Technical information

Molecular Formula: C9H17NO4 · HCl

Molecular Weight: 239.7


(R)-3-Acetoxy-4-(trimethylammonio)butyrate dihydrochloride

L-O-Acetylcarnitine chloride

R(-)-2-Acetyloxy-3-carboxy-N,N,N-trimethyl-1-propanaminium chloride



CAS Number: 5080-50-2

Beilstein Registry Number: 4340103

Solubility: water 100 mg/mL

What is ALC and what does it do?

L-Carnitine is a quarternary amine that is synthesized in the liver, kidney, and muscle from the amino acids L-lysine and L-methionine. Although humans and other mammals are capable of synthesizing L-carnitine, the majority of it is obtained from dietary sources such as meat and dairy products.

L-Carnitine’s major function in the body is to help transport long-chain fatty acids into the mitochondrial matrix where they are oxidized for eventual energy production. L-Carnitine and ALCAR are also involved in helping maintain mitochondrial levels of coenzyme A (CoA), which is essential for a number of metabolic reactions.

ALCAR is formed in the mitochondria when L-carnitine joins an acetyl group from acetyl CoA. The enzyme that catalyzes ALCAR formation is carnitine acetyltransferase. In the mitochondria, ALCAR may serve as a source of acetyl groups.

ALCAR can also be transported, via the enzyme carnitine acetyltranslocase, across the inner mitochondrial membrane, where it can then diffuse out of the mitochondria and into the cytoplasm. In the cytosol of the cell, ALCAR can also act as a donor of acetyl groups to amino acids in peptides and proteins. Acetylation of these proteins can alter both their structure and activity.

In a number of recent studies, researchers have reported modulatory effects of ALCAR on brain energy metabolism, neurotrophic factors, neurohormones, synaptic structure, and neuotransmitters. In controlled clinical studies, researchers have documented the beneficial effects of ALCAR in a number of diverse human conditions including Alzheimer’s disease geriatric depression, cerebellar ataxia, type 2 diabetes, neuropathy, and HIV.

Mitochondrial damage

Bruce Ames

Professor of the Graduate School of Biochemistry & Molecular Biology

“We have shown that mtDNA has more oxidative lesions than nuclear DNA and that the level increases more rapidly with age. Methods have been developed to study mtDNA heterogeneity with age. Mitochondria from old rats have decreased membrane potential, cardiolipin, and oxygen utilization, and have increased production of oxidants. This mitochondrial decay has been partially reversed by feeding old rats a mixture of normal mitochondrial metabolites. The treated old rats have considerably increased energy compared to controls and improved brain function.”

ALA, ALC, mitochondria, aging

Tory M. Hagen, Ph.D.

Principal Investigator, Linus Pauling Institute

Assistant Professor, Department of Biochemistry and Biophysics

“...we have identified certain compounds normally found in cells that decline markedly with age, but can be replenished through dietary supplementation. We have termed these compounds “age-essential” micronutrients and have shown that two of these compounds, acetyl-L-carnitine and lipoic acid, when fed to rats, markedly improve mitochondrial function and ameliorate many signs of aging.”


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ALC: highest dose in clinical use seems to be 3 g/day.

ALA: highest dose in clinical use seems to be 800 mg/day.

ALA: The LD50 was 400-500 mg/kg after an oral dosage in dogs.