更新于：2024-11-04
Fudosteine
福多司坦
更新于：2024-11-04
概要
基本信息
非在研机构- |
最高研发阶段批准上市 |
首次获批日期 日本 (2001-10-02), |
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C6H13NO3S |
InChIKeyKINWYTAUPKOPCQ-YFKPBYRVSA-N |
CAS号13189-98-5 |
关联
10
项与 福多司坦 相关的临床试验福多司坦片人体生物等效性试验
福多司坦片在健康受试者中的随机、开放、单剂量、两制剂、两周期、自身交叉空腹及餐后生物等效性试验
Clinical study of fudosteine in patients with stable COPD of neutrophil type
100 项与 福多司坦 相关的临床结果
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100 项与 福多司坦 相关的转化医学
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100 项与 福多司坦 相关的专利（医药）
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32
项与 福多司坦 相关的文献（医药）2024-01-01Neuroendocrinology
MiR-320a Acts as a Tumor Suppressor in Somatotroph Pituitary Neuroendocrine Tumors by Targeting BCAT1
Article
作者: Zhang, Yazhuo ; Gao, Hua ; Zhao, Sida ; Li, Bin
Introduction: Aberrant miR-320a has been reported to be involved in the tumorigenesis of several cancers. In our previous study, we identified the low expression of circulating miR-320a in patients with somatotroph pituitary neuroendocrine tumor (PitNET); however, the role of miR-320a in somatotroph PitNET proliferation is still unclear. Methods: Cell viability and colony formation assays were used to detect the effect of miR-320a and BCAT1 on GH3 cells. TargetScan was used to identify the target genes of miR-320a. Dual-luciferase reporter gene assay was used to explore the relation between miR-320a and BCAT1. Transcriptome and proteome analyses were performed between somatotroph PitNETs and healthy controls. The expression level of miR-320a in somatotroph PitNETs were detected by RT-qPCR and Western blot. Results: miR-320a mimics inhibit cell proliferation, while miR-320a inhibitors promote cell proliferation in GH3 cells. An overlap analysis using a Venn diagram revealed that BCAT1 is the only target gene of miR-320a overexpressed in somatotroph PitNETs compared to healthy controls, as revealed by both microarray and proteomics results. A dual-luciferase reporter gene assay showed that miR-320a may bind to the BCAT1-3′UTR. The transfection of miR-320a mimics downregulated the expression and miR-320a inhibitors and upregulated the expression of BCAT1 in GH3 cells. The interference of BCAT1 expression in GH3 cells downregulated cell proliferation and growth. Pan-cancer analyses demonstrated that high BCAT1 expression often indicates a poor prognosis. Conclusion: Our findings illustrate that miR-320a may function as a tumor suppressor and BCAT1 may promote tumor progression. miR-320a may inhibit the growth of somatotroph PitNETs by targeting BCAT1.
2023-01-01Clinical pharmacology in drug development
Pharmacokinetics and Bioequivalence of Fudosteine in Healthy Chinese Volunteers Under Fasting and Fed Conditions: A 4‐Way Replicate Crossover Study
Article
作者: Wan, Lei ; Tang, Chengyong ; Zhu, Mingxue ; Tao, Yi ; Zhang, Peilin ; Zhao, Hongtao ; Pu, Junliang
Abstract:
The bioequivalence of a generic fudosteine tablet vs a brand‐named fudosteine tablet under fasting and fed conditions was evaluated in this study. This randomized, open‐label, single‐dose, 4‐way replicate, crossover, bioequivalence study included 64 healthy Chinese subjects (fasting cohort, n = 32; fed cohort, n = 32) who were assigned to receive a single 200‐mg dose of generic or brand‐named fudosteine. Blood samples were collected before dosing and up to 24 hours after dosing. The plasma concentrations of fudosteine were analyzed by high‐performance liquid chromatography–tandem mass spectrometry. Safety was monitored. There were no significant differences in maximum plasma concentration (Cmax), area under the plasma concentration–time curve (AUC) from time 0 to time t (AUC0‐t), or AUC from time 0 to infinity (AUC0‐∞) between the test and reference formulations. However, food showed a significant effect on Cmax, AUC0‐t, and AUC0‐∞ for both generic and brand‐named fudosteine. The 90%CIs of the test/reference ratios of Cmax, AUC0‐t, and AUC0‐∞ were within the range of 80% to 125% under both fasting and fed conditions. No serious adverse events were reported. The bioequivalence between generic and brand‐named fudosteine under fasting and fed conditions was demonstrated. Both of them had good tolerance for healthy Chinese volunteers. In addition, food delayed the absorption of fudosteine, so taking this medicine before meals might be an optimized option.
2022-07-01European journal of pharmacology
Fudosteine attenuates acute lung injury in septic mice by inhibiting pyroptosis via the TXNIP/NLRP3/GSDMD pathway
Article
作者: Yang, Deqing ; Chen, Jun ; Wang, Hao ; Wang, Tao ; Wen, Fuqiang ; Liu, Lian ; Li, Xiaoou ; Xu, Dan ; Chen, Keling ; He, Guangming ; Li, Wenhao ; Hu, Jun
There is a dearth of effective pharmacotherapies for sepsis-induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS) to which oxidative stress and excessive inflammation are major contributors. We hypothesized that fudosteine, a cysteine derivative, may protect against sepsis-induced ALI/ARDS given its anti-oxidant capacity. This study aimed to investigate the effects and mechanisms of fudosteine in a mouse model of sepsis-induced ALI. Sepsis was induced by cecal ligation and puncture (CLP). The intragastrical administration of fudosteine (25 mg/kg, 50 mg/kg, and 100 mg/kg) dose-dependently decreased proinflammatory cytokine levels in bronchoalveolar lavage fluid (BALF) and serum and reduced BALF/serum albumin and lung wet/dry weight ratios in septic mice. The lung injury score was significantly lowered by fudosteine [e.g., 0.18 ± 0.03 (100 mg/kg) vs. 0.42 ± 0.03 (CLP), P < 0.0001]. Fudosteine also reduced the biomarkers of lung epithelial injury in BALF and markedly improved oxidative stress indicators in lung tissues [e.g., malondialdehyde: 337.70 ± 23.78 (100 mg/kg) vs. 686.40 ± 28.36 (CLP) nmol/mg protein, P < 0.0001]. Lung tissue transcriptomics analyses revealed suppressed inflammatory responses and oxidative stress with fudosteine and the involvement of the inflammasome and pyroptosis pathways. Western blot analyses indicated that fudosteine inhibited the sepsis-induced activation of gasdermin D (GSDMD) and caspase-1 and the upregulation of thioredoxin-interacting protein (TXNIP), nucleotide-binding domain, leucine-rich repeat-containing receptor, pyrin domain-containing-3 (NLRP3), and apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC). Fudosteine therefore protects against sepsis-induced ALI in mice, and the inhibition of pyroptosis via the TXNIP/NLRP3/GSDMD pathway may be an underlying mechanism.
100 项与 福多司坦 相关的药物交易
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研发状态
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 呼吸系统疾病 | 中国 | 2005-11-15 | |
| 痰咳 | 日本 | 2001-10-02 |
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