XBiotech Announces Discovery that Blocking Interleukin-1a Reduces Brain Injury and Neurological Deficit After Stroke

Antibody Therapy Targeting Interleukin-1a significantly reduced stroke related brain injury in animals and points to new potential blockbuster therapy

AUSTIN, Texas, July 14, 2020 (GLOBE NEWSWIRE) -- XBiotech Inc. (NASDAQ: XBIT) announced today findings published in the prestigious American Heart Association’s journal, Circulation. The publication titled, Post-Ischemic Administration of IL-1a Neutralizing Antibody Reduces Brain Damage and Neurological Deficit in Experimental Stroke, points to a use for XBiotech’s drug candidate antibody that blocks interleukin-1 alpha (IL-1⍺) for use as a therapeutic to reduce brain damage and neurological deficit after stroke. The research was headed by a world-leading cardiovascular researcher, Dr. Giovanni Camici, Director for the Center for Molecular Cardiology at the University of Zurich in Switzerland. Dr. Camici’s research team tested an anti-IL-1⍺ antibody provided by XBiotech to evaluate its ability to reduce brain injury in animals subjected to an experimental stroke and reperfusion injury. About 15 million people worldwide suffer from a stroke each year. Approximately 795,000 of these people are in the United States. Stroke is the second leading cause of death worldwide.

Dr. Camici commented, “This study demonstrates the importance of IL-1α in mediating the damages caused by ischemic stroke and the efficacy of IL-1α blockade in improving outcome after transient cerebral ischemia in mice. The availability of a clinically approved anti-human IL-1α antibody could offer the possibility to establish new treatment strategies for the management of ischemic stroke patients.  Based on our results, randomized clinical trials should be designed to assess the potential of anti-IL-1α therapy as an adjuvant to interventional or thrombolytic treatment of acute ischemic strokes.”

Dr. Camici’s research team focused on a particular difficult aspect of ischemic stroke, so called reperfusion injury. When patients suffer from a stroke, or a blockage in an artery that provides crucial blood and oxygen to the brain, a portion of the brain typically suffers irreparable damage. However, there is also typically a portion of the brain that has been deprived of oxygen but is functional and may be rescued if the blood clot is removed and normal circulation can be restored. Unfortunately, when the blood clot is removed and blood supply resumes into areas of the brain where oxygen had been deprived, a massive inflammatory response occurs. This ensuing inflammation is believed to be responsible for the so called “reperfusion injury” that is observed with the returning blood supply. The result is widening destruction of brain tissue upon opening of the clogged artery and associated irreparable neurologic deficits. Therefore, decreasing this inflammatory response by inhibiting IL-1⍺ holds promise as an effective treatment for reperfusion injury. There is currently no therapy to treat reperfusion injury.