L-Carnitine 6000mg (10ml)

L-Carnitine (3-hydroxy-4-(trimethylammonio)butanoate) is a quaternary ammonium compound that functions in mammals as an obligate carrier of long-chain fatty-acid acyl groups across the inner mitochondrial membrane, supporting mitochondrial β-oxidation of long-chain fatty acids. The carnitine shuttle — the system of carnitine palmitoyltransferase 1 (CPT1) at the outer mitochondrial membrane, carnitine-acylcarnitine translocase (CACT) at the inner membrane, and carnitine palmitoyltransferase 2 (CPT2) on the matrix side — is the rate-limiting step in long-chain fatty-acid entry into mitochondrial β-oxidation. Carnitine has been studied extensively in mitochondrial biology, exercise physiology, and metabolic-disease research since the carnitine shuttle was characterized in the 1960s-1970s.

This research-supply preparation provides L-carnitine at 600 mg/mL in an aqueous vehicle (6,000 mg per 10 mL vial). The preparation is studied in research-supply context as a standardized aqueous carnitine source for biochemical and metabolic research. Endogenous carnitine biosynthesis occurs in liver, kidney, and brain from lysine and methionine substrates, with the majority of body carnitine stores residing in skeletal muscle.

This page is a research-only educational reference. The preparation is supplied as a research-supply product for laboratory and research-supply use and is not intended for human consumption or any therapeutic application. No medical claims are made on this page.

L-Carnitine is the L-enantiomer of carnitine, a small quaternary ammonium compound with the molecular formula C7H15NO3 and molecular weight 161.2 g/mol. The compound is biologically active only in the L-form; the D-form (D-carnitine) competitively inhibits L-carnitine-dependent processes and is not used in mammalian metabolism. Research-supply L-carnitine preparations specify the L-enantiomer and the typical specifications confirm absence of D-carnitine contamination above defined limits.

The compound is a zwitterion at physiological pH, with a quaternary ammonium nitrogen (positively charged) and a carboxylate (negatively charged). The hydroxyl group at the 3-position of the four-carbon backbone is the acyl-group-attachment site that supports the carnitine-shuttle function: an acyl group from acyl-CoA is transferred to the carnitine hydroxyl, producing acylcarnitine and free coenzyme A. The reverse reaction releases the acyl group as acyl-CoA on the opposite side of the membrane and regenerates free carnitine.

The 600 mg/mL aqueous preparation is at high concentration appropriate for research-supply applications. Endogenous carnitine concentrations in plasma are in the 40-60 μM range (~6-10 μg/mL), so the research-supply preparation is more than four orders of magnitude more concentrated than endogenous plasma levels. The research applications of an aqueous carnitine preparation typically involve dilution into experimental media for cell-culture or enzyme-assay work, rather than direct administration at the per-vial concentration.

Carnitine is a small-molecule metabolic cofactor, not a peptide. It is included in research-supply catalogs that focus on metabolic and mitochondrial research because of its central role in long-chain fatty-acid oxidation and its widespread use as a research tool in mitochondrial biology, exercise physiology, and metabolic-disease modeling.

Carnitine was identified in muscle extracts by Russian biochemists Wladimir Gulewitsch and R. Krimberg in 1905 and named "carnitine" (from the Latin carnis, meaning flesh) reflecting its discovery context in meat extracts. The structural characterization followed over subsequent decades; the absolute configuration as L-carnitine and the chemistry of acyl-carnitine formation were established in the 1940s-1950s.

The mitochondrial function of carnitine was characterized by Irving Fritz at Harvard in the 1950s through experiments demonstrating that carnitine specifically stimulated oxidation of long-chain fatty acids in mitochondrial preparations. Fritz, Bremer, and others over the 1960s-1970s characterized the carnitine palmitoyltransferase enzymes (CPT1 outer mitochondrial membrane, CPT2 inner mitochondrial membrane / matrix-facing) and the carnitine-acylcarnitine translocase that together constitute the carnitine shuttle. The biochemical significance — that long-chain fatty-acyl-CoA cannot cross the inner mitochondrial membrane and must be transported as acylcarnitine through the shuttle — established carnitine as essential for long-chain fatty-acid β-oxidation.

Genetic disorders of the carnitine shuttle and related metabolism were characterized through the 1970s-1990s: primary carnitine deficiency (organic-cation transporter OCTN2 mutations), CPT1 deficiency, CPT2 deficiency, and carnitine-acylcarnitine translocase deficiency. These disorders produce characteristic clinical phenotypes of impaired fatty-acid oxidation (hypoketotic hypoglycemia, cardiomyopathy, rhabdomyolysis) and established the clinical importance of the carnitine shuttle.

Carnitine entered clinical and supplement use through several pathways. Pharmaceutical L-carnitine (Carnitor, levocarnitine) is FDA-approved for primary and secondary carnitine deficiency. Acetyl-L-carnitine (LAC, ALCAR) and propionyl-L-carnitine (PLC) are acylated derivatives that have been studied in research for additional applications. Dietary L-carnitine is widely available as a nutritional supplement, particularly in sports-nutrition contexts where the rationale (with mixed empirical support) is enhancement of fatty-acid oxidation during exercise.

The carnitine shuttle is the obligate transport system for long-chain fatty-acyl groups across the inner mitochondrial membrane. The four key components are:

CPT1 (carnitine palmitoyltransferase 1). Outer mitochondrial membrane enzyme that transfers a long-chain fatty-acyl group from coenzyme A onto carnitine, producing long-chain acylcarnitine and free CoA. CPT1 exists as three tissue-specific isoforms: CPT1A (liver-predominant), CPT1B (muscle-predominant), and CPT1C (brain-predominant, with regulatory rather than catalytic roles). CPT1 is the rate-limiting step of long-chain fatty-acid β-oxidation and is allosterically inhibited by malonyl-CoA, the cytosolic metabolic signal of active fatty-acid synthesis. This malonyl-CoA / CPT1 regulation is one of the central regulatory nodes in mammalian energy metabolism, coordinating fatty-acid oxidation versus fatty-acid synthesis based on cellular energy state.

CACT (carnitine-acylcarnitine translocase). Inner mitochondrial membrane transporter that exchanges cytosolic long-chain acylcarnitine for matrix free carnitine, completing the transport of the acyl group across the inner membrane.

CPT2 (carnitine palmitoyltransferase 2). Inner mitochondrial membrane enzyme on the matrix side that transfers the long-chain fatty-acyl group from carnitine back onto free coenzyme A in the matrix, regenerating long-chain acyl-CoA inside the matrix and free carnitine for return to the cytosol via CACT. The matrix long-chain acyl-CoA then enters β-oxidation through the four enzymatic steps that cleave two carbons per cycle.

Cytosolic short-chain and medium-chain fatty acyl groups (C12 and shorter) can enter mitochondria by alternative carnitine-independent transport mechanisms; the carnitine shuttle is essential specifically for long-chain (C14 and longer) fatty-acid β-oxidation.

The malonyl-CoA / CPT1 regulatory node is the principal mechanism by which fatty-acid oxidation and fatty-acid synthesis are reciprocally regulated. When cytosolic acetyl-CoA carboxylase is active (high insulin / fed state), it converts acetyl-CoA to malonyl-CoA, which both supports fatty-acid synthesis and inhibits CPT1, suppressing fatty-acid oxidation. When AMPK is active (low cellular energy state), it phosphorylates and inhibits acetyl-CoA carboxylase, reducing malonyl-CoA, relieving CPT1 inhibition, and allowing fatty-acid oxidation to proceed.

Beyond the carnitine shuttle, carnitine has additional functions: it buffers the mitochondrial acetyl-CoA / CoA ratio (excess acetyl-CoA can be exported from mitochondria as acetylcarnitine via the carnitine acetyltransferase pathway, allowing the mitochondrion to maintain free CoA for ongoing β-oxidation), and it scavenges acyl groups from accumulated acyl-CoA species in genetic and acquired disorders of fatty-acid oxidation.

Acetyl-L-carnitine (ALCAR, LAC) is a carnitine derivative with the acetyl group esterified to the carnitine hydroxyl. It has been studied for additional research applications including CNS / cognitive research, where the acetylated form is proposed to support cellular acetyl-CoA pools and choline / acetylcholine biosynthesis. Propionyl-L-carnitine (PLC) is another carnitine derivative studied in cardiovascular and muscle research.

L-Carnitine ((R)-3-hydroxy-4-(trimethylammonio)butanoate) has the molecular formula C7H15NO3, molecular weight 161.20 g/mol, and CAS number 541-15-1 for the L-enantiomer (the racemic carnitine has CAS 461-06-3). The compound is a zwitterion at physiological pH, with the quaternary ammonium nitrogen carrying a permanent positive charge and the carboxylate carrying a negative charge under typical conditions. Net charge is therefore zero across a wide pH range, though the molecule has substantial polar surface area and is highly hydrophilic.

The molecule has one stereocenter at the 3-position (the hydroxyl-bearing carbon), with the R-configuration corresponding to the biologically active L-enantiomer. Solid L-carnitine is typically isolated as the inner salt (zwitterion form) or as the L-tartrate, L-fumarate, or hydrochloride salt for improved handling and stability. The free zwitterion is hygroscopic; the tartrate and other salt forms are more amenable to powder handling.

The 600 mg/mL aqueous preparation is at high concentration approaching the saturation limit of L-carnitine in water; the preparation is likely formulated with pH and isotonicity adjustment for stability. The specific formulation excipients and pH appear on the supplier's certificate of analysis.

Research-supply L-carnitine is typically of pharmaceutical-grade or USP-grade purity, with specifications including chiral purity (L-enantiomer content, with limits on D-carnitine contamination), water content, residual solvents from the production process, and microbial limits for aqueous preparations. Production is typically by chemical synthesis or by microbial biosynthesis with appropriate chiral purification. Refer to the supplier's certificate of analysis for the specific lot specifications.

Storage of aqueous L-carnitine preparations is typically at refrigerated temperature (2-8°C) protected from light, with appropriate shelf-life specifications based on stability data. The compound is reasonably stable in solution at neutral to slightly acidic pH; alkaline conditions can promote degradation.

Published research using L-carnitine and the analogous research-supply applications include:

Mitochondrial β-oxidation enzymology. Purified CPT1 and CPT2 enzymes and isolated mitochondrial preparations are studied with carnitine as the obligate acyl-acceptor substrate. Enzyme kinetics, malonyl-CoA inhibition characterization, tissue-isoform comparison, and inhibitor screening (e.g., etomoxir) are foundational research-context applications.

Acylcarnitine profiling. Mass-spectrometric measurement of plasma and tissue acylcarnitine species is a standard tool in inherited-metabolic-disease research and screening, in cardiovascular metabolomics research, and in exercise / metabolic research. The carnitine substrate is foundational to this analytical area, and carnitine isotope labels (e.g., [13C]-carnitine) are used in tracer studies of carnitine and fatty-acid metabolism.

Cell-culture fatty-acid oxidation studies. Cultured cardiomyocytes, hepatocytes, and skeletal-muscle cell lines are studied with carnitine supplementation and depletion to characterize the contribution of long-chain fatty-acid oxidation to cellular energy metabolism. Carnitine-supplemented media support sustained fatty-acid oxidation in cell-culture systems.

Exercise physiology research. The role of muscle carnitine in fatty-acid oxidation during exercise has been extensively studied, particularly in the context of whether oral or intravenous carnitine supplementation increases muscle carnitine stores and affects exercise fatty-acid oxidation. Stable-isotope tracer studies of acyl-carnitine flux during exercise are a standard research methodology.

Inherited metabolic disorder models. Rodent and cell-culture models of carnitine-shuttle disorders (OCTN2 mutations, CPT1 deficiency, CPT2 deficiency, CACT deficiency) and of related fatty-acid oxidation disorders (medium-chain and long-chain acyl-CoA dehydrogenase deficiency) use carnitine and acylcarnitine measurements as endpoints and use exogenous carnitine as a research and therapeutic intervention.

CNS and cognitive research with ALCAR. Acetyl-L-carnitine has been studied in research on cognitive aging, neurodegeneration, and CNS energy metabolism, with rodent and clinical research literature exploring various proposed mechanisms.

Cardiovascular research. Propionyl-L-carnitine has been studied in cardiovascular research particularly in models of ischemic muscle metabolism and peripheral arterial disease.

All applications are research-supply context: laboratory and research-supply use in cells, isolated mitochondria and enzymes, and rodent in-vivo studies. The preparation is not for human consumption. Nothing on this page describes a clinical protocol or therapeutic use.

L-Carnitine sits within the broader carnitine-and-derivatives family and within the mitochondrial fatty-acid-oxidation research toolkit.

L-Carnitine is a small quaternary ammonium compound (~161 Da) that functions as the obligate carrier of long-chain fatty-acid acyl groups across the inner mitochondrial membrane via the carnitine shuttle (CPT1 / CACT / CPT2). The shuttle is the rate-limiting step in long-chain fatty-acid β-oxidation and is the principal site of metabolic regulation coordinating fatty-acid oxidation with fatty-acid synthesis via the malonyl-CoA / CPT1 regulatory node. Carnitine has been studied since the 1960s-1970s as a central mitochondrial metabolism research compound.

This 600 mg/mL aqueous preparation (6,000 mg per 10 mL vial) is supplied for research-supply use in mitochondrial enzymology, acylcarnitine profiling, cell-culture fatty-acid oxidation studies, exercise physiology research, inherited metabolic disorder models, and related metabolic-research applications. The L-enantiomer is the biologically active form; the D-enantiomer is a competitive inhibitor that is not used in mammalian metabolism.

The preparation is supplied as a research-supply product for laboratory and research-supply use, not as a medicine and not as a dietary supplement. Pharmaceutical L-carnitine (Carnitor / levocarnitine) is FDA-approved for primary carnitine deficiency and certain secondary deficiency contexts, but those clinical products are distinct from research-supply preparations. The educational content on this page provides scientific and historical context for the research-supply application only.