Chemokine Therapeutics: Identification of Mechanism for Blood Vessel Growth
Chemokine Therapeutics Corp. announced the publication of an article in Nature medicine, authored by clinical advisory board member and collaborator, Dr. Shahin Rafii of the Weill Medical College of Cornell University, and co-authored by Dr. Hassan Salari, President and CEO of Chemokine Therapeutics.
"More than 200,000 individuals undergo various costly treatments for diseases associated with abnormal vascularization, such as Age-related Macular Degeneration (AMD). Vascularization is a process believed to involve local production of a group of growth factors, cytokines and chemokines. An excess amount of these growth factors leads to abnormal growth of endothelial cells which form new blood vessels. In the article, the team concludes that in the limb ischemia revascularization model, the chemokine SDF-1 is a hub for most growth factors and, without it, there is reduced revascularization, even if other growth factors are present. The discoveries point to the need for the development of SDF-1 inhibitors as a mean to stop unwanted vascularization of tissues and organs. SDF-1 inhibitors may have even greater potential than currently used anti-cytokine/growth factor therapies," stated Dr. Hassan Salari, President and CEO.
The discoveries were made possible in part through the use of a novel SDF-1 antagonist, CTCE-0012 produced by Chemokine Therapeutics. It was shown that CTCE-0012 is as powerful as antibodies to CXCR4, however with the benefits of being a most closely homolog of natural SDF-1 protein which might be used chronically. CTCE-0012 is a powerful inhibitor of SDF-1 and prevents revascularizarion of tissues, leading to a lower number of new blood vessels. This discovery leads the way to the development of CTCE-0012 for diseases that are initiated through excess vascularization, such as Macular Degeneration, etc.
Original publication: "Cytokine-mediated deployment of SDF-1 induces revascularization through recruitment of CXCR4+ hemangiocytes" Nature Medicine 12006, 2(5):557-567.
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