The nuclear hormone receptor RORγt has emerged as the “master” regulator of Th17 cell differentiation and the production of pro-inflammatory cytokines, such as IL-17A and IL-17F. Increased production of these cytokines has been linked to the pathophysiology of psoriasis. Small molecule inhibitors of RORγt have been shown to reduce production of IL-17 in immune cells and are promising therapies for psoriasis and other autoimmune conditions.

With two decades of experience in nuclear hormone receptor drug discovery, our RORγt drugs are “structurally engineered” to provide high potency and specificity in the target tissue and a high safety margin in patients.

RORγt Drugs

Small-molecule inhibition of RORγt has been shown to reduce production of the inflammatory cytokine IL-17, which plays a key role in autoimmune disorders. Inhibitors of RORγt are being developed for the treatment of IL-17 mediated autoimmune diseases, such as psoriasis and associated co-morbidities. RORγt inhibitors have therapeutic opportunities beyond psoriasis, such as psoriatic arthritis, rheumatoid arthritis, lupus, inflammatory bowel disease and multiple sclerosis. Small-molecule inhibitors of RORγt are also called RORγt “inverse agonists”. Data from a recent clinical trial in mild-to-moderate psoriasis patients has validated RORγt as a target for psoriasis therapy.