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Contractility

Through our service, you can assess cardiac contratility in particular disease models as well as in cardiac drug safety. Ncardia offers a non-invasive in vitro assay to measure true contractility of human cardiomyocytes in 2D or 3D with exceptional accuracy under physiological mechanical boundary conditions.

This is the only in vitro contraction assay that mimics physiological tissue elasticity in a multi-well format which allows the studying of compound effects in e.g. cardiomyopathy, or in healthy cardiomyocytes for safety assessment.


Benefits

Tailored to your project needs
Measurements can be produced for monolayers or 3D co-cultures

Physiologically relevant
Assay mimics physiological tissue elasticity in multi-well format

High quality results
Based on 10+ years of Ncardia experience

Description

Our contractility assay combines cell-induced electrical impedance measurements with multi-electrode array technology, to simultaneously assess cardiomyocyte contractility, viability, and electrophysiology, providing a detailed view of cardiomyocyte health. By applying a low voltage between electrodes, we establish an electric current, which enables us to dynamically monitor cardiomyocyte contraction and relaxation.

The assay offers multiplexing methods, using contractility and multi-electrode array techniques to help you gain insight into the toxicity or efficacy of your test compounds in either healthy cardiomyocytes or cardiac disease models.

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.

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.

Assay Capabilities


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Related

Innovation  

CRACK IT InPulse Challenge

A physiologically-relevant hiPSC-CM contractility platform

Poster  

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