New Medication Choice

The goals of vitiligo treatment include stabilizing the condition, achieving repigmentation, and preventing recurrence. Recently, topical JAK inhibitors have been explored as a promising therapeutic option for vitiligo. The activation of the JAK-STAT pathway and the inflammatory cycle led to the destruction of melanocytes, resulting in depigmentation.3

Topical JAK inhibitors block the JAK-STAT pathway, which reduces JAK-STAT signaling and suppresses inflammatory responses. This helps to prevent the body’s attack on melanin-producing cells. Therefore, the JAK-STAT pathway presents a compelling target for therapeutic intervention. 3,4

Clinical studies on the effectiveness of topical JAK inhibitor have shown promising results. In clinical trials, the application of a JAK inhibitor cream resulted in greater repigmentation in non-segmental vitiligo compared to the control group over a 52-week period.*5

Pathophysiology of vitiligo and role of JAK inhibitors3

(Adapted from Utama A 2024)

The process of repigmentation

Repigmentation may take place once the inflammatory response is suppressed and melanocyte precursors are stimulated to proliferate, migrate, and mature into melanocytes, which can gradually start to produce pigment.6

Repigmentation is a gradual process influenced by the severity and location of lesions on the body. The main sources of melanocytes and melanocyte precursors are the hair follicles and the epidermis at the lesion borders. Repigmentation tends to occur more rapidly in areas with a higher density of hair follicles. However, the molecular and cellular mechanisms driving repigmentation are still not fully understood.6

Depigmentation

(Adapted from Frisoli ML 2020)

Repigmentation

(Adapted from Birlea SA 2017)

*There are two phase 3, double-blind, vehicle-controlled trials that involved patients 12 years of age or older who had

non-segmental vitiligo with depigmentation covering 10% or less of total body-surface area.

JAK: Janus Kinase; STAT: signal transducer and activator of transcription.

References:

1. Vitiligo [Internet]. Cleveland Clinic. Available at: https://my.clevelandclinic.org/health/diseases/12419-vitiligo Accessed January 2025.

2. Vitiligo [Internet]. American Academy of Dermatology. Available at: https://www.aad.org/public/diseases/a-z/vitiligo-treatment Accessed January 2025.

3. Utama A et al. Janus Kinase Inhibitors and the Changing Landscape of Vitiligo Management: A Scoping Review. International Journal of Dermatology 2024;63:1020–35.

4. Frisoli ML, et al. Vitiligo: Mechanisms of Pathogenesis and Treatment. Annual Review of Immunology 2020;38:621–48.

5. Rosmarin D, et al; TRuE-V Study Group. Two Phase 3, Randomized, Controlled Trials of Ruxolitinib Cream for Vitiligo. N Engl J Med. 2022;387(16):1445-1455.

6. Birlea SA, et al.Repigmentation through melanocyte regeneration in vitiligo. Dermatol Clin. 2017;35(2):205-218.