Compugen's CGEN-15001 recombinant fusion protein abolishes spontaneous relapses in animal model of MS

Compugen Ltd. (NASDAQ:CGEN) announced today that administration of CGEN-15001 in an animal model of multiple sclerosis (MS) has been shown to completely abolish spontaneous relapses. In addition, administration of this novel molecule prior to disease onset demonstrated a pronounced delay of disease onset and a significant decrease in disease symptoms. These results, together with complementary results from earlier studies, strongly support a significant potential therapeutic utility for CGEN-15001 in the treatment of multiple sclerosis and other autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease, and type 1 diabetes.

CGEN-15001 is a soluble recombinant fusion protein comprised of the extracellular region of a Compugen discovered B7/CD28 family member, designated CGEN-15001T. CGEN-15001T, which itself has potential medical utilities - such as serving as a target for antibody therapeutics - was discovered by Compugen through the use of its LEADS platform and a proprietary algorithm designed to predict novel members of known protein families. Patents have been filed for both CGEN-15001 and CGEN-15001T.

The recently completed study of CGEN-15001 utilized the relapsing-remitting autoimmune encephalomyelitis mouse model. This well-recognized animal model of multiple sclerosis manifests an autoimmune CNS demyelinating disease with clinical and pathologic similarity to human relapsing-remitting multiple sclerosis. Relapsing-remitting multiple sclerosis is the most common form of MS affecting approximately 85% of the 2.5 million people worldwide diagnosed with MS. Relapses in multiple sclerosis patients result in recurring attacks of clinical symptoms which lead to a worsening of existing symptoms or to the appearance of new symptoms. Thus, prevention of relapses is a major goal in the development of treatments for multiple sclerosis, and the demonstrated therapeutic effect of CGEN-15001 in the presence of this established disease, as demonstrated in this animal model, is highly relevant for its potential use in human therapy.

Professor Stephen Miller from Northwestern University, a leading scientist in this field who supervised the studies, stated, "The capacity of CGEN-15001 to prevent the development of disease in this well-recognized animal model for multiple sclerosis, and more significantly to ameliorate its progression when administered in the presence of pre-existing disease is quite dramatic. Furthermore, these beneficial effects were shown to be long lasting and persisted through the study, indicating that CGEN-15001 may prevent disease progression as efficiently as immune tolerance induction, a process whereby the immune system no longer attacks the self antigens that cause the disease. These findings, together with those demonstrated in our earlier studies, are unique among the molecules targeting the B7 family of co-stimulatory molecules that have been published to date."

Compugen's VP R&D, Dr. Zurit Levine stated, "In addition to being an extremely exciting discovery, this is a good example of how our extensive infrastructure of predictive capabilities can be utilized for 'discovery on demand' purposes. In this case, we were interested in finding a new member of the B7 protein family, a family of proteins that are widely believed to have substantial therapeutic potential. However, it was our belief that relying only on commonly used discovery approaches, such as sequence and functional homology, which underlie most such efforts by others, would be unlikely to yield all unknown members for this family."

Dr. Levine continued, "We utilized, therefore, a different predictive discovery approach combining certain components of our LEADS infrastructure platform with a proprietary algorithm that had been developed to predict in silico novel members of a known protein family based on genomic information, protein structure and additional characteristics. This led to the prediction and selection of a number of novel proteins, including CGEN-15001T, and the discovery of CGEN-15001T led to the identification of the CGEN- 15001 protein."