ML9 (0-100 μM; 0-24 hours) has no reduction in cardiomyocyte viability, 50-100 μM significantly induces cell death[2]. ML9 (50 μM; 1-4 hours) significantly increases cleaved caspase-3 levels, decreased STIM1 protein levels by about 42%[2]. Cell Viability Assay[1] Cell Line: Neonatal rat ventricular myocytes (NRVM) cells Concentration: 0, 10, 50 and 100 μM Incubation Time: 0, 1, 4, 8 and 24 hours Result: Decreased cell viability at 50-100 μM concentration. Apoptosis Analysis[1] Cell Line: Neonatal rat ventricular myocytes (NRVM) cells Concentration: 50 μM Incubation Time: 1, 4 and 8 hours Result: Induced cardiomyocyte death through necrosis and apoptosis.
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Ito S, et al. ML-9, a myosin light chain kinase inhibitor, reduces intracellular Ca2+ concentration in guinea pig trachealis.Eur J Pharmacol. 2004 Feb 23;486(3):325-33.
[2]. Shaikh S, et al. The STIM1 inhibitor ML9 disrupts basal autophagy in cardiomyocytes by decreasing lysosome content.Toxicol In Vitro. 2018 Apr;48:121-127.
[3]. Kondratskyi A1, et al.Identification of ML-9 as a lysosomotropic agent targeting autophagy and cell death.Cell Death Dis. 2014 Apr 24;5:e1193.
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