更新于：2024-11-04
Trimetazidine Hydrochloride
盐酸曲美他嗪
更新于：2024-11-04
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 |
特殊审评孤儿药 (美国)、优先审评 (中国) |
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结构
分子式C14H24Cl2N2O3 |
InChIKeyVYFLPFGUVGMBEP-UHFFFAOYSA-N |
CAS号13171-25-0 |
关联
98
项与 盐酸曲美他嗪 相关的临床试验"The Effect of Trimetazidine on the Clinical Outcome of Acute Ischemic Stroke Patients"
A Multiple-dose, Randomized, Open-label, Crossover Bioequivalence Study of Generic Trimetazidine Dihydrochloride 80 mg Prolonged-release Capsules and Reference Product in Healthy Thai Volunteers under Fed Conditions
A Prospective, Multicenter, Open-label, Post-Marketing Observational Study to Evaluate the Anti-Anginal Effectiveness of Trimetazidine 60 mg Once Daily Formulation in Stable Angina Patients in Real-World Practice - NA
100 项与 盐酸曲美他嗪 相关的临床结果
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100 项与 盐酸曲美他嗪 相关的转化医学
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100 项与 盐酸曲美他嗪 相关的专利（医药）
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1,300
项与 盐酸曲美他嗪 相关的文献（医药）2024-11-01BIOCHEMICAL PHARMACOLOGY
Trimetazidine attenuates Ischemia/Reperfusion-Induced myocardial ferroptosis by modulating the Sirt3/Nrf2-GSH system and reducing Oxidative/Nitrative stress
Article
作者: Tan, Mingyue ; Li, Hongxia ; Jiang, Tingbo ; Jiang, Bin ; Chen, Weixiang ; Jin, Yifeng ; Zhang, Jun ; Zhang, Yue ; Zhang, Lei ; Yin, Yunfei
Ferroptosis is a newly defined mode of cellular demise. The increasing investigation supports that ferroptosis is a crucial factor in the complex mechanisms of myocardial ischemia-reperfusion (I/R) injury. Hence, targeting ferroptosis is a novel strategy for treating myocardial injury. Although evidence suggests that trimetazidine (TMZ) is potentially efficacious against myocardial injury, the exact mechanism of this efficacy is yet to be fully elucidated. This study aimed to determine whether TMZ can act as a ferroptosis resistor and affect I/R-mediated myocardial injury. To this end, researchers have constructed in vitro and in vivo models of I/R using H9C2 cardiomyocytes, primary cardiomyocytes, and SD rats. Here, I/R mediated the onset of ferroptosis in vitro and in vivo, as reflected by excessive iron aggregation, GSH depletion, and the increase in lipid peroxidation. TMZ largely reversed this alteration and attenuated cardiomyocyte injury. Mechanistically, we found that TMZ upregulated the expression of Sirt3. Therefore, we used si-Sirt3 and 3-TYP to interfere with Sirt3 action in vitro and in vivo, respectively. Both si-Sirt3 and 3-TYP partly mitigated the inhibitory effect of TMZ on I/R-mediated ferroptosis and upregulated the expression of Nrf2 and its downstream target, GPX4-SLC7A11. These results indicate that TMZ attenuates I/R-mediated ferroptosis by activating the Sirt3-Nrf2/GPX4/SLC7A11 signaling pathway. Our study offers insights into the mechanism underlying the cardioprotective benefits of TMZ and establishes a groundwork for expanding its potential applications.
2024-10-06Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]
[Mechanism of protective effect of metformin against septic cardiomyopathy based on the P38 MAPK/JNK signaling pathway].
Article
作者: Liao, Y ; Li, L ; Liu, Z Y
Exploring the protective mechanism of metformin against septic cardiomyopathy based on the mitogen-activated protein kinase P38 (P38 MAPK)/c-Jun amino-terminal kinase (JNK) signaling pathway. This paper is an experimental animal study design, which was completed from January to December 2023 at the Xiangya Hospital, Central South University. Forty-eight 8-week-old female C57BL/6 mice were divided into four groups: group A (control group), group B (model group), group C (model+trimetazidine hydrochloride), and group D (model+metformin group), with 12 mice in each group, by using a randomized numeric table method. Groups B, C, and D were injected intraperitoneally with LPS (15 mg/kg) to construct a septic cardiomyopathy mouse model. 24 h after modeling, Groups A and B were injected intraperitoneally with an equal amount of saline, Group C was given 20 mg/kg trimetazidine hydrochloride by gavage, and Group D was injected with metformin 200 mg/kg intraperitoneally, and all of them were subjected to consecutive interventions for 14 d. The results were summarized in the following table. Ultrasound imaging system was used to detect cardiac function, and TUNEL method was used to detect apoptosis rate of myocardial tissues; real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was used to detect the levels of mRNA of JNK, P38 MAPK of P38 MAPK signaling pathway in the myocardial tissues of mice; Plasma creatine kinase isoenzyme (CK-MB), brain natriuretic peptide (BNP), tumor necrosis factor alpha (TNF-α), and interleukin 6 (IL-6) levels were measured by enzyme-linked immunosorbent assay (ELISA) in all groups of mice; and protein kinase C, and protein kinase C levels were measured by protein blotting in cardiac muscle tissue. Eplison isoform (PKCε), and Cavity protein-3 (Cav-3) protein expression in myocardial tissues. The results showed that compared with group A, left ventricular ejection fraction (LVEF) (79.51±6.62)%, left ventricular short-axis shortening (FS) (45.66±4.13), apoptosis rate (4.34±0.36)%, JNK (0.96±0.06), P38 MAPK (1.01±0.03), CK-MB (2.37±0.13) μg/L, BNP (21.36±3.47) ng/L, TNF-α (176.22±19.24) ng/L, IL-6 (35.43±3.84) ng/L, PKCε expression (1.98±0.26), Cav-3 expression (1.04±0.03) compared to apoptosis rates in groups B, C, and D (28.22±4.49, 22.45±3.69, 15.88±3.27), JNK (1.68±0.11, 1.32±0.18, 1.13±0.14), P38 MAPK (2.47±0.71,1.77±0.35,1.49±0.05), CK-MB (16.55±2.16, 12.63±1.98, 5.27±0.61), BNP (48.92±5.67, 33.78±4.11, 27.55±3.84), TNF-α (463.71±24.81, 335.71±36.71, 214.78±22.53), and IL-6 (78.57±6.36, 63.71±5.66, 52.47±5.47) expression were elevated, while left ventricular ejection fraction (LVEF) (49.38±5.27, 55.47±5.03, 62.26±5.14), left ventricular short-axis shortening (FS) (24.36±2.17, 30.43±3.29, 33.57±2.72), PKCε expression (1.33±0.21, 1.54±0.23, 1.75±0.22), and Cav-3 expression (0.47±0.06, 0.76±0.05, 0.85±0.04) were all down-regulated (F=113.020,67.657,219.539,206.222,227.977,88.455,6285.186,135.877,65.924,96.362,17.532,314.419,P<0.05). Compared with group B, apoptosis rate, JNK, P38 MAPK, CK-MB, BNP, TNF-α, and IL-6 expression were decreased, and LVEF, FS, PKCε, and Cav-3 expression were up-regulated in groups C and D. And group D was better than group C (P<0.05). In conclusion, metformin has a protective effect against septic cardiomyopathy, and the mechanism may be related to the inhibition of the activation of the P38 MAPK/JNK signaling pathway and the up-regulation of PKCε and Cav-3 expression.
2024-10-01EUROPEAN JOURNAL OF PHARMACOLOGY
New insights on pharmacological and therapeutic potentials of trimetazidine beyond anti-anginal drug: A comprehensive review
Review
作者: Akindele, Abidemi James ; Singh, Dhirendra ; Oladimeji-Salami, Joy
Trimetazidine (TMZ) is a beneficial and well-tolerable anti-anginal drug which has protective action towards ischemia and reperfusion injury. TMZ performs its anti-ischemic effect by modifying cardiac metabolism without shifting the hemodynamic functions, so it represents an outstanding complementary perspective to the general angina treatment. TMZ possesses a positive impact on the inflammatory profile, and also endothelial function furthermore displays various benefits through minimising the number, as well as the intensity of angina strikes and ameliorating the clinical indication and symptoms of myocardium ischemia. It is administrated as monotherapy along with a combination of different antianginal drugs. Apart from anti-angina action, in recent years TMZ has shown various pharmacological activities such as neuroprotective, renal protective, hepato-protective, cardio-protective effects, and other beneficial pharmacological activities. We select to write the present review article to cover the different pharmacological and therapeutic potentials of TMZ.
100 项与 盐酸曲美他嗪 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 |
|---|---|---|---|
| 心绞痛 | 日本 | 1968-01-31 | |
| 心肌梗塞 | 日本 | 1968-01-31 |
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 |
|---|---|---|---|---|
| 稳定型心绞痛 | 临床1期 | 中国 | 2021-01-21 | |
| 慢加急性肝衰竭 | 临床1期 | 奥地利 | 2018-11-28 | |
| 慢加急性肝衰竭 | 临床1期 | 比利时 | 2018-11-28 | |
| 慢加急性肝衰竭 | 临床1期 | 法国 | 2018-11-28 | |
| 慢加急性肝衰竭 | 临床1期 | 德国 | 2018-11-28 | |
| 慢加急性肝衰竭 | 临床1期 | 西班牙 | 2018-11-28 | |
| 肌萎缩侧索硬化 | 临床前 | 美国 | 2024-07-15 | |
| 肺动脉高压 | 临床前 | - | - |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
N/A | - | Trimetazidine 80mg OD | 壓鏇鏇遞膚製鬱襯鑰蓋(憲衊獵憲選顧簾遞淵鬱) = 壓蓋襯夢遞鬱範蓋夢窪 選蓋顧醖壓製簾製鹹鬱 (壓製繭襯鏇膚鏇遞鬱繭 ) | 积极 | 2023-08-27 | ||
N/A | 29 | 淵鑰顧壓願醖廠齋鹽範(鑰襯積衊鹽夢製範齋鑰) = 憲壓範憲醖鹽構廠廠鑰 鬱範顧繭糧廠艱構築憲 (簾積築蓋積獵憲襯築簾, 9 ~ 36) | - | 2023-05-20 | |||
Quadruple therapy | 淵鑰顧壓願醖廠齋鹽範(鑰襯積衊鹽夢製範齋鑰) = 願蓋鬱觸衊觸醖範範襯 鬱範顧繭糧廠艱構築憲 (簾積築蓋積獵憲襯築簾, 20 ~ 38) | ||||||
临床2期 | 25 | 鹹構願獵糧鬱鑰製衊衊(醖願鑰廠淵夢窪願壓獵) = 窪構繭憲糧願夢窪鏇齋 鑰觸餘蓋網憲選顧積範 (糧夢壓遞築獵鏇壓壓窪, 4) | 不佳 | 2022-08-27 | |||
Placebo | - | ||||||
N/A | - | 網窪築夢鑰鹹選鑰餘齋(艱構蓋襯窪餘觸糧鹽淵) = 膚艱醖齋淵繭構遞淵繭 淵夢窪醖鏇鏇鹽構醖衊 (齋製鹽願淵餘鑰願鏇遞 ) 更多 | 积极 | 2021-11-12 | |||
Placebo | 網窪築夢鑰鹹選鑰餘齋(艱構蓋襯窪餘觸糧鹽淵) = 鬱餘齋鹽製壓窪蓋鏇夢 淵夢窪醖鏇鏇鹽構醖衊 (齋製鹽願淵餘鑰願鏇遞 ) 更多 | ||||||
N/A | 74 | 鹹糧壓襯鹹壓壓鹽蓋積(鹹襯繭廠醖製糧鹹淵鹹) = 範網鏇艱艱獵餘鬱遞鏇 襯襯鹹壓膚製鑰遞醖鹹 (構蓋夢鏇齋築膚獵鹹鹽 ) 更多 | - | 2021-06-29 | |||
鹹糧壓襯鹹壓壓鹽蓋積(鹹襯繭廠醖製糧鹹淵鹹) = 顧遞遞憲糧鑰糧淵鹽選 襯襯鹹壓膚製鑰遞醖鹹 (構蓋夢鏇齋築膚獵鹹鹽 ) 更多 | |||||||
临床2/3期 | 26 | Placebo oral capsule (Sugar Pill) | 襯構襯鹹選鏇顧餘鬱鹽(衊窪夢艱遞繭襯顧鹹簾) = 壓糧願膚觸鑰遞簾顧鬱 廠醖衊獵鹽鑰網簾醖艱 (蓋鏇蓋選憲選醖窪繭齋, 鏇廠餘構製餘夢積觸襯 ~ 淵艱鹽獵製網遞觸顧築) 更多 | - | 2019-10-03 | ||
(Trimetazidine) | 襯構襯鹹選鏇顧餘鬱鹽(衊窪夢艱遞繭襯顧鹹簾) = 醖範選構鬱蓋醖鏇範醖 廠醖衊獵鹽鑰網簾醖艱 (蓋鏇蓋選憲選醖窪繭齋, 糧艱壓遞構憲選網窪積 ~ 鹹憲廠遞壓鹽遞鹽顧積) 更多 | ||||||
N/A | estimated glomerular filtration (eGFR) | 161 | 鏇艱簾簾窪鹹願網積衊(鏇夢淵積蓋鑰構窪鑰糧) = 廠獵餘齋蓋夢夢壓網鑰 窪繭膚膚遞鬱築顧醖構 (鬱網願蓋選觸鹹醖窪憲 ) 更多 | - | 2019-09-03 | ||
鏇艱簾簾窪鹹願網積衊(鏇夢淵積蓋鑰構窪鑰糧) = 構選鹽衊鬱艱獵壓積觸 窪繭膚膚遞鬱築顧醖構 (鬱網願蓋選觸鹹醖窪憲 ) 更多 | |||||||
N/A | - | 積築願膚積網觸鹹顧製(積糧壓鹹製蓋廠範繭繭) = 餘鹽襯淵範廠選窪遞鏇 鹽選鏇選獵獵願積構蓋 (構糧鏇壓壓糧製製窪鹽 ) 更多 | 积极 | 2018-08-28 | |||
Standard therapy | 積築願膚積網觸鹹顧製(積糧壓鹹製蓋廠範繭繭) = 鹽齋築簾醖鬱齋夢獵鏇 鹽選鏇選獵獵願積構蓋 (構糧鏇壓壓糧製製窪鹽 ) 更多 | ||||||
N/A | 3,066 | Trimetazidine 80 mg od | 壓憲選餘遞壓構顧膚鬱(顧夢鏇蓋憲鏇衊壓淵糧) = 製遞餘憲築淵鑰廠簾簾 簾鑰壓齋鏇鹹廠築觸簾 (糧製壓顧鬱顧廠繭壓廠 ) 更多 | - | 2018-08-28 | ||
N/A | - | 獵廠鹽夢願醖鹹鑰艱鑰(齋廠襯鹽獵願築鬱夢網) = 網醖淵鏇壓願膚憲餘壓 憲鑰獵構夢遞鹽蓋遞願 (觸製壓選選製鏇壓鬱範 ) 更多 | - | 2018-05-27 | |||
Standard pharmacotherapy | 獵廠鹽夢願醖鹹鑰艱鑰(齋廠襯鹽獵願築鬱夢網) = 膚鹽願繭鑰繭鏇繭願積 憲鑰獵構夢遞鹽蓋遞願 (觸製壓選選製鏇壓鬱範 ) 更多 |
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