Canakinumab, approved for treatment of gouty arthritis, works by specifically neutralising which cytokine that is central to NLRP3 inflammasome-mediated joint inflammation in gout?
- A Tumor necrosis factor alpha (TNF-α)
- B Interleukin-6 (IL-6)
- C Interleukin-1 beta (IL-1β) ✓
- D Interleukin-17 (IL-17)
Explanation
Monosodium urate crystals activate the NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammasome in macrophages and neutrophils, leading to caspase-1 activation and processing of pro-IL-1β into active IL-1β. IL-1β is the principal cytokine driving the acute gouty arthritis cascade. Canakinumab is a fully human monoclonal IgG1 antibody that selectively neutralises IL-1β, preventing it from binding to the IL-1 receptor. It is used for recurrent gouty flares when standard drugs are contraindicated. Anakinra (IL-1 receptor antagonist) is an alternative. TNF-α, IL-6, and IL-17 are not the primary mediators in NLRP3-driven gout inflammation.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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