TARGET PSORIASIS AT IL-23

TARGET THE INFLAMMATORY CYCLE OF PSORIASIS AT
IL-23 WITH ILUMYA® 1-8

ILUMYA® (tildrakizumab-asmn) Mechanism of Action

TARGET THE IL-23 PATHWAY IN THE INFLAMMATORY CYCLE OF PSORIASIS WITH ILUMYA®

An IL-23 inhibitor for moderate-to-severe plaque psoriasis1

By directly targeting IL-23, ILUMYA® (tildrakizumab-asmn):

  • Controls release of both IL-17 and TNF-α to continuously maintain immune homeostasis, even after steady-state concentrations were achieved1,2

  • Decreases the cellular inflammatory infiltrate typically seen within psoriasis lesions3

  • Normalizes the expression of inflammatory genes3

  • Stops plaque formation and resolves tissue damage3

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IL=Interleukin; TNF=tumor necrosis factor.

Cellular diagram illustrating the cycle of psoriasis, from skin stress, to IL-23 activation, to inflammation activation with IL-17 and TNF-α.

IL-23 acts as a key component of the inflammatory cycle of psoriasis by:

  • Maintaining immune cells in an inflammatory state4-8
  • Regulating the release of inflammatory cytokines, including IL-17 and TNF-α5-9
  • Not modifying the effects of IL-12, which naturally functions in protecting against infection and cancer4,8-12

*No formal pharmacodynamics studies have been conducted.1

5 YEARS OF LASTING CLEARANCE2,13

ILUMYA® minimized measurable disease
over 5 years of continuous treatment2,13
Explore Efficacy

INDICATION AND IMPORTANT SAFETY INFORMATION

ILUMYA® (tildrakizumab-asmn) is indicated for the treatment of adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy.

CONTRAINDICATIONS

ILUMYA is contraindicated in patients with a previous serious hypersensitivity reaction to tildrakizumab or to any of the excipients.

WARNINGS AND PRECAUTIONS

Hypersensitivity

Cases of angioedema and urticaria occurred in ILUMYA-treated subjects in clinical trials. If a serious allergic reaction occurs, discontinue ILUMYA immediately and initiate appropriate therapy.

Infections

ILUMYA may increase the risk of infection. Treatment with ILUMYA should not be initiated in patients with a clinically important active infection until the infection resolves or is adequately treated.

Consider the risks and benefits of treatment prior to prescribing ILUMYA in patients with a chronic infection or a history of recurrent infection. Instruct patients receiving ILUMYA to seek medical help if signs or symptoms of clinically important chronic or acute infection occur. If a patient develops a clinically important or serious infection, or is not responding to standard therapy, closely monitor and consider discontinuation of ILUMYA until the infection resolves.

Pretreatment Evaluation for Tuberculosis

Evaluate patients for tuberculosis (TB) infection prior to initiating treatment with ILUMYA. Do not administer ILUMYA to patients with active TB infection. Initiate treatment of latent TB prior to administering ILUMYA. Consider anti-TB therapy prior to initiation of ILUMYA in patients with a past history of latent or active TB in whom an adequate course of treatment cannot be confirmed. Patients receiving ILUMYA should be monitored closely for signs and symptoms of active TB during and after treatment.

Immunizations

Prior to initiating therapy with ILUMYA, consider completion of all age-appropriate immunizations according to current immunization guidelines. Patients treated with ILUMYA should not receive live vaccines.

Adverse Reactions

The most common (≥1%) adverse reactions associated with ILUMYA treatment that were more frequent than in the placebo group are upper respiratory infections, injection-site reactions, and diarrhea.

Please see full Prescribing Information.

 

References: 1. ILUMYA® [package insert]. Princeton, NJ: Sun Pharmaceutical Industries, Inc. 2. Data on File. Sun Pharmaceutical Industries, Inc. 3. Kopp T, Riedl E. Bangert C, et al. Clinical improvement in psoriasis with specific targeting of interleukin-23. Nature. 2015;521(7551):222-226. 4. Campa M, Mansouri B, Warren R, Menter A. A review of biologic therapies targeting IL-23 and IL-17 for use in moderate-to-severe plaque psoriasis. Dermatol Ther (Heidelb). 2016;6(1):1-12. 5. Mahil SK, Capon F, Barker JN. Update on psoriasis immunopathogenesis and targeted immunotherapy. Semin Immunopathol. 2016;38(1):11-27. 6. Lowes MA, Suárez-Fariñas M, Krueger JG. Immunology of psoriasis. Annu Rev Immunol. 2014;32:227-255. 7. Gaspari AA, Tyring S. New and emerging biologic therapies for moderate-to-severe plaque psoriasis: mechanistic rationales and recent clinical data for IL-17 and IL-23 inhibitors. Dermatol Ther. 2015;28(4):179-193. 8. Girolomoni G, Strohal R, Puig L, et al. The role of IL-23 and the IL-23/TH17 immune axis in the pathogenesis of psoriasis. J Eur Acad Dermatol Venereol. 2017;31(10):1616-1626. 9. Marinoni B, Ceribelli A, Massarotti MS, Selmi C. The Th17 axis in psoriatic disease: pathogenetic and therapeutic implications. Auto Immun Highlights. 2014;5(1):9-19. 10. Teng MW, Bowman EP, McElwee JJ, et al. IL-12 and IL-23 cytokines: from discovery to targeted therapies for immune-mediated inflammatory diseases. Nat Med. 2015;21(7):719-729. 11. Kulig P, Musiol S, Freiberger S, et al. IL-12 protects from psoriasiform skin inflammation. Nat Commun. 2016;7:1-14. 12. Ergen E, Yusuf N. Inhibition of interleukin 12 and/or interleukin 23 for treatment of psoriasis: what is the evidence for an effect on malignancy? Experimental Derm. 2018;27(7):737-747. 2021;185(2):323-334. 13. Thaçi D, Piaserico S, Warren RB, et al. Five-year efficacy and safety of tildrakizumab in patients with moderate-to-severe psoriasis who respond at week 28: pooled analyses of two randomized phase III clinical trials (reSURFACE 1 and reSURFACE 2). Br J Dermatol.