ABT-263 (Navitoclax)Catalog No. A10022

Quick Overview

ABT-263 also called Navitoclax is a potent and orally bioavailable Bcl-2 family inhibitor (Ki's of <1 nmol/L for Bcl-2, Bcl-xL, and Bcl-w).ABT-263 maintains a high affinity for Bcl-xL, Bcl-2, and Bcl-w, (Ki ≤1 nmol/L), but binds more weakly to Mcl-1 and A1.^[1]

Products are for laboratory research use only. Not for human use. We do not sell to patients.

ABT-263 (Navitoclax) Citations(10)

Momeny M, .et al. The ERBB receptor inhibitor dacomitinib suppresses proliferation and invasion of pancreatic ductal adenocarcinoma cells, Cell Oncol (Dordr), 2019, Apr 25 PMID: 31025257

Anderson R, .et al. Length-independent telomere damage drives postmitotic cardiomyocyte senescence, EMBO J, 2019, Feb 8. pii: e100492 PMID: 30737259

Shinya Ishida, .et al. Mechanisms for mTORC1 activation and synergistic induction of apoptosis by ruxolitinib and BH3 mimetics or autophagy inhibitors in JAK2-V617F-expressing leukemic cells including newly established PVTL-2, Oncotarget, 2018, Jun 1; 9(42): 26834-26851 PMID: 29928488

Rhys Anderson, .et al. Length-independent telomere damage drives cardiomyocyte senescence, bioRxiv, 2018, 2018

Ryuta Mikawa, .et al. Elimination of p19ARF-expressing cells protects against pulmonary emphysema in mice, Aging Cell, 2018, Oct; 17(5): e12827 PMID: 30058137

Joo Sang Lee, .et al. Harnessing synthetic lethality to predict the response to cancer treatment, Nat Commun, 2018, 9: 2546 PMID: 29959327

Toshiyuki Sumi, .et al. Survivin knockdown induces senescence in TTF-1-expressing, KRAS-mutant lung adenocarcinomas, Int J Oncol, 2018, Jul; 53(1): 33-46 PMID: 29658609

Wei TW, .et al. Aurora A and NF-κB Survival Pathway Drive Chemoresistance in Acute Myeloid Leukemia via the TRAF-Interacting Protein TIFA, Cancer Res, 2017, Jan 15;77(2):494-508 PMID: 28069801

Yusuke Takagi, .et al. SPIB is a novel prognostic factor in diffuse large B-cell lymphoma that mediates apoptosis via the PI3K-AKT pathway, Cancer Sci, 2016, Sep; 107(9): 1270-1280 PMID: 27348272

Matsumoto M, .et al. Cisplatin-induced apoptosis in non-small-cell lung cancer cells is dependent on Bax- and Bak-induction pathway and synergistically activated by BH3-mimetic ABT-263 in p53 wild-type and mutant cells, Biochem Biophys Res Commun, 2016, Apr 29;473(2):490-6 PMID: 26996126

Product Information

Catalog Num	A10022
M. Wt	974.6
Formula	C47H55ClF3N5O6S3
Solubility	DMSO
Purity	>98%
Storage	at -20°C 3 years Powder
CAS No.	923564-51-6
Synonyms	ABT263
SMILES Code	CC1(CCC(=C(C1)CN2CCN(CC2)C3=CC=C(C=C3)C(=O)NS(=O)(=O)C4=CC(=C(C=C4)N[[email protected]](CCN5CCOCC5)CSC6=CC=CC=C6)S(=O)(=O)C(F)(F)F)C7=CC=C(C=C7)Cl)C

Biological activity

Introduction

Targets

Bcl-xL (Cell-free assay)	Bcl-2 (Cell-free assay)	Bcl-w (Cell-free assay)	A1 (Cell-free assay)	Mcl-1 (Cell-free assay)
<=0.5 nM(Ki)	<=1 nM(Ki)	<=1 nM(Ki)	354 nM(Ki)	550 nM(Ki)

Solubility

Solubility (25C)*	In vitro	DMSO	100 mg/mL (102.6 mM)
		Water	<1 mg/mL (<1 mM)
		Ethanol	<1 mg/mL (<1 mM)
	* <1 mg/ml means slightly soluble or insoluble. * Please note that Adooq tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Reference

Tse C, et al. ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor. Cancer Res. 2008 May 1;68(9):3421-8. doi: 10.1158/0008-5472.CAN-07-5836.
Chen J, et al. The Bcl-2/Bcl-X(L)/Bcl-w inhibitor, navitoclax, enhances the activity of chemotherapeutic agents in vitro and in vivo. Mol Cancer Ther. 2011 Dec;10(12):2340-9. doi: 10.1158/1535-7163.MCT-11-0415. Epub 2011 Sep 13.
Shoemaker AR, et al. (2008) Activity of the Bcl-2 family inhibitor ABT-263 in a panel of small cell lung cancer xenograft models. Clin Cancer Res 14(11):3268–3277.
Santi Suryani, et al. Cell and molecular determinants of in vivo efficacy of the BH3 mimetic ABT-263 against pediatric acute lymphoblastic leukemia xenografts. Clin Cancer Res. 2014 Sep 1;20(17):4520-31. doi: 10.1158/1078-0432.CCR-14-0259. Epub 2014 Jul 10.

Return Policy

Contact information

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