Aldagen Presents Data Describing Cell Therapy Products' Mechyanism for Homing to Ischemic Injury
Durham, NC (January 26, 2012) — Aldagen, Inc. today announced that a poster describing the homing properties of its cellular therapies was presented at the Seventh International Conference on Cell Therapy for Cardiovascular Disease. The data further explains the mechanism of action for Aldagen’s cell therapy products, and supports the ability of these cells to home to the site of ischemic injury.
The poster, entitled Mechanisms of Homing of Bone Marrow Derived ALDHbr Stem Cells to Ischemic Injury, describes the multiple mechanisms by which Aldagen’s cell therapy products home to areas of ischemic damage. These mechanisms include the expression of integrins and selectins that can bind to the endothelium and promote transmigration into ischemic tissues.
“This scientific poster provides evidence that our cellular products home to sites of ischemic damage, and give us a better understanding of the mechanisms behind this action. These data, along with the recently published paper describing the pro-angiogenic activity of our cellular therapies, outlines a compelling mechanism of action for our cell products, and supports the potential of our ongoing clinical programs,” said Lyle A. Hohnke, Ph.D., Chief Executive Officer of Aldagen.
Aldagen is a clinical-stage biopharmaceutical company developing proprietary regenerative cell therapies. Our product candidates consist of a specific population of a patient’s own stem cells, which are isolated using our proprietary technology and which we believe have the potential to promote the regeneration of multiple types of cells and tissues, including the growth of new blood vessels. Our initial focus is on developing product candidates to address cardiovascular disease. Our clinical stage cardiovascular product candidates are ALD-301 for the treatment of critical limb ischemia, ALD-201 for the treatment of ischemic heart failure, and ALD-401 for the post-acute treatment of ischemic stroke.