Our Programs
Developing novel and differentiated therapeutics that target both the innate and adaptive immune system.
S1P1R
Dampening the inflammatory response in IBD by sequestering lymphocytes in the lymph nodes
About the S1P1 Receptor
Sphingosine 1 phosphate (S1P) receptors are G-Protein Coupled Receptors involved in the modulation of numerous biological responses, including lymphocyte trafficking from lymph nodes to the peripheral blood. S1P1 receptor (S1P1R) modulators sequester lymphocytes in the lymph nodes, resulting in fewer immune cells in the circulating blood to exacerbate inflammation.
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TYK2
Inhibiting type I interferon and the Th1/Th17 axis for the treatment of psoriasis and other autoimmune diseases
About TYK2
A member of the JAK family, Tyrosine Kinase 2 (TYK2) regulates both innate and adaptive immunity by mediating type I interferon, IL-12 and IL-23 signaling. Selective inhibition of TYK2 without inhibition of other JAK family enzymes provides an optimal balance between reducing inflammation and preserving immune protection.
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NLRP3
Targeting the inflammasome/IL-1β axis to break the inflammation feed-forward loop in autoinflammatory and autoimmune diseases
About NLRP3
NLRP3, the best-characterized inflammasome, is known to be activated by a range of non-infectious tissue damage signals associated with aging, physical inactivity and obesity. Its activation results in the production of inflammatory cytokines (IL-1β and IL-18), as well as a type of cell death called pyroptosis.
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cGAS
Targeting the cGAS/STING pathway for the treatment of type I interferon associated pathologies in autoinflammatory and autoimmune diseases
About cGAS
cGAS is the predominant sensor of abnormal double-stranded DNA in cells. The engagement of cGAS leads to the activation of STING. The cGAS/STING pathway stimulates the production of inflammatory cytokines, including type I interferon. While cGAS plays a role in host defense against invading pathogens, chronic activation by self-DNA can trigger systemic inflammation that exacerbates autoimmune disease progression.
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Gasdermin D
Inhibiting pyroptosis, a pro-inflammatory form of cell death, for the treatment of autoinflammatory diseases
About Gasdermin D
Pyroptosis, a form of cell death caused by lysis (cell membrane rupture), results in the rapid release of proinflammatory mediators. The pore-forming protein gasdermin D (GSDMD) is a central player in this cell death and deleterious inflammation feed-forward loop.
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