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Compugen Presents Experimental Results Supporting Induction Of Immune Tolerance By CGEN-15001 Drug Candidate

In a presentation tomorrow at the Autoimmune & Inflammation Leaders’ Forum in Boston, Massachusetts, Galit Rotman, PhD, Chief Scientist of Therapeutics at Compugen Ltd. (NASDAQ: CGEN), will disclose results from an animal model study in which CGEN-15001, an Fc fusion protein drug candidate derived from a novel immune checkpoint protein discovered by Compugen, demonstrated potential to induce immune tolerance, a much desired goal for treatment of many immunological disorders. The presentation will also disclose recent positive results from a humanized animal model of psoriasis, further expanding the scope of autoimmune conditions potentially treatable by CGEN-15001.

In her presentation, Dr. Rotman will disclose results from a recently completed bone marrow transplantation study in which CGEN-15001 was highly effective in preventing graft rejection, suggesting that this drug candidate acts through an induction of immune tolerance. Establishment of immune tolerance is a key goal in the treatment of autoimmune diseases. In comparison to current therapeutic approaches that generally suppress the immune system, tolerance induction would provide a sustained resolution of the disease without compromising the immune system’s capacity to fight infections and malignancies.

The bone marrow transplantation study was performed as part of Compugen’s ongoing collaboration with Stephen Miller, Professor of microbiology-immunology at Northwestern University Feinberg School of Medicine. In this study, bone marrow cells from male mice were transplanted into female mice of the same strain, followed by monitoring of the number of male cells in their blood. In CGEN-15001 treated animals, successful engraftment of the transplanted bone marrow cells was observed, while in control animals the transplanted cells were rejected. These results suggest that treatment with CGEN-15001 induces immune tolerance towards the transplanted cells. Additional data will also be presented for CGEN-15001 supporting this highly desired mechanism of action in type 1 diabetes and multiple sclerosis animal models.

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