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Submit ReviewABT 263
Description: High affinity Bcl-2 family inhibitor; proapoptotic, senolytic and antitumor
Chemical Name: 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
Purity: ≥98% (HPLC)
Biological Activity for ABT 263
ABT 263 is a high affinity inhibitor of Bcl-2 family proteins (Ki values are 0.5 nM, <1 nM and <1 nM in Bcl-xL, Bcl-2 and Bcl-W respectively). ABT 263 induces G1/G0 phase arrest, apoptosis and autophagy in cancer cells in vitro (IC50 = 3.4 - 12 μM). In vivo, ABT 263 displays a synergistic antitumor effect with rituximab and Bortezomib (Cat. No. 7282), Docetaxel (Cat. No. 4056) and Erlotinib (Cat. No. 7194), and inhibits growth of SCLC xenografts when combined with (+)-JQ1 (Cat. No. 4499). ABT 263 also reduces inflammation and viral-induced senescence in SARS-CoV-2 infection in vivo, and clears senescent cells and rejuvenates aging stem cells. Orally bioavailable.
Technical Data for ABT 263
| M. Wt | 974.62 |
| Formula | C47H55ClF3N5O6S3 |
| Storage | Store at -20°C |
| Purity | ≥98% (HPLC) |
| CAS Number | 923564-51-6 |
| PubChem ID | 24978538 |
| InChI Key | JLYAXFNOILIKPP-KXQOOQHDSA-N |
| Smiles | C(C1=C(CCC(C)(C)C1)C2=CC=C(Cl)C=C2)N3CCN(CC3)C4=CC=C(C(NS(=O)(=O)C5=CC(S(C(F)(F)F)(=O)=O)=C(N[C@H](CCN6CCOCC6)CSC7=CC=CC=C7)C=C5)=O)C=C4 |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for ABT 263
| Solvent | Max Conc. mg/mL | Max Conc. mM | |
|---|---|---|---|
| Solubility | |||
| DMSO | 97.46 | 100 |
Preparing Stock Solutions for ABT 263
The following data is based on the product molecular weight 974.62. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
| Concentration / Solvent Volume / Mass | 1 mg | 5 mg | 10 mg |
|---|---|---|---|
| 1 mM | 1.03 mL | 5.13 mL | 10.26 mL |
| 5 mM | 0.21 mL | 1.03 mL | 2.05 mL |
| 10 mM | 0.1 mL | 0.51 mL | 1.03 mL |
| 50 mM | 0.02 mL | 0.1 mL | 0.21 mL |
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Product Datasheets for ABT 263
References for ABT 263
References are publications that support the biological activity of the product.
Chen et al (2011) The Bcl-2/Bcl-X(L)/Bcl-w inhibitor, navitoclax, enhances the activity of chemotherapeutic agents in vitro and in vivo. Mol.Cancer Ther. 10 2340 PMID: 21914853
Wang et al (2017) JQ1 synergizes with the Bcl-2 inhibitor ABT-263 against MYCN-amplified small cell lung cancer. Oncotarget 8 86312 PMID: 29156797
Tse et al (2008) ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor. Cancer Res. 68 3421 PMID: 18451170
Lee et al (2021) Virus-induced senescence is a driver and therapeutic target in COVID-19. Nature 599 283 PMID: 34517409
Chang et al (2016) Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice. Nat.Med. 22 78 PMID: 26657143
If you know of a relevant reference for ABT 263, please let us know.
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Citations for ABT 263
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Parkinson's Disease Poster
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.
Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.
Pathways for ABT 263
