Company: OCEA
Filing Date: 2025-04-08
Form Type: 10-K
Source: 0001641172-25-003155
Chunk: 3377

Company: Ocean Biomedical, Inc.
Filing Date: 2025-04-08
Form: 10-K
Item: Item 1A
Chunk 3377
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phosphatase and tensin homolog, or PTEN, and p53 thereby removing intracellular controls against unregulated cell growth. These molecules
taken together form the tumor microenvironment, a localized set of conditions that supports the evolution and growth of tumors.

20

In
summary, Chi3l1 contributes to neoplasia, or the uncontrolled and abnormal growth of cells or tissues that is the hallmark of cancer,
by regulating various pro- and anti-oncogenic pathways as shown in the illustration below:

Chi3l1
and its Roles in Disease Biology

Dr.
Elias and other investigators have also found a direct link between Chit1 and fibrotic diseases, such as IPF and HPS. This finding is
the basis for our anti-Chit1 small molecule therapeutic product candidate, OCF-203, detailed later.

OCX-253—Anti-Chi3l1
mAb for Lung Cancer

Recent
published studies have demonstrated that the levels of circulating Chi3l1 are elevated in many malignancies including cancers of the
prostate, colon, rectum, ovary, kidney, breast, as well as GBM and malignant melanoma. In these diseases, the levels of Chi3l1 frequently
correlate directly with disease progression and inversely with disease-free interval and survival. This is particularly striking in lung
cancer where preclinical and clinical studies demonstrated that the serum and tissue levels of Chi3l1 are increased and are associated
with adverse outcomes, such as poor prognosis and shorter survival. Dr Elias and colleagues have found that Chi3l1 plays a critical role
in the pathogenesis of primary and metastatic lung cancer in murine models that 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.