[November 06, 2017]

Mitobridge Presents Preclinical Data Demonstrating Beneficial Effects of PPARd Modulators in Acute Kidney Injury at American Society of Nephrology Annual Meeting

Mitobridge, Inc., dedicated to the discovery and development of therapeutics that improve mitochondrial function, presented results highlighting the potential of selective PPARd modulation to treat acute kidney injury (AKI). AKI is the sudden loss of kidney function that often occurs in hospitalized patients following cardiac and/or vascular surgery, trauma, infection, cardiac disease or treatment with nephrotoxic anti-cancer therapy.

The data, presented last week at the Annual Meeting of the American Society of Nephrology (ASN), demonstrated that Mitobridge's proprietary compound MA-0217 (also known as MTB-2) corrects the mitochondrial deficits and alleviates the renal dysfunction in a rat ischemia reperfusion AKI (IR-AKI) model. Additionally, MA-0204, a close analog of MA-0217, dosed post IR-AKI in a rat model of patients with hypertension, chronic kidney disease and diabetes and thereby at high risk to develop AKI, reduced kidney injury, accelerated recovery of kidney function and decreased the onset of fibrosis and slowed progression of diabetes and chronic kidney disease by 4 weeks. The posters are available on the Company's website: http://www.mitobridge.com/news/publications.

"These proof-of-concept data demonstrated that MA-0217 can enhance mitochondrial fatty acid oxidation in human kidney cells and restore kidney function in animal models of the disease," commented Effie Tozzo, Senior Vice President, Translational Sciences at Mitobridge. "These results are encouraging and support advancing MA-0217 into clinical development as a first-in-class interventional approach for cardiac surgery-associated acute kidney injury (CSA-AKI)."

"AKI is a serious condition and there are no currently approved therapies to help manage patients," said Bruce A. Molitoris, Professor of Medicine and Director of the Indiana Center for Biological Microscopy at Indiana University (News - Alert). "MA-0217 may address the cellular injury, mitochondrial dysfunction and organ damage associated with AKI and represents an innovative option for this life-threatening condition. The presented data are quite promising and I look forward to seeing the compound enter clinical development."

About Mitobridge
Mitobridge is dedicated to delivering therapeutics that improve mitochondrial function. Our team of experienced drug discovery and development scientists is leveraging their exceptional knowledge of mitochondria biology to develop a pipeline of innovative programs for the treatment of kidney and muscle diseases with high unmet medical need. Headquartered in Cambridge, MA, Mitobridge was launched in October 2013 with funding from Astellas Pharma, Inc., MPM Capital and Longwood Ventures. For more information about the Company, please visit www.mitobridge.com.

About MA-0217
MA-0217 (MTB-2) is a potent and highly-selective PPARd modulator and the second program to emerge from Mitobridge's platform. The compound is a potentially first-in-class approach to treating acute kidney injury (AKI). Mitobridge has generated preclinical data demonstrating that intervention with MA-0217 improves mitochondrial function, overall energy metabolism and performance of the kidney following an acute ischemia reperfusion injury.

About AKI
AKI is a sudden loss of kidney function that often occurs in hospitalized patients as a result of cardiac and/or vascular surgery, trauma, infection, cardiac disease or being treated with nephrotoxic anti-cancer therapy. AKI affects more than 13 million people each year worldwide and is associated with extended hospitalization and increased mortality. Currently, there are no therapies to prevent or treat AKI. The clinical manifestations are, in part, due to early onset mitochondrial deficits that drive multiple pathophysiological events that lead to AKI and appear to be linked to the severity of AKI and progression to Chronic Kidney Disease (CKD).

View source version on businesswire.com: http://www.businesswire.com/news/home/20171106005791/en/

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