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Venetoclax; ABT-199; ABT 199; GDC-0199

Quick Overview

CAS No.: 1257044-40-8
Catalog No.: 105148
Purity: 95%
MF: C45H50ClN7O7S
MW: 868.457
Storage: 2-8 degree Celcius
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ABT-199 is a highly potent, selective and orally bioavailable Bcl-2 inhibitor with a Ki of less than 0.01 nM.

IC50 & Target
Ki: <0.01 nM (Bcl-2), 48 nM (Bcl-xl), 245 nM (Bcl-w), >444 nM (Mcl-1)[1]

In Vitro
ABT-199 potently kills FL5.12-BCL-2 cells (EC50=4 nM), ABT-199 shows much weaker activity against FL5.12-BCL-XL cells (EC50=261 nM). ABT-199 also shows selectivity in cellular mammalian two-hybrid assays, where it disrupts BCL-2-BIM complexes (EC50=3 nM) but is much less effective against BCL-XL-BCL-XS (EC50=2.2 μM) or MCL-1-NOXA complexes[1].

In Vivo
After a single oral dose of 12.5 mg per kg body weight in xenografts derived from RS4;11 cells (ALL), ABT-199 causes a maximal tumor growth inhibition (TGImax) of 47% (P<0.001) and tumor growth delay (TGD) of 26% (P<0.05)[1]. Treatment of established xenografted (a mouse xenograft model of the T-ALL cell line LOUCY) tumors with 100 mg ABT-199/kg for 4 days resulted in a significant reduction of leukemic burden (P=0.0048)[2].

[1]. Souers AJ, et al. ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets. Nat Med. 2013 Feb;19(2):202-8.

[2]. Peirs S, et al. ABT-199 mediated inhibition of BCL-2 as a novel therapeutic strategy in T-cell acute lymphoblastic leukemia. Blood. 2014 Dec 11;124(25):3738-47.

[3]. Bi C, et al. Inhibition of 4EBP phosphorylation mediates the cytotoxic effect of mechanistic target of rapamycin kinase inhibitors in aggressive B-cell lymphomas. Haematologica. 2017 Apr;102(4):755-764.
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Memory usage: real: 44826624, emalloc: 43418744
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