# Extended treatment of abrocitinib: evaluation of efficacy and safety in chronic actinic dermatitis

**Authors:** Lu Tang, Lanhai Zhong, Liangzi Liang, Jiande Han, Naiyu Lin

PMC · DOI: 10.3389/fmed.2026.1742273 · Frontiers in Medicine · 2026-02-04

## TL;DR

This study shows abrocitinib, a JAK1 inhibitor, may be effective and safe for treating chronic actinic dermatitis, with potential key inflammatory factors identified.

## Contribution

The study provides new clinical insights into abrocitinib's efficacy for chronic actinic dermatitis and identifies specific inflammatory pathways involved.

## Key findings

- Abrocitinib significantly reduced disease severity in 16 CAD patients over 12 weeks.
- Key inflammatory factors like IL-13 and CCL-4 were significantly altered after treatment.
- No serious adverse events were observed during the treatment period.

## Abstract

JAK inhibitors are well-established for their utilization in the treatment of autoinflammatory diseases, with the JAK1 inhibitor abrocitinib primarily employed in the management of atopic dermatitis. To provide new clinical therapeutic experience for patients with chronic actinic dermatitis (CAD), reveal the inflammatory pathways that may be involved in the treatment of CAD with abrocitinib and to provide clues for exploring the pathogenesis of CAD.

In a 3-month longitudinal study, we recorded and analyzed laboratory test data and clinical severity assessments in 16 patients diagnosed with chronic actinic dermatitis treated with abrocitinib. And the plasma samples of 6 patients before and after treatment were analyzed proteomically using Olink inflammation panel.

After 12 weeks of treatment, there was a significant decrease in disease severity scores of 16 patients. No serious adverse events were identified throughout the course of treatment. Significant changes in several inflammatory factors such as EN-RAGE, MCP-3, MCP-4, IL-13, CCL4, FGF21 and TNFRSF9 were observed after treatment.

The analysis of our data demonstrates that abrocitinib may be an effective therapeutic option in the management of CAD. IL-13 and CCL-4 might be the core effective factors after the therapy.

## Linked entities

- **Proteins:** S100A12 (S100 calcium binding protein A12), CCL7 (C-C motif chemokine ligand 7), CCL13 (C-C motif chemokine ligand 13), IL13 (interleukin 13), CCL4 (C-C motif chemokine ligand 4), FGF21 (fibroblast growth factor 21), TNFRSF9 (TNF receptor superfamily member 9)
- **Chemicals:** abrocitinib (PubChem CID 78323835)
- **Diseases:** chronic actinic dermatitis (MONDO:0018025), atopic dermatitis (MONDO:0004980)

## Full-text entities

- **Genes:** IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}, TSLP (thymic stromal lymphopoietin) [NCBI Gene 85480], CCL7 (C-C motif chemokine ligand 7) [NCBI Gene 6354] {aka FIC, MARC, MCP-3, MCP3, NC28, SCYA6}, CCL4 (C-C motif chemokine ligand 4) [NCBI Gene 6351] {aka ACT2, AT744.1, G-26, HC21, LAG-1, LAG1}, CD46 (CD46 molecule) [NCBI Gene 4179] {aka AHUS2, MCP, MIC10, TLX, TRA2.10}, IL13 (interleukin 13) [NCBI Gene 3596] {aka IL-13, P600}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, JAK1 (Janus kinase 1) [NCBI Gene 3716] {aka AIIDE, JAK1A, JAK1B, JTK3}, FGF21 (fibroblast growth factor 21) [NCBI Gene 26291], S100A1 (S100 calcium binding protein A1) [NCBI Gene 6271] {aka S100, S100-alpha, S100A}, S100A12 (S100 calcium binding protein A12) [NCBI Gene 6283] {aka CAAF1, CAGC, CGRP, ENRAGE, MRP-6, MRP6}, TNFRSF9 (TNF receptor superfamily member 9) [NCBI Gene 3604] {aka 4-1BB, CD137, CDw137, ILA, IMD109}, IL31 (interleukin 31) [NCBI Gene 386653] {aka IL-31}, OSM (oncostatin M) [NCBI Gene 5008], AGER (advanced glycosylation end-product specific receptor) [NCBI Gene 177] {aka RAGE, SCARJ1, sRAGE}, C3 (complement C3) [NCBI Gene 718] {aka AHUS5, ARMD9, ASP, C3a, C3b, CPAMD1}, JAK3 (Janus kinase 3) [NCBI Gene 3718] {aka JAK-3, JAK3_HUMAN, JAKL, L-JAK, LJAK}, CCL13 (C-C motif chemokine ligand 13) [NCBI Gene 6357] {aka CKb10, MCP-4, NCC-1, NCC1, SCYA13, SCYL1}, IL22 (interleukin 22) [NCBI Gene 50616] {aka IL-21, IL-22, IL-D110, IL-TIF, ILTIF, TIFIL-23}
- **Diseases:** skin alterations (MESH:D012868), chronic (MESH:D002908), AD (MESH:D003876), Erythema (MESH:D004890), papules (MESH:D000169), impairment in liver and kidney function (MESH:D056486), cardiac disease (MESH:D006331), liver dysfunction (MESH:D017093), tuberculosis (MESH:D014376), renal damage (MESH:D007674), deep vein thrombosis (MESH:D020246), latent tuberculosis infection (MESH:D055985), CAD (MESH:D010787), eczema (MESH:D004485), hypertension (MESH:D006973), hematological impairment (MESH:D006402), thrombosis (MESH:D013927), itch (MESH:D011537), burn (MESH:D002056), autoinflammatory diseases (MESH:D056660), psoriasis (MESH:D011565), folliculitis (MESH:D005499), COPD (MESH:D029424), pulmonary edema (MESH:D011654), hepatitis B. (MESH:D006509), edema (MESH:D004487), opportunistic infections (MESH:D009894), scaling (MESH:C538175), coronary heart disease (MESH:D003327), dermatoses (MESH:D012871), chronic inflammation (MESH:D007249)
- **Chemicals:** Abrocitinib (MESH:C000634427), metoprolol (MESH:D008790), baricitinib (MESH:C000596027), dupilumab (MESH:C582203), phosphatidylserine (MESH:D010718), Hydroxychloroquine (MESH:D006886), UVA (-), advanced glycation end products (MESH:D017127), ivabradine (MESH:D000077550), tofacitinib (MESH:C479163), isoniazid (MESH:D007538), Upadacitinib (MESH:C000613732)
- **Species:** Homo sapiens (human, species) [taxon 9606], Hepatitis B virus (no rank) [taxon 10407]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12913078/full.md

## References

30 references — full list in the complete paper: https://tomesphere.com/paper/PMC12913078/full.md

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Source: https://tomesphere.com/paper/PMC12913078