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Contractility

Through our service, you can assess cardiac contractility in the cardiac iPSC-based model of your interest to obtain reproducible and clinically relevant results on the safety and efficacy of your compounds. This in vitro assay combines cell-induced electrical impedance measurements with multi-electrode array technology, to simultaneously assess cardiomyocyte contractility, viability, and electrophysiology providing predictive information about how human biology responds to novel drug candidates.

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Assay Capabilities

xCelligence RTCA CardioECR system The xCELLigence RTCA CardioECR system is a non-invasive, label-free platform that records cellular impedance and electrical field potential in parallel to simultaneously assess cardiomyocyte contractility, viability and electrophysiology.

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Case Study

Simultaneous Measurement of Contractility, Electrophysiology, and Troponin I Secretion to Determine Cardiotoxicity of anti-cancer drugs

Many novel oncology therapeutics may induce cardiotoxicity by inhibiting survival pathways which are shared by both tumors and cardiac cells. As complex mechanisms underlie drug-induced toxicity, some compound effects will only become evident after longer incubation times. Multiplexing impedance and MEA with cTnI release assay allows for a simultaneous assessment of short-term and long-term as well as structural and functional drug-induced cardiotoxicity from a single well.

Results

Unlike lapatinib and nilotinib, ponatinib and doxorubicin caused a concentration- and time-dependent increase in cTnI release (right panels, represented as counts, dashed line indicates baseline cTnI levels), which correlated with reduced Cell Index (CI) values (left panels). The CI can also be affected by changes in the morphology or contractility of the cardiomyocyte monolayer as seen after addition of nitrendipine. Therefore, the CI could not be used as a direct measurement for structural cardiotoxicity.

Multiplexing data of cardiotoxic compound effects on Pluricyte cardiomyocytes

Conclusion

Whereas addition of nilotinib and lapatinib caused a (functional) contractile/electrophysiological deficit, doxorubicin exhibited a long-term toxic effect in both MEA and impedance measurements. While lapatinib and nilotinib did not cause structural toxicity as measured by cTnI release, ponatinib and doxorubicin induced a dose- and time-dependent increase in cTnI release which correlated with reduced cell index values.

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Related

Innovation 

A physiologically-relevant hiPSC-CM contractility platform

Poster 

Studying inotropic compounds effects in human iPSC-derived cardiomyocytes using 2D and 3D models