Baricitinib (INCB028050) results in a 50% reduction in hind paw volumes over two weeks of treatment at a dose of 1 mg/kg and a reduction of more than 95% at doses of 3 or 10 mg/kg^[1].

Moreover, mice treated with Baricitinib (0.7 mg/day) display significantly diminished inflammation as evidenced by H&E staining, reduced CD8 infiltration, and lowered expression of MHC class I and II. Importantly, CD8+NKG2D+ cells, pivotal in the pathogenesis of both murine and human alopecia areata (AA), are substantially reduced in Baricitinib-treated mice compared to those receiving vehicle control^[2].

Baricitinib (INCB028050) is demonstrated as a potent inhibitor of Janus kinase (JAK) signaling and functionality in cell-based assays. In peripheral blood mononuclear cells (PBMCs), Baricitinib curtails IL-6-induced phosphorylation of STAT3 (pSTAT3) and the subsequent secretion of the chemokine MCP-1, with IC50 values being 44 nM and 40 nM, respectively. Furthermore, in isolated naive T-cells, it suppresses pSTAT3 activation by IL-23 with an IC50 value of 20 nM, significantly inhibiting the production of IL-17 and IL-22, two cytokines produced by Th17 cells, known for their inflammatory and pathogenic roles, with an IC50 of 50 nM. This is in sharp contrast to structurally similar but less effective JAK1/2 inhibitors INCB027753 and INCB029843, which show no notable effect in these assay systems up to 10 μM^[1].