- HS-20118 has shown promising efficacy signals in the evaluated participants with moderate to severe plaque psoriasis, and a favorable safety profile in both healthy volunteers from China and New Zealand and participants with moderate to severe psoriasis from China.
- The favorable pharmacokinetic profile of HS-20118 supports a once-weekly oral dosing regimen, with no ethnic differences in pharmacokinetics.SHANGHAI,May 15, 2026-Hansoh Pharmaceutical Group Co., Ltd. (“Hansoh Pharma,” 03692.HK) today announced the Phase 1 data of HS-20118 were presented as an oral presentation at the Society for Investigative Dermatology Annual Meeting (SID 2026), held on May 13-16 in Chicago.
HS-20118 is an orally bioavailable IL-23R antagonist under clinical development for the treatment of immune-mediated diseases. At SID 2026, data were presented from two randomized, double-blind, placebo-controlled Phase 1 studies (HS-20118-101 and 102) evaluating the safety, tolerability, pharmacokinetics, and pharmacodynamics of HS-20118 in healthy volunteers and participants with moderate-to-severe psoriasis, in China, New Zealand and U.S..
Both studies included a single ascending dose (SAD) and a multiple ascending dose (MAD) part. A total of 129 participants received treatment, including 48 healthy volunteers in New Zealand, 58 healthy volunteers and 23 patients with psoriasis in China.
Study results showed:
● Encouraging PK profile: the terminal half-life of HS-20118 was 6–7 days, supporting weekly oral dosing regimens. PK profile was comparable between Chinese and New Zealand populations.
● Promising efficacy signals: HS-20118 showed promising efficacy signals coupled with concordant biomarker responses, achieving therapeutic effects comparable to IL-23 monoclonal antibody therapies in participants with psoriasis.
◾ Following only 4 weeks of treatment, HS-20118 demonstrated clinically significantly greater PASI improvements compared to placebo. Furthermore, PASI scores continued to decrease over the subsequent 6 weeks after treatment discontinuation.
□ 100 mg QW cohort: -39.1% at week 4, -58.0% at week 10
□ 25 mg QD cohort: -54.5% at week 4, -90.5% at week 10
◾ At week 8, PASI 75 response rates were 33.3% in the 100 mg QW cohort and 75.0% in the 25 mg QD cohort. A similar trend was observed for IGA 0/1 response rate, with the 25 mg QD cohort achieving a notably high rate of 87.5%.
● Favorable safety profile:Only mild-to-moderate TEAEs were reported, with no dose-dependent relationship observed. Most of TEAEs were transient and resolved/recovered without medical treatment. The rates of moderate TEAEs were similar between SAD parts in China and New Zealand. No SAEs or TEAEs leading to study discontinuation occurred.
● Robust pharmacodynamics:Sustained IL-17 and hBD-2 reduction in psoriasis patients following HS-20118 treatment, confirming effective blockade of IL-23/IL-17 axis. This pharmacodynamic effect correlates with durable clinical efficacy.
Details of the oral presentation are as follows:
● Presentation Title: Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of HS-20118 in Healthy Adults and Psoriasis Patients
● Session: Concurrent Minisymposium 2: Clinical Research – Interventional Research
● Abstract No.: 0459
● Date/Time: May 14, 2026 from 9:35 AM to 9:45 AM(CDT)
● Presenter: Xiangqing Yu, Shanghai Hansoh BioMedical Co., Ltd.
About HS-20118
HS- 20118 is an oral peptide developed by Hansoh Pharma that selectively targets IL-23R. It works by inhibiting the binding of IL-23 to IL-23R, thus blocking the signal transduction and cytokine cascade mediated by IL-23. It is intended for the treatment of patients with psoriasis, and with an oral formulation, it can reduce the pain of injection and improve patient compliance, thus serving as a new option for psoriasis treatment. Phase 2 studies of HS-20118 in participants with moderate to severe psoriasis are currently planning globally.
About Psoriasis
Psoriasis is an immune-mediated chronic, recurrent, inflammatory skin disease influenced by both genetic and environmental factors. The typical clinical manifestations of the skin lesions are scaly erythema or plaques, which can be localized or widely distributed. When accompanied by joint damage, it is referred to as psoriatic arthritis. Patients with moderate to severe psoriasis have an increased risk of developing metabolic syndrome and atherosclerotic cardiovascular disease[1]. The prevalence of psoriasis ranges from 0.5% to 3.15% in the United States and 0.75% to 2.9% in Europe[2, 3]. The prevalence in China is approximately 0.47% to 0.5%[4, 5]. Although psoriasis is not contagious, it is difficult to treat. Patients often suffer from it for a lifetime, leading to impaired quality of life and reduced work capacity. In severe cases, psoriasis can be disabling, imposing a heavy burden on the patient, their family, and society[6, 7].
Currently, there is no cure for psoriasis. The primary treatment methods focus on anti-inflammatory and symptomatic therapies, which include topical medication, phototherapy, conventional systemic medication, and biological agents or small molecule drugs[1]. Topical medications are effective in controlling mild, localized psoriasis, but their use is limited by the duration of treatment and potential adverse effects. Patients with moderate to severe psoriasis often require a combination of phototherapy or systemic medications. The use of phototherapy and conventional systemic medications is limited by long treatment duration and adverse effects such as organ toxicity. Although biological agents offer strong specificity in targeting and have a rapid onset of action, they are not always effective for all patients with psoriasis[8], and their efficacy can diminish over time by varying degrees[9]. Additionally, the high cost and the need for injection administration have somewhat restricted their clinical use, and their long-term safety still needs further evaluation[10, 11]. Small molecule targeted drugs, such as phosphodiesterase 4 (PDE4) inhibitors (apremilast), Janus kinase (JAK1-3) inhibitors (tofacitinib, upadacitinib), and tyrosine kinase (TYK2) inhibitors (deucravacitinib), show great differences in efficacy and safety in the treatment of psoriasis, and also have the risk of adverse reactions and even serious adverse reactions[1]. Existing treatments still fail to meet the medical needs of most patients, and new therapies need to be developed.
References
[1] Psoriasis Committee, Chinese Society of Dermatology and Venereology, Zhang Xuejun. Chinese psoriasis Diagnosis and Treatment Guidelines (2023 edition)[J]. Chinese Journal of Dermatology, 2023,56(7):573-625.
[2] Helmick C G, Lee-Han H, Hirsch S C, et al. Prevalence of psoriasis among adults in the U.S.: 2003-2006 and 2009-2010 National Health and Nutrition Examination Surveys[J]. Am J Prev Med, 2014, 47(1): 37-45.
[3] Zhao Na, WU Wei-Zhi, Yang Ping. Research progress in the epidemiology of psoriasis [J]. Shandong Medicine, 2013, 53(39): 95-97.
[4] Ding X L, Wang T L, Shen Y W, et al. Epidemiological survey of psoriasis in six provinces and cities of China [J]. Chinese Journal of Dermatology and Venereology, 2010, 24(7): 598-603.
[5] Wang Xiao-hui. An epidemiological investigation of psoriasis in 4 provinces of Southwest China [J]. Harbin Med, 2017, 37(5): 426-427.
[6] Armstrong A W, Schupp C, Wu J, et al. Quality of life and work productivity impairment among psoriasis patients: findings from the National Psoriasis Foundation survey data 2003-2011[J]. PLoS One, 2012, 7(12): e52935.
[7] Dubertret L, Mrowietz U, Ranki A, et al. European patient perspectives on the impact of psoriasis: the EUROPSO patient membership survey[J]. Br J Dermatol, 2006, 155(4): 729-36.
[8] Furue K, Ito T, Furue M. Differential efficacy of biologic treatments targeting the TNF-alpha/IL-23/IL-17 axis in psoriasis and psoriatic arthritis[J]. Cytokine, 2018, 111: 182-188.
[9] Jullien D, Prinz J C, Nestle F O. Immunogenicity of biotherapy used in psoriasis: the science behind the scenes[J]. J Invest Dermatol, 2015, 135(1): 31-38.
[10] Boehncke W H, Schon M P. Psoriasis[J]. Lancet, 2015, 386(9997): 983-94.
[11] Mason A R, Mason J M, Cork M J, et al. Topical treatments for chronic plaque psoriasis of the scalp: a systematic review[J]. Br J Dermatol, 2013, 169(3): 519-27.
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