Pyritinol
Encephabol, Encefabol, Cerbon 6 — pyrithioxine, two vitamin B6 molecules joined by a disulfide
Pyritinol (Encephabol, Encefabol, Cerbon 6 — pyrithioxine, two vitamin B6 molecules joined by a disulfide) is a cognitive & mood research compound. Two pyridoxine molecules bridged by a disulfide, which makes it a thiol drug wearing a vitamin's structure. It is not a vitamin B6 supplement and does not behave as one: the disulfide is what gets reduced in the body, and it is also what puts this molecule in the same chemical family as penicillamine and tiopronin — drugs with a well-documented capacity to trigger autoimmune skin and liver reactions. The nootropic claim rests on increased glucose uptake and cholinergic effects reported in old European work rather than on a named receptor.
Pyritinol quick facts
| Route | Oral |
| Frequency | 3x Daily in the clinical literature |
| Half-life | ~2.5 hrs for the parent; the reduced thiol is the reactive species |
| Forms | Oral |
| Evidence level | A prescription or pharmacy medicine in parts of Europe and Asia, never approved in the United States. The randomized evidence that resolves is small and mostly negative. |
Sold as a gentle B6-derived nootropic and chemically nothing of the sort — the disulfide bridge that defines it is the same structural feature that makes penicillamine a drug with a monitoring requirement. The randomized record is thinner than the reputation: the trial that resolves cleanly is a double-blind controlled study in newborns after birth asphyxia, and it found no significant difference at one year. It also turns up in a systematic review of hangover interventions, where the evidence for every agent examined was rated very low quality. Treating it as a vitamin because it is built from vitamins is the error this page exists to prevent.
How Pyritinol works
Two pyridoxine molecules bridged by a disulfide, which makes it a thiol drug wearing a vitamin's structure. It is not a vitamin B6 supplement and does not behave as one: the disulfide is what gets reduced in the body, and it is also what puts this molecule in the same chemical family as penicillamine and tiopronin — drugs with a well-documented capacity to trigger autoimmune skin and liver reactions. The nootropic claim rests on increased glucose uptake and cholinergic effects reported in old European work rather than on a named receptor.
Proposed benefits
Researched for focus, memory, neuroprotection, mood and stress resilience.
Where to get Pyritinol
Buy Pyritinol at RUPharma →The evidence for Pyritinol
Graded by what exists behind each claim.
✅ Clinically validated
- The randomized trial that resolves cleanly is null: a double-blind controlled trial of pyritinol for post-asphyxial encephalopathy in term babies found no statistically significant difference in neurodevelopmental outcomes at one year (Nair 2009).
- Its other randomized appearance is in a systematic review of hangover interventions, whose verdict on every agent examined was very low quality evidence (Roberts 2022).
- No trial has ever been run in healthy adults with a cognitive endpoint — the claim the retail market is built on.
📊 Correlative data
- It had a second career as a disease-modifying antirheumatic drug, which is the setting in which patients took it for years under observation and the serious thiol-drug reactions were recorded. The modern network meta-analysis of that class finds methotrexate the reference standard (Guski 2023).
- Its chemistry places it with penicillamine and tiopronin, the drugs associated with drug-induced pemphigus and lichenoid eruptions (Boch 2021).
🧪 Theoretical / extrapolated
- Two pyridoxine molecules joined by a disulfide — and that bond is both the mechanism and the hazard. It is what makes the molecule lipophilic enough to cross membranes B6 does not, and what makes it a thiol drug.
- It does not act as vitamin B6: the enzyme that phosphorylates pyridoxine to its active form works on the free vitamin, not on a disulfide-linked dimer.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Pyritinol actually does
Two vitamins joined by a bond that makes it not a vitamin. Pyritinol is two molecules of pyridoxine — vitamin B6 — connected through a disulfide bridge. That single bond is the whole pharmacology and the whole safety story. It is what makes the molecule lipophilic enough to cross membranes that pyridoxine does not, and it is what makes it a thiol drug.
Why it does not act as vitamin B6, in one step. Pyridoxine becomes active as pyridoxal 5-phosphate, and the enzyme that phosphorylates it works on the free vitamin. A disulfide-linked dimer with the hydroxymethyl groups engaged is not that substrate. Taking pyritinol is therefore not a way of taking B6, and the reverse is also true: B6 supplementation does not reproduce anything pyritinol does.
The company it keeps chemically. Reduce that disulfide in vivo and the molecule joins the family that includes penicillamine, tiopronin and bucillamine — drugs whose reactive sulfhydryl group is associated with drug-induced pemphigus, lichenoid eruptions and cholestatic liver injury. Boch 2021 reviews lichen planus and its lichenoid drug-induced mimics, which is the dermatological category this chemistry sits in. That is a structural argument about risk, and it is stronger than an argument from the absence of reported harm on a drug nobody studies.
What the nootropic claim actually rests on. An older European literature reporting increased cerebral glucose uptake and cholinergic effects, with no named receptor and no modern binding work. Malik 2022 catalogs it among cognitive enhancers with doses and side effects. Being catalogued is not being characterized, and sixty years on there is no target for this molecule the way there is for a modern drug.
Cell, rodent, human — and where it stops
The randomized trial that resolves cleanly is null. Nair 2009 is a randomized double-blind controlled trial of pyritinol for post-asphyxial encephalopathy in term babies, and it found no statistically significant difference in neurodevelopmental outcomes at one year. That is a hard endpoint, a proper design, and a negative result — and it is the highest quality single piece of evidence about this molecule that a search returns.
The other trial setting it turns up in is a hangover review. Roberts 2022 is a systematic review of randomized placebo-controlled trials of pharmacologically active interventions for hangover symptoms, and its overall verdict is that the evidence for every agent examined is of very low quality. That is where pyritinol's randomized human record largely lives: small trials, in hangover, pooled into a review that declines to recommend anything.
Its second career was as an antirheumatic drug, and that is where the harm was documented. Pyritinol was used as a disease-modifying agent in rheumatoid arthritis, which is the setting in which patients took it for years under observation and in which the serious adverse reactions of the thiol drugs were recorded. Guski 2023 is the modern network meta-analysis of conventional antirheumatic monotherapies and finds methotrexate the reference standard — the field moved on, and the older agents did not survive the comparison.
The transfer this page refuses. A null trial in newborns after birth asphyxia does not prove a drug useless in adults, and a very-low-quality hangover literature does not establish it useful. What both together establish is that after sixty years, nobody has run the trial that the retail claim would need: pyritinol against placebo, in healthy adults, with a cognitive endpoint.
Pyritinol pharmacokinetics — how much of it actually gets in
What degrades it. The disulfide bridge is reduced in vivo, principally by glutathione and thiol-disulfide exchange, and the resulting thiol is the reactive species. Beyond that the molecule is handled by hepatic oxidation and conjugation. The parent's plasma half-life is short, on the order of 2.5 hours, which is why the European regimens dosed it two or three times daily.
The oral barrier, and the thing the disulfide buys. Absorption from the gut is good and the lipophilicity conferred by the dimerization is the reason the molecule reaches the brain where free pyridoxine, a small polar vitamin, is limited by transporter capacity. First-pass metabolism reduces what arrives intact, and the reduced thiol formed in the process is not the molecule that was swallowed.
The arithmetic worth knowing about the tablets. The tablets sold are 100 mg and the clinical literature used around 600 mg a day in divided doses. On a molar basis, 600 mg of pyritinol is roughly 1.8 mmol of pyridoxine-derived material a day, against a recommended B6 intake of a few milligrams. Whether any free pyridoxine is liberated during metabolism is unclear from the published record, and it matters, because chronic high-dose pyridoxine causes a sensory neuropathy.
No injectable comparator, and what that costs. Pyritinol has been available in parenteral form in some markets historically, but no study comparing an injection with a tablet resolves in the literature this page can read. Without it, the size of first-pass loss is inferred from the chemistry rather than measured, and no bioavailable fraction can be quoted for the product on sale.
What would have to be true, and how you would know it was not
Four predictions. Two are efficacy and two are safety, and the safety pair is the reason this page exists.
1. CMP and GGT, baseline and eight weeks. Cholestatic liver injury is the documented serious adverse reaction of the thiol drug family, and liver enzymes are where it shows before anything is felt. This is the single most useful measurement anyone taking this molecule could make, and it is the one nobody thinks to make on something sold as a B6 derivative.
2. CBC, for the same class reason. The antirheumatic thiols are associated with blood dyscrasias, and a full blood count is cheap enough that including it is not a burden. Prediction: unchanged in almost everyone, which is exactly why the rare exception is worth catching.
3. Any cognitive endpoint will not separate from placebo in a healthy adult. That is the prediction the entire published record supports: a null randomized trial on a hard endpoint Nair 2009, and a very-low-quality body of evidence elsewhere Roberts 2022. Falsifying it needs a controlled trial, not a personal impression, because a substance with a mild subjective effect and no measurable one is the standard shape of an active placebo.
4. Against the product, from its own chemistry. If the disulfide is what makes the molecule work, then it is also what makes the molecule risky, and no formulation can separate the two. A hypothetical version with the bond removed would be pyridoxine, which is a vitamin nobody claims does this. The mechanism and the hazard are the same bond.
What nobody has tested yet
Nobody has run the trial the retail claim needs. Pyritinol against placebo, in healthy adults, on a validated cognitive battery. Sixty years, several markets, and no such trial in the literature a search returns.
Nobody has quantified the pemphigus and hepatitis risk. The association between thiol drugs and drug-induced pemphigus and cholestatic injury is established for the class Boch 2021; the incidence attributable to this specific member, at the doses used, in a defined population, has not been published in a form a reader can check. Unquantified is not the same as small.
Nobody has published whether it liberates free pyridoxine. It is a metabolic question with a straightforward answer if anyone measured plasma pyridoxal 5-phosphate after dosing, and it determines whether long-term use carries the sensory neuropathy risk that high-dose B6 does. It has not been reported.
Extrapolation, labeled as such. If the cognitive effect is real and depends on the disulfide crossing into brain, then a comparison against equimolar pyridoxine should show a difference. That is the cheapest possible test of the molecule's central premise, it would take one small crossover study, and nobody has run it.
Pyritinol — its own safety story, not its class's
Three things specific to a thiol drug sold as a vitamin derivative.
The framing error is the hazard. Being built from two vitamin B6 molecules invites the assumption that the safety profile is a vitamin's. It is not. The reduced disulfide is a reactive sulfhydryl, and that chemical group is what links penicillamine, tiopronin and this molecule to drug-induced pemphigus, lichenoid eruptions and cholestatic liver injury Boch 2021. A rash on this drug is not a nuisance to push through.
Where the harm was actually documented, and why that setting matters. The serious reactions were recorded when pyritinol was used as a disease-modifying antirheumatic drug — long courses, monitored patients, a specialty that watches for exactly these reactions. The nootropic market takes the same molecule with none of that observation, and Guski 2023 shows the field that once used it has moved to methotrexate as its reference.
What an absent regulator means here. There is no United States approval, so there is no FDA adverse-reaction table and no American label to read. The safety information that exists comes from European prescribing history and case reports. A reader who develops an unexplained rash, mouth ulceration, itching, pale stools or dark urine on this drug should stop and be assessed rather than look for the answer online; nothing on this page is a diagnosis or a substitute for one.
Sources read for this page
- Nair MK, George B, Jeyaseelan L. Pyritinol for post asphyxial encephalopathy in term babies--a randomized double-blind controlled trial. Indian Pediatrics 2009 · PMID 19279367
- Roberts E, Smith R, Hotopf M, Drummond C. The efficacy and tolerability of pharmacologically active interventions for alcohol-induced hangover symptomatology: a systematic review of the evidence from randomized placebo-controlled trials. Addiction 2022 · PMID 34972259
- Malik M, Tlustos P. Nootropics as Cognitive Enhancers: Types, Dosage and Side Effects of Smart Drugs. Nutrients 2022 · PMID 36014874
- Boch K, Langan EA, Kridin K, Zillikens D, Ludwig RJ, Bieber K. Lichen Planus. Frontiers in Medicine (Lausanne) 2021 · PMID 34790675
- Guski LS, Jurgens G, Pedder H, Levinsen NKG, Andersen SE, Welton NJ, Graudal N. Monotreatment With Conventional Antirheumatic Drugs or Glucocorticoids in Rheumatoid Arthritis: A Network Meta-Analysis. JAMA Network Open 2023 · PMID 37801318
Pyritinol — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- This class is broad, but the predicted problems cluster by mechanism rather than by molecule. Cholinergics (racetams, and anything raising acetylcholine) predict headache — the classic one, from choline demand outrunning supply. Dopaminergics and eugeroics predict tolerance, sleep disruption and a flat mood on the days off. Anything glutamatergic or AMPA-facing carries a theoretical excitotoxicity concern at high doses.
- The pattern worth internalizing: anything that borrows performance from tomorrow eventually presents the bill. Sleep is the most common currency it gets paid in.
What has actually been reported
- Headache is the most reported effect across the racetam family and usually responds to added choline.
- Irritability, blunted affect and a rebound low on cessation are commonly reported with the stimulant-adjacent members.
- Most of this class has little or no controlled human safety data at the doses actually used.
How to reduce the risk
Same mechanism as the prediction.
- Take a choline source with any racetam. The headache is the mechanism running out of substrate, and it is largely preventable rather than something to push through.
- Dose in the morning. Almost everything in this class has a longer functional tail than its half-life suggests, and sleep is the first thing you lose.
- Use them for something, not as a habit. The compounds that carry tolerance genuinely reward intermittent use aimed at a task, and genuinely punish daily use aimed at feeling normal.
- One at a time, and long enough to judge it. This is the class where people stack five and cannot tell you which one is doing anything — and the effects are subjective, so attribution is already hard enough.
- If you need it to feel normal, stop. That is the line where a tool has become a dependency, and it is the one worth watching for.
What it does to your bloodwork
A fact about the assay.
- No routine marker tracks these. Sleep is the assay — if it is degrading, the compound is costing more than it is producing, and that shows up before anything else does.
Don't run this if
- A seizure history — several of these lower the threshold at least theoretically, and it is not worth establishing empirically.
- Bipolar disorder, for the dopaminergic members especially.
- Alongside prescribed psychiatric medication without knowing exactly how the mechanisms overlap.
The honest unknown
- Chronic use is essentially uncharacterized. The specific unmeasured thing is what daily cholinergic or dopaminergic pressure does to baseline function over years — not whether a few weeks is tolerable.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Pyritinol — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Pyritinol moves on your bloodwork
Expected direction, not a measured one.
- Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Most of this class has no predicted marker movement at all, and saying so is more useful than listing markers that will not move.
What to do: A baseline liver panel is reasonable for anything taken daily and long-term. Beyond that there is nothing specific to chase.
- Dose range and how to work up to it
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Pyritinol in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Pyritinol
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| TSH (Thyroid-Stimulating Hormone) | Thyroid disease imitates every cognitive complaint there is |
| Vitamin B12 | Deficiency causes fog long before it causes anemia |
| Methylmalonic Acid (MMA) | Catches the deficiency a normal B12 hides |
| Ferritin | Low iron flattens cognition at levels most labs call fine |
| Vitamin D (25-Hydroxy) | Commonly low, cheap to correct, associated with mood |
The Brain Fog & Cognition panel covers these in one order — 12 markers, $233.06 with the discount applied.
Check results you already have → · All 103 markers A–Z
Pyritinol — frequently asked questions
What is Pyritinol?
Pyritinol (Encephabol, Encefabol, Cerbon 6 — pyrithioxine, two vitamin B6 molecules joined by a disulfide) is a cognitive & mood research compound. Two pyridoxine molecules bridged by a disulfide, which makes it a thiol drug wearing a vitamin's structure. It is not a vitamin B6 supplement and does not behave as one: the disulfide is what gets reduced in the body, and it is also what puts this molecule in the same chemical family as penicillamine and tiopronin — drugs with a well-documented capacity to trigger autoimmune skin and liver reactions. The nootropic claim rests on increased glucose uptake and cholinergic effects reported in old European work rather than on a named receptor.
Where can I find Pyritinol dosing and protocols?
Dosing, the reconstitution calculator and Coach Cam's full Pyritinol protocol are available to members inside Skool. This public page covers what Pyritinol is, how it works and the evidence.
What is the half-life of Pyritinol?
Pyritinol has an approximate half-life of ~2.5 hrs for the parent; the reduced thiol is the reactive species, which is part of what determines how often it's dosed.
What's the evidence behind Pyritinol?
Current evidence level: A prescription or pharmacy medicine in parts of Europe and Asia, never approved in the United States. The randomized evidence that resolves is small and mostly negative.. Pyritinol is offered for research purposes only and is not an approved medicine.
What Pyritinol is used for
Pyritinol appears under 1 goal in the goal router.
Related Cognitive & Mood compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.