ABSTRACT
Introduction
Alopecia areata is a heterogenous, immune-mediated hair loss disorder that can affect any hair-bearing site on the body. Despite being one of the most prevalent autoimmune skin diseases, treatments have historically been limited to off-label medications that have demonstrated limited efficacy, especially in more severe forms of disease. Thus, there has long been an unmet need for rigorously studied therapeutics in alopecia areata.
Areas covered
Janus kinase inhibitors have proven to be an effective class of drugs for treating several inflammatory disorders. One such drug, baricitinib, has recently demonstrated significant hair regrowth in phase 2 and 3 alopecia areata trials. It has since become the first systemic therapy approved for treating severe alopecia areata. This review examines the role of Janus kinase pathways in alopecia areata’s pathogenesis and the safety and efficacy of baricitinib for treating severe alopecia areata.
Expert opinion
The approval of baricitinib for treating severe alopecia areata marks a major milestone in the disease’s history. While baricitinib has proven to be efficacious for this indication and has demonstrated an overall good safety profile, patients’ individual risk factors for serious adverse events should be assessed during shared decision-making with patients before initiating treatment.
Article highlights
Alopecia areata is a heterogenous, autoimmune hair loss disorder with considerable psychosocial comorbidity
Janus kinase inhibitors interfere with inflammatory cascades thought to be central to alopecia areata’s pathogenesis
The JAK-inhibitor, baricitinib, has proven to be efficacious in AA patients with extensive hair loss and is now the first systemic therapy to be FDA-approved for adults with severe AA.
Baricitinib has generally demonstrated a good safety profile in AA; however, patients’ individual risk factors for SAEs should be assessed during shared decision-making with patients before initiating treatment.
Declaration of interest
N Mesinkovska is a principal investigator for the BRAVE-AA1 and BRAVE-AA2 clinical trials sponsored by Eli Lilly with all funds directed to the University of California, Irvine. She is on the speaker bureau and advisory board for Eli Lilly and Company. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose. Eli Lilly provided a scientific accuracy review at the request of the journal editor.