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CAS#: 1257044-40-8

Description: Venetoclax, also known as ABT-199 or GDC0199, is an orally bioavailable, selective small molecule inhibitor of the anti-apoptotic protein Bcl-2, with potential antineoplastic activity. Venetoclax mimics BH3-only proteins, the native ligands of Bcl-2 and apoptosis activators, by binding to the hydrophobic groove of Bcl-2 proteins thereby repressing Bcl-2 activity and restoring apoptotic processes in tumor cells.

ynonym: ABT199; ABT-199; ABT 199; GDC0199; GDC0199; GDC 0199; RG7601; RG7601; RG 7601. Venetoclax.

IUPAC/Chemical Name: 4-(4-{[2-(4-chlorophenyl)-4,4-dimethylcyclohex-1-en-1-yl]methyl}piperazin-1-yl)-N-({3-nitro-4-[(tetrahydro-2H-pyran-4-ylmethyl)amino]phenyl}sulfonyl)-2-(1H-pyrrolo[2,3-b]pyridin-5-yloxy)benzamide


Name: Venetoclax (ABT199)
CAS#: 1257044-40-8
Chemical Formula: C45H50ClN7O7S
Exact Mass: 867.3181
Molecular Weight: 868.44
Elemental Analysis: C, 62.24; H, 5.80; Cl, 4.08; N, 11.29; O, 12.90; S, 3.69


Yellow solid powder
>98% (or refer to the Certificate of Analysis)
Shipping Condition:
Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.
Storage Condition:
Dry, dark and at 0 – 4 C for short term (days to weeks) or -20 C for long term (months to years).
Soluble in DMSO, not in water
Shelf Life:
>2 years if stored properly
Drug Formulation:
This drug may be formulated in DMSO
Stock Solution Storage:
0 – 4 C for short term (days to weeks), or -20 C for long term (months).


GDC-0199 (RG7601) is a novel small molecule Bcl-2 selective inhibitor designed to restore apoptosis, also known as programmed cell death, by blocking the function of a pro-survival Bcl-2 family protein. The Bcl-2 family proteins, which are expressed at high levels in many tumors, play a central role in regulating apoptosis and, consequently, are thought to impact tumor formation, tumor growth and resistance.


1: Seymour J. ABT-199 for Chronic Lymphocytic Leukemia. Clin Adv Hematol Oncol. 2014 Oct;12(10):698-700. PubMed PMID: 25658896.

2: Choudhary GS, Al-Harbi S, Mazumder S, Hill BT, Smith MR, Bodo J, Hsi ED, Almasan A. MCL-1 and BCL-xL-dependent resistance to the BCL-2 inhibitor ABT-199 can be overcome by preventing PI3K/AKT/mTOR activation in lymphoid malignancies. Cell Death Dis. 2015 Jan 15;6:e1593. doi: 10.1038/cddis.2014.525. PubMed PMID: 25590803.

3: Cao Y, Yang G, Hunter ZR, Liu X, Xu L, Chen J, Tsakmaklis N, Hatjiharissi E, Kanan S, Davids MS, Castillo JJ, Treon SP. The BCL2 antagonist ABT-199 triggers apoptosis, and augments ibrutinib and idelalisib mediated cytotoxicity in CXCR4(Wild-type) and CXCR4(WHIM) mutated Waldenstrom macroglobulinaemia cells. Br J Haematol. 2015 Jan 12. doi: 10.1111/bjh.13278. [Epub ahead of print] PubMed PMID: 25582069.

4: Johnson-Farley N, Veliz J, Bhagavathi S, Bertino JR. ABT-199, a BH3 mimetic that specifically targets Bcl-2, enhances the antitumor activity of chemotherapy, bortezomib and JQ1 in “double hit” lymphoma cells. Leuk Lymphoma. 2015 Jan 28:1-7. [Epub ahead of print] PubMed PMID: 25373508.

5: Ko TK, Chuah CT, Huang JW, Ng KP, Ong ST. The BCL2 inhibitor ABT-199 significantly enhances imatinib-induced cell death in chronic myeloid leukemia progenitors. Oncotarget. 2014 Oct 15;5(19):9033-8. PubMed PMID: 25333252; PubMed Central PMCID: PMC4253416.

6: Peirs S, Matthijssens F, Goossens S, Van de Walle I, Ruggero K, de Bock CE, Degryse S, Canté-Barrett K, Briot D, Clappier E, Lammens T, De Moerloose B, Benoit Y, Poppe B, Meijerink JP, Cools J, Soulier J, Rabbitts TH, Taghon T, Speleman F, Van Vlierberghe P. 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. doi: 10.1182/blood-2014-05-574566. Epub 2014 Oct 9. PubMed PMID: 25301704.

7: Zhao X, Bodo J, Sun D, Durkin L, Lin J, Smith MR, Hsi ED. Combination of ibrutinib with ABT-199: synergistic effects on proliferation inhibition and apoptosis in mantle cell lymphoma cells through perturbation of BTK, AKT and BCL2 pathways. Br J Haematol. 2015 Mar;168(5):765-8. doi: 10.1111/bjh.13149. Epub 2014 Oct 4. PubMed PMID: 25284608.

8: ABT-199 shows effectiveness in CLL. Cancer Discov. 2014 Sep;4(9):OF7. doi: 10.1158/2159-8290.CD-NB2014-102. Epub 2014 Jul 3. PubMed PMID: 25185206.

9: Chonghaile TN, Roderick JE, Glenfield C, Ryan J, Sallan SE, Silverman LB, Loh ML, Hunger SP, Wood B, DeAngelo DJ, Stone R, Harris M, Gutierrez A, Kelliher MA, Letai A. Maturation stage of T-cell acute lymphoblastic leukemia determines BCL-2 versus BCL-XL dependence and sensitivity to ABT-199. Cancer Discov. 2014 Sep;4(9):1074-87. doi: 10.1158/2159-8290.CD-14-0353. Epub 2014 Jul 3. PubMed PMID: 24994123; PubMed Central PMCID: PMC4154982.

10: Wei A. ABT-199 partners with azacitidine to contest myeloid malignancies. Leuk Lymphoma. 2015 Jan;56(1):8-9. doi: 10.3109/10428194.2014.919638. Epub 2014 Jul 15. PubMed PMID: 24794804.

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