N-Acetyl-L-Carnitine HCl
Compiled from published pharmacological and botanical literature. Not independently verified by Herbuno. Spotted an error or have a correction? Flag it below →
| Compound | N-Acetyl-L-carnitine hydrochloride (ALCAR HCl) |
|---|---|
| Chemical class | Hydrochloride salt of the acetyl ester of L-carnitine |
| CAS | 5080-50-2 (acetyl-L-carnitine HCl) · 3040-38-8 (acetyl-L-carnitine inner salt) |
| Molecular weight | 239.70 g/mol (ALCAR free 203.24 · L-carnitine 161.20) |
| Equivalence | Approx. 84.8% acetyl-L-carnitine · approx. 67.3% carnitine-equivalent |
| Key distinction | Crosses the blood-brain barrier; donates acetyl groups for acetyl-CoA |
| Claim strength | Moderate for diabetic neuropathy; Emerging for cognitive endpoints |
| Buy from Herbuno | N-Acetyl-L-Carnitine HCl Powder |
| Origin | Processed / Sourced from India |
| MOQ | R&D 100 g / 250 g (subject to stock) · Pilot batch 1–5 kg · Bulk 10 kg, 25 kg and above |
| Lead Time | Dispatch within 72 hrs from stock · fresh-batch production (typically 50 kg+): 10 working days |
| Documentation | CoA & MSDS standard with every lot |
Name origin: The acetyl ester of L-carnitine, formed on the hydroxyl group, supplied as the hydrochloride and almost universally abbreviated ALCAR in the trade. Acetyl-L-carnitine is not a synthetic contrivance: it occurs endogenously as the product of carnitine acetyltransferase, which buffers the mitochondrial acetyl-CoA pool by transferring acetyl groups onto carnitine. The commercial material reproduces a physiological metabolite.
Why the acetyl ester exists as a separate product: The acetyl group changes the molecule's distribution and its functional role. Acetyl-L-carnitine crosses the blood-brain barrier where carnitine itself does so poorly, which shifts the target tissue from skeletal muscle and liver to the central nervous system. It also carries a transferable acetyl group, making it a donor for acetyl-CoA and, by extension, a contributor to acetylcholine synthesis. These are genuinely different properties, not a reformulation of the same ingredient.
Research trajectory: ALCAR has a substantially larger independent clinical literature than any carnitine salt form. The best-developed body of work is in diabetic peripheral neuropathy, where controlled trials have examined ALCAR for pain and nerve regeneration endpoints. Further threads cover age-related cognitive decline, chemotherapy-induced peripheral neuropathy, depression as an adjunct, and male fertility. ALCAR has pharmaceutical status in several European countries, which places it in a different regulatory position from the carnitine salts in some markets.
Commercial source: ALCAR is produced by acetylation of L-carnitine, itself made by chemoenzymatic synthesis or fermentation, then crystallised as the hydrochloride. The hydrochloride is the common article because the inner salt is markedly more hygroscopic. Chirality is as critical here as for carnitine, and free L-carnitine is the relevant process-related impurity.
Evidence for N-Acetyl-L-Carnitine HCl Applications
Blood-brain barrier penetration is the real distinction and the basis for every central application. L-carnitine crosses the blood-brain barrier poorly; acetyl-L-carnitine crosses it readily, apparently via organic cation transport, and raises brain carnitine and acetylcarnitine concentrations. This is why ALCAR, rather than carnitine, is the form used in essentially all of the neurological and cognitive research. A product targeting central effects should specify ALCAR rather than a carnitine salt, and a carnitine salt should not borrow ALCAR's central literature. Claim strength: High.
The acetyl group is functionally active, not a delivery device. Acetyl-L-carnitine donates its acetyl group to coenzyme A, contributing to the mitochondrial acetyl-CoA pool, and acetyl-CoA is the substrate for acetylcholine synthesis via choline acetyltransferase. This gives ALCAR a mechanistic connection to cholinergic transmission that carnitine itself lacks, and it is the basis for pairing ALCAR with choline sources in nootropic formulations. The mechanism is sound; the magnitude of any cholinergic contribution from a supplemental dose is not established. Claim strength: Moderate for the mechanism, Emerging for the functional consequence.
Diabetic peripheral neuropathy is ALCAR's best-developed clinical application. Controlled trials, several of reasonable size and duration, have examined ALCAR at doses in the range of 1 to 3 grams daily for neuropathic pain, nerve conduction parameters and nerve fibre regeneration, with meta-analytic work reporting benefit for pain endpoints. The evidence is not uniform and effect sizes vary, but this is a real clinical literature rather than a mechanistic extrapolation. It is also a disease endpoint, so it cannot be used in supplement claims regardless of its strength. Claim strength: Moderate.
Cognitive endpoints in healthy adults are considerably weaker than the category implies. Meta-analytic work on ALCAR in mild cognitive impairment and age-related cognitive decline has reported modest benefits, but the trials are heterogeneous, generally in older or impaired populations, and the translation to cognitive enhancement in healthy adults is not supported. ALCAR's position in the nootropic market substantially exceeds its evidence in that specific application, and a formulator should know the difference between the impaired-population literature and the claim being made. Claim strength: Emerging.
Chemotherapy-induced peripheral neuropathy is a cautionary case worth knowing. Despite the plausible rationale from the diabetic neuropathy work, a randomised controlled trial of ALCAR for prevention of taxane-induced peripheral neuropathy reported worse neuropathy outcomes in the ALCAR arm. That result does not transfer to other settings, but it does demonstrate that the neuroprotective rationale is not universally reliable and that ALCAR should not be assumed benign in every neurological context. This is the kind of finding that belongs in technical documentation rather than being quietly omitted. Claim strength: Moderate for the specific finding.
Dose arithmetic involves two conversion layers and is commonly handled incorrectly. ALCAR HCl at 239.70 g/mol contains approximately 84.8% acetyl-L-carnitine and approximately 67.3% carnitine-equivalent. A clinical dose of 2 grams of acetyl-L-carnitine therefore requires about 2.36 grams of ALCAR HCl. Whether a label declaring "acetyl-L-carnitine 500 mg" means the hydrochloride or the free acetylcarnitine is frequently unstated, and the 15% difference compounds with the further ambiguity if a customer is converting to carnitine-equivalent. Claim strength: High.
Sourcing N-acetyl-L-carnitine HCl from Herbuno. We supply ALCAR HCl alongside the L-carnitine salts.
Specify whether the declared quantity is ALCAR HCl or free acetyl-L-carnitine — the gap is about 15%, and a further conversion is needed if a customer is reasoning in carnitine-equivalent terms. Note also that ALCAR has pharmaceutical status in several European countries, so the regulatory position differs from the carnitine salts and should be confirmed per target market. All lots ship with CoA and MSDS; request a quotation for pilot or bulk volumes.
Dosage & Formulator Specification
Three figures matter and should never be conflated. ALCAR HCl is 239.70 g/mol; it contains approximately 84.8% acetyl-L-carnitine and approximately 67.3% carnitine-equivalent. Clinical doses in the diabetic neuropathy literature run 1 to 3 grams of acetyl-L-carnitine daily, usually divided, which corresponds to roughly 1.18 to 3.54 grams of ALCAR HCl. Cognitive trials have generally used 1.5 to 3 grams daily. State on the specification which basis the declared quantity uses, because all three appear in the market and the differences are well outside analytical tolerance.
Regulatory status deserves checking before formulation rather than at registration. ALCAR is a registered pharmaceutical in several European countries, which means a supplement containing it may face a different classification than one containing a carnitine salt, and the position differs by market. The diabetic neuropathy evidence, whatever its strength, is a disease endpoint and cannot be used in supplement claims anywhere. For a product intended across several jurisdictions, resolve the most restrictive classification first.
Handling is dominated by hygroscopicity, which the hydrochloride reduces but does not eliminate. The acetyl-L-carnitine inner salt is markedly hygroscopic, which is why the hydrochloride is the commercial article; the hydrochloride is itself moderately hygroscopic and requires sealed, foil-lined packaging with desiccant for extended storage, and humidity control during blending and encapsulation. It is freely soluble in water, giving acidic solutions from the hydrochloride, and has a sharply bitter and slightly sour taste that is difficult to mask at clinical doses. Capsules are the usual format for that reason.
Co-formulation follows the mechanism. Pairing ALCAR with a choline source — citicoline, alpha-GPC or choline bitartrate — is mechanistically coherent, since ALCAR contributes acetyl groups to the acetyl-CoA pool and choline supplies the other substrate for acetylcholine synthesis. Pairing it with alpha-lipoic acid is common in the neuropathy-adjacent space and rests on the mitochondrial rationale. In both cases the combination is a design rationale rather than a tested synergy, and should be described that way. The chloride and acid contribution is modest at typical doses but should be counted in a formula stacking several hydrochlorides.
For analytical control, specify acetyl-L-carnitine identity and assay with the basis stated, optical rotation or chiral chromatography confirming L-configuration, chloride confirming salt stoichiometry, and water content given the material's moisture sensitivity. Free L-carnitine is the critical process-related and degradation impurity — it arises from incomplete acetylation and from hydrolysis in storage, and it is the direct indicator of material quality and handling history, so specify it as a limit test. Standard coverage includes heavy metals, residual solvents, microbiological limits, loss on drying and sulphated ash.
On form selection the distinction is genuinely functional rather than cosmetic, which is unusual in this family. The carnitine salts and ALCAR are not interchangeable: carnitine salts target peripheral fatty acid oxidation and are limited by insulin-dependent muscle uptake, while ALCAR crosses the blood-brain barrier and carries a transferable acetyl group, which is why the neurological literature uses it exclusively. A sports or metabolic formulation should specify a carnitine salt; a cognitive or neuropathy-adjacent formulation should specify ALCAR. Substituting one for the other on price or availability changes what the product does, and the two should not share claim language. Where a formulation wants both targets, both can be included, dosed separately on their respective bases.
Frequently Asked Questions — N-Acetyl-L-Carnitine HCl
How is ALCAR different from L-carnitine?
The acetyl group changes the target tissue and adds a function. Acetyl-L-carnitine crosses the blood-brain barrier readily where carnitine does so poorly, which is why all the neurological and cognitive research uses ALCAR. It also donates its acetyl group to the acetyl-CoA pool, connecting it to acetylcholine synthesis. These are different properties, not a reformulation.
What does a declared quantity actually mean?
Check, because three bases circulate. ALCAR HCl at 239.70 g/mol is about 84.8% acetyl-L-carnitine and about 67.3% carnitine-equivalent. A 2 gram acetyl-L-carnitine clinical dose needs about 2.36 grams of the hydrochloride. State the basis on the specification — the differences are well outside analytical tolerance.
How strong is the cognitive evidence?
Weaker than the nootropic market implies. Meta-analytic work in mild cognitive impairment and age-related decline reports modest benefit, but the trials are heterogeneous and in older or impaired populations. Translation to enhancement in healthy adults is not supported. The diabetic neuropathy literature is the stronger body — and it is a disease endpoint, so unusable in supplement claims.
Is ALCAR always neuroprotective?
No, and this is worth knowing. A randomised controlled trial of ALCAR for prevention of taxane-induced peripheral neuropathy reported worse neuropathy outcomes in the ALCAR arm. It does not transfer to other settings, but it shows the neuroprotective rationale is not universally reliable. It belongs in technical documentation rather than being omitted.
What impurity should I specify?
Free L-carnitine, as a limit test. It arises both from incomplete acetylation during manufacture and from hydrolysis in storage, so it is the direct indicator of material quality and handling history. Also water content, given the material's moisture sensitivity, and optical rotation on the carnitine configuration.
Can I substitute ALCAR for a carnitine salt or vice versa?
Not without changing what the product does. Carnitine salts target peripheral fatty acid oxidation and are limited by insulin-dependent muscle uptake; ALCAR crosses into the CNS and carries a transferable acetyl group. Sports and metabolic formulations want a carnitine salt; cognitive and neuropathy-adjacent ones want ALCAR. They should not share claim language.