Company: OCEA
Filing Date: 2025-04-08
Form Type: 10-K
Source: 0001641172-25-003155
Chunk: 2462

Company: Ocean Biomedical, Inc.
Filing Date: 2025-04-08
Form: 10-K
Item: Item 1
Chunk 2462
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 we believe will enable us to create mutual value for us and potential licensing partners. We
believe this structure, combined with the networks of our leadership team, allows us to opportunistically build a continuous pipeline
of promising product innovations through our existing and potential future relationships with research institutions. Our goal is to optimize
value creation for each of our product candidates, and we intend to continuously assess the best pathway for each as it progresses through
the preclinical and clinical development process—including through internal advancement, partnerships with established companies
and spin-outs or initial public offerings—in order to benefit patients through the commercialization of these products. Our current
active assets are licensed directly or indirectly from Brown University and Rhode Island Hospital. Our scientific co-founders and members
of our board of directors, Dr. Jack A. Elias and Dr. Jonathan Kurtis, are both affiliated with Brown University and with Rhode Island
Hospital.

9

Our
Pipeline

Our
pipeline consists of preclinical programs. We anticipate moving certain preclinical product candidates in our oncology, fibrosis and/or
infectious disease platforms, all licensed exclusively from Brown University and Rhode Island Hospital, into the clinic in the next 12
to 18 months.

Our
programs in oncology and fibrosis are based on discoveries of disease pathways and of related drug targets emerging from pioneering work
in the field of chitinase biology by our scientific co-founder and member of our board of directors, Jack A. Elias, M.D., former Dean
of Medicine and current Special Advisor for Health Affairs to Brown University.

In
oncology, our product candidates are based on Dr. Elias’ findings that a protein called chitinase 3-like-1, or Chi3L1, is a key
driver of multiple disease pathways, including those involved in primary and metastatic tumor development. In animal models of both lung
cancer and glioblastoma, inhibition of Chi3l1 resulted in significant tumor reduction, and the reduction was even greater when the inhibition
of Chi3l1 was combined with immune checkpoint inhibitors, which are used as immuno-therapies to stimulate the body’s immune response
against cancer. Neutralizing antibodies against Chi3l1 have been developed that are highly avid, specific, react with mouse, human and
monkey Chi3l1 and are effectively expressed and humanized. We are developing a mono-specific antibody, or mAb, and two bi-specific monoclonal
antibodies, or BsAbs,