DL-Carnitine HCl
(Synonyms: 混旋肉碱盐酸盐,DL-Carnitine chloride) 目录号 : GC11702
DL-Carnitine HCl 存在两种异构体，称为 D 和 L。
Cas No.:461-05-2
Sample solution is provided at 25 µL, 10mM.
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(±)-Carnitine chloride exists in two isomers, known as D and L. L-carnitine plays an essential role in the β-oxidation of fatty acids and also shows antioxidant, and anti-inflammatory activities.
The main role of L-carnitine is to shuttle long-chain fatty acids across the inner mitochondrial membrane. After L-carnitine and acyl-CoA become acyl-carnitine by activation of carnitine palmitoyl transferase (CPT)-I, the transported acyl-carnitine is changed into acyl-CoA by CPT-II in the mitochondria matrix. Palmitoyl-CoA-induced mitochondrial respiration is increased by L-carnitine treatment, and then is accelerated by the presence of ADP. This acceleration is induced by treatment with L-carnitine in a concentration-dependent manner, and is saturated at 5 mM L-carnitine[1]. Pretreatment with L-carnitine augments Nrf2 nuclear translocation, DNA binding activity and heme oxygenase-1 (HO-1) expression in H2O2-treated HL7702 cells. L-carnitine protects HL7702 cells against H2O2-induced cell damage through Akt-mediated activation of Nrf2 signaling pathway[2].
L-carnitine is found to down-regulate the ubiquitin proteasome pathway and increase IGF-1 concentrations in animal models. L-carnitine administration for 2 weeks of hindlimb suspension alleviates the decrease in weight and fiber size in the soleus muscle. In addition, L-carnitine suppresses atrogin-1 mRNA expression, which has been reported to play a pivotal role in muscle atrophy[3]. Simultaneous treatment with L-carnitine attenuates the renal fibrosis (which correlated with a reduction of plasma TGF-β1 levels) and the pro-oxidative and proinflammatory status reported in L-NAME groups, with a concomitant increase in the expression of PPAR-γ[4].
Reference：
[1]. Oyanagi E, et al. Protective action of L-carnitine on cardiac mitochondrial function and structure against fatty acidstress. Biochem Biophys Res Commun. 2011 Aug 19;412(1):61-7.
[2]. Li J, et al. l-carnitine protects human hepatocytes from oxidative stress-induced toxicity through Akt-mediated activation of Nrf2 signaling pathway. Can J Physiol Pharmacol. 2016 May;94(5):517-25.
[3]. Jang J, et al. l-Carnitine supplement reduces skeletal muscle atrophy induced by prolonged hindlimb suspension in rats. Appl Physiol Nutr Metab. 2016 Dec;41(12):1240-1247.
[4]. Zambrano S, et al. L-carnitine attenuates the development of kidney fibrosis in hypertensive rats by upregulating PPAR-γ. Am J Hypertens. 2014 Mar;27(3):460-70.
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Kinase experiment: |
Mitochondria (0.6 mg protein/mL) are incubated in 2.5 mM Hepes (pH7.4) containing 225 mM mannitol, 75 mM sucrose and 100 μM ethylene glycol tetraacetic acid (EGTA) with or without 5 mM L-carnitine at 25°C. To measure oxygen uptake, 10 min after inorganic phosphate (Pi) 4 mM are added, the mitochondria are treated with palmitoyl-CoA (50 μM) and then ADP is added (200 μM). Oligomycin (5 μM) and rotenone (10 μM) are added 3-4 min after the ADP treatment. HPG (0-10 mM), which can specifically inhibit carnitine palmitoyl transferase (CPT)-I activity in the mitochondria, is added in the Hepes medium before incubation of the mitochondria[1]. |
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Animal experiment: |
Rats: After 1 week of acclimatization, rats are randomly assigned to a hindlimb suspension group, hindlimb suspension with L-carnitine administration group, and a pair-fed group. The L-carnitine group are administered a 1250 mg L-carnitine/kg dissolved in distilled water orally using a sonde. The body weight is measured every morning at 09:00 and L-carnitine solution is ingested every morning at 10:00. The experiment is conducted for 14 days[3]. |
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References: [1]. Oyanagi E, et al. Protective action of L-carnitine on cardiac mitochondrial function and structure against fatty acidstress. Biochem Biophys Res Commun. 2011 Aug 19;412(1):61-7. |
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| Cas No. | 461-05-2 | SDF | |
| 别名 | 混旋肉碱盐酸盐,DL-Carnitine chloride | ||
| 化学名 | (3-carboxy-2-hydroxypropyl)-trimethylazanium;chloride | ||
| Canonical SMILES | C[N+](C)(C)CC(CC(=O)O)O.[Cl-] | ||
| 分子式 | C7H15NO3.HCl | 分子量 | 197.66 |
| 溶解度 | ≥ 9.5mg/mL in DMSO with gentle warming | 储存条件 | Store at 2-8°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.0592 mL | 25.296 mL | 50.5919 mL |
| 5 mM | 1.0118 mL | 5.0592 mL | 10.1184 mL |
| 10 mM | 0.5059 mL | 2.5296 mL | 5.0592 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet