Nuclear receptors (NRs) are ligand-regulated transcription factors that display canonical domain structure with highly conserved DNA-binding and ligand-binding domains. The identification of the endogenous ligands for several receptors remains elusive or is controversial, and thus these receptors are classified as orphans. One such orphan receptor is the retinoic acid receptor-related orphan receptor γ (RORγ). An isoform of RORγ, RORγt, has been shown to be essential for the expression of Interleukin 17 (IL-17) and the differentiation of Th17 cells. Th17 cells have been implicated in the pathology of several autoimmune diseases, including multiple sclerosis (MS) and rheumatoid arthritis (RA). Genetic ablation of RORγ alone or in combination with RORα in mice led to impaired Th17 differentiation and protected the mice from development of experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. Here we describe SR2211, a selective RORγ modulator that potently inhibits production of IL-17 in cells.