Cosentyx secukinumab APPROVED
Drug Profile
ModalityAntibody
RouteSC
Therapy AreaImmunology
Launch2015-01-21
US LOE2030-12-26
Peak Sales Est$8000M
Formulations[{"id":"cosentyx-sc","doses":"300mg (two 150mg injections or single-dose pen)","notes":"Induction: 3
Companies
NVS (ORIGINATOR)100%
Mechanism: IL-17A inhibitor
Expert: mAb neutralizing IL-17A. Rapid onset from direct downstream effector blockade. Does not neutralize IL-17F (expressed at 5-30x higher levels via differential STAT5 regulation, non-redundant inflammatory functions). PASI 90 ~54-59% Wk12, plateaus by Wk52 (~63%). Evidence of waning vs IL-23 inhibitors (IMMerge: secukinumab 57% vs risankizumab 87% PASI 90 at Wk52). Does not deplete TRM17 cells — blocks effector cytokine but not Th17 survival signal. Candidiasis 0.9/100 PY (300mg) — IL-17F backup preserves partial mucosal immunity. No disease modification: median relapse within 6-8 weeks of discontinuation.
Everyday: Blocks IL-17A only — the most potent (per molecule) inflammatory signal in psoriasis, but NOT its more abundant partner IL-17F. IN HEALTHY PEOPLE: IL-17A is a key immune defense protein, particularly important for fighting fungal infections. It is one of two closely related proteins (the other being IL-17F) that call neutrophils to fight threats. IN PSORIASIS: IL-17A is overproduced in skin plaques and directly causes skin cells to multiply too fast. Blocking it produces rapid improvement because you are intercepting inflammation at the final step — right where the damage happens. LIMITATIONS: IL-17F (the more abundant partner) continues driving residual inflammation. This creates a ceiling effect — about 50-60% of patients achieve PASI 90, but response plateaus because IL-17F establishes a new steady state. Cosentyx also does NOT deplete the tissue-resident memory T cells (TRM17) that hide in skin and cause relapse, because it blocks a downstream product rather than the upstream survival signal (IL-23). This is why response does NOT deepen over time the way Skyrizi or Bimzelx does. CANDIDIASIS: Moderate risk (~2-5%) because IL-17F still provides backup mucosal defense against yeast.
Targets: ["IL-17A"]
Revenue History
PeriodRevenue ($M)
2023$5,000M
2024$6,112M
2025$6,670M
Q3 2025$1,698M
Q4 2025$1,807M
Programs (4)
IndicationStageKey StudyRegional Status
Plaque psoriasisAPPROVEDERASURE/FIXTURE[{"stage":"APPROVED","region":"US","approval_date":"2015-01"}]
Psoriatic arthritisAPPROVEDFUTURE 1/2[{"stage":"APPROVED","region":"US","approval_date":"2016-01"}]
Ankylosing spondylitisAPPROVEDMEASURE 1/2[{"stage":"APPROVED","region":"US","approval_date":"2016-01"}]
Polymyalgia rheumaticaPHASE3Phase 3[]
Upcoming Catalysts (1)
Cosentyx - Biosimilar Competition Timeline Ongoing
Notes
First approved IL-17A inhibitor (2015). Rapid onset but response PLATEAUS — does not deepen over time because IL-17F drives residual disease. PASI 90 54-59% Wk12, ~63% Wk52. PASI 100 24-29% Wk12. Beaten by Bimzelx in BE RADIANT (PASI 100: 48.9% vs 61.7% Wk16). Beaten by Skyrizi in IMMerge (PASI 90: 57% vs 87% Wk52). Candidiasis ~2-5% (IL-17F backup preserved). Approved: PsO (2015), PsA, AS, nr-axSpA, HS. US LOE ~2029 (core patent). Peak estimate $8B+. Revenue $6.67B (2025) across all indications.
Data from Supabase · Updated 2026-03-24