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Research compound — not a dietary supplement
Sunifiram (DM-235) is a research compound, not a regulated dietary supplement. It is sold for research or off-label use. The evidence below is largely preclinical (animal and in-vitro) or early-stage, so no evidence score is assigned. This page is provided for transparency and education — it is not a recommendation to use. Consult a qualified healthcare provider, and be aware that purity, dosing, and legal status vary by jurisdiction.
What the evidence says
Most Sunifiram (DM-235) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality studies published 2002–2013.
Based on 5 studies
Confidence
LowBy outcome
The current evidence for Sunifiram (DM-235) is insufficient to assign an evidence score, based on 5 indexed studies. A grey-market 'research chemical' sold online as a potent nootropic — sunifiram (DM-235) is a piperazine-based experimental cognition enhancer, a structural simplification of the racetam piracetam. The CRITICAL fact is the nature of its evidence: the ENTIRE evidence base is rodent and in-vitro pharmacology, with NO human clinical trials of any kind — no efficacy data, no safety data, and no pharmacovigilance on the material people actually buy. In rodents, sunifiram has anti-amnesic and memory-enhancing effects at very low doses, acting by potentiating AMPA receptors (ampakine-like) and the glycine site of NMDA receptors, enhancing cholinergic signalling, and driving downstream CaMKII / PKCα / BDNF cascades that strengthen hippocampal long-term potentiation. None of that has ever been tested in a person. It is sold as an unregulated 'research chemical' with no approval, no human safety data, unknown long-term effects, and unverified identity, purity and dose, with anecdotal reports of stimulation and overstimulation. The presumed harms are excitatory: anxiety, insomnia, headache, and a theoretical excitotoxicity concern from chronically potentiating AMPA/NMDA signalling — all UNSTUDIED in humans. It is NOT an approved medicine, NOT a dietary supplement, and there is no human use this library can recommend. Informational, harm-reduction entry only — the honest takeaway is that sunifiram's benefit and safety in humans are entirely unstudied. Representative study: PMID 12070754.
Sarcosine
Mostly mechanism / observationalAn endogenous glycine derivative that inhibits the type-1 glycine transporter (GlyT-1), enhancing NMDA-receptor co-agonism. It is studied as a prescription-style PSYCHIATRIC ADJUNCT — with genuine add-on RCTs in schizophrenia (and smaller signals in OCD and depression) — not as a casual nootropic. Evidence is real but narrow and emerging.
Tianeptine
Last reviewed June 2026 · evidence from 5 studies · how we score
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
Sunifiram (DM-235; 1-benzoyl-4-propanoylpiperazine) — a piperazine-based experimental nootropic and structural simplification of piracetam, studied ONLY preclinically (rodent / in-vitro) with NO human clinical trials of any kind
A grey-market 'research chemical' sold online as a potent nootropic — sunifiram (DM-235) is a piperazine-based experimental cognition enhancer, a structural simplification of the racetam piracetam. The CRITICAL fact is the nature of its evidence: the ENTIRE evidence base is rodent and in-vitro pharmacology, with NO human clinical trials of any kind — no efficacy data, no safety data, and no pharmacovigilance on the material people actually buy. In rodents, sunifiram has anti-amnesic and memory-enhancing effects at very low doses, acting by potentiating AMPA receptors (ampakine-like) and the glycine site of NMDA receptors, enhancing cholinergic signalling, and driving downstream CaMKII / PKCα / BDNF cascades that strengthen hippocampal long-term potentiation. None of that has ever been tested in a person. It is sold as an unregulated 'research chemical' with no approval, no human safety data, unknown long-term effects, and unverified identity, purity and dose, with anecdotal reports of stimulation and overstimulation. The presumed harms are excitatory: anxiety, insomnia, headache, and a theoretical excitotoxicity concern from chronically potentiating AMPA/NMDA signalling — all UNSTUDIED in humans. It is NOT an approved medicine, NOT a dietary supplement, and there is no human use this library can recommend. Informational, harm-reduction entry only — the honest takeaway is that sunifiram's benefit and safety in humans are entirely unstudied.
Sunifiram (DM-235) is a grey-market 'research chemical' — a piperazine-based experimental nootropic and structural simplification of piracetam — whose ENTIRE evidence base is rodent and in-vitro pharmacology with NO human clinical trials of any kind. The literature cited here is real and consistent in animals: anti-amnesic, memory-enhancing effects at very low doses (Ghelardini 2002; Martini 2009; Guandalini 2012) acting via AMPA-receptor potentiation and the glycine site of the NMDA receptor with downstream CaMKII / PKCα signalling and enhanced hippocampal LTP (Moriguchi 2013a, 2013b). But none of it is human evidence — there are no efficacy, safety or pharmacokinetic trials in people. The dominant signal is therefore an ABSENCE of any human data, against a presumed excitatory harm profile (anxiety, insomnia, overstimulation, theoretical excitotoxicity from chronic AMPA/NMDA potentiation) and grey-market quality risk (unverified identity, purity and dose), so the score sits low.
Sunifiram — development code DM-235, chemically 1-benzoyl-4-propanoylpiperazine — is a piperazine-based experimental nootropic created by simplifying the structure of the racetam piracetam.
In the foundational pharmacology, DM-235 prevented chemically induced amnesia in mice and rats at extraordinarily low doses (roughly a thousand-fold more potent than piracetam in the same models) without impairing motor coordination or spontaneous activity, which is why it was framed as a candidate cognition enhancer and anti-amnesic for conditions like Alzheimer's disease.
Mechanistic work since then has mapped how it does this in rodent tissue: sunifiram potentiates AMPA receptors in an ampakine-like fashion and stimulates the glycine-binding site of the NMDA receptor, enhancing NMDA-dependent hippocampal long-term potentiation; this is coupled to increased phosphorylation of AMPA-receptor subunits via CaMKII and of NMDA-receptor subunits via PKCα (through Src-family kinase signalling), with enhanced cholinergic transmission and downstream BDNF-related plasticity.
The honest description of its evidence base is that it is ENTIRELY PRECLINICAL. There are NO human clinical trials of sunifiram — none for efficacy, none for safety, none for pharmacokinetics.
Every result that vendors and nootropic forums cite comes from rodent behavioural tests (passive-avoidance, Y-maze, novel-object recognition, Morris water maze) and ex-vivo / in-vitro slice electrophysiology and biochemistry.
Promising as that animal signal is, it cannot be transferred to a human dose, and a 'research chemical' bought online is of unverified identity, purity and quantity, so even the rodent dose-response is no guide to what a person is actually taking.
The expected harm profile is likewise inferred, not measured: as an excitatory agent that potentiates AMPA and NMDA signalling, sunifiram is anecdotally reported to be stimulating, with overstimulation effects such as anxiety, insomnia and headache, and it carries a theoretical excitotoxicity concern from chronically driving glutamatergic signalling — none of which has been characterised in humans.
Layered on top is the grey-market reality: an unregulated substance sold (often 'not for human consumption') with no quality system, no medical supervision, no monitoring, and unknown drug interactions.
The evidence score sits low and the level is 'Emerging' precisely because the dominant signal here is the ABSENCE of any human data at all — a real and interesting preclinical pharmacology, but zero translation to people.
This is an informational, harm-reduction entry: the responsible conclusion is that sunifiram is an essentially unstudied-in-humans experimental nootropic sold as a 'research chemical', not a supported intervention, and there is no human use this library endorses.
In rodent hippocampal tissue, sunifiram potentiates AMPA-type glutamate receptors in an ampakine-like fashion, increasing phosphorylation of AMPA-receptor subunits via CaMKII and raising the slope of field excitatory postsynaptic potentials. This strengthens fast excitatory neurotransmission and underlies the enhancement of long-term potentiation seen in animal work — characterised only in rodent/ex-vivo tissue, never in humans.
Sunifiram stimulates the glycine-binding site of the NMDA receptor and enhances NMDA-dependent long-term potentiation in hippocampal CA1, with downstream PKCα activation through Src-family kinase and NMDA-subunit phosphorylation. This glutamatergic-plasticity mechanism explains the rodent memory and anti-amnesic effects — but it is also the basis of the theoretical excitotoxicity concern, and it is entirely preclinical.
In animal models sunifiram restores cholinergic-dependent memory (it reverses scopolamine- and mecamylamine-induced amnesia) and engages CaMKII/PKCα cascades linked to -related synaptic plasticity. These downstream effects are inferred from rodent biochemistry and behaviour; sunifiram's pharmacology in humans is completely uncharacterised.
How Sunifiram (DM-235) works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Tap node to isolate • Pinch to zoom • Tap edge for research
There is no established or legitimate human dose. Sunifiram is an UNSTUDIED-IN-HUMANS grey-market 'research chemical' with no clinical trials, no approval, and no pharmacovigilance — this library does NOT provide a dosing protocol. The only quantitative data are rodent: anti-amnesic effects in mice at roughly 0.001–0.1 mg/kg (intraperitoneal) or 0.01–0.1 mg/kg (oral) and synaptic potentiation in hippocampal slices at nanomolar concentrations, which cannot be converted to a safe human dose. Vendors and forums quote figures in the tens of milligrams orally, but these are unverified extrapolations for a product of unknown identity and purity, taken without medical supervision or monitoring, with anecdotal reports of overstimulation.
Can be taken without food
| Form | Type |
|---|---|
| 💊No human form is endorsed — sunifiram is an experimental 'research chemical' nootropic with no approved or supplement form | Recommended |
There is no over-the-counter, supplement or prescription form of sunifiram. Grey-market powder/capsules are of unverified identity and purity and are frequently sold 'not for human consumption'.
Minimum: 1 weeks
Optimal: 4 weeks
Cycling: Not required
Note: No human timing is endorsed. Sunifiram is an experimental nootropic unstudied in humans, with an inferred excitatory harm profile (overstimulation, anxiety, insomnia, theoretical excitotoxicity). Morning-only framing is harm-reduction to limit insomnia if exposure occurs; this library does not schedule its use.
Dose-response data unavailable. The current published research for Sunifiram (DM-235) does not provide sufficient dose-specific outcome data to generate reliable dose-response curves.
Refer to the Dosage & Timing section above for recommended dose ranges based on available evidence.
There are no published human trials of sunifiram of any kind — no demonstrated cognitive, memory or performance benefit in people, and no safety or pharmacokinetic data. Every result is from rodent behavioural tests and in-vitro / ex-vivo slice pharmacology. Any 'benefit' claimed for sunifiram in humans is an extrapolation from animal work, not a measured human result.
In rodents sunifiram is anti-amnesic and memory-enhancing at very low doses — reversing scopolamine-induced amnesia and improving Y-maze, novel-object-recognition and water-maze performance, with potency roughly a thousand-fold above piracetam in the same model. In humans this is UNPROVEN: no person has ever been tested, so the cognitive benefit is an animal-only inference, not a trial result, and it comes bundled with the excitatory harms below.
Marketed as a focus and clarity nootropic, sunifiram's only support is its rodent procognitive and synaptic-plasticity profile. No human study has tested it for focus or attention, so any such benefit is assumed, not shown, and may not transfer to people at unknown grey-market doses.
As an AMPA/NMDA-potentiating excitatory agent, sunifiram is anecdotally reported to be stimulating, with users describing overstimulation, anxiety, jitteriness and headache. With no human dose-finding and a 'research chemical' of uncertain potency, there is nothing to bound these effects — they are inferred from the mechanism and user reports, not characterised.
A stimulating, excitatory nootropic taken without dosing guidance is widely reported to disrupt sleep, especially later in the day. By extrapolation from its excitatory mechanism and anecdotal stimulation, sunifiram is expected to interfere with falling asleep; there is no human data to quantify the risk.
Chronically potentiating AMPA and NMDA (glutamatergic) signalling raises a theoretical excitotoxicity concern — completely unstudied for sunifiram in humans. Combined with the grey-market reality of unverified identity, purity and dose and unknown drug interactions, the safety picture is fundamentally unknown rather than reassuring.
Avoid — sunifiram is unstudied in humans, of unverified identity and dose, and carries a presumed excitatory harm profile (overstimulation, anxiety, insomnia, theoretical excitotoxicity). There is no human evidence of benefit.
Avoid — sunifiram is an excitatory, anecdotally stimulating agent likely to worsen anxiety and disrupt sleep.
Avoid — potentiating AMPA/NMDA glutamatergic signalling is theoretically pro-excitatory, with no human safety data.
Avoid — no human interaction data exists for an unstudied, CNS-active 'research chemical'.
Avoid entirely — no human safety data of any kind for sunifiram.
Combining sunifiram with caffeine, ADHD stimulants or other sympathomimetics compounds the expected overstimulation, anxiety and insomnia; the additive effect is uncharacterised in a product of unknown potency.
Sunifiram acts on the NMDA glycine site and potentiates AMPA signalling; stacking it with other glutamatergic agents could unpredictably amplify or oppose excitatory neurotransmission, with no human data to bound the interaction.
Tip: Expected of an excitatory, anecdotally stimulating nootropic; there is no validated human dosing to limit it. The only harm-reduction note is that there is no established safe dose, so the conservative choice is to avoid use.
Tip: Commonly reported anecdotally with sunifiram and related ampakine-type nootropics. With an unstudied agent of uncertain potency there is no dose-finding to bound it; stop use if it occurs.
Tip: Expected of a stimulating excitatory agent, especially if taken later in the day; there is no human dosing to limit this, and the only note is that evening exposure is worse than morning.
Tip: Chronically driving glutamatergic signalling raises a theoretical neuronal-injury concern that is completely unstudied for sunifiram in humans. The unknown is the point: avoid chronic exposure rather than assume it is safe.
The commonly studied dose of Sunifiram (DM-235) is There is no established or legitimate human dose. Sunifiram is an UNSTUDIED-IN-HUMANS grey-market 'research chemical' with no clinical trials, no approval, and no pharmacovigilance — this library does NOT provide a dosing protocol. The only quantitative data are rodent: anti-amnesic effects in mice at roughly 0.001–0.1 mg/kg (intraperitoneal) or 0.01–0.1 mg/kg (oral) and synaptic potentiation in hippocampal slices at nanomolar concentrations, which cannot be converted to a safe human dose. Vendors and forums quote figures in the tens of milligrams orally, but these are unverified extrapolations for a product of unknown identity and purity, taken without medical supervision or monitoring, with anecdotal reports of overstimulation.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
The best time to take Sunifiram (DM-235) is in the morning. It can be taken on an empty stomach. As an excitatory, anecdotally stimulating nootropic, sunifiram is taken in the morning to limit insomnia if exposure occurs.
Sunifiram (DM-235) should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are overstimulation, anxiety & jitteriness, headache, insomnia / disrupted sleep. Use caution if any of these apply to you: Any human use — sunifiram is an experimental 'research chemical' UNSTUDIED in humans (no efficacy, safety or pharmacokinetic trials), of unverified identity, purity and dose; it is NOT a dietary supplement and NOT an approved medicine; Anyone seeking it for memory, focus or 'nootropic' enhancement — there is no human evidence of benefit for sunifiram and a presumed excitatory harm profile; Anyone with anxiety, insomnia or a history of overstimulation / panic — sunifiram is an excitatory, anecdotally stimulating agent.
An atypical antidepressant — brand Stablon/Coaxil/Tatinol — approved and prescribed for major depression (and anxious depression) in parts of Europe, Asia and Latin America, where randomized trials show efficacy comparable to SSRIs and tricyclics, often with better tolerability at the therapeutic dose (12.5 mg three times daily). Mechanistically it is unusual: it modulates the stress system and enhances glutamatergic/hippocampal plasticity, and — the critical fact for harm reduction — it is a FULL MU-OPIOID RECEPTOR AGONIST. That opioid action explains both its antidepressant effect AND its abuse potential. In the United States it is NOT FDA-approved; the FDA has warned about it, and it is sold illicitly as an unapproved 'nootropic'/'supplement' ('Tianaa', 'Za Za', 'Pegasus') nicknamed 'gas station heroin'. The dominant recent US literature is not efficacy but ABUSE, DEPENDENCE, opioid-like WITHDRAWAL, overdose/toxicity (usually at supratherapeutic doses far above the clinical dose), and rising poison-center exposures. The honest framing: a genuine antidepressant abroad with proven short-term efficacy at the prescribed dose, but a mu-opioid agonist carrying real dependence/abuse/withdrawal/overdose risk and no US approval. Informational, harm-reduction entry only — not a recommendation, and not a substitute for clinician-supervised treatment.
Because sunifiram is sold as an unregulated 'research chemical', the substance, its purity, its actual dose and its human pharmacokinetics are not assured or known. The rodent dose-response (active in micrograms-to-milligrams per kilogram) cannot be converted to a safe human dose, and what a buyer ingests is not guaranteed to match any label or any published reference.
Stacking a CNS-active 'research chemical' of unknown human pharmacology with psychiatric medications risks additive or unpredictable CNS effects; sunifiram has no interaction data, so the combination is uncharacterised and unsafe to assume benign.
Because sunifiram is pro-excitatory (AMPA/NMDA potentiation), combining it with agents that lower the seizure threshold is a theoretical risk; there is no human evidence either way, so caution is the only defensible stance.
Tip: A 'research chemical' of unverified identity and quantity can deliver the wrong substance or the wrong dose entirely. There is no quality system or assay behind it; the only mitigation is to not consume an unverified compound.