GlycoMimetics (GLYC) Announces Publication of Positive GMI-1271 Data in Post-Heart Attack Inflammatory Response Reduction

August 16, 2016 9:30 AM EDT
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GlycoMimetics, Inc. (Nasdaq: GLYC) announced the publication of results from a preclinical study that showed its drug candidate GMI-1271 reduced the cellular interactions that often lead to a buildup in inflammatory response and unstable atherosclerotic plaque formation after a heart attack. The study, entitled “E-Selectin Inhibition Mitigates Splenic HSC Activation and Myelopoiesis in Hypercholesterolemic Mice With Myocardial Infarction,” was published in the September issue of Arteriosclerosis, Thrombosis, and Vascular Biology.

In the study, researchers demonstrated a wider range of potential clinical applications of the E-selectin antagonist GMI-1271, which is currently being evaluated as a potential treatment for acute myelogenous leukemia (AML) in a Phase 1/2 clinical trial.

“The results in this animal model of myocardial infarction and atherosclerosis demonstrate both the biological activity of GMI-1271 and the possible broader uses of an E-selectin antagonist. While GlycoMimetics is currently focused on developing GMI-1271 for treatment of AML, this drug candidate has shown activity in pre-clinical models of a number of diseases where E-selectin plays a key functional role,” said John L. Magnani, Ph.D., Vice President and Chief Scientific Officer of GlycoMimetics.

Myocardial infarctions are often triggered by unstable atherosclerotic plaque material, the growth of which is initiated by the production and infiltration of inflammatory cells through the action of E-selectin. The study, conducted at Harvard Medical School and Massachusetts General Hospital, found that after a myocardial infarction (MI), GMI-1271 not only reduced the production of inflammatory cells and their hematopoietic stem and progenitor cells, but also their infiltration into atherosclerotic plaques, thereby stabilizing existing plaques and decreasing the risk of a further ischemic injury which can lead to a second MI. The study showed that GMI-1271-induced E-selectin inhibition significantly reduced the numbers of stem and progenitor cells leading to reduced numbers of inflammatory monocytes, and neutrophils in the blood. It also inhibited their infiltration into existing plaques leading to the stabilization of atherosclerotic plaques (smaller plaque size, reduced necrotic core area, and thicker fibrous cap) after an MI in animal models.



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