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Small molecule inhibitors of IRAP

總結: Monash University researchers have identified and validated a novel anti-fibrosis target - IRAP. Inhibition of this target with the proprietary small molecule lead series completely reversed cardiac and renal fibrosis in clinically relevant disease models. We nows eek a partner to develop novel lead candidate inhibitors as safe and effective anti-fibrotic drugs.

技術優勢: - Potential to develop ‘Best in Disease’ anti-fibrotic drugs that reverse existing fibrotic lesions
- ‘Proof of Mechanism’ with in vivo efficacy for small molecule inhibitors
- Differentiated and vasoprotective mechanism of action

詳細技術說明: Researchers from the Monash BioMedicine Discovery Institute (A/Prof. Siew Chai, Prof. Rob Widdop & Dr. Tracey Gaspari) and Monash Institute of Pharmaceutical Sciences (A/Prof. Phil Thompson) have identified IRAP as a new target for the treatment of cardiac, kidney, liver and potentially other organ fibrosis. IRAP is an extracellular protein that is ‘druggable’ with small molecule inhibitors. A compelling body of evidence supporting proof-of-mechanism and validation with a lead series has shown that IRAP inhibition can prevent and reverse fibrosis.
- IRAP deficiency/inhibition protects against the development of cardiac and renal fibrosis in aged mice and cardiac fibrosis in Ang II-treated mice.
- IRAP inhibition completely reverses cardiac fibrosis in aged mice, with corresponding decreases in inflammatory and oxidative stress markers and increases in NO bioavailability.
- IRAP deficiency/inhibition protects against ischemia-reperfusion damage and improves function of aged ischemic hearts.
- IRAP inhibition protects and reverses age mediated renal fibrosis and high salt induced cardiac/renal fibrosis

其他: Monash seeks a partner to optimise the lead series and develop new drug candidates against this exciting target. The Monash team has extensive experience in IRAP and fibrosis biology, having an array of in-house models including in vitro target screen, functional assay, specific knock-out models, fibrosis and other pathological models, pus target SAT and preclinical profiling experience.

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