ChemicalBook--->CAS DataBase List--->6920-35-0

6920-35-0

6920-35-0 Structure

6920-35-0 Structure
IdentificationBack Directory
[Name]

DL-CAPROYLCARNITINE CHLORIDE
[CAS]

6920-35-0
[Synonyms]

Zinc02517065
Hexanoyl-L-carnitine HCl
DL-CAPROYLCARNITINE CHLORIDE
DL-HEXANOYLCARNITINE CHLORIDE
Hexanoyl-DL-carnitine chloride
(+/-)-HEXANOYLCARNITINE CHLORIDE
[Molecular Formula]

C13H26ClNO4
[MDL Number]

MFCD00151472
[MOL File]

6920-35-0.mol
[Molecular Weight]

295.8
Chemical PropertiesBack Directory
[Melting point ]

156-158°C
[storage temp. ]

−20°C
[solubility ]

Methanol (Slightly), Water (Slightly)
[form ]

Solid
[color ]

White to Off-White
Safety DataBack Directory
[Hazard Codes ]

Xn
[Risk Statements ]

22-43
[Safety Statements ]

36/37
[WGK Germany ]

2
Hazard InformationBack Directory
[Uses]

(±)-Hexanoylcarnitine Chloride acts as a potential absorption-enhancing agents when used in drugs that are poorly absorbed, particularly in the gastrointestinal track.
[Biological Activity]

(±)-hexanoylcarnitine 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.(±)-hexanoylcarnitine 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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