THR-123, a novel BMP-7 mimetic that activates Akt phosphorylation and inhibits cardiomyocyte apoptosis and inflammation, protects the heart from myocardial injury in a Rat model - Report - MDSpire
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THR-123, a novel BMP-7 mimetic that activates Akt phosphorylation and inhibits cardiomyocyte apoptosis and inflammation, protects the heart from myocardial injury in a Rat model
Clinical Report: THR-123: A Novel BMP-7 Mimetic for Myocardial Protection
Overview
THR-123, a BMP-7 mimetic, significantly reduces myocardial infarct size and inflammation in a rat model of ischemia-reperfusion injury. It activates Akt phosphorylation and inhibits cardiomyocyte apoptosis.
Background
Acute myocardial infarction (AMI) is a leading cause of heart failure and mortality worldwide. The size of myocardial infarction correlates with patient outcomes.
Data Highlights
Parameter
Effect of THR-123
Myocardial infarct size
Decreased by 84%
Pericardial inflammation
Reduced
Key Findings
THR-123 activates Akt phosphorylation in cardiomyocytes.
THR-123 reduces cardiomyocyte apoptosis and inflammation.
THR-123 decreases myocardial infarct size by 84% in a rat model.
THR-123 promotes tissue regeneration without inducing bone formation.
Administration of exogenous BMP-7 may attenuate cardiac infarction and adverse remodeling.
Clinical Implications
Further studies are warranted to explore the clinical applicability of THR-123.
Conclusion
THR-123 demonstrates significant cardioprotective effects in a rat model of myocardial injury.
