Palmitoyl-L-carnitine (chloride)
(Synonyms: L-氯化棕榈酰肉碱) 目录号 : GC44551
A long-chain acylcarnitine
Cas No.:18877-64-0
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Palmitoyl-L-carnitine is a naturally occurring long-chain acylcarnitine and the L-enantiomer of palmitoyl-DL-carnitine . In cells, palmitoyl-L-carnitine is transported into mitochondria via carnitine palmitoyl transferase II to deliver palmitate for fatty acid oxidation and energy production. It also inhibits lecithin:cholesterol acyltransferase activity in rat, but not human, plasma when used at a concentration of 500 µM. In vivo, palmitoyl-L-carnitine increases intestinal absorption of the antibiotic cefoxitin in rat intestine.
| Cas No. | 18877-64-0 | SDF | |
| 别名 | L-氯化棕榈酰肉碱 | ||
| Canonical SMILES | OC(C[C@H](C[N+](C)(C)C)OC(CCCCCCCCCCCCCCC)=O)=O.[Cl-] | ||
| 分子式 | C23H46NO4•Cl | 分子量 | 436.1 |
| 溶解度 | DMSO : 50 mg/mL (114.66 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble) | 储存条件 | Store at -20°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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.2931 mL | 11.4653 mL | 22.9305 mL |
| 5 mM | 0.4586 mL | 2.2931 mL | 4.5861 mL |
| 10 mM | 0.2293 mL | 1.1465 mL | 2.2931 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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Mitochondria from the hepatopancreas of the marine clam Mercenaria mercenaria: substrate preferences and salt and pH effects on the oxidation of Palmitoyl-L-carnitine and succinate
J Exp Zool 1984 May;230(2):165-74.PMID:6736891DOI:10.1002/jez.1402300202.
A method is presented for the isolation of mitochondria with good respiratory control from the hepatopancreas of the marine clam Mercenaria mercenaria. Palmitoyl-L-carnitine is the preferred substrate of the mitochondria of the hepatopancreas based on state 3 rates of oxidation (in the presence of ADP). Rates of oxidation of pyruvate and glutamate were about one-half that of the lipid substrate in state 3. alpha-Glycerophosphate was oxidized at a rate about one-third that of Palmitoyl-L-carnitine. All Krebs cycle intermediates were oxidized to some extent. Proline was not oxidized at detectable levels. The optimal range of KCl concentrations for the oxidation of Palmitoyl-L-carnitine is between 250 and 500 mM whereas the optimal range of KCl concentration for the oxidation of succinate is between 200 and 350 mM. The optimal range of pH for the oxidation of succinate and for the oxidation of Palmitoyl-L-carnitine lies between pH 6.5 and 7.5 based on the respiratory control ratio.
Enhanced bioavailability of cefoxitin using palmitoyl L-carnitine. I. Enhancer activity in different intestinal regions
Pharm Res 1992 Feb;9(2):191-4.PMID:1553340DOI:10.1023/a:1018977021183.
The conditions under which the absorption enhancer palmitoyl L-carnitine chloride (PCC) improved the bioavailability of the poorly absorbed antibiotic cefoxitin throughout the rat intestine has been studied. Cefoxitin alone was appreciably absorbed only in the duodenum (31% vs less than 7% elsewhere). PCC solutions (3 mg/rat, pH 4.0) enhanced cefoxitin bioavailability (F) by 0-, 22-, 16-, and greater than 32-fold in the duodenum, jejunum, ileum, and colon regions, respectively. The inability of PCC to improve F in the duodenum could not likely be attributed to enzymatic degradation of the enhancer, since coadministration with protease and esterase inhibitors produced similar results (F = 30%). Coadministration of PCC solution with cefoxitin in the unligated or ligated colon, increased F to 33 and 76%, respectively. Qualitatively similar results were seen with PCC suspensions (3 mg/rat, pH 6.0). Maintaining a high concentration of cefoxitin and PCC in a restricted region (i.e., by ligating a 2- to 3-cm section of the colon) afforded a two- to threefold advantage over an unligated colon section. The difference in cefoxitin bioavailability between ligated and unligated colon was probably due to sample spreading and subsequent/simultaneous dilution.
Effects of in vivo treatment of rats with trimethyltin chloride on respiratory properties of rat liver mitochondria
Biochem Pharmacol 2002 Aug 15;64(4):657-67.PMID:12167485DOI:10.1016/s0006-2952(02)01182-6.
Liver mitochondria isolated from rats treated in vivo with trimethyltin chloride show stimulation of respiration using glutamate/malate as substrate, and a transient inhibition on rates of respiration using Palmitoyl-L-carnitine as substrate. This phenomenon was observed with both ADP- and FCCP-stimulated respiration. In contrast, rates of respiration by liver mitochondria isolated from rats treated in vivo with trimethyltin chloride, following prior treatment with clofibrate, were inhibited when glutamate/malate was respiratory substrates. With Palmitoyl-L-carnitine no effect of trimethyltin chloride was observed. In vitro treatment of rat liver mitochondria, or of rat liver homogenates, led to the expected, powerful inhibition of respiration. The synthesis of ATP by liver mitochondria isolated from rats treated in vivo with trimethyltin chloride was not inhibited compared to mitochondria isolated from control rats. Similarly, ATP synthesis by mitochondria isolated from rats treated with clofibrate, before treatment with trimethyltin chloride, was not inhibited. We, therefore, conclude that the powerful inhibitory effects of trimethyltin found in vitro, is not expressed in vivo during the first 36 hr following administration. In vivo treatment of rats with trimethyltin chloride caused a marked increase in hepatic levels of taurine and glycine, while levels of glutathione and glutamine were diminished. This is consistent with an enhanced oxidative stress in the liver. Our findings lead to the conclusion that increased oxidative stress, rather than inhibition of the mitochondrial ATPase, is a likely major cause of the in vivo toxic effects due to trimethyltin chloride.
Ammonium inhibition of fatty acid oxidation in rat liver mitochondria. A possible cause of fatty liver in Reye's syndrome and urea cycle defects
Biochem Biophys Res Commun 1985 Mar 15;127(2):565-70.PMID:3977937DOI:10.1016/s0006-291x(85)80197-2.
NH4C1 inhibited oxygen consumption (State 3, ADP induced) by rat liver mitochondria respiring on Palmitoyl-L-carnitine or octanoic acid but not on succinate or malate + glutamate. The inhibition became apparent at 0.02 mM reaching a plateau (40%) at 2 mM NH4C1. Similar inhibition was observed with uncoupled (in the presence of 2, 4-dinitrophenol) mitochondria. The inhibition of uncoupled mitochondria was reversible as the rate of respiration with Palmitoyl-L-carnitine was further increased by succinate and the total rate was unaffected by NH4C1. Therefore, NH+4 inhibition of mitochondrial respiration may lead to fatty infiltration and be one of the causes of the pathophysiology in children with Reye's syndrome and disorders of urea cycle enzymes.