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BMX kinase (also termed ETK) is a member of the TEC family of non-receptor tyrosine kinases (which also includes ITK, TEC, BTK and TXK), and is the major member of this family expressed in epithelial cells, including prostate epithelium. Similar to the SRC family of kinases, the TEC kinases contain core SH3, SH2 and kinase domains, binds to membrane-associated PIPs in a manner similar to Akt.

BMX is further activated by the subsequent phosphorylation of a tyrosine in its kinase domain by membrane-associated SRC. The activation of BMX in response to PI-3K signaling, which is increased in prostate cancer (PCa) due to PTEN loss, suggests a potential role for BMX in PCa. Indeed, BMX expression is increased in PCa, and transgenic over-expression of BMX in mouse prostate epithelium causes hyperplasia and contributes to development of dysplastic lesions resembling human prostate intraepithelial neoplasia (PIN). The irreversible BMX kinase inhibitor, BMX-IN-1, demonstrates antiproliferation efficacy against prostate cancer cells.



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Cat. No. Product Name CAS No. Information



BMX-IN-1 (CAS 1431525-23-3) is a potent, selective, irreversible inhibitor of BMX kinase with IC50 of 8 nM; also inhibits BTK with IC50 of 10.4 nM and displays 47-656-fold less potent for Blk, JAK3, EGFR, Itk, or Tec; inhibits the proliferation of Tel-BMX-transformed Ba/F3 prostate cancer cells with GI50 of 25 nM, exhibits antiproliferative activity in RV-1, DU-145, PC-3, and VCAP prostate cancer cell lines with GI50 of 2-5 uM.

Prostate cancer




1265823-05-9 CTA095 (CTA-095) is a potent Etk (BMX) and Src dual inhibitor with IC50 of 60 and 120 nM, respectively, shows no significant inhibition on Btk and Yes at 10 uM; induces autophagy and apoptosis, as well as synergistic effects with autophagy modulators in prostate cancer cells; inhibits the phosphorylation of Etk, Src and the downstream signals Stat3 and Akt in prostate cancer cells; CTA095nano inhibits PC3 xenograft tumor growth in vivo.


CTN06 is a potent Etk (BMX) and Btk dual inhibitor with IC50 of 200 and 50 nM, respectively; weakly inhibits Itk (IC50=0.5 uM), and shows no inhibition on Src (IC50=5 uM) and Mer (IC50=10 uM); effectively kills PC3 and other prostate cancer cells, induces autophagy as well as apoptosis in prostate cancer cells; inhibits the phosphorylation of Btk, Etk and the downstream signal PLCγ2, Stat3, Akt in prostate cancer cells; inhibits PC3 xenograft tumor growth in vivo.


1808288-51-8 CHMFL-BMX-078 is a highly selective, potent, type II irreversible BMX kinase inhibitor with IC50 of 11 nM; displays a high selectivity profile (S score(1) = 0.01) against the 468 kinases/mutants in the KINOMEscan evaluation and achieved at least 40-fold selectivity over BTK kinase; CHMFL-BMX-078 is a useful pharmacological tool to elucidate the detailed mechanism of BMX mediated signaling pathways.

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