Expert: Bispecific mAb neutralizing both IL-17A and IL-17F via the same IL-17RA/IL-17RC receptor complex. IL-17F is regulated by STAT5-inducing cytokines (IL-2, IL-7, IL-15) and IL-1beta, leading to preferential IL-17F overproduction in psoriatic lesions (~8-fold elevation vs ~6.7-fold for IL-17A). Dual blockade achieves PASI 100 ~62% Wk16 vs ~35-40% with IL-17A-only. BE RADIANT crossover data confirms IL-17F-driven residual disease: Cosentyx→Bimzelx switch improved PASI 100 from 52.8% to 76.6%. Higher oral candidiasis (10-21%) reflects disruption of both IL-17A and IL-17F-mediated mucosal neutrophil chemotaxis via CXCL1/CXCL5/CXCL8 and antimicrobial peptides (beta-defensins, S100A). Transcriptomic normalization by Wk8; deepening clinical response reflects epidermal remodeling kinetics. Median time to PASI 75 loss after discontinuation: 32 weeks (BE READY), suggesting partial immunological reset.

Everyday: Blocks both IL-17A and IL-17F — two inflammatory proteins that directly damage skin in psoriasis. IN HEALTHY PEOPLE: IL-17A and IL-17F are part of your immune defense system. Both proteins call in neutrophils (first-responder white blood cells) to fight infections, especially yeast (Candida) in your mouth and throat. They signal through the same receptor (IL-17RA/RC) on skin and mucosal cells. IL-17F is actually produced in HIGHER quantities than IL-17A — it is the more abundant defender. IN PSORIASIS: Both IL-17A and IL-17F are massively overproduced in skin plaques. IL-17F levels are elevated ~8-fold in affected skin (vs ~6.7-fold for IL-17A). The inflamed environment of a psoriatic plaque specifically amplifies IL-17F production through STAT5 signaling. Both proteins cause keratinocytes (skin cells) to multiply too fast, recruit more immune cells, and sustain chronic inflammation. WHY DUAL BLOCKADE IS BETTER FOR SKIN: Blocking IL-17A alone (Cosentyx) removes one fuel source, but IL-17F keeps driving residual inflammation — creating a ceiling at ~50-60% PASI 90. Bimzelx blocks BOTH fuels, achieving ~86-91% PASI 90. Direct proof: in BE RADIANT, patients on Cosentyx who switched to Bimzelx saw their remaining patches clear — confirming IL-17F sustained the residual disease. WHY DUAL BLOCKADE CAUSES MORE THRUSH: In your mouth, both IL-17A and IL-17F work as alarm signals calling neutrophils to fight yeast. Cosentyx cuts one alarm wire — IL-17F still works as backup (thrush ~2-5%). Bimzelx cuts BOTH wires — no alarm at all, yeast grows unchecked (thrush ~10-21%, though 99.3% mild/moderate, treatable with antifungals). WHY RESPONSE DEEPENS OVER TIME: By completely normalizing the IL-17 inflammatory gene signature in skin (by week 8 per transcriptomic data), Bimzelx allows the skin to physically remodel — thickening resolves, blood vessels normalize, immune infiltrates clear. This physical healing takes months after the molecular fire is extinguished.

Targets: ["IL-17A","IL-17F"]

Primary EP: [{"id":"pasi90-w12","name":"PASI 90 at Week 12","type":"PRIMARY","unit":"%","results":[{"value":76.5,"arm_id":"son120-arm","p_value":0.001},{"value":77,"arm_id":"son60-arm"},{"value":73.6,"arm_id":"se

Trivalent camelid nanobody (~40 kDa) targeting IL-17A, IL-17F, and IL-17A/F heterodimer via separate domains. Albumin-binding module extends half-life. Phase 2b PsO data: PASI 90 ~77% Wk12 (120mg augmented). Phase 3 focus pivoted to HS (VELA program) and PsA (IZAR). No Phase 3 plaque psoriasis planned. Key difference from bimekizumab: smaller (monovalent domains vs bivalent IgG1), potentially shorter effective half-life, lower functional avidity. VELA HS Phase 3 results mixed (VELA-2 missed primary). IZAR PsA readout expected H1 2026.