Compugen Ltd. announced today that administration of CGEN-15001 in an animal model of rheumatoid arthritis (RA) dramatically ameliorates the clinical symptoms of the disease. These results, combined with earlier results in an animal model of multiple sclerosis (MS), strongly support the therapeutic potential of CGEN-15001 for multiple autoimmune diseases and inflammatory conditions.
The recently completed study of CGEN-15001 utilized the collagen-induced arthritis (CIA) animal model. This well accepted animal model of RA manifests an autoimmune disease with clinical and pathological similarity to human rheumatoid arthritis. Upon treatment of mice with established RA disease, impressive therapeutic effects of CGEN-15001 were observed. Furthermore, CGEN-15001 showed efficacy similar to that observed through TNF-alpha blockade with TNFR-Fc, ENBREL®, a widely used biologic disease modifying anti-rheumatic drug (DMARD). In the study, both ENBREL® and CGEN-15001 were administered at the same dose and frequency.
TNF-alpha blockade therapy has revolutionized the treatment of RA; however, neutralization of TNF in patients receiving TNF blockers therapy leads to increased risk of infection, and particularly, of reactivating latent tuberculosis. In addition, significant proportions of patients do not respond to TNF blockers and require alternative effective treatments. Thus, novel drugs for RA that are devoid of such side effects and benefit additional patient populations remain an unmet clinical need. Among these are drugs targeting negative co-stimulatory pathways, which are of high industry interest.
The CIA model of RA is the second well recognized animal model of autoimmune disease in which CGEN-15001 has shown dramatic therapeutic potential; previous studies with CGEN-15001 demonstrated similar beneficial effects in an animal model of multiple sclerosis. Furthermore, in both the animal models of RA and of MS, the significant clinical potential for this novel molecule was underscored by the pronounced therapeutic effects demonstrated when CGEN-15001 was administered in the presence of established disease. These promising results in the two different autoimmune disease models further support the development of CGEN-15001 as a therapeutic agent for autoimmune and inflammatory diseases, such as multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease.
Dr. Richard Williams from the Kennedy Institute of Rheumatology, Imperial College London UK, a leading scientist in the field of rheumatoid arthritis who supervised the studies, stated, "These preliminary results are very impressive, with CGEN-15001 showing the same level of efficacy as ENBREL®. Furthermore, by testing CGEN-15001 in established disease we are setting the bar quite high, as not many compounds are effective in this setting. Therefore, based on the results seen to date, this molecule definitely should be further studied as a potential therapy for multiple autoimmune diseases."
Dr. Zurit Levine, Compugen's VP of R&D, stated, "We are extremely excited about the pronounced efficacy of CGEN-15001 in an additional autoimmune disease as it substantially broadens the therapeutic potential for this novel molecule and further validates our Protein Family Members Discovery Platform. Modulating the immune system by the use of protein therapeutics targeting B7/CD28-like negative co-stimulatory pathways, such as CGEN-15001 and its membrane protein form, is an area of extensive research and has substantial potential in the development of new therapies for multiple autoimmune and inflammatory diseases, as well as cancer. The high level of interest in this field led to Compugen's recent focus on the B7/CD28 protein family which has resulted thus far in the discovery of nine novel proteins predicted to be previously unknown members of this family. CGEN-15001 is the first of these nine molecules to undergo in vivo validation studies, and has now exhibited impressive therapeutic activity in well recognized animal models of both multiple sclerosis and rheumatoid arthritis."