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(±)-Myristoylcarnitine chloride
cholinergic agonist; important intermediates in lipid metabolism

Catalog No.B6354
Size Price Stock Qty
50mg
$152.00
In stock

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Sample solution is provided at 25 µL, 10mM.

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Chemical structure

(±)-Myristoylcarnitine chloride

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Chemical Properties

Cas No. 14919-38-1 SDF Download SDF
Chemical Name (R)-3-carboxy-N,N,N-trimethyl-2-(tetradecanoyloxy)propan-1-aminium chloride
Canonical SMILES O=C(CCCCCCCCCCCCC)O[[email protected]](CC(O)=O)C[N+](C)(C)C.[Cl-]
Formula C21H42ClNO4 M.Wt 408.02
Solubility Soluble to 25 mM in sterile water Storage Store at -20°C
Physical Appearance White solid Shipping Condition Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request
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.

Background

(±)-Myristoylcarnitine chloride is an agonist for cholinergic and a homolog of acetylcarnitine chloride (Cat No. B6273).

Acetylcholine receptor (AChR) is an integral membrane protein receptor for acetylcholine. There are two kinds of AChRs: nicotinic acetylcholine receptors and muscarinic acetylcholine receptors.

(±)-Myristoylcarnitine chloride is a cholinergic agonist and an intermediate in lipid metabolism [1]. In retinal ganglion cells, acetylcarnitine and acetylcholine inhibited GABAergic responses to exogenous GABA and GABAergic inhibitory postsynaptic currents [2].

In dogs with coronary ligation, (-)-carnitine chloride (LCC) (300 mg/kg) and acetyl (-)-carnitine chloride (ALCC) (300 mg/kg) inhibited the ventricular arrhythmia. Also, LCC and ALCC improved oxidative phosphorylation rate and the mitochondrial function [1]. In the mouse hot plate test, acetyl-l-carnitine (ALCAR) (100 mg/kg) exhibited analgesia. While, U-73122 and neomycin (the phospholipase C (PLC) inhibitors) blocked the increase of the pain threshold induced by ALCAR. LiCl that impairing phosphatidylinositol synthesis antagonized the antinociception in a dose-dependent way. PMA and PDBu (PKC activators) blocked the increase of the pain threshold in a dose-dependent way. These results suggested that ALCAR analgesia required the participation of the PLC-IP3 pathway [3].

References:
[1].  Imai S, Matsui K, Nakazawa M, et al. Anti-arrhythmic effects of (-)-carnitine chloride and its acetyl analogue on canine late ventricular arrhythmia induced by ligation of the coronary artery as related to improvement of mitochondrial function. Br J Pharmacol, 1984, 82(2): 533-542.
[2].  B?hring R, Standhardt H, Martelli EA, et al. GABA-activated chloride currents of postnatal mouse retinal ganglion cells are blocked by acetylcholine and acetylcarnitine: how specific are ion channels in immature neurons? Eur J Neurosci, 1994, 6(7): 1089-1099.
[3].  Galeotti N, Bartolini A, Calvani M, et al. Acetyl-L-carnitine requires phospholipase C-IP3 pathway activation to induce antinociception. Neuropharmacology, 2004, 47(2): 286-294.