# Drug development in psoriatic arthritis: a trialtrove-based landscape analysis (1999–2025)

**Authors:** Gang Wang, Jun Li, Xinling Su, Zhuangwei Fang, Yuting Xu, Juan Zheng, Hao Liu, Ning Wang, Liping Huang

PMC · DOI: 10.3389/fimmu.2026.1722103 · Frontiers in Immunology · 2026-03-12

## TL;DR

This paper analyzes PsA drug trials from 1999 to 2025, showing a shift from TNF inhibitors to newer therapies and highlighting ongoing challenges in trial design and outcomes.

## Contribution

The study provides a comprehensive analysis of PsA drug development trends using Trialtrove data, linking clinical trial patterns to regulatory and translational changes.

## Key findings

- PsA drug development shifted from TNF inhibitors to newer mechanisms like IL-17/IL-23 and JAK1/TYK2 pathways.
- Most trials completed successfully, but outcome reporting was often incomplete or non-standardized.
- The US and China led in trial participation, with academic and top pharmaceutical companies as primary funders.

## Abstract

Psoriatic arthritis (PsA) is a heterogeneous, immune-mediated disease affecting joints, entheses, the axial skeleton, and skin. Although many targeted therapies have emerged, unmet needs remain in musculoskeletal control, comorbidity management, and durable remission.

To map the contemporary clinical-trial landscape of PsA pharmacotherapy and place these data in the context of current evidence, treatment guidelines, regulatory changes, and translational advances.

We analyzed Citeline Trialtrove data on 587 interventional PsA drug trials initiated from 1999 to 2025. Structured variables captured annual trial starts by phase, operational status and outcomes, geographic distribution, funding sources, investigated drugs, molecular targets, and primary endpoints. We characterized trends using descriptive statistics and graphical summaries. To strengthen interpretation of temporal trends, we additionally prespecified count-based trend testing (Poisson/negative binomial regression) and conducted era-stratified summaries (1999–2010 vs 2011–2025) to reflect systemic changes in regulation and transparency.

Trial activity was higher after 2012, with increased early-phase programs and sustained phase III/IV development. Most studies reached completion (82.5%); 22.7% disclosed positive outcomes, while many were labeled undefined because of incomplete or non-standardized reporting. Terminations were driven mainly by business decisions rather than lack of efficacy. The United States (US) and China had the highest absolute trial participation, with Europe providing strong multicenter coordination; population-standardized participation (trials per 10 million population) was higher in the US than in China. Funding was diverse: academic institutions (35.3%) and top-20 pharmaceutical companies (32.9%) predominated, alongside smaller industry and generic sponsors. TNF inhibitors such as adalimumab and etanercept were the most frequently tested agents, but substantial activity involved newer mechanisms including IL-17/IL-23, JAK1/TYK2, and PDE4 pathways.

Over the past two decades PsA drug development has broadened from TNF blockade to multiple targeted axes, supported by balanced academic–industry sponsorship and a rapidly expanding global footprint. Yet challenges remain—heterogeneous endpoints, incomplete outcome reporting, modest musculoskeletal efficacy in some novel classes, and the need to integrate cost considerations as biosimilars and generics enter routine care. Future trials should prioritize harmonized, domain-specific outcomes, precision patient selection, long-term safety (especially for JAK-pathway inhibitors), and pragmatic, treat-to-target designs to translate mechanistic advances into sustainable, patient-centered therapy.

## Linked entities

- **Proteins:** TNF (tumor necrosis factor), IL17A (interleukin 17A), IL37 (interleukin 37), JAK1 (Janus kinase 1), TYK2 (tyrosine kinase 2), PDE4A (phosphodiesterase 4A)
- **Diseases:** psoriatic arthritis (MONDO:0011849)

## 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}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, PDE4A (phosphodiesterase 4A) [NCBI Gene 5141] {aka DPDE2, PDE4, PDE46}, IL23A (interleukin 23 subunit alpha) [NCBI Gene 51561] {aka IL-23, IL-23A, IL23P19, P19, SGRF}, JAK1 (Janus kinase 1) [NCBI Gene 3716] {aka AIIDE, JAK1A, JAK1B, JTK3}
- **Diseases:** immune-mediated (MESH:C567355), PsA (MESH:D015535)
- **Chemicals:** adalimumab (MESH:D000068879)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13017793/full.md

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13017793/full.md

## References

32 references — full list in the complete paper: https://tomesphere.com/paper/PMC13017793/full.md

---
Source: https://tomesphere.com/paper/PMC13017793