Company: OCEA
Filing Date: 2025-04-08
Form Type: 10-K
Source: 0001641172-25-003155
Chunk: 2483

Company: Ocean Biomedical, Inc.
Filing Date: 2025-04-08
Form: 10-K
Item: Item 1
Chunk 2483
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 have the same genetic mutations that are seen in human
disease including activating mutations of the K-Ras oncogene. In murine models primary lung cancer is induced in mice that have activating
mutations of Kras (the G12 D mutation) and null mutations of the tumor suppressor p53. Dr Elias and colleagues have additionally demonstrated
that Chi3l1 is able to replace null mutations of p53 in the generation of primary lung cancer in murine models that only have activating
mutations of the K-Ras oncogene. They also demonstrated that Chi3l1 is induced during pulmonary melanoma and pulmonary breast cancer
metastasis in murine models of these diseases and that Chi3l1 induction is required for the generation of a metastasis permissive pulmonary
microenvironment. 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