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Related Experiment Video

Updated: May 31, 2026

Preclinical Drug Testing in Scalable 3D Engineered Muscle Tissues

Preclinical Drug Testing in Scalable 3D Engineered Muscle Tissues

Published on: April 7, 2023

BMS309403 directly suppresses cardiac contractile function.

Christiane Look¹, Ingo Morano, Monika Ehrhart-Bornstein

¹Medical Clinic III, University of Technology Dresden, Germany. Christiane.Look2@uniklinikum-dresden.de

Naunyn-Schmiedeberg'S Archives of Pharmacology

|July 19, 2011

Summary

This summary is machine-generated.

BMS309403, an adipocyte fatty acid-binding protein inhibitor, may cause cardiac issues. This study found it depresses heart contractility and can cause heart arrest, suggesting caution for therapeutic use.

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Area of Science:

Cardiovascular Pharmacology
Molecular Cardiology
Drug Safety Evaluation

Background:

Adipocyte fatty acid-binding protein (AFABP) inhibitors, like BMS309403, are explored for type 2 diabetes mellitus and atherosclerosis.
Potential cardiovascular side effects of BMS309403 remain largely uncharacterized.
Understanding drug-induced cardiac effects is crucial for therapeutic development.

Purpose of the Study:

To investigate the in vitro cardiovascular effects of BMS309403.
To determine the impact of BMS309403 on cardiac contractility and electrophysiology.
To assess the safety profile of BMS309403 concerning cardiac function.

Main Methods:

Isolated perfused adult rat heart preparations for contractility analysis.
Single adult rat cardiomyocytes for contractile function assessment.
Porcine cardiac skinned muscle fibers to evaluate myofilament Ca(2+) sensitivity.

Main Results:

BMS309403 induced negative inotropy in isolated perfused hearts, leading to cardiac arrest.
Electromechanical dissociation was observed, with no interference in electrocardiographic activity.
BMS309403 exhibited a direct, biphasic inhibitory effect on cardiomyocyte contraction, attenuating Ca(2+) levels at higher concentrations.
The negative inotropic effect was not due to direct action on cardiac myofilaments.

Conclusions:

BMS309403 demonstrates an acute cardiac depressant effect in vitro.
The compound induces heart arrest via electromechanical dissociation.
Further evaluation is necessary before considering BMS309403 for therapeutic applications due to its cardiac side effects.