Targeted inhibiton of protein kinase c beta ameliorates pemphigus-related skin blistering disorders
''Inhibition of PKCßII offers therapeutic potential for ameliorating desmosome-related disorders
Background: Pemphigus is a painful autoimmune blistering disorder caused by autoantibodies developed by the patients to attack desmosomal junction proteins, essential for maintaining cell-cell attachment between keratinocytes in the epidermis and mucous membrane. Treatment strategies for pemphigus involve the use of systemic glucocorticoids and immunosuppressant adjuvant. The use of systemic glucocorticoids often leads to severe side effects and lesions cannot always be cleared clinically. Thus, there is a strong need for the development of novel therapeutic approaches for pemphigus.
Technology Overview: Dr. Jiang Chen at Stony Brook University has established a causal relationship between upregulation of PRKCß and pathophysiology in pemphigus using a patient-IgG induced in vitro pemphigus model and a pemphigus mouse model. Using a proprietary PRKCßspecific inhibitor, Dr. Chen confirmed that inhibiting PRKCß can ameliorate keratinocyte adhesion defects in both an in-vitro model and in pemphigus patients-IgG treated cells. These results suggests that up regulation of PRKCß is a common process down stream of the disruption of desmosomal junctions, and PRKCß inhibition may ameliorate blistering phenotypes in all types of pemphigus.
Advantages: Novel target Tested compounds in clinical trials. Targeted treatment: PRKCß only expressed in diseased keratinocytes
Applications: Therapy for pemphigus
Intellectual Property Summary: Provisional filed
Stage of Development: Animal Data
Licensing Potential: Available for licensing
Licensing Status: Available for License