ChemicalBook--->CAS DataBase List--->14919-38-1

14919-38-1

14919-38-1 Structure

14919-38-1 Structure
IdentificationBack Directory
[Name]

MYRISTOYL-DL-CARNITINE CHLORIDE
[CAS]

14919-38-1
[Synonyms]

MYRISTOYL-DL-CARNITINE CHLORIDE
(+/-)-MYRISTOYLCARNITINE CHLORIDE
[Molecular Formula]

C21H42ClNO4
[MDL Number]

MFCD00063479
[MOL File]

14919-38-1.mol
[Molecular Weight]

408.02
Chemical PropertiesBack Directory
[storage temp. ]

−20°C
[solubility ]

<10.2mg/ml in H2O
[form ]

solid
[color ]

White
Safety DataBack Directory
[Hazard Codes ]

Xn
[Risk Statements ]

22-43
[Safety Statements ]

36/37
[WGK Germany ]

3
Hazard InformationBack Directory
[Uses]

(+/-)-Myristoylcarnitine Chloride is a homolog of Acetylcarnitine Chloride (A171990), and an intermediate in lipid metabolism.
[Biological Activity]

(±)-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.
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