Company: OCEA
Filing Date: 2025-04-08
Form Type: 10-K
Source: 0001641172-25-003155
Chunk: 3378

Company: Ocean Biomedical, Inc.
Filing Date: 2025-04-08
Form: 10-K
Item: Item 1A
Chunk 3378
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 As shown below, both primary tumor growth and metastatic spread were both significantly inhibited via immune inhibition
of Chi3l1 using therapeutic antibodies (Fig. 1). These antibody findings are the basis for Ocean Biomedical’s OCX-253 program in
NSCLC. We plan to initially focus on a subset of patients who exhibit elevated levels of circulating Chi3l1 as they are anticipated to
be the patient population most likely to respond to this product candidate. However, the treatable patient population may eventually
expand as a consequence of the many critical pathways OCX-253 appears to impact (as described and shown in the figure above) and as our
understanding of chitinase biology grows.

21

Figure
1: In Animal Models, Antibodies Against Chi3l1 Show Reduction in Primary and Metastatic Tumors

OCX-410
and OCX-909—Anti-Chi3l1/PD-1 and Anti-Chi3l1/CTLA-4 Bispecific Antibodies for NSCLC and GBM

Novel
immunotherapeutic approaches have improved the prognosis for a number of cancers over the past decade. Cancer cells have unstable genomes
and as a result accumulate genetic mutations that are not seen in normal cells and tissues. These non-self mutations generate non-self
proteins that can be recognized and reacted to by the immune system. Normal white blood cells, particularly T lymphocytes, learn to recognize
these novel antigens and kill the cells that express them. Under normal circumstances, immune responses are activated to deal with pathogens
and non-self antigens but are then inhibited to prevent overexuberant, injury-inducing, immune responses. This immune inhibition is often
mediated by immune checkpoint inhibitor pathways. Unfortunately, some tumors evolve to take advantage of these regulatory pathways to
evade endogenous antitumor immune responses. For example, tumor cells may produce the regulatory protein cell death ligand 1, or PD-L1
or cluster of differentiation proteins 80 or 86. These proteins interact with their corresponding receptors on T cells, PD-1 and CTLA-4,
respectively, to turn off the immune system response to the cancer. Multiple approved immunotherapies disrupt the connection between
PD-1 or CTLA-4 and their ligands to restore immune activity against susceptible cancers.

Dr.
Elias has demonstrated in widely accepted mouse models of cancer that PD-1 and its ligands, PD-L1 and PD-L