Benefit–risk profile of tofacitinib in patients with moderate‐to‐severe chronic plaque psoriasis: pooled analysis across six clinical trials

Strober, Bruce; Gottlieb, Alice B.; Kerkhof, P.C.M. van de; Puig, L.; Bachelez, H.; Chouela, Edgardo; Imafuku, Shinichi; Thaçi, Diamant; Tan, Huaming; Valdez, Hernán; Gupta, Pankaj; Kaur, Mandeep; Frajzyngier, Veronica; Wołk, Robert

doi:10.1111/bjd.17149

Cited by 31 publications

(25 citation statements)

References 38 publications

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“…On the other hand, perifollicular repigmentation was observed in the patient's vitiligo patches in response to tofacitinib. A possible explanation could be that concomitant tofacitinib and NB‐UVB act synergistically, which is supported by studies that have shown that JAK inhibitors are more effective when combined with phototherapy …”

Section: Discussionmentioning

confidence: 94%

Effective use of oral tofacitinib and phototherapy in a patient with concomitant alopecia areata, vitiligo, and plaque and inverse psoriasis

Tajalli

Kabir

Vance

et al. 2020

Clinical Case Reports

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Section: Discussionmentioning

confidence: 94%

Effective use of oral tofacitinib and phototherapy in a patient with concomitant alopecia areata, vitiligo, and plaque and inverse psoriasis

Tajalli

Kabir

Vance

et al. 2020

Clinical Case Reports

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“…Also, an investigation of the effects of tofacitinib on the viral loads of Cytomegalovirus and Epstein-Barr virus pointed to no clinically significant effects of this JAK inhibitor [31]. The risk of infection during treatment with tofacitinib seems to be similar to that during treatment with biologics [6,9], and the overall benefit/risk profile of the drug when used for psoriasis appears to be comparable to those of other systemic treatments [32].…”

Section: Discussionmentioning

confidence: 98%

Systemic Treatment of Psoriasis with JAK Inhibitors: A Review

Kvist-Hansen

Hansen

Skov

2019

Dermatol Ther (Heidelb)

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Psoriasis is a prevalent chronic inflammatory disease. The inflammatory response is driven by T cells and mediated by multiple cytokines such as tumor necrosis factor and the interleukins IL-17 and IL-23. Moderate-to-severe psoriasis is treated systemically, using either biologics or conventional treatments with small-molecule drugs. The newer biologics are very effective and well tolerated, but not all patients respond to treatment with biologics, so there is a need for new treatment options for psoriasis. Janus kinase (JAK) inhibitors are a new drug class that may be of use in this respect. These inhibitors are already on the market for rheumatoid arthritis, psoriatic arthritis, and ulcerative colitis. They block the intracellular signal pathway mediated by JAK and signal transducer and activator of transcription (STAT) proteins, thereby inhibiting gene transcription of proinflammatory cytokines. JAK inhibitors are currently being tested as potential treatments for psoriasis. They have shown clinical efficacy as measured by the Psoriasis Area and Severity Index 75 response in both phase 2 and 3 trials, and appear to be well tolerated overall. This review provides an overview of the mechanisms underlying the actions of JAK inhibitors in psoriasis, together with the results of clinical trials testing their efficacies when used to treat the disease.

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“…Safety profile is considered generally acceptable, infections and laboratory abnormalities can be observed as major adverse events (226). The increased risk of infections was similar to that observed by the use of biologics, with the exception of higher risk for varicella zoster infection which should be taken into consideration.…”

Section: Adverse Events During Jak Inhibitor Treatment In Inflammatormentioning

confidence: 99%

Tyrosine Kinases in Autoimmune and Inflammatory Skin Diseases

2019

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Tyrosine kinases relay signals from diverse leukocyte antigen receptors, innate immune receptors, and cytokine receptors, and therefore mediate the recruitment and activation of various leukocyte populations. Non-receptor tyrosine kinases of the Jak, Src, Syk, and Btk families play major roles in various immune-mediated disorders, and small-molecule tyrosine kinase inhibitors are emerging novel therapeutics in a number of those diseases. Autoimmune and inflammatory skin diseases represent a broad spectrum of immune-mediated diseases. Genetic and pharmacological studies in humans and mice support the role of tyrosine kinases in several inflammatory skin diseases. Atopic dermatitis and psoriasis are characterized by an inflammatory microenvironment which activates cytokine receptors coupled to the Jak-Stat signaling pathway. Jak kinases are also implicated in alopecia areata and vitiligo, skin disorders mediated by cytotoxic T lymphocytes. Genetic studies indicate a critical role for Src-family kinases and Syk in animal models of autoantibody-mediated blistering skin diseases. Here, we review the various tyrosine kinase signaling pathways and their role in various autoimmune and inflammatory skin diseases. Special emphasis will be placed on identification of potential therapeutic targets, as well as on ongoing preclinical and clinical studies for the treatment of inflammatory skin diseases by small-molecule tyrosine kinase inhibitors.

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Benefit–risk profile of tofacitinib in patients with moderate‐to‐severe chronic plaque psoriasis: pooled analysis across six clinical trials

Abstract: Tofacitinib has a benefit-risk profile in moderate-to-severe psoriasis consistent with that of other systemic treatments.

Cited by 31 publications

References 38 publications

Effective use of oral tofacitinib and phototherapy in a patient with concomitant alopecia areata, vitiligo, and plaque and inverse psoriasis

Effective use of oral tofacitinib and phototherapy in a patient with concomitant alopecia areata, vitiligo, and plaque and inverse psoriasis

Systemic Treatment of Psoriasis with JAK Inhibitors: A Review

Tyrosine Kinases in Autoimmune and Inflammatory Skin Diseases

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