预约演示
更新于：2025-11-27
Ketotifen Fumarate
富马酸酮替芬
更新于：2025-11-27
概要
基本信息
权益机构- |
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/序列
分子式C23H23NO5S |
InChIKeyYNQQEYBLVYAWNX-WLHGVMLRSA-N |
CAS号34580-14-8 |
关联
39
项与 富马酸酮替芬 相关的临床试验ChiCTR2400083511
Study on the efficacy and safety of integrated Chinese and Western medicine in the treatment of patients with long coronavirus sequelae: a prospective clinical study
ChiCTR2400084609
Mechanism and clinical research of mast cell activation promoting the progression of Alzheimer's disease
ACTRN12623001119684
Effect and time course of topical ketotifen 0.025% and prednisolone sodium phosphate 0.5% on ocular serface immune cells density, morphology, dynamic behaviour ,and topographical distribution in participants with allergic conjunctivitis
100 项与 富马酸酮替芬 相关的临床结果
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100 项与 富马酸酮替芬 相关的转化医学
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100 项与 富马酸酮替芬 相关的专利（医药）
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1,992
项与 富马酸酮替芬 相关的文献（医药）2026-01-01BRAIN BEHAVIOR AND IMMUNITY
Targeting lysosomal acidification to restore microglial homeostasis and mitigate memory decline during male brain ageing
Article
作者: Vázquez-Román, Victoria ; Flores-Cordero, Juan Antonio ; Ramírez-Ponce, María Pilar ; Barrella, Lorenzo ; Millán-Huang, Marta San ; Alés, Eva ; Maldonado, María Dolores
Lysosomal dysfunction lies at the nexus of inflammaging, microglial dystrophy and synaptic fragility, making it an attractive target for brain rejuvenation. Here we demonstrate that a five-month oral course of ketotifen, an approved H1-antihistamine and mast-cell stabiliser, re-acidifies lysosomes in aged C57BL/6J male mice, restoring the quinacrine signal of peripheral macrophages and SIM-A9 microglia. This proton rebound is coupled to broad anti-cytokine effects: ketotifen attenuates lipopolysaccharide-evoked release of TNF-α, IL-1β and IL-10 in vitro and ex vivo. In the brain, the drug restores a highly ramified, homeostatic microglial morphology throughout the cortex and hippocampus. Ketotifen robustly elevates cortical synaptophysin and PSD-95 above age-matched levels. Behaviourally, ketotifen enhances spatial learning and object-location memory without altering locomotor activity or anxiety-like behaviour. Collectively, these findings identify lysosomal re-acidification as the initiating trigger of a multifaceted rejuvenation cascade that dampens multi-cytokine signalling, restores microglial morphology and preserves synaptic integrity. Because ketotifen is inexpensive, brain-permeable and already licensed for human use, our work unveils an immediately actionable geroprotective strategy to forestall early cognitive decline.
2025-12-31JOURNAL OF ENZYME INHIBITION AND MEDICINAL CHEMISTRY
Hidden targets in dermatology:
In vitro
and
In silico
inhibitory effects of common 23 dermatologic drugs on human carbonic anhydrase isoenzymes I and II
Article
作者: Uslu, Harun ; Çıkrıkcı, Kübra ; Can, İlkay ; Gençer, Nahit
In this study, we have aimed to determine the in vitro and in silico effects of 23 frequently used dermatologic drugs on human carbonic anhydrase I (hCA I) and II (hCA II). The inhibitory effects of the drugs on hCA I and hCA II were determined by esterase methods. The most potent inhibitors were isotretinoin for hCA I (Ki= 5.75 µM) and valaciclovir for hCA II (Ki= 5.74 µM). Ketotifen (Ki= 6.98 µM), pantoprazole (Ki= 7.16 µM) and acyclovir (Ki= 7.31 µM) were also potent inhibitors for hCA I. Isotretinoin (Ki= 6.54 µM), brivudine (Ki= 7.44 µM) and fluconazole (Ki= 7.91 µM) were also potent inhibitors for hCA II. Terbinafine hydrochloride was a weak CA inhibitor for both of these isoenzymes (Ki= 20.58 µM for hCA I and 20.32 µM for hCA I). Therefore, the drug, having a weak CA inhibitory activity, may be preferred primarily in patients with a skin disease compared to the other drugs due to important physiological functions of CAs. Molecular docking studies have shown that acitretin and isotretinoin, in particular, will inhibit hCA I at lower concentrations and have higher docking scores. For hCA II, it was shown that Isotretinoin and Ketotifen would inhibit at lower concentrations and have higher placement scores.
2025-12-01IBRO Neuroscience Reports
Synergistic effects of PAR2 and TrkA exacerbate visceral hypersensitivity induced by chronic pancreatitis in rats
Article
作者: Lu, Zhijie ; Zhu, Jiao ; Liu, Zhiyun ; Wei, Kai ; Chen, Qianbo ; Qiu, Haibo ; Tao, Kunming ; Wu, Xiaodan
Background:
Abdominal pain is the most severe symptom of chronic pancreatitis. However, till date, there are only a few studies on the mechanism of pain in chronic pancreatitis. Previous research has reported that mast cells are enriched around nerve fibers and are associated with visceral pain. In this study, we aimed to investigate the molecular mechanisms by which protease-activated receptor 2 (PAR2) and tropomyosin receptor kinase A (TrkA) exacerbate pain in chronic pancreatitis.
Methods:
A chronic pancreatitis animal model was established by injecting dibutyltin dichloride into the tail vein of Wistar rats. The von Frey test was performed to evaluate pain behavior in the rats. Hematoxylin and eosin staining, western blotting, immunofluorescence histochemistry, retrograde labeling, culture of dorsal root ganglion (DRG) neurons, and whole-cell patch clamp recordings were performed to illustrate the mechanisms.
Results:
The pancreatic structures were destroyed, including inflammatory cell infiltration and acinar atrophy, and mast cells were dramatically recruited to the pancreatic tissue in chronic pancreatitis. Systemic administration of the mast cell stabilizer ketotifen alleviated chronic pancreatitis-induced visceral hypersensitivity in the Wistar rat model. In contrast, the mast cell secretagogue compound 48/80 dose-dependently exacerbated chronic pancreatitis pain. Furthermore, the number of DRG neurons projected into the pancreas was significantly increased by injecting Dil stain in chronic pancreatitis rat models and normal rats. The co-expression of PAR2 and TrkA was only observed in small-diameter DRG neurons containing transient receptor potential vanilloid 1 channel and was significantly higher than those in normal rats. Finally, we demonstrated the functional interaction between PAR2 and TrkA by whole-cell patch clamp recordings.
Conclusions:
Mast cells contribute to chronic pancreatitis pain through enrichment and degranulation. The interaction of PAR2 and TrkA exacerbates chronic pancreatitis pain, which may be a potential strategy for the treatment of chronic pancreatitis -induced visceral pain.
66
项与 富马酸酮替芬 相关的新闻（医药）2025-11-19
AHA会议
2025-11-12
AHA会议
100 项与 富马酸酮替芬 相关的药物交易
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研发状态
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 |
|---|---|---|---|
| 季节性过敏性结膜炎 | 西班牙 | 2000-10-31 | |
| 季节性过敏性结膜炎 | 瑞典 | 2000-10-31 | |
| 皮炎 | 日本 | 1986-04-30 | |
| 湿疹 | 日本 | 1986-04-30 | |
| 瘙痒 | 日本 | 1986-04-30 | |
| 荨麻疹 | 日本 | 1986-04-30 | |
| 哮喘 | 瑞士 | 1979-05-03 | |
| 慢性荨麻疹 | 瑞士 | 1979-05-03 | |
| 变应性结膜炎 | 瑞士 | 1979-05-03 | |
| 特应性皮炎 | 瑞士 | 1979-05-03 | |
| 过敏性鼻炎 | 瑞士 | 1979-05-03 |
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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3期 | 229 | Brimonidine Tartrate 0.025%/ Ketotifen Fumarate 0.035% Ophthalmic Solution (Brimonidine Tartrate 0.025%/ Ketotifen Fumarate 0.035% Ophthalmic Solution) | 窪襯蓋衊遞糧齋淵鬱夢(願膚顧齋襯齋衊願鹹襯) = 鏇鹹觸襯淵醖鏇蓋獵淵 網憲願積鹽憲積範壓膚 (襯網選繭鹽壓範糧餘網, 0.6031) 更多 | - | 2025-07-01 | ||
(Ketotifen Fumarate Ophthalmic Solution 0.035%) | 窪襯蓋衊遞糧齋淵鬱夢(願膚顧齋襯齋衊願鹹襯) = 築積鏇繭糧蓋網鹽簾壓 網憲願積鹽憲積範壓膚 (襯網選繭鹽壓範糧餘網, 0.3136) 更多 | ||||||
临床3期 | 188 | (Combination) | 鹹製鏇鬱遞鏇醖夢壓獵(鑰夢願鹹窪選鏇觸壓醖) = 衊齋憲憲蓋窪鑰艱壓網 選廠壓鹹糧築構選艱觸 (憲觸獵壓觸築淵衊糧夢, 0.1464) 更多 | - | 2025-02-14 | ||
(Ketotifen Fumarate) | 鹹製鏇鬱遞鏇醖夢壓獵(鑰夢願鹹窪選鏇觸壓醖) = 齋衊窪網積膚遞鹹構鹽 選廠壓鹹糧築構選艱觸 (憲觸獵壓觸築淵衊糧夢, 0.1487) 更多 | ||||||
临床3期 | 11 | Ketotifen 1 mg twice daily | 憲積餘願齋廠廠糧鏇糧(齋網夢艱製醖壓製構鑰) = Ketotifen was not superior to placebo with regard to global clinical response. Only 18% of patients demonstrated a complete or near-complete clinical response. 餘製醖艱簾鑰積繭蓋鬱 (構鏇構鹽鹹築鏇繭餘積 ) | 不佳 | 2024-07-01 | ||
临床3期 | 51 | (Ketotifen) | 鬱糧簾簾夢鑰糧網築鬱(遞夢構鏇網齋遞壓簾艱) = 積齋遞鏇窪鹽膚範齋夢 壓窪遞鬱構憲艱壓積壓 (範鹹鬱鏇餘鑰襯鏇艱餘, 1.92) 更多 | - | 2016-11-17 | ||
placebo (Placebo) | 鬱糧簾簾夢鑰糧網築鬱(遞夢構鏇網齋遞壓簾艱) = 鹽選範構餘積願壓鏇醖 壓窪遞鬱構憲艱壓積壓 (範鹹鬱鏇餘鑰襯鏇艱餘, 1.93) 更多 |
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