Small molecule
PubChem CID 9926791
Tofacitinib
Xeljanz
- Mechanism of action
- JAK inhibitor, blocks cytokine signaling that drives inflammation
- In plain language
- Blocks JAK enzymes inside immune cells that relay signals from inflammatory messenger proteins to the cell's nucleus, dialing down an overactive immune system's inflammatory activity.
- How it works
- Tofacitinib (Xeljanz) is a Janus kinase (JAK) inhibitor. Per the FDA label, JAKs are intracellular enzymes that transmit signals from cytokine and growth-factor receptor interactions on the cell membrane to influence cellular processes, including immune cell function; within this pathway, JAKs phosphorylate and activate Signal Transducers and Activators of Transcription (STATs), which modulate gene expression. Tofacitinib modulates this signaling pathway at the point of the JAKs, preventing STAT phosphorylation and activation and dialing down the inflammatory signaling that drives autoimmune disease.
- Therapeutic applications
- Tofacitinib (Xeljanz) is FDA-indicated for moderately to severely active rheumatoid arthritis, active psoriatic arthritis, active ankylosing spondylitis, polyarticular course juvenile idiopathic arthritis, and moderately to severely active ulcerative colitis, generally after an inadequate response or intolerance to one or more TNF blockers. It carries a boxed warning, based on a large postmarketing safety trial in rheumatoid arthritis patients 50 years of age and older with at least one cardiovascular risk factor, for increased risk of serious infections (including tuberculosis), a higher rate of all-cause mortality including sudden cardiovascular death, malignancies including lymphoma and lung cancer, major adverse cardiovascular events, and thrombosis, each compared against TNF blockers.
- Class
- Small molecule
- Therapeutic area
- Immunology
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