Company: OCEA
Filing Date: 2025-04-08
Form Type: 10-K
Source: 0001641172-25-003155
Chunk: 2085

Company: Ocean Biomedical, Inc.
Filing Date: 2025-04-08
Form: 10-K
Item: Item 1A
Chunk 2085
---
 Elias identified a small molecule candidate for the OCF-203 program that prevented and reduced inflammation
and fibrosis in the bleomycin mouse model of IPF (Fig. 5). Importantly, the molecular mediators of fibrosis, fibronectin, Col1A1, and
Col3A1, were also substantially reduced in the IPF model animals that had received the OCF-203 candidate. Results were similar in a mouse
model of HPS (Fig. 6), suggesting that the OCF-203 molecule could benefit this patient population as well. The biochemical pathways known
to be impacted by Chit1 inhibition imply that there may be benefit of this product candidate for the potential treatment of other fibrotic
diseases such as non-alcoholic-steatohepatitis, or NASH, and lysosomal storage disorders.

26

Figure
6: OCF-203 Lead Candidate Treatment Reduces Observed Markers of Fibrosis in an Animal Model of IPF

Figure
7: OCF-203 Lead Candidate Treatment of the Bleomycin HPS-1 Mouse Model results in Normalized Levels of Fibrotic Markers

No
significant toxicity has been observed at therapeutic doses in the animal studies with the OCF-203 lead to date. This candidate molecule
has been previously evaluated (by unrelated parties) in Japan in the mid-1960s for potential use as an antibiotic – though approval
was never pursued. While the clinical data from these studies is not suitable for current regulatory filings, we believe it may support
the safety observations seen in Dr. Elias’ recent animal studies and also provides invaluable information as to the behavior of
this molecule and its derivatives that we can potentially use in the design of future clinical development work. Additionally, we believe
OCF-203’s safety observations in animal studies may be further supported by past published literature which estimates that 6% of
humans do not produce Chit1 and, though they may be more susceptible to infection by chitin-containing parasites, this deficiency may
provide greater longevity and reduced age-related disease burden as compared to people who produce Chit1 normally. Taken together, these
findings suggest that therapies that focus on inhibiting Chit1 may be well tolerated in patients. This is of import to IPF and HPS given
that there are no currently approved drug therapies for HPS, and the currently approved therapies for IPF, pirfenidone and nintedanib,
both