MGH, Duke University and Angion Biomedica partner to develop novel therapeutics for ischemic stroke

Angion Biomedica Corp. announced today the establishment of an alliance with Duke University and Massachusetts General Hospital (MGH) to pursue advanced development and clinical studies of its lead therapeutics for treatment of ischemic stroke. An often debilitating if not fatal consequence of interrupted blood flow in the brain, ischemic stroke has long been deprived of effective treatments as a result of multiple clinical study failures over the past two decades. Angion Biomedica is pursuing novel therapeutic strategies targeting protective and regenerative systems in the brain using a small molecule mimetic of the growth factor called hepatocyte growth factor (HGF), and separately, a small molecule inhibitor of the poly(ADP-ribose) polymerase-1 (PARP-1) pathway.

Based on promising results obtained from preclinical models with its HGF mimetic, BB3, Angion Biomedica and its alliance partners anticipate that these in vivo data will translate into human efficacy. "We forged this alliance after our collaborators at Duke University Medical Center and the Massachusetts General Hospital (MGH) observed encouraging results in preclinical studies with BB3," said David E. Smith, Ph.D., of Angion Biomedica. "Although fully aware of the failures with this indication in the past, they felt strongly that there were sufficient data to support accelerating our research plan to allow the initiation of clinical studies as quickly as possible. Angion Biomedica has already completed critical clinical safety studies on BB3. Thus, moving into the stroke patient population will be expeditious."

Pathologies such as infection, inflammation, and toxic or ischemic injury often lead to organ dysfunction and failure, hampering quality of life and impacting survival. In ischemic stroke, interruption of blood flow deprives brain cells of oxygen directly killing cells in the immediate vicinity of the interruption while initiating an inflammatory response that spreads and destroys brain cells in the surrounding area. This expansion of the injury leads to the devastating consequences of what may be only a temporary blockage of blood flow. The brain, as well as other organs, possesses diverse endogenous repair mechanisms to address these pathologies. One mechanism Angion Biomedica discovered to be particularly responsive to intervention is a pathway involving hepatocyte growth factor (HGF), a kinase that triggers a powerful reparative response. Angion Biomedica's HGF mimetic BB3, already undergoing clinical studies for renal and liver diseases, was found in preclinical ischemic stroke models to offer significant benefit. Because this protective and reparative response is similar between the animal models and humans, direct translation of the benefits is anticipated.

"Through this alliance we will be working to advance BB3 into clinical studies in ischemic stroke," said David S. Warner, M.D., of Duke University Medical Center. "We are well underway in generating data in The Multidisciplinary Neuroprotection Laboratories at Duke under the most exacting standards, with the goal of independently verifying the data generated to date at Angion Biomedica."

"Our hospital sees a large number of stroke patients," said Cenk Ayata, M.D. of the Department of Neurology at MGH and associate professor of Neurology and Radiology at Harvard Medical School. "It is our expectation that studies on BB3 can begin as soon as regulatory requirements are met and we are cautiously optimistic regarding the outcome of such a trial."

"We are excited at the prospect of working with these two great institutions to advance novel treatments for ischemic stroke, a huge unmet need which results in untold damage to lives and families," said Itzhak D. Goldberg, M.D., F.A.C.R., CEO of Angion Biomedica.

Together with its partners, Angion Biomedica is also advancing a novel, small molecule PARP-1 inhibitor for ischemic stroke. With data indicating that PARP-1 is involved in energy consumption, inflammation and necrotic cell death, inhibiting this pathway can limit infarct expansion by mitigating neuronal loss. Preclinical studies validating use of Angion's PARP-1 inhibitor in ischemic stroke are expected to begin shortly.