ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets

By A. Souers, J. Leverson, E. Boghaert, S. Ackler, Nathaniel D. Catron, Jun Chen, B. Dayton, H. Ding, S. Enschede, W. Fairbrother and 30 more. Nature Medicine, 2013

2,856 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/73cfdbc3c1d81c3a5ae0b5e37bddb59f42525b35

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Citations in the corpus

Phase I First-in-Human Study of Venetoclax in Patients With Relapsed or Refractory Non-Hodgkin Lymphoma. (2017, neutral): “Emergent* Any event 103 (97) 21 (96) 33 (100) 49 (96) 59 (56) 14 (64) 21 (64) 24 (47) Nausea 51 (48) 9 (41) 15 (45) 27 (53) 0 0 0 0 Diarrhea 48 (45) 7 (32) 14 (42) 27 (53) 3 (3) 0 2 (6) 1 (2) Fatigue 44 (42) 10 (45) 9 (27) 25 (49) 7 (7) 2 (9) 2 (6) 3 (6) Decreased appetite 23 (22) 4 (18) 4 (12) 15 (”
Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies (2016, background): “So far, nearly a dozen BH3 mimetics are under investigation as Bcl-2 inhibitors in different phases of human clinical trials such as AT-101 (R-(-)-gossypol) [83,84], ABT199 (venetoclax) [85], ABT-737 [86], ABT-263 (navitoclax, orally available derivative of ABT-737) [87,88], GX15-070 (obatoclax) [89”
An interactive resource to identify cancer genetic and lineage dependencies targeted by small molecules (2013, background): “The same selectivity was not observed for ABT-199, a Bcl-2specific inhibitor (Souers et al., 2013) (data not shown), suggesting that inhibition of other Bcl-2 family members underlies the differential response.”
Bax, Bak and beyond — mitochondrial performance in apoptosis (2018, background): “There is an interest in the mechanism of peptides derived from BH3 domains because they are the basis for the design of BH3 mimetic molecules, which have been recently approved for their use in therapy [2, 83].”
Twenty years on: the impact of fragments on drug discovery (2016, background): “4) gave the BCL-2 selective venetoclax, which gained the FDA’s ‘breakthrough therapy’ designation for recalcitrant chronic lymphocytic leukaemia 95 and was approved in the United States in April 2016.”
Broad targeting of resistance to apoptosis in cancer (2015, background): “[36] Souers AJ, Leverson JD, Boghaert ER, Ackler SL, Catron ND, Chen J, et al.”
Directed elimination of senescent cells by inhibition of BCL-W and BCL-XL (2016, neutral): “27).”
BCL-2 family proteins: changing partners in the dance towards death (2017, background): “Small molecule BH3 mimetics, like ABT-263 (Navitoclax) and ABT-199 (Venetoclax), mimic the binding of BH3 peptides to the hydrophobic BH3 domain-binding groove of anti-apoptotic proteins and thus displace BH3-only proteins and active BAX/BAK from anti-apoptotic proteins.(107,108) By binding to the B”