BMS-3

Research use only, not for human use.

BMS-3 is a potent LIMK inhibitor with IC50s of 5 nM and 6 nM for LIMK1 and LIMK2, respectively.

BMS-3 is a LIM kinase 1 (LIMK1) inhibitor. LIMK inhibition with 1 μM BMS-3 damaged MTOC protein localisation to spindle poles, undermined the formation and positioning of functional MTOC and thus disrupted spindle formation and chromosome alignment. These effects were phenocopied by microinjection of LIMK1 antibody into mouse oocytes. LIM kinase 1 (LIMK1) activity is essential for cell migration and cell cycle progression.

BMS-3 (Compound 2) causes a dose-dependent reduction in cell count and induces mitotic arrest by increases in total nuclear DNA intensity and histone H3 phosphorylation after 24 h treatment in A549 human lung cancer cells. BMS-3 inhibits A549 human lung cancer cells with EC50 value of 154 nM. BMS-3 is used to demonstrate the direct participation of LIMK1 in the phosphorylation of Cofilin. Inhibition of p-LIMK with 1-50 μM of BMS-3 results in a dose-dependent decrease of p-Cofilin after 10 min incubation in capacitating conditions. As a control, sperm are also incubated for 10 min under non-capacitating conditions which result in low levels of p-Cofilin. In the presence of 1 or 50 μM of BMS-3, actin polymerization levels are significantly lower compared to controls (DMSO). Mouse sperm are incubated under capacitating conditions for 90 min in the presence or absence of increasing concentrations of p-LIMK inhibitor BMS-3 (0, 1, 10 and 50 μM). The increasing concentrations of BMS-3 result in a strong decrease on the percentage of sperm that undergoes acrosomal exocytosis after stimulation with 20 μM of Progesterone.

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BMS-3 | BMS 3 | BMS3

Others

Other Targets

LIMK1|LIMK2

Cancer

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1338247-30-5

429.27

C17H12Cl2F2N4OS

>98% (HPLC)

DMSO : ≥ 30 mg/mL6; 9.89 mM

O=C(Nc1ncc(s1)c2cc(nn2c3c(Cl)cccc3Cl)C(F)F)C4CC4

N-[5-[2-(2,6-Dichlorophenyl)-5-(difluoromethyl)pyrazol-3-yl]-1,3-thiazol-2-yl]cyclopropanecarboxamide

(-20℃)

With Ice Pack

≥ 2 years