TREMFYA (guselkumab) by Johnson & Johnson is interleukin-23 antagonists [moa]. Approved for interleukin-23 antagonist [epc]. First approved in 2017.
Drug data last refreshed 21h ago · AI intelligence enriched 3w ago
TREMFYA (guselkumab) is a monoclonal antibody developed by Johnson & Johnson that selectively antagonizes interleukin-23 (IL-23), a key cytokine in inflammatory and immune-mediated diseases. Approved by the FDA on July 13, 2017, it is administered via subcutaneous injection. The drug is indicated for treatment of moderate-to-severe plaque psoriasis and other IL-23-driven conditions. It represents a targeted approach to reducing inflammatory signaling in dermatological and systemic diseases.
Interleukin-23 Antagonists
Interleukin-23 Antagonist
Indication data is being enriched from DailyMed and FDA labeling. Check back soon for approved therapeutic uses.
A Study to Assess Real-world Outcomes for Long-Term Use of Guselkumab
A Study of Guselkumab Versus Risankizumab in Participants With Moderately to Severely Active Crohn's Disease
A Real-World Study of Guselkumab in Ulcerative Colitis and Crohn's Disease in Saudi Arabia
An Observational, Multicenter Study to Evaluate the Effectiveness of Guselkumab for the Treatment of Participants With Crohn's Disease After Surgical Resection
A Study of Guselkumab Treatment Persistence in Psoriatic Arthritis Participants
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The information on this page is for informational purposes only and should not be used as a substitute for professional medical advice. Drug information is sourced from FDA, DailyMed, and other government databases. Adverse event data from FAERS does not establish causation. Always consult a healthcare professional for medical decisions.
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TREMFYA currently supports 2 open linked job positions, indicating moderate active hiring. Roles typically include brand managers overseeing commercial strategy, medical science liaisons (MSLs) conducting clinical education, and field sales representatives. Success in these roles requires deep knowledge of psoriasis treatment paradigms, IL-23 biology, payer/formulary dynamics, and ability to differentiate against risankizumab and mirikizumab in a competitive therapeutic class.