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JAK Inhibitor Mechanism — SCE Rheumatology MCQ

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ModerateRheumatology PharmacologyJAK Inhibitor MechanismSCE Rheumatology

A 50-year-old woman with rheumatoid arthritis is considering baricitinib. Which statement best describes its mechanism and the principal pharmacological distinction between baricitinib and biological DMARDs?

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Correct answer: D — It is an oral small molecule that reversibly inhibits intracellular JAK1 and JAK2, reducing STAT activation downstream of several cytokine receptors; biological DMARDs target extracellular or cell-surface molecules.

Baricitinib is an orally administered targeted synthetic DMARD. It selectively and reversibly inhibits intracellular JAK1 and JAK2, reducing phosphorylation and activation of STAT proteins downstream of several cytokine and growth-factor receptors. This allows one small molecule to modulate signalling from multiple JAK-dependent mediators. Biological DMARDs are proteins that instead bind extracellular cytokines, cell-surface receptors or cellular targets—for example TNF inhibitors, IL-6 receptor inhibitors, abatacept and rituximab. Baricitinib is therefore neither a monoclonal antibody nor a fusion protein, excluding A and B. Cyclo-oxygenase inhibition is the mechanism of NSAIDs, excluding D. CD20-positive B-cell depletion is produced by rituximab, a biological DMARD, not by baricitinib, excluding E.

Reference: Electronic Medicines Compendium. Baricitinib Lilly 4 mg film-coated tablets, Summary of Product Characteristics, sections 4.2 and 5.1; text revised 15 May 2026. https://www.medicines.org.uk/emc/product/16006/smpc