Company: OCEA
Filing Date: 2025-04-08
Form Type: 10-K
Source: 0001641172-25-003155
Chunk: 2084

Company: Ocean Biomedical, Inc.
Filing Date: 2025-04-08
Form: 10-K
Item: Item 1A
Chunk 2084
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 pulmonary fibrosis, or HPS-PF, patients. There is no approved drug therapy, and
no treatment except potential lung transplantation. The only pharmacological option for patients is off-label use of Esbriet, which may
slow disease progression but only in patients who retain significant residual lung function. Published clinical studies of Esbriet and
Ofev suggest that bleeding is more likely with Ofev, so its use is generally avoided in the HPS patient population.

We
believe that OCF-203, if approved, has potential to address the need for a HPS therapeutic due to its novel therapeutic approach. It
is also our belief that developing this product candidate for HPS may allow us to enter the broader fibrotic disease space in an expedited
manner by pursuing an ultra-rare disease indication before potentially broadening to adjacent indications.

The
Chitinase Biology Behind Our Fibrosis Product Candidate

Previously,
we described Dr. Elias’ research on chitinase enzymes and CLP, and his discovery of the key role that a CLP called Chi3l1 plays
in cancer. Dr. Elias also discovered that a chitinase called Chit1, also known as chitotriosidase, plays a central role in inflammation
and in fibrotic diseases such as IPF and HPS. Chit1 is expressed in an exaggerated manner in IPF where it correlates inversely with Smad
7. Chit1 is also a critical biomarker and therapeutic target in Scleroderma-associated interstitial lung disease. This finding is the
basis for our anti-Chit1 small molecule therapeutic product candidate, OCF-203.

OCF-203—Small
Molecule Candidate for IPF and HPS

In
animal models, Dr. Elias and his colleagues showed that Chit1 is a master regulator of transforming growth factor beta 1, an extensively-published
biochemical pathway relevant to inflammation, tissue modeling, and fibrosis, and that it mediated fibrosis response through various mechanisms
described below. Animal models of IPF exhibit similar pathology to that of humans, allowing for relevant testing of molecular mechanisms
and potential therapeutics in these models. Transgenic laboratory animals developed in the Elias laboratory to over-express Chit1 were
shown to be far more susceptible to lung fibrosis than their wild type counterparts, which further demonstrates the role of Chit1 as
a factor in IPF.

Using
high throughput screening, Dr.