Ocean Biomed: Allowance for U.S. Patent Application for Breakthrough Pulmonary Fibrosis Treatments

 Ocean Biomedical, Inc. (NASDAQ: OCEA), a biopharma company working to accelerate the development and commercialization of scientifically compelling assets from research universities and medical centers, announced today that its Scientific Co-founder Dr. Jack A. Elias, received a Notice of Allowance from the United States Patent and Trademark Office (“USPTO”) for his U.S. patent application covering a therapeutic molecule that Ocean Biomedical is working to advance into the clinic for patients suffering from pulmonary fibrosis. Discoveries in recent years by Ocean Biomedical’s Scientific Co-founder, Dr. Jack A. Elias, and his colleagues at Brown University, have revealed a new target and a new pathway for treating pulmonary tissue damage in Idiopathic Pulmonary Fibrosis (IPF). This patent allowance covers pulmonary fibrosis caused by multiple conditions including: idiopathic pulmonary fibrosis (IPF), genetic pulmonary fibrosis such as Hermansky-Pudlak Syndrome (HPS), chemotherapy and radiation-induced pulmonary fibrosis, and exposure-induced interstitial lung diseases including asbestosis and silicosis.

A Notice of Allowance is issued after the USPTO examines a patent application and determines that the applicant should be granted a patent from the application. Ocean Biomedical anticipates that a patent will be issued by the USPTO from Dr. Elias’ application in the coming months.

Ocean Biomedical’s novel approach to treating pulmonary fibrosis – a condition with no disease modifying agents currently available – is focused on inhibiting Chitinase 1 (Chit1) with patented “OCF-203.” Chit1 is also a critical biomarker in Scleroderma-associated interstitial lung disease (SSc-ILD) and plays a role in bleomycin- and IL-13-induced pulmonary fibrosis. In four pulmonary fibrosis animal models, Ocean Biomedical’s OCF-203 has shown an 85% – 90% reduction in collagen accumulation. The results of this antifibrotic (termed molecule X: SMX) in the bleomycin model can be seen in the diagram below. Results also showed efficacy in the pale-ear mouse model of HPS, including impressive reductions in fibrosis. As a result, efforts are now moving towards IND-enabling studies.

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