A Pipeline to Explore
the Extraordinary
Odyssey’s pipeline focuses on targets that address patient populations with unmet need within immunology. By leveraging our expertise in immunology and strategically employing two therapeutic modalities—small molecules and protein therapeutics—we aim to develop innovative medicines that make significant advancements over the standard of care. Each program is focused on modulating the root of inflammatory dysregulation through highly selective targeting of key nodes of inflammatory signaling.

Pipeline
Targeting the next wave of innovation by addressing upstream
activation nodes that initiate and sustain inflammation
Mechanism
OD-001 is an oral small molecule RIPK2 scaffolding inhibitor. We believe that blocking RIPK2 scaffolding with XIAP has the potential to block downstream pathway signaling and activation of proinflammatory cells of both the innate and adaptive immune systems that drive pathology and produce high levels of cytokines (e.g., TNF, TNF-like cytokine 1A, or TL1A, and interleukin 23) that each are validated therapeutic targets for inflammatory bowel disease (IBD).
Additional Information on Target
RIPK2 as a Promising Druggable Target for Autoimmune Diseases (paywall)
Receptor Interacting Ser/Thr-Protein Kinase 2 as a New Therapeutic Target (paywall)
RIPK2 NODs to XIAP and IBD (paywall)
Disruption of XIAP-RIP2 Association Blocks NOD2-Mediated Inflammatory Signaling
Small Molecule Inhibitors Reveal an Indispensable Scaffolding Role of RIPK2 in NOD2 Signaling
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Small molecule therapeutic
Cutaneous lupus erythematosus, nephropathies, and B cell-mediated diseases
Mechanism
OD-002 is an oral small molecule SLC15A4 inhibitor designed to selectively block TLR7/8/9-mediated activation of interferon regulatory factor 5, IRF5. IRF5 controls the production of inflammatory cytokines in myeloid cells, proliferation and survival of pathogenic B cells, and production of autoantibodies. Our program is designed to be a first-in-class approach to block disease-relevant signaling while retaining other host defense functions of IRF5. We believe targeting SLC15A4 has the potential to be developed for multiple inflammatory or interferon-mediated diseases, including lupus, Sjögren’s syndrome, dermatomyositis, systemic sclerosis, nephropathies, and other B cell-mediated diseases.
Additional Information on Target
SLC15A4 controls endolysosomal TLR7–9 responses by recruiting the innate immune adaptor TASL
TASL is the SLC15A4-associated adaptor for IRF5 activation by TLR7-9
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Mechanism
OD-003 is a protein therapeutic designed to agonize TNFR2 selectively on Treg. TNFR2 is a surface receptor that is highly expressed on Treg with relatively limited expression on other cell types. Agonizing TNFR2 on Treg can reduce inflammation by increasing Treg number, improving Treg immunosuppressive function and tissue homing, and enabling Treg to retain a stable immunosuppressive phenotype. We believe these features can unlock the full potential of a Treg-targeted therapy and address the shortcomings of historical approaches, such as IL-2.
Additional Information on Target
TNF-Alpha: An Activator of CD4+FoxP3+TNFR2+ Regulatory T cells
Regulatory T cells in the Treatment of Disease (paywall)
Harnessing Regulatory T cells to Establish Immune Tolerance (paywall)
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Mechanism
We are developing a TSLP/IL-33 bispecific antagonist designed to address upstream cytokine redundancy and improve suppression of inflammation. TSLP and IL-33 are two alarmins that are promising targets for the treatment of inflammatory conditions like asthma and COPD because of their redundant function in activating common inflammatory pathways. TSLP antagonists are approved to treat asthma and IL-33 antagonism has shown clinical activity in respiratory diseases.
CloseMechanism
We are developing an oral small molecule IRAK4 scaffolding inhibitor designed to block inflammatory signaling by the myddosome, a protein complex found in multiple cell types across tissues. The myddosome serves as a key junction of inflammatory signaling where innate immune signals converge to initiate a broad downstream cytokine response. Our program is designed to address the shortcomings of other programs targeting IRAK4, including small molecule kinase inhibitors and degraders, by achieving the desired pharmacology to block cytokine production across disease-relevant cell types, both inside and outside of the immune system. We believe IRAK4 scaffolding inhibition has the potential to be developed for multiple inflammatory diseases, including atopic dermatitis and hidradenitis suppurativa.
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Small molecule therapeutic
Cutaneous lupus erythematosus, nephropathies, and B cell-mediated diseases
In collaboration with our partner, Terray, we are developing a small molecule inhibitor of IRF5. IRF5 controls the production of inflammatory cytokines in myeloid cells, proliferation and survival of pathogenic B cells, and production of autoantibodies. We believe IRF5 inhibition represents a complementary strategy to target the interferon pathway alongside our wholly owned SLC15A4 inhibitor as different diseases may benefit from broader or more selective inhibition.
ClosePartnerships
Odyssey collaborates with leading biotech and pharmaceutical companies on challenging targets of mutual interest, leveraging complementary expertise to discover and develop cutting-edge solutions for patients worldwide. Our strategic partnerships are built on shared goals, fostering innovation through joint research, co-development and access to advanced technologies and resources. By partnering with industry leaders, we seek to amplify our impact, enable breakthrough discoveries and deliver transformative healthcare solutions faster and more efficiently.
Our Pipeline
“We are uniquely equipped to address some of the most complex challenges across inflammatory and autoimmune disease, aiming to produce solutions that drive real-world impact for patients.”
