The Effectiveness of Topical Ruxolitinib versus Topical Placebo in the Treatment of Vitiligo: Comparative Study

Background: Vitiligo is thought to be driven by interferon-γ (IFN-γ), which activates the JAK–STAT pathway and promotes recruitment of CD8⁺ T cells that trigger melanocyte apoptosis, resulting in the characteristic depigmented patches. These insights have supported the development of therapeutic strategies targeting JAK inhibition. JAK inhibitors act by binding to the ATP-binding site of JAKs, preventing autophosphorylation and thereby blocking downstream cytokine signaling. Ruxolitinib, a JAK1/2 inhibitor, suppresses IFN-γ–mediated signaling, thereby protecting melanocytes and facilitating repigmentation.. Methods: this study included 15 patients of non-segmental vitiligo of both sexes and their ages above 12 years old. Bilateral & nearly symmetrical patches in same body area were selected in every patient. The patient applied 1.5% ruxolitinib cream topically twice a day, to the right patch (es) (Ruxolitinib patch) for 24 weeks while the left (placebo patch) was received placebo cream (Vaseline) topically twice a day within the same period. Results: There were high statistically significant differences (P<0.01) between the ruxolitinib treated patch (es) and placebo treated patch (es). Ruxolotinib was well tolerable with minimal side effects. Conclusion: our study observed the safety and therapeutic efficacy of topical ruxolitinib for localized lesions of non-segmental vitiligo

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Publication Details

Journal
Zagazig University Medical Journal
Published
2025-11-05
DOI
https://doi.org/10.21608/zumj.2025.429247.4233
Primary Topic
melanin and skin pigmentation
Type
article
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article

The Effectiveness of Topical Ruxolitinib versus Topical Placebo in the Treatment of Vitiligo: Comparative Study

Zagazig University Medical Journal
melanin and skin pigmentation
article

The Effectiveness of Topical Ruxolitinib versus Topical Placebo in the Treatment of Vitiligo: Comparative Study

article en

Abstract

Background: Vitiligo is thought to be driven by interferon-γ (IFN-γ), which activates the JAK–STAT pathway and promotes recruitment of CD8⁺ T cells that trigger melanocyte apoptosis, resulting in the characteristic depigmented patches. These insights have supported the development of therapeutic strategies targeting JAK inhibition. JAK inhibitors act by binding to the ATP-binding site of JAKs, preventing autophosphorylation and thereby blocking downstream cytokine signaling. Ruxolitinib, a JAK1/2 inhibitor, suppresses IFN-γ–mediated signaling, thereby protecting melanocytes and facilitating repigmentation.. Methods: this study included 15 patients of non-segmental vitiligo of both sexes and their ages above 12 years old. Bilateral & nearly symmetrical patches in same body area were selected in every patient. The patient applied 1.5% ruxolitinib cream topically twice a day, to the right patch (es) (Ruxolitinib patch) for 24 weeks while the left (placebo patch) was received placebo cream (Vaseline) topically twice a day within the same period. Results: There were high statistically significant differences (P<0.01) between the ruxolitinib treated patch (es) and placebo treated patch (es). Ruxolotinib was well tolerable with minimal side effects. Conclusion: our study observed the safety and therapeutic efficacy of topical ruxolitinib for localized lesions of non-segmental vitiligo

Zagazig University Medical JournalVol. 0(0)
Zagazig University (EG), Department of Embryology (US)
Good health and well-being
Openalex Percentile: Top 40%
melanin and skin pigmentation
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