A 35-year-old man with moderate-to-severe plaque psoriasis (PASI 22, DLQI 18) is started on secukinumab. After 16 weeks (loading dose + maintenance), PASI 90 response is achieved. Secukinumab's mechanism of action is:
- A Blockade of IL-17A ✓
- B Inhibition of TNF-α
- C Blockade of IL-12/23 (p40 subunit)
- D Inhibition of JAK1/JAK2
Explanation
Secukinumab is a fully human monoclonal IgG1 antibody that selectively binds and neutralises IL-17A, a key effector cytokine in psoriasis pathogenesis produced by Th17 cells. Other IL-17 pathway biologics include ixekizumab (anti-IL-17A) and bimekizumab (anti-IL-17A and IL-17F). Ustekinumab targets the p40 subunit shared by IL-12 and IL-23. Guselkumab, risankizumab, and tildrakizumab target IL-23 p19 subunit specifically. TNF inhibitors (adalimumab, etanercept, infliximab) are first-generation biologics. JAK inhibitors (tofacitinib, deucravacitinib) are small molecule oral therapies.
Reference: Neena Khanna Illustrated Synopsis of Dermatology & STD, 6th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.