MildronateCAS# 76144-81-5 |
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Chemical structure
3D structure
Cas No. | 76144-81-5 | SDF | Download SDF |
PubChem ID | 123868 | Appearance | Powder |
Formula | C6H14N2O2 | M.Wt | 146.2 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | H2O : 50 mg/mL (342.02 mM; Need ultrasonic) | ||
Chemical Name | 3-[(trimethylazaniumyl)amino]propanoate | ||
SMILES | C[N+](C)(C)NCCC(=O)[O-] | ||
Standard InChIKey | PVBQYTCFVWZSJK-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C6H14N2O2/c1-8(2,3)7-5-4-6(9)10/h7H,4-5H2,1-3H3 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Mildronate Dilution Calculator
Mildronate Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 6.8399 mL | 34.1997 mL | 68.3995 mL | 136.7989 mL | 170.9986 mL |
5 mM | 1.368 mL | 6.8399 mL | 13.6799 mL | 27.3598 mL | 34.1997 mL |
10 mM | 0.684 mL | 3.42 mL | 6.8399 mL | 13.6799 mL | 17.0999 mL |
50 mM | 0.1368 mL | 0.684 mL | 1.368 mL | 2.736 mL | 3.42 mL |
100 mM | 0.0684 mL | 0.342 mL | 0.684 mL | 1.368 mL | 1.71 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Mildronate is an inhibitor of biosynthesis of L-carnitine by gamma-butyrobetaine (GBB) hydroxylase and as a competitive inhibitor of renal carnitine reabsorption.
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Crystal structures of binary compounds of meldonium 3-(1,1,1-tri-methyl-hydrazin-1-ium-2-yl)prop-ano-ate with sodium bromide and sodium iodide.[Pubmed:29951240]
Acta Crystallogr E Crystallogr Commun. 2018 May 22;74(Pt 6):829-834.
3-(1,1,1-Tri-methyl-hydrazin-1-ium-2-yl)propano-ate (C6H14N2O2, M, more commonly known under its commercial names Meldonium or Mildronate) co-crystalizes with sodium bromide and sodium iodide forming polymeric hydrates poly[[tetra-mu-aqua-di-aqua-bis-[3-(1,1,1-tri-methyl-hydrazin-1-ium-2-yl)propano- ate]disodium] dibromide tetra-hydrate], [Na2(C6H14N2O2)2(H2O)6]Br2.4H2O, and poly[[di-mu-aqua-di-aqua-[mu-3-(1,1,1-tri-methyl-hydrazin-1-ium-2-yl)propano-ate] disodium] diiodide], [Na2(C6H14N2O2)2(H2O)4]I2. The coordination numbers of the sodium ions are 6; the coordination polyhedra can be described as distorted octa-hedra. Metal ions and M zwitterions are assembled into infinite layers via electrostatic inter-actions and hydrogen-bonded networks. These layers are connected via electrostatic attraction between halogenide ions and positive tri-methyl-hydrazinium groups into a three-dimensional structure.
Inhibited Carnitine Synthesis Causes Systemic Alteration of Nutrient Metabolism in Zebrafish.[Pubmed:29867554]
Front Physiol. 2018 May 9;9:509.
Impaired mitochondrial fatty acid beta-oxidation has been correlated with many metabolic syndromes, and the metabolic characteristics of the mammalian models of mitochondrial dysfunction have also been intensively studied. However, the effects of the impaired mitochondrial fatty acid beta-oxidation on systemic metabolism in teleost have never been investigated. In the present study, we established a low-carnitine zebrafish model by feeding fish with Mildronate as a specific carnitine synthesis inhibitor [0.05% body weight (BW)/d] for 7 weeks, and the systemically changed nutrient metabolism, including carnitine and triglyceride (TG) concentrations, fatty acid (FA) beta-oxidation capability, and other molecular and biochemical assays of lipid, glucose, and protein metabolism, were measured. The results indicated that Mildronate markedly decreased hepatic carnitine concentrations while it had no effect in muscle. Liver TG concentrations increased by more than 50% in Mildronate-treated fish. Mildronate decreased the efficiency of liver mitochondrial beta-oxidation, increased the hepatic mRNA expression of genes related to FA beta-oxidation and lipolysis, and decreased the expression of lipogenesis genes. Mildronate decreased whole body glycogen content, increased glucose metabolism rate, and upregulated the expression of glucose uptake and glycolysis genes. Mildronate also increased whole body protein content and hepatic mRNA expression of mechanistic target of rapamycin (mtor), and decreased the expression of a protein catabolism-related gene. Liver, rather than muscle, was the primary organ targeted by Mildronate. In short, Mildronate-induced hepatic inhibited carnitine synthesis in zebrafish caused decreased mitochondrial FA beta-oxidation efficiency, greater lipid accumulation, and altered glucose and protein metabolism. This reveals the key roles of mitochondrial fatty acid beta-oxidation in nutrient metabolism in fish, and this low-carnitine zebrafish model could also be used as a novel fish model for future metabolism studies.
A fatty acid analogue targeting mitochondria exerts a plasma triacylglycerol lowering effect in rats with impaired carnitine biosynthesis.[Pubmed:29590220]
PLoS One. 2018 Mar 28;13(3):e0194978.
L-carnitine is important for the catabolism of long-chain fatty acids in the mitochondria. We investigated how the triacylglycerol (TAG)-lowering drug 2-(tridec-12-yn-1-ylthio)acetic acid (1-triple TTA) influenced lipid metabolism in carnitine-depleted, 3-(2,2,2-trimethylhydrazinium)propionate dehydrate (Mildronate; meldonium)-treated male Wistar rats. As indicated, carnitine biosynthesis was impaired by Mildronate. However, TAG levels of both plasma and liver were decreased by 1-triple TTA in Mildronate-treated animals. This was accompanied by increased gene expression of proteins involved in mitochondrial activity and proliferation and reduced mRNA levels of Dgat2, ApoB and ApoCIII in liver. The hepatic energy state was reduced in the group of Mildronate and 1-triple TTA as reflected by increased AMP/ATP ratio, reduced energy charge and induced gene expression of uncoupling proteins 2 and 3. The increase in mitochondrial fatty acid oxidation was observed despite low plasma carnitine levels, and was linked to strongly induced gene expression of carnitine acetyltransferase, translocase and carnitine transporter, suggesting an efficient carnitine turnover. The present data suggest that the plasma TAG-lowering effect of 1-triple TTA in Mildronate-treated rats is not only due to increased mitochondrial fatty acid oxidation reflected by increased mitochondrial biogenesis, but also to changes in plasma clearance and reduced TAG biosynthesis.
Rat spinal ganglia in assessment of protective action of antioxidants: A morphological study.[Pubmed:29273287]
Medicina (Kaunas). 2017 Dec;53(5):316-322.
BACKGROUND AND OBJECTIVE: Mercury pollution is one of the most pressing environmental problems. Therefore, the impact of mercury on human body, the nervous system in particular, remains topical. The aim of the study was to identify the morphological characteristics of neurons and neuroglia in spinal ganglia of rats receiving antioxidants in the presence of small doses of mercury (II) chloride. MATERIALS AND METHODS: A total of 100 white Wistar rats were divided into 5 series (10 groups), with 10 animals in each group. The first series comprised intact animals receiving saline solution instead of drugs administered in other series (control). In the second series 10 injections of mercury (II) chloride were performed (group of short-term neurointoxication) and 50 injections (group of long-term neurointoxication). In the third to the fifth series, the short- and long-term neurointoxication was followed by 10 daily injection of the drugs: unithiolum, thiotriazolinum and Mildronate respectively. Spinal ganglia were obtained two weeks after the completion of drugs administration and studied microscopically and ultramicroscopically. RESULTS: Administration of thiotriazolinum, unithiolum and Mildronate mitigated manifestations of toxic effects of mercury (II) chloride on spinal ganglia. Unithiolum and thiotriazolinum activated synthetic processes, while Mildronate had a positive effect on restoration of cells metabolism. CONCLUSIONS: Morphological data show that unithiolum and thiotriazolinum action decreases toxic effects of mercury chloride and are similar. They demonstrate pronounced activation of synthetic processes in sensory neurons and satellite cells of spinal ganglia. Mildronate also restores cell ultrastructure and has more pronounced effect on their energetic processes and interaction between neurons and satellite cells.
Inhibited fatty acid beta-oxidation impairs stress resistance ability in Nile tilapia (Oreochromis niloticus).[Pubmed:28774846]
Fish Shellfish Immunol. 2017 Sep;68:500-508.
Energy metabolism plays important roles in stress resistance and immunity in mammals, however, such functions have not been established in fish. In the present study, Nile tilapia (Oreochromis niloticus) was fed with Mildronate, an inhibitor of mitochondrial fatty acid (FA) beta-oxidation, for six weeks subsequently challenged with Aeromonas hydrophila and ammonia nitrogen exposure. Mildronate treatment reduced significantly l-carnitine concentration and mitochondrial FA beta-oxidation efficiency, while it increased lipid accumulation in liver. The fish with inhibited hepatic FA catabolism had lower survival rate when exposed to Aeromonas hydrophila and ammonia nitrogen. Moreover, fish fed Mildronate supplemented diet had lower immune enzymes activities and anti-inflammatory cytokine genes expressions, but had higher pro-inflammatory cytokine genes expressions. However, the oxidative stress-related biochemical indexes were not significantly affected by Mildronate treatment. Taken together, inhibited mitochondrial FA beta-oxidation impaired stress resistance ability in Nile tilapia mainly through inhibiting immune functions and triggering inflammation. This is the first study showing the regulatory effects of lipid catabolism on stress resistance and immune functions in fish.
Bacteriolytic Activity Of Human Interleukin-2, Chicken Egg Lysozyme In The Presence Of Potential Effectors.[Pubmed:28740730]
Acta Naturae. 2017 Apr-Jun;9(2):82-87.
The bacteriolytic activity of interleukin-2 and chicken egg lysozyme in the presence of various substances has been studied. Glycine and lysine do not affect the activity of interleukin-2 but increase that of lysozyme, showing a bell-shape concentration dependence peaking at 1.5 mM glycine and 18 mM lysine. Arginine and glutamate activate both interleukin-2 and lysozyme with a concentration dependence of the saturation type. Aromatic amino acids have almost no effect on the activity of both interleukin-2 and lysozyme. Aromatic amines, tryptamine, and tyramine activate interleukin-2 but inhibit lysozyme. Peptide antibiotics affect interleukin and lysozyme similarly and exhibit maximum activity in the micromolar range of antibiotics. Taurine has no effect on the activity of interleukin-2 and lysozyme. Mildronate showed no influence on lysozyme, but it activated interleukin-2 with the activity maximum at 3 mM. EDTA activates both interleukin-2 and lysozyme at concentrations above 0.15 mM.