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HA14-1 is a cell-permeable inhibitor of Bcl-2 protein (IC50 ~ 9 μM); acts by binding to the surface pocket. Disrupts Bax/Bcl-2 interaction and induces apoptosis of tumor cells. Also binds to the antiapoptotic Blc-2 proteins Bcl-XL and Bcl-w.
|Storage||Desiccate at -20°C|
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.
References are publications that support the biological activity of the product.
Doshi et al (2006) Structure-activity relationship studies of ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (HA 14-1), an antagonist for antiapoptotic Bcl-2 proteins to overcome drug resistance in cancer. J.Med.Chem. 49 7731 PMID: 17181155
Milella et al (2002) Synergistic induction of apoptosis by simultaneous disruption of the Bcl-2 and MEK/MAPK pathways in acute myelogenous leukemia. Blood 99 3461 PMID: 11964319
Wang et al (2000) Structure-based discovery of an organic compound that binds Bcl-2 protein and induces apoptosis of tumor cells. Proc.Natl.Acad.Sci.U.S.A. 97 7124 PMID: 10860979
Keywords: HA14-1, HA14-1 supplier, Bcl-2, inhibitors, inhibits, induces, apoptosis, Bax, Bcl-XL, Mcl-1, Family, bcl2, inhibitor, 1541, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for HA14-1 include:
Qin et al (2010) Coeloglossum viride var. bracteatum extract protects against amyloid toxicity in rat prefrontal cortex neurons. Blood 3 88 PMID: 20369044
Mohan et al (2009) Bcl-2 inhibitor HA14-1 and genistein together adeptly down regulated survival factors and activated cysteine proteases for apoptosis in human malignant neuroblastoma SK-N-BE2 and SH-SY5Y cells. Brain Res 1283 155 PMID: 19505441
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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.
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