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

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Results support the therapeutic potential of targeting mitochondrial
stress associated with kidney injury and advancement of MA-0217 into
clinical studies

Mitobridge, Inc., dedicated to the discovery and development of
therapeutics that improve mitochondrial function, presented results
highlighting the potential of selective PPARδ 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. "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 PPARδ 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).

 

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