# Oral JAK Inhibitors as a Promising Therapeutic Strategy for Refractory Rosacea: A Systematic Review and Meta‐Analysis

**Authors:** Yu Peng, Mingzi Sun, Jiayu Chen, Xubo Huang, Fengchuan Zhang

PMC · DOI: 10.1111/jocd.70791 · Journal of Cosmetic Dermatology · 2026-03-08

## TL;DR

Oral JAK inhibitors may be a promising treatment for difficult-to-treat rosacea, but more research is needed to confirm their effectiveness and safety.

## Contribution

This study provides the first systematic review and meta-analysis of oral JAK inhibitors for refractory rosacea.

## Key findings

- Oral JAK inhibitors showed an 89.9% pooled clinical response rate in treating refractory rosacea.
- Patients experienced significant improvements in erythema and quality of life measures.
- Adverse events occurred in 10.5% of patients, indicating a generally favorable safety profile.

## Abstract

Rosacea is a chronic inflammatory dermatosis. While standard therapies exist, managing refractory subtypes remains a therapeutic challenge. Oral Janus kinase (JAK) inhibitors have emerged as potential alternatives, but systematic evidence is lacking.

To evaluate the efficacy and safety of oral JAK inhibitors for rosacea through a systematic review and meta‐analysis.

A comprehensive search was conducted in five databases from inception to December 1, 2025. The primary outcome was the pooled clinical response rate. Secondary outcomes included the Investigator's Global Assessment (IGA), Clinician's Erythema Assessment (CEA), and Dermatology Life Quality Index (DLQI).

Eleven studies involving 57 patients were included. The overall pooled response rate was 89.9% (95% CI: 74.4%–99.4%), with low heterogeneity (I
2 = 16.3%). Regarding secondary outcomes, 67.8% of patients achieved an IGA score of ≤ 1, and 74.6% achieved a CEA reduction of ≥ 2 points. DLQI score also decreased from 17.30 ± 3.80 to 10.00 ± 3.43. Adverse events were reported in 10.5% of patients.

Oral JAK inhibitors show promising potential as a therapeutic option for refractory rosacea. However, given the small sample size and single‐arm design, these findings are exploratory. Large‐scale randomized controlled trials are urgently needed to validate these findings and guide stratified treatment.

## Linked entities

- **Proteins:** jak (Janus kinase)
- **Diseases:** rosacea (MONDO:0006604)

## Full-text entities

- **Genes:** CEACAM3 (CEA cell adhesion molecule 3) [NCBI Gene 1084] {aka CD66D, CEA, CGM1, CGM1a, W264, W282}, TLR2 (toll like receptor 2) [NCBI Gene 7097] {aka CD282, TIL4}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, JAK3 (Janus kinase 3) [NCBI Gene 3718] {aka JAK-3, JAK3_HUMAN, JAKL, L-JAK, LJAK}, TRPV1 (transient receptor potential cation channel subfamily V member 1) [NCBI Gene 7442] {aka VR1}, IL15 (interleukin 15) [NCBI Gene 3600] {aka IL-15}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, KLK5 (kallikrein related peptidase 5) [NCBI Gene 25818] {aka KLK-L2, KLKL2, SCTE}, TRPA1 (transient receptor potential cation channel subfamily A member 1) [NCBI Gene 8989] {aka ANKTM1, FEPS, FEPS1, p120}, JAK1 (Janus kinase 1) [NCBI Gene 3716] {aka AIIDE, JAK1A, JAK1B, JTK3}, TPSG1 (tryptase gamma 1) [NCBI Gene 25823] {aka PRSS31, TMT, trpA}, LOC102723407 (immunoglobulin heavy variable 4-38-2-like) [NCBI Gene 102723407] {aka IGHV4, IGHV4-30, IGHV4-38-2, IGHV4-39, IGHV4-b, IGVH4-39}, IL7 (interleukin 7) [NCBI Gene 3574] {aka IL-7, IMD130}, CAMP (cathelicidin antimicrobial peptide) [NCBI Gene 820] {aka CAP-18, CAP18, CRAMP, FALL-39, FALL39, HSD26}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}
- **Diseases:** telangiectasia (MESH:D013684), gastrointestinal symptoms (MESH:D012817), inflammation (MESH:D007249), ETR (MESH:D012393), Skin lesions (MESH:D012871), anorexia (MESH:D000855), anxiety (MESH:D001007), eosinophilia (MESH:D004802), vitiligo (MESH:D014820), nausea (MESH:D009325), vomiting (MESH:D014839), pruritus (MESH:D011537), Flushing (MESH:D005483), Rhinophyma (MESH:D012224), neurovascular dysregulation (MESH:D013901), dermatological diseases (MESH:D000168), depression (MESH:D003866), hepatic abnormalities (MESH:D056486), acne (MESH:D000152), Erythema (MESH:D004890), atopic dermatitis (MESH:D003876), alopecia areata (MESH:D000506), ulcerative colitis (MESH:D003093)
- **Chemicals:** doxycycline (MESH:D004318), ivermectin (MESH:D007559), Upadacitinib (MESH:C000613732), carvedilol (MESH:D000077261), bilirubin (MESH:D001663), metronidazole (MESH:D008795), Tofacitinib (MESH:C479163), Ruxolitinib (MESH:C540383), Demodex (-), hydroxychloroquine (MESH:D006886), brimonidine (MESH:D000068438), Steroid (MESH:D013256), prednisone (MESH:D011241), minocycline (MESH:D008911), Baricitinib (MESH:C000596027), Abrocitinib (MESH:C000634427)
- **Species:** Homo sapiens (human, species) [taxon 9606], Demodex (genus) [taxon 188544]

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## References

35 references — full list in the complete paper: https://tomesphere.com/paper/PMC12968368/full.md

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Source: https://tomesphere.com/paper/PMC12968368