Janus kinase inhibitors may be an effective treatment to reduce skin depigmentation in vitiligo

A clinical decision report appraising Rothstein B, Joshipura D, Saraiya A, Abdat R, Ashkar H, Turkowski Y, Sheth V, Huang V, Au SC, Kachuk C, Dumont N, Gottlieb AB, Rosmarin D. Treatment of vitiligo with the topical Janus kinase inhibitor ruxolitinib. J Am Acad Dermatol.2017 Jun;76(6):1054-1060.e1. https://doi.org/10.1016/j.jaad.2017.02.049 for a patient with worsening vitiligo.

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JAK-Inhibitor and Type I Interferon Ability to Produce Favorable Clinical Outcomes in COVID-19 Patients: A Systematic Review and Meta-Analysis

10.21203/rs.3.rs-64782/v1 ◽

2020 ◽

Cited By ~ 1

Author(s):

Lucas Walz ◽

Avi J. Cohen ◽

Andre P. Rebaza ◽

James Vanchieri ◽

Martin D. Slade ◽

...

Keyword(s):

Clinical Outcomes ◽

Kinase Inhibitors ◽

Kinase Inhibitor ◽

Type I Interferon ◽

Meta Analysis ◽

Janus Kinase ◽

Type I Interferons ◽

Type I ◽

Janus Kinase Inhibitor ◽

Janus Kinase Inhibitors

Abstract Background The spread of a highly pathogenic, novel coronavirus (SARS-CoV-2) has emerged as a once-in-a-century pandemic, having already infected over 17 million. Novel therapies are urgently needed. Janus kinase-inhibitors and Type I interferons have emerged as potential antiviral candidates for COVID-19 patients for their proven efficacy against diseases with excessive cytokine release and due to direct antiviral ability against viruses including coronaviruses, respectively. We conducted a systemic review and meta-analysis to evaluate the effect of Janus kinase-inhibitors and Type I interferons and their ability to produce positive patient outcomes in COVID-19 patients. Methods A search of MEDLINE and MedRxiv was conducted by three investigators from inception until July 30 th 2020, including any study type that compared treatment outcomes of humans treated with JAK-inhibitor or Type I interferon against controls. Inclusion necessitated data with clearly indicated risk estimates or those that permitted their back-calculation. Outcomes were synthesized using RevMan. Results Of 733 searched studies, we included four randomized and eleven non-randomized trials. Five of the studies were unpublished. Those who received Janus kinase-inhibitor had significantly reduced odds of mortality (OR, 0.12; 95% CI, 0.03 – 0.39, p<0.001) and ICU admission (OR, 0.05; 95% CI, 0.01 – 0.26, p<0.001), and had significantly increased odds of hospital discharge (OR, 22.76; 95% CI, 10.68 – 48.54, p<0.00001), when compared to standard treatment group. Type I interferon recipients had significantly reduced odds of mortality (OR, 0.19; 95% CI, 0.04 – 0.85, p<0.05), and increased odds of discharge bordering significance (OR, 1.89; 95% CI, 1.00 – 3.59, p=0.05). Conclusions Janus kinase-inhibitor treatment is significantly associated with positive clinical outcomes in terms of mortality, ICU admission, and discharge. Type I interferon treatment is associated with positive clinical outcomes in regard to mortality and discharge. While these data show promise, additional well-conducted RCTs are needed to further elucidate the relationship between clinical outcomes and Janus kinase-inhibitors and Type I interferons in COVID-19 patients.

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Janus kinase inhibitors: jackpot or potluck?

Oncology Reviews ◽

10.4081/oncol.2012.187 ◽

2012 ◽

pp. e13

Author(s):

Pavithran Keechilat ◽

Shripad Brahmanand Pande

Keyword(s):

High Risk ◽

Polycythemia Vera ◽

Kinase Inhibitors ◽

Kinase Inhibitor ◽

Myeloproliferative Neoplasms ◽

Primary Myelofibrosis ◽

Janus Kinase ◽

Current Evidence ◽

Federal Drug Administration ◽

Janus Kinase Inhibitors

The reports of a unique mutation in the Janus kinase-2 gene (JAK2) in polycythemia vera by several independent groups in 2005 quickly spurred the development of the Janus kinase inhibitors. In one of the great victories of translational research in recent times, the first smallmolecule Janus kinase inhibitor ruxolitinib entered a phase I trial in 2007. With the approval of ruxolitinib by the US Federal Drug Administration in November 2011 for high-risk and intermediate-2 risk myelofibrosis, a change in paradigm has occurred in the management of a subset of myeloproliferative neoplasms (MPN): primary myelofibrosis, post-polycythemia vera myelofibrosis, and post-essential thrombocythemia myelofibrosis. Whereas the current evidence for ruxolitinib only covers high-risk and intermediate-2 risk myelofibrosis, inhibitors with greater potency are likely to offer better disease control and survival advantage in patients belonging to these categories, and possibly to the low-risk and intermediate-1 risk categories of MPN as well. But use of the Janus kinase inhibitors also probably has certain disadvantages, such as toxicity, resistance, withdrawal phenomenon, non-reversal of histology, and an implausible goal of disease clone eradication, some of which could offset the gains. In spite of this, Janus kinase inhibitors are here to stay, and for use in more than just myeloproliferative neoplasms.

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Janus kinase inhibitors: jackpot or potluck?

Oncology Reviews ◽

10.4081/oncol.2012.e13 ◽

2012 ◽

Vol 6 (1) ◽

pp. 13

Author(s):

Pavithran Keechilat ◽

Shripad Brahmanand Pande

Keyword(s):

High Risk ◽

Polycythemia Vera ◽

Kinase Inhibitors ◽

Kinase Inhibitor ◽

Myeloproliferative Neoplasms ◽

Primary Myelofibrosis ◽

Janus Kinase ◽

Current Evidence ◽

Federal Drug Administration ◽

Janus Kinase Inhibitors

The reports of a unique mutation in the Janus kinase-2 gene (<em>JAK2</em>) in polycythemia vera by several independent groups in 2005 quickly spurred the development of the Janus kinase inhibitors. In one of the great victories of translational research in recent times, the first smallmolecule Janus kinase inhibitor ruxolitinib entered a phase I trial in 2007. With the approval of ruxolitinib by the US Federal Drug Administration in November 2011 for high-risk and intermediate-2 risk myelofibrosis, a change in paradigm has occurred in the management of a subset of myeloproliferative neoplasms (MPN): primary myelofibrosis, post-polycythemia vera myelofibrosis, and post-essential thrombocythemia myelofibrosis. Whereas the current evidence for ruxolitinib only covers high-risk and intermediate-2 risk myelofibrosis, inhibitors with greater potency are likely to offer better disease control and survival advantage in patients belonging to these categories, and possibly to the low-risk and intermediate-1 risk categories of MPN as well. But use of the Janus kinase inhibitors also probably has certain disadvantages, such as toxicity, resistance, withdrawal phenomenon, non-reversal of histology, and an implausible goal of disease clone eradication, some of which could offset the gains. In spite of this, Janus kinase inhibitors are here to stay, and for use in more than just myeloproliferative neoplasms.

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