1219798-68-1
Chemical Structure
3-Methylglutaric acid-d4
- CAS 番号: 1219798-68-1
- Formula:C6H6D4O4
- Molecular Weight:150.17
IUPAC Name: 3-methylpentanedioic-2,2,4,4-d4 acid
InChIKey: XJMMNTGIMDZPMU-RRVWJQJTSA-N
SMILES: OC(C([2H])([2H])C(C)C([2H])([2H])C(O)=O)=O
Biological Activity: 3-Methylglutaric acid-d4 is the deuterium labeled 3-Methylglutaric acid (HY-113410). 3-Methylglutaric acid is a non-selective inhibitor of mitochondrial function and Na+, K+-ATPase, with an inhibition rate of 30% on rat cortical synaptosomal Na+, K+-ATPase. 3-Methylglutaric acid can induce reactive oxygen species (ROS) generation, thereby causing oxidative damage and inhibiting mitochondrial redox potential and ion pump function of cell membranes. 3-Methylglutaric acid can be used to study the neuropathological mechanisms of metabolic diseases and the role of oxidative stress-mediated neuronal damage in neurodegeneration[1][2][3][4][5].
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3-Methylglutaric acid-d4 | 3-Methylglutaric acid-d4 is the deuterium labeled 3-Methylglutaric acid (HY-113410). 3-Methylglutaric acid is a non-selective inhibitor of mitochondrial function and Na+, K+-ATPase, with an inhibition rate of 30% on rat cortical synaptosomal Na+, K+-ATPase. 3-Methylglutaric acid can induce reactive oxygen species (ROS) generation, thereby causing oxidative damage and inhibiting mitochondrial redox potential and ion pump function of cell membranes. 3-Methylglutaric acid can be used to study the neuropathological mechanisms of metabolic diseases and the role of oxidative stress-mediated neuronal damage in neurodegeneration. | |||||||||||||||||||||
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3-Methylglutaric acid (Standard) | ≥98% | 3-Methylglutaric acid (Standard) is the analytical standard of 3-Methylglutaric acid (HY-113410). This product is intended for research and analytical applications. 3-Methylglutaric acid is a non-selective inhibitor of mitochondrial function and Na+, K+-ATPase, with an inhibition rate of 30% on rat cortical synaptosomal Na+, K+-ATPase. 3-Methylglutaric acid can induce reactive oxygen species (ROS) generation, thereby causing oxidative damage and inhibiting mitochondrial redox potential and ion pump function of cell membranes. 3-Methylglutaric acid can be used to study the neuropathological mechanisms of metabolic diseases and the role of oxidative stress-mediated neuronal damage in neurodegeneration. | ||||||||||||||||||||
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3-Methylglutaric acid | 98.0% | 3-Methylglutaric acid is a non-selective inhibitor of mitochondrial function and Na+, K+-ATPase, with an inhibition rate of 30% on rat cortical synaptosomal Na+, K+-ATPase. 3-Methylglutaric acid can induce reactive oxygen species (ROS) generation, thereby causing oxidative damage and inhibiting mitochondrial redox potential and ion pump function of cell membranes. 3-Methylglutaric acid can be used to study the neuropathological mechanisms of metabolic diseases and the role of oxidative stress-mediated neuronal damage in neurodegeneration. | ||||||||||||||||||||
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References
- [1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019 Feb;53(2):211-216. [Content Brief]
- [2]. Ribeiro CA, et al. Neurochemical evidence that 3-methylglutaric acid inhibits synaptic Na+,K+-ATPase activity probably through oxidative damage in brain cortex of young rats. Int J Dev Neurosci. 2011 Feb;29(1):1-7. [Content Brief]
- [3]. da Rosa-Junior NT, et al. In vivo evidence that bezafibrate prevents oxidative stress and mitochondrial dysfunction caused by 3-methylglutaric acid in rat liver. Biochimie. 2020 Apr-May;171-172:187-196. [Content Brief]
- [4]. da Rosa-Junior NT, et al. Bezafibrate In Vivo Administration Prevents 3-Methylglutaric Acid-Induced Impairment of Redox Status, Mitochondrial Biogenesis, and Neural Injury in Brain of Developing Rats. Neurotox Res. 2019 May;35(4):809-822. [Content Brief]
- [5]. Colín-González AL, et al. Experimental Evidence that 3-Methylglutaric Acid Disturbs Mitochondrial Function and Induced Oxidative Stress in Rat Brain Synaptosomes: New Converging Mechanisms. Neurochem Res. 2016 Oct;41(10):2619-2626. [Content Brief]
