# Significant improvement with ivarmacitinib after suboptimal response to tofacitinib in severe alopecia areata: a case report and literature review

**Authors:** Zulin Wan, Ying Wang, Dingquan Yang

PMC · DOI: 10.3389/fimmu.2026.1766847 · Frontiers in Immunology · 2026-02-17

## TL;DR

A patient with severe hair loss improved significantly after switching from tofacitinib to ivarmacitinib, a new JAK1 inhibitor, suggesting it could be a better treatment option.

## Contribution

This case report provides real-world evidence that ivarmacitinib may be effective for patients who do not respond well to tofacitinib.

## Key findings

- The patient showed significant improvement with ivarmacitinib after a suboptimal response to tofacitinib.
- Ivarmacitinib's higher JAK1 selectivity may explain its effectiveness in tofacitinib-refractory alopecia areata.
- More research is needed to determine ivarmacitinib's role in treating severe alopecia areata.

## Abstract

Alopecia areata (AA) is a chronic, immune-mediated hair loss disorder, in which the JAK-STAT signaling pathway plays an important pathogenic role. Available agents for AA include minoxidil, corticosteroids, immunosuppressants and Janus kinase (JAK) inhibitors, among others. For adults with severe AA, JAK inhibitors have emerged as cornerstone systemic treatments, but the responses to them are variable. Ivarmacitinib is a novel and highly selective JAK1 inhibitor, which has been approved for AA in China recently with little real-world evidence. We present a case of a patient with severe AA who achieved significant improvement with ivarmacitinib after suboptimal response to tofacitinib, and review previous studies on switching therapy between different JAK inhibitors for AA. This case suggests that ivarmacitinib is a viable alternative for tofacitinib-refractory AA, possibly due to its higher JAK1 selectivity. Further studies are required to define ivarmacitinib’s optimal position in AA treatment algorithm, and to elucidate underlying mechanisms behind JAK inhibitors, which is essential for more personalized and targeted therapy for severe AA.

## Linked entities

- **Chemicals:** ivarmacitinib (PubChem CID 71622431), tofacitinib (PubChem CID 9926791)
- **Diseases:** alopecia areata (MONDO:0004907)

## Full-text entities

- **Genes:** IL15 (interleukin 15) [NCBI Gene 3600] {aka IL-15}, JAK3 (Janus kinase 3) [NCBI Gene 3718] {aka JAK-3, JAK3_HUMAN, JAKL, L-JAK, LJAK}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, JAK2 (Janus kinase 2) [NCBI Gene 3717] {aka JTK10}, JAK1 (Janus kinase 1) [NCBI Gene 3716] {aka AIIDE, JAK1A, JAK1B, JTK3}
- **Diseases:** alopecia universalis (MESH:C537055), ankylosing spondylitis (MESH:D013167), folliculitis (MESH:D005499), Alopecia (MESH:D000505), autoimmune (MESH:D001327), hepatitis B and C virus (MESH:D006509), AU (MESH:C566303), Skin Diseases (MESH:D012871), syphilis (MESH:D013587), inflammatory (MESH:D007249), Infectious disease (MESH:D003141), AA (MESH:D000506), atopic dermatitis (MESH:D003876), tuberculosis (MESH:D014376), immune (MESH:D007154), infections (MESH:D007239), rheumatoid arthritis (MESH:D001172)
- **Chemicals:** ruxolitinib (MESH:C540383), tofacitinib (MESH:C479163), hydrocortisone (MESH:D006854), mupirocin (MESH:D016712), betamethasone (MESH:D001623), dupilumab (MESH:C582203), ritlecitinib (MESH:C000614924), baricitinib (MESH:C000596027), minoxidil (MESH:D008914), lipid (MESH:D008055), Ivarmacitinib (MESH:C000615713)
- **Species:** Homo sapiens (human, species) [taxon 9606], Human immunodeficiency virus (species) [taxon 12721]
- **Mutations:** R1063H

## Full text

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## Figures

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## References

18 references — full list in the complete paper: https://tomesphere.com/paper/PMC12953536/full.md

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Source: https://tomesphere.com/paper/PMC12953536