# Emerging Targets in Psoriatic Arthritis: Dual IL-17A/F and Selective TYK2 Inhibition in a Clinical Perspective

**Authors:** Violeta Dimopoulou, Maria Nitsa, Christos Koutsianas

PMC · DOI: 10.31138/mjr.101025.erh · Mediterranean Journal of Rheumatology · 2026-01-08

## TL;DR

New treatments targeting IL-17A/F and TYK2 show promise for better managing psoriatic arthritis, offering improved joint and skin outcomes.

## Contribution

The paper highlights two novel therapeutic approaches—dual IL-17A/F inhibition and selective TYK2 inhibition—for psoriatic arthritis.

## Key findings

- Bimekizumab, an IL-17A/F inhibitor, showed superior efficacy in Phase III trials with high joint and skin response rates.
- Deucravacitinib, a TYK2 inhibitor, demonstrated significant improvements in PsA symptoms with a favorable safety profile.

## Abstract

Psoriatic arthritis (PsA) is a multifaceted immune-mediated inflammatory disease with several unmet therapeutic needs, and many patients fail to achieve comprehensive disease control with existing treatments. This has driven the exploration of novel therapeutic targets deriving from a better understanding of the immunopathogenetic cascade. Two of the most promising emerging targets are the dual inhibition of interleukin-17A and F (IL-17A/F) and the selective inhibition of tyrosine kinase 2 (TYK2). Bimekizumab, a monoclonal antibody that neutralises both IL-17A and IL-17F, has demonstrated superior efficacy over placebo and a standard-of-care TNF inhibitor in pivotal Phase III trials, achieving high rates of both joint and skin response. Its safety profile is characterised by a manageable increase in mild-to-moderate fungal infections, particularly oral candidiasis. Deucravacitinib, an oral, allosteric TYK2 inhibitor, represents a novel mechanism of action that modulates key cytokine pathways (IL-23, IL-12, Type I IFN) without inhibiting JAKs 1-3. Phase II and preliminary phase III data in PsA show significant improvements in joint and skin symptoms, with a safety profile from long-term psoriasis studies that appears favourable, showing minimal hematologic or laboratory abnormalities. The advent of bimekizumab and deucravacitinib enriches the PsA treatment arsenal and their introduction will help with more personalised management strategies for patients with PsA.

## Linked entities

- **Proteins:** IL17A (interleukin 17A), IL17F (interleukin 17F), TYK2 (tyrosine kinase 2), IL37 (interleukin 37), IL12 (Interleukin 12 level)
- **Chemicals:** deucravacitinib (PubChem CID 134821691)
- **Diseases:** psoriatic arthritis (MONDO:0011849), oral candidiasis (MONDO:0005886)

## Full-text entities

- **Genes:** IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, TYK2 (tyrosine kinase 2) [NCBI Gene 7297] {aka IMD35, JTK1}, IL17F (interleukin 17F) [NCBI Gene 112744] {aka CANDF6, IL-17F, ML-1, ML1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL23A (interleukin 23 subunit alpha) [NCBI Gene 51561] {aka IL-23, IL-23A, IL23P19, P19, SGRF}, IL12B (interleukin 12B) [NCBI Gene 3593] {aka CLMF, CLMF2, IL-12B, IMD28, IMD29, NKSF}
- **Diseases:** hematologic or laboratory abnormalities (MESH:D007757), fungal infections (MESH:D009181), inflammatory disease (MESH:D007249), psoriasis (MESH:D011565), oral candidiasis (MESH:D002180), PsA (MESH:D015535)
- **Chemicals:** Deucravacitinib (MESH:C000628674), Bimekizumab (MESH:C000625981)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12869330/full.md

## References

52 references — full list in the complete paper: https://tomesphere.com/paper/PMC12869330/full.md

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Source: https://tomesphere.com/paper/PMC12869330