Page last updated: 2024-11-13

navitoclax

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

Cross-References

ID SourceID
PubMed CID24978538
CHEMBL ID443684
CHEBI ID131174
CHEBI ID94128
SCHEMBL ID522847
MeSH IDM0553438

Synonyms (76)

Synonym
HY-10087
4-(4-{[2-(4-chlorophenyl)-5,5-dimethylcyclohex-1-en-1-yl]methyl}piperazin-1-yl)-n-({4-({(1r)-3-morpholin-4-yl-1-[(phenylsulfanyl)methyl]propyl}amino)-3-[(trifluoromethyl)sulfonyl]phenyl}sulfonyl)benzamide
abt-263 ,
rg-7433
navitoclax ,
BRD-K82746043-001-03-7
NCGC00188344-02
BRD-K82746043-001-04-5
BRD-K82746043-001-01-1
bdbm50270877
(r)-4-(4-((2-(4-chlorophenyl)-5,5-dimethylcyclohex-1-enyl)methyl)piperazin-1-yl)-n-(4-(4-morpholino-1-(phenylthio)butan-2-ylamino)-3-(trifluoromethylsulfonyl)phenylsulfonyl)benzamide
BRD-K82746043-001-02-9
CHEMBL443684 ,
abt263
4-{4-[(4'-chloro-4,4-dimethyl-3,4,5,6-tetrahydro[biphenyl]-2-yl)methyl]piperazin-1-yl}-n-[(4-{[(2r)-4-(morpholin-4-yl)-1-(phenylsulfanyl)butan-2-yl]amino}-3-[(trifluoromethyl)sulfonyl]phenyl)sulfonyl]benzamide
navitoclaxum
abt 263
923564-51-6
a-855071.0
CHEBI:131174
NCGC00188344-01
NCGC00188344-03
abt-263,navitoclax
navitoclax (usan/inn)
D09935
navitoclax [usan:inn]
benzamide, 4-(4-((2-(4-chlorophenyl)-5,5-dimethyl-1-cyclohexen-1-yl)methyl)-1-piperazinyl)-n-((4-(((1r)-3-(4-morpholinyl)-1-((phenylthio)methyl)propyl)amino)-3-((trifluoromethyl)sulfonyl)phenyl)sulfonyl)-
unii-xkj5vvk2wd
xkj5vvk2wd ,
4-[4-[[2-(4-chlorophenyl)-5,5-dimethyl-1-cyclohexen-1-yl]methyl]-1-piperazinyl]-n-[[4-[[(1r)-3-(4-morpholinyl)-1-[(phenylthio)methyl]propyl]amino]-3-[(trifluoromethyl)sulfonyl]phenyl]sulfonyl]benzamide
4-(4-{[2-(4-chlorophenyl)-5,5-dimethylcyclohex-1-en-1-yl]methyl}piperazin-1-yl)-n-[(4-{[(2r)-4-(morpholin-4-yl)-1-(phenylsulfanyl)butan-2-yl]amino}-3-[(trifluoromethyl)sulfonyl]phenyl)sulfonyl]benzamide
NCGC00188344-05
S1001
AKOS015896297
c47h55clf3n5o6s3
4-(4-((2-(4-chlorophenyl)-5,5-dimethylcyclohex-1-en-1-yl)methyl)piperazin-1-yl)-n-((4-(((2r)-4-(morpholin-4-yl)-1-(phenylsulfanyl)butan-2-yl)amino)-3-((trifluoromethyl)sulfonyl)phenyl)sulfonyl)benzamide
benzamide, 4-(4-((2-(4-chlorophenyl)-5,5-dimethyl-1-cyclohexen-1-yl)methyl)-1- piperazinyl)-n-((4-(((1r)-3-(4-morpholinyl)-1-((phenylthio)methyl)propyl)amino)-3-((trifluoromethyl)sulfonyl)phenyl)sulfonyl)-
navitoclax [who-dd]
4-(4-((2-(4-chlorophenyl)-5,5-dimethylcyclohex-1-en-1-yl)methyl)piperazin-1-yl)-n-(4-(((2r)-4-(morpholin-4-yl)-1-(phenylsulfanyl)butan-2-yl)amino)-3-(trifluoromethanesulfonyl)benzenesulfonyl)benzamide
navitoclax [usan]
navitoclax [jan]
navitoclax [inn]
navitoclax [mi]
4-(4-{[2-(4-chlorophenyl)-5,5-dimethylcyclohex-1-en-1-yl]methyl}piperazin-1-yl)-n-({4-({(1r)-3-(morpholin-4-yl)-1-[(phenylsulfanyl)methyl]propyl}amino)-3-[(trifluoromethyl)sulfonyl]phenyl}sulfonyl)benzamide
MLS006011021
smr004702817
SCHEMBL522847
4-[4-[[2-(4-chlorophenyl)-5,5-dimethyl-cyclohexen-1-yl]methyl]piperazin-1-yl]-n-[4-[[(1r)-3-morpholino-1-(phenylsulfanylmethyl)propyl]amino]-3-(trifluoromethylsulfonyl)phenyl]sulfonyl-benzamide
DTXSID2042640
4-[4-[[2-(4-chlorophenyl)-5,5-dimethylcyclohexen-1-yl]methyl]piperazin-1-yl]-n-[4-[[(2r)-4-morpholin-4-yl-1-phenylsulfanylbutan-2-yl]amino]-3-(trifluoromethylsulfonyl)phenyl]sulfonylbenzamide
gtpl8319
AC-31055
navitoclax (abt-263)
(r)-4-(4-((4'-chloro-4,4-dimethyl-3,4,5,6-tetrahydro-[1,1'-biphenyl]-2-yl)methyl)piperazin-1-yl)-n-((4-((4-morpholino-1-(phenylthio)butan-2-yl)amino)-3-((trifluoromethyl)sulfonyl)phenyl)sulfonyl)benzamide
abt-263 (navitoclax)
J-519525
EX-A055
4-[4-[[2-(4-chlorophenyl)-5,5-dimethyl-1-cyclohexen-1-yl]methyl]-1-piperazinyl]-n-[[4-[[(1r)-3-(4-mo
CHEBI:94128
n-(4-{4-[2-(4-chlorophenyl)-5,5-dimethyl-cyclohex-1-enylmethyl]-piperazin-1-yl}-benzoyl)-4-((r)-3-morpholin-4-yl-1-phenylsulfanylmethyl-propylamino)-3-trifluoromethanesulfonyl-benzenesulfonamide
mfcd12756219
NCGC00188344-08
SW218055-2
DB12340
(r)-4-(4-((2-(4-chlorophenyl)-5,5-dimethylcyclohex-1-enyl)methyl)piperazin-1-yl)-n-(4-(4-morpholino-1-(phenylthio)butan-2-ylamino)-3-(trifluoromethylsulfonyl)p
navitoclax, abt-263
AS-16690
Q18002993
(r)-4-(4-((4-chloro-4,4-dimethyl-3,4,5,6-tetrahydro-[1,1-biphenyl]-2-yl)methyl)piperazin-1-yl)-n-((4-((4-morpholino-1-(phenylthio)butan-2-yl)amino)-3-((trifluoromethyl)sulfonyl)phenyl)sulfonyl)benzamide
4-[4-[[2-(4-chlorophenyl)-5,5-dimet
nsc-759659
nsc759659
navitoclax; abt-263
jlyaxfnoilikpp-kxqooqhdsa-n
abt-263 in bulk
novitoclax

Research Excerpts

Overview

Navitoclax is a first-in-class, orally bioavailable, targeted Bcl-2 family protein inhibitor and promotes apoptosis. It has demonstrated efficacy in haematological tumours alone and in combination with other agents.

ExcerptReferenceRelevance
"Navitoclax, which is a type of senolytic drug, selectively eliminates senescent cells. "( Senolytic Agent Navitoclax Inhibits Angiotensin II-Induced Heart Failure in Mice.
Bao, Y; Dai, Y; Jia, K; Jin, Q; Li, X; Liu, A; Lu, L; Wu, L, 2020
)
2.35
"Navitoclax is a targeted B-cell lymphoma-2 (Bcl-2) family protein inhibitor. "( Effect of co-administration of ketoconazole, a strong CYP3A inhibitor, on the pharmacokinetics, safety and tolerability of navitoclax, a first-in-class oral Bcl-2 family inhibitor, in cancer patients.
Graham, A; Holen, K; Patnaik, A; Pradhan, R; Salem, AH; Xiong, H; Yang, J, 2014
)
2.05
"Navitoclax is a selective, potent, orally bioavailable, small molecule Bcl-2 inhibitor."( A phase I safety and pharmacokinetic study of ABT-263 in combination with carboplatin/paclitaxel in the treatment of patients with solid tumors.
Busman, T; Cosgrove, D; Karantza, V; Mabry, M; Rudersdorf, N; Vlahovic, G; Wang, D; Xiong, H; Yang, J, 2014
)
1.12
"Navitoclax is a first-in-class, orally bioavailable, targeted Bcl-2 family protein inhibitor that has been studied in cancer patients."( Studying navitoclax, a targeted anticancer drug, in healthy volunteers--ethical considerations and risk/benefit assessments and management.
Awni, WM; Gordon, GB; Holen, KD; Humerickhouse, R; Krivoshik, AP; Nada, A; Pradhan, RS; Rhodes, JW; Xiong, H, 2014
)
1.54
"Navitoclax is a first-in-class, orally bioavailable, targeted Bcl-2 family protein inhibitor and promotes apoptosis. "( Mechanism-based pharmacokinetic/pharmacodynamic meta-analysis of navitoclax (ABT-263) induced thrombocytopenia.
Awni, W; Humerickhouse, R; Kaefer, A; Mensing, S; Noertersheuser, P; Xiong, H; Yang, J, 2014
)
2.08
"Navitoclax is a targeted high-affinity small molecule that inhibits the anti-apoptotic activity of BCL-2 and BCL-XL."( Navitoclax, a targeted high-affinity inhibitor of BCL-2, in lymphoid malignancies: a phase 1 dose-escalation study of safety, pharmacokinetics, pharmacodynamics, and antitumour activity.
Busman, T; Chiu, YL; Cui, Y; Czuczman, MS; Dunleavy, K; Elmore, SW; Enschede, SH; Gerecitano, JF; Humerickhouse, RA; Krivoshik, AP; LaCasce, AS; Leonard, JP; O'Connor, OA; Rosenberg, SH; Tulpule, A; Wilson, WH; Xiong, H, 2010
)
2.52
"Navitoclax (ABT-263) is a potent inhibitor of Bcl-2, Bcl-x(L) and Bcl-w, which has demonstrated efficacy in haematological tumours alone and in combination with other agents."( Navitoclax (ABT-263) and bendamustine ± rituximab induce enhanced killing of non-Hodgkin's lymphoma tumours in vivo.
Ackler, S; Boghaert, ER; Chen, J; Clarin, J; Foster, K; Jin, S; Leverson, JD; Mitten, MJ; Phillips, DC; Schlessinger, S; Wang, B, 2012
)
2.54

Effects

ExcerptReferenceRelevance
"Navitoclax has a novel mechanism of peripheral thrombocytopenia and T-cell lymphopenia, attributable to high-affinity inhibition of BCL-XL and BCL-2, respectively. "( Navitoclax, a targeted high-affinity inhibitor of BCL-2, in lymphoid malignancies: a phase 1 dose-escalation study of safety, pharmacokinetics, pharmacodynamics, and antitumour activity.
Busman, T; Chiu, YL; Cui, Y; Czuczman, MS; Dunleavy, K; Elmore, SW; Enschede, SH; Gerecitano, JF; Humerickhouse, RA; Krivoshik, AP; LaCasce, AS; Leonard, JP; O'Connor, OA; Rosenberg, SH; Tulpule, A; Wilson, WH; Xiong, H, 2010
)
3.25

Treatment

ExcerptReferenceRelevance
"Navitoclax treatment increases dependency on MCL-1 and increases BIM protein levels."( Dynamic BH3 profiling identifies pro-apoptotic drug combinations for the treatment of malignant pleural mesothelioma.
Bohl, SR; Bueno, R; Chow, KH; Du, R; Letai, A; Ligon, KL; Potter, DS, 2023
)
1.63

Toxicity

ExcerptReferenceRelevance
" Common toxic effects included grade 1 or 2 anaemia (41 patients), infection (39), diarrhoea (31), nausea (29), and fatigue (21); and grade 3 or 4 thrombocytopenia (29), lymphocytopenia (18), and neutropenia (18)."( Navitoclax, a targeted high-affinity inhibitor of BCL-2, in lymphoid malignancies: a phase 1 dose-escalation study of safety, pharmacokinetics, pharmacodynamics, and antitumour activity.
Busman, T; Chiu, YL; Cui, Y; Czuczman, MS; Dunleavy, K; Elmore, SW; Enschede, SH; Gerecitano, JF; Humerickhouse, RA; Krivoshik, AP; LaCasce, AS; Leonard, JP; O'Connor, OA; Rosenberg, SH; Tulpule, A; Wilson, WH; Xiong, H, 2010
)
1.8
" There were no adverse events related to navitoclax exposure reported in these 2 patients."( Effect of co-administration of ketoconazole, a strong CYP3A inhibitor, on the pharmacokinetics, safety and tolerability of navitoclax, a first-in-class oral Bcl-2 family inhibitor, in cancer patients.
Graham, A; Holen, K; Patnaik, A; Pradhan, R; Salem, AH; Xiong, H; Yang, J, 2014
)
0.88
" The most common treatment-related adverse events were diarrhea, nausea, vomiting, and decreased appetite."( Safety, efficacy, and pharmacokinetics of navitoclax (ABT-263) in combination with erlotinib in patients with advanced solid tumors.
Arzt, J; Busman, TA; Holen, KD; Kirschbrown, W; Lian, G; LoRusso, P; Rosen, LS; Rudersdorf, NS; Tolcher, AW; Vanderwal, CA, 2015
)
0.68
" The most common adverse event in both groups was diarrhea (Q3W 92."( Safety, efficacy, and pharmacokinetics of navitoclax (ABT-263) in combination with irinotecan: results of an open-label, phase 1 study.
Arzt, J; Busman, TA; Holen, KD; Lian, G; LoRusso, P; Rosen, LS; Rudersdorf, NS; Tolcher, AW; Vanderwal, CA; Waring, JF; Yang, J, 2015
)
0.68
" Compared to ABT263, PZ is less toxic to platelets, but equally or slightly more potent against SCs because CRBN is poorly expressed in platelets."( Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity.
Almeida, M; Budamagunta, V; Campisi, J; Chang, J; Elisseeff, JH; He, Y; Khan, S; Kim, HN; Li, W; Liu, X; Lv, D; Ortiz, YT; Song, L; Thummuri, D; Wang, Y; Wiegand, JS; Yuan, Y; Zhang, P; Zhang, X; Zheng, G; Zhou, D, 2020
)
0.8

Pharmacokinetics

Navitoclax showed a pharmacodynamic effect on circulating platelets and T cells. Rifampin did not affect the half-life of navitClax.

ExcerptReferenceRelevance
" We aimed to assess the safety and antitumour activity of navitoclax in patients with lymphoid tumours, and establish the drug's pharmacokinetic and pharmacodynamic profiles."( Navitoclax, a targeted high-affinity inhibitor of BCL-2, in lymphoid malignancies: a phase 1 dose-escalation study of safety, pharmacokinetics, pharmacodynamics, and antitumour activity.
Busman, T; Chiu, YL; Cui, Y; Czuczman, MS; Dunleavy, K; Elmore, SW; Enschede, SH; Gerecitano, JF; Humerickhouse, RA; Krivoshik, AP; LaCasce, AS; Leonard, JP; O'Connor, OA; Rosenberg, SH; Tulpule, A; Wilson, WH; Xiong, H, 2010
)
2.05
" Study endpoints were safety, maximum tolerated dose, pharmacokinetic profile, pharmacodynamic effects on platelets and T cells, and antitumour activity."( Navitoclax, a targeted high-affinity inhibitor of BCL-2, in lymphoid malignancies: a phase 1 dose-escalation study of safety, pharmacokinetics, pharmacodynamics, and antitumour activity.
Busman, T; Chiu, YL; Cui, Y; Czuczman, MS; Dunleavy, K; Elmore, SW; Enschede, SH; Gerecitano, JF; Humerickhouse, RA; Krivoshik, AP; LaCasce, AS; Leonard, JP; O'Connor, OA; Rosenberg, SH; Tulpule, A; Wilson, WH; Xiong, H, 2010
)
1.8
" Navitoclax showed a pharmacodynamic effect on circulating platelets and T cells."( Navitoclax, a targeted high-affinity inhibitor of BCL-2, in lymphoid malignancies: a phase 1 dose-escalation study of safety, pharmacokinetics, pharmacodynamics, and antitumour activity.
Busman, T; Chiu, YL; Cui, Y; Czuczman, MS; Dunleavy, K; Elmore, SW; Enschede, SH; Gerecitano, JF; Humerickhouse, RA; Krivoshik, AP; LaCasce, AS; Leonard, JP; O'Connor, OA; Rosenberg, SH; Tulpule, A; Wilson, WH; Xiong, H, 2010
)
2.71
"Ten patients had evaluable pharmacokinetic data and were, therefore, included in pharmacokinetic statistical analyses."( Effect of co-administration of ketoconazole, a strong CYP3A inhibitor, on the pharmacokinetics, safety and tolerability of navitoclax, a first-in-class oral Bcl-2 family inhibitor, in cancer patients.
Graham, A; Holen, K; Patnaik, A; Pradhan, R; Salem, AH; Xiong, H; Yang, J, 2014
)
0.61
" Primary endpoints assessed the safety and pharmacokinetic (PK) interactions between navitoclax in combination with carboplatin/paclitaxel or paclitaxel alone in patients with solid tumors The study comprised two arms, one a combination of navitoclax with paclitaxel and carboplatin, the second with navitoclax and paclitaxel alone."( A phase I safety and pharmacokinetic study of ABT-263 in combination with carboplatin/paclitaxel in the treatment of patients with solid tumors.
Busman, T; Cosgrove, D; Karantza, V; Mabry, M; Rudersdorf, N; Vlahovic, G; Wang, D; Xiong, H; Yang, J, 2014
)
0.63
" This study evaluated the effects of co-administration of a potent CYP3A4 inducer rifampin on the pharmacokinetic and safety profiles of navitoclax."( Effect of rifampin on the pharmacokinetics, safety and tolerability of navitoclax (ABT-263), a dual inhibitor of Bcl-2 and Bcl-XL , in patients with cancer.
Graham, AM; Holen, KD; Pradhan, RS; Rosen, LS; Xiong, H; Yang, J, 2014
)
0.84
" Rifampin did not affect the half-life of navitoclax."( Effect of rifampin on the pharmacokinetics, safety and tolerability of navitoclax (ABT-263), a dual inhibitor of Bcl-2 and Bcl-XL , in patients with cancer.
Graham, AM; Holen, KD; Pradhan, RS; Rosen, LS; Xiong, H; Yang, J, 2014
)
0.9
" A population pharmacokinetic/pharmacodynamic (PK/PD) model was developed to describe the pharmacokinetic of navitoclax as well as the time course of the platelet counts in cancer patients receiving navitoclax."( Mechanism-based pharmacokinetic/pharmacodynamic meta-analysis of navitoclax (ABT-263) induced thrombocytopenia.
Awni, W; Humerickhouse, R; Kaefer, A; Mensing, S; Noertersheuser, P; Xiong, H; Yang, J, 2014
)
0.85
" Pharmacokinetic analyses revealed no apparent interactions between the drugs."( Phase 1 study of the safety, pharmacokinetics, and antitumour activity of the BCL2 inhibitor navitoclax in combination with rituximab in patients with relapsed or refractory CD20+ lymphoid malignancies.
Advani, RH; Busman, TB; Carney, DA; Enschede, SH; Humerickhouse, RA; Kahl, BS; Persky, D; Roberts, AW; Seymour, JF; Sweetenham, JW; Yang, J, 2015
)
0.64
" Pharmacokinetic analysis showed no apparent interactions between co-administered navitoclax and erlotinib."( Safety, efficacy, and pharmacokinetics of navitoclax (ABT-263) in combination with erlotinib in patients with advanced solid tumors.
Arzt, J; Busman, TA; Holen, KD; Kirschbrown, W; Lian, G; LoRusso, P; Rosen, LS; Rudersdorf, NS; Tolcher, AW; Vanderwal, CA, 2015
)
0.91
" There were no apparent pharmacokinetic interactions between erlotinib and navitoclax."( Safety, efficacy, and pharmacokinetics of navitoclax (ABT-263) in combination with erlotinib in patients with advanced solid tumors.
Arzt, J; Busman, TA; Holen, KD; Kirschbrown, W; Lian, G; LoRusso, P; Rosen, LS; Rudersdorf, NS; Tolcher, AW; Vanderwal, CA, 2015
)
0.91

Compound-Compound Interactions

An open-label dose escalation study included an arm evaluating navitoclax combined with erlotinib, which included a dose escalation cohort and a planned safety expansion cohort. Primary endpoints assessed the safety and pharmacokinetic (PK) interactions between navitClax in combination with carboplatin/paclitaxel or paclitaxe alone.

ExcerptReferenceRelevance
" Taken together, these data suggest the efficacy of agents that target the MAPK and PI3K pathways can be improved by combination with a Bcl-2 family inhibitor."( Bcl-2/Bcl-xL inhibition increases the efficacy of MEK inhibition alone and in combination with PI3 kinase inhibition in lung and pancreatic tumor models.
Belmont, LD; Fairbrother, WJ; Hong, R; Lee, LB; Nannini, MA; Price, S; Sampath, D; Savy, PP; Settleman, J; Tan, N; Williams, K; Wong, M; Yue, P, 2013
)
0.39
" Primary endpoints assessed the safety and pharmacokinetic (PK) interactions between navitoclax in combination with carboplatin/paclitaxel or paclitaxel alone in patients with solid tumors The study comprised two arms, one a combination of navitoclax with paclitaxel and carboplatin, the second with navitoclax and paclitaxel alone."( A phase I safety and pharmacokinetic study of ABT-263 in combination with carboplatin/paclitaxel in the treatment of patients with solid tumors.
Busman, T; Cosgrove, D; Karantza, V; Mabry, M; Rudersdorf, N; Vlahovic, G; Wang, D; Xiong, H; Yang, J, 2014
)
0.63
"To investigate the safety, optimal dosing, pharmacokinetics and clinical activity of a regimen of navitoclax (ABT-263) combined with gemcitabine in patients with solid tumors."( A phase I clinical trial of navitoclax, a targeted high-affinity Bcl-2 family inhibitor, in combination with gemcitabine in patients with solid tumors.
Busman, T; Cleary, JM; Franklin, C; Graham, A; Holen, K; Hurwitz, HI; Lima, CM; Mabry, M; Montero, AJ; Shapiro, GI; Uronis, H; Yang, J, 2014
)
0.91
" No clinically significant pharmacokinetic drug-drug interactions were observed."( A phase I clinical trial of navitoclax, a targeted high-affinity Bcl-2 family inhibitor, in combination with gemcitabine in patients with solid tumors.
Busman, T; Cleary, JM; Franklin, C; Graham, A; Holen, K; Hurwitz, HI; Lima, CM; Mabry, M; Montero, AJ; Shapiro, GI; Uronis, H; Yang, J, 2014
)
0.7
" This phase I study (NCT01009073) evaluated the safety, pharmacokinetics, and preliminary antitumor activity of navitoclax combined with erlotinib in patients with advanced solid tumors."( Safety, efficacy, and pharmacokinetics of navitoclax (ABT-263) in combination with erlotinib in patients with advanced solid tumors.
Arzt, J; Busman, TA; Holen, KD; Kirschbrown, W; Lian, G; LoRusso, P; Rosen, LS; Rudersdorf, NS; Tolcher, AW; Vanderwal, CA, 2015
)
0.89
"An open-label dose escalation study included an arm evaluating navitoclax combined with erlotinib, which included a dose escalation cohort and a planned safety expansion cohort."( Safety, efficacy, and pharmacokinetics of navitoclax (ABT-263) in combination with erlotinib in patients with advanced solid tumors.
Arzt, J; Busman, TA; Holen, KD; Kirschbrown, W; Lian, G; LoRusso, P; Rosen, LS; Rudersdorf, NS; Tolcher, AW; Vanderwal, CA, 2015
)
0.92
"The oral Bcl-2 inhibitor navitoclax demonstrated activity in solid and hematologic malignancies as monotherapy and in combination with other cytotoxic agents in preclinical and early clinical studies."( Safety, efficacy, and pharmacokinetics of navitoclax (ABT-263) in combination with irinotecan: results of an open-label, phase 1 study.
Arzt, J; Busman, TA; Holen, KD; Lian, G; LoRusso, P; Rosen, LS; Rudersdorf, NS; Tolcher, AW; Vanderwal, CA; Waring, JF; Yang, J, 2015
)
0.98
"In this multicenter, open-label, phase 1 dose escalation study, adults with advanced solid tumors received navitoclax (starting dose 150 mg/day) in combination with 1 of 2 irinotecan schedules during a 21-day cycle: a once-every-3-week regimen (Q3W 180, 250, or 350 mg/m(2)) or a once-weekly regimen (QW 75 or 100 mg/m(2))."( Safety, efficacy, and pharmacokinetics of navitoclax (ABT-263) in combination with irinotecan: results of an open-label, phase 1 study.
Arzt, J; Busman, TA; Holen, KD; Lian, G; LoRusso, P; Rosen, LS; Rudersdorf, NS; Tolcher, AW; Vanderwal, CA; Waring, JF; Yang, J, 2015
)
0.89
" In the QW group, the MTD and RPTD for navitoclax were 150 mg when combined with irinotecan 75 mg/m(2)."( Safety, efficacy, and pharmacokinetics of navitoclax (ABT-263) in combination with irinotecan: results of an open-label, phase 1 study.
Arzt, J; Busman, TA; Holen, KD; Lian, G; LoRusso, P; Rosen, LS; Rudersdorf, NS; Tolcher, AW; Vanderwal, CA; Waring, JF; Yang, J, 2015
)
0.95
"The RPTD of navitoclax in combination with irinotecan 75 mg/m(2) QW during a 21-day cycle was 150 mg in these heavily pretreated patients."( Safety, efficacy, and pharmacokinetics of navitoclax (ABT-263) in combination with irinotecan: results of an open-label, phase 1 study.
Arzt, J; Busman, TA; Holen, KD; Lian, G; LoRusso, P; Rosen, LS; Rudersdorf, NS; Tolcher, AW; Vanderwal, CA; Waring, JF; Yang, J, 2015
)
1.06
" To obtain curative therapy, other effective agents, based on HL biology, would have to be given in combination with BV."( Augmented efficacy of brentuximab vedotin combined with ruxolitinib and/or Navitoclax in a murine model of human Hodgkin's lymphoma.
Bamford, RN; Ferrer, M; Guha, R; Ju, W; Petrus, MN; Thomas, CJ; Waldmann, TA; Wilson, KM; Zhang, M; Zhang, X, 2016
)
0.66
" This supports expanded use of CIVO as an in vivo platform for expedited in vivo drug combination validation and sets the stage for performing toxicity-sparing drug combination studies directly in cancer patients with solid malignancies."( A Platform for Rapid, Quantitative Assessment of Multiple Drug Combinations Simultaneously in Solid Tumors In Vivo.
Carleton, M; Casalini, JR; Dey, J; Ditzler, SH; Frazier, JP; Grenley, MO; Kerwin, WS; Klinghoffer, RA; Pierce, DW; Thirstrup, DJ; Tretyak, I, 2016
)
0.43
"To study the effect of apoptotic drug Navitoclax (NTX) combined with chemotherapy drug Daunorubicin (DNR) on apoptosis of erythroleukemia cells."( [Navitoclax Combined with Daunorubicin Promotes Apoptosis of Erythroleukemia Cell Lines K562, HEL and TF-1].
Chen, XY; Duan, YJ; Liu, C; Wu, WQ; Zhang, YC; Zheng, JR; Zhu, XF, 2020
)
1.74
"NTX combined with DNR could significantly inhibit the growth of K562, HEL and TF-1 cells; Apoptosis detection results showed that the apoptotic rate of K562, HEL and TF-1 cells in combination group was significantly higher than that in NTX and DNR single group; the expression level of apoptosis-related genes BAK and BAX in K562 cells in combination group was significantly higher than that in two single drug groups, and the expression level of anti-apoptotic protein genes BCL-2 and BCL-xl was significantly lower than that in two single drug groups (P<0."( [Navitoclax Combined with Daunorubicin Promotes Apoptosis of Erythroleukemia Cell Lines K562, HEL and TF-1].
Chen, XY; Duan, YJ; Liu, C; Wu, WQ; Zhang, YC; Zheng, JR; Zhu, XF, 2020
)
1.47
"NTX combined with DNR can significantly promote the apoptosis of erythroleukemia cell lines K562, HEL and TF-1, and induce the expression of apoptosis-related genes."( [Navitoclax Combined with Daunorubicin Promotes Apoptosis of Erythroleukemia Cell Lines K562, HEL and TF-1].
Chen, XY; Duan, YJ; Liu, C; Wu, WQ; Zhang, YC; Zheng, JR; Zhu, XF, 2020
)
1.47

Bioavailability

Abbott's ABT-737 and an orally bioavailable compound of the same class, navitoclax (ABT-263), have shown promising antitumor efficacy in preclinical and early clinical studies. While these properties are associated with low oral bioavailability (F), both navitClax and ABt-199 showed moderate F in prescientific species. Here we report the re-engineering of navitclax to create a highly potent, orally bio available and BCL-2-selective inhibitor, ABT -199.

ExcerptReferenceRelevance
" Here we report the biological properties of ABT-263, a potent, orally bioavailable Bad-like BH3 mimetic (K(i)'s of <1 nmol/L for Bcl-2, Bcl-xL, and Bcl-w)."( ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor.
Adickes, J; Anderson, MG; Chen, J; Elmore, SW; Fesik, S; Jin, S; Johnson, EF; Marsh, KC; Mitten, MJ; Nimmer, P; Roberts, L; Rosenberg, SH; Shoemaker, AR; Tahir, SK; Tse, C; Xiao, Y; Yang, X; Zhang, H, 2008
)
0.35
"ABT-263 is a potent, orally bioavailable inhibitor of Bcl-2 family proteins that has recently entered clinical trials."( Activity of the Bcl-2 family inhibitor ABT-263 in a panel of small cell lung cancer xenograft models.
Ackler, S; Adickes, J; Bauch, J; Elmore, SW; Ferguson, D; Fesik, SW; Frost, DJ; Marsh, K; Mitten, MJ; O'Connor, JM; Oleksijew, A; Refici, M; Rosenberg, SH; Shoemaker, AR; Tahir, SK; Tse, C; Wang, B; Yang, X, 2008
)
0.35
"ABT-263 is a potent, orally bioavailable inhibitor of the antiapoptotic Bcl-2 family members Bcl-2, Bcl-x(L), and Bcl-w, which is currently in phase I clinical trials."( ABT-263 and rapamycin act cooperatively to kill lymphoma cells in vitro and in vivo.
Ackler, S; Bauch, J; Chemburkar, SR; Elmore, SW; Fesik, SW; Foster, K; Frost, DJ; Mitten, MJ; Oleksijew, A; Refici, M; Rosenberg, SH; Schlessinger, S; Shoemaker, AR; Tse, C; Wang, B; Xiao, Y, 2008
)
0.35
" However, ABT-737, a specific BCL2 inhibitor, is neither orally bioavailable nor metabolically stable."( Diminished sensitivity of chronic lymphocytic leukemia cells to ABT-737 and ABT-263 due to albumin binding in blood.
Cohen, GM; Dyer, MJ; Furdas, SD; Jung, M; Kuwana, T; Vogler, M, 2010
)
0.36
" Modification of ABT-263 may yield a BCL2 inhibitor with greater bioavailability and more favorable pharmacokinetics."( Diminished sensitivity of chronic lymphocytic leukemia cells to ABT-737 and ABT-263 due to albumin binding in blood.
Cohen, GM; Dyer, MJ; Furdas, SD; Jung, M; Kuwana, T; Vogler, M, 2010
)
0.36
" This "addiction" can be exploited therapeutically by combining aurora kinase inhibitors and the orally bioavailable BH3 mimetic, ABT-263, which inhibits Bcl-XL, Bcl-2, and Bcl-w."( Bcl-XL represents a druggable molecular vulnerability during aurora B inhibitor-mediated polyploidization.
Anderson, MG; Chen, J; Donawho, CK; Fesik, SW; Glaser, KB; Huang, X; Li, J; Li, L; Lin, X; McLoughlin, S; Palma, J; Rodriguez, LE; Shah, OJ; Shen, Y; Tang, H; Warder, SE, 2010
)
0.36
"In this study, we demonstrate that ABT-263, a potent and orally bioavailable inhibitor of the Bcl-2 family, was able to reverse the resistance of hepatocarcinoma cell lines to TRAIL-induced apoptosis, while sparing normal liver cells."( ABT-263 sensitizes TRAIL-resistant hepatocarcinoma cells by downregulating the Bcl-2 family of anti-apoptotic protein.
Li, W; Wang, G; Wang, H; Zhan, Y, 2012
)
0.38
"The BH3-mimetic ABT-737 and an orally bioavailable compound of the same class, navitoclax (ABT-263), have shown promising antitumor efficacy in preclinical and early clinical studies."( Bcl-2, Bcl-x(L), and Bcl-w are not equivalent targets of ABT-737 and navitoclax (ABT-263) in lymphoid and leukemic cells.
Anderson, DJ; Belmont, LD; Bouillet, P; Campbell, KJ; Cory, S; Fairlie, WD; Glaser, SP; Huang, DC; Khaw, SL; Lee, EF; Ludlam, MJ; Mérino, D; Phipson, B; Robati, M; Roberts, AW; Vandenberg, CJ; Wong, C; Yue, P, 2012
)
0.84
" Here we report the re-engineering of navitoclax to create a highly potent, orally bioavailable and BCL-2-selective inhibitor, ABT-199."( ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets.
Ackler, SL; Boghaert, ER; Catron, ND; Chen, J; Dayton, BD; Ding, H; Elmore, SW; Enschede, SH; Fairbrother, WJ; Huang, DC; Humerickhouse, RA; Hymowitz, SG; Jin, S; Khaw, SL; Kovar, PJ; Lam, LT; Lee, J; Leverson, JD; Maecker, HL; Marsh, KC; Mason, KD; Mitten, MJ; Nimmer, PM; Oleksijew, A; Park, CH; Park, CM; Phillips, DC; Roberts, AW; Rosenberg, SH; Sampath, D; Seymour, JF; Smith, ML; Souers, AJ; Sullivan, GM; Tahir, SK; Tse, C; Wendt, MD; Xiao, Y; Xue, JC; Zhang, H, 2013
)
0.66
" While these properties are associated with low oral bioavailability (F), both navitoclax and ABT-199 showed moderate F in preclinical species."( The role of lymphatic transport on the systemic bioavailability of the Bcl-2 protein family inhibitors navitoclax (ABT-263) and ABT-199.
Boggs, J; Catron, ND; Choo, EF; Jenkins, G; Lubach, JW; Souers, AJ; Voorman, R; Zhu, C, 2014
)
0.84
"Cell membrane permeability is an important determinant for oral absorption and bioavailability of a drug molecule."( Highly predictive and interpretable models for PAMPA permeability.
Jadhav, A; Kerns, E; Nguyen, K; Shah, P; Sun, H; Xu, X; Yan, Z; Yu, KR, 2017
)
0.46
" Retrospective analysis of past successes and failures in drug discovery bRo5 may shed light on the key principles that contribute to the oral bioavailability of successful bRo5 compounds and improve the efficiency of drug design for future projects."( Beyond the Rule of 5: Lessons Learned from AbbVie's Drugs and Compound Collection.
Chen, HJ; Cox, PB; DeGoey, DA; Wendt, MD, 2018
)
0.48
"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
" Both survival mechanisms can be overcome by the combination of an orally bioavailable BAX activator, BTSA1."( Co-targeting of BAX and BCL-XL proteins broadly overcomes resistance to apoptosis in cancer.
Chi, P; Gavathiotis, E; Gitego, N; Kopp, F; Lopez, A; Miranda-Roman, MA; Narayanagari, SR; Nordstrøm, LU; Reyna, DE; Tsirigos, A; Vilar, E; Zhou, H, 2022
)
0.72
" Steven Elmore from Abbott Laboratories, reported the discovery of the first orally bioavailable BCL2/BCL-xL inhibitor, navitoclax (ABT-263), marking the onset of an era of "BH3 mimetics" in cancer therapeutics and changing the therapeutic landscape especially for leukemia."( BCL-xL Targeting to Induce Apoptosis and to Eliminate Chemotherapy-Induced Senescent Tumor Cells: From Navitoclax to Platelet-Sparing BCL-xL PROTACs.
Konopleva, M; Skwarska, A, 2023
)
1.33

Dosage Studied

navitoclax can extend the lifespan of premature-aged Drosophila and mitigate the aging-related phenotype. We determined that the nav itoclax dose of 250 mg/d in a continuous dosing schedule was optimal for phase II studies.

ExcerptRelevanceReference
" The oral efficacy of ABT-263 should provide dosing flexibility to maximize clinical utility both as a single agent and in combination regimens."( ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor.
Adickes, J; Anderson, MG; Chen, J; Elmore, SW; Fesik, S; Jin, S; Johnson, EF; Marsh, KC; Mitten, MJ; Nimmer, P; Roberts, L; Rosenberg, SH; Shoemaker, AR; Tahir, SK; Tse, C; Xiao, Y; Yang, X; Zhang, H, 2008
)
0.35
" Single agent activity was examined on a continuous dosing schedule in each of these models."( Activity of the Bcl-2 family inhibitor ABT-263 in a panel of small cell lung cancer xenograft models.
Ackler, S; Adickes, J; Bauch, J; Elmore, SW; Ferguson, D; Fesik, SW; Frost, DJ; Marsh, K; Mitten, MJ; O'Connor, JM; Oleksijew, A; Refici, M; Rosenberg, SH; Shoemaker, AR; Tahir, SK; Tse, C; Wang, B; Yang, X, 2008
)
0.35
" A modified Fibonacci 3+3 design was used to assign patients to receive oral navitoclax once daily by one of two dosing schedules: intermittently for the first 14 days of a 21-day cycle (14/21) at doses of 10, 20, 40, 80, 110, 160, 225, 315, or 440 mg/day; or continuously for 21 days of a 21-day cycle (21/21) at doses of 200, 275, 325, or 425 mg/day."( Navitoclax, a targeted high-affinity inhibitor of BCL-2, in lymphoid malignancies: a phase 1 dose-escalation study of safety, pharmacokinetics, pharmacodynamics, and antitumour activity.
Busman, T; Chiu, YL; Cui, Y; Czuczman, MS; Dunleavy, K; Elmore, SW; Enschede, SH; Gerecitano, JF; Humerickhouse, RA; Krivoshik, AP; LaCasce, AS; Leonard, JP; O'Connor, OA; Rosenberg, SH; Tulpule, A; Wilson, WH; Xiong, H, 2010
)
2.03
"55 patients were enrolled (median age 59 years, IQR 51-67), 38 to receive the 14/21 dosing schedule, and 17 to receive the 21/21 dosing schedule."( Navitoclax, a targeted high-affinity inhibitor of BCL-2, in lymphoid malignancies: a phase 1 dose-escalation study of safety, pharmacokinetics, pharmacodynamics, and antitumour activity.
Busman, T; Chiu, YL; Cui, Y; Czuczman, MS; Dunleavy, K; Elmore, SW; Enschede, SH; Gerecitano, JF; Humerickhouse, RA; Krivoshik, AP; LaCasce, AS; Leonard, JP; O'Connor, OA; Rosenberg, SH; Tulpule, A; Wilson, WH; Xiong, H, 2010
)
1.8
" On the basis of these findings, a 150 mg 7-day lead-in dose followed by a 325 mg dose administered on a continuous 21/21 dosing schedule was selected for phase 2 study."( Navitoclax, a targeted high-affinity inhibitor of BCL-2, in lymphoid malignancies: a phase 1 dose-escalation study of safety, pharmacokinetics, pharmacodynamics, and antitumour activity.
Busman, T; Chiu, YL; Cui, Y; Czuczman, MS; Dunleavy, K; Elmore, SW; Enschede, SH; Gerecitano, JF; Humerickhouse, RA; Krivoshik, AP; LaCasce, AS; Leonard, JP; O'Connor, OA; Rosenberg, SH; Tulpule, A; Wilson, WH; Xiong, H, 2010
)
1.8
"Patients enrolled to intermittent dosing cohorts received navitoclax on day -3, followed by dosing on days 1 to 14 of a 21-day cycle."( Phase I study of Navitoclax (ABT-263), a novel Bcl-2 family inhibitor, in patients with small-cell lung cancer and other solid tumors.
Bonomi, P; Busman, T; Camidge, DR; Chiu, YL; Dive, C; Enschede, SH; Gandara, D; Gandhi, L; Hann, CL; Hemken, PM; Humerickhouse, R; Khaira, D; Krivoshik, AP; Litvinovich, E; McKeegan, EM; Nolan, C; Ribeiro de Oliveira, M; Rudin, CM; Shapiro, GI; Xiong, H, 2011
)
0.95
"Forty-seven patients, including 29 with small-cell lung cancer (SCLC) or pulmonary carcinoid, were enrolled between 2007 and 2008, 35 on intermittent and 12 on continuous dosing cohorts."( Phase I study of Navitoclax (ABT-263), a novel Bcl-2 family inhibitor, in patients with small-cell lung cancer and other solid tumors.
Bonomi, P; Busman, T; Camidge, DR; Chiu, YL; Dive, C; Enschede, SH; Gandara, D; Gandhi, L; Hann, CL; Hemken, PM; Humerickhouse, R; Khaira, D; Krivoshik, AP; Litvinovich, E; McKeegan, EM; Nolan, C; Ribeiro de Oliveira, M; Rudin, CM; Shapiro, GI; Xiong, H, 2011
)
0.71
" We determined that the navitoclax dose of 250 mg/d in a continuous dosing schedule was optimal for phase II studies."( Substantial susceptibility of chronic lymphocytic leukemia to BCL2 inhibition: results of a phase I study of navitoclax in patients with relapsed or refractory disease.
Brown, JR; Busman, TA; Carney, DA; Cui, Y; Enschede, SH; He, SZ; Huang, DC; Humerickhouse, R; Khaw, SL; Kipps, TJ; Krivoshik, AP; McKeegan, EM; Roberts, AW; Seymour, JF; Wierda, WG; Xiong, H, 2012
)
0.9
" In platelets from mice dosed with ABT-263 in vivo, clopidogrel or deficiency of P2Y(12) receptor enhanced apoptosis along with increased Bak/Bax activation."( P2Y12 protects platelets from apoptosis via PI3k-dependent Bak/Bax inactivation.
Ding, Z; Kunapuli, SP; Liu, J; Xu, X; Ye, J; Zhang, S; Zhang, SH; Zhang, Y, 2013
)
0.39
"Patients with solid tumors for which gemcitabine was deemed an appropriate therapy were enrolled into one of two different dosing schedules (21-day dosing schedule: navitoclax administered orally on days 1-3 and 8-10,; and gemcitabine 1,000 mg/m(2) on days 1 and 8; 28-day dosing schedule: navitoclax administrated orally on days 1-3, 8-10, and 15-17; and gemcitabine 1,000 mg/m(2) on days 1, 8 and 15)."( A phase I clinical trial of navitoclax, a targeted high-affinity Bcl-2 family inhibitor, in combination with gemcitabine in patients with solid tumors.
Busman, T; Cleary, JM; Franklin, C; Graham, A; Holen, K; Hurwitz, HI; Lima, CM; Mabry, M; Montero, AJ; Shapiro, GI; Uronis, H; Yang, J, 2014
)
0.89
" We used these screening methods to evaluate the dependencies of seven patient-derived cell models: three grown on laminin and four grown as neurospheres, against 56 agents in 17-point dose-response curves in 384-well format in triplicate."( High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
deCarvalho, AC; Mikkelsen, T; Quartararo, CE; Reznik, E; Stockwell, BR, 2015
)
0.42
" Navitoclax dosing remained at 150 mg/day because the maximum tolerated dose was exceeded at this starting dose."( Safety, efficacy, and pharmacokinetics of navitoclax (ABT-263) in combination with erlotinib in patients with advanced solid tumors.
Arzt, J; Busman, TA; Holen, KD; Kirschbrown, W; Lian, G; LoRusso, P; Rosen, LS; Rudersdorf, NS; Tolcher, AW; Vanderwal, CA, 2015
)
1.59
" Dose-response measurements were used to generate multiparameter drug sensitivity scores using R-statistical language."( Comprehensive Drug Testing of Patient-derived Conditionally Reprogrammed Cells from Castration-resistant Prostate Cancer.
Af Hällström, TM; Aittokallio, T; Bychkov, D; Eldfors, S; Heckman, C; Horvath, P; Kallioniemi, O; Mirtti, T; Mpindi, JP; Östling, P; Paavolainen, L; Peehl, DM; Rahkama, V; Rannikko, A; Saeed, K; Wennerberg, K; Yadav, B, 2017
)
0.46
" Importantly, results obtained with CIVO accurately predicted the outcome of systemic dosing studies in the same model where superior tumor regression induced by the Abraxane/ABT-263 combination was observed compared to that induced by either single agent."( A Platform for Rapid, Quantitative Assessment of Multiple Drug Combinations Simultaneously in Solid Tumors In Vivo.
Carleton, M; Casalini, JR; Dey, J; Ditzler, SH; Frazier, JP; Grenley, MO; Kerwin, WS; Klinghoffer, RA; Pierce, DW; Thirstrup, DJ; Tretyak, I, 2016
)
0.43
" Extending our in vitro findings, we found that ABT-263 reduced the growth of HSC-4 cells in vivo at a dosage of 100 mg/kg/day without any change in body weight."( ABT-263 exhibits apoptosis-inducing potential in oral cancer cells by targeting C/EBP-homologous protein.
Cho, NP; Cho, SD; Hong, SD; Jung, JY; Kim, SH; Lee, H; Lee, JY; Shin, JA; Yang, IH; Yoo, ES, 2019
)
0.51
" Our results reveal that pan-mTOR inhibitors can reduce the dosage or timespan of navitoclax necessary for reaching IC50 and LT50 in senescent cells, also extend the lifespan of premature-aged Drosophila and mitigate the aging-related phenotype."( Pan-mTOR inhibitors sensitize the senolytic activity of navitoclax via mTORC2 inhibition-mediated apoptotic signaling.
Chen, H; Gong, C; Gong, H; Huang, N; Li, T; Xiao, H; Xu, W; Yang, M; Yang, Y; Zhang, G; Zhang, J; Zhao, T, 2022
)
1.19
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (3)

RoleDescription
B-cell lymphoma 2 inhibitorAny inhibitor of B-cell lymphoma 2 protein.
apoptosis inducerAny substance that induces the process of apoptosis (programmed cell death) in multi-celled organisms.
antineoplastic agentA substance that inhibits or prevents the proliferation of neoplasms.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (9)

ClassDescription
piperazines
monochlorobenzenesAny member of the class of chlorobenzenes containing a mono- or poly-substituted benzene ring in which only one substituent is chlorine.
morpholinesAny compound containing morpholine as part of its structure.
aryl sulfideAny organic sulfide in which the sulfur is attached to at least one aromatic group.
N-sulfonylcarboxamideA mixed diacylamine resulting from the formal condensation of the nitrogen of a carboxamide with a sulphonic acid.
sulfoneAn organosulfur compound having the structure RS(=O)2R (R =/= H).
organofluorine compoundAn organofluorine compound is a compound containing at least one carbon-fluorine bond.
secondary amino compoundA compound formally derived from ammonia by replacing two hydrogen atoms by organyl groups.
tertiary amino compoundA compound formally derived from ammonia by replacing three hydrogen atoms by organyl groups.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (18)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
TDP1 proteinHomo sapiens (human)Potency0.38140.000811.382244.6684AID686978; AID686979
Smad3Homo sapiens (human)Potency3.16230.00527.809829.0929AID588855
EWS/FLI fusion proteinHomo sapiens (human)Potency19.95720.001310.157742.8575AID1259252; AID1259253; AID1259255; AID1259256
67.9K proteinVaccinia virusPotency10.61010.00018.4406100.0000AID720579; AID720580
heat shock 70kDa protein 5 (glucose-regulated protein, 78kDa)Homo sapiens (human)Potency22.38720.016525.307841.3999AID602332
flap endonuclease 1Homo sapiens (human)Potency89.12510.133725.412989.1251AID588795
tyrosine-protein kinase YesHomo sapiens (human)Potency30.74750.00005.018279.2586AID686947
DNA polymerase eta isoform 1Homo sapiens (human)Potency95.28340.100028.9256213.3130AID720502
DNA polymerase iota isoform a (long)Homo sapiens (human)Potency53.41320.050127.073689.1251AID588590; AID720496
DNA polymerase kappa isoform 1Homo sapiens (human)Potency35.67400.031622.3146100.0000AID588579; AID720501
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Bcl-2-like protein 11Homo sapiens (human)IC50 (µMol)0.00430.00204.45168.9000AID1189618
Apoptosis regulator Bcl-2Homo sapiens (human)IC50 (µMol)0.00910.00100.57634.3000AID1178967; AID1368926; AID1610200
Apoptosis regulator Bcl-2Homo sapiens (human)Ki0.00050.00000.19012.9000AID1293717; AID1352865; AID1388438; AID1525538; AID1545359; AID1599465; AID1674225; AID1710464; AID389261
Bcl-2-like protein 1Homo sapiens (human)IC50 (µMol)0.01680.00031.04829.5400AID1073482; AID1178968; AID1189618; AID1368927; AID1610199
Bcl-2-like protein 1Homo sapiens (human)Ki0.01100.00000.45819.0000AID1293718; AID1352866; AID1388439; AID1545358; AID1599466; AID1710463; AID462446; AID526645
Induced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)IC50 (µMol)20.00000.00442.923510.0000AID1073483; AID1610202
Induced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)Ki0.25830.00101.46539.5400AID1352867; AID1599467; AID1710465
Aspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)IC50 (µMol)1.09250.02002.66099.4300AID1677972; AID1677973; AID1677974; AID1677975
Bcl-2-like protein 2Homo sapiens (human)IC50 (µMol)0.07000.00100.32512.3300AID1610201
Bcl-2-like protein 2Homo sapiens (human)Ki0.24500.00101.25908.1900AID1545360
Bcl2-associated agonist of cell death Homo sapiens (human)Ki0.00080.00050.15890.4900AID389260; AID405509
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Apoptosis regulator Bcl-2Homo sapiens (human)Kd0.60810.00060.95874.8000AID1700823; AID1700824; AID1830310
Bcl-2-like protein 1Homo sapiens (human)Kd0.00210.00010.90252.8000AID1830309
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Other Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, BCL-2-RELATED PROTEIN A1Homo sapiens (human)AbsAC10_uM3.09001.106010.951833.6220AID504346
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (222)

Processvia Protein(s)Taxonomy
intrinsic apoptotic signaling pathway in response to DNA damageBcl-2-like protein 11Homo sapiens (human)
in utero embryonic developmentBcl-2-like protein 11Homo sapiens (human)
B cell homeostasisBcl-2-like protein 11Homo sapiens (human)
kidney developmentBcl-2-like protein 11Homo sapiens (human)
myeloid cell homeostasisBcl-2-like protein 11Homo sapiens (human)
apoptotic processBcl-2-like protein 11Homo sapiens (human)
cell-matrix adhesionBcl-2-like protein 11Homo sapiens (human)
spermatogenesisBcl-2-like protein 11Homo sapiens (human)
male gonad developmentBcl-2-like protein 11Homo sapiens (human)
post-embryonic developmentBcl-2-like protein 11Homo sapiens (human)
mammary gland developmentBcl-2-like protein 11Homo sapiens (human)
positive regulation of protein-containing complex assemblyBcl-2-like protein 11Homo sapiens (human)
response to endoplasmic reticulum stressBcl-2-like protein 11Homo sapiens (human)
tube formationBcl-2-like protein 11Homo sapiens (human)
odontogenesis of dentin-containing toothBcl-2-like protein 11Homo sapiens (human)
regulation of apoptotic processBcl-2-like protein 11Homo sapiens (human)
T cell homeostasisBcl-2-like protein 11Homo sapiens (human)
positive regulation of apoptotic processBcl-2-like protein 11Homo sapiens (human)
positive regulation of neuron apoptotic processBcl-2-like protein 11Homo sapiens (human)
ear developmentBcl-2-like protein 11Homo sapiens (human)
positive regulation of cell cycleBcl-2-like protein 11Homo sapiens (human)
regulation of organ growthBcl-2-like protein 11Homo sapiens (human)
developmental pigmentationBcl-2-like protein 11Homo sapiens (human)
regulation of developmental pigmentationBcl-2-like protein 11Homo sapiens (human)
spleen developmentBcl-2-like protein 11Homo sapiens (human)
thymus developmentBcl-2-like protein 11Homo sapiens (human)
positive regulation of T cell apoptotic processBcl-2-like protein 11Homo sapiens (human)
thymocyte apoptotic processBcl-2-like protein 11Homo sapiens (human)
cellular response to glucocorticoid stimulusBcl-2-like protein 11Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondriaBcl-2-like protein 11Homo sapiens (human)
extrinsic apoptotic signaling pathway in absence of ligandBcl-2-like protein 11Homo sapiens (human)
positive regulation of mitochondrial membrane permeability involved in apoptotic processBcl-2-like protein 11Homo sapiens (human)
positive regulation of endoplasmic reticulum stress-induced intrinsic apoptotic signaling pathwayBcl-2-like protein 11Homo sapiens (human)
apoptotic process involved in embryonic digit morphogenesisBcl-2-like protein 11Homo sapiens (human)
positive regulation of IRE1-mediated unfolded protein responseBcl-2-like protein 11Homo sapiens (human)
positive regulation of fibroblast apoptotic processBcl-2-like protein 11Homo sapiens (human)
meiosis IBcl-2-like protein 11Homo sapiens (human)
protein polyubiquitinationApoptosis regulator Bcl-2Homo sapiens (human)
apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
extrinsic apoptotic signaling pathway via death domain receptorsApoptosis regulator Bcl-2Homo sapiens (human)
response to xenobiotic stimulusApoptosis regulator Bcl-2Homo sapiens (human)
response to toxic substanceApoptosis regulator Bcl-2Homo sapiens (human)
positive regulation of cell growthApoptosis regulator Bcl-2Homo sapiens (human)
response to cytokineApoptosis regulator Bcl-2Homo sapiens (human)
B cell proliferationApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of neuron apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
regulation of calcium ion transportApoptosis regulator Bcl-2Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stressApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of extrinsic apoptotic signaling pathway in absence of ligandApoptosis regulator Bcl-2Homo sapiens (human)
G1/S transition of mitotic cell cycleApoptosis regulator Bcl-2Homo sapiens (human)
ossificationApoptosis regulator Bcl-2Homo sapiens (human)
ovarian follicle developmentApoptosis regulator Bcl-2Homo sapiens (human)
metanephros developmentApoptosis regulator Bcl-2Homo sapiens (human)
branching involved in ureteric bud morphogenesisApoptosis regulator Bcl-2Homo sapiens (human)
behavioral fear responseApoptosis regulator Bcl-2Homo sapiens (human)
B cell homeostasisApoptosis regulator Bcl-2Homo sapiens (human)
B cell apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
release of cytochrome c from mitochondriaApoptosis regulator Bcl-2Homo sapiens (human)
regulation of cell-matrix adhesionApoptosis regulator Bcl-2Homo sapiens (human)
lymphoid progenitor cell differentiationApoptosis regulator Bcl-2Homo sapiens (human)
B cell lineage commitmentApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of B cell apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
response to ischemiaApoptosis regulator Bcl-2Homo sapiens (human)
renal system processApoptosis regulator Bcl-2Homo sapiens (human)
melanin metabolic processApoptosis regulator Bcl-2Homo sapiens (human)
regulation of nitrogen utilizationApoptosis regulator Bcl-2Homo sapiens (human)
autophagyApoptosis regulator Bcl-2Homo sapiens (human)
humoral immune responseApoptosis regulator Bcl-2Homo sapiens (human)
DNA damage responseApoptosis regulator Bcl-2Homo sapiens (human)
actin filament organizationApoptosis regulator Bcl-2Homo sapiens (human)
axonogenesisApoptosis regulator Bcl-2Homo sapiens (human)
female pregnancyApoptosis regulator Bcl-2Homo sapiens (human)
positive regulation of cell population proliferationApoptosis regulator Bcl-2Homo sapiens (human)
male gonad developmentApoptosis regulator Bcl-2Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to oxidative stressApoptosis regulator Bcl-2Homo sapiens (human)
response to radiationApoptosis regulator Bcl-2Homo sapiens (human)
response to xenobiotic stimulusApoptosis regulator Bcl-2Homo sapiens (human)
response to toxic substanceApoptosis regulator Bcl-2Homo sapiens (human)
post-embryonic developmentApoptosis regulator Bcl-2Homo sapiens (human)
response to iron ionApoptosis regulator Bcl-2Homo sapiens (human)
response to UV-BApoptosis regulator Bcl-2Homo sapiens (human)
response to gamma radiationApoptosis regulator Bcl-2Homo sapiens (human)
regulation of gene expressionApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of autophagyApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of calcium ion transport into cytosolApoptosis regulator Bcl-2Homo sapiens (human)
regulation of glycoprotein biosynthetic processApoptosis regulator Bcl-2Homo sapiens (human)
mesenchymal cell developmentApoptosis regulator Bcl-2Homo sapiens (human)
positive regulation of neuron maturationApoptosis regulator Bcl-2Homo sapiens (human)
smooth muscle cell migrationApoptosis regulator Bcl-2Homo sapiens (human)
positive regulation of smooth muscle cell migrationApoptosis regulator Bcl-2Homo sapiens (human)
cochlear nucleus developmentApoptosis regulator Bcl-2Homo sapiens (human)
gland morphogenesisApoptosis regulator Bcl-2Homo sapiens (human)
regulation of transmembrane transporter activityApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of ossificationApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of cell growthApoptosis regulator Bcl-2Homo sapiens (human)
melanocyte differentiationApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of cell migrationApoptosis regulator Bcl-2Homo sapiens (human)
positive regulation of B cell proliferationApoptosis regulator Bcl-2Homo sapiens (human)
hair follicle morphogenesisApoptosis regulator Bcl-2Homo sapiens (human)
axon regenerationApoptosis regulator Bcl-2Homo sapiens (human)
regulation of protein stabilityApoptosis regulator Bcl-2Homo sapiens (human)
endoplasmic reticulum calcium ion homeostasisApoptosis regulator Bcl-2Homo sapiens (human)
glomerulus developmentApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of cellular pH reductionApoptosis regulator Bcl-2Homo sapiens (human)
regulation of protein localizationApoptosis regulator Bcl-2Homo sapiens (human)
myeloid cell apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of myeloid cell apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
T cell differentiation in thymusApoptosis regulator Bcl-2Homo sapiens (human)
positive regulation of peptidyl-serine phosphorylationApoptosis regulator Bcl-2Homo sapiens (human)
osteoblast proliferationApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of osteoblast proliferationApoptosis regulator Bcl-2Homo sapiens (human)
response to nicotineApoptosis regulator Bcl-2Homo sapiens (human)
organ growthApoptosis regulator Bcl-2Homo sapiens (human)
positive regulation of multicellular organism growthApoptosis regulator Bcl-2Homo sapiens (human)
cellular response to glucose starvationApoptosis regulator Bcl-2Homo sapiens (human)
response to hydrogen peroxideApoptosis regulator Bcl-2Homo sapiens (human)
neuron maturationApoptosis regulator Bcl-2Homo sapiens (human)
T cell homeostasisApoptosis regulator Bcl-2Homo sapiens (human)
positive regulation of apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
CD8-positive, alpha-beta T cell lineage commitmentApoptosis regulator Bcl-2Homo sapiens (human)
ear developmentApoptosis regulator Bcl-2Homo sapiens (human)
regulation of viral genome replicationApoptosis regulator Bcl-2Homo sapiens (human)
positive regulation of melanocyte differentiationApoptosis regulator Bcl-2Homo sapiens (human)
retinal cell programmed cell deathApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of retinal cell programmed cell deathApoptosis regulator Bcl-2Homo sapiens (human)
regulation of mitochondrial membrane permeabilityApoptosis regulator Bcl-2Homo sapiens (human)
focal adhesion assemblyApoptosis regulator Bcl-2Homo sapiens (human)
spleen developmentApoptosis regulator Bcl-2Homo sapiens (human)
thymus developmentApoptosis regulator Bcl-2Homo sapiens (human)
digestive tract morphogenesisApoptosis regulator Bcl-2Homo sapiens (human)
oocyte developmentApoptosis regulator Bcl-2Homo sapiens (human)
skeletal muscle fiber developmentApoptosis regulator Bcl-2Homo sapiens (human)
positive regulation of skeletal muscle fiber developmentApoptosis regulator Bcl-2Homo sapiens (human)
pigment granule organizationApoptosis regulator Bcl-2Homo sapiens (human)
stem cell developmentApoptosis regulator Bcl-2Homo sapiens (human)
homeostasis of number of cells within a tissueApoptosis regulator Bcl-2Homo sapiens (human)
B cell receptor signaling pathwayApoptosis regulator Bcl-2Homo sapiens (human)
response to glucocorticoidApoptosis regulator Bcl-2Homo sapiens (human)
neuron apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
defense response to virusApoptosis regulator Bcl-2Homo sapiens (human)
establishment of localization in cellApoptosis regulator Bcl-2Homo sapiens (human)
regulation of mitochondrial membrane potentialApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of mitochondrial depolarizationApoptosis regulator Bcl-2Homo sapiens (human)
hematopoietic stem cell differentiationApoptosis regulator Bcl-2Homo sapiens (human)
calcium ion transport into cytosolApoptosis regulator Bcl-2Homo sapiens (human)
T cell apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of T cell apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
cellular response to organic substanceApoptosis regulator Bcl-2Homo sapiens (human)
cellular response to hypoxiaApoptosis regulator Bcl-2Homo sapiens (human)
reactive oxygen species metabolic processApoptosis regulator Bcl-2Homo sapiens (human)
dendritic cell apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
motor neuron apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
cell-cell adhesionApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorApoptosis regulator Bcl-2Homo sapiens (human)
epithelial cell apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of epithelial cell apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of G1/S transition of mitotic cell cycleApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of reactive oxygen species metabolic processApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of dendritic cell apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of motor neuron apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of anoikisApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of apoptotic signaling pathwayApoptosis regulator Bcl-2Homo sapiens (human)
negative regulation of intrinsic apoptotic signaling pathwayApoptosis regulator Bcl-2Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damageApoptosis regulator Bcl-2Homo sapiens (human)
extrinsic apoptotic signaling pathway in absence of ligandApoptosis regulator Bcl-2Homo sapiens (human)
activation of cysteine-type endopeptidase activity involved in apoptotic processApoptosis regulator Bcl-2Homo sapiens (human)
response to cytokineBcl-2-like protein 1Homo sapiens (human)
negative regulation of apoptotic processBcl-2-like protein 1Homo sapiens (human)
negative regulation of extrinsic apoptotic signaling pathway via death domain receptorsBcl-2-like protein 1Homo sapiens (human)
ovarian follicle developmentBcl-2-like protein 1Homo sapiens (human)
in utero embryonic developmentBcl-2-like protein 1Homo sapiens (human)
release of cytochrome c from mitochondriaBcl-2-like protein 1Homo sapiens (human)
endocytosisBcl-2-like protein 1Homo sapiens (human)
germ cell developmentBcl-2-like protein 1Homo sapiens (human)
spermatogenesisBcl-2-like protein 1Homo sapiens (human)
male gonad developmentBcl-2-like protein 1Homo sapiens (human)
apoptotic mitochondrial changesBcl-2-like protein 1Homo sapiens (human)
fertilizationBcl-2-like protein 1Homo sapiens (human)
regulation of cytokinesisBcl-2-like protein 1Homo sapiens (human)
positive regulation of mononuclear cell proliferationBcl-2-like protein 1Homo sapiens (human)
ectopic germ cell programmed cell deathBcl-2-like protein 1Homo sapiens (human)
regulation of growthBcl-2-like protein 1Homo sapiens (human)
negative regulation of apoptotic processBcl-2-like protein 1Homo sapiens (human)
negative regulation of neuron apoptotic processBcl-2-like protein 1Homo sapiens (human)
dendritic cell proliferationBcl-2-like protein 1Homo sapiens (human)
response to cycloheximideBcl-2-like protein 1Homo sapiens (human)
regulation of mitochondrial membrane permeabilityBcl-2-like protein 1Homo sapiens (human)
epithelial cell proliferationBcl-2-like protein 1Homo sapiens (human)
negative regulation of developmental processBcl-2-like protein 1Homo sapiens (human)
neuron apoptotic processBcl-2-like protein 1Homo sapiens (human)
defense response to virusBcl-2-like protein 1Homo sapiens (human)
regulation of mitochondrial membrane potentialBcl-2-like protein 1Homo sapiens (human)
cellular response to amino acid stimulusBcl-2-like protein 1Homo sapiens (human)
cellular response to alkaloidBcl-2-like protein 1Homo sapiens (human)
cellular response to gamma radiationBcl-2-like protein 1Homo sapiens (human)
apoptotic process in bone marrow cellBcl-2-like protein 1Homo sapiens (human)
negative regulation of release of cytochrome c from mitochondriaBcl-2-like protein 1Homo sapiens (human)
dendritic cell apoptotic processBcl-2-like protein 1Homo sapiens (human)
hepatocyte apoptotic processBcl-2-like protein 1Homo sapiens (human)
negative regulation of execution phase of apoptosisBcl-2-like protein 1Homo sapiens (human)
negative regulation of intrinsic apoptotic signaling pathway in response to DNA damageBcl-2-like protein 1Homo sapiens (human)
negative regulation of endoplasmic reticulum stress-induced intrinsic apoptotic signaling pathwayBcl-2-like protein 1Homo sapiens (human)
negative regulation of protein localization to plasma membraneBcl-2-like protein 1Homo sapiens (human)
negative regulation of reproductive processBcl-2-like protein 1Homo sapiens (human)
negative regulation of dendritic cell apoptotic processBcl-2-like protein 1Homo sapiens (human)
negative regulation of extrinsic apoptotic signaling pathway in absence of ligandBcl-2-like protein 1Homo sapiens (human)
negative regulation of intrinsic apoptotic signaling pathwayBcl-2-like protein 1Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damageBcl-2-like protein 1Homo sapiens (human)
extrinsic apoptotic signaling pathway in absence of ligandBcl-2-like protein 1Homo sapiens (human)
activation of cysteine-type endopeptidase activity involved in apoptotic processBcl-2-like protein 1Homo sapiens (human)
DNA damage responseInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
response to cytokineInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
cell fate determinationInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
negative regulation of autophagyInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
cellular homeostasisInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
positive regulation of apoptotic processInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
negative regulation of apoptotic processInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
protein transmembrane transportInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
extrinsic apoptotic signaling pathway in absence of ligandInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
positive regulation of oxidative stress-induced neuron intrinsic apoptotic signaling pathwayInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
negative regulation of anoikisInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
negative regulation of extrinsic apoptotic signaling pathway in absence of ligandInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
activation of cysteine-type endopeptidase activity involved in apoptotic processInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
mitochondrial fusionInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
release of cytochrome c from mitochondriaInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damageInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
muscle contractionAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
pattern specification processAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
cell population proliferationAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
negative regulation of cell population proliferationAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
regulation of protein stabilityAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
limb morphogenesisAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
positive regulation of proteolysisAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
roof of mouth developmentAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
face morphogenesisAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
activation of cysteine-type endopeptidase activityAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
regulation of protein depolymerizationAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
peptidyl-aspartic acid hydroxylationAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
response to ischemiaBcl-2-like protein 2Homo sapiens (human)
spermatogenesisBcl-2-like protein 2Homo sapiens (human)
negative regulation of mitochondrial membrane permeabilityBcl-2-like protein 2Homo sapiens (human)
regulation of apoptotic processBcl-2-like protein 2Homo sapiens (human)
negative regulation of apoptotic processBcl-2-like protein 2Homo sapiens (human)
Sertoli cell proliferationBcl-2-like protein 2Homo sapiens (human)
cellular response to estradiol stimulusBcl-2-like protein 2Homo sapiens (human)
negative regulation of release of cytochrome c from mitochondriaBcl-2-like protein 2Homo sapiens (human)
cellular response to amyloid-betaBcl-2-like protein 2Homo sapiens (human)
cellular response to glycineBcl-2-like protein 2Homo sapiens (human)
extrinsic apoptotic signaling pathway in absence of ligandBcl-2-like protein 2Homo sapiens (human)
release of cytochrome c from mitochondriaBcl-2-like protein 2Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damageBcl-2-like protein 2Homo sapiens (human)
activation of cysteine-type endopeptidase activity involved in apoptotic processBcl-2-like protein 2Homo sapiens (human)
glucose catabolic processBcl2-associated agonist of cell death Homo sapiens (human)
apoptotic processBcl2-associated agonist of cell death Homo sapiens (human)
activation of cysteine-type endopeptidase activity involved in apoptotic processBcl2-associated agonist of cell death Homo sapiens (human)
extrinsic apoptotic signaling pathway via death domain receptorsBcl2-associated agonist of cell death Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damageBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of autophagyBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of mitochondrial membrane potentialBcl2-associated agonist of cell death Homo sapiens (human)
cytokine-mediated signaling pathwayBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of insulin secretionBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of glucokinase activityBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of insulin secretion involved in cellular response to glucose stimulusBcl2-associated agonist of cell death Homo sapiens (human)
glucose homeostasisBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of apoptotic processBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of cysteine-type endopeptidase activity involved in apoptotic processBcl2-associated agonist of cell death Homo sapiens (human)
type B pancreatic cell proliferationBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of B cell differentiationBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of T cell differentiationBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of proteolysisBcl2-associated agonist of cell death Homo sapiens (human)
ADP metabolic processBcl2-associated agonist of cell death Homo sapiens (human)
ATP metabolic processBcl2-associated agonist of cell death Homo sapiens (human)
regulation of mitochondrial membrane permeabilityBcl2-associated agonist of cell death Homo sapiens (human)
pore complex assemblyBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of epithelial cell proliferationBcl2-associated agonist of cell death Homo sapiens (human)
cellular response to mechanical stimulusBcl2-associated agonist of cell death Homo sapiens (human)
cellular response to nicotineBcl2-associated agonist of cell death Homo sapiens (human)
cellular response to lipidBcl2-associated agonist of cell death Homo sapiens (human)
cellular response to hypoxiaBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondriaBcl2-associated agonist of cell death Homo sapiens (human)
extrinsic apoptotic signaling pathwayBcl2-associated agonist of cell death Homo sapiens (human)
extrinsic apoptotic signaling pathway in absence of ligandBcl2-associated agonist of cell death Homo sapiens (human)
intrinsic apoptotic signaling pathwayBcl2-associated agonist of cell death Homo sapiens (human)
activation of cysteine-type endopeptidase activityBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathway in response to osmotic stressBcl2-associated agonist of cell death Homo sapiens (human)
positive regulation of type B pancreatic cell developmentBcl2-associated agonist of cell death Homo sapiens (human)
release of cytochrome c from mitochondriaBcl2-associated agonist of cell death Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (27)

Processvia Protein(s)Taxonomy
protein bindingBcl-2-like protein 11Homo sapiens (human)
microtubule bindingBcl-2-like protein 11Homo sapiens (human)
protein kinase bindingBcl-2-like protein 11Homo sapiens (human)
protease bindingApoptosis regulator Bcl-2Homo sapiens (human)
protein bindingApoptosis regulator Bcl-2Homo sapiens (human)
channel activityApoptosis regulator Bcl-2Homo sapiens (human)
channel inhibitor activityApoptosis regulator Bcl-2Homo sapiens (human)
ubiquitin protein ligase bindingApoptosis regulator Bcl-2Homo sapiens (human)
identical protein bindingApoptosis regulator Bcl-2Homo sapiens (human)
sequence-specific DNA bindingApoptosis regulator Bcl-2Homo sapiens (human)
protein heterodimerization activityApoptosis regulator Bcl-2Homo sapiens (human)
BH3 domain bindingApoptosis regulator Bcl-2Homo sapiens (human)
protein phosphatase 2A bindingApoptosis regulator Bcl-2Homo sapiens (human)
molecular adaptor activityApoptosis regulator Bcl-2Homo sapiens (human)
DNA-binding transcription factor bindingApoptosis regulator Bcl-2Homo sapiens (human)
BH domain bindingApoptosis regulator Bcl-2Homo sapiens (human)
protein bindingBcl-2-like protein 1Homo sapiens (human)
protein kinase bindingBcl-2-like protein 1Homo sapiens (human)
identical protein bindingBcl-2-like protein 1Homo sapiens (human)
BH3 domain bindingBcl-2-like protein 1Homo sapiens (human)
BH domain bindingBcl-2-like protein 1Homo sapiens (human)
protein bindingInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
protein transmembrane transporter activityInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
protein heterodimerization activityInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
BH3 domain bindingInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
channel activityInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
BH domain bindingInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
structural molecule activityAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
calcium ion bindingAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
protein bindingAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
structural constituent of muscleAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
electron transfer activityAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
peptidyl-aspartic acid 3-dioxygenase activityAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
protein bindingBcl-2-like protein 2Homo sapiens (human)
identical protein bindingBcl-2-like protein 2Homo sapiens (human)
protein-containing complex bindingBcl-2-like protein 2Homo sapiens (human)
disordered domain specific bindingBcl-2-like protein 2Homo sapiens (human)
BH domain bindingBcl-2-like protein 2Homo sapiens (human)
protein bindingBcl2-associated agonist of cell death Homo sapiens (human)
phospholipid bindingBcl2-associated agonist of cell death Homo sapiens (human)
lipid bindingBcl2-associated agonist of cell death Homo sapiens (human)
cysteine-type endopeptidase activator activity involved in apoptotic processBcl2-associated agonist of cell death Homo sapiens (human)
protein kinase bindingBcl2-associated agonist of cell death Homo sapiens (human)
protein phosphatase bindingBcl2-associated agonist of cell death Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (23)

Processvia Protein(s)Taxonomy
mitochondrial outer membraneBcl-2-like protein 11Homo sapiens (human)
cytosolBcl-2-like protein 11Homo sapiens (human)
endomembrane systemBcl-2-like protein 11Homo sapiens (human)
Bcl-2 family protein complexBcl-2-like protein 11Homo sapiens (human)
mitochondrionBcl-2-like protein 11Homo sapiens (human)
mitochondrial outer membraneApoptosis regulator Bcl-2Homo sapiens (human)
endoplasmic reticulum membraneApoptosis regulator Bcl-2Homo sapiens (human)
nucleusApoptosis regulator Bcl-2Homo sapiens (human)
cytoplasmApoptosis regulator Bcl-2Homo sapiens (human)
mitochondrionApoptosis regulator Bcl-2Homo sapiens (human)
mitochondrial outer membraneApoptosis regulator Bcl-2Homo sapiens (human)
endoplasmic reticulumApoptosis regulator Bcl-2Homo sapiens (human)
cytosolApoptosis regulator Bcl-2Homo sapiens (human)
membraneApoptosis regulator Bcl-2Homo sapiens (human)
nuclear membraneApoptosis regulator Bcl-2Homo sapiens (human)
myelin sheathApoptosis regulator Bcl-2Homo sapiens (human)
BAD-BCL-2 complexApoptosis regulator Bcl-2Homo sapiens (human)
protein-containing complexApoptosis regulator Bcl-2Homo sapiens (human)
pore complexApoptosis regulator Bcl-2Homo sapiens (human)
cytoplasmBcl-2-like protein 1Homo sapiens (human)
mitochondrionBcl-2-like protein 1Homo sapiens (human)
mitochondrial outer membraneBcl-2-like protein 1Homo sapiens (human)
mitochondrial inner membraneBcl-2-like protein 1Homo sapiens (human)
mitochondrial matrixBcl-2-like protein 1Homo sapiens (human)
endoplasmic reticulumBcl-2-like protein 1Homo sapiens (human)
centrosomeBcl-2-like protein 1Homo sapiens (human)
cytosolBcl-2-like protein 1Homo sapiens (human)
synaptic vesicle membraneBcl-2-like protein 1Homo sapiens (human)
nuclear membraneBcl-2-like protein 1Homo sapiens (human)
Bcl-2 family protein complexBcl-2-like protein 1Homo sapiens (human)
mitochondrial outer membraneBcl-2-like protein 1Homo sapiens (human)
nucleusInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
nucleoplasmInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
cytoplasmInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
mitochondrionInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
mitochondrial outer membraneInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
cytosolInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
membraneInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
Bcl-2 family protein complexInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
mitochondrial outer membraneInduced myeloid leukemia cell differentiation protein Mcl-1Homo sapiens (human)
endoplasmic reticulumAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
endoplasmic reticulum membraneAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
plasma membraneAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
cortical endoplasmic reticulumAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
sarcoplasmic reticulum membraneAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
endoplasmic reticulumAspartyl/asparaginyl beta-hydroxylaseHomo sapiens (human)
cytosolBcl-2-like protein 2Homo sapiens (human)
Bcl-2 family protein complexBcl-2-like protein 2Homo sapiens (human)
mitochondrial outer membraneBcl-2-like protein 2Homo sapiens (human)
mitochondrionBcl2-associated agonist of cell death Homo sapiens (human)
mitochondrial outer membraneBcl2-associated agonist of cell death Homo sapiens (human)
cytosolBcl2-associated agonist of cell death Homo sapiens (human)
BAD-BCL-2 complexBcl2-associated agonist of cell death Homo sapiens (human)
cytosolBcl2-associated agonist of cell death Homo sapiens (human)
mitochondrionBcl2-associated agonist of cell death Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (176)

Assay IDTitleYearJournalArticle
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347113qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347125qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347119qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347122qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347114qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347126qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347121qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347129qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347123qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508591NCATS Rat Liver Microsome Stability Profiling2020Scientific reports, 11-26, Volume: 10, Issue:1
Retrospective assessment of rat liver microsomal stability at NCATS: data and QSAR models.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347110qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for A673 cells)2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347116qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347118qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347128qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347117qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347112qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1508612NCATS Parallel Artificial Membrane Permeability Assay (PAMPA) Profiling2017Bioorganic & medicinal chemistry, 02-01, Volume: 25, Issue:3
Highly predictive and interpretable models for PAMPA permeability.
AID1347111qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347124qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347115qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347109qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347127qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID389269AUC in CD1 mouse at 50 mg/kg, po2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1388441Antiproliferative activity against human MOLT4 cells in presence of 10% human serum2018Journal of medicinal chemistry, 04-12, Volume: 61, Issue:7
Beyond the Rule of 5: Lessons Learned from AbbVie's Drugs and Compound Collection.
AID661213Induction of apoptosis in human SU-DHL4 cells assessed as BAK oligomerization at 0.1 to 10 uM after 24 hrs by Western blot analysis2012Bioorganic & medicinal chemistry letters, Jun-15, Volume: 22, Issue:12
Identification of a phenylacylsulfonamide series of dual Bcl-2/Bcl-xL antagonists.
AID389263Cytotoxicity against IL3-dependent mouse FL5.12 cells overexpressing human Bcl-XL assessed as cell viability after 24 hrs by MTS assay in absence of serum2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID389260Displacement of fluorescein labeled BAD peptide from Bcl-XL by fluorescence polarization assay2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1250174Cytotoxicity against human Glioma cells (HF2876) after 72 hrs by CelltiterGlo assay in presence of mTOR inhibitor AZD-80552015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID389445Oral bioavailability in Sprague-Dawley rat2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID389277Oral bioavailability in Beagle dog2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1610206Time dependent inhibition of recombinant human C-terminal 6xHis-tagged Bcl-2 (M1 to F212 residues) expressed in Escherichia coli using HyLite Fluor 647-labeled BIM peptide as substrate measured after 240 mins by TR-FRET assay2019Bioorganic & medicinal chemistry letters, 12-01, Volume: 29, Issue:23
Discovery and optimization of covalent Bcl-xL antagonists.
AID1545359Inhibition of BCL-2 (unknown origin) by fluorescence polarization assay2019European journal of medicinal chemistry, Apr-01, Volume: 167Clinical candidates modulating protein-protein interactions: The fragment-based experience.
AID1677973Inhibition of N-His6-tagged human AspH (315-755) expressed in Escherichia coli BL21 (DE3) using 1 uM hFX-CP as substrate mixture with high 200 uM 2OG, 100 uM L-ascorbic acid and 2 uM FAS incubated for 35 mins by MS analysis2020Bioorganic & medicinal chemistry, 10-15, Volume: 28, Issue:20
Small-molecule active pharmaceutical ingredients of approved cancer therapeutics inhibit human aspartate/asparagine-β-hydroxylase.
AID526645Binding affinity to Bcl-xl2010Journal of medicinal chemistry, Oct-14, Volume: 53, Issue:19
Toward the development of innovative bifunctional agents to induce differentiation and to promote apoptosis in leukemia: clinical candidates and perspectives.
AID1293717Binding affinity to Bcl-2 (unknown origin) by fluorescence polarization assay2016Bioorganic & medicinal chemistry letters, May-01, Volume: 26, Issue:9
Selective inhibitors of Bcl-2 and Bcl-xL: Balancing antitumor activity with on-target toxicity.
AID1738438Selectivity ratio of IC50 for human platelets to IC50 for human MyLa1929 cells2020European journal of medicinal chemistry, Aug-01, Volume: 199Discovery of IAP-recruiting BCL-X
AID1710464Inhibition of F-Bak binding to GST-tagged BCL2 (unknown origin) measured after 1 hr by TR-FRET assay
AID1545374Toxicity in mouse xenografted with human haematological tumor at 12.5 mg/kg, po2019European journal of medicinal chemistry, Apr-01, Volume: 167Clinical candidates modulating protein-protein interactions: The fragment-based experience.
AID389268Ratio of AUC for Sprague-Dawley rat at 5 mg/kg, po to EC50 for human NCI-H146 cells in presence of 10% human serum2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID389276Oral bioavailability in CD1 mouse2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1738409Antiproliferative activity against human MyLa1929 cells assessed as cell viability measured after 72 hrs by MTS assay2020European journal of medicinal chemistry, Aug-01, Volume: 199Discovery of IAP-recruiting BCL-X
AID1710467Cytotoxicity against human MOLT-4 cells assessed as reduction in cell viability measured after 48 hrs by celltiter-glo assay
AID1700823Binding affinity to human full-length N-terminal His6-tagged Bcl2 (2 to 206 residues) expressed in Escherichia coli S12 extract by isothermal titration calorimetry
AID1830300Cytotoxicity against human MOLT-4 cells assessed as reduction in cell viability measured after 48 hrs by MTS assay
AID1830295Cytotoxicity against platelets in human PRP assessed as reduction in cell viability measured after 48 hrs by MTS assay
AID389264Cytotoxicity against human NCI-H146 cells assessed as cell viability after 48 hrs in presence of 10% human serum2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID389446Toxicity against human NCI-H146 cells xenografted C.B-17 SCID-bg mouse assessed as weight loss at 100 mg/kg, po daily once for 21 days2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1250171Cytotoxicity against human Glioma cells (HF2476) after 72 hrs by CelltiterGlo assay in presence of mTOR inhibitor AZD-80552015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1352865Inhibition of Bcl-2 (unknown origin) by fluorescence polarization assay2018European journal of medicinal chemistry, Feb-25, Volume: 146Small-molecule Mcl-1 inhibitors: Emerging anti-tumor agents.
AID405509Binding affinity to BH3 binding groove of BclXL2008Journal of medicinal chemistry, Jul-10, Volume: 51, Issue:13
Recent developments in fragment-based drug discovery.
AID701241Induction of apoptosis in human NCI-H146 cells assessed as caspase 3 activation at 30 nM after 24 hrs by Western blot analysis2012Journal of medicinal chemistry, Oct-11, Volume: 55, Issue:19
Structure-based discovery of BM-957 as a potent small-molecule inhibitor of Bcl-2 and Bcl-xL capable of achieving complete tumor regression.
AID1738439Cytotoxicity against human WI-38 cells assessed as cell viability measured after 72 hrs by MTS assay2020European journal of medicinal chemistry, Aug-01, Volume: 199Discovery of IAP-recruiting BCL-X
AID462446Binding affinity to Bcl-xL by competitive fluorescence polarization assay2010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Fragment-based deconstruction of Bcl-xL inhibitors.
AID1352866Inhibition of Bcl-xL (unknown origin) by fluorescence polarization assay2018European journal of medicinal chemistry, Feb-25, Volume: 146Small-molecule Mcl-1 inhibitors: Emerging anti-tumor agents.
AID389262Cytotoxicity against IL3-dependent mouse FL5.12 cells overexpressing human Bcl2 assessed as cell viability after 24 hrs by MTS assay in absence of serum2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1140898Inhibition of BCL2 (unknown origin) overexpressed in E-mu-myc transgenic mouse lymphoma cells assessed as induction of cell death at 0.1 to 10 uM after 15 to 18 hrs by flow cytometric analysis2014Journal of medicinal chemistry, May-22, Volume: 57, Issue:10
3-Substituted-N-(4-hydroxynaphthalen-1-yl)arylsulfonamides as a novel class of selective Mcl-1 inhibitors: structure-based design, synthesis, SAR, and biological evaluation.
AID587094Cytotoxicity against human NCI-H889 after 48 hrs by MTS assay in presence of 10% human serum2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Quinazoline sulfonamides as dual binders of the proteins B-cell lymphoma 2 and B-cell lymphoma extra long with potent proapoptotic cell-based activity.
AID1250173Cytotoxicity against human Glioma cells (HF2303) after 72 hrs by CelltiterGlo assay in presence of mTOR inhibitor AZD-80552015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1700825Binding affinity to human full-length N-terminal His6-tagged Bcl2 R106A/R109A mutant expressed in Escherichia coli S12 extract by isothermal titration calorimetry
AID1710465Inhibition of F-Bak binding to GST-tagged MCL1 (unknown origin) measured after 1 hr by TR-FRET assay
AID1700824Binding affinity to human full-length N-terminal His6-tagged prephosphorylated Bcl2 (2 to 206 residues) expressed in Escherichia coli S12 extract by isothermal titration calorimetry
AID1178968Inhibition of human BCL-xL overexpressed in mouse FDC-P1 cells assessed as cell viability after 24 hrs by Cell Titer Glo assay2014Bioorganic & medicinal chemistry letters, Jul-15, Volume: 24, Issue:14
Towards the next generation of dual Bcl-2/Bcl-xL inhibitors.
AID1140897Inhibition of MCL1 (unknown origin) overexpressed in E-mu-myc transgenic mouse lymphoma cells assessed as induction of cell death at 0.1 to 10 uM after 15 to 18 hrs by flow cytometric analysis2014Journal of medicinal chemistry, May-22, Volume: 57, Issue:10
3-Substituted-N-(4-hydroxynaphthalen-1-yl)arylsulfonamides as a novel class of selective Mcl-1 inhibitors: structure-based design, synthesis, SAR, and biological evaluation.
AID1677971Inhibition of N-His6-tagged human AspH (315-755) expressed in Escherichia coli BL21 (DE3) at 20uM using 1 uM hFX-CP as substrate mixture with 3 uM 2OG, 100 uM L-ascorbic acid and 2 uM FAS incubated for 35 mins by MS analysis2020Bioorganic & medicinal chemistry, 10-15, Volume: 28, Issue:20
Small-molecule active pharmaceutical ingredients of approved cancer therapeutics inhibit human aspartate/asparagine-β-hydroxylase.
AID1599466Inhibition of Flu-Bax peptide binding to Bcl-xL (unknown origin) by time-resolved fluorescence resonance energy transfer assay2019European journal of medicinal chemistry, Sep-01, Volume: 177The chemical biology of apoptosis: Revisited after 17 years.
AID661091Induction of apoptosis in human SU-DHL4 cells assessed as cytochrome c release at 0.1 to 10 uM after 24 hrs by Western blot analysis2012Bioorganic & medicinal chemistry letters, Jun-15, Volume: 22, Issue:12
Identification of a phenylacylsulfonamide series of dual Bcl-2/Bcl-xL antagonists.
AID389267Oral bioavailability in Sprague-Dawley rat at 5 mg/kg2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1250151Cytotoxicity against human Glioma cells (HF2876) after 72 hrs by CelltiterGlo assay2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1610199Inhibition of recombinant human N-terminal GST-tagged Bcl-xl (1 to 209 residues) expressed in Escherichia coli using HyLite Fluor 647-labeled BIM peptide as substrate incubated for 120 to 180 mins by TR-FRET assay2019Bioorganic & medicinal chemistry letters, 12-01, Volume: 29, Issue:23
Discovery and optimization of covalent Bcl-xL antagonists.
AID1250165Induction of apoptosis in human Glioma cells (HF2476) assessed as increase in cleaved caspase-3 level by western blot analysis2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1388437Oral bioavailability in dog2018Journal of medicinal chemistry, 04-12, Volume: 61, Issue:7
Beyond the Rule of 5: Lessons Learned from AbbVie's Drugs and Compound Collection.
AID389272Oral elimination half life in Sprague-Dawley rat2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1250166Induction of apoptosis in human Glioma cells (HF2876) assessed as increase in cleaved caspase-3 level by western blot analysis2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1763283Antiproliferative activity against human MIA PaCa-2 cells assessed as cell growth inhibition at 5 uM measured after 3 days by Prestoblue assay relative to control2021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Aminopyrazole based CDK9 PROTAC sensitizes pancreatic cancer cells to venetoclax.
AID587093Cytotoxicity against human NCI-H146 after 48 hrs by MTS assay in presence of 10% human serum2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Quinazoline sulfonamides as dual binders of the proteins B-cell lymphoma 2 and B-cell lymphoma extra long with potent proapoptotic cell-based activity.
AID1178967Inhibition of human BCL-2 overexpressed in mouse FDC-P1 cells assessed as cell viability after 24 hrs by Cell Titer Glo assay2014Bioorganic & medicinal chemistry letters, Jul-15, Volume: 24, Issue:14
Towards the next generation of dual Bcl-2/Bcl-xL inhibitors.
AID1250153Cytotoxicity against human Glioma cells (HF3013) after 72 hrs by CelltiterGlo assay2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1599465Inhibition of Flu-Bax peptide binding to Bcl2 (unknown origin) by time-resolved fluorescence resonance energy transfer assay2019European journal of medicinal chemistry, Sep-01, Volume: 177The chemical biology of apoptosis: Revisited after 17 years.
AID1189616Reduction in Mcl1 level in human MDA-MB-468 cells at 3 uM2015European journal of medicinal chemistry, Jan-27, Volume: 90Design, synthesis and evaluation of marinopyrrole derivatives as selective inhibitors of Mcl-1 binding to pro-apoptotic Bim and dual Mcl-1/Bcl-xL inhibitors.
AID389275Oral elimination half life in cynomolgus monkey2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1368927Displacement of Bad-derived peptide from Bcl-XL (unknown origin) by fluorescence polarization assay2018Bioorganic & medicinal chemistry, 01-15, Volume: 26, Issue:2
Design, synthesis and pharmacological evaluation of new acyl sulfonamides as potent and selective Bcl-2 inhibitors.
AID1677975Inhibition of N-His6-tagged human AspH (315-755) expressed in Escherichia coli BL21 (DE3) using high 10 uM hFX-CP as substrate mixture with 10 uM 2OG, 100 uM L-ascorbic acid and 2 uM FAS incubated for 35 mins by MS analysis2020Bioorganic & medicinal chemistry, 10-15, Volume: 28, Issue:20
Small-molecule active pharmaceutical ingredients of approved cancer therapeutics inhibit human aspartate/asparagine-β-hydroxylase.
AID1710926Cytotoxicity against human Hep3B cells assessed as reduction in cell viability measured upto 72 hrs by MTT assay2016Bioorganic & medicinal chemistry letters, Feb-01, Volume: 26, Issue:3
Adamantyl-tethered-biphenylic compounds induce apoptosis in cancer cells by targeting Bcl homologs.
AID1738437Cytotoxicity against human platelet assessed as cell viability measured after 72 hrs by MTS assay2020European journal of medicinal chemistry, Aug-01, Volume: 199Discovery of IAP-recruiting BCL-X
AID728129Cytotoxicity against human NCI-H1417 cells assessed as growth inhibition after 4 days by WST assay2013Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7
A potent and highly efficacious Bcl-2/Bcl-xL inhibitor.
AID389266AUC in Sprague-Dawley rat at 5 mg/kg, po2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1599467Inhibition of Flu-Bax peptide binding to MCl-1 (unknown origin) by time-resolved fluorescence resonance energy transfer assay2019European journal of medicinal chemistry, Sep-01, Volume: 177The chemical biology of apoptosis: Revisited after 17 years.
AID1710463Inhibition of F-Bak binding to GST-tagged BCL-XL (unknown origin) measured after 1 hr by TR-FRET assay
AID1610204Inhibition of Bcl-xl in human U266B1 cells assessed as caspase 3/7 activation in presence of 10 % serum for 6 hrs by Caspase 3/7-Glo luminescence assay2019Bioorganic & medicinal chemistry letters, 12-01, Volume: 29, Issue:23
Discovery and optimization of covalent Bcl-xL antagonists.
AID1830322Binding affinity to VHL/BCL-2 in human RS4-11 cells assessed as ternary complex formation at up to 300 nM measured after 12 hrs in presence of VHL-032 by immunoprecipitation assay
AID1610200Inhibition of recombinant human C-terminal 6xHis-tagged Bcl-2 (M1 to F212 residues) expressed in Escherichia coli using HyLite Fluor 647-labeled BIM peptide as substrate incubated for 120 to 180 mins by TR-FRET assay2019Bioorganic & medicinal chemistry letters, 12-01, Volume: 29, Issue:23
Discovery and optimization of covalent Bcl-xL antagonists.
AID389270AUC in Beagle dog at 2.5 mg/kg, iv or po2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1830319Binding affinity to VHL/ BCL-XL in human RS4-11 cells assessed as ternary complex formation at up to 300 nM measured after 12 hrs by immunoprecipitation assay
AID1178965Induction of apoptosis in human RS4:11 cells overexpressing BCL-2 assessed as caspase 3/7 activation after 6 hrs by quantitative luminescence assay2014Bioorganic & medicinal chemistry letters, Jul-15, Volume: 24, Issue:14
Towards the next generation of dual Bcl-2/Bcl-xL inhibitors.
AID1250172Cytotoxicity against human Glioma cells (HF3013) after 72 hrs by CelltiterGlo assay in presence of mTOR inhibitor AZD-80552015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1189618Inhibition of Bcl-xL/Bim (unknown origin) by ELISA2015European journal of medicinal chemistry, Jan-27, Volume: 90Design, synthesis and evaluation of marinopyrrole derivatives as selective inhibitors of Mcl-1 binding to pro-apoptotic Bim and dual Mcl-1/Bcl-xL inhibitors.
AID1250149Cytotoxicity against human Glioma cells (HF2476) after 72 hrs by CelltiterGlo assay2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1073482Displacement of FITC-Bid from GST-tagged human Bcl-xL expressed in Escherichia coli after 2 hrs by TR-FRET assay2013Journal of medicinal chemistry, Dec-12, Volume: 56, Issue:23
Discovery of potent Mcl-1/Bcl-xL dual inhibitors by using a hybridization strategy based on structural analysis of target proteins.
AID1610202Inhibition of recombinant human C-terminal 6xHis-tagged Mcl-1 (E171 ti G327) expressed in Escherichia coli using biotin-labeled BIM peptide as substrate incubated for 120 to 180 mins by TR-FRET assay2019Bioorganic & medicinal chemistry letters, 12-01, Volume: 29, Issue:23
Discovery and optimization of covalent Bcl-xL antagonists.
AID728146Cytotoxicity against human NCI-H1963 cells assessed as growth inhibition after 4 days by WST assay2013Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7
A potent and highly efficacious Bcl-2/Bcl-xL inhibitor.
AID389274Oral elimination half life in Beagle dog2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1368926Displacement of Bax-derived peptide from Bcl-2 (unknown origin) by fluorescence polarization assay2018Bioorganic & medicinal chemistry, 01-15, Volume: 26, Issue:2
Design, synthesis and pharmacological evaluation of new acyl sulfonamides as potent and selective Bcl-2 inhibitors.
AID728130Cytotoxicity against human NCI-H187 cells assessed as growth inhibition after 4 days by WST assay2013Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7
A potent and highly efficacious Bcl-2/Bcl-xL inhibitor.
AID1830309Displacement of biotin-tagged LWAAQRYGRELRRMSDEFEGSFKGL from human BCL-XL expressed in Escherichia coli measured after 2 hrs by AlphaScreen assay
AID1545358Inhibition of BCL-XL (unknown origin) by fluorescence polarization assay2019European journal of medicinal chemistry, Apr-01, Volume: 167Clinical candidates modulating protein-protein interactions: The fragment-based experience.
AID1830311Binding affinity to human BCL-XL expressed in Escherichia coli/recombinant human VHL (54 to end residues) fused to human N-terminal GST-tagged elongin-C/elongin -B/N-terminal His-tagged CUL2/Rbx1 expressed in baculovirus infected Sf21 insect cells measure
AID1830321Binding affinity to VHL/ BCL-XL in human RS4-11 cells assessed as ternary complex formation at up to 300 nM measured after 12 hrs in presence of VHL-032 by immunoprecipitation assay
AID1352867Inhibition of Mcl-1 (unknown origin) by fluorescence polarization assay2018European journal of medicinal chemistry, Feb-25, Volume: 146Small-molecule Mcl-1 inhibitors: Emerging anti-tumor agents.
AID389278Oral bioavailability in cynomolgus monkey2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID389261Displacement of fluorescein labeled Bax peptide from Bcl2 by fluorescence polarization assay2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1610201Inhibition of recombinant human N-terminal 6xHis-tagged Bcl-w (M1 to R171) expressed in Escherichia coli using HyLite Fluor 647-labeled Bim peptide as substrate incubated for 120 to 180 mins by TR-FRET assay2019Bioorganic & medicinal chemistry letters, 12-01, Volume: 29, Issue:23
Discovery and optimization of covalent Bcl-xL antagonists.
AID1677972Inhibition of N-His6-tagged human AspH (315-755) expressed in Escherichia coli BL21 (DE3) using 1 uM hFX-CP as substrate mixture with 3 uM 2OG, 100 uM L-ascorbic acid and 2 uM FAS incubated for 35 mins by MS analysis2020Bioorganic & medicinal chemistry, 10-15, Volume: 28, Issue:20
Small-molecule active pharmaceutical ingredients of approved cancer therapeutics inhibit human aspartate/asparagine-β-hydroxylase.
AID389273Oral elimination half life in CD1 mouse2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1830299Cytotoxicity against human RS4-11 cells assessed as reduction in cell viability measured after 48 hrs by MTS assay
AID1293718Binding affinity to Bcl-XL (unknown origin) by fluorescence polarization assay2016Bioorganic & medicinal chemistry letters, May-01, Volume: 26, Issue:9
Selective inhibitors of Bcl-2 and Bcl-xL: Balancing antitumor activity with on-target toxicity.
AID1710468Cytotoxicity against human RS4-11 cells assessed as reduction in cell viability measured after 48 hrs by celltiter-glo assay
AID1388438Inhibition of Bcl2 (unknown origin)2018Journal of medicinal chemistry, 04-12, Volume: 61, Issue:7
Beyond the Rule of 5: Lessons Learned from AbbVie's Drugs and Compound Collection.
AID701261Induction of apoptosis in human NCI-H146 cells assessed as cell viability after 24 hrs by trypan blue exclusion assay2012Journal of medicinal chemistry, Oct-11, Volume: 55, Issue:19
Structure-based discovery of BM-957 as a potent small-molecule inhibitor of Bcl-2 and Bcl-xL capable of achieving complete tumor regression.
AID1525538Inhibition of Bcl2 (unknown origin)2019Journal of medicinal chemistry, 11-27, Volume: 62, Issue:22
Why Some Targets Benefit from beyond Rule of Five Drugs.
AID701259Induction of apoptosis in human NCI-H146 cells assessed as cell viability at 30 to 100 nM after 24 hrs by trypan blue exclusion assay2012Journal of medicinal chemistry, Oct-11, Volume: 55, Issue:19
Structure-based discovery of BM-957 as a potent small-molecule inhibitor of Bcl-2 and Bcl-xL capable of achieving complete tumor regression.
AID1677974Inhibition of N-His6-tagged human AspH (315-755) expressed in Escherichia coli BL21 (DE3) using 1 uM hFX-CP as substrate mixture with 3 uM 2OG, 100 uM L-ascorbic acid and high 20 uM FAS incubated for 35 mins by MS analysis2020Bioorganic & medicinal chemistry, 10-15, Volume: 28, Issue:20
Small-molecule active pharmaceutical ingredients of approved cancer therapeutics inhibit human aspartate/asparagine-β-hydroxylase.
AID1250147Cytotoxicity against human Glioma cells (HF2303) after 72 hrs by CelltiterGlo assay2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1700826Binding affinity to human full-length N-terminal His6-tagged prephosphorylated Bcl2 R106A/R109A mutant expressed in Escherichia coli S12 extract by isothermal titration calorimetry
AID1710923Cytotoxicity against human HepG2 cells assessed as reduction in cell viability measured upto 72 hrs by MTT assay2016Bioorganic & medicinal chemistry letters, Feb-01, Volume: 26, Issue:3
Adamantyl-tethered-biphenylic compounds induce apoptosis in cancer cells by targeting Bcl homologs.
AID389279Antitumor activity against human NCI-H146 cells xenografted C.B-17 SCID-bg mouse assessed as inhibition of tumor growth at 100 mg/kg, po daily once for 21 days2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID389271AUC in cynomolgus monkey at 2.5 mg/kg, po2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID701242Induction of apoptosis in human NCI-H146 cells assessed as PARP cleavage at 30 nM after 24 hrs by Western blot analysis2012Journal of medicinal chemistry, Oct-11, Volume: 55, Issue:19
Structure-based discovery of BM-957 as a potent small-molecule inhibitor of Bcl-2 and Bcl-xL capable of achieving complete tumor regression.
AID1830310Displacement of biotin-tagged MRPEPATIAQELRRIGDEFNA from C-terminal His-tagged human BCL-2 (1` to 211 residues) expressed in Escherichia coli measured after 2 hrs by AlphaScreen assay
AID1073483Displacement of FITC-Bid from GST-tagged human Mcl-1 expressed in Escherichia coli after 2 hrs by TR-FRET assay2013Journal of medicinal chemistry, Dec-12, Volume: 56, Issue:23
Discovery of potent Mcl-1/Bcl-xL dual inhibitors by using a hybridization strategy based on structural analysis of target proteins.
AID1710925Cytotoxicity against human HuH-7 cells assessed as reduction in cell viability measured upto 72 hrs by MTT assay2016Bioorganic & medicinal chemistry letters, Feb-01, Volume: 26, Issue:3
Adamantyl-tethered-biphenylic compounds induce apoptosis in cancer cells by targeting Bcl homologs.
AID1388440Antiproliferative activity against human RS4:11 cells in presence of 10% human serum2018Journal of medicinal chemistry, 04-12, Volume: 61, Issue:7
Beyond the Rule of 5: Lessons Learned from AbbVie's Drugs and Compound Collection.
AID587095Cytotoxicity against human NCI-H1963 after 48 hrs by MTS assay in presence of 10% human serum2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Quinazoline sulfonamides as dual binders of the proteins B-cell lymphoma 2 and B-cell lymphoma extra long with potent proapoptotic cell-based activity.
AID1368928Selectivity factor, ratio of IC50 for Bad-derived peptide from Bcl-XL (unknown origin) to IC50 for displacement of Bax-derived peptide from Bcl-2 (unknown origin)2018Bioorganic & medicinal chemistry, 01-15, Volume: 26, Issue:2
Design, synthesis and pharmacological evaluation of new acyl sulfonamides as potent and selective Bcl-2 inhibitors.
AID1830320Binding affinity to VHL/BCL-2 in human RS4-11 cells assessed as ternary complex formation at up to 300 nM measured after 12 hrs by immunoprecipitation assay
AID1388439Inhibition of Bcl-xL (unknown origin)2018Journal of medicinal chemistry, 04-12, Volume: 61, Issue:7
Beyond the Rule of 5: Lessons Learned from AbbVie's Drugs and Compound Collection.
AID1830312Binding affinity to C-terminal His-tagged human BCL-2 (1 to 211 residues) expressed in Escherichia coli/recombinant human VHL (54 to end residues) fused to human N-terminal GST-tagged elongin-C/elongin -B/N-terminal His-tagged CUL2/Rbx1 expressed in bacul
AID1674225Inhibition of BCL2 (unknown origin) by TR-FRET assay2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Fragment Linking Strategies for Structure-Based Drug Design.
AID1545360Inhibition of BCL-W (unknown origin) by fluorescence polarization assay2019European journal of medicinal chemistry, Apr-01, Volume: 167Clinical candidates modulating protein-protein interactions: The fragment-based experience.
AID1610203Inhibition of Bcl-xl in human U266B1 cells assessed as caspase 3/7 activation for 6 hrs by Caspase 3/7-Glo luminescence assay2019Bioorganic & medicinal chemistry letters, 12-01, Volume: 29, Issue:23
Discovery and optimization of covalent Bcl-xL antagonists.
AID1645848NCATS Kinetic Aqueous Solubility Profiling2019Bioorganic & medicinal chemistry, 07-15, Volume: 27, Issue:14
Predictive models of aqueous solubility of organic compounds built on A large dataset of high integrity.
AID1347411qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID686947qHTS for small molecule inhibitors of Yes1 kinase: Primary Screen2013Bioorganic & medicinal chemistry letters, Aug-01, Volume: 23, Issue:15
Identification of potent Yes1 kinase inhibitors using a library screening approach.
AID720501qHTS for Inhibitors of Polymerase Kappa: Confirmatory Assay for Cherry-picked Compounds2012PloS one, , Volume: 7, Issue:10
A comprehensive strategy to discover inhibitors of the translesion synthesis DNA polymerase κ.
AID1347159Primary screen GU Rhodamine qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347160Primary screen NINDS Rhodamine qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1346193Human BCL2, apoptosis regulator (B-cell lymphoma 2 (Bcl-2) protein family)2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
AID1346232Human Bcl-2-like 1 (B-cell lymphoma 2 (Bcl-2) protein family)2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Discovery of an orally bioavailable small molecule inhibitor of prosurvival B-cell lymphoma 2 proteins.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (428)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's0 (0.00)18.2507
2000's13 (3.04)29.6817
2010's286 (66.82)24.3611
2020's129 (30.14)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 55.22

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

MetricThis Compound (vs All)
Research Demand Index55.22 (24.57)
Research Supply Index6.10 (2.92)
Research Growth Index5.97 (4.65)
Search Engine Demand Index88.99 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (55.22)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials15 (3.50%)5.53%
Reviews43 (10.02%)6.00%
Case Studies2 (0.47%)4.05%
Observational0 (0.00%)0.25%
Other369 (86.01%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (44)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Phase I/II Study of Dabrafenib, Trametinib, and Navitoclax in BRAF Mutant Melanoma (Phase I and II) and Other Solid Tumors (Phase I Only) [NCT01989585]Phase 1/Phase 275 participants (Anticipated)Interventional2014-03-24Active, not recruiting
A Phase I Study to Assess the Effect of a CYP3A Inducer (Rifampin) on the Pharmacokinetics of ABT-263 (Navitoclax) [NCT01121133]Phase 112 participants (Actual)Interventional2010-05-31Completed
A Phase I Trial of the Combination of Olaparib and Navitoclax in Women With High Grade Serous Epithelial Ovarian Cancer and Triple Negative Breast Cancer [NCT05358639]Phase 136 participants (Anticipated)Interventional2022-11-09Recruiting
A Phase 1b Study of Mivebresib Alone or in Combination With Ruxolitinib or Navitoclax in Subjects With Myelofibrosis [NCT04480086]Phase 11 participants (Actual)Interventional2021-03-17Terminated(stopped due to Strategic considerations)
A Phase 1 Dose Escalation, Open-Label Study of Venetoclax in Combination With Navitoclax and Chemotherapy in Subjects With Relapsed/Refractory Acute Lymphoblastic Leukemia or Relapsed/Refractory Lymphoblastic Lymphoma [NCT03181126]Phase 169 participants (Actual)Interventional2017-11-27Completed
A Phase 1 Study of Triplet Therapy With Navitoclax, Venetoclax, and Decitabine for High-risk Myeloid Malignancies [NCT05455294]Phase 136 participants (Anticipated)Interventional2022-07-18Recruiting
A Phase 2 Open-Label Study Evaluating Tolerability and Efficacy of Navitoclax Alone or in Combination With Ruxolitinib in Subjects With Myelofibrosis (REFINE) [NCT03222609]Phase 2191 participants (Actual)Interventional2017-10-31Active, not recruiting
An Extension Study of Navitoclax (ABT-263) in Subjects With Chronic Lymphocytic Leukemia (CLL) [NCT01557777]Phase 217 participants (Actual)Interventional2012-06-30Completed
A Phase 1/2a Study Evaluating the Safety, Pharmacokinetics and Efficacy of ABT-263 in Subjects With Relapsed or Refractory Lymphoid Malignancies [NCT00406809]Phase 1/Phase 281 participants (Actual)Interventional2006-11-30Completed
A Phase II Study of Genetically Risk-Stratified Combination of Venetoclax, Ibrutinib and Rituximab (With and Without Navitoclax) in Patients With Relapsed and Refractory Mantle Cell Lymphoma (AIM2) [NCT05864742]Phase 240 participants (Anticipated)Interventional2023-09-07Recruiting
A Phase 1/2a Study Evaluating the Safety, Pharmacokinetics, and Efficacy of ABT-263 in Subjects With Small Cell Lung Cancer or Other Non-Hematological Malignancies [NCT00445198]Phase 1/Phase 286 participants (Actual)Interventional2007-04-30Completed
A Phase 2b Monotherapy Study of ABT-263 in Subjects With Relapsed or Refractory B-Cell Chronic Lymphocytic Leukemia [NCT00918450]Phase 2150 participants (Anticipated)Interventional2010-03-31Withdrawn(stopped due to Sponsor has decided to not proceed with this study.)
A Phase 1 Safety and Pharmacokinetic Study of ABT-263 in Combination With Paclitaxel in the Treatment of Subjects With Solid Tumors [NCT00891605]Phase 119 participants (Actual)Interventional2009-07-31Completed
A Randomized, Double-Blind, Placebo-Controlled, Phase 3 Study Of Navitoclax In Combination With Ruxolitinib Versus Ruxolitinib In Subjects With Myelofibrosis (TRANSFORM-1) [NCT04472598]Phase 3252 participants (Actual)Interventional2020-09-29Active, not recruiting
A Phase 1 Study Evaluating the Safety of ABT-263 in Combination With Etoposide/Cisplatin in Subjects With Cancer [NCT00878449]Phase 112 participants (Actual)Interventional2009-10-31Completed
A Randomized, Open-Label, Phase 3 Study Evaluating Efficacy and Safety of Navitoclax in Combination With Ruxolitinib Versus Best Available Therapy in Subjects With Relapsed/Refractory Myelofibrosis (TRANSFORM-2) [NCT04468984]Phase 3330 participants (Anticipated)Interventional2020-08-31Recruiting
Venetoclax-Navitoclax With Cladribine-based Salvage Therapy in Patients With Relapsed/Refractory Acute Myeloid Leukemia [NCT06007911]Phase 136 participants (Anticipated)Interventional2024-02-29Not yet recruiting
A Phase 1 Study Evaluating the Relative Oral Bioavailability of New Formulations of ABT-263 in Subjects With Cancer [NCT00982566]Phase 137 participants (Actual)Interventional2009-10-31Completed
A Phase 1 Study Evaluating the Safety of ABT-263 in Combination With Rituximab in Subjects With CD20-positive Lymphoid Malignancies [NCT00788684]Phase 129 participants (Actual)Interventional2009-07-21Active, not recruiting
A Phase Ib Open Label Study of Navitoclax in Combination With Venetoclax + Decitabine in Relapsed/Refractory Acute Myeloid Leukemia Previously Treated With Venetoclax [NCT05222984]Phase 136 participants (Anticipated)Interventional2022-07-29Recruiting
[NCT01053520]Phase 112 participants (Anticipated)Interventional2009-10-31Completed
Expanded Access to Navitoclax [NCT03592576]0 participants Expanded AccessAvailable
A Single Dose Study Evaluating the Oral Bioavailability and Pharmacokinetics of the Capsule Formulation of ABT-263 in Subjects With Cancer [NCT00743028]Phase 136 participants (Actual)Interventional2008-08-31Completed
A Phase 1 Study Evaluating the Safety of ABT-263 in Combination With Either Fludarabine/Cyclophosphamide/Rituximab (FCR) or Bendamustine/Rituximab (BR) in Subjects With Relapsed or Refractory Chronic Lymphocytic Leukemia [NCT00868413]Phase 132 participants (Actual)Interventional2009-11-30Completed
A Phase 1 Safety and Pharmacokinetic Study of ABT-263 in Combination With Gemzar® (Gemcitabine) in the Treatment of Subjects With Solid Tumors [NCT00887757]Phase 146 participants (Actual)Interventional2009-09-30Completed
A Study of ABT-263 as Single Agent in Women With Platinum Resistant/Refractory Recurrent Ovarian Cancer [NCT02591095]Phase 247 participants (Actual)Interventional2016-01-31Completed
A Phase 1 Study Evaluating the Safety and Pharmacokinetics of ABT-263 in Combination With Erlotinib and ABT-263 in Combination With Irinotecan, and Evaluating the Safety of ABT-263 Monotherapy in Subjects With Cancer [NCT01009073]Phase 151 participants (Actual)Interventional2009-10-31Completed
A Phase 1 Study to Assess the Effect of Ketoconazole on the Pharmacokinetics of ABT-263 (Navitoclax) [NCT01021358]Phase 112 participants (Anticipated)Interventional2010-01-31Completed
A Phase II, Multicenter, Randomized, Controlled, Open-label Study of the Safety, Efficacy and Pharmacokinetics of ABT-263 in Combination With Dose-intensive Rituximab, or Dose-intensive Rituximab Alone, in Previously Untreated Patients With B-Cell, Chroni [NCT01087151]Phase 2118 participants (Actual)Interventional2010-08-31Completed
A Phase 1 Safety and Pharmacokinetic Study of ABT-263 in Combination With Taxotere® (Docetaxel) in the Treatment of Subjects With Solid Tumors [NCT00888108]Phase 141 participants (Actual)Interventional2009-07-31Completed
Intermediate Size Expanded Access Program of Venetoclax (ABT-199) in Combination With Navitoclax (ABT-263) for Pediatric Patients With Relapsed or Refractory Acute Lymphocytic Leukemia (ALL) or Lymphoblastic Lymphoma (LL) [NCT05215405]0 participants Expanded AccessAvailable
A Phase II, Multicenter, Randomized, Controlled, Open-Label Study of Bendamustine + Rituximab With or Without Navitoclax in Patients With Relapsed Diffuse Large B-Cell Lymphoma [NCT01423539]Phase 20 participants (Actual)Interventional2011-10-31Withdrawn(stopped due to The NAVIGATE study has been terminated due to non-safety related reasons.)
A Phase 1 Open-Label Study Evaluating the Safety and Tolerability, and Pharmacokinetics of Navitoclax Monotherapy and in Combination With Ruxolitinib in Myeloproliferative Neoplasm Subjects [NCT04041050]Phase 185 participants (Actual)Interventional2019-11-08Active, not recruiting
Phase 1/2 Study of Navitoclax Plus Vistusertib in Patients With Relapsed Small Cell Lung Cancer (SCLC) and Other Solid Tumors [NCT03366103]Phase 1/Phase 215 participants (Actual)Interventional2018-03-20Terminated(stopped due to Drug supply issues)
International Proof of Concept Therapeutic Stratification Trial of Molecular Anomalies in Relapsed or Refractory HEMatological Malignancies in Children, Subprotocol A: Decitabine / Venetoclax and Navitoclax in Pediatric Patients With Relapsed or Refractor [NCT05740449]Phase 1/Phase 226 participants (Anticipated)Interventional2023-10-01Not yet recruiting
A Phase II Study of ABT-263/Abiraterone (Arm A) or ABT-263/Abiraterone and Hydroxychloroquine (Arm B) in Patients With Metastatic Castrate Refractory Prostate Cancer (CRPC) and Progression Following Chemotherapy and Abiraterone [NCT01828476]Phase 213 participants (Actual)Interventional2013-06-30Terminated(stopped due to The Investigator left the organization.)
A Phase 1/2a Study Evaluating the Safety, Pharmacokinetics, and Efficacy of ABT-263 in Subjects With Relapsed or Refractory Chronic Lymphocytic Leukemia [NCT00481091]Phase 1/Phase 260 participants (Actual)Interventional2007-07-25Completed
An Open Label, Two-Part, Phase Ib/II Study to Investigate the Safety, Pharmacokinetics, Pharmacodynamics, and Clinical Activity of the MEK Inhibitor Trametinib and the BCL2-Family Inhibitor Navitoclax (ABT-263) in Combination in Subjects With KRAS or NRAS [NCT02079740]Phase 1/Phase 2130 participants (Anticipated)Interventional2014-03-26Active, not recruiting
A Phase I Trial of ABT-263 (Navitoclax), a Bcl-2 Inhibitor, and Sorafenib (Nexavar) in Patients With Relapsed or Refractory Solid Organ Tumors [NCT02143401]Phase 129 participants (Actual)Interventional2014-11-07Active, not recruiting
RAVEN: A Phase I/II Trial Treating Relapsed Acute Lymphoblastic Leukemia With Venetoclax and Navitoclax [NCT05192889]Phase 1/Phase 290 participants (Anticipated)Interventional2022-08-25Recruiting
A Phase 1b-2 Trial to Assess the Safety and Efficacy of a Venetoclax and Navitoclax Consolidation in High-risk Patients With T- Cell Acute Lymphoblastic Leukemia Prior to Allogeneic Transplantation Followed by Venetoclax and Navitoclax Post-transplant Mai [NCT05054465]Phase 1/Phase 248 participants (Anticipated)Interventional2021-10-01Not yet recruiting
A Phase 1b Study Of ABBV-744 Alone Or In Combination With Ruxolitinib Or Navitoclax In Subjects With Myelofibrosis [NCT04454658]Phase 121 participants (Actual)Interventional2020-11-11Active, not recruiting
A Phase 1B Study of AZD9291 in Combination With Navitoclax in EGFR-Mutant Non-Small Cell Lung Cancer Following Resistance to Initial EGFR Kinase Inhibitor [NCT02520778]Phase 150 participants (Anticipated)Interventional2016-08-30Active, not recruiting
A Phase Ib/II Study Evaluating Navitoclax After Failure of Hypomethylating Agent and Venetoclax for Treatment of Relapsed or Refractory High-Risk Myelodysplastic Syndrome [NCT05564650]Phase 1/Phase 237 participants (Anticipated)Interventional2023-01-12Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00481091 (15) [back to overview]Phase 1: Maximum Tolerated Dose (MTD) in the Dose Escalation Phase
NCT00481091 (15) [back to overview]Phase 1: Number of Participants With DLTs in the Dose Escalation Phase
NCT00481091 (15) [back to overview]Phase 1: Recommended Phase 2 Dose (RPTD) Determined in the Dose Escalation Phase
NCT00481091 (15) [back to overview]Phase 1: Terminal Phase Elimination Half-life (t1/2) of Navitoclax
NCT00481091 (15) [back to overview]Phase 1: Terminal Phase Elimination Rate Constant (β) for Navitoclax
NCT00481091 (15) [back to overview]Phase 1: Area Under the Plasma Concentration-Time Curve From Time 0 to Hour 24 (AUC24)
NCT00481091 (15) [back to overview]Phase 1: Area Under the Plasma Concentration-Time Curve From Time 0 to Hour 8 (AUC8)
NCT00481091 (15) [back to overview]Phase 1: AUC24/Dose
NCT00481091 (15) [back to overview]Phase 1: AUC8/Dose
NCT00481091 (15) [back to overview]Phase 1: Cmax/Dose
NCT00481091 (15) [back to overview]Phase 1: Maximum Observed Plasma Concentration (Cmax)
NCT00481091 (15) [back to overview]Phase 1: Number of Participants With Treatment Emergent Adverse Events (TEAEs), Serious Adverse Events (SAEs), and Discontinuations Due to Adverse Events (AEs)
NCT00481091 (15) [back to overview]Phase 1: Time to Maximum Observed Plasma Concentration (Tmax) of Navitoclax
NCT00481091 (15) [back to overview]Phase 2: Dose-Normalized Plasma Concentrations After Navitoclax Once Daily Dosing
NCT00481091 (15) [back to overview]Phase 2: Number of Participants With TEAEs, SAEs, and Discontinuations Due to AEs
NCT01828476 (8) [back to overview]Bcl-2 Family Protein Expression (Bcl-2, Bcl-XL, MCL-1) in Paraffin Blocks When Available by Immunohistochemistry
NCT01828476 (8) [back to overview]Biochemical Response to ABT-263 and Abiraterone and to ABT-263 in Combination With Hydroxychloroquine and Abiraterone in Patients That Are Progressing on Abiraterone
NCT01828476 (8) [back to overview]Biomarkers of Autophagy Modulation by EM; and LC3, and/or p62 by Immunoblotting in PBMC and Tumor Tissue When Available
NCT01828476 (8) [back to overview]Circulating Tumor Cells Pre-enrollment and During Therapy
NCT01828476 (8) [back to overview]Measurable Tumor Response in Patients With Measurable Disease
NCT01828476 (8) [back to overview]Overall Survival
NCT01828476 (8) [back to overview]Progression Free Survival
NCT01828476 (8) [back to overview]Time to PSA Progression
NCT03366103 (6) [back to overview]Disease Control Rate (Phase II)
NCT03366103 (6) [back to overview]Overall Survival (OS) at Year 1 (Phase II)
NCT03366103 (6) [back to overview]Progression Free Survival (PFS) (Phase II)
NCT03366103 (6) [back to overview]Number of Participants Experiencing Adverse Events by Grade (Phase II)
NCT03366103 (6) [back to overview]Occurrence of a Bi-directional Pharmacokinetic (PK) Interaction
NCT03366103 (6) [back to overview]Occurrence of a Bi-directional Pharmacokinetic (PK) Interaction

Phase 1: Maximum Tolerated Dose (MTD) in the Dose Escalation Phase

The MTD was defined as the dose at which 30% of participants experienced a DLT during the first cycle. DLTs were graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) version 3.0 (grade 1=mild; grade 2=moderate; grade 3=severe; grade 4=life threatening; grade 5=death). Any of the following events, considered possibly or probably related to the administration of navitoclax, were considered a DLT: Grade 4 thrombocytopenia (< 25,000/mm^3); platelet counts < 25,000/mm^3, Grade 2 or higher bleeding associated with thrombocytopenia; all other Grade 3, 4 or 5 adverse events were considered a DLT. Exceptions included: Grade 3, 4 febrile neutropenia less than 7 days; Grade 3, 4 leukopenia; Grade 3, 4 lymphopenia; Grade 3 nausea, vomiting and/or diarrhea unless unresponsive to treatment; Grade 2 toxicity that requires dose modification or delay of > 1 week. (NCT00481091)
Timeframe: Cycle 1 (Up to 21 days) plus 7 days

Interventionmg (Number)
Participants Receiving 14/21-Day Dosing Schedule in Phase 1200
Participants Receiving 21/21-Day Dosing Schedule in Phase 1250

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Phase 1: Number of Participants With DLTs in the Dose Escalation Phase

DLTs were graded according to NCI CTCAE version 3.0 (grade 1=mild; grade 2=moderate; grade 3=severe; grade 4=life threatening; grade 5=death). Any of the following events, considered possibly or probably related to the administration of navitoclax, were considered a DLT: Grade 4 thrombocytopenia (< 25,000/mm^3); platelet counts < 25,000/mm^3, Grade 2 or higher bleeding associated with thrombocytopenia; all other Grade 3, 4 or 5 adverse events were considered a DLT. Exceptions included: Grade 3, 4 febrile neutropenia less than 7 days; Grade 3, 4 leukopenia; Grade 3, 4 lymphopenia; Grade 3 nausea, vomiting and/or diarrhea unless unresponsive to treatment; Grade 2 toxicity that requires dose modification or delay of > 1 week. (NCT00481091)
Timeframe: Cycle 1 (Up to 21 days) plus 7 days

InterventionParticipants (Count of Participants)
Navitoclax 14/21 Day Cycle: 10 mg0
Navitoclax 14/21 Day Cycle: 110 mg1
Navitoclax 14/21 Day Cycle: 200 mg0
Navitoclax 14/21 Day Cycle: 250 mg2
Navitoclax 21/21 Day Cycle: 125 mg0
Navitoclax 21/21 Day Cycle: 200 mg1
Navitoclax 21/21 Day Cycle: 250 mg1
Navitoclax 21/21 Day Cycle: 300 mg1

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Phase 1: Area Under the Plasma Concentration-Time Curve From Time 0 to Hour 24 (AUC24)

The AUC24 was derived and reported from Cycle 1 Day 1 values and Cycle 1 Day 14 values; the pre-dose value taken on Day 14 was utilized as 24-hour timepoint on Day 14 to generate AUC24 for Day 14. (NCT00481091)
Timeframe: Cycle 1 Day 1: pre-dose, 2, 4, 6, 8, and 24 hours post-dose; Cycle 1 Days 14: pre-dose, 2, 4, 6, 8

,,,,,,,
Interventionμg•hr/mL (Mean)
Cycle 1 Day 1Cycle 1 Day 14
Navitoclax 14/21 Day Cycle: 10 mg2.75.5
Navitoclax 14/21 Day Cycle: 110 mg15.030.9
Navitoclax 14/21 Day Cycle: 200 mg34.068.7
Navitoclax 14/21 Day Cycle: 250 mg67.850.6
Navitoclax 21/21 Day Cycle: 125 mg37.543.5
Navitoclax 21/21 Day Cycle: 200 mg44.056.2
Navitoclax 21/21 Day Cycle: 250 mg49.572.7
Navitoclax 21/21 Day Cycle: 300 mg52.964.8

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Phase 1: Area Under the Plasma Concentration-Time Curve From Time 0 to Hour 8 (AUC8)

(NCT00481091)
Timeframe: Cycle 1 Days 1 and 14: pre-dose, 2, 4, 6, 8 hours post-dose

,,,,,,,
Interventionμg•hr/mL (Mean)
Cycle 1 Day 1Cycle 1 Day 14
Navitoclax 14/21 Day Cycle: 10 mg1.02.2
Navitoclax 14/21 Day Cycle: 110 mg5.711.1
Navitoclax 14/21 Day Cycle: 200 mg10.624.2
Navitoclax 14/21 Day Cycle: 250 mg19.817.8
Navitoclax 21/21 Day Cycle: 125 mg12.015.7
Navitoclax 21/21 Day Cycle: 200 mg12.318.4
Navitoclax 21/21 Day Cycle: 250 mg12.024.4
Navitoclax 21/21 Day Cycle: 300 mg14.321.6

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Phase 1: AUC24/Dose

The AUC24 was derived and reported from Cycle 1 Day 1 values and Cycle 1 Day 14 values; the pre-dose value taken on Day 14 was utilized as 24-hour timepoint on Day 14 to generate AUC24 for Day 14. (NCT00481091)
Timeframe: Cycle 1 Day 1: pre-dose, 2, 4, 6, 8, and 24 hours post-dose; Cycle 1 Days 14: pre-dose, 2, 4, 6, 8

,,,,,,,
Interventionng•hr/mL/mg (Mean)
Cycle 1 Day 1Cycle 1 Day 14
Navitoclax 14/21 Day Cycle: 10 mg268546
Navitoclax 14/21 Day Cycle: 110 mg136281
Navitoclax 14/21 Day Cycle: 200 mg170344
Navitoclax 14/21 Day Cycle: 250 mg271202
Navitoclax 21/21 Day Cycle: 125 mg300348
Navitoclax 21/21 Day Cycle: 200 mg220281
Navitoclax 21/21 Day Cycle: 250 mg198291
Navitoclax 21/21 Day Cycle: 300 mg176216.0

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Phase 1: AUC8/Dose

(NCT00481091)
Timeframe: Cycle 1 Days 1 and 14: pre-dose, 2, 4, 6, 8 hours post-dose

,,,,,,,
Interventionng•hr/mL/mg (Mean)
Cycle 1 Day 1Cycle 1 Day 14
Navitoclax 14/21 Day Cycle: 10 mg99.9215.0
Navitoclax 14/21 Day Cycle: 110 mg52.0101.0
Navitoclax 14/21 Day Cycle: 200 mg53.1121.0
Navitoclax 14/21 Day Cycle: 250 mg79.271.3
Navitoclax 21/21 Day Cycle: 125 mg95.8125.0
Navitoclax 21/21 Day Cycle: 200 mg61.392.1
Navitoclax 21/21 Day Cycle: 250 mg47.997.7
Navitoclax 21/21 Day Cycle: 300 mg47.672.0

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Phase 1: Cmax/Dose

(NCT00481091)
Timeframe: Cycle 1 Days 1 and 14: pre-dose, 2, 4, 6, 8 hours post-dose

,,,,,,,
Interventionng/mL/mg (Mean)
Cycle 1 Day 1Cycle 1 Day 14
Navitoclax 14/21 Day Cycle: 10 mg24.542.3
Navitoclax 14/21 Day Cycle: 110 mg10.717.0
Navitoclax 14/21 Day Cycle: 200 mg13.022.2
Navitoclax 14/21 Day Cycle: 250 mg20.812.8
Navitoclax 21/21 Day Cycle: 125 mg17.921.4
Navitoclax 21/21 Day Cycle: 200 mg13.717.3
Navitoclax 21/21 Day Cycle: 250 mg10.415.0
Navitoclax 21/21 Day Cycle: 300 mg11.010.4

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Phase 1: Maximum Observed Plasma Concentration (Cmax)

(NCT00481091)
Timeframe: Cycle 1 Days 1 and 14: pre-dose, 2, 4, 6, 8 hours post-dose

,,,,,,,
Interventionμg/mL (Mean)
Cycle 1 Day 1Cycle 1 Day 14
Navitoclax 14/21 Day Cycle: 10 mg0.250.42
Navitoclax 14/21 Day Cycle: 110 mg1.191.87
Navitoclax 14/21 Day Cycle: 200 mg2.604.44
Navitoclax 14/21 Day Cycle: 250 mg5.193.21
Navitoclax 21/21 Day Cycle: 125 mg2.242.68
Navitoclax 21/21 Day Cycle: 200 mg2.733.46
Navitoclax 21/21 Day Cycle: 250 mg2.593.74
Navitoclax 21/21 Day Cycle: 300 mg3.303.11

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Phase 1: Number of Participants With Treatment Emergent Adverse Events (TEAEs), Serious Adverse Events (SAEs), and Discontinuations Due to Adverse Events (AEs)

An AE is defined as any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product and which does not necessarily have a causal relationship with this treatment. An SAE is one that: results in death, hospitalization, prolongation of hospitalization, or persistent or significant disability/incapacity; is life-threatening, a congenital anomaly, or other important medical event. Events were graded as 1=mild, 2=moderate, 3=severe, 4=life-threatening, or 5=death. The investigator assessed the relationship of each event to the use of study drug as either probably related, possibly related, probably not related or not related. A treatment-emergent adverse event is defined as any adverse event with onset or worsening reported by a subject from the time that the first dose of study drug is administered until 30 days have elapsed following discontinuation of study drug administration. Deaths category included non treatment emergent deaths. (NCT00481091)
Timeframe: From first dose of study drug to 30 days post-last dose. Participants enrolled in the 14/21-day cycle received a mean of 21.7 treatment cycles; participants enrolled in the 21/21-day cycle received a mean of 19.4 treatment cycles.

,,,,,,,
InterventionParticipants (Count of Participants)
Any AEAny AE at least possibly related to navitoclaxAny AE with NCI CTCAE Grade ≥ 3Any AE with NCI CTCAE Grade 3 or 4Any SAEAny AE leading to navitoclax discontinuationAny AE leading to navitoclax dose reductionAny AE leading to navitoclax interruptionAny AE leading to dose delayAny dose limiting toxicity (DLT)Any fatal AEDeaths
Navitoclax 14/21 Day Cycle: 10 mg332221002000
Navitoclax 14/21 Day Cycle: 110 mg644442143211
Navitoclax 14/21 Day Cycle: 200 mg333320131000
Navitoclax 14/21 Day Cycle: 250 mg332221222200
Navitoclax 21/21 Day Cycle: 125 mg332222010011
Navitoclax 21/21 Day Cycle: 200 mg444441140200
Navitoclax 21/21 Day Cycle: 250 mg333322230200
Navitoclax 21/21 Day Cycle: 300 mg444431042200

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Phase 2: Number of Participants With TEAEs, SAEs, and Discontinuations Due to AEs

An AE is defined as any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product and which does not necessarily have a causal relationship with this treatment. An SAE is one that: results in death, hospitalization, prolongation of hospitalization, or persistent or significant disability/incapacity; is life-threatening, a congenital anomaly, or other important medical event. Events were graded as 1=mild, 2=moderate, 3=severe, 4=life-threatening, or 5=death. The investigator assessed the relationship of each event to the use of study drug as either probably related, possibly related, probably not related or not related. A treatment-emergent adverse event is defined as any adverse event with onset or worsening reported by a subject from the time that the first dose of study drug is administered until 30 days have elapsed following discontinuation of study drug administration. Deaths category included non treatment emergent deaths. (NCT00481091)
Timeframe: From first dose of study drug to 30 days post-last dose. Participants enrolled in Phase 2 received a mean of 15.6 treatment cycles.

,
InterventionParticipants (Count of Participants)
Any AEAny AE at least possibly related to navitoclaxAny AE with NCI CTCAE Grade ≥ 3Any AE with NCI CTCAE Grade 3 or 4Any SAEAny AE leading to navitoclax discontinuationAny AE leading to navitoclax dose reductionAny AE leading to navitoclax interruptionAny AE leading to navitoclax dose delayAny fatal AEDeaths
Phase 2: Navitoclax 100 mg44331112201
Phase 2: Navitoclax 250 mg272623231291016518

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Bcl-2 Family Protein Expression (Bcl-2, Bcl-XL, MCL-1) in Paraffin Blocks When Available by Immunohistochemistry

(NCT01828476)
Timeframe: 5 years

Intervention ()
ARM A0
ARM B0

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Biochemical Response to ABT-263 and Abiraterone and to ABT-263 in Combination With Hydroxychloroquine and Abiraterone in Patients That Are Progressing on Abiraterone

"Characterize biochemical response to ABT-263 and Abiraterone and to ABT-263 in combination with hydroxychloroquine and Abiraterone by looking at PSA levels." (NCT01828476)
Timeframe: 5 years

InterventionParticipants (Count of Participants)
ARM A0

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Biomarkers of Autophagy Modulation by EM; and LC3, and/or p62 by Immunoblotting in PBMC and Tumor Tissue When Available

(NCT01828476)
Timeframe: 5 years

Intervention ()
ARM A0
ARM B0

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Circulating Tumor Cells Pre-enrollment and During Therapy

(NCT01828476)
Timeframe: 5 years

Intervention ()
ARM A0
ARM B0

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Measurable Tumor Response in Patients With Measurable Disease

(NCT01828476)
Timeframe: 5 years

Intervention ()
ARM A0
ARM B0

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Overall Survival

(NCT01828476)
Timeframe: 5 years

Intervention ()
ARM A0
ARM B0

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Progression Free Survival

(NCT01828476)
Timeframe: 5 years

Intervention ()
ARM A - Dose Escalation0
ARM B - Dose Escalation0

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Time to PSA Progression

(NCT01828476)
Timeframe: 5 years

Intervention ()
ARM A0
ARM B0

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Disease Control Rate (Phase II)

Based on RECIST 1.1. The proportion of patients achieving disease control will be reported with exact 95% binomial confidence intervals. (NCT03366103)
Timeframe: Up to 1.5 years

InterventionParticipants (Count of Participants)
Phase 20

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Overall Survival (OS) at Year 1 (Phase II)

Standard life table methods will be used to analyze OS. We will report the one-year and median OS with 95% confidence intervals. (NCT03366103)
Timeframe: At Year 1

InterventionParticipants (Count of Participants)
Phase 20

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Progression Free Survival (PFS) (Phase II)

Based on RECIST 1.1. Standard life table methods will be used to analyze PFS. We will report the one-year and median PFS with 95% confidence intervals. (NCT03366103)
Timeframe: Up to 1.5 years

InterventionParticipants (Count of Participants)
Phase 20

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Number of Participants Experiencing Adverse Events by Grade (Phase II)

Graded by NCI CTCAE v 4.0. The number of participants with toxicities by grade in the phase 2 study will be reported with exact binomial 95% confidence intervals. (NCT03366103)
Timeframe: Up to 1.5 years

Interventionparticipants (Number)
Grade 1 Adverse EventsGrade 2 Adverse EventsGrade 3 Adverse EventsGrade 4 Adverse EventsGrade 5 Adverse Events
Phase 211000

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Occurrence of a Bi-directional Pharmacokinetic (PK) Interaction

Concentrations of each study agent present in the blood at the specified time point are reported for each study agent. (NCT03366103)
Timeframe: Through Day 15

Interventionng/ml (Mean)
Navitoclax average of individual steady-state trough concentration (avg Cmin,ss)Navitoclax Cycle 1 Day 15 Concentration 6 hours after dose (C6h)Navitoclax Cycle 1 Day 15 maximum concentration (Cmax)Vistusertib average of individual steady-state trough concentration (avg Cmin,ss)Vistusertib Cycle 1 Day 15 Concentration 2 hours after dose (C2h)
Navitoclax 250 mg Reduced to 150 mg + Vistusertib 35 mg228334503910238.5273

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Occurrence of a Bi-directional Pharmacokinetic (PK) Interaction

Concentrations of each study agent present in the blood at the specified time point are reported for each study agent. (NCT03366103)
Timeframe: Through Day 15

,
Interventionng/ml (Mean)
Navitoclax average of individual steady-state trough concentration (avg Cmin,ss)Navitoclax Cycle 1 Day 1 Concentration 6 hours after dose (C6h)Navitoclax Cycle 1 Day 15 Concentration 6 hours after dose (C6h)Navitoclax Cycle 1 Day 15 maximum concentration (Cmax)Vistusertib average of individual steady-state trough concentration (avg Cmin,ss)Vistusertib Cycle 1 Day 1 Concentration 2 hours after dose (C2h)Vistusertib Cycle 1 Day 15 Concentration 2 hours after dose (C2h)
Navitoclax 150 mg + Vistusertib 35 mg11451808226023932113721061
Navitoclax 250 mg + Vistusertib 35 mg19663254283030605594191032

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