TARGET PSORIASIS AT IL-23

TARGET PSORIASIS AT IL-231-8

Psoriasis Mechanism of Action Cycle

IN PSORIASIS INFLAMMATION, IL-23*:

  • Maintains immune cells in an inflammatory state2-6
  • Regulates the release of inflammatory cytokines, including IL-17 and TNF-α3-7
  • Does not modify the effects of IL-12, which naturally functions in protecting against infection and cancer2,6-10

BY SELECTIVELY MODULATING IL-23, ILUMYA™:

  • Controls release of both IL-17 and TNF-α to continuously maintain immune homeostasis, even after steady state concentrations were achieved1,11

  • Decreases the cellular inflammatory infiltrate typically seen within psoriasis lesions12

  • Normalizes the expression of inflammatory genes12

  • Stops plaque formation and resolves tissue damage12

ILUMYA™ precisely targets the inflammatory pathway at IL-231

RESPONSE THAT LASTS

See results through Week 14813

Explore Efficacy

SAFETY PROFILE

As demonstrated in Clinical Trial 1 and reSURFACE 1 and 21

See Safety

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 Pharmaceuticals, Inc. 2. 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. 3. Mahil SK, Capon F, Barker JN. Update on psoriasis immunopathogenesis and targeted immunotherapy. Semin Immunopathol. 2016;38(1):11-27. 4. Lowes MA, Suárez-Fariñas M, Krueger JG. Immunology of psoriasis. Annu Rev Immunol. 2014;32:227-255. 5. 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. 6. 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. 7. 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. 8. 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. 9. Kulig P, Musiol S, Freiberger S, et al. IL-12 protects from psoriasiform skin inflammation. Nat Commun. 2016;7:1-14. 10. 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. 11. Data on File. Sun Pharmaceutical Industries, Inc. 12. Kopp T, Riedl E. Bangert C, et al. Clinical improvement in psoriasis with specific targeting of interleukin-23. Nature. 2015;521(7551):222-226. 13. Thaçi D, Iversen L, Pau-Charles I, et al. Long-term efficacy and safety of tildrakizumab in patients with moderate-to-severe psoriasis who were responders at week 28: pooled analysis through 3 years (148 weeks) from reSURFACE 1 and reSURFACE 2 phase 3 trials. Paper presented at: 27th Congress of the European Academy of Dermatology and Venereology (EADV); September 12-16, 2018; Paris, France.