BBI-03 has the potential to modulate the balance of regulatory T cells (TREG) and effector T cells (TEFF), such as TH17 or TH1/TH2 cells, to re-establish immune homeostasis. This novel approach is differentiated from many current topical standard-of-care therapies of dermatologic autoimmune diseases, such as steroids, which are broadly immunosuppressing and may come with side effects including skin thinning, telangiectasias, folliculitis, and contact dermatitis.
In addition, BBI-03 may target innate immune responses through induction of alternative splicing of MyD88 into its short form MyD88s, thereby inhibiting IRAK4-related signaling pathways. This results in significant reduction of cytokines and chemokines including pro-inflammatory IL-6.
BBI-03 has demonstrated efficacy in several preclinical in vivo models of atopic dermatitis and psoriasis and is currently undergoing formulation development for further preclinical assessment.