N,N-Dimethylglycine HCl

CAS Number	2491-06-7 (verified against PubChem CID 75605)
Molecular Formula / MW	C4H9NO2·HCl / 139.58 g/mol (free base: C4H9NO2, 103.12)
Chemical Class	N-methylated glycine derivative — 2-(dimethylamino)acetic acid, as the hydrochloride salt
Metabolic Position	An intermediate in one-carbon metabolism: betaine → DMG → sarcosine → glycine. Formed when betaine donates a methyl group to homocysteine
Endogenous?	Yes — DMG is a normal human metabolite, not a xenobiotic. It is also a proposed biomarker of protein degradation
Typical Standardisation	DMG HCl by HPLC or titration; ≥98–99% commercial grade
Claim Strength (Overview)	Null for autism (RCTs); Null for progressive MS (RCT); Emerging at best for athletic performance
Buy from Herbuno	N N Dimethyl Glycine HCL Powder →

Name origin: N,N-dimethylglycine is exactly what the name describes — glycine bearing two methyl groups on the nitrogen, supplied commercially as the hydrochloride salt for stability and handling. It has also traded under the name "vitamin B15" or "pangamic acid," a designation that deserves to be retired: DMG is not a vitamin, has no deficiency syndrome, and "pangamic acid" was never a chemically coherent substance. Its actual biochemistry is genuine and specific. DMG sits in one-carbon metabolism: betaine (trimethylglycine) donates a methyl group to homocysteine via betaine-homocysteine methyltransferase, regenerating methionine and leaving DMG behind. DMG is then demethylated to sarcosine and thence to glycine. It is a normal human metabolite, an output of a methylation reaction rather than a methyl donor itself — which is a distinction the marketing tends to blur. Research trajectory, and this page’s purpose: DMG has been marketed as a dietary supplement since 1974, promoted heavily for athletic performance and, most prominently, for autism. Both claims have been tested. This page reports what the trials found. Commercial source: Synthetic. DMG HCl is not a botanical extract.

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Evidence for N,N-Dimethylglycine HCl Applications

The autism claim — historically the largest driver of DMG sales — did not survive controlled testing, and the history is instructive. A double-blind, placebo-controlled crossover pilot study explicitly noted that although influential non-medical literature regarded DMG as more effective than usual psychopharmacologic drugs, there had been no studies of DMG using currently accepted research methodology; the investigators then ran one, in eight autistic males across a 3½-month protocol with drug-free baselines and two one-month double-blind DMG-versus-placebo trials, using the Campbell-NIMH rating scale and individualised measures (Bolman 1999). A reputation built entirely on uncontrolled testimonial, then tested, is a familiar shape. An earlier controlled trial by Findling and colleagues reached similarly unsupportive conclusions. Claim strength: Null.

The pattern held when DMG was tested in a different neurological indication. A one-year double-blind, placebo-controlled randomized trial in 30 patients with progressive multiple sclerosis — premised on the proposition that oral DMG enhances tissue oxygen utilisation and reduces fatigue — found no treatment effects between the placebo and DMG groups for disability, fatigue, cognitive, or gait parameters, with no differences between study groups on any evaluated parameter (Wolfsegger 2021). Two indications, two well-designed trials, two nulls. Claim strength: Null.

The athletic performance claim — that DMG improves endurance and oxygen utilisation — rests on a mechanistic story that does not hold up under scrutiny. The proposed mechanism, that DMG "enhances oxygen utilisation by tissue," has no established biochemical basis: DMG is a product of methyl transfer, not an oxygen carrier or a respiratory cofactor, and there is no plausible pathway by which supplementing it would increase tissue oxygen extraction. The human performance literature is old, small, and largely negative. A formulator building an endurance product on DMG is building on a mechanism that was asserted rather than demonstrated. Claim strength: Emerging at best.

What is DMG actually good for, then? The honest answer is that its established roles are analytical and research ones rather than therapeutic. DMG is used in comparative analysis with other N-methylated glycines such as sarcosine and betaine, in the development of glycine-based ionic liquids and emulsifiers, and as a substrate to identify and characterise amino acid methyltransferases. It is potentially useful as a biomarker of protein degradation in COPD patients. It also has a substantial and separate life in veterinary and animal nutrition, where it is widely used — a market Herbuno serves and which does not depend on the human claims. Claim strength: Moderate (research and analytical use).

One coherent thread worth stating without overselling: because DMG is downstream of betaine in the homocysteine remethylation pathway, elevated plasma DMG is a marker of betaine-dependent methylation flux, and the DMG/betaine ratio has been examined as an index of that pathway. This is real biochemistry and it is genuinely interesting. But it makes DMG a readout, not a lever — and it is precisely the reason that supplementing DMG is not a methylation intervention. If a formulator wants to support the betaine-homocysteine pathway, the intervention is betaine, the methyl donor, not DMG, the spent product. Claim strength: High (established biochemistry).

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Dosage & Formulator Specification

Herbuno carries N,N-Dimethyl Glycine HCl Powder. We are listing it with the evidence stated plainly: the autism and multiple sclerosis claims failed in controlled trials, and the athletic-performance mechanism has no established biochemical basis. Herbuno will not support marketing that presents DMG as "vitamin B15" or as a methyl donor. Substantial legitimate demand exists in animal nutrition and in research and analytical applications, and buyers in those categories should say so at enquiry.

Human trial dosing has been modest and the trials that used it found nothing: the autism pilot used low-dose DMG, and the MS trial ran a year at supplement-typical doses without effect on any parameter. Consumer products commonly supply 100–500 mg/day. Because no human indication has been established, no dose can honestly be presented as clinically validated, and escalating the serving is not a route to an effect that the controlled trials did not find at any dose tested. Animal-nutrition inclusion rates are a separate matter and are set by species and application.

Analytical verification should specify DMG HCl by HPLC or titration (≥98–99%), with related substances quantified — sarcosine (the monomethyl homologue), betaine (the trimethyl homologue), and free glycine are the relevant impurities and the ones a synthesis route is most likely to carry. Note that the hydrochloride salt is hygroscopic; moisture control in storage and packaging must be specified. Confirm whether a stated assay refers to the salt (MW 139.58) or the free base (103.12) — a 35% difference that has caused real labelling errors. Residual solvent testing appropriate to the synthetic route applies.

DMG is a normal human metabolite present in the diet and formed endogenously in one-carbon metabolism, and is well tolerated; it has an extensive safety record in both human supplement and animal-feed use, with no significant toxicity signal at customary intakes and no adverse findings reported in the year-long MS trial. The issue with DMG is therefore not safety but efficacy, and a supplier owes a buyer honesty about that. The autism claim, which built the market, failed when properly tested. The MS trial was null across every parameter. The performance mechanism was asserted, not demonstrated. And the "vitamin B15" framing should be abandoned outright: DMG is not a vitamin, there is no deficiency syndrome, and "pangamic acid" was never a coherent chemical entity. An ingredient can be perfectly safe and still not do what it is sold to do.

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Frequently Asked Questions — N,N-Dimethylglycine HCl

Does DMG help autism?
No — and this is the claim that built the market. A double-blind placebo-controlled crossover trial noted that DMG's reputation rested on influential non-medical literature with no studies using accepted methodology. They ran one. It did not support the claim, and an earlier controlled trial by Findling reached similar conclusions. A reputation built on uncontrolled testimonial, then tested.

Does DMG improve athletic endurance?
The mechanism does not hold up. The claim that DMG "enhances tissue oxygen utilisation" has no established biochemical basis — DMG is a product of methyl transfer, not an oxygen carrier or respiratory cofactor, and there is no plausible pathway by which supplementing it would raise oxygen extraction. The human performance literature is old, small, and largely negative.

Is DMG a methyl donor?
No, and this is the key misunderstanding. DMG is what is left over after betaine donates a methyl group to homocysteine — it is the spent product, not the donor. That makes it a readout of methylation flux, not a lever on it. If you want to support the betaine-homocysteine pathway, the intervention is betaine.

Is DMG safe?
Yes — it is a normal human metabolite with an extensive safety record and no significant toxicity signal, including in a year-long MS trial. The problem with DMG is not safety but efficacy. An ingredient can be perfectly safe and still not do what it is sold to do. Legitimate demand does exist in animal nutrition and research applications.

Related compounds: Betaine, Choline, L-Glutathione, Adenosine

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Claim-strength scale – High = multiple human RCTs; Moderate = limited trials or strong preclinical convergence; Emerging = early-stage lab or animal data.

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