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Details

Stereochemistry RACEMIC
Molecular Formula C9H17NO4.ClH
Molecular Weight 239.697
Optical Activity ( + / - )
Defined Stereocenters 0 / 1
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of ACETYLCARNITINE HYDROCHLORIDE, (±)-

SMILES

Cl.CC(=O)OC(CC([O-])=O)C[N+](C)(C)C

InChI

InChIKey=JATPLOXBFFRHDN-UHFFFAOYSA-N
InChI=1S/C9H17NO4.ClH/c1-7(11)14-8(5-9(12)13)6-10(2,3)4;/h8H,5-6H2,1-4H3;1H

HIDE SMILES / InChI

Description

L-acetylcarnitine or acet-L-carnitine, a compound, naturally produced by the body, is necessary for fatty-acid metabolism and energy production. It is often taken as a dietary supplement. The mechanisms of action of acetylcarnitine have not been fully elucidated, but it seems that the main role of acetylcarnitine is to donate an acetyl group during fatty acid metabolism to help transport fatty acids, such as acetyl CoA, into the mitochondrial matrix where fatty acid metabolism occurs. L-acetylcarnitine is an investigational drug, which is approved in some countries, for example in Italy for diabetic neuropathy. Phase IV of clinical trials have revealed, that it also effective agent to treat the Alzheimer's disease. In contrary, the efficacy of L-acetylcarnitine as a prophylaxis in migraine patients did not provide evidence of benefit for efficacy. Besides, Acetyl-L-carnitine was in clinical trial Phase III to investigate its efficacy in the treatment of peripheral sensory neuropathy that anti-cancer chemotherapeutics induce. Recently published article unexpectedly discovered that this drug increased chemotherapy-induced peripheral neuropathy in a randomized trial.

CNS Activity

Approval Year

Targets

Primary TargetPharmacologyConditionPotency

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
Unknown
Palliative
Unknown
Preventing
Unknown
Palliative
Unknown

Doses

AEs

PubMed

Patents

Sample Use Guides

In Vivo Use Guide
orally at a dosage of 2000 mg/day
Route of Administration: Oral
In Vitro Use Guide
The neuroprotective properties of acetyl-L-carnitine (ALCAR) were investigated in primary cell cultures from rat hippocampal formation and cerebral cortex of 17-day-old rat embryos. ALCAR (10-50 microM for 10 days) reduced the cell mortality induced by 24 hr fetal calf serum deprivation. Protection was partial when the neuronal cells, chronically treated with ALCAR (50 microM), were exposed to glutamate (0.25-1 mM) and kainic acid (250-500 microM) for 24 hr. The neurotoxicity induced by N-methyl-D-aspartate (NMDA, 250 microM) was attenuated by the acute co-exposure with ALCAR (1 mM), the chronic treatment with ALCAR (50 microM) significantly reduced the neuronal death induced by NMDA (0.25-1 mM).