Trimetazidine dihydrochlorideTrimetazidine dihydrochloride
MedChemExpress (MCE)
HY-B0968
13171-25-0
99.91%
4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months
-20°C, 1 month (sealed storage, away from moisture)
Room temperature in continental US
may vary elsewhere.
Trimetazidine dihydrochloride is a selective long chain 3-ketoyl coenzyme A thiolase inhibitor with an IC50 of 75 nM, which can inhibit β-oxidation of free fatty acid (FFA). Trimetazidine dihydrochloride is an effective antianginal agent and a cytoprotective agent, has anti-oxidant, anti-inflammatory, antinociceptive and gastroprotective properties. Trimetazidine dihydrochloride triggers autophagy. Trimetazidine dihydrochloride is also a 3-hydroxyacyl-CoA dehydrogenase (HADHA) inhibitor.
Trimetazidine (1 μM-100 μM
24 hours
HUVECs) could enhance the viability of the injured HUVECs induces by oxidation in a certain dose-dependent manner[1].
Trimetazidine (5-20 mg/kg
oral administration
1 hour
Swiss albino male mice) in 10 mg/kg and 20 mg/kg doses significantly raises the seizure-threshold current in the increasing current electroshock seizure (ICES) test in the mice[5].
IC50: 75 nM (long chain 3-ketoyl coenzyme A thiolase)[2] β-oxidation[2] Autophagy[3] 3-hydroxyacyl-CoA dehydrogenase (HADHA)[4] In Vitro Trimetazidine (1 μM-100 μM
24 hours
HUVECs) could enhance the viability of the injured HUVECs induces by oxidation in a certain dose-dependent manner[1]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Trimetazidine dihydrochloride Related Antibodies Cell Viability Assay[1] Cell Line: Human umbilical vein endothelial cells (HUVECs)
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[1]. Shenghu He, et al. Protective effects of trimetazidine against vascular endothelial cell injury induced by oxidation. Journal of Geriatric Cardiology, December 2008 , Vol 5 No 4.
[2]. Chrusciel P, et al. Defining the role of trimetazidine in the treatment of cardiovascular disorders: some insights on its role in heart failure and peripheral artery disease. Drugs. 2014 Jun
74(9):971-80. [Content Brief]
[3]. Kantor PF, et al. The antianginal drug trimetazidine shifts cardiac energy metabolism from fatty acid oxidation to glucose oxidation by inhibiting mitochondrial long-chain 3-ketoacyl coenzyme A thiolase. Circ Res. 2000 Mar 17
86(5):580-8. [Content Brief]
[4]. Hossain F, et al.Inhibition of Fatty Acid Oxidation Modulates Immunosuppressive Functions of Myeloid-Derived Suppressor Cells and Enhances Cancer Therapies. Cancer Immunol Res. 2015 Nov
3(11):1236-47. [Content Brief]
[5]. Jain S, et al. Trimetazidine exerts protection against increasing current electroshock seizure test in mice. Seizure. 2010 Jun
19(5):300-2. [Content Brief]