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    Sunifiram (DM-235) molecular structure

    Sunifiram (DM-235)

    NootropicsPreclinical

    Also known as: DM-235, DM 235, 1-(4-benzoylpiperazin-1-yl)propan-1-one, 1-benzoyl-4-propanoylpiperazine

    Sunifiram, also called DM-235, is a piperazine that came out of an academic medicinal chemistry program at the University of Florence, not out of a pharmaceutical company. It was first reported in 2000 as one of a series of acylpiperazines obtained by simplifying a bicyclic scaffold, and it stood out for potency: it prevented amnesia in the mouse passive avoidance test at doses about a thousand times lower than piracetam-like reference compounds (PMID: 11087574; PMID: 12070754).

    Half-Life: Not established. No pharmacokinetic study in humans or animals has been published, and the group that discovered the compound stated that its long-term toxicity was unknown (PMID: 25831025).Route: OralMW: 246.30 g/molCAS: 314728-85-3
    Last reviewed:
    Nootropics
    Category
    Preclinical
    Research Stage

    Overview

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    At A Glance

    Mechanism

    Sunifiram has no established single target and shows no affinity for the major central receptors or channels in binding assays, yet it prevents amnesia induced through cholinergic, nicotinic, GABAergic and adrenergic manipulations (PMID: 12070754; PMID: 16834757). The clearest do

    Half-Life
    Not established. No pharmacokinetic study in humans or animals has been published, and the group that discovered the compound stated that its long-term toxicity was unknown (PMID: 25831025).
    Routes
    Oral
    Potential Benefits
    Prevented scopolamine-induced amnesia in the passive avoidance test in mice at doses about a thousand times lower than piracetam-like reference compounds (PMID: 12070754)Prevented scopolamine-induced memory impairment in the Morris water maze in rats without impairing motor coordination or spontaneous motility (PMID: 12070754)Reversed amnesia induced by the AMPA receptor antagonist NBQX in mice (PMID: 14600801)Enhanced hippocampal long-term potentiation through the glycine site of the NMDA receptor in mouse hippocampal slices, with a bell-shaped concentration-response curve (PMID: 23733502)Improved Y maze and novel object recognition performance and restored hippocampal long-term potentiation in olfactory bulbectomized mice (PMID: 23295391)

    Overview

    Sunifiram, also called DM-235, is a piperazine that came out of an academic medicinal chemistry program at the University of Florence, not out of a pharmaceutical company. It was first reported in 2000 as one of a series of acylpiperazines obtained by simplifying a bicyclic scaffold, and it stood out for potency: it prevented amnesia in the mouse passive avoidance test at doses about a thousand times lower than piracetam-like reference compounds (PMID: 11087574; PMID: 12070754). Despite the racetam-style name it is not a pyrrolidinone and is not structurally a racetam. The mechanism is not fully resolved. Binding studies found no affinity for the major central receptors or channels, yet sunifiram prevented amnesia induced by drugs acting on several different transmitter systems, including scopolamine, mecamylamine, baclofen and clonidine (PMID: 12070754; PMID: 16834757). Two glutamatergic actions have been documented. Sunifiram and its analog unifiram reversed amnesia induced by the AMPA receptor antagonist NBQX in mice and reversed kynurenic acid blockade of NMDA-mediated noradrenaline release in rat hippocampal slices, an effect abolished by NBQX (PMID: 14600801). Separately, in mouse hippocampal slices sunifiram enhanced long-term potentiation with a bell-shaped concentration-response curve peaking at 10 nanomolar; the enhancement was blocked by an antagonist of the glycine site of the NMDA receptor but not by an antagonist of the polyamine site, and involved protein kinase C alpha, Src family kinase and calcium/calmodulin-dependent protein kinase II (PMID: 23733502). Sunifiram also increased acetylcholine release in rat brain (PMID: 11087574). In disease-model animals, sunifiram improved spatial reference memory in the Y maze and short-term memory in novel object recognition in olfactory bulbectomized mice and restored hippocampal long-term potentiation, with those effects blocked by a glycine site inhibitor; it did not improve depressive behavior in the same animals (PMID: 23295391). There is no human data of any kind. No clinical trial, case series or pharmacokinetic study has been published, and searches of ClinicalTrials.gov return no records. The chemist who led the group that discovered sunifiram and unifiram wrote in 2015 that he had discovered by chance that dozens of websites were selling both compounds as cognitive enhancers for healthy people, even though only a few preclinical studies had been performed and their long-term toxicity was unknown, and that neither compound had been protected by a patent or taken forward by industry (PMID: 25831025). Sunifiram is not approved in any country, is not a controlled substance in the United States and has no established human dose, safety threshold or contraindication list. Everything sold is a research chemical. One frequently cited paper on sunifiram carbamate hybrids as dual acetylcholinesterase inhibitors and NMDA co-agonists was retracted by the journal in 2026 (PMID: 42565552), so any claim traced back to it should be treated as unsupported.

    Potential Research Fields

    Cognitive enhancementNMDA glycine siteAMPA receptor pharmacologyNootropics

    Chemical Information

    IUPAC Name

    Not yet available

    CAS Number

    314728-85-3

    Molecular Formula

    C14H18N2O2

    Molecular Mass

    246.30 g/mol

    Dosing & Protocols

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    Interactions

    Contraindications

    None established, because no human study exists. Mechanism-based cautions: sunifiram acts at the glycine site of the NMDA receptor and enhances long-term potentiation with a bell-shaped concentration-response curve in mouse hippocampal slices, so higher exposure is not simply more of the same effect (PMID: 23733502). Compounds that increase NMDA and AMPA receptor signaling carry a theoretical excitotoxicity and seizure risk, which is relevant to anyone with a seizure disorder or recent brain injury. No reproductive toxicity, genotoxicity, repeat-dose toxicity or drug interaction data have been published in any species.

    Research Disclaimer

    This interaction data is compiled from published research and community reports. It may not be exhaustive. Always consult a healthcare professional before combining compounds.

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    9-Me-BC (9-Methyl-β-carboline)

    NootropicsPreclinical

    9-Methyl--carboline (9-Me-BC) is a synthetic -carboline alkaloid that has drawn nootropic-community interest for a preclinical property that is genuinely unusual among -carbolines: in rodent and cell-culture studies it appears to stimulate the dopaminergic phenotype - raising tyrosine hydroxylase, the number of differentiated dopamine neurons and dopamine content - while also showing neuroprotective, neurorestorative and anti-inflammatory effects, plus in-vitro MAO-A/MAO-B inhibition [PMID:17913302, PMID:20374418, PMID:32285253].

    t½ Not characterized in humans (no pharmacokinetic data). Community/anecdotal only: ~5-25 mg per day, oral. No validated or approved human dose exists.
    6 studiesView Profile

    Aniracetam

    NootropicsApproved (Italy)

    Aniracetam is a pyrrolidinone in the racetam family, developed by Hoffmann-La Roche under the code Ro 13-5057.

    t½ About half an hour for the parent drug in humans. Plasma elimination half-life was 0.47 to 0.49 hours after a single 400 mg oral dose in 20 healthy male volunteers (PMID: 19025058). Aniracetam is extensively metabolized to N-anisoyl-GABA and anisic acid; in six elderly hospitalized patients with cerebrovascular disease and reduced creatinine clearance, metabolite half-life was 4 to 7 times longer than in young volunteers (PMID: 9062694).
    PreclinicalView Profile

    Bemethyl (bemitil)

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    Bemethyl, known in the Russian literature as bemitil and sold in the region under names including Metaprot, Bemactor and Antihot, is 2-ethylthiobenzimidazole, normally handled as the hydrobromide salt.

    t½ Not established in humans; in healthy volunteers given a single 250 mg oral dose of the Metaprot capsule form, peak serum ethylthiobenzimidazole averaged 0.91 microg/mL at about 1.06 h, and no terminal half-life was reported (PMID: 21870773)
    PreclinicalView Profile

    Bromantane

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    Bromantane is an atypical psychostimulant and anxiolytic developed in the 1980s at the Zakusov Institute of Pharmacology of the Russian Academy of Medical Sciences, originally created as an adaptogen for Soviet military and elite athletic use and later approved in Russia for the treatment of neurasthenic and asthenic disorders under the trade name Ladasten.

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    NootropicsPreclinical

    Dihexa is a synthetic peptide analogue of the angiotensin IV metabolite LVV-hemorphin-7, developed at Washington State University.

    t½ Not characterized in humans. Dihexa was engineered for metabolic stability (resistant to plasma and enzymatic degradation) and blood-brain-barrier penetration; in preclinical work its central procognitive effects appear to outlast its plasma presence. 5 to 40 mg oral per day (anecdotal range; no established human dose)
    1 studiesView Profile

    View Full Dosage Guide →

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    1 vendors · 1 listings

    Research Score

    30

    0 PubMed studies

    Quality Indicators

    Data Completeness

    63%
    Description
    Mechanism of Action
    Chemical Data
    Dosing Protocols
    Safety Profile
    PubMed Studies
    Interactions
    Vendor Listings

    Quick Facts

    Half-Life

    Not established. No pharmacokinetic study in humans or animals has been published, and the group that discovered the compound stated that its long-term toxicity was unknown (PMID: 25831025).

    Molecular Weight

    246.30 g/mol

    Administration

    Oral

    CAS Number

    314728-85-3

    Trial Phase

    Preclinical

    0

    Research Disclaimer

    This information is for educational and research purposes only. Not intended as medical advice. Consult a healthcare professional before use.

    Frequently Asked Questions

    What is Sunifiram (DM-235) used for in research?

    Sunifiram, also called DM-235, is a piperazine that came out of an academic medicinal chemistry program at the University of Florence, not out of a pharmaceutical company. It was first reported in 2000 as one of a series of acylpiperazines obtained by simplifying a bicyclic scaffold, and it stood out for potency: it prevented amnesia in the mouse passive avoidance test at doses about a thousand times lower than piracetam-like reference compounds (PMID: 11087574; PMID: 12070754). Despite the racetam-style name it is not a pyrrolidinone and is not structurally a racetam.

    The mechanism is not fully resolved. Binding studies found no affinity for the major central receptors or channels, yet sunifiram prevented amnesia induced by drugs acting on several different transmitter systems, including scopolamine, mecamylamine, baclofen and clonidine (PMID: 12070754; PMID: 16834757). Two glutamatergic actions have been documented. Sunifiram and its analog unifiram reversed amnesia induced by the AMPA receptor antagonist NBQX in mice and reversed kynurenic acid blockade of NMDA-mediated noradrenaline release in rat hippocampal slices, an effect abolished by NBQX (PMID: 14600801). Separately, in mouse hippocampal slices sunifiram enhanced long-term potentiation with a bell-shaped concentration-response curve peaking at 10 nanomolar; the enhancement was blocked by an antagonist of the glycine site of the NMDA receptor but not by an antagonist of the polyamine site, and involved protein kinase C alpha, Src family kinase and calcium/calmodulin-dependent protein kinase II (PMID: 23733502). Sunifiram also increased acetylcholine release in rat brain (PMID: 11087574).

    In disease-model animals, sunifiram improved spatial reference memory in the Y maze and short-term memory in novel object recognition in olfactory bulbectomized mice and restored hippocampal long-term potentiation, with those effects blocked by a glycine site inhibitor; it did not improve depressive behavior in the same animals (PMID: 23295391).

    There is no human data of any kind. No clinical trial, case series or pharmacokinetic study has been published, and searches of ClinicalTrials.gov return no records. The chemist who led the group that discovered sunifiram and unifiram wrote in 2015 that he had discovered by chance that dozens of websites were selling both compounds as cognitive enhancers for healthy people, even though only a few preclinical studies had been performed and their long-term toxicity was unknown, and that neither compound had been protected by a patent or taken forward by industry (PMID: 25831025).

    Sunifiram is not approved in any country, is not a controlled substance in the United States and has no established human dose, safety threshold or contraindication list. Everything sold is a research chemical. One frequently cited paper on sunifiram carbamate hybrids as dual acetylcholinesterase inhibitors and NMDA co-agonists was retracted by the journal in 2026 (PMID: 42565552), so any claim traced back to it should be treated as unsupported.

    What forms does Sunifiram (DM-235) come in?

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    How much does Sunifiram (DM-235) cost?

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    Research Tools

    Related Compounds

    View All

    9-Me-BC (9-Methyl-β-carboline)

    NootropicsPreclinical

    9-Methyl--carboline (9-Me-BC) is a synthetic -carboline alkaloid that has drawn nootropic-community interest for a preclinical property that is genuinely unusual among -carbolines: in rodent and cell-culture studies it appears to stimulate the dopaminergic phenotype - raising tyrosine hydroxylase, the number of differentiated dopamine neurons and dopamine content - while also showing neuroprotective, neurorestorative and anti-inflammatory effects, plus in-vitro MAO-A/MAO-B inhibition [PMID:17913302, PMID:20374418, PMID:32285253].

    t½ Not characterized in humans (no pharmacokinetic data). Community/anecdotal only: ~5-25 mg per day, oral. No validated or approved human dose exists.
    6 studiesView Profile

    Aniracetam

    NootropicsApproved (Italy)

    Aniracetam is a pyrrolidinone in the racetam family, developed by Hoffmann-La Roche under the code Ro 13-5057.

    t½ About half an hour for the parent drug in humans. Plasma elimination half-life was 0.47 to 0.49 hours after a single 400 mg oral dose in 20 healthy male volunteers (PMID: 19025058). Aniracetam is extensively metabolized to N-anisoyl-GABA and anisic acid; in six elderly hospitalized patients with cerebrovascular disease and reduced creatinine clearance, metabolite half-life was 4 to 7 times longer than in young volunteers (PMID: 9062694).
    PreclinicalView Profile

    Bemethyl (bemitil)

    NootropicsApproved (Russia)

    Bemethyl, known in the Russian literature as bemitil and sold in the region under names including Metaprot, Bemactor and Antihot, is 2-ethylthiobenzimidazole, normally handled as the hydrobromide salt.

    t½ Not established in humans; in healthy volunteers given a single 250 mg oral dose of the Metaprot capsule form, peak serum ethylthiobenzimidazole averaged 0.91 microg/mL at about 1.06 h, and no terminal half-life was reported (PMID: 21870773)
    PreclinicalView Profile

    Bromantane

    NootropicsRussia Approved

    Bromantane is an atypical psychostimulant and anxiolytic developed in the 1980s at the Zakusov Institute of Pharmacology of the Russian Academy of Medical Sciences, originally created as an adaptogen for Soviet military and elite athletic use and later approved in Russia for the treatment of neurasthenic and asthenic disorders under the trade name Ladasten.

    34 studiesView Profile

    Cyclazodone

    NootropicsPreclinical

    Cyclazodone is the N-cyclopropyl derivative of pemoline, a 4-oxazolidinone stimulant.

    PreclinicalView Profile

    Dihexa

    NootropicsPreclinical

    Dihexa is a synthetic peptide analogue of the angiotensin IV metabolite LVV-hemorphin-7, developed at Washington State University.

    t½ Not characterized in humans. Dihexa was engineered for metabolic stability (resistant to plasma and enzymatic degradation) and blood-brain-barrier penetration; in preclinical work its central procognitive effects appear to outlast its plasma presence. 5 to 40 mg oral per day (anecdotal range; no established human dose)
    1 studiesView Profile

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