DL-Carnitine - CAS 406-76-8
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Carnitine regulates fatty acid transport in mitochondria, elevates serum carnitine fractions.
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White solid
(3-carboxy-2-hydroxypropyl)trimethyl-,hydroxide,innersalt,dl-ammoniu;1-propanaminium,3-carboxy-2-hydroxy-n,n,n-trimethyl-,hydroxide,innersalt,;DL-CARNITINE;CARNITIN;(±)-(3-carboxy-2-hydroxypropyl)trimethylammonium hydroxide;1-Propanaminium, 3-carboxy-2-h
Soluble in DMSO
Store at 2-8 °C
Regulates fatty acid transport in mitochondria, elevates serum carnitine fractions.
Quality Standard:
Enterprise Standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Canonical SMILES:
1.Mitochondrial gene polymorphisms alter hepatic cellular energy metabolism and aggravate diet-induced non-alcoholic steatohepatitis.
Schröder T1, Kucharczyk D2, Bär F2, Pagel R3, Derer S2, Jendrek ST3, Sünderhauf A2, Brethack AK2, Hirose M4, Möller S5, Künstner A6, Bischof J4, Weyers I7, Heeren J8, Koczan D9, Schmid SM2, Divanovic S10, Giles DA10, Adamski J11, Fellermann K2, Lehnert H2, Köhl J12, Ibrahim S4, Sina C2. Mol Metab. 2016 Feb 2;5(4):283-95. doi: 10.1016/j.molmet.2016.01.010. eCollection 2016.
OBJECTIVE: Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and is associated with an enhanced risk for liver and cardiovascular diseases and mortality. NAFLD can progress from simple hepatic steatosis to non-alcoholic steatohepatitis (NASH). However, the mechanisms predisposing to this progression remain undefined. Notably, hepatic mitochondrial dysfunction is a common finding in patients with NASH. Due to a lack of appropriate experimental animal models, it has not been evaluated whether this mitochondrial dysfunction plays a causative role for the development of NASH.
2.Palmitoyl-DL-carnitine is a multitarget inhibitor of Pseudomonas aeruginosa biofilm development.
Wenderska IB1, Chong M, McNulty J, Wright GD, Burrows LL. Chembiochem. 2011 Dec 16;12(18):2759-66. doi: 10.1002/cbic.201100500. Epub 2011 Nov 2.
Bacteria growing in biofilms are often in metabolic and physiological states that do not respond well to antibiotics, and thus, are major contributors to chronic diseases. Biofilm inhibitors, therefore, have the potential to be used alone or as adjuvants to conventional antibiotic therapies. Here, we screened a chemically diverse collection of protein kinase inhibitors for molecules that perturb biofilm development. Among the inhibitory molecules identified, palmitoyl-DL-carnitine (pDLC) impaired Pseudomonas aeruginosa and Escherichia coli biofilm formation in a dose-dependent manner. The pDLC affected multiple pathways implicated in P. aeruginosa biofilm development; it stimulated motility, inhibited activity of the Las quorum sensing system, and overrode the biofilm-promoting effects of subminimal inhibitory concentrations of aminoglycosides and high levels of the second messenger, cyclic-di-GMP. Palmitic acid, but not carnitine, inhibited biofilm formation but did not stimulate motility, suggesting that pDLC works through unique mechanisms.
3.Effects of L-, D-, and DL-carnitine on morphometric parameters of skeletal muscle and exercise performance of laboratory animals receiving carnitine-deficient diet.
Spasov AA1, Iezhitsa IN, Kravchenko MS, Pisarev VB, Snigur GL. Bull Exp Biol Med. 2006 Oct;142(4):458-60.
Serum concentration of L-carnitine, the mean thickness of the skeletal muscle fiber, and exercise performance in the forced swimming test decreased in rats receiving a carnitine-deficient diet. Treatment with L-carnitine compensated for carnitine deficiency, while racemate and D-stereoisomer did not increase its level. L-Carnitine, but not racemate and D-stereoisomer, promoted recovery of the skeletal muscle fiber thickness and exercise performance of rats.
4.[Comparative evaluation of the effects of carnitine stereoisomers and racemate on the cardio- and hemodynamics of rats on a carnitine-deficient diet].
Spasov AA, Iezhitsa IN, Tiurenkov IN, Perfilova VN, Gurova NA, Kravchenko MS. Vestn Ross Akad Med Nauk. 2006;(7):20-7.
L-carnitine (L-beta-hydroxy-gamma-N,N,N-trimethylaminobutyric acid) is conditionally necessary for mitochondrial transport and metabolism of long-chain fatty acids, and thus for myocardial energetic metabolism. D-carnitine is not biologically active and might interfere with proper utilization of the L isomer, and so there are claims that the racemic mixture (DL-carnitine) should be avoided. The pharmacological effects of carnitine are stereospecific: L-carnitine was effective in various animal and clinical studies, while D- and DL-carnitine was found to be ineffective or even toxic to some cells and tissues, such as muscle cells and the myocardium. DL-carnitine caused symptoms of myasthenia and cardiac arrhythmias, which disappeared after L-carnitine administration. Therefore, the purposes of this work were (1) to study the effect of L-carnitine vs. that of D- and DL-stereoisomers on carnitine restoration rate in blood plasma of carnitine-deficient rats and (2) to evaluate the effect of stereoisomers and racemate of carnitine on the cardio- and hemodynamics of rats on carnitine-deficient diet.
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CAS 406-76-8 DL-Carnitine

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