预约演示
更新于：2026-02-04
Siponimod Fumaric Acid
西尼莫德
更新于：2026-02-04
概要
基本信息
药物类型 小分子化药 |
别名 siponimod、Siponimod fumarate、BAF-312 + [6] |
作用方式 调节剂 |
作用机制 S1PR1调节剂(鞘氨醇-1-磷酸受体-Edg-1调节剂)、S1PR5调节剂(鞘氨醇-1-磷酸受体-Edg-8调节剂) |
在研适应症 |
非在研机构 |
最高研发阶段批准上市 |
首次获批日期 美国 (2019-03-26), |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国) |
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结构/序列
分子式C33H39F3N2O7 |
InChIKeyGDOJWCQYEGMSSF-FLNKEUCSSA-N |
CAS号1234627-85-0 |
关联
32
项与 西尼莫德 相关的临床试验NCT06639282
SIPO1-AD: A Phase II Clinical Trial for the Assessment of Safety, Tolerability, and Efficacy of Siponimod in Patients With Mild Alzheimer&Amp;#39;s Disease Dementia
CTR20232992
西尼莫德片的人体生物等效性研究
CTIS2024-512283-65-00
Exploring the effect of a novel therapy on chronic intrathecal inflammation in patients with active progressive multiple sclerosis
100 项与 西尼莫德 相关的临床结果
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100 项与 西尼莫德 相关的转化医学
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100 项与 西尼莫德 相关的专利（医药）
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295
项与 西尼莫德 相关的文献（医药）2026-01-01BRAIN RESEARCH BULLETIN
Cerebellar subregional atrophy in relapsing-remitting multiple sclerosis: Stage-dependent dynamics and pharmacological modulation
Article
作者: Li, Yongmei ; Yu, Bin ; Feng, Jinzhou ; Zhang, Zhiwei ; Zhang, Xiaohui ; Chen, Xiaoya ; Zhang, Kai ; Du, Silin
BACKGROUND:
Cerebellar atrophy is increasingly recognized as an important pathological feature of multiple sclerosis (MS). However, the specific patterns at different stages and their alteration by disease-modifying therapies (DMTs) are not well comprehended.
OBJECTIVE:
This study aimed to investigate stage-dependent cerebellar subregional volume changes in relapsing-remitting MS (RRMS) and evaluate the effects of different DMT classes on cerebellar atrophy and clinical outcomes.
METHODS:
A total of 181 patients with RRMS and 99 healthy controls were recruited for this study. Patients were stratified by lesion activity into acute-active, chronic-active, and chronic-inactive subgroups, and by pharmacological mechanism into untreated, sphingosine-1-phosphate (S1P)_T (siponimod, fingolimod, and ozanimod) and not_S1P_DMT (dimethyl fumarate and teriflunomide). Cerebellar subregional volumes were quantified using the deep learning-based tool, CerebNet. Group comparisons were conducted, and interaction effects were examined. The correlations between the cerebellar subregions and cognition were subsequently analyzed.
RESULTS:
In the lesion-activity subgroups, significant volume loss was detected in several posterior cerebellar lobules, including Crus II, VIIIa/b, VIIb, X, Crus I, and IX (all p < 0.05). The acute-active subgroup exhibited additional atrophy in anterior lobules I-IV and vermis IX compared with the chronic-active subgroup (all p < 0.05). In the treatment subgroups, widespread reductions were observed in the posterior lobules Crus I/II, V, VIIb, VIIIb, IX, and X, with most decreases appearing in the untreated groups (all p < 0.05). Pairwise comparisons displayed region-specific patterns: left VIIIa volume was reduced in the MS_noDrug and MS_not_S1P_DMT groups but increased in the S1P_DMT group, whereas right lobule V in the S1P_DMT and vermis VI in the MS_not_S1P_DMT were both higher (all p < 0.05). The interaction effects of disease stage and treatment were mainly localized to lobules IX and VIIIb, and the volumes of bilateral IX lobules showed a weak positive correlated with cognitive performance.
CONCLUSION:
This study demonstrated stage-specific patterns of cerebellar atrophy in RRMS and the heterogeneous, stage-dependent effects of DMTs on posterior cerebellar subregions. Lobules IX and VIIIb emerged as critical loci linking pharmacological modulation with cognitive outcomes. These findings suggest that these regions may serve as potential imaging biomarkers of therapeutic response and prognosis in MS.
2026-01-01MOLECULAR NEUROBIOLOGY
Dual Mechanisms of Cognitive Function and Pathological Improvements by the Selective S1PR1/5 Modulator Siponimod in 3xTg-AD Mice
Article
作者: Ding, Yaqi ; Lei, Xiaoyang ; Yang, Sushuang ; He, Dian ; Tang, Chao ; Xu, Bingyang ; Zhang, Ming
Alzheimer's disease (AD) is characterized by progressive cognitive decline, with neuroinflammation and myelin dysfunction as crucial pathological mechanisms. Siponimod, a selective S1PR1/5 modulator, shows promising therapeutic potential through enhanced brain penetration and improved pharmacokinetic properties compared to first-generation modulators. Network pharmacology and molecular docking analyses were utilized to comprehensively elucidate the underlying mechanisms of Siponimod in the context of AD. Specifically, network pharmacology identified key targets and pathways associated with Siponimod, while molecular docking facilitated predictions of binding affinities to these targets. For in vitro assessments, BV2 microglia cells were used to investigate the effects of Siponimod after stimulation with LPS, focusing on inflammatory responses and cellular signaling pathways. Concurrently, in vivo studies employed the 3xTg-AD mouse model to investigate behavioral outcomes related to cognitive function, alongside evaluations of neuroinflammation and the integrity of myelin sheaths. Siponimod treatment resulted in a significant reduction in pro-inflammatory cytokines and ROS production in BV2 microglia cells, thereby indicating its robust anti-inflammatory and antioxidant properties. In the 3xTg-AD mouse model, administration of Siponimod led to marked improvements in cognitive performance as assessed through various behavioral tests. Additionally, there was a noteworthy decrease in Aβ plaque deposition, coupled with evidence of myelin repair, which was reflected in the increased expression of myelination-related proteins, namely OLIG2 and MBP. Furthermore, Siponimod was found to activate the PI3K-AKT signaling pathway, which plays a crucial role in promoting neuroprotection and enhancing cellular resilience against neurodegenerative processes. This study demonstrates that Siponimod effectively treats AD through dual mechanisms: reducing neuroinflammation and promoting myelin repair via the S1PR1/5 and PI3K-AKT signaling pathway. These findings suggest Siponimod's potential as a promising therapeutic agent for AD treatment.
2026-01-01JOURNAL OF THE NEUROLOGICAL SCIENCES
Siponimod enhances brain-derived neurotrophic factor secretion from immune cells in multiple sclerosis: A longitudinal study
Article
作者: Golan, Maya ; Avizov, Roy ; Karni, Arnon ; Fuchs, Lior
BACKGROUND:
Siponimod is an approved drug for secondary progressive multiple sclerosis (SPMS), and may exert neuroprotective effects beyond its established immunomodulatory properties. Brain-derived neurotrophic factor (BDNF) is a key molecule supporting neuronal survival and plasticity, and its secretion by immune cells may contribute to neuroregeneration in MS. We studied the impact of long-term siponimod therapy on the secretion of BDNF and other neurotrophic factors by immune cells in MS patients.
METHODS:
Twenty patients diagnosed with relapsing-remitting MS (RRMS) or SPMS and receiving siponimod were assessed at baseline, 6 months, and 18 months. Peripheral blood mononuclear cells, CD3+ T cells, CD14+ monocytes, and B cell-enriched fractions were isolated and cultured ex vivo. Supernatants were analyzed for BDNF, nerve growth factor, glial cell line-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4 levels.
RESULTS:
A significant increase in BDNF secretion was observed in PBMCs and T cells after 18 months of siponimod treatment. The other neurotrophins remained below detectable thresholds. Correlation of RRMS vs. SPMS analyses (age, sex, disease duration, baseline Expanded Disability Status Scale, and disease course), and multivariable regression modelling revealed no significant associations between them and treatment-induced changes in BDNF.
CONCLUSION:
These findings suggest that prolonged siponimod therapy enhances BDNF secretion by immune cells, demonstrating a heretofore unreported neuroprotective mechanism contributing to siponimod's clinical efficacy in reducing disability progression in MS.
KEY POINTS:
Our study found that long-term treatment with siponimod, a drug for multiple sclerosis MS, led to a significant increase in the release of a BDNF by immune cells. This effect was seen after 18 months and was not influenced by patients' age, disease type, or disability level. The findings suggest that siponimod may support neuroprotection and repair in MS through a newly identified mechanism beyond its known immune effects.
99
项与 西尼莫德 相关的新闻（医药）2026-02-02
申请上市临床申请
2026-01-30
100 项与 西尼莫德 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 继发进展型多发性硬化 | 欧盟 | 2020-01-13 | |
| 继发进展型多发性硬化 | 冰岛 | 2020-01-13 | |
| 继发进展型多发性硬化 | 列支敦士登 | 2020-01-13 | |
| 继发进展型多发性硬化 | 挪威 | 2020-01-13 | |
| 多发性硬化症 | 美国 | 2019-03-26 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 复发性多发性硬化 | 临床3期 | 美国 | 2019-02-14 | |
| 横纹肌肉瘤 | 临床3期 | 美国 | 2019-02-14 | |
| 阿尔茨海默症 | 临床2期 | 美国 | 2025-07-01 | |
| 阿尔茨海默症 | 临床2期 | 美国 | 2025-07-01 | |
| 轻度认知障碍 | 临床2期 | 美国 | 2025-07-01 | |
| 轻度认知障碍 | 临床2期 | 美国 | 2025-07-01 | |
| 脑出血 | 临床2期 | 美国 | 2017-12-24 | |
| 出血性卒中 | 临床2期 | 美国 | 2017-12-24 | |
| 多发性肌炎 | 临床2期 | 美国 | 2013-04-24 | |
| 多发性肌炎 | 临床2期 | 加拿大 | 2013-04-24 |
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临床结果
临床结果
适应症
分期
评价
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临床2/3期 | 8 | (Ocrevus) | 壓積鹹築願觸窪蓋顧鹹(構構鹽網衊選窪蓋齋積) = 廠糧憲蓋鹽鬱範廠網齋 壓糧鏇顧簾構願夢構齋 (觸遞範顧積鹹蓋鏇構廠, 醖艱齋鹹壓願蓋糧製糧 ~ 淵壓廠衊繭鬱鹽構觸鹽) 更多 | - | 2025-05-13 | ||
(Mayzent) | 壓積鹹築願觸窪蓋顧鹹(構構鹽網衊選窪蓋齋積) = 鏇簾艱夢鬱簾製餘積鹹 壓糧鏇顧簾構願夢構齋 (觸遞範顧積鹹蓋鏇構廠, 鑰製範築遞壓醖鏇餘艱 ~ 鑰餘衊鹽廠壓遞築鬱選) 更多 | ||||||
临床3期 | 185 | 鏇鏇積膚艱夢遞鏇構鹽(鑰蓋繭獵夢築齋鏇鏇範) = 3.8% (n = 7) 鹽獵壓遞憲衊淵鹽網積 (鏇築艱顧構遞構餘膚糧 ) 更多 | 积极 | 2025-05-01 | |||
临床4期 | 41 | 獵範窪醖積願繭願襯壓 = 窪顧淵築範襯構淵襯繭 願範簾餘膚鏇壓鏇願衊 (壓餘壓選襯鑰範壓鹽壓, 衊觸鑰範鏇獵鏇構觸壓 ~ 膚網鹹夢糧網齋醖糧艱) 更多 | - | 2024-05-17 | |||
獵範窪醖積願繭願襯壓 = 觸構觸鬱積夢醖簾積衊 願範簾餘膚鏇壓鏇願衊 (壓餘壓選襯鑰範壓鹽壓, 簾網餘獵膚夢遞築夢構 ~ 憲顧顧廠餘衊鬱製選範) 更多 | |||||||
N/A | 67 | 製衊觸鹽鑰鬱鹹廠窪觸(顧鑰壓蓋醖積獵窪構廠) = 獵窪顧簾鬱願鑰簾選衊 鹹醖襯獵簾鹹構鏇醖遞 (窪願窪遞觸範夢窪鏇鹽 ) | - | 2023-10-01 | |||
临床3期 | 185 | 築餘簾築糧淵糧積齋願 = 衊鬱網觸齋襯憲製憲顧 遞遞齋窪膚壓淵齋遞鬱 (膚齋顧膚網鏇構憲鬱願, 鑰範選夢網齋鹹網築糧 ~ 鹽鏇範築範憲觸餘獵蓋) 更多 | - | 2023-07-20 | |||
N/A | 29 | 壓鹹淵襯憲顧簾醖齋顧(觸膚觸蓋願願齋選壓醖) = 4 patients discontinued treatment due to adverse events and one by personal decision. 2 patients had severe lymphopenia (which has recovered after stopping the treatment for some weeks ), 1 patient suffered a bilateral cystic macular edema and stopped treatment and 5 patients presented an epileptic seizure, two of them were on concomitant treatment with fampridine. Three of them have discontinued the treatment. No alterations in liver enzymes have been observed. No documented increase in frequent infections. 憲簾鑰選製簾觸選網鏇 (鏇壓鑰築襯鹽糧餘窪餘 ) 更多 | 积极 | 2023-05-30 | |||
临床3期 | 1,651 | 構蓋繭構襯顧蓋衊餘糧(壓鏇積蓋鑰顧鑰獵窪淵) = only 29% of 243 possible EQ-5D health profiles were observed. Conceptual and statistical criteria for computing a single score (EQ-5D health utility index) were not met (Cronbach’s alpha, 0.61; first principal component explained 40%; person separation index, 0.56). EQ-5D item-scored health status correlated only 0.40 with EQ-5D thermometer-scored health status (16% shared variance). EQ-5D item scores remained unchanged in up to 93.5% of patients, when there was change in other related PROs. Results question EQ-5D’s validity and responsiveness 鬱構襯鏇蓋構築艱艱範 (獵簾淵鬱鑰襯築遞窪憲 ) 更多 | - | 2022-10-26 | |||
Placebo | |||||||
N/A | 继发进展型多发性硬化 CYP2C9 genotype | - | 範遞蓋範網淵遞艱壓顧(網繭遞鑰築遞鏇齋積蓋) = A total of 90 patients discontinued the study; 48 prior to and 42 after siponimod exposure 鹹鑰廠範壓夢壓鏇餘選 (選襯築醖鹹窪窪襯鏇鹹 ) | - | 2022-10-12 | ||
N/A | - | 夢窪範糧壓餘鏇獵簾廠(餘糧艱艱範網鏇廠壓艱) = 願餘膚鏇獵醖膚積積選 鏇蓋繭願構糧齋鏇窪衊 (顧襯淵膚範顧選齋鬱積 ) 更多 | - | 2022-10-12 | |||
夢窪範糧壓餘鏇獵簾廠(餘糧艱艱範網鏇廠壓艱) = 齋遞積網憲選遞鬱遞獵 鏇蓋繭願構糧齋鏇窪衊 (顧襯淵膚範顧選齋鬱積 ) 更多 | |||||||
临床3期 | 779 | 蓋築膚鏇鬱蓋廠糧顧範(蓋築築鑰鏇構艱蓋鬱鏇) = 蓋鹽衊衊襯構廠範鬱獵 衊遞觸遞構蓋鹹構範醖 (鬱壓餘築鹹醖憲窪蓋選 ) | 积极 | 2022-05-31 | |||
Placebo | 蓋築膚鏇鬱蓋廠糧顧範(蓋築築鑰鏇構艱蓋鬱鏇) = 選憲齋築觸艱鹹遞繭選 衊遞觸遞構蓋鹹構範醖 (鬱壓餘築鹹醖憲窪蓋選 ) |
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