Phenylpiracetam Hydrazide.
The banned-by-WADA racetam. Athletes caught with this.
Reviewed March 2026
- Category
- Nootropic
- Also filed under
- StimulationCold toleranceFocus
What Phenylpiracetam Hydrazide is, and what it does.
- Does it work
- Suits people who accept they're handling a research chemical with no human data of its own and who verify identity by certificate of analysis. It is a different molecule from its parent.
- How much to take
- Start with 50mg a day, with 100mg the top of the daily band. The 200mg figure on record is a research condition, not a daily target.
- Time to feel it
- Nobody has published human timing data for this specific molecule. Reports of stimulation within the first hour are experience rather than measurement.
- The first dose
- Reports describe alertness and drive inside the first hour or two, then a taper. None of that has been measured formally in people.
- With regular use
- Most effects take 2-8 weeks. Be patient.
- How well tolerated
- Generally well tolerated. Check with your doctor if on medications.
- How it feels
- Clean stimulation without jitters. Some find it too activating for evening use.
- The overlooked benefit
- Swapping the amide for a hydrazide makes a different molecule, not a stronger version of the parent, so anything written about phenylpiracetam is inference here, not data.
50 to 100mg a day is where Phenylpiracetam Hydrazide works.
Source: Nootropic community reports; no published human trials
The proof, claim by claim.
These words describe the research, not the molecule's worth. Research strength is how much work stands behind one claim, and it is never a product score.
- cognitive and stimulant-type effectsNarrative review
- central nervous system penetration from the phenyl substituentNarrative review
Questions people ask about Phenylpiracetam Hydrazide.
- When should I take it?
- Timing matters less than consistency. Pick a time that works for you and take it daily.
- Can I take it with other supplements?
- Usually fine. The main thing to watch is not doubling up on the same ingredient from different products. If you're on prescription meds, check with your pharmacist first.
- Any side effects to watch for?
- Most people tolerate it well at recommended doses. GI upset is the most common complaint with any supplement. Start with a lower dose and work up. If something feels off, stop and reassess.
- Who benefits most from this?
- Honestly, most people would benefit more from the basics. But if you've got a specific reason to try it, the risk is generally low.
Why these belong in the same formula. Each row says what the basis is, from settled biochemistry through to a trial that measured the pair.
Fonturacetam hydrazide is a racetam-class analogue, and compounds in this class raise acetylcholine turnover at the synapse. Alpha-GPC supplies brain-available choline for that synthesis step, the same reason it accompanies the parent compound.
Choline acetyltransferase needs choline to build acetylcholine, and raised turnover draws on that pool. A choline source is the routine companion for this compound class.
The hydrazide is a structural analogue within the racetam family and shares the same broad mechanism. Running both delivers one class effect twice rather than two separate ones.
Phosphatidylcholine is both a membrane phospholipid and a choline reservoir released by phospholipase D. It supplies choline more slowly than a free choline salt, which is why some formulas prefer it. As with every partner here, no published human pharmacology exists for the hydrazide itself.
Lecithin is a crude phospholipid mixture whose phosphatidylcholine share varies widely by source and grade, so it is a diffuse choline source. It is used in nootropic blends for that reason and as an emulsifier. The choline argument is class-level and untested for this compound.
Sunflower lecithin offers the same phospholipid classes as soy lecithin without the soy allergen and is often chosen on that basis alone. Its choline contribution per gram is modest compared with a choline salt. Nothing has been measured with this hydrazide.
Tyrosine is hydroxylated to L-DOPA and decarboxylated to dopamine, then converted to noradrenaline, and precursor availability matters most when catecholamine turnover is already high. Phenylpiracetam's parent compound is described as stimulant-like, which is the basis for the pairing argument. For the hydrazide analogue this is inference from the parent, not measured pharmacology.
Caffeine blocks adenosine A1 and A2A receptors, producing arousal that stacks with anything else stimulating. Combining two stimulating compounds raises the likelihood of a faster heart rate, restlessness and disturbed sleep in the same session. Because the hydrazide's human pharmacology is not published, the prudent reading is that the additive risk is real and unquantified.
Anhydrous caffeine is the same molecule without crystal water, so per-milligram potency is slightly higher and powder dosing errors are easier to make. The additive stimulation caution is identical to caffeine. Timing away from sleep is the practical point.
Theanine is a glutamate analogue that raises alpha-band activity and is conventionally paired with stimulants to smooth the edge of arousal rather than to add to it. That is the direction of the pairing here. It is class-level reasoning and has not been tested with this compound.
Taurine acts at glycine and GABA-A receptors and functions as an intracellular osmolyte, which is the basis for including it alongside stimulating ingredients. The effect direction is calming rather than additive. No data pairs it with this compound.
Magnesium sits in the NMDA channel pore as a voltage-dependent block and is a cofactor for hundreds of ATP-dependent enzymes, so status affects excitability broadly. That places it as a background condition rather than a direct partner. The pairing is general neurophysiology, not specific pharmacology.
Melatonin signals biological night through MT1 and MT2 receptors, which works directly against an arousing compound taken too late in the day. Anyone combining them is asking the same evening to be both alerting and sleep-permissive. Flagging the opposition is more useful than describing it as a stack.
Supplemental GABA crosses the blood brain barrier poorly, so much of its reported calming effect is attributed to peripheral or enteric signalling. In direction it opposes an arousing compound rather than complementing it. Both halves of this pairing rest on weak human pharmacology.
Huperzine A is a reversible acetylcholinesterase inhibitor, so it raises synaptic acetylcholine by slowing its breakdown rather than by supplying precursor. Stacked with a choline source and a racetam-class compound, the cholinergic load can add up, and cholinergic excess presents as headache, cramping, nausea or vivid dreams. The interaction direction is established pharmacology; the combination has not been studied here.
Phosphatidylserine is an inner-leaflet phospholipid involved in signalling protein docking, and it is a conventional component of cognitive-support blends. Its role here is membrane composition rather than any interaction with the hydrazide. No combination data exists.
Acetyl-L-carnitine carries an acetyl group that can enter acetyl-CoA pools, which is the argument for it contributing to acetylcholine synthesis alongside a choline source. It also shuttles long-chain fatty acids into mitochondria. The acetyl-donation argument is mechanistic and its size in human brain is not established.
Creatine buffers ATP through the phosphocreatine system in tissues with fluctuating energy demand, brain included, which is why it appears in cognitive-support stacks. The mechanism is independent of anything a racetam-class compound does. It is complementary rather than interacting.
Rhodiola is reported to influence monoamine turnover and is used for perceived fatigue, so combined with an arousing compound it points in the same direction. That makes overlapping stimulation, not a distinct mechanism, the thing to watch. Human data for the pairing does not exist.
Bacopa's bacosides are described in preclinical work as affecting cholinergic signalling and dendritic morphology, and its human trials use multi-week dosing rather than acute effects. That makes it a slow-acting partner to an acutely acting compound. The two have not been studied together.
Ginkgo terpene lactones affect platelet activating factor signalling, which is why ginkgo carries a bleeding-risk caution alongside anticoagulants and antiplatelet agents. That caution travels with it into any stack. It is included here as a flag rather than as a benefit pairing.
Ashwagandha is used for stress-axis measures and is generally calming in direction, which is the opposite of an arousing compound. Stacking them is a deliberate attempt to blunt one with the other rather than an additive pairing. No data addresses the combination.
Activated charcoal adsorbs small organic molecules broadly and is not selective, so co-dosing reduces absorption of almost anything taken with it. This applies to a synthetic small molecule as much as to a nutrient. Separating doses by several hours is the practical response.
Nothing specific on file for Phenylpiracetam Hydrazide. Match the label to the daily amount above, and tell your doctor what you take.
Not medical advice. Show the label to your pharmacist.What Phenylpiracetam Hydrazide actually does.
Phenylpiracetam hydrazide, also called fonturacetam hydrazide, is a 2-oxopyrrolidine derivative in which the acetamide group of phenylpiracetam is replaced by an acethydrazide, so it is a structural analogue and not the same molecule.
Replacing an amide with a hydrazide adds a basic, nucleophilic nitrogen, which changes ionisation, hydrogen bonding and metabolic handling; hydrazide functional groups are chemically reactive toward carbonyls and are not pharmacologically interchangeable with the parent amide.
The phenyl substituent on the pyrrolidinone ring raises lipophilicity relative to unsubstituted piracetam, which is the standard structural explanation for greater central nervous system penetration within this chemical class.
The compound is a fully synthetic small molecule with no plant, animal or microbial source, so any description of it as extracted from something is incorrect.
Where Phenylpiracetam Hydrazide comes from.
It is made entirely in a lab from chemical building blocks, with a final step that swaps one part of phenylpiracetam for a hydrazide group, then purified and tested to confirm what it is.
Chemically synthesised. The molecule is identical to the one a plant or an animal makes, and building it deliberately means a known purity, a fixed dose and no crop contaminants. For several nutrients this is the only route that reaches a usable amount.
Built from small synthetic building blocks; there is no botanical, animal or fermentation source for this molecule at any point in its history.
The 4-phenyl-2-oxopyrrolidine ring system is assembled and then N-alkylated to attach the acetic acid side chain, the same core route used for the parent compound.
The ester or amide side chain is reacted with hydrazine to give the acethydrazide, which is the step that distinguishes this compound from phenylpiracetam.
Crude solid is recrystallised from a solvent system to remove residual hydrazine, unreacted intermediates and process solvents; residual hydrazine is the impurity of most concern in a hydrazide synthesis.
Assay by HPLC with identity confirmed by NMR or mass spectrometry, plus residual solvent and heavy metal testing; without these a powder is an unidentified white solid.
Packed as loose powder or dosed into capsules with an excipient for flow.
Residual hydrazine limits, the identity method behind a certificate of analysis, and the testing laboratory are the things most often missing, and for a hydrazide they are the ones that matter.
Getting Phenylpiracetam Hydrazide from food.
The whole-food sources on file. A supplement closes the gap, it does not replace dinner.
A gram-for-gram figure (how much of each you would eat to match a dose) will appear here once it is sourced and reviewed. This page will not print a number it cannot cite.
The forms it comes in.
FDA Disclaimer: These statements have not been evaluated by the Food and Drug Administration. This information is for educational purposes only and is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare provider before starting any supplement regimen.