DL-CAPROYLCARNITINE CHLORIDE Property

Melting point:

156-158°C

storage temp. 

−20°C

solubility 

Methanol (Slightly), Water (Slightly)

form 

Solid

color 

White to Off-White

Water Solubility 

Soluble to 100 mM in water

Stability:

Hygroscopic

Safety

Hazard Codes 

Xn

Risk Statements 

22-43

Safety Statements 

36/37

WGK Germany 

2

Hazard and Precautionary Statements (GHS)

Symbol(GHS)

Signal word

Warning

Hazard statements

H302Harmful if swallowed

H317May cause an allergic skin reaction

Precautionary statements

P280Wear protective gloves/protective clothing/eye protection/face protection.

P302+P352IF ON SKIN: wash with plenty of soap and water.

DL-CAPROYLCARNITINE CHLORIDE Chemical Properties,Usage,Production

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].