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Time2020-04-20 14:40:06 Hits554

Cav1.2 in the heart mediates L-type calcium currents. The influx of calcium causes calcium-induced calcium release from the ER Stores via ryanodine receptors. Calcium ions are the principle intracellular signal ions. In the heart, calcium ions regulate excitation-contraction coupling of cardiac muscles. Cav1.2 channels are activated when the heart is depolarized and the calcium currents help shape the cardiac action potential phase 2 (plateau phase). Mutation of Cav1.2 could lead to various severe diseases and arrhythmia, such as Timothy syndrome, Brugada syndrome, even sudden death. Drug action on Cav1.2 could also cause life-threatening severe arrhythmia, hence it’s important to evaluate drug’s effect on Cav1.2 channel as one of the preclinical safety precautions.

Pharmacore Labs currently provide manual patch clamp assay using acutely isolated animal cardiomyocytes to test drug's inhibition or potentiating effect on Cav1.2 channels. This assay is one of the preclinical cardiac safety assays highly recommended in the pharmaceutical industry.

In vitro electrophysiology ICa assay in primary cardiomyocytes:

Assay platform/method

Conventional patch clamp

Cells used in the assay

Acutely isolated cardiomyocytes from guinea pigs, or rats, or rabbits

Measured parameters

Whole cell current of calcium channels, mainly L-type calcium channels

Test concentrations

4 doses for IC50

Data point repeats

N ≥ 3 for each concentration

Note: 1) Positive control: 0.03 mM CdCl2 is used in the assay to ensure cell quality and normal response of L-type calcium channels.

Effect of inhibitor (CdCl2) on the L-type Ca channel in cardiomyocytes isolated from guinea pig

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