Company: OCEA
Filing Date: 2025-04-08
Form Type: 10-K
Source: 0001641172-25-003155
Chunk: 2076

Company: Ocean Biomedical, Inc.
Filing Date: 2025-04-08
Form: 10-K
Item: Item 1A
Chunk 2076
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 It then feeds back to inhibit tissue injury by inhibiting cell death and apoptosis while stimulating fibroproliferative
repair.

The
levels of circulating and tissue Chi3l1 are increased in many human visceral cancers and animal tumor models including lung cancer and
glioblastoma. In visceral tumors elevated serum levels of Chi3l1 correlate with a poor prognosis and shorter disease-free intervals and
survival. Studies in animal models have also demonstrated that the inhibition of Chi3l1 can dramatically reduce tumor burden. Consequently,
Chi3l1 is now appreciated to be a sensitive biomarker and an attractive therapeutic target for these malignancies. We intend to take
advantage of both of these properties because the inhibition of Chi3l1 is a major focus in OCX-253, —410 and —909, and we
intend to use Chi311’s properties as a biomarker to identify relevant populations for clinical trials of these product candidates.

Chi3l1
interacts with several different cell-surface proteins to mediate its cell and tissue responses. Studies by Dr. Elias and others have
demonstrated that Chi3l1 binds to and signals via a number of cell surface receptors (proteins that pass signals between the outside
and inside of cells) including the interleukin-13 receptor-α 2 and CRTH2. They have also demonstrated that IL-13Rα2 is the
alpha subunit of multimeric receptor complexes that can include galectin 3 and CD44 as ß subunits. Chi3l1 can also interact with
receptor tyrosine kinases, integrins αVß3 and αVß5 / syndecan 1 complexes, and the receptor for advanced glycation
end products. These receptors activate a number of signaling pathways including MAPK kinases, Protein Kinase B/Akt and the Wnt/ß-catenin
pathways and induce the production of VEGF intermediaries. As a result of these complex receptor-ligand interactions it is now known
that Chi3l1 regulates oncogenesis via a number of mechanisms. Dr. Elias has demonstrated that Chi3l1 stimulates malignant responses by
inhibiting tumor cell death, stimulating tumor cell proliferation, stimulating the B-Raf protooncogene, and stimulating the phosphorylation
of cofilin. He has demonstrated that Chi3l1 also inhibits key antineoplastic pathways including those mediated by the tumor suppressors