(R)-9b is an ATP -competitive kinase inhibitor. (R)-9b binds to the ATP-binding site of ACK1 / TNK2, inhibiting their kinase activity and autophosphorylation, with a human IC50 of 56 nM. (R)-9b also inhibits JAK2, Tyk2, ALK, c-Src, ABL1, CHK1, FGFR1, LCK, and ROS/ROS1. (R)-9b can be used for research on prostate cancer [1].
In Vitro, (R)-9b is a potent ACK1 inhibitor with an IC50 of 56 nM in the 33P HotSpot assay[1]. (R)-9b (1 μM) is a potent ACK1 inhibitor with IC50 values in the low nanomolar range for JAK2 (6 nM) and Tyk2 (5 nM), and exhibits good selectivity over other kinases such as ALK (143 nM) and cSrc (438 nM)[1]. (R)-9b (5 μM; 16 h) potently inhibits EGF-induced ACK1 autophosphorylation at Tyr284 in LAPC4 prostate cancer cells, achieving 93.5% inhibition at 5 μM[1]. (R)-9b (2-10 μM; 72 h) effectively suppresses proliferation of LNCaP (IC50 = 1.8 μM) and VCaP (IC50 = 2 μM) prostate cancer cell lines, and shows comparable growth suppression to reference compounds in LAPC4 cells[1].
References:
[1]. Lawrence HR, et al. Development of novel ACK1/TNK2 inhibitors using a fragment-based approach. Journal of medicinal chemistry. 2015 Mar 26;58(6):2746-63.
In Vitro, (R)-9b is a potent ACK1 inhibitor with an IC50 of 56 nM in the 33P HotSpot assay[1]. (R)-9b (1 μM) is a potent ACK1 inhibitor with IC50 values in the low nanomolar range for JAK2 (6 nM) and Tyk2 (5 nM), and exhibits good selectivity over other kinases such as ALK (143 nM) and cSrc (438 nM)[1]. (R)-9b (5 μM; 16 h) potently inhibits EGF-induced ACK1 autophosphorylation at Tyr284 in LAPC4 prostate cancer cells, achieving 93.5% inhibition at 5 μM[1]. (R)-9b (2-10 μM; 72 h) effectively suppresses proliferation of LNCaP (IC50 = 1.8 μM) and VCaP (IC50 = 2 μM) prostate cancer cell lines, and shows comparable growth suppression to reference compounds in LAPC4 cells[1].
References:
[1]. Lawrence HR, et al. Development of novel ACK1/TNK2 inhibitors using a fragment-based approach. Journal of medicinal chemistry. 2015 Mar 26;58(6):2746-63.