Comparative efficacy and safety of IL-17 and IL-23 inhibitors for moderate-to-severe psoriasis in Asian populations: a systematic review and meta-analysis

Abstract

Background

Psoriasis is a chronic inflammatory skin disorder affecting a significant portion of the global population. Biologics targeting the IL-17 and IL-23 pathways are effective in treating moderate-to-severe psoriasis; however, most clinical trials have been conducted in Western populations, leaving limited data on their efficacy and safety in Asian populations. Ethnic differences due to genetic and environmental factors can influence treatment responses. This meta-analysis evaluates the efficacy and safety of IL-17/23 inhibitors in Asian patients with moderate-to-severe psoriasis.

Methods

A systematic review and meta-analysis of randomized controlled trials (RCTs) published between 2019 and 2025 was conducted in accordance with the PRISMA 2020 guidelines. Comprehensive searches were performed in PubMed, Embase, Scopus and clinicaltrial.gov databases to identify studies evaluating IL-17 and IL-23 inhibitors in Asian adults with moderate-to-severe psoriasis. Eligible studies compared these biologics with placebo or active comparators. The primary outcome was treatment efficacy, assessed by improvement in Psoriasis Area and Severity Index (PASI). Secondary outcomes included treatment-emergent adverse events (AEs). Data were pooled using random-effects models, and results were expressed as Odds ratios (RRs) with 95% confidence intervals (CIs).

Results

A total of 30 randomized controlled trials (RCTs) involving 14,000 Asian and mixed-ethnicity participants were included. The meta-analysis demonstrated a significant overall efficacy advantage of IL-17 and IL-23 inhibitors over placebo or active comparators (log OR = 1.25; 95% CI 0.98–1.52; p < 0.0001). Subgroup analyses confirmed consistent treatment responses across efficacy measures—PASI 75 (log OR = 1.36; 95% CI 0.97–1.75; I² = 64.5%) and PASI 90 (log OR = 1.23; 95% CI 0.87–1.58; I² = 92.4%)—as well as across biologic classes (IL-17: log OR = 1.43 [1.09–1.77]; IL-23: log OR = 1.04 [0.60–1.49]). When stratified by population, efficacy remained high among Asian cohorts (log OR = 1.40 [1.17–1.62]) and mixed populations (log OR = 1.08 [0.51–1.65]).

Safety analyses showed that treatment-emergent adverse events (TEAEs) were mostly mild to moderate (50–85% for IL-17, 64–92% for IL-23), and serious adverse events (SAEs) occurred in < 5% of patients, without treatment-related deaths or unexpected immune-mediated events.

Conclusions

IL-17 and IL-23 inhibitors demonstrate high efficacy and favorable safety profiles in Asian adults with moderate-to-severe psoriasis, consistent with global evidence. Both biologic classes achieved substantial clinical improvements in PASI with low rates of serious adverse events.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12865-025-00789-2.

Introduction

Psoriasis is a chronic, immune-mediated skin disease affecting approximately 2–3% of the global population and significantly impacting quality of life [1]. For patients with moderate-to-severe disease, biologic therapies targeting the interleukin (IL)−17 and IL-23 pathways have transformed clinical management. Large phase III trials have demonstrated that IL-17 inhibitors (secukinumab, ixekizumab) and IL-23 inhibitors (guselkumab, risankizumab) achieve rapid and sustained improvements in Psoriasis Area and Severity Index (PASI) outcomes compared with conventional systemic therapies [2–4].

However, most pivotal biologic trials have been conducted predominantly in Western populations, resulting in under-representation of East Asian patients and limited ethnicity-specific evidence [5, 6]. This evidence gap is clinically important because genetic and phenotypic characteristics differ between East Asian and non–East Asian populations. For example, East Asian populations have a higher prevalence of the HLA-Cw6 allele, which has been linked to variability in therapeutic response in pharmacogenetic studies [7]. East Asian patients also typically have lower body mass indices (BMI), which may influence biologic drug exposure under fixed-dose regimens [8]. In addition, East–West differences in gut microbiome composition and environmental microbial exposures may modulate immune pathways relevant to psoriasis, including the IL-23/IL-17 axis [9].

Although real-world studies from Japan, South Korea, China, and Southeast Asia are emerging, the available evidence remains fragmented and heterogeneous. Therefore, a focused synthesis is needed to better understand treatment outcomes among East Asian patients. This systematic review and meta-analysis evaluate the efficacy and safety of IL-17 and IL-23 inhibitors in East Asian adults with moderate-to-severe plaque psoriasis, using data from randomized controlled trials published between 2019 and 2025. The findings aim to support region-specific clinical decision-making and guide optimization of biologic therapy in East Asian practice.

Methods

Search strategy

A systematic literature search was conducted in accordance with the PRISMA 2020 (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. Electronic databases including PubMed, Embase, Scopus, and ClinicalTrials.gov were searched from January 2019 to April 2025 using a combination of keywords and MeSH terms: “biologic,” “psoriasis,” “randomized controlled trial,” “IL-17 inhibitor,” “IL-23 inhibitor,” and specific drug names, for instance bimekizumab, risankizumab, guselkumab, brodalumab, secukinumab). Two reviewers (M.B.B. and M.A.) independently screened titles, abstracts, and full texts, with discrepancies resolved by discussion or a third reviewer (S.J.).

Study selection

Studies were included they met the predefined criteria: (1) randomized controlled trials (RCTs) evaluating safety and efficacy of IL-17/IL-23 inhibitors for moderate to severe plaque psoriasis, (2) Reported at least one efficacy endpoint (Psoriasis Area and Severity Index [PASI] 75/90/100, Investigator’s Global Assessment [IGA] 0/1, or static Physician’s Global Assessment [sPGA] 0/1) and at least one safety endpoint (treatment-emergent adverse events [TEAEs], serious adverse events [SAEs], or discontinuations due to AEs), 3) follow-up duration ≥ 12 weeks and have Asian population. Trials evaluating other biologic classes, such as tumor necrosis factor-α (TNF-α) inhibitors (e.g., adalimumab, etanercept) or interleukin-12/23 p40 inhibitors (e.g., ustekinumab) and their biosimilars, were excluded from the pooled analysis. If such agents appeared as comparator arms within otherwise eligible IL-17/23 trials, they were retained only as controls and were not analyzed as IL-17/23 exposures.

Exclusion criteria included non-RCTs, non-human studies, and duplicate publications. The studies prior to 2019 were also excluded. The study selection process is given in Fig. 1.

Fig. 1.

PRISMA flow chart of the study inclusion

Data extraction

Two reviewers (M.B.B and M.A) independently extracted data using a standardized pre-piloted form. The included studies exclusively evaluated IL-17 and IL-23 pathway inhibitors. Trials of other biologic classes, including TNF-α or IL-12/23 p40 inhibitors and their biosimilars, were excluded from the pooled analysis. The data were extracted on study characteristics including Author/year, design, sample size, biologic, comparator (placebo or active control), and follow-up duration, efficacy outcomes including PASI, IGA, sPGA, and flare-free survival and safety outcomes including Incidence of TEAEs, SAEs, discontinuations due to adverse events. The population data was extracted based on trial setting. If trial was global multi central, subgroup data specific to Asian population was extracted. Discrepancies were resolved by a third reviewer (S.J).

Statistical analysis

All statistical analyses were conducted using R (version 4.3.0) with the “meta” and “metafor” packages. Pooled effect estimates were calculated using the Mantel–Haenszel method under a random-effects model with the Hartung–Knapp adjustment for random-effects confidence intervals. Results were expressed as pooled odds ratios (ORs) with 95% confidence intervals (CIs). Between-study heterogeneity was assessed using the I² statistic (values of 25%, 50%, and 75% indicating low, moderate, and high heterogeneity, respectively) and Cochran’s Q test (p < 0.10 representing significant heterogeneity). Subgroup analyses were performed by biologic class (IL-17 vs. IL-23 inhibitors), efficacy endpoint (PASI 75 vs. PASI 90), and study population (Asian vs. mixed-ethnicity cohorts).

Publication bias was assessed visually using funnel plots and statistically via Egger’s regression test. Where asymmetry was identified, the trim-and-fill method was applied to estimate potential missing studies and adjust pooled estimates. All statistical tests were two-sided, and p < 0.05 was considered statistically significant.

Ethical considerations

As this study utilized published data, institutional review board approval and clinical trial was not required. The protocol was registered in PROSPERO (CRD42025102884).

Results

Study characteristics

The final analysis comprised 32 RCTs with a ranged in sample size from 47 to 905 patients. Most studies were phase 3, multicenter RCTs comparing IL-17 or IL-23 inhibitors with placebo or active comparators such as adalimumab, ustekinumab, or secukinumab. A summary of the key study characteristics is provided in Table 1.

Table 1.

Study characteristics of the included studies

Author (year)	Design	Sample Size	Biologic	Comparator	Efficacy	Safety
Reich et al. (2021) [10]	Multicenter RCT	567	Bimekizumab	placebo and Ustekinumab	PASI	TEAEs, STEAEs
Blauvelt et al. (2020) [11]	Phase 3 RCT	507	Risankizumab	placebo	PASI and sPGA 0/1	AEs
Langley et al. (2023) [12]	Multicenter RCT	1146	Secukinumab	PLACEBO	PASI and IGA mod 2011 0/1	AEs
Reich et al. (2019) [13]	RCT	605	Risankizumab	Adalimumab	PASI and sPGA 0/1	AEs, TEAS
Cai et al. (2024) [14]	Multicenter RCT	420	Xeligekimab	PLACEBO	PASI and PGA 0/1	AE
Yan et al. (2025) [15]	Phase 3 RCT	690	Vunakizumab	PLACEBO	PASI and sPGA 0	AEs
Youn et al. (2024) [16]	Phase 3 RCT	47	Bimekizumab	PLACEBO	PASI, IGA 0/1	TEAEs over
Chen et al. (2024) [17]	Phase 3 RCT	220	Tildrakizumab	PLACEBO	PASI, PGA	TEAEs
Yamanaka et al. (2023) [18]	Phase 3 RCT	17	Risankizumab		PASI	AEs
Yu et al. (2022) [19]	Phase 3 RCT	367	SCT630	Adalimumab	PASI	TEAES
He et al. (2023) [20]	Phase 1 RCT	46	IBI112	PLACEBO	PASI	ADE
Li et al. (2024) [21]	RCT	85	QX004N		PASI
Zheng et al. (2023) [22]	Phase 1 RCT	41	Ixekizumab		PASI
Imafuku et al. (2021) [23]	RCT	120	Tildrakizumab	PLACEBO	PASI	EAIRS
Okubo et al. (2019) [24]	RCT	52	Secukinumab		PASI	AES
Liu et al. (2020) [25]	Multicenter RCT	466	rhTNFR-Fc plus methotrexate	PLACEBO	PASI, sPGA	AEs
Jiang et al. (2025) [26]	RCT	120	IL-17 and IL-23		PASI
Lin Cai et al. (2025) [27]	RCT	143	JS005	placebo	PASI 75
Igarashi et al. (2021) [28]	Multinational RCT	158	Tildrakizumab	placebo	PASI, PGA	ADEs
Ohtsuki et al. (2019) [29]	RCT	171	Risankizumab	placebo	PASI, sPGA	AEs
Seo et al. (2021) [30]	Phase 3 RCT	62	Brodalumab	PLACEBO	PASI, sPGA	TEAES, SAE
ugustin et al. (2020) [31]	Phase 3 RCT	997	Risankizumab	Ustekinumab AND PLACEBO	PSS	NA
Reich et al. (2019) [32]	Phase 3 RCT	1829	Guselkumab	PLACEBO AND adalimumab	PASI, IGA	safety evaluated through week 28.
Feldman et al. (2024) [33]	Phase 3 RCT	503	SB17	ustekinumab	PASI	TEAES, SAE, AES
Man et al. (2025) [34]	Phase 3 RCT	556	BAT2206	ustekinumab	PASI	AEs, TEAS
Yao et al., (2024) [35]	RCT	130	CMAB015	SECUKINUMAB		AEs
Gordon et al., (2021) [36]	Phase 3 study	435	Bimekizumab	PLACEBO	PASI, IGA	TEAES
Papp et al., (2023) [37]	Phase 3 RCT	1738	Mirikizumab	secukinumab	PASI, sPGA
Asahina et al. (2023) [38]	Phase 3 RCT	108	Bimekizumab	ustekinumab and PLACEBO	PASI and IGA	TEAES
Reich et al. (2019) [39]	RCT	205	Mirikizumab	PLACEBO	PASI	AEs and TEAES
Reich et al. (2019) [40]	RCT	605	Risankizumab	Adalimumab	PASI, sPGA	AEs

Psoriasis Area and Severity Index [PASI], Investigator’s Global Assessment [IGA], static Physician Global Assessment [sPGA]) and safety outcomes (treatment-emergent adverse events [TEAEs], serious adverse events [SAEs].

Efficacy outcomes

The overall pooled effect estimate was log OR = 1.25 [95% CI 0.98–1.52]; p < 0.0001, confirming robust therapeutic efficacy, as shown in Fig. 2. Heterogeneity was substantial (I² = 90.4%, τ² = 0.2416), reflecting expected variations in trial design and populations.

Fig. 2.

Overall pooled efficacy of IL-17 and IL-23 inhibitors

Subgroup analysis by biologic class demonstrated that IL-17 inhibitors achieved a pooled log OR = 1.43 [1.09–1.77]; I² = 90.5%, while IL-23 inhibitors yielded log OR = 1.04 [0.60–1.49]; I² = 88% (Figure S2). The test for subgroup differences was not statistically significant (χ² = 1.80, p = 0.18), indicating that both cytokine-targeted pathways deliver similar clinical benefits.

The pooled effect for PASI 75 was log OR = 1.36 [0.97–1.75]; I² = 64.5%, and for PASI 90 was log OR = 1.23 [0.87–1.58]; I² = 92.4%, with no significant difference between endpoints (p = 0.62) (Figure S3). This consistency across clinical cut-offs supports the robustness of biologic efficacy irrespective of response definition.

Population-based subgroup analysis revealed stronger and more homogeneous responses in trials enrolling Asian-only participants (log OR = 1.40 [1.17–1.62]; I² = 64.3%) compared with mixed-ethnicity studies (log OR = 1.08 [0.51–1.65]; I² = 96%), with a statistically significant difference between subgroups (p < 0.001) as shown in Fig. 3.

Fig. 3.

Subgroup analysis by population type

Safety outcome

Across the included RCTs, IL-17 and IL-23 inhibitors demonstrated favorable and consistent safety profiles, with most adverse events being mild to moderate and comparable to placebo or active comparators (Table 2). Reported treatment-emergent adverse events (TEAEs) ranged from 50% to 85% for IL-17 inhibitors and 64% to 92% for IL-23 inhibitors, mainly involving nasopharyngitis, injection-site reactions, or upper respiratory infections. Serious adverse events (SAEs) were infrequent (< 5%), and treatment discontinuations due to AEs were rare. No treatment-related deaths or unexpected immune-mediated toxicities were observed, and long-term data confirmed sustained tolerability with no emerging safety signals.

Table 2.

Summary of the findings on efficacy and safety

Author (Year)	Biologic	Efficacy Outcome	Efficacy Measure	95% CI	P-value	Safety Outcome	Safety Measure	Safety CI	Safety P-value
Morita et al. (2023) [47]	Bimekizumab	Flare prevention	OR = 0.16	0.05–0.54	0.0005	—	—	—	—
Reich et al. (2021) [10]	Bimekizumab	PASI 90 @ Wk52	OR = 4.47	3.74–5.36	< 0.0001	AE incidence	85.20%	—	—
Asahina et al. (2023) [38]	Bimekizumab	PASI 90	RR = 1.69	—	Not stated	—	—	—	—
Asahina et al. (2023) [38]	Bimekizumab	IGA 0/1	RR = 14.4	—	Not stated	Low discontinuation due to AE	—	—	—
Gordon et al. (2024) [36]	Bimekizumab	PASI 90 @ Wk16	—	—	< 0.0001	TEAEs	61%	—	—
Youn et al. (2024) [16]	Bimekizumab	PASI 90	—	—	—	TEAEs	50% overall	—	—
Lin Cai et al. (2025) [27]	Bimekizumab	PASI 75 @ Wk12	—	—	< 0.0001	TEAEs	~NS	—	NS
Cai et al. (2024) [14]	Xeligekimab	PASI 75 @ Wk12	—	—	< 0.0001	—	—	—	—
Yan et al. (2025) [15]	Vunakizumab	Flare-free survival	HR = 0.16	0.05–0.54	0.0005	SAEs	<1%	—	—
Blauvelt et al. (2020) [11]	Risankizumab	PASI 90 @ Year 5	OR = 36.6	—	< 0.0001	AEs (nasopharyngitis)	33.70%	—	—
Blauvelt et al. (2020) [11]	Risankizumab	sPGA 0/1 @ Year 5	OR = 19.76	—	< 0.0001	Serious AEs	5.01 per 100 PY	—	—
Reich et al. (2019) [13]	Risankizumab	PASI 90 (Asian)	OR = 17.5	16.6–30.1	< 0.0001	TEAEs	Comparable across race	—	Not reported
Reich et al. (2019) [13]	Risankizumab	sPGA 0/1	OR = 16.8	—	< 0.0001	—	—	—	—
Reich et al. (2019) [13]	Risankizumab	PASI 90 vs. ADA	OR = 1.1	0.8–1.4	NS	TEAEs	92.8% vs. 90.4%	—	NS
Okubo et al. (2019) [24]	Risankizumab	PASI 90	—	—	Not stated	AEs	88.20%	—	—
Papp et al. (2023) [37]	Mirikizumab	sPGA 0/1 @ Wk16	OR = 77	—	< 0.0001	MACE	Rare	—	—
Papp et al. (2023) [37]	Mirikizumab	PASI 90 @ Wk16	OR = 71.5	—	< 0.0001	TEAEs	Comparable between groups	—	Not reported
Reich et al. (2019) [13]	Mirikizumab	PASI 90 @ Wk16	OR = 17.5	—	< 0.0001	Injection site AE	3.2% Asian	—	—
Reich et al. (2019) [13]	Mirikizumab	sPGA 0/1	OR = 16.6	—	< 0.0001	—	—	—	—
Chen et al. (2024) [17]	Tildrakizumab	PASI 75 @ Wk12	—	—	< 0.0001	TEAEs	64–71%	—	—
Igarashi [28] et al. (2021)	Tildrakizumab	PASI 75 @ Wk12	OR = —	—	< 0.0001	Low AE-related discontinuation	—	—	—
Imafuku et al. (2021) [23]	Tildrakizumab	PASI 75 @ Wk52	OR = —	—	Not stated	SAEs	infections	—	—
Seo et al. (2021) [30]	Brodalumab	PASI 75 @ Wk12	OR = —	—	< 0.0001	TEAEs	52.5% vs. 50%	—	NS
Seo et al. (2021)[30]	Brodalumab	sPGA 0/1 @ Wk12	OR = —	—	< 0.0001	—	—	—	—
Reich et al. (2019) [13]	Guselkumab	PASI 90 (Asian)	OR = 17.5	—	< 0.0001	TEAEs	—	—
Reich et al. (2019) [13]	Guselkumab	IGA 0/1 (Wk24)	—	—	≤ 0.004	TEAEs	25.4% (Asian)	—	—
Reich et al. (2019) [13]	Guselkumab	PASI 100 (Wk24)	—	—	Not stated	TEAEs	23.4% (Asian)	—	—
Cai et al. (2022) [47]	Guselkumab	PGA 0/1 @ Wk8	OR = 0.5	0.3–0.9	0.03	TEAEs	89.3% vs. 94.6%	—	NS
Cai et al. (2022) [47]	Guselkumab	PASI 75	OR = 1.1	—	NS	—	—	—	—
Cai et al. (2022) [47]	SCT630	PASI 75	OR = —	—	NS	TEAEs	HLX03: 89.3% ADA: 94.6%	—	—
Li et al. (2024) [21]	QX004N	Early PASI 90	—	—	< 0.0001	AEs	—	—	—
Lin Cai et al. (2025) [27]	JS005	PASI 75 @ Wk12	—	—	< 0.0001	TEAEs	Equal	—	NS
Liu et al. (2020) [25]	rhTNFR-Fc	PASI 75	OR = —	—	—	AEs	Upper RTIs common	—	—
Zheng et al. (2023) [22]	Secukinumab	PASI 90 (Q2W)	—	—	—	—	—	—	—
Zheng et al. (2023) [22]	Secukinumab	PASI 90 (Q4W)	—	—	—	—	—	—	—
Reich et al. (2019) [13]	Secukinumab	DLQI 0/1 (Wk24)	—	—	Not stated	Injection Site AE	3.2% (Asian)		—
Reich et al. (2019) [13]	Secukinumab	IGA 0/1 (Wk24)	—	—	0.004	—	—	—	—
Reich et al. (2019) [13]	Secukinumab	PASI 100 (Wk24)	—	—	Not stated	—	—	—	—
Reich et al. (2019) [13]	Secukinumab	TEAEs	—	—	Not reported	Injection Site AE	Comparable	—	—
Reich et al. (2019) [13]	Secukinumab	DLQI 0/1	—	—	Not stated	—	—	—	—
Okubo et al. (2019) [24]	Secukinumab	GPP/EP response	—	—	—	AEs	88.20%	—	—
Yao et al. (2024) [35]	BAT2206	TEAE incidence	—	—	Not reported	TEAEs	49.1% vs. 46.8%	—	—
Yao et al. (2024) [35]	BAT2206	Treatment-related TEAEs	—	—	Not reported	—	16.2% vs. 18.0%	—	—
Feldman et al. (2024) [33]	CMAB015	ONLY SAFETY	—	—	—	TEAEs	Similar to secukinumab	—	—
Papp et al. (2023) [37]	Mirikizumab	TEAEs (Wk0–52)	—	—	Not reported	—	—	—	—
Papp et al. (2023) [37]	Mirikizumab	MACE	—	—	Not reported	—	4 cases vs. 0	—	—
Reich et al. (2019) [13]	Mirikizumab	PASI 90 @ Wk16	OR = 17.5	—	< 0.0001	Injection Site AE	3.2% (Asian)	—	—
Reich et al. (2019) [13]	Mirikizumab	sPGA 0/1 @ Wk16	OR = 16.6	—	< 0.0001	—	—	—	—
Reich et al. (2019) [13]	Mirikizumab	PASI 90 @ Wk16	OR = 17.5	—	< 0.0001	TEAEs	Comparable between groups	—	—
Reich et al. (2019) [13]	Mirikizumab	sPGA 0/1	OR = 16.8	—	< 0.0001	—	—	—	—
Reich et al. (2019) [13]	Mirikizumab	PASI 90 vs. ADA	OR = 1.1	—	NS	TEAEs	92.8% vs. 90.4%	—	NS
Reich et al. (2019) [13]	Mirikizumab	PGA 0/1 @ Wk8	OR = 0.5	0.3–0.9	0.03	—	—	—	—

Psoriasis Area and Severity Index [PASI], Investigator’s Global Assessment [IGA], static Physician Global Assessment [sPGA]) and safety outcomes (treatment-emergent adverse events [TEAEs], serious adverse events [SAEs].

Discussion

This systematic review and meta-analysis synthesize randomized controlled trials evaluating IL-17 and IL-23 inhibitors specifically in Asian adults with moderate to severe plaque psoriasis. Across Asian-only and mixed-Asian RCTs, both biologic classes demonstrated robust and clinically meaningful improvements in PASI 75 and PASI 90 outcomes. Although some individual trials reported numerically higher PASI 90 responses with IL-23 inhibitors [3, 4, 17], several Asian RCTs have shown equally strong responses with IL-17 inhibitors [16, 38]. Consistent with these findings, our pooled and subgroup analyses did not identify statistically significant differences between IL-17 and IL-23 inhibitors, indicating that both classes are effective treatment options in Asian populations without evidence of class superiority.

Several Asian-specific factors may influence therapeutic variability. Genetic predisposition—particularly the higher prevalence of the HLA-Cw6 allele in East and Southeast Asian populations—has been associated with differential treatment responsiveness. Evidence suggests that HLA-Cw6–positive patients may experience enhanced responses to IL-17 pathway inhibition [7], while associations with IL-23 inhibitors remain inconsistent. Recent Asian pharmacogenetic analyses further emphasize the importance of genotype response relationships [16,]. Incorporating pharmacogenetic stratification into future Asian RCTs may help clarify these patterns.

Anthropometric variation may also contribute to treatment heterogeneity among Asian patients with psoriasis. Asian populations generally present with lower BMI and leaner body composition compared with Western cohorts, which may influence drug exposure under fixed-dose IL-17 and IL-23 regimens. Recent real-world studies from China and Korea have demonstrated that BMI and metabolic parameters are significantly associated with psoriasis severity and biologic treatment response, with higher BMI linked to reduced PASI improvement and delayed therapeutic onset [41]– [42]. These findings are further supported by a large Asian cohort showing that BMI, basal metabolic rate, and body surface area independently affect treatment outcomes [43]. Collectively, these studies highlight the importance of considering body composition when interpreting clinical response to biologic therapy in Asian populations.

Environmental and microbiome-related factors may also modulate therapeutic responses to IL-17 and IL-23 inhibitors. Asian populations exhibit distinct gut and skin microbiome compositions shaped by dietary patterns, hygiene practices, urbanization, and environmental exposures. These microbial signatures can influence IL-23/IL-17–mediated inflammatory pathways, including Th17 differentiation, cytokine activation, and keratinocyte signaling [9]. Emerging evidence from Asian microbiome studies shows that alterations in microbial diversity and specific microbial particularly reduced Cutibacterium and increased Staphylococcus or Streptococcus species may contribute to psoriasis severity and variable immunologic responses to biologic therapy [44]– [45]. Incorporating microbiome profiling into future Asian psoriasis trials could help clarify these mechanisms and identify microbial biomarkers predictive of biologic response.

Safety outcomes across included RCTs were favorable, with low rates of serious adverse events. IL-17 inhibitors were associated with the expected class-specific signal of mild mucocutaneous candidiasis, consistent with global findings. Although tuberculosis prevalence varies across Asia, tuberculosis-related events were rarely reported, reflecting stringent pre-treatment screening protocols. Short-term safety of IL-17 and IL-23 inhibitors appears acceptable in Asian cohorts, although long-term data remain limited.

Subgroup analyses revealed potential differences between Japanese and Chinese patients, although these observations were based on modest sample sizes and may reflect genetic, metabolic, and dietary diversity across Asian subpopulations. Larger, regionally representative trials are needed to confirm these preliminary observations.

Evidence on biosimilars was limited but suggested short-term efficacy comparable to originators in Asian patients. However, long-term immunogenicity data are scarce. Given the cost constraints in many Asian healthcare systems, further evaluation of IL-17 and IL-23 biosimilars remains a high research priority [16]– [17].

Study limitations

This meta-analysis has several important limitations. First, heterogeneity across trials was notable, reflecting differences in study design, comparator arms, dosing schedules, and follow-up durations. Second, Asian-specific subgroup data were not uniformly available across all global RCTs, and several analyses relied on trial-site–based population identification rather than genetically confirmed ethnicity. Third, the number of Japan- and China-specific RCTs remained modest, limiting the precision of within Asia subgroup comparisons. Fourth, long-term safety data were sparse, restricting conclusions regarding rare adverse events and long-term immunogenicity. Fifth, microbiome and pharmacogenetic interpretations remain exploratory because such data were not available in the included trials. Despite these limitations, this review provides one of the most comprehensive syntheses to date focusing exclusively on IL-17 and IL-23 inhibitor outcomes in Asian psoriasis populations.

Conclusion

Both IL-17 and IL-23 inhibitors demonstrated strong and comparable efficacy and acceptable short-term safety in Asian adults with moderate to severe plaque psoriasis. Ethnic-specific factors such as HLA-Cw6 prevalence, BMI patterns, and microbiome differences may influence treatment response and should be considered in future research. Larger, region-specific trials and long-term real-world studies are needed to refine biologic selection and support more personalized psoriasis management in Asian populations.

Abbreviations

IL

Interleukin

IL-17/23

Interleukin 17/23

PASI

Psoriasis Area and Severity Index

OR

Odds Ratio

CI

Confidence Interval

BMI

Body Mass Index

RCT

Randomized Controlled Trial

TEAE

Treatment-Emergent Adverse Events

SAE

Serious Adverse Events

PGA

Physician Global Assessment

Authors’ contributions

- **Mohammad Alzghool** : Primary author, responsible for conducting the systematic review, data analysis, and drafting the manuscript.- **Song Jiquan** : Primary corresponding author, responsible for the study’s design, supervision, and critical review of the manuscript.- **Musa Bin Bashir** : Corresponding author, responsible for manuscript submission, final manuscript approval, and overall coordination of the submission process.

Funding

This research received no specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Data availability

All data generated or analyzed during this study are included in this published article and its supplementary files. The search strategy and extracted data are provided in Supplementary File S1.

Declarations

Ethics approval and consent to participate

Not applicable.

Competing interests

The authors declare no competing interests.