bmx kinase

BMX-IN-1 (BMX kinase inhibitor) is a selective inhibitor of bone marrow tyrosine kinase on chromosome X (BMX, IC50 = 8 nM) and the related Bruton’s tyrosine kinase (BTK, IC50 = 10.4 nM), but BMX-IN-1 is more than 47-656 fold less potent against Blk, JAK3, EGFR, Itk, or Tec activity.

Aurora kinase inhibitor-3 (Aurora Kinase Inhibitor III) is a potent inhibitor of Aurora A kinase (IC50 = 42 nM).1 It is selective for Aurora A over BMX, BTK, IGF-1R, c-Src, TRKB, SYK, and EGFR.

CHMFL-BMX-078 is a highly potent and selective type II irreversible inhibitor of BMX kinase, with an IC50 of 11 nM.

BTK-IN-22, a BTK inhibitor (IC 50: 0.9 nM), also exhibits inhibition against BLX and BMX with IC 50 values of 1.4 and 1.2 nM, respectively. Demonstrating enhanced kinase selectivity, BTK-IN-22 outperforms Ibrutinib in this regard [1].

BTK-IN-23 is a BTK inhibitor with an IC50 value of 12.8 nM, demonstrating kinase selectivity superior to Ibrutinib [1]. It effectively inhibits BLX and BMX, with IC50 values of 35.6 nM and 5.7 nM, respectively.

Poseltinib is an orally active, selective, and irreversible Bruton's tyrosine kinase (BTK) inhibitor, exhibiting a half-maximal inhibitory concentration (IC 50) of 1.95 nM. It demonstrates 0.3, 2.3, and 2.4-fold greater selectivity for BTK over BMX, TEC, and TXK, respectively. This compound covalently binds to BTK's active site at the cysteine 481 residue, effectively inhibiting signaling pathways mediated by the B cell receptor (BCR), Fc receptor (FcR), and Toll-like receptor (TLR).

(Rac)-PF-06250112 is a racemic form of PF-06250112, a potent and highly selective BTK inhibitor that is orally bioavailable; it also inhibits BMX non-receptor tyrosine kinase and TEC [1].

PF-06250112 is an effective and highly selective BTK inhibitor (IC50: 0.5 nM. PF-06250112 displays an inhibitory effect toward BMX nonreceptor tyrosine kinase and TEC (IC50s: 0.9 nM and 1.2 nM, respectively).