Pyridoxine
Compiled from published pharmacological and botanical literature. Not independently verified by Herbuno. Spotted an error or have a correction? Flag it below →
| Compound | Pyridoxine (one of the vitamin B6 vitamers) |
|---|---|
| Chemical class | Pyridine-ring vitamin — the alcohol vitamer, supplied as the hydrochloride |
| CAS | 58-56-0 (pyridoxine HCl) · 65-23-6 (pyridoxine) |
| Salt equivalence | 205.64 g/mol HCl → ~82.3% pyridoxine |
| Activation route | Pyridoxal kinase, then FMN-dependent PNPO — so riboflavin is required |
| Safety limit | Dose-dependent sensory peripheral neuropathy — EFSA UL revised to 12 mg/day (2023) |
| Claim strength | High for the neuropathy risk and activation chemistry |
| Buy from Herbuno | Liposomal Vitamin B6 (Pyridoxine HCl) Powder · plain pyridoxine HCl / P5P: availability on request |
| 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: From the pyridine ring that forms its core, with the suffix recording its vitamin status. Pyridoxine was isolated in 1938 and was initially taken to be the whole of vitamin B6; the discovery that pyridoxal and pyridoxamine are equally vitamers came later, which is why "vitamin B6" is a family and "pyridoxine" is one member of it.
Why the distinction matters: Vitamin B6 comprises six interconvertible forms — pyridoxine, pyridoxal and pyridoxamine, plus their 5'-phosphates. Only pyridoxal 5'-phosphate is the active cofactor. Pyridoxine, the alcohol form, is the cheapest and most stable and therefore the standard commercial article, but it must be phosphorylated by pyridoxal kinase and then oxidised by pyridoxine-5'-phosphate oxidase to become active. A specification reading "vitamin B6" does not say which vitamer, and the vitamers are not equivalent in safety or in activation requirement.
The activation dependency: Pyridoxine-5'-phosphate oxidase is an FMN-dependent flavoenzyme, which means riboflavin status directly determines how effectively pyridoxine is converted to the active P5P form. A B6 formulation without adequate riboflavin supplies a precursor the body may not be able to activate efficiently, and this is a real mechanistic argument for a B-complex over a single vitamin.
The safety position: Pyridoxine is the only water-soluble vitamin with an upper intake level set on the basis of demonstrated neurotoxicity. High-dose pyridoxine causes a dose-dependent sensory peripheral neuropathy, documented since the 1980s, and regulatory limits have tightened as cases at lower doses have accumulated. EFSA revised its tolerable upper intake level to 12 milligrams daily for adults in 2023, substantially below earlier figures, and Australia and New Zealand introduced mandatory warning labelling above 10 milligrams in 2022.
Evidence for Pyridoxine Applications
The neuropathy risk is the governing fact and the regulatory position has tightened sharply. High-dose pyridoxine causes a dose-dependent sensory peripheral neuropathy — paraesthesia, numbness, gait disturbance, sometimes incompletely reversible — first clearly documented in the 1980s at gram-level intakes, with subsequent cases reported at progressively lower doses. EFSA revised its tolerable upper intake level for adults to 12 milligrams daily in 2023, well below the 25 milligram figure it had previously used and far below the 100 milligram US level, and Australia and New Zealand mandated warning labelling above 10 milligrams in 2022. Any formulation carrying B6 needs the current limit for each target market, not a remembered one. Claim strength: High.
There is an open question about whether pyridoxine specifically, rather than vitamin B6 generally, is the neurotoxic form. The hypothesis is that unphosphorylated pyridoxine can competitively inhibit P5P-dependent enzymes when present at high concentration, so that high-dose pyridoxine produces a functional B6 deficiency at the enzyme level despite high circulating vitamin. If correct, pyridoxal 5'-phosphate would carry a lower risk at equivalent B6 activity. The hypothesis is mechanistically coherent and actively discussed but not settled, and regulatory limits currently apply to B6 as a class rather than to pyridoxine alone. Claim strength: Emerging.
Riboflavin is required to activate pyridoxine, which is a real formulation dependency. Pyridoxine is phosphorylated by pyridoxal kinase and then oxidised to pyridoxal 5'-phosphate by pyridoxine-5'-phosphate oxidase, an FMN-dependent flavoenzyme. Riboflavin status therefore constrains the conversion, and in riboflavin-insufficient individuals pyridoxine supplementation may raise circulating pyridoxine without proportionally raising active P5P. A B6 product without riboflavin is supplying a precursor that may not be efficiently activated. Claim strength: Moderate.
P5P is a separate article with different properties, and the choice between them is not trivial. Pyridoxal 5'-phosphate bypasses the activation steps, which is the argument for it, but it is less stable, more expensive, and in practice is dephosphorylated in the intestine before absorption and rephosphorylated afterwards — so it does not straightforwardly bypass metabolism the way marketing implies. Where it has a stronger case is in the hypothesis above, and in the rare genetic PNPO deficiency where the conversion enzyme is absent. Specify by CAS number and convert the declaration. Claim strength: Moderate.
The cofactor role is extensive and settled biochemistry, which is why both deficiency and excess are consequential. Pyridoxal 5'-phosphate is the cofactor for well over a hundred enzymes, including essentially all transaminases, glycogen phosphorylase, the decarboxylases producing GABA, serotonin, dopamine and histamine, cystathionine beta-synthase in the transsulphuration route, delta-aminolevulinic acid synthase in haem synthesis, and the kynurenine pathway enzymes. No other vitamin-derived cofactor serves so many reactions. Claim strength: High.
The nausea-of-pregnancy use is a drug indication rather than a supplement claim and should not be borrowed. Pyridoxine with doxylamine is an approved pharmaceutical combination for nausea and vomiting of pregnancy in several jurisdictions, and pyridoxine alone has trial support for that indication. It is a disease endpoint, and the doses used sit above the revised EFSA upper limit, which makes it doubly unavailable to a supplement. It belongs in technical documentation only. Claim strength: Moderate for the indication; not usable as a claim.
Sourcing pyridoxine from Herbuno. We hold pyridoxine hydrochloride in a liposomal format; plain pyridoxine HCl and pyridoxal 5'-phosphate are availability on request.
Check the current upper limit for every target market before fixing the inclusion. EFSA revised its adult tolerable upper intake level to 12 milligrams daily in 2023 and Australia and New Zealand mandated warning labelling above 10 milligrams in 2022, so a formulation designed against older figures may now be non-compliant or require label changes. Specify the vitamer by CAS number — "vitamin B6" does not say which. All lots ship with CoA and MSDS; request a quotation for pilot or bulk volumes.
Dosage & Formulator Specification
Dose on pyridoxine content and against the current market limit. Pyridoxine HCl is 205.64 g/mol giving approximately 82.3% pyridoxine, so a 1.4 milligram pyridoxine target requires about 1.70 milligrams of the hydrochloride. Adult reference intakes sit around 1.3 to 1.7 milligrams daily. The binding consideration is not the reference intake but the upper limit: EFSA's revised adult figure is 12 milligrams daily, Australia and New Zealand require warning labelling above 10 milligrams, and other markets differ. Design to the most restrictive target market.
The regulatory change is recent enough that existing formulations need review rather than assumption. Products designed when the working upper limit was 25 or 100 milligrams may now exceed the EFSA figure by a wide margin, and a high-dose B6 or B-complex that was compliant a few years ago may not be today in the European market. This is a reformulation or market-withdrawal question rather than a labelling one at high inclusion rates, and it is worth auditing a portfolio against the current numbers rather than waiting for a registration to fail.
Handling is easy, which is part of why pyridoxine rather than the other vitamers dominates. Pyridoxine hydrochloride is freely soluble in water at around 22 grams per 100 millilitres, stable to heat in the dry state and reasonably stable in solution across a moderate pH range, and only mildly hygroscopic. It is light-sensitive, though less so than riboflavin, so amber or opaque packaging is advisable. It flows well as a crystalline powder, blends uniformly, and is essentially tasteless at nutritional inclusion rates.
Co-formulation has one dependency worth building in deliberately. Pyridoxine's conversion to active P5P requires FMN-dependent pyridoxine-5'-phosphate oxidase, so riboflavin should accompany it rather than being assumed adequate. Beyond that, B6 participates in transsulphuration with folate and B12 in homocysteine management, which is the basis for the conventional folate-B12-B6 combination, and that combination has a coherent mechanistic rationale even where the clinical outcome evidence on homocysteine lowering has been disappointing.
For analytical control, specify the vitamer by CAS number and assay by HPLC with the basis stated — pyridoxine or the hydrochloride. Specify chloride to confirm salt stoichiometry. Standard coverage includes heavy metals, residual solvents, microbiological limits, loss on drying and sulphated ash, with the production route named. Where pyridoxal 5'-phosphate is specified instead, note that it is less stable, requires its own stability data rather than inheriting pyridoxine's, and should be assayed as P5P with free pyridoxal as a degradation limit.
One point of vitamer discipline worth carrying into customer documentation. "Vitamin B6" names a family of six interconvertible compounds, and a specification using that term without naming the vitamer is incomplete: pyridoxine hydrochloride, pyridoxal 5'-phosphate and pyridoxamine dihydrochloride differ in cost, stability, declaration basis and — on the open question above — possibly in safety at equivalent B6 activity. A customer asking for "B6" should be asked which, and a customer asking for P5P on the grounds that it bypasses metabolism should be told that P5P is dephosphorylated in the intestine before absorption and rephosphorylated afterwards, so the bypass is partial at best. The stronger argument for P5P is the inhibition hypothesis and PNPO deficiency, not absorption.
Frequently Asked Questions — Pyridoxine
What is the upper limit for B6 now?
Lower than most formulations assume. EFSA revised its adult tolerable upper intake level to 12 mg daily in 2023, well below the 25 mg it previously used and far below the 100 mg US figure, and Australia and New Zealand mandated warning labelling above 10 mg in 2022. Design to the most restrictive target market and check the current number rather than a remembered one.
Why does B6 have an upper limit at all?
Demonstrated neurotoxicity — it is the only water-soluble vitamin whose UL rests on it. High-dose pyridoxine causes a dose-dependent sensory peripheral neuropathy with paraesthesia, numbness and gait disturbance, sometimes incompletely reversible, first documented at gram intakes in the 1980s with subsequent cases at progressively lower doses.
Is P5P safer than pyridoxine?
Possibly, but it is not settled. The hypothesis is that unphosphorylated pyridoxine can competitively inhibit P5P-dependent enzymes at high concentration, producing a functional B6 deficiency at the enzyme level despite high circulating vitamin. Mechanistically coherent and actively discussed, not established — and regulatory limits currently apply to B6 as a class.
Does P5P bypass metabolism?
Only partially, despite the marketing. P5P is dephosphorylated in the intestine before absorption and rephosphorylated afterwards, so it does not straightforwardly skip the conversion steps. Its stronger arguments are the inhibition hypothesis above and the rare genetic PNPO deficiency, not absorption. It is also less stable and more expensive.
Why does my B6 product need riboflavin?
Because pyridoxine-5'-phosphate oxidase, which performs the final activation step to P5P, is an FMN-dependent flavoenzyme. Riboflavin status therefore constrains the conversion, and in riboflavin-insufficient individuals pyridoxine supplementation can raise circulating pyridoxine without proportionally raising active P5P.
What should a specification say?
Which vitamer, by CAS number. "Vitamin B6" names a family of six interconvertible compounds that differ in cost, stability, declaration basis and possibly safety at equivalent activity. Pyridoxine HCl is 58-56-0 at 82.3% pyridoxine. If a customer asks for "B6", ask which.