New target for development of anti-fibrotic drugs
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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.
- 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
Anti-fibrotic therapeutic to reverse existing lesions.
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
Licensing
29/07/2016 00:00:00
AU2016301113
JA2018-504650
Others
Monash seeks a partner to optimise the lead series and develop new drug candidates against this exciting target.
2015-027
澳洲
