Alopecia areata affects both children and adults and hair of all colours.  Up to 66% of patients are younger than 30 years of age, and only 20% are older than 40 years, with no sex predilection. Alopecia areata is further associated with an increased overall risk of other autoimmune disorders: lupus erythematosus in 0.6% of patients, vitiligo in 4% and autoimmune thyroid disease in up to 28% of cases.
The possibility to use JAK inhibitors for alopecia areata arose from an unusual case report in which a patient with plaque psoriasis being treated with tofacitinib experienced a reversal in alopecia universalis. 
We now know that Janus kinase-signal transducer and activator of transcription (JAK-STAT) is a signalling pathway that is crucial in maintaining the CD8+ NKG2D+ T cell inflammatory infiltrate which is typical of alopecia areata. 
At present, at least 3 JAK inhibitors are under investigation in alopecia areata: tofacitinib, baricitinib and ruxolitinib. 
In a study with tofacitinib in 66 patients (>50% scalp hair loss, alopecia totalis and universalis) treated with tofacitinib 5 mg twice daily, 32% of patients were intermediate responders (improvement in S ALT score ≥5% and ≤50%) and 32% were strong responders (changes in SALT score ≥50%).
Patients with chronic alopecia areata were less likely to be good responders; drug cessation resulted in disease relapse in a mean of 8.5 weeks. 
A small study in 12 patients with moderate-to-severe alopecia areata on oral ruxolitinib, 20 mg twice per day, for 3–6 months, followed by 3 months follow-up off drug reported that after 6 months 75% of patients (9 of 12) had a strong response to treatment (defined as >50% hair regrowth). 
At the end of the treatment, shedding started 3 weeks after cessation of ruxolitinib. 
Most recently, the efficacy, side effects and durability of ruxolitinib was compared to tofacitinib in the treatment of severe alopecia areata. 
Both tofacitinib and ruxolitinib induced remarkable hair regrowth, with a mean change in SALT score of 93.8 ± 3.25 in the ruxolitinib group and 95.2 ± 2.69 in the tofacitinib group.
However, the ruxolitinib group showed a shorter duration for initial hair regrowth.
Baricitinib is an oral selective inhibitor of JAK1 and JAK2, approved for the treatment of rheumatoid arthritis.
To date only isolated case reports have been published on baricitinib in alopecia areata, although a placebo-controlled trial involving 725 subjects comparing baricitinib to placebo in moderate to severe alopecia areata is currently recruiting (NCT03570749).
Apremilast is a disease modifying antirheumatic drugs (DMARD) used in psoriasis; a small retrospective analysis on 15 patients showed that apremilast could be a potential treatment for refractory alopecia areata at doses lower than that approved for psoriasis; however, further study is needed. 
Fumaric acids inhibit T-suppressor cells and T-helper cells by the inhibition of the cytokines INF-γ, IL-2, IL-12 and TNF-α, and block ICAM and the proliferation of keratinocytes.
A retrospective analysis of 13 patients with various types of alopecia showed that those with alopecia totalis showed no response, while 67% those with alopecia universalis partially responded; 50% of alopecia areata patients had full regrowth of hair after a mean period of treatment of 5.2 months. 
However, relapse was seen after a mean of 3.3 months following cessation of therapy.
A number of other agents are in the early stages of investigation.
These include BNZ-1 (a selective and simultaneous inhibitor of cytokines IL-2, IL-9 and IL-15), tralokinumab (an IgG4 humanised monoclonal antibody that specifically binds IL-13) and dupilumab (a Th2 antagonist that blocks IL-4 receptor α, inhibiting IL-4 and IL-13). 
Presented by: Prof. Kristian Reich, Translational Research in Inflammatory Skin Diseases, Institute for Health Services Research in Dermatology and Nursing, University Medical Center Hamburg-Eppendorf, and Skinflammation® Center, Hamburg, Germany