Basic information Safety Supplier Related

MYRISTOYL-DL-CARNITINE CHLORIDE

Basic information Safety Supplier Related

MYRISTOYL-DL-CARNITINE CHLORIDE Basic information

Product Name:
MYRISTOYL-DL-CARNITINE CHLORIDE
Synonyms:
  • MYRISTOYL-DL-CARNITINE CHLORIDE
  • (+/-)-MYRISTOYLCARNITINE CHLORIDE
CAS:
14919-38-1
MF:
C21H42ClNO4
MW:
408.02
Product Categories:
  • Lipid signaling
Mol File:
14919-38-1.mol
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MYRISTOYL-DL-CARNITINE CHLORIDE Chemical Properties

storage temp. 
−20°C
solubility 
<10.2mg/ml in H2O
form 
solid
color 
White
Water Solubility 
Soluble to 25 mM in water
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Safety Information

Hazard Codes 
Xn
Risk Statements 
22-43
Safety Statements 
36/37
WGK Germany 
3

MSDS

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MYRISTOYL-DL-CARNITINE CHLORIDE Usage And Synthesis

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].

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