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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|
((addition))-Apogossypol(Apogossypol; NSC736630) is a potent inhibitor of Bcl-2 family proteins; competing with the BH3 peptide-binding sites on Bcl-2, Bcl-XL, Mcl-1, Bcl-W, and Bcl-B, but not Bfl-1, with IC50s of 0.5 to 2 (mu)M.
A-1155463 is a highly potent and selective BCL-XL inhibitor, A-1155463 shows picomolar binding affinity to BCL-XL (Ki ＜0.01 nM), and >1000-fold weaker binding to BCL-2 (Ki = 80 nM) and related proteins BCL-W (Ki = 19 nM) and MCL-1 (Ki > 440 nM).
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.
ABT-737 is a BH3 mimetic inhibitor of Bcl-xL, Bcl-2 and Bcl-w with EC50 of 78.7 nM, 30.3 nM and 197.8 nM, respectively; no inhibition observed against Mcl-1, Bcl-B or Bfl-1.
BAM 7 is a direct and selective activator of proapoptotic Bax with EC50 of 3.3 (mu)M.
Bax inhibitor peptide V5 is a peptide inhibitor of Bax translocation to mitochondria.
BH3I-1 is an inhibitor of Bcl-xL with IC 50 of 293.95 (mu)M. BH3I-1 is a cell permeable BH3 mimetic that binds to Bcl-xL, BH3I-1 can induce cell death. BH3I-1 is a bak activator.
Gambogic Acid activates caspases with EC50 of 0.78-1.64 (mu)M and competitively inhibits Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1 with IC50 of 1.47, 1.21, 2.02, 0.66, 1.06 and 0.79 (mu)M, respectively.
HA14-1 is a non-peptidic ligand of a Bcl-2 surface pocket with IC50 of ~9 (mu)M.