venetoclax - CAS 1257044-40-8
Catalog number: B0084-462638
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Bcl-2 Family
Venetoclax is a small-molecule inhibitor that has high selectivity for Bcl-2 (Ki < 0.01 nM in cell-free assays) over Mcl-1. It suppresses anti-apoptotic Bcl-2, a protein commonly overexpressed in cancer cells, to induce programmed death of CLL cells. Venetoclax is used as a second-line treatment of chronic lymphocytic leukemia (CLL).
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Catalog Number Size Price Stock Quantity
B0084-462638 500 mg $298 In stock
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Brife Description:
Bcl-2 inhibitor, chronic lymphocytic leukemia (CLL)
ABT199; ABT-199; ABT 199; GDC0199; GDC0199; GDC 0199; RG7601; RG7601; RG 7601. Venetoclax
10mM in DMSO
the treatment of chronic lymphocytic leukemia (CLL)
Shelf Life:
2 years
Canonical SMILES:
Current Developer:
AbbVie; Genentech
1.BCR signaling inhibitors differ in their ability to overcome Mcl-1-mediated resistance of CLL B cells to ABT-199.
Bojarczuk K1, Sasi BK1, Gobessi S1, Innocenti I2, Pozzato G3, Laurenti L2, Efremov DG4. Blood. 2016 Apr 19. pii: blood-2015-10-675009. [Epub ahead of print]
The Bcl-2 antagonist ABT-199 has demonstrated promising clinical activity in patients with CLL. ABT-199 is strongly cytotoxic against unstimulated peripheral blood CLL cellsin vitro, but is much less effective against CLL cells that have received survival signals from the microenvironment. In particular, stimulation of CLL cells with CD40L results in substantial resistance that is mediated by induction of the antiapoptotic Bcl-2 family proteins Bcl-xLand Bfl-1. In the present study we investigated whether resistance to ABT-199 can be conferred by B-cell receptor (BCR) stimulation, which is another important survival signal from the leukemic microenvironment. We show that sustained BCR stimulation results in significant ABT-199-resistance, which correlates with induction of the antiapoptotic protein Mcl-1 and less consistently with downregulation of proapoptotic Bmf, Hrk and BimEL A major role for Mcl-1 in conferring ABT-199 resistance is additionally supported by knockdown and enforced expression experiments with primary CLL cells.
2.Binding of released Bim to Mcl-1 is a mechanism of intrinsic resistance to ABT-199 which can be overcome by combination with daunorubicin or cytarabine in AML cells.
Niu X1, Zhao J2, Ma J1, Xie C3, Edwards H4, Wang G1, Caldwell JT5, Xiang S6, Zhang X7, Chu R8, Wang J9, Lin H10, Taub JW11, Ge Y12. Clin Cancer Res. 2016 Apr 21. pii: clincanres.3057.2015. [Epub ahead of print]
PURPOSE: To investigate the molecular mechanism underlying intrinsic resistance to ABT-199.
3.Complementary dynamic BH3 profiles predict co-operativity between the multi-kinase inhibitor TG02 and the BH3 mimetic ABT-199 in acute myeloid leukaemia cells.
Pallis M1, Burrows F2, Ryan J3, Grundy M1, Seedhouse C4, Abdul-Aziz A4, Montero J3, Letai A3, Russell N1,4. Oncotarget. 2016 Apr 15. doi: 10.18632/oncotarget.8742. [Epub ahead of print]
Direct co-operation between sensitiser molecules BAD and NOXA in mediating apoptosis suggests that therapeutic agents which sensitise to BAD may complement agents which sensitise to NOXA. Dynamic BH3 profiling is a novel methodology that we have applied to the measurement of complementarity between sensitiser BH3 peptide mimetics and therapeutic agents. Using dynamic BH3 profiling, we show that the agent TG02, which downregulates MCL-1, sensitises to the BCL-2-inhibitory BAD-BH3 peptide, whereas the BCL-2 antagonist ABT-199 sensitises to MCL-1 inhibitory NOXA-BH3 peptide in acute myeloid leukaemia (AML) cells. At the concentrations used, the peptides did not trigger mitochondrial outer membrane permeabilisation in their own right, but primed cells to release Cytochrome C in the presence of an appropriate trigger of a complementary pathway. In KG-1a cells TG02 and ABT-199 synergised to induce apoptosis. In heterogeneous AML patient samples we noted a range of sensitivities to the two agents.
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CAS 1257044-40-8 venetoclax

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