Open‐label pilot study of tofacitinib 2% for the treatment of refractory vitiligo

Mobasher, Pezhman; Guerra, Ricardo; Li, Sara J.; Frangos, Jason E.; Ganesan, Anand K.; Huang, Victor

doi:10.1111/bjd.18606

Cited by 40 publications

(36 citation statements)

References 5 publications

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“…They reported successful repigmentation of facial spots, while repigmentation of other anatomical sites showed mixed results (162). Similar results with better responses of facial spots than non-facial spots were reported by a recently published cohort study with 16 patients receiving 2% tofacitinib cream (163). A retrospective case study of 10 patients treated with oral tofacitinib 5 or 10 mg once daily suggests that a combination of phototherapy with JAKi is therapeutically more effective than JAKi monotherapy (164) (Figure 3).…”

Section: Vitiligosupporting

confidence: 88%

Emerging Topical and Systemic JAK Inhibitors in Dermatology

2019

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Accumulating data on cellular and molecular pathways help to develop novel therapeutic strategies in skin inflammation and autoimmunity. Examples are psoriasis and atopic dermatitis, two clinically and immunologically well-defined disorders. Here, the elucidation of key pathogenic factors such as IL-17A/IL-23 on the one hand and IL-4/IL-13 on the other hand profoundly changed our therapeutic practice. The knowledge on intracellular pathways and governing factors is shifting our attention to new druggable molecules. Multiple cytokine receptors signal through Janus kinases (JAKs) and associated signal transducer and activators of transcription (STATs). Inhibition of JAKs can simultaneously block the function of multiple cytokines. Therefore, JAK inhibitors (JAKi) are emerging as a new class of drugs, which in dermatology can either be used systemically as oral drugs or locally in topical formulations. Inhibition of JAKs has been shown to be effective in various skin disorders. The first oral JAKi have been recently approved for the treatment of rheumatoid arthritis and psoriatic arthritis. Currently, multiple inhibitors of the JAK/STAT pathway are being investigated for skin diseases like alopecia areata, atopic dermatitis, dermatomyositis, graft-versus-host-disease, hidradenitis suppurativa, lichen planus, lupus erythematosus, psoriasis, and vitiligo. Here, we aim to discuss the immunological basis and current stage of development of JAKi in dermatology.

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Section: Vitiligosupporting

confidence: 88%

Emerging Topical and Systemic JAK Inhibitors in Dermatology

2019

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“…However, results on other anatomic sites were disappointing, which highlights the importance of concomitant use of anti-inflammatory agents and UV exposure to enhance repigmentation in vitiligo (Figure 2). Similar results have been reported with 2% tofacitinib cream in a case series of 16 patients (Mobasher et al, 2019). Several oral and topical JAK inhibitors are currently under investigation, which suggests that there may soon be effective therapies available for vitiligo.…”

Section: Other Immunosuppressive Drugs In Vitiligo? the Case For Jak Inhibitorssupporting

confidence: 83%

Vitiligo: Targeted Therapies Add Color to Disease Pathophysiology

Ezzedine

Vance

Hamzavi

et al. 2020

Journal of Investigative Dermatology

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There is excitement in the air for patients with vitiligo. For the first time in decades, we have early case studies showing that targeted therapies can repigment vitiliginous skin, and well-powered clinical trials are underway. However, at the time of this writing, there is no Food and Drug Administrationeapproved drug for vitiligo. In a randomized clinical trial by Khemis et al. report negative results on a randomized clinical trial testing the combination of apremilast, a phosphodiesterase 4 inhibitor, and narrowband-ultraviolet B versus placebo and narrowband-ultraviolet B in patients with nonsegmental vitiligo. The results of this trial are a reminder that clinical management of vitiligo is challenging at best, even when combining anti-inflammatory and/or immunomodulating agents with repigmenting agents. However, these negative trials are critical in improving our understanding of this complex and disfiguring disease.

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“…While anti‐interleukin‐17A and apremilast did not demonstrate a significant therapeutic effect, 191,192 the IFN‐γ pathway and its downstream intracellular JAK signal transducer and activator of transcription signaling pathway are key players in the pathophysiology of vitiligo. Case reports and open label studies had recognized the therapeutic potential of JAK inhibitors in vitiligo 147,193,194 . In an open label, proof‐of‐concept trial, topical ruxolitinib 1.5% cream, a JAK‐1/2 inhibitor, was applied twice daily to 11 adult patients with vitiligo over a period of 20 weeks and showed significant repigmentation in photoexposed areas, mainly on face 195 .…”

Section: Stabilization Of Rapidly Progressive Diseasementioning

confidence: 99%

Vitiligo: A focus on pathogenesis and its therapeutic implications

Bergqvist

Ezzedine

2021

The Journal of Dermatology

139

106

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Vitiligo is the most common depigmenting disorder affecting 0.1%–2% of the population worldwide. The characteristic white patches result from the selective loss of melanocytes. Sustained recent efforts have resulted in a detailed understanding of the genetic architecture of vitiligo. About 80% of vitiligo risk is attributable to genetic factors; and the rest (20%) is attributable to the environment. Over the past decade, substantial progress has been made in our understanding of the pathogenesis of vitiligo which is now clearly classified as an autoimmune disease. Melanocytes from patients with vitiligo are more susceptible to oxidative stress which begets the release of exosomes and inflammatory cytokines that will lead to activation of the innate immune response and subsequently to adaptive immune response through activation of autoreactive cytotoxic CD8+ T cells. These produce interferon‐γ (IFN‐γ) which promotes disease progression through IFN‐γ‐induced chemokine secretion from surrounding keratinocytes to further recruit T cells to the skin through a positive feedback loop. CD8 tissue‐resident memory T cells are in turn responsible for long‐term maintenance and potential relapse of vitiligo in human patients through cytokine‐mediated recruitment of T cells from the circulation. This review summarizes the current knowledge on vitiligo and attempt to give an overview of the future in vitiligo treatment.

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Open‐label pilot study of tofacitinib 2% for the treatment of refractory vitiligo

Cited by 40 publications

References 5 publications

Emerging Topical and Systemic JAK Inhibitors in Dermatology

Emerging Topical and Systemic JAK Inhibitors in Dermatology

Vitiligo: Targeted Therapies Add Color to Disease Pathophysiology

Vitiligo: A focus on pathogenesis and its therapeutic implications

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