Page last updated: 2024-12-05

mitoxantrone

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth Market Indicators

Description

Mitoxantrone is a synthetic anthracenedione antineoplastic agent. Its synthesis involves a multi-step process, starting from anthraquinone. It acts by inhibiting DNA topoisomerase II, an enzyme essential for DNA replication and repair. This inhibition leads to double-strand DNA breaks, ultimately causing cell death. Mitoxantrone is used in the treatment of various cancers, including acute non-lymphocytic leukemia, breast cancer, and multiple myeloma. Its importance lies in its ability to target rapidly dividing cells, making it effective against cancers. The study of mitoxantrone continues to focus on optimizing its therapeutic efficacy, reducing its side effects, and exploring its potential applications in other diseases. This ongoing research aims to improve patient outcomes and develop novel therapeutic strategies.'

Mitoxantrone: An anthracenedione-derived antineoplastic agent. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

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. [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]

Cross-References

ID SourceID
PubMed CID4212
CHEMBL ID58
CHEBI ID50729
SCHEMBL ID3000
MeSH IDM0013954

Synonyms (166)

Synonym
smr001549953
mitoxantrone, mitoxantrone hydrochloride, mitoxantrone dihydrochloride, mitoxanthrone hydrochloride
BIDD:PXR0181
9,10-anthracenedione, 1,4-dihydroxy-5,8-bis((2-((2-hydroxyethyl)amino)ethyl)amino)-
1,4-dihydroxy-5,8-bis(5-hydroxy-3-azapentylamino)anthrachinon
mitoxantronum [inn-latin]
5,8-bis((2-((2-hydroxyethyl)amino)ethyl)amino)-1,4-dihydroxyanthraquinone
mitoxantrone [inn]
1,4-dihydroxy-5,8-bis(2-((2-hydroxyethyl)amino)ethylamino)-9,10-anthracenedione
mitozantrone
anthraquinone, 5,8-bis((2-((2-hydroxyethyl)amino)ethyl)amino)-1,4-dihydroxy-
brn 2795126
mitoxanthrone ,
mitoxantrona [inn-spanish]
nsc 279836
ccris 7604
mitoxantron
MLS001333711 ,
AKOS005564036
AB00053716-18
AB00053716-19
BRD-K21680192-300-05-2
ksc-19-204
KUC108634N
smr000058480
MIX ,
1,4-dihydroxy-5,8-bis({2-[(2-hydroxyethyl)amino]ethyl}amino)-9,10-anthracenedione
KBIO1_000516
DIVK1C_000516
NCI60_002535
NCI60_002276
SPECTRUM_001655
BSPBIO_003160
lopac-m-6545
cas-70476-82-3
NCGC00015693-01
NCGC00015693-02
LOPAC0_000779
IDI1_000516
nsc301739
dhad
nsc299195
1,4-dihydroxy-5,8-bis[[2-[(2-hydroxyethyl)amino]ethyl]amino]-9,10-anthracenedione
nsc279836
1,4-dihydroxy-5,8-bis[2-(2-hydroxyethylamino)ethylamino]anthracene-9,10-dione
dhaq (*diacetate salt*)
9, 1,4-dihydroxy-5,8-bis[[2-[(2-hydroxyethyl)amino]ethyl] amino]-
mls002703044 ,
mitoxantrone (free base)
nsc-279836
BPBIO1_000627
PRESTWICK3_000385
NEURO_000153
SPECTRUM5_001205
mitoxantronum
1,4-dihydroxy-5,8-bis({2-[(2-hydroxyethyl)amino]ethyl}amino)anthracene-9,10-dione
mitoxantrona
CHEBI:50729 ,
dhaq
AB00053716
65271-80-9
mitoxantrone
1,4-bis(2-(2-hydroxyethylamino)ethyl)amino)-5,8-dihydroxyanthraquinone
DB01204
2FUM
SMP2_000179
KBIO2_002135
KBIO2_007271
KBIO2_004703
KBIO3_002660
KBIOSS_002135
KBIOGR_001531
SPBIO_002490
SPECTRUM2_000908
PRESTWICK1_000385
NINDS_000516
SPECTRUM4_000866
SPECTRUM3_001590
PRESTWICK0_000385
SPBIO_000756
PRESTWICK2_000385
BSPBIO_000569
NCGC00162251-01
HMS2090D05
BRD-K21680192-300-07-8
NCGC00015693-04
SR-01000076001-7
sr-01000076001
VU0244399-2
misostol
CHEMBL58
misostol (tn)
mitoxantrone (inn)
D08224
STK631833
9,10-anthracenedione, 1,4-dihydroxy-5,8-bis[[2-[(2-hydroxyethyl)amino]ethyl]amino]-
CCG-36371
NCGC00015693-03
NCGC00015693-06
NCGC00015693-05
BRD-K21680192-001-01-5
BCP9000931
unii-bz114nvm5p
mitoxantrone [inn:ban]
bz114nvm5p ,
FT-0630752
BRD-K21680192-001-11-4
S1889
NCGC00015693-08
BRD-K21680192-300-10-2
BRD-K21680192-300-12-8
gtpl7242
1,4-dihydroxy-5,8-bis({2-[(2-hydroxyethyl)amino]ethyl}amino)-9,10-dihydroanthracene-9,10-dione
1,4-bis[2-(2-hydroxyethylamino)ethylamino]-5,8-dihydroxyanthraquinone
1,4-dihydroxy-5,8-bis[[2-(2-hydroxyethylamino)ethyl]amino]anthraquinone
1,4-bis[2-(2-hydroxyethylamino)-ethylamino]-5,8-dihydroxyanthraquinone
mitoxantrone [iarc]
mitoxantrone [vandf]
mitoxantrone [mi]
mitoxantrone [who-dd]
HY-13502
SCHEMBL3000
AB00053716-22
DTXSID4046947 ,
immunex (salt/mix)
1,4-dihydroxy-5,8-bis-[[2-[(2-hydroxyethyl)amino]ethyl]amino]anthraquinone
mitoxantrone hydrochloride (salt/mix)
1,4-bis[2-(2-hydroxyethylamino)ethylamino]-5,8-bis(oxidanyl)anthracene-9,10-dione;hydrochloride
cid_4212
bdbm67690
1,4-dihydroxy-5,8-bis[2-(2-hydroxyethylamino)ethylamino]-9,10-anthraquinone;hydrochloride
cid_5458171
1,4-dihydroxy-5,8-bis[2-(2-hydroxyethylamino)ethylamino]anthracene-9,10-dione;hydrochloride
AB00053716_24
AB00053716_23
HMS3655E20
SBI-0050757.P003
SW196745-6
1,4-dihydroxy-5,8-bis(2-(2-hydroxyethylamino)ethylamino)anthracene-9,10-dione
mitoxantrone; 1,4-dihydroxy-5,8-bis({2-[(2-hydroxyethyl)amino]ethyl}amino)anthra-9,10-quinone
M3133
1,4-dihydroxy-5,8-bis[[2-[(2-hydroxyethyl)amino]ethyl]amino]anthracene-9,10-dione
SY226320
mfcd00242942
FT-0672423
1,4-dihydroxy-5,8-bis((2-((2-hydroxyethyl)amino)ethyl)amino)anthracene-9,10-dione
AS-35321
Q239426
BCP02861
BRD-K21680192-300-09-4
SDCCGSBI-0050757.P004
mitoxantrone free base
NCGC00015693-23
65271-80-9 (free base)
NCGC00015693-13
mitoxantrone base
EN300-117257
1,4-dihydroxy-5,8-bis((2-((2-hydroxyethyl)amino)ethyl)amino)-9,10-anthracenedione
1,3-dihydroxy-5,8-bis((2-((2-hydroxyethyl)amino)ethyl)amino)-9, 10-anthracenedione
mitoxantronum (inn-latin)
l01db07
mitoxantrona (inn-spanish)
dtxcid2026947
mitoxantrone (iarc)
dihydroxyanthracenedione
1,4-dihydroxy-5,8-bis((2-((2-hydroxyethyl)amino)ethyl)amino)-9, 10-anthroquinone

Research Excerpts

Overview

Mitoxantrone is an anticancer anthracenedione that can be activated by formaldehyde to generate covalent drug-DNA adducts. It is a topoisomerase II inhibitor that binds and intercalates with DNA, being used in the treatment of several cancers and multiple sclerosis.

ExcerptReferenceRelevance
"Mitoxantrone is an anticancer anthracenedione that can be activated by formaldehyde to generate covalent drug-DNA adducts. "( Formaldehyde-activated WEHI-150 induces DNA interstrand crosslinks with unique structural features.
Collins, JG; Cutts, SM; Evison, BJ; Kelso, C; Konda, SK; Medan, J; Phillips, DR; Pumuye, PP; Sleebs, BE; Watson, K, 2020
)
2
"Mitoxantrone (MTX) is a topoisomerase II inhibitor used to treat a wide range of tumors and multiple sclerosis but associated with potential neurotoxic effects mediated by hitherto poorly understood mechanisms. "( Chemobrain: mitoxantrone-induced oxidative stress, apoptotic and autophagic neuronal death in adult CD-1 mice.
Bastos, ML; Capela, JP; Carvalho, F; Costa, VM; Dias-Carvalho, A; Fernandes, E; Ferreira, M; Ferreira, R; Reis-Mendes, A; Sá, SI, 2022
)
2.54
"Mitoxantrone (MTX) is an antineoplastic agent used to treat advanced breast cancer, prostate cancer, acute leukemia, lymphoma and multiple sclerosis. "( Autophagy (but not metabolism) is a key event in mitoxantrone-induced cytotoxicity in differentiated AC16 cardiac cells.
Carvalho, F; Costa, VM; de Lourdes Bastos, M; Reis-Mendes, A; Remião, F; Sousa, E, 2023
)
2.61
"Mitoxantrone (MXN) is a synthetic anthracenedione oncogenic therapy. "( An eco-friendly matrix-augmented fluorescence spectroscopic approach for the analysis of mitoxantrone, an oncogenic therapy; application to the dosage form and biological matrices.
Abourehab, MAS; Derayea, SM; Eltoukhi, WE; Hamad, AA; Hassan, YF; Mohammed, BS, 2023
)
2.57
"Mitoxantrone (MX) is a robust chemotherapeutic with well-characterized applications in treating certain leukemias and advanced breast and prostate cancers. "( Design, synthesis, and evaluation of a mitoxantrone probe (MXP) for biological studies.
Borgstahl, GEO; Natarajan, A; Singh, S; Wallin, S, 2023
)
2.62
"Mitoxantrone (MTX) is a topoisomerase II inhibitor that binds and intercalates with DNA, being used in the treatment of several cancers and multiple sclerosis."( A Clinically Relevant Dosage of Mitoxantrone Disrupts the Glutathione and Lipid Metabolic Pathways of the CD-1 Mice Brain: A Metabolomics Study.
Carvalho, F; Costa, VM; Dias-Carvalho, A; Fernandes, E; Guedes de Pinho, P; Margarida-Araújo, A; Pereira, SA; Reis-Mendes, A; Sá, SI; Sequeira, CO, 2023
)
1.92
"Mitoxantrone is a chemotherapeutic agent approved for various diseases. "( A case of mitoxantrone extravasation.
Chang, A, 2020
)
2.4
"Mitoxantrone (MTX) is a synthetic compound used as a second line chemotherapeutic drug for prostate cancer. "( Mitoxantrone triggers immunogenic prostate cancer cell death via p53-dependent PERK expression.
Huo, H; Li, B; Li, C; Lian, F; Liu, F; Liu, Q; Qi, Z; Sun, H; Wang, Y; Wei, W; Ying, K; Zhang, Y, 2020
)
3.44
"Mitoxantrone (MTX) is an antitumor drug that can block type II topoisomerase."( miR-130-3p Promotes MTX-Induced Immune Killing of Hepatocellular Carcinoma Cells by Targeting EPHB4.
Jia, M; Shao, L; Ye, Q, 2021
)
1.34
"Mitoxantrone (MXT) is an androstenedione that is used to treat cancers and progressive forms of multiple sclerosis; however, its use is limited by its cardiotoxicity. "( Pituitary adenylate cyclase-activating polypeptide (PACAP) protects against mitoxantrone-induced cardiac injury in mice.
Bradley, J; Burn, B; Chuang, G; Coy, DH; Maderdrut, JL; Subramaniam, V; Varner, KJ; Xia, H, 2017
)
2.13
"Mitoxantrone (MIT) is an anticancer agent with photosensitive properties that is commonly used in various cancers. "( Polymeric mixed micelles loaded mitoxantrone for overcoming multidrug resistance in breast cancer via photodynamic therapy.
Cai, Y; Chen, M; Li, Z; Yu, H; Zhao, Y; Zhou, H, 2017
)
2.18
"Mitoxantrone (MTX) is an antracycline antibiotic that is used in oncologic treatment of breast, prostate, liver, ovarian and stomach cancer."( BLOOD COUNT IN PATIENTS WITH MULTIPLE SCLEROSIS TREATED WITH MITOXANTRONE IN SHORT TIME OBSERVATION.
Pastuszak, Z; Piusinska-Macoch, R; Stepien, A; Tomczykiewicz, K, 2016
)
1.4
"Mitoxantrone (MTO) is a topoisomerase II inhibitor which has been used to treat various forms of cancer either as a solo chemotherapy regimen or as a component in cocktail treatments. "( Tobacco mosaic virus delivery of mitoxantrone for cancer therapy.
Lin, RD; Steinmetz, NF, 2018
)
2.2
"Mitoxantrone (MTX) is an antitumor agent that causes cardiotoxicity in 18 % patients. "( The metabolic profile of mitoxantrone and its relation with mitoxantrone-induced cardiotoxicity.
Arbo, MD; Costa, VM; de Freitas, V; de Lourdes Bastos, M; de Pinho, PG; Palmeira, C; Remião, F; Rossato, LG; Vilain, L, 2013
)
2.14
"Mitoxantrone is a promising antitumor drug having considerably reduced cardiotoxicity as compared to anthracyclines. "( NMR-based structure of anticancer drug mitoxantrone stacked with terminal base pair of DNA hexamer sequence d-(ATCGAT)2.
Awasthi, P; Barthwal, R; Dogra, S; Nair, MS; Pradeep, TP; Tripathi, S, 2014
)
2.11
"Mitoxantrone is an effective disease-modifying therapy in multiple sclerosis (MS), but its use is limited by cardiotoxicity. "( Subclinical myocardial dysfunction in multiple sclerosis patients remotely treated with mitoxantrone: evidence of persistent diastolic dysfunction.
Goggin, C; Joyce, E; Lynch, T; Mahon, N; McGorrian, C; Melling, J; Mulroy, E; O'Rourke, K; Scott, J, 2013
)
2.05
"Mitoxantrone (MTX) is a chemotherapeutic agent that emerged as an alternative to anthracycline therapy. "( Therapeutic concentrations of mitoxantrone elicit energetic imbalance in H9c2 cells as an earlier event.
Costa, VM; de Lourdes Bastos, M; Palmeira, C; Remião, F; Rolo, A; Rossato, LG; Vilas-Boas, V, 2013
)
2.12
"Mitoxantrone (MTX) is a chemotherapeutic agent, which presents late irreversible cardiotoxicity. "( Mitochondrial cumulative damage induced by mitoxantrone: late onset cardiac energetic impairment.
Amado, F; Arbo, M; Costa, VM; Dallegrave, E; de Lourdes Bastos, M; Dinis-Oliveira, RJ; Duarte, JA; Ferreira, R; Palmeira, C; Remião, F; Rossato, LG; Silva, R, 2014
)
2.11
"Mitoxantrone (MTX) is an antineoplastic agent that can induce hepato- and haematotoxicity. "( Cumulative mitoxantrone-induced haematological and hepatic adverse effects in a subchronic in vivo study.
Arbo, M; Costa, VM; Dallegrave, E; de Lourdes Bastos, M; Dinis-Oliveira, RJ; Duarte, JA; Palmeira, C; Remião, F; Rossato, LG; Santos-Silva, A, 2014
)
2.23
"Mitoxantrone is a reasonable replacement for daunorubicin in times of drug shortage."( Mitoxantrone as a substitute for daunorubicin during induction in newly diagnosed lymphoblastic leukemia and lymphoma.
Bergsagel, J; Cooper, T; Daves, M; Keller, F; Lew, G; Nickel, RS; Sabnis, H, 2014
)
2.57
"Mitoxantrone is an antineoplastic agent approved for clinical use in the secondary progressive phase of multiple sclerosis (MS). "( [Mitoxantrone - an anthraquinone antibiotic with antitumor activity applied for the treatment of multiple sclerosis].
Szwed, M, 2014
)
2.76
"Mitoxantrone is an immunosuppressive drug approved for aggressive relapsing and progressive multiple sclerosis. "( The current role of mitoxantrone in the treatment of multiple sclerosis.
Cocco, E; Marrosu, MG, 2014
)
2.17
"Mitoxantrone is a conventional agent for relapsed or refractory acute lymphoblastic leukemia (ALL). "( Clinical efficacy of mitoxantrone and Ara-C with or without etoposide salvage chemotherapy in adult patients with relapsed or refractory acute lymphoblastic leukemia: retrospective multicenter study of the Korean Adult ALL Working Party.
Ahn, JS; Chung, JS; Jo, DY; Joo, YD; Jung, SH; Kim, DY; Kim, I; Lee, JJ; Lee, KH; Moon, JH; Park, S; Shin, HJ; Sohn, SK; Song, IC; Yang, DH, 2015
)
2.18
"Mitoxantrone is a synthetic anthracenedione originally developed to improve the therapeutic profile of the anthracyclines and is commonly applied in the treatment of breast and prostate cancers, lymphomas, and leukemias. "( Mitoxantrone, More than Just Another Topoisomerase II Poison.
Cutts, SM; Evison, BJ; Phillips, DR; Sleebs, BE; Watson, KG, 2016
)
3.32
"Mitoxantrone (MXT) is an anticancer drug structurally related to anthracyclines, such as doxorubicin (DOX). "( Influence of nucleotide excision repair on mitoxantrone cytotoxicity.
Busatto, FF; de Souza, LK; Rocha, JC; Saffi, J, 2016
)
2.14
"Mitoxantrone (MIT) is a chemotherapeutic agent with promising anticancer efficacy. "( Vitamin E succinate-conjugated F68 micelles for mitoxantrone delivery in enhancing anticancer activity.
Chen, M; Fan, L; He, C; Li, H; Li, P; Liu, Y; Wan, JB; Wu, M; Xu, Y, 2016
)
2.13
"Mitoxantrone is a highly cytotoxic antineoplastic drug, however, its poor penetration of the blood-brain barrier has limited its role in the treatment of brain cancers. "( Safety, feasibility, and optimization of intra-arterial mitoxantrone delivery to gliomas.
Bigio, IJ; Bruce, JN; Cooke, J; Ellis, JA; Emala, CW; Joshi, S; Singh-Moon, RP; Wang, M, 2016
)
2.12
"Mitoxantrone (MTX) is an antineoplastic agent used to treat several types of cancers and on multiple sclerosis, which shows a high incidence of cardiotoxicity. "( Naphthoquinoxaline metabolite of mitoxantrone is less cardiotoxic than the parent compound and it can be a more cardiosafe drug in anticancer therapy.
Bastos, ML; Carvalho, F; Carvalho, RA; Costa, VM; Gomes, AS; Pinto, M; Reis-Mendes, A; Remião, F; Sousa, E, 2017
)
2.18
"Mitoxantrone is a synthetic anticancer drug used clinically in the treatment of different types of cancer. "( Mitoxantrone-Surfactant Interactions: A Physicochemical Overview.
Enache, M; Enache, MI; Toader, AM, 2016
)
3.32
"Mitoxantrone (MTO) is a potent drug used to treat breast cancer; however, efforts to expand its clinical applicability have been restricted because of its high risk for cardiotoxicity. "( Mitoxantrone- and Folate-TPGS2k Conjugate Hybrid Micellar Aggregates To Circumvent Toxicity and Enhance Efficiency for Breast Cancer Therapy.
Chen, M; Guissi, NE; Li, H; Ping, Q; Semcheddine, F; Su, Z; Xu, Y, 2017
)
3.34
"Mitoxantrone is an effective drug used for acute leukemias."( [Effects of mitoxantrone on the activity of human protein kinase CK2 holoenzyme].
Chen, XW; Li, CM; Liang, NC; Lin, XC; Liu, XG, 2008
)
1.45
"Mitoxantrone is a strong inhibitor of recombinant human protein kinase CK2 in vitro. "( [Effects of mitoxantrone on the activity of human protein kinase CK2 holoenzyme].
Chen, XW; Li, CM; Liang, NC; Lin, XC; Liu, XG, 2008
)
2.17
"Mitoxantrone (MTX) is a clinically used antitumor anthracycline, which is made available to the target tissues by transport protein human serum albumin (HSA). "( Interaction of mitoxantrone with human serum albumin: spectroscopic and molecular modeling studies.
Islam, B; Khan, AU; Khan, SN; Subbarao, N; Sultan, A; Yennamalli, R, 2008
)
2.14
"Mitoxantrone (MX) is a potent immunosuppressant for the treatment of active MS."( Mitoxantrone does not restore the impaired suppressive function of natural regulatory T cells in patients suffering from multiple sclerosis. A longitudinal ex vivo and in vitro study.
Diener, HC; Grosse-Wilde, H; Kreuzfelder, E; Kumar, M; Limmroth, V; Putzki, N, 2009
)
2.52
"Mitoxantrone is a potent antitumor drug, widely used in the treatment of various cancers. "( Studies on the binding affinity of anticancer drug mitoxantrone to chromatin, DNA and histone proteins.
Hajihassan, Z; Rabbani-Chadegani, A, 2009
)
2.05
"Mitoxantrone is an approved disease modifying agent for treatment of multiple sclerosis (MS). "( Efficacy and safety of mitoxantrone, as an initial therapy, in multiple sclerosis: experience in an Indian tertiary care setting.
Geeta, S; Hundalani, SG; Menon, S; Singhal, BS,
)
1.88
"Mitoxantrone (MTX) is a synthetic antineoplastic cytotoxic drug, active both on proliferative and non-proliferative cells. "( Mitoxantrone: benefits and risks in multiple sclerosis patients.
Comi, G; Martinelli, V; Radaelli, M; Rodegher, M; Straffi, L, 2009
)
3.24
"Mitoxantrone is a cytotoxic drug with immune modulatory properties used in the treatment of progressive forms of multiple sclerosis (MS). "( Mitoxantrone treatment in multiple sclerosis induces TH2-type cytokines.
Bröker, BM; Dressel, A; Rosenberg, S; Skrzipek, S; Vogelgesang, A, 2010
)
3.25
"Mitoxantrone (MTX) is an immunosuppressive drug approved for multiple sclerosis (MS) treatment."( Comparative study of mitoxantrone efficacy profile in patients with relapsing-remitting and secondary progressive multiple sclerosis.
Comi, G; Esposito, F; Martinelli Boneschi, F; Martinelli, V; Moiola, L; Radaelli, M; Rocca, MA; Rodegher, M; Sormani, MP, 2010
)
2.12
"Mitoxantrone is an anticancer agent that acts as a topoisomerase II poison, however, it can also be activated by formaldehyde to form DNA adducts. "( New anthracenedione derivatives with improved biological activity by virtue of stable drug-DNA adduct formation.
Bilardi, RA; Buck, DP; Collins, JG; Cutts, SM; Evison, BJ; Mansour, OC; Nudelman, A; Phillips, DR; Rephaeli, A; Sleebs, BE; Watson, KG, 2010
)
1.8
"Mitoxantrone (MX) is a potent immunosuppressant that is licensed as escalation therapy for the treatment of active multiple sclerosis (MS)."( Stability of cognitive functions under mitoxantrone therapy in patients with progressive multiple sclerosis: a pilot analysis.
Gold, R; Klotz, P; Lee, DH; Linker, RA; Schröder, A, 2011
)
2.08
"Mitoxantrone is a cytotoxic drug approved for the treatment of MS with adverse effects associated potentially with an increased level of oxidative stress."( Paraoxonase 1 activity in multiple sclerosis patients during mitoxantrone therapy.
Bartosik-Psujek, H; Beltowski, J; Jamroz-Wisniewska, A; Stelmasiak, Z, 2013
)
1.35
"Mitoxantrone is an anthracycline analog with presumed better antineoplastic activity and lesser toxicity."( A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone.
Błasiak, J; Gloc, E; Warszawski, M, 2002
)
1.26
"Mitoxantrone is an anticancer agent for which it is important to know the concentration in blood during therapy. "( Quantitative analysis of mitoxantrone by surface-enhanced resonance Raman scattering.
MacMillan, D; McCardle, C; McLaughlin, C; Smith, WE, 2002
)
2.06
"Mitoxantrone is a drug with potent in vitro activity against malignant brain tumor cell lines; however, its effectiveness as a systemic agent has been hampered by poor central nervous system penetration and dose-limiting myelosuppression. "( Local delivery of mitoxantrone for the treatment of malignant brain tumors in rats.
Brem, H; DiMeco, F; Li, KW; Olivi, A; Tyler, BM; Wolf, AS, 2002
)
2.09
"Mitoxantrone is a recently approved drug for patients with secondary progressive multiple sclerosis (SPMS). "( Rapid onset mitoxantrone-induced cardiotoxicity in secondary progressive multiple sclerosis.
Abbey, EE; Avasarala, JR; Clifford, DB; Cross, AH; Siegel, BA; Singer, BA, 2003
)
2.14
"Mitoxantrone is an anthracenedione, which is active in NHL and its toxicity profile may be more favorable than doxorubicin with respect to alopecia, mucositis and cardiotoxicity."( A randomized trial comparing intensified CNOP vs. CHOP in patients with aggressive non-Hodgkin's lymphoma.
Angelopoulou, MK; Bourantas, KL; Christopoulos, G; Grigorakis, V; Kalmantis, T; Kokkinis, G; Korantzis, J; Michalis, E; Mihalakeas, I; Pangalis, GA; Papayiannis, A; Repousis, P; Roussou, P; Siakantaris, MP; Stamatellou, M; Stefanoudakis, E; Symeonidis, A; Vassilakopoulos, TP; Vrakidou, E, 2003
)
1.04
"Mitoxantrone is an antineoplastic agent that exerts a potent immunosuppresive effect, including suppression of B cell immunity and reduction of T cell numbers. "( [Mitoxantrone].
Montalban, X; Pericot, I,
)
2.48
"Mitoxantrone (Mx) is a drug well known for its antiproliferative properties and is used clinically in oncology and in the treatment of relapsing multiple sclerosis."( The effect of mitoxantrone on anti-pig immunization in baboons.
Ashton-Chess, J; Barreau, N; Blancho, G; Boulday, G; Edan, G; Le Berre, L; Minault, D; Petzold, T; Roussel, JC; Soulillou, JP, 2003
)
1.4
"As mitoxantrone is a recently approved immunosuppressant for managing multiple sclerosis, the number of patients treated with this effective but potentially cardiotoxic anthracenedione derivative will increase substantially. "( Non-invasive functional and biochemical assessment of mitoxantrone cardiotoxicity in patients with multiple sclerosis.
Beer, M; Ertl, G; Gold, R; Hahn, D; Köstler, H; Sandstede, J; Spindler, M; Strotmann, J; Voelker, W; Weilbach, F, 2003
)
1.19
"Mitoxantrone is an immunosuppressive drug usually delivered in severe relapsing remitting multiple sclerosis. "( [Acute heart failure in a patient treated by mitoxantrone for multiple sclerosis].
Ali Chérif, A; Eusebio, A; Feuillet, L; Guedj, E; Malikova, I; Mundler, O; Pelletier, J, 2003
)
2.02
"Mitoxantrone is a rescue therapy reserved to patients with an aggressive, rapidly progressive form of the disease."( A comparison of the benefits of mitoxantrone and other recent therapeutic approaches in multiple sclerosis.
Gonsette, RE, 2004
)
1.33
"Mitoxantrone is a member of the anthracendione family developed to treat malignancies and increasingly used to treat multiple sclerosis (MS). "( Rationale for the use of mitoxantrone in multiple sclerosis.
Edan, G; Le Page, E; Morrissey, S, 2004
)
2.07
"Mitoxantrone (MX) is a cytotoxic drug with proven clinical efficacy in active multiple sclerosis (MS). "( Mitoxantrone induces cell death in peripheral blood leucocytes of multiple sclerosis patients.
Chan, A; Gold, R; Toyka, KV; Weilbach, FX, 2005
)
3.21
"Mitoxantrone is a synthetic anthracenedione recently approved by the FDA for the treatment of worsening relapsing-remitting (RR), secondary progressive (SP), and progressive relapsing (PR) multiple sclerosis (MS). "( Review of mitoxantrone in the treatment of multiple sclerosis.
Herndon, R; Jeffery, DR, 2004
)
2.17
"Mitoxantrone is an approved drug for patients with worsening relapsing-remitting, secondary progressive and progressive relapsing multiple sclerosis (MS). "( Severe delayed heart failure in three multiple sclerosis patients previously treated with mitoxantrone.
Goffette, S; Morandini, E; Sindic, CJ; van Pesch, V; Vanoverschelde, JL, 2005
)
1.99
"Mitoxantrone is an useful and clinically effective drug in MS and its major limitation is the potencial cardiotoxicity due to cumulative dose (140 mg)."( Mitoxantrone in secondarily progressive multiple sclerosis: a series of 18 patients.
Arruda, WO; de Oliveira, Mde S; Montú, MB; Ramina, R, 2005
)
2.49
"Mitoxantrone (MX) is an immunosupressant drug used in secondarily progressive multiple sclerosis (SPMS) and in relapsing-remitting multiple sclerosis (RRMS). "( Acute myeloid leukaemia induced by mitoxantrone: case report.
Arruda, WO; de Oliveira, Mde S; Montú, MB; Ramina, R, 2005
)
2.05
"Mitoxantrone is an anti-neoplastic anthracenedione derivative that, based on its immunosuppressive properties, is approved for the treatment of severe forms of relapsing-remitting or secondary progressive multiple sclerosis (MS). "( Multiple sclerosis: Mitoxantrone promotes differential effects on immunocompetent cells in vitro.
Archelos, JJ; Hartung, HP; Hemmer, B; Kieseier, BC; Neuhaus, O; Stüve, O; Wiendl, H, 2005
)
2.09
"Mitoxantrone is a synthetic anthracenedione, recently approved for the treatment of worsening multiple sclerosis, which is known to induce cardiotoxicity."( Evaluation of the myocardial performance index for early detection of mitoxantrone-induced cardiotoxicity in patients with multiple sclerosis.
Borghetti, A; Montanari, E; Moruzzi, P; Pattoneri, P; Pelà, G; Pesci, I, 2007
)
1.29
"Mitoxantrone is an antineoplastic drug, recently approved for treatment of multiple sclerosis."( Mitoxantrone-induced cardiotoxicity in patients with multiple sclerosis.
Etemadifar, M; Hamzehloo, A, 2006
)
2.5
"Mitoxantrone is an antineoplastic agent also used for the treatment of multiple sclerosis (MS). "( In vivo effects of mitoxantrone on the production of pro- and anti-inflammatory cytokines by peripheral blood mononuclear cells of secondary progressive multiple sclerosis patients.
Angelucci, F; Batocchi, AP; Caggiula, M; Frisullo, G; Mirabella, M; Nociti, V; Patanella, K; Sancricca, C; Tonali, PA, 2006
)
2.1
"Mitoxantrone is a DNA topoisomerase II poison commonly used for the treatment of hormone-refractory prostate cancer. "( Mitoxantrone-related acute myeloblastic leukaemia in a patient with metastatic hormone-refractory prostate cancer.
Bouscary, D; Dômont, J; Goldwasser, F; Martinez, V; Mir, O, 2007
)
3.23
"Mitoxantrone is an antineoplastic agent considered a potential human teratogen because of its mechanism of action and is classified by the US Food and Drug Administration in pregnancy category risk D. "( The first case of mitoxantrone exposure in early pregnancy.
Batocchi, AP; Caruso, A; Cavaliere, AF; De Santis, M; Rosati, P; Straface, G, 2007
)
2.12
"Mitoxantrone (MXR) is a prototypical substrate for the ABCG2 (bcrp1) efflux transporter and is often used as a positive control in bcrp-mediated transport studies. "( Mitoxantrone permeability in MDCKII cells is influenced by active influx transport.
Elmquist, WF; Pan, G,
)
3.02
"Mitoxantrone (MTX) is a water-soluble anticancer drug that poorly penetrates the BBB."( Optical method for real-time monitoring of drug concentrations facilitates the development of novel methods for drug delivery to brain tissue.
A'Amar, O; Bigio, IJ; Joshi, S; Reif, R; Wang, M,
)
0.85
"Mitoxantrone (MTX) is an antineoplastic agent approved for treatment of secondary progressive and rapidly worsening relapsing-remitting multiple sclerosis (MS). "( Mitoxantrone treatment in multiple sclerosis: a 5-year clinical and MRI follow-up.
Borriello, G; Buttinelli, C; Clemenzi, A; Denaro, F; Fieschi, C; Pozzilli, C, 2007
)
3.23
"Mitoxantrone is a similar anticancer agent with an anthracenedion structure that has been shown to be significantly less cardiotoxic."( Mechanisms responsible for reduced cardiotoxicity of mitoxantrone compared to doxorubicin examined in isolated guinea-pig heart preparations.
Chugun, A; Hara, Y; Nagasawa, H; Sasaki, T; Takagishi, K; Temma, K; Tsurimaki, C; Uchide, T; Ueno, S, 2008
)
1.32
"Mitoxantrone is a DNA-topoisomerase 2 inhibitor used as a single agent for treatment of relapsing-remitting or progressive multiple sclerosis (MS). "( Acute promyelocytic leukemia after mitoxantrone therapy for multiple sclerosis.
Baer, MR; Barcos, M; Chadha, MK; Heyman, MR; Ramkumar, B; Sait, SN, 2008
)
2.07
"Mitoxantrone is an active and relatively non-toxic agent which merits further assessment prior to its incorporation in first-line therapy of acute leukaemia."( Sequential studies on the role of mitoxantrone in the treatment of acute leukaemia.
Ho, AD; Ma, DD; Prentice, HG; Robbins, G, 1983
)
1.27
"Mitoxantrone appears to be an effective and well-tolerated agent for breast cancer."( A comparative trial of mitoxantrone and doxorubicin in patients with minimally pretreated breast cancer.
Gochnour, D; Neidhart, JA; Roach, RW; Steinberg, JA; Young, D, 1984
)
1.3
"Mitoxantrone is a relatively new synthetic anthracenedione derivative with intercalating properties. "( Mitoxantrone in relapsed and refractory acute leukemia.
Ho, AD; Ma, DD; Prentice, HG; Robbins, G, 1984
)
3.15
"Mitoxantrone (NSC-301739) is a synthetic amino anthraquinone DNA intercalater active in several experimental tumor systems. "( Phase I study of mitoxantrone on a daily X 5 schedule.
Goldsmith, MA; Greenspan, EM; Holland, JF; Jaffrey, IH; Ohnuma, T, 1984
)
2.05
"Mitoxantrone is an active, well-tolerated new drug in the treatment of advanced breast cancer, but cardiotoxicity may occur in a proportion of patients."( Mitoxantrone in advanced breast cancer--a phase II study with special attention to cardiotoxicity.
Coleman, RE; Knight, RK; Maisey, MN; Rubens, RD, 1984
)
2.43
"Mitoxantrone is an anthracenedione, showing structural similarities to doxorubicin. "( An EORTC phase II study of mitoxantrone in solid tumors and lymphomas.
Armand, JP; Bastit, P; Cappelaere, P; De Jager, R; Earl, H; Fargeot, P; Keiling, R; Renard, J; Rubens, R; van Glabbeke, M, 1984
)
2.01
"Mitoxantrone is an active, well tolerated drug in the treatment of advanced breast cancer and merits further evaluation."( Mitoxantrone (Novantrone) as single agent and in combination chemotherapy in the treatment of advanced breast cancer.
Bozek, T; Pavlidis, N; Smith, IE; Stuart-Harris, R, 1983
)
2.43
"Mitoxantrone is an active well-tolerated agent in the treatment of advanced breast carcinoma, but the risk of neutropenia requires careful supervision."( Mitoxantrone: an active new agent in the treatment of advanced breast cancer.
Bozek, T; Pavlidis, NA; Smith, IE; Stuart-Harris, RC, 1984
)
2.43
"Mitoxantrone is a synthetic anthraquinone that was developed through the doxorubicin analog program in hopes of retaining anticancer activity with less cardiotoxicity. "( Cardiac evaluation of mitoxantrone.
Balcerzak, SP; Bashore, TA; Neidhart, JA; Unverferth, BJ; Unverferth, DV, 1983
)
2.02
"Mitoxantrone (DAD) is a new agent which intercalates into DNA. "( Phase I trial of mitoxantrone by 24-hour continuous infusion.
Anderson, KC; Canellos, GP; Cohen, GI; Frei, E; Garnick, MB; Israel, M; Meshad, MW; Modest, E; Pegg, WJ, 1983
)
2.05
"Mitoxantrone is a promising new agent developed in an attempt to find drugs with a broad spectrum of antitumor activity and devoid of cardiotoxicity. "( Potential cardiotoxicity with mitoxantrone.
Blumenschein, G; Bodey, G; Schell, FC; Valdivieso, M; Yap, HY, 1982
)
2
"Mitoxantrone appears to be a well-tolerated and clinically active agent against advanced breast carcinoma."( Mitoxantrone: a phase II study in the treatment of patients with advanced breast carcinoma and other solid tumours.
Smith, IE; Stuart-Harris, RC, 1982
)
2.43
"Mitoxantrone is an anthracenedion (an anthracycline-related class of compounds) of increased clinical use, which may benefit from selective circadian timing."( Circadian changes in mitoxantrone toxicity in mice: relationship with plasma pharmacokinetics.
Bizi, E; Hallek, M; Lemaigre, G; Lévi, F; Metzger, G; Tampellini, M, 1994
)
1.33
"Mitoxantrone is an effective drug against ovarian cancer cells in vitro and is an attractive agent for IP therapy because of its very low peritoneal clearance."( Intraperitoneal mitoxantrone as consolidation treatment for patients with ovarian carcinoma in pathologic complete remission.
Audhuy, B; Barats, JC; Bergerat, JP; Dellenbach, P; Duclos, B; Dufour, P; Giron, C; Oberling, F; Renaud, R; Ritter, J, 1994
)
1.36
"Mitoxantrone is an effective and safe agent for the post-TUR adjuvant intravesical therapy."( Intravesical mitoxantrone for superficial bladder tumors.
Arikan, N; Yaman, LS; Yaşar, B; Yurdakul, T; Zissis, NP, 1994
)
1.38
"Mitoxantrone hydrochloride is an anthracenodione that has been reported to be useful when used intracavitary for malignant effusion due to gynaecological malignancies."( Mitoxantrone for malignant pleural effusion due to metastatic sarcoma.
Holmes, EC; Kelly, J; Rosen, G, 1993
)
2.45
"Mitoxantrone (MIT) is a new anthraquinone anti-cancer agent. "( [Preoperative intra-arterial injection of mitoxantrone for locally advanced breast cancer].
Hirayama, R; Ichikawa, W; Mishima, Y; Miyanaga, T; Nihei, Z; Sawai, S; Shoji, Y; Yamashita, T; Yoshinaga, K, 1993
)
1.99
"Mitoxantrone is an anthraquinone derivative that has demonstrated encouraging preclinical and clinical activity against a variety of human carcinoma cell lines and malignancies. "( A phase I-II trial of mitoxantrone by hepatic arterial infusion in patients with hepatocellular carcinoma or colorectal carcinoma metastatic to the liver.
Abbruzzese, J; Ajani, JA; Carrasco, CH; Charnsangavej, C; Jones, DV; Levin, B; Patt, YZ; Wallace, S, 1993
)
2.04
"Mitoxantrone is an anthraquinone structurally related to the anthracycline drugs doxorubicin and daunorubicin. "( Reversible cardiopathy after accidental overdose of mitoxantrone.
DeWolf, D; Hachimi-Idrissi, S; Otten, J; Schots, R; Van Belle, SJ,
)
1.82
"Mitoxantrone is a good candidate for local or regional administration because (1) its metabolism is mainly hepatic, (2) it has a steep dose-response curve for multiple solid tumors, and (3) its fixation in tissues is sustained without vesicant effects after extravasation."( Pharmacokinetics and antitumor effects of mitoxantrone after intratumoral or intraarterial hepatic administration in rabbits.
Ardouin, P; Bognel, C; Dzodic, R; Gouyette, A; Munck, JN; Ramirez, LH; Rougier, P; Vassal, G; Zhao, Z, 1996
)
1.28
"Mitoxantrone is an effective and well-tolerated regimen in elderly breast cancer patients presenting with comorbid conditions."( Mitoxantrone in elderly women with advanced breast cancer: a phase II study.
Biancardi, V; Campora, E; Gasco, M; Repetto, L; Rosso, R; Simoni, C; Venturino, A,
)
2.3
"Mitoxantrone is a new antineoplastic that differs from bleomycin in that it binds to membranes."( Comparison of mitoxantrone and tetracycline as pleural sclerosing agents in rabbits.
Despars, JA; Gruer, SE; Light, RW; Sassoon, C; Vargas, FS; Wang, NS, 1996
)
1.38
"Mitoxantrone is an agent with potential to cause t-AML and t-MDS and which is being used increasingly in the treatment of breast cancer."( Myelodysplasia and acute myeloid leukaemia following adjuvant chemotherapy for breast cancer using mitoxantrone and methotrexate with or without mitomycin.
Cremin, P; Daly, PA; Flattery, M; McCann, SR, 1996
)
1.23
"Mitoxantrone is an intravenous anthracenedione structurally related to the anthracycline antibiotics. "( Mitoxantrone in the treatment of acute myelogenous leukemia: a review.
Archimbaud, E; Thomas, X, 1997
)
3.18
"Mitoxantrone (M) is a synthetic aminoanthraquinone with anti-leukemic activity in patients with daunorubicin (D) resistant acute leukemia. "( Sequential mitoxantrone, daunorubicin, and cytosine arabinoside for patients with newly diagnosed acute myelocytic leukemia.
Cuttner, J; Davis, RB; Gottlieb, A; Holland, JF; Martelo, O; Paciucci, PA, 1997
)
2.13
"Mitoxantrone (MIT) is a new anthraquinone anticancer agent. "( [Intra-arterial injection therapy of mitoxantrone for locally advanced breast cancer].
Ichikawa, W; Iida, S; Miyanaga, T; Nihei, Z; Nishi, N; Osanai, T; Shimizu, C; Sugihara, K; Togo, S; Uetake, H; Yamashita, T, 1998
)
2.02
"Mitoxantrone is an anthracenedione with low cardiotoxicity, and seems to be effective when combined with vinorelbine after prior exposure to anthracyclines."( First-line vinorelbine-mitoxantrone combination in metastatic breast cancer patients relapsing after an adjuvant anthracycline regimen: results of a phase II study.
Le Cesne, A; Le Chevalier, T; Llombart-Cussac, A; Pivot, X; Rhor-Alvarado, A; Spielmann, M; Tursz, T,
)
1.16
"Mitoxantrone (Novantrone) is an anthracene derivative that has demonstrated antitumor activity in patients with breast cancer, ovarian cancer, acute leukemia, and lymphoma."( A phase I trial of vinorelbine in combination with mitoxantrone in patients with refractory solid tumors.
Bigley, J; Burris, HA; Dieras, V; Eckardt, JR; Hardy, J; Hohneker, J; Jones, SF; Peacock, NW; Rodriguez, GI; Smith, L; Von Hoff, DD, 1998
)
1.27
"Mitoxantrone is an anthracenedione anti-neoplastic agent that has recently been shown to be effective in ameliorating disease activity in multiple sclerosis (MS) as indicated by clinical and MRI data. "( [Mitoxantrone (Novantron) in therapy of severe multiple sclerosis. A retrospective study of 15 patients].
Cursiefen, S; Flachenecker, P; Rieckmann, P; Toyka, KV, 1999
)
2.66
"Mitoxantrone is an active agent in lymphoma that is not generally used in first-line treatment."( CN3OP: an active regimen in patients with relapsed/refractory Hodgkin's lymphoma.
Kraszewska, E; Krzyzanowska, JB; Lampka, E; Meder, J; Miśkiewicz, Z; Romejko-Jarosińska, J; Walewski, J, 2000
)
1.03
"Mitoxantrone is a minimally toxic chemotherapeutic agent, which justifies its current indication in hormone-resistant advanced prostate cancer."( [Value of mitoxantrone in metastatic hormone-resistant prostate cancer].
Dunet, F; Grise, P; Hellot, MF; Khalaf, A; Moussu, J; Pfister, C, 2002
)
2.16
"Mitoxantrone is a dihydroxyanthracenedione derivative which as intravenous mono- and combination therapy has demonstrated therapeutic efficacy similar to that of standard induction and salvage treatment regimens in advanced breast cancer, non-Hodgkin's lymphoma, acute nonlymphoblastic leukaemia and chronic myelogenous leukaemia in blast crisis; it appears to be an effective alternative to the anthracycline component of standard treatment regimens in these indications. "( Mitoxantrone. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in the chemotherapy of cancer.
Balfour, JA; Chrisp, P; Faulds, D; Langtry, HD, 1991
)
3.17
"Mitoxantrone is a new anthracenodione derivative with a high antineoplastic activity in proliferative diseases of the haemopoietic system. "( [Preliminary results of the treatment of acute leukemia with mitoxantrone].
Apel, D; Hołowiecki, J; Konecki, R; Lawniczek, T; Maj, S; Mariańska, B; Mazur, J; Pałynyczko, G; Rozmysłowicz, T; Rudzka, E, 1991
)
1.97
"Mitoxantrone is an anthracene derivative that acts as a cytostatic in a variety of cancers. "( Novel assay method for mitoxantrone in plasma, and its application in cancer patients.
Chang, SP; Chen, KY; Hu, OY; Law, CK; Song, YB, 1990
)
2.03
"Mitoxantrone is an active agent in the treatment of acute leukemia and demonstrates incomplete cross resistance with duanorubicin."( Mitoxantrone for refractory and relapsed acute leukemia.
Bernasconi, C; Bezwoda, WR; de Bock, R; Hutchinson, RM; Mandelli, F; Winfield, DA, 1990
)
2.44
"Mitoxantrone is a substituted anthraquinone with considerable activity against human acute leukemia. "( Continuous infusion mitoxantrone in relapsed acute nonlymphocytic leukemia.
Choi, KE; Daley, KM; Kaminer, LS; Larson, RA, 1990
)
2.05
"Mitoxantrone (MTX) is a recently synthesized antitumor intercalative molecule, currently in use in chemotherapy. "( Theoretical design of novel, 4 base pair selective derivatives of mitoxantrone.
Gresh, N; Kahn, PH, 1990
)
1.96
"Mitoxantrone (DHAQ) is a new anti-cancer agent. "( [Ion-paired high performance liquid chromatographic determination of mitoxantrone hydrochloride injection].
Guo, P; Song, H; Wu, C, 1990
)
1.96
"Mitoxantrone is a synthetic anthraquinone that is active in the therapy of a number of malignancies. "( Mitoxantrone: potential for use in intensive therapy.
Herzig, R; LeMaistre, CF, 1990
)
3.16
"Mitoxantrone is a new effective antineoplastic agent with activity against a wide range of tumors. "( Accidental overdose of mitoxantrone in three patients.
Büchner, T; Essink, M; Hiddemann, W; Huhn, D; Jung, M; Koppensteiner, R; Marosi, L; Martin, T; Minar, E; Siegert, W, 1989
)
2.03
"Mitoxantrone is an antitumor agent that was synthesized to try to develop a doxorubicinlike drug with a better therapeutic index. "( Mitoxantrone: its development and role in clinical practice.
Weiss, RB, 1989
)
3.16
"Mitoxantrone is a compound that is related to the anthracyclines but has a different mechanism of action."( Phase I and II agents in cancer therapy: I. Anthracyclines and related compounds.
Fuks, JZ; Wadler, S; Wiernik, PH,
)
0.85
"Mitoxantrone is an important new agent with antitumor activity in leukemia, lymphoma, and breast cancer."( Mitoxantrone: a novel anthracycline derivative.
Eble, M; Koeller, J, 1988
)
2.44
"Mitoxantrone is an effective agent in refractory NHL and should be taken into consideration in the design of salvage regimens."( Mitoxantrone: an active agent in refractory non-Hodgkin's lymphomas.
Bajetta, E; Bonadonna, G; Buzzoni, R; Valagussa, P, 1988
)
2.44
"Mitoxantrone is a synthetic aminoanthraquinone we have previously reported to be effective for patients with acute leukemia in relapse. "( Mitoxantrone and ara-C in previously treated patients with acute myelogenous leukemia.
Cuttner, J; Dutcher, JP; Holland, JF; Paciucci, PA; Strauman, JJ; Wiernik, PH, 1987
)
3.16
"Mitoxantrone is an anthraquinone antineoplastic agent with structural similarities to doxorubicin. "( Mitoxantrone.
Poirier, TI, 1986
)
3.16
"Mitoxantrone is an anthracenedione derivative with structural and functional similarities to doxorubicin."( Inhibition of endogenous respiration in rat heart slices as a measure of mitoxantrone cardiac toxicity.
Cini-Neri, G; Neri, B, 1986
)
1.22
"Mitoxantrone thus appears to be a promising drug for the treatment of acute leukemia."( [A phase II study of mitoxantrone in acute leukemia. Hanshin Cooperative Study Group of Hematological Disorders].
Horiuchi, A; Kawagoe, H; Kitani, T; Masaoka, T; Nagai, K; Oguma, S; Shibata, H; Yasunaga, K; Yonezawa, T, 1986
)
1.31
"Mitoxantrone (Novantrone), is an anthracenedione which in preclinical studies demonstrated a spectrum of antitumor activity similar to the anthracyclines, but with less cardiotoxicity. "( Mitoxantrone: an overview of safety and toxicity.
Bernstein, T; Cartwright, K; Dukart, G; Goldberg, J; Posner, LE, 1985
)
3.15
"Mitoxantrone is a new active anthracene-based, DNA intercalator which is undergoing widespread clinical testing for antitumor efficacy in man."( Lack of experimental vesicant activity for the anticancer agents cisplatin, melphalan, and mitoxantrone.
Alberts, DS; Dorr, RT; Soble, M, 1986
)
1.21
"Mitoxantrone (DHAD) is a recently developed cancer chemotherapeutic drug proposed as a possible substitute for the older established chemotherapeutic, doxorubicin (adriamycin, or ADR). "( Comparative toxicity of mitoxantrone and doxorubicin on hematopoietic stem cells.
Buffo, MJ; Kociban, DL; OKunewick, JP, 1985
)
2.02
"Mitoxantrone is an anthracenedione with structural similarities to adriamycin but without the amino-sugar moiety on the parent molecule. "( [Mitoxantrone in the treatment of relapsed and refractory malignant lymphoma].
Hiraki, S; Kimura, I; Miyamoto, H; Murashima, M; Ohnoshi, T; Toyata, K; Ueno, K; Ueoka, H; Yamane, T, 1985
)
2.62
"Mitoxantrone is a new anthracenedione derivative that suppresses cell proliferation in the T-47D human breast tumor cell line as revealed by colony-forming assay in soft agar and growth study in monolayer culture. "( Growth and ultrastructural responses of T-47D human breast tumor cells to treatment with mitoxantrone.
Ballou, RJ; Safa, AR; Tseng, MT, 1985
)
1.93

Effects

Mitoxantrone has a broad anti-tumour activity including lymphoma with potentially less cardiotoxicity than doxorubicin. The molecule also has a very favorable toxicity profile with significantly less nausea and vomiting, alopecia, and stomatitis as compared with anthracyclines.

Mitoxantrone has been extensively used as a disease-modifying therapy for multiple sclerosis. It has not gained widespread acceptance in the veterinary community, primarily due to its cost and single-dose packaging.

ExcerptReferenceRelevance
"The mitoxantrone molecule has an intense binding energy of - 880.536 kcal/mol with AKT1 protein, while the XFE molecule shows a binding energy value of - 83.569 kcal/mol."( Investigation of the inhibitory behavior of XFE and mitoxantrone molecules in interaction with AKT1 protein: a molecular dynamics simulation study.
Abasi Joozdani, F; Amiran, MR; Taghdir, M, 2023
)
1.64
"Mitoxantrone has a broad anti-tumour activity including lymphoma with potentially less cardiotoxicity than doxorubicin, which may be of particular importance in elderly patients. "( CNOP (mitoxantrone) chemotherapy is inferior to CHOP (doxorubicin) in the treatment of patients with aggressive non-Hodgkin lymphoma (meta-analysis).
Ahlbom, A; Anders, A; Andersson, T; Björkholm, M; Eva, O; Magnus, B; Ösby, E; Tomas, A, 2008
)
2.27
"Mitoxantrone also has a very favorable toxicity profile with significantly less nausea and vomiting, alopecia, and stomatitis as compared with anthracyclines."( A phase I trial of vinorelbine in combination with mitoxantrone in patients with refractory solid tumors.
Bigley, J; Burris, HA; Dieras, V; Eckardt, JR; Hardy, J; Hohneker, J; Jones, SF; Peacock, NW; Rodriguez, GI; Smith, L; Von Hoff, DD, 1998
)
1.27
"Mitoxantrone has a role in the treatment of MS patients with frequent exacerbations and rapid disease progression."( A double-blind clinical trial of mitoxantrone versus methylprednisolone in relapsing, secondary progressive multiple sclerosis.
Beguin, C; Carton, H; D'Hooghe, MB; Dooms, G; Lissoir, F; Sindic, CJ; van de Wyngaert, FA, 2001
)
1.31
"Mitoxantrone also has a much slower dissociation rate from poly[d(G-C)]2 than from poly[d(A-T)]2, but its dissociation from both polymers exhibits biphasic kinetics."( Stopped-flow kinetic analysis of the interaction of anthraquinone anticancer drugs with calf thymus DNA, poly[d(G-C)].poly[d(G-C)], and poly[d(A-T)].poly[d(A-T)].
Krishnamoorthy, CR; Lown, JW; Smith, JC; Wilson, WD; Yen, SF, 1986
)
0.99
"Mitoxantrone has proved efficacy in treatment of multiple sclerosis (MS). "( Does physical exercise improve or deteriorate treatment of multiple sclerosis with mitoxantrone? Experimental autoimmune encephalomyelitis study in rats.
Abdallah, DM; El Achy, S; El-Abhar, HS; El-Emam, MA; Gowayed, MA, 2022
)
2.39
"The mitoxantrone molecule has an intense binding energy of - 880.536 kcal/mol with AKT1 protein, while the XFE molecule shows a binding energy value of - 83.569 kcal/mol."( Investigation of the inhibitory behavior of XFE and mitoxantrone molecules in interaction with AKT1 protein: a molecular dynamics simulation study.
Abasi Joozdani, F; Amiran, MR; Taghdir, M, 2023
)
1.64
"Mitoxantrone (MTX) has been used as an effective disease modifying treatment (DMT) in multiple sclerosis (MS). "( Mitoxantrone in relapsing-remitting and rapidly progressive multiple sclerosis: Ten-year clinical outcomes post-treatment with mitoxantrone.
Foo, EC; Ford, HL; Lily, O; Russell, M, 2020
)
3.44
"Mitoxantrone (MITOX) has been used to treat patients with aggressive multiple sclerosis (MS) for decades. "( Clinical follow-up of 411 patients with relapsing and progressive multiple sclerosis 10 years after discontinuing mitoxantrone treatment: a real-life cohort study.
Chartier, N; Dahan, C; Debouverie, M; Epstein, J; Guillemin, F; Mathey, G; Michaud, M; Pittion-Vouyovitch, S; Soudant, M, 2018
)
2.13
"Mitoxantrone (MTX) has been shown to reduce progression of disability and number of clinical exacerbations in patients with progressive multiple sclerosis (MS). "( The N-terminal pro-brain natriuretic peptide as a marker of mitoxantrone-induced cardiotoxicity in multiple sclerosis patients.
Kamińska, AM; Kochanowski, J; Kwieciński, H; Opolski, G; Podlecka-Piętowska, A; Zakrzewska-Pniewska, B, 2014
)
2.09
"Mitoxantrone has been extensively used as a disease-modifying therapy for multiple sclerosis. "( Long-term risk of leukaemia or cardiomyopathy after mitoxantrone therapy for multiple sclerosis.
Goggin, C; Joyce, E; Lynch, T; Mahon, N; Melling, J; Mulroy, E; O'Rourke, K; Scott, J, 2012
)
2.07
"Mitoxantrone has been approved by the FDA for the treatment of multiple sclerosis (MS). "( Mitoxantrone repression of astrocyte activation: relevance to multiple sclerosis.
Burns, SA; Chavis, JA; Drew, PD; Hensley, LL; Lee Archer, R; Tull, CA, 2012
)
3.26
"Mitoxantrone has not gained widespread acceptance in the veterinary community, primarily due to its cost and single-dose packaging in a volume that exceeds the needs of the majority of veterinary cancer patients."( Evaluation of the in vitro cytotoxicity of mitoxantrone following repeated freeze-thaw cycles.
Mauldin, GN; Truax, R, 2002
)
1.3
"Mitoxantrone (MX) has been approved by the Food and Drug Administration (FDA) for the treatment of patients with worsening relapsing-remitting (RR) or secondary progressive (SP) multiple sclerosis (MS). "( Mitoxantrone in progressive multiple sclerosis: when and how to treat?
Gonsette, RE, 2003
)
3.2
"Mitoxantrone has gained largest acceptance."( Clinical practice of immunosuppressive treatments in multiple sclerosis: results of a second international questionnaire.
Hommes, OR; Weiner, HL, 2004
)
1.04
"Mitoxantrone (MX) has been approved by the Food and Drug Administration for the treatment of rapidly progressive multiple sclerosis (MS). "( Pixantrone (BBR2778): a new immunosuppressant in multiple sclerosis with a low cardiotoxicity.
Dubois, B; Gonsette, RE, 2004
)
1.77
"Mitoxantrone (MTZ) has been shown to be effective in the treatment of newly diagnosed acute myeloblastic leukemia (AML). "( A randomized trial of continuous infusion versus bolus mitoxantrone in combination with cytarabine in newly diagnosed patients with acute myeloblastic leukemia.
Canpinar, H; Kansu, E; Kars, A; Koc, Y; Oyan, B; Tekuzman, G, 2004
)
2.01
"Mitoxantrone (mitox) has been shown to be effective for secondary progressive (SP) and relapsing-remitting multiple sclerosis (MS). "( [The effect of combined mitoxantrone and methylprednisolone therapy in primary and secondary progressive multiple sclerosis. An applied study in 65 patients].
Brandt, T; Gross, A; Hohlfeld, R; Jahn, K; Strupp, M; Zingler, VC, 2005
)
2.08
"Mitoxantrone has been approved by the Food and Drug Administration for HRCAP."( Phase II trial of tesmilifene plus mitoxantrone and prednisone for hormone refractory prostate cancer: high subjective and objective response in patients with symptomatic metastases.
Brandes, LJ; Klapp, K; Lieskovsky, G; Quinn, DI; Raghavan, D; Ramsey, EW; Snyder, T; Styles, E; Tsao-Wei, D, 2005
)
1.33
"Mitoxantrone (MX) has been shown to be moderately effective in reducing the clinical outcome measures of disease activity in multiple sclerosis (MS) patients."( Mitoxantrone for multiple sclerosis.
Capra, R; Comi, G; Martinelli Boneschi, F; Rovaris, M, 2005
)
3.21
"Mitoxantrone has been shown to reduce relapses, the number of new lesions visualised on magnetic resonance imaging and stop or reduce the progression of the disease in many patients treated."( The cardiac effects of mitoxantrone: do the benefits in multiple sclerosis outweigh the risks?
Murray, TJ, 2006
)
1.37
"Mitoxantrone has activity similar to that of doxorubicin, is less cardiotoxic, and is widely used to treat prostate cancer."( Phase II study of mitoxantrone and ketoconazole for hormone-refractory prostate cancer.
Bergan, RC; Eklund, J; Gallot, L; Jovanovic, B; Kozloff, M; Mariott, M; Pins, M; Robin, E; Schilder, L; Starr, A; Vlamakis, J, 2006
)
1.39
"Mitoxantrone (MX) has demonstrated efficacy in multiple sclerosis (MS), but its immunologic mechanisms of action are poorly understood. "( Immunological studies of mitoxantrone in primary progressive MS.
Cotleur, AC; Fox, RJ; Lee, JC; Pelfrey, CM; Zamor, N, 2006
)
2.08
"Mitoxantrone has been approved by the FDA for worsening relapsing remitting and secondary progressive Multiple Sclerosis. "( Sequential maintenance treatment with glatiramer acetate after mitoxantrone is safe and can limit exposure to immunosuppression in very active, relapsing remitting multiple sclerosis.
Boggild, M; Das, K; Jacob, A; Ramtahal, J, 2006
)
2.02
"Mitoxantrone has recently been shown to be effective in ameliorating multiple sclerosis activity and reducing the relapse rate."( Mitoxantrone reduced disability in Iranian patients with multiple sclerosis.
Etemadifar, M; Hamzehloo, A, 2007
)
2.5
"Mitoxantrone (MTZ) has potent in vitro activity against malignant glioma cell lines, but it cannot be used effectively as a systemic agent for the treatment of brain tumors because of its poor central nervous system penetration. "( Treatment of malignant gliomas with mitoxantrone-loaded poly (lactide-co-glycolide) microspheres.
Bozdag, S; Capan, Y; Cetin, M; Dalkara, T; Söylemezoglu, F; Vural, I; Yemisci, M, 2006
)
2.05
"Mitoxantrone resistance has been related to the expression of a drug efflux pump breast cancer resistance pump (BCRP) but little is known of the intracellular protein changes. "( Proteomic analysis to dissect mitoxantrone resistance-associated proteins in a squamous lung carcinoma.
Clynes, M; Keenan, J; Murphy, L,
)
1.86
"Mitoxantrone has a broad anti-tumour activity including lymphoma with potentially less cardiotoxicity than doxorubicin, which may be of particular importance in elderly patients. "( CNOP (mitoxantrone) chemotherapy is inferior to CHOP (doxorubicin) in the treatment of patients with aggressive non-Hodgkin lymphoma (meta-analysis).
Ahlbom, A; Anders, A; Andersson, T; Björkholm, M; Eva, O; Magnus, B; Ösby, E; Tomas, A, 2008
)
2.27
"Mitoxantrone has been administered to more than 4000 patients worldwide. "( Clinical safety and tolerance of mitoxantrone.
Crossley, RJ, 1984
)
1.99
"Mitoxantrone has markedly less cardiotoxicity than doxorubicin, and this may be linked to the fact that the drug does not induce free radical formation but inhibits lipid peroxidation."( Biologic and biochemical effects of mitoxantrone.
Durr, FE, 1984
)
1.26
"Mitoxantrone has been given to 335 patients in an i.v."( An EORTC phase II study of mitoxantrone in solid tumors and lymphomas.
Armand, JP; Bastit, P; Cappelaere, P; De Jager, R; Earl, H; Fargeot, P; Keiling, R; Renard, J; Rubens, R; van Glabbeke, M, 1984
)
1.29
"Mitoxantrone has recently been tested to treat effusions, and preliminary results suggest the high efficacy of this drug in the treatment of peritoneal, pericardial and pleural effusions."( Management of peritoneal effusions with intracavitary mitoxantrone or bleomycin.
Maiche, AG, 1994
)
1.26
"Mitoxantrone has been tested recently in the treatment of effusions, and preliminary results suggest high efficacy of this drug in the treatment of peritoneal, pericardial, and pleural effusions."( Bleomycin and mitoxantrone in the treatment of malignant pleural effusions. A comparative study.
Kontkanen, T; Maiche, AG; Möykkynen, K; Porkka, K; Virkkunen, P, 1993
)
1.37
"Mitoxantrone has shown moderate activity in advanced epithelial ovarian cancer following intermittent i.v. "( Continuous mitoxantrone infusion in pretreated epithelial ovarian cancer.
Aversa, S; Azzoni, P; Endrizzi, L; Fiorentino, MV; Koussis, H; Nicoletto, MO; Padrini, R; Palumbo, M; Rosabian, A, 1995
)
2.12
"Mitoxantrone has demonstrable clinical activity when administered intravenously in a wide range of malignancies. "( Phase I/II study of intraperitoneal mitoxantrone in refractory ovarian cancer.
Aartsen, E; Dubbelman, R; Mandjes, I; McVie, JG; Oza, AM; Soepenberg, O; ten Bokkel Huinink, W, 1994
)
2.01
"Mitoxantrone has been shown in vitro to exhibit a steep dose-response relationship with respect to the clonogenic survival of acute myeloid leukemia cells. "( High-dose mitoxantrone induces programmed cell death or apoptosis in human myeloid leukemia cells.
Bhalla, K; Bullock, G; Grant, S; Huang, Y; Ibrado, AM; Mahoney, ME; Ponnathpur, V; Tang, C; Tourkina, E, 1993
)
2.13
"Mitoxantrone (MIT) has not been studied as a single agent in children with untreated leukemia. "( In vitro cytotoxicity of mitoxantrone, daunorubicin and doxorubicin in untreated childhood acute leukemia.
de Waal, FC; Hählen, K; Kaspers, GL; Klumper, E; Pieters, R; van Wering, ER; van Zantwijk, I; Veerman, AJ, 1994
)
2.03
"Mitoxantrone has also been effective in inducing complete remissions in patients with relapsed or refractory ANLL, mainly in combination with other antineoplastic agents."( Mitoxantrone: a review of its pharmacological properties and use in acute nonlymphoblastic leukaemia.
Dunn, CJ; Goa, KL, 1996
)
2.46
"Mitoxantrone also has a very favorable toxicity profile with significantly less nausea and vomiting, alopecia, and stomatitis as compared with anthracyclines."( A phase I trial of vinorelbine in combination with mitoxantrone in patients with refractory solid tumors.
Bigley, J; Burris, HA; Dieras, V; Eckardt, JR; Hardy, J; Hohneker, J; Jones, SF; Peacock, NW; Rodriguez, GI; Smith, L; Von Hoff, DD, 1998
)
1.27
"Mitoxantrone has demonstrated therapeutic efficacy in the regional treatment of intraperitoneal malignancies. "( Evaluation of mitoxantrone-loaded albumin microspheres following intraperitoneal administration to rats.
Eichler, HG; Luftensteiner, CP; Paul, B; Schwendenwein, I; Viernstein, H, 1999
)
2.11
"Mitoxantrone (MXN) has demonstrated therapeutic efficacy in the intraperitoneal treatment of malignancies. "( Toxicity of a particulate formulation for the intraperitoneal application of mitoxantrone.
Eichler, HG; Luftensteiner, CP; Paul, B; Schwendenwein, I; Viernstein, H; Wölfl, G, 1999
)
1.97
"Mitoxantrone has not been compared with palliative care comprising radiotherapy."( Mitoxantrone: new indication. More risky than beneficial in advanced prostate cancer.
, 2001
)
2.47
"Mitoxantrone has a role in the treatment of MS patients with frequent exacerbations and rapid disease progression."( A double-blind clinical trial of mitoxantrone versus methylprednisolone in relapsing, secondary progressive multiple sclerosis.
Beguin, C; Carton, H; D'Hooghe, MB; Dooms, G; Lissoir, F; Sindic, CJ; van de Wyngaert, FA, 2001
)
1.31
"Mitoxantrone has moderate activity in childhood ALL and should be considered for further trials in less heavily pretreated patients."( Phase II trial of mitoxantrone in acute lymphocytic leukemia of childhood. A Pediatric Oncology Group study.
Estrada, J; Graham, ML; Ragab, AH; Rosen, D; Starling, KA; Wilkenson, RW; Wilkerson, RW, 1991
)
1.34
"Mitoxantrone has been reported to lack certain properties that characterize quinone containing antitumor agents that undergo enzymatic reduction. "( Mechanism(s) for the metabolism of mitoxantrone: electron spin resonance and electrochemical studies.
Gutierrez, PL; Nguyen, B, 1990
)
2
"Mitoxantrone (6 mg/m2) has been administrated after effusion aspiration."( [Efficacy and toxicity of intrapleural mitoxantrone: apropos of 18 cases of pleural metastases of breast cancer].
Brun, B; Calitchi, E; Feuilhade, F; Haddad, E; Le Bourgeois, JP; Otzmeguine, Y; Pierquin, B, 1989
)
1.27
"Mitoxantrone has activity in HCC and is well tolerated when administered by HAI."( Hepatic arterial infusion of mitoxantrone in the treatment of primary hepatocellular carcinoma.
Blackstein, ME; Evans, WK; Fine, S; Habal, F; Heathcote, J; Kutas, G; Langer, B; Pritchard, KI; Shepherd, FA; Taylor, B, 1987
)
1.29
"Mitoxantrone has demonstrated clinical efficacy in the treatment of leukemia, lymphoma, and breast cancer."( Mitoxantrone: a novel anthracycline derivative.
Eble, M; Koeller, J, 1988
)
2.44
"Mitoxantrone has been found to fluoresce with excitation maxima at 610 and 660 nm and emission maximum at 685 nm."( Characterization of the fluorescence of the antitumor agent, mitoxantrone.
Bell, DH, 1988
)
1.24
"Both mitoxantrone and etoposide have been shown to be active in monotherapy trials of relapsed and refractory acute myelogenous leukemia (AML). "( Combination of mitoxantrone and etoposide in refractory acute myelogenous leukemia--an active and well-tolerated regimen.
Ehninger, G; Freund, M; Ho, AD; Hunstein, W; Illiger, HJ; Lipp, T; Meyer, P, 1988
)
1.14
"Mitoxantrone has significant activity in the treatment of metastatic breast cancer, acute leukemias, and non-Hodgkin's lymphoma."( Mitoxantrone.
Poirier, TI, 1986
)
2.44
"Mitoxantrone (MIT) has recently been introduced into cancer therapy as a possible substitute for the structurally related drug, adriamycin (ADR), because it causes less cardiotoxicity and fewer gastrointestinal side effects. "( Comparative in vitro toxicity of mitoxantrone and adriamycin in human granulocyte-macrophage progenitor cells.
Brühl, P; Ehninger, G; Heidemann, E; Mergenthaler, HG, 1987
)
2
"Mitoxantrone also has a much slower dissociation rate from poly[d(G-C)]2 than from poly[d(A-T)]2, but its dissociation from both polymers exhibits biphasic kinetics."( Stopped-flow kinetic analysis of the interaction of anthraquinone anticancer drugs with calf thymus DNA, poly[d(G-C)].poly[d(G-C)], and poly[d(A-T)].poly[d(A-T)].
Krishnamoorthy, CR; Lown, JW; Smith, JC; Wilson, WD; Yen, SF, 1986
)
0.99

Actions

Mitoxantrone displays an improved tolerability profile compared with doxorubicin and other anthracyclines. Myelosuppression may occur more frequently in patients with advanced non-squamous carcinoma of the cervix.

ExcerptReferenceRelevance
"Mitoxantrone did not cause signs of congestive heart failure in any of the patients."( Assessment of potential cardiotoxic side effects of mitoxantrone in patients with multiple sclerosis.
Brandt, T; Gross, A; Hohlfeld, R; Jahn, K; Nabauer, M; Strupp, M; Zingler, VC, 2005
)
1.3
"Mitoxantrone may inhibit the migration of inflammatory cells into and within the central nervous system."( Inhibition by mitoxantrone of in vitro migration of immunocompetent cells: a possible mechanism for therapeutic efficacy in the treatment of multiple sclerosis.
Dehmel, T; Hartung, HP; Kieseier, BC; Kopadze, T; Stüve, O, 2006
)
2.14
"Mitoxantrone could cause an intrapleural inflammatory reaction."( [Therapy of pronounced pleural and pericardial effusion in metastatic breast cancer with local mitoxantrone and radiation therapy. Presentation of the intrapleural cytologic findings during this therapy].
Blohmer, JU; Kohls, A; Lau, HU, 1993
)
1.23
"Mitoxantrone displays an improved tolerability profile compared with doxorubicin and other anthracyclines, although myelosuppression may occur more frequently."( Mitoxantrone. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in the chemotherapy of cancer.
Balfour, JA; Chrisp, P; Faulds, D; Langtry, HD, 1991
)
2.45
"Mitoxantrone displays no activity in patients with advanced carcinoma of the vulva or vagina."( Mitoxantrone in the treatment of advanced vulvar and vaginal carcinoma. A gynecologic oncology group study.
Bundy, BN; Christopherson, WA; Muss, HB, 1989
)
2.44
"Mitoxantrone displays minimal activity in patients with advanced non-squamous carcinoma of the cervix."( Mitoxantrone in the treatment of advanced non-squamous carcinoma of the cervix (a phase II trial of the gynecologic oncology group).
Bundy, BN; Homesley, HD; Muss, HB; Wilbanks, G, 1987
)
2.44

Treatment

Mitoxantrone treatment increased the ex vivo production of the TH2 cytokines interleukin-4 (IL-4) and IL-5 (P < 0.001) in phytohemagglutinin-stimulated CD4+ T cells within 18 days of treatment. When B16-F1 cells were used as antigen to inoculate mice, the mice acquired an ability to suppress proliferation of homologous tumor cells.

ExcerptReferenceRelevance
"41 mitoxantrone-treated PPMS-patients, 155 mitoxantrone-treated RP/SPMS-patients and 43 PPMS-controls were retrospectively assessed for clinical therapy-response and in correlation with four single-nucleotide-polymorphisms in ABCB1- and ABCG2-genes."( Lack of efficacy of mitoxantrone in primary progressive Multiple Sclerosis irrespective of pharmacogenetic factors: a multi-center, retrospective analysis.
Chan, A; Comabella, M; Fleischer, V; Gold, R; Grey Née Cotte, S; Kruse, N; Montalban, X; Salmen Née Stroet, A; Starck, M; von Ahsen, N; Winkelmann, A; Zettl, UK; Zipp, F, 2015
)
1.36
"Mitoxantrone treatment increased the ex vivo production of the TH2 cytokines interleukin-4 (IL-4; P < 0.05) and IL-5 (P < 0.001) in phytohemagglutinin-stimulated CD4+ T cells within 18 days of treatment. "( Mitoxantrone treatment in multiple sclerosis induces TH2-type cytokines.
Bröker, BM; Dressel, A; Rosenberg, S; Skrzipek, S; Vogelgesang, A, 2010
)
3.25
"Mitoxantrone treatment in MS enhances the inducibility of TH2-type cytokines, which may contribute to its beneficial effects in MS."( Mitoxantrone treatment in multiple sclerosis induces TH2-type cytokines.
Bröker, BM; Dressel, A; Rosenberg, S; Skrzipek, S; Vogelgesang, A, 2010
)
3.25
"When mitoxantrone-treated B16-F1 cells were used as antigen to inoculate mice, the mice acquired an ability to suppress proliferation of homologous tumor cells."( Mitoxantrone-mediated apoptotic B16-F1 cells induce specific anti-tumor immune response.
Cao, C; Han, Y; Ren, Y; Wang, Y, 2009
)
2.25
"Mitoxantrone treatment induced γH2AX foci and NU7441 increased their longevity (24 h)."( Mitoxantrone in combination with an inhibitor of DNA-dependent protein kinase: a potential therapy for high risk B-cell chronic lymphocytic leukaemia.
Bedwell, C; Crawford, C; Durkacz, BW; Elliott, SL; Evans, P; Mainou-Fowler, T; Mulligan, E; Newton, P; Summerfield, G; Wallis, J; Willmore, E, 2011
)
2.53
"Mitoxantrone treatment in MS is associated with long-term major potential harms - leukaemia (LK) and cardiotoxicity (CT)."( Long-term treatment risks in multiple sclerosis: risk knowledge and risk perception in a large cohort of mitoxantrone-treated patients.
Elias, WG; Heesen, C; Hofmann, A; Kasper, J; Köpke, S; Pauly, I; Repenthin, J; Rosenkranz, T; Stellmann, JP; Ufer, F; Weber, T, 2013
)
1.33
"Mitoxantrone treatment did not improve the Expanded Disability Status Scale score; however, no further significant deterioration appeared."( Efficacy of mitoxantrone and intrathecal triamcinolone acetonide treatment in chronic progressive multiple sclerosis patients.
Brune, N; Hellwig, K; Hoffmann, V; Lukas, C; Müller, T; Przuntek, H; Schimrigk, S,
)
1.23
"On mitoxantrone treatment there was a considerable neurologic recovery."( 3-methylcrotonyl-CoA carboxylase deficiency and severe multiple sclerosis.
Andersen, O; Darin, N; Holme, E; Holmgren, D; Wiklund, LM, 2007
)
0.85
"Mitoxantrone treatment induced two partial remissions (patients with metastatic squamous cell carcinomas of the hypopharynx and rectum) and one mixed response (patient with gastric carcinoma)."( Phase I clinical trial f mitoxantrone: a new anthracenedione anticancer drug.
Alberts, DS; Goodman, GE; Griffith, KS; Herman, TS; Murray, E, 1980
)
1.29
"Mitoxantrone treatment seems able to improve the clinical course of relapsing remitting multiple sclerosis patients."( Noninvasive assessment of mitoxantrone cardiotoxicity in relapsing remitting multiple sclerosis.
Beni, S; Cartoni, D; De Castro, S; Funaro, S; Gasperini, C; Millefiorini, E; Morino, S; Tallarico, D, 1995
)
1.31
"Mitoxantrone treatment and doxorubicin treatment also cause up-regulation of Fas, the cell surface receptor for FasL, in LNCaP cells, but not in DU145 or PC3 cells."( Fas ligand is constitutively secreted by prostate cancer cells in vitro.
Lederman, S; Liu, QY; Omene, C; Rubin, MA; Stein, CA, 1998
)
1.02
"Mitoxantrone-treated animals showed moderate cardiotoxic lesions (but not cumulative) and no increase in serum lipids."( The effect of doxorubicin and its analogue mitoxantrone on cardiac muscle and on serum lipids: an experimental study.
Couris, E; Deliconstantinos, G; Dontas, I; Karayannacos, PE; Koutinos, G; Perrea-Kotsarelis, D; Stathopoulos, GP,
)
1.12
"Mitoxantrone treated NCI-H69 cells were found to accumulate DNA-protein crosslinks during a 4 hr post-treatment incubation period whereas variant cells maintained depressed levels of crosslinking."( Mitoxantrone-DNA binding and the induction of topoisomerase II associated DNA damage in multi-drug resistant small cell lung cancer cells.
Fox, ME; Morgan, SA; Smith, PJ; Watson, JV, 1990
)
2.44
"Treatment with mitoxantrone also led to the appearance of structures resembling agresomes in H1299 cells and to nucleolar segregation in both cell lines."( Cytoskeletal reorganization and cell death in mitoxantrone-treated lung cancer cells.
Gackowska, L; Grzanka, A; Klimaszewska-Wisniewska, A; Pawlik, A; Szczepanski, MA; Zuryn, A, 2016
)
1.03
"The treatment with mitoxantrone is limited by the occurrence of infertility, cardiotoxicy and leukaemia."( Treatment of multiple sclerosis: role of natalizumab.
Comi, G, 2009
)
0.67
"Cotreatment of mitoxantrone with different concentrations of dexamethasone and indomethacin sensitized parental and resistant MCF-7 cells to mitoxantrone cytotoxicity."( Evaluation of indomethacin and dexamethasone effects on BCRP-mediated drug resistance in MCF-7 parental and resistant cell lines.
Behravan, J; Elahian, F; Kalalinia, F, 2010
)
0.7
"Treatment with mitoxantrone in patients with highly relapsing NMO significantly reduces relapse rates, resulting in subsequent functional stabilization or improvement."( Efficacy and safety of mitoxantrone in patients with highly relapsing neuromyelitis optica.
Kim, HJ; Kim, SH; Kim, W; Li, XF; Park, MS; Sohn, EH, 2011
)
1.03
"Treatment with mitoxantrone brought about statistically significant decreases in relapse rates, progression of disability, gadolinium-enhancing, and new lesions on T2-weighted MRI."( Review of mitoxantrone in the treatment of multiple sclerosis.
Herndon, R; Jeffery, DR, 2004
)
1.07
"Treatment with mitoxantrone is associated with certain adverse events, such as cardiotoxicity."( Mitoxantrone for multiple sclerosis in clinical practice.
Fox, EJ; Rizvi, SA; Zwibel, H, 2004
)
2.11
"Treatment with mitoxantrone and cytarabine resulted in two acute myeloid leukemia patients achieving complete remission and one a partial remission; two patients had progressive disease, and one died in induction."( Mitoxantrone as a single agent and in combination chemotherapy in patients with refractory acute leukemia.
Cuttner, J; Holland, JF; Paciucci, PA, 1984
)
2.05
"treatment with mitoxantrone had AUCs and plasma peak levels of the drug that were significantly higher than those in non-responders (P = 0.03, Fisher's exact test)."( Phase I-II intraperitoneal mitoxantrone in advanced pretreated ovarian cancer.
Costa, L; Ferrazzi, E; Monfardini, S; Nascimben, O; Nicoletto, MO; Padrini, R; Palumbo, M; Tumolo, S; Vinante, O; Visonà, E, 1993
)
0.92
"Treatment with mitoxantrone plus prednisone was associated with greater and longer-lasting improvement in several HQL domains and symptoms than treatment with prednisone alone."( Health-related quality of life in men with metastatic prostate cancer treated with prednisone alone or mitoxantrone and prednisone.
Ernst, DS; Neville, AJ; Osoba, D; Tannock, IF, 1999
)
0.87
"treatment with mitoxantrone."( Clinical pharmacokinetics of mitoxantrone after intraperitoneal administration.
Dubbelman, R; McVie, JG; Nagel, JD; ten Bokkel Huinink, WW; Varossieau, FJ, 1992
)
0.91
"Mice treated with mitoxantrone at a dose of 0.5 mg/kg daily for the 10 days following immunization did not develop any clinical signs and had minimal pathologic signs of disease."( Suppression of acute and relapsing experimental allergic encephalomyelitis with mitoxantrone.
Knobler, RL; Lavasa, M; Lublin, FD; Viti, C, 1987
)
0.82

Toxicity

Most pediatric oncology treatment groups assume that the hematologic toxicity of anthracycline agents is equivalent to their cardiotoxicity. These results suggest that intracavity injection of mitoxantrone is feasible and generally safe in most patients.

ExcerptReferenceRelevance
" Generally, the liposomal application form was more effective and less toxic than the free drug."( Evaluation of incorporation characteristics of mitoxantrone into unilamellar liposomes and analysis of their pharmacokinetic properties, acute toxicity, and antitumor efficacy.
Berger, DP; Berger, MR; Fiebig, HH; Schwendener, RA, 1991
)
0.54
" These two DNA intercalators differed significantly in their cytotoxic potential, mitoxantrone being 24-fold more toxic than mAMSA when assayed by the inhibition of clonogenicity."( Long-term inhibition of DNA synthesis and the persistence of trapped topoisomerase II complexes in determining the toxicity of the antitumor DNA intercalators mAMSA and mitoxantrone.
Fox, ME; Smith, PJ, 1990
)
0.7
" From June 1988 to December 1989, 27 previously untreated patients with early-staged Hodgkin's disease with adverse features for disease-free survival received combined-modality therapy."( NOVP: a novel chemotherapeutic regimen with minimal toxicity for treatment of Hodgkin's disease.
Cabanillas, F; Hagemeister, FB; Liang, JC; McLaughlin, P; Meistrich, ML; Redman, JR; Rodríguez, MA; Romaguera, JE; Swan, F; Velásquez, WS, 1990
)
0.28
" In K562 the sequence Ara-C much greater than MX was significantly more toxic (3."( Synergistic cytotoxicity of cytosine arabinoside and mitoxantrone for K562 and CFU-GM.
Büchner, T; Hiddemann, W; Krehmeier, C; Zühlsdorf, M, 1990
)
0.53
" This suggests that mitoxantrone is oxidised to a toxic intermediate by the MFO system."( The role of reductive and oxidative metabolism in the toxicity of mitoxantrone, adriamycin and menadione in human liver derived Hep G2 hepatoma cells.
Duthie, SJ; Grant, MH, 1989
)
0.84
" The toxic effects were compared with those of adriamycin (ADR)."( [A study of acute toxicity of mitoxantrone].
Bao, DY; Li, GR; Liao, J; Liao, NG; Liu, YQ; Miao, SK; Xiao, Y; Zeng, ZX, 1989
)
0.57
" These results suggest that intracavity injection of mitoxantrone is feasible and generally safe in most patients."( [Efficacy and toxicity of intrapleural mitoxantrone: apropos of 18 cases of pleural metastases of breast cancer].
Brun, B; Calitchi, E; Feuilhade, F; Haddad, E; Le Bourgeois, JP; Otzmeguine, Y; Pierquin, B, 1989
)
0.8
" The results indicate that reserpine enhances the cytotoxicity of mitoxantrone and adriamycin in mildly toxic concentrations (1 and 10 micrograms respectively), in CML cells."( Mitoxantrone & adriamycin cytotoxicity enhanced by reserpine in human chronic myeloid leukaemia cells.
Advani, SH; Chitnis, MP; Kamath, NS, 1989
)
1.96
" Moreover, at low concentrations, ADR was less toxic than MIT in both types of GM-CFCs, but was more toxic than MIT when a concentration of 20 ng/ml was used."( Comparative in vitro toxicity of mitoxantrone and adriamycin in human granulocyte-macrophage progenitor cells.
Brühl, P; Ehninger, G; Heidemann, E; Mergenthaler, HG, 1987
)
0.55
" In four randomized trials the adverse experience profile associated with Novantrone was superior to that of Adriamycin with statistically significant lower incidences of mucositis/stomatitis, nausea, vomiting and alopecia."( Mitoxantrone: an overview of safety and toxicity.
Bernstein, T; Cartwright, K; Dukart, G; Goldberg, J; Posner, LE, 1985
)
1.71
" In mice, LD10, LD50 and LD90 values were respectively, 26, 35 and 47 mg kg-1 28 days following single intravenous injection and 22, 67 and 206 mg kg-1 14 days after single intraperitoneal injection."( Preclinical toxicity of the new antineoplastic agent, ametantrone acetate, in mice and dogs.
Anderson, JA; de la Iglesia, FA; Fitzgerald, JE; Jayasekara, U; Kim, SN; Watkins, JR, 1986
)
0.27
" The spleen weight depression assay indicated that, on a mg/kg basis, DHAD was more toxic to the organ than ADR, with 17."( Comparative toxicity of mitoxantrone and doxorubicin on hematopoietic stem cells.
Buffo, MJ; Kociban, DL; OKunewick, JP, 1985
)
0.58
" The most common adverse clinical effects were nausea and vomiting, stomatitis, and alopecia, though the majority of these cases were mild."( Clinical safety and tolerance of mitoxantrone.
Crossley, RJ, 1984
)
0.55
" 10-fold less toxic than doxorubicin and caused only minor electrocardiogram (ECG) changes."( Comparison of cardiotoxicity of two anthracenediones and doxorubicin in rats.
Beilstein, AK; Zbinden, G, 1982
)
0.26
"Cardiotoxicity is a well recognized side effect of anthracyclines (doxorubicin and epirubicin) or antracenadiones (mitoxantrone) at cumulative or high doses."( Late cardiac toxicity of doxorubicin, epirubicin, and mitoxantrone therapy for Hodgkin's disease in adults.
Arévila, N; Avilés, A; Díaz Maqueo, JC; García, R; Gómez, T; Nambo, MJ, 1993
)
0.74
" Neither nanoparticles nor liposomes were able to reduce the toxic side-effects caused by mitoxantrone, namely leucocytopenia."( Influence of polybutylcyanoacrylate nanoparticles and liposomes on the efficacy and toxicity of the anticancer drug mitoxantrone in murine tumour models.
Beck, P; Fichtner, I; Kreuter, J; Reszka, R,
)
0.56
" In the FAMP group, a direct correlation was found between the LD50 values of both FAMP and Mitox and the number of synergistic interactions, while the Pearson correlation coefficient was not significant in the Pento group."( The in vitro cytotoxic effect of mitoxantrone in combination with fludarabine or pentostatin in B-cell chronic lymphocytic leukemia.
Brugiatelli, M; Callea, I; Console, G; Filangeri, M; Iacopino, P; Morabito, F; Musolino, C; Oliva, B; Sculli, G; Stelitano, C,
)
0.41
" Furthermore, we evaluated the times for hematopoietic reconstitution in a group of five BC patients in the high-risk adjuvant situation who underwent HD chemotherapy and hematopoietic rescue with positive/negative selected stem cells and compared it with our own data from 10 BC patients who, after identical HD therapy, received only positively selected CD34+ cells and 14 patients who, after identical HD therapy, received autografts purged by incubation with toxic ether lipids (ET-18-OCH3)."( Efficacy and safety of simultaneous immunomagnetic CD34+ cell selection and breast cancer cell purging in peripheral blood progenitor cell samples used for hematopoietic rescue after high-dose therapy.
Berdel, WE; Cassens, U; Fietz, T; Hilgenfeld, E; Hoffmann, M; Hoppe, B; Kienast, J; Knauf, WU; Koenigsmann, M; Mohr, M; Sibrowski, W; Thiel, E, 1999
)
0.3
"Acute toxic effects of the antineoplastic anthraquinones carminomycin, epirubicin, idarubicin and mitoxantrone were studied in primary cultures of cardiomyocytes, which were isolated from adult rats."( Anthraquinone-induced cell injury: acute toxicity of carminomycin, epirubicin, idarubicin and mitoxantrone in isolated cardiomyocytes.
Andersson, BS; Carlberg, M; Eksborg, S; Sundberg, M; Vidal, RF, 1999
)
0.74
" No toxic deaths have occurred."( Etoposide, mitoxantrone and prednisone: a salvage regimen with low toxicity for refractory or relapsed non-Hodgkin's lymphoma.
Budel, L; Doorduijn, JK; Löwenberg, B; Sonneveld, P; Spruit, P; van Der Holt, B; van't Veer, M, 2000
)
0.7
" With both P388 and HL-60 cells, cryptolepine proved about four times more toxic than its isomer."( Cytotoxicity and cell cycle effects of the plant alkaloids cryptolepine and neocryptolepine: relation to drug-induced apoptosis.
Bailly, C; Dassonneville, L; Lansiaux, A; Mahieu, C; Pieters, L; Van Miert, S; Wattelet, A; Wattez, N, 2000
)
0.31
"Cardiotoxicity, a side-effect that can occur after treatment with an anticancer drug, has severe clinical implications."( In vitro screening of antitumour agents for cardiotoxicity by means of isolated mouse left atria.
Bast, A; Haenen, GR; van Acker, FA; van Acker, SA; van der Vijgh, WJ,
)
0.13
" In CD2F1 mice, LEM was significantly less toxic as compared with MTO."( Improved safety, pharmacokinetics and therapeutic efficacy profiles of a novel liposomal formulation of mitoxantrone.
Ahmad, I; Gokhale, PC; Kasid, U; Pei, J; Rahman, A; Zhang, C,
)
0.35
" A liver biopsy revealed a grade II toxic hepatitis."( Methotrexate-associated liver toxicity in a patient with breast cancer: case report and literature review.
Bogers, J; Schrijvers, D; van den Brande, J; van Marck, E; van Outryve, S; Vermorken, JB; Wilmes, P, 2002
)
0.31
"The toxicity of most drugs is associated with their enzymatic conversion to toxic metabolites."( Saccharomyces cerevisiae as an eukaryotic cell model to assess cytotoxicity and genotoxicity of three anticancer anthraquinones.
Buschini, A; Poli, P; Rossi, C, 2003
)
0.32
" Pixantrone (PIX) is an analogue of MX devoid of toxic effects on cardiac tissue and was developed as a replacement for other anthracenediones in cancer patients."( Pixantrone (BBR2778): a new immunosuppressant in multiple sclerosis with a low cardiotoxicity.
Dubois, B; Gonsette, RE, 2004
)
0.32
" TMJ is a safe and effective regimen when used as a part of autologous stem cell transplant for patients with HD and NHL."( High dose chemotherapy with thiotepa, mitoxantrone and carboplatin (TMJ) followed by autologous stem cell support in 100 consecutive lymphoma patients in a single centre: analysis of efficacy, toxicity and prognostic factors.
Ahmed, T; Hoang, A; Kancherla, R; Liu, D; Qureshi, Z; Seiter, K; Waheed, F, 2004
)
0.59
"Treatment of patients with mitoxantrone for worsening multiple sclerosis (MS) requires careful monitoring for possible adverse events."( Mitoxantrone treatment of multiple sclerosis: safety considerations.
Cohen, BA; Mikol, DD, 2004
)
2.06
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004
)
0.32
" Glatiramer Acetate appears a safe and effective option for continuing disease modification in patients with relapsing remitting multiple sclerosis treated with Mitoxantrone."( Sequential maintenance treatment with glatiramer acetate after mitoxantrone is safe and can limit exposure to immunosuppression in very active, relapsing remitting multiple sclerosis.
Boggild, M; Das, K; Jacob, A; Ramtahal, J, 2006
)
0.77
"To investigate spontaneous reports of TdP present in the public version of the FDA Adverse Event Reporting System (AERS) in the light of what is already known on their TdP-liability."( Drug-induced torsades de pointes: data mining of the public version of the FDA Adverse Event Reporting System (AERS).
De Ponti, F; Moretti, U; Poluzzi, E; Raschi, E, 2009
)
0.35
" Cases were represented by TdP reports, whereas non-cases were all reports of adverse drug reactions other than TdP."( Drug-induced torsades de pointes: data mining of the public version of the FDA Adverse Event Reporting System (AERS).
De Ponti, F; Moretti, U; Poluzzi, E; Raschi, E, 2009
)
0.35
"Large spontaneous reporting databases represent an important source for signal detection of rare adverse drug reactions (ADR), such as TdP."( Drug-induced torsades de pointes: data mining of the public version of the FDA Adverse Event Reporting System (AERS).
De Ponti, F; Moretti, U; Poluzzi, E; Raschi, E, 2009
)
0.35
" The patients were monitored for the adverse effects."( Efficacy and safety of mitoxantrone, as an initial therapy, in multiple sclerosis: experience in an Indian tertiary care setting.
Geeta, S; Hundalani, SG; Menon, S; Singhal, BS,
)
0.44
" The adverse events noted in the entire cohort were leucopenia in four patients and asymptomatic reversible decrease in cardiac ejection fraction in one patient."( Efficacy and safety of mitoxantrone, as an initial therapy, in multiple sclerosis: experience in an Indian tertiary care setting.
Geeta, S; Hundalani, SG; Menon, S; Singhal, BS,
)
0.44
"To evaluate the incidence and potential predictors of adverse events associated with mitoxantrone at the MS Clinic, University of British Columbia, Canada."( Cardiotoxicity and other adverse events associated with mitoxantrone treatment for MS.
Geddes, J; Isserow, S; Kingwell, E; Koch, M; Leung, B; Rieckmann, P; Tremlett, H, 2010
)
0.83
" Generalized estimating equations were used to examine potential predictors of adverse events (graded according to the Common Toxicity Criteria, version 4) in patients with normal baseline and > or =1 follow-up MUGA or laboratory assessment."( Cardiotoxicity and other adverse events associated with mitoxantrone treatment for MS.
Geddes, J; Isserow, S; Kingwell, E; Koch, M; Leung, B; Rieckmann, P; Tremlett, H, 2010
)
0.61
"Cytoreduction with 4 courses of R-FM was safe and highly efficient in patients with recurrent/refractory follicular lymphoma who had high tumor burden; however, better consolidation than FM is needed to further improve outcome."( Efficacy and safety of the combination of rituximab, fludarabine, and mitoxantrone for rituximab-naive, recurrent/refractory follicular non-Hodgkin lymphoma with high tumor burden: a multicenter phase 2 trial by the Groupe d'Etude des Lymphomes de l'Adult
Brice, P; Copin, MC; Fermé, C; Feugier, P; Lamy, T; Morschhauser, F; Mounier, N; Sebban, C; Solal-Celigny, P; Tilly, H, 2010
)
0.59
" The findings of the present study suggest that FLANG salvage chemotherapy is an effective regimen and that it offers a safe bridge to SCT."( FLANG salvage chemotherapy is an effective regimen that offers a safe bridge to transplantation for patients with relapsed or refractory acute myeloid leukemia.
Cho, BS; Cho, SG; Choi, SM; Eom, KS; Kim, CC; Kim, HJ; Kim, YJ; Lee, DG; Lee, JW; Lee, S; Min, CK; Min, WS, 2011
)
0.37
" No patients had serious adverse effects during the mean follow-up period of 41 months after completing therapy."( Efficacy and safety of mitoxantrone in patients with highly relapsing neuromyelitis optica.
Kim, HJ; Kim, SH; Kim, W; Li, XF; Park, MS; Sohn, EH, 2011
)
0.68
" The most common adverse effects were hematologic, with 2 patients experiencing treatment-related myelodysplastic syndrome (MDS), evolving to acute myelogenous leukemia (AML) in 1 patient."( Safety and efficacy of combination therapy with fludarabine, mitoxantrone, and rituximab followed by yttrium-90 ibritumomab tiuxetan and maintenance rituximab as front-line therapy for patients with follicular or marginal zone lymphoma.
Bayer, R; Fung, HC; Gregory, SA; Karmali, R; Kassar, M; O'Brien, T; Shammo, JM; Venugopal, P, 2011
)
0.61
" Redox inactivity in the face of high cardiac uptake suggests that pixantrone might also be safe in doxorubicin-naïve patients."( The novel anthracenedione, pixantrone, lacks redox activity and inhibits doxorubicinol formation in human myocardium: insight to explain the cardiac safety of pixantrone in doxorubicin-treated patients.
Chello, M; Covino, E; Menna, P; Minotti, G; Paz, OG; Salvatorelli, E; Singer, JW, 2013
)
0.39
" Safety and tolerability of fingolimod were evaluated by adverse events monitoring, laboratory tests, and ophthalmological and skin assessment."( Evaluation of efficacy, safety and tolerability of fingolimod in patients with the relapsing form of multiple sclerosis - 12-month observation. A preliminary report.
Maciejek, Z; Niezgodzińska-Maciejek, A; Wawrzyniak, S; Wójcik-Drączkowska, H,
)
0.13
" During fingolimod treatment there was no new relapse in any patient and no patient stopped the treatment because of any adverse event."( Evaluation of efficacy, safety and tolerability of fingolimod in patients with the relapsing form of multiple sclerosis - 12-month observation. A preliminary report.
Maciejek, Z; Niezgodzińska-Maciejek, A; Wawrzyniak, S; Wójcik-Drączkowska, H,
)
0.13
"In our study patients fingolimod was effective, safe and well tolerated independently of disease activity and previous treatment."( Evaluation of efficacy, safety and tolerability of fingolimod in patients with the relapsing form of multiple sclerosis - 12-month observation. A preliminary report.
Maciejek, Z; Niezgodzińska-Maciejek, A; Wawrzyniak, S; Wójcik-Drączkowska, H,
)
0.13
" Two toxic deaths were observed."( High response rate and acceptable toxicity of a combination of rituximab, vinorelbine, ifosfamide, mitoxantrone and prednisone for the treatment of diffuse large B-cell lymphoma in first relapse: results of the R-NIMP GOELAMS study.
Alexis, M; Arakelyan, N; Banos, A; Cartron, G; Courby, S; Damotte, D; Dreyfus, F; Fontan, J; Gressin, R; Gyan, E; Lamy, T; Laribi, K; Le Gouill, S; Maisonneuve, H; Quittet, P; Schmidt-Tanguy, A; Sénécal, D; Solal-Céligny, P; Tournilhac, O, 2013
)
0.61
" Thus, a network of multiple-treatments meta-analysis was performed using four clinical outcomes: 'patients free of relapse', 'patients without disease progression', 'patients without MRI progression' and 'patients with adverse events'."( A network meta-analysis of randomized controlled trials for comparing the effectiveness and safety profile of treatments with marketing authorization for relapsing multiple sclerosis.
Bakalos, G; Doxani, C; Grigoriadis, N; Hadjigeorgiou, GM; Miligkos, M; Mprotsis, T; Papadimitriou, D; Ziakas, P; Zintzaras, E, 2013
)
0.39
" Regarding 'patients with adverse events', no data were available for all comparisons to make fair inferences."( A network meta-analysis of randomized controlled trials for comparing the effectiveness and safety profile of treatments with marketing authorization for relapsing multiple sclerosis.
Bakalos, G; Doxani, C; Grigoriadis, N; Hadjigeorgiou, GM; Miligkos, M; Mprotsis, T; Papadimitriou, D; Ziakas, P; Zintzaras, E, 2013
)
0.39
" One of the treated groups suffered euthanasia on day 22 (MTX22) to evaluate early MTX toxic effects, while the other suffered euthanasia on day 48 (MTX48), to allow the evaluation of MTX late effects."( Cumulative mitoxantrone-induced haematological and hepatic adverse effects in a subchronic in vivo study.
Arbo, M; Costa, VM; Dallegrave, E; de Lourdes Bastos, M; Dinis-Oliveira, RJ; Duarte, JA; Palmeira, C; Remião, F; Rossato, LG; Santos-Silva, A, 2014
)
0.79
" Adverse events included nausea and vomiting, fatigue, alopecia, palpitation, cardiomyopathy and mild leukopenia."( Safety and efficacy of mitoxantrone in pediatric patients with aggressive multiple sclerosis.
Abtahi, SH; Afzali, P; Etemadifar, M; Fereidan-Esfahani, M; Murray, RT; Nourian, SM; Ramagopalan, SV, 2014
)
0.71
" Continuing research is needed to establish its efficacy and safety profile in a multinational collaboration with careful follow-up of adverse events."( Safety and efficacy of mitoxantrone in pediatric patients with aggressive multiple sclerosis.
Abtahi, SH; Afzali, P; Etemadifar, M; Fereidan-Esfahani, M; Murray, RT; Nourian, SM; Ramagopalan, SV, 2014
)
0.71
"The results of our study confirm that MTX therapy is safe for carefully selected and closely monitored MS patients."( The N-terminal pro-brain natriuretic peptide as a marker of mitoxantrone-induced cardiotoxicity in multiple sclerosis patients.
Kamińska, AM; Kochanowski, J; Kwieciński, H; Opolski, G; Podlecka-Piętowska, A; Zakrzewska-Pniewska, B, 2014
)
0.64
"Exploring the relationships among adverse events is important because those that arise from a common mechanism are amenable to a common intervention, which can improve symptom management, quality of life, and treatment adherence."( Identifying Severe Adverse Event Clusters Using the National Cancer Institute's Common Terminology Criteria for Adverse Events.
Hershman, DL; Lee, SM; Lim, EA; Moinpour, CM; Unger, J; Zhong, X, 2016
)
0.43
"The CTCAE data from a randomized clinical trial conducted by SWOG that compared docetaxel plus estramustine versus mitoxantrone plus predinsone in patients with advanced prostate cancer were used to identify severe adverse event clusters."( Identifying Severe Adverse Event Clusters Using the National Cancer Institute's Common Terminology Criteria for Adverse Events.
Hershman, DL; Lee, SM; Lim, EA; Moinpour, CM; Unger, J; Zhong, X, 2016
)
0.64
"A total of 109 adverse event types were captured using the CTCAE."( Identifying Severe Adverse Event Clusters Using the National Cancer Institute's Common Terminology Criteria for Adverse Events.
Hershman, DL; Lee, SM; Lim, EA; Moinpour, CM; Unger, J; Zhong, X, 2016
)
0.43
"Several severe adverse event clusters were identified in patients with advanced prostate cancer."( Identifying Severe Adverse Event Clusters Using the National Cancer Institute's Common Terminology Criteria for Adverse Events.
Hershman, DL; Lee, SM; Lim, EA; Moinpour, CM; Unger, J; Zhong, X, 2016
)
0.43
"In this article, we review the potential adverse effects and recommended laboratory studies as part of the monitoring strategy following initiation of various first generation DMTs and their recently approved versions."( Update on monitoring and adverse effects of first generation disease modifying therapies and their recently approved versions in relapsing forms of multiple sclerosis.
Cano, CA; Dubey, D; Stüve, O, 2016
)
0.43
" MTX was more toxic in equivalent concentrations in all cytotoxicity tests performed [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide reduction, neutral red uptake, and lactate dehydrogenase release assays] and times tested (24 and 48 h)."( Naphthoquinoxaline metabolite of mitoxantrone is less cardiotoxic than the parent compound and it can be a more cardiosafe drug in anticancer therapy.
Bastos, ML; Carvalho, F; Carvalho, RA; Costa, VM; Gomes, AS; Pinto, M; Reis-Mendes, A; Remião, F; Sousa, E, 2017
)
0.74
" We analyzed the main outcomes, including the overall survival (OS), progression-free survival (PFS), prostate-specific antigen (PSA) response, tumor response and severe adverse events (AEs)."( The efficacy and safety comparison of docetaxel, cabazitaxel, estramustine, and mitoxantrone for castration-resistant prostate cancer: A network meta-analysis.
Huang, C; Song, P; Wang, Y, 2018
)
0.71
"Cardiotoxicity was ascertained through adverse event monitoring over the course of follow-up among 1,022 pediatric patients with acute myeloid leukemia treated in the Children's Oncology Group trial AAML0531."( Occurrence of Treatment-Related Cardiotoxicity and Its Impact on Outcomes Among Children Treated in the AAML0531 Clinical Trial: A Report From the Children's Oncology Group.
Alonzo, T; Aplenc, R; Gamis, A; Gerbing, RB; Getz, KD; Ky, B; Leahy, AB; Leger, KJ; Sack, L; Sung, L; Woods, WG, 2019
)
0.51
" Most pediatric oncology treatment groups assume that the hematologic toxicity of anthracycline agents is equivalent to their cardiotoxicity; for example, Children's Oncology Group substitution rules consider daunorubicin and epirubicin isoequivalent to doxorubicin, whereas mitoxantrone and idarubicin are considered 4 to 5 times as toxic as doxorubicin."( Derivation of Anthracycline and Anthraquinone Equivalence Ratios to Doxorubicin for Late-Onset Cardiotoxicity.
Armstrong, GT; Aune, GJ; Chow, EJ; Feijen, EAM; Green, DM; Hudson, MM; Kremer, LCM; Leisenring, WM; Loonen, J; Ness, KK; Oeffinger, KC; Robison, LL; Stratton, KL; van Dalen, EC; van der Pal, HJH; Yasui, Y, 2019
)
0.69
" Yet, it may serve as a safe and reliable alternative in cases where the radioactive technique is unavailable."( Safety and Efficacy of Mitoxantrone Hydrochloride Injection for Identification of Axillary Sentinel Lymph Nodes in Patients with Primary Breast Cancer.
Abdelaal, M; Elzayat, I; Monib, S, 2023
)
1.22
"Cardiotoxicity is among the most important adverse effects of childhood cancer treatment."( Acute and early-onset cardiotoxicity in children and adolescents with cancer: a systematic review.
Bolier, M; Feijen, EAM; Grotenhuis, HB; Hoesein, FAAM; Kouwenberg, TW; Kremer, LCM; Mavinkurve-Groothuis, AMC; Netea, SA; Slieker, MG; van Dalen, EC, 2023
)
0.91

Pharmacokinetics

Median values obtained for the pharmacokinetic parameters of mitoxantrone in peritoneal dialysate were: t1/2 beta (distribution), 56.5 mg/m2. Median terminal half-life was similar to that of the mono- and dicarboxylic acid and was 75 h.

ExcerptReferenceRelevance
" The drug was quantified in plasma with an HPLC assay and pharmacokinetic analysis was performed with the APIS software."( Pharmacokinetics of mitoxantrone in cancer patients treated by high-dose chemotherapy and autologous bone marrow transplantation.
Blaise, D; Cano, JP; Gaspard, MH; Iliadis, A; Just-Landi, S; Launay-Iliadis, MC; Maraninchi, D; Richard, B; Stoppa, AM; Viens, P, 1992
)
0.61
" Median values obtained for the pharmacokinetic parameters of mitoxantrone in peritoneal dialysate were: t1/2 beta (distribution), 56."( Clinical pharmacokinetics of mitoxantrone after intraperitoneal administration.
Dubbelman, R; McVie, JG; Nagel, JD; ten Bokkel Huinink, WW; Varossieau, FJ, 1992
)
0.82
" The pharmacokinetic parameters are described adequately by a three-compartment model with a terminal half-life of 71."( Pharmacokinetic and pharmacodynamic studies with mitoxantrone in the treatment of patients with nasopharyngeal carcinoma.
Chang, SP; Chen, KY; Hu, OY; Jian, JM; Law, CK, 1992
)
0.54
"Phase I and pharmacokinetic studies were performed in order to evaluate the maximum tolerated dose and the efficiency of 120 h continuous venous infusion (CVI) of mitoxantrone."( Phase I/II pharmacokinetic study of mitoxantrone by continuous venous infusion in patients with solid tumours and lymphoproliferative diseases.
Bugat, R; Canal, P; Chevreau, C; de Forni, M; Huguet, F; Lachau, S; Laurent, G; Roche, H, 1991
)
0.75
" This paper reports the pharmacokinetic studies of 3H-mitoxantrone in mice by liquid scintillation."( [A study on pharmacokinetics of 3H-mitoxantrone in experimental animals].
Bao, D; Fang, Z; Kong, G, 1990
)
0.8
" Early pharmacokinetic studies of mitoxantrone in experimental animals using radioactive material showed an extensive tissue distribution and a long terminal plasma half-life."( Pharmacokinetics and metabolism of mitoxantrone. A review.
Blanz, J; Ehninger, G; Proksch, B; Schuler, U; Zeller, KP, 1990
)
0.84
"The pharmacokinetic parameters of mitoxantrone in patients with liver metastasis after intra-arterial 2 h and 24 h infusion (dosage 12 mg/m2) were investigated."( Pharmacokinetics of mitoxantrone in patients after 2 h and 24 h intra-arterial administration.
Czejka, MJ; Georgopoulos, A; Jäger, W; Schüller, J,
)
0.73
" Pharmacokinetic studies were performed by high-performance liquid chromatography (HPLC) with ultraviolet (UV) detection."( A phase I pharmacokinetic study of 21-day continuous infusion mitoxantrone.
de Vries, EG; Greidanus, J; Mulder, NH; Oosterhuis, B; Sleijfer, DT; Uges, DR; Willemse, PH, 1989
)
0.52
" route was studied in a Phase I and pharmacokinetic trial."( Phase I clinical and pharmacokinetic study of mitoxantrone given to patients by intraperitoneal administration.
Alberts, DS; Graham, V; McCloskey, T; McDonald, L; Peng, YM; Rivest, R; Roe, D; Surwit, EA, 1988
)
0.53
" Pharmacokinetic and metabolic research is essential to a better understanding of the pharmacological and toxicological activities of drugs and their metabolites."( Extrapolation of preclinical pharmacokinetic data to therapeutic drug use.
Cano, JP; Fabre, G; Rahmani, R; Richard, B, 1988
)
0.27
" The pharmacokinetic parameters for ametantrone acetate (CI-881) were characterized in six patients concurrently with the phase I clinical trial."( Pharmacokinetics of ametantrone acetate (NSC-287513).
Balmer, CE; Bender, JF; Grillo-Lopez, AJ; Kuhn, JG; Loesch, DM; Ludden, TM; Von Hoff, DD, 1987
)
0.27
" The pharmacokinetic parameters were also defined in five patients who were treated with combination chemotherapy (mitoxantrone 12 mg/m2, methotrexate 30 mg/m2 and vincristine 2 mg)."( Pharmacokinetics of mitoxantrone in humans following single-agent infusion or intra-arterial injection therapy or combined-agent infusion therapy.
de Planque, MM; Deneve, W; McVie, JG; Schoemaker, TJ; Smith, IE; Van Belle, SJ; van Oosterom, AT, 1986
)
0.8
" The pharmacokinetic parameters are adequately described by a three-compartment model with a terminal half-life of 214."( The pharmacokinetics and metabolism of mitoxantrone in man.
Ehninger, G; Heinzel, G; Proksch, B; Schiller, E; Weible, KH; Woodward, DL, 1985
)
0.54
" Distribution and half-life data provide a pharmacological rationale for the use of mitoxantrone on an intermittent dosing schedule."( Pharmacology of mitoxantrone: mode of action and pharmacokinetics.
Alberts, DS; Bowden, GT; Dalton, WS; Mackel, C; Peng, YM, 1985
)
0.84
" There was a large interpatient variability of the area under the time versus concentration curve (AUC) for all three drugs."( Pharmacokinetics of mitoxantrone, etoposide and cytosine arabinoside in leukemic cells during treatment of acute myelogenous leukemia--relationship to treatment outcome and bone marrow toxicity.
Björkholm, M; Gruber, A; Liliemark, E; Liliemark, J; Paul, C; Peterson, C; Tidefelt, U, 1995
)
0.61
" Whereas cellular versus plasma maximum concentration ratio was near 1, the area under the concentration +/- time curve ratio reached 100, suggesting a long elimination half-life from cells."( Plasma and cellular pharmacokinetics of mitoxantrone in high-dose chemotherapeutic regimen for refractory lymphomas.
Attal, M; Bugat, R; Canal, P; Chatelut, E; Guichard, S; Houin, G; Huguet, F; Laurent, G; Muller, C; Schlaifer, D, 1993
)
0.55
" No significant changes in mean mitoxantrone plasma elimination rates (ie, terminal plasma half-life and total-body clearance rate) occurred as the mitoxantrone dose doubled, indicating linear pharmacokinetics."( Phase I clinical and pharmacokinetic evaluation of high-dose mitoxantrone in combination with cytarabine in patients with acute leukemia.
Ahmed, T; Alberts, DS; Arlin, Z; Baier, M; Baskind, P; Feldman, EJ; Mittelman, A; Peng, YM; Plezia, P, 1993
)
0.81
" The pharmacokinetic parameters of DHAQ-PBCA-NP-FDIn and DHAQ-SIn were presented by statistical moment."( [Study on pharmacokinetics of mitoxantrone polycyanoacrylate nanoparticles freeze-dried injection by HPLC column switching technique].
Liao, GT; Ye, LM; Zhang, ZR, 1995
)
0.58
"Two liposomal formulations of mitoxantrone (MTO) were compared with the aqueous solution (free MTO) in terms of their pharmacokinetic behaviour in ICR mice and cytotoxic activity in a nude mouse xenograft model."( Comparative pharmacokinetic and cytotoxic analysis of three different formulations of mitoxantrone in mice.
Hänseler, E; Horber, DH; Rentsch, KM; Schwendener, RA; Wunderli-Allenspach, H, 1997
)
0.81
" Pharmacokinetic parameters of f-MTO and 1-MTO were calculated."( Pharmacokinetic studies of mitoxantrone and one of its metabolites in serum and urine in patients with advanced breast cancer.
Hänseler, E; Pestalozzi, BC; Rentsch, KM; Sauter, C; Schwendener, RA; Wunderli-Allenspach, H, 1998
)
0.6
"1-MTO had a significantly longer half-life of distribution in the deep (third) compartment and thus a larger area under the curve (AUC) than f-MTO."( Pharmacokinetic studies of mitoxantrone and one of its metabolites in serum and urine in patients with advanced breast cancer.
Hänseler, E; Pestalozzi, BC; Rentsch, KM; Sauter, C; Schwendener, RA; Wunderli-Allenspach, H, 1998
)
0.6
"f-MTO and 1-MTO exhibited different distribution patterns in the deep compartment with a significantly increased half-life for 1-MTO."( Pharmacokinetic studies of mitoxantrone and one of its metabolites in serum and urine in patients with advanced breast cancer.
Hänseler, E; Pestalozzi, BC; Rentsch, KM; Sauter, C; Schwendener, RA; Wunderli-Allenspach, H, 1998
)
0.6
" LEM also demonstrated favourable pharmacokinetic profiles."( Improved safety, pharmacokinetics and therapeutic efficacy profiles of a novel liposomal formulation of mitoxantrone.
Ahmad, I; Gokhale, PC; Kasid, U; Pei, J; Rahman, A; Zhang, C,
)
0.35
" The method was used to successfully quantify mitoxantrone in mouse plasma and tissue samples to support a pharmacokinetic study of LEM-ETU in mice."( Improved liquid chromatographic method for mitoxantrone quantification in mouse plasma and tissues to study the pharmacokinetics of a liposome entrapped mitoxantrone formulation.
Abu-Qare, AW; Ahmad, A; Ahmad, I; Ayoub, JE; Johnson, JL; Khan, S; Wang, YF; Zhang, A, 2004
)
0.84
" The recovery of MTO, as well as the precision, linearity, and accuracy of the method for both free and liposomal MTO, appears satisfactory for pharmacokinetic studies."( Separation of liposome-entrapped mitoxantrone from nonliposomal mitoxantrone in plasma: pharmacokinetics in mice.
Ahmad, A; Ahmad, I; Wang, YF, 2005
)
0.61
" 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
"To determine the pharmacokinetic (PK) profile of manganese (Mn) after a 2-hour intravenous infusion of mangafodipir at 5 micromol/kg body weight and to correlate Mn concentrations with oxidative stress, early decrease in serum total bilirubin concentration, and prothrombin time (PT) in chronic alcoholic patients with acute alcoholic hepatitis."( Pharmacokinetic-pharmacodynamic modeling of manganese after a single intravenous infusion of mangafodipir in patients with acute alcoholic hepatitis.
Batteux, F; Debray, M; Hirt, D; Laurent, A; Pavlovic, S; Poupon, J; Richardet, JP; Sogni, P; Treluyer, JM; Urien, S; Weill, B, 2009
)
0.35
" This assay was successfully applied in a pharmacokinetic and tissue distribution study of mitoxantrone in mice."( HPLC analysis of mitoxantrone in mouse plasma and tissues: application in a pharmacokinetic study.
An, G; Morris, ME, 2010
)
0.92
"The objective of this investigation was to compare the observed biliary clearance (CL(b)) and % of dose excreted in the bile (PD(b)) of mitoxantrone with the predicted values obtained from quantitative structure pharmacokinetic relationship (QSPKR) models."( Pharmacokinetics and biliary excretion of mitoxantrone in rats.
Morris, ME; Yang, X, 2010
)
0.83
" Finally, the method was successfully applied to a pharmacokinetic study of mitoxantrone in rats following intravenous administration."( Determination of mitoxantrone in rat plasma by liquid chromatography-tandem mass spectrometry method: Application to a pharmacokinetic study.
He, Z; Ling, G; Pu, X; Sun, J; Sun, Y; Wang, Z; Zhang, P, 2010
)
0.93
" The pharmacokinetic comparability of Prolastin-C to Prolastin was assessed in subjects with AAT deficiency."( Pharmacokinetic comparability of Prolastin®-C to Prolastin® in alpha₁-antitrypsin deficiency: a randomized study.
Brantly, ML; Campos, MA; Chapman, KR; Kueppers, F; Sandhaus, RA; Stocks, JM; Strange, C; Turino, G; Wang-Smith, L, 2010
)
0.36
" Pharmacokinetic plasma samples were drawn over 7 days following last dose in the first treatment period and over 10 days following the last dose in the second period."( Pharmacokinetic comparability of Prolastin®-C to Prolastin® in alpha₁-antitrypsin deficiency: a randomized study.
Brantly, ML; Campos, MA; Chapman, KR; Kueppers, F; Sandhaus, RA; Stocks, JM; Strange, C; Turino, G; Wang-Smith, L, 2010
)
0.36
"09, demonstrating pharmacokinetic equivalence between the 2 products."( Pharmacokinetic comparability of Prolastin®-C to Prolastin® in alpha₁-antitrypsin deficiency: a randomized study.
Brantly, ML; Campos, MA; Chapman, KR; Kueppers, F; Sandhaus, RA; Stocks, JM; Strange, C; Turino, G; Wang-Smith, L, 2010
)
0.36
"Prolastin-C demonstrated pharmacokinetic equivalence and a comparable safety profile to Prolastin."( Pharmacokinetic comparability of Prolastin®-C to Prolastin® in alpha₁-antitrypsin deficiency: a randomized study.
Brantly, ML; Campos, MA; Chapman, KR; Kueppers, F; Sandhaus, RA; Stocks, JM; Strange, C; Turino, G; Wang-Smith, L, 2010
)
0.36
" The pharmacokinetic study of Mit-lipo and Mit-free was performed on dogs following a single intravenous injection."( [Pharmacodynamics, pharmacokinetics and tissue distribution of liposomal mitoxantrone hydrochloride].
Li, CL; Li, YH; Wang, CX; Wei, N; Yang, HY; Zhang, L; Zhao, X, 2010
)
0.59
" We show the feasibility of real-time, direct pharmacodynamic monitoring by flow cytometry during clinical trials combining intensive chemotherapy and signal transduction inhibitors."( Single-cell pharmacodynamic monitoring of S6 ribosomal protein phosphorylation in AML blasts during a clinical trial combining the mTOR inhibitor sirolimus and intensive chemotherapy.
Carroll, M; Kasner, MT; Luger, SM; Perl, AE; Shank, D, 2012
)
0.38
"We conducted a pharmacokinetic (PK) study of mitoxantrone (Novantrone®), a clinically well-established anticancer agent, in mice and developed a mechanism-based PBPK (physiologically based pharmacokinetic) model to describe its disposition."( A physiologically based pharmacokinetic model of mitoxantrone in mice and scale-up to humans: a semi-mechanistic model incorporating DNA and protein binding.
An, G; Morris, ME, 2012
)
0.89
" Samples for pharmacokinetic studies were collected."( Phase I clinical trial of pegylated liposomal mitoxantrone plm60-s: pharmacokinetics, toxicity and preliminary efficacy.
Du, P; Gui, L; Han, X; Li, C; Li, N; Liu, P; Shi, Y; Song, Y; Yang, J; Zhang, S; Zhao, X, 2014
)
0.66
" The pharmacokinetic profile of plm60-s was remarkably altered."( Phase I clinical trial of pegylated liposomal mitoxantrone plm60-s: pharmacokinetics, toxicity and preliminary efficacy.
Du, P; Gui, L; Han, X; Li, C; Li, N; Liu, P; Shi, Y; Song, Y; Yang, J; Zhang, S; Zhao, X, 2014
)
0.66
" Herein, the intracellular pharmacokinetic behavior of D-luciferin was investigated in pancreatic cancer cell lines in real time by using bioluminescence imaging."( Gemcitabine upregulates ABCG2/BCRP and modulates the intracellular pharmacokinetic profiles of bioluminescence in pancreatic cancer cells.
Gu, M; Li, F; Liu, J; Sun, Y; Wei, Y; Xiong, Y; Zhu, L, 2016
)
0.43
"The LHRH-MTO-LIPs demonstrated a superior pharmacokinetic profile relative to free MTO."( Pharmacokinetics, distribution and anti-tumor efficacy of liposomal mitoxantrone modified with a luteinizing hormone-releasing hormone receptor-specific peptide.
Feng, W; He, Y; Ren, Y; Song, C; Wang, Y; Zhang, L, 2018
)
0.72

Compound-Compound Interactions

A trial of the second-generation proteasome inhibitor ixazomib in combination with MEC was conducted in patients with R/R AML. A phase II clinical study was performed to evaluate the effectiveness and toxicity of cladribine (2-CdA) combined with mitoxantrone (CM regimen)

ExcerptReferenceRelevance
"38 patients with advanced breast adenocarcinoma were treated in a phase II study with 5-fluorouracil and high-dose folinic acid combined with cyclophosphamide and mitoxantrone."( A phase II study of 5-fluorouracil and high-dose folinic acid in combination with cyclophosphamide and mitoxantrone for advanced breast cancer.
Aitini, E; Cantore, M; Cavazzini, G; Di Marco, A; Rabbi, C; Rivera, A; Smerieri, F; Togliani, B, 1992
)
0.69
"To investigate the effects of mitoxantrone in combination with other anticancer agents, a human T-cell leukemia cell line, MOLT-3, was incubated for 3 days in the presence of two drugs (mitoxantrone and the combined drug) and cell growth inhibition was determined by assay with 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazonium bromide."( Effects of mitoxantrone in combination with other anticancer agents on a human leukemia cell line.
Akutsu, M; Kano, Y; Suda, K; Suzuki, K, 1992
)
0.96
" Chronic treatment with these drugs or each combined with ICRF-187 did not change the antioxidant levels relative to the control values."( Comparative study of doxorubicin, mitoxantrone, and epirubicin in combination with ICRF-187 (ADR-529) in a chronic cardiotoxicity animal model.
Alderton, PM; Green, MD; Gross, J, 1992
)
0.56
" The low toxicity combined with worthwhile remissions make this an attractive first-line option for elderly patients."( Phase 2 study of mitozantrone in combination with chlorambucil and prednisolone for relapsed and refractory non-Hodgkins lymphoma.
Cotter, FE; Jones, L; Lord, D; Newland, AC,
)
0.13
" Neoadjuvant (cytoreductive) chemotherapy combined with early secondary surgical debulking is feasible, with little severe morbidity, and can leave a high proportion of patients free of macroscopic disease."( Neoadjuvant (cytoreductive) chemotherapy combined with intervention debulking surgery in advanced, unresected epithelial ovarian cancer.
Blackledge, G; Chan, KK; Lawton, FG; Luesley, DM; Redman, CW, 1989
)
0.28
"To determine optimal dosage, Dihydroxyanthracenedione (DHAD) was given once daily for 3 days at dosage levels of 6, 7, 8, and 10 mg/m2 in combination with a 7-day continuous infusion of cytosine arabinoside (Ara-C)."( Toxicity evaluation of dihydroxyanthracenedione (DHAD) in combination with cytosine arabinoside (Ara-C).
Civin, CI; Krischer, J; Land, VJ; Ragab, AH; Steuber, CP; Vietti, TJ, 1987
)
0.27
"The efficacy of mitoxantrone in combination with vinblastine was assessed in 156 patients with metastatic breast cancer who had been treated previously with one or multiple chemotherapeutic regimens."( Chemotherapy with mitoxantrone in combination with continuous infusion vinblastine for metastatic breast cancer.
Blumenschein, GR; Buzdar, AU; Fraschini, G; Hortobagyi, GN; Mann, G; Yap, HY, 1987
)
0.95
" Because of the broad spectrum of activity of these DNA binders against murine tumors and due to their promising clinical utility, we have evaluated these agents in combination with a variety of clinically useful antitumor drugs."( Response of transplantable tumors of mice to anthracenedione derivatives alone and in combination with clinically useful agents.
Corbett, TH; Griswold, DP; Laster, WR; Roberts, BJ; Schabel, FM; Trader, MW, 1982
)
0.26
" The aim of this study was to assess the response of four mesothelioma cell lines, derived from diffuse asbestos-related pleural malignant mesothelioma, to methotrexate alone and in combination with recombinant IFN-alpha and IFN-gamma."( Interferon (IFN)-alpha and IFN-gamma in combination with methotrexate: in vitro sensitivity studies in four human mesothelioma cell lines.
Hand, A; Linnainmaa, K; Mattson, K; Pelin, K, 1995
)
0.29
"High-dose chemotherapy given with autologous bone marrow support has resulted in significant tumor responses in the majority of patients with metastatic breast cancer, a minority of which are durable."( Dose escalation of mitoxantrone given with thiotepa and autologous bone marrow transplantation for metastatic breast cancer.
Adkins, D; Bowers, C; Dunphy, F; Harrison, B; LeMaistre, CF; Spitzer, G, 1993
)
0.61
"To determine the maximally tolerated dose of mitoxantrone in combination with cytarabine in patients with acute leukemia and advanced phases of chronic myelogenous leukemia (CML), and to assess the pharmacokinetics of high-dose mitoxantrone in this patient population."( Phase I clinical and pharmacokinetic evaluation of high-dose mitoxantrone in combination with cytarabine in patients with acute leukemia.
Ahmed, T; Alberts, DS; Arlin, Z; Baier, M; Baskind, P; Feldman, EJ; Mittelman, A; Peng, YM; Plezia, P, 1993
)
0.79
" Mitoxantrone pharmacokinetics were evaluated by high-performance liquid chromatography (HPLC) in 15 patients given a single dose of mitoxantrone ranging from 40 to 80 mg/m2 in combination with cytarabine."( Phase I clinical and pharmacokinetic evaluation of high-dose mitoxantrone in combination with cytarabine in patients with acute leukemia.
Ahmed, T; Alberts, DS; Arlin, Z; Baier, M; Baskind, P; Feldman, EJ; Mittelman, A; Peng, YM; Plezia, P, 1993
)
1.44
"The recommended phase II dose of mitoxantrone is 80 mg/m2 administered over 15 minutes as a single intravenous infusion in combination with cytarabine 3 g/m2/d for 5 days."( Phase I clinical and pharmacokinetic evaluation of high-dose mitoxantrone in combination with cytarabine in patients with acute leukemia.
Ahmed, T; Alberts, DS; Arlin, Z; Baier, M; Baskind, P; Feldman, EJ; Mittelman, A; Peng, YM; Plezia, P, 1993
)
0.81
"193 patients with relapsed or refractory acute myeloid leukemia (AML) were entered into a prospective randomized comparison of high-dose versus intermediate dose cytosine arabinoside (AraC) both combined with mitoxantrone (mitox) according to the previously established sequential HD-AraC/mitox regimen (S-HAM)."( High-dose versus intermediate dose cytosine arabinoside combined with mitoxantrone for the treatment of relapsed and refractory acute myeloid leukemia: results of an age adjusted randomized comparison.
Aul, C; Balleisen, L; Bartholomäus, A; Becker, K; Bettelheim, P; Hiddemann, W; Lathan, B; Ludwig, WD; Maschmeyer, G; Schönrock-Nabulsi, R, 1993
)
0.71
"The maximum tolerated dose of mitoxantrone (MX) administered alone or combined with whole body hyperthermia (WBH) was determined in this nonrandomized, prospective study in dogs with lymphoma."( Phase I evaluation of mitoxantrone alone and combined with whole body hyperthermia in dogs with lymphoma.
Dewhirst, MW; Gillette, EL; Hauck, ML; Johnson, J; Ogilvie, GK; Page, RL; Price, GS; Thrall, DE,
)
0.73
"In this selected group of patients with multiple sclerosis with very active disease, mitoxantrone combined with methylprednisolone was effective in improving both clinical and MRI indices of disease activity over a period of six months whereas methylprednisolone alone was not."( Therapeutic effect of mitoxantrone combined with methylprednisolone in multiple sclerosis: a randomised multicentre study of active disease using MRI and clinical criteria.
Berry, I; Brochet, B; Cabanis, E; Clanet, M; Confavreux, C; Edan, G; Froment, JC; Gandon, JM; Iba-Zizen, MT; Lai, HM; Lubetzki, C; Lyon-Caen, O; Miller, D; Moseley, I; Rolland, Y; Sabouraud, O, 1997
)
0.84
"We conducted a randomized, multicenter study of intravenous cyclophosphamide 500 mg/m2 plus fluorouracil 500 mg/m2 combined with either mitoxantrone (Novantrone, Lederle Cyanamid Canada Ltd, Willowdale, Ontario) 10 mg/m2 (CNF) or doxorubicin (Adriamycin, Adria Laboratories of Canada Ltd, Mississauga, Ontario) 50 mg/m2 (CAF) every 3 weeks in advanced breast cancer."( Cyclophosphamide and fluorouracil combined with mitoxantrone versus doxorubicin for breast cancer: superiority of doxorubicin.
Evans, WK; Martz, K; Pritchard, KI; Shepherd, FA; Stewart, DJ; Trudeau, ME; Wilson, JJ; Wilson, KS, 1997
)
0.76
" The study was designed to determine the safety and maximally tolerated dose of IV vinorelbine used in combination with a fixed dose of mitoxantrone for the treatment of patients with refractory solid tumors."( A phase I trial of vinorelbine in combination with mitoxantrone in patients with refractory solid tumors.
Bigley, J; Burris, HA; Dieras, V; Eckardt, JR; Hardy, J; Hohneker, J; Jones, SF; Peacock, NW; Rodriguez, GI; Smith, L; Von Hoff, DD, 1998
)
0.75
" Because both P-glycoprotein- and platinum-induced resistance appear to be clinically important and can be reversed in vitro with a short exposure of cyclosporin A (CSA) at 2000 and 5000 ng/ml, respectively, we undertook a trial of high-dose chemotherapy with carboplatin (1500mg/m2), mitoxantrone (75 mg/m2), and cyclophosphamide (120 mg/kg) over a 5-day period combined with escalating doses of CSA."( High-dose chemotherapy combined with escalating doses of cyclosporin A and an autologous bone marrow transplant for the treatment of drug-resistant solid tumors: a phase I clinical trial.
Bayer, R; Camarda, M; Kinch, L; Loutfi, S; Peace, D; Rad, N; Sosman, J; Stiff, PJ; Tan, S, 1995
)
0.47
"To define the maximum-tolerated dose (MTD) and the dose-limiting toxicities (DLTs) of docetaxel in combination with mitoxantrone in patients with metastatic breast cancer (MBC)."( Dose-escalation study of docetaxel in combination with mitoxantrone as first-line treatment in patients with metastatic breast cancer.
Androulakis, N; Georgoulias, V; Hatzidaki, D; Kakolyris, S; Katsogridakis, K; Kotsakis, T; Kouroussis, C; Mavroudis, D; Samonis, G; Souglakos, J; Vardakis, N; Vlachonikolis, J, 1999
)
0.76
"This trial shows the activity of paclitaxel and mitoxantrone in ABC and finds that a dose of 14 mg/m2 of mitoxantrone is the MTD in combination with a fixed dose of 175 mg/m2 of paclitaxel without granulocyte colony stimulating factor (G-CSF)."( Dose intensification of mitoxantrone in combination with paclitaxel in advanced breast cancer: a phase II study.
Acito, L; Angiona, S; Bilancia, D; Costanzo, FD; Fioriti, L; Gasperoni, S; Giustini, L; Manzione, L; Sdrobolini, A; Valenti, L, 1999
)
0.87
" These results support that fludarabine in combination with cyclophosphamide and/or mitoxantrone can be highly effective in the treatment of B-CLL."( In vitro evaluation of fludarabine in combination with cyclophosphamide and/or mitoxantrone in B-cell chronic lymphocytic leukemia.
Bellosillo, B; Colomer, D; Gil, J; Montserrat, E; Pons, G; Villamor, N, 1999
)
0.76
"Evaluate response, duration of response, and toxicity of paclitaxel in combination with other drugs known to be effective in non-Hodgkin's lymphoma (NHL)."( Phase II study of paclitaxel in combination with mitoxantrone and ifosfamide/mesna for patients with relapsed or refractory non-Hodgkin's lymphoma after failure to cytarabine/cisplatin combination.
Cabanillas, F; Hagemeister, FB; McLaughlin, P; Preti, A; Rodriguez, J; Rodriguez, MA; Romaguera, JE; Sarris, AH; Younes, A, 1999
)
0.56
" We analyzed the induction of apoptosis by 2-CdA alone (n=5) and in combination with other drugs in peripheral lymphocytes from 25 patients with leukemic low-grade lymphomas and from 25 healthy volunteers."( Induction of apoptosis by 2-chloro-2'deoxyadenosine (2-CdA) alone and in combination with other cytotoxic drugs: synergistic effects on normal and neoplastic lymphocytes by addition of doxorubicin and mitoxantrone.
Boehrer, S; Chow, KU; Hoelzer, D; Jantschke, P; Martin, H; Mitrou, PS; Napieralski, S; Pourebrahim, F; Ries, J; Rummel, MJ; Stein, J; Weidmann, E, 2000
)
0.5
"A dose-escalation study was realized in order to assess the maximally tolerated dose (MTD) of high-dose mitoxantrone in a single injection combined with cytarabine and etoposide (EMA regimen) in refractory or relapsed acute myelogenous leukemia (AML)."( Dose-escalation study of single dose mitoxantrone in combination with timed sequential chemotherapy in patients with refractory or relapsing acute myelogenous leukemia.
Archimbaud, E; Cambier, N; Ecstein-Fraïssé, E; Leblond, V; Pautas, C; Reman, O; Soler-Michel, P; Taksin, AL; Thomas, X; Vekhoff, A, 2000
)
0.79
"Main portal branch transection combined with major liver resection and neoadjuvant and adjuvant locoregional immunochemotherapy fulfilled our expectations firstly for increasing the resectability rate and secondly for increasing the overall survival and the disease-free survival."( Preoperative main portal branch transection combined with liver locoregional transarterial neo and adjuvant immunochemotherapy for patients with hepatocellular carcinoma.
Dedemadi, G; Kontis, A; Lygidakis, NJ; Nestoridis, J; Sgourakis, G; Spentzouris, N,
)
0.13
" Because its toxicities are minimal and do not overlap with the toxicities of standard chemotherapy, it is an appealing agent to use in combination with chemotherapy."( Safety of fludarabine, mitoxantrone, and dexamethasone combined with rituximab in the treatment of stage IV indolent lymphoma.
Cabanillas, F; Dang, NH; Hagemeister, FB; Lee, MS; McAda, N; McLaughlin, P; Pate, O; Preti, AH; Rodriguez, MA; Romaguera, JE; Sarris, AH; Younes, A, 2000
)
0.62
" MV represents a chemotherapy combination with equivalent efficacy to standard FAC/FEC and improved results for patients who have previously received adjuvant chemotherapy."( Results of a phase III prospective, randomised trial, comparing mitoxantrone and vinorelbine (MV) in combination with standard FAC/FEC in front-line therapy of metastatic breast cancer.
Calais, G; Chinet-Charrot, P; Clavère, P; Colin, P; de Gislain, C; Delozier, T; Etienne, PL; Eymard, JC; Ganem, G; Luporsi, E; Maillart, P; Marti, P; Namer, M; Pouillart, P; Prevost, G; Romieu, G; Schraub, S; Serin, D; Soler-Michel, P; Tigaud, D; Trillet-Lenoir, V; Turpin, F; Wendling, JL, 2001
)
0.55
"To evaluate the activity and tolerance of docetaxel in combination with mitoxantrone and granulocyte colony-stimulating factor (G-CSF) as front-line treatment in patients with metastatic breast cancer (MBC)."( Docetaxel in combination with mitoxantrone and granulocyte colony-stimulating factor as front-line chemotherapy in metastatic breast cancer: a multicenter phase II study.
Agelaki, S; Alexopoulos, A; Georgoulias, V; Kakolyris, S; Kalbakis, K; Kosmas, C; Kouroussis, C; Malamos, N; Mavroudis, D; Rigatos, G; Sarra, E; Vlachonicolis, J, 2001
)
0.83
"Docetaxel in combination with mitoxantrone and G-CSF support is an intensified and active front-line regimen for patients with MBC; despite its hematological toxicity, this regimen merits further comparison with other standard anthracycline- and/or taxane-based combinations."( Docetaxel in combination with mitoxantrone and granulocyte colony-stimulating factor as front-line chemotherapy in metastatic breast cancer: a multicenter phase II study.
Agelaki, S; Alexopoulos, A; Georgoulias, V; Kakolyris, S; Kalbakis, K; Kosmas, C; Kouroussis, C; Malamos, N; Mavroudis, D; Rigatos, G; Sarra, E; Vlachonicolis, J, 2001
)
0.89
"A phase II clinical study was performed to evaluate the effectiveness and toxicity of cladribine (2-CdA) combined with mitoxantrone (CM regimen) in the treatment of chronic myeloid leukemia in blastic phase (CML BP)."( Cladribine combined with mitoxantrone in the treatment of blastic phase of chronic myeloid leukemia.
Góra-Tybor, J; Robak, T, 2001
)
0.82
" 2-CdA in combination with DOX significantly increased the percentage of annexin V-positive cells, particularly after 48 h of incubation, as compared with DOX used in monotherapy (median AI for 2-CdA+DOX=37."( Evaluation of apoptosis induced in vitro by cladribine (2-CdA) combined with anthracyclines in lymphocytes from patients with B-cell chronic lymphocytic leukemia.
Najder, M; Robak, T; Smolewski, P; Szmigielska-Kaplon, A, 2002
)
0.31
"Rituximab, a chimeric monoclonal antibody, produces response rates of up to 73% in patients with previously untreated indolent non-Hodgkin's lymphoma (NHL), and has high activity when combined with chemotherapy."( Rituximab in combination with CNOP chemotherapy in patients with previously untreated indolent non-Hodgkin's lymphoma.
Christodoulou, C; Dimopoulos, M; Economopoulos, T; Fountzilas, G; Hamilos, G; Kalantzis, D; Nicolaides, C; Papageorgiou, E; Pavlidis, N, 2003
)
0.32
" Western blot technique combined with videodensitometry was used for Bax and Bcl-2 determination in homogenate, nuclear and postnuclear fractions of mononuclear cells isolated from peripheral blood of B-CLL patients treated with cladribine alone (C), and in combination with cyclophosphamide (CC) or mitoxantrone and cyclophosphamide (CMC)."( Determination of the in vivo effects of cladribine alone and its combination with cyclophosphamide or cyclophosphamide and mitoxantrone on Bax and Bcl-2 protein expression in B-CLL cells.
Blonski, JZ; Hanausek, M; Kilianska, ZM; Kobylinska, A; Robak, T; Walaszek, Z, 2004
)
0.71
" This report examines the efficacy of irofulven alone or in combination with mitoxantrone or docetaxel against androgen-independent prostate cancer cell lines."( Antitumor activity of irofulven monotherapy and in combination with mitoxantrone or docetaxel against human prostate cancer models.
MacDonald, JR; Van Laar, ES; Waters, SJ; Weitman, S, 2004
)
0.79
"These studies demonstrate that irofulven displays strong activity as monotherapy and in combination with mitoxantrone or docetaxel against androgen-independent prostate cancer in vitro and in vivo; thus, supporting the clinical investigation of irofulven against hormone-refractory prostate cancer."( Antitumor activity of irofulven monotherapy and in combination with mitoxantrone or docetaxel against human prostate cancer models.
MacDonald, JR; Van Laar, ES; Waters, SJ; Weitman, S, 2004
)
0.77
" These data provide a proof-of-principle for the clinical use of LErafAON in combination with chemotherapy for cancer treatment."( Combination with liposome-entrapped, ends-modified raf antisense oligonucleotide (LErafAON) improves the anti-tumor efficacies of cisplatin, epirubicin, mitoxantrone, docetaxel and gemcitabine.
Ahmad, I; Dritschilo, A; Gokhale, PC; Kasid, UN; Pei, J; Rahman, A; Zhang, C, 2004
)
0.52
" Cladribine is highly effective as a single agent and in combination with mitoxantrone in the treatment of indolent NHL, and its availability broadens the range of therapeutic options for indolent NHL."( Treatment of indolent non-Hodgkin's lymphoma with cladribine as single-agent therapy and in combination with mitoxantrone.
Armitage, JO; Hoelzer, D; Rummel, MJ; Tobinai, K, 2004
)
0.77
"From 1998 to 2001, 5 consecutive cases of AML/TMDS entered our hospital and achieved complete remission (CR) with continuous drip infusion of low-dose etoposide and low-dose Ara-C combined with mitoxantrone (MEtA regimen)."( [Five cases of de novo acute myeloid leukemia with trilineage myelodysplasia (AML/TMDS) achieved CR with the continuous drip infusion of low-dose etoposide and low-dose cytosine arabinoside combined with mitoxantrone (MEtA)].
Furukawa, Y; Kitani, T; Shibano, M; Tsukaguchi, M, 2004
)
0.7
"To evaluate the efficacy of postoperative intraperitoneal hyperthermic chemoperfusion (IHCP) combined with intravenous chemotherapy for advanced gastric cancer."( [Postoperative intraperitioneal hyperthermic chemoperfusion combined with intravenous chemotherapy for 82 advanced gastric cancer patients].
Lu, JF; Lu, WD; Shen, D; Xu, M; Zuo, Y, 2004
)
0.32
"Eighty-two patients with stage II - IV gastric cancer were postoperatively randomized into two groups; 46 patients in treatment group who received IHCP combined with intravenous chemotherapy for three times and 36 patients in control group who received intravenous chemotherapy only for six times."( [Postoperative intraperitioneal hyperthermic chemoperfusion combined with intravenous chemotherapy for 82 advanced gastric cancer patients].
Lu, JF; Lu, WD; Shen, D; Xu, M; Zuo, Y, 2004
)
0.32
"Intraperitoneal hyperthermic chemoperfusion combined with intravenous chemotherapy can prolong survival and reduce gastrointestinal side-effect which provides an effective treatment option for advanced gastric cancer."( [Postoperative intraperitioneal hyperthermic chemoperfusion combined with intravenous chemotherapy for 82 advanced gastric cancer patients].
Lu, JF; Lu, WD; Shen, D; Xu, M; Zuo, Y, 2004
)
0.32
" From March 1987 to March 1994, 40 newly diagnosed patients with AML were randomized to receive either bolus or CI-MTZ, administered for 3 days at 10 mg/m2/day in combination with CI-cytarabine for 7 days at 100 mg/m2/day."( A randomized trial of continuous infusion versus bolus mitoxantrone in combination with cytarabine in newly diagnosed patients with acute myeloblastic leukemia.
Canpinar, H; Kansu, E; Kars, A; Koc, Y; Oyan, B; Tekuzman, G, 2004
)
0.57
"Docetaxel, a taxane previously approved for the treatment of breast cancer and non-small cell lung cancer, was approved by the United States Food and Drug Administration on May 19, 2004 for use in combination with prednisone for the treatment of metastatic androgen-independent (hormone-refractory) prostate cancer."( Approval summary: Docetaxel in combination with prednisone for the treatment of androgen-independent hormone-refractory prostate cancer.
Abraham, S; Dagher, R; Li, N; Pazdur, R; Rahman, A; Sridhara, R, 2004
)
0.32
" When given with prednisone, docetaxel was also shown to reduce pain and serum prostate specific antigen levels and improve quality of life compared with mitoxantrone/prednisone."( Which drug combination for hormone-refractory prostate cancer?
Doggrell, SA, 2005
)
0.53
" In this study, the efficacy of lintuzumab in combination with induction chemotherapy was compared with chemotherapy alone in adults with first relapsed or primary refractory acute myeloid leukemia (AML)."( Phase III randomized multicenter study of a humanized anti-CD33 monoclonal antibody, lintuzumab, in combination with chemotherapy, versus chemotherapy alone in patients with refractory or first-relapsed acute myeloid leukemia.
Brandwein, J; Brown, R; Chopra, R; De Angelo, D; Ehmann, WC; Feldman, EJ; Frankel, SR; Jurcic, JC; Kalaycio, M; Miller, C; Moore, J; O'Connor, J; Roboz, GJ; Scheinberg, D; Schulman, P; Stone, R; Wedel, N, 2005
)
0.33
"Patients with relapsed or primary resistant AML (duration of first response, zero to 12 months) were randomly assigned to receive either mitoxantrone 8 mg/m(2), etoposide 80 mg/m(2), and cytarabine 1 g/m(2) daily for 6 days (MEC) in combination with lintuzumab 12 mg/m(2), or MEC alone."( Phase III randomized multicenter study of a humanized anti-CD33 monoclonal antibody, lintuzumab, in combination with chemotherapy, versus chemotherapy alone in patients with refractory or first-relapsed acute myeloid leukemia.
Brandwein, J; Brown, R; Chopra, R; De Angelo, D; Ehmann, WC; Feldman, EJ; Frankel, SR; Jurcic, JC; Kalaycio, M; Miller, C; Moore, J; O'Connor, J; Roboz, GJ; Scheinberg, D; Schulman, P; Stone, R; Wedel, N, 2005
)
0.53
"In this prospective randomized trial, we compared the efficacy and toxicity of cladribine (2-CdA) alone to 2-CdA combined with cyclophosphamide (CC) or cyclophosphamide and mitoxantrone (CMC) in untreated progressive chronic lymphocytic leukemia (CLL)."( Cladribine alone and in combination with cyclophosphamide or cyclophosphamide plus mitoxantrone in the treatment of progressive chronic lymphocytic leukemia: report of a prospective, multicenter, randomized trial of the Polish Adult Leukemia Group (PALG C
Blonski, JZ; Calbecka, M; Ceglarek, B; Dmoszynska, A; Dwilewicz-Trojaczek, J; Gora-Tybor, J; Jamroziak, K; Kasznicki, M; Kloczko, J; Konopka, L; Kowal, M; Kuliczkowski, K; Robak, T; Skotnicki, AB; Stella-Holowiecka, B; Sulek, K; Tomaszewska, A; Warzocha, K; Zawilska, K, 2006
)
0.75
" It is possible that lamivudine combined with chemotherapy may have had a therapeutic effect on ATL in this case."( [Development of acute type, CD 8 positive adult T-cell leukemia in a carrier of hepatitis B virus--possible therapeutic effect of lamivudine combined with chemotherapy].
Hasegawa, H; Miyagi, T; Nagasaki, A; Nakachi, S; Shinzato, O; Taira, N; Takasu, N; Tomoyose, T, 2006
)
0.33
" During 2004 and 2005, 45 patients with newly diagnosed Ph+ ALL were treated in the Group for Research on Adult Acute Lymphoblastic Leukemia (GRAAPH) 2003 study, in which imatinib was started with HAM (mitoxantrone with intermediate-dose cytarabine) consolidation in good early responders (corticosensitive and chemosensitive ALL) or earlier during the induction course in combination with dexamethasone and vincristine in poor early responders (corticoresistant and/or chemoresistant ALL)."( Imatinib combined with induction or consolidation chemotherapy in patients with de novo Philadelphia chromosome-positive acute lymphoblastic leukemia: results of the GRAAPH-2003 study.
Buzyn, A; Cayuela, JM; Chalandon, Y; de Labarthe, A; Delabesse, E; Dombret, H; Escoffre, M; Huguet-Rigal, F; Ifrah, N; Lhéritier, V; MacIntyre, E; Maury, S; Pigneux, A; Réa, D; Reman, O; Rousselot, P; Thomas, X; Vekemans, MC; Vernant, JP; Witz, F, 2007
)
0.53
"While gemtuzumab ozogamicin (GTMZ) is commonly used in the treatment of acute myeloid leukemia (AML) in combination with standard chemotherapy agents, the pediatric maximum-tolerated dose (MTD) of GMTZ in combination with chemotherapy has not been determined."( Safety and efficacy of gemtuzumab ozogamicin in combination with chemotherapy for pediatric acute myeloid leukemia: a report from the Children's Oncology Group.
Alonzo, TA; Aplenc, R; Arceci, RJ; Bernstein, I; Buckley, P; Gerbing, RB; Hurwitz, CA; Krimmel, K; Lange, BJ; Sievers, EL; Smith, FO; Wells, RJ, 2008
)
0.35
"The Children's Oncology Group AAML00P2 trial sought to define the MTD of GMTZ in combination with cytarabine and mitoxantrone and cytarabine and l-asparaginase chemotherapy regimens."( Safety and efficacy of gemtuzumab ozogamicin in combination with chemotherapy for pediatric acute myeloid leukemia: a report from the Children's Oncology Group.
Alonzo, TA; Aplenc, R; Arceci, RJ; Bernstein, I; Buckley, P; Gerbing, RB; Hurwitz, CA; Krimmel, K; Lange, BJ; Sievers, EL; Smith, FO; Wells, RJ, 2008
)
0.56
"The MTD for GMTZ in combination with cytarabine and mitoxantrone was 3 mg/m(2) while the MTD in combination with cytarabine and l-asparaginase was 2 mg/m(2)."( Safety and efficacy of gemtuzumab ozogamicin in combination with chemotherapy for pediatric acute myeloid leukemia: a report from the Children's Oncology Group.
Alonzo, TA; Aplenc, R; Arceci, RJ; Bernstein, I; Buckley, P; Gerbing, RB; Hurwitz, CA; Krimmel, K; Lange, BJ; Sievers, EL; Smith, FO; Wells, RJ, 2008
)
0.6
" In vitro, CI-994 in combination with cytarabine (ara-C), daunorubicin and mitoxantrone, resulted in moderate synergism."( CI-994 (N-acetyl-dinaline) in combination with conventional anti-cancer agents is effective against acute myeloid leukemia in vitro and in vivo.
Comijn, EM; Hubeek, I; Kaspers, GJ; Merriman, RL; Padron, JM; Peters, GJ; Van der Wilt, CL, 2008
)
0.58
"To evaluate the preliminary efficacy, safety, and impact on quality of life (QoL) of high-dose calcitriol (DN-101) combined with mitoxantrone and glucocorticoids in androgen-independent prostate cancer (AIPC)."( A phase II study of high-dose calcitriol combined with mitoxantrone and prednisone for androgen-independent prostate cancer.
Beer, TM; Chan, JS; Dehaze, DR; Garzotto, M; Pinski, JK; Quinn, DI; Ryan, CW; Sokoloff, M, 2008
)
0.8
"This prospective phase II clinical trial evaluated the effects of single-dose mitoxantrone (36 mg/m2 on day 1) in combination with continuous infusion intermediate-dose cytarabine plus etoposide in 25 patients with refractory or early relapsed acute myeloid leukemia (AML)."( Single-dose mitoxantrone in combination with continuous infusion intermediate-dose cytarabine plus etoposide for treatment of refractory or early relapsed acute myeloid leukemia.
Chi, HS; Jang, S; Kang, YA; Kim, DY; Kim, SH; Lee, JH; Lee, KH; Lee, SS; Lee, YS; Lim, SN; Park, CJ; Ryu, SG; Seol, M; Yun, SC, 2009
)
0.96
"To observe the clinical efficacy of Chinese drugs combined with chemotherapy in the treatment of acute myeloid leukemia (AML) and to investigate the prognostic relevance of the main parameters in AML treated with integrative medicine."( Effect and prognostic analysis of treatment for acute myeloid leukemia using Chinese drugs combined with chemotherapy.
Hu, NP; Hu, XM; Li, L; Liu, C; Liu, F; Ma, R; Wang, HZ; Xiao, HY; Xu, YG; Yang, XH; Zhang, SS; Zheng, CM, 2009
)
0.35
" While clinical efficacy was limited with the viral mutants alone, outcomes were improved in combination with chemotherapeutics."( Optimisation of replication-selective oncolytic adenoviral mutants in combination with chemotherapeutics.
Halldén, G, 2009
)
0.35
" The aim of this study was to investigate the cytotoxic effects of this agent in combination with conventional antileukemic agents."( The cytotoxic effects of gemtuzumab ozogamicin (mylotarg) in combination with conventional antileukemic agents by isobologram analysis in vitro.
Akutsu, M; Furukawa, Y; Izumi, T; Kano, Y; Mano, H; Miyawaki, S; Tanaka, M; Tsunoda, S; Yazawa, Y, 2009
)
0.35
"The cytotoxic effects of GO in combination with antileukemic agents were studied against human CD33 antigen-positive leukemia HL-60, U937, TCC-S and NALM20 cells."( The cytotoxic effects of gemtuzumab ozogamicin (mylotarg) in combination with conventional antileukemic agents by isobologram analysis in vitro.
Akutsu, M; Furukawa, Y; Izumi, T; Kano, Y; Mano, H; Miyawaki, S; Tanaka, M; Tsunoda, S; Yazawa, Y, 2009
)
0.35
"To find the maximum tolerated dose (MTD) of OSI-461 in combination with mitoxantrone in patients with advanced solid tumors."( A phase I study of OSI-461 in combination with mitoxantrone in patients with advanced solid tumors potentially responsive to mitoxantrone.
Boinpally, R; Carducci, MA; Eisenberger, MA; Franke, A; King, S; Pili, R; Porter, J; Resta, LP; Spitz, A; Sweeney, CJ, 2011
)
0.86
"This was a Phase I study using cohort dose escalation of OSI-461 dosed orally twice daily in combination with mitoxantrone 12 mg/m(2) given on Day 1 of each 21-day cycle."( A phase I study of OSI-461 in combination with mitoxantrone in patients with advanced solid tumors potentially responsive to mitoxantrone.
Boinpally, R; Carducci, MA; Eisenberger, MA; Franke, A; King, S; Pili, R; Porter, J; Resta, LP; Spitz, A; Sweeney, CJ, 2011
)
0.84
" The TTFields were applied alone and in combination with paclitaxel and doxorubicin."( TTFields alone and in combination with chemotherapeutic agents effectively reduce the viability of MDR cell sub-lines that over-express ABC transporters.
Kirson, ED; Palti, Y; Schneiderman, RS; Shmueli, E, 2010
)
0.36
"The results indicate that TTFields alone and in combination with paclitaxel and doxorubicin effectively reduce the viability of both wild type and MDR cell sub-lines and thus can potentially be used as an effective treatment of drug resistant tumors."( TTFields alone and in combination with chemotherapeutic agents effectively reduce the viability of MDR cell sub-lines that over-express ABC transporters.
Kirson, ED; Palti, Y; Schneiderman, RS; Shmueli, E, 2010
)
0.36
" Here we report greatly improved antitumor efficacy for both attenuated (dl1520) and highly potent (dl922–947) oncolytic mutants in combination with the current standard of care for late-stage hormone-independent prostate cancers, mitoxantrone or docetaxel."( Efficacy of oncolytic mutants targeting pRb and p53 pathways is synergistically enhanced when combined with cytotoxic drugs in prostate cancer cells and tumor xenografts.
Ekblad, M; Halldén, G; Holford, A; Lemoine, NR; Miranda, E; Pizarro, MT; Radhakrishnan, S, 2010
)
0.54
"The hepatic organic anion transporting polypeptides (OATPs) influence the pharmacokinetics of several drug classes and are involved in many clinical drug-drug interactions."( Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
Artursson, P; Haglund, U; Karlgren, M; Kimoto, E; Lai, Y; Norinder, U; Vildhede, A; Wisniewski, JR, 2012
)
0.38
"To explore the therapeutic effect of homoharringtonine (HHT) combined with cytarabine (HA regimen) on CML-MBC and its influence on bone marrow CD34+CD7+ cells."( Homoharringtonine combined with cytarabine to treat chronic myelogenous leukemia in myeloid blast crisis and its impact on bone marrow CD34+CD7+ cells.
Deng, Z; Ding, B; Li, Y; Shi, Y; Zho, J, 2014
)
0.4
"Reported response rates of transitional cell carcinoma (TCC) in dogs to piroxicam in combination with either mitoxantrone or carboplatin are similar; however, it is unknown whether either drug might provide superior duration of response."( Randomized phase III trial of piroxicam in combination with mitoxantrone or carboplatin for first-line treatment of urogenital tract transitional cell carcinoma in dogs.
Allstadt, SD; Boostrom, B; Rebhun, RB; Rodriguez, CO; Skorupski, KA, 2015
)
0.87
"This study did not detect a different in outcome in dogs with TCC treated with either mitoxantrone or carboplatin in combination with piroxicam."( Randomized phase III trial of piroxicam in combination with mitoxantrone or carboplatin for first-line treatment of urogenital tract transitional cell carcinoma in dogs.
Allstadt, SD; Boostrom, B; Rebhun, RB; Rodriguez, CO; Skorupski, KA, 2015
)
0.88
"To investigate the efficacy and safety of MA (mitoxantrone and cytarabine) regimen chemotherapy combined with granulocyte-colony stimulating factor (G-CSF)-mobilized family related HLA-haploidentical donor peripheral blood hematopoietic stem cell (G-PBHSC) infusion for the treatment of acute myeloid leukemia (AML) patients aged over 80 years."( [Clinical Analysis of 4 AML Patients Aged Over 80 Years Treated with Chemotherapy Combined with Haploidentical Hematopoietic Stem Cell Infusion].
Hu, HL; Huang, YJ; Li, J; Liu, J; Sun, WJ; Xi, XQ; Zhao, HX, 2015
)
0.68
" We performed an open-label, multi-center, phase II study to investigate the effect and quality of life (QoL) of treatment with vorinostat in combination with fludarabine, mitoxantrone and dexamethasone (V-FND) for relapsed or refractory MCL."( Results of a phase II study of vorinostat in combination with intravenous fludarabine, mitoxantrone, and dexamethasone in patients with relapsed or refractory mantle cell lymphoma: an interim analysis.
Kim, BS; Kim, HJ; Kim, JA; Kim, SJ; Kim, WS; Kong, JH; Park, SK; Park, Y; Shin, DY; Won, JH; Yoon, DH, 2016
)
0.85
"In this study, we compared the efficacy of mitoxantrone in combination with intermediate-dose cytarabine (HAM) with that of high-dose cytarabine alone (HiDAC) as consolidation regimens in non-acute promyelocytic leukemia (APL) acute myeloid leukemia patients with favorable and intermediate cytogenetics."( Comparison of Mitoxantrone in Combination with Intermediate-dose Cytarabine versus High-dose Cytarabine as Consolidation Therapies for Young Non-APL Acute Myeloid Leukemia Patients with Favorable and Intermediate Cytogenetics.
Hu, LN; Li, GQ; Lin, HQ; Shen, Q; Sun, XF; Zhang, XY; Zhou, JH, 2018
)
1.1
" A phase I trial of the second-generation proteasome inhibitor ixazomib in combination with MEC (mitoxantrone, etoposide, and cytarabine) was conducted in patients with R/R AML."( A Phase I/II Trial of MEC (Mitoxantrone, Etoposide, Cytarabine) in Combination with Ixazomib for Relapsed Refractory Acute Myeloid Leukemia.
Advani, AS; Caimi, P; Carew, J; Carraway, H; Chan, R; Cooper, B; de Lima, M; Elson, P; Gerds, A; Hamilton, B; Kalaycio, M; Little, J; Maciejewski, J; Malek, E; Miron, A; Mukherjee, S; Nazha, A; Pink, J; Sekeres, MA; Sobecks, R; Tomlinson, B; Unger, A; Visconte, V; Wei, W, 2019
)
1.03
" The aim of this study was to investigate the cytotoxic and anti-proliferative effects of arvanil and olvanil when administered alone and in combination with cisplatin (CDDP) and mitoxantrone (MTX), using various primary (A375, FM55P) and metastatic (SK-MEL 28, FM55M2) human malignant melanoma cell lines."( Comparison of the Anticancer Effects of Arvanil and Olvanil When Combined with Cisplatin and Mitoxantrone in Various Melanoma Cell Lines-An Isobolographic Analysis.
Drozd, M; Florek-Łuszczki, M; Góralczyk, A; Marzęda, P; Wróblewska-Łuczka, P; Łuszczki, JJ, 2022
)
1.13

Bioavailability

Mitoxantrone is poorly absorbed orally and is most commonly administered intravenously. Novel nanostructured lipid-carrageenan hybrid carriers (NLCCs) were exploited for controlled delivery of water soluble chemotherapeutic agent. MTO has high loading capacity, sustained release property and potential for improving oral bioavailability and antitumor efficacy.

ExcerptReferenceRelevance
" Mitoxantrone is poorly absorbed orally and is most commonly administered intravenously."( Mitoxantrone: a novel anthracycline derivative.
Eble, M; Koeller, J, 1988
)
2.63
" To avoid the confounding drug transport provided by P-glycoprotein (P-gp), the roles of Bcrp1 in the bioavailability of topotecan and the effect of GF120918 were studied in both wild-type and P-gp-deficient mice and their fetuses."( Role of breast cancer resistance protein in the bioavailability and fetal penetration of topotecan.
Beijnen, JH; Brinkhuis, RF; Jonker, JW; Maliepaard, M; Schellens, JH; Schinkel, AH; Smit, JW, 2000
)
0.31
" When both topotecan and GF120918 were administered orally, the bioavailability (i."( Role of breast cancer resistance protein in the bioavailability and fetal penetration of topotecan.
Beijnen, JH; Brinkhuis, RF; Jonker, JW; Maliepaard, M; Schellens, JH; Schinkel, AH; Smit, JW, 2000
)
0.31
" These results may have therapeutic implications because the antitumor efficacy of ST1481 is in part related to a good bioavailability after oral administration, and the drug is currently under Phase I clinical evaluation."( A novel 7-modified camptothecin analog overcomes breast cancer resistance protein-associated resistance in a mitoxantrone-selected colon carcinoma cell line.
Beggiolin, G; Carenini, N; Carminati, P; De Cesare, M; De Isabella, P; Palumbo, M; Perego, P; Pezzoni, G; Pisano, C; Pratesi, G; Scheffer, GL; Tartaglia, L; Zunino, F, 2001
)
0.52
", irinotecan), resulting in increased bioavailability and reduced clearance of these agents."( Cyclosporin A, tacrolimus and sirolimus are potent inhibitors of the human breast cancer resistance protein (ABCG2) and reverse resistance to mitoxantrone and topotecan.
Dai, Y; Gupta, A; Hebert, MF; Mao, Q; Ross, DD; Thummel, KE; Unadkat, JD; Vethanayagam, RR, 2006
)
0.54
"The human ATP-binding cassette transporter, ABCG2, confers resistance to multiple chemotherapeutic agents and also affects the bioavailability of different drugs."( The calcium channel blockers, 1,4-dihydropyridines, are substrates of the multidrug resistance-linked ABC drug transporter, ABCG2.
Ambudkar, SV; Bates, SE; Robey, RW; Shukla, S, 2006
)
0.33
" The pharmacokinetic study in rats showed that LPG significantly prolonged the circulation time and enhanced the bioavailability of MX."( Dual-functional liposome for tumor targeting and overcoming multidrug resistance in hepatocellular carcinoma cells.
Fan, R; Gan, Y; Guo, S; Li, F; Yu, M; Zhang, X; Zhu, C, 2012
)
0.38
" This study investigates the interactions between selected prenylflavonoids and breast cancer resistance protein (BCRP/ABCG2), an efflux transporter important for xenobiotic bioavailability and multidrug resistance (MDR)."( Hop-derived prenylflavonoids are substrates and inhibitors of the efflux transporter breast cancer resistance protein (BCRP/ABCG2).
Birch, NP; Cooney, J; Jensen, D; Li, Y; Paxton, JW; Scheepens, A; Tan, KW, 2014
)
0.4
"The ATP-binding cassette transporter G2/breast cancer resistance protein (ABCG2/BCRP) is an efflux protein involved in the bioavailability and milk secretion of endogenous and exogenous compounds, actively affecting milk composition."( Effect of bovine ABCG2 polymorphism Y581S SNP on secretion into milk of enterolactone, riboflavin and uric acid.
Álvarez, AI; Espín, JC; García-Villalba, R; González-Lobato, L; Merino, G; Miguel, V; Otero, JA; Prieto, JG, 2016
)
0.43
"Novel nanostructured lipid-carrageenan hybrid carriers (NLCCs) were exploited for controlled delivery of water soluble chemotherapeutic agent mitoxantrone hydrochloride (MTO) with high loading capacity, sustained release property, and potential for improving oral bioavailability and antitumor efficacy."( Nanostructured lipid-carrageenan hybrid carriers (NLCCs) for controlled delivery of mitoxantrone hydrochloride to enhance anticancer activity bypassing the BCRP-mediated efflux.
He, Z; Ling, G; Sun, J; Zhang, P; Zhang, T, 2016
)
0.86
" The release in vivo was carried out on the rats, as a result, liposome L3 showed higher bioavailability than traditional intravenous injectable administration, and liposome L3 showed higher elimination ratio after stimulation by ultrasound than L3 without stimulation."( PLGA nanoparticles introduction into mitoxantrone-loaded ultrasound-responsive liposomes: In vitro and in vivo investigations.
Mao, Z; Qi, Q; Xin, Y; Zhan, X, 2017
)
0.73
" However, the limited bioavailability of curcumin prevents its use for modulation of the function of these transporters in the clinical setting."( Synthetic Analogs of Curcumin Modulate the Function of Multidrug Resistance-Linked ATP-Binding Cassette Transporter ABCG2.
Ambudkar, SV; Chufan, EE; Fukuda, M; Ishida, M; Iwabuchi, Y; Kanehara, K; Kudoh, K; Murakami, M; Naitoh, T; Ohnuma, S; Shibata, H; Sugisawa, N; Unno, M, 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
" However, it has several disadvantages such as poor water solubility, low bioavailability and low targeting, which seriously restrict its clinical application."( Delivery of quercetin for breast cancer and targeting potentiation via hyaluronic nano-micelles.
Li, M; Lin, K; Liu, Z; Sun, J; Wang, W; Wang, Z; Zhang, S; Zhao, Y; Zhen, Y, 2023
)
0.91

Dosage Studied

Mitoxantrone has been shown in vitro to exhibit a steep dose-response relationship with respect to the clonogenic survival of acute myeloid leukemia cells.

ExcerptRelevanceReference
" This dosage is only 25% of what a patient with a solid tumour would normally receive during the same time period."( Treatment of multiple sclerosis with mitoxantrone.
Fetzer, U; Kornhuber, HH; Krapf, H; Laufen, H; Mauch, E, 1992
)
0.56
"Twelve patients received intrapleural instilments of the cytostatic agent mitoxantrone in a total dosage of 30 mg for locoregional palliative therapy of malignant pleural effusion."( Local therapy of malignant pleural effusion with mitoxantrone.
Opri, F; Torsten, U; Weitzel, H, 1992
)
0.77
" As mitoxantrone exhibits a steep dose-response curve against ovarian cancer cells and acute myeloid leukemia cells in vitro, we evaluated the safety and efficacy of high dose mitoxantrone with HiDAc in the treatment of ALL."( Short course high dose mitoxantrone with high dose cytarabine is effective therapy for adult lymphoblastic leukemia.
Ahmed, T; Arlin, ZA; Arnold, P; Baskind, P; Cook, P; Feldman, EJ; Finger, LR; Mittelman, A; Puccio, C; Razis, ED, 1991
)
1.15
" All patients were given 4-6 doses of intravesical novantrone at the same dose level at weekly dosing interval."( Phase I-II evaluation of intravesical novantrone (mitoxantrone) in superficial bladder cancer.
Albert, D; Clayton, M; Lamb, D; Lee, M; Sarosdy, M; Sharifi, R; Siami, P; Strub, M, 1991
)
0.53
" A steep mitoxantrone dose-response curve was observed, and increases in drug concentrations at both low and high dose ranges were associated with a significant potentiation of anti-leukemic effects."( Effect of pharmacologically relevant concentrations of mitoxantrone on the in vitro growth of leukemic blast progenitors.
Arlin, Z; Feldman, E; Gewirtz, D; Grant, S, 1991
)
0.95
"Sixteen patients with advanced adenocarcinoma of the stomach were entered into a phase II study of mitoxantrone at a dosage of either 12 mg/m2 or 14 mg/m2 given at 3 weekly intervals."( A phase II study of mitoxantrone in advanced gastric cancer.
Gill, PG; Levi, JA; Presgrave, P, 1990
)
0.82
"In order to reduce the incidence of severe complications noted with regimens containing high-dose cytarabine (HD ARA-C), wer used a combination of mitoxantrone (MTZ) in optimal dosage (12 mg/m2/day for 5 days) and cytarabine in intermediate dosage (1 g/m2 twice daily for 3 or 5 days)."( Mitoxantrone and intermediate-dose cytarabine in relapsed or refractory acute myeloblastic leukemia.
Brière, J; Desablens, B; Ghandour, C; Harousseau, JL; Milpied, N, 1990
)
1.92
"Twenty patients with advanced squamous cell carcinomas (SCC) of the head and neck were entered into a phase II study of mitoxantrone at a dosage of either 12 mg/m2 or 14 mg/m2 given at 3 weekly intervals."( A phase II study of mitoxantrone in advanced squamous cell cancer of the head and neck.
Levi, J; Page, J; Wheeler, H; Woods, RL, 1990
)
0.81
" Modifications in timing and dosage and the addition of hematopoietic growth factors will be evaluated in subsequent trials."( Treatment of refractory Hodgkin's disease with high-dose cytosine arabinoside and mitoxantrone in combination. Results of a clinical phase II study of the German Hodgkin Study Group.
Hiddemann, W; Kirchner, H; Koch, P; Maschmeyer, G; Ollech-Chwoyka, J; Pflüger, KH; Pfreundschuh, M; Schmitz, N; Tirier, C; Wagner, T, 1990
)
0.5
" The dosage of diaziquone was increased for sequential cohorts of seven patients from 20 mg/m2/day to 24 mg/m2/day, and finally to 28 mg/m2/day to determine the maximum tolerated dose for this chemotherapy combination."( Treatment of relapsed and refractory acute myeloid leukemia with diaziquone and mitoxantrone: a CALGB phase I study.
Amrein, PC; Davis, RB; Mayer, RJ; Schiffer, CA, 1990
)
0.51
" These features in conjunction with evidence that mitoxantrone displays a dose-response effect in vitro make it an attractive candidate for intensive therapy regimens."( Mitoxantrone: potential for use in intensive therapy.
Herzig, R; LeMaistre, CF, 1990
)
1.97
" These results are of particular interest in clinical routines to calculate dosage regimens by Bayesian estimation methods."( Population pharmacokinetics of mitoxantrone performed by a NONMEM method.
Iliadis, A; Launay, MC; Richard, B, 1989
)
0.56
"To determine the safety and efficacy of mitoxantrone use in hyperbilirubinemic breast cancer patients, a prospectively determined dosage schedule was evaluated in a multi-center trial."( Mitoxantrone use in breast cancer patients with elevated bilirubin.
Bulcavage, L; Chlebowski, RT; Elashoff, R; Henderson, IC; Rivest, R; Woodcock, T, 1989
)
1.99
" Sharp plateaus in the VpmR-5 dose-response curves for Adriamycin-induced DNA strand breaks and cytotoxicity appear to be related to interference with type II topoisomerase-mediated cleavage of DNA at high concentrations of the intercalator."( Cross-resistance to intercalating agents in an epipodophyllotoxin-resistant Chinese hamster ovary cell line: evidence for a common intracellular target.
Glisson, B; Gupta, R; Hodges, P; Ross, W, 1986
)
0.27
"The chemistry, pharmacology, pharmacokinetics, clinical efficacy, dosage and administration, and adverse effects of mitoxantrone are reviewed."( Mitoxantrone: a novel anthracycline derivative.
Eble, M; Koeller, J, 1988
)
1.93
" Toxicity, particularly alopecia, was appreciably lower in the VMP treated patients, but subclinical cardiotoxicity was seen within the scheduled dosage for both combinations."( Mitoxantrone versus doxorubicin in combination chemotherapy for advanced carcinoma of the breast.
Cornbleet, MA; Hutcheon, AW; Kaye, SB; Kerr, ME; Leonard, RC; Robinson, S; Smyth, JF; Soukop, M; White, G, 1987
)
1.72
"To determine optimal dosage, Dihydroxyanthracenedione (DHAD) was given once daily for 3 days at dosage levels of 6, 7, 8, and 10 mg/m2 in combination with a 7-day continuous infusion of cytosine arabinoside (Ara-C)."( Toxicity evaluation of dihydroxyanthracenedione (DHAD) in combination with cytosine arabinoside (Ara-C).
Civin, CI; Krischer, J; Land, VJ; Ragab, AH; Steuber, CP; Vietti, TJ, 1987
)
0.27
" The recommended dosage regimen for the treatment of breast carcinoma is 12-14 mg/m2 given intravenously once every 21 days."( Pharmacokinetics of mitoxantrone in man and laboratory animals.
Batra, VK; Morrison, JA; Siverd, NS; Woodward, DL; Yacobi, A, 1986
)
0.59
" The combination of mitoxantrone and vinblastine appeared to offer no advantage over single-agent therapy, probably because of the dosage reduction required by the overlapping myelosuppressive toxicity."( Chemotherapy with mitoxantrone in combination with continuous infusion vinblastine for metastatic breast cancer.
Blumenschein, GR; Buzdar, AU; Fraschini, G; Hortobagyi, GN; Mann, G; Yap, HY, 1987
)
0.93
" A dosage of 18 mg/m2 was administered as a short intravenous infusion every 3 weeks."( Novantrone for childhood malignant solid tumors. A pediatric oncology group phase II study.
Etcubanas, E; Krance, RA; Mahoney, DH; Patterson, RB; Pratt, CB; Sexauer, C; Vietti, TJ, 1986
)
0.27
" MIT dosage was intravenous injection of 3-6 mg/m2/day X 5 consecutive days as a rule."( [Phase II study of mitoxantrone in patients with acute leukemia].
Hirano, M; Ikeda, Y; Kimura, K; Kobayashi, M; Ohara, K; Ohta, K; Shirakawa, S; Yamada, K; Yoshikawa, H; Yoshikawa, S, 1986
)
0.6
" However, there were fewer dosage decreases with CNF."( A randomized multicenter trial of cyclophosphamide, Novantrone and 5-fluorouracil (CNF) versus cyclophosphamide, Adriamycin and 5-fluorouracil (CAF) in patients with metastatic breast cancer.
Bennett, JM; Byrne, P; DeConti, R; Desai, A; Doroshow, J; Krementz, E; Muggia, F; Plotkin, D; Vogel, C; White, C, 1985
)
0.27
"Twenty-six evaluable patients with advanced or recurrent squamous cell carcinoma of the uterine cervix were treated with mitoxantrone at a dosage of 12 mg/m2 every 3 weeks."( Mitoxantrone (NSC 301739) in patients with advanced cervical carcinoma. A phase II study of the Gynecologic Oncology Group.
Bundy, B; Hatch, KD; Muss, HB; Sutton, GP, 1985
)
1.92
" A 5-day, consecutive intraperitoneal dosing study yielded 28 day, LD10, LD50 and LD90 values of 18, 21 and 26 mg kg-1, respectively, in mice."( Preclinical toxicity of the new antineoplastic agent, ametantrone acetate, in mice and dogs.
Anderson, JA; de la Iglesia, FA; Fitzgerald, JE; Jayasekara, U; Kim, SN; Watkins, JR, 1986
)
0.27
" These data provide a pharmacological rationale for use of mitoxantrone on an intermittent dosing schedule."( Disposition of mitoxantrone in cancer patients.
Alberts, DS; Davis, TP; Leigh, S; Peng, YM; Woodward, DL, 1985
)
0.87
" Serum samples collected at various time intervals from rats dosed intravenously with mitoxantrone (0."( Radioimmunoassay for mitoxantrone, a new antitumor agent.
Lanzilotti, A; McWilliams, W; Morrison, J; Nicolau, G; Szucs-Myers, V, 1985
)
0.81
" Distribution and half-life data provide a pharmacological rationale for the use of mitoxantrone on an intermittent dosing schedule."( Pharmacology of mitoxantrone: mode of action and pharmacokinetics.
Alberts, DS; Bowden, GT; Dalton, WS; Mackel, C; Peng, YM, 1985
)
0.84
" Fifty-three evaluable patients were treated with this agent at a dosage of 5 mg/M2/week."( Phase II study of mitoxantrone in advanced squamous cell carcinoma of the head and neck. A Southeastern Cancer Study Group trial.
Birch, R; Gams, R; Velez-Garcia, E; Williams, SD, 1985
)
0.6
" Dosage escalations proceeded from 15 mg/m2 to 35 mg/m2."( A phase I trial of ametantrone acetate (NSC-287513).
Bender, JF; Gams, RA; Grillo-López, AJ; Ostroy, F, 1985
)
0.27
" Mitoxantrone was given in form of a 30-minute infusion at a dosage of 14 mg/m2."( [Mitoxantrone in the primary treatment of metastasizing breast cancer].
Dittrich, C; Dudczak, R; Lenzhofer, R; Moser, K; Pirker, P; Rainer, H; Schuster, R, 1984
)
2.09
" We have carried out a phase II trial of mitoxantrone using an every three weeks dosing schedule in patients with advanced head and neck cancers."( Phase II trial of mitoxantrone in head and neck cancer.
Aapro, MS; Alberts, DS, 1984
)
0.87
"Twenty-six evaluable patients with advanced epithelial ovarian cancer were treated with mitoxantrone at a dosage of 12 mg/m2 every three weeks."( Mitoxantrone (NSC-301739) in patients with advanced ovarian carcinoma. A phase II study of the Gynecologic Oncology Group.
Asbury, R; Bundy, B; Ehrlich, CE; Graham, J; Muss, HB, 1984
)
1.93
" However, 24 h after dosing 10."( Pharmacological disposition of 1,4-dihydroxy-5-8-bis[[2 [(2-hydroxyethyl)amino]ethyl]amino]-9,10-anthracenedione dihydrochloride in the dog.
Loo, TL; Lu, K; Savaraj, N, 1984
)
0.27
"Combined chemotherapy and radiotherapy in standard dosage is an acceptable approach following mastectomy for patients with extensive nodal involvement at high risk for local recurrence and distant relapse."( Combined chemotherapy and radiotherapy for patients with breast cancer and extensive nodal involvement.
Barraclough, B; Boyages, J; Langlands, AO; Ung, O, 1995
)
0.29
" A dose-response relationship characterized body-weight loss and survival rate."( Circadian changes in mitoxantrone toxicity in mice: relationship with plasma pharmacokinetics.
Bizi, E; Hallek, M; Lemaigre, G; Lévi, F; Metzger, G; Tampellini, M, 1994
)
0.61
" Once a cumulative dosage of 140 mg/m2 is reached cardiac function tests, including echocardiography with measurement of the left ventricular ejection fraction, should be routinely carried out preceding each treatment administration in all patients."( [Immunosuppressive therapy of multiple sclerosis with mitoxantrone].
Kornhuber, HH; Mauch, E, 1993
)
0.53
" Further studies are needed to explore the potential impact on response and/or toxicity and the requirement of a pharmacokinetic directed adjustment of drug dosage in clinical trials."( New aspects on the pharmacokinetics of mitoxantrone and its two major metabolites.
Hiddemann, W; Kamischke, A; Kaufmann, CC; Schleyer, E; Unterhalt, M, 1994
)
0.56
"Seventeen patients with APL were salvaged with ATRA at a dosage of 50 mg/m2/day for 3 months or until complete remission (CR) was achieved; idarubicin (12 mg/m2/day for 4 days) was added if blast plus promyelocyte count either was or reached > or = 10 x 10(3)/microliters."( All-trans retinoic acid followed by chemotherapy for salvage of refractory or relapsed acute promyelocytic leukemia.
Cortes, JE; Estey, E; Hirsh-Ginsberg, C; Kantarjian, H; Keating, M; Koller, C; O'Brien, S; Robertson, LE; Stass, S, 1994
)
0.29
" Intraperitoneal mitoxantrone was administered at a dosage of 20-30 mg/mq repeated every 28 days if ascites was still present."( Mitoxantrone in the treatment of recurrent ascites of pretreated ovarian carcinoma.
Berardi, F; Catino, A; de Lena, M; Fioretto, A; Gargano, G; Lorusso, V, 1994
)
2.07
"Mitoxantrone has been shown in vitro to exhibit a steep dose-response relationship with respect to the clonogenic survival of acute myeloid leukemia cells."( High-dose mitoxantrone induces programmed cell death or apoptosis in human myeloid leukemia cells.
Bhalla, K; Bullock, G; Grant, S; Huang, Y; Ibrado, AM; Mahoney, ME; Ponnathpur, V; Tang, C; Tourkina, E, 1993
)
2.13
" However, in vitro data demonstrate a steep dose-response curve to a variety of agents, most notably mitoxantrone."( Phase I clinical and pharmacokinetic study of high-dose mitoxantrone combined with carboplatin, cyclophosphamide, and autologous bone marrow rescue: high response rate for refractory ovarian carcinoma.
Alberts, DS; Dolan, JR; McCloskey, T; McKenzie, RS; Rad, N; Sosman, JA; Stiff, PJ, 1994
)
0.75
" For consolidation with NOVE, rhGM-CSF was given according to the same dosage schedule."( Idarubicin/cytosine arabinoside and mitoxantrone/etoposide for the treatment of de novo acute myelogenous leukemia.
Del Valle, F; Döhner, H; Ehrhardt, R; Fischer, JT; Haas, R; Ho, AD; Huberts, H; Hunstein, W; Kaplan, E; Witt, B, 1993
)
0.56
" An increase in the prednisolone dosage led to an improvement."( Interstitial pneumonitis possibly due to mitoxantrone.
Aiso, M; Hagiwara, T; Hayama, T; Horie, T; Kitami, Y; Matsukawa, Y; Ohshima, T; Takeuchi, J, 1993
)
0.55
" Although the primary purpose of this study was to determine a clinically useful dosage and to characterize the toxicoses associated with mitoxantrone administration, each cat was monitored for response to treatment."( Toxicoses and efficacy associated with administration of mitoxantrone to cats with malignant tumors.
Atwater, SW; Ciekot, PE; Elmslie, RE; Klein, MK; Moore, AS; Obradovich, JE; Ogilvie, GK; Salmon, MD; Straw, RC; Vail, DM, 1993
)
0.73
" All patients received a standard IV dose of mitoxantrone (8 mg/m2) every 3 weeks for a total of seven infusions, with dosage adjustments depending on the hematologic profile at the nadir."( An open-trial evaluation of mitoxantrone in the treatment of progressive MS.
Cauvier, H; Grinwich, KD; Harris, BJ; Hopkins, MB; Karlik, SJ; Lee, DH; Noseworthy, JH; Penman, M; Rice, GP; Vandervoort, MK, 1993
)
0.84
" In the trial, the dosage of granisetron tablet was 2 mg once a day, and the drug was given before each chemotherapy for 6 consecutive days."( [Study on the inhibitory effect of oral granisetron against nausea/vomiting induced by cytosine arabinoside containing chemotherapy for tumors in the hematopoietic organs].
Gondo, H; Harada, M; Matsuishi, H; Omori, F; Otsuka, T; Shibuya, T; Taniguchi, S; Teshima, T; Yamano, Y; Yamazaki, K, 1993
)
0.29
" However, because this drug exhibits a steep dose-response curve, a Phase I-II trial of mitoxantrone by hepatic arterial infusion was initiated."( A phase I-II trial of mitoxantrone by hepatic arterial infusion in patients with hepatocellular carcinoma or colorectal carcinoma metastatic to the liver.
Abbruzzese, J; Ajani, JA; Carrasco, CH; Charnsangavej, C; Jones, DV; Levin, B; Patt, YZ; Wallace, S, 1993
)
0.82
" Only one patient required a dosage reduction on the basis of toxicity (neutropenia)."( A phase I-II trial of mitoxantrone by hepatic arterial infusion in patients with hepatocellular carcinoma or colorectal carcinoma metastatic to the liver.
Abbruzzese, J; Ajani, JA; Carrasco, CH; Charnsangavej, C; Jones, DV; Levin, B; Patt, YZ; Wallace, S, 1993
)
0.6
" In addition, ICRF-187 allowed for 50% greater cumulative dosing in normal mice that, nonetheless, showed extensive histological heart damage 7 wk after dosing."( Characterization of experimental mitoxantrone cardiotoxicity and its partial inhibition by ICRF-187 in cultured neonatal rat heart cells.
Alberts, DS; Dawson, BV; Dorr, RT; Hendrix, M; Shipp, NG, 1993
)
0.57
" The dose-response curves of mitoxantrone in a human clonogenic cytotoxicity assay against the RPMI 2780/S human ovarian cell line were virtually identical when the cells were incubated in either 5 or 50% fetal bovine serum, suggesting that protein binding will not significantly impair mitoxantrone-induced tumor cell killing."( Evidence for persistence of mitoxantrone within the peritoneal cavity following intraperitoneal delivery.
Alberts, D; Barakat, R; Brodar, F; Curtin, J; Hakes, T; Jones, W; Lewis, JL; Markman, M; Reichman, B; Rubin, S, 1993
)
0.87
" Mitoxantrone is a good candidate for local or regional administration because (1) its metabolism is mainly hepatic, (2) it has a steep dose-response curve for multiple solid tumors, and (3) its fixation in tissues is sustained without vesicant effects after extravasation."( Pharmacokinetics and antitumor effects of mitoxantrone after intratumoral or intraarterial hepatic administration in rabbits.
Ardouin, P; Bognel, C; Dzodic, R; Gouyette, A; Munck, JN; Ramirez, LH; Rougier, P; Vassal, G; Zhao, Z, 1996
)
1.47
" For both drugs, a loss of linearity of the IC90 and IC50 dose-response curves was found at maximum concentrations."( [Comparison of the cytostatic effect of epirubicin and mitoxantrone on native breast carcinoma cells using the ATP tumor chemosensitivity assay].
Brenne, U; Krebs, D; Kurbacher, CM; Kurbacher, JA; Mallmann, P, 1996
)
0.54
" Dosage in subsequent cycles was adjusted according to hematologic toxicity."( A carboplatin-based regimen for the treatment of patients with advanced transitional cell carcinoma of the urothelium.
Carroll, PR; Ernest, ML; Fippin, LJ; Small, EJ, 1996
)
0.29
" FLANG (27 patients) had a shorter duration (3 days), reduced Ara-C dosage (1 g/sqm) and administration of mitoxantrone (10 mg/sqm) at the end of Ara-C infusion."( High efficacy of fludarabine-containing therapy (FLAG-FLANG) in poor risk acute myeloid leukemia.
Balleari, E; Canepa, L; Carrara, P; Celesti, L; Cerri, R; Clavio, M; Damasio, E; Gatti, AM; Ghio, R; Gobbi, M; Miglino, M; Patrone, F; Pierri, I; Sessarego, M; Vallebella, E,
)
0.34
"Echocardiographic reports on 144 adults receiving anthracycline therapy and 18 controls were reviewed for the possible relationship between dosage and ejection fractions."( [Echocardiographic evaluation of cardiotoxicity induced by anthracycline therapy].
Horikawa, K; Okada, Y; Sano, M, 1997
)
0.3
" DHAD dosage could be increased to 18 mg/m2 in 66 out of 317 cycles of chemotherapy (21%)."( Dose intensification of mitoxantrone in combination with levofolinic acid, fluorouracil, cyclophosphamide and granulocyte colony stimulating factor support in advanced untreated breast cancer patients. A multicentric phase II study of the Southern Italy O
Caruso, M; Colucci, G; Durini, E; Gebbia, N; Gebbia, V; Giotta, F; Pezzella, G; Riccardi, F; Romito, S, 1997
)
0.6
" No difference in toxicity was observed between the two dosage regimens."( A randomized trial of high- vs standard-dose mitoxantrone with cytarabine in elderly patients with acute myeloid leukemia.
Ahmed, T; Beer, M; Case, DC; Damon, L; Feldman, EJ; Linker, C; Ries, C; Rugo, H; Seiter, K, 1997
)
0.56
" Neutropenia is the most common toxicity associated with mitoxantone therapy and may necessitate dosage reduction in some patients."( Mitoxantrone. A review of its pharmacology and clinical efficacy in the management of hormone-resistant advanced prostate cancer.
Spencer, CM; Wiseman, LR, 1997
)
1.74
"Although cytosine arabinoside (AraC) represents the most effective single agent in the treatment of adults with acute myeloid leukemia (AML) when given at doses exceeding 200 to 500 mg per application, its optimal dosage is still a matter of controversial discussion."( Superiority of high-dose over intermediate-dose cytosine arabinoside in the treatment of patients with high-risk acute myeloid leukemia: results of an age-adjusted prospective randomized comparison.
Aul, C; Bartholomäus, A; Bettelheim, P; Büchner, T; Hiddemann, W; Kern, W; Ludwig, WD; Maschmeyer, G; Schönrock-Nabulsi, R; Wörmann, B, 1998
)
0.3
"In the human clonogenic assay, mitoxantrone possesses among the steepest dose-response curves of any cytotoxic agent against ovarian cancer."( Phase 2 trial of moderately high dose single agent mitoxantrone in platinum and paclitaxel-refractory ovarian cancer.
Belinson, J; Ernst, S; Homesley, H; Kennedy, A; Lichtman, SM; Markman, M; Omura, G; Webster, K, 1998
)
0.84
" Data analysis revealed sustained release of mitoxantrone from microspheres into peritoneal fluid in all dosage groups."( Evaluation of mitoxantrone-loaded albumin microspheres following intraperitoneal administration to rats.
Eichler, HG; Luftensteiner, CP; Paul, B; Schwendenwein, I; Viernstein, H, 1999
)
0.92
" Applied MXN dosage was equivalent to 30 mg/m2 body surface area."( Toxicity of a particulate formulation for the intraperitoneal application of mitoxantrone.
Eichler, HG; Luftensteiner, CP; Paul, B; Schwendenwein, I; Viernstein, H; Wölfl, G, 1999
)
0.53
" No apparent dose-response relationship was observed in our study."( Phase I/II trial of high dose mitoxantrone in metastatic breast cancer: the M.D. Anderson Cancer Center experience.
Buzdar, AU; Cristofanilli, M; Esparza, L; Holmes, FA; Hortobagyi, GN; Neidhart, JA; Valero, V, 1999
)
0.59
" The maximal acceptable dosage of mitoxantrone was 10 mg/m2 x 2 due to serious hematologic toxicity."( Mitoxantrone-DHAP with GM-CSF: an active but myelosuppressive salvage therapy for relapsed/refractory aggressive non-Hodgkin's lymphoma.
Berinstein, NL; Franssen, E; Haq, R; Sawka, CA, 1999
)
2.03
" We conclude that CBP at a cumulative dosage of 1 g/m2 together with intercalating agents (IDA/MIT) has antileukemic efficacy in elderly patients."( Continuous-infusion carboplatin in combination with idarubicin or mitoxantrone for high-risk acute myeloid leukemia: a randomised phase II study.
Archimbaud, E; Assouline, D; Belhabri, A; Blanc, M; Fière, D; Michallet, M; Thomas, X; Tigaud, JD; Troncy, J; Wattel, E, 1999
)
0.54
" On the other hand, bacillus Calmette-Guerin (BCG) currently appears to be the most effective agent for intravesical use, especially in patients with high grade and stage neoplasms but the optimum strain, dosage and duration schedule have not been determined."( Intravesical therapy of superficial bladder cancer.
Melekos, MD; Moutzouris, GD, 2000
)
0.31
"The combination CEF using this schedule and dosage in metastatic breast cancer is more effective with less toxicity than CNF, except for alopecia, and was associated with longer survival."( Phase III trial of cyclophosphamide, epirubicin, fluorouracil (CEF) versus cyclophosphamide, mitoxantrone, fluorouracil (CNF) in women with metastatic breast cancer.
Alvarez, E; Buesa, JM; Corral, N; Estaban, E; Estrada, E; Fernández, JL; Lacave, AJ; Muñiz, I; Palacio, I; Vieitez, JM, 1999
)
0.52
" These data suggest that the addition of PSC 833 to an M/E regimen for older patients with untreated AML is well tolerated but requires a reduction in M/E dosing to avoid increased toxicity."( A phase I study of induction chemotherapy for older patients with newly diagnosed acute myeloid leukemia (AML) using mitoxantrone, etoposide, and the MDR modulator PSC 833: a southwest oncology group study 9617.
Anderson, JE; Appelbaum, FR; Chauncey, TR; Chen, I; Godwin, JE; Head, DR; Kalaycio, ME; Kopecky, KJ; Kraut, EH; Leith, CP; Luthardt, FW; Moore, DF; Petersdorf, SH; Rankin, C; Shurafa, MS; Willman, CL, 2000
)
0.52
"The carboplatin-mitoxantrone combination, at the dosage tested in this study, appears to be well tolerated by elderly patients with advanced ovarian cancer and is associated with an acceptable response rate."( Elderly ovarian cancer: treatment with mitoxantrone-carboplatin.
Amichetti, M; Artioli, G; Azzoni, P; Donach, M; Endrizzi, L; Ferrazzi, E; Monfardini, S; Nicoletto, MO; Prosperi, A; Salvagno, L; Sileni, VC; Talamini, R; Tumolo, S; Veronesi, A; Visonà, E, 2001
)
0.93
" Here, in order to determine whether the efficacy of chemotherapy can be enhanced by changing the regimen, we evaluated the effect of the varied timing and dosage of chemotherapy in combination with androgen withdrawal on time to androgen-independent (AI) progression in the human androgen-dependent LNCaP tumour model."( Optimal timing and dosage of chemotherapy as a combined treatment with androgen withdrawal in the human prostate LNCaP tumour model.
Arakawa, S; Hara, I; Hara, S; Kamidono, S; Miyake, H, 2001
)
0.31
" The dose-response curve was represented by a second-degree polynomial without absolute term."( Effect of acetyl-L-carnitine on leukemia L1210 resistant to mitoxantrone.
Mĕlka, M; Niang, M, 2000
)
0.55
" However, some trials showed that increasing the dosage of anthracyclines within induction therapy improved treatment outcome substantially."( Intensified double induction therapy with high dose mitoxantrone, etoposide, m-amsacrine and high dose ara-C for elderly acute myeloid leukemia patients aged 61-65 years.
Aulitzky, W; Bodenstein, H; Clemens, M; Ehninger, G; Illmer, T; Neubauer, A; Repp, R; Schaich, M; Schäkel, U; Soucek, S; Wandt, H, 2002
)
0.57
" Given the potent myelosuppressive activity of mitoxantrone, dosage should be carefully adapted to the body surface and hematological changes."( Mitoxantrone in progressive multiple sclerosis: when and how to treat?
Gonsette, RE, 2003
)
2.02
" With the same dosage (2 mg."( [Preparation of long circulating mitoxantrone liposomes and its pharmacokinetics].
Duan, YS; Yu, BT; Zhang, ZR, 2002
)
0.6
" In phase I, on 23 patients entered on study, dose-limiting toxicity occurred at the dosage of 1200 mg m(-2) gemcitabine and 10 mg m(-2) mitoxantrone, with three out of five patients developing grade 4 neutropenia."( Phase I/II study of gemcitabine plus mitoxantrone as salvage chemotherapy in metastatic breast cancer.
Calabrese, P; Caporusso, L; Catino, A; Crucitta, E; D'Amico, C; De Lena, M; Guida, M; Latorre, A; Lorusso, V; Mazzei, A; Sambiasi, D; Schittulli, F; Silvestris, N, 2003
)
0.79
" These drugs are at different stages of clinical development and additional clinical data are needed to support their use and devise dosage regimens."( New and emerging treatment options for multiple sclerosis.
Polman, CH; Uitdehaag, BM, 2003
)
0.32
" Positive PA317/Tet-on/TRE-BCRP cells, which showed well dose-response in expression of BCRP with different concentration of Dox induction, were selected by both reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot."( [Expression establishment and functional analysis of breast cancer resistance protein with doxycycline induced tet regulating system in mouse fibroblast cell line PA317].
Chen, ZC; He, ZM; Yu, YH; Yuan, JH, 2004
)
0.32
"5 PA317/Tet-on /TRE-BCRP cell clone showed well dose-response in expression of BCRP with different concentration of Dox induction; its drug-resistance against mitoxantrone has positive correlation with BCRP expression (r=0."( [Expression establishment and functional analysis of breast cancer resistance protein with doxycycline induced tet regulating system in mouse fibroblast cell line PA317].
Chen, ZC; He, ZM; Yu, YH; Yuan, JH, 2004
)
0.52
" Early pilot trials using mitoxantrone were carried out using vastly different dosage regimens and patient populations, which may have resulted in conflicting results."( Review of mitoxantrone in the treatment of multiple sclerosis.
Herndon, R; Jeffery, DR, 2004
)
1.03
" This C(i) was designed as a prognostic index by taking the area under the curve as an exact measure of the total dose-response relationship."( Prediction of individual response to chemotherapy in patients with acute myeloid leukaemia using the chemosensitivity index Ci.
Cornely, O; Neurohr, K; Reiser, M; Schinköthe, T; Staib, P; Staltmeier, E, 2005
)
0.33
" However, these approaches will not take into account the possible dose-response relationship on each endpoint, and therefore are less specific and may have lower power."( Multiplicity adjustment for multiple endpoints in clinical trials with multiple doses of an active treatment.
Capizzi, T; Luo, X; Quan, H, 2005
)
0.33
" Dosing was continued at 5 mg/m2 every third month."( A pilot trial of combination therapy with mitoxantrone and interferon beta-1b using monthly gadolinium-enhanced magnetic resonance imaging.
Burdette, J; Chepuri, N; Durden, D; Jeffery, DR, 2005
)
0.59
"MX is moderately effective in reducing the disease progression and the frequency of relapses in patients affected by RR, PR and SP MS in the short-term follow-up (2 years), even if the results are based on trials heterogeneous in terms of drug dosage and inclusion criteria."( Mitoxantrone for multiple sclerosis.
Capra, R; Comi, G; Martinelli Boneschi, F; Rovaris, M, 2005
)
1.77
" Given the increased number of early treatment-related deaths, future treatment protocols should aim to reduce chemotherapy dosage or intensity whilst maintaining low rates of resistant and recurrent disease."( Treatment for myeloid leukaemia of Down syndrome: population-based experience in the UK and results from the Medical Research Council AML 10 and AML 12 trials.
de Graaf, SS; Gibson, BE; Hann, IM; Hills, RK; O'Marcaigh, A; Rao, A; Stiller, C; Webb, DK; Wheatley, K, 2006
)
0.33
" Dogs underwent laser ablation of the primary tumor and were treated with mitoxantrone at a dosage of 5 mg/m2)every 3 weeks for 4 treatments."( Evaluation of carbon dioxide laser ablation combined with mitoxantrone and piroxicam treatment in dogs with transitional cell carcinoma.
Payton, ME; Tangner, CH; Upton, ML, 2006
)
0.81
" GO at a dosage of 3 mg/m2 was administered as a 2-h intravenous infusion on days 1 and 14, cytarabine at 100 mg/m2 on days 1-7, and mitoxantrone at 12 mg/m2 on days 1-3."( Gemtuzumab ozogamicin with cytarabine and mitoxantrone as a third-line treatment in a poor prognosis group of adult acute myeloid leukemia patients: a single-center experience.
Carluccio, P; Giannoccaro, M; Liso, V; Mestice, A; Pastore, D; Rizzi, R; Specchia, G; Spinosa, G, 2007
)
0.81
" MITO was administered at a dosage of 8 mg/m(2) monthly for 3 months, then every 3 months, until a dosage of 120 mg/m(2) was reached."( Intravenous mitoxantrone and cyclophosphamide as second-line therapy in multiple sclerosis: an open-label comparative study of efficacy and safety.
Amato, MP; Hakiki, B; Portaccio, E; Siracusa, G; Sorbi, S; Zipoli, V, 2008
)
0.72
" The most common reason for reduction of the dosage or for cycle delay in the combined scheme was neutropenia."( Feasibility and efficacy of chemotherapy with gemcitabine mono and with paclitaxel/mitoxantron in gynaecological cancers.
Cordes, T; Fischer, D; Friedrich, M; Lüdders, D; Maass, N; Schroer, A; Villena-Heinsen, C, 2007
)
0.34
" Nine patients were enrolled at increasing dosage levels of ara-C (8, 12, and 16 g/m2 per dose level)."( Phase I trial of FLAGM with high doses of cytosine arabinoside for relapsed, refractory acute myeloid leukemia: study of the Japan Adult Leukemia Study Group (JALSG).
Arai, Y; Doki, N; Ishida, F; Kano, Y; Kawai, Y; Komatsu, N; Miyawaki, S; Morii, T; Ogura, M; Ohno, R; Takeshita, A; Usui, N, 2007
)
0.34
"The dosing schedule of docetaxel may affect its clinical activity and toxicity profile."( Biweekly docetaxel-containing chemotherapy may be the optimal schedule.
Cai, Y; Hong, X; Hu, X; Li, J; Ou, Z; Shen, Z; Wang, Z; Yang, X; Zhao, X, 2008
)
0.35
" However, with MTD dosing this drug ratio is not optimal to produce synergy and future studies using ratiometric dosing are required to confirm these findings."( Phase I evaluation of gemcitabine, mitoxantrone, and their effect on plasma disposition of fludarabine in patients with relapsed or refractory acute myeloid leukemia.
Adams, DJ; Decastro, CM; Gockerman, JP; Moore, JO; Peterson, BL; Petros, WP; Rao, AV; Rizzieri, DA; Sand, GJ; Spasojevic, I; Younis, IR, 2008
)
0.62
" Clofarabine dosed at 52 mg/m2 was used in adult patients with refractory ALL to maximize response before allo-HSCT."( The use of higher dose clofarabine in adults with relapsed acute lymphoblastic leukemia.
Brown, AW; McGregor, BA; Osswald, MB; Savona, MR, 2009
)
0.35
"These results suggest that the combination of ixabepilone and mitoxantrone is feasible and active in CRPC and requires dosing with pegfilgrastim."( Phase I study of ixabepilone, mitoxantrone, and prednisone in patients with metastatic castration-resistant prostate cancer previously treated with docetaxel-based therapy: a study of the department of defense prostate cancer clinical trials consortium.
Beer, TM; Harzstark, AL; Hussain, M; Mathew, P; Pagliaro, LC; Rosenberg, JE; Ryan, CJ; Ryan, CW; Sharib, J; Small, EJ; Smith, DC; Weinberg, VK, 2009
)
0.88
" Monitoring and dosing guidelines in the product labeling accompanying this indication include blood counts, liver function, and pregnancy tests at each administration."( Adherence to recommended dosing and monitoring for mitoxantrone in patients with multiple sclerosis: a healthcare claims database study supplemented with medical records--the RETRO study.
Al-Sabbagh, A; Bennett, R; Funch, D; Hillier, J; Norman, H; Seeger, JD; Wong, J, 2010
)
0.61
" Adherence to recommended dosing was higher than for recommended monitoring."( Adherence to recommended dosing and monitoring for mitoxantrone in patients with multiple sclerosis: a healthcare claims database study supplemented with medical records--the RETRO study.
Al-Sabbagh, A; Bennett, R; Funch, D; Hillier, J; Norman, H; Seeger, JD; Wong, J, 2010
)
0.61
" A dose-response effect was not apparent."( Cardiotoxicity and other adverse events associated with mitoxantrone treatment for MS.
Geddes, J; Isserow, S; Kingwell, E; Koch, M; Leung, B; Rieckmann, P; Tremlett, H, 2010
)
0.61
"This was a Phase I study using cohort dose escalation of OSI-461 dosed orally twice daily in combination with mitoxantrone 12 mg/m(2) given on Day 1 of each 21-day cycle."( A phase I study of OSI-461 in combination with mitoxantrone in patients with advanced solid tumors potentially responsive to mitoxantrone.
Boinpally, R; Carducci, MA; Eisenberger, MA; Franke, A; King, S; Pili, R; Porter, J; Resta, LP; Spitz, A; Sweeney, CJ, 2011
)
0.84
" In the Phase I part, dose-limiting toxicities occurred in all three patients, given mitoxantrone at the dosage of 10 mg/m(2)/day, and the recommended mitoxantrone dosage was determined to be 8 mg/m(2)/day."( A phase I/II study of combined chemotherapy with mitoxantrone and uracil/tegafur for advanced hepatocellular carcinoma.
Furuse, J; Ikeda, M; Ishii, H; Mitsunaga, S; Morizane, C; Nakachi, K; Okusaka, T; Suzuki, E; Ueno, H, 2011
)
0.85
" Pharmacokinetics demonstrated a dose-response for total and unbound plasma flavopiridol unrelated to total protein, albumin, peripheral blast count, or toxicity."( Phase 1 and pharmacokinetic study of bolus-infusion flavopiridol followed by cytosine arabinoside and mitoxantrone for acute leukemias.
Alino, K; Bagain, L; Blackford, A; Briel, J; Carraway, H; Doyle, LA; Gore, SD; Greer, JM; Joseph, B; Karp, JE; Levis, MJ; Mackey, K; McDevitt, MA; Moton-Nelson, D; Resar, LS; Rudek, MA; Smith, BD; Wright, JJ; Zhao, M, 2011
)
0.58
" This decrease suggests that daunorubicin, cytosine arabinoside, etoposide and mitoxantrone may impair the metabolism of other active substances metabolized by this isoenzyme, which should be taken into consideration in planning the dosage scheme in individual patients and considering interactions between drugs."( Influence of anticancer therapy on oxidation phenotype and acetylation phenotype in patients with acute myeloblastic leukemia.
Czarnik-Matusewicz, H; Ganczarski, G; Gąsiorowski, J; Głowacka, K; Kuliczkowski, K; Orzechowska-Juzwenko, K; Wiela-Hojeńska, A; Wołowiec, D; Łapiński, Ł, 2011
)
0.6
" Herein, we report the response to treatment with a fixed dosing schedule of ME or MEC in 65 patients treated for primary refractory or relapsed AML with intermediate or unfavorable risk cytogenetics."( Mitoxantrone and etoposide with or without intermediate dose cytarabine for the treatment of primary induction failure or relapsed acute myeloid leukemia.
Altman, J; Carlson-Leuer, K; Coyle, K; Frankfurt, O; Mehta, J; Newman, D; Rademaker, AW; Tallman, MS; Trifilio, SM, 2012
)
1.82
" Angiogenesis was induced in normal adult rat mesentery by intraperitoneal injection of a low dosage of VEGF-A."( Low-dosage metronomic chemotherapy and angiogenesis: topoisomerase inhibitors irinotecan and mitoxantrone stimulate VEGF-A-mediated angiogenesis.
Albertsson, P; Lennernäs, B; Norrby, K, 2012
)
0.6
" We show that real-time flow cytometric quantification of compound-uptake is reliably measured and that analyzing their respective uptake kinetic provides additional valuable information which can be used for improving drug dosage and delivery."( Utilizing inherent fluorescence of therapeutics to analyze real-time uptake and multi-parametric effector kinetics.
Efferth, T; Eichhorn, T; Korn, B; Paulsen, M; Wiench, B, 2012
)
0.38
" We aimed to provide a rationale for optimal dosing and scheduling of this anti-CD20 antibody based on pharmacokinetics."( Rituximab serum concentrations during immuno-chemotherapy of follicular lymphoma correlate with patient gender, bone marrow infiltration and clinical response.
Burgstaller, S; Drach, J; Einberger, C; Fridrik, M; Gaiger, A; Greil, R; Heintel, D; Hopfinger, G; Jäger, U; Mannhalter, C; Oberaigner, W; Porpaczy, E; Putman, M; Raderer, M; Skrabs, C; Zeitlinger, M, 2012
)
0.38
"The results of this pilot trial suggest that more differentiated dosing schedules based on gender and bone marrow infiltration should be explored for rituximab therapy for lymphoma."( Rituximab serum concentrations during immuno-chemotherapy of follicular lymphoma correlate with patient gender, bone marrow infiltration and clinical response.
Burgstaller, S; Drach, J; Einberger, C; Fridrik, M; Gaiger, A; Greil, R; Heintel, D; Hopfinger, G; Jäger, U; Mannhalter, C; Oberaigner, W; Porpaczy, E; Putman, M; Raderer, M; Skrabs, C; Zeitlinger, M, 2012
)
0.38
"These results suggest that the combination of ixabepilone and mitoxantrone is both feasible and active in castration-resistant prostate cancer and requires dosing with pegfilgrastim."( Ixabepilone, mitoxantrone, and prednisone for metastatic castration-resistant prostate cancer after docetaxel-based therapy: a phase 2 study of the Department Of Defense Prostate Cancer Clinical Trials Consortium.
Beer, TM; Harzstark, AL; Liu, G; Pagliaro, LC; Rosenberg, JE; Ryan, CJ; Sharib, J; Small, EJ; Smith, DC; Weinberg, VK, 2011
)
0.98
" Using TR-FRET, we screened the Sigma LOPAC library for MBD2-MBD inhibitors and identified four compounds that also validated in a dose-response series."( Time-Resolved Fluorescence Resonance Energy Transfer Assay for Discovery of Small-Molecule Inhibitors of Methyl-CpG Binding Domain Protein 2.
Giovinazzo, H; Nelson, WG; Walker, D; Wyhs, N; Yegnasubramanian, S, 2014
)
0.4
" However, an effective combination with other drugs and a feasible dosage has not been identified."( Clinical efficacy of mitoxantrone and Ara-C with or without etoposide salvage chemotherapy in adult patients with relapsed or refractory acute lymphoblastic leukemia: retrospective multicenter study of the Korean Adult ALL Working Party.
Ahn, JS; Chung, JS; Jo, DY; Joo, YD; Jung, SH; Kim, DY; Kim, I; Lee, JJ; Lee, KH; Moon, JH; Park, S; Shin, HJ; Sohn, SK; Song, IC; Yang, DH, 2015
)
0.74
" Multiple dosing of liposomal MTO strongly delayed tumor growth compared to free MTO and prolonged mouse survival, whereas among the liposomal MTO treatments, C8-GluCer-MTOL was most effective."( Plasma membrane targeting by short chain sphingolipids inserted in liposomes improves anti-tumor activity of mitoxantrone in an orthotopic breast carcinoma xenograft model.
Cordeiro Pedrosa, LR; Eggermont, AM; Koning, GA; Seynhaeve, AL; Soullié, T; Ten Hagen, TL; van Tellingen, O; Verheij, M, 2015
)
0.63
" In addition, gemcitabine increased the elimination rate of the ABCG2 substrate, D-luciferin, and decreased D-luciferin accumulation in BxPC3 and Panc1 cells in a dose-response manner."( Gemcitabine upregulates ABCG2/BCRP and modulates the intracellular pharmacokinetic profiles of bioluminescence in pancreatic cancer cells.
Gu, M; Li, F; Liu, J; Sun, Y; Wei, Y; Xiong, Y; Zhu, L, 2016
)
0.43
" In this study we assessed the dose-response characteristics as well as the feasibility and safety of mitoxantrone delivery to the brain and specifically to gliomas in a rodent model."( Safety, feasibility, and optimization of intra-arterial mitoxantrone delivery to gliomas.
Bigio, IJ; Bruce, JN; Cooke, J; Ellis, JA; Emala, CW; Joshi, S; Singh-Moon, RP; Wang, M, 2016
)
0.9
" The affected tumors remained dormant long after dosing stopped, resulting in a prolonged progression-free survival and sustained immune surveillance of the host bearing desmoplastic melanoma."( Nanocarrier-Mediated Chemo-Immunotherapy Arrested Cancer Progression and Induced Tumor Dormancy in Desmoplastic Melanoma.
Chen, F; Hou, L; Huang, L; Liu, Q; Shen, L; Wang, D; Zhang, X, 2018
)
0.48
" Ratios based on a continuous linear dose-response relationship were similar for daunorubicin (0."( Derivation of Anthracycline and Anthraquinone Equivalence Ratios to Doxorubicin for Late-Onset Cardiotoxicity.
Armstrong, GT; Aune, GJ; Chow, EJ; Feijen, EAM; Green, DM; Hudson, MM; Kremer, LCM; Leisenring, WM; Loonen, J; Ness, KK; Oeffinger, KC; Robison, LL; Stratton, KL; van Dalen, EC; van der Pal, HJH; Yasui, Y, 2019
)
0.51
"Dual-targeted drug delivery is a new drug dosing strategy that is frequently used to enhance the therapeutic efficacy of anticancer drugs."( New Folate-Modified Human Serum Albumin Conjugated to Cationic Lipid Carriers for Dual Targeting of Mitoxantrone against Breast Cancer.
Azandaryani, AH; Kashanian, S; Mahdavian, E; Rafipour, R; Ridha, AA, 2020
)
0.77
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (2)

RoleDescription
antineoplastic agentA substance that inhibits or prevents the proliferation of neoplasms.
analgesicAn agent capable of relieving pain without the loss of consciousness or without producing anaesthesia. In addition, analgesic is a role played by a compound which is exhibited by a capability to cause a reduction of pain symptoms.
[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]

Drug Classes (1)

ClassDescription
dihydroxyanthraquinone
[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 Targets (147)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, TYROSYL-DNA PHOSPHODIESTERASEHomo sapiens (human)Potency19.95260.004023.8416100.0000AID485290
Chain A, JmjC domain-containing histone demethylation protein 3AHomo sapiens (human)Potency6.30960.631035.7641100.0000AID504339
Chain A, ATP-DEPENDENT DNA HELICASE Q1Homo sapiens (human)Potency20.38650.125919.1169125.8920AID2549; AID2708
Chain A, Ferritin light chainEquus caballus (horse)Potency11.22025.623417.292931.6228AID485281
dopamine D1 receptorHomo sapiens (human)Potency5.17350.00521.30228.1995AID624455
glp-1 receptor, partialHomo sapiens (human)Potency16.54680.01846.806014.1254AID624172; AID624417
15-lipoxygenase, partialHomo sapiens (human)Potency7.87580.012610.691788.5700AID887
WRNHomo sapiens (human)Potency4.93700.168331.2583100.0000AID651768; AID720497
ATAD5 protein, partialHomo sapiens (human)Potency18.61920.004110.890331.5287AID493106; AID493107
Fumarate hydrataseHomo sapiens (human)Potency0.69780.00308.794948.0869AID1347053
USP1 protein, partialHomo sapiens (human)Potency43.01320.031637.5844354.8130AID504865; AID743255
NFKB1 protein, partialHomo sapiens (human)Potency1.99530.02827.055915.8489AID895; AID928
GLS proteinHomo sapiens (human)Potency4.58580.35487.935539.8107AID624146; AID624170
PPM1D proteinHomo sapiens (human)Potency0.93000.00529.466132.9993AID1347411
TDP1 proteinHomo sapiens (human)Potency0.10810.000811.382244.6684AID686978; AID686979
ThrombopoietinHomo sapiens (human)Potency0.02510.02517.304831.6228AID917; AID918
Smad3Homo sapiens (human)Potency1.58490.00527.809829.0929AID588855
apical membrane antigen 1, AMA1Plasmodium falciparum 3D7Potency10.00000.707912.194339.8107AID720542
DNA polymerase III, partialBacillus subtilisPotency1.50031.062114.152826.6795AID485295
hypoxia-inducible factor 1, alpha subunit (basic helix-loop-helix transcription factor)Homo sapiens (human)Potency10.26630.00137.762544.6684AID914; AID915
hypothetical protein, conservedTrypanosoma bruceiPotency39.81070.223911.245135.4813AID624173
regulator of G-protein signaling 4Homo sapiens (human)Potency11.91730.531815.435837.6858AID504845
EWS/FLI fusion proteinHomo sapiens (human)Potency0.10630.001310.157742.8575AID1259252; AID1259253; AID1259255
polyproteinZika virusPotency0.69780.00308.794948.0869AID1347053
67.9K proteinVaccinia virusPotency5.15810.00018.4406100.0000AID720579; AID720580
ParkinHomo sapiens (human)Potency23.10930.819914.830644.6684AID720573
arylsulfatase AHomo sapiens (human)Potency23.93411.069113.955137.9330AID720538
pyruvate kinaseLeishmania mexicana mexicanaPotency15.84890.398113.744731.6228AID945; AID959
IDH1Homo sapiens (human)Potency20.59620.005210.865235.4813AID686970
euchromatic histone-lysine N-methyltransferase 2Homo sapiens (human)Potency6.20900.035520.977089.1251AID504332
heat shock 70kDa protein 5 (glucose-regulated protein, 78kDa)Homo sapiens (human)Potency2.32810.016525.307841.3999AID504836; AID602332
Bloom syndrome protein isoform 1Homo sapiens (human)Potency7.74170.540617.639296.1227AID2528; AID720503
cytochrome P450 2D6 isoform 1Homo sapiens (human)Potency39.81070.00207.533739.8107AID891
NPC intracellular cholesterol transporter 1 precursorHomo sapiens (human)Potency115.82100.01262.451825.0177AID485313
cellular tumor antigen p53 isoform aHomo sapiens (human)Potency7.69980.316212.443531.6228AID902; AID924
atrial natriuretic peptide receptor 1 precursorHomo sapiens (human)Potency23.93410.134610.395030.1313AID1347049
vitamin D3 receptor isoform VDRAHomo sapiens (human)Potency38.95190.354828.065989.1251AID504847
chromobox protein homolog 1Homo sapiens (human)Potency15.37120.006026.168889.1251AID488953; AID540317
nuclear factor erythroid 2-related factor 2 isoform 2Homo sapiens (human)Potency8.19950.00419.984825.9290AID504444
huntingtin isoform 2Homo sapiens (human)Potency10.00000.000618.41981,122.0200AID1688
importin subunit beta-1 isoform 1Homo sapiens (human)Potency31.62285.804836.130665.1308AID540253
mitogen-activated protein kinase 1Homo sapiens (human)Potency3.98110.039816.784239.8107AID995
atrial natriuretic peptide receptor 2 precursorHomo sapiens (human)Potency16.48160.00669.809418.4927AID1347050
flap endonuclease 1Homo sapiens (human)Potency2.53780.133725.412989.1251AID488816; AID588795; AID720498
ubiquitin carboxyl-terminal hydrolase 2 isoform aHomo sapiens (human)Potency14.68920.65619.452025.1189AID463106
ras-related protein Rab-9AHomo sapiens (human)Potency91.99970.00022.621531.4954AID485297
serine/threonine-protein kinase mTOR isoform 1Homo sapiens (human)Potency0.14690.00378.618923.2809AID2668
tyrosine-protein kinase YesHomo sapiens (human)Potency34.49930.00005.018279.2586AID686947
snurportin-1Homo sapiens (human)Potency31.62285.804836.130665.1308AID540253
histone-lysine N-methyltransferase 2A isoform 2 precursorHomo sapiens (human)Potency12.58930.010323.856763.0957AID2662
GTP-binding nuclear protein Ran isoform 1Homo sapiens (human)Potency31.62285.804816.996225.9290AID540253
DNA polymerase eta isoform 1Homo sapiens (human)Potency11.08690.100028.9256213.3130AID588591; AID720502
DNA polymerase iota isoform a (long)Homo sapiens (human)Potency7.10680.050127.073689.1251AID588590; AID720496
DNA polymerase kappa isoform 1Homo sapiens (human)Potency7.87540.031622.3146100.0000AID588579; AID720501
VprHuman immunodeficiency virus 1Potency11.22021.584919.626463.0957AID651644
peripheral myelin protein 22Rattus norvegicus (Norway rat)Potency0.38560.005612.367736.1254AID624032; AID624044
survival motor neuron protein isoform dHomo sapiens (human)Potency0.79430.125912.234435.4813AID1458
cytochrome P450 3A4 isoform 1Homo sapiens (human)Potency25.11890.031610.279239.8107AID884; AID885
M-phase phosphoprotein 8Homo sapiens (human)Potency6.70160.177824.735279.4328AID488949
muscleblind-like protein 1 isoform 1Homo sapiens (human)Potency5.36730.00419.962528.1838AID493199; AID493205
histone acetyltransferase KAT2A isoform 1Homo sapiens (human)Potency25.11890.251215.843239.8107AID504327
muscarinic acetylcholine receptor M1Rattus norvegicus (Norway rat)Potency11.39740.00106.000935.4813AID943; AID944
lamin isoform A-delta10Homo sapiens (human)Potency0.07080.891312.067628.1838AID1487
pyruvate kinase PKM isoform bHomo sapiens (human)Potency19.95262.511912.262825.1189AID954; AID958
Gamma-aminobutyric acid receptor subunit piRattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Polyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)Potency7.87580.316212.765731.6228AID881
Glycoprotein hormones alpha chainHomo sapiens (human)Potency1.12204.46688.344810.0000AID624291
Interferon betaHomo sapiens (human)Potency0.93000.00339.158239.8107AID1347411
Integrin beta-3Homo sapiens (human)Potency6.47760.316211.415731.6228AID924
Integrin alpha-IIbHomo sapiens (human)Potency6.47760.316211.415731.6228AID924
Gamma-aminobutyric acid receptor subunit beta-1Rattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit deltaRattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-2Rattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-5Rattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-3Rattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-1Rattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-2Rattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-4Rattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-3Rattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-6Rattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Histamine H2 receptorCavia porcellus (domestic guinea pig)Potency7.87580.00638.235039.8107AID881
Gamma-aminobutyric acid receptor subunit alpha-1Rattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit beta-3Rattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Guanine nucleotide-binding protein GHomo sapiens (human)Potency22.38721.995325.532750.1187AID624288
Gamma-aminobutyric acid receptor subunit beta-2Rattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Inositol monophosphatase 1Rattus norvegicus (Norway rat)Potency10.00001.000010.475628.1838AID901
GABA theta subunitRattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Ataxin-2Homo sapiens (human)Potency0.31620.011912.222168.7989AID588378
Gamma-aminobutyric acid receptor subunit epsilonRattus norvegicus (Norway rat)Potency25.11891.000012.224831.6228AID885
Single-stranded DNA cytosine deaminaseHomo sapiens (human)Potency33.669828.183860.145389.1251AID1347427; AID1347430
phosphoglycerate kinaseTrypanosoma brucei brucei TREU927Potency21.33130.07578.474229.0628AID504547
2,3-bisphosphoglycerate-independent phosphoglycerate mutaseLeishmania major strain FriedlinPotency23.93417.568615.230621.3313AID504548
ATP-dependent phosphofructokinaseTrypanosoma brucei brucei TREU927Potency4.77550.060110.745337.9330AID485368
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, Probable serine/threonine-protein kinase pknBMycobacterium tuberculosis H37RvIC50 (µMol)0.80000.80000.80000.8000AID977608
nonstructural protein 1Influenza A virus (A/California/07/2009(H1N1))IC50 (µMol)2.04900.200024.4540100.0000AID504329
rac GTPase-activating protein 1 isoform aHomo sapiens (human)IC50 (µMol)14.46007.390057.8904301.2400AID624330
Solute carrier family 22 member 2Homo sapiens (human)IC50 (µMol)73.30000.40003.10009.7000AID721751
Solute carrier family 22 member 1 Homo sapiens (human)IC50 (µMol)43.90000.21005.553710.0000AID721750
Voltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)IC50 (µMol)22.50000.00032.63119.0000AID1207752
5-hydroxytryptamine receptor 4Cavia porcellus (domestic guinea pig)IC50 (µMol)3.56190.00011.00768.7800AID625218
5-hydroxytryptamine receptor 4Cavia porcellus (domestic guinea pig)Ki1.86570.00000.887110.0000AID625218
Solute carrier family 22 member 3Homo sapiens (human)IC50 (µMol)60.50000.09003.72779.5000AID721749
Epidermal growth factor receptorHomo sapiens (human)IC50 (µMol)5.38590.00000.536910.0000AID625184
Receptor tyrosine-protein kinase erbB-2Homo sapiens (human)IC50 (µMol)2.03520.00010.545310.0000AID625186
Tyrosine-protein kinase FynHomo sapiens (human)IC50 (µMol)1.25790.00021.67898.6800AID625185
Aldo-keto reductase family 1 member B1Rattus norvegicus (Norway rat)IC50 (µMol)4.98980.00041.877310.0000AID625207
Aldo-keto reductase family 1 member B1Rattus norvegicus (Norway rat)Ki4.94850.00322.28879.3160AID625207
Muscarinic acetylcholine receptor M2Homo sapiens (human)IC50 (µMol)0.21900.00001.23267.7930AID625152
Muscarinic acetylcholine receptor M2Homo sapiens (human)Ki0.07790.00000.690210.0000AID625152
Muscarinic acetylcholine receptor M4Homo sapiens (human)IC50 (µMol)0.64410.00001.15467.5858AID625154
Muscarinic acetylcholine receptor M4Homo sapiens (human)Ki0.08980.00000.79519.1201AID625154
ATP-dependent translocase ABCB1Homo sapiens (human)IC50 (µMol)1.50100.00022.318510.0000AID1525935
Proto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)IC50 (µMol)2.99870.00010.30056.7000AID1506771
Cytochrome P450 2D6Homo sapiens (human)IC50 (µMol)76.30000.00002.015110.0000AID240619
Muscarinic acetylcholine receptor M1Homo sapiens (human)IC50 (µMol)0.74870.00001.403910.0000AID625151
Muscarinic acetylcholine receptor M1Homo sapiens (human)Ki0.18030.00000.59729.1201AID625151
DNA topoisomerase 2-alphaHomo sapiens (human)IC50 (µMol)5.30000.48004.35649.9400AID381809
Polyunsaturated fatty acid lipoxygenase ALOX15Oryctolagus cuniculus (rabbit)IC50 (µMol)1.78530.11003.26419.0330AID625146
Angiotensin-converting enzymeOryctolagus cuniculus (rabbit)IC50 (µMol)3.58490.00001.612910.0000AID625171
Angiotensin-converting enzymeOryctolagus cuniculus (rabbit)Ki2.93700.00042.03378.6606AID625171
Casein kinase II subunit alpha'Homo sapiens (human)IC50 (µMol)0.66000.00031.432010.0000AID729381
Sodium-dependent noradrenaline transporter Homo sapiens (human)IC50 (µMol)4.98980.00081.541620.0000AID625207
Sodium-dependent noradrenaline transporter Homo sapiens (human)Ki4.94850.00031.465610.0000AID625207
5-hydroxytryptamine receptor 2CHomo sapiens (human)IC50 (µMol)3.56190.00011.03029.0000AID625218
5-hydroxytryptamine receptor 2CHomo sapiens (human)Ki1.86570.00010.954910.0000AID625218
Multidrug resistance-associated protein 1 Homo sapiens (human)IC50 (µMol)0.00810.00153.71109.6600AID1525934; AID681514; AID681515; AID681516
Casein kinase II subunit betaHomo sapiens (human)IC50 (µMol)0.66000.00031.487510.0000AID729381
Casein kinase II subunit alphaHomo sapiens (human)IC50 (µMol)0.66000.00051.333210.0000AID729381
Voltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)IC50 (µMol)22.50000.00032.59559.0000AID1207752
Tyrosine-protein kinase BTKHomo sapiens (human)IC50 (µMol)1.00000.00010.25577.6000AID729382
Potassium voltage-gated channel subfamily H member 2Homo sapiens (human)IC50 (µMol)3.58490.00091.901410.0000AID625171
Potassium voltage-gated channel subfamily H member 2Homo sapiens (human)Ki2.93700.00211.840710.0000AID625171
TAR DNA-binding protein 43Homo sapiens (human)IC50 (µMol)10.000010.000010.000010.0000AID1666489
Voltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)IC50 (µMol)22.50000.00032.63119.0000AID1207752
Voltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)IC50 (µMol)22.50000.00032.25459.6000AID1207752
Nuclear receptor subfamily 3 group C member 3 Bos taurus (cattle)IC50 (µMol)3.58490.10482.83988.3173AID625171
Nuclear receptor subfamily 3 group C member 3 Bos taurus (cattle)Ki2.93700.08582.95428.6606AID625171
Integrase Human immunodeficiency virus 1IC50 (µMol)5.90000.00051.544310.0000AID91425; AID91426
Multidrug and toxin extrusion protein 2Homo sapiens (human)IC50 (µMol)0.68000.16003.95718.6000AID721748; AID721752
Casein kinase II subunit alpha 3Homo sapiens (human)IC50 (µMol)0.66000.00151.966410.0000AID729381
Multidrug and toxin extrusion protein 1Homo sapiens (human)IC50 (µMol)0.37330.01002.765610.0000AID721746; AID721747; AID721754
P2Y purinoceptor 12Homo sapiens (human)Ki10.00000.00202.82209.8300AID375433
Solute carrier organic anion transporter family member 1B3Homo sapiens (human)IC50 (µMol)3.39000.10472.71957.0795AID1197747
Solute carrier organic anion transporter family member 1B3Homo sapiens (human)Ki3.10000.08002.46889.8000AID1197747
Broad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)IC50 (µMol)0.90380.00401.966610.0000AID1525933
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
NEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)EC50 (µMol)1.30000.03001.57673.4000AID1349085
NEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)EC50 (µMol)1.30000.03001.57673.4000AID1349085
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Other Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
LANAHuman gammaherpesvirus 8AC503.19550.042032.4569312.0010AID504726; AID504727
interferon gamma precursorHomo sapiens (human)AC500.16850.128015.173038.6100AID1259418; AID1259420
histone-lysine N-methyltransferase NSD2 isoform 1Homo sapiens (human)AC502.34000.29307.307019.4400AID1053173
protein AF-9 isoform aHomo sapiens (human)AC500.37400.08008.380217.9800AID720495
dual specificity tyrosine-phosphorylation-regulated kinase 1ARattus norvegicus (Norway rat)AC501.24800.00564.693226.6940AID588345
DNA repair protein RAD52 homolog isoform aHomo sapiens (human)AC500.24400.150012.066235.2100AID652116
DNA topoisomerase 2-alphaHomo sapiens (human)IC90 (µMol)1.10001.10001.10001.1000AID211122; AID57199
DNA topoisomerase 2-betaHomo sapiens (human)IC90 (µMol)1.10001.10001.10001.1000AID211122; AID57199
Broad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)Kact7.00001.00003.75007.0000AID678804
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (663)

Processvia Protein(s)Taxonomy
activation of cysteine-type endopeptidase activity involved in apoptotic processSolute carrier family 22 member 2Homo sapiens (human)
positive regulation of gene expressionSolute carrier family 22 member 2Homo sapiens (human)
organic cation transportSolute carrier family 22 member 2Homo sapiens (human)
monoatomic cation transportSolute carrier family 22 member 2Homo sapiens (human)
neurotransmitter transportSolute carrier family 22 member 2Homo sapiens (human)
serotonin transportSolute carrier family 22 member 2Homo sapiens (human)
body fluid secretionSolute carrier family 22 member 2Homo sapiens (human)
organic cation transportSolute carrier family 22 member 2Homo sapiens (human)
quaternary ammonium group transportSolute carrier family 22 member 2Homo sapiens (human)
prostaglandin transportSolute carrier family 22 member 2Homo sapiens (human)
amine transportSolute carrier family 22 member 2Homo sapiens (human)
putrescine transportSolute carrier family 22 member 2Homo sapiens (human)
spermidine transportSolute carrier family 22 member 2Homo sapiens (human)
acetylcholine transportSolute carrier family 22 member 2Homo sapiens (human)
choline transportSolute carrier family 22 member 2Homo sapiens (human)
dopamine transportSolute carrier family 22 member 2Homo sapiens (human)
norepinephrine transportSolute carrier family 22 member 2Homo sapiens (human)
xenobiotic transportSolute carrier family 22 member 2Homo sapiens (human)
epinephrine transportSolute carrier family 22 member 2Homo sapiens (human)
histamine transportSolute carrier family 22 member 2Homo sapiens (human)
serotonin uptakeSolute carrier family 22 member 2Homo sapiens (human)
histamine uptakeSolute carrier family 22 member 2Homo sapiens (human)
norepinephrine uptakeSolute carrier family 22 member 2Homo sapiens (human)
thiamine transmembrane transportSolute carrier family 22 member 2Homo sapiens (human)
purine-containing compound transmembrane transportSolute carrier family 22 member 2Homo sapiens (human)
amino acid import across plasma membraneSolute carrier family 22 member 2Homo sapiens (human)
dopamine uptakeSolute carrier family 22 member 2Homo sapiens (human)
L-arginine import across plasma membraneSolute carrier family 22 member 2Homo sapiens (human)
export across plasma membraneSolute carrier family 22 member 2Homo sapiens (human)
transport across blood-brain barrierSolute carrier family 22 member 2Homo sapiens (human)
L-alpha-amino acid transmembrane transportSolute carrier family 22 member 2Homo sapiens (human)
spermidine transmembrane transportSolute carrier family 22 member 2Homo sapiens (human)
L-arginine transmembrane transportSolute carrier family 22 member 2Homo sapiens (human)
cellular detoxificationSolute carrier family 22 member 2Homo sapiens (human)
xenobiotic transport across blood-brain barrierSolute carrier family 22 member 2Homo sapiens (human)
xenobiotic metabolic processSolute carrier family 22 member 1 Homo sapiens (human)
neurotransmitter transportSolute carrier family 22 member 1 Homo sapiens (human)
serotonin transportSolute carrier family 22 member 1 Homo sapiens (human)
establishment or maintenance of transmembrane electrochemical gradientSolute carrier family 22 member 1 Homo sapiens (human)
organic cation transportSolute carrier family 22 member 1 Homo sapiens (human)
quaternary ammonium group transportSolute carrier family 22 member 1 Homo sapiens (human)
prostaglandin transportSolute carrier family 22 member 1 Homo sapiens (human)
monoamine transportSolute carrier family 22 member 1 Homo sapiens (human)
putrescine transportSolute carrier family 22 member 1 Homo sapiens (human)
spermidine transportSolute carrier family 22 member 1 Homo sapiens (human)
acetylcholine transportSolute carrier family 22 member 1 Homo sapiens (human)
dopamine transportSolute carrier family 22 member 1 Homo sapiens (human)
norepinephrine transportSolute carrier family 22 member 1 Homo sapiens (human)
thiamine transportSolute carrier family 22 member 1 Homo sapiens (human)
xenobiotic transportSolute carrier family 22 member 1 Homo sapiens (human)
epinephrine transportSolute carrier family 22 member 1 Homo sapiens (human)
serotonin uptakeSolute carrier family 22 member 1 Homo sapiens (human)
norepinephrine uptakeSolute carrier family 22 member 1 Homo sapiens (human)
thiamine transmembrane transportSolute carrier family 22 member 1 Homo sapiens (human)
metanephric proximal tubule developmentSolute carrier family 22 member 1 Homo sapiens (human)
purine-containing compound transmembrane transportSolute carrier family 22 member 1 Homo sapiens (human)
dopamine uptakeSolute carrier family 22 member 1 Homo sapiens (human)
monoatomic cation transmembrane transportSolute carrier family 22 member 1 Homo sapiens (human)
transport across blood-brain barrierSolute carrier family 22 member 1 Homo sapiens (human)
(R)-carnitine transmembrane transportSolute carrier family 22 member 1 Homo sapiens (human)
acyl carnitine transmembrane transportSolute carrier family 22 member 1 Homo sapiens (human)
spermidine transmembrane transportSolute carrier family 22 member 1 Homo sapiens (human)
cellular detoxificationSolute carrier family 22 member 1 Homo sapiens (human)
xenobiotic transport across blood-brain barrierSolute carrier family 22 member 1 Homo sapiens (human)
lipid metabolic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
phospholipid metabolic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
apoptotic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
negative regulation of cell population proliferationPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
positive regulation of macrophage derived foam cell differentiationPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
arachidonic acid metabolic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
negative regulation of cell migrationPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
prostate gland developmentPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
regulation of epithelial cell differentiationPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
positive regulation of chemokine productionPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
positive regulation of peroxisome proliferator activated receptor signaling pathwayPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
positive regulation of keratinocyte differentiationPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
negative regulation of cell cyclePolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
negative regulation of growthPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
hepoxilin biosynthetic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
endocannabinoid signaling pathwayPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
cannabinoid biosynthetic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
lipoxin A4 biosynthetic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
linoleic acid metabolic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
lipid oxidationPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
lipoxygenase pathwayPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
visual perceptionVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
detection of light stimulus involved in visual perceptionVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
calcium ion import across plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
histamine metabolic processSolute carrier family 22 member 3Homo sapiens (human)
organic cation transportSolute carrier family 22 member 3Homo sapiens (human)
quaternary ammonium group transportSolute carrier family 22 member 3Homo sapiens (human)
monoatomic ion transportSolute carrier family 22 member 3Homo sapiens (human)
neurotransmitter transportSolute carrier family 22 member 3Homo sapiens (human)
serotonin transportSolute carrier family 22 member 3Homo sapiens (human)
organic cation transportSolute carrier family 22 member 3Homo sapiens (human)
quaternary ammonium group transportSolute carrier family 22 member 3Homo sapiens (human)
organic anion transportSolute carrier family 22 member 3Homo sapiens (human)
monocarboxylic acid transportSolute carrier family 22 member 3Homo sapiens (human)
monoamine transportSolute carrier family 22 member 3Homo sapiens (human)
spermidine transportSolute carrier family 22 member 3Homo sapiens (human)
dopamine transportSolute carrier family 22 member 3Homo sapiens (human)
norepinephrine transportSolute carrier family 22 member 3Homo sapiens (human)
regulation of appetiteSolute carrier family 22 member 3Homo sapiens (human)
xenobiotic transportSolute carrier family 22 member 3Homo sapiens (human)
epinephrine transportSolute carrier family 22 member 3Homo sapiens (human)
histamine transportSolute carrier family 22 member 3Homo sapiens (human)
serotonin uptakeSolute carrier family 22 member 3Homo sapiens (human)
histamine uptakeSolute carrier family 22 member 3Homo sapiens (human)
norepinephrine uptakeSolute carrier family 22 member 3Homo sapiens (human)
epinephrine uptakeSolute carrier family 22 member 3Homo sapiens (human)
purine-containing compound transmembrane transportSolute carrier family 22 member 3Homo sapiens (human)
dopamine uptakeSolute carrier family 22 member 3Homo sapiens (human)
transport across blood-brain barrierSolute carrier family 22 member 3Homo sapiens (human)
spermidine transmembrane transportSolute carrier family 22 member 3Homo sapiens (human)
cellular detoxificationSolute carrier family 22 member 3Homo sapiens (human)
cell surface receptor signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
epidermal growth factor receptor signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
positive regulation of cell population proliferationEpidermal growth factor receptorHomo sapiens (human)
MAPK cascadeEpidermal growth factor receptorHomo sapiens (human)
ossificationEpidermal growth factor receptorHomo sapiens (human)
embryonic placenta developmentEpidermal growth factor receptorHomo sapiens (human)
positive regulation of protein phosphorylationEpidermal growth factor receptorHomo sapiens (human)
hair follicle developmentEpidermal growth factor receptorHomo sapiens (human)
translationEpidermal growth factor receptorHomo sapiens (human)
signal transductionEpidermal growth factor receptorHomo sapiens (human)
epidermal growth factor receptor signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
activation of phospholipase C activityEpidermal growth factor receptorHomo sapiens (human)
salivary gland morphogenesisEpidermal growth factor receptorHomo sapiens (human)
midgut developmentEpidermal growth factor receptorHomo sapiens (human)
learning or memoryEpidermal growth factor receptorHomo sapiens (human)
circadian rhythmEpidermal growth factor receptorHomo sapiens (human)
positive regulation of cell population proliferationEpidermal growth factor receptorHomo sapiens (human)
diterpenoid metabolic processEpidermal growth factor receptorHomo sapiens (human)
peptidyl-tyrosine phosphorylationEpidermal growth factor receptorHomo sapiens (human)
cerebral cortex cell migrationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of cell growthEpidermal growth factor receptorHomo sapiens (human)
lung developmentEpidermal growth factor receptorHomo sapiens (human)
positive regulation of cell migrationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of superoxide anion generationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylationEpidermal growth factor receptorHomo sapiens (human)
response to cobalaminEpidermal growth factor receptorHomo sapiens (human)
response to hydroxyisoflavoneEpidermal growth factor receptorHomo sapiens (human)
cellular response to reactive oxygen speciesEpidermal growth factor receptorHomo sapiens (human)
peptidyl-tyrosine autophosphorylationEpidermal growth factor receptorHomo sapiens (human)
ERBB2-EGFR signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
negative regulation of epidermal growth factor receptor signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
negative regulation of protein catabolic processEpidermal growth factor receptorHomo sapiens (human)
vasodilationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of phosphorylationEpidermal growth factor receptorHomo sapiens (human)
ovulation cycleEpidermal growth factor receptorHomo sapiens (human)
hydrogen peroxide metabolic processEpidermal growth factor receptorHomo sapiens (human)
negative regulation of apoptotic processEpidermal growth factor receptorHomo sapiens (human)
positive regulation of MAP kinase activityEpidermal growth factor receptorHomo sapiens (human)
tongue developmentEpidermal growth factor receptorHomo sapiens (human)
positive regulation of cyclin-dependent protein serine/threonine kinase activityEpidermal growth factor receptorHomo sapiens (human)
positive regulation of DNA repairEpidermal growth factor receptorHomo sapiens (human)
positive regulation of DNA replicationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of bone resorptionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of DNA-templated transcriptionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of vasoconstrictionEpidermal growth factor receptorHomo sapiens (human)
negative regulation of mitotic cell cycleEpidermal growth factor receptorHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIEpidermal growth factor receptorHomo sapiens (human)
regulation of JNK cascadeEpidermal growth factor receptorHomo sapiens (human)
symbiont entry into host cellEpidermal growth factor receptorHomo sapiens (human)
protein autophosphorylationEpidermal growth factor receptorHomo sapiens (human)
astrocyte activationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of fibroblast proliferationEpidermal growth factor receptorHomo sapiens (human)
digestive tract morphogenesisEpidermal growth factor receptorHomo sapiens (human)
positive regulation of smooth muscle cell proliferationEpidermal growth factor receptorHomo sapiens (human)
neuron projection morphogenesisEpidermal growth factor receptorHomo sapiens (human)
epithelial cell proliferationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of epithelial cell proliferationEpidermal growth factor receptorHomo sapiens (human)
regulation of peptidyl-tyrosine phosphorylationEpidermal growth factor receptorHomo sapiens (human)
protein insertion into membraneEpidermal growth factor receptorHomo sapiens (human)
response to calcium ionEpidermal growth factor receptorHomo sapiens (human)
regulation of phosphatidylinositol 3-kinase/protein kinase B signal transductionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transductionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of synaptic transmission, glutamatergicEpidermal growth factor receptorHomo sapiens (human)
positive regulation of glial cell proliferationEpidermal growth factor receptorHomo sapiens (human)
morphogenesis of an epithelial foldEpidermal growth factor receptorHomo sapiens (human)
eyelid development in camera-type eyeEpidermal growth factor receptorHomo sapiens (human)
response to UV-AEpidermal growth factor receptorHomo sapiens (human)
positive regulation of mucus secretionEpidermal growth factor receptorHomo sapiens (human)
regulation of ERK1 and ERK2 cascadeEpidermal growth factor receptorHomo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeEpidermal growth factor receptorHomo sapiens (human)
cellular response to amino acid stimulusEpidermal growth factor receptorHomo sapiens (human)
cellular response to mechanical stimulusEpidermal growth factor receptorHomo sapiens (human)
cellular response to cadmium ionEpidermal growth factor receptorHomo sapiens (human)
cellular response to epidermal growth factor stimulusEpidermal growth factor receptorHomo sapiens (human)
cellular response to estradiol stimulusEpidermal growth factor receptorHomo sapiens (human)
cellular response to xenobiotic stimulusEpidermal growth factor receptorHomo sapiens (human)
cellular response to dexamethasone stimulusEpidermal growth factor receptorHomo sapiens (human)
positive regulation of canonical Wnt signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
liver regenerationEpidermal growth factor receptorHomo sapiens (human)
cell-cell adhesionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of protein kinase C activityEpidermal growth factor receptorHomo sapiens (human)
positive regulation of G1/S transition of mitotic cell cycleEpidermal growth factor receptorHomo sapiens (human)
positive regulation of non-canonical NF-kappaB signal transductionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of prolactin secretionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of miRNA transcriptionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of protein localization to plasma membraneEpidermal growth factor receptorHomo sapiens (human)
negative regulation of cardiocyte differentiationEpidermal growth factor receptorHomo sapiens (human)
neurogenesisEpidermal growth factor receptorHomo sapiens (human)
multicellular organism developmentEpidermal growth factor receptorHomo sapiens (human)
positive regulation of kinase activityEpidermal growth factor receptorHomo sapiens (human)
cell surface receptor protein tyrosine kinase signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
G protein-coupled receptor signaling pathwayGlycoprotein hormones alpha chainHomo sapiens (human)
positive regulation of cell population proliferationGlycoprotein hormones alpha chainHomo sapiens (human)
hormone-mediated signaling pathwayGlycoprotein hormones alpha chainHomo sapiens (human)
regulation of signaling receptor activityGlycoprotein hormones alpha chainHomo sapiens (human)
positive regulation of steroid biosynthetic processGlycoprotein hormones alpha chainHomo sapiens (human)
positive regulation of cell migrationGlycoprotein hormones alpha chainHomo sapiens (human)
thyroid gland developmentGlycoprotein hormones alpha chainHomo sapiens (human)
luteinizing hormone secretionGlycoprotein hormones alpha chainHomo sapiens (human)
organ growthGlycoprotein hormones alpha chainHomo sapiens (human)
follicle-stimulating hormone signaling pathwayGlycoprotein hormones alpha chainHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIGlycoprotein hormones alpha chainHomo sapiens (human)
negative regulation of organ growthGlycoprotein hormones alpha chainHomo sapiens (human)
follicle-stimulating hormone secretionGlycoprotein hormones alpha chainHomo sapiens (human)
thyroid hormone generationGlycoprotein hormones alpha chainHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell activation involved in immune responseInterferon betaHomo sapiens (human)
cell surface receptor signaling pathwayInterferon betaHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to virusInterferon betaHomo sapiens (human)
positive regulation of autophagyInterferon betaHomo sapiens (human)
cytokine-mediated signaling pathwayInterferon betaHomo sapiens (human)
natural killer cell activationInterferon betaHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT proteinInterferon betaHomo sapiens (human)
cellular response to interferon-betaInterferon betaHomo sapiens (human)
B cell proliferationInterferon betaHomo sapiens (human)
negative regulation of viral genome replicationInterferon betaHomo sapiens (human)
innate immune responseInterferon betaHomo sapiens (human)
positive regulation of innate immune responseInterferon betaHomo sapiens (human)
regulation of MHC class I biosynthetic processInterferon betaHomo sapiens (human)
negative regulation of T cell differentiationInterferon betaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIInterferon betaHomo sapiens (human)
defense response to virusInterferon betaHomo sapiens (human)
type I interferon-mediated signaling pathwayInterferon betaHomo sapiens (human)
neuron cellular homeostasisInterferon betaHomo sapiens (human)
cellular response to exogenous dsRNAInterferon betaHomo sapiens (human)
cellular response to virusInterferon betaHomo sapiens (human)
negative regulation of Lewy body formationInterferon betaHomo sapiens (human)
negative regulation of T-helper 2 cell cytokine productionInterferon betaHomo sapiens (human)
positive regulation of apoptotic signaling pathwayInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell differentiationInterferon betaHomo sapiens (human)
natural killer cell activation involved in immune responseInterferon betaHomo sapiens (human)
adaptive immune responseInterferon betaHomo sapiens (human)
T cell activation involved in immune responseInterferon betaHomo sapiens (human)
humoral immune responseInterferon betaHomo sapiens (human)
cell surface receptor signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of protein phosphorylationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
protein phosphorylationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
signal transductionReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
enzyme-linked receptor protein signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
cell surface receptor protein tyrosine kinase signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
heart developmentReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
neuromuscular junction developmentReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
motor neuron axon guidanceReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
Schwann cell developmentReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
peptidyl-tyrosine phosphorylationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of cell growthReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
regulation of microtubule-based processReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
immature T cell proliferation in thymusReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
negative regulation of immature T cell proliferation in thymusReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of Rho protein signal transductionReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
intracellular signal transductionReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ERBB2-ERBB3 signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ERBB2-EGFR signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ERBB2-ERBB4 signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
wound healingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
myelinationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of MAP kinase activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
phosphatidylinositol 3-kinase/protein kinase B signal transductionReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of translationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
regulation of angiogenesisReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of cell adhesionReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of transcription by RNA polymerase IReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
oligodendrocyte differentiationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of epithelial cell proliferationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
regulation of ERK1 and ERK2 cascadeReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
cellular response to growth factor stimulusReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
cellular response to epidermal growth factor stimulusReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
semaphorin-plexin signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of protein targeting to membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
neurotransmitter receptor localization to postsynaptic specialization membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
neurogenesisReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of MAPK cascadeReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
negative regulation of apoptotic processReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of kinase activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
multicellular organism developmentReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of cell population proliferationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
neuron differentiationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
regulation of gene expressionAmyloid-beta precursor proteinHomo sapiens (human)
cognitionAmyloid-beta precursor proteinHomo sapiens (human)
G2/M transition of mitotic cell cycleAmyloid-beta precursor proteinHomo sapiens (human)
microglial cell activationAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of protein phosphorylationAmyloid-beta precursor proteinHomo sapiens (human)
suckling behaviorAmyloid-beta precursor proteinHomo sapiens (human)
astrocyte activation involved in immune responseAmyloid-beta precursor proteinHomo sapiens (human)
regulation of translationAmyloid-beta precursor proteinHomo sapiens (human)
protein phosphorylationAmyloid-beta precursor proteinHomo sapiens (human)
intracellular copper ion homeostasisAmyloid-beta precursor proteinHomo sapiens (human)
endocytosisAmyloid-beta precursor proteinHomo sapiens (human)
response to oxidative stressAmyloid-beta precursor proteinHomo sapiens (human)
cell adhesionAmyloid-beta precursor proteinHomo sapiens (human)
regulation of epidermal growth factor-activated receptor activityAmyloid-beta precursor proteinHomo sapiens (human)
Notch signaling pathwayAmyloid-beta precursor proteinHomo sapiens (human)
axonogenesisAmyloid-beta precursor proteinHomo sapiens (human)
learning or memoryAmyloid-beta precursor proteinHomo sapiens (human)
learningAmyloid-beta precursor proteinHomo sapiens (human)
mating behaviorAmyloid-beta precursor proteinHomo sapiens (human)
locomotory behaviorAmyloid-beta precursor proteinHomo sapiens (human)
axo-dendritic transportAmyloid-beta precursor proteinHomo sapiens (human)
cholesterol metabolic processAmyloid-beta precursor proteinHomo sapiens (human)
negative regulation of cell population proliferationAmyloid-beta precursor proteinHomo sapiens (human)
adult locomotory behaviorAmyloid-beta precursor proteinHomo sapiens (human)
visual learningAmyloid-beta precursor proteinHomo sapiens (human)
regulation of gene expressionAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of gene expressionAmyloid-beta precursor proteinHomo sapiens (human)
negative regulation of gene expressionAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of peptidyl-threonine phosphorylationAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of G2/M transition of mitotic cell cycleAmyloid-beta precursor proteinHomo sapiens (human)
microglia developmentAmyloid-beta precursor proteinHomo sapiens (human)
axon midline choice point recognitionAmyloid-beta precursor proteinHomo sapiens (human)
neuron remodelingAmyloid-beta precursor proteinHomo sapiens (human)
dendrite developmentAmyloid-beta precursor proteinHomo sapiens (human)
regulation of Wnt signaling pathwayAmyloid-beta precursor proteinHomo sapiens (human)
extracellular matrix organizationAmyloid-beta precursor proteinHomo sapiens (human)
forebrain developmentAmyloid-beta precursor proteinHomo sapiens (human)
neuron projection developmentAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of chemokine productionAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of interleukin-1 beta productionAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of interleukin-6 productionAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of tumor necrosis factor productionAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylationAmyloid-beta precursor proteinHomo sapiens (human)
ionotropic glutamate receptor signaling pathwayAmyloid-beta precursor proteinHomo sapiens (human)
regulation of multicellular organism growthAmyloid-beta precursor proteinHomo sapiens (human)
negative regulation of neuron differentiationAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of glycolytic processAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of mitotic cell cycleAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of JNK cascadeAmyloid-beta precursor proteinHomo sapiens (human)
astrocyte activationAmyloid-beta precursor proteinHomo sapiens (human)
regulation of long-term neuronal synaptic plasticityAmyloid-beta precursor proteinHomo sapiens (human)
collateral sprouting in absence of injuryAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of inflammatory responseAmyloid-beta precursor proteinHomo sapiens (human)
regulation of peptidyl-tyrosine phosphorylationAmyloid-beta precursor proteinHomo sapiens (human)
regulation of synapse structure or activityAmyloid-beta precursor proteinHomo sapiens (human)
synapse organizationAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of calcium-mediated signalingAmyloid-beta precursor proteinHomo sapiens (human)
neuromuscular process controlling balanceAmyloid-beta precursor proteinHomo sapiens (human)
synaptic assembly at neuromuscular junctionAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of protein metabolic processAmyloid-beta precursor proteinHomo sapiens (human)
neuron apoptotic processAmyloid-beta precursor proteinHomo sapiens (human)
smooth endoplasmic reticulum calcium ion homeostasisAmyloid-beta precursor proteinHomo sapiens (human)
neuron cellular homeostasisAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeAmyloid-beta precursor proteinHomo sapiens (human)
response to interleukin-1Amyloid-beta precursor proteinHomo sapiens (human)
modulation of excitatory postsynaptic potentialAmyloid-beta precursor proteinHomo sapiens (human)
NMDA selective glutamate receptor signaling pathwayAmyloid-beta precursor proteinHomo sapiens (human)
regulation of spontaneous synaptic transmissionAmyloid-beta precursor proteinHomo sapiens (human)
cytosolic mRNA polyadenylationAmyloid-beta precursor proteinHomo sapiens (human)
negative regulation of long-term synaptic potentiationAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of long-term synaptic potentiationAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of non-canonical NF-kappaB signal transductionAmyloid-beta precursor proteinHomo sapiens (human)
cellular response to amyloid-betaAmyloid-beta precursor proteinHomo sapiens (human)
regulation of presynapse assemblyAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of amyloid fibril formationAmyloid-beta precursor proteinHomo sapiens (human)
amyloid fibril formationAmyloid-beta precursor proteinHomo sapiens (human)
neuron projection maintenanceAmyloid-beta precursor proteinHomo sapiens (human)
positive regulation of T cell migrationAmyloid-beta precursor proteinHomo sapiens (human)
central nervous system developmentAmyloid-beta precursor proteinHomo sapiens (human)
negative regulation of low-density lipoprotein receptor activityIntegrin beta-3Homo sapiens (human)
positive regulation of protein phosphorylationIntegrin beta-3Homo sapiens (human)
positive regulation of endothelial cell proliferationIntegrin beta-3Homo sapiens (human)
positive regulation of cell-matrix adhesionIntegrin beta-3Homo sapiens (human)
cell-substrate junction assemblyIntegrin beta-3Homo sapiens (human)
cell adhesionIntegrin beta-3Homo sapiens (human)
cell-matrix adhesionIntegrin beta-3Homo sapiens (human)
integrin-mediated signaling pathwayIntegrin beta-3Homo sapiens (human)
embryo implantationIntegrin beta-3Homo sapiens (human)
blood coagulationIntegrin beta-3Homo sapiens (human)
positive regulation of endothelial cell migrationIntegrin beta-3Homo sapiens (human)
positive regulation of gene expressionIntegrin beta-3Homo sapiens (human)
negative regulation of macrophage derived foam cell differentiationIntegrin beta-3Homo sapiens (human)
positive regulation of fibroblast migrationIntegrin beta-3Homo sapiens (human)
negative regulation of lipid storageIntegrin beta-3Homo sapiens (human)
response to activityIntegrin beta-3Homo sapiens (human)
smooth muscle cell migrationIntegrin beta-3Homo sapiens (human)
positive regulation of smooth muscle cell migrationIntegrin beta-3Homo sapiens (human)
platelet activationIntegrin beta-3Homo sapiens (human)
positive regulation of vascular endothelial growth factor receptor signaling pathwayIntegrin beta-3Homo sapiens (human)
cell-substrate adhesionIntegrin beta-3Homo sapiens (human)
activation of protein kinase activityIntegrin beta-3Homo sapiens (human)
negative regulation of lipid transportIntegrin beta-3Homo sapiens (human)
regulation of protein localizationIntegrin beta-3Homo sapiens (human)
regulation of actin cytoskeleton organizationIntegrin beta-3Homo sapiens (human)
cell adhesion mediated by integrinIntegrin beta-3Homo sapiens (human)
positive regulation of cell adhesion mediated by integrinIntegrin beta-3Homo sapiens (human)
positive regulation of osteoblast proliferationIntegrin beta-3Homo sapiens (human)
heterotypic cell-cell adhesionIntegrin beta-3Homo sapiens (human)
substrate adhesion-dependent cell spreadingIntegrin beta-3Homo sapiens (human)
tube developmentIntegrin beta-3Homo sapiens (human)
wound healing, spreading of epidermal cellsIntegrin beta-3Homo sapiens (human)
cellular response to platelet-derived growth factor stimulusIntegrin beta-3Homo sapiens (human)
apolipoprotein A-I-mediated signaling pathwayIntegrin beta-3Homo sapiens (human)
wound healingIntegrin beta-3Homo sapiens (human)
apoptotic cell clearanceIntegrin beta-3Homo sapiens (human)
regulation of bone resorptionIntegrin beta-3Homo sapiens (human)
positive regulation of angiogenesisIntegrin beta-3Homo sapiens (human)
positive regulation of bone resorptionIntegrin beta-3Homo sapiens (human)
symbiont entry into host cellIntegrin beta-3Homo sapiens (human)
platelet-derived growth factor receptor signaling pathwayIntegrin beta-3Homo sapiens (human)
positive regulation of fibroblast proliferationIntegrin beta-3Homo sapiens (human)
mesodermal cell differentiationIntegrin beta-3Homo sapiens (human)
positive regulation of smooth muscle cell proliferationIntegrin beta-3Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationIntegrin beta-3Homo sapiens (human)
negative regulation of lipoprotein metabolic processIntegrin beta-3Homo sapiens (human)
negative chemotaxisIntegrin beta-3Homo sapiens (human)
regulation of release of sequestered calcium ion into cytosolIntegrin beta-3Homo sapiens (human)
regulation of serotonin uptakeIntegrin beta-3Homo sapiens (human)
angiogenesis involved in wound healingIntegrin beta-3Homo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeIntegrin beta-3Homo sapiens (human)
platelet aggregationIntegrin beta-3Homo sapiens (human)
cellular response to mechanical stimulusIntegrin beta-3Homo sapiens (human)
cellular response to xenobiotic stimulusIntegrin beta-3Homo sapiens (human)
positive regulation of glomerular mesangial cell proliferationIntegrin beta-3Homo sapiens (human)
blood coagulation, fibrin clot formationIntegrin beta-3Homo sapiens (human)
maintenance of postsynaptic specialization structureIntegrin beta-3Homo sapiens (human)
regulation of postsynaptic neurotransmitter receptor internalizationIntegrin beta-3Homo sapiens (human)
regulation of postsynaptic neurotransmitter receptor diffusion trappingIntegrin beta-3Homo sapiens (human)
positive regulation of substrate adhesion-dependent cell spreadingIntegrin beta-3Homo sapiens (human)
positive regulation of adenylate cyclase-inhibiting opioid receptor signaling pathwayIntegrin beta-3Homo sapiens (human)
regulation of trophoblast cell migrationIntegrin beta-3Homo sapiens (human)
regulation of extracellular matrix organizationIntegrin beta-3Homo sapiens (human)
cellular response to insulin-like growth factor stimulusIntegrin beta-3Homo sapiens (human)
negative regulation of endothelial cell apoptotic processIntegrin beta-3Homo sapiens (human)
positive regulation of T cell migrationIntegrin beta-3Homo sapiens (human)
cell migrationIntegrin beta-3Homo sapiens (human)
response to singlet oxygenTyrosine-protein kinase FynHomo sapiens (human)
neuron migrationTyrosine-protein kinase FynHomo sapiens (human)
stimulatory C-type lectin receptor signaling pathwayTyrosine-protein kinase FynHomo sapiens (human)
adaptive immune responseTyrosine-protein kinase FynHomo sapiens (human)
negative regulation of inflammatory response to antigenic stimulusTyrosine-protein kinase FynHomo sapiens (human)
heart processTyrosine-protein kinase FynHomo sapiens (human)
protein phosphorylationTyrosine-protein kinase FynHomo sapiens (human)
calcium ion transportTyrosine-protein kinase FynHomo sapiens (human)
G protein-coupled glutamate receptor signaling pathwayTyrosine-protein kinase FynHomo sapiens (human)
axon guidanceTyrosine-protein kinase FynHomo sapiens (human)
learningTyrosine-protein kinase FynHomo sapiens (human)
feeding behaviorTyrosine-protein kinase FynHomo sapiens (human)
regulation of cell shapeTyrosine-protein kinase FynHomo sapiens (human)
gene expressionTyrosine-protein kinase FynHomo sapiens (human)
negative regulation of gene expressionTyrosine-protein kinase FynHomo sapiens (human)
negative regulation of hydrogen peroxide biosynthetic processTyrosine-protein kinase FynHomo sapiens (human)
positive regulation of neuron projection developmentTyrosine-protein kinase FynHomo sapiens (human)
protein ubiquitinationTyrosine-protein kinase FynHomo sapiens (human)
peptidyl-tyrosine phosphorylationTyrosine-protein kinase FynHomo sapiens (human)
protein catabolic processTyrosine-protein kinase FynHomo sapiens (human)
forebrain developmentTyrosine-protein kinase FynHomo sapiens (human)
T cell costimulationTyrosine-protein kinase FynHomo sapiens (human)
negative regulation of protein ubiquitinationTyrosine-protein kinase FynHomo sapiens (human)
intracellular signal transductionTyrosine-protein kinase FynHomo sapiens (human)
cellular response to platelet-derived growth factor stimulusTyrosine-protein kinase FynHomo sapiens (human)
Fc-gamma receptor signaling pathway involved in phagocytosisTyrosine-protein kinase FynHomo sapiens (human)
negative regulation of protein catabolic processTyrosine-protein kinase FynHomo sapiens (human)
positive regulation of tyrosine phosphorylation of STAT proteinTyrosine-protein kinase FynHomo sapiens (human)
response to ethanolTyrosine-protein kinase FynHomo sapiens (human)
vascular endothelial growth factor receptor signaling pathwayTyrosine-protein kinase FynHomo sapiens (human)
ephrin receptor signaling pathwayTyrosine-protein kinase FynHomo sapiens (human)
dendrite morphogenesisTyrosine-protein kinase FynHomo sapiens (human)
regulation of peptidyl-tyrosine phosphorylationTyrosine-protein kinase FynHomo sapiens (human)
activated T cell proliferationTyrosine-protein kinase FynHomo sapiens (human)
modulation of chemical synaptic transmissionTyrosine-protein kinase FynHomo sapiens (human)
T cell receptor signaling pathwayTyrosine-protein kinase FynHomo sapiens (human)
leukocyte migrationTyrosine-protein kinase FynHomo sapiens (human)
detection of mechanical stimulus involved in sensory perception of painTyrosine-protein kinase FynHomo sapiens (human)
cellular response to hydrogen peroxideTyrosine-protein kinase FynHomo sapiens (human)
cellular response to transforming growth factor beta stimulusTyrosine-protein kinase FynHomo sapiens (human)
positive regulation of protein targeting to membraneTyrosine-protein kinase FynHomo sapiens (human)
dendritic spine maintenanceTyrosine-protein kinase FynHomo sapiens (human)
positive regulation of protein localization to nucleusTyrosine-protein kinase FynHomo sapiens (human)
regulation of glutamate receptor signaling pathwayTyrosine-protein kinase FynHomo sapiens (human)
negative regulation of oxidative stress-induced intrinsic apoptotic signaling pathwayTyrosine-protein kinase FynHomo sapiens (human)
negative regulation of dendritic spine maintenanceTyrosine-protein kinase FynHomo sapiens (human)
response to amyloid-betaTyrosine-protein kinase FynHomo sapiens (human)
cellular response to amyloid-betaTyrosine-protein kinase FynHomo sapiens (human)
cellular response to L-glutamateTyrosine-protein kinase FynHomo sapiens (human)
cellular response to glycineTyrosine-protein kinase FynHomo sapiens (human)
positive regulation of protein localization to membraneTyrosine-protein kinase FynHomo sapiens (human)
regulation of calcium ion import across plasma membraneTyrosine-protein kinase FynHomo sapiens (human)
positive regulation of cysteine-type endopeptidase activityTyrosine-protein kinase FynHomo sapiens (human)
innate immune responseTyrosine-protein kinase FynHomo sapiens (human)
cell differentiationTyrosine-protein kinase FynHomo sapiens (human)
cell surface receptor protein tyrosine kinase signaling pathwayTyrosine-protein kinase FynHomo sapiens (human)
G protein-coupled receptor signaling pathwayMuscarinic acetylcholine receptor M2Homo sapiens (human)
adenylate cyclase-modulating G protein-coupled receptor signaling pathwayMuscarinic acetylcholine receptor M2Homo sapiens (human)
phospholipase C-activating G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M2Homo sapiens (human)
G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M2Homo sapiens (human)
nervous system developmentMuscarinic acetylcholine receptor M2Homo sapiens (human)
regulation of heart contractionMuscarinic acetylcholine receptor M2Homo sapiens (human)
response to virusMuscarinic acetylcholine receptor M2Homo sapiens (human)
G protein-coupled serotonin receptor signaling pathwayMuscarinic acetylcholine receptor M2Homo sapiens (human)
presynaptic modulation of chemical synaptic transmissionMuscarinic acetylcholine receptor M2Homo sapiens (human)
regulation of smooth muscle contractionMuscarinic acetylcholine receptor M2Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M2Homo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerMuscarinic acetylcholine receptor M2Homo sapiens (human)
chemical synaptic transmissionMuscarinic acetylcholine receptor M2Homo sapiens (human)
signal transductionMuscarinic acetylcholine receptor M4Homo sapiens (human)
cell surface receptor signaling pathwayMuscarinic acetylcholine receptor M4Homo sapiens (human)
G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M4Homo sapiens (human)
regulation of locomotionMuscarinic acetylcholine receptor M4Homo sapiens (human)
G protein-coupled serotonin receptor signaling pathwayMuscarinic acetylcholine receptor M4Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M4Homo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerMuscarinic acetylcholine receptor M4Homo sapiens (human)
chemical synaptic transmissionMuscarinic acetylcholine receptor M4Homo sapiens (human)
G2/M transition of mitotic cell cycleATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic metabolic processATP-dependent translocase ABCB1Homo sapiens (human)
response to xenobiotic stimulusATP-dependent translocase ABCB1Homo sapiens (human)
phospholipid translocationATP-dependent translocase ABCB1Homo sapiens (human)
terpenoid transportATP-dependent translocase ABCB1Homo sapiens (human)
regulation of response to osmotic stressATP-dependent translocase ABCB1Homo sapiens (human)
transmembrane transportATP-dependent translocase ABCB1Homo sapiens (human)
transepithelial transportATP-dependent translocase ABCB1Homo sapiens (human)
stem cell proliferationATP-dependent translocase ABCB1Homo sapiens (human)
ceramide translocationATP-dependent translocase ABCB1Homo sapiens (human)
export across plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
transport across blood-brain barrierATP-dependent translocase ABCB1Homo sapiens (human)
positive regulation of anion channel activityATP-dependent translocase ABCB1Homo sapiens (human)
carboxylic acid transmembrane transportATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic detoxification by transmembrane export across the plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic transport across blood-brain barrierATP-dependent translocase ABCB1Homo sapiens (human)
regulation of chloride transportATP-dependent translocase ABCB1Homo sapiens (human)
positive regulation of leukocyte migrationIntegrin alpha-IIbHomo sapiens (human)
cell-matrix adhesionIntegrin alpha-IIbHomo sapiens (human)
integrin-mediated signaling pathwayIntegrin alpha-IIbHomo sapiens (human)
angiogenesisIntegrin alpha-IIbHomo sapiens (human)
cell-cell adhesionIntegrin alpha-IIbHomo sapiens (human)
cell adhesion mediated by integrinIntegrin alpha-IIbHomo sapiens (human)
regulation of cell growthProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
columnar/cuboidal epithelial cell developmentProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
protein phosphorylationProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
cell surface receptor protein tyrosine kinase signaling pathwayProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
spermatogenesisProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
cell differentiationProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
regulation of TOR signalingProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
regulation of ERK1 and ERK2 cascadeProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
positive regulation of kinase activityProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
multicellular organism developmentProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
xenobiotic metabolic processCytochrome P450 2D6Homo sapiens (human)
steroid metabolic processCytochrome P450 2D6Homo sapiens (human)
cholesterol metabolic processCytochrome P450 2D6Homo sapiens (human)
estrogen metabolic processCytochrome P450 2D6Homo sapiens (human)
coumarin metabolic processCytochrome P450 2D6Homo sapiens (human)
alkaloid metabolic processCytochrome P450 2D6Homo sapiens (human)
alkaloid catabolic processCytochrome P450 2D6Homo sapiens (human)
monoterpenoid metabolic processCytochrome P450 2D6Homo sapiens (human)
isoquinoline alkaloid metabolic processCytochrome P450 2D6Homo sapiens (human)
xenobiotic catabolic processCytochrome P450 2D6Homo sapiens (human)
retinol metabolic processCytochrome P450 2D6Homo sapiens (human)
long-chain fatty acid biosynthetic processCytochrome P450 2D6Homo sapiens (human)
negative regulation of bindingCytochrome P450 2D6Homo sapiens (human)
oxidative demethylationCytochrome P450 2D6Homo sapiens (human)
negative regulation of cellular organofluorine metabolic processCytochrome P450 2D6Homo sapiens (human)
arachidonic acid metabolic processCytochrome P450 2D6Homo sapiens (human)
positive regulation of monoatomic ion transportMuscarinic acetylcholine receptor M1Homo sapiens (human)
signal transductionMuscarinic acetylcholine receptor M1Homo sapiens (human)
G protein-coupled receptor signaling pathwayMuscarinic acetylcholine receptor M1Homo sapiens (human)
protein kinase C-activating G protein-coupled receptor signaling pathwayMuscarinic acetylcholine receptor M1Homo sapiens (human)
phospholipase C-activating G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M1Homo sapiens (human)
G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M1Homo sapiens (human)
neuromuscular synaptic transmissionMuscarinic acetylcholine receptor M1Homo sapiens (human)
nervous system developmentMuscarinic acetylcholine receptor M1Homo sapiens (human)
regulation of locomotionMuscarinic acetylcholine receptor M1Homo sapiens (human)
saliva secretionMuscarinic acetylcholine receptor M1Homo sapiens (human)
cognitionMuscarinic acetylcholine receptor M1Homo sapiens (human)
regulation of postsynaptic membrane potentialMuscarinic acetylcholine receptor M1Homo sapiens (human)
regulation of glial cell proliferationMuscarinic acetylcholine receptor M1Homo sapiens (human)
positive regulation of intracellular protein transportMuscarinic acetylcholine receptor M1Homo sapiens (human)
G protein-coupled serotonin receptor signaling pathwayMuscarinic acetylcholine receptor M1Homo sapiens (human)
postsynaptic modulation of chemical synaptic transmissionMuscarinic acetylcholine receptor M1Homo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerMuscarinic acetylcholine receptor M1Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M1Homo sapiens (human)
chemical synaptic transmissionMuscarinic acetylcholine receptor M1Homo sapiens (human)
hematopoietic progenitor cell differentiationDNA topoisomerase 2-alphaHomo sapiens (human)
DNA topological changeDNA topoisomerase 2-alphaHomo sapiens (human)
DNA ligationDNA topoisomerase 2-alphaHomo sapiens (human)
DNA damage responseDNA topoisomerase 2-alphaHomo sapiens (human)
chromosome segregationDNA topoisomerase 2-alphaHomo sapiens (human)
female meiotic nuclear divisionDNA topoisomerase 2-alphaHomo sapiens (human)
apoptotic chromosome condensationDNA topoisomerase 2-alphaHomo sapiens (human)
embryonic cleavageDNA topoisomerase 2-alphaHomo sapiens (human)
regulation of circadian rhythmDNA topoisomerase 2-alphaHomo sapiens (human)
positive regulation of apoptotic processDNA topoisomerase 2-alphaHomo sapiens (human)
positive regulation of single stranded viral RNA replication via double stranded DNA intermediateDNA topoisomerase 2-alphaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIDNA topoisomerase 2-alphaHomo sapiens (human)
rhythmic processDNA topoisomerase 2-alphaHomo sapiens (human)
negative regulation of DNA duplex unwindingDNA topoisomerase 2-alphaHomo sapiens (human)
resolution of meiotic recombination intermediatesDNA topoisomerase 2-alphaHomo sapiens (human)
sister chromatid segregationDNA topoisomerase 2-alphaHomo sapiens (human)
double-strand break repairCasein kinase II subunit alpha'Homo sapiens (human)
apoptotic processCasein kinase II subunit alpha'Homo sapiens (human)
spermatogenesisCasein kinase II subunit alpha'Homo sapiens (human)
Wnt signaling pathwayCasein kinase II subunit alpha'Homo sapiens (human)
cerebral cortex developmentCasein kinase II subunit alpha'Homo sapiens (human)
negative regulation of proteasomal ubiquitin-dependent protein catabolic processCasein kinase II subunit alpha'Homo sapiens (human)
liver regenerationCasein kinase II subunit alpha'Homo sapiens (human)
regulation of mitophagyCasein kinase II subunit alpha'Homo sapiens (human)
positive regulation of protein targeting to mitochondrionCasein kinase II subunit alpha'Homo sapiens (human)
regulation of chromosome separationCasein kinase II subunit alpha'Homo sapiens (human)
negative regulation of apoptotic signaling pathwayCasein kinase II subunit alpha'Homo sapiens (human)
peptidyl-threonine phosphorylationCasein kinase II subunit alpha'Homo sapiens (human)
peptidyl-serine phosphorylationCasein kinase II subunit alpha'Homo sapiens (human)
monoamine transportSodium-dependent noradrenaline transporter Homo sapiens (human)
neurotransmitter transportSodium-dependent noradrenaline transporter Homo sapiens (human)
chemical synaptic transmissionSodium-dependent noradrenaline transporter Homo sapiens (human)
response to xenobiotic stimulusSodium-dependent noradrenaline transporter Homo sapiens (human)
response to painSodium-dependent noradrenaline transporter Homo sapiens (human)
norepinephrine uptakeSodium-dependent noradrenaline transporter Homo sapiens (human)
neuron cellular homeostasisSodium-dependent noradrenaline transporter Homo sapiens (human)
amino acid transportSodium-dependent noradrenaline transporter Homo sapiens (human)
norepinephrine transportSodium-dependent noradrenaline transporter Homo sapiens (human)
dopamine uptake involved in synaptic transmissionSodium-dependent noradrenaline transporter Homo sapiens (human)
sodium ion transmembrane transportSodium-dependent noradrenaline transporter Homo sapiens (human)
behavioral fear response5-hydroxytryptamine receptor 2CHomo sapiens (human)
intracellular calcium ion homeostasis5-hydroxytryptamine receptor 2CHomo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathway5-hydroxytryptamine receptor 2CHomo sapiens (human)
phospholipase C-activating serotonin receptor signaling pathway5-hydroxytryptamine receptor 2CHomo sapiens (human)
locomotory behavior5-hydroxytryptamine receptor 2CHomo sapiens (human)
feeding behavior5-hydroxytryptamine receptor 2CHomo sapiens (human)
positive regulation of phosphatidylinositol biosynthetic process5-hydroxytryptamine receptor 2CHomo sapiens (human)
cGMP-mediated signaling5-hydroxytryptamine receptor 2CHomo sapiens (human)
regulation of nervous system process5-hydroxytryptamine receptor 2CHomo sapiens (human)
regulation of appetite5-hydroxytryptamine receptor 2CHomo sapiens (human)
regulation of corticotropin-releasing hormone secretion5-hydroxytryptamine receptor 2CHomo sapiens (human)
positive regulation of fat cell differentiation5-hydroxytryptamine receptor 2CHomo sapiens (human)
positive regulation of calcium-mediated signaling5-hydroxytryptamine receptor 2CHomo sapiens (human)
release of sequestered calcium ion into cytosol5-hydroxytryptamine receptor 2CHomo sapiens (human)
positive regulation of ERK1 and ERK2 cascade5-hydroxytryptamine receptor 2CHomo sapiens (human)
G protein-coupled serotonin receptor signaling pathway5-hydroxytryptamine receptor 2CHomo sapiens (human)
serotonin receptor signaling pathway5-hydroxytryptamine receptor 2CHomo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger5-hydroxytryptamine receptor 2CHomo sapiens (human)
chemical synaptic transmission5-hydroxytryptamine receptor 2CHomo sapiens (human)
leukotriene metabolic processMultidrug resistance-associated protein 1 Homo sapiens (human)
xenobiotic metabolic processMultidrug resistance-associated protein 1 Homo sapiens (human)
response to xenobiotic stimulusMultidrug resistance-associated protein 1 Homo sapiens (human)
cobalamin transportMultidrug resistance-associated protein 1 Homo sapiens (human)
sphingolipid biosynthetic processMultidrug resistance-associated protein 1 Homo sapiens (human)
cellular response to oxidative stressMultidrug resistance-associated protein 1 Homo sapiens (human)
heme catabolic processMultidrug resistance-associated protein 1 Homo sapiens (human)
xenobiotic transportMultidrug resistance-associated protein 1 Homo sapiens (human)
phospholipid translocationMultidrug resistance-associated protein 1 Homo sapiens (human)
positive regulation of inflammatory responseMultidrug resistance-associated protein 1 Homo sapiens (human)
transmembrane transportMultidrug resistance-associated protein 1 Homo sapiens (human)
cell chemotaxisMultidrug resistance-associated protein 1 Homo sapiens (human)
transepithelial transportMultidrug resistance-associated protein 1 Homo sapiens (human)
cyclic nucleotide transportMultidrug resistance-associated protein 1 Homo sapiens (human)
leukotriene transportMultidrug resistance-associated protein 1 Homo sapiens (human)
monoatomic anion transmembrane transportMultidrug resistance-associated protein 1 Homo sapiens (human)
sphingolipid translocationMultidrug resistance-associated protein 1 Homo sapiens (human)
export across plasma membraneMultidrug resistance-associated protein 1 Homo sapiens (human)
transport across blood-brain barrierMultidrug resistance-associated protein 1 Homo sapiens (human)
cellular response to amyloid-betaMultidrug resistance-associated protein 1 Homo sapiens (human)
carboxylic acid transmembrane transportMultidrug resistance-associated protein 1 Homo sapiens (human)
xenobiotic transport across blood-brain barrierMultidrug resistance-associated protein 1 Homo sapiens (human)
glutathione transmembrane transportMultidrug resistance-associated protein 1 Homo sapiens (human)
negative regulation of inflammatory response to antigenic stimulusGuanine nucleotide-binding protein GHomo sapiens (human)
renal water homeostasisGuanine nucleotide-binding protein GHomo sapiens (human)
G protein-coupled receptor signaling pathwayGuanine nucleotide-binding protein GHomo sapiens (human)
regulation of insulin secretionGuanine nucleotide-binding protein GHomo sapiens (human)
cellular response to glucagon stimulusGuanine nucleotide-binding protein GHomo sapiens (human)
signal transductionCasein kinase II subunit betaHomo sapiens (human)
negative regulation of cell population proliferationCasein kinase II subunit betaHomo sapiens (human)
Wnt signaling pathwayCasein kinase II subunit betaHomo sapiens (human)
peptidyl-threonine phosphorylationCasein kinase II subunit betaHomo sapiens (human)
negative regulation of proteasomal ubiquitin-dependent protein catabolic processCasein kinase II subunit betaHomo sapiens (human)
positive regulation of activin receptor signaling pathwayCasein kinase II subunit betaHomo sapiens (human)
adiponectin-activated signaling pathwayCasein kinase II subunit betaHomo sapiens (human)
negative regulation of blood vessel endothelial cell migrationCasein kinase II subunit betaHomo sapiens (human)
regulation of DNA bindingCasein kinase II subunit betaHomo sapiens (human)
positive regulation of SMAD protein signal transductionCasein kinase II subunit betaHomo sapiens (human)
endothelial tube morphogenesisCasein kinase II subunit betaHomo sapiens (human)
protein-containing complex assemblyCasein kinase II subunit betaHomo sapiens (human)
symbiont-mediated disruption of host cell PML bodyCasein kinase II subunit betaHomo sapiens (human)
negative regulation of viral life cycleCasein kinase II subunit betaHomo sapiens (human)
double-strand break repairCasein kinase II subunit alphaHomo sapiens (human)
protein phosphorylationCasein kinase II subunit alphaHomo sapiens (human)
apoptotic processCasein kinase II subunit alphaHomo sapiens (human)
DNA damage responseCasein kinase II subunit alphaHomo sapiens (human)
signal transductionCasein kinase II subunit alphaHomo sapiens (human)
positive regulation of cell population proliferationCasein kinase II subunit alphaHomo sapiens (human)
Wnt signaling pathwayCasein kinase II subunit alphaHomo sapiens (human)
negative regulation of translationCasein kinase II subunit alphaHomo sapiens (human)
peptidyl-serine phosphorylationCasein kinase II subunit alphaHomo sapiens (human)
peptidyl-threonine phosphorylationCasein kinase II subunit alphaHomo sapiens (human)
positive regulation of Wnt signaling pathwayCasein kinase II subunit alphaHomo sapiens (human)
positive regulation of cell growthCasein kinase II subunit alphaHomo sapiens (human)
negative regulation of proteasomal ubiquitin-dependent protein catabolic processCasein kinase II subunit alphaHomo sapiens (human)
negative regulation of cysteine-type endopeptidase activity involved in apoptotic processCasein kinase II subunit alphaHomo sapiens (human)
positive regulation of protein catabolic processCasein kinase II subunit alphaHomo sapiens (human)
rhythmic processCasein kinase II subunit alphaHomo sapiens (human)
protein stabilizationCasein kinase II subunit alphaHomo sapiens (human)
chaperone-mediated protein foldingCasein kinase II subunit alphaHomo sapiens (human)
symbiont-mediated disruption of host cell PML bodyCasein kinase II subunit alphaHomo sapiens (human)
positive regulation of aggrephagyCasein kinase II subunit alphaHomo sapiens (human)
regulation of chromosome separationCasein kinase II subunit alphaHomo sapiens (human)
negative regulation of double-strand break repair via homologous recombinationCasein kinase II subunit alphaHomo sapiens (human)
negative regulation of apoptotic signaling pathwayCasein kinase II subunit alphaHomo sapiens (human)
regulation of cell cycleCasein kinase II subunit alphaHomo sapiens (human)
calcium ion transportVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
adenylate cyclase-modulating G protein-coupled receptor signaling pathwayVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
sensory perception of soundVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
positive regulation of adenylate cyclase activityVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
positive regulation of calcium ion transportVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
regulation of atrial cardiac muscle cell membrane repolarizationVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
calcium ion importVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
calcium ion transmembrane transportVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
cardiac muscle cell action potential involved in contractionVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
membrane depolarization during cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
membrane depolarization during SA node cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
regulation of heart rate by cardiac conductionVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
regulation of potassium ion transmembrane transporter activityVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
regulation of potassium ion transmembrane transportVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
calcium ion import across plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
neuron migrationDNA topoisomerase 2-betaHomo sapiens (human)
DNA topological changeDNA topoisomerase 2-betaHomo sapiens (human)
axonogenesisDNA topoisomerase 2-betaHomo sapiens (human)
B cell differentiationDNA topoisomerase 2-betaHomo sapiens (human)
forebrain developmentDNA topoisomerase 2-betaHomo sapiens (human)
positive regulation of single stranded viral RNA replication via double stranded DNA intermediateDNA topoisomerase 2-betaHomo sapiens (human)
cellular response to hydrogen peroxideDNA topoisomerase 2-betaHomo sapiens (human)
cellular response to ATPDNA topoisomerase 2-betaHomo sapiens (human)
cellular senescenceDNA topoisomerase 2-betaHomo sapiens (human)
positive regulation of double-strand break repair via nonhomologous end joiningDNA topoisomerase 2-betaHomo sapiens (human)
sister chromatid segregationDNA topoisomerase 2-betaHomo sapiens (human)
resolution of meiotic recombination intermediatesDNA topoisomerase 2-betaHomo sapiens (human)
neutrophil homeostasisTyrosine-protein kinase BTKHomo sapiens (human)
positive regulation of type III hypersensitivityTyrosine-protein kinase BTKHomo sapiens (human)
positive regulation of type I hypersensitivityTyrosine-protein kinase BTKHomo sapiens (human)
adaptive immune responseTyrosine-protein kinase BTKHomo sapiens (human)
B cell affinity maturationTyrosine-protein kinase BTKHomo sapiens (human)
histamine secretion by mast cellTyrosine-protein kinase BTKHomo sapiens (human)
positive regulation of immunoglobulin productionTyrosine-protein kinase BTKHomo sapiens (human)
regulation of B cell cytokine productionTyrosine-protein kinase BTKHomo sapiens (human)
MyD88-dependent toll-like receptor signaling pathwayTyrosine-protein kinase BTKHomo sapiens (human)
regulation of B cell apoptotic processTyrosine-protein kinase BTKHomo sapiens (human)
protein phosphorylationTyrosine-protein kinase BTKHomo sapiens (human)
mesoderm developmentTyrosine-protein kinase BTKHomo sapiens (human)
peptidyl-tyrosine phosphorylationTyrosine-protein kinase BTKHomo sapiens (human)
calcium-mediated signalingTyrosine-protein kinase BTKHomo sapiens (human)
proteoglycan catabolic processTyrosine-protein kinase BTKHomo sapiens (human)
negative regulation of B cell proliferationTyrosine-protein kinase BTKHomo sapiens (human)
positive regulation of B cell proliferationTyrosine-protein kinase BTKHomo sapiens (human)
response to lipopolysaccharideTyrosine-protein kinase BTKHomo sapiens (human)
negative regulation of interleukin-10 productionTyrosine-protein kinase BTKHomo sapiens (human)
positive regulation of interleukin-6 productionTyrosine-protein kinase BTKHomo sapiens (human)
positive regulation of tumor necrosis factor productionTyrosine-protein kinase BTKHomo sapiens (human)
cellular response to reactive oxygen speciesTyrosine-protein kinase BTKHomo sapiens (human)
intracellular signal transductionTyrosine-protein kinase BTKHomo sapiens (human)
Fc-epsilon receptor signaling pathwayTyrosine-protein kinase BTKHomo sapiens (human)
B cell activationTyrosine-protein kinase BTKHomo sapiens (human)
innate immune responseTyrosine-protein kinase BTKHomo sapiens (human)
positive regulation of B cell differentiationTyrosine-protein kinase BTKHomo sapiens (human)
cell maturationTyrosine-protein kinase BTKHomo sapiens (human)
positive regulation of phagocytosisTyrosine-protein kinase BTKHomo sapiens (human)
B cell receptor signaling pathwayTyrosine-protein kinase BTKHomo sapiens (human)
positive regulation of NF-kappaB transcription factor activityTyrosine-protein kinase BTKHomo sapiens (human)
monocyte proliferationTyrosine-protein kinase BTKHomo sapiens (human)
cellular response to molecule of fungal originTyrosine-protein kinase BTKHomo sapiens (human)
apoptotic signaling pathwayTyrosine-protein kinase BTKHomo sapiens (human)
cellular response to interleukin-7Tyrosine-protein kinase BTKHomo sapiens (human)
positive regulation of interleukin-17A productionTyrosine-protein kinase BTKHomo sapiens (human)
positive regulation of NLRP3 inflammasome complex assemblyTyrosine-protein kinase BTKHomo sapiens (human)
positive regulation of synoviocyte proliferationTyrosine-protein kinase BTKHomo sapiens (human)
eosinophil homeostasisTyrosine-protein kinase BTKHomo sapiens (human)
T cell receptor signaling pathwayTyrosine-protein kinase BTKHomo sapiens (human)
regulation of heart rate by cardiac conductionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of heart rate by hormonePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of membrane potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
positive regulation of DNA-templated transcriptionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion homeostasisPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cardiac muscle contractionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of membrane repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of ventricular cardiac muscle cell membrane repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cellular response to xenobiotic stimulusPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
ventricular cardiac muscle cell action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane depolarization during action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarization during action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarization during cardiac muscle cell action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of heart rate by cardiac conductionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion export across plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarization during ventricular cardiac muscle cell action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
negative regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
positive regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
negative regulation of potassium ion export across plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion import across plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
negative regulation of protein phosphorylationTAR DNA-binding protein 43Homo sapiens (human)
mRNA processingTAR DNA-binding protein 43Homo sapiens (human)
RNA splicingTAR DNA-binding protein 43Homo sapiens (human)
negative regulation of gene expressionTAR DNA-binding protein 43Homo sapiens (human)
regulation of protein stabilityTAR DNA-binding protein 43Homo sapiens (human)
positive regulation of insulin secretionTAR DNA-binding protein 43Homo sapiens (human)
response to endoplasmic reticulum stressTAR DNA-binding protein 43Homo sapiens (human)
positive regulation of protein import into nucleusTAR DNA-binding protein 43Homo sapiens (human)
regulation of circadian rhythmTAR DNA-binding protein 43Homo sapiens (human)
regulation of apoptotic processTAR DNA-binding protein 43Homo sapiens (human)
negative regulation by host of viral transcriptionTAR DNA-binding protein 43Homo sapiens (human)
rhythmic processTAR DNA-binding protein 43Homo sapiens (human)
regulation of cell cycleTAR DNA-binding protein 43Homo sapiens (human)
3'-UTR-mediated mRNA destabilizationTAR DNA-binding protein 43Homo sapiens (human)
3'-UTR-mediated mRNA stabilizationTAR DNA-binding protein 43Homo sapiens (human)
nuclear inner membrane organizationTAR DNA-binding protein 43Homo sapiens (human)
amyloid fibril formationTAR DNA-binding protein 43Homo sapiens (human)
regulation of gene expressionTAR DNA-binding protein 43Homo sapiens (human)
signal transductionNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
mitotic DNA replication checkpoint signalingNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
regulation of apoptotic processNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
regulation of neuron apoptotic processNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
protein neddylationNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
neuron apoptotic processNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
ubiquitin-dependent protein catabolic processNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
protein ubiquitinationNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
DNA damage responseNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
skeletal system developmentVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
extraocular skeletal muscle developmentVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
calcium ion transportVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
muscle contractionVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
striated muscle contractionVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
endoplasmic reticulum organizationVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
myoblast fusionVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
neuromuscular junction developmentVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
skeletal muscle adaptationVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
positive regulation of muscle contractionVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
skeletal muscle fiber developmentVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
release of sequestered calcium ion into cytosolVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
calcium ion transmembrane transportVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
cellular response to caffeineVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
calcium ion import across plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
immune system developmentVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
positive regulation of cytosolic calcium ion concentrationVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
heart developmentVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
regulation of cardiac muscle contraction by regulation of the release of sequestered calcium ionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
embryonic forelimb morphogenesisVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
camera-type eye developmentVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
positive regulation of adenylate cyclase activityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
positive regulation of muscle contractionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calcium ion transport into cytosolVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
cardiac conductionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calcium ion transmembrane transport via high voltage-gated calcium channelVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calcium ion transmembrane transportVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
cardiac muscle cell action potential involved in contractionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
membrane depolarization during cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
membrane depolarization during AV node cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
cell communication by electrical coupling involved in cardiac conductionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
regulation of heart rate by cardiac conductionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
regulation of ventricular cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
membrane depolarization during atrial cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calcium ion import across plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
organic cation transportMultidrug and toxin extrusion protein 2Homo sapiens (human)
transmembrane transportMultidrug and toxin extrusion protein 2Homo sapiens (human)
proton transmembrane transportMultidrug and toxin extrusion protein 2Homo sapiens (human)
xenobiotic detoxification by transmembrane export across the plasma membraneMultidrug and toxin extrusion protein 2Homo sapiens (human)
protein phosphorylationCasein kinase II subunit alpha 3Homo sapiens (human)
positive regulation of cell population proliferationCasein kinase II subunit alpha 3Homo sapiens (human)
positive regulation of cell growthCasein kinase II subunit alpha 3Homo sapiens (human)
positive regulation of protein catabolic processCasein kinase II subunit alpha 3Homo sapiens (human)
peptidyl-threonine phosphorylationCasein kinase II subunit alpha 3Homo sapiens (human)
peptidyl-serine phosphorylationCasein kinase II subunit alpha 3Homo sapiens (human)
regulation of cell cycleCasein kinase II subunit alpha 3Homo sapiens (human)
proteolysisNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
endomitotic cell cycleNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
protein modification processNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
post-translational protein modificationNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
protein neddylationNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
regulation of cell cycleNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
xenobiotic transmembrane transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
organic cation transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
putrescine transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
xenobiotic transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
transmembrane transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
thiamine transmembrane transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
amino acid import across plasma membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
L-arginine import across plasma membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
L-alpha-amino acid transmembrane transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
proton transmembrane transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
L-arginine transmembrane transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
xenobiotic detoxification by transmembrane export across the plasma membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
negative regulation of receptor internalizationAtaxin-2Homo sapiens (human)
regulation of translationAtaxin-2Homo sapiens (human)
RNA metabolic processAtaxin-2Homo sapiens (human)
P-body assemblyAtaxin-2Homo sapiens (human)
stress granule assemblyAtaxin-2Homo sapiens (human)
RNA transportAtaxin-2Homo sapiens (human)
mRNA processingSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
cytidine deaminationSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
somatic diversification of immunoglobulinsSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
somatic hypermutation of immunoglobulin genesSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
B cell differentiationSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
regulation of nuclear cell cycle DNA replicationSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
defense response to bacteriumSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
positive regulation of gene expression via chromosomal CpG island demethylationSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
isotype switchingSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
cellular response to lipopolysaccharideSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
DNA cytosine deaminationSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
DNA demethylationSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
cytidine to uridine editingSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
negative regulation of single stranded viral RNA replication via double stranded DNA intermediateSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
defense response to virusSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
G protein-coupled adenosine receptor signaling pathwayP2Y purinoceptor 12Homo sapiens (human)
monoatomic ion transportP2Y purinoceptor 12Homo sapiens (human)
substrate-dependent cell migration, cell extensionP2Y purinoceptor 12Homo sapiens (human)
G protein-coupled receptor signaling pathwayP2Y purinoceptor 12Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled receptor signaling pathwayP2Y purinoceptor 12Homo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathwayP2Y purinoceptor 12Homo sapiens (human)
hemostasisP2Y purinoceptor 12Homo sapiens (human)
calcium-mediated signalingP2Y purinoceptor 12Homo sapiens (human)
cerebral cortex radial glia-guided migrationP2Y purinoceptor 12Homo sapiens (human)
cell projection organizationP2Y purinoceptor 12Homo sapiens (human)
lamellipodium assemblyP2Y purinoceptor 12Homo sapiens (human)
platelet activationP2Y purinoceptor 12Homo sapiens (human)
positive regulation of integrin activation by cell surface receptor linked signal transductionP2Y purinoceptor 12Homo sapiens (human)
positive regulation of cell adhesion mediated by integrinP2Y purinoceptor 12Homo sapiens (human)
G protein-coupled purinergic nucleotide receptor signaling pathwayP2Y purinoceptor 12Homo sapiens (human)
positive regulation of monoatomic ion transportP2Y purinoceptor 12Homo sapiens (human)
response to axon injuryP2Y purinoceptor 12Homo sapiens (human)
regulation of chemotaxisP2Y purinoceptor 12Homo sapiens (human)
positive regulation of chemotaxisP2Y purinoceptor 12Homo sapiens (human)
establishment of localization in cellP2Y purinoceptor 12Homo sapiens (human)
positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transductionP2Y purinoceptor 12Homo sapiens (human)
platelet aggregationP2Y purinoceptor 12Homo sapiens (human)
cellular response to ATPP2Y purinoceptor 12Homo sapiens (human)
visual system developmentP2Y purinoceptor 12Homo sapiens (human)
positive regulation of ruffle assemblyP2Y purinoceptor 12Homo sapiens (human)
regulation of microglial cell migrationP2Y purinoceptor 12Homo sapiens (human)
positive regulation of microglial cell migrationP2Y purinoceptor 12Homo sapiens (human)
xenobiotic metabolic processSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
monoatomic ion transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
organic anion transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
bile acid and bile salt transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
heme catabolic processSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
sodium-independent organic anion transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
transmembrane transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
lipid transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
organic anion transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
urate transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
biotin transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
sphingolipid biosynthetic processBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
riboflavin transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
urate metabolic processBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
transmembrane transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
transepithelial transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
renal urate salt excretionBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
export across plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
transport across blood-brain barrierBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
cellular detoxificationBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
xenobiotic transport across blood-brain barrierBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (193)

Processvia Protein(s)Taxonomy
amine transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
acetylcholine transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
neurotransmitter transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
monoamine transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
organic anion transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
organic cation transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
prostaglandin transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
L-amino acid transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
pyrimidine nucleoside transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
choline transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
thiamine transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
putrescine transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
efflux transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
spermidine transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
quaternary ammonium group transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
toxin transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
xenobiotic transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
L-arginine transmembrane transporter activitySolute carrier family 22 member 2Homo sapiens (human)
acetylcholine transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
neurotransmitter transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
dopamine:sodium symporter activitySolute carrier family 22 member 1 Homo sapiens (human)
norepinephrine:sodium symporter activitySolute carrier family 22 member 1 Homo sapiens (human)
protein bindingSolute carrier family 22 member 1 Homo sapiens (human)
monoamine transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
secondary active organic cation transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
organic anion transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
organic cation transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
prostaglandin transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
pyrimidine nucleoside transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
thiamine transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
putrescine transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
spermidine transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
quaternary ammonium group transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
toxin transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
identical protein bindingSolute carrier family 22 member 1 Homo sapiens (human)
xenobiotic transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
(R)-carnitine transmembrane transporter activitySolute carrier family 22 member 1 Homo sapiens (human)
iron ion bindingPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
calcium ion bindingPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
protein bindingPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
lipid bindingPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
linoleate 13S-lipoxygenase activityPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
arachidonate 8(S)-lipoxygenase activityPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
arachidonate 15-lipoxygenase activityPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
linoleate 9S-lipoxygenase activityPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
metal ion bindingVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
high voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
neurotransmitter transmembrane transporter activitySolute carrier family 22 member 3Homo sapiens (human)
protein bindingSolute carrier family 22 member 3Homo sapiens (human)
monoamine transmembrane transporter activitySolute carrier family 22 member 3Homo sapiens (human)
organic anion transmembrane transporter activitySolute carrier family 22 member 3Homo sapiens (human)
organic cation transmembrane transporter activitySolute carrier family 22 member 3Homo sapiens (human)
spermidine transmembrane transporter activitySolute carrier family 22 member 3Homo sapiens (human)
quaternary ammonium group transmembrane transporter activitySolute carrier family 22 member 3Homo sapiens (human)
toxin transmembrane transporter activitySolute carrier family 22 member 3Homo sapiens (human)
epidermal growth factor receptor activityEpidermal growth factor receptorHomo sapiens (human)
virus receptor activityEpidermal growth factor receptorHomo sapiens (human)
chromatin bindingEpidermal growth factor receptorHomo sapiens (human)
double-stranded DNA bindingEpidermal growth factor receptorHomo sapiens (human)
MAP kinase kinase kinase activityEpidermal growth factor receptorHomo sapiens (human)
protein tyrosine kinase activityEpidermal growth factor receptorHomo sapiens (human)
transmembrane receptor protein tyrosine kinase activityEpidermal growth factor receptorHomo sapiens (human)
transmembrane signaling receptor activityEpidermal growth factor receptorHomo sapiens (human)
epidermal growth factor receptor activityEpidermal growth factor receptorHomo sapiens (human)
integrin bindingEpidermal growth factor receptorHomo sapiens (human)
protein bindingEpidermal growth factor receptorHomo sapiens (human)
calmodulin bindingEpidermal growth factor receptorHomo sapiens (human)
ATP bindingEpidermal growth factor receptorHomo sapiens (human)
enzyme bindingEpidermal growth factor receptorHomo sapiens (human)
kinase bindingEpidermal growth factor receptorHomo sapiens (human)
protein kinase bindingEpidermal growth factor receptorHomo sapiens (human)
protein phosphatase bindingEpidermal growth factor receptorHomo sapiens (human)
protein tyrosine kinase activator activityEpidermal growth factor receptorHomo sapiens (human)
transmembrane receptor protein tyrosine kinase activator activityEpidermal growth factor receptorHomo sapiens (human)
ubiquitin protein ligase bindingEpidermal growth factor receptorHomo sapiens (human)
identical protein bindingEpidermal growth factor receptorHomo sapiens (human)
cadherin bindingEpidermal growth factor receptorHomo sapiens (human)
actin filament bindingEpidermal growth factor receptorHomo sapiens (human)
ATPase bindingEpidermal growth factor receptorHomo sapiens (human)
epidermal growth factor bindingEpidermal growth factor receptorHomo sapiens (human)
hormone activityGlycoprotein hormones alpha chainHomo sapiens (human)
protein bindingGlycoprotein hormones alpha chainHomo sapiens (human)
follicle-stimulating hormone activityGlycoprotein hormones alpha chainHomo sapiens (human)
cytokine activityInterferon betaHomo sapiens (human)
cytokine receptor bindingInterferon betaHomo sapiens (human)
type I interferon receptor bindingInterferon betaHomo sapiens (human)
protein bindingInterferon betaHomo sapiens (human)
chloramphenicol O-acetyltransferase activityInterferon betaHomo sapiens (human)
growth factor bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
RNA polymerase I core bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
protein tyrosine kinase activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
transmembrane receptor protein tyrosine kinase activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
transmembrane signaling receptor activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
signaling receptor bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
protein bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ATP bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
coreceptor activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
receptor tyrosine kinase bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
identical protein bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ErbB-3 class receptor bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
protein heterodimerization activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingAmyloid-beta precursor proteinHomo sapiens (human)
DNA bindingAmyloid-beta precursor proteinHomo sapiens (human)
serine-type endopeptidase inhibitor activityAmyloid-beta precursor proteinHomo sapiens (human)
signaling receptor bindingAmyloid-beta precursor proteinHomo sapiens (human)
protein bindingAmyloid-beta precursor proteinHomo sapiens (human)
heparin bindingAmyloid-beta precursor proteinHomo sapiens (human)
enzyme bindingAmyloid-beta precursor proteinHomo sapiens (human)
identical protein bindingAmyloid-beta precursor proteinHomo sapiens (human)
transition metal ion bindingAmyloid-beta precursor proteinHomo sapiens (human)
receptor ligand activityAmyloid-beta precursor proteinHomo sapiens (human)
PTB domain bindingAmyloid-beta precursor proteinHomo sapiens (human)
protein serine/threonine kinase bindingAmyloid-beta precursor proteinHomo sapiens (human)
signaling receptor activator activityAmyloid-beta precursor proteinHomo sapiens (human)
fibroblast growth factor bindingIntegrin beta-3Homo sapiens (human)
C-X3-C chemokine bindingIntegrin beta-3Homo sapiens (human)
insulin-like growth factor I bindingIntegrin beta-3Homo sapiens (human)
neuregulin bindingIntegrin beta-3Homo sapiens (human)
virus receptor activityIntegrin beta-3Homo sapiens (human)
fibronectin bindingIntegrin beta-3Homo sapiens (human)
protease bindingIntegrin beta-3Homo sapiens (human)
protein disulfide isomerase activityIntegrin beta-3Homo sapiens (human)
protein kinase C bindingIntegrin beta-3Homo sapiens (human)
platelet-derived growth factor receptor bindingIntegrin beta-3Homo sapiens (human)
integrin bindingIntegrin beta-3Homo sapiens (human)
protein bindingIntegrin beta-3Homo sapiens (human)
coreceptor activityIntegrin beta-3Homo sapiens (human)
enzyme bindingIntegrin beta-3Homo sapiens (human)
identical protein bindingIntegrin beta-3Homo sapiens (human)
vascular endothelial growth factor receptor 2 bindingIntegrin beta-3Homo sapiens (human)
metal ion bindingIntegrin beta-3Homo sapiens (human)
cell adhesion molecule bindingIntegrin beta-3Homo sapiens (human)
extracellular matrix bindingIntegrin beta-3Homo sapiens (human)
fibrinogen bindingIntegrin beta-3Homo sapiens (human)
protein tyrosine kinase activityTyrosine-protein kinase FynHomo sapiens (human)
non-membrane spanning protein tyrosine kinase activityTyrosine-protein kinase FynHomo sapiens (human)
protein bindingTyrosine-protein kinase FynHomo sapiens (human)
ATP bindingTyrosine-protein kinase FynHomo sapiens (human)
phospholipase activator activityTyrosine-protein kinase FynHomo sapiens (human)
enzyme bindingTyrosine-protein kinase FynHomo sapiens (human)
type 5 metabotropic glutamate receptor bindingTyrosine-protein kinase FynHomo sapiens (human)
identical protein bindingTyrosine-protein kinase FynHomo sapiens (human)
alpha-tubulin bindingTyrosine-protein kinase FynHomo sapiens (human)
phospholipase bindingTyrosine-protein kinase FynHomo sapiens (human)
transmembrane transporter bindingTyrosine-protein kinase FynHomo sapiens (human)
metal ion bindingTyrosine-protein kinase FynHomo sapiens (human)
ephrin receptor bindingTyrosine-protein kinase FynHomo sapiens (human)
tau protein bindingTyrosine-protein kinase FynHomo sapiens (human)
tau-protein kinase activityTyrosine-protein kinase FynHomo sapiens (human)
growth factor receptor bindingTyrosine-protein kinase FynHomo sapiens (human)
scaffold protein bindingTyrosine-protein kinase FynHomo sapiens (human)
disordered domain specific bindingTyrosine-protein kinase FynHomo sapiens (human)
signaling receptor bindingTyrosine-protein kinase FynHomo sapiens (human)
G protein-coupled acetylcholine receptor activityMuscarinic acetylcholine receptor M2Homo sapiens (human)
arrestin family protein bindingMuscarinic acetylcholine receptor M2Homo sapiens (human)
G protein-coupled serotonin receptor activityMuscarinic acetylcholine receptor M2Homo sapiens (human)
G protein-coupled serotonin receptor activityMuscarinic acetylcholine receptor M4Homo sapiens (human)
G protein-coupled acetylcholine receptor activityMuscarinic acetylcholine receptor M4Homo sapiens (human)
protein bindingATP-dependent translocase ABCB1Homo sapiens (human)
ATP bindingATP-dependent translocase ABCB1Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
efflux transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
ATP hydrolysis activityATP-dependent translocase ABCB1Homo sapiens (human)
transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
ubiquitin protein ligase bindingATP-dependent translocase ABCB1Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
carboxylic acid transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
phosphatidylcholine floppase activityATP-dependent translocase ABCB1Homo sapiens (human)
phosphatidylethanolamine flippase activityATP-dependent translocase ABCB1Homo sapiens (human)
ceramide floppase activityATP-dependent translocase ABCB1Homo sapiens (human)
floppase activityATP-dependent translocase ABCB1Homo sapiens (human)
protein bindingIntegrin alpha-IIbHomo sapiens (human)
identical protein bindingIntegrin alpha-IIbHomo sapiens (human)
metal ion bindingIntegrin alpha-IIbHomo sapiens (human)
extracellular matrix bindingIntegrin alpha-IIbHomo sapiens (human)
molecular adaptor activityIntegrin alpha-IIbHomo sapiens (human)
fibrinogen bindingIntegrin alpha-IIbHomo sapiens (human)
integrin bindingIntegrin alpha-IIbHomo sapiens (human)
protein tyrosine kinase activityProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
protein bindingProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
ATP bindingProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
protein phosphatase bindingProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
transmembrane receptor protein tyrosine kinase activityProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
monooxygenase activityCytochrome P450 2D6Homo sapiens (human)
iron ion bindingCytochrome P450 2D6Homo sapiens (human)
oxidoreductase activityCytochrome P450 2D6Homo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygenCytochrome P450 2D6Homo sapiens (human)
heme bindingCytochrome P450 2D6Homo sapiens (human)
anandamide 8,9 epoxidase activityCytochrome P450 2D6Homo sapiens (human)
anandamide 11,12 epoxidase activityCytochrome P450 2D6Homo sapiens (human)
anandamide 14,15 epoxidase activityCytochrome P450 2D6Homo sapiens (human)
phosphatidylinositol phospholipase C activityMuscarinic acetylcholine receptor M1Homo sapiens (human)
protein bindingMuscarinic acetylcholine receptor M1Homo sapiens (human)
G protein-coupled acetylcholine receptor activityMuscarinic acetylcholine receptor M1Homo sapiens (human)
G protein-coupled serotonin receptor activityMuscarinic acetylcholine receptor M1Homo sapiens (human)
magnesium ion bindingDNA topoisomerase 2-alphaHomo sapiens (human)
DNA bindingDNA topoisomerase 2-alphaHomo sapiens (human)
chromatin bindingDNA topoisomerase 2-alphaHomo sapiens (human)
RNA bindingDNA topoisomerase 2-alphaHomo sapiens (human)
DNA topoisomerase type II (double strand cut, ATP-hydrolyzing) activityDNA topoisomerase 2-alphaHomo sapiens (human)
protein kinase C bindingDNA topoisomerase 2-alphaHomo sapiens (human)
protein bindingDNA topoisomerase 2-alphaHomo sapiens (human)
ATP bindingDNA topoisomerase 2-alphaHomo sapiens (human)
ATP-dependent activity, acting on DNADNA topoisomerase 2-alphaHomo sapiens (human)
DNA binding, bendingDNA topoisomerase 2-alphaHomo sapiens (human)
protein homodimerization activityDNA topoisomerase 2-alphaHomo sapiens (human)
ubiquitin bindingDNA topoisomerase 2-alphaHomo sapiens (human)
protein heterodimerization activityDNA topoisomerase 2-alphaHomo sapiens (human)
protein serine/threonine kinase activityCasein kinase II subunit alpha'Homo sapiens (human)
protein bindingCasein kinase II subunit alpha'Homo sapiens (human)
ATP bindingCasein kinase II subunit alpha'Homo sapiens (human)
protein serine kinase activityCasein kinase II subunit alpha'Homo sapiens (human)
actin bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
neurotransmitter transmembrane transporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
neurotransmitter:sodium symporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
dopamine:sodium symporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
norepinephrine:sodium symporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
protein bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
monoamine transmembrane transporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
alpha-tubulin bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
metal ion bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
beta-tubulin bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
Gq/11-coupled serotonin receptor activity5-hydroxytryptamine receptor 2CHomo sapiens (human)
G protein-coupled serotonin receptor activity5-hydroxytryptamine receptor 2CHomo sapiens (human)
protein binding5-hydroxytryptamine receptor 2CHomo sapiens (human)
identical protein binding5-hydroxytryptamine receptor 2CHomo sapiens (human)
serotonin binding5-hydroxytryptamine receptor 2CHomo sapiens (human)
1-(4-iodo-2,5-dimethoxyphenyl)propan-2-amine binding5-hydroxytryptamine receptor 2CHomo sapiens (human)
neurotransmitter receptor activity5-hydroxytryptamine receptor 2CHomo sapiens (human)
ATP bindingMultidrug resistance-associated protein 1 Homo sapiens (human)
ABC-type vitamin B12 transporter activityMultidrug resistance-associated protein 1 Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityMultidrug resistance-associated protein 1 Homo sapiens (human)
efflux transmembrane transporter activityMultidrug resistance-associated protein 1 Homo sapiens (human)
ATP hydrolysis activityMultidrug resistance-associated protein 1 Homo sapiens (human)
ATPase-coupled lipid transmembrane transporter activityMultidrug resistance-associated protein 1 Homo sapiens (human)
glutathione transmembrane transporter activityMultidrug resistance-associated protein 1 Homo sapiens (human)
ATPase-coupled transmembrane transporter activityMultidrug resistance-associated protein 1 Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug resistance-associated protein 1 Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityMultidrug resistance-associated protein 1 Homo sapiens (human)
sphingolipid transporter activityMultidrug resistance-associated protein 1 Homo sapiens (human)
carboxylic acid transmembrane transporter activityMultidrug resistance-associated protein 1 Homo sapiens (human)
ABC-type transporter activityMultidrug resistance-associated protein 1 Homo sapiens (human)
ABC-type xenobiotic transporter activityMultidrug resistance-associated protein 1 Homo sapiens (human)
G protein activityGuanine nucleotide-binding protein GHomo sapiens (human)
adenylate cyclase activator activityGuanine nucleotide-binding protein GHomo sapiens (human)
protein serine/threonine kinase activityCasein kinase II subunit betaHomo sapiens (human)
chromatin bindingCasein kinase II subunit betaHomo sapiens (human)
protein serine/threonine kinase activityCasein kinase II subunit betaHomo sapiens (human)
signaling receptor bindingCasein kinase II subunit betaHomo sapiens (human)
protein bindingCasein kinase II subunit betaHomo sapiens (human)
protein kinase regulator activityCasein kinase II subunit betaHomo sapiens (human)
protein domain specific bindingCasein kinase II subunit betaHomo sapiens (human)
protein-macromolecule adaptor activityCasein kinase II subunit betaHomo sapiens (human)
identical protein bindingCasein kinase II subunit betaHomo sapiens (human)
metal ion bindingCasein kinase II subunit betaHomo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingCasein kinase II subunit betaHomo sapiens (human)
protein serine/threonine kinase activityCasein kinase II subunit alphaHomo sapiens (human)
protein bindingCasein kinase II subunit alphaHomo sapiens (human)
ATP bindingCasein kinase II subunit alphaHomo sapiens (human)
kinase activityCasein kinase II subunit alphaHomo sapiens (human)
identical protein bindingCasein kinase II subunit alphaHomo sapiens (human)
Hsp90 protein bindingCasein kinase II subunit alphaHomo sapiens (human)
protein serine kinase activityCasein kinase II subunit alphaHomo sapiens (human)
high voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
protein bindingVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
ankyrin bindingVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
metal ion bindingVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
alpha-actinin bindingVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
voltage-gated calcium channel activity involved in cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
voltage-gated calcium channel activity involved SA node cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
DNA bindingDNA topoisomerase 2-betaHomo sapiens (human)
chromatin bindingDNA topoisomerase 2-betaHomo sapiens (human)
DNA topoisomerase type II (double strand cut, ATP-hydrolyzing) activityDNA topoisomerase 2-betaHomo sapiens (human)
protein bindingDNA topoisomerase 2-betaHomo sapiens (human)
ATP bindingDNA topoisomerase 2-betaHomo sapiens (human)
ribonucleoprotein complex bindingDNA topoisomerase 2-betaHomo sapiens (human)
metal ion bindingDNA topoisomerase 2-betaHomo sapiens (human)
protein tyrosine kinase activityTyrosine-protein kinase BTKHomo sapiens (human)
non-membrane spanning protein tyrosine kinase activityTyrosine-protein kinase BTKHomo sapiens (human)
protein bindingTyrosine-protein kinase BTKHomo sapiens (human)
ATP bindingTyrosine-protein kinase BTKHomo sapiens (human)
phosphatidylinositol-3,4,5-trisphosphate bindingTyrosine-protein kinase BTKHomo sapiens (human)
phospholipase activator activityTyrosine-protein kinase BTKHomo sapiens (human)
identical protein bindingTyrosine-protein kinase BTKHomo sapiens (human)
phospholipase bindingTyrosine-protein kinase BTKHomo sapiens (human)
metal ion bindingTyrosine-protein kinase BTKHomo sapiens (human)
transcription cis-regulatory region bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
inward rectifier potassium channel activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
delayed rectifier potassium channel activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
protein bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
ubiquitin protein ligase bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
identical protein bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
protein homodimerization activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
C3HC4-type RING finger domain bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel activity involved in cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
scaffold protein bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingTAR DNA-binding protein 43Homo sapiens (human)
DNA bindingTAR DNA-binding protein 43Homo sapiens (human)
double-stranded DNA bindingTAR DNA-binding protein 43Homo sapiens (human)
RNA bindingTAR DNA-binding protein 43Homo sapiens (human)
mRNA 3'-UTR bindingTAR DNA-binding protein 43Homo sapiens (human)
protein bindingTAR DNA-binding protein 43Homo sapiens (human)
lipid bindingTAR DNA-binding protein 43Homo sapiens (human)
identical protein bindingTAR DNA-binding protein 43Homo sapiens (human)
pre-mRNA intronic bindingTAR DNA-binding protein 43Homo sapiens (human)
molecular condensate scaffold activityTAR DNA-binding protein 43Homo sapiens (human)
NEDD8 activating enzyme activityNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
protein bindingNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
ubiquitin protein ligase bindingNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
protein heterodimerization activityNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
ubiquitin activating enzyme activityNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
protein bindingVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
calmodulin bindingVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
high voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
small molecule bindingVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
metal ion bindingVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
molecular function activator activityVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
high voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel activity involved in cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
protein bindingVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calmodulin bindingVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
high voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
metal ion bindingVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
alpha-actinin bindingVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel activity involved in cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel activity involved in AV node cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
organic cation transmembrane transporter activityMultidrug and toxin extrusion protein 2Homo sapiens (human)
antiporter activityMultidrug and toxin extrusion protein 2Homo sapiens (human)
transmembrane transporter activityMultidrug and toxin extrusion protein 2Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug and toxin extrusion protein 2Homo sapiens (human)
polyspecific organic cation:proton antiporter activityMultidrug and toxin extrusion protein 2Homo sapiens (human)
protein serine/threonine kinase activityCasein kinase II subunit alpha 3Homo sapiens (human)
protein bindingCasein kinase II subunit alpha 3Homo sapiens (human)
ATP bindingCasein kinase II subunit alpha 3Homo sapiens (human)
protein serine kinase activityCasein kinase II subunit alpha 3Homo sapiens (human)
NEDD8 activating enzyme activityNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
protein bindingNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
ATP bindingNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
NEDD8 activating enzyme activityNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
NEDD8 transferase activityNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
identical protein bindingNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
protein heterodimerization activityNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
protein bindingMultidrug and toxin extrusion protein 1Homo sapiens (human)
organic cation transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
L-amino acid transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
thiamine transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
antiporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
putrescine transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
L-arginine transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
polyspecific organic cation:proton antiporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
RNA bindingAtaxin-2Homo sapiens (human)
epidermal growth factor receptor bindingAtaxin-2Homo sapiens (human)
protein bindingAtaxin-2Homo sapiens (human)
mRNA bindingAtaxin-2Homo sapiens (human)
cytidine deaminase activitySingle-stranded DNA cytosine deaminaseHomo sapiens (human)
protein bindingSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
zinc ion bindingSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
ubiquitin protein ligase bindingSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
identical protein bindingSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
RNA bindingSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
G protein-coupled adenosine receptor activityP2Y purinoceptor 12Homo sapiens (human)
G protein-coupled ADP receptor activityP2Y purinoceptor 12Homo sapiens (human)
guanyl-nucleotide exchange factor activityP2Y purinoceptor 12Homo sapiens (human)
G protein-coupled purinergic nucleotide receptor activityP2Y purinoceptor 12Homo sapiens (human)
serine-type endopeptidase inhibitor activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
bile acid transmembrane transporter activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
protein bindingBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ATP bindingBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
organic anion transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ABC-type xenobiotic transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
urate transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
biotin transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
efflux transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ATP hydrolysis activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
riboflavin transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ATPase-coupled transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
identical protein bindingBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
protein homodimerization activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
xenobiotic transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
sphingolipid transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (144)

Processvia Protein(s)Taxonomy
plasma membraneSolute carrier family 22 member 2Homo sapiens (human)
basal plasma membraneSolute carrier family 22 member 2Homo sapiens (human)
membraneSolute carrier family 22 member 2Homo sapiens (human)
basolateral plasma membraneSolute carrier family 22 member 2Homo sapiens (human)
apical plasma membraneSolute carrier family 22 member 2Homo sapiens (human)
extracellular exosomeSolute carrier family 22 member 2Homo sapiens (human)
presynapseSolute carrier family 22 member 2Homo sapiens (human)
plasma membraneSolute carrier family 22 member 1 Homo sapiens (human)
basal plasma membraneSolute carrier family 22 member 1 Homo sapiens (human)
membraneSolute carrier family 22 member 1 Homo sapiens (human)
basolateral plasma membraneSolute carrier family 22 member 1 Homo sapiens (human)
apical plasma membraneSolute carrier family 22 member 1 Homo sapiens (human)
lateral plasma membraneSolute carrier family 22 member 1 Homo sapiens (human)
presynapseSolute carrier family 22 member 1 Homo sapiens (human)
nucleusPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
cytosolPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
cytoskeletonPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
plasma membranePolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
adherens junctionPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
focal adhesionPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
membranePolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
extracellular exosomePolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
photoreceptor outer segmentVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
membraneVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
perikaryonVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
nuclear outer membraneSolute carrier family 22 member 3Homo sapiens (human)
plasma membraneSolute carrier family 22 member 3Homo sapiens (human)
endomembrane systemSolute carrier family 22 member 3Homo sapiens (human)
membraneSolute carrier family 22 member 3Homo sapiens (human)
basolateral plasma membraneSolute carrier family 22 member 3Homo sapiens (human)
apical plasma membraneSolute carrier family 22 member 3Homo sapiens (human)
mitochondrial membraneSolute carrier family 22 member 3Homo sapiens (human)
neuronal cell bodySolute carrier family 22 member 3Homo sapiens (human)
presynapseSolute carrier family 22 member 3Homo sapiens (human)
endosomeEpidermal growth factor receptorHomo sapiens (human)
plasma membraneEpidermal growth factor receptorHomo sapiens (human)
ruffle membraneEpidermal growth factor receptorHomo sapiens (human)
Golgi membraneEpidermal growth factor receptorHomo sapiens (human)
extracellular spaceEpidermal growth factor receptorHomo sapiens (human)
nucleusEpidermal growth factor receptorHomo sapiens (human)
cytoplasmEpidermal growth factor receptorHomo sapiens (human)
endosomeEpidermal growth factor receptorHomo sapiens (human)
endoplasmic reticulum membraneEpidermal growth factor receptorHomo sapiens (human)
plasma membraneEpidermal growth factor receptorHomo sapiens (human)
focal adhesionEpidermal growth factor receptorHomo sapiens (human)
cell surfaceEpidermal growth factor receptorHomo sapiens (human)
endosome membraneEpidermal growth factor receptorHomo sapiens (human)
membraneEpidermal growth factor receptorHomo sapiens (human)
basolateral plasma membraneEpidermal growth factor receptorHomo sapiens (human)
apical plasma membraneEpidermal growth factor receptorHomo sapiens (human)
cell junctionEpidermal growth factor receptorHomo sapiens (human)
clathrin-coated endocytic vesicle membraneEpidermal growth factor receptorHomo sapiens (human)
early endosome membraneEpidermal growth factor receptorHomo sapiens (human)
nuclear membraneEpidermal growth factor receptorHomo sapiens (human)
membrane raftEpidermal growth factor receptorHomo sapiens (human)
perinuclear region of cytoplasmEpidermal growth factor receptorHomo sapiens (human)
multivesicular body, internal vesicle lumenEpidermal growth factor receptorHomo sapiens (human)
intracellular vesicleEpidermal growth factor receptorHomo sapiens (human)
protein-containing complexEpidermal growth factor receptorHomo sapiens (human)
receptor complexEpidermal growth factor receptorHomo sapiens (human)
Shc-EGFR complexEpidermal growth factor receptorHomo sapiens (human)
basal plasma membraneEpidermal growth factor receptorHomo sapiens (human)
extracellular regionGlycoprotein hormones alpha chainHomo sapiens (human)
extracellular spaceGlycoprotein hormones alpha chainHomo sapiens (human)
Golgi lumenGlycoprotein hormones alpha chainHomo sapiens (human)
follicle-stimulating hormone complexGlycoprotein hormones alpha chainHomo sapiens (human)
pituitary gonadotropin complexGlycoprotein hormones alpha chainHomo sapiens (human)
extracellular spaceGlycoprotein hormones alpha chainHomo sapiens (human)
extracellular spaceInterferon betaHomo sapiens (human)
extracellular regionInterferon betaHomo sapiens (human)
semaphorin receptor complexReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
nucleusReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
nucleoplasmReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
early endosomeReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
cytosolReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
plasma membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
endosome membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
basolateral plasma membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
apical plasma membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
neuromuscular junctionReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ruffle membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
presynaptic membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
myelin sheathReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
perinuclear region of cytoplasmReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ERBB3:ERBB2 complexReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
receptor complexReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
plasma membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
basal plasma membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
extracellular spaceAmyloid-beta precursor proteinHomo sapiens (human)
dendriteAmyloid-beta precursor proteinHomo sapiens (human)
extracellular regionAmyloid-beta precursor proteinHomo sapiens (human)
extracellular spaceAmyloid-beta precursor proteinHomo sapiens (human)
nuclear envelope lumenAmyloid-beta precursor proteinHomo sapiens (human)
cytoplasmAmyloid-beta precursor proteinHomo sapiens (human)
mitochondrial inner membraneAmyloid-beta precursor proteinHomo sapiens (human)
endosomeAmyloid-beta precursor proteinHomo sapiens (human)
early endosomeAmyloid-beta precursor proteinHomo sapiens (human)
endoplasmic reticulumAmyloid-beta precursor proteinHomo sapiens (human)
endoplasmic reticulum lumenAmyloid-beta precursor proteinHomo sapiens (human)
smooth endoplasmic reticulumAmyloid-beta precursor proteinHomo sapiens (human)
Golgi apparatusAmyloid-beta precursor proteinHomo sapiens (human)
Golgi lumenAmyloid-beta precursor proteinHomo sapiens (human)
Golgi-associated vesicleAmyloid-beta precursor proteinHomo sapiens (human)
cytosolAmyloid-beta precursor proteinHomo sapiens (human)
plasma membraneAmyloid-beta precursor proteinHomo sapiens (human)
clathrin-coated pitAmyloid-beta precursor proteinHomo sapiens (human)
cell-cell junctionAmyloid-beta precursor proteinHomo sapiens (human)
synaptic vesicleAmyloid-beta precursor proteinHomo sapiens (human)
cell surfaceAmyloid-beta precursor proteinHomo sapiens (human)
membraneAmyloid-beta precursor proteinHomo sapiens (human)
COPII-coated ER to Golgi transport vesicleAmyloid-beta precursor proteinHomo sapiens (human)
axonAmyloid-beta precursor proteinHomo sapiens (human)
growth coneAmyloid-beta precursor proteinHomo sapiens (human)
platelet alpha granule lumenAmyloid-beta precursor proteinHomo sapiens (human)
neuromuscular junctionAmyloid-beta precursor proteinHomo sapiens (human)
endosome lumenAmyloid-beta precursor proteinHomo sapiens (human)
trans-Golgi network membraneAmyloid-beta precursor proteinHomo sapiens (human)
ciliary rootletAmyloid-beta precursor proteinHomo sapiens (human)
dendritic spineAmyloid-beta precursor proteinHomo sapiens (human)
dendritic shaftAmyloid-beta precursor proteinHomo sapiens (human)
perikaryonAmyloid-beta precursor proteinHomo sapiens (human)
membrane raftAmyloid-beta precursor proteinHomo sapiens (human)
apical part of cellAmyloid-beta precursor proteinHomo sapiens (human)
synapseAmyloid-beta precursor proteinHomo sapiens (human)
perinuclear region of cytoplasmAmyloid-beta precursor proteinHomo sapiens (human)
presynaptic active zoneAmyloid-beta precursor proteinHomo sapiens (human)
spindle midzoneAmyloid-beta precursor proteinHomo sapiens (human)
recycling endosomeAmyloid-beta precursor proteinHomo sapiens (human)
extracellular exosomeAmyloid-beta precursor proteinHomo sapiens (human)
receptor complexAmyloid-beta precursor proteinHomo sapiens (human)
early endosomeAmyloid-beta precursor proteinHomo sapiens (human)
membrane raftAmyloid-beta precursor proteinHomo sapiens (human)
cell surfaceAmyloid-beta precursor proteinHomo sapiens (human)
Golgi apparatusAmyloid-beta precursor proteinHomo sapiens (human)
plasma membraneAmyloid-beta precursor proteinHomo sapiens (human)
glutamatergic synapseIntegrin beta-3Homo sapiens (human)
nucleusIntegrin beta-3Homo sapiens (human)
nucleoplasmIntegrin beta-3Homo sapiens (human)
plasma membraneIntegrin beta-3Homo sapiens (human)
cell-cell junctionIntegrin beta-3Homo sapiens (human)
focal adhesionIntegrin beta-3Homo sapiens (human)
external side of plasma membraneIntegrin beta-3Homo sapiens (human)
cell surfaceIntegrin beta-3Homo sapiens (human)
apical plasma membraneIntegrin beta-3Homo sapiens (human)
platelet alpha granule membraneIntegrin beta-3Homo sapiens (human)
lamellipodium membraneIntegrin beta-3Homo sapiens (human)
filopodium membraneIntegrin beta-3Homo sapiens (human)
microvillus membraneIntegrin beta-3Homo sapiens (human)
ruffle membraneIntegrin beta-3Homo sapiens (human)
integrin alphav-beta3 complexIntegrin beta-3Homo sapiens (human)
melanosomeIntegrin beta-3Homo sapiens (human)
synapseIntegrin beta-3Homo sapiens (human)
postsynaptic membraneIntegrin beta-3Homo sapiens (human)
extracellular exosomeIntegrin beta-3Homo sapiens (human)
integrin alphaIIb-beta3 complexIntegrin beta-3Homo sapiens (human)
glycinergic synapseIntegrin beta-3Homo sapiens (human)
integrin complexIntegrin beta-3Homo sapiens (human)
protein-containing complexIntegrin beta-3Homo sapiens (human)
alphav-beta3 integrin-PKCalpha complexIntegrin beta-3Homo sapiens (human)
alphav-beta3 integrin-IGF-1-IGF1R complexIntegrin beta-3Homo sapiens (human)
alphav-beta3 integrin-HMGB1 complexIntegrin beta-3Homo sapiens (human)
receptor complexIntegrin beta-3Homo sapiens (human)
alphav-beta3 integrin-vitronectin complexIntegrin beta-3Homo sapiens (human)
alpha9-beta1 integrin-ADAM8 complexIntegrin beta-3Homo sapiens (human)
focal adhesionIntegrin beta-3Homo sapiens (human)
cell surfaceIntegrin beta-3Homo sapiens (human)
synapseIntegrin beta-3Homo sapiens (human)
membrane raftTyrosine-protein kinase FynHomo sapiens (human)
dendriteTyrosine-protein kinase FynHomo sapiens (human)
nucleusTyrosine-protein kinase FynHomo sapiens (human)
mitochondrionTyrosine-protein kinase FynHomo sapiens (human)
endosomeTyrosine-protein kinase FynHomo sapiens (human)
cytosolTyrosine-protein kinase FynHomo sapiens (human)
actin filamentTyrosine-protein kinase FynHomo sapiens (human)
plasma membraneTyrosine-protein kinase FynHomo sapiens (human)
postsynaptic densityTyrosine-protein kinase FynHomo sapiens (human)
dendriteTyrosine-protein kinase FynHomo sapiens (human)
perikaryonTyrosine-protein kinase FynHomo sapiens (human)
cell bodyTyrosine-protein kinase FynHomo sapiens (human)
membrane raftTyrosine-protein kinase FynHomo sapiens (human)
perinuclear region of cytoplasmTyrosine-protein kinase FynHomo sapiens (human)
perinuclear endoplasmic reticulumTyrosine-protein kinase FynHomo sapiens (human)
glial cell projectionTyrosine-protein kinase FynHomo sapiens (human)
Schaffer collateral - CA1 synapseTyrosine-protein kinase FynHomo sapiens (human)
plasma membraneTyrosine-protein kinase FynHomo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M2Homo sapiens (human)
membraneMuscarinic acetylcholine receptor M2Homo sapiens (human)
clathrin-coated endocytic vesicle membraneMuscarinic acetylcholine receptor M2Homo sapiens (human)
asymmetric synapseMuscarinic acetylcholine receptor M2Homo sapiens (human)
symmetric synapseMuscarinic acetylcholine receptor M2Homo sapiens (human)
presynaptic membraneMuscarinic acetylcholine receptor M2Homo sapiens (human)
neuronal cell bodyMuscarinic acetylcholine receptor M2Homo sapiens (human)
axon terminusMuscarinic acetylcholine receptor M2Homo sapiens (human)
postsynaptic membraneMuscarinic acetylcholine receptor M2Homo sapiens (human)
glutamatergic synapseMuscarinic acetylcholine receptor M2Homo sapiens (human)
cholinergic synapseMuscarinic acetylcholine receptor M2Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M2Homo sapiens (human)
synapseMuscarinic acetylcholine receptor M2Homo sapiens (human)
dendriteMuscarinic acetylcholine receptor M2Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M4Homo sapiens (human)
postsynaptic membraneMuscarinic acetylcholine receptor M4Homo sapiens (human)
dendriteMuscarinic acetylcholine receptor M4Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M4Homo sapiens (human)
synapseMuscarinic acetylcholine receptor M4Homo sapiens (human)
cytoplasmATP-dependent translocase ABCB1Homo sapiens (human)
plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
cell surfaceATP-dependent translocase ABCB1Homo sapiens (human)
membraneATP-dependent translocase ABCB1Homo sapiens (human)
apical plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
extracellular exosomeATP-dependent translocase ABCB1Homo sapiens (human)
external side of apical plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
plasma membraneIntegrin alpha-IIbHomo sapiens (human)
focal adhesionIntegrin alpha-IIbHomo sapiens (human)
cell surfaceIntegrin alpha-IIbHomo sapiens (human)
platelet alpha granule membraneIntegrin alpha-IIbHomo sapiens (human)
extracellular exosomeIntegrin alpha-IIbHomo sapiens (human)
integrin alphaIIb-beta3 complexIntegrin alpha-IIbHomo sapiens (human)
blood microparticleIntegrin alpha-IIbHomo sapiens (human)
integrin complexIntegrin alpha-IIbHomo sapiens (human)
external side of plasma membraneIntegrin alpha-IIbHomo sapiens (human)
membraneProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
receptor complexProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
plasma membraneProto-oncogene tyrosine-protein kinase ROSHomo sapiens (human)
mitochondrionCytochrome P450 2D6Homo sapiens (human)
endoplasmic reticulumCytochrome P450 2D6Homo sapiens (human)
endoplasmic reticulum membraneCytochrome P450 2D6Homo sapiens (human)
cytoplasmCytochrome P450 2D6Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 2D6Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M1Homo sapiens (human)
membraneMuscarinic acetylcholine receptor M1Homo sapiens (human)
presynaptic membraneMuscarinic acetylcholine receptor M1Homo sapiens (human)
axon terminusMuscarinic acetylcholine receptor M1Homo sapiens (human)
Schaffer collateral - CA1 synapseMuscarinic acetylcholine receptor M1Homo sapiens (human)
postsynaptic density membraneMuscarinic acetylcholine receptor M1Homo sapiens (human)
glutamatergic synapseMuscarinic acetylcholine receptor M1Homo sapiens (human)
cholinergic synapseMuscarinic acetylcholine receptor M1Homo sapiens (human)
synapseMuscarinic acetylcholine receptor M1Homo sapiens (human)
dendriteMuscarinic acetylcholine receptor M1Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M1Homo sapiens (human)
nucleolusDNA topoisomerase 2-alphaHomo sapiens (human)
nuclear chromosomeDNA topoisomerase 2-alphaHomo sapiens (human)
centrioleDNA topoisomerase 2-alphaHomo sapiens (human)
chromosome, centromeric regionDNA topoisomerase 2-alphaHomo sapiens (human)
condensed chromosomeDNA topoisomerase 2-alphaHomo sapiens (human)
male germ cell nucleusDNA topoisomerase 2-alphaHomo sapiens (human)
nucleusDNA topoisomerase 2-alphaHomo sapiens (human)
nucleoplasmDNA topoisomerase 2-alphaHomo sapiens (human)
nucleolusDNA topoisomerase 2-alphaHomo sapiens (human)
cytoplasmDNA topoisomerase 2-alphaHomo sapiens (human)
DNA topoisomerase type II (double strand cut, ATP-hydrolyzing) complexDNA topoisomerase 2-alphaHomo sapiens (human)
protein-containing complexDNA topoisomerase 2-alphaHomo sapiens (human)
ribonucleoprotein complexDNA topoisomerase 2-alphaHomo sapiens (human)
nucleusDNA topoisomerase 2-alphaHomo sapiens (human)
plasma membraneGamma-aminobutyric acid receptor subunit gamma-2Rattus norvegicus (Norway rat)
PcG protein complexCasein kinase II subunit alpha'Homo sapiens (human)
acrosomal vesicleCasein kinase II subunit alpha'Homo sapiens (human)
nucleusCasein kinase II subunit alpha'Homo sapiens (human)
nucleoplasmCasein kinase II subunit alpha'Homo sapiens (human)
cytosolCasein kinase II subunit alpha'Homo sapiens (human)
protein kinase CK2 complexCasein kinase II subunit alpha'Homo sapiens (human)
chromatinCasein kinase II subunit alpha'Homo sapiens (human)
cytosolCasein kinase II subunit alpha'Homo sapiens (human)
nucleusCasein kinase II subunit alpha'Homo sapiens (human)
plasma membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
cell surfaceSodium-dependent noradrenaline transporter Homo sapiens (human)
membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
neuronal cell body membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
presynaptic membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
plasma membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
axonSodium-dependent noradrenaline transporter Homo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 2CHomo sapiens (human)
synapse5-hydroxytryptamine receptor 2CHomo sapiens (human)
G protein-coupled serotonin receptor complex5-hydroxytryptamine receptor 2CHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 2CHomo sapiens (human)
dendrite5-hydroxytryptamine receptor 2CHomo sapiens (human)
plasma membraneMultidrug resistance-associated protein 1 Homo sapiens (human)
basal plasma membraneMultidrug resistance-associated protein 1 Homo sapiens (human)
membraneMultidrug resistance-associated protein 1 Homo sapiens (human)
basolateral plasma membraneMultidrug resistance-associated protein 1 Homo sapiens (human)
apical plasma membraneMultidrug resistance-associated protein 1 Homo sapiens (human)
lateral plasma membraneMultidrug resistance-associated protein 1 Homo sapiens (human)
extracellular exosomeMultidrug resistance-associated protein 1 Homo sapiens (human)
basolateral plasma membraneMultidrug resistance-associated protein 1 Homo sapiens (human)
plasma membraneGamma-aminobutyric acid receptor subunit alpha-1Rattus norvegicus (Norway rat)
plasma membraneGuanine nucleotide-binding protein GHomo sapiens (human)
plasma membraneGamma-aminobutyric acid receptor subunit beta-2Rattus norvegicus (Norway rat)
plasma membraneCasein kinase II subunit betaHomo sapiens (human)
PcG protein complexCasein kinase II subunit betaHomo sapiens (human)
PML bodyCasein kinase II subunit betaHomo sapiens (human)
extracellular regionCasein kinase II subunit betaHomo sapiens (human)
nucleusCasein kinase II subunit betaHomo sapiens (human)
nucleoplasmCasein kinase II subunit betaHomo sapiens (human)
cytoplasmCasein kinase II subunit betaHomo sapiens (human)
cytosolCasein kinase II subunit betaHomo sapiens (human)
protein kinase CK2 complexCasein kinase II subunit betaHomo sapiens (human)
secretory granule lumenCasein kinase II subunit betaHomo sapiens (human)
extracellular exosomeCasein kinase II subunit betaHomo sapiens (human)
ficolin-1-rich granule lumenCasein kinase II subunit betaHomo sapiens (human)
chromatinCasein kinase II subunit betaHomo sapiens (human)
cytoplasmCasein kinase II subunit betaHomo sapiens (human)
PcG protein complexCasein kinase II subunit alphaHomo sapiens (human)
PML bodyCasein kinase II subunit alphaHomo sapiens (human)
nucleusCasein kinase II subunit alphaHomo sapiens (human)
nucleoplasmCasein kinase II subunit alphaHomo sapiens (human)
cytosolCasein kinase II subunit alphaHomo sapiens (human)
plasma membraneCasein kinase II subunit alphaHomo sapiens (human)
protein kinase CK2 complexCasein kinase II subunit alphaHomo sapiens (human)
Sin3-type complexCasein kinase II subunit alphaHomo sapiens (human)
cytosolCasein kinase II subunit alphaHomo sapiens (human)
nucleusCasein kinase II subunit alphaHomo sapiens (human)
plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
Z discVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
L-type voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
nucleolusDNA topoisomerase 2-betaHomo sapiens (human)
heterochromatinDNA topoisomerase 2-betaHomo sapiens (human)
nucleusDNA topoisomerase 2-betaHomo sapiens (human)
nucleoplasmDNA topoisomerase 2-betaHomo sapiens (human)
nucleolusDNA topoisomerase 2-betaHomo sapiens (human)
cytosolDNA topoisomerase 2-betaHomo sapiens (human)
ribonucleoprotein complexDNA topoisomerase 2-betaHomo sapiens (human)
nucleusDNA topoisomerase 2-betaHomo sapiens (human)
nucleusTyrosine-protein kinase BTKHomo sapiens (human)
cytoplasmTyrosine-protein kinase BTKHomo sapiens (human)
cytosolTyrosine-protein kinase BTKHomo sapiens (human)
plasma membraneTyrosine-protein kinase BTKHomo sapiens (human)
cytoplasmic vesicleTyrosine-protein kinase BTKHomo sapiens (human)
membrane raftTyrosine-protein kinase BTKHomo sapiens (human)
perinuclear region of cytoplasmTyrosine-protein kinase BTKHomo sapiens (human)
plasma membraneTyrosine-protein kinase BTKHomo sapiens (human)
plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cell surfacePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
perinuclear region of cytoplasmPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel complexPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
inward rectifier potassium channel complexPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
intracellular non-membrane-bounded organelleTAR DNA-binding protein 43Homo sapiens (human)
nucleusTAR DNA-binding protein 43Homo sapiens (human)
nucleoplasmTAR DNA-binding protein 43Homo sapiens (human)
perichromatin fibrilsTAR DNA-binding protein 43Homo sapiens (human)
mitochondrionTAR DNA-binding protein 43Homo sapiens (human)
cytoplasmic stress granuleTAR DNA-binding protein 43Homo sapiens (human)
nuclear speckTAR DNA-binding protein 43Homo sapiens (human)
interchromatin granuleTAR DNA-binding protein 43Homo sapiens (human)
nucleoplasmTAR DNA-binding protein 43Homo sapiens (human)
chromatinTAR DNA-binding protein 43Homo sapiens (human)
cytosolNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
plasma membraneNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
protein-containing complexNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
cytoplasmNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
nucleusNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
cytoplasmVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
sarcoplasmic reticulumVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
T-tubuleVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
I bandVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
L-type voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
cytoplasmVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
postsynaptic densityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
membraneVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
Z discVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
dendriteVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
perikaryonVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
postsynaptic density membraneVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
L-type voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
plasma membraneMultidrug and toxin extrusion protein 2Homo sapiens (human)
apical plasma membraneMultidrug and toxin extrusion protein 2Homo sapiens (human)
membraneMultidrug and toxin extrusion protein 2Homo sapiens (human)
nucleoplasmCasein kinase II subunit alpha 3Homo sapiens (human)
nucleusCasein kinase II subunit alpha 3Homo sapiens (human)
cytosolCasein kinase II subunit alpha 3Homo sapiens (human)
protein kinase CK2 complexCasein kinase II subunit alpha 3Homo sapiens (human)
nucleusNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
cytosolNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
protein-containing complexNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
cytoplasmNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
nucleusNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
plasma membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
basolateral plasma membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
apical plasma membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
cytoplasmAtaxin-2Homo sapiens (human)
Golgi apparatusAtaxin-2Homo sapiens (human)
trans-Golgi networkAtaxin-2Homo sapiens (human)
cytosolAtaxin-2Homo sapiens (human)
cytoplasmic stress granuleAtaxin-2Homo sapiens (human)
membraneAtaxin-2Homo sapiens (human)
perinuclear region of cytoplasmAtaxin-2Homo sapiens (human)
ribonucleoprotein complexAtaxin-2Homo sapiens (human)
cytoplasmic stress granuleAtaxin-2Homo sapiens (human)
nucleusSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
cytoplasmSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
cytosolSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
protein-containing complexSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
nucleusSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
cytoplasmSingle-stranded DNA cytosine deaminaseHomo sapiens (human)
P-bodySingle-stranded DNA cytosine deaminaseHomo sapiens (human)
plasma membraneP2Y purinoceptor 12Homo sapiens (human)
cell surfaceP2Y purinoceptor 12Homo sapiens (human)
membraneP2Y purinoceptor 12Homo sapiens (human)
cell projection membraneP2Y purinoceptor 12Homo sapiens (human)
cell body membraneP2Y purinoceptor 12Homo sapiens (human)
plasma membraneSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
basal plasma membraneSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
basolateral plasma membraneSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
nucleoplasmBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
apical plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
brush border membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
mitochondrial membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
membrane raftBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
external side of apical plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (933)

Assay IDTitleYearJournalArticle
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID504836Inducers of the Endoplasmic Reticulum Stress Response (ERSR) in human glioma: Validation2002The Journal of biological chemistry, Apr-19, Volume: 277, Issue:16
Sustained ER Ca2+ depletion suppresses protein synthesis and induces activation-enhanced cell death in mast cells.
AID1347057CD47-SIRPalpha protein protein interaction - LANCE assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347058CD47-SIRPalpha protein protein interaction - HTRF assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID588349qHTS for Inhibitors of ATXN expression: Validation of Cytotoxic Assay
AID1347410qHTS for inhibitors of adenylyl cyclases using a fission yeast platform: a pilot screen against the NCATS LOPAC library2019Cellular signalling, 08, Volume: 60A fission yeast platform for heterologous expression of mammalian adenylyl cyclases and high throughput screening.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347045Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot counterscreen GloSensor control cell line2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347059CD47-SIRPalpha protein protein interaction - Alpha assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347151Optimization of GU AMC qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay2020Proceedings 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.
AID1347050Natriuretic polypeptide receptor (hNpr2) antagonism - Pilot subtype selectivity assay2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID588378qHTS for Inhibitors of ATXN expression: Validation
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347405qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS LOPAC collection2020ACS 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.
AID1347049Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot screen2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID504810Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347128qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347112qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347113qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347121qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347115qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347125qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347109qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347137qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D viability screen for Daoy cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347114qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347122qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347126qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347111qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347118qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347123qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347138qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D caspase screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347127qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID686947qHTS for small molecule inhibitors of Yes1 kinase: Primary Screen2013Bioorganic & medicinal chemistry letters, Aug-01, Volume: 23, Issue:15
Identification of potent Yes1 kinase inhibitors using a library screening approach.
AID1347116qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347139qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D viability screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347141qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D viability screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347140qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D viability screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347117qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347136qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D viability screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347129qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347110qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for A673 cells)2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347135qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Orthogonal 3D viability screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings 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.
AID1347119qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347124qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID45645Survivors of CDF1 mice on day 4 after 1st injection of compound at 1.5 mg/kg in six mice; 6/61989Journal of medicinal chemistry, Aug, Volume: 32, Issue:8
Synthesis of unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones as potential antileukemic agents.
AID354543Cytotoxicity against rat C6 cells assessed as cell release at 50 ug/mL to 2.5 mg/mL after 5 hrs by MTT assay in absence of db-cAMP1996Journal of natural products, Dec, Volume: 59, Issue:12
Cell-based screen for identification of inhibitors of tubulin polymerization.
AID99359Tested for inhibitory activity against murine cell line L12110, a strain sensitive to doxorubicin using MTT assay.2000Journal of medicinal chemistry, Aug-10, Volume: 43, Issue:16
Analogues of amonafide and azonafide with novel ring systems.
AID8289In vitro cytotoxic activity against human lung A549 cell line ( standard deviation in parenthesis)2002Journal of medicinal chemistry, Jun-06, Volume: 45, Issue:12
Design, synthesis, and antiproliferative activity of some new pyrazole-fused amino derivatives of the pyranoxanthenone, pyranothioxanthenone, and pyranoacridone ring systems: a new class of cytotoxic agents.
AID1349098Inhibition of NAE in human Caco2 cells assessed as increase in p27 protein levels at 0.1 to 10 uM after 16 hrs by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID1550885Induction of immunogenic cell death in mouse H22 cells assessed as increase in extracellular ATP level at 2 uM measured after 5 hrs by chemiluminescence-based assay2019European journal of medicinal chemistry, Jun-01, Volume: 171Naphthyl quinoxaline thymidine conjugate is a potent anticancer agent post UVA activation and elicits marked inhibition of tumor growth through vaccination.
AID248060Cytotoxicity against human HCT116 cancer cell line was determined after 144 hr2004Journal of medicinal chemistry, Oct-07, Volume: 47, Issue:21
Rational design, synthesis, and biological evaluation of bis(pyrimido[5,6,1-de]acridines) and bis(pyrazolo[3,4,5-kl]acridine-5-carboxamides) as new anticancer agents.
AID624623Apparent permeability (Papp) from basolateral to apical side determined in MDR1-MDCKII cells2001The Journal of pharmacology and experimental therapeutics, Nov, Volume: 299, Issue:2
Rational use of in vitro P-glycoprotein assays in drug discovery.
AID154065Inhibition of P388 leukemia cells in mice, measured as percent treated to the control values with the number of 30 day survivors1987Journal of medicinal chemistry, Jan, Volume: 30, Issue:1
Anthrapyrazole anticancer agents. Synthesis and structure-activity relationships against murine leukemias.
AID466798Growth inhibition of human A549 cells by MTT assay2010Bioorganic & medicinal chemistry letters, Mar-01, Volume: 20, Issue:5
Triterpene compounds isolated from Acer mandshuricum and their anti-inflammatory activity.
AID1883025Antitumor activity against mouse 4T1 cells implanted in Balb/c mouse assessed as nuclei disappearance at 50 mg/kg administered intratumorally every four days for 14 days in the presence of liquid cyanoacrylate2022European journal of medicinal chemistry, Jul-05, Volume: 237Design, synthesis, and evaluation of a novel series of mono-indolylbenzoquinones derivatives for the potential treatment of breast cancer.
AID51931Tested for the cytotoxicity against the repair deficient xrs-6 chinese hamster ovary cell line1994Journal of medicinal chemistry, Oct-28, Volume: 37, Issue:22
Inhibition of topoisomerase II catalytic activity by pyridoacridine alkaloids from a Cystodytes sp. ascidian: a mechanism for the apparent intercalator-induced inhibition of topoisomerase II.
AID683854Antiproliferative activity against human LoVo cells after 72 hrs by SRB assay2012Bioorganic & medicinal chemistry letters, Oct-01, Volume: 22, Issue:19
New derivatives of 11-methyl-6-[2-(dimethylamino)ethyl]-6H-indolo[2,3-b]quinoline as cytotoxic DNA topoisomerase II inhibitors.
AID354542Inhibition of tubulin polymerization in rat C6 cells at 50 ug/mL to 2.5 mg/mL after 4 hrs1996Journal of natural products, Dec, Volume: 59, Issue:12
Cell-based screen for identification of inhibitors of tubulin polymerization.
AID524790Antiplasmodial activity against Plasmodium falciparum 3D7 after 72 hrs by SYBR green assay2009Nature chemical biology, Oct, Volume: 5, Issue:10
Genetic mapping of targets mediating differential chemical phenotypes in Plasmodium falciparum.
AID45657Survivors of CDF1 mice on day 4 after 1st injection of compound at 6 mg/kg in six mice; 6/61989Journal of medicinal chemistry, Aug, Volume: 32, Issue:8
Synthesis of unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones as potential antileukemic agents.
AID1525941Resistance factor, ratio of IC50 for human LCC6MDR cells overexpressing P-gp to IC50 for human LCC6 cells2019Journal of medicinal chemistry, 09-26, Volume: 62, Issue:18
Triazole Bridged Flavonoid Dimers as Potent, Nontoxic, and Highly Selective Breast Cancer Resistance Protein (BCRP/ABCG2) Inhibitors.
AID270856Resistant factor, IC50 for MES-SA/Dx5/ IC50 for MES-SA cells by MTT assay after 72 hrs2006Bioorganic & medicinal chemistry letters, Sep-15, Volume: 16, Issue:18
Synthesis and antiproliferative activity of substituted benzopyranoisoindoles: a new class of cytotoxic compounds.
AID681572TP_TRANSPORTER: drug resistance in BCRP-expressing MEF3.8 cells2003Cancer research, Mar-15, Volume: 63, Issue:6
Mouse breast cancer resistance protein (Bcrp1/Abcg2) mediates etoposide resistance and transport, but etoposide oral availability is limited primarily by P-glycoprotein.
AID84475Inhibitory concentration of compound against proliferation of colon carcinoma HT-29 cell line2002Bioorganic & medicinal chemistry letters, Jun-03, Volume: 12, Issue:11
Design and synthesis of some new pyranoxanthenone aminoderivatives with cytotoxic activity.
AID562245Antimycobacterial activity against Mycobacterium smegmatis grown in nitrogen -limited broth medium assessed as growth inhibition in mid-logarithmic phase by GFP-based fluorescence assay2009Antimicrobial agents and chemotherapy, Dec, Volume: 53, Issue:12
Modifying culture conditions in chemical library screening identifies alternative inhibitors of mycobacteria.
AID272514Antiproliferative activity against adriamycin resistant P388 cells in presence of 5 uM 1,13-bis[4'-((5,7-dihydroxy)-4H-chromen-4-on-2-yl)phenyl]-1,4,7,10,13-pentaoxatridecane by ELISA2006Journal of medicinal chemistry, Nov-16, Volume: 49, Issue:23
Flavonoid dimers as bivalent modulators for P-glycoprotein-based multidrug resistance: synthetic apigenin homodimers linked with defined-length poly(ethylene glycol) spacers increase drug retention and enhance chemosensitivity in resistant cancer cells.
AID55499Concentration required to give 50% fluorescence quenching of bound ethidium for [ethidium]: [(poly dG-dC)]2 DNA in ratio of 0.1:1 at pH 51997Journal of medicinal chemistry, Nov-07, Volume: 40, Issue:23
1-[(omega-aminoalkyl)amino]-4-[N-(omega-aminoalkyl)carbamoyl]-9-oxo-9, 10-dihydroacridines as intercalating cytotoxic agents: synthesis, DNA binding, and biological evaluation.
AID524793Antiplasmodial activity against Plasmodium falciparum Dd2 after 72 hrs by SYBR green assay2009Nature chemical biology, Oct, Volume: 5, Issue:10
Genetic mapping of targets mediating differential chemical phenotypes in Plasmodium falciparum.
AID134572In vitro cytotoxicity against L1210 leukemia cell line1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Synthesis and antitumor properties of an anthraquinone bisubstituted by the copper chelating peptide Gly-Gly-L-His.
AID1130156Antineoplastic activity against mouse Colon 26 cells allografted in CDF1 mouse assessed as survival at 1.08 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID202628Mean percentage reduction in tumor weight at 0.75 mg/kg (cumulative dose 525 mg/Kg) introduced (in vivo) ip; Significant1988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID1130157Antineoplastic activity against mouse Colon 26 cells allografted in CDF1 mouse at 1.08 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1349095Inhibition of NAE in human Caco2 cells harboring p53-luc plasmid assessed as increase in p53 transcriptional activity after 16 hrs by luciferase reporter gene assay2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID132862In vitro for its inhibitory activity against murine L1210 leukemia1988Journal of medicinal chemistry, Aug, Volume: 31, Issue:8
Benzothiopyranoindazoles, a new class of chromophore modified anthracenedione anticancer agents. Synthesis and activity against murine leukemias.
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID219914Cytotoxicity against CHO cell line xrs61995Journal of medicinal chemistry, Oct-27, Volume: 38, Issue:22
Topoisomerase II-mediated DNA cleavage by adocia- and xestoquinones from the Philippine sponge Xestospongia sp.
AID624628Drug-stimulated Pgp ATPase activity ratio determined in MDR1-Sf9 cell membranes with test compound at a concentration of 20uM2001The Journal of pharmacology and experimental therapeutics, Nov, Volume: 299, Issue:2
Rational use of in vitro P-glycoprotein assays in drug discovery.
AID102333In vitro cytotoxicity on human colon adenocarcinoma resistant to doxorubicin (LoVo/Dx ) tumor cell line.1998Journal of medicinal chemistry, Dec-31, Volume: 41, Issue:27
Synthesis and antitumor evaluation of 2,5-disubstituted-indazolo[4, 3-gh]isoquinolin-6(2H)-ones (9-aza-anthrapyrazoles).
AID429650Cytotoxicity against human HL60 cells by MTT assay2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
C29 sterols with a cyclopropane ring at C-25 and 26 from the Vietnamese marine sponge Ianthella sp. and their anticancer properties.
AID39742Optimal dose per injection in mg/kg required to inhibit growth of murine B-16 melanoma in vivo1987Journal of medicinal chemistry, Jan, Volume: 30, Issue:1
Anthrapyrazole anticancer agents. Synthesis and structure-activity relationships against murine leukemias.
AID1221982Fraction absorbed in human2011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1883021Toxicity in Balb/c mouse implanted with mouse 4T1 cells assessed as liver lesions at 50 mg/kg administered intratumorally every four days for 14 days in the presence of liquid cyanoacrylate by H&E staining based histopathological analysis2022European journal of medicinal chemistry, Jul-05, Volume: 237Design, synthesis, and evaluation of a novel series of mono-indolylbenzoquinones derivatives for the potential treatment of breast cancer.
AID103420Tested for inhibitory activity against human tumor cell line MCF7, a strain resistant to mitoxantrone of breast carcinoma using sulforhodamine B assay.2000Journal of medicinal chemistry, Aug-10, Volume: 43, Issue:16
Analogues of amonafide and azonafide with novel ring systems.
AID1506786Induction of apoptosis in human HCC78 cells assessed as necrotic cells level at 10 nM incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry (Rvb = 0.06%)2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID272515Antiproliferative activity against adriamycin resistant P388 cells in presence of 5 uM verapamil by ELISA2006Journal of medicinal chemistry, Nov-16, Volume: 49, Issue:23
Flavonoid dimers as bivalent modulators for P-glycoprotein-based multidrug resistance: synthetic apigenin homodimers linked with defined-length poly(ethylene glycol) spacers increase drug retention and enhance chemosensitivity in resistant cancer cells.
AID223628Tested for inhibitory activity against human tumor cell line OVCAR-3, a resistant ovarian carcinoma using sulforhodamine B assay.2000Journal of medicinal chemistry, Aug-10, Volume: 43, Issue:16
Analogues of amonafide and azonafide with novel ring systems.
AID595061Cytotoxicity against human HCT116 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Design, synthesis and antiproliferative activity of novel aminosubstituted benzothiopyranoisoindoles.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1349093Inhibition of NAE in human Caco2 cells assessed as increase in p53 protein levels at 1 to 10 uM after 16 hrs by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID647963Cytotoxicity against human H1299 cells assessed as cell growth at 10 uM after 48 hrs by MTT assay2012European journal of medicinal chemistry, Apr, Volume: 50Design, synthesis and evaluation of telomerase inhibitory, hTERT repressing, and anti-proliferation activities of symmetrical 1,8-disubstituted amidoanthraquinones.
AID83792Percent inhibition at G2/M phase of cell cycle at a dose of 25 ng/mL after 72 hours of induction in HT-29 cell line1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID588217FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1349084Inhibition of NAE-mediated Ubcl2-NEDD8 conjugation in human Caco2 cells at 10 uM after 16 hrs by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID107941Compound was evaluated in vivo for the antitumor activity at a dose of 1.25 mg/kg & 3.75 mg/kg against mammary adenocarcinoma 16C to assess tumor growth delay (T-C).1984Journal of medicinal chemistry, Mar, Volume: 27, Issue:3
5-[(Aminoalkyl)amino]-substituted anthra[1,9-cd]pyrazol-6(2H)-ones as novel anticancer agents. Synthesis and biological evaluation.
AID1506772Cytotoxicity in human HCC78 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID81486Relative cytotoxicity against Human promyelocytic Leukemia(HL-60) cells; Value is in range, activity expressed as IC501999Journal of medicinal chemistry, Jun-17, Volume: 42, Issue:12
Design and synthesis of modified quinolones as antitumoral acridones.
AID1883016Antitumor activity against mouse 4T1 cells implanted in Balb/c mouse assessed as tumor growth inhibition by measuring T/C ratio at 50 mg/kg administered intratumorally every four days for 14 days in the presence of liquid cyanoacrylate2022European journal of medicinal chemistry, Jul-05, Volume: 237Design, synthesis, and evaluation of a novel series of mono-indolylbenzoquinones derivatives for the potential treatment of breast cancer.
AID363203Antitumor activity against human NCI60 cells after 48 hrs by SRB assay2008Bioorganic & medicinal chemistry, Sep-01, Volume: 16, Issue:17
Design, synthesis, and antitumor activity of new bis-aminomethylnaphthalenes.
AID591077Resistance index, ratio IC50 for human HL60/MX2 cells to IC50 for human HL60 cells2011Bioorganic & medicinal chemistry letters, Apr-15, Volume: 21, Issue:8
Synthesis, cytotoxicity and topoisomerase inhibition properties of multifarious aminoalkylated indeno[1,2-c]isoquinolin-5,11-diones.
AID562244Antimycobacterial activity against Mycobacterium smegmatis grown in carbon-limited broth medium assessed as growth inhibition in mid-logarithmic phase by GFP-based fluorescence assay2009Antimicrobial agents and chemotherapy, Dec, Volume: 53, Issue:12
Modifying culture conditions in chemical library screening identifies alternative inhibitors of mycobacteria.
AID1130148Antineoplastic activity against mouse B16 cells allografted in BDF1 mouse assessed as survival at 2 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1903849Antitumor immunity against human U2OS cells assessed as inhibition of RNA synthesis at 3 uM pretreated for 2.5 hrs by bright field microscopic analysis2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Biological Investigation of a Water-Soluble Isoginkgetin-Phosphate Analogue, Targeting the Spliceosome with
AID729377Effect on total BAD level in human MV411 cells at 10 to 100 nM after 12 hrs by Western blotting analysis2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID536040Cytotoxicity against human HL60/MX2 cells after 72 hrs2010Bioorganic & medicinal chemistry, Nov-15, Volume: 18, Issue:22
Indeno[1,2-c]isoquinolin-5,11-diones conjugated to amino acids: Synthesis, cytotoxicity, DNA interaction, and topoisomerase II inhibition properties.
AID45643Survivors of CDF1 mice on day 4 after 1st injection of compound at 0.75 mg/kg in six mice; 6/61989Journal of medicinal chemistry, Aug, Volume: 32, Issue:8
Synthesis of unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones as potential antileukemic agents.
AID1430730Antitumor activity against mouse 4T1.2 cells implanted in Balb/c mouse assessed as mouse survival time at 3 mg/kg, iv encapsulated within cucurbit[8]uril administered twice weekly for 2 weeks measured up to 33 days2017ACS medicinal chemistry letters, May-11, Volume: 8, Issue:5
Encapsulation of Mitoxantrone within Cucurbit[8]uril Decreases Toxicity and Enhances Survival in a Mouse Model of Cancer.
AID1349102Induction of apoptosis in human Caco2 cells assessed as viable cells at 1 uM after 16 hrs by Annexin V-FITC/propidium iodide staining-based flow cytometric analysis (Rvb = 98.4%)2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID84105In vitro Cytotoxic activity of compound in comparison with reference compounds in human cell line HT-29/Mx1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1381971Antiproliferative activity against human HCT116 cells after 48 hrs by MTT assay2018European journal of medicinal chemistry, Feb-25, Volume: 146The lead optimization of the polyamine conjugate of flavonoid with a naphthalene motif: Synthesis and biological evaluation.
AID1268088Binding affinity to calf thymus double stranded DNA by spectrophotometric titration method2015Journal of medicinal chemistry, Dec-24, Volume: 58, Issue:24
Synthesis and Characterization of 4,11-Diaminoanthra[2,3-b]furan-5,10-diones: Tumor Cell Apoptosis through tNOX-Modulated NAD(+)/NADH Ratio and SIRT1.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID721746Inhibition of human MATE1-mediated [14]-metformin uptake expressed in polarized MDCK2 cells after 5 mins by liquid scintillation counting analysis2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID425653Renal clearance in human2009Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15
Physicochemical determinants of human renal clearance.
AID32544Inhibitory activity against AUC375 cell line1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID307326Growth inhibition of topoisomerase 2 mutated mitoxantrone-resistant MX2 cells by Alamar blue assay2007Bioorganic & medicinal chemistry, Jun-15, Volume: 15, Issue:12
Synthesis and topoisomerase poisoning activity of A-ring and E-ring substituted luotonin A derivatives.
AID102201In vitro cytotoxic activity against human colon adenocarcinoma (LoVo) cells2000Bioorganic & medicinal chemistry letters, Feb-07, Volume: 10, Issue:3
Synthesis and antitumor activities of 5-methyl-1- and 2-[[2-dimethylaminoethyl]amino]-aza-thiopyranoindazoles.
AID1682834Antiproliferative activity against human HepG2 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay2021Bioorganic & medicinal chemistry, 01-01, Volume: 29Structure-activity relationship of novel acridone derivatives as antiproliferative agents.
AID1132472Antitumor activity against mouse P388 cells allografted in BDF1 mouse assessed as increase in survival time at 0.12 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID537735Binding affinity to Candida albicans CaMdr1p expressed in yeast AD1-8u2010European journal of medicinal chemistry, Nov, Volume: 45, Issue:11
Analysis of physico-chemical properties of substrates of ABC and MFS multidrug transporters of pathogenic Candida albicans.
AID1132507Toxicity in mouse P388 cells allografted BDF1 mouse assessed as body weight difference at 2 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID1132492Antitumor activity against mouse P388 cells allografted in BDF1 mouse assessed as mouse survival at 0.06 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID567091Drug absorption in human assessed as human intestinal absorption rate2011European journal of medicinal chemistry, Jan, Volume: 46, Issue:1
Prediction of drug intestinal absorption by new linear and non-linear QSPR.
AID436881Inhibition of VIM2 in imipenem-resistant Escherichia coli BL21(DE3) assessed as potentiation of imipenem-induced bactericidal activity at 50 uM after 18 hrs by twofold serial broth dilution method2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID1506771Inhibition of ROS1 (unknown origin) using poly (Glu,Tyr)4:1 substrate and ATP incubated for 60 mins by ELISA2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID1233373Antiproliferative activity against human MES-SA cells after 72 hrs by MTT assay2015Bioorganic & medicinal chemistry letters, Jul-01, Volume: 25, Issue:13
Synthesis and antiproliferative activity of some novel benzo-fused imidazo[1,8]naphthyridinones.
AID232811Toxicity ratio determined by the quotient of IC50 values in the myocytes divided by the average value in the three tumor lines.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID27139Apparent equilibrium constant for DNA binding (C-T)2003Journal of medicinal chemistry, Jul-03, Volume: 46, Issue:14
Design, synthesis, and biological properties of new bis(acridine-4-carboxamides) as anticancer agents.
AID437514Displacement of fluorescent pyrene-neomycin conjugate from tau stem-loop RNA2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Mitoxantrone analogues as ligands for a stem-loop structure of tau pre-mRNA.
AID729384Inhibition of BTK (unknown origin) using [gamma33P]ATP assessed as residual activity at 1 uM after 120 mins by radiometric assay2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID320432Binding affinity to calf thymus DNA assessed as thermal denaturation temperature at 10 uM2008Bioorganic & medicinal chemistry, Jan-15, Volume: 16, Issue:2
Synthesis, DNA binding, and cytotoxicity of 1,4-bis(2-amino-ethylamino)anthraquinone-amino acid conjugates.
AID1130153Antineoplastic activity against mouse B16 cells allografted in BDF1 mouse at 0.5 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID380013Cytotoxicity against human HCT cells after 48 hrs by MTT assay2000Journal of natural products, May, Volume: 63, Issue:5
New 7,20:14,20-diepoxy ent-kauranoids from Isodon xerophilus.
AID84119Effect of compound as percent survival at dose of 1000 ng/mL on HT-29/Mx cell line after 72 hours1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID681516TP_TRANSPORTER: cell accumulation in MCF7/MRP1-10 cells2006Molecular pharmacology, Apr, Volume: 69, Issue:4
Multidrug resistance protein 1 (MRP1, ABCC1) mediates resistance to mitoxantrone via glutathione-dependent drug efflux.
AID431399Cytotoxicity against human HL60/MX2 cells after 48 hrs by cell titer-blue assay2009Journal of medicinal chemistry, Oct-08, Volume: 52, Issue:19
Structure-activity relationship and molecular mechanisms of ethyl 2-amino-4-(2-ethoxy-2-oxoethyl)-6-phenyl-4h-chromene-3-carboxylate (sha 14-1) and its analogues.
AID588219FDA HLAED, gamma-glutamyl transferase (GGT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID154579Percent ratio of the medium survival time for P388 murine leukemia in CDF1 mice at 6 mg/kg1989Journal of medicinal chemistry, Aug, Volume: 32, Issue:8
Synthesis of unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones as potential antileukemic agents.
AID46133Inhibitory concentration against ethidium:calf thymus DNA (1.26:1) binding at pH 51997Journal of medicinal chemistry, Nov-07, Volume: 40, Issue:23
1-[(omega-aminoalkyl)amino]-4-[N-(omega-aminoalkyl)carbamoyl]-9-oxo-9, 10-dihydroacridines as intercalating cytotoxic agents: synthesis, DNA binding, and biological evaluation.
AID588215FDA HLAED, alkaline phosphatase increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID154575Percent ratio of the medium survival time for P388 murine leukemia in CDF1 mice at 3 mg/kg1989Journal of medicinal chemistry, Aug, Volume: 32, Issue:8
Synthesis of unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones as potential antileukemic agents.
AID1506322Growth inhibition of human umbilical cord cells2018Journal of medicinal chemistry, Aug-09, Volume: 61, Issue:15
Exploring the Structure-Activity Relationship and Mechanism of a Chromene Scaffold (CXL Series) for Its Selective Antiproliferative Activity toward Multidrug-Resistant Cancer Cells.
AID1209592Dissociation constant, pKa of the basic compound by capillary electrophoresis-mass spectrometry analysis2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID592673Cytotoxicity against human HL60 cells by MTT assay2011Bioorganic & medicinal chemistry, Apr-15, Volume: 19, Issue:8
Cytotoxic and anti-inflammatory cembranoids from the Vietnamese soft coral Lobophytum laevigatum.
AID106292Tested against MXF7 breast carcinoma (doxorubicin resistant) cell line in the sulforhodamine B assay.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID404304Effect on human MRP2-mediated estradiol-17-beta-glucuronide transport in Sf9 cells inverted membrane vesicles relative to control2008Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11
Prediction and identification of drug interactions with the human ATP-binding cassette transporter multidrug-resistance associated protein 2 (MRP2; ABCC2).
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID8424In vitro inhibition of tumor cell growth in the human myeloma 8226/ADR system.1992Journal of medicinal chemistry, Nov-13, Volume: 35, Issue:23
Novel non-cross resistant diaminoanthraquinones as potential chemotherapeutic agents.
AID687163Ratio of IC50 for doxorubicin-resistant human HL60 cells to IC50 for human HL60 cells2012Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11
Structure-activity relationship (SAR) study of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and the potential of the lead against multidrug resistance in cancer treatment.
AID272493Antiproliferative activity against adriamycin resistant P388 cells by ELISA2006Journal of medicinal chemistry, Nov-16, Volume: 49, Issue:23
Flavonoid dimers as bivalent modulators for P-glycoprotein-based multidrug resistance: synthetic apigenin homodimers linked with defined-length poly(ethylene glycol) spacers increase drug retention and enhance chemosensitivity in resistant cancer cells.
AID114263In vivo antitumor activity against subcutaneous Colon 38 tumors in mice determined as delay in growth after 3.9 mg/kg/day dose given as 3 times in a day for 4 days2003Journal of medicinal chemistry, Mar-13, Volume: 46, Issue:6
Synthesis and cytotoxic activity of carboxamide derivatives of benzo[b][1,6]naphthyridines.
AID320438Cytotoxicity against DNA topoisomerase-2 deficient human HL60/MX2 cells by MTT assay2008Bioorganic & medicinal chemistry, Jan-15, Volume: 16, Issue:2
Synthesis, DNA binding, and cytotoxicity of 1,4-bis(2-amino-ethylamino)anthraquinone-amino acid conjugates.
AID307328Ratio of GI50 for mitoxantrone-resistant human MX2 cells to GI50 for human HL60 cells2007Bioorganic & medicinal chemistry, Jun-15, Volume: 15, Issue:12
Synthesis and topoisomerase poisoning activity of A-ring and E-ring substituted luotonin A derivatives.
AID380012Cytotoxicity against human HL60 cells after 48 hrs by MTT assay2000Journal of natural products, May, Volume: 63, Issue:5
New 7,20:14,20-diepoxy ent-kauranoids from Isodon xerophilus.
AID214778Anti-tumor activity against human UACC375 melanoma cell lines by using MTT assay1995Journal of medicinal chemistry, Mar-17, Volume: 38, Issue:6
Amino-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H- dibenz[de,h]isoquinoline-1,3-diones. Synthesis, antitumor activity, and quantitative structure--activity relationship.
AID84288In vitro cytotoxic potency against HT-29 (human colon adenocarcinoma) cell line.2002Journal of medicinal chemistry, Jan-31, Volume: 45, Issue:3
2,6-Di(omega-aminoalkyl)-2,5,6,7-tetrahydropyrazolo[3,4,5-mn]pyrimido[5,6,1-de]acridine-5,7-diones: novel, potent, cytotoxic, and DNA-binding agents.
AID562242Antimycobacterial activity against Mycobacterium smegmatis grown in nitrogen -limited broth medium assessed as growth inhibition in mid-logarithmic phase by spectrophotometry2009Antimicrobial agents and chemotherapy, Dec, Volume: 53, Issue:12
Modifying culture conditions in chemical library screening identifies alternative inhibitors of mycobacteria.
AID154568Percent ratio of the medium survival time for P388 murine leukemia in CDF1 mice at 1.5 mg/kg1989Journal of medicinal chemistry, Aug, Volume: 32, Issue:8
Synthesis of unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones as potential antileukemic agents.
AID1439469Cytotoxicity against mouse NIH/3T3 cells assessed as reduction in cell viability after 24 hrs by MTT assay2017European journal of medicinal chemistry, Mar-31, Volume: 129Allylic isothiouronium salts: The discovery of a novel class of thiourea analogues with antitumor activity.
AID54993Compound was evaluated for the increase in melting temperature (delta Tm) for calf Thymus DNA on interaction with Ligand at DNAp to ligand ratio 10:11992Journal of medicinal chemistry, Apr-17, Volume: 35, Issue:8
Anthracene-9,10-diones as potential anticancer agents. Synthesis, DNA-binding, and biological studies on a series of 2,6-disubstituted derivatives.
AID320435Cytotoxicity against human SF268 cells at 4 ug/ml after 48 hrs by SRB assay2008Bioorganic & medicinal chemistry, Jan-15, Volume: 16, Issue:2
Synthesis, DNA binding, and cytotoxicity of 1,4-bis(2-amino-ethylamino)anthraquinone-amino acid conjugates.
AID253344Cytotoxicity against human MKN45 cancer cell line was determined after 1 hr2004Journal of medicinal chemistry, Oct-07, Volume: 47, Issue:21
Rational design, synthesis, and biological evaluation of bis(pyrimido[5,6,1-de]acridines) and bis(pyrazolo[3,4,5-kl]acridine-5-carboxamides) as new anticancer agents.
AID592676Cytotoxicity against human MCF7 cells by MTT assay2011Bioorganic & medicinal chemistry, Apr-15, Volume: 19, Issue:8
Cytotoxic and anti-inflammatory cembranoids from the Vietnamese soft coral Lobophytum laevigatum.
AID1221962Efflux ratio of permeability from apical to basolateral side over basolateral to apical side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of P-gp inhibitor LY3359792011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1711987Antimetastatic activity against mouse H22 cells implanted in Kunming mouse assessed as number of metastatic focus at 0.4 mg/kg, iv administered for 7 consecutive days starting from day 11 post inoculation and measured after 18 days (Rvb = 5.73 +/- 14.6 No2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID1349104Induction of apoptosis in human Caco2 cells assessed as late apoptotic cells at 1 uM after 16 hrs by Annexin V-FITC/propidium iodide staining-based flow cytometric analysis (Rvb = 0.072%)2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID156652In vitro Cytotoxic activity of compound in comparison with reference compounds in human cell line PC31999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID129072Antileukemic activity towards P388 Murine Leukemia at a dose of 0.1 mg/kg, expressed as body weight change1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID98537Compound was tested in vitro for cytotoxicity against L1210 murine cell line (48 hr exposure to compound)1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID102325In vitro Cytotoxic activity of compound in comparison with reference compounds in human cell line LoVo/Dx(RI)1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID681514TP_TRANSPORTER: cell accumulation in MCF7/MRP1-M6 cells2006Molecular pharmacology, Apr, Volume: 69, Issue:4
Multidrug resistance protein 1 (MRP1, ABCC1) mediates resistance to mitoxantrone via glutathione-dependent drug efflux.
AID8690Activity against A549 cancer cell line.1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID201222Bacterial mutagenicity was measured against Salmonella Typhimurium TA1538 at dose range of 0-5 ug/plate1998Journal of medicinal chemistry, Sep-10, Volume: 41, Issue:19
Anthracene-9,10-diones as potential anticancer agents: bacterial mutation studies of amido-substituted derivatives reveal an unexpected lack of mutagenicity.
AID624629Inhibition of Pgp expressed in MDR1-MDCKII cells measured by calcein-AM assay2001The Journal of pharmacology and experimental therapeutics, Nov, Volume: 299, Issue:2
Rational use of in vitro P-glycoprotein assays in drug discovery.
AID588218FDA HLAED, lactate dehydrogenase (LDH) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID83602In vitro Cytotoxic activity of compound in comparison with reference compounds in human cell line HT-291999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID681062TP_TRANSPORTER: Northern blot from primary hepatocytes1996Biochemical pharmacology, Nov-08, Volume: 52, Issue:9
Multidrug resistance gene expression in rodents and rodent hepatocytes treated with mitoxantrone.
AID699539Inhibition of human liver OATP1B1 expressed in HEK293 Flp-In cells assessed as reduction in E17-betaG uptake at 20 uM by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID72412Cytotoxic potency required to inhibit G-361 cell growth by 50%1997Journal of medicinal chemistry, Nov-07, Volume: 40, Issue:23
1-[(omega-aminoalkyl)amino]-4-[N-(omega-aminoalkyl)carbamoyl]-9-oxo-9, 10-dihydroacridines as intercalating cytotoxic agents: synthesis, DNA binding, and biological evaluation.
AID436893Bacteriostatic activity against imipenem-non resistant Escherichia coli BL21(DE3) at 2.1 ug/mL after 24 hrs by broth microdilution method2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID1349096Inhibition of NAE in human Caco2 cells assessed as increase in beta-catenin protein levels after 16 hrs by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID47499Cytotoxic potency required to inhibit CH1 cell growth by 50%1997Journal of medicinal chemistry, Nov-07, Volume: 40, Issue:23
1-[(omega-aminoalkyl)amino]-4-[N-(omega-aminoalkyl)carbamoyl]-9-oxo-9, 10-dihydroacridines as intercalating cytotoxic agents: synthesis, DNA binding, and biological evaluation.
AID1271102Cytotoxicity against rat C6 cells after 24 hrs by MTT assay2016European journal of medicinal chemistry, Jan-01, Volume: 107Synthesis and evaluation of bis-thiazole derivatives as new anticancer agents.
AID1506785Induction of apoptosis in human HCC78 cells assessed as late apoptotic cells level at 10 nM incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry (Rvb = 13.8%)2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID647961Inhibition of human TERT expression in H1299 cells at 100 uM after 24 hrs by secreted alkaline phosphatase reporter gene assay relative to control2012European journal of medicinal chemistry, Apr, Volume: 50Design, synthesis and evaluation of telomerase inhibitory, hTERT repressing, and anti-proliferation activities of symmetrical 1,8-disubstituted amidoanthraquinones.
AID98910Inhibitory activity against resistant murine leukemia L1210 cell lines.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID1271104Cytotoxicity against mouse NIH/3T3 cells after 24 hrs by MTT assay2016European journal of medicinal chemistry, Jan-01, Volume: 107Synthesis and evaluation of bis-thiazole derivatives as new anticancer agents.
AID1550895Antitumor activity against mouse H22 cells allografted in immunocompetent Balb/c mouse assessed as inhibition of tumour formation at 2 uM incubated with cells for 5 hrs prior to 20 mins 2 mW/cm2 UVA irradiation post compound washout followed by vaccinatio2019European journal of medicinal chemistry, Jun-01, Volume: 171Naphthyl quinoxaline thymidine conjugate is a potent anticancer agent post UVA activation and elicits marked inhibition of tumor growth through vaccination.
AID1130617Antitumor activity against mouse P388 cells allografted in mouse assessed as increase of median life span at 6.2 mg/kg, ip on day 1, 5 and 9 measured up to 60 days relative to control1979Journal of medicinal chemistry, Sep, Volume: 22, Issue:9
Antitumor agents. 1. 1,4-Bis[(aminoalkyl)amino]-9,10-anthracenediones.
AID216451Activity against sensitive cell line of WiDr human colon tumor1995Journal of medicinal chemistry, Mar-17, Volume: 38, Issue:6
Amino-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H- dibenz[de,h]isoquinoline-1,3-diones. Synthesis, antitumor activity, and quantitative structure--activity relationship.
AID1130149Antineoplastic activity against mouse B16 cells allografted in BDF1 mouse at 2 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID103088In vitro inhibition of tumor cell growth in the human mammary carcinoma MCF-7/ADR system.1992Journal of medicinal chemistry, Nov-13, Volume: 35, Issue:23
Novel non-cross resistant diaminoanthraquinones as potential chemotherapeutic agents.
AID216595Activity against human colon carcinoma sensitive WiDr cell line.1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID243266Thermal denaturation of calf thymus DNA at 37 degree C2004Bioorganic & medicinal chemistry letters, Oct-04, Volume: 14, Issue:19
Pyrrolo[2,1-c][1,4]benzodiazepine-anthraquinone conjugates. Synthesis, DNA binding and cytotoxicity.
AID1883020Toxicity in Balb/c mouse implanted with mouse 4T1 cells assessed as heart lesions at 50 mg/kg administered intratumorally every four days for 14 days in the presence of liquid cyanoacrylate by H&E staining based histopathological analysis2022European journal of medicinal chemistry, Jul-05, Volume: 237Design, synthesis, and evaluation of a novel series of mono-indolylbenzoquinones derivatives for the potential treatment of breast cancer.
AID721742Ratio of Cmax unbound to IC50 for human MATE1-mediated [14]-metformin uptake expressed in polarized MDCK2 cells2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID1132511Toxicity in mouse P388 cells allografted BDF1 mouse assessed as body weight difference at 0.12 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID1130159Antineoplastic activity against mouse Colon 26 cells allografted in CDF1 mouse at 0.69 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID381805Binding affinity to calf thymus DNA assessed as change in thermal stability at 2 uM in tris-HCl buffer at pH 7.5 by thermal denaturation assay2008Bioorganic & medicinal chemistry, Apr-01, Volume: 16, Issue:7
The structure-based design, synthesis and biological evaluation of DNA-binding bisintercalating bisanthrapyrazole anticancer compounds.
AID540213Half life in human after iv administration2008Drug 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.
AID216450Activity against resistant cell line of WiDr human colon tumor1995Journal of medicinal chemistry, Mar-17, Volume: 38, Issue:6
Amino-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H- dibenz[de,h]isoquinoline-1,3-diones. Synthesis, antitumor activity, and quantitative structure--activity relationship.
AID1209590Drug uptake in Sprague-Dawley rat brain slices at 100 nM after 5 hrs in presence of 20 uM of MK-5712011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID46325Thermal denaturation of calf-thymus DNA was evaluated1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Synthesis and antitumor properties of an anthraquinone bisubstituted by the copper chelating peptide Gly-Gly-L-His.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID47668Concentration required to inhibit CH1-cell growth by 50%1998Journal of medicinal chemistry, Aug-13, Volume: 41, Issue:17
1,4- and 2,6-disubstituted amidoanthracene-9,10-dione derivatives as inhibitors of human telomerase.
AID136070Antileukemic activity towards P388 Murine Leukemia at a dose of 0.2 mg/kg1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID248039Cytotoxicity against human H460M cancer cell line was determined after 144 hr2004Journal of medicinal chemistry, Oct-07, Volume: 47, Issue:21
Rational design, synthesis, and biological evaluation of bis(pyrimido[5,6,1-de]acridines) and bis(pyrazolo[3,4,5-kl]acridine-5-carboxamides) as new anticancer agents.
AID540210Clearance in human after iv administration2008Drug 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.
AID318700Antiproliferative activity against human MDA-MB-231 cells2008Bioorganic & medicinal chemistry, Mar-15, Volume: 16, Issue:6
Design, synthesis and cell growth inhibitory activity of a series of novel aminosubstituted xantheno[1,2-d]imidazoles in breast cancer cells.
AID588975Substrates of transporters of clinical importance in the absorption and disposition of drugs, BCRP2010Nature reviews. Drug discovery, Mar, Volume: 9, Issue:3
Membrane transporters in drug development.
AID1130174Antineoplastic activity against mouse P388 cells allografted in CDF1 mouse assessed as survival at 1 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1132470Antitumor activity against mouse P388 cells allografted in BDF1 mouse assessed as increase in survival time at 0.5 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID102330Inhibitory activity against human colon adenocarcinoma cell line LoVo/Dx.1995Journal of medicinal chemistry, Feb-03, Volume: 38, Issue:3
Chromophore-modified antitumor anthracenediones: synthesis, DNA binding, and cytotoxic activity of 1,4-bis[(aminoalkyl)amino]benzo[g]-phthalazine-5,10-diones.
AID320433Cytotoxicity against human MCF7 cells at 4 ug/ml after 48 hrs by SRB assay2008Bioorganic & medicinal chemistry, Jan-15, Volume: 16, Issue:2
Synthesis, DNA binding, and cytotoxicity of 1,4-bis(2-amino-ethylamino)anthraquinone-amino acid conjugates.
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID624622Apparent permeability (Papp) from apical to basolateral side determined in MDR1-MDCKII cells2001The Journal of pharmacology and experimental therapeutics, Nov, Volume: 299, Issue:2
Rational use of in vitro P-glycoprotein assays in drug discovery.
AID1130163Antineoplastic activity against mouse L1210 cells allografted in CDF1 mouse at 18 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1130171Antineoplastic activity against mouse L1210 cells allografted in CDF1 mouse at 1 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID364460Cytotoxicity against human HeLa cells expressing telomerase after 96 hrs by MTT assay2008Journal of medicinal chemistry, Sep-25, Volume: 51, Issue:18
Aminoacyl-anthraquinone conjugates as telomerase inhibitors: synthesis, biophysical and biological evaluation.
AID320441Cytotoxicity against human NCI-H460 cells after 48 hrs by SRB assay2008Bioorganic & medicinal chemistry, Jan-15, Volume: 16, Issue:2
Synthesis, DNA binding, and cytotoxicity of 1,4-bis(2-amino-ethylamino)anthraquinone-amino acid conjugates.
AID320440Cytotoxicity against human MCF7 cells after 48 hrs by SRB assay2008Bioorganic & medicinal chemistry, Jan-15, Volume: 16, Issue:2
Synthesis, DNA binding, and cytotoxicity of 1,4-bis(2-amino-ethylamino)anthraquinone-amino acid conjugates.
AID121351Therapeutic effect against P388 leukemia in mice on days 1, 5 and 9 after administration of 1.6 mg/kg dose expressed as median survival time of treated and control mice (in vivo)1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Synthesis and antitumor properties of an anthraquinone bisubstituted by the copper chelating peptide Gly-Gly-L-His.
AID1271101Cytotoxicity against human A549 cells after 24 hrs by MTT assay2016European journal of medicinal chemistry, Jan-01, Volume: 107Synthesis and evaluation of bis-thiazole derivatives as new anticancer agents.
AID84437Cytotoxic potency required to inhibit HT-29 cell growth by 50% after cell drug contact for 144 hrs1997Journal of medicinal chemistry, Nov-07, Volume: 40, Issue:23
1-[(omega-aminoalkyl)amino]-4-[N-(omega-aminoalkyl)carbamoyl]-9-oxo-9, 10-dihydroacridines as intercalating cytotoxic agents: synthesis, DNA binding, and biological evaluation.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID270853Antiproliferative activity against HT29 cells by MTT assay after 72 hrs2006Bioorganic & medicinal chemistry letters, Sep-15, Volume: 16, Issue:18
Synthesis and antiproliferative activity of substituted benzopyranoisoindoles: a new class of cytotoxic compounds.
AID1550902Antitumor activity against mouse H22 cells allografted in immunocompetent Balb/c mouse assessed as decrease in lump formation in vaccination site at 2 uM incubated with cells for 5 hrs prior to 20 mins 2 mW/cm2 UVA irradiation post compound washout follow2019European journal of medicinal chemistry, Jun-01, Volume: 171Naphthyl quinoxaline thymidine conjugate is a potent anticancer agent post UVA activation and elicits marked inhibition of tumor growth through vaccination.
AID1233375Ratio of IC50 for human MES-SA/Dx5 cells to IC50 for human MES-SA cells2015Bioorganic & medicinal chemistry letters, Jul-01, Volume: 25, Issue:13
Synthesis and antiproliferative activity of some novel benzo-fused imidazo[1,8]naphthyridinones.
AID1197747Inhibition of human OATP1B3-mediated [3H]CCK-8 after 5 mins by Dixon plot method2015European journal of medicinal chemistry, Mar-06, Volume: 92Interaction of human organic anion transporter polypeptides 1B1 and 1B3 with antineoplastic compounds.
AID1130178Antineoplastic activity against mouse P388 cells allografted in CDF1 mouse assessed as survival at 0.25 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID154372Optimal dose per injection in mg/kg required to inhibit growth of P388 leukemia cells in mice1987Journal of medicinal chemistry, Jan, Volume: 30, Issue:1
Anthrapyrazole anticancer agents. Synthesis and structure-activity relationships against murine leukemias.
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug 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.
AID477017Displacement of ethidium bromide from calf thymus DNA assessed as decrease of fluorescence of bound ethidium bromide by fluorometric assay2010European journal of medicinal chemistry, Apr, Volume: 45, Issue:4
Synthesis, cytotoxicity and DNA-binding of novel bisnaphthalimidopropyl derivatives in breast cancer MDA-MB-231 cells.
AID381807Growth inhibition of etoposide-resistant human K/VP.5 cells after 72 hrs by MTS method2008Bioorganic & medicinal chemistry, Apr-01, Volume: 16, Issue:7
The structure-based design, synthesis and biological evaluation of DNA-binding bisintercalating bisanthrapyrazole anticancer compounds.
AID1130170Antineoplastic activity against mouse L1210 cells allografted in CDF1 mouse assessed as survival at 1 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID98563Cytotoxic potency required to inhibit L1210 cell growth by 50% after cell drug contact for 48 hrs1997Journal of medicinal chemistry, Nov-07, Volume: 40, Issue:23
1-[(omega-aminoalkyl)amino]-4-[N-(omega-aminoalkyl)carbamoyl]-9-oxo-9, 10-dihydroacridines as intercalating cytotoxic agents: synthesis, DNA binding, and biological evaluation.
AID436885Bactericidal activity against imipenem-non resistant Escherichia coli BL21(DE3) at 2.1 ug/mL after 24 hrs by broth microdilution method2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID1550871Cytotoxicity against human Bel7402 cells assessed as reduction in cell viability preincubated for 5 hrs followed by compound washout and measured after 48 hrs by CCK8 assay2019European journal of medicinal chemistry, Jun-01, Volume: 171Naphthyl quinoxaline thymidine conjugate is a potent anticancer agent post UVA activation and elicits marked inhibition of tumor growth through vaccination.
AID687167Ratio of IC50 for human CCRF-CEM/VM-1-5 cells IC50 for human CCRF-CEM cells2012Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11
Structure-activity relationship (SAR) study of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and the potential of the lead against multidrug resistance in cancer treatment.
AID1209591Drug uptake in Sprague-Dawley rat brain slices at 100 nM after 5 hrs in presence of 10 uM of fumitremorgin-C and 20 uM of MK-5712011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID232808The quotient of the IC50 in the myocytes divided by the mean IC50 in the three cell lines1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID134227The compound was tested for antitumor activity against P388 murine leukemia by measuring maximum tolerated dose1994Journal of medicinal chemistry, Mar-18, Volume: 37, Issue:6
6,9-Bis[(aminoalkyl)amino]benzo[g]isoquinoline-5,10-diones. A novel class of chromophore-modified antitumor anthracene-9,10-diones: synthesis and antitumor evaluations.
AID1506773Cytotoxicity in human CCD-19Lu cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID1209582Unbound volume of distribution in Sprague-Dawley rat brain slices at 100 nM after 5 hrs2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID436883Inhibition of VIM2 in imipenem-resistant Escherichia coli BL21(DE3) assessed as potentiation of imipenem-induced bactericidal activity at 2.1 ug/mL after 18 hrs by checkerboard microdilution method2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID1506798Inhibition of ROS1 in human HCC78 cells assessed as reduction in ERK phosphorylation incubated for 48 hrs by Western blot method2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID272491Antiproliferative activity against multidrug resistant MDA435/LCC6 cells by ELISA2006Journal of medicinal chemistry, Nov-16, Volume: 49, Issue:23
Flavonoid dimers as bivalent modulators for P-glycoprotein-based multidrug resistance: synthetic apigenin homodimers linked with defined-length poly(ethylene glycol) spacers increase drug retention and enhance chemosensitivity in resistant cancer cells.
AID733190Antiproliferative activity against human RKOp27 cells after 48 hrs2013Bioorganic & medicinal chemistry letters, Mar-15, Volume: 23, Issue:6
Synthesis and biological evaluation of new cytotoxic indazolo[4,3-gh]isoquinolinone derivatives.
AID1525935Inhibition of MDR in human LCC6MDR cells assessed as reduction in cell viability after 5 days by MTS/PMS assay2019Journal of medicinal chemistry, 09-26, Volume: 62, Issue:18
Triazole Bridged Flavonoid Dimers as Potent, Nontoxic, and Highly Selective Breast Cancer Resistance Protein (BCRP/ABCG2) Inhibitors.
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID524794Antiplasmodial activity against Plasmodium falciparum GB4 after 72 hrs by SYBR green assay2009Nature chemical biology, Oct, Volume: 5, Issue:10
Genetic mapping of targets mediating differential chemical phenotypes in Plasmodium falciparum.
AID436895Inhibition of VIM2 in imipenem-resistant Escherichia coli BL21(DE3) assessed as potentiation of imipenem-induced bactericidal activity at 8.4 ug/mL after 18 hrs by checkerboard microdilution method2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID540211Fraction unbound in human after iv administration2008Drug 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.
AID1506790Induction of apoptosis in human HCC78 cells assessed as necrotic cells level at 20 nM incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry (Rvb = 0.06%)2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID588214FDA HLAED, liver enzyme composite activity2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID681494TP_TRANSPORTER: Northern blot in vivo Wistar rat1996Biochemical pharmacology, Nov-08, Volume: 52, Issue:9
Multidrug resistance gene expression in rodents and rodent hepatocytes treated with mitoxantrone.
AID721748Inhibition of human MATE2K-mediated ASP+ uptake expressed in HEK293 cells up to 500 uM after 1.5 mins by fluorescence assay2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID1132512Toxicity in mouse P388 cells allografted BDF1 mouse assessed as body weight difference at 0.06 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID1130169Antineoplastic activity against mouse L1210 cells allografted in CDF1 mouse at 2 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID334268Cytotoxicity against human K562 cells after 48 hrs by MTT assay2002Journal of natural products, May, Volume: 65, Issue:5
Abietane diterpenoids from Coleus xanthanthus.
AID624606Specific activity of expressed human recombinant UGT1A12000Annual review of pharmacology and toxicology, , Volume: 40Human UDP-glucuronosyltransferases: metabolism, expression, and disease.
AID721750Inhibition of human OCT1-mediated ASP+ uptake expressed in HEK293 cells after 3 mins by fluorescence assay2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID248010Cytotoxicity against human PC3 cancer cell line was determined after 144 hr2004Journal of medicinal chemistry, Oct-07, Volume: 47, Issue:21
Rational design, synthesis, and biological evaluation of bis(pyrimido[5,6,1-de]acridines) and bis(pyrazolo[3,4,5-kl]acridine-5-carboxamides) as new anticancer agents.
AID1349086Inhibition of NAE (unknown origin) assessed as decrease in NAE-mediated Ubc12-NEDD8 conjugation levels preincubated for 10 mins followed by ATP and Mg2+ addition measured after 60 mins by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID679173TP_TRANSPORTER: drug resistance in BCRP-expressing K562 cells2003Molecular cancer therapeutics, Jan, Volume: 2, Issue:1
Reversal of breast cancer resistance protein-mediated drug resistance by estrogen antagonists and agonists.
AID83791Percent inhibition at G2/M phase of cell cycle at a dose of 100n g/mL after 72 hours of induction in HT-29 cell line1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1586108Antiproliferative activity against human A549 cells after 72 hrs by sulforhodamine B assay2018Journal of natural products, 12-28, Volume: 81, Issue:12
A Pair of Enantiomeric Bis- seco-abietane Diterpenoids from Cryptomeria fortunei.
AID1711939Antiproliferative activity against human SMMC-7221 cells assessed as inhibition of cell proliferation at 1 uM measured after 48 hrs by MTT assay relative to control2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1711940Antiproliferative activity against human SMMC-7221 cells assessed as inhibition of cell proliferation at 5 uM measured after 48 hrs by MTT assay relative to control2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID1349110Induction of apoptosis in human Caco2 cells assessed as viable cells at 10 uM after 16 hrs by Annexin V-FITC/propidium iodide staining-based flow cytometric analysis (Rvb = 98.4%)2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID562240Antimycobacterial activity against Mycobacterium smegmatis grown in Luria-Bertani broth medium assessed as growth inhibition in mid-logarithmic phase by spectrophotometry2009Antimicrobial agents and chemotherapy, Dec, Volume: 53, Issue:12
Modifying culture conditions in chemical library screening identifies alternative inhibitors of mycobacteria.
AID524792Antiplasmodial activity against Plasmodium falciparum D10 after 72 hrs by SYBR green assay2009Nature chemical biology, Oct, Volume: 5, Issue:10
Genetic mapping of targets mediating differential chemical phenotypes in Plasmodium falciparum.
AID85757In vitro cytotoxic activity against human colon HT-29 cell line ( standard deviation in parenthesis)2002Journal of medicinal chemistry, Jun-06, Volume: 45, Issue:12
Design, synthesis, and antiproliferative activity of some new pyrazole-fused amino derivatives of the pyranoxanthenone, pyranothioxanthenone, and pyranoacridone ring systems: a new class of cytotoxic agents.
AID103419Tested for inhibitory activity against human tumor cell line D40, a strain resistant to doxorubicin of breast carcinoma using sulforhodamine B assay.2000Journal of medicinal chemistry, Aug-10, Volume: 43, Issue:16
Analogues of amonafide and azonafide with novel ring systems.
AID106296Antitumor activity against human mammary carcinoma mitoxantrone-resistant MXF7 breast cell line.1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID591076Cytotoxicity against human HL60/MX2 cells2011Bioorganic & medicinal chemistry letters, Apr-15, Volume: 21, Issue:8
Synthesis, cytotoxicity and topoisomerase inhibition properties of multifarious aminoalkylated indeno[1,2-c]isoquinolin-5,11-diones.
AID153899In vivo antitumor activity against P388 leukemia cells at a dose of 0.75 mg/kg as a single injection and 1.5 mg/kg as a total1984Journal of medicinal chemistry, Mar, Volume: 27, Issue:3
5-[(Aminoalkyl)amino]-substituted anthra[1,9-cd]pyrazol-6(2H)-ones as novel anticancer agents. Synthesis and biological evaluation.
AID1903854Antitumor immunity against human U2OS cells expressing CALR-GFP fusion protein assessed as accumulation CALR-GFP fusion protein at 3 uM measured upto 24 hrs by live cell microscopic analysis2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Biological Investigation of a Water-Soluble Isoginkgetin-Phosphate Analogue, Targeting the Spliceosome with
AID87741Effective concentration required to inhibit by 50% the growth of HeLa S3 cells1988Journal of medicinal chemistry, Oct, Volume: 31, Issue:10
Synthesis and antineoplastic evaluation of 1,4-bis(aminoalkanamido)-9,10-anthracenediones.
AID540209Volume of distribution at steady state in human after iv administration2008Drug 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.
AID1396805Antiproliferative activity against human HL60 cells after 72 hrs by SRB assay2018Bioorganic & medicinal chemistry letters, 08-15, Volume: 28, Issue:15
Phosphorus-containing isothiocyanate-derived mercapturic acids as a useful alternative for parental isothiocyanates in experimental oncology.
AID404700Cytotoxicity against mitoxantrone-resistant human HL60/MX2 cells after 72 hrs2008Journal of medicinal chemistry, Jun-26, Volume: 51, Issue:12
Synthesis, cytotoxicity, DNA interaction, and topoisomerase II inhibition properties of novel indeno[2,1-c]quinolin-7-one and indeno[1,2-c]isoquinolin-5,11-dione derivatives.
AID404701Resistant index, ratio of IC50 for mitoxantrone-resistant human HL60/MX2 cells to IC50 for mitoxantrone-sensitive human HL60 cells2008Journal of medicinal chemistry, Jun-26, Volume: 51, Issue:12
Synthesis, cytotoxicity, DNA interaction, and topoisomerase II inhibition properties of novel indeno[2,1-c]quinolin-7-one and indeno[1,2-c]isoquinolin-5,11-dione derivatives.
AID320437Cytotoxicity against human HL60 cells after 48 hrs by MTT assay2008Bioorganic & medicinal chemistry, Jan-15, Volume: 16, Issue:2
Synthesis, DNA binding, and cytotoxicity of 1,4-bis(2-amino-ethylamino)anthraquinone-amino acid conjugates.
AID272512Relative fold, IC50 in absence to presence of 1,13-bis[4'-((5,7-dihydroxy)-4H-chromen-4-on-2-yl)phenyl]-1,4,7,10,13-pentaoxatridecane in multidrug resistant MDA435/LCC6 cells2006Journal of medicinal chemistry, Nov-16, Volume: 49, Issue:23
Flavonoid dimers as bivalent modulators for P-glycoprotein-based multidrug resistance: synthetic apigenin homodimers linked with defined-length poly(ethylene glycol) spacers increase drug retention and enhance chemosensitivity in resistant cancer cells.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID1711981Toxicity in Kunming mouse implanted with mouse H22 cells assessed as change in mouse body weight at 0.4 mg/kg, iv administered for 7 consecutive days starting from day 8 post inoculation and measured after 16 days (Rvb = 21 %)2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID477016Binding affinity to calf thymus DNA assessed as temperature required to cause 50% of DNA denatured at 10 uM by thermal denaturation assay2010European journal of medicinal chemistry, Apr, Volume: 45, Issue:4
Synthesis, cytotoxicity and DNA-binding of novel bisnaphthalimidopropyl derivatives in breast cancer MDA-MB-231 cells.
AID135061In vivo antileukemic activity towards P388 Murine Leukemia at a dose of 0.8 mg/kg, expressed as long time survivors tested in 6 animals1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID537734Antifungal activity against yeast AD1-8u expressing Candida albicans CaMdr1p by agar disk diffusion assay2010European journal of medicinal chemistry, Nov, Volume: 45, Issue:11
Analysis of physico-chemical properties of substrates of ABC and MFS multidrug transporters of pathogenic Candida albicans.
AID1711982Toxicity in iv dosed Kunming mouse assessed as maximum tolerated dose2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID202844Concentration required to inhibit SKOV-3-cell growth by 50%1998Journal of medicinal chemistry, Aug-13, Volume: 41, Issue:17
1,4- and 2,6-disubstituted amidoanthracene-9,10-dione derivatives as inhibitors of human telomerase.
AID230412It is the ratio of IC50 for LOVO tumor cell line to that of LOVO/DOXO cell line.1991Journal of medicinal chemistry, Aug, Volume: 34, Issue:8
Synthesis and antitumor evaluations of symmetrically and unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones and 1,4-bis[(aminoalkyl)amino]-5,8-dihydroxyanthracene-9,10-diones.
AID436892Bacteriostatic activity against imipenem-resistant Escherichia coli BL21(DE3) expressing VIM2 gene at 2.1 ug/mL after 24 hrs by broth microdilution method2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID729382Inhibition of BTK (unknown origin)2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID1132508Toxicity in mouse P388 cells allografted BDF1 mouse assessed as body weight difference at 1 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID216575Tested against WiDr colon (sensitive) in the sulforhodamine B assay.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID562243Antimycobacterial activity against Mycobacterium smegmatis grown in Luria-Bertani broth medium assessed as growth inhibition in mid-logarithmic phase by GFP-based fluorescence assay2009Antimicrobial agents and chemotherapy, Dec, Volume: 53, Issue:12
Modifying culture conditions in chemical library screening identifies alternative inhibitors of mycobacteria.
AID1130183Antineoplastic activity against mouse P388 cells allografted in CDF1 mouse at 0.06 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID729385Inhibition of AKT1 (unknown origin) using [gamma33P]ATP assessed as residual activity at 1 uM after 120 mins by radiometric assay2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID1070863Cytotoxicity against human H1299 cells assessed as cell viability at 10 uM after 48 hrs by MTT assay2013European journal of medicinal chemistry, Nov, Volume: 69Structure-based design, synthesis and biological evaluation of novel anthra[1,2-d]imidazole-6,11-dione homologues as potential antitumor agents.
AID733196Antiproliferative activity against human SF268 cells after 48 hrs2013Bioorganic & medicinal chemistry letters, Mar-15, Volume: 23, Issue:6
Synthesis and biological evaluation of new cytotoxic indazolo[4,3-gh]isoquinolinone derivatives.
AID216596Activity against human colon carcinoma multi drug resistant (MDR)-WiDr cell line.1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID1152333Antiproliferative activity against human HepG2 cells after 48 hrs by MTT assay2014Bioorganic & medicinal chemistry, Jun-15, Volume: 22, Issue:12
Novel aromatic-polyamine conjugates as cholinesterase inhibitors with notable selectivity toward butyrylcholinesterase.
AID624626Ratio of apparent permeability from basolateral to apical side over apical to basolateral side determined in MDR1-MDCKII cells2001The Journal of pharmacology and experimental therapeutics, Nov, Volume: 299, Issue:2
Rational use of in vitro P-glycoprotein assays in drug discovery.
AID99088Tested in vitro for inhibitory activity against L1210 murine leukemia1994Journal of medicinal chemistry, Mar-18, Volume: 37, Issue:6
6,9-Bis[(aminoalkyl)amino]benzo[g]isoquinoline-5,10-diones. A novel class of chromophore-modified antitumor anthracene-9,10-diones: synthesis and antitumor evaluations.
AID10003Concentration required to inhibit A2780-cell growth by 50%1998Journal of medicinal chemistry, Aug-13, Volume: 41, Issue:17
1,4- and 2,6-disubstituted amidoanthracene-9,10-dione derivatives as inhibitors of human telomerase.
AID425652Total body clearance in human2009Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15
Physicochemical determinants of human renal clearance.
AID222140Inhibition of cellular growth was evaluated in vitro against human colon carcinoma LOVO.1991Journal of medicinal chemistry, Aug, Volume: 34, Issue:8
Synthesis and antitumor evaluations of symmetrically and unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones and 1,4-bis[(aminoalkyl)amino]-5,8-dihydroxyanthracene-9,10-diones.
AID1883024Toxicity in Balb/c mouse implanted with mouse 4T1 cells assessed as kidney lesions at 50 mg/kg administered intratumorally every four days for 14 days in the presence of liquid cyanoacrylate by H&E staining based histopathological analysis2022European journal of medicinal chemistry, Jul-05, Volume: 237Design, synthesis, and evaluation of a novel series of mono-indolylbenzoquinones derivatives for the potential treatment of breast cancer.
AID1130160Antineoplastic activity against mouse Colon 26 cells allografted in CDF1 mouse assessed as survival at 0.39 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID106430Antitumor activity against human mammary carcinoma doxorubicin-resistant MXF7 breast cell line.1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID253346Cytotoxicity against human HCT116 cancer cell line was determined after 1 hr2004Journal of medicinal chemistry, Oct-07, Volume: 47, Issue:21
Rational design, synthesis, and biological evaluation of bis(pyrimido[5,6,1-de]acridines) and bis(pyrazolo[3,4,5-kl]acridine-5-carboxamides) as new anticancer agents.
AID1525937Antiproliferative activity against human 2008 cells assessed as reduction in cell viability after 5 days by MTS/PMS assay2019Journal of medicinal chemistry, 09-26, Volume: 62, Issue:18
Triazole Bridged Flavonoid Dimers as Potent, Nontoxic, and Highly Selective Breast Cancer Resistance Protein (BCRP/ABCG2) Inhibitors.
AID84124Effect of compound as percent survival at dose of 3000 ng/mL on HT-29/Mx cell line after 72 hours1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID1712013Toxicity in Kunming mouse implanted with mouse H22 cells assessed as mouse mortality at 0.4 mg/kg, iv administered for 7 consecutive days starting from day 8 post inoculation and measured after 16 days2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID83926Effect of compound as percent survival at dose of 100n g/mL on HT-29 cell line after 72 hours1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID54113Increase in Melting temperature (delta Tm) for Micrococcus lysodeikticus DNA on interaction against ligand (mole ratio of 10:1)1992Journal of medicinal chemistry, Apr-17, Volume: 35, Issue:8
Anthracene-9,10-diones as potential anticancer agents. Synthesis, DNA-binding, and biological studies on a series of 2,6-disubstituted derivatives.
AID99358Tested for inhibitory activity against murine cell line L12110, a strain resistant to doxorubicin using MTT assay.2000Journal of medicinal chemistry, Aug-10, Volume: 43, Issue:16
Analogues of amonafide and azonafide with novel ring systems.
AID602039Cytotoxicity against human A549 cells after 24 hrs by MTT assay2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Cytotoxic and PPARs transcriptional activities of sterols from the Vietnamese soft coral Lobophytum laevigatum.
AID364461Cytotoxicity against human 293T cells expressing telomerase after 96 hrs by MTT assay2008Journal of medicinal chemistry, Sep-25, Volume: 51, Issue:18
Aminoacyl-anthraquinone conjugates as telomerase inhibitors: synthesis, biophysical and biological evaluation.
AID136071Antileukemic activity towards P388 Murine Leukemia at a dose of 0.4 mg/kg1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1130154Antineoplastic activity against mouse B16 cells allografted in BDF1 mouse assessed as survival at 0.25 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1132468Antitumor activity against mouse P388 cells allografted in BDF1 mouse assessed as increase in survival time at 2 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID116824Percent increase in life span when given at a dose in P388 leukemia cells of mice1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID153498In vivo antineoplastic activity was determined in BDF1 mice implanted with P388 leukemia and activity is expressed as T/C at 1 mg/kg1987Journal of medicinal chemistry, Sep, Volume: 30, Issue:9
Structural modification study of mitoxantrone (DHAQ). Chloro-substituted mono- and bis[(aminoalkyl)amino]anthraquinones.
AID202642Mean percentage reduction in tumor weight on S180 tumor cell at 0.75 mg/kg (cumulative dose 16 mg/Kg) introduced ip (in vivo)1988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID683860Antiproliferative activity against human HL60 cells after 72 hrs by SRB assay2012Bioorganic & medicinal chemistry letters, Oct-01, Volume: 22, Issue:19
New derivatives of 11-methyl-6-[2-(dimethylamino)ethyl]-6H-indolo[2,3-b]quinoline as cytotoxic DNA topoisomerase II inhibitors.
AID1130150Antineoplastic activity against mouse B16 cells allografted in BDF1 mouse assessed as survival at 1 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1132519Antitumor activity against mouse B16 cells allografted in BDF1 mouse assessed as increase in survival time at 1 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID681132TP_TRANSPORTER: ATP hydrolysis in MDR1-expressing Sf9 cells2001The Journal of pharmacology and experimental therapeutics, Nov, Volume: 299, Issue:2
Rational use of in vitro P-glycoprotein assays in drug discovery.
AID127620The compound was evaluated in vivo for the optimal dose for activity against murine B-16 melanoma1988Journal of medicinal chemistry, Aug, Volume: 31, Issue:8
Benzothiopyranoindazoles, a new class of chromophore modified anthracenedione anticancer agents. Synthesis and activity against murine leukemias.
AID436879Antibacterial activity against imipenem-resistant Escherichia coli BL21(DE3) expressing VIM2 gene after 18 hrs by twofold serial broth dilution method2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID45652Survivors of CDF1 mice on day 4 after 1st injection of compound at 3 mg/kg in six mice; 6/61989Journal of medicinal chemistry, Aug, Volume: 32, Issue:8
Synthesis of unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones as potential antileukemic agents.
AID89435In vitro inhibitory activity against MCF-7 mammary cell line1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Synthesis and antitumor properties of an anthraquinone bisubstituted by the copper chelating peptide Gly-Gly-L-His.
AID153496In vivo antineoplastic activity was determined in BDF1 mice implanted with P388 leukemia and activity is expressed as T/C at 0.25 mg/kg1987Journal of medicinal chemistry, Sep, Volume: 30, Issue:9
Structural modification study of mitoxantrone (DHAQ). Chloro-substituted mono- and bis[(aminoalkyl)amino]anthraquinones.
AID67112Percent colony reduction in cell growth in EBV-positive nasopharyngeal cell lines after administration of 0.1 ug/mL dose1983Journal of medicinal chemistry, Dec, Volume: 26, Issue:12
Bis(bioreductive) alkylating agents: synthesis and biological activity in a nude mouse human carcinoma model.
AID211122Effect of dose dependent inhibition of TOPO II-catalyzed kDNA decatenation in vitro1994Journal of medicinal chemistry, Oct-28, Volume: 37, Issue:22
Inhibition of topoisomerase II catalytic activity by pyridoacridine alkaloids from a Cystodytes sp. ascidian: a mechanism for the apparent intercalator-induced inhibition of topoisomerase II.
AID681563TP_TRANSPORTER: Cytotoxicity in MT-4 and MT-4/DOX500 cells2003Molecular pharmacology, Jan, Volume: 63, Issue:1
Breast cancer resistance protein (BCRP/ABCG2) induces cellular resistance to HIV-1 nucleoside reverse transcriptase inhibitors.
AID436878Antibacterial activity against imipenem-non resistant Escherichia coli BL21(DE3) after 18 hrs by twofold serial broth dilution method2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID54626Apparent equilibrium constant for binding to calf thymus DNA by competitive displacement fluorometric assay2001Journal of medicinal chemistry, Sep-27, Volume: 44, Issue:20
Synthesis, antitumor cytotoxicity, and DNA-binding of novel N-5,2-di(omega-aminoalkyl)-2,6-dihydropyrazolo[3,4,5-kl]acridine-5-carboxamides.
AID1130182Antineoplastic activity against mouse P388 cells allografted in CDF1 mouse assessed as survival at 0.06 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1381975Antiproliferative activity against human HepG2 cells after 48 hrs by MTT assay2018European journal of medicinal chemistry, Feb-25, Volume: 146The lead optimization of the polyamine conjugate of flavonoid with a naphthalene motif: Synthesis and biological evaluation.
AID1525938Antiproliferative activity against human LCC6 cells assessed as reduction in cell viability after 5 days by MTS/PMS assay2019Journal of medicinal chemistry, 09-26, Volume: 62, Issue:18
Triazole Bridged Flavonoid Dimers as Potent, Nontoxic, and Highly Selective Breast Cancer Resistance Protein (BCRP/ABCG2) Inhibitors.
AID9611Inhibitory activity against human tumor cell line A0375 melanoma.1995Journal of medicinal chemistry, Feb-03, Volume: 38, Issue:3
Chromophore-modified antitumor anthracenediones: synthesis, DNA binding, and cytotoxic activity of 1,4-bis[(aminoalkyl)amino]benzo[g]-phthalazine-5,10-diones.
AID1233371Antiproliferative activity against human Ishikawa cells after 72 hrs by MTT assay2015Bioorganic & medicinal chemistry letters, Jul-01, Volume: 25, Issue:13
Synthesis and antiproliferative activity of some novel benzo-fused imidazo[1,8]naphthyridinones.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID135278Net log value for P388 leukemia cell kill in mice was determined1988Journal of medicinal chemistry, Aug, Volume: 31, Issue:8
Benzothiopyranoindazoles, a new class of chromophore modified anthracenedione anticancer agents. Synthesis and activity against murine leukemias.
AID255441Resistant factor as ability to overcome multidrug resistance of MES-SA/Dx5 cells compared to MES-SA cells2005Bioorganic & medicinal chemistry letters, Nov-15, Volume: 15, Issue:22
Design, synthesis, and antiproliferative activity of some novel aminosubstituted xanthenones, able to overcome multidrug resistance toward MES-SA/Dx5 cells.
AID1130152Antineoplastic activity against mouse B16 cells allografted in BDF1 mouse assessed as survival at 0.5 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID43704Cytotoxicity in human leukemic CCRF-CEM cells.2003Journal of medicinal chemistry, Dec-18, Volume: 46, Issue:26
Bisintercalating threading diacridines: relationships between DNA binding, cytotoxicity, and cell cycle arrest.
AID594148Antiproliferative activity against human SKOV3 cells after 48 hrs by XTT assay2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Synthesis and antiproliferative activity of new cytotoxic azanaphthoquinone pyrrolo-annelated derivatives: Part II.
AID1903856Antitumor immunity against human U2OS cells expressing HMGBI-GFP fusion protein assessed as accumulation HMGBI-GFP fusion protein at 3 uM measured upto 24 hrs by live cell microscopic analysis2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Biological Investigation of a Water-Soluble Isoginkgetin-Phosphate Analogue, Targeting the Spliceosome with
AID687165Ratio of IC50 for human K562/HHT300 cells to IC50 for human K562 cells2012Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11
Structure-activity relationship (SAR) study of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and the potential of the lead against multidrug resistance in cancer treatment.
AID536041Resistance index, ratio of IC50 for human HL60/MX2 cells to IC50 for human HL60 cells2010Bioorganic & medicinal chemistry, Nov-15, Volume: 18, Issue:22
Indeno[1,2-c]isoquinolin-5,11-diones conjugated to amino acids: Synthesis, cytotoxicity, DNA interaction, and topoisomerase II inhibition properties.
AID26757DNA binding dissociation constant as KD; No data1984Journal of medicinal chemistry, Apr, Volume: 27, Issue:4
Interactions of antitumor drugs with natural DNA: 1H NMR study of binding mode and kinetics.
AID253343Cytotoxicity against human H460M cancer cell line was determined after 1 hr2004Journal of medicinal chemistry, Oct-07, Volume: 47, Issue:21
Rational design, synthesis, and biological evaluation of bis(pyrimido[5,6,1-de]acridines) and bis(pyrazolo[3,4,5-kl]acridine-5-carboxamides) as new anticancer agents.
AID431400Ratio of GI50 for human HL60/MX2 cells to GI50 for human HL60 cells2009Journal of medicinal chemistry, Oct-08, Volume: 52, Issue:19
Structure-activity relationship and molecular mechanisms of ethyl 2-amino-4-(2-ethoxy-2-oxoethyl)-6-phenyl-4h-chromene-3-carboxylate (sha 14-1) and its analogues.
AID683858Antiproliferative activity against human MESSA/DX5 cells after 72 hrs by SRB assay2012Bioorganic & medicinal chemistry letters, Oct-01, Volume: 22, Issue:19
New derivatives of 11-methyl-6-[2-(dimethylamino)ethyl]-6H-indolo[2,3-b]quinoline as cytotoxic DNA topoisomerase II inhibitors.
AID538479Cytotoxicity against human HL60 cells by MTT assay2010Bioorganic & medicinal chemistry letters, Dec-01, Volume: 20, Issue:23
Oleanane-type triterpenoids from Panax stipuleanatus and their anticancer activities.
AID106294Tested against MXF7 breast carcinoma (sensitive) cell line in the sulforhodamine B assay.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID170463Cardiotoxicity by a neonatal rat heart myocyte assay1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID83759Inhibitory activity against human tumor cell line HT-29.1995Journal of medicinal chemistry, Feb-03, Volume: 38, Issue:3
Chromophore-modified antitumor anthracenediones: synthesis, DNA binding, and cytotoxic activity of 1,4-bis[(aminoalkyl)amino]benzo[g]-phthalazine-5,10-diones.
AID721754Inhibition of human MATE1-mediated ASP+ uptake expressed in HEK293 cells after 1.5 mins by fluorescence assay2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID95160Compound was tested in vitro for cytotoxicity against MDR cell line K562R (72 hr exposure to compound)1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID540212Mean residence time in human after iv administration2008Drug 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.
AID83793Percent inhibition at S phase of cell cycle at a dose of 100n g/mL after 72 hours of induction in HT-29 cell line1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID647964Cytotoxicity against human H1299 cells assessed as cell growth at 100 uM after 48 hrs by MTT assay2012European journal of medicinal chemistry, Apr, Volume: 50Design, synthesis and evaluation of telomerase inhibitory, hTERT repressing, and anti-proliferation activities of symmetrical 1,8-disubstituted amidoanthraquinones.
AID592674Cytotoxicity against human A549 cells by MTT assay2011Bioorganic & medicinal chemistry, Apr-15, Volume: 19, Issue:8
Cytotoxic and anti-inflammatory cembranoids from the Vietnamese soft coral Lobophytum laevigatum.
AID1132509Toxicity in mouse P388 cells allografted BDF1 mouse assessed as body weight difference at 0.5 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID1550896Antitumor activity against mouse H22 cells allografted in immunocompetent Balb/c mouse assessed as decrease in lump formation at challenge site at 2 uM incubated with cells for 5 hrs followed by compound washout prior to vaccination and subsequent H22 cel2019European journal of medicinal chemistry, Jun-01, Volume: 171Naphthyl quinoxaline thymidine conjugate is a potent anticancer agent post UVA activation and elicits marked inhibition of tumor growth through vaccination.
AID678963TP_TRANSPORTER: uptake in BCRP-expressing oocyte cells2003Molecular pharmacology, Dec, Volume: 64, Issue:6
Functional characterization of human breast cancer resistance protein (BCRP, ABCG2) expressed in the oocytes of Xenopus laevis.
AID1349085Inhibition of NAE-mediated Ubcl2-NEDD8 conjugation in human Caco2 cells after 16 hrs by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID84123Effect of compound as percent survival at dose of 250 ng/mL on HT-29/Mx cell line after 72 hours1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1882975Antitumor activity against mouse 4T1 cells implanted in Balb/c mouse assessed as apoptotic rate of dissected tumor cell at 50 mg/kg administered intratumorally every four days for 14 days in the presence of liquid cyanoacrylate by flow cytometric analysis2022European journal of medicinal chemistry, Jul-05, Volume: 237Design, synthesis, and evaluation of a novel series of mono-indolylbenzoquinones derivatives for the potential treatment of breast cancer.
AID1519982Inhibition of Nedd8-cullin1 adduct formation in human A549 cells assessed as decrease in cullin1 neddylation at 75 uM measured after 6 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID381806Growth inhibition of human K562 cells after 72 hrs by MTS method2008Bioorganic & medicinal chemistry, Apr-01, Volume: 16, Issue:7
The structure-based design, synthesis and biological evaluation of DNA-binding bisintercalating bisanthrapyrazole anticancer compounds.
AID733197Antiproliferative activity against human SKOV3 cells after 48 hrs2013Bioorganic & medicinal chemistry letters, Mar-15, Volume: 23, Issue:6
Synthesis and biological evaluation of new cytotoxic indazolo[4,3-gh]isoquinolinone derivatives.
AID98865Percentage increase in lifespan of mice in L1210 leukemia cells (in vivo) at 0.4 mg/kg (cumulative dose 6.8 mg/Kg) with ip day 1,5&9 (once daily)1988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID100154Number of tumor free survivors of mice was measured (in vivo) at a 0.75 mg/kg dose (cumulative dose 225 mg/kg)1988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID202783Percentage of tumor free survivors of mice at 0.75 mg/kg (cumulative dose 525 mg/Kg) introduced (in vivo) ip; value given as 0/101988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID1430726Toxicity in Balb/c mouse assessed as body weight loss at 3 mg/kg, iv encapsulated within cucurbit[8]uril administered twice weekly for 2 weeks2017ACS medicinal chemistry letters, May-11, Volume: 8, Issue:5
Encapsulation of Mitoxantrone within Cucurbit[8]uril Decreases Toxicity and Enhances Survival in a Mouse Model of Cancer.
AID221330Tested for inhibitory activity against human tumor cell line A549 (a non small, drug resistant cell line that does not produce P-glycoprotein) of lung carcinoma using sulforhodamine B assay.2000Journal of medicinal chemistry, Aug-10, Volume: 43, Issue:16
Analogues of amonafide and azonafide with novel ring systems.
AID102203In vitro cytotoxicity on human colon adenocarcinoma (LoVo ) tumor cell line.1998Journal of medicinal chemistry, Dec-31, Volume: 41, Issue:27
Synthesis and antitumor evaluation of 2,5-disubstituted-indazolo[4, 3-gh]isoquinolin-6(2H)-ones (9-aza-anthrapyrazoles).
AID212547Inhibition of Taq polymerase at 50 uM (Total inhibition)1998Journal of medicinal chemistry, Aug-13, Volume: 41, Issue:17
1,4- and 2,6-disubstituted amidoanthracene-9,10-dione derivatives as inhibitors of human telomerase.
AID729386Inhibition of CHK2 (unknown origin) using [gamma33P]ATP assessed as residual activity at 1 uM after 120 mins by radiometric assay2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID145445Inhibitory activity against OVCAR-3 cell line1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID594152Antiproliferative activity against human RKOp27IND cells after 48 hrs by XTT assay2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Synthesis and antiproliferative activity of new cytotoxic azanaphthoquinone pyrrolo-annelated derivatives: Part II.
AID83927Effect of compound as percent survival at dose of 25 ng/mL on HT-29 cell line after 72 hours1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID681121TP_TRANSPORTER: inhibition of Calcein-AM efflux in MDR1-expressing MDCKII cells2001The Journal of pharmacology and experimental therapeutics, Nov, Volume: 299, Issue:2
Rational use of in vitro P-glycoprotein assays in drug discovery.
AID136072Antileukemic activity towards P388 Murine Leukemia at a dose of 0.8 mg/kg1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID230916Ratio of antilog(mean log IC90 in bone marrow sample) and antolog(mean log IC90) in HL-60)1999Journal of medicinal chemistry, Jun-17, Volume: 42, Issue:12
Design and synthesis of modified quinolones as antitumoral acridones.
AID380014Cytotoxicity against human MKN28 cells after 48 hrs by MTT assay2000Journal of natural products, May, Volume: 63, Issue:5
New 7,20:14,20-diepoxy ent-kauranoids from Isodon xerophilus.
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID215072An average for IC50 values in the two solid tumor cell lines.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID721743Ratio of Cmax unbound to IC50 for human MATE1-mediated [14]-metformin uptake expressed in HEK293 cells2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID524791Antiplasmodial activity against Plasmodium falciparum 7G8 after 72 hrs by SYBR green assay2009Nature chemical biology, Oct, Volume: 5, Issue:10
Genetic mapping of targets mediating differential chemical phenotypes in Plasmodium falciparum.
AID588216FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID153497In vivo antineoplastic activity was determined in BDF1 mice implanted with P388 leukemia and activity is expressed as T/C at 0.5 mg/kg1987Journal of medicinal chemistry, Sep, Volume: 30, Issue:9
Structural modification study of mitoxantrone (DHAQ). Chloro-substituted mono- and bis[(aminoalkyl)amino]anthraquinones.
AID102184Inhibitory activity against human colon adenocarcinoma cell line LoVo.1995Journal of medicinal chemistry, Feb-03, Volume: 38, Issue:3
Chromophore-modified antitumor anthracenediones: synthesis, DNA binding, and cytotoxic activity of 1,4-bis[(aminoalkyl)amino]benzo[g]-phthalazine-5,10-diones.
AID320436Cytotoxicity against human PC3 cells after 48 hrs by SRB assay2008Bioorganic & medicinal chemistry, Jan-15, Volume: 16, Issue:2
Synthesis, DNA binding, and cytotoxicity of 1,4-bis(2-amino-ethylamino)anthraquinone-amino acid conjugates.
AID106293Tested against MXF7 breast carcinoma (mitoxantrone resistant)cell line in the sulforhodamine B assay.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID110796Number of mice(with Colon 38 tumors) cured after treatment of 3.9 mg/kg/day dose given as 3 times in a day for 4 days out of 5 mice2003Journal of medicinal chemistry, Mar-13, Volume: 46, Issue:6
Synthesis and cytotoxic activity of carboxamide derivatives of benzo[b][1,6]naphthyridines.
AID1430725Toxicity in Balb/c mouse assessed as body weight loss at 2 mg/kg, iv administered twice weekly for 2 weeks relative to control2017ACS medicinal chemistry letters, May-11, Volume: 8, Issue:5
Encapsulation of Mitoxantrone within Cucurbit[8]uril Decreases Toxicity and Enhances Survival in a Mouse Model of Cancer.
AID594147Antiproliferative activity against human KB/HeLa cells after 48 hrs by XTT assay2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Synthesis and antiproliferative activity of new cytotoxic azanaphthoquinone pyrrolo-annelated derivatives: Part II.
AID236912Permeability Coefficient in 2/4/A1 cell model2005Journal of medicinal chemistry, Jan-27, Volume: 48, Issue:2
Exploring the role of different drug transport routes in permeability screening.
AID1550889Induction of immunogenic cell death in mouse H22 cells assessed as increase in extracellular HMGB1 level at 2 uM incubated for 5 hrs by ELISA2019European journal of medicinal chemistry, Jun-01, Volume: 171Naphthyl quinoxaline thymidine conjugate is a potent anticancer agent post UVA activation and elicits marked inhibition of tumor growth through vaccination.
AID1506782Induction of apoptosis in human HCC78 cells assessed as necrotic cells level at 5 nM incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry (Rvb = 0.06%)2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID1381973Antiproliferative activity against human HeLa cells after 48 hrs by MTT assay2018European journal of medicinal chemistry, Feb-25, Volume: 146The lead optimization of the polyamine conjugate of flavonoid with a naphthalene motif: Synthesis and biological evaluation.
AID127618In vivo for the optimal dose for activity against P388 leukemia per injection1988Journal of medicinal chemistry, Aug, Volume: 31, Issue:8
Benzothiopyranoindazoles, a new class of chromophore modified anthracenedione anticancer agents. Synthesis and activity against murine leukemias.
AID54632Binding affinity towards calf thymus DNA1999Journal of medicinal chemistry, Jul-15, Volume: 42, Issue:14
2,3-Dihydro-1H,7H-pyrimido[5,6,1-de]acridine-1,3,7-trione derivatives, a class of cytotoxic agents active on multidrug-resistant cell lines: synthesis, biological evaluation, and structure-activity relationships.
AID1883023Toxicity in Balb/c mouse implanted with mouse 4T1 cells assessed as lung lesions at 50 mg/kg administered intratumorally every four days for 14 days in the presence of liquid cyanoacrylate by H&E staining based histopathological analysis2022European journal of medicinal chemistry, Jul-05, Volume: 237Design, synthesis, and evaluation of a novel series of mono-indolylbenzoquinones derivatives for the potential treatment of breast cancer.
AID729381Inhibition of human recombinant casein kinase 2 using [gamma-32P] ATP2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID729388Inhibition of CK2alpha2 (unknown origin) using [gamma33P]ATP assessed as residual activity at 1 uM after 120 mins by radiometric assay2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID211285Inhibition of commercially obtained pure Drosophila Topoisomerase II in catalytic DNA unwinding.1995Journal of medicinal chemistry, Oct-27, Volume: 38, Issue:22
Topoisomerase II-mediated DNA cleavage by adocia- and xestoquinones from the Philippine sponge Xestospongia sp.
AID595064Resistant factor, ratio of IC50 for doxorubicin-resistant human MES-SA/Dx5 cells to IC50 for doxorubicin-sensitive human MES-SA cells2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Design, synthesis and antiproliferative activity of novel aminosubstituted benzothiopyranoisoindoles.
AID1525939Resistance factor, ratio of IC50 for human HEK293/R2 cells overexpressing BCRP to IC50 for human HEK293 cells2019Journal of medicinal chemistry, 09-26, Volume: 62, Issue:18
Triazole Bridged Flavonoid Dimers as Potent, Nontoxic, and Highly Selective Breast Cancer Resistance Protein (BCRP/ABCG2) Inhibitors.
AID200624Cytotoxicity against human SCLC cells resistant to cisplatin (SCLC/CDDP)1993Journal of medicinal chemistry, Dec-10, Volume: 36, Issue:25
Design of antineoplastic agents on the basis of the "2-phenylnaphthalene-type" structural pattern. 2. Synthesis and biological activity studies of benzo]b]naphtho[2,3-d]furan-6,11-dione derivatives.
AID270855Antiproliferative activity against doxorubicin-resistant MES-SA/Dx5 cells by MTT assay after 72 hrs2006Bioorganic & medicinal chemistry letters, Sep-15, Volume: 16, Issue:18
Synthesis and antiproliferative activity of substituted benzopyranoisoindoles: a new class of cytotoxic compounds.
AID1381974Antiproliferative activity against human K562 cells after 48 hrs by MTT assay2018European journal of medicinal chemistry, Feb-25, Volume: 146The lead optimization of the polyamine conjugate of flavonoid with a naphthalene motif: Synthesis and biological evaluation.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID253340Cytotoxicity against human PC3 cancer cell line was determined after 1 hr2004Journal of medicinal chemistry, Oct-07, Volume: 47, Issue:21
Rational design, synthesis, and biological evaluation of bis(pyrimido[5,6,1-de]acridines) and bis(pyrazolo[3,4,5-kl]acridine-5-carboxamides) as new anticancer agents.
AID227751Concentration required to reduce ethidium bromide fluorescence to 50% of control in presence of calf thymus DNA; ND is Not Determined.1994Journal of medicinal chemistry, Oct-28, Volume: 37, Issue:22
Inhibition of topoisomerase II catalytic activity by pyridoacridine alkaloids from a Cystodytes sp. ascidian: a mechanism for the apparent intercalator-induced inhibition of topoisomerase II.
AID201633The IC50 value was measured on human breast cancer cell line SK-BR-3.1995Journal of medicinal chemistry, Mar-17, Volume: 38, Issue:6
Synthesis and biological activity of thiazolylindolequinones, analogues of the natural product BE 10988.
AID98403Tested in vitro against murine L1210 leukemia.1987Journal of medicinal chemistry, Jan, Volume: 30, Issue:1
Anthrapyrazole anticancer agents. Synthesis and structure-activity relationships against murine leukemias.
AID1550875Cytotoxicity against human A375 cells assessed as reduction in cell viability preincubated for 5 hrs followed by compound washout and measured after 48 hrs by CCK8 assay2019European journal of medicinal chemistry, Jun-01, Volume: 171Naphthyl quinoxaline thymidine conjugate is a potent anticancer agent post UVA activation and elicits marked inhibition of tumor growth through vaccination.
AID771325Cytotoxicity against human NCI-H460 cells after 48 hrs by resazurin dye assay2013Bioorganic & medicinal chemistry letters, Oct-01, Volume: 23, Issue:19
Synthesis and antiproliferative activity of new cytotoxic tri- and tetraazabenzo[3,2-a]fluorene-5,6-dione derivatives.
AID524796Antiplasmodial activity against Plasmodium falciparum W2 after 72 hrs by SYBR green assay2009Nature chemical biology, Oct, Volume: 5, Issue:10
Genetic mapping of targets mediating differential chemical phenotypes in Plasmodium falciparum.
AID232016Resistance index is the ratio of IC50 of resistant cell line/IC50 of sensitive cell line1994Journal of medicinal chemistry, Mar-18, Volume: 37, Issue:6
6,9-Bis[(aminoalkyl)amino]benzo[g]isoquinoline-5,10-diones. A novel class of chromophore-modified antitumor anthracene-9,10-diones: synthesis and antitumor evaluations.
AID1132488Antitumor activity against mouse P388 cells allografted in BDF1 mouse assessed as mouse survival at 2 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID255803In vitro cytotoxicity against murine leukemia cell line L12102005Bioorganic & medicinal chemistry letters, Nov-15, Volume: 15, Issue:22
Design, synthesis, and antiproliferative activity of some novel aminosubstituted xanthenones, able to overcome multidrug resistance toward MES-SA/Dx5 cells.
AID232812Toxicity ratio of quotient of the IC50 in myocytes divided by the average IC50 for three tumor cell lines1995Journal of medicinal chemistry, Mar-17, Volume: 38, Issue:6
Amino-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H- dibenz[de,h]isoquinoline-1,3-diones. Synthesis, antitumor activity, and quantitative structure--activity relationship.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID46135Inhibitory concentration against ethidium:Calf thymus DNA (1.26:1) binding at pH 71997Journal of medicinal chemistry, Nov-07, Volume: 40, Issue:23
1-[(omega-aminoalkyl)amino]-4-[N-(omega-aminoalkyl)carbamoyl]-9-oxo-9, 10-dihydroacridines as intercalating cytotoxic agents: synthesis, DNA binding, and biological evaluation.
AID680987TP_TRANSPORTER: inhibition of MTX update by Mitoxantrone at a concentration of 50uM in membrane vesicles from BCRP-expressing MCF7 cells2003Cancer research, Sep-01, Volume: 63, Issue:17
Wild-type breast cancer resistance protein (BCRP/ABCG2) is a methotrexate polyglutamate transporter.
AID1197745Inhibition of human OATP1B3-mediated [3H]CCK-8 at 100 uM after 5 mins relative to control2015European journal of medicinal chemistry, Mar-06, Volume: 92Interaction of human organic anion transporter polypeptides 1B1 and 1B3 with antineoplastic compounds.
AID255789In vitro cytotoxicity against uterine sarcoma MES-SA cells2005Bioorganic & medicinal chemistry letters, Nov-15, Volume: 15, Issue:22
Design, synthesis, and antiproliferative activity of some novel aminosubstituted xanthenones, able to overcome multidrug resistance toward MES-SA/Dx5 cells.
AID102168In vitro Cytotoxic activity of compound in comparison with reference compounds in human cell line LoVo1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID272492Antiproliferative activity against MDA435/LCC6 cells by ELISA2006Journal of medicinal chemistry, Nov-16, Volume: 49, Issue:23
Flavonoid dimers as bivalent modulators for P-glycoprotein-based multidrug resistance: synthetic apigenin homodimers linked with defined-length poly(ethylene glycol) spacers increase drug retention and enhance chemosensitivity in resistant cancer cells.
AID95161Compound was tested in vitro for cytotoxicity against MDR cell line K562R (RI) (72 hr exposure to compound)1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID100158Number of tumor free survivors of mice was measured in L1210 leukemia cells (in vivo) at 0.4 mg/kg (cumulative dose 6.8 mg/Kg) with ip day 1,5&9 (once daily)1988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID230914Ratio of antilog(mean log IC50 in bone marrow sample) and antolog(mean log IC50) in HL-60)1999Journal of medicinal chemistry, Jun-17, Volume: 42, Issue:12
Design and synthesis of modified quinolones as antitumoral acridones.
AID1550873Cytotoxicity against human MCF7 cells assessed as reduction in cell viability preincubated for 5 hrs followed by compound washout and measured after 48 hrs by CCK8 assay2019European journal of medicinal chemistry, Jun-01, Volume: 171Naphthyl quinoxaline thymidine conjugate is a potent anticancer agent post UVA activation and elicits marked inhibition of tumor growth through vaccination.
AID681515TP_TRANSPORTER: cell accumulation in MCF7/MRP1-M24 cells2006Molecular pharmacology, Apr, Volume: 69, Issue:4
Multidrug resistance protein 1 (MRP1, ABCC1) mediates resistance to mitoxantrone via glutathione-dependent drug efflux.
AID220579Binding affinity towards [poly(dA-dT)]21999Journal of medicinal chemistry, Jul-15, Volume: 42, Issue:14
2,3-Dihydro-1H,7H-pyrimido[5,6,1-de]acridine-1,3,7-trione derivatives, a class of cytotoxic agents active on multidrug-resistant cell lines: synthesis, biological evaluation, and structure-activity relationships.
AID102033In vitro cytotoxic activity against human colon adenocarcinoma resistant to doxorubicin (LoVo Dx) cells.2000Bioorganic & medicinal chemistry letters, Feb-07, Volume: 10, Issue:3
Synthesis and antitumor activities of 5-methyl-1- and 2-[[2-dimethylaminoethyl]amino]-aza-thiopyranoindazoles.
AID1349101Inhibition of NAE in human Caco2 cells assessed as increase in phosphorylated NF-kappaB protein levels at 0.1 to 10 uM after 16 hrs by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID602041Cytotoxicity against human HL60 cells after 24 hrs by MTT assay2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Cytotoxic and PPARs transcriptional activities of sterols from the Vietnamese soft coral Lobophytum laevigatum.
AID1525940Resistance factor, ratio of IC50 for human 2008/MRP1 cells overexpressing MRP1 to IC50 for human 2008 cells2019Journal of medicinal chemistry, 09-26, Volume: 62, Issue:18
Triazole Bridged Flavonoid Dimers as Potent, Nontoxic, and Highly Selective Breast Cancer Resistance Protein (BCRP/ABCG2) Inhibitors.
AID1130161Antineoplastic activity against mouse Colon 26 cells allografted in CDF1 mouse at 0.39 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1209583Unbound drug partitioning coefficient, Kp of the compound assessed as ratio of unbound concentration in Sprague-Dawley rat brain to unbound concentration in plasma2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID687168Ratio of IC50 for human CCRF-CEM/VLB100 cells IC50 for human CCRF-CEM cells2012Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11
Structure-activity relationship (SAR) study of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and the potential of the lead against multidrug resistance in cancer treatment.
AID1506789Induction of apoptosis in human HCC78 cells assessed as late apoptotic cells level at 20 nM incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry (Rvb = 13.8%)2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID699540Inhibition of human liver OATP1B3 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E17-betaG uptake at 20 uM incubated for 5 mins by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID1167196Intrinsic cytotoxicity against HEK293 cells assessed as reduction in cell viability after 72 hrs by MTT assay2015Journal of medicinal chemistry, Jan-08, Volume: 58, Issue:1
Converting potent indeno[1,2-b]indole inhibitors of protein kinase CK2 into selective inhibitors of the breast cancer resistance protein ABCG2.
AID1474537Cytotoxicity against human HL60 cells after 72 hrs by sulforhodamine B assay2017European journal of medicinal chemistry, May-26, Volume: 132Novel phosphonate analogs of sulforaphane: Synthesis, in vitro and in vivo anticancer activity.
AID594149Antiproliferative activity against human SF268 cells after 48 hrs by XTT assay2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Synthesis and antiproliferative activity of new cytotoxic azanaphthoquinone pyrrolo-annelated derivatives: Part II.
AID98386Antitumor activity against murine leukemia L1210 cell line.1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID1070861Inhibition of human tert transcriptional activity assessed as SEAP activity at 1 uM after 24 hrs by SEAP reporter assay2013European journal of medicinal chemistry, Nov, Volume: 69Structure-based design, synthesis and biological evaluation of novel anthra[1,2-d]imidazole-6,11-dione homologues as potential antitumor agents.
AID436872Inhibition of IMP1 using nitrocefin as substrate at 56 uM after 15 mins by microtiter plate assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID1221961Apparent permeability from basolateral to apical side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of P-gp inhibitor LY3359792011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1711948Cytotoxicity against human QSG7701 cells assessed as inhibition of cell proliferation at 5 uM measured after 48 hrs by MTT assay relative to control2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID1053262Agonist activity at human recombinant dopamine D2 long receptor expressed in CHOK1 cells coexpressing mitochondrial apoaequorin at 100 uM by luminometric analysis relative to quinpirol2013Journal of medicinal chemistry, Nov-14, Volume: 56, Issue:21
Experimental confirmation of new drug-target interactions predicted by Drug Profile Matching.
AID8485Tested against A549 lung carcinoma in the sulforhodamine B assay.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID1271103Cytotoxicity against rat 5RP7 cells after 24 hrs by MTT assay2016European journal of medicinal chemistry, Jan-01, Volume: 107Synthesis and evaluation of bis-thiazole derivatives as new anticancer agents.
AID1711943Antiproliferative activity against human HepG2 cells assessed as inhibition of cell proliferation at 1 uM measured after 48 hrs by MTT assay relative to control2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID437515Binding affinity to tau stem-loop RNA assessed as inhibition of RNA stem-loop unfolding2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Mitoxantrone analogues as ligands for a stem-loop structure of tau pre-mRNA.
AID84114Percent inhibition at S phase of cell cycle at a dose of 1000 ng/mL after 72 hours of induction in HT-29/Mx cell line1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1506779Induction of apoptosis in human HCC78 cells assessed as viable cells level at 5 nM incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry (Rvb = 80.8%)2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID202961Cytotoxic potency required to inhibit SKOV-3 cell growth 50%1997Journal of medicinal chemistry, Nov-07, Volume: 40, Issue:23
1-[(omega-aminoalkyl)amino]-4-[N-(omega-aminoalkyl)carbamoyl]-9-oxo-9, 10-dihydroacridines as intercalating cytotoxic agents: synthesis, DNA binding, and biological evaluation.
AID1349097Inhibition of NAE in human Caco2 cells assessed as increase in c-myc protein levels after 16 hrs by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID54438In vitro inhibition of calf thymus DNA/ethidium bromide complex formation.2002Journal of medicinal chemistry, Jun-06, Volume: 45, Issue:12
Design, synthesis, and antiproliferative activity of some new pyrazole-fused amino derivatives of the pyranoxanthenone, pyranothioxanthenone, and pyranoacridone ring systems: a new class of cytotoxic agents.
AID1439468Cytotoxicity against mouse L1210 cells assessed as reduction in cell viability after 24 hrs by MTT assay2017European journal of medicinal chemistry, Mar-31, Volume: 129Allylic isothiouronium salts: The discovery of a novel class of thiourea analogues with antitumor activity.
AID687166Ratio of IC50 for human CCRF-CEM/C2 cells IC50 for human CCRF-CEM cells2012Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11
Structure-activity relationship (SAR) study of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and the potential of the lead against multidrug resistance in cancer treatment.
AID1520331Cytotoxicity against human A549 cells after 48 hrs by MTT assay2019European journal of medicinal chemistry, Mar-15, Volume: 166All that glitters is not gold: Panning cytotoxic natural products and derivatives with a fused tricyclic backbone by the estimation of their leadlikeness for cancer treatment.
AID97252Compound was tested against L1210 leukemia at % increase in life span (ILS) in mice at 1.6 mg/kg dosage.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID733194Antiproliferative activity against human NCI-H460 cells after 48 hrs2013Bioorganic & medicinal chemistry letters, Mar-15, Volume: 23, Issue:6
Synthesis and biological evaluation of new cytotoxic indazolo[4,3-gh]isoquinolinone derivatives.
AID1506783Induction of apoptosis in human HCC78 cells assessed as viable cells level at 10 nM incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry (Rvb = 80.8%)2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID236914Permeability Coefficient in hexadecane membranes model2005Journal of medicinal chemistry, Jan-27, Volume: 48, Issue:2
Exploring the role of different drug transport routes in permeability screening.
AID681522TP_TRANSPORTER: ATP- and GSH-dependent transport in MCF7/MRP1-10 cells2006Molecular pharmacology, Apr, Volume: 69, Issue:4
Multidrug resistance protein 1 (MRP1, ABCC1) mediates resistance to mitoxantrone via glutathione-dependent drug efflux.
AID683857Antiproliferative activity against human MESSA cells after 72 hrs by SRB assay2012Bioorganic & medicinal chemistry letters, Oct-01, Volume: 22, Issue:19
New derivatives of 11-methyl-6-[2-(dimethylamino)ethyl]-6H-indolo[2,3-b]quinoline as cytotoxic DNA topoisomerase II inhibitors.
AID1221964Transporter substrate index ratio of permeability from basolateral to apical side in human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of P-gp inhibitor LY3359792011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID230379Resistance index measured as the ratio of IC50 of LoVo/Dx cell line to that of LoVo cell line.1998Journal of medicinal chemistry, Dec-31, Volume: 41, Issue:27
Synthesis and antitumor evaluation of 2,5-disubstituted-indazolo[4, 3-gh]isoquinolin-6(2H)-ones (9-aza-anthrapyrazoles).
AID562241Antimycobacterial activity against Mycobacterium smegmatis grown in carbon-limited broth medium assessed as growth inhibition in mid-logarithmic phase by spectrophotometry2009Antimicrobial agents and chemotherapy, Dec, Volume: 53, Issue:12
Modifying culture conditions in chemical library screening identifies alternative inhibitors of mycobacteria.
AID1207752Inhibition of Cav1.2 current measured using QPatch automatic path clamp system in CHO cells expressing Cav1.2, beta-2 and alpha-2/delta-1 subunits2013Scientific reports, , Volume: 3MICE models: superior to the HERG model in predicting Torsade de Pointes.
AID381809Inhibition of human topoisomerase 2alpha decantation activity2008Bioorganic & medicinal chemistry, Apr-01, Volume: 16, Issue:7
The structure-based design, synthesis and biological evaluation of DNA-binding bisintercalating bisanthrapyrazole anticancer compounds.
AID107945In vivo antitumor activity at a single dose of 12.5 mg/kg & 37.5 mg/kg total against mammary adenocarcinoma 16C1984Journal of medicinal chemistry, Mar, Volume: 27, Issue:3
5-[(Aminoalkyl)amino]-substituted anthra[1,9-cd]pyrazol-6(2H)-ones as novel anticancer agents. Synthesis and biological evaluation.
AID137725Percentage ratio of treated animals to cured animals against murine B-16 melanoma (day 60 surv)1988Journal of medicinal chemistry, Aug, Volume: 31, Issue:8
Benzothiopyranoindazoles, a new class of chromophore modified anthracenedione anticancer agents. Synthesis and activity against murine leukemias.
AID1130168Antineoplastic activity against mouse L1210 cells allografted in CDF1 mouse assessed as survival at 2 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID375434Displacement of [3H]PSB0413 from human platelet P2Y12 receptor at 10 uM2009Journal of medicinal chemistry, Jun-25, Volume: 52, Issue:12
High-affinity, non-nucleotide-derived competitive antagonists of platelet P2Y12 receptors.
AID429711Cytotoxicity against human U937 cells by MTT assay2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
C29 sterols with a cyclopropane ring at C-25 and 26 from the Vietnamese marine sponge Ianthella sp. and their anticancer properties.
AID721749Inhibition of human OCT3-mediated ASP+ uptake expressed in HEK293 cells after 3 mins by fluorescence assay2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID429709Cytotoxicity against human MCF7 cells by MTT assay2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
C29 sterols with a cyclopropane ring at C-25 and 26 from the Vietnamese marine sponge Ianthella sp. and their anticancer properties.
AID1130167Antineoplastic activity against mouse L1210 cells allografted in CDF1 mouse at 4 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID537733Binding affinity to Candida albicans CaCdr1p expressed in yeast AD1-8u2010European journal of medicinal chemistry, Nov, Volume: 45, Issue:11
Analysis of physico-chemical properties of substrates of ABC and MFS multidrug transporters of pathogenic Candida albicans.
AID588977Substrates of transporters of clinical importance in the absorption and disposition of drugs, MRP22010Nature reviews. Drug discovery, Mar, Volume: 9, Issue:3
Membrane transporters in drug development.
AID729375Effect on total PIM1 level in human MV411 cells at 10 to 100 nM after 12 hrs by Western blotting analysis2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID137724Percentage ratio of treated animals to cured animals against P388 leukemia (day 30 surv)1988Journal of medicinal chemistry, Aug, Volume: 31, Issue:8
Benzothiopyranoindazoles, a new class of chromophore modified anthracenedione anticancer agents. Synthesis and activity against murine leukemias.
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID242838Concentration required to displace ethidium from CT-DNA was determined from fluorescence binding studies2004Journal of medicinal chemistry, Oct-07, Volume: 47, Issue:21
Rational design, synthesis, and biological evaluation of bis(pyrimido[5,6,1-de]acridines) and bis(pyrazolo[3,4,5-kl]acridine-5-carboxamides) as new anticancer agents.
AID236269Fraction absorbed in human intestine after oral administration compound was measured; NA=Not available2005Journal of medicinal chemistry, Jan-27, Volume: 48, Issue:2
Exploring the role of different drug transport routes in permeability screening.
AID429710Cytotoxicity against human SKOV3 cells by MTT assay2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
C29 sterols with a cyclopropane ring at C-25 and 26 from the Vietnamese marine sponge Ianthella sp. and their anticancer properties.
AID248040Cytotoxicity against human MKN45 cancer cell line was determined after 144 hr2004Journal of medicinal chemistry, Oct-07, Volume: 47, Issue:21
Rational design, synthesis, and biological evaluation of bis(pyrimido[5,6,1-de]acridines) and bis(pyrazolo[3,4,5-kl]acridine-5-carboxamides) as new anticancer agents.
AID135719The compound was tested for antitumor activity against P388 murine leukemia by measuring median survival time of treated mice/median survival time of control x 1001994Journal of medicinal chemistry, Mar-18, Volume: 37, Issue:6
6,9-Bis[(aminoalkyl)amino]benzo[g]isoquinoline-5,10-diones. A novel class of chromophore-modified antitumor anthracene-9,10-diones: synthesis and antitumor evaluations.
AID524795Antiplasmodial activity against Plasmodium falciparum HB3 after 72 hrs by SYBR green assay2009Nature chemical biology, Oct, Volume: 5, Issue:10
Genetic mapping of targets mediating differential chemical phenotypes in Plasmodium falciparum.
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID272510Antiproliferative activity against multidrug resistant MDA435/LCC6 cells in presence of 5 uM 1,13-bis[4'-((5,7-dihydroxy)-4H-chromen-4-on-2-yl)phenyl]-1,4,7,10,13-pentaoxatridecane by ELISA2006Journal of medicinal chemistry, Nov-16, Volume: 49, Issue:23
Flavonoid dimers as bivalent modulators for P-glycoprotein-based multidrug resistance: synthetic apigenin homodimers linked with defined-length poly(ethylene glycol) spacers increase drug retention and enhance chemosensitivity in resistant cancer cells.
AID466796Growth inhibition of human HL60 cells by MTT assay2010Bioorganic & medicinal chemistry letters, Mar-01, Volume: 20, Issue:5
Triterpene compounds isolated from Acer mandshuricum and their anti-inflammatory activity.
AID322369Inhibition of human BCRP mediated mitoxantrone accumulation in wild type MCF7 cells at 5 uM by flow cytometry2008Bioorganic & medicinal chemistry, Jan-01, Volume: 16, Issue:1
Functionalized chalcones as selective inhibitors of P-glycoprotein and breast cancer resistance protein.
AID1129361Unbound fraction in HEK293 cell homogenate at 0.1 uM by equilibrium dialysis based UPLC-MS/MS analysis2014Journal of medicinal chemistry, Apr-10, Volume: 57, Issue:7
A high-throughput cell-based method to predict the unbound drug fraction in the brain.
AID1525934Inhibition of MRP1 in human 2008/MRP1 cells assessed as reduction in cell viability after 5 days by MTS/PMS assay2019Journal of medicinal chemistry, 09-26, Volume: 62, Issue:18
Triazole Bridged Flavonoid Dimers as Potent, Nontoxic, and Highly Selective Breast Cancer Resistance Protein (BCRP/ABCG2) Inhibitors.
AID681085TP_TRANSPORTER: transport in etoposide-selected MCF7 cells2006Molecular pharmacology, Apr, Volume: 69, Issue:4
Multidrug resistance protein 1 (MRP1, ABCC1) mediates resistance to mitoxantrone via glutathione-dependent drug efflux.
AID201223Bacterial mutagenicity was measured against Salmonella Typhimurium TA97a at dose range of 0-400 ug/plate1998Journal of medicinal chemistry, Sep-10, Volume: 41, Issue:19
Anthracene-9,10-diones as potential anticancer agents: bacterial mutation studies of amido-substituted derivatives reveal an unexpected lack of mutagenicity.
AID153494In vivo antineoplastic activity was determined in BDF1 mice implanted with P388 leukemia and activity is expressed as T/C at 0.06 mg/kg1987Journal of medicinal chemistry, Sep, Volume: 30, Issue:9
Structural modification study of mitoxantrone (DHAQ). Chloro-substituted mono- and bis[(aminoalkyl)amino]anthraquinones.
AID153505In vivo antineoplastic activity was determined in BDF1 mice implanted with P388 leukemia and activity is expressed as T/C at 2 mg/kg1987Journal of medicinal chemistry, Sep, Volume: 30, Issue:9
Structural modification study of mitoxantrone (DHAQ). Chloro-substituted mono- and bis[(aminoalkyl)amino]anthraquinones.
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID721752Inhibition of human MATE2K-mediated ASP+ uptake expressed in HEK293 cells after 1.5 mins by fluorescence assay2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID627483Inhibition of ATP-dependent ABCG2 pump assessed as ratio of compound IC50 for HEK/ABCG2-482-R2 cells to IC50 for HEK293/pcDNA3.1 cells after 72 hrs by MTT assay2011Bioorganic & medicinal chemistry letters, Nov-01, Volume: 21, Issue:21
Inhibition of c-Kit, VEGFR-2 (KDR), and ABCG2 by analogues of OSI-930.
AID226658An average for IC50 values in the two solid tumor cell lines and sensitive L1210 leukemia cell line.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID1221958Efflux ratio of permeability from apical to basolateral side over basolateral to apical side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis2011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID280856Antiproliferative activity against human MDA-MB-231 cells by WST-1 method after 72 hrs2007Journal of medicinal chemistry, Apr-05, Volume: 50, Issue:7
Design, synthesis, and evaluation of the antiproliferative activity of a series of novel fused xanthenone aminoderivatives in human breast cancer cells.
AID103421Tested for inhibitory activity against human tumor cell line MCF7, a strain sensitive to doxorubicin of breast carcinoma using sulforhodamine B assay.2000Journal of medicinal chemistry, Aug-10, Volume: 43, Issue:16
Analogues of amonafide and azonafide with novel ring systems.
AID102188Tested in vitro for cytotoxic activity against Human colon Adenocarcinoma sensitive cell line (LoVo)1994Journal of medicinal chemistry, Mar-18, Volume: 37, Issue:6
6,9-Bis[(aminoalkyl)amino]benzo[g]isoquinoline-5,10-diones. A novel class of chromophore-modified antitumor anthracene-9,10-diones: synthesis and antitumor evaluations.
AID8247In vitro inhibition of tumor cell growth in the human myeloma 8226 system.1992Journal of medicinal chemistry, Nov-13, Volume: 35, Issue:23
Novel non-cross resistant diaminoanthraquinones as potential chemotherapeutic agents.
AID216434Tested for inhibitory activity against a multi drug resistant (MDR) strain of human colon carcinoma WiDr using sulforhodamine B assay (it is MRP positive but non-P-glycoprotein).2000Journal of medicinal chemistry, Aug-10, Volume: 43, Issue:16
Analogues of amonafide and azonafide with novel ring systems.
AID1349100Inhibition of NAE in human Caco2 cells assessed as decrease in Bcl2 protein levels at 0.1 to 10 uM after 16 hrs by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID81308Compound was tested in vitro for cytotoxicity against HL60 human leukemia cell line (72 hr exposure to compound)1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID595063Cytotoxicity against human MES-SA/Dx5 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Design, synthesis and antiproliferative activity of novel aminosubstituted benzothiopyranoisoindoles.
AID200620Cytotoxicity against human small-cell lung cancer (SCLC)1993Journal of medicinal chemistry, Dec-10, Volume: 36, Issue:25
Design of antineoplastic agents on the basis of the "2-phenylnaphthalene-type" structural pattern. 2. Synthesis and biological activity studies of benzo]b]naphtho[2,3-d]furan-6,11-dione derivatives.
AID98355Inhibitory concentration of compound against proliferation of murine leukemia L1210 cell line2002Bioorganic & medicinal chemistry letters, Jun-03, Volume: 12, Issue:11
Design and synthesis of some new pyranoxanthenone aminoderivatives with cytotoxic activity.
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID1129639Cytotoxicity against HEK293 cells overexpressing ABCG2 after 72 hrs by MTT assay2014Journal of medicinal chemistry, Apr-10, Volume: 57, Issue:7
Symmetric bis-chalcones as a new type of breast cancer resistance protein inhibitors with a mechanism different from that of chromones.
AID253341Cytotoxicity against human LoVo cancer cell line was determined after 1 hr2004Journal of medicinal chemistry, Oct-07, Volume: 47, Issue:21
Rational design, synthesis, and biological evaluation of bis(pyrimido[5,6,1-de]acridines) and bis(pyrazolo[3,4,5-kl]acridine-5-carboxamides) as new anticancer agents.
AID135709Tested for antitumor activity against P388 murine leukemia1994Journal of medicinal chemistry, Mar-18, Volume: 37, Issue:6
6,9-Bis[(aminoalkyl)amino]benzo[g]isoquinoline-5,10-diones. A novel class of chromophore-modified antitumor anthracene-9,10-diones: synthesis and antitumor evaluations.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1349116Inhibition of SAE-mediated Ubc9-SUMO conjugation in human Caco2 cells up to 10 uM preincubated for 10 mins followed by ATP and Mg2+ addition measured after 60 mins by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID1130165Antineoplastic activity against mouse L1210 cells allografted in CDF1 mouse at 10.8 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID729387Inhibition of PIM1 (unknown origin) using [gamma33P]ATP assessed as residual activity at 1 uM after 120 mins by radiometric assayATP2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID67127EBV-positive nasopharyngeal colony count obtained from the examination of uniform plate surface areas after a dose of 0.1 ug/mL1983Journal of medicinal chemistry, Dec, Volume: 26, Issue:12
Bis(bioreductive) alkylating agents: synthesis and biological activity in a nude mouse human carcinoma model.
AID624609Specific activity of expressed human recombinant UGT1A62000Annual review of pharmacology and toxicology, , Volume: 40Human UDP-glucuronosyltransferases: metabolism, expression, and disease.
AID154566Percent ratio of the medium survival time for P388 murine leukemia in CDF1 mice at 0.75 mg/kg1989Journal of medicinal chemistry, Aug, Volume: 32, Issue:8
Synthesis of unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones as potential antileukemic agents.
AID216573Tested against WiDr colon carcinoma (resistant) in the sulforhodamine B assay.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID98384Antitumor activity against sensitive L1210 murine leukemia cell lines.1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID101065In vitro extracellular concentration required to reduce cell population to 50% against L1210 leukemia cells1992Journal of medicinal chemistry, Apr-17, Volume: 35, Issue:8
Anthracene-9,10-diones as potential anticancer agents. Synthesis, DNA-binding, and biological studies on a series of 2,6-disubstituted derivatives.
AID102597In vitro inhibition of tumor cell growth in the human mammary tumor MCF-7 system1992Journal of medicinal chemistry, Nov-13, Volume: 35, Issue:23
Novel non-cross resistant diaminoanthraquinones as potential chemotherapeutic agents.
AID1129642Cytotoxicity against HEK293 cells after 72 hrs by MTT assay2014Journal of medicinal chemistry, Apr-10, Volume: 57, Issue:7
Symmetric bis-chalcones as a new type of breast cancer resistance protein inhibitors with a mechanism different from that of chromones.
AID1130623Antitumor activity against mouse B16 cells allografted in BDF1 mouse assessed as increase of median life span at 3.1 mg/kg, ip on day 1 to 9 measured up to 80 days relative to control1979Journal of medicinal chemistry, Sep, Volume: 22, Issue:9
Antitumor agents. 1. 1,4-Bis[(aminoalkyl)amino]-9,10-anthracenediones.
AID196905Cardiotoxicity was measured by using Neonatal rat heart myocyte assay1995Journal of medicinal chemistry, Mar-17, Volume: 38, Issue:6
Amino-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H- dibenz[de,h]isoquinoline-1,3-diones. Synthesis, antitumor activity, and quantitative structure--activity relationship.
AID272516Relative fold, IC50 in absence to presence of 1,13-bis[4'-((5,7-dihydroxy)-4H-chromen-4-on-2-yl)phenyl]-1,4,7,10,13-pentaoxatridecane in multidrug resistant P388 cells2006Journal of medicinal chemistry, Nov-16, Volume: 49, Issue:23
Flavonoid dimers as bivalent modulators for P-glycoprotein-based multidrug resistance: synthetic apigenin homodimers linked with defined-length poly(ethylene glycol) spacers increase drug retention and enhance chemosensitivity in resistant cancer cells.
AID1562300Antimycobacterial activity against Mycobacterium smegmatis atR10 assessed as decrease in drug resistance development at 10 nmol/disc after 2 to 3 days by paper disc method2019European journal of medicinal chemistry, Sep-15, Volume: 178Synthesis and antimycobacterial activity of imidazo[1,2-b][1,2,4,5]tetrazines.
AID729379Inhibition of PIM1-mediated BAD phosphorylation in human MV411 cells after 12 hrs by Western blotting analysis2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID1197743Inhibition of human OATP1B1-mediated [3H]estrone 3-sulfate at 100 uM after 5 mins relative to control2015European journal of medicinal chemistry, Mar-06, Volume: 92Interaction of human organic anion transporter polypeptides 1B1 and 1B3 with antineoplastic compounds.
AID466797Growth inhibition of human SKOV3 cells by MTT assay2010Bioorganic & medicinal chemistry letters, Mar-01, Volume: 20, Issue:5
Triterpene compounds isolated from Acer mandshuricum and their anti-inflammatory activity.
AID1550877Dark toxicity against mouse H22 cells assessed as reduction in cell viability preincubated for 5 hrs followed by compound washout and measured after 48 hrs by CCK8 assay2019European journal of medicinal chemistry, Jun-01, Volume: 171Naphthyl quinoxaline thymidine conjugate is a potent anticancer agent post UVA activation and elicits marked inhibition of tumor growth through vaccination.
AID436862Inhibition of VIM2 using nitrocefin as substrate after 15 mins by microtiter plate assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID1506797Inhibition of ROS1 in human HCC78 cells assessed as reduction in AKT phosphorylation incubated for 48 hrs by Western blot method2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID1402046Induction of apoptosis in human Jurkat T cells assessed as downregulation of Bcl2 expression at 10 uM after 48 hrs by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Design, synthesis and evaluation of an anthraquinone derivative conjugated to myelin basic protein immunodominant (MBP
AID1430728Antitumor activity against mouse 4T1.2 cells implanted in Balb/c mouse assessed as tumor growth inhibition at 2 mg/kg, iv administered twice weekly for 2 weeks2017ACS medicinal chemistry letters, May-11, Volume: 8, Issue:5
Encapsulation of Mitoxantrone within Cucurbit[8]uril Decreases Toxicity and Enhances Survival in a Mouse Model of Cancer.
AID1851422Antiproliferative activity against human HeLa cells assessed as inhibition of cell growth2022Bioorganic & medicinal chemistry letters, 10-01, Volume: 73Synthesis and antitumor activity of a series of novel N-aryl-5-(2,2,2-trifluoroethoxy)-1,5-dihydro-2H-pyrrol-2-ones derivatives.
AID466799Growth inhibition of human HT-29 cells by MTT assay2010Bioorganic & medicinal chemistry letters, Mar-01, Volume: 20, Issue:5
Triterpene compounds isolated from Acer mandshuricum and their anti-inflammatory activity.
AID1130179Antineoplastic activity against mouse P388 cells allografted in CDF1 mouse at 0.25 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1132471Antitumor activity against mouse P388 cells allografted in BDF1 mouse assessed as increase in survival time at 0.25 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID240619Inhibitory concentration against cytochrome P450 2D62004Journal of medicinal chemistry, Oct-21, Volume: 47, Issue:22
Validation of model of cytochrome P450 2D6: an in silico tool for predicting metabolism and inhibition.
AID54994Compound was evaluated for the increase in melting temperature (delta Tm) for calf Thymus DNA on interaction with Ligand at DNAp to ligand ratio 20:11992Journal of medicinal chemistry, Apr-17, Volume: 35, Issue:8
Anthracene-9,10-diones as potential anticancer agents. Synthesis, DNA-binding, and biological studies on a series of 2,6-disubstituted derivatives.
AID687159Cytotoxicity against human CCRF-CEM cells assessed as cell viability after 48 hrs by celltiter-blue assay2012Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11
Structure-activity relationship (SAR) study of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and the potential of the lead against multidrug resistance in cancer treatment.
AID1070860Inhibition of human tert transcriptional activity assessed as SEAP activity at 10 uM after 24 hrs by SEAP reporter assay2013European journal of medicinal chemistry, Nov, Volume: 69Structure-based design, synthesis and biological evaluation of novel anthra[1,2-d]imidazole-6,11-dione homologues as potential antitumor agents.
AID683855Antiproliferative activity against human LoVo/DX cells after 72 hrs by SRB assay2012Bioorganic & medicinal chemistry letters, Oct-01, Volume: 22, Issue:19
New derivatives of 11-methyl-6-[2-(dimethylamino)ethyl]-6H-indolo[2,3-b]quinoline as cytotoxic DNA topoisomerase II inhibitors.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID537736Antifungal activity against yeast AD1-8u expressing Candida albicans CaCdr1p by agar disk diffusion assay2010European journal of medicinal chemistry, Nov, Volume: 45, Issue:11
Analysis of physico-chemical properties of substrates of ABC and MFS multidrug transporters of pathogenic Candida albicans.
AID255777In vitro cytotoxicity variant MES-SA/Dx5 multidrug resistant cells2005Bioorganic & medicinal chemistry letters, Nov-15, Volume: 15, Issue:22
Design, synthesis, and antiproliferative activity of some novel aminosubstituted xanthenones, able to overcome multidrug resistance toward MES-SA/Dx5 cells.
AID1550905Induction of immunogenic cell death in mouse H22 cells assessed as increase in intracellular calreticulin level at 2 uM measured after 5 hrs by flow cytometric analysis2019European journal of medicinal chemistry, Jun-01, Volume: 171Naphthyl quinoxaline thymidine conjugate is a potent anticancer agent post UVA activation and elicits marked inhibition of tumor growth through vaccination.
AID1233368Antiproliferative activity against human HCT116 cells after 72 hrs by MTT assay2015Bioorganic & medicinal chemistry letters, Jul-01, Volume: 25, Issue:13
Synthesis and antiproliferative activity of some novel benzo-fused imidazo[1,8]naphthyridinones.
AID39730Tested for activity against murine B-16 melanoma in mice and percent treated to the control values with the number of 60 day survivors1987Journal of medicinal chemistry, Jan, Volume: 30, Issue:1
Anthrapyrazole anticancer agents. Synthesis and structure-activity relationships against murine leukemias.
AID1396804Antiproliferative activity against human HL60/MX2 cells after 72 hrs by SRB assay2018Bioorganic & medicinal chemistry letters, 08-15, Volume: 28, Issue:15
Phosphorus-containing isothiocyanate-derived mercapturic acids as a useful alternative for parental isothiocyanates in experimental oncology.
AID1349094Inhibition of NAE in human Caco2 cells assessed as increase in p53 protein levels by measuring p53 degradation at 10 uM preincubated for 16 hrs followed by cycloheximide addition measured up to 60 mins by Western blot analysis relative to control2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID1130162Antineoplastic activity against mouse L1210 cells allografted in CDF1 mouse assessed as survival at 18 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID255826In vitro cytotoxicity against colorectal adenocarcinoma HT-29 cells2005Bioorganic & medicinal chemistry letters, Nov-15, Volume: 15, Issue:22
Design, synthesis, and antiproliferative activity of some novel aminosubstituted xanthenones, able to overcome multidrug resistance toward MES-SA/Dx5 cells.
AID1132469Antitumor activity against mouse P388 cells allografted in BDF1 mouse assessed as increase in survival time at 1 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID1883022Toxicity in Balb/c mouse implanted with mouse 4T1 cells assessed as spleen lesions at 50 mg/kg administered intratumorally every four days for 14 days in the presence of liquid cyanoacrylate by H&E staining based histopathological analysis2022European journal of medicinal chemistry, Jul-05, Volume: 237Design, synthesis, and evaluation of a novel series of mono-indolylbenzoquinones derivatives for the potential treatment of breast cancer.
AID1883019Antitumor activity against mouse 4T1 cells implanted in Balb/c mouse assessed as tumor growth inhibition at 50 mg/kg administered intratumorally every four days for 14 days in the presence of liquid cyanoacrylate relative to control2022European journal of medicinal chemistry, Jul-05, Volume: 237Design, synthesis, and evaluation of a novel series of mono-indolylbenzoquinones derivatives for the potential treatment of breast cancer.
AID307325Growth inhibition of human HL60 cells by Almar blue assay2007Bioorganic & medicinal chemistry, Jun-15, Volume: 15, Issue:12
Synthesis and topoisomerase poisoning activity of A-ring and E-ring substituted luotonin A derivatives.
AID98871Percentage increase in lifespan of mice was measured (in vivo) at 0.75 mg/kg dose1988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID84111Percent inhibition at G2/M phase of cell cycle at a dose of 100n g/mL after 72 hours of induction in HT-29/Mx cell line1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID152915In vivo antitumor activity was measured on systemic P388 murine leukemia cells. Optimal dose at 3 mg/kg/day1998Journal of medicinal chemistry, Dec-31, Volume: 41, Issue:27
Synthesis and antitumor evaluation of 2,5-disubstituted-indazolo[4, 3-gh]isoquinolin-6(2H)-ones (9-aza-anthrapyrazoles).
AID436876Inhibition of Enterobacter cloacae AmpC using nitrocefin as substrate after 15 mins by microtiter plate assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID201224Bacterial mutagenicity was measured against Salmonella Typhimurium TA98 at dose range of 0-10 ug/plate1998Journal of medicinal chemistry, Sep-10, Volume: 41, Issue:19
Anthracene-9,10-diones as potential anticancer agents: bacterial mutation studies of amido-substituted derivatives reveal an unexpected lack of mutagenicity.
AID771326Cytotoxicity against human SKOV3 cells after 48 hrs by resazurin dye assay2013Bioorganic & medicinal chemistry letters, Oct-01, Volume: 23, Issue:19
Synthesis and antiproliferative activity of new cytotoxic tri- and tetraazabenzo[3,2-a]fluorene-5,6-dione derivatives.
AID538480Cytotoxicity against human HCT116 cells by MTT assay2010Bioorganic & medicinal chemistry letters, Dec-01, Volume: 20, Issue:23
Oleanane-type triterpenoids from Panax stipuleanatus and their anticancer activities.
AID1506323Growth inhibition of human bone marrow cells2018Journal of medicinal chemistry, Aug-09, Volume: 61, Issue:15
Exploring the Structure-Activity Relationship and Mechanism of a Chromene Scaffold (CXL Series) for Its Selective Antiproliferative Activity toward Multidrug-Resistant Cancer Cells.
AID1132510Toxicity in mouse P388 cells allografted BDF1 mouse assessed as body weight difference at 0.25 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID220580Binding affinity towards [poly(dG-dC)]21999Journal of medicinal chemistry, Jul-15, Volume: 42, Issue:14
2,3-Dihydro-1H,7H-pyrimido[5,6,1-de]acridine-1,3,7-trione derivatives, a class of cytotoxic agents active on multidrug-resistant cell lines: synthesis, biological evaluation, and structure-activity relationships.
AID1349091Inhibition of NAE in human Caco2 cells assessed as increase in p53 protein levels at 0.1 to 10 uM after 16 hrs by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID129075Antileukemic activity towards P388 Murine Leukemia at a dose of 0.8 mg/kg, expressed as body weight change1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1132490Antitumor activity against mouse P388 cells allografted in BDF1 mouse assessed as mouse survival at 0.25 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID436867Inhibition of VIM2 using nitrocefin as substrate by rapid dilution method2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID613827Ratio of IC50 for vinblastine100-resistant human CCRF-CEM cells to IC50 for human CCRF-CEM cells2011Journal of medicinal chemistry, Aug-25, Volume: 54, Issue:16
Structure-activity relationship and molecular mechanisms of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and its analogues.
AID100159Number of tumor free survivors of mice was measured in L1210 leukemia cells (in vivo) at 3 mg/kg (cumulative dose 9 mg/kg) with ip day 1-9 (twice daily); value give as 7/101988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID687157Cytotoxicity against human HL60 cells assessed as cell viability after 48 hrs by celltiter-blue assay2012Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11
Structure-activity relationship (SAR) study of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and the potential of the lead against multidrug resistance in cancer treatment.
AID1130166Antineoplastic activity against mouse L1210 cells allografted in CDF1 mouse assessed as survival at 4 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID272494Antiproliferative activity against P388 cells by ELISA2006Journal of medicinal chemistry, Nov-16, Volume: 49, Issue:23
Flavonoid dimers as bivalent modulators for P-glycoprotein-based multidrug resistance: synthetic apigenin homodimers linked with defined-length poly(ethylene glycol) spacers increase drug retention and enhance chemosensitivity in resistant cancer cells.
AID1506784Induction of apoptosis in human HCC78 cells assessed as early apoptotic cells level at 10 nM incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry (Rvb = 6.33%)2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID681447TP_TRANSPORTER: cell accumulation in KOT52 and D320 cells1999Cancer research, Sep-01, Volume: 59, Issue:17
The mouse Bcrp1/Mxr/Abcp gene: amplification and overexpression in cell lines selected for resistance to topotecan, mitoxantrone, or doxorubicin.
AID91425Inhibition of HIV-1 integrase, under 1 uM for the 3''-preprocessing2000Journal of medicinal chemistry, Jun-01, Volume: 43, Issue:11
Developing a dynamic pharmacophore model for HIV-1 integrase.
AID1289283Cytotoxicity against human HaCaT cells by Cell titre-blue assay2016Journal of natural products, Jan-22, Volume: 79, Issue:1
Cylindrofridins A-C, Linear Cylindrocyclophane-Related Alkylresorcinols from the Cyanobacterium Cylindrospermum stagnale.
AID85749Concentration required to inhibit cell growth by 50% in vitro against Human colon adenocarcinoma cell line2001Journal of medicinal chemistry, Sep-27, Volume: 44, Issue:20
Synthesis, antitumor cytotoxicity, and DNA-binding of novel N-5,2-di(omega-aminoalkyl)-2,6-dihydropyrazolo[3,4,5-kl]acridine-5-carboxamides.
AID647960Inhibition of human TERT expression in H1299 cells at 10 uM after 24 hrs by secreted alkaline phosphatase reporter gene assay relative to control2012European journal of medicinal chemistry, Apr, Volume: 50Design, synthesis and evaluation of telomerase inhibitory, hTERT repressing, and anti-proliferation activities of symmetrical 1,8-disubstituted amidoanthraquinones.
AID25619Estimated pKa value of the compound1992Journal of medicinal chemistry, Apr-17, Volume: 35, Issue:8
Anthracene-9,10-diones as potential anticancer agents. Synthesis, DNA-binding, and biological studies on a series of 2,6-disubstituted derivatives.
AID613825Ratio of IC50 for daunorubicin-resistant human HL60 cells to IC50 for human HL60 cells2011Journal of medicinal chemistry, Aug-25, Volume: 54, Issue:16
Structure-activity relationship and molecular mechanisms of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and its analogues.
AID140016The compound was tested for antitumor activity against P388 murine leukemia at 2 (mg/kg/day) dose; 0/82 -no. of toxic deaths/no. of mice1994Journal of medicinal chemistry, Mar-18, Volume: 37, Issue:6
6,9-Bis[(aminoalkyl)amino]benzo[g]isoquinoline-5,10-diones. A novel class of chromophore-modified antitumor anthracene-9,10-diones: synthesis and antitumor evaluations.
AID1851421Antiproliferative activity against human A549 cells assessed as inhibition of cell growth2022Bioorganic & medicinal chemistry letters, 10-01, Volume: 73Synthesis and antitumor activity of a series of novel N-aryl-5-(2,2,2-trifluoroethoxy)-1,5-dihydro-2H-pyrrol-2-ones derivatives.
AID771327Cytotoxicity against human KB/HeLa cells after 48 hrs by resazurin dye assay2013Bioorganic & medicinal chemistry letters, Oct-01, Volume: 23, Issue:19
Synthesis and antiproliferative activity of new cytotoxic tri- and tetraazabenzo[3,2-a]fluorene-5,6-dione derivatives.
AID98310Dose level for 50% inhibition of L1210 cell growth was measured after 24 h.1988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID140020The compound was tested for antitumor activity against P388 murine leukemia at 4 (mg/kg/day) dose; 43/48 -no. of toxic deaths/no. of mice1994Journal of medicinal chemistry, Mar-18, Volume: 37, Issue:6
6,9-Bis[(aminoalkyl)amino]benzo[g]isoquinoline-5,10-diones. A novel class of chromophore-modified antitumor anthracene-9,10-diones: synthesis and antitumor evaluations.
AID436864Inhibition of IMP1 using nitrocefin as substrate after 15 mins by microtiter plate assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID1474538Cytotoxicity against human HL60/MX2 cells after 72 hrs by sulforhodamine B assay2017European journal of medicinal chemistry, May-26, Volume: 132Novel phosphonate analogs of sulforaphane: Synthesis, in vitro and in vivo anticancer activity.
AID96751Effect of dosing on L1210 leukemia in vivo measured as mean at 0.75 mg/kg1988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID55292CT-DNA binding required to produce a 50% drop in fluorescence of DNA-bound ethidium.2002Journal of medicinal chemistry, Jan-31, Volume: 45, Issue:3
2,6-Di(omega-aminoalkyl)-2,5,6,7-tetrahydropyrazolo[3,4,5-mn]pyrimido[5,6,1-de]acridine-5,7-diones: novel, potent, cytotoxic, and DNA-binding agents.
AID98911Inhibitory activity against sensitive L1210 cell lines1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID153495In vivo antineoplastic activity was determined in BDF1 mice implanted with P388 leukemia and activity is expressed as T/C at 0.12 mg/kg1987Journal of medicinal chemistry, Sep, Volume: 30, Issue:9
Structural modification study of mitoxantrone (DHAQ). Chloro-substituted mono- and bis[(aminoalkyl)amino]anthraquinones.
AID380011Cytotoxicity against human K562 cells after 48 hrs by MTT assay2000Journal of natural products, May, Volume: 63, Issue:5
New 7,20:14,20-diepoxy ent-kauranoids from Isodon xerophilus.
AID98203Anti-tumor activity against murine L1210 sensitive cell line by using MTT assay1995Journal of medicinal chemistry, Mar-17, Volume: 38, Issue:6
Amino-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H- dibenz[de,h]isoquinoline-1,3-diones. Synthesis, antitumor activity, and quantitative structure--activity relationship.
AID681063TP_TRANSPORTER: Northern blot in vivo Wistar rat1996Biochemical pharmacology, Nov-08, Volume: 52, Issue:9
Multidrug resistance gene expression in rodents and rodent hepatocytes treated with mitoxantrone.
AID1053260Antagonist activity at human recombinant dopamine D2 long receptor expressed in CHOK1 cells coexpressing mitochondrial apoaequorin assessed as inhibition of agonist-induced effect at 50 uM after 15 mins by luminometric analysis relative to haloperidol2013Journal of medicinal chemistry, Nov-14, Volume: 56, Issue:21
Experimental confirmation of new drug-target interactions predicted by Drug Profile Matching.
AID594150Antiproliferative activity against human NCI-H460 cells after 48 hrs by XTT assay2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Synthesis and antiproliferative activity of new cytotoxic azanaphthoquinone pyrrolo-annelated derivatives: Part II.
AID409954Inhibition of mouse brain MAOA2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Quantitative structure-activity relationship and complex network approach to monoamine oxidase A and B inhibitors.
AID487000Binding affinity to calf thymus DNA assessed as ratio of final absorbance area to the absorbance at 100 uM after 24 hrs by UV spectrophotometer analysis relative to control2010Bioorganic & medicinal chemistry, Jun-15, Volume: 18, Issue:12
Study of benzo[a]phenazine 7,12-dioxide as selective hypoxic cytotoxin-scaffold. Identification of aerobic-antitumoral activity through DNA fragmentation.
AID107214Tested for inhibitory activity against human tumor cell line UA375 of melanoma using sulforhodamine B assay.2000Journal of medicinal chemistry, Aug-10, Volume: 43, Issue:16
Analogues of amonafide and azonafide with novel ring systems.
AID729380Inhibition of PIM1-mediated BAD phosphorylation in human K562 cells after 12 hrs by Western blotting analysis2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID699541Inhibition of human liver OATP2B1 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E3S uptake at 20 uM incubated for 5 mins by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID54998Increase in Melting temperature (delta Tm) for Calf thymus DNA on interaction against ligand (mole ratio of 10:1)1992Journal of medicinal chemistry, Apr-17, Volume: 35, Issue:8
Anthracene-9,10-diones as potential anticancer agents. Synthesis, DNA-binding, and biological studies on a series of 2,6-disubstituted derivatives.
AID613826Ratio of IC50 for homoharringtonine300-resistant human K562 cells to IC50 for human K562 cells2011Journal of medicinal chemistry, Aug-25, Volume: 54, Issue:16
Structure-activity relationship and molecular mechanisms of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and its analogues.
AID1557151Cytotoxicity against human NCI-H460 cells assessed as inhibition of cell viability incubated for 2 hrs by MTT assay2019European journal of medicinal chemistry, Oct-01, Volume: 179Benzoyl indoles with metabolic stability as reversal agents for ABCG2-mediated multidrug resistance.
AID682127TP_TRANSPORTER: Northern blot in vivo NMRI mouse1996Biochemical pharmacology, Nov-08, Volume: 52, Issue:9
Multidrug resistance gene expression in rodents and rodent hepatocytes treated with mitoxantrone.
AID1711944Antiproliferative activity against human HepG2 cells assessed as inhibition of cell proliferation at 5 uM measured after 48 hrs by MTT assay relative to control2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID591075Cytotoxicity against human HL60 cells2011Bioorganic & medicinal chemistry letters, Apr-15, Volume: 21, Issue:8
Synthesis, cytotoxicity and topoisomerase inhibition properties of multifarious aminoalkylated indeno[1,2-c]isoquinolin-5,11-diones.
AID429649Cytotoxicity against human A549 cells by MTT assay2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
C29 sterols with a cyclopropane ring at C-25 and 26 from the Vietnamese marine sponge Ianthella sp. and their anticancer properties.
AID721751Inhibition of human OCT2-mediated ASP+ uptake expressed in HEK293 cells after 3 mins by fluorescence assay2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID436868Inhibition of VIM2 using nitrocefin as substrate at 44 uM after 15 mins by microtiter plate assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID80704Tested for the cytotoxicity to inhibit replication assay against the human colon tumor cell line HCT116; ND is Not Determined1994Journal of medicinal chemistry, Oct-28, Volume: 37, Issue:22
Inhibition of topoisomerase II catalytic activity by pyridoacridine alkaloids from a Cystodytes sp. ascidian: a mechanism for the apparent intercalator-induced inhibition of topoisomerase II.
AID222141Inhibition of cellular growth was evaluated in vitro against human colon carcinoma subline resistant to DOXO (LOVO/DOXO).1991Journal of medicinal chemistry, Aug, Volume: 34, Issue:8
Synthesis and antitumor evaluations of symmetrically and unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones and 1,4-bis[(aminoalkyl)amino]-5,8-dihydroxyanthracene-9,10-diones.
AID247764In vitro cytotoxicity against mouse leukemia L1210 cell lines2004Bioorganic & medicinal chemistry letters, Oct-04, Volume: 14, Issue:19
Pyrrolo[2,1-c][1,4]benzodiazepine-anthraquinone conjugates. Synthesis, DNA binding and cytotoxicity.
AID1562301Antimycobacterial activity against Mycobacterium smegmatis atR17 assessed as decrease in drug resistance at 10 nmol/disc after 2 to 3 days by paper disc method2019European journal of medicinal chemistry, Sep-15, Volume: 178Synthesis and antimycobacterial activity of imidazo[1,2-b][1,2,4,5]tetrazines.
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID436865Inhibition of VIM2 using CCF2 as substrate after 15 mins by FRET assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID375433Displacement of [3H]PSB0413 from human platelet P2Y12 receptor2009Journal of medicinal chemistry, Jun-25, Volume: 52, Issue:12
High-affinity, non-nucleotide-derived competitive antagonists of platelet P2Y12 receptors.
AID436896Inhibition of VIM2 in imipenem-resistant Escherichia coli BL21(DE3) assessed as potentiation of imipenem-induced bactericidal activity at 4.2 ug/mL after 18 hrs by checkerboard microdilution method2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID236913Permeability Coefficient in Caco-2 cell culture model2005Journal of medicinal chemistry, Jan-27, Volume: 48, Issue:2
Exploring the role of different drug transport routes in permeability screening.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID7501In vitro Cytotoxic activity of compound in comparison with reference compounds in human cell line A2780/DX(RI)1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1132491Antitumor activity against mouse P388 cells allografted in BDF1 mouse assessed as mouse survival at 0.12 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID1221956Apparent permeability from apical to basolateral side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis2011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1506781Induction of apoptosis in human HCC78 cells assessed as late apoptotic cells level at 5 nM incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry (Rvb = 13.8%)2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID55500Concentration required to give 50% fluorescence quenching of bound ethidium for [ethidium]: [poly(dA-dT)]2 DNA in ratio of 0.1:1 at pH 51997Journal of medicinal chemistry, Nov-07, Volume: 40, Issue:23
1-[(omega-aminoalkyl)amino]-4-[N-(omega-aminoalkyl)carbamoyl]-9-oxo-9, 10-dihydroacridines as intercalating cytotoxic agents: synthesis, DNA binding, and biological evaluation.
AID1547889Inhibition of MTH1 in human U2OS cells assessed as activation of p53 at 2.25 uM incubated for 4 and 24 hrs by Peggy sue Western blot assay2020ACS medicinal chemistry letters, Mar-12, Volume: 11, Issue:3
Discovery of Potent and Selective MTH1 Inhibitors for Oncology: Enabling Rapid Target (In)Validation.
AID1586107Antiproliferative activity against human HL60 cells after 72 hrs by CCK8 assay2018Journal of natural products, 12-28, Volume: 81, Issue:12
A Pair of Enantiomeric Bis- seco-abietane Diterpenoids from Cryptomeria fortunei.
AID106431Antitumor activity against human mammary carcinoma sensitive MXF7 breast cell line.1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID1506795Inhibition of ROS1 phosphorylation in human HCC78 cells incubated for 48 hrs by Western blot method2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID1519983Inhibition of Nedd8-cullin1 adduct formation in human A549 cells assessed as decrease in cullin1 neddylation at 50 uM measured after 6 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1209589Drug uptake in Sprague-Dawley rat brain slices at 100 nM after 5 hrs in presence of 10 uM of fumitremorgin-C2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID1130180Antineoplastic activity against mouse P388 cells allografted in CDF1 mouse assessed as survival at 0.12 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID45639Survivors of CDF1 mice on day 4 after 1st injection of compound 12 at mg/kg in six mice; 6/61989Journal of medicinal chemistry, Aug, Volume: 32, Issue:8
Synthesis of unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones as potential antileukemic agents.
AID1130177Antineoplastic activity against mouse P388 cells allografted in CDF1 mouse at 0.5 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1349115Cytotoxicity against NAE-knockdown human Caco2 cells after 72 hrs by MTT assay2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID1349109Induction of apoptosis in human Caco2 cells assessed as necrotic cells at 5 uM after 16 hrs by Annexin V-FITC/propidium iodide staining-based flow cytometric analysis (Rvb = 0.12%)2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID436877Inhibition of Enterobacter cloacae AmpC using nitrocefin as substrate at 25 uM after 15 mins by microtiter plate assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID1132473Antitumor activity against mouse P388 cells allografted in BDF1 mouse assessed as increase in survival time at 0.06 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID477295Octanol-water partition coefficient, log P of the compound2010European journal of medicinal chemistry, Apr, Volume: 45, Issue:4
QSPR modeling of octanol/water partition coefficient of antineoplastic agents by balance of correlations.
AID83790Percent inhibition at G1 phase of cell cycle at a dose of 25 ng/mL after 72 hours of induction in HT-29 cell line1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1656533Stabilization of dsBE12 oligonucleotide (unknown origin) assessed as drug-DNA adduct formation at 5 to 50 uM incubated for 4 hrs in presence of formaldehyde using [gamma-32P]ATP by phosphorimaging analysis relative to control2020Bioorganic & medicinal chemistry, 02-01, Volume: 28, Issue:3
Formaldehyde-activated WEHI-150 induces DNA interstrand crosslinks with unique structural features.
AID270854Antiproliferative activity against MES-SA cells by MTT assay after 72 hrs2006Bioorganic & medicinal chemistry letters, Sep-15, Volume: 16, Issue:18
Synthesis and antiproliferative activity of substituted benzopyranoisoindoles: a new class of cytotoxic compounds.
AID1130175Antineoplastic activity against mouse P388 cells allografted in CDF1 mouse at 1 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID431398Cytotoxicity against human HL60 cells after 48 hrs by cell titer-blue assay2009Journal of medicinal chemistry, Oct-08, Volume: 52, Issue:19
Structure-activity relationship and molecular mechanisms of ethyl 2-amino-4-(2-ethoxy-2-oxoethyl)-6-phenyl-4h-chromene-3-carboxylate (sha 14-1) and its analogues.
AID54441In vitro calf thymus DNA binding affinity by ethidium bromide displacement2002Bioorganic & medicinal chemistry letters, Jun-03, Volume: 12, Issue:11
Design and synthesis of some new pyranoxanthenone aminoderivatives with cytotoxic activity.
AID624612Specific activity of expressed human recombinant UGT1A92000Annual review of pharmacology and toxicology, , Volume: 40Human UDP-glucuronosyltransferases: metabolism, expression, and disease.
AID681130TP_TRANSPORTER: transepithelial transport (basal to apical) in MDR1-expressing MDCKII cells2001The Journal of pharmacology and experimental therapeutics, Nov, Volume: 299, Issue:2
Rational use of in vitro P-glycoprotein assays in drug discovery.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID521220Inhibition of neurosphere proliferation of mouse neural precursor cells by MTT assay2007Nature chemical biology, May, Volume: 3, Issue:5
Chemical genetics reveals a complex functional ground state of neural stem cells.
AID1430723Growth inhibition of mouse 4T1.2 cells up to 20000 nM after 48 hrs by MTT assay2017ACS medicinal chemistry letters, May-11, Volume: 8, Issue:5
Encapsulation of Mitoxantrone within Cucurbit[8]uril Decreases Toxicity and Enhances Survival in a Mouse Model of Cancer.
AID687158Cytotoxicity against human K562 cells assessed as cell viability after 48 hrs by celltiter-blue assay2012Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11
Structure-activity relationship (SAR) study of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and the potential of the lead against multidrug resistance in cancer treatment.
AID54104Increase in Melting temperature (delta Tm) for Clostridium perfringens DNA on interaction against ligand (mole ratio of 10:1)1992Journal of medicinal chemistry, Apr-17, Volume: 35, Issue:8
Anthracene-9,10-diones as potential anticancer agents. Synthesis, DNA-binding, and biological studies on a series of 2,6-disubstituted derivatives.
AID102335Resistance index is IC50 ratio of LoVo/Dx to LoVo1999Journal of medicinal chemistry, Jul-15, Volume: 42, Issue:14
2,3-Dihydro-1H,7H-pyrimido[5,6,1-de]acridine-1,3,7-trione derivatives, a class of cytotoxic agents active on multidrug-resistant cell lines: synthesis, biological evaluation, and structure-activity relationships.
AID729389Inhibition of Mycobacterium tuberculosis protein kinase B2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID107942Compound was evaluated in vivo for the antitumor activity at a dose of 2.5 mg/kg & 7.5 mg/kg against mammary adenocarcinoma 16C to assess tumor growth delay (T-C)1984Journal of medicinal chemistry, Mar, Volume: 27, Issue:3
5-[(Aminoalkyl)amino]-substituted anthra[1,9-cd]pyrazol-6(2H)-ones as novel anticancer agents. Synthesis and biological evaluation.
AID320434Cytotoxicity against human NCI-H460 cells at 4 ug/ml after 48 hrs by SRB assay2008Bioorganic & medicinal chemistry, Jan-15, Volume: 16, Issue:2
Synthesis, DNA binding, and cytotoxicity of 1,4-bis(2-amino-ethylamino)anthraquinone-amino acid conjugates.
AID230386Resistance index as the ratio of IC50 value against LoVo/Dx to that of LoVo cell lines.1995Journal of medicinal chemistry, Feb-03, Volume: 38, Issue:3
Chromophore-modified antitumor anthracenediones: synthesis, DNA binding, and cytotoxic activity of 1,4-bis[(aminoalkyl)amino]benzo[g]-phthalazine-5,10-diones.
AID681446TP_TRANSPORTER: cell accumulation in MEF3.8, M32 and T6400 cells1999Cancer research, Sep-01, Volume: 59, Issue:17
The mouse Bcrp1/Mxr/Abcp gene: amplification and overexpression in cell lines selected for resistance to topotecan, mitoxantrone, or doxorubicin.
AID84106Percent inhibition at G1 phase of cell cycle at a dose of 1000 ng/mL after 72 hours of induction in HT-29 cell line1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID84110Percent inhibition at G1 phase of cell cycle at a dose of 250 ng/mL after 72 hours of induction in HT-29/Mx cell line1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID83618In vitro cytotoxicity was tested against human colon adenocarcinoma HT-29 cell line1999Journal of medicinal chemistry, Jul-15, Volume: 42, Issue:14
2,3-Dihydro-1H,7H-pyrimido[5,6,1-de]acridine-1,3,7-trione derivatives, a class of cytotoxic agents active on multidrug-resistant cell lines: synthesis, biological evaluation, and structure-activity relationships.
AID436884Bactericidal activity against imipenem-resistant Escherichia coli BL21(DE3) expressing VIM2 gene at 2.1 ug/mL after 24 hrs by broth microdilution method2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID107946In vivo antitumor activity at a single dose of 6.5 mg/kg & 18.8 mg/kg total against mammary adenocarcinoma 16C1984Journal of medicinal chemistry, Mar, Volume: 27, Issue:3
5-[(Aminoalkyl)amino]-substituted anthra[1,9-cd]pyrazol-6(2H)-ones as novel anticancer agents. Synthesis and biological evaluation.
AID145432Anti-tumor activity against human OVCAR-3 ovarian cancer cell lines by using MTT assay1995Journal of medicinal chemistry, Mar-17, Volume: 38, Issue:6
Amino-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H- dibenz[de,h]isoquinoline-1,3-diones. Synthesis, antitumor activity, and quantitative structure--activity relationship.
AID232336Ratio of BR1 IC50 to xrs-6 IC501995Journal of medicinal chemistry, Oct-27, Volume: 38, Issue:22
Topoisomerase II-mediated DNA cleavage by adocia- and xestoquinones from the Philippine sponge Xestospongia sp.
AID232294Differential cytotoxicity was determined from the ratio between BR1(IC50) and xrs-6 (IC50)1994Journal of medicinal chemistry, Oct-28, Volume: 37, Issue:22
Inhibition of topoisomerase II catalytic activity by pyridoacridine alkaloids from a Cystodytes sp. ascidian: a mechanism for the apparent intercalator-induced inhibition of topoisomerase II.
AID1233372Antiproliferative activity against human Daudi cells after 72 hrs by MTT assay2015Bioorganic & medicinal chemistry letters, Jul-01, Volume: 25, Issue:13
Synthesis and antiproliferative activity of some novel benzo-fused imidazo[1,8]naphthyridinones.
AID1666489Inhibition of TDP-43 (unknown origin) binding to RNA2020Bioorganic & medicinal chemistry letters, 02-15, Volume: 30, Issue:4
Emerging small-molecule therapeutic approaches for amyotrophic lateral sclerosis and frontotemporal dementia.
AID135058In vivo antileukemic activity towards P388 Murine Leukemia at a dose of 0.1 mg/kg, expressed as long time survivors tested in 12 animals1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1682835Antiproliferative activity against human K562 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay2021Bioorganic & medicinal chemistry, 01-01, Volume: 29Structure-activity relationship of novel acridone derivatives as antiproliferative agents.
AID136069Antileukemic activity towards P388 Murine Leukemia at a dose of 0.1 mg/kg1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID91426Tested for inhibition of HIV-1 integrase, under 1 uM for the strand transfer2000Journal of medicinal chemistry, Jun-01, Volume: 43, Issue:11
Developing a dynamic pharmacophore model for HIV-1 integrase.
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1349117Inhibition of UAE1-mediated Ubc10-ubiquitin conjugation in human Caco2 cells up to 10 uM preincubated for 10 mins followed by ATP and Mg2+ addition measured after 60 mins by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID429651Cytotoxicity against human HT-29 cells by MTT assay2009Bioorganic & medicinal chemistry letters, Aug-15, Volume: 19, Issue:16
C29 sterols with a cyclopropane ring at C-25 and 26 from the Vietnamese marine sponge Ianthella sp. and their anticancer properties.
AID90440In vitro cytotoxic activity against human colon adenocarcinoma (HT-29).2003Journal of medicinal chemistry, Jul-03, Volume: 46, Issue:14
Design, synthesis, and biological properties of new bis(acridine-4-carboxamides) as anticancer agents.
AID687162Ratio of IC50 for daunorubicin-resistant human HL60 cells to IC50 for human HL60 cells2012Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11
Structure-activity relationship (SAR) study of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and the potential of the lead against multidrug resistance in cancer treatment.
AID1430724Growth inhibition of mouse 4T1.2 cells up to 20000 nM encapsulated within cucurbit[8]uril after 48 hrs by MTT assay2017ACS medicinal chemistry letters, May-11, Volume: 8, Issue:5
Encapsulation of Mitoxantrone within Cucurbit[8]uril Decreases Toxicity and Enhances Survival in a Mouse Model of Cancer.
AID1381972Antiproliferative activity against human HT-29 cells after 48 hrs by MTT assay2018European journal of medicinal chemistry, Feb-25, Volume: 146The lead optimization of the polyamine conjugate of flavonoid with a naphthalene motif: Synthesis and biological evaluation.
AID130603In vitro inhibitory activity against L1210 leukemia cell line1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Synthesis and antitumor properties of an anthraquinone bisubstituted by the copper chelating peptide Gly-Gly-L-His.
AID1506788Induction of apoptosis in human HCC78 cells assessed as early apoptotic cells level at 20 nM incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry (Rvb = 6.33%)2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID536039Cytotoxicity against human HL60 cells after 72 hrs2010Bioorganic & medicinal chemistry, Nov-15, Volume: 18, Issue:22
Indeno[1,2-c]isoquinolin-5,11-diones conjugated to amino acids: Synthesis, cytotoxicity, DNA interaction, and topoisomerase II inhibition properties.
AID1209581Fraction unbound in Sprague-Dawley rat brain homogenates at 5 uM by equilibrium dialysis analysis2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID1130181Antineoplastic activity against mouse P388 cells allografted in CDF1 mouse at 0.12 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID395134Binding affinity to poly(dA).poly(dT) DNA assessed as change in melting temperature2008European journal of medicinal chemistry, Nov, Volume: 43, Issue:11
Ligand binding to nucleic acids and proteins: Does selectivity increase with strength?
AID1506787Induction of apoptosis in human HCC78 cells assessed as viable cells level at 20 nM incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry (Rvb = 80.8%)2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID129073Antileukemic activity towards P388 Murine Leukemia at a dose of 0.2 mg/kg, expressed as body weight change1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID235123Resistance index was determined by ratio of cytotoxicities of human colon adenocarcinoma (LoVo) cells to human colon adenocarcinoma resistant to doxorubicin (LoVo Dx) cells.2000Bioorganic & medicinal chemistry letters, Feb-07, Volume: 10, Issue:3
Synthesis and antitumor activities of 5-methyl-1- and 2-[[2-dimethylaminoethyl]amino]-aza-thiopyranoindazoles.
AID150676Relative cytotoxicity against Human bone marrow samples; Value is in range, activity expressed as IC501999Journal of medicinal chemistry, Jun-17, Volume: 42, Issue:12
Design and synthesis of modified quinolones as antitumoral acridones.
AID1233369Antiproliferative activity against human HeLa cells after 72 hrs by MTT assay2015Bioorganic & medicinal chemistry letters, Jul-01, Volume: 25, Issue:13
Synthesis and antiproliferative activity of some novel benzo-fused imidazo[1,8]naphthyridinones.
AID354538Cytotoxicity against rat C6 cells at 50 ug/mL to 2.5 mg/mL after 3 days treated 4 hrs before db-cAMP challenge by MTT assay1996Journal of natural products, Dec, Volume: 59, Issue:12
Cell-based screen for identification of inhibitors of tubulin polymerization.
AID1349092Upregulation of p53 protein levels in NAE knockdown human Caco2 cells at 10 uM after 16 hrs by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID729376Inhibition of PIM1-mediated BAD phosphorylation in human K562 cells at 0.1 to 30 uM after 12 hrs by Western blotting analysis2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID729378Inhibition of PIM1-mediated BAD phosphorylation in human MV411 cells at 100 nM after 12 hrs by Western blotting analysis2013Journal of medicinal chemistry, Mar-28, Volume: 56, Issue:6
A new target for an old drug: identifying mitoxantrone as a nanomolar inhibitor of PIM1 kinase via kinome-wide selectivity modeling.
AID1349108Induction of apoptosis in human Caco2 cells assessed as late apoptotic cells at 5 uM after 16 hrs by Annexin V-FITC/propidium iodide staining-based flow cytometric analysis (Rvb = 0.072%)2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID1557152Cytotoxicity against human NCI-H460/MX20 cells assessed as inhibition of cell viability incubated for 2 hrs by MTT assay2019European journal of medicinal chemistry, Oct-01, Volume: 179Benzoyl indoles with metabolic stability as reversal agents for ABCG2-mediated multidrug resistance.
AID1349112Induction of apoptosis in human Caco2 cells assessed as late apoptotic cells at 10 uM after 16 hrs by Annexin V-FITC/propidium iodide staining-based flow cytometric analysis (Rvb = 0.072%)2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID232611Ratio of IC50 against V79 cells in the presence of air to that of nitrogen.1995Journal of medicinal chemistry, Mar-17, Volume: 38, Issue:6
Synthesis and biological activity of thiazolylindolequinones, analogues of the natural product BE 10988.
AID602040Cytotoxicity against human HCT116 cells after 24 hrs by MTT assay2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Cytotoxic and PPARs transcriptional activities of sterols from the Vietnamese soft coral Lobophytum laevigatum.
AID679172TP_TRANSPORTER: drug resistance in BCRP-expressing LLC-PK1 cells2003Molecular pharmacology, Sep, Volume: 64, Issue:3
Breast cancer resistance protein exports sulfated estrogens but not free estrogens.
AID135059In vivo antileukemic activity towards P388 Murine Leukemia at a dose of 0.2 mg/kg, expressed as long time survivors tested in 6 animals1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1711947Cytotoxicity against human QSG7701 cells assessed as inhibition of cell proliferation at 1 uM measured after 48 hrs by MTT assay relative to control2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID1130173Antineoplastic activity against mouse P388 cells allografted in CDF1 mouse at 2 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID150691Relative cytotoxicity against Human bone marrow samples; Value is in range, activity expressed as IC901999Journal of medicinal chemistry, Jun-17, Volume: 42, Issue:12
Design and synthesis of modified quinolones as antitumoral acridones.
AID145436Antitumor activity against human ovarian OVCAR-3 cell lines.1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID236916Percentage of mass balance in hexadecane membranes model2005Journal of medicinal chemistry, Jan-27, Volume: 48, Issue:2
Exploring the role of different drug transport routes in permeability screening.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID227413Dose modifying factor expressed as the ratio of IC50 for the chemotherapy drug to IC50 for drug + GG918; Range = 1.2-18502004Bioorganic & medicinal chemistry letters, Feb-23, Volume: 14, Issue:4
Inhibitors of multidrug resistance (MDR) have affinity for MDR substrates.
AID216273In vitro extracellular concentration required to reduce cell population to 50% against Walker 256 (WS) carcinoma cells1992Journal of medicinal chemistry, Apr-17, Volume: 35, Issue:8
Anthracene-9,10-diones as potential anticancer agents. Synthesis, DNA-binding, and biological studies on a series of 2,6-disubstituted derivatives.
AID436875Inhibition of TEM-1 using nitrocefin as substrate at 25 uM after 15 mins by microtiter plate assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID83794Percent inhibition at S phase of cell cycle at a dose of 25 ng/mL after 72 hours of induction in HT-29 cell line1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID57199In vitro inhibition of partially purified human ovarian carcinoma topoisomerase II of kDNA decatenation1995Journal of medicinal chemistry, Oct-27, Volume: 38, Issue:22
Topoisomerase II-mediated DNA cleavage by adocia- and xestoquinones from the Philippine sponge Xestospongia sp.
AID683861Antiproliferative activity against human HL60/MX2 cells after 72 hrs by SRB assay2012Bioorganic & medicinal chemistry letters, Oct-01, Volume: 22, Issue:19
New derivatives of 11-methyl-6-[2-(dimethylamino)ethyl]-6H-indolo[2,3-b]quinoline as cytotoxic DNA topoisomerase II inhibitors.
AID1349105Induction of apoptosis in human Caco2 cells assessed as necrotic cells at 1 uM after 16 hrs by Annexin V-FITC/propidium iodide staining-based flow cytometric analysis (Rvb = 0.12%)2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID81643Relative cytotoxicity against Human promyelocytic Leukemia(HL-60) cells; Value is in range, activity expressed as IC901999Journal of medicinal chemistry, Jun-17, Volume: 42, Issue:12
Design and synthesis of modified quinolones as antitumoral acridones.
AID1053264Antagonist activity at human recombinant dopamine D1 receptor expressed in CHOK1 cells assessed as inhibition of agonist-induced cAMP accumulation at 100 uM preincubated for 10 mins prior to agonist addition measured after 30 mins by HTRF assay relative t2013Journal of medicinal chemistry, Nov-14, Volume: 56, Issue:21
Experimental confirmation of new drug-target interactions predicted by Drug Profile Matching.
AID320442Cytotoxicity against human SF268 cells after 48 hrs by SRB assay2008Bioorganic & medicinal chemistry, Jan-15, Volume: 16, Issue:2
Synthesis, DNA binding, and cytotoxicity of 1,4-bis(2-amino-ethylamino)anthraquinone-amino acid conjugates.
AID595062Cytotoxicity against human MES-SA cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Design, synthesis and antiproliferative activity of novel aminosubstituted benzothiopyranoisoindoles.
AID1130164Antineoplastic activity against mouse L1210 cells allografted in CDF1 mouse assessed as survival at 10.8 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1711997Toxicity in Kunming mouse implanted with mouse H22 cells assessed as change in body weight at 0.4 mg/kg, iv administered for 7 consecutive days starting from day 11 post inoculation and measured after 18 days (Rvb = 5.2 %)2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID594151Antiproliferative activity against human RKOp27 cells after 48 hrs by XTT assay2011Bioorganic & medicinal chemistry letters, May-15, Volume: 21, Issue:10
Synthesis and antiproliferative activity of new cytotoxic azanaphthoquinone pyrrolo-annelated derivatives: Part II.
AID216435Tested for inhibitory activity against a sensitive strain of human colon carcinoma WiDr using sulforhodamine B assay (it is MRP positive but non-P-glycoprotein).2000Journal of medicinal chemistry, Aug-10, Volume: 43, Issue:16
Analogues of amonafide and azonafide with novel ring systems.
AID681508TP_TRANSPORTER: efflux in MCF7/VP and MCF cells2001Cancer research, Jul-15, Volume: 61, Issue:14
Resistance to mitoxantrone in multidrug-resistant MCF7 breast cancer cells: evaluation of mitoxantrone transport and the role of multidrug resistance protein family proteins.
AID1430727Toxicity in Balb/c mouse implanted with mouse 4T1.2 cells assessed as body weight loss at 3 mg/kg, iv encapsulated within cucurbit[8]uril administered twice weekly for 2 weeks2017ACS medicinal chemistry letters, May-11, Volume: 8, Issue:5
Encapsulation of Mitoxantrone within Cucurbit[8]uril Decreases Toxicity and Enhances Survival in a Mouse Model of Cancer.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID102172In vitro cytotoxicity was tested against human colon adenocarcinoma LoVo cell line1999Journal of medicinal chemistry, Jul-15, Volume: 42, Issue:14
2,3-Dihydro-1H,7H-pyrimido[5,6,1-de]acridine-1,3,7-trione derivatives, a class of cytotoxic agents active on multidrug-resistant cell lines: synthesis, biological evaluation, and structure-activity relationships.
AID1711976Antitumor activity against mouse H22 cells implanted in Kunming mouse assessed as tumor growth inhibition at 0.4 mg/kg, iv administered for 7 consecutive days starting from day 8 post inoculation and measured after 16 days relative to control2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID1474540Resistance index, ratio of IC50 for human HL60/MX2 cells to IC50 for human HL60 cells2017European journal of medicinal chemistry, May-26, Volume: 132Novel phosphonate analogs of sulforaphane: Synthesis, in vitro and in vivo anticancer activity.
AID98312Dose level for 50% inhibition of L1210 cell growth was measured after 48 hr.1988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID10007Cytotoxic potency required to inhibit A2780 cell growth by 50% after cell drug contact for 96 hrs1997Journal of medicinal chemistry, Nov-07, Volume: 40, Issue:23
1-[(omega-aminoalkyl)amino]-4-[N-(omega-aminoalkyl)carbamoyl]-9-oxo-9, 10-dihydroacridines as intercalating cytotoxic agents: synthesis, DNA binding, and biological evaluation.
AID1903852Antitumor immunity against human U2OS cells assessed as decrease in ATP by measuring reduction in quinacrine green fluorescence intensity at 3 uM pretreated for 24 hrs by live fluorescence microscopic analysis2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Biological Investigation of a Water-Soluble Isoginkgetin-Phosphate Analogue, Targeting the Spliceosome with
AID1506796Inhibition of ROS1 in human HCC78 cells assessed as reduction in STAT3 phosphorylation incubated for 48 hrs by Western blot method2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID115197The percent increase in life span of compound was measured against P388 Leukemia cells in mice at at a dose of 1.6 mg/kg on days 1,5 and 91995Journal of medicinal chemistry, Mar-17, Volume: 38, Issue:6
Amino-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H- dibenz[de,h]isoquinoline-1,3-diones. Synthesis, antitumor activity, and quantitative structure--activity relationship.
AID1221965Transporter substrate index of efflux ratio in human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of P-gp inhibitor LY3359792011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID272511Antiproliferative activity against multidrug resistant MDA435/LCC6 cells in presence of 5 uM verapamil by ELISA2006Journal of medicinal chemistry, Nov-16, Volume: 49, Issue:23
Flavonoid dimers as bivalent modulators for P-glycoprotein-based multidrug resistance: synthetic apigenin homodimers linked with defined-length poly(ethylene glycol) spacers increase drug retention and enhance chemosensitivity in resistant cancer cells.
AID214779Antitumor activity against human melanoma UACC375 cell line.1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID1221957Apparent permeability from basolateral to apical side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis2011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1506774Induction of apoptosis in human HCC78 cells incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID589896Cytotoxicity against human A549 cells after 72 hrs2011Bioorganic & medicinal chemistry letters, Apr-01, Volume: 21, Issue:7
Cytotoxic and antioxidant activities of diterpenes and sterols from the Vietnamese soft coral Lobophytum compactum.
AID1130155Antineoplastic activity against mouse B16 cells allografted in BDF1 mouse at 0.25 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID85581Inhibitory activity against human tumor cell line HT1080.1995Journal of medicinal chemistry, Feb-03, Volume: 38, Issue:3
Chromophore-modified antitumor anthracenediones: synthesis, DNA binding, and cytotoxic activity of 1,4-bis[(aminoalkyl)amino]benzo[g]-phthalazine-5,10-diones.
AID1550886Induction of immunogenic cell death in mouse H22 cells assessed as extracellular ATP level at 2 uM measured after 24 hrs by chemiluminescence-based assay2019European journal of medicinal chemistry, Jun-01, Volume: 171Naphthyl quinoxaline thymidine conjugate is a potent anticancer agent post UVA activation and elicits marked inhibition of tumor growth through vaccination.
AID322370Inhibition of human BCRP mediated mitoxantrone accumulation in mitoxantrone resistant MCF7 cells at 5 uM by flow cytometry2008Bioorganic & medicinal chemistry, Jan-01, Volume: 16, Issue:1
Functionalized chalcones as selective inhibitors of P-glycoprotein and breast cancer resistance protein.
AID1656522Stabilization of [32P]-labelled dsDNA (unknown origin) assessed as drug-DNA adduct formation at 5 uM in presence of formaldehyde incubated for 12 hrs by phosphorimaging analysis relative to control2020Bioorganic & medicinal chemistry, 02-01, Volume: 28, Issue:3
Formaldehyde-activated WEHI-150 induces DNA interstrand crosslinks with unique structural features.
AID1221960Apparent permeability from apical to basolateral side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of P-gp inhibitor LY3359792011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1236570Cytotoxicity against human MCF7 cells2015Journal of medicinal chemistry, Aug-13, Volume: 58, Issue:15
Progress Toward the Development of Noscapine and Derivatives as Anticancer Agents.
AID152516Activity against P388 leukemia cells in mice, by intraperitoneal dosing and net log tumor cell kill was reported1987Journal of medicinal chemistry, Jan, Volume: 30, Issue:1
Anthrapyrazole anticancer agents. Synthesis and structure-activity relationships against murine leukemias.
AID135060In vivo antileukemic activity towards P388 Murine Leukemia at a dose of 0.4 mg/kg, expressed as long time survivors tested in 12 animals1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID101787In vitro cytotoxic activity against human breast MDA-MB-231 cell line ( standard deviation in parenthesis)2002Journal of medicinal chemistry, Jun-06, Volume: 45, Issue:12
Design, synthesis, and antiproliferative activity of some new pyrazole-fused amino derivatives of the pyranoxanthenone, pyranothioxanthenone, and pyranoacridone ring systems: a new class of cytotoxic agents.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug 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.
AID97056In vivo effect of dosing on L1210 leukemia measured as range at 0.4 mg/kg (cumulative dose 6.8 mg/Kg) with ip day 1,5&9 (once daily); value range 15 to 201988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID1711971Antitumor activity against mouse H22 cells implanted in Kunming mouse assessed as reduction in tumor weight at 0.4 mg/kg, iv administered for 7 consecutive days starting from day 8 post inoculation and measured after 16 days (Rvb = 2.15 +/- 0.51 g)2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID733200Antiproliferative activity against human KB/HeLa cells after 48 hrs2013Bioorganic & medicinal chemistry letters, Mar-15, Volume: 23, Issue:6
Synthesis and biological evaluation of new cytotoxic indazolo[4,3-gh]isoquinolinone derivatives.
AID647959Inhibition of human TERT expression in H1299 cells at 1 uM after 24 hrs by secreted alkaline phosphatase reporter gene assay relative to control2012European journal of medicinal chemistry, Apr, Volume: 50Design, synthesis and evaluation of telomerase inhibitory, hTERT repressing, and anti-proliferation activities of symmetrical 1,8-disubstituted amidoanthraquinones.
AID1349111Induction of apoptosis in human Caco2 cells assessed as early apoptotic cells at 10 uM after 16 hrs by Annexin V-FITC/propidium iodide staining-based flow cytometric analysis (Rvb = 1.40%)2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID455589Cytotoxicity against human HL60 cells by MTT assay2010Bioorganic & medicinal chemistry letters, Jan-01, Volume: 20, Issue:1
Dammarane-type saponins from the flower buds of Panax ginseng and their effects on human leukemia cells.
AID647962Cytotoxicity against human H1299 cells assessed as cell growth at 1 uM after 48 hrs by MTT assay2012European journal of medicinal chemistry, Apr, Volume: 50Design, synthesis and evaluation of telomerase inhibitory, hTERT repressing, and anti-proliferation activities of symmetrical 1,8-disubstituted amidoanthraquinones.
AID1430721Drug uptake in mouse 4T1.2 cell nucleus at 5 uM encapsulated within cucurbit[8]uril after 4 hrs by laser scanning confocal microscopic method2017ACS medicinal chemistry letters, May-11, Volume: 8, Issue:5
Encapsulation of Mitoxantrone within Cucurbit[8]uril Decreases Toxicity and Enhances Survival in a Mouse Model of Cancer.
AID1586109Antiproliferative activity against human SGC7901 cells after 72 hrs by sulforhodamine B assay2018Journal of natural products, 12-28, Volume: 81, Issue:12
A Pair of Enantiomeric Bis- seco-abietane Diterpenoids from Cryptomeria fortunei.
AID436874Inhibition of TEM-1 using nitrocefin as substrate after 15 mins by microtiter plate assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Inhibitors of VIM-2 by screening pharmacologically active and click-chemistry compound libraries.
AID592675Cytotoxicity against human HCT116 cells by MTT assay2011Bioorganic & medicinal chemistry, Apr-15, Volume: 19, Issue:8
Cytotoxic and anti-inflammatory cembranoids from the Vietnamese soft coral Lobophytum laevigatum.
AID687161Ratio of IC50 for human HL60/ADR cells to IC50 for human HL60 cells2012Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11
Structure-activity relationship (SAR) study of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and the potential of the lead against multidrug resistance in cancer treatment.
AID1349087Inhibition of SAE (unknown origin) assessed as decrease in SAE-mediated Ubc9-SUMO conjugation levels up to 10 uM preincubated for 10 mins followed by ATP and Mg2+ addition measured after 60 mins by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID635081Cytotoxicity against human PC3 cells after 48 hrs by SRB assay2012European journal of medicinal chemistry, Jan, Volume: 47, Issue:1
Synthesis, antiproliferative activities and telomerase inhibition evaluation of novel asymmetrical 1,2-disubstituted amidoanthraquinone derivatives.
AID538150Binding affinity to calf thymus DNA assessed as ratio of final absorbance area to absorbance of compound at 100 uM after 24 hrs by UV spectrophotometer analysis2010European journal of medicinal chemistry, Nov, Volume: 45, Issue:11
Structural modifications on the phenazine N,N'-dioxide-scaffold looking for new selective hypoxic cytotoxins.
AID153900In vivo antitumor activity against P388 leukemia cells at a dose of 1.5 mg/kg as a single injection and 3 mg/kg as a total1984Journal of medicinal chemistry, Mar, Volume: 27, Issue:3
5-[(Aminoalkyl)amino]-substituted anthra[1,9-cd]pyrazol-6(2H)-ones as novel anticancer agents. Synthesis and biological evaluation.
AID10019In vitro Cytotoxic activity of compound in comparison with reference compounds in human cell line A27801999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1883026Antitumor activity against mouse 4T1 cells implanted in Balb/c mouse assessed as TUNEL positive cells at 50 mg/kg administered intratumorally every four days for 14 days in the presence of liquid cyanoacrylate by TUNEL staining analysis2022European journal of medicinal chemistry, Jul-05, Volume: 237Design, synthesis, and evaluation of a novel series of mono-indolylbenzoquinones derivatives for the potential treatment of breast cancer.
AID1209593Dissociation constant, pKa of the acidic compound by capillary electrophoresis-mass spectrometry analysis2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID1132489Antitumor activity against mouse P388 cells allografted in BDF1 mouse assessed as mouse survival at 0.5 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID320439Ratio of GI50 for human HL60/MX2 cells to GI50 for human HL60 cells2008Bioorganic & medicinal chemistry, Jan-15, Volume: 16, Issue:2
Synthesis, DNA binding, and cytotoxicity of 1,4-bis(2-amino-ethylamino)anthraquinone-amino acid conjugates.
AID102331Tested in vitro for cytotoxic activity against Doxorubicin resistant Human colon Adenocarcinoma sensitive cell line1994Journal of medicinal chemistry, Mar-18, Volume: 37, Issue:6
6,9-Bis[(aminoalkyl)amino]benzo[g]isoquinoline-5,10-diones. A novel class of chromophore-modified antitumor anthracene-9,10-diones: synthesis and antitumor evaluations.
AID678804TP_TRANSPORTER: ATP hydrolysis in membrane vesicle from BCRP-expressing Sf9 cells2001Biochemical and biophysical research communications, Jul-06, Volume: 285, Issue:1
Functional characterization of the human multidrug transporter, ABCG2, expressed in insect cells.
AID102334In vitro cytotoxicity was tested against human colon adenocarcinoma LoVo/Dx resistant cell line1999Journal of medicinal chemistry, Jul-15, Volume: 42, Issue:14
2,3-Dihydro-1H,7H-pyrimido[5,6,1-de]acridine-1,3,7-trione derivatives, a class of cytotoxic agents active on multidrug-resistant cell lines: synthesis, biological evaluation, and structure-activity relationships.
AID97831Effective concentration required to inhibit by 50% the growth of L1210 cells1988Journal of medicinal chemistry, Oct, Volume: 31, Issue:10
Synthesis and antineoplastic evaluation of 1,4-bis(aminoalkanamido)-9,10-anthracenediones.
AID202924Number of mice dead with toxic dose was measured on S180 tumor cell at 0.75 mg/kg (cumulative dose 16 mg/kg) introduced (in vivo) ip1988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID83789Percent inhibition at G1 phase of cell cycle at a dose of 100n g/mL after 72 hours of induction in HT-29 cell line1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1233374Antiproliferative activity against human MES-SA/Dx5 cells after 72 hrs by MTT assay2015Bioorganic & medicinal chemistry letters, Jul-01, Volume: 25, Issue:13
Synthesis and antiproliferative activity of some novel benzo-fused imidazo[1,8]naphthyridinones.
AID733186Binding affinity to calf thymus DNA up to 5 mM2013Bioorganic & medicinal chemistry letters, Mar-15, Volume: 23, Issue:6
Synthesis and biological evaluation of new cytotoxic indazolo[4,3-gh]isoquinolinone derivatives.
AID1525936Cytotoxicity against human HEK293 cells assessed as reduction in cell viability after 5 days by MTS/PMS assay2019Journal of medicinal chemistry, 09-26, Volume: 62, Issue:18
Triazole Bridged Flavonoid Dimers as Potent, Nontoxic, and Highly Selective Breast Cancer Resistance Protein (BCRP/ABCG2) Inhibitors.
AID9065Inhibitory concentration of compound against proliferation of lung carcinoma A549 cell line2002Bioorganic & medicinal chemistry letters, Jun-03, Volume: 12, Issue:11
Design and synthesis of some new pyranoxanthenone aminoderivatives with cytotoxic activity.
AID678965TP_TRANSPORTER: drug resistance in BCRP-expressing PA317 cells2003International journal of cancer, Dec-10, Volume: 107, Issue:5
Single amino acid substitutions in the transmembrane domains of breast cancer resistance protein (BCRP) alter cross resistance patterns in transfectants.
AID1439470Selectivity index, ratio of IC50 for mouse NIH/3T3 cells to IC50 for mouse L1210 cells2017European journal of medicinal chemistry, Mar-31, Volume: 129Allylic isothiouronium salts: The discovery of a novel class of thiourea analogues with antitumor activity.
AID106265In vivo antitumor activity was measured on MX-1 human mammary carcinoma cells. TWI%=tumor weight inhibition. Optimal dose at 3 mg/kg/day1998Journal of medicinal chemistry, Dec-31, Volume: 41, Issue:27
Synthesis and antitumor evaluation of 2,5-disubstituted-indazolo[4, 3-gh]isoquinolin-6(2H)-ones (9-aza-anthrapyrazoles).
AID1430722Drug uptake in mouse 4T1.2 cell lysosomes at 5 uM encapsulated within cucurbit[8]uril after 20 mins by LysoTracker Green staining based laser scanning confocal microscopic method2017ACS medicinal chemistry letters, May-11, Volume: 8, Issue:5
Encapsulation of Mitoxantrone within Cucurbit[8]uril Decreases Toxicity and Enhances Survival in a Mouse Model of Cancer.
AID1430731Antitumor activity against mouse 4T1.2 cells implanted in Balb/c mouse assessed as mouse survival rate at 2 mg/kg, iv administered twice weekly for 2 weeks measured up to 33 days (rvb = 30%)2017ACS medicinal chemistry letters, May-11, Volume: 8, Issue:5
Encapsulation of Mitoxantrone within Cucurbit[8]uril Decreases Toxicity and Enhances Survival in a Mouse Model of Cancer.
AID721747Inhibition of human MATE1-mediated [14]-metformin uptake expressed in HEK293 cells after 1.5 mins by scintillation counting analysis2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID1130151Antineoplastic activity against mouse B16 cells allografted in BDF1 mouse at 1 mg/kg qd for 9 days relative to control1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1349103Induction of apoptosis in human Caco2 cells assessed as early apoptotic cells at 1 uM after 16 hrs by Annexin V-FITC/propidium iodide staining-based flow cytometric analysis (Rvb = 1.40%)2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID1349106Induction of apoptosis in human Caco2 cells assessed as viable cells at 5 uM after 16 hrs by Annexin V-FITC/propidium iodide staining-based flow cytometric analysis (Rvb = 98.4%)2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID248024Cytotoxicity against human LoVo cancer cell line was determined after 144 hr2004Journal of medicinal chemistry, Oct-07, Volume: 47, Issue:21
Rational design, synthesis, and biological evaluation of bis(pyrimido[5,6,1-de]acridines) and bis(pyrazolo[3,4,5-kl]acridine-5-carboxamides) as new anticancer agents.
AID680981TP_TRANSPORTER: intracellular accumulation in MCF-7 and MCF-7 AdVp3000 cells2000Journal of cell science, Jun, Volume: 113 ( Pt 11)The multidrug-resistant phenotype associated with overexpression of the new ABC half-transporter, MXR (ABCG2).
AID230915Ratio of antilog(mean log IC50 in bone marrow sample) and antolog(mean log IC90) in HL-60)1999Journal of medicinal chemistry, Jun-17, Volume: 42, Issue:12
Design and synthesis of modified quinolones as antitumoral acridones.
AID129074Antileukemic activity towards P388 Murine Leukemia at a dose of 0.4 mg/kg, expressed as body weight change1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID171537Cardiotoxicity measured by the ATP/protein ratio compared with untreated controls using neonatal rat heart myocyte assay.1996Journal of medicinal chemistry, Dec-06, Volume: 39, Issue:25
2-[2'-(Dimethylamino)ethyl]-1,2-dihydro- 3H-dibenz[de,h]isoquinoline-1,3-diones with substituents at positions 4, 8, 9, 10, and 11. Synthesis, antitumor activity, and quantitative structure-activity relationships.
AID680980TP_TRANSPORTER: intracellular accumulation in S1 and S1-M1-80 cells2000Journal of cell science, Jun, Volume: 113 ( Pt 11)The multidrug-resistant phenotype associated with overexpression of the new ABC half-transporter, MXR (ABCG2).
AID1070859Inhibition of human tert transcriptional activity assessed as SEAP activity at 100 uM after 24 hrs by SEAP reporter assay2013European journal of medicinal chemistry, Nov, Volume: 69Structure-based design, synthesis and biological evaluation of novel anthra[1,2-d]imidazole-6,11-dione homologues as potential antitumor agents.
AID1711992Antimetastatic activity against mouse H22 cells implanted in Kunming mouse assessed as inhibition of metastasis at 0.4 mg/kg, iv administered for 7 consecutive days starting from day 11 post inoculation and measured after 18 days relative to control2016European journal of medicinal chemistry, Oct-04, Volume: 121Synthesis and biological properties of polyamine modified flavonoids as hepatocellular carcinoma inhibitors.
AID154570Percent ratio of the medium survival time for P388 murine leukemia in CDF1 mice at 12 mg/kg1989Journal of medicinal chemistry, Aug, Volume: 32, Issue:8
Synthesis of unsymmetrically substituted 1,4-bis[(aminoalkyl)amino]anthracene-9,10-diones as potential antileukemic agents.
AID1070862Cytotoxicity against human H1299 cells assessed as cell viability at 100 uM after 48 hrs by MTT assay2013European journal of medicinal chemistry, Nov, Volume: 69Structure-based design, synthesis and biological evaluation of novel anthra[1,2-d]imidazole-6,11-dione homologues as potential antitumor agents.
AID96628Antitumor activity against L1210 lymphocytic cells in vitro1984Journal of medicinal chemistry, Mar, Volume: 27, Issue:3
5-[(Aminoalkyl)amino]-substituted anthra[1,9-cd]pyrazol-6(2H)-ones as novel anticancer agents. Synthesis and biological evaluation.
AID1233370Antiproliferative activity against human FM3 cells after 72 hrs by MTT assay2015Bioorganic & medicinal chemistry letters, Jul-01, Volume: 25, Issue:13
Synthesis and antiproliferative activity of some novel benzo-fused imidazo[1,8]naphthyridinones.
AID1221963Transporter substrate index ratio of permeability from apical to basolateral side in human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of P-gp inhibitor LY3359792011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1883018Protection of Balb/c mouse spleen implanted with mouse 4T1 cells at 50 mg/kg administered intratumorally every four days for 14 days in the presence of liquid cyanoacrylate2022European journal of medicinal chemistry, Jul-05, Volume: 237Design, synthesis, and evaluation of a novel series of mono-indolylbenzoquinones derivatives for the potential treatment of breast cancer.
AID312292Cytotoxicity against human K562 cells after 5 days by XTT assay2007Journal of natural products, Dec, Volume: 70, Issue:12
Curcumin induces high levels of topoisomerase I- and II-DNA complexes in K562 leukemia cells.
AID39734Compound was tested against sc B16 melanoma at % tumor growth inhibition(TGI) in mice at 3.2 mg/kg dosage.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID84118Percent inhibition at S phase of cell cycle at a dose of 250 ng/mL after 72 hours of induction in HT-29/Mx cell line1999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID1130172Antineoplastic activity against mouse P388 cells allografted in CDF1 mouse assessed as survival at 2 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1236574Cytotoxicity against human MCF-7 FLV1000 cells expressing ABCB22015Journal of medicinal chemistry, Aug-13, Volume: 58, Issue:15
Progress Toward the Development of Noscapine and Derivatives as Anticancer Agents.
AID1506780Induction of apoptosis in human HCC78 cells assessed as early apoptotic cells level at 5 nM incubated fro 48 hrs by Annexin-V FITC and propidium iodide staining based flow cytometry (Rvb = 6.33%)2017MedChemComm, Mar-01, Volume: 8, Issue:3
Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells.
AID721745Ratio of Cmax unbound to IC50 for human MATE1-mediated ASP+ uptake expressed in HEK293 cells2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID1550891Induction of immunogenic cell death in mouse H22 cells assessed as increase in calreticulin level in cell surface at 2 uM incubated for 5 hrs by Hoechst staining based fluorescence microscopic analysis2019European journal of medicinal chemistry, Jun-01, Volume: 171Naphthyl quinoxaline thymidine conjugate is a potent anticancer agent post UVA activation and elicits marked inhibition of tumor growth through vaccination.
AID1349113Induction of apoptosis in human Caco2 cells assessed as necrotic cells at 10 uM after 16 hrs by Annexin V-FITC/propidium iodide staining-based flow cytometric analysis (Rvb = 0.12%)2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID1349107Induction of apoptosis in human Caco2 cells assessed as early apoptotic cells at 5 uM after 16 hrs by Annexin V-FITC/propidium iodide staining-based flow cytometric analysis (Rvb = 1.40%)2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID1656521Stabilization of [32P]-labelled dsDNA (unknown origin) assessed as drug-DNA adduct formation by measuring adduct half life incubated for 12 hrs in presence of formaldehyde by phosphorimaging analysis2020Bioorganic & medicinal chemistry, 02-01, Volume: 28, Issue:3
Formaldehyde-activated WEHI-150 induces DNA interstrand crosslinks with unique structural features.
AID248858Cytotoxicity is determined as the concentration required to inhibit the growth of human colon adenocarcinoma (HT-29) cell line2004Journal of medicinal chemistry, Oct-07, Volume: 47, Issue:21
Rational design, synthesis, and biological evaluation of bis(pyrimido[5,6,1-de]acridines) and bis(pyrazolo[3,4,5-kl]acridine-5-carboxamides) as new anticancer agents.
AID1053266Agonist activity at human recombinant dopamine D1 receptor expressed in CHOK1 cells assessed as stimulation of cAMP accumulation at 100 uM after 30 mins by HTRF assay relative to SKF812972013Journal of medicinal chemistry, Nov-14, Volume: 56, Issue:21
Experimental confirmation of new drug-target interactions predicted by Drug Profile Matching.
AID1851419Antiproliferative activity against human K562 cells assessed as inhibition of cell growth2022Bioorganic & medicinal chemistry letters, 10-01, Volume: 73Synthesis and antitumor activity of a series of novel N-aryl-5-(2,2,2-trifluoroethoxy)-1,5-dihydro-2H-pyrrol-2-ones derivatives.
AID46169Inhibitory concentration against ethidium:Calf thymus DNA(0.1:1) binding at pH 51997Journal of medicinal chemistry, Nov-07, Volume: 40, Issue:23
1-[(omega-aminoalkyl)amino]-4-[N-(omega-aminoalkyl)carbamoyl]-9-oxo-9, 10-dihydroacridines as intercalating cytotoxic agents: synthesis, DNA binding, and biological evaluation.
AID1132520Antitumor activity against mouse B16 cells allografted in BDF1 mouse assessed as increase in survival time at 0.5 mg/kg administered 24 hrs post challenge relative to control1978Journal of medicinal chemistry, Mar, Volume: 21, Issue:3
Antineoplastic agents. Structure-activity relationship study of bis(substituted aminoalkylamino)anthraquinones.
AID381808Resistance factor, ratio of IC50 for etoposide-resistant human K/VP.5 cells to IC50 for human K562 cells2008Bioorganic & medicinal chemistry, Apr-01, Volume: 16, Issue:7
The structure-based design, synthesis and biological evaluation of DNA-binding bisintercalating bisanthrapyrazole anticancer compounds.
AID212421Inhibition of Taq polymerase at 10 uM (Slight inhibition)1998Journal of medicinal chemistry, Aug-13, Volume: 41, Issue:17
1,4- and 2,6-disubstituted amidoanthracene-9,10-dione derivatives as inhibitors of human telomerase.
AID1130158Antineoplastic activity against mouse Colon 26 cells allografted in CDF1 mouse assessed as survival at 0.69 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID1430729Antitumor activity against mouse 4T1.2 cells implanted in Balb/c mouse assessed as tumor growth inhibition at 3 mg/kg, iv encapsulated within cucurbit[8]uril administered twice weekly for 2 weeks2017ACS medicinal chemistry letters, May-11, Volume: 8, Issue:5
Encapsulation of Mitoxantrone within Cucurbit[8]uril Decreases Toxicity and Enhances Survival in a Mouse Model of Cancer.
AID1130176Antineoplastic activity against mouse P388 cells allografted in CDF1 mouse assessed as survival at 0.5 mg/kg qd for 9 days1979Journal of medicinal chemistry, May, Volume: 22, Issue:5
Structural modification study of bis(substituted aminoalkylamino)anthraquinones. An evaluation of the relationship of the [2-[(2-hydroxyethyl)amino]ethyl]amino side chain with antineoplastic activity.
AID679126TP_TRANSPORTER: transepithelial transport (basal to apical) in MDR1-expressing MDCKII cells2004European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences, Jan, Volume: 21, Issue:1
Exploring the quantitative relationship between the level of MDR1 transcript, protein and function using digoxin as a marker of MDR1-dependent drug efflux activity.
AID1349090Inhibition of NAE (unknown origin) assessed as decrease in NAE-mediated Ubc12-NEDD8 conjugation levels at 10 uM treated for 10 mins post ATP and Mg2+ addition measured after 60 mins by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID153418Compound was tested against P388 leukemia at % increase in life span (ILS) in mice at 1.6 mg/kg dosage.1996Journal of medicinal chemistry, Apr-12, Volume: 39, Issue:8
6- and 7-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H-dibenz[de,h] isoquinoline-1,3-diones: synthesis, nucleophilic displacements, antitumor activity, and quantitative structure-activity relationships.
AID98202Antitumor activity against murine L1210 resistant cell line by using MTT assay1995Journal of medicinal chemistry, Mar-17, Volume: 38, Issue:6
Amino-substituted 2-[2'-(dimethylamino)ethyl]-1,2-dihydro-3H- dibenz[de,h]isoquinoline-1,3-diones. Synthesis, antitumor activity, and quantitative structure--activity relationship.
AID100166Number of mice dead with 0.75 mg/kg dose (in vivo)1988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID733189Antiproliferative activity against human RKOp27IND cells after 48 hrs2013Bioorganic & medicinal chemistry letters, Mar-15, Volume: 23, Issue:6
Synthesis and biological evaluation of new cytotoxic indazolo[4,3-gh]isoquinolinone derivatives.
AID1349099Inhibition of NAE in human Caco2 cells assessed as decrease in cyclin D1 protein levels at 0.1 to 10 uM after 16 hrs by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID1070864Cytotoxicity against human H1299 cells assessed as cell viability at 1 uM after 48 hrs by MTT assay2013European journal of medicinal chemistry, Nov, Volume: 69Structure-based design, synthesis and biological evaluation of novel anthra[1,2-d]imidazole-6,11-dione homologues as potential antitumor agents.
AID101603Inhibitory activity against human tumor cell line MCF-7 breast adenocarcinoma.1995Journal of medicinal chemistry, Feb-03, Volume: 38, Issue:3
Chromophore-modified antitumor anthracenediones: synthesis, DNA binding, and cytotoxic activity of 1,4-bis[(aminoalkyl)amino]benzo[g]-phthalazine-5,10-diones.
AID1396797Resistance index, ratio of IC50 for antiproliferative activity against human HL60/MX2 cells to IC50 for antiproliferative activity against human HL60 cells2018Bioorganic & medicinal chemistry letters, 08-15, Volume: 28, Issue:15
Phosphorus-containing isothiocyanate-derived mercapturic acids as a useful alternative for parental isothiocyanates in experimental oncology.
AID1349089Competitive inhibition of NAE (unknown origin) assessed as decrease in NAE-mediated Ubc12-NEDD8 conjugation levels at 10 uM preincubated for 10 mins followed by Mg2+ and various concentrations of ATP addition measured after 60 mins by Lineweaver-Burk plot2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID683862Resistance index, ratio of IC50 for human HL60/MX2 cells to IC50 for human HL60 cells2012Bioorganic & medicinal chemistry letters, Oct-01, Volume: 22, Issue:19
New derivatives of 11-methyl-6-[2-(dimethylamino)ethyl]-6H-indolo[2,3-b]quinoline as cytotoxic DNA topoisomerase II inhibitors.
AID1349114Cytotoxicity against human Caco2 cells after 72 hrs by MTT assay2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID687160Ratio of IC50 for human HL60/MX2 cells to IC50 for human HL60 cells2012Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11
Structure-activity relationship (SAR) study of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and the potential of the lead against multidrug resistance in cancer treatment.
AID1430720Drug uptake in mouse 4T1.2 cell nucleus at 5 uM after 4 hrs by laser scanning confocal microscopic method2017ACS medicinal chemistry letters, May-11, Volume: 8, Issue:5
Encapsulation of Mitoxantrone within Cucurbit[8]uril Decreases Toxicity and Enhances Survival in a Mouse Model of Cancer.
AID1349088Inhibition of UAE1 (unknown origin) assessed as decrease in UAE1-mediated Ubc10-ubiquitin conjugation levels up to 10 uM preincubated for 10 mins followed by ATP and Mg2+ addition measured after 60 mins by Western blot analysis2018European journal of medicinal chemistry, Jan-01, Volume: 143Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
AID140019The compound was tested for antitumor activity against P388 murine leukemia at 3 (mg/kg/day) dose; 12/132 -no. of toxic deaths/no. of mice1994Journal of medicinal chemistry, Mar-18, Volume: 37, Issue:6
6,9-Bis[(aminoalkyl)amino]benzo[g]isoquinoline-5,10-diones. A novel class of chromophore-modified antitumor anthracene-9,10-diones: synthesis and antitumor evaluations.
AID1525933Inhibition of BCRP in human HEK293/R2 cells assessed as reduction in cell viability after 5 days by MTS/PMS assay2019Journal of medicinal chemistry, 09-26, Volume: 62, Issue:18
Triazole Bridged Flavonoid Dimers as Potent, Nontoxic, and Highly Selective Breast Cancer Resistance Protein (BCRP/ABCG2) Inhibitors.
AID55805In vitro Cytotoxic activity of compound in comparison with reference compounds in human cell line DU1451999Journal of medicinal chemistry, Sep-09, Volume: 42, Issue:18
8,11-dihydroxy-6-[(aminoalkyl)amino]-7H-benzo[e]perimidin-7-ones with activity in multidrug-resistant cell lines: synthesis and antitumor evaluation.
AID687164Ratio of IC50 for doxorubicin-resistant human K562 cells to IC50 for human K562 cells2012Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11
Structure-activity relationship (SAR) study of ethyl 2-amino-6-(3,5-dimethoxyphenyl)-4-(2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (CXL017) and the potential of the lead against multidrug resistance in cancer treatment.
AID96755Effect of dosing on L1210 leukemia in vivo measured as mean at 0.4 mg/kg (cumulative dose 6.8 mg/Kg) with ip day 1,5&9 (once daily)1988Journal of medicinal chemistry, Apr, Volume: 31, Issue:4
Synthesis, molecular modeling, DNA binding, and antitumor properties of some substituted amidoanthraquinones.
AID404699Cytotoxicity against human mitoxantrone-sensitive HL60 cells after 72 hrs2008Journal of medicinal chemistry, Jun-26, Volume: 51, Issue:12
Synthesis, cytotoxicity, DNA interaction, and topoisomerase II inhibition properties of novel indeno[2,1-c]quinolin-7-one and indeno[1,2-c]isoquinolin-5,11-dione derivatives.
AID589897Cytotoxicity against human HL60 cells after 72 hrs2011Bioorganic & medicinal chemistry letters, Apr-01, Volume: 21, Issue:7
Cytotoxic and antioxidant activities of diterpenes and sterols from the Vietnamese soft coral Lobophytum compactum.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID720501qHTS for Inhibitors of Polymerase Kappa: Confirmatory Assay for Cherry-picked Compounds2012PloS one, , Volume: 7, Issue:10
A comprehensive strategy to discover inhibitors of the translesion synthesis DNA polymerase κ.
AID1811Experimentally measured binding affinity data derived from PDB2006FEBS letters, May-29, Volume: 580, Issue:13
The structure of PknB in complex with mitoxantrone, an ATP-competitive inhibitor, suggests a mode of protein kinase regulation in mycobacteria.
AID977608Experimentally measured binding affinity data (IC50) for protein-ligand complexes derived from PDB2006FEBS letters, May-29, Volume: 580, Issue:13
The structure of PknB in complex with mitoxantrone, an ATP-competitive inhibitor, suggests a mode of protein kinase regulation in mycobacteria.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1347411qHTS 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) Libary2020ACS 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.
AID1347412qHTS assay to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: Counter screen cell viability and HiBit confirmation2020ACS 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.
AID1745855NCATS anti-infectives library activity on the primary C. elegans qHTS viability assay2023Disease models & mechanisms, 03-01, Volume: 16, Issue:3
In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
AID1745854NCATS anti-infectives library activity on HEK293 viability as a counter-qHTS vs the C. elegans viability qHTS2023Disease models & mechanisms, 03-01, Volume: 16, Issue:3
In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
AID1346063Human DNA topoisomerase II alpha (5.99.1.2 DNA Topoisomerases)2008Bioorganic & medicinal chemistry, Apr-01, Volume: 16, Issue:7
The structure-based design, synthesis and biological evaluation of DNA-binding bisintercalating bisanthrapyrazole anticancer compounds.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (4,303)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990634 (14.73)18.7374
1990's1184 (27.52)18.2507
2000's1362 (31.65)29.6817
2010's939 (21.82)24.3611
2020's184 (4.28)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 61.03

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index61.03 (24.57)
Research Supply Index8.63 (2.92)
Research Growth Index4.64 (4.65)
Search Engine Demand Index108.58 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (61.03)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials1,042 (22.88%)5.53%
Reviews392 (8.61%)6.00%
Case Studies373 (8.19%)4.05%
Observational12 (0.26%)0.25%
Other2,736 (60.07%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (312)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Phase 3 Randomized Trial for Patients With De Novo AML Comparing Standard Therapy Including Gemtuzumab Ozogamicin (GO) to CPX-351 With GO, and the Addition of the FLT3 Inhibitor Gilteritinib for Patients With FLT3 Mutations [NCT04293562]Phase 31,400 participants (Anticipated)Interventional2020-07-21Recruiting
"A Phase III Trial Comparing ARA-C/High-Dose Mitoxantrone (ALL-2') to A Standard Vincristine/Prednisone Based Regimen ('L-20') as Induction Therapy For Adult Patients With Acute Lymphoblastic Leukemia (ALL): The ALL-4 Protocol" [NCT00002766]Phase 3170 participants (Actual)Interventional1996-03-31Completed
A Clinical Study to Evaluate the Safety, Efficacy and Pharmacokinetics of Mitoxantrone Hydrochloride Liposome Injection Combined With Chemotherapy in Previously Untreated de Novo Acute Myeloid Leukemia [NCT05941585]90 participants (Anticipated)Interventional2023-07-31Not yet recruiting
CLAG-M or FLAG-Ida Chemotherapy Followed Immediately by Related/Unrelated Reduced-Intensity Conditioning (RIC) Allogeneic Hematopoietic Cell Transplantation for Adults With Myeloid Malignancies at High Risk of Relapse: A Phase 1 Study [NCT04375631]Phase 1120 participants (Anticipated)Interventional2020-12-03Recruiting
A Phase I Study of Azacitidine Combined With Mitoxantrone and Etoposide (A-NOVE) Chemotherapy for Patients' Age ≥ 60 With Poor Prognosis Acute Myeloid Leukemia (AML) [NCT01260714]Phase 113 participants (Actual)Interventional2010-12-31Terminated(stopped due to Inadequate accrual rate)
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 160 participants (Anticipated)Interventional2021-10-20Recruiting
Prexasertib in Combination With Mitoxantrone, Etoposide and Cytarabine (MEC) in Relapsed/Refractory Acute Myeloid Leukemia (AML) and High Risk Myelodysplastic Syndrome (MDS) - a Phase I Trial [NCT03735446]Phase 12 participants (Actual)Interventional2019-01-18Terminated(stopped due to Sponsor Decision)
A Phase 1 Study of MLN9708 in Combination With MEC (Mitoxantrone, Etoposide, and Intermediate-Dose Cytarabine) for Relapsed/ Refractory Acute Myelogenous Leukemia (AML) [NCT02070458]Phase 130 participants (Actual)Interventional2014-10-08Completed
Phase I Dose Escalation Study of Mitoxantrone Hydrochloride Liposome Injection in Patients With Malignant Lymphoma [NCT02131688]Phase 130 participants (Anticipated)Interventional2013-05-31Recruiting
A Phase Ib/II Trial of Combined SGN-35 (BrentuximabVedotin) Therapy With Cyclophosphamide, Procarbazine, Prednisone, Etoposide and Mitoxantrone (BrEPEM) for Older Patients With Untreated Hodgkin Lymphoma (HL) [NCT03576378]Phase 1/Phase 241 participants (Actual)Interventional2018-08-08Active, not recruiting
A Randomized, Risk and Age Adapted Comparison of the Dose-Dense Regimen S-HAM (Sequential High Dose Cytosine Arabinoside and Mitoxantrone) Versus Standard Double Induction for Initial Chemotherapy of Adult Patients With Acute Myeloid Leukemia [NCT01382147]Phase 3396 participants (Actual)Interventional2009-07-01Completed
Multicenter Randomised Clinical Trial in Acute Myeloid Leukemia Treatment Based on Three Anthracyclines, Comparing Two Types of Consolidation With Different ARA-C Doses Followed by One Year Maintenance [NCT01587430]Phase 4245 participants (Anticipated)Interventional2010-01-31Active, not recruiting
Phase I Study of the Combination of Midostaurin, Bortezomib, and Chemotherapy in Relapsed/Refractory Acute Myeloid Leukemia [NCT01174888]Phase 134 participants (Actual)Interventional2010-08-31Completed
A Phase III Randomized Trial of Gemtuzumab Ozogamicin (Mylotarg) Combined With Conventional Chemotherapy for De Novo Acute Myeloid Leukemia (AML) in Children, Adolescents, and Young Adults [NCT00372593]Phase 31,070 participants (Actual)Interventional2006-08-31Completed
Addition of Sorafenib to G-CSF, Cladribine, Cytarabine and Mitoxantrone (G-CLAM) in Adults With Newly-Diagnosed Acute Myeloid Leukemia (AML) Independent of FLT3-ITD Status: A Phase 1/2 Study [NCT02728050]Phase 1/Phase 284 participants (Actual)Interventional2016-12-01Completed
TINI 2: Total Therapy for Infants With Acute Lymphoblastic Leukemia II [NCT05848687]Phase 1/Phase 290 participants (Anticipated)Interventional2023-11-01Not yet recruiting
A Phase III Study for Patients With Newly Diagnosed Acute Promyelocytic Leukemia (APL) Using Arsenic Trioxide and All-Trans Retinoic Acid [NCT02339740]Phase 3158 participants (Actual)Interventional2015-07-21Active, not recruiting
Clinical Pharmacokinetics of Mitoxantrone Hydrochloride Liposome Injection in Recurrent/Refractory Lymphoma Subjects [NCT05173545]Phase 124 participants (Actual)Interventional2019-07-29Completed
An Open Label Study to Evaluate the Feasibility of CPI-613 Given With High Dose Cytarabine and Mitoxantrone in Patients With Relapsed or Refractory Acute Myeloid Leukemia (AML) [NCT02484391]Phase 250 participants (Anticipated)Interventional2015-09-30Completed
Open-label Multicenter Trial of Glivec® (Imatinib Mesylate, Formerly Known as STI571) in Combination With Chemotherapy (MTC) in Patients With Refractory or Relapsed Acute Myeloid Leukemia (AML) [NCT00744081]Phase 2130 participants (Anticipated)Interventional2004-07-31Completed
A Phase II, Open-label, Single Arm Study to Evaluate the Safety, Efficacy, and Pharmacokinetics of Twice Daily Midostaurin (PKC412) Combined With Standard Chemotherapy and as a Single Agent Post-consolidation Therapy in Children With Untreated FLT3-mutate [NCT03591510]Phase 223 participants (Anticipated)Interventional2019-03-13Recruiting
Study Impact, on Clinical Outcomes, Quality of Life and Costs of 2 Therapeutic Strategy (Monthly Natalizumab Versus Mitoxantrone Then Immunomodulator) at 3 Years of Follow-up for Aggressive Remitting Multiple Sclerosis [NCT01065727]250 participants (Anticipated)Interventional2010-02-28Recruiting
Evaluation of the Efficacy of Induction-consolidation Treatment Using a Double Induction in Patients With AML <60 Years Old, Depending on the Percentage of Blasts in the 14 Day, Residual Disease and Leukemic Hematopoietic Cells [NCT02072811]Phase 3400 participants (Anticipated)Interventional2014-02-28Recruiting
A Randomized, Open-Label Study of Oral CEP-701 Administered in Sequence With Standard Chemotherapy to Patients With Relapsed Acute Myeloid Leukemia (AML) Expressing FLT-3 Activating Mutations [NCT00079482]Phase 2224 participants (Actual)Interventional2003-10-31Completed
Dose Finding Safety Run-in Phase Followed by a Randomized Phase II Trial of Intensive Chemotherapy With or Without Volasertib (BI 6727) Administered Prior or After Chemotherapy in Patients With Newly Diagnosed High-Risk Myelodysplastic Syndrome (MDS) and [NCT02198482]Phase 26 participants (Actual)Interventional2016-02-29Terminated(stopped due to development program of study drug volasertib was stopped by Boehringer Ingelheim due to manufacturing problems)
A Phase 1b/2 Study to Assess the Safety and Efficacy of AMG 102 in Combination With Mitoxantrone and Prednisone in Subjects With Previously Treated Castrate Resistant Prostate Cancer [NCT00770848]Phase 1/Phase 2162 participants (Actual)Interventional2008-11-30Completed
Adjuvant Androgen Deprivation Versus Mitoxantrone Plus Prednisone Plus Androgen Deprivation in Selected High-Risk Prostate Cancer Patients Following Radical Prostatectomy [NCT00004124]Phase 3983 participants (Actual)Interventional1999-10-15Completed
Phase 1b/2 Study of Carfilzomib in Combination With Induction Chemotherapy in Children With Relapsed or Refractory Acute Lymphoblastic Leukemia [NCT02303821]Phase 1130 participants (Anticipated)Interventional2015-02-16Recruiting
National Multicenter, Controlled, Single-blind Study With Two Parallel Groups Evaluating the Safety and Efficacy of Sequential Treatment With Mitoxantrone and Interferon Beta-1a (REBIF 44mg 3 Times / Week) Versus Interferon Alone in Patients With Strong R [NCT02937285]Phase 335 participants (Actual)Interventional2010-12-06Completed
Dose-Finding Run-in Phase I Followed by a Phase III, Multicenter, Randomized, Double-Blind, Placebo-controlled Study of Crenolanib in Combination With Chemotherapy in Patients With Relapsed or Refractory Acute Myeloid Leukemia and Activating FLT3 Mutation [NCT02298166]Phase 39 participants (Actual)Interventional2016-11-17Terminated(stopped due to The manufacturer Arog Pharmaceuticals Inc has terminated the Agreement Concerning the Support of an Investigator Initiated Trial this became valid on 2020/03/09)
Risk-Stratified Randomized Phase III Testing of Blinatumomab (NSC#765986) in First Relapse of Childhood B-Lymphoblastic Leukemia (B-ALL) [NCT02101853]Phase 3669 participants (Actual)Interventional2014-12-17Active, not recruiting
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 13 participants (Actual)Interventional2010-07-31Completed
A Phase 1 Study of Intravenous EGFR-ErbituxEDVsMIT (EEDVsMit) in Children With Recurrent / Refractory Solid or CNS Tumours Expressing Epidermal Growth Factor Receptor (EGFR) (ECREST Study) [NCT02687386]Phase 19 participants (Actual)Interventional2016-02-08Terminated(stopped due to Study medication no longer in production)
A Multicentre, Open-label, Single-arm, Phase I/II Clinical Study to Evaluate the Safety, Efficacy and Pharmacokinetic Characteristics of Liposomal Mitoxantrone Hydrochloride Injection Combined With Pegaspargase in the Treatment of NKTCL [NCT04509466]Phase 1/Phase 2104 participants (Anticipated)Interventional2020-08-15Not yet recruiting
Single-arm, Open and Multi-center Phase II Study of Liposome-entrapped Mitoxantrone Hydrochloride Injection in Relapsed/Refractory Peripheral T-cell Lymphoma and NK/T-cell Lymphoma [NCT03776279]Phase 2106 participants (Anticipated)Interventional2018-04-02Recruiting
Isolated Thoracic Perfusion With Hemofiltration (ITP-F) for Pretreated and Progressive Malignant Pleural Mesothelioma [NCT02467426]23 participants (Actual)Observational2009-09-30Completed
Fludarabine, Mitoxantrone, and Dexamethasone (FND) Plus Chimeric Anti-CD20 Monoclonal Antibody (Rituximab) for Stage IV Indolent Lymphoma [NCT00577993]Phase 3210 participants (Actual)Interventional1998-03-16Completed
Effect of Priming With Granulocyte-Macrophage Colony-Stimulating Factor During Chemotherapy and Comparison of Timed Sequential Chemotherapy vs 4 Courses of High Dose Cytarabine as Consolidation in Younger Adults With Newly Diagnosed AML [NCT00880243]Phase 3473 participants (Actual)Interventional1999-03-31Completed
A Phase II, Open-Label, Single- Center Study to Assess the Activity of Oshadi D and Oshadi R in Combination With Salvage Chemotherapy for Relapsed or Refractory Acute Myeloid Leukemia (AML) or Lymphoid Leukemia (ALL) Patients [NCT02462265]Phase 215 participants (Anticipated)Interventional2017-01-31Suspended
A PALG Prospective Multicenter Clinical Trial to Compare the Efficacy of Two Standard Induction Therapies (DA-90 vs DAC) and Two Standard Salvage Regimens (FLAG-IDA vs CLAG-M) in AML Patients ≤ 60 Years Old [NCT03257241]Phase 3582 participants (Anticipated)Interventional2017-07-03Recruiting
A Phase II Study of Double Induction Chemotherapy for Newly Diagnosed Non-L3 Adult Acute Lymphoblastic Leukemia With Investigation of Minimal Residual Disease and Risk of Relapse Following Maintenance Chemotherapy [NCT00109837]Phase 279 participants (Actual)Interventional2005-04-30Completed
A Multicenter, Open-label, Phase Ib Study of Mitoxantrone Hydrochloride Liposome Injection in Subjects With Advanced Bone and Soft Tissue Sarcoma Who Has Failed At Least One Prior Line of Therapy [NCT04900766]Phase 150 participants (Anticipated)Interventional2021-06-30Not yet 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 31,645 participants (Actual)Interventional2011-06-20Active, not recruiting
A Prospective, Single-arm, Multicenter Clinical Study of Mitoxantrone Hydrochloride Liposome Combined With Rituximab and Lenalidomide in the Treatment of Relapsed and Refractory Diffuse Large B-cell Lymphoma [NCT05575973]Phase 255 participants (Anticipated)Interventional2022-10-10Not yet recruiting
A Randomized, Double-blind, Placebo-controlled Phase Ⅱ Clinical Study to Evaluate the Efficacy and Safety of Mitoxantrone Hydrochloride Liposome Injection in the Treatment of Neuromyelitis Optica Spectrum Disorder (NMOSD) [NCT05551598]Phase 245 participants (Anticipated)Interventional2022-11-15Not yet recruiting
A Collaboration Phase 2 Study of Venetoclax in Combination With Conventional Chemotherapy in Pediatric Patients With Acute Myeloid Leukemia [NCT05955261]Phase 270 participants (Anticipated)Interventional2023-07-25Recruiting
Clinical Study of Venetoclax Combined With Mitoxantrone Liposome in the Treatment of Relapsed or Refractory Acute Myeloid Leukemia [NCT05522192]Phase 1/Phase 270 participants (Anticipated)Interventional2022-07-21Recruiting
Phase I Study of Induction Therapy With Cytarabine, High-Dose Mitoxantrone and Dasatinib for Patients With Philadelphia-Chromosome Positive (Ph+) Acute Lymphoblastic Leukemia (ALL): ALL-6 Protocol [NCT00940524]Phase 17 participants (Actual)Interventional2009-07-31Completed
A Phase II Trial to Evaluate the Rate of Immune Response Using Idiotype Immunotherapies Produced by Molecular Biological Means for Treatment of Aggressive B Cell Lymphoma [NCT00004197]Phase 20 participants Interventional1999-06-25Completed
Phase I Investigator Sponsored Study to Assess the Tolerability and Efficacy of Selinexor in Combination With High Dose Cytarabine (HiDAC) and Mitoxantrone Chemotherapy for Remission Induction in Acute Myelogenous Leukemia (AML) [NCT02573363]Phase 125 participants (Actual)Interventional2015-10-07Completed
Venetoclax-Navitoclax With Cladribine-based Salvage Therapy in Patients With Relapsed/Refractory Acute Myeloid Leukemia [NCT06007911]Phase 136 participants (Anticipated)Interventional2024-02-29Not yet recruiting
A Phase I Study of Intravenous Plerixafor in Combination With Mitoxantrone Etoposide and Cytarabine for Relapsed or Refractory Acute Myeloid Leukemia [NCT01027923]Phase 16 participants (Actual)Interventional2010-05-31Terminated(stopped due to Withdrawal of support from sponsor)
The Efficacy and Safety of Chidamide Combined With VDDT Regimen(Vinorelbine,Liposomal Doxorubicin,Dexamethasone and Thalidomide) in Relapse and Refractory Patients With Diffuse Large B Cell Lymphoma [NCT02733380]Phase 220 participants (Anticipated)Interventional2016-05-31Recruiting
A Multicenter, Open-label, Phase I Dose-escalation and Dose-expansion Study of Mitoxantrone Hydrochloride Liposome Injection Combination Therapy in Chinese Patients With Advanced Solid Tumors [NCT05344742]Phase 1116 participants (Anticipated)Interventional2022-04-30Not yet recruiting
Phase I/II Study of the Combination of Mitoxantrone, Etoposide and Gemtuzumab Ozogamicin for Patients With Acute Myeloid Leukemia Refractory to Initial Standard Induction Therapy (UPCI 07-154) [NCT00660036]Phase 15 participants (Actual)Interventional2008-09-30Terminated(stopped due to due to new safety information)
ALLR3: An International Collaborative Trial for Relapsed and Refractory Acute Lymphoblastic Leukaemia (ALL) [NCT00967057]Phase 3470 participants (Anticipated)Interventional2002-10-31Completed
A Phase I Study of Combination Chemotherapy With Mitoxantrone and Etoposide (VP-16) Combined With an Autophagy Inhibitor, Hydroxychloroquine (HCQ), for the Treatment of Patients With Relapsed Acute Myelogenous Leukemia (AML) [NCT02631252]Phase 11 participants (Actual)Interventional2016-08-18Terminated(stopped due to Inability to accrue)
A Multi-Center, Randomized, Open Label Study To Evaluate Safety, Tolerability And Efficacy Of Treatment With Mitoxantrone; Pre-Treatment With Glatiramer Acetate (GA) Versus Treatment With GA Alone In Relapsing Forms Of Multiple Sclerosis. [NCT00203073]Phase 240 participants (Actual)Interventional2003-06-30Completed
Liposomal Mitoxantrone Hydrochloride, Gemcitabine, Vinorelbine With or Without Rituximab (GVM±R) in Patients With Relapsed or Refractory Aggressive Non-Hodgkin's Lymphoma [NCT05299164]Phase 124 participants (Anticipated)Interventional2022-05-15Not yet recruiting
A Phase 3 Open-Label, Multicenter, Randomized Study of ASP2215 Versus Salvage Chemotherapy in Patients With Relapsed or Refractory Acute Myeloid Leukemia (AML) With FLT3 Mutation [NCT02421939]Phase 3371 participants (Actual)Interventional2015-10-20Active, not recruiting
A Phase I/II Study of AMD3100 With Mitoxantrone, Etoposide and Cytarabine (AMD3100+MEC) in Relapsed or Refractory AML [NCT00512252]Phase 1/Phase 252 participants (Actual)Interventional2007-07-31Completed
A Phase 2, Multicenter, Open-Label Study of CNTO 328 (Anti-IL-6 Monoclonal Antibody) in Combination With Mitoxantrone Versus Mitoxantrone in Subjects With Metastatic Hormone-Refractory Prostate Cancer (HRPC) [NCT00385827]Phase 2106 participants (Actual)Interventional2006-11-30Terminated(stopped due to Prematurely stopped after Independent Data Monitoring Committee (IDMC) evaluation for lack of efficacy.)
Title: A Pilot Study Evaluating the Safety and Feasibility of Custirsen (OGX-011) in Combination With Second Line Chemotherapy in Patients With Hormone Refractory Prostate Cancer [NCT00327340]Phase 270 participants (Actual)Interventional2006-07-31Completed
A Phase I-II Study of Pentostatin, Cyclophosphamide, Rituximab, and Mitoxantrone in Previously Treated Patients With Chronic Lymphocytic Leukemia and Other Low Grade B-Cell Neoplasms [NCT00546377]Phase 1/Phase 250 participants (Actual)Interventional2005-07-31Completed
Phase II Trial of Combined Immunochemotherapy With Fludarabine, Mitoxantrone, Cyclophosphamide and Alemtuzumab (FMC-Alemtuzumab) in Patients With Previously Treated or Untreated T-Prolymphocytic Leukemia [NCT01186640]Phase 216 participants (Actual)Interventional2010-06-30Completed
Risk Adapted Treatment of Newly Diagnosed Childhood Acute Promyelocytic Leukemia (APL) Using Arsenic Trioxide (Trisenox® ) During Consolidation [NCT00866918]Phase 3106 participants (Actual)Interventional2009-03-09Completed
A Randomized Phase II Study of Mitoxantrone vs. Mitoxantrone With Cetuximab in Metastatic Androgen Independent Prostate Cancer (AIPC) Previously Treated With Docetaxel-based Chemotherapy [NCT00661492]Phase 2115 participants (Actual)Interventional2008-05-31Completed
A Phase 2, Multicenter, Randomized Study of IMC-A12 or IMC-1121B Plus Mitoxantrone and Prednisone in Metastatic Androgen-Independent Prostate Cancer (AIPC) Following Disease Progression on Docetaxel-Based Chemotherapy [NCT00683475]Phase 2138 participants (Actual)Interventional2008-08-31Completed
Risk-Stratified Therapy for Acute Myeloid Leukemia in Down Syndrome [NCT02521493]Phase 3312 participants (Anticipated)Interventional2015-12-23Active, not recruiting
Clofarabine, Etoposide, and Mitoxantrone for Relapsed and Refractory Acute Leukemias [NCT00882076]Phase 122 participants (Actual)Interventional2009-03-31Terminated(stopped due to study closed prematurely)
A Phase II Multicenter Open-label Study of MabThera(Rituximab) Addition to Regularly Prescribed Chemotherapy in Patients With Untreated Mantle Cell Lymphoma [NCT01144403]Phase 28 participants (Actual)Interventional2010-06-30Terminated
A Multicenter and Randomized Prospective Study for Improving the Outcome of Childhood Acute Promyeloid Leukemia [NCT02200978]Phase 4176 participants (Actual)Interventional2011-09-30Completed
Phase II Study of Treatment of Relapsed Agressive Lymphomas [NCT00842595]Phase 250 participants (Actual)Interventional2003-12-31Completed
Impact of Treatment Intensity on Survival, Quality of Life, and Resource Utilization in Medically Less Fit Adults With Acute Myeloid Leukemia and Analogous Myeloid Neoplasms: A Randomized Pilot Study [NCT03012672]Phase 250 participants (Actual)Interventional2016-12-30Completed
A Phase 1 Study of Temsirolimus in Combination With Intensive Re-induction Therapy for Children With Relapsed Acute Lymphoblastic Leukemia and Non-Hodgkin Lymphoma [NCT01403415]Phase 113 participants (Actual)Interventional2011-09-30Completed
Combination of Mitoxantrone, Etoposide and Gemtuzumab Ozogamicin (MEGO) for Patients With Acute Myeloid Leukemia Refractory to Initial Standard Induction Therapy [NCT03839446]Phase 216 participants (Actual)Interventional2019-02-28Completed
An Open-label, Randomized, Phase 3 Study Of Inotuzumab Ozogamicin (Cmc-544) Administered In Combination With Rituximab Compared To A Defined Investigator's Choice Therapy In Subjects With Relapsed Or Refractory, Cd22- Positive, Follicular B-cell Non Hodgk [NCT00562965]Phase 329 participants (Actual)Interventional2007-11-30Terminated(stopped due to See termination reason in detailed description.)
A Phase I Study of M3814 in Combination With MEC in Patients With Relapsed or Refractory Acute Myeloid Leukemia [NCT03983824]Phase 148 participants (Anticipated)Interventional2020-05-05Recruiting
A Prospective Single Institution Pilot Study Evaluating the Pharmacokinetics of Sirolimus in Combination With MEC (Mitoxantrone + Etoposide + Cytarabine) in Patients With High Risk Leukemias [NCT00780104]Phase 116 participants (Actual)Interventional2007-07-31Completed
Multicenter Trial for Treatment of Acute Lymphoblastic Leukemia in Adults (05/93) [NCT00199069]Phase 4720 participants Interventional1993-04-30Completed
Treatment of Relapsed / Refractory Chronic Lymphocytic Leukemia (CLL) WITH Bendamustine / Mitoxantrone (BM) [NCT00274963]Phase 260 participants (Anticipated)Interventional2004-10-31Completed
A Single-arm, Open, Multi-center Phase II Clinical Trial of Mitoxantrone HCL Liposome Injection in Subjects With Relapsed Diffuse Large B-cell Lymphoma and and Peripheral T/NK Lymphomas [NCT02597387]Phase 250 participants (Anticipated)Interventional2015-08-31Recruiting
A PHASE I-II MULTICENTER STUDY OF THE CLORETAZINE-DAUNORUBICIN-ARACYTINE COMBINATION FOR THE TREATMENT OF ACUTE MYELOID LEUKEMIA (AML) WITH UNFAVORABLE CYTOGENETICS [NCT00840684]Phase 1/Phase 2135 participants (Anticipated)Interventional2009-01-31Completed
Phase I and Pharmacokinetic Study of Mitoxantrone Hydrochloride Liposome Injection in Patients With Solid Tumor [NCT02043756]Phase 120 participants (Actual)Interventional2011-08-31Completed
A Randomized Trial for Patients With Acute Myeloid Leukemia or High Risk Myelodysplatic Syndrome Aged 60 or Over [NCT00005823]Phase 32,000 participants (Anticipated)Interventional1998-12-31Completed
Treatment of High Risk Adult Acute Lymphoblastic Leukemia [NCT00853008]Phase 4100 participants (Anticipated)Interventional2003-01-31Completed
Primed Peripheral Blood Stem Cell Autologous Transplantation for Lymphoma and Hodgkin's Disease [NCT00005985]Phase 2213 participants (Actual)Interventional2000-08-31Completed
First Line Treatment of Metastatic Hormone Refractory Prostate Cancer With a Combination of Novantrone-Navelbine [NCT00006114]Phase 20 participants Interventional1999-05-31Active, not recruiting
Autologous Transplantation for Non-Hodgkin's Lymphoma and Hodgkin's Disease Using Retrovirally Marked Peripheral Blood Progenitor Cells Obtained After In Vivo Mobilization Using Hematopoietic Cytokines Plus Chemotherapy [NCT00005998]Phase 20 participants (Actual)Interventional2000-01-31Withdrawn(stopped due to Withdrawn because study never enrolled patients)
"RANDOMIZED COMPARISON OF ALTERNATING TRIPLE THERAPY (ATT) VERUS CHOP IN PATIENTS WITH INTERMEDIATE GRADE LYMPHOMAS AND IMMUNOBLASTIC LYMPHOMAS WITH INTERNATIONAL INDEX 2-5" [NCT00002565]Phase 361 participants (Actual)Interventional1994-05-25Completed
A Single-arm, Open, Multi-center Phase II Clinical Trial of Mitoxantrone HCL Liposome Injection in Subjects With Relapsed Cutaneous T Cell Lymphomas [NCT02597153]Phase 21 participants (Actual)Interventional2015-10-31Terminated(stopped due to Just one subject enrolled in this trial during one and a half years.)
Study Of The Survival Without Degradation To The Quality Of Life During Chemotherapy For Metastatic Breast Cancer In Women [NCT00010075]Phase 20 participants Interventional2000-01-31Active, not recruiting
Autologous Transplantation for Multiple Myeloma: A Research Study of Multiple Myeloma Using Chemotherapy Plus Growth Factor Primed Peripheral Blood Stem Cells Followed by Autologous Transplantation and Post-Transplant Immunotherapy [NCT00005987]Phase 287 participants (Actual)Interventional2000-08-31Terminated(stopped due to Withdrawn because treatment guidelines changed)
A Randomized, Open-label, Positive-controlled, Single-institutional, Phase Ⅱ of Mitoxantrone Hydrochloride Liposome Injection in Advanced Recurrent or Metastatic Breast Cancer [NCT02596373]Phase 260 participants (Anticipated)Interventional2015-06-30Recruiting
A Phase II Study of Gemzar, Novantrone and Rituxan in Relapsed or Refractory Mantle Cell Lymphoma (MCL) (B9E-US-X436) [NCT00656084]Phase 216 participants (Actual)Interventional2004-12-31Completed
A Double-Blind, Three-Armed, Randomized Phase-III-Study, to Compare the Efficacy, Tolerability and Safety of Three Doses of Mitoxantrone in the Treatment of Patients With Secondary Progressive Multiple Sclerosis [NCT00146159]Phase 3336 participants (Anticipated)Interventional2005-03-31Terminated
An Open, Single-arm, Multi-center Clinical Trial of Molecular Subtype-guided R-MINE+X Regimen in the Treatment of Relapsed/Refractory Diffuse Large B-cell Lymphoma (DLBCL) [NCT05784987]60 participants (Anticipated)Interventional2023-04-15Not yet recruiting
AML2003 - Randomized Comparison Between Standard-Therapy and Intensified Therapy for Adult Acute Myeloid Leukemia Patients <= 60 Years. A Prospective, Randomized, Multi-center Therapy-Optimizing-Study. [NCT00180102]Phase 4600 participants (Anticipated)Interventional2003-12-31Completed
A Phase II Study of R-FND, Followed by Zevalin Radioimmunotherapy, and Subsequent Maintenance Rituximab for Advanced Stage Follicular Lymphoma With High-Risk Features [NCT00290511]Phase 249 participants (Actual)Interventional2004-06-29Completed
A Collaborative Trial for the Treatment of Patients With Newly Diagnosed Acute Myeloid Leukemia or Myelodysplasia [NCT00136084]Phase 3238 participants (Actual)Interventional2002-08-31Completed
A Phase II Study of Bortezomib in Combination With Rituximab, Fludarabine, Mitoxantrone, and Dexamethasone (VR-FND) for Relapsed or Refractory Follicular Lymphoma [NCT00510887]Phase 214 participants (Actual)Interventional2007-01-31Terminated(stopped due to Low accrual.)
Phase I/II Trial of Epothilone Analog BMS-247550 (Ixabepilone), Mitoxantrone, and Prednisone in Hormone Refractory Prostate Cancer (HRPC) Patients Previously Treated With Chemotherapy [NCT00331344]Phase 1/Phase 2100 participants (Actual)Interventional2006-04-30Completed
A Phase II Study of Gemcitabine/ Mitoxantrone in Patients With Acute Myeloid Leukemia in First Relapse [NCT00268242]Phase 224 participants (Actual)Interventional2006-01-31Terminated(stopped due to If
A Phase I Study of Lenalidomide Therapy Prior to Re-induction Chemotherapy With Mitoxantrone, Etoposide, and Cytarabine (MEC) for the Treatment of Relapsed or Refractory Acute Myeloid Leukemia (AML) [NCT01904643]Phase 117 participants (Actual)Interventional2014-02-28Terminated(stopped due to Accrual factor)
A Pilot Study of Mitoxantrone for the Treatment of Recurrent Neuromyelitis Optica (Devic's Disease) [NCT00304291]Phase 45 participants Interventional2001-08-31Completed
A Phase 2, Single-arm, Multicenter Trial to Evaluate the Efficacy and Safety of Mitoxantrone Hydrochloride Liposome Injection in Patients With Relapsed/Refractory Diffuse Large B-Cell Lymphoma (DLBCL) [NCT05875428]Phase 2104 participants (Anticipated)Interventional2023-06-01Not yet recruiting
Evaluation of a New Therapeutic Strategy in Early and Active Relapsing-Remitting Multiple Sclerosis: Induction Treatment With Mitoxantrone Followed by Long-Term Treatment With Interferon-beta1b [NCT00219908]Phase 2124 participants Interventional1999-07-31Terminated
Pilot Study of Crenolanib Combined With Standard Salvage Chmetherapy in Subjects With Relapsed/Refractory Acute Myeloid Leukemia [NCT02626338]Phase 1/Phase 216 participants (Actual)Interventional2016-02-29Completed
An Open, Single-arm, Multicenter Study of R-CMOP Protocol for Primary Treatment of Diffuse Large B-cell Lymphoma Based on Cardiac Function Screening [NCT05777369]30 participants (Anticipated)Interventional2023-03-31Not yet recruiting
A Phase 1/2 Study of Mitoxantrone Hydrochloride Liposome Infusion in Patients With Non-Hodgkin's Lymphoma [NCT02856685]Phase 1/Phase 260 participants (Anticipated)Interventional2016-08-31Recruiting
Efficacy and Safety of Mitoxantrone in Patients With Refractory Neuromyelitis Optica and Spectrum Disorders [NCT02021825]Phase 450 participants (Anticipated)Interventional2009-03-31Recruiting
Phase III, Randomized, Multicenter Study to Assess the Efficacy and Safety of HuM195 (Recombinant Humanized Anti-CD33 Monoclonal Antibody) in Combination With Standardized Chemotherapy Compared to Standardized Chemotherapy Alone in the Treatment of Patien [NCT00006045]Phase 30 participants Interventional2000-03-31Active, not recruiting
Randomized Trial of MCD Versus FMD in Untreated Advanced Follicular Lymphoma [NCT00006250]Phase 3500 participants (Anticipated)Interventional2000-05-31Active, not recruiting
A Phase II Trial of Brief Duration Combination Chemotherapy and Rituximab With Prophylactic Pegfilgrastim, Followed by Maintenance Rituximab, in Elderly/Poor Performance Status Patients With Large B-Cell Non-Hodgkin's Lymphoma [NCT00193479]Phase 251 participants (Actual)Interventional2003-04-30Completed
Programma di Terapia Per Pazienti Affetti da Linfoma Diffuso a Grandi Cellule B CD20 Positive [NCT00556127]Phase 294 participants (Actual)Interventional2002-06-30Completed
A Phase II Trial of Epigenetic Priming in Patients With Newly Diagnosed Acute Myeloid Leukemia [NCT03164057]Phase 2206 participants (Actual)Interventional2017-06-15Active, not recruiting
Cyclosporine Modulation of Drug Resistance in Combination With Pravastatin, Mitoxantrone, and Etoposide for Adult Patients With Relapsed/Refractory Acute Myeloid Leukemia (AML): A Phase 1/2 Study [NCT01342887]Phase 1/Phase 26 participants (Actual)Interventional2011-04-30Terminated
A Randomized, Open Label Multi-Center Study of XRP6258 at 25 mg/m^2 in Combination With Prednisone Every 3 Weeks Compared to Mitoxantrone in Combination With Prednisone For The Treatment of Hormone Refractory Metastatic Prostate Cancer Previously Treated [NCT00417079]Phase 3755 participants (Actual)Interventional2007-01-31Completed
A Single-arm, Multi-center Phase II Clinical Study on Pegaspargase Combined With Gemcitabine, Etoposide, Liposomal Mitoxantrone Hydrochloride and Dexamethasone (P-GEMD) in the Treatment of Untreated Early Non-upper Respiratory Tract or Advanced Extranodal [NCT05774028]Phase 250 participants (Anticipated)Interventional2023-04-30Not yet recruiting
A Phase 2 Multicenter Study of First-line Dasatinib Plus Conventional Chemotherapy in Adults With Newly Diagnosed Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia [NCT01004497]Phase 251 participants (Actual)Interventional2010-03-31Completed
Clinical Study of Mitoxantrone Hydrochloride Liposome Injection Combined With Capecitabine in Patients With HER-2 Negative Advanced Breast Cancer [NCT06156761]24 participants (Anticipated)Interventional2023-11-28Not yet recruiting
International Randomised Phase III Clinical Trial in Children With Acute Myeloid Leukaemia - Incorporating an Embedded Dose Finding Study for Gemtuzumab Ozogamicin in Combination With Induction Chemotherapy [NCT02724163]Phase 3700 participants (Anticipated)Interventional2016-04-30Recruiting
Phase 2 Randomized Study Evaluating 3 Chemotherapy Regimens as Second-line Treatment in Patients With Hormone-refractory Metastatic Prostate Cancer [NCT00627354]Phase 290 participants (Anticipated)Interventional2006-09-30Completed
A Phase 1 Clinical Study of DSP-2033 (Alvocidib) in Combination With Cytarabine/Mitoxantrone or Cytarabine/Daunorubicin (7+3) in Patients With Acute Myeloid Leukemia [NCT03563560]Phase 110 participants (Actual)Interventional2018-05-15Completed
A Randomized Phase 2 Study of Human Anti-PDGFRα Monoclonal Antibody IMC-3G3 Plus Mitoxantrone Plus Prednisone or Mitoxantrone Plus Prednisone in Metastatic Castration-Refractory Prostate Cancer Following Disease Progression or Intolerance on Docetaxel-bas [NCT01204710]Phase 2123 participants (Actual)Interventional2010-10-31Completed
Optimal Treatment Strategy Based on Prognostic Groups for Pediatric de Novo Acute Myeloid Leukemia [NCT02848183]Phase 2350 participants Interventional2016-01-31Recruiting
A Phase II Study of Bendamustine, Mitoxantrone, and Rituximab (BMR) for Patients With Untreated High Risk Follicular Lymphoma [NCT00901927]Phase 214 participants (Actual)Interventional2009-05-31Terminated(stopped due to Study was closed early due to toxicity)
Chemosensitization With Plerixafor Plus G-CSF in Relapsed or Refractory Acute Myeloid Leukemia [NCT00906945]Phase 1/Phase 239 participants (Actual)Interventional2011-02-28Completed
A Randomized, Open-label, Active Controlled, Multi-center Phase 3 Clinical Study to Compare the Efficacy and Safety of Mitoxantrone Hydrochloride Liposome Injection With Chidamide in Patients With Relapsed/Refractory PTCL. [NCT04668690]Phase 3190 participants (Anticipated)Interventional2021-01-01Not yet recruiting
A Phase 2 Study of Chidamide, Azacitidine Combined With GM Regimen for Patients With Relapsed and Refractory DLBCL [NCT05823701]Phase 223 participants (Anticipated)Interventional2022-09-30Recruiting
An Multicenter, Randomized Study of Comparison of Docetaxel Plus Prednisone With Mitoxantrone Plus Prednisone in the Patients With Hormone-refractory (Androgen-independent) Metastatic Prostate Cancer [NCT00436839]Phase 3228 participants (Actual)Interventional2007-01-31Completed
Gemtuzumab Ozogamicin (CMA-676) Followed or Not by Intensive Chemotherapy as Initial Treatment for Elderly Patients With Acute Myeloid Leukemia: An EORTC-LG Pilot Phase II Study [NCT00006122]Phase 2106 participants (Actual)Interventional2000-06-30Completed
An Open Label, Multicenter, Non Randomized Phase II Study to Evaluate Anti-tumor Activity and Safety of a Combination of Fludarabine, Mitoxantrone and Rituximab in Relapsed or Primary Failing Advanced Follicular Non-Hodgkin's Lymphoma. [NCT00169208]Phase 250 participants (Actual)Interventional2001-04-30Completed
Risk-Adapted Therapy for Patients With Untreated Age-Adjusted International Prognostic Index Low-Intermediate Risk, High-Intermediate Risk, or High Risk Diffuse Large B Cell Lymphoma [NCT00712582]Phase 296 participants (Actual)Interventional2008-07-01Completed
High-dose Cytarabine/Mitoxantrone Followed by Autotransplantation for Therapy-Related Myelodysplastic Syndrome/Therapy -Related Acute Myeloid Leukemia [NCT00774046]Phase 232 participants (Actual)Interventional2002-12-31Completed
Treatment of Newly Diagnosed Patients With Acute Promyelocytic Leukemia (PETHEMA LPA 2005): Remission Induction With ATRA + Idarubicin. Risk-adapted Consolidation With ATRA and Anthracycline-based Chemotherapy (Idarubicin/Mitoxantrone) With Addition of Ar [NCT00408278]Phase 4300 participants (Anticipated)Interventional2005-07-31Completed
AIDA2000 - Risk-Adapted Therapy for Patients With Acute Promyelocytic Leukemia(APL) [NCT00180128]Phase 480 participants (Anticipated)Interventional2000-01-31Recruiting
Dose-Finding (Phase 1) Study of Continuous Infusion Cladribine, Cytarabine and Mitoxantrone (CI-CLAM) for Adults With Relapsed/Refractory Acute Myeloid Leukemia or Other High-Grade Myeloid Neoplasms Treated at UW/SCCA [NCT04196010]Phase 113 participants (Actual)Interventional2020-05-08Terminated(stopped due to Terminated due to unfavorable risk-benefit ratio of investigational regimen.)
Phase I Study of a Pharmacologically Derived Hybrid Bolus-Infusion Schedule of Flavopiridol (NSC 649890, IND 46,211) Given in Timed Sequential Combination With Cytosine Arabinoside (Ara-C) and Mitoxantrone for Adults With Relapsed and Refractory Acute Leu [NCT00470197]Phase 135 participants (Actual)Interventional2007-04-30Completed
A Randomized Phase II Trial of Fludarabine, Cyclophosphamide and Mitoxantrone (FCM) With or Without Rituximab in Previously Treated Chronic Lymphocytic Leukemia [NCT00337246]Phase 256 participants (Anticipated)Interventional2005-07-31Completed
Phase II Study of DN-101 (High Dose Pulse Calcitriol), Mitoxantrone, Prednisone in Androgen-Independent Prostate Cancer (AIPC) [NCT00182741]Phase 219 participants (Actual)Interventional2004-09-30Completed
A Pilot Phase II Trial of Combination Therapy With Fludarabine, Mitoxantrone and Rituximab in Mantle Cell Lymphoma [NCT00183989]Phase 230 participants (Anticipated)Interventional2000-08-31Terminated(stopped due to Insufficient accrual)
Phase II Trial to Assess the Activity of Ketoconazole and Mitoxantrone Plus GM-CSF in Patients With Progressive Hormone Refractory Prostate Cancer [NCT00447473]Phase 231 participants (Actual)Interventional2006-07-31Terminated(stopped due to PI decision)
Phase II Study of Fludarabine and Mitoxantrone, Followed by GM-CSF(Granulocyte-macrophage Colony-stimulating Factor) and Rituximab in Patients With Low Grade Non-Hodgkins Lymphoma: An Analysis of Efficacy and Tolerability [NCT00208975]Phase 215 participants (Actual)Interventional2002-07-31Terminated(stopped due to slow accrual)
Phase I Investigation of the Feasibility of Combining 5-azacytidine With Highdose Cytarabine (HiDAC) and Mitoxantrone Chemotherapy in a Sequential Manner for Remission Induction in High-risk Acute Myelogenous Leukemia (AML) [NCT01839240]Phase 150 participants (Actual)Interventional2012-06-06Completed
A Phase 1 Study of Azacitidine in Combination With MEC (Mitoxantrone, Etoposide, Cytarabine) in Relapsed and Refractory Acute Myeloid Leukemia [NCT01249430]Phase 124 participants (Actual)Interventional2011-01-20Completed
Study Phase II Non-randomized Prospective Open to Assess the Combination of Rituximab, Bendamustine, Mitoxantrone, Dexamethasone (R-BMD) in Patients With Follicular Lymphoma Refractory or Relapsed [NCT01133158]Phase 261 participants (Actual)Interventional2009-07-31Completed
LAL-Ph-2000: Treatment of Acute Lymphoblastic Leukemia Chromosome Philadelphia Positive [NCT00526305]Phase 4100 participants (Anticipated)Interventional2000-01-31Completed
International Collaborative Treatment Protocol for Infants Under One Year With Acute Lymphoblastic or Biphenotypic Leukemia [NCT00550992]445 participants (Anticipated)Interventional2006-01-31Recruiting
A Phase I/II, Open-label Multicenter Trial to Determine Safety, Pharmacokinetics and Efficacy of GMI-1271 in Combination With Chemotherapy in Patients With Acute Myeloid Leukemia [NCT02306291]Phase 1/Phase 291 participants (Actual)Interventional2015-03-31Completed
Phase I Trial of Brentuximab Vedotin With Re-induction Chemotherapy in Patients With Relapsed, CD30 Expressing, Acute Myeloid Leukemia (AML) [NCT01830777]Phase 122 participants (Actual)Interventional2013-05-31Completed
The Clinical Observationg on HAM for Acute Myeloid Leukemia [NCT04024241]250 participants (Anticipated)Observational2017-09-01Recruiting
MITOXANTRONE (N) VS. 5-FLUOROURACIL, EPIRUBICIN AND CYCLOPHOSPHAMIDE AS FIRST-LINE CHEMOTHERAPY FOR PATIENTS WITH METASTATIC BREAST CANCER AND AN UNFAVORABLE PROGNOSIS [NCT00002544]Phase 3300 participants (Anticipated)Interventional1993-05-31Completed
A PHASE II STUDY OF MITOXANTRONE AND HIGH-DOSE ARA-C FOLLOWED BY INTENSIVE CONSOLIDATION WITH CYCLOPHOSPHAMIDE AND ETOPOSIDE FOR MYELOID BLAST CRISIS OF CHRONIC MYELOGENOUS LEUKEMIA (CML) [NCT00002598]Phase 230 participants (Anticipated)Interventional1994-06-30Completed
ACUTE MYELOID LEUKAEMIA TRIAL 12 [NCT00002658]Phase 32,000 participants (Anticipated)Interventional1994-01-31Active, not recruiting
AML-MVPCYA: ADDITION OF CYCLOSPORIN A TO THE COMBINATION OF MITOXANTRONE AND ETOPOSIDE (VP 16,213) TO OVERCOME RESISTANCE TO CHEMOTHERAPY IN REFRACTORY AML: A RANDOMIZED PHASE II STUDY [NCT00002688]Phase 225 participants (Anticipated)Interventional1995-02-28Active, not recruiting
A RANDOMIZED PHASE III TRIAL COMPARING DEXAMETHASONE WITH PREDNISONE IN INDUCTION TREATMENT AND BONE MARROW TRANSPLANTATION WITH INTENSIVE MAINTENANCE TREATMENT IN ADOLESCENT AND ADULT ACUTE LYMPHOBLASTIC LEUKEMIA (ALL-4) [NCT00002700]Phase 3392 participants (Anticipated)Interventional1995-08-31Completed
A Phase II Trial of Adjuvant Mitoxantrone (NSC #301739) for High Risk Patients Following Radical Prostatectomy [NCT00003858]Phase 20 participants (Actual)InterventionalWithdrawn(stopped due to The study was not activated.)
Chemotherapy (CT) Followed by Donor Lymphocyte Infusion (DLI) Plus Interleukin 2 (IL-2) for Patients With Relapse Acute Myeloid or Lymphoid Leukemia After Allogeneic Hematopoietic Transplant [NCT00005802]Phase 1/Phase 20 participants Interventional1999-06-30Completed
A Phase 1, Multicenter, Open-Label, Safety Study of AG-120 or AG-221 in Combination With Induction Therapy and Consolidation Therapy in Patients With Newly Diagnosed Acute Myeloid Leukemia With an IDH1 and/or IDH2 Mutation [NCT02632708]Phase 1153 participants (Actual)Interventional2015-12-31Active, not recruiting
Intensive Induction for Newly Diagnosed Acute Myelogenous Leukemia [NCT00274807]Phase 240 participants (Actual)Interventional2001-06-30Completed
Abbreviated Fludarabine / Mitoxantrone / Rituximab Chemotherapy Followed by Zevalin for Relapsed Mantle Cell Lymphoma [NCT00119730]Phase 230 participants (Actual)Interventional2005-02-28Completed
A Clinical Study Was Conducted to Evaluate the Efficacy and Safety of the RCMOP Regimen Sequential Therapy as a First-line Treatment for Patients With Intermediate-to-high Risk Diffuse Large B-cell Lymphoma Who Had Incomplete Remission. [NCT05990985]20 participants (Anticipated)Interventional2023-09-01Not yet recruiting
Phase I Dose Escalation and Pharmacokinetics Clinical Trial of Mitoxantrone Hydrochloride Liposome in Children With Relapsed and Refractory Lymphoma and Solid Tumors [NCT05620862]Phase 168 participants (Anticipated)Interventional2022-10-25Recruiting
Phase I Cinical Sudy of Lposomal Mitoxantrone Hydrochloride Combined With Cyclophosphamide, Vincristine, Etoposide and Prednisone (CMOEP) in Previously Untreated Peripheral T-cell Lymphoma [NCT05458180]Phase 118 participants (Anticipated)Interventional2022-07-07Not yet recruiting
Three-Arm Randomized Phase II Clinical Study of Irofulven/Prednisone, Irofulven/Capecitabine/Prednisone or Mitoxantrone/Prednisone in Docetaxel-Pretreated Hormone-Refractory Prostate Cancer Patients [NCT00124566]Phase 2135 participants (Actual)Interventional2004-06-30Completed
Phase I Study of Adoptive Immunotherapy With CD8 Minor Histocompatibility (H) Antigen-Specific CTL Clones for Patients With Relapsed of AML or ALL After Allogeneic Hematopoietic Stem Cell Transplant [NCT00107354]Phase 10 participants Interventional1998-12-31Completed
A Randomised Multicentric Phase III Study for the Treatment of Young Patients With High Risk (IPI 2-3) Diffuse Large B-Cell Lymphoma. Dose Dense Chemotherapy + Rituximab +/- Intensified High Dose Chemoimmunotherapy With Support of Peripheral Autologous St [NCT00499018]Phase 3399 participants (Anticipated)Interventional2006-01-31Active, not recruiting
A Phase I Study Investigating the Combination of RAD001 With Standard Induction and Consolidation Therapy in Older Patients With Newly Diagnosed Acute Myeloid Leukemia (AML) [NCT01154439]Phase 111 participants (Actual)Interventional2010-10-31Completed
Phase II Study on Gemtuzumab Ozogamicin in Combination With All-trans-Retinoic Acid, High-dose Cytarabine and Mitoxantrone in Patients With Primary Refractory Acute Myeloid Leukemia [NCT00143975]Phase 295 participants (Actual)Interventional2004-06-30Completed
A Pilot Study of Mitoxantrone in Combination With Clofarabine (MITCL) in Children, Adolescents and Young Adults (CAYA) With Refractory/Relapsed Acute Leukemia or High Grade Non-Hodgkin Lymphoma [NCT01842672]Phase 1/Phase 241 participants (Actual)Interventional2013-03-31Completed
A Pilot, Pharmacodynamic Correlate, Multi-Institutional Trial of Sirolimus in Combination With Chemotherapy (Mitoxantrone, Etoposide, Cytarabine) for the Treatment of High Risk, Acute Myelogenous Leukemia [NCT01184898]36 participants (Actual)Interventional2010-07-31Completed
Phase III Trial Comparing CHOP ot PMitCEBO in Good Risk Patients With Histologically Aggresive Non Hodgkin's Lymphoma [NCT00005867]Phase 3310 participants (Anticipated)Interventional1998-01-31Completed
Phase II Trial of CLAG-M in Relapsed ALL [NCT01513603]Phase 250 participants (Anticipated)Interventional2012-01-31Recruiting
A Phase II Study of Bortezomib and Vorinostat in Patients With Refractory or Relapsed MLL Rearranged Hematologic Malignancies [NCT02419755]Phase 212 participants (Actual)Interventional2015-04-14Terminated(stopped due to Accrual goals were no longer feasible based on restrictions imposed by the DSMB.)
Brief Induction Chemoimmunotherapy With Rituximab + Bendamustine + Mitoxantrone Followed by Rituximab in Elderly Patients With Advanced Stage Previously Untreated Follicular Lymphoma [NCT01523860]Phase 276 participants (Actual)Interventional2009-06-30Completed
Phase II Study of High Dose Cyclophosphamide, Mitoxantrone, and Carboplatin With Autologous Bone Marrow Transplantation in Refractory or Relapsed Ovarian Carcinoma [NCT00002474]Phase 20 participants Interventional1991-02-28Completed
CMF AND MITOXANTRONE IN ELDERLY PATIENTS WITH ADVANCED BREAST CANCER, A RANDOMIZED PHASE II STUDY [NCT00002498]Phase 20 participants Interventional1992-07-31Active, not recruiting
Study of Topoisomerase Inhibition in the Treatment of Acute Leukemia [NCT00100477]Phase 210 participants (Actual)Interventional1998-08-31Completed
MULTICENTRE TRIAL OF INTENSIFIED THERAPY FOR ADULT ALL (O5/93) [NCT00002531]Phase 20 participants Interventional1993-01-31Active, not recruiting
Pilot Study Of PMitCEBO Plus G-CSF In Good-Prognosis HIV-Related Lymphoma [NCT00032149]Phase 1/Phase 230 participants (Anticipated)Interventional2001-10-31Active, not recruiting
A Phase II Study of the Recombinant Human Monoclonal Anti-Vascular Endothelial Growth Factor Antibody (rhuMAB VEGF) Bevacizumab (NSC #704865, IND # 7,921) Administered in Times Sequential Combination With Cytosine Arabinoside (Ara-C) and Mitoxantrone for [NCT00015951]Phase 20 participants Interventional2001-04-30Completed
A Phase 1/2 Trial of G-CSF, Cladribine, Cytarabine, and Dose-Escalated Mitoxantrone (G-CLAM) in Adults With Newly Diagnosed or Relapsed/Refractory Acute Myeloid Leukemia (AML) or High-Risk Myelodysplastic Syndromes (MDS) [NCT02044796]Phase 1/Phase 2199 participants (Actual)Interventional2014-01-23Completed
High Dose Cytarabine And Mitoxantrone Therapy For Relapsed And Refractory Acute Myeloid And Lymphocytic Leukemia: Effects Of GM-CSF Versus G-CSF On Dendritic Cells And Leukemia Associated Antigen-Specific T-Lymphocytes [NCT00053131]Phase 20 participants Interventional1999-01-31Completed
A Randomized Phase II Study Of BMS 247550 Or Mitoxantrone And Prednisone In Patients With Taxane Resistant Hormone Refractory Prostate Cancer [NCT00058084]Phase 280 participants (Actual)Interventional2003-03-31Completed
Treatment of Newly Diagnosed Childhood Acute Myeloid Leukemia (AML) Using Intensive MRC-Based Therapy and Gemtuzumab Ozogamicin (GMTZ): A COG Pilot Study [NCT00070174]Phase 2350 participants (Actual)Interventional2003-12-31Completed
A Phase II Study VEPEMB In Patients With Hodgkin's Lymphoma Aged ≥ 60 Years; Vinblastine, Cyclophosphamide, Procarbazine, Prednisolone, Etoposide, Mitoxantrone, and Bleomycin in Treating Older Patients With Hodgkin's Lymphoma [NCT00079105]Phase 2175 participants (Actual)Interventional2004-01-31Completed
A Prospective, Open-label, Single-arm Clinical Study of Mitoxantrone Hydrochloride Liposome Injection Combined With Daratumumab and Dexamethasone in the Treatment of Relapsed/Refractory Multiple Myeloma [NCT05857982]Phase 1/Phase 220 participants (Anticipated)Interventional2023-05-20Recruiting
A Phase I/II Study of Flavopiridol (NSC 649890, IND 46,211) in Timed Sequential Combination With Cytosine Arabinoside (Ara-C) and Mitoxantrone for Adults With Poor-Risk Acute Leukemias [NCT00016016]Phase 1/Phase 253 participants (Anticipated)Interventional2001-02-28Completed
[NCT00024492]Phase 140 participants Interventional2001-08-31Completed
A Dose Finding Study of the Safety of Gemtuzumab Ozogamicin Combined With Conventional Chemotherapy for Patients With Relapsed or Refractory Acute Myeloid Leukemia [NCT00028899]Phase 147 participants (Actual)Interventional2002-07-31Completed
A Multicenter, Single-arm, Open Clinical Efficacy Observational Study of Cidapenem Combined With Azacitidine and Mitoxantrone Liposome (CAM) Regimen for Relapsed/Refractory Intra-nodal Follicular Adjuvant T-cell Lymphoma (nTFHL) [NCT05772728]23 participants (Anticipated)Interventional2023-04-30Not yet recruiting
Gemtuzumab Ozogamicin (GO) Combined With Standard Intensive Chemotherapy Versus Standard Intensive Chemotherapy Alone For Induction/Consolidation In Patients 61-75 Years Old With Previously Untreated AML: A Randomized Phase III Trial (AML-17) Of The EORTC [NCT00052299]Phase 3472 participants (Actual)Interventional2002-09-30Completed
Phase I Study of Weekly Intravenous PS-341 (Bortezomib) Plus Mitoxantrone in Patients With Advanced Androgen-Independent Prostate Cancer (AI-PCa) [NCT00059631]Phase 142 participants (Actual)Interventional2003-03-20Completed
A Pilot Study Of Cytarabine And High-Dose Mitoxantrone For Relapsed Or Refractory Hematologic Malignancies [NCT00047021]Phase 23 participants (Actual)Interventional2001-11-30Completed
Phase III - Study on All-Trans Retinoic Acid in Combination With Standard Induction and Consolidation Therapy in Older Patients With Newly Diagnosed Acute Myeloid Leukemia [NCT00151255]Phase 3500 participants (Anticipated)Interventional2004-06-30Completed
Phase I/II Trial of VELCADE® (Bortezomib) in Combination With Mitoxantrone and Etoposide for Relapsed or Refractory Acute Leukemias [NCT00410423]Phase 1/Phase 255 participants (Actual)Interventional2006-01-31Completed
Mitoxantrone, Prednisone Plus Sorafenib in Taxane-Refractory Metastatic Hormone Refractory Prostate Cancer (HRPC) [NCT00452387]Phase 222 participants (Actual)Interventional2007-05-31Terminated(stopped due to Early stopping rule)
Cytosine Arabinoside and Mitoxantrone for Patients With Juvenile Myelomonocytic Leukemia Receiving Repeat Stem Cell Transplantation [NCT00609739]Phase 1/Phase 21 participants (Actual)Interventional1999-06-30Terminated(stopped due to Low accrual)
The Efficiency of CAMS-2016 Trial for the Newly Diagnosed Pediatric Acute Myeloid Leukemia: A Prospective Single Centre Trial From China [NCT03173612]132 participants (Anticipated)Interventional2016-08-31Recruiting
"A Feasibility Study of Early Allogeneic Hematopoietic Cell Transplantation for Relapsed or Refractory High-Grade Myeloid Neoplasms" [NCT02756572]Phase 230 participants (Actual)Interventional2016-09-22Completed
An Multicenter, Randomized, Controlled, Prospective Clinical Study of Mitoxantrone Liposome Combined With PTCy as Conditioning Regimen in Allo-HSCT in Acute Leukemia [NCT05739630]Phase 2/Phase 360 participants (Anticipated)Interventional2023-01-01Recruiting
Clinical Study to Evaluate the Safety, Tolerability, Efficacy and Pharmacokinetics of Liposomal Mitoxantrone Hydrochloride Injection Combined With Cyclophosphamide, Vincristine and Prednisone in the Treatment of Untreated PTCL [NCT04548700]Phase 163 participants (Anticipated)Interventional2020-12-24Recruiting
Treatment of Poor Prognosis Acute Myeloid Leukemia and Blastic Crisis Chronic Myelogenous Leukemia With Mylotarg, High-Dose Cytarabine, Mitozantrone and Ethyol AML/CML 2000-06. [NCT00003407]Phase 20 participants (Actual)Interventional2001-02-13Withdrawn(stopped due to The P.I deceased.)
A Phase I Study of Lenalidomide Plus Chemotherapy With Mitoxantrone, Etoposide, and Cytarabine for the Reinduction of Patients With Acute Myelogenous Leukemia [NCT01681537]Phase 136 participants (Actual)Interventional2012-09-30Completed
Treatment of Advanced Chronic Lymphocytic Leukemia (CLL) Fludarabine, Mitoxantrone and Cyclophosphamide With or Without G-CSF [NCT00416910]Phase 383 participants (Actual)Interventional1999-07-31Terminated(stopped due to low recruitment)
A Multicenter, Open-label, Single-arm, Phase Ib Study to Evaluate the Safety and Efficacy of Mitoxantrone Hydrochloride Liposome Injection in Subjects With Platinum-Resistant or Platinum-Refractory Relapsed Ovarian Cancer [NCT04718376]Phase 130 participants (Anticipated)Interventional2021-01-12Recruiting
Consolidation With Campath-1H After FMC Induction in Patients With T-cell Chronic Lymphocytic Leukemia [NCT00278213]Phase 217 participants (Anticipated)Interventional2002-09-30Completed
A Multicenter, Open-label, Single-arm, Phase Ib Study to Evaluate the Safety and Efficacy of Mitoxantrone Hydrochloride Liposome Injection in Subjects With Advanced Gastric Carcinoma [NCT04718402]Phase 130 participants (Anticipated)Interventional2021-03-30Recruiting
A Phase I Study of Lintuzumab-Ac225 in Combination With CLAG-M Chemotherapy in Patients With Relapsed/Refractory Acute Myeloid Leukemia [NCT03441048]Phase 126 participants (Actual)Interventional2018-05-22Active, not recruiting
A Phase II Proof of Concept Study Evaluating the Reduction of Mitoxantrone-induced Cardiotoxicity and Neurological Outcome in the Combined Use of Mitoxantrone and Dexrazoxane (Cardioxane®) in Multiple Sclerosis (MSCardioPro) [NCT01627938]Phase 250 participants (Anticipated)Interventional2012-04-30Active, not recruiting
Sequencing of Chemotherapy and Radiotherapy in Adjuvant Breast Cancer [NCT00003893]Phase 32,250 participants (Anticipated)Interventional1998-07-31Completed
A Phase II Study of the Efficacy and Pharmacogenomics of Cladribine-based Salvage Chemotherapy in Patients With Relapse/Refractory and Secondary Acute Myeloid Leukemia (AML) and High Risk Myelodysplastic Syndrome (MDS) [NCT03150004]Phase 290 participants (Anticipated)Interventional2017-06-14Recruiting
An Open Label, Dose-Escalation Study to Evaluate Safety, Tolerability, Maximum Tolerated Dose (MTD), Efficacy, and Pharmacokinetics (PKs) of CPI-613 Given With High Dose Cytarabine and Mitoxantrone in Patients With Relapsed or Refractory Acute Myeloid Leu [NCT01768897]Phase 167 participants (Actual)Interventional2013-01-31Completed
HLA-mismatched Allogeneic Cellular Therapy (HMMACT) After Chemotherapy in High Risk Acute Myeloid Leukemia [NCT01801046]Phase 110 participants (Actual)Interventional2013-03-06Terminated(stopped due to Insufficient Accrual)
NOPHO-DBH AML 2012 Protocol. Research Study for Treatment of Children and Adolescents With Acute Myeloid Leukaemia 0-18 Years [NCT01828489]Phase 3300 participants (Anticipated)Interventional2013-03-31Recruiting
"Randomized Phase II Trial of Timed Sequential Therapy (TST) With Alvocidib (Flavopiridol), Ara-C and Mitoxantrone (FLAM) vs. 7+3 for Adults Age 70 and Under With Newly Diagnosed Acute Myelogenous Leukemia (AML)" [NCT01349972]Phase 2172 participants (Actual)Interventional2011-04-30Completed
Phase 1/2 Study of Concurrent Decitabine in Combination With G-CSF, Cladribine, Cytarabine, and Mitoxantrone (G-CLAM) in Adults With Newly Diagnosed Acute Myeloid Leukemia (AML) or High-Risk Myelodysplastic Syndromes (MDS) [NCT02921061]Phase 1/Phase 228 participants (Actual)Interventional2016-11-17Completed
A Phase II Study of Therapy for Pediatric Relapsed or Refractory Precursor B-Cell Acute Lymphoblastic Leukemia and Lymphoma [NCT01700946]Phase 280 participants (Actual)Interventional2013-04-15Completed
A Multicenter, Randomized, Open-label, Phase Ib Study to Evaluate the Safety, Efficacy and Pharmacokinetic Characteristics of Mitoxantrone Hydrochloride Liposome Injection in Subjects With Advanced Solid Tumor [NCT04719065]Phase 190 participants (Anticipated)Interventional2021-01-13Active, not recruiting
Phase II Study of Intravenous Novantrone(R) in the Treatment of AIDS Related Kaposi's Sarcoma [NCT00002259]Phase 20 participants InterventionalCompleted
IDA VS MTZ IN INDUCTION AND INTENSIFICATION TREATMENT OF AML OR MDS IN CHILDREN, A PHASE III RANDOMIZED STUDY [NCT00002517]Phase 30 participants Interventional1993-03-31Completed
A Phase I/II Trial Using Weekly Mitoxantrone Chemotherapy and G-CSF for the Treatment of Metastatic Hormone Refractory Prostate Cancer [NCT00003183]Phase 1/Phase 264 participants (Anticipated)Interventional1997-03-31Active, not recruiting
A Phase II Randomized Trial of Carboplatin and Topotecan; Flavopiridol, Mitoxantrone and Cytosine Arabinoside; and Sirolimus, Mitoxantrone, Etoposide and Cytosine Arabinoside for the Treatment of Adults With Primary Refractory or Initial Relapse of Acute [NCT00634244]Phase 292 participants (Actual)Interventional2008-10-31Completed
Treateament of Newly Diagnosed Acute Monocytic Leukemia in Children: A Prospective Multicenter Study in South China [NCT05313958]Phase 2/Phase 343 participants (Anticipated)Interventional2021-12-01Recruiting
A Single-arm, Multicenter, Prospective Clinical Study of Mitoxantrone Hydrochloride Liposome Injection Combined With Chidamide and Azacitidine in the Treatment of Relapsed and Refractory Peripheral T-cell Lymphoma [NCT05495100]Phase 245 participants (Anticipated)Interventional2022-08-11Recruiting
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 23 participants (Actual)Interventional2016-11-23Terminated(stopped due to Due to slow accrual)
A Randomized Phase III Study to Compare Arsenic Trioxide (ATO) Combined to ATRA and Idarubicin Versus Standard ATRA and Anthracyclines-based Chemotherapy (AIDA Regimen) for Patients With Newly Diagnosed, High-risk Acute Promyelocytic Leukemia [NCT02688140]Phase 3280 participants (Anticipated)Interventional2016-06-30Active, not recruiting
CYTOREDUCTIVE CHEMOTHERAPY WITH MITOXANTRONE, CYTOSINE ARABINOSIDE AND ETOPOSIDE FOLLOWED BY RECOMBINANT HUMAN G-CSF FOR MOBILIZATION OF PERIPHERAL BLOOD STEM CELLS IN PATIENTS WITH CHRONIC MYELOID LEUKEMIA [NCT00002674]Phase 230 participants (Anticipated)Interventional1994-10-31Completed
Study of Combinative Effect of Induction Therapy With Mitoxantrone and Plasmapheresis to Treat Patients With Aggressive Multiple Sclerosis [NCT01214317]40 participants (Actual)Interventional2010-01-31Completed
Medical Research Council Working Party on Leukaemia in Childhood Acute Myeloid Leukaemia Trial 12 [NCT00003436]Phase 32,000 participants (Anticipated)Interventional1998-07-31Completed
Randomized Placebo-Controlled Trial of Mitoxantrone/Prednisone and Clodronate Versus Mitoxantrone/Prednisone Alone in Patients With Hormone Refractory Metastatic Prostate Cancer and Pain [NCT00003232]Phase 3227 participants (Actual)Interventional1997-11-24Completed
A Randomized Controlled Study on the Efficacy and Safety of MA-BUCY2 Protocol in the Conditioning of Haploidentical Stem Cell Transplantation in Patients With High-risk Acute Myeloid Leukemia [NCT05814731]264 participants (Anticipated)Interventional2023-04-15Not yet recruiting
Safety, Tolerability, Pharmacokinetics and Efficacy of Mitoxantrone Hydrochloride Liposome Injection in Chinese Patients With Advanced Solid Tumors: A Multicenter, Open-label, Phase I Dose-escalation and Dose-expansion Study [NCT04921878]Phase 1104 participants (Anticipated)Interventional2021-06-30Not yet recruiting
Evaluation of the Impact of Remission Induction Chemotherapy Prior to Allogeneic Stem Cell Transplantation in Relapsed and Poor-response Patients With AML [NCT02461537]Phase 3281 participants (Actual)Interventional2015-09-17Completed
Phase 1 Study of Selinexor in Combination With Topoisomerase-II Inhibition in Acute Myeloid Leukemia [NCT02299518]Phase 123 participants (Actual)Interventional2015-05-18Completed
Phase I/II Study of Neoadjuvant Weekly Docetaxel and Mitoxantrone Prior to Prostatectomy in Patients With High Risk Localized Prostate Cancer [NCT00017563]Phase 257 participants (Actual)Interventional2000-09-30Completed
Mitoxantrone, Etoposide, and Cytarabine (MEC) Following Epigenetic Priming With Decitabine in Adults With Relapsed/Refractory Acute Myeloid Leukemia (AML) or High-Risk Myelodysplastic Syndromes (MDS): A Phase 1/2 Study [NCT01729845]Phase 1/Phase 252 participants (Actual)Interventional2012-12-20Completed
A Study of Therapy for Pediatric Relapsed or Refractory Acute Lymphoblastic Leukemia [NCT00186875]Phase 247 participants (Actual)Interventional2003-11-30Completed
Clofarabine, Cytarabine and Mitoxantrone (CLAM) for Relapsed or Refractory AML [NCT02686593]Phase 250 participants (Actual)Interventional2016-02-01Completed
A Phase II Investigation of Vorinostat in Combination With Intravenous Fludarabine, Mitoxantrone, and Dexamethasone in Patients With Relapsed or Refractory Mantle Cell Lymphoma [NCT01578343]Phase 220 participants (Actual)Interventional2012-06-30Terminated(stopped due to we collected data of a total of 19 patients for an interim analysis. but there are less than 7 responses out of the initial 19 patients.)
A Phase I Study of Cabazitaxel, Mitoxantrone, and Prednisone (CAMP) for Patients With Metastatic Castration-Resistant Prostate Cancer and no Prior Chemotherapy [NCT01594918]Phase 125 participants (Actual)Interventional2012-06-30Completed
Phase 3 Open-label, Multicenter, Randomized Study of ASP2215 Versus Salvage Chemotherapy in Patients With Relapsed or Refractory Acute Myeloid Leukemia (AML) With FLT3 Mutation [NCT03182244]Phase 3276 participants (Actual)Interventional2018-01-15Active, not recruiting
Treatment Protocol for Relapsed Anaplastic Large Cell Lymphoma of Childhood and Adolescence [NCT00317408]96 participants (Anticipated)Interventional2004-04-30Active, not recruiting
A RANDOMIZED PROSPECTIVE TRIAL OF CHOP VERSUS MCOP IN ELDERLY PATIENTS WITH INTERMEDIATE AND HIGH GRADE NON-HODGKIN'S LYMPHOMA (AGED 65 YEARS AND OVER) [NCT00002576]Phase 3200 participants (Anticipated)Interventional1992-11-30Completed
A Single-arm, Open-label, Single-center Phase Ib Study to Evaluate the Safety and Efficacy of Liposome-entrapped Mitoxantrone Hydrochloride Injection (PLM60) in Advanced Hepatocellular Carcinoma (HCC) [NCT04331743]Phase 118 participants (Anticipated)Interventional2021-06-05Not yet recruiting
A PHASE I COOPERATIVE AGREEMENT PEDIATRIC TRIAL OF MITOXANTRONE, ETOPOSIDE AND PSC-833 (PSC-ME) THERAPY IN PATIENTS WITH RELAPSED AND REFRACTORY ACUTE LEUKEMIA [NCT00002912]Phase 13 participants (Actual)Interventional1997-01-31Completed
A Randomized Trial of High-Dose Chemotherapy and Autologous Stem Cell Therapy Versus Standard Therapy in Women With Metastatic Breast Cancer Who Have Responded to Anthracycline or Taxane-Based Induction Chemotherapy [NCT00003032]Phase 3224 participants (Actual)Interventional1997-04-25Completed
An Out Patient Dose Escalation Trial of High Dose Mitoxantrone, Thiotepa and Cyclophosphamide Plus Autologous Blood Cell Rescue and Amifostine Cytoprotection [NCT00003068]Phase 230 participants (Anticipated)Interventional1997-06-30Completed
A Phase I Trial of Sequential High Dose Chemotherapy Regimens Followed by Autologous or Syngeneic Peripheral Blood Stem Cell (PBSC) Rescue in Patients With Persistent Stage III/IV Ovarian Cancer [NCT00003080]Phase 10 participants Interventional1996-09-30Completed
INDUCTION WITH ALL-TRANS RETINOIC ACID IN COMBINATION WITH IDARUBICIN AND INTENSIVE CONSOLIDATION FOLLOWED BY BONE MARROW TRANSPLANTATION OR A RANDOMIZED MAINTENANCE TREATMENT DEPENDING UPON THE AMOUNT OF MINIMAL RESIDUAL DISEASE IN ACUTE PROMYELOCYTIC LE [NCT00002701]Phase 3750 participants (Anticipated)Interventional1995-10-31Active, not recruiting
RANDOMIZED PHASE III STUDY TO EVALUATE THE VALUE OF rHuG-CSF IN INDUCTION AND OF AN ORAL SCHEDULE AS CONSOLIDATION TREATMENT IN ELDERLY PATIENTS WITH ACUTE MYELOGENOUS LEUMEKIA (AML-13 PROTOCOL) [NCT00002719]Phase 3500 participants (Anticipated)Interventional1995-12-31Completed
A Randomised Study Comparing an Oral Regimen (Idarubicin and Etoposide) With an Intravenous Regimen (MAE) for Consolidation in Patients Over 55 Years With Acute Myeloid Leukaemia in First Complete Remission [NCT00003602]Phase 3400 participants (Anticipated)Interventional1998-03-31Active, not recruiting
Phase III Study of Combination Chemotherapy in Children With T Cell and Pre-B Cell Non-Hodgkin's Lymphoma [NCT00003650]Phase 3179 participants (Actual)Interventional1997-02-28Completed
The Value of Dexamethasone Versus Prednisolone During Induction and Maintenance Therapy of Prolonged Versus Conventional Duration of L-Asparaginase Therapy During Consolidation and Late Intensification, and of Corticosteroid + VCR Pulses During Maintenanc [NCT00003728]Phase 31,500 participants (Anticipated)Interventional1998-12-31Active, not recruiting
PROSPECTIVE NON-RANDOMIZED STUDY WITH CHEMOTHERAPY FOR RELAPSED OR REFRACTORY HIV-RELATED NON-HODGKIN'S LYMPHOMA: VMP REGIMEN FOR RELAPSED PATIENTS, CDE REGIMEN FOR REFRACTORY PATIENTS [NCT00002905]Phase 220 participants (Anticipated)Interventional1995-06-30Active, not recruiting
A Randomized Phase II Trial of Navelbine/Epirubicin Versus Navelbine/Mitozantrone Versus Cyclophosphamide/Adriamycin as Preoperative Chemotherapy in Patients With > or = 3cm Diameter Early Breast Cancer [NCT00004237]Phase 20 participants Interventional1998-10-31Completed
A Randomized, Double-Blind, Placebo-Controlled, Phase III Study of the Matrix Metalloprotease Inhibitor AG3340 in Combination With Mitoxantrone and Prednisone With Provision for Subsequent Change in Therapy in Patients Having Hormone-Refractory Prostate C [NCT00003343]Phase 3525 participants (Anticipated)Interventional1998-03-31Completed
Phase 2, Randomized, Biomarker-driven Clinical Study in Patients With Relapsed or Refractory Acute Myeloid Leukemia (AML) With MCL-1 Dependence ≥30% [NCT02520011]Phase 2104 participants (Actual)Interventional2016-03-14Terminated(stopped due to Due to slow enrollment, the extensive time projected to conclude the study hypothesis rendered the study no longer reasonably feasible to complete.)
Phase II Study of Novantrone(R) (Mitoxantrone) and Etoposide in Patients With HIV Associated Large Cell and Immunoblastic Lymphomas [NCT00002003]Phase 20 participants InterventionalCompleted
RANDOMIZED PHASE III STUDY OF INDUCTION (ICE VS MICE VS DCE) AND INTENSIVE CONSOLIDATION (IDIA VS NOVIA VS DIA) FOLLOWED BY BONE MARROW TRANSPLANTATION IN ACUTE MYELOGENOUS LEUKEMIA: AML 10 PROTOCOL [NCT00002549]Phase 31,520 participants (Anticipated)Interventional1993-11-30Active, not recruiting
A Pilot Clinical Trial of Mitomycin C Modulation of Multidrug Resistance Proteins and a Phase I Evaluation of Mitomycin C and Mitoxantrone in Patients With Acute Myelogenous Leukemia [NCT00003003]Phase 129 participants (Anticipated)Interventional1996-09-30Completed
Treatment Protocol for Patients With Standard Risk Acute Myelogenous Leukemia and Its Variants: Induction Using High-Dose Cytarabine, Mitoxantrone and Ethyol; Consolidation With Cytarabine and Idarubicin and Maintenance With 13 Cis Retinoic Acid and Alpha [NCT00003405]Phase 20 participants (Actual)Interventional1998-04-30Withdrawn(stopped due to No enrollment)
Phase 3 Multicenter Randomized Trial to Evaluate Efficacy and Safety of CPI-613 in Combination With HD Cyt. and Mito. vs HD Cyt. and Mito. Therapy and Control Sub-groups in Older Patients With R/R AML [NCT03504410]Phase 3200 participants (Actual)Interventional2018-11-12Terminated(stopped due to Futile)
A Phase Ⅱ Study to Evaluate the Safety and Efficacy of Mitoxantrone Hydrochloride Liposome Injection for Relapsing Multiple Sclerosis [NCT05496894]Phase 20 participants (Actual)Interventional2022-08-31Withdrawn(stopped due to Due to the company's project adjustment, decided to stop this study)
Acute Myeloid Leukemia Salvage Therapy for Patients in First Relapse or Who Fail to Achieve an Initial Remission or Who Develop AML as a Second Malignant Neoplasm [NCT00002805]Phase 2115 participants (Actual)Interventional1997-08-31Completed
Phase I/II Study of High Dose Topotecan, Mitoxantrone and Thiotepa (TMT) Followed by Autologous Stem Cell Transplant in Patients With Recurrent Platinum Resistant Ovarian Cancer [NCT00003297]Phase 1/Phase 250 participants (Anticipated)Interventional1997-12-31Completed
A Randomized Prospective Study of Early Intensification Versus Alternating Triple Therapy for Patients With Poor Prognosis Lymphoma [NCT00002835]Phase 3116 participants (Actual)Interventional1995-10-30Completed
A Phase II Trial of Multiple Cycles of Sequential High Dose Chemotherapy for Patients With Chemotherapy Sensitive Relapsed Non-Hodgkin's Lymphoma [NCT00003957]Phase 23 participants (Actual)Interventional1998-12-31Completed
Treatment of Prostate Cancer by Induction of Alternate Cell Death Pathways: A Phase I Trial of Docetaxel, Estramustine, Mitoxantrone and Prednisone [NCT00003633]Phase 112 participants (Anticipated)Interventional1998-08-31Active, not recruiting
A Randomized, Open-Label Phase II/III Study of SU101 Plus Mitoxantrone/Prednisone Compared to Mitoxantrone/Prednisone Alone in Patients With Hormone-Refractory Prostate Cancer [NCT00004071]Phase 2/Phase 30 participants Interventional1999-08-31Completed
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 22 participants (Actual)Interventional2015-07-31Terminated(stopped due to Funding source discontinued)
Phase 3 Randomized Trial of DFP-10917 vs Non-Intensive Reinduction (LoDAC, Azacitidine, Decitabine, Venetoclax Combination Regimens) or Intensive Reinduction (High & Intermediate Dose Cytarabine Regimens) for Acute Myelogenous Leukemia Patients in Second, [NCT03926624]Phase 3450 participants (Anticipated)Interventional2019-11-22Recruiting
Phase I/II Clinical Study of Mitoxantrone Hydrochloride Liposomes in Combination With Gemcitabine, Dexamethasone, and Cisplatin in Relapsed/Refractory Peripheral T-cell Lymphoma [NCT05441761]Phase 1/Phase 260 participants (Anticipated)Interventional2022-05-01Recruiting
Phase Ib Trial of Gilteritinib in Combination With Mitoxantrone, Cladribine, Cytarabine and Filgrastim (GM-CLAG) for Relapsed/Refractory FLT3-mutated Acute Myeloid Leukemia [NCT05330377]Phase 10 participants (Actual)Interventional2023-03-31Withdrawn(stopped due to Sponsor withdrew funding)
Phase 2 Study of Mitoxantrone, Etoposide, and Cytarabine (MEC) Plus Lenalidomide for the Treatment of Adult Patients With Relapsed or Refractory Acute Myeloid Leukemia [NCT03118466]Phase 241 participants (Actual)Interventional2017-09-25Active, not recruiting
AN OPEN-LABEL, RANDOMIZED PHASE 3 STUDY OF INOTUZUMAB OZOGAMICIN COMPARED TO A DEFINED INVESTIGATOR'S CHOICE IN ADULT PATIENTS WITH RELAPSED OR REFRACTORY CD22-POSITIVE ACUTE LYMPHOBLASTIC LEUKEMIA (ALL) [NCT01564784]Phase 3326 participants (Actual)Interventional2012-08-02Completed
Phase II Study of Granulocyte-Macrophage Colony Stimulating Factor Plus Mitoxantrone for the Treatment of Hormone Refractory Prostate Cancer [NCT00477087]Phase 210 participants (Actual)Interventional2006-07-31Terminated(stopped due to Low accrual)
Open-Label, PhaseIb/Ⅱ Study of Tislelizumab and Mitoxantrone Hydrochloride Liposome Combination Treatment in Patients With Relapsed or Refractory Extranodal Natural Killer/T Cell Lymphoma(ALLIANCE-022) [NCT05464433]Phase 1/Phase 246 participants (Anticipated)Interventional2022-07-30Recruiting
Venetoclax Combining Chidamide and Azacitidine (VCA) Regimen Followed by Dicitabine Combined With Liposome Mitoxantrone, Cytarabine, and G-CSF (D-MAG) Regimen on the Treatment of Elderly Patients With Newly Diagnosed Acute Myeloid Leukemia (AML) : A Multi [NCT05603884]Phase 266 participants (Anticipated)Interventional2022-12-01Recruiting
A Multicenter, Open-label, Single-arm, Phase Ib Study to Evaluate Safety and Efficacy of Mitoxantrone Hydrochloride Liposome Injection in Subjects With Recurrent/Metastatic Head and Neck Cancers [NCT04902027]Phase 130 participants (Anticipated)Interventional2021-07-01Not yet recruiting
A Multicenter, Single-arm, Prospective Phase I/II Trial of Mitoxantrone Hydrochloride Liposome Injection Combined With Chidamide in Relapsed or Refractory Peripheral T-cell Lymphoma [NCT05527275]Phase 1/Phase 278 participants (Anticipated)Interventional2022-10-01Not yet recruiting
Phase I-II Study of Crenolanib Combined With Standard Salvage Chemotherapy, and Crenolanib Combined With 5-Azacitidine in Acute Myeloid Leukemia Patients With FLT3 Activating Mutations [NCT02400281]Phase 1/Phase 228 participants (Actual)Interventional2015-09-30Completed
Safety, Tolerability, and Efficacy of Mitoxantrone Hydrochloride Liposome Injection in Patients With Advanced Pancreatic Cancer: A Multicenter, Open-label, Phase Ⅱ Study [NCT05100329]Phase 238 participants (Anticipated)Interventional2021-11-30Not yet recruiting
A Randomized Phase II Trial of Mitoxantrone, Estramustine and Navelbine or 13-cis Retinoic Acid, Interferon and Paclitaxel in Patients With Metatstatic Hormone Refractory Prostate Cancer [NCT00005847]Phase 20 participants Interventional2001-04-05Completed
Total Therapy for Infants With Acute Lymphoblastic Leukemia (ALL) I [NCT02553460]Phase 1/Phase 250 participants (Actual)Interventional2016-01-29Active, not recruiting
A Phase I/II Study to Evaluate the Safety, Tolerability, Efficacy, and Pharmacokinetics of Mitoxantrone Hydrochloride Liposome Injection in Subjects With Acute Myeloid Leukemia [NCT05345938]Phase 1/Phase 290 participants (Anticipated)Interventional2022-05-30Not yet recruiting
Dasatinib Plus Multi-agent Chemotherapy for New Diagnosed Philadelphia Chromosome-positive Acute Lymphoblastic Leukemia [NCT02523976]Phase 230 participants (Actual)Interventional2015-08-01Completed
Multicenter Randomized Controlled Clinical Study of Mitoxantrone Hydrochloride Liposome Injection Combined With Carmustine, Etoposide and Cytarabine (Modified BEAM Protocol) for T Cell Lymphoma Underwent Autologous Stem Cell Transplantation [NCT05814718]122 participants (Anticipated)Interventional2023-04-15Not yet recruiting
A Phase 1 Single-Center Trial Combining Venetoclax With G-CSF, Cladribine, Cytarabine, and Mitoxantrone (CLAG-M) for Patients With AML and High-Grade Myeloid Neoplasms [NCT04797767]Phase 120 participants (Anticipated)Interventional2022-02-04Recruiting
Open-label, Single-arm Trial to Evaluate Antitumor Activity, Safety, and Pharmacokinetics of Isatuximab Used in Combination With Chemotherapy in Pediatric Patients From 28 Days to Less Than 18 Years of Age With Relapsed/Refractory B or T Acute Lymphoblast [NCT03860844]Phase 267 participants (Actual)Interventional2019-08-06Terminated(stopped due to Study was prematurely stopped due to sponsor decision (stage 2 efficacy criteria not met); not due to safety concerns.)
A Single-Center Phase 1/2 Study of Single- or Fractioned-Dose Gemtuzumab Ozogamicin in Combination With G-CSF, Cladribine, Cytarabine, and Mitoxantrone for Previously Untreated Adult Acute Myeloid Leukemia or High-Grade Myeloid Neoplasm [NCT03531918]Phase 1/Phase 266 participants (Actual)Interventional2018-09-14Completed
Phase 2 Study of the Activity and Safety of Fludarabine, Cyclophosphamide, and Mitoxantrone Plus Rituximab (FCM-R) With Pegfilgrastim (Neulasta) as Frontline Therapy for Patients < 70 Years With Chronic Lymphocytic Leukemia [NCT00254410]Phase 230 participants (Actual)Interventional2005-03-14Completed
A Phase 3, Randomized, Double-blind, Controlled Trial of Cabozantinib (XL184) Versus Mitoxantrone Plus Prednisone in Men With Previously Treated Symptomatic Castration-resistant Prostate Cancer [NCT01522443]Phase 3119 participants (Actual)Interventional2012-03-31Terminated(stopped due to Stopped after the outcome of cabozantinib Phase 3 CRPC study XL184-307.)
Phase II Study of Adult Acute Lymphoblastic Leukaemia (ALL): Imatinib in Combination With Chemotherapy in Ph+ Patients, and Post-remissional Treatment Intensification in High-risk Ph- Patients, With Minimal Residual Disease Monitoring. [NCT00458848]Phase 2470 participants (Actual)Interventional2004-10-31Completed
Randomized Phase 2 Trial of CPX-351 (Vyxeos) vs. CLAG-M (Cladribine, Cytarabine, G-CSF, and Mitoxantrone) in Medically Less-Fit Adults With Acute Myeloid Leukemia (AML) or Other High-Grade Myeloid Neoplasm [NCT04195945]Phase 260 participants (Anticipated)Interventional2020-03-11Recruiting
A Phase I Dose Escalation Study of Clofarabine Given in Combination With Multi-agent Therapy for Remission Induction in Pediatric Patients With Acute Lymphoblastic Leukemia in First Relapse or Refractory to First Line Therapy - [NCT01279096]Phase 120 participants (Actual)Interventional2010-01-31Completed
A Multicenter, Open-label, Single-arm, Phase II Study of Mitoxantrone Hydrochloride Liposome Injection in Patients With Advanced HER2 Negative Breast Cancer [NCT04927481]Phase 273 participants (Anticipated)Interventional2021-06-11Recruiting
A Phase 2 Multi-Arm Study of Magrolimab Combinations in Patients With Myeloid Malignancies [NCT04778410]Phase 259 participants (Anticipated)Interventional2021-06-28Active, not recruiting
An Open-label, Multi-center Phase II Clinical Trial to Evaluate the Cardiac Safety of Mitoxantrone Hydrochloride Liposome Injection in the Treatment of Advanced Malignant Tumor [NCT05089461]Phase 2120 participants (Anticipated)Interventional2022-03-07Suspended(stopped due to sponsor decided to stop)
A RANDOMIZED, CONTROLLED TRIAL OF SALVAGE THERAPY WITH PACLITAXEL AND CARBOPLATIN VERSU SALVAGE THERAPY WITH STEM CELL SUPPORTED HIGH-DOSE CARBOPLATIN, MITOXANTRONE AND CYCLOPHOSPHAMIDE IN PATIENTS WITH PERSISTENT LOW VOLUME OVARIAN CANCER AND RESPONSE TO [NCT00002819]Phase 30 participants Interventional1996-11-30Terminated
Standard Chemotherapy (CHOP Regimen) Versus Sequential High-Dose Chemotherapy With Autologous Stem Cell Transplantation in Patients With Newly Diagnosed Aggressive Non-Hodgkin's Lymphomas and Poor Prognostic Factors: A Randomized Phase III Study (MISTRAL) [NCT00003215]Phase 3400 participants (Anticipated)Interventional1997-04-30Completed
Docetaxel and Estramustine Versus Mitoxantrone and Prednisone for Advanced, Hormone Refractory Prostate Cancer [NCT00004001]Phase 3770 participants (Actual)Interventional1999-10-31Completed
Phase II Study of Alvocidib (NSC 649890, Flavopiridol) in Timed Sequential Combination With Cytosine Arabinoside (Ara-C) and Mitoxantrone for Adults With Newly Diagnosed, Previously Untreated, Poor-Risk Acute Myelogenous Leukemias [NCT00407966]Phase 245 participants (Actual)Interventional2006-10-31Completed
A Phase I Study of Neoadjuvant Chemotherapy Involving Cabazitaxel, Docetaxel, Mitoxantrone or Satraplatin (CDMS) Followed by Surgery for Patients With High Risk Localized Prostate Cancer [NCT03258320]Phase 150 participants (Anticipated)Interventional2015-01-31Recruiting
Randomized Phase II Study Comparing Two Administration Schedules of Flavopiridol (Alvocidib, NSC 649890, IND 46, 211) Given in Timed Sequential Combination With Cytosine Arabinoside (Ara-C) and Mitoxantrone Hydrochloride for Adults With Newly Diagnosed, P [NCT00795002]Phase 278 participants (Actual)Interventional2008-11-30Completed
Phase III Randomized, Double-blind, Placebo-controlled Study Investigating the Efficacy of the Addition of Crenolanib to Salvage Chemotherapy Versus Salvage Chemotherapy Alone in Subjects ≤ 75 Years of Age With Relapsed/Refractory FLT3 Mutated Acute Myelo [NCT03250338]Phase 3322 participants (Anticipated)Interventional2018-06-05Recruiting
An Open-label, Multi-center Phase Ib/II Study to Evaluate the Tolerance and Efficacy of Mitoxantrone Hydrochloride Liposome Injection Combined With Cytarabine in Patients With Acute Myeloid Leukemia (AML) [NCT05100303]Phase 1/Phase 258 participants (Anticipated)Interventional2021-12-31Not yet recruiting
A Pilot Study of Decitabine and Vorinostat With Chemotherapy for Relapsed ALL [NCT01483690]Phase 1/Phase 223 participants (Actual)Interventional2011-12-31Terminated(stopped due to Toxicity)
A Prospective, Randomized, Controlled Trial of Decitabine Versus Conventional Chemotherapy for Maintenance Therapy of Patients With Acute Myeloid Leukemia With t(8;21) [NCT03026842]Phase 4180 participants (Anticipated)Interventional2017-01-31Active, not recruiting
A Biomarker Validation Study to Establish Whether Serial Flow Cytometric Measurements Predict Clinical Response to Sirolimus and MEC (Mitoxantrone Etoposide Cytarabine) Treatment in Patients With High-Risk Acute Myelogenous Leukemia [NCT02583893]Phase 239 participants (Actual)Interventional2015-10-07Completed
A Randomized, Open-label, Positive-controlled, Multicenter Phase Ш Study Comparing Mitoxantrone Hydrochloride Liposome Injection Combined With Capecitabine Versus Capecitabine Monotherapy in Patients With Recurrent Metastatic Nasopharyngeal Carcinoma Who [NCT05717764]Phase 3500 participants (Anticipated)Interventional2023-02-28Not yet recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00002766 (1) [back to overview]Complete Remission (CR)
NCT00004124 (3) [back to overview]Compare Qualitative and Quantitative Toxicities of These Regimens in These Patients
NCT00004124 (3) [back to overview]Disease Free Survival
NCT00004124 (3) [back to overview]Overall Survival
NCT00017563 (1) [back to overview]Number of Participants With 5-year Freedom From Prostate Specific Antigen (PSA) Recurrence.
NCT00109837 (2) [back to overview]Continuous Complete Remission at 1 Year
NCT00109837 (2) [back to overview]Toxicity
NCT00136084 (7) [back to overview]Relationship of Inhibition of DNA Synthesis and Clinical Response
NCT00136084 (7) [back to overview]To Assess Whether Inhibition of DNA Synthesis is Greater After High-dose Ara-C (HDAC) Than After Low-dose Ara-C (LDAC) Therapy
NCT00136084 (7) [back to overview]Minimal Residual Disease (MRD).
NCT00136084 (7) [back to overview]Proportion of Minimal Residual Disease (MRD)+ Patients Who Become MRD- After One Course of Gemtuzumab Ozogamicin (GO)
NCT00136084 (7) [back to overview]To Estimate the Overall Event-free Survival (EFS) of AML Patients Who Undergo Risk-adapted and Genotype-directed Therapy
NCT00136084 (7) [back to overview]Proportion of MRD Reduction After One Course of Cytarabine + Daunomycin + Etoposide (ADE) + GO
NCT00136084 (7) [back to overview]Proportion of Patients Experienced Toxicity of Cytarabine + Daunomycin + Etoposide (ADE) + GO.
NCT00186875 (4) [back to overview]Overall Survival (OS)
NCT00186875 (4) [back to overview]Minimal Residual Disease (MRD) Compared With Historical Data From TOTXV Protocol (NCT00137111)
NCT00186875 (4) [back to overview]Minimal Residual Disease (MRD) Compared With Historical Data From TOTXV Protocol (NCT00137111)
NCT00186875 (4) [back to overview]Response Rate
NCT00193479 (1) [back to overview]Overall Response Rate (ORR), the Percentage of Patients Who Experience an Objective Benefit From Treatment
NCT00208975 (1) [back to overview]Number of Patients's Who Had Complete Response and Partial Response to the Treatment of Fludarabine and Cyclophosphamide Followed by GM-CSF and Rituximab.
NCT00254410 (4) [back to overview]Molecular Response Rate at 3 Months
NCT00254410 (4) [back to overview]Clinical Response Rate at 6 Months
NCT00254410 (4) [back to overview]Clinical Response Rate at 3 Months
NCT00254410 (4) [back to overview]Molecular Response Rate at 6 Months
NCT00268242 (6) [back to overview]Complete Response Rate
NCT00268242 (6) [back to overview]White Blood Cell Count at Time of Relapse
NCT00268242 (6) [back to overview]Disease-free and Overall Survival
NCT00268242 (6) [back to overview]Laboratory Correlates: Immunohistochemistry
NCT00268242 (6) [back to overview]Duration of the First Complete Response
NCT00268242 (6) [back to overview]Percentage of Patients Making it to Bone Marrow Transplant.
NCT00290511 (7) [back to overview]Tolerance and Efficacy of Maintenance Therapy With Yttrium-90 Ibritumomab Tiuxetan (YIT)
NCT00290511 (7) [back to overview]Tolerance and Efficacy of Maintenance Therapy With Rituximab
NCT00290511 (7) [back to overview]Number of Participants With Time to Progression (TTP)
NCT00290511 (7) [back to overview]Progression Free Survival at 10 Years
NCT00290511 (7) [back to overview]Percentage of Participants With Overall Survival Rate at 10 Years
NCT00290511 (7) [back to overview]Median Progression Free Survival
NCT00290511 (7) [back to overview]Overall Survival
NCT00327340 (4) [back to overview]Safety and Tolerability of Custirsen (OGX-011) in Combination With Either Docetaxel/Prednisone or Mitoxantrone/Prednisone as Second-line Chemotherapy.
NCT00327340 (4) [back to overview]Feasibility of Treatment With Custirsen (OGX-011) in Combination With Second-line Chemotherapy Based on Prostate Specific Antigen (PSA) Response
NCT00327340 (4) [back to overview]Feasibility of Treatment With OGX-011 in Combination With Either Docetaxel/Prednisone or Mitoxantrone/Prednisone as Second Line Chemotherapy Based on Time to Pain Progression
NCT00327340 (4) [back to overview]Relationship Between Changes in Serum Clusterin Levels and Change in Serum PSA Levels When OGX-011 in Combination With Either Docetaxel/Prednisone or Mitoxantrone/Prednisone is Administered as Second Line Chemotherapy.
NCT00331344 (4) [back to overview]Proportion Responding to Treatment With of the Combination of Ixabepilone and Mitoxantrone Hydrochloride With Prednisone in Hormone Refractory Prostate Cancer Patients Who Have Had Prior Taxane Chemotherapy Based Upon a PSA Decline of > 50% (Phase II)
NCT00331344 (4) [back to overview]Dose Limiting Toxicities for Each Dose Level of Ixabepilone, Mitoxantrone Hydrochloride, and Prednisone in Patients With Hormone-refractory Metastatic Prostate Cancer That Progressed During or After Taxane-based Chemotherapy (Phase I).
NCT00331344 (4) [back to overview]Time to Progression (Phase II)
NCT00331344 (4) [back to overview]Safety of the Combination of Ixabepilone, Mitoxantrone Hydrochloride, and Prednisone in Patients With Hormone-refractory Metastatic Prostate Cancer That Progressed During or After Taxane-based Chemotherapy (Phase I)
NCT00372593 (7) [back to overview]Event-free Survival at 3 Years
NCT00372593 (7) [back to overview]Mortality
NCT00372593 (7) [back to overview]Overall Survival at 3 Years
NCT00372593 (7) [back to overview]Remission Induction Rate After 2 Courses of Induction Therapy
NCT00372593 (7) [back to overview]Toxicities, Including Infectious Complications
NCT00372593 (7) [back to overview]Time to Marrow Recovery
NCT00372593 (7) [back to overview]Disease-free Survival (DFS)
NCT00385827 (5) [back to overview]Overall Survival (OS)
NCT00385827 (5) [back to overview]Number of Participants With Prostate Specific Antigen (PSA) Response
NCT00385827 (5) [back to overview]Time to Clinical Deterioration (TtCD)
NCT00385827 (5) [back to overview]Part 1: Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)
NCT00385827 (5) [back to overview]Part 2: Progression Free Survival (PFS)
NCT00407966 (1) [back to overview]Complete Response
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
NCT00417079 (8) [back to overview]PSA (Prostate-Specific Antigen) Response
NCT00417079 (8) [back to overview]Overall Survival
NCT00417079 (8) [back to overview]Overall Tumor Response
NCT00417079 (8) [back to overview]Pain Response
NCT00417079 (8) [back to overview]Time to Pain Progression
NCT00417079 (8) [back to overview]Time to Progression Free Survival (PFS)
NCT00417079 (8) [back to overview]Time to Prostatic Specific Antigen (PSA) Progression
NCT00417079 (8) [back to overview]Time to Tumor Progression
NCT00452387 (3) [back to overview]Quality of Life (QoL)
NCT00452387 (3) [back to overview]Correlation of Biochemical Criteria (PSA, Prostate-specific Antigen) With Objective Imaging
NCT00452387 (3) [back to overview]Median Overall Survival (OS)
NCT00458848 (3) [back to overview]Percentage of Participants Reaching Overall Survival
NCT00458848 (3) [back to overview]Percentage of Participants Reaching Disease Free Survival
NCT00458848 (3) [back to overview]Number of Patients Reaching Complete Hematological Response After Induction Therapy
NCT00477087 (3) [back to overview]Overall Survival (OS)
NCT00477087 (3) [back to overview]Progression-free Survival (PFS)
NCT00477087 (3) [back to overview]Number of Participants With > 50% Decrease in Prostate-specific Antigen Levels (PSA Response)
NCT00510887 (6) [back to overview]Complete and Partial Response
NCT00510887 (6) [back to overview]Number of Participants With Neuropathy, Any Grade
NCT00510887 (6) [back to overview]Duration of Response
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
NCT00512252 (10) [back to overview]Time to Platelet Recovery
NCT00512252 (10) [back to overview]Time to Neutrophil Recovery
NCT00512252 (10) [back to overview]Relapse-free Survival
NCT00512252 (10) [back to overview]Treatment Failure
NCT00512252 (10) [back to overview]Safety and Tolerability of AMD3100 + MEC.
NCT00512252 (10) [back to overview]Phase II Only: Complete Response Rate of AMD3100 + MEC
NCT00512252 (10) [back to overview]Characterize the Mobilization of Leukemic Cells With AMD3100 by Measuring the Peak Mobilization of Total Leukocytes (Phase I)
NCT00512252 (10) [back to overview]Characterize the Mobilization of Leukemic Cells With AMD3100 by Measuring the Peak Mobilization of AML Blasts (Phase I)
NCT00512252 (10) [back to overview]Phase I Only: Optimal Dose of AMD3100 Plus MEC in Patients With Relapsed or Refractory AML
NCT00512252 (10) [back to overview]Overall Survival
NCT00546377 (2) [back to overview]Maximum Tolerated Dose (MTD) of Mitoxantrone
NCT00546377 (2) [back to overview]Overall Response
NCT00562965 (7) [back to overview]Progression-Free Survival (PFS)
NCT00562965 (7) [back to overview]Number of Participants With Clinically Significant Change From Baseline in Vital Signs
NCT00562965 (7) [back to overview]Number of Participants With Grade 3 or 4 Treatment Emergent Adverse Events (TEAEs)
NCT00562965 (7) [back to overview]Number of Participants With Clinically Significant Change From Baseline in QT Interval Findings
NCT00562965 (7) [back to overview]Percentage of Participants With Objective Response (OR)
NCT00562965 (7) [back to overview]Overall Survival Probability at Months 6, 12 and 24
NCT00562965 (7) [back to overview]Number of Participants With Clinically Significant Change From Baseline in Laboratory Findings
NCT00577993 (2) [back to overview]Number of Participants With Progression Free Survival (10 Years) by Treatment
NCT00577993 (2) [back to overview]Number of Participants With Overall Survival (10 Years) by Treatment
NCT00609739 (4) [back to overview]Patients With Graft-Versus-Host-Disease
NCT00609739 (4) [back to overview]Patients Who Relapsed
NCT00609739 (4) [back to overview]Patients With Regimen-Related Toxicity
NCT00609739 (4) [back to overview]Disease-free Survival
NCT00634244 (2) [back to overview]The Rate of Treatment Failure
NCT00634244 (2) [back to overview]The Rate of Complete Remission (CR+CRi)
NCT00656084 (4) [back to overview]Duration of Response
NCT00656084 (4) [back to overview]Objective Response Rate (CR + PR)
NCT00656084 (4) [back to overview]Progression-free Survival Rate at 1 Year.
NCT00656084 (4) [back to overview]Overall Survival (OS) Rate at 1 Year
NCT00661492 (8) [back to overview]Prostate-specific Antigen (PSA) Response Rate
NCT00661492 (8) [back to overview]Prostate-specific Antigen (PSA) Doubling Time
NCT00661492 (8) [back to overview]Objective Response Rate (ORR)
NCT00661492 (8) [back to overview]Median Time to Prostate-specific Antigen (PSA) Progression
NCT00661492 (8) [back to overview]Median Time to Progression (TTP)
NCT00661492 (8) [back to overview]Median Overall Survival (OS)
NCT00661492 (8) [back to overview]2-year Radiographically Evident Progression-free Survival (REPFS).
NCT00661492 (8) [back to overview]Median Progression-free Survival (PFS)
NCT00683475 (9) [back to overview]Objective Response Rate (ORR)
NCT00683475 (9) [back to overview]Prostate Specific Antigen (PSA) Response Rate
NCT00683475 (9) [back to overview]Composite Progression-free Survival (cPFS) at 12-months
NCT00683475 (9) [back to overview]Composite Progression-free Survival (cPFS)
NCT00683475 (9) [back to overview]Overall Survival (OS)
NCT00683475 (9) [back to overview]Composite Progression-free Survival (cPFS) at 9-months
NCT00683475 (9) [back to overview]Composite Progression-free Survival (cPFS) at 6-months
NCT00683475 (9) [back to overview]Summary Listing of Participants Reporting Treatment-Emergent Adverse Events
NCT00683475 (9) [back to overview]Time to Radiographic Evidence of Disease Progression
NCT00712582 (2) [back to overview]2-year PFS From the Start of Induction Therapy Conditional
NCT00712582 (2) [back to overview]Overall Survival at 1 Year
NCT00774046 (7) [back to overview]Response to Induction Chemotherapy (CR or PR)
NCT00774046 (7) [back to overview]Disease-free Survival in Patients Undergoing Autologous Stem Cell Transplant
NCT00774046 (7) [back to overview]Relapse-free Survival
NCT00774046 (7) [back to overview]Feasibility of Stem Cell Collection
NCT00774046 (7) [back to overview]Numbers of Stem Cells Collected
NCT00774046 (7) [back to overview]Overall Survival
NCT00774046 (7) [back to overview]Overall Survival in Patients Undergoing Autologous Stem Cell Transplant
NCT00795002 (3) [back to overview]Complete Response
NCT00795002 (3) [back to overview]Disease-free Survival
NCT00795002 (3) [back to overview]Number of Participants Experiencing Death From Any Cause Within 60 Days of Starting FLAM
NCT00866918 (4) [back to overview]Hematologic Remission Rate
NCT00866918 (4) [back to overview]Overall Survival (OS)
NCT00866918 (4) [back to overview]Hematologic, Molecular, and Cytogenetic Remission Rate
NCT00866918 (4) [back to overview]Event-free Survival (EFS)
NCT00901927 (3) [back to overview]Participants With Adverse Events
NCT00901927 (3) [back to overview]Complete Response Rate of the Combination of BMR (Bendamustine + Mitoxantrone + Rituximab)
NCT00901927 (3) [back to overview]Time to Progression (TTP) for Participants Treated With BMR (Bendamustine, Mitoxantrone, and Rituximab)
NCT00906945 (13) [back to overview]Characterize the Mobilization of Leukemic Cells With Plerixafor Plus G-CSF as Measured by Fold Change in AML Blast Count
NCT00906945 (13) [back to overview]Characterize the Mobilization of Leukemic Cells With Plerixafor Plus G-CSF as Measured by Fold Change in White Blood Cells
NCT00906945 (13) [back to overview]Overall Survival
NCT00906945 (13) [back to overview]Phase I: Maximum Tolerated Dose of Plerixafor Plus G-CSF When Combined With MEC
NCT00906945 (13) [back to overview]Phase II: Complete Response Rate (CR+CRi)
NCT00906945 (13) [back to overview]Relapse Free-survival Rate
NCT00906945 (13) [back to overview]Time to Hematologic Recovery as Measured by Time to Neutrophil Recovery
NCT00906945 (13) [back to overview]Time to Hematologic Recovery as Measured by Time to Neutrophil Recovery
NCT00906945 (13) [back to overview]Time to Hematologic Recovery as Measured by Time to Platelet Recovery
NCT00906945 (13) [back to overview]Time to Hematologic Recovery as Measured by Time to Platelet Recovery
NCT00906945 (13) [back to overview]Phase I and Phase II: Safety and Tolerability of Regimen as Measured by Grade and Frequency of Adverse Events Exceeding 10% in Total Frequency
NCT00906945 (13) [back to overview]Characterize the Effects of Plerixafor Plus G-CSF on Fold Change in CXCR4 Clone 12G5 Relative Mean Fluorescent Intensity
NCT00906945 (13) [back to overview]Characterize the Effects of Plerixafor Plus G-CSF on Fold Change in CXCR4 Clone 1D9 Relative Mean Fluorescent Intensity
NCT01133158 (2) [back to overview]Secondary Endpoints Included an Assessment of the Following Parameters: Progression-Free Survival, Disease-Free Survival, Global Survival, Duration of the Response.
NCT01133158 (2) [back to overview]Response Rate
NCT01144403 (4) [back to overview]Number of Participant With Adverse Event (AE)
NCT01144403 (4) [back to overview]Overall Response Rate (ORR)
NCT01144403 (4) [back to overview]Overall Survival (OS)
NCT01144403 (4) [back to overview]Progression-free Survival (PFS)
NCT01184898 (4) [back to overview]Complete Response in the Absence of Platelet Recovery
NCT01184898 (4) [back to overview]Association Between the Magnitude of mTOR Target Inhibition Post-treatment in Leukemic Blasts and Clinical Response in Patients With High Risk AML Treated With Sirolimus MEC
NCT01184898 (4) [back to overview]Partial Response
NCT01184898 (4) [back to overview]Complete Response
NCT01204710 (11) [back to overview]PFS Based on Baseline Circulating Tumor Cells (CTC) Counts
NCT01204710 (11) [back to overview]Percentage of Participants With Anti-Olaratumab Antibody Assessment (Immunogenicity)
NCT01204710 (11) [back to overview]Percentage of Participants With a ≥50% Decrease in Prostate Specific Androgen (PSA) From Pretreatment to Any Time
NCT01204710 (11) [back to overview]Summary Listing of Participants Reporting Treatment-Emergent Adverse Events (TEAE)
NCT01204710 (11) [back to overview]Percentage of Participants Who Achieved a Best Overall Response of Complete Response (CR) or Partial Response (PR) [Objective Response Rate (ORR)]
NCT01204710 (11) [back to overview]Overall Survival (OS)
NCT01204710 (11) [back to overview]OS Based on Baseline CTC Counts
NCT01204710 (11) [back to overview]Percentage of Participants With a ≥30% Decrease in PSA From Pretreatment to Week 12
NCT01204710 (11) [back to overview]Progression-Free Survival (PFS)
NCT01204710 (11) [back to overview]Number of Participants Who Died During Study
NCT01204710 (11) [back to overview]Number of Participants With Negative Platelet-Derived Growth Factor Receptor Alpha (PDGFRα) Protein Expression by Immunohistochemistry (IHC)
NCT01214317 (2) [back to overview]Expanded Disability Status Score
NCT01214317 (2) [back to overview]Change From Baseline in Mean Number of MS Plaques Found on Brain MRI
NCT01342887 (1) [back to overview]Maximum Tolerated Doses Mitoxantrone Hydrochloride and Etoposide When Combined With Cyclosporine and Pravastatin Sodium
NCT01349972 (6) [back to overview]Complete Response Rate
NCT01349972 (6) [back to overview]Progression-free Survival
NCT01349972 (6) [back to overview]Overall Survival
NCT01349972 (6) [back to overview]Disease-free Survival
NCT01349972 (6) [back to overview]Incidence of Toxicities, Characterized by Number of Events by Treatment and Grade
NCT01349972 (6) [back to overview]Number of Patients With Minimal Residual Disease
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]OS for Patients on Arm C, Cohort 2
NCT01371981 (18) [back to overview]Total Scale Score From Parent-reported Multidimensional Fatigue Scale Module
NCT01371981 (18) [back to overview]EFS for Patients on Arm C, Cohort 2
NCT01371981 (18) [back to overview]EFS for Patients on Arm C, Cohort 1
NCT01371981 (18) [back to overview]OS for Patients on Arm C, Cohort 1
NCT01371981 (18) [back to overview]Change in Shortening Fraction
NCT01371981 (18) [back to overview]Change in Ejection Fraction
NCT01371981 (18) [back to overview]OS for Patients on Arm C, Cohort 3
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]Total Scale Score From Parent-reported Pediatric Quality of Life Inventory Module
NCT01371981 (18) [back to overview]Bortezomib Clearance
NCT01371981 (18) [back to overview]Overall Survival (OS) for Patients Without High Allelic Ratio FLT3/ITD+ Mutations
NCT01371981 (18) [back to overview]Event-free Survival (EFS) for Patients Without High Allelic Ratio FLT3/ITD+ Mutations
NCT01371981 (18) [back to overview]EFS for Patients on Arm C, Cohort 3
NCT01371981 (18) [back to overview]Proportion of Patients Experiencing Grade 3 or Higher Non-hematologic Toxicities and Infections While on Protocol Therapy
NCT01371981 (18) [back to overview]Relapse Rate for Patients Without High Allelic Ratio FLT3/ITD+ Mutations
NCT01483690 (2) [back to overview]Disease Response Rate After Treatment.
NCT01483690 (2) [back to overview]Number of Participants Who Experienced a Dose Limiting Toxicity (DLT).
NCT01522443 (3) [back to overview]Pain Response at Week 6 Confirmed at Week 12, Week 12 Reported
NCT01522443 (3) [back to overview]Bone Scan Response (BSR)
NCT01522443 (3) [back to overview]Overall Survival (OS)
NCT01564784 (12) [back to overview]Duration of Remission (DoR) for Participants Who Achieved CR/CRi (Per Investigator Assessment)
NCT01564784 (12) [back to overview]Cytogenetic Status (Based on Local Laboratory Analysis) of Participants With CR/CRi (Per EAC Assessment)
NCT01564784 (12) [back to overview]Overall Survival (OS)
NCT01564784 (12) [back to overview]Maximum Observed Inotuzumab Ozogamicin Serum Concentration (Cmax) and Pre-Dose Inotuzumab Ozogamicin Serum Concentration (Ctrough) Following Single and Multiple Dosing
NCT01564784 (12) [back to overview]Change From Baseline in EuroQol 5 Dimension Health Questionnaire (EQ-5D) Index Score
NCT01564784 (12) [back to overview]Change From Baseline in European Organization for Research and Treatment of Cancer Quality of Life Questionnaire, Core 30 (EORTC QLQ-C30) Score
NCT01564784 (12) [back to overview]Change From Baseline in EQ-5D VAS
NCT01564784 (12) [back to overview]Progression-Free Survival (PFS)
NCT01564784 (12) [back to overview]Percentage of Participants With Veno-Occlusive Liver Disease (VOD)/Sinusoidal Obstruction Syndrome (SOS) Following Post Study HSCT
NCT01564784 (12) [back to overview]Percentage of Participants With Hematologic Remission (Complete Remission [CR]/Complete Remission With Incomplete Hematologic Recovery [CRi]) as Assessed by the Endpoint Adjudication Committee (EAC)
NCT01564784 (12) [back to overview]Percentage of Participants Who Had a Hematopoietic Stem-Cell Transplant (HSCT)
NCT01564784 (12) [back to overview]Percentage of Participants Achieving MRD Negativity (Based on Central Laboratory Analysis) in Participants Achieving a CR/CRi (Per EAC Assessment)
NCT01700946 (4) [back to overview]3-year Overall Survival Rate of Patients With Relapsed ALL
NCT01700946 (4) [back to overview]Median CD20 Expression Levels
NCT01700946 (4) [back to overview]Mean of CD20 Expression Levels
NCT01700946 (4) [back to overview]3-year Event-free Survival Rates in Patients With Relapsed ALL
NCT01729845 (4) [back to overview]Remission Rate Including CR and CRp
NCT01729845 (4) [back to overview]Duration of Relapse-free Survival (for Patients Achieving CR or CRp)
NCT01729845 (4) [back to overview]Overall Survival
NCT01729845 (4) [back to overview]Most Efficacious and Tolerated Dosage of Decitabine (Period 1)
NCT02044796 (4) [back to overview]Minimal Residual Disease Negative Complete Remission Rate in Patients With Newly Diagnosed Disease (Phase II)
NCT02044796 (4) [back to overview]Number of Participants With Dose Limiting Toxicities of Mitoxantrone (Phase I, Dose Level 4)
NCT02044796 (4) [back to overview]Remission Rate (Complete Remission and Complete Remission With Incomplete Platelet Count Recovery) of This Regimen in Patients With Relapsed/Refractory Disease (Phase II)
NCT02044796 (4) [back to overview]Overall Survival (Phase II)
NCT02101853 (4) [back to overview]Disease Free Survival (DFS) of Low Risk (LR) Relapse Patients
NCT02101853 (4) [back to overview]Disease Free Survival (DFS) of High-risk (HR) and Intermediate-risk (IR) Relapse Patients
NCT02101853 (4) [back to overview]Overall Survival (OS) of HR and IR Relapse Patients
NCT02101853 (4) [back to overview]Overall Survival (OS) of LR Relapse Patients
NCT02339740 (2) [back to overview]EFS in High Risk APL Patients
NCT02339740 (2) [back to overview]Event-free Survival (EFS) in Standard Risk Acute Promyelocytic Leukemia (APL) Patients
NCT02419755 (1) [back to overview]Number of Relevant Toxicities Related to Therapy
NCT02421939 (12) [back to overview]Duration of Overall Survival (OS)
NCT02421939 (12) [back to overview]Percentage of Participants Who Achieved Transfusion Conversion and Maintenance
NCT02421939 (12) [back to overview]Change From Baseline in Brief Fatigue Inventory (BFI)
NCT02421939 (12) [back to overview]Percentage of Participants With Composite Complete Remission (CRc Rate)
NCT02421939 (12) [back to overview]Percentage of Participants With Complete Remission (CR) With Partial Hematological Recovery (CRh)
NCT02421939 (12) [back to overview]Percentage of Participants With Complete Remission (CR) Rate
NCT02421939 (12) [back to overview]Duration of Event-Free Survival (EFS)
NCT02421939 (12) [back to overview]Percentage of Participants Who Underwent Hematopoietic Stem Cell Transplant
NCT02421939 (12) [back to overview]Duration of Remission
NCT02421939 (12) [back to overview]Number of Participants With Adverse Events
NCT02421939 (12) [back to overview]Percentage of Participants With Complete Remission and Complete Remission With Partial Hematological Recovery (CR/CRh) in the Gilteritinib Arm
NCT02421939 (12) [back to overview]Duration of Leukemia-Free Survival (LFS)
NCT02520011 (2) [back to overview]Complete Response (CR) Rate in Patients With Relapsed or Refractory AML
NCT02520011 (2) [back to overview]Response to Treatment
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)
NCT02626338 (1) [back to overview]Clinical Response to Crenolanib With Standard Salvage Chemotherapy
NCT02728050 (8) [back to overview]Overall Response Rate (ORR)
NCT02728050 (8) [back to overview]Overall Survival (OS)
NCT02728050 (8) [back to overview]Phase 1: Maximum Tolerated Dose (MTD)/Recommended Phase 2 Dose (RP2D) of Mitoxantrone
NCT02728050 (8) [back to overview]Phase 1: Maximum Tolerated Dose (MTD)/Recommended Phase 2 Dose (RP2D) of Sorafenib
NCT02728050 (8) [back to overview]Phase I and II: Rate of Minimal Residual Disease Negative (MRDneg) Complete Response (CR)
NCT02728050 (8) [back to overview]Relapse-free Survival (RFS)
NCT02728050 (8) [back to overview]Number of Participants With Adverse Events
NCT02728050 (8) [back to overview]Event-free Survival (EFS)
NCT02756572 (19) [back to overview]Feasibility of Early Allogeneic Hematopoietic Cell Transplant Assessed by Relapsed-free Survival 6 Months After Transplant
NCT02756572 (19) [back to overview]Overall Survival (OS) Among Patients Who Received Early Transplant.
NCT02756572 (19) [back to overview]Overall Survival (OS) Among Patients Who Did Not Receive Early Transplant
NCT02756572 (19) [back to overview]Overall Survival (OS) Among Patients Who Did Not Receive Early Transplant
NCT02756572 (19) [back to overview]Factors That Distinguish Patients Who Received Early Transplant From Those Who Did Not - TREATMENT RELATED MORTALITY
NCT02756572 (19) [back to overview]Factors That Distinguish Patients Who Received Early Transplant From Those Who Did Not - AGE
NCT02756572 (19) [back to overview]Event-free Survival (EFS) Among Patients Who Received Early Transplant
NCT02756572 (19) [back to overview]Demonstrate the Feasibility of Collecting Resource Utilization Data for Trial Participants
NCT02756572 (19) [back to overview]Response Assessments After Early Allogeneic Hematopoietic Cell Transplant, Day 84
NCT02756572 (19) [back to overview]Response Assessments After Early Allogeneic Hematopoietic Cell Transplant, Day 28
NCT02756572 (19) [back to overview]Overall Survival (OS) Among Patients Who Received Early Transplant.
NCT02756572 (19) [back to overview]Relapse-free Survival (RFS) Among Patients Who Received Early Transplant
NCT02756572 (19) [back to overview]Feasibility of Early Allogeneic Hematopoietic Cell Transplant Assessed by Enrollment and Incidence of Early Transplant
NCT02756572 (19) [back to overview]Factors That Distinguish Patients Who Received Early Transplant From Those Who Did Not - GENDER
NCT02756572 (19) [back to overview]Demonstrate the Feasibility of Collecting Patient-reported Outcomes for Trial Participants
NCT02756572 (19) [back to overview]Treatment Related Mortality Among Patients Who Received Early Transplant vs Patients Who Did Not Receive Early Transplant
NCT02756572 (19) [back to overview]Relapse-free Survival (RFS) Among Patients Who Received Early Transplant
NCT02756572 (19) [back to overview]Event-free Survival (EFS) Among Patients Who Received Early Transplant
NCT02756572 (19) [back to overview]Acute Graft Versus Host Disease Among Patients Who Received Early Transplant
NCT02921061 (6) [back to overview]Number of Participants With Event-free Survival
NCT02921061 (6) [back to overview]Number of Participants Who Achieved Remission (Complete Remission [CR]/CR With Incomplete Peripheral Blood Count Recovery [CRi])
NCT02921061 (6) [back to overview]Number of Participants Experiencing Dose Limiting Toxicities (DLTs) at the Maximum Tolerated Dose (MTD) for Decitabine When Given Together With G-CLAM Toxicities (DLTs) (Phase I)
NCT02921061 (6) [back to overview]Number of Participants With Relapse-free Survival
NCT02921061 (6) [back to overview]Number of Participants With Overall Survival
NCT02921061 (6) [back to overview]Number of Participants With Minimal Residual Disease Negative (MRDneg) Complete Remission (Phase II)
NCT03118466 (6) [back to overview]Number of Patients That Achieved ANC Recovery
NCT03118466 (6) [back to overview]Number of Patients That Achieved Platelet Recovery
NCT03118466 (6) [back to overview]Overall Survival
NCT03118466 (6) [back to overview]Treatment-related Mortality
NCT03118466 (6) [back to overview]Transfusion Support: Number of Red Blood Cell and Platelet Transfusions
NCT03118466 (6) [back to overview]Complete Response Rate
NCT03504410 (1) [back to overview]Complete Remission (CR)
NCT03531918 (10) [back to overview]Measurable Residual Disease (MRD) and Remission Rates: Alapasia (MRDneg)
NCT03531918 (10) [back to overview]Measurable Residual Disease (MRD) and Remission Rates: CRi (MRDneg)
NCT03531918 (10) [back to overview]Measurable Residual Disease (MRD) and Remission Rates: MLFS (MRDneg)
NCT03531918 (10) [back to overview]Overall Survival
NCT03531918 (10) [back to overview]Relapse-free Survival of GO3 Cohort
NCT03531918 (10) [back to overview]Event-free Survival (EFS) Rate (Phase 2)
NCT03531918 (10) [back to overview]Measurable Residual Disease (MRD) Rates and Remission Rates: CR
NCT03531918 (10) [back to overview]Maximum Tolerated Dose (MTD) of Gemtuzumab Ozogamicin (GO) When Added to GCLAM (Phase 1)
NCT03531918 (10) [back to overview]30-day All-cause Mortality
NCT03531918 (10) [back to overview]Measurable Residual Disease (MRD) and Remission Rates: CR/CRi
NCT03860844 (13) [back to overview]Number of Participants With Infusion Reactions (IRs)
NCT03860844 (13) [back to overview]Overall Response Rate (ORR)
NCT03860844 (13) [back to overview]Percentage of Participants With Complete Response (CR) Rate
NCT03860844 (13) [back to overview]AML: AUC of Isatuximab
NCT03860844 (13) [back to overview]AML: Ceoi of Isatuximab
NCT03860844 (13) [back to overview]AML: Plasma Concentration Reached by Isatuximab Before Next Dose Administration (Ctrough)
NCT03860844 (13) [back to overview]B-ALL and T-ALL: Area Under the Concentration Time Curve (AUC) of Isatuximab
NCT03860844 (13) [back to overview]B-ALL and T-ALL: Concentrations at the End of Infusion (Ceoi) of Isatuximab
NCT03860844 (13) [back to overview]B-ALL and T-ALL: Plasma Concentration Reached by Isatuximab Before Next Dose Administration (Ctrough)
NCT03860844 (13) [back to overview]CD38 Receptor Occupancy
NCT03860844 (13) [back to overview]CD38 Receptor Occupancy
NCT03860844 (13) [back to overview]Cluster of Differentiation (CD)38 Receptor Density
NCT03860844 (13) [back to overview]Number of Participants With Treatment-Emergent Adverse Events (TEAEs) and Treatment-Emergent Serious Adverse Events (TESAEs)

Complete Remission (CR)

complete remission (CR) Disappearance of all clinical evidence of leukemia for a minimum of four weeks. The patient should have a neutrophil count > 1,000 x 10^6/1, a platelet count > 100,000 x 10^9/1, no circulating blasts, and < than or = to blasts on bone marrow differential in a qualitatively normal or hypercellular marrow. Progressive disease or failure: Increasing bone marrow infiltrate or development of organ failure or extramedullary infiltrates due to leukemia. (NCT00002766)
Timeframe: 2 years

,
Interventionparticipants (Number)
Complete RemissionComplete Response (CR)FailureFailure-ProgressionRelapse
All-25014581
L-20501114100

[back to top]

Compare Qualitative and Quantitative Toxicities of These Regimens in These Patients

Number of patients with adverse events that are related to study drug (NCT00004124)
Timeframe: Up to 22 months from registration

,
InterventionParticipants (Number)
Abdominal pain/crampingAbscessAlkaline phosphatase increaseAllergic reactionAllergic rhinitisAlopeciaAnal incontinenceAnemiaAnorexiaAnxiety/agitationApneaArrhythmia, NOSArthralgiaArthritisAtaxia (incoordination)Bilirubin increaseBlurred visionBone painBruisingCPK increaseCardiac ischemia/infarctionCardiovascular-otherCataractCerebrovascular ischemiaChest pain,not cardio or pleurConduction abnormality/blockConfusionConjunctivitisConstipation/bowel obstructionCoughCreatinine increaseCushingoid appearanceDehydrationDepressionDiarrhea without colostomyDizziness/light headednessDry eyeDry skinDysmenorrheaDyspepsia/heartburnDyspneaDysuriaEar-otherEdemaEndocrine-otherEpistaxisErectile impotenceEryth/rash/eruption/desq, NOSEsophagitis/dysphagiaEye-otherFatigue/malaise/lethargyFebrile neutropeniaFeminization of maleFever without neutropeniaFever, NOSFlatulenceFlu-like symptoms-otherFlushingGGT increaseGI Mucositis, NOSGI-otherGU-otherGastritisGastritis/ulcer, NOSGlaucomaGynecomastiaHeadacheHematologic-otherHematuriaHemolysisHemoptysisHemorrhage-otherHiccoughsHot flashesHypercalcemiaHypercholesterolemiaHyperglycemiaHyperkalemiaHypermagnesemiaHypernatremiaHypertensionHypertriglyceridemiaHypoalbuminemiaHypocalcemiaHypoglycemiaHypokalemiaHypomagnesemiaHyponatremiaHypotensionHypothyroidismHypoxiaIncontinenceInfection w/o 3-4 neutropeniaInfection with 3-4 neutropeniaInfection, unk ANCInner ear-hearing lossInsomniaInvol. movement/restlessnessJoint,muscle,bone-otherLVEF decrease/CHFLeukopeniaLibido lossLocal injection site reactionLung-otherLymphopeniaMale infertilityMelena/ GI bleedingMemory lossMetabolic-otherMiddle ear-hearing loss/otitisMood/consciousness change, NOSMouth drynessMuscle weakness (not neuro)MyalgiaMyalgia/arthralgia, NOSMyocarditisNail changesNauseaNeuro-otherNeuropathic painNeutropenia/granulocytopeniaPRBC transfusionPain-otherPalpitationsPelvic painPericar. effusion/pericarditisPersonality/behavioral changePhlebitisPigmentation changes/yellowingPleural effusionsPneumonitis/infiltratesProctitisProteinuriaPruritusRT-GI mucositis, NOSRT-focal dermatitis, NOSRT-late bladder morbidityRT-late intestinal morbidityRT-painRash/desquamationRectal bleeding/hematocheziaRectal/perirectal painRespiratory infect w/o neutropRespiratory infection, unk ANCRigors/chillsSGOT (AST) increaseSGPT (ALT) increaseSalivary change, NOSSecond primarySeizuresSensory neuropathySexual/reproductive-otherSinus bradycardiaSkin-otherSpeech impairmentStomatitis/pharyngitisSupraventricular arrhythmiaSurgery-wound infectionSweatingSyncopeTaste disturbanceTearingThrombocytopeniaThrombosis/embolismTremorTroponin T (cTnT) increaseUrinary frequency/urgencyUrinary retentionUrinary tr infect w/ neutropUrinary tr infect w/o neutropUrinary tr infection, unk ANCUrine color changeUrticariaVentricular arrhythmiaVertigoVision,NOSVoice change/stridor/larynxVomitingWeakness (motor neuropathy)Weight gainWeight loss
Arm I: Bicalutamide + Goserelin19011129125275210431715319101051111605710700805533111072114040301810212580101225101292021403719001043945440003821108133208850137921101416311042015002105526104265011011219012000043130312146127117422200137201105001380103200861301333110010317912
Arm II: Mitoxantrone + Prednisone + Bivalutamid + Goserelin411115161312141416211641712063414215601901441173417868575715281444911256221462136357209636401020901010082113114442252784143806711112110471102429222783171331724932121131377451215720541239312761111153114123110106310578244226161571411149211293466355211017122444011651615129

[back to top]

Disease Free Survival

Measured from date of randomization to date of first observation of recurrence or death due to any cause. Patients without recurrence are censored at date of last contact. (NCT00004124)
Timeframe: at 10 Years

Interventionpercentage of probability of survival (Number)
Arm I: Bicalutamide + Goserelin72
Arm II: Mitoxantrone + Prednisone + Bivalutamid + Goserelin72

[back to top]

Overall Survival

Measured from date of randomization to date of death from any cause. Patient known to be alive are censored at date of last contact. (NCT00004124)
Timeframe: at 10 Years

Interventionpercentage of probability of survival (Number)
Arm I: Bicalutamide + Goserelin87
Arm II: Mitoxantrone + Prednisone + Bivalutamid + Goserelin86

[back to top]

Number of Participants With 5-year Freedom From Prostate Specific Antigen (PSA) Recurrence.

Number of participants that experienced 5-year freedom from Prostate Specific Antigen (PSA) recurrence (PSA > 0.4 ng/ml confirmed by a second PSA that is higher than the first by any amount (2)) in men with high risk localized prostate cancer treated with neoadjuvant docetaxel/mitoxantrone followed by surgery. (NCT00017563)
Timeframe: Every 3 months after surgery for up to 5 years.

Interventionparticipants (Number)
Docetaxel and Mitox30

[back to top]

Continuous Complete Remission at 1 Year

A patient has a continuous complete remission at 1 year if they achieve a CR and are alive 365 days after registering to the study. (NCT00109837)
Timeframe: After induction, after consolidation, every 3 months during maintenance, and every three months after off treatment for up to a year

Interventionparticipants (Number)
Treatment21

[back to top]

Toxicity

Number of patients with Grade 3-5 adverse events that are related to study drug by given type of adverse event (NCT00109837)
Timeframe: Patients were assessed for adverse events after the induction cycle

InterventionParticipants with a given type of AE (Number)
ALT, SGPT (serum glutamic pyruvic transaminase)AST, SGOT (serum glut oxaloacetic transaminase)Albumin, serum-low (hypoalbuminemia)Alkaline phosphataseAnorexiaAscites (non-malignant)Bilirubin (hyperbilirubinemia)Calcium, serum-low (hypocalcemia)CholecystitisCholesterol, serum-high (hypercholesterolemia)Coagulation-Other (Specify)Colitis, infectious (e.g., Clostridium difficile)ConstipationDIC (disseminated intravascular coagulation)Death not assoc with CTCAE term-Multi-organ failEdema: limbFatigue (asthenia, lethargy, malaise)Febrile neutropeniaFever (in the abs of neutropenia)FibrinogenGlucose, serum-high (hyperglycemia)Glucose, serum-low (hypoglycemia)HemoglobinHypertensionHypotensionHypoxiaIleus, GI (functional obstruction of bowel)Infec(doc clin or mibio) w/ Gr 3/4 neut-AnalInfec(doc clin or mibio) w/ Gr 3/4 neut-BladderInfec(doc clin or mibio) w/ Gr 3/4 neut-BloodInfec(doc clin or mibio) w/ Gr 3/4 neut-BronchusIInfec(doc clin or mibio) w/ Gr 3/4 neut-CatheterInfec(doc clin or mibio) w/ Gr 3/4 neut-Eye NOSInfec(doc clin or mibio) w/ Gr 3/4 neut-LungInfec(doc clin or mibio) w/ Gr 3/4 neut-NoseInfec(doc clin or mibio) w/ Gr 3/4 neut-PharynxInfec(doc clin or mibio) w/ Gr 3/4 neut-Ur tractInfec with nor ANC or Gr 1/2 neut-Lung (pneumonia)Infection-Other (Specify)Leukocytes (total WBC)LipaseLiver dysfunction/failure (clinical)LymphopeniaMagnesium, serum-high (hypermagnesemia)Mucositis/stomatitis (clinical exam) - Oral cavityMucositis/stomatitis (funct/symp) - Oral cavityMucositis/stomatitis (func/symp) - PharynxMuscle weak,gen spec area-Whole bodyNauseaNeuropathy: motorNeutrophils/granulocytes (ANC/AGC)Pain - Abdomen NOSPain - BonePain - NeckPancreatic endocrine: glucose intolerancePancreatitisPhosphate, serum-low (hypophosphatemia)PlateletsPotassium, serum-high (hyperkalemia)Potassium, serum-low (hypokalemia)Rash/desquamationRenal failureSodium, serum-low (hyponatremia)Thrombosis/thrombus/embolismThrombotic microangiopathyTriglyceride, serum-high (hypertriglyceridemia)Tumor lysis syndromeTyphlitis (cecal inflammation)Uric acid, serum-high (hyperuricemia)Vomiting
Induction171332216712111211318111161332321111111111122143121912112314711111144171261215111

[back to top]

Relationship of Inhibition of DNA Synthesis and Clinical Response

Clinical response is defined as MRD (minimal residual disease) measured by flow cytometry at day 22. The MRD at day 22 is classified as positive (with MRD) or negative (no detectable MRD). The relation between inhibition of DNA synthesis and MRD was performed by logistic regression. In the model, logit of probability of MRD positive was regressed on inhibition of DNA synthesis. (NCT00136084)
Timeframe: Measurements were assessed in Induction I chemotherapy

InterventionPercent inhibition of DNA Synthesis (Mean)
Overall66.7

[back to top]

To Assess Whether Inhibition of DNA Synthesis is Greater After High-dose Ara-C (HDAC) Than After Low-dose Ara-C (LDAC) Therapy

Inhibition of DNA synthesis is defined as the percentage of DNA synthesis rate at 24-hour post-araC treatment over DNA synthesis rate pre-araC treatment. (NCT00136084)
Timeframe: Measurements were assessed in Induction I chemotherapy

InterventionPercent Inhibition of DNA Synthesis (Mean)
Arm 1: (HDAC)60.6
Arm 2:(LDAC)72.8

[back to top]

Minimal Residual Disease (MRD).

Detection of Minimal Residual Disease following one course of chemotherapy where positive MRD was defined as one or more leukemic cell per 1000 mononuclear bone-marrow cells (>=0.1%). (NCT00136084)
Timeframe: Day 22 MRD measurement

,
Interventionparticipants (Number)
MRD PositiveMRD Negative
Arm 1: (HDAC)3168
Arm 2:(LDAC)4363

[back to top]

Proportion of Minimal Residual Disease (MRD)+ Patients Who Become MRD- After One Course of Gemtuzumab Ozogamicin (GO)

To estimate the proportion of minimal residual disease (MRD)+ patients who become MRD- after one course of gemtuzumab ozogamicin (GO) (NCT00136084)
Timeframe: Consolidation I

InterventionParticipants (Number)
NegativePositive
Overall114

[back to top]

To Estimate the Overall Event-free Survival (EFS) of AML Patients Who Undergo Risk-adapted and Genotype-directed Therapy

Overall event-free survival (EFS) was defined as the time from study enrollment to induction failure, relapse, secondary malignancy, death, or study withdrawal for any reason, with event-free patients censored on the date of the last follow-up (NCT00136084)
Timeframe: Five Year

InterventionPercentage of Participants (Number)
Overall62.4

[back to top]

Proportion of MRD Reduction After One Course of Cytarabine + Daunomycin + Etoposide (ADE) + GO

To estimate proportion of patients with MRD reduction after one course of Induction II (cytarabine + daunomycin + etoposide (ADE) + GO), who had no response to first course of induction therapy. (NCT00136084)
Timeframe: Induction II

InterventionParticipants (Number)
DecreaseIncrease or no change
Overall272

[back to top]

Proportion of Patients Experienced Toxicity of Cytarabine + Daunomycin + Etoposide (ADE) + GO.

To estimate proportion of patients experiencing CTC Grade 3 or 4 toxicity during Induction II (Cytarabine + Daunomycin + Etoposide (ADE) + GO), who had no response to first course of induction therapy (NCT00136084)
Timeframe: Induction II

InterventionParticipants (Number)
Experienced Grade 3 or 4 toxicitiesDid not experience Grade 3 or 4 toxicities
Overall273

[back to top]

Overall Survival (OS)

OS is measured from the start of on-study to the date of death or to the last date of follow-up. Measurement is determined by Kaplan-Meyer estimate. The probability of survival at 5 years after diagnosis is given. (NCT00186875)
Timeframe: 2 years after last patient completes therapy (approximately 4 years after enrollment)

Interventionprobability (Mean)
Standard Risk0.654
High Risk0.357

[back to top]

Minimal Residual Disease (MRD) Compared With Historical Data From TOTXV Protocol (NCT00137111)

The prevalence of MRD in children undergoing treatment for relapsed ALL and to compare the results to those obtained in children with newly diagnosed ALL. MRD is considered as positive (i.e., prevalent) if its level is >=0.01%. The prevalence of MRD after Block B is defined as the proportion of MRD positives. (NCT00186875)
Timeframe: End of Block B therapy (Day 19)

,,
InterventionParticipants (Count of Participants)
Negative <0.01%Positive ≥0.01%
High Risk210
Standard Risk1111
TOTXV Participants191297

[back to top]

Minimal Residual Disease (MRD) Compared With Historical Data From TOTXV Protocol (NCT00137111)

The prevalence of MRD in children undergoing treatment for relapsed ALL and to compare the results to those obtained in children with newly diagnosed ALL. MRD is considered as positive (i.e., prevalent) if its level is >=0.01%. The prevalence of MRD after Block C is defined as the proportion of MRD positives. (NCT00186875)
Timeframe: End of Block Block C therapy (Day 46)

,,
InterventionParticipants (Count of Participants)
Negative <0.01%Positive ≥0.01%
High Risk18
Standard Risk119
TOTXV Participants390102

[back to top]

Response Rate

"The response rate is defined as the proportion of participants who attain morphological complete remission after the re-induction Block C, inclusive of all patients who begin re-induction. Morphological complete remission was defined as <5% blasts in bone marrow by morphology." (NCT00186875)
Timeframe: End of re-induction Block C (approximately 1 month after the start of therapy)

,
Interventionproportion of participants (Number)
Complete remissionFailure to reach complete remission
High Risk0.7860.214
Standard Risk0.8460.154

[back to top]

Overall Response Rate (ORR), 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. (NCT00193479)
Timeframe: 18 Months

Interventionpercentage of patients (Number)
CNOP (CVP)/Rituximab/Pegfilgrastim Followed by Rituximab81

[back to top]

Number of Patients's Who Had Complete Response and Partial Response to the Treatment of Fludarabine and Cyclophosphamide Followed by GM-CSF and Rituximab.

"Complete Response (CR): Disappearance of all clinical evidence of active tumor for a minimum of eight weeks and absence of any symptoms related to the tumor.~Partial Response (PR):50% decrease in the sum of the product diameters of all lesions that persist for at least four weeks. No lesion can increase in size and no new lesion can appear during this period.~Stable disease (SD):A tumor that is neither growing nor shrinking.No new tumors have developed" (NCT00208975)
Timeframe: 6 months

,
Interventionparticipants (Number)
Complete ResponsePartial ResponseStable Disease
Chronic Lymphocytic Leukemia421
Non Hodgkin Lymphoma520

[back to top]

Molecular Response Rate at 3 Months

Molecular response rate (PCR for immunoglobulin heavy chain (IgH) rearrangements) at 3 months following treatment. Courses will be repeated every 28 to 42 days (+/- 7 days) depending on recovery of peripheral blood counts and toxicities for a maximum of 6 courses. Patients will be evaluated for response after 3 and 6 courses. Bone marrow biopsies will be performed at the end of Cycles 3 and 6 of chemotherapy. (NCT00254410)
Timeframe: End of cycle 3

InterventionParticipants (Count of Participants)
FCM-R + Pegylated Filgrastim17

[back to top]

Clinical Response Rate at 6 Months

Clinical Response Rate (combined morphological [NCI WG criteria] + flow cytometry criteria) at 6 months following treatment. Courses will be repeated every 28 to 42 days (+/- 7 days) depending on recovery of peripheral blood counts and toxicities for a maximum of 6 courses. Patients will be evaluated for response after 3 and 6 courses. Bone marrow biopsies will be performed at the end of Cycles 3 and 6 of chemotherapy. (NCT00254410)
Timeframe: End of Cycle 6

InterventionParticipants (Count of Participants)
FCM-R + Pegylated Filgrastim28

[back to top]

Clinical Response Rate at 3 Months

Clinical Response Rate (combined morphological [NCI Working Group (WG) criteria] + flow cytometry criteria) at 3 months following treatment. Courses will be repeated every 28 to 42 days (+/- 7 days) depending on recovery of peripheral blood counts and toxicities for a maximum of 6 courses. Patients will be evaluated for response after 3 and 6 courses. Bone marrow biopsies will be performed at the end of Cycles 3 and 6 of chemotherapy. (NCT00254410)
Timeframe: End of cycle 3

InterventionParticipants (Count of Participants)
FCM-R + Pegylated Filgrastim29

[back to top]

Molecular Response Rate at 6 Months

Molecular response rate (PCR for IgH rearrangements) at 6 months following treatment. Courses will be repeated every 28 to 42 days (+/- 7 days) depending on recovery of peripheral blood counts and toxicities for a maximum of 6 courses. Patients will be evaluated for response after 3 and 6 courses. Bone marrow biopsies will be performed at the end of Cycles 3 and 6 of chemotherapy. (NCT00254410)
Timeframe: End of 6 months

InterventionParticipants (Count of Participants)
FCM-R + Pegylated Filgrastim10

[back to top]

Complete Response Rate

Assumptions/ hypothesis: A Complete Response (CR) rate of 30% or less is unacceptable, and 50% or more is promising. A two-stage design will be used. Initially, 18 patients will be enrolled. If 5 or fewer achieve CR, the study will be stopped. Otherwise, an additional 22 patients will be accrued. Accrual was not halted while follow-up of the first 18 evaluable patients was under way. Therefore, 24 patients were enrolled. Four weeks is anticipated for observation for response. Only 5 patients (21%) achieved a CR and therefore, the study was terminated. Since response was assessed using the International Working Group criteria, a complete response was determined by Morphologic complete remission: A CR designation requires that the patient achieve the morphologic leukemia-free state and have an absolute neutrophil count of more than 1,000/μL and platelets of ≥ 100,000/μL, a cytogenic CR and a morphologic CR with incomplete blood count recovery (CRi). (NCT00268242)
Timeframe: 4 Weeks

Interventionparticipants (Number)
Gemcitabine + Mitoxantrone5

[back to top]

White Blood Cell Count at Time of Relapse

(NCT00268242)
Timeframe: After a CR is achieved, patient will be followed at 3 month intervals for disease progression, typically for up to 5 years.

Interventioncells per microliter (Median)
Gemcitabine + Mitoxantrone3450

[back to top]

Disease-free and Overall Survival

(NCT00268242)
Timeframe: After a CR is achieved, patients are followed at 3 month intervals for disease progression and survival. If a patient has disease progression after achieving a CR, survival will be captured at 6 month intervals, typically for up to 5 years.

Interventionparticipants (Number)
Patients dead >30 days post-tx, no relapsePatients alive with no evidence of disease relapsePatient death on Day 1 of Protocol TherapyPatients dead >30 days post-tx, after relapse
Gemcitabine + Mitoxantrone14118

[back to top]

Laboratory Correlates: Immunohistochemistry

"Percentage of patients who had a moderate-strong (2-3+) expression of multidrug resistance (MDR) genes by immunohistochemistry.~Multidrug resistance gene 1 (MDR1)~Equilibrative nucleoside transporter 2(SLC29A2)" (NCT00268242)
Timeframe: Baseline

Interventionpercentage of participants (Number)
Participants with GSTP1 Gene ExpressionParticipants with SLC29A2 Gene ExpressionParticipants with MRP1 Gene ExpressionParticipants with LRP1 Gene ExpressionParticipants with MDR1 Gene Expression
Gemcitabine + Mitoxantrone7055433522

[back to top]

Duration of the First Complete Response

(NCT00268242)
Timeframe: After a CR is achieved, patients are followed at 3 month intervals for disease progression and survival. If a patient has disease progression after achieving a CR, survival will be captured at 6 month intervals, typically for up to 5 years.

Interventionmonths (Median)
Gemcitabine + Mitoxantrone7.3

[back to top]

Percentage of Patients Making it to Bone Marrow Transplant.

Assessing the number of patients who were able to have protocol treatment and have a bone marrow transplant after treatment. (NCT00268242)
Timeframe: After completion of protocol therapy

Interventionpercentage of Patients completed a BMT (Number)
Gemcitabine + Mitoxantrone8

[back to top]

Tolerance and Efficacy of Maintenance Therapy With Yttrium-90 Ibritumomab Tiuxetan (YIT)

"To assess the tolerance and efficacy of maintenance therapy with YIT. CR: defined as those who achieve a normal state which includes no detectable evidence of disease on x-rays. CRu: defined as CR unconfirmed on the basis of minimal residual abnormalities on x-ray such as a residual mass <25% of original measurement, and or residual indeterminate bone marrow aggregates. PR: a 50% or more reduction in the sum of the products of the diameters of the 6 largest measurable lesions. No new sites of disease. Progressive disease (PD) is also defined by the appearance of new lymph nodes, of other new or worsening sites of disease, such as > 50% increase in the size of liver and/or spleen, or a > 50% increase in absolute number of circulating lymphocytes." (NCT00290511)
Timeframe: cycle 1 and every 2 weeks thereafter until completion of therapy, an average of 10 years

InterventionParticipants (Count of Participants)
Complete Response (CR)Progressive Disease
R-FIND + Zevalin371

[back to top]

Tolerance and Efficacy of Maintenance Therapy With Rituximab

"To assess the tolerance and efficacy of maintenance therapy with rituximab. Participants proceeded to the rituximab maintenance program of 6 treatments comprising 1 every 2 months. CR: defined as those who achieve a normal state which includes no detectable evidence of disease on x-rays. CRu: defined as CR unconfirmed on the basis of minimal residual abnormalities on x-ray such as a residual mass <25% of original measurement, and or residual indeterminate bone marrow aggregates. PR: a 50% or more reduction in the sum of the products of the diameters of the 6 largest measurable lesions. No new sites of disease. Progressive disease (PD) is also defined by the appearance of new lymph nodes, of other new or worsening sites of disease, such as > 50% increase in the size of liver and/or spleen, or a > 50% increase in absolute number of circulating lymphocytes." (NCT00290511)
Timeframe: cycle 1 and every 2 weeks thereafter until completion of therapy, an average of 10 years

InterventionParticipants (Count of Participants)
Complete Response (CR)Progression Disease (PD)
R-FIND + Zevalin383

[back to top]

Number of Participants With Time to Progression (TTP)

Regimen regarded as a success if median TTP can be prolonged to 36 months or greater. Time to Progression measured by the method of Kaplan and Meier, and accompanied by 95% confidence interval. Complete Response (CR) defined as those who achieve a normal state which includes no detectable evidence of disease on x-rays and Partial Response (PR) is defined as a 50% or more reduction in the sum of the products of the diameters of the 6 largest measurable lesions. No new sites of disease. av (NCT00290511)
Timeframe: baseline, 2 and 4 courses, approximately month 8, 9, and 12 months, then restaging every 4 months, then at 2 years every 4-6 months, then yearly until progressive disease or lost to follow up, average of 10 years

InterventionParticipants (Count of Participants)
Complete Response (CR)Partial Response (PR)
R-FIND + Zevalin424

[back to top]

Progression Free Survival at 10 Years

Progression-free survival time is defined as time from registration/randomization to the date of progression or death from any cause. PFS was estimated by the method of Kaplan and Meier, and accompanied by 95% confidence interval. (NCT00290511)
Timeframe: 10 years

Interventionmonths (Number)
R-FIND + Zevalin49

[back to top]

Percentage of Participants With Overall Survival Rate at 10 Years

OS is defined as the interval from first dose of study treatment to the date of death, irrespective of the cause of death; subjects still alive will be censored at the date of the last contact. Overall Survival Rate estimated by the method of Kaplan and Meier. (NCT00290511)
Timeframe: 10 years

Interventionpercentage of participants (Number)
R-FIND + Zevalin69

[back to top]

Median Progression Free Survival

Progression-free survival time is defined as time from registration/randomization to the date of progression or death from any cause. Median Progression Free Survival estimated by the method of Kaplan and Meier, and accompanied by 95% confidence interval. (NCT00290511)
Timeframe: up to 5 years

Interventionmonths (Median)
R-FIND + Zevalin84

[back to top]

Overall Survival

OS is defined as the interval from first dose of study treatment to the date of death, irrespective of the cause of death; subjects still alive will be censored at the date of the last contact. Median Overall Survival was estimated by the method of Kaplan and Meier, and accompanied by 95% confidence interval. (NCT00290511)
Timeframe: up to 5 years

Interventionmonths (Number)
R-FIND + Zevalin143

[back to top]

Safety and Tolerability of Custirsen (OGX-011) in Combination With Either Docetaxel/Prednisone or Mitoxantrone/Prednisone as Second-line Chemotherapy.

"Safety and tolerability were based on Adverse Events (AE) and Serious Adverse Events (SAE) graded using National Cancer Institute's Common Terminology Criteria for Adverse Events (CTCAE).~The CTCAE has 5 grades with unique clinical descriptions of severity for each AE based on this general guideline: Grade 1=Mild AE; Grade 2=Moderate AE; Grade 3=Severe AE; Grade 4=Life-threatening or disabling AE; and Grade 5=Death related to AE." (NCT00327340)
Timeframe: Subjects were followed for safety from enrollment for up to 8 months (9 three-week cycles plus 30 days after end of treatment)

,
Interventionpercentage of participants (Number)
Percent of Subjects with Serious Adverse EventsPercent of Subjects with Grade 5 Adverse EventsPercent of Subjects with Grade 4 Adverse EventsPercent of Subjects with Grade 3 Adverse EventsPercent of Subjects with Grade 2 Adverse EventsPercent of Subjects with Grade 1 Adverse EventsPercent of Subjects who Discontinued Study Drug
OGX-011 + Docetaxel + Prednisone26415529810017
OGX-011 + Mitoxantrone + Prednisone261326708310022

[back to top]

Feasibility of Treatment With Custirsen (OGX-011) in Combination With Second-line Chemotherapy Based on Prostate Specific Antigen (PSA) Response

PSA or prostate specific antigen is a marker for prostate cancer. A PSA response was defined as a decrease in PSA values of ≥ 50% relative to baseline on two or more consecutive measurements that were 4-6 weeks apart. (NCT00327340)
Timeframe: PSA was evaluated at screening, on Day 1 of each cycle, at the end of treatment visit and during off-treatment follow up (up to 27 months)

Interventionpercentage of participants (Number)
OGX-011 / Mitoxantrone/Prednisone17
OGX-011 / Docetaxel/Prednisone31

[back to top]

Feasibility of Treatment With OGX-011 in Combination With Either Docetaxel/Prednisone or Mitoxantrone/Prednisone as Second Line Chemotherapy Based on Time to Pain Progression

Time to pain progression was defined as the time (months) from the first dose of OGX-011 to the first documentation of pain or analgesic progression or initiation of palliative radiation therapy. Pain response was defined as either a decrease of at least two points on the 11-point Worst Pain Scale, without an increase in analgesic level, maintained for at least two consecutive measurements approximately three weeks apart -or- a decrease in analgesic level, without an increase in pain score, maintained for at least two consecutive measurements approximately three weeks apart. (NCT00327340)
Timeframe: Enrollment until pain progression (up to 21 months)

Interventionmonths (Number)
OGX-011 + Mitoxantrone + Prednisone5.2
OGX-011 + Docetaxel + Prednisone7.2

[back to top]

Relationship Between Changes in Serum Clusterin Levels and Change in Serum PSA Levels When OGX-011 in Combination With Either Docetaxel/Prednisone or Mitoxantrone/Prednisone is Administered as Second Line Chemotherapy.

Serum clusterin samples were collected prior to receiving OGX-011 loading dose 1, prior to study treatment on Day 1 of each cycle, and at the end of treatment. PSA was evaluated at screening, on Day 1 of each cycle, at the end of treatment visit, and during off-treatment follow-up. PSA response was defined in the protocol as a decrease in PSA of ≥ 50% relative to baseline on two or more consecutive measurements 4-6 weeks apart. (NCT00327340)
Timeframe: Enrollment until disease progression (up to 13 months)

,
Interventionpercentage of participants (Number)
Minimum clusterin level < or = to 45 mcg/mLMinimum clusterin level > 45 mcg/mL
OGX-011 + Docetaxel + Prednisone247
OGX-011 + Mitoxantrone + Prednisone224

[back to top]

Proportion Responding to Treatment With of the Combination of Ixabepilone and Mitoxantrone Hydrochloride With Prednisone in Hormone Refractory Prostate Cancer Patients Who Have Had Prior Taxane Chemotherapy Based Upon a PSA Decline of > 50% (Phase II)

"Descriptive statistics will be calculated to characterize the disease and treatment factors including the proportion responding with a 95% confidence interval. If accrual is completed and more than 15 of 58 patients show > 50% Prostate Specific Antigen (PSA) declines after 3 courses, then the null hypothesis of a 20% response proportion will be rejected. PSA declines for individual patients will be plotted in the form of a waterfall diagram of maximal PSA declines.~58 patients were enrolled for phase II, two were ineligible so 56 patients were analyzed." (NCT00331344)
Timeframe: Every 3 courses until cancer progression/excessive toxicity or death

InterventionParticipants (Count of Participants)
Treatment (Combination Chemotherapy)25

[back to top]

Dose Limiting Toxicities for Each Dose Level of Ixabepilone, Mitoxantrone Hydrochloride, and Prednisone in Patients With Hormone-refractory Metastatic Prostate Cancer That Progressed During or After Taxane-based Chemotherapy (Phase I).

Cohorts of 3 patients will be enrolled at each dose level; if 1 dose limiting toxicity (DLT) is observed then the cohort will be expanded to 6 patients. If a second DLT is observed, the previous dose level will be considered the maximum tolerated dose (MTD). If all observed DLT are due to neuropathy (specific to ixabepilone), then we would consider the previous dose level of Ixabepilone the MTD for that drug, and escalate mitoxantrone hydrochloride as described above to a maximum dose of 12 mg/m^2. Toxicities will be tabulated by grade for each dose cohort and overall for all patients accrued to the phase I study. (NCT00331344)
Timeframe: Course 1 (first 21 days)

InterventionParticipants (Count of Participants)
Phase I Group I0
Phase Group II0
Phase I Group III0
Phase I Group IV1
Phase I Group V2
Phase I Group VI2
Phase I Group Va0
Phase I Group VIa1

[back to top]

Time to Progression (Phase II)

Measured from the start of protocol therapy until RECIST (Response Evaluation Criteria In Solid Tumors Criteria) v1.0 progression. Progression is defined 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. (NCT00331344)
Timeframe: Every 3 months until cancer progression/excessive toxicity or death

Interventionmonths (Median)
Treatment (Combination Chemotherapy)4.4

[back to top]

Safety of the Combination of Ixabepilone, Mitoxantrone Hydrochloride, and Prednisone in Patients With Hormone-refractory Metastatic Prostate Cancer That Progressed During or After Taxane-based Chemotherapy (Phase I)

This study will utilize the Common Terminology Criteria for Adverse Events (CTCAE) v3.0 for adverse event monitoring and reporting. The cumulative grade 3 or higher adverse events for all dose levels are noted below and in the table of adverse events. (NCT00331344)
Timeframe: Every 21 days until cancer progression/excessive toxicity or death

InterventionAdverse Events (above threshold) (Number)
Phase I Treatment (Groups I-VIa)62

[back to top]

Event-free Survival at 3 Years

The Kaplan-Meier method will be used to calculate estimates of Event Free Survival (EFS). The log-rank test will be used to compare survival between treatment groups. Analysis of EFS of Down syndrome patients will be performed separately. Monitoring for efficacy of GMTZ with respect to Overall Survival (OS) and EFS will utilize monitoring based on the Lan-DeMets criterion with α-spending function αt^2 (truncated at 3 standard deviations) and 2.5% type I error. (NCT00372593)
Timeframe: Time from study entry to time of induction failure, relapse, or death, assessed at 3 years

Interventionpercentage of participants (Number)
Arm A: Standard Arm - No GMTZ, AML Pts w/Out Down Syndrome46.9
Arm B: Experimental - With GMTZ, AML Pts w/Out Down Syndrome53.1
Arm A: Standard Arm - No GMTZ, AML Patients With Down Syndrome50.0

[back to top]

Mortality

Number of participants who died during the first three courses of therapy. (NCT00372593)
Timeframe: During the first three courses of therapy

InterventionNumber of participants (Number)
Arm A: Standard Arm - No GMTZ, AML Pts w/Out Down Syndrome11
Arm B: Experimental - With GMTZ, AML Pts w/Out Down Syndrome13
Arm A: Standard Arm - No GMTZ, AML Patients With Down Syndrome1

[back to top]

Overall Survival at 3 Years

The Kaplan-Meier method will be used to calculate estimates of OS. Analysis of OS of Down syndrome patients will be performed separately. Monitoring for efficacy of GMTZ with respect to OS and EFS will utilize monitoring based on the Lan-DeMets criterion with α-spending function αt^2 (truncated at 3 standard deviations) and 2.5% type I error. (NCT00372593)
Timeframe: Time from study entry, assessed at 3 years

Interventionpercentage of participants (Number)
Arm A: Standard Arm - No GMTZ, AML Pts w/Out Down Syndrome65.4
Arm B: Experimental - With GMTZ, AML Pts w/Out Down Syndrome69.4
Arm A: Standard Arm - No GMTZ, AML Patients With Down Syndrome50.0

[back to top]

Remission Induction Rate After 2 Courses of Induction Therapy

Patients without an evaluable bone marrow at the end of Induction I will be excluded from the calculation of remission rate after 2 courses of therapy because their responses are not evaluable. The following patients will be considered to not be in complete remission (CR) after 2 courses of therapy: (1) patients who die during Induction I and II; (2) patients with ≥ 5% blasts or extramedullary disease at the end of Induction II. (NCT00372593)
Timeframe: After 2 courses of induction (I and II) therapy, assessed for up to 10 years

InterventionProportion of participants (Number)
Arm A: Standard Arm - No GMTZ, AML Pts w/Out Down Syndrome0.851324
Arm B: Experimental - With GMTZ, AML Pts w/Out Down Syndrome0.882716
Arm A: Standard Arm - No GMTZ, AML Patients With Down Syndrome0.666667

[back to top]

Toxicities, Including Infectious Complications

Number of participants with at least one grade 3 or higher adverse event during therapy. (NCT00372593)
Timeframe: From the time therapy is initiated, assessed up to 10 years

InterventionNumber of participants (Number)
Arm A: Standard Arm - No GMTZ, AML Pts w/Out Down Syndrome482
Arm B: Experimental - With GMTZ, AML Pts w/Out Down Syndrome477
Arm A: Standard Arm - No GMTZ, AML Patients With Down Syndrome5

[back to top]

Time to Marrow Recovery

Mean time to ANC recovery - defined as ANC greater than 500/MicroLiter for 3 consecutive days. (NCT00372593)
Timeframe: At 25 days after treatment with Induction I, Induction II, and Intensification I

,,
InterventionMean days (Mean)
During Induction I (days 0 - 28 of therapy)During Induction II (days 29 - 56 of therapy)During Intensification I (days 57 - 84 of therapy)
Arm A: Standard Arm - No GMTZ, AML Patients With Down Syndrome29.1726.624.5
Arm A: Standard Arm - No GMTZ, AML Pts w/Out Down Syndrome30.5628.5427.51
Arm B: Experimental - With GMTZ, AML Pts w/Out Down Syndrome30.5628.5228.10

[back to top]

Disease-free Survival (DFS)

Time from end of Intensification I to relapse, death or last contact (NCT00372593)
Timeframe: At 3 years from end of Intensification I

InterventionPercentage participants DFS at 3 years (Number)
Arm A: Standard Arm - No GMTZ, AML Pts w/Out Down Syndrome56.6
Arm B: Experimental - With GMTZ, AML Pts w/Out Down Syndrome63.0
Arm A: Standard Arm - No GMTZ, AML Patients With Down Syndrome75.0

[back to top]

Overall Survival (OS)

The OS is defined as the time from the date of start of treatment (for participants in Part 1) or randomization (for participants in Part 2) to death due to any cause. For participants who were alive at the time of analysis, OS was censored at the last contact date. (NCT00385827)
Timeframe: Start of treatment (Part 1)/Randomization (Part 2) until death, up to 2 years

Interventiondays (Median)
Part 1: Mitoxantrone + Prednisone + Siltuximab368.0
Part 2: Mitoxantrone + Prednisone394.0
Part 2: Mitoxantrone + Prednisone + Siltuximab311.0

[back to top]

Number of Participants With Prostate Specific Antigen (PSA) Response

The PSA response is defined as at least a 50% reduction in PSA from the Baseline value, confirmed by a second PSA value at least 3 weeks after initial documentation of PSA response. (NCT00385827)
Timeframe: Start of treatment (Part 1)/Randomization (Part 2), Week 1 of each cycle up to 1 month after last dose administration, and thereafter every 3 months until disease progression, up to 2 years

Interventionparticipants (Number)
Part 1: Mitoxantrone + Prednisone + Siltuximab4
Part 2: Mitoxantrone + Prednisone12
Part 2: Mitoxantrone + Prednisone + Siltuximab7

[back to top]

Time to Clinical Deterioration (TtCD)

The TtCD is defined as the time from the start of treatment (for participants in Part 1) or randomization (for participants in Part 2) until the first documented clinical deterioration (consists of pain requiring palliative (intended to relieve pain) intervention (a treatment given during the course of a research study), or death due to any cause, whichever occurs earlier. (NCT00385827)
Timeframe: Start of treatment (Part 1)/Randomization (Part 2), Week 1 of each cycle up to 1 month after last dose administration, and thereafter every 3 months until clinical deterioration or death, up to 2 years

Interventiondays (Median)
Part 1: Mitoxantrone + Prednisone + Siltuximab199.0
Part 2: Mitoxantrone + Prednisone298.0
Part 2: Mitoxantrone + Prednisone + Siltuximab183.0

[back to top]

Part 1: Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)

An AE is any untoward medical occurrence in a participant participating in a clinical study that does not necessarily have a causal relationship with the pharmaceutical/biological agent under study. An SAE is any AE that results in: death, persistent or significant disability/incapacity, requires inpatient hospitalization or prolongation of existing hospitalization, is life-threatening experience, is a congenital anomaly/birth defect and may jeopardize participant and/or may require medical or surgical intervention to prevent one of the outcomes listed above. (NCT00385827)
Timeframe: Baseline up to 12 weeks after last dose administration

Interventionparticipants (Number)
AEsSAEs
Part 1: Mitoxantrone + Prednisone + Siltuximab95

[back to top]

Part 2: Progression Free Survival (PFS)

The PFS is the time from the date of randomization until the first documented sign of progression (at least a 20 percent increase in the sum of the longest diameter [LD] of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new target or non-target lesions as per Response Evaluation Criteria in Solid Tumors [RECIST] or 3 or more new skeletal lesions on bone scan with confirmation of second bone scan or with clinical deterioration) or death, whichever occurs first. (NCT00385827)
Timeframe: Randomization, Week 12, then every 9 weeks until 1 month after last dose administration, then every 3 months until disease progression or death, up to 2 years

Interventiondays (Median)
Part 2: Mitoxantrone + Prednisone228.0
Part 2: Mitoxantrone + Prednisone + Siltuximab97.0

[back to top]

Complete Response

Bone marrow showing less than 5% myeloblasts with normal maturation of all cell lines, an Absolute Neutrophil Count of at least 1000/mililiter and a platelet count of 100,000 mililiter, absence of blast in peripheral blood, absence of identifiable leukemic cells in the bone marrow, clearance of disease-associated cytogenetic abnormalities, and clearance of any previously existing extramedullary disease. A complete remission must be confirmed 4 to 6 weeks after the initial documentation. If possible, at least one bone marrow biopsy should be performed to confirm the complete remission. (NCT00407966)
Timeframe: 6 months

Interventionparticipants (Number)
Arm A45

[back to top]

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

Interventionpercentage of participants (Number)
Phase 2 - Bortezomib 1.3mg/m^227

[back to top]

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

InterventionParticipants (Count of Participants)
Phase 1 - Bortezomib 0.7mg/m^20
Phase 1 - Bortezomib 1.0 mg/m^20
Phase 1 - Bortezomib 1.3mg/m^20

[back to top]

PSA (Prostate-Specific Antigen) Response

PSA response was defined as a ≥ 50% reduction in serum PSA, determined only for patients with a serum PSA ≥ 20ng/mL at baseline, confirmed by a repeat PSA ≥ 3 weeks later. (NCT00417079)
Timeframe: from baseline up to 104 weeks (study cut-off)

InterventionPercentage of participants (Number)
Mitoxantrone + Prednisone17.8
Cabazitaxel + Prednisone39.2

[back to top]

Overall Survival

"Overall survival was defined as the time interval from the date of randomization to the date of death due to any cause.~In the absence of confirmation of death, the survival time was censored at the last date patient was known to be alive or at the cut-off date, whichever had come first." (NCT00417079)
Timeframe: From the date of randomization up to 104 weeks (study cut-off)

InterventionMonths (Median)
Mitoxantrone + Prednisone12.7
Cabazitaxel + Prednisone15.1

[back to top]

Overall Tumor Response

"Tumor Overall Response Rate (ORR) (only in patients with measurable disease):~Objective responses (Complete Response and Partial Response) for measurable disease as assessed by investigators according to RECIST criteria.~Complete Response (CR) is defined as: Disappearance of all target lesions. Partial Response (PR) is defined as: At least a 30% decrease in the sum of longest diameter (LD) of target lesions taking as reference baseline sum LD.~Confirmation of objective responses will be performed by repeat tumor imaging (CT scans, MRI, bone scans) after the first documentation of response." (NCT00417079)
Timeframe: From the date of randomization up to 104 weeks (study cut-off)

Interventionpercentage of participants (Number)
Mitoxantrone + Prednisone4.4
Cabazitaxel + Prednisone14.4

[back to top]

Pain Response

Pain Response was defined as a two-point or greater reduction from baseline median Present Pain Intensity (PPI) score without an increased Analgesic Score (AS) or a decrease of ≥50% in the AS without an increase in the PPI score, maintained for at least 3 weeks. (NCT00417079)
Timeframe: from baseline up to 104 weeks (study cut-off)

InterventionPercentage of participants (Number)
Mitoxantrone + Prednisone7.7
Cabazitaxel + Prednisone9.2

[back to top]

Time to Pain Progression

"Pain Progression is defined as an increase of ≥1 point in the median Personal Pain Intensity (PPI) from its nadir noted on 2 consecutive 3-week-apart visits or ≥25 % increase in the mean analgesic score compared with the baseline score & noted on 2 consecutive 3-week-apart visits or requirement for local palliative radiotherapy.~Evaluation of the PPI & analgesic scores are based on the short-form McGill Pain Questionnaire which consists of 15 descriptors (11 sensory; 4 affective) which are rated on an intensity scale as 0=none (best) 1=mild 2=moderate 3=severe (worst) (TOTAL: 0=best 45=worst)" (NCT00417079)
Timeframe: from baseline up to 104 weeks (study cut-off)

InterventionMonths (Median)
Mitoxantrone + PrednisoneNA
Cabazitaxel + Prednisone11.1

[back to top]

Time to Progression Free Survival (PFS)

Progression free survival was defined as a composite endpoint evaluated from the date of randomization to the date of tumor progression, PSA progression, pain progression, or death due to any cause, whichever occurred first (NCT00417079)
Timeframe: From the date of randomization up to 104 weeks (study cut-off)

InterventionMonths (Median)
Mitoxantrone + Prednisone1.4
Cabazitaxel + Prednisone2.8

[back to top]

Time to Prostatic Specific Antigen (PSA) Progression

"In PSA non-responders, progression will be defined as a 25% increase over nadir and increase in the absolute value PSA level by at least 5 ng/ml and confirmed by a second value at least 4 weeks later.~In PSA responders and in patients not evaluable for PSA response at baseline, progression will be defined as a ≥50% increase over nadir, provided that the increase is a minimum of 5 ng/ml and confirmed by a second value at least 1 week later." (NCT00417079)
Timeframe: at screening, day 1 of every treatment cycle, up to 104 weeks (study cut-off)

InterventionMonths (Median)
Mitoxantrone + Prednisone3.1
Cabazitaxel + Prednisone6.4

[back to top]

Time to Tumor Progression

Time to tumor progression is defined as the number of months from randomization until evidence of progressive disease (RECIST) (NCT00417079)
Timeframe: From the date of randomization up to 104 weeks (study cut-off)

InterventionMonths (Median)
Mitoxantrone + Prednisone5.4
Cabazitaxel + Prednisone8.8

[back to top]

Quality of Life (QoL)

The subject answers questions from the following 6 categories: general physical symptoms, treatment side effects, distress, despair, impaired performance, and impaired ambulation. Each question has a scale from 0 through 10, where 0 is not a problem and 10 is as bad as possible. The scores for the 6 categories are combined and normalized, and used to describe overall quality of life. Because normalized scores are created using a look-up index, there is no clearly defined maximum value. In practice, the maximum value for the combined scale is 73.5. (NCT00452387)
Timeframe: The Patient Care Monitor questionnaire was administered on day 1 of every cycle (approximately every 3 weeks) during study treatment.

Interventionunits on a scale (Mean)
BaselineCycle 1Cycle 2Cycle 3Cycle 4Cycle 5Cycle 6Cycle 7Cycle 8Cycle 9Cycle 10Cycle 11Cycle 12Cycle 13End of Study (at treatment discontinuation)
Treatment Group: Mitoxantrone, Prednisone, Plus Sorafenib50.2149.7151.0651.2051.6651.2249.7349.5048.2054.3455.8854.9554.0254.6545.13

[back to top]

Correlation of Biochemical Criteria (PSA, Prostate-specific Antigen) With Objective Imaging

The test of association assesses the null hypothesis that the frequency of PSA response is the same for patients with and without a favorable imaging response. PSA response required a 50% reduction of the baseline PSA result that was confirmed three weeks later. Favorable imaging response is defined as stable disease, partial response, or complete response per RECIST guidelines. The Fisher's exact test was used to test this hypothesis. (NCT00452387)
Timeframe: PSA was evaluated on day 1 of every cycle (approximately every 3 weeks) during study treatment. Radiologic imaging was repeated after every 4 cycles (approximately every 12 weeks) during study treatment.

,
InterventionParticipants (Number)
PSA response (> 50% reduction)PSA response (< or = 50% reduction)
Imaging Response (Favorable)36
Imaging Response (Unfavorable)013

[back to top]

Median Overall Survival (OS)

Overall survival is defined as the time from treatment start until death from any cause. The median overall survival time is used to measure OS. (NCT00452387)
Timeframe: Overall survival was measured from day 1 of treatment until the end of treatment and then every 3 months thereafter until death.

InterventionMonths (Median)
Treatment Group: Mitoxantrone, Prednisone, Plus Sorafenib12.32

[back to top]

Percentage of Participants Reaching Overall Survival

Overall survival from diagnosis (NCT00458848)
Timeframe: At 60 months

Interventionpercentage of patients (Number)
Philadelphia Positive, Imatinib Only in Induction Therapy48.8

[back to top]

Percentage of Participants Reaching Disease Free Survival

(NCT00458848)
Timeframe: At 60 months

Interventionpercentage of participants (Number)
Philadelphia Positive, Imatinib Only in Induction Therapy45.8

[back to top]

Number of Patients Reaching Complete Hematological Response After Induction Therapy

(NCT00458848)
Timeframe: At the end of induction, day +50

Interventionparticipants (Number)
Philadelphia Positive, Imatinib Only in Induction Therapy49

[back to top]

Overall Survival (OS)

Assessed as the time from the 1st dose of study drug to death. (NCT00477087)
Timeframe: 18 months

InterventionMonths (Median)
GM-CSF Plus Mitoxantrone7.8

[back to top]

Progression-free Survival (PFS)

Assessed as the time from the 1st dose of study drug to death or disease progression (increase >25% over baseline PSA on 2 consecutive measurements 2 weeks apart, need for palliative therapy, formation/progression of new bone lesions, or decline of >20% KPS) (NCT00477087)
Timeframe: 18 months

Interventionweeks (Median)
GM-CSF Plus Mitoxantrone7.5

[back to top]

Number of Participants With > 50% Decrease in Prostate-specific Antigen Levels (PSA Response)

Defined as the first evidence of a total serum PSA decline of > 50% from baseline, maintained for at least 28 days, and confirmed with 2 consecutive measurements taken 2 weeks apart. (NCT00477087)
Timeframe: 18 months

InterventionParticipants (Count of Participants)
GM-CSF Plus Mitoxantrone3

[back to top]

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

Interventionpercentage of participants (Number)
VR-FND64

[back to top]

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

Interventionparticipants (Number)
VR-FND6

[back to top]

Duration of Response

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

Interventionmonths (Mean)
VR-FND16.47143

[back to top]

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

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

Interventionparticipants (Number)
VR-FND7

[back to top]

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

Interventionpercentage of participants (Number)
VR-FND27

[back to top]

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

Interventionpercentage of participants (Number)
VR-FND17

[back to top]

Time to Platelet Recovery

Defined as the date of the first dose of AMD3100 to the date that the platelet count is >100,000/mm3 in the absence of platelet transfusions. (NCT00512252)
Timeframe: 42 days

Interventiondays (Median)
Phase II Dose Treatment28.5

[back to top]

Time to Neutrophil Recovery

Defined as the date of the first dose of AMD3100 to the date that the absolute neutrophil count >1,000 cells/mm^3. (NCT00512252)
Timeframe: 42 days

Interventiondays (Median)
Phase II Dose Treatment28

[back to top]

Relapse-free Survival

"This is determined only for patients achieving a complete remission. Defined as the interval from the date of the first documentation of a leukemia free state to date of recurrence or death due to any cause.~Kaplain-Meier estimate was used." (NCT00512252)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Phase II Dose Treatment42.9

[back to top]

Treatment Failure

Treatment failures includes those patients for whom treatment has failed to achieve a CR or a CRi. (NCT00512252)
Timeframe: 42 days

,,,
Interventionparticipants (Number)
Persistent leukemiaDeath during aplasiaUnknown
>= Second Relapse/Salvage300
First Relapse, First Salvage1211
Primary Refractory620
Total2131

[back to top]

Safety and Tolerability of AMD3100 + MEC.

Treatment related mortality (deaths occurring during treatment) (NCT00512252)
Timeframe: 42 days

Interventionparticipants (Number)
SepsisAdverse transfusion reaction w/febrile neutropenia
Phase II Dose Treatment21

[back to top]

Phase II Only: Complete Response Rate of AMD3100 + MEC

"Responses were assessed according to the International Working Group Criteria for AML. All patients who received at least one dose of AMD3100 were considered evaluable for response.~Response rate was the rate of complete remission plus complete remission with incomplete blood count recovery (CR + CRi)." (NCT00512252)
Timeframe: 42 days

,,,
Interventionpercentage of participants (Number)
CR + CRiCR only
>= Second Relapse/Salvage2525
First Relapse, First Salvage5647
Primary Refractory2020
Total4639

[back to top]

Characterize the Mobilization of Leukemic Cells With AMD3100 by Measuring the Peak Mobilization of Total Leukocytes (Phase I)

"Measured at 0 hours, 1 hour, 2 hours, 4 hours, 6 hours, 8 hours, 12 hours, and 24 hours after AMD3100 dose on Day 0.~Characterization of the mobilized cells as well as the kinetics of mobilization will be determined by analyzing the surface expression of mobilized cells by flow cytometry at the specified time points in conjunction with their total leukocyte count from the patient's CBC." (NCT00512252)
Timeframe: Day 0

,,
Interventioncells x 10^3/microliter (Median)
Total leukocytes at 0 hoursTotal leukocytes at 1 hourTotal leukocytes at 2 hoursTotal leukocytes at 4 hoursTotal leukocytes at 6 hoursTotal leukocytes at 8 hoursTotal leukocytes at 12 hoursTotal leukocytes at 24 hours
Phase I Dose Escalation - Dose Level 12.54.344.74.84.55.14.3
Phase I Dose Escalation - Dose Level 24.77.08.59.411.312.012.17.9
Phase I Dose Escalation - Dose Level 33.56.47.58.39.58.97.85.8

[back to top]

Characterize the Mobilization of Leukemic Cells With AMD3100 by Measuring the Peak Mobilization of AML Blasts (Phase I)

Measured at 0 hours, 1 hour, 2 hours, 4 hours, 6 hours, 8 hours, 12 hours, and 24 hours after AMD3100 dose on Day 0. (NCT00512252)
Timeframe: Day 0

,,
Interventionpercentage of AML blasts (Median)
AML blasts at 0 hoursAML blasts at 1 hourAML blasts at 2 hoursAML blasts at 4 hoursAML blasts at 6 hoursAML blasts at 8 hoursAML blasts at 12 hoursAML blasts at 24 hours
Phase I Dose Escalation - Dose Level 146.026.026.037.031.032.027.035.0
Phase I Dose Escalation - Dose Level 24.09.037.516.014.019.045.023
Phase I Dose Escalation - Dose Level 343.530.532.530.027.026.035.055

[back to top]

Phase I Only: Optimal Dose of AMD3100 Plus MEC in Patients With Relapsed or Refractory AML

A standard 3+3 design was used in the Phase I portion starting with the AMD3100 dose of 80 mcg/kg and escalating by 80 mcg/kg for each successive cohort up to a maximum of 240 mcg/kg/d. The optimal dose was defined as the highest dose of AMD3100 <= 240 mcg/kg at which 0-1 of 6 patients experienced a dose limiting toxicity. (NCT00512252)
Timeframe: Completion of all patients in Phase I portion (232 days)

Interventionmcg/kg (Number)
Phase I Dose Escalation240

[back to top]

Overall Survival

(NCT00512252)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Phase II Dose Treatment37

[back to top]

Maximum Tolerated Dose (MTD) of Mitoxantrone

The MTD is defined as the highest dose studied for which the incidence of DLT is less than 33%. In the phase I portion of the trial, cohorts of 3-6 pts will receive pentostatin, cyclophosphamide and rituximab along with one of three potential dose levels of mitoxantrone. The following dose escalation scheme will be followed: If none of the initial three pts in a cohort experience a dose-limiting toxicity (grade 4 infection, or grade ≥ 3 non-hematologic toxicity that persists for 7 days or more) then a new cohort of three pts will be treated at the next higher dose level. If one of the three pts in a cohort experiences DLT, then up to three additional pts will be treated at the same dose level. If two or more pts in a cohort experience DLT, then the maximum tolerated dose (MTD) will have been exceeded, and no further dose escalation will occur. The previous dose level will be considered as the MTD. (NCT00546377)
Timeframe: 2 years

Interventionmg/m2 (Number)
Pentostatin,Cyclophosphamide,Rituximab & Mitoxantrone10

[back to top]

Overall Response

Complete response (CR): Absence of lymphadenopathy, hepatomegaly or splenomegaly by physical examination and appropriate radiographic techniques (if abnormal pre-treatment): it is recognized that some patients with lymphoid malignancies who achieve a CR may have mild persistent abnormalities on CT Scan. Such abnormalities if stable on subsequent scanning will not be viewed as persistent disease in patients who otherwise meet the criteria for CR. Response will be assessed on an ongoing basis, but at a minimum of prior to cycle four and following completion of all therapy. Patients who are removed from study early will have response status determined at time of removal from study. The major criteria for determination of response to therapy in patients with CLL include physical examination and examination of the peripheral blood and bone marrow. Radiographic studies are not required but those that were abnormal pre-treatment, will be repeated to document the degree of maximal response. (NCT00546377)
Timeframe: 3 years

Interventionparticipants (Number)
Complete ResponsePartial ResponseStable DiseaseProgression of Disease
Pentostatin,Cyclophosphamide,Rituximab & Mitoxantrone112345

[back to top]

Progression-Free Survival (PFS)

PFS was defined as the time from randomization to disease progression or death due to any cause, whichever occurred first, censored at the last tumor evaluation date. PFS calculated as (Months) = (first event date minus randomization date plus 1) divided by 30.44. (NCT00562965)
Timeframe: Baseline until disease progression or death or up to 1 year after last dose of study drug

Interventionmonths (Median)
Rituximab + Inotuzumab OzogamicinNA
Control Regimens R-CVP + R-FND16.4

[back to top]

Number of Participants With Clinically Significant Change From Baseline in Vital Signs

Criteria for determining significant change from baseline in vital signs abnormalities: heart rate value of <40 beats per minute and value >150 beats per minute, systolic blood pressure (SBP) of <80 or >210 millimeter of mercury (mmHg), diastolic blood pressure (DBP) of <40 or >130 mmHg, temperature <32 or >40 degree centigrade, and body weight>=10% increase or decrease of body weight in kilogram (kg). (NCT00562965)
Timeframe: Baseline up to 42 days post-treatment, disease follow up (every 12 weeks for a minimum of 1 year and up to 2 years)

,
Interventionparticipants (Number)
Baseline up to 42 days post-treatmentDisease follow up
Control Regimens R-CVP + R-FND12
Rituximab + Inotuzumab Ozogamicin03

[back to top]

Number of Participants With Grade 3 or 4 Treatment Emergent Adverse Events (TEAEs)

AE=any untoward medical occurrence in participant who received study drug without regard to possibility of causal relationship. Grade 3 (Severe) events=unacceptable or intolerable events, significantly interrupting usual daily activity, require systemic drug therapy/other treatment. Grade 4 (Life-threatening) events caused participant to be in imminent danger of death. TEAE=between first dose of study drug and up to 42 days after last dose that were absent before treatment or that worsened relative to pretreatment state. (NCT00562965)
Timeframe: Baseline up to 42 days post-treatment

Interventionparticipants (Number)
Rituximab + Inotuzumab Ozogamicin12
Control Regimens R-CVP + R-FND13

[back to top]

Number of Participants With Clinically Significant Change From Baseline in QT Interval Findings

Assessments of QT interval was performed only in rituximab + inotuzumab ozogamicinin group. QT interval corrected using Fridericia's formula (QTcF) and Bazett's formula (QTcB) was analyzed as per common terminology criteria for adverse events (CTCAE) version 3.0, where 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. Number of participants with change in CTCAE grading at post-baseline time point compared to the baseline were presented. The post-baseline value was defined as the maximum grade after the first dose date on or before the end of treatment. (NCT00562965)
Timeframe: Baseline up to 42 days post-treatment

Interventionparticipants (Number)
QTcB: BL normal, post-BL normalQTcB: BL normal, post-BL Grade 1QTcB: BL normal, post-BL Grade 2QTcF: BL normal, post-BL normalQTcF: BL normal, post-BL Grade 1
Rituximab + Inotuzumab Ozogamicin42363

[back to top]

Percentage of Participants With Objective Response (OR)

OR was based on assessment of complete response(CR),unconfirmed CR(Cru),partial response(PR) as per International Response Criteria for Non-Hodgkin's Lymphoma.Confirmed response=response persists on repeat imaging at least 4 weeks after initial response.CR=complete disappearance of all detectable clinical/radiographic evidence of disease,lymph nodes regressed to normal size [at least 1.5 centimeter(cm) or less],spleen regressed,not palpable on physical examination,bone marrow infiltrate cleared on repeat aspiration/biopsy.PR=at least 50 percent (%) decrease in sum of product diameters of 6 greatest dominant nodes,no increase in other nodes,liver/spleen,no new sites of disease. CRu=residual lymph node greater than 1.5 cm in transverse diameter that has regressed more than 75% in product diameter.Individual nodes previously confluent,regressed more than 75% in product diameters.Indeterminate bone marrow (increased number/size of lymph aggregates without cytologic/architectural atypia). (NCT00562965)
Timeframe: Baseline, every 6 to 12 weeks during treatment period, end of treatment (EOT) (42 days after last dose), every 12 weeks during follow-up for up to 1 year after the last dose of study drug

Interventionpercentage of participants (Number)
Rituximab + Inotuzumab Ozogamicin93.3
Control Regimens R-CVP + R-FND64.3

[back to top]

Overall Survival Probability at Months 6, 12 and 24

Overall survival was defined as the time from randomization to death due to any cause, censoring at the date of last contact or the end of the study. Participants who withdrew or lost to follow-up from study without having death documented were censored at the date of last contact. Kaplan-Meier estimates of the probability of survival at 6, 12 and 24 months was used to estimate the survival function. (NCT00562965)
Timeframe: Baseline up to Month 6, 12, 24

,
Interventionpercent chance of survival (Number)
Overall Survival: Baseline up to Month 6Overall Survival: Baseline up to Month 12Overall Survival: Baseline up to Month 24
Control Regimens R-CVP + R-FND92.383.967.1
Rituximab + Inotuzumab Ozogamicin100.086.786.7

[back to top]

Number of Participants With Clinically Significant Change From Baseline in Laboratory Findings

Criteria for laboratory test abnormality: Blood Chemistry (alkaline phosphatase [greater than{>}5*upper limit of normal {ULN}, calcium [less than {<}1.75 millimole per liter {mmol/L}, creatinine [>3*ULN], glucose [>13.9 mmol/L], phosphorous [<0.6 mmol/L], potassium [<3 mmol/L], aspartate transaminase [>5.0*ULN], total bilirubin [>3*ULN]), Coagulation (international normalized ratio [>2*ULN]), Hematology (hemoglobin [<80 grams/Liter], lymphocytes [<0.5*10^9/L], absolute neutrophil count [<1*10^9/L], platelet count [<50*10^9/L], WBC [<2.0*10^9/L]). (NCT00562965)
Timeframe: Baseline up to 42 days post-treatment, disease follow up (every 12 weeks for a minimum of 1 year and up to 2 years)

,
Interventionparticipants (Number)
Baseline up to 42 days post-treatmentDisease follow up
Control Regimens R-CVP + R-FND127
Rituximab + Inotuzumab Ozogamicin118

[back to top]

Number of Participants With Progression Free Survival (10 Years) by Treatment

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. (NCT00577993)
Timeframe: 10 years

InterventionParticipants (Count of Participants)
Fludarabine,Mitoxantrone, and Dexamethasone (FND)-Rituximab59
Rituximab- Fludarabine,Mitoxantrone, and Dexamethasone (FND)58

[back to top]

Number of Participants With Overall Survival (10 Years) by Treatment

Overall Survival is the time from date of treatment start until date of death due to any cause or last Follow-up within 10 years. (NCT00577993)
Timeframe: 10 Years

InterventionParticipants (Count of Participants)
Fludarabine,Mitoxantrone, and Dexamethasone (FND)-Rituximab59
Rituximab- Fludarabine,Mitoxantrone, and Dexamethasone (FND)58

[back to top]

Patients With Graft-Versus-Host-Disease

Number of patients who exhibited acute and/or chronic graft-versus-host disease. (NCT00609739)
Timeframe: Up to 30 Days Post Study Treatment

Interventionparticipants (Number)
Cytarabine + Mitoxantrone1

[back to top]

Patients Who Relapsed

Number of patients whose disease relapsed. (NCT00609739)
Timeframe: 1 Year

Interventionparticipants (Number)
Cytarabine + Mitoxantrone1

[back to top] [back to top]

Disease-free Survival

Number of patients who were free of disease and alive at 1 year. (NCT00609739)
Timeframe: 1 year

InterventionParticipants (Number)
Cytarabine + Mitoxantrone0

[back to top]

The Rate of Treatment Failure

"The definition of treatment failure will include:~≥ 5% leukemic blasts at the time of pre-consolidation marrow~Death during/following induction chemotherapy (pre-consolidation)~Persisting marrow hypoplasia and pancytopenia for ≥ 2 months after chemotherapy~CNS or extramedullary disease at the time of pre-consolidation~Leukemia persistence after completion of induction treatment. Leukemia persistence is defined as greater than 10% residual blasts on marrow biopsy done 5-7 days after completion of induction chemotherapy" (NCT00634244)
Timeframe: Assessed every 3 months for the first 2 years and then every 6 months until relapse or death up to 3 years from registration.

Interventionproportion of participants (Number)
Arm A (Carboplatin+Topotecan Hydrochloride)0.86
Arm B (Alvocidib+Cytarabine+Mitoxantrone)0.72
Arm C (Sirolimus+Mitoxantrone+Etoposide+Cytarabine)0.84

[back to top]

The Rate of Complete Remission (CR+CRi)

CR requires: 1. peripheral blood counts: neutrophil count ≥ 1.0 x 10^9/L, platelet count ≥ 100 x 10^9/L, reduced hemoglobin concentration or hematocrit has no bearing on remission status, and leukemic blasts must not be present in the peripheral blood. 2. bone marrow aspirate and biopsy: maturation of all cell lines must be present, ≤ 5% blasts, auer rods must not be detectable. 3. extramedullary leukemia, such as central nervous system (CNS) or soft tissue involvement, must not be present. CRi requires that all criteria for complete remission be satisfied except patients can have residual neutropenia (<1 x 10^9/L) or thrombocytopenia (<100 x 10^9/L). (NCT00634244)
Timeframe: Assessed every 3 months for the first 2 years and then every 6 months until relapse or death up to 3 years from registration.

Interventionproportion of participants (Number)
Arm A (Carboplatin+Topotecan Hydrochloride)0.143
Arm B (Alvocidib+Cytarabine+Mitoxantrone)0.278
Arm C (Sirolimus+Mitoxantrone+Etoposide+Cytarabine)0.15

[back to top]

Duration of Response

"The duration of response is measured from the time measurement criteria are first met for CR/PR until the first date that recurrent or progressive disease is objectively documented.~CR: Disappearance of all target lesions. PR: At least a 30% decrease in the sum of the LD of target lesions taking as reference the baseline sum LD." (NCT00656084)
Timeframe: From date of randomization until the date of first documented progression or the date of death from any cause, whichever came first, assessed up to 33 months.

Interventionmonths (Median)
Gemzar + Novantrone + Rituxan7.9

[back to top]

Objective Response Rate (CR + PR)

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. (NCT00656084)
Timeframe: 2 years

Interventionpercentage of participants (Number)
Gemzar + Novantrone + Rituxan46.7

[back to top]

Progression-free Survival Rate at 1 Year.

PFS is measured from the date of randomization to the date of first documented disease progression or date of death, whichever comes first. If a patient neither progresses nor dies, this patient will be censored at last contact date. (NCT00656084)
Timeframe: 1 year.

InterventionProbability of Progression-free Survival (Number)
Gemzar + Novantrone + Rituxan0.54

[back to top]

Overall Survival (OS) Rate at 1 Year

OS is measured from the date of randomization to the date of death for a dead patient. If a patient is still alive or is lost to follow up, the patient will be censored at the last contact date. (NCT00656084)
Timeframe: 1 year.

InterventionProbability of Survival (Number)
Gemzar + Novantrone + Rituxan0.57

[back to top]

Prostate-specific Antigen (PSA) Response Rate

Defined as the fraction of patients with a ≥50% reduction in serum PSA confirmed by a second serum PSA at least 3 weeks later (NCT00661492)
Timeframe: 24 months

Interventionpercentage of participants (Number)
Arm 17.7
Arm 217.6

[back to top]

Prostate-specific Antigen (PSA) Doubling Time

PSA doubling time = [log (2)× t] ÷ [log (final PSA) - log (initial PSA)] (NCT00661492)
Timeframe: 24 months

Interventionmonths (Median)
Arm 12.3
Arm 21.5

[back to top]

Objective Response Rate (ORR)

ORR = CR + PR 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. (NCT00661492)
Timeframe: 24 months

Interventionpercentage of participants (Number)
Arm 12.2
Arm 23.8

[back to top]

Median Time to Prostate-specific Antigen (PSA) Progression

Defined as the time from initiation of therapy until the first 25% increase from baseline in non-responders or 50% increase from nadir in responders as defined above. A minimum increase in the PSA of 5 ng/mL will be required for progression. (NCT00661492)
Timeframe: 24 months

InterventionMonths (Median)
Arm 12.7
Arm 22.7

[back to top]

Median Time to Progression (TTP)

TTP will be measured from the start of treatment date to the date the patient is first recorded as having disease progression (even in patients who discontinue study treatment early due to toxicity or death due to disease progression. (NCT00661492)
Timeframe: 24 months

InterventionMonths (Median)
Arm 14.9
Arm 26.6

[back to top]

Median Overall Survival (OS)

OS is measured from the date of randomization to the date of death for a dead patient. If a patient is still alive or is lost to follow up, the patient will be censored at the last contact date. (NCT00661492)
Timeframe: 30 months

Interventionmonths (Median)
Arm 111.9
Arm 215.7

[back to top]

2-year Radiographically Evident Progression-free Survival (REPFS).

"Radiographic progression:~1) For bone scan, 2 unequivocal new lesions confirmed by a subsequent bone scan with at least 1 more new lesion; 2) Skeletal related event (eg, fracture, need for radiation to bone for pain, spinal cord compression, need for surgery to bone to prevent or treat a pathologic fracture)." (NCT00661492)
Timeframe: 24 months.

InterventionProbability of REPFS at 2-year (Number)
Arm 10.73
Arm 20.80

[back to top]

Median Progression-free Survival (PFS)

PFS is measured from the date of randomization to the date of first documented disease progression or date of death, whichever comes first. If a patient neither progresses nor dies, this patient will be censored at last contact date. (NCT00661492)
Timeframe: 24 months

Interventionmonths (Median)
Arm 14.2
Arm 25.5

[back to top]

Objective Response Rate (ORR)

"Objective response is Complete Response (CR) + Partial Response (PR), as classified by the investigators according to the Response Evaluation Criteria In Solid Tumors (RECIST) guidelines. CR is a disappearance of all target and non-target lesions; PR is at least a 30% decrease in the sum of the longest diameter of target lesions without new lesions and progression of non-target lesions.~Objective response rate is calculated as a total number of participants with CR or PR divided by the total number of participants with measurable disease, multiplied by 100." (NCT00683475)
Timeframe: Baseline to date of progressive disease or death up to 36.3 months

Interventionpercentage of participants (Number)
IMC-A12 + Mitoxantrone + Prednisone15.2
IMC-1121B (Ramucirumab) + Mitoxantrone + Prednisone31.6

[back to top]

Prostate Specific Antigen (PSA) Response Rate

PSA response rate is defined as the percentage of participants with a decrease in PSA >= 50 percent from baseline. (NCT00683475)
Timeframe: Baseline up to data cut-off date (up to 36.3 months)

Interventionpercentage of participants (Number)
IMC-A12 + Mitoxantrone + Prednisone18.5
IMC-1121B (Ramucirumab) + Mitoxantrone + Prednisone21.4

[back to top]

Composite Progression-free Survival (cPFS) at 12-months

"Data presented are the percentage of participants without disease progression at 12 months.~Participants who were ongoing with no progression or who discontinued treatment for reasons other than progression were censored at date of last assessment. Participants who started new anticancer treatment before progression were censored at date of last assessment before start of new anti-cancer therapy." (NCT00683475)
Timeframe: 12 months

Interventionpercentage of participants (Number)
IMC-A12 + Mitoxantrone + Prednisone12.4
IMC-1121B (Ramucirumab) + Mitoxantrone + Prednisone20.0

[back to top]

Composite Progression-free Survival (cPFS)

"Defined as the median time from randomization to the earliest of:~Tumor progression by Response Evaluation Criteria in Solid Tumors (RECIST);~Evidence of progression by bone scan, performed after completion of the first 3 cycles, demonstrating the appearance of >=2 new lesions;~New skeletal events (New pathologic bone fracture in the region of metastatic disease; New bone lesion requiring radiation or surgery; Spinal cord or nerve root compression)~Symptomatic progression (for participants without measurable disease);~Other clinical events attributable to prostate cancer that require major interventions; or~Death from any cause~Participants who were ongoing with no progression or who discontinued treatment for reasons other than progression were censored at date of last assessment. Participants who started new anticancer treatment before progression were censored at date of last assessment before start of new anti-cancer therapy." (NCT00683475)
Timeframe: Randomization to composite progressive disease, up to 23.4 months

Interventionmonths (Median)
IMC-A12 + Mitoxantrone + Prednisone4.1
IMC-1121B (Ramucirumab) + Mitoxantrone + Prednisone6.7

[back to top]

Overall Survival (OS)

Overall survival is defined as the time from randomization to the date of death due to any cause. Participants who were alive at the time of study completion were censored at the time the participant was last known to be alive. (NCT00683475)
Timeframe: First dose to death due to any cause up to 36.3 months

Interventionmonths (Median)
IMC-A12 + Mitoxantrone + Prednisone10.8
IMC-1121B (Ramucirumab) + Mitoxantrone + Prednisone13.0

[back to top]

Composite Progression-free Survival (cPFS) at 9-months

"Data presented are the percentage of participants without disease progression at 9 months.~Participants who were ongoing with no progression or who discontinued treatment for reasons other than progression were censored at date of last assessment. Participants who started new anticancer treatment before progression were censored at date of last assessment before start of new anti-cancer therapy." (NCT00683475)
Timeframe: 9 months

Interventionpercentage of participants (Number)
IMC-A12 + Mitoxantrone + Prednisone20.7
IMC-1121B (Ramucirumab) + Mitoxantrone + Prednisone35.9

[back to top]

Composite Progression-free Survival (cPFS) at 6-months

"Data presented are the percentage of participants without disease progression at 6 months.~Participants who were ongoing with no progression or who discontinued treatment for reasons other than progression were censored at date of last assessment. Participants who started new anticancer treatment before progression were censored at date of last assessment before start of new anti-cancer therapy." (NCT00683475)
Timeframe: 6 months

Interventionpercentage of participants (Number)
IMC-A12 + Mitoxantrone + Prednisone37.2
IMC-1121B (Ramucirumab) + Mitoxantrone + Prednisone59.2

[back to top]

Summary Listing of Participants Reporting Treatment-Emergent Adverse Events

Data presented are the number of participants who experienced A12 or 1121B (ramucirumab) related treatment-emergent adverse events (TEAE), treatment related serious adverse events (SAE), or any Grade 3 or higher TEAE; any TEAE leading to discontinuation of A12 or 1121B (ramucirumab) treatment, and any TEAE leading to dose modification of A12 or 1121B (ramucirumab). A summary of SAEs and other nonserious AEs, regardless of causality, is located in the Reported Adverse Event section. (NCT00683475)
Timeframe: Randomization to 36.3 months

,
Interventionparticipants (Number)
A12/1121B Related TEAEA12/1121B Related Serious TEAEA12/1121B Related Grade >= 3 TEAETEAE Leading to Dose Modification of A12/1121BTEAE Leading to Discontinuation of A12/1121B
IMC-1121B (Ramucirumab) + Mitoxantrone + Prednisone6316313525
IMC-A12 + Mitoxantrone + Prednisone6422353518

[back to top]

Time to Radiographic Evidence of Disease Progression

"Time between date of randomization and earliest date of radiographic progression defined as either:~Tumor progression by RECIST;~Evidence of progression by bone scan;~New skeletal events (New pathologic bone fracture in the region of metastatic disease; New bone lesion requiring radiation or surgery; Spinal cord or nerve root compression).~Participants who were ongoing with no radiographic evidence of disease progression, who discontinued treatment for reasons other than progression,or died before progression were censored at date of last tumor or bone radiographic assessment. Participants who started a new anticancer treatment before progression were censored at date of last tumor or bone radiographic assessment before start of new anti-cancer therapy." (NCT00683475)
Timeframe: Randomization to date of radiographic progression, up to 36.3 months

Interventionmonths (Median)
IMC-A12 + Mitoxantrone + Prednisone7.5
IMC-1121B (Ramucirumab) + Mitoxantrone + Prednisone10.2

[back to top]

2-year PFS From the Start of Induction Therapy Conditional

2-year PFS from the start of induction therapy conditional on attaining either a negative FDG-PET or a negative biopsy at the interim evaluation. (NCT00712582)
Timeframe: 2 years

Interventionpercentage of patients (Number)
Consolidation A86.6
Consolidation B90.6
Consolidation C0.4

[back to top]

Overall Survival at 1 Year

Overall survival from the start of induction therapy conditional on attaining either a negative FDG-PET or a negative biopsy at the interim evaluation. (NCT00712582)
Timeframe: 1 year

InterventionPercent of patients (Number)
Consolidation A98.3
Consolidation B96.9
Consolidation C50.0

[back to top]

Response to Induction Chemotherapy (CR or PR)

Complete remission (CR): <5% bone marrow blasts with recovery of peripheral blood counts; complete cytogenetic remission, the disappearance of any pre-existing cytogenetic abnormality Partial remission (PR): >5% bone marrow blasts, but less than the pre-treatment blast percentage within the bone marrow Resistant disease (RD): no significant cytoreduction in bone marrow leukemic cells from pre-treatment levels Not evaluable (NE): patients who died during induction chemotherapy or who withdrew from follow-up before assessment could be made (NCT00774046)
Timeframe: Day 28-40

Interventionpercentage of participants (Number)
All Patients81.2

[back to top]

Disease-free Survival in Patients Undergoing Autologous Stem Cell Transplant

(NCT00774046)
Timeframe: Up to 883 days

InterventionDays (Median)
All Patients367

[back to top]

Relapse-free Survival

Relapse is defined as bone marrow blasts >5% if the patient had achieved a complete remission, or the recurrence of any clonal cytogenetic abnormality. (NCT00774046)
Timeframe: Up to 2000 days

InterventionDays (Median)
All Patients415

[back to top]

Feasibility of Stem Cell Collection

Feasibility is the ability to cryopreserve >=2.0 x 10^6 CD34+ cells/kg (NCT00774046)
Timeframe: 1-5 days from initiation of stem cell collection

Interventionpercentage of participants (Number)
All Patients70

[back to top]

Numbers of Stem Cells Collected

(NCT00774046)
Timeframe: 1-5 days from initiation of stem cell collection

Intervention10^6 CD34+ cells/kg (Median)
All Patients4.50

[back to top]

Overall Survival

(NCT00774046)
Timeframe: Up to 2000 days

InterventionDays (Median)
All Patients399

[back to top]

Overall Survival in Patients Undergoing Autologous Stem Cell Transplant

(NCT00774046)
Timeframe: Up to 817 days

InterventionDays (Median)
All Patients294

[back to top]

Complete Response

Bone marrow showing less than 5% leukemic blasts with normal maturation of all cell lines, an ANC of at least 1000/uL and a platelet count of 100,000/uL, absence of blast in peripheral blood, absence of identifiable leukemic cells in the bone marrow, clearance of disease-associated cytogenetic abnormalities, and clearance of any previously existing extramedullary disease. Repeat marrow confirmation 4-6 weeks following the marrow documenting CR is not required due to the need for continued treatment in CR. (NCT00795002)
Timeframe: 1 year

Interventionparticipants (Number)
Arm I24
Arm II29

[back to top]

Disease-free Survival

This will be defined as the time between study entry and the first date that recurrent or progressive disease is objectively documented, or death from any cause occurs. (NCT00795002)
Timeframe: up to 2 years

Interventionmonths (Median)
Arm I13.6
Arm II12.0

[back to top]

Number of Participants Experiencing Death From Any Cause Within 60 Days of Starting FLAM

Toxicity defined as death from any cause within 60 days of starting FLAM. (NCT00795002)
Timeframe: 60 days

InterventionParticipants (Count of Participants)
Arm I3
Arm II3

[back to top]

Hematologic Remission Rate

Proportion of patients in hematologic remission at end of consolidation, course 1 are reported. (NCT00866918)
Timeframe: End of consolidation, course 1: up to 5 months

InterventionProportion of participants (Number)
Standard Risk1.0000
High Risk0.8824

[back to top]

Overall Survival (OS)

OS - time from study entry to death. (NCT00866918)
Timeframe: At 3 years from study entry

InterventionPercentage of participants (Number)
Standard Risk98.4
High Risk85.7

[back to top]

Hematologic, Molecular, and Cytogenetic Remission Rate

Proportion of patients in hematologic, molecular, and cytogenetic remission at end of consolidation, course 3 and 4 are reported. Patients were determined to be in remission by all three criteria. (NCT00866918)
Timeframe: End of consolidation, course 3; up to 7 months (for Standard Risk) or end of consolidation, course 4; up to 9 months (for High Risk)

InterventionProportion of participants (Number)
Standard Risk0.8095
High Risk0.5882

[back to top]

Event-free Survival (EFS)

EFS - time from study entry until failure to achieve complete remission during consolidation, relapse, or death. For further clarification see definitions provided in the protocol. (NCT00866918)
Timeframe: At 3 years from study entry

InterventionPercentage of participants (Number)
Standard Risk95.4
High Risk82.9

[back to top]

Participants With Adverse Events

To evaluate the toxicity and safety of BMR in participants with untreated follicular lymphoma. (NCT00901927)
Timeframe: 3 months

InterventionParticipants (Count of Participants)
Bendamustine + Mitoxantrone + Rituximab3

[back to top]

Complete Response Rate of the Combination of BMR (Bendamustine + Mitoxantrone + Rituximab)

To evaluate the complete response rate of the combination of BMR in previously untreated follicular non-Hodgkin's lymphoma. CR defined by International Working Group Criteria for Response for Non-Hodgkin's Lymphoma as complete disappearance of all detectable clinical evidence of disease and disease-related symptoms. (NCT00901927)
Timeframe: 3 months

Interventionparticipants (Number)
Bendamustine + Mitoxantrone + Rituximab3

[back to top]

Time to Progression (TTP) for Participants Treated With BMR (Bendamustine, Mitoxantrone, and Rituximab)

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. (NCT00901927)
Timeframe: 5 months

Interventionmonths (Median)
Bendamustine + Mitoxantrone + Rituximab5

[back to top]

Characterize the Mobilization of Leukemic Cells With Plerixafor Plus G-CSF as Measured by Fold Change in AML Blast Count

(NCT00906945)
Timeframe: 6 hours after plerixafor

Interventionfold change in AML blast count (Mean)
Phase I and Phase II Participants9.4

[back to top]

Characterize the Mobilization of Leukemic Cells With Plerixafor Plus G-CSF as Measured by Fold Change in White Blood Cells

(NCT00906945)
Timeframe: 6 hours after plerixafor

Interventionfold change in white blood cells (Mean)
Phase I and Phase II Participants4.6

[back to top]

Overall Survival

Overall survival: Defined as the date of first dose of study drug to the date of death from any cause. (NCT00906945)
Timeframe: Median follow-up was 34.6 months

Interventiondays (Median)
Phase I and Phase II Participants227

[back to top]

Phase I: Maximum Tolerated Dose of Plerixafor Plus G-CSF When Combined With MEC

(NCT00906945)
Timeframe: Completion of Phase I enrollment (17 months)

Interventionmcg/kg/day (Number)
Phase I (Includes Levels 1-5)750

[back to top]

Phase II: Complete Response Rate (CR+CRi)

"Morphologic complete remission (CR): Defined as morphologic leukemia-free state, including <5% blasts in BM aspirate with marrow spicules and a count of > 200 nucleated cells and no blasts with Auer rods, no persistent extramedullary disease, ANC > 1,000/mm3, platelet count > 100,000/mm3.~Morphologic complete remission with incomplete blood count recovery (CRi): Defined as CR with the exception of neutropenia <1,000/mm3 or thrombocytopenia <100,000/mm3." (NCT00906945)
Timeframe: 45 days

Interventionpercentage of participants (Number)
Phase II (MTD)30

[back to top]

Relapse Free-survival Rate

(NCT00906945)
Timeframe: 2 years

Interventionpercentage of participants (Number)
Phase I and Phase II Participants75

[back to top]

Time to Hematologic Recovery as Measured by Time to Neutrophil Recovery

-Neutrophil recovery is defined as absolute neutrophil count (ANC) >= 500/mm^3 (NCT00906945)
Timeframe: Up to 62 days after treatment

Interventiondays (Median)
Phase I and Phase II Participants38

[back to top]

Time to Hematologic Recovery as Measured by Time to Neutrophil Recovery

-Neutrophil recovery is defined as absolute neutrophil count >= 1000/mm^3 (NCT00906945)
Timeframe: Up to 62 days after treatment

Interventiondays (Median)
Phase I and Phase II Participants40

[back to top]

Time to Hematologic Recovery as Measured by Time to Platelet Recovery

-Platelet recovery is defined as platelets >= 100,000/mm3 (NCT00906945)
Timeframe: Up to 62 days after treatment

Interventiondays (Median)
Phase I and Phase II Participants32

[back to top]

Time to Hematologic Recovery as Measured by Time to Platelet Recovery

-Platelet recovery is defined as platelets >= 50,000/mm^3 (NCT00906945)
Timeframe: Up to 62 days after treatment

Interventiondays (Median)
Phase I and Phase II Participants32

[back to top]

Phase I and Phase II: Safety and Tolerability of Regimen as Measured by Grade and Frequency of Adverse Events Exceeding 10% in Total Frequency

(NCT00906945)
Timeframe: 30 days following end of treatment

,,,,
Interventionnumber of events (Number)
AnemiaFebrile neutropeniaAbdominal painConstipationDiarrheaGastroesophageal reflux diseaseMucositis oralNauseaVomitingChillsEdema-limbsFatigueFeverNon-cardiac chest painPainBacteremiaLung infectionSepsisActivated partial thromboplastin time prolongedAlanine aminotransferase increasedAlkaline phosphatase increasedAspartate aminotransferase increasedBlood bilirubin increasedINR increasedNeutrophil count decreasedPlatelet count decreasedWhite blood cell count decreasedAnorexiaHypoalbuminemiaHypocalcemiaHypokalemiaHypomagnesemiaHyponatremiaBone painDizzinessHeadacheParesthesiaInsomniaProteinuriaCoughDyspneaPneumonitisRash maculo-papularHypotension
Grade 10065712211255961200053342700043257444745333134
Grade 2400265330012422010001030000261120021612123334
Grade 3920100010100101045001001000000020120100000002
Grade 40000000000000000040000007151600020000000000000
Grade 500000000000000002400000000000000000000000100

[back to top]

Characterize the Effects of Plerixafor Plus G-CSF on Fold Change in CXCR4 Clone 12G5 Relative Mean Fluorescent Intensity

(NCT00906945)
Timeframe: 6 hours after plerixafor

Interventionfold change in CXCR4 clone 1D9 (Mean)
Phase I and Phase II Participants0.9

[back to top]

Characterize the Effects of Plerixafor Plus G-CSF on Fold Change in CXCR4 Clone 1D9 Relative Mean Fluorescent Intensity

(NCT00906945)
Timeframe: 6 hours after plerixafor

Interventionfold change in CXCR4 clone 1D9 (Mean)
Phase I and Phase II Participants8.0

[back to top]

Secondary Endpoints Included an Assessment of the Following Parameters: Progression-Free Survival, Disease-Free Survival, Global Survival, Duration of the Response.

(NCT01133158)
Timeframe: 7 years

Interventionmonths (Median)
Progression-Free SurvivalDisease-Free SurvivalGlobal SurvivalDuration of the Response
R-BMD5651NA54

[back to top]

Response Rate

"The primary endpoint is the number of Participants with Response according to the criteria of the International Workshop to Standardize Response Criteria for NHL~Complete Remission (CR):~Nodes returned to normal (if GTD >15 mm before therapy, GTD now ≤15 mm; if GTD 11-15 and SA >10 mm before therapy, SA now ≤10 mm) All (non-nodal) target lesions completely resolved~Partial Remission (PR) SPD of target lesions decreased ≥50% from baseline Spleen and liver nodules regress by 50% in SPD or single lesion in GTD~Stable Disease (SD) Not enough shrinkage for PR Not enough growth for PD~Progressive Disease (PD):~SPD increase ≥50% from nadir (smallest value seen during trial) in nodal target lesions overall or in any single nodal target lesion" (NCT01133158)
Timeframe: 7 years

InterventionParticipants (Count of Participants)
Induction Rituximab, Bendamustine, Mitoxantrone, Dexamethasone57
Maintenance Rituximab35

[back to top]

Number of Participant With Adverse Event (AE)

An 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 study treatment. (NCT01144403)
Timeframe: Up to 50 months (approximately)

Interventionparticipants (Number)
Rituximab8

[back to top]

Overall Response Rate (ORR)

Overall Response Rate (ORR) was determined by tumor response according to International Workshop Group to Standardize Response Criteria for mantle cell lymphoma (MCL) criteria from confirmed evaluations of both target, radiographically evaluated, and non-target lesions. A responder is defined as a subject experiencing either a complete (CR)/ unconfirmed complete (Cru), or partial response (PR) by these criteria. As per criteria; CR = disappearance of all evidence of disease; CRu = the sum of the product of the diameters (SPD) of multiple nodes decreased by at least 75%; PR = regression of measurable disease and no new sites. (NCT01144403)
Timeframe: Up to 50 months (approximately)

Interventionpercentage of participants (Number)
Rituximab87.5

[back to top]

Overall Survival (OS)

Overall survival is defined as time from date of enrollment to the date of death, regardless of the cause of death. (NCT01144403)
Timeframe: From the time of enrollment until death due to any cause (up to 50 months [approximately])

Interventiondays (Median)
Rituximab927

[back to top]

Progression-free Survival (PFS)

PFS is defined as the interval between the day of enrollment and the first documentation of progressive disease or death. Progression of disease is defined as at least a 20 percent (%) increase in the sum of longest diameter (LD) of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of 1 or more new lesions. (NCT01144403)
Timeframe: From the time of enrollment until death due to any cause (up to 50 months [approximately])

Interventiondays (Median)
Rituximab653

[back to top]

Complete Response in the Absence of Platelet Recovery

"Complete response in the absence of platelet recovery is defined as:~- Bone marrow (<5% blasts) with adequate bone marrow cellularity, no evidence of circulating blasts or extramedullary disease and normalization of peripheral blood counts except for platelets (neutrophil count =1,000/µL)" (NCT01184898)
Timeframe: Within one week of peripheral count recovery but no later than day 42

Interventionparticipants (Number)
Sirolimus and MEC2

[back to top]

Association Between the Magnitude of mTOR Target Inhibition Post-treatment in Leukemic Blasts and Clinical Response in Patients With High Risk AML Treated With Sirolimus MEC

"Percent change compared between response groups (responder vs nonresponder).~This outcome measure only includes patients who survived to outcome assessment." (NCT01184898)
Timeframe: From pre- to post-treatment

Interventionpercentage change in leukemic blasts (Mean)
Responders (17 pts)Nonresponders (10 pts)
Sirolimus and MEC69-36

[back to top]

Partial Response

"Partial response is defined as:~Requires that all of the criteria for complete remission be satisfied except that the bone marrow may contain ≥ 5% blasts but < 25% blasts.~A marrow with <5% blasts that contain Auer rods will also be considered a PR" (NCT01184898)
Timeframe: Within one week of peripheral count recovery but no later than day 42

Interventionparticipants (Number)
Sirolimus and MEC3

[back to top]

Complete Response

"Complete response is defined as:~Peripheral Blood Counts -Neutrophil count >1 x 109/L.~Platelet count ≥ 100 x 109/L.~Reduced hemoglobin concentration or hematocrit has no bearing on remission status.~Leukemic blasts must not be present in the peripheral blood.~Cellularity of bone marrow biopsy must be > 20% with maturation of all cell lines with < 5% blasts and no Auer rods.~Extramedullary leukemia, such as CNS or soft tissue involvement, must not be present" (NCT01184898)
Timeframe: Within one week of peripheral count recovery but no later than day 42

Interventionparticipants (Number)
Sirolimus and MEC11

[back to top]

PFS Based on Baseline Circulating Tumor Cells (CTC) Counts

High expression (HE) of CTC was defined as having CTC counts ≥5 cells/7.5 milliliter (mL) and low expression (LE) of CTC was defined as having CTC counts <5 cells/7.5 mL. PFS is measured from randomization to the earliest date of the following events: PD according to RECIST criteria v. 1.1, is a ≥20% increase in the sum diameter of the target lesions taking as reference the smallest sum on study and an absolute increase in the sum diameter of ≥5 mm, the appearance of 1 or more new lesions and/or unequivocal progression of existing nontarget lesions, unequivocal evidence of progression by bone scan, clinical progression or death from any cause. (NCT01204710)
Timeframe: Randomization to Measured PD or Death Due to Any Cause Up to 23 Months

Interventionmonths (Median)
Olaratumab + Mitoxantrone (HE)2.32
Mitoxantrone (HE)2.23
Olaratumab + Mitoxantrone (LE)2.38
Mitoxantrone (LE)4.91

[back to top]

Percentage of Participants With Anti-Olaratumab Antibody Assessment (Immunogenicity)

Participants with Treatment Emergent (TE) anti-olaratumab antibodies were participants with a 4-fold increase (2 dilutions) increase over a positive baseline antibody titer or for a negative baseline titer, a participant with an increase from the baseline to a level of 1:20. (NCT01204710)
Timeframe: From Start of Treatment up to 9 Months

Interventionpercent of participants (Number)
Olaratumab + Mitoxantrone3.8
Mitoxantrone0

[back to top]

Percentage of Participants With a ≥50% Decrease in Prostate Specific Androgen (PSA) From Pretreatment to Any Time

Decrease in PSA ≥50% from pretreatment required confirmation no less than 3 weeks after the initial suggestion of response and occurring prior to documentation of PD. Percentage of participants = (number of participants who had ≥50% decrease in PSA at any time) / (number of participants treated) * 100. (NCT01204710)
Timeframe: Pretreatment to PD Up to 23 Months

Interventionpercentage of participants (Number)
Olaratumab + Mitoxantrone22.6
Mitoxantrone18.6

[back to top]

Summary Listing of Participants Reporting Treatment-Emergent Adverse Events (TEAE)

Data presented are the number of participants who experienced serious adverse events (SAEs) and other nonserious adverse events (AEs). For participants in mitoxantrone group who had PD and chose optional IMC-3G3 follow-on treatment, the baseline was defined as the last assessment prior to the start of the olaratumab treatment. A summary of SAEs and other nonserious AEs, regardless of causality, is located in the Reported Adverse Events section. (NCT01204710)
Timeframe: From Start of Treatment Through Study Completion Up to 36 months

,,
Interventionparticipants (Number)
SAEsAEs
Mitoxantrone2151
Mitoxantrone: Optional Olaratumab Monotherapy615
Olaratumab + Mitoxantrone2652

[back to top]

Percentage of Participants Who Achieved a Best Overall Response of Complete Response (CR) or Partial Response (PR) [Objective Response Rate (ORR)]

Best response is categorized using the RECIST v1.1 guidelines. CR is the disappearance of all non-nodal target lesions, with the short axes of any target lymph nodes reduced to <10 mm. PR is a ≥30% decrease in the sum of the diameters of target lesions (including the short axes of any target lymph nodes), taking as reference the pretreatment sum diameter. Percentage of participants = (number of participants who had CR or PR) / (number of participants treated) * 100. (NCT01204710)
Timeframe: Randomization to Objective PD or Death Up to 23 Months

Interventionpercentage of participants (Number)
Olaratumab + Mitoxantrone10.0
Mitoxantrone3.1

[back to top]

Overall Survival (OS)

OS was defined as the time from the date of randomization to the date of death from any cause. If the participants were alive at the end of the follow-up period or were lost to follow-up, OS time was censored on the last date the participant was known to be alive. (NCT01204710)
Timeframe: Randomization to Death Due to Any Cause Up to 36 Months

Interventionmonths (Median)
Olaratumab + Mitoxantrone14.2
Mitoxantrone12.8

[back to top]

OS Based on Baseline CTC Counts

HE of CTC was defined as having CTC counts ≥5 cells/7.5 mL and LE of CTC was defined as having CTC counts <5 cells/7.5 mL. OS was defined as the time from the date of randomization to the date of death from any cause. (NCT01204710)
Timeframe: Randomization to Death Due to Any Cause Up to 36 Months

Interventionmonths (Median)
Olaratumab + Mitoxantrone (HE)12.85
Mitoxantrone (HE)8.10
Olaratumab + Mitoxantrone (LE)16.49
Mitoxantrone (LE)23.00

[back to top]

Percentage of Participants With a ≥30% Decrease in PSA From Pretreatment to Week 12

Percentage of participants = (number of participants who had ≥30% decrease in PSA at Week 12) / (number of participants treated) * 100. (NCT01204710)
Timeframe: Pretreatment through Week 12

Interventionpercentage of participants (Number)
Olaratumab + Mitoxantrone22.6
Mitoxantrone16.9

[back to top]

Progression-Free Survival (PFS)

PFS is measured from randomization to the earliest date of the following events: PD according to Response Evaluation Criteria In Solid Tumors (RECIST) criteria version (v) 1.1, is a ≥20% increase in the sum of diameter of the target lesions taking as reference the smallest sum on study and an absolute increase in the sum diameter of ≥5 millimeter (mm), the appearance of 1 or more new lesions and/or unequivocal progression of existing nontarget lesions, unequivocal evidence of progression by bone scan, clinical progression or death from any cause. For participants who had no documented PD or death or had started new anti-cancer therapy or were lost to follow-up, PFS was censored at their last tumor assessment. (NCT01204710)
Timeframe: Randomization to Measured PD or Death Due to Any Cause Up to 23 Months

Interventionmonths (Median)
Olaratumab + Mitoxantrone2.3
Mitoxantrone2.4

[back to top]

Number of Participants Who Died During Study

(NCT01204710)
Timeframe: From Start of Treatment through Study Completion up to 36 Months

,,
Interventionparticipants (Number)
Due to PDDue to AEsDue to Other reasons
Mitoxantrone2732
Mitoxantrone: Optional Olaratumab Monotherapy1211
Olaratumab + Mitoxantrone4343

[back to top]

Number of Participants With Negative Platelet-Derived Growth Factor Receptor Alpha (PDGFRα) Protein Expression by Immunohistochemistry (IHC)

"PDGFRα protein expression (pretreatment) by IHC was assessed in tumor cells, and was provided as a dichotomous variable with positive and negative expression. Positive corresponds to weak intensity membranous staining comprising greater than 30% of the tumor and/or moderate to strong intensity membranous staining comprising greater than 5% of the tumor. Negative corresponds to staining that does not meet these requirements." (NCT01204710)
Timeframe: Baseline

Interventionparticipants (Number)
Olaratumab + Mitoxantrone14
Mitoxantrone9

[back to top]

Expanded Disability Status Score

"The Kurtzke Expanded Disability Status Scale (EDSS) is a method of quantifying disability in multiple sclerosis and defines functional systems as pyramidalm, cerebellar, brainstem, sensory, bowel and bladder, visual, cerebral and others.~The EDSS scale ranges from 0 to 10 in 0.5 unit increments that represent higher levels of disability." (NCT01214317)
Timeframe: At the end of month 8 after treatment initiation

Interventionscore on a scale (Mean)
Mitoxantrone and Plasmapheresis2.9
Mitoxantrone2.6

[back to top]

Change From Baseline in Mean Number of MS Plaques Found on Brain MRI

Change From Baseline in Mean Number of MS plaques found on Brain MRI 8 months after treatment initiation (NCT01214317)
Timeframe: Month 8 after treatment initiation

InterventionPlaques (Mean)
Mitoxantrone and Plasmapheresis3.5
Mitoxantrone7.3

[back to top]

Maximum Tolerated Doses Mitoxantrone Hydrochloride and Etoposide When Combined With Cyclosporine and Pravastatin Sodium

"Determine the doses of mitoxantrone and etoposide that, when combined with CSA and pravastatin, meet minimum standards for both efficacy and toxicity and have the highest efficacy rate among several mitoxantrone and etoposide doses.~Assessed by the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 4.0." (NCT01342887)
Timeframe: After completion of first 2 courses, up to 22 weeks

Interventiondoses tolerated (Number)
Treatment (Immunosuppression, Enzyme Inhibitor, and Chemo)0

[back to top]

Complete Response Rate

Bone marrow showing less than 5% myeloblasts with normal maturation of all cell lines, an ANC of at least 1000/cu mm and a platelet count of 100,000/cu mm, absence of blast in peripheral blood, absence of identifiable leukemic cells in the bone marrow, clearance of disease-associated cytogenetic abnormalities, and clearance of any previously existing extramedullary disease. These criteria are taken from Dohner H, Estey EH, Amadori S, et al. Diagnosis and management of acute myeloid leukemia in adults: recommendations from an international expert panel, on behalf of the European LeukemiaNet. Blood 2010;115:453-474 (NCT01349972)
Timeframe: 3 years

Interventionparticipants (Number)
Arm I (Alvocidib, Cytarabine, Mitoxantrone Hydrochloride)76
Arm II (Cytarabine, Daunorubicin Hydrochloride)24

[back to top]

Progression-free Survival

Probabilities will be estimated with the Kaplan-Meier estimate. Survival estimates at two years will be estimated. (NCT01349972)
Timeframe: 4 years

Interventionyears (Median)
Arm I (Alvocidib, Cytarabine, Mitoxantrone Hydrochloride)0.81
Arm II (Cytarabine, Daunorubicin Hydrochloride)0.28

[back to top]

Overall Survival

Probabilities will be estimated with the Kaplan-Meier estimate. Survival estimates at two years will be estimated. (NCT01349972)
Timeframe: 4 years

Interventionyears (Median)
Arm I (Alvocidib, Cytarabine, Mitoxantrone Hydrochloride)1.46
Arm II (Cytarabine, Daunorubicin Hydrochloride)1.850

[back to top]

Disease-free Survival

Probabilities will be estimated with the Kaplan-Meier estimate. Survival estimates at two years will be estimated. Disease-free survival Overall survival was defined from date of randomization to death or last known follow-up. Event free survival was defined as date of randomization to the first occurrence of persistent AML after 1 cycle of induction, relapse or death. Patients were censored for event free survival if they had received non-protocol therapy or a stem cell transplant. (NCT01349972)
Timeframe: Time from randomization until death from any cause or relapse or recurrence, assessed up to 2 years

Interventionyears (Median)
Arm I (Alvocidib, Cytarabine, Mitoxantrone Hydrochloride)1.46
Arm II (Cytarabine, Daunorubicin Hydrochloride)1.85

[back to top]

Incidence of Toxicities, Characterized by Number of Events by Treatment and Grade

The descriptions and grading scales found in the revised NCI Common Terminology Criteria for Adverse Events (CTCAE) version 4.0 will be utilized for AE reporting. (NCT01349972)
Timeframe: Up to 14 days after completion of study treatment

InterventionNumber of events (Number)
Arm I (Alvocidib, Cytarabine, Mitoxantrone Hydrochloride)156
Arm II (Cytarabine, Daunorubicin Hydrochloride)77

[back to top]

Number of Patients With Minimal Residual Disease

Comparisons of the treatments with respect to MRD will be based on the number of patients with MRD at day 14 after the start of treatment. (NCT01349972)
Timeframe: From study start to 14 days after the start of treatment

InterventionParticipants (Count of Participants)
Arm I (Alvocidib, Cytarabine, Mitoxantrone Hydrochloride)26
Arm II (Cytarabine, Daunorubicin Hydrochloride)24

[back to top]

Sorafenib Steady State Concentration

Median and range of sorafenib steady state concentration for Induction I. (NCT01371981)
Timeframe: Up to 30 days

InterventionNanogram/Milliliter (Median)
Arm C1090.0

[back to top]

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

InterventionScores on a scale (Mean)
Arm A66.2
Arm B65.8
Arm C (Cohort 1)74.9
Arm C (Cohort 2)63.7

[back to top]

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

Interventionpercentage of patients (Number)
Arm C (Cohort 2)64.77

[back to top]

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

InterventionScores on a scale (Mean)
Arm A60.5
Arm B58.1
Arm C (Cohort 1)71.2
Arm C (Cohort 2)48.2

[back to top]

EFS for Patients on Arm C, Cohort 2

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

Interventionpercentage of patients (Number)
Arm C (Cohort 2)56.12

[back to top]

EFS for Patients on Arm C, Cohort 1

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

Interventionpercentage of patients (Number)
Arm C (Cohort 1)25.00

[back to top]

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

Interventionpercentage of patients (Number)
Arm C (Cohort 1)41.67

[back to top]

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

InterventionPercentage 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

[back to top]

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

InterventionPercentage 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

[back to top]

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

Interventionpercentage of patients (Number)
Arm C (Cohort 3)61.84

[back to top]

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

InterventionProportion of patients (Number)
Arm A0.5000
Arm B0.5238

[back to top]

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

InterventionScores on a scale (Mean)
Arm A68.3
Arm B67.8
Arm C (Cohort 1)71.3
Arm C (Cohort 2)61.6

[back to top]

Bortezomib Clearance

Median and range of bortezomib clearance during Induction II. (NCT01371981)
Timeframe: Day 8 of Induction II

InterventionLiters/hour/m^2 (Median)
Arm B8.42

[back to top]

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

Interventionpercentage of patients (Number)
Arm A65.04
Arm B68.45

[back to top]

Event-free Survival (EFS) for Patients Without High Allelic Ratio FLT3/ITD+ Mutations

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

Interventionpercentage of patients (Number)
Arm A45.64
Arm B46.95

[back to top]

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

Interventionpercentage of patients (Number)
Arm C (Cohort 3)58.18

[back to top]

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

InterventionProportion of patients (Number)
Arm A0.8819
Arm B0.9217
Arm C (Cohort 1)0.9167
Arm C (Cohort 2)0.9394
Arm C (Cohort 3)0.9149
Arm D0.0239

[back to top]

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

Interventionpercentage of patients (Number)
Arm A46.67
Arm B46.65

[back to top]

Disease Response Rate After Treatment.

Bone marrow evaluation was performed on Day 35 of study to evaluate treatment response. CR defined as attaining M1 marrow (<5% blasts) with no evidence of circulating blasts or extramedullary disease in addition to recovery of peripheral blood counts (ANC >750/uL and platelet count >75,000/uL). CRp was defined as attaining an M1 marrow with no evidence of circulating blasts or extramedullary disease in addition to recovery of ANC but insufficient recovery of platelets. CRi was attaining M1 marrow with no evidence of circulating blasts or extramedullary disease but insufficient recovery of ANC with or without sufficient recovery of platelets. PR was defined as no evidence of circulating blasts and achievement of M2 marrow (5-25% blasts) without new sites of disease and with recovery of ANC. SD is for patients who did not meet the criteria for PR, CR, CRp, or CRi. PD is an increase of at least 25% in the absolute number of leukemia cells or development of new sites. (NCT01483690)
Timeframe: 6 weeks

,
InterventionParticipants (Count of Participants)
complete response (CR)complete response without platelet recovery (CRp)complete remission with incomplete recovery (CRi)stable disease (SD)patient not evaluable for response
Initial Dose Level01112
Modified Dose Level13347

[back to top]

Number of Participants Who Experienced a Dose Limiting Toxicity (DLT).

To evaluate the side effects of giving decitabine and vorinostat before and during chemotherapy using the standard drugs vincristine, dexamethasone, PEG-asparaginase and mitoxantrone. (NCT01483690)
Timeframe: 6 weeks

,
InterventionParticipants (Count of Participants)
# of patients with DLT# of patients without DLT# of patients not evaluable
Initial Dose Level221
Modified Dose Level1125

[back to top]

Pain Response at Week 6 Confirmed at Week 12, Week 12 Reported

The pre-specified primary analysis of Pain Response at Week 6 confirmed at Week 12 was defined as ≥ 30% from baseline in the average daily worst pain intensity score during a 7-day reporting period, with neither a concomitant increase in average daily use of any opioid narcotic type, nor addition of any new opioid narcotic type, relative to baseline. Pain Progression at a given time point is defined as ≥ 30% increase compared with baseline in the average daily worst pain intensity score during a 7-day reporting period or either an increase in the average daily use of any type of opioid narcotic or addition of a new opioid narcotic type compared with baseline. (NCT01522443)
Timeframe: Pain response was measured at Week 6 and Week 12 by self-reports of subjects

Interventionpercentage of responders (Number)
Cabozantinib15
Mitoxantrone/Prednisone17

[back to top]

Bone Scan Response (BSR)

BSR is defined as >=30% in the bone scan lesion area (BSLA) compared with baseline. Bones scans were evaluated by an independent radiology facility (IRF) for response. (NCT01522443)
Timeframe: BSR was measured at the end of Week 12 as determined by the IRF

Interventionpercentage of responders (Number)
Cabozantinib31
Mitoxantrone/Prednisone5.2

[back to top]

Overall Survival (OS)

OS was defined as the time from randomization to the date of death (due to any cause). Participants that had not died were censored at last known date alive. The analyses for OS occurred after 78/196 deaths (40% of the total required for the pre-specified primary analysis of OS). The data cut-off date was 06 October 2014. Median OS was calculated using Kaplan-Meier estimates. (NCT01522443)
Timeframe: OS was measured at the time of randomization until 78 deaths

Interventionmonths (Median)
Cabozantinib9.0
Mitoxantrone/Prednisone7.9

[back to top]

Duration of Remission (DoR) for Participants Who Achieved CR/CRi (Per Investigator Assessment)

DoR was defined as time from date of first response in responders (CR/CRi per Investigator assessment) to date of PFS event (i.e. death, progressive disease [objective progression, relapse from CR/CRi or treatment discontinuation due to global deterioration of health status] or starting new induction therapy or post-therapy stem cell transplant [SCT] without achieving CR/CRi). Responders without PFS events were censored at the last valid disease assessment including follow-up. (NCT01564784)
Timeframe: Up to 2 years from randomization

InterventionMonths (Median)
Inotuzumab Ozogamicin5.4
Defined Investigator's Choice of Chemotherapy3.5

[back to top]

Cytogenetic Status (Based on Local Laboratory Analysis) of Participants With CR/CRi (Per EAC Assessment)

Karyotyping was required locally, at screening and at least once during the study in participants who had abnormal cytogenetics at baseline and who achieved CR/CRi. Data presented below are for participants who achieved CR/CRi per EAC and had abnormal karyotype at screening. (NCT01564784)
Timeframe: Up to approximately 4 weeks (EoT) from last dose of study drug

InterventionPercentage of Participants (Number)
Inotuzumab Ozogamicin3.7
Defined Investigator's Choice of Chemotherapy18.2

[back to top]

Overall Survival (OS)

OS was defined as the time from randomization to date of death due to any cause. Participants last known to be alive were censored at date of last contact. (NCT01564784)
Timeframe: Up to 5 years after randomization or 2 years from randomization of the last participant, whichever occurs first.

InterventionMonths (Median)
Inotuzumab Ozogamicin7.7
Defined Investigator's Choice of Chemotherapy6.2

[back to top]

Maximum Observed Inotuzumab Ozogamicin Serum Concentration (Cmax) and Pre-Dose Inotuzumab Ozogamicin Serum Concentration (Ctrough) Following Single and Multiple Dosing

Blood samples were collected and analyzed for inotuzumab ozogamicin serum concentrations using a validated high performance liquid chromatography with tandem mass spectrometry (HPLC/MS/MS) method with a lower limit of quantification of 1.0 nanograms per milliliter (ng/mL). Cmax was the maximum observed concentration occurring between 0-8 hours post-dose. Ctrough was the concentration prior to subsequent dose (pre-dose) occurring after 8 hours. n = number of observations (non-missing concentrations). (NCT01564784)
Timeframe: Days 1, 4, 8, and 15 of Cycle 1, Days 1 and 8 of Cycle 2 and Day 1 of Cycle 4

Interventionng/mL (Mean)
Cmax (Cycle 1 Day 1, 1 hour post-dose) (n=128)Ctrough (Cycle 4 Day 1, pre-dose) (n=46)Cmax (Cycle 4 Day 1, 1 hour post-dose) (n=37)
Inotuzumab Ozogamicin21157.9308

[back to top]

Change From Baseline in EuroQol 5 Dimension Health Questionnaire (EQ-5D) Index Score

"The EQ-5D self-report questionnaire is a standardized measure of health status developed by the EuroQoL Group. It consists of the EQ-5D descriptive system and a visual analogue scale (VAS), EQ-VAS. The EQ-5D descriptive system measures a participants' health state on 5 dimensions: mobility, self-care, usual activities, pain/discomfort, and anxiety/depression. Each dimension has 3 levels, reflecting no problems, some problems, and extreme problems. The EQ-VAS records the respondent's self-rated health on a scale from 0 (worst imaginable health state) to 100 (best imaginable health state); higher scores indicate a better health state. EQ-5D summary index is obtained with a formula that weights each level of the dimensions. The index-based score is interpreted along a continuum of 0 (death) to 1 (perfect health)." (NCT01564784)
Timeframe: Day 1 of each cycle prior to dosing and EoT

,
InterventionScore on a scale (Mean)
Cycle 2, Day 1Cycle 3, Day 1Cycle 4, Day 1Cycle 5, Day 1Cycle 6, Day 1EoT
Defined Investigator's Choice of Chemotherapy0.02-0.080.00NANA-0.04
Inotuzumab Ozogamicin0.000.010.040.040.03-0.01

[back to top]

Change From Baseline in European Organization for Research and Treatment of Cancer Quality of Life Questionnaire, Core 30 (EORTC QLQ-C30) Score

This questionnaire comprised 30 questions within which are 9 multi-item scales & 6 single-item measures. There are 5 functional scales; physical, role, cognitive, emotional & social, 3 symptom scales; fatigue, pain, & nausea & vomiting, & a global health status/quality of life (QoL) scale. There are 5 single item measures assessing additional symptoms commonly reported by cancer patients (loss of appetite, insomnia, constipation, diarrhea, & dyspnea) & a single item concerning perceived financial impact of the disease. Most questions used a 4 point scale (1='not at all' to 4='very much'); 2 questions used a 7-point scale (1='very poor' to 7='excellent'). Scores were averaged & transformed to a scale ranging from 0 to 100; a higher score indicates a better level of functioning or greater degree of symptoms. (NCT01564784)
Timeframe: Day 1 of each cycle prior to dosing and EoT

,
InterventionScore on a scale (Mean)
Physical Functioning C2D1Physical Functioning C3D1Physical Functioning C4D1Physical Functioning C5D1Physical Functioning C6D1Physical Functioning EoTRole Functioning C2D1Role Functioning C3D1Role Functioning C4D1Role Functioning C5D1Role Functioning C6D1Role Functioning EoTEmotional Functioning C2D1Emotional Functioning C3D1Emotional Functioning C4D1Emotional Functioning C5D1Emotional Functioning C6D1Emotional Functioning EoTCognitive Functioning C2D1Cognitive Functioning C3D1Cognitive Functioning C4D1Cognitive Functioning C5D1Cognitive Functioning C6D1Cognitive Functioning EoTSocial Functioning C2D1Social Functioning C3D1Social Functioning C4D1Social Functioning C5D1Social Functioning C6D1Social Functioning EoTGlobal Health Status C2D1Global Health Status C3D1Global Health Status C4D1Global Health Status C5D1Global Health Status C6D1Global Health Status EoTDyspnoea C2D1Dyspnoea C3D1Dyspnoea C4D1Dyspnoea C5D1Dyspnoea C6D1Dyspnoea EoTInsomnia C2D1Insomnia C3D1Insomnia C4D1Insomnia C5D1Insomnia C6D1Insomnia EoTAppetite Loss C2D1Appetite Loss C3D1Appetite Loss C4D1Appetite Loss C5D1Appetite Loss C6D1Appetite Loss EoTConstipation C2D1Constipation C3D1Constipation C4D1Constipation C5D1Constipation C6D1Constipation EoTDiarrhoea C2D1Diarrhoea C3D1Diarrhoea C4D1Diarrhoea C5D1Diarrhoea C6D1Diarrhoea EoTFinancial Difficulties C2D1Financial Difficulties C3D1Financial Difficulties C4D1Financial Difficulties C5D1Financial Difficulties C6D1Financial Difficulties EoTFatigue C2D1Fatigue C3D1Fatigue C4D1Fatigue C5D1Fatigue C6D1Fatigue EotNausea and Vomiting C2D1Nausea and Vomiting C3D1Nausea and Vomiting C4D1Nausea and Vomiting C5D1Nausea and Vomiting C6D1Nausea and Vomiting EoTPain C2D1Pain C3D1Pain C4D1Pain C5D1Pain C6D1Pain EoT
Defined Investigator's Choice of Chemotherapy0.32-13.330.00NANA-8.17-1.59-11.110.00NANA-12.374.76-19.440.00NANA4.350.00-5.5616.67NANA0.54-2.38-27.780.00NANA-2.150.40-16.678.33NANA-0.40-7.9411.110.00NANA0.541.590.000.00NANA0.003.170.000.00NANA11.830.000.000.00NANA-0.54-1.59-11.110.00NANA3.760.000.000.00NANA2.195.8222.22-11.11NANA5.73-0.790.00-16.67NANA3.49-7.14-5.56-33.33NANA-7.26
Inotuzumab Ozogamicin0.483.155.3311.527.22-3.385.4511.8116.6712.8816.671.325.217.415.696.822.78-0.914.055.794.580.76-8.330.834.205.5610.4212.8816.671.823.989.3811.258.710.690.00-5.41-7.41-12.50-3.03-2.78-2.31-2.40-9.26-7.50-4.55-11.11-2.31-4.20-8.33-11.67-6.062.78-1.32-1.210.47-2.500.005.562.64-3.30-5.09-0.83-9.52-2.782.31-1.800.47-1.67-3.03-5.560.33-4.10-8.33-9.17-7.320.00-0.330.15-4.63-3.332.270.00-0.17-8.86-8.56-4.170.76-2.78-1.98

[back to top]

Change From Baseline in EQ-5D VAS

"The EQ-5D self-report questionnaire is a standardized measure of health status developed by the EuroQoL Group. It consists of the EQ-5D descriptive system and a visual analogue scale (VAS), EQ-VAS. The EQ-5D descriptive system measures a participants' health state on 5 dimensions: mobility, self-care, usual activities, pain/discomfort, and anxiety/depression. Each dimension has 3 levels, reflecting no problems, some problems, and extreme problems. The EQ-VAS records the respondent's self-rated health on a scale from 0 (worst imaginable health state) to 100 (best imaginable health state); higher scores indicate a better health state." (NCT01564784)
Timeframe: Day 1 of each cycle prior to dosing and EoT

,
InterventionScore on a scale (Mean)
Cycle 2, Day 1Cycle 3, Day 1Cycle 4, Day 1Cycle 5, Day 1Cycle 6, Day 1EoT
Defined Investigator's Choice of Chemotherapy5.9019.6744.00NANA-0.52
Inotuzumab Ozogamicin5.818.137.137.6215.094.62

[back to top]

Progression-Free Survival (PFS)

PFS was defined as time from date of randomization to earliest date of the following events: death, progressive disease (objective progression, relapse from CR/CRi or treatment discontinuation due to global deterioration of health status) and starting new induction therapy or post-therapy SCT without achieving CR/CRi. Participants without a PFS event at time of analysis were censored at the last valid disease assessment. In addition, participants with documentation of an event after an unacceptably long interval (>28 weeks if there was post-baseline disease assessment, or >12 weeks if there was no post-baseline assessment) since the previous disease assessment were censored at the time of the previous assessment (date of randomization if no post-baseline assessment). Post-study treatment follow-up disease assessments was included. Kaplan-Meier method used and 2-sided 95% confidence interval (CI) calculated based on the Brookmeyer and Crowley method. (NCT01564784)
Timeframe: Up to 2 years from randomization

InterventionMonths (Median)
Inotuzumab Ozogamicin5.0
Defined Investigator's Choice of Chemotherapy1.7

[back to top]

Percentage of Participants With Veno-Occlusive Liver Disease (VOD)/Sinusoidal Obstruction Syndrome (SOS) Following Post Study HSCT

VOD/SOS was defined as the occurrence of 2 out of the following 3 clinical criteria: 1) total serum bilirubin level >34 micromoles per liter (μmol/L) (>2.0 milligrams per deciliter [mg/dL]), 2) an increase in liver size from baseline or development of right upper quadrant pain of liver origin and 3) sudden weight gain >2.5% (eg, within a 72 hour period) because of fluid accumulation in the weeks following infusion of study drug or chemotherapy, or HSCT conditioning/preparative therapy, or development of ascites not present at baseline following such exposures AND the absence of other explanations for these signs and symptoms, OR development of bilirubin elevation, weight gain, or hepatomegaly plus histologic abnormalities on liver biopsy demonstrating hepatocyte necrosis in zone 3 of the liver acinus, sinusoidal fibrosis, and centrilobular hemorrhage, with or without fibrosis of the terminal hepatic venules. (NCT01564784)
Timeframe: Up to 2 years from randomization

InterventionPercentage of Participants (Number)
Inotuzumab Ozogamicin22.8
Defined Investigator's Choice of Chemotherapy8.6

[back to top]

Percentage of Participants With Hematologic Remission (Complete Remission [CR]/Complete Remission With Incomplete Hematologic Recovery [CRi]) as Assessed by the Endpoint Adjudication Committee (EAC)

CR was the disappearance of leukemia indicated by less than (<) 5 percent (%) marrow blasts & absence of peripheral blood leukemic blasts, with recovery of hematopoiesis defined by absolute neutrophil count (ANC) greater than or equal to (≥)1000 per microliter (/μL) & platelets ≥100,000/μL. C1 extramedullary disease status (i.e. complete disappearance of measurable & non-measurable extramedullary disease with the following exceptions: for participants with at least 1 measurable lesion, all nodal masses greater than (>) 1.5 centimeters (cm) in greatest transverse diameter (GTD) at baseline must have regressed to less than or equal to (≤) 1.5 cm in GTD; all nodal masses ≥1 cm & ≤1.5 cm in GTD at baseline must have regressed to <1 cm GTD or reduced by 75% in sum of products of greatest diameters, no new lesions, spleen & other previously enlarged organs must have regressed in size & must not be palpable) was required. CRi was defined as CR except ANC <1000/μL &/or platelets <100,000/μL. (NCT01564784)
Timeframe: Screening, Day 16 to 28 of Cycles 1, 2 and 3, then every 1 to 2 cycles (or as clinically indicated) up to approximately 4 weeks (end of treatment [EoT]) from the last dose

InterventionPercentage of Participants (Number)
Inotuzumab Ozogamicin80.7
Defined Investigator's Choice of Chemotherapy29.4

[back to top]

Percentage of Participants Who Had a Hematopoietic Stem-Cell Transplant (HSCT)

HSCT rate was defined as the percentage of participants who underwent SCT following treatment with inotuzumab ozogamicin or Investigator's choice of chemotherapy. (NCT01564784)
Timeframe: Up to 19 weeks from last dose

InterventionPercentage of Participants (Number)
Inotuzumab Ozogamicin42.7
Defined Investigator's Choice of Chemotherapy11.1

[back to top]

Percentage of Participants Achieving MRD Negativity (Based on Central Laboratory Analysis) in Participants Achieving a CR/CRi (Per EAC Assessment)

MRD analysis was performed at least once in participants with prior assessment of CR or CRi. Bone marrow aspirates, collected at screening and during the study, were sent to the central laboratory and analyzed using multiparametric flow cytometry. The antibody combinations were designed to maximize discrimination between normal and abnormal cells of B-cell lineage and similar maturational stage and included antibodies detecting cluster of differentiation (CD) 9, CD10, CD13, CD19, CD20, CD33, CD34, CD38, CD45, CD58, CD66c, and CD123. A peripheral blood sample was provided if a participant had an inadequate bone marrow aspirate at screening. MRD negativity was considered to have been achieved if the lowest value of MRD from the first date of CR/CRi to EoT was <1 × 10^-4 blasts/nucleated cells. (NCT01564784)
Timeframe: Up to approximately 4 weeks (EoT) from last dose of study drug

InterventionPercentage of Participants (Number)
Inotuzumab Ozogamicin78.4
Defined Investigator's Choice of Chemotherapy28.1

[back to top]

3-year Overall Survival Rate of Patients With Relapsed ALL

Estimate the 3-year survival rate of participants with first relapse or primary refractory precursor B-cell ALL treated with risk-directed therapy. (NCT01700946)
Timeframe: 3 years of follow-up since the on-study date

Interventionpercentage of participants (Number)
STANDARD RISK94.4
HIGH RISK55.5
All Patients Enrolled on the Study72.63

[back to top]

Median CD20 Expression Levels

To estimate median levels of CD20 expression at baseline, during treatment with dexamethasone-containing chemotherapy and following rituximab treatment in Block I of remission induction therapy for relapsed precursor B-cell ALL. (NCT01700946)
Timeframe: Baseline and at the end of Block I (approximately 5 weeks after the on-study date)

,,
Interventionpercentage of CD20 Antigen (Median)
At BaselineAt Block 1
All Patients Enrolled on the Study22.015.58
HIGH RISK23.1319.58
STANDARD RISK16.4011.83

[back to top]

Mean of CD20 Expression Levels

To estimate mean levels of CD20 expression at baseline, during treatment with dexamethasone-containing chemotherapy and following rituximab treatment in Block I of remission induction therapy for relapsed precursor B-cell ALL. (NCT01700946)
Timeframe: Baseline and at the end of Block I (approximately 5 weeks after the on-study date)

,,
Interventionpercentage of CD20 Antigen (Mean)
At BaselineAt Block I
All Patients Enrolled on the Study36.2319.43
HIGH RISK39.8220.10
STANDARD RISK31.1018.54

[back to top]

3-year Event-free Survival Rates in Patients With Relapsed ALL

Estimate the 3-year event-free survival rate of participants with first relapse or primary refractory precursor B-cell ALL treated with risk-directed therapy. (NCT01700946)
Timeframe: 3 years of follow-up since the on-study date

Interventionpercentage of participants (Number)
STANDARD RISK83.3
HIGH RISK55.7
All Patients Enrolled on the Study67.83

[back to top]

Remission Rate Including CR and CRp

"Complete remission (CR) and Complete remission with incomplete platelet recovery (CRp) categorized according to criteria recommended by International Working Groups:~Complete resolution of disease-related symptoms and signs including palpable hepatosplenomegaly; hemoglobin level at least 110 g/L, platelet count at least 100x10^9/L, and absolute neutrophil count at least 1.0 x10^9/L. In addition, all 3 blood counts should be no higher than the upper normal limit; Normal leukocyte differential; Bone marrow histologic remission defined as the presence of age-adjusted normocellularity, no more than 5% myeloblasts, and an osteomyelofibrosis grade no higher than 1." (NCT01729845)
Timeframe: Up to 5 years

InterventionParticipants (Count of Participants)
Dose Level 2: 7-Days of Decitabine-MEC11

[back to top]

Duration of Relapse-free Survival (for Patients Achieving CR or CRp)

Categorized according to criteria recommended by International Working Groups. (NCT01729845)
Timeframe: Up to 5 years

InterventionDays (Median)
Dose Level 2: 7-Days of Decitabine-MEC150

[back to top]

Overall Survival

Survival measured as of day of last contact. Categorized according to criteria recommended by International Working Groups. (NCT01729845)
Timeframe: Up to 5 years

Interventiondays (Median)
Dose Level 2: 7-Days of Decitabine-MEC564

[back to top]

Most Efficacious and Tolerated Dosage of Decitabine (Period 1)

MTD (most tolerated dose) of decitabine, measured in number of dose limiting toxicities. MTD defined as the highest dose in which the incidence of dose limiting toxicity is < 33%, graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events version 4.0 (Phase I) (NCT01729845)
Timeframe: through day 45

,,
InterventionIncidents (Number)
Dose-limiting toxiticiesComplete RemissionComplete Remission, incomplete PLT recoveryComplete Remission, incomplete blood count recoverMorphologic leukemia-free stateResistant DiseaseDeath (among those who received MEC)
Dose Level 1: 5-Days of Decitabine-MEC0120012
Dose Level 2: 7-Days of Decitabine-MEC0511031
Dose Level 3: 10-Days of Decitabine-MEC0320340

[back to top]

Minimal Residual Disease Negative Complete Remission Rate in Patients With Newly Diagnosed Disease (Phase II)

Remission Rate defined as Recist Category of Complete Resposne (CR) Disappearance of all non-target lesions and normalization of tumor marker level. All lymph nodes must be non-pathological in size(<10 mm short axis). (NCT02044796)
Timeframe: Up to day 45 after start of second course of induction chemotherapy

InterventionParticipants (Count of Participants)
Newly Diagnosed Group95
Relapsed/Refractory22

[back to top]

Number of Participants With Dose Limiting Toxicities of Mitoxantrone (Phase I, Dose Level 4)

Defined as the highest dose studied in which the incidence of dose-limiting toxicity is < 33%, graded according to NCI Common Terminology Criteria for Adverse Events version 4.0 (NCT02044796)
Timeframe: Up to day 45 after start of induction chemotherapy

InterventionParticipants (Count of Participants)
Newly Diagnosed Group1
Relapsed/Refractory Group2

[back to top]

Remission Rate (Complete Remission and Complete Remission With Incomplete Platelet Count Recovery) of This Regimen in Patients With Relapsed/Refractory Disease (Phase II)

(NCT02044796)
Timeframe: Up to 5 years

InterventionParticipants (Count of Participants)
Phase 2 Relapsed/Refractory Group 16 mg/m^224

[back to top]

Overall Survival (Phase II)

Number of subjects that have survived (NCT02044796)
Timeframe: From date of randomization until the date of death from any cause, assessed up to 12 months

InterventionParticipants (Number)
Phase 2 Newly Diagnosed Group 18 mg/m^266
Phase 2 Relapsed/Refractory Group 16 mg/m^213

[back to top]

Disease Free Survival (DFS) of Low Risk (LR) Relapse Patients

DFS rates of LR relapse B-ALL patients who are randomized following Block 1 chemotherapy to receive either chemotherapy alone or chemotherapy plus blinatumomab (LR Randomization). DFS is calculated as the time from randomization to date of first event (relapse, second malignancy, remission death) or date of last contact. Three-year DFS estimates will be calculated from date of randomization for both Arm C and Arm D. Two-sided 95% confidence intervals will be calculated. (NCT02101853)
Timeframe: Up to 3 years from date of randomization

Interventionpercentage of participants (Number)
Arm C (LR Control)58.94
Arm D (LR Blinatumomab)67.00

[back to top]

Disease Free Survival (DFS) of High-risk (HR) and Intermediate-risk (IR) Relapse Patients

DFS rates of HR and IR relapse B-ALL patients who are randomized following Induction Block 1 chemotherapy to receive either two intensive chemotherapy blocks or two 5-week blocks of blinatumomab (HR/IR Randomization). DFS is calculated as the time from randomization to date of first event (treatment failure, relapse, second malignancy, remission death) or date of last contact. Two-year DFS estimates will be calculated from date of randomization for both Arm A and Arm B. Two-sided 95% confidence intervals will be calculated. (NCT02101853)
Timeframe: Up to 2 years from date of randomization

Interventionpercentage of participants (Number)
Arm A (HR and IR Control)39.04
Arm B (HR and IR Blinatumomab)54.44

[back to top]

Overall Survival (OS) of HR and IR Relapse Patients

OS rates of HR and IR relapse B-ALL patients who are randomized following Induction Block 1 chemotherapy to receive either two intensive chemotherapy blocks or two 5-week blocks of blinatumomab (HR/IR Randomization). OS is calculated as the time from randomization to date of death or date of last contact. Two-year OS estimates will be calculated from date of randomization for both Arm A and Arm B. Two-sided 95% confidence intervals will be calculated. (NCT02101853)
Timeframe: Up to 2 years from date of randomization

Interventionpercentage of participants (Number)
Arm A (HR and IR Control)58.40
Arm B (HR and IR Blinatumomab)71.33

[back to top]

Overall Survival (OS) of LR Relapse Patients

OS rates of LR relapse B-ALL patients who are randomized following Block 1 chemotherapy to receive either chemotherapy alone or chemotherapy plus blinatumomab (LR Randomization). OS is calculated as the time from randomization to date of death or date of last contact. Three-year OS estimates will be calculated from date of randomization for both Arm C and Arm D. Two-sided 95% confidence intervals will be calculated. (NCT02101853)
Timeframe: Up to 3 years from date of randomization

Interventionpercentage of participants (Number)
Arm C (LR Control)88.29
Arm D (LR Blinatumomab)90.37

[back to top]

EFS in High Risk APL Patients

EFS is defined as the time from on study to failure to achieve hematological CR prior to start of consolidation, persistence of molecular positive disease after MRD positive consolidation course, relapse (molecular, morphologic or extramedullary), or death. The Kaplan-Meier method will be used to estimate 2-year EFS along with 90% log-minus-log transformed confidence limits. (NCT02339740)
Timeframe: Up to 24 months

Interventionpercentage of participants (Number)
High Risk96.1

[back to top]

Event-free Survival (EFS) in Standard Risk Acute Promyelocytic Leukemia (APL) Patients

EFS is defined as the time from on study to failure to achieve hematological complete response (CR) prior to start of consolidation, persistence of molecular positive disease after minimal residual disease (MRD) positive consolidation course, relapse (molecular, morphologic or extramedullary), or death. The Kaplan-Meier method will be used to estimate 2-year EFS along with 90% log-minus-log transformed confidence limits. (NCT02339740)
Timeframe: Up to 24 months

Interventionpercentage of participants (Number)
Standard Risk97.9

[back to top] [back to top]

Duration of Overall Survival (OS)

Overall survival was defined as the time from the date of randomization until the date of death from any cause (death date - randomization date + 1). For a participant who was not known to have died by the end of study follow-up, OS was censored at the date of last contact (date of last contact - randomized date + 1). The date of last contact was the latest date that the participant was known to be alive by the cutoff date. The last contact date was derived for participants alive at the analysis cutoff date. Survival rate and 95% CI were estimated using the Kaplan-Meier method and the Greenwood formula. (NCT02421939)
Timeframe: From randomization until the data cut-off date of 17 Sep 2018, median time of follow-up for OS was 17.8 months

InterventionMonths (Median)
Gilteritinib9.3
Salvage Chemotherapy5.6

[back to top]

Percentage of Participants Who Achieved Transfusion Conversion and Maintenance

Transfusion conversion & maintenance rate was defined for gilteritinib arm. Participants were classified as transfusion independent if there were no RBC or platelet transfusions within 28 days prior to the first dose to 28 days after the first dose; otherwise they were classified as transfusion dependent at baseline. Participants were considered independent postbaseline if they had 1 consecutive 8 week period without any RBC or platelet transfusion from 29 days after the first dose until the last dose date. For participants who were on treatment ≤ 4 weeks or > 4 weeks but < 12 weeks and there was no RBC or platelet transfusion within postbaseline period, they were considered not evaluable; otherwise, they were considered postbaseline transfusion dependent. Transfusion conversion rate was defined for participants who had evaluable postbaseline transfusion status. Transfusion status (independent vs. dependent) at baseline and postbaseline was reported in a 2 by 2 contingency table. (NCT02421939)
Timeframe: From randomization until the data cut-off date of 17 Sep 2018, median treatment duration for gilteritinib was (126.00 [4.0, 885.0]) days versus salvage chemotherapy 28.0 [5.0, 217.0] days)

InterventionPercentage of participants (Number)
Baseline Independent/ Post baseline IndependentBaseline Independent/Post baseline DependentBaseline Independent/Post baseline Not EvaluableBaseline Dependent/Post baseline IndependentBaseline Dependent/Post baseline DependentBaseline Dependent/Post baseline Not Evaluable
Gilteritinib59.224.516.334.555.89.6

[back to top]

Change From Baseline in Brief Fatigue Inventory (BFI)

The Brief Fatigue Inventory (BFI) is a screening tool designed to assess the severity and impact of fatigue on daily functioning of participants with cancer during the 24 hours. There are 9 items on the scale. The first three questions ask participants to rate their fatigues on a scale from 0 (no fatigue) - 10 (as bad as you can imagine), with higher scores indicating worse outcome. The remaining six questions ask participants to rate how much fatigue has interfered with their daily activities on a scale from 0 (Does not interfere) to 10 (Completely interferes). A global fatigue score can be obtained by averaging all the items on the BFI. The global BFI score will be calculated only if at least 5 of the 9 items are answered. A higher BFI fatigue score indicates worse outcome. (NCT02421939)
Timeframe: Baseline and cycle 1, day 8 and cycle 2 day 1 (up to data cut off date of 17 Sep 2018)

,
InterventionUnits on a scale (Mean)
Cycle 1 day 8 (C1D8)Cycle 2 day 1 (C2D1)
Gilteritinib-0.40.0
Salvage Chemotherapy1.00.4

[back to top]

Percentage of Participants With Composite Complete Remission (CRc Rate)

CRc rate was defined as the number of participants who achieved the best response of CRc (CR,complete remission with incomplete platelet recovery (CRp) or complete remission with incomplete hematologic recovery (CRi) divided by the number of participants in the analysis population. (NCT02421939)
Timeframe: From randomization until the data cut-off date of 17 Sep 2018, median time of follow-up for OS was 17.8 months

InterventionPercentage of participants (Number)
Gilteritinib54.3
Salvage Chemotherapy21.8

[back to top]

Percentage of Participants With Complete Remission (CR) With Partial Hematological Recovery (CRh)

CRh rate was defined as the number of participants who achieved CRh at any of the postbaseline visits and did not have a best response of CR divided by the number of participants in the analysis population. (NCT02421939)
Timeframe: From randomization until the data cut-off date of 17 Sep 2018, median time of follow-up for OS was 17.8 months

InterventionPercentage of participants (Number)
Gilteritinib34.0
Salvage Chemotherapy15.3

[back to top]

Percentage of Participants With Complete Remission (CR) Rate

The CR rate was defined as the number of participants who achieved the best response of CR divided by the number of participants in the analysis population. (NCT02421939)
Timeframe: From randomization until the data cut-off date of 17 Sep 2018, all participants included in the primary analysis of CR rate were followed up at least 6 months

InterventionPercentage of participants (Number)
Gilteritinib21.1
Salvage Chemotherapy10.5

[back to top]

Duration of Event-Free Survival (EFS)

"EFS was defined as the time from the date of randomization until the date of documented relapse (excluding relapse after PR), treatment failure or death from any cause within 30 days after the last dose of study drug, whichever occurred first (earliest of [relapse date, treatment failure date, death date] - randomization date + 1). If a participant experienced relapse or death within 30 days after the last dose of study drug, the participant was defined as having an EFS event related to either relapse or death, and the event date was the date of relapse or death. For a participant who was not known to have had a relapse or treatment failure or death event, EFS was censored at the date of last relapse-free disease assessment (last relapse-free disease assessment date - randomization date + 1). Data was estimated based on Kaplan-Meier estimates." (NCT02421939)
Timeframe: From randomization until the data cut-off date of 17 Sep 2018, median time of follow-up for OS was 17.8 months

InterventionMonths (Median)
Gilteritinib2.8
Salvage Chemotherapy0.7

[back to top]

Percentage of Participants Who Underwent Hematopoietic Stem Cell Transplant

Transplantation rate is defined as the percentage of participants undergoing Hematopoietic stem cell transplant (HSCT) during the study period. (NCT02421939)
Timeframe: From randomization until the data cut-off date of 17 Sep 2018, median time of follow-up for OS was 17.8 months

InterventionPercentage of participants (Number)
Gilteritinib25.5
Salvage Chemotherapy15.3

[back to top]

Duration of Remission

Duration of remission included duration of composite complete remission (CRc), duration of complete remission (CR)/ complete remission with partial hematologic recovery (CRh), duration of CRh, duration of CR and duration of response (CRc + partial remission (PR). The duration of response was defined as the time from the date of either first CRc or PR until the date of documented relapse (i.e., the date of first NR after CRc or PR) for participants who achieved CRc or PR (relapse date - first CRc or PR disease assessment date + 1). Participants who died without report of relapse were considered nonevents and censored at their last relapse-free disease assessment date (last relapse-free disease assessment date - first CRc or PR disease assessment date + 1). Other participants who did not relapse during the study were considered nonevents and censored at the last relapse-free assessment date. Duration of CR was only applicable to participants with best overall response of CR. (NCT02421939)
Timeframe: From randomization until the data cut-off date of 17 Sep 2018, median time of follow-up for OS was 17.8 months

InterventionMonths (Median)
Gilteritinib14.8
Salvage Chemotherapy1.8

[back to top]

Number of Participants With Adverse Events

"A treatment-emergent adverse event (TEAE) was defined as an AE observed after starting administration of the study drug (gilteritinib or salvage chemotherapy). If the AE occurred on day 1 and the onset check box was marked Onset after first dose of study drug or the onset check box was left blank, then the AE was considered treatment emergent. If the AE occurred on day 1 and the onset check box was marked Onset before first dose of study drug, then the AE was not considered treatment emergent. Majority of salvage chemotherapy participants finished the study by cycle 2 of treatment, the duration of exposure was longer in the gilteritinib arm compared with the salvage chemotherapy arm (126.00 [4.0, 885.0] days versus 28.0 [5.0, 217.0] days). The NCI-CTCAE is defined as National Cancer Institute-Common Terminology Criteria for Adverse Events." (NCT02421939)
Timeframe: From first dose of study drug up to 30 days after the last dose of study drug (median treatment duration for gilteritinib was (126.00 [4.0, 885.0]) days versus salvage chemotherapy 28.0 [5.0, 217.0] days)

,
InterventionParticipants (Count of Participants)
Drug-related TEAESerious TEAEDrug-related serious TEAETEAE leading to deathDrug-related TEAE leading to deathTEAE leading to withdrawal of treatmentDrug-related TEAE lead withdrawal of treatmentNCI-CTCAE Grade 3 or higher TEAEDrug-related Grade 3 or higher TEAEDeath
Gilteritinib2062058871105827236153170
Salvage Chemotherapy713416165135945781

[back to top]

Percentage of Participants With Complete Remission and Complete Remission With Partial Hematological Recovery (CR/CRh) in the Gilteritinib Arm

The CR/CRh rate was defined as the number of participants who achieved either CR or CRh at any of the postbaseline visits divided by the number of participants in the analysis population. (NCT02421939)
Timeframe: From randomization until the data cut-off date 04 Aug 2017, the 142 patients included in the primary analysis of CR/CRh rate were followed up at least 112 days

InterventionPercentage of participants (Number)
CR/CRh rateCR rateCRh rate
Gilteritinib28.219.09.2

[back to top]

Duration of Leukemia-Free Survival (LFS)

The LFS was defined as the time from the date of first CRc until the date of documented relapse (excluding relapse from PR) or death for participants who achieved CRc (relapse date or death date - first CRc disease assessment date + 1). For a participant who was not known to have relapsed or died, LFS was censored on the date of last relapse-free disease assessment date (last relapse-free disease assessment date - first CRc disease assessment date + 1). For a participant who was not known to have relapsed or died, LFS was censored on the date of last relapse-free disease assessment date (last relapse-free disease assessment date - first CRc disease assessment date + 1). (NCT02421939)
Timeframe: From randomization until the data cut-off date of 17 Sep 2018, median time of follow-up for OS was 17.8 months

InterventionMonths (Median)
Gilteritinib4.4
Salvage Chemotherapy6.7

[back to top]

Complete Response (CR) Rate in Patients With Relapsed or Refractory AML

"Complete Remission (CR) rate = Percentage of patients achieving CR after Cycle 1 as defined in Stage 1 by the International Working Group (IWG) Criteria and 2010 European LeukemiaNet (EN) criteria in patients with relapsed or refractory AML with MCL-1 dependence >30% and in Stage 2 by the 2017 ELN criteria.~The study was terminated in January 2020 due to a steady and marked reduction in enrollment. Thus, the efficacy endpoints could not be analyzed. As sufficient efficacy results were not available to analyze patients based on the percentage of MCL-1 dependency the treatment efficacy was summarized by distributing the safety population into 6 groups based on whether the patients received the ACM vs CM regimen and their disease stages at study entry." (NCT02520011)
Timeframe: Best response after at least 1 cycle through study completion approximately 4 years

,,,,,
Interventionparticipants (Number)
Complete Remission (CR)CR with Incomplete Neutrophil Recovery (Cri)Partial Remission (PR)Resistant/Relapsed DiseaseNot Evaluated
All Stages and Cohorts (Including Randomized Stage): ACM Total271723413
Stage 1 ACM Relapsed/Refractory85156
Stage 1 Newly Diagnosed ACM62141
Stage 2 ACM Relapsed/Refractory23051
Stage 2 CM Relapsed/Refractory60050
Stages 1 and 2 ACM Relapsed/Refractory211513012

[back to top]

Response to Treatment

To determine if treatment with ACM can induce CR in patients with relapsed or refractory AML with MCL-1 dependence of >30% who failed to achieve CR following 1 cycle of CM (NCT02520011)
Timeframe: Best response after at least 1 cycle through study completion approximately 4 years

Interventionparticipants (Number)
Partial Remission (PR)Not Evaluated
Stage 2 CM Relapsed/Refractory AML11

[back to top]

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

InterventionParticipants (Count of Participants)
Treatment Arm1

[back to top]

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

InterventionPercentage of Cells Positive for MRD (Mean)
Treatment Arm0.65

[back to top]

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

InterventionParticipants (Count of Participants)
Treatment Arm2

[back to top]

Number of Subject With Adverse Events

Toxicities were assessed and graded according to CTCAE v 4.0. (NCT02535806)
Timeframe: 36 days

InterventionParticipants (Count of Participants)
Treatment Arm1

[back to top] [back to top]

Clinical Response to Crenolanib With Standard Salvage Chemotherapy

To determine the response rate to crenolanib. Complete remission (CR) response criteria include a post-baseline bone marrow (BM) biopsy or aspiration % blasts <5%, absolute neutrophil count (ANC) >1×10^9/L and platelet count >100×10^9/L. CRi response included all CR criteria met, except participant did not have either platelet recovery or ANC recovery. CRh response included all CR criteria met, except subject only has partial platelet recovery and ANC recovery. Complete CR (CRc) response includes all subjects who achieve a CR, CRi and CRh. Partial Response (PR) response included a decrease of ≥50% in % blasts in the BM aspirate or biopsy from baseline but >5%. Morphologic Leukemia-Free State (MLFS) response included ≤5% in % blasts in the BM aspirate or biopsy. (NCT02626338)
Timeframe: 1 year

,,,
InterventionParticipants (Count of Participants)
Composite complete remission (CR+CRh+CRi)MLFSClinical benefit (CRc+PR+MLFS)
All Subjects737
Arm A: HAM Chemotherapy323
Arm B: FLAG-Ida Chemotherapy404
Arm C: MEC Chemotherapy010

[back to top]

Overall Response Rate (ORR)

ORR, defined as CR+CRi, rates of patients treated with CLAG-M with sorafenib. (NCT02728050)
Timeframe: Up to 5 years

InterventionParticipants (Count of Participants)
Phase 1, Dose Level 16
Phase 1, Dose Level 26
Phase 1, Dose Level 38
Phase 1, Dose Level 45
Phase 1, Dose Level 59
Phase 1, Dose Level 67
Phase 2, Dose Level 634

[back to top]

Overall Survival (OS)

12-month overall survival (NCT02728050)
Timeframe: 12 months

Interventionpercentage of participants (Number)
CLAGM+Sorafenib Phase 286

[back to top]

Phase 1: Maximum Tolerated Dose (MTD)/Recommended Phase 2 Dose (RP2D) of Mitoxantrone

MTD/RP2D will be defined as the highest dose studied in which the incidence of dose-limiting toxicity (DLT) is < 33% assuming at least 6 patients have been treated at this dose. DLTs were defined as: 1) grade ≥3 non-hematologic toxicity lasting >48 hours leading to >7-day delay of the next cycle; 2) grade ≥4 non-hematologic toxicity if no recovery to grade ≤2 in 14 days (both excluding febrile neutropenia/ infection); 3) Absolute neutrophil count <500/ µL or platelet count <50,000/µL for >49 days after CLAGM+S without marrow evidence of AML. Doses were escalated up to dose level six if <2/6 patients out of each cohort of 6 had a DLT (some cohorts were expanded to 12 patients while awaiting completion of DLT monitoring period). The dose level at which dose escalation was stopped was the recommended phase 2 dose (RP2D). (NCT02728050)
Timeframe: First 28 days of treatment

Interventionmg/m^2 (Number)
CLAGM+Sorafenib Phase 118

[back to top]

Phase 1: Maximum Tolerated Dose (MTD)/Recommended Phase 2 Dose (RP2D) of Sorafenib

MTD/RP2D will be defined as the highest dose studied in which the incidence of dose-limiting toxicity (DLT) is < 33% assuming at least 6 patients have been treated at this dose. DLTs were defined as: 1) grade ≥3 non-hematologic toxicity lasting >48 hours leading to >7-day delay of the next cycle; 2) grade ≥4 non-hematologic toxicity if no recovery to grade ≤2 in 14 days (both excluding febrile neutropenia/ infection); 3) Absolute neutrophil count <500/ µL or platelet count <50,000/µL for >49 days after CLAGM+S without marrow evidence of AML. Doses were escalated up to dose level six if <2/6 patients out of each cohort of 6 had a DLT (some cohorts were expanded to 12 patients while awaiting completion of DLT monitoring period). The dose level at which dose escalation was stopped was the recommended phase 2 dose (RP2D). (NCT02728050)
Timeframe: First 28 days of treatment

Interventionmg BID (Number)
CLAGM+Sorafenib Phase 1400

[back to top]

Phase I and II: Rate of Minimal Residual Disease Negative (MRDneg) Complete Response (CR)

We will determine if the addition of sorafenib to CLAG-M improves the rate of MRDneg CR compared to our institution's historical control of CLAG-M alone in adults with newly-diagnosed AML/high-risk MDS. (NCT02728050)
Timeframe: 56 days (2 cycles of induction chemotherapy)

InterventionParticipants (Count of Participants)
Phase 1, Dose Level 13
Phase 1, Dose Level 26
Phase 1, Dose Level 38
Phase 1, Dose Level 44
Phase 1, Dose Level 59
Phase 1, Dose Level 67
Phase 2, Dose Level 631

[back to top]

Relapse-free Survival (RFS)

12-month relapse free survival (RFS) (NCT02728050)
Timeframe: 12 months

Interventionpercentage of participants (Number)
CLAGM+Sorafenib Phase 282

[back to top]

Number of Participants With Adverse Events

Will be assessed using National Cancer Institute Common Terminology Criteria for Adverse Events version 5.0. (NCT02728050)
Timeframe: Up to 5 years

InterventionParticipants (Count of Participants)
Phase 1, Dose Level 16
Phase 1, Dose Level 26
Phase 1, Dose Level 311
Phase 1, Dose Level 48
Phase 1, Dose Level 59
Phase 1, Dose Level 67
Phase 2, Dose Level 632

[back to top]

Event-free Survival (EFS)

12-month event free survival (NCT02728050)
Timeframe: 12 months

Interventionpercentage of participants (Number)
CLAGM+Sorafenib Phase 281

[back to top]

Feasibility of Early Allogeneic Hematopoietic Cell Transplant Assessed by Relapsed-free Survival 6 Months After Transplant

Success will be defined as observing a 40% of higher 6-month relapse-free survival among patients who received early transplant on study. (NCT02756572)
Timeframe: 6 months after early allogeneic HCT on study

InterventionParticipants (Count of Participants)
No relapse within 6 months post-HCT (feasibility success)Relapse within 6 months post-HCT (feasibility failure)
Received Early Allogeneic HCT on Study62

[back to top]

Overall Survival (OS) Among Patients Who Received Early Transplant.

Overall survival among patients who received early allogeneic HCT on study as estimated with the Kaplan-Meier method. (NCT02756572)
Timeframe: Up to 100 days post-transplant

InterventionPercentage of participants (Number)
Received Allogeneic HCT on Study91

[back to top]

Overall Survival (OS) Among Patients Who Did Not Receive Early Transplant

Overall survival among patients who did not receive early allogeneic HCT on study as estimated with the Kaplan-Meier method. (NCT02756572)
Timeframe: Up to 6 months after induction day 1

InterventionPercentage of participants (Number)
Did Not Receive Allogeneic HCT on Study62

[back to top]

Overall Survival (OS) Among Patients Who Did Not Receive Early Transplant

Overall survival among patients who did not receive early allogeneic HCT on study as estimated with the Kaplan-Meier method. (NCT02756572)
Timeframe: Up to 100 days after induction day 1

InterventionPercentage of participants (Number)
Did Not Receive Allogeneic HCT on Study75

[back to top] [back to top]

Factors That Distinguish Patients Who Received Early Transplant From Those Who Did Not - AGE

Patients who receive early transplant will be compared to those that don't using the Wilcoxon rank sum test for the quantitative variable of age. (NCT02756572)
Timeframe: From time of subject's study enrollment to time of subject's feasibility success assessment (i.e. when subject received transplant within 60 days or when it was determined subject would not proceed with transplant on study)

Interventionyears (Median)
Received Allogeneic HCT on Study55
Did Not Receive Allogeneic HCT on Study57

[back to top]

Event-free Survival (EFS) Among Patients Who Received Early Transplant

Event-free survival among patients who received early allogeneic HCT on study as estimated with the Kaplan-Meier method. Events included death, relapse, and grade 3-4 acute graft vs host disease. (NCT02756572)
Timeframe: Up to 6 months post-transplant

InterventionPercentage of participants (Number)
Received Allogeneic HCT on Study82

[back to top]

Demonstrate the Feasibility of Collecting Resource Utilization Data for Trial Participants

The amount of days of hospitalization (the major driver of costs within the first year) will be collected for resource utilization. (NCT02756572)
Timeframe: Within the first year of induction chemotherapy on study

Interventiondays (Median)
Treatment (Chemotherapy, HCT)49

[back to top]

Response Assessments After Early Allogeneic Hematopoietic Cell Transplant, Day 84

"Complete Remission (CR), defined as <5% blasts in bone marrow with hematologic recovery (ANC>1000/ul and platelets >100,000/ml).~CRi, defined as complete remission with insufficient hematologic recovery (ANC<1000/ul or platelets<100,000/ul).~CRp, defined as complete remission but platelets <100,000/ul. Minimal residual disease (MRD), defined as any detectable disease by flow cytometry, cytogenetics, FISH or PCR in a patient otherwise fulfilling remission criteria.~Morphologic leukemia-free state (MLFS), defined as <5% blasts in bone marrow with no hematologic recovery.~Relapse, defined as >5% blasts in bone marrow, flow cytometry, or manual differential; OR treatment for active relapsed disease." (NCT02756572)
Timeframe: Approximately 84 days after early allogeneic HCT

InterventionParticipants (Count of Participants)
CR with MRDCR without MRDCRi with MRDCRi without MRDMLFS with MRDMLFS without MRDRelapse
Received Allogeneic HCT on Study0402002

[back to top]

Response Assessments After Early Allogeneic Hematopoietic Cell Transplant, Day 28

"Complete Remission (CR), defined as <5% blasts in bone marrow with hematologic recovery (ANC>1000/ul and platelets >100,000/ml).~CRi, defined as complete remission with insufficient hematologic recovery (ANC<1000/ul or platelets<100,000/ul).~CRp, defined as complete remission but platelets <100,000/ul. Minimal residual disease (MRD), defined as any detectable disease by flow cytometry, cytogenetics, FISH or PCR in a patient otherwise fulfilling remission criteria.~Morphologic leukemia-free state (MLFS), defined as <5% blasts in bone marrow with no hematologic recovery.~Relapse, defined as >5% blasts in bone marrow, flow cytometry, or manual differential; OR treatment for active relapsed disease." (NCT02756572)
Timeframe: Approximately 28 days after early allogeneic HCT

InterventionParticipants (Count of Participants)
CR with MRDCR without MRDCRi with MRDCRi without MRDMLFS with MRDMLFS without MRDRelapse
Received Allogeneic HCT on Study0701000

[back to top]

Overall Survival (OS) Among Patients Who Received Early Transplant.

Overall survival among patients who received early allogeneic HCT on study as estimated with the Kaplan-Meier method. (NCT02756572)
Timeframe: Up to 6 months post-transplant

InterventionPercentage of participants (Number)
Received Allogeneic HCT on Study82

[back to top]

Relapse-free Survival (RFS) Among Patients Who Received Early Transplant

Relapse-free survival among patients who received early allogeneic HCT on study as estimated with the Kaplan-Meier method. (NCT02756572)
Timeframe: Up to 100 days post-transplant

InterventionPercentage of participants (Number)
Received Allogeneic HCT on Study91

[back to top]

Feasibility of Early Allogeneic Hematopoietic Cell Transplant Assessed by Enrollment and Incidence of Early Transplant

Success will be defined as enrollment of at least 30 patients with transplants occurring in 15 of these 30 (50%) within 60 days of enrollment or start of induction chemotherapy with G-CLAM, whichever is earlier. (NCT02756572)
Timeframe: Up to 60 days after start of chemotherapy

InterventionParticipants (Count of Participants)
Received allogeneic HCT on study within 60 days (feasibility success)Did not receive allogeneic HCT on study within 60 days (feasibility failure)
Treatment (Chemotherapy, HCT)921

[back to top]

Factors That Distinguish Patients Who Received Early Transplant From Those Who Did Not - GENDER

Patients who receive early transplant will be compared to those that don't using the Fisher's exact test for the categorical variables of gender. (NCT02756572)
Timeframe: From time of subject's study enrollment to time of subject's feasibility success assessment (i.e. when subject received transplant within 60 days or when it was determined subject would not proceed with transplant on study)

,
InterventionParticipants (Count of Participants)
FemaleMale
Did Not Receive Allogeneic HCT on Study1011
Received Allogeneic HCT on Study81

[back to top]

Demonstrate the Feasibility of Collecting Patient-reported Outcomes for Trial Participants

The amount of returned patient-reported outcome questionnaires will be summarized for each collection timepoint using percent collection from surviving patients for PRO timepoints. (NCT02756572)
Timeframe: Up to 12 months post-HCT

InterventionParticipants (Count of Participants)
Enrollment PROs returnedPost G-CLAM PROs returnedPre-HCT PROs returned6 months post-HCT PROs returned12 months post-HCT PROs returned
Treatment (Chemotherapy, HCT)2723843

[back to top] [back to top]

Relapse-free Survival (RFS) Among Patients Who Received Early Transplant

Relapse-free survival among patients who received early allogeneic HCT on study as estimated with the Kaplan-Meier method. (NCT02756572)
Timeframe: Up to 6 months post-transplant

InterventionPercentage of participants (Number)
Received Allogeneic HCT on Study82

[back to top]

Event-free Survival (EFS) Among Patients Who Received Early Transplant

Event-free survival among patients who received early allogeneic HCT on study as estimated with the Kaplan-Meier method. Events included death, relapse, and grade 3-4 acute graft vs host disease. (NCT02756572)
Timeframe: Up to 100 days post-transplant

InterventionPercentage of participants (Number)
Received Allogeneic HCT on Study91

[back to top]

Acute Graft Versus Host Disease Among Patients Who Received Early Transplant

Acute graft versus host disease (graded II, III, or IV) among patients who received early allogeneic HCT on study. (NCT02756572)
Timeframe: At day 100

InterventionParticipants (Count of Participants)
Received Allogeneic HCT on Study0

[back to top]

Number of Participants With Event-free Survival

(NCT02921061)
Timeframe: Up to 1 year

Interventionparticipants (Number)
Treatment (Decitabine 20 mg/m2 and G-CLAM)8

[back to top]

Number of Participants Who Achieved Remission (Complete Remission [CR]/CR With Incomplete Peripheral Blood Count Recovery [CRi])

(NCT02921061)
Timeframe: Up to 1 year

Interventionparticipants (Number)
Treatment (Decitabine 20 mg/m2 and G-CLAM)13

[back to top]

Number of Participants Experiencing Dose Limiting Toxicities (DLTs) at the Maximum Tolerated Dose (MTD) for Decitabine When Given Together With G-CLAM Toxicities (DLTs) (Phase I)

"Evaluated according to National Cancer Institute Common Terminology Criteria for Adverse Events version 4.0. MTD is defined as the highest dose studied in which the incidence of DLT is < 33%. Each participant was monitored for DLTs in the first 20 days of treatment. DLTs monitored included~any grade 3 non-hematologic toxicity lasting more than 48 hours that resulted in more than a 7 day delay of the subsequent treatment cycle (except for febrile neutropenia or infection)~any grade 4 or greater non-hematologic toxicity (except febrile neutropenia and infection unless a direct consequence of a treatment-related toxicity, and except constitutional symptoms if they recovered to grade 2 or less within 14 days)~lack of recovery of the absolute neutrophil count to 500/microliter or greater and lack of self-sustained platelet count of at least 50,000/microliter by treatment day +49 with no evidence of residual leukemia" (NCT02921061)
Timeframe: Up to 49 days

InterventionParticipants (Count of Participants)
Treatment (Decitabine 20 mg/m2 and G-CLAM)3

[back to top]

Number of Participants With Relapse-free Survival

(NCT02921061)
Timeframe: Up to 1 year

Interventionparticipants (Number)
Treatment (Decitabine 20 mg/m2 and G-CLAM)8

[back to top]

Number of Participants With Overall Survival

(NCT02921061)
Timeframe: Up to 1 year

Interventionparticipants (Number)
Treatment (Decitabine 20 mg/m2 and G-CLAM)9

[back to top]

Number of Participants With Minimal Residual Disease Negative (MRDneg) Complete Remission (Phase II)

Compared to historical controls of filgrastim, cladribine, cytarabine, and mitoxantrone hydrochloride (G-CLAM) alone. A Simon Minimax two-stage design will be used. (NCT02921061)
Timeframe: Up to 1 year

Interventionparticipants (Number)
Treatment (Decitabine 20 mg/m2 and G-CLAM)13

[back to top]

Number of Patients That Achieved ANC Recovery

The number of patients that achieved a neutrophil count of > 500/mm3 for 3 days within 45 of starting treatment (NCT03118466)
Timeframe: up to 45 days

InterventionParticipants (Count of Participants)
Lenalidomide and MEC Chemotherapy25

[back to top]

Number of Patients That Achieved Platelet Recovery

The number of patients that achieved a stable platelet count > 20,000/mm3 for 3 days within 45 days of starting treatment (NCT03118466)
Timeframe: up to 45 days

InterventionParticipants (Count of Participants)
Lenalidomide and MEC Chemotherapy27

[back to top]

Overall Survival

Overall survival is defined as time from diagnosis of disease until date of death or censored on the last known date alive if patients are still alive. (NCT03118466)
Timeframe: Up to 3 years

InterventionMonths (Median)
Lenalidomide and MEC Chemotherapy16

[back to top] [back to top]

Transfusion Support: Number of Red Blood Cell and Platelet Transfusions

Number of red blood cell and platelet transfusions received within the first 50 days of treatment (NCT03118466)
Timeframe: 50 days

InterventionNumber of Transfusions (Median)
Platelet TransfusionsRed Blood Cell Transfusions
Lenalidomide and MEC Chemotherapy79

[back to top]

Complete Response Rate

"Proportion of patients who have achieve CR or CRp after treatment.~Morphologic Complete Remission (CR): Defined as morphologic leukemia-free state, including <5% blasts in Bone Marrow aspirate with marrow spicules, no persistent extramedullary disease, ANC >1000/mm3 and platelet count >100,000/mm3.~Morphologic Complete Remission without platelet recovery (CRp): Defined as CR with the exception of platelet count < 100,000/mm3 (CRp)." (NCT03118466)
Timeframe: up to 45 days

InterventionParticipants (Count of Participants)
Lenalidomide and MEC Chemotherapy19

[back to top]

Complete Remission (CR)

Complete disappearance of all clinical evidence of disease (NCT03504410)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
CPI-613 + HD Cytarabine and Mitoxantrone20
Control (HAM) and Control Sub-groups (MEC and FLAG)22

[back to top]

Measurable Residual Disease (MRD) and Remission Rates: Alapasia (MRDneg)

"Will be estimated and 95% confidence intervals will be calculated. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors.~o Aplasia rate is defined in this protocol as frequency of patients without blood count recovery after chemotherapy and bone marrow examination showing hypocellularity not meeting cellularity criteria for morphologic leukemia free state (MLFS). MRD negative (MRDneg) status is defined as negative for leukemic markers by multiparameter flow cytometry.~Aplasia was defined as absence of tumoral cells but cellularity not meeting criteria for MLFS.~Statistical significance tests were not performed." (NCT03531918)
Timeframe: 90 days

InterventionParticipants (Count of Participants)
GO1 Dose Level Phase 10
GO3 Dose Level Includes Phase 1 and Phase 22

[back to top]

Measurable Residual Disease (MRD) and Remission Rates: CRi (MRDneg)

"Will be estimated and 95% confidence intervals will be calculated. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors.~Complete response with incomplete hematologic recovery (CRi) rate is defined as the frequency of patients achieving CRi, which is defined by the European LeukemiaNet 2017 guidelines as all CR criteria except for residual neutropenia (ANC <1.0 x 109/L [1000/mL]) or thrombocytopenia (platelet count <100 x 109/L [100,000/mL]). MRD negative (MRDneg) status is defined as negative for leukemic markers by multiparameter flow cytometry.~Aplasia was defined as absence of tumoral cells but cellularity not meeting criteria for MLFS.~Statistical significance tests were not performed." (NCT03531918)
Timeframe: 90 days

InterventionParticipants (Count of Participants)
GO1 Dose Level Phase 11
GO3 Dose Level Includes Phase 1 and Phase 27

[back to top]

Measurable Residual Disease (MRD) and Remission Rates: MLFS (MRDneg)

"Will be estimated and 95% confidence intervals will be calculated. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors.~Morphologic leukemia free state (MLFS) rate is defined as the frequency of patients achieving MLFS, which is defined by the European LeukemiaNet guidelines as bone marrow blasts <5%; absence of blasts with Auer rods; absence of extramedullary disease; no hematologic recovery required. At least 200 cells should be enumerated or cellularity should be at least 10%. MRD negative (MRDneg) status is defined as negative for leukemic markers by multiparameter flow cytometry.~Aplasia was defined as absence of tumoral cells but cellularity not meeting criteria for MLFS.~Statistical significance" (NCT03531918)
Timeframe: 90 days

InterventionParticipants (Count of Participants)
GO1 Dose Level Phase 10
GO3 Dose Level Includes Phase 1 and Phase 22

[back to top]

Overall Survival

OS was calculated for all participants and measured from initial trial therapy to death from any cause. Patients last known ot be alive were censored at date of last contact. Will be estimated using the Kaplan-Meier method. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors. (NCT03531918)
Timeframe: 3 years and 1 month

Interventionpercentage of participants (Number)
GO3 Dose Level60

[back to top]

Relapse-free Survival of GO3 Cohort

RFS was calculated for participants who achieved a complete remission (with or without count recovery; CR or CRi) and measured from the date remission to the first of relapse from CR/CRi or death from any cause. Patients last known to be alive in CR /CRi were censored at date of last contact. Will be estimated using the Kaplan-Meier method. Time to relapse will be estimated using non-parametric estimates of the cumulative incidence curve with death analyzed as a competing event. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors. (NCT03531918)
Timeframe: Up to 5 years. 2-year RFS reported.

Interventionpercentage of participants (Number)
GO3 Dose Level Includes Phase 1 and Phase 251

[back to top]

Event-free Survival (EFS) Rate (Phase 2)

A two-stage design will be used to evaluate the EFS. Patients treated at the maximum tolerated dose (MTD) from the phase 1 portion of the trial will be used in the phase 2 analysis. If censoring occurs, secondary analyses analyzing 6-month or 1-year EFS accounting for censoring will be done, including estimating 6-month or 1-year EFS using the Kaplan-Meier method. The first stage of the two-stage phase 2 design will evaluate 30 patients. If 20 or more of the first 30 patients are alive without event at 6-months after study registration, an additional 30 patients will be enrolled. If 46 or more of the 60 patients treated at the MTD are alive and without event at 6-months after study registration, the study will consider the regimen of interest for further investigation. Patients last known to be alive in CR were censored at date of last contact. (NCT03531918)
Timeframe: From the start of study treatment, assessed at 6 months and 1 year

Interventionpercent of participants (Number)
Event-free Survival (6 months)Event-free survival (12 months)
GO3 Dose Level Includes Phase 1 and Phase 27358

[back to top]

Measurable Residual Disease (MRD) Rates and Remission Rates: CR

"Will be estimated and 95% confidence intervals will be calculated. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors.~Complete response (CR) rate is defined as the frequency of patients achieving CR, which is defined by the European LeukemiaNet 2017 guidelines as bone marrow blasts <5%; absence of circulating blasts and blasts with Auer rods; absence of extramedullary disease; ANC ≥1.0 x 109/L (1000/mL); platelet count ≥100 x 109/L. (100 000/mL). MRD negative (MRDneg) status is defined as negative for leukemic markers by multiparameter flow cytometry.~Aplasia was defined as absence of tumoral cells but cellularity not meeting criteria for MLFS.~Statistical significance tests were not performed." (NCT03531918)
Timeframe: 90 days

,
InterventionParticipants (Count of Participants)
MRDnegMRDpos
GO1 Dose Level Phase 140
GO3 Dose Level Includes Phase 1 and Phase 2387

[back to top]

Maximum Tolerated Dose (MTD) of Gemtuzumab Ozogamicin (GO) When Added to GCLAM (Phase 1)

Defined as the highest dose studied in which the incidence of Dose Limiting Toxicity (DLT) is ≤33% (≤4 of 12 patients experiencing DLT), defined as any Grade 3 non-hematologic toxicity lasting >48 hours that results in >7-day delay of the subsequent treatment cycle, with the exception of febrile neutropenia or infection or toxicities secondary to febrile neutropenia or infection, or any Grade ≥4 non-hematologic toxicity except febrile neutropenia/infection (or toxicities secondary to febrile neutropenia or infection) unless felt to be a direct consequence of treatment-related toxicity (e.g. intestinal infection following mucosal barrier breakdown), and with the exception of constitutional symptoms if recovery to Grade ≤2 within 14 days. The National Cancer Institute Common Terminology Criteria for Adverse Events v5.0 will be used. (NCT03531918)
Timeframe: At time of count recovery, second cycle of treatment, response assessment or removal from protocol (at approximately 1 month).

InterventionParticipants (Count of Participants)
GO1 Dose Level Phase 1NA
GO3 Dose Level Includes Phase 1 and Phase 2NA

[back to top]

30-day All-cause Mortality

"As a summary of adverse events (captured on trial using the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 5.0), 30-day all cause mortality is reported as a percent of patients treated at the MTD/RP2D.~Will be estimated and 95% confidence intervals will be calculated. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors." (NCT03531918)
Timeframe: Up to 5 years. 30-day all-cause mortality is reported

Interventionproportion died on/before day 30 (Number)
GO3 Dose Level Includes Phase 1 and Phase 2.03

[back to top]

Measurable Residual Disease (MRD) and Remission Rates: CR/CRi

"Will be estimated and 95% confidence intervals will be calculated. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors.~Complete response (CR) + complete response with incomplete hematologic recovery (CRi) rate is defined as the frequency of patients achieving CR or CRi per the European LeukemiaNet 2017 criteria as defined above. MRD negative (MRDneg) status is defined as negative for leukemic markers by multiparameter flow cytometry.~Aplasia was defined as absence of tumoral cells but cellularity not meeting criteria for MLFS.~Statistical significance tests were not performed." (NCT03531918)
Timeframe: 90 days

InterventionParticipants (Count of Participants)
GO1 Dose Level Phase 15
GO3 Dose Level Includes Phase 1 and Phase 252

[back to top]

Number of Participants With Infusion Reactions (IRs)

An IR was an AE related to isatuximab typically with onset within 24 hours from the start of the isatuximab infusion and was reported by the investigator. (NCT03860844)
Timeframe: From the time of the first treatment administration (Day 1) up to 30 days after the last treatment (maximum duration of exposure of 13.1 weeks for B-ALL cohort, 10.7 weeks for T-ALL cohort and 7.1 weeks for AML cohort)

InterventionParticipants (Count of Participants)
B-cell Acute Lymphoblastic Leukemia (B-ALL)9
T-cell Acute Lymphoblastic Leukemia (T-ALL)5
Acute Myeloid Leukemia (AML)15

[back to top]

Overall Response Rate (ORR)

ORR:Percentage of participants with CR/CRi or partial response (PR) for blood and bone marrow disease based on NCCN guideline. CR: <5% blasts in BMA with spicules; no circulating blasts (ALL)/no blasts with Auer rods (AML) or extramedullary disease, no lymphadenopathy, splenomegaly, skin/gum infiltration/testicular mass/central nervous system involvement (ALL), trilineage hematopoiesis (ALL);ANC >=1000/mcL; platelets >100000/mcL; RBC transfusion independence. If the physician documented transfusion dependency related to study treatment;not to participant's underlying disease, CRi was reported. CRi met the same criteria as CR, except neutrophils and/or platelets recovery (ANC <1000/mcL or platelets <100000/mcL). PR: >50% decrease in the sum of the product of the greatest perpendicular diameters of the mediastinal enlargement. For participants with a previous positive positron emission tomography (PET) scan, a post-treatment PET was to be positive in at least 1 previously involved site. (NCT03860844)
Timeframe: From enrollment until the primary analysis completion date of 12 Sep 2022; the median duration of exposure was approximately 7 weeks

Interventionpercentage of participants (Number)
B-cell Acute Lymphoblastic Leukemia (B-ALL)52.0
T-cell Acute Lymphoblastic Leukemia (T-ALL)54.5
Acute Myeloid Leukemia (AML)65.2

[back to top]

Percentage of Participants With Complete Response (CR) Rate

The complete response rate (CR + CRi [complete response with incomplete peripheral recovery]) was defined as the percentage of participants achieving complete response (CR + CRi) assessed by the investigator per National Comprehensive Cancer Network (NCCN) guidelines version 1.2018 criteria. CR was defined as <5% blasts in a bone marrow aspirate (BMA) with spicules; no circulating blasts (ALL)/no blasts with Auer rods (AML) or extramedullary disease, no lymphadenopathy, splenomegaly, skin/gum infiltration/testicular mass/central nervous system involvement (ALL), trilineage hematopoiesis (ALL); Absolute neutrophil count (ANC) >=1000/microliter (mcL); platelets >100000/mcL; red blood cell transfusion independence. If the physician documented transfusion dependency related to study treatment and not to the participant's underlying disease, CRi was reported. CRi met the same criteria as for CR, except neutrophils and/or platelets recovery (ANC <1000/mcL or platelets <100000/mcL). (NCT03860844)
Timeframe: From enrollment until the primary analysis completion date of 12 Sep 2022; the median duration of exposure was approximately 7 weeks

Interventionpercentage of participants (Number)
B-cell Acute Lymphoblastic Leukemia (B-ALL)52.0
T-cell Acute Lymphoblastic Leukemia (T-ALL)45.5
Acute Myeloid Leukemia (AML)60.9

[back to top]

AML: AUC of Isatuximab

Plasma samples were collected at specified timepoints to determine the AUC of isatuximab. (NCT03860844)
Timeframe: From Week 0 to Week 1, Week 0 to Week 3, and Week 0 to Week 8

Interventionmg*h/L (Mean)
Week 0 to Week 1Week 0 to Week 3Week 0 to Week 8
Acute Myeloid Leukemia (AML)28592130862291962

[back to top]

AML: Ceoi of Isatuximab

Ceoi is the plasma concentration observed at the end of intravenous infusion of isatuximab. (NCT03860844)
Timeframe: At end of infusion on Cycle 1 Days 1 and 15

Interventionmcg/mL (Mean)
Cycle 1: Day 1Cycle 1: Day 15
Acute Myeloid Leukemia (AML)363562

[back to top] [back to top]

B-ALL and T-ALL: Area Under the Concentration Time Curve (AUC) of Isatuximab

Plasma samples were collected at specified timepoints to determine the AUC of isatuximab. (NCT03860844)
Timeframe: From Week 0 to Week 1, Week 0 to Week 5, and Week 0 to Week 10

,
Interventionmg*hour (h)/Liter (L) (Mean)
Week 0 to Week 1Week 0 to Week 5Week 0 to Week 10
B-cell Acute Lymphoblastic Leukemia (B-ALL)31703299071582686
T-cell Acute Lymphoblastic Leukemia (T-ALL)29057289167540375

[back to top]

B-ALL and T-ALL: Concentrations at the End of Infusion (Ceoi) of Isatuximab

Ceoi is the plasma concentration observed at the end of intravenous infusion of isatuximab. (NCT03860844)
Timeframe: At end of infusion on Cycle 1 Days 1 and 29

,
Interventionmcg/mL (Mean)
Cycle 1: Day 1Cycle 1: Day 29
B-cell Acute Lymphoblastic Leukemia (B-ALL)452835
T-cell Acute Lymphoblastic Leukemia (T-ALL)259745

[back to top] [back to top]

CD38 Receptor Occupancy

Blood samples were collected to assess CD38 receptor occupancy as a pharmacodynamics marker. It was assessed across complete responders and non-complete responders. Multicolor flow cytometry assay was validated for CD38 receptor occupancy (CD38RO) quantification, based on the use of two murine monoclonal antibodies (MAbs), one competing with SAR650984 to determine the number of free CD38 receptors (MAb1) and one recognizing a different binding epitope on CD38 to measure the total number of receptors (MAb2) at the cell surface of the cancer cells. Cells were tagged with either MAb1 (Tube #1) or MAb2 (Tube #2). The percentage RO was calculated using the following equation: % CD38RO = [(sABC MAb2 - sABC MAb1)/sABC MAb2] X 100. (NCT03860844)
Timeframe: Pre-dose on Day 15

Interventionpercent receptor occupancy (Mean)
Blood plasma cells: Non CR/CRi;Blood NK cells: CR/CRiBlood NK cells: Non CR/CRi
B-cell Acute Lymphoblastic Leukemia (B-ALL)44.055.661.3

[back to top]

CD38 Receptor Occupancy

Blood samples were collected to assess CD38 receptor occupancy as a pharmacodynamics marker. It was assessed across complete responders and non-complete responders. Multicolor flow cytometry assay was validated for CD38 receptor occupancy (CD38RO) quantification, based on the use of two murine monoclonal antibodies (MAbs), one competing with SAR650984 to determine the number of free CD38 receptors (MAb1) and one recognizing a different binding epitope on CD38 to measure the total number of receptors (MAb2) at the cell surface of the cancer cells. Cells were tagged with either MAb1 (Tube #1) or MAb2 (Tube #2). The percentage RO was calculated using the following equation: % CD38RO = [(sABC MAb2 - sABC MAb1)/sABC MAb2] X 100. (NCT03860844)
Timeframe: Pre-dose on Day 15

Interventionpercent receptor occupancy (Mean)
Blood plasma cells: CR/CRiBlood plasma cells: Non CR/CRi;Blood NK cells: CR/CRiBlood NK cells: Non CR/CRi
T-cell Acute Lymphoblastic Leukemia (T-ALL)40.555.066.770.0

[back to top]

Cluster of Differentiation (CD)38 Receptor Density

"Blood samples were collected to assess CD38 receptor density as a predictive biomarker. It was assessed across complete responders and non-complete responders. The Antibody Binding Capacity (ABC) was calculated using the following equation: ABC = 10^(Logarithm(Mean Fluorescence Intensity)*a+b) where a was the slope and b was the Y-intercept of the calibration curve equation. Specific and absolute quantitative values (specific antibody-binding capacity [sABC]) of binding of the selected antibodies were calculated after subtraction of the negative isotypic immunoglobulin G (IgG) control." (NCT03860844)
Timeframe: Pre-dose on Day 1

,,
InterventionsABC (Mean)
Blood blast cells: CR/CRiBlood blast cells: Non CR/CRi;Blood immune cells (Natural Killer [NK] cells): CR/CRiBlood immune cells (NK cells): Non CR/CRi
Acute Myeloid Leukemia (AML)19502.09815.011220.322530.0
B-cell Acute Lymphoblastic Leukemia (B-ALL)20345.631080.013506.216650.0
T-cell Acute Lymphoblastic Leukemia (T-ALL)12780.022952.022639.033859.0

[back to top]

Number of Participants With Treatment-Emergent Adverse Events (TEAEs) and Treatment-Emergent Serious Adverse Events (TESAEs)

An AE was defined as any untoward medical occurrence in a participant temporally associated with the use of study treatment, whether or not considered related to the study treatment. SAEs were any untoward medical occurrence that at any dose: resulted in death, was life-threatening, required inpatient hospitalization or prolongation of existing hospitalization, resulted in persistent or significant disability/incapacity, was a congenital anomaly/birth defect, was a medically important event. TEAEs were defined as an AE which occurred after the first dose of study treatment administration until the last dose plus 30 days, or until the start of hematological recovery period or a new anti-leukemia/lymphoma therapy, whichever occurred first. (NCT03860844)
Timeframe: From the time of the first treatment administration (Day 1) up to 30 days after the last treatment (maximum duration of exposure of 13.1 weeks for B-ALL cohort, 10.7 weeks for T-ALL cohort and 7.1 weeks for AML cohort)

,,
InterventionParticipants (Count of Participants)
Any TEAEAny TESAE
Acute Myeloid Leukemia (AML)2616
B-cell Acute Lymphoblastic Leukemia (B-ALL)2719
T-cell Acute Lymphoblastic Leukemia (T-ALL)1312

[back to top]