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(WEHI539 hydrochloride; WEHI 539 hydrochloride)
WEHI-539 hydrochloride Chemical Structure
|Product name: WEHI-539 hydrochloride|
|Cat. No.: HY-15607A|
WEHI-539, has high affinity (subnanomolar) and selectivity for BCL-XL and potently kills cells by selectively antagonizing its prosurvival activity. WEHI-539 has a high affinity for BCL-XL (IC50 = 1.1 nM).
IC50 Value: 1.1 nM (BCL-XL) 
Target: Bcl-2 Family
The prosurvival BCL-2 family protein BCL-XL is often overexpressed in solid tumors and renders malignant tumor cells resistant to anticancer therapeutics. The optimized compound,
WEHI-539 interacts with residues in the P4 pocket and adopts a distinct binding mode compared to ABT-737. WEHI-539 induces apoptosis in MEFs only if they lack MCL-1 supports the notion that cell killing induced by WEHI-539 is due to direct inhibition of BCL-XL. Accordingly, restoring expression of MCL-1 in mcl-1 knockout cells renders them highly resistant to WEHI-539. WEHI-539 could only kill cells that contained BAK (Fig. 6b). This observation was confirmed in MEFs where both the amount and activity of MCL-1 were abrogated by expression of its natural and selective BH3-only ligand NOXA. Cytochrome c release and caspase-3 processing confirmed that WEHI-539 induces apoptosis in BAX-deficient MEF cells expressing BIM2A but not in their BAK-deficient counterparts. Remarkably, WEHI-539 efficiently triggered the killing of platelets purified from mice or humans in culture.
|M.Wt||620.18||Storage||Please store the product under the recommended conditions in the Certificate of Analysis.|
|Solvent & Solubility||
10 mM in DMSO
|1 mg||5 mg||10 mg|
|1 mM||1.6124 mL||8.0622 mL||16.1244 mL|
|5 mM||0.3225 mL||1.6124 mL||3.2249 mL|
|10 mM||0.1612 mL||0.8062 mL||1.6124 mL|
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A-1210477 is an inhibitor of MCL-1 (Ki=0.45 nM in TR-FRET-binding assays), is a much weaker binder of BCL-2 (Ki=0.132 (mu)M) and BCL-XL(Ki>0.660 (mu)M).
ABT-199 (GDC-0199) is a Bcl-2-selective inhibitor with Ki of <0.01 nM, >4800-fold more selective versus Bcl-xL and Bcl-w, and no activity to Mcl-1.
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BAM 7 is a direct and selective activator of proapoptotic Bax with EC50 of 3.3 (mu)M.
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HA14-1 is a non-peptidic ligand of a Bcl-2 surface pocket with IC50 of ~9 (mu)M.
Marinopyrrole (Maritoclax) is a novel and specific Mcl-1 inhibitor with an IC50 value of 10.1 uM, >8 fold selectivity than BCL-xl (IC50 > 80 uM).