Taltz ixekizumab APPROVED
Drug Profile
ModalityAntibody
RouteSC
Therapy AreaImmunology
Launch2016-03-22
US LOE2028-03-01
Peak Sales Est$4000M
Formulations[{"id":"taltz-sc","doses":"80mg (single injection; 160mg loading dose at Wk 0 = two injections)","no
Companies
LLY (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$2,760M
2024$3,260M
Q4 2024$952M
Programs (3)
IndicationStageKey StudyRegional Status
PsOAPPROVEDUNCOVER[{"stage":"APPROVED","region":"US","approval_date":"2016-03-22"},{"stage":"APPRO
PsAAPPROVEDSPIRIT-P1/P2[{"stage":"APPROVED","region":"US","approval_date":"2017-12-05"},{"stage":"APPRO
Mod-sev PsOAPPROVED[]
Clinical Studies (1)
UNCOVER-2 PHASE3
COMPLETED · n=1224
Primary EP: [{"id":"pasi75-w12","name":"PASI 75 at Week 12","type":"PRIMARY","unit":"%","results":[{"value":89.7,"arm_id":"ix80-arm","p_value":0.001},{"value":77.5,"arm_id":"ix80q4-arm"},{"value":41.6,"arm_id":"e
NCT01597245
Upcoming Catalysts (1)
Taltz + Zepbound - PsA/Obesity - FDA Filing H2 2026
Notes
IL-17A inhibitor (2016). Similar mechanism to Cosentyx but slightly different PK. PASI 90 68-71% Wk12 (UNCOVER trials). PASI 100 35-40% Wk12. Strong 5-year data: PASI 90 85% Wk60. Candidiasis ~2% (lower than Bimzelx, similar to Cosentyx). Injection site reactions more common than other IL-17s. Heavy induction: q2w for 12 weeks. Approved: PsO (2016), PsA, AS, nr-axSpA. US LOE late 2020s. Revenue $3.26B (2024).
Data from Supabase · Updated 2026-03-24