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Head-to-head comparison of Nefiracetam and Phenylpiracetam hydrazide — mechanism, side effects, legal status, and pricing.
Nefiracetam is a non-peptide small molecule in the racetam (pyrrolidinone/2-oxopyrrolidine acetamide) class, investigated as a cognitive enhancer. It was never approved by the FDA, EMA, or Japan's PMDA; Daiichi Seiyaku withdrew its Japanese NDA (Translon) in February 2002 after a repeat Phase III trial in dementia failed to demonstrate efficacy. A US/Canada Phase II trial in poststroke depression (600 mg and 900 mg/day) showed no overall separation from placebo, though a subgroup analysis suggested benefit in the most severely depressed patients at 900 mg. No validated therapeutic dose or approved indication exists; it is sold by research-chemical and laboratory-reagent suppliers for research use only.
Phenylpiracetam hydrazide is a non-peptide racetam-class small molecule — specifically a pyrrolidinone acetohydrazide in which the terminal carboxamide of phenylpiracetam (fonturacetam) is replaced by a carbohydrazide group. First synthesized in 1980 by a Russian medicinal-chemistry group screening 4-phenyl-2-pyrrolidinone derivatives for anticonvulsant activity, it has never been approved as a drug in any jurisdiction and has no human clinical trial data. The parent compound phenylpiracetam is explicitly listed on the WADA Prohibited List under S6.A (Non-Specified Stimulants); the hydrazide analog's own it is not on the WADA Prohibited List (only beta-2 agonists are prohibited, Category S3). It is sold by gray-market research-chemical vendors labeled 'not for human consumption.'
Nefiracetam
Phenylpiracetam hydrazide
Category
Legal Status
Mechanism
Side Effects
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Nefiracetam
No pricing data yet.
Check Nefiracetam prices →Phenylpiracetam hydrazide
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Check Phenylpiracetam hydrazide prices →COA corpus from Disclosed Labs — independently tested batches only.
Nefiracetam
2
COAs
99.6%
Avg purity
2
Labs
Phenylpiracetam hydrazide
2
COAs
99.4%
Avg purity
2
Labs
Human clinical data are limited and largely negative or mixed. Japanese Phase II/III trials in dementia/cognitive sequelae after cerebrovascular disorders showed improvement over placebo in some early trials, but a Ministry of Health-mandated repeat Phase III trial under revised guidelines failed to demonstrate efficacy, and Daiichi Seiyaku withdrew its Japanese NDA (Translon) in February 2002. A US/Canada multicenter randomized double-blind Phase II trial (28 sites, 1999–2001, n=159) tested nefiracetam 600 mg and 900 mg/day vs. placebo for poststroke depression; the drug did not separate from placebo overall (response >70%, remission >40% in both arms) but showed significant benefit in the most-severely-depressed subgroup at 900 mg (Robinson et al., J Neuropsychiatry Clin Neurosci 2008). A related post hoc analysis examined apathy outcomes in the same cohort. Preclinical findings include: rat cortical neurons showed potentiation of native α4β2-type nicotinic acetylcholine receptor currents via a G(s)-protein-dependent pathway; rat dorsal root ganglion neurons showed dual concentration-dependent effects on GABA_A receptor-channel currents mediated via cAMP-dependent protein kinase and Gi/Go proteins; rat neuronal preparations showed enhancement of high-voltage-activated N/L-type Ca²⁺ channel currents and modulation of NMDA receptor function via PKC-dependent phosphorylation; rat passive avoidance models showed reversal of apomorphine-induced amnesia and preservation of hippocampal NCAM-mediated memory consolidation during scopolamine disruption.
No human clinical trials have been conducted; no ClinicalTrials.gov record or DrugBank entry exists. The sole preclinical finding is from the 1980 Glozman et al. synthesis paper: an ED<sub>50</sub> of approximately 310 mg/kg for seizure protection in a rodent electroshock assay (species, strain, sex, and route not fully recoverable from accessed sources). No published human toxicology, LD<sub>50</sub>, pharmacokinetics, or adverse-event data were located for this compound.
Nefiracetam and Phenylpiracetam hydrazide are both in the Cognitive category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining research compounds.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
Contraindications
Lab Testing