更新于：2024-11-15
Clemastine Fumarate
富马酸氯马斯汀
更新于：2024-11-15
概要
基本信息
最高研发阶段批准上市 |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构
分子式C25H30ClNO5 |
InChIKeyPMGQWSIVQFOFOQ-YKVZVUFRSA-N |
CAS号14976-57-9 |
关联
21
项与 富马酸氯马斯汀 相关的临床试验Clemastine for Improving White Matter and Boosting Antidepressant Response in Late-life Depression
A Randomized, Double-Blind, Delayed Treatment, Placebo-Controlled Trial to Assess the Changes in Multi-parametric MRI in Patients With Acute Demyelinating Lesions Taking Clemastine Fumarate as a Myelin Repair Therapy
Clemastine Treatment in Individuals With Williams Syndrome- a Double-blind Placebo Control to Assess the Safety and Efficacy
100 项与 富马酸氯马斯汀 相关的临床结果
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100 项与 富马酸氯马斯汀 相关的转化医学
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100 项与 富马酸氯马斯汀 相关的专利（医药）
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478
项与 富马酸氯马斯汀 相关的文献（医药）2025-01-01BRAIN RESEARCH
Clemastine enhances exercise-induced motor improvement in hypoxic ischemic rats
Article
作者: Kunori, Nobuo ; Komaki, Yuji ; Goto, Taichi ; Tsurugizawa, Tomokazu ; Iwaki, Sunao ; Takashima, Ichiro
Neonatal hypoxic ischemia (HI) occurs owing to reduced cerebral oxygen levels and perfusion during the perinatal period. Brain injury after HI triggers neurological manifestations such as motor impairment, and the improvement of impaired brain function remains challenging. Recent studies suggest that cortical myelination plays a role in motor learning, but its involvement in motor improvement after HI injury is not well understood. This study aimed to investigate the impact of myelination on motor improvement following neonatal HI injury. We employed a modified Rice-Vannucci model; the right common carotid artery of postnatal day 7 (P7) Wistar rats was isolated and divided, and the rats were then exposed to hypoxic condition (90 min, 8 % O2). A total of 101 rats (66 males) were divided into four groups: trained-HI (n = 38), trained-Sham (n = 16), untrained-HI (n = 31), and untrained-Sham (n = 16). The trained groups underwent rotarod-based exercise training from P22 to P41 (3 days per week). Structural analysis using magnetic resonance imaging and immunohistochemistry (n = 6 per group) revealed increased fractional anisotropy and myelin density in the primary somatosensory cortex of the trained-HI group. We further evaluated the effect of myelination promotion on rotarod performance by administering clemastine, a myelination-promoting drug, via daily intraperitoneal injections. Clemastine did not enhance motor improvement in untrained-HI rats. However, clemastine-administered trained-HI rats (n = 7) exhibited significantly improved motor performance compared to both saline-administered trained-HI rats (n = 11) and clemastine-administered untrained-HI rats (n = 7). These findings suggest that myelination may be a key mechanism in motor improvement after HI injury and that combining exercise training with clemastine administration could be an effective therapeutic strategy for motor improvement following HI injury.
2024-12-31Molecular & Cellular Oncology
Clemastine and hyperthermia enhance sensitization of osteosarcoma cells for apoptosis
Article
作者: Kumar, Deepak ; Hoang, Hieu ; He, Yiping ; Vandana ; Niture, Suryakant ; Gadi, Sashi ; Obu, Somtochukwu
Clemastine is an antagonist of histamine H1 receptor may provide benefits in the treatment of osteosarcoma (OS). In the current study, we used hyperthermia approach to sensitize OS cells to clemastine-mediated cell death. Osteosarcoma U-2 OS and Saos-2 cells were treated with clemastine at 37°C, followed by 42°C for 2 h, and released at 37°C for 6 h. The impact of clemastine and hyperthermia on OS cell survival and autophagy-mediated cell death was investigated. Exposure of U-2 OS and Saos-2 cells to clemastine and hyperthermia (42°C) inhibited dose-dependent clemastine-mediated cell survival by increasing cell apoptosis. Hyperthermia and clemastine exposure modulated inflammatory and unfolded protein response (UPR) signaling differentially in U-2 OS and Saos-2 cells. Exposure of U-2 OS and Saos-2 cells to hyperthermia and clemastine inhibited AKT/mTOR and induced expression of the autophagy biomarkers LC3B II and LC3-positive puncta formation. The inhibition of autophagy by 3-methyladenine blocked hyperthermia and clemastine-mediated induction of LC3B II, LC3-positive puncta formation, and OS cell apoptosis. These results indicate that clemastine and hyperthermia sensitize OS cell lines by inducing increased autophagic cell death. Collectively, our data suggest that hyperthermia along with antihistamine therapy may provide an improved approach for the treatment of OS.
2024-10-18ANNALS OF NEUROLOGY
Clemastine Induces Oligodendrocyte Progenitor Pool Exhaustion and Senescence in the Context of Chronic Demyelination in a Rabbit Model.
Article
作者: Ravichandar, Roopa ; Buck, Gregory T ; Raymond, Faye D ; Sim, Fraser J ; Frost, Jon R ; Gadelkarim, Farah ; Cooper, James J M ; Muthaiah, Rupadevi
OBJECTIVES:
Clemastine has emerged as a promising therapy for the restoration of neurologic function in patients with multiple sclerosis (MS). However, clemastine and other agents with prodifferentiative effects on oligodendrocyte progenitor cells (OPCs) in rodent models have underperformed in clinical trials. We hypothesized that the preclinical studies showed more robust effects because of the abundance of OPCs in rodent models. To better examine the therapeutic potential of clemastine, we examined its effect on demyelinated white matter lesions in rabbits, which exhibit progenitor densities and limited remyelination more closely matching those found in tissues from patients with MS.
METHODS:
We used lysolecithin to induce demyelination in white matter of New Zealand rabbits and then administered oral clemastine (10mg/kg/day) for various periods before assessing the OPC and oligodendrocyte (OL) populations in these lesions.
RESULTS:
Daily administration of clemastine for the full study period (56 days) increased oligodendrogenesis in white matter lesions. However, shorter durations of treatment failed to increase overall OL density despite enhancing OPC-to-OL differentiation. This effect was due to exhaustion of the OPC pool, as the differentiating progenitors were not replaced because of reduced OPC proliferation. Notably, delayed administration of clemastine led to an accumulation of activated OPCs expressing markers of senescence.
INTERPRETATION:
Although capable of driving OL differentiation, clemastine treatment in rabbits hampered progenitor pool replenishment, induced senescence, and promoted conversion of microglia/macrophages to a proinflammatory phenotype. Whether these effects would also occur in humans or with other prodifferentiative therapies should be studied further, but our data suggest the need to carefully consider progenitor dynamics in the treatment of MS. ANN NEUROL 2024.
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研发状态
批准上市
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 变应性结膜炎 | 美国 | 1977-02-25 | |
| 普通感冒 | 日本 | 1970-01-17 | |
| 湿疹 | 日本 | 1970-01-17 | |
| 瘙痒 | 日本 | 1970-01-17 | |
| 过敏性鼻炎 | 日本 | 1970-01-17 | |
| 荨麻疹 | 日本 | 1970-01-17 |
未上市
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 季节性过敏性鼻炎 | 临床2期 | 美国 | - |
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临床结果
临床结果
适应症
分期
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N/A | - | - | 鹹築鬱蓋膚鹹夢積獵蓋(餘蓋範獵觸糧觸製簾齋) = 醖選範顧繭壓蓋憲網獵 鹹襯鹹鏇糧襯窪鬱網醖 (鬱廠艱製製鏇窪廠齋鏇, -3.4 ~ 1.1) | 积极 | 2024-06-07 | ||
鹹築鬱蓋膚鹹夢積獵蓋(餘蓋範獵觸糧觸製簾齋) = 膚鹹顧蓋願遞遞網顧憲 鹹襯鹹鏇糧襯窪鬱網醖 (鬱廠艱製製鏇窪廠齋鏇, -3.4 ~ 1.1) | |||||||
N/A | 9 | 鏇窪繭艱鬱顧繭製選窪(網顧範壓簾鹹鹽獵艱構) = 簾餘艱鏇獵廠願憲遞蓋 鏇醖積範壓艱觸淵蓋觸 (鹽顧網襯願網遞廠簾衊 ) | 不佳 | 2024-02-29 | |||
临床2期 | 50 | (Clemastine) | 範鏇廠膚夢顧廠憲獵夢(築淵糧鑰積餘製鬱遞壓) = 製鹽餘範製淵膚餘廠壓 網廠繭鏇觸遞遞膚膚築 (艱夢鑰繭蓋獵壓憲窪糧, 齋簾願鑰簾鑰選積構鹹 ~ 構製襯糧壓醖製顧襯鬱) 更多 | - | 2021-07-15 | ||
Placebo+clemastine (Placebo) | 範鏇廠膚夢顧廠憲獵夢(築淵糧鑰積餘製鬱遞壓) = 廠餘範齋選範願願廠觸 網廠繭鏇觸遞遞膚膚築 (艱夢鑰繭蓋獵壓憲窪糧, 憲夢鹹齋築衊齋網鬱蓋 ~ 簾鹹鬱餘構壓選淵選範) 更多 |
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