cladribine profile

Cladribine is a purine nucleoside analog that inhibits DNA synthesis and repair by being incorporated into DNA. It is primarily used to treat hairy cell leukemia, a rare type of leukemia, and is also being investigated for other diseases such as multiple sclerosis and chronic lymphocytic leukemia. The synthesis of cladribine involves multiple chemical steps, beginning with the modification of adenosine, a naturally occurring nucleoside. Cladribine is a potent immunosuppressant, which means it weakens the immune system. This is why it is effective in treating hairy cell leukemia, as the leukemia cells are often targeted by the immune system. Its importance lies in its effectiveness against diseases that are difficult to treat with other medications. Research continues to explore its potential for treating other autoimmune diseases and cancers.'

ID Source	ID
PubMed CID	20279
CHEMBL ID	1619
CHEBI ID	567361
SCHEMBL ID	3775
MeSH ID	M0026332

Synonym
AC-7591
chlorodeoxyadenosine
nsc 105014
2-chloro-6-amino-9-(2-deoxy-beta-d-erythropentofuranosyl)purine
rwj 26251
brn 0624220
cladarabine
MLS001077345
AB00382963-17
MLS000028484
smr000058553
2-chloro-2'-deoxyadenosine
CL9 ,
MLS000028377 ,
(2r,3s,5r)-5-(6-amino-2-chloro-purin-9-yl)-2-(hydroxymethyl)tetrahydrofuran-3-ol
adenosine, 2-chloro-2'-deoxy
4291-63-8
cladribine ,
adenosine, 2-chloro-2'-deoxy-
rwj-26251
2cda
2-cda
nsc-105014
leustatin
2 chlorodeoxyadenosine
2-chloro-2'-deoxyadenosine, antileukemic
MLS000759397
cldado
(2r,3s,5r)-5-(6-amino-2-chloropurin-9-yl)-2-(hydroxymethyl)oxolan-3-ol
2clado
2-chloro-deoxyadenosine
DB00242
2-chloro-2'-deoxy-beta-adenosine
(2r,3s,5r)-5-(6-amino-2-chloro-9h-purin-9-yl)-2-(hydroxymethyl)tetrahydrofuran-3-ol
2-chloro-6-amino-9-(2-deoxy-beta-d-erythro-pentofuranosyl)purine
leustatin (tn)
mavenclad (tn)
cladribine (jan/usp/inn)
D01370
NCGC00164384-01
2-chlorodeoxyadenosine
NCGC00022567-05
HMS2052K13
movectro
mylinax
rwj-26251-000
litak
CHEMBL1619
cladaribine
nsc-05014
nsc-105014-f
cladribinum
cladribina
CHEBI:567361 ,
NCGC00022567-06
NCGC00022567-07
hsdb 7564
47m74x9yt5 ,
unii-47m74x9yt5
ccris 9374
cladribine [usan:usp:inn:ban]
NCGC00254518-01
tox21_300596
2-chloro-2'-deoxyadenosine;(2r,3s,5r)-5-(6-amino-2-chloro-purin-9-yl)-2-(hydroxymethyl)tetrahydrofuran-3-ol
A826062
BCP9000538
MLS001424194
cas-4291-63-8
tox21_110834
dtxsid8022828 ,
dtxcid602828
HMS2232C23
CCG-101116
NCGC00022567-08
cladribine [vandf]
cladribine [hsdb]
cladribine [jan]
cladribine [mi]
cladribine [ema epar]
cladribine [usp-rs]
cladribine [orange book]
cladribine [usp impurity]
cladribine [usan]
cladribine [inn]
cladribine [who-dd]
cladribine [usp monograph]
cladribine [ep monograph]
mavenclad
cladribine [mart.]
AKOS015854898
AKOS015892544
(2r,3s,5r)-5-(6-amino-2-chloro-9h-purin-9-yl)-2-(hydroxymethyl)oxolan-3-ol
gtpl4799
HY-13599
CS-2057
2-chloro-2'-deoxy-adenosine
6-amino-2-chloro-9-(2-deoxy-beta-erythropentofuranosyl)purine
PTOAARAWEBMLNO-KVQBGUIXSA-N
6-amino-2-chloro-9-(2-deoxy-beta-d-erythro-pentofuranosyl)purine
NC00366
SCHEMBL3775
bdbm38920
cid_20279
(2r,3s,5r)-5-(6-amino-2-chloropurin-9-yl)-2-(hydroxymethyl)oxalan-3-ol
OPERA_ID_1191
AB00382963_19
mfcd00153939
2-chloro-2 inverted exclamation marka-deoxyadenosine
sr-01000003063
SR-01000003063-10
cladribine, united states pharmacopeia (usp) reference standard
cladribine for peak identification, european pharmacopoeia (ep) reference standard
cladribine, european pharmacopoeia (ep) reference standard
SR-01000003063-7
HMS3715F17
SW197746-4
Q414030
24757-90-2
AS-12366
BCP02868
AMY22140
BP-25407
cladribine- bio-x
BC164318
cladribine for peak identification

Excerpt	Reference	Relevance
"Cladribine in tablets is a cost-saving alternative for treatment of patients with highly active multiple sclerosis compared to the current treatment practice. "	( [Pharmacoeconomic aspects of using cladribine (in tablets) for treatment of adult patients with remitting multiple sclerosis]. Avxentyev, NA; Davydovskaya, MV; Frolov, MY; Klabukova, DL; Makarova, YV, 2021)	2.34
"Cladribine (CLAD) is a deoxyadenosine analogue prodrug which is given in multiple sclerosis (MS) as two short oral treatment courses 12 months apart. "	( Cladribine Alters Immune Cell Surface Molecules for Adhesion and Costimulation: Further Insights to the Mode of Action in Multiple Sclerosis. Akgün, K; Feige, J; Haschke-Becher, E; Hoepner, L; Moser, T; Schwenker, K; Seiberl, M; Sellner, J; Ziemssen, T, 2021)	3.51
"Cladribine is a synthetic deoxyadenosine analogue with demonstrated efficacy in patients with relapsing-remitting multiple sclerosis (MS). "	( Immunomodulatory Effects Associated with Cladribine Treatment. Boschert, U; Calvo-Barreiro, L; Comabella, M; Eixarch, H; Espejo, C; Fissolo, N; Montalban, X, 2021)	2.33
"Cladribine (2CdA) is a synthetic chlorinated purine nucleoside analogue which acts as a pro-drug requiring intracellular phosphorylation to be activated. "	( 2-Chlorodeoxyadenosine (Cladribine) preferentially inhibits the biological activity of microglial cells. Aybar, F; Correale, J; Eugenia Samman, M; Julia Perez, M; María Pasquini, J; Marrodan, M; Silvina Marcora, M, 2022)	2.47
"Oral cladribine is a novel treatment for Multiple Sclerosis (MS). "	( Anti-HBs titers are not decreased after treatment with oral Cladribine in patients with Multiple Sclerosis vaccinated against Hepatitis B virus. Cola, G; Di Mauro, G; Grimaldi, A; Landi, D; Marfia, GA; Mataluni, G; Nicoletti, CG, 2022)	1.48
"Cladribine is a synthetic deoxyadenosine analogue approved for the treatment of highly active relapsing multiple sclerosis (RMS). "	( Immunological consequences of cladribine treatment in multiple sclerosis: A real-world study. Aslan, D; Hackert, J; Hagenacker, T; Huntemann, N; Kleinschnitz, C; Kleinschnitz, K; Meuth, SG; Pawlitzki, M; Pfeuffer, S; Pul, R; Rolfes, L; Ruck, T; Schmidt, M; Skuljec, J; Su, C, 2022)	2.45
"Cladribine is a synthetic purine nucleoside analog that induces cell death of lymphocytes and oral cladribine treatment leads to a long-lasting disease stabilization, potentially attributable to immune reconstitution."	( Cladribine Treatment for MS Preserves the Differentiative Capacity of Subsequently Generated Monocytes, Whereas Its Administration Aprico, A; Ayoub, S; Binder, MD; Johnson, LJ; Kilpatrick, TJ; Medeiros-Furquim, T; Nwoke, E, 2022)	2.89
"Cladribine is a purine analog used in first-line treatment of hairy cell leukemia and in relapsed/refractory chronic lymphocytic anemia. "	( Increased risk of severe cutaneous adverse reactions when cladribine is used together with other medications with a propensity for skin reactions. Haynes, J; Jackson, M; Smugar, SS, 2022)	2.41
"Oral cladribine is a highly effective pulsed selective immune reconstitution therapy licensed for relapsing multiple sclerosis (RMS) since 2017. "	( Long-term management of multiple sclerosis patients treated with cladribine tablets beyond year 4. Bayas, A; Kallmann, B; Kleinschnitz, C; Linker, R; Mäurer, M; Meuth, SG; Rieckmann, P; Wattjes, MP, 2022)	1.47
"Cladribine tablets are a newly launched short course oral treatment approved for high disease activity (HDA) relapsing multiple sclerosis (RMS). "	( Economic evaluation of cladribine tablets in high disease activity (HDA) relapsing multiple sclerosis (RMS) patients in Lebanon. Fleifel, L; Khamis, C; Koussa, S; Matni, M; Mohamed, O; Sharifi, S; Yamout, B, 2022)	2.47
"Cladribine tablets are a cost-effective and a budget-saving treatment option for the treatment of HDA-RMS patients in Lebanon from the NSSF perspective."	( Economic evaluation of cladribine tablets in high disease activity (HDA) relapsing multiple sclerosis (RMS) patients in Lebanon. Fleifel, L; Khamis, C; Koussa, S; Matni, M; Mohamed, O; Sharifi, S; Yamout, B, 2022)	2.47
"Cladribine is an effective immunomodulatory treatment used for relapsing forms of multiple sclerosis (MS)."	( Cladribine treatment for highly active multiple sclerosis: Real-world clinical outcomes for years 3 and 4. Achiron, A; Didikin, M; Dreyer-Alster, S; Flechter, S; Harari, G; Magalashvili, D; Mandel, M, 2022)	3.61
"Cladribine is a synthetic purine analogue that interferes with DNA synthesis and repair next to disrupting cellular proliferation in actively dividing lymphocytes. "	( Cladribine treatment improves cortical network functionality in a mouse model of autoimmune encephalomyelitis. Bock, S; Budde, T; Cerina, M; Dobelmann, V; Duarte-Silva, E; Fazio, L; Gothan, KSS; Gruchot, J; Henes, A; Herrmann, AM; Hundehege, P; Huntemann, N; Kremer, D; Küry, P; Meuth, SG; Müntefering, T; Narayanan, V; Nelke, C; Pfeuffer, S; Raba, K; Räuber, S; Rolfes, L; Ruck, T; Schroeter, CB; Wiendl, H, 2022)	3.61
"Cladribine is a rational candidate steroid-sparing treatment for presumed neurologic autoimmune conditions such as CLIPPERS."	( CLIPPERS Responsive to Cladribine as a Durable Steroid-Sparing Agent. Atkins, HL; Bergman, H; Brooks, J; Freedman, MS; Thebault, S, 2023)	2.66
"Cladribine is a nucleoside analogue interfering with synthesis and repair of DNA. "	( Real-world experience of cladribine treatment in relapsing-remitting multiple sclerosis: A Danish nationwide study. Heick, A; Joensen, H; Magyari, M; Pihl, CE; Pontieri, L; Rasmussen, PV; Ratzer, R; Schäfer, J; Sellebjerg, F; Sorensen, PS, 2023)	2.66
"Cladribine is a selective and oral immunological reconstitution treatment, approved in Europe for very active multiple sclerosis (MS) with relapses. "	( Safety and Effectiveness of Cladribine in Multiple Sclerosis: Real-World Clinical Experience From 5 Tertiary Hospitals in Portugal. Abreu, P; Brum, M; Capela, C; de Sá, J; Dias, R; Ferreira, J; Guerreiro, R; Ladeira, F; Leitão, L; Sá, MJ; Salgado, V; Santos, M; Sequeira, J, )	1.87
"Cladribine tablets are a highly effective immune reconstitution therapy licensed for treating relapsing multiple sclerosis (RMS) in Europe since 2017. "	( Safety and effectiveness of cladribine tablets for multiple sclerosis: Results from a single-center real-world cohort. Aerts, S; Khan, H; Peeters, LM; Popescu, V; Severijns, D; Van Wijmeersch, B, 2023)	2.65
"Cladribine is an oral disease-modifying drug authorized by the European Medicine Agency for the treatment of highly active relapsing multiple sclerosis (MS)."	( Cladribine tablets in people with relapsing multiple sclerosis: A real-world multicentric study from southeast European MS centers. Abičić, A; Adamec, I; Barun, B; Bašić Kes, V; Brecl Jakob, G; Cindrić, I; Drulović, J; Gabelić, T; Gomezelj, S; Gržinčić, T; Habek, M; Klivényi, P; Krbot Skorić, M; Lazibat, I; Mesaroš, Š; Pekmezović, T; Radulović, L; Rajda, C; Rimac, J, 2023)	3.8
"Cladribine monotherapy is an effective and well-tolerated therapeutic option for XD patients. "	( Clinical and pathological evaluation of cladribine treatment response in a case series of patients with xanthoma disseminatum. Bi, Y; Huang, Y; Li, J; Li, L; Tuan, H; Wang, B; Wang, Y; Yin, H; Yu, F; Zhao, Y; Zhou, EY, 2023)	2.62
"Cladribine is a purine nucleoside found to enhance toxic amyloid protein and cause memory impairment. "	( Cladribine induces apoptosis, neuroinflammation, mitochondrial oxidative stress, tau phosphorylation and Aβ (1-42) pathway in the hippocampus: An in vivo approach. Aran, KR; Gupta, GD; Singh, S, 2023)	3.8
"Cladribine is a nucleoside analogue widely used in the pharmaceutical industry for the treatment of several neoplasms, including hairy-cell leukemia among others. "	( Biotransformation of cladribine using a stabilized biocatalyst in calcium alginate beads. Britos, CN; Lapponi, MJ; Rivero, CW; Trelles, JA, 2020)	2.32
"Cladribine seems to be a safe and effective emergency therapy in a population of patients with refractory MG."	( Cladribine in myasthenia gravis: a pilot open-label study. Baranowski, D; Korchut, A; Rejdak, K; Szklener, S, 2020)	3.44
"Cladribine is a prodrug, a synthetic analogue of deoxyadenosine, approved for use as selective immune reconstitution therapy in very active recurring multiple sclerosis in adults."	( [Recommendations for the use of cladribine tablets in recurring multiple sclerosis]. Álvarez-Cermeño, JC; Estrada-Pérez, V; Fernández, O; García-Merino, JA; Izquierdo, G; Oreja-Guevara, C; Rodríguez-Antigüedad, A; Saiz, A, 2019)	2.24
"Cladribine is a new oral treatment for relapsing-remitting multiple sclerosis."	( [Neurology 2019]. Benninger, D; Diserens, K; Hirt, L; Kuntzer, T; Michel, P; Novy, J; Pantazou, V; Pasquier, RD; Perrenoud, M; Rossetti, AO; Rouaud, O; Ryvlin, P; Theaudin, M, 2020)	1.28
"Cladribine is an approved drug for the treatment of highly active multiple sclerosis. "	( Lichenoid rash: A new side effect of oral Cladribine. Aruta, F; Costa, C; Iodice, R; Iovino, A; Manganelli, F, 2020)	2.27
"Cladribine is an antimetabolite used for the treatment of relapsing-remitting multiple sclerosis. "	( Cladribine transfer into human milk: A case report. Baker, T; Ciplea, AI; Datta, P; Gold, R; Hale, TW; Hellwig, K; Rewers-Felkins, K, 2021)	3.51
"Cladribine is a purine nucleoside analog used to treat B-cell chronic lymphocytic leukemia and hairy cell leukemia, also functions as an inhibitor of DNA synthesis to block the repair of the damaged DNA. "	( Cladribine Induces ATF4 Mediated Apoptosis and Synergizes with SAHA in Diffuse Large B-Cell Lymphoma Cells. Gao, X; Jiao, J; Li, Z; Liu, M; Qin, Y; Sang, W; Song, X; Sun, C; Sun, X; Tian, Y; Xu, K; Xu, L; Yan, D; Yang, P; Zeng, L; Zhu, F, 2020)	3.44
"Oral cladribine is a highly effective pulsed selective immune reconstitution therapy licensed for relapsing multiple sclerosis. "	( Long-term management of multiple sclerosis patients treated with cladribine tablets: an expert opinion. Bayas, A; Kallmann, B; Kleinschnitz, C; Linker, R; Mäurer, M; Meuth, SG; Rieckmann, P, 2020)	1.31
"Cladribine is a highly effective, recently available treatment in multiple sclerosis. "	( Normal antibody response after COVID-19 during treatment with cladribine. Celius, EG, 2020)	2.24
"Cladribine is a purine nucleoside analog initially developed in the 1970s as a treatment for various blood cancers. "	( The Development of Cladribine Tablets for the Treatment of Multiple Sclerosis: A Comprehensive Review. Coyle, PK; Dangond, F; Galazka, A; Grosso, M; Leist, TP; Rammohan, K; Sylvester, E, 2020)	2.33
"Cladribine (Cd) is a purine nucleoside analogue which in an oral formulation is approved for treatment of patients with multiple sclerosis (MS). "	( Cladribine inhibits secretion of pro-inflammatory cytokines and phagocytosis in human monocyte-derived M1 macrophages in-vitro. Gad, M; Larsen, J; Mathiesen, CBK; Pedersen, AE; Rudjord-Levann, AM; Sellebjerg, F, 2021)	3.51
"Cladribine is an approved selective immune reconstitution therapy for relapsing-remitting MS (RRMS). "	( The development and impact of cladribine on lymphoid and myeloid cells in multiple sclerosis. Butzkueven, H; Monif, M; O'Brien, T; Stankovich, J; Voo, VTF, 2021)	2.35
"Oral cladribine is an approved disease-modifying drug for the treatment of relapsing multiple sclerosis. "	( Autoimmune glomerulonephritis in a multiple sclerosis patient after cladribine treatment. Eisenberger, U; Fleischer, M; Gäckler, A; Hackert, J; Hagenacker, T; Kleinschnitz, C; Krämer, J; Kribben, A; Meuth, SG; Pfeuffer, S; Pfister, F; Pul, R; Ruck, T; Schönfelder, K; Schuh, H; Skuljec, J, 2021)	1.37
"Cladribine tablets are a dominant treatment option for patients with HDA-RRMS from the payer perspective in the KSA."	( Economic Evaluation of Cladribine Tablets in Patients With High Disease Activity-Relapsing-Remitting Multiple Sclerosis in the Kingdom of Saudi Arabia. Al Malik, Y; Al-Johani, A; Al-Saqa'aby, M; Alarieh, R; Bohlega, S; Elboghdady, A; Mahajan, K; Mohamed, O; Mughari, MK, 2021)	2.37
"Cladribine is an effective therapy for relapse-onset multiple sclerosis. "	( Cladribine versus fingolimod, natalizumab and interferon β for multiple sclerosis. Barnett, M; Butler, E; Butzkueven, H; Duquette, P; Fabis-Pedrini, M; Ferraro, D; Girard, M; Grammond, P; Grand'Maison, F; Havrdova, E; Hodgkinson, S; Horakova, D; Hupperts, R; Jokubaitis, V; Kalincik, T; Kermode, A; Lechner-Scott, J; Lugaresi, A; McCombe, P; Prat, A; Prevost, J; Shaw, C; Slee, M; Sola, P; Solaro, C; Spelman, T; Terzi, M; Trojano, M, 2018)	3.37
"Cladribine is a purine nucleoside analogue that selectively depletes peripheral lymphocytes without a major impact on cells of the innate immune system. "	( Cladribine to Treat Relapsing Forms of Multiple Sclerosis. Giovannoni, G, 2017)	3.34
"Cladribine tablets are an important addition to the therapeutic landscape in RMS. "	( [Cladribine tablets : Oral immunotherapy of relapsing-remitting multiple sclerosis with short yearly treatment periods]. Aktas, O; Hartung, HP; Meuth, SG; Ruck, T, 2018)	2.83
"Cladribine tablets are a cost-effective alternative to alemtuzumab and natalizumab in the treatment of HDA-RRMS from the perspective of the NHS in England."	( Cost-effectiveness of cladribine tablets, alemtuzumab, and natalizumab in the treatment of relapsing-remitting multiple sclerosis with high disease activity in England. Harty, G; Hettle, R; Wong, SL, 2018)	2.24
"Cladribine is a safe and effective form of induction therapy for relapsing MS. "	( Cladribine: mechanisms and mysteries in multiple sclerosis. Ammoscato, F; Baker, D; Giovannoni, G; Jacobs, BM; Schmierer, K, 2018)	3.37
"Cladribine is a useful immunosuppressive drug for the treatment of autoimmune diseases, leukemias and multiple sclerosis (MS). "	( Expression of caspase 1 and histomorphology of lung after cladribine treatment. Chylińska-Wrzos, P; Jodłowska-Jędrych, B; Lis-Sochocka, M; Wawryk-Gawda, E, 2019)	2.2
"Cladribine is an oral immunosuppressant recently approved in Europe for the treatment of highly active relapsing multiple sclerosis."	( [Cladribine in the treatment of relapsing multiple sclerosis]. Ramio-Torrenta, L; Robles-Cedeno, R, 2018)	2.11
"Oral cladribine is a novel treatment for relapsing multiple sclerosis (MS). "	( Potential mechanisms of action related to the efficacy and safety of cladribine. Baker, D; Herrod, SS; Pryce, G; Schmierer, K, 2019)	1.26
"Cladribine Tablets is a cost-effective treatment, compared to fingolimod, for the treatment of RMS with high disease activity."	( Cost-effectiveness of Cladribine Tablets and fingolimod in the treatment of relapsing multiple sclerosis with high disease activity in Spain. Polanco, A; Poveda, JL; Rubio-Rodríguez, D; Rubio-Terrés, C; Torres, C; Trillo, JL, 2020)	2.32
"Cladribine is a purine nucleoside analog developed to treat lymphoid malignancies. "	( Cladribine exerts an immunomodulatory effect on human and murine dendritic cells. Hubo, M; Jolivel, V; Jonuleit, H; Kraus, SH; Lerch, S; Luessi, F; Paterka, M; Poisa-Beiro, L; Trinschek, B; Zipp, F, 2014)	3.29
"Cladribine is a purine nucleoside analog which initiates the apoptotic mechanism within cells. "	( Intrinsic apoptosis pathway in fallopian tube epithelial cells induced by cladribine. Bulak, K; Chylińska-Wrzos, P; Jodłowska-Jędrych, B; Lis-Sochocka, M; Wawryk-Gawda, E, 2014)	2.08
"Cladribine is a cytotoxic drug which ameliorates the clinical course of relapsing-remitting multiple sclerosis. "	( Cladribine Exposure Results in a Sustained Modulation of the Cytokine Response in Human Peripheral Blood Mononuclear Cells. Bragado Alonso, S; Bröker, BM; Dressel, A; Korsen, M; Peix, L, 2015)	3.3
"Cladribine is a purine substrate analogue that is toxic to lymphocytes and monocytes with good hematoencephalic penetration."	( Successful treatment with cladribine of Erdheim-Chester disease with orbital and central nervous system involvement developing after treatment of Langerhans cell histiocytosis. Antić, B; Jovandić, S; Knezević-Usaj, S; Magić, Z; Perić, P; Radić-Tasić, O; Radovinović-Tasić, S; Sekulović, L; Tarabar, O; Tukić, L; Vasić-Vilić, J, 2016)	1.46
"Cladribine is an effective therapy for these patients and leads to complete response in most of the patients."	( Hairy cell leukemia: clinical, pathological and ultrastructural findings in Asian-Indians. Chatterjee, T; Choudhry, VP; Kumar, R; Mahapatra, M; Naithani, R; Panigrahi, I; Pati, HP; Saxena, R; Wadhwa, S, )	0.85
"Cladribine, which is a preferential lymphocyte-depleting therapy, has the potential to be the first oral agent available for the treatment of relapsing forms of MS."	( Cladribine tablets' potential in multiple: sclerosis treatment. Costello, K; Sipe, JC, 2008)	2.51
"Cladribine is an immunosuppressive drug currently investigated in a phase-III clinical trial for relapsing-remitting MS."	( Cladribine impedes in vitro migration of mononuclear cells: a possible implication for treating multiple sclerosis. Dehmel, T; Döbert, M; Kieseier, BC; Kopadze, T; Leussink, VI, 2009)	2.52
"Cladribine is an immunosuppressant that offers targeted, sustained regulation of the immune system and that has a well-characterized safety profile, derived from more than 15 years of use of the parenteral formulation in oncology indications and MS."	( Development of oral cladribine for the treatment of multiple sclerosis. Aktas, O; Giancarlo Comi, GC; Hartung, HP; Kieseier, B, 2010)	1.41
"Cladribine is an immunomodulator with a long-lasting effect and a well-characterized safety profile based on over 15 years of experience with the parenteral route for MS and other indications."	( [Cladribin. Development of an oral formulation for the treatment of multiple sclerosis]. Aktas, O; Hartung, HP; Kieseier, BC, 2010)	1.08
"Cladribine (2CdA) is a nucleoside analog that has been introduced as a promising agent for treatment of advanced SM."	( In vitro and in vivo growth-inhibitory effects of cladribine on neoplastic mast cells exhibiting the imatinib-resistant KIT mutation D816V. Blatt, K; Böhm, A; Gleixner, KV; Herrmann, H; Pehamberger, H; Peter, B; Pickl, WF; Rabitsch, W; Schernthaner, GH; Schuch, K; Sonneck, K; Sperr, WR; Valent, P, 2010)	1.34
"Cladribine is a synthetic deoxyadenosine analogue in development as an oral multiple sclerosis (MS) therapy."	( Safety and tolerability of cladribine tablets in multiple sclerosis: the CLARITY (CLAdRIbine Tablets treating multiple sclerosis orallY) study. Comi, G; Cook, S; Giovannoni, G; Greenberg, SJ; Hamlett, A; Miret, M; Musch, B; Rammohan, K; Rieckmann, P; Sørensen, PS; Vermersch, P; Viglietta, V; Weiner, J, 2011)	2.11
"Cladribine is a prodrug which is selectively activated intracellularly."	( Hairy cell leukemia: epidemiology, pharmacokinetics of cladribine, and long-term follow-up of subcutaneous therapy. Juliusson, G; Samuelsson, H, 2011)	1.34
"R-cladribine is an effective therapy for previously untreated MCL, and these results validate the use of R-cladribine for the initial treatment of MCL."	( Cladribine plus rituximab is an effective therapy for newly diagnosed mantle cell lymphoma. Abbi, K; Chen, Y; Chen, Z; Epner, EM; Mater, E; Okada, C; Pindyck, T; Spurgeon, SE, 2011)	2.37
"Cladribine is a purine nucleotide analogue, and its efficacy is based on long-term reduction of CD4+ and CD8+ lymphocytes."	( [Current treatment of multiple sclerosis]. Csépány, T, 2011)	1.09
"Cladribine is a highly effective medication used in treating Langerhans cell histiocytosis. "	( [Cladribine is highly effective in the treatment of Langerhans cell histiocytosis and rare histiocytic disorders of the juvenile xanthogranuloma group]. Adam, Z; Koukalová, R; Král, Z; Krejčí, M; Mayer, J; Pour, L; Rehák, Z; Szturz, P; Tomíška, M; Zahradová, L, 2012)	2.73
"Cladribine is a suitable medication for multiorgan and multifocal forms of LCH. "	( [Treatment of Langerhans cells histiocytosis by cladribin reached long-term complete remission in 9 out of 10 adult patients]. Adam, Z; Duraš, J; Hájek, R; Koukalová, R; Král, Z; Krejčí, M; Mayer, J; Navrátil, M; Pour, L; Rehák, Z; Szturz, P, 2012)	1.82
"Cladribine is a prodrug and must be phosphorylated intracellularly to cladribine-monophosphate (MP) by the nuclear/cystosol enzyme deoxycytidine kinase (dCK) and the mitochondrial enzyme deoxyguanosine kinase."	( Pharmacological basis for cladribine resistance. Albertioni, F; Juliusson, G; Lotfi, K, 2003)	1.34
"Cladribine is a newer purine analogue and is of particular interest because it is resistant to deamination by adenosine deaminase."	( 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)	1.3
"Cladribine is a potent immunosuppressive agent and should be included with the list of immunosuppressive agents that may be associated with EBV-related B-cell lymphoproliferative disorders."	( Epstein-Barr virus positive large B-cell lymphoma arising in a patient previously treated with Cladribine for hairy cell leukemia. Barbashina, V; Bhargava, R; Filippa, DA; Teruya-Feldstein, J, 2004)	1.26
"Cladribine is a purine analogue that is resistant to degradation by adenosine deaminase. "	( [Cladribine monotherapy for patients with relapsed or refractory indolent non-Hodgkin lymphoma]. Choi, I; Nakashima, Y; Shimada, T; Uike, N; Yamada, Y; Yufu, Y, 2004)	2.68
"Cladribine is an adenosine deaminase-resistant deoxyadenosine analog with a unique mechanism of action. "	( Cladribine: from the bench to the bedside--focus on hairy cell leukemia. Greyz, N; Saven, A, 2004)	3.21
"Cladribine is a purine analog that demonstrates lymphocytotoxic activity. "	( Cladribine: an investigational immunomodulatory agent for multiple sclerosis. Brousil, JA; Roberts, RJ; Schlein, AL, 2006)	3.22
"Cladribine is a purine nucleoside analogue that is resistant to cellular catabolism."	( Cladribine in indolent non-Hodgkin's lymphoma. Saven, A; Sigal, DS, 2008)	2.51
"Cladribine is an effective therapy for hairy cell leukaemia (HCL), but the standard regime is frequently complicated by neutropenic fever and prolonged T-cell depression. "	( Low-dose cladribine for symptomatic hairy cell leukaemia. Heldal, D; Juliusson, G; Lenkei, R; Liliemark, J; Tjønnfjord, G, 1995)	2.15
"Cladribine is a synthetic analogue of adenine used in the treatment of lymphoid malignancies, commonly associated with a decrease in T lymphocytes."	( Transfusion-associated graft-versus-host disease in a patient treated with Cladribine (2-chlorodeoxyadenosine): demonstration of exogenous DNA in various tissue extracts by PCR analysis. Alberto, P; Betticher, DC; Diebold-Berger, S; Extermann, M; Helg, C; Reymond, JM; Roux, E; Tiercy, JM; Zubler, R; Zulian, GB, 1995)	1.24
"Cladribine is a synthetic purine nucleoside with demonstrated activity in hairy cell leukemia and acute myeloid leukemia. "	( Pharmacokinetics of cladribine (2-chlorodeoxyadenosine) in children with acute leukemia. Blakley, RL; Crom, WR; Kearns, CM; Santana, VM, 1994)	2.05
"Cladribine is a newly developed antimetabolite with promising activity in lymphoproliferative disorders. "	( A limited sampling strategy for estimation of the cladribine plasma area under the concentration versus time curve after intermittent i.v. infusion, s.c. injection, and oral administration. Albertioni, F; Eksborg, S; Juliusson, G; Liliemark, J, 1996)	1.99
"Cladribine is a new purine nucleoside analogue with promising activity in low-grade lymphoproliferative disorders, childhood acute myelogenous leukaemia and multiple sclerosis. "	( The clinical pharmacokinetics of cladribine. Liliemark, J, 1997)	2.02
"Cladribine is a new type of drug with properties of selective lymphocyte suppression that appear to favorably alter the clinical course of progressive multiple sclerosis (MS). "	( Development of cladribine treatment in multiple sclerosis. Beutler, E; Koziol, JA; McMillan, R; Romine, JS; Sipe, JC; Zyroff, J, 1996)	2.09
"Cladribine is an active single agent in the treatment of patients with refractory or relapsed advanced stage indolent lymphoma, with major responses in one third of patients."	( Cladribine in the treatment of advanced relapsed or refractory low and intermediate grade non-Hodgkin's lymphoma. Boswell, W; Espina, BM; Harvey-Buchanan, LA; Khan, AU; Lee, M; Levine, AM; Nathwani, B; Schiller, G; Tulpule, A, 1998)	3.19
"Cladribine is a purine analog with impressive activity in patients with low-grade lymphoproliferative disorders. "	( Cytotoxicity of 2-chlorodeoxadenosine (cladribine, 2-cdA) in combination with other chemotherapy drugs against two lymphoma cell lines. Hoffman, M; Lesser, M; Rai, K; Xu, JC, 1999)	2.02
"Cladribine is an active agent in HCL-V albeit with a lower response rate than in classic HCL."	( Treatment of hairy cell leukemia-variant with cladribine. Robbins, BA; Saven, A; Tetreault, SA, 1999)	1.28
"Cladribine is a lymphocytotoxic purine nucleoside with potential for treatment of autoimmune diseases. "	( Hematological effects of intermittent 2-hour infusions of cladribine in multiple sclerosis patients: a comparison of 2 dosage patterns. Chrapusta, SJ; Grieb, P; Hoser, G; Janisz, M; Kamienowski, J; Kawiak, J; Kuśnierczyk, P, 2001)	2
"Cladribine (2-CdA) is a purine analogue that exhibits activity against a variety of hematological malignancies and has a potent immunosuppressive effect. "	( Therapeutic potential of a reduced-intensity preparative regimen for allogeneic transplantation with cladribine, busulfan, and antithymocyte globulin against advanced/refractory acute leukemia/lymphoma. Kami, M; Kanai, S; Kanda, Y; Kato, K; Kawano, Y; Makimoto, A; Matsubara, H; Mineishi, S; Nakai, K; Ogasawara, T; Ohnishi, T; Saito, T; Shoji, N; Takaue, Y; Tanosaki, R; Tobinai, K; Wakasugi, H, 2002)	1.97

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"Cladribine has a unique pharmacokinetic/pharmacodynamic (PK/PD) profile with a short elimination half-life (~ 1 day) relative to a prolonged PD effect on specific immune cells (most notably a reversible reduction in B and T lymphocyte counts)."	( Model-informed assessment of ethnic sensitivity and dosage justification for Asian populations in the global clinical development and use of cladribine tablets. Li, D; Liu, P; Munafo, A; Terranova, N; Venkatakrishnan, K, 2022)	1.64
"Cladribine has a significant efficacy and encouraging acute and long-term benefits when administered to patients with HCL. "	( Treatment Outcomes Of Patients With Hairy Cell Leukaemia; A 16-Year Experience At A Tertiary Care Center In Pakistan. Ahmad, U; Chaudary, QU; Iftikhar, R; Javed, H; Khan, MA; Shahbaz, N; Yousaf, M, )	1.57
"Cladribine tablets have been approved in many countries for the treatment of patients with various forms of relapsing multiple sclerosis (MS). "	( Model-informed assessment of ethnic sensitivity and dosage justification for Asian populations in the global clinical development and use of cladribine tablets. Li, D; Liu, P; Munafo, A; Terranova, N; Venkatakrishnan, K, 2022)	2.37
"Cladribine has a significant efficacy and encouraging acute and long-term benefits when administered to patients with HCL. "	( Treatment Outcomes Of Patients With Hairy Cell Leukaemia; A 16-Year Experience At A Tertiary Care Center In Pakistan. Ahmad, U; Chaudary, QU; Iftikhar, R; Javed, H; Khan, MA; Shahbaz, N; Yousaf, M, )	1.57
"Cladribine has been approved for the treatment of multiple sclerosis (MS) and its administration results in a long-lasting depletion of lymphocytes. "	( Immune Response to Seasonal Influenza Vaccination in Multiple Sclerosis Patients Receiving Cladribine. Aslan, D; Hagenacker, T; He, X; Kleinschnitz, C; Kleinschnitz, K; Korsen, M; Meuth, SG; Oezalp, SH; Pawlitzki, M; Pfeuffer, S; Pul, R; Rolfes, L; Ruck, T; Skuljec, J; Su, C, 2023)	2.57
"Cladribine has activity in AML, and an enhancing effect on other cytostatic drugs thus may help overcome resistance."	( Long-term follow-up of Cladribine, high-dose Cytarabine, and Idarubicin as salvage treatment for relapsed acute myeloid leukemia and literature review. Brossart, P; Glasmacher, A; Hahn-Ast, C; Mayer, K; Schmidt-Wolf, IGH; Schwab, K; von Lilienfeld-Toal, M, 2020)	1.59
"Cladribine has been shown to lower relapse rates and decrease disease progression in patients with relapsing forms of multiple sclerosis (MS). "	( Retinal cotton wool spot associated with cladribine therapy for multiple sclerosis. Ahmad, B; Gummi, R; Walsh, RD, 2021)	2.33
"Oral cladribine has been approved for the treatment of relapsing multiple sclerosis (MS) yet real-world evidence regarding its effectiveness and safety remains scarce."	( Effectiveness and safety of cladribine in MS: Real-world experience from two tertiary centres. Hackert, J; Kleinschnitz, C; Kleinschnitz, K; Klotz, L; Meuth, SG; Pfeuffer, S; Pul, R; Rolfes, L; Ruck, T; Wiendl, H, 2022)	1.53
"Cladribine has shown efficacy at all stages of MS."	( Treating the ineligible: Disease modification in people with multiple sclerosis beyond NHS England commissioning policies. Adams, A; Allen-Philbey, K; Álvarez-González, C; Baker, D; Campion, T; De Trane, S; Espasandin, M; Giovannoni, G; Gnanapavan, S; Mao, Z; Marta, M; Mathews, J; Schmierer, K; Turner, BP; Yildiz, O, 2019)	1.24
"Cladribine has moderate clinical efficacy in the treatment of ECD and can be considered a treatment option in cases without the BRAF V600E mutation. "	( Clinical and Radiologic Responses to Cladribine for the Treatment of Erdheim-Chester Disease. Call, TG; Go, RS; Goyal, G; Hogan, WJ; Litzow, MR; Shah, MV, 2017)	2.17
"Cladribine has been noted to have particular activity among lymphoid disorders with few effective therapies, specifically, chronic lymphocytic leukemia, lymphoplasmacytic lymphoma, marginal zone lymphoma, and mantle cell lymphoma."	( Beyond hairy cell: the activity of cladribine in other hematologic malignancies. Miller, HJ; Saven, A; Schram, ED; Sigal, DS, 2010)	1.36
"Cladribine has been used in the treatment of hairy cell leukemia for about 30 years. "	( Immunohistochemical evaluation of cell proliferation and apoptosis markers in ovarian surface epithelial cells of cladribine-treated rats. Chylińska-Wrzos, P; Jasiński, L; Jędrych, M; Jodłowska-Jędrych, B; Wawryk-Gawda, E, 2013)	2.04
"Cladribine has been reported to have little activity in fludarabine- refractory chronic lymphocytic leukemia (CLL). "	( A phase II study of cladribine treatment for fludarabine refractory B cell chronic lymphocytic leukemia: results from CALGB Study 9211. Byrd, JC; Larson, RA; Peterson, B; Piro, L; Saven, A; Schiffer, C; Vardiman, JW, 2003)	2.09
"Cladribine has single-drug activity in acute myeloid leukaemia (AML), and may enhance the formation of the active metabolite (ara-CTP) of cytosine arabinoside (ara-C). "	( Increased remissions from one course for intermediate-dose cytosine arabinoside and idarubicin in elderly acute myeloid leukaemia when combined with cladribine. A randomized population-based phase II study. Björkholm, M; Höglund, M; Juliusson, G; Karlsson, K; Löfgren, C; Möllgård, L; Paul, C; Tidefelt, U, 2003)	1.96
"Cladribine has also proven useful in the treatment of a variety of other hematologic malignancies, and its current place in the oncologic therapeutic armamentarium, as well as in potential areas of development, are outlined."	( Cladribine: from the bench to the bedside--focus on hairy cell leukemia. Greyz, N; Saven, A, 2004)	2.49
"Cladribine has epigenetic activity in that it inhibits DNA methylation."	( The epigenetics of mantle cell lymphoma. Epner, E; Yu, M, 2007)	1.06
"Cladribine has shown efficacy against a variety of hematologic malignancies, notably HCL and CLL."	( Cladribine for the treatment of hematologic malignancies. Baltz, JK; Montello, MJ, 1993)	2.45
"Cladribine has shown efficacy in phase-II studies in hairy cell leukemia [response rate (RR) = 75-100% and complete response rate (CR) = 46-92%], chronic lymphocytic leukemia (RR = 37-67% and CR = 4-39%), and lymphocytic lymphoma (RR = 43-52% and CR = 14-20%)."	( Clinical and toxicological aspects of the antineoplastic drug cladribine: a review. Guchelaar, HJ; Richel, DJ; Schaafsma, MR, 1994)	1.25
"Cladribine has shown response rates of nearly 90% in patients with hairy cell leukemia after a single, seven-day continuous infusion. "	( The role of cladribine in the treatment of lymphoid malignancies. Hogan, DK; Nelson, MC, 1995)	2.11
"Cladribine has high efficacy and a favorable acute and long-term toxicity profile when administered to patients with hairy cell leukemia."	( Long-term follow-up of patients with hairy cell leukemia after cladribine treatment. Burian, C; Koziol, JA; Piro, LD; Saven, A, 1998)	1.26
"Cladribine has been known since the 1960s as an intermediate for the synthesis of 2-deoxynucleotides and its potential for the treatment of leukemia was disclosed in 1984."	( Cladribine. Ortho Biotech Inc. Filippi, M; Rovaris, M; Tortorella, C, 2001)	2.47
"Cladribine has in the last decade emerged as the drug of choice for treating hairy cell leukaemia."	( [Hairy cell leukemia treated with cladribine]. Ghanima, W; Heldal, D; Tjønnfjord, GE, 2002)	1.32

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"Cladribine tablets cause a reduction in lymphocytes with a predominant effect on B-cell and T-cell counts. "	( Specific Patterns of Immune Cell Dynamics May Explain the Early Onset and Prolonged Efficacy of Cladribine Tablets: A MAGNIFY-MS Substudy. Achiron, A; Barkhof, F; Boschert, U; Chan, A; Chudecka, A; De Stefano, N; Derfuss, T; Hodgkinson, S; Holmberg, KH; Leocani, L; Montalban, X; Mwape, C; Prat, A; Roy, S; Schmierer, K; Sellebjerg, F; Vermersch, P; Wiendl, H, 2023)	2.57
"Cladribine was found to inhibit growth of primary MC and the MC line HMC-1 in a dose-dependent manner, with lower IC(50) values recorded in HMC-1.2 cells harboring KIT D816V (IC(50): 10 ng/mL) compared to HMC-1.1 cells lacking KIT D816V (IC(50): 300 ng/mL). "	( In vitro and in vivo growth-inhibitory effects of cladribine on neoplastic mast cells exhibiting the imatinib-resistant KIT mutation D816V. Blatt, K; Böhm, A; Gleixner, KV; Herrmann, H; Pehamberger, H; Peter, B; Pickl, WF; Rabitsch, W; Schernthaner, GH; Schuch, K; Sonneck, K; Sperr, WR; Valent, P, 2010)	2.06
"Cladribine therapy, at lower doses than previously reported, was remarkably well tolerated in CPMS, with no significant myelosuppression. "	( Safety and tolerability of subcutaneous cladribine therapy in progressive multiple sclerosis. Brandwein, J; O'Connor, P; Selby, R, 1998)	2.01

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"Oral cladribine is a novel treatment for Multiple Sclerosis (MS). "	( Anti-HBs titers are not decreased after treatment with oral Cladribine in patients with Multiple Sclerosis vaccinated against Hepatitis B virus. Cola, G; Di Mauro, G; Grimaldi, A; Landi, D; Marfia, GA; Mataluni, G; Nicoletti, CG, 2022)	1.48
"Cladribine treated MS patients are able to produce antibodies to the SARS-CoV-2 mRNA vaccine. "	( Effect of cladribine on COVID-19 serology responses following two doses of the BNT162b2 mRNA vaccine in patients with multiple sclerosis. Brill, L; Haham, N; Levin, N; Rechtman, A; Rozenberg, A; Shifrin, A; Vaknin-Dembinsky, A; Zveik, O, 2022)	2.57
"cladribine-based treatment was initiated with satisfactory outcome."	( [Erdheim-Chester disease: an aggressive systemic disease treated with cladribine with favorable outcome (a case report)]. Lahlimi, F; Lasri, N; Tazi, MI, 2022)	1.68
"Cladribine (CLD) treats multiple sclerosis (MS) by selectively and transiently depleting B and T cells with a secondary long-term reconstruction of the immune system. "	( Cytokine Secretion Dynamics of Isolated PBMC after Cladribine Exposure in RRMS Patients. Andone, S; Balasa, R; Hutanu, A; Maier, S; Manu, D; Oiaga, M; Voidazan, S, 2022)	2.42
"Oral cladribine treatment significantly attenuated clinical deficits in EAE mice. "	( Cladribine treatment improves cortical network functionality in a mouse model of autoimmune encephalomyelitis. Bock, S; Budde, T; Cerina, M; Dobelmann, V; Duarte-Silva, E; Fazio, L; Gothan, KSS; Gruchot, J; Henes, A; Herrmann, AM; Hundehege, P; Huntemann, N; Kremer, D; Küry, P; Meuth, SG; Müntefering, T; Narayanan, V; Nelke, C; Pfeuffer, S; Raba, K; Räuber, S; Rolfes, L; Ruck, T; Schroeter, CB; Wiendl, H, 2022)	2.68
"Cladribine treatment discontinuation was registered in 8% of patients, mainly (69.2%) due to disease activity persistence."	( Safety and Effectiveness of Cladribine in Multiple Sclerosis: Real-World Clinical Experience From 5 Tertiary Hospitals in Portugal. Abreu, P; Brum, M; Capela, C; de Sá, J; Dias, R; Ferreira, J; Guerreiro, R; Ladeira, F; Leitão, L; Sá, MJ; Salgado, V; Santos, M; Sequeira, J, )	1.15
"Cladribine treatment reduced significantly relapse rate and MRI activity. "	( A prospective observational longitudinal study with a two-year follow-up of multiple sclerosis patients on Cladribine. Ahmed, SF; Al-Hashel, J; AlMojel, M; Alroughani, R, 2023)	2.57
"Cladribine is a new oral treatment for relapsing-remitting multiple sclerosis."	( [Neurology 2019]. Benninger, D; Diserens, K; Hirt, L; Kuntzer, T; Michel, P; Novy, J; Pantazou, V; Pasquier, RD; Perrenoud, M; Rossetti, AO; Rouaud, O; Ryvlin, P; Theaudin, M, 2020)	1.28
"Cladribine-treated patients with a skin AE were identified."	( Skin Reactions in Patients With Multiple Sclerosis Receiving Cladribine Treatment. Hackert, J; Kleinschnitz, C; Korsen, M; Meuth, SG; Pawlitzki, M; Pfeuffer, S; Pul, R; Rolfes, L; Ruck, T; Sondermann, W; Wiendl, H, 2021)	1.58
"Cladribine treatment was associated with clinical stabilization, as evidenced by significantly decreased ARR and no progression of EDSS score."	( Cladribine suppresses disease activity in neuromyelitis optica spectrum disorder: a 2-year follow-up study. Papuć, E; Rejdak, K, 2021)	2.79
"Cladribine treatment in CLARITY produced efficacy improvements that were maintained in patients treated with placebo in the Extension; in patients treated with cladribine 3.5 mg/kg in CLARITY, approximately 75% remained relapse-free when given placebo during the Extension."	( Safety and efficacy of cladribine tablets in patients with relapsing-remitting multiple sclerosis: Results from the randomized extension trial of the CLARITY study. Adeniji, AK; Comi, G; Cook, S; Dangond, F; Giovannoni, G; Rammohan, K; Rieckmann, P; Soelberg Sorensen, P; Vermersch, P, 2018)	1.51
"Cladribine tablets treatment for 2 years followed by 2 years' placebo treatment produced durable clinical benefits similar to 4 years of cladribine treatment with a low risk of severe lymphopenia or clinical worsening. "	( Safety and efficacy of cladribine tablets in patients with relapsing-remitting multiple sclerosis: Results from the randomized extension trial of the CLARITY study. Adeniji, AK; Comi, G; Cook, S; Dangond, F; Giovannoni, G; Rammohan, K; Rieckmann, P; Soelberg Sorensen, P; Vermersch, P, 2018)	2.23
"Cladribine treatment was well tolerated without any side effects. "	( Disease activity in progressive multiple sclerosis can be effectively reduced by cladribine. Adams, A; Allen-Philbey, K; Baker, D; Dubuisson, N; Giovannoni, G; Gnanapavan, S; Malaspina, A; Mao, Z; Schmierer, K; Yildiz, O, 2018)	2.15
"Oral cladribine is a novel treatment for relapsing multiple sclerosis (MS). "	( Potential mechanisms of action related to the efficacy and safety of cladribine. Baker, D; Herrod, SS; Pryce, G; Schmierer, K, 2019)	1.26
"Cladribine treatment of hairy cell leukemia (HCL) is complicated by neutropenic fever in 42% of patients despite documented infections being relatively uncommon. "	( Filgrastim for cladribine-induced neutropenic fever in patients with hairy cell leukemia. Adusumalli, J; Burian, C; Koziol, JA; Saven, A, 1999)	2.1
"Both cladribine treatments were superior to placebo for the proportion of patients having gadolinium-enhanced T1 lesions and for the mean volume and number of such lesions (p < or = 0.003)."	( Cladribine and progressive MS: clinical and MRI outcomes of a multicenter controlled trial. Cladribine MRI Study Group. Comi, G; Filippi, M; Rice, GP, 2000)	2.2
"Cladribine treatment induced mitochondrial transmembrane potential (DeltaPsi(m)) loss, phosphatidylserine exposure, caspase activation and development of typical apoptotic morphology in JM1 (pre-B), Jurkat (T) and U937 (promonocytic) cells."	( Cladribine induces apoptosis in human leukaemia cells by caspase-dependent and -independent pathways acting on mitochondria. Anel, A; Giraldo, P; Marzo, I; Naval, J; Pérez-Galán, P; Rubio-Félix, D, 2001)	2.47
"Treatment with cladribine tablets (CladT), an immune reconstitution therapy for relapsing multiple sclerosis (RMS), involves two short courses of treatment in Year 1 and Year 2. "	( Expert opinion on the long-term use of cladribine tablets for multiple sclerosis: Systematic literature review of real-world evidence. Brownlee, W; Celius, EG; Centonze, D; Giovannoni, G; Havrdova, EK; Hodgkinson, S; Kleinschnitz, C; Magyari, M; Oreja-Guevara, C; Salloukh, H; Selchen, D; Van Wijmeersch, B; Vermersch, P; Wiendl, H; Yamout, B, 2023)	1.53
"Treatment with cladribine leads to a preferential reduction in lymphocytes, resulting in profound depletion of B-cells with a rapid recovery of naïve B-cells, while T-cell show a lesser but long-lasting depletion It is approved for treatment of relapsing multiple sclerosis (MS)."	( Real-world experience of cladribine treatment in relapsing-remitting multiple sclerosis: A Danish nationwide study. Heick, A; Joensen, H; Magyari, M; Pihl, CE; Pontieri, L; Rasmussen, PV; Ratzer, R; Schäfer, J; Sellebjerg, F; Sorensen, PS, 2023)	1.55
"Treatment with cladribine tablets is indicated in highly active relapsing-remitting multiple sclerosis (RRMS). "	( Cladribine tablets for highly active relapsing-remitting multiple sclerosis in Poland: a real-world, multi-centre, retrospective, cohort study during the COVID-19 pandemic. Adamczyk-Sowa, M; Bartosik-Psujek, H; Chorąży, M; Jamróz-Wiśniewska, A; Kurkowska-Jastrzębska, I; Kułakowska, A; Piasecka-Stryczyńska, K; Pogoda-Wesołowska, A; Puz, P; Rejdak, K; Stępień, A; Słowik, A; Tokarz-Kupczyk, E, 2023)	2.71
"Treatment with cladribine tablets, a high-efficacy disease-modifying therapy (DMT), has been available in England since 2017 for patients with highly active relapsing multiple sclerosis (MS). "	( Real-world use of cladribine tablets (completion rates and treatment persistence) in patients with multiple sclerosis in England: The CLARENCE study. Amin, A; Ashton, L; Brownlee, W; Herbert, A, 2023)	1.6
"Treatment with cladribine temporarily reversed the patient's neutropenia."	( Neutropenia caused by hairy cell leukemia in a patient with myelofibrosis secondary to polycythemia vera: a case report. Dahm, AEA; Dybedal, I; Habberstad, AH; Randen, U; Spetalen, S; Tjønnfjord, GE; Tran, HTT, 2018)	0.82
"Treatment with cladribine tablets 3.5 mg/kg resulted in selective reductions in B and T lymphocytes. "	( Effect of cladribine tablets on lymphocyte reduction and repopulation dynamics in patients with relapsing multiple sclerosis. Comi, G; Cook, S; Dangond, F; Galazka, A; Giovannoni, G; Hicking, C; Nolting, A; Rieckmann, P; Sørensen, PS; Vermersch, P, 2019)	1.27
"Treatment with cladribine (2-chlorodeoxyadenosine) produced a marked and sustained reduction in her symptoms and serum tryptase level."	( Sustained improvement in urticaria pigmentosa and pruritus in a case of indolent systemic mastocytosis treated with cladribine. Lock, AD; McNamara, CJ; Rustin, MH, 2015)	0.97
"Treatment with cladribine (2-chlorodeoxyadenosine) was subsequently successful with radiological resolution of the CNS lesion."	( Successful treatment of central nervous system juvenile xanthogranulomatosis with cladribine. Duncan, A; Parslew, R; Pizer, BL; Rajendra, B, 2009)	0.92
"Treatment with cladribine tablets significantly reduced relapse rates, the risk of disability progression, and MRI measures of disease activity at 96 weeks. "	( A placebo-controlled trial of oral cladribine for relapsing multiple sclerosis. Chang, P; Comi, G; Cook, S; Giovannoni, G; Greenberg, SJ; Hamlett, A; Musch, B; Rammohan, K; Rieckmann, P; Soelberg Sørensen, P; Vermersch, P, 2010)	0.99
"Treatment with cladribine tablets significantly increased the proportion of patients with sustained freedom from disease activity over 96 weeks compared with placebo. "	( Sustained disease-activity-free status in patients with relapsing-remitting multiple sclerosis treated with cladribine tablets in the CLARITY study: a post-hoc and subgroup analysis. Cook, S; Giovannoni, G; Greenberg, S; Hamlett, A; Rammohan, K; Rieckmann, P; Sørensen, PS; Vermersch, P; Viglietta, V, 2011)	0.93
"Treatment with cladribine resulted in a significant G1 arrest in U266 and RPMI8226 cells, but only a minor increase in the G1 phase for MM1.S cells."	( Therapeutic potential of cladribine in combination with STAT3 inhibitor against multiple myeloma. Deng, XS; Lee, CK; Liu, B; Ma, J; Wang, S; Yu, XD; Zhao, M, 2011)	1.01
"Treatment with cladribine followed by rituximab is effective tk;4and may increase CR rate."	( Phase 2 study of cladribine followed by rituximab in patients with hairy cell leukemia. Brandt, M; Burger, J; Challagundla, P; Faderl, S; Ferrajoli, A; Jorgensen, J; Kantarjian, H; Keating, M; Koller, C; Luthra, R; O'Brien, S; Pierce, S; Ravandi, F; Thomas, D; York, S, 2011)	1.05
"The treatment with cladribine, of younger persons and even children, appears to be a major factor stimulating the more exact recognition of its activities."	( Immunohistochemical evaluation of cell proliferation and apoptosis markers in ovarian surface epithelial cells of cladribine-treated rats. Chylińska-Wrzos, P; Jasiński, L; Jędrych, M; Jodłowska-Jędrych, B; Wawryk-Gawda, E, 2013)	0.92
"Treatment with cladribine/mitoxantrone induced a short-lasting partial response and the patient died 6 months after diagnosis."	( CD4+ CD56+ neoplasia: clinical and biological features with emphasis on cytotoxic drug-induced apoptosis and expression of sialyl Lewis X. Chow, KU; Hoelzer, D; Kim, SZ; Kriener, S; Mitrou, PS; Schui, DK; Sterry, W; Weidmann, E; Zollner, TM, 2003)	0.66
"Treatment with cladribine led to an impressive improvement of skin lesions, a significant decrease in tryptase serum levels and stabilization of bone marrow infiltrates."	( ["Smoldering systemic mastocytosis. "Successful therapy with cladribine]. Landthaler, M; Meyer, S; Schleyer, V; Szeimies, RM, 2004)	0.9
"Treatment with cladribine, daunorubicin and cytosine arabinoside, followed by autologous stem cell transplantation, induced complete remission of AML and hematologic remission of HCL for 22 months, when he relapsed with AML."	( Concomitant hairy cell and acute myeloid leukemia. Gratwohl, A; Rimner, T; Tichelli, A; Went, P, 2006)	0.67
"Treatment with cladribine achieved a high overall response rate for patients with HCL and was safe even in elderly patients like ours."	( [Successful use of cladribine in the treatment of an elderly woman with typical hairy cell leukemia]. Hirose, A; Ishiura, Y; Nakao, S; Okumura, H; Saito, K; Terasaki, Y; Yokawa, S, 2007)	1.01
"Pretreatment with cladribine increases the intracellular accumulation of the active metabolite of cytarabine, cytosine arabinoside 5'-triphosphate, by 36 to 40%."	( The clinical pharmacokinetics of cladribine. Liliemark, J, 1997)	0.9

Excerpt	Reference	Relevance
"Deoxyadenosine is known to be toxic to both proliferating and resting lymphocytes that lack adenosine deaminase (ADA) activity."	( Profound toxicity of deoxyadenosine and 2-chlorodeoxyadenosine toward human monocytes in vitro and in vivo. Carrera, CJ; Carson, DA; Lotz, M; Piro, LD; Yamanaka, H, 1989)	0.28
"Deoxyadenosine has been implicated as the toxic metabolite causing profound lymphopenia in immunodeficient children with a genetic deficiency of adenosine deaminase (ADA), and in adults treated with the potent ADA inhibitor deoxycoformycin."	( Mechanism of deoxyadenosine and 2-chlorodeoxyadenosine toxicity to nondividing human lymphocytes. Carrera, CJ; Carson, DA; Kubota, M; Seto, S; Wasson, DB, 1985)	0.27
"2-Chlorodeoxyadenosine (CdA), an adenosine-deaminase-resistant purine deoxynucleoside, is markedly toxic toward human T-lymphoblastoid cell lines in vitro and is an effective agent against L1210 leukemia in vivo."	( Specific toxicity of 2-chlorodeoxyadenosine toward resting and proliferating human lymphocytes. Carson, DA; Taetle, R; Wasson, DB; Yu, A, 1983)	0.27
" In addition, case records from National Cancer Institute (NCI) Group C protocols were reviewed for fludarabine in chronic lymphocytic leukemia (CLL), and cladribine and pentostatin in hairy cell leukemia (HCL), as well as adverse drug reactions reported to the NCI from January 1980 through September 1993."	( Neurotoxicity of purine analogs: a review. Cheson, BD; Foss, FM; Sorensen, JM; Vena, DA, 1994)	0.49
" Although prolonged myelosuppression would have been dose-limiting at 21 mg/m2/d for 5 days, the most important adverse effect was the development of a sensorimotor peripheral neuropathy."	( Therapeutic and neurotoxic effects of 2-chlorodeoxyadenosine in adults with acute myeloid leukemia. Foley, KM; Rosenblum, M; Vahdat, L; Warrell, RP; Wile, MJ; Wong, ET, 1994)	0.29
" Therefore we reviewed our experience with 2-CdA in 16 HCL patients, with special attention to adverse effects."	( Treatment of hairy cell leukaemia (HCL) with 2-chlorodeoxyadenosine (2-CdA): identification of parameters predictive of adverse effects. Delmer, A; Legrand, O; Marie, JP; Vekhoff, A; Zittoun, R, 1997)	0.3
"5 mg/kg per cycle is safe and this dose level should not be exceeded in this patient population."	( Reduced dose of subcutaneous cladribine induces identical response rates but decreased toxicity in pretreated chronic lymphocytic leukaemia. Swiss Group for Clinical Cancer Research (SAKK). Betticher, DC; Cerny, T; Fey, MF; Hess, U; Hsu Schmitz, SF; Ratschiller, D; Tichelli, A; Tobler, A; von Rohr, A; Wernli, M; Zulian, G, 1998)	0.59
" Following an uncomplicated pregnancy, a healthy child was born at full term and careful haematological and immunological monitoring has revealed no adverse effects resulting from exposure to rituximab."	( Safety of rituximab therapy during the first trimester of pregnancy: a case history. Elinder, G; Kimby, E; Sverrisdottir, A, 2004)	0.32
" After 24 h incubation tezacitabine was equally or less toxic compared to cladribine."	( Cytotoxic effects of cladribine and tezacitabine toward HL-60. Grieb, P; Skierski, JS; Stachnik, K, 2005)	0.88
"These results show that while cN-I provides both protective and selective benefits to gene-modified cells in vitro, selection requires a treatment strategy that is likely too toxic to consider cN-I as an in vivo selectable marker."	( Enforced expression of cytosolic 5'-nucleotidase I confers resistance to nucleoside analogues in vitro but systemic chemotherapy toxicity precludes in vivo selection. Archer, DR; Gangadharan, B; Gray, T; Morrey, EL; Spencer, HT; Spychala, J; Sumter, TF, 2006)	0.33
"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
" An understanding of structure-activity relationships (SARs) of chemicals can make a significant contribution to the identification of potential toxic effects early in the drug development process and aid in avoiding such problems."	( Developing structure-activity relationships for the prediction of hepatotoxicity. Fisk, L; Greene, N; Naven, RT; Note, RR; Patel, ML; Pelletier, DJ, 2010)	0.36
" Safety assessments included monitoring for adverse events (AEs), routine physical and neurologic examinations and frequent laboratory parameter assessments."	( Safety and tolerability of cladribine tablets in multiple sclerosis: the CLARITY (CLAdRIbine Tablets treating multiple sclerosis orallY) study. Comi, G; Cook, S; Giovannoni, G; Greenberg, SJ; Hamlett, A; Miret, M; Musch, B; Rammohan, K; Rieckmann, P; Sørensen, PS; Vermersch, P; Viglietta, V; Weiner, J, 2011)	0.67
" Only a few studies have evaluated the long-term adverse effects of purine analogs on the immune system or stem cell toxicity, and most of these are not very recent."	( Purine analog toxicity in patients with hairy cell leukemia. Tadmor, T, 2011)	0.37
"Efficacy and adverse events of patients with refractory or relapsed AML who were treated with one course of CLAG from April 1st, 2014 through December 9th, 2015 in our hospital were retrospectively reviewed."	( [Efficacy and safety analysis of the combination of cladribine, cytarabine, granulocyte colonystimulating factor (CLAG) regime in patients with refractory or relapsed acute myeloid leukemia]. Duan, MH; Feng, J; Han, X; Li, J; Tian, LP; Yang, C; Zhang, L; Zhang, M; Zhang, W; Zhang, Y; Zhou, DB, 2016)	0.68
" Adverse event rates were generally similar between groups, but lymphopenia Grade ⩾ 3 rates were higher with cladribine than placebo (Grade 4 lymphopenia occurred infrequently)."	( Safety and efficacy of cladribine tablets in patients with relapsing-remitting multiple sclerosis: Results from the randomized extension trial of the CLARITY study. Adeniji, AK; Comi, G; Cook, S; Dangond, F; Giovannoni, G; Rammohan, K; Rieckmann, P; Soelberg Sorensen, P; Vermersch, P, 2018)	1
" Mode of action, adverse effects, reported risks for infections and malignancies, and pregnancy related issues are discussed in the review."	( Managing the side effects of multiple sclerosis therapy: pharmacotherapy options for patients. Rommer, PS; Zettl, UK, 2018)	0.48
" A lichenoid drug eruption is a rare side effect which can occur following the administration of several different medications, but it has never been described after treatment with oral Cladribine."	( Lichenoid rash: A new side effect of oral Cladribine. Aruta, F; Costa, C; Iodice, R; Iovino, A; Manganelli, F, 2020)	1.01
" Serious adverse events (SAEs) and predefined SAEs of special interest were recorded."	( Long-term safety data from the cladribine tablets clinical development program in multiple sclerosis. Comi, G; Cook, S; Damian, D; Galazka, A; Giovannoni, G; Leist, T; Montalban, X; Nolting, A; Syed, S, 2020)	0.84
"825) or occurrence of adverse events (OR=0."	( Monitoring of safety and effectiveness of cladribine in multiple sclerosis patients over 50 years. Brescia Morra, V; Carotenuto, A; Disanto, G; Gobbi, C; Moccia, M; Sacco, R; Spiezia, AL; Zecca, C, 2022)	0.99
" Safety assessments, including occurrence of treatment-emergent adverse events (TEAEs; any adverse event reported after drug administration), serious adverse events (SAEs), and lymphocyte counts, were summarized descriptively."	( Treatment satisfaction, safety, and tolerability of cladribine tablets in patients with highly active relapsing multiple sclerosis: CLARIFY-MS study 6-month interim analysis. Alexandri, N; Brochet, B; Havrdova, EK; Hupperts, R; Keller, B; Langdon, D; Lechner-Scott, J; Montalban, X; Nolting, A; Patti, F; Piehl, F; Rejdak, K; Selmaj, K; Solari, A; Valis, M, 2022)	0.97
" This study aims at investigating in a real-world adverse event reporting system whether S1P receptor modulators increase the risk of skin cancer reporting, compared to other DMTs."	( S1P receptor modulators in Multiple Sclerosis: Detecting a potential skin cancer safety signal. Lallas, A; Papadopoulou, A; Papazisis, G; Rigas, A; Stamatellos, VP; Stamoula, E, 2022)	0.72
"Adverse event reports from the FDA Adverse Event Reporting System (FAERS) were extracted, cleaned, and analyzed from 2004Q1 until 2020Q4."	( S1P receptor modulators in Multiple Sclerosis: Detecting a potential skin cancer safety signal. Lallas, A; Papadopoulou, A; Papazisis, G; Rigas, A; Stamatellos, VP; Stamoula, E, 2022)	0.72
"CLARION aims to further evaluate adverse events of special interest in patients who are newly initiating treatment with cladribine tablets for relapsing multiple sclerosis (MS)."	( The CLARION study design and status update: a long-term, registry-based study evaluating adverse events of special interest in patients with relapsing multiple sclerosis newly started on cladribine tablets. Aydemir, A; Bezemer, I; Butzkueven, H; Korhonen, P; Moore, N; Sabidó, M; Sõnajalg, J, 2022)	1.12
"By providing further information on adverse events of special interest during long-term follow-up, CLARION will assist neurologists and patients regarding treatment decision-making for management of relapsing MS."	( The CLARION study design and status update: a long-term, registry-based study evaluating adverse events of special interest in patients with relapsing multiple sclerosis newly started on cladribine tablets. Aydemir, A; Bezemer, I; Butzkueven, H; Korhonen, P; Moore, N; Sabidó, M; Sõnajalg, J, 2022)	0.91
" Skin-related adverse events were common in the studies focusing on safety aspects."	( Real-world evidence for cladribine tablets in multiple sclerosis: further insights into efficacy and safety. Moser, T; Sellner, J; Ziemssen, T, 2022)	1.03
"This study provides level 4 evidence that AHSCT in patients previously treated with alemtuzumab, cladribine or rituximab is safe and efficacious."	( Impact of previous disease-modifying treatment on safety and efficacy in patients with MS treated with AHSCT. Burman, J; Bø, L; Kvistad, SAS; Lehmann, AK; Melve, GK; Tolf, A; Torkildsen, Ø; Zjukovskaja, C, 2022)	0.94
" A higher rate of adverse events (AEs) was revealed for alemtuzumab versus all other high-efficacy DMTs; for alemtuzumab (average probability of an event: 98."	( Comparative safety of high-efficacy disease-modifying therapies in relapsing-remitting multiple sclerosis: a systematic review and network meta-analysis. Holko, P; Kawalec, P; Osiecka, O; Śladowska, K, 2022)	0.72
"To describe the baseline characteristics of patients enrolled in the Argentina Patient Support Program (PSP) for cladribine tablets (Adveva®), with at least 1 treatment course, evaluate treatment persistence, adverse event reports from PSP patients and reported relapses characterization."	( High persistence and low adverse events burden in cladribine treated MS patients from Argentina. Assefi, A; D'Eramo, M; Etchepare, A; Grinspan, A; Iut, VC; Negrotto, L, 2022)	1.19
" In addition, using the pharmacovigilance data, reported adverse events and the time elapsed from treatment initiation to relapse were analyzed."	( High persistence and low adverse events burden in cladribine treated MS patients from Argentina. Assefi, A; D'Eramo, M; Etchepare, A; Grinspan, A; Iut, VC; Negrotto, L, 2022)	0.97
" During follow-up, 425 adverse events were reported, mainly MS relapse (8."	( High persistence and low adverse events burden in cladribine treated MS patients from Argentina. Assefi, A; D'Eramo, M; Etchepare, A; Grinspan, A; Iut, VC; Negrotto, L, 2022)	0.97
" We examined the Expanded Disability Severity Scale (EDSS), the proportion of severe adverse events, and cost in a 5-year period."	( Cost, efficacy, and safety comparison between early intensive and escalating strategies for multiple sclerosis: A systematic review and meta-analysis. Apóstolos-Pereira, SL; Callegaro, D; Mahler, JV; Nascimento, RFV; Pipek, LZ; Silva, GD, 2023)	0.91
" Sixty-two patients presented at least one side effect and globally 111 adverse events were recorded, none of them was serious."	( Effectiveness and safety profile of cladribine in an Italian real-life cohort of relapsing-remitting multiple sclerosis patients: a monocentric longitudinal observational study. Ferrè, L; Filippi, M; Martinelli, V; Meani, A; Moiola, L; Rocca, MA; Zanetta, C, 2023)	1.19
" Our analysis showed that infection is the most common adverse event after cladribine treatment with a pooled prevalence of 10% (95%CI 4%, 18%)."	( Safety and efficacy of cladribine in multiple sclerosis: a systematic review and meta-analysis. Afrashteh, F; Mirmosayyeb, O; Mohamadi, M; Nabizadeh, F; Najdaghi, S; Rahmani, S; Rajabi, R, 2023)	1.45
" Combination of our findings with the results of previous studies which compared cladribine to other disease-modifying therapies (DMTs), cladribine seems to be a safe and effective drug in achieving better treatment for relapsing-remitting MS (RRMS) patients."	( Safety and efficacy of cladribine in multiple sclerosis: a systematic review and meta-analysis. Afrashteh, F; Mirmosayyeb, O; Mohamadi, M; Nabizadeh, F; Najdaghi, S; Rahmani, S; Rajabi, R, 2023)	1.45
" Most frequent adverse reactions were lymphocytopenia (55%), infections (25."	( Safety and Effectiveness of Cladribine in Multiple Sclerosis: Real-World Clinical Experience From 5 Tertiary Hospitals in Portugal. Abreu, P; Brum, M; Capela, C; de Sá, J; Dias, R; Ferreira, J; Guerreiro, R; Ladeira, F; Leitão, L; Sá, MJ; Salgado, V; Santos, M; Sequeira, J, )	0.43
" Safety endpoints included lymphopenia, liver transaminases, and adverse events (AEs) during follow-up."	( Safety and effectiveness of cladribine tablets for multiple sclerosis: Results from a single-center real-world cohort. Aerts, S; Khan, H; Peeters, LM; Popescu, V; Severijns, D; Van Wijmeersch, B, 2023)	1.2
"To compare adverse effects of immunotherapies for people with MS or clinically isolated syndrome (CIS), and to rank these treatments according to their relative risks of adverse effects through network meta-analyses (NMAs)."	( Adverse effects of immunotherapies for multiple sclerosis: a network meta-analysis. Benedetti, MD; Capobussi, M; Castellini, G; Featherstone, R; Filippini, G; Frau, S; Gonzalez-Lorenzo, M; Lucenteforte, E; Perduca, V; Tramacere, I; Virgili, G, 2023)	0.91
" Our review, along with other work in the literature, confirms poor-quality reporting of adverse events from RCTs of interventions."	( Adverse effects of immunotherapies for multiple sclerosis: a network meta-analysis. Benedetti, MD; Capobussi, M; Castellini, G; Featherstone, R; Filippini, G; Frau, S; Gonzalez-Lorenzo, M; Lucenteforte, E; Perduca, V; Tramacere, I; Virgili, G, 2023)	0.91

Excerpt	Reference	Relevance
" The long terminal half-life of CdA after 2-h infusion supports the use of intermittent infusions."	( On the pharmacokinetics of 2-chloro-2'-deoxyadenosine in humans. Juliusson, G; Liliemark, J, 1991)	0.28
" Early pharmacokinetic data suggest that cladribine may be administered by oral and subcutaneous routes, both of which permit convenient outpatient therapy."	( Cladribine. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic potential in haematological malignancies. Bryson, HM; Sorkin, EM, 1993)	1.99
" The terminal phase half-life in 22 patients ranged from 14."	( Pharmacokinetics of cladribine (2-chlorodeoxyadenosine) in children with acute leukemia. Blakley, RL; Crom, WR; Kearns, CM; Santana, VM, 1994)	0.61
" Pharmacokinetic and pharmacodynamic interactions between CdA and ara-C during therapy were investigated."	( Chlorodeoxyadenosine and arabinosylcytosine in patients with acute myelogenous leukemia: pharmacokinetic, pharmacodynamic, and molecular interactions. Chucrallah, A; Estey, E; Gandhi, V; Keating, MJ; Plunkett, W, 1996)	0.29
"The pharmacokinetic parameters of cladribine (CdA) in patient plasma and its intracellular nucleotides CdA 5'-monophosphate (CdAMP) and CdA 5'-triphosphate (CdATP) were delineated in circulating leukemia cells in 17 patients with chronic lymphocytic leukemia, after the last dose intake and up to 72 h thereafter."	( Pharmacokinetics of cladribine in plasma and its 5'-monophosphate and 5'-triphosphate in leukemic cells of patients with chronic lymphocytic leukemia. Albertioni, F; Eriksson, S; Juliusson, G; Liliemark, J; Lindemalm, S; Pettersson, B; Reichelova, V, 1998)	0.9
" Furthermore, a method for pharmacodynamic modeling is introduced that permits a quantitative approach for the assessment of the sensitivity of tumor cells to anticancer drugs and combined treatments."	( Apoptosis- and necrosis-inducing potential of cladribine, cytarabine, cisplatin, and 5-fluorouracil in vitro: a quantitative pharmacodynamic model. Guchelaar, HJ; Haanen, C; Koopmans, RP; Reutelingsperger, CP; Vermes, I, 1998)	0.56
" The primary aim of the study was to evaluate the population distribution of pharmacokinetic parameters in patients undergoing treatment with cladribine and to detect the influence of different covariates on the pharmacokinetic parameters."	( Application of population pharmacokinetics to cladribine. Albertioni, F; Juliusson, G; Karlsson, MO; Liliemark, J; Lindemalm, S; Savic, RM, 2005)	0.79
"This pharmacokinetic study presents the results of a retrospective population pharmacokinetic analysis based on pooled data from 161 patients, who were given cladribine in different administration routes in various dosing regimens."	( Application of population pharmacokinetics to cladribine. Albertioni, F; Juliusson, G; Karlsson, MO; Liliemark, J; Lindemalm, S; Savic, RM, 2005)	0.78
" The half-life for the terminal phase was 16 hours."	( Application of population pharmacokinetics to cladribine. Albertioni, F; Juliusson, G; Karlsson, MO; Liliemark, J; Lindemalm, S; Savic, RM, 2005)	0.59
"To develop and validate a sensitive and specific HPLC assay for cladribine (CdA) in plasma for pharmacokinetic studies in rats."	( Development and validation of a sensitive and specific HPLC assay of cladribine for pharmacokinetics studies in rats. Ferguson, C; Jarrar, A; King, B; Li, ML; Yeung, PK, 2007)	0.81
" The assay was validated for sensitivity, precision, specificity and application for pharmacokinetic study in rats."	( Development and validation of a sensitive and specific HPLC assay of cladribine for pharmacokinetics studies in rats. Ferguson, C; Jarrar, A; King, B; Li, ML; Yeung, PK, 2007)	0.57
" The assay was used to study a single dose pharmacokinetic study of CdA in rats after a 2 mg/kg subcutaneous injection."	( Development and validation of a sensitive and specific HPLC assay of cladribine for pharmacokinetics studies in rats. Ferguson, C; Jarrar, A; King, B; Li, ML; Yeung, PK, 2007)	0.57
"The described HPLC assay has adequate sensitivity and specificity to study pharmacokinetics of CdA in rats, and could be adapted also to clinical pharmacokinetic studies."	( Development and validation of a sensitive and specific HPLC assay of cladribine for pharmacokinetics studies in rats. Ferguson, C; Jarrar, A; King, B; Li, ML; Yeung, PK, 2007)	0.57
" 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
" Topotecan dosing based on simultaneous drug monitoring and pharmacokinetic analysis can yield more accurate and precise estimation of the topotecan systemic exposure than that attainable with the fixed dosing approach."	( Topotecan exposure estimation in pediatric acute myeloid leukemia supported by LC-MS-based drug monitoring and pharmacokinetic analysis. Adamkiewicz-Drożyńska, E; Bączek, T; Balcerska, A; Belka, M; Konieczna, L; Maciejka-Kapuścińska, L; Niedźwiecki, M; Wachowiak, J; Wiśniewski, J, 2012)	0.38

Excerpt	Reference	Relevance
"The influence of 2-CdA administrated alone and in combination with CY or MTX on the survival time of mice bearing L1210 leukemia was investigated."	( Influence of 2-chloro-2'-deoxyadenosine alone and in combination with cyclophosphamide or methotrexate on murine leukemia L1210. Góra-Tybor, J; Grieb, P; Robak, T; Warzocha, K, 1994)	0.29
"The influence of 2-chlorodeoxyadenosine (2-CDA) administered alone or in combination with cyclophosphamide (CY) or methotrexate (MTX) on normal hematopoiesis in mice was investigated."	( The influence of 2-chlorodeoxyadenosine alone and in combination with cyclophosphamide or methotrexate on normal hematopoiesis in mice. Góra-Tybor, J; Robak, T, 1993)	0.29
" Both agents were used alone and in combination with these different concentrations."	( The comparison of 2-chlorodeoxyadenosine (2-Cd A) in combination with interferon alpha (IFN alpha) or interferon gamma (IFN gamma) on granulocyte-macrophage progenitor cells (CFU-GM) and clonogenic blasts in (CFU-L) in vitro cultures. Korycka, A; Robak, T, 1996)	0.29
" When CSA was combined with 2-CDA, no rejection was seen in 80% of the liver allografts and in 60% of heart allografts, and only mild rejection was observed in the remaining animals."	( 2-Chlorodeoxyadenosine (cladribine) in combination with low-dose cyclosporin prevents rejection after allogeneic heart and liver transplantation in the rat. Dietze, O; Fischer, M; Geisen, F; Hechenleitner, P; Klima, G; Konwalinka, G; Margreiter, R; Mark, W; Roberts, K; Schmid, T, 1998)	0.61
" Cladribine was combined with cisplatin, daunorubicin, chlorambucil, paclitaxel or etoposide."	( Cytotoxicity of 2-chlorodeoxadenosine (cladribine, 2-cdA) in combination with other chemotherapy drugs against two lymphoma cell lines. Hoffman, M; Lesser, M; Rai, K; Xu, JC, 1999)	1.48
"We evaluated the influence of amifostine used alone or in combination with 2-chlorodeoxyadenosine (2-CdA) on the colony growth of normal and chronic myeloid leukemia (CML) granulocyte-macrophage progenitor cells (CFU-GM) in semisolid culture in vitro."	( The influence of amifostine used alone or in combination with 2-chlorodeoxyadenosine on normal and chronic myelogenous leukemia granulocyte-macrophage progenitor cells in vitro. Korycka, A; Robak, T, 2000)	0.31
"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)	1.98
" In the second part, where the interaction between CsA and 2-CdA was examined, the animals were administered CsA at a dose of 15 mg/kg, or 2-CdA at a dose of 20 mg/kg, or CsA combined with 2-CdA at the same doses as in monotherapy."	( Cytotoxic effect of cyclosporin A alone and in combination with 2-chlorodeoxyadenosine against P388 murine leukemia in vivo. Józefowicz-Okonkwo, G; Robak, T; Szmigielska-Kapłon, A, 2002)	0.31
" 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)	0.58
"To identify the optimal schedule for infusion of cytarabine (ara-C) given with cladribine (2-CdA) to pediatric patients with acute myeloid leukemia (AML), and to compare the effects of the two schedules on the pharmacokinetics of ara-C triphosphate (ara-CTP) in leukemic cells."	( Interim comparison of a continuous infusion versus a short daily infusion of cytarabine given in combination with cladribine for pediatric acute myeloid leukemia. Behm, FG; Crews, KR; Gandhi, V; Plunkett, W; Pui, CH; Raimondi, SC; Razzouk, BI; Ribeiro, RC; Rubnitz, JE; Srivastava, DK; Stewart, CF; Tong, X, 2002)	0.75
"Intracellular accumulation of ara-CTP is increased when 2-CdA is given with ara-C, but no schedule-dependent differences in this effect were seen."	( Interim comparison of a continuous infusion versus a short daily infusion of cytarabine given in combination with cladribine for pediatric acute myeloid leukemia. Behm, FG; Crews, KR; Gandhi, V; Plunkett, W; Pui, CH; Raimondi, SC; Razzouk, BI; Ribeiro, RC; Rubnitz, JE; Srivastava, DK; Stewart, CF; Tong, X, 2002)	0.53
"The aim of the study was to evaluate the activity and toxicity of cladribine (2-CdA) in combination with cyclophosphamide (CY), the CC schedule, in patients with previously untreated B-cell chronic lymphocytic leukemia (B-CLL)."	( Cladribine combined with cyclophosphamide is highly effective in the treatment of chronic lymphocytic leukemia. Błoński, JZ; Dwilewicz-Trojaczek, J; Góra-Tybor, J; Kasznicki, M; Robak, T; Stella-Hołowiecka, B; Wołowiec, D, 2002)	1.99
" 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)	0.77
" 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)	1.49
"The anti-tumour in vitro activity of proteasome inhibitor bortezomib (PS-341, VELCADE) in combination with purine nucleoside analogues, cladribine (2-CdA) and fludarabine (FA) was tested in lymphocytes derived from 26 patients with B-cell chronic lymphocytic leukaemia (B-CLL)."	( In vitro cytotoxic effect of proteasome inhibitor bortezomib in combination with purine nucleoside analogues on chronic lymphocytic leukaemia cells. Cebula, B; Duechler, M; Linke, A; Robak, T; Schwarzmeier, JD; Shehata, M; Smolewski, P, 2005)	0.53
" The observed increase was especially evident when 5 nm of bortezomib were combined with suboptimal doses of 2-CdA or FA."	( In vitro cytotoxic effect of proteasome inhibitor bortezomib in combination with purine nucleoside analogues on chronic lymphocytic leukaemia cells. Cebula, B; Duechler, M; Linke, A; Robak, T; Schwarzmeier, JD; Shehata, M; Smolewski, P, 2005)	0.33
"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)	2
" The aim of this study was to evaluate the cytotoxicity of SDX-101 combined with agents proven to be effective as first-line treatment of B-CLL: the purine nucleoside analogs, fludarabine (FA) and cladribine (2-CdA), and the monoclonal antibodies, anti-CD52 (alemtuzumab; ALT) and anti-CD20 (rituximab; RIT)."	( Cytotoxic effect of R-etodolac (SDX-101) in combination with purine analogs or monoclonal antibodies on ex vivo B-cell chronic lymphocytic leukemia cells. Cebula, B; Linke, A; Robak, P; Robak, T; Smolewski, P, 2006)	0.52
"S), and its therapeutic potential in combination with a specific inhibitor of the signal transducer and activator of transcription 3 (STAT3)."	( Therapeutic potential of cladribine in combination with STAT3 inhibitor against multiple myeloma. Deng, XS; Lee, CK; Liu, B; Ma, J; Wang, S; Yu, XD; Zhao, M, 2011)	0.67
"S cells may particularly benefit from cladribine monotherapy, whereas cladribine in combination with STAT3 inhibitor exerts a broader therapeutic potential against MM."	( Therapeutic potential of cladribine in combination with STAT3 inhibitor against multiple myeloma. Deng, XS; Lee, CK; Liu, B; Ma, J; Wang, S; Yu, XD; Zhao, M, 2011)	0.94
"Cladribine (C) and fludarabine (F) combined with cyclophosphamide/mafosfamide in vivo, as well as ex vivo trigger apoptosis in CLL cells."	( In vivo and ex vivo responses of CLL cells to purine analogs combined with alkylating agent. Borowiak, A; Błoński, JZ; Cebula-Obrzut, B; Kiliańska, ZM; Kotkowska, A; Robak, T; Rogalińska, M; Smolewski, P; Wawrzyniak, E; Żołnierczyk, JD, 2013)	1.83
" After demonstrating the safety and feasibility in a phase I study, we conducted a phase II clinical study of CLAG (cladribine, cytarabine, granulocyte colony-stimulating factor) regimen combined with IM for patients with RR-AML."	( A Phase II Study of CLAG Regimen Combined With Imatinib Mesylate for Relapsed or Refractory Acute Myeloid Leukemia. Cubitt, C; Komrokji, RS; Lancet, JE; List, AF; Mirza, AS; Nardelli, L; Padron, E; Pinilla-Ibarz, J; Sweet, K, 2017)	0.66
" We evaluated two new lower-intensity regimens with clofarabine (n = 119) or cladribine (n = 129) combined with low-dose cytarabine (LDAC) alternating with decitabine."	( Long-term results of low-intensity chemotherapy with clofarabine or cladribine combined with low-dose cytarabine alternating with decitabine in older patients with newly diagnosed acute myeloid leukemia. Borthakur, G; Burger, J; Daver, N; DiNardo, CD; Estrov, Z; Ferrajoli, A; Garcia-Manero, G; Huang, X; Jabbour, E; Jain, N; Kadia, TM; Kanagal-Shamanna, R; Kantarjian, H; Konopleva, M; Pemmaraju, N; Pierce, S; Popat, U; Rausch, C; Ravandi, F; Verstovsek, S; Wang, X, 2021)	1.09
" Cladribine in monotherapy or in combination with cyclophosphamide were used for first line therapy."	( Therapy of 3 patients with Erdhiem-Chester disease with cladribin or cladribin in combination with cyclophosphamide. Case report and review of the therapy. Adam, Z; Koukalová, R; Král, Z; Krejčí, M; Pour, L; Řehák, Z; Sandecká, V; Ševčíková, S; Štork, M, 2021)	1.53
" Furthermore, CCK-8 was used to determine the effects of HCA, alone or in combination with apoptosis inhibitors, necroptosis inhibitors, ferroptosis inhibitors, or autophagy inhibitors, on the proliferation of HL60 and THP1 cells and to screen for possible HCA-mediated death pathways in AML cells."	( Homoharringtonine combined with cladribine and aclarubicin (HCA) in acute myeloid leukemia: A new regimen of conventional drugs and its mechanism. Chen, P; Wang, D; Wang, F; Xie, M; Yang, M, 2022)	1

Excerpt	Reference	Relevance
" The aim of the present study was to determine the bioavailability of subcutaneously (SC) and orally administered CdA, and to establish an oral dose of CdA that could supersede IV administration."	( On the bioavailability of oral and subcutaneous 2-chloro-2'-deoxyadenosine in humans: alternative routes of administration. Albertioni, F; Hassan, M; Juliusson, G; Liliemark, J, 1992)	0.28
"The bioavailability of SC CdA was 102% +/- 28% (mean +/- SD), and the bioavailability of CdA administered in enteric-coated capsules was 19%, 24%, and 60%."	( On the bioavailability of oral and subcutaneous 2-chloro-2'-deoxyadenosine in humans: alternative routes of administration. Albertioni, F; Hassan, M; Juliusson, G; Liliemark, J, 1992)	0.28
" Food intake did not significantly influence the bioavailability of CdA (42% after food intake vs 46% while fasting) but it did reduce the maximum plasma concentration (Cmax) by 40%; 83 compared to 116 nM while fasting."	( On the bioavailability of 2-chloro-2'-deoxyadenosine (CdA). The influence of food and omeprazole. Albertioni, F; Juliusson, G; Liliemark, J, 1993)	0.29
"This study was designed to evaluate the absolute bioavailability (F value) of 2-chlorodeoxyadenosine (cladribine; 2-CdA) after multiple oral administrations, and the intersubject variability after oral and 2-hour intravenous (IV) administration schedules in patients with malignancy."	( Pharmacokinetic study of oral and bolus intravenous 2-chlorodeoxyadenosine in patients with malignancy. Cheung, WK; Gollard, R; Johannsen, T; Kosty, M; Miller, WE; Moyer, M; Piro, LD; Rose, E; Saven, A; Smith, I, 1996)	0.51
"The F value of 2-CdA after oral administration was approximately 37% and there were no cumulative differences in bioavailability observed on multiple dosing of the drug."	( Pharmacokinetic study of oral and bolus intravenous 2-chlorodeoxyadenosine in patients with malignancy. Cheung, WK; Gollard, R; Johannsen, T; Kosty, M; Miller, WE; Moyer, M; Piro, LD; Rose, E; Saven, A; Smith, I, 1996)	0.29
" We previously established that the oral bioavailability of cladribine is 50%."	( Oral cladribine as primary therapy for patients with B-cell chronic lymphocytic leukemia. Christiansen, I; Elmhorn-Rosenborg, A; Hansen, MM; Johnson, S; Juliusson, G; Kimby, E; Liliemark, J, 1996)	1.05
" The oral bioavailability of cladribine is 37 to 51%, and that of subcutaneous administration is 100%."	( The clinical pharmacokinetics of cladribine. Liliemark, J, 1997)	0.87
" Our pharmacokinetic studies revealed that the bioavailability of subcutaneous cladribine is complete but that the concentration-time profile is very different from intravenous administration."	( Cladribine (2-CDA) given as subcutaneous bolus injections is active in pretreated Waldenström's macroglobulinaemia. Swiss Group for Clinical Cancer Research (SAKK). Betticher, DC; Cerny, T; Egger, T; Fey, MF; Hess, U; Hsu Schmitz, SF; Pugin, P; Ratschiller, D; Stalder, M; von Rohr, A, 1997)	1.97
" The oral bioavailability is only 50%."	( Bioavailability and bacterial degradation of rectally administered 2-chloro-2'-deoxyadenosine. Albertioni, F; Edlund, C; Juliusson, G; Liliemark, J, 1995)	0.29
" Bioavailability was 100% and 35% for subcutaneous and oral administration, respectively, with low interindividual variability."	( Application of population pharmacokinetics to cladribine. Albertioni, F; Juliusson, G; Karlsson, MO; Liliemark, J; Lindemalm, S; Savic, RM, 2005)	0.59
" Subcutaneous injection once daily is simple and effective due to 100% bioavailability and no local side effects from injection, and self-administration is easy."	( Hairy cell leukemia: epidemiology, pharmacokinetics of cladribine, and long-term follow-up of subcutaneous therapy. Juliusson, G; Samuelsson, H, 2011)	0.62
" The oral bioavailability of F-ara-A from 1,2-dimyristoylglycerophosphate derivative 29 was similar to its oral bioavailability from fludarabine phosphate."	( Phospholipid derivatives of cladribine and fludarabine: synthesis and biological properties. Baranovsky, A; Bogushevich, S; Golubeva, M; Kalinichenko, E; Kulak, T; Kuzmitsky, B; Tsybulskaya, I, 2015)	0.71
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."	( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019)	0.51

Excerpt	Relevance	Reference
" In addition, there was a dose-response relationship in all patients with improved cytoreduction of peripheral blast cells at higher doses of 2-CDA."	( A phase I clinical trial of 2-chlorodeoxyadenosine in pediatric patients with acute leukemia. Blakley, RL; Cherrie, J; Harwood, FC; Kalwinsky, D; Mirro, J; Santana, VM; Schell, M, 1991)	0.28
" The enhancement of the killing efficiency of X-rays by CdA was mainly observed in the reduction of quasi-threshold doses (Dq) of the dose-response curves."	( 2-Chlorodeoxyadenosine inhibits the repair of DNA double-strand breaks and does not inhibit the repair of DNA single-strand breaks in X-irradiated Chinese hamster V79 cells. Hiraoka, W; Kuwabara, M; Matsuda, A; Sato, F; Tamura, Y; Tanabe, K; Ueda, T, 1991)	0.28
" At an optimum dosage schedule, 2-BrdAdo and 2-CldAdo have similar therapeutic effects against L1210 in vivo, both producing over 99% cell kill, but the optimum dosage of 2-CldAdo is lower."	( Effects of cytotoxicity of 2-chloro-2'-deoxyadenosine and 2-bromo-2'-deoxyadenosine on cell growth, clonogenicity, DNA synthesis, and cell cycle kinetics. Ashmun, RA; Avery, TL; Blakley, RL; Huang, MC; Kuehl, M, 1986)	0.27
"The mechanism of action, pharmacokinetics, efficacy, adverse effects, storage, dosage and administration, and cost of cladribine are reviewed."	( Cladribine for the treatment of hematologic malignancies. Baltz, JK; Montello, MJ, 1993)	1.94
" Three dosage levels (4, 6, and 8 mg/m2/day) were explored, and patients were observed to determine toxicity."	( A phase I study of intermittent infusion cladribine in patients with solid tumors. Kobayashi, K; O'Brien, SM; Ratain, MJ; Schilsky, RL; Vogelzang, NJ; Vokes, EE, 1994)	0.55
" The median Cycle-1 leukocyte nadirs for the 4, 6, and 8 mg/m2/day dosage levels were 3100, 2300, and 950 cells/microliters (range 800-3500), respectively, and the and 950 cells/microliters (range 800-3500), respectively, and the mean nadir absolute neutrophil counts were 1500, 936, and 482 cells/microliters (range 130-2241), respectively."	( A phase I study of intermittent infusion cladribine in patients with solid tumors. Kobayashi, K; O'Brien, SM; Ratain, MJ; Schilsky, RL; Vogelzang, NJ; Vokes, EE, 1994)	0.55
"The F value of 2-CdA after oral administration was approximately 37% and there were no cumulative differences in bioavailability observed on multiple dosing of the drug."	( Pharmacokinetic study of oral and bolus intravenous 2-chlorodeoxyadenosine in patients with malignancy. Cheung, WK; Gollard, R; Johannsen, T; Kosty, M; Miller, WE; Moyer, M; Piro, LD; Rose, E; Saven, A; Smith, I, 1996)	0.29
" With our dosing and schedule, cladribine seems relatively safe in multiple sclerosis patients."	( Effect of repeated treatments with cladribine (2-chlorodeoxyadenosine) on blood counts in multiple sclerosis patients. Grieb, P; Jakubowska, B; Nowicki, J; Ryba, M; Solski, J; Stelmasiak, Z, 1995)	0.85
" With this agent, a dosage regimen of 25-30 mg/m2 daily over 5 days seems to be the most effective to date."	( Purine analogs in chronic lymphocytic leukemia and Waldenström's macroglobulinemia. Kantarjian, H; Keating, MJ; O'Brien, S, 1996)	0.29
" In addition, no evidence of DNA laddering, indicative of cellular apoptosis, was detected at these dosage levels and treatment times."	( 2-Chloro-2'-deoxyadenosine, an antileukemic drug, has an early effect on cellular mitochondrial function. Hentosh, P; Tibudan, M, 1997)	0.3
"These results demonstrate single-agent activity of cladribine in mantle-cell lymphomas using the intermittent two-hour infusion dosage regimen."	( Treatment of mantle-cell lymphomas with intermittent two-hour infusion of cladribine as first-line therapy or in first relapse. Bergmann, L; Chow, KU; Hansmann, ML; Hoelzer, D; Hossfeld, DK; Jäger, E; Meyer, A; Mitrou, PS; Peters, HD; Rummel, MJ, 1999)	0.79
" Interestingly, it was possible to arrest and even ameliorate the progression of MS by administering as little as 30% of the dosage recently recommended for the treatment of this disease."	( Cladribine treatment of a patient with hairy cell leukemia and concomitant multiple sclerosis. Berger, T; Hilbe, W; Konwalinka, G; Thaler, J, 1999)	1.75
" However, further studies are required to optimize the CdA schedule and dosage in order to ameliorate its toxic profile while maintaining antitumor activity."	( Fludarabine and cladribine in relapsed/refractory low-grade non-Hodgkin's lymphoma: a phase II randomized study. Balzarotti, M; Bonadonna, G; De Paoli, A; Luoni, M; Rampinelli, I; Santoro, A; Tondini, C; Valagussa, P, 2000)	0.65
"Microphthalmia appeared first in the dose-response curve."	( Exposure-disease continuum for 2-chloro-2'-deoxyadenosine, a prototype ocular teratogen. 1. Dose-response analysis. Charlap, JH; Knudsen, TB; Lau, C; Setzer, RW; Wubah, JA, 2001)	0.31
" The clustered dosage produced a lasting decline in granulocyte count, a delayed decrease in monocyte count, and a transient decrease in RBC count."	( Hematological effects of intermittent 2-hour infusions of cladribine in multiple sclerosis patients: a comparison of 2 dosage patterns. Chrapusta, SJ; Grieb, P; Hoser, G; Janisz, M; Kamienowski, J; Kawiak, J; Kuśnierczyk, P, 2001)	0.55
" CsA was used for the interaction study at a dosage of 15 mg/kg, as this was best tolerated by the animals."	( Cytotoxic effect of cyclosporin A alone and in combination with 2-chlorodeoxyadenosine against P388 murine leukemia in vivo. Józefowicz-Okonkwo, G; Robak, T; Szmigielska-Kapłon, A, 2002)	0.31
" More experience in the administration of 2-CdA to patients with renal insufficiency will be necessary to determine the need for dosage adjustment."	( Pharmacokinetics of 2-chlorodeoxyadenosine in a child undergoing hemofiltration and hemodialysis for acute renal failure. Crews, KR; Howard, SC; Hudson, JQ; Razzouk, BI; Ribeiro, RC; Wimmer, PS, 2002)	0.31
"This pharmacokinetic study presents the results of a retrospective population pharmacokinetic analysis based on pooled data from 161 patients, who were given cladribine in different administration routes in various dosing regimens."	( Application of population pharmacokinetics to cladribine. Albertioni, F; Juliusson, G; Karlsson, MO; Liliemark, J; Lindemalm, S; Savic, RM, 2005)	0.78
" Individualized dosing on basis of body surface area or weight does not represent an improvement in this study as compared to administering a fixed dose to all patients."	( Application of population pharmacokinetics to cladribine. Albertioni, F; Juliusson, G; Karlsson, MO; Liliemark, J; Lindemalm, S; Savic, RM, 2005)	0.59
" Because of its simplified dosing schedule, cladribine is commonly used as the initial therapy."	( Hairy cell leukemia: an elusive but treatable disease. de Castro, C; Wanko, SO, )	0.39
" After 1 year from first dose, cladribine dosage was repeated in four patients because of recurrence of relapses with subsequent similar positive clinical results."	( Cladribine in aggressive forms of multiple sclerosis. Cadavid, D; Cook, SD; Martinez-Rodriguez, JE; Pliner, L; Wolansky, LJ, 2007)	2.07
" This oral formulation is administered through intermittent, once-daily dosing to treat relapsing forms of MS."	( Cladribine tablets' potential in multiple: sclerosis treatment. Costello, K; Sipe, JC, 2008)	1.79
" Cladribine given as a single continuous intravenous seven-day infusion is the dosing schedule with the most durable complete remissions and evaluated in the greatest number of patients with HCL."	( Cladribine in the treatment of hairy cell leukemia: initial and subsequent results. Huynh, E; Saven, A; Sigal, D, 2009)	2.71
"The MTD was not reached in Stratum 1, but a DLT occurred at the lowest cladribine dosage (9."	( Combination of cladribine plus topotecan for recurrent or refractory pediatric acute myeloid leukemia. Crews, KR; Inaba, H; Pounds, S; Pui, CH; Razzouk, BI; Ribeiro, RC; Rubnitz, JE; Stewart, CF; Yang, S, 2010)	0.95
" This mechanism of action provides the rationale for use in relapsing-remitting multiple sclerosis (MS) in a short-course annual dosing regimen."	( Cladribine tablets: a potential new short-course annual treatment for relapsing multiple sclerosis. Sipe, JC, 2010)	1.8
" A reduced dosage of cladribine may also be advantageous since it may be associated with reduced toxicity and may set the dose needed for combinations with antibody treatments."	( Alternative methods of cladribine administration. Cencini, E; Forconi, F; Lauria, F, 2011)	1
" Newer methods of cladribine administration and modified dosing schedules have since been studied."	( My treatment approach to hairy cell leukemia. Naik, RR; Saven, A, 2012)	0.71
"Individualization of the topotecan dosing can reduce inter-patient variability, toxicity, and at the same time increases chemotherapy efficacy."	( Topotecan exposure estimation in pediatric acute myeloid leukemia supported by LC-MS-based drug monitoring and pharmacokinetic analysis. Adamkiewicz-Drożyńska, E; Bączek, T; Balcerska, A; Belka, M; Konieczna, L; Maciejka-Kapuścińska, L; Niedźwiecki, M; Wachowiak, J; Wiśniewski, J, 2012)	0.38
" Pharmacokinetic data showed that the 25 mg dosing of midostaurin achieved therapeutic levels with no significant interaction between midostaurin and ATRA."	( Phase I study of cladribine, cytarabine, granulocyte colony stimulating factor (CLAG regimen) and midostaurin and all-trans retinoic acid in relapsed/refractory AML. Abboud, CN; Cashen, A; Dipersio, JF; Fiala, M; McBride, A; Ramsingh, G; Stockerl-Goldstein, K; Uy, G; Vij, R; Westervelt, P, 2014)	0.74
" Therefore, in study AML-BFM 2004 we aimed to improve outcome of HR-patients by adding moderately dosed 2-Chloro-2-Deoxyadenosine (2-CDA) to the respective consolidation treatment backbone without increasing toxicity."	( Randomised Introduction of 2-CDA as Intensification during Consolidation for Children with High-risk AML--results from Study AML-BFM 2004. Bourquin, JP; Creutzig, U; Dworzak, M; Fleischhack, G; Graf, N; Gruhn, B; Klingebiel, T; Kremens, B; Lehrnbecher, T; Reinhardt, D; Stray, J; von Neuhoff, C; von Stackelberg, A; Zimmermann, M, 2015)	0.42
" The dosage was 10 mg/(m2 · d) for 4 days, and one course lasted for 28 days, the third to fifth courses of treatment used Arac in combination, the whole treating time lasted for 5 months."	( [Cladribine treatment of repeatedly-relapsed Langerhans cell histiocytosis: a case report and literature review]. Qing, S; Weihong, Z; Xintian, L; Yao, X; Ying, H, 2015)	1.33
" Expert opinion: Cladribine is well tolerated, it is dosed orally in cycles of one year, the need for regular blood testing during treatment is likely limited, and the two-year efficacy data for treatment of relapsing MS are at least in the same range as the most efficient licensed treatments."	( An update on cladribine for relapsing-remitting multiple sclerosis. Holmøy, T; Myhr, KM; Torkildsen, Ø, 2017)	1.16
" With patient-friendly short dosing periods and a favorable adverse event profile, cladribine tablets provide a sustained and strong reduction of MS disease activity."	( [Cladribine tablets : Oral immunotherapy of relapsing-remitting multiple sclerosis with short yearly treatment periods]. Aktas, O; Hartung, HP; Meuth, SG; Ruck, T, 2018)	1.62
" Personalised dosing led to grade 1-2 lymphopenia in 50% of cases."	( Treating the ineligible: Disease modification in people with multiple sclerosis beyond NHS England commissioning policies. Adams, A; Allen-Philbey, K; Álvarez-González, C; Baker, D; Campion, T; De Trane, S; Espasandin, M; Giovannoni, G; Gnanapavan, S; Mao, Z; Marta, M; Mathews, J; Schmierer, K; Turner, BP; Yildiz, O, 2019)	0.51
"Personalised dosing of cladribine avoided severe lymphopenia in all but one patients and was very well tolerated across a large spectrum of disease severity."	( Treating the ineligible: Disease modification in people with multiple sclerosis beyond NHS England commissioning policies. Adams, A; Allen-Philbey, K; Álvarez-González, C; Baker, D; Campion, T; De Trane, S; Espasandin, M; Giovannoni, G; Gnanapavan, S; Mao, Z; Marta, M; Mathews, J; Schmierer, K; Turner, BP; Yildiz, O, 2019)	0.82
" Therapy of multiple sclerosis is based on the use of anti-inflammatory and immunomodulating substances, however, there are certain disadvantages associated with the constant use of these drugs and a possible change in dosage over time."	( [New directions of immunocorrection in multiple sclerosis]. Boyko, AN; Evdoshenko, EP; Khachanova, NV; Melnikov, MV; Rozenson, OL; Sivertseva, SA; Spirin, NN; Vasilyev, AV, 2020)	0.56
" However, adjustments to dosing schedules may help de-risk the chance of infection further and reduce the concerns of people with MS being treated during the COVID-19 pandemic."	( The underpinning biology relating to multiple sclerosis disease modifying treatments during the COVID-19 pandemic. Amor, S; Baker, D; Giovannoni, G; Kang, AS; Schmierer, K, 2020)	0.56
"5 mg/kg group because this dosage is approved for relapsing forms of MS."	( Subgroup analysis of clinical and MRI outcomes in participants with a first clinical demyelinating event at risk of multiple sclerosis in the ORACLE-MS study. Bowen, JD; Cree, BAC; Damian, D; Dangond, F; Galazka, A; Grosso, M; Hartung, HP; Hughes, B; Hyvert, Y; Jones, DL; Leist, TP; Vermersch, P, 2021)	0.62
" We develop the Synthetic Lethality Knowledge Graph (SLKG), presenting the tumor therapy landscape of synthetic lethality (SL) and synthetic dosage lethality (SDL)."	( The tumor therapy landscape of synthetic lethality. Cai, X; Chen, L; Chen, X; Liu, Q; Sun, S; Tang, C; Wei, Z; Xing, F; Yao, Y; Zhang, B; Zhang, Z; Zhou, C, 2021)	0.62
" This results in a short dosing schedule (up to 20 days over 2 years of treatment) to sustain efficacy for at least another 2 years."	( Model-informed assessment of ethnic sensitivity and dosage justification for Asian populations in the global clinical development and use of cladribine tablets. Li, D; Liu, P; Munafo, A; Terranova, N; Venkatakrishnan, K, 2022)	0.92
" Controlled studies are warranted to examine a view that delaying the dosing interval by 3-6 months may allow more people to potentially seroconvert after vaccination."	( CD19 B cell repopulation after ocrelizumab, alemtuzumab and cladribine: Implications for SARS-CoV-2 vaccinations in multiple sclerosis. Baker, D; Dobson, R; Giovannoni, G; Kang, AS; MacDougall, A; Schmierer, K, 2022)	0.96
" The benefit of convenient dosing may be lost if side effects prevent people with MS from finishing their treatment."	( Side effects that occurred early in people with multiple sclerosis during the first year of treatment with cladribine tablets: a plain language summary. Aldridge, J; Dangond, F; Giovannoni, G; Jack, D; Lebson, LA; Leist, TP; Nolting, A; Oh, J; Walker, B, 2022)	0.93
" CLAD tablets are the first oral therapy with an infrequent dosing schedule, administered in two annual treatment courses, each divided into two treatment cycles comprising 4-5 days of treatment."	( Real-world evidence for cladribine tablets in multiple sclerosis: further insights into efficacy and safety. Moser, T; Sellner, J; Ziemssen, T, 2022)	1.03
"Researchers concluded the recommended 2-year dosing of cladribine tablets may reduce the number and severity of relapses in people with MS for up to 5 years."	( Relapses in people with multiple sclerosis treated with cladribine tablets followed for up to 5 years: a plain language summary. Alexandri, N; Coyle, PK; Dangond, F; Galazka, A; Giovannoni, G; Leist, TP; Rammohan, K; Sormani, MP; Stefano, N, 2022)	1.21
"Although most newborns are healthy, reinforced councelling on effective contraception 6 months after the last cladribine dosing is necessary."	( Cladribine and pregnancy in women with multiple sclerosis: The first cohort study. Ciplea, AI; Dost-Kovalsky, K; Gold, R; Hellwig, K; Thiel, S, 2023)	2.56
" The full treatment dosage of cladribine tablets is completed over two years and so these results may be conservative."	( Comparative effectiveness of cladribine tablets versus fingolimod in the treatment of highly active multiple sclerosis: A real-world study. Brownlee, WJ; Duncan, J; Haghikia, A; Harty, GT; Hayward, B; Kayaniyil, S; Khan, Z; Millar, S; Waser, N, 2023)	1.49

Role	Description
antineoplastic agent	A substance that inhibits or prevents the proliferation of neoplasms.
immunosuppressive agent	An agent that suppresses immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-cells or by inhibiting the activation of helper cells. In addition, an immunosuppressive agent is a role played by a compound which is exhibited by a capability to diminish the extent and/or voracity of an immune response.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Class	Description
purine 2'-deoxyribonucleoside	A 2'-deoxyribonucleoside that has a purine moiety as the nucleobase (the R group in the illustration).
organochlorine compound	An organochlorine compound is a compound containing at least one carbon-chlorine bond.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
glp-1 receptor, partial	Homo sapiens (human)	Potency	12.5893	0.0184	6.8060	14.1254	AID624417
Fumarate hydratase	Homo sapiens (human)	Potency	37.2212	0.0030	8.7949	48.0869	AID1347053
TDP1 protein	Homo sapiens (human)	Potency	0.0706	0.0008	11.3822	44.6684	AID686978; AID686979
GLI family zinc finger 3	Homo sapiens (human)	Potency	0.5736	0.0007	14.5928	83.7951	AID1259369; AID1259392
AR protein	Homo sapiens (human)	Potency	28.1838	0.0002	21.2231	8,912.5098	AID588515
Smad3	Homo sapiens (human)	Potency	35.4813	0.0052	7.8098	29.0929	AID588855
nuclear receptor subfamily 1, group I, member 3	Homo sapiens (human)	Potency	0.1211	0.0010	22.6508	76.6163	AID1224838; AID1224893
EWS/FLI fusion protein	Homo sapiens (human)	Potency	0.3187	0.0013	10.1577	42.8575	AID1259252; AID1259253; AID1259255; AID1259256
retinoic acid nuclear receptor alpha variant 1	Homo sapiens (human)	Potency	4.0217	0.0030	41.6115	22,387.1992	AID1159552; AID1159555
retinoid X nuclear receptor alpha	Homo sapiens (human)	Potency	6.7847	0.0008	17.5051	59.3239	AID1159527; AID1159531
estrogen-related nuclear receptor alpha	Homo sapiens (human)	Potency	33.2378	0.0015	30.6073	15,848.9004	AID1224841; AID1224842; AID1224848; AID1224849; AID1259401; AID1259403
farnesoid X nuclear receptor	Homo sapiens (human)	Potency	0.8650	0.3758	27.4851	61.6524	AID743217
pregnane X nuclear receptor	Homo sapiens (human)	Potency	4.3951	0.0054	28.0263	1,258.9301	AID1346982; AID720659
estrogen nuclear receptor alpha	Homo sapiens (human)	Potency	11.5124	0.0002	29.3054	16,493.5996	AID743069; AID743075; AID743078; AID743079
G	Vesicular stomatitis virus	Potency	26.8370	0.0123	8.9648	39.8107	AID1645842
polyprotein	Zika virus	Potency	37.2212	0.0030	8.7949	48.0869	AID1347053
67.9K protein	Vaccinia virus	Potency	8.5070	0.0001	8.4406	100.0000	AID720579; AID720580
peroxisome proliferator-activated receptor delta	Homo sapiens (human)	Potency	15.8977	0.0010	24.5048	61.6448	AID588535; AID743212
IDH1	Homo sapiens (human)	Potency	0.3663	0.0052	10.8652	35.4813	AID686970
Histone H2A.x	Cricetulus griseus (Chinese hamster)	Potency	17.0459	0.0391	47.5451	146.8240	AID1224845; AID1224896
cellular tumor antigen p53 isoform a	Homo sapiens (human)	Potency	18.8541	0.3162	12.4435	31.6228	AID902; AID924
nuclear factor erythroid 2-related factor 2 isoform 2	Homo sapiens (human)	Potency	2.9089	0.0041	9.9848	25.9290	AID504444; AID720524
thyroid hormone receptor beta isoform 2	Rattus norvegicus (Norway rat)	Potency	0.1765	0.0003	23.4451	159.6830	AID743065; AID743067
huntingtin isoform 2	Homo sapiens (human)	Potency	4.4668	0.0006	18.4198	1,122.0200	AID1688
tyrosine-protein kinase Yes	Homo sapiens (human)	Potency	79.2586	0.0000	5.0182	79.2586	AID686947
nuclear factor erythroid 2-related factor 2 isoform 1	Homo sapiens (human)	Potency	0.0217	0.0006	27.2152	1,122.0200	AID651741
urokinase-type plasminogen activator precursor	Mus musculus (house mouse)	Potency	0.3162	0.1585	5.2879	12.5893	AID540303
plasminogen precursor	Mus musculus (house mouse)	Potency	0.3162	0.1585	5.2879	12.5893	AID540303
urokinase plasminogen activator surface receptor precursor	Mus musculus (house mouse)	Potency	0.3162	0.1585	5.2879	12.5893	AID540303
nuclear receptor ROR-gamma isoform 1	Mus musculus (house mouse)	Potency	19.9526	0.0079	8.2332	1,122.0200	AID2551
geminin	Homo sapiens (human)	Potency	0.9048	0.0046	11.3741	33.4983	AID624296; AID624297
survival motor neuron protein isoform d	Homo sapiens (human)	Potency	7.6111	0.1259	12.2344	35.4813	AID1458
muscleblind-like protein 1 isoform 1	Homo sapiens (human)	Potency	0.1259	0.0041	9.9625	28.1838	AID2675
relaxin receptor 1 isoform 1	Homo sapiens (human)	Potency	19.1180	0.0388	14.3501	43.6206	AID2676
lamin isoform A-delta10	Homo sapiens (human)	Potency	0.5174	0.8913	12.0676	28.1838	AID1487
Interferon beta	Homo sapiens (human)	Potency	26.8370	0.0033	9.1582	39.8107	AID1645842
HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)	Potency	26.8370	0.0123	8.9648	39.8107	AID1645842
Cellular tumor antigen p53	Homo sapiens (human)	Potency	0.5968	0.0023	19.5956	74.0614	AID651631; AID651743; AID720552
Integrin beta-3	Homo sapiens (human)	Potency	25.1189	0.3162	11.4157	31.6228	AID924
Integrin alpha-IIb	Homo sapiens (human)	Potency	25.1189	0.3162	11.4157	31.6228	AID924
Rap guanine nucleotide exchange factor 4	Homo sapiens (human)	Potency	39.8107	3.9811	46.7448	112.2020	AID720708
Inositol hexakisphosphate kinase 1	Homo sapiens (human)	Potency	26.8370	0.0123	8.9648	39.8107	AID1645842
ATPase family AAA domain-containing protein 5	Homo sapiens (human)	Potency	9.4392	0.0119	17.9420	71.5630	AID651632
Ataxin-2	Homo sapiens (human)	Potency	9.4392	0.0119	12.2221	68.7989	AID651632
cytochrome P450 2C9, partial	Homo sapiens (human)	Potency	26.8370	0.0123	8.9648	39.8107	AID1645842
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)	IC50 (µMol)	10.0000	0.0000	1.7767	9.2000	AID1368375
ATP-binding cassette sub-family C member 3	Homo sapiens (human)	IC50 (µMol)	133.0000	0.6315	4.4531	9.3000	AID1473740
Multidrug resistance-associated protein 4	Homo sapiens (human)	IC50 (µMol)	133.0000	0.2000	5.6774	10.0000	AID1473741
Bile salt export pump	Homo sapiens (human)	IC50 (µMol)	133.0000	0.1100	7.1903	10.0000	AID1473738
Adenosine receptor A3	Rattus norvegicus (Norway rat)	Ki	207.0000	0.0003	0.9196	9.0000	AID33337
Canalicular multispecific organic anion transporter 1	Homo sapiens (human)	IC50 (µMol)	133.0000	2.4100	6.3433	10.0000	AID1473739
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Chain A, BCL-2-RELATED PROTEIN A1	Homo sapiens (human)	EC50 (µMol)	350.0000	8.0570	121.1218	338.0000	AID2765
bcl-2-like protein 11 isoform 1	Homo sapiens (human)	EC50 (µMol)	350.0000	8.0570	121.1218	338.0000	AID2765
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Deoxycytidine kinase	Homo sapiens (human)	Km	41.5500	0.4000	3.5790	8.5000	AID344442; AID344443
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
heart valve development	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
ventricular septum development	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
aorta development	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
negative regulation of transcription by RNA polymerase II	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled receptor signaling pathway	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
regulation of cGMP-mediated signaling	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cAMP-mediated signaling	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cGMP-mediated signaling	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cellular response to macrophage colony-stimulating factor stimulus	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
negative regulation of vascular permeability	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
positive regulation of vascular permeability	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
regulation of cAMP-mediated signaling	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cGMP catabolic process	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
positive regulation of inflammatory response	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
establishment of endothelial barrier	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cellular response to mechanical stimulus	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cellular response to cAMP	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cellular response to cGMP	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cellular response to transforming growth factor beta stimulus	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
negative regulation of adenylate cyclase-activating G protein-coupled receptor signaling pathway	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cellular response to 2,3,7,8-tetrachlorodibenzodioxine	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
positive regulation of gene expression	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
negative regulation of cGMP-mediated signaling	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
negative regulation of cAMP-mediated signaling	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
regulation of mitochondrion organization	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
xenobiotic metabolic process	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
xenobiotic transmembrane transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
bile acid and bile salt transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
glucuronoside transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
xenobiotic transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
transmembrane transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
leukotriene transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
monoatomic anion transmembrane transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
transport across blood-brain barrier	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
prostaglandin secretion	Multidrug resistance-associated protein 4	Homo sapiens (human)
cilium assembly	Multidrug resistance-associated protein 4	Homo sapiens (human)
platelet degranulation	Multidrug resistance-associated protein 4	Homo sapiens (human)
xenobiotic metabolic process	Multidrug resistance-associated protein 4	Homo sapiens (human)
xenobiotic transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
bile acid and bile salt transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
prostaglandin transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
urate transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
glutathione transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
cAMP transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
leukotriene transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
monoatomic anion transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
export across plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
transport across blood-brain barrier	Multidrug resistance-associated protein 4	Homo sapiens (human)
guanine nucleotide transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
fatty acid metabolic process	Bile salt export pump	Homo sapiens (human)
bile acid biosynthetic process	Bile salt export pump	Homo sapiens (human)
xenobiotic metabolic process	Bile salt export pump	Homo sapiens (human)
xenobiotic transmembrane transport	Bile salt export pump	Homo sapiens (human)
response to oxidative stress	Bile salt export pump	Homo sapiens (human)
bile acid metabolic process	Bile salt export pump	Homo sapiens (human)
response to organic cyclic compound	Bile salt export pump	Homo sapiens (human)
bile acid and bile salt transport	Bile salt export pump	Homo sapiens (human)
canalicular bile acid transport	Bile salt export pump	Homo sapiens (human)
protein ubiquitination	Bile salt export pump	Homo sapiens (human)
regulation of fatty acid beta-oxidation	Bile salt export pump	Homo sapiens (human)
carbohydrate transmembrane transport	Bile salt export pump	Homo sapiens (human)
bile acid signaling pathway	Bile salt export pump	Homo sapiens (human)
cholesterol homeostasis	Bile salt export pump	Homo sapiens (human)
response to estrogen	Bile salt export pump	Homo sapiens (human)
response to ethanol	Bile salt export pump	Homo sapiens (human)
xenobiotic export from cell	Bile salt export pump	Homo sapiens (human)
lipid homeostasis	Bile salt export pump	Homo sapiens (human)
phospholipid homeostasis	Bile salt export pump	Homo sapiens (human)
positive regulation of bile acid secretion	Bile salt export pump	Homo sapiens (human)
regulation of bile acid metabolic process	Bile salt export pump	Homo sapiens (human)
transmembrane transport	Bile salt export pump	Homo sapiens (human)
cell surface receptor signaling pathway via JAK-STAT	Interferon beta	Homo sapiens (human)
response to exogenous dsRNA	Interferon beta	Homo sapiens (human)
B cell activation involved in immune response	Interferon beta	Homo sapiens (human)
cell surface receptor signaling pathway	Interferon beta	Homo sapiens (human)
cell surface receptor signaling pathway via JAK-STAT	Interferon beta	Homo sapiens (human)
response to virus	Interferon beta	Homo sapiens (human)
positive regulation of autophagy	Interferon beta	Homo sapiens (human)
cytokine-mediated signaling pathway	Interferon beta	Homo sapiens (human)
natural killer cell activation	Interferon beta	Homo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT protein	Interferon beta	Homo sapiens (human)
cellular response to interferon-beta	Interferon beta	Homo sapiens (human)
B cell proliferation	Interferon beta	Homo sapiens (human)
negative regulation of viral genome replication	Interferon beta	Homo sapiens (human)
innate immune response	Interferon beta	Homo sapiens (human)
positive regulation of innate immune response	Interferon beta	Homo sapiens (human)
regulation of MHC class I biosynthetic process	Interferon beta	Homo sapiens (human)
negative regulation of T cell differentiation	Interferon beta	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Interferon beta	Homo sapiens (human)
defense response to virus	Interferon beta	Homo sapiens (human)
type I interferon-mediated signaling pathway	Interferon beta	Homo sapiens (human)
neuron cellular homeostasis	Interferon beta	Homo sapiens (human)
cellular response to exogenous dsRNA	Interferon beta	Homo sapiens (human)
cellular response to virus	Interferon beta	Homo sapiens (human)
negative regulation of Lewy body formation	Interferon beta	Homo sapiens (human)
negative regulation of T-helper 2 cell cytokine production	Interferon beta	Homo sapiens (human)
positive regulation of apoptotic signaling pathway	Interferon beta	Homo sapiens (human)
response to exogenous dsRNA	Interferon beta	Homo sapiens (human)
B cell differentiation	Interferon beta	Homo sapiens (human)
natural killer cell activation involved in immune response	Interferon beta	Homo sapiens (human)
adaptive immune response	Interferon beta	Homo sapiens (human)
T cell activation involved in immune response	Interferon beta	Homo sapiens (human)
humoral immune response	Interferon beta	Homo sapiens (human)
positive regulation of T cell mediated cytotoxicity	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
adaptive immune response	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, TAP-independent	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
regulation of T cell anergy	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
defense response	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
immune response	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
detection of bacterium	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
regulation of interleukin-12 production	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
regulation of interleukin-6 production	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
protection from natural killer cell mediated cytotoxicity	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
innate immune response	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
regulation of dendritic cell differentiation	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class Ib	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
negative regulation of cell population proliferation	Cellular tumor antigen p53	Homo sapiens (human)
regulation of cell cycle	Cellular tumor antigen p53	Homo sapiens (human)
regulation of cell cycle G2/M phase transition	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response	Cellular tumor antigen p53	Homo sapiens (human)
ER overload response	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to glucose starvation	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
regulation of apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of miRNA transcription	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of transcription by RNA polymerase II	Cellular tumor antigen p53	Homo sapiens (human)
mitophagy	Cellular tumor antigen p53	Homo sapiens (human)
in utero embryonic development	Cellular tumor antigen p53	Homo sapiens (human)
somitogenesis	Cellular tumor antigen p53	Homo sapiens (human)
release of cytochrome c from mitochondria	Cellular tumor antigen p53	Homo sapiens (human)
hematopoietic progenitor cell differentiation	Cellular tumor antigen p53	Homo sapiens (human)
T cell proliferation involved in immune response	Cellular tumor antigen p53	Homo sapiens (human)
B cell lineage commitment	Cellular tumor antigen p53	Homo sapiens (human)
T cell lineage commitment	Cellular tumor antigen p53	Homo sapiens (human)
response to ischemia	Cellular tumor antigen p53	Homo sapiens (human)
nucleotide-excision repair	Cellular tumor antigen p53	Homo sapiens (human)
double-strand break repair	Cellular tumor antigen p53	Homo sapiens (human)
regulation of DNA-templated transcription	Cellular tumor antigen p53	Homo sapiens (human)
regulation of transcription by RNA polymerase II	Cellular tumor antigen p53	Homo sapiens (human)
protein import into nucleus	Cellular tumor antigen p53	Homo sapiens (human)
autophagy	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
transforming growth factor beta receptor signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
Ras protein signal transduction	Cellular tumor antigen p53	Homo sapiens (human)
gastrulation	Cellular tumor antigen p53	Homo sapiens (human)
neuroblast proliferation	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of neuroblast proliferation	Cellular tumor antigen p53	Homo sapiens (human)
protein localization	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of DNA replication	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of cell population proliferation	Cellular tumor antigen p53	Homo sapiens (human)
determination of adult lifespan	Cellular tumor antigen p53	Homo sapiens (human)
mRNA transcription	Cellular tumor antigen p53	Homo sapiens (human)
rRNA transcription	Cellular tumor antigen p53	Homo sapiens (human)
response to salt stress	Cellular tumor antigen p53	Homo sapiens (human)
response to inorganic substance	Cellular tumor antigen p53	Homo sapiens (human)
response to X-ray	Cellular tumor antigen p53	Homo sapiens (human)
response to gamma radiation	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of gene expression	Cellular tumor antigen p53	Homo sapiens (human)
cardiac muscle cell apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of cardiac muscle cell apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
glial cell proliferation	Cellular tumor antigen p53	Homo sapiens (human)
viral process	Cellular tumor antigen p53	Homo sapiens (human)
glucose catabolic process to lactate via pyruvate	Cellular tumor antigen p53	Homo sapiens (human)
cerebellum development	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of cell growth	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
mitotic G1 DNA damage checkpoint signaling	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of telomere maintenance via telomerase	Cellular tumor antigen p53	Homo sapiens (human)
T cell differentiation in thymus	Cellular tumor antigen p53	Homo sapiens (human)
tumor necrosis factor-mediated signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
regulation of tissue remodeling	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to UV	Cellular tumor antigen p53	Homo sapiens (human)
multicellular organism growth	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of mitochondrial membrane permeability	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to glucose starvation	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
entrainment of circadian clock by photoperiod	Cellular tumor antigen p53	Homo sapiens (human)
mitochondrial DNA repair	Cellular tumor antigen p53	Homo sapiens (human)
regulation of DNA damage response, signal transduction by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of neuron apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
transcription initiation-coupled chromatin remodeling	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of proteolysis	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of DNA-templated transcription	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of DNA-templated transcription	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of RNA polymerase II transcription preinitiation complex assembly	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Cellular tumor antigen p53	Homo sapiens (human)
response to antibiotic	Cellular tumor antigen p53	Homo sapiens (human)
fibroblast proliferation	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of fibroblast proliferation	Cellular tumor antigen p53	Homo sapiens (human)
circadian behavior	Cellular tumor antigen p53	Homo sapiens (human)
bone marrow development	Cellular tumor antigen p53	Homo sapiens (human)
embryonic organ development	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylation	Cellular tumor antigen p53	Homo sapiens (human)
protein stabilization	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of helicase activity	Cellular tumor antigen p53	Homo sapiens (human)
protein tetramerization	Cellular tumor antigen p53	Homo sapiens (human)
chromosome organization	Cellular tumor antigen p53	Homo sapiens (human)
neuron apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
regulation of cell cycle	Cellular tumor antigen p53	Homo sapiens (human)
hematopoietic stem cell differentiation	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of glial cell proliferation	Cellular tumor antigen p53	Homo sapiens (human)
type II interferon-mediated signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
cardiac septum morphogenesis	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of programmed necrotic cell death	Cellular tumor antigen p53	Homo sapiens (human)
protein-containing complex assembly	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stress	Cellular tumor antigen p53	Homo sapiens (human)
thymocyte apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of thymocyte apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
necroptotic process	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to hypoxia	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to xenobiotic stimulus	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to ionizing radiation	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to gamma radiation	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to UV-C	Cellular tumor antigen p53	Homo sapiens (human)
stem cell proliferation	Cellular tumor antigen p53	Homo sapiens (human)
signal transduction by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
reactive oxygen species metabolic process	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to actinomycin D	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondria	Cellular tumor antigen p53	Homo sapiens (human)
cellular senescence	Cellular tumor antigen p53	Homo sapiens (human)
replicative senescence	Cellular tumor antigen p53	Homo sapiens (human)
oxidative stress-induced premature senescence	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
oligodendrocyte apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of execution phase of apoptosis	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of mitophagy	Cellular tumor antigen p53	Homo sapiens (human)
regulation of mitochondrial membrane permeability involved in apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
regulation of intrinsic apoptotic signaling pathway by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of miRNA transcription	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of G1 to G0 transition	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of miRNA processing	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of glucose catabolic process to lactate via pyruvate	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of pentose-phosphate shunt	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to hypoxia	Cellular tumor antigen p53	Homo sapiens (human)
regulation of fibroblast apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of reactive oxygen species metabolic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of reactive oxygen species metabolic process	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of stem cell proliferation	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of cellular senescence	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of low-density lipoprotein receptor activity	Integrin beta-3	Homo sapiens (human)
positive regulation of protein phosphorylation	Integrin beta-3	Homo sapiens (human)
positive regulation of endothelial cell proliferation	Integrin beta-3	Homo sapiens (human)
positive regulation of cell-matrix adhesion	Integrin beta-3	Homo sapiens (human)
cell-substrate junction assembly	Integrin beta-3	Homo sapiens (human)
cell adhesion	Integrin beta-3	Homo sapiens (human)
cell-matrix adhesion	Integrin beta-3	Homo sapiens (human)
integrin-mediated signaling pathway	Integrin beta-3	Homo sapiens (human)
embryo implantation	Integrin beta-3	Homo sapiens (human)
blood coagulation	Integrin beta-3	Homo sapiens (human)
positive regulation of endothelial cell migration	Integrin beta-3	Homo sapiens (human)
positive regulation of gene expression	Integrin beta-3	Homo sapiens (human)
negative regulation of macrophage derived foam cell differentiation	Integrin beta-3	Homo sapiens (human)
positive regulation of fibroblast migration	Integrin beta-3	Homo sapiens (human)
negative regulation of lipid storage	Integrin beta-3	Homo sapiens (human)
response to activity	Integrin beta-3	Homo sapiens (human)
smooth muscle cell migration	Integrin beta-3	Homo sapiens (human)
positive regulation of smooth muscle cell migration	Integrin beta-3	Homo sapiens (human)
platelet activation	Integrin beta-3	Homo sapiens (human)
positive regulation of vascular endothelial growth factor receptor signaling pathway	Integrin beta-3	Homo sapiens (human)
cell-substrate adhesion	Integrin beta-3	Homo sapiens (human)
activation of protein kinase activity	Integrin beta-3	Homo sapiens (human)
negative regulation of lipid transport	Integrin beta-3	Homo sapiens (human)
regulation of protein localization	Integrin beta-3	Homo sapiens (human)
regulation of actin cytoskeleton organization	Integrin beta-3	Homo sapiens (human)
cell adhesion mediated by integrin	Integrin beta-3	Homo sapiens (human)
positive regulation of cell adhesion mediated by integrin	Integrin beta-3	Homo sapiens (human)
positive regulation of osteoblast proliferation	Integrin beta-3	Homo sapiens (human)
heterotypic cell-cell adhesion	Integrin beta-3	Homo sapiens (human)
substrate adhesion-dependent cell spreading	Integrin beta-3	Homo sapiens (human)
tube development	Integrin beta-3	Homo sapiens (human)
wound healing, spreading of epidermal cells	Integrin beta-3	Homo sapiens (human)
cellular response to platelet-derived growth factor stimulus	Integrin beta-3	Homo sapiens (human)
apolipoprotein A-I-mediated signaling pathway	Integrin beta-3	Homo sapiens (human)
wound healing	Integrin beta-3	Homo sapiens (human)
apoptotic cell clearance	Integrin beta-3	Homo sapiens (human)
regulation of bone resorption	Integrin beta-3	Homo sapiens (human)
positive regulation of angiogenesis	Integrin beta-3	Homo sapiens (human)
positive regulation of bone resorption	Integrin beta-3	Homo sapiens (human)
symbiont entry into host cell	Integrin beta-3	Homo sapiens (human)
platelet-derived growth factor receptor signaling pathway	Integrin beta-3	Homo sapiens (human)
positive regulation of fibroblast proliferation	Integrin beta-3	Homo sapiens (human)
mesodermal cell differentiation	Integrin beta-3	Homo sapiens (human)
positive regulation of smooth muscle cell proliferation	Integrin beta-3	Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylation	Integrin beta-3	Homo sapiens (human)
negative regulation of lipoprotein metabolic process	Integrin beta-3	Homo sapiens (human)
negative chemotaxis	Integrin beta-3	Homo sapiens (human)
regulation of release of sequestered calcium ion into cytosol	Integrin beta-3	Homo sapiens (human)
regulation of serotonin uptake	Integrin beta-3	Homo sapiens (human)
angiogenesis involved in wound healing	Integrin beta-3	Homo sapiens (human)
positive regulation of ERK1 and ERK2 cascade	Integrin beta-3	Homo sapiens (human)
platelet aggregation	Integrin beta-3	Homo sapiens (human)
cellular response to mechanical stimulus	Integrin beta-3	Homo sapiens (human)
cellular response to xenobiotic stimulus	Integrin beta-3	Homo sapiens (human)
positive regulation of glomerular mesangial cell proliferation	Integrin beta-3	Homo sapiens (human)
blood coagulation, fibrin clot formation	Integrin beta-3	Homo sapiens (human)
maintenance of postsynaptic specialization structure	Integrin beta-3	Homo sapiens (human)
regulation of postsynaptic neurotransmitter receptor internalization	Integrin beta-3	Homo sapiens (human)
regulation of postsynaptic neurotransmitter receptor diffusion trapping	Integrin beta-3	Homo sapiens (human)
positive regulation of substrate adhesion-dependent cell spreading	Integrin beta-3	Homo sapiens (human)
positive regulation of adenylate cyclase-inhibiting opioid receptor signaling pathway	Integrin beta-3	Homo sapiens (human)
regulation of trophoblast cell migration	Integrin beta-3	Homo sapiens (human)
regulation of extracellular matrix organization	Integrin beta-3	Homo sapiens (human)
cellular response to insulin-like growth factor stimulus	Integrin beta-3	Homo sapiens (human)
negative regulation of endothelial cell apoptotic process	Integrin beta-3	Homo sapiens (human)
positive regulation of T cell migration	Integrin beta-3	Homo sapiens (human)
cell migration	Integrin beta-3	Homo sapiens (human)
positive regulation of leukocyte migration	Integrin alpha-IIb	Homo sapiens (human)
cell-matrix adhesion	Integrin alpha-IIb	Homo sapiens (human)
integrin-mediated signaling pathway	Integrin alpha-IIb	Homo sapiens (human)
angiogenesis	Integrin alpha-IIb	Homo sapiens (human)
cell-cell adhesion	Integrin alpha-IIb	Homo sapiens (human)
cell adhesion mediated by integrin	Integrin alpha-IIb	Homo sapiens (human)
pyrimidine nucleotide metabolic process	Deoxycytidine kinase	Homo sapiens (human)
CMP biosynthetic process	Deoxycytidine kinase	Homo sapiens (human)
dAMP salvage	Deoxycytidine kinase	Homo sapiens (human)
nucleoside phosphate biosynthetic process	Deoxycytidine kinase	Homo sapiens (human)
adaptive immune response	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
G protein-coupled receptor signaling pathway	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
adenylate cyclase-activating G protein-coupled receptor signaling pathway	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
calcium-ion regulated exocytosis	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
regulation of exocytosis	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
insulin secretion	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
positive regulation of insulin secretion	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
regulation of synaptic vesicle cycle	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
Ras protein signal transduction	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
regulation of insulin secretion	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
inositol phosphate metabolic process	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
phosphatidylinositol phosphate biosynthetic process	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
negative regulation of cold-induced thermogenesis	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol phosphate biosynthetic process	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
xenobiotic metabolic process	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
xenobiotic transmembrane transport	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
negative regulation of gene expression	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
bile acid and bile salt transport	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
bilirubin transport	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
heme catabolic process	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
xenobiotic export from cell	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
transmembrane transport	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
transepithelial transport	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
leukotriene transport	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
monoatomic anion transmembrane transport	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
transport across blood-brain barrier	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
xenobiotic transport across blood-brain barrier	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
cell population proliferation	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
positive regulation of B cell proliferation	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
nuclear DNA replication	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
signal transduction in response to DNA damage	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
isotype switching	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
positive regulation of DNA replication	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
positive regulation of isotype switching to IgG isotypes	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
DNA clamp unloading	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
regulation of mitotic cell cycle phase transition	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
positive regulation of cell cycle G2/M phase transition	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
negative regulation of receptor internalization	Ataxin-2	Homo sapiens (human)
regulation of translation	Ataxin-2	Homo sapiens (human)
RNA metabolic process	Ataxin-2	Homo sapiens (human)
P-body assembly	Ataxin-2	Homo sapiens (human)
stress granule assembly	Ataxin-2	Homo sapiens (human)
RNA transport	Ataxin-2	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
magnesium ion binding	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
3',5'-cyclic-AMP phosphodiesterase activity	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cGMP-stimulated cyclic-nucleotide phosphodiesterase activity	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
protein binding	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
zinc ion binding	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cAMP binding	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cGMP binding	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
TPR domain binding	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
phosphate ion binding	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
protein homodimerization activity	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
3',5'-cyclic-GMP phosphodiesterase activity	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
ATP binding	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ABC-type xenobiotic transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
glucuronoside transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ABC-type bile acid transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ATP hydrolysis activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ATPase-coupled transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
xenobiotic transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
icosanoid transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ABC-type transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
guanine nucleotide transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
protein binding	Multidrug resistance-associated protein 4	Homo sapiens (human)
ATP binding	Multidrug resistance-associated protein 4	Homo sapiens (human)
ABC-type xenobiotic transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
prostaglandin transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
urate transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
purine nucleotide transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ABC-type bile acid transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
efflux transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
15-hydroxyprostaglandin dehydrogenase (NAD+) activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ATP hydrolysis activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
glutathione transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ATPase-coupled transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
xenobiotic transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ABC-type transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
protein binding	Bile salt export pump	Homo sapiens (human)
ATP binding	Bile salt export pump	Homo sapiens (human)
ABC-type xenobiotic transporter activity	Bile salt export pump	Homo sapiens (human)
bile acid transmembrane transporter activity	Bile salt export pump	Homo sapiens (human)
canalicular bile acid transmembrane transporter activity	Bile salt export pump	Homo sapiens (human)
carbohydrate transmembrane transporter activity	Bile salt export pump	Homo sapiens (human)
ABC-type bile acid transporter activity	Bile salt export pump	Homo sapiens (human)
ATP hydrolysis activity	Bile salt export pump	Homo sapiens (human)
cytokine activity	Interferon beta	Homo sapiens (human)
cytokine receptor binding	Interferon beta	Homo sapiens (human)
type I interferon receptor binding	Interferon beta	Homo sapiens (human)
protein binding	Interferon beta	Homo sapiens (human)
chloramphenicol O-acetyltransferase activity	Interferon beta	Homo sapiens (human)
TAP binding	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
signaling receptor binding	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
protein binding	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
peptide antigen binding	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
TAP binding	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
protein-folding chaperone binding	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
transcription cis-regulatory region binding	Cellular tumor antigen p53	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specific	Cellular tumor antigen p53	Homo sapiens (human)
cis-regulatory region sequence-specific DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
core promoter sequence-specific DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
TFIID-class transcription factor complex binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specific	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specific	Cellular tumor antigen p53	Homo sapiens (human)
protease binding	Cellular tumor antigen p53	Homo sapiens (human)
p53 binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
chromatin binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription factor activity	Cellular tumor antigen p53	Homo sapiens (human)
mRNA 3'-UTR binding	Cellular tumor antigen p53	Homo sapiens (human)
copper ion binding	Cellular tumor antigen p53	Homo sapiens (human)
protein binding	Cellular tumor antigen p53	Homo sapiens (human)
zinc ion binding	Cellular tumor antigen p53	Homo sapiens (human)
enzyme binding	Cellular tumor antigen p53	Homo sapiens (human)
receptor tyrosine kinase binding	Cellular tumor antigen p53	Homo sapiens (human)
ubiquitin protein ligase binding	Cellular tumor antigen p53	Homo sapiens (human)
histone deacetylase regulator activity	Cellular tumor antigen p53	Homo sapiens (human)
ATP-dependent DNA/DNA annealing activity	Cellular tumor antigen p53	Homo sapiens (human)
identical protein binding	Cellular tumor antigen p53	Homo sapiens (human)
histone deacetylase binding	Cellular tumor antigen p53	Homo sapiens (human)
protein heterodimerization activity	Cellular tumor antigen p53	Homo sapiens (human)
protein-folding chaperone binding	Cellular tumor antigen p53	Homo sapiens (human)
protein phosphatase 2A binding	Cellular tumor antigen p53	Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor binding	Cellular tumor antigen p53	Homo sapiens (human)
14-3-3 protein binding	Cellular tumor antigen p53	Homo sapiens (human)
MDM2/MDM4 family protein binding	Cellular tumor antigen p53	Homo sapiens (human)
disordered domain specific binding	Cellular tumor antigen p53	Homo sapiens (human)
general transcription initiation factor binding	Cellular tumor antigen p53	Homo sapiens (human)
molecular function activator activity	Cellular tumor antigen p53	Homo sapiens (human)
promoter-specific chromatin binding	Cellular tumor antigen p53	Homo sapiens (human)
fibroblast growth factor binding	Integrin beta-3	Homo sapiens (human)
C-X3-C chemokine binding	Integrin beta-3	Homo sapiens (human)
insulin-like growth factor I binding	Integrin beta-3	Homo sapiens (human)
neuregulin binding	Integrin beta-3	Homo sapiens (human)
virus receptor activity	Integrin beta-3	Homo sapiens (human)
fibronectin binding	Integrin beta-3	Homo sapiens (human)
protease binding	Integrin beta-3	Homo sapiens (human)
protein disulfide isomerase activity	Integrin beta-3	Homo sapiens (human)
protein kinase C binding	Integrin beta-3	Homo sapiens (human)
platelet-derived growth factor receptor binding	Integrin beta-3	Homo sapiens (human)
integrin binding	Integrin beta-3	Homo sapiens (human)
protein binding	Integrin beta-3	Homo sapiens (human)
coreceptor activity	Integrin beta-3	Homo sapiens (human)
enzyme binding	Integrin beta-3	Homo sapiens (human)
identical protein binding	Integrin beta-3	Homo sapiens (human)
vascular endothelial growth factor receptor 2 binding	Integrin beta-3	Homo sapiens (human)
metal ion binding	Integrin beta-3	Homo sapiens (human)
cell adhesion molecule binding	Integrin beta-3	Homo sapiens (human)
extracellular matrix binding	Integrin beta-3	Homo sapiens (human)
fibrinogen binding	Integrin beta-3	Homo sapiens (human)
protein binding	Integrin alpha-IIb	Homo sapiens (human)
identical protein binding	Integrin alpha-IIb	Homo sapiens (human)
metal ion binding	Integrin alpha-IIb	Homo sapiens (human)
extracellular matrix binding	Integrin alpha-IIb	Homo sapiens (human)
molecular adaptor activity	Integrin alpha-IIb	Homo sapiens (human)
fibrinogen binding	Integrin alpha-IIb	Homo sapiens (human)
integrin binding	Integrin alpha-IIb	Homo sapiens (human)
deoxyadenosine kinase activity	Deoxycytidine kinase	Homo sapiens (human)
deoxycytidine kinase activity	Deoxycytidine kinase	Homo sapiens (human)
deoxyguanosine kinase activity	Deoxycytidine kinase	Homo sapiens (human)
ATP binding	Deoxycytidine kinase	Homo sapiens (human)
protein homodimerization activity	Deoxycytidine kinase	Homo sapiens (human)
cytidine kinase activity	Deoxycytidine kinase	Homo sapiens (human)
guanyl-nucleotide exchange factor activity	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
protein binding	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
cAMP binding	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
protein-macromolecule adaptor activity	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
small GTPase binding	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
inositol-1,3,4,5,6-pentakisphosphate kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol hexakisphosphate kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol heptakisphosphate kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol hexakisphosphate 5-kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
protein binding	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
ATP binding	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol hexakisphosphate 1-kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol hexakisphosphate 3-kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol 5-diphosphate pentakisphosphate 5-kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol diphosphate tetrakisphosphate kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
protein binding	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ATP binding	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
organic anion transmembrane transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ABC-type xenobiotic transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
bilirubin transmembrane transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ATP hydrolysis activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ATPase-coupled transmembrane transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
xenobiotic transmembrane transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
ABC-type transporter activity	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
protein binding	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
ATP binding	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
ATP hydrolysis activity	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
DNA clamp unloader activity	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
DNA binding	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
RNA binding	Ataxin-2	Homo sapiens (human)
epidermal growth factor receptor binding	Ataxin-2	Homo sapiens (human)
protein binding	Ataxin-2	Homo sapiens (human)
mRNA binding	Ataxin-2	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
plasma membrane	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
nucleus	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cytoplasm	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
mitochondrial outer membrane	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
mitochondrial inner membrane	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
endoplasmic reticulum	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
Golgi apparatus	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cytosol	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
plasma membrane	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
presynaptic membrane	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
perinuclear region of cytoplasm	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
nucleus	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
mitochondrial inner membrane	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
perinuclear region of cytoplasm	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
mitochondrial outer membrane	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
synaptic membrane	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
cytosol	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
mitochondrial matrix	cGMP-dependent 3',5'-cyclic phosphodiesterase	Homo sapiens (human)
plasma membrane	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
basal plasma membrane	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
basolateral plasma membrane	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
membrane	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
nucleolus	Multidrug resistance-associated protein 4	Homo sapiens (human)
Golgi apparatus	Multidrug resistance-associated protein 4	Homo sapiens (human)
plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
basolateral plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
apical plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
platelet dense granule membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
external side of apical plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
basolateral plasma membrane	Bile salt export pump	Homo sapiens (human)
Golgi membrane	Bile salt export pump	Homo sapiens (human)
endosome	Bile salt export pump	Homo sapiens (human)
plasma membrane	Bile salt export pump	Homo sapiens (human)
cell surface	Bile salt export pump	Homo sapiens (human)
apical plasma membrane	Bile salt export pump	Homo sapiens (human)
intercellular canaliculus	Bile salt export pump	Homo sapiens (human)
intracellular canaliculus	Bile salt export pump	Homo sapiens (human)
recycling endosome	Bile salt export pump	Homo sapiens (human)
recycling endosome membrane	Bile salt export pump	Homo sapiens (human)
extracellular exosome	Bile salt export pump	Homo sapiens (human)
membrane	Bile salt export pump	Homo sapiens (human)
extracellular space	Interferon beta	Homo sapiens (human)
extracellular region	Interferon beta	Homo sapiens (human)
Golgi membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
endoplasmic reticulum	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
Golgi apparatus	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
plasma membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
cell surface	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
ER to Golgi transport vesicle membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
secretory granule membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
phagocytic vesicle membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
early endosome membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
recycling endosome membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
extracellular exosome	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
lumenal side of endoplasmic reticulum membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
MHC class I protein complex	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
extracellular space	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
external side of plasma membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
nuclear body	Cellular tumor antigen p53	Homo sapiens (human)
nucleus	Cellular tumor antigen p53	Homo sapiens (human)
nucleoplasm	Cellular tumor antigen p53	Homo sapiens (human)
replication fork	Cellular tumor antigen p53	Homo sapiens (human)
nucleolus	Cellular tumor antigen p53	Homo sapiens (human)
cytoplasm	Cellular tumor antigen p53	Homo sapiens (human)
mitochondrion	Cellular tumor antigen p53	Homo sapiens (human)
mitochondrial matrix	Cellular tumor antigen p53	Homo sapiens (human)
endoplasmic reticulum	Cellular tumor antigen p53	Homo sapiens (human)
centrosome	Cellular tumor antigen p53	Homo sapiens (human)
cytosol	Cellular tumor antigen p53	Homo sapiens (human)
nuclear matrix	Cellular tumor antigen p53	Homo sapiens (human)
PML body	Cellular tumor antigen p53	Homo sapiens (human)
transcription repressor complex	Cellular tumor antigen p53	Homo sapiens (human)
site of double-strand break	Cellular tumor antigen p53	Homo sapiens (human)
germ cell nucleus	Cellular tumor antigen p53	Homo sapiens (human)
chromatin	Cellular tumor antigen p53	Homo sapiens (human)
transcription regulator complex	Cellular tumor antigen p53	Homo sapiens (human)
protein-containing complex	Cellular tumor antigen p53	Homo sapiens (human)
glutamatergic synapse	Integrin beta-3	Homo sapiens (human)
nucleus	Integrin beta-3	Homo sapiens (human)
nucleoplasm	Integrin beta-3	Homo sapiens (human)
plasma membrane	Integrin beta-3	Homo sapiens (human)
cell-cell junction	Integrin beta-3	Homo sapiens (human)
focal adhesion	Integrin beta-3	Homo sapiens (human)
external side of plasma membrane	Integrin beta-3	Homo sapiens (human)
cell surface	Integrin beta-3	Homo sapiens (human)
apical plasma membrane	Integrin beta-3	Homo sapiens (human)
platelet alpha granule membrane	Integrin beta-3	Homo sapiens (human)
lamellipodium membrane	Integrin beta-3	Homo sapiens (human)
filopodium membrane	Integrin beta-3	Homo sapiens (human)
microvillus membrane	Integrin beta-3	Homo sapiens (human)
ruffle membrane	Integrin beta-3	Homo sapiens (human)
integrin alphav-beta3 complex	Integrin beta-3	Homo sapiens (human)
melanosome	Integrin beta-3	Homo sapiens (human)
synapse	Integrin beta-3	Homo sapiens (human)
postsynaptic membrane	Integrin beta-3	Homo sapiens (human)
extracellular exosome	Integrin beta-3	Homo sapiens (human)
integrin alphaIIb-beta3 complex	Integrin beta-3	Homo sapiens (human)
glycinergic synapse	Integrin beta-3	Homo sapiens (human)
integrin complex	Integrin beta-3	Homo sapiens (human)
protein-containing complex	Integrin beta-3	Homo sapiens (human)
alphav-beta3 integrin-PKCalpha complex	Integrin beta-3	Homo sapiens (human)
alphav-beta3 integrin-IGF-1-IGF1R complex	Integrin beta-3	Homo sapiens (human)
alphav-beta3 integrin-HMGB1 complex	Integrin beta-3	Homo sapiens (human)
receptor complex	Integrin beta-3	Homo sapiens (human)
alphav-beta3 integrin-vitronectin complex	Integrin beta-3	Homo sapiens (human)
alpha9-beta1 integrin-ADAM8 complex	Integrin beta-3	Homo sapiens (human)
focal adhesion	Integrin beta-3	Homo sapiens (human)
cell surface	Integrin beta-3	Homo sapiens (human)
synapse	Integrin beta-3	Homo sapiens (human)
plasma membrane	Integrin alpha-IIb	Homo sapiens (human)
focal adhesion	Integrin alpha-IIb	Homo sapiens (human)
cell surface	Integrin alpha-IIb	Homo sapiens (human)
platelet alpha granule membrane	Integrin alpha-IIb	Homo sapiens (human)
extracellular exosome	Integrin alpha-IIb	Homo sapiens (human)
integrin alphaIIb-beta3 complex	Integrin alpha-IIb	Homo sapiens (human)
blood microparticle	Integrin alpha-IIb	Homo sapiens (human)
integrin complex	Integrin alpha-IIb	Homo sapiens (human)
external side of plasma membrane	Integrin alpha-IIb	Homo sapiens (human)
nucleoplasm	Deoxycytidine kinase	Homo sapiens (human)
cytosol	Deoxycytidine kinase	Homo sapiens (human)
mitochondrion	Deoxycytidine kinase	Homo sapiens (human)
cytoplasm	Deoxycytidine kinase	Homo sapiens (human)
cytosol	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
plasma membrane	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
membrane	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
hippocampal mossy fiber to CA3 synapse	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
plasma membrane	Rap guanine nucleotide exchange factor 4	Homo sapiens (human)
fibrillar center	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
nucleoplasm	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
cytosol	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
nucleus	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
cytoplasm	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
plasma membrane	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
cell surface	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
apical plasma membrane	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
intercellular canaliculus	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
apical plasma membrane	Canalicular multispecific organic anion transporter 1	Homo sapiens (human)
Elg1 RFC-like complex	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
nucleus	ATPase family AAA domain-containing protein 5	Homo sapiens (human)
cytoplasm	Ataxin-2	Homo sapiens (human)
Golgi apparatus	Ataxin-2	Homo sapiens (human)
trans-Golgi network	Ataxin-2	Homo sapiens (human)
cytosol	Ataxin-2	Homo sapiens (human)
cytoplasmic stress granule	Ataxin-2	Homo sapiens (human)
membrane	Ataxin-2	Homo sapiens (human)
perinuclear region of cytoplasm	Ataxin-2	Homo sapiens (human)
ribonucleoprotein complex	Ataxin-2	Homo sapiens (human)
cytoplasmic stress granule	Ataxin-2	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Assay ID	Title	Year	Journal	Article
AID588460	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588460	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set	2006	Cytometry. 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.
AID588460	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588461	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588461	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set	2006	Cytometry. 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.
AID588461	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588459	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588459	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set	2006	Cytometry. 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.
AID588459	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504810	Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign	2010	Endocrinology, Jul, Volume: 151, Issue:7	A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID504812	Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign	2010	Endocrinology, Jul, Volume: 151, Issue:7	A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID588501	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set	2006	Cytometry. 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.
AID588501	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588497	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set	2006	Cytometry. 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.
AID588497	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID651635	Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1745845	Primary qHTS for Inhibitors of ATXN expression
AID588499	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set	2006	Cytometry. 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.
AID588499	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID686947	qHTS for small molecule inhibitors of Yes1 kinase: Primary Screen	2013	Bioorganic & medicinal chemistry letters, Aug-01, Volume: 23, Issue:15	Identification of potent Yes1 kinase inhibitors using a library screening approach.
AID504749	qHTS profiling for inhibitors of Plasmodium falciparum proliferation	2011	Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043	Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID1347092	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347129	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-SH cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347089	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508630	Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay	2021	Cell reports, 04-27, Volume: 35, Issue:4	A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347116	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SJ-GBM2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347114	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for DAOY cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347115	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB-EBc1 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346987	P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347105	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1296008	Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening	2020	SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1	Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347113	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for LAN-5 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347123	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh41 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347127	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Saos-2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347117	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-37 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347110	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for A673 cells)	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347122	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for U-2 OS cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347126	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh30 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347125	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh18 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347124	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for RD cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347128	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for OHS-50 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347119	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for MG 63 (6-TG R) cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347111	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-MC cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347121	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for control Hh wild type fibroblast cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154	Primary screen GU AMC qHTS for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347083	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347101	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347112	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-12 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347109	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB1643 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346986	P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347118	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for TC32 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID625283	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079947	Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID588215	FDA HLAED, alkaline phosphatase increase	2004	Current 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.
AID445376	Cell cycle arrest in human CCRF-CEM assessed as accumulation at G2/M phase at 1 x GIC50 after 24 hrs by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID1174818	Cytotoxicity against human HCT116 cells after 72 hrs by SRB assay	2015	European journal of medicinal chemistry, Jan-07, Volume: 89	Synthesis of novel substituted purine derivatives and identification of the cell death mechanism.
AID1079941	Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1368376	Inhibition of recombinant human PDE2A catalytic domain (580 to 919 residues) expressed in Escherichia coli BL21 (Codonplus) at 1 uM using [3H]cGMP as substrate after 15 mins by liquid scintillation counting method relative to control	2018	Bioorganic & medicinal chemistry, 01-01, Volume: 26, Issue:1	Discovery of novel purine nucleoside derivatives as phosphodiesterase 2 (PDE2) inhibitors: Structure-based virtual screening, optimization and biological evaluation.
AID1079940	Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1236700	Antiproliferative activity against human RPMI8226 cells assessed as cell growth inhibition after 48 hrs by MTT assay	2015	Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13	Phospholipid derivatives of cladribine and fludarabine: synthesis and biological properties.
AID445468	Inhibition of [3H]adenine binding to adenine 1 receptor in rat brain cortical membrane at 100 uM by liquid scintillation counting	2009	Journal of medicinal chemistry, Oct-08, Volume: 52, Issue:19	Structure-activity relationships of adenine and deazaadenine derivatives as ligands for adenine receptors, a new purinergic receptor family.
AID344449	Ratio of Kcat for human deoxycytidine kinase C4S mutant to Km for deoxycytidine kinase C4S mutant in presence of UTP	2008	Journal of medicinal chemistry, Jul-24, Volume: 51, Issue:14	Elucidation of different binding modes of purine nucleosides to human deoxycytidine kinase.
AID1079943	Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1473741	Inhibition of human MRP4 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay	2013	Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1	A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1197746	Stimulation of human OATP1B3-mediated [3H]CCK-8 at 100 uM after 5 mins relative to control	2015	European journal of medicinal chemistry, Mar-06, Volume: 92	Interaction of human organic anion transporter polypeptides 1B1 and 1B3 with antineoplastic compounds.
AID1197742	Stimulation of human OATP1B1-mediated [3H]estrone 3-sulfate at 100 uM after 5 mins relative to control	2015	European journal of medicinal chemistry, Mar-06, Volume: 92	Interaction of human organic anion transporter polypeptides 1B1 and 1B3 with antineoplastic compounds.
AID1474167	Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status	2016	Drug discovery today, Apr, Volume: 21, Issue:4	DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID588218	FDA HLAED, lactate dehydrogenase (LDH) increase	2004	Current 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.
AID1370963	Antiproliferative activity against human HCT116 cells after 72 hrs by SRB assay	2018	Bioorganic & medicinal chemistry letters, 02-01, Volume: 28, Issue:3	Synthesis of novel 6-substituted amino-9-(β-d-ribofuranosyl)purine analogs and their bioactivities on human epithelial cancer cells.
AID425652	Total body clearance in human	2009	Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15	Physicochemical determinants of human renal clearance.
AID344447	Activity of human deoxycytidine kinase C4S mutant in presence of UTP	2008	Journal of medicinal chemistry, Jul-24, Volume: 51, Issue:14	Elucidation of different binding modes of purine nucleosides to human deoxycytidine kinase.
AID625281	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625295	Drug Induced Liver Injury Prediction System (DILIps) validation dataset; compound DILI positive/negative as observed in Pfizer data	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625287	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID425653	Renal clearance in human	2009	Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15	Physicochemical determinants of human renal clearance.
AID588216	FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase	2004	Current 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.
AID1079933	Acute 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
AID1079946	Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID611460	Cytotoxicity against human MDA-MB-231 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID1079949	Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID617760	Cytotoxicity against human CCRF-CEM cells after 72 hrs by MTT assay	2011	Bioorganic & medicinal chemistry, Sep-15, Volume: 19, Issue:18	Synthesis and biological evaluation of 2',4'- and 3',4'-bridged nucleoside analogues.
AID1079948	Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID1079935	Cytolytic 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]
AID31885	Binding affinity to adenosine A1 receptor in rat brain membranes by measuring displacement of specific [3H]PIA as radioligand.	1995	Journal of medicinal chemistry, Mar-31, Volume: 38, Issue:7	Search for new purine- and ribose-modified adenosine analogues as selective agonists and antagonists at adenosine receptors.
AID611469	Cytotoxicity against rat MAT-LyLu cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID625286	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588214	FDA HLAED, liver enzyme composite activity	2004	Current 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.
AID611477	Cytotoxicity against human BJ cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID1473740	Inhibition of human MRP3 overexpressed in Sf9 insect cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 10 mins by membrane vesicle transport assay	2013	Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1	A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID611474	Cytotoxicity against human SK-MEL-2 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID625279	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID155643	Percentage of apoptotic cells in human peripheral blood mononuclear cells after 72 hour incubation at the concentration 1 uM	1998	Bioorganic & medicinal chemistry letters, Sep-22, Volume: 8, Issue:18	Modulation of apoptosis in human lymphocytes by adenosine analogues.
AID445375	Cell cycle arrest in human CCRF-CEM assessed as accumulation at S phase at 5 x GIC50 after 24 hrs by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID540213	Half life in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID611461	Cytotoxicity against human SK-N-AS cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID153257	In vitro inhibitory effect was tested for cytostatic activity on the growth of lymphoid neoplasm P388 leukemic cell lines	1985	Journal of medicinal chemistry, Oct, Volume: 28, Issue:10	Synthesis and biological activity of certain 6-substituted and 2,6-disubstituted 2'-deoxytubercidins prepared via the stereospecific sodium salt glycosylation procedure.
AID1370962	Antiproliferative activity against human HuH7 cells after 72 hrs by SRB assay	2018	Bioorganic & medicinal chemistry letters, 02-01, Volume: 28, Issue:3	Synthesis of novel 6-substituted amino-9-(β-d-ribofuranosyl)purine analogs and their bioactivities on human epithelial cancer cells.
AID1079931	Moderate 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]
AID1236704	Antiproliferative activity against human SK-UT-1B cells assessed as cell growth inhibition after 48 hrs by MTT assay	2015	Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13	Phospholipid derivatives of cladribine and fludarabine: synthesis and biological properties.
AID588213	Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents	2010	Chemical research in toxicology, Jan, Volume: 23, Issue:1	Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID445373	Cell cycle arrest in human CCRF-CEM assessed as accumulation at G1 phase at 5 x GIC50 after 24 hrs by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID1079945	Animal toxicity known. [column 'TOXIC' in source]
AID1079944	Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID445384	Inhibition of DNA synthesis in human CCRF-CEM assessed as assessed as BrdU incorporation after 24 by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID96710	Compound was tested for cytotoxicity against L1210 cell lines	1992	Journal of medicinal chemistry, Jan-24, Volume: 35, Issue:2	Synthesis and biologic activity of 2'-fluoro-2-halo derivatives of 9-beta-D-arabinofuranosyladenine.
AID155439	In vitro antiviral activity was tested against, parainfluenza type 3 (Para 3) virus	1985	Journal of medicinal chemistry, Oct, Volume: 28, Issue:10	Synthesis and biological activity of certain 6-substituted and 2,6-disubstituted 2'-deoxytubercidins prepared via the stereospecific sodium salt glycosylation procedure.
AID625284	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID611454	Cytotoxicity against human BV173 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID344446	Activity of human deoxycytidine kinase C4S mutant in presence of ATP	2008	Journal of medicinal chemistry, Jul-24, Volume: 51, Issue:14	Elucidation of different binding modes of purine nucleosides to human deoxycytidine kinase.
AID678994	TP_TRANSPORTER: uptake in Xenopus laevis oocytes	2000	Biochemical pharmacology, Jul-15, Volume: 60, Issue:2	Role of organic cation transporters in the renal secretion of nucleosides.
AID588217	FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase	2004	Current 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.
AID611452	Cytotoxicity against human K562 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID588219	FDA HLAED, gamma-glutamyl transferase (GGT) increase	2004	Current 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.
AID611473	Cytotoxicity against human SKOV3 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID1474166	Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index	2016	Drug discovery today, Apr, Volume: 21, Issue:4	DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID342000	Antimicrobial activity against Staphylococcus aureus CCM 885 after 20 hrs	2007	Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8	Deoxyribonucleoside kinases activate nucleoside antibiotics in severely pathogenic bacteria.
AID445377	Cell cycle arrest in human CCRF-CEM assessed as accumulation at G2/M phase at 5 x GIC50 after 24 hrs by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID344443	Activity of human wild type deoxycytidine kinase in presence of UTP	2008	Journal of medicinal chemistry, Jul-24, Volume: 51, Issue:14	Elucidation of different binding modes of purine nucleosides to human deoxycytidine kinase.
AID1473738	Inhibition of human BSEP overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-taurocholate in presence of ATP measured after 15 to 20 mins by membrane vesicle transport assay	2013	Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1	A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID44000	Compound was tested for cytotoxicity against CCRF-CEM cell lines	1992	Journal of medicinal chemistry, Jan-24, Volume: 35, Issue:2	Synthesis and biologic activity of 2'-fluoro-2-halo derivatives of 9-beta-D-arabinofuranosyladenine.
AID344442	Activity of human wild type deoxycytidine kinase in presence of ATP	2008	Journal of medicinal chemistry, Jul-24, Volume: 51, Issue:14	Elucidation of different binding modes of purine nucleosides to human deoxycytidine kinase.
AID611462	Cytotoxicity against human U87MG cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID625291	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID33792	Binding affinity to adenosine A2A receptor in rat striatal membranes by measuring displacement of specific [3H]-CGS- 21680 as radioligand	1995	Journal of medicinal chemistry, Mar-31, Volume: 38, Issue:7	Search for new purine- and ribose-modified adenosine analogues as selective agonists and antagonists at adenosine receptors.
AID611453	Cytotoxicity against human paclitaxel resistant K562 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID1370966	Antiproliferative activity against human Mahlavu cells after 72 hrs by SRB assay	2018	Bioorganic & medicinal chemistry letters, 02-01, Volume: 28, Issue:3	Synthesis of novel 6-substituted amino-9-(β-d-ribofuranosyl)purine analogs and their bioactivities on human epithelial cancer cells.
AID611458	Cytotoxicity against human MCF7 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID81745	Compound was tested for cytotoxicity against HEp-2 cell lines	1992	Journal of medicinal chemistry, Jan-24, Volume: 35, Issue:2	Synthesis and biologic activity of 2'-fluoro-2-halo derivatives of 9-beta-D-arabinofuranosyladenine.
AID588211	Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans	2010	Chemical research in toxicology, Jan, Volume: 23, Issue:1	Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID611475	Cytotoxicity against human HPAC cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID1079942	Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1368375	Inhibition of recombinant human PDE2A catalytic domain (580 to 919 residues) expressed in Escherichia coli BL21 (Codonplus) using [3H]cGMP as substrate after 15 mins by liquid scintillation counting method	2018	Bioorganic & medicinal chemistry, 01-01, Volume: 26, Issue:1	Discovery of novel purine nucleoside derivatives as phosphodiesterase 2 (PDE2) inhibitors: Structure-based virtual screening, optimization and biological evaluation.
AID155645	Percentage of apoptotic cells in human peripheral blood mononuclear cells after 72 hour incubation at the concentration 30 uM	1998	Bioorganic & medicinal chemistry letters, Sep-22, Volume: 8, Issue:18	Modulation of apoptosis in human lymphocytes by adenosine analogues.
AID611459	Cytotoxicity against human BT549 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID29734	Toxic level was evaluated	1985	Journal of medicinal chemistry, Oct, Volume: 28, Issue:10	Synthesis and biological activity of certain 6-substituted and 2,6-disubstituted 2'-deoxytubercidins prepared via the stereospecific sodium salt glycosylation procedure.
AID341997	Antimicrobial activity against Streptococcus sp. 07706-1 after 20 hrs	2007	Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8	Deoxyribonucleoside kinases activate nucleoside antibiotics in severely pathogenic bacteria.
AID625282	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1370964	Antiproliferative activity against human MCF7 cells after 72 hrs by SRB assay	2018	Bioorganic & medicinal chemistry letters, 02-01, Volume: 28, Issue:3	Synthesis of novel 6-substituted amino-9-(β-d-ribofuranosyl)purine analogs and their bioactivities on human epithelial cancer cells.
AID445382	Inhibition of DNA synthesis in human CCRF-CEM assessed as assessed as BrdU incorporation at 1 x GIC50 after 24 by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID611463	Cytotoxicity against rat C6 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID445379	Antimitotic activity in human CCRF-CEM cells assessed as decrease in mitotic histone H3 at 5 x GIC50	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID625290	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID611455	Cytotoxicity against human CEM-DNR-bulk cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID1236699	Antiproliferative activity against human K562 cells assessed as cell growth inhibition after 48 hrs by MTT assay	2015	Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13	Phospholipid derivatives of cladribine and fludarabine: synthesis and biological properties.
AID1079934	Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID1079939	Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1370967	Antiproliferative activity against human FOCUS cells after 72 hrs by SRB assay	2018	Bioorganic & medicinal chemistry letters, 02-01, Volume: 28, Issue:3	Synthesis of novel 6-substituted amino-9-(β-d-ribofuranosyl)purine analogs and their bioactivities on human epithelial cancer cells.
AID155644	Percentage of apoptotic cells in human peripheral blood mononuclear cells after 72 hour incubation at the concentration 10 uM	1998	Bioorganic & medicinal chemistry letters, Sep-22, Volume: 8, Issue:18	Modulation of apoptosis in human lymphocytes by adenosine analogues.
AID611465	Cytotoxicity against human HCT116 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID33337	Binding affinity determined by displacement of specific binding of [125I]N-(4-amino-3-iodophenethyl)-adenosine in membranes of CHO cells stably transfected with the rat adenosine A3 receptor	1995	Journal of medicinal chemistry, Mar-31, Volume: 38, Issue:7	Search for new purine- and ribose-modified adenosine analogues as selective agonists and antagonists at adenosine receptors.
AID96819	In vitro inhibitory effect was tested for cytostatic activity on the growth of murine leukemic L1210 cell lines	1985	Journal of medicinal chemistry, Oct, Volume: 28, Issue:10	Synthesis and biological activity of certain 6-substituted and 2,6-disubstituted 2'-deoxytubercidins prepared via the stereospecific sodium salt glycosylation procedure.
AID344445	Ratio of Kcat for human wild type deoxycytidine kinase to Km for human wild type deoxycytidine kinase in presence of UTP	2008	Journal of medicinal chemistry, Jul-24, Volume: 51, Issue:14	Elucidation of different binding modes of purine nucleosides to human deoxycytidine kinase.
AID611476	Cytotoxicity against mouse P388D1 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID344444	Ratio of Kcat for human wild type deoxycytidine kinase to Km for human wild type deoxycytidine kinase in presence of ATP	2008	Journal of medicinal chemistry, Jul-24, Volume: 51, Issue:14	Elucidation of different binding modes of purine nucleosides to human deoxycytidine kinase.
AID617761	Cytotoxicity against human Raji cells after 72 hrs by MTT assay	2011	Bioorganic & medicinal chemistry, Sep-15, Volume: 19, Issue:18	Synthesis and biological evaluation of 2',4'- and 3',4'-bridged nucleoside analogues.
AID1079936	Choleostatic 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]
AID84599	In vitro antiviral activity was tested against, herpes simplex type 2 virus (HSV-2)	1985	Journal of medicinal chemistry, Oct, Volume: 28, Issue:10	Synthesis and biological activity of certain 6-substituted and 2,6-disubstituted 2'-deoxytubercidins prepared via the stereospecific sodium salt glycosylation procedure.
AID1236702	Antiproliferative activity against human MCF7 cells assessed as cell growth inhibition after 48 hrs by MTT assay	2015	Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13	Phospholipid derivatives of cladribine and fludarabine: synthesis and biological properties.
AID611471	Cytotoxicity against human MES-SA cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID611468	Cytotoxicity against human LNCAP cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID611467	Cytotoxicity against human PC3 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID611456	Cytotoxicity against mouse L1210 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID1236703	Antiproliferative activity against human ZR-75-1 cells assessed as cell growth inhibition after 48 hrs by MTT assay	2015	Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13	Phospholipid derivatives of cladribine and fludarabine: synthesis and biological properties.
AID344448	Ratio of Kcat for human deoxycytidine kinase C4S mutant to Km for deoxycytidine kinase C4S mutant in presence of ATP	2008	Journal of medicinal chemistry, Jul-24, Volume: 51, Issue:14	Elucidation of different binding modes of purine nucleosides to human deoxycytidine kinase.
AID445383	Inhibition of DNA synthesis in human CCRF-CEM assessed as assessed as BrdU incorporation at 5 x GIC50 after 24 by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID445380	Inhibition of RNA synthesis in human CCRF-CEM assessed as assessed as BrdU incorporation at 1 x GIC50 after 24 by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID1370965	Antiproliferative activity against human HepG2 cells after 72 hrs by SRB assay	2018	Bioorganic & medicinal chemistry letters, 02-01, Volume: 28, Issue:3	Synthesis of novel 6-substituted amino-9-(β-d-ribofuranosyl)purine analogs and their bioactivities on human epithelial cancer cells.
AID341995	Antimicrobial activity against Escherichia coli ATCC 25922 after 20 hrs	2007	Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8	Deoxyribonucleoside kinases activate nucleoside antibiotics in severely pathogenic bacteria.
AID477295	Octanol-water partition coefficient, log P of the compound	2010	European journal of medicinal chemistry, Apr, Volume: 45, Issue:4	QSPR modeling of octanol/water partition coefficient of antineoplastic agents by balance of correlations.
AID155782	Percentage of apoptotic cells in human peripheral blood mononuclear cells after 72 hour incubation at the concentration 60 uM	1998	Bioorganic & medicinal chemistry letters, Sep-22, Volume: 8, Issue:18	Modulation of apoptosis in human lymphocytes by adenosine analogues.
AID1079938	Chronic 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]
AID1236701	Antiproliferative activity against human SKHEP1 cells assessed as cell growth inhibition after 48 hrs by MTT assay	2015	Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13	Phospholipid derivatives of cladribine and fludarabine: synthesis and biological properties.
AID588212	Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents	2010	Chemical research in toxicology, Jan, Volume: 23, Issue:1	Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID611472	Cytotoxicity against human HeLa cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID445381	Inhibition of RNA synthesis in human CCRF-CEM assessed as assessed as BrdU incorporation at 5 x GIC50 after 24 by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID611466	Cytotoxicity against mouse CT26 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID625285	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1473739	Inhibition of human MRP2 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay	2013	Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1	A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID445362	Inhibition of RNA synthesis in human CCRF-CEM assessed as assessed as BrdU incorporation after 24 by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID540212	Mean residence time in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID341999	Antimicrobial activity against Staphylococcus aureus ATCC 29213 after 20 hrs	2007	Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8	Deoxyribonucleoside kinases activate nucleoside antibiotics in severely pathogenic bacteria.
AID611457	Cytotoxicity against mouse EL4 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID588210	Human drug-induced liver injury (DILI) modelling dataset from Ekins et al	2010	Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 38, Issue:12	A predictive ligand-based Bayesian model for human drug-induced liver injury.
AID679291	TP_TRANSPORTER: uptake in Xenopus laevis oocytes	2000	Biochemical pharmacology, Jul-15, Volume: 60, Issue:2	Role of organic cation transporters in the renal secretion of nucleosides.
AID1079932	Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID540209	Volume of distribution at steady state in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID108459	In vitro antiviral activity was tested against, measles virus	1985	Journal of medicinal chemistry, Oct, Volume: 28, Issue:10	Synthesis and biological activity of certain 6-substituted and 2,6-disubstituted 2'-deoxytubercidins prepared via the stereospecific sodium salt glycosylation procedure.
AID1236698	Antiproliferative activity against human KG1 cells assessed as cell growth inhibition after 48 hrs by MTT assay	2015	Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13	Phospholipid derivatives of cladribine and fludarabine: synthesis and biological properties.
AID540210	Clearance in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID341998	Antimicrobial activity against Streptococcus sp. 07686-2 after 20 hrs	2007	Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8	Deoxyribonucleoside kinases activate nucleoside antibiotics in severely pathogenic bacteria.
AID445378	Antimitotic activity in human CCRF-CEM cells assessed as decrease in mitotic histone H3 at 1 x GIC50	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID445374	Cell cycle arrest in human CCRF-CEM assessed as accumulation at S phase at 1 x GIC50 after 24 hrs by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID445372	Cell cycle arrest in human CCRF-CEM assessed as accumulation at G1 phase at 1 x GIC50 after 24 hrs by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID1236697	Antiproliferative activity against human MOLT3 cells assessed as cell growth inhibition after 48 hrs by MTT assay	2015	Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13	Phospholipid derivatives of cladribine and fludarabine: synthesis and biological properties.
AID1439437	Cytotoxicity against human HuH7 cells assessed as growth inhibition after 72 hrs by SRB assay	2017	European journal of medicinal chemistry, Mar-31, Volume: 129	Synthesis and biological evaluation of novel pyrazolic chalcone derivatives as novel hepatocellular carcinoma therapeutics.
AID445370	Cell cycle arrest in human CCRF-CEM assessed as accumulation at subG1 phase at 1 x GIC50 after 24 hrs by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID445371	Cell cycle arrest in human CCRF-CEM assessed as accumulation at subG1 phase at 5 x GIC50 after 24 hrs by flow cytometry	2010	Journal of medicinal chemistry, Jan-14, Volume: 53, Issue:1	6-(Het)aryl-7-deazapurine ribonucleosides as novel potent cytostatic agents.
AID625280	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1439439	Cytotoxicity against human HCT116 cells assessed as growth inhibition after 72 hrs by SRB assay	2017	European journal of medicinal chemistry, Mar-31, Volume: 129	Synthesis and biological evaluation of novel pyrazolic chalcone derivatives as novel hepatocellular carcinoma therapeutics.
AID611464	Cytotoxicity against human HT-29 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID540211	Fraction unbound in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID625288	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID217824	In vitro antiviral activity was tested against, vaccinia virus (VV)	1985	Journal of medicinal chemistry, Oct, Volume: 28, Issue:10	Synthesis and biological activity of certain 6-substituted and 2,6-disubstituted 2'-deoxytubercidins prepared via the stereospecific sodium salt glycosylation procedure.
AID588209	Literature-mined public compounds from Greene et al multi-species hepatotoxicity modelling dataset	2010	Chemical research in toxicology, Jul-19, Volume: 23, Issue:7	Developing structure-activity relationships for the prediction of hepatotoxicity.
AID625292	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1174819	Cytotoxicity against human T47D cells after 72 hrs by SRB assay	2015	European journal of medicinal chemistry, Jan-07, Volume: 89	Synthesis of novel substituted purine derivatives and identification of the cell death mechanism.
AID342001	Antimicrobial activity against Streptococcus pyogenes AP1 after 20 hrs	2007	Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8	Deoxyribonucleoside kinases activate nucleoside antibiotics in severely pathogenic bacteria.
AID445467	Displacement of [3H]adenine from adenine 1 receptor in rat brain cortical membrane by liquid scintillation counting	2009	Journal of medicinal chemistry, Oct-08, Volume: 52, Issue:19	Structure-activity relationships of adenine and deazaadenine derivatives as ligands for adenine receptors, a new purinergic receptor family.
AID341996	Antimicrobial activity against Streptococcus sp. 07941-1 after 20 hrs	2007	Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8	Deoxyribonucleoside kinases activate nucleoside antibiotics in severely pathogenic bacteria.
AID611470	Cytotoxicity against human NCI-H146 cells after 3 days by MTT assay	2011	Journal of medicinal chemistry, Aug-11, Volume: 54, Issue:15	Synthesis and significant cytostatic activity of 7-hetaryl-7-deazaadenosines.
AID1079937	Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID625289	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1439438	Cytotoxicity against human MCF7 cells assessed as growth inhibition after 72 hrs by SRB assay	2017	European journal of medicinal chemistry, Mar-31, Volume: 129	Synthesis and biological evaluation of novel pyrazolic chalcone derivatives as novel hepatocellular carcinoma therapeutics.
AID1174817	Cytotoxicity against human HuH7 cells after 72 hrs by SRB assay	2015	European journal of medicinal chemistry, Jan-07, Volume: 89	Synthesis of novel substituted purine derivatives and identification of the cell death mechanism.
AID1347411	qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary	2020	ACS chemical biology, 07-17, Volume: 15, Issue:7	High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1159607	Screen for inhibitors of RMI FANCM (MM2) intereaction	2016	Journal 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.
AID1224864	HCS microscopy assay (F508del-CFTR)	2016	PloS one, , Volume: 11, Issue:10	Increasing the Endoplasmic Reticulum Pool of the F508del Allele of the Cystic Fibrosis Transmembrane Conductance Regulator Leads to Greater Folding Correction by Small Molecule Therapeutics.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	24 (1.39)	18.7374
1990's	524 (30.34)	18.2507
2000's	499 (28.89)	29.6817
2010's	416 (24.09)	24.3611
2020's	264 (15.29)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	258 (14.42%)	5.53%
Reviews	334 (18.67%)	6.00%
Case Studies	325 (18.17%)	4.05%
Observational	19 (1.06%)	0.25%
Other	853 (47.68%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (117)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
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 1	120 participants (Anticipated)	Interventional	2020-12-03	Recruiting
A Monocenter Prospective Single Arm Study of Cladribine Plus Homoharringtonine and Cytarabine Regimen (CHA) for Induced Therapy in Adults de Novo Acute Myeloid Leukemia (Non-M3) [NCT05906914]	Phase 2	30 participants (Anticipated)	Interventional	2023-06-29	Recruiting
A 2-year Extension Study to Evaluate Long-term Effectiveness of Mavenclad® in Participants Who Have Completed Trial MS700568_0022 (MAGNIFY MS) (Magnify MS Extension) [NCT04783935]	Phase 4	219 participants (Actual)	Interventional	2021-03-10	Active, not recruiting
Cladribine Combined With G-CSF and Cytarabine as a Salvage Treatment in Refractory/Relapsed Acute Lymphoblastic Leukemia [NCT05578378]	Phase 2/Phase 3	32 participants (Anticipated)	Interventional	2022-01-01	Recruiting
A Prospective Biomarker Study in Active Secondary Progressive Multiple Sclerosis (SPMS)Subjects Treated With Cladribine Tablets [NCT04550455]	Phase 4	30 participants (Anticipated)	Interventional	2020-09-16	Recruiting
Clinical Study of Efficacy and Safety of Chidamide Combined With Cladribine Regimen in Refractory/Relapsed Acute Myeloid Leukemia [NCT05330364]	Phase 2	31 participants (Anticipated)	Interventional	2021-06-01	Recruiting
Phase 1 Study of Cladribine Based Induction Therapy (CLAG) With ATRA (All-Trans Retinoic Acid) and Midostaurin in Relapsed/Refractory AML [NCT01161550]	Phase 1	11 participants (Actual)	Interventional	2010-11-30	Completed
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 2	84 participants (Actual)	Interventional	2016-12-01	Completed
LCH-IV, International Collaborative Treatment Protocol for Children and Adolescents With Langerhans Cell Histiocytosis [NCT02205762]	Phase 2/Phase 3	1,400 participants (Anticipated)	Interventional	2016-11-02	Recruiting
Phase Ib/II Study of Uproleselan Added to Cladribine Plus Low Dose Cytarabine (LDAC) Induction Followed by Consolidation With Uproleselan Plus Cladribine Plus LDAC in Patients With Treated Secondary AML (TS-AML) [NCT04848974]	Phase 1/Phase 2	37 participants (Anticipated)	Interventional	2021-06-11	Recruiting
Allogeneic Transplantation Using Venetoclax, Timed Sequential Busulfan,Cladribine, and Fludarabine Conditioning in Patients With AML and MDS [NCT02250937]	Phase 2	116 participants (Anticipated)	Interventional	2014-10-27	Active, not recruiting
CBA Versus FBA Conditioning Followed by Allogeneic HSCT in Treatment of High Risk and Refractory AML [NCT03384212]	Phase 3	120 participants (Anticipated)	Interventional	2016-08-01	Recruiting
Chidamide Combined With Cladribine/Gemcitabine/Busulfan (ChiCGB) With Autologous Stem-Cell Transplantation in High-risk Hodgkin and Non-Hodgkin Lymphoma [NCT03602131]	Phase 2	30 participants (Anticipated)	Interventional	2019-01-01	Not yet recruiting
Czech Pharmaco-epidemiological Real World Data Study Focused on Effectiveness of Different Disease Modifying Drugs [NCT05762003]		17,478 participants (Actual)	Observational	2019-01-01	Completed
Efficacy and Safety of Cladribine Combined With BEAC ( Semustine, Etoposide, Cytarabine, Cyclophosphamide) Pretreatment Regimen in the Treatment of Peripheral T-cell Lymphoma: a Multicenter Clinical Study [NCT04880746]	Phase 3	266 participants (Anticipated)	Interventional	2020-10-17	Recruiting
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 3	400 participants (Anticipated)	Interventional	2014-02-28	Recruiting
A Randomized, Double-blind, 2-Period, 2-Sequence Crossover Phase I Study With a 1 Month run-in Period to Examine the Effect of Cladribine Tablets on the PK of a Monophasic Oral Contraceptive Containing Ethinyl Estradiol and Levonorgestrel (Microgynon®) in [NCT03745144]	Phase 1	24 participants (Actual)	Interventional	2019-01-17	Completed
Venetoclax, Cladribine Plus Low-dose Cytarabine for Relapsed/Refractory Philadelphia Chromosome-negative (Ph-) B-cell Acute Lymphoblastic Leukemia (B-ALL): a Single-arm, Multicenter Study [NCT05657652]		36 participants (Anticipated)	Interventional	2022-10-01	Recruiting
Phase I-II Study of Low Dose CdA Combined With Valproic Acid (VPA) in Previously Treated B-cell Chronic Lymphocytic Leukemia (CLL) Patients [NCT01295593]	Phase 1/Phase 2	33 participants (Anticipated)	Interventional	2010-12-31	Recruiting
Cladribine Tablets Level of Response Predictors in Clinical Practice (CLODINA) [NCT05797740]		360 participants (Anticipated)	Observational	2023-08-03	Recruiting
Oral CLADribine in Patients That Change From First-line Disease Modifying Treatments for Multiple Sclerosis: a pROspective effectivenesS and Safety Study (CLAD CROSS) [NCT04934800]		256 participants (Actual)	Observational	2019-12-10	Active, not recruiting
An Open-label, Cross Over Study, to Assess the Interactions of Pantoprazole (Proton Pump Inhibitor) With Oral Cladribine Administered in Subjects With Multiple Sclerosis [NCT00938366]	Phase 1	18 participants (Actual)	Interventional	2008-01-31	Completed
Phase I/II Trial of Rituximab, Cladribine, and Temsirolimus (RCT) Therapy in Newly Diagnosed Mantle Cell Lymphoma (MCL) [NCT00787969]	Phase 1	74 participants (Anticipated)	Interventional	2009-04-30	Completed
Phase II Study of 2-Chlorodeoxyadenosine (2CDA) Followed by Rituximab in Hairy Cell Leukemia [NCT00412594]	Phase 2	150 participants (Anticipated)	Interventional	2004-06-10	Recruiting
CBA Versus FBA Conditioning Followed by Haploidentical Allogeneic HSCT in Treatment of High Risk and Refractory AML [NCT03384225]	Phase 3	120 participants (Anticipated)	Interventional	2016-08-01	Recruiting
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 3	582 participants (Anticipated)	Interventional	2017-07-03	Recruiting
Study on the Treatment of Hairy Cell Leukaemia Variant and Relapsing Hairy Cell Leukaemia [NCT02157181]	Phase 2	89 participants (Actual)	Interventional	2004-06-30	Completed
Phase II Study of Cladribine Plus Idarubicin Plus Cytarabine (ARAC) in Patients With AML, HR MDS, or Myeloid Blast Phase of CML [NCT02115295]	Phase 2	458 participants (Anticipated)	Interventional	2014-05-19	Recruiting
Efficacy and Safety of Cladribine in Combination With G-CSF, Low-dose Cytarabine and Aclarubicin in Patients With Refractory/Relapsed Acute Myeloid Leukemia: a Phase 2 Clinical Trial [NCT03181815]	Phase 2	48 participants (Anticipated)	Interventional	2016-01-01	Recruiting
Venetoclax-Navitoclax With Cladribine-based Salvage Therapy in Patients With Relapsed/Refractory Acute Myeloid Leukemia [NCT06007911]	Phase 1	36 participants (Anticipated)	Interventional	2024-02-29	Not yet recruiting
Phase II Prospective Randomized Control Trial of Cladribine and Low-Dose Cytarabine (LoDAC) Alternating With Decitabine vs. Hypomethylating Agents (HMA) Plus Venetoclax as Frontline Therapy for AML or High-Grade MDS in Patients Unfit for Intensive Inducti [NCT05766514]	Phase 2	98 participants (Anticipated)	Interventional	2024-03-31	Not yet recruiting
A Phase II Study of CLAG Regimen in Combination With Imatinib Mesylate (Gleevec) in Refractory or Relapsed Acute Myeloid Leukemia [NCT00594555]	Phase 2	20 participants (Anticipated)	Interventional	2007-11-30	Withdrawn(stopped due to Principal Investigator resigned position with the University of Cincinnati, closing study at this site will reopen study in new position)
A Phase IIIb, Double-Blind, Placebo-Controlled, Multicenter, Parallel Group, Extension Trial to Evaluate the Safety and Tolerability of Oral Cladribine in Subjects With Relapsing-Remitting Multiple Sclerosis Who Have Completed Trial 25643 (CLARITY) [NCT00641537]	Phase 3	867 participants (Actual)	Interventional	2008-02-29	Completed
A Phase III, Randomized, Double-blind, Three-arm, Placebo-controlled, Multi-center Study to Evaluate the Safety and Efficacy of Oral Cladribine in Subjects With Relapsing-remitting Multiple Sclerosis (RRMS) [NCT00213135]	Phase 3	1,326 participants (Actual)	Interventional	2005-04-30	Completed
Phase II Study of Vorinostat (SAHA), Cladribine, and Rituximab (SCR) in Mantle Cell Lymphoma, Chronic Lymphocytic Leukemia, and Relapsed B Cell Non-Hodgkin Lymphoma [NCT00764517]	Phase 2	57 participants (Actual)	Interventional	2008-08-31	Completed
A Phase III, Randomized, Double-blind, Placebo-controlled, Multi-center Clinical Trial of Oral Cladribine in Subjects With a First Clinical Event at High Risk of Converting to MS [NCT00725985]	Phase 3	617 participants (Actual)	Interventional	2008-12-31	Completed
Efficacy and Safety of Cladribine in Combination With G-CSF,Low-dose Cytarabine and Aclarubicin in Newly Diagnosed Unfit Patients With Acute Myeloid Leukemia [NCT04254640]	Phase 2	34 participants (Anticipated)	Interventional	2021-03-01	Not yet recruiting
Primary Treatment of Macroglobulinemic Lymphoma With 2CdA, Cyclophosphamide and Rituximab [NCT00667329]	Phase 1	14 participants (Actual)	Interventional	1999-07-09	Completed
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 2	50 participants (Actual)	Interventional	2016-12-30	Completed
A Phase II Study of Cladribine and Low Dose Cytarabine in Combination With Venetoclax, Alternating With Azacitidine and Venetoclax, in Patients With Higher-risk Myeloproliferative Chronic Myelomonocytic Leukemia or Higher-risk Myelodysplastic Syndromes Wi [NCT05365035]	Phase 2	60 participants (Anticipated)	Interventional	2022-09-23	Recruiting
A Randomized, Open Label Study to Assess the Effect of Maintenance Treatment With Mabthera (Rituximab) Versus No Treatment, After Induction Treatment With Rituximab, Cladribine and Cyclophosphamide (RCC) on Progression-Free Survival in Previously Untreate [NCT00718549]	Phase 3	128 participants (Actual)	Interventional	2009-07-21	Completed
A Phase II, Multicenter, Randomized, Double Blind, Placebo Controlled, Safety, Tolerability and Efficacy Study of Add-on Cladribine Tablet Therapy With Interferon-beta (IFN-β) Treatment in Multiple Sclerosis Subjects With Active Disease [NCT00436826]	Phase 2	172 participants (Actual)	Interventional	2006-11-30	Completed
A Collaborative Trial for the Treatment of Patients With Newly Diagnosed Acute Myeloid Leukemia or Myelodysplasia [NCT00136084]	Phase 3	238 participants (Actual)	Interventional	2002-08-31	Completed
Cladribine Tablets: Observational Evaluation of Effectiveness and PROs in Suboptimally Controlled Patients Previously Taking Injectable DMDs for RMS (CLICK-MS) [NCT03933215]		100 participants (Actual)	Observational	2019-05-21	Active, not recruiting
A Multicenter Randomized Controlled Trial of Best Available Therapy Versus Autologous Hematopoietic Stem Cell Transplant for Treatment-Resistant Relapsing Multiple Sclerosis (ITN077AI) [NCT04047628]	Phase 3	156 participants (Anticipated)	Interventional	2019-12-19	Recruiting
A Phase II Study of Cladribine, Cytarabine, and Granulocyte-Colony Stimulating Factor With Fractionated Gemtuzumab Ozogamicin (CLAG-GO) for the Treatment of Patients With Persistent, Relapsed or Refractory Acute Myeloid Leukemia [NCT04050280]	Phase 2	39 participants (Anticipated)	Interventional	2019-11-01	Recruiting
Cladribine Tablets: Collaborative Study to Evaluate the Impact On Central Nervous System Biomarkers in Multiple Sclerosis [NCT03963375]	Phase 4	47 participants (Actual)	Interventional	2019-10-28	Active, not recruiting
Subcutaneous Cladribine Plus Pegylated Interpheron Alfa-2a in Advanced Systemic Mastocytosis With D816V and Other Exon 17 KIT Mutations. [NCT01602939]	Phase 2/Phase 3	10 participants (Anticipated)	Interventional	2012-05-31	Recruiting
Determining the Effectiveness of earLy Intensive Versus Escalation Approaches for the Treatment of Relapsing-Remitting Multiple Sclerosis [NCT03535298]	Phase 4	800 participants (Anticipated)	Interventional	2019-01-03	Recruiting
Multicenter Trial for Treatment Optimization in T-lymphoblastic Lymphoma in Adults and Adolescents Older Than 15 Years (GMALL T-LBL 1/2004) (Amend 1) [NCT00199017]	Phase 4	75 participants (Anticipated)	Interventional	2004-04-30	Completed
Clinical Observation on the Efficacy and Safety of CLAE Regimen (Cladribine + Cytarabine + Etoposide) in the Treatment of Relapsed/Refractory T- Acute Lymphoblastic Leukemia/Lymphoblastic Lymphoma [NCT04679506]		50 participants (Anticipated)	Observational [Patient Registry]	2020-12-31	Not yet recruiting
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 1	13 participants (Actual)	Interventional	2020-05-08	Terminated(stopped due to Terminated due to unfavorable risk-benefit ratio of investigational regimen.)
Four-Arm Randomized Phase II Study of SGI-110: 5 Days, Versus 10 Days, Versus 5 Days + Idarubicin, Versus 5 Days + Cladribine, in Previously Untreated Patients >/= 70 Years With Acute Myeloid Leukemia [NCT02096055]	Phase 2	44 participants (Actual)	Interventional	2014-04-04	Completed
Phase I Clinical Evaluation of Bryostatin 1 in Combination With 2-CdA in Patients With Relapsed CLL [NCT00003174]	Phase 1	80 participants (Anticipated)	Interventional	1998-05-31	Completed
Evaluation of Efficacy and Tolerance of Cladribine in Symptomatic Patients With Pulmonary Langerhans Cell Histiocytosis and Impairment of Lung Function [NCT01473797]	Phase 2	10 participants (Actual)	Interventional	2011-11-30	Active, not recruiting
Chidamide Combined With Cladribine/Gemcitabine/Busulfan (ChiCGB) With Autologous Stem-Cell Transplantation in Relapsed and Refractory Diffuse Large B Cell Lymphoma [NCT03151876]	Phase 2	93 participants (Anticipated)	Interventional	2017-06-12	Recruiting
Cladribine Tablets After Treatment With Natalizumab (CLADRINA) [NCT04178005]	Phase 4	40 participants (Anticipated)	Interventional	2020-02-19	Active, not recruiting
Cladribine Tablets: Observational Evaluation of Effectiveness and PROs in Suboptimally Controlled Patients Previously Taking Oral or Infusion DMDs for RMS (MASTER-2) [NCT03933202]		295 participants (Actual)	Observational	2019-07-22	Active, not recruiting
A Pragmatic Trial to Evaluate the Intermediate-term Effects of Early, Aggressive Versus Escalation Therapy in People With Multiple Sclerosis [NCT03500328]		900 participants (Anticipated)	Interventional	2018-05-02	Recruiting
A Phase I Study of CLAG Regimen in Combination With Imatinib Mesylate (Gleevec) in Refractory or Relapsed Leukemias [NCT00258271]	Phase 1	18 participants (Anticipated)	Interventional	2005-03-31	Completed
Multicenter Therapy-Optimization Trial AML-BFM 2004 for the Treatment of Acute Myeloid Leukemias in Children and Adolescents [NCT00111345]	Phase 2/Phase 3	550 participants (Actual)	Interventional	2004-03-31	Active, not recruiting
Phase II Study of Cladribine Plus Low Dose Cytarabine (LDAC) Induction Followed By Consolidation With Cladribine Plus LDAC Alternating With Decitabine in Patients With Untreated Acute Myeloid Leukemia (AML) or High-Risk Myelodysplastic Syndrome (MDS) [NCT01515527]	Phase 2	160 participants (Anticipated)	Interventional	2012-02-07	Recruiting
Phase II Study of Cladribine, High-dose Cytarabine and Idarubicin in Patients With Relapsed Acute Myeloid Leukemia [NCT00126321]	Phase 2	50 participants (Anticipated)	Interventional	2004-11-30	Recruiting
Phase II Study: 2-Chlorodeoxyadenosine (2-CdA) and Cytarabine (Ara-C) in Idiopathic Hypereosinophilic Syndrome (HES) [NCT00483067]	Phase 2	13 participants (Actual)	Interventional	1998-03-31	Completed
Venetoclax to Improve Outcomes of Fractionated Busulfan Regimen in Patients With High-Risk AML and MDS [NCT04708054]	Phase 2	100 participants (Anticipated)	Interventional	2021-10-21	Recruiting
Randomized Trial of Cladribine (CdA) With Simultaneous or Delayed Rituximab to Eliminate Hairy Cell Leukemia Minimal Residual Disease [NCT00923013]	Phase 2	208 participants (Anticipated)	Interventional	2008-10-20	Recruiting
ChariotMS - A National (UK) Phase IIb, Multi-centre, Randomised, Double-blind, Placebo Controlled (1:1) Efficacy Trial With Cost-utility Analysis of Cladribine Tablets (3.5mg/kg Over Two Years) in People With Advanced Multiple Sclerosis. Is Cladribine Sup [NCT04695080]	Phase 2/Phase 3	200 participants (Anticipated)	Interventional	2021-06-25	Recruiting
Phase II Trial of CLAG-M in Relapsed ALL [NCT01513603]	Phase 2	50 participants (Anticipated)	Interventional	2012-01-31	Recruiting
2-CDA and Rituximab as Remission Induction and Rituximab as In Vivo Purging Prior to Peripheral Stem Cell Mobilization in Patients With Chronic Lymphocytic Leukemia (CLL) - A Prospective Multicenter Phase II Trial [NCT00072007]	Phase 2	43 participants (Actual)	Interventional	2002-06-30	Completed
Effects of Oral Cladribine on Remyelination and Inflammation in Multiple Sclerosis Patients [NCT05902429]	Phase 4	10 participants (Actual)	Interventional	2021-04-28	Active, not recruiting
A PHASE I STUDY OF 2-CHLORODEOXYADENOSINE AND RADIATION FOR THE TREATMENT OF HIGH GRADE GLIOMA (CDX) [NCT00019071]	Phase 1	0 participants	Interventional	1995-03-31	Completed
Cardioprotection With Dexrazoxane in Acute Myeloid Leukemia (AML), High-Risk Myelodysplastic Syndrome (MDS), Myeloid Blast Phase of Chronic Myeloid Leukemia (CML), Ph+ AML, and Myeloid Blast Phase of Myeloproliferative Neoplasms [NCT03589729]	Phase 2	100 participants (Anticipated)	Interventional	2018-09-19	Recruiting
The Prospective Non-randomized Phase II Clinical Trial of Vemurafenib in Combination With Cytarabine and 2-chlorodeoxyadenosine in Children With Langerhans-cell Hisitocytosis With BRAF V600E Mutation [NCT03585686]	Phase 2	12 participants (Anticipated)	Interventional	2018-06-26	Recruiting
A 2-year Prospective Study to Evaluate the Onset of Action of Mavenclad® in Subjects With Highly Active Relapsing Multiple Sclerosis (MAGNIFY) [NCT03364036]	Phase 4	270 participants (Actual)	Interventional	2018-05-28	Completed
Phase II Trial of Rituximab and 2-Chlorodeoxyadenosine (2-CDA) in Newly Diagnosed Mantle Cell Lymphoma (MCL) [NCT00053027]	Phase 2	30 participants (Actual)	Interventional	2003-02-28	Completed
Safety and Efficacy of Subcutaneous Cladribine for Nonrelapsing, Secondary Progressive Multiple Sclerosis (CLASP-MS): a Randomized, Placebo-controlled, Double-blind, Phase 2 Study. [NCT05961644]	Phase 2/Phase 3	188 participants (Anticipated)	Interventional	2022-10-03	Recruiting
"A Feasibility Study of Early Allogeneic Hematopoietic Cell Transplantation for Relapsed or Refractory High-Grade Myeloid Neoplasms" [NCT02756572]	Phase 2	30 participants (Actual)	Interventional	2016-09-22	Completed
Randomized Autologous heMatopoietic Stem Cell Transplantation Versus Alemtuzumab, Cladribine or Ocrelizumab for Patients With Relapsing Remitting Multiple Sclerosis [NCT03477500]	Phase 3	100 participants (Anticipated)	Interventional	2018-03-21	Recruiting
A Phase I Study of Lintuzumab-Ac225 in Combination With CLAG-M Chemotherapy in Patients With Relapsed/Refractory Acute Myeloid Leukemia [NCT03441048]	Phase 1	26 participants (Actual)	Interventional	2018-05-22	Active, not recruiting
Safety and Efficacy of a Therapy With Cladribine Following a Treatment With Anti CD20 Compounds in Relapsing Multiple Sclerosis Patients: a Pilot Study [NCT04640818]		45 participants (Anticipated)	Observational	2020-12-17	Active, not recruiting
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 2	90 participants (Anticipated)	Interventional	2017-06-14	Recruiting
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 2	28 participants (Actual)	Interventional	2016-11-17	Completed
Norwegian Study of Oral Cladribine and Rituximab in Multiple Sclerosis (NOR-MS) A Prospective Randomized Open-label Blinded Endpoint (PROBE) Multicenter Non-inferiority Study [NCT04121403]	Phase 3	264 participants (Anticipated)	Interventional	2019-10-16	Recruiting
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 2	199 participants (Actual)	Interventional	2014-01-23	Completed
Phase II Study of Venetoclax Added to Cladribine Plus Low Dose Cytarabine (LDAC) Induction Followed by Consolidation With Cladribine Plus LDAC Alternating With 5-Azacitidine With Venetoclax in Patients With Untreated AML [NCT03586609]	Phase 2	145 participants (Anticipated)	Interventional	2018-10-25	Recruiting
Bortezomib (VELCADE), Cladribine and Rituximab (VCR) in Mantle Cell Lymphoma: A Phase I/II Study (PSHCI 10-011) [NCT01439750]	Phase 1	13 participants (Actual)	Interventional	2012-05-31	Active, not recruiting
STATURE: A Prospective Observational Study of the relationShip beTween Oral DMT bURden and adhErence in People With MS [NCT04676204]		323 participants (Anticipated)	Observational	2020-09-25	Enrolling by invitation
Rituximab-2cda and Prolongation of Therapy With Rituximab Alone in Chronic Lymphocytic Leukaemia and Small Lymphocytic Lymphoma [NCT01446900]	Phase 2	25 participants (Actual)	Interventional	2011-01-31	Terminated(stopped due to low rate in patient accrual)
A Phase 1, Open-Label, Sequential Cross-over, Bioavailability/Bioequivalence Study to Compare the Pharmacokinetics of Oral Cladribine With the Reference Listed Drug, Intravenous Cladribine [NCT06021600]	Phase 1	40 participants (Anticipated)	Interventional	2023-10-09	Recruiting
A Phase II, Open-Label Study of Bortezomib (Velcade), Cladribine and Rituximab (VCR) in Advanced, Newly Diagnosed and Relapsed/Refractory Mantle Cell and Indolent Lymphomas [NCT00980395]	Phase 2	24 participants (Actual)	Interventional	2009-07-07	Completed
Treateament of Newly Diagnosed Acute Monocytic Leukemia in Children： A Prospective Multicenter Study in South China [NCT05313958]	Phase 2/Phase 3	43 participants (Anticipated)	Interventional	2021-12-01	Recruiting
Clinical Study of Bcl-2 Inhibitors Combined With Azacytidine and Chemotherapy in Elderly Patients With Previously Untreated Acute Myeloid Leukemia [NCT05053425]		30 participants (Anticipated)	Interventional	2021-10-20	Recruiting
Idarubicin and Cladribine in Recurrent and Refractory Acute Myeloid Leukemia: A POG Phase II Study [NCT00003178]	Phase 2	120 participants (Actual)	Interventional	1998-03-31	Completed
German Multicenter Phase II Trial to Study Effectivity and Feasibility of Alemtuzumab (MabCampath®) in T-ALL and T-Lymphoblastic Lymphomas With Minimal Residual Disease (MRD), in Refractory Relapse or in Primary Failure [NCT00199030]	Phase 2	8 participants (Actual)	Interventional	2004-02-29	Completed
[NCT00004762]	Phase 2	5 participants	Interventional	1994-12-31	Completed
Therapy Optimisation for the Treatment of Hairy Cell Leukemia [NCT02131753]	Phase 2/Phase 3	210 participants (Anticipated)	Interventional	2004-05-31	Recruiting
German Multicenter Study for Treatment Optimisation in Acute Lymphoblastic Leukemia in Adults and Adolescents Above 15 Years (Amend 3) (GMALL 07/2003) [NCT00198991]	Phase 4	1,883 participants (Actual)	Interventional	2003-04-30	Completed
ChiCGB Versus BEAM With Autologous Stem-Cell Transplantation in High-risk Hodgkin and Non-Hodgkin Lymphoma - A Prospective, Multi-centered, Randomized Clinical Trial [NCT05466318]	Phase 3	306 participants (Anticipated)	Interventional	2022-07-01	Recruiting
Assessment of Tolerance and Effectiveness of Total Body Irradiation and Cladribine Before Allogeneic Hematopoietic Cell Transplantation in Patients With Acute Myeloid Leukemia and Myelodysplastic Syndromes [NCT04861207]	Phase 2	40 participants (Anticipated)	Interventional	2021-06-30	Not yet recruiting
"Phase I Study of T Cell Depleted (TCD) Partially Matched Related Donor (PMRD) Hematopoietic Stem Cell Transplantation for High Risk Hematologic Diseases Using Intense Pre and Post Transplant Immunosuppression and Megadose CD34 Veto Cells" [NCT00004904]	Phase 1	0 participants	Interventional	1999-10-31	Completed
Daily Versus Weekly Administration of 2-Chlorodeoxyadenosine (CDA) in Patients With Hairy Cell Leukemia [NCT00003746]	Phase 3	100 participants (Actual)	Interventional	1998-09-30	Completed
Use of G-CSF Stimulated HLA-Identical Allogeneic Peripheral Blood Stem Cells for Patients With High Risk Acute Myelogenous Leukemia or CML in Blast Crisis [NCT00002833]	Phase 2	53 participants (Actual)	Interventional	1994-10-31	Completed
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 2	115 participants (Actual)	Interventional	1997-08-31	Completed
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 3	450 participants (Anticipated)	Interventional	2019-11-22	Recruiting
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 1	0 participants (Actual)	Interventional	2023-03-31	Withdrawn(stopped due to Sponsor withdrew funding)
Efficacy and Safety of Cladribine in Combination With G-CSF, Low-dose Cytarabine and Pegaspargase in Patients With Refractory/Relapsed Acute Lymphoblastic Leukemia: a Phase 2 Clinical Trial [NCT03318419]	Phase 2	50 participants (Anticipated)	Interventional	2016-01-01	Recruiting
Cladribine Dose Escalation in Conditioning Regimen Prior to Allo-HSCT for Refractory Acute Leukemia and Myelodysplastic Syndromes [NCT03235973]	Phase 1	29 participants (Anticipated)	Interventional	2018-04-28	Recruiting
A Phase II Study of CLAG Regimen in Combination With Imatinib Mesylate (Gleevec) in Relapsed or Refractory Acute Myeloid Leukemia [NCT00955916]	Phase 2	38 participants (Actual)	Interventional	2009-08-31	Completed
An Investigator Sponsored Phase I/II Study of CLAG + Selinexor in Relapsed or Refractory Acute Myeloid Leukemia [NCT02416908]	Phase 1/Phase 2	40 participants (Actual)	Interventional	2015-06-16	Completed
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 1	20 participants (Anticipated)	Interventional	2022-02-04	Recruiting
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 2	66 participants (Actual)	Interventional	2018-09-14	Completed
Clinical Study on the Efficacy and Safety of Auto-HSCT in Adult Patients With Burkitt Lymphoma, Lymphoblastic Lymphoma, and Acute Lymphoblastic Leukemia Who Received TCCA Conditioning Regimen [NCT06060782]	Phase 1	28 participants (Anticipated)	Interventional	2023-10-01	Recruiting
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 2	60 participants (Anticipated)	Interventional	2020-03-11	Recruiting
A PHASE II TRIAL OF 2-CDA IN PREVIOUSLY TREATED OR UNTREATED PATIENTS WITH MANTLE CELL LYMPHOMA (MCL) [NCT00002879]	Phase 2	51 participants (Actual)	Interventional	1996-11-30	Completed
A 2-Year Prospective Study to Assess Health-related Quality of Life In Subjects With Highly-Active Relapsing Multiple Sclerosis Treated With Mavenclad® (CLARIFY MS) [NCT03369665]	Phase 4	485 participants (Actual)	Interventional	2018-06-20	Completed
Epacadostat With Cladribine and Cytarabine (ECC) in Relapsed / Refractory AML Patients Fit for Intensive Chemotherapy; a Phase I Study. [NCT03491579]	Phase 1	0 participants (Actual)	Interventional	2018-12-31	Withdrawn(stopped due to IMP will not be further developed)
A Combination of Cladribine, Idarubicin, Cytarabine (CLIA) and Quizartinib for the Treatment of Patients With Newly Diagnosed or Relapsed/Refractory Acute Myeloid Leukemia (AML) and High-Risk Myelodysplastic Syndrome (MDS)) [NCT04047641]	Phase 1/Phase 2	80 participants (Anticipated)	Interventional	2019-10-22	Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT00136084 (7) [back to overview]	Proportion of Patients Experienced Toxicity of Cytarabine + Daunomycin + Etoposide (ADE) + GO.
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]	To Estimate the Overall Event-free Survival (EFS) of AML Patients Who Undergo Risk-adapted and Genotype-directed 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]	Proportion of MRD Reduction After One Course of Cytarabine + Daunomycin + Etoposide (ADE) + GO
NCT00213135 (4) [back to overview]	Time to Disability Progression
NCT00213135 (4) [back to overview]	Mean Number of Combined Unique (CU) Lesions, Active Time Constant 2 (T2) Lesions, and Active Time Constant 1 (T1) Gadolinium-Enhanced (Gd+) Lesions Per Participant Per Scan
NCT00213135 (4) [back to overview]	Annualized Qualifying Relapse Rate
NCT00213135 (4) [back to overview]	Percentage of Relapse-free Participants
NCT00436826 (42) [back to overview]	Double Blind Period: Percentage of Participants With no Active T1 Gd-Enhanced Lesions at Week 96
NCT00436826 (42) [back to overview]	Double Blind Period: Percentage of Participants Qualifying Relapse-free
NCT00436826 (42) [back to overview]	Double Blind Period: Percent Change in Normalized Brain Volume From Baseline to Week 96
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Number of T1 Hypointense Lesions Per Participant Per Scan at Week 96
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Change From Baseline in Vital Signs- Systolic and Diastolic Blood Pressure
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Change in T2 Lesion Volume From Baseline to Week 96
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Change in T1 Hypointense Lesion Volume From Baseline to Week 96
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Change in New T1 Gd+ Lesions From Baseline to Week 96
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Change From Baseline in Vital Signs- Weight
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Change From Baseline in Vital Signs- Temperature
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Change From Baseline in Vital Signs- Pulse Rate
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Change From Baseline in Electrocardiogram (ECG) Parameters- Heart Rate
NCT00436826 (42) [back to overview]	Double Blind Period: Maximum Corrected QT Interval (QTc)
NCT00436826 (42) [back to overview]	Double Blind Period: Annualized Qualifying Relapse Rate
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Changes From Baseline in CD4+ Count, CD8+ Count, and CD19+ to Week 96
NCT00436826 (42) [back to overview]	Open Label Extension Period: Mean Change From Baseline in Vital Signs- Temperature
NCT00436826 (42) [back to overview]	Open Label Extension Period: Mean Change From Baseline in Vital Signs- Weight
NCT00436826 (42) [back to overview]	Double Blind Period and OLE Period: Time to 3-Month Sustained Expanded Disability Status Scale (EDSS) Progression
NCT00436826 (42) [back to overview]	Double Blind Period and OLE Period: Time to First Qualifying Relapse
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Change From Baseline in Electrocardiogram (ECG) Parameters- PR, RR, QRS and OT Interval
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Changes From Baseline in Hemoglobin Level to Week 96
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Changes From Baseline in Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) to Week 96
NCT00436826 (42) [back to overview]	Double Blind Period: Mean Changes in Lymphocytes, White Blood Cells (WBC), Neutrophils and Platelets Values From Baseline to Week 96
NCT00436826 (42) [back to overview]	Double Blind Period: Number of Combined Unique Active (CUA) Lesions, Active Time Constant 2 (T2) Lesions, and Time Constant 1 (T1) Gadolinium Enhanced (Gd+) Lesions Per Participant Per Scan
NCT00436826 (42) [back to overview]	Double Blind Period: Number of Participants With Treatment Emergent Adverse Events (TEAEs) and Serious TEAEs
NCT00436826 (42) [back to overview]	Double Blind Period: Percentage of Participants With Grade 3 or 4 (Common Terminology Criteria for Adverse Events [CTCAE] v 4.0) Hematological or Liver Toxicity
NCT00436826 (42) [back to overview]	Double Blind Period: Time to First Grade 3 or 4 Hematological Toxicity or Liver Toxicity
NCT00436826 (42) [back to overview]	Double Blind Period: Time to First Grade 3 or 4 Hematological Toxicity or Liver Toxicity
NCT00436826 (42) [back to overview]	Double Blind Period: Time to Recovery From Grade 3 or 4 Hematological Toxicity
NCT00436826 (42) [back to overview]	Open Label Extension Period: Mean Change From Baseline in Vital Signs- Pulse Rate
NCT00436826 (42) [back to overview]	OLE and Safety Follow-up Period: Number of Participants With Treatment Emergent Adverse Events (TEAEs) and Serious TEAEs
NCT00436826 (42) [back to overview]	Open Label Extension Period: Mean Change From Baseline in Electrocardiogram (ECG) Parameters- PR, RR, QRS and OT Interval
NCT00436826 (42) [back to overview]	Open Label Extension Period: Mean Change From Baseline in Vital Signs- Systolic and Diastolic Blood Pressure
NCT00436826 (42) [back to overview]	Open Label Extension Period: Time to First Grade 3 or 4 Hematological Toxicity or Liver Toxicity
NCT00436826 (42) [back to overview]	Open Label Extension Period: Time to First Grade 3 or 4 Hematological Toxicity or Liver Toxicity
NCT00436826 (42) [back to overview]	Double Blind Period: Time to Recovery From Grade 3 or 4 Hematological Toxicity
NCT00436826 (42) [back to overview]	Open Label Extension Period: Mean Change From Baseline in Electrocardiogram (ECG) Parameters- Heart Rate
NCT00436826 (42) [back to overview]	Open Label Extension Period: Maximum Corrected QT Interval (Qtc)
NCT00436826 (42) [back to overview]	OLE and Safety Follow-up Period: Percentage of Participants With Treatment Emergent Adverse Events (TEAEs) in Infections and Infestations System Organ Class (SOC)
NCT00436826 (42) [back to overview]	Double Blind Period: Percentage of Participants With Treatment Emergent Adverse Events (TEAEs) in Infections and Infestations System Organ Class (SOC)
NCT00436826 (42) [back to overview]	Double Blind Period: Percentage of Participants With no Active T2 Lesions at Week 96
NCT00436826 (42) [back to overview]	OLE and Safety Follow-up Period: Percentage of Participants With Grade 3 or 4 (Common Terminology Criteria for Adverse Events [CTCAE] v 4.0) Hematological or Liver Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Mean Change From Baseline in Aspartate Aminotransferase and Alanine Aminotransferase at Week 120
NCT00641537 (28) [back to overview]	Safety Population: Mean Change in Corrected QT (QTc) Interval From Baseline
NCT00641537 (28) [back to overview]	Safety Population: Mean Time to Recovery From Grade 3 or 4 Hematological and Liver Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Mean Time to Recovery From Grade 3 or 4 Hematological and Liver Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Mean Time to Recovery From Grade 3 or 4 Hematological and Liver Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Mean Time to Recovery From Grade 3 or 4 Hematological and Liver Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Mean Time to Recovery From Grade 3 or 4 Hematological and Liver Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Median Time to Recovery From Grade 3 or 4 Hematological and Hepatic Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Median Time to Recovery From Grade 3 or 4 Hematological and Hepatic Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Median Time to Recovery From Grade 3 or 4 Hematological and Hepatic Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Median Time to Recovery From Grade 3 or 4 Hematological and Hepatic Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Number of Participants Who Developed Infections (Herpes Viral Infection, Viral Infectious Disorder and Opportunistic Infection), Infection-related Adverse Events and Malignancies
NCT00641537 (28) [back to overview]	Safety Population: Percentage of Participants With at Least 1 Common Terminology Criteria for Adverse Events Version 3.0 (CTCAE) Grade 4 Hematologic and Hepatic Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Time to First Grade 3 or 4 Hematological Toxicity and Liver Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Time to First Grade 3 or 4 Hematological Toxicity and Liver Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Time to First Grade 3 or 4 Hematological Toxicity and Liver Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Number of Participants With Treatment Emergent Adverse Events (TEAEs) and Serious TEAEs
NCT00641537 (28) [back to overview]	Safety Population: Time to First Grade 3 or 4 Hematological Toxicity and Liver Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Time to First Grade 3 or 4 Hematological Toxicity and Liver Toxicity
NCT00641537 (28) [back to overview]	SAFUP Analysis Set: Number of Participants Who Developed Infections (Herpes Viral Infection, Viral Infectious Disorder and Opportunistic Infection), Infection-related Adverse Events and Malignancies
NCT00641537 (28) [back to overview]	SAFUP Analysis Set: Number of Participants With Treatment Emergent Adverse Events (TEAEs) and Serious TEAEs
NCT00641537 (28) [back to overview]	Safety Population: Median Time to Recovery From Grade 3 or 4 Hematological and Hepatic Toxicity
NCT00641537 (28) [back to overview]	Safety Population: Mean Change From Baseline in Bilirubin at Week 120
NCT00641537 (28) [back to overview]	Safety Population: Mean Change From Baseline in Hemoglobin at Week 120
NCT00641537 (28) [back to overview]	Safety Population: Mean Time to Nadir of Absolute Lymphocyte Count
NCT00641537 (28) [back to overview]	Safety Population: Mean Time to Recovery From Nadir of Absolute Lymphocyte Count to Normal Value
NCT00641537 (28) [back to overview]	Safety Population: Median Time to Nadir of Absolute Lymphocyte Count
NCT00641537 (28) [back to overview]	Safety Population: Mean Change From Baseline in Absolute Lymphocyte Count, Platelet, Neutrophils and Leukocytes at Week 120
NCT00718549 (11) [back to overview]	Percentage of Participants With MRD According to Rawstron Criteria in Participants With CR or PR According to Clinical and Biochemical Factors at Week 29
NCT00718549 (11) [back to overview]	Percentage of Participants With MRD According to Rawstron Criteria in Participants With CR or PR According to Clinical and Biochemical Factors at Week 129
NCT00718549 (11) [back to overview]	Percentage of Participants With Disease Progression (PD), Relapse, or Death Due to Any Cause Assessed According to the National Cancer Institute (NCI) Revised Guidelines for the Diagnosis and Treatment of Chronic Lymphocytic Leukemia (CLL)
NCT00718549 (11) [back to overview]	Progression-Fee Survival (PFS) Assessed According to the NCI Revised Guidelines for the Diagnosis and Treatment of CLL
NCT00718549 (11) [back to overview]	Percentage of Participants With CR or PR Assessed According to the NCI Revised Guidelines for the Diagnosis and Treatment of CLL
NCT00718549 (11) [back to overview]	Percentage of Participants With CR or PR Assessed According to the NCI Revised Guidelines for the Diagnosis and Treatment of CLL
NCT00718549 (11) [back to overview]	Percentage of Participants With CR or PR Assessed According to the NCI Revised Guidelines for the Diagnosis and Treatment of CLL According to Clinical and Biochemical Factors at Week 129
NCT00718549 (11) [back to overview]	Percentage of Participants With CR or PR Assessed According to the NCI Revised Guidelines for the Diagnosis and Treatment of CLL According to Clinical and Biochemical Factors at Week 29
NCT00718549 (11) [back to overview]	Percentage of Participants With Minimal Residual Disease (MRD) According to Rawstron Criteria in Participants With CR or PR
NCT00718549 (11) [back to overview]	Percentage of Participants With Minimal Residual Disease (MRD) According to Rawstron Criteria in Participants With CR or PR
NCT00718549 (11) [back to overview]	PFS Assessed According to the NCI Revised Guidelines for the Diagnosis and Treatment of CLL According to Clinical and Biochemical Factors
NCT00725985 (56) [back to overview]	ITP: Number of T1 Hypointense Lesions
NCT00725985 (56) [back to overview]	ITP: Percent Change From Baseline in Brain Volume
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Mean Volume of T1 Gd-Enhanced Lesions and Changes From Baseline in Volume of T1 Gd-Enhanced Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Mean Volume of T1 Gd-Enhanced Lesions and Changes From Baseline in Volume of T1 Gd-Enhanced Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Mean Volume of T2 Lesions and Changes From Baseline in Volume of T2 Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Mean Volume of T2 Lesions and Changes From Baseline in Volume of T2 Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Number of Combined Unique Active (CUA) Magnetic Resonance Imaging (MRI) Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Number of New or Enlarging T2 Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Number of New or Enlarging T2 Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Number of New or Persisting Gd-enhanced Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Number of New or Persisting Gd-enhanced Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Number of T1 Hypointense Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Number of T1 Hypointense Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [Treated at LTFU Entry]): Mean Volume of T1 Gd-Enhanced Lesions and Changes From Baseline in Volume of T1 Gd-Enhanced Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [Treated at LTFU Entry]): Number of Combined Unique Active (CUA) Magnetic Resonance Imaging (MRI) Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [Treated at LTFU Entry]): Number of New or Enlarging T2 Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [Treated at LTFU Entry]): Number of New or Persisting Gd-enhanced Lesions
NCT00725985 (56) [back to overview]	OLMP: Mean Volume of T1 Gd-Enhanced Lesions and Changes From Baseline in Volume of T1 Gd-Enhanced Lesions
NCT00725985 (56) [back to overview]	OLMP: Mean Volume of T2 Lesions and Changes From Baseline in Volume of T2 Lesions
NCT00725985 (56) [back to overview]	OLMP: Number of Combined Unique Active (CUA) Magnetic Resonance Imaging (MRI) Lesions
NCT00725985 (56) [back to overview]	OLMP: Number of New or Enlarging T2 Lesions
NCT00725985 (56) [back to overview]	OLMP: Number of New or Persisting Gd-enhanced Lesions
NCT00725985 (56) [back to overview]	OLMP: Number of T1 Hypointense Lesions
NCT00725985 (56) [back to overview]	OLMP: Percent Change From Baseline in Brain Volume
NCT00725985 (56) [back to overview]	OLMP: Percent Change From Baseline in Brain Volume
NCT00725985 (56) [back to overview]	OLMP: Time to 3 Month Confirmed Expanded Disability Status Scale (EDSS) Progression From Randomization Represented by Kaplan-Meier Estimates of Probability of Disability Progression
NCT00725985 (56) [back to overview]	ITP: Time to Clinically Definite Multiple Sclerosis (CDMS) Conversion Represented by Kaplan-Meier Estimates of the Cumulative Percentage of Participants With CDMS
NCT00725985 (56) [back to overview]	ITP: Change From Baseline in Volume of T1 Gd-Enhanced Lesions
NCT00725985 (56) [back to overview]	ITP: Percentage of Participants Converting to Clinically Definite Multiple Sclerosis (CDMS) as Per Poser Criteria
NCT00725985 (56) [back to overview]	ITP: Percentage of Participants Converting to McDonald Multiple Sclerosis (MS) (2005)
NCT00725985 (56) [back to overview]	ITP: Percentage of Participants With no New or Enlarging T2 Lesions
NCT00725985 (56) [back to overview]	ITP: Percentage of Participants With no New or Persisting T1 Gd-Enhanced Lesions
NCT00725985 (56) [back to overview]	ITP: Time to Develop Multiple Sclerosis (MS) Conversion According to the Revised McDonald Criteria (2005) Represented by Kaplan-Meier Estimates of the Cumulative Percentage of Participants With McDonald MS
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Number of Relapses
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Number of Combined Unique Active (CUA) Magnetic Resonance Imaging (MRI) Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Percentage of Participants With no New or Enlarging T2 Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Percentage of Participants With no New or Persisting T1 Gd-Enhanced Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Time to Conversion to Clinically Definite Multiple Sclerosis (CDMS) According to Poser Criteria
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [No Treatment at LTFU Entry]): Time to Conversion to Multiple Sclerosis (MS) According to the 2005 McDonald Criteria
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [Treated at LTFU Entry]): Mean Volume of T2 Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [Treated at LTFU Entry]): Number of Relapses
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [Treated at LTFU Entry]): Number of T1 Hypointense Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [Treated at LTFU Entry]): Percentage of Participants With no New or Enlarging T2 Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [Treated at LTFU Entry]): Percentage of Participants With no New or Persisting T1 Gd-Enhanced Lesions
NCT00725985 (56) [back to overview]	LTFU (LTFU Analysis Set [Treated at LTFU Entry]): Time to Conversion to Clinically Definite Multiple Sclerosis (CDMS) According to Poser Criteria
NCT00725985 (56) [back to overview]	OLMP: Annualized Relapse Rate
NCT00725985 (56) [back to overview]	OLMP: Number of Relapses
NCT00725985 (56) [back to overview]	OLMP: Percentage of Participants With no New or Enlarging T2 Lesions
NCT00725985 (56) [back to overview]	OLMP: Percentage of Participants With no New or Persisting T1 Gd-Enhanced Lesions
NCT00725985 (56) [back to overview]	OLMP: Percentage of Relapse-Free Participants
NCT00725985 (56) [back to overview]	ITP: Changes From Baseline in Volume of T2 Lesions
NCT00725985 (56) [back to overview]	ITP: Number of Combined Unique Active (CUA) Lesions, New or Enlarging Time Constant 2 (T2) Lesions, and New or Persisting Time Constant 1 (T1) Gadolinium Enhanced (Gd+) Lesions Per Participant Per Scan
NCT00725985 (56) [back to overview]	ITP: Number of Combined Unique Active (CUA) Magnetic Resonance Imaging (MRI) Lesions
NCT00725985 (56) [back to overview]	ITP: Number of New or Enlarging T2 Lesions
NCT00725985 (56) [back to overview]	ITP: Number of New or Persisting Gd-enhanced Lesions
NCT00725985 (56) [back to overview]	ITP: Number of Participants With Treatment-emergent Adverse Events (TEAEs) and Serious TEAEs
NCT00764517 (5) [back to overview]	Toxicities as Assessed Using the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) Version 4.0
NCT00764517 (5) [back to overview]	Tolerability of Treatment
NCT00764517 (5) [back to overview]	Progression-free Survival
NCT00764517 (5) [back to overview]	Objective Response Rate
NCT00764517 (5) [back to overview]	Event-free Survival
NCT00938366 (8) [back to overview]	Time to Reach the Maximum Plasma Concentration (Tmax) of Cladribine
NCT00938366 (8) [back to overview]	Maximum Plasma Concentration (Cmax) of Cladribine
NCT00938366 (8) [back to overview]	Area Under the Plasma Concentration-time Curve From Time Zero to the Last Sampling Time at Which the Concentration is at or Above the Lower Limit of Quantification (AUC0-t) of Cladribine
NCT00938366 (8) [back to overview]	Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of Cladribine
NCT00938366 (8) [back to overview]	Apparent Volume of Distribution During the Terminal Phase Following Extravascular Administration (Vz/f) of Cladribine
NCT00938366 (8) [back to overview]	Apparent Terminal Half-life (t1/2) of Cladribine
NCT00938366 (8) [back to overview]	Total Body Clearance From Plasma Following Extravascular Administration (CL/f) of Cladribine
NCT00938366 (8) [back to overview]	Percentage of Subjects With Any Treatment Emergent Adverse Events (TEAEs), Serious AEs, AEs Leading to Death, and AEs Leading to Discontinuation
NCT00955916 (3) [back to overview]	Overall Response Rate (ORR)
NCT00955916 (3) [back to overview]	Median Progression Free Survival (PFS)
NCT00955916 (3) [back to overview]	Median Overall Survival (OS)
NCT00980395 (4) [back to overview]	Complete Response Rate
NCT00980395 (4) [back to overview]	Overall Survival at 2 Years
NCT00980395 (4) [back to overview]	Progression-free Survival at 2 Years
NCT00980395 (4) [back to overview]	Partial Response
NCT02044796 (4) [back to overview]	Number of Participants With Dose Limiting Toxicities of Mitoxantrone (Phase I, Dose Level 4)
NCT02044796 (4) [back to overview]	Overall Survival (Phase II)
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]	Remission Rate (Complete Remission and Complete Remission With Incomplete Platelet Count Recovery) of This Regimen in Patients With Relapsed/Refractory Disease (Phase II)
NCT02096055 (5) [back to overview]	Leukemia-free Survival
NCT02096055 (5) [back to overview]	Remission Duration
NCT02096055 (5) [back to overview]	Survival
NCT02096055 (5) [back to overview]	Number of Participants With the Most Frequently Reports Grade 3 or 4 Adverse Event.
NCT02096055 (5) [back to overview]	Number of Participants With a Complete Response
NCT02416908 (9) [back to overview]	Complete Remission Rate (CR + CRi)
NCT02416908 (9) [back to overview]	Duration of Remission
NCT02416908 (9) [back to overview]	Event-free Survival
NCT02416908 (9) [back to overview]	Number of Participants Who Were Able to Undergo Hematopoietic Stem Cell Transplantation
NCT02416908 (9) [back to overview]	Overall Survival
NCT02416908 (9) [back to overview]	Relapse-free Survival
NCT02416908 (9) [back to overview]	Time to Neutrophil Engraftment
NCT02416908 (9) [back to overview]	Time to Platelet Engraftment
NCT02416908 (9) [back to overview]	Safety and Tolerability of Treatment as Measured by Incidence of Grade 3-4 Adverse Events Occurring in >5% of Participants
NCT02728050 (8) [back to overview]	Relapse-free Survival (RFS)
NCT02728050 (8) [back to overview]	Phase I and II: Rate of Minimal Residual Disease Negative (MRDneg) Complete Response (CR)
NCT02728050 (8) [back to overview]	Phase 1: Maximum Tolerated Dose (MTD)/Recommended Phase 2 Dose (RP2D) of Sorafenib
NCT02728050 (8) [back to overview]	Overall Response Rate (ORR)
NCT02728050 (8) [back to overview]	Event-free Survival (EFS)
NCT02728050 (8) [back to overview]	Number of Participants With Adverse Events
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
NCT02756572 (19) [back to overview]	Factors That Distinguish Patients Who Received Early Transplant From Those Who Did Not - GENDER
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]	Feasibility of Early Allogeneic Hematopoietic Cell Transplant Assessed by Relapsed-free Survival 6 Months After Transplant
NCT02756572 (19) [back to overview]	Response Assessments After Early Allogeneic Hematopoietic Cell Transplant, Day 28
NCT02756572 (19) [back to overview]	Response Assessments After Early Allogeneic Hematopoietic Cell Transplant, Day 84
NCT02756572 (19) [back to overview]	Acute Graft Versus Host Disease 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]	Event-free Survival (EFS) 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]	Factors That Distinguish Patients Who Received Early Transplant From Those Who Did Not - AGE
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]	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]	Overall Survival (OS) Among Patients Who Received Early Transplant.
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]	Relapse-free Survival (RFS) Among Patients Who Received Early Transplant
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]	Demonstrate the Feasibility of Collecting Patient-reported Outcomes for Trial Participants
NCT02921061 (6) [back to overview]	Number of Participants With Event-free Survival
NCT02921061 (6) [back to overview]	Number of Participants With Minimal Residual Disease Negative (MRDneg) Complete Remission (Phase II)
NCT02921061 (6) [back to overview]	Number of Participants With Overall Survival
NCT02921061 (6) [back to overview]	Number of Participants With Relapse-free Survival
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 Who Achieved Remission (Complete Remission [CR]/CR With Incomplete Peripheral Blood Count Recovery [CRi])
NCT03364036 (6) [back to overview]	Percent Change From Baseline in Counts of Immune Cell Subsets - T Cells at Month 3, 6, 12, 15, 18 and 24
NCT03364036 (6) [back to overview]	Percent Change From Baseline in Counts of Immune Cell Subsets - B Cells at Month 3, 6, 12, 15, 18 and 24
NCT03364036 (6) [back to overview]	Percent Change From Baseline in Counts of Immune Cell Subsets - NK Cells at Month 3, 6, 12, 15, 18 and 24
NCT03364036 (6) [back to overview]	Change From Baseline Period (Period Screening to Baseline) in Counts of Combined Unique Active (CUA) Magnetic Resonance Imaging (MRI) Lesions at Period 3 (Month 3-6)
NCT03364036 (6) [back to overview]	Change From Baseline Period (Period Screening to Baseline) in Counts of Combined Unique Active (CUA) Magnetic Resonance Imaging (MRI) Lesions at Period 2 (Month 2-6)
NCT03364036 (6) [back to overview]	Change From Baseline Period (Period Screening to Baseline) in Counts of Combined Unique Active (CUA) Magnetic Resonance Imaging (MRI) Lesions at Period 1 (Month 1-6)
NCT03369665 (2) [back to overview]	Change From Baseline in Multiple Sclerosis Quality of Life-54 Questionnaire (MSQoL-54) Physical Health Composite Summary and Mental Health Composite Summary Scores at Month 24
NCT03369665 (2) [back to overview]	Treatment Global Satisfaction Determined by Treatment Satisfaction Questionnaire Medication Version 1.4 (TSQM v1.4) Scale at Month 6
NCT03531918 (10) [back to overview]	Maximum Tolerated Dose (MTD) of Gemtuzumab Ozogamicin (GO) When Added to GCLAM (Phase 1)
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: CR/CRi
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]	30-day All-cause Mortality

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

Intervention	Participants (Number)
	Experienced Grade 3 or 4 toxicities	Did not experience Grade 3 or 4 toxicities
Overall	27	3

Intervention	months (Number)
Cladribine 5.25 mg/kg	13.6
Cladribine 3.5 mg/kg	13.6
Placebo	10.8

Intervention	lesions (Least Squares Mean)
	CU lesions	Active T1 Gd+ lesions	Active T2 lesions
Cladribine 3.5 mg/kg	0.43	0.12	0.38
Cladribine 5.25 mg/kg	0.38	0.11	0.33
Placebo	1.72	0.91	1.43

Intervention	relapses per year (Number)
Cladribine 5.25 mg/kg	0.15
Cladribine 3.5 mg/kg	0.14
Placebo	0.33

Intervention	percentage of participants (Number)
Cladribine 5.25 mg/kg	78.9
Cladribine 3.5 mg/kg	79.7
Placebo	60.9

Intervention	Percentage of Participants (Number)
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	86.0
Placebo, IFN-beta (DB Period)	56.3

Intervention	Percentage of Participants (Number)
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	75.0
Placebo, IFN-beta (DB Period)	52.1

Intervention	Percent Change (Mean)
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	-1.01
Placebo, IFN-beta (DB Period)	-1.42

Intervention	Millimeter of mercury (mm*hg) (Mean)
	Systolic Blood Pressure	Diastolic Blood Pressure
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	-0.6	-0.6
Placebo, IFN-beta (DB Period)	0.0	-2.2

Intervention	cubic millimeters (mm^3) (Mean)
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	-2007.2
Placebo, IFN-beta (DB Period)	-1224.6

Intervention	millimeter cubic (Mean)
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	-481.8
Placebo, IFN-beta (DB Period)	-263.0

Intervention	Lesions (Mean)
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	-1.0
Placebo, IFN-beta (DB Period)	-0.3

Intervention	Degree celsius (Mean)
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	-0.1
Placebo, IFN-beta (DB Period)	-0.1

Intervention	beats per minutes (Mean)
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	-3.114
Placebo, IFN-beta (DB Period)	1.981

Intervention	Milliseconds (Mean)
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	0.4381
Placebo, IFN-beta (DB Period)	0.4361

Intervention	Cells per microliter (Mean)
	CD4+	CD8+	CD19+
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	-604.1	-137.8	22.0
Placebo, IFN-beta (DB Period)	7.1	23.9	30.7

Intervention	Days (Number)
	10th percentile	20th percentile
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	244	NA
Cladribine 3.5 mg/kg, IFN-beta, Cladribine 3.5 mg/kg (OL Ext)	87	246
Placebo, IFN-beta (DB Period)	484	0
Placebo, IFN-beta, Cladribine 3.5 mg/kg (OL Ext)	85	0

Intervention	milliseconds (Mean)
	PR Interval	RR Interval	QRS Interval	QT Interval
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	0.0001	0.0361	0.0028	0.0135
Placebo, IFN-beta (DB Period)	0.0033	-0.0272	0.0043	0.0037

Intervention	gram per liter (g/L) (Mean)
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	-2.9
Placebo, IFN-beta (DB Period)	-2.5

Intervention	Units per liter (Mean)
	ALT	AST
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	-3.0	-1.7
Placebo, IFN-beta (DB Period)	1.3	1.1

Intervention	10^9 cells per liter (Mean)
	Lymphocytes	Platelet	WBC	Neutrophils
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	-0.8	-29.8	-1.5	-0.7
Placebo, IFN-beta (DB Period)	0.0	-12.4	-0.4	-0.4

cladribine

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Protein Targets (54)

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Research

Studies (1,727)

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Research Demand Index: 79.75

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Clinical Trials (117)

Trial Overview

Trial Outcomes

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

Relationship of Inhibition of DNA Synthesis and Clinical Response

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

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

Minimal Residual Disease (MRD).

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

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

Time to Disability Progression

Mean Number of Combined Unique (CU) Lesions, Active Time Constant 2 (T2) Lesions, and Active Time Constant 1 (T1) Gadolinium-Enhanced (Gd+) Lesions Per Participant Per Scan

Annualized Qualifying Relapse Rate

Percentage of Relapse-free Participants

Double Blind Period: Percentage of Participants With no Active T1 Gd-Enhanced Lesions at Week 96

Double Blind Period: Percentage of Participants Qualifying Relapse-free

Double Blind Period: Percent Change in Normalized Brain Volume From Baseline to Week 96

Double Blind Period: Mean Number of T1 Hypointense Lesions Per Participant Per Scan at Week 96

Double Blind Period: Mean Change From Baseline in Vital Signs- Systolic and Diastolic Blood Pressure

Double Blind Period: Mean Change in T2 Lesion Volume From Baseline to Week 96

Double Blind Period: Mean Change in T1 Hypointense Lesion Volume From Baseline to Week 96

Double Blind Period: Mean Change in New T1 Gd+ Lesions From Baseline to Week 96

Double Blind Period: Mean Change From Baseline in Vital Signs- Weight

Double Blind Period: Mean Change From Baseline in Vital Signs- Temperature

Double Blind Period: Mean Change From Baseline in Vital Signs- Pulse Rate

Double Blind Period: Mean Change From Baseline in Electrocardiogram (ECG) Parameters- Heart Rate

Double Blind Period: Maximum Corrected QT Interval (QTc)

Double Blind Period: Annualized Qualifying Relapse Rate

Double Blind Period: Mean Changes From Baseline in CD4+ Count, CD8+ Count, and CD19+ to Week 96

Open Label Extension Period: Mean Change From Baseline in Vital Signs- Temperature

Open Label Extension Period: Mean Change From Baseline in Vital Signs- Weight

Double Blind Period and OLE Period: Time to 3-Month Sustained Expanded Disability Status Scale (EDSS) Progression

Double Blind Period and OLE Period: Time to First Qualifying Relapse

Double Blind Period: Mean Change From Baseline in Electrocardiogram (ECG) Parameters- PR, RR, QRS and OT Interval

Double Blind Period: Mean Changes From Baseline in Hemoglobin Level to Week 96

Double Blind Period: Mean Changes From Baseline in Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) to Week 96

Double Blind Period: Mean Changes in Lymphocytes, White Blood Cells (WBC), Neutrophils and Platelets Values From Baseline to Week 96

Double Blind Period: Number of Combined Unique Active (CUA) Lesions, Active Time Constant 2 (T2) Lesions, and Time Constant 1 (T1) Gadolinium Enhanced (Gd+) Lesions Per Participant Per Scan

Double Blind Period: Number of Participants With Treatment Emergent Adverse Events (TEAEs) and Serious TEAEs

Double Blind Period: Percentage of Participants With Grade 3 or 4 (Common Terminology Criteria for Adverse Events [CTCAE] v 4.0) Hematological or Liver Toxicity

Double Blind Period: Time to First Grade 3 or 4 Hematological Toxicity or Liver Toxicity

Double Blind Period: Time to First Grade 3 or 4 Hematological Toxicity or Liver Toxicity

Double Blind Period: Time to Recovery From Grade 3 or 4 Hematological Toxicity

Open Label Extension Period: Mean Change From Baseline in Vital Signs- Pulse Rate

OLE and Safety Follow-up Period: Number of Participants With Treatment Emergent Adverse Events (TEAEs) and Serious TEAEs

Open Label Extension Period: Mean Change From Baseline in Electrocardiogram (ECG) Parameters- PR, RR, QRS and OT Interval

Open Label Extension Period: Mean Change From Baseline in Vital Signs- Systolic and Diastolic Blood Pressure

Open Label Extension Period: Time to First Grade 3 or 4 Hematological Toxicity or Liver Toxicity

Open Label Extension Period: Time to First Grade 3 or 4 Hematological Toxicity or Liver Toxicity

Double Blind Period: Time to Recovery From Grade 3 or 4 Hematological Toxicity

Open Label Extension Period: Mean Change From Baseline in Electrocardiogram (ECG) Parameters- Heart Rate

Intervention	Lesions (Mean)
	T1 Gd+ lesions	CUA lesions	T2 lesions
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	0.06	0.55	0.53
Placebo, IFN-beta (DB Period)	0.34	1.12	1.04

Intervention	Participants (Count of Participants)
	Participants with TEAEs	Participants with Serious TEAEs
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	119	12
Placebo, IFN-beta (DB Period)	36	5

Intervention	Percentage of participants (Number)
	Grade 3 or 4 Lymphocyte toxicity	Grade 3 or 4 Hemoglobin toxicity	Grade 3 or 4 White Blood Cell toxicity	Grade 3 or 4 Neutrophil toxicity	Grade 3 or 4 CD4+ toxicity	Grade 3 or 4 AST toxicity	Grade 3 or 4 ALT toxicity	Grade 3 or 4 Platelet toxicity	Grade 3 or 4 Bilirubin toxicity
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	63.71	2.42	10.48	12.10	50.81	0.81	0.81	0.00	0.00
Placebo, IFN-beta (DB Period)	2.08	0.00	0.00	2.08	2.08	0.00	2.08	0.00	0.00

Intervention	Months (Number)
	10th percentile: Lymphocytes toxicity	20th percentile: Lymphocytes toxicity	10th percentile:Hemoglobin toxicity	20th percentile:Hemoglobin toxicity	10th percentile: White Blood Cell toxicity	20th percentile: White Blood Cell toxicity	10th percentile: Neutrophil toxicity	20th percentile: Neutrophil toxicity	10th percentile: CD4+ count toxicity	20th percentile: CD4+ count toxicity	10th percentile: AST toxicity	20th percentile: AST toxicity	10th percentile: ALT toxicity	20th percentile: ALT toxicity
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	1.61	2.00	NA	NA	17.74	NA	12.55	NA	1.87	2.99	NA	NA	NA	NA

Intervention	Participants (Count of Participants)
	Participants with TEAEs	Participants with Serious TEAEs
Cladribine 3.5 mg/kg, IFN-beta (Safety Follow up)	22	1
Cladribine 3.5 mg/kg, IFN-beta, Cladribine 3.5 mg/kg (OL Ext)	37	0
Placebo, IFN-beta (Safety Follow up)	0	0
Placebo, IFN-beta, Cladribine 3.5 mg/kg (OL Ext)	19	1

Intervention	Days (Mean)
	Hemoglobin	White Blood Cell	Neutrophil	Lymphocyte
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	19.50	31.27	41.17	142.53

Intervention	Milliseconds (Mean)
Cladribine 3.5 mg/kg, IFN-beta, Cladribine 3.5 mg/kg (OL Ext)	0.4370
Placebo, IFN-beta, Cladribine 3.5 mg/kg (OL Ext)	0.4317

Intervention	Percentage of participants (Number)
Cladribine 3.5 mg/kg, IFN-beta, Cladribine 3.5 mg/kg (OL Ext)	38.3
Placebo, IFN-beta, Cladribine 3.5 mg/kg (OL Ext)	21.4
Cladribine 3.5 mg/kg, IFN-beta (Safety Follow up)	11.5
Placebo, IFN-beta (Safety Follow up)	0

Intervention	Percentage of participants (Number)
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	61.3
Placebo, IFN-beta (DB Period)	54.2

Intervention	Percentage of Participants (Number)
Cladribine 3.5 mg/kg, IFN-beta (DB Period)	56.2
Placebo, IFN-beta (DB Period)	29.2