A Phase 3, Multicenter, Double-blind, Randomized, Placebo-controlled, Parallel-group Trial to Assess the Efficacy, Safety and Tolerability of Cenerimod in Adult Patients With Systemic Lupus Erythematosus and Active Lupus Nephritis in Combination With Background Therapy

The goal of this clinical trial is to learn if cenerimod, on top of regular treatment, works to treat active lupus nephritis in adults with systemic lupus erythematosus and active lupus nephritis. It will also learn about the safety of cenerimod. The main questions it aims to answer are:
* Does cenerimod improve kidney function in participants?
* What medical problems do participants have when taking cenerimod?
Researchers will compare cenerimod to a placebo (a look-alike substance that contains no drug) to see how well cenerimod works when it is added to regular treatment.
Participants will:
* Take cenerimod or a placebo every day for 76 weeks (approximately 1.5 years), on top of regular treatment.
* Visit the clinic every 1 to 3 months for checkups and tests.

开始日期2026-02-09

申办/合作机构

Viatris, Inc.

NCT07266090

/ Active, not recruiting临床2期

A Multicenter,Open-label,Single Arm,Multiple-dose Study to Evaluate the Safety,Tolerability,Pharmacokinetics and Pharmacodynamics of Cenerimod in Adult Chinese Participants With Moderate-to-severe Systemic Lupus Erythematosus (SLE) on Top of Background Therapy

The goal of this clinical trial is to learn about the safety, how the body processes the drug, and its effects of a drug called cenerimod in adult Chinese participants (aged 18-75) with moderate to severe Systemic Lupus Erythematosus (SLE) who are already receiving standard background therapy.
The main questions it aims to answer are:
* What is the safety and tolerability of a daily 4 mg dose of cenerimod in Chinese participants with SLE?
* How is cenerimod processed by the body (pharmacokinetics) in this population?
* What is the effect of cenerimod on the level of lymphocytes in the blood (pharmacodynamics)? This is a single-arm study without a comparison group.
Participants will:
* Take one 4 mg cenerimod tablet by mouth once daily for up to 12 months.
* Continue their stable, pre-existing background SLE medications throughout the study.
* Attend regular clinic visits over a period of up to 22 months for tests and check-ups, including blood draws, heart monitoring (12-lead electrocardiogram), vital signs(blood pressure),and physical examinations.
* Undergo a final safety follow-up 6 months after their last dose of the study drug.

开始日期2026-01-14

申办/合作机构

晖致医药有限公司

NCT07301723

/ Completed临床1期

A Single-center, Open-label Trial to Determine the Absolute Bioavailability of Cenerimod Using an Intravenous 14C-radiolabeled Cenerimod Microtracer in Healthy Male Participants

The goal of this clinical trial is to learn about the absolute bioavailability of cenerimod in healthy participants. It will also provide information about the safety of cenerimod.
Participants will receive one tablet with cenerimod, followed by an intravenous (i.v.) infusion with a 14C-radiolabeled cenerimod microtracer (cenerimod with a very low dose of radioactivity) 6 hours later.
Participants will stay at the clinic for a total of 4 days, and will return to the clinic for further tests over the course of approximately 3 months.

开始日期2025-12-11

申办/合作机构

Viatris, Inc.

100 项与 Cenerimod 相关的临床结果

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100 项与 Cenerimod 相关的转化医学

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100 项与 Cenerimod 相关的专利（医药）

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项与 Cenerimod 相关的文献（医药）

2025-02-01·ANNALS OF THE RHEUMATIC DISEASES

Pharmacodynamics of the S1P₁ receptor modulator cenerimod in a phase 2b randomised clinical trial in patients with moderate to severe SLE.

Article

作者: Murphy, Mark Joseph ; Suffiotti, Madeleine ; Keller, Marcel Peter ; Seifer, Gustavo ; Strasser, Daniel Stefan ; Berkani, Ouali ; Cornelisse, Peter ; Brazauskas, Pijus

BACKGROUND:

Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterised by autoreactive T and B lymphocytes. Sphingosine-1- phosphate (S1P) is involved in lymphocyte egress from peripheral lymphoid organs into the circulation. In phase 2a clinical trial, the potent, selective S1P₁ receptor modulator cenerimod reduced circulating antibody-secreting cells and interferon (IFN)-associated biomarkers.

OBJECTIVES:

Pharmacodynamic effects of 2 and 4 mg cenerimod were evaluated in the phase 2b clinical trial (CARE) in moderate to severe patients with SLE (NCT03742037).

METHODS:

Blood samples were collected at baseline and after 6 months of treatment with cenerimod or placebo from CARE. The gene expression signatures for type 1 interferon (IFN-1), IFN-γ and plasma cells were used to assess dose-dependent pharmacodynamic effects of cenerimod. Cell-type deconvolution was performed to estimate cell abundance.

RESULTS:

Cenerimod 4 mg reduced IFN-associated protein and gene signature biomarkers after 6 months compared with placebo. A larger decrease of IFN proteins was evident in IFN-1 high patients compared with IFN-1 low patients. The median IFN-1 score in the IFN-1 high patients was reduced after 6 months of cenerimod 4 mg and the transition from IFN-1 low to high status compared with placebo was prevented. Cenerimod 4 mg exhibited a larger effect size on the pharmacodynamic biomarkers IFN-1, IFN-γ and plasma cells compared with cenerimod 2 mg.

CONCLUSIONS:

This study further characterised the mechanism of action of cenerimod in patients with SLE and substantiated the scientific rationale for cenerimod 4 mg in the phase 3 clinical trials in moderate to severe SLE (OPUS-1/-2).

2025-01-01·Lancet Rheumatology

Cenerimod, a sphingosine-1-phosphate receptor modulator, versus placebo in patients with moderate-to-severe systemic lupus erythematosus (CARE): an international, double-blind, randomised, placebo-controlled, phase 2 trial

Article

作者: Trokan, Luba ; Cahuzac, Clélia ; Merrill, Joan T ; Murphy, Mark J ; Kalunian, Kenneth ; Berkani, Ouali ; Askanase, Anca D ; Navarra, Sandra V ; D'Cruz, David ; Cornelisse, Peter ; Strasser, Daniel S

BACKGROUND:

Sphingosine-1-phosphate (S1P) is a signalling molecule that has an inhibitory role in atherosclerosis, inflammation, cell proliferation, and immunity. Cenerimod is a selective S1P₁ receptor modulator under investigation for the treatment of systemic lupus erythematosus (SLE). We aimed to determine the efficacy, safety, and tolerability of four doses of cenerimod in adults with moderate-to-severe SLE receiving standard of care background therapy.

METHODS:

CARE was a double-blind, randomised, placebo-controlled, phase 2 trial, in adults (aged 18-75 years) with moderate-to-severe SLE (a score of at least 6 out of 105 on the SLE disease activity index-2000, modified to exclude leukopenia [mSLEDAI-2K] score). Participants were recruited from 189 hospitals, specialist centres, and outpatient clinics in 22 countries in Asia Pacific, Latin America, Europe, and the USA. Participants were randomly assigned (1:1:1:1:1), using an interactive response technology via balanced block randomisation (block size of 5) and stratified by oral glucocorticoid dose at randomisation and disease activity at screening, to once-daily oral cenerimod at 0·5 mg, 1·0 mg, 2·0 mg, or 4·0 mg or placebo, in addition to stable background SLE therapy, and followed up for 12 months. After 6 months, participants assigned to cenerimod 4·0 mg were randomly assigned again (1:1) to either cenerimod 2.0 mg or placebo for a further 6 months. The primary endpoint was change from baseline to month 6 in mSLEDAI-2K score, assessed in all participants randomly assigned to treatment (full analysis set). To meet the primary endpoint, the doses had to show a significant improvement over placebo, when adjusting for multiplicity, considering the hierarchical testing strategy, per a prespecified plan. Safety analyses included all participants who received at least one dose of study treatment. This study is registered with ClinicalTrials.gov, NCT03742037, and is complete.

FINDINGS:

Between Dec 21, 2018, and Aug 25, 2022, 810 patients were screened and 427 were randomly assigned to 0·5 mg (n=85), 1·0 mg (n=85), 2·0 mg (n=86), and 4·0 mg (n=85) cenerimod or placebo (n=86). Median age was 42 years (IQR 33-51), 406 (95%) of 427 participants were women, 21 (5%) were men, and 337 (79%) were White. At month 6, the least squares mean change from baseline in mSLEDAI-2K score was -2·85 (95% CI -3·60 to -2·10) for the placebo group and -3·24 (-3·98 to -2·49; difference vs placebo -0·39 [95% CI -1·45 to 0·68]; p=0·47) for the cenerimod 0·5 mg group, -3·41 (-4·16 to -2·67; difference vs placebo -0·57 [-1·62 to 0·49]; p=0·29) for the 1·0 mg group, -2·84 (-3·58 to -2·09; difference vs placebo 0·01 [-1·05 to 1·08]; p=0·98) for the 2·0 mg group, and -4·04 (-4·79 to -3·28; difference vs placebo -1·19 [-2·25 to -0·12]; p=0·029) for the 4·0 mg group; hence, the primary endpoint was not met. Treatment-emergent adverse events up to 12 months had no clear treatment-related or dose-related pattern across the groups. At month 6, treatment-emergent lymphopenia was reported in one (1%) of 85 patients who received cenerimod 0·5 mg, five (6%) of 85 patients who received 1·0 mg, nine (10%) of 86 patients who received 2·0 mg, 12 (14%) of 84 patients who received 4·0 mg, and no patients who received placebo. Two deaths due to adverse events occurred (both in the cenerimod 1·0 mg group; one due to acute coronary syndrome and the other due to upper gastrointestinal haemorrhage), and were determined to be unrelated to study treatment.

INTERPRETATION:

The primary endpoint was not met. Cenerimod was well tolerated over 12 months. Cenerimod 4·0 mg is being investigated for the treatment of SLE in two ongoing phase 3 trials (NCT05648500, NCT05672576).

FUNDING:

Idorsia Pharmaceuticals.

2024-12-03·Cureus Journal of Medical Science

Evolving Treatment Strategies for Systemic Lupus Erythematosus in Clinical Practice: A Narrative Review

Review

作者: Upshaw, William C ; Varrassi, Giustino ; Burroughs, Caroline R ; Mosieri, Chizoba N ; Tassin, Joseph P ; Patel, Chandni R ; Shekoohi, Sahar ; Bembenick, Kristin Nicole ; Kaye, Alan D ; Kaye, Adam M ; Ahmadzadeh, Shahab ; Hawkins, Alison M

Systemic lupus erythematosus (SLE) is an autoimmune disease that more commonly affects African American people, although it is seen in people of all racial backgrounds. This condition is characterized by a dysregulated immune response resulting in widespread inflammation. Clinical manifestations caused by this inflammation include arthritis, anemia, cutaneous rashes, pleuritis, and nephritis. Treatment for SLE aims to reduce disease activity and maintain a state of low inflammation. In this regard, numerous treatments are used, such as hydroxychloroquine, glucocorticoids, and non-glucocorticoid immunosuppressants such as methotrexate. Related to these drugs resulting in significant adverse effects and being ineffective in controlling SLE symptoms in some patients, new biologic agents have been created in hopes of better treating SLE. This includes belimumab and anifrolumab, monoclonal antibodies directed against the cytokine, and type 1 interferon receptor, respectively. These agents are indicated in patients with SLE whose symptoms are inadequately controlled by standard therapy alone. Clinical trials have shown that these agents effectively reduce SLE symptoms as judged using standardized metrics of disease activity. These biological agents have also been shown to have generally mild side effects when taken by patients with SLE, making them safe for use. In addition to the above medications, new treatments are being developed for SLE patients, such as cenerimod, litifilimab, chimeric antigen receptor T cells, and DS-7011a (anti-toll-like receptor 7 monoclonal antibody). These new treatments have shown promise in clinical trials. However, more information regarding their safety and efficacy is needed before they are available for the treatment of SLE.

项与 Cenerimod 相关的新闻（医药）

2026-10-12

·GlobeNewswire-Health Care

Aprocitentan efficacy data reinforce endothelin pathway blockade as a distinct therapeutic approach across the cardiometabolic disease spectrum including obesity

Two oral presentations at AHA Hypertension 2026 demonstrate the pronounced efficacy of aprocitentan in two groups of patients with notoriously difficult to control hypertension from the PRECISION study: patients with obesity and patients across the cardiovascular-kidney-metabolic (CKM) continuum. In both groups of patients, aprocitentan induced a rapid double-digit reduction in blood pressure and was associated with improved UACR and stable renal function, suggesting a potential kidney protective effect. A trend towards improvement was also observed in several metabolic biomarkers. The robust effects observed in patients with obesity or CKM disease further underscore the importance of blocking the upregulated endothelin system in difficult-to-control hypertension. Allschwil, Switzerland – October 12, 2026Idorsia Ltd (SIX: IDIA) shared positive findings from two new analyses of the pivotal Phase 3 PRECISION study of aprocitentan in patients with resistant hypertension, at the American Heart Association Hypertension Scientific Sessions 2026 on October 10. Amer Joseph, MD, Chief Medical Officer and Head of Global Clinical Development“For us, these results are an important step in understanding where targeting the endothelin pathway makes the greatest difference for patients with uncontrolled hypertension. In PRECISION, aprocitentan produced a double-digit blood pressure reduction in the overall population. We are encouraged to see consistent blood pressure reductions in patients with obesity and across earlier and more advanced stages of CKM, given their complex and overlapping clinical risks. Together with the reduction in UACR, stable eGFR and safety profile, this adds to the growing evidence that the endothelin pathway matters in patients across the broader spectrum of uncontrolled hypertension.” An estimated 1.4 billion people worldwide live with hypertension, yet many do not achieve adequate control, increasing their risk of cardiovascular and kidney complications and premature death.1 The burden is particularly high among people with obesity or CKM.2-4 A 5-10 mmHg reduction in systolic blood pressure can reduce the risk of major cardiovascular events by approximately 10%-20%.5 Yet, despite the well-established benefits of lowering blood pressure, many patients remain above target despite multiple therapies, underscoring the need for treatments that address additional pathways involved in hypertension. When the endothelin system is upregulated, endothelin-1 drives vasoconstriction, vascular and cardiac hypertrophy, fibrosis, inflammation and aldosterone production. It is especially the case in populations prone to difficult-to-control hypertension such as obesity, type 2 diabetes, and renal failure. There is a strong correlation between ET-1 and markers of metabolic syndrome (body mass index, triglycerides, insulin resistance), and between ET-1 and kidney function. By blocking ETA and ETB receptors, aprocitentan targets this distinct pathway beyond the renin-angiotensin-aldosterone system.6,7 Aprocitentan shows marked benefits in patients with obesity and hypertension Endothelin is a driver of hypertension in individuals with obesity: A post hoc analysis of the PRECISION study. Presented by Dr Michael A Weber, MDMarkus Schlaich, Martine Clozel, Ruth Collins, Parisa Danaietash, John M. Flack, Johann Laurent, Krzysztof Narkiewicz, Ji-Guang Wang and Michael A Weber.Abstract available online This post hoc analysis compared 506 patients with obesity defined as body mass index ≥30 kg/m² with 224 patients without obesity. At baseline, office blood pressure was similar between groups, while patients with obesity carried a higher burden of several comorbidities, including diabetes, chronic kidney disease, ischemic heart disease, congestive heart failure and obstructive sleep apnea. Key findings: Aprocitentan 12.5 mg and 25 mg reduced office systolic blood pressure at Week 4 in patients with obesity by 15.4 and 16.0 mmHg respectively, consistent with the reduction observed in the overall PRECISION population. Double-digit absolute reductions were maintained during the 32-week single-blind treatment period to Week 36.Night-time ambulatory systolic blood pressure decreased in patients with obesity, with the reduction maintained during longer-term treatment.UACR decreased in patients with obesity, eGFR remained stable while uric acid showed favorable changes with aprocitentan versus placebo.Safety profile was consistent between the two cohorts Dr. Michael A. Weber, Professor of Medicine at the SUNY Downstate College of Medicine in Brooklyn, New York, commented:“Obesity and hypertension are major, interconnected drivers of cardiovascular risk. As the endothelin pathway is upregulated in uncontrolled hypertension and adipose tissue can contribute to endothelin production, it represents a compelling therapeutic target in patients with obesity and resistant hypertension. In this post hoc analysis of PRECISION, aprocitentan substantially reduced office systolic blood pressure in patients with obesity, consistent with the double-digit reduction observed in the overall PRECISION population and was also associated with signs of kidney protection, a vital objective in this population. These findings reinforce the role of the endothelin pathway in obesity-associated resistant hypertension.” Aprocitentan showed marked benefits in patients with CKM and hypertension Endothelin as a therapeutic target across the cardiovascular-kidney-metabolic continuum: A post hoc analysis of the PRECISION study. Presented by Dr John M. FlackMarkus Schlaich, Martine Clozel, Parisa Danaietash, Johann Laurent, Alessandro Maresta, Krzysztof Narkiewicz, Ji-Guang Wang, Michael A Weber and John M. Flack.Abstract available online This post hoc analysis focused on 410 patients in CKM stage 2 and 273 patients in CKM stage 4a. Patients in stage 4a were older and had a greater burden of diabetes, chronic kidney disease, ischemic heart disease, heart failure and cerebrovascular disease, while baseline office and ambulatory blood pressure were similar between cohorts. Key findings: Aprocitentan 12.5 mg reduced office systolic blood pressure at Week 4, by 15.1 mmHg in patients with CKM stage 2 and by 16.6 mmHg in those with stage 4a.At Week 4, daytime and night-time ambulatory systolic blood pressure decreased in both CKM cohorts. Increase of the UACR is associated with higher risks of mortality in patients with CKM.8 Aprocitentan reduced UACR by almost 50% across earlier and more advanced CKM stages in patients with albuminuria. Urate showed also favorable trends versus placebo in both CKM cohorts. Estimated glomerular filtration rate remained stable over the duration of the study in both cohorts. NT-proBNP was also stable, and no increase in electrolyte abnormalities was observed. The safety profile was consistent between CKM stages 2 and 4a. Dr. John M. Flack, Professor and Chair of the Departments of Medicine and Population Science at Southern Illinois University School of Medicine, commented:“Patients with hypertension across the CKM spectrum face a considerable burden of morbidity and mortality. The risk of cardiovascular death increases markedly with CKM progression, nearly tripling from earlier stages to stage 4. Since endothelin is implicated in blood pressure regulation, kidney function, adiposity and other CKM-related processes, we wanted to understand whether blocking this pathway could provide consistent benefits across different stages of CKM. Aprocitentan substantially reduced blood pressure, consistent with the double-digit reduction observed in the overall PRECISION population. Importantly, it also reduced UACR by approximately 50% across both earlier and more advanced CKM stages. Knowing that an increase of UACR is associated with a higher risk of all-cause and cardiovascular-related mortality, these findings highlight the potential importance of targeting the endothelin system in uncontrolled hypertension.” Notes to the editor About Dr Michael A. Weber, MDDr. Weber is Professor of Medicine at the SUNY Downstate College of Medicine in Brooklyn, New York. He received his medical degree from Sydney University in Australia. His career has been focused primarily on hypertension and preventive cardiology. He has published numerous research articles in medical literature and has authored or edited several books. Dr. Weber was the Editor-in-Chief of The Journal of Clinical Hypertension for over 10 years. Dr. Weber was one of the founders of The American Society of Hypertension and has served as its President. He also served as Chair of the ASH Hypertension Specialists Program. He is a Fellow of The American College of Physicians, The American College of Cardiology and The American Heart Association. He has served on the Cardiovascular and Renal Drugs Advisory Board of the Food and Drug Administration. He has also served for ten years as Chairman of the Formulary Committee of a major pharmacy benefits provider serving many of the leading health plans in the United States. His main current research interests are in clinical trials of patients at high risk of cardiovascular events or strokes. He is also participating actively in trials in patients with metabolic disorders such as diabetes and kidney disease. Dr. Weber currently serves on the Steering Committees of several national and international clinical trials. Dr. Weber serves as a consultant to Idorsia. About Dr. John M. Flack, MDDr. Flack, an Alpha Omega Alpha (AOA) graduate of the University of Oklahoma School of Medicine, is the Sergio Rabinovich Endowed Chair of Internal Medicine and the Professor and Chair of the Departments of Medicine and Population Science at Southern Illinois University School of Medicine. He is also Director of the Hypertension Clinic. He is a board-certified Internal Medicine specialist and an internationally renowned hypertension specialist/cardiovascular epidemiologist with widely recognized clinical/research expertise in hypertension in African Americans, resistant/refractory hypertension, device-based therapies for hypertension and racial cardiovascular health disparities. Dr. Flack is the current President of the American Hypertension Specialist Certification Program. He has published over 250 peer-reviewed manuscripts and book chapters and is an Associate Editor for the journal Hypertension. He maintains an active clinical practice in complex hypertension at SIU where he teaches and mentors medical students and residents and undertakes innovative, cutting-edge research. Dr. Flack has received numerous awards including the Distinguished Research Award (1993) from the International Society on Hypertension in Blacks (ISHIB), the Daniel D. Savage Memorial Scientific Award (1998) from the Association of Black Cardiologist (ABC), the F. Dewey Dodrill Award for Excellence (2007) from the American Heart Association (AHA), the Detroit News Michiganian of the Year (2009), and the University of Oklahoma Academic Physician of the Year (2012). Also, he has been repeatedly named to Top Doctor, Best Doctor, and Super Doctor lists. Previously, he served as a voting member of the FDA Cardio-Renal Advisory Board. Dr. Flack was recently conferred the status of Master by the American College of Physicians (ACP); he also previously served as a member of the ACP Board of Regents. Dr. Flack serves as a consultant to Idorsia. About aprocitentanAprocitentan is a once-daily, orally active, dual endothelin receptor antagonist, which inhibits the binding of ET-1 to ETA and ETB receptors. Aprocitentan is approved as TRYVIO® in the US for the treatment of systemic hypertension in combination with other antihypertensive drugs, to lower blood pressure in adult patients who are not adequately controlled on other drugs, and has been commercially available since October 2024. For more information see the Full Prescribing Information including BOXED Warning (PI and Medication Guide). TRYVIO is now included in the American College of Cardiology’s (ACC) and the American Heart Association’s (AHA) new comprehensive clinical practice guidelines for the management of high blood pressure. Aprocitentan is approved as JERAYGO™ for the treatment of resistant hypertension in combination with other antihypertensives in the European Union, the UK, Switzerland, and Canada. About PRECISION9,10 (NCT03541174)PRECISION was a multicenter, blinded, randomized, parallel-group, Phase 3 study, which was performed in Europe, North America, Asia, and Australia. Patients were eligible for randomization if their sitting systolic blood pressure was 140 mm Hg or higher despite taking standardized background therapy consisting of three antihypertensive drugs, including a diuretic. The study consisted of three sequential parts: Part 1 was the 4-week double-blind, randomized, and placebo-controlled part, in which 730 patients were randomized to aprocitentan 12.5 mg (n=243), aprocitentan 25 mg (n=243), or placebo (n=244) in a 1:1:1 ratio; Part 2 was a 32-week single (patient)-blind part, in which all patients received aprocitentan 25 mg (n=704); and Part 3 was a 12-week double-blind, randomized, and placebo-controlled withdrawal part, in which patients were re-randomized to aprocitentan 25 mg (n=307) or placebo (n=307) in a 1:1 ratio. The primary and key secondary endpoints were changes in unattended office systolic blood pressure from baseline to week 4 and from withdrawal baseline to week 40, respectively. Secondary endpoints included 24-h ambulatory blood pressure changes. At baseline, 69.2% of patients were obese or severely obese, 54.1% had diabetes, 22.2% had stage 3-4 chronic kidney disease and 19.6% had congestive heart failure. 63% of randomized patients were receiving at least 4 anti-hypertensive therapies at screening. References World Health Organization. Global report on hypertension 2025: high stakes: turning evidence into action. Geneva: World Health Organization; 2025.Mavromatis LA, et al. Epidemiology of cardiovascular-kidney-metabolic syndrome. Nat Rev Nephrol. Published online May 7, 2026. doi:10.1038/s41581-026-01078-w.Haddadin F, et al. The prevalence and predictors of resistant hypertension in high-risk overweight and obese patients: A cross-sectional study based on the 2017 ACC/AHA guidelines. J Clin Hypertens (Greenwich). 2019 Oct;21(10):1507-1515. doi: 10.1111/jch.13666. Epub 2019 Aug 26. PMID: 31448866; PMCID: PMC8030605.Chen Y, et al. Prevalence and mortality association of different stages of cardiovascular-kidney-metabolic syndrome. JACC Adv. 2025;4(6 Pt 2):101843. doi:10.1016/j.jacadv.2025.101843.McCormack T, et al. Uncontrolled Hypertension Prevalence, Characteristic Profiles, and Risk of Cardiorenal and Metabolic Outcomes: Insights from the EnligHTN Study. Adv Ther. Published online July 13, 2026. doi:10.1007/s12325-026-03681-6Weil BR, et al. Enhanced endothelin-1 system activity with overweight and obesity. Am J Physiol Heart Circ Physiol. 2011;301(3):H689-H695. doi:10.1152/ajpheart.00206.2011.Parvanova A, et al. Mechanisms and treatment of obesity-related hypertension. Part 2: Treatments. Clin Kidney J. 2025;18(3):sfaf035. doi:10.1093/ckj/sfaf035.Xu J, Wang P, et al. The urine albumin-to-creatinine ratio is associated with advanced cardiovascular-kidney-metabolic syndrome stages and mortality: an analysis of NHANES 1999-2018. J Diabetes Metab Disord. 2026;25(1):63. Published 2026 Feb 17. doi:10.1007/s40200-026-01892-wDanaietash P et al. Identifying and treating resistant hypertension in PRECISION: A randomized long-term clinical trial with aprocitentan. J Clin Hypertension 2022 Jul;24(7):804-813.Schlaich MP, et al. A randomized controlled trial of the dual endothelin antagonist aprocitentan for resistant hypertension. The Lancet, 2022; Dec 3;400(10367):1927-1937. About IdorsiaThe purpose of Idorsia is to discover, develop and commercialize innovative medicines to help more patients. To achieve this, we will develop Idorsia into a leading biopharmaceutical company, with a strong scientific core. Headquartered near Basel, Switzerland – a European biotech hub – Idorsia has a highly experienced team of dedicated professionals, covering all disciplines from bench to bedside; QUVIVIQ™ (daridorexant), a different kind of insomnia treatment with the potential to revolutionize this mounting public health concern; strong partners to maximize the value of our portfolio; a promising in-house development pipeline; and a specialized drug discovery engine focused on small-molecule drugs that can change the treatment paradigm for many patients. Idorsia is listed on the SIX Swiss Exchange (ticker symbol: IDIA). For further information, please contact:Investor & Media RelationsIdorsia Pharmaceuticals Ltd, Hegenheimermattweg 91, CH-4123 Allschwil+41 58 844 10 10investor.relations@idorsia.com – media.relations@idorsia.com – www.idorsia.com The above information contains certain "forward-looking statements", relating to the company's business, which can be identified by the use of forward-looking terminology such as “intend”, "estimates", "believes", "expects", "may", "are expected to", "will", "will continue", "should", "would be", "seeks", "pending" or "anticipates" or similar expressions, or by discussions of strategy, plans or intentions. Such statements include descriptions of the company's investment and research and development programs, business development activities and anticipated expenditures in connection therewith, descriptions of new products expected to be introduced by the company and anticipated customer demand for such products and products in the company's existing portfolio. Such statements reflect the current views of the company with respect to future events and are subject to certain risks, uncertainties and assumptions. Many factors could cause the actual results, performance or achievements of the company to be materially different from any future results, performances or achievements that may be expressed or implied by such forward-looking statements. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those described herein as anticipated, believed, estimated or expected. Idorsia has transferred its rights for aprocitentan, cenerimod and selatogrel to Idorsia Investments SARL to allow the repayment of notes issued in connection with the repurchase offer completed in August 2025. More details on the transfer can be found in the latest Financial Report. Attachment Press Release PDF

临床结果临床3期上市批准AHA会议

2026-10-10

·药化小白

S1P1受体药物研究进展

S1P1受体药物研究进展：从非选择性到高选择性，从海外到国产突围靶点机制 · 已上市药物 · 国内外管线 · 临床数据 · 最新文献一、靶点概述：S1P受体家族如何调控免疫鞘氨醇-1-磷酸（Sphingosine-1-phosphate, S1P）是一种由鞘氨醇激酶生成的溶血磷脂类信号分子，通过结合五个G蛋白偶联受体亚型 S1PR1–S1PR5（又称 Edg-1/5/3/6/8）发挥生物学作用1,2。其中 S1PR1 是调控 T、B 淋巴细胞向外周迁移的核心受体：体内存在明显的 S1P 浓度梯度——血浆中较高（约 1 µM），淋巴组织间质中较低（约 100 nM）。淋巴细胞借助 S1PR1 感知该梯度，从而迁出淋巴结进入体循环1,2。合成的小分子 S1P1 调节剂（激动剂/功能性拮抗剂）与 S1PR1 结合后，诱导受体内化并被降解，使淋巴细胞"听不见"外周 S1P 梯度，从而滞留于淋巴结、无法进入外周血与炎症组织。这一"药理性的淋巴细胞隔离"正是其抑制中枢神经系统、肠道与皮肤炎症的共同机制1,2。五个亚型功能各异：S1PR1 主导淋巴细胞迁移；S1PR3 与心动过缓、房室（AV）传导阻滞等心血管不良反应相关，是第二代药物重点规避的"脱靶"；S1PR5 主要表达于少突胶质细胞，常与 S1PR1 联用（1/5 选择性）；S1PR2 参与血管与发育调控2,3。因此，提升对 S1PR1 的选择性、尤其是规避 S1PR3，成为该领域药物化学的核心命题。图 1 S1P1 受体调节剂的作用机制。左图：生理状态下 S1P 浓度梯度（淋巴结内低、体液/循环中高）驱动 CCR7+ naive / central memory T、B 淋巴细胞从淋巴结迁出；S1PR1 调节剂诱导 S1PR1 内化/功能拮抗，阻断淋巴细胞沿 S1P 梯度离开淋巴结，从而减轻外周组织（肠、脑、皮肤等）炎症。右图：已上市/在研 S1PR1 调节剂（ozanimod、etrasimod、VTX002 等）对 S1PR1–5 的选择性差异及相应功能。引自 Bencardino, S.; et al. J. Clin. Med. 2023, 12 (15), 5014[33]（MDPI，CC BY 4.0）。二、适应症版图：靶向不同亚型，能治什么以 S1PR1 为核心的调节剂已覆盖多类自身免疫与炎症疾病：多发性硬化（MS，包括复发缓解型 RRMS 与继发进展型 SPMS）、溃疡性结肠炎（UC）、克罗恩病（CD）、银屑病、系统性红斑狼疮（SLE）、以及移植物抗宿主病（GvHD）/造血干细胞移植3,5,6,10,15。但安全性始终是天花板——已知风险包括首剂心动过缓、AV 阻滞、黄斑水肿、肝酶升高、淋巴细胞减少，以及芬戈莫德特有的进行性多灶性脑白质脑病（PML）与感染风险1,2。其中芬戈莫德与珀奈莫德需首剂心电监测与剂量滴定；奥扎莫德与依曲莫德因对 S1P3 活性极弱，通常无需首剂心脏监测，临床便捷性更优3,10,11。正因 S1PR3 关联心脏毒性，第二代药物普遍追求"高 S1P3 选择性"以降低心血管事件2,3,13,14。三、已上市药物：从非选择性到高选择性的演进 S1P 调节剂的上市史是一条"选择性递进"的清晰轨迹：芬戈莫德（非选择性 1/3/4/5）→ 西尼莫德/奥扎莫德（1/5 选择性）→ 珀奈莫德/依曲莫德（1 选择性/高 S1P1 亲和）。下表汇总五款已上市药物的关键信息。表1 已上市 S1P 受体调节剂汇总名称（商品名）靶点选择性开发公司首次上市年中国上市（年）主要适应症优缺点参考文献芬戈莫德Fingolimod（捷灵亚/Gilenya） S1PR1/3/4/5（非选择性） Novartis 2010（美国） 2019-07 RRMS 优：首个口服 MS 疾病修正药（DMT），开创靶点。缺：非选择性→首剂心动过缓、黄斑水肿、肝毒、PML、需首剂心电监测1,2 西尼莫德Siponimod（万立能/Mayzent） S1PR1/5 Novartis 2019（美国） 2020-05 SPMS（及 RRMS）优：首个口服 SPMS 药物；较芬戈莫德 S1P3 选择性提高。缺：首剂心脏监测、黄斑水肿、肝酶升高3,4 奥扎莫德Ozanimod（Zeposia/奥扎莫德） S1PR1/5 BMS/Celgene/Receptos 2020（美国 MS） 2023-02 RRMS、UC 优：口服、无需复杂滴定。缺：UC 疗效"天花板"明显；启动前需 LFT/CBC/眼科；CD 的 III 期 YELLOWSTONE 未达主要终点175,6,7,17 珀奈莫德Ponesimod（Ponvory） S1PR1（高选择性） Janssen/Actelion 2021（美国）未上市（台湾 2022-01、香港 2022-10） RMS 优：已上市中对 S1P3 选择性最高（约 650 倍）、整体 S1P1 选择性突出；停药约 1 周淋巴细胞恢复（可逆快）；首个头对头优于特立氟胺者8。缺：首剂心动过缓/AV 阻滞、黄斑水肿、肝毒；中国大陆不可及8,9 依曲莫德Etrasimod（维适平/VELSIPITY） S1PR1/4/5（高亲和 1/4/5，极少 S1P3，无 S1P2） Pfizer/Arena→云顶新耀（中国权益） 2023（美国） 2026-02 中重度 UC 优：best-in-disease 潜力、深度黏膜愈合、起效快、无激素缓解、无需复杂滴定、安全性佳。缺：S1P4 参与（多属良性）；CD 的 CULTIVATE 因疗效不足中止1810,11,12,18,21 图 2 已获批上市的 5 个 S1P 受体调节剂（结构取自 PubChem 权威记录；奥扎莫德 (1S)、珀奈莫德 (2R)、依曲莫德 (3R) 为单一对映体，已按核查后的绝对构型以实楔/虚楔绘制；芬戈莫德、西尼莫德无手性中心）四、国内外在研管线（按 III / II / I 期）国外企业 III 期进行中：Mocravimod（Priothera / Kyorin，原 KRP203）——口服 S1P1 调节剂，用于急性髓系白血病（AML）异基因造血干细胞移植后 GvHD 预防。全球 III 期 MO-TRANS（NCT05429632）正在入组，预计 2027–2028 年读出，并已获 FDA/EMA 孤儿药认定19。其作用特点是在保留移植物抗白血病（GvL）效应的同时降低 GvHD，是 S1P 机制在血液肿瘤领域的差异化拓展。 III 期受挫（重要警示）：奥扎莫德 CD 的 YELLOWSTONE III 期诱导研究未达临床缓解主要终点，项目已终止17；依曲莫德 CD 的 CULTIVATE II/III 期因亚组疗效不足提前终止18。这提示 S1P 调节剂在 CD 这一适应症上集体遭遇瓶颈。 II 期及以前：Amiselimod（MT-1303，三菱田边→Biogen）——高选择性 S1P1 前药，CD II 期未优于安慰剂（CDAI100 应答 48.7% vs 54.1%）15，MS（MOMENTUM）因策略原因停止；Ceralifimod（ONO-4641，Ono/Merck）——S1P1/5、S1P3-sparing，MS II 期（DreaMS）显示病变减少但未推进 III 期（策略原因）14；CS-0777（Daiichi Sankyo）——选择性 S1P1，MS II 期（已停）13。国内企业（按进展排序） III 期在望 / II 期后期：TT-01688（药捷安康 / TransThera，源自 LG Chem）——高选择性口服 S1P1 调节剂。溃疡性结肠炎 Ib/II 期已完成、即将启动 III 期注册临床；特应性皮炎（AD）处于 II 期。这是目前国产 S1P1 进展最快的品种22。 II 期：HE009（南昌弘益）——选择性 S1P1 调节剂（拮抗剂），用于系统性红斑狼疮（SLE）。II 期（IIa/IIb）于 2025-08 组长单位（北京大学人民医院）启动，多中心推进中23。 II 期：CBP-307 / Icanbelimod（康乃德，苏州）——选择性 S1P1 调节剂，中重度 UC 的 II 期剂量探索研究（CN002，NCT04700449）已完成，并公布诱导期与 48 周维持期阳性数据；公司 2026 年披露将推进下一阶段临床20。 I 期 / IND：艾托莫德 Ethoximod（渐宽生物，苏州，联合中国医学科学院药物研究所）——高选择性 S1PR1 激动剂，用于银屑病。已完成健康受试者 Ia（单次给药）与 Ib（多次给药）PK/PD 研究，显示剂量依赖性降低外周淋巴细胞；2026-08-03 递交银屑病 IND 并获 CDE 受理24。全球在研 S1P1 调节剂结构总览为便于一览全球在研分子，下文给出整合管线表（表 2）与对应结构总览（图 3）。Cenerimod（Idorsia/Viatris）和 Mocravimod（Kyorin/Asahi Kasei）为全球 III 期在研：Cenerimod 用于系统性红斑狼疮（SLE，OPUS-1/2）19,25；Mocravimod 用于急性髓系白血病异基因移植后 GvHD 预防（MO-TRANS）19。TT-01688（药捷安康/LG Chem）是国产最快 S1P1，UC 注册性 II/III 期在望、AD II 期22；CBP-307（康乃德）UC II 期已完成阳性数据20；HE009（南昌弘益）SLE II 期已启动，但结构未公开，详见其专利 WO2021/175225 / CN115210223B31。其余中小型 I/II 期项目（Amiselimod、ONO-4641、ASP4058、CS-0777、Udifitimod、Vibozilimod、SAR247799、GSK2018682、AKP11、艾托莫德等）多处于停滞或已终止状态，反映该靶点临床开发门槛较高15,14,28,13,26,27,29,30,32,24。图 3 全球临床在研 S1P1 受体调节剂结构（11 个有公开结构 + 1 个 HE009 专利占位；GSK2018682、AKP11 等见下表）。立体化学标注说明：奥扎莫德等之外的在研分子中，Cenerimod、ASP4058 各含 1 个手性中心（均为 S 构型），CS-0777 为 (3R)，Udifitimod 含 3 个手性中心，CBP-307 为 cis-(1s,3s)-3-氨基环丁烷-1-甲酸头基（1,3-二取代环丁烷的两个环碳非 CIP 手性中心，只能以 cis/trans 描述，无法给出 R/S）——以上均按 PubChem/ChEMBL 权威记录以楔键绘制；Mocravimod、TT-01688(zectivimod)、Amiselimod、ONO-4641、Vibozilimod、SAR247799、GSK2018682 无手性中心，故不标立体化学符号。表 2 全球临床在研 S1P1 受体调节剂汇总（含结构来源 / 专利）编号代号（通用名）研发公司（国家/地区）最高阶段·适应症结构来源（PubChem CID / 专利）参考文献 1 Cenerimod(ACT-334441) Idorsia / Viatris（瑞士/美） SLE III 期（OPUS-1 NCT05648500；OPUS-2 NCT05672576） PubChem CID 4987197325 2 Mocravimod(KRP-203) Kyorin / Asahi Kasei（日） AML 异基因移植后 GvHD 预防 III 期（MO-TRANS NCT05429632） PubChem CID 1115587419 3 TT-01688(zectivimod) 药捷安康 / LG Chem（中/韩） UC 注册性 II/III 期（2024-12 NMPA 批）；AD II 期（2025-01 完成） PubChem CID 9035630722 4 CBP-307(icanbelimod) 康乃德生物 Connect（中） UC II 期（NCT04700449 完成）；Crohn、AD PubChem CID 139266790（C24H26FN3O3；cis-(1s,3s)-3-氨基环丁烷-1-甲酸头基）20 5 HE009 南昌弘益药业（中） SLE II 期（2025-08 启动）结构未公开：专利 WO2021/175225 / CN115210223B31 6 Amiselimod(MT-1303) Mitsubishi Tanabe（日） CD II 期（未优于安慰剂）；MS / PsO PubChem CID 1612948315 7 Udifitimod(BMS-986166) Bristol-Myers Squibb（美） AD II 期（NCT05014438）；UC I 期（NCT03038711） PubChem CID 11887751626 8 Vibozilimod(SCD-044) Sun Pharma Advanced Research（印） PsO / AD II 期（SOLARES 未达终点，终止） PubChem CID 6657456427 9 ONO-4641(ceralifimod) Ono / Merck KGaA（日/德） MS II 期（2014 终止） PubChem CID 1150299614 10 ASP4058 Astellas（日） I 期（NCT01998646 完成） PubChem CID 1675514328 11 CS-0777 Mitsubishi Tanabe / Daiichi Sankyo（日） MS I 期（NCT00616733） PubChem CID 1137129013 12 SAR247799 Sanofi（法） I 期（已终止；G 蛋白偏向型，不致脱敏/淋巴细胞减少） PubChem CID 5331212729 13 GSK2018682 GSK（英） MS / 健康人 I 期（NCT01387217 等） PubChem CID 2498820130 14 AKP11 Kyorin / Asahi Kasei（日）外用 PsO I/II 期（ANZCTR ACTRN12613001226796 等）结构/代号待公司披露32五、临床数据分析表 3 关键注册临床研究疗效汇总药物研究适应症关键疗效（活性药 vs 安慰剂）备注参考文献奥扎莫德 RADIANCE RRMS 年化复发率（ARR）0.17/0.22 vs 0.28（IFNβ-1a）复发率显著降低5 奥扎莫德 True North UC 临床缓解：诱导 18.4% vs 6.0%；维持 37.0% vs 18.5% NEJM 20216 珀奈莫德 OPTIMUM RMS ARR 0.202 vs 0.290（特立氟胺），相对降低 30.5% 头对头优于活性对照8 依曲莫德 ELEVATE UC 52 UC 临床缓解：12 周 27.0% vs 7.0%；52 周 32.1% vs 6.7% Lancet 202310 依曲莫德 ENLIGHT UC UC（亚洲）维持 40 周临床缓解 48.1% vs 12.5%；黏膜愈合 51.9% vs 8.8% Lancet Gastroenterol Hepatol 202511 奥扎莫德 YELLOWSTONE CD 诱导 12 周临床缓解未达主要终点项目终止17 依曲莫德 CULTIVATE CD 亚组 1 内镜应答低（2 mg 21%、3 mg 10%）因疗效不足提前终止18 Amiselimod CD II 期 CD CDAI100 应答 48.7% vs 54.1% 未优于安慰剂15哪些分子最优？ UC 领域：依曲莫德（Etrasimod）数据最优——ENLIGHT UC 黏膜愈合率达 51.9%、维持期临床缓解 48.1%，且起效快、无需滴定、安全性特征良好，被普遍认为具 best-in-disease 潜力10,11；奥扎莫德 True North 维持缓解约 37%，疗效天花板明显，且 CD 已失败6,17。MS 领域：珀奈莫德在头对头研究（OPTIMUM）中优于特立氟胺，是已上市品种中 S1P1 选择性最高、可逆性最好者；西尼莫德则是首个口服 SPMS 药物3,8。总体趋势是"1 选择性 / 高 S1P3 选择性"，但 CD 已成为 S1P 调节剂集体折戟的适应症。国内进展最快、药效最好的是谁？自研进度：药捷安康 TT-01688 领跑（UC 即将 III 期、AD II 期），南昌弘益 HE009、康乃德 CBP-307 紧随其后20,22,23。若论"中国可及的 S1P1 商业化成功"，云顶新耀引进的依曲莫德（维适平）于 2026-02 在中国获批，是当前国产权益下最成功的 S1P1 相关药物21。六、最新文献（2024–2026）：代表性小分子（年份 / 数据优点 / 参考文献）以下汇总 2024–2026 年发表的高选择性 S1P1（及 S1P1/5）激动剂代表性工作。核心方向有二：① 继续提升对 S1P3 的选择性以根除心动过缓等心血管风险；② 探索偏向性（β-arrestin biased）或计算设计的新机制 / 新骨架。表中标注发表年份；代表性分子结构见图 4（化合物 28 结构暂以原文献为准）。表 4 代表性 S1P1 / S1P1·5 调节剂文献汇总（2024–2026）编号年份分子数据 / 优点参考文献 1 2024 HY-X-1011（R 型）计算设计 S1PR1高选择性激动剂（任若冰/竺立哲等，复旦·港中大深圳）物理驱动自动化路径搜索（PNAS 2024）计算设计的全新骨架；BRET 证实其激活 S1PR1 达纳摩尔级，对 S1PR3/5 选择性约 100 倍（2 个数量级）；S/R 两构型均高选择性激活 S1PR1，为“仅靶向 S1PR1”的超选择性激动剂提供计算方法范式。其 S1PR1–Gi 复合物冷冻电镜结构已解析，配体坐标见 PDB 9VNZ。 Ti R, Pang B, Yu L, et al.; Ren R, Zhu L, Warshel A. Fine-tuning activation specificity of GPCRs via automated path searching. Proc Natl Acad Sci U S A. 2024;121(8):e2317893121. DOI:10.1073/pnas.2317893121. PMID:38346183. 2 2025 Y18（叶天宇/李洪林等，华东理工）反转型 1,2,4-噁二唑骨架（氮杂环丁烷-3-甲酸头、2-氯苄基连接、4-异丁基-3-三氟甲基苯尾，分子式 C24H23ClF3N3O3）；对 S1PR1 EC50 = 0.98 nM，对 S1PR2/3/5 > 10,000 倍选择性、对 S1PR4 109 倍选择性；强效诱导受体内化并阻断回收，从源头规避心血管风险。 Ye T, Zhu L, Li H, et al. Discovery and SAR study of highly selective and potent 1,2,4-oxadiazole-based S1PR1 agonists. Eur J Med Chem. 2025;300:118097. DOI:10.1016/j.ejmech.2025.118097. PMID:40911968. 3 2025 化合物 28（S1P1 agonist 7）（Lee 等，KIST，韩国）首个 β-arrestin 偏向性 S1P1 激动剂；EC50(G-protein)=12.7 nM、EC50(β-arrestin)=3.23 nM，偏向因子 4.51（vs 芬戈莫德）；外周淋巴细胞降至基线 24.4%，iPSC 心肌细胞无心率影响；EAE 模型有效。 Lee CY, Gotina L, Kim J, et al. Discovery of Novel β-Arrestin Biased Sphingosine-1-Phosphate-1 Receptor Agonists for the Treatment of Multiple Sclerosis. J Med Chem. 2025;68(17):18289–18313. DOI:10.1021/acs.jmedchem.5c00859. PMID:40853740. 4 2026 TYY-31（叶天宇/贺欢/李洪林等，华东理工） 3-芳基-5-双芳基-1,2,4-噁二唑；对 S1PR1 EC50 = 1.13 pM（单 digit pM），对 S1PR2/3/5 EC50 > 10 μM、对 S1PR4 > 30,000 倍选择性；DSS 结肠炎 0.3 mg/kg ≈ 奥扎莫德 1 mg/kg；斑马鱼心脏安全性优异。 Ye T, Xiao Y, Tang C, et al. Rational Design, Synthesis, and Biological Evaluation of Potent, Highly Selective 1,2,4-Oxadiazole-Based S1PR1 Agonists for UC Treatment. J Med Chem. 2026;69(9):10660–10684. DOI:10.1021/acs.jmedchem.5c03837. PMID:41996212. 5 2026 化合物 19（S1PR1/S1PR5 agonist-1）（魏欣欣/柳红/王江等，上海药物所）头基为 trans-4-甲基吡咯烷-3-羧酸（图中按原文献所绘对映体，指定为 (3R,4R)；原文仅命名相对构型 trans）；3-(萘-1-基)-1,2,4-噁二唑；S1PR1/5 双重激动，EC50 = 40.0 / 22.9 nM，对 S1PR2/3/4 的 EC50 均 > 10,000 nM（基于 S1PR1 EC50 40.0 nM，计算选择性 > 250 倍；原文摘要报道 > 1000 倍选择性）、无 S1PR3 活性；对小鼠心率影响极小；DSS-IBD 显著缓解。 Wei X, Yuan K, Zhao J, et al. Discovery of Novel Selective Dual Agonists Targeting S1PR1 and S1PR5 for the Treatment of Inflammatory Bowel Disease. J Med Chem. 2026;69(5):5575–5593. DOI:10.1021/acs.jmedchem.5c02690. PMID:41712781. 6 2026 化合物 37（S1PR1/S1PR5 agonist-2）（魏欣欣/柳红/王江等，上海药物所）头基同为 trans-4-甲基吡咯烷-3-羧酸（图中指定为 (3R,4R)）；3-(萘-1-基)-1,2,4-噁二唑；化合物 19 的正丙氧基（n-propoxy）异构体；S1PR1/5 双重激动，EC50 = 33 / 173.8 nM，对 S1PR2/3/4 的 EC50 均 > 10,000 nM；DSS-IBD 与化合物 19 疗效相当、对小鼠心率影响极小。 Wei X, Yuan K, Zhao J, et al. Discovery of Novel Selective Dual Agonists Targeting S1PR1 and S1PR5 for the Treatment of Inflammatory Bowel Disease. J Med Chem. 2026;69(5):5575–5593. DOI:10.1021/acs.jmedchem.5c02690. PMID:41712781. 图 4 代表性 S1P1 调节剂结构（HY-X-1011、Y18、TYY-31、化合物 19、化合物 37）。注：① 化合物 19 与 37 共用同一手性砌块 trans-4-甲基吡咯烷-3-羧酸，原文化合物名仅标注相对构型“trans”，图中按其结构图所绘对映体绘制，RDKit 指定为 (3R,4R)；其对映体 (3S,4S) 亦属 trans，若原文实际使用另一对映体，两者互为镜像，相对构型描述不受影响。② TYY-31 的 cis 相对构型（COOH 与 NH 位于环丁烷平面同侧）已用三维几何验证；1,3-二取代环丁烷的两个环碳并非 CIP 手性中心，故只能以 cis/trans 描述而无 R/S。③ Y18 的头基氮杂环丁烷-3-甲酸无手性中心（C3 的两个环 CH2 等价）。④ HY-X-1011 结构取自其与 S1PR1–Gi 复合物的冷冻电镜结构（PDB 9VNZ，配体 A1ESY，磷酸酯形式 C25H28F4N3O6P），该记录中手性碳标注为 (2S)，而 PNAS 原文称 HY-X-1011 为 R 型（S 型为 HY-X-1010），此处按 PDB 沉积结构绘制。七、总结与未来方向现有结果：已有 5 款 S1P 调节剂上市，选择性沿"非选择性→1/5→1 选择性"递进。UC 是 S1P 调节剂最成功的新战场，其中依曲莫德疗效与安全性综合最佳；MS 领域珀奈莫德、西尼莫德各有定位；而 CD 则是该机制集体受挫的适应症。国产力量正在崛起——自研的 TT-01688、HE009、CBP-307、艾托莫德与商业化引进的依曲莫德（维适平）共同构成中国 S1P1 赛道的多点布局20,21,22,23,24。未来方向：① 继续提升 S1P3 选择性（如 Y18 对 S1P3 >10000 倍），从源头规避心动过缓与 AV 阻滞；② 拓展适应症边界（SLE、AD、GvHD/移植、银屑病）；③ 明确口服小分子相对生物制剂的定位与联用策略；④ 积累真实世界长期安全性数据；⑤ 推进国产替代与本地化生产，提升可及性16,24。S1P1 靶点已从"概念验证"走向"差异化竞争"，高选择性、口服便捷与更广适应症，将是下一阶段的主旋律。参考文献参考文献 [1] Kappos, L.; Radue, E.; O'Connor, P.; Polman, C.; Hohlfeld, R.; Calabresi, P.; Selmaj, K.; Agoropoulou, C.; Leyk, M.; Zhang-Auberson, L.; Burtin, P. A Placebo-Controlled Trial of Oral Fingolimod in Relapsing Multiple Sclerosis. N. Engl. J. Med. 2010, 362 (5), 387-401. DOI: 10.1056/nejmoa0909494 [2] Brinkmann, V.; Billich, A.; Baumruker, T.; Heining, P.; Schmouder, R.; Francis, G.; Aradhye, S.; Burtin, P. Fingolimod (FTY720): Discovery and Development of an Oral Drug To Treat Multiple Sclerosis. Nat. Rev. Drug Discov. 2010, 9 (11), 883-897. DOI: 10.1038/nrd3248 [3] Kappos, L.; Bar-Or, A.; Cree, B. A. C.; Fox, R. J.; Giovannoni, G.; Gold, R.; Vermersch, P.; Arnold, D. L.; Arnould, S.; Scherz, T.; et al. Siponimod versus Placebo in Secondary Progressive Multiple Sclerosis (EXPAND): A Double-Blind, Randomised, Phase 3 Study. Lancet 2018, 391 (10127), 1263-1273. DOI: 10.1016/S0140-6736(18)30475-6 [4] Pan, S.; Gray, N. S.; Gao, W.; Mi, Y.; Fan, Y.; Wang, X.; Tuntland, T.; Che, J.; Lefebvre, S.; Chen, Y.; Chu, A.; Hinterding, K.; Gardin, A.; End, P.; Heining, P.; Bruns, C.; Cooke, N. G.; Nuesslein-Hildesheim, B. 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L.; Clemons, B.; Brooks, J.; Brahmachary, E.; Powell, R.; Dedman, H.; Desale, H. G.; Timony, G. A.; Martinborough, E.; Rosen, H.; Roberts, E.; Boehm, M. F.; Peach, R. J. Ozanimod (RPC1063) Is a Potent Sphingosine-1-Phosphate Receptor-1 (S1P1) and Receptor-5 (S1P5) Agonist with Autoimmune Disease-Modifying Activity. Br. J. Pharmacol. 2016, 173 (11), 1778-1792. DOI: 10.1111/bph.13476 [8] Kappos, L.; Fox, R. J.; Burcklen, M.; Freedman, M. S.; Havrdova, E. K.; Hennessy, B.; Hohlfeld, R.; Lublin, F.; Montalban, X.; Pozzilli, C.; Scherz, T.; D'Ambrosio, D.; Linscheid, P.; Vaclavkova, A.; Pirozek-Lawniczek, M.; Kracker, H.; Sprenger, T. Ponesimod Compared With Teriflunomide in Patients With Relapsing Multiple Sclerosis in the Active-Comparator Phase 3 OPTIMUM Study. JAMA Neurol. 2021, 78 (5), 558-572. DOI: 10.1001/jamaneurol.2021.0405 [9] Bolli, M. H.; Abele, S.; Binkert, C.; Bravo, R.; Buchmann, S.; Bur, D.; Gatfield, J.; Hess, P.; Kohl, C.; Mangold, C.; et al. 2-Imino-thiazolidin-4-one Derivatives as Potent, Orally Active S1P1 Receptor Agonists. J. Med. Chem. 2010, 53 (10), 4198-4211. DOI: 10.1021/jm100181s [10] Sandborn, W. J.; Vermeire, S.; Peyrin-Biroulet, L.; Dubinsky, M. C.; Panes, J.; Yarur, A.; Ritter, T.; Baert, F.; Schreiber, S.; Sloan, S.; Cataldi, F.; Shan, K.; Rabbat, C. J.; Chiorean, M.; Wolf, D. C.; Sands, B. E.; D'Haens, G.; Danese, S.; Goetsch, M.; Feagan, B. G. Etrasimod as Induction and Maintenance Therapy for Ulcerative Colitis (ELEVATE): Two Randomised, Double-Blind, Placebo-Controlled, Phase 3 Studies. Lancet 2023, 401 (10383), 1159-1171. DOI: 10.1016/S0140-6736(23)00061-2 [11] Wu, K.; Zheng, C.; Cao, Q.; Ding, Y.; Gao, X.; Zhong, J.; Chiu, C.; Zhang, H.; Wang, X.; Wang, B.; et al. 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DOI: 10.1021/ml100301k [14] Kurata, H.; Kusumi, K.; Otsuki, K.; Suzuki, R.; Kurono, M.; Komiya, T.; Hagiya, H.; Mizuno, H.; Shioya, H.; Ono, T.; Takada, Y.; Maeda, T.; Matsunaga, N.; Kondo, T.; Tominaga, S.; Nunoya, K.; Kiyoshi, H.; Komeno, M.; Nakade, S.; Habashita, H. Discovery of a 1-Methyl-3,4-dihydronaphthalene-Based Sphingosine-1-Phosphate (S1P) Receptor Agonist Ceralifimod (ONO-4641). A S1P1 and S1P5 Selective Agonist for the Treatment of Autoimmune Diseases. J. Med. Chem. 2017, 60 (23), 9508-9530. DOI: 10.1021/acs.jmedchem.7b00785 [15] D'Haens, G.; Danese, S.; Davies, M.; Watanabe, M.; Hibi, T. A Phase II, Multicentre, Randomised, Double-Blind, Placebo-Controlled Study to Evaluate Safety, Tolerability, and Efficacy of Amiselimod in Patients with Moderate to Severe Active Crohn's Disease. J. Crohns Colitis 2022, 16 (5), 746-756. DOI: 10.1093/ecco-jcc/jjab201 [16] Ye, T.; Yu, J.; Fang, Y.; Xu, Z.; Guo, S.; Zhao, Z.; Li, H.; He, H.; Zhu, L. 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HE009 — 新型高选择性 S1P1 调节剂. 中国专利 CN115210223B (PCT/CN2021/078744, WO2021/175225; 优先权 2020-03 / 2020-05). 结构未公开（见通式(I)与三环类化合物）. PubMed PMID: 41051739 (Phase 1 PK/PD). [32] Kyorin / Asahi Kasei. AKP11 - Topical S1P1 Modulator; Phase 1 (ANZCTR ACTRN12613001226796) and Phase 2 Psoriasis (ACTRN12616000293460). Structure / Compound Code to Be Confirmed by Company Disclosures. [33] Bencardino, S.; D'Amico, F.; Faggiani, I.; Bernardi, F.; Allocca, M.; Furfaro, F.; Parigi, T. L.; Zilli, A.; et al. Efficacy and Safety of S1P1 Receptor Modulator Drugs for Patients with Moderate-to-Severe Ulcerative Colitis. J. Clin. Med. 2023, 12 (15), 5014. DOI: 10.3390/jcm12155014

2026-10-08

·idorsia.com

New results across pediatric, adult and real-world insomnia settings highlight the expanding clinical evidence for daridorexant at Sleep Europe 2026

Phase 2 results with daridorexant in pediatric insomnia disorder will be presented in a late-breaking "Impactful Clinical Trial" session. These are the first and only investigational data of a dual orexin receptor antagonist in children. A growing body of real-world evidence will examine the use of daridorexant in routine clinical practice, including sleep outcomes, daytime functioning, quality of life and work productivity. Further research will examine daridorexant in adults with insomnia and short sleep duration, and the evolving use of insomnia medications across six countries. Investigator-initiated studies will explore daridorexant in menopausal women with insomnia and in patients with insomnia and epilepsy, major depressive disorder or sedative-hypnotic use disorder. Allschwil, Switzerland – October 8, 2026 Idorsia Ltd (SIX: IDIA) continues its commitment to advancing the science of sleep and insomnia at Sleep Europe 2026, a leading European congress for sleep medicine and research, taking place in Maastricht, the Netherlands, from October 20 to 23, 2026. The scientific program features the first clinical study of a dual orexin receptor antagonist in pediatric insomnia disorder, new real-world evidence on daridorexant outcomes in routine practice, and analyses exploring the impact of dual orexin receptor antagonists on the treatment landscape of insomnia. Late-breaking research in pediatric insomnia Pediatric insomnia is associated with impaired sleep, daytime functioning, academic performance and quality of life, particularly in children with neurodevelopmental disorders such as Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD). Pharmacological treatment options for pediatric insomnia are very limited, with no approved medication in the US and only prolonged-release melatonin approved for certain pediatric populations in Europe. The placebo-controlled, Phase 2, two-week dose-finding study evaluated daridorexant 10, 25 and 50 mg in children and adolescents aged 10 to under 18 years with insomnia disorder, including participants with neurodevelopmental disorders such as ASD and ADHD. The study extends the scientific understanding of orexin signaling in insomnia to a younger and clinically complex population, particularly children and adolescents with neurodevelopmental disorders. The detailed results were selected by the European Sleep Research Society (ESRS) for inclusion in the “Impactful Clinical Trial Session II” and will be presented by Professor Carmen M. Schröder. The findings will also be presented in a poster session later that day. Session II of “Impactful Clinical Trial”. Friday, October 23. Auditorium 2. 11:45-12:10 CEST The dual orexin receptor antagonist daridorexant in pediatric insomnia disorder. Carmen Schröder, Akinyemi Ajayi, Oliviero Bruni, Yves Dauvilliers, Ingo Fietze, Katharina Lederer, Judith Owens, Adela Fraile, Fabio Pizza, Martine Clozel, Chiara De Stefani, Michael Meinel, Emanuele Noseda, Cedric Vaillant, Daniel Coury. Poster presentation. Friday, October 23. Poster Area 2, Level 1, F282 A growing body of real-world evidence for daridorexant Two poster presentations will provide complementary perspectives from routine clinical practice, examining outcomes across the 24-hour burden of insomnia, from night-time symptoms to daytime functioning, quality of life and work productivity. Interim findings from the prospective ProDiGyA study in Germany and Austria will be presented on real-world treatment patterns, as well as changes in insomnia severity and depressive symptoms during the first months of daridorexant treatment: ProDiGyA: Interim Analysis of a Real-world, Prospective, Noninterventional Study Evaluating Daridorexant in Patients with Insomnia Disorder. Yaroslav Winter, Jens Kuhn, Göran Hajak, Stefan Ries, Corinna Frohn, Cornelius Bachman, Henry Memczak, Julia Kleylein-Sohn, Michael Saletu, Lucie Bartova. Wednesday, October 21. Poster Area 1, Level 1, W130 Results of a Canadian noninterventional study will be presented on quality of life and work productivity in patients prescribed daridorexant: Effect of Daridorexant on Quality of Life and Work Productivity in Patients with Insomnia in a Canadian Real-World Setting. Wilfred Alonso, Julie Patenaude, Ariane Légaré, Marc Véronneau, Björn Steiniger-Brach, Jean Lachaine, Joseph Michaels. Wednesday, October 21. Poster Area 3, Level 0, W501 Further insights from the adult pivotal program A new analysis of a pivotal adult Phase 3 study will examine the efficacy and safety of daridorexant in individuals with insomnia and objectively measured short sleep duration. Efficacy and Safety of Daridorexant in individuals with Insomnia with Short Sleep Duration. Julio Fernandez-Mendoza, Paul Saskin, Orestis Briasoulis, Joana Marques-Barros, Fjola Sigurdardottir, Yves Dauvilliers. Wednesday, October 21. Poster Area 3, Level 0, W500 How DORAs are changing the treatment landscape of insomnia A six-country analysis will examine how the introduction of dual orexin receptor antagonists (DORAs) has influenced the use of traditional sedative-hypnotics, and how reimbursement and healthcare system policies have shaped their adoption. Impact of the Introduction of Dual Orexin Receptor Antagonists on the Usage of Prescription Medications for Insomnia. Dieter Kunz, Marco Di Nicola, Pierre-Alexis Geoffroy, Eddy Aelen, Francois Aerts, Björn Steiniger-Brach, Antonio Olivieri, David Taylor. Thursday, October 22. Poster Area 2, Level 1, T403 Investigator-Initiated research on daridorexant At least six investigator-initiated studies of daridorexant will be presented at Sleep Europe 2026, reflecting continued scientific interest beyond the Idorsia-supported program. Together, these studies advance understanding of insomnia management, generate insights relevant to clinical practice, and help expand the scientific knowledge base on sleep and insomnia. Presentations include the following investigator-initiated studies: Daridorexant for Chronic Insomnia in Menopausal Women: A Retrospective Real-World Study. Claudio Liguori Daridorexant in Adult People with Epilepsy and Chronic Insomnia: Preliminary Real-World Findings. Silvia Maio Daridorexant for chronic insomnia in patients with sedative-hypnotic use disorder and major depression: a comparative longitudinal study. Laura Palagini Hyperarousal Modulates Circadian Heart Rate Variations Associated to Daridorexant Treatment: An Explorative, Real-world, Observational Study. Alessandro Colitta Two Birds with One Stone: Efficacy of Daridorexant in Patients with MDD Comorbid with Insomnia. Meiyi Guo Daridorexant for Insomnia Disorder: outcomes across two years of treatment and post discontinuation findings. Laura Palagini Additional investigator-initiated research and case reports involving daridorexant will also be presented. The full list of daridorexant-related presentations as well as their dates, times, and locations, is available online. About Sleep Europe 2026 Sleep Europe 2026, the 28th Congress of the European Sleep Research Society, will take place in Maastricht, the Netherlands, from October 20 to 23, 2026. Held every two years, the congress brings together more than 3000 clinicians, researchers, scientists and other sleep professionals to share and discuss the latest advances in sleep medicine and sleep research. Notes to the editor About daridorexant – a different kind of insomnia treatment Insomnia affects millions worldwide, yet commonly used treatments can lead to next day drowsiness, dependence, and withdrawal symptoms – leaving a clear unmet need for safer, effective alternatives. Discovered by Idorsia, daridorexant works differently from traditional hypnotics. As a dual orexin receptor antagonist, it selectively targets the orexin system, helping to regulate overactive wake signaling without broadly suppressing brain activity. Its optimized pharmacokinetics promote restorative sleep throughout the entire night, reducing morning sleepiness and improving daytime functioning. Clinical trials published in The Lancet Neurology demonstrated that daridorexant significantly improved sleep onset, sleep maintenance, and self-reported total sleep time in adult patients with insomnia at 25mg and 50mg doses compared to placebo. Daridorexant 50 mg also demonstrated a significant improvement in daytime functioning compared to placebo. About Idorsia The purpose of Idorsia is to discover, develop and commercialize innovative medicines to help more patients. To achieve this, we will develop Idorsia into a leading biopharmaceutical company, with a strong scientific core. Headquartered near Basel, Switzerland – a European biotech hub – Idorsia has a highly experienced team of dedicated professionals, covering all disciplines from bench to bedside; QUVIVIQ™ (daridorexant), a different kind of insomnia treatment with the potential to revolutionize this mounting public health concern; strong partners to maximize the value of our portfolio; a promising in-house development pipeline; and a specialized drug discovery engine focused on small-molecule drugs that can change the treatment paradigm for many patients. Idorsia is listed on the SIX Swiss Exchange (ticker symbol: IDIA). For further information, please contact: Investor & Media Relations Idorsia Pharmaceuticals Ltd, Hegenheimermattweg 91, CH-4123 Allschwil +41 58 844 10 10 investor.relations@idorsia.com – media.relations@idorsia.com – www.idorsia.com The above information contains certain "forward-looking statements", relating to the company's business, which can be identified by the use of forward-looking terminology such as “intend”, "estimates", "believes", "expects", "may", "are expected to", "will", "will continue", "should", "would be", "seeks", "pending" or "anticipates" or similar expressions, or by discussions of strategy, plans or intentions. Such statements include descriptions of the company's investment and research and development programs, business development activities and anticipated expenditures in connection therewith, descriptions of new products expected to be introduced by the company and anticipated customer demand for such products and products in the company's existing portfolio. Such statements reflect the current views of the company with respect to future events and are subject to certain risks, uncertainties and assumptions. Many factors could cause the actual results, performance or achievements of the company to be materially different from any future results, performances or achievements that may be expressed or implied by such forward-looking statements. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those described herein as anticipated, believed, estimated or expected. Idorsia has transferred its rights for aprocitentan, cenerimod and selatogrel to Idorsia Investments SARL to allow the repayment of notes issued in connection with the repurchase offer completed in August 2025. More details on the transfer can be found in the current Financial Report. Attachment Press Release PDF

临床2期临床3期

100 项与 Cenerimod 相关的药物交易

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KEGG	Wiki	ATC	Drug Bank
D11283	-	-	DB12705

研发状态

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适应症	最高研发状态	国家/地区	公司	日期
狼疮性肾炎	临床3期	中国	Corden Pharma GmbH	2026-01-16
狼疮性肾炎	临床3期	中国	爱多希（北京）医药有限公司	2026-01-16
狼疮性肾炎	临床3期	中国	Viatris, Inc.	2026-01-16
系统性红斑狼疮	临床3期	日本	Viatris, Inc.	2022-12-13
系统性红斑狼疮	临床3期	阿根廷	Viatris, Inc.	2022-12-13
系统性红斑狼疮	临床3期	巴西	Viatris, Inc.	2022-12-13
系统性红斑狼疮	临床3期	保加利亚	Viatris, Inc.	2022-12-13
系统性红斑狼疮	临床3期	哥伦比亚	Viatris, Inc.	2022-12-13
系统性红斑狼疮	临床3期	法国	Viatris, Inc.	2022-12-13
系统性红斑狼疮	临床3期	希腊	Viatris, Inc.	2022-12-13

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT03742037 (CARE, ACR2025)	临床2期	系统性红斑狼疮	427	Cenerimod 4 mg	構顧範夢築遞繭膚糧艱(網壓醖夢廠觸繭淵壓醖) = 艱範築製顧憲衊觸獵鑰窪顧餘壓積簾糧願膚糧 (壓遞鹽簾糧鏇遞築觸憲 ) 更多	积极	2025-10-24
				Placebo	構顧範夢築遞繭膚糧艱(網壓醖夢廠觸繭淵壓醖) = 築齋獵鑰憲鹹餘繭糧遞窪顧餘壓積簾糧願膚糧 (壓遞鹽簾糧鏇遞築觸憲 ) 更多
NCT03742037 (CARE, EULAR2025)	临床2期	系统性红斑狼疮	427	Cenerimod 0.5 mg	鬱簾簾憲糧餘鬱構築窪(鹹窪壓淵繭製鹹淵醖築) = 築窪範膚夢鹹獵積壓淵壓願網鑰顧築鏇憲膚襯 (壓艱製鏇鹽艱齋蓋繭膚 )	积极	2025-06-11
				Placebo	鬱簾簾憲糧餘鬱構築窪(鹹窪壓淵繭製鹹淵醖築) = 憲觸築遞顧鑰壓觸衊餘壓願網鑰顧築鏇憲膚襯 (壓艱製鏇鹽艱齋蓋繭膚 )
NCT03742037 (CARE, EULAR2023)	临床2期	IFN-1 gene expression signature \| anti-dsDNA antibody levels	427	Cenerimod 4 mg	製遞糧淵襯範蓋鹽鏇鹽(繭膚製壓艱衊憲網餘觸) = 夢構鏇鹽選積夢範膚艱壓網衊鬱獵餘製醖夢網 (壓鹽醖願蓋築淵襯襯淵 ) 更多	积极	2023-05-31
				Placebo	製遞糧淵襯範蓋鹽鏇鹽(繭膚製壓艱衊憲網餘觸) = 鬱窪簾鹽範襯夢積憲範壓網衊鬱獵餘製醖夢網 (壓鹽醖願蓋築淵襯襯淵 ) 更多
NCT03742037 (ACR2022) 人工标引	临床2期	系统性红斑狼疮	427	Cenerimod	壓膚遞願製獵蓋夢鑰簾(壓膚壓繭醖淵繭艱壓淵) = AEs were similar across treatment groups. The % of reported hypertension AEs was higher in the cenerimod 1 and 4 mg groups vs PBO 獵鏇簾夢襯選遞願衊糧 (夢鏇選窪選膚蓋鹽餘網 )	-	2022-09-12
NCT02472795 (CTgov)	临床1/2期	系统性红斑狼疮	105	Cenerimod (Cenerimod 0.5 mg (Part A))	夢鏇夢顧鏇窪構顧範夢(構繭鬱蓋憲齋憲糧選鬱) = 願繭壓夢鏇廠願範衊餘窪糧製獵蓋築憲顧窪醖 (鑰淵觸獵餘壓遞築選顧, 0.48) 更多	-	2020-02-26
				Cenerimod (Cenerimod 1 mg (Part A))	夢鏇夢顧鏇窪構顧範夢(構繭鬱蓋憲齋憲糧選鬱) = 鏇積願積構簾鑰膚壓築窪糧製獵蓋築憲顧窪醖 (鑰淵觸獵餘壓遞築選顧, 0.68) 更多
NCT02472795 (Pubmed \| Lupus Sci Med)	临床1/2期	系统性红斑狼疮	105	Cenerimod 0.5 mg	壓範壓鏇顧鏇簾選觸醖(餘獵顧鏇淵鏇鏇蓋膚齋) = 鑰願膚齋鑰窪夢醖繭齋廠觸蓋蓋鹽製餘糧遞獵 (鹹簾夢齋築壓築簾鬱選 )	积极	2019-01-01
				Cenerimod 1 mg	壓範壓鏇顧鏇簾選觸醖(餘獵顧鏇淵鏇鏇蓋膚齋) = 鏇衊觸餘憲鏇廠蓋窪艱廠觸蓋蓋鹽製餘糧遞獵 (鹹簾夢齋築壓築簾鬱選 )