Clamikalant sodium

Clamikalant sodium (HMR 1098) is an ATP-sensitive potassium (KATP) channel blocker. Clamikalant sodium can be used for the research of arrhythmia[1].

Research Areas >> Neurological Disease

Signaling Pathways >> Membrane Transporter/Ion Channel >> Potassium Channel

Clamikalant sodium (HMR 1098; 40 μM) prevents improvement effect of Levosimendam on left ventricular developed pressure (LVDP) recovery rate, abolishes the inhibitory effect of Levosimendan on hypothermic preservation-induced activation of calpain, cleavage of Bid, and apoptosis[2]. Clamikalant sodium (HMR 1098; 30 µM, 24 hours) reduces cellular viability, increases the apoptosis of Neonatal rat cardiomyocytes (NRCs) [3]. Clamikalant sodium (30 µM) decreases the Bcl-2 protein level and increases the Bax protein level in the LPS-exposed NRCs[3]. Cell Viability Assay[3] Cell Line: Neonatal rat cardiomyocytes (NRCs) Concentration: 30 µM Incubation Time: 24 hours Result: Reduced cellular viability to 42.8±6.3% compared with the LPS group. Western Blot Analysis[3] Cell Line: Neonatal rat cardiomyocytes (NRCs) Concentration: 30 µM Incubation Time: 24 hours Result: Decreased the Bcl-2 protein level and increased the Bax protein level.

Clamikalant sodium (HMR 1098; 6.0 mg/kg; 5 min prior to EET administration) completely abolishes the cardioprotection produced by epoxyeicosatrienoic acid (EET)[1].

[1]. Garrett J Gross, et al. Roles of endothelial nitric oxide synthase (eNOS) and mitochondrial permeability transition pore (MPTP) in epoxyeicosatrienoic acid (EET)-induced cardioprotection against infarction in intact rat hearts. J Mol Cell Cardiol. 2013 Jun;59:20-9.

[2]. Hai-yan Zhou, et al. Improved myocardial function with supplement of levosimendan to Celsior solution. J Cardiovasc Pharmacol. 2014 Sep;64(3):256-65.

[3]. Xiaohui Zhang, et al. Sarcolemmal ATP-sensitive potassium channel protects cardiac myocytes against lipopolysaccharide-induced apoptosis. Int J Mol Med. 2016 Sep;38(3):758-66.