Compugen Ltd. (NASDAQ: CGEN), announced today that CGEN-15001 was the subject of a presentation by Joseph Podojil, Ph.D. of the Feinberg School of Medicine Northwestern University, at the 2nd International Conference on Immune Tolerance, now being held in Amsterdam. This is the first time that scientific information related to CGEN-15001's therapeutic potential is being presented to the scientific community. In his talk, Dr. Podojil presented data demonstrating that administration of CGEN-15001 in the experimental autoimmune encephalitis (EAE) animal model of multiple sclerosis (MS) resulted in a dramatic improvement of disease symptoms and abolishment of spontaneous relapses. In addition, the study results demonstrated that short-term treatment with CGEN-15001 lead to long-term inhibition of disease symptoms as well as of the underlying spread of pathological immune responses.
Dr. Podojil, a Research Assistant Professor in the laboratory of Professor Stephen Miller at Northwestern University, showed that CGEN-15001 appears to exert its beneficial therapeutic effect by modulating the immune system and preventing infiltration of reactive immune T cells into the central nervous system. CGEN-15001 thereby inhibits the underlying mechanisms which cause the debilitating disease symptoms and its relapsing nature. Similar beneficial effects were observed in two MS models, an EAE model actively induced by immunization with a myelin antigen and an adoptive transfer EAE model created by injection of immune cells specifically reactive to myelin. The results reported are from studies performed under an agreement with Northwestern University and Prof. Miller, a leading scientist in the fields of immunology and autoimmune diseases who supervised the studies.
In his talk, Dr. Podojil presented data demonstrating that the effects of CGEN-15001 include modulating the activity of a sub-group of white blood cells called T helper cells, which are known to provide signals for orchestrating the immune response. In particular, CGEN-15001 inhibits the pro-inflammatory T helper cells Th1 and Th17, while at the same time promoting anti-inflammatory Th2 responses. T cell modulation can be therapeutically beneficial in the treatment of T cell mediated autoimmune diseases.