A Pipeline to Explore
the Extraordinary
Odyssey’s pipeline focuses on targets that address patient populations with significant 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-07656 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, or IL-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
Atopic dermatitis, hidradenitis suppurativa, osteoarthritis
Mechanism
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, hidradenitis suppurativa and osteoarthritis.
Additional Information on Target
Understanding Early TLR Signaling Through the Myddosome (paywall)
Targeting IRAK4 for Degradation with PROTACs
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Mechanism
OD-00910 is a monospecific tetravalent V-body 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, improve Treg immunosuppressive function and tissue homing, and enable 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)
News
CloseMechanism
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 Type 2 and non-Type 2 asthma 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 a small molecule inhibitor of NLRP1, an innate immune sensor designed to activate an inflammasome complex that controls the production of IL-1β, IL-18 and a form of cell death called pyroptosis. Upon activation caused by cellular stress (e.g., ribotoxic stress), NLRP1 initiates proinflammatory responses that can lead to autoinflammatory and autoimmune diseases.
CloseMechanism
We are developing a small molecule inhibitor of MDA5, an innate immune sensor responsible for detecting RNA. Upon detection of endogenous RNA, MDA5 initiates proinflammatory responses that lead to autoinflammatory and autoimmune disease.
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 including Pfizer, Johnson & Johnson and Terray Therapeutics, 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.”
