT01088048 (15) [back to overview]	Plasma Concentration of IDELA (Cohort 4)
NCT01088048 (15) [back to overview]	Overall Survival
NCT01088048 (15) [back to overview]	Overall Response Rate
NCT01088048 (15) [back to overview]	Sub-study: Plasma Concentration of IDELA (Cohorts 1-4)
NCT01088048 (15) [back to overview]	Plasma Concentration of Lenalidomide
NCT01088048 (15) [back to overview]	Progression-free Survival
NCT01088048 (15) [back to overview]	Duration of Exposure to IDELA
NCT01090921 (1) [back to overview]	Number of Participants With Dose Reductions in Bortezomib, Dexamethasone or Both
NCT01100242 (3) [back to overview]	Progression Free Survival (PFS)
NCT01100242 (3) [back to overview]	Overall Response Rate (ORR)
NCT01100242 (3) [back to overview]	Toxicity Profile
NCT01103778 (4) [back to overview]	Proteinuria
NCT01103778 (4) [back to overview]	Number of Participants With Complete Remission, Partial Response, or no Response.
NCT01103778 (4) [back to overview]	Number of Participants With Abnormal Lab Values or Infections Related to Exposure to Study Medication.
NCT01103778 (4) [back to overview]	Serum Creatinine
NCT01109004 (10) [back to overview]	FACT-G Total Score
NCT01109004 (10) [back to overview]	FACT-BMT Trial Outcome Index
NCT01109004 (10) [back to overview]	FACT-BMT Score
NCT01109004 (10) [back to overview]	Percentage of Participants With Treatment-related Mortality (TRM)
NCT01109004 (10) [back to overview]	Percentage of Participants With Overall Survival (OS)
NCT01109004 (10) [back to overview]	Percentage of Participants With Disease Progression
NCT01109004 (10) [back to overview]	MOS SF-36 Mental Component Summary
NCT01109004 (10) [back to overview]	Percentage of Participants With Progression-free Survival (PFS)
NCT01109004 (10) [back to overview]	Number of Participants With Treatment Response
NCT01109004 (10) [back to overview]	MOS SF-36 Physical Component Summary
NCT01119794 (1) [back to overview]	Overall Response Rate (ORR) of the Combination of Ofatumumab and Bortezomib in Patients Receiving Study Treatment
NCT01125293 (10) [back to overview]	PTEN Mutation Rate [Phase II]
NCT01125293 (10) [back to overview]	Phase II Duration of Response (DoR)
NCT01125293 (10) [back to overview]	Phase II Overall Response Rate
NCT01125293 (10) [back to overview]	Treatment-Emergent Sensory Neuropathy Rate [Phase I]
NCT01125293 (10) [back to overview]	Very-good-partial-response-or-better Rate [Phase II]
NCT01125293 (10) [back to overview]	Everolimus Dose Limiting Toxicity (DLT) [Phase I]
NCT01125293 (10) [back to overview]	Everolimus Maximum Tolerated Dose (MTD) Stage B [Phase I]
NCT01125293 (10) [back to overview]	Everolimus Maximum Tolerated Dose (MTD) Stage A [Phase I]
NCT01125293 (10) [back to overview]	2 Year Progression-free-survival [Phase II]
NCT01125293 (10) [back to overview]	2-year Time-to-progression Probability (TTP) [Phase II]
NCT01142401 (6) [back to overview]	Number of Participants With Progression Free Survival (PFS) at 6 Months
NCT01142401 (6) [back to overview]	Progression Free Survival at 24 Weeks (Arm C)
NCT01142401 (6) [back to overview]	Frequency of Most Common Toxicities
NCT01142401 (6) [back to overview]	Number of Participants Who Survived Until Study End (up to 7 Years)
NCT01142401 (6) [back to overview]	Clinical Benefit Rate (CBR) of Adding Bortezomib to Fulvestrant in Arm C
NCT01142401 (6) [back to overview]	Number of Participants With Progression Free Survival (PFS) at 12 Months
NCT01146834 (3) [back to overview]	Number of Patients Able to Collect >=6 x 106 CD34+ Cells/kg in <= 2 Collections.
NCT01146834 (3) [back to overview]	Number of Patients Who Achieved Neutrophil Recovery After Melphalan 200 Based Transplant
NCT01146834 (3) [back to overview]	Number of Patients Who Achieved Platelet Recovery After Melphalan 200 Based Transplant
NCT01160484 (7) [back to overview]	Follow-up Time
NCT01160484 (7) [back to overview]	Time to Best Response
NCT01160484 (7) [back to overview]	International Myeloma Working Group (IMWG) Response Criteria
NCT01160484 (7) [back to overview]	Time to Progression
NCT01160484 (7) [back to overview]	Duration of Response
NCT01160484 (7) [back to overview]	Progression-free Survival
NCT01160484 (7) [back to overview]	Time to First Response
NCT01163786 (3) [back to overview]	Exercise Tolerance- 6 Minute Walk
NCT01163786 (3) [back to overview]	Change in Pulmonary Function as Measured by Forced Expiratory Volume in 1 Second (FEV1) Decline
NCT01163786 (3) [back to overview]	Short Form (SF)-36 Health Survey
NCT01177683 (6) [back to overview]	Phase I: MTD of Bendamustine When Combined With Bortezomib and Pegylated Liposomal Doxorubicin.
NCT01177683 (6) [back to overview]	Phase I & Phase II : Toxicity of Treatment Regimen
NCT01177683 (6) [back to overview]	Phase II: Progression-free Survival (PFS)
NCT01177683 (6) [back to overview]	Phase II: Overall Survival
NCT01177683 (6) [back to overview]	Phase II: Duration of Survival
NCT01177683 (6) [back to overview]	Phase II : Time to Progression
NCT01186458 (1) [back to overview]	Toxicity
NCT01208662 (17) [back to overview]	Quality-Adjusted Life Years (QALYs)
NCT01208662 (17) [back to overview]	Subsequent Therapy Rate
NCT01208662 (17) [back to overview]	Median Treatment Duration
NCT01208662 (17) [back to overview]	Median Progression-Free Survival (PFS)
NCT01208662 (17) [back to overview]	Median Maintenance Treatment Duration
NCT01208662 (17) [back to overview]	Median Event Free Survival (EFS)
NCT01208662 (17) [back to overview]	Change From Baseline on the European Organization for Research and Treatment of Cancer Quality-of-Life Questionnaire Core 30 (EORTC QLQ-C30): Global Health Status/Quality of Life (QoL) Sub-scale
NCT01208662 (17) [back to overview]	Change From Baseline on the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity (FACT/GOG-NTX)
NCT01208662 (17) [back to overview]	Partial Response (PR) Rate
NCT01208662 (17) [back to overview]	Median Duration of Response: Partial Response (DOR PR)
NCT01208662 (17) [back to overview]	Very Good Partial Response (VGPR) Rate
NCT01208662 (17) [back to overview]	Grade 3 or Higher Treatment-Related Non-Hematologic Adverse Event (AE) Rate
NCT01208662 (17) [back to overview]	Complete Response (CR) Rate
NCT01208662 (17) [back to overview]	5-Year Time to Progression (TTP)
NCT01208662 (17) [back to overview]	5-Year Overall Survival (OS)
NCT01208662 (17) [back to overview]	5-year Cumulative Incidence of Second Primary Malignancy (SPM)
NCT01208662 (17) [back to overview]	Next Generation Sequencing (NGS) Minimal Residual Disease Negative (MRD-) Rate at Maintenance Start
NCT01212952 (3) [back to overview]	Find Maximum Tolerated Dose (MTD) of Bortezomib in Combination With Pomalidomide and Dexamethasone Out to 2.5 Years, by Count of Patients With Dose Limiting Toxicities.
NCT01212952 (3) [back to overview]	Number of Participants With Adverse Events
NCT01212952 (3) [back to overview]	Progression Free Survival
NCT01215344 (2) [back to overview]	The Percent of Patients With Minimal Residual Disease (MRD) Status Changing to Negative at Day 100 (Post-AHCT), Among Patients With MRD Positive at the End of Induction (EOI).
NCT01215344 (2) [back to overview]	Progression Free Survival by MRD Status at Day 100.
NCT01216683 (25) [back to overview]	Functional Assessment of Cancer Therapy - Lymphoma (FACT-Lym) Subscale Score at End of Induction Treatment
NCT01216683 (25) [back to overview]	Functional Assessment of Cancer Therapy - General (FACT-G) Total Score at Baseline
NCT01216683 (25) [back to overview]	Complete Remission (CR) Rate
NCT01216683 (25) [back to overview]	Complete Remission (CR) Rate
NCT01216683 (25) [back to overview]	Complete Remission (CR) Rate
NCT01216683 (25) [back to overview]	5-year Overall Survival Rate
NCT01216683 (25) [back to overview]	5-year Overall Survival Rate
NCT01216683 (25) [back to overview]	5-year Overall Survival Rate
NCT01216683 (25) [back to overview]	3-year Progression-free Survival Rate
NCT01216683 (25) [back to overview]	Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-Fatigue) Subscale Score at Mid-induction Treatment
NCT01216683 (25) [back to overview]	3-year Progression-free Survival Rate
NCT01216683 (25) [back to overview]	1-year Post-induction Disease-free Survival (DFS) Rate
NCT01216683 (25) [back to overview]	1-year Disease-free Survival (DFS) Rate
NCT01216683 (25) [back to overview]	1-year Disease-free Survival (DFS) Rate
NCT01216683 (25) [back to overview]	Proportion of Patients With Grade 3 or Higher Peripheral Neuropathy
NCT01216683 (25) [back to overview]	Progression-free Survival
NCT01216683 (25) [back to overview]	Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-Fatigue) Subscale Score at End of Induction Treatment
NCT01216683 (25) [back to overview]	Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-Fatigue) Subscale Score at Baseline
NCT01216683 (25) [back to overview]	Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - Neurotoxicity (FACT-GOG-NTX) Subscale Score at the End of Induction Treatment
NCT01216683 (25) [back to overview]	Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - Neurotoxicity (FACT-GOG-NTX) Subscale Score at Mid-induction Treatment
NCT01216683 (25) [back to overview]	Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - Neurotoxicity (FACT-GOG-NTX) Subscale Score at Baseline
NCT01216683 (25) [back to overview]	Functional Assessment of Cancer Therapy - Lymphoma (FACT-Lym) Subscale Score at Mid-induction Treatment
NCT01216683 (25) [back to overview]	Functional Assessment of Cancer Therapy - Lymphoma (FACT-Lym) Subscale Score at Baseline
NCT01216683 (25) [back to overview]	Functional Assessment of Cancer Therapy - General (FACT-G) Total Score at Mid-treatment
NCT01216683 (25) [back to overview]	Functional Assessment of Cancer Therapy - General (FACT-G) Total Score at End of Induction Treatment
NCT01242267 (4) [back to overview]	Toxicity Assessment
NCT01242267 (4) [back to overview]	Maximum Tolerated Dose of Thalidomide
NCT01242267 (4) [back to overview]	Treatment Free Interval/PFS
NCT01242267 (4) [back to overview]	Complete Response (CR) and Very Good Partial Response (VgPR) Rate
NCT01267812 (3) [back to overview]	Two-year Overall Survival
NCT01267812 (3) [back to overview]	Grade 3 or 4 Toxicities of Bortezomib and Rituximab Treatment
NCT01267812 (3) [back to overview]	Two-year Disease-free Survival
NCT01281917 (5) [back to overview]	Overall Response Rate
NCT01281917 (5) [back to overview]	Overall Survival
NCT01281917 (5) [back to overview]	Progression Free Survival
NCT01281917 (5) [back to overview]	Duration of Response
NCT01281917 (5) [back to overview]	Complete Response Rate
NCT01286077 (15) [back to overview]	Overall Survival
NCT01286077 (15) [back to overview]	Tumor Response: Percentage of Participants With Very Good Partial Response (VGPR) or Stringent Complete Response (sCR) or Complete Response (CR) Based on International Myeloma Working Group (IMWG) Response Criteria
NCT01286077 (15) [back to overview]	Tumor Response: Percentage of Participants With Stable Disease (SD) or Progressive Disease (PD) Based on International Myeloma Working Group (IMWG) Response Criteria
NCT01286077 (15) [back to overview]	Number of Patients With Skeletal Events
NCT01286077 (15) [back to overview]	Change From Baseline in Bone Mineral Density (BMD) in the Femur at End of Treatment
NCT01286077 (15) [back to overview]	Change From Baseline in Biochemical Bone Markers: Dickkopf Homolog 1 (DKK-1)
NCT01286077 (15) [back to overview]	Change From Baseline in Bone Mineral Density (BMD) in the Spine at End of Treatment (EOT)
NCT01286077 (15) [back to overview]	Change From Baseline in Biochemical Bone Markers: Carboxyterminal Collagen Crosslinks (CTX-I)
NCT01286077 (15) [back to overview]	Appearance of New Bone Lesions Compared to Baseline
NCT01286077 (15) [back to overview]	Change From Baseline in Quality of Life Assessed by Euro Quality of Life (EQ-5D)
NCT01286077 (15) [back to overview]	Change From Baseline in Spine T-score
NCT01286077 (15) [back to overview]	Karnofsky Performance Status
NCT01286077 (15) [back to overview]	Tumor Response: Percentage of Participants With Partial Response (PR) Based on International Myeloma Working Group (IMWG) Response Criteria
NCT01286077 (15) [back to overview]	Change From Baseline in Biochemical Bone Markers:Carboxyterminal Telopeptide of Type I Collagen (ICTP), Osteocalcin, Bone-specific Alkaline Phosphatase (BAP)
NCT01286077 (15) [back to overview]	Progression Free Survival
NCT01286272 (3) [back to overview]	The Number of Patients Who Experienced Grade 3+ Hematologic and Non-hematologic Adverse Events at Least Possibly Related to Treatment
NCT01286272 (3) [back to overview]	Progression-free Survival (PFS)
NCT01286272 (3) [back to overview]	Complete Response Rate
NCT01312818 (2) [back to overview]	Number of Subjects Who Achieved Complete Remission of Their Disease
NCT01312818 (2) [back to overview]	Number of Subjects Experiencing Drug Related Adverse Events
NCT01313897 (1) [back to overview]	Therapeutic Efficacy
NCT01323920 (4) [back to overview]	The Cumulative Incidence of Chronic GVHD Requiring Systemic Immune Suppression up to 1 Year After Stem Cell Infusion
NCT01323920 (4) [back to overview]	The Non-relapse Mortality, Progression-free and Overall Survival up to 1 Year After Stem Cell Infusion
NCT01323920 (4) [back to overview]	The Percentage Donor Engraftment up to Day 30 Post Stem Cell Infusion
NCT01323920 (4) [back to overview]	The Cumulative Incidence of Grade II-IV Acute GVHD up to Day 100 After Stem Cell Infusion
NCT01371981 (18) [back to overview]	Proportion of High Risk Children Without HR FLT3/ITD+ Converting From Positive MRD at End of Induction I to Negative MRD at the End of Induction II
NCT01371981 (18) [back to overview]	EFS for Patients on Arm C, Cohort 3
NCT01371981 (18) [back to overview]	OS for Patients on Arm C, Cohort 1
NCT01371981 (18) [back to overview]	Event-free Survival (EFS) for Patients Without High Allelic Ratio FLT3/ITD+ Mutations
NCT01371981 (18) [back to overview]	OS for Patients on Arm C, Cohort 3
NCT01371981 (18) [back to overview]	Relapse Rate for Patients Without High Allelic Ratio FLT3/ITD+ Mutations
NCT01371981 (18) [back to overview]	Change in Ejection Fraction
NCT01371981 (18) [back to overview]	Overall Survival (OS) for Patients Without High Allelic Ratio FLT3/ITD+ Mutations
NCT01371981 (18) [back to overview]	OS for Patients on Arm C, Cohort 2
NCT01371981 (18) [back to overview]	Bortezomib Clearance
NCT01371981 (18) [back to overview]	Change in Shortening Fraction
NCT01371981 (18) [back to overview]	Sorafenib Steady State Concentration
NCT01371981 (18) [back to overview]	Total Scale Score From Parent-reported Cancer Module
NCT01371981 (18) [back to overview]	Total Scale Score From Parent-reported Multidimensional Fatigue Scale Module
NCT01371981 (18) [back to overview]	Total Scale Score From Parent-reported Pediatric Quality of Life Inventory Module
NCT01371981 (18) [back to overview]	EFS for Patients on Arm C, Cohort 1
NCT01371981 (18) [back to overview]	EFS for Patients on Arm C, Cohort 2
NCT01371981 (18) [back to overview]	Proportion of Patients Experiencing Grade 3 or Higher Non-hematologic Toxicities and Infections While on Protocol Therapy
NCT01381692 (1) [back to overview]	Phase I: The Maximum Tolerated Dose (MTD) of Temsirolimus in Combination With Bortezomib, Rituximab and Dexamethasone
NCT01383759 (3) [back to overview]	Progression Free Survival at 24 Months
NCT01383759 (3) [back to overview]	Percentage of Participants Experiencing Progression Free Survival at 12 Months
NCT01383759 (3) [back to overview]	Participants Evaluated for Toxicity
NCT01397591 (2) [back to overview]	Response Rate of Ofatumumab in Combination With Bortezomib in Patients With Relapsed CD20+ (Cluster of DIfferentiation Antigen 20) Diffuse Large B Cell Lymphoma, Follicular Lymphoma, or Mantle Cell Lymphoma
NCT01397591 (2) [back to overview]	Number of Participants With Adverse Events (Toxicity)
NCT01420926 (5) [back to overview]	Progression-free Survival
NCT01420926 (5) [back to overview]	Adverse Events
NCT01420926 (5) [back to overview]	Complete Remission Rate (CR and CRi)
NCT01420926 (5) [back to overview]	Disease-free Survival (DFS)
NCT01420926 (5) [back to overview]	Overall Survival (OS) Time
NCT01438177 (3) [back to overview]	Median Duration of Response of This Regimen
NCT01438177 (3) [back to overview]	Number of Participants With Adverse Events of Grade 3 or Higher
NCT01438177 (3) [back to overview]	Response Rate (CR + PR After 2 Cycles)
NCT01453088 (2) [back to overview]	Overall Survival Rate
NCT01453088 (2) [back to overview]	Progression Free Survival Rate
NCT01453101 (3) [back to overview]	Progression Free Survival
NCT01453101 (3) [back to overview]	Overall Response Rate
NCT01453101 (3) [back to overview]	Overall Survival (OS)
NCT01462773 (2) [back to overview]	Determine Dose Limiting Toxicities (DLTs) of VELCADE When Administered in Combination With IFN-α-2b to Patients With Metastatic Malignant Melanoma.
NCT01462773 (2) [back to overview]	Document Any Objective Anti-tumor Responses and Time to Tumor Progression That May Occur in Response to This Treatment Regimen.
NCT01465386 (1) [back to overview]	Progression Free Survival (PFS)
NCT01478048 (6) [back to overview]	1 Year Progression-Free Survival Rate - Randomized Participants
NCT01478048 (6) [back to overview]	Investigator-Assessed Objective Response Rate (ORR) - All Randomized Participants
NCT01478048 (6) [back to overview]	Investigator-Assessed Objective Response Rate in Randomized Participants With at Least One FcγRIIIa V Allele
NCT01478048 (6) [back to overview]	Median Investigator-Assessed Progression-free Survival (PFS) Time (Months) From Randomization to Date of First Tumor Progression or Death Due to Any Cause - Randomized Participants
NCT01478048 (6) [back to overview]	Number of Investigator-Assessed Progression-free Survival Events From Randomization to Date of First Tumor Progression or Death Due to Any Cause - All Randomized Participants
NCT01478048 (6) [back to overview]	Median Progression-free Survival Time (Months) From Randomization to Date of First Tumor Progression or Death Due to Any Cause, in Randomized Participants With at Least One FcγRIIIa V Allele
NCT01497275 (3) [back to overview]	Number of Participants With Progression Free Survival
NCT01497275 (3) [back to overview]	Response Rate (Complete Response + Partial Response)
NCT01497275 (3) [back to overview]	Overall Survival at 1 Year
NCT01504477 (5) [back to overview]	Maximum Tolerated Dose
NCT01504477 (5) [back to overview]	Percent of Patients With Disease Control
NCT01504477 (5) [back to overview]	Percent of of Patients With a Complete or Partial Response
NCT01504477 (5) [back to overview]	Maximum Tolerated Dose
NCT01504477 (5) [back to overview]	Duration of Disease Control
NCT01531998 (2) [back to overview]	Maximum Tolerated Dose (MTD) of Siltuximab
NCT01531998 (2) [back to overview]	Number of Participants With Response
NCT01534260 (4) [back to overview]	Phase II - Percentage of Patients With a Partial Response or Greater
NCT01534260 (4) [back to overview]	Phase II - Time to Relapse
NCT01534260 (4) [back to overview]	Phase II - Treatment-Related Adverse Events Grade 3 or Higher
NCT01534260 (4) [back to overview]	Number of Patients With Dose Limiting Toxicity
NCT01536067 (1) [back to overview]	Frequency and Severity of Toxicity as Graded According to the Cancer Therapeutic Evaluation Program (CTEP) Common Toxicity Criteria (CTC) Version 4.0
NCT01539083 (8) [back to overview]	Overall Survival (OS)
NCT01539083 (8) [back to overview]	Progression Free Survival (PFS)
NCT01539083 (8) [back to overview]	Consolidation Phase: Change From Baseline in AQOL-6D Scores at the End of the Consolidation Phase
NCT01539083 (8) [back to overview]	Consolidation Phase: Percentage of Participants With Complete Response (CR) at Months 3, 6, 9 and 12
NCT01539083 (8) [back to overview]	Consolidation Phase: Percentage of Participants With Stringent Complete Response (sCR) at Months 3, 6, 9 and 12
NCT01539083 (8) [back to overview]	Disease-free Survival (DFS)
NCT01539083 (8) [back to overview]	Consolidation Phase: Percentage of Participants With Complete Response (CR) and Very Good Partial Response (VGPR) at Month 12
NCT01539083 (8) [back to overview]	Consolidation Phase: Change From Baseline in FACT/GOG-NTX Total Score at the End of the Consolidation Phase
NCT01548573 (4) [back to overview]	Number of Grade 3 Non-hematologic and Grade 4 Hematologic Serious Adverse Events Associated With the Addition of Bortezomib, Thalidomide, and Dexamethasone Into Autologous Transplant Regimens.
NCT01548573 (4) [back to overview]	Overall Survival
NCT01548573 (4) [back to overview]	Event-Free Survival (EFS)
NCT01548573 (4) [back to overview]	Identification of Drug Resistant Genes
NCT01556347 (9) [back to overview]	Percentage of Patients Who Suffer Mortality, a Serious Adverse Event, or Other Adverse Event During the Study Period
NCT01556347 (9) [back to overview]	Percentage of Patients Who Experience CMV, PTLD, and PML
NCT01556347 (9) [back to overview]	Percentage of Patients Transplanted
NCT01556347 (9) [back to overview]	Percentage of Patients Who Experience Grade 3 and Above Non-Hematologic Toxicities
NCT01556347 (9) [back to overview]	The Percentage of Patients Who Experience Either a Respiratory Tract Infection or a Urinary Tract Infection
NCT01556347 (9) [back to overview]	Percentage of Patients With Grade 4 Hematologic Toxicities
NCT01556347 (9) [back to overview]	Percentage of Patients With a Reduction in CPRA to Less Than 20%
NCT01556347 (9) [back to overview]	The Percentage of Patients Who Experience Exacerbations Cardiac Dysrhythmias or Heart Failure
NCT01556347 (9) [back to overview]	The Percentage of Patients Who Experience Any Grade of Peripheral Neuropathy
NCT01556438 (8) [back to overview]	Pharmacodynamics (PD): Change From Baseline in B-cell Subset Fractions
NCT01556438 (8) [back to overview]	Pharmacokinetics (PK): Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-∞) of Tabalumab (LY2127399)
NCT01556438 (8) [back to overview]	Pharmacokinetics (PK): Maximum Plasma Concentration (Cmax) for Tabalumab (LY2127399)
NCT01556438 (8) [back to overview]	Number of Participants With One or More Drug Related Adverse Events (AEs) or Any Serious AEs
NCT01556438 (8) [back to overview]	Duration of Response (DoR)
NCT01556438 (8) [back to overview]	Time to Progression (TTP)
NCT01556438 (8) [back to overview]	Number of Participants With Tumor Response (Tumor Response Rate)
NCT01556438 (8) [back to overview]	Pharmacokinetics (PK): Area Under the Plasma Concentration-time Curve From Time Zero to the Last Measurable Plasma Concentration (AUC0-tlast) of Tabalumab (LY2127399)
NCT01568866 (8) [back to overview]	Percentage of Participants With a Significant Reduction in Left Ventricular Ejection Fraction (LVEF)
NCT01568866 (8) [back to overview]	Overall Survival
NCT01568866 (8) [back to overview]	Overall Response
NCT01568866 (8) [back to overview]	Percentage of Participants With ≥ Grade 2 Peripheral Neuropathy
NCT01568866 (8) [back to overview]	Progression-free Survival
NCT01568866 (8) [back to overview]	Change From Baseline in Pulmonary Artery Systolic Pressure (PASP)
NCT01568866 (8) [back to overview]	Change From Baseline in Right Ventricular Fractional Area Change (FAC)
NCT01568866 (8) [back to overview]	Duration of Response
NCT01602224 (13) [back to overview]	Number of Participants With >30% Reduction in Brief Pain Inventory (BPI) - Worst Pain Score
NCT01602224 (13) [back to overview]	Overall Response Rate (ORR)
NCT01602224 (13) [back to overview]	Overall Survival
NCT01602224 (13) [back to overview]	Progression Free Survival (PFS)
NCT01602224 (13) [back to overview]	Time to Next Treatment (TNT)
NCT01602224 (13) [back to overview]	Time to Progression (TTP)
NCT01602224 (13) [back to overview]	Number of Participants With a Given Best Objective Myeloma Response (Quality of Response [QoR])
NCT01602224 (13) [back to overview]	Time to First Skeletal-Related Event (SRE)
NCT01602224 (13) [back to overview]	PK: Time to Maximum Plasma Concentration (Tmax) of Tabalumab
NCT01602224 (13) [back to overview]	Pharmacokinetics (PK): Maximum Concentration (Cmax) of Tabalumab
NCT01602224 (13) [back to overview]	PK: Area Under the Curve Over the Dosing Interval (AUC-T) for Tabalumab
NCT01602224 (13) [back to overview]	Participants With Best Overall Response (BOR) in Each Category
NCT01602224 (13) [back to overview]	Duration of Response (DoR)
NCT01605032 (5) [back to overview]	Overall Survival
NCT01605032 (5) [back to overview]	Progression-free Survival
NCT01605032 (5) [back to overview]	Rate of Complete Response as Determined by the IMWG Criteria
NCT01605032 (5) [back to overview]	Overall Response Rate
NCT01605032 (5) [back to overview]	Mortality
NCT01653418 (9) [back to overview]	Toxicity of V-BEAM
NCT01653418 (9) [back to overview]	Complete Response Rate (Complete Response + Stringent Complete Response)
NCT01653418 (9) [back to overview]	Very Good Partial Response Rate (VGPR+nCR+sCR+CR)
NCT01653418 (9) [back to overview]	Number of Participants With Overall Survival (OS)
NCT01653418 (9) [back to overview]	Number of Participants With Progression-free Survival (PFS)
NCT01653418 (9) [back to overview]	Time to Platelet Engraftment After V-BEAM.
NCT01653418 (9) [back to overview]	Overall Response Rate (ORR)
NCT01653418 (9) [back to overview]	Time to Neutrophil Engraftment After V-BEAM.
NCT01653418 (9) [back to overview]	Treatment Related Mortality (TRM) of V-BEAM
NCT01668719 (5) [back to overview]	Progression-free Survival
NCT01668719 (5) [back to overview]	Phase I: Maximum Tolerated Dose (MTD) of Elotuzumab in Combination With Bortezomib, Lenalidomide and Dexamethasone
NCT01668719 (5) [back to overview]	Overall Survival
NCT01668719 (5) [back to overview]	Number of Participants With Gr 3 Through 5 Adverse Events That Are Related to Study Drugs
NCT01668719 (5) [back to overview]	Response (Partial Response [PR] or Better) Rate
NCT01672736 (1) [back to overview]	Maximum Tolerated Dose of the Combination of ASP7487 (OSI-906) With Velcade and Dexamethasone
NCT01695330 (1) [back to overview]	The Primary Objective of This Study Will be to Investigate the Incidence and Severity of Peripheral Neuropathy Caused by a Prior Intravenous VELCADE-containing Regimen in Comparison to That Caused by a Subcutaneous VELCADE-containing Regimen.
NCT01706666 (3) [back to overview]	Progression-free Survival
NCT01706666 (3) [back to overview]	Proportion of Patients Experiencing a Stringent Complete Response (sCR) After 12 Cycles, 24 Months
NCT01706666 (3) [back to overview]	Survival Time
NCT01720043 (1) [back to overview]	Efficacy of Velcade
NCT01729338 (11) [back to overview]	QLQ-C30 Question 30
NCT01729338 (11) [back to overview]	Maximum Depth of Response During Maintenance Therapy
NCT01729338 (11) [back to overview]	Maximum Depth of Response During Induction Therapy
NCT01729338 (11) [back to overview]	Severe Adverse Event Rate
NCT01729338 (11) [back to overview]	Overall Response Rate (ORR) During Induction Therapy
NCT01729338 (11) [back to overview]	Median Progression-free Survival
NCT01729338 (11) [back to overview]	Median Overall Survival
NCT01729338 (11) [back to overview]	Median Duration of Response
NCT01729338 (11) [back to overview]	Functionality as Assessed Using the Cancer and Leukemia Group B (CALGB) Geriatric Assessment Tool
NCT01729338 (11) [back to overview]	Median Time to Response
NCT01729338 (11) [back to overview]	QLQ-C30 Question 29
NCT01734928 (6) [back to overview]	Overall Response Rate by Independent Response Adjudication Committee (IRAC)
NCT01734928 (6) [back to overview]	Progression Free Survival by Independent Response Adjudication Committee (IRAC)
NCT01734928 (6) [back to overview]	Overall Survival (OS)
NCT01734928 (6) [back to overview]	Number of Participants With Grade 5 Treatment Emergent Adverse Events (TEAE)
NCT01734928 (6) [back to overview]	Number of Participants With Grade 3-4 Treatment Emergent Adverse Events (TEAE)
NCT01734928 (6) [back to overview]	Duration of Response by Independent Response Adjudication Committee (IRAC)
NCT01736943 (3) [back to overview]	Toxicity Information Recorded Will Include the Type, Severity, Time of Onset, Time of Resolution, and the Probable Association With the Study Regimen.
NCT01736943 (3) [back to overview]	Overall Survival
NCT01736943 (3) [back to overview]	Progression Free Survival
NCT01754389 (5) [back to overview]	Percentage of Participants With Incidence of Grade II-IV GVHD
NCT01754389 (5) [back to overview]	Percentage of Participants With Non-relapse Mortality
NCT01754389 (5) [back to overview]	Percentage of Participants With Chronic Graft Versus Host Disease
NCT01754389 (5) [back to overview]	Percentage of Participants With Progression-free and Overall Survival
NCT01754389 (5) [back to overview]	Percentage of Participants With Relapse
NCT01769209 (7) [back to overview]	Related Adverse Events (Grade 3, 4, 5)
NCT01769209 (7) [back to overview]	Response Rate (RR)
NCT01769209 (7) [back to overview]	Progression-free Survival (PFS)
NCT01769209 (7) [back to overview]	Failure-free Survival (FFS)
NCT01769209 (7) [back to overview]	Overall Survival (OS)
NCT01769209 (7) [back to overview]	Complete Response (CR)
NCT01769209 (7) [back to overview]	Complete Response Without Platelet Recovery (CRp)
NCT01782963 (6) [back to overview]	Objective Response Rate
NCT01782963 (6) [back to overview]	Mean Plasma Bortezomib Concentration Following Intravenous and and Subcutaneous Injection
NCT01782963 (6) [back to overview]	Median Time to Response
NCT01782963 (6) [back to overview]	Median Progression Free Survival
NCT01782963 (6) [back to overview]	Median Overall Survival
NCT01782963 (6) [back to overview]	Number of Participants With Grade 3 or Higher Treatment Related Adverse Events
NCT01801436 (29) [back to overview]	Systemic Clearance (CL) of Bortezomib on Day 11 of Cycle 1
NCT01801436 (29) [back to overview]	Time to Reach Maximum Observed Plasma Concentration (Tmax) of Bortezomib on Day 1 of Cycle 1
NCT01801436 (29) [back to overview]	Volume of Distribution at Steady-State (Vss) of Bortezomib on Day 11 of Cycle 1
NCT01801436 (29) [back to overview]	Area Under the Plasma Concentration-Time Curve From Time Zero to Infinite Time (AUC[0-infinity]) of Bortezomib on Day 11 of Cycle 1
NCT01801436 (29) [back to overview]	Area Under the Plasma Concentration-Time Curve From Time Zero to Time at Last Observed Quantifiable Concentration (AUC[0-t]) of Bortezomib on Day 1 of Cycle 1
NCT01801436 (29) [back to overview]	Number of Participants With Response to Treatment at Day 11 of Cycle 8
NCT01801436 (29) [back to overview]	Number of Participants With Response to Treatment at Day 1 of Cycle 7
NCT01801436 (29) [back to overview]	Number of Participants With Response to Treatment at Day 1 of Cycle 5
NCT01801436 (29) [back to overview]	Number of Participants With KPS Score at Day 11 of Cycle 8
NCT01801436 (29) [back to overview]	Number of Participants With KPS Score at Day 1 of Cycle 7
NCT01801436 (29) [back to overview]	Number of Participants With KPS Score at Day 1 of Cycle 5
NCT01801436 (29) [back to overview]	Number of Participants With KPS Score at Day 1 of Cycle 3
NCT01801436 (29) [back to overview]	Number of Participants With KPS Score at Day 1 of Cycle 1
NCT01801436 (29) [back to overview]	Number of Participants With Karnofsky Performance Status (KPS) Score at Baseline
NCT01801436 (29) [back to overview]	Area Under the Plasma Concentration-Time Curve From Time Zero to Time at Last Observed Quantifiable Concentration (AUC[0-t]) of Bortezomib on Day 11 of Cycle 1
NCT01801436 (29) [back to overview]	Volume of Distribution at Steady-State (Vss) of Bortezomib on Day 1 of Cycle 1
NCT01801436 (29) [back to overview]	Time to Reach Maximum Observed Plasma Concentration (Tmax) of Bortezomib on Day 11 of Cycle 1
NCT01801436 (29) [back to overview]	Elimination Half-Life Period (T1/2) of Bortezomib on Day 1 of Cycle 1
NCT01801436 (29) [back to overview]	Terminal Rate Constant (Lambda[z]) of Bortezomib on Day 11 of Cycle 1
NCT01801436 (29) [back to overview]	Terminal Rate Constant (Lambda[z]) of Bortezomib on Day 1 of Cycle 1
NCT01801436 (29) [back to overview]	Area Under First Moment Plasma Concentration-Time Curve (AUMC) of Bortezomib on Day 1 of Cycle 1
NCT01801436 (29) [back to overview]	Area Under First Moment Plasma Concentration-Time Curve (AUMC) of Bortezomib on Day 11 of Cycle 1
NCT01801436 (29) [back to overview]	Area Under the Plasma Concentration-Time Curve From Time Zero to Infinite Time (AUC[0-infinity]) of Bortezomib on Day 1 of Cycle 1
NCT01801436 (29) [back to overview]	Elimination Half-Life Period (T1/2) of Bortezomib on Day 11 of Cycle 1
NCT01801436 (29) [back to overview]	Maximum Observed Plasma Concentration (Cmax) of Bortezomib on Day 1 of Cycle 1
NCT01801436 (29) [back to overview]	Maximum Observed Plasma Concentration (Cmax) of Bortezomib on Day 11 of Cycle 1
NCT01801436 (29) [back to overview]	Mean Residence Time (MRT) of Bortezomib in the Body on Day 1 of Cycle 1
NCT01801436 (29) [back to overview]	Mean Residence Time (MRT) of Bortezomib in the Body on Day 11 of Cycle 1
NCT01801436 (29) [back to overview]	Systemic Clearance (CL) of Bortezomib on Day 1 of Cycle 1
NCT01818752 (7) [back to overview]	Complete Response Rate
NCT01818752 (7) [back to overview]	Overall Response Rate
NCT01818752 (7) [back to overview]	Overall Survival (OS)
NCT01818752 (7) [back to overview]	Percentage of Participants With ≥ Grade 2 Peripheral Neuropathy
NCT01818752 (7) [back to overview]	Progression-Free Survival (PFS)
NCT01818752 (7) [back to overview]	Number of Participants With Adverse Events
NCT01818752 (7) [back to overview]	European Organisation for Research and Treatment of Cancer Quality of Life Core Module (EORTC QLQ-C30) Global Health Status/Quality of Life (QOL) Scores
NCT01833143 (3) [back to overview]	Participants Evaluated for Toxicity
NCT01833143 (3) [back to overview]	Overall Survival
NCT01833143 (3) [back to overview]	Progression Free Survival
NCT01849783 (4) [back to overview]	Percentage of Participants With Serious Treatment-Related Complications
NCT01849783 (4) [back to overview]	Mean Change in Quality-Of-Life Indicators Post-Transplant
NCT01849783 (4) [back to overview]	Percentage of Participants Able to Complete Full Course Therapy
NCT01849783 (4) [back to overview]	Median Progression Free Survival (mPFS)
NCT01860170 (3) [back to overview]	GVHD
NCT01860170 (3) [back to overview]	Dose Limiting Toxicity
NCT01860170 (3) [back to overview]	Engraftment
NCT01891968 (1) [back to overview]	Overall Response (OR)
NCT01929980 (1) [back to overview]	Number of Participants With Response
NCT02037256 (2) [back to overview]	>= 2 Fold Increase in Circulating PBSC's
NCT02037256 (2) [back to overview]	Time to Neutrophil Engraftment
NCT02100657 (12) [back to overview]	Recommended Dose of Dexamethasone in Combination With Plitidepsin and Bortezomib
NCT02100657 (12) [back to overview]	Progression-free Survival Rates
NCT02100657 (12) [back to overview]	Overall Response Rate
NCT02100657 (12) [back to overview]	Event-free Survival Rates
NCT02100657 (12) [back to overview]	Time to Progression
NCT02100657 (12) [back to overview]	Number of Participants Who Experienced Dose-Limiting Toxicities (DLTs)
NCT02100657 (12) [back to overview]	Event-free Survival
NCT02100657 (12) [back to overview]	Duration of Response
NCT02100657 (12) [back to overview]	Recommended Dose of Plitidepsin in Combination With Bortezomib and Dexamethasone
NCT02100657 (12) [back to overview]	Recommended Dose of Bortezomib in Combination With Plitidepsin and Dexamethasone
NCT02100657 (12) [back to overview]	Progression-free Survival
NCT02100657 (12) [back to overview]	Time to Progression Rates
NCT02112916 (6) [back to overview]	Event-free Survival (EFS) for Modified Augmented Berlin-Frankfurt-Munster Backbone With or Without Bortezomib in All Randomized Patients
NCT02112916 (6) [back to overview]	EFS for Very High Risk (VHR) T-LLy Patients Treated With HR Berlin-Frankfurt-Munster (BFM) Intensification Blocks Who Have Complete or Partial Remission and Those Who do Not Respond
NCT02112916 (6) [back to overview]	EFS for Very High Risk (VHR) T-ALL Patients Treated With High Risk (HR) Berlin-Frankfurt-Munster (BFM) Intensification Blocks Who Become Minimal Residual Disease (MRD) Negative and Those Who Remain MRD Positive at the End of HR Block 3
NCT02112916 (6) [back to overview]	EFS for Standard (SR) and Intermediate Risk (IR) T-ALL Patients on the Non-bortezomib Containing Arm on This Study (no Cranial Radiation Therapy [CRT]) and Similar Patients on AALL0434 (Received CRT)
NCT02112916 (6) [back to overview]	Toxicity Rates Associated With Modified Standard Therapy, Including Dexamethasone and Additional Pegaspargase
NCT02112916 (6) [back to overview]	Cumulative Incidence Rates of Isolated Central Nervous System (CNS) Relapse for SR and IR T-ALL Patients on the Non-bortezomib Containing Arm on This Study (no CRT) and Similar Patients on AALL0434 (Receive CRT)
NCT02136134 (6) [back to overview]	Progression-free Survival (PFS)
NCT02136134 (6) [back to overview]	Time to Disease Progression (TTP)
NCT02136134 (6) [back to overview]	Overall Response Rate (ORR)
NCT02136134 (6) [back to overview]	Overall Survival (OS)
NCT02136134 (6) [back to overview]	Percentage of Participants With a Very Good Partial Response (VGPR) or Better
NCT02136134 (6) [back to overview]	Percentage of Participants With Negative Minimal Residual Disease (MRD)
NCT02195479 (16) [back to overview]	Percentage of Participants With Best M-protein Response
NCT02195479 (16) [back to overview]	Change From Baseline in EuroQol-5 Dimensions-5 Levels (EQ-5D-5L): Visual Analogue Scale (VAS)
NCT02195479 (16) [back to overview]	Change From Baseline in EuroQol 5 Dimensions-5 Level (EQ-5D-5L) Utility Score
NCT02195479 (16) [back to overview]	Change From Baseline in European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ)-C30: Emotional Functioning Score
NCT02195479 (16) [back to overview]	Overall Survival (OS)
NCT02195479 (16) [back to overview]	Percentage of Participants With Complete Response (CR) or Better
NCT02195479 (16) [back to overview]	Percentage of Participants With Negative Minimal Residual Disease (MRD)
NCT02195479 (16) [back to overview]	Percentage of Participants With Stringent Complete Response (sCR)
NCT02195479 (16) [back to overview]	Overall Response Rate (ORR)
NCT02195479 (16) [back to overview]	Percentage of Participants With Very Good Partial Response (VGPR) or Better
NCT02195479 (16) [back to overview]	Progression Free Survival (PFS)
NCT02195479 (16) [back to overview]	Progression Free Survival on Next Line of Therapy (PFS2)
NCT02195479 (16) [back to overview]	Time to Disease Progression (TTP)
NCT02195479 (16) [back to overview]	Time to Next Treatment (TNT)
NCT02195479 (16) [back to overview]	Time to Response
NCT02195479 (16) [back to overview]	Duration of Response (DOR)
NCT02208037 (13) [back to overview]	Percentage of Participants With Platelet Recovery
NCT02208037 (13) [back to overview]	Percentage of Participants With Transplant-Related Mortality (TRM)
NCT02208037 (13) [back to overview]	Percentage of Participants With GVHD/Relapse or Progression-free Survival (GRFS)
NCT02208037 (13) [back to overview]	Percentage of Participants With GVHD-free Survival
NCT02208037 (13) [back to overview]	Percentage of Participants With Grade III-IV Acute GVHD
NCT02208037 (13) [back to overview]	Percentage of Participants With Grade II-IV Acute GVHD
NCT02208037 (13) [back to overview]	Percentage of Participants With Disease-free Survival
NCT02208037 (13) [back to overview]	Percentage of Participants With Disease Relapse or Progression
NCT02208037 (13) [back to overview]	Percentage of Participants With Chronic GVHD Requiring Immunosupressive Therapy
NCT02208037 (13) [back to overview]	Percentage of Participants With Chronic GVHD
NCT02208037 (13) [back to overview]	Percentage of Participants With Neutrophil Recovery
NCT02208037 (13) [back to overview]	Percentage of Participants With Overall Survival
NCT02208037 (13) [back to overview]	Donor Cell Engraftment
NCT02224729 (5) [back to overview]	Count of Participants That Experience Overall Survival (OS)
NCT02224729 (5) [back to overview]	Incidence of Grade 3-4 Adverse Events From the Combination of Bendamustine Hydrochloride, Bortezomib, and Dexamethasone Based on the Common Terminology Criteria Version 4.0
NCT02224729 (5) [back to overview]	Count of Participants That Experience Overall Response Following 4 Cycles of the Combination Regimen BBd
NCT02224729 (5) [back to overview]	Count of Participants That Experience Progression-free Survival (PFS)
NCT02224729 (5) [back to overview]	Count of Participants That Experience Very Good Partial Remission (VGPR)
NCT02254551 (1) [back to overview]	Maximum Tolerated Dose (MTD) of LDE225 Plus Bortezomib
NCT02265510 (10) [back to overview]	Phase 1a, 1b, and Phase 2: Tmax: Time to Maximum Plasma Concentration for INCB052793
NCT02265510 (10) [back to overview]	Phase 1a, 1b, and Phase 2: Cmax: Maximum Observed Plasma Concentration of Itacitinib
NCT02265510 (10) [back to overview]	Phase 1a, 1b, and Phase 2: Cmax: Maximum Observed Plasma Concentration for INCB052793
NCT02265510 (10) [back to overview]	Phase 1a, 1b, and Phase 2: AUC0-τ: Area Under the Plasma Concentration-time Curve Over Dosing Interval for Itacitinib
NCT02265510 (10) [back to overview]	Phase 1a, 1b, and Phase 2: AUC0-τ: Area Under the Plasma Concentration-time Curve Over Dosing Interval for INCB052793
NCT02265510 (10) [back to overview]	Phase 1A and 1B: Percentage of Participants With Response as Determined by Investigator's Assessment
NCT02265510 (10) [back to overview]	Phase 1a and 1b: Number of Participants With at Least One Treatment-Emergent Adverse Event (TEAE) and Serious Adverse Event (SAE)
NCT02265510 (10) [back to overview]	Phase 2: Number of Participants With at Least One TEAE and SAE
NCT02265510 (10) [back to overview]	Phase 2: Objective Response Rate (ORR) in Hematological Malignancies
NCT02265510 (10) [back to overview]	Phase 1a, 1b, and Phase 2: Tmax: Time to Maximum Plasma Concentration for Itacitinib
NCT02290431 (16) [back to overview]	Minimal Response Rate (MRR) Per Investigator
NCT02290431 (16) [back to overview]	Overall Survival (OS)
NCT02290431 (16) [back to overview]	Overall Response Rate (ORR)
NCT02290431 (16) [back to overview]	Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: Lambda_z
NCT02290431 (16) [back to overview]	Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: T1/2
NCT02290431 (16) [back to overview]	Time to Response (TTR) Per Investigator
NCT02290431 (16) [back to overview]	Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: Vz/F
NCT02290431 (16) [back to overview]	Quality of Life (QoL) as Measured by FACT/GOG-Ntx Total Score
NCT02290431 (16) [back to overview]	Percentage of Participants With Near Complete Response (nCR)/ Complete Response (CR) Rate
NCT02290431 (16) [back to overview]	Progression Free Survival (PFS)
NCT02290431 (16) [back to overview]	Time to Progression/Relapse (TTP) Per Investigator
NCT02290431 (16) [back to overview]	Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: AUClast, AUC0-24h, AUC0-48h, AUCinf
NCT02290431 (16) [back to overview]	Duration of Response (DOR) Per Investigator
NCT02290431 (16) [back to overview]	Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: Cmax
NCT02290431 (16) [back to overview]	Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: CL/F
NCT02290431 (16) [back to overview]	Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: Tmax
NCT02370693 (3) [back to overview]	Change of Lung Function Measured by Forced Vital Capacity (FVC) Between Baseline and 24 Weeks
NCT02370693 (3) [back to overview]	Change of Skin Fibrosis Measured by the Rodnan Skin Score Between Baseline and 24 Weeks
NCT02370693 (3) [back to overview]	Number of Participants With Serious Adverse Events
NCT02375555 (6) [back to overview]	Grade 3 and 4 Treatment-Emergent Adverse Event (TEAE) Rate
NCT02375555 (6) [back to overview]	4 Cycle Response Rate
NCT02375555 (6) [back to overview]	4 Cycle Ever Dose Modification (DM) Rate
NCT02375555 (6) [back to overview]	Median Time to Response
NCT02375555 (6) [back to overview]	Successful Stem Cell Mobilization (SC Mob) Rate
NCT02375555 (6) [back to overview]	Objective Response Rate (ORR) at End of 8 Cycles of Induction Therapy.
NCT02419755 (1) [back to overview]	Number of Relevant Toxicities Related to Therapy
NCT02424851 (5) [back to overview]	Haematological and Non-haematological Toxicity in Both Treatment Arms
NCT02424851 (5) [back to overview]	Quality of Life Measured by the EQ-5D-3L Questionnaire at Baseline and 1 Month Follow up
NCT02424851 (5) [back to overview]	Renal Response After Two Cycles of Trial Treatment
NCT02424851 (5) [back to overview]	Overall Survival
NCT02424851 (5) [back to overview]	Number of Participants With >50% Reduction From Baseline in Serum Free Light Chain
NCT02440464 (14) [back to overview]	Percentage of Participants With Progression-Free Survival
NCT02440464 (14) [back to overview]	Percentage of Participants With Overall Survival (OS)
NCT02440464 (14) [back to overview]	Percentage of Participants With Infections Post-randomization by Time Point
NCT02440464 (14) [back to overview]	Percentage of Participants With Infections Post-randomization by Infection Type
NCT02440464 (14) [back to overview]	Percentage of Participants With Disease Progression
NCT02440464 (14) [back to overview]	Percentage of Participants With Chronic GVHD
NCT02440464 (14) [back to overview]	Medical Outcomes Study (MOS) - Short Form 36 (SF-36) Score
NCT02440464 (14) [back to overview]	Functional Assessment of Cancer Therapy (FACT) - Bone Marrow Transplant (BMT) Total Score
NCT02440464 (14) [back to overview]	Percentage of Participants With Acute GVHD (Grades III-IV)
NCT02440464 (14) [back to overview]	Percentage of Participants With Toxicities Post-randomization by Time Point
NCT02440464 (14) [back to overview]	Percentage of Participants With Response to Treatment
NCT02440464 (14) [back to overview]	Percentage of Participants With Best Response to Treatment After Randomization
NCT02440464 (14) [back to overview]	Percentage of Participants With Treatment-Related Mortality (TRM)
NCT02440464 (14) [back to overview]	Percentage of Participants With Toxicities Post-randomization by Toxicity Type
NCT02481934 (2) [back to overview]	Number of Participants With Peripheral Blood Monoclonal Protein Reduction or Stabilization
NCT02481934 (2) [back to overview]	Number of Participants With Adverse Events During NKAE Treatment
NCT02489500 (3) [back to overview]	Overall Survival
NCT02489500 (3) [back to overview]	Toxicities
NCT02489500 (3) [back to overview]	Number of Participants With Hematologic Response
NCT02535806 (4) [back to overview]	2-year Overall Survival Seen With Using Bortezomib in Combination With the ALL R3 Re-induction Regimen in Pediatric Patients With Relapsed or Refractory ALL or LL.
NCT02535806 (4) [back to overview]	Post-induction Level of Minimal Residual Disease Seen With Using Bortezomib in Combination With the ALL R3 Re-induction Regimen in Pediatric Patients With Relapsed or Refractory ALL or LL.
NCT02535806 (4) [back to overview]	Remission Rate Seen With Using Bortezomib in Combination With the ALL R3 Re-induction Regimen in Pediatric Patients With Relapsed or Refractory ALL or LL.
NCT02535806 (4) [back to overview]	Number of Subject With Adverse Events
NCT02553460 (1) [back to overview]	Percentage of Treatment-related Mortality (TRM)
NCT02703779 (3) [back to overview]	Cluster of Differentiation 34 (CD34) Enumeration
NCT02703779 (3) [back to overview]	Multiparametric Flow Cytometry - Cluster of Differentiation 34 (CD34)Assessment
NCT02703779 (3) [back to overview]	Multiparametric Flow Cytometry - Minimum Residual Disease
NCT02755597 (12) [back to overview]	Progression-Free Survival (PFS) in Participants With High B-cell Lymphoma 2 (BCL-2) Expression
NCT02755597 (12) [back to overview]	Overall Response Rate (ORR)
NCT02755597 (12) [back to overview]	Mean Change From Baseline in Physical Functioning Scale of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30)
NCT02755597 (12) [back to overview]	Mean Change From Baseline in Patient Reported Outcomes Measurement Information System [PROMIS] Cancer Fatigue Short Form [SF] Score
NCT02755597 (12) [back to overview]	Overall Survival (OS).
NCT02755597 (12) [back to overview]	Progression-free Survival (PFS)
NCT02755597 (12) [back to overview]	Mean Change From Baseline in Global Health Status/Quality of Life Scale of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30)
NCT02755597 (12) [back to overview]	Mean Change From Baseline in Brief Pain Inventory - Short Form (BPI-SF) Worst Pain
NCT02755597 (12) [back to overview]	Very Good Partial Response (VGPR) or Better Response Rate
NCT02755597 (12) [back to overview]	Time to Progression (TTP)
NCT02755597 (12) [back to overview]	Minimal Residual Disease (MRD) Negativity Rate
NCT02755597 (12) [back to overview]	Duration of Response (DOR)
NCT02874742 (16) [back to overview]	Time to Progression (TTP)
NCT02874742 (16) [back to overview]	Time to Partial Response (PR) or Better
NCT02874742 (16) [back to overview]	Time to Complete Response or Better
NCT02874742 (16) [back to overview]	Progression-free Survival (PFS)
NCT02874742 (16) [back to overview]	Percentage of Participants With Stringent Complete Response (sCR)
NCT02874742 (16) [back to overview]	Overall Survival (OS)
NCT02874742 (16) [back to overview]	Percentage of Participants Who Achieved Very Good Partial Response (VGPR) or Better
NCT02874742 (16) [back to overview]	Time to Stringent Complete Response (sCR)
NCT02874742 (16) [back to overview]	Duration of Stringent Complete Response (sCR)
NCT02874742 (16) [back to overview]	Duration of Response
NCT02874742 (16) [back to overview]	Duration of Complete Response or Better
NCT02874742 (16) [back to overview]	Percentage of Participants With Negative Minimal Residual Disease (MRD)
NCT02874742 (16) [back to overview]	Percentage of Participants With Overall Response Rate (ORR)
NCT02874742 (16) [back to overview]	Percentage of Participants With Overall Stringent Complete Response (sCR)
NCT02874742 (16) [back to overview]	Time to Very Good Partial Response (VGPR) or Better
NCT02874742 (16) [back to overview]	Percentage of Participants With Complete Response (CR) or Better
NCT02877082 (2) [back to overview]	Number of Patients Alive and Free of Severe Acute GVHD Following HLA Matched Related or Unrelated Donor Hematopoietic Peripheral Blood Transplant
NCT02877082 (2) [back to overview]	Total Number of Serious Adverse Events and Adverse Events Related to This Immunosuppressive Regimen
NCT02902965 (7) [back to overview]	Progression Free Survival (PFS) at Landmark Points - 20 Months
NCT02902965 (7) [back to overview]	Safety and Tolerability of Ibrutinib in Combination With Bortezomib and Dexamethasone as Measured by the Number of Participants With Adverse Events.
NCT02902965 (7) [back to overview]	Time to Progression (TTP)
NCT02902965 (7) [back to overview]	Duration of Response (DOR)
NCT02902965 (7) [back to overview]	Median Progression-Free Survival (PFS)
NCT02902965 (7) [back to overview]	Overall Response Rate (ORR)
NCT02902965 (7) [back to overview]	Overall Survival (OS) at 24 Months
NCT02928029 (3) [back to overview]	Phase 1: The Number of Subjects With Treatment-emergent Adverse Events (TEAEs), Drug-related TEAEs, and Treatment-emergent Serious AE
NCT02928029 (3) [back to overview]	Phase 1: The Number of Subjects With Complete Response (CR) and Very Good Partial Response (VGPR)
NCT02928029 (3) [back to overview]	Phase 1: MTD/RP2D Determined by the Incidence of DLTs
NCT02951819 (9) [back to overview]	Overall Survival (OS)
NCT02951819 (9) [back to overview]	Duration of Response (DOR)
NCT02951819 (9) [back to overview]	Percentage of Participants With Treatment Emergent-Adverse Event
NCT02951819 (9) [back to overview]	Time to Disease Progression (TTP)
NCT02951819 (9) [back to overview]	Progression Free Survival (PFS)
NCT02951819 (9) [back to overview]	Percentage of Participants Who Achieved Complete Response (CR) or Very Good Partial Response (VGPR)
NCT02951819 (9) [back to overview]	Overall Response Rate (ORR)
NCT02951819 (9) [back to overview]	Time to Very Good Partial Response (VGPR) or Better
NCT02951819 (9) [back to overview]	Time to Partial Response (PR) or Better
NCT03110562 (1) [back to overview]	Progression-free Survival (PFS) as Assessed by IRC
NCT03117361 (19) [back to overview]	Clinical Benefit Rate
NCT03117361 (19) [back to overview]	Duration of Response
NCT03117361 (19) [back to overview]	Disease Control Rate
NCT03117361 (19) [back to overview]	Percentage of Participants With Event-free Survival at 6 Months
NCT03117361 (19) [back to overview]	Percentage of Participants With Overall Survival at 12 Months
NCT03117361 (19) [back to overview]	Percentage of Participants With Overall Survival at 6 Months
NCT03117361 (19) [back to overview]	Percentage of Participants With Progression Disease at 6 Months
NCT03117361 (19) [back to overview]	Percentage of Participants With Progression-free Survival at 12 Months
NCT03117361 (19) [back to overview]	Percentage of Participants With Progression-free Survival at 3 Months
NCT03117361 (19) [back to overview]	Progression-free Survival
NCT03117361 (19) [back to overview]	Percentage of Participants With Event-free Survival at 3 Months
NCT03117361 (19) [back to overview]	Percentage of Participants With Event-free Survival at 12 Months
NCT03117361 (19) [back to overview]	Time to Progression
NCT03117361 (19) [back to overview]	Percentage of Participants With Progression-free Survival at 6 Months
NCT03117361 (19) [back to overview]	Percentage of Participants With Progression Disease at 12 Months
NCT03117361 (19) [back to overview]	Percentage of Participants With Progression Disease at 3 Months
NCT03117361 (19) [back to overview]	Overall Survival
NCT03117361 (19) [back to overview]	Overall Response Rate
NCT03117361 (19) [back to overview]	Event-free Survival
NCT03201965 (1) [back to overview]	Percentage of Participants With Overall Complete Hematologic Response (CHR)
NCT03412565 (14) [back to overview]	D-VMP, D-Rd and D-Kd Cohorts: Duration of Response (DOR)
NCT03412565 (14) [back to overview]	D-VMP, D-Rd, and D-Kd Cohorts: Overall Response Rate (ORR)
NCT03412565 (14) [back to overview]	D-VMP, D-Rd, and D-Kd Cohorts: Percentage of Participants With VGPR or Better Response
NCT03412565 (14) [back to overview]	Percentage of Participants With Anti-rHuPH20 Antibodies
NCT03412565 (14) [back to overview]	Percentage of Participants With Anti-Daratumumab Antibodies
NCT03412565 (14) [back to overview]	Percentage of Participants With CR or Better Response
NCT03412565 (14) [back to overview]	D-VRd Cohort: Overall Response Rate (ORR)
NCT03412565 (14) [back to overview]	D-VMP, D-Rd, and D-Kd Cohorts: Percentage of Participants With Minimal Residual Disease (MRD) Negative Rate
NCT03412565 (14) [back to overview]	Percentage of Participants With Infusion-Related Reactions (IRRs)
NCT03412565 (14) [back to overview]	Maximum Observed Serum Concentration (Cmax) of Daratumumab
NCT03412565 (14) [back to overview]	Maximum Observed Serum Concentration (Cmax) of Daratumumab
NCT03412565 (14) [back to overview]	Maximum Observed Serum Concentration (Cmax) of Daratumumab
NCT03412565 (14) [back to overview]	Maximum Observed Serum Concentration (Cmax) of Daratumumab
NCT03412565 (14) [back to overview]	D-VRd Cohort: Percentage of Participants With Very Good Partial Response (VGPR) or Better Response
NCT03416374 (21) [back to overview]	Percentage of Participants With Bone Lesions (Bone Evaluation)
NCT03416374 (21) [back to overview]	PFS From the Start of Study Treatment
NCT03416374 (21) [back to overview]	Progression-Free Survival (PFS) Rate at 12 Months From the Start of Study Treatment
NCT03416374 (21) [back to overview]	Time to Next Treatment (TTNT)
NCT03416374 (21) [back to overview]	Number of Participants With Minimal Residual Disease (MRD) Positive or Negative in Bone Marrow in Participants Who Achieved CR
NCT03416374 (21) [back to overview]	Patient-Reported Outcome Health-Related Quality of Life (HRQoL) Based on Global Health Status Scale of European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-C30 (EORTC QLQ-C30)
NCT03416374 (21) [back to overview]	Patient-Reported Outcome Health-Related Quality of Life (HRQoL) Based on Global Health Status Scale of European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-C30 (EORTC QLQ-C30)
NCT03416374 (21) [back to overview]	Patient-Reported Outcome HRQoL Based on EORTC Multiple Myeloma Module (EORTC QLQ-MY20) Score
NCT03416374 (21) [back to overview]	Percentage of Participants Who Achieve or Maintain Any Best Response
NCT03416374 (21) [back to overview]	Relative Dose Intensity (RDI)
NCT03416374 (21) [back to overview]	Overall Survival (OS) From the Start of Study Treatment
NCT03416374 (21) [back to overview]	Healthcare Resource Utilization (HCRU): Duration of Hospital Stay Per Participants
NCT03416374 (21) [back to overview]	Patient-Reported Outcome HRQoL Based on EORTC Multiple Myeloma Module (EORTC QLQ-MY20) Score
NCT03416374 (21) [back to overview]	Healthcare Resource Utilization (HCRU): Number of Events With Hospitalization Per Participants-Month
NCT03416374 (21) [back to overview]	Number of Participants Reporting One or More Treatment-Emergent AEs (TEAEs)
NCT03416374 (21) [back to overview]	Percentage of Participants Continuing Treatment With Ixazomib at 12 Months From the Start of Study Treatment
NCT03416374 (21) [back to overview]	Overall Response Rate (ORR)
NCT03416374 (21) [back to overview]	Percentage of Participants Who Achieved VGPR or Better (CR + VGPR)
NCT03416374 (21) [back to overview]	Duration of Response (DOR)
NCT03416374 (21) [back to overview]	Duration of Therapy (DOT)
NCT03416374 (21) [back to overview]	Evaluation of Modified Quality-Adjusted Life-Years (QALYs)
NCT03481556 (12) [back to overview]	Time to Next Treatment (TTNT)
NCT03481556 (12) [back to overview]	Overall Survival (OS)
NCT03481556 (12) [back to overview]	Time to Response (TTR)
NCT03481556 (12) [back to overview]	Best Response (BR)
NCT03481556 (12) [back to overview]	Number of Participants Who Experienced a Treatment-emergent Adverse Event (TEAE)
NCT03481556 (12) [back to overview]	Time to Progression (TTP)
NCT03481556 (12) [back to overview]	Duration of Clinical Benefit (DOCB)
NCT03481556 (12) [back to overview]	Clinical Benefit Rate (≥ Minimal Response)
NCT03481556 (12) [back to overview]	Phase 1: Number of Participants Who Experienced a Dose Limiting Toxicity (DLT)
NCT03481556 (12) [back to overview]	Phase 2: Overall Response Rate (ORR)
NCT03481556 (12) [back to overview]	Progression-Free Survival (PFS)
NCT03481556 (12) [back to overview]	Duration of Response (DOR)
NCT03945591 (2) [back to overview]	Percentage of Participants Who Experience Acute GvHD
NCT03945591 (2) [back to overview]	Percentage of Participants Who Experience Moderate to Severe Chronic GvHD

Number of Participants With Adverse Events

Here is the number of participants with adverse events. For a detailed list of adverse events see the adverse event module. (NCT00006184)
Timeframe: 9 years

Intervention	Participants (Count of Participants)
Recipient - Chemotherapy Group	10
Donor - Vaccination Generation Group	10

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Immune Response

Immune cell depletion is defined as immunosuppression of participants T cells prior to transplant measured by cluster of differentiation 4 (CD4) counts (i.e. cells) > 50 cells per ul.Immune T-cell depletion helps to reduce the ability to reject allogeneic cells in participants and is required for engraftment. Engraftment is the body's ability to accept donor cells. (NCT00006184)
Timeframe: 105 days

Intervention	Particpants (Number)
Recipient - Chemotherapy Group	7

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Overall Survival

(NCT00023712)
Timeframe: From study entry, up to 5 years following disease progression

Intervention	months (Median)
Cohort 1 - Bortezomib 1.5 (mg/m2)	18.2
Cohort 2 - Bortezomib (1.3 mg/m2)	27.2

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Progression-Free Survival

Progression is defined according to RECIST v1.0 as at least a 20% increase in the sum of LD target lesions taking as reference the smallest sum LD recorded since study entry, the appearance of one or more new lesions, death due to disease without prior objective documentation of progression, global deterioration in health status attributable to the disease requiring a change in therapy without objective evidence of progression, or unequivocal progression of existing non-target lesions. (NCT00023712)
Timeframe: From study entry up to 5 years

Intervention	months (Median)
Cohort 1 - Bortezomib 1.5 (mg/m2)	1.5
Cohort 2 - Bortezomib (1.3 mg/m2)	1.4

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Tumor Response Duration

RECIST 1.0 defines complete response as the disappearance of all target lesions and non-target lesions and no evidence of new lesions documented by two disease assessments at least 4 weeks apart. Partial response is defined as at least a 30% decrease in the sum of longest dimensions (LD) of all target measurable lesions taking as reference the baseline sum of LD. There can be no unequivocal progression of non-target lesions and no new lesions. Documentation by two disease assessments at least 4 weeks apart is required. In the case where the ONLY target lesion is a solitary pelvic mass measured by physical exam, which is not radiographically measurable, a 50% decrease in the LD is required. These patients will have their response classified according to the definitions stated above. Complete and partial responses are included in the objective tumor response rate. (NCT00023712)
Timeframe: From study entry, up to 5 years

Intervention	months (Median)
Cohort 1 - Bortezomib 1.5 (mg/m2)	3.9
Cohort 2 - Bortezomib (1.3 mg/m2)	24.1

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Frequency and Severity of Observed Adverse Events

(NCT00023712)
Timeframe: Up to 5 years

,,,,,,,,,

Intervention	Participants (Count of Participants)
	Platelets	Absolute neutrophil count (ANC)	Fatigue	Rash	Diarrhea	Constipation	Genitourinary/renal	Hepatic	Infection	Metabolic	Neuropathy (sensory)	Pain	Pulmonary
Grade 0 AEs Cohort 1 - Bortezomib 1.5 (mg/m2)	14	18	4	14	13	17	24	21	23	21	14	12	21
Grade 0 AEs Cohort 2 - Bortezomib (1.3 mg/m2)	16	21	7	17	21	11	25	22	25	24	15	15	26
Grade 1 AEs (CTCAE v 2.0) Cohort 2 - Bortezomib (1.3 mg/m2)	10	5	11	9	5	7	3	6	2	4	8	5	0
Grade 1 AEs (CTCAE v.2.0) Cohort 1 - Bortezomib 1.5 (mg/m2)	9	5	10	6	7	4	1	3	1	3	6	8	0
Grade 2 AEs (CTCAE v 2.0) Cohort 1 - Bortezomib 1.5 (mg/m2)	0	2	10	4	2	5	0	1	1	0	3	5	3
Grade 2 AEs (CTCAE v 2.0) Cohort 2 - Bortezomib (1.3 mg/m2)	3	3	6	3	3	9	1	1	2	1	4	7	2
Grade 3 AEs (CTCAE v 2.0) Cohort 1 - Bortezomib 1.5 (mg/m2)	3	1	1	2	4	0	1	0	0	2	3	1	2
Grade 3 AEs (CTCAE v 2.0) Cohort 2 - Bortezomib (1.3 mg/m2)	0	0	5	0	0	0	0	0	0	0	2	2	1
Grade 4 AEs (CTCAE v 2.0) Cohort 1 - Bortezomib 1.5 (mg/m2)	0	0	1	0	0	0	0	1	1	0	0	0	0
Grade 4 AEs (CTCAE v 2.0) Cohort 2- Bortezomib (1.3 mg/m2)	0	0	0	0	0	2	0	0	0	0	0	0	0

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Objective Partial/Complete Tumor Response Based on the Gynecologic Oncology Group (GOG) Response Evaluation Criteria in Solid Tumors (RECIST) Criteria

Number of participants who experienced an objective tumor response up to 5 years. Per RECIST version 1.0 criteria: each target lesion must be >= 20 mm when measured by conventional techniques, including palpation, plain x-ray, CT, and MRI, or >= 10 mm when measured by spiral CT. Complete Response is a disappearance of all target and non-target lesions. Partial Response is at least a 30% decrease in the sum of longest dimensions (LD) of all target measurable lesions, taking as reference the baseline sum of LD. (NCT00023712)
Timeframe: From study entry until disease progression/intolerable toxicity/study withdrawal

Intervention	participants (Number)
Cohort 1 - Bortezomib 1.5 (mg/m2)	1
Cohort 2 - Bortezomib (1.3 mg/m2)	2

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Response Rate

The response probability will be estimated. The 95% confidence interval will be provided. (NCT00023764)
Timeframe: Up to 3 years

Intervention	participants (Number)
PS-341 (Bortezomib)-Relapsed Patients	11
PS-341 (Bortezomib)-Refractory Patients	6

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Number of Participants With Adverse Events

Here is the number of participants with adverse events. For the detailed list of adverse events see the adverse event module. (NCT00054665)
Timeframe: 43 months

Intervention	Participants (Number)
Part A: PS-341 Alone	23
Part B: PS-341 & EPOCH	44

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Clinical Response Rate

Clinical Response Rate is the number of participants with a partial and complete response assessed by the criteria for lymphoma. A complete response is complete disappearance of all detectable clinical and radiographic evidence of disease and disappearance of all disease-related symptoms if present before therapy and normalization of those biochemical abnormalities. Partial response is a greater than or equal to 50% decrease in the sum of the products of the greatest diameters of 6 largest dominant nodes or nodal masses. No increase in size of nodes, liver or spleen and no new sites of disease (NCT00054665)
Timeframe: 18 weeks

Intervention	Participants (Number)
	Partial response	Complete response
Part A: PS-341 Alone	1	0
Part B: PS-341 & EPOCH	7	8

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Change in Patterns of Gene Expression Pre- and Post-treatment Performed by GeneChip Analysis

Number of Participants with a Change in Gene Expression from Pre to Post Treatment (NCT00061932)
Timeframe: Baseline to 6 years

Intervention	Participants (Count of Participants)
Stratum 1 (Previously Untreated)	2
Stratum 2 (Previously Treated)	2

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True Response Rate Evaluated for the Combination of Irinotecan and PS341 by Response Evaluation Criteria in Solid Tumors (RECIST)

CT or MRI imaging scans of measurable lesions were obtained at baseline and every 8 weeks thereafter. Responses were classified according to RECIST criteria (version 1.0) (NCT00061932)
Timeframe: Up to 6 years

Intervention	participants (Number)
Stratum 1 (Previously Untreated)	3
Stratum 2 (Previously Treated)	1

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1-year Progression Free Survival Probability

Progression-free survival is defined as time from randomization to disease progression or death from any cause, whichever occurred first. Disease progression is defined using the ECOG Myeloma Response Criteria. Kaplan-Meier method is used to estimate the 1-year progression-free survival probability. 42 eligible and treated patients were included in the analysis. (NCT00075881)
Timeframe: Every 3 months if patient is <2 years from study entry, every 6 months if patient is 2-6 years from study entry, no specific requirment if patient is more than 6 years from study entry

Intervention	percentage of participants (Number)
PS-341	36.4

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Response Rate on Reinduction

ECOG Myeloma Response Criteria that follows the standard European Group for Blood and Bone Marrow Transplant criteria was used to evaluate patient response and progression. Patients who have complete disappearance of an M-protein and no evidence of myeloma in the bone marrow are considered to have complete response. 7 eligible and treated patients were included in the analysis. (NCT00075881)
Timeframe: participants were evaluated prior to each cycle, up to 23 cycles with a median number of 3 cycles. 1 cycle=21 days

Intervention	percentage of participants (Number)
PS-341	28.6

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Response Rate on Maintenance

ECOG Myeloma Response Criteria that follows the standard European Group for Blood and Bone Marrow Transplant criteria was used to evaluate patient response and progression. Patients who have complete disappearance of an M-protein and no evidence of myeloma in the bone marrow are considered to have complete response. 15 eligible and treated patients were included in the analysis. (NCT00075881)
Timeframe: participants were evaluated prior to each cycle, up to 45 cycles with a median number of 9 cycles. 1 cycle=21 days

Intervention	percentage of participants (Number)
PS-341	66.7

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Response Rate on Induction

Eastern Cooperative Oncology Group (ECOG) Myeloma Response Criteria that follows the standard European Group for Blood and Bone Marrow Transplant criteria was used to evaluate patient response and progression. Patients who have complete disappearance of an M-protein and no evidence of myeloma in the bone marrow are considered to have complete response. 42 eligible and treated patients were included in the analysis. (NCT00075881)
Timeframe: participants were evaluated prior to each cycle, up to 8 cycles with a median number of 6 cycles. 1 cycle=21 days

Intervention	percentage of participants (Number)
PS-341	47.6

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Percentage of Participants With Progression-Free Survival (PFS) at 3 Years From Initiation of Study Treatment

In patients with no confirmed Partial Response, Near Complete Response, or Complete Response, progression was defined as a >25% increase from baseline in myeloma protein production or other signs of disease progression such as hypercalcemia, etc. (NCT00081939)
Timeframe: 3 years

Intervention	percentage of participants (Number)
Study Treatment	77

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Overall Survival

Overall survival is defined as time from registration to death from any cause. Patients alive were censored at follow up. Analysis was conducted in the 38 eligible and treated patients. (NCT00083226)
Timeframe: assessed every 3 months for 2 years and then every 6 months for 1 year

Intervention	months (Median)
Treatment (Doxorubicin+Bortezomib)	6.4

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Progression Free Survival

Time from registration to disease progression or death, whichever occurred earlier. Patients alive and progression-free were censored at last follow up. 36 eligible and treated patients were included in the analysis. The other 2 eligible and treated patients had no disease status information. (NCT00083226)
Timeframe: assessed every 3 cycles while on treatment. After discontinuing treatment, assessed every 3 months for 2 years and then every 6 months for 1 year.

Intervention	months (Median)
Treatment (Doxorubicin+Bortezomib)	2.2

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Objective Response Rate Measured by Response Evaluation Criteria In Solid Tumors (RECIST)

Tumor response was measured by Response Evaluation Criteria In Solid Tumors (RECIST) v1.0. Objective response rate included complete response (disappearance of all tumor lesions) and partial response (At least a 30% decrease in the sum of the longest diameters of target lesions, taking as reference the baseline sum longest diameter.). (NCT00083226)
Timeframe: assessed every 3 cycles while on treatment. After discontinuing treatment, assessed every 3 months for 2 years and then every 6 months for 1 year

Intervention	percentage of participants (Number)
Treatment (Doxorubicin+Bortezomib)	3

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Overall Survival

(NCT00084747)
Timeframe: up to 5 years from time of consent

Intervention	months (Median)
Bortezomib	55

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Progression-free Survival

Disease Progression: The day when bone marrow recurrence and/or new lytic bone marrow lesions on radiograph and/or progressive M-component paraprotein (~ 25% increase) were detected. Paraprotein progression will be confirmed labs on the consecutive month. (NCT00084747)
Timeframe: signed consent to progression or end of trial. Up to 5 years.

Intervention	months (Median)
Bortezomib	29

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Time to Disease Progression

Time from initiation of therapy to first progressive disease. (NCT00085410)
Timeframe: Up to 1 year

Intervention	months (Median)
Arm I	5.8

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Objective Response Rate

Objective Response Rate (ORR) was determined by best response on radiologic assessment (computed tomography or magnetic resonance imaging) according to Response Evaluation Criteria in Solid Tumors (RECIST) 1.0. (NCT00085410)
Timeframe: Up to 1 year

Intervention	Participants (Count of Participants)
	Stable Disease	Partial Response (Unconfirmed)	Progressive Disease	Withdrew Consent Before Evaluation
Arm I	10	1	8	1

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Clinical Benefit Rate

Best response to study treatment was confirmed complete response, partial response, or stable disease. Unconfirmed partial response was not included. The outcome measure data table is stratified into patients who a) received prior therapy b) did not receive prior therapy. (NCT00085410)
Timeframe: Up to 1 year

Intervention	percentage of patients (Number)
	Patients who received prior therapy	Patients who did not receive prior therapy
Arm I	21	32

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1-year Survival

The time from initiation of initiation of therapy to 1 year beyond. (NCT00085410)
Timeframe: 1 year

Intervention	percentage of patients (Number)
Arm I	38

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6-Month Survival

The time from initiation of therapy to 6 months beyond. (NCT00085410)
Timeframe: 6 months

Intervention	percentage of patients (Number)
Arm I	70

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Overall Survival

The time from initiation of therapy to death or last follow-up. (NCT00085410)
Timeframe: Up to 1 year

Intervention	months (Median)
Arm I	9

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6-Month and 1-Year Survival: Patients Who Did Not Derive Clinical Benefit From Study Treatment

The time from initiation of therapy to 6 months beyond. Only patients who did not derive clinical benefit from study treatment (progressive disease or unconfirmed partial response was best response) were included. (NCT00085410)
Timeframe: Up to 1 year

Intervention	percentage of patients (Number)
	6-Month Survival	1-Year Survival
Arm I	44	11

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6-Month and 1-Year Survival for Patients Who Derived Clinical Benefit From Study Treatment

The time from initiation of therapy to 6 months beyond. Only patients who derived benefit from study treatment (stable disease, partial response, or complete response was best response) were included. (NCT00085410)
Timeframe: Up to 1 year

Intervention	percentage of patients (Number)
	6-Month Survival	1-Year Survival
Arm I	90	69

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The Primary Endpoint of This Trial is the Proportion of Patients Alive at 1 Year. Phase II Patients Only.

The primary endpoint of this trial is the proportion of patients alive at 1 year (i.e., 365 days) after study registration. Proportion of successes, defined as the number of patients alive at one year divided by the total number of evaluable patients. (NCT00093756)
Timeframe: At 1 year

Intervention	proportion of Participants (Number)
PhaseII	0.73

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Progression-free Survival

The distribution of progression-free survival (PFS) is defined as the time from registration to the time of progression or death, whichever comes first. The PFS will be estimated using the method of Kaplan-Meier. (NCT00093756)
Timeframe: From study registration to the first of either death due to any cause or progression, up to 5 years

Intervention	months (Median)
Phase II	8.4

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Frequency and Severity of Observed Toxicity, Graded by Common Terminology Criteria for Adverse Events (CTCAE)

Toxicity was reported after the first 21 days of treatment and after each 28 day cycle thereafter. Events were graded according to the Common Terminology Criteria for Adverse Events (CTCAE) v3.0. The number of patients reporting grade 3 and higher are tabulated. (NCT00093756)
Timeframe: Up to 5 years

Intervention	Participants (Count of Participants)
	Grade 3 Adverse Event	Grade 4 Adverse Event
Phase II	22	15

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Overall Survival

Overall Survival is defined as the time from registration to the time to death due to any cause. The distribution of survival time will be estimated using the method of Kaplan-Meier. (NCT00093756)
Timeframe: From registration to death due to any cause, up to 5 years

Intervention	months (Median)
Phase II	25

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Confirmed Tumor Response

Response was assessed using the RECIST v1.1 criteria. Patients were evaluated at 4 weeks post-RT, 3 months post-RT, every 3 months for 1 year post-RT, and every 6 months thereafter for a maximum of 5 years from time of registration. A Complete Response (CR) is defined as the disappearance of all target lesions. A Partial Response (PR) is defined as at least a 20% decrease in the sum of the longest diameter of target lesions from baseline. A confirmed response is defined as a CR or PR as the objective status on 2 consecutive evaluations at least 4 weeks apart. (NCT00093756)
Timeframe: Up to 5 years

Intervention	Participants (Count of Participants)
	Complete Response (CR)	Partial Response (PR)
PhaseII	3	4

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Response Rate on Step 1

Tumor response was evaluated via Response Evaluation Criteria In Solid Tumors (RECIST) v1.0, and response rate was defined as the proportion of patients with a complete response or partial response among all eligible and treated patients. Complete response was defined as disappearance of all tumor lesions. Partial response was defined as at least a 30% decrease in the sum of the longest diameters of target lesions. (NCT00103259)
Timeframe: Tumor response was assessed every 2 cycles until progression or intolerable toxicity with maximum of 3 years

Intervention	percentage of participants (Number)
Arm I (Bortezomib+Irinotecan)	13.1
Arm II (Bortezomib)	2.6

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Progression-free Survival on Step 1

Progression-free survival was defined as time from registration to step 1 to disease recurrence or death from any cause, whichever occurred first. Disease progression was measured by Response Evaluation Criteria In Solid Tumors (RECIST) v1.0, and defined as at least a 20% increase in the sum of the longest diameters of target lesions. (NCT00103259)
Timeframe: Every 3 months for first 2 years from protocol entry, then every 6 months until 3 years from study entry

Intervention	months (Median)
Arm I (Bortezomib+Irinotecan)	1.6
Arm II (Bortezomib)	1.5

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Overall Survival on Step 1

Overall survival was defined as time from registration on step 1 to death from any cause. It was evaluated in all 61 eligible and treated patients. (NCT00103259)
Timeframe: Survival was assessed every 3 month within 2 years and every 6 months betwen 2 and 3 years

Intervention	months (Median)
Arm I (Bortezomib+Irinotecan)	9.1
Arm II (Bortezomib)	7.3

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Response Rate on Step 2

Tumor response was evaluated via Response Evaluation Criteria In Solid Tumors (RECIST) v1.0, and response rate was defined as the proportion of patients with a complete response or partial response among all eligible and treated patients. Complete response was defined as disappearance of all tumor lesions. Partial response was defined as at least a 30% decrease in the sum of the longest diameters of target lesions. (NCT00103259)
Timeframe: Tumor response was assessed after every 2 cycles until progression or intolerable toxicity with maximum of 3 years

Intervention	percentage of participants (Number)
Cross-over From Bortezomib to Combined Arm	0

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Prostate-specific Antigen (PSA) Response

(NCT00103376)
Timeframe: 3 months after the start of treatment

Intervention	participants (Number)
Part A: Velcade	1
Part B: (Velcade+LH-RH Antagonist+Adrogen Receptor)	6
Part A + Part B	5

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Number of Patients Who Experienced an Adverse Event by CTCAE v. 2.0

(NCT00103376)
Timeframe: From start of treatment until end of study, up to 6 months

Intervention	participants (Number)
Part A Only: Velcade	8
Part B (Velcade+Lh-RH Antagonist+ Androgen Receptor)	7
Part A + Part B	8

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Time to PSA Progression

PSA progression is defined as a PSA increase of 50% over the nadir CR or CR/PR value on three successive PSA measurements two months apart to a value of >= 1.0 ng/ml. (NCT00103376)
Timeframe: From on study until time of PSA progression for up to two years

Intervention	months (Median)
Part B and Part A + Part B	5.49

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Time to Progression (TTP)

Median time to progression of disease is assessed according to International Myeloma Working Group (IMWG) criteria or death from any cause. IMWG criteria: increase of >=25% from lowest level in Serum M-component or (the absolute increase must be >=0.5 gram per deciliter [g/dL]); Urine M component or (the absolute increase must be >=200 milligram per 24 hour. Only in participants without measurable serum and urine M-protein levels: the difference between involved and uninvolved free light chain levels. The absolute increase >10 mg/dL. Bone marrow plasma cell percentage >=10%. Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing. Development of hypercalcemia. Participants who died or dropped out due to any reason without progression will be censored with the day of death or drop-out, respectively and who are alive at the end of the study without any progression was censored with the last available date. (NCT00103506)
Timeframe: Up to 1 year and 4 months (From date of first participant randomization [20 December 2004] up to interim analysis cut-off date [28 April 2006])

Intervention	Months (Median)
Velcade (Bortezomib) Monotherapy	6.5
Doxil/Caelyx Plus Velcade (Bortezomib)	9.3

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Overall Survival

The OS is defined as the time from the date of first dose of study drug to date of death from any cause. If the participant is alive or the vital status is unknown, the participant will be censored at the date the participant will be last known to be alive. (NCT00103506)
Timeframe: Up to 9 years and 5 months (From date of first participant randomization [20 December 2004] to cut-off date for final survival analysis (16 May 2014)

Intervention	months (Median)
Velcade (Bortezomib) Monotherapy	30.8
Doxil/Caelyx Plus Velcade (Bortezomib)	33.0

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Number of Participants With Serious Adverse Events (SAEs)

A serious adverse event (SAE) was an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly. (NCT00103506)
Timeframe: Up to 1 year and 11 months (From date of first participant randomization [20 December 2004] to cut-off date for safety update (28 November 2006)

Intervention	Participants (Number)
Velcade (Bortezomib) Monotherapy	105
Doxil/Caelyx Plus Velcade (Bortezomib)	120

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Participant Tumor Response Assessed by RECIST

Baseline scan and confirmatory scans obtained 6 weeks following initial documentation of objective response using Response Evaluation Criteria in Solid Tumors (RECIST). Complete Response (CR): Disappearance of all target lesions; Partial Response (PR): >30% decrease in sum longest diameter (LD) of target lesions, taking as reference the baseline sum LD; Progressive Disease (PD): At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions; Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started. (NCT00104871)
Timeframe: Baseline to 12 weeks (minimum of 4 treatment cycles (or 12 weeks))

Intervention	participants (Number)
	Complete Response	Partial Response	Stable Disease	Progressive Disease
Bortezomib	0	0	11	9

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Progression-free Survival Assessed by RECIST

Intervention	Participants (Count of Participants)
Bortezomib	4

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Objective Tumor Response Rate Assessed by RECIST

Response Rate calculated as number of participants with Complete or Partial Response divided by total participants. Baseline scan and confirmatory scans obtained 6 weeks following initial documentation of objective response using Response Evaluation Criteria in Solid Tumors (RECIST). Complete Response (CR): Disappearance of all target lesions; Partial Response (PR): >30% decrease in sum longest diameter (LD) of target lesions, taking as reference the baseline sum LD; Progressive Disease (PD): At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions; Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started. (NCT00104871)
Timeframe: Baseline to 12 weeks

Intervention	participants (Number)
Bortezomib	0

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Number of Participants With Adverse Events

Here is the number of participants with adverse events. For a detailed list of adverse events, see the adverse event module. (NCT00108069)
Timeframe: 7.5 years

Intervention	Participants (Number)
GBM (Glioblastoma Multiforme)	30
AG (Anaplastic Glioma)	12

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Adverse Event Grades

The combined serious and non-serious adverse event Table describes count of patients whose highest grade adverse event for any CTC (common terminology criteria) term was related to study drugs for the GBM (Glioblastoma multiforme) and AG (Anaplastic glioma) cohorts. (NCT00108069)
Timeframe: 7.5 years

,,,,,

Intervention	participants (Number)
	thrombocytopenia	lymphopenia	hypophosphatemia	ALT/sGPT	anemia (Decreased Hgb)	hyponatremia	headache	leukopenia	AST/sGOT	dyspnea	fatigue	fever	hyperkalemia	cough	depression (mood alteration)	diarrhea	dizziness	venous thrombosis	edema	hyperbilirubinemia	hypermagnesemia	hypocalcemia	hypokalemia	hypotension	elevated creatinine	infection with unknown ANC	neutropenia	pain	rash	hemorrhage (rectal)	somnolence	urinary frequency
Grade 1	19	4	0	6	6	4	0	1	2	1	2	1	2	1	0	0	1	0	1	1	1	1	1	1	1	0	0	0	1	1	0	1
Grade 2	3	4	6	1	0	0	2	2	0	0	0	1	0	0	1	1	0	0	0	0	0	0	0	0	0	0	1	1	0	0	0	0
Grade 3	1	4	3	0	0	1	1	0	0	1	0	0	0	0	0	0	0	1	0	0	0	0	0	0	0	1	0	0	0	0	1	0
Grade 4	1	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0
Grade 5	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0
Total	24	12	9	7	6	5	3	3	2	2	2	2	2	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1

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Response, Defined as Stable Disease or Objective (Partial or Complete) Response.

Complete response (CR) is complete disappearance of all measurable and evaluable disease. No new lesions. No evidence of non-evaluable disease. All measurable, evaluable and non-evaluable lesions and site must be assessed using the same techniques as baseline. Patients who respond must be on the same or decreasing doses of dexamethasone. Partial response (PR) is greater than or equal to a 50% decrease compared to baseline in the sum of products of perpendicular diameters of all measurable disease. No new lesions. All measurable and evaluable lesions and sites must be assessed using same techniques as baseline. Responders must be on the same decreasing doses of dexamethasone. Stable disease (SD) does not qualify for CR, PR, or progression (e.g., a 25% increase in the sum of products of all measurable lesions). The designation of stable/no response requires a minimum of 6 weeks duration. All measurable and evaluable sites must be assessed using the same techniques as baseline. (NCT00108069)
Timeframe: Patients were followed for an average of six weeks for assessment of response

Intervention	Participants (Number)
	Complete response	Partial response	Stable disease	Progressive disease
AG (Anaplastic Glioma)	0	0	0	12
GBM (Glioblastoma Multiforme)	0	0	1	27

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Laboratory AE Summary

"An AE was defined as any unfavorable/unintended change in the structure/function/chemistry of the body temporally associated with the use of study drug, or any worsening of a preexisting condition.~A SAE was any AE that resulted in death, was life threatening, resulted in a persistent or significant disability/incapacity, resulted in or prolonged an existing inpatient hospitalization, was a congenital anomaly/birth defect, was a new cancer, or was an overdose.~A lab (S)AE was any lab value considered clinically significant in the investigator's judgment." (NCT00111813)
Timeframe: Day 1 up to disease progression, toxicity, or death, assessed up to 29 months

,,,,,

Intervention	Participants (Number)
	With one or more laboratory AEs	With no laboratory AEs	With drug-related laboratory AEs	With laboratory Serious AEs (SAEs)	With drug-related laboratory SAEs	Who died	Who discontinued due to laboratory AEs	Who discontinued due to drug-related lab AEs	Who discontinued due to laboratory SAEs	Who discontinued due to drug-related lab SAEs
Vorinostat 200 mg + Bortezomib 0.7 mg/m^2	1	2	1	0	0	0	0	0	0	0
Vorinostat 200 mg + Bortezomib 0.9 mg/m^2	1	2	0	0	0	0	0	0	0	0
Vorinostat 300 mg + Bortezomib 1.3 mg/m^2	3	7	2	0	0	0	0	0	0	0
Vorinostat 400 mg + Bortezomib 0.9 mg/m^2	0	6	0	0	0	0	0	0	0	0
Vorinostat 400 mg + Bortezomib 1.1 mg/m^2	2	4	1	0	0	0	0	0	0	0
Vorinostat 400 mg + Bortezomib 1.3 mg/m^2	3	3	3	0	0	0	0	0	0	0

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Clinical AE Summary

"An AE was defined as any unfavorable/unintended change in the structure/function/chemistry of the body temporally associated with the use of study drug, or any worsening of a preexisting condition.~A serious AE (SAE) was any AE that resulted in death, was life threatening, resulted in a persistent or significant disability/incapacity, resulted in or prolonged an existing inpatient hospitalization, was a congenital anomaly/birth defect, was a new cancer, or was an overdose." (NCT00111813)
Timeframe: Day 1 up to disease progression, toxicity, or death, assessed up to 30 days after end of treatment (up to 30 months)

,,,,,

Intervention	Participants (Number)
	With one or more AEs	With no AEs	With drug-related AEs	With Serious AEs (SAEs)	With drug-related SAEs	Who died	Who discontinued due to AEs	Who discontinued due to drug-related AEs	Who discontinued due to SAEs	Who discontinued due to drug-related SAEs
Vorinostat 200 mg + Bortezomib 0.7 mg/m^2	3	0	2	0	0	0	1	0	0	0
Vorinostat 200 mg + Bortezomib 0.9 mg/m^2	3	0	3	1	0	0	2	2	0	0
Vorinostat 300 mg + Bortezomib 1.3 mg/m^2	10	0	10	2	1	0	4	3	1	1
Vorinostat 400 mg + Bortezomib 0.9 mg/m^2	6	0	6	4	4	0	2	2	2	2
Vorinostat 400 mg + Bortezomib 1.1 mg/m^2	6	0	6	4	2	0	1	1	0	0
Vorinostat 400 mg + Bortezomib 1.3 mg/m^2	6	0	6	2	1	0	2	1	1	0

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Mean Time to First AE Resulting in a Dose Modification in Either Vorinostat or Bortezomib

An AE was defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the sponsor's product, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which was temporally associated with the use of the sponsor's product, was also an adverse experience. (NCT00111813)
Timeframe: Day 1 to disease progression, toxicity, or death, assessed up to 29 months

Intervention	Days (Mean)
Vorinostat 200 mg + Bortezomib 0.7 mg/m^2	NA
Vorinostat 200 mg + Bortezomib 0.9 mg/m^2	NA
Vorinostat 300 mg + Bortezomib 1.3 mg/m^2	58
Vorinostat 400 mg + Bortezomib 0.9 mg/m^2	58
Vorinostat 400 mg + Bortezomib 1.1 mg/m^2	128
Vorinostat 400 mg + Bortezomib 1.3 mg/m^2	32

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Number of Participants With Dose Modifications of Either Vorinostat or Bortezomib Due to Adverse Experiences (AEs) After Treatment With Study Drug

An adverse experience (AE) was defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the sponsor's product, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which was temporally associated with the use of the sponsor's product, was also an adverse experience. (NCT00111813)
Timeframe: Day 1 to disease progression, toxicity, or death, assessed up to 29 months

,,,,,

Intervention	Participants (Number)
	No dose modification	One dose modification	Two or more dose modifications
Vorinostat 200 mg + Bortezomib 0.7 mg/m^2	3	0	0
Vorinostat 200 mg + Bortezomib 0.9 mg/m^2	3	0	0
Vorinostat 300 mg + Bortezomib 1.3 mg/m^2	8	2	0
Vorinostat 400 mg + Bortezomib 0.9 mg/m^2	4	2	0
Vorinostat 400 mg + Bortezomib 1.1 mg/m^2	3	1	2
Vorinostat 400 mg + Bortezomib 1.3 mg/m^2	3	0	3

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Mean Duration of Treatment With Vorinostat

"Event causing discontinuation from the study was defined as (1) progressive disease OR (2) intolerable toxicity.~Progressive disease was defined as:~>25% increase in the level of serum monoclonal paraprotein.~25% increase in 24-hour urinary light chain excretion.~>25% increase in plasma cells in a bone marrow aspirate or on trephine~biopsy.~Development of new bone lesions or soft tissue plasmacytomas.~Development of hypercalcemia.~Intolerable toxicity was based on the clinical judgment of the investigator." (NCT00111813)
Timeframe: Day 1 to an event causing discontinuation from the study, assessed up to 29 months

Intervention	Days (Mean)
	200 mg	300 mg	400 mg
All Participants	4.6	72.6	107.1

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Overall Progression Free Survival

Time interval from start of treatment to documented evidence of disease progression. Progression is defined by at least one of the following: ≥50% increase in the sum of the products of at least two lymph nodes, appearance of new lymph nodes, ≥50% increase in the size of the liver and/or spleen as determined by measurement below the respective costal margin, appearance of new palpable hepatomegaly or splenomegaly that was not previously present, and ≥50% increase in the absolute number of circulating lymphocytes. (NCT00114738)
Timeframe: up to 9.9 years

Intervention	Months (Median)
EPOCH-R+Bortezomib	29.3

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Overall Survival

Overall Survival is the time between the first day of treatment to the day of death. The primary evaluation will be a Kaplan-Meier analysis with a two tailed log rank test. (NCT00114738)
Timeframe: up to 9.9 years

Intervention	Months (Median)
Bortezomib Maintenance	78.6
Observation	87.5
Not Randomized	31.6

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Progression Free Survival (PFS)

Intervention	Months (Median)
Bortezomib Maintenance	27.2
Observation	33.5
Not Randomized	7.8

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Clinical Response

Clinical response is assessed by the response criteria for lymphomas and is defined as a fraction of patients who have a complete response (CR) or a complete response (CR) + partial response (PR). A complete response is disappearance of all detectable clinical and radiographic evidence of disease and disappearance of all disease-related symptoms if present before therapy, and normalization of those biochemical abnormalities (e.g. lactate dehydrogenase) definitely assignable to the lymphoma. Partial response is ≥50% decreased in the sum of the products of the greatest diameters of 6 largest dominant nodes or nodal masses. No increase in size of nodes, liver or spleen and no new sites of disease. Progressive disease is defined by at least one of the following: ≥50% increase in the sum of the products of at least two lymph nodes appearance of new lymph nodes, ≥50% increase in the size of the liver and/or spleen, ≥50% increase in the absolute number of circulating lymphocytes. (NCT00114738)
Timeframe: up to 22 weeks after initiation of therapy

Intervention	Percentage of patients (Number)
	Overall Response (CR+PR)	Complete Response	Stable Disease	Progressive Disease	Not Evaluable
EPOCH-R+Bortezomib	92.5	86.7	3.8	1.9	1.9

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Count of Participants With Serious and Non-Serious Adverse Events

Here is the count of participants with serious and non-serious adverse events assessed by the Common Terminology Criteria in Adverse Events (CTCAE v4.0). A non-serious adverse event is any untoward medical occurrence. A serious adverse event is an adverse event or suspected adverse reaction that results in death, a life threatening adverse drug experience, hospitalization, disruption of the ability to conduct normal life functions, congenital anomaly/birth defect or important medical events that jeopardize the patient or subject and may require medical or surgical intervention to prevent one of the previous outcomes mentioned. (NCT00114738)
Timeframe: Date treatment consent signed to date off study, approximately 143 months and 7 days

Intervention	Participants (Count of Participants)
EPOCH-R+Bortezomib	53

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Median Overall Survival (OS)

Intervention	Months (Median)
EPOCH-R+Bortezomib	80.4

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Objective Response Rate With Bortezomib Evaluated by Both RECIST Criteria and Computer-assisted Image Analysis.

A response rate of 20% or more with bortezomib would be of interest for further evaluation, whereas a response rate of less than 5% would be of no interest. Response defined as a confirmed CR or PR. (NCT00118144)
Timeframe: Up to 5 years

Intervention	percentage of responders (Number)
Arm 1	5

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Overall Survival

Overall Suvival using the product-limit method of Kaplan and Meier. (NCT00118144)
Timeframe: Up to 5 years

Intervention	Months (Mean)
Arm I	13.6

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Progression-free Survival

Progression Free Survival using the product-limit method of Kaplan and Meier (NCT00118144)
Timeframe: Up to 5 years

Intervention	Months (Median)
Arm 1	5.5

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Overall Response Rate Complete Remission (CR), Remission (R), and Partial Remission (PR).

"Responses are defined as follows:~Complete Remission: Absence of bone marrow or blood findings of multiple myeloma. This includes disappearance of all evidence of serum and urine M-proteins on immunofixation electrophoresis studies. Normalization of serum concentrations of normal immunoglobulins is not required for CR. There must also be no evidence of increasing anemia. Bone marrow cellularity must be ≥ 20% with plasma cells ≤ 5%.~Remission: A ≥ 75% reduction in the serum M-protein, and if a urine M-protein (Bence-Jones protein) is present, either a ≥ 90% reduction in this protein, or a urine M-protein < 0.2gm/day. Bone marrow plasma cells must be ≤ 5%.~Partial Remission: A ≥ 50% reduction in the serum M-protein, and if present, a ≥ 50% reduction in the urine M-protein (Bence-Jones protein). Bone marrow plasma cells must not be increased from baseline level." (NCT00124579)
Timeframe: 1 year

Intervention	percentage of participants (Number)
Bortezomib With Thalidomide and Dexamethasone	14

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Progression-Free Survival

From date of initial registration to date of progression/relapse of disease (> 25% increase from baseline in myeloma protein production or other signs of disease progression such as hypercalcemia, etc.) or death from any cause, whichever came first, up to 5 years (NCT00124579)
Timeframe: about 12-18 months

Intervention	Months (Median)
Bortezomib With Thalidomide and Dexamethasone	8

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Toxicity Evaluation

To evaluate the qualitative and quantitative toxicities associated with this regimen. (NCT00124579)
Timeframe: From date of protocol therapy start to date of protocol therapy end, i.e., up to about 3.5 years

Intervention	Participants (Number)
	Albumin, serum-low (hypoalbuminemia)	Allergy/Immunology-Other	Bilirubin (hyperbilirubinemia)	Edema: limb	Extremity-lower (gait/walking)	Fatigue (asthenia, lethargy, malaise)	Hemoglobin	Inf (clin/microbio) w/Gr 3-4 neuts - Lung	Leukocytes (total WBC)	Lymphopenia	Muscle weakness, not d/t neuropathy - Extrem-lower	Muscle weakness, not d/t neuropathy - body/general	Neuropathy: motor	Neuropathy: sensory	Neutrophils/granulocytes (ANC/AGC)	Platelets
Bortezomib + Thal/Dex	1	1	1	1	1	1	1	1	1	1	1	1	1	1	2	1

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Number of Participants With a Positive Response to Bortezomib Measured by Bone Marker Osteocalcin

Osteocalcin: Any Osteocalcin increase means positive response. (NCT00128921)
Timeframe: 6 months

Intervention	participants (Number)
Cohort A	4
Cohort B	3

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Number of Participants With a Positive Response to Bortezomib Measured by Bone Markers Like Phosphate.

Phosphate: any Phosphate increase would refer to a positive response. (NCT00128921)
Timeframe: 6 months

Intervention	participants (Number)
Cohort A	0
Cohort B	0

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Number of Participants With a Positive Response to Bortezomib Measured by the Bone Marker Parathyroid Hormone

Parathyroid hormone: Any increase in PTH was considered response (NCT00128921)
Timeframe: 6 months

Intervention	participants (Number)
Cohort A	4
Cohort B	3

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Number of Participants With a Positive Response to Bortezomib Measured by Bone Markers Like Magnesium

Magnesium: Any Magnesium increase would refer to a positive response. (NCT00128921)
Timeframe: 6 months

Intervention	participants (Number)
Cohort A	0
Cohort B	0

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Number of Participants With a Positive Response to Bortezomib Measured by Bone Markers Like Calcium

Calcium: any Calcium increase would refer to a positive response. (NCT00128921)
Timeframe: 6 months

Intervention	participants (Number)
Cohort A	0
Cohort B	0

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Number of Participants With a Positive Response to Bortezomib Measured by Bone Marker Alkaline Phosphatase

Alkaline phosphatase: If the Alkaline phosphatase increases it's considered positive response (NCT00128921)
Timeframe: 6 months

Intervention	participants (Number)
Cohort A	4
Cohort B	3

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Efficacy of Drug Combination as Therapy for Myeloma (Overall Response Rate)

Myeloma response criteria developed by Bladé et al. was used to categorize response. (NCT00148317)
Timeframe: Best response at any point during each respective study phase was collected - once after consolidation/prior to mobilization (approximately 6 cycles after start of treatment), and once after mobilization

Intervention	participants (Number)
	Stringent Complete Response (sCR)	Complete Response (CR)	Very Good Partial response (VGPR)	Partial Response (PR)	Other Response (progression, stable disease, etc)
Treatment Arm - Post Mobilization	4	3	6	13	1
Treatment Arm - Responses Prior to Mobilization	0	1	1	2	6

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Progression Free Survival

"Response was assessed using IMWG guidelines, which for progressive disease are as follows:~Increase of > 25% from lowest response value in any one or more of the following:~Serum M-component and/or (the absolute increase must be > 0.5 g/dL)*~Urine M-component and/or (the absolute increase must be > 200 mg/24 h)~Only in patients without measurable serum and urine M-protein levels; the difference between involved and uninvolved FLC levels. The absolute increase must be > 10 mg/dL~Bone marrow plasma cell percentage; the absolute percentage must be > 10%~Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas~Development of hypercalcaemia (corrected serum calcium > 11.5 mg/dL or 2.65 mmol/L) that can be attributed solely to the plasma cell proliferative disorder IF starting M protein component is > 5g/dL, then absolute increase of 1g is sufficient for progression." (NCT00148317)
Timeframe: Date of progression, assessed from start of trial to Final data cut off date (15 April 2011)

Intervention	months (Median)
Treatment Arm (All Patients)	46.6

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Yield of CD34+ Stem Cells

This is the yield of CD34+ stem cells collection after high dose cyclophosphamide. (NCT00148317)
Timeframe: Occurred after mobilization, and prior to Stem cell transplant; a 7 day limit was imposed on stem cell collection

Intervention	10^6 cells/kg (Median)
Treatment Arm - Post Bortezomib-based Mobilization	23.2

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ORR

Overall Response Rate (NCT00151320)
Timeframe: 6 cycles (18 weeks)

Intervention	percentage of patients (Number)
Untreated DLBCL	88
Untreated MCL	81

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Progression-Free Survival (PFS)

PFS based on the Kaplan-Meier method is defined as the time from study entry to the earliest documentation of disease progression (PD) or death. Participants alive without evidence of PD were censored at the earliest date of last disease assessment or date of initiation of non-protocol therapy. PD was established based European Group for Blood and Marrow Transplantation criteria (Blade J et al Br J Haematol 1998). PD required 1 or more of the following: >25% increase in serum monoclonal protein with absolute minimum of 0.5 g/dL (confirmed on repeat investigation); >25% increase in 24-hour urinary light chain excretion with minimum absolute increase of 200 mg/24 hrs (confirmed on repeat investigation); >25% increase in bone marrow plasma cells with minimum absolute increase of 10%; Definite increase in size of existing soft tissue plasmacytomas and/or lytic lesions or new; Development of hypercalcemia (corrected serum calcium >11.5 mg/dL not attributable to other cause). (NCT00153920)
Timeframe: Disease was assessed every two cycles on treatment and every 6 weeks in long-term follow-up. Median follow-up was 29 months as of the data analysis.

Intervention	months (Median)
Bortezomib	17.0

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Objective Response (OR) Rate

Objective response was defined as complete response (CR) or partial response (PR) according to European Group for Blood and Marrow Transplantation criteria (Blade J et al Br J Haematol 1998). CR required all of the following: Negative immunofixation on the serum and urine at two consecutive times for minimum 6 weeks; Disappearance of soft tissue plasmacytomas for at least 6 weeks; <5% plasma cells in bone marrow on 2 determinations for a minimum of 6 weeks; No increase in the size or number of lytic bone lesions. PR required all the following: ≥50% reduction in the level of the serum monoclonal protein on 2 determinations for minimum 6 weeks; If present, reduction in 24-hour urinary light chain excretion either by ≥90% or to <200 mg on 2 determinations for minimum 6 weeks; ≥50% reduction size of soft tissue plasmacytomas for minimum 6 weeks; No increase in the number or size of lytic bone lesions. Development of a compression fracture does not exclude response in either category. (NCT00153920)
Timeframe: Response was assessed every two cycles on treatment. Treatment duration in months was a median (range) of 5.1 (0.8-6.1).

Intervention	proportion of participants (Number)
Bortezomib	0.41

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Number of Participants With Treatment-Emergent Neuropathic Pain

Number of participants experiencing any grade treatment-emergent neuropathic pain events based on CTCAEv3 as reported on case report forms. (NCT00153920)
Timeframe: Assessed each cycle throughout treatment from time of first dose and up to day 30 post-treatment. Treatment duration in months was a median (range) of 5.1 (0.8-6.1).

Intervention	participants (Number)
Bortezomib	8

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Time to Progression (TTP)

TTP based on the Kaplan-Meier method is defined as the time from start of treatment to documentation of disease progression (PD). Participants without evidence of PD were censored at the latest date of last disease assessment or date of initiation of non-protocol therapy. PD was established based European Group for Blood and Marrow Transplantation criteria (Blade J et al Br J Haematol 1998). PD required 1 or more of the following: >25% increase in serum monoclonal protein with absolute minimum of 0.5 g/dL (confirmed on repeat investigation); >25% increase in 24-hour urinary light chain excretion with minimum absolute increase of 200 mg/24 hrs (confirmed on repeat investigation); >25% increase in bone marrow plasma cells with minimum absolute increase of 10%; Definite increase in size of existing or new soft tissue plasmacytomas and/or lytic lesions; Development of hypercalcemia (corrected serum calcium >11.5 mg/dL not attributable to other cause). (NCT00153920)
Timeframe: Disease was assessed every two cycles on treatment and every 6 weeks in long-term follow-up. Median follow-up was 29 months.

Intervention	months (Median)
Bortezomib	17.3

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Very Good Partial Response (VGPR) Rate

Very good partial response or better was defined per International Uniform Response criteria (Durie B, Harousseau JL, Miquel JS, et al Leukemia 2006). See CR requirements in primary outcome measure plus if serum and urine M protein were unmeasurable then immunoglobulin free light chain (FLC) must be in a normal ratio of 0.26-1.65 at two consecutive times. VGPR required the following: Serum and urine M-component detectable by immunofixation but not on electrophoresis; >=90% reduction in serum M-component plus urine M-component <100 mg per 24 hours (by SPEP and UPEP); if the serum and urine M protein were unmeasurable then a >90% decrease in the difference between involved and uninvolved FLC levels. (NCT00153920)
Timeframe: Response was assessed every two cycles on treatment. Treatment duration in months was a median (range) of 5.1 (0.8-6.1).

Intervention	proportion of participants (Number)
Bortezomib	.17

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Number of Participants With Treatment-Emergent Sensory Neuropathy

Number of participants experiencing any grade treatment-emergent sensory neuropathy events based on CTCAEv3 as reported on case report forms. (NCT00153920)
Timeframe: Assessed each cycle throughout treatment from time of first dose and up to day 30 post-treatment. Treatment duration in months was a median (range) of 5.1 (0.8-6.1).

Intervention	participants (Number)
Bortezomib	41

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Assess the Toxicity of Combination Rituximab and Velcade™ in Patients With Previously Treated Mantle Cell and Follicular Lymphoma.

The descriptions and grading scales found in the revised NCI Common Terminology Criteria for Adverse Events (CTCAE) version 3.0 will be utilized for adverse event reporting. (NCT00201877)
Timeframe: Day 1 of each cycle

Intervention	patients (Number)
Velcade and Rituximab	13

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Overall Response Rate

To determine the overall survival in patients with relapsed or refractory mantle cell and follicular lymphoma following treatment with rituximab and Velcade™. (NCT00201877)
Timeframe: Every 3 months

Intervention	percentage of patients (Number)
	All patients	Patients with follicular lymphoma	Patients with MCL
Velcade and Rituximab	40	55	29

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Progression-free Survival(PFS)

To correlate serial plasma rituximab levels with response and progression-free survival. (NCT00201877)
Timeframe: 2 years

Intervention	percentage of patients (Number)
	All patients	Responding patients
Velcade and Rituximab	24	60

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Time to Progression

Progressive Disease (PD) will be defined as a greater than 25% increase in serum IgM monoclonal protein levels from the lowest attained response value as determined by serum electrophoresis, confirmed by at least one other investigation, or progression of clinically significant disease related symptom(s). (NCT00250926)
Timeframe: 42 months

Intervention	months (Median)
Bortezomib, Dexamethasone, Rituximab	NA

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Response Rate

"This outcome measure was to determine the response rate along with attainment of stable disease and time to disease progression following treatment with this patient population. The response rates were defined as follows.~A complete response (CR) was defined as having resolution of all symptoms, normalization of serum IgM levels with complete disappearance of IgM paraprotein by immunofixation, absence of bone marrow disease by bone marrow biopsy and aspiration, and resolution of any adenopathy or splenomegaly. A near complete response (nCR) was defined as fulfilling all CR criteria in the presence of a positive immunofixation study. Patients with very good partial response (VGPR), partial response (PR), and minor response (MR) were defined as having a ≥ 90%, ≥ 50%, and 25% to 49% reduction in serum IgM levels, respectively. Progressive disease (PD) occurred when a more than 25% increase in serum IgM level or progression of clinically significant disease parameters was observed." (NCT00250926)
Timeframe: 33.2 months

Intervention	participants (Number)
	Complete Response (CR)	Near Complete Response (nCR)	Very Good Partial Response (VGPR)	Partial Response (PR)	Minor Response (MR)	Stable Disease
Bortezomib, Dexamethasone, Rituximab	3	2	3	11	3	1

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Number of Participants With Adverse Events

This outcome measure was to assess the safety and tolerability of bortezomib, dexamethasone and rituximab in patients with untreated Waldenstroms macroglobulinemia. (NCT00250926)
Timeframe: 33.2 months

Intervention	participants (Number)
Bortezomib, Dexamethasone, Rituximab	23

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Time to Best Response

(NCT00250926)
Timeframe: 33.2 months

Intervention	Months (Median)
Bortezomib, Dexamethasone, Rituximab	15

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Progression Free Survival

(NCT00256776)
Timeframe: 3 year

Intervention	months (Median)
Thal + Dex + Velcade	18.3
Thal + Dex	13.6

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Median Time to Progression (TTP)

(NCT00256776)
Timeframe: 3 year

Intervention	months (Median)
Thal + Dex + Velcade	19.5
Thal + Dex	13.8

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Response Rate After 2 Courses of Therapy

Response was evaluated after two cycles of therapy using the 1999 Cheson response criteria. All responses were based on CT scans. The criteria that were developed include anatomic definitions of response, with normal lymph node size after treatment of 1.5 cm in the longest transverse diameter by computer-assisted tomography scan. A designation of complete response/unconfirmed was adopted to include patients with a greater than 75% reduction in tumor size after therapy but with a residual mass, to include patients-especially those with large-cell NHL-who may not have residual disease. For patients who had FDG-PET imaging, metabolic response was defined as a decrease in the standardized uptake value in target lesions (regions of abnormal FDG uptake on pretreatment FDG-PET images) to below three on posttreatment FDG-PET imaging). All PET scans were reviewed and interpreted by a single radiologist (SV). (NCT00262860)
Timeframe: 21 Days/course for up to 2 courses

Intervention	participants (Number)
Bortezomib, Gemcitabine Hydrochloride	4

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Change in Proteasome Activity Compared to Baseline (Cycle 1)

Peripheral blood (40 ml) was collected on cycle 1, day 1 of prebortezomib at baseline and 2 hrs post-bortezomib treatment. The samples were refrigerated at 4C and processed within 36 h of collection. Frozen cell lysates were thawed and the proteasome activity in 10 microliters was determined using a spectroflourometric 20S proteasome assay kit. Samples were run in triplicate on two separate days. The percent change between baseline and 2 hrs (day1, cycle 1) was calculated. (NCT00262860)
Timeframe: baseline to 2 hours

Intervention	Percentage of change in proteosome activ (Median)
Bortezomib, Gemcitabine Hydrochloride	-50

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Change in Proteasome Activity Compared to Baseline (Cycle 2)

Peripheral blood (40 ml) was collected at baseline and 1-2 weeks after cycle 2, day 11 post-bortezomib treatment. The samples were refrigerated at 4C and processed within 36 h of collection. Frozen cell lysates were thawed and the proteasome activity in 10 microliters was determined using a spectroflourometric 20S proteasome assay kit. Samples were run in triplicate on two separate days. The percent change between baseline and 2 hrs (day1, cycle 1) was calculated. (NCT00262860)
Timeframe: baseline and 1-2 weeks after cycle 2, day 11

Intervention	percentage of change in proteosome activ (Median)
Bortezomib, Gemcitabine Hydrochloride	-57

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Average Number of Erthroid Burst Forming Units in Bone Marrow

Colony forming unit-granulocyte-macrophage (CFU-GM) progenitors, erythroid burst forming units (BFU-E), and leukemia colony forming units (CFU-L) were measured at day 0 and day 14 of cycle 1. Five × 10(4) light density cell for granulocyte-macrophage colony forming unit (CFU-GM) or erythroid burst forming unit (BFU-E) assays were plated in 0.9% methylcellulose, 30% FCS, 2 mmol/L L-glutamine, 10-4 mol/L β-mercaptoethanol, and 1% BSA with 3U/ml human erythropoietin, 10 ng/ml GM-CSF, 10 ng/ml IL-3, and 50 ng/ml stem cell factor (SCF) (c-kit ligand). For leukemia colony forming units (CFU-Ls), the plating mixture was comparable with the exception that the cytokines utilized were 4 U/ml erythropoietin, 10 ng/ml GM-CSF, 10 ng/ml IL-3, 100 ng/ml c-kit ligand, and 100 ng/ml Flt3 ligand. The methylcellulose mixture and associated reagents were purchased from Stem Cell Technologies (Vancouver, BC). Colonies were scored at Day 14 and were defined as > 20 grouped cells. (NCT00262873)
Timeframe: day 14

Intervention	number of colonies per 50000 cell plated (Mean)
	pre bortezomib	post bortezomib
Bortezomib	14.75	14.75

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Average Number of Leukemia Forming Units in Bone Marrow

Intervention	number of colonies per 50000 cell plated (Mean)
	pre bortezomib	post bortezomib
Bortezomib	27.65	54.28

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Average Percentage of Light Density Cells in Apoptosis

The CD34+ fraction of light density marrow obtained from patients at baseline and while receiving bortezomib were assessed through measurement of Annexin V (assay obtained form R&D Systems) and by flow cytometry analysis. (NCT00262873)
Timeframe: day 14

Intervention	percentage of apoptotic cells (Mean)
	pre bortezomib	post bortezomib
Bortezomib	6.68	11.37

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Interleukin 6 Levels in Serum

"interleukin-6 levels were measured by enzyme-linked immunosorbant assay ELISA in serum from participants exposed to bortezomib.~Levels were measured at Day 0 and Day 14 of cycle 1 of the clinical trial." (NCT00262873)
Timeframe: day 14

Intervention	pg/ml (Mean)
	pre bortezomib	post bortezomib
Bortezomib	6.8	8.6

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Vascular Endothelial Growth Factor (VEGF) Levels in Serum

VEGF levels were measured by ELISA (R&DSystems) in serum from participants exposed to bortezomib. Levels were measured at Day 0 and Day 14 of cycle 1 of the clinical trial. (NCT00262873)
Timeframe: day 14

Intervention	pg/ml (Mean)
	pre bortezomib	post bortezomib
Bortezomib	402	254

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Average Number of Colony Forming Unit-granulocyte-macrophages in Bone Marrow

Intervention	number of colonies per 50000 cell plated (Mean)
	pre bortezomib	post bortezomib
Bortezomib	16.1	28.6

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Number of Participants Who Experienced an Adverse Event

(NCT00262873)
Timeframe: For 21 days/course for up to 12 courses

Intervention	participants (Number)
Bortezomib	6

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Objective Response Rate as Measured by RECIST Criteria After Every 2 Courses of Treatment for up to 6 Courses

(NCT00276614)
Timeframe: 2 months

Intervention	participants (Number)
Bortezomib	2

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Clinical Response to Treatment

Clinical evaluations of disease response were determined with each cycle. Bone marrow biopsies were done at baseline and at study termination. Clinical responses were defined by the International Myeloma Working Group criteria: Stringent Complete Response (SCR), CR and normal free light chain ratio and no clonal cells in bone marrow; Complete Response (CR), Negative serum and urine on immunofixation, disappearance of any soft tissue plasmacytomas and ≤ 5% plasma cells in bone marrow; Very Good Partial Response (VGPR), Serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥ 90% reduction in serum M-protein and urine M-protein level < 100 mg/24 hours; Partial Response (PR), ≥ 50% reduction of serum M-Protein and reduction in urinary M-protein by ≥ 90% or to < 200 mg/24 hours. Objective response is defined as a best overall response of SCR, CR, VGPR, or PR. (NCT00287872)
Timeframe: 1-6 months

Intervention	percentage of participants (Number)
Bortezomib and Thalidomide	81.5

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Peripheral Motor and Sensory Neuropathy (Grade 2 and Higher)

Neuropathy was monitored using Total Neuropathy Score reduced (TNSr). (NCT00287872)
Timeframe: 1-6 months

Intervention	participants (Number)
Bortezomib and Thalidomide	19

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The Time to Response

(NCT00287872)
Timeframe: 1-6 months

Intervention	months (Median)
Bortezomib and Thalidomide	2

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Response Rate in Patients With Relapsed or Refractory B- and T-cell NHL With Gemcitabine and Bortezomib Combination Treatment.

"Response rate in patients with relapsed or refractory B- and T-cell NHL with Gemcitabine and Bortezomib combination treatment will be defined as the number of patients with Complete Remission [CR] and Partial Remission [PR]. CT scans at screening and after completing cycle 3, cycle 6 and 30 days after Cycle 8 assessed by the Response Criteria for Non-hodgkins Lymphoma will be used to determine response where:~CR=Complete disappearance of all detectable clinical and radiographic evidence of disease PR=> 50% decrease in SPD of the six largest dominant nodes or nodal masses" (NCT00290706)
Timeframe: At screening and after completing cycle 3, cycle 6 and 30 days after Cycle 8

Intervention	participants (Number)
Phase II Gemcitabine 800 mg/m2 + Bortezomib 1.6 mg/m2 D1+D8	1
Phase II Gemcitabine 800 mg/m2 + Bortezomib 1.6 mg/m2 D1+D15	2

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Toxicity of Participants Receiving Bortezomib, Rituximab, Cyclophosphamide, and Prednisone for Treatment of Non-Hodgkin's Lymphoma

Toxicity assessed using NCI-CTC v. 3.0 (NCT00295932)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
1.3 mg/m2 Bortezomib; 750 mg/m2 Cyclophosphamide	4
1.6 mg/m2 Bortezomib; 750 mg/m2 Cyclophosphamide	6
1.6 mg/m2 Bortezomib; 1000 mg/m2 Cyclophosphamide	3
1.8 mg/m2 Bortezomib; 1000 mg/m2 Cyclophosphamide	4
Dose Level 1- 1.0 mg/m2 Bortezomib; 750 mg/m2 Cyclophosphamid	2
Dose Level 2 - 1.3 mg/m2 Bortezomib; 750 mg/m2 Cyclophosphamid	18
Dose Level 3 - 1.3 mg/m2 Bortezomib; 1000 mg/m2 Cyclophospham	3
Dose Level 4 - 1.5 mg/m2 Bortezomib; 1000 mg/m2 Cyclophosphami	4
Dose Level 5 - 1.3 mg/m2 Bortezomib; 1000 mg/m2 Cyclophospham	10
Weekly Bortezomib Dosing Schedule	12
Twice-weekly Bortezomib Dosing Schedule	13

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Maximum Tolerated Dose

Maximum tolerated dose of Bortezomib in combination with Rituximab, Cyclophosphamide and Prednisone in Phase I participants (NCT00295932)
Timeframe: 2 years

Intervention	mg/m^2 of Bortezomib (Number)
	Weekly Bortezomib	Twice-Weekly Bortezomib
Arm I	1.8	1.5

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Subjects With Treatment Emergent Adverse Events Leading to Treatment Termination

Treatment emergent adverse events observed during outcome measure time frame leading to treatment termination (NCT00298766)
Timeframe: from first study-related procedure to 30 days after last dose of study medication

Intervention	participants (Number)
Single Agent VELCADE	23

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Best Confirmed Hematologic Responders

Hematologic response was determined by the investigator per the response criteria for immunoglobulin light chain amyloidosis by Gertz (2005). It include Complete and Partial Responders (CR+PR). CR requires serum and urine negative for a monoclonal protein by immunofixation and free light chain ratio normal. PR requires: 1. reduction in quantitative serum M-protein by 50% if baseline value is at least 0.5 g/dL, 2. if light chain is detected in the urine (with a consistent peak and >100 mg/ 24 hours), then 50% reduction is required, 3. if free light chain >10 mg/dL, reduction by 50% is required. (NCT00298766)
Timeframe: from first dose of study medication to end of study visit

Intervention	participants responded (Number)
Single Agent VELCADE	33

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Maximum Tolerated Dose

"Maximum Tolerated Dose (MTD) was defined as the highest dose level that has 0/1 out of 6 patients experiences Dose Limited Toxicity (DLT). MTD is defined separately for QW and BIQ dose cohorts.~DLT was defined as adverse events occurring during Cycle 1 and: (1) related to VELCADE, (2) Grade 4 thrombocytopenia or neutropenia, (3) Grade 3 or higher nonhematologic toxicity." (NCT00298766)
Timeframe: 5 weeks in once weekly (QW) dose cohorts and 3 weeks in twice weekly (BIW) dose cohorts

Intervention	participants with DLT (Number)
Single Agent VELCADE	2

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Subjects Grade 3/4/5 Treatment Emergent Adverse Events

"Grade 3/4/5 treatment emergent adverse events observed during outcome measure time frame.~Grade is determined according to Common Terminology Criteria for Adverse Event (CTCAE) Version 3.0." (NCT00298766)
Timeframe: from first study-related procedure to 30 days after last dose of study medication

Intervention	participants (Number)
Single Agent VELCADE	43

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Subjects With Serious Treatment Emergent Adverse Events

Serious treatment emergent adverse events observed during outcome measure time frame (NCT00298766)
Timeframe: from first study-related procedure to 30 days after last dose of study medication

Intervention	participants (Number)
Single Agent VELCADE	25

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Subjects With Treatment Emergent Adverse Events

Treatment emergent adverse events observed during outcome measure time frame (NCT00298766)
Timeframe: from first study-related procedure to 30 days after last dose of study medication

Intervention	participants (Number)
Single Agent VELCADE	70

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Overall Survival (OS)

Median overall survival after first peripheral blood stem cell transplant (PBSCT). (NCT00307086)
Timeframe: 40 months post transplant

Intervention	months (Median)
Autologous PBSCT	40

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Number of Participants With Complete Response Intensive Chemo-immunotherapy Plus Maintenance or Consolidation Bortezomib

"Complete response is:~Complete disappearance of all detectable clinical and radiographic evidence of target lesions and disappearance of all disease-related symptoms if present prior to therapy and normalization of biochemical abnormalities definitely assignable to NHL~All lymph nodes and nodal masses must have regressed to normal size (<= 1.5 cm in the greatest transverse diameter (GTD) for nodes > 1.5 cm prior to therapy) or <= 1 cm for nodes that were 1.1-1.5 cm in the GTD prior to therapy or by more than 75% in the sum of the products of the GTD~The spleen, if enlarged before therapy, must have regressed in size and must not be palpable on physical examination. Any macroscopic nodules in any organs detectable on imaging studies should no longer be present. Other organs enlarged prior to therapy due to involvement of lymphoma must have decreased in size~If bone marrow was involved by lymphoma prior to treatment, infiltrate must be cleared on repeat bone marrow aspirate" (NCT00310037)
Timeframe: Up to 10 years

Intervention	participants (Number)
Arm A Maintenance Therapy	31
Arm B Consolidation Therapy	35

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Number of Participants With Grade 3, 4 or 5 Adverse Event at Least Possibly Related to Treatment.

The National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) version 3. Grade 1: Mild; Grade 2: Moderate; Grade 3: Severe; Grade 4: Life Threatening; Grade 5: Death. (NCT00310037)
Timeframe: Duration of treatment (up to approximately 2 years)

Intervention	participants (Number)
Arm A Maintenance Therapy	52
Arm B Consolidation Therapy	50

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Overall Survival

Overall Survival (OS) was measured from the date of study entry to date of death due to any cause. The median OS with 95% CI was estimated using the Kaplan-Meier method. (NCT00310037)
Timeframe: Up to 10 years

Intervention	years (Median)
Arm A Maintenance Therapy	NA
Arm B Consolidation Therapy	8.9

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Progression-free Survival Rate at 18 Months

Progression free survival (PFS) rate at 18 months was defined as the proportion of patients that were alive and progression-free 18 months after registration into the study. The Kaplan-Meier method of 18 month progression-free survival was calculated.. (NCT00310037)
Timeframe: At 18 months

Intervention	percentage of participants (Number)
Arm A Maintenance Therapy	88.5
Arm B Consolidation Therapy	96

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Progression Free Survival

Progression free survival is defined as time from randomization to progressive disease or death due to any cause, whichever occurs first. (NCT00312845)
Timeframe: Subjects are followed until progressive disease/death or the end of the study. The median follow up time is 33.9 months.

Intervention	days (Median)
Bortezomib + Rituximab	389
Rituximab	334

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Overall Response Rate

Overall response rate is defined as Complete Response (CR) + Complete Response Unconfirmed (CRu) + Partial Response (PR) using International Working Group Criteria (IWGC) and Independent Radiographic Review results and clinical results. The IWGC CR requires complete disappearance of all detectable clinical and radiographic evidence of disease and disappearance of all disease-related symptoms, and normalization of lactic dehydrogenase and bone marrow involvement. CRu requires more than 75% reduction in sum of product of nodes (SPD). PR requires moer than 50% reduction in SPD. (NCT00312845)
Timeframe: Subjects are followed until progressive disease/death or the end of the study. The median follow up time is 33.9 months.

Intervention	participants (Number)
Bortezomib + Rituximab	199
Rituximab	160

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Disease Control Rate

Disease control rate was defined as the rate of partial response (PR) plus stable disease (SD; for at least 2 cycles). (NCT00362882)
Timeframe: Up to 4 years

Intervention	percentage of participants (Number)
Arm 1	50
Arm 2	49

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Overall Response Rate

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by CT, MRI or X-ray: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT00362882)
Timeframe: Up to 4 years

Intervention	percentage of participants (Number)
Arm 1	10
Arm 2	10

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Overall Survival

Will be estimated using the product-limit method of Kaplan and Meier. (NCT00362882)
Timeframe: From first day of treatment to time of death due to any cause, up to 4 years

Intervention	Months (Median)
Arm 1	13.3
Arm 2	7.8

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Progression-free Survival @ 6 Months

Estimated using the product-limit method of Kaplan and Meier. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT00362882)
Timeframe: 6 months

Intervention	percent of participants (Number)
Arm 1	30
Arm 2	17

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Relative Dose Intensity of Bortezomib

Relative dose intensity is defined as actual dose/scheduled dose. Bortezomib is administered on Days 1, 4, 15, and 18 every 28 days. (NCT00366106)
Timeframe: Each dose of bortezomib (days 1, 4, 15, and 18 every 28 days)

Intervention	Relative dose intensity (Mean)
	Cycle 1 / Week 1	Cycle 1 / Week 1 Day 4	Cycle 1 / Week 3	Cycle 1 / Week 3 Day 18	Cycle 2 / Week 5	Cycle 2 / Week 5 Day 4	Cycle 2 / Week 7	Cycle 2 / Week 7 Day 18	Cycle 3 / Week 9	Cycle 3 / Week 9 Day 4	Cycle 3 / Week 11	Cycle 3 / Week 11 Day 18	Cycle 4 / Week 13	Cycle 4 / Week 13 Day 4	Cycle 4 / Week 15	Cycle 4 / Week 15 Day 18	Cycle 5 / Week 17	Cycle 5 / Week 17 Day 4	Cycle 5 / Week 19	Cycle 5 / Week 19 Day 18	Cycle 6 / Week 21	Cycle 6 / Week 21 Day 4	Cycle 6 / Week 23	Cycle 6 / Week 23 Day 18	Cycle 7 / Week 25	Cycle 7 / Week 25 Day 4	Cycle 7 / Week 27	Cycle 7 / Week 27 Day 18	Cycle 8 / Week 29	Cycle 8 / Week 29 Day 4	Cycle 8 / Week 31	Cycle 8 / Week 31 Day 18	Cycle 9 / Week 33	Cycle 9 / Week 33 Day 4	Cycle 9 / Week 35	Cycle 10 / Week 37	Cycle 10 / Week 37 Day 4	Cycle 10 / Week 39	Cycle 10 / Week 39 Day 18	Cycle 11 / Week 41	Cycle 11 / Week 41 Day 4	Cycle 11 / Week 43	Cycle 11 / Week 43 Day 18
Treatment Group	0.97	0.98	0.97	0.97	0.95	0.96	0.95	0.96	0.99	0.97	0.97	0.95	0.99	0.96	0.99	0.96	0.98	0.96	1.00	0.97	1.01	0.98	1.01	0.99	1.11	1.03	1.08	1.03	1.05	0.99	1.05	1.04	1.10	0.75	1.15	1.22	1.00	1.22	1.00	1.22	1.00	1.44	1.00

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Time to Progression (TTP)

(NCT00366106)
Timeframe: TTP was measured from day 1 of treatment until time of progression, assessed up to 40 months

Intervention	Months (Mean)
Treatment Group	23.07

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Number of Participants With Treatment Response

Complete Response (CR), Partial Response (PR), and Minor Response (MR) each required stable bone disease and normal calcium levels. CR also required 100% serum protein electrophoresis (SPEP) reduction, negative immunofixation (IF), 100% urine protein electrophoresis (UPEP)reduction, and <5% plasma cells in bone marrow. PR also required >=50% SPEP reduction, >=90% UPEP reduction, and >=50% reduction in plasma cells in bone marrow. MR also required >=25% SPEP reduction, >=50% UPEP reduction, and > 25% reduction in plasma cells. (NCT00366106)
Timeframe: Every 8 weeks from start of treatment until end of treatment

Intervention	Participants (Number)
Treatment Group	NA

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Incidence of Treatment-emergent Peripheral Neuropathy

(NCT00366106)
Timeframe: Every 4 weeks from start of treatment until end of treatment

Intervention	Participants (Number)
Treatment Group	11

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Incidence of Grade II-IV Acute Graft Versus Host Disease (GVHD) by Day 100.

(NCT00369226)
Timeframe: by day 100 after peripheral blood stem cell (PBSC) infusion

Intervention	percentage of participants (Number)
Phase I and Phase II	22

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Incidence of Chronic Graft Versus Host Disease (Chronic GVHD).

Number of participants with chronic GVHD at 1 year post transplant. (NCT00369226)
Timeframe: by 1 year after PBSC infusion

Intervention	percentage of participants (Number)
Phase I and Phase II	29

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Successful Initial Engraftment by Day 45 Post Peripheral Blood Stem Cell (PBSC) Infusion and Administration of Bortezomib (Velcade), Tacrolimus and Methotrexate

Percentage of participants who did not experience failure to engraft or relapse or death before assessment. (NCT00369226)
Timeframe: by day 45 post PBSC infusion

Intervention	percentage of participants (Number)
Combined Phase I Plus Phase II	97

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Sustained Engraftment Following Transplant.

As measured by median total donor chimerism at day 100. (NCT00369226)
Timeframe: by day 100 post transplant

Intervention	percentage of participants (Number)
Phase I and Phase II	97

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The Maximally Tolerated Dose (MTD) of Bortezomib (Velcade) That Can be Administered With Tacrolimus and Methotrexate After Mismatched Allogeneic Non-myeloablative Peripheral Blood Stem Cell (PBSC) Transplantation

"The MTD of bortezomib was evaluated at 3 dose levels:~Dose level 1: 1.0 mg/m^2 Dose level 2: 1.3 mg/m^2 Dose level 3: 1.5 mg/m^2 Cohorts of 3-5 pts were enrolled at each dose level. At any dose level, if no DLT in the first 3, 4, or 5 pts, then dose escalation would occur.~If 3 evaluable pts in cohort, and 1 of 3 experiences DLT then 2 additional pts treated at the same dose level. If >=1 of 2 additional pts experience DLT then previous dose level will be MTD. If no DLT in additional 2 pts then dose escalation will occur. If 4 evaluable pts in cohort, and 1 of the 4 experiences DLT then 1 additional pt treated at same dose level. If this additional pt experiences DLT then the previous dose will be declared to be the MTD. If additional pt does not experience DLT, then dose escalation will take place. If 5 evaluable pts in cohort, and 1 experiences DLT, then dose escalation will take place. If >=2 of first 3, 4, or 5 pts experience DLT then the previous dose will be declared MTD." (NCT00369226)
Timeframe: by day 45 post PBSC infusion

Intervention	mg/m^2 (Number)
Phase I	1.3

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Overall Survival and Progression-free Survival.

Progression is defined as disease relapse or disease progression since transplant. (NCT00369226)
Timeframe: by 1 year after PBSC infusion

Intervention	percentage of participants (Number)
Progression-free Survival (PFS)	60
Overall Survival (OS)	76

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Overall Survival Rate

Overall survival (OS) will be measured from the time of first treatment to death from any cause. (NCT00369707)
Timeframe: Median follow up for all patients was 50 months (range 12-78 months) and on intent to treat, OS rate for all patients is reported at 4 years.

Intervention	percentage of patients (Number)
Bortezomib and Rituximab	87

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Number of Patients That Experience Adverse Events With Bortezomib/Rituximab Combination Treatment

"Assess the safety and tolerance of bortezomib/rituximab as induction and maintenance therapy. Data will be collected for grade 3 and grade 4 adverse events experienced by patients that are determined to be at least possibly related to at least one study drug. Toxicity data for bortezomib/rituximab will be collected on day 1 of every cycle (1 cycle = 35 days) for up to 7 cycles during treatment according to the National Cancer Institute's Common Toxicity Criteria for adverse events version 3.0 (CTCAE v3.0). In general adverse events (AEs) will be graded according to the following:~Grade 1 Mild AE Grade 2 Moderate AE Grade 3 Severe AE Grade 4 Life-threatening or disabling AE Grade 5 Death related to AE" (NCT00369707)
Timeframe: Day 1 of each cycle and at the completion of cycles 1 and 3, during treatment up to 12 months

Intervention	Participants (Count of Participants)
	Neutropenia	Fever	Infection	Infusion reaction (rituximab)	Cardiac	Fatigue	Throbocytopenia	Diarrhea	Hypokalemia	Bowel obstruction	Dehydration
Bortezomib and Rituximab	2	2	2	2	2	2	1	1	1	1	1

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Correlation of Tumor Burden

"Correlation of tumor burden according to Groupe D'Etude des Lymphomes Follicularies (GELF) with recently developed Follicular Lymphoma International Prognostic Index (FLIPI) prognostic index. All patients enrolled in the study were required to have high tumor burden (HTB) as defined by GELF, where HTB is defined as representing higher risk disease and poorer outcomes than low tumor burden (LTB). Patients were put into low risk or high risk FLIPI groups. Low risk group with a score of 0-2 and high risk group with a score of 3-5.~A FLIPI score of 0 to 1 = low risk with a 10 year overall survival of 70%. A score of 2= intermediate risk with a 10 year overall survival of 50%. Finally, a score of ≥ 3 is considered high risk with a 10 year overall survival of 35%. Data was collected in connection with high or low risk FLIPI and Progression Free Survival (PFS) or Overall Survival (OS) and is reported as percentage patient with high/low risk that are progression free or alive." (NCT00369707)
Timeframe: At the start of treatment and at Median follow up for all patients was 50 months (range 12-78 months) and on intent to treat, PFS and OS for all patients is reported at 4 years.

Intervention	percentage of patients (Number)
	4 year PFS high risk FLIPI	4 year PFS low risk FLIPI	4 year OS high risk FLIPI	4 year OS low risk FLIPI
Bortezomib and Rituximab	26	60	81	92

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Progression Free Survival (PFS) Rate

"Progression Free Survival is measured from the time of first induction infusion to disease progression, relapse, second tumor, or death from any cause.~Progressive disease (PD) requires the following:~Appearance of any new lesion or increase by > 50% in the size of previously involved sites.~Increase of > 50% in the SPD from nadir measurement of all involved dominant lymph nodes and liver nodules and spleen nodules or unequivocal progression in any non measurable disease or nondominant site.~> 50% increase in greatest diameter of any previously identified node greater than 1 cm in its short axis or in the SPD of more than one node" (NCT00369707)
Timeframe: Median follow up for all patients was 50 months (range 12-78 months) and on intent to treat, PFS for all patients is reported at 4 years.

Intervention	percentage of patients (Number)
Bortezomib and Rituximab	44

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Percentage of Patients With Treatment Failure

Time to Treatment Failure (TTF) rate measured, from the time of first treatment to disease progression, relapse, second tumor, death from any cause, treatment toxicity requiring termination from the study, or for any reason treatment is discontinued permanently. (NCT00369707)
Timeframe: Median follow up for all patients was 50 months and on intent to treat, TTF rate for all patients is reported at 4 years.

Intervention	percentage of patients (Number)
Bortezomib and Rituximab	26

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Overall Response Rate After Completion of Maintenance Therapy

"Overall response rate at completion of bortezomib/rituximab maintenance therapy.~Overall response rate at this time point will be defined as complete response [CR] plus partial response [PR]) after 3 cycles of bortezomib/rituximab induction therapy and up to 4 cycles of maintenance for patients with previously untreated low-grade, B-cell NHL.~Complete response requires complete disappearance of all detectable clinical and radiographic evidence of disease and disappearance of all disease-related symptoms if present before therapy, and normalization of those biochemical abnormalities (e.g., lactate dehydrogenase [LDH]) definitely assignable to NHL. There must also be complete disappearance of lymphoma involvement in the bone marrow (if initially present).~Partial response (PR) requires 50% decrease in SPD of the six largest dominant nodes or nodal masses and no increase in the size of the other nodes, liver, or spleen." (NCT00369707)
Timeframe: At baseline and every 2 months during treatment of up to 3 cycles of induction (1 cycle =35days) and 4 cycles of maintenance (1 cycle =2 months) for up to 12 months.

Intervention	percentage of patients (Number)
Bortezomib and Rituximab	71

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Overall Response Rate After 1 Course of Induction Therapy

"Overall response rate (ORR) after 1 cycle of bortezomib/rituximab induction therapy.~Overall response rate at this time point will be defined as complete response [CR] plus partial response [PR]) after 1 cycle of bortezomib/rituximab induction therapy for patients with previously untreated low-grade, B-cell NHL.~Complete response requires complete disappearance of all detectable clinical and radiographic evidence of disease and disappearance of all disease-related symptoms if present before therapy, and normalization of those biochemical abnormalities (e.g., lactate dehydrogenase [LDH]) definitely assignable to NHL. There must also be complete disappearance of lymphoma involvement in the bone marrow (if initially present).~Partial response (PR) requires 50% decrease in SPD of the six largest dominant nodes or nodal masses and no increase in the size of the other nodes, liver, or spleen." (NCT00369707)
Timeframe: At baseline and at the completion of cycle 1 (1 cycle =35 days)

Intervention	percentage of patients (Number)
Bortezomib and Rituximab	33

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Overall Response Rate (Complete Response and Partial Response) After Three Inductions Cycles of Treatment.

"The primary objective of this study is to assess the overall response rate. Overall response rate at this time point will be defined as complete response [CR] plus partial response [PR]) after 3 cycles of bortezomib/rituximab induction therapy for patients with previously untreated low-grade, B-cell NHL.~Complete response requires complete disappearance of all detectable clinical and radiographic evidence of disease and disappearance of all disease-related symptoms if present before therapy, and normalization of those biochemical abnormalities (e.g., lactate dehydrogenase [LDH]) definitely assignable to NHL. There must also be complete disappearance of lymphoma involvement in the bone marrow (if initially present).~Partial response (PR) requires 50% decrease in SPD of the six largest dominant nodes or nodal masses and no increase in the size of the other nodes, liver, or spleen." (NCT00369707)
Timeframe: At baseline and at the completion of 3 cycles of treatment where 1 cycle equals 35 days.

Intervention	percentage of patients (Number)
Bortezomib and Rituximab	71

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Maximum Tolerated Dose (MTD) and Tolerability of Bortezomib Combined With Y-90-Ibritumomab Tiuxetan Determined by Number of Dose Limiting Toxicities in a Cohort.

"To determine the MTD using a 3+3 dose escalating design. There will be 3 dose cohorts:1.0mg/m2,1.3mg/m2 and1.6 mg/m2. 3 patients will be enrolled at dose of 1.0mg/m2 bortezomib. If no dose limiting toxicities (DLTs) are seen in the first 3 patients then dose will be escalated to next level and 3 patients will be treated at that dose level. If a DLT is seen at any dose, then 3 more patients will be enrolled at that dose level. If 1 patient out of 6, experience a DLT then MTD will be determined to be at this dose level. If 2 or more DLTs are seen in first 3 patients at that dose, then MTD will be one dose lower to the level where the DLTs were experienced.~DLTs were defined using the National Cancer Institute Common Toxicity Criteria Version 3.0.~DLTs=grade 3 nausea, vomiting, diarrhea or ileus more than 96h; grade 4 nausea, vomiting, diarrhea or ileus,neuropathic pain, peripheral sensory neuropathy, neutropenia, thrombocytopenia." (NCT00372905)
Timeframe: During induction therapy, the first 28 days of treatment.

Intervention	DLT (Number)
Cohort 1: 1.0mg/m2 Bortezomib	0
Cohort 2: 1.3mg/m2 Bortezomib	0
Cohort 3: 1.6mg/m2 Bortezomib	2

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Median Progression Free Survival

"Median progression free survival (PFS) will be assessed by CT scans after induction therapy, consolidation therapy, every 3 months for the first year following treatment and every 6 months for the second year.~Progressive disease is defined as the appearance of any new lesion more than 1.5 cm in any axis during or at the end of therapy, even if other lesions are decreasing in size or at least a 50% increase in the longest diameter of any single previously identified node or extranodal mass more than 1 cm in its short axis." (NCT00372905)
Timeframe: At start of treatment, at completion of induction therapy, at completion of consolidation therapy, every 3 months for 1 year, and every 6 months for 1 year

Intervention	Months (Median)
Cohort 1+ Cohort 2+ Cohort 3	6.5

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Overall Response Rate

"The overall response rate at the completion of treatment was defined as complete response plus partial response.~Complete response (CR)=A post-treatment residual mass of any size is permitted as long as it is PET-negative and normalization of those biochemical abnormalities.~Partial response (PR)=50% decrease in SPD of the six largest dominant nodes or nodal masses, no increase in the size of the other nodes, liver or spleen, and no new sites of disease.~Stable disease=Failing to attain the criteria for PR or CR, but not fulfilling those for progressive disease.~Progressive disease(PD)=At least a 50% increase from nadir in the SPD of any previously involved nodes or extranodal masses, or in a single involved node or extranodal mass, or the size of other lesions. Appearance of any new lesion more than 1.5 cm in any axis during or at the end of therapy, even if other lesions are decreasing in size." (NCT00372905)
Timeframe: At baseline, after induction cycle (1 cycle =28 days) and consolidation therapy of a maximum of 3 cycles (1cycle =28 days), up to approximately 6 months

Intervention	percentage of patients (Number)
Cohort 1+ Cohort 2+ Cohort 3	89

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Number of Patients With Adverse Events Related to Treatment of Bortezomib Combined With Y-90-ibritumomab Tiuxetan

"To further explore the toxicity bortezomib combined with Y-90-ibritumomab tiuxetan by collecting data on adverse events (AE) reported by patient or collected lab results that are grade 3 or grade 4 that were determined to be at least possible related to any of the studies drugs.~Toxicity will be collected on treatment days according to the National Cancer Institute's Common Toxicity Criteria for adverse events version 3.0 (CTCAE v3.0). In general adverse events (AEs) will be graded according to the following:~Grade 1 Mild AE Grade 2 Moderate AE Grade 3 Severe AE Grade 4 Life-threatening or disabling AE Grade 5 Death related to AE" (NCT00372905)
Timeframe: At start of treatment on days 1, 8, 15, 22 of induction, days 36 and 50 of recovery, days 1, 8, 15 of consolidation cycles for up to 3 cycles and 4 weeks after the completion of treatment.

Intervention	Participants (Count of Participants)
	Leukopenia	Lymphopenia	Neutropenia	Thrombocytopenia	Cardiac
Cohort 1+ Cohort 2+ Cohort 3	3	3	5	4	1

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Response Rate in Patients Treated With Rituximab-CHOPbortezomib Induction Therapy (R-CHOP-V) Followed by Bortezomib Maintenance Therapy(VM).

Complete Response(CR) is a complete disappearance of all disease with the exception of nodes. No new lesions. previously enlarged organs must have regressed and not be palpable. Bone marrow(BM) must be negative if positive at baseline. Normalization of markers. CR Unconfirmed (CRU) does not qualify for CR above, due to a residual nodal mass or an indeterminate BM. Partial Response(PR) is a 50% decrease in the sum of products of greatest diameters (SPD) for up to 6 identified dominant lesions, including spleenic and hepatic nodules from baseline. No new lesions and no increase in the size of liver, spleen or other nodes. (NCT00376961)
Timeframe: At the time of restaging (between Cycles 6 and 7), every 6 months during Cycles 7-14, and at the end of protocol treatment

Intervention	participants (Number)
	Complete Response	Partial Response	Unconfirmed Complete Response	Unconfirmed Partial Response	No Response	Assessment Inadequate
R-CHOP-V Followed by VM	17	16	13	1	4	14

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2-year Progression-free Survival in Patients Treated With Rituximab-CHOP-bortezomib Induction Therapy (RCHOP-V) Followed by Bortezomib Maintenance Therapy (VM)

Measured from date of registration to date of first observation of relapsed or progressive disease, or death due to any cause. (NCT00376961)
Timeframe: 0-2 years

Intervention	percentage of participants (Number)
R-CHOP-V Followed by VM	62

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Number of Patients With Grade 3 Through Grade 5 Adverse Events That Are Related to Study Drug

Adverse Events (AEs) are reported by the NCI Common Terminology Criteria for Adverse Events (CTCAE) version 3.0. For each patient, worst grade of each event type is reported. Grade 3 = Severe, Grade 4 = Life-threatening, Grade 5 = Fatal. (NCT00376961)
Timeframe: Assessed prior to each cycle (for Cycles 2-6), at restaging (between Cycle 6 and 7), every 3 months ( for Cycle 7-14), and at the end of protocol treatment.

Intervention	Participants (Number)
	Albumin, serum-low (hypoalbuminemia)	Anorexia	Calcium, serum-low (hypocalcemia)	Constipation	Dehydration	Diarrhea	Dizziness	Dyspnea (shortness of breath)	Edema: limb	Fatigue (asthenia, lethargy, malaise)	Febrile neutropenia	GGT (gamma-glutamyl transpeptidase)	Glucose, serum-high (hyperglycemia)	Hemoglobin	Hypoxia	Inf (clin/microbio) w/Gr 3-4 neuts - Lung	Inf (clin/microbio) w/Gr 3-4 neuts - Oral cav-gums	Inf (clin/microbio) w/Gr 3-4 neuts - Sinus	Inf w/normal ANC or Gr 1-2 neutrophils - Ext ear	Inf w/normal ANC or Gr 1-2 neutrophils - Lung	Inf w/normal ANC or Gr 1-2 neutrophils - Oral cav	Inf w/normal ANC or Gr 1-2 neutrophils - Sinus	Inf w/normal ANC or Gr 1-2 neutrophils -Nerve-peri	Infection-Other (Specify)	Leukocytes (total WBC)	Lymphopenia	Mucositis/stomatitis (functional/symp) - Oral cav	Muscle weakness, not d/t neuropathy - body/general	Nausea	Neuropathy: CN V Motor-jaw muscles; Sensory-facial	Neuropathy: motor	Neuropathy: sensory	Neutrophils/granulocytes (ANC/AGC)	Pain - Head/headache	Phosphate, serum-low (hypophosphatemia)	Platelets	Pneumonitis/pulmonary infiltrates	Potassium, serum-low (hypokalemia)	Pruritus/itching	Renal failure	Syncope (fainting)	Thrombosis/embolism (vascular access-related)	Thrombosis/thrombus/embolism	Uric acid, serum-high (hyperuricemia)	Urticaria (hives, welts, wheals)
Bortezomib Maintenance (VM)	0	0	0	0	0	0	0	1	0	1	0	1	0	0	0	0	0	0	0	0	0	1	0	0	0	2	0	0	0	0	0	1	0	1	0	0	0	0	0	0	0	0	0	0	1
Rituximab-CHOP-Bortezomib (R-CHOP-V) Induction	1	1	1	1	1	3	1	1	1	6	12	1	3	3	1	3	1	1	1	1	1	0	1	1	26	15	1	1	2	1	2	2	34	0	1	11	1	2	1	1	2	1	1	1	0

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2-year Overall Survival in Patients Treated With Rituximab-CHOP-bortezomib Induction Therapy (RCHOP-V) Followed by Bortezomib Maintenance Therapy (VM)

Measured from date of registration to date of death due to any cause or last contact (NCT00376961)
Timeframe: 0-2 years

Intervention	percentage of participants (Number)
R-CHOP-V Followed by VM	85

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Objective Response Rate of the Drug Combination in This Patient Populations.

Overall Response (OR) was defined as partial response (PR) or better. Response was assessed according to European Group for Blood and Marrow Transplant criteria, modified to include nCR and VGPR, from the International Uniform Response Criteria. (NCT00378105)
Timeframe: Full response assessment was conducted at the end of cycle 8 (average of168 days) and after cycle 4 (84 days) for patients proceeding to transplant.

Intervention	percentage of participants (Number)
Phase 1 Population	100
Phase II Population	100
Total	100

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Estimated 18-month Progression Free Survival (PFS) Rate

"PD from European Bone Marrow Transplant (EBMT) Response Criteria Required one or more:~>25% increased in the level of serum monoclonal paraprotein, which must also be an absolute increase of at least 5 g/L and confirmed on a repeat investigation, or >25% increased in 24-hour urinary light chain excretion (must also be an absolute increase of at least 200 mg/24 h and confirmed on a repeat investigation), or >25% increased in plasma cells in a bone marrow aspirate or biopsy (must also be an absolute increase of at least 10%) Definite increase in the size of existing lytic bone lesions or soft tissue plasmacytomas.~Development of new bone lesions or soft tissue plasmacytomas (not including compression fracture).~Development of hypercalcemia (corrected serum calcium >11.5 mg/dL or 2.8 mmol/L not attributable to any other cause).~PFS was measured from treatment initiation to progression or death, censored at the date patients were last known to be alive and disease free" (NCT00378105)
Timeframe: PFS rate at 18 months

Intervention	Percentage of participants (Number)
All Patients	75

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Estimated 18-month Overall Survival Rate

Overall survival was measured from treatment initiation to death, censored at the date patients were last known to be alive for those who had not died. (NCT00378105)
Timeframe: Survival rate at 18 months

Intervention	Percentage of participants (Number)
All Patients	97

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Percentage of Patients Who Remained in Response for More Than 18 Months

Duration of response was measured from first response to progression or death, censored at the date patients were last known to be alive and disease free for patients who had not progressed or died. (NCT00378105)
Timeframe: Response rate at 18 months

Intervention	Percentage of participants (Number)
All Patients	68

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Duration of Response

Duration of response will be measured as the time from initiation of a response to first documentation of disease progression or death, or date last known progression-free and alive for those who have not progressed or died. (NCT00378209)
Timeframe: Assessed at a median follow-up of 44 months

Intervention	months (Median)
Lenalidomide, Dexamethasone, Bortezomib Combination	8.7

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Objective Response Rate

"Response assessed by the European Group for Blood and Marrow Transplant (EBMT) criteria, modified to include nCR and VGPR from the international uniform response criteria (IMWG).~Objective response was defined by the achievement of at least Partial Response (PR) or better (CR-complete response, nCR-near complete response, and VGPR-very good partial response)." (NCT00378209)
Timeframe: Assessed every cycle for up to 8 cycles and best response was reported

Intervention	percentage of treated patients (Number)
Lenalidomide, Dexamethasone, Bortezomib Combination	64

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Overall Survival

defined as time from treatment initiation to death, or last known to be alive for those who had not died (NCT00378209)
Timeframe: assesed at a median follow-up of 44 months

Intervention	month (Median)
Lenalidomide, Dexamethasone, Bortezomib Combination	30

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Progression Free Survival

Progression-free survival is defined as the time from registration to the disease progression or death from any cause, censored at date last known progression-free for those who have not progressed or died. (NCT00378209)
Timeframe: aassesed at a median follow-up of 44 months

Intervention	months (Median)
Lenalidomide, Dexamethasone, Bortezomib Combination	9.5

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The Proportion of Patients Alive and Without Progressive Disease (PD) for ≥6 Months

"Response assessed by the European Group for Blood and Marrow Transplant (EBMT) criteria, modified to include nCR and VGPR from the international uniform response criteria (IMWG).~Progressive disease (PD) required one or more of the following:~>25% increased in serum monoclonal paraprotein (must also be an absolute increase of at least 5 g/L and confirmed on a repeat investigation) >25% increased in 24-hour urinary light chain excretion (must also be an absolute increase of at least 200 mg/24 h and confirmed on a repeat investigation) >25% increased in plasma cells in a bone marrow aspirate or on trephine biopsy (must also be an absolute increase of at least 10%) Definite increase in the size of existing lytic bone lesions or soft tissue plasmacytomas.~Development of new bone lesions or soft tissue plasmacytomas (not including compression fracture).~Development of hypercalcemia (corrected serum calcium >11.5 mg/dL or 2.8 mmol/L not attributable to any other cause)." (NCT00378209)
Timeframe: 6 months after therapy

Intervention	percentage of treated patients (Number)
Lenalidomide, Dexamethasone, Bortezomib Combination	75

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Number of Patients Who Experienced Adverse Events

(NCT00379574)
Timeframe: 6 months

Intervention	participants (Number)
Bortezomib + CHOP Every 2 Weeks	49

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Number of Patients Who Achieved Complete Response

All patients,9 patients of phase I study and 40 patietns in phase II stuay, were assessed with International Working Group response criteria assessed by CT; Complete Response (CR), Disappearance of all detectable clinical and radiographic evidence of disease and diappearance of all disease-related symptoms. (NCT00379574)
Timeframe: 14 weeks

Intervention	participants (Number)
Bortezomib + CHOP Every 2 Weeks	32

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Complete Response (CR)

CR is defined as at least 80% reduction in the sum of the products of the perpendicular diameters of each of the nodal masses or return to normal size, along with negative nuclear medicine imaging. (NCT00381940)
Timeframe: After 2 cycles of treatment

Intervention	participants (Number)
	With CR	Without CR
Treatment (Ifosfamide, Vinorelbine, Bortezomib)	2	21

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Induction Success Rate

Induction success is defined as achieving CR or PR without a targeted primary toxicity. Primary toxicity includes toxic death (which is any death predominantly attributable to treatment-related toxicities or complications, occurring during or within one month of the completion of therapy), Non-hematologic grades 3 or 4 toxicities attributable to drug (with the specific exclusion of 1) Grade 3 or 4 nausea or vomiting, 2) grade 3 transaminases (AST/ALT) elevations which return to < grade 1 prior to the time of the next treatment course, 3) grade 3 or 4 fever or infection, and 4) Grade 3 mucositis.) and Hematologic toxicity (Delay of >2 weeks in the start of re-induction cycle 2 or in hematologic recovery after cycle 2 secondary to severe myelosuppression, infection, or sepsis.) (NCT00381940)
Timeframe: After 2 cycles and 4 cycles

Intervention	Participants (Count of Participants)
	Induction Success Rate (After 2 cycles)	Induction Success Rate (After 4 cycles)
Treatment (Ifosfamide, Vinorelbine, Bortezomib)	19	12

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Overall Response Rate

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT00381940)
Timeframe: After 2 cycles and 4 cycles

Intervention	Participants (Count of Participants)
	Overall Response Rate (After 2 cycles)	Overall Response Rate (After 4 cycles)
Treatment (Ifosfamide, Vinorelbine, Bortezomib)	19	12

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Number of Participants With Grade 3 or 4 Toxicity

Grade 3 and 4 non-hematologic toxicity during protocol therapy. The number of patients that experience CTC Version 4 grade 3 or higher non-hematologic at any time during protocol therapy (NCT00381940)
Timeframe: 4 weeks following completion of therapy

Intervention	Participants (Count of Participants)
Treatment (Ifosfamide, Vinorelbine, Bortezomib)	9

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Rate of Successful PBSC Harvest

Success is defined as the ability to harvest 2x10^6 CD34+ cells/kg within 5 collection days. (NCT00381940)
Timeframe: After 2 cycles

Intervention	Participants (Count of Participants)
Treatment (Ifosfamide, Vinorelbine, Bortezomib)	19

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Maximum Tolerated Dose of Bortezomib in Combination With Pemetrexel (Phase I)

(NCT00389805)
Timeframe: Up to 36 months

Intervention	Mg/m^2 (Number)
Arm A	1.3
Arm B	1.6

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Number of Patients With Grade ≥ 3 Toxicity (Phase I)

Grade 3/4 toxicity occurring in a patient within 1 cycle. (NCT00389805)
Timeframe: First cycle of treatment (3 weeks)

Intervention	participants (Number)
	Neutropenia	Anemia	Thrombocytopenia	Increased transaminases	Fatigue
Arm A	12	1	0	1	2
Arm B	1	0	1	0	0

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Number of Patients Experiencing a Dose-limiting Toxicity (Phase I)

Grade 4 thrombocytopenia or grade 3 thrombocytopenia associated with bleeding, requirement for transfusion or lasting >7 days; febrile neutropenia; grade 3 neutropenia associated with infection; any other grade >/=3 non-hematologic toxicity considered by the investigator to be related to study drug. (NCT00389805)
Timeframe: Up to 36 months

Intervention	Participants (Count of Participants)
Arm A	3
Arm B	0

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Number of Participants Who Experience Adverse Events (Phase I)

Number of participants with treatment-related adverse events as assessed by CTCAE v3.0 (Phase I). (NCT00389805)
Timeframe: Throughout the entire study (up to 36 months).

Intervention	Participants (Count of Participants)
Arm A	15
Arm B	12

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Number of Patients With Toxicity by NCI CTC v3.0 (Phase I)

Adverse events possibly related to treatment, graded according to the NCI CTCAE v3.0. (NCT00389805)
Timeframe: Up to 36 months

Intervention	participants (Number)
	Neutropenia	Anemia	Thrombocytopenia	Increased transaminases	Anorexia	Constipation	Cough	Dehydration	Diarrhea	Dizziness	Edema	Fatigue	Fever	Infection	Nausea +/- vomiting	Neuropathy	Rash	Renal impairment	Weakness
Arm A	12	1	0	12	4	5	5	4	2	5	4	15	3	6	10	4	6	5	0
Arm B	1	0	1	5	6	3	4	1	3	4	4	11	3	4	6	6	5	1	2

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Number of Participants With Adverse Events (AEs) or Serious Adverse Events (SAEs)

An AE is any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. An SAE is an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; lifethreatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly. (NCT00401843)
Timeframe: up to 5 years

Intervention	participants (Number)
	Adverse Events (AEs)	Serious Adverse Events (SAEs)
Part 1 - Bortezomib + Siltuximab	21	10
Part 2 - Bortezomib + Placebo	138	44
Part 2 - Bortezomib + Siltuximab	140	47

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Progression-free Survival

Progression-free survival was defined as the time interval between randomization and the first documented sign of disease progression (including relapse from complete response [CR]) by the European Bone Marrow Transplant (EBMT) criteria or death, whichever occurred first. Relapse from CR requires at least 1 of the following: Reappearance of serum or urinary M-protein on immunofixation or routine electrophoresis, confirmed by at least 1 further investigation and excluding oligoclonal immune reconstitution; Greater than or equal to (>=) 5 percent (%) plasma cells either in a bone marrow aspirate or on trephine bone biopsy; Development of new lytic bone lesions or soft tissue plasmacytomas or definite increase in the size of residual bone lesions (development of a compression fracture does not exclude continued response and may not indicate progression); Development of hypercalcemia not attributable to any other cause. (NCT00401843)
Timeframe: Randomization until disease progression or death, which ever occured first (maximum up to 5 years)

Intervention	days (Median)
Part 2 - Bortezomib + Placebo	232
Part 2 - Bortezomib + Siltuximab	245

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Percentage of Participants With Confirmed Complete Response (CR Rate)

CR rate was defined as the percentage of participants who achieved a confirmed CR before dexamethasone was added. CR: Absence of original M-protein in serum/urine by immunofixation,maintained for minimum of 6 weeks. The presence of oligoclonal bands consistent with oligoclonal immune reconstitution does not exclude CR; Less than 5 percent (%) plasma cells in bone marrow aspirate and also on trephine bone biopsy if biopsy is performed; No increase in size/number of lytic bone lesions; Disappearance of soft tissue plasmacytomas. (NCT00401843)
Timeframe: Randomization until disease progression (maximum up to 5 years)

Intervention	percentage of participants (Number)
Part 2 - Bortezomib + Placebo	7.3
Part 2 - Bortezomib + Siltuximab	10.7

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Percentage of Participants With Best Confirmed Response of Complete Response (CR) or Partial Response (PR) (Overall Response Rate)

Overall response rate was defined as best response (CR/PR confirmed) for a participant recorded from first administration of study agent or randomization (Part 2) until disease progression/recurrence and before dexamethasone was added. CR: Absence of original M-protein in serum/urine by immunofixation,maintained for minimum of 6 weeks. The presence of oligoclonal bands consistent with oligoclonal immune reconstitution does not exclude CR; Less than 5 percent (%) plasma cells in bone marrow aspirate and also on trephine bone biopsy if biopsy is performed; No increase in size/number of lytic bone lesions; Disappearance of soft tissue plasmacytomas. PR: Greater than or equal to (>=) 50% reduction in level of serum M-protein, maintained for minimum of 6 weeks. Reduction in 24 hour urinary light chain excretion either by >= 90% or to < 200 mg, maintained for minimum of 6 weeks; >= 50% reduction in size of soft tissue plasmacytomas; No increase in size/number of lytic bone lesions. (NCT00401843)
Timeframe: Randomization until disease progression (maximum up to 5 years)

Intervention	percentage of participants (Number)
Part 2 - Bortezomib + Placebo	46.7
Part 2 - Bortezomib + Siltuximab	55.0

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Overall Survival

Overall survival was defined as the interval between the first administration of study agent or randomization (Part 2) and the participant's death from any cause. For participants with unknown survival status as of the data cut-off date, overall survival was censored at the last date known to be alive. (NCT00401843)
Timeframe: up to 5 years

Intervention	days (Median)
Part 2 - Bortezomib + Placebo	1121
Part 2 - Bortezomib + Siltuximab	937

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Response to Bortezomib (VELCADE®)

"Response is the primary endpoint of this study and will be scored on day 21 (3 weeks after the first dose of VELCADE) and every 3 weeks subsequently. Patients who progress or expire before the end of the study will be considered non-responders.~Patients are evaluated for response in an organ if they have AGVHD in that organ at the start of treatment with VELCADE or if AGVHD develops after the start of VELCADE, but before the time period of evaluation. Complete response in an organ is defined as no evidence clinical or biochemical signs of AGVHD. For the overall assessment, it is defined as complete resolution of rash, abnormal LFTs, and absence of diarrhea attributed to AGVHD.~Partial response is defined as a one stage decrease in any organ system without worsening in other organ systems." (NCT00408928)
Timeframe: Through 30 days post-treatment

Intervention	participants (Number)
	Complete response	Partial response	No response
Bortezomib for Treatment of GHVD	2	2	4

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Number of Toxicities Related to Bortezomib (VELCADE®)

Observe the toxicities of VELCADE® when administered to recipients of allogeneic hematopoietic stem cell transplant in the setting of steroid refractory or steroid dependent acute graft-versus-host disease. (NCT00408928)
Timeframe: Through 30 days post-traeatment

Intervention	toxicities (Number)
Bortezomib for Treatment of GHVD	18

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Complete Response Rate to 1.3mg/m^2 of Bortezomib With Mitoxantrone and Etoposide in Phase II

"Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions.~The percentage of participants that experienced complete response will be reported." (NCT00410423)
Timeframe: Up to 7 years

Intervention	percentage of participants (Number)
Phase 2 - Bortezomib 1.3mg/m^2	27

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Number of Participants With Dose Limiting Toxicity in Phase I

Dose limiting toxicity (DLT) is defined as grade-3 toxicity definitely related to bortezomib or grade-4 toxicity probably or definitely related to bortezomib. (NCT00410423)
Timeframe: 30-90 days

Intervention	Participants (Count of Participants)
Phase 1 - Bortezomib 0.7mg/m^2	0
Phase 1 - Bortezomib 1.0 mg/m^2	0
Phase 1 - Bortezomib 1.3mg/m^2	0

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Overall Survival

The study was closed prematurely due to slow accrual. When the study closed only two patients had died, making the OS 83%. (NCT00413959)
Timeframe: 4 years

Intervention	percentage of participants (Number)
Velcade, Rituximab,Cyclophosphamide & Decadron	83

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Overall Response Rate Using This Regimen in Patients With Low-grade B-Cell Non-Hodgkin's Lymphoma.

Percentage of complete responders plus percentage of partial responders equals overall response rate. (NCT00413959)
Timeframe: 4 years

Intervention	percentage of patients (Number)
Velcade, Rituximab,Cyclophosphamide & Decadron	90

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Overall Survival Rate at 6 Months

Overall survival (OS) at 6 months with the combination of bortezomib and carboplatin in participants who previously received 1 prior regimen for metastatic pancreatic cancer from date of randomization until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 6 months. Rate equals number of participants living at 6 months following treatment divided by the total number of participants. (NCT00416793)
Timeframe: up to 6 months

Intervention	Proportion of participants (Number)
Bortezomib + Carboplatin	0

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Overall Response Rate

Overall Response Rate measured by number of patients per the total treatment population who partially or completely responded to treatment. Participants reevaluated for response every 6 weeks. In addition to a baseline scan, confirmatory scans at 4 weeks following initial documentation of objective response. (NCT00416793)
Timeframe: from assignment of treatment until the date of first documented progression, assessed up to 17 months

Intervention	Participants (Count of Participants)
Bortezomib + Carboplatin	0

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Duration of Response in Patients With WM

Time from documentation of first response to progressive disease. (NCT00422799)
Timeframe: 5 Years

Intervention	years (Median)
Bortezomib and Rituximab	1.4

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Time to Progression in Patients With WM

Time to progresion is the defined as the time from study entry to disease progression (PD) or death. Patients without PD are censored at the date of last disease evaluation. PD is defined as a greater than 25% increase in serum monoclonal IgM electrophoresis confirmed by a second measurement at least 2 weeks apart, or progression of clinically significant findings due to disease or symptoms attributable to WM. (NCT00422799)
Timeframe: 5 Years

Intervention	years (Median)
Bortezomib and Rituximab	1.6

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Overall Response Rate of Bortezomib and Rituximab (VR) in Patients With Relapsed or Refractory Waldenstrom's Macroglobulinemia (WM)

Overall Response Rate= Minor response (>25%-50% reduction in monoclonal IgM from baseline + Partial Response (>50-90% reduction in monoclonal IgM from baseline)+ Complete Response (Disappearance of monoclonal protein by immunofixation; no histologic evidence of bone marrow involvement, resolution of any adenopathy/organomegaly (confirmed by CT scan), or signs or symptoms attributable to WM. Reconfirmation of the CR status is required at least 6 weeks apart with a second immunofixation.) (NCT00422799)
Timeframe: 2 Years

Intervention	Participants (Count of Participants)
Bortezomib and Rituximab	30

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Overall Response Rate of Bortezomib and Rituximab (VR) in Patients With Previously Untreated Waldenstrom's Macroglobulinemia (WM)

Intervention	Participants (Count of Participants)
Bortezomib and Rituximab	23

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Number of Subjects Who Require Dose Delay/Reduction in Dose of Bortezomibin the First Cycle

Dose limiting toxicity at Level 1,2 and 3: Number of subjects who required dose delay/reduction in dose of bortezomib in the first cycle of treatment. DLT defined by any of the following during first cycle: (1) GR4 neutropenia or thrombocytopenia, (2) Greater than GR3 non-hematological toxicity except alopecia or inadequately treated nausea or vomiting or (3) neurosensory toxicity of GR2 with pain or any neurotoxicity greater than GR2. (NCT00424840)
Timeframe: up to 21 days for each dosing cycle

Intervention	participants (Number)
Phase I: Dose Level 1	0
Phase 1 Dose Level II:	0
Phase I Dose Level III	0

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The Purpose of the Present Study is to Assess the Safety of PS-341 as a Pretreatment in Patients Who Are to Undergo a Radical Prostatectomy. Poor Wound Healing and Excessive Bleeding, With Historical Rates of <1% and 10% Respectively Will be Measured.

Pour wound healing is defined in the protocol as dehiscence of fascia during the first postoperative week. Excessive bleeding is defined in the protocol as greater than 2 units of blood required during the first 24 hours after surgery. (NCT00425503)
Timeframe: Poor wound healing (dehiscence of fascia during the first postoperative week) and bleeding 24 hours after surgery

Intervention	Events (Number)
	Poor wound healing	Excessive bleeding
PS-341	0	0

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Patient Response to Treatment

Progressive disease (PD): >=20% increase in sum of longest diameter (LD) of target lesion(s), taking as reference smallest sum LD recorded since treatment started. Complete response (CR): disappearance of all target lesions. Partial response (PR): >=30% decrease in sum of LD of target lesion(s), taking as reference baseline sum LD. Stable disease (SD): neither sufficient shrinkage to qualify as PR nor sufficient increase to qualify as PD. (NCT00425750)
Timeframe: 7.55 months (average duration, on study to off study)

Intervention	participants (Number)
	Partial Response	Progressive Disease	Stable Disease	Not Evaluable
Bortezomib; Docetaxel	1	10	10	4

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Progression-free Survival

Median duration of survival without disease progression, calculated as on-study date to date of progression or date of death (censored) or off-study date (censored) (NCT00425750)
Timeframe: 7.55 months (average duration, on study to off study)

Intervention	Month (Median)
Bortezomib; Docetaxel	2.27

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Overall Survival

Median survival time of patients, calculated as on-study date to date of death or off-study date (censored) (NCT00425750)
Timeframe: 7.55 months (average duration, on study to off study)

Intervention	Month (Median)
Bortezomib; Docetaxel	5.13

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Optimal Bendamustine Dosage for Further Studies

(NCT00426855)
Timeframe: Three weeks after treatment termination

Intervention	mg/m^2 (Number)
Group 1	60

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3-year Overall Survival (OS)

OS for patients who received maintenance rituximab or ASCT after VcR-CVAD induction is defined as time from start of maintenance rituximab or ASCT to death. Patients alive at last follow-up were censored. (NCT00433537)
Timeframe: Assessed every 6 months for 5 years, and then yearly thereafter.

Intervention	probability (Number)
VcR-CVAD Induction Followed by Maintenance Rituximab	0.91
VcR-CVAD Induction Followed by ASCT	0.96

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2-year Progression-free Survival (PFS)

PFS for patients who received maintenance rituximab or ASCT after VcR-CVAD induction is defined as time from start of maintenance rituximab or ASCT to earlier of disease progression or death. Patients alive and progression-free at last follow-up were censored. (NCT00433537)
Timeframe: Assessed every 6 months for 5 years, and then yearly thereafter.

Intervention	probability (Number)
VcR-CVAD Induction Followed by Maintenance Rituximab	0.79
VcR-CVAD Induction Followed by ASCT	0.76

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Complete Response (CR) Rate

Number of eligible, treated participants who achieve complete response. Response criteria are based upon the criteria from the Revised Response Criteria for Malignant Lymphoma (Cheson et al., 2007). Complete response is defined as complete disappearance of all detectable clinical evidence of disease, and disease-related symptoms if present prior to therapy. (NCT00433537)
Timeframe: Assessed after VcR-CVAD cycles 2, 4, and 6.

Intervention	proportion (Number)
VcR-CVAD Induction	0.68

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Number of Participants With Dose Limiting Toxicity (DLT)

To determine the maximum tolerated dose(MTD) of velcade and dose limiting toxicity(DLT). A dose limiting toxicity (DLT) was defined as a grade 3-4 neurological toxicity, graft failure, or death due to GvHD. The Commom Terminlogy Criteria for Adverse Events v3.0 was used. (NCT00439556)
Timeframe: From start of treatment to 90 days after the start of treatment

Intervention	Participants (Count of Participants)
Treatment (Chemotherapy, Transplant, Filgrastim, Tacrolimus)	0
Velcade Dose Level 2	0
Velcade Dose Level 3	0

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Disease-free Survival

To determine DFS at 1 year post transplant. (NCT00439556)
Timeframe: At 1 year

Intervention	Participants (Count of Participants)
Velcade Dose Level 1	16
Velcade Dose Level 2	0
Velcade Dose Level 3	0

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Duration of Response (DOR)

DOR was defined as the duration from the date of the best confirmed response for subjects who achieved CR or PR to the date of first documented evidence of PD (or relapse for subjects who experienced CR) over the duration of the study. DOR = ([Date of PD or date of censoring - Date of best response]+1)/30.44. (NCT00441168)
Timeframe: every 28 days during treatment period for up to 6 to 8 cycles

Intervention	months (Number)
	patient 1	patient 2	patient 3	patient 4	patient 5	patient 6
PAD Treatment	2.83	7.69	5.52	6.57	4.96	7.42
VAD Treatment	1.68	6.18	3.71	5.42	4.73	NA

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Best Confirmed Disease Response

The primary efficacy analysis was based on the best response obtained during the treatment period according to the European Group for Blood and Marrow Transplantation (EBMT) criteria as assessed by the investigator. The best confirmed response was defined as 2 separate and consecutive evaluations of response, at least 6 weeks apart (for progressive disease [PD], 1 to 3 weeks apart). The ordering of the responses was: complete response (CR), partial response (PR), minimal response (MR), no change (NC) and PD. CR was the best response and the poorest response was PD. (NCT00441168)
Timeframe: every 28 days during treatment period for up to 6 to 8 cycles

Intervention	participants (Number)
	CR	PR	Response Rate (CR + PR)	MR	Overall Response (CR + PR + MR)	NC	PD	Unknown/Unable to Assess
PAD Treatment	1	6	7	0	7	1	1	4
VAD Treatment	0	5	5	2	7	3	1	4

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Best Reported Disease Response

The primary efficacy analysis was based on the best response obtained during the treatment period according to the EBMT criteria as assessed by the investigator. The ordering of the responses was: CR, PR, MR, NC and PD. CR was the best response and the poorest response was PD. (NCT00441168)
Timeframe: every 28 days during treatment period for up to 6 to 8 cycles

Intervention	participants (Number)
	CR	PR	Response Rate (CR + PR)	MR	Overall Response (CR + PR + MR)	NC	PD	Unknown/Unable to Assess
PAD Treatment	3	4	7	3	10	3	0	0
VAD Treatment	1	6	7	2	9	5	0	1

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Disease Response

The response of myeloma to BDDTD will be assessed by standard electrophoretic and immunofixation tests of blood and urine for a monoclonal protein (M protein), and bone marrow aspirate and biopsy. These tests will be performed at enrollment and at the conclusion of therapy. (NCT00458705)
Timeframe: 2 years

Intervention	participants (Number)
	Complete Response	Near Complete Response	Partial Response	Stable Disease	Progression of Disease	Very Good Partial Response
Combination Therapy	10	8	10	2	3	7

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Hematologic and Organ Response

patients will be assessed for hematologic response (the response of the clonal plasma cell disease). If the plasma cell disease persists, then they will receive 6 cycles of adjuvant therapy with bortezomib and dexamethasone; patients with peripheral neuropathy will receive dexamethasone alone because of the risk of neuropathy associated with bortezomib. Symptomatic organ involvement with amyloid as defined below. Patients must have symptomatic involvement of no more than 2 of the following 4 visceral organ-systems: kidneys, liver/GI, peripheral/autonomic nervous system, and heart. (NCT00458822)
Timeframe: 2-3 months post transplant

Intervention	participants (Number)
	Complete Hematologic Response	Partial Response	Stable Disease
All Patients	11	7	18

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Overall Survival (OS) - Number of Participants Alive at Study Completion

The secondary objective of this study is to assess the safely and tolerability of the combination treatment of bevacizumnab and bortezomnib. Adjustments in the dosing schedule of bortezomib would be made for patients with adequate response as per Blade criteria and continue until disease progression or 18 months (NCT00464178)
Timeframe: 18 months

Intervention	participants (Number)
Bortezomilb and Bevacizumab	5

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Median Number of Cycles to Tumor Progression (TTP)

Study Schema: Bortezomib will be administered on Days 1. 4, 8, and 11. Response will be assessed subsequent to each 21-day cycle. Progression is defined using the Bladé criteria, defined progression as an increase of >25% in paraprotein or urinary light chain excretion (or marrow plasma cell percentage in the marrow (NCT00464178)
Timeframe: 18 months

Intervention	Cycles Prior to Tumor Progression (Median)
Bortezomib and Bevacizumab	1.5

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Number of Patients Reaching Complete Response (CR)

Number of participants with CR at Day 180 who had maintained CR for at minimum of 4 weeks, and who had: No monoclonal protein in urine/serum when analyzed by immunofixation electrophoresis; bone marrow normal by morphological examination with <5% plasma cells, <1% aneuploid light chain restricted population by flow cytometry for DNA/cIg; and, while healing of bony lesion is not required, no new lytic lesion should appear. Further compression fracture of spine not considered progressive disease. (NCT00469209)
Timeframe: Baseline through Day 180, with assessments at Day 90 and Day 180

Intervention	participants (Number)
No Bortezomib	4
Bortezomib 1.0 mg/m^2	1
Bortezomib 1.5 mg/m^2	4

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Number of Participants With Selected Adverse Events (AEs)

Adverse events were graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE), v3.0. All serious adverse events are listed in the Adverse Event Reporting section. (NCT00473590)
Timeframe: Participants were monitored for AEs from initiation of treatment to 30 days after treatment termination (up to 122 weeks).

Intervention	Participants (Number)
	Arterial thromboembolic events (any grade)	Bleeding other than pulmonary or CNS (Grade >=3)	Febrile neutropenia (any grade)	Gastrointestinal Perforation (Any Grade)	Hypertension (Grade >= 3)	Left Ventricular Systolic Dysfunction (Grade >= 3)	Neutropenia (Grade >= 3)	Osteonecrosis of the Jaw	Peripheral Neuropathy (Grade >= 3)	Pulmonary and CNS Bleeding (Any Grade)	Thrombocytopenia (Grade >= 3)	Vernous Thromboembolic Events (Grade >=3)
BORT + BV	1	2	1	0	8	0	10	1	8	1	15	0
BORT + P	0	1	1	1	0	1	6	0	7	0	15	1

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Progression-free Survival (PFS)

Progression-free survival (PFS) was defined as the time from randomization to disease progression or death on study from any cause within 30 days of the last response assessment. Disease progression was determined by the investigator using the International Myeloma Working Group's (IMWG) uniform response criteria. Median PFS was estimated using Kaplan-Meier methodology. For patients who were alive at the time of the analysis and whose disease had not yet progressed, PFS was censored at the time of the last response assessment. (NCT00473590)
Timeframe: From randomization to disease progression or death on study (up to 116 weeks).

Intervention	months (Median)
BORT + P	5.1
BORT + BV	6.2

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Percentage of Participants With an Overall Response

Overall response was defined as a stringent complete response, complete response, very good partial response, or partial response (sCR, CR, VGPR, and PR) determined on two consecutive assessments ≤ 6 weeks apart and before the initiation of any new anti-tumor therapy, as assessed by the investigator using the IMWG's uniform response criteria. Patients without a post-baseline response assessment or who died prior to their first scheduled response assessment were considered non-responders. (NCT00473590)
Timeframe: From randomization to the end of study (clinical cut-off; up to 116 weeks).

Intervention	Percentage of Participants (Number)
BORT + P	43.4
BORT + BV	51.0

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Overall Survival (OS)

Overall survival was defined as the duration of time from randomization until death from any cause. All deaths were included, whether they occurred on study treatment or following treatment discontinuation. Overall survival was estimated using Kaplan-Meier. For patients who had not died, overall survival was censored at the date that the patient was last known to be alive. (NCT00473590)
Timeframe: From randomization until death from any cause, up until the end of study (clinical cut-off; up to 116 weeks).

Intervention	Months (Median)
BORT + P	24.0
BORT + BV	NA

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Number of Participants With an Overall Response

Overall response was defined as a stringent complete response, complete response, very good partial response, or partial response (sCR, CR, VGPR, and PR, respectively) determined on two consecutive assessments ≤ 6 weeks apart and before the initiation of any new anti-tumor therapy, as assessed by the investigator using the International Myeloma Working Group's (IMWG's) uniform response criteria. Patients without a post-baseline response assessment or who died prior to their first scheduled response assessment were considered non-responders. (NCT00473590)
Timeframe: From randomization to the end of study (clinical cut-off; up to 116 weeks).

Intervention	participants (Number)
BORT + P	23
BORT + BV	25

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Duration of Response

Duration of response was defined as the time from the initial response to disease progression or death on study. Disease progression was determined by the investigator using the IMWG's uniform response criteria and defined as an increase of ≥25% from best response in: Serum M-protein and/or Urine M-protein and/or Marrow plasma cells; or new or increased plasmacytomas or bone lesions; or hypercalcemia due to myeloma. Duration of response was estimated using Kaplan-Meier. For patients who had not progressed or died, duration of response was censored at the date of the last response assessment. (NCT00473590)
Timeframe: From randomization to the end of study (clinical cut-off; up to 116 weeks).

Intervention	Months (Median)
BORT + P	6.0
BORT + BV	6.9

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Time to Failure (Phase II)

Failure will be defined as recurrence/progression of disease or death from either disease or toxicity. Bayesian toxicity monitoring schema will be used to monitor severe toxicity profile in combined therapy. Severe toxicity is defined as at least two episodes of neutropenic fever during treatment courses. (NCT00477412)
Timeframe: First date of diagnosis up to 5 years

Intervention	months (Median)
Phase II- Treatment (Combination Chemotherapy)	55

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Overall Survival

Overall survival is the time in number of months from start of study treatment to date of death due to any cause. (NCT00477412)
Timeframe: Date of diagnosis to last known date of survival, up to 5 years

Intervention	months (Median)
Phase II- Treatment (Combination Chemotherapy)	44

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Number of Participants With Overall Response Rate

Response rate is determined by CT scans of the chest, abdomen, and pelvis, unilateral BM biopsy and aspirate with lymphoma markers (if initially positive) and colonoscopy/endoscopy if applicable. (NCT00477412)
Timeframe: Up to 5 years

Intervention	Participants (Count of Participants)
Phase II- Treatment (Combination Chemotherapy)	87

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Maximum Tolerated Dose of Bortezomib (Phase I)

Determine the safety and the maximum tolerated dose (MTD) of bortezomib when added to the combination of rituximab, methotrexate, and cytarabine alternating with bortezomib, rituximab-hyperCVAD in patients with untreated aggressive mantle cell lymphoma. (NCT00477412)
Timeframe: Cycle 1 Day 1 - End of Cycle 2 up to 60 days.

Intervention	mg/m^2 (Number)
Phase 1 Maximum Tolerated Dose (MTD)	1.3

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Progression-Free Survival

Median time to progression or death (NCT00483262)
Timeframe: 10 months

Intervention	month (Median)
CCI779 PFS Phase I	5.7
CCI779 PFS Phase II	5.0

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Toxicity. Number of Patients With Specific Toxicities Are Reported.

Toxicity of CCI-779 (Temsirolimus) and bortezomib (Velcade) in patients with multiple myeloma. (NCT00483262)
Timeframe: 10 months

Intervention	percentage of patients (Number)
CCI779 Toxicity Phase I	90
CCI779 Toxicity Phase II	79

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Best Response to Combination Treatment

Response rate of PR or better to the combination treatment of CCI-779 (Temsirolimus) and bortezomib (Velcade) in patients with relapsed or refractory multiple myeloma (NCT00483262)
Timeframe: 10 months

Intervention	percentage of patients (Number)
CCI779 Response Phase I	10
CCI779 Response Phase II	33

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Response Rate After 2 Cycles of Treatment With Bortezomib and Rituximab

Partial response (PR) defined as at least > 50 % reduction of serum monoclonal IgM concentration determined by protein electrophoresis, > 50% decrease in adenopathy / organomegaly on physical examination or on CT scan, and no new symptoms or signs of active disease. Complete response (CR) defined as a disappearance of serum and urine monoclonal protein determined by immunofixation, absence of malignant cells in bone marrow determined by histologic evaluation, resolution of adenopathy/organomegaly (confirmed by computed tomography [CT] scan), and no signs or symptoms attributable to WM. Stable disease defined as neither grown nor shrunk; the amount of disease has not changed.Participants will be followed for < 6 months after receiving bortezomib/rituximab or rituximab-modified hyper-CVAD to be considered unresponsive to therapy in accordance with the guidelines of the Consensus Panel of the Third International Workshop on Waldenstrom's Macroglobulinemia. (NCT00492050)
Timeframe: After 2 (35 day) cycles of treatment

Intervention	Participants (Count of Participants)
	Stable Disease	Partial Response	Progressive Disease	No Response
All Participants	20	11	2	3

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Response Rate After 3 Cycles of Treatment With Bortezomib and Rituximab

Partial response (PR) defined as at least > 50 % reduction of serum monoclonal IgM concentration determined by protein electrophoresis, > 50% decrease in adenopathy / organomegaly on physical examination or on CT scan, and no new symptoms or signs of active disease. Complete response (CR) defined as a disappearance of serum and urine monoclonal protein determined by immunofixation, absence of malignant cells in bone marrow determined by histologic evaluation, resolution of adenopathy/organomegaly (confirmed by computed tomography [CT] scan), and no signs or symptoms attributable to WM. Stable disease defined as neither grown nor shrunk; the amount of disease has not changed. Participants will be followed for < 6 months after receiving bortezomib/rituximab or rituximab-modified hyper-CVAD to be considered unresponsive to therapy in accordance with the guidelines of the Consensus Panel of the Third International Workshop on Waldenstrom's Macroglobulinemia. (NCT00492050)
Timeframe: After 3 (35 day) cycles of treatment

Intervention	Participants (Count of Participants)
	Stable Disease	Partial Response	No Response
All Participants	7	16	2

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Participants Ability to Collect Stem Cells After Treatment With Bortezomib and Rituximab

Number of Participants who were able to collect stem cells successfully or unable to collect after treatment with bortezomib and rituximab. (NCT00492050)
Timeframe: 4 weeks

Intervention	Participants (Count of Participants)
	Participants Collected Successfully	Participants Unable to Collect
All Participants	30	7

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Complete Response

Complete Response (NCT00504751)
Timeframe: 26 months

Intervention	participants (Number)
Study Treatment	3

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Percentage of Participants With a Complete Response

Participants with a best overall response of complete response, defined as negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas, and <5% plasma cells in bone marrow. Response was assessed by the Investigator using the IMWG uniform response criteria. (NCT00507416)
Timeframe: Response assessed every other cycle, for up to 13 cycles (49 weeks).

Intervention	percentage of participants (Number)
Bortezomib and Dexamethasone	3
Bortezomib, Thalidomide, and Dexamethasone	4
Bortezomib, Melphalan and Prednisone	4

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Time to Alternative Therapy

Time to alternative therapy is defined as the time between randomization and alternative therapy. Participants who did not receive alternative therapy were censored at the time of last contact. (NCT00507416)
Timeframe: From randomization until alternative therapy. Median follow-up time was 43 months.

Intervention	months (Median)
Bortezomib and Dexamethasone	19.7
Bortezomib, Thalidomide, and Dexamethasone	24.5
Bortezomib, Melphalan and Prednisone	19.0

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Percentage of Participants With an Overall Response

"Overall response defined as a best overall response of complete response (CR), very good partial response (VGPR) or partial response (PR), assessed by the Investigator using the IMWG uniform response criteria.~CR: Negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas, and <5% plasma cells in bone marrow.~VGPR: Serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥ 90% reduction in serum M-protein plus urine M-protein level <100 mg per 24 hours (h).~PR requires 1 of the following:~≥50% reduction of serum M-protein and 24-h urinary M-protein by ≥ 90% or to <200 mg/24 h, or~If M-protein not measurable, a ≥50% decrease in the difference between involved and uninvolved FLC levels, or~If FLC not measurable, a ≥ 50% reduction in plasma cells, provided baseline bone marrow plasma cell percentage was ≥30%.~If present at baseline, a ≥50% reduction in the size of soft tissue plasmacytomas is also required." (NCT00507416)
Timeframe: Response assessed every other cycle for up to 13 cycles (49 weeks).

Intervention	percentage of participants (Number)
Bortezomib and Dexamethasone	73
Bortezomib, Thalidomide, and Dexamethasone	80
Bortezomib, Melphalan and Prednisone	70

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Overall Survival

Overall survival is defined as the time between randomization and death. Participants still alive at the cutoff date or lost to follow-up were censored at the date of last contact. (NCT00507416)
Timeframe: From randomization until death. Median follow-up time was 43 months.

Intervention	months (Median)
Bortezomib and Dexamethasone	49.8
Bortezomib, Thalidomide, and Dexamethasone	51.5
Bortezomib, Melphalan and Prednisone	53.1

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Progression Free Survival (PFS)

"PFS is defined as the time from randomization to disease progression or death, whichever occurs first. Participants who did not progress and were still alive at the cut-off date were censored at the date of last contact. Response was assessed by the Investigator using the International Myeloma Working Group (IMWG) uniform response criteria.~Progressive disease requires 1 of the following:~Increase of ≥ 25% from nadir in:~Serum M-component (absolute increase ≥ 0.5 g/dl)~Urine M-component (absolute increase ≥ 200 mg/24 hours)~In patients without measurable serum and urine M-protein levels the difference between involved and uninvolved free light chain (FLC) levels (absolute increase > 100 mg/dl)~Bone marrow plasma cell percentage (absolute % ≥ 10%)~Development of new or increase in the size of existing bone lesions or soft tissue plasmacytomas.~Development of hypercalcemia (corrected serum calcium > 11.5 mg/dl) attributed solely to plasma cell proliferative disease" (NCT00507416)
Timeframe: From randomization until disease progression. Median follow-up time was 43 months.

Intervention	months (Median)
Bortezomib and Dexamethasone	14.7
Bortezomib, Thalidomide, and Dexamethasone	15.4
Bortezomib, Melphalan and Prednisone	17.3

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Duration of Response

Duration of response is defined in participants with an overall response as the time between first documentation of response and disease progression. Responders without disease progression were censored at the last clinical assessment of response. (NCT00507416)
Timeframe: From first documented response until disease progression. Median follow-up time was 43 months.

Intervention	months (Median)
Bortezomib and Dexamethasone	18.3
Bortezomib, Thalidomide, and Dexamethasone	22.4
Bortezomib, Melphalan and Prednisone	19.8

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Percentage of Participants With a Complete Response or a Very Good Partial Response

"Complete response is defined by negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas, and <5% plasma cells in bone marrow.~Very good partial response is defined by serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein plus urine M-protein level <100 mg per 24 hours.~Response was assessed by the Investigator using the IMWG uniform response criteria." (NCT00507416)
Timeframe: Response assessed every other cycle for up to 13 cycles (49 weeks).

Intervention	percentage of participants (Number)
Bortezomib and Dexamethasone	37
Bortezomib, Thalidomide, and Dexamethasone	51
Bortezomib, Melphalan and Prednisone	41

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Change From Baseline in EORTC QLQ-C30 - Global Health Status

"The European Organisation for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact).~The EORTC QLQ-C30 Global Health Status/QOL Scale is scored between 0 and 100, where higher scores indicate better Global Health Status/QOL. Negative changes from baseline indicate deterioration in QOL or functioning and positive changes indicate improvement." (NCT00507416)
Timeframe: Baseline and Day 1 of Cycles 3, 5, 7, 9, 11 and 13

Intervention	units on a scale (Mean)
	Cycle 3, Day 1 (n=129, 115, 125)	Cycle 5, Day 1 (n=114, 98, 107)	Cycle 7, Day 1 (n=89, 79, 84)	Cycle 9, Day 1 (n=87, 66, 67)	Cycle 11, Day 1 (n=71, 61, 65)	Cycle 13, Day 1 (n=67, 52, 61)
Bortezomib and Dexamethasone	1.3	-4.9	-3.3	-4.2	-11.6	-10.2
Bortezomib, Melphalan and Prednisone	2.0	-0.4	-4.7	-1.0	2.8	1.0
Bortezomib, Thalidomide, and Dexamethasone	-4.4	-6.1	-8.6	-8.1	-7.9	-8.5

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Overall Survival

Overall survival is defined as time from the date of randomization to the date of death (NCT00507442)
Timeframe: Up to 48 weeks or until death

Intervention	days (Median)
V-DR	NA
VDCR	NA
V-DC	NA
VDC-mod	NA

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Number of Patients With Stringent Complete Response Rate

Stringent Complete Response is defined as complete response plus normal free light chain (kappa/lambda) ratio and absence of clonal cells in bone marrow by immunohistochemistry or immunofluorescence. (NCT00507442)
Timeframe: Up to 48 weeks or until disease progression

Intervention	participants (Number)
V-DR	7
VDCR	6
V-DC	3
VDC-mod	5

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Number of Patients With Overall Response

"Overall Response includes complete response and partial response.~Complete response requires negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and < 5% plasma cells in bone marrow.~Partial response requires at least 50% reduction of serum M-protein and reduction in 24-h urinary M-protein by at least 90% or to < 200 mg per 24 hour." (NCT00507442)
Timeframe: Up to 48 weeks or until disease progression

Intervention	participants (Number)
V-DR	35
VDCR	35
V-DC	24
VDC-mod	17

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Number of Patients With Combined Complete Response and Very Good Partial Response

"Complete response requires negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and < 5% plasma cells in bone marrow.~Very good partial response requires serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein plus urine M-protein level < 100 mg per 24 h" (NCT00507442)
Timeframe: Up to 48 weeks or until disease progression

Intervention	participants (Number)
V-DR	21
VDCR	23
V-DC	13
VDC-mod	9

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Number of Patients With Adverse Events (AEs)

Evaluate the safety and tolerability of the combination therapy (NCT00507442)
Timeframe: From first dose of study drug through the 30 day post-treatment AE assessment visit

Intervention	participants (Number)
V-DR	42
VDCR	65
V-DC	33
VDC-mod	17

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Duration of Response

"Duration of response is the time from date of first documented confirmed response to date of first documented progressive disease. A confirmed response is a response that has been observed on at least two consecutive assessments.~Disease progression requires any one or more of the following: serum m-protein increase >= 25% from nadir(absolute increase >= 0.5 g/dL); Urine m-protein increase >= 25% from nadir(absolute increase >= 200 mg/24 hr), bone marrow plasma cell percentage increase >= 25% from nadir(absolute increase >= 10%), new bone lesion or soft tissue plasmacytomas." (NCT00507442)
Timeframe: Up to 48 weeks or until disease progression

Intervention	days (Median)
V-DR	NA
VDCR	NA
V-DC	NA
VDC-mod	NA

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Number of Patients With Complete Response Rate + Near Complete Response Rate

"Complete response requires negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and < 5% plasma cells in bone marrow.~Near Complete response requires positive immunofixation on the serum and/or urine and disappearance of any soft tissue plasmacytomas and < 5% plasma cells in bone marrow." (NCT00507442)
Timeframe: Up to 48 weeks or until disease progression

Intervention	participants (Number)
V-DR	17
VDCR	14
V-DC	10
VDC-mod	8

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Time to Response

Time to response is defined as time from date of randomization to the date of the first documentation of a confirmed response. confirmed response is a response that has been observed on at least two consecutive assessments. (NCT00507442)
Timeframe: Up to 48 weeks or until disease response

Intervention	days (Median)
V-DR	49
VDCR	50
V-DC	55
VDC-mod	49

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Time to Disease Progression

"Time to disease progression is defined as time from the date of randomization to the date of first documented progressive disease.~Disease progression requires any one or more of the following: serum m-protein increase >= 25% from nadir(absolute increase >= 0.5 g/dL); Urine m-protein increase >= 25% from nadir(absolute increase >= 200 mg/24 hr), bone marrow plasma cell percentage increase >= 25% from nadir(absolute increase >= 10%), new bone lesion or soft tissue plasmacytomas." (NCT00507442)
Timeframe: Up to 48 weeks or until disease progression

Intervention	days (Median)
V-DR	NA
VDCR	NA
V-DC	NA
VDC-mod	NA

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Progression-free Survival

"Progression-free survival is defined as time from the date of randomization to the date of the first documented progressive disease or death.~Disease progression requires any one or more of the following: serum m-protein increase >= 25% from nadir(absolute increase >= 0.5 g/dL); Urine m-protein increase >= 25% from nadir(absolute increase >= 200 mg/24 hr), bone marrow plasma cell percentage increase >= 25% from nadir(absolute increase >= 10%), new bone lesion or soft tissue plasmacytomas." (NCT00507442)
Timeframe: Up to 48 weeks or until disease progression/death

Intervention	days (Median)
V-DR	NA
VDCR	631
V-DC	NA
VDC-mod	NA

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Probability of 1-year Survival

(NCT00507442)
Timeframe: survival probability at 1 year after randomization

Intervention	percentage of patients (Number)
V-DR	100
VDCR	91.6
V-DC	100
VDC-mod	100

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Complete and Partial Response

"Complete Response: Complete disappearance of all detectable clinical and radiographic evidence of disease, disappearance of all disease-related symptoms and normalization of biochemical abnormalities (eg. LDH) definitely assignable to follicular lymphoma.~Partial Response requires the following:~greater than or equal to 50% decrease in the SPD of the 6 largest dominant nodes of nodal masses.~No increase in size of other nodes, liver, or spleen.~Splenic and hepatic nodes must regress by at least 50% in sum of the products (SPD).~Bone marrow assessment in irrelevant for determination of Partial Response since it is not measurable disease; however, if positive the type of cell should be reported.~No new lesions." (NCT00510887)
Timeframe: 1 year

Intervention	percentage of participants (Number)
VR-FND	64

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Duration of Response

Duration of response is measured from time of treatment to time of disease progression (NCT00510887)
Timeframe: up to 4 years

Intervention	months (Mean)
VR-FND	16.47143

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Number of Participants With Neuropathy, Any Grade

Before each drug dose, the patient will be evaluated for possible toxicities that may have occurred after the previous dose(s). Toxicities are to be assessed according to the NCI Common Toxicity Criteria (CTC). (NCT00510887)
Timeframe: up to 1 year

Intervention	participants (Number)
VR-FND	6

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Number of Participants With a Grade 3-4 Hematologic Toxicity.

Intervention	participants (Number)
VR-FND	7

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Percentage of Subjects Experiencing Overall Survival

Overall survival is from the day of enrollment to date of death from any cause. (NCT00510887)
Timeframe: up to 2 years

Intervention	percentage of participants (Number)
VR-FND	27

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Percentage of Subjects Experiencing Progression Free Survival

Progression free survival is measured from treatment to progression or death, whichever comes first. Progressive disease is measured as: 50% or greater increase from nadir in the sum of the products (SPD) of any previously identified abnormal node and the appearance of any new lesions during or at the end of treatment. (NCT00510887)
Timeframe: up to 2 years

Intervention	percentage of participants (Number)
VR-FND	17

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Patients With Inhibition in NF-kB Activation (Phase I)

Patient with a minimum of 50% reduction from baseline on day 8 or day 29 in NF-kB, measured by picograms/milliliter in peripheral mononuclear blood cells (NCT00512798)
Timeframe: at baseline, on day 8 and on day 29

Intervention	participants (Number)
Phase I	0

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Patients With Inhibition of NF-kB (Phase II)

Intervention	participants (Number)
Phase II	0

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Number of Patients With Clinical Anti-tumor Activity Phase II)

Per RECIST criteria v. 1.0: measurable lesions: complete response (CR) disappearance of target lesions, partial response (PR) > 30% decrease in the sum of the longest diameter (LD) of target lesions, progressive disease (PD) > 20% increase in the sum of the LD of target lesions or appearance of new lesions, stable disease (SD) neither sufficient decrease nor increase of the sum of smallest sum of the LD of target lesions. Patients with CR + PR + SD (NCT00512798)
Timeframe: every 9 weeks to a maximum of 54 weeks

Intervention	participants (Number)
	Complete Response	Partial Response	Stable Disease	Progressive Disease
Phase II	0	1	5	22

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Optimal Doses of Temozolomide and Bortezomib (Phase I)

The optimal biologic dose (OBD) defined as the dose that achieves the greatest degree of inhibition of NF-κB activation in peripheral blood mononuclear cells when co-administered with Temozolomide (NCT00512798)
Timeframe: up to 42 days

Intervention	mg/m2 (Number)
	bortezomib	temozolomide
Phase I	1.3	75

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Patients With Clinical Anti-tumor Activity (Phase I)

Per RECIST criteria v. 1.0: measurable lesions: complete response (CR) disappearance of target lesions, partial response (PR) > 30% decrease in the sum of the longest diameter (LD) of target lesions, progressive disease (PD) > 20% increase in the sum of the LD of target lesions or appearance of new lesions, stable disease (SD) neither sufficient decrease nor increase of the sum of smallest sum of the LD of target lesions (NCT00512798)
Timeframe: every 9 weeks up to a maximum of 54 weeks

Intervention	participants (Number)
	Complete Response	Partial Response	Stable Disease	Progressive Disease
Phase I	0	4	1	14

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Overall Survival

time from day of registration until day of death. (NCT00520767)
Timeframe: time from day of registration until 72 months.

Intervention	month (Median)
Melphalan, Dexamethasone, Bortezomib,	31.1

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Time to Treatment Failure (TTF)

Time from start of treatment until date of documented disease progression, removal from protocol due to toxicity, or death from any cause. (NCT00520767)
Timeframe: start of treatment until 72 months

Intervention	month (Median)
Melphalan, Dexamethasone, Bortezomib,	18.1

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Complete Hematologic Response

(NCT00520767)
Timeframe: Up to 12 months

Intervention	participants (Number)
Melphalan, Dexamethasone, Bortezomib,	16

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Progression-free Survival (PFS)

"Progression-free survival was defined as the time from randomization to the earliest documentation of disease progression (PD) or death. If a patient died without evidence of PD, the patient was considered an event if death occurred within 3 months of the last disease assessment. Patients who died outside of the specified interval or patients who were alive without evidence of PD were censored at the date of last disease assessment.~The PFS results are based on data as of August 2012, while overall survival (OS) was updated in April 2014. Given the early termination and limited sample size, data management efforts to update PFS were not pursued." (NCT00522392)
Timeframe: Assessed every 3 months if patient is < 2 years from study entry, every 6 months if patient is 2-5 years from study entry, every 12 months if patient is 6-10 years from study entry, up to 10 years

Intervention	Months (Median)
Arm A (VRD)	NA
Arm B (VD)	17.4

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Response Rates (Complete Response [CR] or Very Good Partial Response [VGPR])

"CR:~Patients with complete disappearance of an M-protein and no evidence of myeloma in the bone marrow are considered to have CR. To be considered CR, patients must meet all of the following criteria:~Negative immunofixation on the serum and urine at two consecutive times~Disappearance of any soft tissue plasmacytomas~≤5% plasma cells in bone marrow~If serum and urine M protein are unmeasurable and the immunoglobulin free light chain (FLC) parameter is being used, patients must have a normal ratio of 0.26-1.65 at two consecutive times~VGPR:~Serum and urine M-component detectable by immunofixation but not on electrophoresis OR~>=90% reduction in serum M-component plus urine M-component <100 mg per 24 hours (by SPEP and UPEP)~If the serum and urine M protein are unmeasurable and the immunoglobulin FLC parameter is being used, a >90% decrease in the difference between involved and uninvolved FLC levels is required in place of the M protein criteria" (NCT00522392)
Timeframe: Assessed at the end of each cycle, every 3 months if patient is < 2 years from study entry, every 6 months if patient is 2-5 years from study entry, every 12 months if patient is 6-10 years from study entry, up to 10 years

Intervention	Proportion of patients (Number)
Arm A (VRD)	0.625
Arm B (VD)	0.188

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Change in Quality of Life (QOL) From Baseline to 6 Months Post Consolidation as Assessed by the Functional Assessment of Cancer Therapy-Neurotoxicity Trial Outcome Index (FACT-Ntx TOI)

The combined score on the FACT-Ntx TOI is of interest. The FACT-Ntx TOI has 25 items and the score ranges from 0 (worst possible quality of life) -100 (best possible quality of life). The primary QOL endpoint is defined as the change in the FACT-Ntx TOI score from registration to 6 months post consolidation treatment. (NCT00522392)
Timeframe: Baseline and 6 months post consolidation treatment

Intervention	units on a scale (Mean)
Arm A (VRD)	-7.9
Arm B (VD)	-2.6

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Overall Survival (OS)

Overall survival is defined as the time from randomization to death or date of last known alive. The OS results are based on data as of April 2014. (NCT00522392)
Timeframe: Assessed every 3 months if patient is < 2 years from study entry, every 6 months if patient is 2-5 years from study entry, every 12 months if patient is 6-10 years from study entry, up to 10 years

Intervention	Months (Median)
Arm A (VRD)	64.0
Arm B (VD)	NA

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Time to Disease Progression

(NCT00523848)
Timeframe: Every 3 monthsntil the date of first documented progression or date of death from any cause, whichever came first

Intervention	months (Median)
VDT: VELCADE, Doxil and Low-dose Thalidomide	27.8

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Overall Response Rate (Complete and Partial)

(NCT00523848)
Timeframe: Every 3 months

Intervention	percentage of participants (Number)
VDT: VELCADE, Doxil and Low-dose Thalidomide	77.50

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Complete Response Rate

(NCT00523848)
Timeframe: Every 3 months

Intervention	percentage of participants (Number)
VDT: VELCADE, Doxil and Low-dose Thalidomide	22.50

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Percent of Participants Achieving Overall Combined Complete Response (CR) Following High-dose Chemotherapy (HDT)/Stem Cell Transplantation (SCT)

"Percent of Participants Achieving Overall Combined Complete Response (CR) (CR w/normalized serum κ:λ ratio + CR + Near Complete Response (nCR)) following stem cell transplantation.~CR criteria: negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas and <5% plasma cells in bone marrow.~κ:λ ratio: normal free light chain (FLC) ratio~nCR criteria: positive immunofixation analysis of serum or urine as the only evidence of disease; disappearance of any soft tissue plasmacytomas and <5% plasma cells in bone marrow." (NCT00531453)
Timeframe: all data included in clinical database as of 10 April 2009

Intervention	percentage of participants (Number)
Three Drug Regimen (VDT)	76
Four Drug Regimen (VDTC)	78

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Percent of Particpants Achieving Overall Combined Complete Response (CR) Following Induction

"Percent of Particpants Achieving Overall combined complete response (CR w/normalized serum κ:λ ratio + CR + near complete response (nCR)) following induction therapy.~CR criteria: negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas and <5% plasma cells in bone marrow.~κ:λ ratio: normal free light chain (FLC) ratio~nCR criteria: positive immunofixation analysis of serum or urine as the only evidence of disease; disappearance of any soft tissue plasmacytomas and <5% plasma cells in bone marrow." (NCT00531453)
Timeframe: all data included in clinical database as of 10 April 2009

Intervention	percentage of participants (Number)
Three Drug Regimen (VDT)	51
Four Drug Regimen (VDTC)	44

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Objective Response Rate (ORR), the Percentage of Patients Who Experience an Objective Benefit From Treatment

The percentage of patients who experience an objective benefit from treatment, determined by the treating physician after reviewing key laboratory values from blood and urine. (NCT00536575)
Timeframe: 24 months

Intervention	percentage of participants (Number)
Sorafenib/Bortezomib	15

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Toxicity of Drug Combination in the Subjects

(NCT00547534)
Timeframe: Two years

Intervention	Lymphoma Subjects (Number)
Lymphoma Subjects	13

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Overall Response Rate (ORR)

Overall response rate (ORR)to protocol treatment - Partial response, Complete response, etc. (NCT00547534)
Timeframe: Two years

Intervention	Lymphoma Subjects (Number)
Lymphoma Subjects	13

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Number of Participants With Progression Free Survival at 2 Years

To determine the progression-free survival following treatment with the BVR combination in patients with relapsed or refractory indolent and mantle cell non-Hodgkin lymphoma. (NCT00547534)
Timeframe: Two years

Intervention	Participants (Number)
Lymphoma Subjects	13

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Overall Survival

(NCT00548717)
Timeframe: 1 year

Intervention	percentage of participants (Number)
Siro/MMF	39
Siro/MMF/Bort	0

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Incidence of 100 Day Mortality

(NCT00548717)
Timeframe: 100 days

Intervention	percentage of participants (Number)
Siro/MMF	31
Siro/MMF/Bort	0

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To Determine the Rate of Grade II-IV Acute GVHD When Sirolimus and Mycophenolate Mofetil or Sirolimus, Mycophenolate Mofetil and Bortezomib is Used for GVHD Prophylaxis After Allogeneic Stem Cell Transplantation in Patients With Hematologic Malignancies

(NCT00548717)
Timeframe: 150 days

Intervention	percentage of participants (Number)
Siro/MMF	77
Siro/MMF/Bort	100

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The Rate of Renal Insufficiency

"Renal function will be measured weekly after transplant for 4 weeks, at 8 weeks and then at 3 month intervals from transplantation. Sentinel renal events such as the occurrence of thrombotic microangiopathy will be noted.~The rationale for the substitution of mycophenolate mofetil for tacrolimus is to continue to prevent acute GVHD, but minimize renal toxicity after transplantation. We will thus monitor renal toxicity closely in this study. In our previous experience, the rate of grade III-V renal toxicity by day 100 after transplantation was about 10%. Here, grade III is defined as a creatinine level between 3.1 to 6 times the normal level, grade IV is defined as a creatinine level 6 times or more the normal level, and grade V is defined as a fatality due to renal toxicity." (NCT00548717)
Timeframe: 1 year

Intervention	participants (Number)
Siro/MMF	1
Siro/MMF/Bort	0

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Incidence of Chronic GVHD

"Chronic GVHD will be graded according to the modified Seattle criteria. Chronic GVHD divided into limited and extensive and evaluated across the following systems: skin, cutaneous structures, liver, mouth, eyes, esophagus, intestines, lung, musculoskeletal, serous, nervous, urologic, vagina, hematopoietic, and immune.~Localized skin involvement with or without hepatic dysfunction is classified as limited disease.~Generalized skin involvement or limited disease plus eye involvement, oral involvement, hepatic dysfunction with abnormal liver histology, or involvement of any other target organ was classified as extensive disease.~Lee SJ, Vogelsang G, Flowers ME. Chronic graft-versus-host disease. Biol Blood Marrow Transplant.~2003;9:215-33." (NCT00548717)
Timeframe: 1 year

Intervention	percentage of participants (Number)
Siro /MMF	15
Siro/MMF/Bort	50

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Donor Stem Cell Engraftment, Including Donor-host Hematopoietic Chimerism Studies Post Transplant

Engraftment of donor cells by week 4 after transplantation. Assessment of donor stem cell engraftment will include donor-host hematopoietic chimerism analyses at 4 weeks and every 3 months after transplantation. Chimerism measured from peripheral blood or from bone marrow. (NCT00548717)
Timeframe: 30 days

Intervention	participants (Number)
Siro/MMF	9
Siro/MMF/Bort	2

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To Correlate the Serum Concentrations of Mycophenolate Mofetil and Its Metabolites With Acute GVHD Incidence

This outcome measure was presented as a comparison between incidence of Grade 0-I aGVHD and Grade II-IV aGVHD across 5 time points (Weeks 1,2,3,8, and 12). (NCT00548717)
Timeframe: 1 year

Intervention	ng/mL (Mean)
	Week 1 MMF level (0-I aGVHD), n=3	Week 1 MMF level (II-IV aGVHD), n=8	Week 2 MMF level (0-I aGVHD), n=3	Week 2 MMF level (II-IV aGVHD), n=6	Week 3 MMF level (0-I aGVHD), n=3	Week 3 MMF level (II-IV aGVHD), n=6	Week 8 MMF level (0-I aGVHD), n=3	Week 8 MMF level (II-IV aGVHD), n=4	Week 12 MMF level (0-I aGVHD), n=2	Week 12 MMF level (II-IV aGVHD), n=4
Siro/MMF	2.43	2.70	3.40	3.07	2.57	2.85	2.37	2.13	1.75	2.20

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Number of Participants With an Overall Response Defined as Complete Response and Partial Response

"Response is assessed by investigator according to International Working Group (IWG) criteria.~A complete response requires disappearance of all evidence of disease. A partial response is a >/= 50% decrease in the sum of products of 6 largest dominant nodes or nodal masses as well as for splenic and hepatic nodules. No increase in size of nodes, liver or spleen and no new sites of disease." (NCT00553644)
Timeframe: Duration of treatment (assessed up to 6 years)

Intervention	participants (Number)
Treatment (Antiangiogenesis Therapy, Enzyme Inhibitor Therapy)	21

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Overall Survival

Overall survival (OS) is defined as the time from study entry until death. The median OS with 95% CI was estimated using the Kaplan-Meier method.. (NCT00553644)
Timeframe: Assessed up to 6 years

Intervention	years (Median)
Treatment (Antiangiogenesis Therapy, Enzyme Inhibitor Therapy)	2.17

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Incidence of Adverse Events

Number of participants who experienced a maximum grade 3, 4 or 5 adverse event. The grading scales found in the revised NCI CTCAE version 4.0 was utilized for adverse event reporting (NCT00553644)
Timeframe: Duration of Treatment (up to 6 years)

Intervention	participants (Number)
	Grade 2	Grade 3	Grade 4	Grade 5
Treatment (Antiangiogenesis Therapy, Enzyme Inhibitor Therapy)	4	29	17	1

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Time to Progression

Time to progression (TTP) is defined as the time from study entry until progression or death due to any cause. The median TTP with 95% CI was estimated using the Kaplan-Meier method. (NCT00553644)
Timeframe: Assessed up to 6 years

Intervention	years (Median)
Treatment (Antiangiogenesis Therapy, Enzyme Inhibitor Therapy)	0.58

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Recommended Phase II Dose (RP2D) of PD-0332991: Phase 1

RP2D was determined based on the MTD, safety and tolerability profile of the study treatment. (NCT00555906)
Timeframe: Day 1 up to Day 28 during Cycle 1 in schedule A, Day 1 up to Day 21 during Cycle 1 in schedule B

Intervention	milligram (mg) (Number)
Palbociclib + Bortezomib + Dexamethasone (Phase1:Schedule A)	NA
Palbociclib + Bortezomib + Dexamethasone (Phase1:ScheduleB)	100

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Progression-free Survival (PFS): Phase 2

"PFS was the time from start of study treatment to date progressive disease was documented or death due to any cause, whichever occurred first. PFS was calculated as (first event date minus the date of first dose of study medication plus 1) divided by 30.44. Tumor progression was determined from oncologic assessment data (where data meet the criteria for progressive disease [PD]), or from adverse event (AE) data (where the outcome was Death). PD: >=25% increase from lowest response level in serum M-component or urine M-component, >=10% bone marrow plasma cell percentage, definite development of new bone lesions/soft tissue plasmacytomas/definite increase in size of existing bone lesions/soft tissue plasmacytomas, development of hypercalcemia, attributed solely to plasma cell proliferative disorder." (NCT00555906)
Timeframe: Cycle 1 Day 1 (baseline) up to 28 days after last dose of palbociclib

Intervention	months (Median)
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase2:Schedule B)	3.9

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Percentage of Participants With Objective Response (OR): Phase 2

OR: confirmed stringent complete response(sCR),complete response(CR),very good partial response(VGPR) or partial response(PR) as per International Myeloma Working Group Uniform Response Criteria (IMWGURC). sCR: normal serum free light chain (FLC) ratio, absence of clonal cells in bone marrow. CR: disappearance of any soft tissue plasmacytomas, <5 percent (%) plasma cells in bone marrow, negative immunofixation on serum, urine. VGPR: serum, urine M-protein detectable by immunofixation but not on electrophoresis, >= 90% reduction in serum M-protein, <100 mg/24 hour (hr) urine M-protein. PR: >=50% reduction in serum M-protein, reduction in 24-hr urinary M-protein by >=90% or to <200 mg/24 hr, >=50% decrease in difference between involved and uninvolved FLC levels if serum, urine M-protein were unmeasurable, >= 50% reduction in plasma cells, provided baseline bone marrow plasma cell was >=30% if serum, urine M-protein were unmeasurable and serum free light assay was unmeasureable. (NCT00555906)
Timeframe: Cycle 1 Day 1 (baseline) up to end of study (up to cycle 22 for schedule B)

Intervention	percentage of participants (Number)
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase2:ScheduleB)	20

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Overall Survival (OS): Phase 2

OS was defined as the time from first dose of study medication to first documentation of death due to any cause. OS was calculated as (the death date or last known alive date [if death date unavailable] minus the date of first dose of study medication plus 1) divided by 30.44. (NCT00555906)
Timeframe: Cycle 1 Day 1 (baseline) up to end of study (up to Cycle 22 for schedule B), thereafter every 3 months until 1 year after the last dose of palbociclib

Intervention	months (Median)
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase2:Schedule B)	21.1

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Number of Participants With Laboratory Abnormalities: Phase 2

Laboratory parameters included hematology (hemoglobin, platelets, leukocytes, total neutrophils, eosinophils, basophils, lymphocytes, monocytes); liver function (total bilirubin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, albumin, total protein); renal function (creatinine, blood urea nitrogen, uric acid); electrolytes (sodium, potassium, chloride, bicarbonate, calcium, magnesium and phosphate); urinalysis (protein and immunology [C reactive protein]), and clinical chemistry (glucose). Total number of participants with laboratory abnormalities was reported. (NCT00555906)
Timeframe: Cycle 1 Day 1 (baseline) up to 28 days after last dose of palbociclib

Intervention	participants (Number)
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase2:Schedule B)	30

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Maximum Tolerated Dose (MTD) of PD-0332991: Phase 1

MTD=highest dose level for which no more than 1 out of 6 participants experienced dose-limiting toxicity (DLT). DLT=any of the following treatment-related events: Absolute neutrophil count (ANC) less than (<)1000/microliter (mcL) (Grade 3 neutropenia) associated with documented infection/fever >=38.5degrees Celsius (C); Grade >=3 nonhematologic treatment-related toxicity, except those that were not maximally treated or considered tolerable, Grade 3 corrected QT interval (QTc) prolongation (QTc >500 millisecond [msec]) in asymptomatic participants even after repeat testing to exclude confounding factors and correction of reversible causes; Delay in the administration of Cycle 2 for more than 1 week of the planned date due to platelet count <25,000/mcL and/or ANC <500/mcL, or due to prolonged nonhematologic toxicities of Grade >=3; Inability to deliver at least 80 percent (%) of the planned PD 0332991 or bortezomib doses during Cycle 1 due to toxicity. (NCT00555906)
Timeframe: Day 1 up to Day 28 during Cycle 1 in schedule A, Day 1 up to Day 21 during Cycle 1 in schedule B

Intervention	milligram (mg) (Number)
Palbociclib + Bortezomib + Dexamethasone (Phase1:Schedule A)	NA
Palbociclib + Bortezomib + Dexamethasone (Phase1:ScheduleB)	100

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Duration of Objective Response (DR): Phase 2

DR was defined as time from first documentation of objective tumor response (sCR, CR, VGPR or PR) that was subsequently confirmed to first documentation of objective tumor progression or death due to any cause since treatment started. sCR: normal FLC ratio, absence of clonal cells in bone marrow. CR: disappearance of any soft tissue plasmacytomas, <5% plasma cells in bone marrow, negative immunofixation on serum, urine. VGPR: serum, urine M-protein detectable by immunofixation but not on electrophoresis, >=90% reduction in serum M-protein, <100 mg/24hr urine M-protein. PR:>=50% reduction in serum M-protein, reduction in 24-hr urinary M-protein by >=90% or to <200 mg/24 hr. PD: >=25% increase from lowest response level in serum M-component, urine M-component, >=10% bone marrow plasma cell percentage, development of new bone lesions/soft tissue plasmacytomas/increase in size of existing bone lesions, development of hypercalcemia, attributed solely to plasma cell proliferative disorder. (NCT00555906)
Timeframe: Cycle 1 Day 1 (baseline) up to 28 days after last dose of palbociclib

Intervention	months (Median)
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase2:Schedule B)	4.63

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Quality of Life Questionnaire Multiple Myeloma Module (QLQ-MY20): Phase 2

The QLQ-MY20 consisted of 20 items addressing 4 domains of health-related quality of life (HRQoL) important to participants with multiple myeloma: future perspective (2 items), pain/disease symptoms (6 items), social support /body image (2 items), and treatment side-effects (10 items). All items used 4 point scale (1 'Not at all' to 4 'Very much'). Scores for HRQoL domains were calculated as an average of the individual items, transformed to 0 to 100 range. Higher scores on symptom scales (disease symptoms and side effects of treatment) indicated a higher level of symptoms/problems. Higher scores on functional scales (future perspective and body image) indicated a higher level of QoL/functioning. (NCT00555906)
Timeframe: C1D1 (baseline), C1D8, C1D15, C2D1, C3D1, C4D1, C5D1, C6D1, C7D1, C8D1, C9D1, C10D1, C11D1, C12D1, C13D1, C14D1, C15D1, C16D1, C17D1, C18D1, C19D1, C20D1, C21D1, C22D1, End of Treatment (assessment at early withdrawal occurring up to Cycle 22)

Intervention	units on a scale (Mean)
	C1D1: Disease Symptoms (n=27)	C1D1: Side Effects of Treatment (n=27)	C1D1: Future Perspective (n=27)	C1D1: Body Image (n=27)	C1D8: Disease Symptoms (n=25)	C1D8: Side Effects of Treatment (n=25)	C1D8: Future Perspective (n=25)	C1D8: Body Image (n=25)	C1D15: Disease Symptoms (n=25)	C1D15: Side Effects of Treatment (n=25)	C1D15: Future Perspective (n=25)	C1D15: Body Image (n=25)	C2D1: Disease Symptoms (n=25)	C2D1: Side Effects of Treatment (n=25)	C2D1: Future Perspective (n=25)	C2D1: Body Image (n=25)	C3D1: Disease Symptoms (n=21)	C3D1: Side Effects of Treatment (n=21)	C3D1: Future Perspective (n=21)	C3D1: Body Image (n=21)	C4D1: Disease Symptoms (n=18)	C4D1: Side Effects of Treatment (n=18)	C4D1: Future Perspective (n=18)	C4D1: Body Image (n=18)	C5D1: Disease Symptoms (n=17)	C5D1: Side Effects of Treatment (n=17)	C5D1: Future Perspective (n=17)	C5D1: Body Image (n=17)	C6D1: Disease Symptoms (n=15)	C6D1: Side Effects of Treatment (n=15)	C6D1: Future Perspective (n=15)	C6D1: Body Image (n=15)	C7D1: Disease Symptoms (n=11)	C7D1: Side Effects of Treatment (n=11)	C7D1: Future Perspective (n=11)	C7D1: Body Image (n=11)	C8D1: Disease Symptoms (n=10)	C8D1: Side Effects of Treatment (n=10)	C8D1: Future Perspective (n=10)	C8D1: Body Image (n=10)	C9D1: Disease Symptoms (n=9)	C9D1: Side Effects of Treatment (n=9)	C9D1: Future Perspective (n=9)	C9D1: Body Image (n=9)	C10D1: Disease Symptoms (n=6)	C10D1: Side Effects of Treatment (n=6)	C10D1: Future Perspective (n=6)	C10D1: Body Image (n=6)	C11D1: Disease Symptoms (n=6)	C11D1: Side Effects of Treatment (n=6)	C11D1: Future Perspective (n=6)	C11D1: Body Image (n=6)	C12D1: Disease Symptoms (n=5)	C12D1: Side Effects of Treatment (n=5)	C12D1: Future Perspective (n=5)	C12D1: Body Image (n=5)	C13D1: Disease Symptoms (n=6)	C13D1: Side Effects of Treatment (n=6)	C13D1: Future Perspective (n=6)	C13D1: Body Image (n=6)	C14D1: Disease Symptoms (n=6)	C14D1: Side Effects of Treatment (n=6)	C14D1: Future Perspective (n=6)	C14D1: Body Image (n=6)	C15D1: Disease Symptoms (n=6)	C15D1: Side Effects of Treatment (n=6)	C15D1: Future Perspective (n=6)	C15D1: Body Image (n=6)	C16D1: Disease Symptoms (n=6)	C16D1: Side Effects of Treatment (n=6)	C16D1: Future Perspective (n=6)	C16D1: Body Image (n=6)	C17D1: Disease Symptoms (n=6)	C17D1: Side Effects of Treatment (n=6)	C17D1: Future Perspective (n=6)	C17D1: Body Image (n=6)	C18D1: Disease Symptoms (n=6)	C18D1: Side Effects of Treatment (n=6)	C18D1: Future Perspective (n=6)	C18D1: Body Image (n=6)	C19D1: Disease Symptoms (n=4)	C19D1: Side Effects of Treatment (n=4)	C19D1: Future Perspective (n=4)	C19D1: Body Image (n=4)	C20D1: Disease Symptoms (n=2)	C20D1: Side Effects of Treatment (n=2)	C20D1: Future Perspective (n=2)	C20D1: Body Image (n=2)	C21D1: Disease Symptoms (n=1)	C21D1: Side Effects of Treatment (n=1)	C21D1: Future Perspective (n=1)	C21D1: Body Image (n=1)	C22D1: Disease Symptoms (n=1)	C22D1: Side Effects of Treatment (n=1)	C22D1: Future Perspective (n=1)	C22D1: Body Image (n=1)	End of Treatment: Disease Symptoms (n=17)	End of Treatment: Side Effects of Treatment (n=17)	End of Treatment: Future Perspective (n=17)	End of Treatment: Body Image (n=17)
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase2:Schedule B)	35.68	25.61	46.50	24.69	35.51	23.90	44.44	13.33	32.31	26.89	48.89	28.00	29.82	24.73	46.22	17.33	25.13	25.01	44.44	20.63	28.71	26.64	44.45	25.93	27.78	27.52	45.75	25.49	24.08	25.04	40.74	20.00	25.96	26.77	44.44	30.30	18.56	26.41	35.56	30.00	19.14	19.75	39.51	25.93	25.93	18.83	33.33	16.67	18.52	18.52	38.89	22.22	28.89	24.30	53.33	40.00	25.00	18.70	37.04	33.33	19.45	18.64	35.19	16.67	23.15	18.09	38.89	16.67	27.78	16.91	37.04	22.22	24.07	19.26	38.89	22.22	41.85	18.52	38.89	33.33	43.06	25.74	38.89	41.67	44.45	35.19	66.67	50.00	77.78	36.67	44.44	33.33	61.11	33.33	44.44	66.67	37.58	29.51	46.41	29.41

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Modified Version of Brief Pain Inventory - Short Form (m-BPI-sf) Questionnaire: Phase 2

"m-BPI-sf was a questionnaire designed to assess the severity of pain and the impact of pain on daily functions. m-BPI-sf contained questions that assessed pain severity (worst, least, average, right now) and pain interference (general activity, mood, walking ability, normal work, relations with other people, sleep, and enjoyment of life). Each question was answered on a scale ranging from 0 No pain to 10 Pain as bad as you can imagine. The 4 pain severity questions were averaged to derive an index of pain severity and the 7 function questions were averaged to derive an index for pain interference. Total score range for pain severity and interference indices: 0 to 10, where higher score indicated higher severity/interference." (NCT00555906)
Timeframe: C1D1 (baseline), C1D8, C1D15, C2D1, C3D1, C4D1, C5D1, C6D1, C7D1, C8D1, C9D1, C10D1, C11D1, C12D1, C13D1, C14D1, C15D1, C16D1, C17D1, C18D1, C19D1, C20D1, C21D1, C22D1, End of Treatment (assessment at early withdrawal occurring up to Cycle 22)

Intervention	units on a scale (Mean)
	C1D1: Pain Severity (n=26)	C1D8: Pain Severity (n=25)	C1D15: Pain Severity (n=24)	C2D1: Pain Severity (n=24)	C3D1: Pain Severity (n=21)	C4D1: Pain Severity (n=17)	C5D1: Pain Severity (n=16)	C6D1: Pain Severity (n=14)	C7D1: Pain Severity (n=10)	C8D1: Pain Severity (n=9)	C9D1: Pain Severity (n=9)	C10D1: Pain Severity (n=6)	C11D1: Pain Severity (n=5)	C12D1: Pain Severity (n=5)	C13D1: Pain Severity (n=6)	C14D1: Pain Severity (n=6)	C15D1: Pain Severity (n=6)	C16D1: Pain Severity (n=6)	C17D1: Pain Severity (n=6)	C18D1: Pain Severity (n=6)	C19D1: Pain Severity (n=4)	C20D1: Pain Severity (n=2)	C21D1: Pain Severity (n=1)	C22D1: Pain Severity (n=1)	End of Treatment: Pain Severity (n=16)	C1D1: Pain Interference (n=25)	C1D8: Pain Interference (n=25)	C1D15: Pain Interference (n=23)	C2D1: Pain Interference (n=23)	C3D1: Pain Interference (n=21)	C4D1: Pain Interference (n=17)	C5D1: Pain Interference (n=16)	C6D1: Pain Interference (n=14)	C7D1: Pain Interference (n=10)	C8D1: Pain Interference (n=9)	C9D1: Pain Interference (n=9)	C10D1: Pain Interference (n=6)	C11D1: Pain Interference (n=5)	C12D1: Pain Interference (n=5)	C13D1: Pain Interference (n=6)	C14D1: Pain Interference (n=6)	C15D1: Pain Interference (n=6)	C16D1: Pain Interference (n=6)	C17D1: Pain Interference (n=6)	C18D1: Pain Interference (n=6)	C19D1: Pain Interference (n=4)	C20D1: Pain Interference (n=2)	C21D1: Pain Interference (n=1)	C22D1: Pain Interference (n=1)	End of Treatment: Pain Interference (n=16)
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase2:Schedule B)	2.32	2.62	2.44	2.30	2.12	2.02	2.22	1.66	1.98	2.47	1.81	1.08	1.45	1.67	0.93	1.42	1.04	1.46	1.67	2.88	3.69	3.50	4.00	4.50	3.30	2.53	2.58	3.06	2.64	2.34	2.54	2.74	2.26	2.94	2.60	2.13	2.07	2.40	2.91	1.90	0.98	1.31	1.83	1.50	2.86	4.07	5.07	2.57	6.71	3.46

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Number of Participants With Adverse Events (AEs) by Severity: Phase 2

An AE was any untoward medical occurrence attributed to study medication in a participant who received study medication. A serious AE (SAE) was an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly. Adverse events were graded according to the common terminology criteria for adverse events (CTCAE) criteria as 1=mild AE, 2=moderate AE, 3=severe AE, 4=life-threatening or disabling AE, 5=Death related to AE. The most severe grade was used in case of multiple occurrences of the same event. (NCT00555906)
Timeframe: Cycle 1 Day 1 (baseline) up to 28 days after last dose of palbociclib

Intervention	participants (Number)
	Grade 2	Grade 3	Grade 4	Grade 5
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase2:Schedule B)	2	9	18	1

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Number of Participants With Treatment-Emergent Adverse Events (TEAEs) by Relationship to Study Medication: Phase 2

An AE was any untoward medical occurrence attributed to study medication in a participant who received study medication. An SAE was an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly. Treatment-emergent are events between first dose of study medication until 28 days after the last dose of study medication that were absent before treatment or that worsened relative to pretreatment state. All causality AEs included SAEs as well as non-serious AEs, without regard to relationship to the study medication, which occurred during the trial. Treatment-related were adverse events (serious as well as non-serious adverse events) considered related to study medication by the investigator. Number of participants with treatment related TEAEs and all causality TEAEs were summarized. (NCT00555906)
Timeframe: Cycle 1 Day 1 (baseline) up to 28 days after last dose of palbociclib

Intervention	participants (Number)
	All Causality	Treatment Related
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase2:Schedule B)	30	27

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European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (EORTC QLQ-C30): Phase 2

EORTC QLQ-C30: included functional scales (physical, role, cognitive, emotional, and social), global health status, symptom scales (fatigue, pain, nausea/vomiting) and single items (dyspnea, appetite loss, insomnia, constipation, diarrhea and financial difficulties). Most questions used 4 point scale (1 'Not at all' to 4 'Very much'); 2 questions used 7-point scale (1 'very poor' to 7 'Excellent'). Scores for functional scales, global health status and symptom scales were calculated as an average of individual items, transformed to 0-100 scale; higher score=better level of functioning, health status or greater degree of symptoms. Score of the single items were transformed to 0-100 scale; higher score=greater degree of symptom/difficulty. (NCT00555906)
Timeframe: C1D1 (baseline), C1D8, C1D15, C2D1, C3D1, C4D1, C5D1, C6D1, C7D1, C8D1, C9D1, C10D1, C11D1, C12D1, C13D1, C14D1, C15D1, C16D1, C17D1, C18D1, C19D1, C20D1, C21D1, C22D1, End of Treatment (assessment at early withdrawal occurring up to Cycle 22)

Intervention	units on a scale (Mean)
	C1D1: Global Health Status (n=27)	C1D1: Physical Functioning (n=27)	C1D1: Role Functioning (n=27)	C1D1: Emotional Functioning (n=27)	C1D1: Cognitive Functioning (n=27)	C1D1: Social Functioning (n=27)	C1D1: Fatigue (n=27)	C1D1: Nausea and Vomiting (n=27)	C1D1: Pain (n=27)	C1D1: Dyspnea (n=27)	C1D1: Insomnia (n=27)	C1D1: Appetite Loss (n=27)	C1D1: Constipation (n=27)	C1D1: Diarrhea (n=27)	C1D1: Financial Problems (n=26)	C1D8: Global Health Status (n=26)	C1D8: Physical Functioning (n=26)	C1D8: Role Functioning (n=26)	C1D8: Emotional Functioning (n=26)	C1D8: Cognitive Functioning (n=26)	C1D8: Social Functioning (n=26)	C1D8: Fatigue (n=26)	C1D8: Nausea and Vomiting (n=26)	C1D8: Pain (n=26)	C1D8: Dyspnea (n=26)	C1D8: Insomnia (n=26)	C1D8: Appetite Loss (n=26)	C1D8: Constipation (n=26)	C1D8: Diarrhea (n=26)	C1D8: Financial Problems	C1D15: Global Health Status	C1D15: Physical Functioning (n=25)	C1D15: Role Functioning (n=25)	C1D15: Emotional Functioning (n=25)	C1D15: Cognitive Functioning (n=25)	C1D15: Social Functioning (n=25)	C1D15: Fatigue (n=25)	C1D15: Nausea and Vomiting (n=25)	C1D15: Pain (n=25)	C1D15: Dyspnea (n=25)	C1D15: Insomnia (n=25)	C1D15: Appetite Loss (n=25)	C1D15: Constipation (n=25)	C1D15: Diarrhea (n=25)	C1D15: Financial Problems (n=25)	C2D1: Global Health Status (n=25)	C2D1: Physical Functioning (n=25)	C2D1: Role Functioning (n=25)	C2D1: Emotional Functioning (n=25)	C2D1: Cognitive Functioning (n=25)	C2D1: Social Functioning (n=25)	C2D1: Fatigue (n=25)	C2D1: Nausea and Vomiting (n=25)	C2D1: Pain (n=25)	C2D1: Dyspnea (n=25)	C2D1: Insomnia (n=25)	C2D1: Appetite Loss (n=25)	C2D1: Constipation (n=25)	C2D1: Diarrhea (n=25)	C2D1: Financial Problems (n=25)	C3D1: Global Health Status (n=25)	C3D1: Physical Functioning (n=25)	C3D1: Role Functioning (n=22)	C3D1: Emotional Functioning (n=22)	C3D1: Cognitive Functioning (n=22)	C3D1: Social Functioning (n=22)	C3D1: Fatigue (n=22)	C3D1: Nausea and Vomiting (n=22)	C3D1: Pain (n=22)	C3D1: Dyspnea (n=22)	C3D1: Insomnia (n=22)	C3D1: Appetite Loss (n=22)	C3D1: Constipation (n=22)	C3D1: Diarrhea (n=22)	C3D1: Financial Problems (n=22)	C4D1: Global Health Status (n=18)	C4D1: Physical Functioning (n=18)	C4D1: Role Functioning (n=18)	C4D1: Emotional Functioning (n=18)	C4D1: Cognitive Functioning (n=18)	C4D1: Social Functioning (n=18)	C4D1: Fatigue (n=18)	C4D1: Nausea and Vomiting (n=18)	C4D1: Pain (n=18)	C4D1: Dyspnea (n=18)	C4D1: Insomnia (n=18)	C4D1: Appetite Loss (n=18)	C4D1: Constipation (n=18)	C4D1: Diarrhea (n=18)	C4D1: Financial Problems (n=18)	C5D1:Global Health Status (n=17)	C5D1: Physical Functioning (n=17)	C5D1: Role Functioning (n=17)	C5D1: Emotional Functioning (n=17)	C5D1: Cognitive Functioning (n=17)	C5D1: Social Functioning (n=17)	C5D1: Fatigue (n=17)	C5D1: Nausea and Vomiting (n=17)	C5D1: Pain (n=17)	C5D1: Dyspnea (n=17)	C5D1: Insomnia (n=17)	C5D1: Appetite Loss (n=17)	C5D1: Constipation (n=17)	C5D1: Diarrhea (n=17)	C5D1: Financial Problems (n=17)	C6D1: Global Health Status (n=15)	C6D1: Physical Functioning (n=15)	C6D1: Role Functioning (n=15)	C6D1: Emotional Functioning (n=15)	C6D1: Cognitive Functioning (n=15)	C6D1: Social Functioning (n=15)	C6D1: Fatigue (n=15)	C6D1: Nausea and Vomiting (n=15)	C6D1: Pain (n=15)	C6D1: Dyspnea (n=15)	C6D1: Insomnia (n=15)	C6D1: Appetite Loss (n=15)	C6D1: Constipation (n=15)	C6D1: Diarrhea (n=15)	C6D1: Financial Problems (n=15)	C7D1: Global Health Status (n=11)	C7D1: Physical Functioning (n=11)	C7D1: Role Functioning (n=11)	C7D1: Emotional Functioning (n=11)	C7D1: Cognitive Functioning (n=11)	C7D1: Social Functioning (n=11)	C7D1: Fatigue (n=11)	C7D1: Nausea and Vomiting (n=11)	C7D1: Pain (n=11)	C7D1: Dyspnea (n=11)	C7D1: Insomnia (n=11)	C7D1: Appetite Loss (n=11)	C7D1: Constipation (n=11)	C7D1: Diarrhea (n=11)	C7D1: Financial Problems (n=11)	C8D1: Global Health Status (n=10)	C8D1: Physical Functioning (n=10)	C8D1: Role Functioning (n=10)	C8D1: Emotional Functioning (n=10)	C8D1: Cognitive Functioning (n=10)	C8D1: Social Functioning (n=10)	C8D1: Fatigue (n=10)	C8D1: Nausea and Vomiting (n=10)	C8D1: Pain (n=10)	C8D1: Dyspnea (n=10)	C8D1: Insomnia (n=10)	C8D1: Appetite Loss (n=10)	C8D1: Constipation (n=10)	C8D1: Diarrhea (n=10)	C8D1: Financial Problems (n=10)	C9D1: Global Health Status (n=9)	C9D1: Physical Functioning (n=9)	C9D1: Role Functioning (n=9)	C9D1: Emotional Functioning (n=9)	C9D1: Cognitive Functioning (n=9)	C9D1: Social Functioning (n=9)	C9D1: Fatigue (n=9)	C9D1: Nausea and Vomiting (n=9)	C9D1: Pain (n=9)	C9D1: Dyspnea (n=9)	C9D1: Insomnia (n=9)	C9D1: Appetite Loss (n=9)	C9D1: Constipation (n=9)	C9D1: Diarrhea (n=9)	C9D1: Financial Problems (n=9)	C10D1: Global Health Status (n=6)	C10D1: Physical Functioning (n=6)	C10D1: Role Functioning (n=6)	C10D1: Emotional Functioning (n=6)	C10D1: Cognitive Functioning (n=6)	C10D1: Social Functioning (n=6)	C10D1: Fatigue (n=6)	C10D1: Nausea and Vomiting (n=6)	C10D1: Pain (n=6)	C10D1: Dyspnea (n=6)	C10D1: Insomnia (n=6)	C10D1: Appetite Loss (n=6)	C10D1: Constipation (n=6)	C10D1: Diarrhea (n=6)	C10D1: Financial Problems (n=6)	C11D1: Global Health Status (n=5)	C11D1: Physical Functioning (n=5)	C11D1: Role Functioning (n=5)	C11D1: Emotional Functioning (n=5)	C11D1: Cognitive Functioning (n=5)	C11D1: Social Functioning (n=5)	C11D1: Fatigue (n=5)	C11D1: Nausea and Vomiting (n=5)	C11D1: Pain (n=5)	C11D1: Dyspnea (n=5)	C11D1: Insomnia (n=5)	C11D1: Appetite Loss (n=5)	C11D1: Constipation (n=5)	C11D1: Diarrhea (n=5)	C11D1: Financial Problems (n=5)	C12D1: Global Health Status (n=15)	C12D1: Physical Functioning (n=15)	C12D1: Role Functioning (n=15)	C12D1: Emotional Functioning (n=15)	C12D1: Cognitive Functioning (n=15)	C12D1: Social Functioning (n=15)	C12D1: Fatigue (n=15)	C12D1: Nausea and Vomiting (n=15)	C12D1: Pain (n=15)	C12D1: Dyspnea (n=15)	C12D1: Insomnia (n=15)	C12D1: Appetite Loss (n=15)	C12D1: Constipation (n=15)	C12D1: Diarrhea (n=15)	C12D1: Financial Problems (n=15)	C13D1: Global Health Status (n=6)	C13D1: Physical Functioning (n=6)	C13D1: Role Functioning (n=6)	C13D1: Emotional Functioning (n=6)	C13D1: Cognitive Functioning (n=6)	C13D1: Social Functioning (n=6)	C13D1: Fatigue (n=6)	C13D1: Nausea and Vomiting (n=6)	C13D1: Pain (n=6)	C13D1: Dyspnea (n=6)	C13D1: Insomnia (n=6)	C13D1: Appetite Loss (n=6)	C13D1: Constipation (n=6)	C13D1: Diarrhea (n=6)	C13D1: Financial Problems (n=6)	C14D1: Global Health Status (n=6)	C14D1: Physical Functioning (n=6)	C14D1: Role Functioning (n=6)	C14D1: Emotional Functioning (n=6)	C14D1: Cognitive Functioning (n=6)	C14D1: Social Functioning (n=6)	C14D1: Fatigue (n=6)	C14D1: Nausea and Vomiting (n=6)	C14D1: Pain (n=6)	C14D1: Dyspnea (n=6)	C14D1: Insomnia (n=6)	C14D1: Appetite Loss (n=6)	C14D1: Constipation (n=6)	C14D1: Diarrhea (n=6)	C14D1: Financial Problems (n=6)	C15D1: Global Health Status (n=6)	C15D1: Physical Functioning (n=6)	C15D1: Role Functioning (n=6)	C15D1: Emotional Functioning (n=6)	C15D1: Cognitive Functioning (n=6)	C15D1: Social Functioning (n=6)	C15D1: Fatigue (n=6)	C15D1: Nausea and Vomiting (n=6)	C15D1: Pain (n=6)	C15D1: Dyspnea (n=6)	C15D1: Insomnia (n=6)	C15D1: Appetite Loss (n=6)	C15D1: Constipation (n=6)	C15D1: Diarrhea (n=6)	C15D1: Financial Problems (n=6)	C16D1: Global Health Status (n=6)	C16D1: Physical Functioning (n=6)	C16D1: Role Functioning (n=6)	C16D1: Emotional Functioning (n=6)	C16D1: Cognitive Functioning (n=6)	C16D1: Social Functioning (n=6)	C16D1: Fatigue (n=6)	C16D1: Nausea and Vomiting (n=6)	C16D1: Pain (n=6)	C16D1: Dyspnea (n=6)	C16D1: Insomnia (n=6)	C16D1: Appetite Loss (n=6)	C16D1: Constipation (n=6)	C16D1: Diarrhea (n=6)	C16D1: Financial Problems (n=6)	C17D1: Global Health Status (n=6)	C17D1: Physical Functioning (n=6)	C17D1: Role Functioning (n=6)	C17D1: Emotional Functioning (n=6)	C17D1: Cognitive Functioning (n=6)	C17D1: Social Functioning (n=6)	C17D1: Fatigue (n=6)	C17D1: Nausea and Vomiting (n=6)	C17D1: Pain (n=6)	C17D1: Dyspnea (n=6)	C17D1: Insomnia (n=6)	C17D1: Appetite Loss (n=6)	C17D1: Constipation (n=6)	C17D1: Diarrhea (n=6)	C17D1: Financial Problems (n=6)	C18D1: Global Health Status (n=6)	C18D1: Physical Functioning (n=6)	C18D1: Role Functioning (n=6)	C18D1: Emotional Functioning (n=6)	C18D1: Cognitive Functioning (n=6)	C18D1: Social Functioning (n=6)	C18D1: Fatigue (n=6)	C18D1: Nausea and Vomiting (n=6)	C18D1: Pain (n=6)	C18D1: Dyspnea (n=6)	C18D1: Insomnia (n=6)	C18D1: Appetite Loss (n=6)	C18D1: Constipation (n=6)	C18D1: Diarrhea (n=6)	C18D1: Financial Problems (n=6)	C19D1: Global Health Status (n=4)	C19D1: Physical Functioning (n=4)	C19D1: Role Functioning (n=4)	C19D1: Emotional Functioning (n=4)	C19D1: Cognitive Functioning (n=4)	C19D1: Social Functioning (n=4)	C19D1: Fatigue (n=4)	C19D1: Nausea and Vomiting (n=4)	C19D1: Pain (n=4)	C19D1: Dyspnea (n=4)	C19D1: Insomnia (n=4)	C19D1: Appetite Loss (n=4)	C19D1: Constipation (n=4)	C19D1: Diarrhea (n=4)	C19D1: Financial Problems (n=4)	C20D1: Global Health Status (n=2)	C20D1: Physical Functioning (n=2)	C20D1: Role Functioning (n=2)	C20D1: Emotional Functioning (n=2)	C20D1: Cognitive Functioning (n=2)	C20D1: Social Functioning (n=2)	C20D1: Fatigue (n=2)	C20D1: Nausea and Vomiting (n=2)	C20D1: Pain (n=2)	C20D1: Dyspnea (n=2)	C20D1: Insomnia (n=2)	C20D1: Appetite Loss (n=2)	C20D1: Constipation (n=2)	C20D1: Diarrhea (n=2)	C20D1: Financial Problems (n=2)	C21D1: Global Health Status (n=1)	C21D1: Physical Functioning (n=1)	C21D1: Role Functioning (n=1)	C21D1: Emotional Functioning (n=1)	C21D1: Cognitive Functioning (n=1)	C21D1: Social Functioning (n=1)	C21D1: Fatigue (n=1)	C21D1: Nausea and Vomiting (n=1)	C21D1: Pain (n=1)	C21D1: Dyspnea (n=1)	C21D1: Insomnia (n=1)	C21D1: Appetite Loss (n=1)	C21D1: Constipation (n=1)	C21D1: Diarrhea (n=1)	C21D1: Financial Problems (n=1)	C22D1: Global Health Status (n=1)	C22D1: Physical Functioning (n=1)	C22D1: Role Functioning (n=1)	C22D1: Emotional Functioning (n=1)	C22D1: Cognitive Functioning (n=1)	C22D1: Social Functioning (n=1)	C22D1: Fatigue (n=1)	C22D1: Nausea and Vomiting (n=1)	C22D1: Pain (n=1)	C22D1: Dyspnea (n=1)	C22D1: Insomnia (n=1)	C22D1: Appetite Loss (n=1)	C22D1: Constipation (n=1)	C22D1: Diarrhea (n=1)	C22D1: Financial Problems (n=1)	End of treatment: Global health status (n=17)	End of Treatment: Physical Functioning (n=17)	End of Treatment: Role Functioning (n=17)	End of Treatment: Emotional Functioning (n=17)	End of Treatment: Cognitive Functioning (n=17)	End of Treatment: Social Functioning (n=17)	End of Treatment: Fatigue (n=17)	End of Treatment: Nausea and Vomiting (n=17)	End of Treatment: Pain (n=17)	End of Treatment: Dyspnea (n=17)	End of Treatment: Insomnia (n=17)	End of Treatment: Appetite Loss (n=17)	End of Treatment: Constipation (n=17)	End of Treatment: Diarrhea (n=17)	End of Treatment: Financial Problems (n=17)
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase2:Schedule B)	60.80	64.20	59.88	70.37	72.22	69.14	29.63	6.79	35.80	32.10	43.21	20.99	27.16	11.11	33.33	60.58	67.18	59.62	72.76	69.87	70.51	27.24	12.82	42.31	30.77	43.59	24.36	34.62	15.38	28.20	55.33	62.93	52.67	67.00	68.00	64.00	33.00	20.67	45.33	42.67	40.00	29.33	32.00	20.00	29.33	52.33	63.73	60.67	65.67	72.00	64.67	34.33	12.67	43.33	33.33	40.00	22.67	21.33	6.67	29.33	56.82	68.18	62.88	68.56	71.97	70.45	31.44	14.39	30.30	36.36	36.36	22.73	36.36	6.06	34.85	59.72	63.15	60.19	67.13	71.30	64.81	32.87	9.26	30.56	37.04	35.19	20.37	33.33	5.56	33.33	52.45	58.04	56.86	65.20	67.65	59.80	34.80	11.76	31.37	45.10	27.45	17.65	35.29	9.80	27.45	61.11	65.78	61.11	73.89	72.22	71.11	26.11	7.78	27.78	31.11	31.11	11.11	28.89	4.44	26.67	53.79	56.36	51.52	66.67	74.24	68.18	33.33	12.12	37.88	20.00	30.30	6.06	27.27	12.12	27.27	62.50	56.00	58.33	78.33	78.33	73.33	21.67	5.00	31.67	30.00	36.67	10.00	20.00	0.00	40.00	56.48	57.78	68.52	75.00	72.22	74.07	25.00	5.56	25.92	33.33	40.74	11.11	18.52	7.41	40.74	52.78	52.22	50.00	70.83	75.00	83.33	29.17	2.78	33.33	33.33	44.45	16.67	16.67	0.00	38.89	61.67	54.67	53.33	65.00	73.33	66.66	35.00	6.67	30.00	20.00	40.00	13.33	13.33	6.67	26.67	45.00	52.00	43.33	63.33	70.00	50.00	36.67	6.67	43.33	40.00	33.33	26.67	6.67	13.33	46.67	54.17	53.34	55.56	69.44	69.44	61.11	30.56	5.56	27.78	22.22	27.78	16.67	16.67	22.22	38.89	61.11	54.45	50.00	73.61	83.33	69.45	26.39	2.78	33.33	22.22	22.22	0.00	16.67	5.56	33.33	66.67	52.23	61.11	61.11	72.22	66.67	22.22	2.78	27.78	27.78	22.22	5.56	16.67	5.56	44.45	52.78	55.56	50.00	76.39	77.78	69.44	23.61	0.00	33.33	27.78	27.78	5.56	11.11	22.22	44.45	55.56	51.11	58.34	73.61	72.22	72.22	26.39	2.78	30.56	22.22	50.00	5.56	22.22	5.56	44.45	61.11	48.89	50.00	70.83	61.11	63.89	29.17	8.33	61.11	33.33	33.33	22.22	22.22	5.56	44.44	45.83	45.00	37.50	66.67	45.83	50.00	33.33	12.50	58.33	25.00	41.67	25.00	50.00	0.00	41.67	37.50	46.67	33.33	33.33	16.67	41.67	66.67	16.67	66.67	33.34	50.00	33.33	16.67	16.67	83.34	41.67	53.33	50.00	66.67	0.00	33.33	33.33	33.33	66.67	0.00	66.67	33.33	0.00	0.00	100.00	16.67	53.33	50.00	83.33	33.33	33.33	16.67	33.33	83.33	0.00	33.33	0.00	0.00	0.00	100.00	49.02	56.08	56.86	62.26	62.75	65.69	37.74	16.67	43.14	41.18	49.02	25.49	43.14	5.88	45.10

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Best Overall Response: Phase 1

Best overall response: best confirmed response on study after first study dose as per IMWGURC. sCR: normal FLC ratio, absence of clonal cells in bone marrow. CR: negative immunofixation on serum and urine, disappearance of any soft tissue plasmacytomas, <5% plasma cells in bone marrow. VGPR: serum and urine M-protein detectable by immunofixation but not on electrophoresis, >=90% reduction in serum M-protein, <100 mg/24 hr urine M-protein. PR: >=50% reduction of serum M-protein, reduction in 24-hr urinary M-protein by >=90% or to <200mg/24 hr. Progressive disease (PD): >=25% increase from lowest response level in serum M-component or urine M-component, >=10% bone marrow plasma cell percentage, definite development of new bone lesions/soft tissue plasmacytomas/definite increase in size of existing bone lesions/soft tissue plasmacytomas, development of hypercalcemia, attributed solely to plasma cell proliferative disorder. Stable disease (SD): criteria for CR, VGPR, PR or PD not met. (NCT00555906)
Timeframe: Cycle 1 Day 1 (baseline), assessed on Day 1 of every cycle up to end of study (up to Cycle 22 for schedule A and schedule B)

,,,

Intervention	participants (Number)
	Stringent Complete Response	Complete Response	Very Good Partial Response	Partial Response	Stable Disease	Progressive Disease	Indeterminate
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase1:Schedule A)	0	0	0	0	0	1	0
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase1:Schedule B)	0	0	0	0	4	3	0
Palbociclib 125mg+Bortezomib+Dexamethasone(Phase1:Schedule B)	0	0	1	0	2	1	1
Palbociclib 75mg+Bortezomib+Dexamethasone(Phase1:Schedule A)	0	0	1	0	1	3	0

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Time to Tumor Progression (TTP): Phase 2

TTP was defined as the time from first dose of study medication to first documentation of objective tumor progression. TTP was calculated as (first event date minus the date of first dose of study medication plus 1) divided by 30.44. Tumor progression was determined from oncologic assessment data (where data meet the criteria for progressive disease [PD] per IMWGURC). PD: >=25% increase from lowest response level in serum M-component or urine M-component, >=10% bone marrow plasma cell percentage, definite development of new bone lesions/soft tissue plasmacytomas/definite increase in size of existing bone lesions/soft tissue plasmacytomas, development of hypercalcemia, attributed solely to plasma cell proliferative disorder. (NCT00555906)
Timeframe: Cycle 1 Day 1 (baseline) up to 28 days after last dose of palbociclib

Intervention	months (Median)
Palbociclib 100mg+Bortezomib+Dexamethasone(Phase2:Schedule B)	3.9

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Maximum Tolerated Dose (MTD) and Recommended MTD of Dasatinib in Combination With Bortezomib and Dexamethasone

MTD is defined as the dose level combination below the dose level that produces a dose-limiting toxicity in at least 2 out of 6 or fewer participants in that cohort. If MTD is not reached, the recommended MTD is the maximum dose that the participants received. (NCT00560352)
Timeframe: Days 1 to 21

Intervention	mg QD (Number)
	MTD dasatinib	Recommended MTD dasatinib
All Treated	NA	140

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MTD and Recommended MTD of Bortezomib in Combination With Dasatinib and Dexamethasone

MTD is defined as the dose level combination below the dose level that produces a dose-limiting toxicity in at least 2 out of 6 or fewer participants in that cohort. If MTD is not reached, the recommended dose is the maximum dose that the participants received. (NCT00560352)
Timeframe: Days 1 to 21

Intervention	mg/m^2 (Number)
	MTD of bortezomib	Recommended MTD of bortezomib
All Treated	NA	1.3

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Progression-free Survival

Progression-free survival was defined as the time from start of treatment until progression or death, whichever occurred first. Participants were to be followed-up for 12 months following the last dose of dasatinib for progression and survival. PFS was analyzed for the all-treated population. (NCT00560352)
Timeframe: Day 1 to disease progression or death, whichever came first (maximum reached: 14 months)

Intervention	Months (Median)
All Treated	6.3

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Best Overall Tumor Response Rate (RR) As Assessed Using International Uniform Response Criteria for Multiple Myeloma and Criteria of the European Bone Marrow Transplant Registry

S=serum; U=urine; MP=M-protein; ST=soft tissue, PC=plasmacytomas; IF=immunofixation; BL=baseline. RR calculated on best response any time. CR=MP undetectable by IF, ≤5% plasma cells in bone marrow, and no ST PC. VGPR=MP detectable by IF, or ≥90% drop in S MP and U MP<100 mg/24h. PR= ≥50% drop in S MP and ≥90% drop in U MP or U protein <200 mg/24h, ≥50% drop in BL ST PC size. MR= ≥25% to <50% drop in S MP and ≥50% to <90% drop in U MP and ≥25% to <50% drop in BL ST PC. SD=Not CR, VGPR, PR, or MR. PD= ≥25% rise in S or U M-component; new/increased size of bone lesions, ST PC, or hypercalcemia. (NCT00560352)
Timeframe: Day 1 until last tumor assessment (maximum reached: 9 months)

Intervention	Percentage of participants (Number)
	Complete response (CR)	Very good partial response (VGPR)	Partial response (PR)	Minimal response (MR)	Stable disease (SD)	Progressive disease (PD)	Unable to determine	Not reported
Dasatinib, 100 mg QD	0	0	0	0	0	33.3	33.3	33.3
Dasatinib, 140 mg QD	0	0	0	25	0	0	25	50
Dasatinib, 50 mg BID	0	0	14.3	0	57.1	14.3	0	14.3

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Duration of Response

Duration of response calculated for those with best response=CR (M-protein [MP] undetectable by immunofixation [IF], ≤5% plasma cells in bone marrow, no soft tissue plasmacytomas); VGPR (MP detectable by IF, or ≥90% drop in serum [S] MP and urine [U] MP<100 mg/24h); PR(≥50% drop in S MP and ≥90% drop in U MP or U protein <200 mg/24h, ≥50% drop in BL ST PC size); or MR (≥25% to <50% drop in S MP and ≥50% to <90% drop in U MP and ≥25% to <50% drop in BL ST PC). Duration of response calculated from day criteria for CR, VGPR, PR, and MR were met until progression or death, whichever came first. (NCT00560352)
Timeframe: First occurrence of response to disease progression or death, whichever occurred first (maximum reached: 12.2 months)

Intervention	Months (Number)
	Partial response (PR)	Minimal response (MR)
Dasatinib, 140 mg QD	0	12.2
Dasatinib, 50 mg BID	5.4	NA

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Number of Participants With Death As Outcome, Serious Adverse Events (SAEs), Drug-related SAEs, Drug-related Adverse Events (AEs) Leading to Discontinuation, AEs Leading to Discontinuation, AEs, and Drug-related AEs by Grade

An AE is any new unfavorable symptom, sign, or disease or worsening of a preexisting condition that does not necessarily have a causal relationship with treatment. An SAE is any unfavorable medical event that at any dose results in death, persistent or significant disability/incapacity, or drug dependency or abuse; is life-threatening, an important medical event, or a congenital anomaly/birth defect; or requires or prolongs hospitalization. Drug-related=possibly, probably, or certainly related to or of unknown relationship to study treatment. Grade 3=severe; Grade 4=life-threatening. (NCT00560352)
Timeframe: Continuously from Day 1 until last day of study medication + 30 days (maximum reached: 10 months)

Intervention	Participants (Number)
	Death	SAEs	Drug-related SAEs	Drug-related AEs leading to discontinuation	AEs leading to discontinuation	AEs	AEs, Grades 3 and 4	Drug-related AEs	Drug-related AEs, Grades 3 and 4
Dasatinib, 100 mg QD	2	2	0	0	1	3	3	2	2
Dasatinib, 140 mg QD	2	1	0	1	2	4	4	4	4
Dasatinib, 50 mg BID	3	6	2	3	5	7	3	6	4

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Progression-free Survival (PFS), and Overall Survival (OS)

To obtain a preliminary estimate of PFS and OS. Overall survival (OS) is defined as time from the first chemotherapy administered on the transplant trial until death from any cause. Progression free survival (PFS)is defined as time from therapy until relapse, progression, or death from any cause. (NCT00571493)
Timeframe: one year post autologous hematopoietic stem cell transplantation (ASCT) , 5 years post ASCT

Intervention	percentage of participants (Number)
	Progression Free Survival 1 year after transplant	Overall Survival 1 year after transplant	Progression Free Survival 5 years after transplant	Overall Survival 5 years after transplant
Phase II: Progression Free Survival and Overall Survival	83	91	32	67

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Preliminary Estimate of Overall Response Rate (ORR)

To obtain a preliminary estimate of overall response rate (ORR). The overall response rate is calculated as the number of patients who achieved complete response (CR) and partial response (PR) divided by the total number of evaluable patients. (NCT00571493)
Timeframe: 100 day post autologous hematopoietic stem cell transplantation (ASCT), one year post ASCT

Intervention	participants (Number)
	Overall Response Rate (100 days after transplant)	Overall Response Rate (1 year after transplant)
Phase II: Overall Response Rate	38	33

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Maximum Tolerated Dose (MTD) of Bortezomib

The maximum tolerated dose (MTD) is defined to be the dose cohort below which 3 of 6 patients experience dose limiting toxicity (DLT), or the highest dose cohort of 1.5 mg/m², if 2 DLT were not observed at any dose cohort. (NCT00571493)
Timeframe: 14 months

Intervention	mg/m² (Number)
Phase I	1.5
Phase II	1.0

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Median Duration of Stable Disease Response

Median number of months of Stable Disease Response Per RECIST v1.0 (Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started) (NCT00581360)
Timeframe: Up to 36 months

Intervention	months (Median)
Bortezomib + Doxorubicin	8

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Objective Response Rate (ORR)

ORR is the number participants experiencing partial response (PR) + the number participants experiencing complete response (CR) / the number participants experiencing partial response (PR) + the number participants experiencing complete response (CR) + the number participants experiencing stable disease (SD) + the number participants experiencing progressive disease (PD). RECIST v1.0 criteria for Target Lesions was used: Complete Response (CR): Disappearance of all target lesions; Partial Response (PR): At least a 30% decrease in the sum of the LD of target lesions, taking as reference the baseline sum LD; Progressive Disease (PD): At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions; Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest s (NCT00581360)
Timeframe: Up to 5 years

Intervention	percentage of participants (Number)
Bortezomib + Doxorubicin	0

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Stable Disease Rate

Using RECIST v1.0 criteria, stable disease rate is the number participants experiencing stable disease (SD) / the number participants experiencing partial response (PR) + the number participants experiencing complete response (CR) + the number participants experiencing stable disease (SD) + the number participants experiencing progressive disease (PD). (NCT00581360)
Timeframe: Up to 5 years

Intervention	percentage of participants (Number)
Bortezomib + Doxorubicin	100

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Number of Months of Progression-free Survival (PFS)

Number of months that participants experienced stable disease (the disease does not progress per RECIST v1.0 criteria - Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started) (NCT00581360)
Timeframe: Up to 5 years

Intervention	months (Number)
	Participant 1	Participant 2	Participant 3	Participant 4	Participant 5	Participant 6	Participant 7	Participant 8	Participant 9
Bortezomib + Doxorubicin	8	23	36	4	2	8	26	5	1

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Number of Months of Survival

Number of months that the participant was alive. (NCT00581360)
Timeframe: Up to 5 years

Intervention	months (Number)
	Participant 1	Participant 2	Participant 3	Participant 4	Participant 5	Participant 6	Participant 7	Participant 8	Participant 9
Bortezomib + Doxorubicin	29.13	23.40	34.50	8.03	12.20	16.10	25.93	24.97	1.27

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3 Year Progression Free Survival

This is the percent of subjects who had not had any recurrence or relapse of disease as of 3 years after enrollment in the study. (NCT00581776)
Timeframe: 36 months

Intervention	percent of participants (Number)
VCR-CVAD With Rituximab Maintenance	63

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3 Year Overall Survival (OS)

This is the percent of participants who were still alive at 3 years after study entry. (NCT00581776)
Timeframe: 36 months

Intervention	Percent of participants (Number)
VCR-CVAD With Rituximab Maintenance	86

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Overall Response Rate (ORR) at the Completion of Induction Chemotherapy, Which is the Percent of Complete Responses (CR) Plus Percent of Partial Responses (PR).

"Patients were considered evaluable for response if they completed at least 2 cycles of therapy and had undergone an initial response evaluation, or had disease progression after 1 cycle of therapy.~1999 International Working Group criteria defines a CR as patients with complete disappearance of disease, or regression of all lymph nodes to 1.5 cm in greatest diameter or less. Partial Response indicates patients responded to treatment with a reduction in the amount of tumor (50 percent or more). Overall response rate is the percent of complete responses plus the percent of partial responses." (NCT00581776)
Timeframe: At completion of induction therapy (21 weeks)

Intervention	Percent of participants (Number)
VCR-CVAD With Rituximab Maintenance	90

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Complete Response Rate (CR) at the End of Induction Chemotherapy

Complete Response Rate (CRR) as defined by 1999 International Working Group criteria, is defined as patients with complete disappearance of disease, or regression of all lymph nodes to 1.5 cm in greatest diameter or less. All subjects who had completed 2 cycles of therapy and had at least one disease evaluation, or had completed 1 cycle of therapy with progressive disease, were considered evaluable. (NCT00581776)
Timeframe: at 21 weeks

Intervention	percent of participants (Number)
VCR-CVAD With Rituximab Maintenance	77

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Area Under the Plasma Concentration-time Curve (AUC) 0-72 Hours

(NCT00608907)
Timeframe: Cycle 3 day 14 (72 hours post last dose)

Intervention	ng*h/mL (Mean)
VELCADE + Rifampicin	123
VELCADE + Dexamethasone	170
VELCADE	215

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Duration of Response

Duration of response was calculated from the documentation (date) of first response (CR, nCR, VGPR, or PR) until the date of progression or last follow-up in the subset of patients who responded. (NCT00609167)
Timeframe: Duration of study (up to 12 cycles)

Intervention	months (Median)
CyBorD (Bortezomib 1.3mg/m^2)	NA
CyBorD (Bortezomib 1.5mg/m^2)	NA

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Number of Participants Who Achieved a Confirmed Responses Defined as a Complete Response (CR), Near CR or Very Good Partial Response (VGPR) After the First 4 Months of Treatment

"Response that was confirmed on 2 consecutive evaluations during the first 4 months of treatment.~Complete Response(CR): Complete disappearance of M-protein from serum and urine on immunofixation, normalization of Free Light Chain (FLC) ratio and <5% plasma cells in bone marrow.~near Complete Response (nCR): Patients who meet all criteria for CR except a positive immunofixation will be classified as nCR.~Very Good Partial Response(VGPR): >=90% reduction in serum M-component; Urine M-Component <100mg per 24hours; <=5% plasma cells in bone marrow." (NCT00609167)
Timeframe: After 4 months of treatment

Intervention	participants (Number)
CyBorD (Bortezomib 1.3mg/m^2)	20
CyBorD (Bortezomib 1.5mg/m^2)	18

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Number of Participants Who Responded to Treatment (Complete Response,CR; Near Complete Response, nCR; Very Good Partial Response, VGPR; or Partial Response, PR) After 4 Cycles

"Response that was confirmed on 2 consecutive evaluations after 8 months of treatment.~CR, nCR and VGPR as defined in the primary outcome.~Partial Response(PR): >=50% reduction in serum M-component and/or~Urine M-Component >=90% reduction or <200mg per 24hours; or >=50% decrease in difference between involved and uninvolved FLC levels." (NCT00609167)
Timeframe: 4 cycles

Intervention	participants (Number)
CyBorD (Bortezomib 1.3mg/m^2)	29
CyBorD (Bortezomib 1.5mg/m^2)	28

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Number of Participants Who Responded to Treatment (CR, nCR, VGPR or PR) After 8 Cycles

"Response that was confirmed on 2 consecutive evaluations after 8 cycles of treatment.~Criteria for CR, nCR, VGPR and PR are defined in prior outcomes." (NCT00609167)
Timeframe: After 8 cycles of treatment

Intervention	participants (Number)
CyBorD (Bortezomib 1.5mg/m^2)	1

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Number of Participants With Severe Adverse Events

Severe adverse events were defined as grade 3 or higher, regardless of attribution to study drugs. Adverse events were graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) version 3. (NCT00609167)
Timeframe: Every cycle during treatment (up to 12 cycles)

Intervention	participants (Number)
CyBorD (Bortezomib 1.3mg/m^2)	16
CyBorD (Bortezomib 1.5mg/m^2)	11

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Overall Survival (OS)

OS was defined as the time from registration to death of any cause. (NCT00609167)
Timeframe: From date of registration until death (up to 5 years)

Intervention	months (Median)
CyBorD (Bortezomib 1.3mg/m^2)	NA
CyBorD (Bortezomib 1.5mg/m^2)	NA

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Participants Who Successfully Completed Collection of Peripheral Blood Stem Cells for Transplant

Evaluation of the ability to successfully collect peripheral blood stem cells following four months (cycles) of combination therapy. (NCT00609167)
Timeframe: After 4 cycles of treatment

Intervention	participants (Number)
CyBorD (Bortezomib 1.3mg/m^2)	33
CyBorD (Bortezomib 1.5mg/m^2)	17

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Progression Free Survival (PFS)

"PFS was defined as the time from registration to progression or death due to any cause.~Progression was defined as any one or more of the following:~An increase of 25% from lowest confirmed response in:~Serum M-component (absolute increase >= 0.5g/dl)~Urine M-component (absolute increase >= 200mg/24hour~Difference between involved and uninvolved Free Light Chain levels (absolute increase >= 10mg/dl)~Bone marrow plasma cell percentage (absolute increase of >=10%)~Definite development of new bone lesion or soft tissue plasmacytomas" (NCT00609167)
Timeframe: up to 5 years

Intervention	months (Median)
CyBorD (Bortezomib 1.3mg/m^2)	NA
CyBorD (Bortezomib 1.5mg/m^2)	NA

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Median Overall Survival (OS)

Time in months from the start of study treatment to the date of death. Patients alive as of the last follow-up had OS censored at the last follow-up date. Median OS was estimated using a Kaplan-Meier curve. (NCT00611325)
Timeframe: Time in months from the start of study treatment to date of death due to any cause. Assessed up to 60 months.

Intervention	months (Median)
EIAED	8
Non-EIAED	6

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Median Progression Free Survival (PFS)

Time in months from the start of study treatment to the date of first progression according to Macdonald criteria, or to death due to any cause. Per Macdonald, progression is a ≥ 25% increase in the sum of the products of perpendicular diameters of enhancing lesions, any new lesion, or clinical deterioration. Patients alive who had not progressed as of the last follow-up had PFS censored at the last follow-up date. Median PFS was estimated using a Kaplan-Meier curve. (NCT00611325)
Timeframe: Time in months from the start of study treatment to the date of first progression or death. Assessed up to 60 months.

Intervention	months (Median)
EIAED	2
Non-EIAED	2.5

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Number of Patients With Grade 3 or Greater, Treatment-related, Non-hematologic Toxicities

Number of patients with grade 3 or greater, treatment-related, non-hematologic toxicities based on Common Terminology Criteria for Adverse Events (CTCAE) version 3.0. (NCT00611325)
Timeframe: 60 months

Intervention	participants (Number)
EIAED	27
Non-EIAED	24

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Radiographic Response Rate

The percentage of participants with a complete or partial response at any assessment as determined by the Macdonald criteria. A confirmation of response was not required. Per Macdonald criteria, complete response (CR) was the disappearance of all target lesions and partial response (PR) was a ≥50% decrease in the sum of the longest diameter of target lesions, no new lesions and stable or decreasing steroid dose. Objective response =CR+PR. Tumor assessments were done at baseline and at the end of each 6 week treatment cycle, and overall best response was recorded. (NCT00611325)
Timeframe: 60 months

Intervention	percentage of participants (Number)
EIAED	7.1
Non-EIAED	39.3

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6-month Progression-free Survival (PFS)

Percentage of participants surviving six months from the initiation of treatment without progression of disease. PFS was defined as the time from the initiation of treatment to the date of the first documented progression according to the Macdonald criteria, or to death due to any cause. Per Macdonald, progression is a ≥ 25% increase in the sum of the products of perpendicular diameters of enhancing lesions, any new lesion or clinical deterioration. (NCT00611325)
Timeframe: 6 months

Intervention	percentage of participants (Number)
EIAED	25
Non-EIAED	28.6

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Time to Best Response of Previously Treated and Previously Untreated Participants

Measured from the time of study entry to the documented beginning of response (CR or PR). This is measured in responders per Non-Hodgkin's Lymphoma Revised Response Criteria for Malignant Lymphoma (Cheson et al. 2007.) CR: complete disappearance of detectable clinical evidence of disease and disease-related symptoms; PR: 50% or greater decrease in sum of product of diameters (SPD) of up to 6 of the largest dominant nodes or nodal masses, no increase in size of other nodes, liver or spleen, no new disease sites, patients with CR and persistent morphologic bone marrow involvement. (NCT00633594)
Timeframe: Every 3 months (+/- 2 weeks) after discontinuation of study treatment for 2 years

Intervention	months (Median)
Previously Treated Participants	2.04
Previously Untreated Participants	2.37

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Time to Best Response of Phase I and Phase II Participants

"Measured from the time of study entry to the documented beginning of response (CR or PR). This is measured in responders per Non-Hodgkin's Lymphoma Revised Response Criteria for Malignant Lymphoma (Cheson et al. 2007.) CR: complete disappearance of detectable clinical evidence of disease and disease-related symptoms; PR: 50% or greater decrease in sum of product of diameters (SPD) of up to 6 of the largest dominant nodes or nodal masses, no increase in size of other nodes, liver or spleen, no new disease sites, patients with CR and persistent morphologic bone marrow involvement.~Time to Best Response will be examined using time-to-event analysis methods. Kaplan-Meier figures will be generated and the log-rank test will be used to examine differences existing between various levels of stratification." (NCT00633594)
Timeframe: Every 3 months (+/- 2 weeks) after discontinuation of study treatment for 2 years

Intervention	days (Median)
Phase I Participants (10 mg/15 mg Lenalidomide)	63.50
Phase II Participants (10 mg Lenalidomide)	71.50

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Progression Free Survival (PFS) of Previously Treated and Previously Untreated Participants

"Defined as the time from entry onto study until lymphoma progression or death from any cause.~Progression Free Survival will be examined using time-to-event analysis methods. Kaplan-Meier figures will be generated and the log-rank test will be used to examine differences existing between various levels of stratification." (NCT00633594)
Timeframe: Every 3 months (+/- 2 weeks) after discontinuation of study treatment for 2 years, then every 6 months after documented disease progression

Intervention	months (Median)
Previously Treated Participants	12.4517
Previously Untreated Participants	25.2649

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Progression Free Survival (PFS) of Phase I and Phase II Participants

Intervention	months (Median)
Phase I Participants (10 mg/15 mg Lenalidomide)	27.70
Phase II Participants (10 mg Lenalidomide)	19.35

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Overall Survival of Previously Treated and Previously Untreated Participants

"Defined as the date of study entry to the date of death.~Overall Survival will be examined using time-to-event analysis methods. Kaplan-Meier figures will be generated and the log-rank test will be used to examine differences existing between various levels of stratification" (NCT00633594)
Timeframe: Every 3 months (+/- 2 weeks) after discontinuation of study treatment for 2 years, then every 6 months after documented disease progression

Intervention	months (Median)
Previously Treated Participants	28.4189
Previously Untreated Participants	71.2608

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Overall Survival of Phase I and Phase II Participants

Intervention	months (Median)
Phase I Participants (10 mg/15 mg Lenalidomide)	51.45
Phase II Participants (10 mg Lenalidomide)	35.35

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Overall Response Rate (ORR) of Previously Treated and Previously Untreated Participants

Response to treatment (Complete Response (CR) or Partial Response (PR)) determined using Non-Hodgkin's Lymphoma Revised Response Criteria for Malignant Lymphoma (Cheson et al. 2007.) CR: complete disappearance of all detectable clinical evidence of disease and disease-related symptoms; PR: 50% or greater decrease in sum of the product of the diameters (SPD) of up to 6 of the largest dominant nodes or extranodal masses, no increase in the size of other nodes, liver or spleen, no new sites of disease, patients who achieve CR but have persistent morphologic bone marrow involvement; Stable Disease (SD): failing to attain PR or CR, but not fulfilling criteria for progressive disease; Progressive Disease (PD)/Relapse: appearance of new lesions more than 1.5 cm in any axis, 50% or greater increase from nadir SPD of any previously involved sites, 50% or greater increase in the longest diameter of any single previously identified node or extranodal mass more than 1 cm in short axis. (NCT00633594)
Timeframe: Every 6 weeks until treatment discontinuation then every 3 months thereafter, projected average 24 months

Intervention	Participants (Count of Participants)
Previously Treated Participants	8
Previously Untreated Participants	25

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Incidence of Non-Serious Adverse Events as a Measure of Safety and Tolerability, Phase II

"A count of affected participants with non-serious adverse events (regardless of relationship to study treatments) occurring in >= 15% of treated patients enrolled in the Phase II section of the study.~Lenalidomide DL-1 dose (10 mg orally, once daily (PO QD)) Day 1-14 followed by 7 days of rest, Rituximab 375 mg/m2 IV Days 1, 8, and 15 of Cycle 1; Cycles 2-6: 375 mg/m2 IV Day 1, Bortezomib 1.3 mg/m2 subcutaneous Days 1, 4, 8, and 11 for Cycles 1-6" (NCT00633594)
Timeframe: Collected from day of first dose to 30 days after the last dose of study medication, a maximum of 18 weeks and 30 days after last study treatment

Intervention	participants (Number)
	Rash	Fatigue	Thrombocytopenia	Leukopenia	Nausea	Diarrhea	Edema	Hyperglycemia	Peripheral Neuropathy	Neutropenia	Hypoalbuminemia	Constipation	Hypocalcemia	Pain in Extremity	Anemia	Cough	Fever	Dehydration	Pruritus	Dyspnea	Hyponatremia	Insomnia	Abdominal Pain	Dizziness	Hypokalemia	Weight Loss	Anorexia	Erythema	Hypomagnesemia	Allergic Reaction	Chills	Hyperhidrosis	Myalgia	Headache	Mucositis	Hypoglycemia
Phase II - Lenalidomide 10mg PO QD	19	18	16	13	12	11	11	11	10	10	10	9	9	9	8	8	8	7	7	7	7	6	6	6	6	6	5	5	5	5	5	5	4	4	4	4

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Duration of Response (DoR) of Previously Treated and Previously Untreated Participants

Measured from the documented beginning of response (CR or PR) to the time of relapse. This is measured in responders per Non-Hodgkin's Lymphoma Revised Response Criteria for Malignant Lymphoma (Cheson et al. 2007.) CR: complete disappearance of detectable clinical evidence of disease and disease-related symptoms; PR: 50% or greater decrease in sum of product of diameters (SPD) of up to 6 of the largest dominant nodes or nodal masses, no increase in size of other nodes, liver or spleen, no new disease sites, patients with CR and persistent morphologic bone marrow involvement. (NCT00633594)
Timeframe: Every 3 months (+/- 2 weeks) after discontinuation of study treatment for 2 years or until documented disease progression

Intervention	months (Median)
Previously Treated Participants	17.94
Previously Untreated Participants	21.09

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Maximum Tolerated Dose of Lenalidomide Combined With Bortezomib and Rituximab in Phase I Participants

"Determination of the maximum tolerated dose (MTD) of lenalidomide combined with bortezomib and rituximab, defined as the highest dose at which ≤1 of 6 patients experiences a dose-limiting toxicity according to the NCI CTCAE v. 4.03.~MTD of Lenalidomide was tested, included with 1.3 mg/m2 subcutaneous (D1, 4, 8, 11) bortezomib, 375 mg/m2 (D1, 8, 15 of Cycle 1, D1 on subsequent cycles) rituximab.~Three dose limiting toxicities were reported in two patients (grade 4 neutropenia and grade 3 neuropathy, grade 3 rash)" (NCT00633594)
Timeframe: Collected from day of first dose to the end of the first treatment cycle, up to 21 days

Intervention	mg lenalidomide, orally, daily, day 1-14 (Number)
Phase I Participants (10 mg/15 mg Lenalidomide)	10

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Duration of Response (DoR) of Phase I and Phase II Participants

"Measured from the documented beginning of response (CR or PR) to the time of relapse. This is measured in responders per Non-Hodgkin's Lymphoma Revised Response Criteria for Malignant Lymphoma (Cheson et al. 2007.) CR: complete disappearance of detectable clinical evidence of disease and disease-related symptoms; PR: 50% or greater decrease in sum of product of diameters (SPD) of up to 6 of the largest dominant nodes or nodal masses, no increase in size of other nodes, liver or spleen, no new disease sites, patients with CR and persistent morphologic bone marrow involvement.~Duration of Response will be examined using time-to-event analysis methods. Kaplan-Meier figures will be generated and the log-rank test will be used to examine differences existing between various levels of stratification." (NCT00633594)
Timeframe: Every 3 months (+/- 2 weeks) after discontinuation of study treatment for 2 years or until documented disease progression

Intervention	months (Median)
Phase I Participants (10 mg/15 mg Lenalidomide)	25.72
Phase II Participants (10 mg Lenalidomide)	17.81

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Overall Response Rate (ORR) of Phase I and Phase II Participants

Intervention	Participants (Count of Participants)
Phase I Participants (10 mg/15 mg Lenalidomide)	12
Phase II Participants (10 mg Lenalidomide)	21

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Maximal Tolerated Doses of Bortezomib and Vincristine When Used in Combination of Bortezomib, Rituximab and the CHOP Chemotherapy Regimen (Phase I)

INDUCTION: Patients receive bortezomib IV on days 1 and 8; rituximab IV, doxorubicin hydrochloride IV over 3-5 minutes, cyclophosphamide IV over 60 minutes, and vincristine sulfate IV over 10 minutes on day 1; and prednisone PO on days 1-5. Treatment repeats every 21 days for up to 8 courses in the absence of disease progression. (NCT00634179)
Timeframe: Cycle 1 for MTD, following completion of therapy for CR, up to 24 weeks

Intervention	mg/m^2 (Number)
MTD of Bortezomib With Vincristine Capped at 1.5 mg	1.62

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An Estimate of the Overall Response Rate (ORR)(Complete Response [CR] + CR Unconfirmed [CRu] + Partial Response [PR]) to Bortezomib and Rituximab (VR)-CHOP According to International Workshop to Standardize Response Criteria (IWRC) Criteria

Response was assessed by computerized tomography (CT) after every 2 cycles of induction therapy, one time at least 4 weeks after completing induction (i.e., prior to maintenance), and then every 3 months while on maintenance therapy. At the conclusion of maintenance therapy, patients underwent one post-treatment scan, with further scans completed at the discretion of the treating physician. Positron emission tomography was permitted but only CT measurements were used to determine response. (NCT00634179)
Timeframe: Following completion of therapy, up to 2 years

Intervention	participants (Number)
	Complete Response (CR)	Partial Response (PR)	Overall Response Rate (ORR)
Phase I: Induction	13	6	19
Phase II: Maintenance	19	10	29

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Number of Participants With Complete Response

Response is assessed by investigator according to International Working Group (IWG) criteria. Complete response requires disappearance of all evidence of disease. (NCT00636792)
Timeframe: 12 weeks after the last subject completes their end of treatment visit.

Intervention	participants (Number)
VELCADE, Bendamustine, Rituximab (VBR) Treatment	32

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Number of Participants With Overall Response (Complete and Partial Response)

Response is assessed by investigator according to International Working Group (IWG) criteria. Complete response requires disappearance of all evidence of disease. Partial response requires regression of measurable disease and no new sites. (NCT00636792)
Timeframe: 12 weeks after the last subject completes their end of treatment visit

Intervention	participants (Number)
VELCADE, Bendamustine, Rituximab (VBR) Treatment	53

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Proportion of Confirmed Tumor Response Defined as an Objective Status of Confirmed Response (CR), Partial Response (PR), or Regression (REGR) on Two Consecutive Evaluations

"Confidence intervals for the true proportion will be calculated using the exact binomial method.~Measurable patients must achieve at least a 50% reduction in the product of perpendicular diameters of contrast enhancement or mass with no new lesions with the patient being on stable or decreased steroid dose.~Evaluable patients must achieve unequivocal reduction in size of contrast-enhancement or decrease in mass effect as agreed upon independently by primary physician and quality control physicians; no new lesions. Patient should be on stable or decreased steroid dose." (NCT00641706)
Timeframe: Assessed up to 5 years

Intervention	proportion of patients (Number)
Arm A (Not Undergoing Surgery)	0.027

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Time to Progression

Estimated using Kaplan-Meier survival curve. Patients who died were considered to have disease progression at the time of death unless there was documented evidence that no progression occurred before death. For patients with bidimensionally measurable disease (measurable disease), progression is defined as > 25% increase in product of perpendicular diameters of contrast enhancement or mass or appearance of new lesions. For patients without bidimensionally measurable disease (evaluable disease), progression is defined as unequivocal increase in size of contrast enhancement or increase in mass effect as agreed upon independently by primary physician and quality control physicians or appearance of new lesions. (NCT00641706)
Timeframe: From study registration to date of progression (up to 5 years)

Intervention	months (Median)
Arm A (Not Undergoing Surgery)	1.5
Arm B (Undergoing Surgery)	4.2

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Progression-free Survival at 6 Months

Estimated using the Binomial point estimator (number of successes divided by the total number of evaluable patients). A patient is classified as a success if alive and progression-free at 6 months. For patients with bidimensionally measurable disease (measurable disease), progression is defined as > 25% increase in product of perpendicular diameters of contrast enhancement or mass or appearance of new lesions. For patients without bidimensionally measurable disease (evaluable disease), progression is defined as unequivocal increase in size of contrast enhancement or increase in mass effect as agreed upon independently by primary physician and quality control physicians or appearance of new lesions. (NCT00641706)
Timeframe: At 6 months

Intervention	percentage of patients (Number)
Arm A (Not Undergoing Surgery)	0
Arm B (Undergoing Surgery)	29

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Overall Survival

Estimated using Kaplan-Meier survival curve. (NCT00641706)
Timeframe: From study registration to date of death due to any cause or last follow-up (up to 5 years)

Intervention	months (Median)
Arm A (Not Undergoing Surgery)	3.2
Arm B (Undergoing Surgery)	8.7

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Response Rates ()

The response rate was calculated as the number of patients with documented confirmed partial response (PR) or better, which includes confirmed/unconfirmed stringent complete response (sCR), confirmed/unconfirmed complete response (CR), confirmed/unconfirmed very good partial response (VGPR), or confirmed partial response (PR), as best response divided by the total number of evaluable patients, in each arm. Patients with measurable disease, as defined in the protocol, are evaluable. Response rates were compared between the two treatment arms using a stratified Cochran-Mantel-Haenszel test. Response designations were based on the International Uniform Response Criteria for Multiple Myeloma. Due to the complexity of these criteria, the details of these criteria have been omitted. (NCT00644228)
Timeframe: Up to 6 years

Intervention	Participants (Count of Participants)
Arm I (Dexamethasone and Lenalidomide)	153
Arm II (Dexamethasone, Lenalidomide, Bortezomib)	176

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Progression-free Survival

Unstratified median progression-free survival in months. (NCT00644228)
Timeframe: From date of registration to date of first documentation of progression or symptomatic deterioration, or death due to any cause, assessed up to 6 years

Intervention	Months (Median)
Arm I (Dexamethasone and Lenalidomide)	30
Arm II (Dexamethasone, Lenalidomide, Bortezomib)	43

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Overall Survival

Unstratified median overall survival in months. (NCT00644228)
Timeframe: Up to 6 years

Intervention	Months (Median)
Arm I (Dexamethasone and Lenalidomide)	64
Arm II (Dexamethasone, Lenalidomide, Bortezomib)	75

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Dose Limiting Toxicity

Number of participants with dose limiting toxicity. (NCT00666588)
Timeframe: During Course 1

Intervention	participants (Number)
Bortezomib 1.3mg/m2-assess Efficacy-low Anthracycline Exposure	0
Bortezomib 1.0mg/m2-assess Feasibility High Anthracycline Exp	1
Bortezomib 1.3 mg/m2-assess Feasibility High Anthracycline Exp	0
Bortezomib 1.3 mg/m2-assess Efficacy High Anthracycline Exp	0

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NF-kB Activity by Enzyme-linked Immunosorbent Assay (ELISA)

NF-kB activity will be measured as a continuous variable (ng NF-kB/Mg protein). Differences in NF-κB activity between time points will be assessed using summary statistics such as mean, standard deviation, and range. We may perform exploratory analyses to determine if single time point measurements, or the difference between time points, correlate with treatment response. (NCT00666588)
Timeframe: At baseline, prior to and up to 24 hours after bortezomib treatment

,,,

Intervention	ng/Mg protein (Mean)
	Baseline	24 Hrs after treatment
Bortezomib 1.0mg/m2-assess Feasibility High Anthracycline Exp	655.4	345.46
Bortezomib 1.3 mg/m2-assess Efficacy High Anthracycline Exp	408.144	497.31
Bortezomib 1.3 mg/m2-assess Feasibility High Anthracycline Exp	974.66	855.96
Bortezomib 1.3mg/m2-assess Efficacy-low Anthracycline Exposure	718.218	774.1925

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Feasibility of Stem Cell Quantitation: Percentage of Leukemia Initiation Cells (LIC) Depletion

Descriptive statistics to assess mean +/- standard deviation for the percentage leukemia initiation cells (LIC) depletion. (NCT00666588)
Timeframe: At baseline and after completion of course 1

Intervention	percentage of LIC depletion (Mean)
	Prior to Treatment	Post Treatment
Bortezomib 1.3 mg/m2-assess Efficacy High Anthracycline Exp	1.6385	0.0435
Bortezomib 1.3 mg/m2-assess Feasibility High Anthracycline Exp	0.2	0.43
Bortezomib 1.3mg/m2-assess Efficacy-low Anthracycline Exposure	0.013667	0.021

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Overall Response (Complete Remission [CR] and CR With Partial Recovery [CRp]) During Course 1

Overall response (complete remission [CR] and CR with partial recovery [CRp]) during course 1. (NCT00666588)
Timeframe: After course 1

Intervention	participants (Number)
Bortezomib 1.3mg/m2-assess Efficacy-low Anthracycline Exposure	4
Bortezomib 1.0mg/m2-assess Feasibility High Anthracycline Exp	2
Bortezomib 1.3 mg/m2-assess Feasibility High Anthracycline Exp	2
Bortezomib 1.3 mg/m2-assess Efficacy High Anthracycline Exp	9

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Proteasome Inhibition Activity

Mean and standard deviation of β1 and β5- Results are ratios (proteasome subunit/β-actin based on loading of 15 µg total protein, normalized to CEM). (NCT00666588)
Timeframe: At baseline

Intervention	ratio (Mean)
	Baseline β1	Baseline β5
Bortezomib 1.0mg/m2-assess Feasibility High Anthracycline Exp	0.7894	0.2576
Bortezomib 1.3 mg/m2-assess Efficacy High Anthracycline Exp	0.2895143	0.3721286
Bortezomib 1.3mg/m2-assess Efficacy-low Anthracycline Exposure	0.08115	0.121575

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Duration of Response

The duration of response, defined only among the responders, is measured from start of achieving Partial Response (PR) [first observation of PR before confirmation] to the time of disease progression, with deaths owing to causes other than progression not counted as events, but censored (Durie et al., 2006). Duration of response will be estimated and plotted with the Kaplan-Meier method. The median will be calculated with 95% confidence intervals. (NCT00691704)
Timeframe: 6 years

Intervention	months (Mean)
High-risk Multiple Myeloma	11

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Progression Free Survival

Progression free survival (PFS) is defined for all subjects as the time from the date of initiation of treatment to the date of first documentation of relapse, progression, or death due to any cause. Full restaging was performed at 6, 12, 18, 24, 36, 48, 60, 72 months). PFS survival will be estimated and plotted with the Kaplan-Meier method. The median will be calculated with 95% confidence intervals. (NCT00691704)
Timeframe: 2 years

Intervention	participants (Number)
	PFS at 2 years	PFS at 1 year
High-risk Multiple Myeloma	3	9

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Time to Response

Time to response will be measured in the population of subjects with a confirmed response as the time from the date of initiation of treatment to the date of the first documentation of a confirmed response. Full restaging was performed at 6, 12, 18, 24, 36, 48, 60, 72 months). Time to response will be estimated and plotted with the Kaplan-Meier method. The median will be calculated with 95% confidence intervals. (NCT00691704)
Timeframe: 6 months

Intervention	months (Mean)
High-risk Multiple Myeloma	2

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Time to Progression

Time to progression (TTP) is defined for all patients as the time from initiation of treatment to disease progression with deaths owing to causes other than progression not counted as events, but censored (Durie et al., 2006). (NCT00691704)
Timeframe: 6 years

Intervention	months (Mean)
High-risk Multiple Myeloma	11

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Overall Survival

Overall survival is defined as the time from the date of initiation of treatment to the date of death due to any cause. Overall response rate will be estimated with its 80% confidence interval, and the numbers of subjects achieving a sustained complete response (sCR), complete response (CR), very good partial response (VGPR), partial response (PR), or stable disease (SD) will be tabulated. Overall survival will be estimated and plotted with the Kaplan-Meier method. The median will be calculated with 95% confidence intervals. (NCT00691704)
Timeframe: 6 years

Intervention	months (Mean)
High-risk Multiple Myeloma	36

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Best Response

Number of participants per category: Partial Response (PR), Stable Disease (SD), Progressive Disease (PD). PR: Regression of measurable disease and no new sites. SD: Failure to attain Complete Response (CR), /PR or PD. Relapsed or Progressive Disease: Any new lesion or increase by ≥ 50% of previously involved sites from nadir. (NCT00703664)
Timeframe: Up to 9 years

Intervention	Participants (Count of Participants)
	Partial Response	Stable Disease	Progressive Disease
Cohort A - MCL	7	5	7
Cohort B - MCL	0	2	2
Cohort C - DLBCL	3	8	23

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Progression-free Survival (PFS)

Median progression-free survival in months per cohort. (NCT00703664)
Timeframe: Up to 9 years

Intervention	months (Median)
Cohort A - MCL	7.6
Cohort C - DLBCL	1.8

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Overall Response Rate (ORR)

ORR: Complete Response (CR) + Partial Response (PR) assessed according to the Revised Response Criteria for Malignant Lymphoma. (NCT00703664)
Timeframe: Up to 9 years

Intervention	percentage of participants (Number)
Cohort A - MCL	31.8
Cohort B - MCL	0
Cohort C - DLBCL	7.7

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Duration of Stable Disease

Median duration of stable disease per cohort. (NCT00703664)
Timeframe: Up to 9 years

Intervention	months (Median)
Cohort A - MCL	3.8
Cohort B - MCL	3.8
Cohort C - DLBCL	1.3

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Duration of Partial Response

Median duration of response per cohort. (NCT00703664)
Timeframe: Up to 9 years

Intervention	months (Median)
Cohort A - MCL	4.2
Cohort C - DLBCL	2.1

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Duration of Response

Duration of response is defined for all evaluable patients who have achieved an objective response as the date at which the patient's earliest objective status is first noted to be either a CR or PR to the earliest date progression is documented. MR for Waldenstrom lymphoma will not be included as a response. Median duration of response and the confidence interval for the median duration will be computed. (NCT00711828)
Timeframe: Up to 3 years from registration

Intervention	months (Median)
Treatment	25.9

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Overall Survival

Survival time is defined as the time from registration to death due to any cause. The distribution of survival time will be estimated using the method of Kaplan-Meier. (NCT00711828)
Timeframe: Up to 3 years from registration

Intervention	months (Median)
Treatment	54.8

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Progression-free Survival

Progression-free survival time is defined as the time from registration to the earliest date of documentation of disease progression or death, whichever occurs first. Progression is defines as having any new lesion or increase by 50% of previously involved sites from nadir. The distribution of progression-free survival time will be estimated using the method of Kaplan-Meier. (NCT00711828)
Timeframe: Up to 3 years from registration

Intervention	months (Median)
Treatment	11.6

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Time to Treatment Failure

Time to treatment failure is defined to be the time from registration to the date at which the patient is removed from treatment due to progression, adverse events, or refusal. If the patient is considered to be a major treatment violation or is taken off study as a non-protocol failure, the patient will be censored on the date they are removed from treatment. The distribution of time to treatment failure will be estimated using the method of Kaplan-Meier. (NCT00711828)
Timeframe: Up to 3 years from registration

Intervention	months (Median)
Treatment	6.6

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Adverse Events

Adverse events were assessed according to the NCI Common Terminology Criteria for Adverse Events (CTCAE), Version 3.0 after each cycle of treatment. The maximum grade for each type of adverse event were recorded for each patient, and frequency tables were reviewed to determine patterns. For this endpoint, the number of patients receiving a Grade 3, Grade 4, or Grade 5 as their highest reported grade regardless of attribution are reported. A full list of adverse events are reported in the Adverse Events section of this report. (NCT00711828)
Timeframe: up to 12 cycles (28 days per cycle) of treatment

Intervention	participants (Number)
	Grade 3	Grade 4	Grade 5
Treatment	19	8	0

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Proportion of Responses (Complete Response or Partial Response)

A response is defined to be a Complete Response (CR) or Partial Response (PR) noted as the objective status on any evaluation (i.e., best response). The proportion of successes will be estimated by the number of successes divided by the total number of evaluable patients. A confidence interval for the true success proportion will be calculated according to the properties of the binomial distribution. (NCT00711828)
Timeframe: up to 12 cycles

Intervention	percentage of participants (Number)
	Complete Response (CR)	Partial Response (PR)
Treatment	19.0	42.9

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Number of Patients Who Experienced at Least One Serious Adverse Event

(NCT00715208)
Timeframe: From completion of informed consent through 30 days after the last dose of study drug

Intervention	participants (Number)
VELCADE R-CAP	2
VELCADE R-CP	12

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Percentage of Participants With Progression-free Survival (PFS) at 1 Year

PFS was defined as the time from the first dose to the date of progressive disease (PD)/relapse or death, whichever comes first. For a participant who had not progressed/relapsed or died, PFS was censored at the last response assessment that was stable disease (failure to attain complete response/partial response or PD or better). (NCT00715208)
Timeframe: Assessed at at the end of Cycle 2, at end of treatment visit, and every 12± 1 weeks for the first year (4 visits) until PD

Intervention	percentage of participants (Number)
VELCADE R-CAP	67
VELCADE R-CP	63

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Number of Patients With Complete Response (CR)

Disappearance of all evidence of disease assessed by computed tomography (CT) and PET (position-emission tomography) according to the revised International Working Group (IWG) Criteria. (NCT00715208)
Timeframe: 30 weeks

Intervention	participants (Number)
VELCADE R-CAP	1
VELCADE R-CP	13

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Duration of Response

"Time (in months) from the first documentation of a response (CR or partial response [PR]) to the date of first documentation of progressive disease or relapse from complete response.~CR is defined as disappearance of all evidence of disease assessed by CT or PET; PR is defined as regression of measurable disease and no new sites assessed by CT or PET according to the revised International Working Group (IWG) Criteria." (NCT00715208)
Timeframe: 2 years

Intervention	Months (Median)
VELCADE R-CP	21.9

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Number of Participants With Overall Response (OR)

"OR = Complete Response (CR) + Partial Response (PR)according to the revised International Working Group (IWG) Criteria.~CR is the disappearance of all evidence of disease assessed by CT and PET. PR is the regression of measurable disease and no new sites assessed by CT and PET." (NCT00715208)
Timeframe: 30 weeks

Intervention	participants (Number)
VELCADE R-CAP	6
VELCADE R-CP	37

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Number of Dose-limiting Toxicity (DLT) Incidents (Phase I)

DLT was defined as any events that is determined to be possibly, probably, or definitely related to the combination of bortezomib and GX15-070 (as determined by the investigator) and occurring during the first cycle of treatment, irrespective of whether the toxicity resolved. Hematologic DLT measures were assessed using the continuous variables as the outcome measures (primarily nadir and percent change from baseline values) as well as categorization via Common Terminology Criteria for Adverse Events (CTCAE) version 3 standard toxicity grading. (NCT00719901)
Timeframe: Up to 21 days of every first course

Intervention	Toxicity Incidents (Number)
Treatment (Enzyme Inhibitor Therapy)	4

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Number of Patients Who Have at Least a Partial Response (Phase I)

In order to be classified as a hematologic response, confirmation of serum monoclonal protein, serum immunoglobulin free light chain (when primary determinant of response) and urine monoclonal protein (when primary determinant of response) results must be made by verification on two consecutive determinations. (NCT00719901)
Timeframe: From baseline to up to 3 years

Intervention	participants (Number)
Treatment (Enzyme Inhibitor Therapy)	4

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Number of Participants Experiencing an Adverse Event (AE)

An AE was defined as any untoward medical occurrence associated with the use of a drug, whether or not considered drug related. AEs were collected from the first dose of study drug through 30 days after the last dose of study drug. Treatment was administered for up to 8 cycles (24 weeks) and AEs were collected for up to 30 days following the last dose of study drug. (NCT00722137)
Timeframe: Up to 107.4 months

Intervention	Participants (Number)
R-CHOP	239
VcR-CAP	240

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Time to Next Anti-lymphoma Treatment (TTNT)

The time to next anti-lymphomatreatment was measured from the date of initiation of study treatment as per protocol to the start date of new anti-lymphoma treatment. Death due to disease progression prior to subsequent therapy was considered as an event. Otherwise, time to next anti lymphoma treatment was censored at the date of death or the last date known to be alive. (NCT00722137)
Timeframe: : Median duration of follow-up of 40 months

Intervention	Days (Median)
R-CHOP	756.0
VcR-CAP	1353.0

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Time to Progression (TTP)

Time to progression was defined as the duration from the date of randomization until the date of first documented evidence of progressive disease (PD) or date of relapse for subjects who experienced complete response (CR) or complete response, unconfirmed (CRu). PD and response were based on the assessment of an Independent Review Committee. (NCT00722137)
Timeframe: Median duration of follow-up of 40 months

Intervention	Days (Median)
R-CHOP	490.0
VcR-CAP	929.0

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Treatment-free Interval (TFI)

The TFI was defined as the duration from the date of last dose plus 1 day to the start date of the new treatment. Death due to disease progression prior to subsequent therapy was considered as an event. Otherwise, treatment-free interval was censored at the date of death or the last date known to be alive. (NCT00722137)
Timeframe: Median duration of follow-up of 40 months

Intervention	Days (Median)
R-CHOP	624.0
VcR-CAP	1236.0

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Duration of Response

The duration of treatment response was defined as the time from the date of the first response to the date of PD or death due to PD for those participants with a best response of CR, CRu, or PR as determined by the Independent Review Committee. The duration of response for complete responders was defined as the time from the date of the first response to the date of PD or death due to PD for those participants with a best response of CR or CRu verified by bone marrow and lactate dehydrogenase (LDH). (NCT00722137)
Timeframe: Median duration of follow-up of 40 months

Intervention	Days (Median)
	Duration of response	Duration for Complete responders
R-CHOP	459.0	563.0
VcR-CAP	1110.0	1282.0

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Progression Free Survival (PFS)

PFS was defined as the interval between the date of randomization and the date of progressive disease (PD) or death, whichever occurred first. PD was based on the assessment of an Independent Review Committee. (NCT00722137)
Timeframe: Median duration of follow-up of 40 months

Intervention	Days (Median)
R-CHOP	437.0
VcR-CAP	751.0

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Overall Complete Response (CR + CRu)

Overall complete response was defined as the number of participants with complete response (CR) and those with unconfirmed complete response (CRu). Response assessment was carried out every 6 weeks for 18 weeks; thereafter, every 8 weeks until PD/initiation of alternate therapy/withdrawal from study/death. (NCT00722137)
Timeframe: Median duration of follow-up of 40 months

Intervention	Participants (Number)
	Overall complete response	CR	CRu
R-CHOP	95	79	16
VcR-CAP	122	106	16

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Overall Survival (OS) in Long Term Follow-up Period

OS was measured from the date of randomization to the date of the participant's death. If the participant was alive or the vital status was unknown, OS was censored at the date that the subject was last known to be alive. (NCT00722137)
Timeframe: Up to 107.4 months

Intervention	Days (Median)
R-CHOP	1695.0
VcR-CAP	2760.0

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Overall Survival (OS)

Intervention	Days (Median)
R-CHOP	1714.0
VcR-CAP	NA

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Overall Response Rate (ORR)

ORR was defined as complete response (CR) + complete response, unconfirmed (CRu) + partial response (PR) as determined by the Independent Review Committee. Response assessment was carried out every 6 weeks for 18 weeks; thereafter, every 8 weeks until PD/initiation of alternate therapy/withdrawal from study/death. (NCT00722137)
Timeframe: Median duration of follow-up of 40 months

Intervention	Participants (Number)
R-CHOP	204
VcR-CAP	211

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18-Month Survival

18-month survival was defined as the estimated probability of survival at 18 months (Kaplan-Meier estimate). (NCT00722137)
Timeframe: Up to month 18 from the time of randomization

Intervention	Percentage of Participants (Mean)
R-CHOP	83.8
VcR-CAP	84.9

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Number of Patients With Overall Response (Complete Response + Partial Response)

"Disease response was measured according to European Group for Blood and Marrow Transplantation (EBMT) criteria with the addition of the response categories of nCR and VGPR.~Complete response requires disappearance of monoclonal protein from the blood and urine and <5% plasma cells in the bone marrow on at least 2 determinations for a minimum of 6 weeks.~Partial Response requires ≥50% reduction in serum m-protein for at least 2 determinations at least 6 weeks apart and if present, reduction in 24-hour urinary light chain excretion by either ≥90% or to <200 mg" (NCT00722566)
Timeframe: Over 4 cycles (prior to the addition of dexamethasone)

Intervention	Participants (Number)
VELCADE Subcutaneuous	61
VELCADE Intravenous	31

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Number of Patients With Complete Response

Intervention	Participants (Number)
VELCADE Subcutaneous	9
VELCADE Intravenous	6

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Response to Bortezomib Monotherapy

Response to treatment with Bortezomib (BTZ) alone was defined as a reduction in serum Donor Specific Alloantibody (DSA) levels following treatment. DSA levels were measured prior to treatment and after treatment. A good response occurred if all DSA were reduced. A partial response when a reduction was observed in at least one DSA, but not all DSA. No response occurred when no reduction of any DSA was attained. (NCT00722722)
Timeframe: 6 months

Intervention	participants (Number)
	Good Response	Partial Response	No Response
16 Dose Group	0	1	4
32 Dose Group	0	6	3
4 Dose Group	0	1	2

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The Percentage of Patients That Achieved Partial or Complete Response to Treatment.

"Partial Response:~50% reduction in the level of serum monoclonal protein for at least two determinations six weeks apart.~If present, reduction in 24-hour urinary light chain excretion by either, greater than or equal to 90%, or to <200 mg for at least two determinations six weeks apart.~50% reduction in the size of soft tissue plasmacytomas (by clinical or radiographic examination) for at least six weeks.~No increase in size or number of lytic bone lesions (development of compression fracture does not exclude response).~Complete Response:~Disappearance of the original monoclonal protein from the blood and urine on at least two determinations for a minimum of six weeks.~<5% plasma cells in the bone marrow on at least two determinations for a minimum of six weeks.~No increase in the size or number of lytic bone lesions." (NCT00724568)
Timeframe: 24 weeks (8, 21-day cycles)

Intervention	percentage of patients (Number)
Combination Drug Therapy	96

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Maximum Tolerated Dose (MTD) of Combination Therapy With VELCADE, Dexamethasone, and Doxil, (RVDD)

"Dose Level 1:~15 mg Revlimid daily on days 1-14 followed by 7-day rest every 21 days 1.3 mg/m2 Velcade daily on days 1, 4, 8 and 11 20 mg dexamethasone daily on Days 1, 2, 4, 5, 8, 9, 11, 12* and 20 mg/m2 Doxil daily on day 4~Dose Level 2:~20 mg Revlimid daily on days 1-14 followed by 7-day rest every 21 days 1.3 mg/m2 Velcade daily on days 1, 4, 8 and 11 20 mg dexamethasone daily on Days 1, 2, 4, 5, 8, 9, 11, 12* and 20 mg/m2 Doxil daily on day 4~Dose Level 3:~25 mg Revlimid daily on days 1-14 followed by 7-day rest every 21 days 1.3 mg/m2 Velcade daily on days 1, 4, 8 and 11 20 mg dexamethasone daily on Days 1, 2, 4, 5, 8, 9, 11, 12* and 20 mg/m2 Doxil daily on day 4~Dose Level 4:~25 mg Revlimid daily on days 1-14 followed by 7-day rest every 21 days 1.3 mg/m2 Velcade daily on days 1, 4, 8 and 11 20 mg dexamethasone daily on Days 1, 2, 4, 5, 8, 9, 11, 12* and 30 mg/m2 Doxil daily on day 4" (NCT00724568)
Timeframe: 1 month post treatment

Intervention	mg (Number)
	Revlimid	VELCADE	Dexamethasone	Doxil
Combination Drug Therapy	25	1.3	20	30

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Response

Overall response rate equals complete response and partial response per Southwest Oncology Group Criteria. Measurable, quantifiable protein criteria must be present. Acceptable protein criteria are quantitative immunoglobulin IgG, IgA, IgD, IgE or IgM and/or urine M-component (Bence-Jones protein). If both are present, the quantitative immunoglobulin will be followed for response. Complete Remission: The absence of bone marrow or blood findings of multiple myeloma. This includes disappearance of all evidence of serum and urine M-components on electrophoresis as by immunofixation studies. There must also be no evidence of increasing anemia. Partial Remission: A 50-74% reduction in the quantitative immunoglobulin, and if present, a 50-89% reduction in the urine M-component (Bence-Jones protein). Stable/No Remission): A <50% reduction I nthe quantitative immunoglobulin, or if the patient has light-chain disease only, a <50% reduction in the urine M-component (Bence-Jones protein. (NCT00734149)
Timeframe: 6 weeks following completion of treatment

Intervention	participants (Number)
Bortezomib+Melphalan+Prednisone	42

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Number of Patients With Any Grade or Severe Adverse Event

Number of patients with any grade or severe, defined as ≥ grade 3 by Common Terminology Criteria for Adverse Events (CTCAE) v4.0, adverse events as a measure of safety (NCT00734149)
Timeframe: At any time during the study and up to 30 days after stopping the study drug

Intervention	participants (Number)
Bortezomib+Melphalan+Prednisone	34

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Median Duration of Response

Duration of response is measured from date of first confirmed response until date of disease progression. (NCT00734149)
Timeframe: up to 4 years

Intervention	months (Median)
Bortezomib+Melphalan+Prednisone: Non-ASCT	19.8
Bortezomib+Melphalan+Prednisone: ASCT	27.9

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Disease-free Survival

Disease-free survival (DFS) was measured as the interval from achievement of CR until relapse or death, regardless of cause. DFS was estimated using the Kaplan Meier method. (NCT00742625)
Timeframe: Duration of study (up to 10 years)

Intervention	months (Median)
Bortezomib + Daunorubicin + Cytarabine	8

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Participants Experiencing a Dose-limiting Toxicity (DLT) of Bortezomib When Administered in Combination With Intermediate-dose Cytarabine

"DLTs were considered only during the first cycle of consolidation therapy and included grade 3 or 4 sensory or autonomic neuropathy, persistent grade 4 thrombocytopenia or neutropenia at day 42 in the absence of AML,any grade 4 or 5 nonhematologic toxicity, and any grade 3 nonhematologic toxicity (excluding neuropathy and toxicities secondary to neutropenia and sepsis) that did not resolve to grade 2 by day 42 unless attributable to persistent or recurrent AML. Grade 4 anorexia (requiring total parenteral nutrition) and grade 4 fatigue (requiring bed rest) were not considered DLTs.~Toxicity was graded per National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 3.0. Grading scale is as follows: grade 1: mild; grade 2: moderate; grade 3: Severe; grade 4: Life Threatening; grade 5: Death." (NCT00742625)
Timeframe: during consolidation cycle 1 (42 days)

Intervention	participants (Number)
Bortezomib (0.7 mg/m^2) + Int-DAC	0
Bortezomib (1.0 mg/m^2) + Int-DAC	0
Bortezomib (1.3 mg/m^2) + Int-DAC	1

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Remission Induction Response

"Response was calculated according to Revised International Working Group (IWG) criteria for Acute myeloid leukemia (AML)~A response was defined as the portion of participants who achieved a complete response (CR) or CR with incomplete platelet recovery(CRp) during induction.~A CR is defined as those with > 20% cellularity of bone marrow biopsy, no presence of extramedullary leukemia for AML, <5 % myeloblast cells for bone marrow with peripheral blood and normal complete blood count (absolute neutrophils > 1000 mL and platelets >= 100,000 mL).~A CRp is defined as a CR except platelets < 100,000 mL without need for transfusion." (NCT00742625)
Timeframe: 2 months

Intervention	participants (Number)
	Complete response	Complete response with incomplete platelet recover
Bortezomib + Daunorubicin + Cytarabine	62	4

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Overall Survival

Overall survival (OS) as the interval from the on-study date until death. OS was estimated using the Kaplan Meier method. (NCT00742625)
Timeframe: Duration of study (up to 10 years)

Intervention	months (Median)
Bortezomib + Daunorubicin + Cytarabine	12

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Phase II: Two Year Overall Survival (OS)

Overall survival by disease risk stratification after CVDD. OS: time from initiation of therapy until death from any cause. (NCT00750815)
Timeframe: 2 years

Intervention	percentage of participants (Number)
High-Risk Myeloma	88.9
Standard-Risk Myeloma	91.1

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Phase II: Progression-Free Survival (PFS)

"Progression-free survival after CVDD in participants with newly diagnosed active multiple myeloma. PFS: time from the initiation of therapy to progression, relapse or death from any causes.~Progressive Disease (PD): Progressive Disease requires any one or more of the following:~Increase of ≥ 25% from baseline in:~serum M-component and /or (the absolute increase must be ≥ 0.5 g/dL)~urine M-component and/or (the absolute increase must be ≥ 200 mg/24 h)" (NCT00750815)
Timeframe: Up to 50.9 months

Intervention	months (Median)
All Participants	31.3

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Phase I - Maximum Planned Dose (MPD) Level

"Maximum Phase II planned dose of cyclophosphamide when given in combination with bortezomib, pegylated liposomal doxorubicin and Dexamethasone (CVDD) in participants with newly diagnosed active multiple myeloma. Dose levels 1, 2, 3, 4 as outlined in Treatment Arm A.~If no dose limiting toxicity (DLT) was reported in the first 3 participants at a dose level, that dose level was to be considered safe and 3 participants would be enrolled at the next dose level. If 1/3 participants in a cohort at a dose level had dose limiting toxicity (DLT), the dose level would be expanded to obtain 6 evaluable participants. MPD reflects the highest dose of drug that did not cause a DLT in 33% of participants." (NCT00750815)
Timeframe: 9 months

Intervention	Dosing Level (Number)
A. Phase I Dose Escalation	4

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Phase II: Overall Response Rate (ORR)

Best response to CVDD chemotherapy. Overall Response: Partial Response (PR) + Very Good Partial Response (VGPR) + Complete Response (CR). PR: ≥ 50% reduction of serum M-protein and reduction in 24 hour urinary M-protein by ≥ 90% or to < 200 mg per 24 hours; VGPR: Serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein with urine M-protein level < 100 mg per 24 hours; CR: Negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas, and ≤ 5% plasma cells in bone marrow. (NCT00750815)
Timeframe: Up to 6 months

Intervention	participants (Number)
	Participants with Partial Response	Participants with Very Good Partial Response	Participants with Complete Response
All Participants	16	23	15

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Participants With Treatment-emergent Adverse Events (TEAEs)

Counts of participants with TEAEs, and subset by relation to drug, grade of severity, serious, TEAEs leading to discontinuation or leading to death. AEs were graded for severity according to the National Cancer Institute Common Terminology Criteria (NCI CTCAE), V 3.0: Grade 1: Mild; Grade 2: Moderate; Grade 3: Severe (prevents normal everyday activities); Grade 4: Life-threatening or disabling; Grade 5: Death. (NCT00765102)
Timeframe: up to 9 months

Intervention	participants (Number)
	At least 1 TEAE	At least 1 drug-related TEAE	At least 1 Romidepsin-related TEAE	At least 1 Bortezomib-related TEAE	At least 1 >=Grade 3 TEAE	At least 1 Grade 4 TEAE	At least 1 serious TEAE	At least 1 TEAE leading to discontinuation	At least 1 TEAE leading to death
Romidepsin + Bortezomib	32	30	28	30	28	5	14	6	2

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Area Under the Concentration-time Curve From Time 0 Extrapolated to Infinity (AUC0-∞)

AUC (0 - ∞) = Area under the plasma concentration versus time curve (AUC) from time zero (pre-dose) to extrapolated infinite time (0 - ∞) of Romidepsin based on plasma samples. (NCT00765102)
Timeframe: Day 1 (cycle 1): 1 hour prior to romidepsin administration, 0.25, 0.5, 1, 2, 3, 4, 6, and 24 hours after initiation of romidepsin infusion

Intervention	ng*hr/mL (Geometric Mean)
Romidepsin 8 mg/m^2 + Bortezomib	1209.1
Romidepsin 10 mg/m^2 + Bortezomib	1149.5

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Maximum Observed Concentration (Cmax)

Maximum observed concentration of Romidepsin (NCT00765102)
Timeframe: Day 1 (cycle 1): 1 hour prior to romidepsin administration, 0.25, 0.5, 1, 2, 3, 4, 6, and 24 hours after initiation of romidepsin infusion

Intervention	ng/mL (Geometric Mean)
Romidepsin 8 mg/m^2 + Bortezomib	913.9
Romidepsin 10 mg/m^2 + Bortezomib	1002.7

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Terminal Half-life (t1/2)

Terminal half-life of Romidepsin (NCT00765102)
Timeframe: Day 1 (cycle 1): 1 hour prior to romidepsin administration, 0.25, 0.5, 1, 2, 3, 4, 6, and 24 hours after initiation of romidepsin infusion

Intervention	hr (Geometric Mean)
Romidepsin 8 mg/m^2 + Bortezomib	4.1
Romidepsin 10 mg/m^2 + Bortezomib	3.6

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Time to Maximum Observed Concentration (Tmax)

Time to maximum observed concentration of Romidepsin (NCT00765102)
Timeframe: Day 1 (cycle 1): 1 hour prior to romidepsin administration, 0.25, 0.5, 1, 2, 3, 4, 6, and 24 hours after initiation of romidepsin infusion

Intervention	hr (Median)
Romidepsin 8 mg/m^2 + Bortezomib	1.04
Romidepsin 10 mg/m^2 + Bortezomib	0.58

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Total Clearance (CL)

Total clearance of Romidepsin (NCT00765102)
Timeframe: Day 1 (cycle 1): 1 hour prior to romidepsin administration, 0.25, 0.5, 1, 2, 3, 4, 6, and 24 hours after initiation of romidepsin infusion

Intervention	L/hr (Geometric Mean)
Romidepsin 8 mg/m^2 + Bortezomib	11.3
Romidepsin 10 mg/m^2 + Bortezomib	16.4

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Total Volume of Distribution (Vz)

Total volume of distribution of Romidepsin (NCT00765102)
Timeframe: Day 1 (cycle 1): 1 hour prior to romidepsin administration, 0.25, 0.5, 1, 2, 3, 4, 6, and 24 hours after initiation of romidepsin infusion

Intervention	L (Geometric Mean)
Romidepsin 8 mg/m^2 + Bortezomib	66.5
Romidepsin 10 mg/m^2 + Bortezomib	85.9

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Number of Patients in Each Group With Any of the Following: Rejection Reversal or Recurrent Rejection

"Rejection Reversal is a return of serum creatinine to within 115% of the baseline value, or histologic reversal occurring within 14 days of initiation of treatment.~Recurrent Rejection is histologic evidence of rejection noted on a biopsy specimen obtained up to 3 months after documented rejection reversal." (NCT00771875)
Timeframe: 1 year

Intervention	participants (Number)
	Rejection Recurrence	Rejection Reversal
Rabbit Antithymocyte Globulin (RATG)	0	2
RATG/Bortezomib	0	1
RATG/Rituximab	0	1

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Mean Serum Creatinine

Renal allograft function as determined by change (∆) in Calculated creatinine clearance by Cockcroft-Gault at 7, 14, 28, 60, and 90 days and 1 year post therapy initiation (NCT00771875)
Timeframe: 7, 14, 28, 60, 90 days and 1 year post therapy initiation

Intervention	mg/dL (Mean)
	7 days	14 days	28 days	60 days	90 days	1 year
Rabbit Antithymocyte Globulin (RATG)	3.04	3.25	2.9	2.62	2.48	2.19
RATG/Bortezomib	2.31	2.20	2.18	2.38	2.13	2.87
RATG/Rituximab	2.32	2.35	2.35	2.32	2.12	2.07

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Renal Allograft Survival

(NCT00771875)
Timeframe: 1 year after rejection treatment

Intervention	participants (Number)
Rabbit Antithymocyte Globulin (RATG)	7
RATG/Rituximab	7
RATG/Bortezomib	10

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Number of Patients With Allografts With C4d Focal Positive Pretreatment Biopsy

(NCT00771875)
Timeframe: Day 1

Intervention	participants (Number)
Rabbit Antithymocyte Globulin (RATG)	2
RATG/Rituximab	2
RATG/Bortezomib	4

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Incidence of Post Transplant Lymphoproliferative Disorder (PTLD)

(NCT00771875)
Timeframe: 1 year

Intervention	participants (Number)
Rabbit Antithymocyte Globulin (RATG)	0
RATG/Rituximab	0
RATG/Bortezomib	0

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Incidence of Death

(NCT00771875)
Timeframe: 90 days

Intervention	participants (Number)
Rabbit Antithymocyte Globulin (RATG)	0
RATG/Rituximab	0
RATG/Bortezomib	0

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Number of Patients With Allografts With C4d Diffuse Positive Pretreatment Biopsy

(NCT00771875)
Timeframe: 90 days

Intervention	participants (Number)
Rabbit Antithymocyte Globulin (RATG)	3
RATG/Rituximab	3
RATG/Bortezomib	5

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Overall Survival (OS)

Overall survival (OS) will be measured as the time from date of enrollment to death from any cause. For patients who remain alive, survival time will be censored at the date of last contact. (NCT00772668)
Timeframe: Up to 5 years

Intervention	months (Number)
RCVELP	NA

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Progression-free Survival (PFS)

Progression free-survival will be assessed according to according to the International Workshop Criteria (IWC). Progression-free survival will be measured as the time from date of enrollment to relapse, progression or death due to follicular lymphoma (FL) or marginal zone lymphoma (MZL), whichever occurs first. Participants who do not experience relapse or progression, and those who die from causes other than cancer, will be censored at the date of last contact. (NCT00772668)
Timeframe: Up to 5 years

Intervention	months (Number)
RCVELP	NA

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Rate of Toxicity in Study Participants

Safety and tolerance to protocol therapy as evidenced by the rate of toxicity (serious adverse events and study-related adverse events) in study participants (NCT00772668)
Timeframe: Up to 5 years

Intervention	participants (Number)
RCVELP	1

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Overall Survival

Overall survival was measured from the start of the treatment to death due to any cause. Overall Survival is represented as the number of deaths per 100-person- months and was computed by dividing the number of participants with an event of death that occurred during the study follow-up period by the total duration of follow-up (in 100 months) for all the participants in each cohort since participants had different lengths of follow-up. (NCT00773747)
Timeframe: From randomization up to 32 months (final study analysis)

Intervention	Events/100-person Months (Number)
Vorinostat + Bortezomib	1.7
Placebo + Bortezomib	1.9

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Objective Response Rate

Objective response rate was measured as the proportion of patients who achieved a confirmed partial response or better during the course of the study. Response to study therapy was assessed using EBMT Criteria and confirmed by Independent Adjudication Review. (NCT00773747)
Timeframe: Baseline and at the end of each 21-day Cycle assessed up to 32 months (final study analysis)

Intervention	Percentage of Participants (Number)
Vorinostat + Bortezomib	56.2
Placebo + Bortezomib	40.6

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Progression-Free Survival (PFS)

Progression-free survival was measured from the start of the treatment to the time when the criteria for progression was met or death due to any cause (whichever is first recorded). Response to study therapy was assessed using European Blood and Marrow Transplantation Group (EBMT) Criteria. A stratified Cox proportional hazards model was used with Efron's likelihood approximation to account for ties in event times. (NCT00773747)
Timeframe: From randomization to event of disease progression or death assessed up to 32 months (final study analysis)

Intervention	Months (Median)
Vorinostat + Bortezomib	7.63
Placebo + Bortezomib	6.83

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Time to Progression

Time to progression was measured from the start of the treatment to the time when the criteria for progression was met or death due to myeloma (whichever is first recorded). Response to study therapy was assessed using European Blood and Marrow Transplantation Group (EBMT) Criteria. A stratified Cox proportional hazards model was used with Efron's likelihood approximation to account for ties in event times. (NCT00773747)
Timeframe: Baseline and at the end of each 21-day Cycle assessed up to 32 months (final study analysis)

Intervention	Months (Median)
Vorinostat + Bortezomib	7.73
Placebo + Bortezomib	7.03

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Number of Participants With Grade 3-5 Clinical or Laboratory Adverse Events (AEs)

An adverse event (AE) was defined as any untoward medical occurrence in a participant administered a pharmaceutical product and which did not necessarily have to have a causal relationship with this treatment. An AE could therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal product/protocol-specified procedure, whether or not considered related to the medicinal product/protocol-specified procedure. Any worsening of a preexisting condition temporally associated with the use of the product was also an AE. Grades come from the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 3.0. Per protocol, clinical and laboratory AEs are presented as a combined total for each grade. (NCT00773747)
Timeframe: Up to 722 days

Intervention	Participants (Count of Participants)
	Grade 3	Grade 4	Grade 5
Placebo + Bortezomib	240	85	17
Vorinostat + Bortezomib	272	108	11

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Objective Response Rate (RR)

Objective RR was defined as percentage (%) of participants with complete response (CR: disappearance of original monoclonal (M) paraprotein from blood & urine on at least 2 determinations for at least 6 weeks (WKs) by immunofixation studies, <5% plasma cells in bone marrow on at least 1 determination, no increase in size/number of lytic bone lesions (LBLs) & disappearance of soft tissue plasmacytomas (STP) for at least 6 WKs on skeletal survey (SS) if available) or partial response (PR: ≥50% reduction in serum M protein for at least 2 determinations 6 WKs apart, if present, reduction in 24-hour urinary light chain excretion by ≥90% or ≤200 mg for at least 2 determinations 6 WKs apart, ≥50% reduction in STP size for at least 6 WKs, & no increase in size/number of LBLs on SS if available) as assessed by Independent Adjudication Committee (IAC) per European Blood & Marrow Transplant (EBMT) criteria. To report RR & 95% confidence intervals (CIs), exact test of binomial parameter was used. (NCT00773838)
Timeframe: Up to approximately 30 months (through Final Analysis data cut-off of 16-May-2011)

Intervention	Percentage of Participants (Number)
Vorinostat + Bortezomib	11.3

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TTP as Assessed by Investigator Per EBMT Criteria

TTP was defined as the time from allocation to the first documented PD as assessed by investigator per EBMT criteria or death due to myeloma, whichever occurred first. PD: >25% increase in level of serum Mparaprotein, which must also be an absolute increase of at least 5g/L (500 mg/dL) and confirmed on a repeat investigation or 25% increase in 24-hour urinary light chain excretion, which must also be an absolute increase of at least 200mg/24hour and confirmed on a repeat investigation or >25% increase in plasma cells in a bone marrow aspirate or on trephine biopsy, which must also be an absolute increase of at least 10% or definitive increase in size of existing LBLs or STP or development of hypercalcemia (corrected serum calcium >11.5 mg/dL or 2.8 mmol/L not attributable to any other cause). To report the median TTP (in months) and associated 95% CIs Kaplan-Meier method was used. (NCT00773838)
Timeframe: Up to approximately 30 months (through Final Analysis data cut-off of 16-May-2011)

Intervention	Months (Median)
Vorinostat + Bortezomib	3.07

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Number of Participants Who Discontinued Study Treatment Due to an AE

An AE is defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the Sponsor's product, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which is temporally associated with the use of the Sponsor's product, is also an AE. The number of participants who discontinued study treatment due to an AE were reported. (NCT00773838)
Timeframe: Up to approximately 18 months

Intervention	Participants (Count of Participants)
Vorinostat + Bortezomib	28

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Number of Participants Who Experienced an Adverse Event (AE)

An AE is defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the Sponsor's product, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which is temporally associated with the use of the Sponsor's product, is also an AE. The number of participants who experienced an AE were reported. (NCT00773838)
Timeframe: Up to approximately 22 months

Intervention	Participants (Count of Participants)
Vorinostat + Bortezomib	142

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Progression-Free Survival (PFS) as Determined by IAC Per EBMT Criteria

PFS was defined as the time from allocation to the first documents PD as determined by IAC per EBMT criteria or death due to any cause, whichever occurs first. PD: >25% increase in level of serum M-paraprotein, which must also be an absolute increase of at least 5g/L (500 mg/dL) and confirmed on a repeat investigation or 25% increase in 24-hour urinary light chain excretion, which must also be an absolute increase of at least 200mg/24hour and confirmed on a repeat investigation or >25% increase in plasma cells in a bone marrow aspirate or on trephine biopsy, which must also be an absolute increase of at least 10% or definitive increase in size of existing LBLs or STP or development of hypercalcemia (corrected serum calcium >11.5 mg/dL or 2.8 mmol/L not attributable to any other cause). To report the median PFS (in months) and associated 95%CIs Kaplan-Meier method was used. (NCT00773838)
Timeframe: Up to approximately 30 months (through Final Analysis data cut-off of 16-May-2011)

Intervention	Months (Median)
Vorinostat + Bortezomib	3.13

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PFS as Assessed by Investigator Per EBMT Criteria

PFS was defined as the time from allocation to the first documents PD as assessed by investigator per EBMT criteria or death due to any cause, whichever occurs first. PD: >25% increase in level of serum M-paraprotein, which must also be an absolute increase of at least 5g/L (500 mg/dL) and confirmed on a repeat investigation or 25% increase in 24-hour urinary light chain excretion, which must also be an absolute increase of at least 200mg/24hour and confirmed on a repeat investigation or >25% increase in plasma cells in a bone marrow aspirate or on trephine biopsy, which must also be an absolute increase of at least 10% or definitive increase in size of existing LBLs or STP or development of hypercalcemia (corrected serum calcium >11.5 mg/dL or 2.8 mmol/L not attributable to any other cause). To report the median PFS (in months) and associated 95%CIs Kaplan-Meier method was used. (NCT00773838)
Timeframe: Up to approximately 30 months (through Final Analysis data cut-off of 16-May-2011)

Intervention	Months (Median)
Vorinostat + Bortezomib	2.83

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Overall Survival (OS)

OS was defined as the time from allocation to death due to any cause. To report the median survival (in months) and the associated 95%CIs were reported using Kaplan-Meier method was used. Participants without documented death at the time of final analysis were censored at the date of the last follow up. (NCT00773838)
Timeframe: Up to approximately 40 months (through End of Trial data cut-off of 09-Apr-2012)

Intervention	Months (Median)
Vorinostat + Bortezomib	11.23

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Time To Disease Progression (TTP) as Determined by IAC Per EBMT Criteria

TTP was defined as the time from allocation to the first documented disease progression (PD) as determined by IAC per EBMT criteria or death due to myeloma, whichever occurred first. PD: >25% increase in level of serum Mparaprotein, which must also be an absolute increase of at least 5g/L (500 mg/dL) and confirmed on a repeat investigation or 25% increase in 24-hour urinary light chain excretion, which must also be an absolute increase of at least 200mg/24hour and confirmed on a repeat investigation or >25% increase in plasma cells in a bone marrow aspirate or on trephine biopsy, which must also be an absolute increase of at least 10% or definitive increase in size of existing LBLs or STP or development of hypercalcemia (corrected serum calcium >11.5 mg/dL or 2.8 mmol/L not attributable to any other cause). To report the median TTP (in months) and associated 95% CIs Kaplan-Meier method was used. (NCT00773838)
Timeframe: Up to approximately 30 months (through Final Analysis data cut-off of 16-May-2011)

Intervention	Months (Median)
Vorinostat + Bortezomib	3.47

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Antibody-mediated Rejection by Banff '97 Criteria (Updated 2005)

"Antibody mediated rejection demonstrated to be due to, atleast in part, to anti-donor antibody at 6 months by Banff 97' criteria. Rejection due, at least in part, to documented anti-donor antibody ('suspicious for' if antibody not demonstrated); may coincide with categories 3, 4 and 5.~Grade I. ATN-like - C4d+, minimal inflammation Grade II. Capillary- margination and/or thromboses, C4d+ Grade III. Arterial - v3, C4d+" (NCT00782821)
Timeframe: 6 months

Intervention	participants (Number)
Rabbit Antithymocyte Globulin (RATG)	1
RATG/Rituxan	0
RATG/Velcade	3
RATG/Rituxan/Velcade	1

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Acute Cellular Rejection by Banff '97 Criteria (Updated 2005)

"Acute cellular rejection IA - cases with significant interstitial infiltration (>25% of parenchyma affected) and foci of moderate tubulitis (>4 mononuclear cells/tubular cross section or group of 10 tubular cells).~IB - cases with significant interstitial infiltration (>25% of parenchyma affected) and foci of severe tubulitis (>10 mononuclear cells/tubular cross section or group of 10 tubular cells) IIA - cases with mild to moderate intimal arteritis (v1) IIB - cases with server intimal arteritis comprising >25% of the luminal area (v2) III - case with transmural arteritis and/or arterial fibrinoid change and necrosis of medical smooth muscle cells (v3 with accompanying lymphoctic inflammation)" (NCT00782821)
Timeframe: 6 months

Intervention	participants (Number)
Rabbit Antithymocyte Globulin (RATG)	1
RATG/Rituxan	0
RATG/Velcade	1
RATG/Rituxan/Velcade	0

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Patient Allograft Survival at 12 Months

Patient's allograft was still functioning at 12 months post study enrollment (NCT00782821)
Timeframe: 12 months

Intervention	participants (Number)
Rabbit Antithymocyte Globulin (RATG)	10
RATG/Rituxan	10
RATG/Velcade	9
RATG/Rituxan/Velcade	9

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Incidence of Acute Rejection (Banff '97) or Antibody Mediated Rejection

"Antibody mediated rejection demonstrated to be due to, atleast in part, to anti-donor antibody at 6 months by Banff 97' criteria.~Acute rejection IA - cases with significant interstitial infiltration (>25% of parenchyma affected) and foci of moderate tubulitis (>4 mononuclear cells/tubular cross section or group of 10 tubular cells).~IB - cases with significant interstitial infiltration (>25% of parenchyma affected) and foci of severe tubulitis (>10 mononuclear cells/tubular cross section or group of 10 tubular cells) IIA - cases with mild to moderate intimal arteritis (v1) IIB - cases with server intimal arteritis comprising >25% of the luminal area (v2) III - case with transmural arteritis and/or arterial fibrinoid change and necrosis of medical smooth muscle cells (v3 with accompanying lymphoctic inflammation)" (NCT00782821)
Timeframe: 6 months

Intervention	participants (Number)
Rabbit Antithymocyte Globulin (RATG)	2
RATG/Rituxan	0
RATG/Velcade	5
RATG/Rituxan/Velcade	3

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Patient Survival at 12 Months

Patient was still alive 12 months post study enrollment. (NCT00782821)
Timeframe: 12 months

Intervention	participants (Number)
Rabbit Antithymocyte Globulin (RATG)	10
RATG/Rituxan	10
RATG/Velcade	10
RATG/Rituxan/Velcade	9

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The Maximum Tolerated Dose of Bortezomib (MTD)

The Maximum Tolerated Dose of Bortezomib (MTD) Will be Defined as the Dose Level Prior to That Resulting in Two Out of Six Patients Experiencing a DLT (NCT00784823)
Timeframe: During dosing of Bortezomib on Day -4 to Day -1 of ASCT

Intervention	mg/m2 of bortezomib (Number)
Combined Dose Intense Melphalan With Bortezomib (MTD)	1.6

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Response Rate of the Combination of Bortezomib and Melphalan in Patients With AML and High-risk MDS.

Determine disease response to treatment using Cheson 2000 report of an international working group to standardize response criteria for myelodysplastic syndromes. (NCT00789256)
Timeframe: Post Cycle 1 through 28 days post-treatment

Intervention	participants (Number)
Strata 1	5
Strata 2	2

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Number of Participants Surviving at 1 Year

(NCT00790647)
Timeframe: one year from transplant

Intervention	participants (Number)
Stem Cell Transplantation With Bortezomib and Melphalan	9

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Number of Participants Surviving at 100 Days From Transplant

(NCT00790647)
Timeframe: 100 Days from transplant date

Intervention	participants (Number)
Stem Cell Transplant With Bortezomib and Melphalan	9

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Number of Participants With Hematologic Response

"complete and partial hematologic response defined as: Complete response: absence of detectable monoclonal protein in serum and urine, and bone marrow biopsy <5% plasma cells with no clonal predominance of kappa or lambda isotype.~Partial response: any one of the following~For patients with detectable and quantifiable marrow plasmacytosis, a reduction of 50% or more in plasma cells as a percentage of nucleated bone marrow cells.~For patients with a detectable monoclonal peak on serum protein electropheresis or urine protein electropheresis, a reduction in the peak height of 50% or more.~For patients with quantifiable urinary kappa or lambda chain concentration, a reduction in daily light chain excretion (concentration x 24-hr urine volume)." (NCT00790647)
Timeframe: one year

Intervention	participants (Number)
Stem Cell Transplant With Bortezomib and Melphalan	6

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Number of Participants Surviving at 2 Years

(NCT00790647)
Timeframe: 2 years from transplant

Intervention	Participants (Count of Participants)
Stem Cell Transplant With Bortezomib and Melphalan	9

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One Year Overall Survival

One year overall survival estimated using the product-limit method of Kaplan and Meier. Defined as the percentage of patients alive at year one after starting treatment. (NCT00792142)
Timeframe: From date of treatment initiation until death from any cause, assessed up to one year.

Intervention	percentage of participants (Number)
Treatment (Stem Cell Transplant, Maintenance Treatment)	95

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One Year Progression-free Survival (PFS)

"PFS estimated using the product-limit method of Kaplan and Meier. Defined as the percentage of patients progression-free at year one after starting treatment.~International Myeloma Working Group uniform response criteria for disease progression:~Increase of > 25% from baseline in Serum M-component and/or (the absolute increase must be > 0.5 g/dl); Urine M-component and/or (the absolute increase must be > 200 mg/24 h; Only in patients without measurable serum and urine M-protein levels:~the difference between involved and uninvolved FLC levels. The absolute increase must be >l0mg/dl.~Bone marrow plasma cell percentage: the absolute % must be > 10%C; Definite development of new bone lesions or soft tissue plasmacytomas.~or definite increase in the size of existing bone lesions or soft tissue plasmacytomas Development of hypercalcemia (corrected serum calcium >11.5 mg/dl or 2.65 mmol/l) that can be attributed solely to the plasma cell proliferative disorder." (NCT00792142)
Timeframe: From start of treatment initiation until disease progression, relapse or death from any cause, assessed up to 1 year.

Intervention	percentage of participants (Number)
Treatment (Stem Cell Transplant, Maintenance Treatment)	88

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Number of Participants With Adverse Events

All grade 3 and above treatment-related adverse events (AEs) during bortezomib/dexamethasone treatment cycles. (NCT00792142)
Timeframe: After 4 months of maintenance therapy

Intervention	Participants (Count of Participants)
	Leukopenia	Lymphopenia	Neutropenia	Thrombocytopenia	Cataract	Fatigue	Upper respiratory infection	Anxiety	Pain in extremity	Sinus bradycardia	Hyperglycemia	Hypophosphatemia
Treatment (Stem Cell Transplant, Maintenance Treatment)	1	13	2	1	1	2	1	1	1	1	4	3

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Number of Patients Surviving Overall

Number of subjects surviving two years post autologous transplant. (NCT00793572)
Timeframe: At 2 years after the autograft

Intervention	Participants (Count of Participants)
Tandem Auto-/Nonmyeloablative Allo-HCT and Maintenance Therapy	21

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Number of Patients Surviving Progression-free

"Number of subjects surviving without progressive disease post-transplant.~Progressive disease criteria:~Greater than 25% increase in serum (absolute increase must be ≥0.5 g/dL) or urine (absolute increase must be ≥200 mg/24h) M proteins compared to best response status after autologous transplant.~Appearance of new lytic bone lesions or plasmacytomas." (NCT00793572)
Timeframe: At 2 years after the autograft

Intervention	Participants (Count of Participants)
Tandem Auto-/Nonmyeloablative Allo-HCT and Maintenance Therapy	14

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Number of Patients With Chronic GVHD

Number of subjects with classic chronic or chronic extensive GVHD post allogeneic transplant. (NCT00793572)
Timeframe: 1 year post allo

Intervention	Participants (Count of Participants)
Tandem Auto-/Nonmyeloablative Allo-HCT and Maintenance Therapy	10

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Number of Patients With Toxicities Related to Bortezomib Maintenance Therapy

Number of subjects with toxicities related to bortezomib maintenance therapy post-transplant. (NCT00793572)
Timeframe: Up to 100 days after the autograft or allograft

Intervention	Participants (Count of Participants)
Tandem Auto-/Nonmyeloablative Allo-HCT and Maintenance Therapy	1

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Number of Patients With Non-relapse Mortality

Number of subjects with non-relapse mortalities post allogeneic transplant. (NCT00793572)
Timeframe: 200 and 365 days after allo

Intervention	Participants (Count of Participants)
	200 days post allo	1 Year post allo
Tandem Auto-/Nonmyeloablative Allo-HCT and Maintenance Therapy	1	1

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Number of Patients With Grade II-IV Acute GVHD

"Number of patients who developed acute GVHD post allogeneic transplant.~aGVHD Stages~Skin:~- a maculopapular eruption involving < 25% BSA~- a maculopapular eruption involving 25 - 50% BSA~- generalized erythroderma~- generalized erythroderma w/ bullous formation and often w/ desquamation~Liver:~- bilirubin 2.0 - 3.0 mg/100 mL~- bilirubin 3 - 5.9 mg/100 mL~- bilirubin 6 - 14.9 mg/100 mL~- bilirubin > 15 mg/100 mL~Gut:~Diarrhea is graded 1 - 4 in severity. Nausea and vomiting and/or anorexia caused by GVHD is assigned as 1 in severity. The severity of gut involvement is assigned to the most severe involvement noted. Patients with visible bloody diarrhea are at least stage 2 gut and grade 3 overall.~aGVHD Grades Grade II: Stage 1 - 2 skin w/ no gut/liver involvement Grade III: Stage 2 - 4 gut involvement and/or stage 2 - 4 liver involvement Grade IV: Pattern and severity of GVHD similar to grade 3 w/ extreme constitutional symptoms or death" (NCT00793572)
Timeframe: 100 days post allo transplant

Intervention	Participants (Count of Participants)
Tandem Auto-/Nonmyeloablative Allo-HCT and Maintenance Therapy	14

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Safety and Engraftment

Peripheral blood progenitor cells were collected with either chemo-mobilization (27 of 39, 69%) or growth factor mobilization (12 of 39, 31%). Patients received an average of 9.0 × 10^6/kg CD34+ cells (range, 2.3-65) as their transplant graft. (NCT00793650)
Timeframe: Day 30 after transplant

Intervention	days (Median)
	Median time for platelet recovery	Median time for neutrophil recovery
Bortezomib After HD melphalanAll	16	12
Bortezomib Before HD Melphalan	16	12

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Response Rate Using EBMT(European Group for Blood and Bone Marrow Transplan) Criteria at Day +100 After Transplant.

"CR :Negative immunofixation on the serum and urine and Disappearance of any soft tissue plasmacytomas and <=5% plasma cells in bone marrow.~VGPR: Serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein plus urine M-protein level <100mg per 24 hour.~Partial Response:>=50% reduction of serum M-protein and reduction in 24-hour urinary M-protein by >=90% or to <200mg per 24 hour." (NCT00793650)
Timeframe: 100 days after transplant

Intervention	participants (Number)
	Complete response (CR)	VGPR-Very good partial remission	Partial Response
Bortezomib After Melphalan	6	11	7
Bortezomib Before Melphalan	2	9	6

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Three-month Progression-free Survival

"Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST), as a 20% increase in the sum of the longest diameter of target lesions, taking as reference the smallest sum of the longest diameter recorded since the treatment started or the appearance of one or more new lesions." (NCT00798720)
Timeframe: Three-months post-treatment

Intervention	percentage of participants (Number)
Vorinostat + Bortezomib	11.1

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Median Overall Survival

(NCT00798720)
Timeframe: 5 years

Intervention	months (Median)
Vorinostat + Bortezomib	4.7

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Response Rate

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) for target lesions and assessed by MRI, CT, or chest x-ray: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR+PR. (NCT00798720)
Timeframe: Until disease progression, up to 2 years

Intervention	participants (Number)
	Partial response	Stable disease	Progressive disease
Vorinostat + Bortezomib	0	5	13

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Toxicity

Graded using the NCI Common Terminology Criteria for Adverse Events (CTCAE) version 3.0 (NCT00798720)
Timeframe: 30 days post-treatment

Intervention	participants (Number)
	Thrombocytopenia Grade 3	Thrombocytopenia Grade 4	Lymphopenia Grade 3	Fatigue Grade 3	Fatigue Grade 4	Vomiting Grade 3	Dizziness Grade 3	Syncope Grade 3	Neuropathy Grade 3	Hyponatremia Grade 3
Vorinostat + Bortezomib	7	1	3	4	1	2	2	2	2	3

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Number of Patients With Response

Computed tomography scans and/or Positron emission tomography (PET) scans obtained every two cycles to evaluate response using International Workshop Criteria of Complete Response, Partial Response, Progressive Disease, or Stable Disease. (NCT00810576)
Timeframe: Every two 21-day cycles

Intervention	participants (Number)
	Complete Response	Partial Response	Progressive Disease	Stable Disease
Vorinostat + Bortezomib	0	0	1	0

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Time to Progression of Disease

'Median time to progression of disease is assessed according to International Myeloma Working Group (IMWG) criteria or death from any cause. IMWG criteria: increase of >=25% from lowest level in Serum M-component or (the absolute increase must be >=0.5 gram per deciliter [g/dL]); Urine M component or (the absolute increase must be >=200 milligram per 24 hour. Only in participants without measurable serum and urine M-protein levels: the difference between involved and uninvolved free light chain levels. The absolute increase >10 mg/dL. Bone marrow plasma cell percentage >=10%. Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing. Development of hypercalcemia. Participants who died or dropped out due to any reason without progression will be censored with the day of death or drop-out, respectively and who are alive at the end of the study without any progression was censored with the last available date. (NCT00813150)
Timeframe: From the date of randomization until the disease progression or participant's death from any cause whichever occurred first, as assessed up to 72 weeks after end of treatment visit (ie, 46 days after last dose of study medication)

Intervention	Months (Median)
Vd (Bortezomib + Dexamethasone)	12.6
Vcd (Bortezomib + Low-dose Dexamethasone + Cyclophosphamide)	9.9

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Overall Survival (OS)

Time interval in months time from randomisation to death from any cause. (NCT00813150)
Timeframe: From the date of randomization until Month 49

Intervention	Months (Median)
Vd (Bortezomib + Dexamethasone)	NA
Vcd (Bortezomib + Low-dose Dexamethasone + Cyclophosphamide)	41.50

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Progression-Free Survival (PFS)

PFS is defined as time from randomization to myeloma progression according to International Myeloma Working Group (IMWG) criteria or death from any cause. IMWG criteria: increase of ≥25 percent from lowest response level in Serum M-component and/or (the absolute increase must be ≥0.5 g/dL) Urine M-component and/or (the absolute increase must be ≥200 mg/24 hour. Only in participants without measurable serum and urine M-protein levels: the difference between involved and uninvolved free light chain levels. The absolute increase must be >10 mg/dL. Bone marrow plasma cell percentage: the absolute percent must be ≥10 percent. Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas. Development of hypercalcemia (corrected serum calcium >11.5 mg/dL or 2.65mmol/L) that can be attributed solely to the plasma cell proliferative disorder. PFS included disease progression as well as death. (NCT00813150)
Timeframe: From the date of randomization until the disease progression or participant's death from any cause whichever occured first, as assessed up to 72 weeks after end of treatment visit (ie, 46 days after last dose of study medication)

Intervention	Months (Median)
Vd (Bortezomib + Dexamethasone)	12.6
Vcd (Bortezomib + Low-dose Dexamethasone + Cyclophosphamide)	9.9

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Overall Response Rate (ORR) - International Myeloma Working Group (IMWG) Response Criteria

Percentage of participants who achieved stringent complete response (sCR), complete response (CR), very good partial response (VGPR) or partial response (PR) is reported in the below table. IMWG criteria- CR: Negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and <5% plasma cells in bone marrow; sCR: CR+Normal free light chain ratio and absence of clonal cells in bone marrow by immunohistochemistry or immunofluorescencec; PR: ≥50% reduction of serum M-protein and reduction in 24-hour urinary M-protein by ≥90%; VGPR: Serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein plus urine M-protein level <100mg per 24 hour. (NCT00813150)
Timeframe: Up to 46 days after last bortezomib dose, or as soon as possible after early discontinuation of study treatment or before start of alternative anti-myeloma therapy

Intervention	Percentage of participants (Number)
Vd (Bortezomib + Dexamethasone)	74.4
Vcd (Bortezomib + Low-dose Dexamethasone + Cyclophosphamide)	70.2

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Proportion of Patients Tolerating >50% Steroid Dose Reduction After a 15 Week Course of Bortezomib Plus Prednisone in Patients With cGVHD

The participants' total daily steroid dose was recorded at baseline and after a 15 week course of treatment. Starting at a dose of 0.5-1 mg/kg, dose reduction of steroids was permitted after 1 cycle of therapy. The suggested taper was 10-25% every 1-2 weeks. . (NCT00815919)
Timeframe: After 15 weeks of bortezomib plus prednisone therapy

Intervention	participants (Number)
Velcade (Bortezomib)	14

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Overall Response Rate After a 15 Week Course of Bortezomib Plus Prednisone in Patients With cGVHD

"Participants had their cGVHD evaluated per NIH consensus criteria:~Complete response: resolution of all reversible manifestations of cGVHD.~Partial response: a decrease ≥ 1 point on a 3-point organ-specific scale or 2 points or more on a 10-point global scale without progression in any organ sites.~Stable disease: no evidence of cGVHD response without evidence of progressive cGVHD.~Progressive cGVHD: increase of ≥ 1 point on an organ-specific 3-point scale, addition of a new immunosuppressive agent prior to the completion of 15 weeks of combination therapy, or requirement an increase in the total daily dose of corticosteroids above a participant's baseline corticosteroid dose during the 15-week combined treatment period.~Mixed response: a response in primary sites of cGVHD involvement but interval progressive cGVHD in other organs or sites.~Responses were not scored for oral or ocular cGVHD, since topical therapies were permitted during the study." (NCT00815919)
Timeframe: Patients had their cGVHD assessed at Baseline and at 15 weeks or end of therapy

Intervention	participants (Number)
	Participants with a complete response in cGVHD	Participants with an partial response in cGVHD	Participants with stable cGVHD	Participants with progressive cGVHD	Participants with mixed response
Velcade (Bortezomib)	2	14	1	2	1

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Proportion of cGVHD Patients Requiring Prednisone by 1 Year After Therapy

Participants who were still being followed 1 year after the start of therapy had their prednisone dose recorded. (NCT00815919)
Timeframe: 1 year after the start of study treatment

Intervention	participants (Number)
	Participants still requiring prednisone	Participants off prednisone
Velcade (Bortezomib)	11	6

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Overall and cGVHD Progression-free Survival by 1 Year After Therapy

(NCT00815919)
Timeframe: 2 years

Intervention	percentage of participants (Number)
	2-year Cum-incidence of Non-relapse mortality	2-year Cum-incidence of malignant relapse	2 year progression-free survival	2-year Overall survival
Velcade (Bortezomib)	14	14	73	73

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The Toxicity of a 15 Week Course of Bortezomib Plus Prednisone in Patients With cGVHD

Participants' toxicities were graded based on the CTCAE version 3.0. The toxicities were then given an attribution to the velcade treatment: unrelated, unlikely, possible, probable, definite. (NCT00815919)
Timeframe: Toxicities were collected from the start of treatment through 15 weeks of therapy or end of study treatmetn

Intervention	participants (Number)
	Participants with >= Grade 3, unrelated/unlikely	Participants with >= Grade 3, possible	Participants with >= Grade 3, probable/definite
Velcade (Bortezomib)	7	1	0

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Number of Patients by Best Clinical Response

Assessed by the International Working Group response criteria: Complete Remission - <5% myeloblasts with normal maturation of all cell lines; Partial Remission - bone marrow blasts decreased by > 50% over pre-treatment but still >5%; and Hematologic Improvement - hemoglobin increase by > 1.5g/dl or decreased transfusions by at least 4/8 week period, platelet absolute increase of >30 X 10^9/L for those starting at >20 X 10^9/L . For those < 20 X 10^9 /L at baseline increase by 100%. (NCT00818649)
Timeframe: At Completion of Course 3 (Day 63)

Intervention	Patients (Number)
	Complete Remission	Progressive Disease	Stable Disease
Evaluable Patients	1	6	5

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Percentage of Participants With Complete Response + Partial Response in Relation to Cytogenetic Subgroups (Per-protocol Set)

Response rate was defined as the percentage of participants with response of combined CR+PR according to the EBMT criteria. As per the EBMT criteria, CR is defined as the absence of serum and urine monoclonal paraprotein and no increase in size or number of lytic bone lesions; PR is defined as not all CR criteria and 50 percentage or more reduction in serum monoclonal paraprotein. Percentage of participants with complete or partial response that carried the indicated cytogenetic marker is reported. Same participant could count in more than one category due to multiple responses possible. (NCT00833560)
Timeframe: Up to Day 63

Intervention	Percentage of participants (Number)
	13q- (n=92)	t (4;14) (n=34)	17p- (n=24)	Other (n=87)	No changes (n=87)
Cyclophosphamide + Bortezomib + Dexamethasone	92.4	91.2	87.5	88.5	85.1

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Participants With Complete Response (CR) + Partial Response (PR) (Per-protocol Analysis Set)

CR and PR are defined by the local investigator according to the current European Group for Blood and Marrow Transplantation (EBMT) criteria. According to EBMT criteria, CR is defined as the absence of serum and urine monoclonal paraprotein + no increase in size or number of lytic bone lesions; and PR is defined as not all CR criteria + 50 percentage or more reduction in serum monoclonal paraprotein. (NCT00833560)
Timeframe: Up to Day 63

Intervention	Participants (Number)
Cyclophosphamide + Bortezomib + Dexamethasone	284

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Percentage of Participants With Complete Response + Partial Response in Relation to Cytogenetic Subgroups (Efficacy Set)

Intervention	Percentage of participants (Number)
	13q- (n=112)	t (4;14) (n=38)	17p- (n=31)	Other (n=104)	No changes (n=102)
Cyclophosphamide + Bortezomib + Dexamethasone	90.2	89.5	74.2	87.5	84.3

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Participants With Complete Response (CR) + Partial Response (PR) (Efficacy Set)

Intervention	Participants (Number)
Cyclophosphamide + Bortezomib + Dexamethasone	334

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Time to Disease Progression in Patients Who Progressed

Patients will be followed for initial response to therapy and for progression of disease. Response criteria will be scored according to International Myeloma Working Group uniform response criteria. (NCT00839956)
Timeframe: Up to 5 years

Intervention	years (Median)
Arm I (Bortezomib and Vorinostat)	2.1

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Median Follow-up Survival for All Patients

(NCT00839956)
Timeframe: Up to 5 years

Intervention	years (Median)
Arm I (Bortezomib and Vorinostat)	5.15

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Survival for All Patients

(NCT00839956)
Timeframe: Up to 5 years

Intervention	Participants (Count of Participants)
Arm I (Bortezomib and Vorinostat)	25

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Toxicity as Assessed by National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) v3.0

The first three months of therapy will be used as the time period in which toxicity will be evaluated and stopping rules for unacceptable toxicity will be implemented. Rules for stopping the study will be based on the rate of withdrawal due to significant toxicity (grade IV, non-hematological, non-metabolic, nonperipheral neuropathy). (NCT00839956)
Timeframe: The first three months of therapy

Intervention	Participants (Count of Participants)
Arm I (Bortezomib and Vorinostat)	0

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Maximum Tolerated Dose of This Combination of Drugs as Assessed by the NCI Common Terminology Criteria for Adverse Events (CTCAE) Version 3.0 (Cohort 1) [MTD Cyclophosphamide, MTD Bortezmib, MTD Docxorubicin]

If 3 patients of cohort 1 require dose reduction of one or more of the medications for toxicity attributed to the drug or drugs, then the starting dose level will be reduced for that drug or drugs for future patients. The initial dosing of drugs for cohort 2 will be permitted to be one dose level above the maximal tolerated doses of cohort 1. Note that this Outcome Measure shows MTD for cyclophosphamide, bortezomib and doxorubicin. MTD for dexamethasone is include in a separate table due to the different Unit of Measure. (NCT00849251)
Timeframe: Up to 90 days after initiation of study treatment

Intervention	mg/m2 (Number)
	MTD cyclophosphamide	MTD bortezomib	MTD liposomal doxorubicin
Relapsed Disease	300	1.6	30

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Maximum Tolerated Dose of This Combination of Drugs as Assessed by the NCI Common Terminology Criteria for Adverse Events (CTCAE) Version 3.0 (Cohort 1). [Dexamethasone MTD]

If 3 patients of cohort 1 require dose reduction of one or more of the medications for toxicity attributed to the drug or drugs, then the starting dose level will be reduced for that drug or drugs for future patients. The initial dosing of drugs for cohort 2 will be permitted to be one dose level above the maximal tolerated doses of cohort 1. Note that this Outcome Measure will only describe the MTD for dexamethasone. Dexamethasone could not be reported with the MTD for the other three drugs due to a different Unit of Measure. (NCT00849251)
Timeframe: Up to 90 days after initiation of study treatment

Intervention	mg (Number)
Relapsed Disease (Cohort I)	40

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Complete Response Rate

The proportion of response-evaluable subjects who achieved a confirmed complete response (CR) or complete response unconfirmed (CRu). Disease response and progression were evaluated according to modified International Workshop Response Criteria (IWRC) criteria by radiographic imaging and other procedures as necessary. (NCT00850499)
Timeframe: Up to 8 cycles (1 cycle is 35 days: 280 days)

Intervention	participants (Number)
Velcade + Fludarabine	2
Rituximab + Fludarabine	3

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Overall Response Rate

The proportion of subjects who achieve CR, CRu, or partial response (PR) relative to the response evaluable population. Disease response and progression were evaluated according to the modified IWRC criteria by radiographic imaging and other procedures as necessary. (NCT00850499)
Timeframe: Up to 8 cycles (1 cycle is 35 days: 280 days)

Intervention	participants (Number)
Velcade + Fludarabine	3
Rituximab + Fludarabine	6

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Number of Participants With an Adverse Event (AE)

The number of participants with ≥1 AE is reported. An AE is any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the study product(s), whether or not considered related to the use of the product(s). (NCT00858234)
Timeframe: Up to 346 days (up to 30 days after the final dose of study treatment)

Intervention	Participants (Count of Participants)
Vorinostat + Bortezomib	9

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Area Under the Plasma Concentration-Time Curve From 0 to 24 Hours Postdose (AUC0-24hr) of Vorinostat Administered With Bortezomib on Days 1 and 11

The AUC0-24hr of vorinostat in plasma on Days 1 and 11 is reported in participants who also received bortezomib. (NCT00858234)
Timeframe: Predose and 0.8, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 10, 12, and 24 hours postdose on Days 1 and 11

Intervention	µM*hr (Least Squares Mean)
	Day 1	Day 11
Vorinostat + Bortezomib	5.41	5.84

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Number of Participants With Dose-Limiting Toxicity (DLT) During Cycle 1

The number of participants with ≥1 DLT during Cycle 1 is reported. A DLT is defined as an event considered by the investigator to be related to study treatment, and either: 1) a Grade 3 or 4 non-hematologic event (except for manageable toxicity by supportive care or non-prohibited therapies, or a transient increase in alanine aminotransferase [ALT]/aspartate aminotransferase [AST]); or 2) a Grade 4 hematologic toxicity except neutropenia or hemoglobin decreased (neutropenia was a DLT if it was Grade 3-4 with fever ≥38.5°C; Grade 3-4 with an infection requiring antibiotic/antifungal therapy; or Grade 4 and lasting ≥5 days). (NCT00858234)
Timeframe: Up to 21 days

Intervention	Participants (Count of Participants)
Vorinostat + Bortezomib	1

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Number of Subject With Complete Response

Per standard lymphoma response criteria (Cheson): Complete Response (CR), 1. Complete disappearance of all detectable clinical and radiographic evidence of disease and disappearance of all disease related symptoms if present before therapy, with normalization of LDH if elevated prior to therapy. 2. All lymph nodes and masses must regress to normal size (<1.5 cm in greatest transverse diameter if >1.5 cm prior to treatment). 3. The spleen, if enlarged prior to therapy, must have regressed to normal size. 3. If bone marrow was involved by lymphoma, it must be cleared as documented by biopsy at the same location. (NCT00863369)
Timeframe: Up to 1 year

Intervention	Participants (Count of Participants)
Dose Level 1 Tx Schema I - Velcade 1.0 mg/m2, Gemcitabine 1000 mg/m2	1
Dose Level Tx Schema I -1 - Velcade 1.0 mg/m2, Gemcitabine 800 mg/m2	0
Dose Level 3B Tx Schema II - Velcade 1.0 mg/m2, Gemcitabine 800 mg/m2	0
Dose Level 4B Tx Schema II - Velcade 1.3 mg/m2, Gemcitabine 800 mg/m2	0
Dose Level 5B Tx Schema II - Velcade 1.3 mg/m2, Gemcitabine 1000 mg/m2	1
Dose Level 5B Tx Schema II - Velcade 1.3 mg/m2, Gemcitabine 1000 mg/m2, Rituximab 375 mg/m2	1

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Recommended Phase II Dose

The maximum tolerated dose (MTD) of Gemcitabine in combination with 1.3 mg/m2 of velcade on days 1 and 15 is based on toxicities observed during the first cycle and is defined as the highest dose tested in which fewer than 33% of patients experience an attributable DLT to the study drug, when at least 6 patients are treated at that dose and are evaluable for toxicity. Dose escalations proceeded according to a standard 3+3 design. (NCT00863369)
Timeframe: 28 days from start of treatment, up to 2 years.

Intervention	mg/m^2 (Number)
Treatment (Velcade, Gemcitabine Hydrochloride, Rituximab)	1000

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Number of Participants With at Least One Dose Limiting Toxicity (DLT)

Adverse events were graded by NCI CTCAE, Version 3.0. DLT defined as grade 4 thrombocytopenia, or grade 3 thrombocytopenia lasting greater than 7 days. Grade 4 neutropenia lasting 7 days or more despite use of growth factors. Febrile neutropenia only is it occurs after 7 days of neutropenia. Any grade 3 or higher non-hematologic toxicity related to the study drug, with the exception of alopecia, inadequately treated nausea, vomiting and/or diarrhea and fatigue. (NCT00863369)
Timeframe: 28 days from start of treatment, up to 2 years.

Intervention	Participants (Count of Participants)
Dose Level 1 Tx Schema I - Velcade 1.0 mg/m2, Gemcitabine 1000 mg/m2	3
Dose Level Tx Schema I -1 - Velcade 1.0 mg/m2, Gemcitabine 800 mg/m2	1
Dose Level 3B Tx Schema II - Velcade 1.0 mg/m2, Gemcitabine 800 mg/m2	0
Dose Level 4B Tx Schema II - Velcade 1.3 mg/m2, Gemcitabine 800 mg/m2	0
Dose Level 5B Tx Schema II - Velcade 1.3 mg/m2, Gemcitabine 1000 mg/m2	0
Dose Level 5B Tx Schema II - Velcade 1.3 mg/m2, Gemcitabine 1000 mg/m2, Rituximab 375 mg/m2	0

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Remission Duration Among Patients Who Respond to Treatment

(NCT00869323)
Timeframe: Day 1 to 8 Months Post Treatment

Intervention	months (Median)
Treated Study Participants	45

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Relapse-free Survival

(NCT00869323)
Timeframe: at 2 years

Intervention	participants (Number)
Treated Study Participants	2

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Overall Survival

(NCT00869323)
Timeframe: at 2 years

Intervention	participants (Number)
Treated Study Participants	1

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Number of Patients With Overall (Complete and Partial) Response Rates

(NCT00869323)
Timeframe: Day 1 to 2 Years Post Treatment

Intervention	participants (Number)
Treated Study Participants	2

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Time to Treatment Failure

(NCT00869323)
Timeframe: Day 1 to Time of Disease Progression

Intervention	months (Number)
Treated Study Participants	1

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Toxic Death Rate

The proportion of toxic death rate among all eligible patients. (NCT00873093)
Timeframe: 4 months

Intervention	percentage of participants (Number)
Overall	2.1

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Rate of Minimal Residual Disease (MRD) < 0.01% at End Block 1

Percentage of eligible and evaluable patients with MRD < 0.01% among those who had successful MRD determination at the end of Block 1. (NCT00873093)
Timeframe: End of Block 1 (Day 36 of Block 1) of re-induction therapy

Intervention	percentage of participants (Number)
Pre-B ALL Relapse 18-36 Mths From Dx (Chemotherapy)Age<=21 Yrs	35.4
Pre-B ALL Relapse <18 Mths From Dx (Chemotherapy) Age <=21 Yrs	25

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Rate of Minimal Residual Disease (MRD) < 0.01% at End Block 2

Percentage of eligible and evaluable patients with MRD < 0.01% among those who had successful MRD determination at the end of Block 2. (NCT00873093)
Timeframe: End of Block 2 (Day 36 of Block 2) of re-induction therapy

Intervention	percentage of participants (Number)
Pre-B ALL Relapse 18-36 Mths From Dx (Chemotherapy)Age<=21 Yrs	66.7
Pre-B ALL Relapse <18 Mths From Dx (Chemotherapy) Age <=21 Yrs	42.1

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Rate of Minimal Residual Disease (MRD) < 0.01% at End Block 3

Percentage of eligible and evaluable patients with MRD < 0.01% among those who had successful MRD determination at the end of Block 3. (NCT00873093)
Timeframe: End of Block 3 (Day 36 of Block 3) of re-induction therapy

Intervention	Percentage of participants (Number)
Pre-B ALL Relapse 18-36 Mths From Dx (Chemotherapy)Age<=21 Yrs	80
Pre-B ALL Relapse <18 Mths From Dx (Chemotherapy) Age <=21 Yrs	63.6

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Severe Adverse Events (SAE) Rate.

The proportion of SAE rate among all eligible patients (NCT00873093)
Timeframe: 4 months

Intervention	percentage of participants (Number)
Overall	8.2

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Event Free Survival

Percentage of patients who were event free at 4 months (NCT00873093)
Timeframe: 4 months after enrollment

Intervention	Percentage of participants (Number)
Pre-B ALL Relapse 18-36 Mths From Dx (Chemotherapy)Age<=21 Yrs	68.5
Pre-B ALL Relapse <18 Mths From Dx (Chemotherapy) Age <=21 Yrs	37.8

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Second Complete Remission Rate at the End of Block 1 Reinduction Chemotherapy

The percentage of eligible and evaluable patients who have achieved complete response at the end Block 1 of re-induction therapy. (NCT00873093)
Timeframe: The outcome is measured the end of Block 1 (Day 36 of Block 1) of re-induction therapy.

Intervention	Percentage of participants (Number)
Pre-B ALL Relapse 18-36 Mths From Dx (Chemotherapy)Age<=21 Yrs	72.2
Pre-B ALL Relapse <18 Mths From Dx (Chemotherapy) Age <=21 Yrs	63

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Response Rate of Plerixafor, Bortezomib, and Dexamethasone in Relapsed or Relapsed/ Refractory Multiple Myeloma (ORR) [Phase I and Phase II]

Overall response was established based on International Myeloma Working Group (IMWG) criteria with 6 potential categories: Complete Response (CR) which is a complete disappearance of monoclonal paraprotein based on negative immunofixation on the serum M-component and urine M-component and no evidence of myeloma in bone marrow, Very Good Partial Response (VGPR) defined as serum and urine M-component detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-component plus urine M-component <100 mg per 24 hours, Partial Response (PR) ≥50% reduction in serum M-component or ≥90% reduction urine M-component or urine M-component <200 mg per 24 hours, Minimal Response (MR) ≥25% reduction in serum or urine M-component, Stable Disease (SD) defined as failure to meet any response criteria, and Progressive Disease (PD) ≥ 25% increase from lowest value reported in serum M-component (absolute ≥0.5 g/dL) and/or urine M-component (absolute ≥200 mg/24 hours). (NCT00903968)
Timeframe: Disease was assessed for response every cycle on treatment. The maximum number of cycles received was 25.

,,,,,,,

Intervention	Participants (Count of Participants)
	Complete Response	Very Good Partial Response	Partial Response	Minimal Response	Stable Disease	Progressive Disease
All Phase II Participants	1	3	12	4	11	2
Phase I Dose Level 1	0	0	0	0	3	0
Phase I Dose Level 2	0	0	0	0	2	1
Phase I Dose Level 3	1	0	0	0	2	0
Phase I Dose Level 4	0	0	0	2	0	1
Phase I Dose Level 5	0	0	0	0	4	0
Phase I Dose Level 5B	0	0	1	1	3	1
Phase I Dose Level 6	0	1	0	0	2	0

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Time to Progression (TTP) [Phase II]

TTP estimated using the Kaplan-Meier method is defined as the time from registration to progression based on IMWG criteria or date last known progression-free for those who have not progressed. [Durie BG et al. Leukemia. 2006] Progression (PD): ≥ 25% increase from lowest value reported in serum M-component (absolute increase ≥0.5 g/dL) and/or urine M-component (absolute increase ≥200 mg/24 hours); if appropriate, a ≥25% increase above the lowest level in the difference between involved and uninvolved FLC levels (absolute increase >10 mg/dL); If none of these are measurable then ≥25% increase in bone marrow plasma cell percentage above the lowest response level (absolute ≥10%); Definite development of new bone lesions or soft tissue plasmacytomas OR increase in size of existing (NCT00903968)
Timeframe: DIsease was assessed to document progression every cycle on treatment and post-treatment every 12 weeks until progression.

Intervention	Months (Median)
All Phase II Participants	12.6

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Plerixafor Maximum Tolerated Dose (MTD) [Phase I]

The MTD plerixafor in combination with bortezomib is determined by the number of patients who experience a dose limiting toxicity (DLT). See subsequent primary outcome measure for the DLT definition. The MTD is defined as highest dose level at which fewer than one-third of patients experience a DLT. The MTD was reached at dose level 5B. The maximum tolerated dose of plerixafor was given on days 1, 2, 3, 6, 10, 13 of 21 each cycle. (NCT00903968)
Timeframe: Participants were assessed every 3 weeks while on study; The observation period for MTD evaluation was the first 21 days of treatment.

Intervention	ug/kg (Number)
All Phase I Particiapnts	320

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Number of Participants With Dose Limiting Toxicity (DLT) [Phase I]

A DLT was defined as (a) grade 3 or greater non-hematologic toxicity, considered by the investigator to be related to plerixafor or bortezomib, with the exception of nausea, vomiting or diarrhea unless receiving maximal medical therapy, (b) grade 4 hematologic toxicity defined as: thrombocytopenia with platelets <10,000 on more than one occasion within first cycle despite transfusion. Grade 4 neutropenia must occur for more than 5 days and/or result in neutropenic fever with elevated temperature (defined as > 101 degrees F). (c) inability to receive Day 1 dose for Cycle 2 due to toxicity. All adverse events were graded according to the CTEP Common Toxicity Criteria (CTCAE v.3.0). (NCT00903968)
Timeframe: Participants were assessed every 3 weeks while on study; The observation period for MTD evaluation was the first 21 days of treatment.

Intervention	Participants (Count of Participants)
Phase I Dose Level 1	0
Phase I Dose Level 2	0
Phase I Dose Level 3	0
Phase I Dose Level 4	0
Phase I Dose Level 5	0
Phase I Dose Level 5B	0
Phase I Dose Level 6	2

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Duration of Response (DOR) [Phase II]

DOR is defined as the time from response to disease progression or death, or date last known progression-free and alive for those who have not progressed or died. DOR was estimated using the Kaplan-Meier method. (NCT00903968)
Timeframe: DIsease was assessed to document response every cycle on treatment and post-treatment every 12 weeks until progression.

Intervention	Months (Median)
All Phase II Participants	12.9

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Bortezomib Maximum Tolerated Dose (MTD) [Phase I]

The MTD plerixafor in combination with bortezomib is determined by the number of patients who experience a dose limiting toxicity (DLT). See subsequent primary outcome measure for the DLT definition. The MTD is defined as highest dose level at which fewer than one-third of patients experience a DLT. The MTD was reached at dose level 5B. The maximum tolerated dose of bortezomib was given on days 3, 6, 10, 13 of 21 each cycle. (NCT00903968)
Timeframe: Participants were assessed every 3 weeks while on study; The observation period for MTD evaluation was the first 21 days of treatment.

Intervention	mg/m2 (Number)
All Phase I Particiapnts	1.3

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Time to Progression

Is calculated as the time from start of treatment to the date of the first observation of disease progression or relapse from CR. Deaths owing to causes other than progression not counted, but censored. Subjects who withdraw from the study or die will be censored at the time of last disease assessment. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0). (NCT00908232)
Timeframe: At Day 1 of each treatment cycle, at the End of Treatment visit until there is evidence of Progressive Disease or relapse from Complete Response (CR), Median Follow-up of 16.9 months

Intervention	days (Median)
Complete to Partial Response: Bortezomib + Dexamethasone	366.0
Stable Disease After 4 Cycles: VD, VDC, VDL	214.0

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Progression Free Survival

"Time from start of treatment to date of disease progression, relapse from CR or death. Estimated using the kaplan-meier method. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions, or similar definition as accurate and appropriate." (NCT00908232)
Timeframe: At Day 1 of each treatment cycle, at the End of Treatment visit until there is evidence of Progressive Disease or relapse from Complete Response (CR). Median Follow-Up of 16.9 months

Intervention	days (Median)
Complete to Partial Response: Bortezomib + Dexamethasone	311.0
Stable Disease After 4 Cycles: VD, VDC, VDL	214.0

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Overall Best Confirmed Response

Overall Best Confirmed Response is the best Overall Response Rate with borezomib-dexamathasone (+/-cyclophosphamide or lenalidomide) recorded between baseline and end of treatment. Response was assessed using the International Myeloma working Group (IMWG) Uniform Response Criteria and validated by an Independent Monitoring Committee. (NCT00908232)
Timeframe: Prior to treatment at day 1 of each cycle and at the end of treatment (day 21 of cycle 8), up to 168 days

Intervention	number of participants (Number)
Complete to Partial Response: Bortezomib + Dexamethasone	101
Stable Disease After 4 Cycles: VD, VDC, VDL	6

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One Year Survival

Percent Probability of Survival at 1 year from the start of treatment, estimated using Kaplan-Meier analysis. (NCT00908232)
Timeframe: At each visit from baseline to end of treatment. After treatment, monthly visit until progression or relapse or until the start of alternative MMY therapy, up to 1 year

Intervention	percent probability (Number)
Complete to Partial Response: Bortezomib + Dexamethasone	80
Stable Disease After 4 Cycles: VD, VDC, VDL	89

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Median Time to First Confirmed Response

Time from start of treatment to the date of the first documentation of a confirmed response. Estimated using the Kaplan-Meier method. Response was assessed using the International Myeloma Working Group (IMWG) Uniform Response Criteria and validated by an Independent Monitoring Committee. (NCT00908232)
Timeframe: At Day 1 of each treatment cycle, at the End of Treatment visit until there is evidence of Progressive Disease or relapse from Complete Response (CR), up to 168 days

Intervention	days (Median)
Complete to Partial Response: Bortezomib + Dexamethasone	43.0
Stable Disease After 4 Cycles: VD, VDC, VDL	NA

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Overall Survival

Is defined as the time interval from start of treatment to the date of death due to any cause. In the absence of confirmation of death (including subjects lost to follow-up), survival time will be censored at the last date the subject is known to be alive (NCT00908232)
Timeframe: At each visit from baseline to end of treatment. After treatment, monthly visit until progression or relapse or until the start of alternative MMY therapy. Further follow up by monthly phone call until the last patient was treated and followed for 1 year

Intervention	days (Median)
Complete to Partial Response: Bortezomib + Dexamethasone	NA
Stable Disease After 4 Cycles: VD, VDC, VDL	NA

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Number of Living Donor Transplant Candidates That Are Transplanted

Number of living donor transplant candidates who convert to a negative flow T- and B-cell crossmatch via desensitization and are subsequently transplanted (NCT00908583)
Timeframe: 1 year post baseline

Intervention	participants (Number)
All Study Participants	19

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Overall Safety of Bortezomib

Incidence of grade 3 and above non-hematologic toxicities. Incidence of grade 4 hematologic toxicities. Incidence of all grades of peripheral neuropathy. Incidence of Cytomegalovirus (CMV), Polyomavirus Allograft Nephropathy (PVN), and Posttransplant Lymphoproliferative Disorder (PTLD). (NCT00908583)
Timeframe: Study Day 62

,,,,,,,

Intervention	participants (Number)
	Incidence of CTCAE Grade 3 Anemia (<8.0-6.5 g/dL)	Incidence of CTCAE Grade 4 Anemia (<6.5g/dL)	Incidence of CTCAE Grade 3 Thrombocytopenia	Incidence of CTCAE Grade 4 Thrombocytopenia	Incidence of CTCAE Grade 3 Neutropenia	Incidence of CTCAE Grade 4 Neutropenia	Incidence of new onset level 1 PN	Incidence of new onset level 2 PN	Incidence of new onset level 3 PN	Incidence of new onset level 4 PN	Incidence of new onset level 5 PN	CMV D+/R- Status	CMV Viremia or Invasive Disease	Polyomavirus Allograft Nephropathy (PVN)	Malignancy
Phase 1 Cycle 2	2	0	2	0	1	0	0	3	3	1	0	0	0	0	0
Phase 1, Cycle 1	1	0	1	0	0	0	1	5	1	0	1	0	0	0	0
Phase 2 Cycle 2	0	0	0	0	0	0	2	3	0	0	0	0	0	0	0
Phase 2, Cycle 1	1	0	0	0	0	0	3	2	0	1	0	0	0	0	0
Phase 3, Cycle 1	0	0	1	0	0	0	0	2	1	0	0	0	0	0	0
Phase 3, Cycle 2	0	0	1	0	0	0	1	1	0	0	1	0	0	0	0
Phase 4, Single Stage	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0
Phase 5, Single Stage	1	0	0	0	0	0	1	0	0	0	0	0	0	0	0

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Acute Rejection Rate

Acute rejection rate at 6 months of all desensitized and transplanted patients (NCT00908583)
Timeframe: 6 months post transplant

Intervention	participants (Number)
All Transplanted Participants	3

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Number of Patients Whose Cytotoxic Panel Reactive Antibody (PRA) is Decreased by 50%

Number of patients on the waiting list whose cytotoxic PRA is decreased by 50%. (NCT00908583)
Timeframe: 46 days

Intervention	participants (Number)
All Study Participants	6

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1-year Survival Rate

Percentage of participants who are alive at the end of year 1 after randomization (NCT00911859)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Part 2: VMP (Velcade+Melphalan+Prednisone)	87.8
Part 2: VMP (Velcade+Melphalan+Prednisone) + Siltuximab	87.5

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1-year Progression-Free Survival (PFS) Rate

The 1-year PFS rate was defined as the percentage of participants surviving 1 year after randomization without disease progression or death. (NCT00911859)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Part 2: VMP (Velcade+Melphalan+Prednisone)	77.5
Part 2: VMP (Velcade+Melphalan+Prednisone) + Siltuximab	72.1

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Percentage of Participants Who Achieved Stringent Complete Response (sCR) - International Myeloma Working Group (IMWG) Criteria

sCR was assesses by IMWG Criteria: Negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas, <=5% plasma cells in bone marrow, normal free light chain ratio, absence of clonal cells in bone marrow by immunohistochemistry or immunofluorescence. sCR is a CR that has been confirmed by immunofixation + free light chain assay + either bone marrow immunohistochemistry or immunofluorescence (NCT00911859)
Timeframe: Up to disease progression, approximately 3 years

Intervention	Percentage of participants (Number)
Part 2: VMP (Velcade+Melphalan+Prednisone)	6.1
Part 2: VMP (Velcade+Melphalan+Prednisone) + Siltuximab	4.1

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Percentage of Participants Who Achieved Overall Response ie, Complete Response (CR) or Partial Response (PR) - European Group for Blood and Marrow Transplantation (EBMT) Criteria

CR or PR was assessed using EBMT criteria. CR: disappearance of the original monoclonal paraprotein from the blood and urine on at least 2 determinations for a minimum of 6 weeks by immunofixation studies, <5% plasma cells in the bone marrow on at least 1 determination, if skeletal survey is available: no increase in the size or number of lytic bone lesions (development of a compression fracture does not exclude response), disappearance of soft tissue plasmacytomas for at least 6 weeks; PR: >=50% reduction in the level of serum monoclonal paraprotein for at least 2 determinations 6 weeks apart, if present, reduction in 24-hour urinary light chain excretion by either >=90% or to <200 mg for at least 2 determinations 6 weeks apart, >=50% reduction in the size of soft tissue plasmacytomas (by clinical or radiographic examination) for at least 6 weeks, if skeletal survey is available: no increase in size or number of lytic bone lesions (NCT00911859)
Timeframe: Up to disease progression, approximately 3 years

Intervention	Percentage of participants (Number)
Part 2: VMP (Velcade+Melphalan+Prednisone)	79.6
Part 2: VMP (Velcade+Melphalan+Prednisone) + Siltuximab	87.8

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Percentage of Participants Who Achieved Complete Response (CR) - European Group for Blood and Marrow Transplantation (EBMT) Criteria

CR was assessed using EMBT criteria: disappearance of the original monoclonal paraprotein from the blood and urine on at least 2 determinations for a minimum of 6 weeks by immunofixation studies, <5% plasma cells in the bone marrow on at least 1 determination, if skeletal survey is available: no increase in the size or number of lytic bone lesions (development of a compression fracture does not exclude response), disappearance of soft tissue plasmacytomas for at least 6 weeks. (NCT00911859)
Timeframe: Up to disease progression, approximately 3 years

Intervention	Percentage of participants (Number)
Part 2: VMP (Velcade+Melphalan+Prednisone)	22.4
Part 2: VMP (Velcade+Melphalan+Prednisone) + Siltuximab	26.5

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Overall Survival

Overall survival is defined as the time interval in days between the date of randomization and the participant's death from any cause. (NCT00911859)
Timeframe: From the date of randomization till the date of death, as assessed up to the end of study (approximately 3 years)

Intervention	Days (Median)
Part 2: VMP (Velcade+Melphalan+Prednisone)	NA
Part 2: VMP (Velcade+Melphalan+Prednisone) + Siltuximab	NA

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Duration of Response (DOR)

DOR was defined as length from the earliest date a participant achieved a complete response (CR) or partial response (PR) to either date for disease progression (including relapse from CR) or the censoring date for progressive disease. Responders without disease progression were censored at the last efficacy assessment for disease progression. (NCT00911859)
Timeframe: From the date participants achieved CR or PR to either date for disease progression (including relapse from CR) or the censoring date for progressive disease, as assessed Up to 30 days after last dose of study medication

Intervention	Days (Median)
Part 2: VMP (Velcade+Melphalan+Prednisone)	497
Part 2: VMP (Velcade+Melphalan+Prednisone) + Siltuximab	583

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Progression-Free Survival (PFS)

PFS was defined as the time between randomization and either disease progression or death, whichever occurred first. (NCT00911859)
Timeframe: From the date of randomization until disease progression or death, whichever occurred first, as assessed up to the last efficacy assessment for disease progression (approximately 3 years)

Intervention	Days (Median)
Part 2: VMP (Velcade+Melphalan+Prednisone)	518
Part 2: VMP (Velcade+Melphalan+Prednisone) + Siltuximab	519

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Change From Baseline to Cycle 9 in Global Health Status/Quality of Life Subscale of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Core 30 (EORTC QLQ C30)

"Global health status/quality of life is a subscale of the EORTC QOL C30, which comprises two questions related to overall health/quality of life during the past week. The raw score to each question ranged from 1 (very poor) to 7 (excellent). The raw mean score of health status/quality of life subscale is calculated for each participant and a linear transformation applied to standardize the raw score, so that scores range from 0 to 100; a higher score represents a higher (better) health and quality of life." (NCT00911859)
Timeframe: Baseline (Day 1 predose) and Cycle 9 (Week 54)

Intervention	Scores on a scale (Mean)
Part 2: VMP (Velcade+Melphalan+Prednisone)	14.78
Part 2: VMP (Velcade+Melphalan+Prednisone) + Siltuximab	8.33

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Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)

An AE is defined as any untoward medical occurrence in a clinical investigation participant, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of a medicinal product. An SAE is defined as any untoward medical occurrence that, at any dose, results in death, is life threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity, or is a congenital anomaly/birth defect, or is an important medical events that jeopardize the participants or may require medical or surgical intervention to prevent one of the other outcomes listed in the above definition, or a drug-induced liver injury. (NCT00920556)
Timeframe: Approximately up to 12 cycles of 3 weeks each

Intervention	Participants (Count of Participants)
	Any AE	Any SAE
SRT501 + Bortezomib	9	3
SRT501 Monotherapy	24	12

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Change From in Baseline Biochemistry: Serum Creatinine, Total Bilirubin

Blood samples were collected to evaluate hematology parameters serum creatinine and total bilirubin. Change from Baseline was defined as the value of baseline minus from the End of study visit. Baseline was defined as Day 1. (NCT00920556)
Timeframe: Baseline (Day 1) and End of Study assessments/follow-up approximately 28 days (+/- 7 days) following the last dose of SRT501 or SRT501 and bortezomib (approximately 280 days)

Intervention	Micromole per liter (Mean)
	Serum creatinine	Total bilirubin
SRT501 + Bortezomib	3.60	0.80
SRT501 Monotherapy	59.8	1.6

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Change From Baseline in Hematology: White Blood Cell (WBC) Count, Neutrophils, Lymphocytes, Platelets

Blood samples collected to evaluate the hematology parameters were WBC count, neutrophils, lymphocytes and platelets. Change from Baseline was defined as the value of Baseline minus from the End of study visit. Baseline was defined as Day 1. (NCT00920556)
Timeframe: Baseline (Day 1) and End of Study assessments/follow-up approximately 28 days (+/- 7 days) following the last dose of SRT501 or SRT501 and bortezomib (approximately 280 days)

Intervention	10^9 cells per liter (L) (Mean)
	WBC count	Neutrophils	Lymphocytes	Platelets
SRT501 + Bortezomib	0.07	0.32	-0.34	-9.3
SRT501 Monotherapy	0.55	0.27	0.09	-12.1

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Change From Baseline in Biochemistry -Urea, Bicarbonate

Blood samples were collected to evaluate the biochemistry parameter urea and bicarbonate. Change from Baseline was defined as the value of Baseline minus from the End of study visit. Baseline was defined as Day 1. (NCT00920556)
Timeframe: Baseline (Day 1) and End of Study assessments/follow-up approximately 28 days (+/- 7 days) following the last dose of SRT501 or SRT501 and bortezomib (approximately 280 days)

Intervention	millimole per liter (Mean)
	Bicarbonate	Urea
SRT501 + Bortezomib	0.64	-0.18
SRT501 Monotherapy	-0.81	3.50

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Time to Disease Progression

Time to disease progression was defined as the time from first dose until objective tumor progression. Participants who did not experience tumor progression were censored at their last known date in the study. It was estimated using Kaplan-Meier methodology. Participants who did not experience tumor progression were censored at their last known date in the study. The first quartile for time to disease progression was evaluated when 25th percentile of participants of mITT population reported disease progression. Similarly, median and 75th percentile of participants of MITT population was planned to be reported. If, less than 75th percentile of participants reported disease progression at the end of the study period, then the observation was censored for the purpose of this analysis and in such case the data was planned to be reported as not evaluable (NA). (NCT00920556)
Timeframe: From Day 1 till disease progression (approximately 12 cycles of 3 weeks each)

Intervention	Months (Median)
SRT501 Monotherapy	2.8
SRT501 + Bortezomib	2.8

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Change From Baseline in Biochemistry: Prothrombin Time (PT)/ International Normalized Ratio (INR)

Blood samples were collected to evaluate the biochemistry parameter PT/INR. Change from Baseline was defined as the value of Baseline minus from the End of study visit. Baseline was defined as Day 1. (NCT00920556)
Timeframe: Baseline (Day 1) and End of Study assessments/follow-up approximately 28 days (+/- 7 days) following the last dose of SRT501 or SRT501 and bortezomib (approximately 280 days)

Intervention	Ratio of PT/INR (Mean)
SRT501 Monotherapy	0.11
SRT501 + Bortezomib	0.05

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Change From Baseline in Hematology: Hematocrit

Blood samples were collected to evaluate the hematology parameter hematocrit. Change from Baseline was defined as the value of baseline minus from the End of study visit. Baseline was defined as Day 1. (NCT00920556)
Timeframe: Baseline (Day 1) and End of Study assessments/follow-up approximately 28 days (+/- 7 days) following the last dose of SRT501 or SRT501 and bortezomib (approximately 280 days)

Intervention	Proportion of red blood cells in blood (Mean)
SRT501 Monotherapy	-0.04
SRT501 + Bortezomib	-0.03

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Change From Baseline in Hematology: Hemoglobin

Blood samples were collected to evaluate the hematology parameter hemoglobin. Change from Baseline was defined as the value of Baseline minus from the End of study visit. Baseline was defined as Day 1. (NCT00920556)
Timeframe: Baseline (Day 1) and End of Study assessments/follow-up approximately 28 days (+/- 7 days) following the last dose of SRT501 or SRT501 and bortezomib (approximately 280 days)

Intervention	Gram per litre (Mean)
SRT501 Monotherapy	-11.4
SRT501 + Bortezomib	-9.17

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Change From Baseline in Hematology: Red Blood Cell (RBC)

Blood samples were collected to evaluate the hematology parameter RBC. Change from Baseline was defined as the value of Baseline minus from the End of study visit. Baseline was defined as Day 1. (NCT00920556)
Timeframe: Baseline (Day 1) and End of Study assessments/follow-up approximately 28 days (+/- 7 days) following the last dose of SRT501 or SRT501 and bortezomib (approximately 280 days)

Intervention	10^12 cells per liter (Mean)
SRT501 Monotherapy	-0.30
SRT501 + Bortezomib	-0.16

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Number of Participants With Minor Response (MR) as Best Response (BR)

MR includes some, but not all, criteria for PR providing the remaining criteria satisfied: ≥25% to ≤ 49% reduction in the level of serum monoclonal paraprotein for at least 2 immunofixation determinations for a minimum of 6 weeks, If present, a 50 to 89% reduction in 24 hr light chain excretion, which still exceeds 200 mg/24 hr, for at least 2 determinations for a minimum of 6 weeks, 25-49% reduction in the size of plasmacytomas (by clinical or radiographic examination) for a minimum of 6 weeks, No increase in size or number of lytic bone lesions (development of compression fracture does not exclude response). (NCT00920556)
Timeframe: Up to 12 cycles of 3 weeks each

Intervention	Participants (Count of Participants)
SRT501 Monotherapy	0
SRT501 + Bortezomib	1

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Number of Participants With Overall Response Rate

Overall response rate, defines proportion of participants with Complete response (CR), Partial response (PR) or Minimal response (MR) as best response for all cycles. In atleast 2 determinations for minimum of 6 week (Wks) for every criteria listed. CR defined as disappearance of original monoclonal (MC) paraprotein (PP) in blood and urine on immunofixation determinations (IFD); < 5 % plasma cells in bone marrow; no increase in size or number of lytic bone lesions (LBLs); disappearance of soft tissue plasmacytomas (STP). PR defined as >= 50% reduction (RE) in level of serum MC PP for 2 IFDs; if present RE in 24 hour urinary light chain excretion (ULCE) by >= 90% RE or <200 mg; >= 50% RE in STP for; no increase in size or number of LBLs. MR criteria defined were >= 25% to <=49% RE serum MC PP; if present 50 to 89% RE in 24 hour LCE exceeding 200 mg/24 hour; 25% to 49% RE in size of STP; no increase in size or number of LBLs. (NCT00920556)
Timeframe: Approximately up to 12 cycles of 3 weeks

Intervention	Participants (Count of Participants)
SRT501 Monotherapy	0
SRT501 + Bortezomib	3

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Number of Participants With Partial Response (PR) as Best Response (BR)

PR includes some, but not all, criteria for CR providing the remaining criteria are satisfied: ≥50% reduction in the level of serum monoclonal paraprotein for at least 2 immunofixation determinations for a minimum of 6 weeks, If present, reduction in 24 hr urinary light chain excretion by either ≥90% or to <200 mg for at least 2 determinations for a minimum of 6 weeks, ≥50% reduction in the size of soft tissue plasmacytomas (by clinical or radiographic examination) for a minimum of 6 weeks, No increase in size or number of lytic bone lesions (development of compression fracture does not exclude response). (NCT00920556)
Timeframe: Up to 12 cycles of 3 weeks each

Intervention	Participants (Count of Participants)
SRT501 Monotherapy	0
SRT501 + Bortezomib	2

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Number of Participants With Partial Response (PR) as Last Observed Response (LOR)

Intervention	Participants (Count of Participants)
SRT501 Monotherapy	0
SRT501 + Bortezomib	1

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Number of Participants With Progressive Disease (PD) PD as Best Response (BR)

PD includes one or more of the following criteria: >25% increase in the level of serum monoclonal paraprotein, which must also be an absolute increase of at least 5 g/L and confirmed on a repeat investigation, >25% increase in 24 hr urinary light chain excretion, which must also be an absolute increase of at least 200 mg/24 hr and confirmed on a repeat investigation, >25% increase in plasma cells in a bone marrow aspirate or on trephine biopsy, which must also be an absolute increase of at least 10%., Definite increase in the size of existing lytic bone lesions or soft tissue plasmacytomas, Development of new bone lesions or soft tissue plasmacytomas (not including compression fracture), Development of hypercalcemia (corrected serum calcium >11.5 mg/dL or 2.8 mmol/L not attributable to any other cause). (NCT00920556)
Timeframe: Up to 12 cycles of 3 weeks each

Intervention	Participants (Count of Participants)
SRT501 Monotherapy	1
SRT501 + Bortezomib	2

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Number of Participants With Progressive Disease (PD) PD as Last Observed Response (LOR)

Intervention	Participants (Count of Participants)
SRT501 Monotherapy	2
SRT501 + Bortezomib	4

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Number of Participants With Stable Disease (SD) as Best Response (BR)

Stable disease included not meeting the criteria for MR or PD. (NCT00920556)
Timeframe: Up to 12 cycles of 3 weeks each

Intervention	Participants (Count of Participants)
SRT501 Monotherapy	3
SRT501 + Bortezomib	4

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Number of Participants With Stable Disease (SD) as Last Observed Response (LOR)

Stable disease included not meeting the criteria for MR or PD. (NCT00920556)
Timeframe: Up to 12 cycles of 3 weeks each

Intervention	Participants (Count of Participants)
SRT501 Monotherapy	2
SRT501 + Bortezomib	4

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Kaplan-Meier Estimate for Duration of Response

Duration of response (DR) is defined as the time from the first response to progressive disease (PD). See outcome #4 for a PD definition. (NCT00920855)
Timeframe: up to 8.5 months

Intervention	months (Median)
Bendamustine and Bortezomib - Overall	NA

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Kaplan-Meier Estimate for Progression-Free Survival

Progression free survival is the time between the date of initiation of therapy to progressive disease (PD) or death from any cause, whichever occurs first. See outcome #4 for a definition of PD. (NCT00920855)
Timeframe: up to 23 months

Intervention	months (Median)
Bendamustine and Bortezomib - Overall	15.21

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Summary of Participants With Adverse Events (AEs)

Counts of participants who had AEs are summarized in a variety of categories. Severity and relatedness to study drug are in the opinion of the investigator according to the National Cancer Institute's Common Terminology Criteria for Adverse Events (NCI CTCAE) v3.0. Severity is rated on a 5-point scale: 1=mild, 2=moderate, 3=severe, 4=life threatening or disabling, and 5= death related to AE. Relatedness is assessed on a 5-point scale: not related, unlikely, possible, probable and definite. Definite, probable and possible answers are reported as 'related' to study medication. Deaths are reported up to 18 months. All the deaths occurred beyond the treatment-emergent timeframe since they occurred 6.5-16 months after the final dosing. All other parts of the summary represent the treatment-emergent timeframe (up to 8.5 months) which is the treatment period plus 30 days. (NCT00920855)
Timeframe: up to 8.5 months. Deaths are reported up to 18 months

Intervention	participants (Number)
	Any adverse event	Any non-haematologic adverse event	Severe adverse event (grade 3 or 4)	Treatment-related adverse events	Deaths	Serious adverse events	Withdrawn from study due to AE
Bendamustine 50 mg/m^2 Cohort	5	5	3	4	1	0	2
Bendamustine 70 mg/m^2 Cohort	4	4	3	4	0	1	2
Bendamustine 90 mg/m^2 Cohort	31	31	22	31	5	7	5

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Participants' Best Tumor Response as Assessed by the Investigator

Abbreviated criteria for response categories: CR includes the disappearance of the original monoclonal protein (M-protein) from blood and urine, and <5% plasma cells in the bone marrow, and no increase in size/number of lytic bone lesions, and disappearance of soft tissue plasmacytomas for >=4 weeks. VGPR includes serum and urine M-protein detectable by immunofixation but not electrophoresis, and reduction in 24-hr urinary light chain excretion by <100 mg, and disappearance of soft tissue plasmacytomas for >= 4 weeks, and no increase in size/number of lytic bone lesions. PR includes a >=50% reduction in serum M-protein, and reduction in 24-hr urinary light chain excretion by either >=90% or to <200 mg, and >=50% reduction in size of soft tissue plasmacytomas, and no increase in size/number of lytic bone lesions. MR includes a >=25% and <=49% reduction in serum M-protein. SD does not meet criteria for the other response categories. See outcome #4 for a definition of PD. (NCT00920855)
Timeframe: up to 7.5 months (eight 28-day cycles)

Intervention	participants (Number)
	Complete response (CR)	Very good partial response (VGPR)	Partial response (PR)	Minimal response (MR)	Stable disease (SD)	Progressive disease (PD)
Bendamustine 50 mg/m^2 Cohort	0	0	1	1	2	1
Bendamustine 70 mg/m^2 Cohort	0	0	0	1	2	1
Bendamustine 90 mg/m^2 Cohort	1	2	8	5	13	2

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Time to the First Response

Time to first response is defined as the time from the initiation of therapy to the first evidence of a confirmed response (ie, CR, VGPR, PR, or MR). (NCT00920855)
Timeframe: up to 8.5 months

Intervention	months (Mean)
Bendamustine and Bortezomib - Overall	1.9

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Percentage of Participants With An Overall Tumor Response As Assessed By the Investigator

Overall tumor response is the sum of a complete response (CR), very good partial response (VGPR), partial response (PR) and minimal response (MR). A modified version of the Bladé criteria for response was used. Abbreviated definitions for the response categories can be found in the description of outcome #3. (NCT00920855)
Timeframe: Up to 7.5 months (eight 28-day cycles)

Intervention	percentage of participants (Number)
Bendamustine 50 mg/m^2 Cohort	40.0
Bendamustine 70 mg/m^2 Cohort	25.0
Bendamustine 90 mg/m^2 Cohort	51.6

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Participants With Dose Limiting Toxicity (DLT)

"Maximum tolerated dose was the dose that was 1 step lower than the dose where at least one third of patients experienced DLT. A DLT was defined as any of the following occurring during the first cycle:~grade 4 hematologic toxicity without regard for relationship to study drug treatment~thrombocytopenia grade 3 with grade 3 or grade 4 hemorrhage~grade 3 febrile neutropenia~grade 3 or grade 4 nausea and vomiting refractory to anti emetic therapy~any study drug related grade 3 or grade 4 nonhematologic toxicity~any drug related death~Toxicity grades (3=severe AE and 4=life-threatening or disabling AE) were assessed using the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) v3." (NCT00920855)
Timeframe: Day 1 - 28

Intervention	participants (Number)
Bendamustine 50 mg/m^2 Cohort	0
Bendamustine 70 mg/m^2 Cohort	0
Bendamustine 90 mg/m^2 Cohort	0

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Kaplan-Meier Estimate for Time to Progression (TTP)

"Time to progression was defined as the time from initiation of therapy to progressive disease (PD). PD requires at least one of the following:~>25% increase in serum monoclonal paraprotein (which must also be an absolute increase of at least 5 g/L),~>25% increase in 24-hour urinary light chain excretion (which must also be an absolute increase of at least 200 mg/24 h),~>25% increase in plasma cells in a bone marrow aspirate or on trephine biopsy (which must also be an absolute increase of at least 10%),~definite increase in the size of existing lytic bone lesions or soft tissue plasmacytomas,~the development of new bone lesions or soft tissue plasmacytomas,~the development of hypercalcemia (corrected serum calcium > 11.5 mg/dL or 2.8 mmol/L not attributable to any other cause)." (NCT00920855)
Timeframe: up to 8.6 months

Intervention	months (Median)
Bendamustine and Bortezomib - Overall	8.4

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Kaplan-Meier Estimate for Overall Survival (OS)

Overall survival is defined as the time from initiation of therapy to death from any cause or last follow-up visit. (NCT00920855)
Timeframe: up to 23 months

Intervention	months (Median)
Bendamustine and Bortezomib - Overall	17.82

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Terminal Half-Life (T1/2) of Bortezomib

The time it takes for the measured concentration of the drug to drop by half. (NCT00923247)
Timeframe: Cycle 1 day 1, and cycle 3 day 1 (an average of 61 days); and Pre-dose and 1, 2, 4, 6, 8, 10, and 24 hours post dose

Intervention	hour (Geometric Mean)
	Before Vandetanib	After Vandetanib
Phase 1	9.4	12.5

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Phase I: Maximum Tolerated Dose (MTD) of Daily Oral Bortezomib

A maximum tolerated dose for bortezomib will be determined if dose limiting toxicity is observed in 2 or more patients at one of the dose levels being evaluated. The MTD will be the dose level immediately preceding the dose level at which DLT (e.g. defined as neutrophil count below 1000/ µL (grade 3) on 2 consecutive measurements drawn at least 72 hours OR a single neutrophil count below 500/µL occurred. Platelet count below 50,000 µL (grade 3) on 2 consecutive measurements drawn at least 72 hours apart OR a singe platelet count below 25,000/µL. A platelet transfusion administered when platelet count is below 50,000/µL is dose limiting thrombocytopenia, unless the transfusion is being administered for peri-operative coverage. (NCT00923247)
Timeframe: 80 days

Intervention	mg/m^2 (Number)
Phase 1	1.3

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Phase I: Maximum Tolerated Dose (MTD) of Daily Oral Vandetanib

A maximum tolerated dose for vandetanib will be determined if dose limiting toxicity is observed in 2 or more patients at one of the dose levels being evaluated. The MTD will be the dose level immediately preceding the dose level at which DLT (e.g. defined as neutrophil count below 1000/ µL (grade 3) on 2 consecutive measurements drawn at least 72 hours OR a single neutrophil count below 500/µL occurred. Platelet count below 50,000 µL (grade 3) on 2 consecutive measurements drawn at least 72 hours apart OR a singe platelet count below 25,000/µL. A platelet transfusion administered when platelet count is below 50,000/µL is dose limiting thrombocytopenia, unless the transfusion is being administered for peri-operative coverage. (NCT00923247)
Timeframe: 80 days

Intervention	mg (Number)
Phase 1	300

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Progression Free Survival (PFS)

Progression free survival is defined as the duration of time from start of treatment to time of progression. Comparison of PFS between cohorts 1, 2A and 2B was to be assessed by the Response Evaluation Criteria in Solid Tumors (RECIST). Progressive disease is at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. (NCT00923247)
Timeframe: 2-3 years

Intervention	Months (Median)
Phase 1	30.2
Phase 2A	3.02

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Area Under the Bortezomib Plasma Concentration Versus Time Curve From Time Zero to Infinity/Dose (AUCinf/D)

The area under the concentration-time curve (AUC) extrapolated to infinity (AUCinf) was calculated using the linear up-log down trapezoidal method via extrapolation of AUC(LAST) (AUC to the last quantifiable time point) by dividing C(LAST) (the last measurable drug concentration, typically at 24 hour post-dose) by the rate constant of the terminal phase, lambda z. This constant was determined from the slope of the terminal phase of the concentration-time curve using weighted least-squares as the estimation procedure. (NCT00923247)
Timeframe: Cycle 1 day 1, and cycle 3 day 1 (an average of 61 days); and Pre-dose and 1, 2, 4, 6, 8, 10, and 24 hours post dose

Intervention	hr*ng/mL/mg (Geometric Mean)
	Before Vandetanib	After Vandetanib
Phase 1 - Vandetanib and Bortezomib	1.27	2.39

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Bortezomib Volume of Distribution (Vss)

Vss represents the volume into which the drug distributes into once given to the patient at steady-state. This volume parameter provides a measure of where in the body the drug is going, based on fluid volume. (NCT00923247)
Timeframe: Cycle 1 day 1, and cycle 3 day 1 (an average of 61 days); and Pre-dose and 1, 2, 4, 6, 8, 10, and 24 hours post dose

Intervention	Liter (Geometric Mean)
	Before Vandetanib	After Vandetanib
Phase 1	1167	749

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Comparison of Steady State Vandetanib Exposure With Relevant Literature Values

"Because vandetanib PK exposure was only measured during a single 8-hr window during daily dosing, the only comparison to assess the effect of bortezomib is to compare these values to published literature." (NCT00923247)
Timeframe: Cycle 3 day 1 (an average of 60 days); and Pre-dose and 1, 2, 4, 6, 8, 10, and 24 hours post dose

Intervention	ng/mL/mg (Mean)
	Published Literature	Study 090089 Results
Phase 1 - Vandetanib and Bortezomib	4.77	3.96

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Maximum Bortezomib Plasma Concentration Normalized to Dose (Cmax/D)

Geometric mean for Bortezomib pharmacokinetic (PK) parameters both before (cycle 1 day 1) and during steady-state Vandetanib (cycle 3 day 1; exposures are dose normalized). Bortezomib plasma concentrations were measured using a validated LC-MS/MS assay with a lower limit of quantification (LLOQ) of 1 ng/mL. Only measured concentrations above the LLOQ were used in the calculation of PK parameters. The maximum plasma concentration (Cmax) was recorded as observed values. (NCT00923247)
Timeframe: Cycle 1 day 1, and cycle 3 day 1 (an average of 61 days); and Pre-dose, 1, 2,4, 6, 8, 10 and 24 hours post dose

Intervention	ng/mL/mg (Geometric Mean)
	Before Vandetanib	After Vandetanib
Phase 1 - Vandetanib and Bortezomib	0.98	1.92

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Response Rate (Complete Response (CR) + Partial Response (PR) of Adults With a Diagnosis of MTC Treated With Either of Two Regimens: (1) Daily Oral Vandetanib and Bortezomib or (2) Daily Oral Vandetanib

Comparison of response between cohorts 1, 2A and 2B was to be determined by computed tomography scan reviews using the Response Evaluation Criteria in Solid Tumors (RECIST). Complete response is disappearance of all target lesions. Partial response is at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD. (NCT00923247)
Timeframe: 2-3 years

Intervention	Participants (Count of Participants)
	Complete Response	Partial Response
Phase 1	0	6
Phase 2A	0	0

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Phase 2: Progression Free Survival in Adults With a Diagnosis of Medullary Thyroid Cancer (MTC) Treated With Daily Oral Vandetanib and Bortezomib

"Progression free survival is defined as the duration of time from start of treatment to time of progression. Progression is assessed by the Response Evaluation Criteria in Solid Tumors (RECIST) and is defined as the appearance of one or more new lesions or unequivocal progression of existing non-target lesions. Although a clear progression of non-target lesions only is exceptional, the opinion of the treating physician should prevail in such circumstances, and the progression status should be confirmed at a later time by the review panel (or Principal Investigator)." (NCT00923247)
Timeframe: 4 months

Intervention	months (Median)
Phase 2 A - Vandetanib and Bortezomib at the MTD	3.67

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Total Systemic Clearance (CL) of Bortezomib

Total systemic clearance = dose/area under curve extrapolated to infinity (AUCinf.). This measurement represents the rate at which plasma is systematically cleared of drug. (NCT00923247)
Timeframe: Cycle 1 day 1, and cycle 3 day 1 (an average of 61 days); and Pre-dose and 1, 2, 4, 6, 8, 10, and 24 hours post dose

Intervention	L/hr (Geometric Mean)
	Before Vandetanib	After Vandetanib
Phase 1	78.7	42.9

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Number of Participants With Adverse Events

Here is the number of participants with adverse events assessed by the Common Terminology Criteria in Adverse Events (CTCAE) v4.0. For the detailed list of adverse events see the adverse event module. (NCT00923247)
Timeframe: Date treatment consent signed to date off study, approximately 7 years and 9 days

Intervention	Participants (Count of Participants)
Phase 1	21
Phase 2 A	0

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Duration of Response

Duration of response is defined as the time (in months) from the date of first documentation of confirmed complete response (CR) or partial response (PR) to the date of first documentation of progressive disease (PD), relapse from CR or death related to disease. For a participant who has not progressed and is not known to have died due to disease under study at the end of his/her study follow-up or at the time of start of an alternate therapy (whichever is first), duration of response is censored at the last overall response assessment that is stable disease or better, and which is prior to the start of the alternate therapy, if any. Disease response was assessed using IWG-revised response criteria for malignant lymphoma. CR=Disappearance of all evidence of disease and PR=Regression of measurable disease and no new sites and PD= any new lesion or increase by > 50% of previously involved sites from nadir. (NCT00931918)
Timeframe: Median Follow-up of 34.3 months for RCHOP arm and 34.4 months for Vc-RCHOP arm

Intervention	months (Median)
RCHOP	NA
Vc-RCHOP	NA

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Overall Survival

Overall survival is defined as the time from the date of randomization to the date of death from any cause. A participant who is alive at the end of his/her study follow-up is censored at the date of last contact. (NCT00931918)
Timeframe: Median Follow-up of 34.3 months for RCHOP arm and 34.4 months for Vc-RCHOP arm

Intervention	months (Median)
RCHOP	NA
Vc-RCHOP	NA

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Progression-Free Survival (PFS) in Patients With Non-germinal Center B-cell-like (Non-GCB) Diffuse Large B-cell Lymphoma (DLBCL)

PFS is defined as the time in months from the date of randomization to the date of first documentation of progressive disease (PD) or death from any cause. The date of progression is the earliest date of a computed tomography/positron emission tomography (CT/PET) scan that shows evidence of PD. For a participant that has not progressed and is alive at the end of his/her study follow-up or at the time of start of an alternate therapy (whichever is first), PFS is censored at the last overall response assessment that is stable disease or better, and which is prior to the start of the alternate therapy, if any. Disease response was assessed using International Working Group (IWG)-revised response criteria for malignant lymphoma. PD= any new lesion or increase by > 50% of previously involved sites from nadir. (NCT00931918)
Timeframe: Median Follow-up of 34.3 months for RCHOP arm and 34.4 months for Vc-RCHOP arm

Intervention	months (Median)
RCHOP	NA
Vc-RCHOP	NA

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Progression-Free Survival Rate

PFS is defined as the time in months from the date of randomization to the date of first documentation of progressive disease (PD) or death from any cause. The date of progression is the earliest date of a computed tomography/positron emission tomography (CT/PET) scan that shows evidence of PD. For a participant that has not progressed and is alive at the end of his/her study follow-up or at the time of start of an alternate therapy (whichever is first), PFS is censored at the last overall response assessment that is stable disease or better, and which is prior to the start of the alternate therapy, if any. Disease response was assessed using International Working Group (IWG)-revised response criteria for malignant lymphoma. PD= any new lesion or increase by > 50% of previously involved sites from nadir. The progression-free survival rate is defined as the Kaplan-Meier (KM) estimate of progression-free survival at 2 years. (NCT00931918)
Timeframe: 2 Years (Median Follow-up of 34.3 months for RCHOP arm and 34.4 months for Vc-RCHOP arm)

Intervention	percentage of participants (Number)
RCHOP	78
Vc-RCHOP	82

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Time to Progression (TTP)

TTP is defined as the time from the date of randomization to the date of first documentation of progressive disease, relapse from CR, or death related to disease under study if participant did not have any documentation of disease progression prior to death caused by lymphoma or complications thereof. For a participant who has not progressed and is not known to have died due to disease under study at the end of his/her study follow-up or at the time of start of an alternate therapy (whichever is first), TTP is censored at the last overall response assessment that is stable disease or better, and which is prior to the start of the alternate therapy, if any. Disease response was assessed using International Working Group (IWG)-revised response criteria for malignant lymphoma. PD= any new lesion or increase by > 50% of previously involved sites from nadir. (NCT00931918)
Timeframe: Median Follow-up of 34.3 months for RCHOP arm and 34.4 months for Vc-RCHOP arm

Intervention	months (Median)
RCHOP	NA
Vc-RCHOP	NA

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Complete Response Rate

Complete Response Rate is defined as the percentage of participants with the best response of Complete Response (CR). Disease response was assessed using International Working Group (IWG)-revised response criteria for malignant lymphoma. CR=Disappearance of all evidence of disease. (NCT00931918)
Timeframe: End of Cycle 2, End of Treatment (Cycle 6) [Median of 16 weeks on treatment]

Intervention	percentage of participants (Number)
	End of Cycle 2	End of Treatment (Cycle 6)	Best Complete Response Rate
RCHOP	23	45	49
Vc-RCHOP	16	56	56

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Fluorodeoxyglucose Positron Emission Tomography (FDG-PET) Negative Rate

FDG-PET negative rate is defined as the percentage of participants FDG-PET negative at the given time-point. (NCT00931918)
Timeframe: End of Cycle 2 and End of Treatment (Cycle 6) [Median of 16 weeks on treatment]

Intervention	percentage of participants (Number)
	End of Cycle 2	End of Treatment (Cycle 6)
RCHOP	42	53
Vc-RCHOP	37	59

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Overall Response Rate (ORR)

ORR is defined as the percentage of participants with the best overall response complete response (CR) + partial response (PR). Disease response was assessed using International Working Group (IWG)-revised response criteria for malignant lymphoma. CR=disappearance of all evidence of disease and PR=regression of measurable disease and no new sites. (NCT00931918)
Timeframe: End of Cycle 2, End of Treatment (Cycle 6) [Median of 16 weeks on treatment]

Intervention	percentage of participants (Number)
	End of Cycle 2	End of Treatment (Cycle 6)	Best Overall Response Rate
RCHOP	93	88	98
Vc-RCHOP	90	84	96

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Percentage of Participants With Chemistry and Hematology Laboratory Values Grade 3 or Higher

Percentage of participants who shifted from a National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) Grade 0, 1, or 2 at Baseline to a Grade 3 or higher on study (worst post-baseline grade). Grade 1=Mild, Grade 2=Moderate, Grade 3=Severe or medically significant but not immediately life-threatening, Grade 4=Life-threatening consequences and 5=Death related to AE. (NCT00931918)
Timeframe: Days 1, 4 and 10 of each cycle and end of treatment visit (Median of 16 weeks on treatment)

Intervention	percentage of participants (Number)
	Lymphocytes	WBC Count	Neutrophils	Platelets	Hemoglobin	Hyperglycemia	Hypokalemia	Hypophosphatemia	Hyponatremia	Alanine aminotransferase (ALT) increased	Aspartate aminotransferase (AST) increased
RCHOP	70	68	65	18	10	14	13	7	4	2	1
Vc-RCHOP	86	69	70	39	15	9	14	10	3	1	2

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Percentage of Participants With Treatment Emergent Adverse Events (TEAEs) by Category

Percentage of participants in the following categories: • At least 1 TEAE • Drug-related, TEAEs • Grade 3 or higher TEAEs. Grade 3 are AEs of Severe Intensity • Grade 3 or higher drug-related, TEAEs • TEAEs resulting in study drug discontinuation • Serious TEAEs An Adverse Event (AE) is defined as any untoward medical occurrence in a clinical investigation participant administered a drug; it does not necessarily have to have a causal relationship with this treatment. A treatment-emergent adverse event (TEAE) is defined as an adverse event with an onset that occurs after receiving study drug. A Serious Adverse Event (SAE) is any experience that suggests a significant hazard, contraindication, side effect or precaution that: results in death, is life-threatening, required in-patient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect or is medically significant. (NCT00931918)
Timeframe: First dose of study drug through 30 days after the last dose of study drug (Up to 26 Weeks)

Intervention	percentage of participants (Number)
	At Least 1 TEAE	Drug-related, TEAEs	Grade 3 or higher TEAEs	Grade 3 or Higher Drug-related, TEAEs	TEAEs Resulting in Study Drug Discontinuation	Serious TEAEs
RCHOP	100	88	71	55	4	31
Vc-RCHOP	99	95	79	68	6	34

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Overall Survival

The distribution of survival time will be estimated using the method of Kaplan-Meier. (NCT00937495)
Timeframe: Time from registration to death due to any cause, assessed up to 2 years

Intervention	months (Median)
Treatment (Vorinostat, Bortezomib)	16.4

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Confirmed Tumor Responses

"The number of confirmed tumor responses is defined as a complete response (CR) or partial response (PR) according to Response Evaluation Criteria in Solid Tumors (RECIST) on two consecutive evaluations at least six weeks apart.~Complete Response (CR): Disappearance of all target lesions. Partial Response (PR): At least a 30% decrease in the sum of the longest dimension (LD) of target lesions taking as reference the baseline sum LD." (NCT00937495)
Timeframe: Up to 2 years

Intervention	participants (Number)
	Complete Response (CR)	Partial Response (PR)
Treatment (Vorinostat, Bortezomib)	0	0

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Progression Free Survival

Progression-free survival is defined as the time from registration to the time of progression or death, whichever comes first. The distribution and median of progression-free survival times will be estimated using the method of Kaplan-Meier. (NCT00937495)
Timeframe: Up to 2 years

Intervention	months (Median)
Treatment (Vorinostat, Bortezomib)	1.5

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Overall Survival (OS) Rate

Overall survival in participants with multiple myeloma treated with Bortezomib (Velcade®) containing conditioning regimen and autologous as well as allogeneic transplantation. (NCT00948922)
Timeframe: End of 2 year, post transplant follow-up

Intervention	percentage (Number)
A: Allogeneic Stem Cell Transplant	79.2
B: Autologous Stem Cell Transplant	89.2
BE: Group B Expansion	97.3

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Progression Free Survival (PFS)

PFS: Number of participants, per treatment arm with progression free survival at time of analysis. Survival time will be measured from the date of transplant to the date of progression, death or the last follow-up, whichever comes first. Progressive Disease (PD): Increase of ≥ 25% from lowest response value in any one or more of the following: Serum M-component and/or; Urine M-component and/or; Only in patients without measurable serum and urine M-protein levels; the difference between involved and uninvolved FLC levels. The absolute increase must be > 10 mg/dL; Bone marrow plasma cell percentage; absolute percentage ≥ 10%; Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas; Development of hypercalcemia that can be attributed solely to the plasma cell proliferative disorder. (NCT00948922)
Timeframe: End of 2 year, post transplant follow-up

Intervention	Participants (Count of Participants)
A: Allogeneic Stem Cell Transplant	17
B: Autologous Stem Cell Transplant	25
BE: Group B Expansion	19

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Percentage of Participants With Acute or Chronic Graft-versus-host Disease (GVHD) Following Transplant

Percentage of participants with Acute or Chronic GVHD following transplant (NCT00948922)
Timeframe: End of 2 year, post transplant follow-up

Intervention	percentage of participants (Number)
A: Allogenic Stem Cell Transplant	34

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Response Rate

Response rate to regimen defined as the percentage of number of complete response or partial response in total number of participants treated. The response assessed after the first 2 cycles. Response (complete and partial remission) according to International Workshop Response Criteria for Non-Hodgkin's Lymphoma: A complete response is the complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present before therapy. A partial response is regression of measurable disease and no new sites of disease. Stable disease is failure to attain a complete response/partial response or progressive disease. A cycle is 21 days with 6-8 cycles administered depending on response. (NCT00958256)
Timeframe: Evaluation of disease after 2 cycles (approximately 6 weeks).

Intervention	percentage of participants (Number)
	Complete Response (CR)	Partial Response (PR)	Progressive Disease (PD)	Stable Disease (SD)
Bortezomib With Cyclophosphamide and Rituximab	52	0	19	5

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Overall Response After 3 Cycles of Botezomib Plus ICE (BICE) Versus Ifosfamide, Carboplatin, Etoposide (ICE) in Patients With Relapsed/Refractory Classical Hodgkin Lymphoma

Response rates for Bortezomib, Ifosfamide, Carboplatin, Etoposide (BICE) and Ifosfamide, Carboplatin, Etoposide (ICE) treatment groups were assessed by the 1999 International Working Group (IWG)(CT alone) (Cheson et al., 1999) and compared to 2007 IWG (CT plus PET) (Cheson et al., 2007) criteria. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT00967369)
Timeframe: From baseline to 3 cycles of treatment

Intervention	Participants (Count of Participants)
	Overall Response	Complete Response (CR)	Partial Response (PR)	Progressive Disease (PD)	Stable Disease (SD)
BICE (Bortezomib, Ifosfamide, Carboplatin, Etoposide)	7	3	4	0	1
ICE (Ifosfamide, Carboplatin, Etoposide)	6	1	5	0	3

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PET Scan Response After 3 Cycles of BICE Versus ICE Chemotherapy.

Response rates for BICE and ICE treatment groups will be assessed by 1999 IWG (CT alone) (Cheson et al., 1999) and compared to 2007 IWG (CT plus PET) (Cheson et al., 2007) criteria. (NCT00967369)
Timeframe: Baseline up to 1 year

Intervention	Participants (Count of Participants)
	PET negativity : Complete Response (CR)	PET negativity : Partial Response (PR)	PET negativity : Stable Disease (SD)	PET positivity : Partial Response (PR)	PET positivity : Stable Disease (SD)	PET positivity : Progressive Disease (PD)
BICE (Bortezomib, Ifosfamide, Carboplatin, Etoposide)	3	0	0	4	1	2
ICE (Ifosfamide, Carboplatin, Etoposide)	6	4	1	2	2	0

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Progression Free Survival (PFS) Rate at 12 Months

Progression free survival time is defined as the time interval from treatment start to progression or death due to any cause whichever happens first. Participants will be censored at the last follow-up date, if an event(progression/death) is not observed during the follow-up. (NCT00967369)
Timeframe: From date of randomization until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 100 months

Intervention	percentage of participants (Number)
BICE (Bortezomib, Ifosfamide, Carboplatin, Etoposide)	50
ICE (Ifosfamide, Carboplatin, Etoposide)	70

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Overall Survival (OS) Rate at 24 Months

Overall Survival is time from date of treatment start until date of death due to any cause or last Follow-up within 24 months. (NCT00967369)
Timeframe: 24 months

Intervention	percentage of participants (Number)
BICE (Bortezomib, Ifosfamide, Carboplatin, Etoposide)	70
ICE (Ifosfamide, Carboplatin, Etoposide)	89

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Skeletal Survey for New Osteolytic Lesions/Fractures

Skeletal survey was measured using conventional radiography [imaging of the whole skeleton (skull, cervical spine, thoracic spine, lumbar spine, pelvis, humeri, femoral bones)] on day 21 of cycle 8 (day 168) (NCT00972959)
Timeframe: day 168

Intervention	participants (Number)
Bortezomib/Dexamethasone/Zoledronic Acid	0

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Bone Remodelling

Bone remodelling was studied by the measurement of the following serum indices on day 21 of cycle 4 (day 84) using an enzyme-linked immunosorbent assay (ELISA) bone formation marker [bone-specific alkaline phosphatase (bALP)]. (NCT00972959)
Timeframe: day 84

Intervention	U/L (Median)
Bortezomib/Dexamethasone/Zoledronic Acid	22.5

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Bone Pain

"Bone pain was measured with the use of the Visual Analogue Scale on day 21 of cycle 8 (day 168).~Bone pain was measured with the use of the Visual Analogue Scale. The visual analogue scale or visual analog scale (VAS) is a psychometric response scale which can be used in questionnaires. It is a measurement instrument for subjective characteristics or attitudes that cannot be directly measured.~The VAS for Bone Pain was constructed as follows:~None Mild Moderate Severe Worst possible 1,2 3,4 5,6 7,8 9,10 Lower values are considered to be of a better outcome, higher values are considered to be of a worst outcome." (NCT00972959)
Timeframe: On the day 168

Intervention	units on a scale (Median)
Bortezomib/Dexamethasone/Zoledronic Acid	0.3

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Bone Remodelling

Bone remodelling was studied by the measurement of the following serum indices on day 21 of cycle 4 (day 84) using an enzyme-linked immunosorbent assay (ELISA): bone formation marker [bone-specific alkaline phosphatase (bALP) ]. (NCT00972959)
Timeframe: day 168

Intervention	U/L (Median)
Bortezomib/Dexamethasone/Zoledronic Acid	24.8

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Bone Pain

"Bone pain was measured with the use of the Visual Analogue Scale on day 21 of cycle 4 (day 84).~Bone pain was measured with the use of the Visual Analogue Scale. The visual analogue scale or visual analog scale (VAS) is a psychometric response scale which can be used in questionnaires. It is a measurement instrument for subjective characteristics or attitudes that cannot be directly measured.~The VAS for Bone Pain was constructed as follows:~None Mild Moderate Severe Worst possible 1,2 3,4 5,6 7,8 9,10 Lower values are considered to be of a better outcome, higher values are considered to be of a worst outcome." (NCT00972959)
Timeframe: On the day 84

Intervention	units on a scale (Median)
Bortezomib/Dexamethasone/Zoledronic Acid	1.5

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Skeletal Survey for New Osteolytic Lesions/Fractures

Skeletal survey was measured using conventional radiography [imaging of the whole skeleton (skull, cervical spine, thoracic spine, lumbar spine, pelvis, humeri, femoral bones)] every 6 months for up to 18 months (NCT00972959)
Timeframe: 18 months

Intervention	participants (Number)
Bortezomib/Dexamethasone/Zoledronic Acid	0

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Bone Mineral Density (BMD)

BMD of the lumbar spine (L1-L4, anteroposterior view) and femoral neck (FN) was measured by Dual Energy X-Absorptiometry scan (DEXA-scan) using a Hologic QDR-1000 scanner on day 21 of cycle 8 (day 168) (NCT00972959)
Timeframe: day 168

Intervention	T-score (Median)
	Lumbar spine (L1-L4)	Femoral neck (FN)
Bortezomib/Dexamethasone/Zoledronic Acid	1.63	-1.44

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New Skeletal-related Events (SRE: Pathologic Fractures, Need for Bone Radiation Therapy or Surgery)

New Skeletal-related events (SRE: pathologic fractures, need for bone radiation therapy or surgery) following 8 cycles (day 168) of therapy (NCT00972959)
Timeframe: day 168

Intervention	participants (Number)
Bortezomib/Dexamethasone/Zoledronic Acid	0

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New Skeletal-related Events (SRE: Pathologic Fractures, Need for Bone Radiation Therapy or Surgery)

New Skeletal-related Events (SRE: Pathologic Fractures, Need for Bone Radiation Therapy or Surgery) after 18 months post VD (NCT00972959)
Timeframe: 18 months

Intervention	participants (Number)
Bortezomib/Dexamethasone/Zoledronic Acid	0

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Bone Mineral Density (BMD)

BMD of the lumbar spine (L1-L4, anteroposterior view) and femoral neck (FN) was measured by dual energy X-ray absorptiometry (DXA) using a Hologic QDR-1000 scanner on day 21 of cycle 4 (day 84) (NCT00972959)
Timeframe: day 84

Intervention	T-scores (Median)
	Lumbar spine (L1-L4)	Femoral neck (FN)
Bortezomib/Dexamethasone/Zoledronic Acid	0.14	-2.68

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Bone Remodelling

Bone remodelling was studied by the measurement of the following serum indices on day 21 of cycle 4 (day 84) using an enzyme-linked immunosorbent assay (ELISA): i) bone resorption marker C-terminal cross-linking telopeptide of collagen type I (CTX) and ii) bone formation markers [osteocalcin (OC)]. (NCT00972959)
Timeframe: day 84

Intervention	ng/ml (Median)
	CTX	OC
Bortezomib/Dexamethasone/Zoledronic Acid	0.25	7.4

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Bone Remodelling

Bone remodelling was studied by the measurement of the following serum indices on day 21 of cycle 8 (day 168) using an enzyme-linked immunosorbent assay (ELISA): i) bone resorption marker C-terminal cross-linking telopeptide of collagen type I (CTX) and ii) bone formation marker [osteocalcin (OC)]. (NCT00972959)
Timeframe: day 168

Intervention	ng/ml (Median)
	CTX	OC
Bortezomib/Dexamethasone/Zoledronic Acid	0.17	10.2

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Complete Response Rate

(NCT00980395)
Timeframe: Two years

Intervention	Participants (Count of Participants)
VCR (Velcade, Cladribine and Rituximab)	8

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Progression-free Survival at 2 Years

PFS was calculated from the first dose of study drug to the first documentation of disease progression, death regardless of cause, or change in therapy due to disease progression, whichever occurred first. If disease progression did not occur by the end of treatment, patients were evaluated every 3 months until progression with physical examination, laboratory studies, and conventional computed tomographic imaging, up to a maximum of 2 years. The Kaplan-Meier product-limit method will be used to estimate progression-free survival in the presence of censoring. (NCT00980395)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
VCR (Velcade, Cladribine and Rituximab)	15

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Overall Survival at 2 Years

(NCT00980395)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
VCR (Velcade, Cladribine and Rituximab)	18

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Partial Response

(NCT00980395)
Timeframe: Two years

Intervention	Participants (Count of Participants)
VCR (Velcade, Cladribine and Rituximab)	14

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Bone Anabolic Effect of Bortezomib in Patients With Smoldering Myeloma.

The primary endpoint is the change in bone Alkaline Phosphatase at baseline and 6 weeks. (NCT00983346)
Timeframe: Baseline and 6 weeks

Intervention	Percentage of Baseline Value (Number)
	% Base Line Patient 1	% Base Line Patient 3	% Base Line Patient 4	% Base Line Patient 6	% Base Line Patient 7	% Base Line Patient 8	% Base Line Patient 10	% Base Line Patient 11	% Base Line Patient 13	% Base Line Patient 14	% Base Line Patient 15	% Base Line Patient 16	% Base Line Patient 17
Arm 1 Bortezomib	178	105	105	99	95	119	128	84	125	120	96	98	431

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Number of Participants With Dose Limiting Toxicities (DLT) (Phase 1)

Safety assessments will be evaluated as the proportion of patients experiencing the following: treatment-related grade 3 or higher toxicity (hematologic and nonhematologic) and treatment-related death. (NCT00985907)
Timeframe: Up to 2 cycles of treatment, approximately 56 days

Intervention	Participants (Count of Participants)
Doxil® + Melphalan + Velcade (DMV)	0

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Maximum Observed Plasma Concentration (Cmax) of Bortezomib (JNJ-26866138 Alone) - Phase I

Cmax of bortezomib following intravenous administration of JNJ-26866138 at dose of 0.7, 1.0, and 1.3 mg/m2 on Cycle 1/Day 25 (JNJ-26866138 alone) (NCT00985959)
Timeframe: Day 25 of Cycle 1

Intervention	ng/mL (Mean)
Phase I - JNJ-26866138 0.7 mg/m2 Group	45.43
Phase I - JNJ-26866138 1.0 mg/m2 Group	59.42
Phase I - JNJ-26866138 1.3 mg/m2 Group	120.3

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Maximum Observed Plasma Concentration (Cmax) of Bortezomib (JNJ-26866138 in Combination With Melphalan and Prednisolone) - Phase I

Cmax of bortezomib following intravenous administration of JNJ-26866138 at dose of 0.7, 1.0, and 1.3 mg/m2 on Cycle 2/Day 4 (combination with melphalan and prednisolone) (NCT00985959)
Timeframe: Day 4 of Cycle 2

Intervention	ng/mL (Mean)
Phase I - JNJ-26866138 0.7 mg/m2 Group	34.40
Phase I - JNJ-26866138 1.0 mg/m2 Group	69.50
Phase I - JNJ-26866138 1.3 mg/m2 Group	88.87

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Maximum Observed Plasma Concentration (Cmax) of Melphalan - Phase I

Cmax of melphalan at dose of 9 mg/m2 on Cycle 2/Day 4 (NCT00985959)
Timeframe: Day 4 of Cycle 2

Intervention	ng/mL (Mean)
Melphalan	100.2

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Maximum Observed Plasma Concentration (Cmax) of Prednisolone - Phase I

Cmax of Prednisolone at dose of 60 mg/m2 on Cycle 2/Day 4 (NCT00985959)
Timeframe: Day 4 of Cycle 2

Intervention	ng/mL (Mean)
Prednisolone	1131

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Median Time to First Response - Phase II

Time to first response is the duartion of time required to achieve first response to treatment (NCT00985959)
Timeframe: up to 54 weeks

Intervention	Days (Median)
Phase II - JNJ-26866138 1.3 mg/m2 Group	51

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Number of Participants With Dose Limiting Toxicity During the Phase I (Cycle 1)

Dose limiting toxicity defined as an adverse event or adverse drug reaction experienced by the participants during 6 weeks of treatment Cycle 1 (NCT00985959)
Timeframe: 6 weeks

Intervention	Participants (Number)
Phase I - JNJ-26866138 0.7 mg/m2 Group	0
Phase I - JNJ-26866138 1.0 mg/m2 Group	0
Phase I - JNJ-26866138 1.3 mg/m2 Group	1

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Number of Participants With Overall Response (Complete Response [CR] + Partial Response [PR]) - Phase I and II

Response is evaluated as per the criteria for evaluating disease response and progression in patients with multiple myeloma treated by high-dose therapy and haemopoietic stem cell transplantation (Blade et al. 1998). CR: disappearance of the original monoclonal protein from the blood and urine and <5% plasma cells in the bone marrow on at least 2 determinations for a minimum of 6 weeks; no increase in the size or number of lytic bone lesions; disappearance of soft tissue plasmacytomas for at least 6 weeks. PR: ≥50% reduction in the level of serum monoclonal protein for at least 2 determinations 6 weeks apart; If present, reduction in 24-hour urinary light chain excretion by either ≥90% or to <200 mg for at least 2 determinations 6 weeks apart; ≥50% reduction in the size of soft tissue plasmacytomas for at least 6 weeks; no increase in size or number of lytic bone lesions (NCT00985959)
Timeframe: 54 weeks

Intervention	Participants (Number)
Phase I - JNJ-26866138 0.7 mg/m2 Group	6
Phase I - JNJ-26866138 1.0 mg/m2 Group	5
Phase I - JNJ-26866138 1.3 mg/m2 Group	4
Phase II - JNJ-26866138 1.3 mg/m2 Group	60
Total	71

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Overall Survival (in Days)

(NCT00990652)
Timeframe: Days 1, 4, 8 pre-surgery, once per cycle (every 4 weeks) while on treatment post-surgery, and then every 3 months up to 2 years during follow-up

Intervention	days (Median)
Bortezomib + Temozolomide	248

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Number of Grade 1, 2, 3, 4, and 5 Adverse Events Observed During Study Treatment (Defined by CTCAE v 3.0)

"Adverse events (AEs) were graded according to the National Cancer Institute's Common Toxicity Criteria for Adverse Events (CTCAE) version 3.0. In general, AEs are graded according to the following:~Grade 1 Mild AE Grade 2 Moderate AE Grade 3 Severe AE Grade 4 Life-threatening or disabling AE Grade 5 Death related to AE" (NCT00990652)
Timeframe: Days 1, 4, 8 pre-surgery, and then at the start of every cycle (approximately every 4 weeks) post-surgery while on treatment

Intervention	adverse events (Number)
	Grade 1	Grade 2	Grade 3	Grade 4	Grade 5
Bortezomib + Temozolomide	80	30	11	1	0

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Overall Survival Rate at 6 Months

The rate of overall survival at 6 months (regardless of disease progression) was calculated. (NCT00990652)
Timeframe: After 6 months on study

Intervention	percentage of participants (Number)
Bortezomib + Temozolomide	69

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Number of Patients Surviving Without Disease Progression After 6 Months

"Patients will be monitored from date of first treatment to the date of first observation of progressive disease, non-reversible neurologic progression or increasing steroid requirements, death due to any cause, or early discontinuation of treatment. Progression-free survival will be defined as the absence of any of the above after 6 months.~Progression (defined by MacDonald Criteria) is a 25% increase in the sum of products of all measurable lesions over smallest sum observed compared to baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to the cancer)." (NCT00990652)
Timeframe: From date of first treatment until disease progression, death, or early discontinuation of treatment (up to 24 months)

Intervention	participants (Number)
Bortezomib + Temozolomide	0

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Number of Participants Achieving a Response to Treatment (Either Complete or Partial Response) as Defined by MacDonald Criteria

"This measure was assessed only in patients who had residual tumor post-operatively. Per MacDonald Criteria:~Complete Response requires complete disappearance of all measurable & evaluable disease, no new lesions, no evidence of non-evaluable disease, and only minimal or no use of steroids.~Partial Response is defined as >= 50% decrease compared to baseline in the sum of products of perpendicular diameters of all measurable lesions, no progression of evaluable disease, and no new lesions. Responders must be on the same or decreasing doses of steroid.~Response was assessed by imaging (MRI or CT with contrast)." (NCT00990652)
Timeframe: Day of treatment post-surgery and then approximately every 8 weeks thereafter until off treatment

Intervention	participants (Number)
Bortezomib + Temozolomide	0

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Overall Survival

Number of patients alive who received maintenance therapy (NCT00992446)
Timeframe: 6.64 Years Post-Transplant

Intervention	participants (Number)
	Alive	Dead
Treatment (Chemotherapy, ASCT, Bortezomib, Vorinostat))	16	3

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Event-free Survival

Number of patients alive without disease progression/relapse (NCT00992446)
Timeframe: 6.64 Years Post-Transplant

Intervention	Participants (Count of Participants)
	Alive without disease porgression	alive with disease progression
Treatment (Chemotherapy, ASCT, Bortezomib, Vorinostat))	14	5

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Toxicity of Vorinostat Bortezomib Maintenance Therapy After Autologous Transplant

Number of patients on maintenance therapy post-transplant who experienced grade 3 or higher toxicity per NCI-Common Terminology Criteria for Adverse Events, version 3. The first three months of bortezomib and vorinostat therapy will be used as the time period to evaluate toxicity for stopping rules of the study. Toxicity that meets stopping rules will be determined based on the number of patients that are withdrawn from study for significant toxicity (grade IV, non-hematological, non-metabolic, non-peripheral neuropathy). (NCT00992446)
Timeframe: 3 months after start of maintenance therapy

Intervention	Participants (Count of Participants)
Treatment (Chemotherapy, ASCT, Bortezomib, Vorinostat))	19

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Median Time to Disease Progression

median days from transplant to relapse/progression (NCT00992446)
Timeframe: time post ASCT to progression

Intervention	years (Median)
Treatment (Chemotherapy, ASCT, Bortezomib, Vorinostat))	1.05

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Survival at 1 Year

Overall Survival at 12 months from completion of radiation treatment (NCT00998010)
Timeframe: 1 year

Intervention	percentage of participants (Median)
Experimental	87.5

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Overall Survival

Estimate the overall survival in subjects with newly-diagnosed glioblastoma (GBM) treated with bortezomib/temozolomide/radiation followed by bortezomib/temozolomide for 24 cycles until progression is detected or for up to 24 cycles (~2 years). (NCT00998010)
Timeframe: 2 years

Intervention	months (Mean)
Experimental	19.1

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Toxicity Assessed According to the NCI Common Terminology Criteria for Adverse Events (CTCAE) Version 3.

(NCT00998010)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
	Radiotherapy phase72241098			Post Radiotherapy phase72241098	Follow-up phase72241098
	Grade 4 Toxicity	< Grade 3 Toxicity	Grade 3 toxicity
Experimental	6
Experimental	1
Experimental	17
Experimental	7
Experimental	0
Experimental	24

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Tumor Progression as Assessed by Magnetic Resonance Imaging (MRI) and Neurologic Exam

MRI will be done 2 weeks after completion of radiation and then every 8 weeks. Neurologic exam to be performed every 2 weeks during radiation therapy, then every every 4 weeks after radiation is completed. (NCT00998010)
Timeframe: at 6, 12, 18 and 24 months from completion of radiation treatment.

Intervention	percentage of participants (Median)
	Progression Free Survival rate at 6 months	Progression Free Survival rate at 12 months	Progression Free Survival rate at 18 months	Progression Free Survival rate at 24 moths
Experimental	54.2	29.2	25.0	25

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Time to Progression

"Median time to tumor progression. Because many newly-diagnosed patients are likely not to have evaluable disease due to gross total resections. A 7-point scale was used to guide Magnetic resonance imaging (MRI) assessment to determine progression in this study. A -2 or -3 assessment will be taken as progression.~The 7-point scale is listed below. complete resolution of tumor: 3 tumor definitely smaller: 2 tumor probably smaller: 1 tumor unchanged: 0 tumor probably worse: -1 tumor definitely worse: -2 new lesion: -3" (NCT00998010)
Timeframe: From the completion of radiation treatment to tumor progression

Intervention	months (Median)
Experimental	6.2

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Efficacy of Treatment as Measured by Best Overall Response

-The response definitions used for this study are the 2007 Cheson criteria. (NCT01000285)
Timeframe: Up to 4 years following completion of therapy

Intervention	participants (Number)
	Progressive Disease	Stable disease	Partial response	Complete response
EPOCH Chemotherapy & Bortezomib	3	3	9	3

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Effects of on HTLV-1 DNA After Treatment as Measured by Proviral Loads

(NCT01000285)
Timeframe: 6 months

Intervention	copies/peripheral blood mononuclear cell (Mean)
	Baseline	Study completion
Non-responders	0.417	0.033
Responders	0.372	0.0128

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Effects of HTLV-1 RNA Load After Treatment as Measured by Hbz Messenger RNA

(NCT01000285)
Timeframe: 6 months

Intervention	copies/peripheral blood mononuclear cell (Mean)
	Baseline	Study completion
Non-responders	41.9	35.7
Responders	37.0	7.33

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Effects of HTLV-1 Integration Sites After Treatment

(NCT01000285)
Timeframe: 6 months

Intervention	number of integration sites (Mean)
	Baseline	Study completion
EPOCH Chemotherapy & Bortezomib	1.31	1.00

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Effects of HTLV-1 Integrase Gene Sequence After Treatment as Measured by Nucleotide Divergence

(NCT01000285)
Timeframe: 6 months

Intervention	percentage of nucleotide divergence (Mean)
	Baseline	Study completion
EPOCH Chemotherapy & Bortezomib	0.49	0.52

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Time to Progression

-The progression definitions used for this study are from the 2007 Cheson criteria. (NCT01000285)
Timeframe: Up to 4 years following completion of therapy

Intervention	days (Median)
	Best response of complete response	Best response of partial response	Best response of stable disease	All participants
EPOCH Chemotherapy & Bortezomib	199	143	88	127

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Tolerability of Treatment as Measured by Number of Participants With Grade 3 or Higher Adverse Events

The descriptions and grading scales found in the revised NCI Common Terminology Criteria for Adverse Events (CTCAE) version 3.0 will be utilized for all toxicity reporting. (NCT01000285)
Timeframe: Up to 30 days after completion of treatment

Intervention	participants (Number)
	Fatigue	Vomiting	Spontaneous bacterial peritonitis	Abdominal distension	Hemoglobin	Leukocytes (WBC)	Lymphopenia	Neutrophils	Platelets	Infection without neutropenia	Infection with neutropenia	Omaya port infection	IV port infection	Sepsis	Neutropenic fever	Hypoglycemia	Hyperglycemia	Magnesium	Hypokalemia	Hypertriglyceridemia	Confusion	Headache	Encephalitis	Abdominal pain	Cough	Dyspnea
EPOCH Chemotherapy & Bortezomib	1	1	1	2	6	7	1	6	6	1	1	1	1	2	3	1	2	1	1	1	1	1	1	1	1	1

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Relation of NFκB Gene Expression Profile on Response

Standard error represents the standard error of the fold expression of protein coding transcripts for each gene indicated. (NCT01000285)
Timeframe: 6 months

,,,,,,,

Intervention	fold expression (Mean)
	BLK	CADMI	CD25	CD4	CD45
Patient A (Responder) Post-Therapy	0.178	0.011	0.035	1.380	1.718
Patient A (Responder) Pre-Therapy	1.000	1.000	1.000	1.000	1.000
Patient B (Responder) Post-Therapy	0.172	0.007	0.015	0.607	0.959
Patient B (Responder) Pre-Therapy	0.889	0.623	0.303	1.437	2.049
Patient C (Non-responder) Post-Therapy	77.590	1.816	0.691	1.923	1.640
Patient C (Non-responder) Pre-Therapy	68.856	1.494	0.862	1.319	1.163
Patient D (Non-responder) Post-Therapy	46.801	0.470	0.512	0.648	0.714
Patient D (Non-responder) Pre-Therapy	233.179	2.013	2.897	3.057	0.594

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Percent Difference Between Area Under Curve (AUC) and Target AUC

A test dose of IV busulfan 0.8 mg/kg was infused at Baseline (Day -12 to -9) to verify a target busulfan integrated AUC of 20,000 μM*min with a range of 16,000 to 24,000. If necessary the dose could be adjusted. The PK-directed dose recommendation based on the test dose was administered at Day -5. Blood samples for PK analysis were collected at 0, 15, 30 minutes after the End of Infusion and 240, 300, 360 minutes after start of the infusion. GC-MS was used to determine the busulfan level in plasma. The percent difference was calculated between AUC and the Target AUC. (NCT01009840)
Timeframe: Baseline (Day -12 to -9), Day -5

Intervention	Percent difference (Median)
IV Busulfan	-0.22

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Overall Survival

Overall Survival was defined as the time in days from transplantation to death due to all causes. (NCT01009840)
Timeframe: 6 Months

Intervention	Days (Median)
IV Busulfan	NA

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Percent Change in IV Busulfan Dose

The percent change in dose is relative to the busulfan dose administered at the Baseline Visit (Day -12 to -9) when a dose of 0.8 mg/kg was administered and on Day -5 when the Seattle Cancer Care Alliance recommended PK-adjusted dose was administered. (NCT01009840)
Timeframe: Baseline (Day -12 to -9), Day -5

Intervention	Percent change (Median)
IV Busulfan	7.55

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Percentage of Participants With Hepatic Veno-Occlusive Disease Based on Baltimore Criteria

The Baltimore criteria for veno-occlusive disease was defined as the development of hyperbilirubinemia with serum bilirubin > 2 mg/dl within 21 days after transplantation and at least 2 of the following clinical signs and symptoms: (1) hepatomegaly, usually painful, (2) > 5% weight gain, or (3) ascites. (NCT01009840)
Timeframe: 6 Months

Intervention	Percentage of participants (Number)
IV Busulfan	0.0

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Percentage of Participants With Overall Disease Response at Month 6

The percentage of participants reported in each disease category by International Myeloma Working Group (IMWG) uniform response criteria for Multiple Myeloma 6 months after autologous Hematopoietic stem cell transplant. Overall Disease Response categories were: [stringent Complete Response (sCR)=CR + normal Free Light Chain (FLC) ratio + absence of clonal cells in bone marrow], [Complete Response (CR)=Negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and ≤5% plasma cells in bone marrow], [Very Good Partial Response (VGPR)=Serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein + urine M-protein level <100 mg/24 hour], [Partial Response (PR)=≥50% reduction of serum M-protein and reduction in 24 hour urine M-protein by ≥90% or to <200 mg per 24 hour], [Stable Disease (SD)=Not meeting criteria for CR, VGPR, PR or progressive disease] or [Progressive Disease (PD)]. (NCT01009840)
Timeframe: 6 Months

Intervention	Percentage of participants (Number)
	sCR or CR or VGPR	PR or SD or PD	Not Assessed
IV Busulfan	20.0	70.0	10.0

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Ratio Area Under Curve (AUC)/Target AUC

A test dose of IV busulfan 0.8 mg/kg was infused at Baseline (Day -12 to -9) to verify a target busulfan integrated AUC of 20,000 μM*min with a range of 16,000 to 24,000. If necessary the dose could be adjusted. The PK-directed dose recommendation based on the test dose was administered at Day -5. Blood samples for PK analysis were collected at 0, 15, 30 minutes after the End of Infusion and 240, 300, 360 minutes after start of the infusion. Gas chromatography with mass selective detection (GC-MS) was used to determine the busulfan level in plasma. The ratio was calculated: AUC/Target AUC. (NCT01009840)
Timeframe: Baseline (Day -12 to -9), Day -5

Intervention	Ratio (Median)
IV Busulfan	1.00

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Progression-free Survival

Progression-free Survival (PFS) defined as the time from transplantation to the occurrence of the event that was death or first recurrence of progressive disease (PD) by IMWG criteria. PD was defined as an Increase of ≥25% from the lowest response value in any one or more of the following: 1)Serum M-component and/or (the absolute increase must be ≥0.5 g/dL), 2)Urine M-component and/or (the absolute increase must be ≥200 mg/24 hr), 3)In patients without measurable serum and urine M-protein levels; the difference between involved and uninvolved FLC levels. The absolute increase must be >10 mg/dL, 4)Bone marrow plasma cell percentage; the absolute percentage must be ≥10%, 5)Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas and/or 6)Development of hypercalcaemia that can be attributed solely to the plasma cell proliferative diso (NCT01009840)
Timeframe: 6 Months

Intervention	Days (Median)
IV Busulfan	191

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Percentage of Participants With Transplant-Related Mortality

The percentage of participants with death related to transplant. (NCT01009840)
Timeframe: 6 Months

Intervention	Percentage of participants (Number)
IV Busulfan	3.3

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Percentage of Participants With Progression-free Survival Events

Progression-free survival events are death or first recurrence of progressive disease by International Myeloma Working Group Criteria. (NCT01009840)
Timeframe: 6 Months

Intervention	Percentage of participants (Number)
IV Busulfan	50.0

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Percentage of Participants With Overall Survival Events

Overall Survival Event was death. (NCT01009840)
Timeframe: 6 Months

Intervention	Percentage of participants (Number)
IV Busulfan	13.3

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Functional Assessment of Chronic Illness Therapy (FACIT) Measurement System : FACT/GOG-NTX-Change From Baseline by Treatment Group

Chronic Illness Therapy (FACIT) Measurement System and focuses on four general quality of life domains for physical well being, functional well-being, social/family well-being, and emotional well-being, and includes additional items to characterize treatment-related neurotoxicity. Higher subscales/total scores represent higher QOL. In the case of the neurotoxicity subscale, lower scores correspond to higher neurotoxicity. The recall period referenced in the questionnaire is the past 7 days.Ranges for FACT-G subscales are as follows:.PWB, scale 0 -28, , NtxS scale 0-44, FACT/GOG-Ntx trial outcome index scale is 0-100 and FACT-G scale is also scaled 0-100. An increase from baseline in these scores indicate improvement. (NCT01023308)
Timeframe: 12, 24 and 48 weeks

Intervention	score on a scale (Least Squares Mean)
	Neurotoxicity wk 12 change baseline (n=212,240)	Neurotoxicity wk 24 change baseline (n=148,174)	Neurotoxicity wk 48 change baseline (n=35,26)	Physical wellbeing wk 12 chge (n=215,240)	Physical wellbeingwk 24 chge (n=150,176)	Physical wellbeing wk 48 chge (n=38,26)	Trial Outcomes wk 12 chge (n=209,236)	Trial Outcomes wk 24 chge (n=148,173)	Trial Outcomes wk 48 chge (n=35,26)	FACT-G Total wk 12 chge (n=213,240)	FACT-G Totalwk 24 chge (n=147,175)	FACT-G Total wk 48 chge (n=37,26)	FACT/GOGNTX Total wk 12 chge (n=206,230)	FACT/GOGNTX Total wk 24 chge (n=146,172)	FACT/GOGNTX Total wk 48 chge (n=35,26)
Panobinostat + Bortezomib	-4.481	-4.564	-3.158	-3.29	-3.044	-2.037	-10.573	-9.84	-6.633	-6.658	-6.076	-2.704	-11.176	-10.581	-5.871
Placebo + Bortezomib	-3.337	-4.739	-2.133	-1.952	-2.259	0.203	-6.874	-8.894	-2.821	-4.106	-4.609	-1.435	-7.524	-9.179	-3.151

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European Organization for Research and Treatment of Cancer Multiple Myeloma Module (EORTC) QLQ-MY20-Change From Baseline by Treatment Group

"Higher values in the disease symptoms and side effects of treatment scores indicate worsening. Higher scores in the future perspective and body image scores indicate improvement. LS Means and SEM are estimated from the repeated measures model. Following factors and covariates are included in the repeated measurement model: time, treatment, treatment by time interaction, number of prior lines of anti-MM therapy (1/ 2 and 3), prior use of BTZ (Yes/ No), baseline score.Disease Symptom is the sum of 20 questions, total score ranges from 0 (best possible outcome) to 100 (worst possible outcome), All subscales of EORTC QLQ-MY20 have the same score range of 0 -100. Decrease in symptom scores from baseline indicate improvement in symptoms." (NCT01023308)
Timeframe: 12, 24 and 48 weeks

Intervention	score on a scale (Least Squares Mean)
	Disease Symptom wk 12 change baseline (n=215,243)	Disease Symptom wk 24 change baseline (n=148,177)	Disease Symptom wk 48 change baseline (n=37,26)	Side effects of treatment wk 12 chge (n=213,242)	Side effects of treatment wk 24 chge (n=148,175)	Side effects of treatment wk 48 chge (n=37,26)	Future perspective wk 12 chge (n=214,242)	Future perspective wk 24 chge (n=148,176)	Future perspective wk 48 chge (n=37,26)	Body image wk 12 chge (n=213,240)	Body image wk 24 chge (n=147,175)	Body image wk 48 chge (n=37,26)
Panobinostat + Bortezomib	-4.795	-4.401	-2.836	8.162	9.016	3.357	5.319	3.877	4.331	-7.178	-11.463	-2.161
Placebo + Bortezomib	-4.865	-6.797	-6.626	5.524	7.731	3.654	6.194	5.839	6.951	-6.22	-7.358	-4.666

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Time to Response Per Investigator Assessment (mEBMT Criteria) of Response Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone.

(NCT01023308)
Timeframe: 45 months

Intervention	time to response in months (Median)
Panobinostat + Bortezomib	1.51
Placebo + Bortezomib	2.00

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European Organization for Research and Treatment of Cancer Multiple Myeloma Module (EORTC ) QLQ-C30 - Summary Statistics by Treatment Group

"The EORTC QLQ-C30 measures functional dimensions (physical, role, emotional, cognitive, and social), three multi-item symptom scales (fatigue, nausea/vomiting, and pain), six single-item symptom scales (dyspnea, sleep disturbance, appetite loss, constipation, diarrhea and financial impact) and a global health status/QoL scale. Disease Symptom is the sum of 30 questions, total score ranges from 0 (best possible outcome) to 100 (worst possible outcome), All subscales of EORTC QLQ-C30 have the same score range of 0 -100. For global health status and other functional scales,an increase from baseline indicates improvement of QoL. Whereas for symptoms scales, fatigue, dyspnea, insomnia, appetite loss, constipation and diarrhea, decrease in scores from baseline indicate improvement in symptoms." (NCT01023308)
Timeframe: 12, 24 and 48 weeks

Intervention	score on a scale (Least Squares Mean)
	Global health wk 12 change baseline (n=216,239)	Global health wk 24 change baseline (n=150,176)	Global health wk 48 change baseline (n=38,26)	Physical functioning wk 12 chge (n=217,242)	Physical functioning wk 24 chge (n=151,177)	Physical functioning wk 48 chge (n=38,26)	Role functioning wk 12 chge (n=215,237)	Role functioning wk 24 chge (n=150,176)	Role functioning wk 48 chge (n=38,26)	Cognitive functioning wk 12 chge (n=216,240)	Cognitive functioning wk 24 chge (n=149,176)	Cognitive functioning wk 48 chge (n=38,26)	Social functioning wk 12 chge (n=216,240)	Social functioning wk 24 chge (n=148,171)	Social functioning wk 48 chge (n=37,26)	Fatigue wk 12 chge (n=217,241)	Fatigue wk 24 chge (n=151,176)	Fatigue wk 48 chge(n=38,26)	Dyspnea wk 12 chge (n=217,240)	Dyspnea wk 24 chge (n=151,177)	Dyspnea wk 48 chge (n=38,26)	Insomnia wk 12 chge (n=216,239)	Insomnia wk 24 chge (n=149,176)	Insomnia wk 48 chge (n=38,26)	Appetite loss wk 12 chge (n=217,239)	Appetite loss wk 24 chge (n=151,176)	Appetite loss wk 48 chge (n=38,26)	Constipation wk 12 chge (n=215,240)	Constipation wk 24 chge (n=151,177)	Constipation wk 48 chge (n=38,25)	Diarrhea wk 12 chge (n=217,241)	Diarrhea wk 24 chge (n=150,177)	Diarrhea wk 48 chge (n=38,26)
Panobinostat + Bortezomib	-9.853	-7.867	-2.986	-9.67	-9.516	-2.88	-11.159	-11.875	-5.927	-4.464	-6.053	-5.568	-8.502	-8.925	-6.104	15.122	12.677	4.646	13.964	7.939	4.118	6.283	10.023	-2.464	15.167	16.574	3.999	4.135	-0.153	-0.358	18.888	23.163	20.48
Placebo + Bortezomib	-4.044	-1.518	4.345	-5.393	-6.456	2.037	-6.762	-11.263	-0.401	-1.023	-3.542	-4.042	-3.991	-6.338	4.617	7.939	9.203	-2.625	6.266	5.308	2.82	7.625	6.104	-3.442	5.383	5.861	-2.963	6.42	0.524	-0.946	10.206	16.406	10.996

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Overall Response Rate in Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone.

Best overall response based on mEBMT criteria per investigator assessment (NCT01023308)
Timeframe: 45 months

Intervention	% participants with response (Number)
Panobinostat + Bortezomib	60.7
Placebo + Bortezomib	54.6

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Duration of Response Per Investigator Assessment (mEBMT Criteria) Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone.

(NCT01023308)
Timeframe: 45 months

Intervention	duration of response in months (Median)
Panobinostat + Bortezomib	13.14
Placebo + Bortezomib	10.87

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Overall Survival in Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone

Number of OS events (NCT01023308)
Timeframe: 45 months

Intervention	Number of OS events (Number)
Panobinostat + Bortezomib	134
Placebo + Bortezomib	152

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Overall Survival in Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone

survival time in months (NCT01023308)
Timeframe: 45 months

Intervention	months (Median)
Panobinostat + Bortezomib	40.28
Placebo + Bortezomib	35.78

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Progression Free Survival in Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone.

(NCT01023308)
Timeframe: 45 months

Intervention	months (Median)
Panobinostat + Bortezomib	11.99
Placebo + Bortezomib	8.80

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Time to Progression/Relapse Per Investigator Assessment (mEBMT Criteria) Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone.

(NCT01023308)
Timeframe: 45 months

Intervention	months (Median)
Panobinostat + Bortezomib	12.71
Placebo + Bortezomib	8.54

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Progression-free Survival Events in Patients Treated With Panobinostat in Combination With Bortezomib and Dexamethasone vs. Patients Treated by Placebo in Combination With Bortezomib and Dexamethasone.

(NCT01023308)
Timeframe: 45 months

Intervention	number of events (Number)
Panobinostat + Bortezomib	207
Placebo + Bortezomib	260

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Median Progression-free Survival

The Length of Time, in Months, That Patients Were Alive From Their First Date of Protocol Treatment Until Worsening of Their Disease. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT01029730)
Timeframe: at 3 and 6 months, then every 3 months post-treatment for 1 year and every 6 months thereafter until disease progression; projected 2 years.

Intervention	months (Median)
Bendamustine/Bortezomib/Rituximab	NA

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Complete Response Rate

Percentage of patients experiencing a complete response (CR) per RECIST. CR = disappearance of all target lesions. (NCT01029730)
Timeframe: 18 months

Intervention	percentage of evaluable participants (Number)
Bendamustine/Bortezomib/Rituximab	65

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Number of Participants With Adverse Events as a Measure of Safety.

Toxicity grades will be assessed using National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) v4.0. Includes adverse events occurring in >1 patient (NCT01029730)
Timeframe: Days 1,8, and 15 of each 28-day cycle for 6 months, then every 3 months for a year, projected 2 years.

Intervention	participants (Number)
	Leukopenia	Neutropenia	Lymphopenia	Thrombocytopenia	Anemia	Peripheral Neuropathy	Diarrhea	Fatigue	Nausea/Vomiting	Cough	Rash	Syncope	Hypocalcemia/Hyponatremia
Bendamustine/Bortezomib/Rituximab	16	16	9	4	3	5	4	4	3	2	2	2	2

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Overall Response Rate

The Percentage of Patients Who Experience an Objective Benefit From Treatment. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI or CT: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT01029730)
Timeframe: At 3 and 6 months during treatment, then 6 months post-treatment.

Intervention	percentage of evaluable participants (Number)
Bendamustine/Bortezomib/Rituximab	94

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Overall Response Rate to the Combination of MLN8237 and Bortezomib in Patients With Relapsed or Refractory Multiple Myeloma.

sCR: Normal serum FLC ratio, and absence of clonal cells in bone marrow by immunohistochemistry or immunofluorescence, negative immunofixation of the serum and urine, <5% plasma cells in bone marrow, disappearance of any soft tissue plasmacytomas, and normalization of FLC ratio. VGPR:PR and serum and urine M-component detectable by immunofixation but not on electrophoresis, or if serum measurable,≥90% or greater reduction in serum M-component plus urine M-component <100 mg per 24h and if only measurable non-bone marrow parameter was FLC,≥90% or greater reduction in difference from involved and uninvolved FLC levels. PR:≥50% reduction of serum M-protein or reduction in 24-h urinary M-protein by ≥90% or to <200 mg per 24h or if FLC, ≥50% decrease in the difference between involved and uninvolved FLC levels or ≥50% reduction in bone marrow plasma cells is required in place of M-protein, provided baseline percentage was ≥30%, and ≥50% reduction in the size of soft tissue plasmacytomas (NCT01034553)
Timeframe: Every 28 day cycle(up to 10 cycles)

,,,

Intervention	percentage of patients per dose level (Number)
	Strong Complete Response	Very Good Partial Response	Partial Response
Dose Level 0	14.3	0	14.3
Dose Level 1	0	33.3	0
Dose Level 2	0	0	0
Dose Level 3	0	7.7	23.1

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Dose-limiting Toxicity (DLT) (Phase I)

"Patients were evaluated over the first cycle of treatment for Dose Limiting Toxicities. For this trail DLTs are as follows:~An AE attributed (definitely, probably, or possibly) to study treatment during cycle 1 and the following criteria:~Grade 4 Neutropenia Grade 4 Thrombocytopenia, or grade 3 with bleeding Febrile neutropenia Creatinine serum great than 2 times baseline or upper limit of normal Grade 3 or higher Fatigue Grade 3 or higher nausea, vomiting, or diarrhea Any grade 3 or higher Non-hematologic toxicity per NCI CTCAE V4.0 Inability to initiate the scheduled cycle 2, day 1 due to toxicity~The maximum tolerated dose level (MTD) will be defined as the highest safely tolerated dose." (NCT01034553)
Timeframe: 28 days

Intervention	participants (Number)
Dose 0**	0
Dose 0	0
Dose 1	0
Dose 2	0
Dose 3	0

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Overall Survival

(NCT01034553)
Timeframe: Every 28 day cycle(up to 10 cycles) then follow-up for up to 2 years

Intervention	Months (Median)
All Patients	23.6

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Progression-free Survival

(NCT01034553)
Timeframe: Every 28 day cycle(up to 10 cycles) then follow-up for up to 2 years

Intervention	Months (Median)
All Patients	5.9

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Rate of Durable Complete Response

Proportion of subjects who achieved a CR with duration of at least 6 months (NCT01040871)
Timeframe: Median follow up approx 12 months

Intervention	percentage of participants (Number)
VR-CAP	44.7
R-CHOP	47.3

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Rate of Durable Response

Proportion of subjects who achieved a CR or PR with duration of at least 6 months. Duration of response (CR or PR) was calculated from the date of initial documentation of a response to the date of first documented evidence of disease progression or death due to disease progression. Response was evaluated by an Independent Radiology Review Committee using available computed tomography (CT) and positron emission tomography (PET) scans collected at Baseline, end of cycle 3, end of cycle 6 (or end of treatment) based on the Revised Response Criteria for Malignant Lymphoma. (NCT01040871)
Timeframe: Median follow up approx. 12 months

Intervention	percentage of participants (Number)
VR-CAP	53.9
R-CHOP	67.6

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Subsequent Anti-lymphoma Therapy Rate at 1-year

Kaplan-meier estimate of subsequent anti-lymphoma therapy at 1-year. Time to subsequent anti-lymphoma therapy was measured from the date of randomization to the start date of new treatment. Death due to disease progression prior to subsequent therapy was considered as an event. Otherwise, time to next anti-lymphoma treatment was censored at the date of death or the last date known to be alive. (NCT01040871)
Timeframe: 1 year

Intervention	percentage of participants (Number)
VR-CAP	71.1
R-CHOP	80.2

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Overall Survival Rate at 1-year

Kaplan-meier estimate of overall survival at 1-year measured from date of randomization. (NCT01040871)
Timeframe: 1 year

Intervention	percentage of partipants (Number)
VR-CAP	94.1
R-CHOP	84.2

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Overall Response Rate

"Overall response = Complete Response (CR) + Partial Response (PR) Response was evaluated by an Independent Radiology Review Committee using available computed tomography (CT) and positron emission tomography (PET) scans collected at Baseline, end of cycle 3, and end of cycle 6 (or end of treatment) based on the Revised Response Criteria for Malignant Lymphoma.~Complete Response: see primary endpoint Partial Response: At least a 50% decrease in the sum of the product of the diameters (SPD) of up to 6 of the largest dominant nodes or nodal masses." (NCT01040871)
Timeframe: 6 cycles

Intervention	percentage of participants (Number)
VR-CAP	93.4
R-CHOP	98.6

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Complete Response (CR) Rate

"Complete response was evaluated by an Independent Radiology Review Committee using available computed tomography (CT) and positron emission tomography (PET) scans collected at Baseline, end of cycle 3, and end of cycle 6 (or end of treatment) based on the Revised Response Criteria for Malignant Lymphoma.~Complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present before therapy.~PET scan was negative.~The spleen and/or liver, if enlarged before therapy on the basis of physical examination or CT scan, was not palpable on physical examination and was considered normal size by imaging studies; all splenic and hepatic nodules related to lymphomas disappeared.~If bone marrow was involved before treatment, the infiltrate cleared on repeated bone marrow biopsy.~No new sites of disease were detected." (NCT01040871)
Timeframe: 6 cycles

Intervention	percentage of participants (Number)
VR-CAP	64.5
R-CHOP	63.5

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Progression-free Survival (PFS)Rate at 1-year

Kaplan-meier estimate of progression-free survival at 1-year. Progression-free survival was defined as the interval between the date of randomization and the date of first documented evidence of disease progression or death. (NCT01040871)
Timeframe: 1 year

Intervention	percentage of partipants (Number)
VR-CAP	78.9
R-CHOP	83.9

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Complete Response Rate

Defined as the percent of patients having a complete response (CR) to treatment, assessed using the International Myeloma Working Group (IMWG) Uniform Response Criteria. CR=disappearance of soft tissue plasmacytomas and 5% or less plasma cells in bone marrow. (NCT01056276)
Timeframe: every 8 weeks for approximately 48 months

Intervention	percentage of participants (Number)
Original BBD Regimen	0
Modified BBD Regimen	13

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Overall Survival

Defined as the interval of time, in months, from first study treatment until the earlier of the date of death or date last known alive. (NCT01056276)
Timeframe: every 4 weeks until progressive disease then every 12 weeks, projected 48 months

Intervention	months (Median)
Original BBD Regimen	NA
BBD Treatment	NA

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Number of Patients Who Experienced Serious and Non-serious Adverse Events

All serious adverse events (SAEs) and non-serious adverse events (AEs) were assessed using National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) v4.0, and were collected from start of study treatment until 30 days after last dose of study medication. Refer to the Adverse Event module for specific terms. (NCT01056276)
Timeframe: approximately 36 weeks

Intervention	participants (Number)
	SAEs	AEs
Modified BBD Regimen	17	38
Original BBD Regimen	7	18

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Overall Response Rate

The number of patients with observed complete or partial response (CR or PR) assessed by International Myeloma Working Group (IMWG) Uniform Response Criteria. PR=50% or greater reduction from baseline in serum M-protein and 90% or greater reduction from baseline in 24-hour urinary M-protein. (NCT01056276)
Timeframe: every 4 weeks for approximately 2 years

Intervention	participants (Number)
	CR	PR
Modified BBD Regimen	5	8
Originl BBD Regimen	0	5

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Progression Free Survival

Defined as the interval of time (in months) that patient are alive from date of first protocol treatment to date of documented tumor progression or date of death from any cause. Progressive disease, assessed according to International Myeloma Working Group Uniform Response Criteria, is defined as at least a 25% increase from the nadir in any one of the following criteria: serum M-protein, urine M-protein, or bone marrow plasma cell percentage of 10% or greater. (NCT01056276)
Timeframe: every 8 weeks for up to 48 months

Intervention	months (Median)
Original BBD Regimen	11.1
Modified BBD Regimen	18.9

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Progression-Free Survival

Median number of months before disease progressed in patient on gemcitabine when treated with the combination of panobinostat and bortezomib. Progression free survival is measured from randomization until the subject has documented disease progression by an objective measure. Subjects must be alive with no more than 20% increase in tumor size to qualify for progression free survival. Changes in tumor size are defined by RECIST criteria. (NCT01056601)
Timeframe: Up to 1 Year

Intervention	Months (Median)
Pancreatic Cancer Patients	2.1

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Number of Participants by Tumor Response

Number of patients whose tumor has responded to study therapy is determined using Response Evaluation Criteria In Solid Tumors. Progressive Disease (PD) is assessed if the sum of the diameters has increased by ≥ 20% and ≥ 5 mm from nadir (including baseline if it is the smallest sum). Objective response is measured by tumor reduction as defined in the RECIST criteria. Tumor shrinkage must be at least 30% to qualify as an objective response. (NCT01056601)
Timeframe: Up to 1 Year

Intervention	Participants (Number)
	Progressive Disease	No data available	Objective Response
Pancreatic Cancer Patients	5	2	0

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Duration of Response

Duration of response is calculated as (Date of First Disease Progression or Death as a Result of any Cause whichever Comes First - Date of First Objective Status Assessment of Confirmed Complete or Partial Response as defined by RECIST criteria). (NCT01056601)
Timeframe: Up to 1 Year

Intervention	Weeks (Number)
Pancreatic Cancer Patients	0

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Treatment Related Toxicities

The toxicities experienced by participants that were deemed to be related to the study treatment. Data is shown as the number of participants that experienced any grade toxicity that was deemed to be related to treatment. Toxicities were assessed with the use of Common Toxicology Criteria for Adverse Events (CTCAE). (NCT01058239)
Timeframe: 2 years

Intervention	participants (Number)
	Febrile Neutropenia	Leukocytosis	Lymph Node Pain	Abdominal Pain	Nausea	Neutrophil Count Decreased	Platelet Count Decreased	Alkalosis	Anorexia	Peripheral Sensory Neuropathy
Rituximab Plus Bortezomib	1	1	2	1	1	2	4	1	1	2

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Overall Survival

The percent of participants surviving at 6 months and 1 year. (NCT01058239)
Timeframe: 6 months, 1 year

Intervention	percentage of participants (Number)
	6 month	12 Month
Rituximab Plus Bortezomib	86	86

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Effects of Bortezomib/Rituximab on EBV Quantitative Viral Load

The Mean epstein barr virus (EBV) viral load at the given time points. (NCT01058239)
Timeframe: baseline, 21, 42, 63, 84 days (end of cycles 1, 2, 3, 4)

Intervention	Log2[(viral copies/ milliliter blood)+1] (Mean)
	Baseline	End of Cycle 1 (21 days)	End of Cycle 2 (42 days)	End of Cycle 3 (63 days)	End of Cycle 4 (84 days)
Rituximab Plus Bortezomib	13.02	10.12	9.11	8.98	7.85

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Six-Month Progression Free Survival

"Percent of participants with progression free survival (alive without disease progression) six months after registration. Progression was evaluated using the International Working Group criteria for lymphoma response.~> Progressive Disease (PD) or Relapsed Disease (RD):~Appearance of any new lesion > 1.5 cm in any axis during or at end of therapy. Increased Radiolabeled[18F]-2-fluoro-2-deoxy-D-glucose (FDG) uptake in a previously unaffected site will be considered PD/RD only after confirmation by other modalities.~≥ 50% increase from nadir in the sum of the products of the largest diameters (SPD) of any previously involved node, or in a single involved node, or in the sizes of other lesions.~≥ 50% increase in the longest diameter of any single previously identified node > 1 cm in its short axis.~PET (positron emission tomography) positive prior to therapy: post-treatment PET should be positive unless lesion is too small to be detected with current PET sys" (NCT01058239)
Timeframe: six months

Intervention	percentage of participants (Number)
Rituximab Plus Bortezomib	43

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Overall Response Rate

"Overall response rate includes both complete and partial responses assessed by PET/CT following completion of therapy. Response was evaluated using the International Working Group criteria for lymphoma response. The complete list of criteria used to evaluate response is too long to be detailed in the allotted space here, but response is defined more generally as:~Complete Response (CR): Complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present before therapy.~Partial Response (PR): ≥ 50% decrease in the sum of the products of the diameters (SPD) of up to six of the largest dominant nodes or nodal masses." (NCT01058239)
Timeframe: 4 months

Intervention	Participants (Count of Participants)
Rituximab Plus Bortezomib	3

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Complete Response Rate

"The number of participants with complete responses as assessed by PET/CT following completion of therapy. Response was evaluated using the International Working Group criteria for lymphoma response.~Complete Response (CR): Complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present before therapy." (NCT01058239)
Timeframe: 4 Months

Intervention	Participants (Count of Participants)
Rituximab Plus Bortezomib	3

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Maximum Percent Change From Baseline in Intact Parathyroid Hormone Levels on Day 1

All patients received 0.7 mg/m2 of bortezomib on days 1, 4, 8 and 11 of a 21 day cycle, for maximum of three cycles for an average of 18 months. Intact Parathyroid hormone was measured in patients with relapsed/refractory myeloma for osteoblast activation. Other bone markers were examined using similar methods. (NCT01062230)
Timeframe: Baseline and Day 1

Intervention	% change (Number)
	Subject 1	Subject 2	Subject 3	Subject 4	Subject 5	Subject 6
All Patients	113.5	-9.09	30.7	-50	93.6	-53.5

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To Establish the Safety, Tolerability, and RP2D (Phase 1); To Assess the Overall Response Rate in Subjects With Advanced Multiple Myeloma (Phase 2).

"The safety of KW-2478 was determined by reported TEAEs, observed DLTs, changes in PEs, vital sign measurements, ECGs, and laboratory analyses.~The ORR, was defined as the best response over a specified number of cycles (calculated and summarized).~Disease control rate (DCR) was defined as the best response over a specified number of cycles (calculated and summarized). Progression-free survival was defined as the time from the first day of treatment until the date of disease progression or death is first reported (calculated and summarized)." (NCT01063907)
Timeframe: 21 day cycle, up to 52 weeks

,,,,,

Intervention	participants (Number)
	Subjects with Any TEAE	Related TEAE	Moderate (CTCAE 2) TEAE	Severe (CTCAE 3) TEAE	Life Threatening TEAE	Serious Treatment-Emergent AE	Subjects with Any DLT
Phase 1 & 2: KW-2478 175 mg/m^2 and Bortezomib 1.3mg/m^2	95	88	22	54	13	48	1
Phase 1 Cohort 1: KW-2478 130 mg/m^2 and Bortezomib 1.0mg/m^2	3	3	0	3	0	2	0
Phase 1 Cohort 2: KW-2478 130 mg/m^2 and Bortezomib 1.3mg/m^2	3	3	0	2	1	3	0
Phase 1 Cohort 3: KW-2478 175 mg/m^2 and Bortezomib 1.0mg/m^2	3	2	0	2	0	3	1
Phase 1 Cohort 4: KW-2478 175 mg/m^2 and Bortezomib 1.3mg/m^2	6	6	0	5	0	4	0
Phase 2: KW-2478 175 mg/m^2 and Bortezomib 1.3mg/m^2	80	74	22	42	12	36	0

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Phase 1: PK Exposure Cmax ng/mL Day 11

Descriptive summary statistics (number, arithmetic mean, standard deviation [SDev], coefficient of variation [CV%]) for concentration and PK data for KW-2478 and Bortezomib in Phase 1 were presented by cohort, dose level and day. (NCT01063907)
Timeframe: PK collected Day 11 of 21-day cycle

Intervention	ng/mL (Mean)
Phase 1 Cohort 1: KW-2478 130 mg/m^2 and Bortezomib 1.0mg/m^2	7910
Phase 1 Cohort 2: KW-2478 130 mg/m^2 and Bortezomib 1.3mg/m^2	41000
Phase 1 Cohort 3: KW-2478 175 mg/m^2 and Bortezomib 1.0mg/m^2	5990
Phase 1 Cohort 4: KW-2478 175 mg/m^2 and Bortezomib 1.3mg/m^2	5280

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Phase 1: PK Elimination t½ hr Day 11

Intervention	hr (Mean)
Phase 1 Cohort 1: KW-2478 130 mg/m^2 and Bortezomib 1.0mg/m^2	1.88
Phase 1 Cohort 2: KW-2478 130 mg/m^2 and Bortezomib 1.3mg/m^2	2.02
Phase 1 Cohort 3: KW-2478 175 mg/m^2 and Bortezomib 1.0mg/m^2	1.84
Phase 1 Cohort 4: KW-2478 175 mg/m^2 and Bortezomib 1.3mg/m^2	1.77

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Phase 1: PK Absorption Tmax hr Day 11

Intervention	hr (Mean)
Phase 1 Cohort 1: KW-2478 130 mg/m^2 and Bortezomib 1.0mg/m^2	1.03
Phase 1 Cohort 2: KW-2478 130 mg/m^2 and Bortezomib 1.3mg/m^2	1.03
Phase 1 Cohort 3: KW-2478 175 mg/m^2 and Bortezomib 1.0mg/m^2	1.11
Phase 1 Cohort 4: KW-2478 175 mg/m^2 and Bortezomib 1.3mg/m^2	1.07

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Phase 1: PK Exposure AUC0-t hr*ng/mL Day 11

Intervention	hr*ng/mL (Mean)
Phase 1 Cohort 1: KW-2478 130 mg/m^2 and Bortezomib 1.0mg/m^2	7940
Phase 1 Cohort 2: KW-2478 130 mg/m^2 and Bortezomib 1.3mg/m^2	26200
Phase 1 Cohort 3: KW-2478 175 mg/m^2 and Bortezomib 1.0mg/m^2	7190
Phase 1 Cohort 4: KW-2478 175 mg/m^2 and Bortezomib 1.3mg/m^2	6040

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Number of Participants With a Confirmed Hematologic Response

"Response that was confirmed on 2 consecutive evaluations during treatment.~Complete Response(CR): Complete disappearance of M-protein from serum and urine on immunofixation, normalization of Free Light Chain (FLC) ratio and <5% plasma cells in bone marrow.~Very Good Partial Response(VGPR): >=90% reduction in serum M-component; Urine M-Component <=100 mg per 24 hours.~Partial Response(PR): >=50% reduction in serum M-component and/or Urine M-Component >=90% reduction or <200 mg per 24 hours; or >=50% decrease in difference between involved and uninvolved FLC levels." (NCT01072773)
Timeframe: Duration of treatment (up to 12 cycles/months)

Intervention	participants (Number)
	Complete Response (CR)	Very Good Partial Response (VGPR)	Partial Response (PR)
Bortez/Cyc/Dex	0	0	0

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Number of Participants With Treatment Related Adverse Events.

"Adverse events (AE) that are classified as either possibly, probably, or definitely related to study treatment according to the National Cancer Institute Common Toxicity Criteria for Adverse Events (NCI CTCAE version 3.0). The maximum grade for each type of AE will be recorded for each patient. Grade refers to the severity of the AE.~Grade 1: Mild AE, Grade 2: Moderate AE, Grade 3: Severe AE, Grade 4: Life-threatening or disabling AE, Grade 5: Death related AE~Adverse events will be assessed using NCI Common Toxicity Criteria for Adverse Effects (CTCAE) v3.0." (NCT01072773)
Timeframe: Duration on treatment (up to 12 cycles/months)

Intervention	participants (Number)
	Grade 1-2	Grade 3-4	Grade 5
Bortez/Cyc/Dex	2	0	0

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Overall Survival

Survival time is defined as the time from registration to death due to any cause. (NCT01072773)
Timeframe: Duration of Study (up to 5 years)

Intervention	Months (Median)
Bortez/Cyc/Dex	1.45

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Time to Disease Progression

Time to disease progression is defined as the time from registration to the earliest date of documented disease progression. If a patient dies without a documentation of disease progression the patient will be considered to have had tumor progression at the time of their death (NCT01072773)
Timeframe: Duration of Study (up to 5 years)

Intervention	Months (Median)
Bortez/Cyc/Dex	1.45

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Number of Participants With an Organ Response.

The number of patients that acheived a response in an affected organ. (NCT01072773)
Timeframe: Duration on treatment (up to 12 cycles/months)

Intervention	participants (Number)
Bortez/Cyc/Dex	0

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One-year Survival in Patients Treated With This Regimen.

Proportion of patients who are still alive at 1 year after registration. (NCT01078441)
Timeframe: Assessed at 1 year

Intervention	Proportion of patients (Number)
Treatment (Combination Chemotherapy)	0.5

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Proportion of Patients With Hematologic Overall Response (Partial Response [PR]+ Very Good PR [VGPR]+ Amyloid Complete Response [ACR]+ Stringent Complete Response [sCR]) After 3 Months (3 Cycles) of Therapy

sCR: ACR and no clonal cells in bone marrow (BM) ACR: Negative serum/urine immunofixation (IF), <5% plasma cells in BM, and normal serum FLC ratio VGPR: 1. PR and any of the following; 2. serum/urine M-protein detectable by IF but not measurable (NM) on electrophoresis (EP); (3) ≥90% reduction in serum M-component and urine M-protein <100 mg/24 hr if baseline serum measurable; (4) urine M-component <100 mg/24 hr and NM serum M-protein on serum protein EP if baseline urine measurable; (5) ≥90% drop in the difference between involved and uninvolved FLC levels if only FLC measurable PR: (1) ≥50% drop of serum M-protein and 24-hr urinary M-protein drop by ≥90% or to <200 mg/24 hr if baseline serum/urine measurable; or (2) ≥50% drop of serum M-protein if only serum measurable at baseline; or (3) 24-hr urinary M-protein drop by ≥90% or to <200 mg/24 hr if baseline urine measurable; or (4) ≥ 50% drop in the difference between involved and uninvolved FLC if only FLC measu (NCT01078454)
Timeframe: Assessed at 3 months

Intervention	Proportion of patients (Number)
Arm A (Mel-Dex)	0.33
Arm B (B-Mel-Dex)	0.60

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Number of Participants Surviving at 5 Years

(NCT01083316)
Timeframe: 5 years

Intervention	Participants (Count of Participants)
Bortezomib and Dexamethasone	29

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Number of Participants Proceeding to Transplant Following Induction

(NCT01083316)
Timeframe: 2 months

Intervention	Participants (Count of Participants)
Bortezomib and Dexamethasone	30

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Number of Participants Surviving at 100 Days Post Transplant

(NCT01083316)
Timeframe: 100 days

Intervention	Participants (Count of Participants)
Bortezomib and Dexamethasone	27

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Number of Participants With Disease Response

Complete response: Normal serum free light chain ratio and Negative serum and urine immunofixation electrophoresis Very good partial response: Difference in serum free light chains less than 40 mg/L Partial Response: >50% Reduction in the difference in serum free light chains (NCT01083316)
Timeframe: One year

Intervention	Participants (Count of Participants)
Bortezomib and Dexamethasone	20

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Over All Survival

Kaplan Meier estimates- median time to event (NCT01083602)
Timeframe: 24 weeks

Intervention	Days (Median)
Panobinostat + Bortezomib & Dexamethasone	559.0

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Responders to Treatment

The primary endpoint for this phase II study of patients with bortezomib-refractory MM is response after a maximum of 8 cycles of therapy as defined by the modified EBMT criteria. (NCT01083602)
Timeframe: after eight cycyles of treatment (24 weeks)

Intervention	participants (Number)
	Complete Response (CR)	near Complete Response(nCR)	Partial Response (PR)	Minimal Response (MR)	No Change	Pregressive Disease (PD)	Unknown
Panobinostat + Bortezomib & Dexamethasone	0	1	18	10	20	3	3

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Progression-free Survival

Progression-free survival (PFS) was defined as the time from the date of first study treatment to first occurrence of documented progressive disease /relapse or death. Time from randomization until disease progression or death by Kaplan-Meier estimates (NCT01083602)
Timeframe: 24 weeks

Intervention	days (Median)
Panobinostat + Bortezomib & Dexamethasone	164.0

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Time to Progression

Time from randomization until objective tumor progression; does not include deaths-- Kaplan-Meier estimates (NCT01083602)
Timeframe: 24 weeks

Intervention	Days (Median)
Panobinostat + Bortezomib & Dexamethasone	164.0

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Time to Response (Greater Than or Equal to PR) Based on Investigator Assessment

Time to response is defined as the time from the date of first administration of study treatment to the date of first documented evidence of CR or nCR or PR (whichever status is recorded first). Patients who do not have a response of PR or better by the data cut-off date are censored. (NCT01083602)
Timeframe: after eight cycyles of treatment (24 weeks)

Intervention	Days (Mean)
Panobinostat + Bortezomib & Dexamethasone	51.8

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Overall Response Rate (PR+nCR+CR)

Overall response rate=(PR+nCR+CR) CR= < 5% plasma cells in bone marrow. No confirmation on bone marrow plasma cell (additional assessment) is needed to document CR except patients with non-secretory myeloma where the bone marrow examination must be repeated after an interval of at least 6 weeks, Absence of M-protein in serum and urine by immunofixation,nCR same as CR without out Absence of M-protein in serum and urine by immunofixation,PR+ 50% reduction of serum M-protein and sofft tissue Plasmacytomas all for more than 6 weeks. (NCT01083602)
Timeframe: after eight cycyles of treatment (24 weeks)

Intervention	percentage of participants (Number)
Panobinostat + Bortezomib & Dexamethasone	34.5

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Time to Response

Time to response (TTR) was defined as the interval from the start of study drug to the first documentation of CR or PR. (NCT01088048)
Timeframe: Up to 5 years

Intervention	months (Median)
Idelalisib + Rituximab	1.9
Idelalisib + Bendamustine	1.9
Idelalisib + Everolimus	1.9
Idelalisib + Bortezomib	1.9
Idelalisib + Rituximab + Bendamustine	1.9
Idelalisib + Ofatumumab	1.9
Idelalisib + Fludarabine	1.9
Idelalisib + Chlorambucil	1.9
Idelalisib + Rituximab + Chlorambucil	1.9
Idelalisib + Rituximab + Lenalidomide	3.0

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Duration of Response

Duration of response (DOR) was defined as the interval from the first documentation of CR or PR to the earlier of the first documentation of disease progression or death from any cause. (NCT01088048)
Timeframe: Up to 5 years

Intervention	months (Median)
Idelalisib + Rituximab	NA
Idelalisib + Bendamustine	NA
Idelalisib + Everolimus	5.6
Idelalisib + Bortezomib	9.3
Idelalisib + Rituximab + Bendamustine	NA
Idelalisib + Ofatumumab	NA
Idelalisib + Fludarabine	NA
Idelalisib + Chlorambucil	NA
Idelalisib + Rituximab + Chlorambucil	NA
Idelalisib + Rituximab + Lenalidomide	NA

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Plasma Concentration of Everolimus

(NCT01088048)
Timeframe: Predose, 1.5 hours postdose at Weeks 0 and 4

Intervention	ng/mL (Mean)
	Pre-dose (Week 0)	1.5 hr post-dose (Week 0)	Pre-dose (Week 4)	1.5 hr post-dose (Week 4)
Everolimus (Cohort 5a)	NA	93.0	3.0	56.3

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Plasma Concentration of Bendamustine

(NCT01088048)
Timeframe: Predose, 0.25, 0.5, 0.75, 1.0, 1.25, 1.5, 2.0, 3.0, 4.0, 5.0, 6.0 hours postdose at Week 0

Intervention	ng/mL (Mean)
	Pre-dose (Week 0)	0.25 hr post-dose (Week 0)	0.5 hr post-dose (Week 0)	0.75 hr post-dose (Week 0)	1.0 hr post-dose (Week 0)	1.25 hr post-dose (Week 0)	1.5 hr post-dose (Week 0)	2.0 hr post-dose (Week 0)	3.0 hr post-dose (Week 0)	4.0 hr post-dose (Week 0)	5.0 hr post-dose (Week 0)	6.0 hr post-dose (Week 0)
Bendamustine (Cohorts 1b, 2b, 3a, 3b, 3f, 3g, 4b, 5c)	NA	3484.1	4694.7	3433.2	2847.2	1916.4	1211.2	514.0	463.4	78.5	15.3	4.4

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Plasma Concentration of IDELA (Cohort 7)

(NCT01088048)
Timeframe: Predose, 1.5 hours postdose at Weeks 0, 5 and 13

Intervention	ng/mL (Mean)
	Pre-dose (Week 0)	1.5 hr post-dose (Week 0)	Pre-dose (Week 5)	1.5 hr post-dose (Week 5)	Pre-dose (Week 13)	1.5 hr post-dose (Week 13)
Idelalisib 150 mg (Cohort 7)	NA	1603.1	20.7	1621.3	354.8	592.7

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Plasma Concentration of IDELA (Cohort 6)

(NCT01088048)
Timeframe: Predose, 1.5 hours postdose at Weeks 0, 4, 12 and 24

Intervention	ng/mL (Mean)
	Pre-dose (Week 0)	1.5 hr post-dose (Week 0)	Pre-dose (Week 4)	1.5 hr post-dose (Week 4)	Pre-dose (Week 12)	1.5 hr post-dose (Week 12)	Pre-dose (Week 24)	1.5 hr post-dose (Week 24)
Idelalisib 150 mg (Cohort 6)	0.0	1930.7	530.8	1869.8	677.9	1733.0	346.8	1710.7

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Toxicity of Administration of IDELA

Percentage of participants experiencing toxicities of administration of IDELA were measured according to the Common Terminology Criteria for Adverse Events v4.02 (NCT01088048)
Timeframe: First dose date up to 5 years

Intervention	percentage of participants (Number)
Idelalisib + Rituximab	100.0
Idelalisib + Bendamustine	100.0
Idelalisib + Everolimus	100.0
Idelalisib + Bortezomib	83.33
Idelalisib + Rituximab + Bendamustine	100.0
Idelalisib + Ofatumumab	100.0
Idelalisib + Fludarabine	100.0
Idelalisib + Chlorambucil	100.0
Idelalisib + Rituximab + Chlorambucil	100.0
Idelalisib + Rituximab + Lenalidomide	100.0

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Plasma Concentration of IDELA (Cohort 1, Cohorts 2 and 3, Cohort 5)

(NCT01088048)
Timeframe: Predose, 0.5, 1.0, 1.5, 2.0, 3.0, 4.0, 6.0 hours postdose at Week 0; predose, 1.5 hours postdose at Weeks 4, 12, and 24

Intervention	ng/mL (Mean)
	Pre-dose (Week 0)	0.5 hr post-dose (Week 0)	1.0 hr post-dose (Week 0)	1.5 hr post-dose (Week 0)	2.0 hr post-dose (Week 0)	3.0 hr post-dose (Week 0)	4.0 hr post-dose (Week 0)	6.0 hr post-dose (Week 0)	Pre-dose (Week 4)	1.5 hr post-dose (Week 4)	Pre-dose (Week 12)	1.5 hr post-dose (Week 12)	Pre-dose (Week 24)	1.5 hr post-dose (Week 24)
Idelalisib 100 mg (Cohort 1)	0.4	437.6	1022.4	1434.0	1282.7	1001.0	788.4	523.7	416.5	1297.2	361.9	1309.5	369.9	1061.6
Idelalisib 150 mg (Cohort 5)	0.0	1380.0	1600.0	1564.7	1400.0	1170.0	795.0	517.0	408.0	1877.9	433.9	1426.8	549.1	885.6
Idelalisib 150 mg (Cohorts 2 and 3)	68.8	1231.4	1789.3	2017.3	1732.8	1296.1	910.0	486.0	364.1	1808.1	351.4	1883.0	419.7	1840.1

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Plasma Concentration of IDELA (Cohort 4)

(NCT01088048)
Timeframe: Predose at Week 0; predose, 0.5, 1.0, 1.5, 2.0, 3.0, 4.0, 6.0 hours postdose at Week 4; predose, 1.5 hours postdose at Week 12; and predose, 1.5 hours postdose at Week 24

Intervention	ng/mL (Mean)
	Pre-dose (Week 0)	Pre-dose (Week 4)	0.5 hr post-dose (Week 4)	1.0 hr post-dose (Week 4)	1.5 hr post-dose (Week 4)	2.0 hr post-dose (Week 4)	3.0 hr post-dose (Week 4)	4.0 hr post-dose (Week 4)	6.0 hr post-dose (Week 4)	Pre-dose (Week 12)	1.5 hr post-dose (Week 12)	Pre-dose (Week 24)	1.5 hr post-dose (Week 24)
Idelalisib 150 mg (Cohort 4)	0.0	0.0	1119.5	994.5	1758.2	737.0	605.0	547.0	524.0	401.9	2018.2	752.5	2251.1

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Overall Survival

Overall Survival (OS) was defined as the interval from the start of study drug to death from any cause. (NCT01088048)
Timeframe: Up to 5 years

Intervention	months (Median)
Idelalisib + Rituximab	NA
Idelalisib + Bendamustine	NA
Idelalisib + Everolimus	NA
Idelalisib + Bortezomib	NA
Idelalisib + Rituximab + Bendamustine	NA
Idelalisib + Ofatumumab	NA
Idelalisib + Fludarabine	NA
Idelalisib + Chlorambucil	NA
Idelalisib + Rituximab + Chlorambucil	NA
Idelalisib + Rituximab + Lenalidomide	NA

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Overall Response Rate

"Overall Response Rate (ORR) was defined as the percentage of participants achieving a complete response (CR) or partial response (PR).~The response definitions were based on the following standard criteria established for each indication:~CLL: International Workshop on chronic lymphocytic leukemia (IWCLL),2008~iNHL & MCL: Cheson, 2007" (NCT01088048)
Timeframe: Up to 5 years

Intervention	percentage of participants (Number)
Idelalisib + Rituximab	78.4
Idelalisib + Bendamustine	84.3
Idelalisib + Everolimus	44.4
Idelalisib + Bortezomib	61.1
Idelalisib + Rituximab + Bendamustine	81.8
Idelalisib + Ofatumumab	71.4
Idelalisib + Fludarabine	91.7
Idelalisib + Chlorambucil	66.7
Idelalisib + Rituximab + Chlorambucil	93.3
Idelalisib + Rituximab + Lenalidomide	71.4

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Sub-study: Plasma Concentration of IDELA (Cohorts 1-4)

(NCT01088048)
Timeframe: pre dose and 0.5, 1, 1.5, 2.0, 3.0, 4.0, and 6.0 hours post dose

Intervention	ng/mL (Mean)
	Pre-dose	0.5 hr post-dose	1.0 hr post-dose	1.5 hr post-dose	2.0 hr post-dose	3.0 hr post-dose	4.0 hr post-dose	6.0 hr post-dose
Idelalisib 100 mg (Cohort 1a, 1b)	1.5	437.6	1022.4	1264.7	1282.7	1001.0	788.4	523.7
Idelalisib 150 mg (Cohorts 2a, 2b, 3a, 3c, 3d, 3e, 3f, 3g, 4a, 4b)	0.0	1222.1	1723.1	1599.2	1646.2	1238.5	879.8	489.3

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Plasma Concentration of Lenalidomide

(NCT01088048)
Timeframe: Predose, 1.5 hours postdose at Week 1 and predose at Week 5

Intervention	ng/mL (Mean)
	Pre-dose (Week 1)	1.5 hr post-dose (Week 1)	Pre-dose (Week 5)
Lenalidomide (Cohort 7a, 7b, 7c)	NA	51.6	NA

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Progression-free Survival

"Progression free survival (PFS) was defined as the interval from the start of study drug to the earlier of the first documentation of disease progression or death from any cause.~The response definitions were based on the following standard criteria established for each indication:~CLL: International Workshop on chronic lymphocytic leukemia (IWCLL), 2008~iNHL & MCL: Cheson, 2007" (NCT01088048)
Timeframe: Up to 5 years

Intervention	months (Median)
Idelalisib + Rituximab	NA
Idelalisib + Bendamustine	NA
Idelalisib + Everolimus	4.3
Idelalisib + Bortezomib	8.1
Idelalisib + Rituximab + Bendamustine	NA
Idelalisib + Ofatumumab	NA
Idelalisib + Fludarabine	NA
Idelalisib + Chlorambucil	NA
Idelalisib + Rituximab + Chlorambucil	NA
Idelalisib + Rituximab + Lenalidomide	NA

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Duration of Exposure to IDELA

Duration of exposure to IDELA was summarized using descriptive statistics. (NCT01088048)
Timeframe: First dose date up to 12 months

Intervention	months (Mean)
Idelalisib + Rituximab	8.1
Idelalisib + Bendamustine	7.6
Idelalisib + Everolimus	4.2
Idelalisib + Bortezomib	5.1
Idelalisib + Rituximab + Bendamustine	8.0
Idelalisib + Ofatumumab	8.3
Idelalisib + Fludarabine	8.9
Idelalisib + Chlorambucil	8.8
Idelalisib + Rituximab + Chlorambucil	8.7
Idelalisib + Rituximab + Lenalidomide	7.7

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Number of Participants With Dose Reductions in Bortezomib, Dexamethasone or Both

To evaluate the toxicity (safety and tolerability) of weekly bortezomib + dexamethasone in patients with newly diagnosed multiple myeloma who are ineligible for transplant or who are eligible but wish to postpone autologous stem cell transplant. (NCT01090921)
Timeframe: Data was collected for each subject for the duration of the participation in the study, which was an average of 4.8 cycles.

Intervention	Participants (Count of Participants)
	Bortezomib reductions	Dexamethasone reductions	Bortezomib and Dexamethasone reductions
Bortezomib and Dexamethasone	8	14	4

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Progression Free Survival (PFS)

Progression free survival will be measured from the beginning of treatment until there is evidence of progressive disease or death from any cause. Progression is evaluated according to Response Evaluation Criteria in Solid Tumors (RECIST) (version 1.0). Target lesions are assessed by computerized tomography (CT) or magnetic resonance imaging (MRI): Progressive Disease (PD), 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT01100242)
Timeframe: 36 weeks

Intervention	weeks (Median)
VELCADE and Sorafenib	13.71

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Overall Response Rate (ORR)

Tumor response is evaluated according to Response Evaluation Criteria in Solid Tumors (RECIST) (version 1.0). Target lesions are assessed by computerized tomography (CT) or magnetic resonance imaging (MRI:) Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions. Overall response rate (ORR) is the percentage of patients who achieve a CR or PR (NCT01100242)
Timeframe: 42 days

Intervention	percentage of participants (Number)
	Complete response (CR)	Partial response (PR)	Overall response rate (CR + PR)
VELCADE and Sorafenib	0	5.9	5.9

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Toxicity Profile

Toxicity is assessed using National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE) version 3.0. Toxicity profile is reported as the number of patients who received at least one dose of on-study treatment and experienced a grade 3 or grade 4 adverse event (AE). For a more complete listing of all AEs experienced by patients on study, please see the Adverse Event section. (NCT01100242)
Timeframe: 42 days

Intervention	participants (Number)
	Abdominal pain	Anorexia (loss of appetite)	Dehydration	Fatigue	Hand and foot syndrome	Hemoglobin	Hyperglycemia	Hypertension	Hypoalbuminemia	Hypokalemia	Hyponatremia	Hypophosphatemia	Lymphopenia	Pain - Other (All over body)	Pain in extremity	Decreased platelets	Weight loss
VELCADE and Sorafenib	2	2	1	2	1	2	1	1	3	1	5	4	4	1	1	1	2

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Proteinuria

Quantification of urinary protein will be made after treatment by measuring 24 hr urine protein. (NCT01103778)
Timeframe: Baseline and 1 year

Intervention	grams per 24 hrs (Median)
	Baseline	1 year
Velcade® Therapy	2.52	1.43

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Number of Participants With Complete Remission, Partial Response, or no Response.

"Complete remission was defined as daily proteinuria of less than 300mg measured by 24 hr urine collection.~Partial response was defined as any reduction in daily proteinuria from baseline as measure by 24 hr urine collection." (NCT01103778)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
	Complete Remission	Partial Response	No Response
Velcade Arm	3	1	3

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Number of Participants With Abnormal Lab Values or Infections Related to Exposure to Study Medication.

Complete blood count will be checked at regular intervals to monitor for anemia; liver panel; serum immunoglobulin profile will also be followed. (NCT01103778)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Velcade Arm	1

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Serum Creatinine

Preservation of renal function will be assessed. (NCT01103778)
Timeframe: Baseline and 1 year

Intervention	milligram per deciliter (Median)
	Baseline	1 year
Velcade Arm	1.35	1.52

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FACT-G Total Score

The Functional Assessment of Cancer Therapy-General (FACT-G) is a quality of life instrument that assesses the effects of cancer therapy on a patient's physical, social/family, emotional, and functional well-being. The assessment has 27 questions, each scored on a Likert scale from 0-4. The overall score is computed by adding scores of the questions and falls in the range 0-108, with higher scores indicating higher levels of overall well-being. (NCT01109004)
Timeframe: Up to 3 years post-randomization

Intervention	score on a scale (Mean)
	Baseline	1 Year	2 Years	3 Years
Lenalidomide Maintenance	77	83	85	85
RVD Consolidation	79	84	84	84
Tandem Auto Transplant	79	84	84	85

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FACT-BMT Trial Outcome Index

The Functional Assessment of Cancer Therapy (FACT) Trial Outcome Index is a quality of life instrument that assesses the impact of bone marrow transplantation (BMT) on a patient's physical and functional well-being while taking into consideration BMT-specific concerns. The assessment has 24 questions, each scored on a Likert scale from 0-4. The overall score is computed by adding scores of the questions and falls in the range 0-96, with higher scores indicating higher levels of overall well-being. (NCT01109004)
Timeframe: Up to 3 years post-randomization

Intervention	score on a scale (Mean)
	Baseline	1 Year	2 Years	3 Years
Lenalidomide Maintenance	63	71	73	73
RVD Consolidation	65	72	73	71
Tandem Auto Transplant	64	70	73	73

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FACT-BMT Score

The Functional Assessment of Cancer Therapy-Bone Marrow Transplant scale (FACT-BMT) is a quality of life instrument that assesses the effects of bone marrow transplantation (BMT) on a patient's physical, social/family, emotional, and functional well-being while taking into consideration BMT-specific concerns. The assessment has 37 questions, each scored on a Likert scale from 0-4. The overall score is computed by adding scores of the questions and falls in the range 0-148, with higher scores indicating higher levels of overall well-being. (NCT01109004)
Timeframe: Up to 3 years post-randomization

Intervention	score on a scale (Mean)
	Baseline	1 Year	2 Years	3 Years
Lenalidomide Maintenance	105	113	115	115
RVD Consolidation	107	115	115	114
Tandem Auto Transplant	107	113	114	115

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Percentage of Participants With Treatment-related Mortality (TRM)

TRM is defined as death prior to progression of multiple myeloma. To account for loss to follow-up of a few participants, the cumulative incidence of TRM at 38 months post-randomization was estimated using the Aalen-Johansen estimator, treating disease progression as a competing risk. (NCT01109004)
Timeframe: Up to 38 months post-randomization

Intervention	percentage of participants (Number)
Tandem Auto Transplant	1.7
RVD Consolidation	1.2
Lenalidomide Maintenance	0.5

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Percentage of Participants With Overall Survival (OS)

Overall survival is defined as survival of death from any cause. To account for loss to follow-up of a few participants, the Kaplan-Meier estimator was used to estimate overall survival at 38 months post-randomization. (NCT01109004)
Timeframe: 38 months post-randomization

Intervention	percentage of participants (Number)
Tandem Auto Transplant	81.8
RVD Consolidation	85.4
Lenalidomide Maintenance	83.7

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Percentage of Participants With Disease Progression

"Disease Progression is defined as progression of multiple myeloma, including one or more of the following:~A reappearance of serum monoclonal paraprotein, with a level of at least 0.5 g/dL~24-hour urine protein electrophoresis with at least 200 mg paraprotein/24 hours~Abnormal free light chain levels of >10 mg/dl, only in patients without measurable paraprotein in the serum and urine~At least 10% plasma cells in a bone marrow aspirate or on trephine biopsy~Definite increase in the size of existing bone lesions or soft tissue plasmacytomas~Development of new bone lesions or soft tissue plasmacytomas~Development of hypercalcemia (corrected serum Ca >11.5 mg/dL or >2.8 mmol/L) not attributable to any other cause~To account for loss to follow-up of a few participants, the cumulative incidence of TRM at 38 months post-randomization was estimated using the Aalen-Johansen estimator, treating death prior to disease progression as a competing risk." (NCT01109004)
Timeframe: 38 months post-randomization

Intervention	percentage of participants (Number)
Tandem Auto Transplant	39.8
RVD Consolidation	41.0
Lenalidomide Maintenance	45.6

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MOS SF-36 Mental Component Summary

The Medical Outcome Study (MOS) SF-36 Mental Component Summary is a subscale of the SF-36 intended to measure mental well-being. It is scored on a scale of 0-100, with higher scores indicating higher levels of well-being. (NCT01109004)
Timeframe: Up to 3 years post-randomization

Intervention	score on a scale (Mean)
	Baseline	1 Year	2 Years	3 Years
Lenalidomide Maintenance	48	50	50	51
RVD Consolidation	48	51	50	50
Tandem Auto Transplant	49	50	50	51

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Percentage of Participants With Progression-free Survival (PFS)

Progression-free survival is defined as survival without disease progression or initiation of non-protocol anti-myeloma therapy. To account for loss to follow-up of a few participants, the Kaplan-Meier estimator was used to estimate progression-free survival at 38 months post-randomization. (NCT01109004)
Timeframe: 38 months post-randomization

Intervention	percentage of participants (Number)
Tandem Auto Transplant	58.5
RVD Consolidation	57.8
Lenalidomide Maintenance	53.9

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Number of Participants With Treatment Response

"The number of participants with very good partial response (VGPR) or better [complete response (CR), near CR (nCR), and stringent CR (sCR)] according to the International Uniform Response Criteria will be calculated. The Worse than VGPR group includes PR, stable disease, and progressive disease.~sCR requires, in addition to CR: Normal free light chain ratio (FLC), Absence of clonal cells in bone marrow CR requires, in addition to nCR: Absence of the original monoclonal paraprotein (PPN), Disappearance of soft tissue plasmacytomas nCR is defined as: < 5% plasma cells in a bone marrow aspirate, No increase in lytic bone lesions VGPR requires: Serum or urine PPN not detectable on electrophoresis OR >=90% reduction in serum PPN plus urine PPN <100 mg/24hrs, >= 50% reduction in the level of serum monoclonal PPN or reduction in 24 hour urinary monoclonal PPN either >= 90% or to <200 mg/24 hours in light chain disease, >= 50% reduction in the size of soft tissue plasmacytomas" (NCT01109004)
Timeframe: 1 and 2 years post-randomization

Intervention	Participants (Count of Participants)
	1 Year72572685			1 Year72572686	1 Year72572687	2 Years72572685	2 Years72572687	2 Years72572686
	Worse than VGPR	CR or sCR	VGPR or nCR
Tandem Auto Transplant	97
RVD Consolidation	122
Lenalidomide Maintenance	98
Tandem Auto Transplant	56
RVD Consolidation	50
Lenalidomide Maintenance	60
Tandem Auto Transplant	39
Lenalidomide Maintenance	50
Tandem Auto Transplant	98
RVD Consolidation	117
Lenalidomide Maintenance	93
RVD Consolidation	37
Lenalidomide Maintenance	41
Tandem Auto Transplant	20
RVD Consolidation	21
Lenalidomide Maintenance	26

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MOS SF-36 Physical Component Summary

The Medical Outcome Study (MOS) SF-36 Physical Component Summary is a subscale of the SF-36 intended to measure physical well-being. It is scored on a scale of 0-100, with higher scores indicating higher levels of well-being. (NCT01109004)
Timeframe: Up to 3 years post-randomization

Intervention	score on a scale (Mean)
	Baseline	1 Year	2 Years	3 Years
Lenalidomide Maintenance	38	42	43	43
RVD Consolidation	39	43	44	42
Tandem Auto Transplant	37	43	44	42

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Overall Response Rate (ORR) of the Combination of Ofatumumab and Bortezomib in Patients Receiving Study Treatment

"Response was assessed based on Bone marrow biopsy and CT scan. Best responses are used for Response Rate and CR and PR only.~Complete Response - CR:~• Complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present before therapy.~Partial Response - PR:~• At least a 50% decrease in sum of the product of the diameters (SPD) of up to six of the largest dominant nodes or nodal masses.~Stable Disease - SD:~• A patient is considered to have SD when he or she fails to attain the criteria needed for a CR or PR, but does not fulfill those for progressive disease~Relapsed Disease:~• Lymph nodes should be considered abnormal if the long axis is more than 1.5 cm regardless of the short axis." (NCT01119794)
Timeframe: Bone Marrow Biopsy: Every 2 months for 1 year then every 4 months until progression for approximately 1 year/Via CT scan: every 4 months until progression, for a total of approximately 2 years

Intervention	participants (Number)
	CR	PR	SD	Progression
Ofatumumab IV,	2	1	3	2

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PTEN Mutation Rate [Phase II]

The PTEN mutation rate is the percentage of patients with PTEN mutation identified in pre-therapy and post-therapy bone marrow samples per established methods. (NCT01125293)
Timeframe: Samples were collected pre-therapy before the beginning therapy (baseline) and post-therapy after finishing the 6th treatment cycle (168 days).

Intervention	percentage of participants (Number)
	MYD88/L265P mutation	CXCR4/C1013G mutation
Phase II	80	5

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Phase II Duration of Response (DoR)

"The DoR is defined as the elapsed time from date when the measurement criteria are first met for a complete or partial response (whichever status is recorded first) until the date of first observation of objective disease progression. Analysis of DoR will be as follows:~For responding patients who die without objective PD (including death from study disease), DoR will be censored at the date of the last objective progression-free disease assessment.~For responding patients not known to have died as of the data cut-off date and who do not have objective PD, DoR will be censored at the date of the last objective progression-free disease assessment.~For responding patients who receive subsequent systemic anticancer therapy (after discontinuation from the study chemotherapy) prior to objectively determined disease progression, DoR will be censored at the date of the last objective progression-free disease assessment prior to post discontinuation therapy." (NCT01125293)
Timeframe: Patients were assessed for disease every cycle while on treatment (168 days) and every three months while on maintenance therapy. In long-term follow-up, disease was monitored every 3 months. Study cohort median (range) follow-up was 15 (1 - 23) months.

Intervention	months (Median)
Phase II	14

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Phase II Overall Response Rate

"Overall response rate is percentage of participants with complete (CR), very good partial (VGPR), partial (PR), or minimal response (MR) as best response during treatment.~CR:~No serum monoclonal IgM protein by immunofixation~Normal IgM level~Complete resolution of extramedullary disease, i.e., lymphadenopathy and splenomegaly if present at baseline~Morphologically normal bone marrow aspirate and trephine biopsy~VGPR:~Monoclonal IgM protein is detectable ≥90% reduction in IgM level from baseline~Complete resolution of extramedullary disease, i.e., lymphadenopathy/splenomegaly if present at baseline~No new signs/symptoms of active disease~PR:~Monoclonal IgM protein is detectable ≥50% but <90% reduction in IgM level from baseline~Reduction in extramedullary disease~No new signs/symptoms of active disease~MR:~Monoclonal IgM protein is detectable ≥25% but <50% reduction in IgM level from baseline~No new signs/symptoms of active disease" (NCT01125293)
Timeframe: Up to 6 cycles (Day 168)

Intervention	percentage of participants (Number)
Phase II	87

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Treatment-Emergent Sensory Neuropathy Rate [Phase I]

Percentage of participants experiencing Grade 1 - Grade 3 treatment-emergent peripheral (sensory) neuropathy events based on CTCAEv3 as reported on case report forms for phase I participants. (NCT01125293)
Timeframe: Adverse events were assessed each cycle (ever 28 days) for 6 cycles then every 3 months on maintenance. Duration of therapy for the Phase I study up to 41 months.

Intervention	percentage of participants (Number)
Phase I Stage A Level 1	33
Phase I Stage A Level 2	33
Phase I Stage B Level 1	100
Phase I Stage B Level 2	67
Phase I Dose Expansion	50
Phase II	48

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Very-good-partial-response-or-better Rate [Phase II]

"Very-good-partial-response-or-better rate is the percentage of participants with complete response (CR) or very good partial response (VGPR) on to the combination of everolimus/bortezomib/rituximab. The combination regimen was received for up to 6 cycles.~CR:~Absence of serum monoclonal IgM protein by immunofixation~Normal serum IgM level~Complete resolution of extramedullary disease, i.e., lymphadenopathy and splenomegaly if present at baseline~Morphologically normal bone marrow aspirate and trephine biopsy~VGPR:~Monoclonal IgM protein is detectable ≥90% reduction in serum IgM level from baseline*~Complete resolution of extramedullary disease, i.e." (NCT01125293)
Timeframe: Up to 6 cycles (Day 168)

Intervention	percentage of participants (Number)
Phase II	4.3

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Everolimus Dose Limiting Toxicity (DLT) [Phase I]

"The following qualify as dose limiting toxicities:~Grade 3 or greater non-hematologic toxicity, considered by the investigator to be related to study drugs.~Grade 4 hematologic toxicity defined as: thrombocytopenia with platelets <10,000 µ/L on more than one occasion despite transfusion support; grade 4 neutropenia occurring for more than 7 days and/or resulting in neutropenic fever with elevated temperature (defined as > 101 degrees F). Lymphopenia, a recognized side effect of bortezomib, is not considered a DLT.~Inability to receive Day 1 dose for Cycle 2 due to toxicity" (NCT01125293)
Timeframe: Assessed within the first cycle (28 days) of the study.

Intervention	participants (Number)
Phase I Stage A Level 1	0
Phase I Stage A Level 2	0
Phase I Stage B Level 1	0
Phase I Stage B Level 2	0

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Everolimus Maximum Tolerated Dose (MTD) Stage B [Phase I]

The MTD of Everolimus/Bortezomib/Rituximab combination is determined by the number of patients who have dose limiting toxicity (DLT). See DLT primary outcome measure for definition. MTD is defined as the highest dose where <1/3 participants experience a DLT. If no DLT's are observed on Level 1, 3 subjects will be enrolled in the Level 2. If >1/3 subjects in a cohort have DLT, that dose will not be considered safe, with no escalation (MTD exceeded). If 1/3 subjects experience DLT, the cohort will be expanded to 6 subjects. If <2 subjects with a DLT among the expanded cohort of 6 evaluable subjects a cohort of 3 subjects will be enrolled in the next higher dose level. If 2 or more subjects with a DLT among the expanded cohort of 6 subjects, that dose level will not be considered safe, no escalation (MTD exceeded).If no DLT's observed, then the MTD is not reached. The MTD was not reached with 0/3 participants experiencing a DLT in the highest level. Higher doses were not planned/tested. (NCT01125293)
Timeframe: Assessed within the first cycle (28 days) of the study.

Intervention	mg (Number)
Phase I Stage B Level 1 & 2 and Dose Expansion	10

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Everolimus Maximum Tolerated Dose (MTD) Stage A [Phase I]

The MTD of Everolimus/Rituximab combination is determined by the number of patients who have dose limiting toxicity (DLT). See DLT primary outcome measure for definition. MTD is defined as the highest dose where <1/3 participants experience a DLT. If no DLT's are observed on Level 1, 3 subjects will be enrolled in the Level 2. If >1/3 subjects in a cohort have DLT, that dose will not be considered safe, with no escalation (MTD exceeded). If 1/3 subjects experience DLT, the cohort will be expanded to 6 subjects. If <2 subjects with a DLT among the expanded cohort of 6 evaluable subjects a cohort of 3 subjects will be enrolled in the next higher dose level. If 2 or more subjects with a DLT among the expanded cohort of 6 subjects, that dose level will not be considered safe, no escalation (MTD exceeded). If no DLT's are observed, then the MTD is not reached. The MTD was not reached with 0/3 participants experiencing a DLT in the highest dose level. Higher doses were not planned/tested. (NCT01125293)
Timeframe: Assessed within the first cycle (28 days) of the study.

Intervention	mg (Number)
Phase I Stage A Level 1 and 2	10

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2 Year Progression-free-survival [Phase II]

2-year progression free survival (PFS) is the probability of participants alive and progression free at 2 years from study entry estimated using Kaplan-Meier methods. PFS is defined as the time from enrollment to progressive disease (PD) or death. PD is defined as ≥25% increase in serum IgM level from lowest nadir and/or progression in clinical features attributable the disease. Patients alive without PD and not reporting use of non-protocol therapy prior to PD are censored at date of last objective progression-free disease assessment. Patients reporting use of non-protocol therapy prior to PD are censored at date of last objective progression-free disease assessment date prior to post-discontinuation therapy. (NCT01125293)
Timeframe: Patients were assessed for disease every cycle while on treatment (168 days) and every three months while on maintenance therapy. In long-term follow-up, disease was monitored every 3 months. Study cohort median (range) follow-up was 15 (1 - 23) months.

Intervention	percent probability of PFS (Number)
Phase II	28

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2-year Time-to-progression Probability (TTP) [Phase II]

2-year TTP probability is based on Kaplan-Meier methods. TTP is defined as time from enrollment to the date of progressive disease (PD). PD is defined as ≥25% increase in serum IgM level from lowest nadir and/or progression in clinical features attributable the disease. Patients without PD and not reporting use of non-protocol therapy prior to PD are censored at date of last objective progression-free disease assessment. Patients reporting use of non-protocol therapy prior to PD are censored at date of last objective progression-free disease assessment date prior to post-discontinuation therapy. (NCT01125293)
Timeframe: Patients were assessed for disease every cycle while on treatment (168 days) and every three months while on maintenance therapy. In long-term follow-up, disease was monitored every 3 months. Study cohort median (range) follow-up was 15 (1 - 23) months.

Intervention	percent probability of progression (Number)
Phase II	28

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Number of Participants With Progression Free Survival (PFS) at 6 Months

(NCT01142401)
Timeframe: At 6 months

Intervention	Participants (Count of Participants)
Arm A: Fulvestrant	16
Arm B: Fulvestrant + Bortezomib	22

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Progression Free Survival at 24 Weeks (Arm C)

(NCT01142401)
Timeframe: At 24 weeks

Intervention	Participants (Count of Participants)
Arm C: Crossover From Arm A at Progression to Fulvestrant + Bortezomib	5

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Frequency of Most Common Toxicities

Most common toxicities in the fulvestrant arm alone (Arm A) and the fulvestrant/bortezomib combination arm (Arm B). Most common toxicities are defined as adverse events having occurred in >10% of the participants within either (or both) Arm A or Arm B. (NCT01142401)
Timeframe: Up to 7 years

Intervention	percentage of participants (Number)
	Hemoglobin-Low	White Blood Cell-Low	Hyperglycemia/Glucose-High	Hypoglycemia/Glucose-Low	SGOT (AST-High)	SGPT (ALT-High)	Neutrophil Count Decreased/ANC-low	Platelet Count Decreased/Platelets-Low	Hypocalcemia/Calcium-Low	Hyponatremia/Sodium-Low	Nausea	Vomiting	Diarrhea	Constipation	Heartburn/Dyspepsia	Anorexia	Headache	Pain (general)	Peripheral Neuropathy (Motor, Pain, Sensory)	Injection Site Reaction	Dyspnea	Cough	Fatigue	Limb Edema	Insomnia	Hot Flashes	Dizziness	Arthralgia	Myalgia	Anxiety	Fever	Pruritis	Rash/Desquamation	Depression	Anemia	Dry Eye	Hypertension	Rash (General)	Eye Disorders (not otherwise specified)	Urinary Disorders (General)	Thrombocytopenia	Neutropenia	Upper Respiratory Disorders (General)	Musculoskeletal Pain Disorders (not otherwise specified)	Mucositis Oral
Arm A: Fulvestrant	41	32	44	5	25	14	10	8	10	8	29	14	8	34	10	15	12	59	31	24	32	29	56	19	25	37	7	36	10	8	15	7	8	8	32	0	12	7	7	15	41	8	12	17	8
Arm B: Fulvestrant + Bortezomib	61	42	51	12	32	21	12	30	12	12	63	32	47	46	18	23	25	54	49	12	19	23	56	37	35	32	19	28	18	19	12	16	11	16	42	12	21	23	12	11	61	30	23	18	11

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Number of Participants Who Survived Until Study End (up to 7 Years)

Tabulation of the number of participants who survived from the date of first treatment until study end (up to 7 years). (NCT01142401)
Timeframe: From first treatment day until study end, assessed up to 7 years

Intervention	Participants (Count of Participants)
Arm A: Fulvestrant Alone	39
Arm B: Fulvestrant + Bortezomib	42

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Clinical Benefit Rate (CBR) of Adding Bortezomib to Fulvestrant in Arm C

This outcome measure determined if the addition of bortezomib to fulvestrant improved the clinical benefit rate (defined as objective response plus stable disease for at least 24 weeks from day+1). Clinical Benefit Rate (CBR) is defined as the percentage of patients with advanced or metastatic cancer who have achieved complete response, partial response and stable disease to a therapeutic intervention in clinical trials of anticancer agents. (NCT01142401)
Timeframe: Up to 24 weeks

Intervention	Participants (Count of Participants)
Arm C: Crossover From Arm A at Progression to Fulvestrant + Bortezomib	5

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Number of Participants With Progression Free Survival (PFS) at 12 Months

The number of patients, treated with fulvestrant alone and fulvestrant plus bortezomib, who remained progression-free (Arms A vs. B). Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT01142401)
Timeframe: At 12 months

Intervention	Participants (Count of Participants)
Arm A: Fulvestrant	8
Arm B: Fulvestrant + Bortezomib	16

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Number of Patients Able to Collect >=6 x 106 CD34+ Cells/kg in <= 2 Collections.

The primary endpoint in all five treatment arms is the percentage of patients who are able to achieve greater than 6 x 106 CD34+ stems cells/kg harvested (defined as effectiveness). Note that no patients were enrolled Arm D and Arm E. (NCT01146834)
Timeframe: 36 months

Intervention	Participants (Count of Participants)
Arm A: VELCADE, CYCLOPHOSPHAMIDE, & G-CSF	11
Arm B: VELCADE & G-CSF	0
Arm C: CYCLOPHOSPHAMIDE & G-CSF	14

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Number of Patients Who Achieved Neutrophil Recovery After Melphalan 200 Based Transplant

Number of patients who achieved neutrophil recovery after Melphalan 200 based transplant in 20 days or fewer. Neutrophil recovery is defined as an absolute neutrophil count of greater than 0.5 k/uL for three consecutive days. (NCT01146834)
Timeframe: 20 days post-transplant

Intervention	Participants (Count of Participants)
Arm A: VELCADE, CYCLOPHOSPHAMIDE, & G-CSF	7
Arm B: VELCADE & G-CSF	4
Arm C: CYCLOPHOSPHAMIDE & G-CSF	11
Arm D: PLERIXAFOR & G-CSF	0
Arm E: PLERIXAFOR, VELCADE, & G-CSF	0

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Number of Patients Who Achieved Platelet Recovery After Melphalan 200 Based Transplant

Number of patients who achieved platelet recovery after Melphalan 200 based transplant in 20 days or fewer. Platelet recovery is defined as a platelet count of greater than 20,000, untransfused, for three consecutive days. (NCT01146834)
Timeframe: 20 days post-transplant

Intervention	Participants (Count of Participants)
Arm A: VELCADE, CYCLOPHOSPHAMIDE, & G-CSF	4
Arm B: VELCADE & G-CSF	1
Arm C: CYCLOPHOSPHAMIDE & G-CSF	9
Arm D: PLERIXAFOR & G-CSF	0
Arm E: PLERIXAFOR, VELCADE, & G-CSF	0

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Follow-up Time

time that patients were monitored for disease progression and overall survival (NCT01160484)
Timeframe: Follow-up visits for disease progression and overall survival every 3 months after study discontinuation. After progression, follow-up visits for survival status every 6 months or until alternate therapy needs to be started or death intervenes

Intervention	months (Median)
DVD-R Single Arm	11

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Time to Best Response

(NCT01160484)
Timeframe: Up to 7.5 months (eight 28-day cycles)

Intervention	months (Median)
DVD-R Single Arm	2

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International Myeloma Working Group (IMWG) Response Criteria

The investigator will evaluate each patient for response to therapy according to criteria augmented from those developed by Bladé et al., 1998 presented below (Table 7-1). Assessment of disease response will be performed prior to drug administration on Day 1 of Cycles 2 8 and at the End of Study Treatment visit. If a patient is determined to have complete response (CR), very good partial response (VGPR), partial response (PR), or minor response (MR), then assessment of disease response is to be performed 4 weeks later to confirm the response. (NCT01160484)
Timeframe: Up to 7.5 months (eight 28-day cycles)

Intervention	participants (Number)
	CR	VGPR	PR	Objective Response (CR+VGPR+PR)	MR	Clinical Benefit (CR+VGPR+PR+MR)	Estable disease	Progressive disease
DVD-R Single Arm	8	4	7	19	14	33	4	2

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Time to Progression

(NCT01160484)
Timeframe: Time from the start of treatment to progressive disease

Intervention	months (Median)
DVD-R Single Arm	9

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Duration of Response

(NCT01160484)
Timeframe: First evidence of PR or better (for overall response) and MR or better (for clinical benefit response) to start of disease progression or death.

Intervention	months (Median)
DVD-R Single Arm	12

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Progression-free Survival

(NCT01160484)
Timeframe: Time from the start of treatment to progressive disease or until death

Intervention	months (Median)
DVD-R Single Arm	9

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Time to First Response

(NCT01160484)
Timeframe: Up to 7.5 months (eight 28-day cycles)

Intervention	months (Median)
DVD-R Single Arm	1

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Exercise Tolerance- 6 Minute Walk

Patients will have an exercise tolerance assessment defined as a 6 minute walk completed at cycle 1 (week 1) and cycle 2 (week 5) of treatment and visit 9 (12 weeks) and visit 10 (18 weeks). (NCT01163786)
Timeframe: Up to 18 weeks from baseline

Intervention	participants (Number)
	Cycle 1 (Visit 1): Started 6 Minute walk	Cycle 1 (Visit 1): Stopped before 6 minutes	Cycle 1(Visit 1):Declined walk	Cycle 2 (Visit 5) : Started 6 Minute walk	Cycle 2 (Visit 5) : Stopped before 6 minutes	Cycle 2(Visit 5):Declined walk	Follow up/Visit 9: Started 6 Minute walk	Follow up/Visit 9 : Stopped before 6 minutes	Follow up/Visit 9: Declined walk	Follow up/Visit 10 : Started 6 Minute walk	Follow up/Visit 10 : Stopped before 6 minutes	Follow up/Visit 10: Declined walk
Bortezomib	13	3	0	3	0	0	6	1	1	5	1	1

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Change in Pulmonary Function as Measured by Forced Expiratory Volume in 1 Second (FEV1) Decline

FEV1 will be measured by spirometry assessments at baseline (pre-transplant baseline - prior to pulmonary chronic graft-versus-host disease (p-CGVHD)) during treatment (10 weeks) and at follow up visit 9 (at 12 weeks) and at follow up visit 10 (at 18 weeks) with patients having spirometry tested up to 6 times from screening to the end of the study. FEV1 is reported as slopes computed by dividing difference in FEV1 by time in months. (NCT01163786)
Timeframe: Mean time to diagnosis (from transplant to p-CGVHD ) of 3.36 years (+/- 1.88 years) and up to 18 weeks after baseline

Intervention	percentage per month (Median)
	Prior to diagnosis of p-CGVHD	During Treatment with Bortezomib
Bortezomib	-1.06	-0.25

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Short Form (SF)-36 Health Survey

"This is a quality of life questionnaire which yields scores for 8 domains (physical functioning, role-physical, bodily pain, general health, vitality, social functioning, role-emotional and mental health). This questionnaire will be completed by patients on Visit 1 (week 1), Visit 5 (week 5), Visit 8 (week 8), Visit 9 (12 weeks), and Visit 10 (18 weeks).~Questionnaires were scored per the scoring rules for the RAND 36-Item Health Survey (version 1.0) A high score defines a more favorable health state. In addition, each item is scored on a 0 to 100 range so that the lowest and highest possible scores are 0 and 100, respectively. Scores represent the percentage of total possible score achieved. Items that are left blank (missing data) are not taken into account when calculating the scale scores. Hence, scale scores represent the average for all items in the scale that the respondent answered." (NCT01163786)
Timeframe: up to 18 weeks

Intervention	Average Score (Number)
	Pt #01 Physical Functioning : Visit 1	Pt #01 Physical Functioning : Visit 5	Pt #01 Physical Functioning : Visit 8	Pt #01 Physical Functioning : Visit 9	Pt #01 Physical Functioning : Visit 10	Pt #01 Role-physical : Visit 1	Pt #01 Role-physical : Visit 5	Pt #01 Role-physical : Visit 8	Pt #01 Role-physical : Visit 9	Pt #01 Role-physical : Visit 10	Pt #01 Role-emotional : Visit 1	Pt #01 Role-emotional : Visit 5	Pt #01 Role-emotional : Visit 8	Pt #01 Role-emotional : Visit 9	Pt #01 Role-emotional : Visit 10	Pt #01 Energy/fatigue : Visit 1	Pt #01 Energy/fatigue : Visit 5	Pt #01 Energy/fatigue : Visit 8	Pt #01 Energy/fatigue : Visit 9	Pt #01 Energy/fatigue : Visit 10	Pt #01 Emotional Well-being : Visit 1	Pt #01 Emotional Well-being : Visit 5	Pt #01 Emotional Well-being : Visit 8	Pt #01 Emotional Well-being : Visit 9	Pt #01 Emotional Well-being : Visit 10	Pt #01 Social Functioning : Visit 1	Pt #01 Social Functioning : Visit 5	Pt #01 Social Functioning : Visit 8	Pt #01 Social Functioning : Visit 9	Pt #01 Social Functioning : Visit 10	Pt #01 Pain : Visit 1	Pt #01 Pain : Visit 5	Pt #01 Pain : Visit 8	Pt #01 Pain : Visit 9	Pt #01 Pain : Visit 10	Pt #01 General Health : Visit 1	Pt #01 General Health : Visit 5	Pt #01 General Health : Visit 8	Pt #01 General Health : Visit 9	Pt #01 General Health : Visit 10	Pt #2 Physical Functioning : Visit 1	Pt #2 Physical Functioning : Visit 5	Pt #2 Physical Functioning : Visit 8	Pt #2 Physical Functioning : Visit 9	Pt #2 Physical Functioning : Visit 10	Pt #2 Role-physical : Visit 1	Pt #2 Role-physical : Visit 5	Pt #2 Role-physical : Visit 8	Pt #2 Role-physical : Visit 9	Pt #2 Role-physical : Visit 10	Pt #2 Role-emotional : Visit 1	Pt #2 Role-emotional : Visit 5	Pt #2 Role-emotional : Visit 8	Pt #2 Role-emotional : Visit 9	Pt #2 Role-emotional : Visit 10	Pt #2 Energy/fatigue : Visit 1	Pt #2 Energy/fatigue : Visit 5	Pt #2 Energy/fatigue : Visit 8	Pt #2 Energy/fatigue : Visit 9	Pt #2 Energy/fatigue : Visit 10	Pt #2 Emotional Well-being : Visit 1	Pt #2 Emotional Well-being : Visit 5	Pt #2 Emotional Well-being : Visit 8	Pt #2 Emotional Well-being : Visit 9	Pt #2 Emotional Well-being : Visit 10	Pt #2 Social Functioning : Visit 1	Pt #2 Social Functioning : Visit 5	Pt #2 Social Functioning : Visit 8	Pt #2 Social Functioning : Visit 9	Pt #2 Social Functioning : Visit 10	Pt #2 Pain : Visit 1	Pt #2 Pain : Visit 5	Pt #2 Pain : Visit 8	Pt #2 Pain : Visit 9	Pt #2 Pain : Visit 10	Pt #2 General Health : Visit 1	Pt #2 General Health : Visit 5	Pt #2 General Health : Visit 8	Pt #2 General Health : Visit 9	Pt #2 General Health : Visit 10	Pt #3 Physical Functioning : Visit 1	Pt #3 Physical Functioning : Visit 5	Pt #3 Physical Functioning : Visit 8	Pt #3 Physical Functioning : Visit 9	Pt #3 Physical Functioning : Visit 10	Pt #3: Role-physical : Visit 1	Pt #3: Role-physical : Visit 5	Pt #3: Role-physical : Visit 8	Pt #3: Role-physical : Visit 9	Pt #3: Role-physical : Visit 10	Pt #3: Role-emotional : Visit 1	Pt #3: Role-emotional : Visit 5	Pt #3: Role-emotional : Visit 8	Pt #3: Role-emotional : Visit 9	Pt #3: Role-emotional : Visit 10	Pt #3: Energy/fatigue : Visit 1	Pt #3: Energy/fatigue : Visit 5	Pt #3: Energy/fatigue : Visit 8	Pt #3: Energy/fatigue : Visit 9	Pt #3: Energy/fatigue : Visit 10	Pt #3: Emotional Well-being : Visit 1	Pt #3: Emotional Well-being : Visit 5	Pt #3: Emotional Well-being : Visit 8	Pt #3: Emotional Well-being : Visit 9	Pt #3: Emotional Well-being : Visit 10	Pt #3 : Social Functioning : Visit 1	Pt #3 : Social Functioning : Visit 5	Pt #3 : Social Functioning : Visit 8	Pt #3 : Social Functioning : Visit 9	Pt #3 : Social Functioning : Visit 10	Pt #3 Pain : Visit 1	Pt #3 Pain : Visit 5	Pt #3 Pain : Visit 8	Pt #3 Pain : Visit 9	Pt #3 Pain : Visit 10	Pt #3 : General Health : Visit 1	Pt #3 : General Health : Visit 5	Pt #3 : General Health : Visit 8	Pt #3 : General Health : Visit 9	Pt #3 : General Health : Visit 10	Pt #4 : Physical Functioning : Visit 1	Pt #4 : Physical Functioning : Visit 5	Pt #4 : Physical Functioning : Visit 8	Pt #4 : Physical Functioning : Visit 9	Pt #4 : Physical Functioning : Visit 10	Pt #4 : Role-physcial : Visit 1	Pt #4 : Role-physcial : Visit 5	Pt #4 : Role-physcial : Visit 8	Pt #4 : Role-physcial : Visit 9	Pt #4 : Role-physcial : Visit 10	Pt #4 : Role-emotional : Visit 1	Pt #4 : Role-emotional : Visit 5	Pt #4 : Role-emotional : Visit 8	Pt #4 : Role-emotional : Visit 9	Pt #4 : Role-emotional : Visit 10	Pt #4 : Energy/fatigue : Visit 1	Pt #4 : Energy/fatigue : Visit 5	Pt #4 : Energy/fatigue : Visit 8	Pt #4 : Energy/fatigue : Visit 9	Pt #4 : Energy/fatigue : Visit 10	Pt #4 : Emotional Well-being : Visit 1	Pt #4 : Emotional Well-being : Visit 5	Pt #4 : Emotional Well-being : Visit 8	Pt #4 : Emotional Well-being : Visit 9	Pt #4 : Emotional Well-being : Visit 10	Pt #4 : Social Functioning : Visit 1	Pt #4 : Social Functioning : Visit 5	Pt #4 : Social Functioning : Visit 8	Pt #4 : Social Functioning : Visit 9	Pt #4 : Social Functioning : Visit 10	Pt #4 : Pain : Visit 1	Pt #4 : Pain : Visit 5	Pt #4 : Pain : Visit 8	Pt #4 : Pain : Visit 9	Pt #4 : Pain : Visit 10	Pt #4 : General Health : Visit 1	Pt #4 : General Health : Visit 5	Pt #4 : General Health : Visit 8	Pt #4 : General Health : Visit 9	Pt #4 : General Health : Visit 10	Pt #5: Physical Functioning : Visit 1	Pt #5: Physical Functioning : Visit 5	Pt #5: Physical Functioning : Visit 8	Pt #5: Physical Functioning : Visit 9	Pt #5: Physical Functioning : Visit 10	Pt #5: Role-physical : Visit 1	Pt #5: Role-physical : Visit 5	Pt #5: Role-physical : Visit 8	Pt #5: Role-physical : Visit 9	Pt #5: Role-physical : Visit 10	Pt #5: Role-emotional : Visit 1	Pt #5: Role-emotional : Visit 5	Pt #5: Role-emotional : Visit 8	Pt #5: Role-emotional : Visit 9	Pt #5: Role-emotional : Visit 10	Pt #5: Energy/fatigue : Visit 1	Pt #5: Energy/fatigue : Visit 5	Pt #5: Energy/fatigue : Visit 8	Pt #5: Energy/fatigue : Visit 9	Pt #5: Energy/fatigue : Visit 10	Pt #5: Emotional Well-being : Visit 1	Pt #5: Emotional Well-being : Visit 5	Pt #5: Emotional Well-being : Visit 8	Pt #5: Emotional Well-being : Visit 9	Pt #5: Emotional Well-being : Visit 10	Pt #5: Social Functioning : Visit 1	Pt #5: Social Functioning : Visit 5	Pt #5: Social Functioning : Visit 8	Pt #5: Social Functioning : Visit 9	Pt #5: Social Functioning : Visit 10	Pt #5: Pain : Visit 1	Pt #5: Pain : Visit 5	Pt #5: Pain : Visit 8	Pt #5: Pain : Visit 9	Pt #5: Pain : Visit 10	Pt #5: General Health : Visit 1	Pt #5: General Health : Visit 5	Pt #5: General Health : Visit 8	Pt #5: General Health : Visit 9	Pt #5: General Health : Visit 10	Pt #6: Physical Functioning : Visit 1	Pt #6: Physical Functioning : Visit 5	Pt #6: Physical Functioning : Visit 8	Pt #6: Physical Functioning : Visit 9	Pt #6: Physical Functioning : Visit 10	Pt #6: Role-physical : Visit 1	Pt #6: Role-physical : Visit 5	Pt #6: Role-physical : Visit 8	Pt #6: Role-physical : Visit 9	Pt #6: Role-physical : Visit 10	Pt #6: Role-emotional : Visit 1	Pt #6: Role-emotional : Visit 5	Pt #6: Role-emotional : Visit 8	Pt #6: Role-emotional : Visit 9	Pt #6: Role-emotional : Visit 10	Pt #6: Energy/fatigue : Visit 1	Pt #6: Energy/fatigue : Visit 5	Pt #6: Energy/fatigue : Visit 8	Pt #6: Energy/fatigue : Visit 9	Pt #6: Energy/fatigue : Visit 10	Pt #6: Emotional Well-being : Visit 1	Pt #6: Emotional Well-being : Visit 5	Pt #6: Emotional Well-being : Visit 8	Pt #6: Emotional Well-being : Visit 9	Pt #6: Emotional Well-being : Visit 10	Pt #6: Social Functioning : Visit 1	Pt #6: Social Functioning : Visit 5	Pt #6: Social Functioning : Visit 8	Pt #6: Social Functioning : Visit 9	Pt #6: Social Functioning : Visit 10	Pt #6: Pain : Visit 1	Pt #6: Pain : Visit 5	Pt #6: Pain : Visit 8	Pt #6: Pain : Visit 9	Pt #6: Pain : Visit 10	Pt #6: General Health : Visit 1	Pt #6: General Health : Visit 5	Pt #6: General Health : Visit 8	Pt #6: General Health : Visit 9	Pt #6: General Health : Visit 10	Pt #7: Physical Functioning : Visit 1	Pt #7: Physical Functioning : Visit 5	Pt #7: Physical Functioning : Visit 8	Pt #7: Physical Functioning : Visit 9	Pt #7: Physical Functioning : Visit 10	Pt #7: Role-physical : Visit 1	Pt #7: Role-physical : Visit 5	Pt #7: Role-physical : Visit 8	Pt #7: Role-physical : Visit 9	Pt #7: Role-physical : Visit 10	Pt #7: Role-emotional : Visit 1	Pt #7: Role-emotional : Visit 5	Pt #7: Role-emotional : Visit 8	Pt #7: Role-emotional : Visit 9	Pt #7: Role-emotional : Visit 10	Pt #7: Energy/fatigue : Visit 1	Pt #7: Energy/fatigue : Visit 5	Pt #7: Energy/fatigue : Visit 8	Pt #7: Energy/fatigue : Visit 9	Pt #7: Energy/fatigue : Visit 10	Pt #7: Emotional Well-being : Visit 1	Pt #7: Emotional Well-being : Visit 5	Pt #7: Emotional Well-being : Visit 8	Pt #7: Emotional Well-being : Visit 9	Pt #7: Emotional Well-being : Visit 10	Pt #7: Social Functioning : Visit 1	Pt #7: Social Functioning : Visit 5	Pt #7: Social Functioning : Visit 8	Pt #7: Social Functioning : Visit 9	Pt #7: Social Functioning : Visit 10	Pt #7: Pain : Visit 1	Pt #7: Pain : Visit 5	Pt #7: Pain : Visit 8	Pt #7: Pain : Visit 9	Pt #7: Pain : Visit 10	Pt #7: General Health : Visit 1	Pt #7: General Health : Visit 5	Pt #7: General Health : Visit 8	Pt #7: General Health : Visit 9	Pt #7: General Health : Visit 10	Pt #8: Physical Functioning : Visit 1	Pt #8: Physical Functioning : Visit 5	Pt #8: Physical Functioning : Visit 8	Pt #8: Physical Functioning : Visit 9	Pt #8: Physical Functioning : Visit 10	Pt #8 Role-physcial : Visit 1	Pt #8 Role-physcial : Visit 5	Pt #8 Role-physcial : Visit 8	Pt #8 Role-physcial : Visit 9	Pt #8 Role-physcial : Visit 10	Pt #8: Role-emotional : Visit 1	Pt #8: Role-emotional : Visit 5	Pt #8: Role-emotional : Visit 8	Pt #8: Role-emotional : Visit 9	Pt #8: Role-emotional : Visit 10	Pt #8: Energy/fatigue : Visit 1	Pt #8: Energy/fatigue : Visit 5	Pt #8: Energy/fatigue : Visit 8	Pt #8: Energy/fatigue : Visit 9	Pt #8: Energy/fatigue : Visit 10	Pt #8 : Emotional Well-being : Visit 1	Pt #8 : Emotional Well-being : Visit 5	Pt #8 : Emotional Well-being : Visit 8	Pt #8 : Emotional Well-being : Visit 9	Pt #8 : Emotional Well-being : Visit 10	Pt #8: Social Functioning : Visit 1	Pt #8: Social Functioning : Visit 5	Pt #8: Social Functioning : Visit 8	Pt #8: Social Functioning : Visit 9	Pt #8: Social Functioning : Visit 10	Pt #8 Pain : Visit 1	Pt #8 Pain : Visit 5	Pt #8 Pain : Visit 8	Pt #8 Pain : Visit 9	Pt #8 Pain : Visit 10	Pt #8: General Health : Visit 1	Pt #8: General Health : Visit 5	Pt #8: General Health : Visit 8	Pt #8: General Health : Visit 9	Pt #8: General Health : Visit 10	Pt #9: Physical Functioning : Visit 1	Pt #9: Physical Functioning : Visit 5	Pt #9: Physical Functioning : Visit 8	Pt #9: Physical Functioning : Visit 9	Pt #9: Physical Functioning : Visit 10	Pt #9: Role-physical : Visit 1	Pt #9: Role-physical : Visit 5	Pt #9: Role-physical : Visit 8	Pt #9: Role-physical : Visit 9	Pt #9: Role-physical : Visit 10	Pt #9: Role-emotional : Visit 1	Pt #9: Role-emotional : Visit 5	Pt #9: Role-emotional : Visit 8	Pt #9: Role-emotional : Visit 9	Pt #9: Role-emotional : Visit 10	Pt #9: Energy/fatigue : Visit 1	Pt #9: Energy/fatigue : Visit 5	Pt #9: Energy/fatigue : Visit 8	Pt #9: Energy/fatigue : Visit 9	Pt #9: Energy/fatigue : Visit 10	Pt #9: Emotional Well-being : Visit 1	Pt #9: Emotional Well-being : Visit 5	Pt #9: Emotional Well-being : Visit 8	Pt #9: Emotional Well-being : Visit 9	Pt #9: Emotional Well-being : Visit 10	Pt #9: Social Functioning : Visit 1	Pt #9: Social Functioning : Visit 5	Pt #9: Social Functioning : Visit 8	Pt #9: Social Functioning : Visit 9	Pt #9: Social Functioning : Visit 10	Pt #9: Pain : Visit 1	Pt #9: Pain : Visit 5	Pt #9: Pain : Visit 8	Pt #9: Pain : Visit 9	Pt #9: Pain : Visit 10	Pt #9: General Health : Visit 1	Pt #9: General Health : Visit 5	Pt #9: General Health : Visit 8	Pt #9: General Health : Visit 9	Pt #9: General Health : Visit 10	Pt #10: Physical Functioning : Visit 1	Pt #10: Physical Functioning : Visit 5	Pt #10: Physical Functioning : Visit 8	Pt #10: Physical Functioning : Visit 9	Pt #10: Physical Functioning : Visit 10	Pt #10: Role-physical : Visit 1	Pt #10: Role-physical : Visit 5	Pt #10: Role-physical : Visit 8	Pt #10: Role-physical : Visit 9	Pt #10: Role-physical : Visit 10	Pt #10: Role-emotional : Visit 1	Pt #10: Role-emotional : Visit 5	Pt #10: Role-emotional : Visit 8	Pt #10: Role-emotional : Visit 9	Pt #10: Role-emotional : Visit 10	Pt #10: Energy/fatigue : Visit 1	Pt #10: Energy/fatigue : Visit 5	Pt #10: Energy/fatigue : Visit 8	Pt #10: Energy/fatigue : Visit 9	Pt #10: Energy/fatigue : Visit 10	Pt #10: Emotional Well-being : Visit 1	Pt #10: Emotional Well-being : Visit 5	Pt #10: Emotional Well-being : Visit 8	Pt #10: Emotional Well-being : Visit 9	Pt #10: Emotional Well-being : Visit 10	Pt #10 : Social Functioning : Visit 1	Pt #10 : Social Functioning : Visit 5	Pt #10 : Social Functioning : Visit 8	Pt #10 : Social Functioning : Visit 9	Pt #10 : Social Functioning : Visit 10	Pt #10 Pain : Visit 1	Pt #10 Pain : Visit 5	Pt #10 Pain : Visit 8	Pt #10 Pain : Visit 9	Pt #10 Pain : Visit 10	Pt #10 Visit 1 : General Health : Visit 1	Pt #10 Visit 1 : General Health : Visit 5	Pt #10 Visit 1 : General Health : Visit 8	Pt #10 Visit 1 : General Health : Visit 9	Pt #10 Visit 1 : General Health : Visit 10	Pt #11 Visit 1 : Physical Functioning : Visit 1	Pt #11 Visit 1 : Physical Functioning : Visit 5	Pt #11 Visit 1 : Physical Functioning : Visit 8	Pt #11 Visit 1 : Physical Functioning : Visit 9	Pt #11 Visit 1 : Physical Functioning : Visit 10	Pt #11 Visit 1 : Role-physical : Visit 1	Pt #11 Visit 1 : Role-physical : Visit 5	Pt #11 Visit 1 : Role-physical : Visit 8	Pt #11 Visit 1 : Role-physical : Visit 9	Pt #11 Visit 1 : Role-physical : Visit 10	Pt #11 Visit 1 : Role-emotional : Visit 1	Pt #11 Visit 1 : Role-emotional : Visit 5	Pt #11 Visit 1 : Role-emotional : Visit 8	Pt #11 Visit 1 : Role-emotional : Visit 9	Pt #11 Visit 1 : Role-emotional : Visit 10	Pt #11 Visit 1 : Energy/fatigue : Visit 1	Pt #11 Visit 1 : Energy/fatigue : Visit 5	Pt #11 Visit 1 : Energy/fatigue : Visit 8	Pt #11 Visit 1 : Energy/fatigue : Visit 9	Pt #11 Visit 1 : Energy/fatigue : Visit 10	Pt #11 Emotional Well-being : Visit 1	Pt #11 Emotional Well-being : Visit 5	Pt #11 Emotional Well-being : Visit 8	Pt #11 Emotional Well-being : Visit 9	Pt #11 Emotional Well-being : Visit 10	Pt #11 Social Functioning : Visit 1	Pt #11 Social Functioning : Visit 5	Pt #11 Social Functioning : Visit 8	Pt #11 Social Functioning : Visit 9	Pt #11 Social Functioning : Visit 10	Pt #11 Visit 1 : Pain : Visit 1	Pt #11 Visit 1 : Pain : Visit 5	Pt #11 Visit 1 : Pain : Visit 8	Pt #11 Visit 1 : Pain : Visit 9	Pt #11 Visit 1 : Pain : Visit 10	Pt #11 General Health : Visit 1	Pt #11 General Health : Visit 5	Pt #11 General Health : Visit 8	Pt #11 General Health : Visit 9	Pt #11 General Health : Visit 10	Pt #12 Physical Functioning : Visit 1	Pt #12 Physical Functioning : Visit 5	Pt #12 Physical Functioning : Visit 8	Pt #12 Physical Functioning : Visit 9	Pt #12 Physical Functioning : Visit 10	Pt #12 Role-physical : Visit 1	Pt #12 Role-physical : Visit 5	Pt #12 Role-physical : Visit 8	Pt #12 Role-physical : Visit 9	Pt #12 Role-physical : Visit 10	Pt #12 Role-emotional : Visit 1	Pt #12 Role-emotional : Visit 5	Pt #12 Role-emotional : Visit 8	Pt #12 Role-emotional : Visit 9	Pt #12 Role-emotional : Visit 10	Pt #12 Energy/fatigue : Visit 1	Pt #12 Energy/fatigue : Visit 5	Pt #12 Energy/fatigue : Visit 8	Pt #12 Energy/fatigue : Visit 9	Pt #12 Energy/fatigue : Visit 10	Pt #12 Emotional Well-being : Visit 1	Pt #12 Emotional Well-being : Visit 5	Pt #12 Emotional Well-being : Visit 8	Pt #12 Emotional Well-being : Visit 9	Pt #12 Emotional Well-being : Visit 10	Pt #12 Social Functioning : Visit 1	Pt #12 Social Functioning : Visit 5	Pt #12 Social Functioning : Visit 8	Pt #12 Social Functioning : Visit 9	Pt #12 Social Functioning : Visit 10	Pt #12 Pain : Visit 1	Pt #12 Pain : Visit 5	Pt #12 Pain : Visit 8	Pt #12 Pain : Visit 9	Pt #12 Pain : Visit 10	Pt #12 General Health : Visit 1	Pt #12 General Health : Visit 5	Pt #12 General Health : Visit 8	Pt #12 General Health : Visit 9	Pt #12 General Health : Visit 10	Pt#13 Physical Functioning : Visit 1	Pt#13 Physical Functioning : Visit 5	Pt#13 Physical Functioning : Visit 8	Pt#13 Physical Functioning : Visit 9	Pt#13 Physical Functioning : Visit 10	Pt #13 Role-physical : Visit 1	Pt #13 Role-physical : Visit 5	Pt #13 Role-physical : Visit 8	Pt #13 Role-physical : Visit 9	Pt #13 Role-physical : Visit 10	Pt #13 Role-emotional : Visit 1	Pt #13 Role-emotional : Visit 5	Pt #13 Role-emotional : Visit 8	Pt #13 Role-emotional : Visit 9	Pt #13 Role-emotional : Visit 10	Pt #13 Energy/fatigue : Visit 1	Pt #13 Energy/fatigue : Visit 5	Pt #13 Energy/fatigue : Visit 8	Pt #13 Energy/fatigue : Visit 9	Pt #13 Energy/fatigue : Visit 10	Pt #13 Emotional Well-being : Visit 1	Pt #13 Emotional Well-being : Visit 5	Pt #13 Emotional Well-being : Visit 8	Pt #13 Emotional Well-being : Visit 9	Pt #13 Emotional Well-being : Visit 10	Pt #13 Social Functioning : Visit 1	Pt #13 Social Functioning : Visit 5	Pt #13 Social Functioning : Visit 8	Pt #13 Social Functioning : Visit 9	Pt #13 Social Functioning : Visit 10	Pt #13 Pain : Visit 1	Pt #13 Pain : Visit 5	Pt #13 Pain : Visit 8	Pt #13 Pain : Visit 9	Pt #13 Pain : Visit 10	Pt #13 General Health : Visit 1	Pt #13 General Health : Visit 5	Pt #13 General Health : Visit 8	Pt #13 General Health : Visit 9	Pt #13 General Health : Visit 10	Pt #14 Physical Functioning : Visit 1	Pt #14 Physical Functioning : Visit 5	Pt #14 Physical Functioning : Visit 8	Pt #14 Physical Functioning : Visit 9	Pt #14 Physical Functioning : Visit 10	Pt #14 Role-physical : Visit 1	Pt #14 Role-physical : Visit 5	Pt #14 Role-physical : Visit 8	Pt #14 Role-physical : Visit 9	Pt #14 Role-physical : Visit 10	Pt #14 Role-emotional : Visit 1	Pt #14 Role-emotional : Visit 5	Pt #14 Role-emotional : Visit 8	Pt #14 Role-emotional : Visit 9	Pt #14 Role-emotional : Visit 10	Pt #14 Energy/fatigue : Visit 1	Pt #14 Energy/fatigue : Visit 5	Pt #14 Energy/fatigue : Visit 8	Pt #14 Energy/fatigue : Visit 9	Pt #14 Energy/fatigue : Visit 10	Pt #14 Emotional Well-being : Visit 1	Pt #14 Emotional Well-being : Visit 5	Pt #14 Emotional Well-being : Visit 8	Pt #14 Emotional Well-being : Visit 9	Pt #14 Emotional Well-being : Visit 10	Pt #14 Social Functioning : Visit 1	Pt #14 Social Functioning : Visit 5	Pt #14 Social Functioning : Visit 8	Pt #14 Social Functioning : Visit 9	Pt #14 Social Functioning : Visit 10	Pt #14 Pain : Visit 1	Pt #14 Pain : Visit 5	Pt #14 Pain : Visit 8	Pt #14 Pain : Visit 9	Pt #14 Pain : Visit 10	Pt #14 General Health : Visit 1	Pt #14 General Health : Visit 5	Pt #14 General Health : Visit 8	Pt #14 General Health : Visit 9	Pt #14 General Health : Visit 10	Pt #15 Physical Functioning : Visit 1	Pt #15 Physical Functioning : Visit 5	Pt #15 Physical Functioning : Visit 8	Pt #15 Physical Functioning : Visit 9	Pt #15 Physical Functioning : Visit 10	Pt #15 Role-physical : Visit 1	Pt #15 Role-physical : Visit 5	Pt #15 Role-physical : Visit 8	Pt #15 Role-physical : Visit 9	Pt #15 Role-physical : Visit 10	Pt #15 Role-emotional : Visit 1	Pt #15 Role-emotional : Visit 5	Pt #15 Role-emotional : Visit 8	Pt #15 Role-emotional : Visit 9	Pt #15 Role-emotional : Visit 10	Pt #15 Energy/fatigue : Visit 1	Pt #15 Energy/fatigue : Visit 5	Pt #15 Energy/fatigue : Visit 8	Pt #15 Energy/fatigue : Visit 9	Pt #15 Energy/fatigue : Visit 10	Pt #15 Emotional Well-being : Visit 1	Pt #15 Emotional Well-being : Visit 5	Pt #15 Emotional Well-being : Visit 8	Pt #15 Emotional Well-being : Visit 9	Pt #15 Emotional Well-being : Visit 10	Pt #15 Social Functioning : Visit 1	Pt #15 Social Functioning : Visit 5	Pt #15 Social Functioning : Visit 8	Pt #15 Social Functioning : Visit 9	Pt #15 Social Functioning : Visit 10	Pt #15 Pain : Visit 1	Pt #15 Pain : Visit 5	Pt #15 Pain : Visit 8	Pt #15 Pain : Visit 9	Pt #15 Pain : Visit 10	Pt #15 General Health : Visit 1	Pt #15 General Health : Visit 5	Pt #15 General Health : Visit 8	Pt #15 General Health : Visit 9	Pt #15 General Health : Visit 10	Pt #16 Physical Functioning : Visit 1	Pt #16 Physical Functioning : Visit 5	Pt #16 Physical Functioning : Visit 8	Pt #16 Physical Functioning : Visit 9	Pt #16 Physical Functioning : Visit 10	Pt #16 Role-physical : Visit 1	Pt #16 Role-physical : Visit 5	Pt #16 Role-physical : Visit 8	Pt #16 Role-physical : Visit 9	Pt #16 Role-physical : Visit 10	Pt #16 Role-emotional : Visit 1	Pt #16 Role-emotional : Visit 5	Pt #16 Role-emotional : Visit 8	Pt #16 Role-emotional : Visit 9	Pt #16 Role-emotional : Visit 10	Pt #16 Energy/fatigue : Visit 1	Pt #16 Energy/fatigue : Visit 5	Pt #16 Energy/fatigue : Visit 8	Pt #16 Energy/fatigue : Visit 9	Pt #16 Energy/fatigue : Visit 10	Pt #16 Emotional Well-being : Visit 1	Pt #16 Emotional Well-being : Visit 5	Pt #16 Emotional Well-being : Visit 8	Pt #16 Emotional Well-being : Visit 9	Pt #16 Emotional Well-being : Visit 10	Pt #16 Social Functioning : Visit 1	Pt #16 Social Functioning : Visit 5	Pt #16 Social Functioning : Visit 8	Pt #16 Social Functioning : Visit 9	Pt #16 Social Functioning : Visit 10	Pt #16 Pain : Visit 1	Pt #16 Pain : Visit 5	Pt #16 Pain : Visit 8	Pt #16 Pain : Visit 9	Pt #16 Pain : Visit 10	Pt #16 General Health : Visit 1	Pt #16 General Health : Visit 5	Pt #16 General Health : Visit 8	Pt #16 General Health : Visit 9	Pt #16 General Health : Visit 10	Pt #17 Physical Functioning : Visit 1	Pt #17 Physical Functioning : Visit 5	Pt #17 Physical Functioning : Visit 8	Pt #17 Physical Functioning : Visit 9	Pt #17 Physical Functioning : Visit 10	Pt #17 Role-physical : Visit 1	Pt #17 Role-physical : Visit 5	Pt #17 Role-physical : Visit 8	Pt #17 Role-physical : Visit 9	Pt #17 Role-physical : Visit 10	Pt #17 Role-emotional : Visit 1	Pt #17 Role-emotional : Visit 5	Pt #17 Role-emotional : Visit 8	Pt #17 Role-emotional : Visit 9	Pt #17 Role-emotional : Visit 10	Pt #17 Energy/fatigue : Visit 1	Pt #17 Energy/fatigue : Visit 5	Pt #17 Energy/fatigue : Visit 8	Pt #17 Energy/fatigue : Visit 9	Pt #17 Energy/fatigue : Visit 10	Pt #17 Emotional Well-being : Visit 1	Pt #17 Emotional Well-being : Visit 5	Pt #17 Emotional Well-being : Visit 8	Pt #17 Emotional Well-being : Visit 9	Pt #17 Emotional Well-being : Visit 10	Pt #17 Social Functioning : Visit 1	Pt #17 Social Functioning : Visit 5	Pt #17 Social Functioning : Visit 8	Pt #17 Social Functioning : Visit 9	Pt #17 Social Functioning : Visit 10	Pt #17 Pain : Visit 1	Pt #17 Pain : Visit 5	Pt #17 Pain : Visit 8	Pt #17 Pain : Visit 9	Pt #17 Pain : Visit 10	Pt #17 General Health : Visit 1	Pt #17 General Health : Visit 5	Pt #17 General Health : Visit 8	Pt #17 General Health : Visit 9	Pt #17 General Health : Visit 10
Bortezomib	30	55	NA	NA	NA	0	25	NA	NA	NA	100	66.67	NA	NA	NA	50	35	NA	NA	NA	88	84	NA	NA	NA	87.5	75	NA	NA	NA	100	55	NA	NA	NA	65	55	NA	NA	NA	30	NA	30	30	75	0	NA	0	0	100	0	NA	100	100	100	25	NA	40	20	55	84	NA	88	92	76	87.5	NA	87.5	87.5	87.5	32.5	NA	45	45	45	25	NA	35	31.25	30	16.67	NA	30	40	30	25	NA	0	0	0	NA	NA	100	100	100	20	NA	5	5	5	88	NA	68	68	72	75	NA	62.5	87.5	75	90	NA	100	100	90	10	20	31.25	20	20	45	60	33.33	50	50	NA	25	100	NA	75	33.33	0	0	33.33	33.33	25	35	35	30	35	60	56	72	66.67	60	25	37.5	50	NA	50	22.5	20	67.5	NA	55	35	35	30	40	30	10	20	15	10	15	0	0	0	0	0	33.33	0	33.33	33.33	33.33	25	30	20	0	15	72	76	68	64	68	12.5	50	37.5	12.5	12.5	22.5	35	22.5	32.5	10	25	20	15	20	25	22.22	27.78	20	15	0	NA	NA	0	0	0	NA	NA	0	100	33.3	10	10	15	10	0	46.67	60	64	64	36	NA	NA	25	37.5	25	NA	NA	100	100	55	20	20	20	15	15	20	55	NA	NA	NA	100	25	NA	NA	NA	100	100	NA	NA	NA	65	10	NA	NA	NA	72	88	NA	NA	NA	50	87.5	NA	NA	NA	77.5	77.5	NA	NA	NA	30	35	NA	NA	NA	45	75	45	70	45	0	33.33	66.67	100	100	0	50	50	45	50	40	50	50	45	50	52	60	52	92	92	50	50	50	75	87.5	45	45	45	80	90	45	50	55	80	65	75	NA	70	70	80	0	NA	0	25	100	100	NA	100	100	100	70	NA	60	70	75	84	NA	80	92	80	75	NA	62.5	87.5	75	77.5	NA	45	77.5	67.5	70	NA	31.25	40	56.25	80	90	83.33	85	85	0	25	100	25	100	100	100	100	100	100	60	75	80	65	80	88	84	84	92	92	87.5	87.5	87.5	75	87.5	100	77.5	77.5	77.5	100	80	65	65	65	65	15	NA	10	5	10	25	NA	25	0	25	0	NA	100	0	66.67	30	NA	40	20	20	60	NA	84	60	68	50	NA	87.5	37.5	62.5	0	NA	22.5	10	22.5	5	NA	15	10	15	35	50	NA	40	44.44	0	0	NA	75	0	33.33	100	NA	100	100	40	60	NA	65	70	68	80	NA	72	80	50	87.5	NA	87.5	87.5	77.5	55	NA	67.5	77.5	60	45	NA	50	55	20	NA	15	10	15	25	NA	0	0	0	33.33	NA	0	100	100	40	NA	25	25	10	60	NA	60	64	72	62.5	NA	62.5	62.5	62.5	67.5	NA	10	32.5	45	20	NA	10	15	15	80	NA	45	50	60	100	NA	0	0	50	0	NA	0	33.33	100	60	NA	50	35	75	56	NA	64	52	92	100	NA	62.5	62.5	62.5	100	NA	32.5	45	32.5	50	NA	50	40	60	10	NA	NA	5	11.11	0	NA	NA	0	25	66.67	NA	NA	66.67	100	0	NA	NA	0	0	88	NA	NA	88	80	37.5	NA	NA	50	50	NA	NA	NA	70	22.5	15	NA	NA	15	10	30	NA	NA	NA	NA	25	NA	NA	NA	NA	0	NA	NA	NA	NA	20	NA	NA	NA	NA	48	NA	NA	NA	NA	0	NA	NA	NA	NA	22.5	NA	NA	NA	NA	25	NA	NA	NA	NA	95	NA	88.89	85	NA	50	NA	100	75	NA	66.67	NA	100	100	NA	70	NA	40	35	NA	96	NA	76	76	NA	87.5	NA	50	50	NA	100	NA	100	75	NA	55	NA	70	55	NA

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Phase I: MTD of Bendamustine When Combined With Bortezomib and Pegylated Liposomal Doxorubicin.

In the first phase, MTD of bendamustine was determined in combination with bortezomib and pegylated liposomal doxorubicin to gain a better idea of safe dosing before proceeding with the second phase to assess efficacy. Assuming myelosuppression being a dose-limiting effect that could have been overcome with growth factor support, MTD of the combination with myeloid growth factor support was also tested. (NCT01177683)
Timeframe: From C1D1 up to a maximum of 7 months or until death

Intervention	mg/m^2 (Number)
Phase I Level 1:Bendamustine at 90 mg/m^2 With Bortezomib and Pegylated Liposomal Doxorubicin.	120
Phase I Level 2:Bendamustine at 120 mg/m^2 With Bortezomib and Pegylated Liposomal	120

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Phase I & Phase II : Toxicity of Treatment Regimen

Toxicity profile (for all patients) were presented by rate of overall toxicity and rates of grade 3 or 4 toxicities analyzed separately and combined. (NCT01177683)
Timeframe: From C1D1 until death or up to a maximum of 54 months

Intervention	Participants (Count of Participants)
	Number of patients had at least one adverse event of any grade	Number of patients had at least one grade 3 or greater adverse event	Number of patients had at least one grade 3 or greater treatment related adverse event	Number of patients having serious adverse event
Phase I Level 1 : Bendamustine at 90mg/m^2 With Bortezomib and Pegylated Liposomal Doxorubicin.	3	2	2	1
Phase I Level 2 : Bendamustine at 120mg/m^2 With Bortezomib and Pegylated Liposomal Doxorubicin.	3	3	3	1
Phase II : Bendamustine in Combination With Bortezomib and Pegylated Liposomal Doxorubicin.	24	19	14	8

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Phase II: Progression-free Survival (PFS)

"The time from the start of treatment of MM patients treated with bendamustine, bortezomib and pegylated liposomal doxorubicin. to disease progression or death (regardless of cause of death), whichever comes first. Censoring date will be the last disease evaluation date.Per modified International Myeloma Working Group criteria: Progressive disease (PD) is reported if any one of the following criteria is met:~Increase of 25% or more in serum or urine M-protein from baseline;Serum M-protein and/or the absolute increase must be ≥0.5 g/dL;Urine M-protein and/or absolute increase must be ≥200 mg/24 hours ; Development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas;Development of hyperc." (NCT01177683)
Timeframe: From C1D1 up to a maximum of 54 months until death

Intervention	months (Median)
Phase II : Bendamustine in Combination With Bortezomib and Pegylated Liposomal Doxorubicin.	18.96

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Phase II: Overall Survival

The time from the start of treatment to death from any cause with last date known alive as censoring date. (NCT01177683)
Timeframe: From C1D1 up to a maximum of 54 months or until death

Intervention	months (Median)
Phase II : Bendamustine in Combination With Bortezomib and Pegylated Liposomal Doxorubicin.	30.13

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Phase II: Duration of Survival

Duration of MM patients treated with bendamustine, bortezomib and pegylated liposomal doxorubicin. from first date of at least partial response to the time of progression or death due to disease progression as events, with disease progression and death due to disease progression as events and deaths due to causes other than progression as censored. Censoring date will be the last disease evaluation date or date of death due to other causes as appropriate. (NCT01177683)
Timeframe: From C1D1 up to a maximum of 52 months

Intervention	months (Median)
Phase II : Bendamustine in Combination With Bortezomib and Pegylated Liposomal Doxorubicin.	13.80

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Phase II : Time to Progression

"The time from the start of treatment (i.e., first dose) of MM patients treated with bendamustine, bortezomib and pegylated liposomal doxorubicin to disease progression, with disease progression and death due to disease progression as events and deaths due to causes other than progression as censored. Censoring date will be the last disease evaluation date for patient without progression/death or date of death due to other diseases for patients' deaths due to other causes.Per modified International Myeloma Working Group criteria: Progressive disease (PD) is reported if any one of the following criteria is met:~Increase of 25% or more in serum or urine M-protein from baseline;Serum M-protein and/or the absolute increase must be ≥0.5 g/dL;Urine M-protein and/or absolute increase must be ≥200 mg/24 hours ; Development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas;Development of hyperc." (NCT01177683)
Timeframe: From C1D1 up to a maximum of 54 months or until death

Intervention	months (Median)
Phase II : Bendamustine in Combination With Bortezomib and Pegylated Liposomal Doxorubicin.	20.53

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Toxicity

To evaluate the toxicity profile of this regimen. Adverse event counts by grade are presented. (NCT01186458)
Timeframe: 6 months

Intervention	number of adverse events (Number)
	Total Adverse Events	Grade 1 Adverse Events	Grade 2 Adverse Events	Grade 3 Adverse Events	Grade 4 Adverse Events	Grade 5 Adverse Events
Fludarabine, Velcade and Rituximab	122	77	35	9	1	0

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Quality-Adjusted Life Years (QALYs)

QALYs were estimated with a model beginning at initiation of first-line therapy by arm. A lifetime horizon, as well as subsequent lines of therapy, was examined using open-source Amua 0.3.0 software. Base case analysis was performed using 10,000 first-order Monte Carlo simulations. Conditional probabilities were extracted from Kaplan-Meier curves from pivotal clinical trials using WebPlotDigitizer. Costs were estimated from RED BOOK and DFCI charge reporting in US Dollars ($) after inflation adjustment to 2022 and 3% discounting, and QALYs effects were measured using EQ-5D data from Hatswell et al. (NCT01208662)
Timeframe: Maximum observation of survival for this study cohort was 129.4 months.

Intervention	years gained (Mean)
RVD Alone	5.67
RVD Plus ASCT	6.10

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Subsequent Therapy Rate

Subsequent therapy rate was the percentage of participants who discontinued treatment and initiated subsequent non-protocol therapy. (NCT01208662)
Timeframe: Up to 129 months

Intervention	Participants (Count of Participants)
RVD Alone	222
RVD Plus ASCT	192

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Median Treatment Duration

Treatment duration estimated using the KM method is defined as the time from registration (C1) to the time off treatment (event) or censored at date of last treatment. (NCT01208662)
Timeframe: Up to 134 months

Intervention	months (Median)
RVD Alone	28.2
RVD Plus ASCT	36.8

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Median Progression-Free Survival (PFS)

PFS was estimated using the Kaplan-Meier (KM) method and defined as time from randomization to the earlier of disease progression (PD) as determined by central review or death from any cause (events). Patients who started non-protocol therapy (NPT) were censored at the date of NPT initiation if available or date treatment ended if date of NPT was missing. Deaths occurring beyond 1 year from the date last known progression-free are not counted as events and censored at date of last disease evaluation. Patients who had not started NPT, progressed, or died were censored at the date of last disease evaluation. PD was based upon the International Myeloma Working Group (IMWG) uniform response criteria. [Kumar S, et al Lancet Oncol 2016;17(8):e328-e346]. (NCT01208662)
Timeframe: On treatment, disease was assessed every cycle up to maintenance and every 3 cycles on maintenance. In long-term follow-up, disease was assessed every 2 months until PD or death. Median (maximum) PFS follow-up was 70 and 129 months.

Intervention	months (Median)
RVD Alone	46.2
RVD Plus ASCT	67.5

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Median Maintenance Treatment Duration

Maintenance treatment duration estimated using the KM method is defined as the time from start of maintenance to the time off maintenance (event) or censored at date of last maintenance treatment. (NCT01208662)
Timeframe: Up to 128 months

Intervention	months (Median)
RVD Alone	36.4
RVD Plus ASCT	41.5

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Median Event Free Survival (EFS)

EFS was estimated using the KM method and defined as the time from randomization to the earliest of IMWG disease progression, death, or initiation of non-protocol therapy (events); patients were censored date of last disease evaluation. (NCT01208662)
Timeframe: Assessed up to approximately 130 months.

Intervention	months (Median)
RVD Alone	32.0
RVD Plus ASCT	47.3

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Change From Baseline on the European Organization for Research and Treatment of Cancer Quality-of-Life Questionnaire Core 30 (EORTC QLQ-C30): Global Health Status/Quality of Life (QoL) Sub-scale

The EORTC QLQ-C30 assessment consists of 30 questions that are used to construct 15 distinct sub-scales (five function scales, nine symptom scales, and a global health status/QoL scale). The global health status/QoL scale is comprised of two questions each with a range of 6 (1=Very Poor to 7=Excellent). Scores on all sub-scales range from 0 to 100 after linear transformation of the raw scores, with higher scores representing better global health status and quality of life. (NCT01208662)
Timeframe: Cycle 1 (Baseline), Cycle 2, Pre-Mobilization, Cycle 5 Arm A / Post Auto-HSCT Arm B, Cycle 8 Arm A /Cycle 5 Arm B, Maintenance Day 1, 2 years from baseline, 3 years from baseline

Intervention	units on a scale (Mean)
	Cycle 2	Pre-Mobilization	Cycle 5 Arm A / Post Auto-HSCT Arm B	Cycle 8 Arm A /Cycle 5 Arm B	Maintenance Day 1	2 years from baseline	3 years from baseline
RVD Alone	0.1	0.4	3.0	1.2	5.3	5.1	3.5
RVD Plus ASCT	4.3	4.4	-11.1	8.3	9.9	11.1	12.7

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Change From Baseline on the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity (FACT/GOG-NTX)

The FACT/GOG-NTX assessment consists of 11 questions that are all used to construct 1 subscale to summarize symptoms of peripheral neuropathy, including sensory, motor, and auditory problems and cold sensitivity. (https://www.facit.org/measures/FACT-GOG-NTX) Each question has 4 possible responses from 0 (Not at all) to 4 (Very Much) which are reverse-scored and summed. This sum is then scaled by the number of questions answered by multiplying by 11 and then dividing by the number of questions that are non-blank, in order to keep all final scores proportional to one another even if some questions are left blank. The aggregate score ranges from 0 to 44, with higher scores indicating less neurotoxicity and lower scores indicating more neurotoxicity. Change from baseline is the difference (NCT01208662)
Timeframe: Cycle 1 (Baseline), Cycle 2, Pre-Mobilization, Cycle 5 Arm A / Post Auto-HSCT Arm B, Cycle 8 Arm A /Cycle 5 Arm B, Maintenance Day 1, 2 years from baseline, 3 years from baseline

Intervention	units on a scale (Mean)
	Cycle 2	Pre-Mobilization	Cycle 5 Arm A / Post Auto-HSCT Arm B	Cycle 8 Arm A /Cycle 5 Arm B	Maintenance Day 1	2 years from baseline	3 years from baseline
RVD Alone	-1.8	-3.9	-4.4	-4.7	-3.7	-4.9	-4.6
RVD Plus ASCT	-1.3	-3.5	-4.4	-2.5	-2.3	-2.6	-3.2

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Partial Response (PR) Rate

The PR rate is the percentage of participants achieving PR or better on treatment and was evaluated based on the IMWG criteria. PR was defined as > 50% reduction of serum M-protein and reduction in 24-h urinary M-protein by > 90% or to < 200mg per 24 hours. If the serum and urine M-protein are unmeasurable, a > 50% decrease in the difference between involved and uninvolved free light chain levels is required in place of the M-protein criteria. If serum and urine M-protein are unmeasurable, and serum free light assay is also unmeasurable, >50% reduction in plasma cells is required in place of M-protein, provided baseline bone marrow plasma cell percentage was > 30%. In addition to the above listed criteria, if present at baseline, a > 50% reduction in the size of soft tissue plasmacytomas was also required. Exact (Clopper-Pearson) confidence limits of 98.2857% represents Bonferroni adjustment for 7 tests (1-0.05/7) per statistical analysis plan for key secondary outcomes. (NCT01208662)
Timeframe: Disease was assessed every cycle up to maintenance and every 3 cycles on maintenance. Median treatment duration (months) from randomization 28.2 (RVD Alone) and 36.1 (RVD plus ASCT). Maximum treatment duration was 133.5 months in this study cohort.

Intervention	percentage of participants (Number)
RVD Alone	95
RVD Plus ASCT	97.5

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Median Duration of Response: Partial Response (DOR PR)

DOR PR was estimated using the KM method and defined as the time from documented best response as CR to documented disease progression per IMWG criteria. Patients who have not progressed or died were censored at the date last known progression-free. (NCT01208662)
Timeframe: On treatment, disease was assessed every cycle up to maintenance and every 3 cycles on maintenance. In long-term follow-up, disease was assessed every 2 months until PD or death. Median (maximum) DOR PR follow-up was 62.9 and 122.9 months.

Intervention	months (Median)
RVD Alone	38.9
RVD Plus ASCT	56.4

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Very Good Partial Response (VGPR) Rate

The VGPR rate is the percentage of participants achieving VGPR or better on treatment and was evaluated based on IMWG criteria. VGPR was defined as serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein plus urine M-protein level <100mg per 24 hours. (NCT01208662)
Timeframe: Disease was assessed every cycle up to maintenance and every 3 cycles on maintenance. Median treatment duration (months) from randomization 28.2 (RVD Alone) and 36.1 (RVD plus ASCT). Maximum treatment duration was 134 months in this study cohort.

Intervention	percentage of patients (Number)
RVD Alone	79.6
RVD Plus ASCT	82.7

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Grade 3 or Higher Treatment-Related Non-Hematologic Adverse Event (AE) Rate

Safety was evaluated throughout trial treatment, including ASCT, and through 30 days after receipt of the last dose of a trial drug. Treatment attribution and grade were based on the NCI CTCAE v4. The Grade 3 or Higher Treatment-Related Non-Hematologic AE Rate is percentage of participants who experienced any grade 3-5 treatment-related (possible, probable or definite attribution) non-hematologic adverse event based on CTCAEv4 as reported on case report forms. The difference in the rate of all grade 3 or higher toxicities was compared between the two groups using Fisher's exact test. (NCT01208662)
Timeframe: AEs was assessed every cycle on treatment. Median treatment duration (months) from randomization 28.2 (RVD Alone) and 36.1 (RVD plus ASCT). Maximum treatment duration was 133.5 months in this study cohort.

Intervention	percentage of participants (Number)
RVD Alone	78.2
RVD Plus ASCT	94.2

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Complete Response (CR) Rate

The CR rate is the percentage of participants achieving CR or better on treatment and was evaluated based on IMWG criteria. CR was defined as the negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and <5% plasma cells in bone marrow. Confirmation with repeat bone marrow biopsy was not needed. (NCT01208662)
Timeframe: Disease was assessed every cycle up to maintenance and every 3 cycles on maintenance. Median treatment duration (months) from randomization 28.2 (RVD Alone) and 36.1 (RVD plus ASCT). Maximum treatment duration was 134 months in this study cohort.

Intervention	percentage of patients (Number)
RVD Alone	42.0
RVD Plus ASCT	46.8

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5-Year Time to Progression (TTP)

TTP was estimated using the KM method and defined as time from randomization to time of documented IMWG disease progression or censoring time (time of last disease evaluation for those alive, time to death among those who died). Patients initiating non-protocol therapy prior to progression or death were censored at the date of non-protocol therapy in the TTP analysis. The 5-year TTP endpoint is a probability. (NCT01208662)
Timeframe: On treatment, disease was assessed every cycle up to maintenance and every 3 cycles on maintenance. In long-term follow-up, disease was assessed every 2 months until PD or death. Median TTP follow-up was 70 months. The probability estimate is at 5 years.

Intervention	percent probability (Number)
RVD Alone	41.6
RVD Plus ASCT	58.4

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5-Year Overall Survival (OS)

OS was estimated using the KM method and defined as time from randomization to death due to any cause. Patients alive were censored at date last known alive. The 5-year OS endpoint is a probability. (NCT01208662)
Timeframe: In long-term follow-up, survival follow-up every 2 months until death. Median (maximum) OS follow-up was 76 and 129 months.The probability estimate is at 5 years.

Intervention	percent probability (Number)
RVD Alone	79.2
RVD Plus ASCT	80.7

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5-year Cumulative Incidence of Second Primary Malignancy (SPM)

Second primary malignancy (SPM) is defined as the development of another new, unrelated cancer, regardless of treatment for previous malignancy attribution. The cumulative incidence of SPMs was estimated with death as a competing risk. SPMs were collected using an SAE form or MEDWATCH 3500A form, with intensity determined by using the NCI CTCAE version 4 as a guideline. (NCT01208662)
Timeframe: 5 years

Intervention	percentage of patients (Number)
RVD Alone	4.9
RVD Plus ASCT	6.5

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Next Generation Sequencing (NGS) Minimal Residual Disease Negative (MRD-) Rate at Maintenance Start

Bone marrow aspirate samples were obtained from patients prior to the start of lenalidomide maintenance. NGS MRD- rate is the percentage of evaluable participants with MRD level of <1 x 10-5 (indicating detection of 1 malignant plasma cell in 100,000 bone marrow cells) using the validated, US Food and Drug Administration approved clonoSEQ® NGS platform (Adaptive Biotechnologies) with a minimum sensitivity of 1 x 10-5. (NCT01208662)
Timeframe: Maintenance treatment occurred after induction, up to 11.5 months.

Intervention	percentage of participants (Number)
RVD Alone	39.8
RVD Plus ASCT	54.4

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Find Maximum Tolerated Dose (MTD) of Bortezomib in Combination With Pomalidomide and Dexamethasone Out to 2.5 Years, by Count of Patients With Dose Limiting Toxicities.

MTD is defined as the dose level below the lowest dose that induces dose-limiting toxicity in at least one-third of patients (at least 2 of a maximum of 6 new patients). (NCT01212952)
Timeframe: 2.5 years

Intervention	Participants (Count of Participants)
Phase 1 Dose Level 1	0
Phase 1 Dose Level 2	1

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Number of Participants With Adverse Events

Reported in Adverse Events section of the results (NCT01212952)
Timeframe: 2.5 years

Intervention	Participants (Count of Participants)
Phase I - Dose Level 1	3
Phase I - Dose Level 2	6
Phase II	41

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Progression Free Survival

The progression-free survival (PFS) time is defined as the time from registration to progression or death due to any cause. The distribution of progression-free survival will be estimated using the method of Kaplan-Meier. PD: Increase of > 25% from lowest response value in any one or more of the following: Serum M-component and/or (the absolute increase must be > 0.5 g/dL), Urine M-component and/or (the absolute increase must be > 200 mg/24 h) (NCT01212952)
Timeframe: 2.5 years

Intervention	months (Median)
Phase I - Dose Level 1	13.9
Phase I - Dose Level 2	18.1
Phase II	10.7

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The Percent of Patients With Minimal Residual Disease (MRD) Status Changing to Negative at Day 100 (Post-AHCT), Among Patients With MRD Positive at the End of Induction (EOI).

Patients were treated with induction therapy (VRD) followed by autologous hematopoietic cell transplant (AHCT). MRD status of a patient with at least partial response was evaluated at the end of induction (EOI) and day 100 (post-AHCT). MRD of a patient is measured by seven-color flow cytometry. (NCT01215344)
Timeframe: 6-months post ASCT

Intervention	percentage of participants (Number)
VELCADE, Lenalidomide, Dexamethasone (VRD)	30

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Progression Free Survival by MRD Status at Day 100.

Intervention	years (Median)
MRD Negative at Day 100	2.64
MRD Status Positive at Day 100 (Post-AHCT)	NA

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Functional Assessment of Cancer Therapy - Lymphoma (FACT-Lym) Subscale Score at End of Induction Treatment

The Functional Assessment of Cancer Therapy - Lymphoma (FACT-Lym) is a 15-item questionnaire that evaluates disease-related symptoms and concerns specific to lymphoma with a scale of 0-4. The FACT-Lym subscale score ranges between 0 and 60. The higher the score, the better the quality of life. (NCT01216683)
Timeframe: Assessed at cycle 6, approximately 6 months

Intervention	score on a scale (Mean)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	48.9
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	48.4
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	47.2

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Functional Assessment of Cancer Therapy - General (FACT-G) Total Score at Baseline

The Functional Assessment of Cancer Therapy - General (FACT-G) is a 27-item questionnaire that has four areas of measurements (physical well-being, social/family well-being, emotional well-being and functional well-being) with a scale of 0-4. The FACT-G total score ranges between 0 and 108. The higher the score, the better the quality of life. (NCT01216683)
Timeframe: Assessed at baseline

Intervention	score on a scale (Mean)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	83.9
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	84.7
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	86.0

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Complete Remission (CR) Rate

"Complete remission is defined as complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present prior to therapy.~This analysis was conducted among 250 evaluable patients with Cumulative Illness Rating Scale (CIRS) data available. The proportion of patients with complete remission was compared between patients with CIRS <10 and patients with CIRS >=10. Higher CIRS scores indicate higher severity with max score of 56 points." (NCT01216683)
Timeframe: Assessed every 4 weeks during induction treatment and every 8 weeks during continuation treatment, up to 2 years

Intervention	proportion of participants (Number)
CIRS <10	0.70
CIRS >=10	0.70

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Complete Remission (CR) Rate

"Complete remission is defined as complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present prior to therapy.~This analysis was conducted among 222 evaluable patients. The proportion of patients with complete remission was compared between patients with Follicular Lymphoma International Prognostic Index (FLIPI) of 3-5 and patients with FLIPI of 0-2/unknown.~The FLIPI was developed in order to predict prognosis of patients with newly diagnosed follicular lymphoma (FL). The five FLIPI risk factors were: age > 60 years, Ann Arbor stage III-IV, hemoglobin level < 12 gm/dL, >4 nodal areas, and serum LDH level above normal. The FLIPI score was calculated by summing the number of risk factors. The higher the FLIPI score, the worse the prognosis." (NCT01216683)
Timeframe: Assessed every 4 weeks during induction treatment and every 8 weeks during continuation treatment, up to 2 years

Intervention	proportion of participants (Number)
FLIPI 0-2/Unknown	0.71
FLIPI 3-5	0.64

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Complete Remission (CR) Rate

"Complete remission is defined as complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present prior to therapy.~This analysis was conducted among 222 evaluable patients for the primary analysis. The purpose of this analysis is to compare the complete remission rate of rituximab + bendamustine vs. bortezomib + rituximab + bendamustine as induction therapy, therefore, the proportion of patients with complete remission was compared between Arm B (bortezomib + rituximab + bendamustine) and Arms A and C combined (rituximab + bendamustine)." (NCT01216683)
Timeframe: Assessed every 4 weeks during induction treatment and every 8 weeks during continuation treatment, up to 2 years

Intervention	proportion of participants (Number)
Arm A and Arm C (Induction With Bendamustine + Rituximab)	0.62
Arm B (Induction With Bendamustine + Rituximab + Bortezomib)	0.75

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5-year Overall Survival Rate

Overall survival is defined as the time from randomization to death or date last known alive. 5-year overall survival rate is the proportion of patients who were alive at 5 years estimated using the method of Kaplan-Meier. (NCT01216683)
Timeframe: Assessed every cycle during treatment and every 6 months between 2 and 5 years from study entry

Intervention	proportion of participants (Number)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	0.87
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	0.86
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	0.83

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5-year Overall Survival Rate

"Overall survival is defined as the time from randomization to death or date last known alive. 5-year overall survival rate is the proportion of patients who were alive at 5 years estimated using the method of Kaplan-Meier.~The FLIPI was developed in order to predict prognosis of patients with newly diagnosed follicular lymphoma (FL). The five FLIPI risk factors were: age > 60 years, Ann Arbor stage III-IV, hemoglobin level < 12 gm/dL, >4 nodal areas, and serum LDH level above normal. The FLIPI score was calculated by summing the number of risk factors. The higher the FLIPI score, the worse the prognosis." (NCT01216683)
Timeframe: Assessed every cycle during treatment and every 6 months between 2 and 5 years from study entry

Intervention	proportion of participants (Number)
FLIPI 0-2/Unknown	0.90
FLIPI 3-5	0.81

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5-year Overall Survival Rate

"Overall survival is defined as the time from randomization to death or date last known alive. 5-year overall survival rate is the proportion of patients who were alive at 5 years estimated using the method of Kaplan-Meier.~The 5-year overall survival rate is reported by Cumulative Illness Rating Scale (CIRS) score (<10 vs. >=10). Higher CIRS scores indicate higher severity with max score of 56 points." (NCT01216683)
Timeframe: Assessed every cycle during treatment and every 6 months between 2 and 5 years from study entry

Intervention	proportion of participants (Number)
CIRS <10	0.87
CIRS >=10	0.80

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3-year Progression-free Survival Rate

"Progression-free survival is defined as the time from registration of induction treatment to progression, relapse or death, whichever occurs first. Patients alive without documented progression are censored at last disease assessment. 3-year progression-free survival rate is the proportion of patients who were progression-free and alive at 3 years estimated using the method of Kaplan-Meier.~Progression/relapse is defined as appearance of any new lesion more than 1.5 cm in any axis during or at the end of therapy, >=50% increase from nadir in the SPD of any previously involved nodes or extranodal masses or the size of other lesions, or >=50% increase in the longest diameter of any single previously identified node or extranodal mass more than 1 cm in its short axis.~The 3-year progression-free survival rate is reported by Cumulative Illness Rating Scale (CIRS) score (<10 vs. >=10). Higher CIRS scores indicate higher severity with max score of 56 points." (NCT01216683)
Timeframe: Assessed every cycle during treatment and every 6 months between 2 and 5 years from study entry

Intervention	proportion of participants (Number)
CIRS <10	0.83
CIRS >=10	0.68

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Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-Fatigue) Subscale Score at Mid-induction Treatment

"The Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-Fatigue) is comprised of 13 items that assess fatigue and its impact with a scale of 0-4. The FACIT-Fatigue subscale score ranges between 0 and 52. The higher the score, the better the quality of life.~FACIT-Fatigue subscale score at cycle 3 is considered as mid-treatment score. If FACIT-Fatigue subscale score at cycle 3 is not available, the score at cycle 4 will be used as the mid-treatment score." (NCT01216683)
Timeframe: Assessed at cycle 3 or cycle 4, approximately 3 or 4 months

Intervention	score on a scale (Mean)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	39.2
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	34.5
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	36.3

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3-year Progression-free Survival Rate

"Progression-free survival is defined as the time from registration of induction treatment to progression, relapse or death, whichever occurs first. Patients alive without documented progression are censored at last disease assessment. 3-year progression-free survival rate is the proportion of patients who were progression-free and alive at 3 years estimated using the method of Kaplan-Meier.~Progression/relapse is defined as appearance of any new lesion more than 1.5 cm in any axis during or at the end of therapy, >=50% increase from nadir in the SPD of any previously involved nodes or extranodal masses or the size of other lesions, or >=50% increase in the longest diameter of any single previously identified node or extranodal mass more than 1 cm in its short axis." (NCT01216683)
Timeframe: Assessed every cycle during treatment and every 6 months between 2 and 5 years from study entry

Intervention	proportion of participants (Number)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	0.77
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	0.82
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	0.76

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1-year Post-induction Disease-free Survival (DFS) Rate

"1-year post induction disease-free survival rate is defined as the proportion of patients achieving complete remission during induction treatment and are alive and maintaining complete remission at 1 year after induction completion.~The purpose of this analysis is to compare the 1-year post-induction disease-free survival (DFS) rate with rituximab plus lenalidomide to rituximab alone as continuation therapy following induction treatment of bendamustine+rituximab, therefore, patients with induction treatment of bendamustine + rituximab + bortezomib were not included in this analysis." (NCT01216683)
Timeframe: Assessed at 1 year post-induction, approximately 1.5 years

Intervention	proportion of participants (Number)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	0.85
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	0.67

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1-year Disease-free Survival (DFS) Rate

Intervention	proportion of participants (Number)
CIRS <10	0.62
CIRS >=10	0.65

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1-year Disease-free Survival (DFS) Rate

"1-year post induction disease-free survival rate is defined as the proportion of patients achieving complete remission during induction treatment and are alive and maintaining complete remission at 1 year after induction completion.~This analysis was conducted among 203 evaluable patients in the continuation treatment portion of the study. The 1-year post induction disease-free survival rate was compared between patients with FLIPI of 3-5 and patients with FLIPI of 0-2/unknown.~The FLIPI was developed in order to predict prognosis of patients with newly diagnosed follicular lymphoma (FL). The five FLIPI risk factors were: age > 60 years, Ann Arbor stage III-IV, hemoglobin level < 12 gm/dL, >4 nodal areas, and serum LDH level above normal. The FLIPI score was calculated by summing the number of risk factors. The higher the FLIPI score, the worse the prognosis." (NCT01216683)
Timeframe: Assessed at 1 year post-induction, approximately 1.5 years

Intervention	proportion of participants (Number)
FLIPI 0-2/Unknown	0.84
FLIPI 3-5	0.74

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Proportion of Patients With Grade 3 or Higher Peripheral Neuropathy

Peripheral neuropathy was assessed using NCI Common Terminology Criteria for Adverse Events (CTCAE) version 4.0. Proportion of patients with grade 3 or higher peripheral neuropathy was compared between patients with subcutaneous bortezomib and patients with intravenous bortezomib. (NCT01216683)
Timeframe: Assessed every cycle during treatment and for 30 days after discontinuation of treatment, up to 15 years

Intervention	proportion of participants (Number)
Subcutaneous Bortezomib	0.06
Intravenous Bortezomib	0.12

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Progression-free Survival

"Progression-free survival is defined as the time from registration of induction treatment to progression, relapse or death, whichever occurs first. Patients alive without documented progression are censored at last disease assessment. Progression/relapse is defined as appearance of any new lesion more than 1.5 cm in any axis during or at the end of therapy, >=50% increase from nadir in the SPD of any previously involved nodes or extranodal masses or the size of other lesions, or >=50% increase in the longest diameter of any single previously identified node or extranodal mass more than 1 cm in its short axis.~The five FLIPI risk factors were: age > 60 years, Ann Arbor stage III-IV, hemoglobin level < 12 gm/dL, >4 nodal areas, and serum LDH level above normal. The FLIPI score was calculated by summing the number of risk factors. The higher the FLIPI score, the worse the prognosis." (NCT01216683)
Timeframe: Assessed every cycle during treatment and every 6 months between 2 and 5 years from study entry

Intervention	years (Median)
FLIPI 0-2/Unknown	6.1
FLIPI 3-5	6.2

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Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-Fatigue) Subscale Score at End of Induction Treatment

The Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-Fatigue) is comprised of 13 items that assess fatigue and its impact with a scale of 0-4. The FACIT-Fatigue subscale score ranges between 0 and 52. The higher the score, the better the quality of life. (NCT01216683)
Timeframe: Assessed at cycle 6, approximately 6 months

Intervention	score on a scale (Mean)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	39.9
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	39.1
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	36.3

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Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-Fatigue) Subscale Score at Baseline

Intervention	score on a scale (Mean)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	38.6
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	37.9
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	38.1

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Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - Neurotoxicity (FACT-GOG-NTX) Subscale Score at the End of Induction Treatment

The Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - Neurotoxicity (FACT-GOG-NTX) subscale is comprised of 11 items that assess neurotoxicity with a scale of 0-4. The FACT-GOG-NTX subscale score ranges between 0 and 44. The higher the score, the better the quality of life. (NCT01216683)
Timeframe: Assessed at end of induction treatment (cycle 6), approximately 6 months

Intervention	score on a scale (Mean)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	39.8
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	36.1
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	39.0

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Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - Neurotoxicity (FACT-GOG-NTX) Subscale Score at Mid-induction Treatment

Intervention	score on a scale (Mean)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	40.0
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	38.6
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	39.1

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Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - Neurotoxicity (FACT-GOG-NTX) Subscale Score at Baseline

Intervention	score on a scale (Mean)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	39.9
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	38.7
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	38.8

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Functional Assessment of Cancer Therapy - Lymphoma (FACT-Lym) Subscale Score at Mid-induction Treatment

"The Functional Assessment of Cancer Therapy - Lymphoma (FACT-Lym) is a 15-item questionnaire that evaluates disease-related symptoms and concerns specific to lymphoma with a scale of 0-4. The FACT-Lym subscale score ranges between 0 and 60. The higher the score, the better the quality of life.~FACT-Lym subscale score at cycle 3 is considered as mid-treatment score. If FACT-Lym subscale score at cycle 3 is not available, the score at cycle 4 will be used as the mid-treatment score." (NCT01216683)
Timeframe: Assessed at cycle 3 or cycle 4, approximately 3 or 4 months

Intervention	score on a scale (Mean)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	47.9
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	46.8
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	46.5

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Functional Assessment of Cancer Therapy - Lymphoma (FACT-Lym) Subscale Score at Baseline

Intervention	score on a scale (Mean)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	43.8
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	44.3
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	44.9

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Functional Assessment of Cancer Therapy - General (FACT-G) Total Score at Mid-treatment

"The Functional Assessment of Cancer Therapy - General (FACT-G) is a 27-item questionnaire that has four areas of measurements (physical well-being, social/family well-being, emotional well-being and functional well-being) with a scale of 0-4. The FACT-G total score ranges between 0 and 108. The higher the score, the better the quality of life.~FACT-G total score at cycle 3 is considered as mid-treatment score. If FACT-G total score at cycle 3 is not available, the score at cycle 4 will be used as the mid-treatment score." (NCT01216683)
Timeframe: Assessed at cycle 3 or cycle 4, approximately 3 or 4 months

Intervention	score on a scale (Mean)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	85.5
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	84.2
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	85.2

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Functional Assessment of Cancer Therapy - General (FACT-G) Total Score at End of Induction Treatment

Intervention	score on a scale (Mean)
Arm A Then Arm D (Induction With Bendamustine + Rituximab; Continuation With Rituximab)	86.0
Arm B Then Arm E (Induction With Bendamustine + Rituximab + Bortezomib; Continuation With Rituximab)	86.5
Arm C Then Arm F (Induction With Bendamustine+Rituximab; Continuation With Lenalidomide + Rituximab)	84.9

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Toxicity Assessment

Assessment of the toxicities resulting from administration of combinations of thalidomide, bortezomib and melphalan (NCT01242267)
Timeframe: Patients will be hospitalized or in the outpatient transplant facility until engraftment and resolution of serious adverse events, a median of 16 (range, 11-24) days

Intervention	Serious Adverse Events (Number)
Phase I - Thalidomide Dose Level 600 mg	1
Phase I - Thalidomide Dose Level 800 mg	0
Phase I - Thalidomide Dose Level 1000 mg	0
Phase 2	3

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Maximum Tolerated Dose of Thalidomide

Maximum tolerated dose of thalidomide used in conjunction with dose-intense melphalan, bortezomib and autologous (syngeneic) HSC support in the salvage therapy of patients who failed a prior treatment with dose-intense melphalan (NCT01242267)
Timeframe: Dose escalation will be based on the assessment of tolerability determined after the last patient of each cohort reaches day +21.

Intervention	mg (Number)
Phase 1	1000
Phase 2	1000

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Treatment Free Interval/PFS

The treatment-free interval after treatment with the combination of thalidomide, bortezomib and melphalan (NCT01242267)
Timeframe: PFS was defined as the time from ASCT to disease progression or death from any cause, an average of 9 months

Intervention	months (Median)
Phase 1/Phase 2	9.3

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Complete Response (CR) and Very Good Partial Response (VgPR) Rate

The complete response (CR) and very good partial response (VgPR) rate in patients undergoing ASCT using thalidomide, bortezomib and melphalan (NCT01242267)
Timeframe: Assessments will be made from Day +28 after transplantation for 3 months and then at 3 month intervals until demonstration of disease progression and initiation of further therapy, an average of 9 months

Intervention	Participants (Count of Participants)
Phase I - Thalidomide Dose Level 600 mg	0
Phase I - Thalidomide Dose Level 800 mg	3
Phase I - Thalidomide Dose Level 1000 mg	1
Phase 2	13

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Two-year Overall Survival

Assessed by Kaplan-Meier survival analysis. 95% confidence intervals will be calculated using Greenwood's formula. (NCT01267812)
Timeframe: Participants were followed up to 5 years after initial treatment and Kaplan-Meier survival analysis was used to generate the two-year overall survival estimate presented.

Intervention	percentage of participants (Number)
Treatment (Bortezomib and Rituximab)	95

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Grade 3 or 4 Toxicities of Bortezomib and Rituximab Treatment

Observed toxicities will be summarized in terms of type, severity (graded by NCI CTCAE version 4.0) and attribution. (NCT01267812)
Timeframe: Participants were followed up to 5 years after initial treatment.

Intervention	Participants (Count of Participants)
	Neutropenia	Lymphopenia	Pneumonia	Anemia	Lung infection	Skin infection	Wound infection	Hypertension	Thrombocytopenia
Treatment (Bortezomib and Rituximab)	17	8	2	2	2	1	1	1	1

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Two-year Disease-free Survival

Intervention	percentage of participants (Number)
Treatment (Bortezomib and Rituximab)	90

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Overall Response Rate

The primary objective of this study is to determine whether Velcade in combination with temsirolimus provides benefit to subjects with relapsed or refractory B-cell non-Hodgkin lymphoma as assessed by overall response rate (ORR) to therapy. ORR is the sum of patients with a Complete Response and Partial Response to therapy. Per Response Evaluation Criteria in Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete REsponse (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT01281917)
Timeframe: Up to 60 months

Intervention	Percentage of participants (Median)
Velcade Plus Temsirolimus	31

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Overall Survival

Length of time from enrollment until death. (NCT01281917)
Timeframe: Up to 60 months

Intervention	Months (Median)
Velcade Plus Temsirolimus	14.1

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Progression Free Survival

Intervention	Months (Median)
Velcade Plus Temsirolimus	4.7

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Duration of Response

Duration of Response is how long a response to therapy is held before a subject has progressive disease. (NCT01281917)
Timeframe: Up to 60 months

Intervention	months (Median)
Velcade Plus Temsirolimus	7

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Complete Response Rate

The complete response rate (CR) to therapy as defined by International Lymphoma Response Criteria. (NCT01281917)
Timeframe: Up to 60 months

Intervention	Participants (Count of Participants)
Velcade Plus Temsirolimus	3

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Overall Survival

Overall survival defined as time from first treatment of MMY, i.e. day of first dose of induction therapy for MMY to date of death (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	Months (Median)
Bortezomib	49.90
Non-treated Control	47.26

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Tumor Response: Percentage of Participants With Very Good Partial Response (VGPR) or Stringent Complete Response (sCR) or Complete Response (CR) Based on International Myeloma Working Group (IMWG) Response Criteria

Tumor response was assessed as VGPR based on IMWG response criteria if, a) serum/urine M protein detectable by immunofixation but not on electrophoresis or; b) greater than or equal to 90% reduction in serum M protein plus urine M protein level less than 100 milligram/24 hour. CR=normal free light chain (FLC) ratio and absence of phenotypically aberrant plasma cells (PC) in bone marrow with a minimum of 3000 total PC analyzed by multiparametric flow cytometry; Complete response (CR) negative immunofixation on the serum and urine and, disappearance of any soft tissue plasmocytomas and <5% plasma cells in bone marrow. (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	Percentage of participants (Number)
Bortezomib	82.6
Non-treated Control	72.3

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Tumor Response: Percentage of Participants With Stable Disease (SD) or Progressive Disease (PD) Based on International Myeloma Working Group (IMWG) Response Criteria

Tumor response was assessed as SD based on IMWG response criteria as not meeting criteria for CR, VGPR, PR, or progressive disease; PD as Increase of >=25% from lowest response level in any one or more of the following: serum M protein (absolute increase >=0.5 g/dl)c or urine M protein (absolute increase >=200 mg/24 h); or serum/urine M protein unmeasurable: difference between involved and uninvolved free light chain (FLC) levels; absolute increase >10 mg/dL; or % bone marrow plasma cells: absolute value >=10% or definite development of new bone lesions or soft tissue plasmocytomas or definite increase in the size of existing bone lesions or soft tissue plasmocytomas; or development of hypercalcemia attributed solely to the plasma cell proliferative disorder. (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	Percentage of participants (Number)
Bortezomib	6.5
Non-treated Control	19.1

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Number of Patients With Skeletal Events

Number of patients with skeletal-related events (i.e. pathological fracture (vertebral, non-vertebral, combined), radiotherapy, spinal cord compression, orthopaedic surgery, hypercalcaemia) occurring over 24 months study period (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	patients (Number)
Bortezomib	0
Non-treated Control	0

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Change From Baseline in Bone Mineral Density (BMD) in the Femur at End of Treatment

Change from baseline in bone mineral density (BMD) will be assessed by dual energy x-ray absorptiometry scans at baseline and the end of treatment EOT visit (NCT01286077)
Timeframe: at screening (i.e. between 14 and 1 days prior to start of treatment) and at end of treatment (EOT), i.e. 24 weeks after randomization or until start of alternative MMY therapy, if earlier

Intervention	g/mm2 (Mean)
	Femur neck	Femur total
Bortezomib	0.0053	0.0071
Non-treated Control	0.0044	0.0138

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Change From Baseline in Biochemical Bone Markers: Dickkopf Homolog 1 (DKK-1)

Bone markers Dickkopf homolog 1 (DKK-1) was measured on serum samples. (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	Picomole per liter (Mean)
Bortezomib	-39.31
Non-treated Control	-25.15

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Change From Baseline in Bone Mineral Density (BMD) in the Spine at End of Treatment (EOT)

Change from baseline in bone mineral density (BMD) will be assessed by dual energy x-ray absorptiometry scans at baseline and the EOT visit (NCT01286077)
Timeframe: at screening (i.e. between 14 and 1 days prior to start of treatment) and at end of treatment (EOT), i.e. 24 weeks after randomization or until start of alternative MMY therapy, if earlier

Intervention	g/mm2 (Mean)
Bortezomib	0.0214
Non-treated Control	0.0167

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Change From Baseline in Biochemical Bone Markers: Carboxyterminal Collagen Crosslinks (CTX-I)

Change from Baseline in Biochemical Bone Markers: CTX-I was assessed (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	Nanogram per liter (Mean)
Bortezomib	-66.50
Non-treated Control	-77.68

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Appearance of New Bone Lesions Compared to Baseline

Appearance of new bone lesions assessed by skeletal survey compared to baseline (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	subjects (Number)
Bortezomib	0
Non-treated Control	0

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Change From Baseline in Quality of Life Assessed by Euro Quality of Life (EQ-5D)

Subjects were asked to rate their general state of health on a Visual analog scale (in millimeter [mm]) ranging from 0 (worst state of health) to 100 (best conceivable state of health) mm. (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	millimeter (mm) (Mean)
Bortezomib	-0.3
Non-treated Control	2.9

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Change From Baseline in Spine T-score

T score is used to calculate bone mineral density (calcium and other types of minerals) in an area of the bone. T score is the number of standard deviations above or below the mean for a healthy 30 year old adult of the same sex and ethnicity as a participant. This score is calculated from participant's age, gender and race and skeletal site. T score has a mean of '50' and a standard deviation of '10'. T score lower than its mean indicate low bone mineral density. (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	T score (Mean)
Bortezomib	1.2028
Non-treated Control	1.1811

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Karnofsky Performance Status

"The Karnofsky performance status is a way to quantify cancer patients' general well-being and activities of daily life and runs from 100 to 0, where 100 is perfect health and 0 is death." (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	Units on a scale (Mean)
	Screening	Follow-up
Bortezomib	92.4	0.0
Non-treated Control	91.7	0.4

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Tumor Response: Percentage of Participants With Partial Response (PR) Based on International Myeloma Working Group (IMWG) Response Criteria

Tumor response was assessed as PR based on IMWG response criteria as >=50% reduction of serum and reduction in 24-h urinary M protein by >=90% or to <200 mg/24 h; or serum/urine M protein unmeasurable:>=50% decrease in the difference between involved and uninvolved FLC levels; or serum/urine M protein and FLC assay unmeasurable: >=50% reduction in plasma cells provided baseline bone marrow plasma cell percentage was >=30%; or plus if present at baseline: >=50% reduction in size of soft tissue plasmocytomas. (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	Percentage of participants (Number)
Bortezomib	8.7
Non-treated Control	8.5

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Change From Baseline in Biochemical Bone Markers:Carboxyterminal Telopeptide of Type I Collagen (ICTP), Osteocalcin, Bone-specific Alkaline Phosphatase (BAP)

Bone markers (carboxyterminal telopeptide of type I collagen (ICTP), osteocalcin (Oc) and bone-specific alkaline phosphatase (BAP) was measured on serum samples. (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	Microgram per liter (Mean)
	ICTP (n= 44, 42)	Osteocalcin (44, 42)	BAP (42, 40)
Bortezomib	-4.11	20.15	-0.48
Non-treated Control	-3.51	14.59	-2.11

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Progression Free Survival

The Progression-Free Survival (PFS) was assessed as median number of months from baseline until the first documented sign of disease progression (increase in disease; radiographic, clinical, or both) or death due to any cause, whichever occurred earlier. (NCT01286077)
Timeframe: Baseline up to end of study (approximately 4 years 7 months)

Intervention	Months (Mean)
Bortezomib	39.56
Non-treated Control	31.66

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The Number of Patients Who Experienced Grade 3+ Hematologic and Non-hematologic Adverse Events at Least Possibly Related to Treatment

The number of patients who experienced grade 3+ hematologic and non-hematologic adverse events at least possibly related to treatment assessed according to National Cancer Institute Common Terminology Criteria for Adverse Events version 4.0 (NCT01286272)
Timeframe: From date of randomization until patient stops treatment for any reason, up to 484 days post-randomization

Intervention	Participants (Count of Participants)
	Hematologic	Non-Hematologic
Arm A (Ofatumumab, Bendamustine Hydrochloride)	45	17
Arm B (Ofatumumab, Bendamustine Hydrochloride, Bortezomib)	41	33

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Progression-free Survival (PFS)

Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. PFS rates (percentages) at 1, 2, ,3 and 4 years are defined as the percentage of patients who are alive and progression-free at the respective time points. The p-values of the log-rank test will be calculated to compare PFS between the two arms. (NCT01286272)
Timeframe: Up to 4 years

Intervention	percentage of patients (Number)
	PFS at 1 year	PFS at 2 years	PFS at 3 years	PFS at 4 years
Arm A (Ofatumumab, Bendamustine Hydrochloride)	93.8	80.3	65.9	57.3
Arm B (Ofatumumab, Bendamustine Hydrochloride, Bortezomib)	84.8	75.6	67.1	64.7

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Complete Response Rate

"A complete response was defined using International Harmonization Project Response Criteria as the complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present before therapy. If the bone marrow was involved by lymphoma before treatment, the infiltrate must have cleared on repeat bone marrow biopsy.~The complete response (CR) rate was calculated in newly diagnosed untreated follicular lymphoma patients receiving 6 cycles of ofatumumab-bendamustine (ARM A) and 6 cycles of ofatumumab, bortezomib, and bendamustine (ARM B).~The complete response rate was calculated as the number of patients with a complete response divided by the number of patients eligible for evaluation." (NCT01286272)
Timeframe: From date of randomization until patient stops treatment for any reason, up to 484 days post-randomization

Intervention	proportion of patients (Number)
Arm A (Ofatumumab, Bendamustine Hydrochloride)	.621
Arm B (Ofatumumab, Bendamustine Hydrochloride, Bortezomib)	.597

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Number of Subjects Who Achieved Complete Remission of Their Disease

Complete Remission (CR): A CR requires that the following be recorded concurrently: an absolute neutrophil count (segs and bands) > 1000/μL, no circulating blasts, platelets > 100,000/μL; adequate bone marrow cellularity with trilineage hematopoiesis, and < 5% marrow leukemia blast cells. All previous extramedullary manifestations of disease must be absent. If patients continue on with treatment, there can be no evidence of recurrence of ALL for at least 4 weeks. (NCT01312818)
Timeframe: Day 30

Intervention	participants (Number)
ALL Treated Patients	0

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Number of Subjects Experiencing Drug Related Adverse Events

To characterize the toxicities of bortezomib, vorinostat and dexamethasone when used in combination. Toxicity will be graded using the NCI's Common Terminology Criteria for Adverse Events (CTCAE 4.0). (NCT01312818)
Timeframe: Day 1 of Treatment to 30 Days Post Treatment

Intervention	participants (Number)
ALL Treated Patients	1

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Therapeutic Efficacy

Number of participants with an objective response of Partial Response (PR) or better according to European Society for Blood and Marrow Transplantation (EBMT) criteria within 180 days post Expanded Natural Killer Cell Infusion. The minimum criteria to meet the EBMT definition of PR or better included: >= 50% reduction in size of soft tissue plasmacytomas (if assessed); AND >= 50% reduction in plasma cells in bone marrow biopsy (if biopsy was performed and if >= 30% plasma cells at baseline); AND >=50% reduction in serum M protein and reduction in urine M protein >= 90% or to 200 mg/24hr OR >= 50% decrease in the difference between involved and uninvolved serum free light chain levels (if serum M protein < 1 g/dL, urine < 200 mg/24 hrs, and an involved serum free light chain level >= 10 mg/dL at baseline). (NCT01313897)
Timeframe: 180 days

Intervention	Participants (Count of Participants)
Velcade for Anti-MM Therapy	1

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The Cumulative Incidence of Chronic GVHD Requiring Systemic Immune Suppression up to 1 Year After Stem Cell Infusion

(NCT01323920)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Velcade/Tac/MTX	53

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The Non-relapse Mortality, Progression-free and Overall Survival up to 1 Year After Stem Cell Infusion

Progression free and overall survival by 1 year after stem cell infusion will be assessed using the method of Kaplan and Meier. Progression-free survival will be defined as the time from stem cell infusion to the time of disease progression or death from any cause. Overall survival will be defined as the time from stem cell infusion to the time to death from any cause. Patients will be censored at the time last documented alive. Cumulative incidence and Kaplan-Meier curves will be constructed as appropriate. Progression is defined per clinical presentation, not protocol specified, and vary per disease, e.g. blasts in bone marrow or peripheral blood for AML/MDS; lymphoma + on PET/CT re-staging etc. (NCT01323920)
Timeframe: 1 year

Intervention	Percent of participants (Number)
	non-relapse mortality	progression-free survival	overall survival
Velcade/Tac/MTX	8.8	85	84

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The Percentage Donor Engraftment up to Day 30 Post Stem Cell Infusion

To assess the percentage donor engraftment up to day 30 post stem cell infusion, defined as the first of 3 consecutive days tested of documented absolute netrophil count (ANC) >/= 500 cells/u/L (NCT01323920)
Timeframe: Day 30

Intervention	Percentage of participants (Number)
Velcade/Tac/MTX	94

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The Cumulative Incidence of Grade II-IV Acute GVHD up to Day 100 After Stem Cell Infusion

The primary outcome of this study is the cumulative incidence of grade II-IV acute GVHD up to Day 100 after stem cell infusion. Acute GHVD is graded according to the modified Glucksberg criteria (adapted from Thomas et al., NEJM ,1975, pp. 895-90), which is based on criteria by which the provider classifies acute GVHD per its objective organ staging. Acute GVHD is assessed in weekly standard of care visits post stem cell infusion and is captured in the protocol EDC upon evaluation of clinical notes up to Day 100. Data for acute GVHD organ staging and etiologies are collected in an acute GVHD separate case report form and do not include system organ class, expectedness or attribution. (NCT01323920)
Timeframe: Day 100

Intervention	Percentage of participants (Number)
Velcade/Tac/MTX	32

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Proportion of High Risk Children Without HR FLT3/ITD+ Converting From Positive MRD at End of Induction I to Negative MRD at the End of Induction II

The proportion of high risk children without HR FLT3/ITD+ converting from positive MRD at end of Induction I to negative MRD at the end of Induction II will be estimated as well as the corresponding 95% confidence interval determined using a binomial exact method. (NCT01371981)
Timeframe: Up to 8 weeks

Intervention	Proportion of patients (Number)
Arm A	0.5000
Arm B	0.5238

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EFS for Patients on Arm C, Cohort 3

The Kaplan-Meier method will be used to estimate 3-year EFS, defined as the time from study entry until induction failure, relapse, secondary malignancy, or death. (NCT01371981)
Timeframe: Up to 3 years

Intervention	percentage of patients (Number)
Arm C (Cohort 3)	58.18

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OS for Patients on Arm C, Cohort 1

The Kaplan-Meier method will be used to estimate 3-year OS, defined as the time from study entry until death. (NCT01371981)
Timeframe: Up to 3 years

Intervention	percentage of patients (Number)
Arm C (Cohort 1)	41.67

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Event-free Survival (EFS) for Patients Without High Allelic Ratio FLT3/ITD+ Mutations

Intervention	percentage of patients (Number)
Arm A	45.64
Arm B	46.95

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OS for Patients on Arm C, Cohort 3

The Kaplan-Meier method will be used to estimate 3-year OS, defined as the time from study entry until death. (NCT01371981)
Timeframe: Up to 3 years

Intervention	percentage of patients (Number)
Arm C (Cohort 3)	61.84

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Relapse Rate for Patients Without High Allelic Ratio FLT3/ITD+ Mutations

Cumulative incidence estimates 3 year relapse rate defined as time from study entry to induction failure or relapse where deaths or secondary malignancies are competing events. (NCT01371981)
Timeframe: Up to 3 years

Intervention	percentage of patients (Number)
Arm A	46.67
Arm B	46.65

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Change in Ejection Fraction

The mean percentage change in ejection fraction from baseline to the end of Induction I will be determined for eligible patients enrolled on Arms A, B and C. (NCT01371981)
Timeframe: Up to 4 weeks

Intervention	Percentage change (Mean)
Arm A	-2.0272
Arm B	-2.3453
Arm C (Cohort 1)	-7.5000
Arm C (Cohort 2)	-5.1997
Arm C (Cohort 3)	-3.4624

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Overall Survival (OS) for Patients Without High Allelic Ratio FLT3/ITD+ Mutations

The Kaplan-Meier method will be used to estimate 3-year OS, defined as the time from study entry until death. (NCT01371981)
Timeframe: Up to 3 years

Intervention	percentage of patients (Number)
Arm A	65.04
Arm B	68.45

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OS for Patients on Arm C, Cohort 2

The Kaplan-Meier method will be used to estimate 3-year OS, defined as the time from study entry until death. (NCT01371981)
Timeframe: Up to 3 years

Intervention	percentage of patients (Number)
Arm C (Cohort 2)	64.77

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Bortezomib Clearance

Median and range of bortezomib clearance during Induction II. (NCT01371981)
Timeframe: Day 8 of Induction II

Intervention	Liters/hour/m^2 (Median)
Arm B	8.42

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Change in Shortening Fraction

Mean percentage change in shortening fraction from baseline to the end of Induction I will be determined for eligible patients enrolled on Arms A, B and C. (NCT01371981)
Timeframe: Up to 4 weeks

Intervention	Percentage change (Mean)
Arm A	-1.8445
Arm B	-2.6298
Arm C (Cohort 1)	-2.2333
Arm C (Cohort 2)	-3.6700
Arm C (Cohort 3)	-3.4246

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Sorafenib Steady State Concentration

Median and range of sorafenib steady state concentration for Induction I. (NCT01371981)
Timeframe: Up to 30 days

Intervention	Nanogram/Milliliter (Median)
Arm C	1090.0

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Total Scale Score From Parent-reported Cancer Module

"Results represent the total scale scores from the parent report of the PedsQL™ 3.0 Cancer Module for timepoint 1 (up to 14 days from start of therapy). Items are reverse-scored and linearly transformed to a 0-100 scale as follows: 0=100, 1=75, 2=50, 3=25, 4=0. Therefore, a higher number is a better outcome. The total score is the sum of all the items divided by the number of items answered on all the scales. Scores on a scale is used for a unit of measure." (NCT01371981)
Timeframe: Up to 14 days

Intervention	Scores on a scale (Mean)
Arm A	66.2
Arm B	65.8
Arm C (Cohort 1)	74.9
Arm C (Cohort 2)	63.7

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Total Scale Score From Parent-reported Multidimensional Fatigue Scale Module

"Results represent the total scale scores from the parent report of the PedsQL™ Multidimensional Fatigue Scale for timepoint 1 (up to 14 days from start of therapy). Items are reverse-scored and linearly transformed to a 0-100 scale as follows: 0=100, 1=75, 2=50, 3=25, 4=0. Therefore, a higher number is a better outcome. The total score is the sum of all the items divided by the number of items answered on all the scales. Scores on a scale is used for a unit of measure." (NCT01371981)
Timeframe: Up to 14 days

Intervention	Scores on a scale (Mean)
Arm A	60.5
Arm B	58.1
Arm C (Cohort 1)	71.2
Arm C (Cohort 2)	48.2

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Total Scale Score From Parent-reported Pediatric Quality of Life Inventory Module

"Results represent the total scale scores from the parent report of the PedsQL™ 4.0 Generic Core Scales for timepoint 1 (up to 14 days from start of therapy). Items are reverse-scored and linearly transformed to a 0-100 scale as follows: 0=100, 1=75, 2=50, 3=25, 4=0. Therefore, a higher number is a better outcome. The total score is the sum of all the items divided by the number of items answered on all the scales. Scores on a scale is used for a unit of measure." (NCT01371981)
Timeframe: Up to 14 days

Intervention	Scores on a scale (Mean)
Arm A	68.3
Arm B	67.8
Arm C (Cohort 1)	71.3
Arm C (Cohort 2)	61.6

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EFS for Patients on Arm C, Cohort 1

Intervention	percentage of patients (Number)
Arm C (Cohort 1)	25.00

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EFS for Patients on Arm C, Cohort 2

Intervention	percentage of patients (Number)
Arm C (Cohort 2)	56.12

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Proportion of Patients Experiencing Grade 3 or Higher Non-hematologic Toxicities and Infections While on Protocol Therapy

The proportion of patients experiencing at least one grade 3 or higher non-hematologic toxicity and infection while on protocol therapy will be estimated along with the corresponding 95% confidence interval determined using a binomial exact method. Toxicity will be assessed by Common Terminology Criteria for Adverse Events version 4.0 (CTCAE v4.0). (NCT01371981)
Timeframe: Up to 2 years

Intervention	Proportion of patients (Number)
Arm A	0.8819
Arm B	0.9217
Arm C (Cohort 1)	0.9167
Arm C (Cohort 2)	0.9394
Arm C (Cohort 3)	0.9149
Arm D	0.0239

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Phase I: The Maximum Tolerated Dose (MTD) of Temsirolimus in Combination With Bortezomib, Rituximab and Dexamethasone

Temsirolimus in combination with bortezomib, rituximab, dexamethasone were to be escalated using a standard 3+3 design. The MTD was defined as the highest dose level at which no more than 0 in 3 or 1 in 6 participants experienced a dose-limiting toxicity (DLT) during the first 28-day cycle of treatment. (NCT01381692)
Timeframe: Assessed during cycle 1 (28 days)

Intervention	mg (Number)
Arm A (Phase I: Temsirolimus Dose Level 1, Rituximab, Bortezomib, Dexamethasone)	NA
Arm B (Phase I: Temsirolimus Dose Level 2, Rituximab, Bortezomib, Dexamethasone)	NA

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Progression Free Survival at 24 Months

following the 3-phase comprehensive treatment approach including induction with BD, followed by risk adapted HDM/ASCT, followed by consolidation/maintenance therapy with BD in patients with AL amyloidosis. (NCT01383759)
Timeframe: 24 months

Intervention	percentage of patients (Number)
Amyloidosis	68

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Percentage of Participants Experiencing Progression Free Survival at 12 Months

of a 3-phase comprehensive treatment approach including induction with BD followed by risk adapted HDM/ASCT, followed by consolidation/maintenance therapy with BD in patients with AL amyloidosis. (NCT01383759)
Timeframe: 12 months

Intervention	percentage of patients (Number)
Amyloidosis	84

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Participants Evaluated for Toxicity

Toxicities will be assessed according to the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE), version 4.0. (NCT01383759)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Amyloidosis	19
Monoclonal Ig DepositionDisease (MIDD)	1

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Response Rate of Ofatumumab in Combination With Bortezomib in Patients With Relapsed CD20+ (Cluster of DIfferentiation Antigen 20) Diffuse Large B Cell Lymphoma, Follicular Lymphoma, or Mantle Cell Lymphoma

Based on International Working Group (IWG) criteria, recorded in four categories: Complete Response (CR), disappearance of all evidence of disease; Partial Response (PR), regression of measurable disease and no new sites of disease; Progressive Disease (PD), Any new lesion or increase by >= 50% of previously involved sites from nadir. Stable Disease (SD), failure to attain CR/PR or PD. A response is defined to be either CR/PR. A failure in response includes SD/PD. (NCT01397591)
Timeframe: Every 2 cycles during treatment and then every 3 months for 2 years

Intervention	participants (Number)
Treatment (Monoclonal Antibody and Enzyme Inhibitor Therapy)	2

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Number of Participants With Adverse Events (Toxicity)

Toxicities and adverse experiences will be assessed at each visit using the NCI Common Toxicity Criteria for Adverse Events v4.0 Interim analyses on toxicity will be implemented based on the toxicity endpoints of the first 6 patients, and will be conducted sequentially 4 weeks after the treatment of each patient, or when serious toxicity has been observed for the patient, whichever comes earlier. we assume a non-informative prior distribution (Beta (0.001, 0.001)) for toxicity rate, and compute the posterior distribution of toxicity rate sequentially. (NCT01397591)
Timeframe: Days 1, 8, and 15 of each course and 4-6 weeks after final treatment

Intervention	participants (Number)
Treatment (Monoclonal Antibody and Enzyme Inhibitor Therapy)	2

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Progression-free Survival

Progression free survival (PFS) was defined as the time from study entry to progression or death. Progression free and surviving patients were censored at the date of last follow-up. The median DFS with 95% CI was estimated using the Kaplan Meier method. (NCT01420926)
Timeframe: 48 months

Intervention	months (Median)
Arm I (Decitabine)	7.3
Arm II (Decitabine and Bortezomib)	8.0

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Adverse Events

Adverse Events: Incidence of adverse events, assessed using National Cancer Institute Common Terminology Criteria for Adverse Events version 4.0. Adverse events were collected every cycle during treatment and up to one month after treatment. Adverse events were summarized using summary statistics and frequency tables for each separate cohort. Per protocol, analysis was descriptive in nature. In this section, the number of patients that reported a grade 4 or higher event are summarized. A complete listing of Adverse Events is provided in the Adverse Events section below. (NCT01420926)
Timeframe: 48 months

Intervention	participants (Number)
Arm I (Decitabine)	51
Arm II (Decitabine and Bortezomib)	45

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Complete Remission Rate (CR and CRi)

Defined as the number of patients who achieve a CR or CRi divided by the total number of evaluable patients. A Complete remission (CR) requires: <5% marrow blast, > 200 nucleated cells, no blasts with auer rods, no extramedullary disease, ANC >1,000/mm^3 and platelets > 100,000/mm^3. A CR with incomplete blood count recovery (CRi) is defined as CR with exception of ANC < 1,000/mm^3 or platelets < 100,000/mm^3. (NCT01420926)
Timeframe: 48 months

Intervention	percentage of participants (Number)
Arm I (Decitabine)	40
Arm II (Decitabine and Bortezomib)	38

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Disease-free Survival (DFS)

Disease free survival (DFS) was defined as the time from CR to relapse or death. Relapse free and surviving patients were censored at the date of last follow-up. The median DFS with 95% CI was estimated using the Kaplan Meier method. Relapse is defined as the reappearance of blood blasts or >= 5% marrow blasts after achieving a CR or CRi. (NCT01420926)
Timeframe: 48 months

Intervention	months (Median)
Arm I (Decitabine)	8.5
Arm II (Decitabine and Bortezomib)	15.3

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Overall Survival (OS) Time

Overall survival (OS) was defined as the time from study entry to death of any cause. Surviving patients were censored at the date of last follow-up. The median OS with 95% CI was estimated using the Kaplan Meier method. (NCT01420926)
Timeframe: 48 months

Intervention	months (Median)
Arm I (Decitabine)	9.3
Arm II (Decitabine and Bortezomib)	8.8

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Median Duration of Response of This Regimen

Duration of response is the time from response (CR or PR) until progression of disease or relapse. Responses and progression were evaluated based on the criteria published by the International Myeloma Working Group (Durie, et al, 2006). (NCT01438177)
Timeframe: up to 2 years

Intervention	months (Median)
Velcade+Cyclophosphamide+Chloroquine	4.4

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Number of Participants With Adverse Events of Grade 3 or Higher

Adverse events reported here were at least possibly related to the protocol therapy. (NCT01438177)
Timeframe: Treatment period plus 30 days post-treatment

Intervention	participants (Number)
	Fatigue	Hemoglobin	Nasal cavity/paranasal reactions	ANC/AGC	Pain: pleural	Platelets
Velcade+Cyclophosphamide+Chloroquine	2	1	1	4	1	5

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Response Rate (CR + PR After 2 Cycles)

"Response rate is defined as the percentage of patients who have a complete response (CR) or partial response (PR). Responses were assessed every two cycles of treatment, based on the criteria published by the International Myeloma Working Group (Durie, et al, 2006). Per International Myeloma Working Group response criteria:~CR: Negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and < 5% plasma cells in bone marrow PR: > 50% reduction of serum M-protein and reduction in 24 hours urinary M-protein by >90% or to < 200 mg/24 h" (NCT01438177)
Timeframe: Up to 2 years

Intervention	percentage of participants (Number)
Velcade+Cyclophosphamide+Chloroquine	30

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Overall Survival Rate

(NCT01453088)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Auto Transplant High Dose Melphalan	27
Auto Transplant High Dose Melphalan+Bortezomib	27

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Progression Free Survival Rate

Progression free survival of elderly patients with multiple myeloma treated with either high-dose melphalan versus high-dose melphalan and bortezomib at 3 years (NCT01453088)
Timeframe: Participants will be followed post transplant for a minimum of 3 years, and after that may be monitored as part of the study indefinitely

Intervention	Participants (Count of Participants)
Auto Transplant High Dose Melphalan	13
Auto Transplant High Dose Melphalan+Bortezomib	11

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Progression Free Survival

The main primary endpoint of this study is two-year progression free survival. Patients are considered a failure with respect to PFS if they die or experience disease progression or relapse. The time to this event is the time from transplantation to relapse/progression, initiation of non-protocol anti-myeloma therapy, or death from any cause. Subjects alive without confirmed disease progression will be censored at the time of last disease evaluation. Deaths without progression are treated as failures no matter when they occur. (NCT01453101)
Timeframe: Subjects will be followed for progression-free survival for at least 36 months

Intervention	Months (Median)
Fludarabine, Melphalan, Bortezomib	16.7

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Overall Response Rate

"Overall response rate: Defined as the composite endpoint of response to treatment which includes Complete Response (CR), Partial Response (PR), stable disease (SD) as defined in International Response Criteria.~International Myeloma Working Group Response Criteria for Multiple Myeloma:~CR: Negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and < 5% plasma cells in bone marrow PR: > 50% reduction of serum M-protein and reduction in 24 hours urinary M-protein by >90% or to < 200 mg/24 h SD: Not meeting criteria for CR, VGPR, PR, or progressive disease" (NCT01453101)
Timeframe: Up to 3 years

Intervention	Participants (Count of Participants)
Fludarabine, Melphalan, Bortezomib	45

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Overall Survival (OS)

Overall survival (OS): Defined as time from the first dose of administration to death from any cause (NCT01453101)
Timeframe: Up to 3 years

Intervention	percentage (Number)
Fludarabine, Melphalan, Bortezomib	42

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Determine Dose Limiting Toxicities (DLTs) of VELCADE When Administered in Combination With IFN-α-2b to Patients With Metastatic Malignant Melanoma.

A standard method for the design of this study. Initially, three patients will be treated at a starting dose of VELCADE (1.0 mg/m2). If one of the three patients demonstrates a DLT, then an additional 3 patients will be treated at that dose level. If only one of the six show DLT, then the next cohort of three patients will be entered at the next dose level (1.3 mg/m2). If two or more of the six demonstrate DLT, no further patients will be treated at that dose level. The highest dose level at which less than 2 patients experienced DLT will be expanded to six patients. (NCT01462773)
Timeframe: up to 25 weeks or until disease progression

Intervention	toxicities (Number)
	Grade 4 fatigue	Grade 4 Lymphopenia
Bortezomib & Interferon-a	3	1

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Document Any Objective Anti-tumor Responses and Time to Tumor Progression That May Occur in Response to This Treatment Regimen.

"Measure levels of the cell cycle proteins p21 and p27 in PBMCs and tumor biopsies obtained pre-study and during week 4 of Cycle 1 (Day 26).~Conduct histologic evaluations of microvessel density, tumor apoptosis and lymphocytic infiltrates within tumor biopsies obtained pre- and post-study.~Measure plasma levels of bFGF and VEGF over the course of the study.~Monitor the effects of proteasome inhibition on the biological activity of IFN-α within immune cells by measuring Jak-STAT signal transduction in patient PBMCs." (NCT01462773)
Timeframe: up to 25 weeks

Intervention	patients (Number)
	partial response	stable disease
Bortezomib & Interferon-a	1	7

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Progression Free Survival (PFS)

Number of days from enrollment to recurrence of acute myeloid leukemia as determined by the reappearance of blasts in the blood or marrow (NCT01465386)
Timeframe: Up to 2 years

Intervention	days (Median)
Treated Patients	107

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1 Year Progression-Free Survival Rate - Randomized Participants

PFS rate=Percentage probability of participants experiencing no progression or death up to 1 year, estimated using the Kaplan-Meier method. Response assessed by the investigator: Day 1 (± 7 days) of each cycle per modified IMWG criteria; assessed using ATA (ie, serum and urine M-protein tests performed within 14 days of each other; imaging done if baseline measurable extramedullary plasmacytoma existed). Progression: Any of the following: Increase of 25% from lowest response in 1 or more: serum and/or urine M-component; in those without measurable serum and urine M-protein levels, difference between involved and uninvolved FLC levels (absolute increase > 100 mg/L) ; Bone marrow plasma cell percentage (≥10%). Definite new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing lesions or plasmacytomas. Development of hypercalcemia attributed solely to the plasma cell proliferative disorder. (NCT01478048)
Timeframe: Year 1 after last participant was randomized

Intervention	percentage probability (Number)
Elotuzumab + Bortezomib + Dexamethasone	0.39
Bortezomib + Dexamethasone	0.33

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Investigator-Assessed Objective Response Rate (ORR) - All Randomized Participants

ORR was calculated for participants with a best overall response (BOR) of partial response (PR) or better, including stringent complete response (sCR), complete response (CR), and very good partial response (VGPR). BOR was determined by the investigator based on myeloma tumor assessments using IMWG criteria: CR=Negative immunofixation of serum and urine and disappearance of any soft tissue plasmacytomas, and < 5% plasma cells in bone marrow; sCR= CR + normal FLC ratio and absence of clonal cells in bone marrow; VGPR=Serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-protein level + urine M-protein level < 100 mg per 24 hour; PR= ≥50% reduction of serum M-protein and reduction in 24-hour urinary M-protein by ≥ 90% or to < 200 mg per 24 hour. ORR= number of participants responding divided by total number of participants randomized, measured as a percentage. (NCT01478048)
Timeframe: Randomization until 111 events, up to May 2014, approximately 2 years

Intervention	percentage of participants (Number)
Elotuzumab + Bortezomib + Dexamethasone	64.9
Bortezomib + Dexamethasone	62.7

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Investigator-Assessed Objective Response Rate in Randomized Participants With at Least One FcγRIIIa V Allele

ORR was calculated for participants with a BOR of PR or better, sCR, CR, and VGPR. BOR was determined by the investigator based on myeloma tumor assessments using IMWG criteria: CR=Negative immunofixation of serum and urine and disappearance of any soft tissue plasmacytomas, and < 5% plasma cells in bone marrow; sCR= CR + normal FLC ratio and absence of clonal cells in bone marrow; VGPR=Serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-protein level + urine M-protein level < 100 mg per 24 hour; PR= ≥50% reduction of serum M-protein and reduction in 24-hour urinary M-protein by ≥ 90% or to < 200 mg per 24 hour. ORR= number of participants responding divided by total number of participants randomized, measured as a percentage. Randomized participants with at least 1 FcγRIIIa V allele were a sub-set of all randomized participants. (NCT01478048)
Timeframe: Randomization until 111 events, up to May 2014, approximately 2 years

Intervention	percentage of participants (Number)
Elotuzumab + Bortezomib + Dexamethasone	60.0
Bortezomib + Dexamethasone	61.1

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Median Investigator-Assessed Progression-free Survival (PFS) Time (Months) From Randomization to Date of First Tumor Progression or Death Due to Any Cause - Randomized Participants

PE was planned for after at least 103 events; it was analyzed after 111 events. Response was assessed: Day 1 (± 7 days) of each cycle per modified International Myeloma Working Group (IMWG) criteria; assessed using adequate tumor assessment (ATA) (ie, serum and urine M-protein tests performed within 14 days of each other; imaging if baseline measurable extramedullary plasmacytoma existed). Progression: Any of following: Increase of 25% from lowest response in 1 or more: serum and/or urine M-component; in those without measurable serum and urine M-protein levels, difference between involved and uninvolved free light chain (FLC) levels (absolute increase > 100 mg/L); Bone marrow plasma cell percentage (≥10%). Definite new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing lesions or plasmacytomas. Development of hypercalcemia attributed solely to the plasma cell proliferative disorder. (NCT01478048)
Timeframe: Randomization until 111 events (disease progression or death), up to May 2014, approximately 2 years

Intervention	Months (Median)
Elotuzumab + Bortezomib + Dexamethasone	9.7
Bortezomib + Dexamethasone	6.9

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Number of Investigator-Assessed Progression-free Survival Events From Randomization to Date of First Tumor Progression or Death Due to Any Cause - All Randomized Participants

PE planned for after at least 103 events (progression/death); analyzed at 111 events. Those who neither progressed nor died were censored on the date of last adequate tumor assessment (ATA), which requires both serum and urine M-protein tests. If no post-baseline tumor assessments/no death, then censored on randomization day. Response assessed: Day 1 (± 7 days) each cycle; 30 and 60 days post treatment. Modified IMWG criteria used. Progression: Any of following: Increase of 25% in serum and/or urine M-component; if no measurable serum, urine M-protein levels, then difference between involved and uninvolved free light chain (FLC) levels (absolute increase > 100 mg/L) ; Bone marrow plasma cell percentage (≥10%). New bone lesions or soft tissue plasmacytomas or increase in size of existing lesions, plasmacytomas. Development of hypercalcemia attributed solely to plasma cell proliferative disorder. First dose occurs within 3 days of randomization. (NCT01478048)
Timeframe: Randomization until 111 events, up to May 2014, approximately 2 years

Intervention	Events (progression or death) (Number)
Elotuzumab + Bortezomib + Dexamethasone	52
Bortezomib + Dexamethasone	59

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Median Progression-free Survival Time (Months) From Randomization to Date of First Tumor Progression or Death Due to Any Cause, in Randomized Participants With at Least One FcγRIIIa V Allele

PE was planned for after at least 103 events; it was analyzed after 111 events. Response was assessed: Day 1 (± 7 days) of each cycle per modified IMWG criteria; assessed using adequate tumor assessment (ATA) (ie, serum and urine M-protein tests performed within 14 days of each other; imaging if baseline measurable extramedullary plasmacytoma existed). Progression: Any of following: Increase of 25% from lowest response in 1 or more: serum and/or urine M-component; in those without measurable serum and urine M-protein levels, difference between involved and uninvolved FLC levels (absolute increase > 100 mg/L); Bone marrow plasma cell percentage (≥10%). Definite new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing lesions or plasmacytomas. Development of hypercalcemia attributed solely to the plasma cell proliferative disorder. Randomized participants with at least 1 FcγRIIIa V allele were a sub-set of all randomized participants. (NCT01478048)
Timeframe: Randomization until 111 events, up to May 2014, approximately 2 years

Intervention	Months (Median)
Elotuzumab + Bortezomib + Dexamethasone	9.9
Bortezomib + Dexamethasone	8.1

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Number of Participants With Progression Free Survival

Progression-free survival will be defined as time from on-study to disease progression or death, whichever comes first (NCT01497275)
Timeframe: 6 months

Intervention	participants (Number)
Zevalin + Velcade	0

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Response Rate (Complete Response + Partial Response)

"Disease will be assessed every 3 months.~The Cheson criteria will be used to define response:~Complete Response = Complete disappearance of all detectable clinical and radiographic evidence of disease and disappearance of all disease-related symptoms if present prior to therapy.~Partial Response = A decrease of ≥ 50% in the sum of the products of their greatest transverse diameters (SPD) of up to six of the largest dominant nodes or nodal masses. These nodes or masses should be selected according to the following features: a) they should be clearly measurable in at least two perpendicular measurements; b) they should be from as disparate regions of the body as possible; and c) they should include mediastinal and retroperitoneal areas of disease whenever these sites are involved." (NCT01497275)
Timeframe: 3 months

Intervention	participants (Number)
Zevalin + Velcade	0

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Overall Survival at 1 Year

Number of participants who were alive at the 1 year time point. (Overall survival will be defined as the time from on-study to death due to any cause.) (NCT01497275)
Timeframe: 1 year

Intervention	participants (Number)
Zevalin + Velcade	2

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Maximum Tolerated Dose

The maximum tolerated dose of panitumumab (to be used in combination with bortezomib) (NCT01504477)
Timeframe: 12 months

Intervention	mg/kg (Number)
Combination of Panitumumab and Bortezomib	6

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Percent of Patients With Disease Control

Stable disease after 2 cycles, partial response or complete response as determined by RECIST v1.0 (NCT01504477)
Timeframe: 16 weeks

Intervention	percentage of participants (Number)
Combination of Panitumumab and Bortezomib	0

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Percent of of Patients With a Complete or Partial Response

Partial response plus complete response as per RECIST v1.0 (NCT01504477)
Timeframe: 16 weeks

Intervention	Participants (Count of Participants)
Combination of Panitumumab and Bortezomib	0

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Maximum Tolerated Dose

The maximum tolerated dose of bortezomib (to be used in combination with panitumumab) (NCT01504477)
Timeframe: 12 months

Intervention	mg/m2 (Number)
Combination of Panitumumab and Bortezomib	1.6

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Duration of Disease Control

Time from study registration until progressive disease (NCT01504477)
Timeframe: 2 years

Intervention	Days (Median)
Combination of Panitumumab and Bortezomib	35.5

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Maximum Tolerated Dose (MTD) of Siltuximab

Maximum tolerated dose (MTD) defined as follows: At first dose level, if greater than 1 out of 3 patients or greater than 1 out of 6 patients experience dose limiting toxicity (DLT), the dose level exceeds the maximum tolerated dose (MTD). Dose limiting toxicity (DLT) defined as toxicities graded in severity according to the guidelines outlined in the NCI-Common Toxicity Criteria for Adverse Effects (CTCAE) version 4.0. (NCT01531998)
Timeframe: 21 days

Intervention	mg/kg (Number)
Siltuximab + Bortezomib + Lenalidomide	8.3

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Number of Participants With Response

Overall response defined as number of participants with International Myeloma Working Group Uniform Response Criteria: Complete Response (CR): Negative immunofixation serum & urine, Disappearance soft tissue plasmacytomas & =/<5% plasma cells in bone marrow; Stringent Complete Remission: CR + Normal Normal free light chain (FLC) ratio & Absence clonal cells in bone marrow by Immunohistochemistry/ immunofluorescence; Very Good Partial Response (VGPR): Serum & urine M-protein detectable by immunofixation but not on electrophoresis or 90%> reduction in serum M-protein +urine M-protein level <100mg per 24 hour; Partial Remission (PR): =/>50% reduction serum M-protein & reduction in 24-hour urinaryMprotein by >90% or to < 200mg per 24 hour, =/>50% reduction of serum M-protein & reduction in 24-hour urinary Mprotein by >90%/or <200mg, and if present at baseline, a >50% reduction in size of soft tissue plasmacytomas; Stable Disease: Not CR, VGPR, PR Or Progressive disease (NCT01531998)
Timeframe: Evaluated after eight cycles of 21 days.

Intervention	participants (Number)
	Complete Remission (CR)	Stringent Complete Remission	Very good partial remission (VGPR)	Partial Remission (PR)	Stable Disease
Siltuximab + Bortezomib + Lenalidomide	2	0	2	6	0

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Phase II - Percentage of Patients With a Partial Response or Greater

Evaluate the overall response rate of patients receiving therapy. Patients are considered as having a response if their overall response is Partial Response or better. The percentage of patients achieving this and the exact 95% confidence interval will be calculated. Responses will be defined using the response criteria determined by the International Working Group for AML. (NCT01534260)
Timeframe: up to 9 months

Intervention	percentage of participants (Number)
Phase II at MTD	40.0

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Phase II - Time to Relapse

Will be examined using Kaplan-Meier estimates. Time from date of confirmed complete remission to date of relapse. The observations of patients who died or remained alive and relapse free were censored at date of death or last disease evaluation, respectively. (NCT01534260)
Timeframe: Up to one year

Intervention	days (Median)
Phase II at MTD	32

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Phase II - Treatment-Related Adverse Events Grade 3 or Higher

Number of unique patients who had a treatment-related (possible, probable or definite) adverse events that were graded 3 or higher. (NCT01534260)
Timeframe: Up to one year

Intervention	Participants (Count of Participants)
Phase II at MTD	4

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Number of Patients With Dose Limiting Toxicity

The number of patients who had a DLT during the dose finding/confirming portion (Phase I) of the trial for the safety of the combination of sorafenib, vorinostat, and bortezomib. (NCT01534260)
Timeframe: up to 9 months

Intervention	Participants (Count of Participants)
Phase I Dose Escalating	0

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Frequency and Severity of Toxicity as Graded According to the Cancer Therapeutic Evaluation Program (CTEP) Common Toxicity Criteria (CTC) Version 4.0

Maximum grade per participant of any AE. (NCT01536067)
Timeframe: Every 30 days for 2 months

Intervention	participants (Number)
	Grade 1	Grade 2	Grade 3
Treatment (Monoclonal Antibody Therapy)	0	0	3

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Overall Survival (OS)

OS was defined as the time between randomization and death. Death of a participant regardless of the cause was considered as an event. (NCT01539083)
Timeframe: Up to 5 years

Intervention	months (Median)
Thalidomide + Prednisolone [TP Consolidation]	NA
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]	NA

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Progression Free Survival (PFS)

PFS, calculated as the time between randomization to disease progression or death (regardless of cause), whichever occurred first. Progressive disease as per IMWG criteria: increase of >= 25 percent from lowest response level in Serum M-component and/or (the absolute increase must be >=0.5 gram per deciliter [g/dL]) Urine M-component and/or (the absolute increase must be >=200 mg/24 hour. Only in participants without measurable serum and urine M-protein levels: the difference between involved and uninvolved free light chain levels. The absolute increase must be >10 mg/dL. Bone marrow plasma cell percentage: the absolute percent must be >=10 percent. Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas. Development of hypercalcemia (corrected serum calcium >11.5 mg/dL or 2.65 millimole per liter (mmol/L) that can be attributed solely to the plasma cell proliferative disorder. (NCT01539083)
Timeframe: Baseline until progressive disease (up to 5 years)

Intervention	months (Median)
Thalidomide + Prednisolone [TP Consolidation]	22.05
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]	22.51

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Consolidation Phase: Change From Baseline in AQOL-6D Scores at the End of the Consolidation Phase

The assessment of quality of life-6D (AQoL-6D) is a multi-attribute health-related quality of life instrument (QoL). It comprises dimension scores for independent living, relationships, mental health, coping, pain, senses, and utility score for AQol-6D. Each scale ranges between 1 (best QoL) and -0.04 (worst possible QoL). (NCT01539083)
Timeframe: Baseline, Month 12

Intervention	units on a scale (Mean)
	Independent Living	Relationships	Mental Health	Coping	Pain	Senses	AQoL-6D Utility score
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]	0.14	0.05	0.18	0.05	0.20	0.00	0.11
Thalidomide + Prednisolone [TP Consolidation]	0.15	0.06	0.18	0.08	0.20	0.03	0.11

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Consolidation Phase: Percentage of Participants With Complete Response (CR) at Months 3, 6, 9 and 12

CR as per IMWG criteria is negative immunofixation on serum and urine and disappearance of soft tissue plasmacytomas and <5 percent plasma cells in bone marrow. (NCT01539083)
Timeframe: Months 3, 6, 9 and 12

Intervention	percentage of participants (Number)
	Month 3	Month 6	Month 9	Month 12
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]	36.7	44.9	52.0	53.1
Thalidomide + Prednisolone [TP Consolidation]	36.5	44.8	49.0	51.0

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Consolidation Phase: Percentage of Participants With Stringent Complete Response (sCR) at Months 3, 6, 9 and 12

sCR as per IMWG criteria is CR plus normal free light chain (FLC) ratio and absence of clonal cells in bone marrow. CR is negative immunofixation on serum and urine and disappearance of soft tissue plasmacytomas and <5 percent plasma cells in bone marrow. (NCT01539083)
Timeframe: Months 3, 6, 9 and 12

Intervention	percentage of participants (Number)
	Month 3	Month 6	Month 9	Month 12
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]	23.5	28.6	30.6	28.6
Thalidomide + Prednisolone [TP Consolidation]	20.8	27.1	26.0	26.0

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Disease-free Survival (DFS)

DFS, defined as the duration from the start of CR to the time of relapse from CR. DFS applied only to participants in CR. CR as per IMWG criteria is negative immunofixation on serum and urine and disappearance of soft tissue plasmacytomas and <5 percent plasma cells in bone marrow. Relapse from CR: reappearance of serum or urine M-protein by immunofixation or electrophoresis; development of >= 5 percent plasma cells in the bone marrow; appearance of any other sign of progression (ie, new plasmacytoma, lytic bone lesion, or hypercalcaemia). (NCT01539083)
Timeframe: Up to 5 years

Intervention	months (Median)
Thalidomide + Prednisolone [TP Consolidation]	18.53
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]	13.37

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Consolidation Phase: Percentage of Participants With Complete Response (CR) and Very Good Partial Response (VGPR) at Month 12

CR as per IMWG criteria is defined as negative immunofixation on the serum and urine and disappearance of soft tissue plasmacytomas and less than (<) 5 percent plasma cells in bone marrow. VGPR as per IMWG criteria is defined as serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90 percent or greater reduction in serum M-protein plus urine M-protein level <100 milligram (mg) per 24 hours. (NCT01539083)
Timeframe: Month 12

Intervention	percentage of participants (Number)
Thalidomide + Prednisolone [TP Consolidation]	81.3
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]	92.9

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Consolidation Phase: Change From Baseline in FACT/GOG-NTX Total Score at the End of the Consolidation Phase

Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity (FACT/GOG-NTX) consists of 10 items and evaluates symptoms and concerns associated specifically with chemotherapy-induced neuropathy. 1 FACT/GOG-NTX total score has a range of 0 to 108 with a higher score indicating better quality of life. (NCT01539083)
Timeframe: Baseline, Month 12

Intervention	units on a scale (Mean)
Thalidomide + Prednisolone [TP Consolidation]	2.9
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]	1.0

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Number of Grade 3 Non-hematologic and Grade 4 Hematologic Serious Adverse Events Associated With the Addition of Bortezomib, Thalidomide, and Dexamethasone Into Autologous Transplant Regimens.

To determine whether bortezomib, thalidomide and dexamethasone with transplant 1 and velcade/gemcitabine with transplant 2 can be safely incorporated into well-tested pre-transplant regimens of high-dose melphalan and carmustine/melphalan in doses equivalent to the BEAM(BCNU, etoposide, arabinoside, melphalan)regimen. Treatment-related toxicities will be compared to those reported in the literature using similar intensive approaches. (NCT01548573)
Timeframe: 2 years

Intervention	()
Tandem Transplant in MM <12 Mos of Prior Treatment	0

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Overall Survival

To determine the median overall survival based on an intent-to-treat analysis, which should exceed 10 years, based on the projected 10-year survival of Total Therapy III, keeping in mind that participants are included in this protocol with up to 12 months of prior therapy. (NCT01548573)
Timeframe: 10 years

Intervention	()
Tandem Transplant in MM <12 Mos of Prior Treatment	0

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Event-Free Survival (EFS)

To determine whether, in comparison to Total Therapy II, the median Event-Free Survival (EFS) can be increased from 4.8 years to 7.2 years, which represents an increase in median EFS of approximately 50%, based on an intent-to-treat analysis. (NCT01548573)
Timeframe: 8 years

Intervention	()
Tandem Autologous Stem Cell Transplant	0

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Identification of Drug Resistant Genes

To determine whether repeated bone marrow samples analyzed for gene expression profiling (GEP) can identify genes related to drug resistance in myeloma. The drug resistant genes or the gene products might then be targeted specifically to eradicate myeloma cells surviving tandem transplantation. (NCT01548573)
Timeframe: 5 years

Intervention	()
Tandem Transplant in MM <12 Mos of Prior Treatment	0

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Percentage of Patients Who Suffer Mortality, a Serious Adverse Event, or Other Adverse Event During the Study Period

Percentage of study patients who experience a serious safety issue during the three phases of the study as measured by all cause mortality, serious adverse reactions and other adverse reactions. (NCT01556347)
Timeframe: 583 days

Intervention	Participants (Count of Participants)
All Cause Mortality	0
Serious Adverse Events	2
Other Adverse Events	2

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Percentage of Patients Who Experience CMV, PTLD, and PML

Percentage of patients who experience cytomegalovirus (CMV), post-transplant lymphoproliferative disease (PTLD), or progressive multifocal leukoencephalopathy (PML) during the study period. (NCT01556347)
Timeframe: 583 days

Intervention	Participants (Count of Participants)
Incidnce of CMV, PTLD, PML	0

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Percentage of Patients Transplanted

Percentage of patients, who are transplanted within one year of finishing the Bortezomib treatment phase. (NCT01556347)
Timeframe: 365 days

Intervention	Participants (Count of Participants)
Highly Sensitized Heart Transplant Candidates	0

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Percentage of Patients Who Experience Grade 3 and Above Non-Hematologic Toxicities

Percentage of patients who experience of grade 3 and above non-hematologic toxicities as measured by the incidence of hypersensitivity reaction, fever, nausea and vomiting or dehydration during the study period. (NCT01556347)
Timeframe: 583 days

Intervention	Participants (Count of Participants)
	Hypersensitivity Reaction	Fever	Nausea and Vomiting	Dehydration
Percentage of Patients With Grade and Above Non-Hematologic Ti	1	1	1	1

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The Percentage of Patients Who Experience Either a Respiratory Tract Infection or a Urinary Tract Infection

The percentage of study patients who experience infectious complications in either the respiratory or urinary tracts during the study period. (NCT01556347)
Timeframe: 583 days

Intervention	Participants (Count of Participants)
Respiratory Tract Infections	1
Urinary Tract Infections	1

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Percentage of Patients With Grade 4 Hematologic Toxicities

A Grade 4 hematologic toxicity includes a platelet count < 25,000/mm3 or an absolute neutrophil count < 500/mm3 (NCT01556347)
Timeframe: 583 days

Intervention	Participants (Count of Participants)
Percentage of Patients With Grade 4 Hemotologic Toxicities	0

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Percentage of Patients With a Reduction in CPRA to Less Than 20%

Percentage of highly sensitized heart transplant candidates, (patients with a CPRA greater than 50%), who have desensitization therapy, and then achieve a reduction in alloantibody such that their CPRA falls below 20%. For an individual patient, the outcome measure time frame is the one year of the Recovery Phase which begins after 218 days from the time that the patient begins the Induction Immunotherapy Phase, which is the same as the end of the Bortezomib Treatment Phase. (NCT01556347)
Timeframe: 365 days

Intervention	Participants (Count of Participants)
Highly Sensitized Heart Transplant Candidates	0

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The Percentage of Patients Who Experience Exacerbations Cardiac Dysrhythmias or Heart Failure

The percentage of study patients who experience an exacerbation of cardiac dysrhythmias and heart failure during the study period (NCT01556347)
Timeframe: 583 days

Intervention	Participants (Count of Participants)
Percentage of Patients With Exacerbation of Heart Failure	0
Percentage of Patients With Exacerbation of Dysrythmias	0

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The Percentage of Patients Who Experience Any Grade of Peripheral Neuropathy

The percentage of patients in the study who experience any grade of peripheral neuropathy during the study period (NCT01556347)
Timeframe: 583 days

Intervention	Participants (Count of Participants)
Highly Sensitized Heart Transplant Candidates	1

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Pharmacodynamics (PD): Change From Baseline in B-cell Subset Fractions

CD19+ peripheral B-cells counts are based on the percentage of total leukocyte population and absolute cell counts. (NCT01556438)
Timeframe: Baseline, Cycle 1 and Cycle 7: prior to first tabalumab dose.

Intervention	percentage of b-cell change (Mean)
	Baseline	Cycle 1, Day 1	Cycle 7, Day 1
100 mg Tabalumab+BTZ IV+Dex	9.3	1.1	NA
300 mg Tabalumab+BTZ IV+Dex	12.5	0.3	-14.4

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Pharmacokinetics (PK): Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-∞) of Tabalumab (LY2127399)

(NCT01556438)
Timeframe: Cycle 1, Day 1: 6 + or - hours after bortezomib (BTZ); Cycle 7, Day 1: immediately post BTZ dose and 2 hours after tabalumab

Intervention	ng*hr/mL (Geometric Mean)
	Cycle 1 Day 1	Cycle 7 Day 1
100 mg Tabalumab+BTZ IV+Dex	13300	NA
300 mg Tabalumab+ IV BTZ +Dex	64200	84100
300 mg Tabalumab+ SC BTZ +Dex	50900	131000

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Pharmacokinetics (PK): Maximum Plasma Concentration (Cmax) for Tabalumab (LY2127399)

(NCT01556438)
Timeframe: Cycle 1, Day 1: 6 + or - hours after bortezomib (BTZ); Cycle 7, Day 1: immediately post BTZ dose and 2 hours after tabalumab

Intervention	microgram per milliliter (μg/mL) (Geometric Mean)
	Cycle 1 Day 1	Cycle 7 Day 1
100 mg Tabalumab+BTZ IV+Dex	38.5	70.5
300 mg Tabalumab+ IV BTZ +Dex	154	179
300 mg Tabalumab+ SC BTZ +Dex	139	220

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Number of Participants With One or More Drug Related Adverse Events (AEs) or Any Serious AEs

A summary of other non-serious AEs, and all SAE's, regardless of causality, is located in the Reported Adverse Events section. (NCT01556438)
Timeframe: Baseline through 8 months

Intervention	Participants (Count of Participants)
100 mg Tabalumab+BTZ IV+Dex	4
300 mg Tabalumab+BTZ +Dex	12

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Duration of Response (DoR)

DoR is defined as the time from the date when the measurement criteria are met for CR, CRu, or PR (whichever status is recorded first) until the date of first observation of measured progressive disease. For responding participants who die without progressive disease (including death from study disease),DoR will be censored at the date of death. For responding participants not known to have died as of the data cut-off date and who do not have progressive disease, DoR will be censored at the last objective progression-free assessment date prior to the data cut-off date. (NCT01556438)
Timeframe: Time from Response until measured Progressive Disease (up to 455 days)

Intervention	months (Number)
100 mg Tabalumab+BTZ IV+Dex	NA
300 mg Tabalumab+BTZ +Dex	NA

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Time to Progression (TTP)

TTP is defined as the time from the date of study enrollment to the date of objectively determined progressive disease. TTP will be censored at the date of the last objective progression free disease assessment. (NCT01556438)
Timeframe: Baseline to date of Progressive Disease (up to 455 days)

Intervention	months (Median)
100 mg Tabalumab+BTZ IV+Dex	NA
300 mg Tabalumab+BTZ +Dex	NA

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Number of Participants With Tumor Response (Tumor Response Rate)

"Stringent Complete Response- Complete response in addition to normal free light chain ration and no clonal cells in bone marrow.~Complete Response- no monoclonal protein (mp) in blood, no serum or urine mp, less than 5% plasma cells in bone marrow.~Very Good Partial Response-more than 90% decrease in mp and urine protein. Partial Response- over 50% decrease in serum mp. Stable Disease- less than 25 percent decrease of monoclonal protein. Progressive Disease- 25% increase compared to lowest value of serum mp, urine mp, no measurable mp." (NCT01556438)
Timeframe: Baseline to disease progression (up to 421 days)

Intervention	Participants (Count of Participants)
	Numbers of Responders	Stringent Complete Response (sCR)	Complete Response (CR)	Very Good Partial Response (VGPR)	Partial Response(PR)	Stable Disease(SD)	Progressive Disease
100 mg Tabalumab+BTZ IV+Dex	4	0	0	2	2	0	0
300 mg Tabalumab+ IV BTZ +Dex	5	0	0	1	4	2	3

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Pharmacokinetics (PK): Area Under the Plasma Concentration-time Curve From Time Zero to the Last Measurable Plasma Concentration (AUC0-tlast) of Tabalumab (LY2127399)

(NCT01556438)
Timeframe: Cycle 1, Day 1: 6 + or - hours after bortezomib (BTZ); Cycle 7, Day 1: immediately post BTZ dose and 2 hours after tabalumab

Intervention	hours times nanograms per milliliter (Geometric Mean)
	Cycle 1 Day 1	Cycle 7 Day 1
100 mg Tabalumab+BTZ IV+Dex	8100	9400
300 mg Tabalumab IV BTZ +Dex	34600	27300
300 mg Tabalumab+ SC BTZ +Dex	26900	22900

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Percentage of Participants With a Significant Reduction in Left Ventricular Ejection Fraction (LVEF)

"A significant reduction in LVEF was defined as a ≥ 10% decrease (absolute change) from baseline in participants whose baseline LVEF is ≤ 55%.~For participants with LVEF > 55% at baseline, a significant change was defined as a decrease in LVEF to < 45%." (NCT01568866)
Timeframe: Baseline and 24 weeks

Intervention	percentage of participants (Number)
Bortezomib + DEX	2.6
Carfilzomib + DEX	0.0

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Overall Survival

"Overall survival (OS) is defined as the time from randomization to the date of death (whatever the cause). Participants who were alive or lost to follow-up as of the data analysis cut-off date were censored at the patient's date of last contact (last known to be alive).~Median overall survival was estimated using the Kaplan-Meier method." (NCT01568866)
Timeframe: From randomization until the data cut-off date of 03 January 2017; median follow-up time for OS was 36.9 and 37.5 months for each treatment group respectively.

Intervention	months (Median)
Bortezomib + DEX	40.0
Carfilzomib + DEX	47.6

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Overall Response

"Disease response was evaluated according to the IMWG-URC by the IRC. Overall response was defined as the percentage of participants with a best overall response of partial response (PR), very good PR (VGPR), complete response (CR) or stringent CR (sCR).~sCR: As for CR, normal serum free light chain (SFLC) ratio and no clonal cells in bone marrow (BM).~CR: No immunofixation on serum and urine, disappearance of any soft tissue plasmacytomas and < 5% plasma cells in BM biopsy; VGPR: Serum and urine M-protein detectable by immunofixation but not electrophoresis or ≥ 90% reduction in serum M-protein with urine M-protein <100 mg/24 hours. A ≥ 50% reduction in the size of soft tissue plasmacytomas if present at baseline.~PR: ≥ 50% reduction of serum M-protein and reduction in urine M-protein by ≥ 90% or to < 200 mg/24 hours. A ≥ 50% reduction in the size of soft tissue plasmacytomas if present at baseline." (NCT01568866)
Timeframe: Disease response was assessed every 28 days until end of treatment or the data cut-off date of 10 November 2014; median duration of treatment was 27 weeks in the bortezomib group and 40 weeks in the carfilzomib treatment group.

Intervention	percentage of participants (Number)
Bortezomib + DEX	62.6
Carfilzomib + DEX	76.9

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Percentage of Participants With ≥ Grade 2 Peripheral Neuropathy

"Neuropathy events were defined as Grade 2 or higher peripheral neuropathy as specified by peripheral neuropathy Standardised Medical Dictionary for Regulatory Activities (MedDRA) Query, narrow (scope) (SMQN) terms.~Peripheral neuropathy was assessed by neurologic exam and graded according to National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) Version 4.03:~Grade 1: Asymptomatic; Grade 2: Moderate symptoms, limiting instrumental activities of daily living (ADL) Grade 3: Severe symptoms; limiting self-care ADL; Grade 4: Life-threatening consequences, urgent intervention indicated; Grade 5: Death." (NCT01568866)
Timeframe: From the first dose of study drug up to 30 days after the last dose of study drug as of the data cut-off date of 10 November 2014; median duration of treatment was 27 weeks in the bortezomib group and 40 weeks in the carfilzomib treatment group.

Intervention	percentage of participants (Number)
Bortezomib + DEX	32.0
Carfilzomib + DEX	6.0

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Progression-free Survival

"Progression-free survival (PFS) was defined as the time from randomization to the earlier of disease progression or death due to any cause. Participants were evaluated for disease response and progression according to the International Myeloma Working Group-Uniform Response Criteria (IMWG-URC) as assessed by an Independent Review Committee (IRC).~Median PFS was estimated using the Kaplan-Meier method. Participants with no baseline disease assessments, starting a new anticancer therapy before documentation of disease progression or death, death or disease progression immediately after more than 1 consecutively missed disease assessment visit, or alive without documentation of disease progression before the data cut-off date were censored." (NCT01568866)
Timeframe: From randomization until the data cut-off date of 10 November 2014; median follow-up time for PFS was 11.1.and 11.9 months in the bortezomib and carfilzomib arms respectively

Intervention	months (Median)
Bortezomib + DEX	9.4
Carfilzomib + DEX	18.7

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Change From Baseline in Pulmonary Artery Systolic Pressure (PASP)

Pulmonary artery pressure was measured using transthoracic echocardiogram. (NCT01568866)
Timeframe: Baseline and Weeks 12, 24 and 36 and at end of treatment (median duration of treatment was 27 weeks in the bortezomib group and 40 weeks in the carfilzomib treatment group).

Intervention	mmHg (Mean)
	Week 12 (n=34, 30)	Week 24 (n=22, 20)	Week 36 (n=12, 14)	End of Treatment (n=21, 14)
Bortezomib + DEX	0.3	1.7	4.0	3.4
Carfilzomib + DEX	2.8	3.4	2.6	0.9

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Change From Baseline in Right Ventricular Fractional Area Change (FAC)

Right ventricular function was assessed by measuring fractional area change (FAC) on echocardiogram. (NCT01568866)
Timeframe: Baseline and Weeks 12, 24 and 36 and at end of treatment (median duration of treatment was 27 weeks in the bortezomib group and 40 weeks in the carfilzomib treatment group).

Intervention	percent fractional area change (Mean)
	Week 12 (n=40, 40)	Week 24 (n=26, 31)	Week 36 (n=15, 18)	End of Treatment (n=23, 18)
Bortezomib + DEX	-0.7	0.7	-0.5	0.4
Carfilzomib + DEX	-1.1	-1.0	-0.5	-1.9

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Duration of Response

Duration of response (DOR) was calculated for participants who achieved an sCR, CR, VGPR, or PR. Duration of response is defined as the time from first evidence of PR or better to confirmation of disease progression or death due to any cause. Median duration of response was estimated using the Kaplan-Meier method. Participants with no baseline disease assessments, starting a new anticancer therapy before documentation of disease progression or death, death or disease progression immediately after more than 1 consecutively missed disease assessment visit, or alive without documentation of disease progression before the data cut-off date were censored. (NCT01568866)
Timeframe: From randomization until the data cut-off date of 10 November 2014; median follow-up time for DOR was 9.4 and 10.4 months for each treatment group respectively.

Intervention	months (Median)
Bortezomib + DEX	10.4
Carfilzomib + DEX	21.3

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Number of Participants With >30% Reduction in Brief Pain Inventory (BPI) - Worst Pain Score

"BPI is assessed by 7 questions rated 0 for no pain and higher numbers indicated more pain." (NCT01602224)
Timeframe: Baseline through End of Treatment (19 months)

Intervention	Participants (Count of Participants)
100 mg Tabalumab+Dexamethasone+Bortezomib	37
300 mg Tabalumab+Dexamethasone+Bortezomib	30
Placebo Comparator: Placebo + Dexamethasone + Bortezomib	30

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Overall Response Rate (ORR)

Overall Response Rate (ORR) is the percentage of participants that had a response. (NCT01602224)
Timeframe: Baseline to Objective Disease Progression or Initiation of New Cancer Treatment (28 Months)

Intervention	percentage of participants (Number)
100 mg Tabalumab+Dexamethasone+Bortezomib	58.1
300 mg Tabalumab+Dexamethasone+Bortezomib	59.5
Placebo Comparator: Placebo + Dexamethasone + Bortezomib	61.1

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Overall Survival

Overall survival is the duration from enrollment to death from any cause. For participants who were alive, overall survival was censored at the last contact. (NCT01602224)
Timeframe: Baseline to Death From Any Cause (assessed up to 19 months)

Intervention	months (Median)
100 mg Tabalumab+Dexamethasone+Bortezomib	NA
300 mg Tabalumab+Dexamethasone+Bortezomib	NA
Placebo Comparator: Placebo + Dexamethasone + Bortezomib	NA

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Progression Free Survival (PFS)

PFS is defined as the time from date of first dose to the first observation of disease progression or death due to any cause. If a participant does not have a complete baseline disease assessment, then the PFS time is censored at the enrollment date, regardless of whether or not objectively determined disease progression (Increase of > 25% from lowest response in serum M component, urine M component, bone marrow plasma cell percentage, development of bone lesions) or death has been observed for the participant. If a participant is not known to have died or have objective progression as of the data inclusion cutoff date for the analysis, the PFS time is censored at the last complete objective progression-free disease assessment date. (NCT01602224)
Timeframe: Baseline up to Objective Disease Progression or Death From Any Cause (assessed up to 9 months)

Intervention	months (Median)
100 mg Tabalumab+Dexamethasone+Bortezomib	6.6
300 mg Tabalumab+Dexamethasone+Bortezomib	7.5
Placebo Comparator: Placebo + Dexamethasone + Bortezomib	7.6

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Time to Next Treatment (TNT)

TNT is defined as the time from the date of randomization to the date of initiation of the first poststudy treatment course of anticancer therapy or death from any cause. Time to next treatment will be censored at the date of the last visit for participant who did not initiate additional anticancer therapy. (NCT01602224)
Timeframe: Baseline to Initiation of New Cancer Treatment or Death From Any Cause (18 Months)

Intervention	months (Median)
100 mg Tabalumab+Dexamethasone+Bortezomib	10.1
300 mg Tabalumab+Dexamethasone+Bortezomib	9.9
Placebo Comparator: Placebo + Dexamethasone + Bortezomib	11.7

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Time to Progression (TTP)

Time to progression is defined as the time from the date of randomization to the date of first observed objective progression or death due to study disease. Time to progression will be censored as for PFS for those participants not known to have progressed or that died from other causes. (NCT01602224)
Timeframe: Baseline to Objective Disease Progression or Death (assessed up to 9 months)

Intervention	months (Median)
100 mg Tabalumab+Dexamethasone+Bortezomib	6.6
300 mg Tabalumab+Dexamethasone+Bortezomib	8.2
Placebo Comparator: Placebo + Dexamethasone + Bortezomib	8.1

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Number of Participants With a Given Best Objective Myeloma Response (Quality of Response [QoR])

Response categories in order of decreasing quality are: Stringent Complete Response(sCR),Complete Response(CR), Very Good Partial Response(VGPR),Partial Response(PR),Minimal Response(MR),Stable Disease(SD), or Progressive Disease(PD), according to the International Uniform Response Criteria for Multiple Myeloma.SCR:normal free light chain ration and no clonal cells in bone marrow;CR-no monoclonal protein(mp) in blood, no serum/urine,<5% plasma cells in bone marrow; VGPR-more than 90% decrease in mp and urine protein; PR->50% decrease in serum MP;SD-<25% decrease in mp; PD-25% increase compared to lowest value of serum mp, urine mp and no measurable mp. (NCT01602224)
Timeframe: Baseline to Objective Disease Progression or Initiation of New Cancer Treatment (up to 28 Months)

Intervention	participants (Number)
	Stringent Complete Response	Complete Response	Very Good Partial Response	Partial Response	Minimal Response	Stable Disease	Progressive Disease
100 mg Tabalumab+Dexamethasone+Bortezomib	1	10	10	23	6	14	6
300 mg Tabalumab+Dexamethasone+Bortezomib	0	4	16	23	8	10	7
Placebo Comparator: Placebo + Dexamethasone + Bortezombib	2	4	9	29	6	12	6

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Time to First Skeletal-Related Event (SRE)

Time to first SRE is defined as time from randomization to any one of the following related to multiple myeloma: New Pathological Fracture, Spinal Cord Compression, Surgery to the Bone, Radiation to the Bone collected until participant death, study closure or lost to follow up. Participants not known to have had an SRE at the time of the analysis were censored at the date of their last complete documented assessment for SRE. (NCT01602224)
Timeframe: Baseline to Date of First Skeletal Related Event (assessed up to 19 months)

Intervention	months (Median)
100 mg Tabalumab+Dexamethasone+Bortezomib	NA
300 mg Tabalumab+Dexamethasone+Bortezomib	NA
Placebo Comparator: Placebo + Dexamethasone + Bortezomib	NA

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PK: Time to Maximum Plasma Concentration (Tmax) of Tabalumab

(NCT01602224)
Timeframe: C1 D1: Predose, 3O minutes, 2 hours Postdose; C1 D4, 8, 11: Predose, (D11 only, 30 minutes Postdose); C2 and C6-C10 D1: Predose and immediately Postdose; C2 D 4, 8, 11: Anytime

Intervention	hours (Mean)
	Cycle 1	Cycle 2	Steady State (Cycle 6-10)
100 mg Tabalumab+Dexamethasone+Bortezomib	1.5	0.92	0.75
300 mg Tabalumab+Dexamethasone+Bortezomib	1.58	0.76	0.73

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Pharmacokinetics (PK): Maximum Concentration (Cmax) of Tabalumab

Maximum Concentration (Cmax) of Tabalumab. (NCT01602224)
Timeframe: Cycle (C)1 Day (D)1: Predose, 3O minutes, 2 hours Postdose; C1 D4, 8, 11: Predose, (D11 only, 30 minutes Postdose); C2 and C6-C10 D1: Predose and immediately Postdose; C2 D 4, 8, 11: Anytime

Intervention	micrograms per milliliter (Geometric Mean)
	Cycle 1	Cycle 2	Steady State (Cycle 6-10)
100 mg Tabalumab+Dexamethasone+Bortezomib	38.0	47.9	69.0
300 mg Tabalumab+Dexamethasone+Bortezomib	103	131	189

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PK: Area Under the Curve Over the Dosing Interval (AUC-T) for Tabalumab

Intervention	micrograms times hour per milliliter (Geometric Mean)
	Cycle 1	Cycle 2	Steady State (Cycle 6-10)
100 mg Tabalumab+Dexamethasone+Bortezomib	7790	11600	25300
300 mg Tabalumab+Dexamethasone+Bortezomib	2220	35400	70100

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Participants With Best Overall Response (BOR) in Each Category

Stringent Complete Response-Complete Response and normal free light chain ration and no clonal cells in bone marrow Complete Response- no monoclonal protein (mp) in blood, no serum or urine mp, less than 5% plasma cells in bone marrow Very Good Partial Response-more than 90% decrease in mp and urine protein Partial Response- over 50% decrease in serum mp Stable Disease- less than 25 percent decrease of monoclonal protein Progressive Disease- 25% increase compared to lowest value of serum mp, urine mp, no measurable mp (NCT01602224)
Timeframe: Baseline to Objective Disease Progression or Initiation of New Cancer Treatment (28 Months)

Intervention	Participants (Count of Participants)
	Stringent Complete Response	Complete Response	Very Good Partial Response	Partial Response	Minimal Response	Stable Disease	Progressive Disease
100 mg Tabalumab+Dexamethasone+Bortezomib	1	10	10	23	6	14	6
300 mg Tabalumab+Dexamethasone+Bortezomib	0	4	16	23	8	10	7
Placebo Comparator: Placebo + Dexamethasone + Bortezomib	2	4	9	29	6	12	6

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Duration of Response (DoR)

DOR is measured by the International Myeloma Working Group Uniform Response Criteria: from the date of first evidence of a confirmed response to the date of objective progression or the date of death due to any cause, whichever is earlier. If a responder is not known to have died or have objective progression as of the data inclusion cutoff date, the DOR time will be censored at the last complete objective progression-free disease assessment date. Progressive disease is an increase of 25% from baseline in Serum M, Urine M, bone marrow plasma cell increase of 10 %, development of new bone lesions, development of new soft tissue plasmacytomas or bone lesions, hypercalcemia >11.5 milligrams per deciliter, decrease in hemoglobin of 2 grams per deciliter, rise in serum creatinine by 2 mg/deciliter. (NCT01602224)
Timeframe: Time from Response to Objective Disease Progression (assessed up to 38 months)

Intervention	months (Median)
100 mg Tabalumab+Dexamethasone+Bortezomib	7.9
300 mg Tabalumab+Dexamethasone+Bortezomib	8.6
Placebo Comparator: Placebo + Dexamethasone + Bortezomib	7.7

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Overall Survival

The overall survival of patients was measured of a period of 2 years. (NCT01605032)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Treatment (Busulfan, Melphalan, Bortezomib, Autologous PBSCT)	18

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Progression-free Survival

The progression free survival was assessed over a period of 2 years (NCT01605032)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Treatment (Busulfan, Melphalan, Bortezomib, Autologous PBSCT)	11

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Rate of Complete Response as Determined by the IMWG Criteria

Number of patients achieved complete response after the treatment regimen (NCT01605032)
Timeframe: Day 100

Intervention	Participants (Count of Participants)
Treatment (Busulfan, Melphalan, Bortezomib, Autologous PBSCT)	2

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Overall Response Rate

Intervention	Participants (Count of Participants)
	Complete response	Partial response
Treatment (Busulfan, Melphalan, Bortezomib, Autologous PBSCT)	2	17

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Mortality

(NCT01605032)
Timeframe: Up to day 100

Intervention	Participants (Count of Participants)
Treatment (Busulfan, Melphalan, Bortezomib, Autologous PBSCT)	1

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Toxicity of V-BEAM

"Graded per the NCI Common Terminology Criteria for Adverse Events (CTCAE) version 4.0.~Patients are evaluated from first receiving study treatment until a 30-day follow-up after the conclusion of treatment for adverse events not resulting in death. Adverse events resulting in death will be evaluated through Day +100.~This outcomes measures the common toxicities observed. Please refer to the Serious Adverse Event and Other Adverse Event sections of the results for further details." (NCT01653418)
Timeframe: 30 days after end of treatment / Day +100

Intervention	participants (Number)
	Neutropenic fever	Clostridium difficile colitis	Neutropenic colitis without Clostridium difficile	Sepsis	Mucositis (grade 1-2)	Mucositis (grade 3-4)	Diarrhea (grade 3-4)	Hepatic toxicity (grade 3-4)	Peripheral neuropathy (grade 1-2)	Toxic death
V-BEAM + Stem Cell Infusion	10	3	3	3	8	2	10	1	2	2

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Complete Response Rate (Complete Response + Stringent Complete Response)

Defined by the International Myeloma Working Group (IMWG) criteria (NCT01653418)
Timeframe: Day +100

Intervention	participants (Number)
V-BEAM + Stem Cell Infusion	6

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Very Good Partial Response Rate (VGPR+nCR+sCR+CR)

Response will be assessed per the International Myeloma Working Group (IMWG) Response Criteria. (NCT01653418)
Timeframe: Day +100

Intervention	participants (Number)
V-BEAM + Stem Cell Infusion	8

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Number of Participants With Overall Survival (OS)

OS is defined as the duration from the time of transplant to death or last follow-up. (NCT01653418)
Timeframe: Median follow-up of 6 months (range: 6-12 months)

Intervention	participants (Number)
	Expired Day +3	Expired Day +18	Alive
V-BEAM + Stem Cell Infusion	1	1	8

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Number of Participants With Progression-free Survival (PFS)

"PFS is defined as the duration from transplant to time of first progression, death, relapse after CR, or the date the patient was last known to be in remission.~Response will be assessed per the International Myeloma Working Group (IMWG) Response Criteria." (NCT01653418)
Timeframe: Median follow-up of 6 months (range: 6.0-12.0 months)

Intervention	participants (Number)
	No relapse/progression	Relapse/progression at 12 months
V-BEAM + Stem Cell Infusion	7	1

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Time to Platelet Engraftment After V-BEAM.

Time to platelet engraftment is defined as the duration between Day 0 to the first day of platelet count sustained at > 20x109/L without transfusion. The median time to neutrophil and platelet engraftment will be reported. (NCT01653418)
Timeframe: Day +100

Intervention	days (Median)
	More than 20 x 10^9/L	More than 50 x 10^9/L
V-BEAM + Stem Cell Infusion	22.5	23

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Overall Response Rate (ORR)

"ORR includes Partial Response (PR) + Very Good Partial Response (VGPR) + Complete Response (CR)~Response will be assessed per the International Myeloma Working Group (IMWG) Response Criteria." (NCT01653418)
Timeframe: 3 months following Day +100 visit

Intervention	participants (Number)
	Partial response	Very good partial response	Complete response
V-BEAM + Stem Cell Infusion	0	2	6

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Time to Neutrophil Engraftment After V-BEAM.

Time to neutrophil engraftment is defined as duration between Day 0 to the first day of ANC > 0.5x109/L post transplant when it is sustained for more than three consecutive days. (NCT01653418)
Timeframe: Day +100

Intervention	days (Median)
V-BEAM + Stem Cell Infusion	10

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Progression-free Survival

"From date of registration to date of first documentation of progression or death due to any cause.~Per the International Uniform Response Criteria for Multiple Myeloma, progression is defined as >=1 of Serum M protein increase >= 25% from lowest response level, with an absolute increase of >= 0.5g/dL; Urine M protein increase >= 25% from lowest response level, with an absolute increase of >= 200 mg/24 hrs; If participant had serum M protein <1 g/dL, urine M protein <200 mg/24 hrs, and an involved serum free light chain level >= 10mg/dL at baseline: >= 25% increase in the difference between involved and uninvolved serum free light chain level with an absolute increase of >= 10 mg/dL; Bone marrow plasma cell % increase =25% from baseline with the absolute plasma cell % >=10%; New bone lesions or soft tissue plasmocytomas, or definite increase in size of existing bone lesions or soft tissue plasmocytomas; Development of hypercalcemia that can be attributed solely to multiple myeloma" (NCT01668719)
Timeframe: Up to 6 years post registration

Intervention	months (Median)
Arm I (Bortezomib, Lenalidomide, Dexamethasone)	33.6
Arm II (Bortezomib, Lenalidomide, Dexamethasone, Elotuzumab)	31.5

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Phase I: Maximum Tolerated Dose (MTD) of Elotuzumab in Combination With Bortezomib, Lenalidomide and Dexamethasone

"Assess safety of elotuzumab in combination with bortezomib, lenalidomide and dexamethasone and select the optimal dose of elotuzumab for the Phase II portion from 10mg/kg on each cycle, to 5mg/kg on each cycle MTD reflects the highest dose that had a dose-limiting toxicity (DLT) rate of ≤ 1/6 participants. DLTs were defined as treatment regimen related: grade ≥ 3 non-hematologic toxicity; grade 3 nausea or diarrhea despite anti-emetic and anti-diarrheal therapy; grade 3 hyperglycemia if symptomatic or glucose level > 300mg/ml despite insulin and/or oral diabetic therapy; grade 4 neutropenia ≥ 7 days or grade 3/4 neutropenia with fever (≥ 38.5 oC); grade 4 thrombocytopenia ≥ 7 days or associated with hemorrhage; delay of treatment with any agent by > 2 weeks due to drug related toxicity.~DLT were graded using the NCI CTCAE version 4.0~Note:~i) the second, lower dose level was not tested as the first dose level was deemed safe ii) 6 participants were evaluable at phase I analysis" (NCT01668719)
Timeframe: time from first participants randomized until at least 6 patients were evaluable for DLTs. DLTs were assessed only during Cycle 1 (21 days)

Intervention	mg/kg (Phase II dosing for elotuzumab) (Number)
Phase I Dose Level 1 (Elotuzumab, 10mg, and Bortezomib, Lenalidomide and Dexamethasone)	10

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Overall Survival

From date of registration to date of death due to any cause (NCT01668719)
Timeframe: Up to 6 years post registration

Intervention	months (Median)
Arm I (Bortezomib, Lenalidomide, Dexamethasone)	NA
Arm II (Bortezomib, Lenalidomide, Dexamethasone, Elotuzumab)	68

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Number of Participants With Gr 3 Through 5 Adverse Events That Are Related to Study Drugs

Adverse Events (AEs) are reported by CTCAE Version 4.0. Only adverse events that are possibly, probably or definitely related to study drug are reported. (NCT01668719)
Timeframe: Duration of treatment and follow up until death or 6 years post registration, whichever occurs first.

Intervention	Participants (Number)
	Abdominal pain	Acute kidney injury	Agitation	Alanine aminotransferase increased	Alkaline phosphatase increased	Allergic reaction	Anemia	Aspartate aminotransferase increased	Atrial fibrillation	Back pain	Blood bilirubin increased	Bone pain	Cataract	Creatinine increased	Diarrhea	Dizziness	Dry skin	Dyspnea	Edema limbs	Encephalopathy	Eye disorders - Other, specify	Fall	Fatigue	Febrile neutropenia	Fracture	Gait disturbance	Gastrointestinal disorders - Other, specify	Generalized muscle weakness	Hyperglycemia	Hyperkalemia	Hypertension	Hypoalbuminemia	Hypokalemia	Hyponatremia	Hypophosphatemia	Hypotension	Hypoxia	INR increased	Infections and infestations - Other, specify	Infusion related reaction	Insomnia	Lung infection	Lymphocyte count decreased	Multi-organ failure	Muscle weakness lower limb	Muscle weakness trunk	Musculoskeletal and connective tiss disorder - Other	Nausea	Neck pain	Neuralgia	Neutrophil count decreased	Osteonecrosis of jaw	Pain	Pain in extremity	Peripheral motor neuropathy	Peripheral sensory neuropathy	Platelet count decreased	Pneumonitis	Portal vein thrombosis	Pulmonary edema	Rash acneiform	Rash maculo-papular	Resp, thoracic and mediastinal disorders - Other	Respiratory failure	Sepsis	Skin infection	Stroke	Supraventricular tachycardia	Syncope	Thromboembolic event	Tremor	Urinary tract infection	Urine output decreased	Vomiting	Weight loss	White blood cell decreased
Arm I (Bortezomib, Lenalidomide, Dexamethasone)	1	1	0	0	0	0	8	0	3	0	0	0	0	0	5	1	1	0	2	1	0	1	6	2	0	1	0	1	2	1	2	0	0	3	1	2	1	0	3	0	0	3	14	0	2	0	1	1	0	0	8	1	0	1	1	4	10	0	0	1	1	2	0	2	2	0	0	0	1	4	1	2	0	1	0	4
Arm II (Bortezomib, Lenalidomide, Dexamethasone, Elotuzumab)	0	0	1	2	1	1	6	2	0	1	1	2	1	1	1	0	0	2	0	0	1	0	5	1	1	0	1	1	4	1	1	1	4	1	0	4	1	1	4	3	2	5	13	1	0	1	0	0	1	1	5	0	1	0	4	6	10	1	1	0	0	3	1	1	1	1	1	1	2	1	0	0	1	0	1	5

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Response (Partial Response [PR] or Better) Rate

Percentage of participants with PR or better to treatment per the International Uniform Response Criteria for Multiple Myeloma stringent Complete Response- CR criteria + normal serum free light chain (FLC) ratio + absence of clonal cells in bone marrow (BM) by immunohistochemistry or immunofluorescence CR- Negative immunofixation (IFX) on serum & urine M proteins + <5% plasma cells in BM + disappearance of soft tissue plasmocytomas (STP) very good PR- PR criteria + serum & urine M proteins detectable by IFX but not on electrophoresis or >=90% reduction (RED) in serum M protein & urine M protein <100 g/24 hrs PR- >=50% RED in size of STP, if present at baseline & >=50% RED in plasma cells, if >=30% plasma cells in BM at baseline: & RED in serum M protein of >=50% & in urine M protein of >= 90% or to 200 mg/24hr OR if serum M protein <1 g/dL, urine M protein <200 mg/24 hrs, & involved serum FLC level >= 10 mg/dl at baseline: >= 50% RED in (involved-uninvolved) serum FLC levels (NCT01668719)
Timeframe: Up to 6 years post registration

Intervention	Percentage of participants (Number)
Arm I (Bortezomib, Lenalidomide, Dexamethasone)	88
Arm II (Bortezomib, Lenalidomide, Dexamethasone, Elotuzumab)	83

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Maximum Tolerated Dose of the Combination of ASP7487 (OSI-906) With Velcade and Dexamethasone

"Phase 1: To determine the maximum tolerated dose (MTD) of ASP7487 (OSI-906) administered in combination with the recommended dose and schedule of bortezomib and dexamethasone;~Phase 2: To evaluate the antitumor activity of ASP7487 (OSI-906) in combination with bortezomib and dexamethasone at the MTD established from the Phase 1 component." (NCT01672736)
Timeframe: 45 months

Intervention	milligrams (Number)
	Linsitinib starting dose in milligrams	Linsitinib maximum dose in milligrams
ASP7487, Velcade, Dexamethasone	75	150

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The Primary Objective of This Study Will be to Investigate the Incidence and Severity of Peripheral Neuropathy Caused by a Prior Intravenous VELCADE-containing Regimen in Comparison to That Caused by a Subcutaneous VELCADE-containing Regimen.

"Definition of incidence: the number of participants enrolled in the study experiencing treatment-emergent peripheral neuropathy. Emergence of peripheral neuropathy is determined via neurological assessment conducted on Day 1 and Day 11 of each treatment cycle as well as during the End of Study visit.~Definition of severity: the severity of any treatment-emergent peripheral neuropathy experienced by a patient on-study. Peripheral neuropathy severity is determined via neurological assessment conducted on Day 1 and Day 11 of each treatment cycle as well as the End of Study visit and is graded on a 0-4 scale based on CTCAE criteria.~Incidence of Peripheral Neuropathy Definition: the number of participants enrolled in the study experiencing treatment-emergent peripheral neuropathy. Emergence of peripheral neuropathy is determined via neurological assessment conducted on Day 1 and Day 11 of each treatment cycle as well as during the End of Study visit." (NCT01695330)
Timeframe: Subjects eligible for this study will receive treatment with study drug for a maximum of eight 28 day treatment cycles.

Intervention	Participants (Count of Participants)
Subcutaneous Bortezomib	5

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Progression-free Survival

The distribution of progression-free survival will be estimated by arm using the method of Kaplan-Meier. (NCT01706666)
Timeframe: From registration to the earliest date of documentation of disease progression or death due to any cause, assessed up to 3 years

Intervention	Months to Progression (Number)
Arm A	NA
Arm B	9.2
Arm C	NA

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Proportion of Patients Experiencing a Stringent Complete Response (sCR) After 12 Cycles, 24 Months

Estimated by the number of sCRs divided by the total number of evaluable patients in each arm. Exact binomial confidence intervals for the true sCR rate will be calculated by arm. Stringent complete response (sCR) is defined as a complete response plus normal serum free light chain ratio and the absence of clonal cells in bone marrow by flow cytometry. (NCT01706666)
Timeframe: 24 months

Intervention	percentage of participants (Number)
Arm A	100
Arm B	0
Arm C	100

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Survival Time

The distribution of survival time will be estimated by arm using the method of Kaplan-Meier. (NCT01706666)
Timeframe: From registration to death due to any cause, assessed up to 3 years

Intervention	Months to death (Number)
Arm A	NA
Arm B	NA
Arm C	NA

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Efficacy of Velcade

Effect of VELCADE at 1.0-1.3 mg/m2 dose on platelet aggregation at 24 and 48 hour post-infusion in patients with multiple myeloma. The following components of platelet aggregation were evaluated at varying levels: Collagen, Adenine di-Phosphate (ADP), Arachidonic acid, and Ristocetin. (NCT01720043)
Timeframe: 48 hours

Intervention	percentage (Mean)
	Collagen 5.g.ml, 24 hrs	Collagen 2.g.ml, 24 hrs	ADP.10.M, 24 hrs	ADP.5.M, 24 hrs	ADP.3.M, 24 hrs	Arach.Acid.0.5.mg.ml, 24 hrs	Ristocetin1.5.mg.ml, 24 hrs	Ristocetin.0.5.mg.ml, 24 hrs	Collagen.5.g.mL, 48 hrs	Collagen.2.g.mL, 48 hrs	ADP.10.M, 48 hrs	ADP.5.M, 48 hrs	ADP.3.M, 48 hrs	Arach.Acid.0.5.mg.mL, 48 hrs	Ristocetin.1.5.mg.mL, 48 hrs	Ristocetin.0.5.mg.mL, 48 hrs
All Participants	-4.143	-4.429	-4.571	-6.429	-7.571	-11.143	-1.429	-2.429	-2.429	-0.857	-3.429	-3.571	1.571	-2.286	.0143	-2.000

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QLQ-C30 Question 30

"Measured as mean quality of life in study subjects, quantitatively scored using the standardized and validated European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ). Question 30: How would you rate your overall quality of life during the past week?~7 point scores are standardized to a scale of 0-100, where 100 means highest possible quality." (NCT01729338)
Timeframe: baseline, 3 months, 5 months

Intervention	units on a scale (Mean)
	Baseline	3 months	5 months
Velcade, Cyclophosphamide, Revlimid	51.7	66.7	66.7

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Maximum Depth of Response During Maintenance Therapy

"Defined as maximum depth of response (ranging from partial response to complete response by International Myeloma Working Group (IMWG) criteria at any point during post-induction maintenance therapy.~IMWG: Complete Response (CR): negative immunofixation on the serum and urine, no soft tissue plasmacytomas and <5% plasma cells in the bone marrow; stringent CR: CR+normal free light chain ratio, no clonal cells in bone marrow by immunohistochemistry or immunofluorescence; Very Good Partial Response: serum and urine M-protein detected by immunofixation but not electrophoresis, >90% in serum M-protein+urine, M-protein level <100 mg/24hour; Partial Response (PR): ≥50% decrease of serum and M-protein, 24 hour urinary M-protein decrease by ≥90% or <200 mg/24hour. Stable disease mean that the patient has not achieved CR, VGPR, PR or progressive disease." (NCT01729338)
Timeframe: Up to 3 years

Intervention	percentage of participants (Number)
	Stable Disease	Partial Response	Very good partial response	Complete Response/Stringent complete response	Progressive Disease/no response
Velcade, Cyclophosphamide, Revlimid	13	0	50	38	0

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Maximum Depth of Response During Induction Therapy

Maximum depth of response is defined as: ranging from partial response to complete response by International Myeloma Working Group (IMWG). Described as number of patients achieving each level of response. IMWG: CR: negative immunofixation on the serum and urine, no soft tissue plasmacytomas and <5% plasma cells in the bone marrow; sCR: CR+normal free light chain ratio, no clonal cells in bone marrow by immunohistochemistry or immunofluorescence; VGPR: serum and urine M-protein detected by immunofixation but not electrophoresis, >90% in serum M-protein+urine, M-protein level <100 mg/24hour; PR: ≥50% decrease of serum and M-protein, 24 hour urinary M-protein decrease by ≥90% or <200 mg/24hour. Stable disease mean that the patient has not achieved CR, VGPR, PR or progressive disease. (NCT01729338)
Timeframe: Up to 8 months

Intervention	percentage of participants (Number)
	Stable Disease	Partial Response	Very good partial response (VGPR)	Complete Response/Stringent complete response	Progressive Disease/no response
Velcade, Cyclophosphamide, Revlimid	21	7	29	29	14

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Severe Adverse Event Rate

Defined as number of patients experiencing any grade or severe (≥ grade 3 by common toxicity criteria for adverse events (CTCAE) v4.0 criteria) adverse events at any time during the study (NCT01729338)
Timeframe: Up to 3 years

Intervention	percentage of participants (Number)
Velcade, Cyclophosphamide, Revlimid	64

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Overall Response Rate (ORR) During Induction Therapy

"Defined as percentage of patients achieving a partial response or better by International Myeloma Working Group (IMWG) standard criteria:~IMWG: Complete Response (CR): negative immunofixation on the serum and urine, no soft tissue plasmacytomas and <5% plasma cells in the bone marrow; stringent CR: CR+normal free light chain ratio, no clonal cells in bone marrow by immunohistochemistry or immunofluorescence; Very Good Partial Response: serum and urine M-protein detected by immunofixation but not electrophoresis, >90% in serum M-protein+urine, M-protein level <100 mg/24hour; Partial Response (PR): ≥50% decrease of serum and M-protein, 24 hour urinary M-protein decrease by ≥90% or <200 mg/24hour." (NCT01729338)
Timeframe: Up to 8 months

Intervention	percentage of participants (Number)
Velcade, Cyclophosphamide, Revlimid	64

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Median Progression-free Survival

Defined as median time elapsed in study subjects between initiation of study therapy and either disease progression or death, regardless of cause of death. (NCT01729338)
Timeframe: 4 years

Intervention	months (Median)
Velcade, Cyclophosphamide, Revlimid	24.2

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Median Overall Survival

Defined as median time elapsed in study subjects between initiation of study therapy and death, regardless of cause. (NCT01729338)
Timeframe: Up to 3 years

Intervention	months (Median)
Velcade, Cyclophosphamide, Revlimid	29.7

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Median Duration of Response

Defined as median time elapsed in study subjects between achievement of response and disease progression. (NCT01729338)
Timeframe: From date of first confirmed response until date of disease progression or up to 3 years

Intervention	months (Median)
Velcade, Cyclophosphamide, Revlimid	26.2

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Functionality as Assessed Using the Cancer and Leukemia Group B (CALGB) Geriatric Assessment Tool

"Mean functionality in study subjects, quantitatively scored using the standardized and validated Cancer and Leukemia Group B (CALGB) Geriatric Assessment Tool, which comprehensively assesses aspects of a patient's functionality such as symptoms (e.g., pain, anxiety), social support (e.g., someone to turn to for help), and ability to carry out routine activities (e.g., grocery shopping) or physical exertion (e.g., climbing stairs) was assessed at baseline.~The score is obtained by inserting patient-specific data into the online calculator found at http://www.mycarg.org/Chemo_Toxicity_Calculator, which is based on the risk score described in Hurria A, Togawa K, Mohile SG, et al. Predicting chemotherapy toxicity in older adults with cancer: a prospective multicenter study. J Clin Oncol. 2011;29(25):3457-3465.~The risk score ranges from 0-19, with 0-5 indicating low risk, 6-9 intermediate risk, and 10-19 high risk for severe (grade >2) toxicity." (NCT01729338)
Timeframe: baseline

Intervention	Scores on a scale (Mean)
Velcade, Cyclophosphamide, Revlimid	10

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Median Time to Response

Defined as median time to achievement of response (partial remission or better by International Myeloma Working Group standard criteria), in study subjects during 8 months of induction chemotherapy. (NCT01729338)
Timeframe: Up to 8 months

Intervention	months (Median)
Velcade, Cyclophosphamide, Revlimid	2

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QLQ-C30 Question 29

Measured as mean quality of life in study subjects, quantitatively scored using the standardized and validated European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ). Question 29: how would you rate your overall health during the past week? 7 point scores are standardized to a scale of 0-100, where 100 means highest possible quality. (NCT01729338)
Timeframe: baseline, 3 months, 5 months

Intervention	units on a scale (Mean)
	Baseline	3 months	5 months
Velcade, Cyclophosphamide, Revlimid	58.3	65	68.3

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Overall Response Rate by Independent Response Adjudication Committee (IRAC)

"The ORR together with the relative proportions in each response category (ie, stringent CR [sCR], CR, very good PR [VGPR], PR, SD, and PD) by treatment using the IMWG criteria will be examined.~Complete Response: Negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and ≤ 5% plasma cells in bone marrow~SCR: CR+ Normal FLC ratio and Absence of clonal cells in bone marrow by immunohistochemistry or immunofluorescence~VGPR: Serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein plus urine Mprotein level < 100 mg per 24 hours~PR: ≥ 50% reduction of serum M-Protein and reduction in 24-hour urinary M-protein by ≥ 90% or to < 200 mg per 24 hours~Progressive Disease: Please refer to Primary outcome measure for definition~SD: Not meeting criteria for CR, VGPR, PR, or progressive disease" (NCT01734928)
Timeframe: From randomization to progressive disease or death during the IRAC assessment period, up to approximately 42 months

Intervention	Participants (Count of Participants)
	Stringent complete response	Complete Reponse	Very Good Partial Response	Partial Response	Stable Disease	Progressive Disease	Not Evaluable
Treatment 1: POM+BTZ+LD-DEX	9	35	104	83	32	11	7
Treatment 2: BTZ+LD-DEX	2	9	40	88	106	16	17

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Progression Free Survival by Independent Response Adjudication Committee (IRAC)

"Progression free survival (PFS) will be calculated as the time between the randomization and progressive disease (PD) or death.~Progressive Disease is defined as an Increase of ≥ 25% from nadir in:~Serum M-component and/or (the absolute increase must be ≥ 0.5 g/dL)g~Urine M-component and/or (the absolute increase must be ≥ 200 mg/24 hours)~In patients without measurable serum and urine M-protein levels the difference between involved and uninvolved FLC levels, the absolute increase must be > 100 mg/dL.~Bone marrow plasma cell percentage, the absolute % must be ≥ 10%h~Definite development of new bone lesions or soft tissue plasmacytomas increase in the size of existing bone lesions or soft tissue plasmacytomas. -Development of hypercalcemia (corrected serum calcium > 11.5 mg/dL or 2.65 mmol/L) that can be attributed solely to the plasma cell proliferative disorder." (NCT01734928)
Timeframe: From randomization to progressive disease or death during the IRAC assessment period, up to approximately 42 months

Intervention	Months (Median)
Treatment 1: POM+BTZ+LD-DEX	11.20
Treatment 2: BTZ+LD-DEX	7.10

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Overall Survival (OS)

Overall survival (OS) is calculated as the time from randomization to death from any cause. (NCT01734928)
Timeframe: From randomization to date of death, up to approximately 65 months

Intervention	Months (Median)
Treatment 1: POM+BTZ+LD-DEX	35.58
Treatment 2: BTZ+LD-DEX	31.61

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Number of Participants With Grade 5 Treatment Emergent Adverse Events (TEAE)

Treatment-emergent adverse events (TEAEs) are defined as any AE occurring or worsening on or after the first dose date of the study treatment and within 28 days after the last dose date. (NCT01734928)
Timeframe: From first dose to 28 days after the last dose (up to approximately 44 months

Intervention	Participants (Count of Participants)
Treatment 1: POM+BTZ+LD-DEX	29
Treatment 2: BTZ+LD-DEX	12

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Number of Participants With Grade 3-4 Treatment Emergent Adverse Events (TEAE)

Intervention	Participants (Count of Participants)
Treatment 1: POM+BTZ+LD-DEX	259
Treatment 2: BTZ+LD-DEX	194

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Duration of Response by Independent Response Adjudication Committee (IRAC)

"Duration of myeloma response is defined as the duration from the time when the IMWG response criteria are first met for sCR or CR or VGPR or PR until the first date the response criteria are met for PD or until the subject died from any cause, whichever occurs first.~Complete Response: Negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and ≤ 5% plasma cells in bone marrow~SCR: CR+ Normal FLC ratio and Absence of clonal cells in bone marrow by immunohistochemistry or immunofluorescence~VGPR: Serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein plus urine Mprotein level < 100 mg per 24 hours~PR: ≥ 50% reduction of serum M-Protein and reduction in 24-hour urinary M-protein by ≥ 90% or to < 200 mg per 24 hours~Progressive Disease: Please refer to Primary outcome measure for definition~SD: Not meeting criteria for CR, VGPR, PR, or progressive disease" (NCT01734928)
Timeframe: From randomization to progressive disease or death during the IRAC assessment period, up to approximately 42 months

Intervention	Months (Median)
Treatment 1: POM+BTZ+LD-DEX	13.70
Treatment 2: BTZ+LD-DEX	10.94

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Toxicity Information Recorded Will Include the Type, Severity, Time of Onset, Time of Resolution, and the Probable Association With the Study Regimen.

Toxicity will be evaluated based on the standard NCI Common Toxicity Criteria for Adverse Effects CTCAE) V.4.0 grading criteria. (NCT01736943)
Timeframe: Up to two years

Intervention	participants (Number)
	Abdominal pain	Alanine aminotransferase increased	Anemia	Anorexia	Aspartate aminotransferase increased	Chills	Constipation	Cough	Diarrhea	Dizziness	Dyspnea	Edema limbs	Epitaxis	Fatigue	Febrile neutopenia	Gastrointestinal disorders - Other, gum tenderness	Generalized muscle weakness	Headache	Hypoalbuminemia	Hypocalcemia	Hypokalemia	Hyponatremia	Hypotension	Infections and infestations - Other, bacteremia	Insomnia	Lymphocyte count decreased	Malaise	Mucositis oral	Nausea	Neutrophil count decreased	Peripheral sensory neuropathy	Platelet count decreased	Respiratory, thoracic and mediastinal disorders - Other, tachypnea	Skin and subcutaneous tissue disorders - Other, Ecchymoses	Vomiting	White blood cell decreased
Bortezomib + Doxil	4	3	17	7	4	4	4	4	9	8	10	3	4	15	12	3	4	5	6	4	3	7	4	3	4	12	4	4	15	10	4	18	3	4	8	14

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Overall Survival

Overall survival wil be measured as the time from start of treatment to the Date of death or the last date the patient was known to be alive (NCT01736943)
Timeframe: Up to two years

Intervention	Days (Median)
Bortezomib + Doxil	50

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Progression Free Survival

The time from first day of treatment to the first observation of disease progression or death due to any cause. If a patient has not progressed or died, progression-free survival is censored at the time of last follow-up. (NCT01736943)
Timeframe: Up to 2 years

Intervention	days (Median)
Bortezomib + Doxil	21

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Percentage of Participants With Incidence of Grade II-IV GVHD

The primary outcome of this study is the cumulative incidence of grade II-IV acute GVHD up to Day 180 after stem cell infusion. Acute GHVD is graded according to the modified Glucksberg criteria (adapted from Thomas et al., NEJM ,1975, pp. 895-90), which is based on criteria by which the provider classifies acute GVHD per its objective organ staging. Acute GVHD is assessed in weekly standard of care visits post stem cell infusion and is captured in the protocol EDC upon evaluation of clinical notes up to Day 100. Data for acute GVHD organ staging and etiologies are collected in an acute GVHD separate case report form and do not include system organ class, expectedness or attribution. (NCT01754389)
Timeframe: 6 months

Intervention	Percentage of participants (Number)
Arm A (Standard of Care)	33
Arm B (Experimental)	31
Arm C (Experimental)	21

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Percentage of Participants With Non-relapse Mortality

Non-relapse mortality by 1 year after stem cell infusion. (NCT01754389)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Arm A (Standard of Care)	11
Arm B (Experimental)	15
Arm C (Experimental)	6.5

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Percentage of Participants With Chronic Graft Versus Host Disease

Rates of chronic GVHD 1 year after stem cell infusion (NCT01754389)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Arm A (Standard of Care)	59
Arm B (Experimental)	55
Arm C (Experimental)	55

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Percentage of Participants With Progression-free and Overall Survival

Progression-free and overall survival 1 year post stem cell infusion (NCT01754389)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
	Progression free survival	Overall survival
Arm A (Standard of Care)	64	72
Arm B (Experimental)	57	63
Arm C (Experimental)	57	70

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Percentage of Participants With Relapse

Relapse relapse-cum-immunosuppression-free survival at 1 year after stem cell infusion (NCT01754389)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Arm A (Standard of Care)	24
Arm B (Experimental)	28
Arm C (Experimental)	36

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Related Adverse Events (Grade 3, 4, 5)

Toxicity was assessed as related grade 3, 4, or 5 adverse events (AEs) per National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) v4.03. The outcome is reported as the total numbers of events (without dispersion) by CTCAE Body System, and whether the event was a hematologic toxicity or non-hematologic toxicity. (NCT01769209)
Timeframe: 45 days

Intervention	Treatment-related adverse events (Number)
	Blood and Lymphatic System Disorders	Gastrointestinal Disorders	Hepatobiliary disorders	Infections and Infestations	Investigations	Metabolism and Nutrition Disorders	Nervous System Disorders	Respiratory, Thoracic and Mediastinal Disorders	Vascular Disorders	Hematologic Toxicity	Non-hematologic Toxicity
Bortezomib + Chemotherapy	109	9	2	17	78	49	1	1	2	63	52

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Response Rate (RR)

"Response Rate (RR) was determined as the sum of complete response (CR) and partial response (PR). Due to overlap, complete response rate without platelet recovery (CRp) is not included in Response Rate (RR). The outcome is reported as the total number without dispersion.~CR = No circulating blasts or extramedullary disease; trilineage hematopoiesis; absolute neutrophil count (ANC) > 1,000/microliter; platelets > 100,000/microliter; < 5% blasts in bone marrow.~CRp = Meets all criteria for CR except platelet count.~PR = Meets all criteria for CR except bone marrow contains 5 to 25% leukemia cells." (NCT01769209)
Timeframe: Day 29

Intervention	Participants (Count of Participants)
Bortezomib + Chemotherapy	11

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Progression-free Survival (PFS)

"Progression-free survival (PFS) was assessed as survival without progression at 2 years. The outcome is reported as the number (without dispersion) of the participants alive without progression.~Progression = More than 25% increase in circulating and/or bone marrow blasts, or the development of extramedullary disease." (NCT01769209)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Bortezomib + Chemotherapy	3

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Failure-free Survival (FFS)

"Failure-free survival (FFS) was assessed as survival without progression or the addition of another systemic therapy, at or within 2 years. The outcome is reported as the number (without dispersion) of the participants alive without progression. Progression is defined below.~Progression = More than 25% increase in circulating and/or bone marrow blasts, or the development of extramedullary disease." (NCT01769209)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Bortezomib + Chemotherapy	3

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Overall Survival (OS)

Overall survival (OS) was assessed as participants remaining alive 2 years after induction therapy. The outcome is reported as the number of participants (without dispersion). (NCT01769209)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Bortezomib + Chemotherapy	5

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Complete Response (CR)

"Complete response (CR) was determined the number of participants who achieved CR by Day 29 after induction treatment. The outcome is reported as the total number without dispersion. CR is defined as:~CR = No circulating blasts or extramedullary disease; trilineage hematopoiesis; absolute neutrophil count (ANC) > 1,000/microliter; platelets > 100,000/microliter; < 5% blasts in bone marrow.~Not CR = All statuses and conditions if less than or not as defined." (NCT01769209)
Timeframe: Day 29

Intervention	Participants (Count of Participants)
Bortezomib + Chemotherapy	11

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Complete Response Without Platelet Recovery (CRp)

"Complete response without platelet recovery (CR) was determined as the number of participants who achieved CRp by Day 29 after induction treatment. The outcome is reported as the total number without dispersion. The outcome reflects only those subjects that meet all complete response (CR) criteria except platelet count; participants that meet all criteria including platelet count are not included in this outcome. CR and CRp are defined below.~CR =.No circulating blasts or extramedullary disease; trilineage hematopoiesis; absolute neutrophil count (ANC) > 1,000/microliter; platelets > 100,000/microliter; < 5% blasts in bone marrow.~CRp = Meets all criteria for CR except platelet count." (NCT01769209)
Timeframe: Day 29

Intervention	Participants (Count of Participants)
Bortezomib + Chemotherapy	1

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Objective Response Rate

"Participants are considered to have achieved an objective response if they meet the International Myeloma Working Group uniform response criteria for any of the following:~Stringent CR: Same as CR plus normal free light chain ratio and absence of clonal cells plasma cells in bone marrow (BM)~CR: Negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and <5% plasma cells in BM~VGPR: Serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein plus urine M-protein level <100 mg per 24 hours~PR: ≥50% reduction of serum M-protein and reduction in 24-h urinary M-protein by ≥90% or to <200 mg per 24 hours. If the serum and urinary M-protein are not measurable, additional criteria are used to assess PR that will not fit in the space provided here. If present at baseline, a ≥50% reduction in the size of plasmacytomas is also required" (NCT01782963)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
	Stringent Complete Response	Complete Response (CR)	Very Good Partial Response (VGPR)	Partial Response (PR)
Treatment Arm	6	16	11	10

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Mean Plasma Bortezomib Concentration Following Intravenous and and Subcutaneous Injection

The pharmacokinetic profile of intravenous and subcutaneous bortezomib administration in combination with lenalidomide and dexamethasone. (NCT01782963)
Timeframe: Day 1 (5 min, 30min, 5 hours post dose), Days 8, 15, Day 22 (pre dose and 5 min, 30 min, 5 hrs post dose), cycle 2 day 1 pre dose

Intervention	ng/mL (Mean)
	Day 1, 5 minutes (min) post dose	Day 1, 30 min post dose	Day 1, 5 hours post dose	Day 8 pre-dose	Day 15 pre-dose	Day 22 pre-dose	Day 22, 5 min post-dose	Day 22, 30 min post-dose	Day 22, 5 hours post-dose	Cycle 2 Day 1, pre-dose
Intravenous	98.84	8.73	1.82	0.44	0.66	0.83	114.3	14.9	2.85	0.53
Subcutaneous	13	20.5	1.96	0.33	0.49	0.66	10.29	21.69	4.16	0.49

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Median Time to Response

"Median amount of time from the start of treatment until first documented response as defined by the International Myeloma Working Group uniform response criteria~Stringent CR: Same as CR plus normal free light chain ratio and absence of clonal cells plasma cells in bone marrow (BM) CR: Negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and <5% plasma cells in BM VGPR: Serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein plus urine M-protein level <100 mg per 24 hours PR: ≥50% reduction of serum M-protein and reduction in 24-h urinary M-protein by ≥90% or to <200 mg per 24 hours. If the serum and urinary M-protein are not measurable, additional criteria are used to assess PR that will not fit in the space provided here. If present at baseline, a ≥50% reduction in the size of plasmacytomas is also required" (NCT01782963)
Timeframe: From the start of treatment until the time of first documented response, median duration of 1.1 months

Intervention	Months (Median)
Treatment Arm	1.1

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Median Progression Free Survival

"The median amount of time as measured from the start of treatment until either death or progression.~Progressive disease requires 1 or more of the following:~>=25% increase from lowest response level in serum M-protein (>=0.5 g/dL absolute increase) and/or urine M-component (>=200 mg/24hr absolute increase)~>=25% increase in the difference between involved and uninvolved FLC levels (absolute increase >10 mg/dL). Only for use in patients without measurable serum and M-protein levels.~>=25% increase in bone marrow plasma cell percentage (absolute percentage >=10%)~New or increase in existing bone lesions or soft tissue plasmacytomas~Hypercalcemia (serum calcium >11.5 mg/dL) due solely to the plasma cell proliferative disorder." (NCT01782963)
Timeframe: From the start of treatment until death or progression or until 3 years after the last participant is enrolled

Intervention	Months (Median)
Treatment Arm	35.1

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Median Overall Survival

The median overall survival as measured from the start of treatment until the time of death due to any cause. (NCT01782963)
Timeframe: From the start of treatment until death or until 5 years after the time of disease progression

Intervention	years (Median)
Treatment Arm	NA

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Number of Participants With Grade 3 or Higher Treatment Related Adverse Events

A summary of the number of participants with grade 3 or higher treatment related adverse events for adverse events that had an overall incidence of greater than 15% (any grade) as assessed by Common Terminology Criteria for Adverse Events (CTCAE 4). (NCT01782963)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
	Fatigue	Peripheral Neuropathy	Hypophosphatemia	Neutropenia	Diarrhea	Peripheral Edema	Insomnia	Rash	Anemia	Thrombocytopenia	Constipation	Dysgeusia	Hyperglycemia	Nausea	Depression	Psychiatric Disorder, other	Generalized Muscle Weakness
Treatment Arm	8	1	17	7	0	1	1	5	1	1	0	0	2	0	0	2	2

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Systemic Clearance (CL) of Bortezomib on Day 11 of Cycle 1

Systemic CL is a quantitative measure of the rate at which a drug substance is removed from the body. The total systemic clearance after intravenous dose was estimated by dividing the total administered dose by the plasma AUC(0-infinity). (NCT01801436)
Timeframe: 0 hour (Pre-dose) and 0.08, 0.25, 0.5, 1, 2, 4, 6, 8, 12, 24, 48, 72 hours (post-dose) on Day 11 of Cycle 1

Intervention	Liter per Hour (Mean)
Bortezomib	4.68

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Time to Reach Maximum Observed Plasma Concentration (Tmax) of Bortezomib on Day 1 of Cycle 1

Tmax is the time when Cmax is observed, taken directly from the plasma concentration-time profile. (NCT01801436)
Timeframe: 0 hour (Pre-dose) and 0.08, 0.25, 0.5, 1, 2, 4, 6, 8, 12, 24, 48, 72 hours (post-dose) on Day 1 of Cycle 1

Intervention	Hours (Mean)
Bortezomib	0.08

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Volume of Distribution at Steady-State (Vss) of Bortezomib on Day 11 of Cycle 1

Volume of distribution is defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired blood concentration of a drug. Steady state volume of distribution (Vss) is the apparent volume of distribution at steady-state which is estimated by (D/AUC[0-infinity])*(AUMC[0-infinity])/AUC[0-infinity]) where D is the dose of study drug, AUMC(0-infinity) is the area under the first moment curve extrapolated to infinity and AUC(0-infinity) is the area under the plasma concentration-time curve from time zero to infinite time. (NCT01801436)
Timeframe: 0 hour (Pre-dose) and 0.08, 0.25, 0.5, 1, 2, 4, 6, 8, 12, 24, 48, 72 hours (post-dose) on Day 11 of Cycle 1

Intervention	Liter (Mean)
Bortezomib	331.68

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Area Under the Plasma Concentration-Time Curve From Time Zero to Infinite Time (AUC[0-infinity]) of Bortezomib on Day 11 of Cycle 1

The AUC(0-infinity) is area under the plasma concentration-time curve from time zero to infinite time, calculated as the sum of AUC(last) and C(last)/lambda(z), in which C(last) is the last observed quantifiable concentration. (NCT01801436)
Timeframe: 0 hour (Pre-dose) and 0.08, 0.25, 0.5, 1, 2, 4, 6, 8, 12, 24, 48, 72 hours (post-dose) on Day 11 of Cycle 1

Intervention	Hour*ng per ml (Mean)
Bortezomib	349.62

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Area Under the Plasma Concentration-Time Curve From Time Zero to Time at Last Observed Quantifiable Concentration (AUC[0-t]) of Bortezomib on Day 1 of Cycle 1

The AUC(0-t) is area under the plasma concentration-time curve from time zero to the last quantifiable concentration determined by the trapezoidal rule. (NCT01801436)
Timeframe: 0 hour (Pre-dose) and 0.08, 0.25, 0.5, 1, 2, 4, 6, 8, 12, 24, 48, 72 hours (post-dose) on Day 1 of Cycle 1

Intervention	Hour*ng per ml (Mean)
Bortezomib	51.86

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Number of Participants With Response to Treatment at Day 11 of Cycle 8

Response to treatment was based on the changes in monoclonal protein (M-protein) in serum and urine. Response categories were complete response: complete clearance of M-protein for at least 6 weeks, response: at least 75 percent reduction in M-protein for at least 2 determinations 6 weeks apart, partial response: 50 to 74 percent reduction in M-protein, minimal response: 25 to 49 percent reduction in M-protein, stable disease: not qualifying minimal response or progression and progression: increased M-protein level in serum or urine or clinical signs of disease progression. (NCT01801436)
Timeframe: Day 11 of Cycle 8

Intervention	Participants (Number)
	Response	Partial response	Minimal response	Stable disease	Progression
Bortezomib	2	3	2	1	6

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Number of Participants With Response to Treatment at Day 1 of Cycle 7

Intervention	Participants (Number)
	Response	Partial Response	Stable disease
Bortezomib	1	3	1

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Number of Participants With Response to Treatment at Day 1 of Cycle 5

Intervention	Participants (Number)
	Complete response	Response	Partial Response	Stable disease	Progression
Bortezomib	1	2	2	1	1

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Number of Participants With KPS Score at Day 11 of Cycle 8

The KPS Index allows participants to be classified as per their functional impairment (abnormal function). This can be used to compare effectiveness of different therapies (medicine or medical care given to a participant for a disease or condition) and to assess the prognosis (outlook, probable outcomes) in individual participants. KPS was recorded on an 11-point scale (0, 10, 20, 30, 40, 50, 60, 70, 80, 90, and 100.) where '0=Dead' and '100=Normal, no complaints, no evidence of disease'. The lower the Karnofsky score, the worse the survival for most serious illnesses. (NCT01801436)
Timeframe: Day 11 of Cycle 8

Intervention	Participants (Number)
	KPS Score = 50	KPS Score = 60	KPS Score = 70	KPS Score = 80	KPS Score = 90	KPS Score = 100
Bortezomib	2	4	1	3	2	2

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Number of Participants With KPS Score at Day 1 of Cycle 7

Intervention	Participants (Number)
	KPS Score = 60	KPS Score = 80	KPS Score = 90	KPS Score = 100
Bortezomib	1	2	1	1

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Number of Participants With KPS Score at Day 1 of Cycle 5

Intervention	Participants (Number)
	KPS Score = 60	KPS Score = 70	KPS Score = 80	KPS Score = 100
Bortezomib	1	1	4	1

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Number of Participants With KPS Score at Day 1 of Cycle 3

Intervention	Participants (Number)
	KPS Score = 60	KPS Score = 70	KPS Score = 80	KPS Score = 90	KPS Score = 100
Bortezomib	1	1	6	2	2

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Number of Participants With KPS Score at Day 1 of Cycle 1

Intervention	Participants (Number)
	KPS Score = 70	KPS Score = 80	KPS Score = 90	KPS Score = 100
Bortezomib	2	5	5	2

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Number of Participants With Karnofsky Performance Status (KPS) Score at Baseline

Intervention	Participants (Number)
	KPS Score = 70	KPS Score = 80	KPS Score = 90	KPS Score = 100
Bortezomib	2	3	7	2

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Area Under the Plasma Concentration-Time Curve From Time Zero to Time at Last Observed Quantifiable Concentration (AUC[0-t]) of Bortezomib on Day 11 of Cycle 1

The AUC(0-t) is area under the plasma concentration-time curve from zero to the last quantifiable concentration determined by the trapezoidal rule. (NCT01801436)
Timeframe: 0 hour (Pre-dose) and 0.08, 0.25, 0.5, 1, 2, 4, 6, 8, 12, 24, 48, 72 hours (post-dose) on Day 11 of Cycle 1

Intervention	Hour*ng per mL (Mean)
Bortezomib	190.39

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Volume of Distribution at Steady-State (Vss) of Bortezomib on Day 1 of Cycle 1

Intervention	Liter (Mean)
Bortezomib	483.71

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Time to Reach Maximum Observed Plasma Concentration (Tmax) of Bortezomib on Day 11 of Cycle 1

Intervention	Hours (Mean)
Bortezomib	0.08

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Elimination Half-Life Period (T1/2) of Bortezomib on Day 1 of Cycle 1

The T1/2 is the time measured for the plasma concentration to decrease by 1 half to its original concentration. It is associated with the terminal rate-constant (lambda[z]) of the semi logarithmic drug concentration-time curve, and is calculated as 0.693/lambda(z). (NCT01801436)
Timeframe: 0 hour (Pre-dose) and 0.08, 0.25, 0.5, 1, 2, 4, 6, 8, 12, 24, 48, 72 hours (post-dose) on Day 1 of Cycle 1

Intervention	Hours (Mean)
Bortezomib	0.08

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Terminal Rate Constant (Lambda[z]) of Bortezomib on Day 11 of Cycle 1

Lambda(z) is defined as terminal rate-constant which reflect the speed of drug elimination in vivo (within the living), and is estimated by log-linear regression analysis of the terminal phase of the plasma concentration versus time curve for at least 3 points. (NCT01801436)
Timeframe: 0 hour (Pre-dose) and 0.08, 0.25, 0.5, 1, 2, 4, 6, 8, 12, 24, 48, 72 hours (post-dose) on Day 11 of Cycle 1

Intervention	Per Hour (Mean)
Bortezomib	0.01

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Terminal Rate Constant (Lambda[z]) of Bortezomib on Day 1 of Cycle 1

Intervention	Per Hour (Mean)
Bortezomib	0.08

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Area Under First Moment Plasma Concentration-Time Curve (AUMC) of Bortezomib on Day 1 of Cycle 1

AUMC is defined as the area under first moment plasma concentration-time curve from time of dosing up to definite time t, to infinity, or to the time of last measurable concentration determined by the following equation: AUMC(0 to infinity)=Cntn/k elimination(el) + Cn/k(el^2) summation[(tn - tn^-1) (Cn^-1) (tn^-1)] + Cntn/2 where Cn=last quantifiable concentration, tn=time at which Cn is measured, k=rate constant. (NCT01801436)
Timeframe: 0 hour (Pre-dose) and 0.08, 0.25, 0.5, 1, 2, 4, 6, 8, 12, 24, 48, 72 hours (post-dose) on Day 1 of Cycle 1

Intervention	Hour square*ng per ml (Mean)
Bortezomib	20678.41

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Area Under First Moment Plasma Concentration-Time Curve (AUMC) of Bortezomib on Day 11 of Cycle 1

Intervention	Hour square*ng per ml (Mean)
Bortezomib	39414.06

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Area Under the Plasma Concentration-Time Curve From Time Zero to Infinite Time (AUC[0-infinity]) of Bortezomib on Day 1 of Cycle 1

Intervention	Hour*ng per ml (Mean)
Bortezomib	106.99

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Elimination Half-Life Period (T1/2) of Bortezomib on Day 11 of Cycle 1

Intervention	Hours (Mean)
Bortezomib	51.55

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Maximum Observed Plasma Concentration (Cmax) of Bortezomib on Day 1 of Cycle 1

The Cmax is observed maximum plasma concentration, taken directly from the plasma concentration-time profile. (NCT01801436)
Timeframe: 0 hour (Pre-dose) and 0.08, 0.25, 0.5, 1, 2, 4, 6, 8, 12, 24, 48, 72 hours (post-dose) on Day 1 of Cycle 1

Intervention	Nanogram per millileter (ng per ml) (Mean)
Bortezomib	76.43

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Maximum Observed Plasma Concentration (Cmax) of Bortezomib on Day 11 of Cycle 1

Intervention	ng per ml (Mean)
Bortezomib	127.02

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Mean Residence Time (MRT) of Bortezomib in the Body on Day 1 of Cycle 1

The MRT is the average time at which the number of absorbed molecules reside in the body, after single-dose administration, and calculated as AUMC(infinity)/AUC(infinity) where AUMC(infinity) is area under the plasma concentration-time first moment curve from time zero to infinite time and AUC(infinity) is the area under the plasma concentration-time curve from time zero to infinite time. (NCT01801436)
Timeframe: 0 hour (Pre-dose) and 0.08, 0.25, 0.5, 1, 2, 4, 6, 8, 12, 24, 48, 72 hours (post-dose) on Day 1 of Cycle 1

Intervention	Hour (Mean)
Bortezomib	65.97

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Mean Residence Time (MRT) of Bortezomib in the Body on Day 11 of Cycle 1

Intervention	Hour (Mean)
Bortezomib	88.74

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Systemic Clearance (CL) of Bortezomib on Day 1 of Cycle 1

Intervention	Liter per Hour (Mean)
Bortezomib	25.99

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Complete Response Rate

"Complete response rate was defined as the percentage of participants in each treatment group who achieved a sCR or CR per the IMWG-URC as their best response.~sCR: As for CR, normal serum free light chain (SFLC) ratio and no clonal cells in bone marrow (BM).~CR: No immunofixation on serum and urine, disappearance of any soft tissue plasmacytomas and < 5% plasma cells in BM biopsy." (NCT01818752)
Timeframe: Disease response was assessed every 3 weeks during the first 54 weeks and every 6 weeks thereafter until PD or the data cut-off date of 15 July 2016; median follow-up time was 21.6.and 22.2 months in the bortezomib and carfilzomib arms respectively.

Intervention	percentage of participants (Number)
Bortezomib, Melphalan, Prednisone	23.1
Carfilzomib, Melphalan, Prednisone	25.9

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Overall Response Rate

"Disease response was evaluated according to the IMWG-URC using a validated computer algorithm. Overall response was defined as the percentage of participants with a best overall response of stringent complete response (sCR), complete response (CR), very good partial response (VGPR), or partial response (PR).~sCR: As for CR, normal serum free light chain (SFLC) ratio and no clonal cells in bone marrow (BM).~CR: No immunofixation on serum and urine, disappearance of any soft tissue plasmacytomas and < 5% plasma cells in BM biopsy; VGPR: Serum and urine M-protein detectable by immunofixation but not electrophoresis or ≥ 90% reduction in serum M-protein with urine M-protein <100 mg/24 hours. A ≥ 50% reduction in the size of soft tissue plasmacytomas if present at baseline.~PR: ≥ 50% reduction of serum M-protein and reduction in urine M-protein by ≥ 90% or to < 200 mg/24 hours. A ≥ 50% reduction in the size of soft tissue plasmacytomas if present at baseline." (NCT01818752)
Timeframe: Disease response was assessed every 3 weeks during the first 54 weeks and every 6 weeks thereafter until PD or the data cut-off date of 15 July 2016; median follow-up time was 21.6.and 22.2 months in the bortezomib and carfilzomib arms respectively.

Intervention	percentage of participants (Number)
Bortezomib, Melphalan, Prednisone	78.8
Carfilzomib, Melphalan, Prednisone	84.3

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Overall Survival (OS)

"Overall survival (OS) was defined as the time from randomization to the date of death (whatever the cause). Participants who were alive or lost to follow-up as of the data analysis cut-off date were censored on the date the patient was last known to be alive.~Median overall survival was estimated using the Kaplan-Meier method." (NCT01818752)
Timeframe: From randomization until the data cut-off date of 15 July 2016; median follow-up time for OS was 22.2 and 22.5 months in the bortezomib and carfilzomib arms respectively.

Intervention	months (Median)
Bortezomib, Melphalan, Prednisone	NA
Carfilzomib, Melphalan, Prednisone	NA

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Percentage of Participants With ≥ Grade 2 Peripheral Neuropathy

"Neuropathy events were defined as Grade 2 or higher peripheral neuropathy as specified by peripheral neuropathy Standardised Medical Dictionary for Regulatory Activities (MedDRA) Query, narrow (scope) (SMQN) terms.~Peripheral neuropathy was assessed by neurologic exam and graded according to National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) Version 4.03:~Grade 1: Asymptomatic; Grade 2: Moderate symptoms, limiting instrumental activities of daily living (ADL) Grade 3: Severe symptoms; limiting self-care ADL; Grade 4: Life-threatening consequences, urgent intervention indicated; Grade 5: Death." (NCT01818752)
Timeframe: From the first dose of any study drug up to 30 days after the last dose of any study drug as of the data cut-off date of 15 July 2016; median duration of treatment was 52 weeks in both treatment groups.

Intervention	percentage of participants (Number)
Bortezomib, Melphalan, Prednisone	35.1
Carfilzomib, Melphalan, Prednisone	2.5

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Progression-Free Survival (PFS)

"Progression-free survival was defined as the time from randomization to the earlier of documented disease progression or death due to any cause. PFS was analyzed using Kaplan-Meier methods. The duration of PFS was censored for participants with no baseline and/or post-baseline disease assessments, who started a new anti-cancer therapy before documentation of disease progression or death, death or disease progression after missed disease assessment of 100 consecutive days or longer, or who were alive without documentation of disease progression before the data cutoff date, including lost to follow-up prior to disease progression.~Participants were evaluated for disease response and progression according to the International Myeloma Working Group Uniform Response Criteria (IMWG-URC), determined centrally using a validated computer algorithm in a blinded manner." (NCT01818752)
Timeframe: From randomization until the data cut-off date of 15 July 2016; median follow-up time for PFS was 21.6.and 22.2 months in the bortezomib and carfilzomib arms respectively.

Intervention	months (Median)
Bortezomib, Melphalan, Prednisone	22.1
Carfilzomib, Melphalan, Prednisone	22.3

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Number of Participants With Adverse Events

"Adverse events (AEs)were graded using National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE), version 4.03, where GRADE 1 = Mild; GRADE 2 = Moderate; GRADE 3 = Severe; GRADE 4 = Life-threatening; GRADE 5 = Fatal.~A serious adverse event is an adverse event that met 1 or more of the following criteria:~Death~Life-threatening~Required inpatient hospitalization or prolongation of an existing hospitalization~Resulted in persistent or significant disability/incapacity~Congenital anomaly/birth defect~Important medical event that jeopardized the participant and may have required medical or surgical intervention to prevent 1 of the outcomes listed above.~Treatment-related adverse events are adverse events considered related to at least 1 investigational product by the investigator, including those with unknown relationship." (NCT01818752)
Timeframe: From the first dose of any study drug up to 30 days after the last dose of any study drug as of the data cut-off date of 15 July 2016; median duration of treatment was 52 weeks in both treatment groups.

Intervention	participants (Number)
	All adverse events	AEs ≥ grade 3	Serious adverse events	Leading to discontinuation of study drug	Fatal adverse events	Treatment-related adverse events (TRAEs)	TRAEs ≥ grade 3	Treatment-related serious adverse events	TRAE leading to discontinuation of study drug	Treatment-related fatal adverse events
Bortezomib, Melphalan, Prednisone	454	358	198	73	20	431	285	102	51	5
Carfilzomib, Melphalan, Prednisone	460	354	235	83	31	408	268	136	54	10

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European Organisation for Research and Treatment of Cancer Quality of Life Core Module (EORTC QLQ-C30) Global Health Status/Quality of Life (QOL) Scores

"The EORTC QLQ-C30 is a validated self-rating questionnaire including 30 items used to assess the overall quality of life in cancer patients.~It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact).~The EORTC QLQ-C30 Global Health Status/QOL scale was scored between 0 and 100, with higher scores indicating better Global Health Status/QOL." (NCT01818752)
Timeframe: Baseline, weeks 6, 12, 18, 24, 30, 36, 42 and 48

Intervention	units on a scale (Mean)
	Baseline (n = 425, 425)	Week 6 (n = 412, 407)	Week 12 (n = 376, 389)	Week 18 (n = 341, 369)	Week 24 (n = 320, 345)	Week 30 (n = 298, 317)	Week 36 (n = 285, 308)	Week 42 (n = 275, 288)	Week 48 (n = 261, 265)
Bortezomib, Melphalan, Prednisone	53.3	56.2	55.3	55.7	57.3	61.6	61.9	63.3	62.9
Carfilzomib, Melphalan, Prednisone	53.9	61.1	62.4	63.2	63.3	63.0	64.0	65.0	65.1

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Participants Evaluated for Toxicity

Intervention	Participants (Count of Participants)
Bortezomib	17

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Overall Survival

(NCT01833143)
Timeframe: 2 years

Intervention	months (Median)
Bortezomib	13

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Progression Free Survival

Intervention	months (Median)
Bortezomib	1

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Percentage of Participants With Serious Treatment-Related Complications

Percentage of participants with severe complications defined at ICU admission and death, graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) version 4.0. (NCT01849783)
Timeframe: From the start of DPACE for all participants who have had at least one day of protocol treatment. Up to 6 years.

Intervention	Participants (Count of Participants)
Autologous Stem Cell Transplant	4

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Mean Change in Quality-Of-Life Indicators Post-Transplant

Measured using the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ-C30) and Multiple Myeloma module (QLQ-MY20). The EORTC QLQ-C30 includes functional scales (physical, role, emotional, cognitive, and social) and global health status. The EORTC QLQ-MY20 includes disease symptoms and treatment side effects scales. Scores are averaged and transformed to 0-100 scale. For functional and global health status, a positive change from baseline (pre-DPACE) indicates improvement whereas for the symptom scales a negative change from baseline (pre-DPACE) indicates improvement. (NCT01849783)
Timeframe: Pre-DPACE, Pre-maintenance, every 6 months for up to 2 years during maintenance. Up to 6 years.

Intervention	score on a scale (Mean)
	Change in Physical Functioning at Pre-Maintenance	Change in Physical Functioning at Maintenance Cycle 6	Change in Physical Functioning at Maintenance Cycle 12	Change in Physical Functioning at Maintenance Cycle 18	Change in Physical Functioning at Maintenance Cycle 24	Change in Role Functioning at Pre-Maintenance	Change in Role Functioning at Maintenance Cycle 6	Change in Role Functioning at Maintenance Cycle 12	Change in Role Functioning at Maintenance Cycle 18	Change in Role Functioning at Maintenance Cycle 24	Change in Emotional Functioning at Pre-Maintenance	Change in Emotional Functioning at Maintenance Cycle 6	Change in Emotional Functioning at Maintenance Cycle 12	Change in Emotional Functioning at Maintenance Cycle 18	Change in Emotional Functioning at Maintenance Cycle 24	Change in Cognitive Functioning at Pre-Maintenance	Change in Cognitive Functioning at Maintenance Cycle 6	Change in Cognitive Functioning at Maintenance Cycle 12	Change in Cognitive Functioning at Maintenance Cycle 18	Change in Cognitive Functioning at Maintenance Cycle 24	Change in Social Functioning at Pre-Maintenance	Change in Social Functioning at Maintenance Cycle 6	Change in Social Functioning at Maintenance Cycle 12	Change in Social Functioning at Maintenance Cycle 18	Change in Social Functioning at Maintenance Cycle 24	Change in Global Health Status at Pre-Maintenance	Change in Global Health Status at Maintenance Cycle 6	Change in Global Health Status at Maintenance Cycle 12	Change in Global Health Status at Maintenance Cycle 18	Change in Global Health Status at Maintenance Cycle 24	Change in Distress Symptoms at Pre-Maintenance	Change in Distress Symptoms at Maintenance Cycle 6	Change in Distress Symptoms at Maintenance Cycle 12	Change in Distress Symptoms at Maintenance Cycle 18	Change in Distress Symptoms at Maintenance Cycle 24	Change in Side Effects of Treatment at Pre-Maintenance	Change in Side Effects of Treatment at Maintenance Cycle 6	Change in Side Effects of Treatment at Maintenance Cycle 12	Change in Side Effects of Treatment at Maintenance Cycle 18	Change in Side Effects of Treatment at Maintenance Cycle 24
Autologous Stem Cell Transplant	1.3	-0.6	1.1	5.4	4.6	7.4	8.7	4.4	7.0	6.0	8.7	5.5	1.4	5.8	8.3	0.4	-4.6	-5.1	-6.0	-3.6	-1.0	2.7	-4.9	0.8	-1.5	5.4	0.2	-3.1	-0.1	3.4	6.2	5.9	5.7	3.8	5.3	-3.3	-0.7	-5.1	-2.4	-2.7

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Percentage of Participants Able to Complete Full Course Therapy

Percentage of participants able to complete the full course of therapy. (NCT01849783)
Timeframe: Up to 6 years

Intervention	Participants (Count of Participants)
Autologous Stem Cell Transplant	24

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Median Progression Free Survival (mPFS)

PFS is defined as the time from the start of DPACE to the date of first documentation of disease progression as assessed by the International Myeloma Working Group response criteria or death due to any cause. Progression is defined using the International Myeloma Working Group response criteria, an increase of greater than or equal to 25% from the lower response value. (NCT01849783)
Timeframe: From the start of DPACE for all participants who have had at least one day of protocol treatment. Up to 6 years.

Intervention	months (Median)
Autologous Stem Cell Transplant	76.4

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GVHD

"aGVHD onset at a certain grade will be used to calculate the cumulative incidence for that grade (e.g., onset of grade 70 post-transplant , time to grade III is 70 days). This end point will be evaluated through day 150 post-transplant. The diagnosis of aGVHD is based on clinical and pathological evaluation by the treating physician.~The first day of cGVHD will be used to calculate the cumulative incidence of cGVHD. The diagnosis of cGVHD is based on clinical and pathological evaluation by the treating physician." (NCT01860170)
Timeframe: Assessed routinely by clinical and pathological evaluation. Acute GVHD will be assessed up to day 150 post-transplant. Chronic GVHD will be assess up to 2 years post-transplant.

Intervention	participants (Number)
	Acute GvHD Grade II-IV	Acute GvHD Grade III-IV	Chronic GvHD
Cohort 1-Bortezomib (Velcade®)	0	0	1
Cohort 2-Bortezomib (Velcade®)	0	0	1
Cohort 3-Bortezomib (Velcade®)	10	3	5

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Dose Limiting Toxicity

Grade 3 non-hematologic Common Toxicity Criteria toxicity directly related to bortezomib (such as peripheral neuropathy) or Grade 2 or > hepatic bilirubin Common Toxicity Criteria Graft failure (NCT01860170)
Timeframe: Assessed daily (while inpatient) through clinical and laboratory examination up to 90 days.

Intervention	Participants (Count of Participants)
Cohort 1-Bortezomib (Velcade®)	0
Cohort 2-Bortezomib (Velcade®)	0
Cohort 3-Bortezomib (Velcade®)	0

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Engraftment

"Neutrophil engraftment is defined as achieving an absolute neutrophil count (ANC) > 0.5 109/L for 3 consecutive measurements on different days. The first of the 3 days will be considered the day of neutrophil engraftment.~Platelet engraftment is defined as platelet count > 20 109/L for 3 consecutive measurements over at least 3 days. The first of the 3 days will be considered the day of platelet engraftment.~In this study, graft failure is defined as lack of achieving neutrophil engraftment by day 22 and donor chimerism > 50% by day 45." (NCT01860170)
Timeframe: Assessed daily by laboratory evaluation until engraftment or up to 90 days.

Intervention	Participants (Count of Participants)
	Neutrophil Engraftment	Platelet Engraftment	Graft Failure
Cohort 1-Bortezomib (Velcade®)	3	3	0
Cohort 2-Bortezomib (Velcade®)	3	1	0
Cohort 3-Bortezomib (Velcade®)	22	22	0

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Overall Response (OR)

Primary outcome is overall response (OR) including hematologic improvement defined by International Working Group (IWG), complete remission, partial remission and marrow complete remission. (NCT01891968)
Timeframe: 8 weeks

Intervention	Participants (Count of Participants)
Bortezomib	3

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Number of Participants With Response

"For Autoimmune Hemolytic Anemia- At least 3 of 5 criteria should be met.~Stabilization of hemoglobin without transfusions by 2 weeks~Conversion of DAT from + to - by 6 weeks~Normalization of serum haptoglobin levels by 6 weeks~Normalization of indirect bilirubin levels by 6 weeks~Reduction in the frequency of transfusions by 50% by 4 weeks~For Autoimmune Neutropenia- At least 2 of 3 criteria should be met.~Stabilization of absolute neutrophil count by 2 weeks~Undetectable antineutrophil antibodies by 6 weeks~Reduction in GCSF dose by 50% by 6 weeks~For Autoimmune Thrombocytopenia- At least 2 of 3 criteria should be met.~Stabilization of platelet count without platelet transfusions by 2 weeks~Undetectable antiplatelet antibodies by 6 weeks~Reduction in the frequency of platelet transfusions by 50% from pre-bortezomib values by 6 weeks" (NCT01929980)
Timeframe: 6 weeks

Intervention	participants (Number)
	Neutropenia (n=3)	Thrombocytopenia (n=2)	Hemolytic Anemia (n=1)
Bortezomib	3	2	1

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>= 2 Fold Increase in Circulating PBSC's

Participants with >= 2 fold increase in circulating PBSC's in blood and in apheresis collections in up to 4-days collection (NCT02037256)
Timeframe: Up to 6 months

Intervention	Participants (Count of Participants)
	Doubling	Less than doubling
Group A: Bortezomib 1.3 mg/m2	0	3
Group B Bortezomib 1/3 mg/m2	4	13

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Time to Neutrophil Engraftment

Estimated Median Time to Neutrophil Engraftment, ANC 500 (NCT02037256)
Timeframe: Up to 6 months

Intervention	days to ANC 500 (Median)
Arm A Standard of Care Mobilization	12
Arm B Alternative Mobilization	13

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Recommended Dose of Dexamethasone in Combination With Plitidepsin and Bortezomib

To determine the recommended dose (RD) of plitidepsin in combination with bortezomib and dexamethasone in patients with relapsed and/or refractory multiple myeloma (MM). To define the RD, patients will be evaluated for DLTs during the first 28-day cycle. The RD will be the highest DL at which fewer than two out of six (33%) of evaluable patients experience a DLT during the first 28-day cycle. (NCT02100657)
Timeframe: After 28-day cycle

Intervention	mg of dexamethasone (Number)
All Participants	40.0

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Progression-free Survival Rates

Progression-free survival (PFS) was calculated from the date of the first infusion to the date of documented PD or death (regardless of the reason), whichever comes first (NCT02100657)
Timeframe: From the date of the first infusion to the date of documented PD or death, up to 4 years

Intervention	percentage of participants (Mean)
	At 3 months	At 6 months	At 12 months
Plitidepsin (4 mg/m2)+BTZ (1 mg/m2)+DXM (40 mg)	85.7	71.4	35.7
Plitidepsin (4 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	100.0	66.7	66.7
Plitidepsin (5 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	44.4	26.7	13.3

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Overall Response Rate

Overall response rate (ORR), including stringent complete response (sCR), complete response (CR), very good partial response (VGPR) and partial response (PR) according to the International Myeloma Working Group (IMWG) criteria (NCT02100657)
Timeframe: Response or disease progression was assessed on Day 1 of each cycle, assessed up to 4 years

Intervention	percentage of participants (Mean)
Plitidepsin (4 mg/m2)+BTZ (1 mg/m2)+DXM (40 mg)	57.1
Plitidepsin (4 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	66.7
Plitidepsin (5 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	22.2

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Event-free Survival Rates

Event-free survival (EFS) was calculated from the date of first infusion to the date of documented PD or death, but could include additional events besides death and PD that were considered of importance (NCT02100657)
Timeframe: from the date of first infusion to the date of documented PD or death, up to 4 years

Intervention	percentage of participants (Mean)
	At 3 months	At 6 months	At 12 months
Plitidepsin (4 mg/m2)+BTZ (1 mg/m2)+DXM (40 mg)	85.7	71.4	35.7
Plitidepsin (4 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	100.0	66.7	66.7
Plitidepsin (5 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	44.4	26.7	13.3

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Time to Progression

Time to progression (TTP) was calculated from the date of the first infusion to the date of documented PD or death due to PD. (NCT02100657)
Timeframe: From the date of the first infusion to the date of documented PD or death due to PD, up to 4 years

Intervention	months (Median)
Plitidepsin (4 mg/m2)+BTZ (1 mg/m2)+DXM (40 mg)	10.4
Plitidepsin (4 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	13.6
Plitidepsin (5 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	2.8

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Number of Participants Who Experienced Dose-Limiting Toxicities (DLTs)

"DLTs were defined as:~Hematological Toxicity~Grade 3/4 neutropenia associated with fever or lasting>7 days related to the study treatment~Grade 3/4 thrombocytopenia accompanied by grade 3/4 hemorrhage~Extensive bone marrow (BM) infiltration, DLT was defined as grade 4 thrombocytopenia with grade 3/4 hemorrhage or grade 4 neutropenia lasting >7 days or with fever Non-hematological Toxicity~Grade 3/4 nausea and vomiting refractory to antiemetic therapy~Grade≥3 muscular Adverse events (AE) (myalgia, muscular weakness, muscle cramps, myopathy)~Grade≥3 alanine aminotransferase (ALT)/Aspartate aminotransferase (AST) lasting more than 1 week~Grade≥3 bilirubin increase~Grade≥3 creatine phosphokinase (CPK) increase~Cardiac toxicity~Symptomatic or treatment-requiring grade ≥1 cardiac arrhythmia related to plitidepsin~Grade≥1 left ventricular systolic dysfunction related to plitidepsin~Neuropathic pain and peripheral sensory neuropathy related to BTZ" (NCT02100657)
Timeframe: After 28-day cycle

Intervention	Participants (Count of Participants)
Plitidepsin (4 mg/m2)+BTZ (1 mg/m2)+DXM (40 mg)	0
Plitidepsin (4 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	0
Plitidepsin (5 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	2

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Event-free Survival

Event-free survival (EFS) was calculated from the date of first infusion to the date of documented PD or death, but could include additional events besides death and PD that were considered of importance (NCT02100657)
Timeframe: From the date of first infusion to the date of documented PD or death, up to 4 years

Intervention	months (Median)
Plitidepsin (4 mg/m2)+BTZ (1 mg/m2)+DXM (40 mg)	10.4
Plitidepsin (4 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	13.6
Plitidepsin (5 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	2.8

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Duration of Response

Duration of response (DR) was analyzed for all patients in whom a response had been observed and was calculated from the date of the first documentation of response to the date of PD or further therapy or death (NCT02100657)
Timeframe: From the date of the first documentation of response to the date of PD or further therapy or death, up to 4 years

Intervention	months (Median)
Plitidepsin (4 mg/m2)+BTZ (1 mg/m2)+DXM (40 mg)	21.0
Plitidepsin (4 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	12.6
Plitidepsin (5 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	12.3

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Recommended Dose of Plitidepsin in Combination With Bortezomib and Dexamethasone

Intervention	mg/m^2 of plitidepsin (Number)
All Participants	5.0

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Recommended Dose of Bortezomib in Combination With Plitidepsin and Dexamethasone

Intervention	mg/m^2 of bortezomib (Number)
All Participants	1.3

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Progression-free Survival

Progression-free survival (PFS) was calculated from the date of the first infusion to the date of documented PD or death (regardless of the reason), whichever comes first (NCT02100657)
Timeframe: from the date of the first infusion to the date of documented PD or death, up to 4 years

Intervention	months (Mean)
Plitidepsin (4 mg/m2)+BTZ (1 mg/m2)+DXM (40 mg)	10.4
Plitidepsin (4 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	13.6
Plitidepsin (5 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	2.8

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Time to Progression Rates

Intervention	percentage of participants (Mean)
	At 3 months	At 6 months	At 12 months
Plitidepsin (4 mg/m2)+BTZ (1 mg/m2)+DXM (40 mg)	85.7	71.4	35.7
Plitidepsin (4 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	100.0	66.7	66.7
Plitidepsin (5 mg/m2)+BTZ (1.3 mg/m2)+DXM (40 mg)	44.4	26.7	13.3

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Event-free Survival (EFS) for Modified Augmented Berlin-Frankfurt-Munster Backbone With or Without Bortezomib in All Randomized Patients

EFS is calculated as time from randomization at study entry to first event (induction failure, induction death, relapse, second malignancy, remission death) or date of last contact. Three-year EFS rates will be calculated for both groups. (NCT02112916)
Timeframe: 3 years

Intervention	Percentage of participants (Number)
Arm A (Combination Chemotherapy)	81.7
Arm B (Combination Chemotherapy, Bortezomib)	85.1

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EFS for Very High Risk (VHR) T-LLy Patients Treated With HR Berlin-Frankfurt-Munster (BFM) Intensification Blocks Who Have Complete or Partial Remission and Those Who do Not Respond

EFS for very high risk (VHR) T-LLy patients treated with HR Berlin-Frankfurt-Munster (BFM) intensification blocks who have complete or partial remission and those who do not respond (NCT02112916)
Timeframe: 3 years

Intervention	Percentage of participants (Number)
VHR T-LLy (CR/PR)	0

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EFS for Very High Risk (VHR) T-ALL Patients Treated With High Risk (HR) Berlin-Frankfurt-Munster (BFM) Intensification Blocks Who Become Minimal Residual Disease (MRD) Negative and Those Who Remain MRD Positive at the End of HR Block 3

EFS will be calculated as time from the end of the three high-risk blocks of therapy to first event (relapse, second malignancy, remission death) or date of last contact. (NCT02112916)
Timeframe: 3 years

Intervention	Percentage of participants (Number)
VHR T-ALL MRD Undetectable	25.0
VHR T-ALL MRD Detectable	88.9

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EFS for Standard (SR) and Intermediate Risk (IR) T-ALL Patients on the Non-bortezomib Containing Arm on This Study (no Cranial Radiation Therapy [CRT]) and Similar Patients on AALL0434 (Received CRT)

Intervention	Percentage of participants (Number)
AALL1231 T-ALL Patients	88.3
AALL0434 T-ALL Patients	88.8

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Toxicity Rates Associated With Modified Standard Therapy, Including Dexamethasone and Additional Pegaspargase

Percentage of patients who experienced Grade 3 or higher Toxicity Assessed by the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) Version 4.0 (NCT02112916)
Timeframe: 3 years from start of therapy by patient

Intervention	Percentage of participants (Number)
Total Patients	78.0

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Cumulative Incidence Rates of Isolated Central Nervous System (CNS) Relapse for SR and IR T-ALL Patients on the Non-bortezomib Containing Arm on This Study (no CRT) and Similar Patients on AALL0434 (Receive CRT)

Cumulative incidence of isolated CNS relapse adjusting for competing risks using the method of: Gray R, A class of K-sample tests for comparing the cumulative incidence of a competing risk. Ann Stat 1141:1154, 1988 (NCT02112916)
Timeframe: 3 years

Intervention	Percentage of participants (Number)
	Isolated CNS Relapse	Isolated Bone Marrow Relapse	Combined Bone Marrow Relapse
AALL0434 T-ALL Patients	2.2	3.0	1.8
AALL1231 T-ALL Patients	3.6	1.4	1.3

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Progression-free Survival (PFS)

PFS was defined as duration from date of randomization to either progressive disease (PD)/death, whichever occurred first. PD was defined as meeting any one of following criteria: Increase of greater than equal to (>=)25 percent (%) in level of serum M-protein from lowest response value and absolute increase must be >=0.5 gram per deciliter (g/dL); Increase of >=25% in 24-hour urinary light chain excretion (urine M-protein) from lowest response value and absolute increase must be >=200 mg/24hours; Only in participants without measurable serum and urine M-protein levels: increase of >=25% in difference between involved and uninvolved FLC levels from lowest response value and absolute increase must be >10 mg/dL; Definite increase in size of existing bone lesions or soft tissue plasmacytomas; Definite development of new bone lesions or soft tissue plasmacytomas; Development of hypercalcemia (corrected serum calcium >11.5 mg/dL) that can be attributed solely to PC proliferative disorder. (NCT02136134)
Timeframe: From the date of randomization to either progressive disease or death, whichever occurs first (approximately 3 years)

Intervention	months (Median)
Bortezomib + Dexamethasone (Vd)	7.16
Daratumumab + Bortezomib and Dexamethasone (DVd)	NA

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Time to Disease Progression (TTP)

TTP was defined as time from date of randomization to date of first documented evidence of progressive disease (PD). PD was defined as meeting any one of following criteria: Increase of >=25% in level of serum M-protein from lowest response value and absolute increase must be >=0.5 g/dL; Increase of >=25% in 24-hour urinary light chain excretion (urine M-protein) from lowest response value and absolute increase must be >=200 mg/24hours; Only in participants without measurable serum and urine M-protein levels: increase of >=25% in difference between involved and uninvolved free light chain (FLC) levels from lowest response value and absolute increase must be >10 milligram per deciliter (mg/dL); Definite increase in size of existing bone lesions or soft tissue plasmacytomas; Definite development of new bone lesions or soft tissue plasmacytomas; Development of hypercalcemia (corrected serum calcium >11.5 mg/dL) that can be attributed solely to Plasma Cell (PC) proliferative disorder. (NCT02136134)
Timeframe: From the date of randomization to the date of first documented evidence of progression or death due to PD whichever occurs first (approximately 3 years)

Intervention	months (Median)
Bortezomib + Dexamethasone (Vd)	7.29
Daratumumab + Bortezomib and Dexamethasone (DVd)	NA

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Overall Response Rate (ORR)

The Overall response rate was defined as the percentage of participants who achieved stringent complete response (sCR), complete response (CR), very good partial response (VGPR), or partial response (PR) according to the International Myeloma Working Group (IMWG) criteria, during the study or during follow up. IMWG criteria for PR: >=50% reduction of serum M-protein and reduction in 24 hour urinary M-protein by >=90% or to <200 mg/24 hours, if the serum and urine M-protein are not measurable, a decrease of >=50% in the difference between involved and uninvolved FLC levels is required in place of the M-protein criteria, in addition to the above criteria, if present at baseline, a >=50% reduction in the size of soft tissue plasmacytomas is also required. (NCT02136134)
Timeframe: Up to disease progression (approximately of 3 years)

Intervention	percentage of participants (Number)
Bortezomib + Dexamethasone (Vd)	63.2
Daratumumab + Bortezomib and Dexamethasone (DVd)	82.9

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Overall Survival (OS)

Overall Survival was measured from the date of randomization to the date of the participant's death. (NCT02136134)
Timeframe: Up to the end of the study (approximately of 3 years)

Intervention	months (Median)
Bortezomib + Dexamethasone (Vd)	NA
Daratumumab + Bortezomib and Dexamethasone (DVd)	NA

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Percentage of Participants With a Very Good Partial Response (VGPR) or Better

Response rate of VGPR or better was defined as the percentage of participants who achieved VGPR and CR (including sCR) according to the IMWG criteria during or after the study treatment. IMWG criteria for VGPR: Serum and urine M-component detectable by immunofixation but not on electrophoresis, or >=90% reduction in serum M-protein plus urine M-protein <100 mg/24 hours, if the serum and urine M-protein are not measurable, a decrease of >90% in the difference between involved and uninvolved FLC levels is required in place of the M-protein criteria, in addition to the above criteria, if present at baseline, a >=50% reduction in the size of soft tissue plasmacytomas is also required; CR: Negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas, and <5% PCs in bone marrow; sCR: CR and normal FLC ratio, absence of clonal PCs by immunohistochemistry, immunofluorescence or 2 to 4 color flow cytometry. (NCT02136134)
Timeframe: Up to disease progression (approximately of 3 years)

Intervention	percentage of participants (Number)
Bortezomib + Dexamethasone (Vd)	29.1
Daratumumab + Bortezomib and Dexamethasone (DVd)	59.2

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Percentage of Participants With Negative Minimal Residual Disease (MRD)

The Minimal Residual Disease negativity rate was defined as the percentage of participants who had negative MRD assessment at any timepoint after the first dose of study drugs by evaluation of bone marrow aspirates or whole blood. MRD was assessed in participants who achieved complete response or stringent complete response (CR/sCR). IMWG criteria for CR: Negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas, and <5% PCs in bone marrow; sCR: CR plus normal FLC ratio, absence of clonal PCs by immunohistochemistry, immunofluorescence or 2 to 4 color flow cytometry. (NCT02136134)
Timeframe: Up to disease progression (approximately of 3 years)

Intervention	percentage of participants (Number)
Bortezomib + Dexamethasone (Vd)	2.8
Daratumumab + Bortezomib and Dexamethasone (DVd)	13.5

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Percentage of Participants With Best M-protein Response

Percentage of participants with Best M- protein response of 100% reduction and >=90% to < 100% reduction were assessed. Best M-protein response was defined as the maximal percent reduction or the lowest percent increase from baseline in serum M-protein for participants with measurable heavy chain at baseline or urine M-protein for participants without measurable heavy chain, but with measurable light chain disease at baseline. For participants without measurable heavy chain and light chain disease at baseline, best response in serum free light chain (FLC) was defined as the maximal percent reduction or the lowest percent increase from baseline in the difference between involved and uninvolved serum FLC level (dFLC). (NCT02195479)
Timeframe: Approximately up to 2.4 years

Intervention	Percentage of participants (Number)
	Best M-protein response in serum: 100% reduction	Best M-protein response in serum:>= 90 to < 100%	Best M-protein response in urine:100% reduction	Best M-protein response in urine:>=90 to < 100%	Best response in dFLC:100% reduction	Best response in dFLC: >=90% to < 100% reduction
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	58.5	15.2	90.5	7.1	0	100.0
Velcade, Melphalan and Prednisone (VMP)	38.7	14.6	69.4	13.9	0	77.8

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Change From Baseline in EuroQol-5 Dimensions-5 Levels (EQ-5D-5L): Visual Analogue Scale (VAS)

Intervention	Units on a scale (Mean)
	Baseline	Month 3	Month 6	Month 9	Month 12	Month 18
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	57.90	9.28	10.83	12.50	10.79	12.04
Velcade, Melphalan and Prednisone (VMP)	60.33	4.20	7.40	9.89	10.80	7.65

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Change From Baseline in EuroQol 5 Dimensions-5 Level (EQ-5D-5L) Utility Score

EQ-5D-5L is a standardized, participant-rated questionnaire to assess health-related quality of life. The EQ-5D-5L includes 2 components: the EQ-5D-5L health state profile (descriptive system) and the EQ-5D-5L Visual Analog Scale. The EQ-5D-5L descriptive system provides a profile of the participant's health state 5 dimensions: mobility, self-care, usual activities, pain/discomfort and anxiety/depression. Each dimension has 5 response options (no problems, slight problems, moderate problems, severe problems and extreme problems) that reflect increasing levels of difficulty. The participant was asked to indicate his/her current health state by selecting the most appropriate level in each of the 5 dimensions. Responses to the 5 dimension scores were combined and converted into a single preference-weighted health utility index score 0 (0.0- worst health state) to 1 (1.0- better health state) representing the general health status of the individual based on the UK scoring algorithm. (NCT02195479)
Timeframe: Baseline, Months 3, 6, 9, 12 and 18

Intervention	Units on a scale (Mean)
	Baseline	Month 3	Month 6	Month 9	Month 12	Month 18
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	0.57	0.12	0.13	0.16	0.17	0.13
Velcade, Melphalan and Prednisone (VMP)	0.59	0.09	0.12	0.16	0.15	0.13

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Change From Baseline in European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ)-C30: Emotional Functioning Score

"The EORTC QLQ-C30 is a 30 items self-reporting questionnaire, with a 1 week recall period, resulting in 5 functional scales (physical functioning, role functioning, emotional functioning, cognitive functioning, and social functioning), 1 Global Health Status (GHS) scale, 3 symptom scales (fatigue, nausea and vomiting, and pain), and 6 single symptom items (dyspnea, insomnia, appetite loss, constipation, diarrhea, and financial difficulties). The questionnaire includes 28 items with 4-point Likert type responses from 1-not at all to 4-very much to assess functioning and symptoms; 2 items with 7-point Likert scales (1= poor and 7= excellent) for global health and overall QoL. Scores are transformed to a 0 to 100 scale, with higher scores representing better GHS, better functioning, and more symptoms. Negative change from baseline values indicate deterioration in quality of life or functioning and positive values indicate improvement." (NCT02195479)
Timeframe: Baseline, Months 3, 6, 9, 12 and 18

Intervention	Units on a scale (Least Squares Mean)
	Month 3	Month 6	Month 9	Month 12	Month 18
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	8.8	10.6	11.1	12.6	11.4
Velcade, Melphalan and Prednisone (VMP)	9.4	10.5	11.9	11	12.7

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Overall Survival (OS)

Overall Survival (OS) was defined as the number of days the date of randomization to date of death. Median Overall Survival was estimated by using the Kaplan-Meier method. (NCT02195479)
Timeframe: From randomization to death (up to approximately 2.4 years)

Intervention	Months (Median)
Velcade, Melphalan and Prednisone (VMP)	NA
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	NA

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Percentage of Participants With Complete Response (CR) or Better

CR or better rate was defined as the percentage of participants with a CR or better (i.e. CR and sCR) as per IMWG criteria. CR: as negative immunofixation on the serum and urine and disappearance of soft tissue plasmacytomas and less than (<) 5 percent plasma cells in bone marrow; sCR: CR plus normal free light chain (FLC) ratio and absence of clonal PCs by immunohistochemistry, immunofluorescence or 2- to 4-color flow cytometry. (NCT02195479)
Timeframe: From randomization to disease progression (up to 2.4 years)

Intervention	Percentage of participants (Number)
Velcade, Melphalan and Prednisone (VMP)	24.4
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	42.6

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Percentage of Participants With Negative Minimal Residual Disease (MRD)

The Minimal Residual Disease negativity rate was defined as the percentage of participants who had negative MRD (detection of less than 1 malignant cell among 100,000 normal cells) assessment at any timepoint after the first dose of study drugs by evaluation of bone marrow aspirates or whole blood at 10^-5 threshold. MRD was evaluated by using Deoxyribonucleic acid (DNA) sequencing of immunoglobulin genes. MRD was assessed in participants who achieved complete response or stringent complete response (CR/sCR). (NCT02195479)
Timeframe: From randomization to disease progression (up to 2.4 years)

Intervention	Percentage of participants (Number)
Velcade, Melphalan and Prednisone (VMP)	6.2
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	22.3

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Percentage of Participants With Stringent Complete Response (sCR)

sCR as per IMWG criteria is CR plus normal free light chain (FLC) ratio and absence of clonal PCs by immunohistochemistry, immunofluorescence or 2- to 4-color flow cytometry. CR: Negative immunofixation on the serum and urine; Disappearance of any soft tissue plasmacytomas; <5% plasma cells (PCs) in bone marrow. (NCT02195479)
Timeframe: From randomization to disease progression (up to 2.4 years)

Intervention	Percentage of participants (Number)
Velcade, Melphalan and Prednisone (VMP)	9.3
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	20.3

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Overall Response Rate (ORR)

The Overall response rate was defined as the percentage of participants who achieved a partial response (PR) or better, according to the International Myeloma Working Group (IMWG) criteria, during the study or during follow up. IMWG criteria for PR: greater than or equal to (>=) 50 percentage(%) reduction of serum M-protein and reduction in 24 hour urinary M-protein by >=90% or to <200 mg/24 hours, if the serum and urine M-protein are not measurable, a decrease of >=50% in the difference between involved and uninvolved free light chain (FLC) levels is required in place of the M-protein criteria, If serum and urine M-protein are not measurable, and serum free light assay is also not measurable, >=50% reduction in bone marrow plasma cells (PCs) is required in place of M-protein, provided baseline bone marrow plasma cell percentage was >=30%, in addition to the above criteria, if present at baseline, a >=50% reduction in the size of soft tissue plasmacytomas is also required. (NCT02195479)
Timeframe: From randomization to disease progression (up to 2.4 years)

Intervention	Percentage of participants (Number)
Velcade, Melphalan and Prednisone (VMP)	73.9
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	90.9

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Percentage of Participants With Very Good Partial Response (VGPR) or Better

VGPR or better rate was defined as the percentage of participants who achieved VGPR or complete response (CR) (including stringent complete response[sCR]) according to the IMWG criteria during or after the study treatment. VGPR: Serum and urine component detectable by immunofixation but not on electrophoresis, or >= 90% reduction in serum M-protein plus urine M-protein level less than (<) 100 milligram (mg) per 24 hour; CR: negative immunofixation on the serum and urine, Disappearance of any soft tissue plasmacytomas and < 5% plasms cells (PCs) in bone marrow; sCR: CR in addition to having a normal FLC ratio and an absence of clonal cells in bone marrow by immunohistochemistry, immunofluorescence, 2-4 color flow cytometry. (NCT02195479)
Timeframe: From randomization to disease progression (up to 2.4 years)

Intervention	Percentage of participants (Number)
Velcade, Melphalan and Prednisone (VMP)	49.7
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	71.1

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Progression Free Survival (PFS)

PFS- duration from date of randomization to Progressive disease (PD)/death, whichever occurs first. PD per IMWG criteria-Increase of 25% from lowest response value in one of following: Serum and urine M-component (absolute increase >=0.5 gram per deciliter [g/dL] and >=200 milligram [mg]/24 hours respectively); Only participants without measurable serum and urine M-protein levels: difference between involved and uninvolved free light chain (FLC) levels (absolute increase>10 mg/dL); Only participants without measurable serum and urine M-protein levels,without measurable disease by FLC levels,bone marrow Plasma cells (PC) %(absolute % >=10%);Bone marrow PC%: absolute% >10%; Definite development of new bone lesions/soft tissue plasmacytomas/definite increase in size of existing bone lesions/soft tissue plasmacytomas and Development of hypercalcemia (corrected serum calcium >11.5 mg/dL) that can be attributed solely to the PC proliferative disorder. (NCT02195479)
Timeframe: From randomization to either disease progression or death whichever occurs first (up to 2.4 years)

Intervention	Months (Median)
Velcade, Melphalan and Prednisone (VMP)	18.14
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	NA

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Progression Free Survival on Next Line of Therapy (PFS2)

Progression-free survival after next-line therapy is defined as the time from randomization to progression on the next line of subsequent antimyeloma therapy or death due to any cause (prior to start of second line of antimyeloma therapy), whichever comes first. Disease progression on next line of treatment was based on investigator judgment. (NCT02195479)
Timeframe: From randomization to either disease progression or death whichever occurs first (up to 2.4 years)

Intervention	Months (Median)
Velcade, Melphalan and Prednisone (VMP)	NA
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	NA

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Time to Disease Progression (TTP)

TTP: Time from date of randomization to date of first documented evidence of PD or death due to PD, whichever occurs first. PD per IMWG criteria- Increase of 25 % from lowest response value in one of following: Serum and urine M-component (absolute increase >=0.5 gram per deciliter [g/dL] and >=200 mg/24 hours respectively); Only in participants without measurable serum and urine M-protein levels: difference between involved and uninvolved FLC levels (absolute increase >10 milligram per deciliter [mg/dL]); Only in participants without measurable serum and urine M-protein levels and without measurable disease by FLC levels, bone marrow plasma cells (PC)% (absolute % >=10%); Bone marrow PC %: absolute % >10%; Definite development of new bone lesions/soft tissue plasmacytomas or definite increase in size of existing bone lesions/soft tissue plasmacytomas and Development of hypercalcemia (corrected serum calcium >11.5 mg/dL) that can be attributed solely to the PC proliferative disorder. (NCT02195479)
Timeframe: From randomization to either disease progression or death due to PD whichever occurs first (up to 2.4 years)

Intervention	Months (Median)
Velcade, Melphalan and Prednisone (VMP)	19.35
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	NA

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Time to Next Treatment (TNT)

Time to next treatment is defined as the time from randomization to the start of the next-line treatment. (NCT02195479)
Timeframe: Approximately up to 2.4 years

Intervention	Months (Median)
Velcade, Melphalan and Prednisone (VMP)	NA
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	NA

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Time to Response

Time to response, defined as the time between the date of randomization and the first efficacy evaluation that the participant has met all criteria for PR or better. PR: >=50% reduction of serum M-protein and reduction in 24-hour urinary M-protein by >=90% or to <200 mg/24 hours; If the serum and urine M-protein are not measurable, a decrease of >=50% in the difference between involved and uninvolved FLC levels is required in place of the M-protein criteria; If serum and urine M-protein are not measurable, and serum free light assay is also not measurable, >=50% reduction in bone marrow PCs is required in place of M-protein, provided baseline bone marrow plasma cell percentage was >=30%. (NCT02195479)
Timeframe: From randomization to first documented PR or better (up to 2.4 years)

Intervention	Months (Median)
Velcade, Melphalan and Prednisone (VMP)	0.82
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	0.79

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Duration of Response (DOR)

DOR: participants with a confirmed response (PR or better) as time between first documentation of response and disease progression, IMWG response criteria, or death due to PD, whichever occurs first. PD: Increase of 25% from lowest response value in any one of following: Serum M-component (absolute increase>=0.5 g/dL); Urine M-component (absolute increase>=200 mg/24 hours); Only participants without measurable serum and urine M-protein levels: difference between involved and uninvolved FLC levels (absolute increase >10 mg/dL); Only participants without measurable serum and urine M-protein levels and without measurable disease by FLC levels, bone marrow PC%(absolute%>=10%); Bone marrow PC's %: absolute%>10%; Definite development of new bone lesions/soft tissue plasmacytomas/definite increase in the size of existing bone lesions or soft tissue plasmacytomas and Development of hypercalcemia (corrected serum calcium >11.5 mg/dL) that can be attributed solely to PC proliferative disorder. (NCT02195479)
Timeframe: Up to 2.4 years

Intervention	Months (Median)
Velcade, Melphalan and Prednisone (VMP)	21.3
Daratumumab, Velcade, Melphalan and Prednisone (D-VMP)	NA

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Percentage of Participants With Platelet Recovery

Platelet recovery is defined as the first day of a sustained platelet count >20,000/mm^3 with no platelet transfusion in the preceding seven days. (NCT02208037)
Timeframe: Days 60 and 100 Post-transplant

Intervention	percentage of participants (Number)
	Day 60	Day 100
Tacrolimus/Methotrexate/Bortezomib	91	91
Tacrolimus/Methotrexate/Maraviroc	92	92
Tacrolimus/MMF/Cyclophosphamide	90	96

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Percentage of Participants With Transplant-Related Mortality (TRM)

TRM is defined as death without prior disease relapse or progression. (NCT02208037)
Timeframe: 1 Year Post-transplant

Intervention	percentage of participants (Number)
Tacrolimus/Methotrexate/Bortezomib	17
Tacrolimus/Methotrexate/Maraviroc	16
Tacrolimus/MMF/Cyclophosphamide	11

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Percentage of Participants With GVHD/Relapse or Progression-free Survival (GRFS)

GRFS is defined as being free of grade III-IV acute GVHD onset, chronic GVHD onset requiring systemic immunosuppressive therapy, disease relapse or progression, and death from any cause. (NCT02208037)
Timeframe: 1 Year Post-transplant

Intervention	percentage of participants (Number)
Tacrolimus/Methotrexate/Bortezomib	35.5
Tacrolimus/Methotrexate/Maraviroc	27.2
Tacrolimus/MMF/Cyclophosphamide	44.1

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Percentage of Participants With GVHD-free Survival

GVHD-free survival is defined as being alive without previous onset of Grade III-IV acute GVHD or chronic GVHD requiring immunosuppressive therapy. (NCT02208037)
Timeframe: 1 Year Post-transplant

Intervention	percentage of participants (Number)
Tacrolimus/Methotrexate/Bortezomib	43
Tacrolimus/Methotrexate/Maraviroc	34
Tacrolimus/MMF/Cyclophosphamide	53

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Percentage of Participants With Grade III-IV Acute GVHD

"Acute GVHD is graded according to the scoring system proposed by Przepiorka et al.1995:~Skin stage:~0: No rash~Rash <25% of body surface area~Rash on 25-50% of body surface area~Rash on > 50% of body surface area~Generalized erythroderma with bullous formation~Liver stage (based on bilirubin level)*:~0: <2 mg/dL 1.2-3 mg/dL 2.3.01-6 mg/dL 3.6.01-15.0 mg/dL 4.>15 mg/dL~GI stage*:~0: No diarrhea or diarrhea <500 mL/day~Diarrhea 500-999 mL/day or persistent nausea with histologic evidence of GVHD~Diarrhea 1000-1499 mL/day~Diarrhea >1500 mL/day~Severe abdominal pain with or without ileus * If multiple etiologies are listed for liver or GI, the organ system is downstaged by 1.~GVHD grade:~0: All organ stages 0 or GVHD not listed as an etiology I: Skin stage 1-2 and liver and GI stage 0 II: Skin stage 3 or liver or GI stage 1 III: Liver stage 2-3 or GI stage 2-4 IV: Skin or liver stage 4" (NCT02208037)
Timeframe: Day 180 Post-transplant

Intervention	percentage of participants (Number)
Tacrolimus/Methotrexate/Bortezomib	8
Tacrolimus/Methotrexate/Maraviroc	9
Tacrolimus/MMF/Cyclophosphamide	2

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Percentage of Participants With Grade II-IV Acute GVHD

"Acute GVHD is graded according to the scoring system proposed by Przepiorka et al.1995:~Skin stage:~0: No rash~Rash <25% of body surface area~Rash on 25-50% of body surface area~Rash on > 50% of body surface area~Generalized erythroderma with bullous formation~Liver stage (based on bilirubin level)*:~0: <2 mg/dL~2-3 mg/dL~3.01-6 mg/dL~6.01-15.0 mg/dL~>15 mg/dL~GI stage*:~0: No diarrhea or diarrhea <500 mL/day~Diarrhea 500-999 mL/day or persistent nausea with histologic evidence of GVHD~Diarrhea 1000-1499 mL/day~Diarrhea >1500 mL/day~Severe abdominal pain with or without ileus * If multiple etiologies are listed for liver or GI, the organ system is downstaged by 1.~GVHD grade:~0: All organ stages 0 or GVHD not listed as an etiology I: Skin stage 1-2 and liver and GI stage 0 II: Skin stage 3 or liver or GI stage 1 III: Liver stage 2-3 or GI stage 2-4 IV: Skin or liver stage 4" (NCT02208037)
Timeframe: Day 180 Post-transplant

Intervention	percentage of participants (Number)
Tacrolimus/Methotrexate/Bortezomib	26
Tacrolimus/Methotrexate/Maraviroc	32
Tacrolimus/MMF/Cyclophosphamide	27

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Percentage of Participants With Disease-free Survival

Disease-free survival is defined as being alive and free of disease relapse or progression. (NCT02208037)
Timeframe: 1 Year Post-transplant

Intervention	percentage of participants (Number)
Tacrolimus/Methotrexate/Bortezomib	58
Tacrolimus/Methotrexate/Maraviroc	56
Tacrolimus/MMF/Cyclophosphamide	60

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Percentage of Participants With Disease Relapse or Progression

Relapse is defined by either morphological or cytogenetic evidence of acute leukemia or MDS consistent with pretransplant features, or radiologic evidence of lymphoma. Progression of disease applies to patients with lymphoproliferative diseases (lymphoma or chronic lymphocytic leukemia) not in remission prior to transplantation and is defined as increase in size of prior sites of disease or evidence of new sites of disease. (NCT02208037)
Timeframe: 1 Year Post-transplant

Intervention	percentage of participants (Number)
Tacrolimus/Methotrexate/Bortezomib	24
Tacrolimus/Methotrexate/Maraviroc	31
Tacrolimus/MMF/Cyclophosphamide	28

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Percentage of Participants With Chronic GVHD Requiring Immunosupressive Therapy

Chronic GVHD is classified per 2005 NIH Consensus Criteria (Filipovich et al. 2005) into categories of severity: none, mild, moderate, and severe. Occurrence of chronic GVHD is defined as the occurrence of mild, moderate, or severe chronic GVHD per this classification. This endpoint considers the occurrence of chronic GVHD that necessitated initiation of immunosuppressive therapy for treatment. (NCT02208037)
Timeframe: 1 Year Post-transplant

Intervention	percentage of participants (Number)
Tacrolimus/Methotrexate/Bortezomib	29
Tacrolimus/Methotrexate/Maraviroc	33
Tacrolimus/MMF/Cyclophosphamide	22

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Percentage of Participants With Chronic GVHD

Intervention	percentage of participants (Number)
Tacrolimus/Methotrexate/Bortezomib	39
Tacrolimus/Methotrexate/Maraviroc	43
Tacrolimus/MMF/Cyclophosphamide	28

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Percentage of Participants With Neutrophil Recovery

Neutrophil recovery is defined as achieving an absolute neutrophil count (ANC) ≥ 500/mm^3 for three consecutive measurements on three different days. (NCT02208037)
Timeframe: Days 28 and 100 Post-transplant

Intervention	percentage of participants (Number)
	Day 28	Day 100
Tacrolimus/Methotrexate/Bortezomib	94	96
Tacrolimus/Methotrexate/Maraviroc	93	95
Tacrolimus/MMF/Cyclophosphamide	95	98

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Percentage of Participants With Overall Survival

(NCT02208037)
Timeframe: 1 Year Post-transplant

Intervention	percentage of participants (Number)
Tacrolimus/Methotrexate/Bortezomib	68
Tacrolimus/Methotrexate/Maraviroc	66
Tacrolimus/MMF/Cyclophosphamide	71

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Donor Cell Engraftment

Donor cell engraftment will be assessed with donor/recipient chimerism. Chimerism may be evaluated in bone marrow, whole blood, or CD3 fractions. Full donor chimerism is defined as the presence of ≥ 95% of donor cells as a proportion of total cells. Mixed chimerism is defined as the presence of donor cells, as a proportion of total cells, of < 95% but > 5% in the bone marrow or peripheral blood. Full and mixed chimerism will be evidence of donor cell engraftment. Donor cells of ≤ 5% will be considered as graft rejection. (NCT02208037)
Timeframe: Days 28 and 100 Post-transplant

Intervention	Participants (Count of Participants)
	Day 2872130179					Day 2872130181	Day 2872130180	Day 10072130180	Day 10072130181	Day 10072130179
	Full Chimerism	Mixed Chimerism	Graft Rejection	Dead	No Assay Performed
Tacrolimus/Methotrexate/Bortezomib	58
Tacrolimus/MMF/Cyclophosphamide	64
Tacrolimus/Methotrexate/Bortezomib	11
Tacrolimus/MMF/Cyclophosphamide	8
Tacrolimus/Methotrexate/Bortezomib	1
Tacrolimus/Methotrexate/Maraviroc	1
Tacrolimus/MMF/Cyclophosphamide	2
Tacrolimus/Methotrexate/Bortezomib	2
Tacrolimus/Methotrexate/Maraviroc	4
Tacrolimus/MMF/Cyclophosphamide	0
Tacrolimus/Methotrexate/Bortezomib	17
Tacrolimus/Methotrexate/Maraviroc	21
Tacrolimus/MMF/Cyclophosphamide	18
Tacrolimus/Methotrexate/Bortezomib	63
Tacrolimus/Methotrexate/Maraviroc	56
Tacrolimus/MMF/Cyclophosphamide	62
Tacrolimus/Methotrexate/Bortezomib	14
Tacrolimus/Methotrexate/Maraviroc	17
Tacrolimus/MMF/Cyclophosphamide	13
Tacrolimus/Methotrexate/Bortezomib	5
Tacrolimus/Methotrexate/Maraviroc	3
Tacrolimus/MMF/Cyclophosphamide	3
Tacrolimus/Methotrexate/Bortezomib	4
Tacrolimus/Methotrexate/Maraviroc	10
Tacrolimus/MMF/Cyclophosphamide	5
Tacrolimus/Methotrexate/Bortezomib	3
Tacrolimus/Methotrexate/Maraviroc	6
Tacrolimus/MMF/Cyclophosphamide	9

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Count of Participants That Experience Overall Survival (OS)

The amount of participants that start treatment with BBd and survive at least one year post treatment completion. (NCT02224729)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Bendamustine, Bortezomib, Dexamethasone (Standard)	2

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Incidence of Grade 3-4 Adverse Events From the Combination of Bendamustine Hydrochloride, Bortezomib, and Dexamethasone Based on the Common Terminology Criteria Version 4.0

All adverse events are tracked during the course of the trial. Adverse events with a grade of 3-4 will be tracked and recorded. (NCT02224729)
Timeframe: Up to 1 year

Intervention	Adverse Events (Number)
Bendamustine, Bortezomib, Dexamethasone (Standard)	22

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Count of Participants That Experience Overall Response Following 4 Cycles of the Combination Regimen BBd

ORR (partial remission or better) to induction therapy following 4 cycles of the combination regimen BBd. (NCT02224729)
Timeframe: At least 140 days

Intervention	Participants (Count of Participants)
Bendamustine, Bortezomib, Dexamethasone (Standard)	13

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Count of Participants That Experience Progression-free Survival (PFS)

The amount of participants that survive one year after treatment with BBd and do not experience worsening disease. (NCT02224729)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Bendamustine, Bortezomib, Dexamethasone (Standard)	2

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Count of Participants That Experience Very Good Partial Remission (VGPR)

Very good partial remission (VGPR) to induction therapy following 4 cycles of the combination regimen BBd. As defined as no dectable M-protein on SPEP (Serum protein electrophoresis) but positive IFX (Immunofixation) on serum or urine and >90% reduction of M-protein in serum and urine (NCT02224729)
Timeframe: Up to 1 year

Intervention	Participants (Count of Participants)
Bendamustine, Bortezomib, Dexamethasone (Standard)	9

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Maximum Tolerated Dose (MTD) of LDE225 Plus Bortezomib

During the safety lead-in, a standard 3+3 dose escalation design was used to establish the MTD for LDE225 in combination with bortezomib. The MTD would be determined by the highest dose at which ≤1 of 6 patients experiences a dose-limiting toxicity (DLT) during one cycle (21 days) of therapy. If 2 of 6 patients within a dose level experienced a DLT, that dose level would be defined as exceeding MTD and no further dose escalation would occur. The previous dose level would be considered the MTD. (NCT02254551)
Timeframe: every 3 weeks up to 48 weeks

Intervention	(Number)
LDE225 Plus Bortezomib	NA

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Phase 1a, 1b, and Phase 2: Tmax: Time to Maximum Plasma Concentration for INCB052793

Tmax is the time to maximum (peak) observed plasma drug concentration. Summary of Steady-State, Day 15, was evaluated by dosing regimen. For PK analyses subjects in TGA and TGB are combined by dosage group because only 3 subjects were enrolled in each dose group in TGB and 4 subject for first dose in TGB 50 mg. (NCT02265510)
Timeframe: Cycle 1, Day 15: predose and 0.5, 1, 2, 4, 6 hours postdose in Phase 1a; 0 (predose), 0.08, 0.5, 1, 2, 4, 6 and 8 hours postdose in Phase 1b and Phase 2

Intervention	hours (hr) (Median)
Phase 1a TGA - INCB052793 15 mg	1.1
Phase 1a TGA - INCB052793 25 mg	0.76
Phase 1a TGA - INCB052793 35 mg	2.0
Phase 1a TGA - INCB052793 50 mg	1.1
Phase 1a TGA - INCB052793 75 mg	2.2
Phase 1a TGA - INCB052793 100 mg	2.0
Phase 1b Cohort B - INCB052793 25 mg + Dexamethasone 40 mg	1.0
Phase 1b Cohort F - INCB052793 25 mg + Azacytidine 75 mg/m^2	1.1
Phase 1b Cohort F - INCB052793 35 mg + Azacytidine 75 mg/m^2	1.1
Phase 2 Cohort I - INCB052793 35 mg + Azacytidine 75 mg/m^2	0.51

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Phase 1a, 1b, and Phase 2: Cmax: Maximum Observed Plasma Concentration of Itacitinib

Cmax is defined as the maximum observed plasma concentration measured at steady state (Day 15). (NCT02265510)
Timeframe: Cycle 1, Day 15: predose and 0.5, 1, 2, 4, 6 hours postdose in Phase 1a; 0 (predose), 0.08, 0.5, 1, 2, 4, 6 and 8 hours postdose in Phase 1b and Phase 2

Intervention	nM (Mean)
Phase 2 Cohort J - Itacitinib 300 mg + Azacitidine 75 mg/m^2	1310

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Phase 1a, 1b, and Phase 2: Cmax: Maximum Observed Plasma Concentration for INCB052793

Cmax is defined as the maximum observed plasma concentration measured at steady state (Day 15). For PK analyses subjects in TGA and TGB are combined by dosage group because only 3 subjects were enrolled in each dose group in TGB and 4 subject for first dose in TGB 50 mg. (NCT02265510)
Timeframe: Cycle 1, Day 15: predose and 0.5, 1, 2, 4, 6 hours postdose in Phase 1a; 0 (predose), 0.08, 0.5, 1, 2, 4, 6 and 8 hours postdose in Phase 1b and Phase 2

Intervention	nM (Mean)
Phase 1a TGA - INCB052793 15 mg	522
Phase 1a TGA - INCB052793 25 mg	1110
Phase 1a TGA - INCB052793 35 mg	1120
Phase 1a TGA - INCB052793 50 mg	2050
Phase 1a TGA - INCB052793 75 mg	1840
Phase 1a TGA - INCB052793 100 mg	2890
Phase 1b Cohort B - INCB052793 25 mg + Dexamethasone 40 mg	928
Phase 1b Cohort F - INCB052793 25 mg + Azacytidine 75 mg/m^2	1270
Phase 1b Cohort F - INCB052793 35 mg + Azacytidine 75 mg/m^2	1480
Phase 2 Cohort I - INCB052793 35 mg + Azacytidine 75 mg/m^2	1610

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Phase 1a, 1b, and Phase 2: AUC0-τ: Area Under the Plasma Concentration-time Curve Over Dosing Interval for Itacitinib

AUC0-τ is the area under the plasma concentration-time curve from time = 0 to the last measurable concentration at time = t measured at steady state (Day 15). (NCT02265510)
Timeframe: Cycle 1, Day 15: predose and 0.5, 1, 2, 4, 6 hours postdose in Phase 1a; 0 (predose), 0.08, 0.5, 1, 2, 4, 6 and 8 hours postdose in Phase 1b and Phase 2

Intervention	nM*hr (Mean)
Phase 2 Cohort J - Itacitinib 300 mg + Azacitidine 75 mg/m^2	9870

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Phase 1a, 1b, and Phase 2: AUC0-τ: Area Under the Plasma Concentration-time Curve Over Dosing Interval for INCB052793

AUC0-τ is the area under the plasma concentration-time curve from time = 0 to the last measurable concentration at time = t measured at steady state (Day 15). For PK analyses subjects in TGA and TGB are combined by dosage group because only 3 subjects were enrolled in each dose group in TGB and 4 subject for first dose in TGB 50 mg. (NCT02265510)
Timeframe: Cycle 1, Day 15: predose and 0.5, 1, 2, 4, 6 hours postdose in Phase 1a; 0 (predose), 0.08, 0.5, 1, 2, 4, 6 and 8 hours postdose in Phase 1b and Phase 2

Intervention	nM*hr (Mean)
Phase 1a TGA - INCB052793 15 mg	4750
Phase 1a TGA - INCB052793 25 mg	9170
Phase 1a TGA - INCB052793 35 mg	8430
Phase 1a TGA - INCB052793 50 mg	14700
Phase 1a TGA - INCB052793 75 mg	18300
Phase 1a TGA - INCB052793 100 mg	27800
Phase 1b Cohort B - INCB052793 25 mg + Dexamethasone 40 mg	6390
Phase 1b Cohort F - INCB052793 25 mg + Azacytidine 75 mg/m^2	9580
Phase 1b Cohort F - INCB052793 35 mg + Azacytidine 75 mg/m^2	10200
Phase 2 Cohort I - INCB052793 35 mg + Azacytidine 75 mg/m^2	9380

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Phase 1A and 1B: Percentage of Participants With Response as Determined by Investigator's Assessment

Response rate is defined as the percentage of participants who achieved best overall response (BOR) as determined by IWG response criteria of investigator's assessment. A participant was considered an objective responder based on the following- Solid tumors: participant had a best overall response (BOR) of CR or PR, Lymphoma: participant had a BOR of complete radiologic response/complete metabolic response or partial remission/partial metabolic response, AML: participant had a BOR of CR, CRi, morphological leukemia-free state (MLFS), or PR, MDS: participant had a BOR of CR, PR, or marrow CR, MDS/myeloproliferative neoplasm (MPN): participant had a BOR of CR, PR, or marrow response, MM: participant had a BOR of stringent CR, CR, very good PR, PR, or MR. Subjects are combined by tumor type for this analysis. (NCT02265510)
Timeframe: Baseline through end of study (Up to approximately 4.5 years)

Intervention	Participants (Count of Participants)
Phase 1a TGA - INCB052793 in Solid Tumors	0
Phase 1a TGB - INCB052793 in Lymphoma	0
Phase 1a TGB - INCB052793 in MDS/MPN	1
Phase 1a TGB - INCB052793 in MM	0
Phase 1b Cohort B - INCB052793 + Dexamethasone in MM	2
Phase 1b Cohort F-INCB052793 +Azacytidine in AML	4
Phase 1b Cohort F-INCB052793 +Azacytidine in MDS	3
Phase 1b Cohort F-INCB052793 +Azacytidine in MDS/MPN	2

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Phase 1a and 1b: Number of Participants With at Least One Treatment-Emergent Adverse Event (TEAE) and Serious Adverse Event (SAE)

An AE is any untoward medical occurrence in a subject administered a medicinal investigational drug. The untoward medical occurrence does not necessarily have to have a causal relationship with treatment. An SAE is any untoward medical occurrence that results in death; is life-threatening; requires inpatient hospitalization or prolongation of present hospitalization; results in persistent or significant disability/incapacity; is a congenital anomaly/birth defect or is a medically important event that may not be immediately life-threatening or result in death or hospitalization. A TEAE was defined as any AE either reported for the first time or worsening of a pre-existing event after first dose of study drug and within 30 days of the last dose of study drug. (NCT02265510)
Timeframe: From first dose of study drug up to 30 days after last dose of study drug (Up to approximately 3.4 years)

,,,,,,,,,,,

Intervention	Participants (Count of Participants)
	TEAE	SAE
Phase 1a TGA - INCB052793 100 mg	6	2
Phase 1a TGA - INCB052793 15 mg	3	0
Phase 1a TGA - INCB052793 25 mg	3	1
Phase 1a TGA - INCB052793 35 mg	6	0
Phase 1a TGA - INCB052793 50 mg	4	2
Phase 1a TGA - INCB052793 75 mg	3	3
Phase 1a TGB - INCB052793 25 mg	3	1
Phase 1a TGB - INCB052793 35 mg	4	2
Phase 1a TGB - INCB052793 50 mg	4	2
Phase 1b Cohort B - INCB052793 25 mg + Dexamethasone 40 mg	7	5
Phase 1b Cohort F - INCB052793 25 mg + Azacytidine 75 mg/m^2	5	4
Phase 1b Cohort F - INCB052793 35 mg + Azacytidine 75 mg/m^2	16	14

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Phase 2: Number of Participants With at Least One TEAE and SAE

Intervention	Participants (Count of Participants)
	TEAE	SAE
Phase 2 Cohort I - INCB052793 35 mg + Azacytidine 75 mg/m^2	9	7
Phase 2 Cohort J - Itacitinib 300 mg + Azacitidine 75 mg/m^2	10	8

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Phase 2: Objective Response Rate (ORR) in Hematological Malignancies

ORR is defined as the proportion of participants who achieved complete response (CR), CR with incomplete hematologic recovery (CRi), partial response (PR), or hematologic improvement (HI), using the IWG response criteria. (NCT02265510)
Timeframe: Baseline through end of study (Up to approximately 4.5 years)

Intervention	Participants (Count of Participants)
Phase 2 Cohort I-INCB052793 +Azacytidine (AML)	0
Phase 2 Cohort I-INCB052793 +Azacytidine (MDS)	1
Phase 2 Cohort J-Itacitinib +Azacitidine (AML)	1
Phase 2 Cohort J-Itacitinib +Azacitidine (MDS)	0

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Phase 1a, 1b, and Phase 2: Tmax: Time to Maximum Plasma Concentration for Itacitinib

Tmax is the time to maximum (peak) observed plasma drug concentration. (NCT02265510)
Timeframe: Cycle 1, Day 15: predose and 0.5, 1, 2, 4, 6 hours postdose in Phase 1a; 0 (predose), 0.08, 0.5, 1, 2, 4, 6 and 8 hours postdose in Phase 1b and Phase 2

Intervention	hr (Median)
Phase 2 Cohort J - Itacitinib 300 mg + Azacitidine 75 mg/m^2	3.5

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Minimal Response Rate (MRR) Per Investigator

MRR is based on modified EBMT criteria per investigator assessment (NCT02290431)
Timeframe: after 24 weeks (8 cycles; cycle = 21 days)

Intervention	Percentage of participants (Number)
LBH589 + Bortezomib + Dexamethasone	9.7

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Overall Survival (OS)

OS is defined as time from first dose of study treatment to death (NCT02290431)
Timeframe: up to 30 days after end of study, approx. 4 years

Intervention	months (Median)
LBH589 + Bortezomib + Dexamethasone	NA

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Overall Response Rate (ORR)

ORR is defined as the proportion of participants with CR, nCR or partial response (PR) based on modified EBMT criteria per investigator assessment (NCT02290431)
Timeframe: 24 weeks (8 cycles; cycle = 21 days)

Intervention	Percentage of participants (Number)
LBH589 + Bortezomib + Dexamethasone	80.6

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Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: Lambda_z

Lambda_z: The terminal elimination rate constant (h-1) (NCT02290431)
Timeframe: Predose, 0.5h, 1h, 2h, 3h, 4h 8h, 24h 48h post dose

Intervention	1/hour (1/h) (Geometric Mean)
	PAN: C1D1	PAN: C1D8
LBH589 + Bortezomib + Dexamethasone	0.0506	0.0421

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Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: T1/2

T1/2: The elimination half-life associated with the terminal slope (Lambda_z) of a semi logarithmic concentration-time curve (NCT02290431)
Timeframe: Predose, 0.5h, 1h, 2h, 3h, 4h 8h, 24h 48h post dose

Intervention	hour (h) (Geometric Mean)
	PAN: C1D1	PAN: C1D8
LBH589 + Bortezomib + Dexamethasone	13.7	16.5

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Time to Response (TTR) Per Investigator

TTR is defined as the time from the date of first dose of study treatment to first documented response (PR or nCR or CR) per modified EBMT criteria as assessed by investigator (NCT02290431)
Timeframe: duration of study up to approx. 4 years

Intervention	months (Median)
LBH589 + Bortezomib + Dexamethasone	1.4

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Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: Vz/F

Vz/F: The apparent volume of distribution during terminal phase (associated with Lambda_z) (NCT02290431)
Timeframe: Predose, 0.5h, 1h, 2h, 3h, 4h 8h, 24h 48h post dose

Intervention	Litre (L) (Geometric Mean)
	PAN: C1D1	PAN: C1D8
LBH589 + Bortezomib + Dexamethasone	3390	2720

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Quality of Life (QoL) as Measured by FACT/GOG-Ntx Total Score

QoL as measured by Functional Assessment of Cancer Therapy/ Gynecology Oncology Group Neurotoxicity (FACT/GOG-NTX) scale calculated scores and changes from baseline were summarized by visit. The FACT/GOG-Ntx is a measure to assess neurotoxicity from systemic chemotherapy. The recall period for this measure is the past 7 days. FACT/GOG-Ntx Total Score: 0 - 152 (28 + 28 + 24 + 28 + 44 = 152). (FACT-G Physical Well-Being Score: 0 - 28, FACT-G Social/Family Well-Being Score: 0 - 28, FACT-G Emotional Well-Being Score: 0 - 24, FACT-G Functional Well-Being Score: 0 - 28, FACT/GOG-Ntx Neurotoxicity Subscale Score: 0 - 44). 4. The scales are combined. The higher the score, the better the QOL. (NCT02290431)
Timeframe: Baseline, Weeks 12, 24, 36, 48, 60, 72, 84, 96, 108, 120, 132, and 156

Intervention	scores on a scale (Median)
	Baseline	Week 12	Week 24	Week 36	Week 48	Week 60	Week 72	Week 84	Week 96	Week 108	Week 120	Week 132	Week 156
LBH589 + Bortezomib + Dexamethasone	112.33	91.75	100.33	125.83	114.25	109.92	108.00	101.00	121.67	120.17	125.25	114.00	119.8

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Percentage of Participants With Near Complete Response (nCR)/ Complete Response (CR) Rate

nCR plus CR rate after 8 cycles of therapy as defined by the modified European Society for Bone and Marrow Transplantation (EBMT) criteria per investigator assessment as the proportion of participants with nCR or CR as their best overall response. (NCT02290431)
Timeframe: after 24 weeks (8 cycles; cycle = 21 days)

Intervention	Percentage of participants (Number)
LBH589 + Bortezomib + Dexamethasone	48.4

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Progression Free Survival (PFS)

PFS is defined as time from first dose of study treatment to progression or death due to any cause, based on modified European Society for Bone and Marrow Transplantation (EBMT) criteria per Investigator's assessment (NCT02290431)
Timeframe: duration of study up to approx. 4 years

Intervention	months (Median)
LBH589 + Bortezomib + Dexamethasone	15.3

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Time to Progression/Relapse (TTP) Per Investigator

TTP is defined as the time from the date of the first dose of study treatment to the date of the first documented disease progression or relapse (NCT02290431)
Timeframe: duration of study up to approx. 4 years

Intervention	months (Median)
LBH589 + Bortezomib + Dexamethasone	15.3

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Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: AUClast, AUC0-24h, AUC0-48h, AUCinf

PK sample collection was performed in subjects who agreed to blood samplings for the PK assessments of PAN and BTZ. The order of administration of the 3 study treatment components was 1) PAN, 2) Dex, and 3) BTZ. (NCT02290431)
Timeframe: Predose, 0.5h, 1h, 2h, 3h, 4h 8h, 24h, 48h post dose

Intervention	h.ng/mL (Geometric Mean)
	PAN: AUClast C1D1	PAN: AUClast C1D8	BJB432: AUClast C1D1	BJB432: AUClast C1D8	PAN: AUC0-24h C1D1	PAN: AUC0-24h C1D8	BJB432: AUC0-24h C1D1	BJB432: AUC0-24h C1D8	PAN: AUC0-48h C1D1	PAN: AUC0-48h C1D8	BJB432: AUC0-48h C1D1	BJB432: AUC0-48h C1D8	PAN: AUCinf C1D1	PAN: AUCinf C1D8
LBH589 + Bortezomib + Dexamethasone	106	156	37.8	166	87.1	125	18.5	83.8	106	156	36.8	169	116	175

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Duration of Response (DOR) Per Investigator

DOR is defined as the time from date of the first documented CR/nCR or PR to the date of the first documented progression or relapse or death due to MM (NCT02290431)
Timeframe: duration of study up to approx. 4 years

Intervention	months (Median)
LBH589 + Bortezomib + Dexamethasone	22.7

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Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: Cmax

Cmax: The maximum (peak) observed plasma concentration. PK sample collection was performed in subjects who agreed to blood samplings for the PK assessments of PAN and BTZ. The order of administration of the 3 study treatment components was 1) PAN, 2) Dex, and 3) BTZ. (NCT02290431)
Timeframe: Predose, 0.5h, 1h, 2h, 3h, 4h 8h, 24h, 48h post dose

Intervention	ng/mL (Geometric Mean)
	PAN: Cycle 1 Day 1 (C1D1)	PAN: Cycle 1 Day 8 (C1D8)	BJB432: C1D1	BJB432: C1D8
LBH589 + Bortezomib + Dexamethasone	11.5	18.2	1.06	4.38

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Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: CL/F

CL/F: The apparent total body clearance of drug from the plasma (NCT02290431)
Timeframe: Predose, 0.5h, 1h, 2h, 3h, 4h 8h, 24h 48h post dose

Intervention	Litre/hour (L/h) (Geometric Mean)
	PAN: C1D1	PAN: C1D8
LBH589 + Bortezomib + Dexamethasone	172	114

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Composite PharmacoKinetics (PK) of Panobinostat and Bortezomib: Tmax

Tmax: The time to reach maximum (peak) plasma concentration. PK sample collection was performed in subjects who agreed to blood samplings for the PK assessments of PAN and BTZ. The order of administration of the 3 study treatment components was 1) PAN, 2) Dex, and 3) BTZ. (NCT02290431)
Timeframe: Predose, 0.5h, 1h, 2h, 3h, 4h 8h, 24h, 48h post dose

Intervention	hour (h) (Median)
	PAN: C1D1	PAN: C1D8	BJB432: C1D1	BJB432: C1D8
LBH589 + Bortezomib + Dexamethasone	2.00	2.00	24.0	24.0

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Change of Lung Function Measured by Forced Vital Capacity (FVC) Between Baseline and 24 Weeks

Forced vital capacity, or FVC, is the amount in liters of air that can be forcibly exhaled from the lungs after taking the deepest breath possible. It measures the effect that lung disease has on a person's ability to inhale and exhale. Higher values are better, and decreases over time can indicate disease progression. (NCT02370693)
Timeframe: 24 weeks

Intervention	Percentage of change in FVC %predicted (Mean)
Bortezomib Plus Mycophenolate Mofetil	0.51
Placebo Plus Mycophenolate Mofetil	-0.69

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Change of Skin Fibrosis Measured by the Rodnan Skin Score Between Baseline and 24 Weeks

The Modified Rodnan Skin Score (mRSS) is a measure of skin thickness that sums individual scores of skin thickness (0 - No Thickening, 1 - Mild Thickening, 2 - Moderate Thickening, 3 - Severe Thickening) measured at 17 body sites to reach a total score (Range: 0 to 51, higher value representing thicker skin). The Score is used as a surrogate for disease activity and severity, and a worsening score over time is associated with worse outcomes. (NCT02370693)
Timeframe: 24 weeks

Intervention	Score on a Scale (Mean)
Bortezomib Plus Mycophenolate Mofetil	-3.00
Placebo Plus Mycophenolate Mofetil	-0.33

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Number of Participants With Serious Adverse Events

To assess the safety and tolerability of bortezomib with mycophenolate mofetil assessed by the incidence of serious adverse events. (NCT02370693)
Timeframe: First dosing day to last study visit day: Mean duration 8 months.

Intervention	Number of Participants with Serious Adve (Mean)
Bortezomib Plus Mycophenolate Mofetil	0.33
Placebo Plus Mycophenolate Mofetil	0.25

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Grade 3 and 4 Treatment-Emergent Adverse Event (TEAE) Rate

Grade 3 and 4 TEA rate was defined as the proportion of participants who experienced a grade 3 or 4 adverse event of any attribution based on NCI Common Toxicity Criteria for Adverse Events Version 4 (CTCAEv4) on treatment. (NCT02375555)
Timeframe: The adverse event observation period defined as the time on treatment (+30d) is 278 weeks.

Intervention	proportion of participants (Number)
Elotuzumab, Lenalidomide, Bortezomib, and Dexamethasone	0.70

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4 Cycle Response Rate

Disease response was defined as the proportion of patients who achieved a response of partial response or better using International Myeloma Working Group (IMWG) response criteria. Partial Response (PR) defined as 50% reduction of serum M-protein and reduction in 24h urinary M-protein by ≥90% or to <200mg/24h; Very Good Partial Response (VGPR) defined as serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-protein plus urine M-protein level <100mg/24h; Complete Response (CR) defined as negative immunofixation on serum and urine and, disappearance of any soft tissue plasmacytomas and, <5% plasma cells in BM; Stringent Complete Response (sCR) defined as normal FLC ratio and absence of clonal cells in BM by immunohistochemistry or 2-4 color flow cytometry. The Clopper and Pearson method was used to estimate the 95% CIs for the response rate at Week 12. (NCT02375555)
Timeframe: Participants were followed up to 12 weeks.

Intervention	proportion of participants (Number)
Elotuzumab, Lenalidomide, Bortezomib, and Dexamethasone	0.971

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4 Cycle Ever Dose Modification (DM) Rate

The 4 cycle ever DM rate is the proportion of participants who started therapy and required dose modification of any study drug during the first four cycles of E-RVD. (NCT02375555)
Timeframe: Participants were followed up to 12 weeks.

Intervention	proportion of participants (Number)
Elotuzumab, Lenalidomide, Bortezomib, and Dexamethasone	.40

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Median Time to Response

Time to response is defined as the time from the first dose of study drug to the first documentation of response partial response (PR) or better. Disease response was assessed using International Myeloma Working Group (IMWG) response criteria: Partial Response (PR) defined as 50% reduction of serum M-protein and reduction in 24h urinary M-protein by ≥90% or to <200mg/24h; Very Good Partial Response (VGPR) defined as serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-protein plus urine M-protein level <100mg/24h; Complete Response (CR) defined as negative immunofixation on serum and urine and, disappearance of any soft tissue plasmacytomas and, <5% plasma cells in BM; Stringent Complete Response (sCR) defined as normal FLC ratio and absence of clonal cells in BM by immunohistochemistry or 2-4 color flow cytometry. (NCT02375555)
Timeframe: Participants were followed up to 92 days.

Intervention	days (Median)
Elotuzumab, Lenalidomide, Bortezomib, and Dexamethasone	22.0

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Successful Stem Cell Mobilization (SC Mob) Rate

Successful SC Mob defined as the proportion of participants with the ability to collect a total of at least 2*10^6 CD34+ cells/kg. (NCT02375555)
Timeframe: The most distant time of stem cell mobilization from time of registration is 21.4 weeks with a median of 15.14 weeks.

Intervention	proportion of participants (Number)
Elotuzumab, Lenalidomide, Bortezomib, and Dexamethasone	0.968

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Objective Response Rate (ORR) at End of 8 Cycles of Induction Therapy.

ORR was defined as the proportion of patients who achieved a disease response of partial response (PR) or better using IMWG response criteria. PR defined as 50% reduction of serum M-protein and reduction in 24h urinary M-protein by ≥90% or to <200mg/24h; Very Good Partial Response (VGPR) defined as serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-protein plus urine M-protein level <100mg/24h; Complete Response (CR) defined as negative immunofixation on serum and urine and, disappearance of any soft tissue plasmacytomas and, <5% plasma cells in BM; Stringent Complete Response (sCR) defined as normal FLC ratio and absence of clonal cells in BM by immunohistochemistry or 2-4 color flow cytometry. (NCT02375555)
Timeframe: Participants were followed up to 24 weeks.

Intervention	proportion of participants (Number)
All Patients Treated With E-RVD.	0.950

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Number of Relevant Toxicities Related to Therapy

"Events were graded using CTCAE v. 4.0. All toxicities will be monitored until the completion of therapy (up to 500 days) for patients that do not go on to bone marrow transplant. If a patient goes on to receive a bone marrow transplant, at that point, they will no longer be monitored for toxicity, as any further toxicities may be secondary to the transplant and not the study regimen.~This outcome reports those toxicities that are that were possibly, probably or definitely related to therapy. Participants were separately monitored for frequency of grade 5 events, grade 4 sepsis, grade 4 hemorrhage, and grade 4 hepatic toxicity across all patients in the stratum. Grade 4 and 5 events that are clearly and incontrovertibly due to extraneous causes or disease progression will be excluded. Higher grade events are considered more severe than lower grade." (NCT02419755)
Timeframe: From on-therapy date up to 18 months

Intervention	events (Number)
	Grade 5: death	Grade 4: sepsis	Grade 4: hemorrhage	Grade 4: hepatic toxicity
Stratum 1: Myeloid Malignancies	1	0	0	0
Stratum 2: ALL and MLM	3	2	1	0

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Haematological and Non-haematological Toxicity in Both Treatment Arms

(NCT02424851)
Timeframe: End of weeks 3, 6, 9, 12 (after receiving 4 cycles of therapy), 30 days after final treatment and 12 months after randomisation

Intervention	Events (Number)
	Serious adverse events	Adverse events
Arm A (BBD)	2	3
Arm B (BTD)	0	6

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Quality of Life Measured by the EQ-5D-3L Questionnaire at Baseline and 1 Month Follow up

"The EQ-5D-3L descriptive system comprises the following five dimensions: mobility, self-care, usual activities, pain/discomfort and anxiety/depression. Each dimension is scored on a scale of 1 to 3: 1 (no problems), 2 (some problems), and 3 (extreme problems). Higher score equates to a worse outcome.~As stated in the official EQ-5D user guide, patient responses to the 5 questions were converted into a single index value as per Dolan P (1997). Modeling valuations for EuroQol health states. Med Care 35(11):1095-108. These index values, with country specific value sets, facilitate the calculation of quality-adjusted life years (QALYs) that are used to inform economic evaluations of health care interventions. In the UK, the values range from -0.594 to +1." (NCT02424851)
Timeframe: Baseline and 1 month follow up

Intervention	Units on a scale (Mean)
	Baseline	1 month FU
Arm A (BBD)	0.72	0.69
Arm B (BTD)	0.69	0.80

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Renal Response After Two Cycles of Trial Treatment

(NCT02424851)
Timeframe: End of 2nd treatment cycle, week 6

Intervention	Participants (Count of Participants)
	Partial response	Minor response	No repsonse
Arm A (BBD)	2	9	4
Arm B (BTD)	0	7	6

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Overall Survival

(NCT02424851)
Timeframe: 1 month post end of treatment and 1 year post randomisation

Intervention	Participants (Count of Participants)
Arm A (BBD)	9
Arm B (BTD)	13

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Number of Participants With >50% Reduction From Baseline in Serum Free Light Chain

(NCT02424851)
Timeframe: End of week 6 (after receiving two cycles of therapy)

Intervention	Participants (Count of Participants)
Arm A (BBD)	13
Arm B (BTD)	3

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Percentage of Participants With Progression-Free Survival

The primary endpoint compares progression-free survival as a time to event endpoint from randomization between patients randomized to ixazomib and placebo maintenance in high risk multiple myeloma. Participants are considered a failure of the primary endpoint if they die or suffer from disease progression or if they initiate non-protocol anti-myeloma therapy. Disease progression was evaluated using the International Uniform Response Criteria. Participants must meet one of the criteria for disease progression specified in the protocol. The time to this event is the time from randomization to progression, death, or initiation of non-protocol anti myeloma therapy whichever comes first. The Kaplan-Meier estimator was used to estimate progression-free survival during the 2 year post-transplant follow-up period. Participants who were event-free at two years post-transplant are censored at that time. (NCT02440464)
Timeframe: 12 months and 21 months post-randomization

Intervention	percentage of participants (Number)
	12 Months Post-randomization	21 Months Post-randomization
Ixazomib Maintenance	65.3	55.3
Placebo	72.7	59.1

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Percentage of Participants With Overall Survival (OS)

Overall survival (OS) is defined as freedom from death from any cause. OS post-randomization is estimated for each arm using the Kaplan-Meier estimator and compared between arms using the log rank test. Participants who are alive at two years post-transplant are censored at that time. Confidence intervals for values of 100% were not calculated and are shown as 100%. (NCT02440464)
Timeframe: 12 months and 21 months post-randomization

Intervention	percentage of participants (Number)
	12 Months Post-randomization	21 Months Post-randomization
Ixazomib Maintenance	100.0	94.7
Placebo	90.9	86.4

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Percentage of Participants With Infections Post-randomization by Time Point

All Grade 2 and 3 infections are reported according to the BMT CTN MOP (Manual of Procedures) where a higher grade corresponds to more severe symptoms. The cumulative incidence of severe, life-threatening, or fatal infections (Grade 3), treating death as a competing event, are estimated at 6, 12 and 18 months post randomization using Aalen-Johansen estimators for each treatment group. Comparison of cumulative incidence between the two treatment arms was done using a Z test at fixed time points. (NCT02440464)
Timeframe: 6, 12 and 18 months post-randomization

Intervention	percentage of participants (Number)
	6 Months Post-randomization	12 Months Post-randomization	18 Months Post-randomization
Ixazomib Maintenance	4.8	4.8	4.8
Placebo	0.0	0.0	0.2

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Percentage of Participants With Infections Post-randomization by Infection Type

All Grade 2 and 3 infections are reported according to the BMT CTN MOP (Manual of Procedures) where a higher grade corresponds to more severe symptoms. The number of participants with post-randomization infections in each treatment arm is described by severity and type of infection. (NCT02440464)
Timeframe: 2 years post-randomization

Intervention	Participants (Count of Participants)
	Participants with Infections	Maximum Severity: Grade 2	Maximum Severity: Grade 3	Participants with Bacterial Infection	Participants with Viral Infection	Participants with Fungal Infection	Participants with Other Infection
Ixazomib Maintenance	8	6	2	3	6	0	1
Placebo	11	10	1	2	11	1	0

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Percentage of Participants With Disease Progression

Disease progression was evaluated using the International Uniform Response Criteria. Participants in sCR/CR must meet at least one of the criteria for disease progression specified in the protocol for sCR/CR participants; those not in sCR/CR must meet at least one of the disease progression criteria specified in the protocol for those not in sCR/CR. The cumulative incidence of progression from randomization will be estimated for each treatment arm using the Aalen-Johansen estimator, with death in remission treated as a competing risk. Initiation of anti-myeloma therapy will be considered evidence of progression. Participants who were event-free at two years post-transplant are censored at that time. (NCT02440464)
Timeframe: 12 months and 21 months post-randomization

Intervention	percentage of participants (Number)
	12 Months Post-randomization	21 Months Post-randomization
Ixazomib Maintenance	34.7	44.7
Placebo	27.3	36.4

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Percentage of Participants With Chronic GVHD

Cumulative incidences of chronic GVHD were determined using the Aalen-Johansen estimator. Death prior to chronic GVHD is treated as the competing risk. Cumulative incidences are compared between treatment arms using Gray's test. Data of chronic GVHD were collected from providers and chart review according to the recommendations of the 2014 NIH Consensus Criteria. Eight organs are scored on a 0-3 scale to reflect degree of chronic GVHD involvement; 3 indicates the worst symptom. Liver and pulmonary function test results and use of systemic therapy for treatment of chronic GVHD are also recorded. (NCT02440464)
Timeframe: 12 months and 21 months post-randomization

Intervention	percentage of participants (Number)
	12 Months Post-randomization	21 Months Post-randomization
Ixazomib Maintenance	68.6	68.6
Placebo	63.6	63.6

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Medical Outcomes Study (MOS) - Short Form 36 (SF-36) Score

The MOS SF-36 instrument is a general assessment of health quality of life with eight components: Physical Functioning, Role Physical, Pain Index, General Health Perceptions, Vitality, Social Functioning, Role Emotional, and Mental Health Index. The scale is 0 to 100 where 0 is maximum disability and 100 is no disability, so the higher the score the more positive the outcome. The Physical Component Summary (PCS) and Mental Component Summary (MCS) were used as the outcome measures in summarizing the SF-36 data for this study. This self-reported questionnaire was completed at transplant, randomization, 6 months following the start of maintenance therapy (which corresponds to 6 months post-randomization), and 24 months post-transplant. Comparisons between treatment groups were performed prior to maintenance, 6 months post-randomization and at 24 months after transplant. Only English and Spanish speaking patients were eligible to participate in the quality of life component of this trial. (NCT02440464)
Timeframe: Randomization, 6 months post-randomization, 24 months post-transplant

Intervention	score on a scale (Median)
	PCS: Randomization	PCS: 6 Months Post-randomization	PCS: 24 Months Post-transplant	PCS: Change from Randomization to 6 Months Post-randomization	PCS: Change from Randomization to 24 Months Post-transplant	MCS: Randomization	MCS: 6 Months Post-randomization	MCS: 24 Months Post-transplant	MCS: Change from Randomization to 6 Months Post-randomization	MCS: Change from Randomization to 24 Months Post-transplant
Ixazomib Maintenance	38.7	47.9	45.1	3.3	4.7	51.5	54.8	56.1	-0.6	4.9
Placebo	41.5	41.2	45.7	1.0	7.8	49.9	54.5	49.5	5.3	-2.5

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Functional Assessment of Cancer Therapy (FACT) - Bone Marrow Transplant (BMT) Total Score

The FACT-BMT version 4.0 instrument is comprised of the Functional Assessment of Cancer Therapy - General (FACT-G), which evaluates the health-related quality of life (HQL) of patients receiving treatment for cancer, and the BMT Concerns module, that addresses disease and treatment-related questions specific to bone marrow transplant. This scale goes from 0 to 196 where higher scores indicate better functioning. The FACT-BMT Total, which has all items in the FACT-G and BMT modules, was used as the outcome measure. This self-reported questionnaire was completed at transplant, randomization, 6 months following the start of maintenance therapy (which corresponds to 6 months post-randomization), and 24 months post-transplant. Comparisons between treatment groups were performed prior to maintenance, 6 months post-randomization and at 24 months after transplant. Only English and Spanish speaking patients were eligible to participate in the quality of life component of this trial. (NCT02440464)
Timeframe: Randomization, 6-months post-randomization, 24 months post-transplant

Intervention	score on a scale (Median)
	Randomization	6 Months Post-randomization	24 Months Post-transplant	Change from Randomization to 6 Months Post-randomization	Change from Randomization to 24 Months Post-transplant
Ixazomib Maintenance	100.0	121.4	121.5	5.0	12.6
Placebo	110.0	114.0	109.0	7.0	3.0

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Percentage of Participants With Acute GVHD (Grades III-IV)

Cumulative incidences of grade III-IV acute GVHD were determined using the Aalen-Johansen estimator. Death prior to acute GVHD is treated as the competing risk. Cumulative incidences are compared between treatment arms using Gray's test. Grading of acute GVHD was derived by consensus grading per BMT Clinical Trials Network (CTN) manual of procedures (MOP). The acute GVHD algorithm calculates the grade based on the organ (skin, GI and liver) stage and etiology/biopsy reported on the weekly GVHD form. Grade I aGVHD is defined as Skin stage of 1-2 and stage 0 for both GI and liver organs. Grade II aGVHD is stage 3 of skin, or stage 1 of GI, or stage 1 of liver. Grade III is stage 2-4 for GI, or stage 2-3 of liver. Grade IV is stage 4 of skin, or stage 4 of liver. Grade 4 is the worst outcome. (NCT02440464)
Timeframe: 100 days post-randomization

Intervention	percentage of participants (Number)
Ixazomib Maintenance	9.5
Placebo	0.0

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Percentage of Participants With Toxicities Post-randomization by Time Point

Toxicities are graded using NCI Common Terminology Criteria for Adverse Events (CTCAE), Version 4.0. Higher grades correspond to worse symptoms with the minimum grade being a 0 and the maximum grade being a 5. The cumulative incidence of Grade ≥ 3 toxicity was estimated at 6, 12 and 18 months post randomization using Aalen-Johansen estimators for each treatment group. Death from a cause other than toxicity was treated as a competing risk. Comparison of cumulative incidence between the two treatment arms was done using a Z test at fixed time points. (NCT02440464)
Timeframe: 6, 12 and 18 months post-randomization

Intervention	percentage of participants (Number)
	6 Months Post-randomization	12 Months Post-randomization	18 Months Post-randomization
Ixazomib Maintenance	57.1	61.9	61.9
Placebo	63.6	68.2	72.7

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Percentage of Participants With Response to Treatment

Response was assessed using the International Uniform Response Criteria. All disease classifications are relative to the patient's disease status prior to allogeneic transplant (i.e. study entry). Response to treatment after randomization (sCR, CR, VGPR, or PR) is summarized in each arm post-transplant at 18 months and 24 months post-transplant. These response data were summarized separately for patients in sCR/CR at the time of randomization vs. those who were not in sCR/CR at the time of randomization. (NCT02440464)
Timeframe: 18 months and 24 months post-transplant

Intervention	Participants (Count of Participants)
	Response to Treatment at 18 Months Post-transplant for Participants in sCR/CR at Randomization72551676								Response to Treatment at 18 Months Post-transplant for Participants in sCR/CR at Randomization72551677	Response to Treatment at 18 Months Post-transplant for Participants Not in sCR/CR at Randomization72551676	Response to Treatment at 18 Months Post-transplant for Participants Not in sCR/CR at Randomization72551677	Response to Treatment at 24 Months Post-transplant for Participants in sCR/CR at Randomization72551676	Response to Treatment at 24 Months Post-transplant for Participants in sCR/CR at Randomization72551677	Response to Treatment at 24 Months Post-transplant for Participants Not in sCR/CR at Randomization72551677	Response to Treatment at 24 Months Post-transplant for Participants Not in sCR/CR at Randomization72551676
	Stringent Complete Response (sCR)	Complete Response (CR)	Very Good Partial Response (VGPR)	Not Evaluable	Partial Response (PR)	Stable Disease (SD)	Progressive Disease (PD)	Died Before Evaluation
Ixazomib Maintenance	3
Placebo	3
Placebo	2
Placebo	0
Ixazomib Maintenance	2
Placebo	4
Ixazomib Maintenance	4
Placebo	1
Placebo	6
Ixazomib Maintenance	0
Ixazomib Maintenance	1
Ixazomib Maintenance	5

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Percentage of Participants With Best Response to Treatment After Randomization

Response was assessed using the International Uniform Response Criteria. Best response is the best of all the disease response status at each assessment time point after randomization. The order from best to worst is: Stringent Complete Response (sCR), Complete Response (CR), Very Good Partial Response (VGPR), Partial Response (PR), Stable Disease (SD), and Progressive Disease (PD). All disease classifications are relative to the patient's disease status prior to allogeneic transplant (i.e. study entry). This outcome was compared between treatment groups using all response data up to 2 years post-transplant. These response data were summarized separately for patients in sCR/CR at the time of randomization vs. those who were not in sCR/CR at the time of randomization. Within each group (in sCR/CR vs not in sCR/CR at randomization), best response to treatment was compared between treatment groups using a Fisher's Exact test instead of a chi-square test because of the small sample size. (NCT02440464)
Timeframe: 2 years post-transplant

Intervention	Participants (Count of Participants)
	Participants in sCR/CR at Randomization72551676						Participants in sCR/CR at Randomization72551677	Participants Not in sCR/CR at Randomization72551677	Participants Not in sCR/CR at Randomization72551676
	Partial Response (PR)	Stable Disease (SD)	Progressive Disease (PD)	Stringent Complete Response (sCR)	Complete Response (CR)	Very Good Partial Response (VGPR)
Ixazomib Maintenance	6
Placebo	5
Ixazomib Maintenance	2
Ixazomib Maintenance	0
Placebo	0
Placebo	1
Ixazomib Maintenance	3
Placebo	4
Placebo	3
Ixazomib Maintenance	4
Ixazomib Maintenance	1

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Percentage of Participants With Treatment-Related Mortality (TRM)

Treatment-related mortality is defined as death occurring in a patient from causes other than disease relapse or progression. The cumulative incidence of treatment-related mortality (TRM) post-randomization is estimated for each treatment arm using the Aalen-Johansen estimator, with progression treated as a competing risk. Participants who were event-free at two years post-transplant are censored at that time. Confidence intervals for values of 0% were not calculated. (NCT02440464)
Timeframe: 12 months and 21 months post-randomization

Intervention	percentage of participants (Number)
	12 Months Post-randomization	21 Months Post-randomization
Ixazomib Maintenance	0	0
Placebo	0	4.5

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Percentage of Participants With Toxicities Post-randomization by Toxicity Type

Toxicities are graded using National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE), Version 4.0. Higher grades correspond to worse symptoms with the minimum grade being a 0 and the maximum grade being a 5. Toxicities post-randomization are described for each treatment arm by the type of toxicity as well as peak overall grade. (NCT02440464)
Timeframe: 2 years post-randomization

Intervention	Participants (Count of Participants)
	Maximum Toxicity Grade : 0 - 2	Maximum Toxicity Grade : 3	Maximum Toxicity Grade : 4	Maximum Toxicity Grade : 5	Abnormal Liver Symptoms	Dysgeusia	Encephalopathy	Grade 3-5 Allergic Reaction	Grade 3-5 Anaphylaxis	Grade 3-5 Blood/Lymphatic Toxicity	Grade 3-5 Cardiac Toxicity	Grade 3-5 Fatigue	Grade 3-5 Fever	Grade 3-5 GI Toxicity	Grade 3-5 Hearing Loss	Grade 3-5 Hemorrhage	Grade 3-5 Hepatobiliary/Pancreas	Grade 3-5 Hyperthyroidism	Grade 3-5 Hypothyroidism	Grade 3-5 Metabolic Toxicity	Grade 3-5 Musculoskeletal Toxicity	Grade 3-5 Nervous System Toxicity	Grade 3-5 Ocular Toxicity	Grade 3-5 Renal Toxicity	Grade 3-5 Respiratory Toxicity	Grade 3-5 Skin/Subcutaneous Tissue Toxicity	Grade 3-5 Vascular Toxicity	Hepatitis	Intestinal Obstruction	Liver Failure	Severe Muscle Weakness/Paralysis	Sudden Vision Loss	Tumor Lysis Syndrome
Ixazomib Maintenance	8	13	0	0	3	1	0	0	0	5	6	3	0	6	0	0	1	0	0	4	1	4	0	0	2	1	2	0	1	0	0	0	1
Placebo	6	14	1	1	2	2	0	1	0	8	7	3	0	7	0	0	7	0	1	6	3	4	2	5	8	5	3	1	0	0	1	0	0

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Number of Participants With Peripheral Blood Monoclonal Protein Reduction or Stabilization

Efficacy will be assessed monthly during NKAE treatment (4 months) by peripheral blood monoclonal protein monitoring. During follow-up, efficacy will be evaluated monthly the first 6 months. After that, quarterly until one year of follow-up. (NCT02481934)
Timeframe: 16 months

Intervention	participants (Number)
NKAE Cells Infusion + Chemotherapy	5

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Number of Participants With Adverse Events During NKAE Treatment

Toxicity will be assessed by adverse events count during NKAE treatment monitoring peripheral blood absolute neutrophil count (cells/μl). Toxicity will be evaluated monthly during NKAE treatment (4 months). During follow-up, it will be assessed monthly the first 6 months. After that, quarterly until one year of follow-up, based on Common Toxicity Criteria for Adverse Events of the National Cancer Institute (CTCAE) to v.4.03. (NCT02481934)
Timeframe: 16 months

Intervention	participants (Number)
NKAE Cells Infusion + Chemotherapy	2

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Overall Survival

duration of overall survival measured in days (NCT02489500)
Timeframe: 5 years

Intervention	days (Number)
Melphalan	43
Melphalan + Bortezomib	29

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Toxicities

Number of serious adverse events per participant based on Common Terminology Criteria for Adverse Events (CTCAE) Version 4.0 (NCT02489500)
Timeframe: 100 days

Intervention	events per participant (Mean)
Melphalan	8.5
Melphalan + Bortezomib	15

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Number of Participants With Hematologic Response

Hematologic response defined as: at least 50% improvement in the difference between involved and uninvolved free light chains (NCT02489500)
Timeframe: 6 months

Intervention	Participants (Count of Participants)
Melphalan	0
Melphalan + Bortezomib	0

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2-year Overall Survival Seen With Using Bortezomib in Combination With the ALL R3 Re-induction Regimen in Pediatric Patients With Relapsed or Refractory ALL or LL.

(NCT02535806)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Treatment Arm	1

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Post-induction Level of Minimal Residual Disease Seen With Using Bortezomib in Combination With the ALL R3 Re-induction Regimen in Pediatric Patients With Relapsed or Refractory ALL or LL.

Percent of Cells Positive for Minimal residual disease measured by multiparameter flow cytometry (NCT02535806)
Timeframe: 36 days

Intervention	Percentage of Cells Positive for MRD (Mean)
Treatment Arm	0.65

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Remission Rate Seen With Using Bortezomib in Combination With the ALL R3 Re-induction Regimen in Pediatric Patients With Relapsed or Refractory ALL or LL.

Number of patients with bone marrow blast percentage <5% after treatment (NCT02535806)
Timeframe: 36 days

Intervention	Participants (Count of Participants)
Treatment Arm	2

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Number of Subject With Adverse Events

Toxicities were assessed and graded according to CTCAE v 4.0. (NCT02535806)
Timeframe: 36 days

Intervention	Participants (Count of Participants)
Treatment Arm	1

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Percentage of Treatment-related Mortality (TRM)

"Number of treatment related deaths divided by total number of patients during induction or reinduction therapy.~Presented as percentage" (NCT02553460)
Timeframe: At the end of reinduction (up to 5 months after start of therapy)

Intervention	Participants (Count of Participants)
Stratum 1	1

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Cluster of Differentiation 34 (CD34) Enumeration

Estimate the percentage of Cluster of Differentiation 34 (CD34) positive cells in circulating peripheral blood as a measure of mobilization on the days of collection. (NCT02703779)
Timeframe: Within the first 30 days after stem cell collection

Intervention	percentage of CD34 positive cells (Mean)
Stem Cell Collection Without In-vivo Purging With Bortezomib	8.9
Stem Cell Collection With In-vivo Purging With Bortezomib	7.8

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Multiparametric Flow Cytometry - Cluster of Differentiation 34 (CD34)Assessment

Estimate the proportion of subjects who have a successful collection of stem cells (> 2 million Cluster of Differentiation 34 (CD34) cells/Kg of body weight) for autologous transplant in both treatment groups. (NCT02703779)
Timeframe: Within the first 30 days after stem cell collection

Intervention	Participants (Count of Participants)
Stem Cell Collection Without In-vivo Purging With Bortezomib	51
Stem Cell Collection With In-vivo Purging With Bortezomib	50

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Multiparametric Flow Cytometry - Minimum Residual Disease

Estimate the proportion of subjects with plasma cell contamination (defined as >0.01% and at least 100 cellular events) of harvested stem cell product by multi parametric flow cytometry (MFC) from patients with myeloma undergoing autologous stem cell collection 1) by standard of care mobilization using Granulocyte colony-stimulating factor (G-CSF) with or without Mozobil and 2) after two doses of bortezomib as in vivo purging plus standard of care using G-CSF with or without Mozobil. (NCT02703779)
Timeframe: Day 0 for all subjects (Day 0 is the day of stem cell collection)

Intervention	Participants (Count of Participants)
Stem Cell Collection Without In-vivo Purging With Bortezomib	11
Stem Cell Collection With In-vivo Purging With Bortezomib	13

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Progression-Free Survival (PFS) in Participants With High B-cell Lymphoma 2 (BCL-2) Expression

"PFS is defined as the number of days from the date the participant was randomized to the date of the first documented progressive disease (PD) per investigator assessment or death due to any cause, whichever occurs first. PFS was analyzed by Kaplan-Meier methodology.~BCL-2 expression was determined through central laboratory testing by immunohistochemistry (IHC) and based on a pre-specified scoring algorithm. High clinical score of 2+: ≥50% of tumor cells with moderate or higher cytoplasmic staining but < 50% of tumor cells with strong staining intensity; high clinical score of 3+: ≥50% of tumor cells with strong cytoplasmic staining." (NCT02755597)
Timeframe: Median duration of follow-up was 28.6 months for the venetoclax group and 28.6 months for the placebo group

Intervention	months (Median)
Venetoclax + Bortezomib and Dexamethasone	23.8
Placebo + Bortezomib and Dexamethasone	11.4

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Overall Response Rate (ORR)

Overall response rate is defined as the percentage of participants with documented best overall response of Partial Response (PR) or better (PR, Very good partial response [VGPR], Complete response [CR], or Stringent complete response [sCR]) per International Myeloma Working Group (IMWG) criteria as determined by an Independent Review Committee (IRC). (NCT02755597)
Timeframe: Response was assessed at Cycle 1, Day 1, and on Day 1 of every cycle thereafter; median time on follow-up was 28.6 months for the venetoclax group and 28.6 months for the placebo group

Intervention	percentage of participants (Number)
Venetoclax + Bortezomib and Dexamethasone	81.4
Placebo + Bortezomib and Dexamethasone	69.1

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Mean Change From Baseline in Physical Functioning Scale of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30)

"The QLQ-C30 is a 30-item subject self-report questionnaire composed of both multi-item and single scales, including five functional scales (physical, role, emotional, social, and cognitive), three symptom scales (fatigue, nausea and vomiting, and pain), a global health status/quality of life scale, and six single items (dyspnea, insomnia, appetite loss, constipation, diarrhea, and financial difficulties). For the Physical Functioning scale, participants rate five items on a four-point scale, with 1 as not at all and 4 as very much. The Physical Functioning Scale scores range from 0 to 100 and were calculated per the EORTC QLQ-C30 Scoring Manual (3rd edition), version 3.0. A high scale score represents high/healthy level of functioning. Positive changes from baseline indicate improvement." (NCT02755597)
Timeframe: Baseline; Cycle 3 (Cycles 1 - 8 are 21 days, Cycles 9 and beyond are 35 days) through Cycle 47, collected on Day 1 of every other cycle and at the Treatment Completion Visit (TCV) while participant is on treatment

Intervention	units on a scale (Mean)
	Cycle 3, Day 1	Cycle 5, Day 1	Cycle 7, Day 1	Cycle 9, Day 1	Cycle 11, Day 1	Cycle 13, Day 1	Cycle 15, Day 1	Cycle 17, Day 1	Cycle 19, Day 1	Cycle 21, Day 1	Cycle 23, Day 1	Cycle 25, Day 1	Cycle 27, Day 1	Cycle 29, Day 1	Cycle 31, Day 1	Cycle 33, Day 1	Cycle 35, Day 1	Cycle 37, Day 1	Cycle 39, Day 1	Cycle 41, Day 1	Cycle 43, Day 1	Cycle 45, Day 1	Cycle 47, Day 1	Final visit
Placebo + Bortezomib and Dexamethasone	-4.6	-7.8	-8.6	-8.0	-7.5	-8.8	-7.3	-8.6	-7.0	-8.5	-7.5	0.5	-3.3	-4.0	2.2	-4.8	4.4	15.0	8.9	13.3	13.3	13.3	0.0	-10.0
Venetoclax + Bortezomib and Dexamethasone	-5.0	-3.9	-6.1	-3.5	-1.5	-3.2	-2.3	-1.8	-2.5	-1.5	-3.4	-3.8	-8.6	-8.7	-2.8	-4.0	-7.0	-7.5	-10.1	-13.0	-7.8	-1.3	0.0	-11.8

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Mean Change From Baseline in Patient Reported Outcomes Measurement Information System [PROMIS] Cancer Fatigue Short Form [SF] Score

PROMIS Cancer Fatigue SF is a seven item questionnaire that assesses the impact and experience of fatigue over the past 7 days. All questions employ the following five response options: 1 = Not at all, 2 = A little bit, 3 = Somewhat, 4 = Quite a bit, and 5 = Very much. The total raw score is the sum of the responses to each question and is converted to a T-score. The T-score re-scales the total raw score to a standardized score with a mean of 50 and a standard deviation of 10. The [PROMIS] Cancer Fatigue Short Form [SF] 7a T-Scores range from 29.4 to 83.2, with higher scores indicating more fatigue. Negative changes from baseline indicate improvement. (NCT02755597)
Timeframe: Baseline; Cycle 3 (Cycles 1 - 8 are 21 days, Cycles 9 and beyond are 35 days) through Cycle 47, collected on Day 1 of every other cycle and at the Treatment Completion Visit (TCV) while participant is on treatment

Intervention	T-score (Mean)
	Cycle 3, Day 1	Cycle 5, Day 1	Cycle 7, Day 1	Cycle 9, Day 1	Cycle 11, Day 1	Cycle 13, Day 1	Cycle 15, Day 1	Cycle 17, Day 1	Cycle 19, Day 1	Cycle 21, Day 1	Cycle 23, Day 1	Cycle 25, Day 1	Cycle 27, Day 1	Cycle 29, Day 1	Cycle 31, Day 1	Cycle 33, Day 1	Cycle 35, Day 1	Cycle 37, Day 1	Cycle 39, Day 1	Cycle 41, Day 1	Cycle 43, Day 1	Cycle 45, Day 1	Cycle 47, Day 1	Final visit
Placebo + Bortezomib and Dexamethasone	1.8	2.4	2.6	2.6	3.1	2.3	2.1	2.6	0.9	1.2	1.5	-0.1	-0.1	0.8	-0.3	3.7	1.1	-3.0	4.1	-0.7	4.4	1.8	0.0	2.9
Venetoclax + Bortezomib and Dexamethasone	2.2	3.3	3.2	2.3	0.6	1.8	1.5	1.2	0.7	1.6	2.0	2.0	3.4	3.9	2.8	2.0	3.4	4.1	3.6	3.3	5.3	-0.3	-2.5	5.0

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Overall Survival (OS).

OS is defined as the number of days from the date of randomization to the date of death due to any cause. All events of death were to be included, regardless of whether the event occurred while the participant was still taking study drug or after the participant discontinued study drug. If a participant is not known to have died, OS was censored at the date of last contact. The distribution of OS was estimated using Kaplan-Meier methodology. (NCT02755597)
Timeframe: Median duration of follow-up was 45.6 months for the venetoclax group and 45.6 months for the placebo group

Intervention	months (Median)
Venetoclax + Bortezomib and Dexamethasone	NA
Placebo + Bortezomib and Dexamethasone	NA

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Progression-free Survival (PFS)

PFS is defined as the number of days from the date the participant was randomized to the date of the first documented progressive disease (PD) as determined by an Independent Review Committee (IRC) or death due to any cause, whichever occurs first. PFS was analyzed by Kaplan-Meier methodology. (NCT02755597)
Timeframe: Median duration of follow-up was 28.6 months for the venetoclax group and 28.6 months for the placebo group

Intervention	months (Median)
Venetoclax + Bortezomib and Dexamethasone	23.2
Placebo + Bortezomib and Dexamethasone	11.5

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Mean Change From Baseline in Global Health Status/Quality of Life Scale of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30)

"The QLQ-C30 is a 30-item subject self-report questionnaire composed of both multi-item and single scales, including five functional scales (physical, role, emotional, social, and cognitive), three symptom scales (fatigue, nausea and vomiting, and pain), a global health status/quality of life scale, and six single items (dyspnea, insomnia, appetite loss, constipation, diarrhea, and financial difficulties). For the Global Health Status/Quality of Life scale, participants rate two items on a seven point scale, with 1 as very poor and 7 as excellent. The Global Health Status/Quality of Life scale ranges from 0 to 100 and was calculated per the EORTC QLQ-C30 Scoring Manual (3rd edition), version 3.0. A high score for the global health status/QoL represents a high QoL. Positive changes from baseline indicate improvement." (NCT02755597)
Timeframe: Baseline; Cycle 3 (Cycles 1 - 8 are 21 days, Cycles 9 and beyond are 35 days) through Cycle 47, collected on Day 1 of every other cycle and at the Treatment Completion Visit (TCV) while participant is on treatment

Intervention	units on a scale (Mean)
	Cycle 3, Day 1	Cycle 5, Day 1	Cycle 7, Day 1	Cycle 9, Day 1	Cycle 11, Day 1	Cycle 13, Day 1	Cycle 15, Day 1	Cycle 17, Day 1	Cycle 19, Day 1	Cycle 21, Day 1	Cycle 23, Day 1	Cycle 25, Day 1	Cycle 27, Day 1	Cycle 29, Day 1	Cycle 31, Day 1	Cycle 33, Day 1	Cycle 35, Day 1	Cycle 37, Day 1	Cycle 39, Day 1	Cycle 41, Day 1	Cycle 43, Day 1	Cycle 45, Day 1	Cycle 47, Day 1	Final visit
Placebo + Bortezomib and Dexamethasone	-2.2	-2.5	-6.7	-6.7	-5.2	-1.7	0.5	-7.7	0.8	-5.6	-1.0	-4.5	4.2	-1.1	5.6	-7.1	4.2	10.4	0.0	8.3	-8.3	4.2	-8.3	-6.7
Venetoclax + Bortezomib and Dexamethasone	-1.9	-5.1	-8.3	-6.9	-0.5	-1.0	-4.9	-5.1	-1.3	-6.6	-2.9	-4.7	-9.0	-6.9	-4.8	-7.7	-3.8	-13.7	-9.3	-11.0	2.0	-1.7	10.4	-8.1

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Mean Change From Baseline in Brief Pain Inventory - Short Form (BPI-SF) Worst Pain

"The BPI-SF is a pain-specific measure developed to assess patient-reported severity (or intensity) of pain (4 items) and the impact of pain on daily functioning (7 items) in patients with cancer pain. The four pain severity items assess pain at its worst in last 24 hours, least in last 24 hours, average, and now (current pain). For these items, participants are asked to rate their pain on an 11-point numeric rating scale with anchors of 0 (no pain) and 10 (pain as bad as you can imagine). The Worst Pain scores range from 0 to 10, with higher scores indicating severe pain. Negative changes from baseline indicate improvement." (NCT02755597)
Timeframe: Baseline; Cycle 3 (Cycles 1 - 8 are 21 days, Cycles 9 and beyond are 35 days) through Cycle 47, collected on Day 1 of every other cycle and at the Treatment Completion Visit (TCV) while participant is on treatment

Intervention	units on a scale (Mean)
	Cycle 3, Day 1	Cycle 5, Day 1	Cycle 7, Day 1	Cycle 9, Day 1	Cycle 11, Day 1	Cycle 13, Day 1	Cycle 15, Day 1	Cycle 17, Day 1	Cycle 19, Day 1	Cycle 21, Day 1	Cycle 23, Day 1	Cycle 25, Day 1	Cycle 27, Day 1	Cycle 29, Day 1	Cycle 31, Day 1	Cycle 33, Day 1	Cycle 35, Day 1	Cycle 37, Day 1	Cycle 39, Day 1	Cycle 41, Day 1	Cycle 43, Day 1	Cycle 45, Day 1	Cycle 47, Day 1	Final visit
Placebo + Bortezomib and Dexamethasone	-0.5	-0.2	0.2	0.0	0.1	-0.1	-0.0	-0.1	-0.2	-0.3	-0.2	0.2	0.1	0.3	0.6	0.4	-0.2	1.5	-0.3	0.3	0.5	1.0	1.0	0.4
Venetoclax + Bortezomib and Dexamethasone	-0.6	0.0	-0.1	-0.2	-0.4	-0.2	-0.2	-0.3	-0.1	-0.1	-0.0	0.4	0.2	-0.2	0.0	-0.2	0.1	0.4	0.1	0.1	-0.1	-0.7	-2.8	0.3

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Very Good Partial Response (VGPR) or Better Response Rate

The percentage of participants with documented best overall response of Very Good Partial Response (VGPR) or better (VGPR, Complete response [CR], or Stringent complete response [sCR]) per 2016 standard International Myeloma Working Group (IMWG) criteria as determined by an Independent Review Committee (IRC) was computed. (NCT02755597)
Timeframe: Response was assessed at Cycle 1, Day 1, and on Day 1 of every cycle thereafter; median time on follow-up was 28.6 months for the venetoclax group and 28.6 months for the placebo group

Intervention	percentage of participants (Number)
Venetoclax + Bortezomib and Dexamethasone	60.3
Placebo + Bortezomib and Dexamethasone	38.1

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Time to Progression (TTP)

TTP is defined as the number of days from the date of randomization to the date of first documented progressive disease (PD) as determined by an Independent Review Committee (IRC) or death due to multiple myeloma, whichever occurs first. TTP was analyzed by Kaplan-Meier methodology. (NCT02755597)
Timeframe: Median time on follow-up up was 28.6 months for the venetoclax group and 28.6 months for the placebo group

Intervention	months (Median)
Venetoclax + Bortezomib and Dexamethasone	25.4
Placebo + Bortezomib and Dexamethasone	12.2

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Minimal Residual Disease (MRD) Negativity Rate

MRD negativity rate is defined as the percentage of participants who have negative MRD by bone marrow aspirate at any time point after randomization and before progression or starting subsequent therapy. MRD negativity was defined at 10^-5 threshold (less than one residual myeloma cell per 10^5 total nucleated cells) as measured by centralized testing of bone marrow aspirate by Next Generation Sequencing (NGS). MRD positive participants include those of which all tested samples were found to be MRD positive or indeterminate. Participants with missing or unevaluable MRD status were considered as MRD positive. (NCT02755597)
Timeframe: Assessed at Screening; to confirm a stringent Complete Response (sCR) or Complete Response (CR); at 6 months and 12 months post-confirmed CR/sCR

Intervention	percentage of participants (Number)
Venetoclax + Bortezomib and Dexamethasone	15.5
Placebo + Bortezomib and Dexamethasone	2.1

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Duration of Response (DOR)

DOR is defined as the number of days from the participant's date of first documented response (partial response [PR] or better) to the date of first documented progressive disease (PD) as determined by an Independent Review Committee (IRC) or death due to multiple myeloma, whichever occurs first. DOR was analyzed by Kaplan-Meier methodology. (NCT02755597)
Timeframe: Response was assessed at Cycle 1, Day 1, and on Day 1 of every cycle thereafter; median time on follow-up was 28.6 months for the venetoclax group and 28.6 months for the placebo group

Intervention	months (Median)
Venetoclax + Bortezomib and Dexamethasone	NA
Placebo + Bortezomib and Dexamethasone	12.8

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Time to Progression (TTP)

TTP is defined as the duration from the date of randomization to the date of first documented evidence of progressive disease according to the IMWG criteria. (NCT02874742)
Timeframe: From randomization to the date of first documented evidence of progressive disease (up to 5 years)

Intervention	Months (Median)
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	NA
Randomized: Daratumumab+RVd (D-RVd)	NA
Safety Run-in: D-RVd	NA

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Time to Partial Response (PR) or Better

Time to PR or better is the duration from the date of randomization to the date of initial documentation of PR or better, which was confirmed by a repeated measurement as required by the IMWG criteria. (NCT02874742)
Timeframe: From randomization to the date of initial documentation of PR or better (up to 5 years)

Intervention	Months (Median)
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	0.8
Randomized: Daratumumab+RVd (D-RVd)	0.8
Safety Run-in: D-RVd	0.8

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Time to Complete Response or Better

Time to CR or better is the duration from the date of randomization to the date of initial documentation of CR or better, which was confirmed by a repeated measurement as required by the IMWG criteria. (NCT02874742)
Timeframe: From randomization to the date of initial documentation of CR (up to 5 years)

Intervention	Months (Median)
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	9.6
Randomized: Daratumumab+RVd (D-RVd)	8.9
Safety Run-in: D-RVd	7.7

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Progression-free Survival (PFS)

PFS is defined as the duration from the date of randomization to the date of first documented evidence of progressive disease or death, whichever comes first. PD is defined as an increase of 25 % from the lowest response value in one of the following: serum and urine M-component (absolute increase must be >= 0.5 g/dL and >=200 mg/24 hours respectively); Only in participants without measurable serum and urine M-protein levels the difference between involved and uninvolved FLC levels (absolute increase must be > 10 mg/dL); Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas; Development of hypercalcemia (corrected serum calcium >11.5 mg/dL) that can be attributed solely to PC proliferative disorder. (NCT02874742)
Timeframe: From randomization to the date of first documented evidence of progressive disease or death (up to 5 years)

Intervention	Months (Median)
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	NA
Randomized: Daratumumab+RVd (D-RVd)	NA
Safety Run-in: D-RVd	NA

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Percentage of Participants With Stringent Complete Response (sCR)

Percentage of participants who had achieved sCR as determined by the validated computer algorithm according to the International Myeloma Working Group (IMWG) criteria, by the end of post-autologous stem cell transplantation (post-ASCT) consolidation treatment were reported. Complete response (CR) is defined as negative immunofixation on the serum and urine, and disappearance of any soft tissue plasmacytomas, and less than (<) 5 percent (%) PCs in bone marrow. sCR is defined as in addition to CR a normal FLC ratio, and absence of clonal plasma cells (PCs) by immunohistochemistry or immunofluorescence or 2 to 4-color flow cytometry. (NCT02874742)
Timeframe: From randomization to post-ASCT consolidation (after Cycle 6) before maintenance treatment (up to 10 months)

Intervention	Percentage of participants (Number)
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	32.0
Randomized: Daratumumab+RVd (D-RVd)	42.4

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Overall Survival (OS)

OS is measured from the date of randomization to the date of the participant's death. (NCT02874742)
Timeframe: From randomization to the date of initial documentation of participant's death (up to 5 years)

Intervention	Months (Median)
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	NA
Randomized: Daratumumab+RVd (D-RVd)	NA
Safety Run-in: D-RVd	NA

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Percentage of Participants Who Achieved Very Good Partial Response (VGPR) or Better

VGPR or better rate is defined as the percentage of participants who achieved VGPR or better, according to the IMWG criteria. VGPR is defined as serum and urine M-component detectable by immunofixation but not on electrophoresis, or >= 90% reduction in serum M-protein plus urine M-protein <100 mg/24 hours. (NCT02874742)
Timeframe: From randomization to end of following: induction treatment, ASCT, post-ASCT consolidation (after Cycle 6) and at the end of maintenance period of 24 months (overall duration up to 34 months)

Intervention	Percentage of participants (Number)
	At the end of induction prior to ASCT	At the end of ASCT prior to consolidation	At the end of post-ASCT consolidation	At the End of Maintenance Period (up to 24 Months)
Randomized: Daratumumab+RVd (D-RVd)	71.7	86.9	90.9	96.0
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	56.7	66.0	73.2	77.6
Safety Run-in: D-RVd	68.8	100	100	100.0

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Time to Stringent Complete Response (sCR)

Time to sCR is the duration from the date of randomization to the date of initial documentation of sCR, which was confirmed by a repeated measurement as required by the IMWG criteria. (NCT02874742)
Timeframe: From randomization to the date of initial documentation of sCR (up to 5 years)

Intervention	Months (Median)
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	14.3
Randomized: Daratumumab+RVd (D-RVd)	10.2
Safety Run-in: D-RVd	8.4

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Duration of Stringent Complete Response (sCR)

Duration of sCR is the duration from the date of initial documentation of a sCR response, according to the IMWG criteria, to the date of first documented evidence of progressive disease, or relapse from sCR. PD is defined as an increase of 25 % from the lowest response value in one of the following: serum and urine M component (absolute increase must be >= 0.5 g/dL and >=200 mg/24 hours respectively); Only in participants without measurable serum and urine M-protein levels the difference between involved and uninvolved FLC levels (absolute increase must be > 10 mg/dL); Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas; Development of hypercalcemia (corrected serum calcium >11.5 mg/dL) that can be attributed solely to PC proliferative disorder. (NCT02874742)
Timeframe: From randomization to the date of first documented evidence of progressive disease or relapse from sCR (up to 5 years)

Intervention	Months (Median)
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	NA
Randomized: Daratumumab+RVd (D-RVd)	NA
Safety Run-in: D-RVd	NA

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Duration of Response

Duration of response is defined as the duration from the date of initial documentation of a response (PR or better) according to the IMWG criteria to the date of first documented evidence of progressive disease according to the IMWG criteria. PD is defined as an increase of 25 % from the lowest response value in one of the following: serum and urine M-component (absolute increase must be >= 0.5 g/dL and >=200 mg/24 hours respectively); Only in participants without measurable serum and urine M-protein levels the difference between involved and uninvolved FLC levels (absolute increase must be > 10 mg/dL); Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas; Development of hypercalcemia (corrected serum calcium >11.5 mg/dL) that can be attributed solely to PC proliferative disorder. (NCT02874742)
Timeframe: From the date of initial documentation of a response (PR or better) to the date of first documented evidence of progressive (up to 5 years)

Intervention	Months (Median)
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	NA
Randomized: Daratumumab+RVd (D-RVd)	NA
Safety Run-in: D-RVd	NA

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Duration of Complete Response or Better

Duration of CR or better is the duration from the date of initial documentation of a CR or sCR response, according to the IMWG criteria, to the date of first documented evidence of progressive disease (PR), or relapse from CR. PD is defined as an increase of 25 % from the lowest response value in one of the following: serum and urine M-component (absolute increase must be greater than or equal to [>=] 0.5 gram per deciliter [g/dL] and >=200 milligrams [mg]/24 hours respectively); Only in participants without measurable serum and urine M-protein levels the difference between involved and uninvolved FLC levels (absolute increase must be > 10 mg/dL); Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas; Development of hypercalcemia (corrected serum calcium >11.5 mg/dL) that can be attributed solely to plasma cells (PCs) proliferative disorder. (NCT02874742)
Timeframe: From randomization to the date of first documented evidence of progressive disease or relapse from CR (up to 5 years)

Intervention	Months (Median)
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	NA
Randomized: Daratumumab+RVd (D-RVd)	NA
Safety Run-in: D-RVd	NA

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Percentage of Participants With Negative Minimal Residual Disease (MRD)

Minimal residual disease negative rate is defined as the percentage of participants who achieve MRD negative status by the respective time point. Minimal residual disease was evaluated in participants who achieved CR or sCR (including participants with VGPR or better and suspected daratumumab interference) using next-generation sequencing which utilizes multiple myeloma cell DNA from bone marrow aspirates at a threshold of less than (<) 10^5. (NCT02874742)
Timeframe: From randomization to end of following: induction treatment, post-ASCT consolidation (after Cycle 6) (up to 4.5 months), and at the end of maintenance period of 24 months (overall duration up to 34 months)

Intervention	Percentage of participants (Number)
	MRD from randomization to prior to ASCT (10^5)	Post ASCT consolidation (10^5)	At the End of Maintenance Period (up to 24 Months) (10^5)
Randomized: Daratumumab+RVd (D-RVd)	22.1	50.0	64.4
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	7.8	20.4	30.1
Safety Run-in: D-RVd	18.8	50.0	81.3

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Percentage of Participants With Overall Response Rate (ORR)

ORR- percentage of participants who achieved partial response (PR) or better (PR, Very Good Partial Response [VGPR], CR or sCR) based on computerized algorithm as per IMWG criteria. PR -greater than or equal to (>=) 50% reduction of serum M-protein and reduction in 24-hour urinary M-protein by >=90% or to <200 mg//24 hours. If serum and urine M-protein are not measurable, a decrease of >=50% in the difference between involved and uninvolved FLC levels is required. A >=50% reduction in the size of soft tissue plasmacytomas is also required; VGPR-serum and urine M-component detectable by immunofixation but not on electrophoresis, or >= 90% reduction in serum M-protein plus urine M-protein <100 mg/24 hours; CR-negative immunofixation on the serum and urine, and disappearance of any soft tissue plasmacytomas, and <5% PCs in bone marrow. sCR- in addition to CR a normal FLC ratio, and absence of clonal PCs by immunohistochemistry or immunofluorescence or 2 to 4-color flow cytometry. (NCT02874742)
Timeframe: From randomization to end of following: induction treatment, ASCT, post-ASCT consolidation (after Cycle 6) and at the end of maintenance treatment of 24 months (overall duration up to 34 months)

Intervention	Percentage of participants (Number)
	At the end of induction prior to ASCT	At the end of ASCT prior to consolidation	At the end of post-ASCT consolidation	At the End of Maintenance Treatment (up to 24 Months)
Randomized: Daratumumab+RVd (D-RVd)	98.0	99.0	99.0	99.0
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	91.8	91.8	91.8	91.8
Safety Run-in: D-RVd	100	100	100	100.0

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Percentage of Participants With Overall Stringent Complete Response (sCR)

Overall sCR rate is defined as the percentage of participants who achieved sCR, according to the IMWG criteria. CR is defined as negative immunofixation on the serum and urine, and disappearance of any soft tissue plasmacytomas, and < 5 % PCs in bone marrow. sCR is defined as in addition to CR a normal FLC ratio, and absence of clonal PCs by immunohistochemistry or immunofluorescence or 2 to 4-color flow cytometry. (NCT02874742)
Timeframe: From randomization to end of following: induction treatment, ASCT, post-ASCT consolidation (after Cycle 6) and at the end of maintenance treatment of 24 months (overall duration up to 34 months)

Intervention	Percentage of participants (Number)
	At the end of induction prior to ASCT	At the end of ASCT prior to consolidation	At the end of post-ASCT consolidation	At the end of Maintenance Treatment (up to 24 Months)
Randomized: Daratumumab+RVd (D-RVd)	12.1	21.2	42.4	67.0
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	7.2	14.4	32.0	48.0
Safety Run-in: D-RVd	0	43.8	56.3	93.8

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Time to Very Good Partial Response (VGPR) or Better

Time to VGPR or better is the duration from the date of randomization to the date of initial documentation of VGPR or better, which was confirmed by a repeated measurement as required by the IMWG criteria. (NCT02874742)
Timeframe: From randomization to the date of initial documentation of VGPR or better (up to 5 years)

Intervention	Months (Median)
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	3.0
Randomized: Daratumumab+RVd (D-RVd)	2.2
Safety Run-in: D-RVd	2.1

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Percentage of Participants With Complete Response (CR) or Better

CR or better rate is defined as the percentage of participants who achieve CR or sCR, according to the IMWG criteria. CR is negative immunofixation on the serum and urine, and disappearance of any soft tissue plasmacytomas, and < 5% PCs in bone marrow. sCR is defined as in addition to CR a normal FLC ratio, and absence of clonal plasma cells (PCs) by immunohistochemistry or immunofluorescence or 2 to 4-color flow cytometry. For 2 participants (1 in each randomized treatment group), data were updated by the study sites which resulted in their inclusion to the response-evaluable analysis set after the primary analysis. (NCT02874742)
Timeframe: From randomization to end of following: induction treatment, ASCT, post-ASCT consolidation (after Cycle 6) and at the end of maintenance period of 24 months (overall duration up to 34 months)

Intervention	Percentage of participants (Number)
	At the end of induction prior to ASCT	At the end of ASCT prior to consolidation	At the end of post-ASCT consolidation	At the end of maintenance period (up to 24 Months)
Randomized: Daratumumab+RVd (D-RVd)	19.2	27.3	51.5	83.0
Randomized: Lenalidomide+Bortezomib+Dexamethasone (RVd)	13.4	19.6	42.3	60.2
Safety Run-in: D-RVd	12.5	56.3	68.8	93.8

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Number of Patients Alive and Free of Severe Acute GVHD Following HLA Matched Related or Unrelated Donor Hematopoietic Peripheral Blood Transplant

Will use patient counts for the number of patients alive and free of severe acute graft versus host disease (GVHD) following human leukocyte antigen (HLA) matched related or unrelated donor hematopoietic peripheral blood transplant. (NCT02877082)
Timeframe: At 6 months post-transplant

Intervention	Participants (Count of Participants)
Tacrolimus, Bortezomib, Thymoglobulin	1

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Total Number of Serious Adverse Events and Adverse Events Related to This Immunosuppressive Regimen

"An adverse event (AE) is defined as any untoward medical experience or change of an existing condition that occurs during or after treatment. All AEs occurring during this study, whether observed by the physician, nurse, or reported by the patient, will be graded per NCI CTCAE version 4.0 and recorded on protocol-specific case report forms. A serious adverse event (SAE) is defined as any expected or unexpected adverse event (AE, generally equivalent to CTCAE grades 3, 4 or 5) that results in any of the following outcomes:~Death~Life-threatening event~In-patient hospitalization (not required as part of the treatment) or prolongation of existing hospitalization~Persistent or significant disability/incapacity~Congenital anomaly/birth defect~Cancer~Overdose" (NCT02877082)
Timeframe: Up to 6 months post-transplant

Intervention	events (Number)
Tacrolimus, Bortezomib, Thymoglobulin	9

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Progression Free Survival (PFS) at Landmark Points - 20 Months

PFS at landmark points are the percentage of participants without progression (i.e., KM estimates) at the landmark time endpoints. (NCT02902965)
Timeframe: The median time on study was 19.6 months (range: 0.16+, 24.64), with the 20 month Progression-Free Survival (PFS) rate presented based on Kaplan-Meier estimates.

Intervention	percentage of participants (Number)
Ibrutinib+ Bortezomib+ Dexamethasone	6.6

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Safety and Tolerability of Ibrutinib in Combination With Bortezomib and Dexamethasone as Measured by the Number of Participants With Adverse Events.

Safety and tolerability of ibrutinib in combination with bortezomib and dexamethasone as measured by the frequency and type of adverse events graded using the NCI CTCAE v 4.03. Frequency and Type of Adverse Events are reported in the Adverse Events module (NCT02902965)
Timeframe: From first dose of Ibrutinib to within 30 days of last dose for each participant or until study closure. This is the median treatment duration for Ibrutinib of 5.7 months (range: 0.1 - 23.7 months) +30 days (Adverse Events collection period).

Intervention	Participants (Count of Participants)
Ibrutinib+ Bortezomib+ Dexamethasone	74

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Time to Progression (TTP)

Time from date of first dose of study treatment to the date of first documented evidence of PD or date of censoring for the participants not progressed. The censoring date is the last adequate tumor assessment date. (NCT02902965)
Timeframe: The median time on study was 19.6 months (range: 0.16+, 24.64).

Intervention	Months (Median)
Ibrutinib+ Bortezomib+ Dexamethasone	10.6

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Duration of Response (DOR)

The time interval between the date of initial documentation of a response (PR or better) and the date of first documented evidence of PD, death, or date of censoring for the participants not progressed/died. The censoring date is the last adequate tumor assessment date. (NCT02902965)
Timeframe: The median time on study was 19.6 months (range: 0.16+, 24.64).

Intervention	Months (Median)
Ibrutinib+ Bortezomib+ Dexamethasone	9.5

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Median Progression-Free Survival (PFS)

The primary efficacy endpoint of this study is mPFS. Progression free survival is defined as the time from the date of first dose of study treatment to confirmed disease progression or death from any cause, whichever occurs first. (NCT02902965)
Timeframe: The median time on study was 19.6 months (range: 0.16+, 24.64). Participants were evaluated for Progression-Free Survival (PFS) during their entire time on the study.

Intervention	Months (Median)
Ibrutinib+ Bortezomib+ Dexamethasone	8.5

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Overall Response Rate (ORR)

Overall Response Rate is the percentage of participants who achieve a PR or better over the course of the study but prior to initiation of subsequent anti-cancer therapy (NCT02902965)
Timeframe: The median time on study was 19.6 months (range: 0.16+, 24.64). Participants were evaluated for Overall Response (OR) during the entire time on the study.

Intervention	percentage of participants (Number)
Ibrutinib+ Bortezomib+ Dexamethasone	56.8

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Overall Survival (OS) at 24 Months

As the median overall survival has not been reached, the data for the landmark analysis at 24 months are provided. (NCT02902965)
Timeframe: The median time on study was 19.6 months (0.16+, 24.64), with the 24 month Overall Survival (OS) rate presented based on Kaplan-Meier estimates.

Intervention	percentage of participants (Number)
Ibrutinib+ Bortezomib+ Dexamethasone	53.6

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Phase 1: The Number of Subjects With Treatment-emergent Adverse Events (TEAEs), Drug-related TEAEs, and Treatment-emergent Serious AE

A treatment-emergent adverse event (TEAE) is defined as any event arising or worsening after start of study drug administration until the end of the treatment period (NCT02928029)
Timeframe: From the start of study drug (radium-223 dichloride) to 30 days after last dose of study treatment (radium-223 dichloride, BOR, or DEX, whichever is last), assessed up to approximately 2 years

Intervention	Participants (Count of Participants)
	Any TEAE	Any drug-related TEAE	Any treatment-emergent serious AE
Radium-223 Dichloride 33 kBq/kg + Bortezomib and Dexamethasone	3	3	2
Radium-223 Dichloride 55 kBq/kg + Bortezomib and Dexamethasone	4	4	1

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Phase 1: The Number of Subjects With Complete Response (CR) and Very Good Partial Response (VGPR)

"Determined by International Myeloma Working Group (IMWG) uniform response criteria.~CR: Negative immunofixation of serum and urine, disappearance of any soft-tissue plasmacytomas, and <5% plasma cells in bone marrow; in patients for whom only measurable disease is by serum free light chain (FLC) level, normal FLC ratio of 0.26 to 1.65 in addition to CR criteria is required; 2 consecutive assessments are needed.~VGPR: Serum and urine M-component detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-component plus urine M-component <100 mg/24 hours (hrs); in patients for whom only measurable disease is by serum FLC level, >90% decrease in difference between involved and uninvolved FLC levels, in addition to VGPR criteria, is required; 2 consecutive assessments are needed" (NCT02928029)
Timeframe: Up to approximately 2 years

Intervention	Participants (Count of Participants)
Radium-223 Dichloride 33 kBq/kg + Bortezomib and Dexamethasone	NA
Radium-223 Dichloride 55 kBq/kg + Bortezomib and Dexamethasone	NA

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Phase 1: MTD/RP2D Determined by the Incidence of DLTs

Maximum tolerated dose (MTD) or recommended phase 2 dose (RP2D) determined by incidence of dose limiting toxicity (DLT) using Common Terminology Criteria for Adverse Events (CTCAE) version 4.03 for the severity grade (NCT02928029)
Timeframe: From the start of study medication through 3 weeks after administration of the second dose of radium-223 dichloride, assessed up to 9 weeks

Intervention	KBq/kg (Number)
Radium-223 Dichloride 33 kBq/kg + Bortezomib and Dexamethasone	NA
Radium-223 Dichloride 55 kBq/kg + Bortezomib and Dexamethasone	NA

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Overall Survival (OS)

Overall survival (OS) was measured from the date of first dose (start of induction) to the date of death due to any cause. (NCT02951819)
Timeframe: Up to 36 months

Intervention	Months (Median)
Newly Diagnosed Multiple Myeloma (NDMM)	NA
Relapsed Multiple Myeloma (RMM)	NA

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Duration of Response (DOR)

DOR was defined for participants with a confirmed response (PR or better) as the duration from the date of initial documentation of a response (PR or better) according to the IMWG criteria to the date of first documented evidence of progressive disease according to the IMWG criteria or death due to progressive disease. PR:>=50% reduction of serum M-protein and reduction in 24hours urinary M-protein by >=90% or to <200 mg/24hours. If serum and urine M-protein are unmeasurable, a >=50% decrease in difference involved and uninvolved FLC levels required in place of M-protein criteria. If serum and urine M-protein are not measurable, and serum free light assay is also not measurable, >=50% reduction in PCs is required in place of M-protein, provided baseline bone marrow PCs % was >=30%. In addition to the above criteria, if present at baseline, a >=50% reduction in the size of soft tissue plasmacytomas is also required. (NCT02951819)
Timeframe: Up to 36 months

Intervention	Months (Median)
Newly Diagnosed Multiple Myeloma (NDMM)	NA
Relapsed Multiple Myeloma (RMM)	20.7

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Percentage of Participants With Treatment Emergent-Adverse Event

An adverse event (AE) was any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. Treatment-emergent were events between administration of study drug and approximately up to 36 months that were absent before treatment or that worsened relative to pre-treatment state. (NCT02951819)
Timeframe: Up to 36 months

Intervention	Percentage of participants (Number)
Newly Diagnosed Multiple Myeloma (NDMM)	100.0
Relapsed Multiple Myeloma (RMM)	100.0

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Time to Disease Progression (TTP)

TTP was defined as the time between the date of first dose (start of induction) and the date of first documented evidence of confirmed PD, as defined in the IMWG response criteria. PD per IMWG criteria: Increase of 25% from lowest response value in one of following: Serum and urine M-component (absolute increase >=0.5 g/deciliter (dL) and >=200 mg/24 hours respectively); Only participants without measurable serum and urine M-protein levels: difference between involved and uninvolved FLC levels (absolute increase>10 mg/dL); Only participants without measurable serum and urine M-protein levels, without measurable disease by FLC levels, bone marrow PC% (absolute % >=10%); Bone marrow PC%: absolute% >10%; Definite development of new bone lesions/soft tissue plasmacytomas/definite increase in size of existing bone lesions/soft tissue plasmacytomas and Development of hypercalcemia (corrected serum calcium >11.5 mg/dL) that can be attributed solely to the PC proliferative disorder. (NCT02951819)
Timeframe: Approximately 15 months

Intervention	Months (Median)
Newly Diagnosed Multiple Myeloma (NDMM)	NA
Relapsed Multiple Myeloma (RMM)	13.31

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Progression Free Survival (PFS)

PFS: duration from date of first dose (start of induction) to date of first documented evidence of progressive disease (PD) based on computerized algorithm per IMWG criteria or death due to any cause, whichever occurred first. PD: 25% increase from lowest response value in one of following: Serum and urine M-component (absolute increase >=0.5 g/dL and >=200 mg/24 hours respectively);Only participants without measurable serum and urine M-protein levels: difference between involved and uninvolved FLC levels (absolute increase>10 mg/dL);Only participants without measurable serum and urine M-protein levels, without measurable disease by FLC levels, bone marrow PC% (absolute % >=10%); Bone marrow PC%: absolute% >10%; Definite development of new bone lesions/soft tissue plasmacytomas/definite increase in size of existing bone lesions/soft tissue plasmacytomas, Development of hypercalcemia (corrected serum calcium >11.5 mg/dL) that can be attributed solely to PC proliferative disorder. (NCT02951819)
Timeframe: Up to 36 months

Intervention	Months (Median)
Newly Diagnosed Multiple Myeloma (NDMM)	NA
Relapsed Multiple Myeloma (RMM)	21.7

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Percentage of Participants Who Achieved Complete Response (CR) or Very Good Partial Response (VGPR)

Percentage of participants who achieved CR or VGPR (as per International Myeloma Working Group [IMWG] criteria) was reported. CR: negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and less than (<) 5 percent (%) plasma cells (PC) in bone marrow. VGPR: serum and urine M-protein detectable by immunofixation but not on electrophoresis or greater than or equal to (>=) 90% reduction in serum M-protein plus urine M-protein level < 100 milligram per 24 hours (mg/24hours). (NCT02951819)
Timeframe: After 4 cycles of Induction (Approximately 4 months)

Intervention	Percentage of Participants (Number)
Newly Diagnosed Multiple Myeloma (NDMM)	44.2
Relapsed Multiple Myeloma (RMM)	57.1

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Overall Response Rate (ORR)

ORR: percentage of participants achieved PR or better (PR,VGPR,CR,sCR) per IMWG. CR:negative immunofixation on serum, urine, disappearance of soft tissue plasmacytomas,<5% PCs in bone marrow(BM). sCR:CR plus normal FLC ratio,absence of clonal cells in BM by immunohistochemistry, immunofluorescence. VGPR:Serum, urine M-protein detectable by immunofixation but not on electrophoresis or >=90% reduction in serum M-protein plus urine M-protein level <100 mg/24hours. PR:>=50% reduction of serum M-protein and reduction in 24hours urinary M-protein by >=90% or to <200mg/24hours. If serum, urine M-protein unmeasurable, a>=50% decrease in difference involved and uninvolved FLC levels required in place of M-protein criteria. If serum, urine M-protein not measurable, serum free light assay is not measurable,>=50% reduction in PCs required in place of M-protein,provided baseline bone marrow PCs% >=30%, if present at baseline, a >=50% reduction in size of soft tissue plasmacytomas is also required. (NCT02951819)
Timeframe: After 4 Cycles of Induction (4 months), at End of Induction (4 to 8 months) and at the End of Maintenance (12 months)

Intervention	Percentage of participants (Number)
	After 4 Cycles of Induction	At the End of Induction	At the End of Maintenance
Newly Diagnosed Multiple Myeloma (NDMM)	79.1	87.2	89.5
Relapsed Multiple Myeloma (RMM)	71.4	78.6	85.7

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Time to Very Good Partial Response (VGPR) or Better

Time to VGPR or Better response was defined as duration from the date of first dose (start of induction) to the date of initial documentation of the response (VGPR or better) which was confirmed by a repeated measurement as required by the IMWG criteria. VGPR is defined by IMWG criteria as serum and urine M-protein detectable by immunofixation but not on electrophoresis or greater than or equal to (>=) 90 % reduction in serum M-protein plus urine M-protein level < 100 milligram/24 hours (mg/24 hours). (NCT02951819)
Timeframe: Up to 36 months

Intervention	Months (Median)
Newly Diagnosed Multiple Myeloma (NDMM)	3.8
Relapsed Multiple Myeloma (RMM)	1.8

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Time to Partial Response (PR) or Better

Time to PR or Better response was defined as duration from the date of first dose (start of induction) to the date of initial documentation of the response (PR or better) which was confirmed by a repeated measurement as required by the IMWG criteria. PR is defined as per IMWG criteria as >= 50% reduction of serum M-protein and reduction in 24 hours urinary M-protein by >= 90% or to < 200 mg/24hours. If the serum and urine M-protein are unmeasurable, a>= 50% decrease in the difference between involved and uninvolved Free light chain (FLC) levels is required in the place of the M-protein criteria. If serum and urine M-protein are not measurable, and serum free light assay is also not measurable, >=50% reduction in plasma cells is required in place of M-protein, provided baseline bone marrow plasma cells percentage was >=30%. In addition to the above listed criteria, if present at baseline, a >= 50% reduction in the size of soft tissue plasmacytomas is also required. (NCT02951819)
Timeframe: Up to 12 months

Intervention	Months (Median)
Newly Diagnosed Multiple Myeloma (NDMM)	1.0
Relapsed Multiple Myeloma (RMM)	1.0

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Progression-free Survival (PFS) as Assessed by IRC

PFS was defined as time from date of randomization until the first date of IRC-confirmed PD, per International Myeloma Working Group (IMWG) response criteria, or death due to any cause, whichever occurs first. PD included increase of 25% from lowest confirmed response value in 1 or more of the following criteria: a) serum M-protein with absolute increase of >= 0.5 gram per deciliter (g/dL); b) serum M-protein increase >= 1 g/dL if the lowest M-component was >=5 g/dL; c) urine M-protein (absolute increase must be >= 200 mg per 24 hours); d) in participants without measurable serum and urine M-protein levels: the difference between involved and uninvolved free light chain (FLC) levels (absolute increase must be greater than [>] 10 mg/dL); e) in participants without measurable serum and urine M-protein levels and without measurable involved FLC levels: bone marrow plasma cell percentage irrespective of baseline status (absolute increase must be >=10%). (NCT03110562)
Timeframe: From date of randomization until IRC-confirmed documented PD or death, censored date, whichever occurred first (up to 32 months)

Intervention	Months (Median)
SVd Arm: Selinexor + Bortezomib + Dexamethasone	13.93
Vd Arm: Bortezomib + Dexamethasone	9.46

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Clinical Benefit Rate

Clinical benefit rate defined as minimal response or better (NCT03117361)
Timeframe: From the date of first drug administration to the date of at least one disease assessment, up to 100 weeks

Intervention	percentage of participants (Number)
Experimental	25.0

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Duration of Response

Duration of Response defined as the time, in months, from the date of first documentation of response to the date of disease progression. Response was assessed according to the IMWG classification response criteria. (NCT03117361)
Timeframe: From the date of first documentation of response to the date of disease progression, up to 100 weeks

Intervention	months (Number)
Experimental	9.2

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Disease Control Rate

Disease control rate defined as stable disease [SD] or better (NCT03117361)
Timeframe: From the date of first drug administration to the date of at least one disease assessment, up to 100 weeks

Intervention	percentage of participants (Number)
Experimental	87.5

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Percentage of Participants With Event-free Survival at 6 Months

"Event-free survival (EFS) was defined as the first drug-related event leading to treatment discontinuation, documented PD or death.~Progressive disease (PD): 25% increase from the lowest response value in any of the following: serum M-protein, urine M-protein, BM plasma cell percentage, or difference in the kappa and lambda FLC. PD also diagnosed when an increase size or new bone lesions." (NCT03117361)
Timeframe: From the date of first drug administration to the date of onset of the first drug-related event leading to treatment discontinuation, documented PD or death, up to 6 months

Intervention	percentage of participants (Number)
Experimental	25.0

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Percentage of Participants With Overall Survival at 12 Months

Overall survival (OS) was defined as death of any cause. (NCT03117361)
Timeframe: From the date of first drug administration to the date of death (of any cause) or last patient contact, up to 12 months

Intervention	percentage of participants (Number)
Experimental	55.6

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Percentage of Participants With Overall Survival at 6 Months

Intervention	percentage of participants (Number)
Experimental	55.6

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Percentage of Participants With Progression Disease at 6 Months

Progression disease was defined as documented PD or death due to PD. Progressive disease (PD): 25% increase from the lowest response value in any of the following: serum M-protein, urine M-protein, BM plasma cell percentage, or difference in the kappa and lambda FLC. PD also diagnosed when an increase size or new bone lesions (NCT03117361)
Timeframe: From the date of the first infusion to the date of documented PD or death due to PD, up to 6 months

Intervention	percentage of participants (Number)
Experimental	25.0

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Percentage of Participants With Progression-free Survival at 12 Months

Progression-free survival (PFS) was defined as the time, in months, from the date of first drug administration to the date of documented PD, or death (of any cause). If any patient was lost to follow-up before PD or received another antitumor therapy, PFS was to be censored on the date of the last tumor assessment. If there were no tumor assessments, these parameters were to be censored on the date of the first drug administration Progressive disease (PD): 25% increase from the lowest response value in any of the following: serum M-protein, urine M-protein, BM plasma cell percentage, or difference in the kappa and lambda FLC. PD also diagnosed when an increase size or new bone lesions. (NCT03117361)
Timeframe: From the date of first drug administration to the date of documented PD, or death (of any cause), up to 12 months

Intervention	percentage of participants (Number)
Experimental	25.0

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Percentage of Participants With Progression-free Survival at 3 Months

Progression-free Survival was defined as documented PD, or death of any cause. Progressive disease (PD): 25% increase from the lowest response value in any of the following: serum M-protein, urine M-protein, BM plasma cell percentage, or difference in the kappa and lambda FLC. PD also diagnosed when an increase size or new bone lesions. (NCT03117361)
Timeframe: From the date of first drug administration to the date of documented PD, or death (of any cause), up to 3 months

Intervention	percentage of participants (Number)
Experimental	37.5

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Progression-free Survival

"Progression-free survival (PFS) was defined as the time, in months, from the date of first drug administration to the date of documented PD, or death (of any cause). If any patient was lost to follow-up before PD or received another antitumor therapy, PFS was to be censored on the date of the last tumor assessment. If there were no tumor assessments, these parameters were to be censored on the date of the first drug administration.~Progressive disease (PD): 25% increase from the lowest response value in any of the following: serum M-protein, urine M-protein, BM plasma cell percentage, or difference in the kappa and lambda FLC. PD also diagnosed when an increase size or new bone lesions." (NCT03117361)
Timeframe: From the date of first drug administration to the date of documented PD, or death (of any cause), up to 100 weeks

Intervention	months (Median)
Experimental	2.7

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Percentage of Participants With Event-free Survival at 3 Months

"Event-free survival (EFS) was defined as the first drug-related event leading to treatment discontinuation, documented PD or death.~rogressive disease (PD): 25% increase from the lowest response value in any of the following: serum M-protein, urine M-protein, BM plasma cell percentage, or difference in the kappa and lambda FLC. PD also diagnosed when an increase size or new bone lesions." (NCT03117361)
Timeframe: From the date of first drug administration to the date of onset of the first drug-related event leading to treatment discontinuation, documented PD or death, up to 3 months

Intervention	percentage of participants (Number)
Experimental	37.5

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Percentage of Participants With Event-free Survival at 12 Months

Intervention	percentage of participants (Number)
Experimental	25.0

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Time to Progression

"Time to progression (TTP) was defined as the time, in months, from the date of the first infusion to the date of documented PD or death due to PD. TTP was to be censored on the date of the last tumor assessment or on the date of the first drug administration if there were no tumor assessments.~Progressive disease (PD): 25% increase from the lowest response value in any of the following: serum M-protein, urine M-protein, BM plasma cell percentage, or difference in the kappa and lambda FLC. PD also diagnosed when an increase size or new bone lesions." (NCT03117361)
Timeframe: From the date of the first infusion to the date of documented PD or death due to PD, up to 100 weeks

Intervention	months (Median)
Experimental	2.7

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Percentage of Participants With Progression-free Survival at 6 Months

Intervention	percentage of participants (Number)
Experimental	25.0

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Percentage of Participants With Progression Disease at 12 Months

Progression disease was defined as documented PD or death due to PD. Progressive disease (PD): 25% increase from the lowest response value in any of the following: serum M-protein, urine M-protein, BM plasma cell percentage, or difference in the kappa and lambda FLC. PD also diagnosed when an increase size or new bone lesions. (NCT03117361)
Timeframe: From the date of the first infusion to the date of documented PD or death due to PD, up to 12 months

Intervention	percentage of participants (Number)
Experimental	25.0

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Percentage of Participants With Progression Disease at 3 Months

Progression disease was defined as documented PD or death due to PD Progressive disease (PD): 25% increase from the lowest response value in any of the following: serum M-protein, urine M-protein, BM plasma cell percentage, or difference in the kappa and lambda FLC. PD also diagnosed when an increase size or new bone lesions. (NCT03117361)
Timeframe: From the date of the first infusion to the date of documented PD or death due to PD, up to 3 months

Intervention	percentage of participants (Number)
Experimental	37.5

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Overall Survival

Overall survival (OS) was defined as the time, in months, from the date of first drug administration to the date of death (of any cause) or last patient contact (in this case, survival was to be censored on that date). (NCT03117361)
Timeframe: From the date of first drug administration to the date of death (of any cause) or last patient contact, up to 100 weeks

Intervention	months (Median)
Experimental	NA

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Overall Response Rate

The primary endpoint was overall response rate (ORR) (including stringent complete response [sCR], complete response [CR], very good partial response [VGPR] and partial response [PR]), according to the IMWG response criteria. (NCT03117361)
Timeframe: From the date of first drug administration to the date of at least one disease assessment, up to 100 weeks

Intervention	percentage of participants (Number)
Experimental	12.5

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Event-free Survival

Event-free survival (EFS) was defined as the time, in months, from the date of first drug administration to the date of onset of the first drug-related event leading to treatment discontinuation, documented PD or death. The censoring rules defined above for PFS were used for EFS (NCT03117361)
Timeframe: From the date of first drug administration to the date of onset of the first drug-related event leading to treatment discontinuation, documented PD or death, up to 100 weeks

Intervention	months (Median)
Experimental	2.7

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Percentage of Participants With Overall Complete Hematologic Response (CHR)

Overall CHR rate was defined as percentage of participants who achieved CHR, according to the International Amyloidosis Consensus Criteria. CHR: normalization of free light chain levels and ratio, negative serum, and urine immunofixation. If involved free light chain (iFLC) is less than (<) upper limit of normal (ULN) and serum and urine Immunofixation electrophoresis (IFE) are negative, then neither a normal uninvolved free light chain (uFLC) level nor a normal free light chain (FLC) ratio are required for complete response (CR). (NCT03201965)
Timeframe: Up to 2.4 years

Intervention	percentage of participants (Number)
CyBorD	18.1
Daratumumab Plus CyBorD	53.3

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D-VMP, D-Rd and D-Kd Cohorts: Duration of Response (DOR)

DOR was defined as the time from the date of initial documented response (PR or better response) to the date of first documented evidence of progressive disease (PD) or death due to PD. PD is defined as an increase of 25% from the lowest response value in one of the following: serum and urine M-component (absolute increase must be >=0.5 gram per deciliter [g/dL] and >=200 mg/24 hours respectively); only in participants without measurable serum and urine M-protein levels the difference between involved and uninvolved FLC levels (absolute increase must be >10 mg/dL); definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas; development of hypercalcemia (corrected serum calcium >11.5 mg/dL) that can be attributed solely to PC proliferative disorder. (NCT03412565)
Timeframe: From baseline up to 2 years 7 months

Intervention	months (Median)
D + Bortezomib + Melphalan + Prednisone (D-VMP)	NA
Daratumumab + Lenalidomide + Dexamethasone (D-Rd)	NA
Daratumumab + Carfilzomib + Dexamethasone (D-Kd)	NA

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D-VMP, D-Rd, and D-Kd Cohorts: Overall Response Rate (ORR)

ORR was defined as the percentage of participants who achieved partial response (PR) or better according to international myeloma working group (IMWG) criteria. IMWG criteria for PR: greater than or equal to (>=) 50 percent (%) reduction of serum M-protein and reduction in 24-hour urinary M-protein by >=90% or to less than (<) 200 milligrams (mg) per 24 hours, If the serum and urine M-protein are not measurable, a decrease of >=50% in the difference between involved and uninvolved free light chain (FLC) levels is required in place of the M-protein criteria, If serum and urine M-protein are not measurable, and serum free light assay is also not measurable, >=50% reduction in bone marrow plasma cells (PCs) is required in place of M-protein, provided baseline bone marrow plasma cell percentage was >=30%. In addition to the above criteria, if present at baseline, a >=50% reduction in the size of soft tissue plasmacytomas is also required. (NCT03412565)
Timeframe: Up to 2 years 3 months

Intervention	percentage of participants (Number)
D + Bortezomib + Melphalan + Prednisone (D-VMP)	88.1
Daratumumab + Lenalidomide + Dexamethasone (D-Rd)	90.8
Daratumumab + Carfilzomib + Dexamethasone (D-Kd)	84.8

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D-VMP, D-Rd, and D-Kd Cohorts: Percentage of Participants With VGPR or Better Response

VGPR or better rate was defined as the percentage of participants who achieved VGPR or CR (including sCR) according to the IMWG criteria during or after the study treatment. VGPR: Serum and urine component detectable by immunofixation but not on electrophoresis, or >= 90% reduction in serum M-protein plus urine M-protein level <100 mg per 24 hour; CR: negative immunofixation on the serum and urine, Disappearance of any soft tissue plasmacytomas and <5% PCs in bone marrow; sCR: CR in addition to having a normal FLC ratio and an absence of clonal cells in bone marrow by immunohistochemistry, immunofluorescence, 2-4 color flow cytometry. (NCT03412565)
Timeframe: From baseline up to 2 years 7 months

Intervention	percentage of participants (Number)
D + Bortezomib + Melphalan + Prednisone (D-VMP)	77.6
Daratumumab + Lenalidomide + Dexamethasone (D-Rd)	80.0
Daratumumab + Carfilzomib + Dexamethasone (D-Kd)	77.3

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Percentage of Participants With Anti-rHuPH20 Antibodies

Percentage of participants with antibodies to rHuPH20 were reported. (NCT03412565)
Timeframe: For D-VRD Arm: Baseline up to 2 years 3 months; For D-VMP, D-Rd and D-Kd Arms: Baseline up to 2 years 7 months

Intervention	percentage of participants (Number)
Daratumumab (D)+Bortezomib+Lenalidomide+Dexamethasone (D-VRd)	6.1
D + Bortezomib + Melphalan + Prednisone (D-VMP)	3.1
Daratumumab + Lenalidomide + Dexamethasone (D-Rd)	4.8
Daratumumab + Carfilzomib + Dexamethasone (D-Kd)	4.7

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Percentage of Participants With Anti-Daratumumab Antibodies

Percentage of participants with antibodies to daratumumab were reported. (NCT03412565)
Timeframe: For D-VRD Arm: Baseline up to 2 years 3 months; For D-VMP, D-Rd and D-Kd Arms: Baseline up to 2 years 7 months

Intervention	percentage of participants (Number)
Daratumumab (D)+Bortezomib+Lenalidomide+Dexamethasone (D-VRd)	0
D + Bortezomib + Melphalan + Prednisone (D-VMP)	0
Daratumumab + Lenalidomide + Dexamethasone (D-Rd)	0
Daratumumab + Carfilzomib + Dexamethasone (D-Kd)	0

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Percentage of Participants With CR or Better Response

CR or better rate was defined as the percentage of participants with a CR or better response (that is, CR and sCR) as per IMWG criteria. CR: as negative immunofixation on the serum and urine and disappearance of soft tissue plasmacytomas and less than (<) 5 percent plasma cells in bone marrow; sCR: CR plus normal FLC ratio and absence of clonal PCs by immunohistochemistry, immunofluorescence or 2- to 4-color flow cytometry. (NCT03412565)
Timeframe: For D-VRD Arm: Baseline up to 2 years 3 months; For D-VMP, D-Rd and D-Kd Arms: Baseline up to 2 years 7 months

Intervention	percentage of participants (Number)
Daratumumab (D)+Bortezomib+Lenalidomide+Dexamethasone (D-VRd)	16.4
D + Bortezomib + Melphalan + Prednisone (D-VMP)	55.2
Daratumumab + Lenalidomide + Dexamethasone (D-Rd)	50.8
Daratumumab + Carfilzomib + Dexamethasone (D-Kd)	42.4

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D-VRd Cohort: Overall Response Rate (ORR)

ORR was defined as the percentage of participants who achieved a PR or better, IMWG criteria, during the study or during follow up. IMWG criteria for PR >= 50% reduction of serum M-protein and reduction in 24 hour urinary M-protein by >=90% or to <200 mg/24 hours, if the serum and urine M-protein are not measurable, a decrease of >=50% in the difference between involved and uninvolved FLC levels is required in place of the M-protein criteria, If serum and urine M-protein are not measurable, and serum free light assay is also not measurable, >=50% reduction in bone marrow PCs is required in place of M-protein, provided baseline bone marrow plasma cell percentage was >=30%, in addition to the above criteria, if present at baseline, a >=50% reduction in the size of soft tissue plasmacytomas is also required. (NCT03412565)
Timeframe: Up to 2 years and 3 months

Intervention	percentage of participants (Number)
Daratumumab (D)+Bortezomib+Lenalidomide+Dexamethasone (D-VRd)	97.0

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D-VMP, D-Rd, and D-Kd Cohorts: Percentage of Participants With Minimal Residual Disease (MRD) Negative Rate

MRD negativity rate was defined as the percentage of participants who were considered MRD negative after MRD testing at any timepoint after the first dose by bone marrow aspirate. MRD negativity rate was assessed by next-generation sequencing at a threshold of <10^5. (NCT03412565)
Timeframe: Up to 2 years and 3 months

Intervention	percentage of participants (Number)
D + Bortezomib + Melphalan + Prednisone (D-VMP)	25.4
Daratumumab + Lenalidomide + Dexamethasone (D-Rd)	21.5
Daratumumab + Carfilzomib + Dexamethasone (D-Kd)	27.3

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Percentage of Participants With Infusion-Related Reactions (IRRs)

Percentage of Participants with IRRs were reported. The administration-related systemic reactions are referred to as IRRs. (NCT03412565)
Timeframe: For D-VRD Arm: Baseline up to 2 years 3 months; For D-VMP, D-Rd and D-Kd Arms: Baseline up to 2 years 7 months

Intervention	percentage of participants (Number)
Daratumumab (D)+Bortezomib+Lenalidomide+Dexamethasone (D-VRd)	9.0
D + Bortezomib + Melphalan + Prednisone (D-VMP)	9.0
Daratumumab + Lenalidomide + Dexamethasone (D-Rd)	4.6
Daratumumab + Carfilzomib + Dexamethasone (D-Kd)	4.5

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Maximum Observed Serum Concentration (Cmax) of Daratumumab

Cmax was defined as maximum serum concentration observed following daratumumab administration. Each cycle for: D-VRd cohort is of 21 days, D-VMP cohort is of 42 days and D-Rd and D-Kd cohorts is of 28 days. Each cohort have a treatment period of 84 days. (NCT03412565)
Timeframe: D-VRd: Day 4 of Cycles 1 and 4 and post treatment at Week 8; D-VMP: Day 4 of Cycles 1 and 2 and post treatment at Week 8; D-Rd and D-Kd: Day 4 of Cycles 1 and 3 and post treatment at Week 8

Intervention	micrograms per milliliter (mcg/mL) (Mean)
	Cycle 1 Day 4	Cycle 3 Day 4
Daratumumab + Lenalidomide + Dexamethasone (D-Rd)	108	648

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Maximum Observed Serum Concentration (Cmax) of Daratumumab

Intervention	micrograms per milliliter (mcg/mL) (Mean)
	Cycle 1 Day 4	Cycle 2 Day 4	Post-treatment Phase Week 8
D + Bortezomib + Melphalan + Prednisone (D-VMP)	98.6	612	162

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Maximum Observed Serum Concentration (Cmax) of Daratumumab

Intervention	micrograms per milliliter (mcg/mL) (Mean)
	Cycle 1 Day 4	Cycle 3 Day 4	Post-treatment Phase Week 8
Daratumumab + Carfilzomib + Dexamethasone (D-Kd)	137	869	49.3

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Maximum Observed Serum Concentration (Cmax) of Daratumumab

Intervention	micrograms per milliliter (mcg/mL) (Mean)
	Cycle 1 Day 4	Cycle 4 Day 4	Post-treatment Phase Week 8
Daratumumab (D)+Bortezomib+Lenalidomide+Dexamethasone (D-VRd)	100	746	263

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D-VRd Cohort: Percentage of Participants With Very Good Partial Response (VGPR) or Better Response

VGPR or better rate was defined as the percentage of participants who achieved VGPR or complete response (CR) (including stringent complete response [sCR]) according to the IMWG criteria during or after the study treatment. VGPR: Serum and urine component detectable by immunofixation but not on electrophoresis, or >= 90% reduction in serum M-protein plus urine M-protein level <100 mg/24 hour; CR: negative immunofixation on the serum and urine, Disappearance of any soft tissue plasmacytomas and <5% PCs in bone marrow; sCR: CR in addition to having a normal FLC ratio and an absence of clonal cells in bone marrow by immunohistochemistry, immunofluorescence, 2-4 color flow cytometry. (NCT03412565)
Timeframe: Up to 2 years and 3 months

Intervention	percentage of participants (Number)
Daratumumab (D)+Bortezomib+Lenalidomide+Dexamethasone (D-VRd)	71.6

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Percentage of Participants With Bone Lesions (Bone Evaluation)

(NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Percentage of Participants (Number)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	100.0
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	59.1
[Overall]; Combination Therapy + Ixazomib Therapy	64.0

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PFS From the Start of Study Treatment

PFS was defined as the period from the first dose of treatment in Treatment Period I to the time of confirmed PD or confirmed death (regardless of the cause of death), whichever is earlier. PFS was assessed by IMWG Criteria. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Months (Median)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	NA
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	28.96
[Overall]; Combination Therapy + Ixazomib Therapy	28.96

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Progression-Free Survival (PFS) Rate at 12 Months From the Start of Study Treatment

PFS rate was defined as the percentage of participants who were alive and have not had disease progression at 12 months after the date of first dose of treatment in Treatment Period I. PFS was assessed by International Myeloma Working Group (IMWG) Criteria (2014 version). Per IMWG criteria, progressive disease (PD): serum M-component increase ≥0.5 g/dl or urine M-component increase ≥200 mg/24-hour/ difference between involved and uninvolved free light chain (FLC) levels increase >10 mg/dl or bone marrow plasma cell ≥10%/ development of new/ increase in size of existing bone lesions or soft tissue plasmacytoma or development of hypercalcemia. (NCT03416374)
Timeframe: Up to 12 months

Intervention	Percentage of Participants (Number)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	50.0
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	48.7
[Overall]; Combination Therapy + Ixazomib Therapy	48.9

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Time to Next Treatment (TTNT)

TTNT is defined as the period from the start of study treatment Period I to the start of next line treatment. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Months (Median)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	21.59
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	32.26
[Overall]; Combination Therapy + Ixazomib Therapy	32.26

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Number of Participants With Minimal Residual Disease (MRD) Positive or Negative in Bone Marrow in Participants Who Achieved CR

MRD was measured by the flow cytometry method using bone marrow aspiration. Reported data were numbers of participants with MRD positive and negative in bone marrow in participants who achieved CR. MRD positive was categorized into three sensitivity levels with the numbers of cells counted (10^-4 to - Max; 10^-5 to 10^-4; 10^-6 to 10^-5). MRD negativity is defined as absence of MRD and MRD positivity is defined as presence of MRD. If a participant is MRD-positive at their first evaluation and MRD-negative after re-examination, the participant will be considered to be MRD-negative. CR will be assessed by IMWG Criteria. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Participants (Count of Participants)
	Sensitivity Level; 10^-4=< - Max	Sensitivity Level; 10^-5=< - <10^-4	Sensitivity Level; 10^-6=< - <10^-5	Negative
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	1	2	1	5
[Overall]; Combination Therapy + Ixazomib Therapy	1	3	2	5
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	0	1	1	0

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Patient-Reported Outcome Health-Related Quality of Life (HRQoL) Based on Global Health Status Scale of European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-C30 (EORTC QLQ-C30)

EORTC QLQ-C30 contains 30 items across 5 functional scales (physical, role, cognitive, emotional, and social), 9 symptom scales (fatigue, nausea and vomiting, pain, dyspnea, sleep disturbance, appetite loss, constipation, diarrhea, and financial difficulties) and a global health status/QOL scale (Global Health Status). EORTC QLQ-C30 contains 28 questions (4-point scale where 1=Not at all [best] to 4=Very Much [worst]) and 2 questions (7-point scale where 1=Very poor [worst] to 7= Excellent [best]). Raw scores are converted into scale scores ranging from 0 to 100. For the functional scales and the global health status/QOL scale, higher scores represent better QOL; for the symptom scales, lower scores represent better QOL. (NCT03416374)
Timeframe: Baseline and End of Treatment (Up to 23 cycles for VRd Group, Up to 32 cycles for KRd and Overall Group, each cycle was of 28 days)

Intervention	Score on a Scale (Mean)
	Baseline	Cycle 23
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	44.44	0

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Patient-Reported Outcome Health-Related Quality of Life (HRQoL) Based on Global Health Status Scale of European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-C30 (EORTC QLQ-C30)

Intervention	Score on a Scale (Mean)
	Baseline	Cycle 23	Cycle 32
[Overall]; Combination Therapy + Ixazomib Therapy	60.74	46.43	50.00
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	63.25	54.17	50.00

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Patient-Reported Outcome HRQoL Based on EORTC Multiple Myeloma Module (EORTC QLQ-MY20) Score

EORTC QLQ-MY20 has 20 items across 4 independent subscales, 2 functional subscales (body image, future perspective), and 2 symptoms scales (disease symptoms, and side effects of treatment). Scores are averaged, and transformed to 0-100 scale. For the functional scales, high scores represent improvement. For the symptom scales, higher scores represent worsening. (NCT03416374)
Timeframe: Baseline and End of Treatment (Up to 23 cycles for VRd Group, Up to 32 cycles for KRd and Overall Group, each cycle was of 28 days)

Intervention	Score on a Scale (Mean)
	Disease Symptoms: Baseline	Disease Symptoms: Cycle 23	Disease Symptoms: Cycle 32	Side-Effects of Treatment: Baseline	Side-Effects of Treatment: Cycle 23	Side-Effects of Treatment: Cycle 32	Body Image: Baseline	Body Image: Cycle 23	Body Image: Cycle 32	Future Perspective: Baseline	Future Perspective: Cycle 23	Future Perspective: Cycle 32
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	19.23	4.63	2.78	16.60	16.05	18.52	23.08	16.67	16.67	44.16	35.19	27.78
[Overall]; Combination Therapy + Ixazomib Therapy	19.88	3.97	2.78	16.61	14.29	18.52	25.93	14.29	16.67	47.16	31.75	27.78

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Percentage of Participants Who Achieve or Maintain Any Best Response

Best response is defined as the cumulative numbers of participants who achieve each level of best response including PR, VGPR and CR assessed with IMWG Criteria, after each cycle of treatment. Per IMWG criteria, PR (partial response): ≥50% reduction of serum M protein+reduction in 24-hour urinary M protein by ≥90%/ to <200 mg/24-hour or ≥50% decrease in difference between involved and uninvolved free light chain (FLC) levels/ ≥50% reduction in bone marrow plasma cells, if ≥30% at baseline/ ≥50% reduction in size of soft tissue plasmacytomas. VGPR (very good PR): serum+urine M-protein detectable by immunofixation but not on electrophoresis/ ≥90% reduction in serum M-protein+urine Mprotein level <100 mg/24-hour. CR (complete response): negative immunofixation on serum+urine+disappearance of soft tissue plasmacytomas+<5% plasma cells in bone marrow. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Percentage of Participants (Number)
	CR	VGPR	PR
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	23.1	20.5	28.2
[Overall]; Combination Therapy + Ixazomib Therapy	24.4	17.8	31.1
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	33.3	0	50.0

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Relative Dose Intensity (RDI)

RDI for each study drug is defined as 100*(Total amount of dose taken)/(Total prescribed dose of treated cycles), where total prescribed dose equals [dose prescribed at enrollment* number of prescribed doses per cycle* the number of treated cycles]. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Percent (Median)
	Bortezomib, Ixazomib	Carfilzomib, Ixazomib	Bortezomib/Carfilzomib, Ixazomib	Lenalidomide	Dexamethasone
[Overall]; Combination Therapy + Ixazomib Therapy	71.93	87.70	83.24	47.18	48.61

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Overall Survival (OS) From the Start of Study Treatment

OS was defined as the period from the first dose of treatment in Treatment Period I to the time when death (regardless of the cause of death) was confirmed. Participants who were still alive were censored at the last confirmed date of survival or the date of data cut-off, whichever was earlier. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Months (Median)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	NA
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	NA
[Overall]; Combination Therapy + Ixazomib Therapy	NA

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Healthcare Resource Utilization (HCRU): Duration of Hospital Stay Per Participants

HCRU was calculated from Exposure-adjusted rate of hospitalization events (per participants-months) and the duration of hospitalization among participants in Treatment Period I and Treatment Period II. Duration of hospital stay per participants in Treatment Period I and Treatment Period II was reported. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Days (Mean)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	14.8
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	19.4
[Overall]; Combination Therapy + Ixazomib Therapy	18.8

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Patient-Reported Outcome HRQoL Based on EORTC Multiple Myeloma Module (EORTC QLQ-MY20) Score

Intervention	Score on a Scale (Mean)
	Disease Symptoms: Baseline	Disease Symptoms: Cycle 23	Side-Effects of Treatment: Baseline	Side-Effects of Treatment: Cycle 23	Body Image: Baseline	Body Image: Cycle 23	Future Perspective: Baseline	Future Perspective: Cycle 23
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	24.07	0	16.67	3.70	44.44	0	66.67	11.11

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Healthcare Resource Utilization (HCRU): Number of Events With Hospitalization Per Participants-Month

HCRU was calculated from Exposure-adjusted rate of hospitalization events (per participants-months) and the duration of hospitalization among participants in Treatment Period I and Treatment Period II. Number of events with hospitalization per participants-month in Treatment Period I and Treatment Period II was reported. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Number of Events per Participants-Month (Number)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	1.9
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	2.9
[Overall]; Combination Therapy + Ixazomib Therapy	2.7

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Number of Participants Reporting One or More Treatment-Emergent AEs (TEAEs)

An adverse event (AE) is defined as any untoward medical occurrence in a clinical investigation participant administered a drug; it does not necessarily have to have a causal relationship with this treatment. A TEAE is defined as an adverse event with an onset that occurs after receiving study drug. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Participants (Count of Participants)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	6
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	35
[Overall]; Combination Therapy + Ixazomib Therapy	41

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Percentage of Participants Continuing Treatment With Ixazomib at 12 Months From the Start of Study Treatment

(NCT03416374)
Timeframe: 12 months

Intervention	Percentage of Participants (Number)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	50.0
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	35.9
[Overall]; Combination Therapy + Ixazomib Therapy	37.8

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Overall Response Rate (ORR)

ORR is defined as the percentage of participants who achieve a best response of PR or better including stringent complete response (sCR), VGPR and PR assessed with IMWG Criteria, after the start of the study treatment. Per IMWG criteria, PR (partial response): ≥50% reduction of serum M protein+reduction in 24-hour urinary M protein by ≥90%/ to <200 mg/24-hour or ≥50% decrease in difference between involved and uninvolved free light chain (FLC) levels/ ≥50% reduction in bone marrow plasma cells, if ≥30% at baseline/ ≥50% reduction in size of soft tissue plasmacytomas. VGPR (very good PR): serum+urine M-protein detectable by immunofixation but not on electrophoresis/ ≥90% reduction in serum M-protein+urine Mprotein level <100 mg/24-hour. CR (complete response): negative immunofixation on serum+urine+disappearance of soft tissue plasmacytomas+<5% plasma cells in bone marrow. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Percentage of Participants (Number)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	83.3
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	71.8
[Overall]; Combination Therapy + Ixazomib Therapy	73.3

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Percentage of Participants Who Achieved VGPR or Better (CR + VGPR)

VGPR or better (CR + VGPR) were assessed by IMWG Criteria. Per IMWG criteria, PR (partial response): ≥50% reduction of serum M protein+reduction in 24-hour urinary M protein by ≥90%/ to <200 mg/24-hour or ≥50% decrease in difference between involved and uninvolved free light chain (FLC) levels/ ≥50% reduction in bone marrow plasma cells, if ≥30% at baseline/ ≥50% reduction in size of soft tissue plasmacytomas. VGPR (very good PR): serum+urine M-protein detectable by immunofixation but not on electrophoresis/ ≥90% reduction in serum M-protein+urine Mprotein level <100 mg/24-hour. CR (complete response): negative immunofixation on serum+urine+disappearance of soft tissue plasmacytomas+<5% plasma cells in bone marrow. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Percentage of Participants (Number)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	33.3
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	43.6
[Overall]; Combination Therapy + Ixazomib Therapy	42.2

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Duration of Response (DOR)

DOR is defined as the time from the date of first documentation of response ≥PR to the date of first documentation of PD or death due to any cause. PR and PD will be assessed with IMWG Criteria. Per IMWG criteria, PR (partial response): ≥50% reduction of serum M protein+reduction in 24-hour urinary M protein by ≥90%/ to <200 mg/24-hour or ≥50% decrease in difference between involved and uninvolved free light chain (FLC) levels/ ≥50% reduction in bone marrow plasma cells, if ≥30% at baseline/ ≥50% reduction in size of soft tissue plasmacytomas. VGPR (very good PR): serum+urine M-protein detectable by immunofixation but not on electrophoresis/ ≥90% reduction in serum M-protein+urine Mprotein level <100 mg/24-hour. CR (complete response): negative immunofixation on serum+urine+disappearance of soft tissue plasmacytomas+<5% plasma cells in bone marrow. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Months (Median)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	15.31
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	28.03
[Overall]; Combination Therapy + Ixazomib Therapy	28.03

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Duration of Therapy (DOT)

DOT is defined as the treatment duration of study drug at study treatment Period I. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Months (Median)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	14.69
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	12.43
[Overall]; Combination Therapy + Ixazomib Therapy	12.43

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Evaluation of Modified Quality-Adjusted Life-Years (QALYs)

Modified QALYs was calculated from the score of EORTC QLQ-C30. The health-related quality of life scale score of EORTC QLQ-C30 was converted into a utility value ranging from 0 (dead) to 1 (perfect health), and used to adjust the value of survival years; this value was assessed as the modified QALY. (NCT03416374)
Timeframe: Up to 39 months as a maximum

Intervention	Quality-Adjusted Life-Years (Median)
[VRd]; Bortezomib + Lenalidomide + Dexamethasone Therapy	0.467
[KRd]; Carfilzomib + Lenalidomide + Dexamethasone Therapy	0.534
[Overall]; Combination Therapy + Ixazomib Therapy	0.518

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Time to Next Treatment (TTNT)

Defined as time from date of initiation of therapy to start of next line of therapy. (NCT03481556)
Timeframe: Until death or initiation of subsequent therapy (a maximum of 194.3 weeks)

Intervention	months (Median)
A (Melflufen+Bortezomib+Dex) 30 mg	33.50
A (Melflufen+Bortezomib+Dex) 40 mg	14.70
B (Melflufen+Daratumumab+Dex) 30 mg	26.25
B (Melflufen+Daratumumab+Dex) 40 mg	9.5

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Overall Survival (OS)

Time from the first dose of melflufen to death due to any cause. (NCT03481556)
Timeframe: Up to 24 months following confirmed disease progression, or initiation of subsequent therapy (a maximum of 198.9 weeks)

Intervention	months (Median)
A (Melflufen+Bortezomib+Dex) 30 mg	33.5
A (Melflufen+Bortezomib+Dex) 40 mg	NA
B (Melflufen+Daratumumab+Dex) 30 mg	35.0
B (Melflufen+Daratumumab+Dex) 40 mg	18.3

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Time to Response (TTR)

Time from Cycle 1 Day 1 to a response of PR or better. (NCT03481556)
Timeframe: Until disease progression, death or initiation of subsequent therapy (a maximum of 194.3 weeks)

Intervention	months (Median)
A (Melflufen+Bortezomib+Dex) 30 mg	3.0
A (Melflufen+Bortezomib+Dex) 40 mg	2.2
B (Melflufen+Daratumumab+Dex) 30 mg	3.3
B (Melflufen+Daratumumab+Dex) 40 mg	1.1

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Best Response (BR)

BR defined by International Myeloma Working Group Uniform Response Criteria. BR= Complete Response (CR)/Stringent CR (sCR) defined as below negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and < 5% plasma cells in bone marrow/plus normal free light chain (FLC) ratio and absence of clonal cells in bone marrow by immunohistochemistry or immunofluorescence, Very Good Partial Response (VGPR)= serum and urine M-protein detectable by immunofixation but not on electrophoresis or > 90% reduction in serum M-protein plus urine M-protein level < 100 mg/24 hours, Partial Response (PR)= a > 50% reduction of serum M-protein and reduction in 24 hours urinary M-protein by > 90% or to < 200 mg/24 hours, Minimal Response (MR), Stable Disease (SD)= not meeting the criteria for other response options, Progressive Disease (PD)= increase of > 25% from lowest response value in serum/urine M-component or bone marrow plasma cell percentage, or non-evaluable. (NCT03481556)
Timeframe: Until disease progression, death or initiation of subsequent therapy (a maximum of 194.3 weeks)

,,,

Intervention	Participants (Count of Participants)
	CR	sCR	VGPR	PR	MR	SD	PD	Non-evaluable	Missing
Regimen A - Melflufen 30mg + Bortezomib + Dexamethasone	1	0	2	9	1	1	0	0	1
Regimen A - Melflufen 40mg + Bortezomib + Dexamethasone	0	1	3	2	0	1	0	0	1
Regimen B - Melflufen 30mg + Daratumumab + Dexamethasone	1	0	2	2	0	0	0	0	1
Regimen B - Melflufen 40mg + Daratumumab + Dexamethasone	1	1	6	11	1	2	1	0	4

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Number of Participants Who Experienced a Treatment-emergent Adverse Event (TEAE)

TEAEs were defined as adverse events (AEs) that started after the first dose of study medication was administered and within 30 days of the last administration of the study treatment or before start of subsequent anticancer treatment (whichever occurred first) or that worsened after the first dose of study medication was administered. (NCT03481556)
Timeframe: Cycle 1 Day 1 up to a maximum of 198.9 weeks

,,,

Intervention	Participants (Count of Participants)
	Any TEAEs	Any Grade 3 or Higher TEAEs
A (Melflufen+Bortezomib+Dex) 30 mg	15	15
A (Melflufen+Bortezomib+Dex) 40 mg	8	8
B (Melflufen+Daratumumab+Dex) 30 mg	6	6
B (Melflufen+Daratumumab+Dex) 40 mg	27	26

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Time to Progression (TTP)

TTP defined as time from first dose to first documented confirmed progression. (NCT03481556)
Timeframe: Until disease progression, death or initiation of subsequent therapy (a maximum of 194.3 weeks)

Intervention	months (Median)
A (Melflufen+Bortezomib+Dex) 30 mg	17.6
A (Melflufen+Bortezomib+Dex) 40 mg	24.3
B (Melflufen+Daratumumab+Dex) 30 mg	29.2
B (Melflufen+Daratumumab+Dex) 40 mg	11.5

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Duration of Clinical Benefit (DOCB)

DOCB was defined as time in months from the first evidence of confirmed assessment of sCR, CR, VGPR, PR or MR to first confirmed disease progression, or to death due to any cause. (NCT03481556)
Timeframe: Until disease progression, death or initiation of subsequent therapy (a maximum of 194.3 weeks)

Intervention	months (Median)
A (Melflufen+Bortezomib+Dex) 30 mg	15.7
A (Melflufen+Bortezomib+Dex) 40 mg	21.3
B (Melflufen+Daratumumab+Dex) 30 mg	27.20
B (Melflufen+Daratumumab+Dex) 40 mg	10.9

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Clinical Benefit Rate (≥ Minimal Response)

≥ Minimal response for participants included sCR, CR, VGPR, PR and MR. (NCT03481556)
Timeframe: Until disease progression, death or initiation of subsequent therapy (a maximum of 194.3 weeks)

Intervention	percentage of participants (Number)
A (Melflufen+Bortezomib+Dex) 30 mg	86.7
A (Melflufen+Bortezomib+Dex) 40 mg	75.0
B (Melflufen+Daratumumab+Dex) 30 mg	83.3
B (Melflufen+Daratumumab+Dex) 40 mg	74.1

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Phase 1: Number of Participants Who Experienced a Dose Limiting Toxicity (DLT)

"Toxicity was graded according to the National Cancer Institute - Common Terminology Criteria for Adverse Events Version 4.03.~DLT criteria that apply to Regimens A and B:~Grade 3 non-hematologic toxicity preventing the administration of > 1 dose of bortezomib or daratumumab during the 1st cycle.~Grade 4 or greater non-hematologic toxicity.~Grade 4 thrombocytopenia (platelet count < 25,000 cells/ mm^3) preventing the administration of > 1 dose of bortezomib or daratumumab during the 1st cycle or with clinically significant bleeding during the 1st cycle.~Grade 4 neutropenia (ANC < 500 cells/mm^3), lasting more than 7 days during the 1st cycle.~Greater than 14 days' delay to meet the criteria for the start of a new cycle (Cycle 2) due to toxicity." (NCT03481556)
Timeframe: Cycle 1: Day 1 to Day 28

Intervention	Participants (Count of Participants)
Regimen A - Melflufen 30mg + Bortezomib + Dexamethasone	0
Regimen A - Melflufen 40mg + Bortezomib + Dexamethasone	0
Regimen B - Melflufen 30mg + Daratumumab + Dexamethasone	0
Regimen B - Melflufen 40mg + Daratumumab + Dexamethasone	0

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Phase 2: Overall Response Rate (ORR)

ORR was defined as the percentage of participants who achieved a best confirmed response of Partial Response (PR) or better. (NCT03481556)
Timeframe: Until disease progression, death or initiation of subsequent therapy (a maximum of 194.3 weeks)

Intervention	percentage of participants (Number)
Regimen A - Melflufen 30mg + Bortezomib + Dexamethasone	80
Regimen A - Melflufen 40mg + Bortezomib + Dexamethasone	75
Regimen B - Melflufen 30mg + Daratumumab + Dexamethasone	83.3
Regimen B - Melflufen 40mg + Daratumumab + Dexamethasone	70.4

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Progression-Free Survival (PFS)

PFS was defined as the time in months from date of initiation of therapy to the earlier of confirmed disease progression or death due to any cause. (NCT03481556)
Timeframe: Until disease progression, death or initiation of subsequent therapy (a maximum of 194.3 weeks)

Intervention	months (Median)
A (Melflufen+Bortezomib+Dex) 30 mg	10.0
A (Melflufen+Bortezomib+Dex) 40 mg	24.30
B (Melflufen+Daratumumab+Dex) 30 mg	28.4
B (Melflufen+Daratumumab+Dex) 40 mg	9.7

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Duration of Response (DOR)

DOR is defined for participants with confirmed objective response (PR or better, which includes PR, VGPR, CR and sCR) as the time from the first documentation of objective response to the first documentation of objective progression or to death due to any cause, whichever occurs first. (NCT03481556)
Timeframe: Until disease progression, death or initiation of subsequent therapy (a maximum of 194.3 weeks)

Intervention	months (Median)
A (Melflufen+Bortezomib+Dex) 30 mg	9.0
A (Melflufen+Bortezomib+Dex) 40 mg	NA
B (Melflufen+Daratumumab+Dex) 30 mg	24.2
B (Melflufen+Daratumumab+Dex) 40 mg	9.9

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Percentage of Participants Who Experience Acute GvHD

Rate of acute GvHD post-transplant. All participants that received a transplant and received any prophylactic treatment will be included in the analysis. (NCT03945591)
Timeframe: Day 120 Post-Transplant

Intervention	percentage of participants (Number)
Cyclophosphamide and Bortezomib	38.46

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Percentage of Participants Who Experience Moderate to Severe Chronic GvHD

Rate of chronic GvHD post-transplant. All participants that received a transplant and received any prophylactic treatment will be included in the analysis. (NCT03945591)
Timeframe: Day 365 Post-Transplant

Intervention	percentage of participants (Number)
Cyclophosphamide and Bortezomib	36.36

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Substance	Relationship Strength	Studies	Trials	Classes	Roles
acetylcarnitine Acetylcarnitine: An acetic acid ester of CARNITINE that facilitates movement of ACETYL COA into the matrices of mammalian MITOCHONDRIA during the oxidation of FATTY ACIDS.	3.87	2	1	O-acylcarnitine	human metabolite
3-hydroxyanthranilic acid 3-Hydroxyanthranilic Acid: An oxidation product of tryptophan metabolism. It may be a free radical scavenger and a carcinogen.. 3-hydroxyanthranilic acid : An aminobenzoic acid that is benzoic acid substituted at C-2 by an amine group and at C-3 by a hydroxy group. It is an intermediate in the metabolism of the amino acid tryptophan.. 3-hydroxyanthranilate : A hydroxybenzoate that is the conjugate base of 3-hydroxyanthranilic acid.	2.06	1	0	aminobenzoic acid; monohydroxybenzoic acid	human metabolite; mouse metabolite
phosphoserine Phosphoserine: The phosphoric acid ester of serine.	2.75	3	0	non-proteinogenic alpha-amino acid; O-phosphoamino acid; serine derivative	human metabolite
3-phenylpropionic acid 3-phenylpropionic acid: RN given refers to parent cpd. 3-phenylpropionic acid : A monocarboxylic acid that is propionic acid substituted at position 3 by a phenyl group.	2.25	1	0	benzenes; monocarboxylic acid	antifungal agent; human metabolite; plant metabolite
gamma-aminobutyric acid gamma-Aminobutyric Acid: The most common inhibitory neurotransmitter in the central nervous system.. gamma-aminobutyric acid : A gamma-amino acid that is butanoic acid with the amino substituent located at C-4.	2.99	4	0	amino acid zwitterion; gamma-amino acid; monocarboxylic acid	human metabolite; neurotransmitter; Saccharomyces cerevisiae metabolite; signalling molecule
aminolevulinic acid Aminolevulinic Acid: A compound produced from succinyl-CoA and GLYCINE as an intermediate in heme synthesis. It is used as a PHOTOCHEMOTHERAPY for actinic KERATOSIS.. 5-aminolevulinic acid : The simplest delta-amino acid in which the hydrogens at the gamma position are replaced by an oxo group. It is metabolised to protoporphyrin IX, a photoactive compound which accumulates in the skin. Used (in the form of the hydrochloride salt)in combination with blue light illumination for the treatment of minimally to moderately thick actinic keratosis of the face or scalp.	2.6	1	0	4-oxo monocarboxylic acid; amino acid zwitterion; delta-amino acid	antineoplastic agent; dermatologic drug; Escherichia coli metabolite; human metabolite; mouse metabolite; photosensitizing agent; plant metabolite; prodrug; Saccharomyces cerevisiae metabolite
acetic acid Acetic Acid: Product of the oxidation of ethanol and of the destructive distillation of wood. It is used locally, occasionally internally, as a counterirritant and also as a reagent. (Stedman, 26th ed). acetic acid : A simple monocarboxylic acid containing two carbons.	2.05	1	0	monocarboxylic acid	antimicrobial food preservative; Daphnia magna metabolite; food acidity regulator; protic solvent
acetamide acetimidic acid : A carboximidic acid that is acetic acid in which the carbonyl oxygen is replaced by an imino group.	2.05	1	0	acetamides; carboximidic acid; monocarboxylic acid amide; N-acylammonia
adenine [no description available]	13.03	43	4	6-aminopurines; purine nucleobase	Daphnia magna metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
allantoin [no description available]	2.05	1	0	imidazolidine-2,4-dione; ureas	Escherichia coli metabolite; human metabolite; Saccharomyces cerevisiae metabolite; vulnerary
ammonium hydroxide azane : Saturated acyclic nitrogen hydrides having the general formula NnHn+2.	2.59	2	0	azane; gas molecular entity; mononuclear parent hydride	EC 3.5.1.4 (amidase) inhibitor; metabolite; mouse metabolite; neurotoxin; NMR chemical shift reference compound; nucleophilic reagent; refrigerant
quinacrine Quinacrine: An acridine derivative formerly widely used as an antimalarial but superseded by chloroquine in recent years. It has also been used as an anthelmintic and in the treatment of giardiasis and malignant effusions. It is used in cell biological experiments as an inhibitor of phospholipase A2.. quinacrine : A member of the class of acridines that is acridine substituted by a chloro group at position 6, a methoxy group at position 2 and a [5-(diethylamino)pentan-2-yl]nitrilo group at position 9.	2.74	3	0	acridines; aromatic ether; organochlorine compound; tertiary amino compound	antimalarial; EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor
benzene [no description available]	4.8	1	1	aromatic annulene; benzenes; volatile organic compound	carcinogenic agent; environmental contaminant; non-polar solvent
betaine glycine betaine : The amino acid betaine derived from glycine.	3.59	2	0	amino-acid betaine; glycine derivative	fundamental metabolite
butyric acid Butyric Acid: A four carbon acid, CH3CH2CH2COOH, with an unpleasant odor that occurs in butter and animal fat as the glycerol ester.. butyrate : A short-chain fatty acid anion that is the conjugate base of butyric acid, obtained by deprotonation of the carboxy group.. butyric acid : A straight-chain saturated fatty acid that is butane in which one of the terminal methyl groups has been oxidised to a carboxy group.	2.17	1	0	fatty acid 4:0; straight-chain saturated fatty acid	human urinary metabolite; Mycoplasma genitalium metabolite
carbon monoxide Carbon Monoxide: Carbon monoxide (CO). A poisonous colorless, odorless, tasteless gas. It combines with hemoglobin to form carboxyhemoglobin, which has no oxygen carrying capacity. The resultant oxygen deprivation causes headache, dizziness, decreased pulse and respiratory rates, unconsciousness, and death. (From Merck Index, 11th ed). carbon monoxide : A one-carbon compound in which the carbon is joined only to a single oxygen. It is a colourless, odourless, tasteless, toxic gas.	2.21	1	0	carbon oxide; gas molecular entity; one-carbon compound	biomarker; EC 1.9.3.1 (cytochrome c oxidase) inhibitor; human metabolite; ligand; metabolite; mitochondrial respiratory-chain inhibitor; mouse metabolite; neurotoxin; neurotransmitter; P450 inhibitor; probe; signalling molecule; vasodilator agent
carnitine [no description available]	7.47	2	0	amino-acid betaine	human metabolite; mouse metabolite
catechol [no description available]	3.22	5	0	catechols	allelochemical; genotoxin; plant metabolite
choline [no description available]	2.03	1	0	cholines	allergen; Daphnia magna metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; neurotransmitter; nutrient; plant metabolite; Saccharomyces cerevisiae metabolite
citric acid, anhydrous Citric Acid: A key intermediate in metabolism. It is an acid compound found in citrus fruits. The salts of citric acid (citrates) can be used as anticoagulants due to their calcium chelating ability.. citric acid : A tricarboxylic acid that is propane-1,2,3-tricarboxylic acid bearing a hydroxy substituent at position 2. It is an important metabolite in the pathway of all aerobic organisms.	2.05	1	0	tricarboxylic acid	antimicrobial agent; chelator; food acidity regulator; fundamental metabolite
coumarin 2H-chromen-2-one: coumarin derivative	2.6	1	0	coumarins	fluorescent dye; human metabolite; plant metabolite
salicylic acid Scalp: The outer covering of the calvaria. It is composed of several layers: SKIN; subcutaneous connective tissue; the occipitofrontal muscle which includes the tendinous galea aponeurotica; loose connective tissue; and the pericranium (the PERIOSTEUM of the SKULL).	2.54	2	0	monohydroxybenzoic acid	algal metabolite; antifungal agent; antiinfective agent; EC 1.11.1.11 (L-ascorbate peroxidase) inhibitor; keratolytic drug; plant hormone; plant metabolite
bupropion Bupropion: A propiophenone-derived antidepressant and antismoking agent that inhibits the uptake of DOPAMINE.. bupropion : An aromatic ketone that is propiophenone carrying a tert-butylamino group at position 2 and a chloro substituent at position 3 on the phenyl ring.	3.59	2	0	aromatic ketone; monochlorobenzenes; secondary amino compound	antidepressant; environmental contaminant; xenobiotic
aminocaproic acid Aminocaproic Acid: An antifibrinolytic agent that acts by inhibiting plasminogen activators which have fibrinolytic properties.. 6-aminohexanoic acid : An epsilon-amino acid comprising hexanoic acid carrying an amino substituent at position C-6. Used to control postoperative bleeding, and to treat overdose effects of the thrombolytic agents streptokinase and tissue plasminogen activator.	3.86	3	0	amino acid zwitterion; epsilon-amino acid; omega-amino fatty acid	antifibrinolytic drug; hematologic agent; metabolite
creatine [no description available]	2.46	2	0	glycine derivative; guanidines; zwitterion	geroprotector; human metabolite; mouse metabolite; neuroprotective agent; nutraceutical
cytosine [no description available]	4.02	2	0	aminopyrimidine; pyrimidine nucleobase; pyrimidone	Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
lactic acid Lactic Acid: A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed). 2-hydroxypropanoic acid : A 2-hydroxy monocarboxylic acid that is propanoic acid in which one of the alpha-hydrogens is replaced by a hydroxy group.	3.6	8	0	2-hydroxy monocarboxylic acid	algal metabolite; Daphnia magna metabolite
dimethyl sulfoxide Dimethyl Sulfoxide: A highly polar organic liquid, that is used widely as a chemical solvent. Because of its ability to penetrate biological membranes, it is used as a vehicle for topical application of pharmaceuticals. It is also used to protect tissue during CRYOPRESERVATION. Dimethyl sulfoxide shows a range of pharmacological activity including analgesia and anti-inflammation.. dimethyl sulfoxide : A 2-carbon sulfoxide in which the sulfur atom has two methyl substituents.	3.23	5	0	sulfoxide; volatile organic compound	alkylating agent; antidote; Escherichia coli metabolite; geroprotector; MRI contrast agent; non-narcotic analgesic; polar aprotic solvent; radical scavenger
formaldehyde paraform: polymerized formaldehyde; RN given refers to parent cpd; used in root canal therapy	2.05	1	0	aldehyde; one-carbon compound	allergen; carcinogenic agent; disinfectant; EC 3.5.1.4 (amidase) inhibitor; environmental contaminant; Escherichia coli metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
glycine [no description available]	19.85	67	7	alpha-amino acid; amino acid zwitterion; proteinogenic amino acid; serine family amino acid	EC 2.1.2.1 (glycine hydroxymethyltransferase) inhibitor; fundamental metabolite; hepatoprotective agent; micronutrient; neurotransmitter; NMDA receptor agonist; nutraceutical
glycerol Moon: The natural satellite of the planet Earth. It includes the lunar cycles or phases, the lunar month, lunar landscapes, geography, and soil.	2.05	1	0	alditol; triol	algal metabolite; detergent; Escherichia coli metabolite; geroprotector; human metabolite; mouse metabolite; osmolyte; Saccharomyces cerevisiae metabolite; solvent
hydroquinone [no description available]	2.05	1	0	benzenediol; hydroquinones	antioxidant; carcinogenic agent; cofactor; Escherichia coli metabolite; human xenobiotic metabolite; mouse metabolite; skin lightening agent
indoleacetic acid indoleacetic acid: RN given refers to unlabeled parent cpd; structure in Merck Index, 9th ed, #4841. auxin : Any of a group of compounds, both naturally occurring and synthetic, that induce cell elongation in plant stems (from Greek alphaupsilonxialphanuomega, "to grow").. indole-3-acetic acid : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens has been replaced by a 1H-indol-3-yl group.	2.25	1	0	indole-3-acetic acids; monocarboxylic acid	auxin; human metabolite; mouse metabolite; plant hormone; plant metabolite
itaconic acid itaconic acid : A dicarboxylic acid that is methacrylic acid in which one of the methyl hydrogens is substituted by a carboxylic acid group.	2.11	1	0	dicarboxylic acid; dicarboxylic fatty acid; olefinic compound	fungal metabolite; human metabolite
thioctic acid Thioctic Acid: An octanoic acid bridged with two sulfurs so that it is sometimes also called a pentanoic acid in some naming schemes. It is biosynthesized by cleavage of LINOLEIC ACID and is a coenzyme of oxoglutarate dehydrogenase (KETOGLUTARATE DEHYDROGENASE COMPLEX). It is used in DIETARY SUPPLEMENTS.	3.57	7	0	dithiolanes; heterocyclic fatty acid; thia fatty acid	fundamental metabolite; geroprotector
pyruvaldehyde Pyruvaldehyde: An organic compound used often as a reagent in organic synthesis, as a flavoring agent, and in tanning. It has been demonstrated as an intermediate in the metabolism of acetone and its derivatives in isolated cell preparations, in various culture media, and in vivo in certain animals.. methylglyoxal : A 2-oxo aldehyde derived from propanal.	2.15	1	0	2-oxo aldehyde; propanals	Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
inositol Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction.. inositol : Any cyclohexane-1,2,3,4,5,6-hexol.. 1D-chiro-inositol : Belonging to the inositol family of compounds, D-chiro-inositol (DCI) is an isomer of glucose. It is an important secondary messenger in insulin signal transduction.. muco-inositol : An inositol that is cyclohexane-1,2,3,4,5,6-hexol having a (1R,2R,3r,4R,5S,6r)-configuration.	2.05	1	0	cyclitol; hexol
melatonin [no description available]	3.59	2	0	acetamides; tryptamines	anticonvulsant; central nervous system depressant; geroprotector; hormone; human metabolite; immunological adjuvant; mouse metabolite; radical scavenger
naphthalene [no description available]	2.17	1	0	naphthalenes; ortho-fused bicyclic arene	apoptosis inhibitor; carcinogenic agent; environmental contaminant; mouse metabolite; plant metabolite; volatile oil component
nickel Nickel: A trace element with the atomic symbol Ni, atomic number 28, and atomic weight 58.69. It is a cofactor of the enzyme UREASE.. nickel ion : A nickel atom having a net electric charge.. nickel atom : Chemical element (nickel group element atom) with atomic number 28.	4.8	1	1	metal allergen; nickel group element atom	epitope; micronutrient
niacinamide nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.	11.98	24	9	pyridine alkaloid; pyridinecarboxamide; vitamin B3	anti-inflammatory agent; antioxidant; cofactor; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor; EC 3.5.1.98 (histone deacetylase) inhibitor; Escherichia coli metabolite; geroprotector; human urinary metabolite; metabolite; mouse metabolite; neuroprotective agent; Saccharomyces cerevisiae metabolite; Sir2 inhibitor
niacin Niacin: A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.. vitamin B3 : Any member of a group of vitamers that belong to the chemical structural class called pyridines that exhibit biological activity against vitamin B3 deficiency. Vitamin B3 deficiency causes a condition known as pellagra whose symptoms include depression, dermatitis and diarrhea. The vitamers include nicotinic acid and nicotinamide (and their ionized and salt forms).. nicotinic acid : A pyridinemonocarboxylic acid that is pyridine in which the hydrogen at position 3 is replaced by a carboxy group.	3.91	3	0	pyridine alkaloid; pyridinemonocarboxylic acid; vitamin B3	antidote; antilipemic drug; EC 3.5.1.19 (nicotinamidase) inhibitor; Escherichia coli metabolite; human urinary metabolite; metabolite; mouse metabolite; plant metabolite; vasodilator agent
nitroxyl nitroxyl: hydroxamic acid oxidized to nitroxyl free radical. nitroxyl : A nitrogen oxoacid consisting of an oxygen atom double-bonded to an NH group.	4.8	1	1	nitrogen oxoacid
orotic acid Orotic Acid: An intermediate product in PYRIMIDINE synthesis which plays a role in chemical conversions between DIHYDROFOLATE and TETRAHYDROFOLATE.. orotic acid : A pyrimidinemonocarboxylic acid that is uracil bearing a carboxy substituent at position C-6.	2.05	1	0	pyrimidinemonocarboxylic acid	Escherichia coli metabolite; metabolite; mouse metabolite
4-aminobenzoic acid 4-Aminobenzoic Acid: An aminobenzoic acid isomer that combines with pteridine and GLUTAMIC ACID to form FOLIC ACID. The fact that 4-aminobenzoic acid absorbs light throughout the UVB range has also resulted in its use as an ingredient in SUNSCREENS.. 4-ammoniobenzoate : A zwitterion obtained by transfer of a proton from the carboxy to the amino group of 4-aminobenzoic acid.. 4-aminobenzoic acid : An aminobenzoic acid in which the amino group is para to the carboxy group.	2.05	1	0	aminobenzoic acid; aromatic amino-acid zwitterion	allergen; Escherichia coli metabolite; plant metabolite
palmitic acid Palmitic Acid: A common saturated fatty acid found in fats and waxes including olive oil, palm oil, and body lipids.. hexadecanoic acid : A straight-chain, sixteen-carbon, saturated long-chain fatty acid.	7.13	1	0	long-chain fatty acid; straight-chain saturated fatty acid	algal metabolite; Daphnia magna metabolite; EC 1.1.1.189 (prostaglandin-E2 9-reductase) inhibitor; plant metabolite
phenol [no description available]	2.05	1	0	phenols	antiseptic drug; disinfectant; human xenobiotic metabolite; mouse metabolite
phenylacetic acid phenylacetic acid : A monocarboxylic acid that is toluene in which one of the hydrogens of the methyl group has been replaced by a carboxy group.	2.05	1	0	benzenes; monocarboxylic acid; phenylacetic acids	allergen; Aspergillus metabolite; auxin; EC 6.4.1.1 (pyruvate carboxylase) inhibitor; Escherichia coli metabolite; human metabolite; plant growth retardant; plant metabolite; Saccharomyces cerevisiae metabolite; toxin
phosphorylcholine Phosphorylcholine: Calcium and magnesium salts used therapeutically in hepatobiliary dysfunction.. phosphocholine : The phosphate of choline; and the parent compound of the phosphocholine family.	9.3	15	3	phosphocholines	allergen; epitope; hapten; human metabolite; mouse metabolite
picolinic acid picolinic acid: iron-chelating agent that inhibits DNA synthesis; may interfere with iron-dependent production of stable free organic radical which is essential for ribonucleotide reductase formation of deoxyribonucleotides; RN given refers to parent cpd; structure in Merck Index, 9th ed, #7206. picolinic acid : A pyridinemonocarboxylic acid in which the carboxy group is located at position 2. It is an intermediate in the metabolism of tryptophan.	2.76	2	0	pyridinemonocarboxylic acid	human metabolite; MALDI matrix material
pteridines [no description available]	3.03	4	0	azaarene; mancude organic heterobicyclic parent; ortho-fused heteroarene; pteridines
pyrazinamide pyrazinecarboxamide : A monocarboxylic acid amide resulting from the formal condensation of the carboxy group of pyrazinoic acid (pyrazine-2-carboxylic acid) with ammonia. A prodrug for pyrazinoic acid, pyrazinecarboxamide is used as part of multidrug regimens for the treatment of tuberculosis.	4.08	4	0	monocarboxylic acid amide; N-acylammonia; pyrazines	antitubercular agent; prodrug
pyrazinoic acid pyrazinoic acid: active metabolite of pyrazinamide; structure. pyrazine-2-carboxylic acid : The parent compound of the class of pyrazinecarboxylic acids, that is pyrazine bearing a single carboxy substituent. The active metabolite of the antitubercular drug pyrazinamide.	2.49	2	0	pyrazinecarboxylic acid	antitubercular agent; drug metabolite
pyridoxal phosphate Pyridoxal Phosphate: This is the active form of VITAMIN B 6 serving as a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, aminolevulinic acid. During transamination of amino acids, pyridoxal phosphate is transiently converted into pyridoxamine phosphate (PYRIDOXAMINE).. pyridoxal 5'-phosphate : The monophosphate ester obtained by condensation of phosphoric acid with the primary hydroxy group of pyridoxal.	2.05	1	0	methylpyridines; monohydroxypyridine; pyridinecarbaldehyde; vitamin B6 phosphate	coenzyme; cofactor; EC 2.7.7.7 (DNA-directed DNA polymerase) inhibitor; Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
pyridoxine 4,5-bis(hydroxymethyl)-2-methylpyridin-3-ol: structure in first source. vitamin B6 : Any member of the group of pyridines that exhibit biological activity against vitamin B6 deficiency. Vitamin B6 deficiency is associated with microcytic anemia, electroencephalographic abnormalities, dermatitis with cheilosis (scaling on the lips and cracks at the corners of the mouth) and glossitis (swollen tongue), depression and confusion, and weakened immune function. Vitamin B6 consists of the vitamers pyridoxine, pyridoxal, and pyridoxamine and their respective 5'-phosphate esters (and includes their corresponding ionized and salt forms).	4.6	4	0	hydroxymethylpyridine; methylpyridines; monohydroxypyridine; vitamin B6	cofactor; Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
selenious acid Selenious Acid: A selenium compound with the molecular formula H2SO3. It used as a source of SELENIUM, especially for patients that develop selenium deficiency following prolonged PARENTERAL NUTRITION.	2.08	1	0	selenium oxoacid
succinic acid Succinic Acid: A water-soluble, colorless crystal with an acid taste that is used as a chemical intermediate, in medicine, the manufacture of lacquers, and to make perfume esters. It is also used in foods as a sequestrant, buffer, and a neutralizing agent. (Hawley's Condensed Chemical Dictionary, 12th ed, p1099; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1851). succinic acid : An alpha,omega-dicarboxylic acid resulting from the formal oxidation of each of the terminal methyl groups of butane to the corresponding carboxy group. It is an intermediate metabolite in the citric acid cycle.	4.8	1	1	alpha,omega-dicarboxylic acid; C4-dicarboxylic acid	anti-ulcer drug; fundamental metabolite; micronutrient; nutraceutical; radiation protective agent
taurine [no description available]	2.6	1	0	amino sulfonic acid; zwitterion	antioxidant; Escherichia coli metabolite; glycine receptor agonist; human metabolite; mouse metabolite; nutrient; radical scavenger; Saccharomyces cerevisiae metabolite
thiamine thiamine(1+) : A primary alcohol that is 1,3-thiazol-3-ium substituted by (4-amino-2-methylpyrimidin-5-yl)methyl, methyl and 2-hydroxyethyl groups at positions 3, 4 and 5, respectively.	3.93	3	0	primary alcohol; vitamin B1	Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
toluene methylbenzene : Any alkylbenzene that is benzene substituted with one or more methyl groups.	5.03	2	1	methylbenzene; toluenes; volatile organic compound	cholinergic antagonist; fuel additive; neurotoxin; non-polar solvent
uracil 2,4-dihydroxypyrimidine: a urinary biomarker for bipolar disorder	2.05	1	0	pyrimidine nucleobase; pyrimidone	allergen; Daphnia magna metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; prodrug; Saccharomyces cerevisiae metabolite
uric acid Uric Acid: An oxidation product, via XANTHINE OXIDASE, of oxypurines such as XANTHINE and HYPOXANTHINE. It is the final oxidation product of purine catabolism in humans and primates, whereas in most other mammals URATE OXIDASE further oxidizes it to ALLANTOIN.. uric acid : An oxopurine that is the final oxidation product of purine metabolism.. 6-hydroxy-1H-purine-2,8(7H,9H)-dione : A tautomer of uric acid having oxo groups at C-2 and C-8 and a hydroxy group at C-6.. 7,9-dihydro-1H-purine-2,6,8(3H)-trione : An oxopurine in which the purine ring is substituted by oxo groups at positions 2, 6, and 8.	5.17	2	1	uric acid	Escherichia coli metabolite; human metabolite; mouse metabolite
urea pseudourea: clinical use; structure. isourea : A carboximidic acid that is the imidic acid tautomer of urea, H2NC(=NH)OH, and its hydrocarbyl derivatives.	5.51	4	1	isourea; monocarboxylic acid amide; one-carbon compound	Daphnia magna metabolite; Escherichia coli metabolite; fertilizer; flour treatment agent; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
vanillin Vanilla: A plant genus of the family ORCHIDACEAE that is the source of the familiar flavoring used in foods and medicines (FLAVORING AGENTS).	2.07	1	0	benzaldehydes; monomethoxybenzene; phenols	anti-inflammatory agent; anticonvulsant; antioxidant; flavouring agent; plant metabolite
catechin [no description available]	2.45	2	0	hydroxyflavan
menthol Menthol: A monoterpene cyclohexanol produced from mint oils.	7.45	2	0	p-menthane monoterpenoid; secondary alcohol	volatile oil component
pk 11195 PK-11195 : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 1-(2-chlorophenyl)isoquinoline-3-carboxylic acid with the amino group of sec-butylmethylamine	3.36	2	0	aromatic amide; isoquinolines; monocarboxylic acid amide; monochlorobenzenes	antineoplastic agent
1-(3-chlorophenyl)piperazine 1-(3-chlorophenyl)piperazine: supposed metabolite of TRAZODONE; RN given refers to parent cpd; structure. 1-(3-chlorophenyl)piperazine : A N-arylpiperazine that is piperazine carrying a 3-chlorophenyl substituent at position 1. It is a metabolite of the antidepressant drug trazodone.	2.46	2	0	monochlorobenzenes; N-arylpiperazine	drug metabolite; environmental contaminant; serotonergic agonist; xenobiotic
pd 173074 [no description available]	2.08	1	0	aromatic amine; biaryl; dimethoxybenzene; pyridopyrimidine; tertiary amino compound; ureas	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; fibroblast growth factor receptor antagonist
2-aminoethoxydiphenyl borate 2-aminoethoxydiphenyl borate: is a novel membrane-penetrable modulator and transient receptor potential channel blocker; structure in first source; do not confuse with 2-APB cpd. 2-aminoethoxydiphenylborane : An organoboron compound that is diphenylborane in which the borane hydrogen is replaced by a 2-aminoethoxy group.	2.17	1	0	organoboron compound; primary amino compound	calcium channel blocker; IP3 receptor antagonist; potassium channel opener
3-aminobenzamide [no description available]	2.6	1	0	benzamides; substituted aniline	EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
3-methylcholanthrene Methylcholanthrene: A carcinogen that is often used in experimental cancer studies.. 3-methylcholanthrene : A pentacyclic ortho- and peri-fused polycyclic arene consisting of a dihydrocyclopenta[ij]tetraphene ring system with a methyl substituent at the 3-position.	2.06	1	0	ortho- and peri-fused polycyclic arene	aryl hydrocarbon receptor agonist; carcinogenic agent
enprofylline enprofylline : Xanthine bearing a propyl substituent at position 3. A bronchodilator, it is used for the symptomatic treatment of asthma and chronic obstructive pulmonary disease, and in the management of cerebrovascular insufficiency, sickle cell disease, and diabetic neuropathy.	2.04	1	0	oxopurine	anti-arrhythmia drug; anti-asthmatic drug; bronchodilator agent; non-steroidal anti-inflammatory drug
pleconaril WIN 63843: structure given in first source	2.6	1	0
4-(2-aminoethyl)benzenesulfonylfluoride [no description available]	2.59	2	0
phenytoin [no description available]	3.93	3	0	imidazolidine-2,4-dione	anticonvulsant; drug allergen; sodium channel blocker; teratogenic agent
oxyquinoline Oxyquinoline: An antiseptic with mild fungistatic, bacteriostatic, anthelmintic, and amebicidal action. It is also used as a reagent and metal chelator, as a carrier for radio-indium for diagnostic purposes, and its halogenated derivatives are used in addition as topical anti-infective agents and oral antiamebics.. quinolin-8-ol : A monohydroxyquinoline that is quinoline substituted by a hydroxy group at position 8. Its fungicidal properties are used for the control of grey mould on vines and tomatoes.	2.15	1	0	monohydroxyquinoline	antibacterial agent; antifungal agrochemical; antiseptic drug; iron chelator
tacrine Tacrine: A cholinesterase inhibitor that crosses the blood-brain barrier. Tacrine has been used to counter the effects of muscle relaxants, as a respiratory stimulant, and in the treatment of Alzheimer's disease and other central nervous system disorders.. tacrine : A member of the class of acridines that is 1,2,3,4-tetrahydroacridine substituted by an amino group at position 9. It is used in the treatment of Alzheimer's disease.	2.46	2	0	acridines; aromatic amine	EC 3.1.1.7 (acetylcholinesterase) inhibitor
abt 702 [no description available]	2.08	1	0	bipyridines
acebutolol Acebutolol: A cardioselective beta-1 adrenergic antagonist with little effect on the bronchial receptors. The drug has stabilizing and quinidine-like effects on cardiac rhythm, as well as weak inherent sympathomimetic action.. acebutolol : An ether that is the 2-acetyl-4-(butanoylamino)phenyl ether of the primary hydroxy group of 3-(propan-2-ylamino)propane-1,2-diol.	3.86	3	0	aromatic amide; ethanolamines; ether; monocarboxylic acid amide; propanolamine; secondary amino compound	anti-arrhythmia drug; antihypertensive agent; beta-adrenergic antagonist; sympathomimetic agent
acetaminophen Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.. paracetamol : A member of the class of phenols that is 4-aminophenol in which one of the hydrogens attached to the amino group has been replaced by an acetyl group.	4.28	5	0	acetamides; phenols	antipyretic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; cyclooxygenase 3 inhibitor; environmental contaminant; ferroptosis inducer; geroprotector; hepatotoxic agent; human blood serum metabolite; non-narcotic analgesic; non-steroidal anti-inflammatory drug; xenobiotic
acetazolamide Acetazolamide: One of the CARBONIC ANHYDRASE INHIBITORS that is sometimes effective against absence seizures. It is sometimes useful also as an adjunct in the treatment of tonic-clonic, myoclonic, and atonic seizures, particularly in women whose seizures occur or are exacerbated at specific times in the menstrual cycle. However, its usefulness is transient often because of rapid development of tolerance. Its antiepileptic effect may be due to its inhibitory effect on brain carbonic anhydrase, which leads to an increased transneuronal chloride gradient, increased chloride current, and increased inhibition. (From Smith and Reynard, Textbook of Pharmacology, 1991, p337)	4.71	8	0	monocarboxylic acid amide; sulfonamide; thiadiazoles	anticonvulsant; diuretic; EC 4.2.1.1 (carbonic anhydrase) inhibitor
acetohexamide Acetohexamide: A sulfonylurea hypoglycemic agent that is metabolized in the liver to 1-hydrohexamide.. acetohexamide : An N-sulfonylurea that is urea in which a hydrogen attached to one of the nitrogens is replaced by a p-acetylphenylsulfonyl group, while a hydrogen attached to the other nitrogen is replaced by a cyclohexyl group.	2.05	1	0	acetophenones; N-sulfonylurea	hypoglycemic agent; insulin secretagogue
acetohydroxamic acid acetohydroxamic acid: urease inhibitor. oxime : Compounds of structure R2C=NOH derived from condensation of aldehydes or ketones with hydroxylamine. Oximes from aldehydes may be called aldoximes; those from ketones may be called ketoximes.. N-hydroxyacetimidic acid : A carbohydroximic acid consisting of acetimidic acid having a hydroxy group attached to the imide nitrogen.. acetohydroxamic acid : A member of the class of acetohydroxamic acids that is acetamide in which one of the amino hydrogens has been replaced by a hydroxy group.	3.59	2	0	acetohydroxamic acids; carbohydroximic acid	algal metabolite; EC 3.5.1.5 (urease) inhibitor
alaproclate alaproclate: specific 5-hydroxytryptamine uptake inhibitors; RN given refers to (DL)-isomer	3.23	1	0	alpha-amino acid ester
albendazole [no description available]	11.23	5	1	aryl sulfide; benzimidazoles; benzimidazolylcarbamate fungicide; carbamate ester	anthelminthic drug; microtubule-destabilising agent; tubulin modulator
albuterol Albuterol: A short-acting beta-2 adrenergic agonist that is primarily used as a bronchodilator agent to treat ASTHMA. Albuterol is prepared as a racemic mixture of R(-) and S(+) stereoisomers. The stereospecific preparation of R(-) isomer of albuterol is referred to as levalbuterol.. albuterol : A member of the class of phenylethanolamines that is 4-(2-amino-1-hydroxyethyl)-2-(hydroxymethyl)phenol having a tert-butyl group attached to the nirogen atom. It acts as a beta-adrenergic agonist used in the treatment of asthma and chronic obstructive pulmonary disease (COPD).	4.08	4	0	phenols; phenylethanolamines; secondary amino compound	beta-adrenergic agonist; bronchodilator agent; environmental contaminant; xenobiotic
alendronate alendronic acid : A 1,1-bis(phosphonic acid) that is methanebis(phosphonic acid) in which the two methylene hydrogens are replaced by hydroxy and 3-aminopropyl groups.	4.13	4	0	1,1-bis(phosphonic acid); primary amino compound	bone density conservation agent; EC 2.5.1.1 (dimethylallyltranstransferase) inhibitor
alfuzosin alfuzosin: structure given in first source	4.06	4	0	monocarboxylic acid amide; quinazolines; tetrahydrofuranol	alpha-adrenergic antagonist; antihypertensive agent; antineoplastic agent
alosetron alosetron : A pyrido[4,3-b]indole compound having a 5-methyl-1H-imidazol-4-ylmethyl group at the 2-position.	3.58	2	0	imidazoles; pyridoindole	antiemetic; gastrointestinal drug; serotonergic antagonist
alprazolam Alprazolam: A triazolobenzodiazepine compound with antianxiety and sedative-hypnotic actions, that is efficacious in the treatment of PANIC DISORDERS, with or without AGORAPHOBIA, and in generalized ANXIETY DISORDERS. (From AMA Drug Evaluations Annual, 1994, p238). alprazolam : A member of the class of triazolobenzodiazepines that is 4H-[1,2,4]triazolo[4,3-a][1,4]benzodiazepine carrying methyl, phenyl and chloro substituents at positions 1, 6 and 8 respectively. Alprazolam is only found in individuals that have taken this drug.	3.58	2	0	organochlorine compound; triazolobenzodiazepine	anticonvulsant; anxiolytic drug; GABA agonist; muscle relaxant; sedative; xenobiotic
alprenolol Alprenolol: One of the ADRENERGIC BETA-ANTAGONISTS used as an antihypertensive, anti-anginal, and anti-arrhythmic agent.. alprenolol : A secondary alcohol that is propan-2-ol substituted by a 2-allylphenoxy group at position 1 and an isopropylamino group at position 3. It is a beta-adrenergic antagonist used as a antihypertensive, anti-arrhythmia and a sympatholytic agent.	2.8	3	0	secondary alcohol; secondary amino compound	anti-arrhythmia drug; antihypertensive agent; beta-adrenergic antagonist; sympatholytic agent
altretamine Altretamine: A hexamethyl-2,4,6-triamine derivative of 1,3,5-triazine.	3.23	1	0	triamino-1,3,5-triazine
amantadine amant: an antiviral compound consisting of an adamantane derivative chemically linked to a water-solube polyanioic matrix; structure in first source	4.11	4	0	adamantanes; primary aliphatic amine	analgesic; antiparkinson drug; antiviral drug; dopaminergic agent; NMDA receptor antagonist; non-narcotic analgesic
ambenonium ambenonium : A symmetrical oxalamide-based bis-quaternary ammonium ion having ethyl and 2-chlorobenzyl groups attached to the nitrogens.	3.23	1	0	quaternary ammonium ion	EC 3.1.1.8 (cholinesterase) inhibitor
ambroxol Ambroxol: A metabolite of BROMHEXINE that stimulates mucociliary action and clears the air passages in the respiratory tract. It is usually administered as the hydrochloride.	2.05	1	0	aromatic amine
diatrizoic acid Diatrizoate: A commonly used x-ray contrast medium. As DIATRIZOATE MEGLUMINE and as Diatrizoate sodium, it is used for gastrointestinal studies, angiography, and urography.. amidotrizoic acid : A member of the class of benzoic acids that is benzoic acid having iodo substituents at the 2-, 4- and 6-positions and acetamido substituents at the 3- and 5-positions. It is used, mainly as its N-methylglucamine and sodium salts, as an X-ray contrast medium in gastrointestinal studies, angiography, and urography.	3.87	3	0	acetamides; benzoic acids; organoiodine compound	environmental contaminant; radioopaque medium; xenobiotic
amifostine anhydrous Amifostine: A phosphorothioate proposed as a radiation-protective agent. It causes splenic vasodilation and may block autonomic ganglia.. amifostine : An organic thiophosphate that is the S-phospho derivative of 2-[(3-aminopropyl)amino]ethanethiol. A prodrug for the free thiol, WR-1065, which is used as a cytoprotectant in cancer chemotherapy and radiotherapy.	3.61	2	0	diamine; organic thiophosphate	antioxidant; prodrug; radiation protective agent
aminoglutethimide Aminoglutethimide: An aromatase inhibitor that is used in the treatment of advanced BREAST CANCER.. aminoglutethimide : A dicarboximide that is a six-membered cyclic compound having ethyl and 4-aminophenyl substituents at the 3-position.	2.47	2	0	dicarboximide; piperidones; substituted aniline	adrenergic agent; anticonvulsant; antineoplastic agent; EC 1.14.14.14 (aromatase) inhibitor
pimagedine pimagedine: diamine oxidase & nitric oxide synthase inhibitor; an advanced glycosylation end product inhibitor; used in the treatment of diabetic complications; structure. aminoguanidine : A one-carbon compound whose unique structure renders it capable of acting as a derivative of hydrazine, guanidine or formamide.	2.05	1	0	guanidines; one-carbon compound	EC 1.14.13.39 (nitric oxide synthase) inhibitor; EC 1.4.3.4 (monoamine oxidase) inhibitor
p-aminohippuric acid p-Aminohippuric Acid: The glycine amide of 4-aminobenzoic acid. Its sodium salt is used as a diagnostic aid to measure effective renal plasma flow (ERPF) and excretory capacity.. p-aminohippurate : A hippurate that is the conjugate base of p-aminohippuric acid, arising from deprotonation of the carboxy group.. p-aminohippuric acid : An N-acylglycine that is the 4-amino derivative of hippuric acid; used as a diagnostic agent in the measurement of renal plasma flow.	3.68	2	0	N-acylglycine	Daphnia magna metabolite
theophylline [no description available]	4.08	4	0	dimethylxanthine	adenosine receptor antagonist; anti-asthmatic drug; anti-inflammatory agent; bronchodilator agent; drug metabolite; EC 3.1.4.* (phosphoric diester hydrolase) inhibitor; fungal metabolite; human blood serum metabolite; immunomodulator; muscle relaxant; vasodilator agent
2-aminothiazole 2-aminothiazole: RN given refers to parent cpd; structure. 1,3-thiazol-2-amine : A primary amino compound that is 1,3-thiazole substituted by an amino group at position 2.	2.6	1	0	1,3-thiazoles; primary amino compound
amiodarone Amiodarone: An antianginal and class III antiarrhythmic drug. It increases the duration of ventricular and atrial muscle action by inhibiting POTASSIUM CHANNELS and VOLTAGE-GATED SODIUM CHANNELS. There is a resulting decrease in heart rate and in vascular resistance.. amiodarone : A member of the class of 1-benzofurans that is 1-benzofuran substituted by a butyl group at position 2 and a 4-[2-(diethylamino)ethoxy]-3,5-diiodobenzoyl group at position 3. It is a cardiovascular drug used for the treatment of cardiac dysrhythmias.	4.08	4	0	1-benzofurans; aromatic ketone; organoiodine compound; tertiary amino compound	cardiovascular drug
dan 2163 [no description available]	2.54	2	0	aromatic amide; aromatic amine; benzamides; pyrrolidines; sulfone	environmental contaminant; second generation antipsychotic; xenobiotic
amitriptyline Amitriptyline: Tricyclic antidepressant with anticholinergic and sedative properties. It appears to prevent the re-uptake of norepinephrine and serotonin at nerve terminals, thus potentiating the action of these neurotransmitters. Amitriptyline also appears to antagonize cholinergic and alpha-1 adrenergic responses to bioactive amines.. amitriptyline : An organic tricyclic compound that is 10,11-dihydro-5H-dibenzo[a,d][7]annulene substituted by a 3-(dimethylamino)propylidene group at position 5.	6.59	8	1	carbotricyclic compound; tertiary amine	adrenergic uptake inhibitor; antidepressant; environmental contaminant; tropomyosin-related kinase B receptor agonist; xenobiotic
amlexanox amlexanox: SRA-A antagonist;structure given in first source. amlexanox : A pyridochromene-derived monocarboxylic acid having an amino substituent at the 2-position, an oxo substituent at the 5-position and an isopropyl substituent at the 7-position.	2.08	1	0	monocarboxylic acid; pyridochromene	anti-allergic agent; anti-ulcer drug; non-steroidal anti-inflammatory drug
amlodipine Amlodipine: A long-acting dihydropyridine calcium channel blocker. It is effective in the treatment of ANGINA PECTORIS and HYPERTENSION.. amlodipine : A fully substituted dialkyl 1,4-dihydropyridine-3,5-dicarboxylate derivative, which is used for the treatment of hypertension, chronic stable angina and confirmed or suspected vasospastic angina.	4.08	4	0	dihydropyridine; ethyl ester; methyl ester; monochlorobenzenes; primary amino compound	antihypertensive agent; calcium channel blocker; vasodilator agent
amobarbital Amobarbital: A barbiturate with hypnotic and sedative properties (but not antianxiety). Adverse effects are mainly a consequence of dose-related CNS depression and the risk of dependence with continued use is high. (From Martindale, The Extra Pharmacopoeia, 30th ed, p565). amobarbital : A member of the class of barbiturates that is pyrimidine-2,4,6(1H,3H,5H)-trione substituted by a 3-methylbutyl and an ethyl group at position 5. Amobarbital has been shown to exhibit sedative and hypnotic properties.	2.05	1	0	barbiturates
amodiaquine Amodiaquine: A 4-aminoquinoline compound with anti-inflammatory properties.. amodiaquine : A quinoline having a chloro group at the 7-position and an aryl amino group at the 4-position.	2.6	1	0	aminoquinoline; organochlorine compound; phenols; secondary amino compound; tertiary amino compound	anticoronaviral agent; antimalarial; drug allergen; EC 2.1.1.8 (histamine N-methyltransferase) inhibitor; non-steroidal anti-inflammatory drug; prodrug
amoxapine Amoxapine: The N-demethylated derivative of the antipsychotic agent LOXAPINE that works by blocking the reuptake of norepinephrine, serotonin, or both; it also blocks dopamine receptors. Amoxapine is used for the treatment of depression.. amoxapine : A dibenzooxazepine compound having a chloro substituent at the 2-position and a piperazin-1-yl group at the 11-position.	3.61	2	0	dibenzooxazepine	adrenergic uptake inhibitor; antidepressant; dopaminergic antagonist; geroprotector; serotonin uptake inhibitor
amsacrine Amsacrine: An aminoacridine derivative that intercalates into DNA and is used as an antineoplastic agent.. amsacrine : A sulfonamide that is N-phenylmethanesulfonamide substituted by a methoxy group at position 3 and an acridin-9-ylamino group at position 4. It exhibits antineoplastic activity.	2.97	4	0	acridines; aromatic ether; sulfonamide	antineoplastic agent; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
anastrozole [no description available]	4.59	4	0	nitrile; triazoles	antineoplastic agent; EC 1.14.14.14 (aromatase) inhibitor
anethole trithione Anethole Trithione: Choleretic used to allay dry mouth and constipation due to tranquilizers.	2.05	1	0	methoxybenzenes
anthralin Anthralin: An anthracene derivative that disrupts MITOCHONDRIA function and structure and is used for the treatment of DERMATOSES, especially PSORIASIS. It may cause FOLLICULITIS.. anthralin : An anthracene compound derived by the substitution of -OH groups for hydrogen at C-1 and C-8, and with an oxo group at C-9.	2.47	2	0	anthracenes	antipsoriatic
antipyrine Antipyrine: An analgesic and antipyretic that has been given by mouth and as ear drops. Antipyrine is often used in testing the effects of other drugs or diseases on drug-metabolizing enzymes in the liver. (From Martindale, The Extra Pharmacopoeia, 30th ed, p29). antipyrine : A pyrazolone derivative that is 1,2-dihydropyrazol-3-one substituted with methyl groups at N-1 and C-5 and with a phenyl group at N-2.	2.74	3	0	pyrazolone	antipyretic; cyclooxygenase 3 inhibitor; environmental contaminant; non-narcotic analgesic; non-steroidal anti-inflammatory drug; xenobiotic
aristolochic acid i aristolochic acid I: phospholipase A inhibitor. aristolochic acid A : An aristolochic acid that is phenanthrene-1-carboxylic acid that is substituted by a methylenedioxy group at the 3,4 positions, by a methoxy group at position 8, and by a nitro group at position 10. It is the most abundant of the aristolochic acids and is found in almost all Aristolochia (birthworts or pipevines) species. It has been tried in a number of treatments for inflammatory disorders, mainly in Chinese and folk medicine. However, there is concern over their use as aristolochic acid is both carcinogenic and nephrotoxic.	2.15	1	0	aristolochic acids; aromatic ether; C-nitro compound; cyclic acetal; monocarboxylic acid; organic heterotetracyclic compound	carcinogenic agent; metabolite; mutagen; nephrotoxin; toxin
aspirin Aspirin: The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5). acetylsalicylate : A benzoate that is the conjugate base of acetylsalicylic acid, arising from deprotonation of the carboxy group.. acetylsalicylic acid : A member of the class of benzoic acids that is salicylic acid in which the hydrogen that is attached to the phenolic hydroxy group has been replaced by an acetoxy group. A non-steroidal anti-inflammatory drug with cyclooxygenase inhibitor activity.	8.04	14	1	benzoic acids; phenyl acetates; salicylates	anticoagulant; antipyretic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; drug allergen; EC 1.1.1.188 (prostaglandin-F synthase) inhibitor; geroprotector; non-narcotic analgesic; non-steroidal anti-inflammatory drug; plant activator; platelet aggregation inhibitor; prostaglandin antagonist; teratogenic agent
astemizole Astemizole: Antihistamine drug now withdrawn from the market in many countries because of rare but potentially fatal side effects.. astemizole : A piperidine compound having a 2-(4-methoxyphenyl)ethyl group at the 1-position and an N-[(4-fluorobenzyl)benzimidazol-2-yl]amino group at the 4-position.	2.08	1	0	benzimidazoles; piperidines	anti-allergic agent; anticoronaviral agent; H1-receptor antagonist
atenolol Atenolol: A cardioselective beta-1 adrenergic blocker possessing properties and potency similar to PROPRANOLOL, but without a negative inotropic effect.. atenolol : An ethanolamine compound having a (4-carbamoylmethylphenoxy)methyl group at the 1-position and an N-isopropyl substituent.	4.08	4	0	ethanolamines; monocarboxylic acid amide; propanolamine	anti-arrhythmia drug; antihypertensive agent; beta-adrenergic antagonist; environmental contaminant; sympatholytic agent; xenobiotic
azathioprine Azathioprine: An immunosuppressive agent used in combination with cyclophosphamide and hydroxychloroquine in the treatment of rheumatoid arthritis. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance has been listed as a known carcinogen. (Merck Index, 11th ed). azathioprine : A thiopurine that is 6-mercaptopurine in which the mercapto hydrogen is replaced by a 1-methyl-4-nitroimidazol-5-yl group. It is a prodrug for mercaptopurine and is used as an immunosuppressant, prescribed for the treatment of inflammatory conditions and after organ transplantation and also for treatment of Crohn's didease and MS.	4.1	4	0	aryl sulfide; C-nitro compound; imidazoles; thiopurine	antimetabolite; antineoplastic agent; carcinogenic agent; DNA synthesis inhibitor; hepatotoxic agent; immunosuppressive agent; prodrug
azelastine azelastine: azeptin is azelastine hydrochloride; structure; eye drop formulation effective in relieving symptoms of allergic conjunctivitis; do not confuse with 5-loxin which is an extract of Boswellia. azelastine : A phthalazine compound having an oxo substituent at the 1-position, a 1-methylazepan-4-yl group at the 2-position and a 4-chlorobenzyl substituent at the 4-position.	2.04	1	0	monochlorobenzenes; phthalazines; tertiary amino compound	anti-allergic agent; anti-asthmatic drug; bronchodilator agent; EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor; H1-receptor antagonist; platelet aggregation inhibitor
baclofen [no description available]	4.13	4	0	amino acid zwitterion; gamma-amino acid; monocarboxylic acid; monochlorobenzenes; primary amino compound	central nervous system depressant; GABA agonist; muscle relaxant
barbital 5,5-diethylbarbituric acid : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by two ethyl groups. Formerly used as a hypnotic (sleeping aid).	2.05	1	0	barbiturates	drug allergen
bendazac bendazac : A monocarboxylic acid that is glycolic acid in which the hydrogen attached to the 2-hydroxy group is replaced by a 1-benzyl-1H-indazol-3-yl group. Although it has anti-inflammatory, antinecrotic, choleretic and antilipidaemic properties and has been used for the treatment of various inflammatory skin disorders, its principal effect is to inhibit the denaturation of proteins. Its lysine salt is used in the management of cataracts.	3.59	2	0	indazoles; monocarboxylic acid	non-steroidal anti-inflammatory drug; radical scavenger
bendroflumethiazide Bendroflumethiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. It has been used in the treatment of familial hyperkalemia, hypertension, edema, and urinary tract disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p810). bendroflumethiazide : A sulfonamide consisting of 7-sulfamoyl-3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide in which the hydrogen at position 6 is substituted by a trifluoromethyl group and that at position 3 is substituted by a benzyl group.	3.23	1	0	benzothiadiazine; sulfonamide	antihypertensive agent; diuretic
benzamide benzamide : An aromatic amide that consists of benzene bearing a single carboxamido substituent. The parent of the class of benzamides.	2.6	1	0	benzamides
benzbromarone Benzbromarone: Uricosuric that acts by increasing uric acid clearance. It is used in the treatment of gout.. benzbromarone : 1-Benzofuran substituted at C-2 and C-3 by an ethyl group and a 3,5-dibromo-4-hydroxybenzoyl group respectively. An inhibitor of CYP2C9, it is used as an anti-gout medication.	3.87	3	0	1-benzofurans; aromatic ketone	uricosuric drug
benzocaine Benzocaine: A surface anesthetic that acts by preventing transmission of impulses along NERVE FIBERS and at NERVE ENDINGS.. dextran sulfate sodium : An organic sodium salt of dextran sulfate. It induces colitis in mice.. benzocaine : A benzoate ester having 4-aminobenzoic acid as the acid component and ethanol as the alcohol component. A surface anaesthetic, it is used to suppress the gag reflex, and as a lubricant and topical anaesthetic on the larynx, mouth, nasal cavity, respiratory tract, oesophagus, rectum, urinary tract, and vagina.	2.08	1	0	benzoate ester; substituted aniline	allergen; antipruritic drug; sensitiser; topical anaesthetic
benzothiazide benzothiazide: structure. benzthiazide : 7-Sulfamoyl-1,2,4-benzothiadiazine 1,1-dioxide in which the hydrogen at position 6 is substituted by chlorine and that at position 3 is substituted by a benzylsulfanylmethyl group. A diuretic, it is used to treat hypertension and edema.	2.13	1	0	benzothiadiazine; sulfonamide	antihypertensive agent; diuretic
benzyl isothiocyanate benzyl isothiocyanate: inhibits carcinogen-induced neoplasia; structure in Negwer, 5th ed, #715; also promotes urinary bladder carcinoma	2.21	1	0	benzenes; isothiocyanate	antibacterial drug
berberine [no description available]	2.93	3	0	alkaloid antibiotic; berberine alkaloid; botanical anti-fungal agent; organic heteropentacyclic compound	antilipemic drug; antineoplastic agent; antioxidant; EC 1.1.1.141 [15-hydroxyprostaglandin dehydrogenase (NAD(+))] inhibitor; EC 1.1.1.21 (aldehyde reductase) inhibitor; EC 1.13.11.52 (indoleamine 2,3-dioxygenase) inhibitor; EC 1.21.3.3 (reticuline oxidase) inhibitor; EC 2.1.1.116 [3'-hydroxy-N-methyl-(S)-coclaurine 4'-O-methyltransferase] inhibitor; EC 2.1.1.122 [(S)-tetrahydroprotoberberine N-methyltransferase] inhibitor; EC 2.7.11.10 (IkappaB kinase) inhibitor; EC 3.1.1.4 (phospholipase A2) inhibitor; EC 3.1.1.7 (acetylcholinesterase) inhibitor; EC 3.1.1.8 (cholinesterase) inhibitor; EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor; EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; geroprotector; hypoglycemic agent; metabolite; potassium channel blocker
betaxolol [no description available]	3.58	2	0	propanolamine	antihypertensive agent; beta-adrenergic antagonist; sympatholytic agent
bethanechol Bethanechol: A slowly hydrolyzing muscarinic agonist with no nicotinic effects. Bethanechol is generally used to increase smooth muscle tone, as in the GI tract following abdominal surgery or in urinary retention in the absence of obstruction. It may cause hypotension, HEART RATE changes, and BRONCHIAL SPASM.. bethanechol : The carbamic acid ester of 2-methylcholine. A slowly hydrolysed muscarinic agonist with no nicotinic effects, it is used as its chloride salt to increase smooth muscle tone, as in the gastrointestinal tract following abdominal surgery, treatment of gastro-oesophageal reflux disease, and as an alternative to catheterisation in the treatment of non-obstructive urinary retention.	3.23	1	0	carbamate ester; quaternary ammonium ion	muscarinic agonist
bevantolol bevantolol: structure given in first source. bevantolol : A propanolamine that is 3-aminopropane-1,2-diol in which the hydrogen of the primary hydroxy group is substituted by 3-methylphenyl and one of the hydrogens attached to the nitrogen is substituted by 2-(3,4-dimethoxyphenyl)ethyl. A beta1 adrenoceptor antagonist, it has been shown to be as effective as other beta-blockers for the treatment of angina pectoris and hypertension.	2.04	1	0	propanolamine	anti-arrhythmia drug; antihypertensive agent; beta-adrenergic antagonist; calcium channel blocker
bicalutamide bicalutamide: approved for treatment of advanced prostate cancer. N-[4-cyano-3-(trifluoromethyl)phenyl]-3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanamide : A member of the class of (trifluoromethyl)benzenes that is 4-amino-2-(trifluoromethyl)benzonitrile in which one of the amino hydrogens is substituted by a 3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanoyl group.. bicalutamide : A racemate comprising of equal amounts of (R)-bicalutamide and (S)-bicalutamide. It is an oral non-steroidal antiandrogen used in the treatment of prostate cancer and hirsutism.	4.43	6	0	(trifluoromethyl)benzenes; monocarboxylic acid amide; monofluorobenzenes; nitrile; sulfone; tertiary alcohol
bay h 4502 bifonazole : A racemate comprising equimolar amounts of R- and S-bifonazole. It is a broad spectrum antifungal drug used for the treatment of fungal skin and nail infections.. 1-[biphenyl-4-yl(phenyl)methyl]imidazole : A member of the class of imidazoles carrying an alpha-(biphenyl-4-yl)benzyl substituent at position 1.	2.47	2	0	biphenyls; imidazoles
biperiden Biperiden: A muscarinic antagonist that has effects in both the central and peripheral nervous systems. It has been used in the treatment of arteriosclerotic, idiopathic, and postencephalitic parkinsonism. It has also been used to alleviate extrapyramidal symptoms induced by phenothiazine derivatives and reserpine.. biperiden : A member of the class of piperidines that is N-propylpiperidine in which the methyl hydrogens have been replaced by hydroxy, phenyl, and 5-norbornen-2-yl groups. A muscarinic antagonist affecting both the central and peripheral nervous systems, it is used in the treatment of all forms of Parkinson's disease.	3.58	2	0	piperidines; tertiary alcohol; tertiary amino compound	antidote to sarin poisoning; antidyskinesia agent; antiparkinson drug; muscarinic antagonist; parasympatholytic
bisacodyl Bisacodyl: A diphenylmethane stimulant laxative used for the treatment of CONSTIPATION and for bowel evacuation. (From Martindale, The Extra Pharmacopoeia, 30th ed, p871)	3.61	2	0	diarylmethane
bisoprolol Bisoprolol: A cardioselective beta-1 adrenergic blocker. It is effective in the management of HYPERTENSION and ANGINA PECTORIS.	3.86	3	0	secondary alcohol; secondary amine	anti-arrhythmia drug; antihypertensive agent; beta-adrenergic antagonist; sympatholytic agent
bromazepam Bromazepam: One of the BENZODIAZEPINES that is used in the treatment of ANXIETY DISORDERS.	2.04	1	0	organic molecular entity
bromopride bromopride: RN given refers to parent cpd; structure	2.46	2	0	benzamides
bromisovalum Bromisovalum: A sedative and mild hypnotic with potentially toxic effects.. bromisoval : A racemate comprising equimolar amounts of (R)- and (S)-bromisoval. It was previously used for its hypnotic and sedative properties but the use of bromides is now deprecated due to the possibility of the toxic accumulation of bromine in the body.. 2-bromo-N-carbamoyl-3-methylbutanamide : An N-acylurea that is urea in which one of the hydrogens is replaced by a 2-bromo-3-methybutanoyl group.	2.05	1	0	N-acylurea; organobromine compound
bronopol [no description available]	2.08	1	0	nitro compound
brotizolam brotizolam: structure	2.45	2	0	organic molecular entity
buflomedil buflomedil: RN given refers to parent cpd; synonym LL 1656 refers to HCl; structure	2.04	1	0	aromatic ketone
bumetanide [no description available]	4.08	4	0	amino acid; benzoic acids; sulfonamide	diuretic; EC 3.6.3.49 (channel-conductance-controlling ATPase) inhibitor
bunazosin bunazosin: structure	2.04	1	0	quinazolines
bupivacaine Bupivacaine: A widely used local anesthetic agent.. 1-butyl-N-(2,6-dimethylphenyl)piperidine-2-carboxamide : A piperidinecarboxamide obtained by formal condensation of the carboxy group of N-butylpipecolic acid with the amino group of 2,6-dimethylaniline.. bupivacaine : A racemate composed of equimolar amounts of dextrobupivacaine and levobupivacaine. Used (in the form of its hydrochloride hydrate) as a local anaesthetic.	2.45	2	0	aromatic amide; piperidinecarboxamide; tertiary amino compound
buspirone Buspirone: An anxiolytic agent and serotonin receptor agonist belonging to the azaspirodecanedione class of compounds. Its structure is unrelated to those of the BENZODIAZAPINES, but it has an efficacy comparable to DIAZEPAM.. buspirone : An azaspiro compound that is 8-azaspiro[4.5]decane-7,9-dione substituted at the nitrogen atom by a 4-(piperazin-1-yl)butyl group which in turn is substituted by a pyrimidin-2-yl group at the N(4) position.	3.59	2	0	azaspiro compound; N-alkylpiperazine; N-arylpiperazine; organic heteropolycyclic compound; piperidones; pyrimidines	anxiolytic drug; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; sedative; serotonergic agonist
busulfan [no description available]	8.62	13	4	methanesulfonate ester	alkylating agent; antineoplastic agent; carcinogenic agent; insect sterilant; teratogenic agent
secbutabarbital secbutabarbital: Butabarbital (a synonym for Secbutabarbital) should be distinguished from Butobarbital	3.23	1	0	barbiturates
butalbital butalbital: management of butalbital withdrawal can be simplified by using a phenobarbital-loading protocol; RN given refers to parent cpd. butalbital : A member of the class of barbiturates that is barbituric acid in which the hydrogens at position 5 are substituted by an allyl group and an isobutyl group. Frequently combined with other medicines, such as aspirin, paracetamol and codeine, it is used for treatment of pain and headache.	2.05	1	0	barbiturates	analgesic; sedative
caffeine [no description available]	4.08	4	0	purine alkaloid; trimethylxanthine	adenosine A2A receptor antagonist; adenosine receptor antagonist; adjuvant; central nervous system stimulant; diuretic; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor; EC 3.1.4.* (phosphoric diester hydrolase) inhibitor; environmental contaminant; food additive; fungal metabolite; geroprotector; human blood serum metabolite; mouse metabolite; mutagen; plant metabolite; psychotropic drug; ryanodine receptor agonist; xenobiotic
verapamil Verapamil: A calcium channel blocker that is a class IV anti-arrhythmia agent.. verapamil : A racemate comprising equimolar amounts of dexverapamil and (S)-verapamil. An L-type calcium channel blocker of the phenylalkylamine class, it is used (particularly as the hydrochloride salt) in the treatment of hypertension, angina pectoris and cardiac arrhythmia, and as a preventive medication for migraine.. 2-(3,4-dimethoxyphenyl)-5-{[2-(3,4-dimethoxyphenyl)ethyl](methyl)amino}-2-(propan-2-yl)pentanenitrile : A tertiary amino compound that is 3,4-dimethoxyphenylethylamine in which the hydrogens attached to the nitrogen are replaced by a methyl group and a 4-cyano-4-(3,4-dimethoxyphenyl)-5-methylhexyl group.	9.67	8	0	aromatic ether; nitrile; polyether; tertiary amino compound
metrizoate Metrizoic Acid: A diagnostic radiopaque that usually occurs as the sodium salt.	2.04	1	0	monocarboxylic acid	radioopaque medium
camostat camostat : A benzoate ester resulting from the formal condensation of the carboxy group of 4-guanidinobenzoic acid with the hydroxy group of 2-(dimethylamino)-2-oxoethyl (4-hydroxyphenyl)acetate. It is a potent inhibitor of the human transmembrane protease serine 2 (TMPRSS2) and its mesylate salt is currently under investigation for its effectiveness in COVID-19 patients.	2.6	1	0	benzoate ester; carboxylic ester; diester; guanidines; tertiary carboxamide	anti-inflammatory agent; anticoronaviral agent; antifibrinolytic drug; antihypertensive agent; antineoplastic agent; antiviral agent; serine protease inhibitor
camphor, (+-)-isomer [no description available]	2.6	1	0	bornane monoterpenoid; cyclic monoterpene ketone	plant metabolite
candesartan cilexetil candesartan cilexetil: a prodrug which is metabolized to an active form candesartan to exert its biological effects	2.05	1	0	biphenyls
candesartan candesartan: a nonpeptide angiotensin II receptor antagonist. candesartan : A benzimidazolecarboxylic acid that is 1H-benzimidazole-7-carboxylic acid substituted by an ethoxy group at position 2 and a ({2'-(1H-tetrazol-5-yl)[1,1'-biphenyl]-4-yl}methyl) group at position 1. It is a angiotensin receptor antagonist used for the treatment of hypertension.	3.73	2	0	benzimidazolecarboxylic acid; biphenylyltetrazole	angiotensin receptor antagonist; antihypertensive agent; environmental contaminant; xenobiotic
carbamazepine Carbamazepine: A dibenzazepine that acts as a sodium channel blocker. It is used as an anticonvulsant for the treatment of grand mal and psychomotor or focal SEIZURES. It may also be used in the management of BIPOLAR DISORDER, and has analgesic properties.. carbamazepine : A dibenzoazepine that is 5H-dibenzo[b,f]azepine carrying a carbamoyl substituent at the azepine nitrogen, used as an anticonvulsant.	4.61	4	0	dibenzoazepine; ureas	analgesic; anticonvulsant; antimanic drug; drug allergen; EC 3.5.1.98 (histone deacetylase) inhibitor; environmental contaminant; glutamate transporter activator; mitogen; non-narcotic analgesic; sodium channel blocker; xenobiotic
carbinoxamine carbinoxamine: Note: tradenames that start with Histex refer to more than one drug. carbinoxamine : An organochlorine compound that is 2-(4-chlorobenzyl)pyridine in which one of the benzylic hydrogens is substituted by 2-(dimethylamino)ethoxy group. It is an ethanolamine-type antihistamine, used as its maleate salt for treating hay fever, as well as mild cases of Parkinson's disease.	3.23	1	0	monochlorobenzenes; pyridines; tertiary amino compound	anti-allergic agent; antiparkinson drug; H1-receptor antagonist; muscarinic antagonist
carisoprodol Carisoprodol: A centrally acting skeletal muscle relaxant whose mechanism of action is not completely understood but may be related to its sedative actions. It is used as an adjunct in the symptomatic treatment of musculoskeletal conditions associated with painful muscle spasm. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1202). carisoprodol : A carbamate ester that is the mono-N-isopropyl derivative of meprobamate (which is a significant metabolite). Carisoprodol interrupts neuronal communication within the reticular formation and spinal cord, resulting in sedation and alteration in pain perception. It is used as a muscle relaxant in the symptomatic treatment of musculoskeletal conditions associated with painful muscle spasm.	3.59	2	0	carbamate ester	muscle relaxant
carmofur [no description available]	2.41	1	0	organohalogen compound; pyrimidines
carmustine Carmustine: A cell-cycle phase nonspecific alkylating antineoplastic agent. It is used in the treatment of brain tumors and various other malignant neoplasms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p462) This substance may reasonably be anticipated to be a carcinogen according to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (From Merck Index, 11th ed). carmustine : A member of the class of N-nitrosoureas that is 1,3-bis(2-chloroethyl)urea in which one of the nitrogens is substituted by a nitroso group.	6.09	10	3	N-nitrosoureas; organochlorine compound	alkylating agent; antineoplastic agent
carprofen carprofen: RN given refers to cpd without isomeric designation. carprofen : Propanoic acid in which one of the methylene hydrogens is substituted by a 6-chloro-9H-carbazol-2-yl group. A non-steroidal anti-inflammatory drug, it is no longer used in human medicine but is still used for treatment of arthritis in elderly dogs.	2.47	2	0	carbazoles; organochlorine compound	EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-steroidal anti-inflammatory drug; photosensitizing agent
carvedilol [no description available]	4.08	4	0	carbazoles; secondary alcohol; secondary amino compound	alpha-adrenergic antagonist; antihypertensive agent; beta-adrenergic antagonist; cardiovascular drug; vasodilator agent
celecoxib [no description available]	7.16	10	1	organofluorine compound; pyrazoles; sulfonamide; toluenes	cyclooxygenase 2 inhibitor; geroprotector; non-narcotic analgesic; non-steroidal anti-inflammatory drug
cetirizine Cetirizine: A potent second-generation histamine H1 antagonist that is effective in the treatment of allergic rhinitis, chronic urticaria, and pollen-induced asthma. Unlike many traditional antihistamines, it does not cause drowsiness or anticholinergic side effects.. cetirizine : A member of the class of piperazines that is piperazine in which the hydrogens attached to nitrogen are replaced by a (4-chlorophenyl)(phenyl)methyl and a 2-(carboxymethoxy)ethyl group respectively.	3.85	3	0	ether; monocarboxylic acid; monochlorobenzenes; piperazines	anti-allergic agent; environmental contaminant; H1-receptor antagonist; xenobiotic
cetylpyridinium Cetylpyridinium: Cationic bactericidal surfactant used as a topical antiseptic for skin, wounds, mucous membranes, instruments, etc.; and also as a component in mouthwash and lozenges.	2.6	1	0	pyridinium ion
cgp 37157 CGP 37157: benzothiazepine derivative of clonazepam; inhibits the in vitro activity of mitochondrial sodium-calcium exchange	2.07	1	0	benzothiazepine
chelerythrine chelerythrine : A benzophenanthridine alkaloid isolated from the root of Zanthoxylum simulans, Chelidonium majus L., and other Papaveraceae.	2.08	1	0	benzophenanthridine alkaloid; organic cation	antibacterial agent; antineoplastic agent; EC 2.7.11.13 (protein kinase C) inhibitor
chloral hydrate [no description available]	2.05	1	0	aldehyde hydrate; ethanediol; organochlorine compound	general anaesthetic; mouse metabolite; sedative; xenobiotic
chlorambucil Chlorambucil: A nitrogen mustard alkylating agent used as antineoplastic for chronic lymphocytic leukemia, Hodgkin's disease, and others. Although it is less toxic than most other nitrogen mustards, it has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (Merck Index, 11th ed). chlorambucil : A monocarboxylic acid that is butanoic acid substituted at position 4 by a 4-[bis(2-chloroethyl)amino]phenyl group. A chemotherapy drug that can be used in combination with the antibody obinutuzumab for the treatment of chronic lymphocytic leukemia.	10.82	6	1	aromatic amine; monocarboxylic acid; nitrogen mustard; organochlorine compound; tertiary amino compound	alkylating agent; antineoplastic agent; carcinogenic agent; drug allergen; immunosuppressive agent
chlorcyclizine chlorcyclizine: was heading 1964-94 (Prov 1964-73); CHLOROCYCLIZINE & HISTACHLORAZINE were see CHLORCYCLIZINE 1977-94; use PIPERAZINES to search CHLORCYCLIZINE 1966-94; histamine H1-blocker used both orally and topically in allergies and also for the prevention of motion sickness	3.23	1	0	diarylmethane
chlordiazepoxide Chlordiazepoxide: An anxiolytic benzodiazepine derivative with anticonvulsant, sedative, and amnesic properties. It has also been used in the symptomatic treatment of alcohol withdrawal.. chlordiazepoxide : A benzodiazepine that is 3H-1,4-benzodiazepine 4-oxide substituted by a chloro group at position 7, a phenyl group at position 5 and a methylamino group at position 2.	4.08	4	0	benzodiazepine
chlormezanone Chlormezanone: A non-benzodiazepine that is used in the management of anxiety. It has been suggested for use in the treatment of muscle spasm.. chlormezanone : A 1,3-thiazine that is 1,3-thiazinan-4-one S,S-dioxide in which a hydrogen at position 2 is substituted by a 4-chlorophenyl group and the hydrogen attached to the nitrogen is substituted by methyl. A non-benzodiazepine muscle relaxant, it was used in the management of anxiety and in the treatment of muscle spasms until being discontinued worldwide by its manufacturer in 1996, due to rare but serious cutaneous reactions.	3.59	2	0	1,3-thiazine; lactam; monochlorobenzenes; sulfone	antipsychotic agent; anxiolytic drug; muscle relaxant
chloroquine Chloroquine: The prototypical antimalarial agent with a mechanism that is not well understood. It has also been used to treat rheumatoid arthritis, systemic lupus erythematosus, and in the systemic therapy of amebic liver abscesses.. chloroquine : An aminoquinoline that is quinoline which is substituted at position 4 by a [5-(diethylamino)pentan-2-yl]amino group at at position 7 by chlorine. It is used for the treatment of malaria, hepatic amoebiasis, lupus erythematosus, light-sensitive skin eruptions, and rheumatoid arthritis.	7.82	16	1	aminoquinoline; organochlorine compound; secondary amino compound; tertiary amino compound	anticoronaviral agent; antimalarial; antirheumatic drug; autophagy inhibitor; dermatologic drug
chlorothiazide Chlorothiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p812). thiazide : Heterocyclic compound with sulfur and nitrogen in the ring.. chlorothiazide : 4H-1,2,4-benzothiadiazine 1,1-dioxide in which the hydrogen at position is substituted by chlorine and that at position 7 is substituted by a sulfonamide group. A diuretic, it is used for treatment of oedema and hypertension.	3.23	1	0	benzothiadiazine	antihypertensive agent; diuretic
chloroxylenol chloroxylenol: topical antiseptic; RN given refers to parent cpd; structure. 4-chloro-3,5-dimethylphenol : A member of the class of phenols that is 3,5-xylenol which is substituted at position 4 by chlorine. It is bactericidal against most Gram-positive bacteria but less effective against Staphylococci and Gram-negative bacteria, and often inactive against Pseudomonas species. It is ineffective against bacterial spores.	2.54	2	0	monochlorobenzenes; phenols	antiseptic drug; disinfectant; molluscicide
chlorpheniramine Chlorpheniramine: A histamine H1 antagonist used in allergic reactions, hay fever, rhinitis, urticaria, and asthma. It has also been used in veterinary applications. One of the most widely used of the classical antihistaminics, it generally causes less drowsiness and sedation than PROMETHAZINE.. chlorphenamine : A tertiary amino compound that is propylamine which is substituted at position 3 by a pyridin-2-yl group and a p-chlorophenyl group and in which the hydrogens attached to the nitrogen are replaced by methyl groups. A histamine H1 antagonist, it is used to relieve the symptoms of hay fever, rhinitis, urticaria, and asthma.	4.08	4	0	monochlorobenzenes; pyridines; tertiary amino compound	anti-allergic agent; antidepressant; antipruritic drug; H1-receptor antagonist; histamine antagonist; serotonin uptake inhibitor
chlorpromazine Chlorpromazine: The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking DOPAMINE RECEPTORS. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup.. chlorpromazine : A substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropanamine moiety.	4.29	5	0	organochlorine compound; phenothiazines; tertiary amine	anticoronaviral agent; antiemetic; dopaminergic antagonist; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; phenothiazine antipsychotic drug
chlorpropamide Chlorpropamide: A sulfonylurea hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. (From Martindale, The Extra Pharmacopoeia, 30th ed, p277). chlorpropamide : An N-sulfonylurea that is urea in which a hydrogen attached to one of the nitrogens is substituted by 4-chlorobenzenesulfonyl group and a hydrogen attached to the other nitrogen is substituted by propyl group. Chlorpropamide is a hypoglycaemic agent used in the treatment of type 2 (non-insulin-dependent) diabetes mellitus not responding to dietary modification.	4.08	4	0	monochlorobenzenes; N-sulfonylurea	hypoglycemic agent; insulin secretagogue
chlorthalidone Chlorthalidone: A benzenesulfonamide-phthalimidine that tautomerizes to a BENZOPHENONES form. It is considered a thiazide-like diuretic.	3.87	3	0	isoindoles; monochlorobenzenes; sulfonamide
chlorzoxazone Chlorzoxazone: A centrally acting central muscle relaxant with sedative properties. It is claimed to inhibit muscle spasm by exerting an effect primarily at the level of the spinal cord and subcortical areas of the brain. (From Martindale, The Extra Pharmacopoea, 30th ed, p1202). chlorzoxazone : A member of the class of 1,3-benzoxazoles that is 1,3-benzoxazol-2-ol in which the hydrogen atom at position 5 is substituted by chlorine. A centrally acting muscle relaxant with sedative properties, it is used for the symptomatic treatment of painful muscle spasm.	3.87	3	0	1,3-benzoxazoles; heteroaryl hydroxy compound; organochlorine compound	muscle relaxant; sedative
cifenline [no description available]	2.46	2	0	diarylmethane
ciclopirox [no description available]	7.55	2	0	cyclic hydroxamic acid; hydroxypyridone antifungal drug; pyridone	antibacterial agent; antiseborrheic
ciglitazone ciglitazone: structure given in second source; PPAR agonist used for type II diabetes. ciglitazone : An aromatic ether that consists of 1,3-thiazolidine-2,4-dione with position 5 substituted by a 4-[(1-methylcyclohexyl)methoxy]benzyl group. A selective PPARgamma agonist.	2.08	1	0	aromatic ether; thiazolidinone	antineoplastic agent; insulin-sensitizing drug
cilostazol [no description available]	3.61	2	0	lactam; tetrazoles	anticoagulant; bronchodilator agent; EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor; fibrin modulating drug; neuroprotective agent; platelet aggregation inhibitor; vasodilator agent
cimetidine Cimetidine: A histamine congener, it competitively inhibits HISTAMINE binding to HISTAMINE H2 RECEPTORS. Cimetidine has a range of pharmacological actions. It inhibits GASTRIC ACID secretion, as well as PEPSIN and GASTRIN output.. cimetidine : A member of the class of guanidines that consists of guanidine carrying a methyl substituent at position 1, a cyano group at position 2 and a 2-{[(5-methyl-1H-imidazol-4-yl)methyl]sulfanyl}ethyl group at position 3. It is a H2-receptor antagonist that inhibits the production of acid in stomach.	4.08	4	0	aliphatic sulfide; guanidines; imidazoles; nitrile	adjuvant; analgesic; anti-ulcer drug; H2-receptor antagonist; P450 inhibitor
cinoxacin Cinoxacin: Synthetic antimicrobial related to OXOLINIC ACID and NALIDIXIC ACID and used in URINARY TRACT INFECTIONS.. cinoxacin : A member of the class of cinnolines that is 6,7-methylenedioxycinnolin-4(1H)-one bearing an ethyl group at position 1 and a carboxylic acid group at position 3. An analogue of oxolinic acid, it has similar antibacterial actions. It was formerly used for the treatment of urinary tract infections.	2.05	1	0	cinnolines; oxacycle; oxo carboxylic acid	antibacterial drug; antiinfective agent
ciprofibrate [no description available]	2.81	3	0	cyclopropanes; monocarboxylic acid; organochlorine compound	antilipemic drug
ciprofloxacin Ciprofloxacin: A broad-spectrum antimicrobial carboxyfluoroquinoline.. ciprofloxacin : A quinolone that is quinolin-4(1H)-one bearing cyclopropyl, carboxylic acid, fluoro and piperazin-1-yl substituents at positions 1, 3, 6 and 7, respectively.	4.08	4	0	aminoquinoline; cyclopropanes; fluoroquinolone antibiotic; N-arylpiperazine; quinolinemonocarboxylic acid; quinolone antibiotic; quinolone; zwitterion	antibacterial drug; antiinfective agent; antimicrobial agent; DNA synthesis inhibitor; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; environmental contaminant; topoisomerase IV inhibitor; xenobiotic
cisapride Cisapride: A substituted benzamide used for its prokinetic properties. It is used in the management of gastroesophageal reflux disease, functional dyspepsia, and other disorders associated with impaired gastrointestinal motility. (Martindale The Extra Pharmacopoeia, 31st ed). cisapride : The amide resulting from formal condensation of 4-amino-5-chloro-2-methoxybenzoic acid with cis-1-[3-(4-fluorophenoxy)propyl]-3-methoxypiperidin-4-amine. It has been used (as its monohydrate or as its tartrate) for the treatment of gastro-oesophageal reflux disease and for non-ulcer dyspepsia, but its propensity to cause cardiac arrhythmias resulted in its complete withdrawal from many countries, including the U.K., and restrictions on its use elsewhere.	2.05	1	0	benzamides
citalopram Citalopram: A furancarbonitrile that is one of the serotonin uptake inhibitors used as an antidepressant. The drug is also effective in reducing ethanol uptake in alcoholics and is used in depressed patients who also suffer from TARDIVE DYSKINESIA in preference to tricyclic antidepressants, which aggravate dyskinesia.. citalopram : A racemate comprising equimolar amounts of (R)-citalopram and its enantiomer, escitalopram. It is used as an antidepressant, although only escitalopram is active.. 1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrile : A nitrile that is 1,3-dihydro-2-benzofuran-5-carbonitrile in which one of the hydrogens at position 1 is replaced by a p-fluorophenyl group, while the other is replaced by a 3-(dimethylamino)propyl group.	4.08	4	0	2-benzofurans; cyclic ether; nitrile; organofluorine compound; tertiary amino compound
clioquinol Clioquinol: A potentially neurotoxic 8-hydroxyquinoline derivative long used as a topical anti-infective, intestinal antiamebic, and vaginal trichomonacide. The oral preparation has been shown to cause subacute myelo-optic neuropathy and has been banned worldwide.. 5-chloro-7-iodoquinolin-8-ol : A monohydroxyquinoline that is quinolin-8-ol in which the hydrogens at positions 5 and 7 are replaced by chlorine and iodine, respectively. It has antibacterial and atifungal properties, and is used in creams for the treatment of skin infections. It has also been investigated as a chelator of copper and zinc ions for the possible treatment of Alzheimer's disease.	3.86	3	0	monohydroxyquinoline; organochlorine compound; organoiodine compound	antibacterial agent; antifungal agent; antimicrobial agent; antineoplastic agent; antiprotozoal drug; chelator; copper chelator
clobazam Clobazam: A benzodiazepine derivative that is a long-acting GABA-A RECEPTOR agonist. It is used as an antiepileptic in the treatment of SEIZURES, including seizures associated with LENNOX-GASTAUT SYNDROME. It is also used as an anxiolytic, for the short-term treatment of acute ANXIETY.. clobazam : 7-Chloro-1H-1,5-benzodiazepine-2,4(3H,5H)-dione in which the hydrogen attached to the nitrogen at position 1 is substituted by a methyl group, whilst that attached to the other nitrogen is substituted by a phenyl group. It is used for the short-term management of acute anxiety and as an adjunct in the treatment of epilepsy in association with other antiepileptics.	2.47	2	0	1,4-benzodiazepinone; organochlorine compound	anticonvulsant; anxiolytic drug; GABA modulator
clofazimine Clofazimine: A fat-soluble riminophenazine dye used for the treatment of leprosy. It has been used investigationally in combination with other antimycobacterial drugs to treat Mycobacterium avium infections in AIDS patients. Clofazimine also has a marked anti-inflammatory effect and is given to control the leprosy reaction, erythema nodosum leprosum. (From AMA Drug Evaluations Annual, 1993, p1619). clofazimine : 3-Isopropylimino-3,5-dihydro-phenazine in which the hydrogen at position 5 is substituted substituted by a 4-chlorophenyl group, and that at position 2 is substituted by a (4-chlorophenyl)amino group. A dark red crystalline solid, clofazimine is an antimycobacterial and is one of the main drugs used for the treatment of multi-bacillary leprosy. However, it can cause red/brown discolouration of the skin, so other treatments are often preferred in light-skinned patients.	2.47	2	0	monochlorobenzenes; phenazines	dye; leprostatic drug; non-steroidal anti-inflammatory drug
clofibrate angiokapsul: contains clofibrate & insoitolnicotinate	3.87	3	0	aromatic ether; ethyl ester; monochlorobenzenes	anticholesteremic drug; antilipemic drug; geroprotector; PPARalpha agonist
clomiphene [no description available]	3.87	3	0	tertiary amine	estrogen antagonist; estrogen receptor modulator
clomipramine Clomipramine: A tricyclic antidepressant similar to IMIPRAMINE that selectively inhibits the uptake of serotonin in the brain. It is readily absorbed from the gastrointestinal tract and demethylated in the liver to form its primary active metabolite, desmethylclomipramine.. clomipramine : A dibenzoazepine that is 10,11-dihydro-5H-dibenzo[b,f]azepine which is substituted by chlorine at position 3 and in which the hydrogen attached to the nitrogen is replaced by a 3-(dimethylamino)propyl group. One of the more sedating tricyclic antidepressants, it is used as the hydrochloride salt for the treatment of depression as well as obsessive-compulsive disorder and phobias.	4.13	4	0	dibenzoazepine	anticoronaviral agent; antidepressant; EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor; serotonergic antagonist; serotonergic drug; serotonin uptake inhibitor
clonazepam Clonazepam: An anticonvulsant used for several types of seizures, including myotonic or atonic seizures, photosensitive epilepsy, and absence seizures, although tolerance may develop. It is seldom effective in generalized tonic-clonic or partial seizures. The mechanism of action appears to involve the enhancement of GAMMA-AMINOBUTYRIC ACID receptor responses.. clonazepam : 1,3-Dihydro-2H-1,4-benzodiazepin-2-one in which the hydrogens at positions 5 and 7 are substituted by 2-chlorophenyl and nitro groups, respectively. It is used in the treatment of all types of epilepsy and seizures, as well as myoclonus and associated abnormal movements, and panic disorders. However, its use can be limited by the development of tolerance and by sedation.	9.08	4	0	1,4-benzodiazepinone; monochlorobenzenes	anticonvulsant; anxiolytic drug; GABA modulator
clonidine Clonidine: An imidazoline sympatholytic agent that stimulates ALPHA-2 ADRENERGIC RECEPTORS and central IMIDAZOLINE RECEPTORS. It is commonly used in the management of HYPERTENSION.. clonidine (amino form) : A clonidine that is 4,5-dihydro-1H-imidazol-2-amine in which one of the amino hydrogens is replaced by a 2,6-dichlorophenyl group.	4.08	4	0	clonidine; imidazoline
4-chloro-N-(2,6-dimethyl-1-piperidinyl)-3-sulfamoylbenzamide [no description available]	2.08	1	0	sulfonamide
chlorazepate clorazepic acid : A 1,4-benzodiazepinone in which the oxo group is at position 2, and which is substituted at positions 3, 5, and 7 by carboxy, phenyl and chloro groups, respectively.	3.58	2	0	1,4-benzodiazepinone	anticonvulsant; anxiolytic drug; GABA modulator; prodrug
clotiazepam clotiazepam: was heading 1975-94 (see under AZEPINES 1978-90; was Y 6047 see under AZEPINES 1975-77); Y 6047 was see CLOTIAZEPAM 1978-94; use AZEPINES to search CLOTIAZEPAM 1975-94; thienodiazepine derivative with actions similar to those of benzodiazepines	2.05	1	0	organic molecular entity
clotrimazole [no description available]	3.59	2	0	conazole antifungal drug; imidazole antifungal drug; imidazoles; monochlorobenzenes	antiinfective agent; environmental contaminant; xenobiotic
cyclandelate Cyclandelate: A direct-acting SMOOTH MUSCLE relaxant used to dilate BLOOD VESSELS.. cyclandelate : The ester obtained by formal condensation of mandelic acid and 3,3,5-tricyclohexanol. It is a direct-acting smooth muscle relaxant used to dilate blood vessels.	2.05	1	0	carboxylic ester; secondary alcohol	vasodilator agent
cyclobenzaprine cyclobenzaprine: RN given refers to parent cpd; Lisseril is synonymous for HCl; structure. cyclobenzaprine : 5-Methylidene-5H-dibenzo[a,d]cycloheptene in which one of the hydrogens of the methylidene group is substituted by a 2-(dimethylamino)ethyl group. A centrally acting skeletal muscle relaxant, it is used as its hydrochloride salt in the symptomatic treatment of painful muscle spasm.	3.23	1	0	carbotricyclic compound	antidepressant; muscle relaxant; tranquilizing drug
cyclofenil Cyclofenil: A gonadal stimulant and inducer of ovulation. It is used in the treatment of infertility and amenorrhea, but is thought to be less effective than CLOMIPHENE.	3.23	1	0	organic molecular entity
cyproheptadine Cyproheptadine: A serotonin antagonist and a histamine H1 blocker used as antipruritic, appetite stimulant, antiallergic, and for the post-gastrectomy dumping syndrome, etc.. cyproheptadine : The product resulting from the formal oxidative coupling of position 5 of 5H-dibenzo[a,d]cycloheptene with position 4 of 1-methylpiperidine resulting in the formation of a double bond between the two fragments. It is a sedating antihistamine with antimuscarinic and calcium-channel blocking actions. It is used (particularly as the hydrochloride sesquihydrate) for the relief of allergic conditions including rhinitis, conjunctivitis due to inhalant allergens and foods, urticaria and angioedema, and in pruritic skin disorders. Unlike other antihistamines, it is also a seratonin receptor antagonist, making it useful in conditions such as vascular headache and anorexia.	8.86	3	0	piperidines; tertiary amine	anti-allergic agent; antipruritic drug; gastrointestinal drug; H1-receptor antagonist; serotonergic antagonist
cystamine [no description available]	2.31	1	0	organic disulfide; primary amino compound	EC 2.3.2.13 (protein-glutamine gamma-glutamyltransferase) inhibitor
danthron danthron: structure. chrysazin : A dihydroxyanthraquinone that is anthracene-9,10-dione substituted by hydroxy groups at positions 1 and 8.	2.54	2	0	dihydroxyanthraquinone	apoptosis inducer; plant metabolite
dapsone [no description available]	4.29	5	0	substituted aniline; sulfone	anti-inflammatory drug; antiinfective agent; antimalarial; leprostatic drug
deferiprone Deferiprone: A pyridone derivative and iron chelator that is used in the treatment of IRON OVERLOAD in patients with THALASSEMIA.. deferiprone : A member of the class of 4-pyridones that is pyridin-4(1H)-one substituted at positions 1 and 2 by methyl groups and at position 3 by a hydroxy group. A lipid-soluble iron-chelator used for treatment of thalassaemia.	2.6	1	0	4-pyridones	iron chelator; protective agent
deferoxamine Deferoxamine: Natural product isolated from Streptomyces pilosus. It forms iron complexes and is used as a chelating agent, particularly in the mesylate form.. desferrioxamine B : An acyclic desferrioxamine that is butanedioic acid in which one of the carboxy groups undergoes formal condensation with the primary amino group of N-(5-aminopentyl)-N-hydroxyacetamide and the second carboxy group undergoes formal condensation with the hydroxyamino group of N(1)-(5-aminopentyl)-N(1)-hydroxy-N(4)-[5-(hydroxyamino)pentyl]butanediamide. It is a siderophore native to Streptomyces pilosus biosynthesised by the DesABCD enzyme cluster as a high affinity Fe(III) chelator.	3.59	2	0	acyclic desferrioxamine	bacterial metabolite; ferroptosis inhibitor; iron chelator; siderophore
desipramine Desipramine: A tricyclic dibenzazepine compound that potentiates neurotransmission. Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. This compound also possesses minor anticholinergic activity, through its affinity to muscarinic receptors.. desipramine : A dibenzoazepine consisting of 10,11-dihydro-5H-dibenzo[b,f]azepine substituted on nitrogen with a 3-(methylamino)propyl group.	3.87	3	0	dibenzoazepine; secondary amino compound	adrenergic uptake inhibitor; alpha-adrenergic antagonist; antidepressant; cholinergic antagonist; drug allergen; EC 3.1.4.12 (sphingomyelin phosphodiesterase) inhibitor; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; H1-receptor antagonist; serotonin uptake inhibitor
nordazepam Nordazepam: An intermediate in the metabolism of DIAZEPAM to OXAZEPAM. It may have actions similar to those of diazepam.. nordazepam : A 1,4-benzodiazepinone having phenyl and chloro substituents at positions 5 and 7 respectively; it has anticonvulsant, anxiolytic, muscle relaxant and sedative properties but is used primarily in the treatment of anxiety.	2.04	1	0	1,4-benzodiazepinone; organochlorine compound	anticonvulsant; anxiolytic drug; GABA modulator; human metabolite; sedative
amphetamine Amphetamine: A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is DEXTROAMPHETAMINE.. 1-phenylpropan-2-amine : A primary amine that is isopropylamine in which a hydrogen attached to one of the methyl groups has been replaced by a phenyl group.. amphetamine : A racemate comprising equimolar amounts of (R)-amphetamine (also known as levamphetamine or levoamphetamine) and (S)-amphetamine (also known as dexamfetamine or dextroamphetamine.	3.86	3	0	primary amine
eflornithine Eflornithine: An inhibitor of ORNITHINE DECARBOXYLASE, the rate limiting enzyme of the polyamine biosynthetic pathway.. eflornithine : A fluoroamino acid that is ornithine substituted by a difluoromethyl group at position 2.	2.05	1	0	alpha-amino acid; fluoroamino acid	trypanocidal drug
diazepam Diazepam: A benzodiazepine with anticonvulsant, anxiolytic, sedative, muscle relaxant, and amnesic properties and a long duration of action. Its actions are mediated by enhancement of GAMMA-AMINOBUTYRIC ACID activity.. diazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a chloro group at position 7, a methyl group at position 1 and a phenyl group at position 5.	4.28	5	0	1,4-benzodiazepinone; organochlorine compound	anticonvulsant; anxiolytic drug; environmental contaminant; sedative; xenobiotic
diazoxide Diazoxide: A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group.. diazoxide : A benzothiadiazine that is the S,S-dioxide of 2H-1,2,4-benzothiadiazine which is substituted at position 3 by a methyl group and at position 7 by chlorine. A peripheral vasodilator, it increases the concentration of glucose in the plasma and inhibits the secretion of insulin by the beta- cells of the pancreas. It is used orally in the management of intractable hypoglycaemia and intravenously in the management of hypertensive emergencies.	4.08	4	0	benzothiadiazine; organochlorine compound; sulfone	antihypertensive agent; beta-adrenergic agonist; bronchodilator agent; cardiotonic drug; diuretic; K-ATP channel agonist; sodium channel blocker; sympathomimetic agent; vasodilator agent
diclofenac Diclofenac: A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt.. diclofenac : A monocarboxylic acid consisting of phenylacetic acid having a (2,6-dichlorophenyl)amino group at the 2-position.	3.86	3	0	amino acid; aromatic amine; dichlorobenzene; monocarboxylic acid; secondary amino compound	antipyretic; drug allergen; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; environmental contaminant; non-narcotic analgesic; non-steroidal anti-inflammatory drug; xenobiotic
ddt 1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane: structure in first source	2.05	1	0	benzenoid aromatic compound; chlorophenylethane; monochlorobenzenes; organochlorine insecticide	bridged diphenyl acaricide; carcinogenic agent; endocrine disruptor; persistent organic pollutant
dichlorphenamide Dichlorphenamide: A carbonic anhydrase inhibitor that is used in the treatment of glaucoma.. diclofenamide : A sulfonamide that is benzene-1,3-disulfonamide in which the hydrogens at positions 4 and 5 are substituted by chlorine. An oral carbonic anhydrase inhibitor, it partially suppresses the secretion (inflow) of aqueous humor in the eye and so reduces intraocular pressure. It is used for the treatment of glaucoma.	3.23	1	0	dichlorobenzene; sulfonamide	antiglaucoma drug; EC 4.2.1.1 (carbonic anhydrase) inhibitor; ophthalmology drug
dicyclomine Dicyclomine: A muscarinic antagonist used as an antispasmodic and in urinary incontinence. It has little effect on glandular secretion or the cardiovascular system. It does have some local anesthetic properties and is used in gastrointestinal, biliary, and urinary tract spasms.. dicyclomine : The ester resulting from the formal condensation of 1-cyclohexylcyclohexanecarboxylic acid with 2-(diethylamino)ethanol. An anticholinergic, it is used as the hydrochloride to treat or prevent spasm in the muscles of the gastrointestinal tract, particularly that associated with irritable bowel syndrome.	3.23	1	0	carboxylic ester; tertiary amine	antispasmodic drug; muscarinic antagonist; parasympatholytic
pentetic acid Pentetic Acid: An iron chelating agent with properties like EDETIC ACID. DTPA has also been used as a chelator for other metals, such as plutonium.	3.62	2	0	pentacarboxylic acid	copper chelator
diflunisal Diflunisal: A salicylate derivative and anti-inflammatory analgesic with actions and side effects similar to those of ASPIRIN.. diflunisal : An organofluorine compound comprising salicylic acid having a 2,4-difluorophenyl group at the 5-position.	3.86	3	0	monohydroxybenzoic acid; organofluorine compound	non-narcotic analgesic; non-steroidal anti-inflammatory drug
dimercaprol Dimercaprol: An anti-gas warfare agent that is effective against Lewisite (dichloro(2-chlorovinyl)arsine) and formerly known as British Anti-Lewisite or BAL. It acts as a chelating agent and is used in the treatment of arsenic, gold, and other heavy metal poisoning.. dimercaprol : A dithiol that is propane-1,2-dithiol in which one of the methyl hydrogens is replaced by a hydroxy group. a chelating agent originally developed during World War II as an experimental antidote against the arsenic-based poison gas Lewisite, it has been used clinically since 1949 for the treatment of poisoning by arsenic, mercury and gold. It can also be used for treatment of poisoning by antimony, bismuth and possibly thallium, and (with sodium calcium edetate) in cases of acute leaad poisoning. Administration is by (painful) intramuscular injection of a suspension of dimercaprol in peanut oil, typically every 4 hours for 2-10 days depending on the toxicity. In the past, dimercaprol was also used for the treatment of Wilson's disease, a severely debilitating genetic disorder in which the body tends to retain copper, with resultant liver and brain injury.	3.23	1	0	dithiol; primary alcohol	chelator
diphenhydramine Diphenhydramine: A histamine H1 antagonist used as an antiemetic, antitussive, for dermatoses and pruritus, for hypersensitivity reactions, as a hypnotic, an antiparkinson, and as an ingredient in common cold preparations. It has some undesired antimuscarinic and sedative effects.. diphenhydramine : An ether that is the benzhydryl ether of 2-(dimethylamino)ethanol. It is a H1-receptor antagonist used as a antipruritic and antitussive drug.. antitussive : An agent that suppresses cough. Antitussives have a central or a peripheral action on the cough reflex, or a combination of both. Compare with expectorants, which are considered to increase the volume of secretions in the respiratory tract, so facilitating their removal by ciliary action and coughing, and mucolytics, which decrease the viscosity of mucus, facilitating its removal by ciliary action and expectoration.	4.1	4	0	ether; tertiary amino compound	anti-allergic agent; antidyskinesia agent; antiemetic; antiparkinson drug; antipruritic drug; antitussive; H1-receptor antagonist; local anaesthetic; muscarinic antagonist; oneirogen; sedative
dipyridamole Dipyridamole: A phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells. Dipyridamole also potentiates the antiaggregating action of prostacyclin. (From AMA Drug Evaluations Annual, 1994, p752). dipyridamole : A pyrimidopyrimidine that is 2,2',2'',2'''-(pyrimido[5,4-d]pyrimidine-2,6-diyldinitrilo)tetraethanol substituted by piperidin-1-yl groups at positions 4 and 8 respectively. A vasodilator agent, it inhibits the formation of blood clots.	9.31	5	0	piperidines; pyrimidopyrimidine; tertiary amino compound; tetrol	adenosine phosphodiesterase inhibitor; EC 3.5.4.4 (adenosine deaminase) inhibitor; platelet aggregation inhibitor; vasodilator agent
disopyramide Disopyramide: A class I anti-arrhythmic agent (one that interferes directly with the depolarization of the cardiac membrane and thus serves as a membrane-stabilizing agent) with a depressant action on the heart similar to that of guanidine. It also possesses some anticholinergic and local anesthetic properties.. disopyramide : A monocarboxylic acid amide that is butanamide substituted by a diisopropylamino group at position 4, a phenyl group at position 2 and a pyridin-2-yl group at position 2. It is used as a anti-arrhythmia drug.	4.08	4	0	monocarboxylic acid amide; pyridines; tertiary amino compound	anti-arrhythmia drug
disulfiram [no description available]	5.68	13	0	organic disulfide; organosulfur acaricide	angiogenesis inhibitor; antineoplastic agent; apoptosis inducer; EC 1.2.1.3 [aldehyde dehydrogenase (NAD(+))] inhibitor; EC 3.1.1.1 (carboxylesterase) inhibitor; EC 3.1.1.8 (cholinesterase) inhibitor; EC 5.99.1.2 (DNA topoisomerase) inhibitor; ferroptosis inducer; fungicide; NF-kappaB inhibitor
valproic acid Valproic Acid: A fatty acid with anticonvulsant and anti-manic properties that is used in the treatment of EPILEPSY and BIPOLAR DISORDER. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of VOLTAGE-GATED SODIUM CHANNELS.. valproic acid : A branched-chain saturated fatty acid that comprises of a propyl substituent on a pentanoic acid stem.	7.62	13	0	branched-chain fatty acid; branched-chain saturated fatty acid	anticonvulsant; antimanic drug; EC 3.5.1.98 (histone deacetylase) inhibitor; GABA agent; neuroprotective agent; psychotropic drug; teratogenic agent
domperidone Domperidone: A specific blocker of dopamine receptors. It speeds gastrointestinal peristalsis, causes prolactin release, and is used as antiemetic and tool in the study of dopaminergic mechanisms.. domperidone : 1-[3-(Piperidin-1-yl)propyl]-1,3-dihydro-2H-benzimidazol-2-one in which the 4-position of the piperidine ring is substituted by a 5-chloro-1,3-dihydro-2H-benzimidazol-2-on-1-yl group. A dopamine antagonist, it is used as an antiemetic for the short-term treatment of nausea and vomiting, and to control gastrointestinal effects of dopaminergic drugs given in the management of parkinsonism. The free base is used in oral suspensions, while the maleate salt is used in tablet preparations.	2.46	2	0	benzimidazoles; heteroarylpiperidine	antiemetic; dopaminergic antagonist
donepezil Donepezil: An indan and piperidine derivative that acts as a selective and reversible inhibitor of ACETYLCHOLINESTERASE. Donepezil is highly selective for the central nervous system and is used in the management of mild to moderate DEMENTIA in ALZHEIMER DISEASE.. donepezil : A racemate comprising equimolar amounts of (R)- and (S)-donepezil. A centrally acting reversible acetylcholinesterase inhibitor, its main therapeutic use is in the treatment of Alzheimer's disease where it is used to increase cortical acetylcholine.. 2-[(1-benzylpiperidin-4-yl)methyl]-5,6-dimethoxyindan-1-one : A member of the class of indanones that is 5,6-dimethoxyindan-1-one which is substituted at position 2 by an (N-benzylpiperidin-4-yl)methyl group.	3.61	2	0	aromatic ether; indanones; piperidines; racemate	EC 3.1.1.7 (acetylcholinesterase) inhibitor; EC 3.1.1.8 (cholinesterase) inhibitor; nootropic agent
doxapram Doxapram: A central respiratory stimulant with a brief duration of action. (From Martindale, The Extra Pharmocopoeia, 30th ed, p1225). doxapram : A member of the class of pyrrolidin-2-ones that is N-ethylpyrrolidin-2-one in which both of the hydrogens at the 3 position (adjacent to the carbonyl group) are substituted by phenyl groups, and one of the hydrogens at the 4 position is substituted by a 2-(morpholin-4-yl)ethyl group. A central and respiratory stimulant with a brief duration of action, it is used (generally as the hydrochloride or the hydrochloride hydrate) as a temporary treatment of acute respiratory failure, particularly when superimposed on chronic obstructive pulmonary disease, and of postoperative respiratory depression. It has also been used for treatment of postoperative shivering.	3.58	2	0	morpholines; pyrrolidin-2-ones	central nervous system stimulant
doxazosin Doxazosin: A prazosin-related compound that is a selective alpha-1-adrenergic blocker.. doxazosin : A member of the class of quinazolines that is quinazoline substituted by an amino group at position 4, methoxy groups at positions 6 and 7 and a piperazin-1-yl group at position 2 which in turn is substituted by a 2,3-dihydro-1,4-benzodioxin-2-ylcarbonyl group at position 4. An antihypertensive agent, it is used in the treatment of high blood pressure.	3.91	3	0	aromatic amine; benzodioxine; monocarboxylic acid amide; N-acylpiperazine; N-arylpiperazine; quinazolines	alpha-adrenergic antagonist; antihyperplasia drug; antihypertensive agent; antineoplastic agent; vasodilator agent
doxepin Doxepin: A dibenzoxepin tricyclic compound. It displays a range of pharmacological actions including maintaining adrenergic innervation. Its mechanism of action is not fully understood, but it appears to block reuptake of monoaminergic neurotransmitters into presynaptic terminals. It also possesses anticholinergic activity and modulates antagonism of histamine H(1)- and H(2)-receptors.. doxepin : A dibenzooxepine that is 6,11-dihydrodibenzo[b,e]oxepine substituted by a 3-(dimethylamino)propylidene group at position 11. It is used as an antidepressant drug.	4.08	4	0	dibenzooxepine; tertiary amino compound	antidepressant
doxylamine Doxylamine: Histamine H1 antagonist with pronounced sedative properties. It is used in allergies and as an antitussive, antiemetic, and hypnotic. Doxylamine has also been administered in veterinary applications and was formerly used in PARKINSONISM.	3.23	1	0	pyridines; tertiary amine	anti-allergic agent; antiemetic; antitussive; cholinergic antagonist; H1-receptor antagonist; histamine antagonist; sedative
droperidol Droperidol: A butyrophenone with general properties similar to those of HALOPERIDOL. It is used in conjunction with an opioid analgesic such as FENTANYL to maintain the patient in a calm state of neuroleptanalgesia with indifference to surroundings but still able to cooperate with the surgeon. It is also used as a premedicant, as an antiemetic, and for the control of agitation in acute psychoses. (From Martindale, The Extra Pharmacopoeia, 29th ed, p593). droperidol : An organofluorine compound that is haloperidol in which the hydroxy group has been eliminated with the introduction of a double bond in the piperidine ring, and the 4-chlorophenyl group has been replaced by a benzimidazol-2-on-1-yl group. It is used in the management of chemotherapy-induced nausea and vomiting, and in conjunction with an opioid analgesic such as fentanyl to maintain the patient in a calm state of neuroleptanalgesia with indifference to surroundings but still able to cooperate with the surgeon.	3.59	2	0	aromatic ketone; benzimidazoles; organofluorine compound	anaesthesia adjuvant; antiemetic; dopaminergic antagonist; first generation antipsychotic
dyclonine [no description available]	7.1	1	0	aromatic ketone; piperidines	topical anaesthetic
dyphylline Dyphylline: A THEOPHYLLINE derivative with broncho- and vasodilator properties. It is used in the treatment of asthma, cardiac dyspnea, and bronchitis.. dyphylline : An oxopurine that is theophylline bearing a 2,3-dihydroxypropyl group at the 7 position. It has broncho- and vasodilator properties, and is used in the treatment of asthma, cardiac dyspnea, and bronchitis. It is also an ingredient in preparations that have been promoted for coughs.	3.58	2	0	oxopurine; propane-1,2-diols	bronchodilator agent; EC 3.1.4.* (phosphoric diester hydrolase) inhibitor; muscle relaxant; vasodilator agent
ebastine [no description available]	2.08	1	0	organic molecular entity
ebselen ebselen : A benzoselenazole that is 1,2-benzoselenazol-3-one carrying an additional phenyl substituent at position 2. Acts as a mimic of glutathione peroxidase.	2.9	2	0	benzoselenazole	anti-inflammatory drug; antibacterial agent; anticoronaviral agent; antifungal agent; antineoplastic agent; antioxidant; apoptosis inducer; EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor; EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor; EC 1.3.1.8 [acyl-CoA dehydrogenase (NADP(+))] inhibitor; EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor; EC 2.5.1.7 (UDP-N-acetylglucosamine 1-carboxyvinyltransferase) inhibitor; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; EC 3.1.3.25 (inositol-phosphate phosphatase) inhibitor; EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor; EC 3.5.4.1 (cytosine deaminase) inhibitor; EC 5.1.3.2 (UDP-glucose 4-epimerase) inhibitor; enzyme mimic; ferroptosis inhibitor; genotoxin; hepatoprotective agent; neuroprotective agent; radical scavenger
econazole Econazole: An imidazole derivative that is commonly used as a topical antifungal agent.. econazole : A racemate composed of equimolar amounts of (R)- and (S)-econazole. Used (as its nitrate salt) to treat skin infections such as athlete's foot, jock itch, ringworm and other fungal skin infections.. 1-{2-(4-chlorobenzyloxy)-2-(2,4-dichlorophenyl)ethyl}imidazole : A member of the class of imidazoles that is 1-(2,4-dichlorophenyl)-2-(imidazol-1-yl)ethanol in which the hydroxyl hydrogen is replaced by a 4-chlorobenzyl group.	2.05	1	0	dichlorobenzene; ether; imidazoles; monochlorobenzenes
edrophonium Edrophonium: A rapid-onset, short-acting cholinesterase inhibitor used in cardiac arrhythmias and in the diagnosis of myasthenia gravis. It has also been used as an antidote to curare principles.. edrophonium : A quaternary ammonium ion that is N-ethyl-N,N-dimethylanilinium in which one of the meta positions is substituted by a hydroxy group. It is a reversible inhibitor of cholinesterase, with a rapid onset (30-60 seconds after injection) but a short duration of action (5-15 minutes). The chloride salt is used in myasthenia gravis both diagnostically and to distinguish between under- or over-treatment with other anticholinesterases. It has also been used for the reversal of neuromuscular blockade in anaesthesia, and for the management of poisoning due to tetrodotoxin, a neuromuscular blocking toxin found in puffer fish and other marine animals.	3.23	1	0	phenols; quaternary ammonium ion	antidote; diagnostic agent; EC 3.1.1.8 (cholinesterase) inhibitor
enflurane Enflurane: An extremely stable inhalation anesthetic that allows rapid adjustments of anesthesia depth with little change in pulse or respiratory rate.. enflurane : An ether in which the oxygen atom is connected to 2-chloro-1,1,2-trifluoroethyl and difluoromethyl groups.	2.05	1	0	ether; organochlorine compound; organofluorine compound	anaesthetic
enoxacin Enoxacin: A broad-spectrum 6-fluoronaphthyridinone antibacterial agent that is structurally related to NALIDIXIC ACID.. enoxacin : A 1,8-naphthyridine derivative that is 1,4-dihydro-1,8-naphthyridine with an ethyl group at the 1 position, a carboxy group at the 3-position, an oxo sustituent at the 4-position, a fluoro substituent at the 5-position and a piperazin-1-yl group at the 7 position. An antibacterial, it is used in the treatment of urinary-tract infections and gonorrhoea.	2.75	3	0	1,8-naphthyridine derivative; amino acid; fluoroquinolone antibiotic; monocarboxylic acid; N-arylpiperazine; quinolone antibiotic	antibacterial drug; DNA synthesis inhibitor
erythrosine Fluoresceins: A family of spiro(isobenzofuran-1(3H),9'-(9H)xanthen)-3-one derivatives. These are used as dyes, as indicators for various metals, and as fluorescent labels in immunoassays.	2.57	2	0
estazolam Estazolam: A benzodiazepine with anticonvulsant, hypnotic, and muscle relaxant properties. It has been shown in some cases to be more potent than DIAZEPAM or NITRAZEPAM.. estazolam : A triazolo[4,3-a][1,4]benzodiazepine having a phenyl group at position 6 and a chloro substituent at position 8. A short-acting benzodiazepine with general properties similar to diazepam, it is given by mouth as a hypnotic in the short-term management of insomnia.	3.59	2	0	triazoles; triazolobenzodiazepine	anticonvulsant; anxiolytic drug; GABA modulator
ethacrynic acid Ethacrynic Acid: A compound that inhibits symport of sodium, potassium, and chloride primarily in the ascending limb of Henle, but also in the proximal and distal tubules. This pharmacological action results in excretion of these ions, increased urinary output, and reduction in extracellular fluid. This compound has been classified as a loop or high ceiling diuretic.. etacrynic acid : An aromatic ether that is phenoxyacetic acid in which the phenyl ring is substituted by chlorines at positions 2 and 3, and by a 2-methylidenebutanoyl group at position 4. It is a loop diuretic used to treat high blood pressure resulting from diseases such as congestive heart failure, liver failure, and kidney failure. It is also a glutathione S-transferase (EC 2.5.1.18) inhibitor.	4.08	4	0	aromatic ether; aromatic ketone; dichlorobenzene; monocarboxylic acid	EC 2.5.1.18 (glutathione transferase) inhibitor; ion transport inhibitor; loop diuretic
ethosuximide Ethosuximide: An anticonvulsant especially useful in the treatment of absence seizures unaccompanied by other types of seizures.. ethosuximide : A dicarboximide that is pyrrolidine-2,5-dione in which the hydrogens at position 3 are substituted by one methyl and one ethyl group. An antiepileptic, it is used in the treatment of absence seizures and may be used for myoclonic seizures, but is ineffective against tonic-clonic seizures.	3.61	2	0	dicarboximide; pyrrolidinone	anticonvulsant; geroprotector; T-type calcium channel blocker
ethotoin ethotoin: was heading 1966-94 (see under HYDANTOINS 1966-90); use HYDANTOINS to search ETHOTOIN 1966-94. ethotoin : An imidazolidine-2,4-dione that is hydantoin substituted by ethyl and phenyl at positions 3 and 5, respectively. An antiepileptic, it is less toxic than phenytoin but also less effective.	3.23	1	0	imidazolidine-2,4-dione	anticonvulsant
ethoxzolamide Ethoxzolamide: A carbonic anhydrase inhibitor used as diuretic and in glaucoma. It may cause hypokalemia.. ethoxzolamide : A sulfonamide that is 1,3-benzothiazole-2-sulfonamide which is substituted by an ethoxy group at position 6. A carbonic anhydrase inhibitor, it has been used in the treatment of glaucoma, and as a diuretic.	2.05	1	0	aromatic ether; benzothiazoles; sulfonamide	antiglaucoma drug; diuretic; EC 4.2.1.1 (carbonic anhydrase) inhibitor
etidronate Etidronic Acid: A diphosphonate which affects calcium metabolism. It inhibits ectopic calcification and slows down bone resorption and bone turnover.. etidronic acid : A 1,1-bis(phosphonic acid) that is (ethane-1,1-diyl)bis(phosphonic acid) having a hydroxy substituent at the 1-position. It inhibits the formation, growth, and dissolution of hydroxyapatite crystals by chemisorption to calcium phosphate surfaces.	3.93	3	0	1,1-bis(phosphonic acid)	antineoplastic agent; bone density conservation agent; chelator
etilefrine Etilefrine: A phenylephrine-related beta-1 adrenergic and alpha adrenergic agonist used as a cardiotonic and antihypotensive agent.	2.04	1	0	phenols
etodolac Etodolac: A non-steroidal anti-inflammatory agent and cyclooxygenase-2 (COX-2) inhibitor with potent analgesic and anti-arthritic properties. It has been shown to be effective in the treatment of OSTEOARTHRITIS; RHEUMATOID ARTHRITIS; ANKYLOSING SPONDYLITIS; and in the alleviation of postoperative pain (PAIN, POSTOPERATIVE).. etodolac : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is substituted by a 1,8-diethyl-1,3,4,9-tetrahydropyrano[3,4-b]indol-1-yl moiety. A preferential inhibitor of cyclo-oxygenase 2 and non-steroidal anti-inflammatory, it is used for the treatment of rheumatoid arthritis and osteoarthritis, and for the alleviation of postoperative pain. Administered as the racemate, only the (S)-enantiomer is active.	3.59	2	0	monocarboxylic acid; organic heterotricyclic compound	antipyretic; cyclooxygenase 2 inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug
2-hexyloxybenzamide 2-hexyloxybenzamide: structure	2.6	1	0	aromatic ether; benzamides	antifungal agent
brl 42810 [no description available]	4.13	4	0	2-aminopurines; acetate ester	antiviral drug; prodrug
felbamate Felbamate: A PEGylated phenylcarbamate derivative that acts as an antagonist of NMDA RECEPTORS. It is used as an anticonvulsant, primarily for the treatment of SEIZURES in severe refractory EPILEPSY.. felbamate : The bis(carbamate ester) of 2-phenylpropane-1,3-diol. An anticonvulsant, it is used in the treatment of epilepsy.	3.59	2	0	carbamate ester	anticonvulsant; neuroprotective agent
4-biphenylylacetic acid biphenyl-4-ylacetic acid : A monocarboxylic acid in which one of the alpha-hydrogens is substituted by a biphenyl-4-yl group. An active metabolite of fenbufen, it is used as a topical medicine to treat muscle inflammation and arthritis.	2.08	1	0	biphenyls; monocarboxylic acid	non-steroidal anti-inflammatory drug
felodipine Felodipine: A dihydropyridine calcium antagonist with positive inotropic effects. It lowers blood pressure by reducing peripheral vascular resistance through a highly selective action on smooth muscle in arteriolar resistance vessels.. felodipine : The mixed (methyl, ethyl) diester of 4-(2,3-dichlorophenyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylic acid. A calcium-channel blocker, it lowers blood pressure by reducing peripheral vascular resistance through a highly selective action on smooth muscle in arteriolar resistance vessels. It is used in the management of hypertension and angina pectoris.	4.08	4	0	dichlorobenzene; dihydropyridine; ethyl ester; methyl ester	anti-arrhythmia drug; antihypertensive agent; calcium channel blocker; vasodilator agent
fenofibrate Pharmavit: a polyvitamin product, comprising vitamins A, D2, B1, B2, B6, C, E, nicotinamide, & calcium pantothene; may be a promising agent for application to human populations exposed to carcinogenic and genetic hazards of ionizing radiation; RN from CHEMLINE	3.87	3	0	aromatic ether; chlorobenzophenone; isopropyl ester; monochlorobenzenes	antilipemic drug; environmental contaminant; geroprotector; xenobiotic
fenoldopam Fenoldopam: A dopamine D1 receptor agonist that is used as an antihypertensive agent. It lowers blood pressure through arteriolar vasodilation.	3.23	1	0	benzazepine	alpha-adrenergic agonist; antihypertensive agent; dopamine agonist; dopaminergic antagonist; vasodilator agent
fenoprofen Fenoprofen: A propionic acid derivative that is used as a non-steroidal anti-inflammatory agent.. fenoprofen : A monocarboxylic acid that is propanoic acid in which one of the hydrogens at position 2 is substituted by a 3-phenoxyphenyl group. A non-steroidal anti-inflammatory drug, the dihydrate form of the calcium salt is used for the management of mild to moderate pain and for the relief of pain and inflammation associated with disorders such as arthritis. It is pharmacologically similar to aspirin, but causes less gastrointestinal bleeding.	3.23	1	0	monocarboxylic acid	antipyretic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; drug allergen; non-narcotic analgesic; non-steroidal anti-inflammatory drug
berotek Fenoterol: A synthetic adrenergic beta-2 agonist that is used as a bronchodilator and tocolytic.. fenoterol : A member of the class resorcinols that is 5-(1-hydroxyethyl)benzene-1,3-diol in which one of the methyl hydrogens is replaced by a 1-(4-hydroxyphenyl)propan-2-amino group. A beta2-adrenergic agonist, it is used (as the hydrobromide salt) as a bronchodilator in the management of reversible airway obstruction.	2.04	1	0	resorcinols; secondary alcohol; secondary amino compound	beta-adrenergic agonist; bronchodilator agent; sympathomimetic agent; tocolytic agent
fenspiride fenspiride: was heading 1975-94 (see under SPIRO COMPOUNDS 1975-90); use SPIRO COMPOUNDS to search FENSPIRIDE 1975-94; bronchodilator agent used in asthma	2.04	1	0	azaspiro compound
fentanyl Fentanyl: A potent narcotic analgesic, abuse of which leads to habituation or addiction. It is primarily a mu-opioid agonist. Fentanyl is also used as an adjunct to general anesthetics, and as an anesthetic for induction and maintenance. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1078). fentanyl : A monocarboxylic acid amide resulting from the formal condensation of the aryl amino group of N-phenyl-1-(2-phenylethyl)piperidin-4-amine with propanoic acid.	2.45	2	0	anilide; monocarboxylic acid amide; piperidines	adjuvant; anaesthesia adjuvant; anaesthetic; intravenous anaesthetic; mu-opioid receptor agonist; opioid analgesic
fexofenadine fexofenadine: a second generation antihistamine; metabolite of the antihistaminic drug terfenadine; structure in first source; RN refers to HCl. fexofenadine : A piperidine-based anti-histamine compound.	3.23	1	0	piperidines; tertiary amine	anti-allergic agent; H1-receptor antagonist
fipexide fipexide: regulates dopaminergic systems at macromolecular level	3.23	1	0	benzodioxoles
flavoxate Flavoxate: A drug that has been used in various urinary syndromes and as an antispasmodic. Its therapeutic usefulness and its mechanism of action are not clear. It may have local anesthetic activity and direct relaxing effects on smooth muscle as well as some activity as a muscarinic antagonist.. flavoxate : A carboxylic ester resulting from the formal condensation of 3-methylflavone-8-carboxylic acid with 2-(1-piperidinyl)ethanol.	3.23	1	0	carboxylic ester; flavones; piperidines; tertiary amino compound	antispasmodic drug; muscarinic antagonist; parasympatholytic
flecainide Flecainide: A potent anti-arrhythmia agent, effective in a wide range of ventricular and atrial ARRHYTHMIAS and TACHYCARDIAS.. flecainide : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 2,5-bis(2,2,2-trifluoroethoxy)benzoic acid with the primary amino group of piperidin-2-ylmethylamine. An antiarrhythmic agent used (in the form of its acetate salt) to prevent and treat tachyarrhythmia (abnormal fast rhythm of the heart).	3.86	3	0	aromatic ether; monocarboxylic acid amide; organofluorine compound; piperidines	anti-arrhythmia drug
fleroxacin Fleroxacin: A broad-spectrum antimicrobial fluoroquinolone. The drug strongly inhibits the DNA-supercoiling activity of DNA GYRASE.. fleroxacin : A fluoroquinolone antibiotic that is 4-oxo-1,4-dihydroquinoline which is substituted at positions 1, 3, 6, 7 and 8 by 2-fluoroethyl, carboxy, fluoro, 4-methylpiperazin-1-yl and fluoro groups, respectively. It is active against many Gram-positive and Gram-negative bacteria.	2.46	2	0	difluorobenzene; fluoroquinolone antibiotic; monocarboxylic acid; N-alkylpiperazine; quinolines	antibacterial drug; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; topoisomerase IV inhibitor
fluconazole Fluconazole: Triazole antifungal agent that is used to treat oropharyngeal CANDIDIASIS and cryptococcal MENINGITIS in AIDS.. fluconazole : A member of the class of triazoles that is propan-2-ol substituted at position 1 and 3 by 1H-1,2,4-triazol-1-yl groups and at position 2 by a 2,4-difluorophenyl group. It is an antifungal drug used for the treatment of mucosal candidiasis and for systemic infections including systemic candidiasis, coccidioidomycosis, and cryptococcosis.	4.59	7	0	conazole antifungal drug; difluorobenzene; tertiary alcohol; triazole antifungal drug	environmental contaminant; P450 inhibitor; xenobiotic
flucytosine Flucytosine: A fluorinated cytosine analog that is used as an antifungal agent.. flucytosine : An organofluorine compound that is cytosine that is substituted at position 5 by a fluorine. A prodrug for the antifungal 5-fluorouracil, it is used for the treatment of systemic fungal infections.	4.08	4	0	aminopyrimidine; nucleoside analogue; organofluorine compound; pyrimidine antifungal drug; pyrimidone	prodrug
flufenamic acid Flufenamic Acid: An anthranilic acid derivative with analgesic, anti-inflammatory, and antipyretic properties. It is used in musculoskeletal and joint disorders and administered by mouth and topically. (From Martindale, The Extra Pharmacopoeia, 30th ed, p16). flufenamic acid : An aromatic amino acid consisting of anthranilic acid carrying an N-(trifluoromethyl)phenyl substituent. An analgesic and anti-inflammatory, it is used in rheumatic disorders.	2.05	1	0	aromatic amino acid; organofluorine compound	antipyretic; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug
fluphenazine [no description available]	3.73	2	0	N-alkylpiperazine; organofluorine compound; phenothiazines	anticoronaviral agent; dopaminergic antagonist; phenothiazine antipsychotic drug
flumazenil Flumazenil: A potent benzodiazepine receptor antagonist. Since it reverses the sedative and other actions of benzodiazepines, it has been suggested as an antidote to benzodiazepine overdoses.. flumazenil : An organic heterotricyclic compound that is 5,6-dihydro-4H-imidazo[1,5-a][1,4]benzodiazepine which is substituted at positions 3, 5, 6, and 8 by ethoxycarbonyl, methyl, oxo, and fluoro groups, respectively. It is used as an antidote to benzodiazepine overdose.	4.08	4	0	ethyl ester; imidazobenzodiazepine; organofluorine compound	antidote to benzodiazepine poisoning; GABA antagonist
flunitrazepam Flunitrazepam: A benzodiazepine with pharmacologic actions similar to those of DIAZEPAM that can cause ANTEROGRADE AMNESIA. Some reports indicate that it is used as a date rape drug and suggest that it may precipitate violent behavior. The United States Government has banned the importation of this drug.. flunitrazepam : A 1,4-benzodiazepinone that is nitrazepam substituted by a methyl group at position 1 and by a fluoro group at position 2'. It is a potent hypnotic, sedative, and amnestic drug used to treat chronic insomnia.	2.45	2	0	1,4-benzodiazepinone; C-nitro compound; monofluorobenzenes	anxiolytic drug; GABAA receptor agonist; sedative
fluorescite fluorescein (acid form) : A xanthene dye that is highly fluorescent and commonly used as a fluorescent tracer.	3.87	3	0	benzoic acids; cyclic ketone; hydroxy monocarboxylic acid; organic heterotricyclic compound; phenols; xanthene dye	fluorescent dye; radioopaque medium
fluorouracil Fluorouracil: A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.. 5-fluorouracil : A nucleobase analogue that is uracil in which the hydrogen at position 5 is replaced by fluorine. It is an antineoplastic agent which acts as an antimetabolite - following conversion to the active deoxynucleotide, it inhibits DNA synthesis (by blocking the conversion of deoxyuridylic acid to thymidylic acid by the cellular enzyme thymidylate synthetase) and so slows tumour growth.	9.85	20	4	nucleobase analogue; organofluorine compound	antimetabolite; antineoplastic agent; environmental contaminant; immunosuppressive agent; radiosensitizing agent; xenobiotic
fluoxetine Fluoxetine: The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants.. fluoxetine : A racemate comprising equimolar amounts of (R)- and (S)-fluoxetine. A selective serotonin reuptake inhibitor (SSRI), it is used (generally as the hydrochloride salt) for the treatment of depression (and the depressive phase of bipolar disorder), bullimia nervosa, and obsessive-compulsive disorder.. N-methyl-3-phenyl-3-[4-(trifluoromethyl)phenoxy]propan-1-amine : An aromatic ether consisting of 4-trifluoromethylphenol in which the hydrogen of the phenolic hydroxy group is replaced by a 3-(methylamino)-1-phenylpropyl group.	3.87	3	0	(trifluoromethyl)benzenes; aromatic ether; secondary amino compound
flurazepam Flurazepam: A benzodiazepine derivative used mainly as a hypnotic.. flurazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a 2-(diethylamino)ethyl group, 2-fluorophenyl group and chloro group at positions 1, 5 and 7, respectively. It is a partial agonist of GABAA receptors and used for the treatment of insomnia.	3.23	1	0	1,4-benzodiazepinone; monofluorobenzenes; organochlorine compound; tertiary amino compound	anticonvulsant; anxiolytic drug; GABAA receptor agonist; sedative
flurbiprofen Flurbiprofen: An anti-inflammatory analgesic and antipyretic of the phenylalkynoic acid series. It has been shown to reduce bone resorption in periodontal disease by inhibiting CARBONIC ANHYDRASE.. flurbiprofen : A monocarboxylic acid that is a 2-fluoro-[1,1'-biphenyl-4-yl] moiety linked to C-2 of propionic acid. A non-steroidal anti-inflammatory, analgesic and antipyretic, it is used as a pre-operative anti-miotic as well as orally for arthritis or dental pain.	3.59	2	0	fluorobiphenyl; monocarboxylic acid	antipyretic; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug
flutamide Flutamide: An antiandrogen with about the same potency as cyproterone in rodent and canine species.	3.87	3	0	(trifluoromethyl)benzenes; monocarboxylic acid amide	androgen antagonist; antineoplastic agent
fomepizole Fomepizole: A pyrazole and competitive inhibitor of ALCOHOL DEHYDROGENASE that is used for the treatment of poisoning by ETHYLENE GLYCOL or METHANOL.. fomepizole : A member of the class of pyrazoles that is 1H-pyrazole substituted by a methyl group at position 4.	3.59	2	0	pyrazoles	antidote; EC 1.1.1.1 (alcohol dehydrogenase) inhibitor; protective agent
foscarnet Foscarnet: An antiviral agent used in the treatment of cytomegalovirus retinitis. Foscarnet also shows activity against human herpesviruses and HIV.. phosphonoformic acid : Phosphoric acid in which one of the hydroxy groups is replaced by a carboxylic acid group. It is used as the trisodium salt as an antiviral agent in the treatment of cytomegalovirus retinitis (CMV retinitis, an inflamation of the retina that can lead to blindness) and as an alternative to ganciclovir for AIDS patients who require concurrent antiretroviral therapy but are unable to tolerate ganciclovir due to haematological toxicity.	3.58	2	0	carboxylic acid; one-carbon compound; phosphonic acids	antiviral drug; geroprotector; HIV-1 reverse transcriptase inhibitor; sodium-dependent Pi-transporter inhibitor
furosemide Furosemide: A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.. furosemide : A chlorobenzoic acid that is 4-chlorobenzoic acid substituted by a (furan-2-ylmethyl)amino and a sulfamoyl group at position 2 and 5 respectively. It is a diuretic used in the treatment of congestive heart failure.	4.27	5	0	chlorobenzoic acid; furans; sulfonamide	environmental contaminant; loop diuretic; xenobiotic
gabapentin Gabapentin: A cyclohexane-gamma-aminobutyric acid derivative that is used for the treatment of PARTIAL SEIZURES; NEURALGIA; and RESTLESS LEGS SYNDROME.. gabapentin : A gamma-amino acid that is cyclohexane substituted at position 1 by aminomethyl and carboxymethyl groups. Used for treatment of neuropathic pain and restless legs syndrome.	9.27	5	0	gamma-amino acid	anticonvulsant; calcium channel blocker; environmental contaminant; xenobiotic
gabexate Gabexate: A serine proteinase inhibitor used therapeutically in the treatment of pancreatitis, disseminated intravascular coagulation (DIC), and as a regional anticoagulant for hemodialysis. The drug inhibits the hydrolytic effects of thrombin, plasmin, and kallikrein, but not of chymotrypsin and aprotinin.	2.76	2	0	benzoate ester
gemfibrozil [no description available]	3.87	3	0	aromatic ether	antilipemic drug
glafenine Glafenine: An anthranilic acid derivative with analgesic properties used for the relief of all types of pain.. glafenine : A carboxylic ester that is 2,3-dihydroxypropyl anthranilate in which the amino group is substituted by a 7-chloroquinolin-4-yl group. A non-steroidal anti-inflammatory drug, glafenine and its hydrochloride salt were used for the relief of all types of pain, but high incidence of anaphylactic reactions resulted in their withdrawal from the market.	3.59	2	0	aminoquinoline; carboxylic ester; glycol; organochlorine compound; secondary amino compound	inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug
gliclazide Gliclazide: An oral sulfonylurea hypoglycemic agent which stimulates insulin secretion.	2.47	2	0	N-sulfonylurea	hypoglycemic agent; insulin secretagogue; radical scavenger
glimepiride glimepiride: structure given in first source	3.87	3	0	sulfonamide
glipizide Glipizide: An oral hypoglycemic agent which is rapidly absorbed and completely metabolized.. glipizide : An N-sulfonylurea that is glyburide in which the (5-chloro-2-methoxybenzoyl group is replaced by a (5-methylpyrazin-2-yl)carbonyl group. An oral hypoglycemic agent, it is used in the treatment of type 2 diabetes mellitus.	3.87	3	0	aromatic amide; monocarboxylic acid amide; N-sulfonylurea; pyrazines	EC 2.7.1.33 (pantothenate kinase) inhibitor; hypoglycemic agent; insulin secretagogue
glutaral Glutaral: One of the protein CROSS-LINKING REAGENTS that is used as a disinfectant for sterilization of heat-sensitive equipment and as a laboratory reagent, especially as a fixative.. glutaraldehyde : A dialdehyde comprised of pentane with aldehyde functions at C-1 and C-5.	2.6	1	0	dialdehyde	cross-linking reagent; disinfectant; fixative
glutethimide Glutethimide: A hypnotic and sedative. Its use has been largely superseded by other drugs.	2.05	1	0	piperidines
glyburide Glyburide: An antidiabetic sulfonylurea derivative with actions like those of chlorpropamide. glyburide : An N-sulfonylurea that is acetohexamide in which the acetyl group is replaced by a 2-(5-chloro-2-methoxybenzamido)ethyl group.	4.08	4	0	monochlorobenzenes; N-sulfonylurea	anti-arrhythmia drug; EC 2.7.1.33 (pantothenate kinase) inhibitor; EC 3.6.3.49 (channel-conductance-controlling ATPase) inhibitor; hypoglycemic agent
2-cyclopentyl-2-hydroxy-2-phenylacetic acid (1,1-dimethyl-3-pyrrolidin-1-iumyl) ester [no description available]	3.23	1	0	benzenes
gossypol Gossypol: A dimeric sesquiterpene found in cottonseed (GOSSYPIUM). The (-) isomer is active as a male contraceptive (CONTRACEPTIVE AGENTS, MALE) whereas toxic symptoms are associated with the (+) isomer.	4.54	7	0
granisetron [no description available]	3.58	2	0	aromatic amide; indazoles
guaiazulene guaiazulene: structure	2.05	1	0	sesquiterpene
guaifenesin Guaifenesin: An expectorant that also has some muscle relaxing action. It is used in many cough preparations.	3.23	1	0	methoxybenzenes
guanethidine Guanethidine: An antihypertensive agent that acts by inhibiting selectively transmission in post-ganglionic adrenergic nerves. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues.. guanethidine : A member of the class of guanidines in which one of the hydrogens of the amino group has been replaced by a 2-azocan-1-ylethyl group.. guanethidine sulfate : A organic sulfate salt composed of two molecules of guanethidine and one of sulfuric acid.	3.23	1	0	azocanes; guanidines	adrenergic antagonist; antihypertensive agent; sympatholytic agent
guanfacine Guanfacine: A centrally acting antihypertensive agent with specificity towards ADRENERGIC ALPHA-2 RECEPTORS.	3.87	3	0	acetamides
guanidine Guanidine: A strong organic base existing primarily as guanidium ions at physiological pH. It is found in the urine as a normal product of protein metabolism. It is also used in laboratory research as a protein denaturant. (From Martindale, the Extra Pharmacopoeia, 30th ed and Merck Index, 12th ed) It is also used in the treatment of myasthenia and as a fluorescent probe in HPLC.. guanidine : An aminocarboxamidine, the parent compound of the guanidines.	3.73	2	0	carboxamidine; guanidines; one-carbon compound
fasudil fasudil: intracellular calcium antagonist; structure in first source. fasudil : An isoquinoline substituted by a (1,4-diazepan-1-yl)sulfonyl group at position 5. It is a Rho-kinase inhibitor and its hydrochloride hydrate form is approved for the treatment of cerebral vasospasm and cerebral ischemia.	2.81	3	0	isoquinolines; N-sulfonyldiazepane	antihypertensive agent; calcium channel blocker; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor; geroprotector; neuroprotective agent; nootropic agent; vasodilator agent
ha14-1 ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate: a BH3 mimetic; synergistic induction of apoptosis by simultaneous disruption of the Bcl-2 and MEK/MAPK pathways in acute myelogenous leukemia	2.74	3	0	1-benzopyran
haloperidol Haloperidol: A phenyl-piperidinyl-butyrophenone that is used primarily to treat SCHIZOPHRENIA and other PSYCHOSES. It is also used in schizoaffective disorder, DELUSIONAL DISORDERS, ballism, and TOURETTE SYNDROME (a drug of choice) and occasionally as adjunctive therapy in INTELLECTUAL DISABILITY and the chorea of HUNTINGTON DISEASE. It is a potent antiemetic and is used in the treatment of intractable HICCUPS. (From AMA Drug Evaluations Annual, 1994, p279). haloperidol : A compound composed of a central piperidine structure with hydroxy and p-chlorophenyl substituents at position 4 and an N-linked p-fluorobutyrophenone moiety.	4.29	5	0	aromatic ketone; hydroxypiperidine; monochlorobenzenes; organofluorine compound; tertiary alcohol	antidyskinesia agent; antiemetic; dopaminergic antagonist; first generation antipsychotic; serotonergic antagonist
halothane [no description available]	2.05	1	0	haloalkane; organobromine compound; organochlorine compound; organofluorine compound	inhalation anaesthetic
hexachlorophene Hexachlorophene: A chlorinated bisphenol antiseptic with a bacteriostatic action against Gram-positive organisms, but much less effective against Gram-negative organisms. It is mainly used in soaps and creams and is an ingredient of various preparations used for skin disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p797). hexachlorophene : An organochlorine compound that is diphenylmethane in which each of the phenyl groups is substituted by chlorines at positions 2, 3, and 5, and by a hydroxy group at position 6. An antiseptic that is effective against Gram-positive organisms, it is used in soaps and creams for the treatment of various skin disorders. It is also used in agriculture as an acaricide and fungicide, but is not approved for such use within the European Union.	2.52	2	0	bridged diphenyl fungicide; polyphenol; trichlorobenzene	acaricide; antibacterial agent; antifungal agrochemical; antiseptic drug
miltefosine miltefosine: hexadecyl phosphocholine derivative of cisplatin; did not substantially activate HIV long terminal repeat; less toxic than cisplatin. miltefosine : A phospholipid that is the hexadecyl monoester of phosphocholine.	2.86	3	0	phosphocholines; phospholipid	anti-inflammatory agent; anticoronaviral agent; antifungal agent; antineoplastic agent; antiprotozoal drug; apoptosis inducer; immunomodulator; protein kinase inhibitor
hexestrol [no description available]	2.05	1	0	stilbenoid
hexetidine Hexetidine: A bactericidal and fungicidal antiseptic. It is used as a 0.1% mouthwash for local infections and oral hygiene. (From Martindale, The Extra Pharmacopoeia, 30th ed, p797)	2.05	1	0	organic heteromonocyclic compound; organonitrogen heterocyclic compound
hexobarbital Hexobarbital: A barbiturate that is effective as a hypnotic and sedative.. hexobarbital : A member of the class of barbiturates taht is barbituric acid substituted at N-1 by methyl and at C-5 by methyl and cyclohex-1-enyl groups.	2.45	2	0	barbiturates
hexylresorcinol [no description available]	2.6	1	0	resorcinols
beta-thujaplicin beta-thujaplicin: structure. beta-thujaplicin : A monoterpenoid that is cyclohepta-2,4,6-trien-1-one substituted by a hydroxy group at position 2 and an isopropyl group at position 4. Isolated from Thuja plicata and Chamaecyparis obtusa, it exhibits antimicrobial activities.	2.6	1	0	cyclic ketone; enol; monoterpenoid	antibacterial agent; antifungal agent; antineoplastic agent; antiplasmodial drug; plant metabolite
hycanthone Hycanthone: Potentially toxic, but effective antischistosomal agent, it is a metabolite of LUCANTHONE.. hycanthone : A thioxanthen-9-one compound having a hydroxymethyl substituent at the 1-position and a 2-[(diethylamino)ethyl]amino substituent at the 4-position. It was formerly used (particularly as the monomethanesulfonic acid salt) as a schistosomicide for individual or mass treatement of infection with Schistosoma haematobium and S. mansoni, but due to its toxicity and concern about possible carcinogenicity, it has been replaced by other drugs such as praziquantel.	2.6	1	0	thioxanthenes	mutagen; schistosomicide drug
hydralazine Hydralazine: A direct-acting vasodilator that is used as an antihypertensive agent.. hydralazine : The 1-hydrazino derivative of phthalazine; a direct-acting vasodilator that is used as an antihypertensive agent.	3.86	3	0	azaarene; hydrazines; ortho-fused heteroarene; phthalazines	antihypertensive agent; vasodilator agent
hydrochlorothiazide Hydrochlorothiazide: A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It is used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism.. hydrochlorothiazide : A benzothiadiazine that is 3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide substituted by a chloro group at position 6 and a sulfonamide at 7. It is diuretic used for the treatment of hypertension and congestive heart failure.	4.13	4	0	benzothiadiazine; organochlorine compound; sulfonamide	antihypertensive agent; diuretic; environmental contaminant; xenobiotic
hydroflumethiazide Hydroflumethiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p822). hydroflumethiazide : A benzothiadiazine consisting of a 3,4-dihydro-HH-1,2,4-benzothiadiazine bicyclic system dioxygenated on sulfur and carrying trifluoromethyl and aminosulfonyl groups at positions 6 and 7 respectively. A diuretic with actions and uses similar to those of hydrochlorothiazide.	3.87	3	0	benzothiadiazine; thiazide	antihypertensive agent; diuretic
hydroxychloroquine Hydroxychloroquine: A chemotherapeutic agent that acts against erythrocytic forms of malarial parasites. Hydroxychloroquine appears to concentrate in food vacuoles of affected protozoa. It inhibits plasmodial heme polymerase. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p970). hydroxychloroquine : An aminoquinoline that is chloroquine in which one of the N-ethyl groups is hydroxylated at position 2. An antimalarial with properties similar to chloroquine that acts against erythrocytic forms of malarial parasites, it is mainly used as the sulfate salt for the treatment of lupus erythematosus, rheumatoid arthritis, and light-sensitive skin eruptions.	8.67	9	2	aminoquinoline; organochlorine compound; primary alcohol; secondary amino compound; tertiary amino compound	anticoronaviral agent; antimalarial; antirheumatic drug; dermatologic drug
hydroxyurea [no description available]	6.08	8	1	one-carbon compound; ureas	antimetabolite; antimitotic; antineoplastic agent; DNA synthesis inhibitor; EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor; genotoxin; immunomodulator; radical scavenger; teratogenic agent
hydroxyzine Hydroxyzine: A histamine H1 receptor antagonist that is effective in the treatment of chronic urticaria, dermatitis, and histamine-mediated pruritus. Unlike its major metabolite CETIRIZINE, it does cause drowsiness. It is also effective as an antiemetic, for relief of anxiety and tension, and as a sedative.. hydroxyzine : A N-alkylpiperazine that is piperzine in which the nitrogens atoms are substituted by 2-(2-hydroxyethoxy)ethyl and (4-chlorophenyl)(phenyl)methyl groups respectively.	3.59	2	0	hydroxyether; monochlorobenzenes; N-alkylpiperazine	anticoronaviral agent; antipruritic drug; anxiolytic drug; dermatologic drug; H1-receptor antagonist
hypericin [no description available]	2.04	1	0
ibuprofen Midol: combination of cinnamedrine, phenacetin, aspirin & caffeine	4.31	5	0	monocarboxylic acid	antipyretic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; drug allergen; environmental contaminant; geroprotector; non-narcotic analgesic; non-steroidal anti-inflammatory drug; radical scavenger; xenobiotic
phenelzine Phenelzine: One of the MONOAMINE OXIDASE INHIBITORS used to treat DEPRESSION; PHOBIC DISORDERS; and PANIC.	3.59	2	0	primary amine
lidocaine Lidocaine: A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE.. lidocaine : The monocarboxylic acid amide resulting from the formal condensation of N,N-diethylglycine with 2,6-dimethylaniline.	4.08	4	0	benzenes; monocarboxylic acid amide; tertiary amino compound	anti-arrhythmia drug; drug allergen; environmental contaminant; local anaesthetic; xenobiotic
alverine alverine : A tertiary amine having one ethyl and two 3-phenylprop-1-yl groups attached to the nitrogen. An antispasmodic that acts directly on intestinal and uterine smooth muscle, it is used (particularly as the citrate salt) in the treatment of irritable bowel syndrome.	2.05	1	0	tertiary amine	antispasmodic drug
idebenone [no description available]	2.05	1	0	1,4-benzoquinones; primary alcohol	antioxidant; ferroptosis inhibitor
ifosfamide [no description available]	9.21	12	5	ifosfamides	alkylating agent; antineoplastic agent; environmental contaminant; immunosuppressive agent; xenobiotic
imipramine Imipramine: The prototypical tricyclic antidepressant. It has been used in major depression, dysthymia, bipolar depression, attention-deficit disorders, agoraphobia, and panic disorders. It has less sedative effect than some other members of this therapeutic group.. imipramine : A dibenzoazepine that is 5H-dibenzo[b,f]azepine substituted by a 3-(dimethylamino)propyl group at the nitrogen atom.	4.08	4	0	dibenzoazepine	adrenergic uptake inhibitor; antidepressant; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
amrinone Amrinone: A positive inotropic cardiotonic (CARDIOTONIC AGENTS) with vasodilator properties, phosphodiesterase 3 inhibitory activity, and the ability to stimulate calcium ion influx into the cardiac cell.. amrinone : A 3,4'-bipyridine substituted at positions 5 and 6 by an amino group and a keto function respectively. A pyridine phosphodiesterase 3 inhibitor, it is a drug that may improve the prognosis in patients with congestive heart failure.	4.08	4	0	bipyridines	EC 3.1.4.* (phosphoric diester hydrolase) inhibitor
indapamide Indapamide: A benzamide-sulfonamide-indole derived DIURETIC that functions by inhibiting SODIUM CHLORIDE SYMPORTERS.. indapamide : A sulfonamide formed by condensation of the carboxylic group of 4-chloro-3-sulfamoylbenzoic acid with the amino group of 2-methyl-2,3-dihydro-1H-indol-1-amine.	3.87	3	0	indoles; organochlorine compound; sulfonamide	antihypertensive agent; diuretic
indirubin-3'-monoxime indirubin-3'-monoxime: has antiangiogenic activity. indirubin-3'-monoxime : A member of the class of biindoles that is indirubin in which the keto group at position 3' has undergone condensation with hydroxylamine to form the corresponding oxime.	2.85	3	0
indole-3-carbinol indole-3-carbinol: occurs in edible cruciferous vegetables. indole-3-methanol : An indolyl alcohol carrying a hydroxymethyl group at position 3. It is a constituent of the cruciferous vegetables and had anticancer activity.	7.07	1	0	indolyl alcohol	antineoplastic agent; plant metabolite
indomethacin Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits CYCLOOXYGENASE, which is necessary for the formation of PROSTAGLANDINS and other AUTACOIDS. It also inhibits the motility of POLYMORPHONUCLEAR LEUKOCYTES.. indometacin : A member of the class of indole-3-acetic acids that is indole-3-acetic acid in which the indole ring is substituted at positions 1, 2 and 5 by p-chlorobenzoyl, methyl, and methoxy groups, respectively. A non-steroidal anti-inflammatory drug, it is used in the treatment of musculoskeletal and joint disorders including osteoarthritis, rheumatoid arthritis, gout, bursitis and tendinitis.	4.29	5	0	aromatic ether; indole-3-acetic acids; monochlorobenzenes; N-acylindole	analgesic; drug metabolite; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; environmental contaminant; gout suppressant; non-steroidal anti-inflammatory drug; xenobiotic metabolite; xenobiotic
iohexol Iohexol: An effective non-ionic, water-soluble contrast agent which is used in myelography, arthrography, nephroangiography, arteriography, and other radiographic procedures. Its low systemic toxicity is the combined result of low chemotoxicity and low osmolality.. iohexol : A benzenedicarboxamide compound having N-(2,3-dihydroxypropyl)carbamoyl groups at the 1- and 3-positions, iodo substituents at the 2-, 4- and 6-positions and an N-(2,3-dihydroxypropyl)acetamido group at the 5-position.	2.75	3	0	benzenedicarboxamide; organoiodine compound	environmental contaminant; radioopaque medium; xenobiotic
iopromide iopromide: structure given in first source. iopromide : A dicarboxylic acid diamide that consists of N-methylisophthalamide bearing three iodo substituents at positions 2, 4 and 6, a methoxyacetyl substituent at position 5 and two 2,3-dihydroxypropyl groups attached to the amide nitrogens. A water soluble x-ray contrast agent for intravascular administration.	2.04	1	0	dicarboxylic acid diamide; organoiodine compound	environmental contaminant; nephrotoxic agent; radioopaque medium; xenobiotic
iothalamic acid Iothalamic Acid: A contrast medium in diagnostic radiology with properties similar to those of diatrizoic acid. It is used primarily as its sodium and meglumine (IOTHALAMATE MEGLUMINE) salts.	2.04	1	0	organic molecular entity
iodipamide Iodipamide: A water-soluble radiographic contrast media for cholecystography and intravenous cholangiography.. adipiodone : An organoiodine compound that is 3-amino-2,4,6-triiodobenzoic acid in which one of the amino hydrogens is substituted by a 6-(3-carboxy-2,4,6-triiodoanilino)-6-oxohexanoyl group. It is a water-soluble radiographic contrast media for cholecystography and intravenous cholangiography.	2.05	1	0	benzoic acids; organoiodine compound; secondary carboxamide	radioopaque medium
ioversol [no description available]	3.23	1	0	amidobenzoic acid
iproniazid [no description available]	3.87	3	0	carbohydrazide; pyridines
avapro Irbesartan: A spiro compound, biphenyl and tetrazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION, and in the treatment of kidney disease.. irbesartan : A biphenylyltetrazole that is an angiotensin II receptor antagonist used mainly for the treatment of hypertension.	4.29	5	0	azaspiro compound; biphenylyltetrazole	angiotensin receptor antagonist; antihypertensive agent; environmental contaminant; xenobiotic
isocarboxazid Isocarboxazid: An MAO inhibitor that is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in the treatment of panic disorder and the phobic disorders. (From AMA, Drug Evaluations Annual, 1994, p311)	3.23	1	0	benzenes
isoflurane Isoflurane: A stable, non-explosive inhalation anesthetic, relatively free from significant side effects.	2.05	1	0	organofluorine compound	inhalation anaesthetic
isoniazid Hydra: A genus of freshwater polyps in the family Hydridae, order Hydroida, class HYDROZOA. They are of special interest because of their complex organization and because their adult organization corresponds roughly to the gastrula of higher animals.. hydrazide : Compounds derived from oxoacids RkE(=O)l(OH)m (l =/= 0) by replacing -OH by -NRNR2 (R groups are commonly H). (IUPAC).	4.08	4	0	carbohydrazide	antitubercular agent; drug allergen
2-propanol 2-Propanol: An isomer of 1-PROPANOL. It is a colorless liquid having disinfectant properties. It is used in the manufacture of acetone and its derivatives and as a solvent. Topically, it is used as an antiseptic.. propan-2-ol : A secondary alcohol that is propane in which one of the hydrogens attached to the central carbon is substituted by a hydroxy group.	2.05	1	0	secondary alcohol; secondary fatty alcohol	protic solvent
isoproterenol Isoproterenol: Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.. isoprenaline : A secondary amino compound that is noradrenaline in which one of the hydrogens attached to the nitrogen is replaced by an isopropyl group. A sympathomimetic acting almost exclusively on beta-adrenergic receptors, it is used (mainly as the hydrochloride salt) as a bronghodilator and heart stimulant for the management of a variety of cardiac disorders.	3.86	3	0	catechols; secondary alcohol; secondary amino compound	beta-adrenergic agonist; bronchodilator agent; cardiotonic drug; sympathomimetic agent
isoxsuprine Isoxsuprine: A beta-adrenergic agonist that causes direct relaxation of uterine and vascular smooth muscle. Its vasodilating actions are greater on the arteries supplying skeletal muscle than on those supplying skin. It is used in the treatment of peripheral vascular disease and in premature labor.	3.59	2	0	alkylbenzene
isradipine Isradipine: A potent antagonist of CALCIUM CHANNELS that is highly selective for VASCULAR SMOOTH MUSCLE. It is effective in the treatment of chronic stable angina pectoris, hypertension, and congestive cardiac failure.	4.08	4	0	benzoxadiazole; dihydropyridine; isopropyl ester; methyl ester
itraconazole [no description available]	4.29	5	0	piperazines
7-amino-4-chloro-3-methoxy-2-benzopyran-1-one [no description available]	2.08	1	0	isocoumarins
ketamine Ketamine: A cyclohexanone derivative used for induction of anesthesia. Its mechanism of action is not well understood, but ketamine can block NMDA receptors (RECEPTORS, N-METHYL-D-ASPARTATE) and may interact with sigma receptors.. ketamine : A member of the class of cyclohexanones in which one of the hydrogens at position 2 is substituted by a 2-chlorophenyl group, while the other is substituted by a methylamino group.	4.26	5	0	cyclohexanones; monochlorobenzenes; secondary amino compound	analgesic; environmental contaminant; intravenous anaesthetic; neurotoxin; NMDA receptor antagonist; xenobiotic
ketanserin Ketanserin: A selective serotonin receptor antagonist with weak adrenergic receptor blocking properties. The drug is effective in lowering blood pressure in essential hypertension. It also inhibits platelet aggregation. It is well tolerated and is particularly effective in older patients.. ketanserin : A member of the class of quinazolines that is quinazoline-2,4(1H,3H)-dione which is substituted at position 3 by a 2-[4-(p-fluorobenzoyl)piperidin-1-yl]ethyl group.	2.75	3	0	aromatic ketone; organofluorine compound; piperidines; quinazolines	alpha-adrenergic antagonist; antihypertensive agent; cardiovascular drug; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; serotonergic antagonist
ketoconazole 1-acetyl-4-(4-{[2-(2,4-dichlorophenyl)-2-(1H-imidazol-1-ylmethyl)-1,3-dioxolan-4-yl]methoxy}phenyl)piperazine : A dioxolane that is 1,3-dioxolane which is substituted at positions 2, 2, and 4 by imidazol-1-ylmethyl, 2,4-dichlorophenyl, and [para-(4-acetylpiperazin-1-yl)phenoxy]methyl groups, respectively.	11.59	5	1	dichlorobenzene; dioxolane; ether; imidazoles; N-acylpiperazine; N-arylpiperazine
ketoprofen Ketoprofen: An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis.. ketoprofen : An oxo monocarboxylic acid that consists of propionic acid substituted by a 3-benzoylphenyl group at position 2.	3.86	3	0	benzophenones; oxo monocarboxylic acid	antipyretic; drug allergen; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; environmental contaminant; non-steroidal anti-inflammatory drug; xenobiotic
ketorolac Ketorolac: A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed). ketorolac : A racemate comprising equimolar amounts of (R)-(+)- and (S)-(-)-5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid. While only the (S)-(-) enantiomer is a COX1 and COX2 inhibitor, the (R)-(+) enantiomer exhibits potent analgesic activity. A non-steroidal anti-inflammatory drug, ketorolac is mainly used (generally as the tromethamine salt) for its potent analgesic properties in the short-term management of post-operative pain, and in eye drops to relieve the ocular itching associated with seasonal allergic conjunctivitis. It was withdrawn from the market in many countries in 1993 following association with haemorrhage and renal failure.. 5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid : A member of the class of pyrrolizines that is 2,3-dihydro-1H-pyrrolizine which is substituted at positions 1 and 5 by carboxy and benzoyl groups, respectively.	3.58	2	0	amino acid; aromatic ketone; monocarboxylic acid; pyrrolizines; racemate	analgesic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; non-steroidal anti-inflammatory drug
ketotifen Ketotifen: A cycloheptathiophene blocker of histamine H1 receptors and release of inflammatory mediators. It has been proposed for the treatment of asthma, rhinitis, skin allergies, and anaphylaxis.. ketotifen : An organic heterotricyclic compound that is 4,9-dihydro-10H-benzo[4,5]cyclohepta[1,2-b]thiophen-10-one which is substituted at position 4 by a 1-methylpiperidin-4-ylidene group. A blocker of histamine H1 receptors with a stabilising action on mast cells, it is used (usually as its hydrogen fumarate salt) for the treatment of asthma, where it may take several weeks to exert its full effect.	7.21	1	0	cyclic ketone; olefinic compound; organic heterotricyclic compound; organosulfur heterocyclic compound; piperidines; tertiary amino compound	anti-asthmatic drug; H1-receptor antagonist
khellin Khellin: A vasodilator that also has bronchodilatory action. It has been employed in the treatment of angina pectoris, in the treatment of asthma, and in conjunction with ultraviolet light A, has been tried in the treatment of vitiligo. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1024). khellin : A furanochrome in which the basic tricyclic skeleton is substituted at positions 4 and 9 with methoxy groups and at position 7 with a methyl group. A major constituent of the plant Ammi visnaga it is a herbal folk medicine used for various illnesses, its main effect being as a vasodilator.	2.05	1	0	furanochromone; organic heterotricyclic compound; oxacycle	anti-asthmatic agent; bronchodilator agent; cardiovascular drug; vasodilator agent
kojic acid [no description available]	2.6	1	0	4-pyranones; enol; primary alcohol	Aspergillus metabolite; EC 1.10.3.1 (catechol oxidase) inhibitor; EC 1.10.3.2 (laccase) inhibitor; EC 1.13.11.24 (quercetin 2,3-dioxygenase) inhibitor; EC 1.14.18.1 (tyrosinase) inhibitor; EC 1.4.3.3 (D-amino-acid oxidase) inhibitor; NF-kappaB inhibitor; skin lightening agent
labetalol Labetalol: A salicylamide derivative that is a non-cardioselective blocker of BETA-ADRENERGIC RECEPTORS and ALPHA-1 ADRENERGIC RECEPTORS.. labetalol : A diastereoisomeric mixture of approximately equal amounts of all four possible stereoisomers ((R,S)-labetolol, (S,R)-labetolol, (S,S)-labetalol and (R,R)-labetalol). It is an adrenergic antagonist used to treat high blood pressure.. 2-hydroxy-5-{1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl}benzamide : A member of the class of benzamides that is benzamide substituted by a hydroxy group at position 2 and by a 1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl group at position 5.	3.86	3	0	benzamides; benzenes; phenols; primary carboxamide; salicylamides; secondary alcohol; secondary amino compound
lamotrigine [no description available]	3.87	3	0	1,2,4-triazines; dichlorobenzene; primary arylamine	anticonvulsant; antidepressant; antimanic drug; calcium channel blocker; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; environmental contaminant; excitatory amino acid antagonist; geroprotector; non-narcotic analgesic; xenobiotic
lansoprazole Lansoprazole: A 2,2,2-trifluoroethoxypyridyl derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS. Lansoprazole is a racemic mixture of (R)- and (S)-isomers.	4.28	5	0	benzimidazoles; pyridines; sulfoxide	anti-ulcer drug; EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor
lapachol lapachol : A hydroxy-1,4-naphthoquinone that is 1,4-naphthoquinone substituted by hydroxy and 3-methylbut-2-en-1-yl groups at positions 2 and 3, respectively. It is a natural compound that exhibits antibacterial and anticancer properties, first isolated in 1882 from the bark of Tabebuia avellanedae.	2.76	2	0
beta-lapachone beta-lapachone: antineoplastic inhibitor of reverse transcriptase, DNA topoisomerase, and DNA polymerase. beta-lapachone : A benzochromenone that is 3,4-dihydro-2H-benzo[h]chromene-5,6-dione substituted by geminal methyl groups at position 2. Isolated from Tabebuia avellanedae, it exhibits antineoplastic and anti-inflammatory activities.	2.05	1	0	benzochromenone; orthoquinones	anti-inflammatory agent; antineoplastic agent; plant metabolite
leflunomide Leflunomide: An isoxazole derivative that inhibits dihydroorotate dehydrogenase, the fourth enzyme in the pyrimidine biosynthetic pathway. It is used an immunosuppressive agent in the treatment of RHEUMATOID ARTHRITIS and PSORIATIC ARTHRITIS.. leflunomide : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 5-methyl-1,2-oxazole-4-carboxylic acid with the anilino group of 4-(trifluoromethyl)aniline. The prodrug of teriflunomide.	5.54	8	0	(trifluoromethyl)benzenes; isoxazoles; monocarboxylic acid amide	antineoplastic agent; antiparasitic agent; EC 1.3.98.1 [dihydroorotate oxidase (fumarate)] inhibitor; EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor; hepatotoxic agent; immunosuppressive agent; non-steroidal anti-inflammatory drug; prodrug; pyrimidine synthesis inhibitor; tyrosine kinase inhibitor
letrozole [no description available]	4.77	5	0	nitrile; triazoles	antineoplastic agent; EC 1.14.14.14 (aromatase) inhibitor
lg 100268 LG 100268: a retinoid X receptor (RXR) selective compound; structure given in first source	2.08	1	0
lofepramine Lofepramine: A psychotropic IMIPRAMINE derivative that acts as a tricyclic antidepressant and possesses few anticholinergic properties. It is metabolized to DESIPRAMINE.	2.47	2	0	aromatic ketone; dibenzoazepine; monochlorobenzenes; tertiary amino compound	antidepressant
lomefloxacin lomefloxacin: structure given in first source. lomefloxacin : A fluoroquinolone antibiotic, used (generally as the hydrochloride salt) to treat bacterial infections including bronchitis and urinary tract infections. It is also used to prevent urinary tract infections prior to surgery.	3.68	2	0	fluoroquinolone antibiotic; N-arylpiperazine; quinolinemonocarboxylic acid; quinolone antibiotic; quinolone	antimicrobial agent; antitubercular agent; photosensitizing agent
lomustine [no description available]	3.87	3	0	N-nitrosoureas; organochlorine compound	alkylating agent; antineoplastic agent
loperamide Loperamide: One of the long-acting synthetic ANTIDIARRHEALS; it is not significantly absorbed from the gut, and has no effect on the adrenergic system or central nervous system, but may antagonize histamine and interfere with acetylcholine release locally.. loperamide : A synthetic piperidine derivative, effective against diarrhoea resulting from gastroenteritis or inflammatory bowel disease.	9.16	4	0	monocarboxylic acid amide; monochlorobenzenes; piperidines; tertiary alcohol	anticoronaviral agent; antidiarrhoeal drug; mu-opioid receptor agonist
loratadine Loratadine: A second-generation histamine H1 receptor antagonist used in the treatment of allergic rhinitis and urticaria. Unlike most classical antihistamines (HISTAMINE H1 ANTAGONISTS) it lacks central nervous system depressing effects such as drowsiness.. loratadine : A benzocycloheptapyridine that is 6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridine substituted by a chloro group at position 8 and a 1-(ethoxycarbonyl)piperidin-4-ylidene group at position 11. It is a H1-receptor antagonist commonly employed in the treatment of allergic disorders.	3.95	3	0	benzocycloheptapyridine; ethyl ester; N-acylpiperidine; organochlorine compound; tertiary carboxamide	anti-allergic agent; cholinergic antagonist; geroprotector; H1-receptor antagonist
lorazepam Lorazepam: A benzodiazepine used as an anti-anxiety agent with few side effects. It also has hypnotic, anticonvulsant, and considerable sedative properties and has been proposed as a preanesthetic agent.	3.58	2	0	benzodiazepine
losartan Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.. losartan : A biphenylyltetrazole where a 1,1'-biphenyl group is attached at the 5-position and has an additional trisubstituted imidazol-1-ylmethyl group at the 4'-position	4.31	5	0	biphenylyltetrazole; imidazoles	angiotensin receptor antagonist; anti-arrhythmia drug; antihypertensive agent; endothelin receptor antagonist
loxapine Loxapine: An antipsychotic agent used in SCHIZOPHRENIA.	3.23	1	0	dibenzooxazepine	antipsychotic agent; dopaminergic antagonist
2-(4-morpholinyl)-8-phenyl-4h-1-benzopyran-4-one 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one: specific inhibitor of phosphatidylinositol 3-kinase; structure in first source	3.34	6	0	chromones; morpholines; organochlorine compound	autophagy inhibitor; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; geroprotector
4-(dimethylamino)-n-(7-(hydroxyamino)-7-oxoheptyl)benzamide 4-(dimethylamino)-N-(7-(hydroxyamino)-7-oxoheptyl)benzamide: structure in first source. 4-(dimethylamino)-N-[7-(hydroxyamino)-7-oxoheptyl]benzamide : A benzamide resulting from the formal condensation of the carboxy group of 4-(dimethylamino)benzoic acid with the amino group of 7-amino-N-hydroxyheptanamide. It is a potent inhibitor of histone deacetylases and induces cell cycle arrest and apoptosis in several human cancer cell lines.	2.6	1	0	benzamides; hydroxamic acid; secondary carboxamide; tertiary amino compound	antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor
mafenide Mafenide: A sulfonamide that inhibits the enzyme CARBONIC ANHYDRASE and is used as a topical anti-bacterial agent, especially in burn therapy.	2.6	1	0	aromatic amine
malathion Malathion: A wide spectrum aliphatic organophosphate insecticide widely used for both domestic and commercial agricultural purposes.. malathion : A racemate comprising equimolar amounts of (R) and (S)-malathion. It is a broad spectrum organophosphate proinsecticide used to control a wide range of pests including Coleoptera, Diptera, fruit flies, mosquitos and spider mites.. diethyl 2-[(dimethoxyphosphorothioyl)thio]succinate : A diester that is diethyl succinate in which position 2 is substituted by a (dimethoxyphosphorothioyl)thio group.	2.05	1	0	diester; ethyl ester; organic thiophosphate
diisopropyl 1,3-dithiol-2-ylidenemalonate diisopropyl 1,3-dithiol-2-ylidenemalonate: structure in first source	2.05	1	0	isopropyl ester
maprotiline Maprotiline: A bridged-ring tetracyclic antidepressant that is both mechanistically and functionally similar to the tricyclic antidepressants, including side effects associated with its use.	3.87	3	0	anthracenes
mazindol Mazindol: Tricyclic anorexigenic agent unrelated to and less toxic than AMPHETAMINE, but with some similar side effects. It inhibits uptake of catecholamines and blocks the binding of cocaine to the dopamine uptake transporter.	2.05	1	0	organic molecular entity
edaravone [no description available]	2.04	1	0	pyrazolone	antioxidant; radical scavenger
mebendazole Mebendazole: A benzimidazole that acts by interfering with CARBOHYDRATE METABOLISM and inhibiting polymerization of MICROTUBULES.. mebendazole : A carbamate ester that is methyl 1H-benzimidazol-2-ylcarbamate substituted by a benzoyl group at position 5.	4.08	4	0	aromatic ketone; benzimidazoles; carbamate ester	antinematodal drug; microtubule-destabilising agent; tubulin modulator
mecamylamine Mecamylamine: A nicotinic antagonist that is well absorbed from the gastrointestinal tract and crosses the blood-brain barrier. Mecamylamine has been used as a ganglionic blocker in treating hypertension, but, like most ganglionic blockers, is more often used now as a research tool.	3.23	1	0	primary aliphatic amine
mechlorethamine nitrogen mustard : Compounds having two beta-haloalkyl groups bound to a nitrogen atom, as in (X-CH2-CH2)2NR.	3.23	1	0	nitrogen mustard; organochlorine compound	alkylating agent
meclizine Meclizine: A histamine H1 antagonist used in the treatment of motion sickness, vertigo, and nausea during pregnancy and radiation sickness.	3.59	2	0	diarylmethane
meclofenamic acid Meclofenamic Acid: A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis.. meclofenamic acid : An aminobenzoic acid that is anthranilic acid in which one of the hydrogens attached to the nitrogen is replaced by a 2,6-dichloro-3-methylphenyl group. A non-steroidal anti-inflammatory drug, it is used as the sodium salt for the treatment of dysmenorrhoea (painful periods), osteoarthritis and rheumatoid arthritis.	3.23	1	0	aminobenzoic acid; organochlorine compound; secondary amino compound	analgesic; anticonvulsant; antineoplastic agent; antipyretic; antirheumatic drug; EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-steroidal anti-inflammatory drug
meclofenoxate Meclofenoxate: An ester of DIMETHYLAMINOETHANOL and para-chlorophenoxyacetic acid.	2.05	1	0	monocarboxylic acid
mefenamic acid Mefenamic Acid: A non-steroidal anti-inflammatory agent with analgesic, anti-inflammatory, and antipyretic properties. It is an inhibitor of cyclooxygenase.. mefenamic acid : An aminobenzoic acid that is anthranilic acid in which one of the hydrogens attached to the nitrogen is replaced by a 2,3-dimethylphenyl group. Although classed as a non-steroidal anti-inflammatory drug, its anti-inflammatory properties are considered to be minor. It is used to relieve mild to moderate pain, including headaches, dental pain, osteoarthritis and rheumatoid arthritis.	3.87	3	0	aminobenzoic acid; secondary amino compound	analgesic; antipyretic; antirheumatic drug; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; environmental contaminant; non-steroidal anti-inflammatory drug; xenobiotic
memantine [no description available]	3.23	1	0	adamantanes; primary aliphatic amine	antidepressant; antiparkinson drug; dopaminergic agent; neuroprotective agent; NMDA receptor antagonist
vitamin k 3 Vitamin K 3: A synthetic naphthoquinone without the isoprenoid side chain and biological activity, but can be converted to active vitamin K2, menaquinone, after alkylation in vivo.	2.05	1	0	1,4-naphthoquinones; vitamin K	angiogenesis inhibitor; antineoplastic agent; EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor; human urinary metabolite; nutraceutical
mepenzolate mepenzolic acid: anticholinergic, antispasmodic agent; RN given refers to parent cpd; structure	3.23	1	0	diarylmethane
meperidine Meperidine: A narcotic analgesic that can be used for the relief of most types of moderate to severe pain, including postoperative pain and the pain of labor. Prolonged use may lead to dependence of the morphine type; withdrawal symptoms appear more rapidly than with morphine and are of shorter duration.. pethidine : A piperidinecarboxylate ester that is piperidine which is substituted by a methyl group at position 1 and by phenyl and ethoxycarbonyl groups at position 4. It is an analgesic which is used for the treatment of moderate to severe pain, including postoperative pain and labour pain.	3.86	3	0	ethyl ester; piperidinecarboxylate ester; tertiary amino compound	antispasmodic drug; kappa-opioid receptor agonist; mu-opioid receptor agonist; opioid analgesic
mephenytoin Mephenytoin: An anticonvulsant effective in tonic-clonic epilepsy (EPILEPSY, TONIC-CLONIC). It may cause blood dyscrasias.. mephenytoin : An imidazolidine-2,4-dione (hydantoin) in which the imidazolidine nucleus carries a methyl group at N-3 and has ethyl and phenyl substituents at C-5. An anticonvulsant, it is no longer available in the USA or the UK but is still studied largely because of its interesting hydroxylation polymorphism.	3.59	2	0	imidazolidine-2,4-dione	anticonvulsant
mepivacaine Mepivacaine: A local anesthetic that is chemically related to BUPIVACAINE but pharmacologically related to LIDOCAINE. It is indicated for infiltration, nerve block, and epidural anesthesia. Mepivacaine is effective topically only in large doses and therefore should not be used by this route. (From AMA Drug Evaluations, 1994, p168). mepivacaine : A piperidinecarboxamide in which N-methylpipecolic acid and 2,6-dimethylaniline have combined to form the amide bond. It is used as a local amide-type anaesthetic.	3.86	3	0	piperidinecarboxamide	drug allergen; local anaesthetic
meprobamate Meprobamate: A carbamate with hypnotic, sedative, and some muscle relaxant properties, although in therapeutic doses reduction of anxiety rather than a direct effect may be responsible for muscle relaxation. Meprobamate has been reported to have anticonvulsant actions against petit mal seizures, but not against grand mal seizures (which may be exacerbated). It is used in the treatment of ANXIETY DISORDERS, and also for the short-term management of INSOMNIA but has largely been superseded by the BENZODIAZEPINES. (From Martindale, The Extra Pharmacopoeia, 30th ed, p603)	3.86	3	0	organic molecular entity
mesalamine Mesalamine: An anti-inflammatory agent, structurally related to the SALICYLATES, which is active in INFLAMMATORY BOWEL DISEASE. It is considered to be the active moiety of SULPHASALAZINE. (From Martindale, The Extra Pharmacopoeia, 30th ed). mesalamine : A monohydroxybenzoic acid that is salicylic acid substituted by an amino group at the 5-position.	3.86	3	0	amino acid; aromatic amine; monocarboxylic acid; monohydroxybenzoic acid; phenols	non-steroidal anti-inflammatory drug
mesoridazine Mesoridazine: A phenothiazine antipsychotic with effects similar to CHLORPROMAZINE.. mesoridazine : A phenothiazine substituted at position 2 (para to the S atom) by a methylsulfinyl group, and on the nitrogen by a 2-(1-methylpiperidin-2-yl)ethyl group.	3.23	1	0	phenothiazines; sulfoxide; tertiary amino compound	dopaminergic antagonist; first generation antipsychotic
metaproterenol Metaproterenol: A beta-2 adrenergic agonist used in the treatment of ASTHMA and BRONCHIAL SPASM.. orciprenaline : A racemate composed of equimolar amounts of (R)- and (S)-orciprenaline. Used (as its sulfate salt) to relax the airway muscles and improve breathing for patients suffering from asthma or bronchitis.. 5-[1-hydroxy-2-(isopropanylamino)ethyl]benzene-1,3-diol : A member of the class of resorcinols bearing an additional 1-hydroxy-2-(isopropanylamino)ethyl substituent at position 5 of resorcinol itself.	3.23	1	0	aralkylamino compound; phenylethanolamines; resorcinols; secondary alcohol; secondary amino compound
metformin Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289). metformin : A member of the class of guanidines that is biguanide the carrying two methyl substituents at position 1.	8.12	15	1	guanidines	environmental contaminant; geroprotector; hypoglycemic agent; xenobiotic
methadone Methadone: A synthetic opioid that is used as the hydrochloride. It is an opioid analgesic that is primarily a mu-opioid agonist. It has actions and uses similar to those of MORPHINE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1082-3). methadone : A racemate comprising equimolar amounts of dextromethadone and levomethadone. It is a opioid analgesic which is used as a painkiller and as a substitute for heroin in the treatment of heroin addiction.. 6-(dimethylamino)-4,4-diphenylheptan-3-one : A ketone that is heptan-3-one substituted by a dimethylamino group at position 6 and two phenyl groups at position 4.	3.86	3	0	benzenes; diarylmethane; ketone; tertiary amino compound
methapyrilene Methapyrilene: Histamine H1 antagonist with sedative action used as a hypnotic and in allergies.. methapyrilene : A member of the class of ethylenediamine derivatives that is ethylenediamine in which one of the nitrogens is substituted by two methyl groups, and the other nitrogen is substituted by a 2-pyridyl group and a (2-thienyl)methyl group.	2.04	1	0	ethylenediamine derivative	anti-allergic agent; carcinogenic agent; H1-receptor antagonist; sedative
methazolamide Methazolamide: A carbonic anhydrase inhibitor that is used as a diuretic and in the treatment of glaucoma.	3.73	2	0	sulfonamide; thiadiazoles
methocarbamol Methocarbamol: A centrally acting muscle relaxant whose mode of action has not been established. It is used as an adjunct in the symptomatic treatment of musculoskeletal conditions associated with painful muscle spasm. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1206). methocarbamol : A racemate comprising equimolar amounts of (R)- and (S)-methocarbamol. A centrally acting skeletal muscle relaxant, it is used as an adjunct in the short-term symptomatic treatment of painful muscle spasm. The (R)-enantiomer is more active than the (S)-enantiomer.. 2-hydroxy-3-(2-methoxyphenoxy)propyl carbamate : A carbamate ester that is glycerol in which one of the primary alcohol groups has been converted to its 2-methoxyphenyl ether while the other has been converted to the corresponding carbamate ester.	3.73	2	0	aromatic ether; carbamate ester; secondary alcohol
methoxsalen Methoxsalen: A naturally occurring furocoumarin compound found in several species of plants, including Psoralea corylifolia. It is a photoactive substance that forms DNA ADDUCTS in the presence of ultraviolet A irradiation.. methoxsalen : A member of the class of psoralens that is 7H-furo[3,2-g]chromen-7-one in which the 9 position is substituted by a methoxy group. It is a constituent of the fruits of Ammi majus. Like other psoralens, trioxsalen causes photosensitization of the skin. It is administered topically or orally in conjunction with UV-A for phototherapy treatment of vitiligo and severe psoriasis.	3.59	2	0	aromatic ether; psoralens	antineoplastic agent; cross-linking reagent; dermatologic drug; photosensitizing agent; plant metabolite
methoxyflurane Methoxyflurane: An inhalation anesthetic. Currently, methoxyflurane is rarely used for surgical, obstetric, or dental anesthesia. If so employed, it should be administered with NITROUS OXIDE to achieve a relatively light level of anesthesia, and a neuromuscular blocking agent given concurrently to obtain the desired degree of muscular relaxation. (From AMA Drug Evaluations Annual, 1994, p180). methoxyflurane : An ether in which the two groups attached to the central oxygen atom are methyl and 2,2-dichloro-1,1-difluoroethyl.	2.05	1	0	ether; organochlorine compound; organofluorine compound	hepatotoxic agent; inhalation anaesthetic; nephrotoxic agent; non-narcotic analgesic
methyclothiazide Methyclothiazide: A thiazide diuretic with properties similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p825)	3.23	1	0	benzothiadiazine
nocodazole [no description available]	2.07	1	0	aromatic ketone; benzimidazoles; carbamate ester; thiophenes	antimitotic; antineoplastic agent; microtubule-destabilising agent; tubulin modulator
methyl salicylate methyl salicylate: used in over-the-counter liniments, ointments, lotions for relief of musculoskeletal aches and pains; has hemolytic effect on human & sheep erythrocytes; RN given refers to parent cpd; structure in Merck Index, 9th ed, #5990. methyl salicylate : A benzoate ester that is the methyl ester of salicylic acid.	2.05	1	0	benzoate ester; methyl ester; salicylates	flavouring agent; insect attractant; metabolite
methylphenidate Methylphenidate: A central nervous system stimulant used most commonly in the treatment of ATTENTION DEFICIT DISORDER in children and for NARCOLEPSY. Its mechanisms appear to be similar to those of DEXTROAMPHETAMINE. The d-isomer of this drug is referred to as DEXMETHYLPHENIDATE HYDROCHLORIDE.. methylphenidate : A racemate comprising equimolar amounts of the two threo isomers of methyl phenyl(piperidin-2-yl)acetate. A central stimulant and indirect-acting sympathomimetic, is used (generally as the hydrochloride salt) in the treatment of hyperactivity disorders in children and for the treatment of narcolepsy.. methyl phenyl(piperidin-2-yl)acetate : A amino acid ester that is methyl phenylacetate in which one of the hydrogens alpha to the carbonyl group is replaced by a piperidin-2-yl group.	3.86	3	0	beta-amino acid ester; methyl ester; piperidines
methyprylon methyprylon: was heading 1973-94 (see under HYPNOTICS AND SEDATIVES 1963-72); use PIPERIDONES to search METHYPRYLON 1973-94	2.05	1	0	organic molecular entity
metoclopramide Metoclopramide: A dopamine D2 antagonist that is used as an antiemetic.. metoclopramide : A member of the class of benzamides resulting from the formal condensation of 4-amino-5-chloro-2-methoxybenzoic acid with the primary amino group of N,N-diethylethane-1,2-diamine.	4.08	4	0	benzamides; monochlorobenzenes; substituted aniline; tertiary amino compound	antiemetic; dopaminergic antagonist; environmental contaminant; gastrointestinal drug; xenobiotic
metolazone Metolazone: A quinazoline-sulfonamide derived DIURETIC that functions by inhibiting SODIUM CHLORIDE SYMPORTERS.. metolazone : A quinazoline that consists of 1,2,3,4-tetrahydroquinazolin-4-one bearing additional methyl, 2-tolyl, sulfamyl and chloro substituents at positions 2, 3, 6 and 7 respectively. A quinazoline diuretic, with properties similar to thiazide diuretics.	3.58	2	0	organochlorine compound; quinazolines; sulfonamide	antihypertensive agent; diuretic; ion transport inhibitor
metoprolol Metoprolol: A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.. metoprolol : A propanolamine that is 1-(propan-2-ylamino)propan-2-ol substituted by a 4-(2-methoxyethyl)phenoxy group at position 1.	4.08	4	0	aromatic ether; propanolamine; secondary alcohol; secondary amino compound	antihypertensive agent; beta-adrenergic antagonist; environmental contaminant; geroprotector; xenobiotic
metronidazole Metronidazole: A nitroimidazole used to treat AMEBIASIS; VAGINITIS; TRICHOMONAS INFECTIONS; GIARDIASIS; ANAEROBIC BACTERIA; and TREPONEMAL INFECTIONS.. metronidazole : A member of the class of imidazoles substituted at C-1, -2 and -5 with 2-hydroxyethyl, nitro and methyl groups respectively. It has activity against anaerobic bacteria and protozoa, and has a radiosensitising effect on hypoxic tumour cells. It may be given by mouth in tablets, or as the benzoate in an oral suspension. The hydrochloride salt can be used in intravenous infusions. Metronidazole is a prodrug and is selective for anaerobic bacteria due to their ability to intracellularly reduce the nitro group of metronidazole to give nitroso-containing intermediates. These can covalently bind to DNA, disrupting its helical structure, inducing DNA strand breaks and inhibiting bacterial nucleic acid synthesis, ultimately resulting in bacterial cell death.	4.26	5	0	C-nitro compound; imidazoles; primary alcohol	antiamoebic agent; antibacterial drug; antimicrobial agent; antiparasitic agent; antitrichomonal drug; environmental contaminant; prodrug; radiosensitizing agent; xenobiotic
metyrapone Metyrapone: An inhibitor of the enzyme STEROID 11-BETA-MONOOXYGENASE. It is used as a test of the feedback hypothalamic-pituitary mechanism in the diagnosis of CUSHING SYNDROME.. metyrapone : An aromatic ketone that is 3,3-dimethylbutan-2-one in which the methyl groups at positions 1 and 4 are replaced by pyridin-3-yl groups. A steroid 11beta-monooxygenase (EC 1.14.15.4) inhibitor, it is used in the diagnosis of adrenal insufficiency.	3.59	2	0	aromatic ketone	antimetabolite; diagnostic agent; EC 1.14.15.4 (steroid 11beta-monooxygenase) inhibitor
mexiletine Mexiletine: Antiarrhythmic agent pharmacologically similar to LIDOCAINE. It may have some anticonvulsant properties.. mexiletine : An aromatic ether which is 2,6-dimethylphenyl ether of 2-aminopropan-1-ol.	4.1	4	0	aromatic ether; primary amino compound	anti-arrhythmia drug
mianserin Mianserin: A tetracyclic compound with antidepressant effects. It may cause drowsiness and hematological problems. Its mechanism of therapeutic action is not well understood, although it apparently blocks alpha-adrenergic, histamine H1, and some types of serotonin receptors.. mianserin : A dibenzoazepine (specifically 1,2,3,4,10,14b-hexahydrodibenzo[c,f]pyrazino[1,2-a]azepine) methyl-substituted on N-2. Closely related to (and now mostly superseded by) the tetracyclic antidepressant mirtazapinean, it is an atypical antidepressant used in the treatment of depression throughout Europe and elsewhere.	2.05	1	0	dibenzoazepine	adrenergic uptake inhibitor; alpha-adrenergic antagonist; antidepressant; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; geroprotector; H1-receptor antagonist; histamine agonist; sedative; serotonergic antagonist
miconazole Miconazole: An imidazole antifungal agent that is used topically and by intravenous infusion.. 1-[2-(2,4-dichlorobenzyloxy)-2-(2,4-dichlorophenyl)ethyl]imidazole : A member of the class of imidazoles that is 1-(2,4-dichlorophenyl)-2-(imidazol-1-yl)ethanol in which the hydroxyl hydrogen is replaced by a 2,4-dichlorobenzyl group.. miconazole : A racemate composed of equimolar amounts of (R)- and (S)-miconazole. Used (as its nitrate salt) to treat skin infections such as athlete's foot, jock itch, ringworm and other fungal skin infections. It inhibits the synthesis of ergosterol, a critical component of fungal cell membranes.	2.05	1	0	dichlorobenzene; ether; imidazoles
midazolam Midazolam: A short-acting hypnotic-sedative drug with anxiolytic and amnestic properties. It is used in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. The short duration and cardiorespiratory stability makes it useful in poor-risk, elderly, and cardiac patients. It is water-soluble at pH less than 4 and lipid-soluble at physiological pH.. midazolam : An imidazobenzodiazepine that is 4H-imidazo[1,5-a][1,4]benzodiazepine which is substituted by a methyl, 2-fluorophenyl and chloro groups at positions 1, 6 and 8, respectively.	4.08	4	0	imidazobenzodiazepine; monofluorobenzenes; organochlorine compound	anticonvulsant; antineoplastic agent; anxiolytic drug; apoptosis inducer; central nervous system depressant; GABAA receptor agonist; general anaesthetic; muscle relaxant; sedative
midodrine Midodrine: An ethanolamine derivative that is an adrenergic alpha-1 agonist. It is used as a vasoconstrictor agent in the treatment of HYPOTENSION.. midodrine : An aromatic ether that is 1,4-dimethoxybenzene which is substituted at position 2 by a 2-(glycylamino)-1-hydroxyethyl group. A direct-acting sympathomimetic with selective alpha-adrenergic agonist activity, it is used (generally as its hydrochloride salt) as a peripheral vasoconstrictor in the treatment of certain hypotensive states. The main active moiety is its major metabolite, deglymidodrine.	3.23	1	0	amino acid amide; aromatic ether; secondary alcohol	alpha-adrenergic agonist; prodrug; sympathomimetic agent; vasoconstrictor agent
milrinone [no description available]	3.58	2	0	bipyridines; nitrile; pyridone	cardiotonic drug; EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor; platelet aggregation inhibitor; vasodilator agent
minoxidil Minoxidil: A potent direct-acting peripheral vasodilator (VASODILATOR AGENTS) that reduces peripheral resistance and produces a fall in BLOOD PRESSURE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p371). minoxidil : A pyrimidine N-oxide that is pyrimidine-2,4-diamine 3-oxide substituted by a piperidin-1-yl group at position 6.	3.87	3	0	dialkylarylamine; tertiary amino compound
mirtazapine Mirtazapine: A piperazinoazepine tetracyclic compound that enhances the release of NOREPINEPHRINE and SEROTONIN through blockage of presynaptic ALPHA-2 ADRENERGIC RECEPTORS. It also blocks both 5-HT2 and 5-HT3 serotonin receptors and is a potent HISTAMINE H1 RECEPTOR antagonist. It is used for the treatment of depression, and may also be useful for the treatment of anxiety disorders.	4.29	5	0	benzazepine; tetracyclic antidepressant	alpha-adrenergic antagonist; anxiolytic drug; H1-receptor antagonist; histamine antagonist; oneirogen; serotonergic antagonist
mitotane Mitotane: A derivative of the insecticide DICHLORODIPHENYLDICHLOROETHANE that specifically inhibits cells of the adrenal cortex and their production of hormones. It is used to treat adrenocortical tumors and causes CNS damage, but no bone marrow depression.	3.89	3	0	diarylmethane
mitoxantrone Mitoxantrone: An anthracenedione-derived antineoplastic agent.. mitoxantrone : A dihydroxyanthraquinone that is 1,4-dihydroxy-9,10-anthraquinone which is substituted by 6-hydroxy-1,4-diazahexyl groups at positions 5 and 8.	7.31	17	0	dihydroxyanthraquinone	analgesic; antineoplastic agent
moclobemide Moclobemide: A reversible inhibitor of monoamine oxidase type A; (RIMA); (see MONOAMINE OXIDASE INHIBITORS) that has antidepressive properties.. moclobemide : A member of the class of benzamides that is benzamide substituted by a chloro group at position 4 and a 2-(morpholin-4-yl)ethyl group at the nitrogen atom. It acts as a reversible monoamine oxidase inhibitor and is used in the treatment of depression.	2.46	2	0	benzamides; monochlorobenzenes; morpholines	antidepressant; environmental contaminant; xenobiotic
modafinil Modafinil: A benzhydryl acetamide compound, central nervous system stimulant, and CYP3A4 inducing agent that is used in the treatment of NARCOLEPSY and SLEEP WAKE DISORDERS.. modafinil : A racemate comprising equimolar amounts of armodafinil and (S)-modafinil. A central nervous system stimulant, it is used for the treatment of sleeping disorders such as narcolepsy, obstructive sleep apnoea, and shift-work sleep disorder. The optical enantiomers of modafinil have similar pharmacological actions in animals.. 2-[(diphenylmethyl)sulfinyl]acetamide : A sulfoxide that is dimethylsulfoxide in which two hydrogens attached to one of the methyl groups are replaced by phenyl groups, while one hydrogen attached to the other methyl group is replaced by a carbamoyl (aminocarbonyl) group.	3.59	2	0	monocarboxylic acid amide; sulfoxide
mofezolac mofezolac: Cyclooxygenase 1 inhibitor; structure in first source; RN from Toxlit	7.21	1	0	methoxybenzenes
moxisylyte Moxisylyte: An alpha-adrenergic blocking agent that is used in Raynaud's disease. It is also used locally in the eye to reverse the mydriasis caused by phenylephrine and other sympathomimetic agents. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1312)	3.59	2	0	monoterpenoid
entinostat [no description available]	9.42	7	0	benzamides; carbamate ester; primary amino compound; pyridines; substituted aniline	antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor
deet N,N-diethyl-m-toluamide : A monocarboxylic acid amide resulting from the formal condensation of the carboxy group of m-toluic acid with the nitrogen of diethylamine. First developed by the U.S. Army in 1946 for use by military personnel in insect-infested areas, it is the most widely used insect repellent worldwide.	2.05	1	0	benzamides; monocarboxylic acid amide	environmental contaminant; insect repellent; xenobiotic
acecainide Acecainide: A major metabolite of PROCAINAMIDE. Its anti-arrhythmic action may cause cardiac toxicity in kidney failure.. N-acetylprocainamide : A benzamide obtained via formal condensation of 4-acetamidobenzoic acid and 2-(diethylamino)ethylamine.	2.46	2	0	acetamides; benzamides	anti-arrhythmia drug
ethylmaleimide Ethylmaleimide: A sulfhydryl reagent that is widely used in experimental biochemical studies.	2.6	1	0	maleimides	anticoronaviral agent; EC 1.3.1.8 [acyl-CoA dehydrogenase (NADP(+))] inhibitor; EC 2.1.1.122 [(S)-tetrahydroprotoberberine N-methyltransferase] inhibitor; EC 2.7.1.1 (hexokinase) inhibitor
nabumetone Nabumetone: A butanone non-steroidal anti-inflammatory drug and cyclooxygenase-2 (COX2) inhibitor that is used in the management of pain associated with OSTEOARTHRITIS and RHEUMATOID ARTHRITIS.. nabumetone : A methyl ketone that is 2-butanone in which one of the methyl hydrogens at position 4 is replaced by a 6-methoxy-2-naphthyl group. A prodrug that is converted to the active metabolite, 6-methoxy-2-naphthylacetic acid, following oral administration. It is shown to have a slightly lower risk of gastrointestinal side effects than most other non-steroidal anti-inflammatory drugs.	3.93	3	0	methoxynaphthalene; methyl ketone	cyclooxygenase 2 inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug; prodrug
nadolol [no description available]	3.61	2	0	tetralins
nafamostat nafamostat: inhibitor of trypsin, plasmin, pancreatic kallikrein, plasma kallikrein & thrombin; strongly inhibits esterolytic activities of C1r & C1 esterase complement-mediated hemolysis; antineoplastic	3.71	2	0	benzoic acids; guanidines
nalidixic acid [no description available]	3.87	3	0	1,8-naphthyridine derivative; monocarboxylic acid; quinolone antibiotic	antibacterial drug; antimicrobial agent; DNA synthesis inhibitor
naratriptan naratriptan: structure given in first source	3.58	2	0	heteroarylpiperidine; sulfonamide; tryptamines	serotonergic agonist; vasoconstrictor agent
nefazodone nefazodone: may be useful as an opiate adjunct	4.08	4	0	aromatic ether; monochlorobenzenes; N-alkylpiperazine; N-arylpiperazine; triazoles	alpha-adrenergic antagonist; analgesic; antidepressant; serotonergic antagonist; serotonin uptake inhibitor
nefopam Nefopam: Non-narcotic analgesic chemically similar to ORPHENADRINE. Its mechanism of action is unclear. It is used for the relief of acute and chronic pain. (From Martindale, The Extra Pharmacopoeia, 30th ed, p26). nefopam : A racemate comprising equal amounts of (R)- and (S)-nefopam. The hydrochloride is a centrally acting non-opiate analgesic commonly used for the treatment of moderate to severe pain.. 5-methyl-1-phenyl-3,4,5,6-tetrahydro-1H-2,5-benzoxazocine : A member of the class of benzoxazocines that is 3,4,5,6-tetrahydro-1H-2,5-benzoxazocine substituted by phenyl and methyl groups at positions 1 and 5 respectively.	2.46	2	0	benzoxazocine; tertiary amino compound
neostigmine Neostigmine: A cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike PHYSOSTIGMINE, does not cross the blood-brain barrier.. neostigmine : A quaternary ammonium ion comprising an anilinium ion core having three methyl substituents on the aniline nitrogen, and a 3-[(dimethylcarbamoyl)oxy] substituent at position 3. It is a parasympathomimetic which acts as a reversible acetylcholinesterase inhibitor.	2.08	1	0	quaternary ammonium ion	antidote to curare poisoning; EC 3.1.1.7 (acetylcholinesterase) inhibitor
nevirapine Nevirapine: A potent, non-nucleoside reverse transcriptase inhibitor used in combination with nucleoside analogues for treatment of HIV INFECTIONS and AIDS.. nevirapine : A dipyridodiazepine that is 5,11-dihydro-6H-dipyrido[3,2-b:2',3'-e][1,4]diazepine which is substituted by methyl, oxo, and cyclopropyl groups at positions 4, 6, and 11, respectively. A non-nucleoside reverse transcriptase inhibitor with activity against HIV-1, it is used in combination with other antiretrovirals for the treatment of HIV infection.	4.29	5	0	cyclopropanes; dipyridodiazepine	antiviral drug; HIV-1 reverse transcriptase inhibitor
nialamide Nialamide: An MAO inhibitor that is used as an antidepressive agent.	3.59	2	0	organonitrogen compound; organooxygen compound
nicardipine Nicardipine: A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents.. nicardipine : A racemate comprising equimolar amounts of (R)- and (S)-nicardipine. It is a calcium channel blocker which is used to treat hypertension.. 2-[benzyl(methyl)amino]ethyl methyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate : A dihydropyridine that is 1,4-dihydropyridine substituted by a methyl, {2-[benzyl(methyl)amino]ethoxy}carbonyl, 3-nitrophenyl, methoxycarbonyl and methyl groups at positions 2, 3, 4, 5 and 6, respectively.	3.87	3	0	benzenes; C-nitro compound; diester; dihydropyridine; methyl ester; tertiary amino compound
niceritrol Niceritrol: An ester of nicotinic acid that lowers cholesterol and triglycerides in total plasma and in the VLD- and LD-lipoprotein fractions.	2.05	1	0	organic molecular entity
nifedipine Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.	4.08	4	0	C-nitro compound; dihydropyridine; methyl ester	calcium channel blocker; human metabolite; tocolytic agent; vasodilator agent
niflumic acid Niflumic Acid: An analgesic and anti-inflammatory agent used in the treatment of rheumatoid arthritis.	2.05	1	0	aromatic carboxylic acid; pyridines
nilutamide [no description available]	3.59	2	0	(trifluoromethyl)benzenes; C-nitro compound; imidazolidinone	androgen antagonist; antineoplastic agent
nimesulide nimesulide: structure. nimesulide : An aromatic ether having phenyl and 2-methylsulfonamido-5-nitrophenyl as the two aryl groups.	4.11	4	0	aromatic ether; C-nitro compound; sulfonamide	cyclooxygenase 2 inhibitor; non-steroidal anti-inflammatory drug
nimodipine Nimodipine: A calcium channel blockader with preferential cerebrovascular activity. It has marked cerebrovascular dilating effects and lowers blood pressure.. nimodipine : A dihydropyridine that is 1,4-dihydropyridine which is substituted by methyl groups at positions 2 and 6, a (2-methoxyethoxy)carbonyl group at position 3, a m-nitrophenyl group at position 4, and an isopropoxycarbonyl group at position 5. An L-type calcium channel blocker, it acts particularly on cerebral circulation, and is used both orally and intravenously for the prevention and treatment of subarachnoid hemorrhage from ruptured intracranial aneurysm.	4.28	5	0	2-methoxyethyl ester; C-nitro compound; dicarboxylic acids and O-substituted derivatives; diester; dihydropyridine; isopropyl ester	antihypertensive agent; calcium channel blocker; cardiovascular drug; vasodilator agent
nisoldipine Nisoldipine: A dihydropyridine calcium channel antagonist that acts as a potent arterial vasodilator and antihypertensive agent. It is also effective in patients with cardiac failure and angina.. nisoldipine : A racemate consisting of equimolar amounts of (R)- and (S)-nisoldipine. A calcium channel blocker, it is used in the treatment of hypertension and angina pectoris.. methyl 2-methylpropyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate : A dihydropyridine that is 1,4-dihydropyridine which is substituted by methyl groups at positions 2 and 6, a methoxycarbonyl group at position 3, an o-nitrophenyl group at position 4, and an isobutoxycarbonyl group at position 5. The racemate, a calcium channel blocker, is used in the treatment of hypertension and angina pectoris.	4.08	4	0	C-nitro compound; dicarboxylic acids and O-substituted derivatives; diester; dihydropyridine; methyl ester
nitrazepam Nitrazepam: A benzodiazepine derivative used as an anticonvulsant and hypnotic.. nitrazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one which is substituted at positions 5 and 7 by phenyl and nitro groups, respectively. It is used as a hypnotic for the short-term management of insomnia and for the treatment of epileptic spasms in infants (West's syndrome).	2.75	3	0	1,4-benzodiazepinone; C-nitro compound	anticonvulsant; antispasmodic drug; drug metabolite; GABA modulator; sedative
nitrendipine Nitrendipine: A calcium channel blocker with marked vasodilator action. It is an effective antihypertensive agent and differs from other calcium channel blockers in that it does not reduce glomerular filtration rate and is mildly natriuretic, rather than sodium retentive.. nitrendipine : A dihydropyridine that is 1,4-dihydropyridine substituted by methyl groups at positions 2 and 6, a 3-nitrophenyl group at position 4, a ethoxycarbonyl group at position 3 and a methoxycarbonyl group at position 5. It is a calcium-channel blocker used in the treatment of hypertension.	2.75	3	0	C-nitro compound; dicarboxylic acids and O-substituted derivatives; diester; dihydropyridine; ethyl ester; methyl ester	antihypertensive agent; calcium channel blocker; geroprotector; vasodilator agent
nitroglycerin Nitroglycerin: A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.. nitroglycerol : A nitrate ester that is glycerol in which nitro group(s) replace the hydrogen(s) attached to one or more of the hydroxy groups.. nitroglycerin : A nitroglycerol that is glycerol in which the hydrogen atoms of all three hydroxy groups are replaced by nitro groups. It acts as a prodrug, releasing nitric oxide to open blood vessels and so alleviate heart pain.	3.87	3	0	nitroglycerol	explosive; muscle relaxant; nitric oxide donor; prodrug; tocolytic agent; vasodilator agent; xenobiotic
nizatidine [no description available]	3.86	3	0	1,3-thiazoles; C-nitro compound; carboxamidine; organic sulfide; tertiary amino compound	anti-ulcer drug; cholinergic drug; H2-receptor antagonist
nomifensine Nomifensine: An isoquinoline derivative that prevents dopamine reuptake into synaptosomes. The maleate was formerly used in the treatment of depression. It was withdrawn worldwide in 1986 due to the risk of acute hemolytic anemia with intravascular hemolysis resulting from its use. In some cases, renal failure also developed. (From Martindale, The Extra Pharmacopoeia, 30th ed, p266). nomifensine : An N-methylated tetrahydroisoquinoline carrying phenyl and amino substituents at positions C-4 and C-8, respectively.	3.58	2	0	isoquinolines	dopamine uptake inhibitor
masoprocol nordihydroguaretic acid: antioxidant compound found in the creosote bush (Larrea tridentata)	2.05	1	0	catechols; lignan; tetrol	antioxidant; ferroptosis inhibitor; geroprotector; plant metabolite
norfloxacin Norfloxacin: A synthetic fluoroquinolone (FLUOROQUINOLONES) with broad-spectrum antibacterial activity against most gram-negative and gram-positive bacteria. Norfloxacin inhibits bacterial DNA GYRASE.. norfloxacin : A quinolinemonocarboxylic acid with broad-spectrum antibacterial activity against most gram-negative and gram-positive bacteria. Norfloxacin is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase.	3.87	3	0	fluoroquinolone antibiotic; N-arylpiperazine; quinolinemonocarboxylic acid; quinolone antibiotic; quinolone	antibacterial drug; DNA synthesis inhibitor; environmental contaminant; xenobiotic
nortriptyline Nortriptyline: A metabolite of AMITRIPTYLINE that is also used as an antidepressive agent. Nortriptyline is used in major depression, dysthymia, and atypical depressions.. nortriptyline : An organic tricyclic compound that is 10,11-dihydro-5H-dibenzo[a,d][7]annulene substituted by a 3-(methylamino)propylidene group at position 5. It is an active metabolite of amitriptyline.	4.08	4	0	organic tricyclic compound; secondary amine	adrenergic uptake inhibitor; analgesic; antidepressant; antineoplastic agent; apoptosis inducer; drug metabolite
n-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide: structure given in first source. NS-398 : A C-nitro compound that is N-methylsulfonyl-4-nitroaniline bearing an additional cyclohexyloxy substituent at position 2.	2.08	1	0	aromatic ether; C-nitro compound; sulfonamide	antineoplastic agent; cyclooxygenase 2 inhibitor
ofloxacin Ofloxacin: A synthetic fluoroquinolone antibacterial agent that inhibits the supercoiling activity of bacterial DNA GYRASE, halting DNA REPLICATION.. 9-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid : An oxazinoquinoline that is 2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinolin-7-one substituted by methyl, carboxy, fluoro, and 4-methylpiperazin-1-yl groups at positions 3, 6, 9, and 10, respectively.. ofloxacin : A racemate comprising equimolar amounts of levofloxacin and dextrofloxacin. It is a synthetic fluoroquinolone antibacterial agent which inhibits the supercoiling activity of bacterial DNA gyrase, halting DNA replication.	6.01	4	1	3-oxo monocarboxylic acid; N-arylpiperazine; N-methylpiperazine; organofluorine compound; oxazinoquinoline
olprinone olprinone: RN refers to HCl; structure given in first source	2.08	1	0	bipyridines
omeprazole Omeprazole: A 4-methoxy-3,5-dimethylpyridyl, 5-methoxybenzimidazole derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits an H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.. omeprazole : A racemate comprising equimolar amounts of (R)- and (S)-omeprazole.. 5-methoxy-2-{[(4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl}-1H-benzimidazole : A member of the class of benzimidazoles that is 1H-benzimidazole which is substituted by a [4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl group at position 2 and a methoxy group at position 5.	11.08	8	1	aromatic ether; benzimidazoles; pyridines; sulfoxide
ondansetron Ondansetron: A competitive serotonin type 3 receptor antagonist. It is effective in the treatment of nausea and vomiting caused by cytotoxic chemotherapy drugs, including cisplatin, and has reported anxiolytic and neuroleptic properties.	4.08	4	0	carbazoles
orphenadrine Orphenadrine: A muscarinic antagonist used to treat drug-induced parkinsonism and to relieve pain from muscle spasm.. orphenadrine : A tertiary amino compound which is the phenyl-o-tolylmethyl ether of 2-(dimethylamino)ethanol.	3.59	2	0	ether; tertiary amino compound	antidyskinesia agent; antiparkinson drug; H1-receptor antagonist; muscarinic antagonist; muscle relaxant; NMDA receptor antagonist; parasympatholytic
osalmide osalmide: structure	2.6	1	0	organic molecular entity
oxonic acid Oxonic Acid: Antagonist of urate oxidase.	3.12	1	0	1,3,5-triazines; monocarboxylic acid
oxamniquine Oxamniquine: An anthelmintic with schistosomicidal activity against Schistosoma mansoni, but not against other Schistosoma spp. Oxamniquine causes worms to shift from the mesenteric veins to the liver where the male worms are retained; the female worms return to the mesentery, but can no longer release eggs. (From Martindale, The Extra Pharmacopoeia, 31st ed, p121). oxamniquine : A racemate comprising equimolar amounts of (R)- and (S)-oxamniquine. An anthelmintic, it is administered orally for the treatment of schistomiasis caused by Schistosoma mansoni (but not by other Schistosoma species); intramuscular administration is no longer used as it causes severe pain at the injection site.. {2-[(isopropylamino)methyl]-7-nitro-1,2,3,4-tetrahydroquinolin-6-yl}methanol : A member of the class of quinolines that is 1,2,3,4-tetrahydroquinoline which is substituted at positions 2, 6, and 7 by (isopropylamino)methyl, hydroxymethyl, and nitro groups, respectively.	2.05	1	0	aromatic primary alcohol; C-nitro compound; quinolines; secondary amino compound
oxaprozin Oxaprozin: An oxazole-propionic acid derivative, cyclooxygenase inhibitor, and non-steroidal anti-inflammatory drug that is used in the treatment of pain and inflammation associated with of OSTEOARTHRITIS; RHEUMATOID ARTHRITIS; and ARTHRITIS, JUVENILE.. oxaprozin : A monocarboxylic acid that is a propionic acid derivative having a 4,5-diphenyl-1,3-oxazol-2-yl substituent at position 3. It is non-steroidal anti-inflammatory drug commonly used to relieve the pain and inflammatory responses associated with osteoarthritis and rheumatoid arthritis.	3.87	3	0	1,3-oxazoles; monocarboxylic acid	analgesic; non-steroidal anti-inflammatory drug
oxazepam Oxazepam: A benzodiazepine used in the treatment of anxiety, alcohol withdrawal, and insomnia.. oxazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a chloro group at position 7, a hydroxy group at position 3 and phenyl group at position 5.	3.86	3	0	1,4-benzodiazepinone; organochlorine compound	anxiolytic drug; environmental contaminant; xenobiotic
oxethazaine [no description available]	2.54	2	0	amino acid amide
oxiracetam oxiracetam: structure in first source	2.04	1	0	organonitrogen compound; organooxygen compound
oxprenolol Oxprenolol: A beta-adrenergic antagonist used in the treatment of hypertension, angina pectoris, arrhythmias, and anxiety.	2.05	1	0	aromatic ether
oxybenzone oxybenzone : A hydroxybenzophenone that is benzophenone which is substituted at the 2- and 4-positions of one of the benzene rings by hydroxy and methoxy groups respectively.	2.05	1	0	hydroxybenzophenone; monomethoxybenzene	dermatologic drug; environmental contaminant; protective agent; ultraviolet filter; xenobiotic
oxybutynin oxybutynin: RN given refers to parent cpd. oxybutynin : A racemate comprising equimolar amounts of (R)-oxybutynin and esoxybutynin. An antispasmodic used for the treatment of overactive bladder.	3.87	3	0	acetylenic compound; carboxylic ester; racemate; tertiary alcohol; tertiary amino compound	antispasmodic drug; calcium channel blocker; local anaesthetic; muscarinic antagonist; muscle relaxant; parasympatholytic
oxyphenbutazone Oxyphenbutazone: A non-steroidal anti-inflammatory drug. Oxyphenbutazone eyedrops have been used abroad in the management of postoperative ocular inflammation, superficial eye injuries, and episcleritis. (From AMA, Drug Evaluations Annual, 1994, p2000) It had been used by mouth in rheumatic disorders such as ankylosing spondylitis, osteoarthritis, and rheumatoid arthritis but such use is no longer considered justified owing to the risk of severe hematological adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p27). oxyphenbutazone : A metabolite of phenylbutazone obtained by hydroxylation at position 4 of one of the phenyl rings. Commonly used (as its hydrate) to treat pain, swelling and stiffness associated with arthritis and gout, it was withdrawn from the market 1984 following association with blood dyscrasis and Stevens-Johnson syndrome.	2.05	1	0	phenols; pyrazolidines	antimicrobial agent; antineoplastic agent; antipyretic; drug metabolite; gout suppressant; non-narcotic analgesic; non-steroidal anti-inflammatory drug; xenobiotic metabolite
aminosalicylic acid Aminosalicylic Acid: An antitubercular agent often administered in association with ISONIAZID. The sodium salt of the drug is better tolerated than the free acid.. 4-aminosalicylic acid : An aminobenzoic acid that is salicylic acid substituted by an amino group at position 4.	3.59	2	0	aminobenzoic acid; phenols	antitubercular agent
palmidrol palmidrol: a cannabinoid receptor-inactive eCB-related molecule used as prophylactic in helping to prevent respiratory viral infection. palmitoyl ethanolamide : An N-(long-chain-acyl)ethanolamine that is the ethanolamide of palmitic (hexadecanoic) acid.	2.6	1	0	endocannabinoid; N-(long-chain-acyl)ethanolamine; N-(saturated fatty acyl)ethanolamine	anti-inflammatory drug; anticonvulsant; antihypertensive agent; neuroprotective agent
pamidronate [no description available]	5.37	7	0	phosphonoacetic acid
pantoprazole Pantoprazole: 2-pyridinylmethylsulfinylbenzimidazole proton pump inhibitor that is used in the treatment of GASTROESOPHAGEAL REFLUX and PEPTIC ULCER.. pantoprazole : A member of the class of benzimidazoles that is 1H-benzimidazole substituted by a difluoromethoxy group at position 5 and a [(3,4-dimethoxypyridin-2-yl)methyl]sulfinyl group at position 2.	3.86	3	0	aromatic ether; benzimidazoles; organofluorine compound; pyridines; sulfoxide	anti-ulcer drug; EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor; environmental contaminant; xenobiotic
papaverine Papaverine: An alkaloid found in opium but not closely related to the other opium alkaloids in its structure or pharmacological actions. It is a direct-acting smooth muscle relaxant used in the treatment of impotence and as a vasodilator, especially for cerebral vasodilation. The mechanism of its pharmacological actions is not clear, but it apparently can inhibit phosphodiesterases and it may have direct actions on calcium channels.. papaverine : A benzylisoquinoline alkaloid that is isoquinoline substituted by methoxy groups at positions 6 and 7 and a 3,4-dimethoxybenzyl group at position 1. It has been isolated from Papaver somniferum.	4.13	4	0	benzylisoquinoline alkaloid; dimethoxybenzene; isoquinolines	antispasmodic drug; vasodilator agent
pd 153035 4-((3-bromophenyl)amino)-6,7-dimethoxyquinazoline: structure given in first source. PD-153035 : A member of the class of quinazolines carrying a 3-bromophenylamino substituent at position 4 and two methoxy substituents at positions 6 and 7.	2.03	1	0	aromatic amine; aromatic ether; bromobenzenes; quinazolines; secondary amino compound	EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; epidermal growth factor receptor antagonist
pd168393 PD 168393 : A member of the class of quinazolines carrying bromoanilino and acrylamido substituents at positions 4 and 6 respectively.	2.03	1	0	acrylamides; bromobenzenes; quinazolines; secondary carboxamide; substituted aniline	epidermal growth factor receptor antagonist
pd 98059 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one: inhibits MAP kinase kinase (MEK) activity, p42 MAPK and p44 MAPK; structure in first source. 2-(2-amino-3-methoxyphenyl)chromen-4-one : A member of the class of monomethoxyflavones that is 3'-methoxyflavone bearing an additional amino substituent at position 2'.	2.79	3	0	aromatic amine; monomethoxyflavone	EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor; geroprotector
pemoline Pemoline: A central nervous system stimulant used in fatigue and depressive states and to treat hyperkinetic disorders in children.. pemoline : A member of the class of 1,3-oxazoles that is 1,3-oxazol-4(5H)-one which is substituted by an amino group at position 2 and by a phenyl group at position 5. A central nervous system stimulant, it was used to treat hyperactivity disorders in children, but withdrawn from use following reports of serious hepatotoxicity.	3.87	3	0	1,3-oxazoles	central nervous system stimulant
pentamidine Pentamidine: Antiprotozoal agent effective in trypanosomiasis, leishmaniasis, and some fungal infections; used in treatment of PNEUMOCYSTIS pneumonia in HIV-infected patients. It may cause diabetes mellitus, central nervous system damage, and other toxic effects.. pentamidine : A diether consisting of pentane-1,5-diol in which both hydroxyl hydrogens have been replaced by 4-amidinophenyl groups. A trypanocidal drug that is used for treatment of cutaneous leishmaniasis and Chagas disease.	3.87	3	0	aromatic ether; carboxamidine; diether	anti-inflammatory agent; antifungal agent; calmodulin antagonist; chemokine receptor 5 antagonist; EC 2.3.1.48 (histone acetyltransferase) inhibitor; NMDA receptor antagonist; S100 calcium-binding protein B inhibitor; trypanocidal drug; xenobiotic
pentobarbital Pentobarbital: A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236). pentobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by ethyl and sec-pentyl groups.	3.86	3	0	barbiturates	GABAA receptor agonist
pentoxifylline [no description available]	4.29	5	0	oxopurine
perazine Perazine: A phenothiazine antipsychotic with actions and uses similar to those of CHLORPROMAZINE. Extrapyramidal symptoms may be more common than other side effects.. perazine : A phenothiazine derivative in which 10H-phenothiazinecarries a 3-(4-methylpiperazin-1-yl)propyl substituent at the N-10 position.	2.05	1	0	N-alkylpiperazine; N-methylpiperazine; phenothiazines	dopaminergic antagonist; phenothiazine antipsychotic drug
perhexiline Perhexiline: 2-(2,2-Dicyclohexylethyl)piperidine. Coronary vasodilator used especially for angina of effort. It may cause neuropathy and hepatitis.	3.73	2	0	piperidines	cardiovascular drug
perphenazine Perphenazine: An antipsychotic phenothiazine derivative with actions and uses similar to those of CHLORPROMAZINE.. perphenazine : A phenothiazine derivative in which the phenothiazine tricycle carries a chloro substituent at the 2-position and a 3-[4-(2-hydroxyethyl)piperazin-1-yl]propyl group at N-10.	4.08	4	0	N-(2-hydroxyethyl)piperazine; N-alkylpiperazine; organochlorine compound; phenothiazines	antiemetic; dopaminergic antagonist; phenothiazine antipsychotic drug
phenacetin Saridon: contains phenacetin, caffeine, propyphenazone & pyrithyldione	2.75	3	0	acetamides; aromatic ether	cyclooxygenase 3 inhibitor; non-narcotic analgesic; peripheral nervous system drug
phenazopyridine Phenazopyridine: A local anesthetic that has been used in urinary tract disorders. Its use is limited by problems with toxicity (primarily blood disorders) and potential carcinogenicity.. phenazopyridine : A diaminopyridine that is 2,6-diaminopyridine substituted at position 3 by a phenylazo group. A local anesthetic that has topical analgesic effect on mucosa lining of the urinary tract. Its use is limited by problems with toxicity (primarily blood disorders) and potential carcinogenicity.	2.6	1	0	diaminopyridine; monoazo compound	anticoronaviral agent; carcinogenic agent; local anaesthetic; non-narcotic analgesic
phenobarbital Phenobarbital: A barbituric acid derivative that acts as a nonselective central nervous system depressant. It potentiates GAMMA-AMINOBUTYRIC ACID action on GABA-A RECEPTORS, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations.. phenobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by ethyl and phenyl groups.	4.08	4	0	barbiturates	anticonvulsant; drug allergen; excitatory amino acid antagonist; sedative
phenolphthalein Phenolphthalein: An acid-base indicator which is colorless in acid solution, but turns pink to red as the solution becomes alkaline. It is used medicinally as a cathartic.	2.05	1	0	phenols
phenoxybenzamine Phenoxybenzamine: An alpha-adrenergic antagonist with long duration of action. It has been used to treat hypertension and as a peripheral vasodilator.	3.59	2	0	aromatic amine
phentermine Phentermine: A central nervous system stimulant and sympathomimetic with actions and uses similar to those of DEXTROAMPHETAMINE. It has been used most frequently in the treatment of obesity.	3.23	1	0	primary amine	adrenergic agent; appetite depressant; central nervous system drug; central nervous system stimulant; dopaminergic agent; sympathomimetic agent
4-phenylbutyric acid 4-phenylbutyric acid: RN refers to the parent cpd. 4-phenylbutyric acid : A monocarboxylic acid the structure of which is that of butyric acid substituted with a phenyl group at C-4. It is a histone deacetylase inhibitor that displays anticancer activity. It inhibits cell proliferation, invasion and migration and induces apoptosis in glioma cells. It also inhibits protein isoprenylation, depletes plasma glutamine, increases production of foetal haemoglobin through transcriptional activation of the gamma-globin gene and affects hPPARgamma activation.	3.73	2	0	monocarboxylic acid	antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor; prodrug
phenylbutazone Phenylbutazone: A butyl-diphenyl-pyrazolidinedione that has anti-inflammatory, antipyretic, and analgesic activities. It has been used in ANKYLOSING SPONDYLITIS; RHEUMATOID ARTHRITIS; and REACTIVE ARTHRITIS.. phenylbutazone : A member of the class of pyrazolidines that is 1,2-diphenylpyrazolidine-3,5-dione carrying a butyl group at the 4-position.	2.05	1	0	pyrazolidines	antirheumatic drug; EC 1.1.1.184 [carbonyl reductase (NADPH)] inhibitor; metabolite; non-narcotic analgesic; non-steroidal anti-inflammatory drug; peripheral nervous system drug
phenylmethylsulfonyl fluoride Phenylmethylsulfonyl Fluoride: An enzyme inhibitor that inactivates IRC-50 arvin, subtilisin, and the fatty acid synthetase complex.. phenylmethanesulfonyl fluoride : An acyl fluoride with phenylmethanesulfonyl as the acyl group.	2.6	1	0	acyl fluoride	serine proteinase inhibitor
moxonidine moxonidine: structure given in first source	2.45	2	0	organohalogen compound; pyrimidines
pifithrin pifithrin: a tetrahydrobenzothiazol; inhibitor of P53 that protects mice from the side effects of cancer therapy; structure in first source	2.07	1	0	aromatic ketone
pimobendan pimobendan: produces arterial & venous dilatation in dogs; structure given in first source	2.52	2	0	benzimidazoles; pyridazinone	cardiotonic drug; EC 3.1.4.* (phosphoric diester hydrolase) inhibitor; vasodilator agent
pinacidil Pinacidil: A guanidine that opens POTASSIUM CHANNELS producing direct peripheral vasodilatation of the ARTERIOLES. It reduces BLOOD PRESSURE and peripheral resistance and produces fluid retention. (Martindale The Extra Pharmacopoeia, 31st ed)	2.05	1	0	pyridines
pindolol Pindolol: A moderately lipophilic beta blocker (ADRENERGIC BETA-ANTAGONISTS). It is non-cardioselective and has intrinsic sympathomimetic actions, but little membrane-stabilizing activity. (From Martindale, The Extra Pharmocopoeia, 30th ed, p638). pindolol : A member of the class of indols which is the 2-hydroxy-3-(isopropylamino)propyl ether derivative of 1H-indol-4-ol.	3.87	3	0	indoles; secondary amine	antiglaucoma drug; antihypertensive agent; beta-adrenergic antagonist; serotonergic antagonist; vasodilator agent
pioglitazone Pioglitazone: A thiazolidinedione and PPAR GAMMA agonist that is used in the treatment of TYPE 2 DIABETES MELLITUS.. pioglitazone : A member of the class of thiazolidenediones that is 1,3-thiazolidine-2,4-dione substituted by a benzyl group at position 5 which in turn is substituted by a 2-(5-ethylpyridin-2-yl)ethoxy group at position 4 of the phenyl ring. It exhibits hypoglycemic activity.	3.89	3	0	aromatic ether; pyridines; thiazolidinediones	antidepressant; cardioprotective agent; EC 2.7.1.33 (pantothenate kinase) inhibitor; EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor; ferroptosis inhibitor; geroprotector; hypoglycemic agent; insulin-sensitizing drug; PPARgamma agonist; xenobiotic
pipemidic acid Pipemidic Acid: Antimicrobial against Gram negative and some Gram positive bacteria. It is protein bound and concentrated in bile and urine and used for gastrointestinal, biliary, and urinary infections.. pipemidic acid : A pyridopyrimidine that is 5-oxo-5,8-dihydropyrido[2,3-d]pyrimidine-6-carboxylic acid substituted at position 2 by a piperazin-1-yl group and at position 8 by an ethyl group. A synthetic broad-spectrum antibacterial, it is used for treatment of gastrointestinal, biliary, and urinary infections.	2.05	1	0	amino acid; monocarboxylic acid; N-arylpiperazine; pyridopyrimidine; quinolone antibiotic	antibacterial drug; DNA synthesis inhibitor
piperazine [no description available]	2.05	1	0	azacycloalkane; piperazines; saturated organic heteromonocyclic parent	anthelminthic drug
piracetam Piracetam: A compound suggested to be both a nootropic and a neuroprotective agent.	2.51	2	0	organonitrogen compound; organooxygen compound
piretanide piretanide: potent inhibitor of chloride transport; structure	2.04	1	0	aromatic ether
piribedil Piribedil: A dopamine D2 agonist. It is used in the treatment of parkinson disease, particularly for alleviation of tremor. It has also been used for circulatory disorders and in other applications as a D2 agonist.	2.08	1	0	N-arylpiperazine
pj-34 PJ34 : A member of the class of phenanthridines that is 5,6-dihydrophenanthridine substituted at positions 2 and 6 by (N,N-dimethylglycyl)amino and oxo groups, respectively. It is a potent inhibitor of poly(ADP-ribose) polymerases PARP1 and PARP2 (IC50 of 110 nM and 86 nM, respectively) and exhibits anti-cancer, cardioprotective and neuroprotective properties.	2.6	1	0	phenanthridines; secondary carboxamide; tertiary amino compound	angiogenesis inhibitor; anti-inflammatory agent; antiatherosclerotic agent; antineoplastic agent; apoptosis inducer; cardioprotective agent; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor; neuroprotective agent
polythiazide [no description available]	3.23	1	0	benzothiadiazine
duodote duodote: consists of atropine and pralidoxime chloride; for treating those exposed to organophosphorus-containing nerve agents	3.23	1	0	pyridinium ion	antidote to organophosphate poisoning; antidote to sarin poisoning; cholinergic drug; cholinesterase reactivator
ono 1078 pranlukast: SRS-A antagonist; leukotriene D4 receptor antagonist	2.08	1	0	chromones
pyranoprofen pyranoprofen: RN given refers to unlabled parent cpd; structure given in first source	2.08	1	0	pyridochromene
praziquantel azinox: Russian drug	4.13	4	0	isoquinolines
prazosin Prazosin: A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.. prazosin : A member of the class of piperazines that is piperazine substituted by a furan-2-ylcarbonyl group and a 4-amino-6,7-dimethoxyquinazolin-2-yl group at positions 1 and 4 respectively.	4.08	4	0	aromatic ether; furans; monocarboxylic acid amide; piperazines; quinazolines	alpha-adrenergic antagonist; antihypertensive agent; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
prilocaine Prilocaine: A local anesthetic that is similar pharmacologically to LIDOCAINE. Currently, it is used most often for infiltration anesthesia in dentistry.. prilocaine : An amino acid amide in which N-propyl-DL-alanine and 2-methylaniline have combined to form the amide bond; used as a local anaesthetic.	2.04	1	0	amino acid amide; monocarboxylic acid amide	anticonvulsant; local anaesthetic
primaquine Primaquine: An aminoquinoline that is given by mouth to produce a radical cure and prevent relapse of vivax and ovale malarias following treatment with a blood schizontocide. It has also been used to prevent transmission of falciparum malaria by those returning to areas where there is a potential for re-introduction of malaria. Adverse effects include anemias and GI disturbances. (From Martindale, The Extra Pharmacopeia, 30th ed, p404). primaquine : An N-substituted diamine that is pentane-1,4-diamine substituted by a 6-methoxyquinolin-8-yl group at the N(4) position. It is a drug used in the treatment of malaria and Pneumocystis pneumonia.	4.08	4	0	aminoquinoline; aromatic ether; N-substituted diamine	antimalarial
primidone Primidone: A barbiturate derivative that acts as a GABA modulator and anti-epileptic agent. It is partly metabolized to PHENOBARBITAL in the body and owes some of its actions to this metabolite.. primidone : A pyrimidone that is dihydropyrimidine-4,6(1H,5H)-dione substituted by an ethyl and a phenyl group at position 5. It is used as an anticonvulsant for treatment of various types of seizures.	3.87	3	0	pyrimidone	anticonvulsant; environmental contaminant; xenobiotic
probenecid Probenecid: The prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy.. probenecid : A sulfonamide in which the nitrogen of 4-sulfamoylbenzoic acid is substituted with two propyl groups.	4.29	5	0	benzoic acids; sulfonamide	uricosuric drug
probucol Probucol: A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993).. probucol : A dithioketal that is propane-2,2-dithiol in which the hydrogens attached to both sulfur atoms are replaced by 3,5-di-tert-butyl-4-hydroxyphenyl groups. An anticholesteremic drug with antioxidant and anti-inflammatory properties, it is used to treat high levels of cholesterol in blood.	2.54	2	0	dithioketal; polyphenol	anti-inflammatory drug; anticholesteremic drug; antilipemic drug; antioxidant; cardiovascular drug
procainamide Procainamide: A class Ia antiarrhythmic drug that is structurally-related to PROCAINE.. procainamide : A benzamide that is 4-aminobenzamide substituted on the amide N by a 2-(diethylamino)ethyl group. It is a pharmaceutical antiarrhythmic agent used for the medical treatment of cardiac arrhythmias.	4.08	4	0	benzamides	anti-arrhythmia drug; platelet aggregation inhibitor; sodium channel blocker
procarbazine Procarbazine: An antineoplastic agent used primarily in combination with mechlorethamine, vincristine, and prednisone (the MOPP protocol) in the treatment of Hodgkin's disease.. procarbazine : A benzamide obtained by formal condensation of the carboxy group of 4-[(2-methylhydrazino)methyl]benzoic acid with the amino group of isopropylamine. An antineoplastic chemotherapy drug used for treatment of Hodgkin's lymphoma. Metabolism yields azo-procarbazine and hydrogen peroxide, which results in the breaking of DNA strands.	4.36	3	0	benzamides; hydrazines	antineoplastic agent
prochlorperazine Prochlorperazine: A phenothiazine antipsychotic used principally in the treatment of NAUSEA; VOMITING; and VERTIGO. It is more likely than CHLORPROMAZINE to cause EXTRAPYRAMIDAL DISORDERS. (From Martindale, The Extra Pharmacopoeia, 30th ed, p612). prochlorperazine : A member of the class of phenothiazines that is 10H-phenothiazine having a chloro substituent at the 2-position and a 3-(4-methylpiperazin-1-yl)propyl group at the N-10 position.	4.08	4	0	N-alkylpiperazine; N-methylpiperazine; organochlorine compound; phenothiazines	alpha-adrenergic antagonist; antiemetic; cholinergic antagonist; dopamine receptor D2 antagonist; dopaminergic antagonist; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; first generation antipsychotic
procyclidine Procyclidine: A muscarinic antagonist that crosses the blood-brain barrier and is used in the treatment of drug-induced extrapyramidal disorders and in parkinsonism.. procyclidine : A tertiary alcohol that consists of propan-1-ol substituted by a cyclohexyl and a phenyl group at position 1 and a pyrrolidin-1-yl group at position 3.	3.87	3	0	pyrrolidines; tertiary alcohol	antidyskinesia agent; antiparkinson drug; muscarinic antagonist
promazine Promazine: A phenothiazine with actions similar to CHLORPROMAZINE but with less antipsychotic activity. It is primarily used in short-term treatment of disturbed behavior and as an antiemetic.. promazine : A phenothiazine deriative in which the phenothiazine tricycle has a 3-(dimethylaminopropyl) group at the N-10 position.	2.52	2	0	phenothiazines; tertiary amine	antiemetic; dopaminergic antagonist; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; H1-receptor antagonist; muscarinic antagonist; phenothiazine antipsychotic drug; serotonergic antagonist
promethazine Promethazine: A phenothiazine derivative with histamine H1-blocking, antimuscarinic, and sedative properties. It is used as an antiallergic, in pruritus, for motion sickness and sedation, and also in animals.. promethazine : A tertiary amine that is a substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropan-2-amine moiety.	4.29	5	0	phenothiazines; tertiary amine	anti-allergic agent; anticoronaviral agent; antiemetic; antipruritic drug; H1-receptor antagonist; local anaesthetic; sedative
propafenone Propafenone: An antiarrhythmia agent that is particularly effective in ventricular arrhythmias. It also has weak beta-blocking activity.. propafenone : An aromatic ketone that is 3-(propylamino)propane-1,2-diol in which the hydrogen of the primary hydroxy group is replaced by a 2-(3-phenylpropanoyl)phenyl group. It is a class 1C antiarrhythmic drug with local anesthetic effects, and is used as the hydrochloride salt in the management of supraventricular and ventricular arrhythmias.	3.87	3	0	aromatic ketone; secondary alcohol; secondary amino compound	anti-arrhythmia drug
propantheline Propantheline: A muscarinic antagonist used as an antispasmodic, in rhinitis, in urinary incontinence, and in the treatment of ulcers. At high doses it has nicotinic effects resulting in neuromuscular blocking.	3.23	1	0	xanthenes
propofol Propofol: An intravenous anesthetic agent which has the advantage of a very rapid onset after infusion or bolus injection plus a very short recovery period of a couple of minutes. (From Smith and Reynard, Textbook of Pharmacology, 1992, 1st ed, p206). Propofol has been used as ANTICONVULSANTS and ANTIEMETICS.. propofol : A phenol resulting from the formal substitution of the hydrogen at the 2 position of 1,3-diisopropylbenzene by a hydroxy group.	3.86	3	0	phenols	anticonvulsant; antiemetic; intravenous anaesthetic; radical scavenger; sedative
propranolol Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.. propranolol : A propanolamine that is propan-2-ol substituted by a propan-2-ylamino group at position 1 and a naphthalen-1-yloxy group at position 3.	4.29	5	0	naphthalenes; propanolamine; secondary amine	anti-arrhythmia drug; antihypertensive agent; anxiolytic drug; beta-adrenergic antagonist; environmental contaminant; human blood serum metabolite; vasodilator agent; xenobiotic
protriptyline Protriptyline: Tricyclic antidepressant similar in action and side effects to IMIPRAMINE. It may produce excitation.	3.23	1	0	carbotricyclic compound	antidepressant
pyridinolcarbamate Pyridinolcarbamate: A drug that has been given by mouth in the treatment of atherosclerosis and other vascular disorders, hyperlipidemias, and thrombo-embolic disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1408)	2.05	1	0	pyridines
pyridostigmine [no description available]	3.58	2	0	pyridinium ion
pyrimethamine Maloprim: contains above 2 cpds	6	4	1	aminopyrimidine; monochlorobenzenes	antimalarial; antiprotozoal drug; EC 1.5.1.3 (dihydrofolate reductase) inhibitor
pyroxamide [no description available]	3.1	1	0	aromatic amide
sch 16134 quazepam: structure given in first source	3.23	1	0	benzodiazepine
quetiapine [no description available]	3.23	1	0	dibenzothiazepine; N-alkylpiperazine; N-arylpiperazine	adrenergic antagonist; dopaminergic antagonist; histamine antagonist; second generation antipsychotic; serotonergic antagonist
rabeprazole Rabeprazole: A 4-(3-methoxypropoxy)-3-methylpyridinyl derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.	3.88	3	0	benzimidazoles; pyridines; sulfoxide	anti-ulcer drug; EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor
3-[(3,5-dibromo-4-hydroxyphenyl)methylidene]-5-iodo-1H-indol-2-one [no description available]	2.08	1	0	indoles
raloxifene raloxifene : A member of the class of 1-benzothiophenes that is 1-benzothiophene in which the hydrogens at positions 2, 3, and 6 have been replaced by p-hydroxyphenyl, p-[2-(piperidin-1-yl)ethoxy]benzoyl, and hydroxy groups, respectively.	3.23	1	0	1-benzothiophenes; aromatic ketone; N-oxyethylpiperidine; phenols	bone density conservation agent; estrogen antagonist; estrogen receptor modulator
ranitidine [no description available]	2.75	3	0	aralkylamine
opc 12759 rebamipide: structure in first source; RN refers to (+-)-isomer; inhibits gastric xanthine oxidase	2.05	1	0	secondary carboxamide
riluzole Riluzole: A glutamate antagonist (RECEPTORS, GLUTAMATE) used as an anticonvulsant (ANTICONVULSANTS) and to prolong the survival of patients with AMYOTROPHIC LATERAL SCLEROSIS.	4.1	4	0	benzothiazoles
rimantadine Rimantadine: An RNA synthesis inhibitor that is used as an antiviral agent in the prophylaxis and treatment of influenza.	3.73	2	0	alkylamine
risperidone Risperidone: A selective blocker of DOPAMINE D2 RECEPTORS and SEROTONIN 5-HT2 RECEPTORS that acts as an atypical antipsychotic agent. It has been shown to improve both positive and negative symptoms in the treatment of SCHIZOPHRENIA.. risperidone : A member of the class of pyridopyrimidines that is 2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one carrying an additional 2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl group at position 2.	4.08	4	0	1,2-benzoxazoles; heteroarylpiperidine; organofluorine compound; pyridopyrimidine	alpha-adrenergic antagonist; dopaminergic antagonist; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; H1-receptor antagonist; psychotropic drug; second generation antipsychotic; serotonergic antagonist
rizatriptan rizatriptan: structure given in first source; RN given refers to benzoate	3.58	2	0	tryptamines	anti-inflammatory drug; serotonergic agonist; vasoconstrictor agent
rofecoxib [no description available]	2.47	2	0	butenolide; sulfone	analgesic; cyclooxygenase 2 inhibitor; non-steroidal anti-inflammatory drug
rolipram [no description available]	2.6	1	0	pyrrolidin-2-ones	antidepressant; EC 3.1.4.* (phosphoric diester hydrolase) inhibitor
ropinirole [no description available]	3.23	1	0	indolones; tertiary amine	antidyskinesia agent; antiparkinson drug; central nervous system drug; dopamine agonist
salicylamide salamide: a major impurity of hydrochlorothiazide; structure in first source	2.05	1	0	phenols; salicylamides	antirheumatic drug; non-narcotic analgesic
sanguinarine benzophenanthridine alkaloid : A specific group of isoquinoline alkaloids that occur only in higher plants and are constituents mainly of the Papaveraceae family.	7.05	1	0	alkaloid antibiotic; benzophenanthridine alkaloid; botanical anti-fungal agent
salicylsalicylic acid salicylsalicylic acid: structure. salsalate : A dimeric benzoate ester obtained by intermolecular condensation between the carboxy of one molecule of salicylic acid with the phenol group of a second. It is a prodrug for salycylic acid that is used for treatment of rheumatoid arthritis and osteoarthritis and also shows activity against type II diabetes.	3.23	1	0	benzoate ester; benzoic acids; phenols; salicylates	antineoplastic agent; antirheumatic drug; EC 3.5.2.6 (beta-lactamase) inhibitor; hypoglycemic agent; non-narcotic analgesic; non-steroidal anti-inflammatory drug; prodrug
sb 206553 SB 206553: a high-affinity 5-HT(2C/2B) antagonist; structure given in first source	2.08	1	0	pyrroloindole
sb 220025 SB 220025: inhibits p38 mitogen-activated protein kinase; structure in first source. SB220025 : Am member of the class of imidazoles carrying piperidin-4-yl, 4-fluophenyl and 2-aminopyrimidin-4-yl substituents at posiitons 1, 4 and 5 respectively.	2.08	1	0	aminopyrimidine; imidazoles; organofluorine compound; piperidines	angiogenesis inhibitor; anti-inflammatory agent; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
sb 202190 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole: structure given in first source; inhibits p38 MAP kinase	2.46	2	0	imidazoles; organofluorine compound; phenols; pyridines	apoptosis inducer; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
suberoyl bis-hydroxamic acid suberoyl bis-hydroxamic acid: antineoplastic, Histone Deacetylase inhibitor	2.1	1	0	hydroxamic acid
scriptaid scriptide: provokes translocation of GLUT4 to increase glucose uptake; structure in first source	7.69	2	0	isoquinolines
sebacic acid sebacic acid : An alpha,omega-dicarboxylic acid that is the 1,8-dicarboxy derivative of octane.	2.6	1	0	alpha,omega-dicarboxylic acid; dicarboxylic fatty acid	human metabolite; plant metabolite
secobarbital Secobarbital: A barbiturate that is used as a sedative. Secobarbital is reported to have no anti-anxiety activity.. secobarbital : A member of the class of barbiturates that is barbituric acid in which the hydrogens at position 5 are substituted by prop-2-en-1-yl and pentan-2-yl groups.	3.23	1	0	barbiturates	anaesthesia adjuvant; GABA modulator; sedative
sevoflurane Sevoflurane: A non-explosive inhalation anesthetic used in the induction and maintenance of general anesthesia. It does not cause respiratory irritation and may also prevent PLATELET AGGREGATION.. sevoflurane : An ether compound having fluoromethyl and 1,1,1,3,3,3-hexafluoroisopropyl as the two alkyl groups.	2.05	1	0	ether; organofluorine compound	central nervous system depressant; inhalation anaesthetic; platelet aggregation inhibitor
sibutramine sibutramine: serotonin and norepinephrine transporter inhibitor; Meridia is tradename for sibutramine hydrochloride	3.59	2	0	organochlorine compound; tertiary amino compound	anti-obesity agent; serotonin uptake inhibitor
sulfadiazine Sulfadiazine: One of the short-acting SULFONAMIDES used in combination with PYRIMETHAMINE to treat toxoplasmosis in patients with acquired immunodeficiency syndrome and in newborns with congenital infections.. sulfadiazine : A sulfonamide consisting of pyrimidine with a 4-aminobenzenesulfonamido group at the 2-position.. diazine : The parent structure of the diazines.	4.08	4	0	pyrimidines; substituted aniline; sulfonamide antibiotic; sulfonamide	antiinfective agent; antimicrobial agent; antiprotozoal drug; coccidiostat; drug allergen; EC 1.1.1.153 [sepiapterin reductase (L-erythro-7,8-dihydrobiopterin forming)] inhibitor; EC 2.5.1.15 (dihydropteroate synthase) inhibitor; environmental contaminant; xenobiotic
sk&f 86002 6-(4-fluorophenyl)-2,3-dihydro-5-(4-pyridinyl)imidazo(2,1-b)thiazole: inhibits p38 MAP kinase	2.08	1	0	imidazoles
sodium fluoride [no description available]	4.8	1	1	fluoride salt	mutagen
risedronic acid Risedronic Acid: A pyridine and diphosphonic acid derivative that acts as a CALCIUM CHANNEL BLOCKER and inhibits BONE RESORPTION.	3.58	2	0	pyridines
sotalol Sotalol: An adrenergic beta-antagonist that is used in the treatment of life-threatening arrhythmias.. sotalol : A sulfonamide that is N-phenylmethanesulfonamide in which the phenyl group is substituted at position 4 by a 1-hydroxy-2-(isopropylamino)ethyl group. It has both beta-adrenoreceptor blocking (Vaughan Williams Class II) and cardiac action potential duration prolongation (Vaughan Williams Class III) antiarrhythmic properties. It is used (usually as the hydrochloride salt) for the management of ventricular and supraventricular arrhythmias.	4.08	4	0	ethanolamines; secondary alcohol; secondary amino compound; sulfonamide	anti-arrhythmia drug; beta-adrenergic antagonist; environmental contaminant; xenobiotic
4-phenylbutyric acid, sodium salt sodium phenylbutyrate : The organic sodium salt of 4-phenylbutyric acid. A prodrug for phenylacetate, it is used to treat urea cycle disorders.	2.05	1	0	organic sodium salt	EC 3.5.1.98 (histone deacetylase) inhibitor; geroprotector; neuroprotective agent; orphan drug; prodrug
fenofibrate [no description available]	2.6	1	0	benzochromenone; delta-lactone; naphtho-alpha-pyrone	platelet aggregation inhibitor; Sir2 inhibitor
imatinib [no description available]	4.3	5	0	aromatic amine; benzamides; N-methylpiperazine; pyridines; pyrimidines	antineoplastic agent; apoptosis inducer; tyrosine kinase inhibitor
vorinostat Vorinostat: A hydroxamic acid and anilide derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used in the treatment of CUTANEOUS T-CELL LYMPHOMA and SEZARY SYNDROME.. vorinostat : A dicarboxylic acid diamide comprising suberic (octanedioic) acid coupled to aniline and hydroxylamine. A histone deacetylase inhibitor, it is marketed under the name Zolinza for the treatment of cutaneous T cell lymphoma (CTCL).	15.25	86	19	dicarboxylic acid diamide; hydroxamic acid	antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor
succinylcholine Succinylcholine: A quaternary skeletal muscle relaxant usually used in the form of its bromide, chloride, or iodide. It is a depolarizing relaxant, acting in about 30 seconds and with a duration of effect averaging three to five minutes. Succinylcholine is used in surgical, anesthetic, and other procedures in which a brief period of muscle relaxation is called for.. succinylcholine : A quaternary ammonium ion that is the bis-choline ester of succinic acid.	3.23	1	0	quaternary ammonium ion; succinate ester	drug allergen; muscle relaxant; neuromuscular agent
sulfadimethoxine Sulfadimethoxine: A sulfanilamide that is used as an anti-infective agent.. sulfadimethoxine : A sulfonamide consisting of pyrimidine having methoxy substituents at the 2- and 6-positions and a 4-aminobenzenesulfonamido group at the 4-position.	2.05	1	0	aromatic ether; pyrimidines; substituted aniline; sulfonamide antibiotic; sulfonamide	antiinfective agent; antimicrobial agent; drug allergen; environmental contaminant; xenobiotic
sulfamerazine [no description available]	2.05	1	0	pyrimidines; sulfonamide antibiotic; sulfonamide	antiinfective agent; drug allergen
sulfameter Sulfameter: Long acting sulfonamide used in leprosy, urinary, and respiratory tract infections.. sulfamethoxydiazine : A sulfonamide consisting of pyrimidine having a methoxy substituent at the 5-position and a 4-aminobenzenesulfonamido group at the 2-position.	2.05	1	0	pyrimidines; sulfonamide antibiotic; sulfonamide	antiinfective agent; leprostatic drug; renal agent
sulfamethazine Sulfamethazine: A sulfanilamide anti-infective agent. It has a spectrum of antimicrobial action similar to other sulfonamides.. sulfamethazine : A sulfonamide consisting of pyrimidine with methyl substituents at the 4- and 6-positions and a 4-aminobenzenesulfonamido group at the 2-position.	2.05	1	0	pyrimidines; sulfonamide antibiotic; sulfonamide	antibacterial drug; antiinfective agent; antimicrobial agent; carcinogenic agent; drug allergen; EC 2.5.1.15 (dihydropteroate synthase) inhibitor; environmental contaminant; ligand; xenobiotic
sulfamethizole Sulfamethizole: A sulfathiazole antibacterial agent.. sulfamethizole : A sulfonamide consisting of a 1,3,4-thiadiazole nucleus with a methyl substituent at C-5 and a 4-aminobenzenesulfonamido group at C-2.	3.59	2	0	sulfonamide antibiotic; sulfonamide; thiadiazoles	antiinfective agent; antimicrobial agent; drug allergen; EC 2.5.1.15 (dihydropteroate synthase) inhibitor
sulfamethoxazole Sulfamethoxazole: A bacteriostatic antibacterial agent that interferes with folic acid synthesis in susceptible bacteria. Its broad spectrum of activity has been limited by the development of resistance. (From Martindale, The Extra Pharmacopoeia, 30th ed, p208). sulfamethoxazole : An isoxazole (1,2-oxazole) compound having a methyl substituent at the 5-position and a 4-aminobenzenesulfonamido group at the 3-position.	2.75	3	0	isoxazoles; substituted aniline; sulfonamide antibiotic; sulfonamide	antibacterial agent; antiinfective agent; antimicrobial agent; drug allergen; EC 1.1.1.153 [sepiapterin reductase (L-erythro-7,8-dihydrobiopterin forming)] inhibitor; EC 2.5.1.15 (dihydropteroate synthase) inhibitor; environmental contaminant; epitope; P450 inhibitor; xenobiotic
sulfanilamide [no description available]	2.05	1	0	substituted aniline; sulfonamide antibiotic; sulfonamide	antibacterial agent; drug allergen; EC 4.2.1.1 (carbonic anhydrase) inhibitor
sulfanitran [no description available]	2.08	1	0	sulfonamide
sulfaphenazole Sulfaphenazole: A sulfonilamide anti-infective agent.. sulfaphenazole : A sulfonamide that is sulfanilamide in which the sulfonamide nitrogen is substituted by a 1-phenyl-1H-pyrazol-5-yl group. It is a selective inhibitor of cytochrome P450 (CYP) 2C9 isozyme, and antibacterial agent.	2.05	1	0	primary amino compound; pyrazoles; substituted aniline; sulfonamide antibiotic; sulfonamide	antibacterial drug; EC 1.14.13.181 (13-deoxydaunorubicin hydroxylase) inhibitor; EC 1.14.13.67 (quinine 3-monooxygenase) inhibitor; P450 inhibitor
sulfapyridine Sulfapyridine: Antibacterial, potentially toxic, used to treat certain skin diseases.. sulfapyridine : A sulfonamide consisting of pyridine with a 4-aminobenzenesulfonamido group at the 2-position.	2.05	1	0	pyridines; substituted aniline; sulfonamide antibiotic; sulfonamide	antiinfective agent; dermatologic drug; drug allergen; environmental contaminant; xenobiotic
sulfasalazine Sulfasalazine: A drug that is used in the management of inflammatory bowel diseases. Its activity is generally considered to lie in its metabolic breakdown product, 5-aminosalicylic acid (see MESALAMINE) released in the colon. (From Martindale, The Extra Pharmacopoeia, 30th ed, p907). sulfasalazine : An azobenzene consisting of diphenyldiazene having a carboxy substituent at the 4-position, a hydroxy substituent at the 3-position and a 2-pyridylaminosulphonyl substituent at the 4'-position.	4.57	7	0
sulfathiazole Sulfathiazole: A sulfathiazole compound that is used as a short-acting anti-infective agent. It is no longer commonly used systemically due to its toxicity, but may still be applied topically in combination with other drugs for the treatment of vaginal and skin infections, and is still used in veterinary medicine.. sulfathiazole : A 1,3-thiazole compound having a 4-aminobenzenesulfonamido group at the 2-position.	3.23	1	0	1,3-thiazoles; substituted aniline; sulfonamide antibiotic; sulfonamide	antiinfective agent; drug allergen; EC 2.5.1.15 (dihydropteroate synthase) inhibitor; environmental contaminant; xenobiotic
sulfinpyrazone Sulfinpyrazone: A uricosuric drug that is used to reduce the serum urate levels in gout therapy. It lacks anti-inflammatory, analgesic, and diuretic properties.	2.45	2	0	pyrazolidines; sulfoxide	uricosuric drug
sulfisoxazole Sulfisoxazole: A short-acting sulfonamide antibacterial with activity against a wide range of gram- negative and gram-positive organisms.. sulfisoxazole : A sulfonamide antibacterial with an oxazole substituent. It has antibiotic activity against a wide range of gram-negative and gram-positive organisms.	2.46	2	0	isoxazoles; sulfonamide antibiotic; sulfonamide	antibacterial drug; drug allergen
sulforaphane sulforaphane: from Cardaria draba L.. sulforaphane : An isothiocyanate having a 4-(methylsulfinyl)butyl group attached to the nitrogen.	2.06	1	0	isothiocyanate; sulfoxide	antineoplastic agent; antioxidant; EC 3.5.1.98 (histone deacetylase) inhibitor; plant metabolite
2-(octylamino)-1-[4-(propan-2-ylthio)phenyl]-1-propanol [no description available]	3.59	2	0	alkylbenzene
sulpiride Sulpiride: A dopamine D2-receptor antagonist. It has been used therapeutically as an antidepressant, antipsychotic, and as a digestive aid. (From Merck Index, 11th ed). sulpiride : A member of the class of benzamides obtained from formal condensation between the carboxy group of 2-methoxy-5-sulfamoylbenzoic acid and the primary amino group of (1-ethylpyrrolidin-2-yl)methylamine.	2.05	1	0	benzamides; N-alkylpyrrolidine; sulfonamide	antidepressant; antiemetic; antipsychotic agent; dopaminergic antagonist
sumatriptan Sumatriptan: A serotonin agonist that acts selectively at 5HT1 receptors. It is used in the treatment of MIGRAINE DISORDERS.. sumatriptan : A sulfonamide that consists of N,N-dimethyltryptamine bearing an additional (N-methylsulfamoyl)methyl substituent at position 5. Selective agonist for a vascular 5-HT1 receptor subtype (probably a member of the 5-HT1D family). Used (in the form of its succinate salt) for the acute treatment of migraine with or without aura in adults.	3.87	3	0	sulfonamide; tryptamines	serotonergic agonist; vasoconstrictor agent
suprofen Suprofen: An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It inhibits prostaglandin synthesis and has been proposed as an anti-arthritic.. suprofen : An aromatic ketone that is thiophene substituted at C-2 by a 4-(1-carboxyethyl)benzoyl group.	2.78	3	0	aromatic ketone; monocarboxylic acid; thiophenes	antirheumatic drug; drug allergen; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug; peripheral nervous system drug
suramin Suramin: A polyanionic compound with an unknown mechanism of action. It is used parenterally in the treatment of African trypanosomiasis and it has been used clinically with diethylcarbamazine to kill the adult Onchocerca. (From AMA Drug Evaluations Annual, 1992, p1643) It has also been shown to have potent antineoplastic properties.. suramin : A member of the class of phenylureas that is urea in which each of the amino groups has been substituted by a 3-({2-methyl-5-[(4,6,8-trisulfo-1-naphthyl)carbamoyl]phenyl}carbamoyl)phenyl group. An activator of both the rabbit skeletal muscle RyR1 and sheep cardiac RyR2 isoform ryanodine receptor channels, it has been used for the treatment of human African trypanosomiasis for over 100 years.	2.77	3	0	naphthalenesulfonic acid; phenylureas; secondary carboxamide	angiogenesis inhibitor; antinematodal drug; antineoplastic agent; apoptosis inhibitor; EC 2.7.11.13 (protein kinase C) inhibitor; GABA antagonist; GABA-gated chloride channel antagonist; purinergic receptor P2 antagonist; ryanodine receptor agonist; trypanocidal drug
2-[4-(1,2-diphenylbut-1-enyl)phenoxy]-N,N-dimethylethanamine [no description available]	2.08	1	0	stilbenoid
gatifloxacin Gatifloxacin: A fluoroquinolone antibacterial agent and DNA TOPOISOMERASE II inhibitor that is used as an ophthalmic solution for the treatment of BACTERIAL CONJUNCTIVITIS.. gatifloxacin : A monocarboxylic acid that is 4-oxo-1,4-dihydroquinoline-3-carboxylic acid which is substituted on the nitrogen by a cyclopropyl group and at positions 6, 7, and 8 by fluoro, 3-methylpiperazin-1-yl, and methoxy groups, respectively. Gatifloxacin is an antibiotic of the fourth-generation fluoroquinolone family, that like other members of that family, inhibits the bacterial topoisomerase type-II enzymes.	2.75	3	0	N-arylpiperazine; organofluorine compound; quinolinemonocarboxylic acid; quinolone antibiotic; quinolone	antiinfective agent; antimicrobial agent; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
tazarotene tazarotene: a topical acetylenic retinoid; a topical kerytolytic. tazarotene : The ethyl ester of tazarotenic acid. A prodrug for tazarotenic acid, it is used for the treatment of psoriasis, acne, and sun-damaged skin.	2.08	1	0	acetylenic compound; ethyl ester; pyridines; retinoid; thiochromane	keratolytic drug; prodrug; teratogenic agent
tegafur [no description available]	3.54	2	0	organohalogen compound; pyrimidines
temazepam Temazepam: A benzodiazepine that acts as a GAMMA-AMINOBUTYRIC ACID modulator and anti-anxiety agent.	3.59	2	0	benzodiazepine
temozolomide [no description available]	10.72	24	5	imidazotetrazine; monocarboxylic acid amide; triazene derivative	alkylating agent; antineoplastic agent; prodrug
terazosin Terazosin: induces decreased blood pressure; used in the treatment of benign prostatic hyperplasia	3.87	3	0	furans; piperazines; primary amino compound; quinazolines	alpha-adrenergic antagonist; antihypertensive agent; antineoplastic agent
terbutaline Terbutaline: A selective beta-2 adrenergic agonist used as a bronchodilator and tocolytic.. terbutaline : A member of the class of phenylethanolamines that is catechol substituted at position 5 by a 2-(tert-butylamino)-1-hydroxyethyl group.	4.08	4	0	phenylethanolamines; resorcinols	anti-asthmatic drug; beta-adrenergic agonist; bronchodilator agent; EC 3.1.1.7 (acetylcholinesterase) inhibitor; hypoglycemic agent; sympathomimetic agent; tocolytic agent
terfenadine Terfenadine: A selective histamine H1-receptor antagonist devoid of central nervous system depressant activity. The drug was used for ALLERGY but withdrawn due to causing LONG QT SYNDROME.	2.47	2	0	diarylmethane
tetracaine Tetracaine: A potent local anesthetic of the ester type used for surface and spinal anesthesia.. tetracaine : A benzoate ester in which 4-N-butylbenzoic acid and 2-(dimethylamino)ethanol have combined to form the ester bond; a local ester anaesthetic (ester caine) used for surface and spinal anaesthesia.	2.05	1	0	benzoate ester; tertiary amino compound	local anaesthetic
thalidomide Thalidomide: A piperidinyl isoindole originally introduced as a non-barbiturate hypnotic, but withdrawn from the market due to teratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppressive and anti-angiogenic activity. It inhibits release of TUMOR NECROSIS FACTOR-ALPHA from monocytes, and modulates other cytokine action.. thalidomide : A racemate comprising equimolar amounts of R- and S-thalidomide.. 2-(2,6-dioxopiperidin-3-yl)-1H-isoindole-1,3(2H)-dione : A dicarboximide that is isoindole-1,3(2H)-dione in which the hydrogen attached to the nitrogen is substituted by a 2,6-dioxopiperidin-3-yl group.	26.34	991	172	phthalimides; piperidones
thiabendazole Tresaderm: dermatologic soln containing dexamethasone, thiabendazole & neomycin sulfate	3.59	2	0	1,3-thiazoles; benzimidazole fungicide; benzimidazoles	antifungal agrochemical; antinematodal drug
thioridazine Thioridazine: A phenothiazine antipsychotic used in the management of PHYCOSES, including SCHIZOPHRENIA.. thioridazine : A phenothiazine derivative having a methylsulfanyl subsitituent at the 2-position and a (1-methylpiperidin-2-yl)ethyl] group at the N-10 position.	3.59	2	0	phenothiazines; piperidines	alpha-adrenergic antagonist; dopaminergic antagonist; EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; first generation antipsychotic; H1-receptor antagonist; serotonergic antagonist
thiotepa Thiotepa: A very toxic alkylating antineoplastic agent also used as an insect sterilant. It causes skin, gastrointestinal, CNS, and bone marrow damage. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), thiotepa may reasonably be anticipated to be a carcinogen (Merck Index, 11th ed).	3.87	3	0	aziridines
tiapride [no description available]	2.08	1	0	benzamides
tiaprofenic acid tiaprofenic acid: RN given refers to parent cpd; structure. tiaprofenic acid : An aromatic ketone that is thiophene substituted at C-2 by benzoyl and at C-4 by a 1-carboxyethyl group.	2.05	1	0	aromatic ketone; monocarboxylic acid; thiophenes	drug allergen; non-steroidal anti-inflammatory drug
ticlopidine Ticlopidine: An effective inhibitor of platelet aggregation commonly used in the placement of STENTS in CORONARY ARTERIES.. ticlopidine : A thienopyridine that is 4,5,6,7-tetrahydrothieno[3,2-c]pyridine in which the hydrogen attached to the nitrogen is replaced by an o-chlorobenzyl group.	3.93	3	0	monochlorobenzenes; thienopyridine	anticoagulant; fibrin modulating drug; hematologic agent; P2Y12 receptor antagonist; platelet aggregation inhibitor
tilorone Tilorone: An antiviral agent used as its hydrochloride. It is the first recognized synthetic, low-molecular-weight compound that is an orally active interferon inducer, and is also reported to have antineoplastic and anti-inflammatory actions.. tilorone : A member of the class of fluoren-9-ones that is 9H-fluoren-9-one which is substituted by a 2-(diethylamino)ethoxy group at positions 2 and 7. It is an interferon inducer and a selective alpha7 nicotinic acetylcholine receptor (alpha7 nAChR) agonist. Its hydrochloride salt is used as an antiviral drug.	2.08	1	0	aromatic ether; diether; fluoren-9-ones; tertiary amino compound	anti-inflammatory agent; antineoplastic agent; antiviral agent; interferon inducer; nicotinic acetylcholine receptor agonist
tinidazole Tinidazole: A nitroimidazole alkylating agent that is used as an antitrichomonal agent against TRICHOMONAS VAGINALIS; ENTAMOEBA HISTOLYTICA; and GIARDIA LAMBLIA infections. It also acts as an antibacterial agent for the treatment of BACTERIAL VAGINOSIS and anaerobic bacterial infections.. tinidazole : 1H-imidazole substituted at C-1 by a (2-ethylsulfonyl)ethyl group, at C-2 by a methyl group and at C-5 by a nitro group. It is used as an antiprotozoal, antibacterial agent.	3.87	3	0	imidazoles	antiamoebic agent; antibacterial drug; antiparasitic agent; antiprotozoal drug
tiopronin Tiopronin: Sulfhydryl acylated derivative of GLYCINE.	3.59	2	0	N-acyl-amino acid
tizanidine tizanidine: RN given refers to parent cpd; structure. tizanidine : 2,1,3-Benzothiadiazole substituted at C-4 by a Delta(1)-imidazolin-2-ylamino group and at C-4 by a chloro group. It is an agonist at alpha2-adrenergic receptor sites.	4.08	4	0	benzothiadiazole; imidazoles	alpha-adrenergic agonist; muscle relaxant
nikethamide Nikethamide: A central nervous system stimulant. It was formerly used in the treatment of barbiturate overdose but is now considered to be of no value for such purposes and may be dangerous. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1229)	2.08	1	0	pyridinecarboxamide
tolazamide Tolazamide: A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE.. tolazamide : An N-sulfonylurea that is 1-tosylurea in which a hydrogen attached to the nitrogen at position 3 is replaced by an azepan-1-yl group. A hypoglycemic agent, it is used for the treatment of type 2 diabetes mellitus.	3.59	2	0	N-sulfonylurea	hypoglycemic agent; potassium channel blocker
tolbutamide Tolbutamide: A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290). tolbutamide : An N-sulfonylurea that consists of 1-butylurea having a tosyl group attached at the 3-position.	4.08	4	0	N-sulfonylurea	human metabolite; hypoglycemic agent; insulin secretagogue; potassium channel blocker
tolmetin Tolmetin: A non-steroidal anti-inflammatory agent (ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL) similar in mode of action to INDOMETHACIN.. tolmetin : A monocarboxylic acid that is (1-methylpyrrol-2-yl)acetic acid substituted at position 5 on the pyrrole ring by a 4-methylbenzoyl group. Used in the form of its sodium salt dihydrate as a nonselective nonsteroidal anti-inflammatory drug.	3.23	1	0	aromatic ketone; monocarboxylic acid; pyrroles	EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-steroidal anti-inflammatory drug
tolnaftate [no description available]	2.08	1	0	monothiocarbamic ester	antifungal drug
tolperisone Tolperisone: A centrally acting muscle relaxant that has been used for the symptomatic treatment of spasticity and muscle spasm. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1211)	2.05	1	0	aromatic ketone
ultram 2-[(dimethylamino)methyl]-1-(3-methoxyphenyl)cyclohexanol : A tertiary alcohol that is cyclohexanol substituted at positions 1 and 2 by 3-methoxyphenyl and dimethylaminomethyl groups respectively.	3.86	3	0	aromatic ether; tertiary alcohol; tertiary amino compound
tranexamic acid Tranexamic Acid: Antifibrinolytic hemostatic used in severe hemorrhage.	3.86	3	0	amino acid
trazodone Trazodone: A serotonin uptake inhibitor that is used as an antidepressive agent. It has been shown to be effective in patients with major depressive disorders and other subsets of depressive disorders. It is generally more useful in depressive disorders associated with insomnia and anxiety. This drug does not aggravate psychotic symptoms in patients with schizophrenia or schizoaffective disorders. (From AMA Drug Evaluations Annual, 1994, p309). trazodone : An N-arylpiperazine in which one nitrogen is substituted by a 3-chlorophenyl group, while the other is substituted by a 3-(3-oxo[1,2,4]triazolo[4,3-a]pyridin-2(3H)-yl)propyl group.	4.08	4	0	monochlorobenzenes; N-alkylpiperazine; N-arylpiperazine; triazolopyridine	adrenergic antagonist; antidepressant; anxiolytic drug; H1-receptor antagonist; sedative; serotonin uptake inhibitor
triamterene Triamterene: A pteridinetriamine compound that inhibits SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS.. triamterene : Pteridine substituted at positions 2, 4 and 7 with amino groups and at position 6 with a phenyl group. A sodium channel blocker, it is used as a diuretic in the treatment of hypertension and oedema.	4.13	4	0	pteridines	diuretic; sodium channel blocker
triazolam Triazolam: A short-acting benzodiazepine used in the treatment of insomnia. Some countries temporarily withdrew triazolam from the market because of concerns about adverse reactions, mostly psychological, associated with higher dose ranges. Its use at lower doses with appropriate care and labeling has been reaffirmed by the FDA and most other countries.	3.58	2	0	triazolobenzodiazepine	sedative
triclosan [no description available]	2.05	1	0	aromatic ether; dichlorobenzene; monochlorobenzenes; phenols	antibacterial agent; antimalarial; drug allergen; EC 1.3.1.9 [enoyl-[acyl-carrier-protein] reductase (NADH)] inhibitor; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; fungicide; persistent organic pollutant; xenobiotic
trifluoperazine [no description available]	9.06	3	0	N-alkylpiperazine; N-methylpiperazine; organofluorine compound; phenothiazines	antiemetic; calmodulin antagonist; dopaminergic antagonist; EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor; EC 5.3.3.5 (cholestenol Delta-isomerase) inhibitor; phenothiazine antipsychotic drug
triflupromazine Triflupromazine: A phenothiazine used as an antipsychotic agent and as an antiemetic.. triflupromazine : A member of the class of phenothiazines that is 10H-phenothiazine having a trifluoromethyl subsitituent at the 2-position and a 3-(dimethylamino)propyl group at the N-10 position.	2.54	2	0	organofluorine compound; phenothiazines; tertiary amine	anticoronaviral agent; antiemetic; dopaminergic antagonist; first generation antipsychotic
trigonelline trigonelline: in hydra among other organisms; RN given refers to hydroxide inner salt; structure. N-methylnicotinic acid : A pyridinium ion consisting of nicotinic acid having a methyl substituent on the pyridine nitrogen.. N-methylnicotinate : An iminium betaine that is the conjugate base of N-methylnicotinic acid, arising from deprotonation of the carboxy group.	2.6	1	0	alkaloid; iminium betaine	food component; human urinary metabolite; plant metabolite
trihexyphenidyl Trihexyphenidyl: One of the centrally acting MUSCARINIC ANTAGONISTS used for treatment of PARKINSONIAN DISORDERS and drug-induced extrapyramidal movement disorders and as an antispasmodic.	3.23	1	0	amine
trimethadione Trimethadione: An anticonvulsant effective in absence seizures, but generally reserved for refractory cases because of its toxicity. (From AMA Drug Evaluations Annual, 1994, p378). trimethadione : An oxazolidinone that is 1,3-oxazolidine-2,4-dione substituted by methyl groups at positions 3, 5 and 5. It is an antiepileptic agent.	3.59	2	0	oxazolidinone	anticonvulsant; geroprotector
trimethobenzamide trimethobenzamide: major descriptor (64-84); on-line search BENZAMIDES (64-84); Index Medicus search TRIMETHOBENZAMIDE (64-84); RN given refers to parent cpd. trimethobenzamide : The amide obtained by formal condensation of 3,4,5-trihydroxybenzoic acid with 4-[2-(N,N-dimethylamino)ethoxy]benzylamine. It is used to prevent nausea and vomitting in humans.	3.73	2	0	benzamides; tertiary amino compound	antiemetic
trimethoprim Trimethoprim: A pyrimidine inhibitor of dihydrofolate reductase, it is an antibacterial related to PYRIMETHAMINE. It is potentiated by SULFONAMIDES and the TRIMETHOPRIM, SULFAMETHOXAZOLE DRUG COMBINATION is the form most often used. It is sometimes used alone as an antimalarial. TRIMETHOPRIM RESISTANCE has been reported.. trimethoprim : An aminopyrimidine antibiotic whose structure consists of pyrimidine 2,4-diamine and 1,2,3-trimethoxybenzene moieties linked by a methylene bridge.	4.29	5	0	aminopyrimidine; methoxybenzenes	antibacterial drug; diuretic; drug allergen; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; environmental contaminant; xenobiotic
trimetrexate Trimetrexate: A nonclassical folic acid inhibitor through its inhibition of the enzyme dihydrofolate reductase. It is being tested for efficacy as an antineoplastic agent and as an antiparasitic agent against PNEUMOCYSTIS PNEUMONIA in AIDS patients. Myelosuppression is its dose-limiting toxic effect.	3.58	2	0
trimipramine Trimipramine: Tricyclic antidepressant similar to IMIPRAMINE, but with more antihistaminic and sedative properties.. trimipramine : A dibenzoazepine that is 10,11-dihydro-5H-dibenzo[b,f]azepine substituted by a 3-(dimethylamino)-2-methylpropyl group at the nitrogen atom. It is used as an antidepressant.	3.58	2	0	dibenzoazepine; tertiary amino compound	antidepressant; environmental contaminant; xenobiotic
troglitazone Troglitazone: A chroman and thiazolidinedione derivative that acts as a PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS (PPAR) agonist. It was formerly used in the treatment of TYPE 2 DIABETES MELLITUS, but has been withdrawn due to hepatotoxicity.	5.34	6	0	chromanes; thiazolidinone	anticoagulant; anticonvulsant; antineoplastic agent; antioxidant; EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor; ferroptosis inhibitor; hypoglycemic agent; platelet aggregation inhibitor; vasodilator agent
thenoyltrifluoroacetone Thenoyltrifluoroacetone: Chelating agent and inhibitor of cellular respiration.	2.08	1	0
tyramine [no description available]	4.99	4	0	monoamine molecular messenger; primary amino compound; tyramines	EC 3.1.1.8 (cholinesterase) inhibitor; Escherichia coli metabolite; human metabolite; mouse metabolite; neurotransmitter
tyrphostin a9 [no description available]	2.6	1	0	alkylbenzene	geroprotector
delavirdine Delavirdine: A potent, non-nucleoside reverse transcriptase inhibitor with activity specific for HIV-1.. delavirdine : The amide resulting from the formal condensation of 5-[(methylsulfonyl)amino]-1H-indole-2-carboxylic acid and 4-amino group of 1-[3-(isopropylamino)pyridin-2-yl]piperazine, delavirdine is a non-nucleoside reverse transcriptase inhibitor with activity specific for HIV-1. Viral resistance emerges rapidly when delavirdine is used alone, so it is therefore used (as the methanesulfonic acid salt) with other antiretrovirals for combination therapy of HIV infection.	3.73	2	0	aminopyridine; indolecarboxamide; N-acylpiperazine; sulfonamide	antiviral drug; HIV-1 reverse transcriptase inhibitor
undecylenic acid undecylenic acid: a fatty acid with a terminal double bond. 10-undecenoic acid : An undecenoic acid having its double bond in the 10-position. It is derived from castor oil and is used for the treatment of skin problems.. undecenoic acid : A C11, straight-chain fatty acid carrying a C=C double bond at any position.	2.08	1	0	undecenoic acid	antifungal drug; plant metabolite
urapidil [no description available]	2.46	2	0	piperazines
urethane [no description available]	2.06	1	0	carbamate ester	fungal metabolite; mutagen
venlafaxine venlafaxine : A tertiary amino compound that is N,N-dimethylethanamine substituted at position 1 by a 1-hydroxycyclohexyl and 4-methoxyphenyl group.	4.08	4	0	cyclohexanols; monomethoxybenzene; tertiary alcohol; tertiary amino compound	adrenergic uptake inhibitor; analgesic; antidepressant; dopamine uptake inhibitor; environmental contaminant; serotonin uptake inhibitor; xenobiotic
vesnarinone [no description available]	2.54	2	0	organic molecular entity
vigabatrin [no description available]	3.87	3	0	gamma-amino acid	anticonvulsant; EC 2.6.1.19 (4-aminobutyrate--2-oxoglutarate transaminase) inhibitor
viloxazine Viloxazine: A morpholine derivative used as an antidepressant. It is similar in action to IMIPRAMINE.	2.04	1	0	aromatic ether
pirinixic acid pirinixic acid: structure	2.08	1	0	aryl sulfide; organochlorine compound; pyrimidines
ici 204,219 zafirlukast: a leukotriene D4 receptor antagonist	3.87	3	0	carbamate ester; indoles; N-sulfonylcarboxamide	anti-asthmatic agent; leukotriene antagonist
zaleplon zaleplon: an azabicyclo(4.3.0)nonane; a nonbenzodiazepine; one of the so-called of Z drugs (zopiclone, eszopiclone, zolpidem, and zaleplon) for which there is some correlation with tumors; a hypnotic with less marked effect on psychomotor functions compared to lorazepam. zaleplon : A pyrazolo[1,5-a]pyrimidine having a nitrile group at position 3 and a 3-(N-ethylacetamido)phenyl substituent at the 7-position.	3.87	3	0	nitrile; pyrazolopyrimidine	anticonvulsant; anxiolytic drug; central nervous system depressant; sedative
zolpidem Zolpidem: An imidazopyridine derivative and short-acting GABA-A receptor agonist that is used for the treatment of INSOMNIA.. zolpidem : An imidazo[1,2-a]pyridine compound having a 4-tolyl group at the 2-position, an N,N-dimethylcarbamoylmethyl group at the 3-position and a methyl substituent at the 6-position.	3.86	3	0	imidazopyridine	central nervous system depressant; GABA agonist; sedative
zonisamide Zonisamide: A benzisoxazole and sulfonamide derivative that acts as a CALCIUM CHANNEL blocker. It is used primarily as an adjunctive antiepileptic agent for the treatment of PARTIAL SEIZURES, with or without secondary generalization.. zonisamide : A 1,2-benzoxazole compound having a sulfamoylmethyl substituent at the 3-position.	3.61	2	0	1,2-benzoxazoles; sulfonamide	anticonvulsant; antioxidant; central nervous system drug; protective agent; T-type calcium channel blocker
zopiclone zopiclone: S(+)-enantiomer of racemic zopiclone; azabicyclo(4.3.0)nonane; a nonbenzodiazepine; one of the so-called of Z drugs (zopiclone, eszopiclone, zolpidem, and zaleplon) for which there is some correlation with tumors; was term of zopiclone 2004-2007. zopiclone : A pyrrolo[3,4-b]pyrazine compound having a 4-methylpiperazine-1-carboxyl group at the 5-position, a 5-chloropyridin-2-yl group at the 6-position and an oxo-substituent at the 7-position.	2.46	2	0	monochloropyridine; pyrrolopyrazine	central nervous system depressant; sedative
guanidine hydrochloride [no description available]	2.05	1	0	one-carbon compound; organic chloride salt	protein denaturant
hydrocortisone acetate hydrocortisone acetate: RN given refers to cpd without isomeric designation	2.05	1	0	cortisol ester; tertiary alpha-hydroxy ketone
cortisone acetate Cortisone Acetate: The acetate ester of cortisone that is used mainly for replacement therapy in adrenocortical insufficiency and in the treatment of many allergic and inflammatory disorders.	3.59	2	0	corticosteroid hormone
mitomycin Mitomycin: An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.. mitomycin : A family of aziridine-containing natural products isolated from Streptomyces caespitosus or Streptomyces lavendulae.	12.16	8	0	mitomycin	alkylating agent; antineoplastic agent
prednisolone Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.. prednisolone : A glucocorticoid that is prednisone in which the oxo group at position 11 has been reduced to the corresponding beta-hydroxy group. It is a drug metabolite of prednisone.	12.59	48	9	11beta-hydroxy steroid; 17alpha-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; C21-steroid; glucocorticoid; primary alpha-hydroxy ketone; tertiary alpha-hydroxy ketone	adrenergic agent; anti-inflammatory drug; antineoplastic agent; drug metabolite; environmental contaminant; immunosuppressive agent; xenobiotic
estriol hormonin: estrogen replacement; each tablet contains 600 ug micronized 17beta-estradiol, 270 ug estriol and 1.4 mg estrone. chlorapatite : A phosphate mineral with the formula Ca5(PO4)3Cl.	2.05	1	0	16alpha-hydroxy steroid; 17beta-hydroxy steroid; 3-hydroxy steroid	estrogen; human metabolite; human xenobiotic metabolite; mouse metabolite
reserpine Reserpine: An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria. Reserpine inhibits the uptake of norepinephrine into storage vesicles resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals. It has been used as an antihypertensive and an antipsychotic as well as a research tool, but its adverse effects limit its clinical use.. reserpine : An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria.	3.87	3	0	alkaloid ester; methyl ester; yohimban alkaloid	adrenergic uptake inhibitor; antihypertensive agent; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; environmental contaminant; first generation antipsychotic; plant metabolite; xenobiotic
cephaloridine Cephaloridine: A cephalosporin antibiotic.. cefaloridine : A cephalosporin compound having pyridinium-1-ylmethyl and 2-thienylacetamido side-groups. A first-generation semisynthetic derivative of cephalosporin C.	2.45	2	0	beta-lactam antibiotic allergen; cephalosporin; semisynthetic derivative	antibacterial drug
phentolamine Phentolamine: A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of RAYNAUD DISEASE and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease.. phentolamine : A substituted aniline that is 3-aminophenol in which the hydrogens of the amino group are replaced by 4-methylphenyl and 4,5-dihydro-1H-imidazol-2-ylmethyl groups respectively. An alpha-adrenergic antagonist, it is used for the treatment of hypertension.	3.59	2	0	imidazoles; phenols; substituted aniline; tertiary amino compound	alpha-adrenergic antagonist; vasodilator agent
sorbitol D-glucitol : The D-enantiomer of glucitol (also known as D-sorbitol).	3.59	2	0	glucitol	cathartic; Escherichia coli metabolite; food humectant; human metabolite; laxative; metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite; sweetening agent
2,5-dichlorobenzoic acid 2,5-dichlorobenzoic acid : A chlorobenzoic acid that is benzoic acid in which the ring hydrogens at positions 2 and 5 are substituted by chloro groups.	2.25	1	0	chlorobenzoic acid; dichlorobenzene
floxuridine Floxuridine: An antineoplastic antimetabolite that is metabolized to fluorouracil when administered by rapid injection; when administered by slow, continuous, intra-arterial infusion, it is converted to floxuridine monophosphate. It has been used to treat hepatic metastases of gastrointestinal adenocarcinomas and for palliation in malignant neoplasms of the liver and gastrointestinal tract.. floxuridine : A pyrimidine 2'-deoxyribonucleoside compound having 5-fluorouracil as the nucleobase; used to treat hepatic metastases of gastrointestinal adenocarcinomas and for palliation in malignant neoplasms of the liver and gastrointestinal tract.	2.05	1	0	nucleoside analogue; organofluorine compound; pyrimidine 2'-deoxyribonucleoside	antimetabolite; antineoplastic agent; antiviral drug; radiosensitizing agent
piperonyl butoxide [no description available]	2.05	1	0	benzodioxoles	pesticide synergist
bromouracil Bromouracil: 5-Bromo-2,4(1H,3H)-pyrimidinedione. Brominated derivative of uracil that acts as an antimetabolite, substituting for thymine in DNA. It is used mainly as an experimental mutagen, but its deoxyriboside (BROMODEOXYURIDINE) is used to treat neoplasms.. 5-bromouracil : A pyrimidine having keto groups at the 2- and 4-positions and a bromo group at the 5-position. Used mainly as an experimental mutagen.	2.05	1	0	nucleobase analogue; pyrimidines	mutagen
3,3',5-triiodothyroacetic acid tiratricol : A monocarboxylic acid that is (4-hydroxy-3,5-diiodophenyl)acetic acid in which the phenolic hydroxy group has been replaced by a 4-hydroxy-3-iodophenoxy group. It is a thyroid hormone analogue that has been used in the treatment of thyroid hormone resistance syndrome.	2.05	1	0
hydroxyproline Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ASCORBIC ACID can result in impaired hydroxyproline formation.. hydroxyproline : A proline derivative that is proline substituted by at least one hydroxy group.	2.04	1	0	4-hydroxyproline; L-alpha-amino acid zwitterion	human metabolite; mouse metabolite; plant metabolite
histamine dihydrochloride Ceplene: Tradename for histamine dihydrochloride.	2.05	1	0
thyroxine Thyroxine: The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (MONOIODOTYROSINE) and the coupling of iodotyrosines (DIIODOTYROSINE) in the THYROGLOBULIN. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form TRIIODOTHYRONINE which exerts a broad spectrum of stimulatory effects on cell metabolism.. thyroxine : An iodothyronine compound having iodo substituents at the 3-, 3'-, 5- and 5'-positions.	4.29	5	0	2-halophenol; iodophenol; L-phenylalanine derivative; non-proteinogenic L-alpha-amino acid; thyroxine zwitterion; thyroxine	antithyroid drug; human metabolite; mouse metabolite; thyroid hormone
dextroamphetamine Dextroamphetamine: The d-form of AMPHETAMINE. It is a central nervous system stimulant and a sympathomimetic. It has also been used in the treatment of narcolepsy and of attention deficit disorders and hyperactivity in children. Dextroamphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulating release of monamines, and inhibiting monoamine oxidase. It is also a drug of abuse and a psychotomimetic.. (S)-amphetamine : A 1-phenylpropan-2-amine that has S configuration.	3.59	2	0	1-phenylpropan-2-amine	adrenergic agent; adrenergic uptake inhibitor; dopamine uptake inhibitor; dopaminergic agent; neurotoxin; sympathomimetic agent
carbachol Carbachol: A slowly hydrolyzed CHOLINERGIC AGONIST that acts at both MUSCARINIC RECEPTORS and NICOTINIC RECEPTORS.	2.05	1	0	ammonium salt; carbamate ester	cardiotonic drug; miotic; muscarinic agonist; nicotinic acetylcholine receptor agonist; non-narcotic analgesic
norethindrone acetate norethisterone acetate : A 3-oxo Delta(4)-steroid that is norethisterone in which the hydroxy group has been converted to its acetate ester.	2.05	1	0	3-oxo-Delta(4) steroid; acetate ester; terminal acetylenic compound	progestin; synthetic oral contraceptive
spironolactone Spironolactone: A potassium sparing diuretic that acts by antagonism of aldosterone in the distal renal tubules. It is used mainly in the treatment of refractory edema in patients with congestive heart failure, nephrotic syndrome, or hepatic cirrhosis. Its effects on the endocrine system are utilized in the treatments of hirsutism and acne but they can lead to adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p827). spironolactone : A steroid lactone that is 17alpha-pregn-4-ene-21,17-carbolactone substituted by an oxo group at position 3 and an alpha-acetylsulfanyl group at position 7.	3.59	2	0	3-oxo-Delta(4) steroid; oxaspiro compound; steroid lactone; thioester	aldosterone antagonist; antihypertensive agent; diuretic; environmental contaminant; xenobiotic
cyclobarbital cyclobarbital: was heading 1977-94 (see under BARBITURATES 1977-90); CYCLOBARBITONE, HEXEMAL, & TETRAHYDROPHENOBARBITAL were see CYCLOBARBITAL 1977-94; use BARBITURATES to search CYCLOBARBITAL 1977-94; short to intermediate duration barbiturate used as hypnotic and sedative	2.05	1	0	barbiturates
aldosterone [no description available]	7.15	1	0	11beta-hydroxy steroid; 18-oxo steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(4) steroid; C21-steroid hormone; mineralocorticoid; primary alpha-hydroxy ketone; steroid aldehyde	human metabolite; mouse metabolite
allobarbital allobarbital: was heading 1976-94 (see under BARBITURATES 1976-90); ALLOBARBITONE, DIALLYLBARBITAL, DIALLYLBARBITURIC ACID, & DIALLYLMAL were see ALLOBARBITAL 1976-94; use BARBITURATES to search ALLOBARBITAL 1976-94; a barbiturate derivative with effects of intermediate duration; at lower doses, it is used as a sedative; at higher doses, it displays hypnotic effects	2.05	1	0	barbiturates
penicillamine Penicillamine: 3-Mercapto-D-valine. The most characteristic degradation product of the penicillin antibiotics. It is used as an antirheumatic and as a chelating agent in Wilson's disease.. penicillamine : An alpha-amino acid having the structure of valine substituted at the beta position with a sulfanyl group.	3.87	3	0	non-proteinogenic alpha-amino acid; penicillamine	antirheumatic drug; chelator; copper chelator; drug allergen
trichlorfon Trichlorfon: An organochlorophosphate cholinesterase inhibitor that is used as an insecticide for the control of flies and roaches. It is also used in anthelmintic compositions for animals. (From Merck, 11th ed). trichlorfon : A phosphonic ester that is dimethyl phosphonate in which the hydrogen atom attched to the phosphorous is substituted by a 2,2,2-trichloro-1-hydroxyethyl group.	2.05	1	0	organic phosphonate; organochlorine compound; phosphonic ester	agrochemical; anthelminthic drug; EC 3.1.1.7 (acetylcholinesterase) inhibitor; EC 3.1.1.8 (cholinesterase) inhibitor; insecticide
cysteine [no description available]	3.23	1	0	cysteine zwitterion; cysteine; L-alpha-amino acid; proteinogenic amino acid; serine family amino acid	EC 4.3.1.3 (histidine ammonia-lyase) inhibitor; flour treatment agent; human metabolite
prednisone Prednisone: A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.. prednisone : A synthetic glucocorticoid drug that is particularly effective as an immunosuppressant, and affects virtually all of the immune system. Prednisone is a prodrug that is converted by the liver into prednisolone (a beta-hydroxy group instead of the oxo group at position 11), which is the active drug and also a steroid.	20.72	216	77	11-oxo steroid; 17alpha-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; C21-steroid; glucocorticoid; primary alpha-hydroxy ketone; tertiary alpha-hydroxy ketone	adrenergic agent; anti-inflammatory drug; antineoplastic agent; immunosuppressive agent; prodrug
estrone Hydroxyestrones: Estrone derivatives substituted with one or more hydroxyl groups in any position. They are important metabolites of estrone and other estrogens.	3.59	2	0	17-oxo steroid; 3-hydroxy steroid; phenolic steroid; phenols	antineoplastic agent; bone density conservation agent; estrogen; human metabolite; mouse metabolite
oxandrolone Oxandrolone: A synthetic hormone with anabolic and androgenic properties.	3.59	2	0	17beta-hydroxy steroid; 3-oxo steroid; anabolic androgenic steroid; oxa-steroid	anabolic agent; androgen
dehydroepiandrosterone Dehydroepiandrosterone: A major C19 steroid produced by the ADRENAL CORTEX. It is also produced in small quantities in the TESTIS and the OVARY. Dehydroepiandrosterone (DHEA) can be converted to TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE. Most of DHEA is sulfated (DEHYDROEPIANDROSTERONE SULFATE) before secretion.. dehydroepiandrosterone : An androstanoid that is androst-5-ene substituted by a beta-hydroxy group at position 3 and an oxo group at position 17. It is a naturally occurring steroid hormone produced by the adrenal glands.	2.05	1	0	17-oxo steroid; 3beta-hydroxy-Delta(5)-steroid; androstanoid	androgen; human metabolite; mouse metabolite
nad [no description available]	2.05	1	0	NAD	geroprotector
penicillin g Penicillin G: A penicillin derivative commonly used in the form of its sodium or potassium salts in the treatment of a variety of infections. It is effective against most gram-positive bacteria and against gram-negative cocci. It has also been used as an experimental convulsant because of its actions on GAMMA-AMINOBUTYRIC ACID mediated synaptic transmission.. benzylpenicillin : A penicillin in which the substituent at position 6 of the penam ring is a phenylacetamido group.	3.86	3	0	penicillin allergen; penicillin	antibacterial drug; drug allergen; epitope
idoxuridine [no description available]	2.6	1	0	organoiodine compound; pyrimidine 2'-deoxyribonucleoside	antiviral drug; DNA synthesis inhibitor
pilocarpine Pilocarpine: A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma.. (+)-pilocarpine : The (+)-enantiomer of pilocarpine.	3.59	2	0	pilocarpine	antiglaucoma drug
triiodothyronine Triiodothyronine: A T3 thyroid hormone normally synthesized and secreted by the thyroid gland in much smaller quantities than thyroxine (T4). Most T3 is derived from peripheral monodeiodination of T4 at the 5' position of the outer ring of the iodothyronine nucleus. The hormone finally delivered and used by the tissues is mainly T3.. 3,3',5-triiodo-L-thyronine : An iodothyronine compound having iodo substituents at the 3-, 3'- and 5-positions. Although some is produced in the thyroid, most of the 3,3',5-triiodo-L-thyronine in the body is generated by mono-deiodination of L-thyroxine in the peripheral tissues. Its metabolic activity is about 3 to 5 times that of L-thyroxine. The sodium salt is used in the treatment of hypothyroidism.	4.29	5	0	2-halophenol; amino acid zwitterion; iodophenol; iodothyronine	human metabolite; mouse metabolite; thyroid hormone
diethylnitrosamine Diethylnitrosamine: A nitrosamine derivative with alkylating, carcinogenic, and mutagenic properties.. N-nitrosodiethylamine : A nitrosamine that is N-ethylethanamine substituted by a nitroso group at the N-atom.	2.07	1	0	nitrosamine	carcinogenic agent; hepatotoxic agent; mutagen
carbon tetrachloride Carbon Tetrachloride: A solvent for oils, fats, lacquers, varnishes, rubber waxes, and resins, and a starting material in the manufacturing of organic compounds. Poisoning by inhalation, ingestion or skin absorption is possible and may be fatal. (Merck Index, 11th ed). tetrachloromethane : A chlorocarbon that is methane in which all the hydrogens have been replaced by chloro groups.	2.08	1	0	chlorocarbon; chloromethanes	hepatotoxic agent; refrigerant
serine Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from GLYCINE or THREONINE. It is involved in the biosynthesis of PURINES; PYRIMIDINES; and other amino acids.. serine : An alpha-amino acid that is alanine substituted at position 3 by a hydroxy group.	10.45	5	1	L-alpha-amino acid; proteinogenic amino acid; serine family amino acid; serine zwitterion; serine	algal metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
4-nitroquinoline-1-oxide 4-nitroquinoline N-oxide : A quinoline N-oxide carrying a nitro substituent at position 4.	2.21	1	0	C-nitro compound; quinoline N-oxide	carcinogenic agent
chloramphenicol Amphenicol: Chloramphenicol and its derivatives.	4.29	5	0	C-nitro compound; carboxamide; diol; organochlorine compound	antibacterial drug; antimicrobial agent; Escherichia coli metabolite; geroprotector; Mycoplasma genitalium metabolite; protein synthesis inhibitor
glutamine Glutamine: A non-essential amino acid present abundantly throughout the body and is involved in many metabolic processes. It is synthesized from GLUTAMIC ACID and AMMONIA. It is the principal carrier of NITROGEN in the body and is an important energy source for many cells.. L-glutamine : An optically active form of glutamine having L-configuration.. glutamine : An alpha-amino acid that consists of butyric acid bearing an amino substituent at position 2 and a carbamoyl substituent at position 4.	6.23	5	1	amino acid zwitterion; glutamine family amino acid; glutamine; L-alpha-amino acid; polar amino acid zwitterion; proteinogenic amino acid	EC 1.14.13.39 (nitric oxide synthase) inhibitor; Escherichia coli metabolite; human metabolite; metabolite; micronutrient; mouse metabolite; nutraceutical; Saccharomyces cerevisiae metabolite
lysine Lysine: An essential amino acid. It is often added to animal feed.. lysine : A diamino acid that is caproic (hexanoic) acid bearing two amino substituents at positions 2 and 6.. L-lysine : An L-alpha-amino acid; the L-isomer of lysine.	4.3	5	0	aspartate family amino acid; L-alpha-amino acid zwitterion; L-alpha-amino acid; lysine; organic molecular entity; proteinogenic amino acid	algal metabolite; anticonvulsant; Escherichia coli metabolite; human metabolite; micronutrient; mouse metabolite; nutraceutical; plant metabolite; Saccharomyces cerevisiae metabolite
cetrimonium bromide cetyltrimethylammonium bromide : The organic bromide salt that is the bromide salt of cetyltrimethylammonium; one of the components of the topical antiseptic cetrimide.	2.05	1	0	organic bromide salt; quaternary ammonium salt	detergent; surfactant
cyanides Cyanides: Inorganic salts of HYDROGEN CYANIDE containing the -CN radical. The concept also includes isocyanides. It is distinguished from NITRILES, which denotes organic compounds containing the -CN radical.. cyanides : Salts and C-organyl derivatives of hydrogen cyanide, HC#N.. isocyanide : The isomer HN(+)#C(-) of hydrocyanic acid, HC#N, and its hydrocarbyl derivatives RNC (RN(+)#C(-)).. cyanide : A pseudohalide anion that is the conjugate base of hydrogen cyanide.	3.58	2	0	pseudohalide anion	EC 1.9.3.1 (cytochrome c oxidase) inhibitor
vincristine [no description available]	3.86	3	0	acetate ester; formamides; methyl ester; organic heteropentacyclic compound; organic heterotetracyclic compound; tertiary alcohol; tertiary amino compound; vinca alkaloid	antineoplastic agent; drug; microtubule-destabilising agent; plant metabolite; tubulin modulator
physostigmine Physostigmine: A cholinesterase inhibitor that is rapidly absorbed through membranes. It can be applied topically to the conjunctiva. It also can cross the blood-brain barrier and is used when central nervous system effects are desired, as in the treatment of severe anticholinergic toxicity.	3.59	2	0	carbamate ester; indole alkaloid	antidote to curare poisoning; EC 3.1.1.8 (cholinesterase) inhibitor; miotic
sucrose Saccharum: A plant genus of the family POACEAE widely cultivated in the tropics for the sweet cane that is processed into sugar.	2.05	1	0	glycosyl glycoside	algal metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; osmolyte; Saccharomyces cerevisiae metabolite; sweetening agent
ethinyl estradiol Ethinyl Estradiol: A semisynthetic alkylated ESTRADIOL with a 17-alpha-ethinyl substitution. It has high estrogenic potency when administered orally, and is often used as the estrogenic component in ORAL CONTRACEPTIVES.. 17alpha-ethynylestradiol : A 3-hydroxy steroid that is estradiol substituted by a ethynyl group at position 17. It is a xenoestrogen synthesized from estradiol and has been shown to exhibit high estrogenic potency on oral administration.	2.75	3	0	17-hydroxy steroid; 3-hydroxy steroid; terminal acetylenic compound	xenoestrogen
testosterone propionate Testosterone Propionate: An ester of TESTOSTERONE with a propionate substitution at the 17-beta position.. androgen : A sex hormone that stimulates or controls the development and maintenance of masculine characteristics in vertebrates by binding to androgen receptors.	2.05	1	0	steroid ester
tubocurarine Tubocurarine: A neuromuscular blocker and active ingredient in CURARE; plant based alkaloid of Menispermaceae.. tubocurarine : A benzylisoquinoline alkaloid muscle relaxant which constitutes the active component of curare.. isoquinoline alkaloid : Any alkaloid that has a structure based on an isoquinoline nucleus. They are derived from the amino acids like tyrosine and phenylalanine.	2.08	1	0	bisbenzylisoquinoline alkaloid	drug allergen; muscle relaxant; nicotinic antagonist
9,10-dimethyl-1,2-benzanthracene 9,10-Dimethyl-1,2-benzanthracene: Polycyclic aromatic hydrocarbon found in tobacco smoke that is a potent carcinogen.. 7,12-dimethyltetraphene : A tetraphene having methyl substituents at the 7- and 12-positions. It is a potent carcinogen and is present in tobacco smoke.	2.11	1	0	ortho-fused polycyclic arene; tetraphenes	carcinogenic agent
apomorphine Apomorphine: A derivative of morphine that is a dopamine D2 agonist. It is a powerful emetic and has been used for that effect in acute poisoning. It has also been used in the diagnosis and treatment of parkinsonism, but its adverse effects limit its use.	4.08	4	0	aporphine alkaloid	alpha-adrenergic drug; antidyskinesia agent; antiparkinson drug; dopamine agonist; emetic; serotonergic drug
aminopyrine Aminopyrine: A pyrazolone with analgesic, anti-inflammatory, and antipyretic properties but has risk of AGRANULOCYTOSIS. A breath test with 13C-labeled aminopyrine has been used as a non-invasive measure of CYTOCHROME P-450 metabolic activity in LIVER FUNCTION TESTS.. aminophenazone : A pyrazolone that is 1,2-dihydro-3H-pyrazol-3-one substituted by a dimethylamino group at position 4, methyl groups at positions 1 and 5 and a phenyl group at position 2. It exhibits analgesic, anti-inflammatory, and antipyretic properties.	2.05	1	0	pyrazolone; tertiary amino compound	antipyretic; environmental contaminant; non-narcotic analgesic; non-steroidal anti-inflammatory drug; xenobiotic
methyltestosterone Methyltestosterone: A synthetic hormone used for androgen replacement therapy and as an hormonal antineoplastic agent (ANTINEOPLASTIC AGENTS, HORMONAL).. methyltestosterone : A 17beta-hydroxy steroid that is testosterone bearing a methyl group at the 17alpha position.	3.59	2	0	17beta-hydroxy steroid; 3-oxo-Delta(4) steroid; enone	anabolic agent; androgen; antineoplastic agent
tetrabenazine 9,10-dimethoxy-3-isobutyl-1,3,4,6,7,11b-hexahydro-2H-pyrido[2,1-a]isoquinolin-2-one : A benzoquinolizine that is 1,2,3,4,4a,9,10,10a-octahydrophenanthrene in which the carbon at position 10a is replaced by a nitrogen and which is substituted by an isobutyl group at position 2, an oxo group at position 3, and methoxy groups at positions 6 and 7.	3.59	2	0	benzoquinolizine; cyclic ketone; tertiary amino compound
adenosine diphosphate Adenosine Diphosphate: Adenosine 5'-(trihydrogen diphosphate). An adenine nucleotide containing two phosphate groups esterified to the sugar moiety at the 5'-position.	2.21	1	0	adenosine 5'-phosphate; purine ribonucleoside 5'-diphosphate	fundamental metabolite; human metabolite
cephalothin Cephalothin: A cephalosporin antibiotic.. cefalotin : A semisynthetic, first-generation cephalosporin antibiotic with acetoxymethyl and (2-thienylacetyl)nitrilo moieties at positions 3 and 7, respectively, of the core structure. Administered parenterally during surgery and to treat a wide spectrum of blood infections.	2.45	2	0	azabicycloalkene; beta-lactam antibiotic allergen; carboxylic acid; cephalosporin; semisynthetic derivative; thiophenes	antibacterial drug; antimicrobial agent
uridine [no description available]	2.46	2	0	uridines	drug metabolite; fundamental metabolite; human metabolite
kanamycin a Kanamycin: Antibiotic complex produced by Streptomyces kanamyceticus from Japanese soil. Comprises 3 components: kanamycin A, the major component, and kanamycins B and C, the minor components.. kanamycin : Kanamycin is a naturally occurring antibiotic complex from Streptomyces kanamyceticus that consists of several components: kanamycin A, the major component (also usually designated as kanamycin), and kanamycins B, C, D and X the minor components.	4.08	4	0	kanamycins	bacterial metabolite
carbostyril Quinolones: A group of derivatives of naphthyridine carboxylic acid, quinoline carboxylic acid, or NALIDIXIC ACID.. quinolin-2(1H)-one : A quinolone that is 1,2-dihydroquinoline substituted by an oxo group at position 2.	7.12	8	2	monohydroxyquinoline; quinolone	bacterial xenobiotic metabolite
phenylephrine Phenylephrine: An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.. phenylephrine : A member of the class of the class of phenylethanolamines that is (1R)-2-(methylamino)-1-phenylethan-1-ol carrying an additional hydroxy substituent at position 3 on the phenyl ring.	2.05	1	0	phenols; phenylethanolamines; secondary amino compound	alpha-adrenergic agonist; cardiotonic drug; mydriatic agent; nasal decongestant; protective agent; sympathomimetic agent; vasoconstrictor agent
levodopa Levodopa: The naturally occurring form of DIHYDROXYPHENYLALANINE and the immediate precursor of DOPAMINE. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to DOPAMINE. It is used for the treatment of PARKINSONIAN DISORDERS and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system.. L-dopa : An optically active form of dopa having L-configuration. Used to treat the stiffness, tremors, spasms, and poor muscle control of Parkinson's disease	2.75	3	0	amino acid zwitterion; dopa; L-tyrosine derivative; non-proteinogenic L-alpha-amino acid	allelochemical; antidyskinesia agent; antiparkinson drug; dopaminergic agent; hapten; human metabolite; mouse metabolite; neurotoxin; plant growth retardant; plant metabolite; prodrug
edetic acid Edetic Acid: A chelating agent that sequesters a variety of polyvalent cations such as CALCIUM. It is used in pharmaceutical manufacturing and as a food additive.	3.23	1	0	ethylenediamine derivative; polyamino carboxylic acid; tetracarboxylic acid	anticoagulant; antidote; chelator; copper chelator; geroprotector
phenylethyl alcohol Phenylethyl Alcohol: An antimicrobial, antiseptic, and disinfectant that is used also as an aromatic essence and preservative in pharmaceutics and perfumery.. 2-phenylethanol : A primary alcohol that is ethanol substituted by a phenyl group at position 2.	2.61	2	0	benzenes; primary alcohol	Aspergillus metabolite; fragrance; plant growth retardant; plant metabolite; Saccharomyces cerevisiae metabolite
tyrosine Tyrosine: A non-essential amino acid. In animals it is synthesized from PHENYLALANINE. It is also the precursor of EPINEPHRINE; THYROID HORMONES; and melanin.. tyrosine : An alpha-amino acid that is phenylalanine bearing a hydroxy substituent at position 4 on the phenyl ring.	11.18	9	1	amino acid zwitterion; erythrose 4-phosphate/phosphoenolpyruvate family amino acid; L-alpha-amino acid; proteinogenic amino acid; tyrosine	EC 1.3.1.43 (arogenate dehydrogenase) inhibitor; fundamental metabolite; micronutrient; nutraceutical
cysteamine Cysteamine: A mercaptoethylamine compound that is endogenously derived from the COENZYME A degradative pathway. The fact that cysteamine is readily transported into LYSOSOMES where it reacts with CYSTINE to form cysteine-cysteamine disulfide and CYSTEINE has led to its use in CYSTINE DEPLETING AGENTS for the treatment of CYSTINOSIS.. cysteamine : An amine that consists of an ethane skeleton substituted with a thiol group at C-1 and an amino group at C-2.	3.23	1	0	amine; thiol	geroprotector; human metabolite; mouse metabolite; radiation protective agent
acetylcholine chloride acetylcholine chloride : The chloride salt of acetylcholine, and a parasympatomimetic drug.	3.23	1	0	quaternary ammonium salt
mepazine mepazine: major descriptor (66-85); on-line search PHENOTHIAZINES (66-85); Index Medicus search MEPAZINE (66-85); RN given refers to parent cpd. pacatal : A phenothiazine derivative in which 10H-phenothiazine has an N-methylpiperidin-4-ylmethyl substituent at the N-10 position.	3.23	1	0	phenothiazines
methicillin Methicillin: One of the PENICILLINS which is resistant to PENICILLINASE but susceptible to a penicillin-binding protein. It is inactivated by gastric acid so administered by injection.. methicillin : A penicillin that is 6-aminopenicillanic acid in which one of the amino hydrogens is replaced by a 2,6-dimethoxybenzoyl group.	2.04	1	0	penicillin allergen; penicillin	antibacterial drug
niridazole Niridazole: An antischistosomal agent that has become obsolete.	2.05	1	0	1,3-thiazoles; C-nitro compound
cloxacillin Cloxacillin: A semi-synthetic antibiotic that is a chlorinated derivative of OXACILLIN.. cloxacillin : A semisynthetic penicillin antibiotic carrying a 3-(2-chlorophenyl)-5-methylisoxazole-4-carboxamido group at position 6.	3.23	1	0	penicillin allergen; penicillin; semisynthetic derivative	antibacterial agent; antibacterial drug
zoxazolamine Zoxazolamine: A uricosuric and muscle relaxant. Zoxazolamine acts centrally as a muscle relaxant, but the mechanism of its action is not understood.	2.6	1	0	benzoxazole
leucine Leucine: An essential branched-chain amino acid important for hemoglobin formation.. leucine : A branched-chain amino acid that consists of glycine in which one of the hydrogens attached to the alpha-carbon is substituted by an isobutyl group.	3.31	6	0	amino acid zwitterion; L-alpha-amino acid; leucine; proteinogenic amino acid; pyruvate family amino acid	algal metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; plant metabolite; Saccharomyces cerevisiae metabolite
4-nitrobenzoic acid 4-nitrobenzoic acid: RN given refers to parent cpd. 4-nitrobenzoic acid : A nitrobenzoic acid having the nitro group at the 4-position.	2.25	1	0	nitrobenzoic acid
calcium acetate calcium acetate: a principal compound used as phosphate binders in patients with chronic renal failure; used like sevelamer. calcium acetate : The calcium salt of acetic acid. It is used, commonly as a hydrate, to treat hyperphosphataemia (excess phosphate in the blood) in patients with kidney disease: the calcium ion combines with dietary phosphate to form (insoluble) calcium phosphate, which is excreted in the faeces.	3.23	1	0	calcium salt	chelator
carbaryl Carbaryl: A carbamate insecticide and parasiticide. It is a potent anticholinesterase agent belonging to the carbamate group of reversible cholinesterase inhibitors. It has a particularly low toxicity from dermal absorption and is used for control of head lice in some countries.. carbaryl : A carbamate ester obtained by the formal condensation of 1-naphthol with methylcarbamic acid.	2.05	1	0	carbamate ester; naphthalenes	acaricide; agrochemical; carbamate insecticide; EC 3.1.1.7 (acetylcholinesterase) inhibitor; EC 3.1.1.8 (cholinesterase) inhibitor; plant growth retardant
lactose Lactose: A disaccharide of GLUCOSE and GALACTOSE in human and cow milk. It is used in pharmacy for tablets, in medicine as a nutrient, and in industry.. lactose : A glycosylglucose disaccharide, found most notably in milk, that consists of D-galactose and D-glucose fragments bonded through a beta-1->4 glycosidic linkage. The glucose fragment can be in either the alpha- or beta-pyranose form, whereas the galactose fragment can only have the beta-pyranose form.. beta-lactose : The beta-anomer of lactose.	2.05	1	0	lactose
methionine Methionine: A sulfur-containing essential L-amino acid that is important in many body functions.. methionine : A sulfur-containing amino acid that is butyric acid bearing an amino substituent at position 2 and a methylthio substituent at position 4.	3.59	2	0	aspartate family amino acid; L-alpha-amino acid; methionine zwitterion; methionine; proteinogenic amino acid	antidote to paracetamol poisoning; human metabolite; micronutrient; mouse metabolite; nutraceutical
phenylalanine Phenylalanine: An essential aromatic amino acid that is a precursor of MELANIN; DOPAMINE; noradrenalin (NOREPINEPHRINE), and THYROXINE.. L-phenylalanine : The L-enantiomer of phenylalanine.. phenylalanine : An aromatic amino acid that is alanine in which one of the methyl hydrogens is substituted by a phenyl group.	3.02	4	0	amino acid zwitterion; erythrose 4-phosphate/phosphoenolpyruvate family amino acid; L-alpha-amino acid; phenylalanine; proteinogenic amino acid	algal metabolite; EC 3.1.3.1 (alkaline phosphatase) inhibitor; Escherichia coli metabolite; human xenobiotic metabolite; micronutrient; mouse metabolite; nutraceutical; plant metabolite; Saccharomyces cerevisiae metabolite
Mebutamate [no description available]	2.05	1	0	organic molecular entity
colchicine (S)-colchicine : A colchicine that has (S)-configuration. It is a secondary metabolite, has anti-inflammatory properties and is used to treat gout, crystal-induced joint inflammation, familial Mediterranean fever, and many other conditions.	4.57	7	0	alkaloid; colchicine	anti-inflammatory agent; gout suppressant; mutagen
mebanazine mebanazine: RN given refers to parent cpd without isomeric designation; structure	3.23	1	0	benzenes
oxacillin Oxacillin: An antibiotic similar to FLUCLOXACILLIN used in resistant staphylococci infections.. oxacillin : A penicillin antibiotic carrying a 5-methyl-3-phenylisoxazole-4-carboxamide group at position 6beta.	3.58	2	0	penicillin	antibacterial agent; antibacterial drug
cycloheximide Cycloheximide: Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.. cycloheximide : A dicarboximide that is 4-(2-hydroxyethyl)piperidine-2,6-dione in which one of the hydrogens attached to the carbon bearing the hydroxy group is replaced by a 3,5-dimethyl-2-oxocyclohexyl group. It is an antibiotic produced by the bacterium Streptomyces griseus.	3.77	10	0	antibiotic fungicide; cyclic ketone; dicarboximide; piperidine antibiotic; piperidones; secondary alcohol	anticoronaviral agent; bacterial metabolite; ferroptosis inhibitor; neuroprotective agent; protein synthesis inhibitor
ficusin Ficusin: A naturally occurring furocoumarin, found in PSORALEA. After photoactivation with UV radiation, it binds DNA via single and double-stranded cross-linking.. psoralen : The simplest member of the class of psoralens that is 7H-furo[3,2-g]chromene having a keto group at position 7. It has been found in plants like Psoralea corylifolia and Ficus salicifolia.	2.6	1	0	psoralens	plant metabolite
fluocinolone acetonide Fluocinolone Acetonide: A glucocorticoid derivative used topically in the treatment of various skin disorders. It is usually employed as a cream, gel, lotion, or ointment. It has also been used topically in the treatment of inflammatory eye, ear, and nose disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p732). fluocinolone acetonide : A fluorinated steroid that is flunisolide in which the hydrogen at position 9 is replaced by fluorine. A corticosteroid with glucocorticoid activity, it is used (both as the anhydrous form and as the dihydrate) in creams, gels and ointments for the treatment of various skin disorders.	2.06	1	0	11beta-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; cyclic ketal; fluorinated steroid; glucocorticoid; organic heteropentacyclic compound; primary alpha-hydroxy ketone	anti-inflammatory drug; antipruritic drug
triamcinolone diacetate triamcinolone diacetate: lysyl oxidase antagonist; Polcortolon may also refers to triamcinolone	2.08	1	0	corticosteroid hormone
norethindrone Norethindrone: A synthetic progestational hormone with actions similar to those of PROGESTERONE but functioning as a more potent inhibitor of ovulation. It has weak estrogenic and androgenic properties. The hormone has been used in treating amenorrhea, functional uterine bleeding, endometriosis, and for CONTRACEPTION.. norethisterone : A 17beta-hydroxy steroid that is testosterone in which the hydrogen at position 17 is replaced by an ethynyl group and in which the methyl group attached to position 10 is replaced by hydrogen.	2.05	1	0	17beta-hydroxy steroid; 3-oxo-Delta(4) steroid; terminal acetylenic compound; tertiary alcohol	progestin; synthetic oral contraceptive
norethynodrel Norethynodrel: A synthetic progestational hormone with actions and uses similar to those of PROGESTERONE. It has been used in the treatment of functional uterine bleeding and ENDOMETRIOSIS. As a contraceptive (CONTRACEPTIVE AGENTS), it has usually been administered in combination with MESTRANOL.	2.05	1	0	oxo steroid
cycloserine Cycloserine: Antibiotic substance produced by Streptomyces garyphalus.. D-cycloserine : A 4-amino-1,2-oxazolidin-3-one that has R configuration. It is an antibiotic produced by Streptomyces garyphalus or S. orchidaceus and is used as part of a multi-drug regimen for the treatment of tuberculosis when resistance to, or toxicity from, primary drugs has developed. An analogue of D-alanine, it interferes with bacterial cell wall synthesis in the cytoplasm by competitive inhibition of L-alanine racemase (which forms D-alanine from L-alanine) and D-alanine--D-alanine ligase (which incorporates D-alanine into the pentapeptide required for peptidoglycan formation and bacterial cell wall synthesis).	3.23	1	0	4-amino-1,2-oxazolidin-3-one; organonitrogen heterocyclic antibiotic; organooxygen heterocyclic antibiotic; zwitterion	antiinfective agent; antimetabolite; antitubercular agent; metabolite; NMDA receptor agonist
benziodarone benziodarone: minor descriptor (75-89); on-line & INDEX MEDICUS search BENZOFURANS (68-89) & IODOBENZOATES (74)	3.59	2	0	aromatic ketone
tubercidin Tubercidin: An antibiotic purine ribonucleoside that readily substitutes for adenosine in the biological system, but its incorporation into DNA and RNA has an inhibitory effect on the metabolism of these nucleic acids.. tubercidin : An N-glycosylpyrrolopyrimidine that is adenosine in which the in the 5-membered ring that is not attached to the ribose moiety is replaced by a carbon. Tubercidin is produced in the culture broth of Streptomyces tubericidus.	2.57	2	0	antibiotic antifungal agent; N-glycosylpyrrolopyrimidine; ribonucleoside	antimetabolite; antineoplastic agent; bacterial metabolite
ampicillin Ampicillin: Semi-synthetic derivative of penicillin that functions as an orally active broad-spectrum antibiotic.. ampicillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-amino-2-phenylacetamido group.	3.86	3	0	beta-lactam antibiotic; penicillin allergen; penicillin	antibacterial drug
mannitol [no description available]	9.35	5	0	mannitol	allergen; antiglaucoma drug; compatible osmolytes; Escherichia coli metabolite; food anticaking agent; food bulking agent; food humectant; food stabiliser; food thickening agent; hapten; metabolite; osmotic diuretic; sweetening agent
cytarabine [no description available]	13.72	50	13	beta-D-arabinoside; monosaccharide derivative; pyrimidine nucleoside	antimetabolite; antineoplastic agent; antiviral agent; immunosuppressive agent
trifluridine Trifluridine: An antiviral derivative of THYMIDINE used mainly in the treatment of primary keratoconjunctivitis and recurrent epithelial keratitis due to HERPES SIMPLEX virus. (From Martindale, The Extra Pharmacopoeia, 30th ed, p557). trifluridine : A pyrimidine 2'-deoxyribonucleoside compound having 5-trifluoromethyluracil as the nucleobase. An antiviral drug used mainly in the treatment of primary keratoconjunctivitis and recurrent epithelial keratitis.	2.6	1	0	nucleoside analogue; organofluorine compound; pyrimidine 2'-deoxyribonucleoside	antimetabolite; antineoplastic agent; antiviral drug; EC 2.1.1.45 (thymidylate synthase) inhibitor
dinitrofluorobenzene Dinitrofluorobenzene: Irritants and reagents for labeling terminal amino acid groups.. 1-fluoro-2,4-dinitrobenzene : The organofluorine compound that is benzene with a fluoro substituent at the 1-position and two nitro substituents in the 2- and 4-positions.	2.06	1	0	C-nitro compound; organofluorine compound	agrochemical; allergen; chromatographic reagent; EC 2.7.3.2 (creatine kinase) inhibitor; protein-sequencing agent; spectrophotometric reagent
asparagine Asparagine: A non-essential amino acid that is involved in the metabolic control of cell functions in nerve and brain tissue. It is biosynthesized from ASPARTIC ACID and AMMONIA by asparagine synthetase. (From Concise Encyclopedia Biochemistry and Molecular Biology, 3rd ed). asparagine : An alpha-amino acid in which one of the hydrogens attached to the alpha-carbon of glycine is substituted by a 2-amino-2-oxoethyl group.	2.21	1	0	amino acid zwitterion; asparagine; aspartate family amino acid; L-alpha-amino acid; proteinogenic amino acid	Escherichia coli metabolite; human metabolite; micronutrient; mouse metabolite; nutraceutical; plant metabolite; Saccharomyces cerevisiae metabolite
medroxyprogesterone acetate [no description available]	2.47	2	0	20-oxo steroid; 3-oxo-Delta(4) steroid; acetate ester; corticosteroid; steroid ester	adjuvant; androgen; antineoplastic agent; antioxidant; female contraceptive drug; inhibitor; progestin; synthetic oral contraceptive
valine Valine: A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway.. valine : A branched-chain amino acid that consists of glycine in which one of the hydrogens attached to the alpha-carbon is substituted by an isopropyl group.. L-valine : The L-enantiomer of valine.	2.5	2	0	L-alpha-amino acid zwitterion; L-alpha-amino acid; proteinogenic amino acid; pyruvate family amino acid; valine	algal metabolite; Escherichia coli metabolite; human metabolite; micronutrient; mouse metabolite; nutraceutical; Saccharomyces cerevisiae metabolite
threonine Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins.. threonine : An alpha-amino acid in which one of the hydrogens attached to the alpha-carbon of glycine is substituted by a 1-hydroxyethyl group.	7.7	16	0	amino acid zwitterion; aspartate family amino acid; L-alpha-amino acid; proteinogenic amino acid; threonine	algal metabolite; Escherichia coli metabolite; human metabolite; micronutrient; mouse metabolite; nutraceutical; plant metabolite; Saccharomyces cerevisiae metabolite
mestranol [no description available]	2.05	1	0	17beta-hydroxy steroid; aromatic ether; terminal acetylenic compound	prodrug; xenoestrogen
methaqualone Methaqualone: A quinazoline derivative with hypnotic and sedative properties. It has been withdrawn from the market in many countries because of problems with abuse. (From Martindale, The Extra Pharmacopoeia, 30th ed, p604). methaqualone : A member of the class of quinazolines that is quinazolin-4-one substituted at positions 2 and 3 by methyl and o-tolyl groups respectively. A depressant that increases the activity of the GABA receptors in the brain and nervous system, it is used as a sedative and hypnotic medication. It became popular as a recreational drug and club drug in the late 1960s and 1970s.	2.05	1	0	quinazolines	GABA agonist; sedative
trypan blue VisionBlue: A trypan blue ophthalmic solution.	2.05	1	0
cordycepin [no description available]	2.05	1	0	3'-deoxyribonucleoside; adenosines	antimetabolite; nucleoside antibiotic
tryptophan Tryptophan: An essential amino acid that is necessary for normal growth in infants and for NITROGEN balance in adults. It is a precursor of INDOLE ALKALOIDS in plants. It is a precursor of SEROTONIN (hence its use as an antidepressant and sleep aid). It can be a precursor to NIACIN, albeit inefficiently, in mammals.. tryptophan : An alpha-amino acid that is alanine bearing an indol-3-yl substituent at position 3.	2.47	2	0	erythrose 4-phosphate/phosphoenolpyruvate family amino acid; L-alpha-amino acid zwitterion; L-alpha-amino acid; proteinogenic amino acid; tryptophan zwitterion; tryptophan	antidepressant; Escherichia coli metabolite; human metabolite; micronutrient; mouse metabolite; nutraceutical; plant metabolite; Saccharomyces cerevisiae metabolite
4-chlorobenzoic acid 4-chlorobenzoic acid: RN given refers to parent cpd. 4-chlorobenzoic acid : A monochlorobenzoic acid carrying a chloro substituent at position 4.	2.25	1	0	monochlorobenzoic acid	bacterial xenobiotic metabolite
arginine Arginine: An essential amino acid that is physiologically active in the L-form.. arginine : An alpha-amino acid that is glycine in which the alpha-is substituted by a 3-guanidinopropyl group.	4.09	4	0	arginine; glutamine family amino acid; L-alpha-amino acid; proteinogenic amino acid	biomarker; Escherichia coli metabolite; micronutrient; mouse metabolite; nutraceutical
boranes Boranes: The collective name for the boron hydrides, which are analogous to the alkanes and silanes. Numerous boranes are known. Some have high calorific values and are used in high-energy fuels. (From Grant & Hackh's Chemical Dictionary, 5th ed). borane : The simplest borane, consisting of a single boron atom carrying three hydrogens.. boranes : The molecular hydrides of boron.	3.91	3	0	boranes; mononuclear parent hydride
trichloroacetic acid Trichloroacetic Acid: A strong acid used as a protein precipitant in clinical chemistry and also as a caustic for removing warts.. trichloroacetic acid : A monocarboxylic acid that is acetic acid in which all three methyl hydrogens are substituted by chlorine.	2.05	1	0	monocarboxylic acid; organochlorine compound	carcinogenic agent; metabolite; mouse metabolite
perflutren Definity: a fluorocarbon-filled ultrasonic contrast agent; Definity is tradename. octafluoropropane : A fluorocarbon that is propane in which all of the hydrogens have been replaced by fluorines.	3.23	1	0	fluoroalkane; fluorocarbon
triamcinolone acetonide Triamcinolone Acetonide: An esterified form of TRIAMCINOLONE. It is an anti-inflammatory glucocorticoid used topically in the treatment of various skin disorders. Intralesional, intramuscular, and intra-articular injections are also administered under certain conditions.. triamcinolone acetonide : A synthetic glucocorticoid that is the 16,17-acetonide of triamcinolone. Used to treat various skin infections.	2.75	3	0	11beta-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(4) steroid; cyclic ketal; fluorinated steroid; glucocorticoid; primary alpha-hydroxy ketone	anti-allergic agent; anti-inflammatory drug
fluoxymesterone Fluoxymesterone: An anabolic steroid that has been used in the treatment of male HYPOGONADISM, delayed puberty in males, and in the treatment of breast neoplasms in women.	3.23	1	0	11beta-hydroxy steroid; 17beta-hydroxy steroid; 3-oxo-Delta(4) steroid; anabolic androgenic steroid; fluorinated steroid	anabolic agent; antineoplastic agent
allylpropymal allylpropymal: RN given refers to parent cpd. aprobarbital : A member of the class of barbiturates that is pyrimidine-2,4,6(1H,3H,5H)-trione substituted by an isopropyl and a prop-1-en-3-yl group at position 5.	2.05	1	0	barbiturates
phencyclidine Phencyclidine: A hallucinogen formerly used as a veterinary anesthetic, and briefly as a general anesthetic for humans. Phencyclidine is similar to KETAMINE in structure and in many of its effects. Like ketamine, it can produce a dissociative state. It exerts its pharmacological action through inhibition of NMDA receptors (RECEPTORS, N-METHYL-D-ASPARTATE). As a drug of abuse, it is known as PCP and Angel Dust.. phencyclidine : A member of the class of piperidines that is piperidine in which the nitrogen is substituted with a 1-phenylcyclohexyl group. Formerly used as an anaesthetic agent, it exhibits both hallucinogenic and neurotoxic effects.	4.99	2	1	benzenes; piperidines	anaesthetic; neurotoxin; NMDA receptor antagonist; psychotropic drug
butobarbital butobarbital: Butobarbital should be distinguished from Butabarbital (a synonym for Secbutabarbital)	2.05	1	0	barbiturates
methsuximide methsuximide: anticonvulsant effective in petit mal & psychomotor epilepsy; has a number of unpleasant & toxic side effects; minor descriptor (75-86); on-line & INDEX MEDICUS search SUCCINIMIDES (75-86); RN given refers to parent cpd without isomeric designation	3.23	1	0	organic molecular entity
tromethamine Tromethamine: An organic amine proton acceptor. It is used in the synthesis of surface-active agents and pharmaceuticals; as an emulsifying agent for cosmetic creams and lotions, mineral oil and paraffin wax emulsions, as a biological buffer, and used as an alkalizer. (From Merck, 11th ed; Martindale, The Extra Pharmacopoeia, 30th ed, p1424)	3.23	1	0	primary amino compound; triol	buffer
trichloroethylene Trichloroethylene: A highly volatile inhalation anesthetic used mainly in short surgical procedures where light anesthesia with good analgesia is required. It is also used as an industrial solvent. Prolonged exposure to high concentrations of the vapor can lead to cardiotoxicity and neurological impairment.. triol : A chemical compound containing three hydroxy groups.	2.05	1	0	chloroethenes	inhalation anaesthetic; mouse metabolite
acrylic acid acrylic acid: RN given refers to parent cpd. acrylic acid : A alpha,beta-unsaturated monocarboxylic acid that is ethene substituted by a carboxy group.	4.8	1	1	alpha,beta-unsaturated monocarboxylic acid	metabolite
dichloroacetic acid [no description available]	2.46	2	0	monocarboxylic acid; organochlorine compound	astringent; marine metabolite
dehydrocholic acid Dehydrocholic Acid: A semisynthetic bile acid made from cholic acid. It is used as a cholagogue, hydrocholeretic, diuretic, and as a diagnostic aid.. 3,7,12-trioxo-5beta-cholanic acid : An oxo-5beta-cholanic acid in which three oxo substituents are located at positions 3, 7 and 12 on the cholanic acid skeleton.	2.05	1	0	12-oxo steroid; 3-oxo-5beta-steroid; 7-oxo steroid; oxo-5beta-cholanic acid	gastrointestinal drug
taurocholic acid Taurocholic Acid: The product of conjugation of cholic acid with taurine. Its sodium salt is the chief ingredient of the bile of carnivorous animals. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as a cholagogue and cholerectic.. taurocholate : An organosulfonate oxoanion that is the conjugate base of taurocholic acid.. taurocholic acid : A bile acid taurine conjugate of cholic acid that usually occurs as the sodium salt of bile in mammals.	2.17	1	0	amino sulfonic acid; bile acid taurine conjugate	human metabolite
rhodamine b rhodamine B: RN & N1 from 9th CI Form Index; RN given refers to parent cpd; structure in Merck Index, 9th ed, #7973; TETRAETHYLRHODAMINE was see RHODAMINES 1975-93; use RHODAMINES to search TETRAETHYLRHODAMINE 1975-93. rhodamine B : An organic chloride salt having N-[9-(2-carboxyphenyl)-6-(diethylamino)-3H-xanthen-3-ylidene]-N-ethylethanaminium as the counterion. An amphoteric dye commonly used as a fluorochrome.	5.04	2	1	organic chloride salt; xanthene dye	fluorescent probe; fluorochrome; histological dye
methylprednisolone Methylprednisolone: A PREDNISOLONE derivative with similar anti-inflammatory action.. 6alpha-methylprednisolone : The 6alpha-stereoisomer of 6-methylprednisolone.	8.38	21	3	6-methylprednisolone; primary alpha-hydroxy ketone; tertiary alpha-hydroxy ketone	adrenergic agent; anti-inflammatory drug; antiemetic; environmental contaminant; neuroprotective agent; xenobiotic
rotenone Derris: A plant genus of the family FABACEAE. The root is a source of rotenoids (ROTENONE) and flavonoids. Some species of Pongamia have been reclassified to this genus and some to MILLETTIA. Some species of Deguelia have been reclassified to this genus.. rotenoid : Members of the class of tetrahydrochromenochromene that consists of a cis-fused tetrahydrochromeno[3,4-b]chromene skeleton and its substituted derivatives. The term was originally restricted to natural products, but is now also used to describe semi-synthetic and fully synthetic compounds.	3.05	4	0	organic heteropentacyclic compound; rotenones	antineoplastic agent; metabolite; mitochondrial NADH:ubiquinone reductase inhibitor; phytogenic insecticide; piscicide; toxin
9,10-anthraquinone 9,10-anthraquinone : An anthraquinone that is anthracene in which positions 9 and 10 have been oxidised to carbonyls.	2.6	1	0	anthraquinone
brompheniramine Brompheniramine: Histamine H1 antagonist used in treatment of allergies, rhinitis, and urticaria.. brompheniramine : Pheniramine in which the hydrogen at position 4 of the phenyl substituent is substituted by bromine. A histamine H1 receptor antagonist, brompheniramine is used (commonly as its maleate salt) for the symptomatic relief of allergic conditions, including rhinitis and conjunctivitis.	3.23	1	0	organobromine compound; pyridines	anti-allergic agent; H1-receptor antagonist
penicillin v Penicillin V: A broad-spectrum penicillin antibiotic used orally in the treatment of mild to moderate infections by susceptible gram-positive organisms.. phenoxymethylpenicillin : A penicillin compound having a 6beta-(phenoxyacetyl)amino side-chain.	3.58	2	0	penicillin allergen; penicillin
salicylanilide salicylanilide: RN given refers to parent cpd. salicylanilide : An amide of salicylic acid and of aniline; it is therefore both a salicylamide and an anilide.	2.6	1	0	benzanilide fungicide; salicylamides; salicylanilides
isosorbide dinitrate Isosorbide Dinitrate: A vasodilator used in the treatment of ANGINA PECTORIS. Its actions are similar to NITROGLYCERIN but with a slower onset of action.	3.86	3	0	glucitol derivative; nitrate ester	nitric oxide donor; vasodilator agent
gramine gramine : An aminoalkylindole that is indole carrying a dimethylaminomethyl substituent at postion 3.	2.6	1	0	aminoalkylindole; indole alkaloid; tertiary amino compound	antibacterial agent; antiviral agent; plant metabolite; serotonergic antagonist
n-vinyl-2-pyrrolidinone N-vinyl-2-pyrrolidinone: monomer of POVIDONE; structure given in first source	4.8	1	1	pyrrolidin-2-ones
aminacrine Aminacrine: A highly fluorescent anti-infective dye used clinically as a topical antiseptic and experimentally as a mutagen, due to its interaction with DNA. It is also used as an intracellular pH indicator.. 9-aminoacridine : An aminoacridine that is acridine in which the hydrogen at position 9 is replaced by an amino group. A fluorescent dyd and topical antiseptic agent, it is used (usually as the hydrochloride salt) in eye drops for the treatment of superficial eye infections.	2.6	1	0	aminoacridines; primary amino compound	acid-base indicator; antiinfective agent; antiseptic drug; fluorescent dye; MALDI matrix material; mutagen
pseudoephedrine Pseudoephedrine: A phenethylamine that is an isomer of EPHEDRINE which has less central nervous system effects and usage is mainly for respiratory tract decongestion.. pseudoephedrine : A member of the class of the class of phenylethanolamines that is (1S)-2-(methylamino)-1-phenylethan-1-ol in which the pro-S hydrogen at position 2 is replaced by a methyl group.	3.23	1	0	phenylethanolamines; secondary alcohol; secondary amino compound	anti-asthmatic drug; bronchodilator agent; central nervous system drug; nasal decongestant; plant metabolite; sympathomimetic agent; vasoconstrictor agent; xenobiotic
diethylpropion Diethylpropion: A appetite depressant considered to produce less central nervous system disturbance than most drugs in this therapeutic category. It is also considered to be among the safest for patients with hypertension. (From AMA Drug Evaluations Annual, 1994, p2290). diethylpropion : An aromatic ketone that is propiophenone in which one of the hydrogens alpha- to the carbonyl is substituted by a diethylamino group. A central stimulant and indirect-acting sympathomimetic, it is an appetite depressant and is used as the hydrochloride as an anoretic in the short term management of obesity.	3.23	1	0	aromatic ketone; tertiary amine	appetite depressant
quinoxalines quinoxaline : A naphthyridine in which the nitrogens are at positions 1 and 4.	3.33	6	0	mancude organic heterobicyclic parent; naphthyridine; ortho-fused heteroarene
2-methylquinoline 2-methylquinoline: RN given refers to parent cpd. methylquinoline : Any member of the class of quinolines carrying at least one methyl substituent.. quinaldine : A quinoline compound in which the quinoline skeleton is substituted at C-2 with a methyl group.	2.13	1	0	quinolines
quinaldic acid [no description available]	2.25	1	0	quinolinemonocarboxylic acid	human metabolite; Saccharomyces cerevisiae metabolite
synephrine [no description available]	2.05	1	0	ethanolamines; phenethylamine alkaloid; phenols	alpha-adrenergic agonist; plant metabolite
benzoyl peroxide Benzoyl Peroxide: A peroxide derivative that has been used topically for BURNS and as a dermatologic agent in the treatment of ACNE and POISON IVY DERMATITIS. It is used also as a bleach in the food industry.	2.05	1	0	carbonyl compound
4-tert-butylbenzoic acid 4-tert-butylbenzoic acid: RN given refers to parent cpd	2.25	1	0	alkylbenzene
3-toluic acid 3-toluic acid: RN given refers to parent cpd; structure	2.25	1	0	methylbenzoic acid	human xenobiotic metabolite
methyl gallate methyl gallate: has both immunosuppressive and phytogenic antineoplastic activities; isolated from Acer saccharinum. methyl 3,4,5-trihydroxybenzoate : A gallate ester obtained by the formal condensation of gallic acid with methanol. It exhibits anti-oxidant, anti-tumor, anti-microbial and anti-inflammatory properties.	2.6	1	0	gallate ester	anti-inflammatory agent; antioxidant; plant metabolite
3,5-dinitrobenzoic acid 3,5-dinitrobenzoic acid : A member of the class of benzoic acids that is benzoic acid in which the hydrogens at positions 3 and 5 are replaced by nitro groups.	2.25	1	0	benzoic acids; C-nitro compound
4-anisic acid 4-methoxybenzoic acid: structure in first source. 4-methoxybenzoic acid : A methoxybenzoic acid substituted with a methoxy group at position C-4.	2.25	1	0	methoxybenzoic acid	plant metabolite
ethylbenzene [no description available]	4.8	1	1	alkylbenzene
quinuclidines Quinuclidines: A class of organic compounds which contain two rings that share a pair of bridgehead carbon atoms and contains an amine group.	2.02	1	0	quinuclidines; saturated organic heterobicyclic parent
boric acid [no description available]	2.04	1	0	boric acids	astringent
monobenzone monobenzone: structure. monobenzone : The monobenzyl ether of hydroquinone. It is used as a topical drug for medical depigmentation.	2.6	1	0	benzyl ether	allergen; dermatologic drug; melanin synthesis inhibitor
benzonatate benzonatate: structure in Merck Index, 9th ed, #1107. benzonatate : The ester obtained by formal condensation of 4-butylaminobenzoic acid with nonaethylene glycol monomethyl ether. Structurally related to procaine and benzocaine, it has an anaesthetic effect on the stretch sensors in the lungs, and is used as a non-narcotic cough suppressant.	3.23	1	0	benzoate ester; secondary amino compound; substituted aniline	anaesthetic; antitussive
glyoxal [no description available]	2.03	1	0	dialdehyde	agrochemical; allergen; pesticide; plant growth regulator
cyclohexanol Cyclohexanols: Monohydroxy derivatives of cyclohexanes that contain the general formula R-C6H11O. They have a camphorlike odor and are used in making soaps, insecticides, germicides, dry cleaning, and plasticizers.. cyclohexanols : An alcohol in which one or more hydroxy groups are attached to a cyclohexane skeleton.	3.21	1	0	cyclohexanols; secondary alcohol	solvent
pyrroles 1H-pyrrole : A tautomer of pyrrole that has the double bonds at positions 2 and 4.. pyrrole : A five-membered monocyclic heteroarene comprising one NH and four CH units which forms the parent compound of the pyrrole group of compounds. Its five-membered ring structure has three tautomers. A 'closed class'.. azole : Any monocyclic heteroarene consisting of a five-membered ring containing nitrogen. Azoles can also contain one or more other non-carbon atoms, such as nitrogen, sulfur or oxygen.	12.29	55	2	pyrrole; secondary amine
furan furan : A monocyclic heteroarene with a structure consisting of a 5-membered ring containing four carbons and one oxygen, with formula C4H4O. It is a toxic, flammable, low-boiling (31degreeC) colourless liquid.	2.05	1	0	furans; mancude organic heteromonocyclic parent; monocyclic heteroarene	carcinogenic agent; hepatotoxic agent; Maillard reaction product
thiophenes Thiophenes: A monocyclic heteroarene furan in which the oxygen atom is replaced by a sulfur.. thiophenes : Compounds containing at least one thiophene ring.	5.92	12	0	mancude organic heteromonocyclic parent; monocyclic heteroarene; thiophenes; volatile organic compound	non-polar solvent
ergotamine Ergotamine: A vasoconstrictor found in ergot of Central Europe. It is a serotonin agonist that has been used as an oxytocic agent and in the treatment of MIGRAINE DISORDERS.. ergotamine : A peptide ergot alkaloid that is dihydroergotamine in which a double bond replaces the single bond between positions 9 and 10.	2.45	2	0	peptide ergot alkaloid	alpha-adrenergic agonist; mycotoxin; non-narcotic analgesic; oxytocic; serotonergic agonist; vasoconstrictor agent
methylergonovine Methylergonovine: A homolog of ERGONOVINE containing one more CH2 group. (Merck Index, 11th ed)	3.23	1	0	ergoline alkaloid
neostigmine bromide neostigmine bromide : The bromide salt of neostigmine.	2.45	2	0	bromide salt
phenformin Phenformin: A biguanide hypoglycemic agent with actions and uses similar to those of METFORMIN. Although it is generally considered to be associated with an unacceptably high incidence of lactic acidosis, often fatal, it is still available in some countries. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290). phenformin : A member of the class of biguanides that is biguanide in which one of the terminal nitrogen atoms is substituted by a 2-phenylethyl group. It was used as an anti-diabetic drug but was later withdrawn from the market due to potential risk of lactic acidosis.	2.79	3	0	biguanides	antineoplastic agent; geroprotector; hypoglycemic agent
mephobarbital Mephobarbital: A barbiturate that is metabolized to PHENOBARBITAL. It has been used for similar purposes, especially in EPILEPSY, but there is no evidence mephobarbital offers any advantage over PHENOBARBITAL.. mephobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at N-1 by a methyl group and at C-5 by ethyl and phenyl groups.	2.05	1	0	barbiturates	anticonvulsant
hexachlorobenzene Hexachlorobenzene: An agricultural fungicide and seed treatment agent.. hexachlorobenzene : A member of the class of chlorobenzenes that is benzene in which all of the hydrogens are replaced by chlorines. An agricultural fungicide introduced in the mid-1940s and formerly used as a seed treatment, its use has been banned since 1984 under the Stockholm Convention on Persistent Organic Pollutants.	2.05	1	0	aromatic fungicide; chlorobenzenes	antifungal agrochemical; carcinogenic agent; persistent organic pollutant
2-chlorobenzoic acid 2-chlorobenzoic acid: RN given refers to parent cpd. chlorobenzoic acid : Any member of the class of benzoic acids in which the benzene ring is substituted by at least one chloro group.. 2-chlorobenzoic acid : A monochlorobenzoic acid having the chloro group at the 2-position.	2.25	1	0	2-halobenzoic acid; monochlorobenzoic acid	plant hormone; plant metabolite
trinitrotoluene Trinitrotoluene: A 2,4,6-trinitrotoluene, which is an explosive chemical that can cause skin irritation and other toxic consequences.. 2,4,6-trinitrotoluene : A trinitrotoluene having the nitro groups at positions 2, 4 and 6.	2.05	1	0	trinitrotoluene	explosive
framycetin Framycetin: A component of NEOMYCIN that is produced by Streptomyces fradiae. On hydrolysis it yields neamine and neobiosamine B. (From Merck Index, 11th ed). framycetin : A tetracyclic antibacterial agent derived from neomycin, being a glycoside ester of neamine and neobiosamine B.	5.01	2	1	aminoglycoside	allergen; antibacterial drug; Escherichia coli metabolite
pyrazolanthrone pyrazolanthrone: JNK (c-Jun N-terminal kinase) inhibitor; structure in first source. anthra[1,9-cd]pyrazol-6(2H)-one : A member of the class of anthrapyrazoles that is anthra[1,9-cd]pyrazole substituted at position 6 by an oxo group. An inhibitor of c-Jun N-terminal kinase.	3.44	7	0	anthrapyrazole; aromatic ketone; cyclic ketone	antineoplastic agent; c-Jun N-terminal kinase inhibitor; geroprotector
meglumine Meglumine: 1-Deoxy-1-(methylamino)-D-glucitol. A derivative of sorbitol in which the hydroxyl group in position 1 is replaced by a methylamino group. Often used in conjunction with iodinated organic compounds as contrast medium.. N-methylglucamine : A hexosamine that is D-glucitol in which the hydroxy group at position 1 is substituted by the nitrogen of a methylamino group. A crystalline base, it is used in preparing salts of certain acids for use as diagnostic radiopaque media, while its antimonate is used as an antiprotozoal in the treatment of leishmaniasis.	2.05	1	0	hexosamine; secondary amino compound
cinchophen cinchophen: was heading 1963-94; ACIPHENOCHINOLIUM was see CHINOPHEN 1978-94; use QUINOLINES to search CINCHOPHEN 1966-94	3.59	2	0	quinolines
2-naphthol 2-naphthol: RN given refers to parent cpd. 2-naphthol : A naphthol carrying a hydroxy group at position 2.. naphthols : Any hydroxynaphthalene derivative that has a single hydroxy substituent.	2.58	2	0	naphthol	antinematodal drug; genotoxin; human urinary metabolite; human xenobiotic metabolite; mouse metabolite; radical scavenger
yohimbine Yohimbine: A plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of ERECTILE DYSFUNCTION.. yohimbine : An indole alkaloid with alpha2-adrenoceptor antagonist activity. It is produced by Corynanthe johimbe and Rauwolfia serpentina.	2.05	1	0	methyl 17-hydroxy-20xi-yohimban-16-carboxylate	alpha-adrenergic antagonist; dopamine receptor D2 antagonist; serotonergic antagonist
nafcillin Nafcillin: A semi-synthetic antibiotic related to penicillin.. nafcillin : A penicillin in which the substituent at position 6 of the penam ring is a (2-ethoxy-1-naphthoyl)amino group.	3.58	2	0	penicillin allergen; penicillin	antibacterial drug
ditiocarb Ditiocarb: A chelating agent that has been used to mobilize toxic metals from the tissues of humans and experimental animals. It is the main metabolite of DISULFIRAM.. diethyldithiocarbamic acid : A member of the class of dithiocarbamic acids that is diethylcarbamic acid in which both of the oxygens are replaced by sulfur.	4.13	4	0	dithiocarbamic acids	chelator; copper chelator
1,2-dihydroxybenzene-3,5-disulfonic acid disodium salt 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt: A colorimetric reagent for iron, manganese, titanium, molybdenum, and complexes of zirconium. (From Merck Index, 11th ed)	2.72	3	0	organic molecular entity
mequinol mequinol: depigmenting agent; RN given refers to parent cpd	2.05	1	0	methoxybenzenes; phenols	metabolite
methohexital Methohexital: An intravenous anesthetic with a short duration of action that may be used for induction of anesthesia.. methohexital : A barbiturate, the structure of which is that of barbituric acid substituted at N-1 by a methyl group and at C-5 by allyl and 1-methylpent-2-ynyl groups.	3.58	2	0	acetylenic compound; barbiturates	drug allergen; intravenous anaesthetic
quinestrol Quinestrol: The 3-cyclopentyl ether of ETHINYL ESTRADIOL. After gastrointestinal absorption, it is stored in ADIPOSE TISSUE, slowly released, and metabolized principally to the parent compound. It has been used in ESTROGEN REPLACEMENT THERAPY. (From AMA Drug Evaluations Annual, 1992, p1011)	2.05	1	0	17-hydroxy steroid; terminal acetylenic compound	xenoestrogen
dydrogesterone [no description available]	2.05	1	0	20-oxo steroid; 3-oxo-Delta(4) steroid	progestin
catechin Catechin: An antioxidant flavonoid, occurring especially in woody plants as both (+)-catechin and (-)-epicatechin (cis) forms.. catechin : Members of the class of hydroxyflavan that have a flavan-3-ol skeleton and its substituted derivatives.. rac-catechin : A racemate comprising equimolar amounts of (+)- and (-)-catechin. (+)-catechin : The (+)-enantiomer of catechin and a polyphenolic antioxidant plant metabolite.	4.59	7	0	catechin	antioxidant; plant metabolite
quinazolines Quinazolines: A group of aromatic heterocyclic compounds that contain a bicyclic structure with two fused six-membered aromatic rings, a benzene ring and a pyrimidine ring.. quinazoline : A mancude organic heterobicyclic parent that is naphthalene in which the carbon atoms at positions 1 and 3 have been replaced by nitrogen atoms.. quinazolines : Any organic heterobicyclic compound based on a quinazoline skeleton and its substituted derivatives.	12.17	42	3	azaarene; mancude organic heterobicyclic parent; ortho-fused heteroarene; quinazolines
indazoles Indazoles: A group of heterocyclic aromatic organic compounds consisting of the fusion of BENZENE and PYRAZOLES.	5.83	3	1	indazole
benzoxazoles 1,3-benzoxazole : A benzoxazole in which the benzene ring is fused to a 1,3-oxazole ring across positions 4 and 5.. benzoxazole : Compounds based on a fused 1,2- or 1,3-oxazole and benzene bicyclic ring skeleton.	2.17	1	0	1,3-benzoxazoles; mancude organic heterobicyclic parent
adamantane Adamantane: A tricyclo bridged hydrocarbon.	2.99	4	0	adamantanes; polycyclic alkane
cyclopentane Cyclopentanes: A group of alicyclic hydrocarbons with the general formula R-C5H9.. cyclopentanes : Cyclopentane and its derivatives formed by substitution.	3.36	6	0	cycloalkane; cyclopentanes; volatile organic compound	non-polar solvent
isoxazoles Isoxazoles: Azoles with an OXYGEN and a NITROGEN next to each other at the 1,2 positions, in contrast to OXAZOLES that have nitrogens at the 1,3 positions.. isoxazole : A monocyclic heteroarene with a structure consisting of a 5-membered ring containing three carbon atoms and an oxygen and nitrogen atom adjacent to each other. It is the parent of the class of isoxazoles.. isoxazoles : Oxazoles in which the N and O atoms are adjacent.	7.26	6	1	isoxazoles; mancude organic heteromonocyclic parent; monocyclic heteroarene
thiazoles [no description available]	8.93	24	2	1,3-thiazoles; mancude organic heteromonocyclic parent; monocyclic heteroarene
pyrazines Pyrazines: A heterocyclic aromatic organic compound with the chemical formula C4H4N2.. pyrazine : A diazine that is benzene in which the carbon atoms at positions 1 and 4 have been replaced by nitrogen atoms.	30.81	3,962	618	diazine; pyrazines	Daphnia magna metabolite
ephedrine Ephedrine: A phenethylamine found in EPHEDRA SINICA. PSEUDOEPHEDRINE is an isomer. It is an alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. It has been used for asthma, heart failure, rhinitis, and urinary incontinence, and for its central nervous system stimulatory effects in the treatment of narcolepsy and depression. It has become less extensively used with the advent of more selective agonists.. (-)-ephedrine : A phenethylamine alkaloid that is 2-phenylethanamine substituted by a methyl group at the amino nitrogen and a methyl and a hydroxy group at position 2 and 1 respectively.	3.59	2	0	phenethylamine alkaloid; phenylethanolamines	bacterial metabolite; environmental contaminant; nasal decongestant; plant metabolite; sympathomimetic agent; vasoconstrictor agent; xenobiotic
hydrazine diamine : Any polyamine that contains two amino groups.	10.59	18	4	azane; hydrazines	EC 4.3.1.10 (serine-sulfate ammonia-lyase) inhibitor
chlormadinone acetate Chlormadinone Acetate: An orally active synthetic progestational hormone used often in combinations as an oral contraceptive (CONTRACEPTIVES, ORAL).	2.05	1	0	corticosteroid hormone
pirinitramide Pirinitramide: A diphenylpropylamine with intense narcotic analgesic activity of long duration. It is a derivative of MEPERIDINE with similar activity and usage.	2.04	1	0	nitrile
edrophonium bromide [no description available]	2.04	1	0
2,3-dimercaptosuccinic acid [no description available]	2.05	1	0
dexamethasone 21-phosphate dexamethasone 21-phosphate: has anti-inflammatory activity. dexamethasone phosphate : A steroid phosphate that is the 21-O-phospho derivative of dexamethasone.	2.07	1	0	11beta-hydroxy steroid; 17-hydroxy steroid; 3-oxo-Delta(4) steroid; fluorinated steroid; steroid phosphate; tertiary alpha-hydroxy ketone	glucocorticoid receptor agonist
evans blue Evans Blue: An azo dye used in blood volume and cardiac output measurement by the dye dilution method. It is very soluble, strongly bound to plasma albumin, and disappears very slowly.. Evans blue : An organic sodium salt that is the tetrasodium salt of 6,6'-{(3,3'-dimethyl[1,1'-biphenyl]-4,4'-diyl)bis[diazene-2,1-diyl]}bis(4-amino-5-hydroxynaphthalene-1,3-disulfonate). It is sometimes used as a counterstain, especially in fluorescent methods to suppress background autofluorescence.	2.46	2	0	organic sodium salt	fluorochrome; histological dye; sodium channel blocker; teratogenic agent
monocrotaline Monocrotaline: A pyrrolizidine alkaloid and a toxic plant constituent that poisons livestock and humans through the ingestion of contaminated grains and other foods. The alkaloid causes pulmonary artery hypertension, right ventricular hypertrophy, and pathological changes in the pulmonary vasculature. Significant attenuation of the cardiopulmonary changes are noted after oral magnesium treatment.	3.03	4	0	pyrrolizidine alkaloid
testosterone enanthate [no description available]	2.05	1	0	heptanoate ester; sterol ester	androgen
5-fluorouridine [no description available]	2.05	1	0	organofluorine compound; uridines	mutagen
aminophylline Aminophylline: A drug combination that contains THEOPHYLLINE and ethylenediamine. It is more soluble in water than theophylline but has similar pharmacologic actions. It's most common use is in bronchial asthma, but it has been investigated for several other applications.. aminophylline : A mixture comprising of theophylline and ethylenediamine in a 2:1 ratio.	3.87	3	0	mixture	bronchodilator agent; cardiotonic drug
azacitidine Azacitidine: A pyrimidine analogue that inhibits DNA methyltransferase, impairing DNA methylation. It is also an antimetabolite of cytidine, incorporated primarily into RNA. Azacytidine has been used as an antineoplastic agent.. 5-azacytidine : An N-glycosyl-1,3,5-triazine that is 4-amino-1,3,5-triazin-2(1H)-one substituted by a beta-D-ribofuranosyl residue via an N-glycosidic linkage. An antineoplastic agent, it is used in the treatment of myeloid leukaemia.	15.75	22	4	N-glycosyl-1,3,5-triazine; nucleoside analogue	antineoplastic agent
phenyramidol phenyramidol: considered as a drug that possibly causes hepatotoxicity	2.05	1	0	aminopyridine
carbutamide Carbutamide: A sulfonylurea antidiabetic agent with similar actions and uses to CHLORPROPAMIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p277)	2.05	1	0	benzenes; sulfonamide
galantamine Galantamine: A benzazepine derived from norbelladine. It is found in GALANTHUS and other AMARYLLIDACEAE. It is a cholinesterase inhibitor that has been used to reverse the muscular effects of GALLAMINE TRIETHIODIDE and TUBOCURARINE and has been studied as a treatment for ALZHEIMER DISEASE and other central nervous system disorders.. galanthamine : A benzazepine alkaloid isolated from certain species of daffodils.	3.87	3	0	benzazepine alkaloid fundamental parent; benzazepine alkaloid; organic heterotetracyclic compound; tertiary amino compound	antidote to curare poisoning; cholinergic drug; EC 3.1.1.7 (acetylcholinesterase) inhibitor; EC 3.1.1.8 (cholinesterase) inhibitor; plant metabolite
nandrolone decanoate Nandrolone Decanoate: Decanoic acid ester of nandrolone that is used as an anabolic agent to prevent or treat WASTING SYNDROME associated with severe chronic illness or HIV infection (HIV WASTING SYNDROME). It may also be used in the treatment of POSTMENOPAUSAL OSTEOPOROSIS.	3.59	2	0	steroid ester
bucladesine [no description available]	2.05	1	0	3',5'-cyclic purine nucleotide; butanamides; butyrate ester	agonist; cardiotonic drug; vasodilator agent
procarbazine hydrochloride procarbazine hydrochloride : A hydrochloride obtained by combining procarbazine with one equivalent of hydrochloric acid. An antineoplastic chemotherapy drug used for treatment of Hodgkin's lymphoma. Metabolism yields azo-procarbazine and hydrogen peroxide, which results in the breaking of DNA strands.	2.08	1	0	hydrochloride	antineoplastic agent
betamethasone Betamethasone: A glucocorticoid given orally, parenterally, by local injection, by inhalation, or applied topically in the management of various disorders in which corticosteroids are indicated. Its lack of mineralocorticoid properties makes betamethasone particularly suitable for treating cerebral edema and congenital adrenal hyperplasia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p724)	7.98	4	0	11beta-hydroxy steroid; 17alpha-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; fluorinated steroid; glucocorticoid; primary alpha-hydroxy ketone; tertiary alpha-hydroxy ketone	anti-asthmatic agent; anti-inflammatory drug; immunosuppressive agent
perflubron perflubron: potential anti-obesity compound; reduces food adsorption; 8-carbon perfluorocarbon radiopaque compound; an oral contrast agent for use with MRI to enhance delineation of the bowel distinguishing it from adjacent organs. perflubron : A haloalkane that is perfluorooctane in which a fluorine attached to one of the terminal carbons has been replaced by a bromine.	2.05	1	0	haloalkane; organobromine compound; perfluorinated compound	blood substitute; radioopaque medium
cyproterone acetate [no description available]	2.05	1	0	20-oxo steroid; 3-oxo-Delta(4) steroid; acetate ester; chlorinated steroid; steroid ester	androgen antagonist; geroprotector; progestin
4-fluorobenzoic acid [no description available]	2.25	1	0	fluorobenzoic acid	bacterial xenobiotic metabolite
hydantoins Hydantoins: Compounds based on imidazolidine dione. Some derivatives are ANTICONVULSANTS.. imidazolidine-2,4-dione : An imidazolidinone with oxo groups at position 2 and 4.	4.8	1	1	imidazolidine-2,4-dione
fluorobenzenes Fluorobenzenes: Derivatives of BENZENE that contain FLUORINE.. monofluorobenzene : The simplest member of the class of monofluorobenzenes that is benzene carrying a single fluoro substituent.. fluorobenzenes : Any fluoroarene that is a benzene or a substituted benzene carrying at least one fluoro group.	2.02	1	0	monofluorobenzenes	NMR chemical shift reference compound
dextropropoxyphene Dextropropoxyphene: A narcotic analgesic structurally related to METHADONE. Only the dextro-isomer has an analgesic effect; the levo-isomer appears to exert an antitussive effect.. propoxyphene : A racemate of the (1R,2R)- and (1S,2R)- diastereoisomers.. dextropropoxyphene : The (1S,2R)-(+)-diastereoisomer of propoxyphene.	3.86	3	0	1-benzyl-3-(dimethylamino)-2-methyl-1-phenylpropyl propanoate	mu-opioid receptor agonist; opioid analgesic
ketobemidone ketobemidone: structure	2.04	1	0	piperidines
glycyrrhetinic acid [no description available]	2.05	1	0	cyclic terpene ketone; hydroxy monocarboxylic acid; pentacyclic triterpenoid	immunomodulator; plant metabolite
chenodeoxycholic acid Chenodeoxycholic Acid: A bile acid, usually conjugated with either glycine or taurine. It acts as a detergent to solubilize fats for intestinal absorption and is reabsorbed by the small intestine. It is used as cholagogue, a choleretic laxative, and to prevent or dissolve gallstones.. chenodeoxycholic acid : A dihydroxy-5beta-cholanic acid that is (5beta)-cholan-24-oic acid substituted by hydroxy groups at positions 3 and 7 respectively.. chenodeoxycholate : Conjugate base of chenodeoxycholic acid; major species at pH 7.3.	3.59	2	0	bile acid; C24-steroid; dihydroxy-5beta-cholanic acid	human metabolite; mouse metabolite
indirubin [no description available]	2.15	1	0
lucanthone Lucanthone: One of the SCHISTOSOMICIDES, it has been replaced largely by HYCANTHONE and more recently PRAZIQUANTEL. (From Martindale The Extrapharmacopoeia, 30th ed., p46). lucanthone : A thioxanthen-9-one compound having a methyl substituent at the 1-position and a 2-[(diethylamino)ethyl]amino substituent at the 4-position. Formerly used for the treatment of schistosomiasis. It is a prodrug, being metabolised to hycanthone.	2.6	1	0	thioxanthenes	adjuvant; antineoplastic agent; EC 5.99.1.2 (DNA topoisomerase) inhibitor; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; mutagen; photosensitizing agent; prodrug; schistosomicide drug
cepharanthine cepharanthine: isoquinoline alkaloid from tubers of STEPHANIA; stimulates recovery of immunologic function in lymphatic system after administration of antineoplastic agents or x-irradiation. cepharanthine : A bisbenzylisoquinoline alkaloid from tubers of Stephania; stimulates recovery of immunologic function in lymphatic system after administration of antineoplastic agents or x-irradiation.	2.6	1	0	bisbenzylisoquinoline alkaloid; isoquinolines
aloe emodin aloe emodin: structure distinct from emodin; this does not mean emodin from aloe. Aloe emodin : A dihydroxyanthraquinone that is chrysazin carrying a hydroxymethyl group at position 3. It has been isolated from plant species of the genus Aloe.	2.6	1	0	aromatic primary alcohol; dihydroxyanthraquinone	antineoplastic agent; plant metabolite
chrysophanic acid chrysophanic acid: RN given refers to parent cpd; structure in Merck, 9th ed, #2260. chrysophanol : A trihydroxyanthraquinone that is chrysazin with a methyl substituent at C-3. It has been isolated from Aloe vera and exhibits antiviral and anti-inflammatory activity.	2.6	1	0	dihydroxyanthraquinone	anti-inflammatory agent; antiviral agent; plant metabolite
emetine Emetine: The principal alkaloid of ipecac, from the ground roots of Uragoga (or Cephaelis) ipecacuanha or U. acuminata, of the Rubiaceae. It is used as an amebicide in many different preparations and may cause serious cardiac, hepatic, or renal damage and violent diarrhea and vomiting. Emetine inhibits protein synthesis in EUKARYOTIC CELLS but not PROKARYOTIC CELLS.. emetine : A pyridoisoquinoline comprising emetam having methoxy substituents at the 6'-, 7'-, 10- and 11-positions. It is an antiprotozoal agent and emetic. It inhibits SARS-CoV2, Zika and Ebola virus replication and displays antimalarial, antineoplastic and antiamoebic properties.	2.58	2	0	isoquinoline alkaloid; pyridoisoquinoline	antiamoebic agent; anticoronaviral agent; antiinfective agent; antimalarial; antineoplastic agent; antiprotozoal drug; antiviral agent; autophagy inhibitor; emetic; expectorant; plant metabolite; protein synthesis inhibitor
osthol osthol: from Cnidium monnieri and Angelica pubescens (both Apiaceae); structure given in first source	2.6	1	0	botanical anti-fungal agent; coumarins	metabolite
dihydralazine Dihydralazine: 1,4-Dihydrazinophthalazine. An antihypertensive agent with actions and uses similar to those of HYDRALAZINE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p354)	2.05	1	0	phthalazines
reticulin Reticulin: A scleroprotein fibril consisting mostly of type III collagen. Reticulin fibrils are extremely thin, with a diameter of between 0.5 and 2 um. They are involved in maintaining the structural integrity in a variety of organs.	2.31	1	0	benzylisoquinoline alkaloid; benzyltetrahydroisoquinoline; isoquinolinol	plant metabolite
flavanone flavanone: RN given refers to cpd with unspecified isomeric designation; structure in first source. flavanone : The simplest member of the class of flavanones that consists of flavan bearing an oxo substituent at position 4.	2.6	1	0	flavanones
thymoquinone thymoquinone: constituent of cedarwood; can cause dermatitis; structure. thymoquinone : A member of the class of 1,4-benzoquinones that is 1,4-bezoquinone in which the hydrogens at positions 2 and 5 are replaced by methyl and isopropyl groups, respectively. It is a natural compound isolated from Nigella sativa which has demonstrated promising chemotherapeutic activity.	7.48	2	0	1,4-benzoquinones	adjuvant; anti-inflammatory agent; antidepressant; antineoplastic agent; antioxidant; cardioprotective agent; plant metabolite
phenylpropanolamine Phenylpropanolamine: A sympathomimetic that acts mainly by causing release of NOREPINEPHRINE but also has direct agonist activity at some adrenergic receptors. It is most commonly used as a nasal vasoconstrictor and an appetite depressant.. phenylpropanolamine : An amphetamine in which the parent 1-phenylpropan-2-amine skeleton is substituted at position 1 with an hydroxy group. A decongestant and appetite suppressant, it is commonly used in prescription and over-the-counter cough and cold preparations.. (-)-norephedrine : An amphetamine that is propylbenzene substituted by a hydroxy group at position 1 and by an amino group at position 2 (the 1R,2S-stereoisomer). It is a plant alkaloid.	2.05	1	0	amphetamines; phenethylamine alkaloid	plant metabolite
phloretic acid phloretic acid: structure. N-hydroxysuccinimide ester : An ester of N-hydroxysuccinimide.. phloretic acid : A hydroxy monocarboxylic acid consisting of propionic acid having a 4-hydroxyphenyl group at the 3-position.	2.6	1	0	hydroxy monocarboxylic acid	plant metabolite
4-hydroxybutyric acid 4-hydroxybutyric acid: was an entry term to Sodium Oxybate (74-98). 4-hydroxybutyric acid : A 4-hydroxy monocarboxylic acid that is butyric acid in which one of the hydrogens at position 4 is replaced by a hydroxy group.	3.23	1	0	4-hydroxy monocarboxylic acid; hydroxybutyric acid	general anaesthetic; GHB receptor agonist; neurotoxin; sedative
alpha-aminopyridine alpha-aminopyridine: RN given refers to parent cpd; structure in Merck Index, 9th ed, #485. aminopyridine : Compounds containing a pyridine skeleton substituted by one or more amine groups.	4.74	8	0
oleanolic acid [no description available]	2.49	2	0	hydroxy monocarboxylic acid; pentacyclic triterpenoid	plant metabolite
dihydroergotamine Dihydroergotamine: A 9,10alpha-dihydro derivative of ERGOTAMINE. It is used as a vasoconstrictor, specifically for the therapy of MIGRAINE DISORDERS.. dihydroergotamine : Ergotamine in which a single bond replaces the double bond between positions 9 and 10. A semisynthetic ergot alkaloid with weaker oxytocic and vasoconstrictor properties than ergotamine, it is used (as the methanesulfonic or tartaric acid salts) for the treatment of migraine and orthostatic hypotension.	3.59	2	0	ergot alkaloid; semisynthetic derivative	dopamine agonist; non-narcotic analgesic; serotonergic agonist; sympatholytic agent; vasoconstrictor agent
elemene elemene: a sclerosing and antineoplastic agent isolated from Curcuma wenyujin & Rhizoma zedoariae; beta- and delta- elemene are also available	7.6	1	0
podophyllotoxin Podophyllum: A genus of poisonous American herbs, family BERBERIDACEAE. The roots yield PODOPHYLLOTOXIN and other pharmacologically important agents. The plant was formerly used as a cholagogue and cathartic. It is different from the European mandrake, MANDRAGORA.	4.38	4	1	furonaphthodioxole; lignan; organic heterotetracyclic compound	antimitotic; antineoplastic agent; keratolytic drug; microtubule-destabilising agent; plant metabolite; tubulin modulator
hesperidin Hesperidin: A flavanone glycoside found in CITRUS fruit peels.. hesperidin : A disaccharide derivative that consists of hesperetin substituted by a 6-O-(alpha-L-rhamnopyranosyl)-beta-D-glucopyranosyl moiety at position 7 via a glycosidic linkage.	2.05	1	0	3'-hydroxyflavanones; 4'-methoxyflavanones; dihydroxyflavanone; disaccharide derivative; flavanone glycoside; monomethoxyflavanone; rutinoside	mutagen
medroxyprogesterone [no description available]	3.23	1	0	17alpha-hydroxy steroid; 20-oxo steroid; 3-oxo-Delta(4) steroid; tertiary alpha-hydroxy ketone	contraceptive drug; progestin; synthetic oral contraceptive
angelicin angelicin: used as tranquillizer; sedative; or anticonvulsant; structure	2.6	1	0	furanocoumarin
dimenhydrinate gravinol: has antioxidant and ant-inflammatory activities; structure in first source	3.61	2	0	diarylmethane
copper gluconate Gluconates: Derivatives of gluconic acid (the structural formula HOCH2(CHOH)4COOH), including its salts and esters.	2.21	1	0	organic molecular entity
azomycin azomycin: RN given refers to parent cpd with specified locant; structure	2.08	1	0	C-nitro compound; imidazoles	antitubercular agent
chlormethiazole Chlormethiazole: A sedative and anticonvulsant often used in the treatment of alcohol withdrawal. Chlormethiazole has also been proposed as a neuroprotective agent. The mechanism of its therapeutic activity is not entirely clear, but it does potentiate GAMMA-AMINOBUTYRIC ACID receptors response and it may also affect glycine receptors.	2.73	3	0	thiazoles
methoxyhydroxyphenylglycol Methoxyhydroxyphenylglycol: Synthesized from endogenous epinephrine and norepinephrine in vivo. It is found in brain, blood, CSF, and urine, where its concentrations are used to measure catecholamine turnover.	2.07	1	0	methoxybenzenes; phenols
perillyl alcohol perillyl alcohol: inhibits geranylgeranyl transferase; structure in first source. perillyl alcohol : A limonene monoterpenoid consists of a cyclohexene ring substituted by a hydroxymethyl and a prop-1-en-2-yl group at positions 1 and 4 respectively. It is a constituent of a variety of essential oils including lavender.	2.07	1	0	limonene monoterpenoid	plant metabolite; volatile oil component
cumic acid cumic acid : A member of the class of benzoic acids that is cumene substituted by at least one carboxy group.. p-cumic acid : A cumic acid that consists of benzoic acid substituted by an isopropyl group at position 4.	2.25	1	0	cumic acid	plant metabolite
diperodon diperodon: RN given refers to parent cpd; structure given in first source	2.6	1	0	carbamate ester
methamphetamine Methamphetamine: A central nervous system stimulant and sympathomimetic with actions and uses similar to DEXTROAMPHETAMINE. The smokable form is a drug of abuse and is referred to as crank, crystal, crystal meth, ice, and speed.. methamphetamine : A member of the class of amphetamines in which the amino group of (S)-amphetamine carries a methyl substituent.	3.86	3	0	amphetamines; secondary amine	central nervous system stimulant; environmental contaminant; neurotoxin; psychotropic drug; xenobiotic
levocarnitine (R)-carnitine : The (R)-enantiomer of carnitine.	3.23	1	0	carnitine	antilipemic drug; nootropic agent; nutraceutical; Saccharomyces cerevisiae metabolite; water-soluble vitamin (role)
sulfanilylurea sulfanilylurea: antimicrobial agent; structure	3.23	1	0	benzenes; sulfonamide
trinitrobenzenesulfonic acid Trinitrobenzenesulfonic Acid: A reagent that is used to neutralize peptide terminal amino groups.. 2,4,6-trinitrobenzenesulfonic acid : The arenesulfonic acid that is benzenesulfonic acid with three nitro substituents in the 2-, 4- and 6-positions.	2.1	1	0	arenesulfonic acid; C-nitro compound	epitope; explosive; reagent
eosine yellowish-(ys) Eosine Yellowish-(YS): A versatile red dye used in cosmetics, pharmaceuticals, textiles, etc., and as tissue stain, vital stain, and counterstain with HEMATOXYLIN. It is also used in special culture media.. eosin YS dye : An organic sodium salt that is 2',4',5',7'-tetrabromofluorescein in which the carboxy group and the phenolic hydroxy group have been deprotonated and the resulting charge is neutralised by two sodium ions.	2.04	1	0	organic sodium salt; organobromine compound	fluorochrome; histological dye
gentian violet Gentian Violet: A dye that is a mixture of violet rosanilinis with antibacterial, antifungal, and anthelmintic properties.. crystal violet : An organic chloride salt that is the monochloride salt of crystal violet cation. It has been used in creams for the topical treatment of bacterial and fungal infections, being effective against some Gram-positive bacteria (notably Staphylococcus species) and some pathogenic fungi (including Candida species) but use declined following reports of animal carcinogenicity. It has also been used for dying wood, silk, and paper, as well as a histological stain.	2.05	1	0	organic chloride salt	anthelminthic drug; antibacterial agent; antifungal agent; antiseptic drug; histological dye
1-naphthylisothiocyanate 1-Naphthylisothiocyanate: A tool for the study of liver damage which causes bile stasis and hyperbilirubinemia acutely and bile duct hyperplasia and biliary cirrhosis chronically, with changes in hepatocyte function. It may cause skin and kidney damage.	2.08	1	0	isothiocyanate	insecticide
hematoporphyrin Hematoporphyrins: Iron-free derivatives of heme with 4 methyl groups, 2 hydroxyethyl groups and 2 propionic acid groups attached to the pyrrole rings. Some of these PHOTOSENSITIZING AGENTS are used in the PHOTOTHERAPY of malignant NEOPLASMS.. hematoporphyrin : A dicarboxylic acid that is protoporphyrin in which the vinyl groups at positions 7 and 12 are replaced by 1-hydroxyethyl groups.	2.05	1	0
lithium carbonate Lithium Carbonate: A lithium salt, classified as a mood-stabilizing agent. Lithium ion alters the metabolism of BIOGENIC MONOAMINES in the CENTRAL NERVOUS SYSTEM, and affects multiple neurotransmission systems.	2.04	1	0	carbonate salt; lithium salt	antimanic drug
formestane [no description available]	2.08	1	0	17-oxo steroid; 3-oxo-Delta(4) steroid; enol; hydroxy steroid	antineoplastic agent; EC 1.14.14.14 (aromatase) inhibitor
lactulose [no description available]	3.59	2	0	glycosylfructose	gastrointestinal drug; laxative
8-aminoquinoline [no description available]	2.15	1	0
4-acetylbenzoic acid 4-acetylbenzoic acid: structure in first source	2.25	1	0
3-bromopropionic acid [no description available]	2.25	1	0
megestrol acetate [no description available]	2.81	3	0	20-oxo steroid; 3-oxo-Delta(4) steroid; acetate ester; steroid ester	antineoplastic agent; appetite enhancer; contraceptive drug; progestin; synthetic oral contraceptive
alpha-naphthoflavone alpha-naphthoflavone: inhibits P4501A1 and P4501A2; stimulates some activities of P4503A4. alpha-naphthoflavone : An extended flavonoid resulting from the formal fusion of a benzene ring with the h side of flavone. A synthetic compound, it is an inhibitor of aromatase (EC 1.14.14.14).	2.07	1	0	extended flavonoid; naphtho-gamma-pyrone; organic heterotricyclic compound	aryl hydrocarbon receptor agonist; aryl hydrocarbon receptor antagonist; EC 1.14.14.14 (aromatase) inhibitor
pamabrom [no description available]	3.23	1	0
toyocamycin Toyocamycin: 4-Amino-5-cyano-7-(D-ribofuranosyl)-7H- pyrrolo(2,3-d)pyrimidine. Antibiotic antimetabolite isolated from Streptomyces toyocaensis cultures. It is an analog of adenosine, blocks RNA synthesis and ribosome function, and is used mainly as a tool in biochemistry.. toyocamycin : An N-glycosylpyrrolopyrimidine that is tubercidin in which the hydrogen at position 5 of the pyrrolopyrimidine moiety has been replaced by a cyano group.	3.6	2	0	antibiotic antifungal agent; N-glycosylpyrrolopyrimidine; nitrile; ribonucleoside	antimetabolite; antineoplastic agent; apoptosis inducer; bacterial metabolite
8-methylquinoline [no description available]	2.15	1	0	methylquinoline
3-methylquinoline [no description available]	2.13	1	0	methylquinoline	xenobiotic
acetylcysteine N-acetyl-L-cysteine : An N-acetyl-L-amino acid that is the N-acetylated derivative of the natural amino acid L-cysteine.	11.04	43	0	acetylcysteine; L-cysteine derivative; N-acetyl-L-amino acid	antidote to paracetamol poisoning; antiinfective agent; antioxidant; antiviral drug; ferroptosis inhibitor; geroprotector; human metabolite; mucolytic; radical scavenger; vulnerary
ethyl pyruvate [no description available]	2.05	1	0	oxo carboxylic acid
dicarbethoxydihydrocollidine Dicarbethoxydihydrocollidine: 1,4-Dihydro-2,4,6-trimethyl-3,5-pyridinedicarboxylic acid diethyl ester.. 3,5-diethoxycarbonyl-1,4-dihydrocollidine : A dihydropyridine that is 2,4,6-trimethyl-1,4-dihydropyridine substituted by ethoxycarbonyl groups at positions 3 and 5.	2.02	1	0	dihydropyridine; ethyl ester	hepatic steatosis inducing agent
erythromycin stearate [no description available]	2.05	1	0	aminoglycoside
erythromycin Erythromycin: A bacteriostatic antibiotic macrolide produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.. erythromycin : Any of several wide-spectrum macrolide antibiotics obtained from actinomycete Saccharopolyspora erythraea (formerly known as Streptomyces erythraeus).. erythromycin A : An erythromycin that consists of erythronolide A having 2,6-dideoxy-3-C-methyl-3-O-methyl-alpha-L-ribo-hexopyranosyl and 3,4,6-trideoxy-3-(dimethylamino)-beta-D-xylo-hexopyranosyl residues attahced at positions 4 and 6 respectively.	4.27	5	0	cyclic ketone; erythromycin
2-piperidone 2-piperidone: structure given in first source. piperidin-2-one : A delta-lactam that is piperidine which is substituted by an oxo group at position 2.	3.73	9	0	delta-lactam; piperidones	EC 1.2.1.88 (L-glutamate gamma-semialdehyde dehydrogenase) inhibitor
2-hydroxy-1-naphthaldehyde 2-hydroxynaphthaldehyde: structure in first source. 2-hydroxy-1-naphthaldehyde : A member of the class of naphthaldehydes that is naphthalene-1-carbaldehyde substituted by a hydroxy group at position 2. Active core of sirtinol (CHEBI:73158).	2.1	1	0	naphthaldehydes; naphthols
hydroxychloroquine sulfate [no description available]	2.83	3	0
levonorgestrel Levonorgestrel: A synthetic progestational hormone with actions similar to those of PROGESTERONE and about twice as potent as its racemic or (+-)-isomer (NORGESTREL). It is used for contraception, control of menstrual disorders, and treatment of endometriosis.	6.01	4	1	17beta-hydroxy steroid; 3-oxo-Delta(4) steroid; terminal acetylenic compound	contraceptive drug; female contraceptive drug; progestin; synthetic oral contraceptive
lormetazepam lormetazepam: RN given refers to cpd with specified locant for methyl group; structure given in first source. lormetazepam : A 1,4-benzodiazepinone compound having a methyl substituent at the 1-position, a hydroxy substituent at the 3-position, a 2-chlorophenyl group at the 5-position and a chloro substituent at the 7-position.	2.04	1	0	1,4-benzodiazepinone; organochlorine compound	sedative
vinblastine [no description available]	2.74	3	0
hydroxyethyl methacrylate hydroxyethyl methacrylate: many of cited refs are for gel which refers to polymeric form of above cpd: POLYHYDROXYETHYL METHACRYLATE. 2-hydroxyethyl methacrylate : An enoate ester that is the monomethacryloyl derivative of ethylene glycol.	2.11	1	0	enoate ester	allergen; polymerisation monomer
diphenoxylate Diphenoxylate: A MEPERIDINE congener used as an antidiarrheal, usually in combination with ATROPINE. At high doses, it acts like morphine. Its unesterified metabolite difenoxin has similar properties and is used similarly. It has little or no analgesic activity.. diphenoxylate : A piperidinecarboxylate ester that is the ethyl ester of difenoxin.	3.23	1	0	ethyl ester; nitrile; piperidinecarboxylate ester; tertiary amine	antidiarrhoeal drug
dodecylamine dodecylamine: RN given refers to parent cpd	2.11	1	0	primary aliphatic amine
deoxycytidine [no description available]	13.64	60	19	pyrimidine 2'-deoxyribonucleoside	Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
estradiol valerate [no description available]	2.05	1	0	steroid ester
cytidine diphosphate choline Cytidine Diphosphate Choline: Donor of choline in biosynthesis of choline-containing phosphoglycerides.	2.03	1	0	nucleotide-(amino alcohol)s; phosphocholines	human metabolite; mouse metabolite; neuroprotective agent; psychotropic drug; Saccharomyces cerevisiae metabolite
ethambutol hydrochloride ethambutol dihydrochloride : The dihydrchloride salt of ethambutol. A bacteriostatic antimycobacterial drug, it is effective against Mycobacterium tuberculosis and some other mycobacteria. It is used in combination with other antituberculous drugs in the treatment of pulmonary and extrapulmonary tuberculosis; resistant strains of M. tuberculosis are readily produced if ethambutol dihydrochloride is used alone.	2.08	1	0	hydrochloride	antitubercular agent
ethambutol Ethambutol: An antitubercular agent that inhibits the transfer of mycolic acids into the cell wall of the tubercle bacillus. It may also inhibit the synthesis of spermidine in mycobacteria. The action is usually bactericidal, and the drug can penetrate human cell membranes to exert its lethal effect. (From Smith and Reynard, Textbook of Pharmacology, 1992, p863). ethambutol : An ethylenediamine derivative that is ethane-1,2-diamine in which one hydrogen attached to each of the nitrogens is sutstituted by a 1-hydroxybutan-2-yl group (S,S-configuration). It is a bacteriostatic antimycobacterial drug, effective against Mycobacterium tuberculosis and some other mycobacteria. It is used (as the dihydrochloride salt) in combination with other antituberculous drugs in the treatment of pulmonary and extrapulmonary tuberculosis; resistant strains of M. tuberculosis are readily produced if ethambutol is used alone.	3.91	3	0	ethanolamines; ethylenediamine derivative	antitubercular agent; environmental contaminant; xenobiotic
nicotinamide mononucleotide Nicotinamide Mononucleotide: 3-Carbamoyl-1-beta-D-ribofuranosyl pyridinium hydroxide-5'phosphate, inner salt. A nucleotide in which the nitrogenous base, nicotinamide, is in beta-N-glycosidic linkage with the C-1 position of D-ribose. Synonyms: Nicotinamide Ribonucleotide; NMN.	2.21	1	0	nicotinamide mononucleotide	Escherichia coli metabolite; mouse metabolite
metformin hydrochloride metformin hydrochloride : A hydrochloride resulting from the reaction of metformin with one molar equivalent of hydrogen chloride.	2.6	1	0	hydrochloride	environmental contaminant; hypoglycemic agent; xenobiotic
calcium peroxide [no description available]	4.8	1	1	calcium oxides
durapatite Durapatite: The mineral component of bones and teeth; it has been used therapeutically as a prosthetic aid and in the prevention and treatment of osteoporosis.. hydroxylapatite : A phosphate mineral with the formula Ca5(PO4)3(OH).	2.17	1	0
manganese dioxide [no description available]	4.8	1	1	manganese molecular entity; metal oxide
zinc oxide Zinc Oxide: A mild astringent and topical protectant with some antiseptic action. It is also used in bandages, pastes, ointments, dental cements, and as a sunblock.	4.8	1	1	zinc molecular entity
cupric sulfide copper(II) sulfide : A copper sulfide in which the metal is in the +2 oxidation state.	2.25	1	0
arsenic trioxide Arsenic Trioxide: An inorganic compound with the chemical formula As2O3 that is used for the treatment of ACUTE PROMYELOCYTIC LEUKEMIA in patients who have relapsed from, or are resistant to, conventional drug therapy.	13.26	50	5
antimycin a [no description available]	2.58	2	0	benzamides; formamides; macrodiolide; phenols	antifungal agent; mitochondrial respiratory-chain inhibitor; piscicide
vancomycin Vancomycin: Antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to RISTOCETIN that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear.. vancomycin : A complex glycopeptide from Streptomyces orientalis. It inhibits a specific step in the synthesis of the peptidoglycan layer in the Gram-positive bacteria Staphylococcus aureus and Clostridium difficile.	4.1	4	0	glycopeptide	antibacterial drug; antimicrobial agent; bacterial metabolite
nsc 65346 sangivamycin: RN given refers to parent cpd. sangivamycin : A nucleoside analogue that is adenosine in which the nitrogen at position 7 is replaced by a carbamoyl-substituted carbon. It is a potent inhibitor of protein kinase C.	2.07	1	0	nucleoside analogue	protein kinase inhibitor
d-alpha tocopherol Vitamin E: A generic descriptor for all TOCOPHEROLS and TOCOTRIENOLS that exhibit ALPHA-TOCOPHEROL activity. By virtue of the phenolic hydrogen on the 2H-1-benzopyran-6-ol nucleus, these compounds exhibit varying degree of antioxidant activity, depending on the site and number of methyl groups and the type of ISOPRENOIDS.. tocopherol : A collective name for a group of closely related lipids that contain a chroman-6-ol nucleus substituted at position 2 by a methyl group and by a saturated hydrocarbon chain consisting of three isoprenoid units. They are designated as alpha-, beta-, gamma-, and delta-tocopherol depending on the number and position of additional methyl substituents on the aromatic ring. Tocopherols occur in vegetable oils and vegetable oil products, almost exclusively with R,R,R configuration. Tocotrienols differ from tocopherols only in having three double bonds in the hydrocarbon chain.. vitamin E : Any member of a group of fat-soluble chromanols that exhibit biological activity against vitamin E deficiency. The vitamers in this class consists of a chroman-6-ol core which is substituted at position 2 by a methyl group and (also at position 2) either a saturated or a triply-unsaturated hydrocarbon chain consisting of three isoprenoid units. The major function of vitamin E is to act as a natural antioxidant by scavenging free radicals and molecular oxygen.. (R,R,R)-alpha-tocopherol : An alpha-tocopherol that has R,R,R configuration. The naturally occurring stereoisomer of alpha-tocopherol, it is found particularly in sunflower and olive oils.	4.29	5	0	alpha-tocopherol	algal metabolite; antiatherogenic agent; anticoagulant; antioxidant; antiviral agent; EC 2.7.11.13 (protein kinase C) inhibitor; immunomodulator; micronutrient; nutraceutical; plant metabolite
pregnenolone carbonitrile Pregnenolone Carbonitrile: A catatoxic steroid and microsomal enzyme inducer having significant effects on the induction of cytochrome P450. It has also demonstrated the potential for protective capability against acetaminophen-induced liver damage.	2.08	1	0	aliphatic nitrile
ibufenac ibufenac: used in the treatment of rheumatism; also possesses antipyretic properties; minor descriptor (75-84); on-line & Index Medicus search PHENYLACETATES (75-84); RN given refers to parent cpd. ibufenac : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is replaced by a 4-isobutylphenyl group. Although it was shown to be effective in treatment of rheumatoid arthritis, the clinical use of ibufenac was discontinued due to hepatotoxic side-effects.	3.23	1	0	monocarboxylic acid	EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; hepatotoxic agent; non-narcotic analgesic; non-steroidal anti-inflammatory drug
metylperon metylperon: RN given refers to parent cpd	2.46	2	0	aromatic ketone
metaxalone [no description available]	3.23	1	0	aromatic ether
spectinomycin Spectinomycin: An antibiotic produced by Streptomyces spectabilis. It is active against gram-negative bacteria and used for the treatment of GONORRHEA.. spectinomycin dihydrochloride : A hydrochloride obtained by combining spectinomycin with two molar equivalents of hydrochloric acid. An antibiotic that is active against gram-negative bacteria and used (as its pentahydrate) to treat gonorrhea.. spectinomycin : A pyranobenzodioxin and antibiotic that is active against gram-negative bacteria and used (as its dihydrochloride pentahydrate) to treat gonorrhea. It is produced by the bacterium Streptomyces spectabilis.	3.58	2	0	cyclic acetal; cyclic hemiketal; cyclic ketone; pyranobenzodioxin; secondary alcohol; secondary amino compound	antibacterial drug; antimicrobial agent; bacterial metabolite
5,5'-dimethyl-2,2'-bipyridyl 5,5'-dimethyl-2,2'-bipyridyl: structure in first source	2.6	1	0	bipyridines
dichlorobenzyl alcohol 2,4-dichlorobenzyl alcohol : A member of the class of benzyl alcohols that is benzyl alcohol in which the hydrogens at positions 2 and 4 are replaced by chlorines.	2.6	1	0	benzyl alcohols; dichlorobenzene	antiseptic drug
paraquat Paraquat: A poisonous dipyridilium compound used as contact herbicide. Contact with concentrated solutions causes irritation of the skin, cracking and shedding of the nails, and delayed healing of cuts and wounds.. paraquat : An organic cation that consists of 4,4'-bipyridine bearing two N-methyl substituents loctated at the 1- and 1'-positions.	2.41	1	0	organic cation	geroprotector; herbicide
dronabinol Dronabinol: A psychoactive compound extracted from the resin of Cannabis sativa (marihuana, hashish). The isomer delta-9-tetrahydrocannabinol (THC) is considered the most active form, producing characteristic mood and perceptual changes associated with this compound.. Delta(9)-tetrahydrocannabinol : A diterpenoid that is 6a,7,8,10a-tetrahydro-6H-benzo[c]chromene substituted at position 1 by a hydroxy group, positions 6, 6 and 9 by methyl groups and at position 3 by a pentyl group. The principal psychoactive constituent of the cannabis plant, it is used for treatment of anorexia associated with AIDS as well as nausea and vomiting associated with cancer chemotherapy.	3.86	3	0	benzochromene; diterpenoid; phytocannabinoid; polyketide	cannabinoid receptor agonist; epitope; hallucinogen; metabolite; non-narcotic analgesic
amiloride hydrochloride, anhydrous amiloride hydrochloride : A hydrochloride obtained by combining amiloride with one molar equivalent of hydrochloric acid.	2.08	1	0	hydrochloride	diuretic; sodium channel blocker
amiloride Amiloride: A pyrazine compound inhibiting SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS. This inhibition creates a negative potential in the luminal membranes of principal cells, located in the distal convoluted tubule and collecting duct. Negative potential reduces secretion of potassium and hydrogen ions. Amiloride is used in conjunction with DIURETICS to spare POTASSIUM loss. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p705). amiloride : A member of the class of pyrazines resulting from the formal monoacylation of guanidine with the carboxy group of 3,5-diamino-6-chloropyrazine-2-carboxylic acid.	3.59	2	0	aromatic amine; guanidines; organochlorine compound; pyrazines	diuretic; sodium channel blocker
pimozide Pimozide: A diphenylbutylpiperidine that is effective as an antipsychotic agent and as an alternative to HALOPERIDOL for the suppression of vocal and motor tics in patients with Tourette syndrome. Although the precise mechanism of action is unknown, blockade of postsynaptic dopamine receptors has been postulated. (From AMA Drug Evaluations Annual, 1994, p403). pimozide : A member of the class of benzimidazoles that is 1,3-dihydro-2H-benzimidazol-2-one in which one of the nitrogens is substituted by a piperidin-4-yl group, which in turn is substituted on the nitrogen by a 4,4-bis(p-fluorophenyl)butyl group.	3.59	2	0	benzimidazoles; heteroarylpiperidine; organofluorine compound	antidyskinesia agent; dopaminergic antagonist; first generation antipsychotic; H1-receptor antagonist; serotonergic antagonist
benperidol Benperidol: A butyrophenone with general properties similar to those of HALOPERIDOL. It has been used in the treatment of aberrant sexual behavior. (From Martindale, The Extra Pharmacopoeia, 30th ed, p567)	2.04	1	0	aromatic ketone
phenethyl isothiocyanate phenethyl isothiocyanate: a dietary liver aldehyde dehydrogenase inhibitor; promotes urinary bladder carcinoma. phenethyl isothiocyanate : An isothiocyanate having a phenethyl group attached to the nitrogen. It is a naturally occurring compound found in some cruciferous vegetables (e.g. watercress) and is known to possess anticancer properties.	2.53	2	0	isothiocyanate	antineoplastic agent; EC 1.2.1.3 [aldehyde dehydrogenase (NAD(+))] inhibitor; metabolite
methylprednisolone hemisuccinate Methylprednisolone Hemisuccinate: A water-soluble ester of METHYLPREDNISOLONE used for cardiac, allergic, and hypoxic emergencies.	2.08	1	0	corticosteroid hormone; hemisuccinate
dexbrompheniramine dexbrompheniramine : The (pharmacologically active) (S)-(+)-enantiomer of brompheniramine. A histamine H1 receptor antagonist, it is used (commonly as its maleate salt) for the symptomatic relief of allergic conditions, including rhinitis and conjunctivitis.	3.23	1	0	brompheniramine	anti-allergic agent; H1-receptor antagonist
sulfadoxine Sulfadoxine: A long acting sulfonamide that is used, usually in combination with other drugs, for respiratory, urinary tract, and malarial infections.. sulfadoxine : A sulfonamide consisting of pyrimidine having methoxy substituents at the 5- and 6-positions and a 4-aminobenzenesulfonamido group at the 4-position. In combination with the antiprotozoal pyrimethamine (CHEBI:8673) it is used as an antimalarial.	2.05	1	0	pyrimidines; sulfonamide	antibacterial drug; antimalarial
acadesine [no description available]	2.47	2	0	1-ribosylimidazolecarboxamide; aminoimidazole; nucleoside analogue	antineoplastic agent; platelet aggregation inhibitor
1,2-benzisothiazoline-3-one 1,2-benzisothiazoline-3-one: a preservative in water-based solutions such as paints, cutting fluids, printing inks, cleaning agents, polyvinyl chloride gloves, etc.. benzo[d]isothiazol-3-one : An organic heterobicyclic compound based on a fused 1,2-thiazole and benzene bicyclic ring skeleton, with the S atom positioned adjacent to one of the positions of ring fusion.	2.41	1	0	organic heterobicyclic compound; organonitrogen heterocyclic compound	disinfectant; drug allergen; environmental contaminant; platelet aggregation inhibitor; sensitiser; xenobiotic
2-(dimethylamino)ethyl methacrylate 2-(dimethylamino)ethyl methacrylate: reducing agent; structure given in first source	2.21	1	0
chlordesmethyldiazepam [no description available]	2.04	1	0	benzodiazepine
stavudine Stavudine: A dideoxynucleoside analog that inhibits reverse transcriptase and has in vitro activity against HIV.. stavudine : A nucleoside analogue obtained by formal dehydration across positions 2 and 3 of thymidine. An inhibitor of HIV-1 reverse transcriptase	4.29	5	0	dihydrofuran; nucleoside analogue; organic molecular entity	antimetabolite; antiviral agent; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
doxifluridine doxifluridine : A pyrimidine 5'-deoxyribonucleoside that is 5-fluorouridine in which the hydroxy group at the 5' position is replaced by a hydrogen. It is an oral prodrug of the antineoplastic agent 5-fluorouracil. Designed to circumvent the rapid degradation of 5-fluorouracil by dihydropyrimidine dehydrogenase in the gut wall, it is converted into 5-fluorouracil in the presence of pyrimidine nucleoside phosphorylase.	2.45	2	0	organofluorine compound; pyrimidine 5'-deoxyribonucleoside	antimetabolite; antineoplastic agent; prodrug
dicloxacillin Dicloxacillin: One of the PENICILLINS which is resistant to PENICILLINASE.. dicloxacillin : A penicillin that is 6-aminopenicillanic acid in which one of the amino hydrogens is replaced by a 3-(2,6-dichlorophenyl)-5-methyl-1,2-oxazol-4-yl]formyl group.	3.87	3	0	dichlorobenzene; penicillin	antibacterial drug
dithiothreitol 1,4-dimercaptobutane-2,3-diol : A glycol that is butane-2,3-diol in which a hydrogen from each of the methyl groups is replaced by a thiol group.. 1,4-dithiothreitol : The threo-diastereomer of 1,4-dimercaptobutane-2,3-diol.	2.02	1	0	1,4-dimercaptobutane-2,3-diol; butanediols; dithiol; glycol; thiol	chelator; human metabolite; reducing agent
iproclozide iproclozide: structure	2.05	1	0	aromatic ether
megestrol Megestrol: A progestational hormone used most commonly as the acetate ester. As the acetate, it is more potent than progesterone both as a progestagen and as an ovulation inhibitor. It has also been used in the palliative treatment of breast cancer.. megestrol : A 3-oxo Delta(4)-steroid that is pregna-4,6-diene-3,20-dione substituted by a methyl group at position 6 and a hydroxy group at position 17.	3.23	1	0	17alpha-hydroxy steroid; 20-oxo steroid; 3-oxo-Delta(4) steroid; tertiary alpha-hydroxy ketone	antineoplastic agent; appetite enhancer; contraceptive drug; progestin; synthetic oral contraceptive
streptomycin [no description available]	3.86	3	0	antibiotic antifungal drug; antibiotic fungicide; streptomycins	antibacterial drug; antifungal agrochemical; antimicrobial agent; antimicrobial drug; bacterial metabolite; protein synthesis inhibitor
nitroxoline nitroxoline: structure in Merck Index, 9th ed, #6475; RN given refers to parent cpd. nitroxoline : A monohydroxyquinoline in which the hydroxy group is positioned at C-8 with a nitro group trans to it at C-5.	3.51	1	0	C-nitro compound; monohydroxyquinoline	antifungal agent; antiinfective agent; antimicrobial agent; renal agent
dideoxyadenosine Dideoxyadenosine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is an inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal side effect is nephrotoxicity. In vivo, dideoxyadenosine is rapidly metabolized to DIDANOSINE (ddI) by enzymatic deamination; ddI is then converted to dideoxyinosine monophosphate and ultimately to dideoxyadenosine triphosphate, the putative active metabolite.	2.6	1	0	adenosines; purine 2',3'-dideoxyribonucleoside	EC 3.5.4.4 (adenosine deaminase) inhibitor; EC 4.6.1.1 (adenylate cyclase) inhibitor
clonidine hydrochloride [no description available]	2.15	1	0	dichlorobenzene
cladribine [no description available]	9.81	12	3	organochlorine compound; purine 2'-deoxyribonucleoside	antineoplastic agent; immunosuppressive agent
carbenicillin Carbenicillin: Broad-spectrum semisynthetic penicillin derivative used parenterally. It is susceptible to gastric juice and penicillinase and may damage platelet function.. carbenicillin : A penicillin antibiotic having a 6beta-2-carboxy-2-phenylacetamido side-chain.	3.58	2	0	penicillin allergen; penicillin	antibacterial drug
carbenicillin disodium [no description available]	2.05	1	0	organic sodium salt
dehydroemetine dehydroemetine: was MH 1991-94 (see under EMETINE 1976-90); use EMETINE to search DEHYDROEMETINE 1976-94; amebicide, derivative of emetine. dehydroemetine : A pyridoisoquinoline which was developed in response to the cardiovascular toxicity associated with emetine and results from the dehydrogenation of the heterotricylic ring of emetine. It is an antiprotozoal agent and displays antimalarial, antiamoebic, and antileishmanial properties.	2.05	1	0	aromatic ether; isoquinolines; pyridoisoquinoline	antileishmanial agent; antimalarial; antiprotozoal drug
benorilate benorilate: was heading 1980-94 (see under SALICYLATES 1980-90); was BENORYLATE see under SALICYLATES 1975-79; BENORYLATE was see BENORILATE 1980-94; use SALICYLATES to search BENORILATE 1980-90 & BENORYLATE 1975-79; an ester of aspirin and paracetamol with analgesic, antipyretic, and anti-inflammatory activity used in the treatment of rheumatoid diseases; it has less severe side effects than aspirin	2.05	1	0	carbonyl compound
trimetazidine Trimetazidine: A vasodilator used in angina of effort or ischemic heart disease.	2.05	1	0	aromatic amine
metocurine metocurine: from Chinese herb Cyclea hainanensis Mrr	2.08	1	0	isoquinolines
floxacillin Floxacillin: Antibiotic analog of CLOXACILLIN.. flucloxacillin : A penicillin compound having a 6beta-[3-(2-chloro-6-fluorophenyl)-5-methyl-1,2-oxazole-4-carboxamido] side-chain.	2.45	2	0	penicillin allergen; penicillin	antibacterial drug
clomacran clomacran: RN given refers to parent cpd; structure	3.23	1	0	acridines
beclomethasone dipropionate beclomethasone dipropionate : A steroid ester comprising beclomethasone having propionyl groups at the 17- and 21-positions.	2.04	1	0	11beta-hydroxy steroid; 20-oxo steroid; 3-oxo-Delta(1),Delta(4)-steroid; chlorinated steroid; corticosteroid; enone; glucocorticoid; propanoate ester; steroid ester	anti-arrhythmia drug; anti-asthmatic drug; anti-inflammatory drug; prodrug
vidarabine adenine arabinoside : A purine nucleoside in which adenine is attached to arabinofuranose via a beta-N(9)-glycosidic bond.	11.2	25	5	beta-D-arabinoside; purine nucleoside	antineoplastic agent; bacterial metabolite; nucleoside antibiotic
methenamine hippurate methenamine hippurate: both parts of molecule contribute to its antibacterial action	3.23	1	0	N-acylglycine
olsalazine olsalazine: cpd with 2 salicylate molecules linked together by an azo bond. olsalazine : An azobenzene that consists of two molecules of 4-aminosalicylic acid joined by an azo linkage. A prodrug for mesalazine, an anti-inflammatory drug, it is used (as the disodium salt) in the treatment of inflammatory bowel disease.	3.58	2	0	azobenzenes; dicarboxylic acid	non-steroidal anti-inflammatory drug; prodrug
3-deazaadenosine 3-deazaadenosine: RN given refers to parent cpd.	2.6	1	0
tiadenol tiadenol: structure	2.05	1	0	aliphatic sulfide
terodiline [no description available]	2.04	1	0	diarylmethane
1-(4-carboxyphenyl)-3,3-dimethyltriazene 1-(4-carboxyphenyl)-3,3-dimethyltriazene: RN given refers to parent cpd	2.04	1	0
etidronate disodium etidronate disodium : An organic sodium salt resulting from the replacement of two protons from etidronic acid (one from from each of the phosphonic acid groups) by sodium ions.	2.08	1	0	organic sodium salt	antineoplastic agent; bone density conservation agent; chelator
manganese Manganese: A trace element with atomic symbol Mn, atomic number 25, and atomic weight 54.94. It is concentrated in cell mitochondria, mostly in the pituitary gland, liver, pancreas, kidney, and bone, influences the synthesis of mucopolysaccharides, stimulates hepatic synthesis of cholesterol and fatty acids, and is a cofactor in many enzymes, including arginase and alkaline phosphatase in the liver. (From AMA Drug Evaluations Annual 1992, p2035). manganese(4+) : A manganese cation that is monoatomic and has a formal charge of +4.	5.02	2	1	elemental manganese; manganese group element atom	Escherichia coli metabolite; micronutrient
mercury Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to MERCURY POISONING. Because of its toxicity, the clinical use of mercury and mercurials is diminishing.. mercury(0) : Elemental mercury of oxidation state zero.	4.8	1	1	elemental mercury; zinc group element atom	neurotoxin
molybdenum Molybdenum: A metallic element with the atomic symbol Mo, atomic number 42, and atomic weight 95.95. It is an essential trace element, being a component of the enzymes xanthine oxidase, aldehyde oxidase, and nitrate reductase.	4.8	1	1	chromium group element atom	micronutrient
platinum Platinum: A heavy, soft, whitish metal, resembling tin, with atomic number 78, atomic weight 195.084, symbol Pt. It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as alutiae.	8.89	2	1	elemental platinum; nickel group element atom; platinum group metal atom
samarium Samarium: An element of the rare earth family of metals. It has the atomic symbol Sm, atomic number 62, and atomic weight 150.36. The oxide is used in the control rods of some nuclear reactors.	9.35	1	1	f-block element atom; lanthanoid atom
silver Silver: An element with the atomic symbol Ag, atomic number 47, and atomic weight 107.87. It is a soft metal that is used medically in surgical instruments, dental prostheses, and alloys. Long-continued use of silver salts can lead to a form of poisoning known as ARGYRIA.	5.3	2	1	copper group element atom; elemental silver	Escherichia coli metabolite
titanium Titanium: A dark-gray, metallic element of widespread distribution but occurring in small amounts with atomic number, 22, atomic weight, 47.867 and symbol, Ti; specific gravity, 4.5; used for fixation of fractures.	5.7	5	1	titanium group element atom
gadolinium Gadolinium: An element of the rare earth family of metals. It has the atomic symbol Gd, atomic number 64, and atomic weight 157.25. Its oxide is used in the control rods of some nuclear reactors.	2.05	1	0	f-block element atom; lanthanoid atom
gold Gold: A yellow metallic element with the atomic symbol Au, atomic number 79, and atomic weight 197. It is used in jewelry, goldplating of other metals, as currency, and in dental restoration. Many of its clinical applications, such as ANTIRHEUMATIC AGENTS, are in the form of its salts.	11	7	1	copper group element atom; elemental gold
zalcitabine Zalcitabine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy.. zalcitabine : A pyrimidine 2',3'-dideoxyribonucleoside compound having cytosine as the nucleobase.	3.01	4	0	pyrimidine 2',3'-dideoxyribonucleoside	antimetabolite; antiviral drug; HIV-1 reverse transcriptase inhibitor
galactosamine 2-amino-2-deoxy-D-galactopyranose : The pyranose form of D-galactosamine.. D-galactosamine : The D-stereoisomer of galactosamine.	4.95	2	1	D-galactosamine; primary amino compound	toxin
metocurine iodide [no description available]	2.04	1	0	aromatic ether
camptothecin NSC 100880: carboxylate (opened lactone) form of camptothecin; RN refers to (S)-isomer; structure given in first source	16.26	25	4	delta-lactone; pyranoindolizinoquinoline; quinoline alkaloid; tertiary alcohol	antineoplastic agent; EC 5.99.1.2 (DNA topoisomerase) inhibitor; genotoxin; plant metabolite
zinc sulfate Zinc Sulfate: A compound given in the treatment of conditions associated with zinc deficiency such as acrodermatitis enteropathica. Externally, zinc sulfate is used as an astringent in lotions and eye drops. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995). zinc sulfate : A metal sulfate compound having zinc(2+) as the counterion.	4.8	1	1	metal sulfate; zinc molecular entity	fertilizer
tricalcium phosphate tricalcium phosphate: a form of tricalcium phosphate used as bioceramic bone replacement material; see also records for alpha-tricalcium phosphate, beta-tricalcium phosphate, calcium phosphate; apatitic tricalcium phosphate Ca9(HPO4)(PO4)5(OH) is the calcium orthophosphate leading to beta tricalcium phosphate Ca3(PO4)2 (b-TCP). calcium phosphate : A calcium salt composed of calcium and phosphate/diphosphate ions; present in milk and used for the mineralisation of calcified tissues.	5.6	4	1	calcium phosphate
sodium thiosulfate sodium thiosulfate: do not confuse synonym sodium hyposulfite with sodium hyposulfite, synonym for di-Na salt of dithionous acid. sodium thiosulfate : An inorganic sodium salt composed of sodium and thiosulfate ions in a 2:1 ratio.	3.23	1	0	inorganic sodium salt	antidote to cyanide poisoning; antifungal drug; nephroprotective agent
sodium selenite disodium selenite : An inorganic sodium salt composed of sodium and selenite ions in a 2:1 ratio.	2.04	1	0	inorganic sodium salt; selenite salt	nutraceutical
ancitabine Ancitabine: Congener of CYTARABINE that is metabolized to cytarabine and thereby maintains a more constant antineoplastic action.. ancitabine : An organic heterotricyclic compound resulting from the formal condensation of the oxo group of cytidine to the 2' position with loss of water to give the corresponding cyclic ether. A prodrug, it is metabolised to the antineoplastic agent cytarabine, so is used to maintain a more constant antineoplastic action.	2.6	1	0	diol; organic heterotricyclic compound	antimetabolite; antineoplastic agent; prodrug
trolamine salicylate Arthritis: Acute or chronic inflammation of JOINTS.	2.49	2	0
stanozolol Stanozolol: A synthetic steroid that has anabolic and androgenic properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1194). stanozolol : An organic heteropentacyclic compound resulting from the formal condensation of the 3-keto-aldehyde moiety of oxymetholone with hydrazine. Like oxymetholone, it is a synthetic anabolic steroid. It has both anabolic and androgenic properties, and has been used to treat hereditary angioedema and various vascular disorders. It has also been widely abused by professional athletes.	2.05	1	0	17beta-hydroxy steroid; anabolic androgenic steroid; organic heteropentacyclic compound; tertiary alcohol	anabolic agent; androgen
chloropyramine chloropyramine: RN given refers to parent cpd; structure	2.6	1	0	aminopyridine
clodronic acid Clodronic Acid: A diphosphonate which affects calcium metabolism. It inhibits bone resorption and soft tissue calcification.. clodronic acid : An organochlorine compound that is methylene chloride in which both hydrogens are replaced by phosphonic acid groups. It inhibits bone resorption and soft tissue calcification, and is used (often as the disodium salt tetrahydrate) as an adjunct in the treatment of severe hypercalcaemia associated with malignancy, and in the management of osteolytic lesions and bone pain associated with skeletal metastases.	2.46	2	0	1,1-bis(phosphonic acid); one-carbon compound; organochlorine compound	antineoplastic agent; bone density conservation agent
mafenide acetate [no description available]	2.08	1	0	carboxylic acid
titanium dioxide titanium dioxide: used medically as protectant against externally caused irritation & sunlight; high concentrations of dust may cause irritation to respiratory tract; RN given refers to titanium oxide (TiO2); structure. titanium dioxide : A titanium oxide with the formula TiO2. A naturally occurring oxide sourced from ilmenite, rutile and anatase, it has a wide range of applications.	4.8	1	1	titanium oxides	food colouring
apazone Apazone: An anti-inflammatory agent used in the treatment of rheumatoid arthritis. It also has uricosuric properties and has been used to treat gout.. apazone : A member of the class of benzotriazines that is 1,2-dihydro-1,2,4-benzotriazine bearing a dimethylamino substitutent at position 3 and a methyl substituent at position 7 and in which the nitrogens at positions 1 and 2 are both acylated by a carboxy group of propylmalonic acid.	2.04	1	0	benzotriazines	non-steroidal anti-inflammatory drug; uricosuric drug
diacerein diacerein: chelates with bivalent metals; a quinone which possesses redox properties; metabolized to active rhein; proposed mechanisms include inhibiting IL1 and metalloproteinases; called a slow acting symptomatic drug in osteoarthritis; no effect of cyclooxygenase;	2.08	1	0	anthraquinone
tiletamine hydrochloride Cyclohexanones: Cyclohexane ring substituted by one or more ketones in any position.. cyclohexanones : Any alicyclic ketone based on a cyclohexane skeleton and its substituted derivatives thereof.	3.84	3	0
xipamide Xipamide: A sulfamoylbenzamide analog of CLOPAMIDE. It is diuretic and saluretic with antihypertensive activity. It is bound to PLASMA PROTEINS, thus has a delayed onset and prolonged action.	2.05	1	0	benzamides
selegiline Selegiline: A selective, irreversible inhibitor of Type B monoamine oxidase that is used for the treatment of newly diagnosed patients with PARKINSON DISEASE, and for the treatment of depressive disorders. The compound without isomeric designation is Deprenyl.	3.86	3	0	selegiline; terminal acetylenic compound	geroprotector
selegiline hydrochloride, (r)-isomer [no description available]	2.08	1	0	hydrochloride; terminal acetylenic compound	antiparkinson drug; dopaminergic agent; EC 1.4.3.4 (monoamine oxidase) inhibitor
levamisole Levamisole: An antihelminthic drug that has been tried experimentally in rheumatic disorders where it apparently restores the immune response by increasing macrophage chemotaxis and T-lymphocyte function. Paradoxically, this immune enhancement appears to be beneficial in rheumatoid arthritis where dermatitis, leukopenia, and thrombocytopenia, and nausea and vomiting have been reported as side effects. (From Smith and Reynard, Textbook of Pharmacology, 1991, p435-6). levamisole : A 6-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b][1,3]thiazole that has S configuration. It is used (generally as the monohydrochloride salt) to treat parasitic worm infections in pigs, sheep and cattle and was formerly used in humans as an adjuvant to chemotherapy for the treatment of various cancers. It is also widely used as an adulterant to coccaine.	2.54	2	0	6-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b][1,3]thiazole	antinematodal drug; antirheumatic drug; EC 3.1.3.1 (alkaline phosphatase) inhibitor; immunological adjuvant; immunomodulator
clemastine Clemastine: A histamine H1 antagonist used as the hydrogen fumarate in hay fever, rhinitis, allergic skin conditions, and pruritus. It causes drowsiness.. clemastine : 2-[(2R)-1-Methylpyrrolidin-2-yl]ethanol in which the hydrogen of the hydroxy group is substituted by a 1-(4-chlorophenyl)-1-phenylethyl group (R configuration). An antihistamine with antimuscarinic and moderate sedative properties, it is used as its fumarate salt for the symptomatic relief of allergic conditions such as rhinitis, urticaria, conjunctivitis and in pruritic (severe itching) skin conditions.	3.23	1	0	monochlorobenzenes; N-alkylpyrrolidine	anti-allergic agent; antipruritic drug; H1-receptor antagonist; muscarinic antagonist
thiamphenicol [no description available]	2.47	2	0	monocarboxylic acid amide; sulfone	antimicrobial agent; immunosuppressive agent
pancuronium bromide pancuronium bromide : A bromide salt consisting of two bromide ions and one pancuronium dication.	2.08	1	0	bromide salt	cholinergic antagonist; muscle relaxant; nicotinic antagonist
pizotyline Pizotyline: Serotonin antagonist used against MIGRAINE DISORDERS and vascular headaches.. pizotifen : A benzocycloheptathiophene that is 9,10-dihydro-4H-benzo[4,5]cyclohepta[1,2-b]thiophene 4-ylidene)-1-methylpiperidine which is joined from the 4 position to the 4 position of an N-methylpiperidine moiety by a double bond. It is a sedating antihistamine, with strong serotonin antagonist and weak antimuscarinic activity. It is generally used as the malate salt for the treatment of migraine and the prevention of headache attacks during cluster periods.	2.05	1	0	benzocycloheptathiophene	histamine antagonist; muscarinic antagonist; serotonergic antagonist
cephalexin Cephalexin: A semisynthetic cephalosporin antibiotic with antimicrobial activity similar to that of CEPHALORIDINE or CEPHALOTHIN, but somewhat less potent. It is effective against both gram-positive and gram-negative organisms.. cephalexin : A semisynthetic first-generation cephalosporin antibiotic having methyl and beta-(2R)-2-amino-2-phenylacetamido groups at the 3- and 7- of the cephem skeleton, respectively. It is effective against both Gram-negative and Gram-positive organisms, and is used for treatment of infections of the skin, respiratory tract and urinary tract.	3.58	2	0	beta-lactam antibiotic allergen; cephalosporin; semisynthetic derivative	antibacterial drug
isosorbide-5-mononitrate isosorbide-5-mononitrate: for prevention of angina pectoris; structure given in first source; a Russian drug	2.45	2	0	glucitol derivative; nitrate ester	nitric oxide donor; vasodilator agent
n'-nitrosonornicotine N'-nitrosonornicotine: structure; a potent carcinogen in laboratory animals	2.6	1	0	pyridines; pyrrolidines
tetradecanoylphorbol acetate Tetradecanoylphorbol Acetate: A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.. phorbol ester : Esters of phorbol, originally found in croton oil (from Croton tiglium, of the family Euphorbiaceae). A number of phorbol esters possess activity as tumour promoters and activate the mechanisms associated with cell growth. Some of these are used in experiments as activators of protein kinase C.. phorbol 13-acetate 12-myristate : A phorbol ester that is phorbol in which the hydroxy groups at the cyclopropane ring juction (position 13) and the adjacent carbon (position 12) have been converted into the corresponding acetate and myristate esters. It is a major active constituent of the seed oil of Croton tiglium. It has been used as a tumour promoting agent for skin carcinogenesis in rodents and is associated with increased cell proliferation of malignant cells. However its function is controversial since a decrease in cell proliferation has also been observed in several cancer cell types.	2.53	2	0	acetate ester; diester; phorbol ester; tertiary alpha-hydroxy ketone; tetradecanoate ester	antineoplastic agent; apoptosis inducer; carcinogenic agent; mitogen; plant metabolite; protein kinase C agonist; reactive oxygen species generator
ornidazole Ornidazole: A nitroimidazole antiprotozoal agent used in ameba and trichomonas infections. It is partially plasma-bound and also has radiation-sensitizing action.. ornidazole : A C-nitro compound that is 5-nitroimidazole in which the hydrogens at positions 1 and 2 are replaced by 3-chloro-2-hydroxypropyl and methyl groups, respectively. It is used in the treatment of susceptible protozoal infections and for the treatment of anaerobic bacterial infections.	2.08	1	0	C-nitro compound; imidazoles; organochlorine compound; secondary alcohol	antiamoebic agent; antibacterial drug; antiinfective agent; antiprotozoal drug; antitrichomonal drug; epitope
danazol Danazol: A synthetic steroid with antigonadotropic and anti-estrogenic activities that acts as an anterior pituitary suppressant by inhibiting the pituitary output of gonadotropins. It possesses some androgenic properties. Danazol has been used in the treatment of endometriosis and some benign breast disorders.	3.87	3	0	17beta-hydroxy steroid; terminal acetylenic compound	anti-estrogen; estrogen antagonist; geroprotector
fenclozic acid fenclozic acid: an analgesic & antipyretic with anti-inflammatory properties; minor descriptor (75-86); on-line & INDEX MEDICUS search THIAZOLES (75-86); RN given refers to parent cpd	3.23	1	0
laxagetten 4,4'-diacetoxydiphenylpyridylemethane [no description available]	3.23	1	0
iodine [no description available]	2.05	1	0	halide anion; monoatomic iodine	human metabolite
daunorubicin Daunorubicin: A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.. anthracycline : Anthracyclines are polyketides that have a tetrahydronaphthacenedione ring structure attached by a glycosidic linkage to the amino sugar daunosamine.. daunorubicin : A natural product found in Actinomadura roseola.	6.6	14	1	aminoglycoside antibiotic; anthracycline; p-quinones; tetracenequinones	antineoplastic agent; bacterial metabolite
cephapirin Cephapirin: Cephalosporin antibiotic, partly plasma-bound, that is effective against gram-negative and gram-positive organisms.. cephapirin : A cephalosporin with acetoxymethyl and 2(pyridin-4-ylsulfanyl)acetamido substituents at positions 3 and 7, respectively, of the cephem skeleton. It is used (as its sodium salt) as an antibiotic, being effective against gram-negative and gram-positive organisms.	2.04	1	0	cephalosporin	antibacterial drug
fludarabine phosphate fludarabine phosphate: structure given in first source. fludarabine phosphate : A purine arabinonucleoside monophosphate having 2-fluoroadenine as the nucleobase. A prodrug, it is rapidly dephosphorylated to 2-fluoro-ara-A and then phosphorylated intracellularly by deoxycytidine kinase to the active triphosphate, 2-fluoro-ara-ATP. Once incorporated into DNA, 2-fluoro-ara-ATP functions as a DNA chain terminator. It is used for the treatment of adult patients with B-cell chronic lymphocytic leukemia (CLL) who have not responded to, or whose disease has progressed during, treatment with at least one standard alkylating-agent containing regimenas.	4.37	3	0	nucleoside analogue; organofluorine compound; purine arabinonucleoside monophosphate	antimetabolite; antineoplastic agent; antiviral agent; DNA synthesis inhibitor; immunosuppressive agent; prodrug
alclofenac alclofenac: was heading 1975-94 (was see under PHENYLACETATES 1975-90); use PHENYLACETATES to search ALCLOFENAC 1975-94; an anti-inflammatory agent used in the treatment of rheumatoid arthritis; acts also as an analgesic and an antipyretic. alclofenac : An aromatic ether in which the ether oxygen links an allyl group to the 4-position of (3-chlorophenyl)acetic acid.A non-steroidal anti-inflammatory drug, it was withdrawn from the UK market in 1979 due to concerns with its association with vasculitis and rash.	3.23	1	0	aromatic ether; monocarboxylic acid; monochlorobenzenes	drug allergen; non-narcotic analgesic; non-steroidal anti-inflammatory drug
carbimazole Carbimazole: An imidazole antithyroid agent. Carbimazole is metabolized to METHIMAZOLE, which is responsible for the antithyroid activity.. carbimazole : A member of the class of imidazoles that is methimazole in which the nitrogen bearing a hydrogen is converted into its ethoxycarbonyl derivative. A prodrug for methimazol, carbimazole is used for the treatment of hyperthyroidism.	2.05	1	0	1,3-dihydroimidazole-2-thiones; carbamate ester	antithyroid drug; prodrug
bromocriptine Bromocriptine: A semisynthetic ergotamine alkaloid that is a dopamine D2 agonist. It suppresses prolactin secretion.	3.59	2	0	indole alkaloid	antidyskinesia agent; antiparkinson drug; dopamine agonist; hormone antagonist
phenyl acetate phenyl acetate: The ester formed between phenol and acetic acid. Don't confuse with phenylacetic acid derivatives listed under PHENYLACETATES.. phenyl acetate : An acetate ester obtained by the formal condensation of phenol with acetic acid.	3.69	3	0	benzenes; phenyl acetates
cetylpyridinium chloride anhydrous tserigel: according to first source contains polyvinylbutyral & cetylpyridinium chloride; UD only lists cetylpyridinium chloride as constituent. cetylpyridinium chloride : A pyridinium salt that has N-hexadecylpyridinium as the cation and chloride as the anion. It has antiseptic properties and is used in solutions or lozenges for the treatment of minor infections of the mouth and throat.	2.46	2	0	chloride salt; organic chloride salt	antiseptic drug; surfactant
triamcinolone Triamcinolone: A glucocorticoid given, as the free alcohol or in esterified form, orally, intramuscularly, by local injection, by inhalation, or applied topically in the management of various disorders in which corticosteroids are indicated. (From Martindale, The Extra Pharmacopoeia, 30th ed, p739). triamcinolone : A C21-steroid hormone that is 1,4-pregnadiene-3,20-dione carrying four hydroxy substituents at positions 11beta, 16alpha, 17alpha and 21 as well as a fluoro substituent at position 9. Used in the form of its 16,17-acetonide to treat various skin infections.	2.05	1	0	11beta-hydroxy steroid; 16alpha-hydroxy steroid; 17alpha-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(4) steroid; C21-steroid hormone; fluorinated steroid; glucocorticoid; primary alpha-hydroxy ketone; tertiary alpha-hydroxy ketone	anti-allergic agent; anti-inflammatory drug
oxyphenisatin [no description available]	3.59	2	0	indoles
tetrachloroethylene Tetrachloroethylene: A chlorinated hydrocarbon used as an industrial solvent and cooling liquid in electrical transformers. It is a potential carcinogen.	2.05	1	0	chlorocarbon; chloroethenes	nephrotoxic agent
fludrocortisone Fludrocortisone: A synthetic mineralocorticoid with anti-inflammatory activity.	3.23	1	0	11beta-hydroxy steroid; 17alpha-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(4) steroid; C21-steroid; fluorinated steroid; mineralocorticoid	adrenergic agent; anti-inflammatory drug
ursodeoxycholic acid Ursodeoxycholic Acid: An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic.. ursodeoxycholic acid : A bile acid found in the bile of bears (Ursidae) as a conjugate with taurine. Used therapeutically, it prevents the synthesis and absorption of cholesterol and can lead to the dissolution of gallstones.. ursodeoxycholate : A bile acid anion that is the conjugate base of ursodeoxycholic acid, obtained by deprotonation of the carboxy group; major species at pH 7.3.	8.91	3	0	bile acid; C24-steroid; dihydroxy-5beta-cholanic acid	human metabolite; mouse metabolite
pregnanolone Pregnanolone: A pregnane found in the urine of pregnant women and sows. It has anesthetic, hypnotic, and sedative properties.. 3alpha-hydroxy-5beta-pregnan-20-one : The 3alpha-stereoisomer of 3-hydroxy-5beta-pregnan-20-one.	2.04	1	0	3-hydroxy-5beta-pregnan-20-one; 3alpha-hydroxy steroid	human metabolite; intravenous anaesthetic; sedative
benzonidazole benzonidazole: used in treatment of Chagas' disease. benznidazole : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of (2-nitroimidazol-1-yl)acetic acid with the aromatic amino group of benzylamine. Used for treatment of Chagas disease.	2.08	1	0	C-nitro compound; imidazoles; monocarboxylic acid amide	antiprotozoal drug
butachlor butachlor : An aromatic amide that is 2-choro-N-(2,6-diethylphenyl)acetamide in which the amide nitrogen has been replaced by a butoxymethyl group.	2.05	1	0	aromatic amide; organochlorine compound; tertiary carboxamide	environmental contaminant; herbicide; xenobiotic
du-21220 Ritodrine: An adrenergic beta-2 agonist used to control PREMATURE LABOR.. 4-[2-[[1-hydroxy-1-(4-hydroxyphenyl)propan-2-yl]amino]ethyl]phenol : A secondary amino compound that is 4-(2-amino-1-hydroxypropyl)phenol in which one of the hydrogens attached to the nitrogen is replaced by a 2-(4-hydroxyphenyl)ethyl group.	2.04	1	0	benzyl alcohols; polyphenol; secondary alcohol; secondary amino compound
transferrin Transferrin: An iron-binding beta1-globulin that is synthesized in the LIVER and secreted into the blood. It plays a central role in the transport of IRON throughout the circulation. A variety of transferrin isoforms exist in humans, including some that are considered markers for specific disease states.	2.11	1	0
rose bengal b disodium salt [no description available]	2.05	1	0
glutamic acid Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.. glutamic acid : An alpha-amino acid that is glutaric acid bearing a single amino substituent at position 2.	2.48	2	0	glutamic acid; glutamine family amino acid; L-alpha-amino acid; proteinogenic amino acid	Escherichia coli metabolite; ferroptosis inducer; micronutrient; mouse metabolite; neurotransmitter; nutraceutical
dexchlorpheniramine dexchlorpheniramine: RN given refers to parent cpd(S)-isomer	3.23	1	0	chlorphenamine
ribostamycin Ribostamycin: A broad-spectrum antimicrobial isolated from Streptomyces ribosifidicus.. ribostamycin : An amino cyclitol glycoside that is 4,6-diaminocyclohexane-1,2,3-triol having a 2,6-diamino-2,6-dideoxy-alpha-D-glucosyl residue attached at position 1 and a beta-D-ribosyl residue attached at position 2. It is an antibiotic produced by Streptomyces ribosidificus (formerly S. thermoflavus).	2.04	1	0	amino cyclitol glycoside; aminoglycoside antibiotic	antibacterial drug; antimicrobial agent; metabolite
clometacin clometacin: structure	3.23	1	0	N-acylindole
cefazolin Cefazolin: A semisynthetic cephalosporin analog with broad-spectrum antibiotic action due to inhibition of bacterial cell wall synthesis. It attains high serum levels and is excreted quickly via the urine.. cefazolin : A first-generation cephalosporin compound having [(5-methyl-1,3,4-thiadiazol-2-yl)sulfanyl]methyl and (1H-tetrazol-1-ylacetyl)amino side-groups at positions 3 and 7 respectively.	3.86	3	0	beta-lactam antibiotic allergen; cephalosporin; tetrazoles; thiadiazoles	antibacterial drug
amoxicillin Amoxicillin: A broad-spectrum semisynthetic antibiotic similar to AMPICILLIN except that its resistance to gastric acid permits higher serum levels with oral administration.. amoxicillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-amino-2-(4-hydroxyphenyl)acetamido group.	4.27	5	0	penicillin allergen; penicillin	antibacterial drug
timolol (S)-timolol (anhydrous) : The (S)-(-) (more active) enantiomer of timolol. A beta-adrenergic antagonist, both the hemihydrate and the maleate salt are used in the mangement of glaucoma, hypertension, angina pectoris and myocardial infarction, and for the prevention of migraine.	4.08	4	0	timolol	anti-arrhythmia drug; antiglaucoma drug; antihypertensive agent; beta-adrenergic antagonist
indoramin Indoramin: An alpha-1 adrenergic antagonist that is commonly used as an antihypertensive agent.	2.46	2	0	tryptamines
tramadol Tramadol: A narcotic analgesic proposed for severe pain. It may be habituating.. tramadol : A racemate consisting of equal amounts of (R,R)- and (S,S)-tramadol. A centrally acting synthetic opioid analgesic, used (as the hydrochloride salt) to treat moderately severe pain. The (R,R)-enantiomer exhibits ten-fold higher analgesic potency than the (S,S)-enantiomer. Originally developed by Gruenenthal GmbH and launched in 1977, it was subsequently isolated from the root bark of the South African tree Nauclea latifolia.. (R,R)-tramadol : A 2-[(dimethylamino)methyl]-1-(3-methoxyphenyl)cyclohexanol in which both stereocentres have R-configuration; the (R,R)-enantiomer of the racemic opioid analgesic tramadol, it exhibits ten-fold higher analgesic potency than the (S,S)-enantiomer.	8.93	3	0	2-[(dimethylamino)methyl]-1-(3-methoxyphenyl)cyclohexanol	adrenergic uptake inhibitor; antitussive; capsaicin receptor antagonist; delta-opioid receptor agonist; kappa-opioid receptor agonist; metabolite; mu-opioid receptor agonist; muscarinic antagonist; nicotinic antagonist; NMDA receptor antagonist; opioid analgesic; serotonergic antagonist; serotonin uptake inhibitor
nicergoline Nicergoline: An ergot derivative that has been used as a cerebral vasodilator and in peripheral vascular disease. It may ameliorate cognitive deficits in CEREBROVASCULAR DISORDERS.	2.05	1	0	organic heterotetracyclic compound; organonitrogen heterocyclic compound
oxcarbazepine Oxcarbazepine: A carbamazepine derivative that acts as a voltage-gated sodium channel blocker. It is used for the treatment of PARTIAL SEIZURES with or without secondary generalization. It is also an inducer of CYTOCHROME P-450 CYP3A4.. oxcarbazepine : A dibenzoazepine derivative, having a carbamoyl group at the ring nitrogen, substituted with an oxo group at C-4 of the azepeine ring which is also hydrogenated at C-4 and C-5. It is a anticholinergic anticonvulsant and mood stabilizing drug, used primarily in the treatment of epilepsy.	4.61	4	0	cyclic ketone; dibenzoazepine	anticonvulsant; drug allergen
carbidopa carbidopa (anhydrous) : 3-(3,4-Dihydroxyphenyl)propanoic acid in which the hydrogens alpha- to the carboxyl group are substituted by hydrazinyl and methyl groups (S-configuration). Carbidopa is a dopa decarboxylase inhibitor, so prevents conversion of levodopa to dopamine. It has no antiparkinson activity by itself, but is used (commonly as its hydrate) in the management of Parkinson's disease to reduce peripheral adverse effects of levodopa.	3.61	2	0	catechols; hydrazines; monocarboxylic acid	antiparkinson drug; dopaminergic agent; EC 4.1.1.28 (aromatic-L-amino-acid decarboxylase) inhibitor
toloxatone toloxatone: oxazolidinone derivative; psychotropic drug; structure. toloxatone : A racemate consisting of equimolar amounts of (R)- and (S)-toloxatone. It is a reversible monoamine oxidase A inhibitor and antidepressant.. 5-(hydroxymethyl)-3-(3-methylphenyl)-1,3-oxazolidin-2-one : A member of the class of oxazolidinones that is 5-(hydroxymethyl)-1,3-oxazolidin-2-one substituted by a 3-methylphenyl group at position 3.	2.04	1	0	oxazolidinone; primary alcohol; toluenes
moricizine Moricizine: An antiarrhythmia agent used primarily for ventricular rhythm disturbances.. moricizine : A phenothiazine substituted on the nitrogen by a 3-(morpholin-4-yl)propanoyl group, and at position 2 by an (ethoxycarbonyl)amino group.	3.23	1	0	carbamate ester; morpholines; phenothiazines	anti-arrhythmia drug
vidarabine phosphate Vidarabine Phosphate: An adenosine monophosphate analog in which ribose is replaced by an arabinose moiety. It is the monophosphate ester of VIDARABINE with antiviral and possibly antineoplastic properties.	3.12	1	0
amineptin amineptin: used in treatment of neuroses with psychoasthenic, anxio-phobic & depressive manifestations; synonym S 1694 refers to HCl; structure. amineptine : A carbocyclic fatty acid that is 5-aminoheptanoic acid in which one of the hydrogens attached to the nitrogen is replaced by a 10,11-dihydro-5H-dibenzo[a,d][7]annulen-5-yl group. A tricyclic antidepressant, it was never approved in the US and was withdrawn from the French market in 1999 due to concerns over abuse, dependence and severe acne.	3.59	2	0	amino acid; carbocyclic fatty acid; carbotricyclic compound; secondary amino compound	antidepressant; dopamine uptake inhibitor
zidovudine Zidovudine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIV-induced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia.. zidovudine : A pyrimidine 2',3'-dideoxyribonucleoside compound having a 3'-azido substituent and thymine as the nucleobase.	4.44	6	0	azide; pyrimidine 2',3'-dideoxyribonucleoside	antimetabolite; antiviral drug; HIV-1 reverse transcriptase inhibitor
feprazone Feprazone: A pyrazole that has analgesic, anti-inflammatory, and antipyretic properties. It has been used in mild to moderate pain, fever, and inflammation associated with musculoskeletal and joint disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p15)	2.08	1	0	organic molecular entity
pirprofen pirprofen: anti-inflammatory agent used in therapy of rheumatoid arthritis; prostaglandin synthetase inhibitor; more potent than indomethacin; structure	3.59	2	0	pyrroline
sisomicin Sisomicin: Antibiotic produced by Micromonospora inyoensis. It is closely related to gentamicin C1A, one of the components of the gentamicin complex (GENTAMICINS).	2.04	1	0	amino cyclitol glycoside; aminoglycoside antibiotic; beta-L-arabinoside; monosaccharide derivative
amdinocillin Amdinocillin: An amidinopenicillanic acid derivative with broad spectrum antibacterial action.. mecillinam : A penicillin in which the 6beta substituent is [(azepan-1-yl)methylidene]amino; an extended-spectrum penicillin antibiotic that binds specifically to penicillin binding protein 2 (PBP2), and is only considered to be active against Gram-negative bacteria.	2.04	1	0	penicillin	antibacterial drug; antiinfective agent
tobramycin Tobramycin: An aminoglycoside, broad-spectrum antibiotic produced by Streptomyces tenebrarius. It is effective against gram-negative bacteria, especially the PSEUDOMONAS species. It is a 10% component of the antibiotic complex, NEBRAMYCIN, produced by the same species.. tobramycin : A amino cyclitol glycoside that is kanamycin B lacking the 3-hydroxy substituent from the 2,6-diaminoglucose ring.	2.75	3	0	amino cyclitol glycoside	antibacterial agent; antimicrobial agent; toxin
paclitaxel Taxus: Genus of coniferous yew trees or shrubs, several species of which have medicinal uses. Notable is the Pacific yew, Taxus brevifolia, which is used to make the anti-neoplastic drug taxol (PACLITAXEL).	12.01	50	8	taxane diterpenoid; tetracyclic diterpenoid	antineoplastic agent; human metabolite; metabolite; microtubule-stabilising agent
buspirone hydrochloride buspirone hydrochloride : A hydrochloride salt resulting from the reaction of equimolar amounts of buspirone and hydrogen chloride.	2.15	1	0	hydrochloride	anxiolytic drug; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; sedative; serotonergic agonist
etoposide [no description available]	12.69	49	12	beta-D-glucoside; furonaphthodioxole; organic heterotetracyclic compound	antineoplastic agent; DNA synthesis inhibitor
substance p [no description available]	7.53	2	0	peptide	neurokinin-1 receptor agonist; neurotransmitter; vasodilator agent
dobutamine Dobutamine: A catecholamine derivative with specificity for BETA-1 ADRENERGIC RECEPTORS. It is commonly used as a cardiotonic agent after CARDIAC SURGERY and during DOBUTAMINE STRESS ECHOCARDIOGRAPHY.. dobutamine : A catecholamine that is 4-(3-aminobutyl)phenol in which one of the hydrogens attached to the nitrogen is substituted by a 2-(3,4-dihydroxyphenyl)ethyl group. A beta1-adrenergic receptor agonist that has cardiac stimulant action without evoking vasoconstriction or tachycardia, it is used as the hydrochloride to increase the contractility of the heart in the management of acute heart failure.	3.59	2	0	catecholamine; secondary amine	beta-adrenergic agonist; cardiotonic drug; sympathomimetic agent
ticarcillin Ticarcillin: An antibiotic derived from penicillin similar to CARBENICILLIN in action.. ticarcillin : A penicillin compound having a 6beta-[(2R)-2-carboxy-2-thiophen-3-ylacetyl]amino side-group.	2.04	1	0	penicillin allergen; penicillin	antibacterial drug
trimazosin trimazosin: RN given refers to parent cpd; structure	2.04	1	0	N-arylpiperazine
1,2,3,4,6,7,8-heptachlorodibenzodioxin 1,2,3,4,6,7,8-heptachlorodibenzodioxin: contaminant of pentachlorophenol	2.41	1	0	polychlorinated dibenzodioxine
penbutolol Penbutolol: A nonselective beta-blocker used as an antihypertensive and an antianginal agent.	3.23	1	0	ethanolamines
ribavirin Rebetron: Rebetron is tradename	4.47	6	0	1-ribosyltriazole; aromatic amide; monocarboxylic acid amide; primary carboxamide	anticoronaviral agent; antiinfective agent; antimetabolite; antiviral agent; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
adinazolam adinazolam: structure in first source. adinazolam : A triazolo[4,3-a][1,4]benzodiazepine having a dimethylaminomethyl group at the 1-position, a phenyl group at the 6-position and a chloro substituent at the 8-position.	2.04	1	0	triazolobenzodiazepine	anticonvulsant; antidepressant; anxiolytic drug; sedative
amikacin Amikacin: A broad-spectrum antibiotic derived from KANAMYCIN. It is reno- and oto-toxic like the other aminoglycoside antibiotics.. amikacin : An amino cyclitol glycoside that is kanamycin A acylated at the N-1 position by a 4-amino-2-hydroxybutyryl group.	4.8	5	0	alpha-D-glucoside; amino cyclitol glycoside; aminoglycoside; carboxamide	antibacterial drug; antimicrobial agent; nephrotoxin
tolamolol [no description available]	2.04	1	0
cephradine Cephradine: A semi-synthetic cephalosporin antibiotic.. cephradine : A first-generation cephalosporin antibiotic with a methyl substituent at position 3, and a (2R)-2-amino-2-cyclohexa-1,4-dien-1-ylacetamido substituent at position 7, of the cephem skeleton.	3.58	2	0	beta-lactam antibiotic allergen; cephalosporin	antibacterial drug
ticrynafen Ticrynafen: A novel diuretic with uricosuric action. It has been proposed as an antihypertensive agent.. tienilic acid : An aromatic ketone that is 2,3-dichlorophenoxyacetic acid in which the hydrogen at position 4 on the benzene ring is replaced by a thiophenecarbonyl group. A loop diuretic used to treat hypertension, it was withdrawn from the market in 1982 due to links with hepatitis.	3.59	2	0	aromatic ether; aromatic ketone; dichlorobenzene; monocarboxylic acid; thiophenes	antihypertensive agent; hepatotoxic agent; loop diuretic
methyldopa Methyldopa: An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.. alpha-methyl-L-dopa : A derivative of L-tyrosine having a methyl group at the alpha-position and an additional hydroxy group at the 3-position on the phenyl ring.	3.86	3	0	L-tyrosine derivative; non-proteinogenic L-alpha-amino acid	alpha-adrenergic agonist; antihypertensive agent; hapten; peripheral nervous system drug; sympatholytic agent
pyridoxal phosphate [no description available]	2.6	1	0	pyridinecarbaldehyde
tocainide Tocainide: An antiarrhythmic agent which exerts a potential- and frequency-dependent block of SODIUM CHANNELS.. tocainide : A monocarboxylic acid amide in which 2,6-dimethylphenylaniline and isobutyric acid have combined to form the amide bond; used as a local anaesthetic.	2.04	1	0	monocarboxylic acid amide	anti-arrhythmia drug; local anaesthetic; sodium channel blocker
sulbenicillin Sulbenicillin: Semisynthetic penicillin-type antibiotic.. sulbenicillin : A penicillin antibiotic having a 6beta-[phenyl(sulfo)acetamido] side-chain.	2.04	1	0	penicillin
bezafibrate [no description available]	2.05	1	0	aromatic ether; monocarboxylic acid amide; monocarboxylic acid; monochlorobenzenes	antilipemic drug; environmental contaminant; geroprotector; xenobiotic
sq-11725 Nadolol: A non-selective beta-adrenergic antagonist with a long half-life, used in cardiovascular disease to treat arrhythmias, angina pectoris, and hypertension. Nadolol is also used for MIGRAINE DISORDERS and for tremor.. nadolol : Nadolol is a diastereoisomeric mixture consisting of equimolar amounts of the four possible 2,3-cis-isomers of 5-[3-(tert-butylamino)-2-hydroxypropoxy]-1,2,3,4-tetrahydronaphthalene-2,3-diol.	2.45	2	0
diltiazem Diltiazem: A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of CALCIUM ion on membrane functions.. diltiazem : A 5-[2-(dimethylamino)ethyl]-2-(4-methoxyphenyl)-4-oxo-2,3,4,5-tetrahydro-1,5-benzothiazepin-3-yl acetate in which both stereocentres have S configuration. A calcium-channel blocker and vasodilator, it is used as the hydrochloride in the management of angina pectoris and hypertension.	4.27	5	0	5-[2-(dimethylamino)ethyl]-2-(4-methoxyphenyl)-4-oxo-2,3,4,5-tetrahydro-1,5-benzothiazepin-3-yl acetate	antihypertensive agent; calcium channel blocker; vasodilator agent
lonidamine lonidamine: structure. lonidamine : A member of the class of indazoles that is 1H-indazole that is substituted at positions 1 and 3 by 2,4-dichlorobenzyl and carboxy groups, respectively.	2.08	1	0	dichlorobenzene; indazoles; monocarboxylic acid	antineoplastic agent; antispermatogenic agent; EC 2.7.1.1 (hexokinase) inhibitor; geroprotector
vecuronium bromide Vecuronium Bromide: Monoquaternary homolog of PANCURONIUM. A non-depolarizing neuromuscular blocking agent with shorter duration of action than pancuronium. Its lack of significant cardiovascular effects and lack of dependence on good kidney function for elimination as well as its short duration of action and easy reversibility provide advantages over, or alternatives to, other established neuromuscular blocking agents.. vecuronium bromide : The organic bromide salt of a 5alpha-androstane compound having 3alpha-acetoxy-, 17beta-acetoxy-, 2beta-piperidinino- and 16beta-N-methylpiperidinium substituents.	2.46	2	0	organic bromide salt; quaternary ammonium salt	muscle relaxant; neuromuscular agent; nicotinic antagonist
vecuronium vecuronium : A 5alpha-androstane compound having 3alpha-acetoxy-, 17beta-acetoxy-, 2beta-piperidino- and 16beta-N-methylpiperidinium substituents.	3.23	1	0	acetate ester; androstane; quaternary ammonium ion	drug allergen; muscle relaxant; neuromuscular agent; nicotinic antagonist
ng-nitroarginine methyl ester NG-Nitroarginine Methyl Ester: A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.	2.15	1	0	alpha-amino acid ester; L-arginine derivative; methyl ester; N-nitro compound	EC 1.14.13.39 (nitric oxide synthase) inhibitor
benoxaprofen benoxaprofen: RN given refers to parent cpd; structure. benoxaprofen : A monocarboxylic acid that is propionic acid substituted at position 2 by a 2-(4-chlorophenyl)-1,3-benzoxazol-5-yl group. It was used as a non-steroidal anti-inflammatory drug until 1982 when it was withdrawn from the market due to adverse side-effects including liver necrosis, photosensitivity, and carcinogenicity in animals.	3.59	2	0	1,3-benzoxazoles; monocarboxylic acid; monochlorobenzenes	antipsoriatic; antipyretic; EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor; hepatotoxic agent; nephrotoxin; non-narcotic analgesic; non-steroidal anti-inflammatory drug; protein kinase C agonist
permethrin hemoglobin Atlanta-Coventry: Leu replaced by Pro at beta75 and Leu deleted at beta141	2.05	1	0	cyclopropanecarboxylate ester; cyclopropanes	agrochemical; ectoparasiticide; pyrethroid ester acaricide; pyrethroid ester insecticide; scabicide
exifone [no description available]	3.23	1	0	benzophenones
decamethrin decamethrin: pyrethroid insecticide; RN given refers to cpd without isomeric designation; structure	2.08	1	0	aromatic ether; cyclopropanecarboxylate ester; nitrile; organobromine compound	agrochemical; antifeedant; calcium channel agonist; EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor; pyrethroid ester insecticide
pirfenidone pirfenidone : A pyridone that is 2-pyridone substituted at positions 1 and 5 by phenyl and methyl groups respectively. An anti-inflammatory drug used for the treatment of idiopathic pulmonary fibrosis.	2.05	1	0	pyridone	antipyretic; non-narcotic analgesic; non-steroidal anti-inflammatory drug
mefloquine (-)-(11S,2'R)-erythro-mefloquine : An optically active form of [2,8-bis(trifluoromethyl)quinolin-4-yl]-(2-piperidyl)methanol having (-)-(11S,2'R)-erythro-configuration. An antimalarial agent, used in racemic form, which acts as a blood schizonticide; its mechanism of action is unknown.	3.65	2	0	[2,8-bis(trifluoromethyl)quinolin-4-yl]-(2-piperidyl)methanol	antimalarial
vindesine Vindesine: Vinblastine derivative with antineoplastic activity against CANCER. Major side effects are myelosuppression and neurotoxicity. Vindesine is used extensively in chemotherapy protocols (ANTINEOPLASTIC COMBINED CHEMOTHERAPY PROTOCOLS).	2.25	1	0	methyl ester; organic heteropentacyclic compound; organic heterotetracyclic compound; primary carboxamide; tertiary alcohol; tertiary amino compound; vinca alkaloid	antineoplastic agent
desogestrel Desogestrel: A synthetic progestational hormone used often as the progestogenic component of combined oral contraceptive agents (ORAL CONTRACEPTIVES, COMBINED).	2.05	1	0	17beta-hydroxy steroid; terminal acetylenic compound	contraceptive drug; progestin; synthetic oral contraceptive
meptazinol Meptazinol: A narcotic antagonist with analgesic properties. It is used for the control of moderate to severe pain.	2.04	1	0	azepanes
muzolimine Muzolimine: A pyrazole diuretic with long duration and high capacity of action. It was proposed for kidney failure and hypertension but was withdrawn worldwide because of severe neurological effects.	2.05	1	0	dichlorobenzene
nitazoxanide nitazoxanide: a 5-nitrothiazolyl derivative used for a broad range of intestinal parasitic infections including CRYPTOSPORIDIUM and GIARDIA; it is a redox-active nitrothiazolyl-salicylamide prodrug	3.95	3	0	benzamides; carboxylic ester
sufentanil Sufentanil: An opioid analgesic that is used as an adjunct in anesthesia, in balanced anesthesia, and as a primary anesthetic agent.. sufentanil : An anilide resulting from the formal condensation of the aryl amino group of 4-(methoxymethyl)-N-phenyl-1-[2-(2-thienyl)ethyl]piperidin-4-amine with propanoic acid.	3.58	2	0	anilide; ether; piperidines; thiophenes	anaesthesia adjuvant; intravenous anaesthetic; mu-opioid receptor agonist; opioid analgesic
acarbose [no description available]	3.61	2	0	tetrasaccharide derivative	EC 3.2.1.1 (alpha-amylase) inhibitor; EC 3.2.1.20 (alpha-glucosidase) inhibitor; geroprotector; hypoglycemic agent
torsemide Torsemide: A pyridine and sulfonamide derivative that acts as a sodium-potassium chloride symporter inhibitor (loop diuretic). It is used for the treatment of EDEMA associated with CONGESTIVE HEART FAILURE; CHRONIC RENAL INSUFFICIENCY; and LIVER DISEASES. It is also used for the management of HYPERTENSION.. torasemide : An N-sulfonylurea obtained by formal condensation of [(3-methylphenyl)amino]pyridine-3-sulfonic acid with the free amino group of N-isopropylurea. It is a potent loop diuretic used for the treatment of hypertension and edema in patients with congestive heart failure.	3.58	2	0	aminopyridine; N-sulfonylurea; secondary amino compound	antihypertensive agent; loop diuretic
medroxalol medroxalol: RN given refers to parent cpd without isomeric designation	2.04	1	0	salicylamides
epirubicin Epirubicin: An anthracycline which is the 4'-epi-isomer of doxorubicin. The compound exerts its antitumor effects by interference with the synthesis and function of DNA.	7.61	13	2	aminoglycoside; anthracycline antibiotic; anthracycline; deoxy hexoside; monosaccharide derivative; p-quinones; primary alpha-hydroxy ketone; tertiary alpha-hydroxy ketone	antimicrobial agent; antineoplastic agent; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
cefmetazole Cefmetazole: A semisynthetic cephamycin antibiotic with a broad spectrum of activity against both gram-positive and gram-negative microorganisms. It has a high rate of efficacy in many types of infection and to date no severe side effects have been noted.. cefmetazole : A second-generation cephalosporin antibiotic having N(1)-methyltetrazol-5-ylthiomethyl, {[(cyanomethyl)sulfanyl]acetyl}amino and methoxy side-groups at positions 3, 7beta and 7alpha respectively of the parent cephem bicyclic structure.	2.04	1	0	cephalosporin	antibacterial drug
desflurane Desflurane: A fluorinated ether that is used as a volatile anesthetic for maintenance of general anesthesia.	2.05	1	0	organofluorine compound	inhalation anaesthetic
lorcainide [no description available]	2.46	2	0	acetamides
idarubicin Idarubicin: An orally administered anthracycline antineoplastic. The compound has shown activity against BREAST NEOPLASMS; LYMPHOMA; and LEUKEMIA.	9.16	11	3	anthracycline antibiotic; deoxy hexoside; monosaccharide derivative
propiconazole Orbit: Bony cavity that holds the eyeball and its associated tissues and appendages.	2.08	1	0	conazole fungicide; cyclic ketal; dichlorobenzene; triazole fungicide; triazoles	antifungal agrochemical; EC 1.14.13.70 (sterol 14alpha-demethylase) inhibitor; environmental contaminant; xenobiotic
ceforanide ceforanide: RN given refers to (6R-(trans))-isomer. ceforanide : A second-generation cephalosporin antibiotic with {[1-(carboxymethyl)-1H-tetrazol-5-yl]sulfanyl}methyl and 2-(aminomethyl)phenylacetamido groups at positions 3 and 7, respectively, of the cephem skeleton. It is effective against many coliforms, including Escherichia coli, Klebsiella, Enterobacter and Proteus, and most strains of Salmonella, Shigella, Hemophilus, Citrobacter and Arizona species.	2.04	1	0	cephalosporin	antibacterial drug
piperacillin Piperacillin: Semisynthetic, broad-spectrum, AMPICILLIN derived ureidopenicillin antibiotic proposed for PSEUDOMONAS infections. It is also used in combination with other antibiotics.. piperacillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-[(4-ethyl-2,3-dioxopiperazin-1-yl)carboxamido]-2-phenylacetamido group.	3.86	3	0	penicillin allergen; penicillin	antibacterial drug
paroxetine Paroxetine: A serotonin uptake inhibitor that is effective in the treatment of depression.. paroxetine : A benzodioxole that consists of piperidine bearing 1,3-benzodioxol-5-yloxy)methyl and 4-fluorophenyl substituents at positions 3 and 4 respectively; the (3S,4R)-diastereomer. Highly potent and selective 5-HT uptake inhibitor that binds with high affinity to the serotonin transporter (Ki = 0.05 nM). Ki values are 1.1, 350 and 1100 nM for inhibition of [3H]-5-HT, [3H]-l-NA and [3H]-DA uptake respectively. Displays minimal affinity for alpha1-, alpha2- or beta-adrenoceptors, 5-HT2A, 5-HT1A, D2 or H1 receptors at concentrations below 1000 nM, however displays weak affinity for muscarinic ACh receptors (Ki = 42 nM). Antidepressant and anxiolytic in vivo.	3.86	3	0	aromatic ether; benzodioxoles; organofluorine compound; piperidines	antidepressant; anxiolytic drug; hepatotoxic agent; P450 inhibitor; serotonin uptake inhibitor
captopril Captopril: A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.. captopril : A L-proline derivative in which L-proline is substituted on nitrogen with a (2S)-2-methyl-3-sulfanylpropanoyl group. It is used as an anti-hypertensive ACE inhibitor drug.	4.29	5	0	alkanethiol; L-proline derivative; N-acylpyrrolidine; pyrrolidinemonocarboxylic acid	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
cefoperazone Cefoperazone: Semisynthetic broad-spectrum cephalosporin with a tetrazolyl moiety that is resistant to beta-lactamase. It may be used to treat Pseudomonas infections.. cefoperazone : A semi-synthetic parenteral cephalosporin with a tetrazolyl moiety that confers beta-lactamase resistance.	3.86	3	0	cephalosporin	antibacterial drug
staurosporine [no description available]	3.37	6	0	indolocarbazole alkaloid; organic heterooctacyclic compound	apoptosis inducer; bacterial metabolite; EC 2.7.11.13 (protein kinase C) inhibitor; geroprotector
foscarnet sodium trisodium phosphonoformate : The trisodium salt of phosphonoformic acid. It is used as an antiviral agent in the treatment of cytomegalovirus retinitis (CMV retinitis, an inflamation of the retina that can lead to blindness) and as an alternative to ganciclovir for AIDS patients who require concurrent antiretroviral therapy but are unable to tolerate ganciclovir due to haematological toxicity.	2.47	2	0	one-carbon compound; organic sodium salt	antiviral drug
oltipraz oltipraz : A 1,2-dithiole that is 3H-1,2-dithiole-3-thione substituted at positions 4 and 5 by methyl and pyrazin-2-yl groups respectively.	2.6	1	0	1,2-dithiole; pyrazines	angiogenesis modulating agent; antimutagen; antineoplastic agent; antioxidant; EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor; neurotoxin; protective agent; schistosomicide drug
atracurium Atracurium: A non-depolarizing neuromuscular blocking agent with short duration of action. Its lack of significant cardiovascular effects and its lack of dependence on good kidney function for elimination provide clinical advantage over alternate non-depolarizing neuromuscular blocking agents.. atracurium : A diester compound consisting of pentane-1,5-diol with both hydroxyls bearing 3-[1-(3,4-dimethoxybenzyl)-6,7-dimethoxy-2-methyl-3,4-dihydroisoquinolinium-2(1H)-yl]propanoyl groups.	3.58	2	0	diester; quaternary ammonium ion	muscle relaxant; nicotinic antagonist
atracurium besylate atracurium besylate : The bisbenzenesulfonate salt of atracurium.	2.08	1	0	organosulfonate salt; quaternary ammonium salt	muscle relaxant; nicotinic antagonist
moxalactam Moxalactam: Broad- spectrum beta-lactam antibiotic similar in structure to the CEPHALOSPORINS except for the substitution of an oxaazabicyclo moiety for the thiaazabicyclo moiety of certain CEPHALOSPORINS. It has been proposed especially for the meningitides because it passes the blood-brain barrier and for anaerobic infections.. moxalactam : A broad-spectrum oxacephem antibiotic in which the oxazine ring is substituted with a tetrazolylthiomethyl group and the azetidinone ring carries methoxy and 2-carboxy-2-(4-hydroxyphenyl)acetamido substituents.	2.45	2	0	cephalosporin; oxacephem	antibacterial drug
nicorandil Nicorandil: A derivative of the NIACINAMIDE that is structurally combined with an organic nitrate. It is a potassium-channel opener that causes vasodilatation of arterioles and large coronary arteries. Its nitrate-like properties produce venous vasodilation through stimulation of guanylate cyclase.. nicorandil : A pyrimidinecarboxamide that is nicotinamide in which one of the hydrogens attached to the carboxamide nitrogen is replaced by a 2-(nitrooxy)ethyl group. It has both nitrate-like and ATP-sensitive potassium channel activator properties, and is used for the prevention and treatment of angina pectoris.	2.47	2	0	nitrate ester; pyridinecarboxamide	potassium channel opener; vasodilator agent
endralazine BQ 22-708: RN given refers to parent cpd	2.04	1	0	benzamides
pergolide Pergolide: A long-acting dopamine agonist which has been used to treat PARKINSON DISEASE and HYPERPROLACTINEMIA but withdrawn from some markets due to potential for HEART VALVE DISEASES.. pergolide : A diamine that is ergoline in which the beta-hydrogen at position 8 is replaced by a (methylthio)methyl group and the hydrogen attached to the piperidine nitrogen (position 6) is replaced by a propyl group. A dopamine D2 receptor agonist which also has D1 and D2 agonist properties, it is used as the mesylate salt in the management of Parkinson's disease, although it was withdrawn from the U.S. and Canadian markets in 2007 due to an increased risk of cardiac valve dysfunction.	3.23	1	0	diamine; methyl sulfide; organic heterotetracyclic compound	antiparkinson drug; dopamine agonist
pergolide mesylate pergolide mesylate : A methanesulfonate salt obtained from pergolide by mixing eqimolar amount of pergolide and methanesulfonic acid. A dopamine D2 receptor agonist which also has D1 and D2 agonist properties, it is used in the management of Parkinson's disease, although it was withdrawn from the U.S. and Canadian markets in 2007 due to an increased risk of cardiac valve dysfunction.	2.08	1	0	methanesulfonate salt	antiparkinson drug; dopamine agonist; geroprotector
cefadroxil anhydrous Cefadroxil: Long-acting, broad-spectrum, water-soluble, CEPHALEXIN derivative.. cefadroxil : A cephalosporin bearing methyl and (2R)-2-amino-2-(4-hydroxyphenyl)acetamido groups at positions 3 and 7, respectively, of the cephem skeleton.	4.08	4	0	cephalosporin	antibacterial drug
encainide Encainide: One of the ANTI-ARRHYTHMIA AGENTS, it blocks VOLTAGE-GATED SODIUM CHANNELS and slows conduction within the His-Purkinje system and MYOCARDIUM.. encainide : 4-Methoxy-N-phenylbenzamide in which the hydrogen at the 2 position of the phenyl group is substituted by a 2-(1-methylpiperidin-2-yl)ethyl group. A class Ic antiarrhythmic, the hydrochloride was used for the treatment of severe or life-threatening ventricular arrhythmias, but it was associated with increased death rates in patients who had asymptomatic heart rhythm abnormalities after a recent heart attack and was withdrawn from the market.	2.45	2	0	benzamides; piperidines	anti-arrhythmia drug; sodium channel blocker
talniflumate talniflumate: an anti-inflammatory molecule for the treatment of cystic fibrosis, chronic obstructive pulmonary disease and asthma	2.08	1	0	benzofurans
fenoldopam mesylate [no description available]	2.08	1	0	benzazepine
fiacitabine fiacitabine: anti-herpes virus agent which also inhibits growth of certain human tumor cell lines in vitro.	2.6	1	0
fialuridine [no description available]	3.85	3	0
cefaclor anhydrous Cefaclor: Semisynthetic, broad-spectrum antibiotic derivative of CEPHALEXIN.. cefaclor : A cephalosporin bearing chloro and (R)-2-amino-2-phenylacetamido groups at positions 3 and 7, respectively, of the cephem skeleton.	3.87	3	0	cephalosporin	antibacterial drug; drug allergen
pefloxacin Pefloxacin: A synthetic broad-spectrum fluoroquinolone antibacterial agent active against most gram-negative and gram-positive bacteria.. pefloxacin : A quinolone that is 4-oxo-1,4-dihydroquinoline which is substituted at positions 1, 3, 6 and 7 by ethyl, carboxy, fluorine, and 4-methylpiperazin-1-yl groups, respectively.	2.46	2	0	fluoroquinolone antibiotic; monocarboxylic acid; N-alkylpiperazine; N-arylpiperazine; quinolone antibiotic; quinolone	antibacterial drug; antiinfective agent; DNA synthesis inhibitor
alfentanil Alfentanil: A short-acting opioid anesthetic and analgesic derivative of FENTANYL. It produces an early peak analgesic effect and fast recovery of consciousness. Alfentanil is effective as an anesthetic during surgery, for supplementation of analgesia during surgical procedures, and as an analgesic for critically ill patients.. alfentanil : A member of the class of piperidines that is piperidine having a 2-(4-ethyl-5-oxo-4,5-dihydro-1H-tetrazol-1-yl)ethyl group at the 1-position as well as N-phenylpropanamido- and methoxymethyl groups at the 4-position.	3.58	2	0	monocarboxylic acid amide; piperidines	central nervous system depressant; intravenous anaesthetic; mu-opioid receptor agonist; opioid analgesic; peripheral nervous system drug
fenoxycarb fenoxycarb: used against mosquitoes (Diptera:Culicidae); structure given in first source. fenoxycarb : A carbamate ester that is the O-ethyl carbamate of 2-(4-phenoxyphenoxy)ethylamine.	2.11	1	0	aromatic ether; carbamate ester	environmental contaminant; insecticide; juvenile hormone mimic; xenobiotic
miglustat miglustat: a glucosylceramide synthase inhibitor. miglustat : A hydroxypiperidine that is deoxynojirimycin in which the amino hydrogen is replaced by a butyl group.	3.59	2	0	piperidines; tertiary amino compound	anti-HIV agent; EC 2.4.1.80 (ceramide glucosyltransferase) inhibitor
haloperidol decanoate [no description available]	3.23	1	0	organic molecular entity
cefotetan Cefotetan: A semisynthetic cephamycin antibiotic that is administered intravenously or intramuscularly. The drug is highly resistant to a broad spectrum of beta-lactamases and is active against a wide range of both aerobic and anaerobic gram-positive and gram-negative microorganisms.. cefotetan : A semi-synthetic second-generation cephamycin antibiotic with [(1-methyl-1H-tetrazol-5-yl)sulfanyl]methyl, methoxy and {[4-(2-amino-1-carboxy-2-oxoethylidene)-1,3-dithietan-2-yl]carbonyl}amino groups at the 3, 7alpha, and 7beta positions, respectively, of the cephem skeleton. It is resistant to a wide range of beta-lactamases and is active against a broad spectrum of aerobic and anaerobic Gram-positive and Gram-negative microorganisms.	4.08	4	0
recainam recainam: structure given in first source	2.04	1	0
lovastatin Lovastatin: A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.. lovastatin : A fatty acid ester that is mevastatin carrying an additional methyl group on the carbobicyclic skeleton. It is used in as an anticholesteremic drug and has been found in fungal species such as Aspergillus terreus and Pleurotus ostreatus (oyster mushroom).	10.06	7	0	delta-lactone; fatty acid ester; hexahydronaphthalenes; polyketide; statin (naturally occurring)	anticholesteremic drug; antineoplastic agent; Aspergillus metabolite; prodrug
flupirtine flupirtine: RN given refers to parent cpd without isomeric designation	2.46	2	0	aminopyridine
tolrestat tolrestat: RN & structure given in first source	3.23	1	0	naphthalenes	EC 1.1.1.21 (aldehyde reductase) inhibitor
enoximone Enoximone: A selective phosphodiesterase inhibitor with vasodilating and positive inotropic activity that does not cause changes in myocardial oxygen consumption. It is used in patients with CONGESTIVE HEART FAILURE.	2.75	3	0	aromatic ketone
stepronin [no description available]	2.08	1	0	N-acyl-amino acid
piritrexim piritrexim: RN given refers to parent cpd; structure given in first source	2.05	1	0
simvastatin Simvastatin: A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.. simvastatin : A member of the class of hexahydronaphthalenes that is lovastatin in which the 2-methylbutyrate ester moiety has been replaced by a 2,2-dimethylbutyrate ester group. It is used as a cholesterol-lowering and anti-cardiovascular disease drug.	11.19	9	1	delta-lactone; fatty acid ester; hexahydronaphthalenes; statin (semi-synthetic)	EC 1.1.1.34/EC 1.1.1.88 (hydroxymethylglutaryl-CoA reductase) inhibitor; EC 3.4.24.83 (anthrax lethal factor endopeptidase) inhibitor; ferroptosis inducer; geroprotector; prodrug
idazoxan Idazoxan: A benzodioxane-linked imidazole that has alpha-2 adrenoceptor antagonist activity.. idazoxan : A benzodioxine that is 2,3-dihydro-1,4-benzodioxine in which one of the hydrogens at position 2 has been replaced by a 4,5-dihydro-1H-imidazol-2-yl group.	2.46	2	0	benzodioxine; imidazolines	alpha-adrenergic antagonist
remoxipride Remoxipride: An antipsychotic agent that is specific for dopamine D2 receptors. It has been shown to be effective in the treatment of schizophrenia.	2.46	2	0	dimethoxybenzene
balsalazide balsalazide: a mesalamine 5-aminosalicylate prodrug; 99% of ingested drug remains intact through the stomach and is delivered to and activated in the colon; used for inflammatory bowel disease, ulcerative colitis and radiation-induced proctosigmoiditis but avoided in patients with known hypersensitivity reaction to salicylates or mesalamine; structure in first source. balsalazide : A monohydroxybenzoic acid consisting of 5-aminosalicylic acid (mesalazine) linked to 4-aminobenzoyl-beta-alanine via an azo bond.	3.23	1	0
pravastatin Pravastatin: An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).. pravastatin : A carboxylic ester resulting from the formal condensation of (S)-2-methylbutyric acid with the hydroxy group adjacent to the ring junction of (3R,5R)-7-[(1S,2S,6S,8S,8aR)-6,8-dihydroxy-2-methyl-1,2,6,7,8,8a-hexahydronaphthalen-1-yl]-3,5-dihydroxyheptanoic acid. Derived from microbial transformation of mevastatin, pravastatin is a reversible inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA). The sodium salt is used for lowering cholesterol and preventing cardiovascular disease. It is one of the lower potency statins, but has the advantage of fewer side effects compared with lovastatin and simvastatin.	4.08	4	0	3-hydroxy carboxylic acid; carbobicyclic compound; carboxylic ester; hydroxy monocarboxylic acid; secondary alcohol; statin (semi-synthetic)	anticholesteremic drug; environmental contaminant; metabolite; xenobiotic
cabergoline Cabergoline: An ergoline derivative and dopamine D2-agonist that inhibits PROLACTIN secretion. It is used in the management of HYPERPROLACTINEMIA, and to suppress lactation following childbirth for medical reasons. Cabergoline is also used in the management of PARKINSON DISEASE.. cabergoline : An N-acylurea that is (8R)-ergoline-8-carboxamide in which the hydrogen attached to the piperidine nitrogen (position 6) is substituted by an allyl group and the hydrogens attached to the carboxamide nitrogen are substituted by a 3-(dimethylamino)propyl group and an N-ethylcarbamoyl group. A dopamine D2 receptor agonist, cabergoline is used in the management of Parkinson's disease and of disorders associated with hyperprolactinaemia.	3.61	2	0	N-acylurea	antineoplastic agent; antiparkinson drug; dopamine agonist
bambuterol bambuterol: selective inhibitor of butyrylcholinesterase & acetylcholinesterase. bambuterol : A carbamate ester that is terbutaline in which both of the phenolic hydroxy groups have been protected as the corresponding N,N-dimethylcarbamates. A long acting beta-adrenoceptor agonist used in the treatment of asthma, it is a prodrug for terbutaline.	2.04	1	0	carbamate ester; phenylethanolamines	anti-asthmatic drug; beta-adrenergic agonist; bronchodilator agent; EC 3.1.1.7 (acetylcholinesterase) inhibitor; prodrug; sympathomimetic agent; tocolytic agent
atomoxetine hydrochloride Atomoxetine Hydrochloride: A propylamine derivative and selective ADRENERGIC UPTAKE INHIBITOR that is used in the treatment of ATTENTION DEFICIT HYPERACTIVITY DISORDER.. atomoxetine hydrochloride : The hydrochloride salt of atomoxetine.	2.78	3	0	hydrochloride	adrenergic uptake inhibitor; antidepressant
atomoxetine atomoxetine : A secondary amino compound having methyl and 3-(2-methylphenoxy)-3-phenylpropan-1-yl substituents.	3.58	2	0	aromatic ether; secondary amino compound; toluenes	adrenergic uptake inhibitor; antidepressant; environmental contaminant; xenobiotic
quinapril Quinapril: A tetrahydroisoquinoline derivative and ANGIOTENSIN CONVERTING ENZYME inhibitor that is used in the treatment of HYPERTENSION and HEART FAILURE.. quinapril : A member of the class of isoquinolines that is (3S)-2-L-alanyl-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid in which the alpha-amino group of the alanyl residue has been substituted by a 1-ethoxycarbonyl-4-phenylbutan-2-yl group (the all-S isomer). A prodrug for quinaprilat (by hydrolysis of the ethyl ester to the corresponding carboxylic acid), it is used as an angiotensin-converting enzyme inhibitor (ACE inhibitor) used (generally as the hydrochloride salt) for the treatment of hypertension and congestive heart failure.	3.87	3	0	dicarboxylic acid monoester; ethyl ester; isoquinolines; tertiary carboxamide	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; prodrug
alpidem [no description available]	3.23	1	0	imidazoles
raloxifene hydrochloride Raloxifene Hydrochloride: A second generation selective estrogen receptor modulator (SERM) used to prevent osteoporosis in postmenopausal women. It has estrogen agonist effects on bone and cholesterol metabolism but behaves as a complete estrogen antagonist on mammary gland and uterine tissue.. raloxifene hydrochloride : A hydrochloride salt resulting from the reaction of equimolar amounts of raloxifene and hydrogen chloride.	2.47	2	0	hydrochloride	bone density conservation agent; estrogen antagonist; estrogen receptor modulator
gepirone gepirone: RN given refers to parent cpd; structure given in first source	2.05	1	0	N-arylpiperazine
mifepristone Mifepristone: A progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua. As a glucocorticoid receptor antagonist, the drug has been used to treat hypercortisolism in patients with nonpituitary CUSHING SYNDROME.	4.08	4	0	3-oxo-Delta(4) steroid; acetylenic compound; tertiary amino compound	abortifacient; contraceptive drug; hormone antagonist; synthetic oral contraceptive
itraconazole Itraconazole: A triazole antifungal agent that inhibits cytochrome P-450-dependent enzymes required for ERGOSTEROL synthesis.. itraconazole : An N-arylpiperazine that is cis-ketoconazole in which the imidazol-1-yl group is replaced by a 1,2,4-triazol-1-yl group and in which the actyl group attached to the piperazine moiety is replaced by a p-[(+-)1-sec-butyl-5-oxo-1,5-dihydro-4H-1,2,4-triazol-4-yl]phenyl group. A potent P-glycoprotein and CYP3A4 inhibitor, it is used as an antifungal drug for the treatment of various fungal infections, including aspergillosis, blastomycosis, candidiasis, chromoblastomycosis, coccidioidomycosis, cryptococcosis, histoplasmosis, and sporotrichosis.	3.19	5	0	aromatic ether; conazole antifungal drug; cyclic ketal; dichlorobenzene; dioxolane; N-arylpiperazine; triazole antifungal drug; triazoles	EC 3.6.3.44 (xenobiotic-transporting ATPase) inhibitor; Hedgehog signaling pathway inhibitor; P450 inhibitor
trospectomycin trospectomycin: active against Neisseria gonorrhoeae; RN refers to 2R-(2alpha,4abeta,5abeta,6beta,7beta,8beta,9beta,9alpha,9aalpha,10abeta)-(9CI)-isomer	2.04	1	0	dioxanes
fosphenytoin fosphenytoin: structure given in first & second source	3.23	1	0	imidazolidine-2,4-dione
pravadoline [no description available]	2.08	1	0
salmeterol xinafoate Salmeterol Xinafoate: A selective ADRENERGIC BETA-2 RECEPTOR agonist that functions as a BRONCHODILATOR when administered by inhalation. It is used to manage the symptoms of ASTHMA and CHRONIC OBSTRUCTIVE PULMONARY DISEASE.	5.04	2	1	naphthoic acid
ranolazine Ranolazine: An acetanilide and piperazine derivative that functions as a SODIUM CHANNEL BLOCKER and prevents the release of enzymes during MYOCARDIAL ISCHEMIA. It is used in the treatment of ANGINA PECTORIS.. N-(2,6-dimethylphenyl)-2-{4-[2-hydroxy-3-(2-methoxyphenoxy)propyl]piperazin-1-yl}acetamide : An aromatic amide obtained by formal condensation of the carboxy group of 2-{4-[2-hydroxy-3-(2-methoxyphenoxy)propyl]piperazin-1-yl}acetic acid with the amino group of 2,6-dimethylaniline.. ranolazine : A racemate comprising equal amounts of (R)- and (S)-ranolazine. Used for treatment of chronic angina.	3.73	2	0	aromatic amide; monocarboxylic acid amide; monomethoxybenzene; N-alkylpiperazine; secondary alcohol
brequinar brequinar : A quinolinemonocarboxylic acid that is quinoline substituted by 2'-fluoro[1,1'-biphenyl]-4-yl, methyl, carboxy and fluoro groups at positions 2, 3, 4, and 6, respectively. It is an inhibitor of dihydroorotate dehydrogenase, an enzyme that is required for de novo pyrimidine biosynthesis. The compound exhibits antineoplastic and antiviral properties.	2.6	1	0	biphenyls; monocarboxylic acid; monofluorobenzenes; quinolinemonocarboxylic acid	anticoronaviral agent; antimetabolite; antineoplastic agent; antiviral agent; EC 1.3.5.2 [dihydroorotate dehydrogenase (quinone)] inhibitor; immunosuppressive agent; pyrimidine synthesis inhibitor
finasteride Finasteride: An orally active 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE inhibitor. It is used as a surgical alternative for treatment of benign PROSTATIC HYPERPLASIA.. finasteride : An aza-steroid that is a synthetic drug for the treatment of benign prostatic hyperplasia.	3.87	3	0	3-oxo steroid; aza-steroid; delta-lactam	androgen antagonist; antihyperplasia drug; EC 1.3.1.22 [3-oxo-5alpha-steroid 4-dehydrogenase (NADP(+))] inhibitor
imiquimod Imiquimod: A topically-applied aminoquinoline immune modulator that induces interferon production. It is used in the treatment of external genital and perianal warts, superficial CARCINOMA, BASAL CELL; and ACTINIC KERATOSIS.. imiquimod : An imidazoquinoline fused [4,5-c] carrying isobutyl and amino substituents at N-1 and C-4 respectively. A prescription medication, it acts as an immune response modifier and is used to treat genital warts, superficial basal cell carcinoma, and actinic keratosis.	2.81	3	0	imidazoquinoline	antineoplastic agent; interferon inducer
sematilide sematilide: RN refers to HCl; structure given in first source	2.04	1	0
esmolol methyl 3-{4-[2-hydroxy-3-(propan-2-ylamino)propoxy]phenyl}propanoate : A methyl ester that is methyl 3-(4-hydroxyphenyl)propanoate in which the hydrogen attached to the phenolic hydroxy group is substituted by a 2-hydroxy-3-(isopropylamino)propyl group.. esmolol : A racemate comprising equimolar amounts of (R)- and (S)-esmolol. A cardioselective and short-acting beta1 receptor blocker with rapid onset but lacking intrinsic sympathomimetic and membrane-stabilising properties, it is used as the hydrochloride salt in the management of supraventricular arrhythmias, and for the control of hypertension and tachycardia during surgery. While the S enantiomer possesses all of the heart rate control, both enantiomers contribute to lowering blood pressure.	3.58	2	0	aromatic ether; ethanolamines; methyl ester; secondary alcohol; secondary amino compound
clinafloxacin clinafloxacin: structure given in first source; RN given is for monoHCl	2.04	1	0	quinolines
sertindole sertindole : A phenylindole that is 1H-indole which is substituted on the nitrogen by a p-chlorophenyl group, at position 5 by chlorine, and at position 3 by a piperidin-4-yl group, which is itself substituted on the nitrogen by a 2-(2-oxoimidazolidin-1-yl)ethyl group.	2.08	1	0	heteroarylpiperidine; imidazolidinone; organochlorine compound; organofluorine compound; phenylindole	alpha-adrenergic antagonist; H1-receptor antagonist; second generation antipsychotic; serotonergic antagonist
adapalene Adapalene: A naphthalene derivative that has specificity for RETINOIC ACID RECEPTORS. It is used as a DERMATOLOGIC AGENT for the treatment of ACNE.. adapalene : A naphthoic acid that is CD437 in which the phenolic hydroxy group has been converted to its methyl ether.	2.08	1	0	adamantanes; monocarboxylic acid; naphthoic acid	dermatologic drug; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor; non-steroidal anti-inflammatory drug
adefovir adefovir: inhibitor of African swine fever virus. adefovir(1-) : A organophosphonate oxoanion obtained by removal of a proton from the phosphonate group of adefovir, a nucleoside reverse transcriptase inhibitor. It is the major microspecies at pH 7.3 (according to Marvin v 6.2.0.).. adefovir : A member of the class of phosphonic acids that is methylphosphonic acid in which one of the methyl hydrogens has been replaced by a 2-(6-amino-9H-purin-9-yl)ethoxy group. An inhibitor of HIV-1 reverse transcriptase, the bis(t-butoxycarbonyloxymethyl) ester (dipivoxil ester) prodrug is used to treat chronic hepatitis B viral infection.	3.91	3	0	6-aminopurines; ether; phosphonic acids	antiviral drug; DNA synthesis inhibitor; drug metabolite; HIV-1 reverse transcriptase inhibitor; nephrotoxic agent
loxiglumide loxiglumide: cholecystokinin receptor antagonist; RN refers to (+-)-isomer; structure in first source	2.04	1	0	organic molecular entity
aromasil [no description available]	4.37	3	0	17-oxo steroid; 3-oxo-Delta(1),Delta(4)-steroid	antineoplastic agent; EC 1.14.14.14 (aromatase) inhibitor; environmental contaminant; xenobiotic
sparfloxacin [no description available]	2.75	3	0	fluoroquinolone antibiotic; N-arylpiperazine; quinolinemonocarboxylic acid; quinolone antibiotic; quinolone
zileuton [no description available]	4.1	4	0	1-benzothiophenes; ureas	anti-asthmatic drug; EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor; ferroptosis inhibitor; leukotriene antagonist; non-steroidal anti-inflammatory drug
niguldipine [no description available]	2.08	1	0	diarylmethane
clopidogrel Clopidogrel: A ticlopidine analog and platelet purinergic P2Y receptor antagonist that inhibits adenosine diphosphate-mediated PLATELET AGGREGATION. It is used to prevent THROMBOEMBOLISM in patients with ARTERIAL OCCLUSIVE DISEASES; MYOCARDIAL INFARCTION; STROKE; or ATRIAL FIBRILLATION.. clopidogrel : A thienopyridine that is 4,5,6,7-tetrahydrothieno[3,2-c]pyridine in which the hydrogen attached to the nitrogen is replaced by an o-chlorobenzyl group, the methylene hydrogen of which is replaced by a methoxycarbonyl group (the S enantiomer). A P2Y12 receptor antagonist, it is used to inhibit blood clots and prevent heart attacks.	3.59	2	0	methyl ester; monochlorobenzenes; thienopyridine	anticoagulant; P2Y12 receptor antagonist; platelet aggregation inhibitor
cidofovir anhydrous Cidofovir: An acyclic nucleoside phosphonate that acts as a competitive inhibitor of viral DNA polymerases. It is used in the treatment of RETINITIS caused by CYTOMEGALOVIRUS INFECTIONS and may also be useful for treating HERPESVIRUS INFECTIONS.. cidofovir anhydrous : Cytosine substituted at the 1 position by a 3-hydroxy-2-(phosphonomethoxy)propyl group (S configuration). A nucleoside analogue, it is an injectable antiviral used for the treatment of cytomegalovirus (CMV) retinitis in AIDS patients.	4.29	5	0	phosphonic acids; pyrimidone	anti-HIV agent; antineoplastic agent; antiviral drug; photosensitizing agent
tiagabine Tiagabine: A nipecotic acid derivative that acts as a GABA uptake inhibitor and anticonvulsant agent. It is used in the treatment of EPILEPSY, for refractory PARTIAL SEIZURES.. tiagabine : A piperidinemonocarboxylic acid that is (R)-nipecotic acid in which the hydrogen attached to the nitrogen has been replaced by a 1,1-bis(3-methyl-2-thienyl)but-1-en-4-yl group. A GABA reuptake inhibitor, it is used (generally as the hydrochloride salt) for the treatment of epilepsy.	3.58	2	0	beta-amino acid; piperidinemonocarboxylic acid; tertiary amino compound; thiophenes	anticonvulsant; GABA reuptake inhibitor
mibefradil Mibefradil: A benzimidazoyl-substituted tetraline that selectively binds and inhibits CALCIUM CHANNELS, T-TYPE.	2.04	1	0	tetralins	T-type calcium channel blocker
topotecan Topotecan: An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA TOPOISOMERASES, TYPE I.. topotecan : A pyranoindolizinoquinoline used as an antineoplastic agent. It is a derivative of camptothecin and works by binding to the topoisomerase I-DNA complex and preventing religation of these 328 single strand breaks.	9.47	14	4	pyranoindolizinoquinoline	antineoplastic agent; EC 5.99.1.2 (DNA topoisomerase) inhibitor
eliprodil 1-(4-chlorophenyl)-2-[4-(4-fluorobenzyl)piperidin-1-yl]ethanol : A member of the class of piperidines that is piperidine substituted by a 2-(4-chlorophenyl)-2-hydroxyethyl group at position 1 and by a 4-fluorobenzyl group at position 4.	2.08	1	0	monochlorobenzenes; monofluorobenzenes; piperidines; secondary alcohol; tertiary amino compound
bromfenac bromfenac: bromfenac sodium is the active cpd; structure in first source. bromfenac : Amfenac in which the the hydrogen at the 4 position of the benzoyl group is substituted by bromine. It is used for the management of ocular pain and treatment of postoperative inflammation in patients who have undergone cataract extraction. It was withdrawn from the US market in 1998, following concerns over off-label abuse and hepatic failure.	4.08	4	0	aromatic amino acid; benzophenones; organobromine compound; substituted aniline	non-narcotic analgesic; non-steroidal anti-inflammatory drug
celgosivir celgosivir: inhibits glycoprotein processing & the growth of HIVs	2.6	1	0
gemcitabine hydrochloride [no description available]	2.08	1	0	hydrochloride; organofluorine compound	anticoronaviral agent; antimetabolite; antineoplastic agent; antiviral drug; EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor; immunosuppressive agent; radiosensitizing agent
gemcitabine gemcitabine : A 2'-deoxycytidine having geminal fluoro substituents in the 2'-position. An inhibitor of ribonucleotide reductase, gemcitabine is used in the treatment of various carcinomas, particularly non-small cell lung cancer, pancreatic cancer, bladder cancer and breast cancer.	13.26	59	16	organofluorine compound; pyrimidine 2'-deoxyribonucleoside	antimetabolite; antineoplastic agent; antiviral drug; DNA synthesis inhibitor; EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor; environmental contaminant; immunosuppressive agent; photosensitizing agent; prodrug; radiosensitizing agent; xenobiotic
ibutilide ibutilide: RN & structure in first source; RN refers to the fumarate salt	3.58	2	0	benzenes; organic amino compound
aripiprazole Aripiprazole: A piperazine and quinolone derivative that is used primarily as an antipsychotic agent. It is a partial agonist of SEROTONIN RECEPTOR, 5-HT1A and DOPAMINE D2 RECEPTORS, where it also functions as a post-synaptic antagonist, and an antagonist of SEROTONIN RECEPTOR, 5-HT2A. It is used for the treatment of SCHIZOPHRENIA and BIPOLAR DISORDER, and as an adjunct therapy for the treatment of depression.. aripiprazole : An N-arylpiperazine that is piperazine substituted by a 4-[(2-oxo-1,2,3,4-tetrahydroquinolin-7-yl)oxy]butyl group at position 1 and by a 2,3-dichlorophenyl group at position 4. It is an antipsychotic drug used for the treatment of Schizophrenia, and other mood disorders.	3.87	3	0	aromatic ether; delta-lactam; dichlorobenzene; N-alkylpiperazine; N-arylpiperazine; quinolone	drug metabolite; H1-receptor antagonist; second generation antipsychotic; serotonergic agonist
remifentanil Remifentanil: A piperidine-propionate derivative and opioid analgesic structurally related to FENTANYL. It functions as a short-acting MU OPIOID RECEPTOR agonist, and is used as an analgesic during induction or maintenance of general anesthesia, following surgery, during childbirth, and in mechanically ventilated patients under intensive care.. remifentanil : A piperidinecarboxylate ester that is methyl piperidine-4-carboxylate in which the hydrogen attached to the nitrogen is substituted by a 3-methoxy-3-oxopropyl group and the hydrogen at position 4 is substituted the nitrogen of N-propanoylaniline.	3.58	2	0	alpha-amino acid ester; anilide; monocarboxylic acid amide; piperidinecarboxylate ester	intravenous anaesthetic; mu-opioid receptor agonist; opioid analgesic; sedative
atorvastatin calcium anhydrous [no description available]	2.08	1	0	organic calcium salt
atorvastatin [no description available]	3.9	3	0	aromatic amide; dihydroxy monocarboxylic acid; monofluorobenzenes; pyrroles; statin (synthetic)	environmental contaminant; xenobiotic
lamivudine [no description available]	4.44	6	0	monothioacetal; nucleoside analogue; oxacycle; primary alcohol	allergen; anti-HBV agent; antiviral drug; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor; HIV-1 reverse transcriptase inhibitor; prodrug
duloxetine hydrochloride Duloxetine Hydrochloride: A thiophene derivative and selective NEUROTRANSMITTER UPTAKE INHIBITOR for SEROTONIN and NORADRENALINE (SNRI). It is an ANTIDEPRESSIVE AGENT and ANXIOLYTIC, and is also used for the treatment of pain in patients with DIABETES MELLITUS and FIBROMYALGIA.. (S)-duloxetine hydrochloride : A duloxetine hydrochloride in which the duloxetine moiety has S configuration.	4.34	5	0	duloxetine hydrochloride	antidepressant
duloxetine [no description available]	3.59	2	0	duloxetine
irinotecan [no description available]	11.19	18	4	carbamate ester; delta-lactone; N-acylpiperidine; pyranoindolizinoquinoline; ring assembly; tertiary alcohol; tertiary amino compound	antineoplastic agent; apoptosis inducer; EC 5.99.1.2 (DNA topoisomerase) inhibitor; prodrug
valsartan Valsartan: A tetrazole derivative and ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to treat HYPERTENSION.. valsartan : A monocarboxylic acid amide consisting of L-valine in which the amino hydrogens have been replaced by a pentanoyl and a [2'-(1H-tetrazol-5-yl)biphenyl]-4-yl]methyl group. It exhibits antihypertensive activity.	4.29	5	0	biphenylyltetrazole; monocarboxylic acid amide; monocarboxylic acid	angiotensin receptor antagonist; antihypertensive agent; environmental contaminant; xenobiotic
ibandronic acid Ibandronic Acid: Aminobisphosphonate that is a potent inhibitor of BONE RESORPTION. It is used in the treatment of HYPERCALCEMIA associated with malignancy, for the prevention of fracture and bone complications in patients with breast cancer and bone metastases, and for the treatment and prevention of POSTMENOPAUSAL OSTEOPOROSIS.	3.58	2	0
ziprasidone ziprasidone: a benzisothiazoylpiperazine derivative; has combined dopamine and serotonin receptor antagonist activity; structurally related to tiospirone. ziprasidone : A piperazine compound having 1,2-benzothiazol-3-yl- and 2-(6-chloro-1,3-dihydro-2-oxindol-5-yl)ethyl substituents attached to the nitrogen atoms.	3.58	2	0	1,2-benzisothiazole; indolones; organochlorine compound; piperazines	antipsychotic agent; dopaminergic antagonist; histamine antagonist; muscarinic antagonist; psychotropic drug; serotonergic antagonist
zanamivir Zanamivir: A guanido-neuraminic acid that is used to inhibit NEURAMINIDASE.	2.52	2	0	guanidines	antiviral agent; EC 3.2.1.18 (exo-alpha-sialidase) inhibitor
zolmitriptan zolmitriptan: an antimigraine compound; a serotonin (5HT)-1D receptor agonist. zolmitriptan : A member of the class of tryptamines that is N,N-dimethyltryptamine in which the hydrogen at position 5 of the indole ring has been replaced by a [(4S)-2-oxo-1,3-oxazolidin-4-yl]methyl group. A serotonin 5-HT1 B and D receptor agonist, it is used for the treatment of migraine.	3.87	3	0	oxazolidinone; tryptamines	anti-inflammatory drug; serotonergic agonist; vasoconstrictor agent
adefovir dipivoxil bis(pivaloyloxymethyl)-9-(2-phosphonylmethoxyethyl)adenine: structure given in first source. adefovir pivoxil : An organic phosphonate that is the dipivoxil ester of adefovir. A prodrug for adefovir, an HIV-1 reverse transcriptase inhibitor, adefovir pivoxil is used to treat chronic hepatitis B viral infection.	2.81	3	0	6-aminopurines; carbonate ester; ether; organic phosphonate	antiviral drug; DNA synthesis inhibitor; HIV-1 reverse transcriptase inhibitor; nephrotoxic agent; prodrug
emtricitabine Emtricitabine: A deoxycytidine analog and REVERSE TRANSCRIPTASE INHIBITOR with antiviral activity against HIV-1 and HEPATITIS B viruses. It is used to treat HIV INFECTIONS.. emtricitabine : An organofluorine compound that is 5-fluorocytosine substituted at the 1 position by a 2-(hydroxymethyl)-1,3-oxathiolan-5-yl group (2R,5S configuration). It is used in combination therapy for the treatment of HIV-1 infection.	3.95	3	0	monothioacetal; nucleoside analogue; organofluorine compound; pyrimidone	antiviral drug; HIV-1 reverse transcriptase inhibitor
tasosartan tasosartan: angiotensin II antagonist; structure given in first source	3.23	1	0	biphenyls
tiludronic acid tiludronic acid: a bone resorption inhibitor; an antihypercalcemic agent; used in the tratment of Paget's disease; used in the treatment and prevention of osteoporosis; structure given in first source	3.23	1	0	organochlorine compound
tirofiban Tirofiban: Tyrosine analog and PLATELET GLYCOPROTEIN GPIIB-IIIA COMPLEX antagonist that inhibits PLATELET AGGREGATION and is used in the treatment of ACUTE CORONARY SYNDROME.. tirofiban : A member of the class of piperidines that is L-tyrosine in which a hydrogen attached to the amino group is replaced by a butylsulfonyl group and in which the hydrogen attached to the phenolic hydroxy group is replaced by a 4-(piperidin-4-yl)butyl group.	3.58	2	0	L-tyrosine derivative; piperidines; sulfonamide	anticoagulant; fibrin modulating drug; platelet glycoprotein-IIb/IIIa receptor antagonist
capecitabine Capecitabine: A deoxycytidine derivative and fluorouracil PRODRUG that is used as an ANTINEOPLASTIC ANTIMETABOLITE in the treatment of COLON CANCER; BREAST CANCER and GASTRIC CANCER.. capecitabine : A carbamate ester that is cytidine in which the hydrogen at position 5 is replaced by fluorine and in which the amino group attached to position 4 is converted into its N-(penyloxy)carbonyl derivative. Capecitabine is a antineoplastic agent used in the treatment of cancers.	7.32	7	2	carbamate ester; cytidines; organofluorine compound	antimetabolite; antineoplastic agent; prodrug
adenosine quinquefolan B: isolated from roots of Panax quinquefolium L.; RN not in Chemline 10/87; RN from Toxlit	6.03	4	1	adenosines; purines D-ribonucleoside	analgesic; anti-arrhythmia drug; fundamental metabolite; human metabolite; vasodilator agent
octyl gallate [no description available]	2.6	1	0	gallate ester	food antioxidant; hypoglycemic agent; plant metabolite
vanadates Vanadates: Oxyvanadium ions in various states of oxidation. They act primarily as ion transport inhibitors due to their inhibition of Na(+)-, K(+)-, and Ca(+)-ATPase transport systems. They also have insulin-like action, positive inotropic action on cardiac ventricular muscle, and other metabolic effects.. vanadate(3-) : A vanadium oxoanion that is a trianion with formula VO4 in which the vanadium is in the +5 oxidation state and is attached to four oxygen atoms.	2.05	1	0	trivalent inorganic anion; vanadium oxoanion	EC 3.1.3.1 (alkaline phosphatase) inhibitor; EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor; EC 3.1.3.41 (4-nitrophenylphosphatase) inhibitor; EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor
acridine orange Acridine Orange: A cationic cytochemical stain specific for cell nuclei, especially DNA. It is used as a supravital stain and in fluorescence cytochemistry. It may cause mutations in microorganisms.. acridine orange : Fluorescent dye useful for cell cycle determination. It is cell-permeable, and interacts with DNA and RNA by intercalation or electrostatic attractions respectively.. acridine orange free base : A member of the class of aminoacridines that is acridine carrying two dimethylamino substituents at positions 3 and 6. The hydrochloride salt is the fluorescent dye 'acridine orange', used for cell cycle determination.	2.08	1	0	aminoacridines; aromatic amine; tertiary amino compound	fluorochrome; histological dye
paroxetine hydrochloride paroxetine hydrochloride : The hydrochloride salt of paroxetine. It is an antidepressant drug.	2.08	1	0	hydrochloride	antidepressant; anxiolytic drug; hepatotoxic agent; P450 inhibitor; serotonin uptake inhibitor
bupropion hydrochloride [no description available]	2.08	1	0	aromatic ketone
cisatracurium cisatracurium: RN refers to (1R-(1alpha,2alpha(1'R,2'R)))-isomer. cisatracurium : A diester that is the (1R,1'R,2R,2'R)-diastereoisomer of atracurium, a quaternary ammonium ion consisting of pentane-1,5-diol with both hydroxy functions bearing 3-[1-(3,4-dimethoxybenzyl)-6,7-dimethoxy-2-methyl-3,4-dihydroisoquinolinium-2(1H)-yl]propanoyl groups. The active species in the skeletal muscle relaxant cisatracurium besylate.	2.04	1	0	diester; quaternary ammonium ion	muscle relaxant; nicotinic antagonist
halofuginone [no description available]	2.05	1	0	quinazolines
venlafaxine hydrochloride Venlafaxine Hydrochloride: A cyclohexanol and phenylethylamine derivative that functions as a SEROTONIN AND NORADRENALINE REUPTAKE INHIBITOR (SNRI) and is used as an ANTIDEPRESSIVE AGENT.	3.21	1	0	hydrochloride
trazodone hydrochloride Triticum: A plant genus of the family POACEAE that is the source of EDIBLE GRAIN. A hybrid with rye (SECALE CEREALE) is called TRITICALE. The seed is ground into FLOUR and used to make BREAD, and is the source of WHEAT GERM AGGLUTININS.. trazodone hydrochloride : A hydrochloride salt prepared from equimolar amounts of trazodone and hydrogen chloride.	2.08	1	0	hydrochloride	adrenergic antagonist; antidepressant; H1-receptor antagonist; sedative; serotonin uptake inhibitor
fosinoprilat fosinoprilat: active phosphinic acid metabolite of prodrug fosenopril, which is activated by esterases in vivo; structure given in first source; binds zinc with phosphinic acid group. fosinoprilat : A phosphinic acid-containing N-acyl derivative of (4S)-cyclohexyl-L-proline. An inhibitor of angiotensin converting enzyme (ACE), it is used as the phosphinate ester pro-drug fosinopril for treatment of hypertension and chronic heart failure.	2.04	1	0	L-proline derivative; phosphinic acids	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
ortho-cept ethinyl estradiol-desogestrel combination: Ethinyl Estradiol and Desogestrell given in fixed proportions; has proved to be an effective & well-tolerated oral contraceptive, which improves cycle control & has a beneficial effect on acne	2.05	1	0
trovafloxacin trovafloxacin: a trifluoronaphthyridone derivative of 7-(3-azabicyclo(3.1.0)hexyl)naphthyridone; has antineoplastic activity. trovafloxacin : A 1,8-naphthyridine derivative that is 4-oxo-1,4-dihydro-1,8-naphthyridine-3-carboxylic acid bearing additional 2,4-difluorophenyl, fluoro and 6-amino-3-azabicyclo[3.1.0]hex-3-yl substituents at positions 1, 6 and 7 respectively. A broad-spectrum antibiotic that was withdrawn from the market due to risk of liver failure.	3.58	2	0
verapamil hydrochloride verapamil hydrochloride : A racemate comprising equimolar amounts of dexverapamil hydrochloride and (S)-verapamil hydrochloride.	2.08	1	0
cefprozil [no description available]	3.86	3	0	cephalosporin; semisynthetic derivative	antibacterial drug
doxazosin mesylate Cardura: Trade name in United States.	2.08	1	0	methanesulfonate salt	geroprotector
4-[1-[4-[2-(dimethylamino)ethoxy]phenyl]-2-phenylbut-1-enyl]phenol [no description available]	2.05	1	0	stilbenoid
efavirenz efavirenz: HIV-1 reverse transcriptase inhibitor. efavirenz : 1,4-Dihydro-2H-3,1-benzoxazin-2-one substituted at the 4 position by cyclopropylethynyl and trifluoromethyl groups (S configuration) and at the 6 position by chlorine. A non-nucleoside reverse transcriptase inhibitor with activity against HIV, it is used with other antiretrovirals for combination therapy of HIV infection.	4.31	5	0	acetylenic compound; benzoxazine; cyclopropanes; organochlorine compound; organofluorine compound	antiviral drug; HIV-1 reverse transcriptase inhibitor
nelfinavir Nelfinavir: A potent HIV protease inhibitor. It is used in combination with other antiviral drugs in the treatment of HIV in both adults and children.. nelfinavir : An aryl sulfide that is used (as its mesylate salt) for treatment of HIV and also exhibits some anticancer properties.	8.56	14	2	aryl sulfide; benzamides; organic heterobicyclic compound; phenols; secondary alcohol; tertiary amino compound	antineoplastic agent; HIV protease inhibitor
doxapram hydrochloride [no description available]	2.05	1	0	hydrochloride	central nervous system stimulant
glucose, (beta-d)-isomer beta-D-glucose : D-Glucopyranose with beta configuration at the anomeric centre.. (1->4)-beta-D-glucan : A beta-D-glucan in which the glucose units are connected by (1->4) linkages.. (1->3)-beta-D-glucan : A beta-D-glucan in which the glucose units are connected by (1->3) linkages.	5.59	4	1	D-glucopyranose	epitope; mouse metabolite
mevastatin mevastatin: antifungal metabolite from Penicillium brevicopactum; potent inhibitory activity to sterol synthesis; structure. mevastatin : A carboxylic ester that is pravastatin that is lacking the allylic hydroxy group. A hydroxymethylglutaryl-CoA reductase inhibitor (statin) isolated from Penicillium citrinum and from Penicillium brevicompactum, its clinical use as a lipid-regulating drug ceased following reports of toxicity in animals.	2.08	1	0	2-pyranones; carboxylic ester; hexahydronaphthalenes; polyketide; statin (naturally occurring)	antifungal agent; apoptosis inducer; EC 3.4.24.83 (anthrax lethal factor endopeptidase) inhibitor; fungal metabolite; Penicillium metabolite
bupivacaine hydrochloride bupivacaine hydrochloride (anhydrous) : A racemate composed of equimolar amounts of dextrobupivacaine hydrochloride and levobupivacaine hydrochloride. The monohydrate form is commonly used as a local anaesthetic.. 1-butyl-N-(2,6-dimethylphenyl)piperidine-2-carboxamide hydrochloride : A hydrochloride obtained by combining 1-butyl-N-(2,6-dimethylphenyl)piperidine-2-carboxamide with one molar equivalent of hydrochloric acid.	2.08	1	0	hydrochloride; racemate	adrenergic antagonist; amphiphile; EC 3.1.1.8 (cholinesterase) inhibitor; EC 3.6.3.8 (Ca(2+)-transporting ATPase) inhibitor; local anaesthetic
fenofibric acid fenofibric acid: RN given refers to parent cpd without isomeric designation; structure. fenofibric acid : A monocarboxylic acid that is 2-methylpropanoic acid substituted by a 4-(4-chlorobenzoyl)phenoxy group at position 2. It is a metabolite of the drug fenofibrate.	3.23	1	0	aromatic ketone; chlorobenzophenone; monocarboxylic acid	drug metabolite; marine xenobiotic metabolite
1,5-anhydroglucitol 1,5-anhydroglucitol: structure. 1,5-anhydro-D-glucitol : An anhydro sugar of D-glucitol.	2.05	1	0	anhydro sugar	human metabolite
thiazolyl blue thiazolyl blue: RN & II refers to bromide. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide : The bromide salt of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium.	3.66	9	0	organic bromide salt	colorimetric reagent; dye
betulinic acid [no description available]	2.79	3	0	hydroxy monocarboxylic acid; pentacyclic triterpenoid	anti-HIV agent; anti-inflammatory agent; antimalarial; antineoplastic agent; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; plant metabolite
arctigenin arctigenin: precursor to catechols; in many plants	2.6	1	0	lignan
baicalin [no description available]	2.6	1	0	dihydroxyflavone; glucosiduronic acid; glycosyloxyflavone; monosaccharide derivative	antiatherosclerotic agent; antibacterial agent; anticoronaviral agent; antineoplastic agent; antioxidant; cardioprotective agent; EC 2.7.7.48 (RNA-directed RNA polymerase) inhibitor; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; ferroptosis inhibitor; neuroprotective agent; non-steroidal anti-inflammatory drug; plant metabolite; prodrug
prostratin prostratin: RN given refers to the (1aR-(1aalpha,1bbeta,4abeta,7aalpha,7balpha,8alpha,9aalpha))-isomer	7.02	1	0
plerixafor plerixafor: a bicyclam derivate, highly potent & selective inhibitor of HIV-1 & HIV-2. plerixafor : An azamacrocycle consisting of two cyclam rings connected by a 1,4-phenylenebis(methylene) linker. It is a CXCR4 chemokine receptor antagonist and a hematopoietic stem cell mobilizer. It is used in combination with grulocyte-colony stimulating factor (G-CSF) to mobilize hematopoietic stem cells to the perpheral blood for collection and subsequent autologous transplantation in patients with non-Hodgkin's lymphoma and multiple myeloma.	13.46	12	2	azacycloalkane; azamacrocycle; benzenes; crown amine; secondary amino compound; tertiary amino compound	anti-HIV agent; antineoplastic agent; C-X-C chemokine receptor type 4 antagonist; immunological adjuvant
amprenavir [no description available]	4.13	4	0	carbamate ester; sulfonamide; tetrahydrofuryl ester	antiviral drug; HIV protease inhibitor
oseltamivir Oseltamivir: An acetamido cyclohexene that is a structural homolog of SIALIC ACID and inhibits NEURAMINIDASE.. oseltamivir : A cyclohexenecarboxylate ester that is the ethyl ester of oseltamivir acid. An antiviral prodrug (it is hydrolysed to the active free carboxylic acid in the liver), it is used to slow the spread of influenza.	3.73	2	0	acetamides; amino acid ester; cyclohexenecarboxylate ester; primary amino compound	antiviral drug; EC 3.2.1.18 (exo-alpha-sialidase) inhibitor; environmental contaminant; prodrug; xenobiotic
epigallocatechin gallate epigallocatechin gallate: a steroid 5alpha-reductase inhibitor and antimutagen in green tea (Camellia sinensis). (-)-epigallocatechin 3-gallate : A gallate ester obtained by the formal condensation of gallic acid with the (3R)-hydroxy group of (-)-epigallocatechin.	9.69	8	0	flavans; gallate ester; polyphenol	antineoplastic agent; antioxidant; apoptosis inducer; geroprotector; Hsp90 inhibitor; neuroprotective agent; plant metabolite
deoxyuridine triphosphate [no description available]	2.41	1	0	deoxyuridine phosphate; pyrimidine 2'-deoxyribonucleoside 5'-triphosphate	Arabidopsis thaliana metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite
rhodamine 123 [no description available]	2.17	1	0	organic chloride salt; xanthene dye	fluorochrome
1,2,3,4,6-pentakis-O-galloyl-beta-D-glucose pentagalloylglucose: pentahydroxy gallic acid ester of glucose; a phytogenic antineoplastic agent and antibacterial agent. 1,2,3,4,6-pentakis-O-galloyl-beta-D-glucose : A galloyl-beta-D-glucose compound having five galloyl groups in the 1-, 2-, 3-, 4- and 6-positions.	2.6	1	0	gallate ester; galloyl beta-D-glucose	anti-inflammatory agent; antineoplastic agent; geroprotector; hepatoprotective agent; plant metabolite; radiation protective agent; radical scavenger
cephalotaxine [no description available]	2.6	1	0	benzazepine alkaloid fundamental parent; benzazepine alkaloid; cyclic acetal; enol ether; organic heteropentacyclic compound; secondary alcohol; tertiary amino compound
desipramine hydrochloride desipramine hydrochloride : The hydrochloride salt of desipramine.	2.6	1	0	hydrochloride	drug allergen
mefloquine hydrochloride [no description available]	2.6	1	0	hydrochloride
ticlopidine hydrochloride [no description available]	2.08	1	0	hydrochloride
epirubicin hydrochloride [no description available]	2.08	1	0
pyrrolidine dithiocarbamate pyrrolidine dithiocarbamic acid: spelled pyrolidine in J Nutr 1979 reference; RN given refers to parent cpd. pyrrolidine dithiocarbamate : A member of the class of dithiocarbamic acids that is the N-dithiocarboxy derivative of pyrrolidine.	3.15	5	0	dithiocarbamic acids; pyrrolidines	anticonvulsant; antineoplastic agent; geroprotector; neuroprotective agent; NF-kappaB inhibitor; radical scavenger
glutathione disulfide Glutathione Disulfide: A GLUTATHIONE dimer formed by a disulfide bond between the cysteine sulfhydryl side chains during the course of being oxidized.	2.05	1	0	glutathione derivative; organic disulfide	Escherichia coli metabolite; mouse metabolite
iopamidol Iopamidol: A non-ionic, water-soluble contrast agent which is used in myelography, arthrography, nephroangiography, arteriography, and other radiological procedures.. iopamidol : A benzenedicarboxamide compound having N-substituted carbamoyl groups at the 1- and 3-positions, iodo substituents at the 2-, 4- and 6-positions and a (2S)-2-hydroxypropanamido group at the 5-position.	2.04	1	0	benzenedicarboxamide; organoiodine compound; pentol	environmental contaminant; radioopaque medium; xenobiotic
histamine phosphate histamine phosphate : A phosphate salt that is the diphosphate salt of histamine.	3.23	1	0	phosphate salt	histamine agonist
tetraiodothyroacetic acid tetraiodothyroacetic acid: RN given refers to parent cpd; structure. 3,3',5,5'-tetraiodothyroacetic acid : A monocarboxylic acid that is thyroacetic acid carrying four iodo substituents at positions 3, 3', 5 and 5'.	2.1	1	0	2-halophenol; aromatic ether; iodophenol; monocarboxylic acid	apoptosis inducer; human metabolite; thyroid hormone
imipramine n-oxide imipramine N-oxide: RN given refers to parent cpd; structure	2.04	1	0	dibenzooxazepine
tilbroquinol [no description available]	3.23	1	0	organohalogen compound; quinolines
bendamustine [no description available]	3.87	3	0	benzimidazoles
erdosteine [no description available]	2.05	1	0	N-acyl-amino acid
aloxistatin aloxistatin: a membrane-permeable cysteine protease inhibitor. aloxistatin : An L-leucine derivative that is the amide obtained by formal condensation of the carboxy group of (2S,3S)-3-(ethoxycarbonyl)oxirane-2-carboxylic acid with the amino group of N-(3-methylbutyl)-L-leucinamide.	2.6	1	0	epoxide; ethyl ester; L-leucine derivative; monocarboxylic acid amide	anticoronaviral agent; cathepsin B inhibitor
droxicam droxicam: structure given in first source. droxicam : An organic heterotricyclic compound that is 2H,5H-[1,3]oxazino[5,6-c][1,2]benzothiazine-2,4(3H)-dione 6,6-dioxide substituted at positions 3 and 5 by pyridin-2-yl and methyl groups respectively. A prodrug of piroxicam, it is used for the relief of pain and inflammation in musculoskeletal disorders such as rheumatoid arthritis and osteoarthritis.	3.23	1	0	organic heterotricyclic compound; pyridines	cyclooxygenase 1 inhibitor; hepatotoxic agent; non-narcotic analgesic; non-steroidal anti-inflammatory drug; platelet aggregation inhibitor; prodrug
propazole propazole: RN given refers to parent cpd; structure	2.6	1	0	benzimidazoles
caroverine caroverine: structure	2.08	1	0	quinoxaline derivative
lercanidipine [no description available]	7.21	1	0	diarylmethane
ebrotidine ebrotidine: an H2-receptor antagonist and gastric mucosa protector	3.23	1	0	sulfonamide
mizolastine [no description available]	2.05	1	0	benzimidazoles
cgs 9343b [no description available]	2.08	1	0	benzimidazoles
dexloxiglumide dexloxiglumide: a CCK receptor antagonist; structure given in first source	2.04	1	0	glutamic acid derivative
prulifloxacin prulifloxacin: structure given in first source	2.6	1	0	fluoroquinolone antibiotic; quinolone antibiotic
intoplicine intoplicine: structure in first source	2.45	2	0	pyridoindole
pazufloxacin [no description available]	2.08	1	0	quinolines
repaglinide [no description available]	3.87	3	0	piperidines
telmisartan Telmisartan: A biphenyl compound and benzimidazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION.. telmisartan : A member of the class of benzimidazoles used widely in the treatment of hypertension.	4.44	6	0	benzimidazoles; biphenyls; carboxybiphenyl	angiotensin receptor antagonist; antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; environmental contaminant; xenobiotic
bergenin bergenin: RN refers to (2R-(2alpha,3beta,4alpha,4aalpha,10bbeta))-isomer; structure	2.6	1	0	trihydroxybenzoic acid	metabolite
dexfenfluramine Dexfenfluramine: The S-isomer of FENFLURAMINE. It is a serotonin agonist and is used as an anorectic. Unlike fenfluramine, it does not possess any catecholamine agonist activity.. (S)-fenfluramine : The S-enantiomer of fenfluramine. It stimulates the release of serotonin and selectively inhibits its reuptake, but unlike fenfluramine it does not possess catecholamine agonist activity. It was formerly given by mouth as the hydrochloride in the treatment of obesity, but, like fenfluramine, was withdrawn wolrdwide following reports of valvular heart defects.	2.45	2	0	fenfluramine	appetite depressant; serotonergic agonist; serotonin uptake inhibitor
2-methoxyestradiol 2-methoxy-17beta-estradiol : A 17beta-hydroxy steroid, being 17beta-estradiol methoxylated at C-2.	3.56	8	0	17beta-hydroxy steroid; 3-hydroxy steroid	angiogenesis modulating agent; antimitotic; antineoplastic agent; human metabolite; metabolite; mouse metabolite
benzeneboronic acid [no description available]	2.54	2	0	boronic acids
ethinyl estradiol-17-sulfate ethinyl estradiol-17-sulfate: RN given refers to the (17alpha)-isomer	2.04	1	0
1,7-phenanthroline [no description available]	2.15	1	0	phenanthroline
triazoles Triazoles: Heterocyclic compounds containing a five-membered ring with two carbon atoms and three nitrogen atoms with the molecular formula C2H3N3.. triazoles : An azole in which the five-membered heterocyclic aromatic skeleton contains three N atoms and two C atoms.	10.77	25	3	1,2,3-triazole
pinocembrin pinocembrin : A dihydroxyflavanone in which the two hydroxy groups are located at positions 5 and 7. A natural product found in Piper sarmentosum and Cryptocarya chartacea.	2.06	1	0	(2S)-flavan-4-one; dihydroxyflavanone	antineoplastic agent; antioxidant; metabolite; neuroprotective agent; vasodilator agent
2,6-dimethoxy-1,4-benzoquinone 2,6-dimethoxy-1,4-benzoquinone: structure given in first source	2.41	1	0
miconazole nitrate miconazole nitrate : A racemate composed of equimolar amounts of (R)- and (S)-miconazole nitrate. An antifungal used for the treatment of athlete's foot, jock itch, ringworm and other fungal skin infections. It inhibits the synthesis of ergosterol, a critical component of fungal cell membranes.	2.08	1	0
ethinylestradiol-3-sulfate ethinylestradiol-3-sulfate: binds to albumin at 2 sites	2.04	1	0	17beta-hydroxy steroid; steroid sulfate	antineoplastic agent; estrogen
medetomidine Medetomidine: An agonist of RECEPTORS, ADRENERGIC ALPHA-2 that is used in veterinary medicine for its analgesic and sedative properties. It is the racemate of DEXMEDETOMIDINE.	2.05	1	0	imidazoles
fluorodeoxyglucose f18 Fluorodeoxyglucose F18: The compound is given by intravenous injection to do POSITRON-EMISSION TOMOGRAPHY for the assessment of cerebral and myocardial glucose metabolism in various physiological or pathological states including stroke and myocardial ischemia. It is also employed for the detection of malignant tumors including those of the brain, liver, and thyroid gland. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1162)	9.05	11	3	2-deoxy-2-((18)F)fluoro-D-glucose; 2-deoxy-2-fluoro-aldehydo-D-glucose
sertraline Sertraline: A selective serotonin uptake inhibitor that is used in the treatment of depression.. sertraline : A member of the class of tetralins that is tetralin which is substituted at positions 1 and 4 by a methylamino and a 3,4-dichlorophenyl group, respectively (the S,S diastereoisomer). A selective serotonin-reuptake inhibitor (SSRI), it is administered orally as the hydrochloride salt as an antidepressant for the treatment of depression, obsessive-compulsive disorder, panic disorder and post-traumatic stress disorder.	3.59	2	0	dichlorobenzene; secondary amino compound; tetralins	antidepressant; serotonin uptake inhibitor
picosulfate sodium picosulfate sodium: contains two active ingredients, sodium picosulfate and magnesium citrate, which are both laxatives; structure	2.05	1	0	aryl sulfate; pyridines
cefcanel cefcanel: RN given refers to (6R-(6 alpha,7 beta(R*)))-isomer; structure	2.04	1	0
zoledronic acid Zoledronic Acid: An imidobisphosphonate inhibitor of BONE RESORPTION that is used for the treatment of malignancy-related HYPERCALCEMIA; OSTEITIS DEFORMANS; and OSTEOPOROSIS.. zoledronic acid : An imidazole compound having a 2,2-bis(phosphono)-2-hydroxyethane-1-yl substituent at the 1-position.	7.54	27	0	1,1-bis(phosphonic acid); imidazoles	bone density conservation agent
epristeride epristeride: structure given in first source	2.04	1	0	steroid acid
talinolol [no description available]	2.04	1	0	ureas
artemisinin (+)-artemisinin : A sesquiterpene lactone obtained from sweet wormwood, Artemisia annua, which is used as an antimalarial for the treatment of multi-drug resistant strains of falciparum malaria.	2.58	2	0	organic peroxide; sesquiterpene lactone	antimalarial; plant metabolite
brinzolamide brinzolamide: an antiglaucoma agent	2.58	2	0	sulfonamide; thienothiazine	antiglaucoma drug; EC 4.2.1.1 (carbonic anhydrase) inhibitor
dienogest [no description available]	2.05	1	0	17beta-hydroxy steroid; 3-oxo-Delta(4) steroid; aliphatic nitrile; steroid hormone	progesterone receptor agonist; progestin; synthetic oral contraceptive
drospirenone drospirenone: a progestational compound with antimineralocorticoid and antiandrogenic activity; structure given in first source	2.08	1	0	3-oxo-Delta(4) steroid; steroid lactone	aldosterone antagonist; contraceptive drug; progestin
artemether Artemether: An artemisinin derivative that is used in the treatment of MALARIA.. artemether : An artemisinin derivative that is artemisinin in which the lactone has been converted to the corresponding lactol methyl ether. It is used in combination with lumefantrine as an antimalarial for the treatment of multi-drug resistant strains of falciparum malaria.	2.08	1	0	artemisinin derivative; cyclic acetal; organic peroxide; semisynthetic derivative; sesquiterpenoid	antimalarial
morphazinamide morphazinamide: RN given refers to parent cpd; RN in Chemline for mono-HCL: 1473-73-0; structure in Merck Index	2.05	1	0	morpholines; pyrazines; secondary carboxamide
dipropylacetamide dipropylacetamide: structure. valpromide : A fatty amide derived from valproic acid.	2.6	1	0	fatty amide	geroprotector; metabolite; teratogenic agent
denaverine denaverine: RN given refers to parent cpd; structure	2.04	1	0	diarylmethane
acamprosate Acamprosate: Structural analog of taurine that is used for the prevention of relapse in individuals with ALCOHOLISM.. acamprosate : An organosulfonic acid that is propane-1-sulfonic acid substituted by an acetylamino group at position 3.	3.23	1	0	acetamides; organosulfonic acid	environmental contaminant; neurotransmitter agent; xenobiotic
isaxonine isaxonine: promotes nerve growth	3.23	1	0	aminopyrimidine
oxprenolol hydrochloride [no description available]	2.6	1	0
diprafenone diprafenone: structure given in first source	2.04	1	0	aromatic compound
nebivolol 2,2'-iminobis[1-(6-fluoro-3,4-dihydro-2H-chromen-2-yl)ethanol] : A member of the class of chromanes that is 2,2'-iminodiethanol in which one hydrogen attached to each hydroxy-bearing carbon is replaced by a 6-fluorochroman-2-yl group.	3.58	2	0	chromanes; diol; organofluorine compound; secondary alcohol; secondary amino compound
uk 68798 [no description available]	3.87	3	0	aromatic ether; sulfonamide; tertiary amino compound	anti-arrhythmia drug; potassium channel blocker
ljc 10627 biapenem: structure given in first source. biapenem : A carbapenem antibiotic in which the azetidine and pyrroline rings carry 1-hydroxymethyl and pyrazolo[1,2-a][1,2,4]triazolium-6-ylthio substituents respectively.	2.04	1	0	carbapenems; organic sulfide; pyrazolotriazole	antibacterial drug
hp 873 iloperidone: an atypical, negative symptom antipsychotic agent. iloperidone : A member of the class of piperidines that is the 4-acetyl-2-methoxyphenyl ether of 3-(piperidin-1-yl)propan-1-ol which is substituted at position 4 of the piperidine ring by a 6-fluoro-1,2-benzoxazol-3-yl group. A member of the group of second generation antipsychotics (also known as an atypical antipsychotics), it is used for the treatment of schizophrenia.	3.61	2	0	1,2-benzoxazoles; aromatic ether; aromatic ketone; methyl ketone; monoamine; organofluorine compound; piperidines; tertiary amino compound	dopaminergic antagonist; second generation antipsychotic; serotonergic antagonist
dexrazoxane Dexrazoxane: The (+)-enantiomorph of razoxane.	3.86	3	0	razoxane	antineoplastic agent; cardiovascular drug; chelator; immunosuppressive agent
loxapine succinate [no description available]	2.08	1	0	succinate salt	geroprotector
guanfacine hydrochloride [no description available]	2.15	1	0	acetamides	geroprotector
fenoxypropazine [no description available]	3.23	1	0	aromatic ether
opipramol hydrochloride [no description available]	2.6	1	0
voriconazole Voriconazole: A triazole antifungal agent that specifically inhibits STEROL 14-ALPHA-DEMETHYLASE and CYTOCHROME P-450 CYP3A.. voriconazole : A triazole-based antifungal agent used for the treatment of esophageal candidiasis, invasive pulmonary aspergillosis, and serious fungal infections caused by Scedosporium apiospermum and Fusarium spp. It is an inhibitor of cytochrome P450 2C9 (CYP2C9) and CYP3A4.	4.42	6	0	conazole antifungal drug; difluorobenzene; pyrimidines; tertiary alcohol; triazole antifungal drug	P450 inhibitor
betamipron [no description available]	2.46	2	0	organonitrogen compound; organooxygen compound
moroxydine [no description available]	2.6	1	0	biguanides
bufuralol bufuralol: RN given refers to cpd without isomeric designation; structure	2.04	1	0	benzofurans
uroxatral [no description available]	2.08	1	0	hydrochloride
aceclofenac [no description available]	3.61	2	0	amino acid; carboxylic ester; dichlorobenzene; monocarboxylic acid; secondary amino compound	EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug
nitrefazole [no description available]	3.23	1	0	imidazoles
alacepril [no description available]	2.08	1	0	dipeptide; thioacetate ester	EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
panipenem panipenem: synthetic cpd; structure given in first source	2.04	1	0	organic molecular entity
perindoprilat perindoprilat : A dipeptide obtained by formal condensation of one of the carboxy groups of N-[(1S)-1-carboxyethyl]-L-norvaline with the amino group of (2S,3aS,7aS)-octahydroindole-2-carboxylic acid. The major active metabolite of perindopril.	2.04	1	0	dicarboxylic acid; dipeptide; L-alanine derivative; organic heterobicyclic compound	antihypertensive agent; drug metabolite; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
cyclobutyrol cyclobutyrol: RN given refers to parent cpd; structure. cyclobutyrol : A hydroxy monocarboxylic acid in which the hydroxy group is geminal to a 1-carboxypropyl group on a cyclohexane ring.	2.05	1	0	hydroxy monocarboxylic acid	bile therapy drug
thiocolchicoside [no description available]	2.08	1	0	glycoside
terlipressin terlivaz: first FDA approved injection to improve kidney function in adults with hepatorenal syndrome (HRS) with rapid reduction in kidney function.	2.05	1	0	polypeptide
thioxolone tioxolone : A 1,3-benzoxathiole having a hydroxy substituent at the 6-position.	2.6	1	0	benzoxathiole	antiseborrheic
ubenimex ubenimex: growth inhibitor	2.08	1	0
7-hydroxystaurosporine [no description available]	3.53	2	0
epicatechin (-)-epicatechin : A catechin with (2R,3R)-configuration.	2.03	1	0	catechin; polyphenol	antioxidant
gallocatechol (-)-epigallocatechin : A flavan-3,3',4',5,5',7-hexol having (2R,3R)-configuration.	2.03	1	0	catechin; flavan-3,3',4',5,5',7-hexol	antioxidant; food component; plant metabolite
methotrimeprazine Methotrimeprazine: A phenothiazine with pharmacological activity similar to that of both CHLORPROMAZINE and PROMETHAZINE. It has the histamine-antagonist properties of the antihistamines together with CENTRAL NERVOUS SYSTEM effects resembling those of chlorpromazine. (From Martindale, The Extra Pharmacopoeia, 30th ed, p604). methotrimeprazine : A member of the class of phenothiazines that is 10H-phenothiazine substituted by a (2R)-3-(dimethylamino)-2-methylpropyl group and a methoxy group at positions 10 and 2 respectively.	2.04	1	0	phenothiazines; tertiary amine	anticoronaviral agent; cholinergic antagonist; dopaminergic antagonist; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; non-narcotic analgesic; phenothiazine antipsychotic drug; serotonergic antagonist
honokiol [no description available]	2.6	1	0	biphenyls
isoflavone [no description available]	2.05	1	0	isoflavones
clevudine [no description available]	2.05	1	0
nobiletin nobiletin : A methoxyflavone that is flavone substituted by methoxy groups at positions 5, 6, 7, 8, 3' and 4' respectively.	2.6	1	0	methoxyflavone	antineoplastic agent; plant metabolite
lycorine lycorine: from bulbs of LYCORIS & other plants; RN given refers to (1 alpha,2 beta)-isomer; structure in Merck Index, 9th ed, #5444. lycorine : An indolizidine alkaloid that is 3,12-didehydrogalanthan substituted by hydroxy groups at positions and 2 and a methylenedioxy group across positions 9 and 10. Isolated from Crinum asiaticum, it has been shown to exhibit antimalarial activity.	7.63	2	0	indolizidine alkaloid	anticoronaviral agent; antimalarial; plant metabolite; protein synthesis inhibitor
9-aminocamptothecin [no description available]	2.04	1	0	pyranoindolizinoquinoline
leupeptin [no description available]	2.6	1	0	aldehyde; tripeptide	bacterial metabolite; calpain inhibitor; cathepsin B inhibitor; EC 3.4.21.4 (trypsin) inhibitor; serine protease inhibitor
sch 34343 Sch 34343: structure given in first source; RN given refers to (5R-(5alpha,6alpha))-isomer	2.04	1	0
squalamine squalamine: from dogfish shark Squalus acanthias; structure given in first source	2.04	1	0	bile acid
alantolactone alantolactone: allergenic sesquiterpene lactone; crystalline mixture of alantolactones from group of sesquiterpenes; structure. alantolactone : A sesquiterpene lactone that is 3a,5,6,7,8,8a,9,9a-octahydronaphtho[2,3-b]furan-2-one bearing two methyl substituents at positions 5 and 8a as well as a methylidene substituent at position 3.	7.11	1	0	naphthofuran; olefinic compound; sesquiterpene lactone	antineoplastic agent; apoptosis inducer; plant metabolite
tetrandrine tetrandrine: a bisbenzylisoquinoline that exhibits antifibrogenic activity	2.54	2	0	bisbenzylisoquinoline alkaloid; isoquinolines
3-deazaneplanocin 3-deazaneplanocin: S-adenosylhomocysteine hydrolase antagonist	2.1	1	0
tosyllysine chloromethyl ketone Tosyllysine Chloromethyl Ketone: An inhibitor of SERINE ENDOPEPTIDASES. Acts as an alkylating agent and is known to interfere with the translation process.	2.25	1	0	sulfonic acid derivative
doripenem Doripenem: A carbapenem derivative antibacterial agent that is more stable to renal dehydropeptidase I than IMIPENEM, but does not need to be given with an enzyme inhibitor such as CILASTATIN. It is used in the treatment of infections such as HOSPITAL-ACQUIRED PNEUMONIA, and complicated intra-abdominal or urinary-tract infections, including PYELONEPHRITIS.	3.61	2	0	carbapenems
calpeptin [no description available]	2.6	1	0	amino acid amide
fangchinoline [no description available]	2.6	1	0	aromatic ether; bisbenzylisoquinoline alkaloid; macrocycle	anti-HIV-1 agent; anti-inflammatory agent; antineoplastic agent; antioxidant; neuroprotective agent; plant metabolite
maslinic acid (2Alpha,3beta)-2,3-dihydroxyolean-12-en-28-oic acid: from Luehea divaricata and Agrimonia eupatoria	2.6	1	0	dihydroxy monocarboxylic acid; pentacyclic triterpenoid	anti-inflammatory agent; antineoplastic agent; antioxidant; plant metabolite
atovaquone Atovaquone: A hydroxynaphthoquinone that has antimicrobial activity and is being used in antimalarial protocols.. atovaquone : A naphthoquinone compound having a 4-(4-chlorophenyl)cyclohexyl group at the 2-position and a hydroxy substituent at the 3-position.	3.91	3	0	hydroxy-1,2-naphthoquinone
2-Chloronicotinic acid [no description available]	2.25	1	0	aromatic carboxylic acid; pyridines
bendamustine hydrochloride [no description available]	15.47	55	13
4'-methoxyflavone 4'-methoxyflavone: from seeds of Psoralea corylifolia (Fabaceae); structure in first source	2.08	1	0	ether; flavonoids
rivastigmine [no description available]	3.58	2	0	carbamate ester; tertiary amino compound	cholinergic drug; EC 3.1.1.8 (cholinesterase) inhibitor; neuroprotective agent
frovatriptan [no description available]	3.58	2	0	carbazoles
eletriptan eletriptan: 5-HT(1B/1D) receptor agonist; structure in first source. eletriptan : An N-alkylpyrrolidine, that is N-methylpyrrolidine in which the pro-R hydrogen at position 2 is replaced by a {5-[2-(phenylsulfonyl)ethyl]-1H-indol-3-yl}methyl group.	3.58	2	0	indoles; N-alkylpyrrolidine; sulfone	non-steroidal anti-inflammatory drug; serotonergic agonist; vasoconstrictor agent
rosiglitazone [no description available]	4.79	5	0	aminopyridine; thiazolidinediones	EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor; ferroptosis inhibitor; insulin-sensitizing drug
tamiflu [no description available]	2.08	1	0	phosphate salt
gamma-glutamine-4-nitroanilide gamma-glutamine-4-nitroanilide: substrate for glutaminase B.; RN given refers to (L)-isomer	2.31	1	0
bexarotene [no description available]	3.94	3	0	benzoic acids; naphthalenes; retinoid	antineoplastic agent
s20098 [no description available]	2.52	2	0	acetamides
flunisolide flunisolide: flunisolide HFA is a formulation of flunisolide using hydrofluoroalkane (HFA) as propellant in place of chlorofluorocarbon (CFC) ones	2.08	1	0	11beta-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; cyclic ketal; fluorinated steroid; primary alpha-hydroxy ketone	anti-asthmatic drug; anti-inflammatory drug; immunosuppressive agent
ketorolac tromethamine Ketorolac Tromethamine: A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is a non-steroidal anti-inflammatory agent used for analgesia for postoperative pain and inhibits cyclooxygenase activity.. ketorolac tromethamine : An organoammonium salt resulting from the mixture of equimolar amounts of ketorolac and tromethamine (tris). It has potent non-sedating analgesic and moderate anti-inflammatory effects. It is used in the short-term management of post-operative pain, and in eye drops to relieve the ocular itching associated with seasonal allergic conjunctivitis.	2.08	1	0	organoammonium salt	analgesic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor
clarithromycin Clarithromycin: A semisynthetic macrolide antibiotic derived from ERYTHROMYCIN that is active against a variety of microorganisms. It can inhibit PROTEIN SYNTHESIS in BACTERIA by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation.. clarithromycin : The 6-O-methyl ether of erythromycin A, clarithromycin is a macrolide antibiotic used in the treatment of respiratory-tract, skin and soft-tissue infections. It is also used to eradicate Helicobacter pylori in the treatment of peptic ulcer disease. It prevents bacteria from growing by interfering with their protein synthesis.	7.37	12	1	macrolide antibiotic	antibacterial drug; environmental contaminant; protein synthesis inhibitor; xenobiotic
ferroin ferroin: RN given refers to parent cpd	2.15	1	0
loganin [no description available]	2.6	1	0	beta-D-glucoside; cyclopentapyran; enoate ester; iridoid monoterpenoid; methyl ester; monosaccharide derivative; secondary alcohol	anti-inflammatory agent; EC 3.1.1.7 (acetylcholinesterase) inhibitor; EC 3.2.1.20 (alpha-glucosidase) inhibitor; EC 3.4.23.46 (memapsin 2) inhibitor; neuroprotective agent; plant metabolite
nicotine (S)-nicotine : A 3-(1-methylpyrrolidin-2-yl)pyridine in which the chiral centre has S-configuration. The naturally occurring and most active enantiomer of nicotine, isolated from Nicotiana tabacum.	2.75	3	0	3-(1-methylpyrrolidin-2-yl)pyridine	anxiolytic drug; biomarker; immunomodulator; mitogen; neurotoxin; nicotinic acetylcholine receptor agonist; peripheral nervous system drug; phytogenic insecticide; plant metabolite; psychotropic drug; teratogenic agent; xenobiotic
fibrinogen Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.. D-iditol : The D-enantiomer of iditol.	6.12	4	2	iditol	fungal metabolite
moexipril [no description available]	3.73	2	0	peptide
aucubin [no description available]	2.6	1	0	organic molecular entity	metabolite
catalpol [no description available]	2.6	1	0	organic molecular entity	metabolite
3,4-dihydroxyphenylglycol 3,4-dihydroxyphenylglycol: noradrenaline metabolite in mouse brain; RN given refers to cpd without isomeric designation. 3,4-dihydroxyphenylethyleneglycol : A tetrol composed of ethyleneglycol having a 3,4-dihydroxyphenyl group at the 1-position.	2.07	1	0	catechols; tetrol	metabolite; mouse metabolite
homocysteine Homocysteine: A thiol-containing amino acid formed by a demethylation of METHIONINE.. homocysteine : A sulfur-containing amino acid consisting of a glycine core with a 2-mercaptoethyl side-chain.. L-homocysteine : A homocysteine that has L configuration.	2.21	1	0	amino acid zwitterion; homocysteine; serine family amino acid	fundamental metabolite; mouse metabolite
gliquidone gliquidone: structure; RN given refers to parent cpd	2.08	1	0	isoquinolines
7-amino-4-methylcoumarin 7-amino-4-methylcoumarin: RN given refers to parent cpd	2.17	1	0	7-aminocoumarins	fluorochrome
lekoptin (S)-verapamil : A 2-(3,4-dimethoxyphenyl)-5-{[2-(3,4-dimethoxyphenyl)ethyl](methyl)amino}-2-(propan-2-yl)pentanenitrile that has S configuration.	2.6	1	0	2-(3,4-dimethoxyphenyl)-5-{[2-(3,4-dimethoxyphenyl)ethyl](methyl)amino}-2-(propan-2-yl)pentanenitrile
mci 9038 [no description available]	3.58	2	0	peptide
lopinavir [no description available]	2.99	4	0	amphetamines; dicarboxylic acid diamide	anticoronaviral agent; antiviral drug; HIV protease inhibitor
gamma-tocopherol gamma-Tocopherol: A natural tocopherol with less antioxidant activity than ALPHA-TOCOPHEROL. It exhibits antioxidant activity by virtue of the phenolic hydrogen on the 2H-1-benzopyran-6-ol nucleus. As in BETA-TOCOPHEROL, it also has three methyl groups on the 6-chromanol nucleus but at different sites.. gamma-tocopherol : A tocopherol in which the chroman-6-ol core is substituted by methyl groups at positions 7 and 8. It is found particularly in maize (corn) oil and soya bean (soybean) oils.	2.05	1	0	tocopherol; vitamin E	algal metabolite; food antioxidant; plant metabolite
norcantharidin norcantharidin: structure given in first source; RN given refers to cpds without isomeric designation	7.08	1	0	furofuran
8-mercaptoquinoline 8-mercaptoquinoline: structure given in first source	2.15	1	0
4-hydroxybenzylamine 4-hydroxybenzylamine: RN given refers to parent cpd	2.21	1	0	aromatic amine
cellulose sulfate cellulose sulfate: RN given refers to cpd with unknown MF; vaginal gel being developed as both a contraceptive and blockage to STD somewhat like nonoxynol-9	2.11	1	0	ether; flavonoids
4-hydroxycyclophosphamide 4-hydroxycyclophosphamide: primary activation metabolite of cyclophosphamide; RN given refers to cpd without isomeric designation. 4-hydroxycyclophosphamide : A phosphorodiamide that consists of 2-amino-1,3,2-oxazaphosphinan-4-ol 2-oxide having two 2-chloroethyl groups attached to the exocyclic nitrogen.	4.44	3	0	nitrogen mustard; organochlorine compound; phosphorodiamide	alkylating agent; metabolite
nimbolide nimbolide: isolated from Nigerian medicinal plant Azadirachta indica; RN given refers to 4alpha,5alpha,6alpha,7alpha,15beta,17alpha-isomer; structure given in first source	7.11	1	0
combretastatin combretastatin: cytotoxic principle from South African tree COMBRETUM caffrum; structure given in first source; acts at COLCHICINE site of TUBULIN	3.17	1	0
arctiin arctiin: from fruits of Arctium lappa L; RN given refers to (3R-trans)-isomer; RN for cpd without isomeric designation not avail 12/92	7.21	1	0	glycoside; lignan
moxifloxacin hydrochloride moxifloxacin hydrochloride : A hydrochloride comprising equimolar amounts of moxifloxacin and hydrogen chloride.	2.08	1	0	hydrochloride	antibacterial drug
n-methyladenosine N-methyladenosine: is a inhibitor of cell differentiation. N(6)-methyladenosine : A methyladenosine compound with one methyl group attached to N(6) of the adenine nucleobase.	2.6	1	0	methyladenosine
fulvestrant Fulvestrant: An estradiol derivative and estrogen receptor antagonist that is used for the treatment of estrogen receptor-positive, locally advanced or metastatic breast cancer.. fulvestrant : A 3-hydroxy steroid that is 17beta-estradiol in which the 7alpha hydrogen has been replaced by a nonyl group in which one of the hydrogens of the terminal methyl has been replaced by a (4,4,5,5,5-pentafluoropentyl)sulfinyl group. An estrogen receptor antagonist, it is used in the treatment of breast cancer.	11.47	7	1	17beta-hydroxy steroid; 3-hydroxy steroid; organofluorine compound; sulfoxide	antineoplastic agent; estrogen antagonist; estrogen receptor antagonist
yttrium radioisotopes Yttrium Radioisotopes: Unstable isotopes of yttrium that decay or disintegrate emitting radiation. Y atoms with atomic weights 82-88 and 90-96 are radioactive yttrium isotopes.	3.85	2	1
mizoribine [no description available]	2.08	1	0	imidazoles	anticoronaviral agent
fotemustine fotemustine: structure given in first source. fotemustine : A racemate comprising equimolar amounts of (R)- and (S)-fotemustine. It is an alkylating agent used in the treatment of malignant melanoma.. diethyl (1-{[(2-chloroethyl)(nitroso)carbamoyl]amino}ethyl)phosphonate : A member of the class of N-nitrosoureas that is ethyl diethylphosphonate in the hydrogen at position 1 of the ethyl group attached to the phosphorus has been replaced by a [(2-chloroethyl)(nitroso)carbamoyl]amino group.	8.47	1	1	N-nitrosoureas; organic phosphonate; organochlorine compound
arginyl-glycyl-aspartic acid arginyl-glycyl-aspartic acid: amino acid sequence of basic unit of widespread cellular recognition system	2.59	2	0	oligopeptide
imipenem, anhydrous Imipenem: Semisynthetic thienamycin that has a wide spectrum of antibacterial activity against gram-negative and gram-positive aerobic and anaerobic bacteria, including many multiresistant strains. It is stable to beta-lactamases. Clinical studies have demonstrated high efficacy in the treatment of infections of various body systems. Its effectiveness is enhanced when it is administered in combination with CILASTATIN, a renal dipeptidase inhibitor.. imipenem : A broad-spectrum, intravenous beta-lactam antibiotic of the carbapenem subgroup.	2.04	1	0	beta-lactam antibiotic allergen; carbapenems; zwitterion	antibacterial drug
sn 38 SN-38 : A member of the class of pyranoindolizinoquinolines that is (4S)-pyrano[3',4':6,7]indolizino[1,2-b]quinoline-3,14-dione bearing two additional ethyl substituents at positions 4 and 11 as well as two additional hydroxy substituents at positions 4 and 9. It is the active metabolite of irinotecan and is ~1000 times more active than irinotecan itself.	2.41	1	0	delta-lactone; phenols; pyranoindolizinoquinoline; tertiary alcohol	antineoplastic agent; apoptosis inducer; drug metabolite; EC 5.99.1.2 (DNA topoisomerase) inhibitor
sr141716 [no description available]	2.47	2	0	amidopiperidine; carbohydrazide; dichlorobenzene; monochlorobenzenes; pyrazoles	anti-obesity agent; appetite depressant; CB1 receptor antagonist
bosentan anhydrous Bosentan: A sulfonamide and pyrimidine derivative that acts as a dual endothelin receptor antagonist used to manage PULMONARY HYPERTENSION and SYSTEMIC SCLEROSIS.	4.44	6	0	primary alcohol; pyrimidines; sulfonamide	antihypertensive agent; endothelin receptor antagonist
diacetyldichlorofluorescein diacetyldichlorofluorescein: stable storage form of dichlorofluorescein	2.1	1	0
paxilline paxilline: structure given in first source; RN given refers to (2R-(2alpha,4bbeta,6aalpha,12bbeta,12calpha,14abeta))-isomer. paxilline : An indole diterpene alkaloid with formula C27H33NO4 isolated from Penicillium paxilli. It is a potent inhibitor of large conductance Ca2(+)- and voltage-activated K(+) (BK)-type channels.	2.04	1	0	diterpene alkaloid; enone; organic heterohexacyclic compound; terpenoid indole alkaloid; tertiary alcohol	anticonvulsant; Aspergillus metabolite; EC 3.6.3.8 (Ca(2+)-transporting ATPase) inhibitor; genotoxin; geroprotector; mycotoxin; Penicillium metabolite; potassium channel blocker
prolinedithiocarbamate prolinedithiocarbamate: do not confuse with pyrrolidine dithiocarbamate which is also abbreviated PDTC	2.05	1	0
selenomethionine [no description available]	2.05	1	0	amino acid zwitterion; selenomethionine	plant metabolite
vinpocetine [no description available]	2.08	1	0
sivelestat sivelestat: inhibitor of neutrophil elastase; structure given in first source	2.6	1	0	N-acylglycine; pivalate ester
racecadotril racecadotril: parenterally active enkephalinase inhibitor	2.08	1	0	N-acyl-amino acid
pyronaridine [no description available]	2.6	1	0	aminoquinoline
perindopril Perindopril: An angiotensin-converting enzyme inhibitor. It is used in patients with hypertension and heart failure.. perindopril : An alpha-amino acid ester that is the ethyl ester of N-{(2S)-1-[(2S,3aS,7aS)-2-carboxyoctahydro-1H-indol-1-yl]-1-oxopropan-2-yl}-L-norvaline	3.59	2	0	alpha-amino acid ester; dicarboxylic acid monoester; ethyl ester; organic heterobicyclic compound	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
geniposide [no description available]	2.6	1	0	terpene glycoside
epicatechin gallate epicatechin gallate: a steroid 5alpha-reductase inhibitor; RN given refers to the (cis)-isomer; structure given in first source; isolated from green tea. (-)-epicatechin-3-O-gallate : A gallate ester obtained by formal condensation of the carboxy group of gallic acid with the (3R)-hydroxy group of epicatechin. A natural product found in Parapiptadenia rigida.	2.03	1	0	catechin; gallate ester; polyphenol	EC 3.2.1.1 (alpha-amylase) inhibitor; EC 3.2.1.20 (alpha-glucosidase) inhibitor; metabolite
asulacrine asulacrine: derivative of amsacrine; structure given in first source	2.04	1	0	acridines
deguelin deguelin: a natural product from Mundulea sericea; RN refers to (7aS-cis)-isomer; structure given in first source. deguelin : A rotenone that is 13,13a-dihydro-3H-chromeno[3,4-b]pyrano[2,3-h]chromen-7(7aH)-one substituted by methoxy groups at positions 9 and 10, and by two methyl groups at position 3 (the 7aS,13aS-stereoisomer). It exists in abundant quantities in the bark, roots, and leaves of the Leguminosae family of plants and reported to exert anti-tumour effects in various cancers.	7.5	2	0	aromatic ether; diether; organic heteropentacyclic compound; rotenones	angiogenesis inhibitor; anti-inflammatory agent; antineoplastic agent; antiviral agent; apoptosis inducer; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor; mitochondrial NADH:ubiquinone reductase inhibitor; plant metabolite
hydroxycotinine hydroxycotinine: metabolite of nicotine; RN given refers to (S)-isomer; structure. trans-3-hydroxycotinine : An N-alkylpyrrolidine that is cotinine substituted at position C-3 by a hydroxy group (the 3R,5S-diastereomer).	2.04	1	0	N-alkylpyrrolidine; pyridines; pyrrolidin-2-ones; pyrrolidine alkaloid
fingolimod hydrochloride Fingolimod Hydrochloride: A sphingosine-derivative and IMMUNOSUPPRESSIVE AGENT that blocks the migration and homing of LYMPHOCYTES to the CENTRAL NERVOUS SYSTEM through its action on SPHINGOSINE 1-PHOSPHATE RECEPTORS. It is used in the treatment of MULTIPLE SCLEROSIS.. fingolimod hydrochloride : The hydrochloride salt of 2-amino-2-[2-(4-octylphenyl) ethyl]-1,3-propanediol (fingolimod).	5.35	6	0	hydrochloride	immunosuppressive agent; prodrug; sphingosine-1-phosphate receptor agonist
fingolimod fingolimod : An aminodiol that consists of propane-1,3-diol having amino and 2-(4-octylphenyl)ethyl substituents at the 2-position. It is a sphingosine 1-phosphate receptor modulator used for the treatment of relapsing-remitting multiple sclerosis. A prodrug, fingolimod is phosphorylated by sphingosine kinase to active metabolite fingolimod-phosphate, a structural analogue of sphingosine 1-phosphate.	2.05	1	0	aminodiol; primary amino compound	antineoplastic agent; CB1 receptor antagonist; immunosuppressive agent; prodrug; sphingosine-1-phosphate receptor agonist
daidzin daidzin: a potent, selective, and reversible inhibitor of human mitochondrial aldehyde dehydrogenase. daidzein 7-O-beta-D-glucoside : A glycosyloxyisoflavone that is daidzein attached to a beta-D-glucopyranosyl residue at position 7 via a glycosidic linkage. It is used in the treatment of alcohol dependency (antidipsotropic).	7.72	2	0	7-hydroxyisoflavones 7-O-beta-D-glucoside; hydroxyisoflavone; monosaccharide derivative	plant metabolite
triptolide [no description available]	7.98	4	0	diterpenoid; epoxide; gamma-lactam; organic heteroheptacyclic compound	antispermatogenic agent; plant metabolite
quinaprilat quinaprilat: metabolite of quinapril. quinaprilat : A dicarboxylic acid resulting from the hydrolysis of the ethyl ester group of quinapril to give the corresponding dicarboxylic acid. The active angiotensin-converting enzyme inhibitor (ACE inhibitor) of the prodrug quinapril.	2.04	1	0	dicarboxylic acid; isoquinolines; tertiary carboxamide	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; vasodilator agent
cobaltiprotoporphyrin cobaltiprotoporphyrin: RN given refers to cobalt protoporphyrin IX	2.03	1	0
2-hydroxyimipramine 2-hydroxyimipramine: RN given refers to parent cpd	2.04	1	0	dibenzoazepine
tamibarotene tamibarotene: has retinoid-binding activity. tamibarotene : A dicarboxylic acid monoamide resulting from the condensation of one of the carboxy groups of terephthalic acid with the amino group of 5,5,8,8-tetramethyl-5,6,7,8-tetrahydronaphthalen-2-amine.	3.15	1	0	dicarboxylic acid monoamide; retinoid; tetralins	antineoplastic agent; retinoic acid receptor alpha/beta agonist
ecteinascidin 743 [no description available]	4.9	6	0	acetate ester; azaspiro compound; bridged compound; hemiaminal; isoquinoline alkaloid; lactone; organic heteropolycyclic compound; organic sulfide; oxaspiro compound; polyphenol; tertiary amino compound	alkylating agent; angiogenesis modulating agent; anti-inflammatory agent; antineoplastic agent; marine metabolite
tadalafil [no description available]	3.61	2	0	benzodioxoles; pyrazinopyridoindole	EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor; vasodilator agent
1-phenyl-2-decanoylamino-3-morpholino-1-propanol RV 538: noninactivating inhibitor of ceramide-UDPG glucosyltransferase; RN given for unspecified HCl; structure given in first source	2.1	1	0
homoorientin homoorientin: isolated from Swertia japonica; structure given in first source	4.8	1	1	flavone C-glycoside; tetrahydroxyflavone	antineoplastic agent; radical scavenger
paliperidone 3-{2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl}-9-hydroxy-2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one : A member of the class of pyridopyrimidines that is 9-hydroxy-2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one carrying an additional 2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl group at position 2.. paliperidone : A racemate comprising equimolar amounts of (R)- and (S)-paliperidone. Paliperidone is the primary active metabolite of the older antipsychotic risperidone and is used for treatment of schizophrenia.	3.23	1	0	1,2-benzoxazoles; heteroarylpiperidine; organofluorine compound; pyridopyrimidine; secondary alcohol
sophocarpine [no description available]	2.6	1	0
nitisinone [no description available]	3.59	2	0	(trifluoromethyl)benzenes; C-nitro compound; cyclohexanones; mesotrione	EC 1.13.11.27 (4-hydroxyphenylpyruvate dioxygenase) inhibitor
plavix [no description available]	2.08	1	0	azaheterocycle sulfate salt; organoammonium sulfate salt	anticoagulant; P2Y12 receptor antagonist; platelet aggregation inhibitor
marimastat marimastat: a matrix metalloproteinase inhibitor active in patients with advanced carcinoma of the pancreas, prostate, or ovary. marimastat : A secondary carboxamide resulting from the foraml condensation of the carboxy group of (2R)-2-[(1S)-1-hydroxy-2-(hydroxyamino)-2-oxoethyl]-4-methylpentanoic acid with the alpha-amino group of N,3-dimethyl-L-valinamide.	2.54	2	0	hydroxamic acid; secondary carboxamide	antineoplastic agent; matrix metalloproteinase inhibitor
1'-acetoxychavicol acetate 1'-acetoxychavicol acetate: antifungal component of Alpinia galanga; structure given in first source. 1'-acetoxychavicol acetate : An acetate ester that is chavicol acetate substituted by an acetoxy group at position 1'.	2.11	1	0	acetate ester; phenylpropanoid	antineoplastic agent; NF-kappaB inhibitor; plant metabolite
clofarabine [no description available]	5.84	7	0	adenosines; organofluorine compound	antimetabolite; antineoplastic agent
sr 48692 SR 48692: structure in first source; a neurotensin receptor-1 antagonist	2.08	1	0	N-acyl-amino acid
elacridar Elacridar: inhibitor of MDR1 PROTEIN; structure given in first source	2.58	2	0
pramipexole Pramipexole: A benzothiazole derivative and dopamine agonist with antioxidant properties that is used in the treatment of PARKINSON DISEASE and RESTLESS LEGS SYNDROME.. pramipexole : A member of the class of benzothiazoles that is 4,5,6,7-tetrahydro-1,3-benzothiazole in which the hydrogens at the 2 and 6-pro-S-positions are substituted by amino and propylamino groups, respectively.	3.61	2	0	benzothiazoles; diamine	antidyskinesia agent; antiparkinson drug; dopamine agonist; radical scavenger
valdecoxib [no description available]	3.61	2	0	isoxazoles; sulfonamide	antipyretic; antirheumatic drug; cyclooxygenase 2 inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug
calpain inhibitor 2 calpain inhibitor 2: inhibits degradation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase and some other cysteine proteinases	2.92	1	0	peptide
mitiglinide mitiglinide: a rapid and short-acting hypoglycemic agent; acts on sulfonylurea receptor closing KATP channels; considered one of the glinides-an imprecise grouping; structure given in first source	2.05	1	0	benzenes; monocarboxylic acid
celastrol [no description available]	3.96	3	0	monocarboxylic acid; pentacyclic triterpenoid	anti-inflammatory drug; antineoplastic agent; antioxidant; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; Hsp90 inhibitor; metabolite
peroxynitrous acid Peroxynitrous Acid: A potent oxidant synthesized by the cell during its normal metabolism. Peroxynitrite is formed from the reaction of two free radicals, NITRIC OXIDE and the superoxide anion (SUPEROXIDES).	2.08	1	0	nitrogen oxoacid
imatinib mesylate imatinib methanesulfonate : A methanesulfonate (mesylate) salt that is the monomesylate salt of imatinib. Used for treatment of chronic myelogenous leukemia and gastrointestinal stromal tumours.	8.82	40	0	methanesulfonate salt	anticoronaviral agent; antineoplastic agent; apoptosis inducer; tyrosine kinase inhibitor
almotriptan almotriptan : An indole compound having a 2-(dimethylamino)ethyl group at the 3-position and a (pyrrolidin-1-ylsulfonyl)methyl group at the 5-position.	3.58	2	0	indoles; sulfonamide; tertiary amine	non-steroidal anti-inflammatory drug; serotonergic agonist; vasoconstrictor agent
mk 0663 [no description available]	2.46	2	0	bipyridines; organochlorine compound; sulfone	cyclooxygenase 2 inhibitor; non-steroidal anti-inflammatory drug
gefitinib [no description available]	7.94	28	0	aromatic ether; monochlorobenzenes; monofluorobenzenes; morpholines; quinazolines; secondary amino compound; tertiary amino compound	antineoplastic agent; epidermal growth factor receptor antagonist
n-(n-(3-carboxyoxirane-2-carbonyl)leucyl)isoamylamine N-(N-(3-carboxyoxirane-2-carbonyl)leucyl)isoamylamine: inhibits calcium-activated neutral protease; see also record for E-64; RN given refers to (2-S-(2alpha,3beta)(R*)-isomer)	2.6	1	0	leucine derivative
n(6)-(3-iodobenzyl)-5'-n-methylcarboxamidoadenosine N(6)-(3-iodobenzyl)-5'-N-methylcarboxamidoadenosine: structure given in first source; a selective A(3) adenosine receptor agonist. 3-iodobenzyl-5'-N-methylcarboxamidoadenosine : A derivative of adenosine in which the 5'-hydroxymethyl group is replaced by N-ethylcarboxamido and one of the hydrogens of the exocyclic amino function is substituted by a 3-iodobenzyl group.	2.05	1	0	adenosines; monocarboxylic acid amide; organoiodine compound	adenosine A3 receptor agonist
bay x 1005 2-(4-(quinolin-2-yl-methoxy)phenyl)-2-cyclopentylacetic acid: inhibits synthesis of leukotriene B4 and 5-hydroxyeicosatetraenoic acid; inhibits five-lipoxygenase activating protein(FLAP)and leukotriene A4 hydrolase(LTA4H); structure given in first source;	2.08	1	0
vadimezan vadimezan : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is replaced by a 5,6-dimethyl-9-oxoxanthen-4-yl group.	2.6	1	0	monocarboxylic acid; xanthones	antineoplastic agent
e 64 E 64: cysteine protease inhibitor of microbial origin, which inhibits cathepsin B (EC 3.4.22.1) and cathepsin L (EC 3.4.22.-)	2.9	3	0	dicarboxylic acid monoamide; epoxy monocarboxylic acid; guanidines; L-leucine derivative; zwitterion	antimalarial; antiparasitic agent; protease inhibitor
gluconamide [no description available]	2.21	1	0
desloratadine desloratadine: major metabolite of loratadine. desloratadine : Loratadine in which the ethoxycarbonyl group attached to the piperidine ring is replaced by hydrogen. The major metabolite of loratidine, desloratadine is an antihistamine which is used for the symptomatic relief of allergic conditions including rhinitis and chronic urticaria. It does not readily enter the central nervous system, so does not cause drowsiness.	3.61	2	0	benzocycloheptapyridine	anti-allergic agent; cholinergic antagonist; drug metabolite; H1-receptor antagonist
desvenlafaxine O-desmethylvenlafaxine : A tertiary amino compound that is N,N-dimethylethanamine substituted at position 1 by a 1-hydroxycyclohexyl and 4-hydroxyphenyl group. It is a metabolite of the drug venlafaxine.	3.23	1	0	cyclohexanols; phenols; tertiary amino compound	antidepressant; drug metabolite; marine xenobiotic metabolite
lestaurtinib [no description available]	3.14	1	0	indolocarbazole
gyki 53655 GYKI 53655: an AMPA (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate) receptor antagonist	2.08	1	0
methotrexate [no description available]	10.77	18	5	dicarboxylic acid; monocarboxylic acid amide; pteridines	abortifacient; antimetabolite; antineoplastic agent; antirheumatic drug; dermatologic drug; DNA synthesis inhibitor; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; immunosuppressive agent
alanyl-alanyl-phenylalanine chloromethyl ketone [no description available]	2	1	0
tamsulosin [no description available]	3.58	2	0	5-(2-{[2-(2-ethoxyphenoxy)ethyl]amino}propyl)-2-methoxybenzenesulfonamide	alpha-adrenergic antagonist; antineoplastic agent
rufinamide rufinamide: for treatment of Lennox-Gastaut syndrome; structure in first source	3.23	1	0	aromatic amide; heteroarene
antiprimod azaspirane: structure given in first source	2.47	2	0
sulbactam [no description available]	2.75	3	0	penicillanic acids
olmesartan medoxomil Olmesartan Medoxomil: An ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to manage HYPERTENSION.	3.87	3	0	biphenyls
dexpanthenol dexpanthenol: The alcohol of pantothenic acid	3.23	1	0	amino alcohol; monocarboxylic acid amide	cholinergic drug; provitamin
umifenovir umifenovir: an antiviral agent	2.6	1	0	indolyl carboxylic acid
fosamprenavir fosamprenavir: a prodrug of the protease inhibitor amprenavir. fosamprenavir : A sulfonamide with a structure based on that of sulfanilamide substituted on the sulfonamide nitrogen by a (2R,3S)-4-phenyl-2-(phosphonooxy)-3-({[(3S)-tetrahydrofuran-3-yloxy]carbonyl}amino)butyl group. It is a pro-drug of the HIV protease inhibitor and antiretroviral drug amprenavir.	3.23	1	0	sulfonamide	prodrug
safinamide safinamide: short-acting inhibitor of MOA-B; FCE 26743 is (S)-isomer, FCE 28073 is (R)-isomer; structure in first source	2.6	1	0	amino acid amide
ilomastat CS 610: matrix metalloproteinase inhibitor; structure in first source. ilomastat : An N-acyl-amino acid obtained by formal condensation of the carboxy group of (2R)-2-[2-(hydroxyamino)-2-oxoethyl]-4-methylpentanoic acid with the amino group of N-methyl-L-tryptophanamide. A cell permeable broad-spectrum matrix metalloproteinase (MMP) inhibitor	2.54	2	0	hydroxamic acid; L-tryptophan derivative; N-acyl-amino acid	anti-inflammatory agent; antibacterial agent; antineoplastic agent; EC 3.4.24.24 (gelatinase A) inhibitor; neuroprotective agent
hemorphin 7 hemorphin 7: opioid peptide fragment of hemoglobin; blood plasma levels of hemorphin-7 increases after long distance running; acts as neurotransmitter antagonist	2.07	1	0
abiraterone [no description available]	2.08	1	0	3beta-hydroxy-Delta(5)-steroid; 3beta-sterol; pyridines	antineoplastic agent; EC 1.14.99.9 (steroid 17alpha-monooxygenase) inhibitor
ml-3000 [no description available]	2.08	1	0
febuxostat Febuxostat: A thiazole derivative and inhibitor of XANTHINE OXIDASE that is used for the treatment of HYPERURICEMIA in patients with chronic GOUT.. febuxostat : A 1,3-thiazolemonocarboxylic acid that is 4-methyl-1,3-thiazole-5-carboxylic acid which is substituted by a 3-cyano-4-(2-methylpropoxy)phenyl group at position 2. It is an orally-active, potent, and selective xanthine oxidase inhibitor used for the treatment of chronic hyperuricaemia in patients with gout.	3.61	2	0	1,3-thiazolemonocarboxylic acid; aromatic ether; nitrile	EC 1.17.3.2 (xanthine oxidase) inhibitor
dilevalol (R,R)-labetalol : A 2-hydroxy-5-{1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl}benzamide that has 1R,2R-configuration.	2.04	1	0	2-hydroxy-5-{1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl}benzamide
aspartame [no description available]	2.25	1	0	carboxylic acid; dipeptide zwitterion; dipeptide; methyl ester	apoptosis inhibitor; EC 3.1.3.1 (alkaline phosphatase) inhibitor; environmental contaminant; micronutrient; nutraceutical; sweetening agent; xenobiotic
pomalidomide 3-aminophthalimidoglutarimide: structure in first source	16.82	77	16	aromatic amine; dicarboximide; isoindoles; piperidones	angiogenesis inhibitor; antineoplastic agent; immunomodulator
cd 437 CD 437: selective for retinoic acid receptors gamma. CD437 : A naphthoic acid that is 6-phenylnaphthylene-2-carboxyic acid in which the phenyl substituent has been substituted at positions 3 and 4 by adamant-1-yl and hydroxy groups, respectively. It acts as a selective agonist of retinoic acid receptor (RAR)gamma and induces cell cycle arrest and apoptosis in various cancer cells.	2.08	1	0	adamantanes; monocarboxylic acid; naphthoic acid; phenols	apoptosis inducer; retinoic acid receptor gamma agonist
1,3,5-triaza-7-phosphaadamantane 1,3,5-triaza-7-phosphaadamantane: structure in first source	2.17	1	0
proline Proline: A non-essential amino acid that is synthesized from GLUTAMIC ACID. It is an essential component of COLLAGEN and is important for proper functioning of joints and tendons.. proline : An alpha-amino acid that is pyrrolidine bearing a carboxy substituent at position 2.	2.05	1	0	amino acid zwitterion; glutamine family amino acid; L-alpha-amino acid; proline; proteinogenic amino acid	algal metabolite; compatible osmolytes; Escherichia coli metabolite; micronutrient; mouse metabolite; nutraceutical; Saccharomyces cerevisiae metabolite
escitalopram Escitalopram: S-enantiomer of CITALOPRAM. Belongs to a class of drugs known as SELECTIVE SEROTONIN REUPTAKE INHIBITORS, used to treat depression and generalized anxiety disorder.. escitalopram : A 1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrile that has S-configuration at the chiral centre. It is the active enantiomer of citalopram.	3.23	1	0	1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrile	antidepressant; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
lexapro Lexapro: Trade name of escitalopram, the active S-enantiomer of the racemic citalopram.	2.08	1	0
10-propargyl-10-deazaaminopterin 10-propargyl-10-deazaaminopterin: structure in first source. pralatrexate : A pteridine that is the N-4-[1-(2,4-diaminopteridin-6-yl)pent-4-yn-2-yl]benzoyl derivative of L-glutamic acid. Used for treatment of Peripheral T-Cell Lymphoma, an aggressive form of non-Hodgkins lymphoma.	7.95	7	2	N-acyl-L-glutamic acid; pteridines; terminal acetylenic compound	antimetabolite; antineoplastic agent; EC 1.5.1.3 (dihydrofolate reductase) inhibitor
docetaxel [no description available]	2.74	3	0	hydrate; secondary alpha-hydroxy ketone	antineoplastic agent
docetaxel anhydrous Docetaxel: A semisynthetic analog of PACLITAXEL used in the treatment of locally advanced or metastatic BREAST NEOPLASMS and NON-SMALL CELL LUNG CANCER.. docetaxel anhydrous : A tetracyclic diterpenoid that is paclitaxel with the N-benzyloxycarbonyl group replaced by N-tert-butoxycarbonyl, and the acetoxy group at position 10 replaced by a hydroxy group.	12.34	37	10	secondary alpha-hydroxy ketone; tetracyclic diterpenoid	antimalarial; antineoplastic agent; photosensitizing agent
perifosine [no description available]	9.3	15	3	ammonium betaine; phospholipid	EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
irofulven irofulven: structure in first source	2.43	2	0	cyclohexenones
atazanavir atazanavir : A heavily substituted carbohydrazide that is an antiretroviral drug of the protease inhibitor (PI) class used to treat infection of human immunodeficiency virus (HIV).	3.93	3	0	carbohydrazide	antiviral drug; HIV protease inhibitor
lonafarnib lonafarnib: inhibitor of farnesyl protein transferase. lonafarnib : A 4-{2-[4-(3,10-dibromo-8-chloro-6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridin-11-yl)piperidin-1-yl]-2-oxoethyl}piperidine-1-carboxamide that has R configuration. It is used as oral farnesyltransferase inhibitor.	9.46	2	0	4-{2-[4-(3,10-dibromo-8-chloro-6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridin-11-yl)piperidin-1-yl]-2-oxoethyl}piperidine-1-carboxamide	antineoplastic agent; EC 2.5.1.58 (protein farnesyltransferase) inhibitor
ym 872 YM 872: structure in first source	2.04	1	0
tariquidar [no description available]	2.54	2	0	benzamides
levofloxacin Levofloxacin: The L-isomer of Ofloxacin.. levofloxacin : An optically active form of ofloxacin having (S)-configuration; an inhibitor of bacterial topoisomerase IV and DNA gyrase.	10.19	5	0	9-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid; fluoroquinolone antibiotic; quinolone antibiotic	antibacterial drug; DNA synthesis inhibitor; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; topoisomerase IV inhibitor
ezetimibe Ezetimibe: An azetidine derivative and ANTICHOLESTEREMIC AGENT that inhibits intestinal STEROL absorption. It is used to reduce total CHOLESTEROL; LDL CHOLESTEROL, and APOLIPOPROTEINS B in the treatment of HYPERLIPIDEMIAS.. ezetimibe : A beta-lactam that is azetidin-2-one which is substituted at 1, 3, and 4 by p-fluorophenyl, 3-(p-fluorophenyl)-3-hydroxypropyl, and 4-hydroxyphenyl groups, respectively (the 3R,3'S,4S enantiomer).	3.87	3	0	azetidines; beta-lactam; organofluorine compound	anticholesteremic drug; antilipemic drug; antimetabolite
4-boronophenylalanine 4-boronophenylalanine: neutron absorbing (10)B-cpd used in thermal neutron capturetherapy of malignant melanoma; RN given refers to (L)-isomer; structure given in first source	2.11	1	0
ertapenem Ertapenem: A carbapenem derivative antibacterial agent that is more stable to renal dehydropeptidase I than IMIPENEM, but does not need to be given with an enzyme inhibitor such as CILASTATIN. It is used in the treatment of Gram-positive and Gram-negative bacterial infections including intra-abdominal infections, acute gynecological infections, complicated urinary tract infections, skin infections, and respiratory tract infections. It is also used to prevent infection in colorectal surgery.. ertapenem : Meropenem in which the one of the two methyl groups attached to the amide nitrogen is replaced by hydrogen while the other is replaced by a 3-carboxyphenyl group. The sodium salt is used for the treatment of moderate to severe susceptible infections including intra-abdominal and acute gynaecological infections, pneumonia, and infections of the skin and of the urinary tract.	3.58	2	0	carbapenemcarboxylic acid; pyrrolidinecarboxamide	antibacterial drug
dx 8951 [no description available]	2.04	1	0	pyranoindolizinoquinoline
cox 189 lumiracoxib: a COX-2 inhibitor. lumiracoxib : An amino acid that is phenylacetic acid which is substituted at position 2 by the nitrogen of 2-chloro-6-fluoroaniline and at position 5 by a methyl group. A highly selective cyclooxygenase 2 inhibitor, it was briefly used for the treatment of osteoarthritis, but was withdrawn due to concersns of hepatotoxicity.	3.61	2	0	amino acid; monocarboxylic acid; organochlorine compound; organofluorine compound; secondary amino compound	cyclooxygenase 2 inhibitor; non-steroidal anti-inflammatory drug
cilomilast [no description available]	2.04	1	0	methoxybenzenes
conivaptan conivaptan : The amide resulting from the formal condensation of 4-[(biphenyl-2-ylcarbonyl)amino]benzoic acid with the benzazepine nitrogen of 2-methyl-1,4,5,6-tetrahydroimidazo[4,5-d][1]benzazepine. It is an antagonist for two of the three types of arginine vasopressin (AVP) receptors, V1a and V2. It is used as its hydrochloride salt for the treatment of hyponatraemia (low blood sodium levels) caused by syndrome of inappropriate antidiuretic hormone (SIADH).	3.58	2	0	benzazepine	aquaretic; vasopressin receptor antagonist
cariporide cariporide: a selective sodium-hydrogen exchange subtype 1 inhibitor; structure in first source	2.05	1	0
tezosentan tezosentan: structure in first source	2.45	2	0
mk 767 5-((2,4-dioxo-5-thiazolidinyl)methyl)-2-methoxy-N-((4-(trifluoromethyl)phenyl)methyl)benzamide: an antihyperlipidemic agent that also functions as an insulin sensitizer, PPARalpha agonist, and PPARgamma agonist; structure in first source	2.08	1	0
vatalanib [no description available]	4.02	2	0	monochlorobenzenes; phthalazines; pyridines; secondary amino compound	angiogenesis inhibitor; antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; vascular endothelial growth factor receptor antagonist
sabarubicin sabarubicin: structure given in first source	2.04	1	0
moxifloxacin Moxifloxacin: A fluoroquinolone that acts as an inhibitor of DNA TOPOISOMERASE II and is used as a broad-spectrum antibacterial agent.. moxifloxacin : A quinolone that consists of 4-oxo-1,4-dihydroquinoline-3-carboxylic acid bearing a cyclopropyl substituent at position 1, a fluoro substitiuent at position 6, a (4aS,7aS)-octahydro-6H-pyrrolo[3,4-b]pyridin-6-yl group at position 7 and a methoxy substituent at position 8. A member of the fluoroquinolone class of antibacterial agents.	3.86	3	0	aromatic ether; cyclopropanes; fluoroquinolone antibiotic; pyrrolidinopiperidine; quinolinemonocarboxylic acid; quinolone antibiotic; quinolone	antibacterial drug
vx 497 N-3-(3-(3-methoxy-4-oxazol-5-ylphenyl)ureido)benzylcarbamic acid tetrahydrofuran-3-yl ester: structure in first source	2.6	1	0
pralnacasan pralnacasan: NSAID, ICE inhibitor & metastasis inhibitor; RN & structure in first source	3.23	1	0
clevidipine clevidipine: a calcium channel blocker and antihypertensive agent; structure in first source	3.58	2	0	dihydropyridine
jtt 501 JTT 501: an insulin sensitizer; structure in first source	2.05	1	0
solifenacin [no description available]	3.58	2	0	isoquinolines
dexmethylphenidate dexmethylphenidate : A methyl phenyl(piperidin-2-yl)acetate in which both stereocentres have R configuration. It is the active enantiomer in the racemic drug methylphenidate.	3.23	1	0	methyl phenyl(piperidin-2-yl)acetate	adrenergic agent
bcx 1812 [no description available]	2.6	1	0	3-hydroxy monocarboxylic acid; acetamides; cyclopentanols; guanidines	antiviral drug; EC 3.2.1.18 (exo-alpha-sialidase) inhibitor
bazedoxifene acetate [no description available]	2.08	1	0
xamoterol Xamoterol: A phenoxypropanolamine derivative that is a selective beta-1-adrenergic agonist.	2.46	2	0	morpholines
naproxen Naproxen: An anti-inflammatory agent with analgesic and antipyretic properties. Both the acid and its sodium salt are used in the treatment of rheumatoid arthritis and other rheumatic or musculoskeletal disorders, dysmenorrhea, and acute gout.. naproxen : A methoxynaphthalene that is 2-methoxynaphthalene substituted by a carboxy ethyl group at position 6. Naproxen is a non-steroidal anti-inflammatory drug commonly used for the reduction of pain, fever, inflammation and stiffness caused by conditions such as osteoarthritis, kidney stones, rheumatoid arthritis, psoriatic arthritis, gout, ankylosing spondylitis, menstrual cramps, tendinitis, bursitis, and for the treatment of primary dysmenorrhea. It works by inhibiting both the COX-1 and COX-2 enzymes.	4.13	4	0	methoxynaphthalene; monocarboxylic acid	antipyretic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; drug allergen; environmental contaminant; gout suppressant; non-narcotic analgesic; non-steroidal anti-inflammatory drug; xenobiotic
canertinib [no description available]	2.08	1	0	monochlorobenzenes; morpholines; organofluorine compound; quinazolines	antineoplastic agent; tyrosine kinase inhibitor
cinacalcet cinacalcet : A secondary amino compound that is (1R)-1-(naphthalen-1-yl)ethanamine in which one of the hydrogens attached to the nitrogen is substituted by a 3-[3-(trifluoromethyl)phenyl]propyl group.	3.23	1	0	(trifluoromethyl)benzenes; naphthalenes; secondary amino compound	calcimimetic; P450 inhibitor
birb 796 [no description available]	7.46	2	0	aromatic ether; morpholines; naphthalenes; pyrazoles; ureas	EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor; immunomodulator
lubiprostone [no description available]	3.23	1	0
olmesartan olmesartan: an active metabolite of CS 866	2.6	1	0	biphenylyltetrazole	angiotensin receptor antagonist; antihypertensive agent
telbivudine [no description available]	3.95	3	0	pyrimidine 2'-deoxyribonucleoside	antiviral drug; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
tipifarnib [no description available]	7.22	9	2	imidazoles; monochlorobenzenes; primary amino compound; quinolone	antineoplastic agent; apoptosis inducer; EC 2.5.1.58 (protein farnesyltransferase) inhibitor
celastrol methyl ester celastrol methyl ester: isolated from Tripterygium wilfordii; potent inhibitory activity on both Kir2.1 and ERG1 potassium channels, leading to LONG QT SYNDROME	2.6	1	0	carboxylic ester
atrasentan Atrasentan: A pyrrolidine and benzodioxole derivative that acts a RECEPTOR, ENDOTHELIN A antagonist. It has therapeutic potential as an antineoplastic agent and for the treatment of DIABETIC NEPHROPATHIES.	3.53	2	0	pyrrolidines
resiquimod S 28463: structure given in first source	2.6	1	0	imidazoquinoline
ukrain ukrain: a phytogenic antineoplastic agent; semisynthetic product from alkaloids of Chelidonium majus L. & thiophosphoric triaciridide acid	7.1	1	0
cyc 202 seliciclib : 2,6-Diaminopurine carrying benzylamino, (2R)-1-hydroxybutan-2-yl and isopropyl substituents at C-6, C-2-N and N-9 respectively. It is an experimental drug candidate in the family of pharmacological cyclin-dependent kinase (CDK) inhibitors.	4.08	4	0	2,6-diaminopurines	antiviral drug; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
methylselenic acid methylseleninic acid : An organoselenium compound that is seleninic acid in which the hydrogen attached to selenium is replaced by a methyl group.	2.07	1	0	one-carbon compound; organoselenium compound	antineoplastic agent; EC 3.5.1.98 (histone deacetylase) inhibitor; human xenobiotic metabolite
withanolide d withanolide D: structure. withanolide D : A withanolide that is 5,6:22,26-diepoxyergosta-2,24-diene-1,26-dione substituted by hydroxy groups at positions 4 and 22 (the 4beta,5beta,6beta,22R stereoisomer). Isolated from Tubocapsicum anomalum and Withania somnifera, it exhibits cytotoxic activity.	2.31	1	0	20-hydroxy steroid; 4-hydroxy steroid; delta-lactone; enone; epoxy steroid; ergostanoid; secondary alcohol; tertiary alcohol; withanolide	antineoplastic agent
sclareol sclareol: structure given in first source. sclareol : A labdane diterpenoid that is labd-14-ene substituted by hydroxy groups at positions 8 and 13. It has been isolated from Salvia sclarea.	7.15	1	0	labdane diterpenoid	antifungal agent; antimicrobial agent; apoptosis inducer; fragrance; plant metabolite
abanoquil [no description available]	2.04	1	0
tanshinone ii a tashinone IIA: a cardiovascular agent with antineoplastic activity; isolated from Salvia miltiorrhiza; structure in first source	2.6	1	0	abietane diterpenoid
2-phenyl-1,2-benzisothiazol-3-(2h)-one 2-phenyl-1,2-benzisothiazol-3-(2H)-one: structure given in first source; sulfur analog of ebselen	2.41	1	0
paromomycin Paromomycin: An aminoglycoside antibacterial and antiprotozoal agent produced by species of STREPTOMYCES.. paromomycin : An amino cyclitol glycoside that is the 1-O-(2-amino-2-deoxy-alpha-D-glucopyranoside) and the 3-O-(2,6-diamino-2,6-dideoxy-beta-L-idopyranosyl)-beta-D-ribofuranoside of 4,6-diamino-2,3-dihydroxycyclohexane (the 1R,2R,3S,4R,6S diastereoisomer). It is obtained from various Streptomyces species. A broad-spectrum antibiotic, it is used (generally as the sulfate salt) for the treatment of acute and chronic intestinal protozoal infections, but is not effective for extraintestinal protozoal infections. It is also used as a therapeutic against visceral leishmaniasis.	3.59	2	0	amino cyclitol glycoside; aminoglycoside antibiotic	anthelminthic drug; antibacterial drug; antiparasitic agent; antiprotozoal drug
anidulafungin Anidulafungin: Echinocandin antifungal agent that is used in the treatment of CANDIDEMIA and CANDIDIASIS.. anidulafungin : A semisynthetic echinocandin anti-fungal drug. It is active against Aspergillus and Candida species and is used for the treatment of invasive candidiasis.	3.58	2	0	antibiotic antifungal drug; azamacrocycle; echinocandin; heterodetic cyclic peptide; semisynthetic derivative
avasimibe [no description available]	2.05	1	0	monoterpenoid
anacardic acid anacardic acid: isolated from Anacardium occidentale; monophenol monooxygenase inhibitor. anacardic acid : A hydroxybenzoic acid that is salicylic acid substituted by a pentadecyl group at position 6. It is a major component of cashew nut shell liquid and exhibits an extensive range of bioactivities.	2.6	1	0	hydroxy monocarboxylic acid; hydroxybenzoic acid	anti-inflammatory agent; antibacterial agent; anticoronaviral agent; apoptosis inducer; EC 2.3.1.48 (histone acetyltransferase) inhibitor; EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor; neuroprotective agent; plant metabolite
beta-solamarine beta-solamarine: RN given refers to (3beta,22beta,25S)-isomer; structure given in first source	2.41	1	0	steroid saponin
aminopterin Aminopterin: A folic acid derivative used as a rodenticide that has been shown to be teratogenic.	7.3	6	2	dicarboxylic acid	EC 1.5.1.3 (dihydrofolate reductase) inhibitor; mutagen
17 alpha-hydroxyprogesterone caproate 17 alpha-Hydroxyprogesterone Caproate: Hydroxyprogesterone derivative that acts as a PROGESTIN and is used to reduce the risk of recurrent MISCARRIAGE and of PREMATURE BIRTH. It is also used in combination with ESTROGEN in the management of MENSTRUATION DISORDERS.	3.23	1	0	corticosteroid hormone
varenicline Varenicline: A benzazepine derivative that functions as an ALPHA4-BETA2 NICOTINIC RECEPTOR partial agonist. It is used for SMOKING CESSATION.. varenicline : An organic heterotetracyclic compound that acts as a partial agonist for nicotinic cholinergic receptors and is used (in the form of its tartate salt) as an aid to giving up smoking.	3.23	1	0
biotin vitamin B7 : Any member of a group of vitamers that belong to the chemical structural class called biotins that exhibit biological activity against vitamin B7 deficiency. Vitamin B7 deficiency is very rare in individuals who take a normal balanced diet. Foods rich in biotin are egg yolk, liver, cereals, vegetables (spinach, mushrooms) and rice. Symptoms associated with vitamin B7 deficiency include thinning hair, scaly skin rashes around eyes, nose and mouth, and brittle nails. The vitamers include biotin and its ionized and salt forms.	2.05	1	0	biotins; vitamin B7	coenzyme; cofactor; Escherichia coli metabolite; fundamental metabolite; human metabolite; mouse metabolite; nutraceutical; prosthetic group; Saccharomyces cerevisiae metabolite
carbobenzyloxyleucyl-tyrosine chloromethyl ketone [no description available]	2.25	1	0
angiotensin ii Giapreza: injectable form of angiotensin II used to increase blood pressure in adult patients with septic or other distributive shock. Ile(5)-angiotensin II : An angiotensin II that acts on the central nervous system (PDB entry: 1N9V).	5.88	6	1	amino acid zwitterion; angiotensin II	human metabolite
fiduxosin fiduxosin: fiduxosin (ABT-980) is the (3aR,9bR)-isomer; structure in first source	3.23	1	0
atropine tropan-3alpha-yl 3-hydroxy-2-phenylpropanoate : A tropane alkaloid that is (1R,5)-8-methyl-8-azabicyclo[3.2.1]octane substituted by a (3-hydroxy-2-phenylpropanoyl)oxy group at position 3.	4.08	4	0
ropivacaine Ropivacaine: An anilide used as a long-acting local anesthetic. It has a differential blocking effect on sensory and motor neurons.. ropivacaine : The piperidinecarboxamide obtained by the formal condensation of N-propylpipecolic acid and 2,6-dimethylaniline.. (S)-ropivacaine : A piperidinecarboxamide-based amide-type local anaesthetic (amide caine) in which (S)-N-propylpipecolic acid and 2,6-dimethylaniline are combined to form the amide bond.	2.04	1	0	piperidinecarboxamide; ropivacaine	local anaesthetic
migalastat migalastat: a potent inhibitor of glycolipid biosynthesis	2.6	1	0	piperidines
sb 203580 [no description available]	2.75	3	0	imidazoles; monofluorobenzenes; pyridines; sulfoxide	EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor; geroprotector; Hsp90 inhibitor; neuroprotective agent
enzastaurin [no description available]	7.13	8	2	indoles; maleimides
erlotinib [no description available]	3.95	3	0	aromatic ether; quinazolines; secondary amino compound; terminal acetylenic compound	antineoplastic agent; epidermal growth factor receptor antagonist; protein kinase inhibitor
erlotinib hydrochloride [no description available]	7.82	17	2	hydrochloride; terminal acetylenic compound	antineoplastic agent; protein kinase inhibitor
piboserod Serotonin 5-HT4 Receptor Antagonists: Drugs that bind to but do not activate SEROTONIN 5-HT4 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN RECEPTOR AGONISTS.	2.08	1	0
organophosphonates hydrogenphosphite : A divalent inorganic anion resulting from the removal of a proton from two of the hydroxy groups of phosphorous acid.	6.48	2	2	divalent inorganic anion; phosphite ion
l 163191 [no description available]	2.08	1	0
limonin [no description available]	2.6	1	0	epoxide; furans; hexacyclic triterpenoid; lactone; limonoid; organic heterohexacyclic compound	inhibitor; metabolite; volatile oil component
dichamanetin dichamanetin: structure in first source	2.06	1	0	diarylheptanoid	metabolite
melagatran [no description available]	2.04	1	0	azetidines; carboxamidine; dicarboxylic acid monoamide; non-proteinogenic alpha-amino acid; secondary amino compound	anticoagulant; EC 3.4.21.5 (thrombin) inhibitor; serine protease inhibitor
scutellarin scutellarin: see scutellarein for aglycone. scutellarin : The glycosyloxyflavone which is the 7-O-glucuronide of scutellarein.	2.6	1	0	glucosiduronic acid; glycosyloxyflavone; monosaccharide derivative; trihydroxyflavone	antineoplastic agent; proteasome inhibitor
bd 1047 N-(2-(3,4-Dichlorphenyl)ethyl)-N,N',N'-trimethyl-1,2-ethandiamin: sigma receptor ligand; putative sigma receptor antagonist with antidystonic activity	2.08	1	0	primary amine
carboxyebselen carboxyebselen: a nitric oxide synthase inhibitor	2.41	1	0
etravirine [no description available]	3.73	2	0	aminopyrimidine; aromatic ether; dinitrile; organobromine compound	antiviral agent; HIV-1 reverse transcriptase inhibitor
pi 083 PI 083: from Streptomyces matensis A-6621	2.45	2	0
chelidonine chelidonine: benzophenanthridine derived from scoulerine from Chelidonium majus; RN given refers to parent cpd (chelidonine, (5bR-(5balpha,6beta,12alpha))-isomer)	2.6	1	0	alkaloid antibiotic; alkaloid fundamental parent; benzophenanthridine alkaloid
troleandomycin Troleandomycin: A macrolide antibiotic that is similar to ERYTHROMYCIN.. troleandomycin : A semi-synthetic macrolide antibiotic obtained by acetylation of the three free hydroxy groups of oleandomycin. Troleandomycin is only found in individuals that have taken the drug.	2.05	1	0	acetate ester; epoxide; macrolide antibiotic; monosaccharide derivative; polyketide; semisynthetic derivative	EC 1.14.13.97 (taurochenodeoxycholate 6alpha-hydroxylase) inhibitor; xenobiotic
4-n-butylresorcinol 4-n-butylresorcinol: structure in first source	2.6	1	0	resorcinols
dronedarone Dronedarone: A non-iodinated derivative of amiodarone that is used for the treatment of ARRHYTHMIA.. dronedarone : A member of the class of 1-benzofurans used for the treatment of cardiac arrhythmias.	3.23	1	0	1-benzofurans; aromatic ether; aromatic ketone; sulfonamide; tertiary amino compound	anti-arrhythmia drug; environmental contaminant; xenobiotic
tesaglitazar tesaglitazar: structure in first source	2.04	1	0
ramelteon ramelteon: melatonin MT1/MT2 receptor agonist	3.61	2	0	indanes
lapatinib [no description available]	9.01	13	1	furans; organochlorine compound; organofluorine compound; quinazolines	antineoplastic agent; tyrosine kinase inhibitor
darunavir Darunavir: An HIV PROTEASE INHIBITOR that is used in the treatment of AIDS and HIV INFECTIONS. Due to the emergence of ANTIVIRAL DRUG RESISTANCE when used alone, it is administered in combination with other ANTI-HIV AGENTS.. darunavir : An N,N-disubstituted benzenesulfonamide bearing an unsubstituted amino group at the 4-position, used for the treatment of HIV infection. A second-generation HIV protease inhibitor, darunavir was designed to form robust interactions with the protease enzyme from many strains of HIV, including those from treatment-experienced patients with multiple resistance mutations to other protease inhibitors.	3.73	2	0	carbamate ester; furofuran; sulfonamide	antiviral drug; HIV protease inhibitor
dapivirine Dapivirine: effectively prevented human immunodeficiency virus (HIV) infection in cocultures of monocyte-derived dendritic cells and T cells, representing primary targets in sexual transmission	2.6	1	0
deferasirox Deferasirox: A triazole and benzoate derivative that acts as a selective iron chelator. It is used in the management of chronic IRON OVERLOAD due to blood transfusion or non-transfusion dependent THALASSEMIA.. deferasirox : A member of the class of triazoles, deferasirox is 1,2,4-triazole substituted by a 4-carboxyphenyl group at position 1 and by 2-hydroxyphenyl groups at positions 3 and 5. An orally active iron chelator, it is used to manage chronic iron overload in patients receiving long-term blood transfusions.	9.59	4	0	benzoic acids; monocarboxylic acid; phenols; triazoles	iron chelator
bms204352 BMS204352: a calcium-sensitive opener of maxi-K potassium channels; structure in first source	2.46	2	0
fosfluconazole fosfluconazole: prodrug of fluconazole	2.04	1	0	conazole antifungal drug; triazole antifungal drug; triazoles	prodrug
tbc-11251 sitaxsentan: endothelin A receptor antagonist; structure in first source	3.87	3	0	benzodioxoles
tolvaptan [no description available]	3.61	2	0	benzazepine; benzenedicarboxamide	aquaretic; vasopressin receptor antagonist
sorafenib [no description available]	12.69	31	10	(trifluoromethyl)benzenes; aromatic ether; monochlorobenzenes; phenylureas; pyridinecarboxamide	angiogenesis inhibitor; anticoronaviral agent; antineoplastic agent; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor; ferroptosis inducer; tyrosine kinase inhibitor
lenalidomide [no description available]	25.71	847	131	aromatic amine; dicarboximide; isoindoles; piperidones	angiogenesis inhibitor; antineoplastic agent; immunomodulator
N-[4-(3-chloro-4-fluoroanilino)-3-cyano-7-ethoxy-6-quinolinyl]-4-(dimethylamino)-2-butenamide [no description available]	2.08	1	0	aminoquinoline
regadenoson [no description available]	3.23	1	0	purine nucleoside
sr 142806 [no description available]	2.08	1	0
lacosamide Lacosamide: An acetamide derivative that acts as a blocker of VOLTAGE-GATED SODIUM CHANNELS. It is used as an anticonvulsant, for adjunctive or monotherapy, in the treatment of PARTIAL SEIZURES.	3.61	2	0	N-acyl-amino acid
cp 101,606 traxoprodil mesylate: a selective NMDA antagonist; structure given in first source	2.04	1	0
1-methylpropyl-2-imidazolyl disulfide 1-methylpropyl-2-imidazolyl disulfide: a thioredoxin inhibitor with antineoplastic activity	2.11	1	0	imidazoles
sitosterol, (3beta)-isomer Sobatum: tradename; active fraction of Solanum trilobatum; reduces side-effects of radiation-induced toxicity. sitosterol : A member of the class of phytosterols that is stigmast-5-ene substituted by a beta-hydroxy group at position 3.	2.05	1	0	3beta-hydroxy-Delta(5)-steroid; 3beta-sterol; C29-steroid; phytosterols; stigmastane sterol	anticholesteremic drug; antioxidant; mouse metabolite; plant metabolite; sterol methyltransferase inhibitor
gossypol acetic acid [no description available]	2.48	2	0
3-nitrotyrosine 3-nitrotyrosine: RN given refers to parent cpd without isomeric designation. 3-nitrotyrosine : A nitrotyrosine comprising tyrosine having a nitro group at the 3-position on the phenyl ring.	2.03	1	0	2-nitrophenols; C-nitro compound; nitrotyrosine; non-proteinogenic alpha-amino acid
vincaleukoblastine [no description available]	4.16	4	0	acetate ester; indole alkaloid fundamental parent; methyl ester; organic heteropentacyclic compound; organic heterotetracyclic compound; tertiary alcohol; tertiary amino compound; vinca alkaloid	antineoplastic agent; immunosuppressive agent; microtubule-destabilising agent; plant metabolite
blastmycin blastmycin: structure	2.03	1	0	amidobenzoic acid
vincristine sulfate [no description available]	2.08	1	0	organic sulfate salt	antineoplastic agent; geroprotector
nsc 74859 NSC 74859: inhibits Stat3 binding activity; structure in first source. S3I-201 : An amidobenzoic acid obtained by formal condensation of the carboxy group of [(4-methylbenzene-1-sulfonyl)oxy]acetic acid with the amino group of 4-amino-2-hydroxybenzoic acid.	2.69	2	0	amidobenzoic acid; monohydroxybenzoic acid; tosylate ester	STAT3 inhibitor
anisomycin Anisomycin: An antibiotic isolated from various Streptomyces species. It interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system.. (-)-anisomycin : An antibiotic isolated from various Streptomyces species. It interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system.	2.01	1	0	monohydroxypyrrolidine; organonitrogen heterocyclic antibiotic	anticoronaviral agent; antimicrobial agent; antineoplastic agent; antiparasitic agent; bacterial metabolite; DNA synthesis inhibitor; protein synthesis inhibitor
benzofurans Benzofurans: Compounds that contain a BENZENE ring fused to a furan ring.	2.05	1	0
benzarone benzarone: antihemorrhagic agent; structure	3.59	2	0	1-benzofurans
nsc-89199 estramustine phosphate : A steroid phosphate which is the 17-O-phospho derivative of estramustine.	2.04	1	0	carbamate ester; organochlorine compound; steroid phosphate
estramustine Estramustine: A nitrogen mustard linked to estradiol, usually as phosphate; used to treat prostatic neoplasms; also has radiation protective properties.. estramustine : A carbamate ester obtained by the formal condensation of the hydroxy group of 17beta-estradiol with the carboxy group of bis(2-chloroethyl)carbamic acid.	3.59	2	0	17beta-hydroxy steroid; carbamate ester; organochlorine compound	alkylating agent; antineoplastic agent; radiation protective agent
withaferin a withaferin A: an antiestrogen and phytogenic antineoplastic agent isolated from leaves of Withania somnifera Dun.; structure. withaferin A : A withanolide that is 5,6:22,26-diepoxyergosta-2,24-diene-1,26-dione substituted by hydroxy groups at positions 4 and 27 (the 4beta,5beta,6beta,22R stereoisomer). Isolated from Physalis longifolia, it exhibits cytotoxic activity.	2.81	3	0	27-hydroxy steroid; 4-hydroxy steroid; delta-lactone; enone; epoxy steroid; ergostanoid; primary alcohol; secondary alcohol; withanolide	antineoplastic agent; apoptosis inducer
phenethicillin phenethicillin: minor descriptor (85); major descriptor (63-84); on-line search PENICILLIN, PHENOXYMETHYL/AA (66-85); Index Medicus search PHENETHICILLIN (63-84); RN given refers to (2S-(2alpha,5alpha,6beta))-isomer. phenethicillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-phenoxypropanamido group.	2.04	1	0	penicillin allergen; penicillin
berbamine [no description available]	2.6	1	0	bisbenzylisoquinoline alkaloid; isoquinolines
noscapine Noscapine: A naturally occurring opium alkaloid that is a centrally acting antitussive agent.. (-)-noscapine : A benzylisoquinoline alkaloid that is 1,2,3,4-tetrahydroisoquinoline which is substituted by a 4,5-dimethoxy-3-oxo-1,3-dihydro-2-benzofuran-1-yl group at position 1, a methylenedioxy group at positions 6-7 and a methoxy group at position 8. Obtained from plants of the Papaveraceae family, it lacks significant painkilling properties and is primarily used for its antitussive (cough-suppressing) effects.	2.05	1	0	aromatic ether; benzylisoquinoline alkaloid; cyclic acetal; isobenzofuranone; organic heterobicyclic compound; organic heterotricyclic compound; tertiary amino compound	antineoplastic agent; antitussive; apoptosis inducer; plant metabolite
Harringtonine harringtonin: alkaloid C from Caphalotaxus fortunei	2.44	2	0	alkaloid
homoharringtonine Homoharringtonine: Semisynthetic derivative of harringtonine that acts as a protein synthesis inhibitor and induces APOPTOSIS in tumor cells. It is used in the treatment of MYELOID LEUKEMIA, CHRONIC.. omacetaxine mepesuccinate : A cephalotaxine-derived alkaloid ester obtained from Cephalotaxus harringtonia; used for the treatment of chronic or accelerated phase chronic myeloid leukaemia.	3.47	7	0	alkaloid ester; enol ether; organic heteropentacyclic compound; tertiary alcohol	anticoronaviral agent; antineoplastic agent; apoptosis inducer; protein synthesis inhibitor
acivicin [no description available]	2.04	1	0	isoxazoles; non-proteinogenic L-alpha-amino acid; organochlorine compound	antileishmanial agent; antimetabolite; antimicrobial agent; antineoplastic agent; EC 2.3.2.2 (gamma-glutamyltransferase) inhibitor; glutamine antagonist; metabolite
elesclomol [no description available]	2.08	1	0	carbohydrazide; thiocarbonyl compound	antineoplastic agent; apoptosis inducer
u-104 SLC-0111: a carbonic anhydrase inhibitor; structure in first source	2.6	1	0
wortmannin [no description available]	2.49	2	0	acetate ester; cyclic ketone; delta-lactone; organic heteropentacyclic compound	anticoronaviral agent; antineoplastic agent; autophagy inhibitor; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; geroprotector; Penicillium metabolite; radiosensitizing agent
2,2-bis(hydroxymethyl)-1-azabicyclo(2,2,2,)octan-3-one 2,2-bis(hydroxymethyl)-1-azabicyclo(2,2,2,)octan-3-one: structure in first source	2.1	1	0	cyclic ketone; quinuclidines
withanolides Withanolides: Ergostane derivatives of 28 carbons with oxygens at C1, C22, and C26 positions and the side chain cyclized. They are found in WITHANIA plant genus and have cytotoxic and other effects.	2.04	1	0
rocaglamide rocaglamide: RN refers to (1alpha,2alpha,3beta,3abeta,8bbeta)-isomer; isolated from stems of Aglaia elliptifolia; structure given in first source. rocaglamide : An organic heterotricyclic compound that is 2,3,3a,8b-tetrahydro-1H-benzo[b]cyclopenta[d]furan substituted by hydroxy groups at positions 1 and 8b, methoxy groups at positions 6 and 8, a 4-methoxyphenyl group at position 3a, a phenyl group at position 3 and a N,N-dimethylcarbamoyl group at position 1. Isolated from Aglaia odorata and Aglaia duperreana, it exhibits antineoplastic activity.	2.05	1	0	monocarboxylic acid amide; monomethoxybenzene; organic heterotricyclic compound	antileishmanial agent; antineoplastic agent; metabolite
trimethoprim, sulfamethoxazole drug combination Trimethoprim, Sulfamethoxazole Drug Combination: A drug combination with broad-spectrum antibacterial activity against both gram-positive and gram-negative organisms. It is effective in the treatment of many infections, including PNEUMOCYSTIS PNEUMONIA in AIDS.. co-trimoxazole : A two-component mixture comprising trimethoprim and sulfamethoxazole.	6.38	3	1
girolline girolline: has antineoplastic activity	3.15	1	0
7-hydroxy-5-methyl-2-(2-oxopropyl)-8-[3,4,5-trihydroxy-6-(hydroxymethyl)-2-oxanyl]-1-benzopyran-4-one [no description available]	2.6	1	0	glycoside
acylfulvene acylfulvene: an antineoplastic agent; structure given in first source; an analog of illudin	2.6	1	0
o-(chloroacetylcarbamoyl)fumagillol O-(Chloroacetylcarbamoyl)fumagillol: Semisynthetic analog of fumagillin (a cyclohexane-sesquiterpene antibiotic isolated from ASPERGILLUS FUMIGATUS) that inhibits angiogenesis.. O-(chloroacetylcarbamoyl)fumagillol : A carbamate ester that is fumagillol in which the hydroxy group has been converted to the corresponding N-(chloroacetyl)carbamate derivative.	2.05	1	0	carbamate ester; organochlorine compound; semisynthetic derivative; sesquiterpenoid; spiro-epoxide	angiogenesis inhibitor; antineoplastic agent; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; methionine aminopeptidase 2 inhibitor; retinoic acid receptor alpha antagonist
nsc 663284 NSC 663284: structure in first source	2.08	1	0	quinolone
nsc 680410 NSC 680410: a bcr/abl kinase inhibitor; structure in first source	2.44	2	0
calcein am calcein AM: a non-fluorescent compound cleaved to a fluorescent compound by non-specific intracellular esterases. calcein am : An organic heteropentacyclic compound that is calcein in which all four carboxy group hydrogens have been substituted by (acetyloxy)methoxy groups and the hyrodgens of the two hydroxy groups have been substituted by acetyl groups. It is a a non-fluorescent probe cleaved to a fluorescent probe by non-specific intracellular esterases.	2.31	1	0	2-benzofurans; acetate ester; gamma-lactone; organic heteropentacyclic compound; oxaspiro compound; xanthene dye	fluorochrome
ritonavir Ritonavir: An HIV protease inhibitor that works by interfering with the reproductive cycle of HIV. It also inhibits CYTOCHROME P-450 CYP3A.. ritonavir : An L-valine derivative that is L-valinamide in which alpha-amino group has been acylated by a [(2-isopropyl-1,3-thiazol-4-yl)methyl]methylcarbamoyl group and in which a hydrogen of the carboxamide amino group has been replaced by a (2R,4S,5S)-4-hydroxy-1,6-diphenyl-5-{[(1,3-thiazol-5-ylmethoxy)carbonyl]amino}hexan-2-yl group. A CYP3A inhibitor and antiretroviral drug from the protease inhibitor class used to treat HIV infection and AIDS, it is often used as a fixed-dose combination with another protease inhibitor, lopinavir. Also used in combination with dasabuvir sodium hydrate, ombitasvir and paritaprevir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.	5.07	7	0	1,3-thiazoles; carbamate ester; carboxamide; L-valine derivative; ureas	antiviral drug; environmental contaminant; HIV protease inhibitor; xenobiotic
rocaglaol rocaglaol: a cytotoxic cyclopenta(b)benzofuran from the bark of Aglaia crassinervia; structure in first source	2.05	1	0
tizoxanide tizoxanide: major metabolite of nitazoxanide; structure in first source	2.6	1	0	salicylamides
sc 144 SC 144: an antineoplastic agent; structure in first source	2.21	1	0
bardoxolone methyl methyl 2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oate: structure in first source	2.08	1	0	cyclohexenones
1-hydroxy-2,1-benzoxaborole 1-hydroxy-2,1-benzoxaborole : A member of the class of benzoxaboroles that is 2,1-benzoxaborole in which the hydrogen attached to the boron atom is replaced by a hydroxy group.	2.15	1	0	benzoxaborole
nexavar [no description available]	2.05	1	0	organosulfonate salt
dihydropyridines Dihydropyridines: Pyridine moieties which are partially saturated by the addition of two hydrogen atoms in any position.	2.63	2	0
nsc 23766 [no description available]	2.08	1	0	aminopyrimidine; aminoquinoline; primary amino compound; secondary amino compound; tertiary amino compound	antiviral agent; apoptosis inducer; EC 3.6.5.2 (small monomeric GTPase) inhibitor; muscarinic antagonist
5-amino-8-hydroxyquinoline 5-amino-8-hydroxyquinoline: structure in first source	3.87	3	0
gant 61 GANT 61: a sonic hedgehog pathway inhibitor and Gli inhibitor; structure in first source. GANT61 : An aminal that is hexahydropyrimidine which is substituted on each nitrogen by a 2-(dimethylamino)benzyl group, and at the aminal carbon by a pyridin-4-yl group. A Hedgehog signaling pathway and Gli protein inhibitor.	3.51	1	0	aminal; dialkylarylamine; pyridines; substituted aniline; tertiary amino compound	antineoplastic agent; apoptosis inducer; glioma-associated oncogene inhibitor; Hedgehog signaling pathway inhibitor
leupeptins Leupeptins: A group of acylated oligopeptides produced by Actinomycetes that function as protease inhibitors. They have been known to inhibit to varying degrees trypsin, plasmin, KALLIKREINS, papain and the cathepsins.	10.11	98	0
carboplatin [no description available]	12.08	28	17
glycogen glycogen : A polydisperse, highly branched glucan composed of chains of D-glucopyranose residues in alpha(1->4) glycosidic linkage, joined together by alpha(1->6) glycosidic linkages. A small number of alpha(1->3) glycosidic linkages and some cumulative alpha(1->6) links also may occur. The branches in glycogen typically contain 8 to 12 glucose residues.	2.1	1	0
n-acetylneuraminic acid N-Acetylneuraminic Acid: An N-acyl derivative of neuraminic acid. N-acetylneuraminic acid occurs in many polysaccharides, glycoproteins, and glycolipids in animals and bacteria. (From Dorland, 28th ed, p1518). N-acetylneuraminic acid : An N-acylneuraminic acid where the N-acyl group is specified as acetyl.	2.63	2	0	N-acetylneuraminic acids	antioxidant; bacterial metabolite; EC 3.2.1.18 (exo-alpha-sialidase) inhibitor; human metabolite; mouse metabolite
glucosamine D-glucosamine : An amino sugar whose structure comprises D-glucose having an amino substituent at position 2.. 2-amino-2-deoxy-D-glucopyranose : A D-glucosamine whose structure comprises D-glucopyranose having an amino substituent at position 2.	2.05	1	0	D-glucosamine	Escherichia coli metabolite; geroprotector; mouse metabolite
mevalonic acid Mevalonic Acid: A dihydroxy monocarboxylic acid and precursor in the biosynthetic pathway known as the mevalonate pathway, which produces terpenes and steroids that are vital for diverse cellular functions.. mevalonic acid : A racemate composed of equimolar amounts of (R)- and (S)-mevalonic acid.. (R)-mevalonic acid : The (R)-enantiomer of mevalonic acid.	2.31	1	0	3,5-dihydroxy-3-methylpentanoic acid
oxytocin Oxytocin: A nonapeptide hormone released from the neurohypophysis (PITUITARY GLAND, POSTERIOR). It differs from VASOPRESSIN by two amino acids at residues 3 and 8. Oxytocin acts on SMOOTH MUSCLE CELLS, such as causing UTERINE CONTRACTIONS and MILK EJECTION.. oxytocin : A cyclic nonapeptide hormone with amino acid sequence CYIQNCPLG that also acts as a neurotransmitter in the brain; the principal uterine-contracting and milk-ejecting hormone of the posterior pituitary. Together with the neuropeptide vasopressin, it is believed to influence social cognition and behaviour.	3.23	1	0	heterodetic cyclic peptide; peptide hormone	oxytocic; vasodilator agent
puromycin [no description available]	2.06	1	0	puromycins	antiinfective agent; antimicrobial agent; antineoplastic agent; EC 3.4.11.14 (cytosol alanyl aminopeptidase) inhibitor; EC 3.4.14.2 (dipeptidyl-peptidase II) inhibitor; nucleoside antibiotic; protein synthesis inhibitor
tosylphenylalanyl chloromethyl ketone Tosylphenylalanyl Chloromethyl Ketone: An inhibitor of Serine Endopeptidases. Acts as alkylating agent and is known to interfere with the translation process.. N-tosyl-L-phenylalanyl chloromethyl ketone : The N-tosyl derivative of L-phenylalanyl chloromethyl ketone.	3.38	2	0	alpha-chloroketone; sulfonamide	alkylating agent; serine proteinase inhibitor
pentostatin Pentostatin: A potent inhibitor of ADENOSINE DEAMINASE. The drug induces APOPTOSIS of LYMPHOCYTES, and is used in the treatment of many lymphoproliferative malignancies, particularly HAIRY CELL LEUKEMIA. It is also synergistic with some other antineoplastic agents and has immunosuppressive activity.. pentostatin : A member of the class of coformycins that is coformycin in which the hydroxy group at position 2' is replaced with a hydrogen. It is a drug used for the treatment of hairy cell leukaemia.	4.81	5	0	coformycins	antimetabolite; antineoplastic agent; Aspergillus metabolite; bacterial metabolite; EC 3.5.4.4 (adenosine deaminase) inhibitor
eriodictyol eriodictyol: structure. eriodictyol : A tetrahydroxyflavanone that is flavanone substituted by hydroxy groups at positions 5, 7, 3' and 4' respectively.	2.25	1	0	3'-hydroxyflavanones; tetrahydroxyflavanone
arbutin hydroquinone O-beta-D-glucopyranoside : A monosaccharide derivative that is hydroquinone attached to a beta-D-glucopyranosyl residue at position 4 via a glycosidic linkage.	2.6	1	0	beta-D-glucoside; monosaccharide derivative	Escherichia coli metabolite; plant metabolite
strychnine Strychnine: An alkaloid found in the seeds of STRYCHNOS NUX-VOMICA. It is a competitive antagonist at glycine receptors and thus a convulsant. It has been used as an analeptic, in the treatment of nonketotic hyperglycinemia and sleep apnea, and as a rat poison.. strychnine : A monoterpenoid indole alkaloid that is strychnidine bearing a keto substituent at the 10-position.	2.07	1	0	monoterpenoid indole alkaloid; organic heteroheptacyclic compound	avicide; cholinergic antagonist; glycine receptor antagonist; neurotransmitter agent; rodenticide
quinidine Quinidine: An optical isomer of quinine, extracted from the bark of the CHINCHONA tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular ACTION POTENTIALS, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission.. quinidine : A cinchona alkaloid consisting of cinchonine with the hydrogen at the 6-position of the quinoline ring substituted by methoxy.	4.29	5	0	cinchona alkaloid	alpha-adrenergic antagonist; anti-arrhythmia drug; antimalarial; drug allergen; EC 1.14.13.181 (13-deoxydaunorubicin hydroxylase) inhibitor; EC 3.6.3.44 (xenobiotic-transporting ATPase) inhibitor; muscarinic antagonist; P450 inhibitor; potassium channel blocker; sodium channel blocker
conessine conessine : A steroid alkaloid that is con-5-enine substituted by a N,N-dimethylamino group at position 3. It has been isolated from the plant species of the family Apocynaceae.	2.6	1	0	steroid alkaloid; tertiary amino compound	antibacterial agent; antimalarial; H3-receptor antagonist; plant metabolite
meropenem Meropenem: A thienamycin derivative antibacterial agent that is more stable to renal dehydropeptidase I than IMIPENEM, but does not need to be given with an enzyme inhibitor such as CILASTATIN. It is used in the treatment of bacterial infections, including infections in immunocompromised patients.. meropenem : A carbapenemcarboxylic acid in which the azetidine and pyrroline rings carry 1-hydroxymethyl and in which the azetidine and pyrroline rings carry 1-hydroxymethyl and 5-(dimethylcarbamoyl)pyrrolidin-3-ylthio substituents respectively.	4.8	5	0	alpha,beta-unsaturated monocarboxylic acid; carbapenemcarboxylic acid; organic sulfide; pyrrolidinecarboxamide	antibacterial agent; antibacterial drug; drug allergen
griseofulvin Griseofulvin: An antifungal agent used in the treatment of TINEA infections.. griseofulvin : An oxaspiro compound produced by Penicillium griseofulvum. It is used by mouth as an antifungal drug for infections involving the scalp, hair, nails and skin that do not respond to topical treatment.	3.59	2	0	1-benzofurans; antibiotic antifungal drug; benzofuran antifungal drug; organochlorine compound; oxaspiro compound	antibacterial agent; Penicillium metabolite
cefoxitin Cefoxitin: A semisynthetic cephamycin antibiotic resistant to beta-lactamase.. cefoxitin : A semisynthetic cephamycin antibiotic which, in addition to the methoxy group at the 7alpha position, has 2-thienylacetamido and carbamoyloxymethyl side-groups. It is resistant to beta-lactamase.	3.58	2	0	beta-lactam antibiotic allergen; cephalosporin; cephamycin; semisynthetic derivative	antibacterial drug
digitoxin Digitoxin: A cardiac glycoside sometimes used in place of DIGOXIN. It has a longer half-life than digoxin; toxic effects, which are similar to those of digoxin, are longer lasting. (From Martindale, The Extra Pharmacopoeia, 30th ed, p665). digitoxin : A cardenolide glycoside in which the 3beta-hydroxy group of digitoxigenin carries a 2,6-dideoxy-beta-D-ribo-hexopyranosyl-(1->4)-2,6-dideoxy-beta-D-ribo-hexopyranosyl-(1->4)-2,6-dideoxy-beta-D-ribo-hexopyranosyl trisaccharide chain.	2.75	3	0	cardenolide glycoside	EC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor
saquinavir Saquinavir: An HIV protease inhibitor which acts as an analog of an HIV protease cleavage site. It is a highly specific inhibitor of HIV-1 and HIV-2 proteases, and also inhibits CYTOCHROME P-450 CYP3A.. saquinavir : An aspartic acid derivative obtained by formal condensation of the primary amino group of (2S,3R)-4-[(3S,4aS,8aS)-3-(tert-butylcarbamoyl)octahydroisoquinolin-2(1H)-yl]-3-hydroxy-1-phenylbutan-2-ylamine with the carboxy group of N(2)(-quinolin-2-ylcarbonyl)-L-asparagine. An inhibitor of HIV-1 protease.	4.29	5	0	L-asparagine derivative; quinolines	antiviral drug; HIV protease inhibitor
pancuronium Pancuronium: A bis-quaternary steroid that is a competitive nicotinic antagonist. As a neuromuscular blocking agent it is more potent than CURARE but has less effect on the circulatory system and on histamine release.. pancuronium : A steroid ester in which a 5alpha-androstane skeleton is C-3alpha- and C-17beta-disubstituted with acetoxy groups and 2beta- and 16beta-disubstituted with 1-methylpiperidinium-1-yl groups. It is a non-depolarizing curare-mimetic muscle relaxant.	3.58	2	0	acetate ester; steroid ester	cholinergic antagonist; muscle relaxant; nicotinic antagonist
rocuronium Rocuronium: An androstanol non-depolarizing neuromuscular blocking agent. It has a mono-quaternary structure and is a weaker nicotinic antagonist than PANCURONIUM.. rocuronium : A 5alpha-androstane compound having 3alpha-hydroxy-, 17beta-acetoxy-, 2beta-morpholino- and 16beta-N-allyllyrrolidinium substituents.	2.04	1	0	3alpha-hydroxy steroid; acetate ester; androstane; morpholines; quaternary ammonium ion; tertiary amino compound	drug allergen; muscle relaxant; neuromuscular agent
abacavir abacavir: a carbocyclic nucleoside with potent selective anti-HIV activity. abacavir : A 2,6-diaminopurine that is (1S)-cyclopent-2-en-1-ylmethanol in which the pro-R hydrogen at the 4-position is substituted by a 2-amino-6-(cyclopropylamino)-9H-purin-9-yl group. A nucleoside analogue reverse transcriptase inhibitor (NRTI) with antiretroviral activity against HIV, it is used (particularly as the sulfate) with other antiretrovirals in combination therapy of HIV infection.	3.91	3	0	2,6-diaminopurines	antiviral drug; drug allergen; HIV-1 reverse transcriptase inhibitor
netilmicin Netilmicin: Semisynthetic 1-N-ethyl derivative of SISOMYCIN, an aminoglycoside antibiotic with action similar to gentamicin, but less ear and kidney toxicity.	2.45	2	0
trimethaphan camsylate trimethaphan camsylate : The (S)-camphorsulfonate salt of trimethaphan.	2.05	1	0
perindopril erbumine [no description available]	2.08	1	0	addition compound	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
miglitol [no description available]	3.87	3	0	piperidines
metyrosine alpha-methyl-L-tyrosine : An L-tyrosine derivative that consists of L-tyrosine bearing an additional methyl substituent at position 2. An inhibitor of the enzyme tyrosine 3-monooxygenase, and consequently of the synthesis of catecholamines. It is used to control the symptoms of excessive sympathetic stimulation in patients with pheochromocytoma.	3.23	1	0	L-tyrosine derivative; non-proteinogenic L-alpha-amino acid	antihypertensive agent; EC 1.14.16.2 (tyrosine 3-monooxygenase) inhibitor
rocuronium bromide rocuronium bromide : The organic bromide salt of a 5alpha androstane compound having 3alpha-hydroxy-, 17beta-acetoxy-, 2beta-morpholino- and 16beta-N-allyllyrrolidinium substituents.	2.08	1	0	organic bromide salt; quaternary ammonium salt	muscle relaxant; neuromuscular agent
erythromycin estolate Erythromycin Estolate: A macrolide antibiotic, produced by Streptomyces erythreus. It is the lauryl sulfate salt of the propionic ester of erythromycin. This erythromycin salt acts primarily as a bacteriostatic agent. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.	2.05	1	0	aminoglycoside sulfate salt; erythromycin derivative	enzyme inhibitor
linezolid [no description available]	4.13	4	0	acetamides; morpholines; organofluorine compound; oxazolidinone	antibacterial drug; protein synthesis inhibitor
brucine brucine: was heading 1991-94 (see under STRYCHNINE 1975-90); DIMETHOXYSTRYCHNINE was see BRUCINE 1975-94; use STRYCHNINE to search BRUCINE 1975-94; very toxic alkaloid from Nux vomica similar to strychnine; used as reagent in analytical chemistry; was MH 1991-94	2.07	1	0	monoterpenoid indole alkaloid; organic heteroheptacyclic compound
decursin decursin: activates protein kinase C; isolated from the root of Angelica gigas; RN given for (S)-isomer; structure in first source	2.06	1	0	coumarins
cephaelin cephaelin: do not confuse with cephalin of brain; after emetine this is the most important alkaloid of ipecac; protein synthesis inhibitor. cephaeline : A pyridoisoquinoline comprising emetam having a hydroxy group at the 6'-position and methoxy substituents at the 7'-, 10- and 11-positions.	2.6	1	0	pyridoisoquinoline
genipin [no description available]	2.06	1	0	iridoid monoterpenoid	anti-inflammatory agent; antioxidant; apoptosis inhibitor; cross-linking reagent; hepatotoxic agent; uncoupling protein inhibitor
(-)-usnic acid (-)-usnic acid : The (-)-enantiomer of usnic acid.	2.6	1	0	usnic acid	EC 1.13.11.27 (4-hydroxyphenylpyruvate dioxygenase) inhibitor
cyclopamine [no description available]	2.05	1	0	piperidines	glioma-associated oncogene inhibitor
acetylleucyl-leucyl-norleucinal acetylleucyl-leucyl-norleucinal: a proteasome inhibitor. acetylleucyl-leucyl-norleucinal : A tripeptide composed of N-acetylleucyl, leucyl and norleucinal residues joined in sequence.	4.37	7	0	aldehyde; tripeptide	cysteine protease inhibitor
bq 123 cyclo(Trp-Asp-Pro-Val-Leu): derived from the modification of a natural lead of BE-18257B, an endothelin A receptor antagonist; has neuroprotective activity; amino acid sequence given in first source	2.13	1	0	cyclic peptide
devazepide Devazepide: A derivative of benzodiazepine that acts on the cholecystokinin A (CCKA) receptor to antagonize CCK-8's (SINCALIDE) physiological and behavioral effects, such as pancreatic stimulation and inhibition of feeding.. devazepide : An indolecarboxamide obtained by formal condensation of the carboxy group of indole-2-carboxylic acid with the exocyclic amino group of (3S)-3-amino-1-methyl-5-phenyl-1,3-dihydro-1,4-benzodiazepin-2-one. A cholecystokinin antagonist used for treatment of gastrointestinal disorders.	2.05	1	0	1,4-benzodiazepinone; indolecarboxamide	antineoplastic agent; apoptosis inducer; cholecystokinin antagonist; gastrointestinal drug
clindamycin phosphate [no description available]	3.23	1	0
sodium arsenite sodium arsenite : An inoganic sodium salt with formula with formula NaAsO2.	2.02	1	0	arsenic molecular entity; inorganic sodium salt	antibacterial agent; antifungal agent; antineoplastic agent; carcinogenic agent; herbicide; insecticide; rodenticide
pemirolast potassium salt [no description available]	2.08	1	0
eplerenone Eplerenone: A spironolactone derivative and selective ALDOSTERONE RECEPTOR antagonist that is used in the management of HYPERTENSION and CONGESTIVE HEART FAILURE, post-MYOCARDIAL INFARCTION.	3.61	2	0	3-oxo-Delta(4) steroid; epoxy steroid; gamma-lactone; methyl ester; organic heteropentacyclic compound; oxaspiro compound; steroid acid ester	aldosterone antagonist; antihypertensive agent
tolterodine [no description available]	3.86	3	0	tertiary amine	antispasmodic drug; muscarinic antagonist; muscle relaxant
doxorubicin hydrochloride [no description available]	3.62	2	0	anthracycline
erythromycin ethylsuccinate Erythromycin Ethylsuccinate: A macrolide antibiotic, produced by Streptomyces erythreus. This compound is an ester of erythromycin base and succinic acid. It acts primarily as a bacteriostatic agent. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.. erythromycin ethylsuccinate : A erythromycin derivative that is erythromycin A in which the hydroxy group at position 3R is substituted by a (4-ethoxy-4-oxobutanoyl)oxy group. It is used for the treatment of a wide variety of bacterial infections.	2.05	1	0	cyclic ketone; erythromycin derivative; ethyl ester; succinate ester
ao 128 AO 128: alpha-glucosidase inhibitor; structure given in first source	2.47	2	0	organic molecular entity
loteprednol etabonate Loteprednol Etabonate: An androstadiene derivative corticosteroid that is used as an ANTI-ALLERGIC AGENT for the treatment of inflammatory and allergic eye conditions.	2.08	1	0	11beta-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; etabonate ester; organochlorine compound; steroid acid ester; steroid ester	anti-inflammatory drug
darifenacin darifenacin : 2-[(3S)-1-Ethylpyrrolidin-3-yl]-2,2-diphenylacetamide in which one of the hydrogens at the 2-position of the ethyl group is substituted by a 2,3-dihydro-1-benzofuran-5-yl group. It is a selective antagonist for the M3 muscarinic acetylcholine receptor, which is primarily responsible for bladder muscle contractions, and is used as the hydrobromide salt in the management of urinary incontinence.	3.58	2	0	1-benzofurans; monocarboxylic acid amide; pyrrolidines	antispasmodic drug; muscarinic antagonist
fluticasone propionate fluticasone propionate : A trifluorinated corticosteroid that consists of 6alpha,9-difluoro-11beta,17alpha-dihydroxy-17beta-{[(fluoromethyl)sulfanyl]carbonyl}-16-methyl-3-oxoandrosta-1,4-diene bearing a propionyl substituent at position 17; has anti-inflammatory, anti-asthmatic and anti-allergic activity.	2.46	2	0	11beta-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; corticosteroid; fluorinated steroid; propanoate ester; steroid ester; thioester	adrenergic agent; anti-allergic agent; anti-asthmatic drug; anti-inflammatory drug; bronchodilator agent; dermatologic drug
acarbose [no description available]	2.45	2	0	amino cyclitol; glycoside
ergosterol [no description available]	2.04	1	0	3beta-hydroxy-Delta(5)-steroid; 3beta-sterol; ergostanoid; phytosterols	fungal metabolite; Saccharomyces cerevisiae metabolite
trichostatin a trichostatin A: chelates zinc ion in the active site of histone deacetylases, resulting in preventing histone unpacking so DNA is less available for transcription; do not confuse with TRICHOSANTHIN which is a protein; found in STREPTOMYCES	4.09	14	0	antibiotic antifungal agent; hydroxamic acid; trichostatin	bacterial metabolite; EC 3.5.1.98 (histone deacetylase) inhibitor; geroprotector
tretinoin Tretinoin: An important regulator of GENE EXPRESSION during growth and development, and in NEOPLASMS. Tretinoin, also known as retinoic acid and derived from maternal VITAMIN A, is essential for normal GROWTH; and EMBRYONIC DEVELOPMENT. An excess of tretinoin can be teratogenic. It is used in the treatment of PSORIASIS; ACNE VULGARIS; and several other SKIN DISEASES. It has also been approved for use in promyelocytic leukemia (LEUKEMIA, PROMYELOCYTIC, ACUTE).. retinoic acid : A retinoid consisting of 3,7-dimethylnona-2,4,6,8-tetraenoic acid substituted at position 9 by a 2,6,6-trimethylcyclohex-1-en-1-yl group (geometry of the four exocyclic double bonds is not specified).. all-trans-retinoic acid : A retinoic acid in which all four exocyclic double bonds have E- (trans-) geometry.	7.22	16	0	retinoic acid; vitamin A	anti-inflammatory agent; antineoplastic agent; antioxidant; AP-1 antagonist; human metabolite; keratolytic drug; retinoic acid receptor agonist; retinoid X receptor agonist; signalling molecule
arachidonic acid icosa-5,8,11,14-tetraenoic acid : Any icosatetraenoic acid with the double bonds at positions 5, 8, 11 and 14.. arachidonate : A long-chain fatty acid anion resulting from the removal of a proton from the carboxy group of arachidonic acid.	2.1	1	0	icosa-5,8,11,14-tetraenoic acid; long-chain fatty acid; omega-6 fatty acid	Daphnia galeata metabolite; EC 3.1.1.1 (carboxylesterase) inhibitor; human metabolite; mouse metabolite
alpha-cyclodextrin alpha-cyclodextrin : A cycloamylose composed of six alpha-(1->4) linked D-glucopyranose units.	2.13	1	0	cyclodextrin
farnesol Farnesol: A colorless liquid extracted from oils of plants such as citronella, neroli, cyclamen, and tuberose. It is an intermediate step in the biological synthesis of cholesterol from mevalonic acid in vertebrates. It has a delicate odor and is used in perfumery. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed). (2-trans,6-trans)-farnesol : The (2-trans,6-trans)-stereoisomer of farnesol.. farnesol : A farnesane sesquiterpenoid that is dodeca-2,6,10-triene substituted by methyl groups at positions 3, 7 and 11 and a hydroxy group at position 1.	7.11	1	0	farnesol	plant metabolite
resveratrol trans-resveratrol : A resveratrol in which the double bond has E configuration.	7.78	11	1	resveratrol	antioxidant; phytoalexin; plant metabolite; quorum sensing inhibitor; radical scavenger
retinol Vitamin A: Retinol and derivatives of retinol that play an essential role in metabolic functioning of the retina, the growth of and differentiation of epithelial tissue, the growth of bone, reproduction, and the immune response. Dietary vitamin A is derived from a variety of CAROTENOIDS found in plants. It is enriched in the liver, egg yolks, and the fat component of dairy products.. vitamin A : Any member of a group of fat-soluble retinoids produced via metabolism of provitamin A carotenoids that exhibit biological activity against vitamin A deficiency. Vitamin A is involved in immune function, vision, reproduction, and cellular communication.. all-trans-retinol : A retinol in which all four exocyclic double bonds have E- (trans-) geometry.. retinol : A retinoid consisting of 3,7-dimethylnona-2,4,6,8-tetraen-1-ol substituted at position 9 by a 2,6,6-trimethylcyclohex-1-en-1-yl group (geometry of the four exocyclic double bonds is not specified).	3.59	2	0	retinol; vitamin A	human metabolite; mouse metabolite; plant metabolite
alpha-D-fructofuranose 1,6-bisphosphate alpha-D-fructofuranose 1,6-bisphosphate : A D-fructofuranose 1,6-bisphosphate with an alpha-configuration at the anomeric position.	2.05	1	0	D-fructofuranose 1,6-bisphosphate
docosahexaenoate efalex: a mixture of fish oil and primrose oil; used as a high-docosahexaenoic acid fatty acid supplement. docosahexaenoic acid : Any C22 polyunsaturated fatty acid containing six double bonds.. docosahexaenoate : A polyunsaturated fatty acid anion that is the conjugate base of docosahexaenoic acid, obtained by deprotonation of the carboxy group; major species at pH 7.3.. all-cis-docosa-4,7,10,13,16,19-hexaenoic acid : A docosahexaenoic acid having six cis-double bonds at positions 4, 7, 10, 13, 16 and 19.	2.05	1	0	docosahexaenoic acid; omega-3 fatty acid	algal metabolite; antineoplastic agent; Daphnia tenebrosa metabolite; human metabolite; mouse metabolite; nutraceutical
oleic acid Oleic Acid: An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed). oleic acid : An octadec-9-enoic acid in which the double bond at C-9 has Z (cis) stereochemistry.	2.05	1	0	octadec-9-enoic acid	antioxidant; Daphnia galeata metabolite; EC 3.1.1.1 (carboxylesterase) inhibitor; Escherichia coli metabolite; mouse metabolite; plant metabolite; solvent
tacrolimus Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro.. tacrolimus (anhydrous) : A macrolide lactam containing a 23-membered lactone ring, originally isolated from the fermentation broth of a Japanese soil sample that contained the bacteria Streptomyces tsukubaensis.	15.76	17	4	macrolide lactam	bacterial metabolite; immunosuppressive agent
ferulic acid ferulate : A monocarboxylic acid anion obtained by the deprotonation of the carboxy group of ferulic acid.	2.31	1	0	ferulic acids	anti-inflammatory agent; antioxidant; apoptosis inhibitor; cardioprotective agent; MALDI matrix material; plant metabolite
cerivastatin cerivastatin: cerivastatin is the ((E)-(+))-isomer; structure given in first source. cerivastatin : (3R,5S)-3,5-dihydroxyhept-6-enoic acid in which the (7E)-hydrogen is substituted by a 4-(4-fluorophenyl)-2,6-diisopropyl-5-(methoxymethyl)pyridin-3-yl group. Formerly used (as its sodium salt) to lower cholesterol and prevent cardiovascular disease, it was withdrawn from the market worldwide in 2001 following reports of a severe form of muscle toxicity.	2.45	2	0	dihydroxy monocarboxylic acid; pyridines; statin (synthetic)
rosuvastatin rosuvastatin : A dihydroxy monocarboxylic acid that is (6E)-7-{4-(4-fluorophenyl)-2-[methyl(methylsulfonyl)amino]-6-(propan-2-yl)pyrimidin-5-yl} hept-6-enoic acid carrying two hydroxy substituents at positions 3 and 5 (the 3R,5S-diastereomer).	3.86	3	0	dihydroxy monocarboxylic acid; monofluorobenzenes; pyrimidines; statin (synthetic); sulfonamide	anti-inflammatory agent; antilipemic drug; cardioprotective agent; CETP inhibitor; environmental contaminant; xenobiotic
cocaine Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake.. cocaine : A tropane alkaloid obtained from leaves of the South American shrub Erythroxylon coca.	2.45	2	0	benzoate ester; methyl ester; tertiary amino compound; tropane alkaloid	adrenergic uptake inhibitor; central nervous system stimulant; dopamine uptake inhibitor; environmental contaminant; local anaesthetic; mouse metabolite; plant metabolite; serotonin uptake inhibitor; sodium channel blocker; sympathomimetic agent; vasoconstrictor agent; xenobiotic
eicosapentaenoic acid icosapentaenoic acid : Any straight-chain, C20 polyunsaturated fatty acid having five C=C double bonds.. all-cis-5,8,11,14,17-icosapentaenoic acid : An icosapentaenoic acid having five cis-double bonds at positions 5, 8, 11, 14 and 17.	3.26	5	0	icosapentaenoic acid; omega-3 fatty acid	anticholesteremic drug; antidepressant; antineoplastic agent; Daphnia galeata metabolite; fungal metabolite; micronutrient; mouse metabolite; nutraceutical
thapsigargin Thapsigargin: A sesquiterpene lactone found in roots of THAPSIA. It inhibits SARCOPLASMIC RETICULUM CALCIUM-TRANSPORTING ATPASES.. thapsigargin : An organic heterotricyclic compound that is a hexa-oxygenated 6,7-guaianolide isolated fron the roots of Thapsia garganica L., Apiaceae. A potent skin irritant, it is used in traditional medicine as a counter-irritant. Thapsigargin inhibits Ca(2+)-transporting ATPase mediated uptake of calcium ions into sarcoplasmic reticulum and is used in experimentation examining the impacts of increasing cytosolic calcium concentrations.	3.94	12	0	butyrate ester; organic heterotricyclic compound; sesquiterpene lactone	calcium channel blocker; EC 3.6.3.8 (Ca(2+)-transporting ATPase) inhibitor
mycophenolic acid Mycophenolic Acid: Compound derived from Penicillium stoloniferum and related species. It blocks de novo biosynthesis of purine nucleotides by inhibition of the enzyme inosine monophosphate dehydrogenase (IMP DEHYDROGENASE). Mycophenolic acid exerts selective effects on the immune system in which it prevents the proliferation of T-CELLS, LYMPHOCYTES, and the formation of antibodies from B-CELLS. It may also inhibit recruitment of LEUKOCYTES to sites of INFLAMMATION.. mycophenolate : A monocarboxylic acid anion resulting from the removal of a proton from the carboxy group of mycophenolic acid.. mycophenolic acid : A member of the class of 2-benzofurans that is 2-benzofuran-1(3H)-one which is substituted at positions 4, 5, 6, and 7 by methyl, methoxy, (2E)-5-carboxy-3-methylpent-2-en-1-yl, and hydroxy groups, respectively. It is an antibiotic produced by Penicillium brevi-compactum, P. stoloniferum, P. echinulatum and related species. An immunosuppressant, it is widely used (partiularly as its sodium salt and as the 2-(morpholin-4-yl)ethyl ester prodrug, mycophenolate mofetil) to prevent tissue rejection following organ transplants and for the treatment of certain autoimmune diseases.	10.84	11	0	2-benzofurans; gamma-lactone; monocarboxylic acid; phenols	anticoronaviral agent; antimicrobial agent; antineoplastic agent; EC 1.1.1.205 (IMP dehydrogenase) inhibitor; environmental contaminant; immunosuppressive agent; mycotoxin; Penicillium metabolite; xenobiotic
mupirocin Mupirocin: A topically used antibiotic from a strain of Pseudomonas fluorescens. It has shown excellent activity against gram-positive staphylococci and streptococci. The antibiotic is used primarily for the treatment of primary and secondary skin disorders, nasal infections, and wound healing.. mupirocin : An alpha,beta-unsaturated ester resulting from the formal condensation of the alcoholic hydroxy group of 9-hydroxynonanoic acid with the carboxy group of (2E)-4-[(2S)-tetrahydro-2H-pyran-2-yl]-3-methylbut-2-enoic acid in which the tetrahydropyranyl ring is substituted at positions 3 and 4 by hydroxy groups and at position 5 by a {(2S,3S)-3-[(2S,3S)-3-hydroxybutan-2-yl]oxiran-2-yl}methyl group. Originally isolated from the Gram-negative bacterium Pseudomonas fluorescens, it is used as a topical antibiotic for the treatment of Gram-positive bacterial infections.	2.08	1	0	alpha,beta-unsaturated carboxylic ester; epoxide; monocarboxylic acid; oxanes; secondary alcohol; triol	antibacterial drug; bacterial metabolite; protein synthesis inhibitor
clindamycin Clindamycin: An antibacterial agent that is a semisynthetic analog of LINCOMYCIN.. clindamycin : A carbohydrate-containing antibiotic that is the semisynthetic derivative of lincomycin, a natural antibiotic.	3.86	3	0
lycopene [no description available]	2.6	1	0	acyclic carotene	antioxidant; plant metabolite
fosfomycin Fosfomycin: An antibiotic produced by Streptomyces fradiae.. fosfomycin : A phosphonic acid having an (R,S)-1,2-epoxypropyl group attached to phosphorus.	3.86	3	0	epoxide; phosphonic acids	antimicrobial agent; EC 2.5.1.7 (UDP-N-acetylglucosamine 1-carboxyvinyltransferase) inhibitor
zithromax Azithromycin: A semi-synthetic macrolide antibiotic structurally related to ERYTHROMYCIN. It has been used in the treatment of Mycobacterium avium intracellulare infections, toxoplasmosis, and cryptosporidiosis.. azithromycin : A macrolide antibiotic useful for the treatment of bacterial infections.	4.58	7	0	macrolide antibiotic	antibacterial drug; environmental contaminant; xenobiotic
geranylgeranyl pyrophosphate geranylgeranyl pyrophosphate: RN given refers to (E,E,E)-isomer. geranylgeranyl diphosphate : A polyprenol diphosphate having geranylgeranyl as the polyprenyl component.. 2-trans,6-trans,10-trans-geranylgeranyl diphosphate : The all-trans-isomer of geranylgeranyl diphosphate.	7.51	2	0	geranylgeranyl diphosphate	mouse metabolite
drf 2725 ragaglitazar: a phenoxazine analogue of phenyl propanoic acid; Ragaglitazar is a coligand of PPARalpha and PPARgamma	2.05	1	0
gw 3965 GW 3965: a liver X receptor ligand	2.08	1	0	diarylmethane
epothilone b [no description available]	2.44	2	0	epothilone; epoxide	antineoplastic agent; apoptosis inducer; microtubule-stabilising agent
y 27632 Y 27632: RN given for di-HCl salt; inhibits Rho-associated protein kinase; inhibits calcium sensitization to affect smooth muscle relaxation; structure in first source. Y-27632 : A monocarboxylic acid amide that is trans-[(1R)-1-aminoethyl]cyclohexanecarboxamide in which one of the nitrogens of the aminocarbony group is substituted by a pyridine nucleus. It has been shown to exhibit inhibitory activity against Rho-associated protein kinase (ROCK) enzyme.	2.81	3	0	aromatic amide
diethylstilbestrol Diethylstilbestrol: A synthetic nonsteroidal estrogen used in the treatment of menopausal and postmenopausal disorders. It was also used formerly as a growth promoter in animals. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), diethylstilbestrol has been listed as a known carcinogen. (Merck, 11th ed). diethylstilbestrol : An olefinic compound that is trans-hex-3-ene in which the hydrogens at positions 3 and 4 have been replaced by p-hydroxyphenyl groups.	2.05	1	0	olefinic compound; polyphenol	antifungal agent; antineoplastic agent; autophagy inducer; calcium channel blocker; carcinogenic agent; EC 1.1.1.146 (11beta-hydroxysteroid dehydrogenase) inhibitor; EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor; endocrine disruptor; xenoestrogen
bms 214662 7-cyano-2,3,4,5-tetrahydro-1-(1H-imidazol-4-ylmethyl)-3-(phenylmethyl)-4-(2-thienylsulfonyl)-1H-1,4-benzodiazepine: a farnesyltransferase inhibitor; structure in first source. BMS-214662 : A member of the class of benzodiazepines that is 2,3,4,5-tetrahydro-1H-1,4-benzodiazepine substituted by (1H-imidazol-5-yl)methyl, benzyl, (thiophen-2-yl)sulfonyl, and cyano groups at positions 1, 3R, 4 and 7, respectively. It is a potent inhibitor of farnesyltransferase (IC50 = 1.35nM) which was under clinical development for the treatment of solid tumors.	3.55	2	0	benzenes; benzodiazepine; imidazoles; nitrile; sulfonamide; thiophenes	antineoplastic agent; apoptosis inducer; EC 2.5.1.58 (protein farnesyltransferase) inhibitor
octreotide [no description available]	3.23	1	0
epothilone a Epothilones: A group of 16-member MACROLIDES which stabilize MICROTUBULES in a manner similar to PACLITAXEL. They were originally found in the myxobacterium Sorangium cellulosum, now renamed to Polyangium (MYXOCOCCALES).	6.22	9	0	epothilone; epoxide	antineoplastic agent; metabolite; microtubule-stabilising agent; tubulin modulator
eptifibatide [no description available]	3.58	2	0	homodetic cyclic peptide; macrocycle; organic disulfide	anticoagulant; platelet aggregation inhibitor
6-bromoindirubin-3'-oxime 6-bromoindirubin-3'-oxime: structure in first source. 6-bromoindirubin-3'-oxime : A member of the class of biindoles that is indirubin substituted at position 6 by a bromo group and in which the keto group at position 3' has undergone condensation with hydroxylamine to form the corresponding oxime.	2.52	2	0
purvalanol b purvalanol B: protein kinase inhibitor; structure in first source	2.08	1	0	purvalanol	protein kinase inhibitor
y-700 [no description available]	2.08	1	0
repsox RepSox: inhibits TGF-beta signaling; structure in first source appears to be incorrect	2.08	1	0	pyrazolopyridine
alitretinoin Alitretinoin: A retinoid that is used for the treatment of chronic hand ECZEMA unresponsive to topical CORTICOSTEROIDS. It is also used to treat cutaneous lesions associated with AIDS-related KAPOSI SARCOMA.	2.49	2	0	retinoic acid	antineoplastic agent; keratolytic drug; metabolite; retinoid X receptor agonist
roflumilast [no description available]	2.76	2	0	aromatic ether; benzamides; chloropyridine; cyclopropanes; organofluorine compound	anti-asthmatic drug; phosphodiesterase IV inhibitor
L-cycloserine L-cycloserine : A 4-amino-1,2-oxazolidin-3-one that has S configuration. An antibiotic isolated from Erwinia uredovora.	2.6	1	0	4-amino-1,2-oxazolidin-3-one	anti-HIV agent; anticonvulsant; EC 2.3.1.50 (serine C-palmitoyltransferase) inhibitor
h 89 N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide: structure given in first source. N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide : A member of the class of isoquinolines that is the sulfonamide obtained by formal condensation of the sulfo group of isoquinoline-5-sulfonic acid with the primary amino group of N(1)-[3-(4-bromophenyl)prop-2-en-1-yl]ethane-1,2-diamine. It is a protein kinase A inhibitor.. (E)-N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide : A N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide in which the double bond adopts a trans-configuration.	2.69	2	0	N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide
gs 4071 GS 4071: The acid form.. oseltamivir acid : A cyclohexenecarboxylic acid that is cyclohex-1-ene-1-carboxylic acid which is substituted at positions 3, 4, and 5 by pentan-3-yloxy, acetamido, and amino groups, respectively (the 3R,4R,5S enantiomer). An antiviral drug, it is used as the corresponding ethyl ester prodrug, oseltamivir, to slow the spread of influenza.	2.04	1	0	acetate ester; amino acid; cyclohexenecarboxylic acid; primary amino compound	antiviral drug; EC 3.2.1.18 (exo-alpha-sialidase) inhibitor; marine xenobiotic metabolite
afimoxifene afimoxifene : A tertiary amino compound that is tamoxifen in which the phenyl group which is in a Z- relationship to the ethyl substituent is hydroxylated at the para- position. It is the active metabolite of tamoxifen.	2.02	1	0	phenols; tertiary amino compound	antineoplastic agent; estrogen receptor antagonist; metabolite
decitabine [no description available]	10	17	2	2'-deoxyribonucleoside
sm 8668 Sch 39304: Sch 42427 is the active entantiomer of the antifungal agent Sch 39304 which consists of Sch 42426 & Sch 42427; Sch 42426, the (S,S)-isomer, is inactive	2.04	1	0
teniposide [no description available]	4.08	4	0	aromatic ether; beta-D-glucoside; cyclic acetal; furonaphthodioxole; gamma-lactone; monosaccharide derivative; phenols; thiophenes	antineoplastic agent; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
iridoids Iridoids: A type of MONOTERPENES, derived from geraniol. They have the general form of cyclopentanopyran, but in some cases, one of the rings is broken as in the case of secoiridoid. They are different from the similarly named iridals (TRITERPENES).	2.06	1	0
troxacitabine troxacitabine: shows good anti-HIV activity without cytotoxicity	4.32	3	0	carbohydrate derivative; nucleobase-containing molecular entity
valrubicin [no description available]	2.08	1	0	anthracycline; trifluoroacetamide
cefamandole Cefamandole: Semisynthetic wide-spectrum cephalosporin with prolonged action, probably due to beta-lactamase resistance. It is used also as the nafate.. cefamandole : A cephalosporin compound having (R)-mandelamido and N-methylthiotetrazole side-groups.	2.04	1	0	cephalosporin; semisynthetic derivative	antibacterial drug
dactinomycin Dactinomycin: A compound composed of a two CYCLIC PEPTIDES attached to a phenoxazine that is derived from STREPTOMYCES parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015)	4.31	5	0	actinomycin	mutagen
bevirimat bevirimat: an HIV inhibitor; disrupts late step in processing HIV Major Core Protein p24, preventing the capsid precursor p25 from being converted to mature capsid p24. bevirimat : A pentacyclic triterpenoid obtained by the formal condensation of 2,2-dimethylsuccinic acid with the 3-hydroxy group of betulinic acid. It is isolated from the Chinese herb Syzygium claviflorum. The first in the class of HIV-1 maturation inhibitors to be studied in humans, bevirimat was identified as a potent HIV drug candidate and several clinical trials were conducted, but development into a new drug was plagued by numerous resistance-related problems.	2.6	1	0	dicarboxylic acid monoester; monocarboxylic acid; pentacyclic triterpenoid	HIV-1 maturation inhibitor; metabolite
tiazofurin tiazofurin: RN given refers to (beta-D)-isomer; structure given in first source. tiazofurine : A C-glycosyl compound that is 1,3-thiazole-4-carboxamide in which the hydrogen at position 2 has been replaced by a beta-D-ribofuranosyl group. It is metabolised to thiazole-4-carboxamide adenine dinucleotide (TAD), a selective inhibitor of inosine monophosphate dehydrogenase (IMP dehydrogenase).	2.45	2	0	1,3-thiazoles; C-glycosyl compound; monocarboxylic acid amide	antineoplastic agent; EC 1.1.1.205 (IMP dehydrogenase) inhibitor; prodrug
melphalan Melphalan: An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - MELPHALAN, the racemic mixture - MERPHALAN, and the dextro isomer - MEDPHALAN; toxic to bone marrow, but little vesicant action; potential carcinogen.. melphalan : A phenylalanine derivative comprising L-phenylalanine having [bis(2-chloroethyl)amino group at the 4-position on the phenyl ring.	22.59	391	112	L-phenylalanine derivative; nitrogen mustard; non-proteinogenic L-alpha-amino acid; organochlorine compound	alkylating agent; antineoplastic agent; carcinogenic agent; drug allergen; immunosuppressive agent
sitafloxacin [no description available]	2.04	1	0	fluoroquinolone antibiotic; quinolines; quinolone antibiotic
benzyloxycarbonylleucyl-leucyl-leucine aldehyde benzyloxycarbonylleucyl-leucyl-leucine aldehyde: proteasome inhibitor. N-benzyloxycarbonyl-L-leucyl-L-leucyl-L-leucinal : A tripeptide that is L-leucyl-L-leucyl-L-leucine in which the C-terminal carboxy group has been reduced to the corresponding aldehyde and the N-terminal amino group is protected as its benzyloxycarbonyl derivative.	9.94	105	0	amino aldehyde; carbamate ester; tripeptide	proteasome inhibitor
tenofovir tenofovir (anhydrous) : A member of the class of phosphonic acids that is methylphosphonic acid in which one of the methyl hydrogens is replaced by a [(2R)-1-(6-amino-9H-purin-9-yl)propan-2-yl]oxy group. An inhibitor of HIV-1 reverse transcriptase, the bis(isopropyloxycarbonyloxymethyl) ester (disoproxil ester) prodrug is used as the fumaric acid salt in combination therapy for the treatment of HIV infection.	4.11	4	0	nucleoside analogue; phosphonic acids	antiviral drug; drug metabolite; HIV-1 reverse transcriptase inhibitor
posaconazole [no description available]	3.95	3	0	aromatic ether; conazole antifungal drug; N-arylpiperazine; organofluorine compound; oxolanes; triazole antifungal drug; triazoles	trypanocidal drug
dibekacin Dibekacin: Analog of KANAMYCIN with antitubercular as well as broad-spectrum antimicrobial properties.. dibekacin : A kanamycin that is kanamycin B lacking the 3- and 4-hydroxy groups on the 2,6-diaminosugar ring.	2.04	1	0	kanamycins	antibacterial agent; protein synthesis inhibitor
gw 257406x maribavir: has antiviral activity against human cytomegalovirus	2.6	1	0
rubitecan rubitecan: RN refers to (+-)-isomer; anti-HIV agent; DNA Topoisomerases, Type I inhibitor. rubitecan : A pyranoindolizinoquinoline that is camptothecin in which the hydrogen at position 9 has been replaced by a nitro group. It is a prodrug for 9-aminocamptothecin.	2.47	2	0	C-nitro compound; delta-lactone; pyranoindolizinoquinoline; semisynthetic derivative; tertiary alcohol	antineoplastic agent; EC 5.99.1.2 (DNA topoisomerase) inhibitor; prodrug
micafungin Micafungin: A cyclic lipo-hexapeptide echinocandin antifungal agent that is used for the treatment and prevention of CANDIDIASIS.. micafungin : A cyclic hexapeptide echinocandin antibiotic which exerts its effect by inhibiting the synthesis of 1,3-beta-D-glucan, an integral component of the fungal cell wall. It is used as the sodium salt for the treatment of invasive candidiasis, and of aspergillosis in patients who are intolerant of other therapy.	4.08	4	0	antibiotic antifungal drug; echinocandin	antiinfective agent
shikonin shikonin: a naphthazarin; has antineoplastic and angiogenesis inhibiting activities	2.91	3	0	hydroxy-1,4-naphthoquinone
4,4-difluoro-N-[(1S)-3-[3-(3-methyl-5-propan-2-yl-1,2,4-triazol-4-yl)-8-azabicyclo[3.2.1]octan-8-yl]-1-phenylpropyl]-1-cyclohexanecarboxamide [no description available]	2.58	2	0	tropane alkaloid
cmx 001 [no description available]	2.6	1	0
amd 8664 [no description available]	2.6	1	0
bay 41-4109 BAY 41-4109: structure in first source	2.6	1	0
mg 262 MG 262: a proteasome inhibitor	4.33	7	0
bay 57-1293 pritelivir: herpes simplex virus 1 helicase-primase inhibitor	2.6	1	0
riboflavin vitamin B2 : Any member of a group of vitamers that belong to the chemical structural class called flavins that exhibit biological activity against vitamin B2 deficiency. Symptoms associated with vitamin B2 deficiency include glossitis, seborrhea, angular stomaitis, cheilosis and photophobia. The vitamers include riboflavin and its phosphate derivatives (and includes their salt, ionised and hydrate forms).	3.59	2	0	flavin; vitamin B2	anti-inflammatory agent; antioxidant; cofactor; Escherichia coli metabolite; food colouring; fundamental metabolite; human urinary metabolite; mouse metabolite; photosensitizing agent; plant metabolite
2'-c-methylcytidine 2'-C-methylcytidine: structure in first source	2.6	1	0
isoxanthohumol isoxanthohumol: structure in first source	2.6	1	0	flavanones
sodium bicarbonate Sodium Bicarbonate: A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions.	3.59	2	0	one-carbon compound; organic sodium salt	antacid; food anticaking agent
sodium acetate, anhydrous Sodium Acetate: The trihydrate sodium salt of acetic acid, which is used as a source of sodium ions in solutions for dialysis and as a systemic and urinary alkalizer, diuretic, and expectorant.	2.05	1	0	organic sodium salt	NMR chemical shift reference compound
sodium benzoate Sodium Benzoate: The sodium salt of BENZOIC ACID. It is used as an antifungal preservative in pharmaceutical preparations and foods. It may also be used as a test for liver function.. sodium benzoate : An organic sodium salt resulting from the replacement of the proton from the carboxy group of benzoic acid by a sodium ion.	2.05	1	0	organic sodium salt	algal metabolite; antimicrobial food preservative; drug allergen; EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor; EC 3.1.1.3 (triacylglycerol lipase) inhibitor; human xenobiotic metabolite; plant metabolite
arsenic trioxide Tetraarsenic Oxide: A form of As2O3 that exists as As4O6 in the solid state. It dissociates to As2O3 upon heating to the vapor phase above 800 degrees Celsius.	3.23	1	0	arsenic oxide	antineoplastic agent; insecticide
IPA-3 IPA-3 : An organic disulfide obtained by oxidative dimerisation of 1-sulfanylnaphthalen-2-ol.	2.25	1	0	naphthols; organic disulfide	EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor
dipyrone Dipyrone: A drug that has analgesic, anti-inflammatory, and antipyretic properties. It is the sodium sulfonate of AMINOPYRINE.. metamizole sodium : An organic sodium salt of antipyrine substituted at C-4 by a methyl(sulfonatomethyl)amino group, commonly used as a powerful analgesic and antipyretic.	2.05	1	0	organic sodium salt	anti-inflammatory agent; antipyretic; antirheumatic drug; cyclooxygenase 3 inhibitor; non-narcotic analgesic; peripheral nervous system drug; prodrug
ditiocarb sodium [no description available]	2.05	1	0	organic molecular entity
bromochloroacetic acid Keratins: A class of fibrous proteins or scleroproteins that represents the principal constituent of EPIDERMIS; HAIR; NAILS; horny tissues, and the organic matrix of tooth ENAMEL. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms a coiled-coil alpha helical structure consisting of TYPE I KERATIN and a TYPE II KERATIN, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. alpha-Keratins have been classified into at least 20 subtypes. In addition multiple isoforms of subtypes have been found which may be due to GENE DUPLICATION.. bromochloroacetic acid : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is replaced by bromine while a second is replaced by chlorine. A low-melting (27.5-31.5degreeC), hygroscopic crystalline solid, it can be formed during the disinfection (by chlorination) of water that contains bromide ions and organic matter, so can occur in drinking water as a byproduct of the disinfection process.	2.42	2	0	2-bromocarboxylic acid; monocarboxylic acid; organochlorine compound
4-(4-chloro-2-methylphenoxy)-n-hydroxybutanamide 4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide: a c-FLIP inhibitor; structure in first source	2.6	1	0	aromatic ether
mecarbinate [no description available]	2.6	1	0
artemisin [no description available]	2.17	1	0
sr 90107 fondaparinux sodium : An organic sodium salt, being the decasodium salt of fondaparinux.	3.23	1	0
carbenoxolone sodium Carbenoxolone: An agent derived from licorice root. It is used for the treatment of digestive tract ulcers, especially in the stomach. Antidiuretic side effects are frequent, but otherwise the drug is low in toxicity.	2.11	1	0	triterpenoid
carbenoxolone [no description available]	2.05	1	0
meglumine iodipamide [no description available]	3.23	1	0	organoammonium salt	radioopaque medium
tenatoprazole Tenatoprazole: structure in first source	2.15	1	0	imidazopyridine
nemorosone [no description available]	2.08	1	0
dimethyl fumarate [no description available]	2.61	2	0	diester; enoate ester; methyl ester	antipsoriatic; immunomodulator
chalcone trans-chalcone : The trans-isomer of chalcone.	2.07	1	0	chalcone	EC 3.2.1.1 (alpha-amylase) inhibitor
isomethyleugenol Methylation: Addition of methyl groups. In histo-chemistry methylation is used to esterify carboxyl groups and remove sulfate groups by treating tissue sections with hot methanol in the presence of hydrochloric acid. (From Stedman, 25th ed)	3.94	3	0	isomethyleugenol
piplartine piplartine: Antineoplastic Agent, Phytogenic; alkaloid from Piper; structure in first source	2.63	2	0	cinnamamides; dicarboximide
stilbenes Stilbenes: Organic compounds that contain 1,2-diphenylethylene as a functional group.. trans-stilbene : The trans-isomer of stilbene.	8.43	12	1	stilbene
thyrotropin-releasing hormone PR 546: no other info available 9/89. protirelin : A tripeptide composed of L-pyroglutamyl, L-histidyl and L-prolinamide residues joined in sequence.	3.23	1	0	peptide hormone; tripeptide	human metabolite
xanthohumol xanthohumol: from hop plant, Humulus lupulus. xanthohumol : A member of the class of chalcones that is trans-chalcone substituted by hydroxy groups at positions 4, 2' and 4', a methoxy group at position 6' and a prenyl group at position 3'. Isolated from Humulus lupulus, it induces apoptosis in human malignant glioblastoma cells.	2.69	2	0	aromatic ether; chalcones; polyphenol	anti-HIV-1 agent; antineoplastic agent; antiviral agent; apoptosis inducer; EC 2.3.1.20 (diacylglycerol O-acyltransferase) inhibitor; metabolite
discodermolide [no description available]	2.05	1	0	diterpenoid
cannabidiol Cannabidiol: Compound isolated from Cannabis sativa extract.. cannabidiol : An cannabinoid that is cyclohexene which is substituted by a methyl group at position 1, a 2,6-dihydroxy-4-pentylphenyl group at position 3, and a prop-1-en-2-yl group at position 4.	7.48	2	0	olefinic compound; phytocannabinoid; resorcinols	antimicrobial agent; plant metabolite
arginine vasopressin Arginine Vasopressin: The predominant form of mammalian antidiuretic hormone. It is a nonapeptide containing an ARGININE at residue 8 and two disulfide-linked cysteines at residues of 1 and 6. Arg-vasopressin is used to treat DIABETES INSIPIDUS or to improve vasomotor tone and BLOOD PRESSURE.. argipressin : The predominant form of mammalian vasopressin (antidiuretic hormone). It is a nonapeptide containing an arginine at residue 8 and two disulfide-linked cysteines at residues of 1 and 6.	3.61	2	0	vasopressin	cardiovascular drug; hematologic agent; mitogen
s 1033 [no description available]	5.32	9	0	(trifluoromethyl)benzenes; imidazoles; pyridines; pyrimidines; secondary amino compound; secondary carboxamide	anticoronaviral agent; antineoplastic agent; tyrosine kinase inhibitor
acetyl-aspartyl-glutamyl-valyl-aspartal acetyl-aspartyl-glutamyl-valyl-aspartal: a capase inhibitor. Ac-Asp-Glu-Val-Asp-H : A tetrapeptide consisting of two L-aspartic acid residues, an L-glutamyl residue and an L-valine residue with an acetyl group at the N-terminal and with the C-terminal carboxy group reduced to an aldehyde. It is an inhibitor of caspase-3/7.	2.6	1	0	tetrapeptide	protease inhibitor
mezlocillin Mezlocillin: Semisynthetic ampicillin-derived acylureido penicillin. It has been proposed for infections with certain anaerobes and may be useful in inner ear, bile, and CNS infections.. mezlocillin : A penicillin in which the substituent at position 6 of the penam ring is a (2R)-2-[3-(methanesulfonyl)-2-oxoimidazolidine-1-carboxamido]-2-phenylacetamido group.	2.04	1	0	penicillin allergen; penicillin	antibacterial drug
trilostane trilostane: inhibits conversion of pregnenolone to progesterone; adrenal blocking agent used in treatment of Cushing's syndrome. trilostane : An epoxy steroid that is 3,17beta-dihydroxy-5alpha-androst-2-ene-2-carbonitrile in which the oxygen of the epoxy group is joined to the 4alpha and 5 alpha positions.	2.08	1	0	17beta-hydroxy steroid; 3-hydroxy steroid; androstanoid; epoxy steroid; nitrile	abortifacient; antineoplastic agent; EC 1.1.1.210 [3beta(or 20alpha)-hydroxysteroid dehydrogenase] inhibitor
tropisetron Tropisetron: An indole derivative and 5-HT3 RECEPTOR antagonist that is used for the prevention of nausea and vomiting.. tropisetron : An indolyl carboxylate ester obtained by formal condensation of the carboxy group of indole-3-carboxylic acid with the hydroxy group of tropine.	2.04	1	0	indolyl carboxylic acid
leuprolide acetate leuprolide acetate : An acetate salt obtained by combining the nonapeptide leuprolide with acetic acid. A long lasting GnRH analog, LH-Rh agonist. It is a synthetic nonapeptide analogue of gonadotropin-releasing hormone, and is used as a subcutaneous hydrogel implant for the treatment of prostate cancer and for the suppression of gonadal sex hormone production in children with central precocious puberty.	2.08	1	0	acetate salt	antineoplastic agent; gonadotropin releasing hormone agonist
leuprolide Leuprolide: A potent synthetic long-acting agonist of GONADOTROPIN-RELEASING HORMONE that regulates the synthesis and release of pituitary gonadotropins, LUTEINIZING HORMONE and FOLLICLE STIMULATING HORMONE.. leuprolide : An oligopeptide comprising pyroglutamyl, histidyl, tryptophyl, seryl, tyrosyl, D-leucyl, leucyl, arginyl, and N-ethylprolinamide residues joined in sequence. It is a synthetic nonapeptide analogue of gonadotropin-releasing hormone, and is used as a subcutaneous hydrogel implant (particularly as the acetate salt) for the treatment of prostate cancer and for the suppression of gonadal sex hormone production in children with central precocious puberty.	3.53	2	0	oligopeptide	anti-estrogen; antineoplastic agent; gonadotropin releasing hormone agonist
octotropine methylbromide octotropine methylbromide: minor descriptor (65-86); on line & INDEX MEDICUS search TROPANES (69-86); RN given refers to endo-isomer. anisotropine methylbromide : A quaternary ammonium salt resulting from the reaction of the amino group of anisotropine with methyl bromide.	2.6	1	0
fludarabine [no description available]	11.07	22	5	purine nucleoside
propylthiouracil Propylthiouracil: A thiourea antithyroid agent. Propythiouracil inhibits the synthesis of thyroxine and inhibits the peripheral conversion of throxine to tri-iodothyronine. It is used in the treatment of hyperthyroidism. (From Martindale, The Extra Pharmacopeoia, 30th ed, p534). 6-propyl-2-thiouracil : A pyrimidinethione consisting of uracil in which the 2-oxo group is substituted by a thio group and the hydrogen at position 6 is substituted by a propyl group.	4.08	4	0	pyrimidinethione	antidote to paracetamol poisoning; antimetabolite; antioxidant; antithyroid drug; carcinogenic agent; EC 1.14.13.39 (nitric oxide synthase) inhibitor; hormone antagonist
prothionamide Prothionamide: Antitubercular agent similar in action and side effects to ETHIONAMIDE. It is used mostly in combination with other agents.	2.05	1	0	pyridines
sesquiterpenes [no description available]	2.98	4	0
etomidate Etomidate: Imidazole derivative anesthetic and hypnotic with little effect on blood gases, ventilation, or the cardiovascular system. It has been proposed as an induction anesthetic.. etomidate : The ethyl ester of 1-[(1R)-1-phenylethyl]-1H-imidazole-5-carboxylic acid. It is an intravenous general anaesthetic with no analgesic activity.	3.86	3	0	ethyl ester; imidazoles	intravenous anaesthetic; sedative
mercaptopurine Mercaptopurine: An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by inhibiting purine metabolism and is used, usually in combination with other drugs, in the treatment of or in remission maintenance programs for leukemia.. purine-6-thiol : A thiol that is the tautomer of mercaptopurine.. mercaptopurine : A member of the class of purines that is 6,7-dihydro-1H-purine carrying a thione group at position 6. An adenine analogue, it is used in the treatment of acute lymphocytic leukemia (ALL), chronic myeloid leukemia (CML), Crohn's disease, and ulcerative colitis.	4.44	6	0	aryl thiol; purines; thiocarbonyl compound	anticoronaviral agent; antimetabolite; antineoplastic agent
jrf 12 N2,N4-dibenzylquinazoline-2,4-diamine: a selective, potent, reversible, and ATP-competitive p97 inhibitor	2.6	1	0
(e)-3-(4-t-butylphenyl)-n-(2,3-dihydrobenzo(b)(1,4)dioxin-6-yl)acrylamide 3-(4-t-butylphenyl)-N-(2,3-dihydrobenzo(b)(1,4)dioxin-6-yl)acrylamide: a vanilloid receptor 1 antagonist and antihyperalgesic agent; structure in first source	2.25	1	0
levosulpiride (S)-(-)-sulpiride : An optically active form of sulpiride having (S)-configuration. The active enantiomer of the racemic drug sulpiride. Selective D2-like dopamine antagonist (Ki values are ~ 0.015. ~ 0.013, 1, ~ 45 and ~ 77 muM at D2, D3, D4, D1 and D5 receptors respectively).	2.08	1	0	sulpiride	antidepressant; antiemetic; antipsychotic agent; dopaminergic antagonist
3,4'-dihydroxyflavone 3,4'-dihydroxyflavone: an antioxidant; structure in first source	2.6	1	0
caffeic acid trans-caffeic acid : The trans-isomer of caffeic acid.	7.69	2	0	caffeic acid	geroprotector; mouse metabolite
rg108 RG108: DNA methyltransferase inhibitor; structure in first source	2.08	1	0	indolyl carboxylic acid
pyrantel Pyrantel: A depolarizing neuromuscular-blocking agent, that causes persistent nicotinic activation resulting in spastic paralysis of susceptible nematodes. It is a drug of second-choice after benzimidazoles for treatment of ascariasis, hookworm, and pinworm infections, being effective after a single dose. (From Smith and Reynard, Textbook of Pharmacology, 1992, p920). pyrantel : A carboxamidine that is 1,4,5,6-tetrahydropyrimidine that is substituted at position 1 by a methyl group and at position 2 by an (E)-2-(2-thienyl)vinyl group. It is used, particularly as the embonate [4,4'-methylenebis(3-hydroxy-2-naphthoate)] salt, as an anthelmintic that is effective against intestinal nematodes including threadworms, roundworms and hookworms, and is included in the WHO 'Model List of Essential Medicines'.	3.23	1	0	1,4,5,6-tetrahydropyrimidines; carboxamidine; thiophenes	antinematodal drug
3-(3,4-dimethoxyphenyl)propenoic acid 3-(3,4-dimethoxyphenyl)propenoic acid: structure given in first source; RN given refers to parent cpd. 3,4-dimethoxycinnamic acid : A methoxycinnamic acid that is trans-cinnamic acid substituted by methoxy groups at positions 3' and 4' respectively.	2.6	1	0	methoxycinnamic acid
stf 083010 [no description available]	2.08	1	0
isoferulic acid isoferulic acid: isomer of ferulic acid; structure. isoferulic acid : A ferulic acid consisting of trans-cinnamic acid bearing methoxy and hydroxy substituents at positions 4 and 3 respectively on the phenyl ring.	2.6	1	0	ferulic acids	antioxidant; biomarker; metabolite
N-(3-cyano-4,5,6,7-tetrahydro-1-benzothiophen-2-yl)-1-naphthalenecarboxamide [no description available]	2.08	1	0	naphthalenecarboxamide
cyclouridine cyclouridine: structure given in third source	2.6	1	0
4-iodo-6-phenylpyrimidine 4-iodo-6-phenylpyrimidine: acts on macrophage migration inhibitory factor; structure in first source. 4-iodo-6-phenylpyrimidine : A member of the class of pyrimidines carrying iodo and phenyl substituents at positions 4 and 6 respectively.	2.13	1	0	biaryl; organoiodine compound; pyrimidines	antineoplastic agent; apoptosis inducer; macrophage migration inhibitory factor inhibitor
cotinine Cotinine: The N-glucuronide conjugate of cotinine is a major urinary metabolite of NICOTINE. It thus serves as a biomarker of exposure to tobacco SMOKING. It has CNS stimulating properties.. (-)-cotinine : An N-alkylpyrrolidine that consists of N-methylpyrrolidinone bearing a pyridin-3-yl substituent at position C-5 (the 5S-enantiomer). It is an alkaloid commonly found in Nicotiana tabacum.	2.04	1	0	N-alkylpyrrolidine; pyridines; pyrrolidin-2-ones; pyrrolidine alkaloid	antidepressant; biomarker; human xenobiotic metabolite; plant metabolite
parthenolide, (1ar-(1ar,4e,7as,10as,10br))-isomer [no description available]	2.31	1	0	germacranolide
thiothixene [no description available]	3.23	1	0	N-methylpiperazine	anticoronaviral agent
eszopiclone Eszopiclone: A pyridine, pyrazine, and piperazine derivative that is used as a HYPNOTIC AND SEDATIVE in the treatment of INSOMNIA.. eszopiclone : The (5S)- (active) enantiomer of zopiclone. Unlike almost all other hypnotic sedatives, which are approved only for the relief of short-term (6-8 weeks) insomnia, eszopiclone is approved by the U.S. Food and Drug Administration for long-term use.	3.61	2	0	zopiclone	central nervous system depressant; sedative
curcumin Curcumin: A yellow-orange dye obtained from tumeric, the powdered root of CURCUMA longa. It is used in the preparation of curcuma paper and the detection of boron. Curcumin appears to possess a spectrum of pharmacological properties, due primarily to its inhibitory effects on metabolic enzymes.. curcumin : A beta-diketone that is methane in which two of the hydrogens are substituted by feruloyl groups. A natural dyestuff found in the root of Curcuma longa.	7.66	18	1	aromatic ether; beta-diketone; diarylheptanoid; enone; polyphenol	anti-inflammatory agent; antifungal agent; antineoplastic agent; biological pigment; contraceptive drug; dye; EC 1.1.1.205 (IMP dehydrogenase) inhibitor; EC 1.1.1.21 (aldehyde reductase) inhibitor; EC 1.1.1.25 (shikimate dehydrogenase) inhibitor; EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor; EC 1.8.1.9 (thioredoxin reductase) inhibitor; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor; EC 3.5.1.98 (histone deacetylase) inhibitor; flavouring agent; food colouring; geroprotector; hepatoprotective agent; immunomodulator; iron chelator; ligand; lipoxygenase inhibitor; metabolite; neuroprotective agent; nutraceutical; radical scavenger
cct018159 CCT018159: structure in first source. CCT-018159 : A member of the class of pyrazoles that is 1H-pyrazole carrying 1,4-benzodioxane-6-yl and 5-ethyl-2,4-dihydroxyphenyl substituents at positions 4 and 5 respectively.	2.08	1	0	benzodioxine; pyrazoles; resorcinols	antineoplastic agent; apoptosis inducer; Hsp90 inhibitor
secinh3 SecinH3: a small molecule antagonist of cytohesins; structure in first source	2.08	1	0	triazoles
jk184 JK184: structure in first source	2.08	1	0
hc 030031 2-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4-isopropylphenyl)acetamide: a TRPA1 channel blocker	2.53	2	0
benztropine Benztropine: A centrally active muscarinic antagonist that has been used in the symptomatic treatment of PARKINSON DISEASE. Benztropine also inhibits the uptake of dopamine.. benzatropine : Tropane in which a hydrogen at position 3 is substituted by a diphenylmethoxy group (endo-isomer). An acetylcholine receptor antagonist, it is used (particularly as its methanesulphonate salt) in the treatment of Parkinson's disease, and to reduce parkinsonism and akathisia side effects of antipsychotic treatments.	3.23	1	0	diarylmethane
thiohydantoins Thiohydantoins: Sulfur analogs of hydantoins with one or both carbonyl groups replaced by thiocarbonyl groups.	4.8	1	1
methimazole Methimazole: A thioureylene antithyroid agent that inhibits the formation of thyroid hormones by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin. This is done by interfering with the oxidation of iodide ion and iodotyrosyl groups through inhibition of the peroxidase enzyme.. methimazole : A member of the class of imidazoles that it imidazole-2-thione in which a methyl group replaces the hydrogen which is attached to a nitrogen.	4.08	4	0	1,3-dihydroimidazole-2-thiones	antithyroid drug
cinnarizine Cinnarizine: A piperazine derivative having histamine H1-receptor and calcium-channel blocking activity with vasodilating and antiemetic properties but it induces PARKINSONIAN DISORDERS.	2.08	1	0	diarylmethane; N-alkylpiperazine; olefinic compound	anti-allergic agent; antiemetic; calcium channel blocker; geroprotector; H1-receptor antagonist; histamine antagonist; muscarinic antagonist
sulindac Sulindac: A sulfinylindene derivative prodrug whose sulfinyl moiety is converted in vivo to an active NSAID analgesic. Specifically, the prodrug is converted by liver enzymes to a sulfide which is excreted in the bile and then reabsorbed from the intestine. This helps to maintain constant blood levels with reduced gastrointestinal side effects.. sulindac : A monocarboxylic acid that is 1-benzylidene-1H-indene which is substituted at positions 2, 3, and 5 by methyl, carboxymethyl, and fluorine respectively, and in which the phenyl group of the benzylidene moiety is substituted at the para position by a methylsulfinyl group. It is a prodrug for the corresponding sulfide, a non-steroidal anti-inflammatory drug, used particularly in the treatment of acute and chronic inflammatory conditions.	9.76	5	0	monocarboxylic acid; organofluorine compound; sulfoxide	analgesic; antineoplastic agent; antipyretic; apoptosis inducer; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug; prodrug; tocolytic agent
zucapsaicin [no description available]	2.6	1	0	methoxybenzenes; phenols
capsaicin ALGRX-4975: an injectable capsaicin (TRPV1 receptor agonist) formulation for longlasting pain relief. capsaicinoid : A family of aromatic fatty amides produced as secondary metabolites by chilli peppers.	2.45	2	0	capsaicinoid	non-narcotic analgesic; TRPV1 agonist; voltage-gated sodium channel blocker
terbinafine [no description available]	3.59	2	0	acetylenic compound; allylamine antifungal drug; enyne; naphthalenes; tertiary amine	EC 1.14.13.132 (squalene monooxygenase) inhibitor; P450 inhibitor; sterol biosynthesis inhibitor
epalrestat epalrestat : A monocarboxylic acid that is 1,3-thiazolidine which is substituted on the nitrogen by a carboxymethyl group, at positions 2 and 4 by thioxo and oxo groups, respectively, and at position 5 by a 2-methyl-3-phenylprop-2-en-1-ylidene group. It is an inhibitor of aldose reductase (which catalyses the conversion of glucose to sorbitol) and is used for the treatment of some diabetic complications, including neuropathy.	2.08	1	0	monocarboxylic acid; thiazolidines	EC 1.1.1.21 (aldehyde reductase) inhibitor
nbd 556 [no description available]	2.6	1	0
drotaverin drotaverin: Hungarian drug; RN given refers to parent cpd; structure	2.46	2	0	isoquinolines
chlorogenic acid caffeoylquinic acid: Antiviral Agent; structure in first source. chlorogenate : A monocarboxylic acid anion that is the conjugate base of chlorogenic acid; major species at pH 7.3.	10.25	2	1	cinnamate ester; tannin	food component; plant metabolite
thioguanine anhydrous Thioguanine: An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia.. tioguanine : A 2-aminopurine that is the 6-thiono derivative of 2-amino-1,9-dihydro-6H-purine. Incorporates into DNA and inhibits synthesis. Used in the treatment of leukaemia.	3.93	3	0	2-aminopurines	anticoronaviral agent; antimetabolite; antineoplastic agent
tacrine hydrochloride [no description available]	2.05	1	0
thiourea Thiourea: A photographic fixative used also in the manufacture of resins. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance may reasonably be anticipated to be a carcinogen (Merck Index, 9th ed). Many of its derivatives are ANTITHYROID AGENTS and/or FREE RADICAL SCAVENGERS.. thiourea : The simplest member of the thiourea class, consisting of urea with the oxygen atom substituted by sulfur.	4.8	1	1	one-carbon compound; thioureas; ureas	antioxidant; chromophore
sodium propionate sodium propionate: was term of propionic acid (1986-2006). sodium propionate : An organic sodium salt comprising equal numbers of sodium and propionate ions.	2.05	1	0	organic sodium salt	antifungal drug; food preservative
thioacetamide Thioacetamide: A crystalline compound used as a laboratory reagent in place of HYDROGEN SULFIDE. It is a potent hepatocarcinogen.. thioacetamide : A thiocarboxamide consiting of acetamide having the oxygen replaced by sulfur.	2	1	0	thiocarboxamide	hepatotoxic agent
succimer Succimer: A mercaptodicarboxylic acid used as an antidote to heavy metal poisoning because it forms strong chelates with them.. succimer : A sulfur-containing carboxylic acid that is succinic acid bearing two mercapto substituents at positions 2 and 3. A lead chelator used as an antedote to lead poisoning.	3.62	2	0	dicarboxylic acid; dithiol; sulfur-containing carboxylic acid	chelator
digoxin Digoxin: A cardiotonic glycoside obtained mainly from Digitalis lanata; it consists of three sugars and the aglycone DIGOXIGENIN. Digoxin has positive inotropic and negative chronotropic activity. It is used to control ventricular rate in ATRIAL FIBRILLATION and in the management of congestive heart failure with atrial fibrillation. Its use in congestive heart failure and sinus rhythm is less certain. The margin between toxic and therapeutic doses is small. (From Martindale, The Extra Pharmacopoeia, 30th ed, p666). digoxin : A cardenolide glycoside that is digitoxin beta-hydroxylated at C-12. A cardiac glycoside extracted from the foxglove plant, Digitalis lanata, it is used to control ventricular rate in atrial fibrillation and in the management of congestive heart failure with atrial fibrillation, but the margin between toxic and therapeutic doses is small.	3.86	3	0	cardenolide glycoside; steroid saponin	anti-arrhythmia drug; cardiotonic drug; EC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor; epitope
4,5,6,7-tetrachloroindan-1,3-dione 4,5,6,7-tetrachloroindan-1,3-dione: inhibits ubiquitin C-terminal hydrolase L1	2.6	1	0
8-ethoxy-2-(4-fluorophenyl)-3-nitro-2h-chromene 8-ethoxy-2-(4-fluorophenyl)-3-nitro-2H-chromene: an antineoplastic agent that inhibits the expression of cyclins D1, D2, and D3 and arrests cells at the G0/G1 phase	2.11	1	0
streptozocin [no description available]	3.59	2	0
tamoxifen citrate [no description available]	2.08	1	0	citrate salt	angiogenesis inhibitor; anticoronaviral agent
tamoxifen [no description available]	7.85	11	2	stilbenoid; tertiary amino compound	angiogenesis inhibitor; antineoplastic agent; bone density conservation agent; EC 1.2.3.1 (aldehyde oxidase) inhibitor; EC 2.7.11.13 (protein kinase C) inhibitor; estrogen antagonist; estrogen receptor antagonist; estrogen receptor modulator
hc-067047 HC-067047: a TRPA1 antagonist; structure in first source	2.08	1	0
bi-78d3 [no description available]	2.08	1	0	aryl sulfide
ethionamide Ethionamide: A second-line antitubercular agent that inhibits mycolic acid synthesis.. ethionamide : A thiocarboxamide that is pyridine-4-carbothioamide substituted by an ethyl group at position 2. A prodrug that undergoes metabolic activation by conversion to the corresponding S-oxide.	3.59	2	0	pyridines; thiocarboxamide	antilipemic drug; antitubercular agent; fatty acid synthesis inhibitor; leprostatic drug; prodrug
stattic [no description available]	7.6	1	0	1-benzothiophenes; C-nitro compound; sulfone	antineoplastic agent; radiosensitizing agent; STAT3 inhibitor
srpin340 SRPIN340: Serine-Arginine-Rich Protein Kinase Inhibitor	2.6	1	0
gsk 3787 [no description available]	2.08	1	0
sc 514 SC 514: inhibits IkappaB kinase-2; structure in first source	2.08	1	0	ring assembly; thiophenes
pr-619 [no description available]	2.72	2	0
p5091 P5091: inhibits ubiquitin-specific protease 7; structure in first source	4	3	0
cancidas [no description available]	3.58	2	0
sirtinol [no description available]	2.15	1	0	aldimine; benzamides; naphthols	anti-inflammatory agent; EC 3.5.1.98 (histone deacetylase) inhibitor; Sir2 inhibitor
methyl-thiohydantoin-tryptophan methyl-thiohydantoin-tryptophan: structure in first source	2.5	2	0	organonitrogen compound; organooxygen compound
ace-011 ACE-011: a dimeric fusion protein consisting of the extracellular domain of the human ActRIIA linked to the Fc portion of human IgG1 and may be an effective therapy in a variety of diseases involving bone loss	3.19	1	0
2-[2-chloro-6-ethoxy-4-[(3-methyl-5-oxo-1-phenyl-4-pyrazolylidene)methyl]phenoxy]acetic acid methyl ester [no description available]	2.08	1	0	monocarboxylic acid
4-(5-(4-methoxyphenyl)-3-phenyl-4,5-dihydro-1h-pyrazol-1-yl)benzenesulfonamide [no description available]	2.08	1	0	sulfonamide
monastrol monastrol: stops mitosis by fostering formation of monopolar spindles; structure in first source. (S)-monastrol : An ethyl 4-(3-hydroxyphenyl)-6-methyl-2-thioxo-1,2,3,4-tetrahydropyrimidine-5-carboxylate that has S configuration.. monastrol : A racemate comprising equimolar amounts of R- and S-monastrol.. ethyl 4-(3-hydroxyphenyl)-6-methyl-2-thioxo-1,2,3,4-tetrahydropyrimidine-5-carboxylate : A member of the class of thioureas that is 3,4-dihydropyrimidine-2(1)-thione substituted by a 3-hydroxyphenyl group at position 4, an ethoxycarbonyl group at position 5, and a methyl group at position 6.	7.15	1	0	enoate ester; ethyl ester; phenols; racemate; thioureas	antileishmanial agent; antimitotic; antineoplastic agent; EC 3.5.1.5 (urease) inhibitor
fusidic acid Fusidic Acid: An antibiotic isolated from the fermentation broth of Fusidium coccineum. (From Merck Index, 11th ed). It acts by inhibiting translocation during protein synthesis.. fusidic acid : A steroid antibiotic that is isolated from the fermentation broth of Fusidium coccineum.	2.47	2	0	11alpha-hydroxy steroid; 3alpha-hydroxy steroid; alpha,beta-unsaturated monocarboxylic acid; steroid acid; steroid antibiotic; sterol ester	EC 2.7.1.33 (pantothenate kinase) inhibitor; Escherichia coli metabolite; protein synthesis inhibitor
lincomycin Lincomycin: An antibiotic produced by Streptomyces lincolnensis var. lincolnensis. It has been used in the treatment of staphylococcal, streptococcal, and Bacteroides fragilis infections.. lincomycin : A carbohydrate-containing antibiotic produced by the actinomyces Streptomyces lincolnensis.	3.58	2	0	carbohydrate-containing antibiotic; L-proline derivative; monocarboxylic acid amide; pyrrolidinecarboxamide; S-glycosyl compound	antimicrobial agent; bacterial metabolite
valinomycin Valinomycin: A cyclododecadepsipeptide ionophore antibiotic produced by Streptomyces fulvissimus and related to the enniatins. It is composed of 3 moles each of L-valine, D-alpha-hydroxyisovaleric acid, D-valine, and L-lactic acid linked alternately to form a 36-membered ring. (From Merck Index, 11th ed) Valinomycin is a potassium selective ionophore and is commonly used as a tool in biochemical studies.. valinomycin : A twelve-membered cyclodepsipeptide composed of three repeating D-alpha-hydroxyisovaleryl-D-valyl-L-lactoyl-L-valyl units joined in sequence. An antibiotic found in several Streptomyces strains.	2.08	1	0	cyclodepsipeptide; macrocycle	antimicrobial agent; antiviral agent; bacterial metabolite; potassium ionophore
thiopental Thiopental: A barbiturate that is administered intravenously for the induction of general anesthesia or for the production of complete anesthesia of short duration.. thiopental : A barbiturate, the structure of which is that of 2-thiobarbituric acid substituted at C-5 by ethyl and sec-pentyl groups.	2.04	1	0	barbiturates	anticonvulsant; drug allergen; environmental contaminant; intravenous anaesthetic; sedative; xenobiotic
trovirdine trovirdine: HIV-1 reverse transcriptase inhibitor	2.6	1	0
estrone sulfate estrone sulfate: sulfoconjugated estrone; RN given refers to parent cpd	2.05	1	0	17-oxo steroid; steroid sulfate	human metabolite; mouse metabolite
ranitidine Ranitidine: A non-imidazole blocker of those histamine receptors that mediate gastric secretion (H2 receptors). It is used to treat gastrointestinal ulcers.. ranitidine : A member of the class of furans used to treat peptic ulcer disease (PUD) and gastroesophageal reflux disease.	3.23	1	0	C-nitro compound; furans; organic sulfide; tertiary amino compound	anti-ulcer drug; drug allergen; environmental contaminant; H2-receptor antagonist; xenobiotic
aplaviroc aplaviroc: a spiro-diketo-piperazine; a potent noncompetitive allosteric antagonist of the CCR5 receptor with concomitantly potent antiviral effects for HIV-1; structure in first source	3.23	1	0
hmr 3647 [no description available]	4.08	4	0
latoconazole latoconazole: RN refers to cpd without isomeric designation; latoconazole is (E)-isomer; structure given in first source	2.08	1	0	conazole antifungal drug; imidazole antifungal drug
maraviroc [no description available]	3.89	3	0	tropane alkaloid
LSM-1318 [no description available]	2.08	1	0	oxa-steroid
fti 277 [no description available]	2.6	1	0
toremifene citrate [no description available]	2.08	1	0	stilbenoid	anticoronaviral agent
toremifene Toremifene: A first generation selective estrogen receptor modulator (SERM). Like TAMOXIFEN, it is an estrogen agonist for bone tissue and cholesterol metabolism but is antagonistic on mammary and uterine tissue.	3.59	2	0	aromatic ether; organochlorine compound; tertiary amine	antineoplastic agent; bone density conservation agent; estrogen antagonist; estrogen receptor modulator
u 0126 U 0126: protein kinase kinase inhibitor; structure in first source	3.08	4	0	aryl sulfide; dinitrile; enamine; substituted aniline	antineoplastic agent; antioxidant; apoptosis inducer; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor; osteogenesis regulator; vasoconstrictor agent
rwj 67657 RWJ 67657: inhibits p38 mitogen-activated protein kinase; structure in first source	2.08	1	0
vicriviroc vicriviroc: structure in first source	2.6	1	0	(trifluoromethyl)benzenes
telaprevir [no description available]	2.54	2	0	cyclopentapyrrole; cyclopropanes; oligopeptide; pyrazines	antiviral drug; hepatitis C protease inhibitor; peptidomimetic
nelarabine nelarabine: prodrug of ara-G. nelarabine : A purine nucleoside in which O-methylguanine is attached to arabinofuranose via a beta-N(9)-glycosidic bond. Inhibits DNA synthesis and causes cell death; a prodrug of 9-beta-D-arabinofuranosylguanine (ara-G).	4.61	4	0	beta-D-arabinoside; monosaccharide derivative; purine nucleoside	antineoplastic agent; DNA synthesis inhibitor; prodrug
2-[(2-ethoxyphenoxy)-phenylmethyl]morpholine [no description available]	2.04	1	0	aromatic ether
6-methyl-2-(phenylethynyl)pyridine 6-methyl-2-(phenylethynyl)pyridine: an mGlu5 antagonist. 2-methyl-6-(phenylethynyl)pyridine : A methylpyridine that coinsists of 2-methylp[yridine bearing an additional phenylethynyl group at position 6. Potent and highly selective non-competitive antagonist at the mGlu5 receptor subtype (IC50 = 36 nM) and a positive allosteric modulator at mGlu4 receptors. Centrally active following systemic administration in vivo. Reverses mechanical hyperalgesia in the inflamed rat hind paw.	2.49	2	0	acetylenic compound; methylpyridines	anxiolytic drug; metabotropic glutamate receptor antagonist
bms 387032 N-(5-(((5-(1,1-dimethylethyl)-2-oxazolyl)methyl)thio)-2-thiazolyl)-4-piperidinecarboxamide: a CDK2 inhibitor with antineoplastic activity; structure in first source. N-(5-{[(5-tert-butyl-1,3-oxazol-2-yl)methyl]sulfanyl}-1,3-thiazol-2-yl)piperidine-4-carboxamide : A secondary carboxamide resulting from the formal condensation of the carboxy group of piperidine-4-carboxylic acid with the amino group of 5-{[(5-tert-butyl-1,3-oxazol-2-yl)methyl]sulfanyl}-1,3-thiazol-2-amine. It is an ATP-competitive inhibitor of CDK2, CDK7 and CDK9 kinases and exhibits anti-cancer properties.	2.08	1	0	1,3-oxazoles; 1,3-thiazoles; organic sulfide; piperidinecarboxamide; secondary carboxamide	angiogenesis inhibitor; antineoplastic agent; apoptosis inducer; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
lithium Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight [6.938; 6.997]. Salts of lithium are used in treating BIPOLAR DISORDER.	3.19	1	0	alkali metal atom
dermatan sulfate Dermatan Sulfate: A naturally occurring glycosaminoglycan found mostly in the skin and in connective tissue. It differs from CHONDROITIN SULFATE A (see CHONDROITIN SULFATES) by containing IDURONIC ACID in place of glucuronic acid, its epimer, at carbon atom 5. (from Merck, 12th ed). alpha-L-IdopA-(1->3)-beta-D-GalpNAc4S : An oligosaccharide sulfate that is 2-acetamido-2-deoxy-4-O-sulfo-beta-D-galactopyranose in which the hydroxy group at position 3 has been converted to the corresponding alpha-L-idopyranuronoside.. dermatan sulfate : Any of a group of glycosaminoglycans with repeating units consisting of variously sulfated beta1->4-linked L-iduronyl-(alpha1->3)-N-acetyl-D-galactosamine units.	3.23	1	0	amino disaccharide; glycosylgalactose derivative; iduronic acids; oligosaccharide sulfate
droloxifene [no description available]	2.05	1	0	stilbenoid
dolasetron [no description available]	3.58	2	0	indolyl carboxylic acid
or 1259 [no description available]	2.45	2	0	hydrazone; nitrile; pyridazinone	anti-arrhythmia drug; cardiotonic drug; EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor; vasodilator agent
gestodene Gestodene: synthetic steroid with progestational activity; RN given refers to (17alpha)-isomer	2.75	3	0	steroid	estrogen
orlistat Orlistat: A lactone derivative of LEUCINE that acts as a pancreatic lipase inhibitor to limit the absorption of dietary fat; it is used in the management of obesity.. orlistat : A carboxylic ester resulting from the formal condensation of the carboxy group of N-formyl-L-leucine with the hydroxy group of (3S,4S)-3-hexyl-4-[(2S)-2-hydroxytridecyl]oxetan-2-one. A pancreatic lipase inhibitor, it is used as an anti-obesity drug.	4.3	5	0	beta-lactone; carboxylic ester; formamides; L-leucine derivative	anti-obesity agent; bacterial metabolite; EC 2.3.1.85 (fatty acid synthase) inhibitor; EC 3.1.1.3 (triacylglycerol lipase) inhibitor
idoxifene idoxifene: structure given in first source	2.05	1	0	stilbenoid
quinine [no description available]	3.87	3	0	cinchona alkaloid	antimalarial; muscle relaxant; non-narcotic analgesic
amrubicin amrubicin: structure in first source; a 9-amino-anthracycline antibiotic. amrubicin : A synthetic anthracycline antibiotic with molecular formula C25H25NO9. A specific inhibitor of topoisomerase II, it is used (particularly as the hydrochloride salt) in the treatment of cancer, especially lung cancer, where it is a prodrug for the active metabolite, ambrucinol.	3.12	1	0	anthracycline antibiotic; methyl ketone; primary amino compound; quinone; tetracenes	antineoplastic agent; prodrug; topoisomerase II inhibitor
isepamicin [no description available]	2.04	1	0
ifetroban ifetroban: thromboxane receptor antagonist; structure given in first source; a 7-oxabicyclo(2.2.1)heptane derivative	2.04	1	0	benzenes; monocarboxylic acid
lamifiban lamifiban: a nonpeptide glycoprotein IIb/IIIa antagonist; prevents platelet loss during experimental cardiopulmonary bypass	2.04	1	0	N-acylglycine
fospropofol [no description available]	3.23	1	0	alkylbenzene
tandutinib [no description available]	2.08	1	0	aromatic ether; N-arylpiperazine; N-carbamoylpiperazine; phenylureas; piperidines; quinazolines; tertiary amino compound	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
vx-745 [no description available]	2.08	1	0	aryl sulfide; dichlorobenzene; difluorobenzene; pyrimidopyridazine	anti-inflammatory drug; apoptosis inducer; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
corlanor ivabradine hydrochloride : A hydrochloride obtained by combining ivabradine with one molar equivalent of hydrochloric acid. Used to treat patients with angina who have intolerance to beta blockers and/or heart failure.	2.08	1	0	hydrochloride	cardiotonic drug
azilect [no description available]	2.08	1	0
rasagiline [no description available]	3.23	1	0	indanes; secondary amine; terminal acetylenic compound	EC 1.4.3.4 (monoamine oxidase) inhibitor; neuroprotective agent
dasatinib N-(2-chloro-6-methylphenyl)-2-((6-(4-(2-hydroxyethyl)piperazin-1-yl)-2-methylpyrimidin-4-yl)amino)-1,3-thiazole-5-carboxamide: a dasatinib prodrug; structure in first source. dasatinib (anhydrous) : An aminopyrimidine that is 2-methylpyrimidine which is substituted at position 4 by the primary amino group of 2-amino-1,3-thiazole-5-carboxylic acid and at position 6 by a 4-(2-hydroxyethyl)piperazin-1-yl group, and in which the carboxylic acid group has been formally condensed with 2-chloro-6-methylaniline to afford the corresponding amide. A multi-targeted kinase inhibitor, it is used, particularly as the monohydrate, for the treatment of chronic, accelerated, or myeloid or lymphoid blast phase chronic myeloid leukemia. Note that the name 'dasatinib' is used to refer to the monohydrate (USAN) as well as to anhydrous dasatinib (INN).	8.6	18	1	1,3-thiazoles; aminopyrimidine; monocarboxylic acid amide; N-(2-hydroxyethyl)piperazine; N-arylpiperazine; organochlorine compound; secondary amino compound; tertiary amino compound	anticoronaviral agent; antineoplastic agent; tyrosine kinase inhibitor
zd 6474 CH 331: structure in first source	7.82	8	1	aromatic ether; organobromine compound; organofluorine compound; piperidines; quinazolines; secondary amine	antineoplastic agent; tyrosine kinase inhibitor
telavancin telavancin: an anti-infective agent; structure in first source. telavancin : A glycopeptide that is vancomycin substituted at position N-3'' by a 2-(decylamino)ethyl group and at position C-29 by a (phosphonomethyl)aminomethyl group. Used as its hydrochloride salt for treatment of adults with complicated skin and skin structure infections caused by bacteria.	2.04	1	0	glycopeptide	antibacterial drug; antimicrobial agent
nitinol nitinol: RN given refers to cpd with MF of Ni-Ti; do not confuse with titanium nickelide; other nitinols (nitinol SE and nitinol 55) are Co-Ni-Ti alloys	2.17	1	0
silybin [no description available]	2.05	1	0
compound 968 compound 968: a glutaminase inhibitor. 5-[3-bromo-4-(dimethylamino)phenyl]-2,2-dimethyl-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one : A partially hydrogenated benzophenanthridine carrying an oxo group at C-4, geminal methyl groups at C-2 and a 3-bromo-4-(dimethylamino)phenyl group at C-5.	2.08	1	0	benzophenanthridine	EC 3.5.1.2 (glutaminase) inhibitor
yya-021 YYA-021: an HIV entry inhibitor; structure in first source	2.6	1	0
ovalbumin Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily.	2.44	2	0
sb-224289 SB 224289 : A member of the class of benzamides obtained by formal condensation of the carboxy group of 2'-methyl-4'-(5-methyl-1,2,4-oxadiazol-3-yl)biphenyl-4-carboxylic acid with the secondary amino group of 1'-methyl-6,7-dihydro-5H-spiro[furo[2,3-f]indole-3,4'-piperidine]. Selective 5-HT1B receptor antagonist (pKi = 8.2). Displays >60-fold selectivity over 5-HT1D, 5-HT1A, 5-HT1E, 5-HT1F, 5-HT2A and 5-HT2C receptors in radioligand binding and functional assays. Centrally active following oral administration in vivo.	2.08	1	0	1,2,4-oxadiazole; azaspiro compound; benzamides; organic heterotetracyclic compound	serotonergic antagonist
gw 7647 GW 7647: a PPAR-alpha agonist; structure in first source. GW 7647 : A monocarboxylic acid that is 2-(phenylsulfanyl)isobutyric acid in which the phenyl group is substituted at the para- position by a 3-aza-7-cyclohexylhept-1-yl group in which the nitrogen is acylated by a (cyclohexylamino)carbonyl group.	2.08	1	0	aryl sulfide; monocarboxylic acid; ureas	PPARalpha agonist
fh535 FH535: inhibits Wnt signaling	2.25	1	0	sulfonamide
mtt formazan MTT formazan: a blue MEM-insoluble mitochondrial byproduct; used to determine viability of cells with active mitochondrial dehydrogenase enzymes	2.47	2	0
chloramine-t chloramine-T: RN given refers to unlabeled parent cpd. chloramine T : An organic sodium salt derivative of toluene-4-sulfonamide with a chloro substituent in place of an amino hydrogen.	2.05	1	0	organic sodium salt	allergen; antifouling biocide; disinfectant
l 663536 MK-886: orally active leukotriene biosynthesis inhibitor. 3-[3-(tert-butylsulfanyl)-1-(4-chlorobenzyl)-5-(propan-2-yl)-1H-indol-2-yl]-2,2-dimethylpropanoic acid : A member of the class of indoles that is 1H-indole substituted by a isopropyl group at position 5, a tert-butylsulfanediyl group at position 3, a 4-chlorobenzyl group at position 1 and a 2-carboxy-2-methylpropyl group at position 2. It acts as an inhibitor of arachidonate 5-lipoxygenase.	2.08	1	0	aryl sulfide; indoles; monocarboxylic acid; monochlorobenzenes	antineoplastic agent; EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor; leukotriene antagonist
1-[6-(4-chlorophenyl)-5-imidazo[2,1-b]thiazolyl]-N-[(3,4-dichlorophenyl)methoxy]methanimine [no description available]	2.08	1	0	imidazoles
zinc protoporphyrin ix [no description available]	2.25	1	0
N4-ethyl-N6,1,2-trimethyl-N4-phenylpyrimidin-1-ium-4,6-diamine [no description available]	2.08	1	0	aromatic amine; tertiary amino compound
alpha-chymotrypsin Chymotrypsin: A serine endopeptidase secreted by the pancreas as its zymogen, CHYMOTRYPSINOGEN and carried in the pancreatic juice to the duodenum where it is activated by TRYPSIN. It selectively cleaves aromatic amino acids on the carboxyl side.	7.14	19	1
2-[[2-[2-(2,3-dihydro-1,4-benzodioxin-6-ylamino)-2-oxoethyl]-1-oxo-5-isoquinolinyl]oxy]propanoic acid ethyl ester [no description available]	2.08	1	0	isoquinolines
4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione: a GSK3beta inhibitor. TDZD-8 : A member of the class of thiadiazolidines that is 1,2,4-thiadiazolidine-3,5-dione which is substituted by a methyl group at position 2 and by a benzyl group at position 4. It is a non-ATP competitive inhibitor of glycogen synthase kinase 3beta (GSK3beta). An experimental compound which was being developed for the potential treatment of Alzheimer's disease.	2.41	1	0	benzenes; thiadiazolidine	anti-inflammatory agent; antineoplastic agent; apoptosis inducer; EC 2.7.11.26 (tau-protein kinase) inhibitor; neuroprotective agent
sb 415286 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione: a glycogen synthase kinase-3 inhibitor; structure in first source	2.6	1	0	C-nitro compound; maleimides; monochlorobenzenes; phenols; secondary amino compound; substituted aniline	antioxidant; apoptosis inducer; EC 2.7.11.26 (tau-protein kinase) inhibitor; neuroprotective agent
naphthoquinones Naphthoquinones: Naphthalene rings which contain two ketone moieties in any position. They can be substituted in any position except at the ketone groups.	3.01	4	0
sch 79797 [no description available]	2.08	1	0	quinazolines
sitagliptin sitagliptin : A triazolopyrazine that exhibits hypoglycemic activity.	4.32	5	0	triazolopyrazine; trifluorobenzene	EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor; environmental contaminant; hypoglycemic agent; serine proteinase inhibitor; xenobiotic
osteoprotegerin Osteoprotegerin: A secreted member of the TNF receptor superfamily that negatively regulates osteoclastogenesis. It is a soluble decoy receptor of RANK LIGAND that inhibits both CELL DIFFERENTIATION and function of OSTEOCLASTS by inhibiting the interaction between RANK LIGAND and RECEPTOR ACTIVATOR OF NUCLEAR FACTOR-KAPPA B.	7.07	10	1	long-chain fatty acid
icodextrin Icodextrin: A glucan that is structurally related to maltodextrin, with more than 85% of its molecules having molecular weights between 1640 and 45 000 Daltons (Da), and a weight-average molecular weight of about 20 000 Da; it is used in dialysis fluids as an alternative to glucose-based solutions, and to reduce adhesions after gynecological or abdominal surgery. It has also been used as a vehicle for drugs given via the peritoneal cavity.	2.02	1	0
flosequinan [no description available]	2.05	1	0	quinolines
4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1h-imidazol-2-yl)benzamide 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide: a TGF-beta type I receptor kinase activity inhibitor	2.08	1	0	benzamides; benzodioxoles; imidazoles; pyridines	EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
rhodamine 123 Rhodamine 123: A fluorescent probe with low toxicity which is a potent substrate for ATP BINDING CASSETTE TRANSPORTER, SUBFAMILY B, MEMBER 1 and the bacterial multidrug efflux transporter. It is used to assess mitochondrial bioenergetics in living cells and to measure the efflux activity of ATP BINDING CASSETTE TRANSPORTER, SUBFAMILY B, MEMBER 1 in both normal and malignant cells. (Leukemia 1997;11(7):1124-30). rhodamine 123(1+) : A cationic fluorescent dye derived from 9-phenylxanthene.	2.08	1	0	organic cation; xanthene dye	fluorochrome
tolcapone Tolcapone: A benzophenone and nitrophenol compound that acts as an inhibitor of CATECHOL O-METHYLTRANSFERASE, an enzyme involved in the metabolism of DOPAMINE and LEVODOPA. It is used in the treatment of PARKINSON DISEASE in patients for whom levodopa is ineffective or contraindicated.. tolcapone : Benzophenone substituted on one of the phenyl rings at C-3 and C-4 by hydroxy groups and at C-5 by a nitro group, and on the other phenyl ring by a methyl group at C-4. It is an inhibitor of catechol O-methyltransferase.	4.08	4	0	2-nitrophenols; benzophenones; catechols	antiparkinson drug; EC 2.1.1.6 (catechol O-methyltransferase) inhibitor
myelin basic protein Myelin Basic Protein: An abundant cytosolic protein that plays a critical role in the structure of multilamellar myelin. Myelin basic protein binds to the cytosolic sides of myelin cell membranes and causes a tight adhesion between opposing cell membranes.	2.13	1	0
1-(4-Fluorophenyl)-3-(3-(4-fluorophenyl)-3-hydroxypropyl)-4-(4-hydroxyphenyl)azetidin-2-one [no description available]	2.08	1	0	monobactam
imd 0354 N-(3,5-bis(trifluoromethyl)phenyl)-5-chloro-2-hydroxybenzamide: a cardioprotective agent that inhibits IkappaB kinase beta (IKKbeta); structure in first source	2.08	1	0	benzamides
ex 527 6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide: structure in first source. 6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide : A member of the class of carbazoles that is 2,3,4,9-tetrahydro-1H-carbazole which is substituted at position 1 by an aminocarbohyl group and at position 6 by a chlorine.	2.08	1	0	carbazoles; monocarboxylic acid amide; organochlorine compound
diethyl maleate diethyl maleate : A maleate ester resulting from the formal condensation of both carboxy groups of maleic acid with ethanol. A colourless liquid at room temperature (m.p. -10degreeC) with boiling point 220degreeC at 1 atm., it is commonly used as a dienophile for Diels-Alder-type cycloaddition reactions in organic synthesis.	2.06	1	0	ethyl ester; maleate ester	glutathione depleting agent
tak-220 TAK-220: structure in first source	2.6	1	0
jtk-303 [no description available]	2.6	1	0	aromatic ether; monochlorobenzenes; organofluorine compound; quinolinemonocarboxylic acid; quinolone	HIV-1 integrase inhibitor
nbd 557 [no description available]	2.6	1	0
sphingosine sphing-4-enine : A sphingenine in which the C=C double bond is located at the 4-position.. sphingenine : A 2-aminooctadecene-1,3-diol having (2S,3R)-configuration.. sphingoid : Sphinganine, its homologs and stereoisomers, and the hydroxy and unsaturated derivatives of these compounds.. 2-aminooctadec-4-ene-1,3-diol : A 2-aminooctadecene-1,3-diol having its double bond at position 4.	4.13	2	0	sphing-4-enine	human metabolite; mouse metabolite
quercetin [no description available]	3.33	6	0	7-hydroxyflavonol; pentahydroxyflavone	antibacterial agent; antineoplastic agent; antioxidant; Aurora kinase inhibitor; chelator; EC 1.10.99.2 [ribosyldihydronicotinamide dehydrogenase (quinone)] inhibitor; geroprotector; phytoestrogen; plant metabolite; protein kinase inhibitor; radical scavenger
bilirubin [no description available]	7.72	2	0	biladienes; dicarboxylic acid	antioxidant; human metabolite; mouse metabolite
dinoprostone prostaglandin E2 : Prostaglandin F2alpha in which the hydroxy group at position 9 has been oxidised to the corresponding ketone. Prostaglandin E2 is the most common and most biologically potent of mammalian prostaglandins.	2.49	2	0	prostaglandins E	human metabolite; mouse metabolite; oxytocic
dinoprost Dinoprost: A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.. prostaglandin F2alpha : A prostaglandins Falpha that is prosta-5,13-dien-1-oic acid substituted by hydroxy groups at positions 9, 11 and 15. It is a naturally occurring prostaglandin used to induce labor.	2.05	1	0	monocarboxylic acid; prostaglandins Falpha	human metabolite; mouse metabolite
formononetin [no description available]	7.21	1	0	4'-methoxyisoflavones; 7-hydroxyisoflavones	phytoestrogen; plant metabolite
apigenin Chamomile: Common name for several daisy-like plants (MATRICARIA; TRIPLEUROSPERMUM; ANTHEMIS; CHAMAEMELUM) native to Europe and Western Asia, now naturalized in the United States and Australia.	2.11	1	0	trihydroxyflavone	antineoplastic agent; metabolite
luteolin [no description available]	10.52	3	1	3'-hydroxyflavonoid; tetrahydroxyflavone	angiogenesis inhibitor; anti-inflammatory agent; antineoplastic agent; apoptosis inducer; c-Jun N-terminal kinase inhibitor; EC 2.3.1.85 (fatty acid synthase) inhibitor; immunomodulator; nephroprotective agent; plant metabolite; radical scavenger; vascular endothelial growth factor receptor antagonist
calcitriol dihydroxy-vitamin D3: as a major in vitro metabolite of 1alpha,25-dihydroxyvitamin D3, produced in primary cultures of neonatal human keratinocytes	5.06	7	0	D3 vitamins; hydroxycalciol; triol	antineoplastic agent; antipsoriatic; bone density conservation agent; calcium channel agonist; calcium channel modulator; hormone; human metabolite; immunomodulator; metabolite; mouse metabolite; nutraceutical
beta carotene beta Carotene: A carotenoid that is a precursor of VITAMIN A. Beta carotene is administered to reduce the severity of photosensitivity reactions in patients with erythropoietic protoporphyria (PORPHYRIA, ERYTHROPOIETIC).. provitamin A : A provitamin that can be converted into vitamin A by enzymes from animal tissues.	2.05	1	0	carotenoid beta-end derivative; cyclic carotene	antioxidant; biological pigment; cofactor; ferroptosis inhibitor; human metabolite; mouse metabolite; plant metabolite; provitamin A
leukotriene b4 Leukotriene B4: The major metabolite in neutrophil polymorphonuclear leukocytes. It stimulates polymorphonuclear cell function (degranulation, formation of oxygen-centered free radicals, arachidonic acid release, and metabolism). (From Dictionary of Prostaglandins and Related Compounds, 1990). leukotriene B4 : A leukotriene composed of (6Z,8E,10E,14Z)-icosatetraenoic acid having (5S)- and (12R)-hydroxy substituents. It is a lipid mediator of inflammation that is generated from arachidonic acid via the 5-lipoxygenase pathway.	2.07	1	0	dihydroxy monocarboxylic acid; hydroxy polyunsaturated fatty acid; leukotriene; long-chain fatty acid	human metabolite; mouse metabolite; plant metabolite; vasoconstrictor agent
5'-o-caffeoylquinic acid trans-5-O-caffeoyl-D-quinic acid : A cinnamate ester obtained by formal condensation of the carboxy group of trans-caffeic acid with the 5-hydroxy group of quinic acid.	2.6	1	0	cinnamate ester; cyclitol carboxylic acid	plant metabolite
luteolin-7-glucoside luteolin-7-glucoside: has both antiasthmatic and antineoplastic activities; has 3C protease inhibitory activity; isolated from Ligustrum lucidum. luteolin 7-O-beta-D-glucoside : A glycosyloxyflavone that is luteolin substituted by a beta-D-glucopyranosyl moiety at position 7 via a glycosidic linkage.	2.6	1	0	beta-D-glucoside; glycosyloxyflavone; monosaccharide derivative; trihydroxyflavone	antioxidant; plant metabolite
alprostadil [no description available]	2.77	3	0	prostaglandins E	anticoagulant; human metabolite; platelet aggregation inhibitor; vasodilator agent
cyclosporine [no description available]	2.6	1	0
vitamin d 2 Ergocalciferols: Derivatives of ERGOSTEROL formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. They differ from CHOLECALCIFEROL in having a double bond between C22 and C23 and a methyl group at C24.. vitamin D2 : A vitamin D supplement and has been isolated from alfalfa.	3.61	2	0	hydroxy seco-steroid; seco-ergostane; vitamin D	bone density conservation agent; nutraceutical; plant metabolite; rodenticide
cholecalciferol Cholecalciferol: Derivative of 7-dehydroxycholesterol formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. It differs from ERGOCALCIFEROL in having a single bond between C22 and C23 and lacking a methyl group at C24.. calciol : A hydroxy seco-steroid that is (5Z,7E)-9,10-secocholesta-5,7,10(19)-triene in which the pro-S hydrogen at position 3 has been replaced by a hydroxy group. It is the inactive form of vitamin D3, being hydroxylated in the liver to calcidiol (25-hydroxyvitamin D3), which is then further hydroxylated in the kidney to give calcitriol (1,25-dihydroxyvitamin D3), the active hormone.	2.47	2	0	D3 vitamins; hydroxy seco-steroid; seco-cholestane; secondary alcohol; steroid hormone	geroprotector; human metabolite
kaempferol [no description available]	2.25	1	0	7-hydroxyflavonol; flavonols; tetrahydroxyflavone	antibacterial agent; geroprotector; human blood serum metabolite; human urinary metabolite; human xenobiotic metabolite; plant metabolite
gamma-linolenic acid gamma-Linolenic Acid: An omega-6 fatty acid produced in the body as the delta 6-desaturase metabolite of linoleic acid. It is converted to dihomo-gamma-linolenic acid, a biosynthetic precursor of monoenoic prostaglandins such as PGE1. (From Merck Index, 11th ed). gamma-linolenic acid : A C18, omega-6 acid fatty acid comprising a linolenic acid having cis- double bonds at positions 6, 9 and 12.	2.08	1	0	linolenic acid; omega-6 fatty acid	human metabolite; mouse metabolite; plant metabolite
harmine Harmine: Alkaloid isolated from seeds of PEGANUM HARMALA; ZYGOPHYLLACEAE. It is identical to banisterine, or telepathine, from Banisteria caapi and is one of the active ingredients of hallucinogenic drinks made in the western Amazon region from related plants. It has no therapeutic use, but (as banisterine) was hailed as a cure for postencephalitic PARKINSON DISEASE in the 1920's.. harmine : A harmala alkaloid in which the harman skeleton is methoxy-substituted at C-7.	2.6	1	0	harmala alkaloid	anti-HIV agent; EC 1.4.3.4 (monoamine oxidase) inhibitor; metabolite
genistein [no description available]	4.37	3	0	7-hydroxyisoflavones	antineoplastic agent; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; geroprotector; human urinary metabolite; phytoestrogen; plant metabolite; tyrosine kinase inhibitor
amphotericin b Amphotericin B: Macrolide antifungal antibiotic produced by Streptomyces nodosus obtained from soil of the Orinoco river region of Venezuela.. amphotericin B : A macrolide antibiotic used to treat potentially life-threatening fungal infections.	3.59	2	0	antibiotic antifungal drug; macrolide antibiotic; polyene antibiotic	antiamoebic agent; antiprotozoal drug; bacterial metabolite
clavulanic acid Clavulanic Acid: A beta-lactam antibiotic produced by the actinobacterium Streptomyces clavuligerus. It is a suicide inhibitor of bacterial beta-lactamase enzymes. Administered alone, it has only weak antibacterial activity against most organisms, but given in combination with other beta-lactam antibiotics it prevents antibiotic inactivation by microbial lactamase.. clavulanate : The conjugate base of clavulanic acid.. clavulanic acid : Antibiotic isolated from Streptomyces clavuligerus. It acts as a suicide inhibitor of bacterial beta-lactamase enzymes.	2.45	2	0	oxapenam	antibacterial drug; anxiolytic drug; bacterial metabolite; EC 3.5.2.6 (beta-lactamase) inhibitor
pulmicort Budesonide: A glucocorticoid used in the management of ASTHMA, the treatment of various skin disorders, and allergic RHINITIS.. budesonide : A glucocorticoid steroid having a highly oxygenated pregna-1,4-diene structure. It is used mainly in the treatment of asthma and non-infectious rhinitis and for treatment and prevention of nasal polyposis.	4.08	4	0	11beta-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; cyclic acetal; glucocorticoid; primary alpha-hydroxy ketone	anti-inflammatory drug; bronchodilator agent; drug allergen
oxymetholone Oxymetholone: A synthetic hormone with anabolic and androgenic properties. It is used mainly in the treatment of anemias. According to the Fourth Annual Report on Carcinogens (NTP 85-002), this compound may reasonably be anticipated to be a carcinogen. (From Merck Index, 11th ed). oxymetholone : A 3-oxo-5alpha- steroid that is 4,5alpha-dihydrotestosterone which is substituted by a hydroxymethylidene group at position 2 and by a methyl group at the 17alpha position. A synthetic androgen, it was mainly used for the treatment of anaemias until being replaced by treatments with fewer side effects.	3.87	3	0
eprosartan eprosartan: angiotensin II receptor antagonist. eprosartan : A member of the class of imidazoles and thiophenes that is an angiotensin II receptor antagonist used for the treatment of high blood pressure.	4.13	4	0	dicarboxylic acid; imidazoles; thiophenes	angiotensin receptor antagonist; antihypertensive agent; environmental contaminant; xenobiotic
montelukast montelukast: a leukotriene D4 receptor antagonist	3.86	3	0	aliphatic sulfide; monocarboxylic acid; quinolines	anti-arrhythmia drug; anti-asthmatic drug; leukotriene antagonist
mivacurium Mivacurium: An isoquinoline derivative that is used as a short-acting non-depolarizing agent.	3.58	2	0	isoquinolines
brompheniramine maleate brompheniramine maleate : The maleic acid salt of brompheniramine. A histamine H1 receptor antagonist, it is used for the symptomatic relief of allergic conditions, including rhinitis and conjunctivitis.	2.08	1	0	maleate salt	anti-allergic agent
dexchlorpheniramine maleate [no description available]	2.08	1	0	organic molecular entity
hemabate carboprost tromethamine : The tromethamine salt of carboprost. It is used as an abortifacient agent that is effective in both the first and second trimesters of pregnancy.	3.23	1	0
mycophenolate mofetil mycophenolate mofetil : A carboxylic ester resulting from the formal condensation between the carboxylic acid group of mycophenolic acid and the hydroxy group of 2-(morpholin-4-yl)ethanol. In the liver, it is metabolised to mycophenolic acid, an immunosuppressant for which it is a prodrug. It is widely used to prevent tissue rejection following organ transplants as well as for the treatment of certain autoimmune diseases.	4.13	4	0	carboxylic ester; ether; gamma-lactone; phenols; tertiary amino compound	anticoronaviral agent; EC 1.1.1.205 (IMP dehydrogenase) inhibitor; immunosuppressive agent; prodrug
entacapone entacapone: structure given in first source. entacapone : A monocarboxylic acid amide that is N,N-diethylprop-2-enamide in which the hydrogen at position 2 is substituted by a cyano group and the hydrogen at the 3E position is substituted by a 3,4-dihydroxy-5-nitrophenyl group.	4.29	5	0	2-nitrophenols; catechols; monocarboxylic acid amide; nitrile	antidyskinesia agent; antiparkinson drug; central nervous system drug; EC 2.1.1.6 (catechol O-methyltransferase) inhibitor
paricalcitol [no description available]	3.58	2	0	hydroxy seco-steroid; seco-cholestane	antiparathyroid drug
astaxanthine astaxanthine: a keto form of carotene; pigment in flesh of Scottish salmon (Salmo salar) crustacoa-lobster (Homarus gammarus, flamingo feathers; structure; a carotenoid without vitamin A activity, has shown anti-oxidant and anti-inflammatory activities. astaxanthin : A carotenone that consists of beta,beta-carotene-4,4'-dione bearing two hydroxy substituents at positions 3 and 3' (the 3S,3'S diastereomer). A carotenoid pigment found mainly in animals (crustaceans, echinoderms) but also occurring in plants. It can occur free (as a red pigment), as an ester, or as a blue, brown or green chromoprotein.	2.05	1	0	carotenol; carotenone	animal metabolite; anticoagulant; antioxidant; food colouring; plant metabolite
cucurbitacin i cucurbitacin I: toxic constituent in edible gourd; see also records for cucurbitacins & specific cucurbitacins. cucurbitacin I : A cucurbitacin that is 9,10,14-trimethyl-4,9-cyclo-9,10-secocholesta-2,5,23-triene substituted by hydroxy groups at positions 2, 16, 20 and 25 and oxo groups at positions 1, 11 and 22.	3.48	1	1	cucurbitacin; tertiary alpha-hydroxy ketone	antineoplastic agent; plant metabolite
geranylgeraniol (E,E,E)-geranylgeraniol : A geranylgeraniol in which all four double bonds have E- (trans-) geometry.	2.17	1	0	geranylgeraniol
humulene humulene: structure given in first source. (1E,4E,8E)-alpha-humulene : The (1E,4E,8E)-isomer of alpha-humulene.	4.8	1	1	alpha-humulene
zearalenone Zearalenone: (S-(E))-3,4,5,6,8,10-Hexahydro-14,16-dihydroxy-3-methyl-1H-2-benzoxacyclotetradecin-1,7(8H)-dione. One of a group of compounds known under the general designation of resorcylic acid lactones. Cis, trans, dextro and levo forms have been isolated from the fungus Gibberella zeae (formerly Fusarium graminearum). They have estrogenic activity, cause toxicity in livestock as feed contaminant, and have been used as anabolic or estrogen substitutes.. zearalenone : A macrolide comprising a fourteen-membered lactone fused to 1,3-dihydroxybenzene; a potent estrogenic metabolite produced by some Giberella species.	2.13	1	0	macrolide; resorcinols	fungal metabolite; mycoestrogen
amentoflavone [no description available]	2.6	1	0	biflavonoid; hydroxyflavone; ring assembly	angiogenesis inhibitor; antiviral agent; cathepsin B inhibitor; P450 inhibitor; plant metabolite
baicalein [no description available]	2.6	1	0	trihydroxyflavone	angiogenesis inhibitor; anti-inflammatory agent; antibacterial agent; anticoronaviral agent; antifungal agent; antineoplastic agent; antioxidant; apoptosis inducer; EC 1.13.11.31 (arachidonate 12-lipoxygenase) inhibitor; EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor; EC 4.1.1.17 (ornithine decarboxylase) inhibitor; ferroptosis inhibitor; geroprotector; hormone antagonist; plant metabolite; prostaglandin antagonist; radical scavenger
diosmin [no description available]	2.05	1	0	dihydroxyflavanone; disaccharide derivative; glycosyloxyflavone; monomethoxyflavone; rutinoside	anti-inflammatory agent; antioxidant
galangin 5,7-dihydroxyflavonol: antimicrobial from the twigs of Populus nigra x Populus deltoides; structure in first source. galangin : A 7-hydroxyflavonol with additional hydroxy groups at positions 3 and 5 respectively; a growth inhibitor of breast tumor cells.	2.25	1	0	7-hydroxyflavonol; trihydroxyflavone	antimicrobial agent; EC 3.1.1.3 (triacylglycerol lipase) inhibitor; plant metabolite
genkwanin genkwanin: structure. genkwanin : A monomethoxyflavone that is apigenin in which the hydroxy group at position 7 is methylated.	2.6	1	0	dihydroxyflavone; monomethoxyflavone	metabolite
hyperoside quercetin 3-O-beta-D-galactopyranoside : A quercetin O-glycoside that is quercetin with a beta-D-galactosyl residue attached at position 3. Isolated from Artemisia capillaris, it exhibits hepatoprotective activity.	2.6	1	0	beta-D-galactoside; monosaccharide derivative; quercetin O-glycoside; tetrahydroxyflavone	hepatoprotective agent; plant metabolite
mangostin mangostin: xanthone from rind of Garcinia mangostana Linn. fruit. alpha-mangostin : A member of the class of xanthones that is 9H-xanthene substituted by hydroxy group at positions 1, 3 and 6, a methoxy group at position 7, an oxo group at position 9 and prenyl groups at positions 2 and 8. Isolated from the stems of Cratoxylum cochinchinense, it exhibits antioxidant, antimicrobial and antitumour activities.	2.6	1	0	aromatic ether; phenols; xanthones	antimicrobial agent; antineoplastic agent; antioxidant; plant metabolite
3-methylquercetin isorhamnetin : A monomethoxyflavone that is quercetin in which the hydroxy group at position 3' is replaced by a methoxy group.	2.6	1	0	7-hydroxyflavonol; monomethoxyflavone; tetrahydroxyflavone	anticoagulant; EC 1.14.18.1 (tyrosinase) inhibitor; metabolite
kaempferide kaempferide: structure in first source. kaempferide : A monomethoxyflavone that is the 4'-O-methyl derivative of kaempferol.	2.76	2	0	7-hydroxyflavonol; monomethoxyflavone; trihydroxyflavone	antihypertensive agent; metabolite
morin morin: a light yellowish pigment found in the wood of old fustic (Chlorophora tinctoria). morin : A pentahydroxyflavone that is 7-hydroxyflavonol bearing three additional hydroxy substituents at positions 2' 4' and 5.	2.25	1	0	7-hydroxyflavonol; pentahydroxyflavone	angiogenesis modulating agent; anti-inflammatory agent; antibacterial agent; antihypertensive agent; antineoplastic agent; antioxidant; EC 5.99.1.2 (DNA topoisomerase) inhibitor; hepatoprotective agent; metabolite; neuroprotective agent
orientin orientin: structure given in first source; RN given refers to the (D-glucopyranosyl)-isomer. orientin : A C-glycosyl compound that is luteolin substituted by a beta-D-glucopyranosyl moiety at position 8.	2.6	1	0	3'-hydroxyflavonoid; C-glycosyl compound; tetrahydroxyflavone	antioxidant; metabolite
scutellarein scutellarein: aglycone of scutellarin from Scutellaria baicalensis; carthamidin is 2S isomer of scutellarein; do not confuse with isoscutellarein and/or isocarthamidin which are respective regioisomers, or with the scutelarin protein. scutellarein : Flavone substituted with hydroxy groups at C-4', -5, -6 and -7.	2.76	2	0	tetrahydroxyflavone	metabolite
wogonin wogonin: structure in first source. wogonin : A dihydroxy- and monomethoxy-flavone in which the hydroxy groups are positioned at C-5 and C-7 and the methoxy group is at C-8.	2.25	1	0	dihydroxyflavone; monomethoxyflavone	angiogenesis inhibitor; antineoplastic agent; cyclooxygenase 2 inhibitor; plant metabolite
daidzein [no description available]	2.25	1	0	7-hydroxyisoflavones	antineoplastic agent; EC 2.7.7.7 (DNA-directed DNA polymerase) inhibitor; EC 3.2.1.20 (alpha-glucosidase) inhibitor; phytoestrogen; plant metabolite
trans-2,3',4,5'-tetrahydroxystilbene trans-2,3',4,5'-tetrahydroxystilbene: hydroxystilbene oxyresveratrol	2.6	1	0	stilbenoid
polydatin trans-piceid : A stilbenoid that is trans-resveratrol substituted at position 3 by a beta-D-glucosyl residue.	2.6	1	0	beta-D-glucoside; monosaccharide derivative; polyphenol; stilbenoid	anti-arrhythmia drug; antioxidant; geroprotector; hepatoprotective agent; metabolite; nephroprotective agent; potassium channel modulator
pterostilbene [no description available]	2.53	2	0	diether; methoxybenzenes; stilbenol	anti-inflammatory agent; antineoplastic agent; antioxidant; apoptosis inducer; hypoglycemic agent; neuroprotective agent; neurotransmitter; plant metabolite; radical scavenger
chicoric acid chicoric acid: inhibits HIV-1 integrase	2.6	1	0	organooxygen compound	geroprotector; HIV-1 integrase inhibitor
cynarine cynarine: active principle of the artichoke; functions primarily as a cholagogue and choleretic and also as antilipemic agent	2.05	1	0	alkyl caffeate ester; quinic acid	plant metabolite
caffeic acid phenethyl ester phenethyl caffeate : An alkyl caffeate ester in which 2-phenylethyl is the alkyl component.	2.11	1	0	alkyl caffeate ester	anti-inflammatory agent; antibacterial agent; antineoplastic agent; antioxidant; antiviral agent; immunomodulator; metabolite; neuroprotective agent
acteoside acteoside: a protein kinase C inhibitor with hepatoprotective, anti-asthmatic, and analgesic activities; a phenylethanoid glycoside related to isoacteoside; from leaves of Lippia multiflora (Verbenaceae). acteoside : A glycoside that is the alpha-L-rhamnosyl-(1->3)-beta-D-glucoside of hydroxytyrosol in which the hydroxy group at position 4 of the glucopyranosyl moiety has undergone esterification by formal condensation with trans-caffeic acid.	2.6	1	0	catechols; cinnamate ester; disaccharide derivative; glycoside; polyphenol	anti-inflammatory agent; antibacterial agent; antileishmanial agent; neuroprotective agent; plant metabolite
wedelolactone wedelolactone: antihepatotoxic coumestan from Eclipta prostrata and Wedelia calendulacea (both Asteraceae); structure given in first source. wedelolactone : A member of the class of coumestans that is coumestan with hydroxy substituents as positions 1, 8 and 9 and a methoxy substituent at position 3.	2.04	1	0	aromatic ether; coumestans; delta-lactone; polyphenol	antineoplastic agent; apoptosis inducer; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; hepatoprotective agent; metabolite
maytansine Maytansine: An ansa macrolide isolated from the MAYTENUS genus of East African shrubs.. maytansine : An organic heterotetracyclic compound and 19-membered macrocyclic lactam antibiotic originally isolated from the Ethiopian shrub Maytenus serrata but also found in other Maytenus species. It exhibits cytotoxicity against many tumour cell lines.	2.25	1	0	alpha-amino acid ester; carbamate ester; epoxide; maytansinoid; organic heterotetracyclic compound; organochlorine compound	antimicrobial agent; antimitotic; antineoplastic agent; plant metabolite; tubulin modulator
rottlerin rottlerin: an angiogenesis inhibitor; an inhibitor of protein kinase Cdelta (PKCdelta) and calmodulin kinase III; RN refers to (E)-isomer; do not confuse this chalcone with an anthraquinone that is also called rottlerin (RN 481-72-1);. rottlerin : A chromenol that is 2,2-dimethyl-2H-chromene substituted by hydroxy groups at positions 5 and 7, a 3-acetyl-2,4,6-trihydroxy-5-methylbenzyl group at position 6 and a (1E)-3-oxo-1-phenylprop-1-en-3-yl group at position 8. A potassium channel opener, it is isolated from Mallotus philippensis.	2.74	3	0	aromatic ketone; benzenetriol; chromenol; enone; methyl ketone	anti-allergic agent; antihypertensive agent; antineoplastic agent; apoptosis inducer; K-ATP channel agonist; metabolite
sdz psc 833 valspodar: nonimmunosuppressive cyclosporin analog which is a potent multidrug resistance modifier; 7-10 fold more potent than cyclosporin A; a potent P glycoprotein inhibitor; MW 1215	2.72	3	0	homodetic cyclic peptide
l 660,711 [no description available]	2.08	1	0	quinolines
coenzyme q10 coenzyme Q10: Ubiquinone ring with a chain of 10 isoprene units; redox equilibrium with ubiqunol serving in mitochondrial inner membrane to transfer electrons; presence during reconstitution of acetylcholine receptor into phospholipid vesicles yields vesicles active in catalyzing carbamylcholine-sensitive Na+ flux; coenzyme Q10 depletion has been noted with use of statins. coenzyme Q10 : A ubiquinone having a side chain of 10 isoprenoid units. In the naturally occurring isomer, all isoprenyl double bonds are in the E- configuration.	7.53	2	0	ubiquinones	antioxidant; ferroptosis inhibitor; human metabolite
cerulenin Cerulenin: An epoxydodecadienamide isolated from several species, including ACREMONIUM, Acrocylindrum, and Helicoceras. It inhibits the biosynthesis of several lipids by interfering with enzyme function.. cerulenin : An epoxydodecadienamide isolated from several species, including Acremonium, Acrocylindrum and Helicoceras. It inhibits the biosynthesis of several lipids by interfering with enzyme function.	2.07	1	0	epoxide; monocarboxylic acid amide	antifungal agent; antiinfective agent; antilipemic drug; antimetabolite; antimicrobial agent; fatty acid synthesis inhibitor
travoprost Travoprost: A cloprostenol derivative that is used as an ANTIHYPERTENSIVE AGENT in the treatment of OPEN-ANGLE GLAUCOMA and OCULAR HYPERTENSION.. travoprost : The isopropyl ester of prostaglandin F2alpha in which the pentyl group is replaced by a 3-(trifluoromethyl)phenoxymethyl group. A synthetic analogue of prostaglandin F2alpha, ophthalmic solutions of travoprost are used as a topical medication for controlling the progression of open-angle glaucoma and ocular hypertension, by reducing intraocular pressure. It is a pro-drug; the isopropyl ester group is hydrolysed by esterases in the cornea to the biologically active free acid, fluprostenol.	2.08	1	0	(trifluoromethyl)benzenes; isopropyl ester; prostaglandins Falpha	antiglaucoma drug; antihypertensive agent; ophthalmology drug; prodrug; prostaglandin receptor agonist
tranilast tranilast: antiallergic drug; potent inhibitor of homologous passive cutaneous anaphylaxis. tranilast : An amidobenzoic acid that is anthranilic acid in which one of the anilino hydrogens is replaced by a 3,4-dimethoxycinnamoyl group.	2.47	2	0	amidobenzoic acid; cinnamamides; dimethoxybenzene; secondary carboxamide	anti-allergic agent; anti-asthmatic drug; antineoplastic agent; aryl hydrocarbon receptor agonist; calcium channel blocker; hepatoprotective agent; nephroprotective agent
7432 s Ceftibuten: A cephalosporin antibacterial agent that is used in the treatment of infections, including urinary-tract and respiratory-tract infections.. ceftibuten : A third-generation cephalosporin antibiotic with a [(2Z)-2-(2-amino-1,3-thiazol-4-yl)-4-carboxybut-2-enoyl]amino substituent at the 7 position of the cephem skeleton. An orally-administered agent, ceftibuten is used as the dihydrate to treat urinary-tract and respiratory-tract infections.	3.23	1	0	cephalosporin; dicarboxylic acid	antibacterial drug
tocotrienol, alpha alpha-tocotrienol : A tocotrienol that is chroman-6-ol substituted by methyl groups at positions 2, 5, 7 and 8 and a farnesyl chain at position 2. It has been found in palm oil derived from Elaeis guineensis.	2.6	1	0	tocotrienol; vitamin E	ferroptosis inhibitor; human metabolite; neuroprotective agent; plant metabolite
imipenem [no description available]	2.08	1	0	carbapenems
etretinate retinoid : Oxygenated derivatives of 3,7-dimethyl-1-(2,6,6-trimethylcyclohex-1-enyl)nona-1,3,5,7-tetraene and derivatives thereof.	2.47	2	0	enoate ester; ethyl ester; retinoid	keratolytic drug
isotretinoin Isotretinoin: A topical dermatologic agent that is used in the treatment of ACNE VULGARIS and several other skin diseases. The drug has teratogenic and other adverse effects.. isotretinoin : A retinoic acid that is all-trans-retinoic acid in which the double bond which is alpha,beta- to the carboxy group is isomerised to Z configuration. A synthetic retinoid, it is used for the treatment of severe cases of acne and other skin diseases.	3.87	3	0	retinoic acid	antineoplastic agent; keratolytic drug; teratogenic agent
misoprostol Misoprostol: A synthetic analog of natural prostaglandin E1. It produces a dose-related inhibition of gastric acid and pepsin secretion, and enhances mucosal resistance to injury. It is an effective anti-ulcer agent and also has oxytocic properties.. misoprostol : A diastereoisomeric mixture composed of approximately equal amounts of a double racemate of four of the sixteen possible diastereoisomers of methyl (13E)-11,16-dihydroxy-16-methyl-9-oxoprost-13-en-1-oate that is racemic prostaglandin E1 which is lacking the hydroxy group at position 15, but which has an additional hydroxy group at position 16. It is a synthetic prostaglandin E1 analogue, used in the treatment of gastric and duodenal ulcers. A weak abortifacient, it is also used for cervical ripening prior to surgical termination of pregnancy. The (11R,16S)-diastereoisomer is the pharmacologically active form.	2.05	1	0
ketotifen fumarate ketotifen fumarate : An organoammonium salt consisting of equimolar amounts of ketotifen(1+) and fumarate(1-) ions. A blocker of histamine H1 receptors with a stabilising action on mast cells, it is a non-bronchodilator anti-asthmatic drug.	2.08	1	0	organoammonium salt	anti-asthmatic drug; H1-receptor antagonist
epoprostenol [no description available]	3.23	1	0	prostaglandins I	mouse metabolite
indocyanine green [no description available]	3.58	2	0	1,1-diunsubstituted alkanesulfonate; benzoindole; cyanine dye
dinoprost tromethamine [no description available]	2.08	1	0	organic molecular entity
ozagrel ozagrel: RN refers to (E)-isomer	2.05	1	0	cinnamic acids
triprolidine Triprolidine: Histamine H1 antagonist used in allergic rhinitis; ASTHMA; and URTICARIA. It is a component of COUGH and COLD medicines. It may cause drowsiness.. triprolidine : An N-alkylpyrrolidine that is acrivastine in which the pyridine ring is lacking the propenoic acid substituent. It is a sedating antihistamine that is used (generally as the monohydrochloride monohydrate) for the relief of the symptoms of uticaria, rhinitis, and various pruritic skin disorders.	3.23	1	0	N-alkylpyrrolidine; olefinic compound; pyridines	H1-receptor antagonist
pitavastatin pitavastatin : A dihydroxy monocarboxylic acid that is (6E)-7-[2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl]hept-6-enoic acid in which the two hydroxy groups are located at positions 3 and 5 (the 3R,5S-stereoisomer). Used as its calcium salt for treatment of hypercholesterolemia (elevated levels of cholesterol in the blood) on patients unable to sufficiently lower their cholesterol levels by diet and exercise.	3.89	3	0	cyclopropanes; dihydroxy monocarboxylic acid; monofluorobenzenes; quinolines; statin (synthetic)	antioxidant
rosuvastatin calcium S 4522: structure in first source	2.08	1	0	N-acyl-15-methylhexadecasphinganine-1-phosphoethanolamine; organic calcium salt	anti-inflammatory agent; cardioprotective agent; CETP inhibitor
terbinafine hydrochloride terbinafine hydrochloride : A hydrochloride obtained by reaction of terbinafine with one molar equivalent of hydrogen chloride.	2.08	1	0	allylamine antifungal drug; hydrochloride	EC 1.14.13.132 (squalene monooxygenase) inhibitor; P450 inhibitor
ethamolin monoethanolamine oleate: used for treatment of pyogenic granuloma	3.23	1	0	long-chain fatty acid
alatrofloxacin mesylate [no description available]	3.59	2	0
sphingosine 1-phosphate sphingosine 1-phosphate: RN given refers to (R-(R,S-(E)))-isomer; RN for cpd without isomeric designation not available 8/89. sphingosine 1-phosphate : A phosphosphingolipid that consists of sphingosine having a phospho group attached at position 1	3.35	1	0	sphingoid 1-phosphate	mouse metabolite; signalling molecule; sphingosine-1-phosphate receptor agonist; T-cell proliferation inhibitor; vasodilator agent
codeine [no description available]	3.86	3	0	morphinane alkaloid; organic heteropentacyclic compound	antitussive; drug allergen; environmental contaminant; opioid analgesic; opioid receptor agonist; prodrug; xenobiotic
cyclosporine ramihyphin A: one of the metabolites produced by Fusarium sp. S-435; RN given refers to cpd with unknown MF	4.08	4	0	homodetic cyclic peptide	anti-asthmatic drug; anticoronaviral agent; antifungal agent; antirheumatic drug; carcinogenic agent; dermatologic drug; EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor; geroprotector; immunosuppressive agent; metabolite
mitolactol Mitolactol: Alkylating antineoplastic toxic to bone marrow; used in breast cancer, also in combination with other drugs.	2.07	1	0	alcohol; organobromine compound
natamycin [no description available]	2.47	2	0	antibiotic antifungal drug; dicarboxylic acid monoester; epoxide; macrolide antibiotic; monosaccharide derivative; polyene antibiotic	antifungal agrochemical; antimicrobial food preservative; apoptosis inducer; bacterial metabolite; ophthalmology drug
acitretin Acitretin: An oral retinoid effective in the treatment of psoriasis. It is the major metabolite of ETRETINATE with the advantage of a much shorter half-life when compared with etretinate.. acitretin : A retinoid that consists of 3,7-dimethylnona-2,4,6,8-tetraenoic acid having a 4-methoxy-2,3,6-trimethylphenyl group attached at position 9.	3.87	3	0	acitretin; alpha,beta-unsaturated monocarboxylic acid; retinoid	keratolytic drug
dorzolamide dorzolamide: topically effective ocular hypotensive carbonic anhydrase inhibitor; RN refers to mono-HCl (4S-trans)-isomer. dorzolamide : 5,6-Dihydro-4H-thieno[2,3-b]thiopyran-2-sulfonamide 7,7-dioxide in which hydrogens at the 4 and 6 positions are substituted by ethylamino and methyl groups, respectively (4S, trans-configuration). A carbonic anhydrase inhibitor, it is used as the hydrochloride in ophthalmic solutions to lower increased intraocular pressure in the treatment of open-angle glaucoma and ocular hypertension.	2.6	1	0	sulfonamide; thiophenes	antiglaucoma drug; antihypertensive agent; EC 4.2.1.1 (carbonic anhydrase) inhibitor
dothiepin [no description available]	2.05	1	0	dothiepin
estropipate estropipate: used therapeutically in menopausal patients	3.23	1	0	piperazinium salt; steroid sulfate
hydromorphone Hydromorphone: An opioid analgesic made from MORPHINE and used mainly as an analgesic. It has a shorter duration of action than morphine.. hydromorphone : A morphinane alkaloid that is a hydrogenated ketone derivative of morphine. A semi-synthetic drug, it is a centrally acting pain medication of the opioid class.	3.58	2	0	morphinane alkaloid; organic heteropentacyclic compound	mu-opioid receptor agonist; opioid analgesic
levetiracetam Levetiracetam: A pyrrolidinone and acetamide derivative that is used primarily for the treatment of SEIZURES and some movement disorders, and as a nootropic agent.. levetiracetam : A pyrrolidinone and carboxamide that is N-methylpyrrolidin-2-one in which one of the methyl hydrogens is replaced by an aminocarbonyl group, while another is replaced by an ethyl group (the S enantiomer). An anticonvulsant, it is used for the treatment of epilepsy in both human and veterinary medicine.	4.11	4	0	pyrrolidin-2-ones	anticonvulsant; environmental contaminant; xenobiotic
ly 163892 loracarbef: 1-carbacephem antibiotic; has a broad spectrum of antimicrobial activity; structure given in first source; carbacephems differ from cephalosporins in the substitution of a sulfur atom in the dihydrothiazine ring with a methylene group to form a tetrahydropyridine ring. loracarbef : A synthetic "carba" analogue of cefaclor, with carbon replacing sulfur at position 1. Used to treat a wide range of infections caused by both gram-positive and gram-negative bacteria.	3.23	1	0	carbacephem; zwitterion	antibacterial drug; antimicrobial agent
nabilone nabilone: cannabinol deriv; RN given refers to cpd without isomeric designation; structure	3.23	1	0
nalmefene nalmefene: RN given refers to 5-alpha isomer	2.46	2	0	morphinane alkaloid
nalorphine Nalorphine: A narcotic antagonist with some agonist properties. It is an antagonist at mu opioid receptors and an agonist at kappa opioid receptors. Given alone it produces a broad spectrum of unpleasant effects and it is considered to be clinically obsolete.	2.05	1	0	morphinane alkaloid
naloxone Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.. naloxone : A synthetic morphinane alkaloid that is morphinone in which the enone double bond has been reduced to a single bond, the hydrogen at position 14 has been replaced by a hydroxy group, and the methyl group attached to the nitrogen has been replaced by an allyl group. A specific opioid antagonist, it is used (commonly as its hydrochloride salt) to reverse the effects of opioids, both following their use of opioids during surgery and in cases of known or suspected opioid overdose.	4.08	4	0	morphinane alkaloid; organic heteropentacyclic compound; tertiary alcohol	antidote to opioid poisoning; central nervous system depressant; mu-opioid receptor antagonist
oxycodone Oxycodone: A semisynthetic derivative of CODEINE.. oxycodone : A semisynthetic opioid of formula C18H21NO4 that is derived from thebaine. It is a moderately potent opioid analgesic, generally used for relief of moderate to severe pain.	8.86	3	0	organic heteropentacyclic compound; semisynthetic derivative	antitussive; mu-opioid receptor agonist; opioid analgesic
oxymorphone Oxymorphone: An opioid analgesic with actions and uses similar to those of MORPHINE, apart from an absence of cough suppressant activity. It is used in the treatment of moderate to severe pain, including pain in obstetrics. It may also be used as an adjunct to anesthesia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1092)	3.59	2	0	morphinane alkaloid
vitamin k 1 Vitamin K 1: A family of phylloquinones that contains a ring of 2-methyl-1,4-naphthoquinone and an isoprenoid side chain. Members of this group of vitamin K 1 have only one double bond on the proximal isoprene unit. Rich sources of vitamin K 1 include green plants, algae, and photosynthetic bacteria. Vitamin K1 has antihemorrhagic and prothrombogenic activity.. phylloquinone : A member of the class of phylloquinones that consists of 1,4-naphthoquinone having methyl and phytyl groups at positions 2 and 3 respectively. The parent of the class of phylloquinones.	3.23	1	0	phylloquinones; vitamin K	cofactor; human metabolite; plant metabolite
sirolimus Sirolimus: A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to IMMUNOPHILINS. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties.. sirolimus : A macrolide lactam isolated from Streptomyces hygroscopicus consisting of a 29-membered ring containing 4 trans double bonds, three of which are conjugated. It is an antibiotic, immunosupressive and antineoplastic agent.	13.54	57	7	antibiotic antifungal drug; cyclic acetal; cyclic ketone; ether; macrolide lactam; organic heterotricyclic compound; secondary alcohol	antibacterial drug; anticoronaviral agent; antineoplastic agent; bacterial metabolite; geroprotector; immunosuppressive agent; mTOR inhibitor
topiramate Topiramate: A sulfamate-substituted fructose analog that was originally identified as a hypoglycemic agent. It is used for the treatment of EPILEPSY and MIGRAINE DISORDERS, and may also promote weight loss.. topiramate : A hexose derivative that is 2,3:4,5-di-O-isopropylidene-beta-D-fructopyranose in which the hydroxy group has been converted to the corresponding sulfamate ester. It blocks voltage-dependent sodium channels and is used as an antiepileptic and for the prevention of migraine.	4.13	4	0	cyclic ketal; ketohexose derivative; sulfamate ester	anticonvulsant; sodium channel blocker
trospium chloride trospium chloride : An organic chloride salt of trospium. It is an antispasmodic drug used for the treatment of overactive bladder.	3.23	1	0
brefeldin a [no description available]	7.98	4	0	macrolide antibiotic	Penicillium metabolite
alvocidib alvocidib: structure given in first source. alvocidib : A synthetic dihydroxyflavone that is 5,7-dihydroxyflavone which is substituted by a 3-hydroxy-1-methylpiperidin-4-yl group at position 8 and by a chlorine at the 2' position (the (-)-3S,4R stereoisomer). A cyclin-dependent kinase 9 (CDK9) inhibitor, it has been studied for the treatment of acute myeloid leukaemia, arthritis and atherosclerotic plaque formation.	7.81	12	2	dihydroxyflavone; hydroxypiperidine; monochlorobenzenes; tertiary amino compound	antineoplastic agent; antirheumatic drug; apoptosis inducer; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
seocalcitol seocalcitol: structure given in first source	2.05	1	0
fenretinide Fenretinide: A synthetic retinoid that is used orally as a chemopreventive against prostate cancer and in women at risk of developing contralateral breast cancer. It is also effective as an antineoplastic agent.. 4-hydroxyphenyl retinamide : A retinoid obtained by formal condensation of the carboxy group of all-trans retinoic acid and the anilino group of 4-hydroxyaniline. Synthetic retinoid agonist. Antiproliferative, antioxidant and anticancer agent with a long half-life in vivo. Apoptotic effects appear to be mediated by a mechanism distinct from that of 'classical' retinoids.	5.18	14	0	monocarboxylic acid amide; retinoid	antineoplastic agent; antioxidant
geldanamycin [no description available]	2.05	1	0	1,4-benzoquinones; ansamycin; carbamate ester; organic heterobicyclic compound	antimicrobial agent; antineoplastic agent; antiviral agent; cysteine protease inhibitor; Hsp90 inhibitor
17-(dimethylaminoethylamino)-17-demethoxygeldanamycin 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin: structure in first source. alvespimycin : A 19-membered macrocyle that is geldanamycin in which the methoxy group attached to the benzoquinone moiety has been replaced by a 2-(N,N-dimethylamino)ethylamino group.	2.49	2	0	1,4-benzoquinones; ansamycin; carbamate ester; secondary amino compound; tertiary amino compound	Hsp90 inhibitor
morphine Meconium: The thick green-to-black mucilaginous material found in the intestines of a full-term fetus. It consists of secretions of the INTESTINAL GLANDS; BILE PIGMENTS; FATTY ACIDS; AMNIOTIC FLUID; and intrauterine debris. It constitutes the first stools passed by a newborn.	4.3	5	0	morphinane alkaloid; organic heteropentacyclic compound; tertiary amino compound	anaesthetic; drug allergen; environmental contaminant; geroprotector; mu-opioid receptor agonist; opioid analgesic; plant metabolite; vasodilator agent; xenobiotic
demycarosylturimycin h [no description available]	2.47	2	0
ter 199 [no description available]	2.08	1	0
acipimox acipimox: lipolysis inhibitor	2.08	1	0	pyrazinecarboxylic acid
arachidonylcyclopropylamide arachidonylcyclopropylamide: a potent and selective agonist of neuronal cannabinoid receptor; structure in first source	2.08	1	0
atosiban [no description available]	2.08	1	0	oligopeptide
benzphetamine Benzphetamine: A sympathomimetic agent with properties similar to DEXTROAMPHETAMINE. It is used in the treatment of obesity. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1222). benzphetamine : Dextroamphetamine in which the the hydrogens attached to the amino group are substituted by a methyl and a benzyl group. A sympathomimetic agent with properties similar to dextroamphetamine, it is used as its hydrochloride salt in the treatment of obesity.	3.23	1	0	amphetamines; tertiary amine	adrenergic uptake inhibitor; appetite depressant; dopamine uptake inhibitor; sympathomimetic agent
bimatoprost Bimatoprost: A cloprostenol-derived amide that is used as an ANTIHYPERTENSIVE AGENT in the treatment of OPEN-ANGLE GLAUCOMA and OCULAR HYPERTENSION.	2.08	1	0	monocarboxylic acid amide	antiglaucoma drug; antihypertensive agent
cicaprost cicaprost: RN given refers to (3aS-(2E,3aalpha,4alpha(3R,4R),5beta,6aalpha))-isomer	2.04	1	0	monoterpenoid
deamino arginine vasopressin Deamino Arginine Vasopressin: A synthetic analog of the pituitary hormone, ARGININE VASOPRESSIN. Its action is mediated by the VASOPRESSIN receptor V2. It has prolonged antidiuretic activity, but little pressor effects. It also modulates levels of circulating FACTOR VIII and VON WILLEBRAND FACTOR.	3.23	1	0	heterodetic cyclic peptide	diagnostic agent; renal agent; vasopressin receptor agonist
desonide Desonide: A nonfluorinated corticosteroid anti-inflammatory agent used topically for DERMATOSES.. desonide : Triamcinolone acetonide with hydrogen instead of the fluorine substituent at position 9. A corticosteroid anti-inflammatory, it is used topically as a cream, ointment or lotion for the treatment of various skin disorders.	2.05	1	0	11beta-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; corticosteroid; cyclic ketal; primary alpha-hydroxy ketone	anti-inflammatory drug
dexmedetomidine [no description available]	3.58	2	0	medetomidine	alpha-adrenergic agonist; analgesic; non-narcotic analgesic; sedative
fluticasone Fluticasone: A STEROID with GLUCOCORTICOID RECEPTOR activity that is used to manage the symptoms of ASTHMA; ALLERGIC RHINITIS, and ATOPIC DERMATITIS.. fluticasone : A trifluorinated corticosteroid used in the form of its propionate ester for treatment of allergic rhinitis.	4.8	1	1	11beta-hydroxy steroid; 17alpha-hydroxy steroid; 3-oxo-Delta(4) steroid; corticosteroid; fluorinated steroid; thioester	anti-allergic agent; anti-asthmatic drug
fr 173657 FR 173657: structure given in first source	2.31	1	0
fr 190997 FR 190997: structure given in first source	2.31	1	0
goserelin Goserelin: A synthetic long-acting agonist of GONADOTROPIN-RELEASING HORMONE. Goserelin is used in treatments of malignant NEOPLASMS of the prostate, uterine fibromas, and metastatic breast cancer.	3.23	1	0	organic molecular entity
benzyloxycarbonyl-phe-ala-fluormethylketone cathepsin B inhibitor : A cysteine protease inhibitor which inhibits cathepsin B (EC 3.4.22.1).	2.6	1	0
iloprost Iloprost: An eicosanoid, derived from the cyclooxygenase pathway of arachidonic acid metabolism. It is a stable and synthetic analog of EPOPROSTENOL, but with a longer half-life than the parent compound. Its actions are similar to prostacyclin. Iloprost produces vasodilation and inhibits platelet aggregation.. iloprost : A carbobicyclic compound that is prostaglandin I2 in which the endocyclic oxygen is replaced by a methylene group and in which the (1E,3S)-3-hydroxyoct-1-en-1-yl side chain is replaced by a (3R)-3-hydroxy-4-methyloct-1-en-6-yn-1-yl group. A synthetic analogue of prostacyclin, it is used as the trometamol salt (generally by intravenous infusion) for the treatment of peripheral vascular disease and pulmonary hypertension.	2.45	2	0	carbobicyclic compound; monocarboxylic acid; secondary alcohol	platelet aggregation inhibitor; vasodilator agent
latanoprost Latanoprost: A prostaglandin F analog used to treat OCULAR HYPERTENSION in patients with GLAUCOMA.. latanoprost : A prostaglandin Falpha that is the isopropyl ester prodrug of latanoprost free acid. Used in the treatment of open-angle glaucoma and ocular hypertension.	2.08	1	0	isopropyl ester; prostaglandins Falpha; triol	antiglaucoma drug; antihypertensive agent; EC 4.2.1.1 (carbonic anhydrase) inhibitor; prodrug
ly 320135 LY 320135: cannabinoid receptor antagonist; structure in first source	2.08	1	0	benzofurans
n-(n-(3,5-difluorophenacetyl)alanyl)phenylglycine tert-butyl ester DAPT : A dipeptide consisting of alanylphenylglycine derivatised as a 3,5-difluorophenylacetamide at the amino terminal and a tert-butyl ester at the carboxy terminal. A gamma-secretase inhibitor.	2.6	1	0	carboxylic ester; difluorobenzene; dipeptide; tert-butyl ester	EC 3.4.23.46 (memapsin 2) inhibitor
nalbuphine Nalbuphine: A narcotic used as a pain medication. It appears to be an agonist at KAPPA RECEPTORS and an antagonist or partial agonist at MU RECEPTORS.	3.58	2	0	organic heteropentacyclic compound	mu-opioid receptor antagonist; opioid analgesic
nateglinide Nateglinide: A phenylalanine and cyclohexane derivative that acts as a hypoglycemic agent by stimulating the release of insulin from the pancreas. It is used in the treatment of TYPE 2 DIABETES.. nateglinide : An N-acyl-D-phenylalanine resulting from the formal condensation of the amino group of D-phenylalanine with the carboxy group of trans-4-isopropylcyclohexanecarboxylic acid. An orally-administered, rapidly-absorbed, short-acting insulinotropic agent, it is used for the treatment of type 2 diabetes mellitus.	3.87	3	0	phenylalanine derivative
pd 166285 [no description available]	2.08	1	0
vinorelbine [no description available]	3.86	3	0	acetate ester; methyl ester; organic heteropentacyclic compound; organic heterotetracyclic compound; ring assembly; vinca alkaloid	antineoplastic agent; photosensitizing agent
silodosin silodosin: an alpha(1a)-adrenoceptor-selective antagonist; structure given in first source	3.23	1	0	indolecarboxamide
kn 62 KN 62: inhibitor of Ca/calmodulin-dependent protein kinase II	2.08	1	0	piperazines
su 6656 SU 6656: a c-Src kinase inhibitor; used to probe growth signaling; structure in first source. SU6656 : A member of the class of oxindoles that is 3-methyleneoxindole in which the hydrogeh at position 5 has been replaced by a dimethylaminosulfonyl group and in which one of the hydrogens of the methylene group has been replaced by a 4,5,6,7-tetrahydro-indol-2-yl group. It is a specific inhibitor of Src family kinase.	2.08	1	0
casticin casticin: from fruit of Vitex rotundifolia; structure in second source. casticin : A tetramethoxyflavone that consists of quercetagetin in which the hydroxy groups at positions 3, 6, 7 and 4' have been replaced by methoxy groups. It has been isolated from Eremophila mitchellii.	2.6	1	0	dihydroxyflavone; tetramethoxyflavone	apoptosis inducer; plant metabolite
andrographolide [no description available]	7.11	1	0	carbobicyclic compound; gamma-lactone; labdane diterpenoid; primary alcohol; secondary alcohol	anti-HIV agent; anti-inflammatory drug; antineoplastic agent; metabolite
icaritin icaritin: structure in first source	2.15	1	0
licochalcone a licochalcone A: has both anti-inflammatory and antineoplastic activities; structure given in first source; isolated from root of Glycyrrhiza inflata; RN given refers to (E)-isomer	2.25	1	0	chalcones
octadecyl caffeate caffeic acid n-octadecyl ester: isolated from Daphne acutiloba Rehd; structure in first source	2.41	1	0
5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one 5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one: isolated from the Chinese herb Scutellariae radix. oroxylin A : A dihydroxy- and monomethoxy-flavone in which the hydroxy groups are positioned at C-5 and C-7 and the methoxy group is at C-6.	2.6	1	0	dihydroxyflavone; monomethoxyflavone	antineoplastic agent; EC 1.14.13.39 (nitric oxide synthase) inhibitor
atractylenolide i atractylenolide I: from Atractylodes macrocephala Koidz; structure in first source	7.25	1	0
(E)-2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucoside 2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucopyranoside: Tyrosinase inhibitor from Polygonum multiflorum; structure in first source. (E)-2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucoside : A stilbenoid that is trans-stilbene which has been substituted by hydroxy groups at positions 2, 3, 5, and 4', and in which the hydroxy group at positon 2 has then been converted to the corresponding the beta-D-glucoside.	2.6	1	0	beta-D-glucoside; resorcinols; stilbenoid	anti-inflammatory agent; antioxidant; apoptosis inhibitor; cardioprotective agent; cyclooxygenase 2 inhibitor; platelet aggregation inhibitor
furazolidone [no description available]	2.05	1	0
fluvoxamine Fluvoxamine: A selective serotonin reuptake inhibitor that is used in the treatment of DEPRESSION and a variety of ANXIETY DISORDERS.. fluvoxamine : An oxime O-ether that is benzene substituted by a (1E)-N-(2-aminoethoxy)-5-methoxypentanimidoyl group at position 1 and a trifluoromethyl group at position 4. It is a selective serotonin reuptake inhibitor that is used for the treatment of obsessive-compulsive disorder.	3.59	2	0	(trifluoromethyl)benzenes; 5-methoxyvalerophenone O-(2-aminoethyl)oxime	antidepressant; anxiolytic drug; serotonin uptake inhibitor
casein kinase ii Casein Kinase II: A ubiquitous casein kinase that is comprised of two distinct catalytic subunits and dimeric regulatory subunit. Casein kinase II has been shown to phosphorylate a large number of substrates, many of which are proteins involved in the regulation of gene expression.	2.51	2	0
tyrphostin ag 555 [no description available]	2.6	1	0
ag-490 [no description available]	2.07	1	0	catechols; enamide; monocarboxylic acid amide; nitrile; secondary carboxamide	anti-inflammatory agent; antioxidant; apoptosis inducer; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor; geroprotector; STAT3 inhibitor
bosutinib 4-((2,4-dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methyl-1-piperazinyl)propoxy)-3-quinolinecarbonitrile: a Src kinase inhibitor; structure in first source	3.23	1	0	aminoquinoline; aromatic ether; dichlorobenzene; N-methylpiperazine; nitrile; tertiary amino compound	antineoplastic agent; tyrosine kinase inhibitor
semaxinib semaxanib : An oxindole that is 3-methyleneoxindole in which one of the hydrogens of the methylene group is replaced by a 3,5-dimethylpyrrol-2-yl group.	4.05	4	0	olefinic compound; oxindoles; pyrroles	angiogenesis modulating agent; antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; vascular endothelial growth factor receptor antagonist
orantinib orantinib: an antiangiogenic agent. orantinib : An oxindole that is 3-methyleneoxindole in which one of the hydrogens of the methylene group is substituted by a 2-(2-carboxyethyl)-3,5-dimethylpyrrol-3-yl group. It is an ATP-competitive inhibitor of the tyrosine kinase activity of fibroblast growth factor receptor 1.	2.05	1	0
su 11248 [no description available]	7.72	12	1	monocarboxylic acid amide; pyrroles	angiogenesis inhibitor; antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; immunomodulator; neuroprotective agent; vascular endothelial growth factor receptor antagonist
palbociclib [no description available]	11.75	6	1	aminopyridine; aromatic ketone; cyclopentanes; piperidines; pyridopyrimidine; secondary amino compound; tertiary amino compound	antineoplastic agent; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
jnj-7706621 [no description available]	2.08	1	0	sulfonamide
nifuroxazide nifuroxazide: structure	2.25	1	0	benzoic acids
fosbretabulin fosbretabulin: a microtubule destabilizing agent isolated from Combretum caffrum; structure in first source	4.05	2	0
ergothioneine ergothioneine thione form : A L-histidine derivative that is N(alpha),N(alpha),N(alpha)-trimethyl-L-histidine in which the hydrogen at position 2 on the imdazole ring is replaced by a thioxo group.	2.04	1	0	1,3-dihydroimidazole-2-thiones; amino-acid betaine; L-histidine derivative; sulfur-containing amino acid	antioxidant; chelator; fungal metabolite; plant metabolite; xenobiotic metabolite
romidepsin depsipeptide : A natural or synthetic compound having a sequence of amino and hydroxy carboxylic acid residues (usually alpha-amino and alpha-hydroxy acids), commonly but not necessarily regularly alternating.	2.04	1	0	cyclodepsipeptide; heterocyclic antibiotic; organic disulfide	antineoplastic agent; EC 3.5.1.98 (histone deacetylase) inhibitor
bay 11-7082 (E)-3-tosylacrylonitrile : A nitrile that is acrylonitrile in which the hydrogen located beta,trans to the cyano group is replaced by a tosyl group. It is an inhibitor of cytokine-induced IkappaB-alpha phosphorylation in cells.	3.66	9	0	nitrile; sulfone	apoptosis inducer; EC 2.7.11.10 (IkappaB kinase) inhibitor; EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor; non-steroidal anti-inflammatory drug; platelet aggregation inhibitor
bay 11-7085 BAY11-7085 : A sulfone that is benzene substituted by [(E)-2-cyanoethenyl]sulfonyl and tert-butyl groups at position 1 and 4, respectively. It is an irreversible inhibitor of IkappaB-alpha phosphorylation in cells (IC50 = 10 muM) and prevents the activation of NF-kappaB.	2.5	2	0	benzenes; nitrile; sulfone	anti-inflammatory agent; antibacterial agent; antineoplastic agent; apoptosis inducer; autophagy inducer; EC 2.7.11.10 (IkappaB kinase) inhibitor; ferroptosis inducer; NF-kappaB inhibitor
carboxycinnamic acid bishydroxamide carboxycinnamic acid bishydroxamide: inhibits histone decacetylase I & 3; structure in first source	2.02	1	0
(6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid (6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid : A dihydroxy monocarboxylic acid that is N-isopropylindole which is substituted at position 3 by a p-fluorophenyl group and at position 2 by a 6-carboxy-3,5-dihydroxyhex-1-en-1-yl group. It has four possible diastereoisomers.	4.08	4	0	dihydroxy monocarboxylic acid; indoles; organofluorine compound
molsidomine [no description available]	2.47	2	0	ethyl ester; morpholines; oxadiazole; zwitterion	antioxidant; apoptosis inhibitor; cardioprotective agent; nitric oxide donor; vasodilator agent
pd 151746 [no description available]	2.6	1	0
flavokawain b flavokawain B: from Piper methysticum Forst (Kava Kava) roots; structure in first source. flavokawain B : A member of the class of chalcones that consists of trans-chalcone substituted by hydroxy group at positions 2' and methoxy groups at positions 4' and 6'. Isolated from Piper methysticum and Piper rusbyi, it exhibits antileishmanial, anti-inflammatory and antineoplastic activities.	7.21	1	0	chalcones; dimethoxybenzene; phenols	anti-inflammatory agent; antileishmanial agent; antineoplastic agent; apoptosis inducer; metabolite
levorphanol Levorphanol: A narcotic analgesic that may be habit-forming. It is nearly as effective orally as by injection.	3.23	1	0	morphinane alkaloid
strontium Strontium: An element of the alkaline earth family of metals. It has the atomic symbol Sr, atomic number 38, and atomic weight 87.62.	4.8	1	1	alkaline earth metal atom
bismuth Bismuth: A metallic element that has the atomic symbol Bi, and atomic number 83. Its principal isotope is Bismuth 209.	4.8	1	1	metal atom; pnictogen
arsenic Arsenic: A shiny gray element with atomic symbol As, atomic number 33, and atomic weight 75. It occurs throughout the universe, mostly in the form of metallic arsenides. Most forms are toxic. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), arsenic and certain arsenic compounds have been listed as known carcinogens. (From Merck Index, 11th ed)	12.71	49	4	metalloid atom; pnictogen	micronutrient
naltrexone Naltrexone: Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of NALOXONE. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence.. naltrexone : An organic heteropentacyclic compound that is naloxone substituted in which the allyl group attached to the nitrogen is replaced by a cyclopropylmethyl group. A mu-opioid receptor antagonist, it is used to treat alcohol dependence.	4.09	4	0	cyclopropanes; morphinane-like compound; organic heteropentacyclic compound	antidote to opioid poisoning; central nervous system depressant; environmental contaminant; mu-opioid receptor antagonist; xenobiotic
morphine-6-glucuronide morphine-6-glucuronide: RN given refers to (5alpha,6alpha)-isomer	2.04	1	0	morphinane alkaloid
dextromethorphan Dextromethorphan: Methyl analog of DEXTRORPHAN that shows high affinity binding to several regions of the brain, including the medullary cough center. This compound is an NMDA receptor antagonist (RECEPTORS, N-METHYL-D-ASPARTATE) and acts as a non-competitive channel blocker. It is one of the widely used ANTITUSSIVES, and is also used to study the involvement of glutamate receptors in neurotoxicity.. dextromethorphan : A 6-methoxy-11-methyl-1,3,4,9,10,10a-hexahydro-2H-10,4a-(epiminoethano)phenanthrene in which the sterocenters at positions 4a, 10 and 10a have S-configuration. It is a prodrug of dextrorphan and used as an antitussive drug for suppressing cough.	3.59	2	0	6-methoxy-11-methyl-1,3,4,9,10,10a-hexahydro-2H-10,4a-(epiminoethano)phenanthrene	antitussive; environmental contaminant; neurotoxin; NMDA receptor antagonist; oneirogen; prodrug; xenobiotic
butorphanol Butorphanol: A synthetic morphinan analgesic with narcotic antagonist action. It is used in the management of severe pain.. butorphanol : Levorphanol in which a hydrogen at position 14 of the morphinan skeleton is substituted by hydroxy and one of the hydrogens of the N-methyl group is substituted by cyclopropyl. A semi-synthetic opioid agonist-antagonist analgesic, it is used as its (S,S)-tartaric acid salt for relief or moderate to severe pain.	3.87	3	0	morphinane alkaloid	antitussive; kappa-opioid receptor agonist; mu-opioid receptor agonist; opioid analgesic
cefodizime cefodizime: RN given refers to (6R-(6alpha,7beta(Z)))-isomer. cefodizime : A cephalosporin compound having 5-(carboxymethyl)-4-methyl-1,3-thiazol-2-yl]sulfanyl}methyl and [2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetyl]amino side groups located at positions 3 and 7 respectively.	2.04	1	0	1,3-thiazoles; cephalosporin; oxime O-ether	antibacterial drug; EC 1.14.18.1 (tyrosinase) inhibitor
methylnaltrexone methylnaltrexone: RN given refers to parent cpd(5alpha)-isomer	2.04	1	0	phenanthrenes
cefixime [no description available]	4.08	4	0	cephalosporin	antibacterial drug; drug allergen
lisinopril Lisinopril: One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.	4.29	5	0	dipeptide	EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
benazepril benazepril: structure given in first source. benazepril : A benzazepine that is benazeprilat in which the carboxy group of the 2-amino-4-phenylbutanoic acid moiety has been converted to the corresponding ethyl ester. It is used (generally as its hydrochloride salt) as a prodrug for the angiotensin-converting enzyme inhibitor benazeprilat in the treatment of hypertension and heart failure.	3.23	1	0	benzazepine; dicarboxylic acid monoester; ethyl ester; lactam	EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; prodrug
ramipril Ramipril: A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.. ramipril : A dipeptide that is the prodrug for ramiprilat, the active metabolite obtained by hydrolysis of the ethyl ester group. An angiotensin-converting enzyme (ACE) inhibitor, used to treat high blood pressure and congestive heart failure.. quark : Quarks comprise one of two classes of the fundamental particles. Quarks possess fractional electric charges and are not observed in free state. The word "quark" first appears in James Joyce's Finnegans Wake and has been chosen by Murray Gell-Mann as a name for fundamental building blocks of particles.	3.87	3	0	azabicycloalkane; cyclopentapyrrole; dicarboxylic acid monoester; dipeptide; ethyl ester	bradykinin receptor B2 agonist; cardioprotective agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; matrix metalloproteinase inhibitor; prodrug
verteporfin (2R,2(1)S)-8-ethenyl-2(1),2(2)-bis(methoxycarbonyl)-17-(3-methoxy-3-oxopropyl)-2,7,12,18-tetramethyl-2,2(1)-dihydrobenzo[b]porphyrin-13-propanoic acid : The 2(1),2(2),17-trimethyl ester of (2R,2(1)S)-2(1),2(2)-dicarboxy-8-ethenyl-2,7,12,18-tetramethyl-2,2(1)-dihydrobenzo[b]porphyrin-13,17-dipropanoic acid.	3.73	2	0
batimastat batimastat: structure given in first source; a synthetic matrix metalloproteinase inhibitor. batimastat : A secondary carboxamide resulting from the formal condensation of the carboxy group of (2S,3R)-5-methyl-3-{[(2S)-1-(methylamino)-1-oxo-3-phenylpropan-2-yl]carbamoyl}-2-[(thiophen-2-ylsulfanyl)methyl]hexanoic acid with the amino group of hydroxylamine. It a broad-spectrum matrix metalloprotease inhibitor.	2.6	1	0	hydroxamic acid; L-phenylalanine derivative; organic sulfide; secondary carboxamide; thiophenes; triamide	angiogenesis inhibitor; antineoplastic agent; matrix metalloproteinase inhibitor
indinavir sulfate Indinavir: A potent and specific HIV protease inhibitor that appears to have good oral bioavailability.	4.29	5	0	dicarboxylic acid diamide; N-(2-hydroxyethyl)piperazine; piperazinecarboxamide	HIV protease inhibitor
sulfur Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight [32.059; 32.076]. It is found in the amino acids cysteine and methionine.	5.76	2	1	chalcogen; nonmetal atom	macronutrient
geldanamycin [no description available]	3.64	9	0
zimeldine Zimeldine: One of the SEROTONIN UPTAKE INHIBITORS formerly used for depression but was withdrawn worldwide in September 1983 because of the risk of GUILLAIN-BARRE SYNDROME associated with its use. (From Martindale, The Extra Pharmacopoeia, 29th ed, p385)	3.23	1	0	styrenes
7-hydroxy-4-trifluoromethylcoumarin 7-hydroxy-4-trifluoromethylcoumarin: structure given in first source	2.15	1	0
enalapril maleate enalapril maleate : The maleic acid salt of enalapril. It contains one molecule of maleic acid for each molecule of enalapril. Following oral administration, the ethyl ester group of enalapril is hydrolysed to afford the corresponding carboxylic acid, enalaprilat, an angiotensin-converting enzyme (ACE) inhibitor. Enalapril is thus a prodrug for enalaprilat (which, unlike enalapril, is not absorbed by mouth), and its maleate is used in the treatment of hypertension and heart failure, for reduction of proteinuria and renal disease in patients with nephropathies, and for the prevention of stroke, myocardial infarction, and cardiac death in high-risk patients.	2.08	1	0	maleate salt	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; prodrug
enalapril Enalapril: An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.. enalapril : A dicarboxylic acid monoester that is ethyl 4-phenylbutanoate in which a hydrogen alpha to the carboxy group is substituted by the amino group of L-alanyl-L-proline (S-configuration).	3.59	2	0	dicarboxylic acid monoester; dipeptide	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; geroprotector; prodrug
nitrofurazone Nitrofurazone: A topical anti-infective agent effective against gram-negative and gram-positive bacteria. It is used for superficial WOUNDS AND INJURIES and skin infections. Nitrofurazone has also been administered orally in the treatment of TRYPANOSOMIASIS.. nitrofurazone : A semicarbazone resulting from the formal condensation of semicarbazide with 5-nitrofuraldehyde. A broad spectrum antibacterial drug, although with little activity against Pseudomonas species, it is used as a local application for burns, ulcers, wounds and skin infections.	2.05	1	0
trientine hydrochloride [no description available]	3.23	1	0
cytochalasin e cytochalasin E: structure	7.17	1	0	cytochalasan alkaloid	metabolite
n-methylscopolamine bromide scopolamine methobromide : A quaternary ammonium salt resulting from the reaction of the amino group of scopolamine with methyl bromide.	3.23	1	0
cisplatin [no description available]	2.08	1	0	diamminedichloroplatinum	antineoplastic agent; apoptosis inducer; cross-linking reagent; ferroptosis inducer; genotoxin; mutagen; nephrotoxin; photosensitizing agent
bleomycin [no description available]	3.59	2	0	bleomycin	antineoplastic agent; metabolite
cysteine Cysteine: A thiol-containing non-essential amino acid that is oxidized to form CYSTINE.. L-cysteinium : The L-enantiomer of cysteinium.. cysteine : A sulfur-containing amino acid that is propanoic acid with an amino group at position 2 and a sulfanyl group at position 3.	8.01	4	0	cysteinium	fundamental metabolite
silicon Silicon: A trace element that constitutes about 27.6% of the earth's crust in the form of SILICON DIOXIDE. It does not occur free in nature. Silicon has the atomic symbol Si, atomic number 14, and atomic weight [28.084; 28.086].	3.51	1	0	carbon group element atom; metalloid atom; nonmetal atom
phosphorus Phosphorus: A non-metal element that has the atomic symbol P, atomic number 15, and atomic weight 31. It is an essential element that takes part in a broad variety of biochemical reactions.	3.51	1	0	monoatomic phosphorus; nonmetal atom; pnictogen	macronutrient
boron Boron: A trace element with the atomic symbol B, atomic number 5, and atomic weight [10.806; 10.821]. Boron-10, an isotope of boron, is used as a neutron absorber in BORON NEUTRON CAPTURE THERAPY.	10.64	6	0	boron group element atom; metalloid atom; nonmetal atom	micronutrient
enalaprilat anhydrous Enalaprilat: The active metabolite of ENALAPRIL and one of the potent, intravenously administered, ANGIOTENSIN-CONVERTING ENZYME INHIBITORS. It is an effective agent for the treatment of essential hypertension and has beneficial hemodynamic effects in heart failure. The drug produces renal vasodilation with an increase in sodium excretion.. enalaprilat dihydrate : The dihydrate form of enalaprilat, an angiotensin-converting enzyme (ACE) inhibitor that is used (often in the form of its prodrug, enalapril) in the treatment of hypertension and heart failure, for reduction of proteinuria and renal disease in patients with nephropathies, and for the prevention of stroke, myocardial infarction, and cardiac death in high-risk patients. Unlike enalapril, enalaprilat is not absorbed by mouth but is administered by intravenous injection.. enalaprilat (anhydrous) : Enalapril in which the ethyl ester group has been hydrolysed to the corresponding carboxylic acid. Enalaprilat is an angiotensin-converting enzyme (ACE) inhibitor and is used (often in the form of its prodrug, enalapril) in the treatment of hypertension and heart failure, for reduction of proteinuria and renal disease in patients with nephropathies, and for the prevention of stroke, myocardial infarction, and cardiac death in high-risk patients. Unlike enalapril, enalaprilat is not absorbed by mouth but is given by intravenous injection, usually as the dihydrate.	4.08	4	0	dicarboxylic acid; dipeptide	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
imidapril imidapril: structure given in first source. imidapril : A member of the class of imidazolidines that is (4S)-1-methyl-2-oxoimidazolidine-4-carboxylic acid in which the hydrogen of the imidazolidine nitrogen has been substituted by (1S)-1-{[(2S)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino}ethyl group. It is the prodrug for imidaprilat, an ACE inhibitor used for the treatment of chronic heart failure.	2.05	1	0	dicarboxylic acid monoester; dipeptide; ethyl ester; imidazolidines; N-acylurea; secondary amino compound	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; prodrug
sulindac sulfone sulindac sulfone: inhibits K-ras-dependent cyclooxygenase-2; sulfated analog of indomethacin;; CP248 is an antineoplastic agent that fosters microtubule depolymerization; structure in first source. sulindac sulfone : A sulfone metabolite of sulindac that inhibits cell growth by inducing apoptosis independently of cyclooxygenase inhibition. It inhibits the development and induces regression of premalignant adenomatous polyps. Lipoxygenase and Cox-2 inhibitor.	3.54	2	0	monocarboxylic acid; organofluorine compound; sulfone	apoptosis inducer; cyclooxygenase 2 inhibitor; EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor
pinostilbene pinostilbene: structure in first source. 3-methoxy-4',5-dihydroxy-trans-stilbene : A stilbenoid that is trans-resveratrol in which one of the meta-hydroxy groups is converted to the corresponding methyl ether.	7.6	1	0	stilbenol
solanesol solanesol : A nonaprenol that is hexatriaconta-2,6,10,14,18,22,26,30,34-nonaen-1-ol substituted by 9 methyl groups at positions 3, 7, 11, 15, 19, 23, 27, 31 and 35 (the all-trans0stereoisomer).	2.6	1	0	nonaprenol; primary alcohol	plant metabolite
pepstatin pepstatin: inhibits the aspartic protease endothiapepsin	2.6	1	0	pentapeptide; secondary carboxamide	bacterial metabolite; EC 3.4.23.* (aspartic endopeptidase) inhibitor
ximelagatran ximelagatran: prodrug (via hydroxylation) of melagatran & a direct thrombin inhibitor; liver toxicity concerns so AZD0837 being developed to replace this. ximelagatran : A member of the class of azetidines that is melagatran in which the carboxylic acid group has been converted to the corresponding ethyl ester and in which the amidine group has been converted into the corresponding amidoxime. A prodrug for melagatran, ximelagatran was the first orally available direct thrombin inhibitor to be brought to market as an anticoagulant, but was withdrawn in 2006 following reports of it causing liver damage.	3.59	2	0	amidoxime; azetidines; carboxamide; ethyl ester; hydroxylamines; secondary amino compound; secondary carboxamide; tertiary carboxamide	anticoagulant; EC 3.4.21.5 (thrombin) inhibitor; prodrug; serine protease inhibitor
cefuroxime [no description available]	3.58	2	0	3-(carbamoyloxymethyl)cephalosporin; furans; oxime O-ether	drug allergen
ceftriaxone [no description available]	3.86	3	0	1,2,4-triazines; 1,3-thiazoles; cephalosporin; oxime O-ether	antibacterial drug; drug allergen; EC 3.5.2.6 (beta-lactamase) inhibitor
cefepime Cefepime: A fourth-generation cephalosporin antibacterial agent that is used in the treatment of infections, including those of the abdomen, urinary tract, respiratory tract, and skin. It is effective against PSEUDOMONAS AERUGINOSA and may also be used in the empiric treatment of FEBRILE NEUTROPENIA.. cefepime : A cephalosporin bearing (1-methylpyrrolidinium-1-yl)methyl and (2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetamido groups at positions 3 and 7, respectively, of the cephem skeleton.	3.58	2	0	cephalosporin; oxime O-ether	antibacterial drug
hr 810 cefpirome: structure in first source. cefpirome : A fourth-generation cephalosporin antibiotic having 6,7-dihydro-5H-cyclopenta[b]pyridinium-1-ylmethyl and [(2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetyl]amino side groups located at positions 3 and 7 respectively.	2.04	1	0	cephalosporin; cyclopentapyridine
l 685458 L 685458: a gamma-secretase inhibitor; structure in first source. L-685,458 : A peptide and carboxamide that is L-leucyl-L-phenylalaninamide, L-Leu-L-Phe-NH2, which has been acylated on the N-terminus by a Phe-Phe hydroxyethylene dipeptide isotere, 2R-benzyl-5S-tert-butoxycarbonylamino-4R-hydroxy-6-phenylhexanoic acid. Compounds based on the structure of L-685,458 are potent inhibitors of gamma-secretase, which mediates the final catalytic step that generates the amyloid beta-peptide (Abeta), which assembles into the neurotoxic aggregates in the brains of sufferers of Alzheimer's disease.	2.6	1	0	carbamate ester; monocarboxylic acid amide; peptide; secondary alcohol	EC 3.4.23.46 (memapsin 2) inhibitor; peptidomimetic
pafuramidine pafuramidine: a prodrug of furamidine	3.23	1	0
norbinaltorphimine norbinaltorphimine: kappa opiate receptor antagonist; structure given in first source	2.11	1	0	isoquinolines
ceftazidime [no description available]	3.58	2	0	cephalosporin; oxime O-ether	antibacterial drug; drug allergen; EC 2.4.1.129 (peptidoglycan glycosyltransferase) inhibitor
trandolapril trandolapril : A heterobicylic compound that is (2S,3aR,7aS)-1-[(2S)-2-aminopropanoyl]octahydro-1H-indole-2-carboxylic acid in which the hydrogen of the amino group is substituted by a (2R)-1-ethoxy-1-oxo-4-phenylbutan-2-yl group. It is a angiotensin-converting enzyme inhibitor and a prodrug used for the treatment of hypertension.	3.87	3	0	dicarboxylic acid monoester; dipeptide; ethyl ester; organic heterobicyclic compound; secondary amino compound; tertiary carboxamide	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; prodrug
pregabalin Pregabalin: A gamma-aminobutyric acid (GABA) derivative that functions as a CALCIUM CHANNEL BLOCKER and is used as an ANTICONVULSANT as well as an ANTI-ANXIETY AGENT. It is also used as an ANALGESIC in the treatment of NEUROPATHIC PAIN and FIBROMYALGIA.. pregabalin : A gamma-amino acid that is gamma-aminobutyric acid (GABA) carrying an isobutyl substitutent at the beta-position (the S-enantiomer). Binds with high affinity to the alpha2-delta site (an auxiliary subunit of voltage-gated calcium channels) in central nervous system tissues.	4.11	4	0	gamma-amino acid	anticonvulsant; calcium channel blocker
cefetamet cefetamet: active against Neisseria gonorrhoeae; structure given in first source. cefetamet : A cephalosporin compound having methyl and [(2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetyl]amino side-groups; a cephalosporin antibiotic active against Neisseria gonorrhoeae.	2.04	1	0	cephalosporin
alvimopan anhydrous alvimopan: mu opioid receptor antagonist; intended to treat constipation in patients taking opiates for pain	3.61	2	0	peptide
baohuoside i baohuoside I: structure given in first source; isolated from the herb Epimedium davidii	2.06	1	0	glycosyloxyflavone	anti-inflammatory agent; antineoplastic agent; apoptosis inducer; plant metabolite
aliskiren aliskiren: orally active nonpeptidic renin inhibitor. aliskiren : A monomethoxybenzene compound having a 3-methoxypropoxy group at the 2-position and a multi-substituted branched alkyl substituent at the 4-position.	3.23	1	0	monocarboxylic acid amide; monomethoxybenzene	antihypertensive agent
vx680 [no description available]	3.86	3	0	N-arylpiperazine
bms 806 BMS 806: prevents entry of HIV into cells by binding HIV envelope protein gp120; no further info available 4/2002	2.6	1	0
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone [no description available]	2.6	1	0
guanabenz acetate [no description available]	2.05	1	0	dichlorobenzene	geroprotector
famotidine [no description available]	4.08	4	0	1,3-thiazoles; guanidines; sulfonamide	anti-ulcer drug; H2-receptor antagonist; P450 inhibitor
tulobuterol hydrochloride [no description available]	2.6	1	0	organic molecular entity
bafilomycin a [no description available]	2.31	1	0
resiniferatoxin resiniferatoxin: phorbol related diterpene ester; potent agonist of vanilloid TRPV1 receptors. resiniferatoxin : A heteropentacyclic compound found in Euphorbia poissonii with molecular formula C37H40O9. It is an agonist of the transient receptor potential cation channel subfamily V member 1 (TrpV1).	2.17	1	0	carboxylic ester; diterpenoid; enone; monomethoxybenzene; organic heteropentacyclic compound; ortho ester; phenols; tertiary alpha-hydroxy ketone	analgesic; neurotoxin; plant metabolite; TRPV1 agonist
salubrinal salubrinal: prevents dephosphorylation of eIF2alpha; structure in first source. salubrinal : A member of the class of quinolines that is a mixed aminal resulting from the formal condensation oftrichloroacetaldehyde with the amide nitrogen of trans-cinnamamide and the primary amino group of 1-quinolin-8-ylthiourea. It is a selective inhibitor of cellular complexes that dephosphorylate eukaryotic translation initiation factor 2 subunit alpha (eIF2alpha).	2.6	1	0	aminal; organochlorine compound; quinolines; secondary carboxamide; thioureas
cefotaxime Cefotaxime: Semisynthetic broad-spectrum cephalosporin.. cefotaxime : A cephalosporin compound having acetoxymethyl and [2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetyl]amino side groups.	3.86	3	0	1,3-thiazoles; cephalosporin; oxime O-ether	antibacterial drug; drug allergen
aztreonam [no description available]	3.86	3	0	beta-lactam antibiotic allergen; monobactam	antibacterial drug; drug allergen; EC 2.4.1.129 (peptidoglycan glycosyltransferase) inhibitor
proguanil Proguanil: A biguanide compound which metabolizes in the body to form cycloguanil, an anti-malaria agent.. proguanil : A biguanide compound which has isopropyl and p-chlorophenyl substituents on the terminal N atoms. A prophylactic antimalarial drug, it works by inhibiting the enzyme dihydrofolate reductase, which is involved in the reproduction of the malaria parasites Plasmodium falciparum and P. vivax within the red blood cells.	2.05	1	0	biguanides; monochlorobenzenes	antimalarial; antiprotozoal drug; EC 1.5.1.3 (dihydrofolate reductase) inhibitor
cci 15641 [no description available]	2.08	1	0	cephalosporin
monorden monorden: inhibits HSP90 Heat-Shock Proteins, DNA topoisomerase VI and human Topoisomerase II	2.21	1	0	cyclic ketone; enone; epoxide; macrolide antibiotic; monochlorobenzenes; phenols	antifungal agent; metabolite; tyrosine kinase inhibitor
rifamycin sv rifamycin SV: RN given refers to parent cpd; structure in Merck Index, 9th ed, #8009. rifamycin SV : A member of the class of rifamycins that exhibits antibiotic and antitubercular properties.	2.05	1	0	acetate ester; cyclic ketal; lactam; macrocycle; organic heterotetracyclic compound; polyphenol; rifamycins	antimicrobial agent; antitubercular agent; bacterial metabolite
ginkgolide b [no description available]	2.04	1	0
radium Radium: A radioactive element of the alkaline earth series of metals. It has the atomic symbol Ra and atomic number 88. Radium is the product of the disintegration of URANIUM and is present in pitchblende and all ores containing uranium. It is used clinically as a source of beta and gamma-rays in radiotherapy, particularly BRACHYTHERAPY.	7.31	1	0	alkaline earth metal atom
cefpodoxime [no description available]	3.23	1	0	carboxylic acid; cephalosporin	antibacterial drug
palonosetron Palonosetron: Isoquinoline and quinuclidine derivative that acts as a 5-HT3 RECEPTOR antagonist. It is used in the prevention of nausea and vomiting induced by cytotoxic chemotherapy, and for the prevention of post-operative nausea and vomiting.. palonosetron : An organic heterotricyclic compound that is an antiemetic used (as its hydrochloride salt) in combination with netupitant (under the trade name Akynzeo) to treat nausea and vomiting in patients undergoing cancer chemotherapy.	3.84	3	0	azabicycloalkane; delta-lactam; organic heterotricyclic compound	antiemetic; serotonergic antagonist
(3S,5S,6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid Fluvastatin: An indole-heptanoic acid derivative that inhibits HMG COA REDUCTASE and is used to treat HYPERCHOLESTEROLEMIA. In contrast to other statins, it does not appear to interact with other drugs that inhibit CYP3A4.. (3S,5S,6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid : A (6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid diastereoisomer in which both chiral centres have S configuration.. fluvastatin : A racemate comprising equimolar amounts of (3R,5S)- and (3S,5R)-fluvastatin. An HMG-CoA reductase inhibitor, it is used (often as the corresponding sodium salt) to reduce triglycerides and LDL-cholesterol, and increase HDL-chloesterol, in the treatment of hyperlipidaemia.	2.31	1	0	(6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid
epoprostenol sodium [no description available]	2.05	1	0	prostanoid
tenofovir disoproxil fumarate tenofovir disoproxil fumarate : A fumarate salt prepared from equimolar amounts of tenofovir disoproxil and fumaric acid. It is used in combination therapy for the treatment of HIV infection.	2.08	1	0	fumarate salt	antiviral drug; HIV-1 reverse transcriptase inhibitor; prodrug
cefatrizine Cefatrizine: Orally active semisynthetic cephalosporin antibiotic with broad-spectrum activity.. cefatrizine : A cephalosporin compound having (1H-1,2,3-triazol-4-ylsulfanyl)methyl and [(2R)-2-amino-2-(4-hydroxyphenyl)]acetamido side-groups. An antibacterial drug first prepared in the 1970s, it has more recently been found to be an inhibitor of eukaryotic elongation factor-2 kinase (eEF2K), which is known to regulate apoptosis, autophagy and ER stress in many types of human cancers.	2.04	1	0	amino acid amide; carboxylic acid; cephalosporin; phenols; semisynthetic derivative; triazoles	antibacterial drug; EC 2.7.11.20 (elongation factor 2 kinase) inhibitor
d 4476 [no description available]	2.08	1	0	imidazoles
cyc 116 4-methyl-5-(2-(4-morpholinophenylamino)pyrimidin-4-yl)thiazol-2-amine: an aurora kinase inhibitor; structure in first source	2.08	1	0
eniporide eniporide: inhibits NHE-1 isoform; structure in first source	2.04	1	0
bay 19-8004 BAY 19-8004: a PDE4 inhibitor; structure in first source	2.08	1	0
dexbrompheniramine maleate dexbrompheniramine maleate : The maleic acid salt of the (pharmacologically active) (S)-(+)-enantiomer of brompheniramine. A histamine H1 receptor antagonist, it is used for the symptomatic relief of allergic conditions, including rhinitis and conjunctivitis.	2.08	1	0	brompheniramine maleate	anti-allergic agent; H1-receptor antagonist
cilastatin [no description available]	2.04	1	0	carboxamide; L-cysteine derivative; non-proteinogenic L-alpha-amino acid; organic sulfide	EC 3.4.13.19 (membrane dipeptidase) inhibitor; environmental contaminant; protease inhibitor; xenobiotic
citreoviridin citreoviridin: formed from Penicillium toxicarium, Penicillium citeoviride; Penicillium ochrosalmoneum on rice during storage	2.1	1	0	2-pyranones
rifaximin [no description available]	3.61	2	0	acetate ester; cyclic ketal; lactam; macrocycle; organic heterohexacyclic compound; rifamycins; semisynthetic derivative	antimicrobial agent; gastrointestinal drug; orphan drug
bafilomycin a1 bafilomycin A1: from Streptomyces griseus; structure given in first source. bafilomycin A1 : The most used of the bafilomycins, a family of toxic macrolide antibiotics derived from Streptomyces griseus.	7.78	3	0	cyclic hemiketal; macrolide antibiotic; oxanes	apoptosis inducer; autophagy inhibitor; bacterial metabolite; EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor; EC 3.6.3.14 (H(+)-transporting two-sector ATPase) inhibitor; ferroptosis inhibitor; fungicide; potassium ionophore; toxin
falcarindiol falcarindiol: from leaves of Schefflera digitata (Araliaceae) and in carrots; inhibits germination of spores of most common dermatophyte fungi	2.15	1	0	organic molecular entity	metabolite
germacrone germacrone: isolated from Curcuma wenyujin	2.6	1	0	germacrane sesquiterpenoid; olefinic compound	androgen antagonist; anti-inflammatory agent; antifeedant; antifungal agent; antimicrobial agent; antineoplastic agent; antioxidant; antitussive; antiviral agent; apoptosis inducer; autophagy inducer; hepatoprotective agent; insecticide; neuroprotective agent; plant metabolite; volatile oil component
(2e,4e,6e,10e)-3,7,11,15-tetramethyl-2,4,6,10,14-hexadecapentaenoic acid (2E,4E,6E,10E)-3,7,11,15-tetramethyl-2,4,6,10,14-hexadecapentaenoic acid: an acyclic retinoid that suppresses hepatocellular carcinoma recurrence; structure in first source	2.6	1	0
concanamycin a concanamycin A: from Streptomyces diastatochromogenes S-45; inhibits vacuolar H+ ATPase. concanamycin A : A concanamycin in which the lactone ring contains 4 double bonds and is substituted by 4 methyl groups, 2 hydroxy groups, 2 methoxy groups and an ethyl group.	2.08	1	0	carbamate ester; concanamycin	antifungal agent; EC 3.6.3.14 (H(+)-transporting two-sector ATPase) inhibitor; metabolite
plastochromanol 8 plastochromanol 8: has antiproliferative activity against 3T3-L1 cells and anti-adipogenic activity; structure; plastochromanol 3 is gamma-tocotrienol	2.05	1	0
pregna-4,17-diene-3,16-dione pregna-4,17-diene-3,16-dione: steroid from guggulu extract; RN & N1 from C1 Form index; RN given refers to cpd without isomeric designation; structure in first source; antagonist of farnesoid X receptor	3.21	1	0	3-hydroxy steroid	androgen
lithospermic acid [no description available]	2.6	1	0
everolimus [no description available]	11.25	24	4	cyclic acetal; cyclic ketone; ether; macrolide lactam; primary alcohol; secondary alcohol	anticoronaviral agent; antineoplastic agent; geroprotector; immunosuppressive agent; mTOR inhibitor
tiglyl-coenzyme a 2-methylbut-2-enoyl-coenzyme A : An alk-2-enoyl-CoA that results from the formal condensation of the thiol group of coenzyme A with the carboxy group of 2-methylbut-2-enoic acid.	2.6	1	0	2-enoyl-CoA; monounsaturated fatty acyl-CoA
laq824 LAQ824: Histone deacetylase inhibitor	2.52	2	0
ixabepilone [no description available]	4.78	5	0	1,3-thiazoles; beta-hydroxy ketone; epoxide; lactam; macrocycle	antineoplastic agent; microtubule-destabilising agent
ekb 569 EKB 569: an EGF receptor kinase inhibitor	2.6	1	0	aminoquinoline; monocarboxylic acid amide; monochlorobenzenes; nitrile	protein kinase inhibitor
cdw17 antigen [no description available]	2.21	1	0
axitinib [no description available]	9.14	4	0	aryl sulfide; benzamides; indazoles; pyridines	antineoplastic agent; tyrosine kinase inhibitor; vascular endothelial growth factor receptor antagonist
pai 039 tiplaxtinin: inhibitor of plasminogen activator inhibitor-1	2.08	1	0	indole-3-acetic acids
rilpivirine [no description available]	2.6	1	0	aminopyrimidine; nitrile	EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor; HIV-1 reverse transcriptase inhibitor
(1Ar,7aS,10aS,10bS)-1a,5-dimethyl-8-methylidene-2,3,6,7,7a,8,10a,10b-octahydrooxireno[9,10]cyclodeca[1,2-b]furan-9(1aH)-one [no description available]	2.6	1	0	germacranolide
4,5-di-O-caffeoylquinic acid [no description available]	2.6	1	0	quinic acid
indigo carmine 3,5-di-O-(E)-caffeoylquinic acid: from roots of Lychnophora ericoides; structure in first source. 3,5-di-O-caffeoyl quinic acid : A carboxylic ester that is the diester obtained by the condensation of the hydroxy groups at positions 3 and 5 of (-)-quinic acid with the carboxy group of trans-caffeic acid. Isolated from Brazilian propolis and Suaeda glauca, it exhibits hepatoprotective and cytotoxic activities.	2.6	1	0
azlocillin Azlocillin: A semisynthetic ampicillin-derived acylureido penicillin.. azlocillin : A semisynthetic penicillin having a 6beta-{(2R)-2-[(2-oxoimidazolidine-1-carbonyl)amino]-2-phenylacetyl}amino side-group. It is an antibiotic used in treating infections caused by Pseudomonas aeruginosa, Escherichia coli and Haemophilus influenzae.	2.45	2	0	penicillin allergen; penicillin; semisynthetic derivative	antibacterial drug
tanespimycin CP 127374: analog of herbimycin A	9.63	23	4	1,4-benzoquinones; ansamycin; carbamate ester; organic heterobicyclic compound; secondary amino compound	antineoplastic agent; apoptosis inducer; Hsp90 inhibitor
verlukast verlukast: LTD4 receptor antagonist	2.04	1	0
cefpodoxime proxetil cefpodoxime proxetil: structure given in first source; prodrug for cefpodoxime. cefpodoxime proxetil : The 1-[(isopropoxycarbonyl)oxy]ethyl (proxetil) ester prodrug of cefpodoxime. After swallowing, hydrolysis of the ester group occurs in the intestinal epithelium, to release active cefpodoxime in the bloodstream. It is used to treat acute otitis media, pharyngitis, and sinusitis.	2.08	1	0	carboxylic acid; carboxylic ester; cephalosporin	antibacterial drug; prodrug
ceftizoxime [no description available]	3.58	2	0	cephalosporin	antibacterial drug
1-methyl-d-lysergic acid butanolamide [no description available]	3.23	1	0	ergot alkaloid; monocarboxylic acid amide	serotonergic antagonist; sympatholytic agent; vasoconstrictor agent
carumonam carumonam: structure given in first source; RN given refers to (2S-(2alpha,3alpha(Z))-isomer. carumonam : An N-sulfonated monobactam antibiotic.	2.04	1	0	monobactam	antibacterial drug
beta-escin [no description available]	3.33	1	0
fluphenazine [no description available]	2.08	1	0
gw2974 GW2974: quinazoline derivative, which is able to block the activation of both the EGFR and erbB2	2.08	1	0	pyridopyrimidine
dantrolene sodium dantrolene sodium (anhydrous) : The anhydrous sodium salt of dantrolene.	2.05	1	0
nitrofurantoin Nitrofurantoin: A urinary anti-infective agent effective against most gram-positive and gram-negative organisms. Although sulfonamides and antibiotics are usually the agents of choice for urinary tract infections, nitrofurantoin is widely used for prophylaxis and long-term suppression.. nitrofurantoin : An imidazolidine-2,4-dione that is hydantoin substituted at position 1 by a [(5-nitro-2-furyl)methylene]amino group. An antibiotic that damages bacterial DNA.	4.29	5	0	imidazolidine-2,4-dione; nitrofuran antibiotic; organonitrogen heterocyclic antibiotic; organooxygen heterocyclic antibiotic	antibacterial drug; antiinfective agent; hepatotoxic agent
am 404 [no description available]	2.17	1	0	anilide
lactacystin [no description available]	9.62	29	0	lactam; S-substituted L-cysteine
tubacin tubacin: inhibits histone deacetylase 6; structure in first source	3.45	7	0	1,3-oxazoles
nifurtimox Nifurtimox: A nitrofuran thiazine that has been used against TRYPANOSOMIASIS.	2.05	1	0	nitrofuran antibiotic
ispinesib [no description available]	2.08	1	0	benzamides
eritoran eritoran : A lipid A derivative used for the treatment of severe sepsis.	2.04	1	0	lipid As
dantrolene [no description available]	3.58	2	0
fk 866 N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide: inhibits nicotinamide phosphoribosyltransferase; structure in first source	2.08	1	0	benzamides; N-acylpiperidine
roxithromycin (E)-roxithromycin : A major geometrical isomer of roxithromycin.	2.47	2	0	roxithromycin	environmental contaminant; xenobiotic
inecalcitol [no description available]	2.08	1	0
mdl 201053 MDL 201053: Immunosuppressive Agent; RN given refers to compound with no isomeric designation	2.08	1	0
cefdinir [no description available]	3.61	2	0	cephalosporin; ketoxime	antibacterial drug
etonogestrel [no description available]	3.23	1	0	17beta-hydroxy steroid; 3-oxo-Delta(4) steroid; terminal acetylenic compound	contraceptive drug; female contraceptive drug; progestin
bisoprolol, fumarate (1:1) salt [no description available]	2.08	1	0
artesunate artesunic acid: RN given for (3R-(3alpha,5abeta,6beta,8abeta,9alpha,10alpha,12beta,(2aR*))-isomer; succinic ester of artemether	2.8	3	0	artemisinin derivative; cyclic acetal; dicarboxylic acid monoester; hemisuccinate; semisynthetic derivative; sesquiterpenoid	antimalarial; antineoplastic agent; ferroptosis inducer
beraprost beraprost: stable prostacyclin analog; structure given in first source. beraprost : An organic heterotricyclic compound that is (3aS,8bS)-2,3,3a,8b-tetrahydro-1H-benzo[b]cyclopenta[d]furan in which the hydrogens at positions 1R, 2R and 5 are replaced by (3S)-3-hydroxy-4-methyloct-1-en-6-yn-1-yl, hydroxy and 3-carboxypropyl groups, respectively. It is a prostaglandin receptor agonist which is approved to treat pulmonary arterial hypertension in Asia.	2.05	1	0	enyne; monocarboxylic acid; organic heterotricyclic compound; secondary alcohol; secondary allylic alcohol	anti-inflammatory agent; antihypertensive agent; platelet aggregation inhibitor; prostaglandin receptor agonist; vasodilator agent
lanreotide [no description available]	2.05	1	0
etoposide phosphate [no description available]	2.08	1	0	furonaphthodioxole
dexniguldipine niguldipine: structure given in first source; clinical modulator of multidrug resistance	2.04	1	0	diarylmethane
ciclesonide ciclesonide: nasal spray approved for seasonal and perennial allergic rhinitis	2.08	1	0	organic molecular entity
ru 58668 RU 58668: a steroidal antiestrogen; induces a long-term regression of human mammary MCF-7 tumors implanted in nude mice; structure given in first source. RU 58668 : A 17beta-hydroxy steroid that is 17beta-estradiol in the the hydrogen at the 11beta position has been replaced by a p-({5-[(4,4,5,5,5-pentafluoropentyl)sulfonyl]pentyl}oxy)phenyl group. RU 58668 is a pure anti-estrogen that downregulates estrogen receptor expression (IC50 = 0.04 nM).	2.04	1	0	17beta-hydroxy steroid; 3-hydroxy steroid; aromatic ether; organofluorine compound; sulfone	anti-estrogen; antineoplastic agent; estrogen receptor antagonist
napsagatran napsagatran: structure given in first source	2.04	1	0
temsirolimus [no description available]	4.09	4	0	macrolide lactam
dutasteride Dutasteride: A 5-ALPHA-REDUCTASE INHIBITOR that is reported to inhibit both type-1 and type2 isoforms of the enzyme and is used to treat BENIGN PROSTATIC HYPERPLASIA.. dutasteride : An aza-steroid that is inasteride in which the tert-butyl group is replaced by a 2,5-bis(trifluoromethyl)phenyl group. A synthetic 4-azasteroid, dutasteride is a selective inhibitor of both the type 1 and type 2 isoforms of steroid 5alpha-reductase, an intracellular enzyme that converts testosterone to 5alpha-dihydrotestosterone. Dutasteride is used for the treatment of symptomatic benign prostatic hyperplasia in men with an enlarged prostate gland.	3.61	2	0	(trifluoromethyl)benzenes; aza-steroid; delta-lactam	antihyperplasia drug; EC 1.3.1.22 [3-oxo-5alpha-steroid 4-dehydrogenase (NADP(+))] inhibitor
(3S,6S,9S,12R)-3-[(2S)-Butan-2-yl]-6-[(1-methoxyindol-3-yl)methyl]-9-(6-oxooctyl)-1,4,7,10-tetrazabicyclo[10.4.0]hexadecane-2,5,8,11-tetrone [no description available]	2.6	1	0	oligopeptide
cvt 313 CVT 313: a potent inhibitor of CDK2 that prevents neointimal proliferation; structure given in first source	2.21	1	0
tekturna [no description available]	2.08	1	0	fumarate salt	antihypertensive agent
pd 184352 2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide: inhibits MAP kinase kinase; structure in first source	2.49	2	0	aminobenzoic acid
voclosporin voclosporin: semi-synthetic cyclosporine A analog & calcineurin inhibitor; FDA approved use to treat lupus nephritis.	3.41	1	0	homodetic cyclic peptide
lu 208075 ambrisentan: an ET(A) receptor antagonist and antihypertensive agent; studied for use in pulmonary arterial hypertension	3.59	2	0	diarylmethane
bms188797 [no description available]	2.04	1	0
jwh-133 1,1-dimethylbutyl-1-deoxy-Delta(9)-THC: a CB2 receptor agonists; no further information available on 8/2001. JWH-133 : A dibenzopyran that is Delta(9)-tetrahydrocannabinol which is lacking the hydroxy group and in which the pentyl group at position 3 has been replaced by a 1,1-dimethylbutyl group. A potent and highly selective CB2 receptor agonist.	2.17	1	0	benzochromene; dibenzopyran; organic heterotricyclic compound	analgesic; anti-inflammatory agent; antineoplastic agent; apoptosis inhibitor; CB2 receptor agonist; opioid analgesic; vasodilator agent
bibx 1382bs BIBX 1382BS: an ErbB receptor kinase inhibitor; no further information available 4/2001	3.61	2	0	substituted aniline
vildagliptin [no description available]	2.58	2	0	amino acid amide
fesoterodine fesoterodine: a muscarinic antagonist for treatment of overactive bladder	3.23	1	0	diarylmethane
talabostat talabostat: an antineoplastic agent; structure in first source	2.08	1	0
belinostat [no description available]	4.95	8	1	hydroxamic acid; olefinic compound; sulfonamide	antineoplastic agent; EC 3.5.1.98 (histone deacetylase) inhibitor
pep005 3-ingenyl angelate: protein kinase C agonist and antineoplastic; structure in first source	2.05	1	0
on 01910 ON 01910: a Plk1 inhibitor with antineoplastic activity; structure in first source. N-[2-methoxy-5-({[2-(2,4,6-trimethoxyphenyl)ethenyl]sulfonyl}methyl)phenyl]glycine : A glycine derivative that is glycine in which one of the hydrogens of the amino group is substituted by a 2-methoxy-5-({[2-(2,4,6-trimethoxyphenyl)ethenyl]sulfonyl}methyl)phenyl group.. rigosertib : An N-[2-methoxy-5-({[2-(2,4,6-trimethoxyphenyl)ethenyl]sulfonyl}methyl)phenyl]glycine in which the double bond has E-configuration. It is a non-ATP-competitive inhibitor of PLK1 with an IC50 of 9 nM and exhibits anti-cancer properties.	2.25	1	0	N-[2-methoxy-5-({[2-(2,4,6-trimethoxyphenyl)ethenyl]sulfonyl}methyl)phenyl]glycine	antineoplastic agent; apoptosis inducer; EC 2.7.11.21 (polo kinase) inhibitor; microtubule-destabilising agent
panobinostat Panobinostat: An indole and hydroxamic acid derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used as an antineoplastic agent in combination with BORTEZOMIB and DEXAMETHASONE for the treatment of MULTIPLE MYELOMA.. panobinostat : A hydroxamic acid obtained by formal condensation of the carboxy group of (2E)-3-[4-({[2-(2-methylindol-3-yl)ethyl]amino}methyl)phenyl]prop-2-enoic acid with the amino group of hydroxylamine. A histone deacetylase inhibitor used (as its lactate salt) in combination with bortezomib and dexamethasone for the treatment of multiple myeloma.	16.32	73	22	cinnamamides; hydroxamic acid; methylindole; secondary amino compound	angiogenesis modulating agent; antineoplastic agent; EC 3.5.1.98 (histone deacetylase) inhibitor
hdac-42 HDAC-42: structure in first source	2.81	3	0	amidobenzoic acid
acetylcarnitine O-acetyl-L-carnitine : An O-acyl-L-carnitine where the acyl group specified is acetyl. It facilitates movement of acetyl-CoA into the matrices of mammalian mitochondria during the oxidation of fatty acids.	2.05	1	0	O-acetylcarnitine; saturated fatty acyl-L-carnitine	human metabolite; Saccharomyces cerevisiae metabolite
staurosporine staurosporinium : Conjugate acid of staurosporine.	4.97	4	0	ammonium ion derivative
bufalin bufalin: cardiotonic; powerful anesthetic & one of the active constituents of the Chinese drug ch'an su(senso); in Japan prepared from skin of Bufo bufo garfarizans; RN given refers to (3beta,5beta)-isomer. bufalin : A 14beta-hydroxy steroid that is bufan-20,22-dienolide having hydroxy substituents at the 5beta- and 14beta-positions. It has been isolated from the skin of the toad Bufo bufo.	7.04	1	0	14beta-hydroxy steroid; 3beta-hydroxy steroid	animal metabolite; anti-inflammatory agent; antineoplastic agent; cardiotonic drug
taxane taxane: produced by Taxomyces andreanae	2.54	2	0	diterpene; terpenoid fundamental parent
9h-purine-9-propanamine, 6-amino-8-((6-iodo-1,3-benzodioxol-5-yl)thio)-n-(1-methylethyl)- 9H-purine-9-propanamine, 6-amino-8-((6-iodo-1,3-benzodioxol-5-yl)thio)-N-(1-methylethyl)-: an epichaperome (purine-scaffold) inhibitor; structure in first source	3.48	1	1
[4-[[4-(1-benzothiophen-2-yl)-2-pyrimidinyl]amino]phenyl]-[4-(1-pyrrolidinyl)-1-piperidinyl]methanone [no description available]	2.08	1	0	benzamides; N-acylpiperidine
chlorhexidine Chlorhexidine: A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.. chlorhexidine : A bisbiguanide compound with a structure consisting of two (p-chlorophenyl)guanide units linked by a hexamethylene bridge.	2.63	2	0	biguanides; monochlorobenzenes	antibacterial agent; antiinfective agent
sgd 301-76 [no description available]	2.08	1	0	conazole antifungal drug; imidazole antifungal drug; organic nitrate salt	antiinfective agent
fluvoxamine maleate [no description available]	2.08	1	0	(trifluoromethyl)benzenes
formazans Formazans: Colored azo compounds formed by the reduction of tetrazolium salts. Employing this reaction, oxidoreductase activity can be determined quantitatively in tissue sections by allowing the enzymes to act on their specific substrates in the presence of tetrazolium salts.	2.47	2	0
thioacetazone Thioacetazone: A thiosemicarbazone that is used in association with other antimycobacterial agents in the initial and continuation phases of antituberculosis regimens. Thiacetazone containing regimens are less effective than the short-course regimen recommended by the International Union Against Tuberculosis and are used in some developing countries to reduce drug costs. (From Martindale, The Extra Pharmacopoeia, 30th ed, p217). thiosemicarbazone : A hydrazone resulting from the formal condensation of an aldehyde or ketone with the non-thioacylated nitrogen of thiosemicarbazide or its substituted derivatives.	2.08	1	0
azimilide azimilide: structure given in first source; RN given refers to dihydrochloride	2.04	1	0	imidazolidine-2,4-dione
nifurtoinol nifurtoinol : An imidazolidine-2,4-dione that is hydantoin substituted at position 1 by a [(5-nitro-2-furyl)methylene]amino group and at position 3 by a hydroxymethyl group.	2.05	1	0	hydrazone; imidazolidine-2,4-dione; nitrofuran antibiotic; organonitrogen heterocyclic antibiotic	antibacterial drug; antiinfective agent; hepatotoxic agent
gemifloxacin Gemifloxacin: A naphthyridine and fluoroquinolone derivative antibacterial agent and DNA TOPOISOMERASE II inhibitor that is used for the treatment of community-acquired pneumonia and acute bacterial infections associated with chronic bronchitis.. gemifloxacin : A 1,4-dihydro-1,8-naphthyridine with a carboxy group at the 3-position, an oxo sustituent at the 4-position, a fluoro substituent at the 5-position and a substituted pyrrolin-1-yl group at the 7-position.	3.23	1	0	1,8-naphthyridine derivative; fluoroquinolone antibiotic; monocarboxylic acid; quinolone antibiotic	antibacterial drug; antimicrobial agent; topoisomerase IV inhibitor
gs-7340 tenofovir alafenamide: component of Biktarvy. tenofovir alafenamide : An L-alanine derivative that is isopropyl L-alaninate in which one of the amino hydrogens is replaced by an (S)-({[(2R)-1-(6-amino-9H-purin-9-yl)propan-2-yl]oxy}methyl)(phenoxy)phosphoryl group. A prodrug for tenofovir, it is used (as the fumarate salt) in combination therapy for the treatment of HIV-1 infection.	2.6	1	0	6-aminopurines; ether; isopropyl ester; L-alanine derivative; phosphoramidate ester	antiviral drug; HIV-1 reverse transcriptase inhibitor; prodrug
st 1481 ST 1481: structure in first source	2.02	1	0
dexlansoprazole Dexlansoprazole: The R-isomer of lansoprazole that is used to treat severe GASTROESOPHAGEAL REFLUX DISEASE.	3.91	3	0	benzimidazoles; sulfoxide
gemifloxacin mesylate gemifloxacin mesylate : The mesylate salt of gemifloxacin.	2.08	1	0	methanesulfonate salt	antimicrobial agent; topoisomerase IV inhibitor
fosinopril [no description available]	3.59	2	0
armodafinil armodafinil : A 2-[(diphenylmethyl)sulfinyl]acetamide that has R configuration at the sulfur atom. Like its racemate, modafinil, it is used for the treatment of sleeping disorders such as narcolepsy, obstructive sleep apnoea, and shift-work sleep disorder. Peak concentration in the blood later occurs later following administration than with modafinil, so it is thought that armodafinil may be more effective than modafinil in treating people with excessive daytime sleepiness.	3.23	1	0	2-[(diphenylmethyl)sulfinyl]acetamide	central nervous system stimulant; eugeroic
clasto-lactacystin beta-lactone clasto-lactacystin beta-lactone: active metabolite of lactacystin; inhibits 20 S proteasome; structure in first source	2.49	2	0
iniparib [no description available]	2.58	2	0	carbonyl compound; organohalogen compound
n-(2-amino-5-fluorobenzyl)-4-(n-(pyridine-3-acrylyl)aminomethyl)benzamide [no description available]	2.6	1	0
pri-2205 [no description available]	2.6	1	0
mk 0752 [no description available]	2.58	2	0
gw 501516 GW 501516: a selective PPARdelta agonist; structure in first source. GW 501516 : An aromatic ether that is phenoxyacetic acid in which the phenyl group is substituted at position 2 by a methyl group and at position 4 by a (1,3-thiazol-5-ylmethyl)sulfanediyl group, and in which the 1,3-thiazolyl group is substituted at positions 2 and 4 by p-trifluoromethylphenyl and methyl groups, respectively.	2.08	1	0	1,3-thiazoles; aromatic ether; aryl sulfide; monocarboxylic acid; organofluorine compound	carcinogenic agent; PPARbeta/delta agonist
eflucimibe eflucimibe: a powerful and systemic acylcoenzyme A: cholesterol acyltransferase inhibitor	2.05	1	0
givinostat [no description available]	2.6	1	0	carbamate ester
av 412 [no description available]	2.08	1	0
ag-041r AG-041R: structure in first source	2.08	1	0
telatinib [no description available]	2.08	1	0
tomopenem [no description available]	2.04	1	0
cp 547632 3-(4-bromo-2,6-difluorobenzyloxy)-5-(3-(4-pyrrolidin-1-ylbutyl)ureido)isothiazole-4-carboxylic acid amide: inhibits vascular endothelial growth factor receptor-2 tyrosine kinase; structure in first source	2.08	1	0
plitidepsin plitidepsin: a cyclodepsipeptide isolated from Aplidium albicans; has a pyruvoyl-proline residue instead of the lactyl-proline residue found in the linear peptide moiety of didemnin B. plitidepsin : A didemnin that is didemin B in which the hydroxy group of the 1-(2-hydroxypropanoyl)-L-prolinamide moiety has been oxidised to the corresponding ketone. It was originally isolated from the Mediterranean tunicate Aplidium albicans.	3.94	2	1	didemnin	anticoronaviral agent; antineoplastic agent; marine metabolite
bms345541 4(2'-aminoethyl)amino-1,8-dimethylimidazo(1,2-a)quinoxaline: structure in first source	3.16	5	0	quinoxaline derivative
pd 144418 [no description available]	2.6	1	0
spc-839 SPC-839: an inhibitor of activator protein 1; structure in first source	2.46	2	0
bicyclol bicyclol: an antihepatitis drug, on the metabolism and hepatotoxicity of aflatoxin B1 (AFB1) in rats.	2.6	1	0
lenvatinib lenvatinib : A member of the class of quinolines that is the carboxamide of 4-{3-chloro-4-[(cyclopropylcarbamoyl)amino]phenoxy}-7-methoxyquinoline-6-carboxylic acid. A multi-kinase inhibitor and orphan drug used (as its mesylate salt) for the treatment of various types of thyroid cancer that do not respond to radioiodine.	3.58	2	0	aromatic amide; aromatic ether; cyclopropanes; monocarboxylic acid amide; monochlorobenzenes; phenylureas; quinolines	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; fibroblast growth factor receptor antagonist; orphan drug; vascular endothelial growth factor receptor antagonist
andarine [no description available]	2.08	1	0	acetamides; anilide
gw843682x [no description available]	2.08	1	0	(trifluoromethyl)benzenes
pd 0325901 mirdametinib: has antineoplastic activity; appears to be a MEK inhibitor. PD 0325901 : A hydroxamic acid ester that is benzhydroxamic acid (N-hydroxybenzamide) in which the hydroxamic acid group has been converted to the corresponding 2,3-dihydroxypropyl ester and in which the benzene ring has been substituted at position 2 by a (2-fluoro-4-iodophenyl)amino group and at positions 3 and 4 by fluorines (the R enantiomer).	2.53	2	0	difluorobenzene; hydroxamic acid ester; monofluorobenzenes; organoiodine compound; propane-1,2-diols; secondary amino compound	antineoplastic agent; EC 2.7.12.2 (mitogen-activated protein kinase kinase) inhibitor
midostaurin midostaurin : An organic heterooctacyclic compound that is the N-benzoyl derivative of staurosporine.	8.95	4	0	benzamides; gamma-lactam; indolocarbazole; organic heterooctacyclic compound	antineoplastic agent; EC 2.7.11.13 (protein kinase C) inhibitor
sincalide Sincalide: An octapeptide hormone present in the intestine and brain. When secreted from the gastric mucosa, it stimulates the release of bile from the gallbladder and digestive enzymes from the pancreas.	3.23	1	0	oligopeptide
tapentadol Tapentadol: An opioid analgesic, MU OPIOID RECEPTOR agonist, and noradrenaline reuptake inhibitor that is used in the treatment of moderate to severe pain, and of pain associated with DIABETIC NEUROPATHIES.	3.23	1	0	alkylbenzene
pd 150606 PD 150606: a calpain inhibitor; structure given in first source. (Z)-3-(4-iodophenyl)-2-mercaptoacrylic acid : An organoiodine compound that is acrylic acid in which the vinylic hydrogens at positions 2 and 3 are replaced by mercapto and 4-iodophenyl groups respectively (the Z geoisomer).	2.92	1	0	cinnamic acids; organoiodine compound; thioenol	apoptosis inhibitor; calpain inhibitor
ag 14361 [no description available]	2.08	1	0	benzimidazoles
etomoxir [no description available]	2.47	2	0	aromatic ether
sb 265610 [no description available]	2.08	1	0
ly 450139 [no description available]	2.6	1	0	peptide
gallium maltolate gallium maltolate: has antineoplastic activity	2.05	1	0
jorumycin jorumycin: structure in first source	3.41	1	0
bb-83698 BB-83698: peptide deformylase inhibitor	2.04	1	0
gambogic acid gambogic acid: RN given refers to (1R-(1alpha,1(Z),3abeta,5alpha,11beta,14aS*))-isomer	2.51	2	0	pyranoxanthones	metabolite
pentagastrin Pentagastrin: A synthetic pentapeptide that has effects like gastrin when given parenterally. It stimulates the secretion of gastric acid, pepsin, and intrinsic factor, and has been used as a diagnostic aid.	3.59	2	0	organic molecular entity
knk 437 KNK 437: inhibits thermotolerance acquisition and heat shock protein induction in colon carcinoma cells; structure in first source	2.49	2	0
fr 148083 5Z-7-oxozeaenol : A macrolide that is the 7-oxo derivative of zeaenol (the 5Z stereoisomer). Isolated from Fungi, it exhibits cytotoxic, antibacterial and inhibitory activity against NF-kappaB.	2.08	1	0	aromatic ether; macrolide; phenols; secondary alcohol; secondary alpha-hydroxy ketone	antibacterial agent; antineoplastic agent; metabolite; NF-kappaB inhibitor
mocetinostat mocetinostat: undergoing phase II clinical trials for treatment of cancer. mocetinostat : A benzamide obtained by formal condensation of the carboxy group of 4-({[4-(pyridin-3-yl)pyrimidin-2-yl]amino}methyl)benzoic acid with one of the amino groups of benzene-1,2-diamine. It is an orally active and isotype-selective HDAC inhibitor which exhibits antitumour activity (IC50 = 0.15, 0.29, 1.66 and 0.59 muM for HDAC1, HDAC2, HDAC3 and HDAC11).	3.02	4	0	aminopyrimidine; benzamides; pyridines; secondary amino compound; secondary carboxamide; substituted aniline	antineoplastic agent; apoptosis inducer; autophagy inducer; cardioprotective agent; EC 3.5.1.98 (histone deacetylase) inhibitor; hepatotoxic agent
osi 930 OSI 930: inhibits both receptor tyrosine kinase Kit and kinase insert domain receptor; structure in first source	2.08	1	0	aromatic amide
ki 20227 [no description available]	2.08	1	0
cefditoren cefditoren: structure given in first source; RN given refers to the (6R-(3(Z),6alpha,7beta(Z)))-isomer. cefditoren : A broad spectrum, third-generation cephalosporin antibiotic with (Z)-2-(4-methyl-1,3-thiazol-5-yl)ethenyl and (2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetamido groups at positions 3 and 7, respectively, of the cephem skeleton. Generally administered as its orally absorbed pivaloyloxymethyl ester prodrug, it is used for the treatment of mild to moderate infections caused by susceptible strains of microorganisms in acute bacterial exacerbation of chronic bronchitis, community-acquired pneumonia, pharyngitis/tonsillitis, and uncomplicated skin and skin-structure infections.	3.23	1	0	carboxylic acid; cephalosporin	antibacterial drug
scio-469 SCIO-469: a small-molecule p38 mitogen-activated protein (MAP) kinase inhibitor for potential oral therapy for inflammatory disorders; in phase lib clinical trials for rheumatoid arthritis 4/2004. talmapimod : An indolecarboxamide obtained by formal condensation of the carboxy group of 6-chloro-3-[(dimethylamino)(oxo)acetyl]-1-methylindole-5-carboxylic acid with the secondary amino group of (2S,5R)-1-[(4-fluorophenyl)methyl]-2,5-dimethylpiperazine. It is a potent inhibitor of MAPK and exhibits anti-cancer properties.	2.74	3	0	aromatic amide; aromatic ketone; chloroindole; dicarboxylic acid diamide; indolecarboxamide; monofluorobenzenes; N-acylpiperazine; N-alkylpiperazine	antineoplastic agent; apoptosis inducer; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
ssr 69071 SSR 69071: structure in first source	2.08	1	0	pyridopyrimidine
k 7174 K 7174: inhibits binding of monocytes to cytokine-stimulated endothelial cells; structure in first source	3.47	1	1
tmc-95a TMC-95A: produced by Apiospora montagnei Sacc.TC 1093; structure in first source. TMC-95A : A 17-membered macrocyclic lactam that incorporates a phenol and a substituted indole moiety. It includes a R-hydroxy group at position 11 and a (3-methyl-2-oxopentanoyl)amino group at position at position 18 with a S-methyl group. It acts as a proteasome inhibitor and is obtained from Apiospora montagnei Sacc. TC 1093, isolated from a soil sample.	3.14	1	0	indoles; lactam; macrocycle; phenols; secondary alcohol; tertiary alcohol	antimicrobial agent; antineoplastic agent; bacterial metabolite; fungal metabolite; proteasome inhibitor
rivaroxaban Rivaroxaban: A morpholine and thiophene derivative that functions as a FACTOR XA INHIBITOR and is used in the treatment and prevention of DEEP-VEIN THROMBOSIS and PULMONARY EMBOLISM. It is also used for the prevention of STROKE and systemic embolization in patients with non-valvular ATRIAL FIBRILLATION, and for the prevention of atherothrombotic events in patients after an ACUTE CORONARY SYNDROME.. rivaroxaban : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 5-chlorothiophene-2-carboxylic acid with the amino group of 4-{4-[(5S)-5-(aminomethyl)-2-oxo-1,3-oxazolidin-3-yl]phenyl}morpholin-3-one. An anticoagulant used for prophylaxis of venous thromboembolism in patients with knee or hip replacement surgery.	2.88	3	0	aromatic amide; lactam; monocarboxylic acid amide; morpholines; organochlorine compound; oxazolidinone; thiophenes	anticoagulant; EC 3.4.21.6 (coagulation factor Xa) inhibitor
zotarolimus zotarolimus: synthetic analog of rapamycin; structure in first source	2.04	1	0	lactam; macrolide
dehydroxymethylepoxyquinomicin dehydroxymethylepoxyquinomicin: an NF-kappaB inhibitor; structure in first source	3.54	2	0
sb 3ct compound SB 3CT compound: a matrix metalloproteinase-2 inhibitor; structure in first source	2.66	2	0	aromatic ether
pi103 PI103: pyridofuropyrimidine antineoplastic; a potent inhibitor of class I phosphatidylinositide 3-kinases (PI3K); structure in first soruce	2.08	1	0	aromatic amine; morpholines; organic heterotricyclic compound; phenols; tertiary amino compound	antineoplastic agent; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; mTOR inhibitor
sb 210313 [no description available]	2.08	1	0
3,5-bis(2-fluorobenzylidene)piperidin-4-one 3,5-bis(2-fluorobenzylidene)piperidin-4-one: an antineoplastic agent; structure in first source	2.1	1	0
gw 4064 [no description available]	2.08	1	0	stilbenoid
mart-1 antigen MART-1 Antigen: A melanosome-specific protein that plays a role in the expression, stability, trafficking, and processing of GP100 MELANOMA ANTIGEN, which is critical to the formation of Stage II MELANOSOMES. The protein is used as an antigen marker for MELANOMA cells.	2.07	1	0
ginsenoside rb1 [no description available]	2.6	1	0	ginsenoside; glycoside; tetracyclic triterpenoid	anti-inflammatory drug; anti-obesity agent; apoptosis inhibitor; neuroprotective agent; plant metabolite; radical scavenger
gentamicin sulfate [no description available]	2.45	2	0
sa 4503 [no description available]	2.08	1	0
ic 87114 IC 87114: structure in first source	2.08	1	0	6-aminopurines; biaryl; quinazolines	EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
bn 52020 [no description available]	2.04	1	0
zibotentan ZD4054: a potent endothelin receptor A antagonist that inhibits ovarian carcinoma cell proliferation	2.08	1	0	phenylpyridine
mcc-950 [no description available]	2.41	1	0
tivozanib N-(2-chloro-4-((6,7-dimethoxy-4-quinolyl)oxy)phenyl)-N'-(5-methyl-3-isoxazolyl)urea: KNR-951 is the HCl, monohydrate salt; an antineoplastic agent; structure in first source	2.08	1	0	aromatic ether
hki 272 [no description available]	2.49	2	0	nitrile; quinolines	antineoplastic agent; tyrosine kinase inhibitor
secoisolariciresinol diglucoside secoisolariciresinol diglucoside: major precursor of mammalian lignans; structure given in first source; RN given refers to B-D-GLUCO isomer	7.07	1	0
tofacitinib tofacitinib : A pyrrolopyrimidine that is pyrrolo[2,3-d]pyrimidine substituted at position 4 by an N-methyl,N-(1-cyanoacetyl-4-methylpiperidin-3-yl)amino moiety. Used as its citrate salt to treat moderately to severely active rheumatoid arthritis.	2.49	2	0	N-acylpiperidine; nitrile; pyrrolopyrimidine; tertiary amino compound	antirheumatic drug; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
bibr 1532 [no description available]	2.58	2	0
n-(6-chloro-7-methoxy-9h-beta-carbolin-8-yl)-2-methylnicotinamide [no description available]	2.08	1	0
rucaparib AG14447: Poly(ADP-ribose) polymerase inhibitor; structure in first source	2.58	2	0	azepinoindole; caprolactams; organofluorine compound; secondary amino compound	antineoplastic agent; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
cediranib [no description available]	2.08	1	0	aromatic ether
gw0742 GW 610742: structure in first source	2.08	1	0	monocarboxylic acid
melflufen melflufen: structure in first source	2.41	1	0
sb 743921 [no description available]	2.11	1	0
6h-thieno[3,2-f][1,2,4]triazolo[4,3-a][1,4]diazepine-6-acetamide, 4-(4-chlorophenyl)-n-(4-hydroxyphenyl)-2,3,9-trimethyl-, (6s)- [no description available]	2.6	1	0	organonitrogen heterocyclic compound; organosulfur heterocyclic compound
reversin 121 reversin 121: high affinity peptide chemosensitizer	2.54	2	0
ps1145 PS1145: IkappaB kinase inhibitor; structure in first source	8.28	6	0	beta-carbolines
cetilistat cetilistat: lipase inhibitor in randomized, placebo-controlled study of weight reduction in obese patients (3/2007)	2.6	1	0	benzoxazine
bay 41-8543 BAY 41-8543: structure in first source	2.08	1	0	pyrazolopyridine
chir 99021 Chir 99021: structure in first source. CHIR 99021 : A member of the class of aminopyrimidines that is 2-aminopyrimidine substituted at positions N2, 5 and 6 by (5-cyanopyridin-2-yl)ethyl, 4-methylimidazol-2-yl and 2,4-dichlorophenyl groups respectively.	2.08	1	0	aminopyridine; aminopyrimidine; cyanopyridine; diamine; dichlorobenzene; imidazoles; secondary amino compound	EC 2.7.11.26 (tau-protein kinase) inhibitor
ym 201636 6-amino-N-(3-(4-(4-morpholinyl)pyrido(3',2'-4,5)furo(3,2-d)pyrimidin-2-yl)phenyl)-3-pyridinecarboxamide: an antiviral agent; structure in first source	2.6	1	0	aromatic amide
benzyloxycarbonyl-isoleucyl-glutamyl(o-tert-butyl)-alanyl-leucinal benzyloxycarbonyl-isoleucyl-glutamyl(O-tert-butyl)-alanyl-leucinal: inhibits chymotrypsin activity of the proteasome	2.45	2	0
sb 525334 6-(2-tert-butyl-5-(6-methylpyridin-2-yl)-1H-imidazol-4-yl)quinoxaline: a TGF-betaR kinase inhibitor	2.08	1	0	quinoxaline derivative
aluminum oxide Aluminum Oxide: An oxide of aluminum, occurring in nature as various minerals such as bauxite, corundum, etc. It is used as an adsorbent, desiccating agent, and catalyst, and in the manufacture of dental cements and refractories.	5.17	2	1
way-362450 [no description available]	2.08	1	0	indoles
cgc 11093 CGC 11093: may prove useful in promoting regression of choroidal neovascularization	2.04	1	0
masitinib [no description available]	2.08	1	0	1,3-thiazoles; benzamides; N-alkylpiperazine; pyridines	antineoplastic agent; antirheumatic drug; tyrosine kinase inhibitor
bx795 BX795: structure in first source	2.08	1	0	ureas
linagliptin Linagliptin: A purine and quinazoline derivative that functions as an INCRETIN and DIPEPTIDYL-PEPTIDASE IV INHIBTOR. It is used as a HYPOGLYCEMIC AGENT in the treatment of TYPE II DIABETES MELLITUS.. linagliptin : A xanthine that is 7H-xanthine bearing (4-methylquinazolin-2-yl)methyl, methyl, but-2-yn-1-yl and 3-aminopiperidin-1-yl substituents at positions 1, 3, 7 and 8 respectively (the R-enantiomer). Used for treatment of type II diabetes.	2.6	1	0	aminopiperidine; quinazolines	EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor; hypoglycemic agent
pazopanib pazopanib: a protein kinase inhibitor. pazopanib : A pyrimidine that is 5-(pyrimidin-2-yl}amino-2-methylbenzenesulfonamide substituted at position 4 by a (2,3-dimethylindazol-6-yl)(methyl)amino group. Used as its hydrochloride salt for treatment of kidney cancer.	4.61	4	0	aminopyrimidine; indazoles; sulfonamide	angiogenesis modulating agent; antineoplastic agent; tyrosine kinase inhibitor; vascular endothelial growth factor receptor antagonist
sepantronium sepantronium: a survivin suppressant with antineoplastic activity. sepantronium : An organic cation that is 1-(2-methoxyethyl)-2-methyl-1H-naphtho[2,3-d]imidazole-4,9-dione in which the nitrogen at position 3 of the napthoimidazole moiety has been alkylated by a pyrazin-2-ylmethyl group.	2.48	2	0	organic cation
azd 6244 AZD 6244: a MEK inhibitor	4.73	6	1	benzimidazoles; bromobenzenes; hydroxamic acid ester; monochlorobenzenes; organofluorine compound; secondary amino compound	anticoronaviral agent; antineoplastic agent; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
odanacatib odanacatib: a selective inhibitor of cathepsin K for the treatment of post-menopausal osteoporosis; structure in first source	2.6	1	0
prasugrel hydrochloride Prasugrel Hydrochloride: A piperazine derivative and PLATELET AGGREGATION INHIBITOR that is used to prevent THROMBOSIS in patients with ACUTE CORONARY SYNDROME; UNSTABLE ANGINA and MYOCARDIAL INFARCTION, as well as in those undergoing PERCUTANEOUS CORONARY INTERVENTIONS.. prasugrel hydrochloride : A racemate comprising equal amounts of (R)- and (S)-prasugrel hydrochloride. Used to prevent blood clots in people with acute coronary syndrome who are undergoing a procedure after a recent heart attack or stroke, and in people with certain disorders of the heart or blood vessels.	3.23	1	0
1-(2-(1-adamantyl)ethyl)-1-pentyl-3-(3-(4-pyridyl)propyl)urea 1-(2-(1-adamantyl)ethyl)-1-pentyl-3-(3-(4-pyridyl)propyl)urea: structure in first source	2.08	1	0
apilimod [no description available]	2.6	1	0
apixaban [no description available]	2.6	1	0	aromatic ether; lactam; piperidones; pyrazolopyridine	anticoagulant; EC 3.4.21.6 (coagulation factor Xa) inhibitor
bibw 2992 [no description available]	2.17	1	0	aromatic ether; enamide; furans; monochlorobenzenes; organofluorine compound; quinazolines; secondary carboxamide; tertiary amino compound	antineoplastic agent; tyrosine kinase inhibitor
N-(3-cyanophenyl)-2'-methyl-5'-(5-methyl-1,3,4-oxadiazol-2-yl)biphenyl-4-carboxamide N-(3-cyanophenyl)-2'-methyl-5'-(5-methyl-1,3,4-oxadiazol-2-yl)biphenyl-4-carboxamide : A member of the class of biphenyls that is the amide obtained by formal condensation of the carboxy group of 2'-methyl-5'-(5-methyl-1,3,4-oxadiazol-2-yl)[1,1'-biphenyl]-4-carboxylic acid with the amino group of 3-cyanoaniline.	2.08	1	0	1,3,4-oxadiazoles; benzamides; biphenyls; nitrile	EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
nu 6140 4-(6-cyclohexylmethoxy-9H-purin-2-ylamino)-N,N-diethylbenzamide: a cyclin-dependent kinase inhibitor; structure in first source	2.15	1	0
ar c155858 AR C155858: an MCT1 inhibitor; structure in first source	2.08	1	0
succinyl-leucyl-leucyl-valyl-tyrosyl-methylcoumarinamide succinyl-leucyl-leucyl-valyl-tyrosyl-methylcoumarinamide: fluorogenic substrate for ingensin. succinyl-Leu-Leu-Val-Tyr-7-amino-4-methylcoumarin : A tetrapeptide compound with a succinyl group at the N-terminal and a 7-amino-4-methylcoumarin group at the C-terminal.	2.04	1	0	7-aminocoumarins; tetrapeptide	fluorochrome
betrixaban betrixaban: a highly potent, selective, and orally efficacious factor Xa inhibitor; structure in first source. betrixaban : A secondary carboxamide obtained by formal condensation of the carboxy group of 4-(N,N-dimethylcarbamimidoyl)benzoic acid with the amino group of 2-amino-N-(5-chloropyridin-2-yl)-5-methoxybenzamide. A synthetic anticoagulant compound that targets activated factor Xa in the coagulation cascade.	2.6	1	0	benzamides; guanidines; monochloropyridine; monomethoxybenzene; secondary carboxamide	anticoagulant; EC 3.4.21.6 (coagulation factor Xa) inhibitor
edoxaban edoxaban : A monocarboxylic acid amide that is used (as its tosylate monohydrate) for the treatment of deep vein thrombosis and pulmonary embolism.	2.66	2	0	chloropyridine; monocarboxylic acid amide; tertiary amino compound; thiazolopyridine	anticoagulant; EC 3.4.21.6 (coagulation factor Xa) inhibitor; platelet aggregation inhibitor
aee 788 AEE 788: structure in first source	2.08	1	0	6-{4-[(4-ethylpiperazin-1-yl)methyl]phenyl}-N-(1-phenylethyl)-7H-pyrrolo[2,3-d]pyrimidin-4-amine	angiogenesis inhibitor; antineoplastic agent; apoptosis inducer; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; epidermal growth factor receptor antagonist; trypanocidal drug
saracatinib [no description available]	2.58	2	0	aromatic ether; benzodioxoles; diether; N-methylpiperazine; organochlorine compound; oxanes; quinazolines; secondary amino compound	anticoronaviral agent; antineoplastic agent; apoptosis inducer; autophagy inducer; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor; radiosensitizing agent
alpha-synuclein alpha-Synuclein: A synuclein that is a major component of LEWY BODIES and plays a role in SYNUCLEINOPATHIES, neurodegeneration and neuroprotection.	2.25	1	0
sd-208 [no description available]	2.53	2	0
n-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide boceprevir : A synthetic tripeptide consisting of N-(tert-butylcarbamoyl)-3-methyl-L-valyl, a cyclopropyl-fused prolyl and 3-amino-4-cyclobutyl-2-oxobutanamide residues joined in sequence. Used for treatment of chronic hepatitis C virus genotype 1 infection.	2.6	1	0	tripeptide; ureas	antiviral drug; hepatitis C protease inhibitor; peptidomimetic
7-aminoactinomycin d 7-aminoactinomycin D: staining reagent used in flow cytometry	2.03	1	0
vx 702 VX 702: a p38 MAP kinase inhibitor	2.08	1	0	phenylpyridine
cylindrocyclophane a cylindrocyclophane A: structure in first source	2.05	1	0
bpr0l075 [no description available]	2.15	1	0
ly 411575 [no description available]	2.6	1	0	dibenzoazepine; difluorobenzene; lactam; secondary alcohol	EC 3.4.23.46 (memapsin 2) inhibitor
galidesivir [no description available]	2.6	1	0
volasertib BI 6727: a polo-like kinase inhibitor with broad antitumor activity; structure in first source	2.52	2	0
PB28 PB28 : A member of the class of tetralins that is tetralin that is substituted by 3-(4-cyclohexylpiperazin-1-yl)propyl and methoxy groups at positions 1 and 5, respectively. It is a sigma 2 (sigma2) receptor agonist (Ki = 0.68 nM) and exhibits antineoplastic and anti SARS-CoV-2 activities.	2.58	2	0	aromatic ether; piperazines; tetralins	anticoronaviral agent; antineoplastic agent; apoptosis inducer; sigma-2 receptor agonist
renieramycin m renieramycin M: from the Thai sponge Xestospongia sp.; structure in first source	3.41	1	0
amg 009 AMG 009: an anti-inflammatory agent; structure in first source	2.08	1	0
oxadiazoles Oxadiazoles: Compounds containing five-membered heteroaromatic rings containing two carbons, two nitrogens, and one oxygen atom which exist in various regioisomeric forms.	2.61	2	0
vinflunine vinflunine: inhibits tubulin assembly; structure in first source. vinflunine : An organic heteropentacyclic compound and an organic heterotetracyclic compound that is vinorelbine in which the tetrahydropyridine moiety of the heterotetracyclic part of the molecule has been redced to the corresponding piperidine, and in which the ethyl group attached to this ring has been replaced by a 1,1-difluoroethyl group.	2.05	1	0	acetate ester; methyl ester; organic heteropentacyclic compound; organic heterotetracyclic compound; semisynthetic derivative; vinca alkaloid	antineoplastic agent
belactosin c belactosin C: isolated from Streptomyces; structure in first source	2.48	2	0
cefotaxime sodium [no description available]	2.08	1	0	organic sodium salt
baci-im [no description available]	3.59	2	0	homodetic cyclic peptide; polypeptide; zwitterion	antibacterial agent; antimicrobial agent
acebutolol alpha-D-glucosyl-(1->4)-alpha-D-mannose : An alpha-D-glucosyl-(1->4)-D-mannopyranose in which the anomeric hydroxy group has alpha configuration.	2.11	1	0	alpha-D-glucosyl-(1->4)-D-mannopyranose
azd 7762 [no description available]	2.08	1	0	aromatic amide; thiophenes
krp-203 [no description available]	2.08	1	0
mk 0354 [no description available]	2.08	1	0
regorafenib [no description available]	2.08	1	0	(trifluoromethyl)benzenes; aromatic ether; monochlorobenzenes; monofluorobenzenes; phenylureas; pyridinecarboxamide	antineoplastic agent; hepatotoxic agent; tyrosine kinase inhibitor
acetic acid 2-[4-methyl-8-(4-morpholinylsulfonyl)-1,3-dioxo-2-pyrrolo[3,4-c]quinolinyl]ethyl ester [no description available]	2.08	1	0	pyrroloquinoline
6-[[5-fluoro-2-(3,4,5-trimethoxyanilino)-4-pyrimidinyl]amino]-2,2-dimethyl-4H-pyrido[3,2-b][1,4]oxazin-3-one [no description available]	2.08	1	0	methoxybenzenes; substituted aniline
degrasyn degrasyn: a JAK2 kinase inhibitor that induces rapid degradation of c-Myc protein in MM-1 multiple myeloma and other tumor cell lines; structure in first source	7.85	3	0
epoxomicin [no description available]	6.21	24	0	morpholines; tripeptide	proteasome inhibitor
abt-737 [no description available]	5.3	16	0	aromatic amine; aryl sulfide; biphenyls; C-nitro compound; monochlorobenzenes; N-arylpiperazine; N-sulfonylcarboxamide; secondary amino compound; tertiary amino compound	anti-allergic agent; anti-inflammatory agent; antineoplastic agent; apoptosis inducer; B-cell lymphoma 2 inhibitor
brivanib [no description available]	2.08	1	0	aromatic ether; diether; fluoroindole; pyrrolotriazine; secondary alcohol	angiogenesis inhibitor; antineoplastic agent; apoptosis inducer; drug metabolite; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; fibroblast growth factor receptor antagonist
icg 001 [no description available]	2.08	1	0	peptide
bms 477118 [no description available]	3.73	2	0	adamantanes; azabicycloalkane; monocarboxylic acid amide; nitrile; tertiary alcohol	EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor; hypoglycemic agent
pha 680632 PHA 680632: Aurora kinase inhibitor with potent antitumoral activity; structure in first source	2.6	1	0
tmc 353121 [no description available]	2.6	1	0
amd 070 mavorixafor: a derivative of AMD3100; a CXCR4 blocker	2.6	1	0	aminoquinoline
103d5r 103D5R: small-molecule inhibitor of the hypoxia-inducible factor 1 pathway; structure in first source	2.47	2	0
mp470 [no description available]	2.08	1	0	N-arylpiperazine
danoprevir [no description available]	2.6	1	0
nystatin a1 Nystatin: Macrolide antifungal antibiotic complex produced by Streptomyces noursei, S. aureus, and other Streptomyces species. The biologically active components of the complex are nystatin A1, A2, and A3.. nystatin : A heterogeneous mixture of polyene compounds produced by cultures of Streptomyces noursei. It mainly consists of three biologically active components designated nystatin A1, nystatin A2, and nystatin A3. It is used to treat oral and dermal fungal infections.. nystatin A1 : A polyene macrolide antibiotic; part of the nystatin complex produced by several Streptomyces species. It is an antifungal antibiotic used for the treatment of topical fungal infections caused by a broad spectrum of fungal pathogens comprising yeast-like and filamentous species.	3.6	2	0	nystatins
pirarubicin [no description available]	7.49	2	0	anthracycline
bms-626529 [no description available]	2.6	1	0
bms-663068 fostemsavir: an HIV-1 attachment inhibitor; structure in first source	2.6	1	0
nu 7441 8-dibenzothiophen-4-yl-2-morpholin-4-yl-chromen-4-one: structure in first source	2.08	1	0	dibenzothiophenes
at 7519 4-(2,6-dichlorobenzamido)-N-(piperidin-4-yl)-pyrazole-3-carboxamide : A member of the class of pryrazoles that is 4-amino-1H-pyrazole-3-carboxylic acid in which the primary amino group has been acylated by a 2,6-dichlorobenzoyl group and in which the carboxylic acid has been converted into a carboxamide by formal condensation with the primary amino group of 4-aminopiperidine.	2.08	1	0	dichlorobenzene; piperidines; pyrazoles; secondary carboxamide	antineoplastic agent; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
marizomib marizomib: a proteasome inhibitor from a marine bacterium Salinospora; structure in first source	14.64	35	0	beta-lactone; gamma-lactam; organic heterobicyclic compound; organochlorine compound; salinosporamide	antineoplastic agent; proteasome inhibitor
cyt997 [no description available]	2.06	1	0	ureas
er-086526 eribulin: a halichondrin B derivative that suppresses microtubule growth and acts as an antimitotic agent; structure in first source. eribulin : A fully synthetic macrocyclic ketone analogue of marine sponge natural products. Inhibits growth phase of microtubules via tubulin-based antimitotic mechanism, which leads to G2/M cell-cycle block, disruption of mitotic spindles, and, ultimately, apoptotic cell death after prolonged mitotic blockage	2.31	1	0	cyclic ketal; cyclic ketone; macrocycle; polycyclic ether; polyether; primary amino compound	antineoplastic agent; microtubule-destabilising agent
bi 2536 [no description available]	2.77	3	0
inno-406 [no description available]	2.03	1	0	biaryl
mitoquinone mitoquinone: has antineoplastic activity	2.41	1	0
amenamevir ASP2151: a herpesvirus helicase-primase inhibitor, in a guinea pig model of genital herpes; structure in first source	2.6	1	0
vx 765 belnacasan: a NSAID	2.6	1	0	dipeptide
Dihydrotanshinone I dihydrotanshinone I: extracted from Radix Salviae	2.6	1	0	abietane diterpenoid	anticoronaviral agent
nutlin-3a nutlin 3: an MDM2 antagonist; structure in first source	3.47	7	0	stilbenoid
danusertib [no description available]	2.08	1	0	piperazines
alogliptin alogliptin: structure in first source. alogliptin : A piperidine that is 3-methyl-2,4-dioxo-3,4-dihydropyrimidine carrying additional 2-cyanobenzyl and 3-aminopiperidin-1-yl groups at positions 1 and 2 respectively (the R-enantiomer). Used in the form of its benzoate salt for treatment of type 2 diabetes.	2.6	1	0	nitrile; piperidines; primary amino compound; pyrimidines	EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor; hypoglycemic agent
N-[4-(2-tert-butylphenyl)sulfonylphenyl]-2,3,4-trihydroxy-5-[(2-propan-2-ylphenyl)methyl]benzamide [no description available]	2.08	1	0	benzamides
N-[5-[[5-[(4-acetyl-1-piperazinyl)-oxomethyl]-4-methoxy-2-methylphenyl]thio]-2-thiazolyl]-4-[(3,3-dimethylbutan-2-ylamino)methyl]benzamide [no description available]	2.08	1	0	benzamides
episilvestrol episilvestrol: isolated from the fruit and twig of Aglaia silvestris; structure in first source. epi-silvestrol : An organic heterotricyclic compound that is a 5'''-epimer of silvestrol. Isolated from Aglaia silvestris, it exhibits antineoplastic activity.	2.15	1	0	dioxanes; ether; methyl ester; organic heterotricyclic compound	antineoplastic agent; metabolite
abt 869 [no description available]	2.08	1	0	aromatic amine; indazoles; phenylureas	angiogenesis inhibitor; antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
fr 180204 FR 180204: structure in first source	2.6	1	0	pyrazoles; ring assembly
arq 197 [no description available]	2.11	1	0	indoles
tavaborole tavaborole: has antifungal activity; structure in first source. tavaborole : A member of the class of benzoxaboroles that is 1,3-dihydro-1-hydroxy-2,1-benzoxaborole substituted at position 5 by a fluoro group. A topical antifungal agent used for the treatment of onychomycosis (fungal infection of the toenails and fingernails).	3.78	2	0	benzoxaborole; organofluorine compound	antifungal agent; EC 6.1.1.4 (leucine--tRNA ligase) inhibitor; protein synthesis inhibitor
ridaforolimus [no description available]	3.15	1	0	macrolide lactam
dorsomorphin dorsomorphin: an AMPK inhibitor. dorsomorphin : A pyrazolopyrimidine that is pyrazolo[1,5-a]pyrimidine which is substituted at positions 3 and 6 by pyridin-4-yl and p-[2-(piperidin-1-yl)ethoxy]phenyl groups, respectively. It is a potent, selective, reversible, and ATP-competitive inhibitor of AMPK (AMP-activated protein kinase, EC 2.7.11.31) and a selective inhibitor of bone morphogenetic protein (BMP) signaling.	2.08	1	0	aromatic ether; piperidines; pyrazolopyrimidine; pyridines	bone morphogenetic protein receptor antagonist; EC 2.7.11.31 {[hydroxymethylglutaryl-CoA reductase (NADPH)] kinase} inhibitor
ac 261066 [no description available]	2.08	1	0
quisinostat [no description available]	10.12	3	1	indoles
2,5-dimethylcelecoxib 2,5-dimethylcelecoxib: non-COX-2 inhibitory structural analog of celecoxib	7.04	1	0
carfilzomib [no description available]	19.84	229	26	epoxide; morpholines; tetrapeptide	antineoplastic agent; proteasome inhibitor
hcv 796 HCV 796: inhibits HCV RdRp; structure in first source	2.6	1	0
gw9508 GW9508: structure in first source	2.08	1	0	aromatic amine
digeranyl bisphosphonate digeranyl bisphosphonate: structure in first source	2.17	1	0
jnj 26854165 [no description available]	2.08	1	0
resminostat resminostat: a histone deacetylase inhibitor; structure in first source	2.6	1	0
pf 573228 6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one: structure in first source	2.08	1	0	quinolines
nsc-287088 [no description available]	2.07	1	0
gw 2580 5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine: a cFMS kinase inhibitor; structure in first source	2.08	1	0
milnacipran [no description available]	3.23	1	0	acetamides
idelalisib idelalisib: an antineoplastic agent and p110delta inhibitor; structure in first source. idelalisib : A member of the class of quinazolines that is 5-fluoro-3-phenylquinazolin-4-one in which the hydrogen at position 2 is replaced by a (1S)-1-(3H-purin-6-ylamino)propyl group. used for for the treatment of refractory indolent non-Hodgkin's lymphoma and relapsed chronic lymphocytic leukemia.	3.21	5	0	aromatic amine; organofluorine compound; purines; quinazolines; secondary amino compound	antineoplastic agent; apoptosis inducer; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
crizotinib Crizotinib: A piperidine and aminopyridine derivative that acts as an inhibitor of RECEPTOR PROTEIN-TYROSINE KINASES, including ANAPLASTIC LYMPHOMA KINASE (ALK) and HEPATOCYTE GROWTH FACTOR RECEPTOR (HGFR; c-Met). It is used in the treatment of NON-SMALL CELL LUNG CANCER.. crizotinib : A 3-[1-(2,6-dichloro-3-fluorophenyl)ethoxy]-5-[1-(piperidin-4-yl)pyrazol-4-yl]pyridin-2-amine that has R configuration at the chiral centre. The active enantiomer, it acts as a kinase inhibitor and is used for the treatment of patients with locally advanced or metastatic non-small cell lung cancer (NSCLC)	3.06	4	0	3-[1-(2,6-dichloro-3-fluorophenyl)ethoxy]-5-[1-(piperidin-4-yl)pyrazol-4-yl]pyridin-2-amine	antineoplastic agent; biomarker; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
5-(5,6-dimethoxy-1-benzimidazolyl)-3-[(2-methylsulfonylphenyl)methoxy]-2-thiophenecarbonitrile [no description available]	2.08	1	0	benzimidazoles
4-[2-(2-chloro-4-fluoroanilino)-5-methyl-4-pyrimidinyl]-N-[(1S)-1-(3-chlorophenyl)-2-hydroxyethyl]-1H-pyrrole-2-carboxamide Vx-11e: ERK1-2 inhibitor	2.08	1	0	aromatic amide; heteroarene
osi 906 [no description available]	2.08	1	0	cyclobutanes; quinolines
vindesine [no description available]	2.04	1	0
zstk474 ZSTK-474 : A triamino-1,3,5-triazine that is 1,3,5-triazine in which two of the hydrogens have been replaced by morpholin-4-yl groups while the third hydrogen has been replaced by a 2-(difluoromethyl)benzimidazol-1-yl group. It is an inhibitor of phosphatidylinositol 3-kinase.	2.1	1	0	benzimidazoles; morpholines; organofluorine compound; triamino-1,3,5-triazine	antineoplastic agent; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
ly2109761 [no description available]	2.51	2	0
chir-265 [no description available]	2.08	1	0	aromatic ether
motesanib [no description available]	2.08	1	0	pyridinecarboxamide
az-628 AZ-628: a multikinase inhibitor; structure in first source	2.08	1	0	benzamides
zk 756326 2-(2-(4-(3-phenoxybenzyl)piperazin-1-yl)ethoxy)ethanol: a CC chemokine receptor CCR8 agonist; structure in first source	2.6	1	0	aromatic ether
balapiravir balapiravir: a prodrug of R1479; structure in first source	2.6	1	0
trametinib [no description available]	3.06	4	0	acetamides; aromatic amine; cyclopropanes; organofluorine compound; organoiodine compound; pyridopyrimidine; ring assembly	anticoronaviral agent; antineoplastic agent; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor; geroprotector
mln8054 [no description available]	2.07	1	0	benzazepine
pf-562,271 [no description available]	2.08	1	0	indoles
tyropeptin a tyropeptin A: proteasome inhibitors produced by Kitasatospora sp. MK993-dF2; structure in first source	4.13	2	0	dipeptide
deoxyarbutin 4-((tetrahydro-2H-pyran-2-yl)oxy)phenol: has antineoplastic activity; structure in first source	2.6	1	0
abexinostat abexinostat: structure in first source	2.53	2	0	benzofurans
losartan potassium Erythropoietin: Glycoprotein hormone, secreted chiefly by the KIDNEY in the adult and the LIVER in the FETUS, that acts on erythroid stem cells of the BONE MARROW to stimulate proliferation and differentiation.	6.05	11	0
silvestrol silvestrol: isolated from the fruit and twig of Aglaia silvestris. silvestrol : An organic heterotricyclic compound that consists of a 2,3,3a,8b-tetrahydro-H-benzo[b]cyclopenta[d]furan framework substituted by hydroxy groups at positions C-1 and C-8b, a methoxycarbonyl group at C-2, a phenyl group at C-3, a 4-methoxyphenyl group at C-3a, a methoxy group at C-8 and a 1,4-dioxan-2-yloxy group at position C-6 which in turn is substituted by a methoxy group at position 3 and a 1,2-dihydroxyethyl group at position 6. Isolated from Aglaia silvestris, it exhibits antineoplastic activity.	2.53	2	0	dioxanes; ether; methyl ester; organic heterotricyclic compound	antineoplastic agent; metabolite
alpha-Neup5Ac-(2->3)-beta-D-Galp-(1->4)-[alpha-L-Fucp-(1->3)]-D-GlcpNAc Sialyl Lewis X Antigen: A sialylated version of Lewis X antigen expressed on cell surfaces. It is a ligand for SELECTINS.. alpha-Neup5Ac-(2->3)-beta-D-Galp-(1->4)-[alpha-L-Fucp-(1->3)]-D-GlcpNAc : A branched amino tetrasaccharide consisting of a sialyl residue, linked (2->3) to a galactosyl residue that in turn is linked (1->4) to a glucosaminyl residue, which is also carrying a fucosyl residue at the 3-position.	2.41	1	0	amino tetrasaccharide; glucosamine oligosaccharide	epitope
narlaprevir narlaprevir: an antiviral agent that inhibits hepatitis C virus NS3 protease. narlaprevir : An azabicyclohexane that is (1R,5S)-6,6-dimethyl-3-azabicyclo[3.1.0]hexane substituted by [(3S)-1-(cyclopropylamino)-1,2-dioxoheptan-3-yl]aminoacyl and N-({1-[(tert-butylsulfonyl)methyl]cyclohexyl}carbamoyl)-3-methyl-L-valyl groups at positions 2S and 3, respectively. It is a hepatitis C virus (HCV) NS3/4A serine protease inhibitor (Ki = 6 nM) that is used for the treatment of chronic hepatitis C.	2.6	1	0	azabicyclohexane; cyclopropanes; pyrrolidinecarboxamide; secondary carboxamide; sulfone; tertiary carboxamide; ureas	anticoronaviral agent; antiviral drug; EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor; hepatitis C protease inhibitor
n-acetylmannosamine N-acetylmannosamine: RN given refers to cpd without isomeric designation. N-acetylmannosamine : Any mannosamine carrying an N-acetyl substituent	2.25	1	0
empagliflozin [no description available]	4.8	1	1	aromatic ether; C-glycosyl compound; monochlorobenzenes; tetrahydrofuryl ether	hypoglycemic agent; sodium-glucose transport protein subtype 2 inhibitor
teneligliptin [no description available]	2.6	1	0	amino acid amide
dextrothyroxine [no description available]	3.01	2	0
veliparib [no description available]	2.58	2	0	benzimidazoles	EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
ku-0060648 [no description available]	2.08	1	0	dibenzothiophenes
indocyanine green Indocyanine Green: A tricarbocyanine dye that is used diagnostically in liver function tests and to determine blood volume and cardiac output.	7.91	3	0	1,1-diunsubstituted alkanesulfonate; benzoindole; cyanine dye
scopolamine hydrobromide [no description available]	3.58	2	0
dactolisib dactolisib: antineoplastic agent that inhibits both phosphatidylinositol 3-kinase and mTOR. dactolisib : An imidazoquinoline that is 3-methyl-2-oxo-2,3-dihydro-1H-imidazo[4,5-c]quinoline substituted at position 1 by a 4-(1-cyanoisopropyl)phenyl group and at position 8 by a quinolin-3-yl group. A dual PI3K/mTOR inhibitor used in cancer treatment.	3.32	6	0	imidazoquinoline; nitrile; quinolines; ring assembly; ureas	antineoplastic agent; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; mTOR inhibitor
th 302 TH 302: an hypoxia-activated prodrug of bromo-isophosphoramide mustard; an antineoplastic agent	2.08	1	0
palomid 529 [no description available]	2.08	1	0
pf 03491390 [no description available]	2.54	2	0
bsc2118 BSc2118: a proteasome inhibitor	2.11	1	0
inositol 3,4,5-trisphosphate [no description available]	2.05	1	0
arabinofuranosyluracil Arabinofuranosyluracil: A pyrimidine nucleoside formed in the body by the deamination of CYTARABINE.	2.44	2	0
6-o-angeloylprenolin 6-O-angeloylprenolin: from Centipeda minima was found to show inhibitory activity on farnesyl protein transferase (FPTase); structure in first source	2.06	1	0
alloin [no description available]	2.6	1	0	anthracenes; C-glycosyl compound; cyclic ketone; phenols	laxative; metabolite
acid phosphatase Acid Phosphatase: An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.2.	2.03	1	0
mefloquine Mefloquine: A phospholipid-interacting antimalarial drug (ANTIMALARIALS). It is very effective against PLASMODIUM FALCIPARUM with very few side effects.. mefloquine : A racemate composed of (+)-(11R,2'S)- and (-)-(11S,2'R)-enantiomers of mefloquine. An antimalarial agent which acts as a blood schizonticide; its mechanism of action is unknown.	2.6	1	0
rabeprazole sodium [no description available]	2.08	1	0	organic sodium salt
tosedostat [no description available]	2.08	1	0	carboxylic ester; hydroxamic acid; secondary carboxamide
nad NAD(1-) : An anionic form of nicotinamide adenine dinucleotide arising from deprotonation of the two OH groups of the diphosphate moiety.	7.88	3	0	organophosphate oxoanion	cofactor; human metabolite; hydrogen acceptor; Saccharomyces cerevisiae metabolite
rrx-001 RRx-001: has antineoplastic activity; structure in first source	3.71	2	0
mdv 3100 [no description available]	2.9	3	0	(trifluoromethyl)benzenes; benzamides; imidazolidinone; monofluorobenzenes; nitrile; thiocarbonyl compound	androgen antagonist; antineoplastic agent
ku 60019 [no description available]	2.08	1	0
gsk 461364 GSK 461364: an antineoplastic agent that inhibits polo-like kinase 1	2.08	1	0	(trifluoromethyl)benzenes
n-(3,4-difluoro-2-(2-fluoro-4-iodophenylamino)-6-methoxyphenyl)-1-(2,3-dihydroxypropyl)cyclopropane-1-sulfonamide N-(3,4-difluoro-2-(2-fluoro-4-iodophenylamino)-6-methoxyphenyl)-1-(2,3-dihydroxypropyl)cyclopropane-1-sulfonamide: a MEK inhibitor; structure in first source	2.08	1	0
nvp-tae684 [no description available]	2.08	1	0	piperidines
amodiaquine hydrochloride [no description available]	2.05	1	0
cytochrome c-t Cytochromes c: Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.	5.15	17	0
bms-650032 asunaprevir: an NS3 protease inhibitor against hepatitis C virus	2.6	1	0	oligopeptide
gw 4869 GW 4869: inhibits neutral sphingomyelinase; structure in first source	2.17	1	0
4-methyl-3-(2-(2-morpholinoethylamino)quinazolin-6-yl)-n-(3-(trifluoromethyl)phenyl)benzamide 4-methyl-3-(2-(2-morpholinoethylamino)quinazolin-6-yl)-N-(3-(trifluoromethyl)phenyl)benzamide: structure in first source	2.08	1	0
bisaramil [no description available]	2.04	1	0
gsk 269962a [no description available]	2.08	1	0
3,4-dimethoxy-n-((2,2-dimethyl-2h-chromen-6-yl)methyl)-n-phenylbenzenesulfonamide 3,4-dimethoxy-N-((2,2-dimethyl-2H-chromen-6-yl)methyl)-N-phenylbenzenesulfonamide: has antineoplastic activity; structure in first source	2.47	2	0
rg 7128 2'-fluoro-2'-methyl-3',5'-diisobutyryldeoxycytidine: inhibits HCV polymerase; structure in first source	2.6	1	0
ceruletide Ceruletide: A specific decapeptide obtained from the skin of Hila caerulea, an Australian amphibian. Caerulein is similar in action and composition to CHOLECYSTOKININ. It stimulates gastric, biliary, and pancreatic secretion; and certain smooth muscle. It is used in paralytic ileus and as diagnostic aid in pancreatic malfunction.. ceruletide : A decapeptide comprising 5-oxoprolyl, glutamyl, aspartyl, O-sulfotyrosyl, threonyl, glycyl, tryptopyl, methionyl, aspartyl and phenylalaninamide residues in sequence. Found in the skins of certain Australian amphibians, it is an analogue of the gastrointestinal peptide hormone cholecystokinin and stimulates gastric, biliary, and pancreatic secretion. It is used in cases of paralysis of the intestine (paralytic ileus) and as a diagnostic aid in pancreatic malfunction.	2.5	2	0	oligopeptide	diagnostic agent; gastrointestinal drug
bivalirudin bivalirudin: designed to bind to the alpha-thrombin catalytic site and anion-binding exosite for fibrin(ogen) recognition. bivalirudin : A synthetic peptide of 20 amino acids, comprising D-Phe, Pro, Arg, Pro, Gly, Gly, Gly, Gly, Asn, Gly, Asp, Phe, Glu, Glu, Ile, Pro, Glu, Glu, Tyr, and Leu in sequence. A congener of hirudin (a naturally occurring drug found in the saliva of the medicinal leech), it a specific and reversible inhibitor of thrombin, and is used as an anticoagulant.	3.61	2	0	polypeptide	anticoagulant; EC 3.4.21.5 (thrombin) inhibitor
somatostatin [no description available]	2.08	1	0	heterodetic cyclic peptide; peptide hormone
teicoplanin teicoplanin A2-1 : A teicoplanin A2 that has (4Z)-dec-4-enoyl as the variable N-acyl group.	2.04	1	0
tannins gallotannin : A class of hydrolysable tannins obtained by condensation of the carboxy group of gallic acid (and its polymeric derivatives) with the hydroxy groups of a monosaccharide (most commonly glucose).	2.05	1	0	tannin
enfuvirtide Enfuvirtide: A synthetic 36-amino acid peptide that corresponds to the heptad repeat sequence of HIV-1 gp41. It blocks HIV cell fusion and viral entry and is used with other anti-retrovirals for combination therapy of HIV INFECTIONS and AIDS.. enfuvirtide : A synthetic 36-amino acid peptide consisting of N-acetyltyrosyl, threonyl, seryl, leucyl, isoleucyl, histidyl, seryl, leucyl, isoleucyl, alpha-glutamyl, alpha-glutamyl, seryl, glutaminyl, asparaginyl, glutaminyl, glutaminyl, alpha-glutamyl, lysyl, asparaginyl, alpha-glutamyl, alpha-glutamyl, alpha-glutamyl, leucyl, leucyl, alpha-glutamyl, leucyl, alpha-aspartyl, lysyl, tryptophyl, alanyl, seryl, leucyl, tryptophyl, asparaginyl, tryptophyl, and phenylalaninamide residues joined in sequence. An HIV fusion inhibitor, it was the first of a novel class of antiretroviral drugs used in combination therapy for the treatment of HIV-1 infection. It interferes with entry of HIV into cells by binding to the gp41 sub-unit of the viral envelope glycoprotein, so inhibiting fusion of viral and cellular membranes.	3.23	1	0
ganirelix [no description available]	3.23	1	0	polypeptide
cs1 peptide CS1 peptide: used as a diagnostic probe for activity of the type III connecting segment of fibronectin; amino acid sequence given in first source	2.08	1	0
abarelix abarelix: RN & structure in first source. abarelix : A polypeptide compound composed of ten natural and non-natural amino acid resiudes in a linear sequence.	3.12	1	0	polypeptide	antineoplastic agent; hormone antagonist
humanin humanin: suppresses neuronal cell death induced by the Swedish mutant of amyloid precursor protein; suppresses neuronal cell death induced by three different types of FAD genes and amyloid beta; amino acid sequence in first source	7.5	2	0
teriparatide [no description available]	3.23	1	0	polypeptide
salmon calcitonin [no description available]	3.23	1	0	heterodetic cyclic peptide; peptide hormone; polypeptide	bone density conservation agent; metabolite
tannins Tannins: Polyphenolic compounds with molecular weights of around 500-3000 daltons and containing enough hydroxyl groups (1-2 per 100 MW) for effective cross linking of other compounds (ASTRINGENTS). The two main types are HYDROLYZABLE TANNINS and CONDENSED TANNINS. Historically, the term has applied to many compounds and plant extracts able to render skin COLLAGEN impervious to degradation. The word tannin derives from the Celtic word for OAK TREE which was used for leather processing.	2.21	1	0
oligonucleotides [no description available]	5.14	5	0
ly-146032 [no description available]	3.87	3	0	heterodetic cyclic peptide; lipopeptide antibiotic; lipopeptide; macrocycle; macrolide	antibacterial drug; bacterial metabolite; calcium-dependent antibiotics
dalbavancin [no description available]	2.04	1	0	carbohydrate acid derivative; glycopeptide; monosaccharide derivative; semisynthetic derivative	antibacterial drug; antimicrobial agent
ap 1903 reagent AP 1903 reagent: a dimerizer drug	2.1	1	0
acetyl-2-naphthylalanyl-3-chlorophenylalanyl-1-oxohexadecyl-seryl-4-aminophenylalanyl(hydroorotyl)-4-aminophenylalanyl(carbamoyl)-leucyl-ilys-prolyl-alaninamide acetyl-2-naphthylalanyl-3-chlorophenylalanyl-1-oxohexadecyl-seryl-4-aminophenylalanyl(hydroorotyl)-4-aminophenylalanyl(carbamoyl)-leucyl-ILys-prolyl-alaninamide: FE-200486 is the acetate salt	3.23	1	0	polypeptide
oritavancin oritavancin : A semisynthetic glycopeptide used (as its bisphosphate salt) for the treatment of acute bacterial skin and skin structure infections caused or suspected to be caused by susceptible isolates of designated Gram-positive microorganisms including MRSA.	2.6	1	0	disaccharide derivative; glycopeptide; semisynthetic derivative	antibacterial drug; antimicrobial agent
exenatide [no description available]	3.23	1	0
ctce-9908 CTCE-9908: antineoplastic; a small peptide CXCR4 antagonist	3.23	1	0
pr 39 PR 39: antibacterial peptide from pig intestine; MW 4.719 kDa; contains 39 amino acid residues; has high activity against E coli & Bacillus megaterium; amino acid sequence given in first source. PR-39 : A 39 amino acid porcine cathelicidin that is rich in proline and arginine residues. It plays a pivotal role in the innate immune defence of the pig against infections and exhibits antimicrobial and immunomodulatory activities.	2.01	1	0
warfarin sodium warfarin sodium : A racemate comprising equal amounts of (R)- and (S)-warfarin sodium. Extensively used as both an anticoagulant drug and as a pesticide against rats and mice.	2.08	1	0
cellulose DEAE-Cellulose: Cellulose derivative used in chromatography, as ion-exchange material, and for various industrial applications.	5.06	2	1	glycoside
endothelin-1 Endothelin-1: A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)	9.3	5	0
a-83-01 A-83-01: an ALK-5 inhibitor; structure in first source	2.08	1	0
3-[(1-methyl-3-indolyl)methylidene]-1H-pyrrolo[3,2-b]pyridin-2-one [no description available]	2.08	1	0	indoles
vx-770 ivacaftor: a CFTR potentiator; structure in first source. ivacaftor : An aromatic amide obtained by formal condensation of the carboxy group of 4-oxo-1,4-dihydroquinoline-3-carboxylic acid with the amino group of 5-amino-2,4-di-tert-butylphenol. Used for the treatment of cystic fibrosis.	2.08	1	0	aromatic amide; monocarboxylic acid amide; phenols; quinolone	CFTR potentiator; orphan drug
buparlisib NVP-BKM120: a pan class I PI3 kinase inhibitor with antineoplastic activity; structure in first source	2.52	2	0	aminopyridine; aminopyrimidine; morpholines; organofluorine compound	antineoplastic agent; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
azd 1480 [no description available]	2.52	2	0
pevonedistat pevonedistat: a potent and selective inhibitor of NAE (NEDD8-activating enzyme). pevonedistat : A pyrrolopyrimidine that is 7H-pyrrolo[2,3-d]pyrimidine which is substituted by a (1S)-2,3-dihydro-1H-inden-1-ylnitrilo group at position 4 and by a (1S,3S,4S)-3-hydroxy-4-[(sulfamoyloxy)methyl]cyclopentyl group at position 7. It is a potent and selective NEDD8-activating enzyme inhibitor with an IC50 of 4.7 nM, and currently under clinical investigation for the treatment of acute myeloid leukemia (AML) and myelodysplastic syndromes.	4.86	9	0	cyclopentanols; indanes; pyrrolopyrimidine; secondary amino compound; sulfamidate	antineoplastic agent; apoptosis inducer
fedratinib fedratinib: a selective small-molecule inhibitor of JAK2	2.08	1	0	sulfonamide
gsk690693 [no description available]	2.08	1	0	1,2,5-oxadiazole; acetylenic compound; aromatic amine; aromatic ether; imidazopyridine; piperidines; primary amino compound; tertiary alcohol	antineoplastic agent; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor
cnf 2024 [no description available]	2.08	1	0	2-aminopurines; aromatic ether; organochlorine compound; pyridines	antineoplastic agent; Hsp90 inhibitor
ku 0063794 Ku 0063794: an mTOR inhibitor; structure in first source	2.08	1	0	benzyl alcohols; monomethoxybenzene; morpholines; pyridopyrimidine; tertiary amino compound	antineoplastic agent; mTOR inhibitor
uk 453,061 UK 453,061: a reverse transcriptase inhibitor/anti-HIV agent; structure in first source	2.6	1	0	aromatic ether
14-methyl-20-oxa-5,7,14,26-tetraazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8(27),9,11,16,21,23-decaene 14-methyl-20-oxa-5,7,14,26-tetraazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8(27),9,11,16,21,23-decaene: has antineoplastic activity; also inhibits Fms-like tyrosine kinase-3; structure in first source	2.08	1	0
azd 7545 AZD 7545: an anilide tertiary carbinol; a pyruvate dehydrogenase kinase 2 inhibitor. AZD7545 : A sulfone that is benzene substituted by [4-(dimethylcarbamoyl)phenyl]sulfonyl, chloro and [(2R)-3,3,3-trifluoro-2-hydroxy-2-methylpropanoyl]amino groups at positions 1, 3 and 4, respectively. It is a potent and non-ATP-competitive inhibitor of pyruvate dehydrogenase kinase 2 (PDHK2) with IC50 of 6.4 nM and exhibits glucose-lowering activity. Also inhibits PDHK1 at higher levels (IC50 = 36.8 nM).	2.08	1	0	benzamides; monochlorobenzenes; organofluorine compound; secondary carboxamide; sulfone; tertiary alcohol; tertiary carboxamide	EC 2.7.11.2 - [pyruvate dehydrogenase (acetyl-transferring)] kinase inhibitor; hypoglycemic agent
nutlin-3b [no description available]	2.08	1	0	Nutlin; piperazinone	anticoronaviral agent
pravastatin sodium pravastatin sodium : An organic sodium salt that is the sodium salt of pravastatin. A reversible inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA), it is used for lowering cholesterol and preventing cardiovascular disease. It is one of the lower potency statins, but has the advantage of fewer side effects compared with lovastatin and simvastatin.	2.08	1	0	organic sodium salt; statin (semi-synthetic)	anticholesteremic drug
alendronate sodium [no description available]	2.08	1	0
sphingosine kinase [no description available]	2.79	3	0
N-(2-aminophenyl)-2-pyrazinecarboxamide [no description available]	2.6	1	0	aromatic amide
ubiquinone Ubiquinone: A lipid-soluble benzoquinone which is involved in ELECTRON TRANSPORT in mitochondrial preparations. The compound occurs in the majority of aerobic organisms, from bacteria to higher plants and animals.	2.82	2	0
pf 04217903 [no description available]	2.08	1	0	quinolines
kd 5170 KD 5170: a histone deacetylase inhibitor; structure in first source	2.04	1	0
gdc 0941 pictrelisib : A sulfonamide composed of indazole, morpholine, and methylsulfonyl-substituted piperazine rings bound to a thienopyrimidine ring.	2.53	2	0	indazoles; morpholines; piperazines; sulfonamide; thienopyrimidine	EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
sm 164 SM 164: a bivalent Smac mimetic with antineoplastic activity; structure in first source	2.08	1	0	benzenes; organic heterobicyclic compound; secondary carboxamide; triazoles	antineoplastic agent; apoptosis inducer; radiosensitizing agent
sl 80.0750 [no description available]	2.08	1	0
igk IgK: abnormal immunoglobin in leprous-Rubino negative sera; partly related to Fc fragment of IgA & to FAB fragments; possesses Kappa but not lambda light polypeptide chains	2.17	1	0
calpain Calpain: Cysteine proteinase found in many tissues. Hydrolyzes a variety of endogenous proteins including NEUROPEPTIDES; CYTOSKELETAL PROTEINS; proteins from SMOOTH MUSCLE; CARDIAC MUSCLE; liver; platelets; and erythrocytes. Two subclasses having high and low calcium sensitivity are known. Removes Z-discs and M-lines from myofibrils. Activates phosphorylase kinase and cyclic nucleotide-independent protein kinase. This enzyme was formerly listed as EC 3.4.22.4.	4.23	6	0
chitosan [no description available]	7.53	2	0
ph 797804 PH 797804: an NSAID; structure in first source. PH 797804 : A member of the class of benzamides obtained by formal condensation of the carboxy group of 3-{3-bromo-4-[(2,4-difluorobenzyl)oxy]-6-methyl-2-oxopyridin-1-yl}-4-methylbenzoic acid with the amino group of methylamine.	2.08	1	0	aromatic ether; benzamides; organobromine compound; organofluorine compound; pyridone	anti-inflammatory agent; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
pha 408 PHA 408: an IKK-2 antagonist; structure in first source	2.08	1	0
kw-2478 [no description available]	8.53	1	1
gsk 1016790a GSK1016790A : A tertiary carboxamide that is piperazine in which one of the amino groups has undergone condensation with the carboxy group of N-[(2,4-dichlorophenyl)sulfonyl]-L-serine, while the other has undergone condensation with the carboxy group of N-(1-benzothiophen-2-ylcarbonyl)-L-leucine. It is a cell-permeable, potent and selective agonist of the TRPV4 (transient receptor potential vanilloid 4) channel.	2.08	1	0	1-benzothiophenes; aromatic primary alcohol; dichlorobenzene; N-acylpiperazine; sulfonamide; tertiary carboxamide	TRPV4 agonist
pr-957 [no description available]	2.54	2	0
p276-00 P276-00: antineoplastic, cyclin-dependent kinase inhibitor; structure in first source	2.46	2	0
tegobuvir tegobuvir: a non-structural protein 5B polymerase inhibitor	2.6	1	0
eliglustat eliglustat: a potent inhibitor of glucosylceramide synthase. eliglustat : A carboxamide obtained by formal condensation of the carboxy group of octanoic acid with the primary amino group of (1R,2R)-2-amino-1-(2,3-dihydro-1,4-benzodioxin-6-yl)-3-(pyrrolidin-1-yl)propan-1-ol. A ceramide glucosyltransferase inhibitor used (as its tartrate salt) for treatment of Gaucher's disease.	2.21	1	0	benzodioxine; carboxamide; N-alkylpyrrolidine; secondary alcohol	EC 2.4.1.80 (ceramide glucosyltransferase) inhibitor
pf-429242 PF-429242: a subtilisin kexin isozyme-1/site-1 protease inhibitor	2.6	1	0
mesna Mesna: A sulfhydryl compound used to prevent urothelial toxicity by inactivating metabolites from ANTINEOPLASTIC AGENTS, such as IFOSFAMIDE or CYCLOPHOSPHAMIDE.	3.87	3	0	organosulfonic acid
sodium oxybate Sodium Oxybate: The sodium salt of 4-hydroxybutyric acid. It is used for both induction and maintenance of ANESTHESIA.	3.81	2	0
cerivastatin sodium cerivastatin sodium : The sodium salt of cerivastatin. Formerly used to lower cholesterol and prevent cardiovascular disease, it was withdrawn from the market worldwide in 2001 following reports of a severe form of muscle toxicity.	2.05	1	0	organic sodium salt; statin (synthetic)
clavulanate potassium potassium clavulanate : A potassium salt having clavulanate as the counterion. It acts as a suicide inhibitor of bacterial beta-lactamase enzymes and has only weak anitbiotic activity when administered alone. However it can be used in combination with amoxicillin trihydrate (under the trade name Augmentin) for treatment of a variety of bacterial infections, where it prevents antibiotic inactivation by microbial lactamases.	2.08	1	0	potassium salt	antibacterial drug; antimicrobial agent; EC 3.5.2.6 (beta-lactamase) inhibitor
sodium lactate Sodium Lactate: The sodium salt of racemic or inactive lactic acid. It is a hygroscopic agent used intravenously as a systemic and urinary alkalizer.. sodium lactate : An organic sodium salt having lactate as the counterion.	3.23	1	0	lactate salt; organic sodium salt	food acidity regulator; food preservative
piperacillin sodium [no description available]	2.08	1	0	organic sodium salt
monensin [no description available]	2.05	1	0
sodium iothalamate [no description available]	3.23	1	0
oxacillin sodium [no description available]	2.47	2	0	organic sodium salt
raltegravir potassium Raltegravir Potassium: A pyrrolidinone derivative and HIV INTEGRASE INHIBITOR that is used in combination with other ANTI-HIV AGENTS for the treatment of HIV INFECTION.	2.13	1	0
sodium diatrizoate histopaque: used for separating mononuclear & other cells. sodium amidotrizoate : The sodium salt of a benzoic acid having iodo substituents at the 2-, 4- and 6-positions and acetamido substituents at the 3- and 5-positions. It is used, often as a mixture with the meglumine salt, as an X-ray contrast medium in gastrointestinal studies, angiography, and urography.	2.05	1	0	organic sodium salt; organoiodine compound	radioopaque medium
cefazolin sodium cefazolin sodium : A cephalosporin organic sodium salt having [(5-methyl-1,3,4-thiadiazol-2-yl)sulfanyl]methyl and (1H-tetrazol-1-ylacetyl)amino side-groups.	2.08	1	0	organic sodium salt
ro13-9904 Ceftriaxone: A broad-spectrum cephalosporin antibiotic and cefotaxime derivative with a very long half-life and high penetrability to meninges, eyes and inner ears.. ceftriaxone : A third-generation cephalosporin compound having 2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetylamino and [(2-methyl-5,6-dioxo-1,2,5,6-tetrahydro-1,2,4-triazin-3-yl)sulfanyl]methyl side-groups.	2.51	2	0
azlocillin sodium [no description available]	2.08	1	0	organic sodium salt
chiniofon Hydroxyquinolines: The 8-hydroxy derivatives inhibit various enzymes and their halogenated derivatives, though neurotoxic, are used as topical anti-infective agents, among other uses.	3.56	2	0
arginine Teniposide: A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent cells from entering into the mitotic phase of the cell cycle, and lead to cell death. Teniposide acts primarily in the G2 and S phases of the cycle.. teniposide : A furonaphthodioxole that is a synthetic derivative of podophyllotoxin with anti-tumour activity; causes single- and double-stranded breaks in DNA and DNA-protein cross-links and prevents repair by topoisomerase II binding.	2.54	2	0
syringolin a syringolin A: a cyclic dipeptide composed of the two non-proteinogenic amino acids. syringolin A : A syrbactin that has a (3E,9E)-2,7-dioxo-1,6-diazacyclododeca-3,9-diene skeleton that is substituted by an isopropyl group at position 5 and by a [(2S)-2-({[(1S)-1-carboxy-2-methylpropyl]carbamoyl}amino)-3-methylbutanoyl]nitrilo group at the 8-pro-S position. It is produced by the pathogenic bacterium Pseudomonas syringae pv. syringae.	7.78	3	0	dipeptide
olaparib [no description available]	3.1	4	0	cyclopropanes; monofluorobenzenes; N-acylpiperazine; phthalazines	antineoplastic agent; apoptosis inducer; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
thiostrepton Thiostrepton: One of the CYCLIC PEPTIDES from Streptomyces that is active against gram-positive bacteria. In veterinary medicine, it has been used in mastitis caused by gram-negative organisms and in dermatologic disorders.. thiostrepton : A heterodetic cyclic peptide, in which the cyclisation step involves a formal lactonisation between the carboxy group of a quinaldic acid-based residue and a secondary alcohol. An antibiotic that inhibits bacterial protein synthesis. Also acts as an antitumor agent.	3.45	7	0
srt1720 [no description available]	2.48	2	0
plx 4720 PLX 4720: a B-Raf(V600E) kinase inhibitor; structure in first source	2.08	1	0	aromatic ketone; difluorobenzene; organochlorine compound; pyrrolopyridine; sulfonamide	antineoplastic agent; B-Raf inhibitor
cx 4945 [no description available]	3.05	4	0
pci 34051 PCI 34051: an HDAC8 inhibitor	2.6	1	0	indolecarboxamide
cudc 101 7-(4-(3-ethynylphenylamino)-7-methoxyquinazolin-6-yloxy)-N-hydroxyheptanamide: a histone deacetylase inhibitor; structure in first source	2.58	2	0
mln 8237 MLN 8237: an aurora kinase A inhibitor	4.16	3	1	benzazepine
snx 2112 SNX 2112: an orally available small molecule Hsp90 inhibitor; structure in first source	2.08	1	0
lde225 sonidegib: specific Smoothened/Smo antagonist. sonidegib : A member of the classo of biphenyls that is the amide obtained by formal condensation of the carboxy group of 2-methyl-4'-(trifluoromethoxy)[1,1'-biphenyl]-3-carboxylic acid with the amino group of 6-(2,6-dimethylmorpholin-4-yl)pyridin-3-amine. Used (as its phosphate salt) for treatment of locally advanced basal cell carcinoma.	2.78	3	0	aminopyridine; aromatic ether; benzamides; biphenyls; morpholines; organofluorine compound; tertiary amino compound	antineoplastic agent; Hedgehog signaling pathway inhibitor; SMO receptor antagonist
gdc 0449 HhAntag691: inhibits the hedgehog pathway and ABC transporters; has antineoplastic activity	2.08	1	0	benzamides; monochlorobenzenes; pyridines; sulfone	antineoplastic agent; Hedgehog signaling pathway inhibitor; SMO receptor antagonist; teratogenic agent
sgx 523 [no description available]	2.08	1	0	aryl sulfide; biaryl; pyrazoles; quinolines; triazolopyridazine	c-Met tyrosine kinase inhibitor; nephrotoxic agent
bms 777607 N-(4-(2-amino-3-chloropyridin-4-yloxy)-3-fluorophenyl)-4-ethoxy-1-(4-fluorophenyl)-2-oxo-1,2-dihydropyridine-3-carboxamide: a Met kinase inhibitor; structure in first source	2.08	1	0	aromatic amide
sgi 1776 SGI 1776: a Pim kinase inhibitor; structure in first source	2.53	2	0	imidazoles
lomibuvir lomibuvir: an antiviral agent with polymerase NS5 inhibitory activity	2.6	1	0	thiophenecarboxylic acid
delanzomib [no description available]	7.16	20	0	C-terminal boronic acid peptide; phenylpyridine; secondary alcohol; threonine derivative	antineoplastic agent; apoptosis inducer; proteasome inhibitor
pci 32765 ibrutinib: a Btk protein inhibitor. ibrutinib : A member of the class of acrylamides that is (3R)-3-[4-amino-3-(4-phenoxyphenyl)pyrazolo[3,4-d]pyrimidin-1-yl]piperidine in which the piperidine nitrogen is replaced by an acryloyl group. A selective and covalent inhibitor of the enzyme Bruton's tyrosine kinase, it is used for treatment of B-cell malignancies.	12.68	33	4	acrylamides; aromatic amine; aromatic ether; N-acylpiperidine; pyrazolopyrimidine; tertiary carboxamide	antineoplastic agent; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
ponatinib [no description available]	7.49	2	0	(trifluoromethyl)benzenes; acetylenic compound; benzamides; imidazopyridazine; N-methylpiperazine	antineoplastic agent; tyrosine kinase inhibitor
pitavastatin(1-) pitavastatin(1-) : A hydroxy monocarboxylic acid anion that is the conjugate base of pitavastatin, obtained by deprotonation of the carboxy group.	2.6	1	0	hydroxy monocarboxylic acid anion
amg 900 N-(4-((3-(2-amino-4-pyrimidinyl)-2-pyridinyl)oxy)phenyl)-4-(4-methyl-2-thienyl)-1-phthalazinamine: a pan-aurora kinase inhibitor; structure in first source	2.08	1	0
mk-1775 adavosertib: a Wee1 kinase inhibitor; structure in first source	4.38	5	0	piperazines
bag956 BAG956: an imidazo[4,5-c]quinoline; dual PI3K/PDK-1 inhibitor, used in antileukemic therapies	2.08	1	0
quizartinib [no description available]	3.57	2	0	benzoimidazothiazole; isoxazoles; morpholines; phenylureas	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; necroptosis inhibitor
GRL-0617 GRL-0617 : A benzamide resulting from the formal condensation of the carboxy group of 5-amino-2-methylbenzoic acid with the amino group of (1R)-1-(naphthalen-1-yl)ethan-1-amine. It is a potent noncovalent inhibitor (IC50 = 600 nM) of severe acute respiratory syndrome-coronavirus papain-like protease (SARS-CoV PLpro).	2.6	1	0	benzamides; naphthalenes; secondary carboxamide; substituted aniline	anticoronaviral agent; protease inhibitor
N-[4-[3-[[[7-(hydroxyamino)-7-oxoheptyl]amino]-oxomethyl]-5-isoxazolyl]phenyl]carbamic acid tert-butyl ester CAY10603: a HDAC6 inhibitor	2.58	2	0	carbamate ester
niraparib niraparib: structure in first source. niraparib : A 2-[4-(piperidin-3-yl)phenyl]-2H-indazole-7-carboxamide that has S-configuration. It is a potent inhibitor of PARP1 and PARP2 (IC50 of 3.8 and 2.1 nM, respectively) and approved as a first-line maintenance treatment for women with advanced ovarian cancer after responding to platinum-based chemotherapy.	5.3	2	1	2-[4-(piperidin-3-yl)phenyl]-2H-indazole-7-carboxamide	antineoplastic agent; apoptosis inducer; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor; radiosensitizing agent
tak 733 [no description available]	2.08	1	0
mk 2206 MK 2206: a protein kinase inhibitor and antineoplastic agent	2.08	1	0	organic heterotricyclic compound	EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
navitoclax [no description available]	4.48	6	0	aryl sulfide; monochlorobenzenes; morpholines; N-sulfonylcarboxamide; organofluorine compound; piperazines; secondary amino compound; sulfone; tertiary amino compound	antineoplastic agent; apoptosis inducer; B-cell lymphoma 2 inhibitor
sns 314 SNS 314: an aurora kinase inhibitor; structure in first source	2.08	1	0	ureas
jzl 184 JZL 184: inhibits monoacylglycerol lipase; structure in first source	2.58	2	0	benzodioxoles
gsk 650394 [no description available]	2.6	1	0	phenylpyridine
belactosin a belactosin A: isolated from Streptomyces; structure in first source	3	4	0
4,4-difluoro-4-bora-3a,4a-diaza-s-indacene [no description available]	3.9	3	0	BODIPY compound
doxo-emch DOXO-EMCH: albumin-binding prodrug of doxorubicin	2.07	1	0
n-(cyanomethyl)-4-(2-((4-(4-morpholinyl)phenyl)amino)-4-pyrimidinyl)benzamide N-(cyanomethyl)-4-(2-((4-(4-morpholinyl)phenyl)amino)-4-pyrimidinyl)benzamide: a Janus kinase 1 and Janus kinase 2 inhibitor; structure in first source. momelotinib : A benzamide obtained by formal condensation of the carboxy group of 4-{2-[4-(morpholin-4-yl)anilino]pyrimidin-4-yl}benzoic acid with the primary amino group of aminoacetonitrile. It is an ATP-competitive JAK1/JAK2 inhibitor with IC50 of 11 nM and 18 nM, respectively. Used for the treatment of patients with intermediate- or high-risk myelofibrosis.	2.48	2	0	aminopyrimidine; benzamides; morpholines; nitrile; secondary amino compound; tertiary amino compound	anti-anaemic agent; antineoplastic agent; apoptosis inducer; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
dcc-2036 rebastinib: an inhibitor of Tie2 tyrosine kinase receptor and antineoplastic agent	2.08	1	0	organofluorine compound; phenylureas; pyrazoles; pyridinecarboxamide; quinolines	tyrosine kinase inhibitor
oprozomib ONX 0912: antineoplastic; an orally active proteasome inhibitor; structure in first source	8.47	21	1
cetrorelix cetrorelix: LHRH antagonist. cetrorelix : A synthetic ten-membered oligopeptide comprising N-acetyl-3-(naphthalen-2-yl)-D-alanyl, 4-chloro-D-phenylalanyl, 3-(pyridin-3-yl)-D-alanyl, L-seryl, L-tyrosyl, N(5)-carbamoyl-D-ornithyl, L-leucyl, L-arginyl, L-prolyl, and D-alaninamide residues coupled in sequence. A gonadotrophin-releasing hormone (GnRH) antagonist, it is used for treatment of infertility and of hormone-sensitive cancers of the prostate and breast.	3.58	2	0	oligopeptide	antineoplastic agent; GnRH antagonist
az 960 [no description available]	2.6	1	0
cabozantinib cabozantinib: a multikinase inhibitor. cabozantinib : A dicarboxylic acid diamide that is N-phenyl-N'-(4-fluorophenyl)cyclopropane-1,1-dicarboxamide in which the hydrogen at position 4 on the phenyl ring is substituted by a (6,7-dimethoxyquinolin-4-yl)oxy group. A multi-tyrosine kinase inhibitor, used (as its malate salt) for the treatment of progressive, metastatic, medullary thyroid cancer.	4.39	3	0	aromatic ether; dicarboxylic acid diamide; organofluorine compound; quinolines	antineoplastic agent; tyrosine kinase inhibitor
golgicide a golgicide A: inhibits the cis-golgi ArfGEF GBF1; structure in first source. golgicide A : A diastereoisomeric mixture comprising racemic cis- and racemic trans-goglioside A in a 10:1 ratio. It is a potent and rapidly reversible GBF1 (Golgi-specific brefeldin A-resistance guanine nucleotide exchange factor 1) inhibitor. The (3aS,4R,9bR) isomer is the most active (see Bioorg. Med. Chem. Lett., 2012, 22, 5177-5181).	2.6	1	0	diastereoisomeric mixture	cis-Golgi ArfGEF GBF inhibitor
N-(2,6-difluorophenyl)-5-[3-[2-[5-ethyl-2-methoxy-4-[4-(4-methylsulfonyl-1-piperazinyl)-1-piperidinyl]anilino]-4-pyrimidinyl]-2-imidazo[1,2-a]pyridinyl]-2-methoxybenzamide [no description available]	2.08	1	0	benzamides
incb-018424 [no description available]	5.26	5	0	nitrile; pyrazoles; pyrrolopyrimidine	antineoplastic agent; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
bix 01294 [no description available]	2.08	1	0	piperidines
cobicistat [no description available]	2.6	1	0	1,3-thiazoles; carbamate ester; monocarboxylic acid amide; morpholines; ureas	P450 inhibitor
bms-790052 daclatasvir: an HCV NS5A inhibitor. daclatasvir : A member of the class of biphenyls that is a potent inhibitor of nonstructural protein 5A and is used (as its hydrochloride salt) for treatment of hepatitis C.	2.6	1	0	biphenyls; carbamate ester; carboxamide; imidazoles; valine derivative	antiviral drug; nonstructural protein 5A inhibitor
pf 3845 PF 3845: inhibits fatty acid amide hydrolase	2.08	1	0	piperidines
gsk 2126458 omipalisib: inhibitor of mTOR protein. omipalisib : A member of the class of quinolines that is quinoline which is substituted by pyridazin-4-yl and 5-[(2,4-difluorobenzene-1-sulfonyl)amino]-6-methoxypyridin-3-yl groups at positions 4 and 6, respectively. It is a highly potent inhibitor of PI3K and mTOR developed by GlaxoSmithKline and was previously in human phase 1 clinical trials for the treatment of idiopathic pulmonary fibrosis and solid tumors.	2.08	1	0	aromatic ether; difluorobenzene; pyridazines; pyridines; quinolines; sulfonamide	anticoronaviral agent; antineoplastic agent; autophagy inducer; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; mTOR inhibitor; radiosensitizing agent
ixazomib ixazomib: a proteasome inhibitor with antineoplastic activity; MLN2238 is the biologically active form of MLN9708; structure in first source. ixazomib : A glycine derivative that is the amide obtained by formal condensation of the carboxy group of N-(2,5-dichlorobenzoyl)glycine with the amino group of [(1R)-1-amino-3-methylbutyl]boronic acid. The active metabolite of ixazomib citrate, it is used in combination therapy for treatment of multiple myeloma.	15.01	74	7	benzamides; boronic acids; dichlorobenzene; glycine derivative	antineoplastic agent; apoptosis inducer; drug metabolite; orphan drug; proteasome inhibitor
ldn 193189 LDN 193189: inhibits bone morphogenetic protein signaling	2.08	1	0	pyrimidines
ver 155008 VER 155008: structure in first source	2.87	3	0	purine nucleoside
ucph 101 2-amino-4-(4-methoxyphenyl)-7-(naphthalen-1-yl)-5-oxo-5,6,7,8-tetrahydro-4H-chromene-3-carbonitrile: structure in first source	2.6	1	0
(5-(2,4-bis((3s)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol (5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol: a potent, selective, and orally bioavailable ATP-competitive mammalian target of rapamycin kinase inhibitor with in vitro and in vivo antitumor activity; structure in first source	2.11	1	0	benzyl alcohols; morpholines; pyridopyrimidine; tertiary amino compound	antineoplastic agent; apoptosis inducer; mTOR inhibitor
plx4032 [no description available]	6.23	5	1	aromatic ketone; difluorobenzene; monochlorobenzenes; pyrrolopyridine; sulfonamide	antineoplastic agent; B-Raf inhibitor
2,3-bis(2-hydroxyethylsulfanyl)-(1,4)naphthoquinone 2,3-bis(2-hydroxyethylsulfanyl)-(1,4)naphthoquinone: CDC25A & B inhibitor	2.05	1	0
(2S)-2-[[2-(2,3-dihydro-1H-inden-5-yloxy)-9-[(4-phenylphenyl)methyl]-6-purinyl]amino]-3-phenyl-1-propanol [no description available]	2.08	1	0	biphenyls
gsk 1363089 GSK 1363089: a multikinase inhibitor that acts on Met, RON, Axl, and VEGFR; structure in first source	2.08	1	0	aromatic ether
kin-193 [no description available]	2.08	1	0	pyridopyrimidine
5-(3-methylsulfonylphenyl)-4-[(1-methyl-5-tetrazolyl)thio]thieno[2,3-d]pyrimidine [no description available]	2.6	1	0	aryl sulfide; thienopyrimidine
glycolipids [no description available]	2.21	1	0
bay 869766 [no description available]	2.08	1	0
baricitinib [no description available]	2.82	2	0	azetidines; nitrile; pyrazoles; pyrrolopyrimidine; sulfonamide	anti-inflammatory agent; antirheumatic drug; antiviral agent; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor; immunosuppressive agent
4-[6-[4-(methoxycarbonylamino)phenyl]-4-(4-morpholinyl)-1-pyrazolo[3,4-d]pyrimidinyl]-1-piperidinecarboxylic acid methyl ester WYE-354: an mTOR inhibitor; structure in first source	2.08	1	0	carbamate ester
arry 520 filanesib: a kinesin spindle protein inhibitor	5.3	2	1
KOM70144 KOM70144 : A benzamide that is GRL-0617 in which one of the hydrogen's of the primary amino group is replaced by an acetyl group. It an inhibitor of SARS-CoV and SARS-CoV-2 papain-like protease (PLpro) with an IC50 of 2.6 muM and 5.0 muM, respectively. It also inhibits SARS-CoV and SARS-CoV-2 infection of Vero E6 cells in vitro (EC50 values are 13.1 and 21 muM, respectively).	2.6	1	0	acetamides; benzamides; naphthalenes; secondary carboxamide	anticoronaviral agent; protease inhibitor
piperidines Piperidines: A family of hexahydropyridines.	14.64	54	8
6-[(3-aminophenyl)methyl]-4-methyl-2-methylsulfinyl-5-thieno[3,4]pyrrolo[1,3-d]pyridazinone ML-265: a small molecule activator of PKM2	2.08	1	0	organic heterobicyclic compound; organonitrogen heterocyclic compound; organosulfur heterocyclic compound
e-52862 [no description available]	2.6	1	0
ly2811376 [no description available]	2.6	1	0
interleukin-8 Interleukin-8: A member of the CXC chemokine family that plays a role in the regulation of the acute inflammatory response. It is secreted by variety of cell types and induces CHEMOTAXIS of NEUTROPHILS and other inflammatory cells.	9.56	23	0
dabrafenib [no description available]	3.63	2	0	1,3-thiazoles; aminopyrimidine; organofluorine compound; sulfonamide	anticoronaviral agent; antineoplastic agent; B-Raf inhibitor
anagliptin anagliptin: anagliptin hydrochloride salt is the active compound	2.6	1	0	amino acid amide
3-[[4-(2,3-dihydro-1,4-benzodioxin-6-ylsulfonyl)-1,4-diazepan-1-yl]sulfonyl]aniline [no description available]	2.08	1	0	benzenes; sulfonamide
cp 466722 [no description available]	2.08	1	0	quinazolines
2,3-dihydro-3beta-O-sulfate withaferin A 2,3-dihydro-3beta-O-sulfate withaferin A : A withanolide that is 2,3-dihydrowithaferin A substituted by a sulfoxy group at position 3. Isolated from Physalis longifolia, it exhibits antineoplastic activity.	2.31	1	0	27-hydroxy steroid; 4-hydroxy steroid; delta-lactone; epoxy steroid; ergostanoid; primary alcohol; steroid sulfate; withanolide	antineoplastic agent; metabolite; plant metabolite
an2728 crisaborole: NSAID, Dermatologic Agent; structure in first source. crisaborole : A member of the class of benzoxaboroles that is 5-hydroxy-1,3-dihydro-2,1-benzoxaborole in which the phenolic hydrogen has been replaced by a 4-cyanophenyl group. A phosphodiesterase 4 inhibitor that is used for treatment of mild to moderate atopic dermatitis in children and adults.	3.78	2	0	aromatic ether; benzoxaborole; nitrile	antipsoriatic; non-steroidal anti-inflammatory drug; phosphodiesterase IV inhibitor
gardiquimod [no description available]	2.6	1	0
CAY10626 [no description available]	2.08	1	0	ureas
grazoprevir grazoprevir: has antiviral activity; component of Zepatier. grazoprevir : An azamacrocyclic compound that is a hepatitis C protease inhibitor used in combination with elbasvir (under the brand name Zepatier) for treatment of chronic HCV genotypes 1 or 4 infection in adults.	2.6	1	0	aromatic ether; azamacrocycle; carbamate ester; cyclopropanes; lactam; N-sulfonylcarboxamide; quinoxaline derivative	antiviral drug; hepatitis C protease inhibitor; hepatoprotective agent
thiopental sodium [no description available]	2.08	1	0	organochlorine compound; piperazines; pyrimidines	antineoplastic agent; tyrosine kinase inhibitor
ribociclib ribociclib: inhibits both CDK4 and CDK6	2.31	1	0
abt-450 paritaprevir: inhibits HCV NS3 protease. paritaprevir : An azamacrocycle which is used which is in combination with dasabuvir sodium hydrate, ombitasvir and ritonavir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.	2.6	1	0
letermovir letermovir: has antiviral activity; structure in first source	2.6	1	0
gx 15-070 obatoclax: a pan-Bcl-2 inhibitor potentially useful in treating mantle cell lymphoma	4.97	8	1
sofosbuvir Sofosbuvir: A uridine monophosphate analog inhibitor of HEPATITIS C VIRUS (HCV) polymerase NS5B that is used as an ANTIVIRAL AGENT in the treatment of CHRONIC HEPATITIS C.. sofosbuvir : A nucleotide conjugate that is used in combination with ledipasvir (under the trade name Harvoni) for the treatment of chronic hepatitis C genotype 1 infection.	2.6	1	0	isopropyl ester; L-alanyl ester; nucleotide conjugate; organofluorine compound; phosphoramidate ester	antiviral drug; hepatitis C protease inhibitor; prodrug
5-(4-amino-1-propan-2-yl-3-pyrazolo[3,4-d]pyrimidinyl)-1,3-benzoxazol-2-amine sapanisertib: an mTOR inhibitor	2.69	2	0	benzoxazole
blz 945 [no description available]	2.6	1	0
pha 793887 [no description available]	2.08	1	0	piperidinecarboxamide
azd3839 AZD3839: a BACE1 inhibitor; structure in first source	2.6	1	0
pr-957 PR-957: immunoproteasome inhibitor; inhibits Lmp7 protein; structure in first source	5.6	15	1
pf 3084014 nirogacestat: an antineoplastic agent. nirogacestat : A member of the class of imidazoles that is 1H-imidazole substituted by a 1-[(2,2-dimethylpropyl)amino]-2-methylpropan-2-yl group at position 1 and a {N-[(2S)-6,8-difluoro-1,2,3,4-tetrahydronaphthalen-2-yl]-L-norvalyl}amino group at position 4. It is a gamma-secretase inhibitor whose hydrobromide salt is indicated for adult patients with progressing desmoid tumours who require systemic treatment.	2.6	1	0
unc 0638 UNC 0638: inhibits lysine methyltransferases G9a and GLP; structure in first source	2.6	1	0	quinazolines
gs-9620 [no description available]	2.6	1	0
nvp-bsk805 [no description available]	2.08	1	0
afuresertib [no description available]	2.25	1	0	amphetamines
xmd 8-92 XMD8-92 : A dimethylpyrimido[4,5-b][1,4]benzodiazepin-6-one carrying at C-2 on the pyrimidine ring a [2-ethoxy-4-(4-hydroxypiperidin-1-yl)phenyl]amino substituent. It is an inhibitor of the BMK1 kinase pathway.	2.08	1	0	pyrimidobenzodiazepine	protein kinase inhibitor
n-((5-(methanesulfonyl)pyridin-2-yl)methyl)-6-methyl-5-(1-methyl-1h-pyrazol-5-yl)-2-oxo-1-(3-(trifluoromethyl)phenyl)-1,2-dihydropyridine-3-carboxamide N-((5-(methanesulfonyl)pyridin-2-yl)methyl)-6-methyl-5-(1-methyl-1H-pyrazol-5-yl)-2-oxo-1-(3-(trifluoromethyl)phenyl)-1,2-dihydropyridine-3-carboxamide: structure in first source	2.6	1	0
bms 708163 BMS 708163: structure in first source	2.6	1	0	oxadiazole; ring assembly
psammaplysin f psammaplysin F: isolated from sponge, Aplysinella sp.; structure given in first source	7.21	1	0
jq1 compound [no description available]	2.58	2	0	carboxylic ester; organochlorine compound; tert-butyl ester; thienotriazolodiazepine	angiogenesis inhibitor; anti-inflammatory agent; antineoplastic agent; apoptosis inducer; bromodomain-containing protein 4 inhibitor; cardioprotective agent; ferroptosis inducer
jnj38877605 [no description available]	2.08	1	0	quinolines
N-[3-(1,3-benzothiazol-2-yl)-5,6-dihydro-4H-thieno[2,3-c]pyrrol-2-yl]acetamide [no description available]	2.08	1	0	benzothiazoles
dinaciclib [no description available]	2.58	2	0	pyrazolopyrimidine
1-(5-((2,4-difluorophenyl)thio)-4-nitrothiophen-2-yl)ethanone 1-(5-((2,4-difluorophenyl)thio)-4-nitrothiophen-2-yl)ethanone: a USP7 inhibitor; structure in first source	2.6	1	0
gsk525762a molibresib: mimicks acetylated histones; structure in first source	2.6	1	0	benzodiazepine
alectinib [no description available]	2.17	1	0	aromatic ketone; morpholines; nitrile; organic heterotetracyclic compound; piperidines	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
ML240 ML240 : A member of the class of quinazolines that is quinazoline which is substituted at positions 2, 5 and 8 by 2-amino-1H-benzimidazol-1-yl, benzylnitrilo and methoxy groups, respectively. It is a ATP-competetive inhibitor of AAA ATPase p97, also known as valosin-containing protein (VCP).	2.61	2	0	aromatic amine; aromatic ether; benzimidazoles; primary amino compound; quinazolines; secondary amino compound	antineoplastic agent
birinapant birinapant: a Smac mimetic with antineoplastic activity	2.6	1	0	dipeptide
torin 1 torin 1 : A member of the class of pyridoquinolines that is 9-(quinolin-3-yl)benzo[h][1,6]naphthyridin-2-one bearing an additional 4-(4-propionylpiperazin-1-yl)-3-(trifluoromethyl)phenyl substituent at position 1. It is a potent inhibitor of mTOR and exhibits anti-cancer properties.	2.08	1	0	N-acylpiperazine; N-arylpiperazine; organofluorine compound; pyridoquinoline; quinolines	antineoplastic agent; mTOR inhibitor
ly2886721 [no description available]	2.6	1	0
nms-p118 NMS-P118: a PARP-1 inhibitor; structure in first source	2.6	1	0
abt-199 venetoclax: A BCL-2 inhibitor with antineoplastic activity that is used in the treatment of CHRONIC LYMPHOCYTIC LEUKEMIA associated with chromosome 17p deletion; structure in first source.. venetoclax : A member of the class of pyrrolopyridines that is a potent inhibitor of the antiapoptotic protein B-cell lymphoma 2. It is used for treamtment of chronic lymphocytic leukemia with 17p deletion.	16.95	27	4	aromatic ether; C-nitro compound; monochlorobenzenes; N-alkylpiperazine; N-arylpiperazine; N-sulfonylcarboxamide; oxanes; pyrrolopyridine	antineoplastic agent; apoptosis inducer; B-cell lymphoma 2 inhibitor
ly2940680 [no description available]	2.08	1	0
tubastatin a [no description available]	2.87	3	0	hydroxamic acid; pyridoindole; tertiary amino compound	EC 3.5.1.98 (histone deacetylase) inhibitor
1-[4-fluoro-3-(trifluoromethyl)phenyl]-3-(5-pyridin-4-yl-1,3,4-thiadiazol-2-yl)urea [no description available]	2.08	1	0	ureas
pracinostat pracinostat : A hydroxamic acid that is N-hydroxyacrylamide which is substituted at position 3 by a 2-butyl-1-[2-(diethylamino)ethyl]-1H-benzimidazol-5-yl group (the E isomer). An orally available pan-histone deacetylase inhibitor with demonstrated activity in the treatment of advanced solid tumours.	2.6	1	0	benzimidazole; hydroxamic acid; olefinic compound; tertiary amino compound	antimalarial; antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor
ro 4929097 [no description available]	2.08	1	0	dibenzoazepine; dicarboxylic acid diamide; lactam; organofluorine compound	EC 3.4.23.46 (memapsin 2) inhibitor
mln 9708 [no description available]	3.04	4	0
gsk4112 GSK4112: a Rev-erbalpha agonist; structure in first source	2.08	1	0
spautin-1 [no description available]	2.6	1	0
torin 2 torin 2 : A member of the class of pyridoquinolines that is benzo[h][1,6]naphthyridin-2-one carrying additional 3-(trifluoromethyl)phenyl and 6-aminopyridin-3-yl substituents at positions 1 and 9 respectively. It is a potent inhibitor of mTOR and exhibits anti-cancer properties.	2.08	1	0	aminopyridine; organofluorine compound; primary amino compound; pyridoquinoline	antineoplastic agent; mTOR inhibitor
pf-4708671 [no description available]	2.08	1	0
ldn 57444 LDN 57444: inhibitor of ubiquitin C-terminal hydrolase-L1; structure in first source	2.6	1	0
gsk1210151a GSK1210151A: inhibitor of the BET family of proteins; structure in first source	2.6	1	0	imidazoquinoline
i-bet726 [no description available]	2.6	1	0
natriuretic peptide, brain Natriuretic Peptide, Brain: A PEPTIDE that is secreted by the BRAIN and the HEART ATRIA, stored mainly in cardiac ventricular MYOCARDIUM. It can cause NATRIURESIS; DIURESIS; VASODILATION; and inhibits secretion of RENIN and ALDOSTERONE. It improves heart function. It contains 32 AMINO ACIDS.	7.23	15	0	polypeptide
acy-1215 ricolinostat: an HDAC6 inhibitor; structure in first source	4.53	6	0	pyrimidinecarboxylic acid
heme Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins.. ferroheme : Any iron(II)--porphyrin coordination complex.. ferroheme b : Heme b in which the iron has oxidation state +2.. heme : A heme is any tetrapyrrolic chelate of iron.	2.11	1	0
N-[4-(1-benzoyl-4-piperidinyl)butyl]-3-(3-pyridinyl)-2-propenamide [no description available]	2.08	1	0	benzamides; N-acylpiperidine
2-methoxy-N-[3-[4-[3-methyl-4-[(6-methyl-3-pyridinyl)oxy]anilino]-6-quinazolinyl]prop-2-enyl]acetamide 2-methoxy-N-[3-[4-[3-methyl-4-[(6-methyl-3-pyridinyl)oxy]anilino]-6-quinazolinyl]prop-2-enyl]acetamide : A member of the class of quinazolines that is quinazoline substituted by {3-methyl-4-[(6-methylpyridin-3-yl)oxy]phenyl}amino and 3-(2-methoxyacetamido)prop-1-en-1-yl groups at positions 4 and 6, respectively.	2.08	1	0	aromatic ether; methylpyridines; olefinic compound; quinazolines; secondary amino compound; secondary carboxamide; toluenes
belinostat [no description available]	2.08	1	0	olefinic compound
cudc-907 [no description available]	2.61	2	0
ascorbic acid Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant.. L-ascorbic acid : The L-enantiomer of ascorbic acid and conjugate acid of L-ascorbate.. L-ascorbate : The L-enantiomer of ascorbate and conjugate base of L-ascorbic acid, arising from selective deprotonation of the 3-hydroxy group. Required for a range of essential metabolic reactions in all animals and plants.. vitamin C : Any member of a group of vitamers that belong to the chemical structural class called butenolides that exhibit biological activity against vitamin C deficiency in animals. The vitamers include L-ascorbic acid and its salt, ionized and oxidized forms.	8.71	15	4	ascorbic acid; vitamin C	coenzyme; cofactor; flour treatment agent; food antioxidant; food colour retention agent; geroprotector; plant metabolite; skin lightening agent
raltegravir [no description available]	3.23	1	0	1,2,4-oxadiazole; dicarboxylic acid amide; hydroxypyrimidine; monofluorobenzenes; pyrimidone; secondary carboxamide	antiviral drug; HIV-1 integrase inhibitor
novobiocin Novobiocin: An antibiotic compound derived from Streptomyces niveus. It has a chemical structure similar to coumarin. Novobiocin binds to DNA gyrase, and blocks adenosine triphosphatase (ATPase) activity. (From Reynolds, Martindale The Extra Pharmacopoeia, 30th ed, p189). novobiocin : A coumarin-derived antibiotic obtained from Streptomyces niveus.	2.05	1	0	carbamate ester; ether; hexoside; hydroxycoumarin; monocarboxylic acid amide; monosaccharide derivative; phenols	antibacterial agent; antimicrobial agent; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; Escherichia coli metabolite; hepatoprotective agent
tetracycline Tetracycline: A naphthacene antibiotic that inhibits AMINO ACYL TRNA binding during protein synthesis.. tetracycline : A broad-spectrum polyketide antibiotic produced by the Streptomyces genus of actinobacteria.	4.08	4	0
chlortetracycline Chlortetracycline: A TETRACYCLINE with a 7-chloro substitution.. chlortetracycline : A member of the class of tetracyclines with formula C22H23ClN2O8 isolated from Streptomyces aureofaciens.	2.45	2	0
oxytetracycline, anhydrous Oxytetracycline: A TETRACYCLINE analog isolated from the actinomycete STREPTOMYCES RIMOSUS and used in a wide variety of clinical conditions.. oxytetracycline : A tetracycline used for treatment of infections caused by a variety of Gram positive and Gram negative microorganisms including Mycoplasma pneumoniae, Pasteurella pestis, Escherichia coli, Haemophilus influenzae (respiratory infections), and Diplococcus pneumoniae.	3.86	3	0
minocycline Minocycline: A TETRACYCLINE analog, having a 7-dimethylamino and lacking the 5 methyl and hydroxyl groups, which is effective against tetracycline-resistant STAPHYLOCOCCUS infections.. minocycline : A tetracycline analogue having a dimethylamino group at position 7 and lacking the methyl and hydroxy groups at position 5.	10.08	7	0
dicumarol Dicumarol: An oral anticoagulant that interferes with the metabolism of vitamin K. It is also used in biochemical experiments as an inhibitor of reductases.	2.05	1	0	hydroxycoumarin	anticoagulant; EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor; Hsp90 inhibitor; vitamin K antagonist
piroxicam [no description available]	3.87	3	0	benzothiazine; monocarboxylic acid amide; pyridines	analgesic; antirheumatic drug; cyclooxygenase 1 inhibitor; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-steroidal anti-inflammatory drug
roquinimex roquinimex: structure in first source	2.46	2	0	aromatic amide
acenocoumarol Acenocoumarol: A coumarin that is used as an anticoagulant. Its actions and uses are similar to those of WARFARIN. (From Martindale, The Extra Pharmacopoeia, 30th ed, p233). acenocoumarol : A hydroxycoumarin that is warfarin in which the hydrogen at position 4 of the phenyl substituent is replaced by a nitro group.	2.05	1	0	C-nitro compound; hydroxycoumarin; methyl ketone	anticoagulant; EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor
mobic Meloxicam: A benzothiazine and thiazole derivative that acts as a NSAID and cyclooxygenase-2 (COX-2) inhibitor. It is used in the treatment of RHEUMATOID ARTHRITIS; OSTEOARTHRITIS; and ANKYLOSING SPONDYLITIS.. meloxicam : A benzothiazine that is piroxicam in which the pyridin-2-yl group is replaced by a 5-methyl-1,3-thiazol-2-yl group. A non-steroidal anti-inflammatory drug and selective inhibitor of COX-2, it is used particularly for the management of rheumatoid arthritis.	4.46	6	0	1,3-thiazoles; benzothiazine; monocarboxylic acid amide	analgesic; antirheumatic drug; cyclooxygenase 2 inhibitor; non-steroidal anti-inflammatory drug
laquinimod [no description available]	3.21	1	0	aromatic amide
mobiflex tenoxicam : A thienothiazine-derived monocarboxylic acid amide obtained by formal condensation of the carboxy group of 4-hydroxy-2-methylthieno[2,3-e][1,2]thiazine-3-carboxylic acid 1,1-dioxide with the amino group of 2-aminopyridine. Used for the treatment of pain and inflammation in osteoarthritis and rheumatoid arthritis. It is also indicated for short term treatment of acute musculoskeletal disorders including strains, sprains and other soft-tissue injuries.	2.75	3	0	heteroaryl hydroxy compound; monocarboxylic acid amide; pyridines; thienothiazine	antipyretic; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug
isoxicam isoxicam : A monocarboxylic acid amide that is piroxicam in which the pyrid-2-yl group is replaced by a 5-methyl-1,2-oxazol-3-yl group. A non-steroidal anti-inflammatory drug, it was withdrawn from the market in the 1980s following its association with cases of Stevens-Johnson syndrome.	2.46	2	0	benzothiazine; isoxazoles; monocarboxylic acid amide	antirheumatic drug; non-steroidal anti-inflammatory drug
ethyl 1-benzyl-3-hydroxy-2(5h)-oxopyrrole-4-carboxylate ethyl 1-benzyl-3-hydroxy-2(5H)-oxopyrrole-4-carboxylate: RN & structure given in first source	2.08	1	0	carboxylic acid; pyrroline
warfarin Warfarin: An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide.. warfarin : A racemate comprising equal amounts of (R)- and (S)-warfarin. Extensively used as both an anticoagulant drug and as a pesticide against rats and mice.. 4-hydroxy-3-(3-oxo-1-phenylbutyl)-1-benzopyran-2-one : A member of the class of coumarins that is 4-hydroxycoumarin which is substituted at position 3 by a 1-phenyl-3-oxo-1-butyl group.	4.96	11	0	benzenes; hydroxycoumarin; methyl ketone
demeclocycline Demeclocycline: A TETRACYCLINE analog having a 7-chloro and a 6-methyl. Because it is excreted more slowly than tetracycline, it maintains effective blood levels for longer periods of time.. demeclocycline : Tetracycline which lacks the methyl substituent at position 7 and in which the hydrogen para- to the phenolic hydroxy group is substituted by chlorine. Like tetracycline, it is an antibiotic, but being excreted more slowly, effective blood levels are maintained for longer. It is used (mainly as the hydrochloride) for the treatment of Lyme disease, acne and bronchitis, as well as for hyponatraemia (low blood sodium concentration) due to the syndrome of inappropriate antidiuretic hormone (SIADH) where fluid restriction alone has been ineffective.	3.58	2	0
phenprocoumon Phenprocoumon: Coumarin derivative that acts as a long acting oral anticoagulant.. phenprocoumon : A hydroxycoumarin that is 4-hydroxycoumarin which is substituted at position 3 by a 1-phenylpropyl group.	2.05	1	0	hydroxycoumarin	anticoagulant; EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor
tipranavir tipranavir: inhibits HIV-1 protease. tipranavir : A pyridine-2-sulfonamide substituted at C-5 by a trifluoromethyl group and at the sulfonamide nitrogen by a dihydropyrone-containing m-tolyl substituent. It is an HIV-1 protease inhibitor.	3.73	2	0	sulfonamide	antiviral drug; HIV protease inhibitor
tasquinimod tasquinimod: a lead second generation quinoline-3-carboxamide anti-angiogenic agent for the treatment of prostate cancer; structure in first source	2.6	1	0
rolitetracycline Rolitetracycline: A pyrrolidinylmethyl TETRACYCLINE.. rolitetracycline : A derivative of tetracycline in which the amide function is substituted with a pyrrolidinomethyl group.	2.45	2	0
minocycline hydrochloride [no description available]	2.08	1	0
tigecycline [no description available]	3.87	3	0
lornoxicam lornoxicam : A thienothiazine-derived monocarboxylic acid amide obtained by formal condensation of the carboxy group of 6-chloro-4-hydroxy-2-methylthieno[2,3-e][1,2]thiazine-3-carboxylic acid 1,1-dioxide with the amino group of 2-aminopyridine. Used for the treatment of pain, primarily resulting from inflammatory diseases of the joints, osteoarthritis, surgery, sciatica and other inflammations.	2.47	2	0	heteroaryl hydroxy compound; monocarboxylic acid amide; organochlorine compound; pyridines; thienothiazine	antipyretic; non-narcotic analgesic; non-steroidal anti-inflammatory drug
lfm a13 LFM A13: inhibits Bruton's tyrosine kinase; structure in first source	3	1	0
a 769662 [no description available]	2.08	1	0	biphenyls
gsk1265744 [no description available]	2.6	1	0	difluorobenzene; monocarboxylic acid amide; organic heterotricyclic compound; secondary carboxamide	HIV-1 integrase inhibitor
s 1 (combination) S 1 (combination): consists of tegafur, 5-chloro-2,4-dihydroxyuridine & potassium oxonate; an inhibitor of fluorouracil(5-FU) degradation; prolongs the blood 5-FU level as well as increases selective toxicity to tumor; used for the treatment of colon cancer	3.12	1	0
abt-267 ombitasvir: inhibits HCV NS5A protein, component of Viekirax. ombitasvir : A dipeptide derivative which is used which is in combination with dasabuvir sodium hydrate, paritaprevir and ritonavir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.	2.6	1	0	aromatic amide; carbamate ester; dipeptide; pyrrolidines	antiviral drug; hepatitis C virus nonstructural protein 5A inhibitor
abt-333 dasabuvir: an antiviral agent. dasabuvir : A member of the class of pyrimidone, which is (as the monohydrate of its sodium salt) in combination with ombitasvir, paritaprevir and ritonavir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.	2.6	1	0	aromatic ether; naphthalenes; pyrimidone; sulfonamide	antiviral drug; nonnucleoside hepatitis C virus polymerase inhibitor
byl719 [no description available]	5.45	3	1	proline derivative
rpx7009 RPX7009: a beta-lactamase inhibitor; structure in first source	2.41	1	0
rgfp966 [no description available]	2.6	1	0
rg2833 RG2833: a histone deacetylase inhibitor; structure in first source	2.6	1	0
epidermal growth factor Epidermal Growth Factor: A 6-kDa polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. Epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and EPITHELIAL CELLS. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form.	2.74	3	0
normosol r normosol R: diluent for packed erythrocytes; Abbott Labs, contains NaCl, Na acetate, Na gluconate, KCl, MgCl (Am Drug Ind)	2.11	1	0
transforming growth factor beta Transforming Growth Factor beta: A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.	10.64	22	0
pi-1840 PI-1840: has both antineoplastic and proteasome inhibitory activities; structure in first source	2.59	2	0
LimKi 3 LIMKi3: LIMK inhibitor. LimKi 3 : A member of the class of pyrazoles that is 1-(2,6-dichlorophenyl)-1H-pyrazole which is substituted by a difluoromethyl group at position 3 and by a 2-(isobutyrylamino)-1,3-thiazol-5-yl group at position 5. It is a a potent cell-permeable inhibitor of LIM kinase 1 and 2.	2.08	1	0	1,3-thiazoles; dichlorobenzene; organofluorine compound; pyrazoles; secondary carboxamide	LIM kinase inhibitor
1-[4-amino-7-[3-(2-methoxyethylamino)propyl]-5-(4-methylphenyl)-6-pyrrolo[2,3-d]pyrimidinyl]-2-fluoroethanone [no description available]	2.08	1	0	pyrroles
okadaic acid Okadaic Acid: A specific inhibitor of phosphoserine/threonine protein phosphatase 1 and 2a. It is also a potent tumor promoter. It is produced by DINOFLAGELLATES and causes diarrhetic SHELLFISH POISONING.. okadaic acid : A polycyclic ether that is produced by several species of dinoflagellates, and is known to accumulate in both marine sponges and shellfish. A polyketide, polyether derivative of a C38 fatty acid, it is one of the primary causes of diarrhetic shellfish poisoning (DSP). It is a potent inhibitor of specific protein phosphatases and is known to have a variety of negative effects on cells.	2.47	2	0	ketal
2-[5-[(3,5-dimethyl-1H-pyrrol-2-yl)methylidene]-4-methoxy-2-pyrrolylidene]indole [no description available]	2.08	1	0	dipyrrins
acy-738 [no description available]	2.6	1	0
pelabresib CPI-0610: a bromodomain and extra-terminal protein inhibitor with antineoplastic activity; structure in first source	2.6	1	0	monochlorobenzenes; organic heterotricyclic compound; primary carboxamide	antineoplastic agent; bromodomain-containing protein 4 inhibitor
N-hydroxy-3-[4-[[2-(2-methyl-1H-indol-3-yl)ethylamino]methyl]phenyl]-2-propenamide [no description available]	2.08	1	0	tryptamines
3-[(5-tert-butyl-1H-imidazol-4-yl)methylidene]-6-(phenylmethylene)piperazine-2,5-dione [no description available]	2.08	1	0	pyrazines
gsk837149a GSK837149A: structure in first source	2.08	1	0
N-[4-(3-chloro-4-fluoroanilino)-7-[[(3S)-3-oxolanyl]oxy]-6-quinazolinyl]-4-(dimethylamino)-2-butenamide [no description available]	2.08	1	0	quinazolines
N-[4-(3-chloro-4-fluoroanilino)-7-methoxy-6-quinazolinyl]-4-(1-piperidinyl)-2-butenamide [no description available]	2.08	1	0	quinazolines
wnt-c59 2-(4-(2-methylpyridin-4-yl)phenyl)-N-(4-(pyridin-3-yl)phenyl)acetamide: a PORCN acyltransferase inhibitor; structure in first source	2.08	1	0
5-[1-(2-hydroxyethyl)-3-pyridin-4-yl-4-pyrazolyl]-2,3-dihydroinden-1-one oxime [no description available]	2.08	1	0	indanes
gs-5806 presatovir: a respiratory syncytial virus entry inhibitor	2.6	1	0
doravirine [no description available]	2.6	1	0
pyrethrins [no description available]	2.08	1	0
gn6958 GN6958: inhibits SUMO-sentrin specific protease 1 (SENP1); structure in first source	2.6	1	0
vx-787 pimodivir: non‐nucleotide inhibitor of the polymerase basic protein 2 (PB2) subunit of the influenza A that is active against H1N1, H7N9 and H5N1, as well as influenza A strains with reduced susceptibility to NAIs	2.6	1	0
tas-116 [no description available]	7.52	2	0
ledipasvir ledipasvir : A benzimidazole derivative that is used in combination with sofosbuvir (under the trade name Harvoni) for the treatment of chronic hepatitis C genotype 1 infection.	2.6	1	0	azaspiro compound; benzimidazole; bridged compound; carbamate ester; carboxamide; fluorenes; imidazoles; L-valine derivative; N-acylpyrrolidine; organofluorine compound	antiviral drug; hepatitis C protease inhibitor
gs-5816 velpatasvir: an NS5A inhibitor used for treating hepatitis C infections. velpatasvir : A complex organic heteropentacyclic compound that is a hepatitis C virus nonstructural protein 5A inhibitor used in combination with sofosbuvir (under the brand name Epclusa) for treatment of patients with chronic hepatitis C of all six major genotypes.	2.6	1	0	carbamate ester; ether; imidazoles; L-valine derivative; N-acylpyrrolidine; organic heteropentacyclic compound; ring assembly	antiviral drug; hepatitis C virus nonstructural protein 5A inhibitor
g007-lk G007-LK: potent and specific small-molecule tankyrase inhibitor; structure in first source	2.6	1	0
gsk-2816126 GSK-2816126: inhibits EZH2 methyltransferase; structure in first source	2.85	3	0	piperazines; pyridines
ajmaline [no description available]	2.05	1	0
thailandepsin a thailandepsin A: isolated from Burkholderia thailandensis; structure in first source	2.11	1	0	cyclodepsipeptide	metabolite
gsk2830371 GSK2830371: inhibits Wip1 phosphatase; structure in first source	2.13	1	0
acp-196 acalabrutinib: inhibits Bruton’s tyrosine kinase; has antineoplastic activity. acalabrutinib : A member of the class of imidazopyrazines that is imidazo[1,5-a]pyrazine substituted by 4-(pyridin-2-ylcarbamoyl)phenyl, (2S)-1-(but-2-ynoyl)pyrrolidin-2-yl, and amino groups at positions 1, 3 and 8, respectively. It is an irreversible second-generation Bruton's tyrosine kinase (BTK) inhibitor that is approved by the FDA for the treatment of adult patients with mantle cell lymphoma (MCL) who have received at least one prior therapy.	3.31	1	0	aromatic amine; benzamides; imidazopyrazine; pyridines; pyrrolidinecarboxamide; secondary carboxamide; tertiary carboxamide; ynone	antineoplastic agent; apoptosis inducer; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
cpi203 CPI203: a BET protein bromodomain inhibitor	7.11	1	0
sc 26196 [no description available]	2.31	1	0
(r)-pfi-2 (R)-PFI-2: a potent and selective inhibitor of SETD7 methyltransferase; structure in first source	2.25	1	0
leu-ser-lys-leu peptide [no description available]	2.13	1	0
rome Rome: The capital city of Italy.. (2R)-2-amino-2-(methoxymethyl)-4-(4-octylphenyl)butan-1-ol : A 2-amino-2-(methoxymethyl)-4-(4-octylphenyl)butan-1-ol that has R-configuration. It is a sphingosine kinase-2 inhibitor.	2.07	1	0	2-amino-2-(methoxymethyl)-4-(4-octylphenyl)butan-1-ol	EC 2.7.1.91 (sphingosine kinase) inhibitor
4-((1-butyl-3-phenylureido)methyl)-n-hydroxybenzamide 4-((1-butyl-3-phenylureido)methyl)-N-hydroxybenzamide: inhibits HDAC6; structure in first source	2.6	1	0
selinexor selinexor: inhibits karyopherin XPO1	10.83	20	3
verdinexor verdinexor: a selective inhibitor of nuclear export	2.6	1	0
cb-839 [no description available]	2.6	1	0
mk-8742 elbasvir: inhibits NS5A protein of hepatitis C virus. elbasvir : A complex organic heterotetracyclic compound that is a hepatitis C virus nonstructural protein 5A inhibitor used in combination with grazoprevir (under the brand name Zepatier) for treatment of chronic HCV genotypes 1 or 4 infection in adults.	2.6	1	0	carbamate ester; imidazoles; L-valine derivative; N-acylpyrrolidine; organic heterotetracyclic compound; ring assembly	antiviral drug; hepatitis C virus nonstructural protein 5A inhibitor; hepatoprotective agent
atglistatin atglistatin: inhibits adipose triglyceride lipase; structure in first source. atglistatin : A biphenyl that is 1,1'-biphenyl substituted by (dimethylcarbamoyl)amino and dimethylamino groups at positions 3 and 4', respectively. It is a potent inhibitor of adipose triglyceride lipase activity (IC50 = 700nM).	2.6	1	0
xen445 [no description available]	2.6	1	0
imetelstat [no description available]	3.17	1	0
santacruzamate a santacruzamate A: HDAC2 inhibitor from the Panamanian marine cyanobacterium cf. Symploca sp.; structure in first source	2.6	1	0	organonitrogen compound; organooxygen compound
cyclin d1 Cyclin D1: Protein encoded by the bcl-1 gene which plays a critical role in regulating the cell cycle. Overexpression of cyclin D1 is the result of bcl-1 rearrangement, a t(11;14) translocation, and is implicated in various neoplasms.	7.35	32	0
ter 286 TER 286: a glutathione-based glutathione S-transferase-activated cytotoxin; TLK-286 is the ((R)-(-))-isomer	3.13	1	0
fertinex [no description available]	3.23	1	0
ldc4297 LDC4297: a CDK7 inhibitor with antineoplastic activity; structure in first source. LDC4297 : A pyrazolotriazine that is pyrazolo[1,5-a][1,3,5]triazine substituted by a piperidin-3-yloxy group, [2-(1H-pyrazol-1-yl)benzyl]nitrilo group and an isopropyl group at positions 2, 4 and 8 respectively. It is a potent and selective CDK7 inhibitor and exhibits antiviral activity.	2.6	1	0	aromatic ether; piperidines; pyrazoles; pyrazolotriazine; secondary amino compound	antineoplastic agent; antiviral agent; apoptosis inducer; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone: an interleukin-1beta converting enzyme (ICE)-like protease inhibitor	5.03	9	0
nitrophenols Nitrophenols: PHENOLS carrying nitro group substituents.	4.14	15	0
enasidenib [no description available]	7.82	2	0	1,3,5-triazines; aminopyridine; aromatic amine; organofluorine compound; secondary amino compound; tertiary alcohol	antineoplastic agent; EC 1.1.1.42 (isocitrate dehydrogenase) inhibitor
lewis x antigen Lewis X Antigen: A trisaccharide antigen expressed on glycolipids and many cell-surface glycoproteins. In the blood the antigen is found on the surface of NEUTROPHILS; EOSINOPHILS; and MONOCYTES. In addition, Lewis X antigen is a stage-specific embryonic antigen.	2.08	1	0
epoetin alfa Epoetin Alfa: A recombinant glycosylated form of erythropoietin which stimulates the differentiation and proliferation of erythroid precursors. It is used for the treatment of ANEMIA associated with CHRONIC RENAL FAILURE in dialysis and predialysis patients.	3.11	1	0
sbi-0206965 SBI-0206965: inhibits ULK1 kinase; structure in first source	2.21	1	0
nct-501 NCT-501: inhibits aldehyde dehydrogenase 1A1; structure in first source	2.17	1	0
peoniflorin peoniflorin: from Radix and of Paeonia suffruticosa	2.41	1	0
vitamin b 12 Vitamin B 12: A cobalt-containing coordination compound produced by intestinal micro-organisms and found also in soil and water. Higher plants do not concentrate vitamin B 12 from the soil and so are a poor source of the substance as compared with animal tissues. INTRINSIC FACTOR is important for the assimilation of vitamin B 12.	5	2	1
oblimersen oblimersen: targets the Bcl-2 oncogene good efficacy with low toxicity tumour regressions	10.79	4	0
s 8932 [no description available]	2.6	1	0	aromatic amine; C-nucleoside; carboxylic ester; nitrile; phosphoramidate ester; pyrrolotriazine	anticoronaviral agent; antiviral drug; prodrug
cyclosporine Cyclosporine: A cyclic undecapeptide from an extract of soil fungi. It is a powerful immunosupressant with a specific action on T-lymphocytes. It is used for the prophylaxis of graft rejection in organ and tissue transplantation. (From Martindale, The Extra Pharmacopoeia, 30th ed).	9.2	18	3
apicidin apicidin: structure in first source	2.1	1	0
siomycin a siomycin A: see also records for siomycin & siomycin D1	2.05	1	0
myelin oligodendrocyte glycoprotein (35-55) [no description available]	2.04	1	0
thromboplastin Thromboplastin: Constituent composed of protein and phospholipid that is widely distributed in many tissues. It serves as a cofactor with factor VIIa to activate factor X in the extrinsic pathway of blood coagulation.	4.15	3	1
exudates Malaysia: A parliamentary democracy with a constitutional monarch in southeast Asia, consisting of 11 states (West Malaysia) on the Malay Peninsula and two states (East Malaysia) on the island of BORNEO. It is also called the Federation of Malaysia. Its capital is Kuala Lumpur. Before 1963 it was the Union of Malaya. It reorganized in 1948 as the Federation of Malaya, becoming independent from British Malaya in 1957 and becoming Malaysia in 1963 as a federation of Malaya, Sabah, Sarawak, and Singapore (which seceded in 1965). The form Malay- probably derives from the Tamil malay, mountain, with reference to its geography. (From Webster's New Geographical Dictionary, 1988, p715 & Room, Brewer's Dictionary of Names, 1992, p329)	4.41	1	1
angiogenin angiogenin: human tumor protein which stimulates growth of blood vessels; contains 123 amino acids; member of the pancreatic ribonuclease superfamily; MW 14,400	2.02	1	0
tautomycin tautomycin: an inhibitor of protein phosphatases 1 and 2A; isolated from Streptomyces spiroverticillatus; MF: C42-H70-O12; exists as a tautomeric mixture in solution	2	1	0
entecavir entecavir (anhydrous) : Guanine substituted at the 9 position by a 4-hydroxy-3-(hydroxymethyl)-2-methylidenecyclopentyl group. A synthetic analogue of 2'-deoxyguanosine, it is a nucleoside reverse transcriptase inhibitor with selective antiviral activity against hepatitis B virus. Entecavir is phosphorylated intracellularly to the active triphosphate form, which competes with deoxyguanosine triphosphate, the natural substrate of hepatitis B virus reverse transcriptase, inhibiting every stage of the enzyme's activity, although it has no activity against HIV. It is used for the treatment of chronic hepatitis B.	4.33	5	0	2-aminopurines; oxopurine; primary alcohol; secondary alcohol	antiviral drug; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
chir 258 [no description available]	2.08	1	0
acyclovir Acyclovir: A GUANOSINE analog that acts as an antimetabolite. Viruses are especially susceptible. Used especially against herpes.. acyclovir : An oxopurine that is guanine substituted by a (2-hydroxyethoxy)methyl substituent at position 9. Used in the treatment of viral infections.	7.83	20	1	2-aminopurines; oxopurine	antimetabolite; antiviral drug
stf 083010 STF 083010: inhibits Ire1 endonuclease; structure in first source	2.8	3	0
osi 027 OSI 027: inhibits both mTORC1 and mTORC2; structure in first source	2.08	1	0
nu 1025 NU 1064: structure in first source	2.6	1	0	phenols; quinazolines	EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
levoleucovorin Levoleucovorin: A folate analog consisting of the pharmacologically active isomer of LEUCOVORIN.. (6S)-5-formyltetrahydrofolic acid : The pharmacologically active (6S)-stereoisomer of 5-formyltetrahydrofolic acid.	5.07	3	1	5-formyltetrahydrofolic acid	antineoplastic agent; metabolite
guanosine diphosphate Guanosine Diphosphate: A guanine nucleotide containing two phosphate groups esterified to the sugar moiety.	2.31	1	0	guanosine 5'-phosphate; purine ribonucleoside 5'-diphosphate	Escherichia coli metabolite; mouse metabolite; uncoupling protein inhibitor
guanosine triphosphate Guanosine Triphosphate: Guanosine 5'-(tetrahydrogen triphosphate). A guanine nucleotide containing three phosphate groups esterified to the sugar moiety.	2.31	1	0	guanosine 5'-phosphate; purine ribonucleoside 5'-triphosphate	Escherichia coli metabolite; mouse metabolite; uncoupling protein inhibitor
guanine [no description available]	9.13	11	2	2-aminopurines; oxopurine; purine nucleobase	algal metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
inosine [no description available]	2.53	2	0	inosines; purines D-ribonucleoside	Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
sapropterin sapropterin: RN given refers to parent cpd; co-factor required for catalytic activity of nitric oxide synthases. (6R)-5,6,7,8-tetrahydrobiopterin : A 5,6,7,8-tetrahydrobiopterin in which the stereocentre at position 6 has R-configuration.. sapropterin : A tetrahydropterin that is 2-amino-5,6,7,8-tetrahydropteridin-4(3H)-one in which a hydrogen at position 6 is substituted by a 1,2-dihydroxypropyl group (6R,1'R,2'S-enantiomer).	2.41	1	0	5,6,7,8-tetrahydrobiopterin	coenzyme; cofactor; diagnostic agent; human metabolite
folic acid folcysteine: used to promote fertility in chickens. vitamin B9 : Any B-vitamin that exhibits biological activity against vitamin B9 deficiency. Vitamin B9 refers to the many forms of folic acid and its derivatives, including tetrahydrofolic acid (the active form), methyltetrahydrofolate (the primary form found in blood), methenyltetrahydrofolate, folinic acid amongst others. They are present in abundance in green leafy vegetables, citrus fruits, and animal products. Lack of vitamin B9 leads to anemia, a condition in which the body cannot produce sufficient number of red blood cells. Symptoms of vitamin B9 deficiency include fatigue, muscle weakness, and pale skin.	4.34	5	0	folic acids; N-acyl-amino acid	human metabolite; mouse metabolite; nutrient
3-methyladenine N3-methyladenine: structure in first source	4.89	10	0
rifampin Rifampin: A semisynthetic antibiotic produced from Streptomyces mediterranei. It has a broad antibacterial spectrum, including activity against several forms of Mycobacterium. In susceptible organisms it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis. Rifampin is bactericidal, and acts on both intracellular and extracellular organisms. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1160)	5.82	6	1	cyclic ketal; hydrazone; N-iminopiperazine; N-methylpiperazine; rifamycins; semisynthetic derivative; zwitterion	angiogenesis inhibitor; antiamoebic agent; antineoplastic agent; antitubercular agent; DNA synthesis inhibitor; EC 2.7.7.6 (RNA polymerase) inhibitor; Escherichia coli metabolite; geroprotector; leprostatic drug; neuroprotective agent; pregnane X receptor agonist; protein synthesis inhibitor
clozapine Clozapine: A tricylic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent.. clozapine : A benzodiazepine that is 5H-dibenzo[b,e][1,4]diazepine substituted by a chloro group at position 8 and a 4-methylpiperazin-1-yl group at position 11. It is a second generation antipsychotic used in the treatment of psychiatric disorders like schizophrenia.	4.08	4	0	benzodiazepine; N-arylpiperazine; N-methylpiperazine; organochlorine compound	adrenergic antagonist; dopaminergic antagonist; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; environmental contaminant; GABA antagonist; histamine antagonist; muscarinic antagonist; second generation antipsychotic; serotonergic antagonist; xenobiotic
dacarbazine (E)-dacarbazine : A dacarbazine in which the N=N double bond adopts a trans-configuration.	15.19	20	5	dacarbazine
didanosine Didanosine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. Didanosine is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase; ddI is then metabolized to dideoxyadenosine triphosphate, its putative active metabolite.. didanosine : A purine 2',3'-dideoxyribonucleoside that is inosine in which the hydroxy groups at both the 2' and the 3' positions on the sugar moiety have been replaced by hydrogen. An antiviral drug, it is used as a medication to treat HIV/AIDS.	4.29	5	0	purine 2',3'-dideoxyribonucleoside	antimetabolite; antiviral drug; EC 2.4.2.1 (purine-nucleoside phosphorylase) inhibitor; geroprotector; HIV-1 reverse transcriptase inhibitor
ganciclovir [no description available]	4.69	8	0	2-aminopurines; oxopurine	antiinfective agent; antiviral drug
valtrex [no description available]	2.08	1	0	organic molecular entity
valacyclovir Valacyclovir: A prodrug of acyclovir that is used in the treatment of HERPES ZOSTER and HERPES SIMPLEX VIRUS INFECTION of the skin and mucous membranes, including GENITAL HERPES.	9.16	4	0	L-valyl ester	antiviral drug
sildenafil sildenafil : A pyrazolo[4,3-d]pyrimidin-7-one having a methyl substituent at the 1-position, a propyl substituent at the 3-position and a 2-ethoxy-5-[(4-methylpiperazin-1-yl)sulfonyl]phenyl group at the 5-position.	3.86	3	0	piperazines; pyrazolopyrimidine; sulfonamide	EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor; vasodilator agent
olanzapine Olanzapine: A benzodiazepine derivative that binds SEROTONIN RECEPTORS; MUSCARINIC RECEPTORS; HISTAMINE H1 RECEPTORS; ADRENERGIC ALPHA-1 RECEPTORS; and DOPAMINE RECEPTORS. It is an antipsychotic agent used in the treatment of SCHIZOPHRENIA; BIPOLAR DISORDER; and MAJOR DEPRESSIVE DISORDER; it may also reduce nausea and vomiting in patients undergoing chemotherapy.. olanzapine : A benzodiazepine that is 10H-thieno[2,3-b][1,5]benzodiazepine substituted by a methyl group at position 2 and a 4-methylpiperazin-1-yl group at position 4.	3.87	3	0	benzodiazepine; N-arylpiperazine; N-methylpiperazine	antiemetic; dopaminergic antagonist; histamine antagonist; muscarinic antagonist; second generation antipsychotic; serotonergic antagonist; serotonin uptake inhibitor
penciclovir penciclovir : A member of the class of 2-aminopurines that is guanine in which the hydrogen at position 9 is substituted by a 4-hydroxy-3-(hydroxymethyl)but-1-yl group. An antiviral drug, it is administered topically for treatment of herpes labialis. A prodrug, famciclovir, is used for oral administration.	2.78	3	0	2-aminopurines; propane-1,3-diols	antiviral drug
oxypurinol Oxypurinol: A xanthine oxidase inhibitor.. alloxanthine : A pyrazolopyrimidine that is 4,5,6,7-tetrahydro-H-pyrazolo[3,4-d]pyrimidine substituted by oxo groups at positions 4 and 6.	2.05	1	0	pyrazolopyrimidine	drug metabolite; EC 1.17.3.2 (xanthine oxidase) inhibitor
raltitrexed [no description available]	3.84	3	0	N-acyl-amino acid
vardenafil vardenafil : The sulfonamide resulting from formal condensation of the sulfo group of 4-ethoxy-3-(5-methyl-7-propylimidazo[5,1-f][1,2,4]triazin-4(1H)-one-2-yl)benzenesulfonic acid and the secondary amino group of 4-ethylpiperazine.	3.58	2	0	imidazotriazine; N-alkylpiperazine; N-sulfonylpiperazine	EC 3.1.4.* (phosphoric diester hydrolase) inhibitor; vasodilator agent
allopurinol Allopurinol: A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.. allopurinol : A bicyclic structure comprising a pyrazole ring fused to a hydroxy-substituted pyrimidine ring.	4.08	4	0	nucleobase analogue; organic heterobicyclic compound	antimetabolite; EC 1.17.3.2 (xanthine oxidase) inhibitor; gout suppressant; radical scavenger
hli 373 [no description available]	2.08	1	0
citrovorum factor [no description available]	3.61	2	0	tetrahydrofolic acid
leucovorin 5-formyltetrahydrofolic acid : A formyltetrahydrofolic acid in which the formyl group is located at position 5.	3.86	3	0	formyltetrahydrofolic acid	Escherichia coli metabolite; mouse metabolite
rifapentine rifapentine: cyclopentyl derivative of rifampicin	3.61	2	0	N-alkylpiperazine; N-iminopiperazine; rifamycins	antitubercular agent; leprostatic drug
4-hydroxyquinazoline 4-oxo-3,4-dihydroquinazoline: structure in first source	2.6	1	0	quinazolines
alanosine [no description available]	2.05	1	0
bl 4162a anagrelide: imidazoquinazoline derivative which lowers platelet count probably by inhibiting thrombopoiesis and reduces platelet aggregation; used for thrombocythemia; structure in first source. anagrelide : A 1,5-dihydroimidazo[2,1-]quinazoline having an oxo substituent at the 2-position and chloro substituents at the 6- and 7-positions.	3.23	1	0	imidazoquinazoline	anticoagulant; antifibrinolytic drug; cardiovascular drug; platelet aggregation inhibitor
forodesine forodesine: structure in first source	4.95	2	1	dihydroxypyrrolidine; pyrrolopyrimidine
tegaserod tegaserod: a nonbenzamide 5-hydroxytryptamine(4) agonist; used in treatment of irritable bowel syndrome; marketing suspended 2007 in US due to higher incidence of MI, stroke, and unstable angina; structure given in first source	3.91	3	0	carboxamidine; guanidines; hydrazines; indoles	gastrointestinal drug; serotonergic agonist
norclozapine norclozapine: structure given in first source. N-desmethylclozapine : A dibenzodoazepine substituted with chloro and piperazino groups which is a major metabolite of clozapine; a potent and selective 5-HT2C serotonin receptor antagonist.	2.6	1	0	dibenzodiazepine; organochlorine compound; piperazines	delta-opioid receptor agonist; metabolite; serotonergic antagonist
pemetrexed pemetrexed disodium : An organic sodium salt that is the disodium salt of N-{4-[2-(2-amino-4-oxo-4,7-dihydro-1H-pyrrolo[2,3-d]pyrimidin-5-yl)ethyl]benzoyl}-L-glutamic acid. Inhibits thymidylate synthase (TS), 421 dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT).	9.54	13	2	N-acyl-L-glutamic acid; pyrrolopyrimidine	antimetabolite; antineoplastic agent; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; EC 2.1.1.45 (thymidylate synthase) inhibitor; EC 2.1.2.2 (phosphoribosylglycinamide formyltransferase) inhibitor
tirapazamine Tirapazamine: A triazine derivative that introduces breaks into DNA strands in hypoxic cells, sensitizing tumor cells to the cytotoxic activity of other drugs and radiation.. tirapazamine : A member of the class of benzotriazines that is 1,2,4-benzotriazine carrying an amino substituent at position 3 and two oxido substituents at positions 1 and 4.	2.45	2	0	aromatic amine; benzotriazines; N-oxide	antibacterial agent; antineoplastic agent; apoptosis inducer
lometrexol lometrexol: RN & structure given in first source;	3.1	1	0
sildenafil citrate Sildenafil Citrate: A PHOSPHODIESTERASE TYPE-5 INHIBITOR; VASODILATOR AGENT and UROLOGICAL AGENT that is used in the treatment of ERECTILE DYSFUNCTION and PRIMARY PULMONARY HYPERTENSION.. sildenafil citrate : The citrate salt of sildenafil.	2.49	2	0	citrate salt	EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor; vasodilator agent
valganciclovir Valganciclovir: A ganciclovir prodrug and antiviral agent that is used to treat CYTOMEGALOVIRUS RETINITIS in patients with AIDS, and for the prevention of CYTOMEGALOVIRUS INFECTIONS in organ transplant recipients who have received an organ from a CMV-positive donor.. valganciclovir : The L-valinyl ester of ganciclovir, into which it is rapidly converted by intestinal and hepatic esterases. It is a synthetic analogue of 2'-deoxyguanosine.	3.58	2	0	L-valyl ester; purines	antiviral drug; prodrug
aprepitant Aprepitant: A morpholine neurokinin-1 (NK1) receptor antagonist that is used in the management of nausea and vomiting caused by DRUG THERAPY, and for the prevention of POSTOPERATIVE NAUSEA AND VOMITING.. aprepitant : A morpholine-based antiemetic, which is or the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of highly emetogenic cancer chemotherapy. Aprepitant is a selective high-affinity antagonist of human substance P/neurokinin 1 (NK1) receptors.	4.43	6	0	(trifluoromethyl)benzenes; cyclic acetal; morpholines; triazoles	antidepressant; antiemetic; neurokinin-1 receptor antagonist; peripheral nervous system drug; substance P receptor antagonist
fosaprepitant fosaprepitant: a pro-drug form of aprepitant. fosaprepitant : A morpholine derivative that is the (1R)-1-[3,5-bis(trifluoromethyl)phenyl]ethyl ether of (3-{[(2R,3S)-3-(4-fluorophenyl)-2-hydroxymorpholin-4-yl]methyl}-5-oxo-4,5-dihydro-1H-1,2,4-triazol-1-yl)phosphonic acid.	3.23	1	0	(trifluoromethyl)benzenes; cyclic acetal; morpholines; phosphoramide; triazoles	antiemetic; neurokinin-1 receptor antagonist; prodrug
tegaserod maleate [no description available]	2.08	1	0	maleate salt	serotonergic agonist
ceftobiprole ceftobiprole: BAL5788 is Ceftobiprole medocaril sodium. ceftobiprole : A fifth-generation cephalosporin antibiotic having (E)-[(3'R)-2-oxo[1,3'-bipyrrolidin]-3-ylidene]methyl and [(2Z)-2-(5-amino-1,2,4-thiadiazol-3-yl)-2-(hydroxyimino)acetyl]amino side groups located at positions 3 and 7 respectively; developed for the treatment of hospital-acquired pneumonia (HAP, excluding ventilator-associated pneumonia, VAP) and community-acquired pneumonia (CAP).	2.04	1	0	cephalosporin; thiadiazoles	antimicrobial agent
rifabutin [no description available]	4.08	4	0
azilsartan azilsartan: an angiotensin type 1 receptor blocker; receptor blocker. azilsartan : A benzimidazolecarboxylic acid that is benzimidazole-7-carboxylic acid substituted at position 2 by a methoxy group and at position 1 by a 2'-[(5-oxo-4,5-dihydro-1,2,4-oxadiazol-3-yl)biphenyl-4-yl]methyl group. Used (as the prodrug, azilsartan medoxomil) for treatment of hypertension.	2.6	1	0	1,2,4-oxadiazole; aromatic ether; benzimidazolecarboxylic acid	angiotensin receptor antagonist; antihypertensive agent
xav939 XAV939: selectively inhibits beta-catenin-mediated transcription; structure in first source. XAV939 : A thiopyranopyrimidine in which a 7,8-dihydro-5H-thiopyrano[4,3-d]pyrimidine skeleton is substituted at C-4 by a hydroxy group and at C-2 by a para-(trifluoromethyl)phenyl group.	2.08	1	0	(trifluoromethyl)benzenes; thiopyranopyrimidine	tankyrase inhibitor
2-carboxyarabinitol 1-phosphate [no description available]	2.08	1	0
hesperadin [no description available]	2.6	1	0
trypan blue Trypan Blue: A diazo-naphthalene sulfonate that is widely used as a stain.. trypan blue : An organosulfonate salt that is the tetrasodium salt of 3,3'-[(3,3'-dimethylbiphenyl-4,4'-diyl)didiazene-2,1-diyl]bis(5-amino-4-hydroxynaphthalene-2,7-disulfonic acid).	2.07	1	0
nintedanib nintedanib : A member of the class of oxindoles that is a kinase inhibitor used (in the form of its ethylsulfonate salt) for the treatment of idiopathic pulmonary fibrosis and cancer.	2.08	1	0
zd 9331 ZD 9331: BGC9331 was formerly known as ZD9331; structure in first source	2.01	1	0
6-bromoindirubin-3'-acetoxime 6-bromoindirubin-3'-acetoxime: a synthetic derivative of a compound from the Mediterranean mollusk Hexaplex trunculus, protects cells from varicella infection	2.6	1	0
amg531 [no description available]	3.14	1	0
n'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthahydrazide [no description available]	2.6	1	0	catechols; hydrazide; hydrazone; naphthols	EC 3.6.5.5 (dynamin GTPase) inhibitor
ver 52296 luminespib : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 5-(2,4-dihydroxy-5-isopropylphenyl)-4-[4-(morpholin-4-ylmethyl)phenyl]-1,2-oxazole-3-carboxylic acid with the amino group of ethylamine.	2.08	1	0	aromatic amide; isoxazoles; monocarboxylic acid amide; morpholines; resorcinols	angiogenesis inhibitor; antineoplastic agent; Hsp90 inhibitor
levomefolate calcium levomefolate calcium: an ingredient in Contraceptives, Oral, Combined. levomefolate calcium : An organic calcium salt of (6S)-5-methyltetrahydrofolic acid.	3.23	1	0	organic calcium salt	antidepressant
sb-590885 N-{5-[2-{4-[2-(dimethylamino)ethoxy]phenyl}-4-(pyridin-4-yl)-1H-imidazol-5-yl]-2,3-dihydro-1H-inden-1-ylidene}hydroxylamine : A ketoxime that is the oxime of indan-1-one in which the hydrogen at position 5 has been replaced by an imidazol-5-yl group which has itself been substituted at positions 2 and 4 by p-[2-(dimethylamino)ethoxy]phenyl and pyridin-4-yl groups, respectively.	2.08	1	0	aromatic ether; imidazoles; ketoxime; pyridines; tertiary amino compound
XL413 XL413 : A benzofuropyrimidine that is 3,4-dihydro[1]benzofuro[3,2-d]pyrimidine substituted by (2S)-pyrrolidin-2-yl, oxo and chloro groups at positions 2, 4, and 8, respectively. It is a potent ATP competitive inhibitor of Cdc7 kinase (IC50 = 3.4 nM) and exhibits anticancer properties.	2.6	1	0	benzofuropyrimidine; organochlorine compound; pyrrolidines	antineoplastic agent; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor
pf-477736 PF 00477736: a Chk1 inhibitor; structure in first source. PF-00477736 : A diazepinoindole that is 8-amino-4,5-dihydro-6H-[1,2]diazepino[4,5,6-cd]indol-6-one which is substituted at position 2 by a 1-methylpyrazol-4-yl group and in which the amino group at position 8 has undergone condensation with the carboxy group of (2R)-2-cyclohexylglycine to give the corresponding carboxamide. It is an inhibitor of checkpoint kinase 1 (Chk 1).	2.08	1	0
pp242 torkinib : A member of the class of pyrazolopyrimidines that is 1H-pyrazolo[3,4-d]pyrimidine substituted by isopropyl, 5-hydroxyindol-2-yl and amino groups at positions 1, 3 and 4 respectively. It is a potent inhibitor of mTOR and exhibits anti-cancer properties.	2.08	1	0	aromatic amine; biaryl; hydroxyindoles; phenols; primary amino compound; pyrazolopyrimidine	antineoplastic agent; mTOR inhibitor
defibrotide defibrotide: Single-stranded polydeoxyribonucleotide extracted from mammalian organs and used in the treatment of HEPATIC VENO-OCCLUSIVE DISEASE in patients with kidney or lung abnormalities following HEMATOPOIETIC STEM CELL TRANSPLANTATION	2.02	1	0
me0328 ME0328: inhibits ARTD3; structure in first source	2.6	1	0
fenobam fenobam: in USAN fenobam refers to monohydrate	2.08	1	0	ureas
nvp-tnks656 [no description available]	2.6	1	0
syringolin b syringolin B: a proteasome inhibitor isolated from Pseudomonas syringae; structure in first source	2.07	1	0
salarin c salarin C: has antineoplastic activity; isolated from the sponge Fascaplysinopsis; structure in first source	2.13	1	0
leptin Leptin: A 16-kDa peptide hormone secreted from WHITE ADIPOCYTES. Leptin serves as a feedback signal from fat cells to the CENTRAL NERVOUS SYSTEM in regulation of food intake, energy balance, and fat storage.	4.8	1	1
pyrimidinones Pyrimidinones: Heterocyclic compounds known as 2-pyrimidones (or 2-hydroxypyrimidines) and 4-pyrimidones (or 4-hydroxypyrimidines) with the general formula C4H4N2O.	6.09	8	1
phenanthrenes Phenanthrenes: POLYCYCLIC AROMATIC HYDROCARBONS composed of three fused BENZENE rings.. phenanthrenes : Any benzenoid aromatic compound that consists of a phenanthrene skeleton and its substituted derivatives thereof.	2.76	3	0

bortezomib

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Change in Patterns of Gene Expression Pre- and Post-treatment Performed by GeneChip Analysis

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The Primary Endpoint of This Trial is the Proportion of Patients Alive at 1 Year. Phase II Patients Only.

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