BOULDER, Colo., Bolder BioTechnology, Inc. announced today publication of preclinical research demonstrating utility of interleukin-11 (IL-11) and the company's long-acting IL-11 analog to prevent kidney damage from ischemia reperfusion injury in mice. This work may lead to new therapeutic approaches to prevent acute kidney injury and ischemia reperfusion injury to multiple organ types.
The studies were performed in the laboratory of H. Thomas Lee, M.D., Ph.D., Professor and Director of Transplantation Anesthesiology, Department of Anesthesiology, Columbia University, New York, and published as an Advance Online Publication in the American Journal of Physiology – Renal Physiology (http://ajprenal.physiology.org; published ahead of printAugust 1, 2012, doi:10.1152/ajprenal.00220.2012).
George (Joe) Cox, Ph.D., Company President stated "IL-11 is a multifunctional protein that is used clinically to treat thrombocytopenia (low platelet counts) in cancer patients receiving chemotherapy. Dr. Lee's experiments show for the first time that IL-11 also can prevent kidney damage that results when blood flow to the kidneys is temporarily blocked and then restarted (ischemia-reperfusion), such as occurs during many types of major surgeries.
Restoring blood flow to the ischemic kidney initiates an inflammatory response that damages the healthy kidney and can lead to acute kidney injury and renal failure. Renal ischemia-reperfusion injury is a major clinical problem that is associated with a high incidence of permanent kidney damage and high mortality in certain patient populations. There are no effective therapies for reducing the incidence of surgery-associated acute kidney injury.
Dr. Lee's studies showed that administration of IL-11 or our biosuperior, long-acting IL-11 analog prior to, or shortly after renal ischemia-reperfusion preserved kidney function and significantly reduced the amount of kidney cell necrosis, cell death and inflammation compared to a placebo. Dr. Lee's studies also elucidated the intracellular signaling pathways triggered by IL-11 that are responsible for protecting the kidney from ischemia-reperfusion injury.
PR Newswire