Date of Presentation
5-2-2024 12:00 AM
College
Rowan-Virtua School of Osteopathic Medicine
Poster Abstract
Up to 70 million people worldwide suffer from vitiligo, an autoimmune disease characterized by the destruction of melanin. Current treatment options vary in efficacy. The disease manifests clinically as white circular macules of depigmentation seen primarily on the face and appendages.1 The pathophysiology of vitiligo is multifactorial and still being studied. One proposed mechanism behind the pathophysiology of vitiligo involves the upregulation of interferon gamma (IFN-γ) with downstream effects on JAK/STAT pathways resulting in CXCL10 transcription.1,2 Here we discuss Ruxolitinib, a topical JAK inhibitor, that recently passed its clinical trial phase, and Ritlecitinib, an oral JAK inhibitor which is currently undergoing clinical trials.3,4 These drugs are a reflection of the recent increase in targeted therapies for dermatologic diseases. The promising results of these drugs are widening the possible treatment options for patients that suffer from vitiligo.
Keywords
vitiligo, JAK inhibitors, ruxolitinib, ritlecitinib, Janus Kinase Inhibitors
Disciplines
Dermatology | Enzymes and Coenzymes | Integumentary System | Medicine and Health Sciences | Pathological Conditions, Signs and Symptoms | Skin and Connective Tissue Diseases | Therapeutics
Document Type
Poster
DOI
10.31986/issn.2689-0690_rdw.stratford_research_day.180_2024
Included in
Dermatology Commons, Enzymes and Coenzymes Commons, Integumentary System Commons, Pathological Conditions, Signs and Symptoms Commons, Skin and Connective Tissue Diseases Commons, Therapeutics Commons
Janus Kinase (JAK) Inhibitors: A New Frontier in the Treatment of Vitiligo
Up to 70 million people worldwide suffer from vitiligo, an autoimmune disease characterized by the destruction of melanin. Current treatment options vary in efficacy. The disease manifests clinically as white circular macules of depigmentation seen primarily on the face and appendages.1 The pathophysiology of vitiligo is multifactorial and still being studied. One proposed mechanism behind the pathophysiology of vitiligo involves the upregulation of interferon gamma (IFN-γ) with downstream effects on JAK/STAT pathways resulting in CXCL10 transcription.1,2 Here we discuss Ruxolitinib, a topical JAK inhibitor, that recently passed its clinical trial phase, and Ritlecitinib, an oral JAK inhibitor which is currently undergoing clinical trials.3,4 These drugs are a reflection of the recent increase in targeted therapies for dermatologic diseases. The promising results of these drugs are widening the possible treatment options for patients that suffer from vitiligo.