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Innovation Pharmaceuticals Brilacidin as a Novel Inhibitor of Phosphodiesterase 4 (PDE4) Supports its Potential to Treat Autoimmune and Inflammatory Diseases; Company Invited to Present at Upcoming Crohn’s & Colitis Foundation Conference
Innovation Pharmaceuticals Brilacidin as a Novel Inhibitor of Phosphodiesterase 4 (PDE4) Supports its Potential to Treat Autoimmune and Inflammatory Diseases; Company Invited to Present at Upcoming Crohn’s & Colitis Foundation Conference.
About this update from Innovation Pharmaceuticals Inc.
[{"type":"text","content":"\nBEVERLY, Mass., Oct. 12, 2018 (GLOBE NEWSWIRE) -- Innovation Pharmaceuticals, (OTCQB:IPIX) (“the Company”), a clinical stage biopharmaceutical company, is pleased to provide this update on Brilacidin as a novel inhibitor of Phosphodiesterase 4 (PDE4), an important aspect of its mechanism of action. PDE4 inhibitors, such as apremilast and crisaborole—the latter having been acquired by Pfizer in 2016 from Anacor—for dermatological conditions, are a well-established and actively marketed class of drugs used to treat a variety of autoimmune and inflammatory diseases. PDE4 inhibition is being studied as a novel therapeutic avenue in treating Inflammatory Bowel Disease (IBD).\n Brilacidin’s Inhibition of PDE4 Due to multiple immunoregulatory functions, defensins—small antimicrobial peptides widely expressed and produced in skin and mucosal surfaces, as well as in neutrophils—play a critical role in mediating human health and disease. Brilacidin, the design of which was modeled on defensins, has been shown to be a potent regulator of immune response (data on file). It suppresses various pro-inflammatory mediators (e.g., TNF-α, IL-1β, IL-8, IL-6, MMP-9, MCP-1). One potentially central aspect of Brilacidin’s mechanism of action concerns its modulation of the cyclic adenosine monophosphate (cAMP) pathway, an established therapeutic target, through its ability to inhibit Phosphodiesterase 4 (PDE4) as well as Phosphodiesterase 3 (PDE3). In more detail, pre-clinical studies have demonstrated that Brilacidin inhibits PDE4B2 and PDE3A in vitro, in a dose dependent manner. Brilacidin demonstrated similar IC50 values against both PDE4 (biochemical) and cytokine release in cell-based assays, suggesting Brilacidin has good cell membrane permeability. Localized clinical administration enables Brilacidin concentrations that markedly exceed in vitro IC50 values, and, consequently, provides for increased concentrations of cAMP. The overall effect of Brilacidin’s ability to modulate cAMP levels—complementing other aspects of its broad immunomodulatory profile—supports its potential to treat a number of chronic, autoimmune and inflammatory diseases related to issues of innate immunity, such as: IBD, atopic dermatitis, and others. While Brilacidin inhibition of PDE4, similar to...