Cognitive Peptides

Dihexa (PNB-0408, angiotensin IV analog)

Dihexa is an angiotensin IV-derived small molecule studied preclinically for synaptogenesis: it binds hepatocyte growth factor (HGF) and facilitates HGF/c-Met activation, driving dendritic spine formation in rodent models. All evidence is animal-stage — no human trial of dihexa has been conducted, one influential 2014 mechanism paper was retracted in 2025, and the related clinical analog fosgonimeton (Athira Pharma) failed its Phase 2/3 endpoint in 2024. It is research-only with no established human safety or efficacy; the platform indexes lab-verified COAs and pricing per source so researchers can vet material provenance.

Selank (TP-7)

Selank is a synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) developed at the Institute of Molecular Genetics (Russian Academy of Sciences) by extending tuftsin with a Pro-Gly-Pro stability sequence. It is registered in Russia as a prescription anxiolytic (0.15% nasal solution) for generalized anxiety disorder and asthenic conditions; it is not approved by the FDA or EMA and the clinical evidence base is primarily Russian-language literature. Research has focused on positive allosteric modulation of GABA-A receptors, inhibition of enkephalin degradation, BDNF expression, and tuftsin-derived immunomodulation. Russian clinical dosing is approximately 300mcg per dose (2–3 drops per nostril of the 0.15% solution) 2–3 times daily in 2–4 week cycles. Grey-market subcutaneous dosing (250–1000mcg/day) is not clinically validated.

Semax (ACTH(4-10) analog, Met-Glu-His-Phe-Pro-Gly-Pro)

Semax is a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) consisting of the ACTH(4-7) core with a Pro-Gly-Pro C-terminal extension that blocks enzymatic degradation. It was synthesized at the Institute of Molecular Genetics (Russian Academy of Sciences) by the Ashmarin/Myasoedov group and registered in Russia in 1994 as intranasal drops in 0.1% (cognitive/asthenic indications) and 1% (acute ischemic stroke, optic nerve disease) concentrations. Research has focused on BDNF/TrkB upregulation, NGF expression, melanocortin receptor activity, and modulation of monoaminergic tone. Because Semax lacks the C-terminal steroidogenic portion of ACTH, it does not activate the hypothalamic-pituitary-adrenal axis. Russian clinical dosing ranges from ~200–600mcg/day intranasal for cognitive/asthenic use up to ~6000mcg/day for acute stroke protocols. Grey-market subcutaneous use (250–1000mcg/day) is not clinically validated. BDNF and validated cognitive scales are the biomarkers most often tracked in research; the primary evidence base is Russian-language literature.

Racetam Nootropic (Cyclic GABA Analog)

Piracetam is a non-peptide racetam (cyclic GABA analog) approved in the EU/UK solely for cortical myoclonus; it has no FDA approval and is not a legal dietary supplement in the US, despite gray-market availability. Mechanism is incompletely understood but includes weak positive allosteric modulation of AMPA receptors at a distinct dimer-interface site, plus proposed effects on cholinergic/glutamatergic transmission and neuronal membrane fluidity. Human trials for age-related cognitive decline, post-stroke aphasia, and post-CABG cognition yielded mixed results; a Cochrane review found no support for use in dementia beyond a global-impression measure. Preclinical rodent ischemia models showed ~36% infarct-volume reduction and improved neurological outcomes. Oral bioavailability is near 100%, with renal excretion unchanged and no identified metabolites. Reported adverse effects include nervousness, insomnia, agitation, drowsiness, GI upset, and rash.

AMPA Receptor Potentiator (Racetam Nootropic)

Aniracetam is a non-peptide racetam derivative that acts as a positive allosteric modulator (“AMPAkine”) of AMPA-type glutamate receptors, binding at the receptor dimer interface to stabilize the closed-cleft conformation and slow desensitization. X-ray crystallographic and electrophysiological studies confirm this mechanism is distinct from piracetam’s binding site. One 6-month placebo-controlled trial in 109 elderly Alzheimer’s patients showed significant improvement in psychobehavioral parameters with excellent reported tolerability, though no itemized adverse-event data were published. The compound is marketed by prescription in Greece (Referan, Memodrin) and Italy (Ampamet, Draganon) but was withdrawn in Japan after a failed confirmatory study and has never been FDA-approved in the US. Despite this, it is widely sold online as a nootropic supplement, with independent testing revealing substantial label inaccuracies (75% of products with declared amounts were incorrect, ranging 0.5–502 mg vs. a 200–750 mg pharmaceutical range).

Racetam Nootropic (AMPA Receptor Modulator)

Oxiracetam is a non-peptide racetam (pyrrolidinone derivative) structurally related to piracetam, proposed to modulate AMPA-type glutamate receptors and enhance acetylcholine release in preclinical models. Approved as a prescription drug for cognitive disorders in Italy (brand Neuromet, 1984) and China, it has been studied in placebo-controlled human trials for dementia, traumatic brain injury, and organic brain syndrome. In the United States, oxiracetam is NOT FDA-approved for any indication; FDA determined (2019) it is a ‘new drug’ requiring approval and does not qualify as a dietary supplement. Oral bioavailability is ~56% in humans, with predominantly renal excretion of unchanged drug; elderly patients show doubled AUC due to reduced renal clearance. Sold in the US exclusively as an unregulated research chemical, with documented product-identity risks.

Racetam-Class Nootropic (2-Oxopyrrolidone Derivative)

Pramiracetam is a non-peptide racetam-class synthetic nootropic (2-oxopyrrolidone derivative) previously marketed in Italy and Eastern Europe for memory deficits in dementia but not FDA-approved in the US. In rat hippocampal synaptosomes, it significantly increased sodium-dependent high-affinity choline uptake without altering monoamine levels. Human data consist of small 1985–1996 trials: a placebo-controlled study in young males with head-injury/anoxia-related memory deficits found improved delayed recall at 400 mg TID; a scopolamine-challenge study showed partial mitigation of induced amnesia at 600 mg BID; an Alzheimer’s dose-finding trial (up to 4,000 mg) found no convincing benefit. No modern (post-2000) randomized controlled trials were located. Sold as a gray-market research chemical in the US; phenylpiracetam (a related racetam) is WADA-prohibited, but pramiracetam’s status is unresolved.

Racetam Nootropic (Pyrrolidinone Derivative)

Nefiracetam (DM-9384) is a non-peptide racetam-class compound studied for cognitive enhancement and poststroke depression. Japanese Phase II/III trials in dementia due to cerebrovascular disease led to a withdrawn NDA in 2002 after a repeat Phase III trial failed to show efficacy. A US/Canada multicenter Phase II trial (n=159) tested 600 mg and 900 mg/day vs. placebo for poststroke depression; no overall benefit was observed, though a post hoc subgroup analysis suggested improvement in the most severely depressed patients at 900 mg. Nefiracetam has never been approved by the FDA, EMA, or Japan’s PMDA, and no validated human dose or indication exists. It is available from research-chemical and laboratory-reagent vendors marketed “for research use only.”

Racetam-Class Pyrrolidinone Acetohydrazide (Phenylpiracetam Analog)

Phenylpiracetam hydrazide is a non-peptide racetam-class small molecule — the hydrazide analog of phenylpiracetam (fonturacetam) — in which the parent compound’s terminal carboxamide is replaced by a carbohydrazide (-C(=O)NHNH₂) group. First synthesized in 1980 as part of a Russian anticonvulsant screening program, it showed an ED₅₀ of ~310 mg/kg for seizure protection in a rodent electroshock assay. No mechanism of action has been experimentally established for this specific hydrazide derivative, and no human clinical trials exist; it is not an approved drug in any jurisdiction. The parent compound phenylpiracetam is explicitly named on the WADA Prohibited List under S6.A (Non-Specified Stimulants); whether the hydrazide analog is separately captured remains unconfirmed. Gray-market vendors sell it as a research chemical labeled ‘not for human consumption.’

Synthetic Eugeroic (Bis-fluorinated Adrafinil Analog)

Fladrafinil (CRL-40,941) is a non-peptide synthetic eugeroic structurally derived from adrafinil by bis(4-fluorophenyl) ring substitution, retaining the N-hydroxyacetamide moiety. Never approved or marketed pharmaceutically, it remains an unregulated research chemical with no clinical trials for any therapeutic indication. A 2026 pharmacokinetics study conducted for anti-doping purposes confirmed fladrafinil acts as a prodrug for flmodafinil (not modafinil). Animal studies from a 1984 patent disclosed stimulant, anti-fatigue, and anti-aggressive effects in mice and rats, but no experimentally confirmed human mechanism of action has been published. WADA added fladrafinil to its S6 non-specified stimulants list effective 1 January 2026, prohibiting in-competition use.

Fluorene Derivative (Investigational Eugeroic)

Hydrafinil (9-fluorenol) is a non-peptide fluorene derivative (C₁₃H₁₀O) investigated as a candidate next-generation eugeroic (wakefulness-promoting) compound, structurally unrelated to modafinil. A Cephalon Inc. medicinal-chemistry study in rats reported that a potent fluorene analog’s wake-promoting activity was attributed to an active metabolite; secondary sources identify that metabolite as fluorenol and cite plausible dopamine-transporter reuptake inhibition, though these details are not independently confirmed in the primary abstract. No human efficacy or safety trials exist; the only human data is a 2021 pilot study in three volunteers given a single 50 mg oral dose to characterize urinary metabolites for anti-doping detection. Hydrafinil is a WADA-prohibited S6.A stimulant (in-competition only) and is not approved by any regulatory body.

Eugeroic (Wakefulness-Promoting Agent) — Unapproved Designer Analog

Modafiendz (CAS 1613222-54-0) is an unapproved non-peptide eugeroic — a diphenylmethylsulfinylacetamide analog of modafinil bearing N-methylation and bis(4-fluoro) ring substitutions. It has never been marketed as a pharmaceutical and has no ClinicalTrials.gov record, DrugBank entry, or INN designation. No peer-reviewed human or controlled-animal pharmacology, toxicology, or efficacy data exists for this specific compound. Sold by analytical/forensic reference-standard suppliers labeled “for research/forensic use only,” it was included in an FDA-adjacent LC-HRMS surveillance method targeting novel modafinil analogs in dietary supplements, though adrafinil (not Modafiendz) was the analog confirmed present in tested products. Its closest structural relatives (flmodafinil, fladrafinil) are explicitly named WADA-prohibited S6 stimulants; Modafiendz itself is not explicitly listed but may be captured by WADA’s generic “similar structure/effect” clause.

Choline-Containing Phospholipid (Acetylcholine Precursor)

Alpha-GPC (L-alpha-glycerylphosphorylcholine) is a non-peptide choline-containing phospholipid derivative sold in the US as an unregulated nootropic and sports-performance supplement. It is marketed as a prescription cognitive drug in some countries. Human studies include a 12-week RCT in 100 amnestic mild cognitive impairment subjects (600 mg/day improved ADAS-cog by 2.34 points vs placebo), a 2-week trial in 39 healthy volunteers (400 mg/day increased self-reported motivation), and a small acute-dose study in 7 resistance-trained men (600 mg increased post-exercise growth hormone and peak bench-press force). A large Korean retrospective cohort (>12 million adults ≥50) found chronic use associated with elevated 10-year stroke risk (total stroke aHR 1.43, ischemic aHR 1.34) in a dose-dependent pattern. No validated human dosing standard exists; studied doses range 400–1200 mg/day.

eIF2B Activator (Integrated Stress Response Inhibitor)

ISRIB is a non-peptide small-molecule eIF2B activator that antagonizes the integrated stress response (ISR) by stabilizing the eIF2B guanine-nucleotide exchange factor complex and restoring translation initiation suppressed by phosphorylated eIF2α. In mice, ISRIB enhanced spatial and fear-associated long-term memory, reversed traumatic brain injury–induced cognitive deficits weeks post-injury, and reset age-related memory decline in aged animals with a brief 3-day dosing course. It also prevented neurodegeneration in prion-disease mice and, combined with imatinib, eliminated therapy-resistant chronic myeloid leukemia cells in vitro and in a mouse model. ISRIB has no completed human clinical trials, no validated human pharmacokinetic or safety data, and is not an approved drug. Chemically distinct eIF2B-activator analogs (DNL343, ABBV-CLS-7262) have human trial data, but DNL343 missed primary endpoints in a Phase 2/3 ALS trial (January 2025).

Aminoalkyl Benzoic Acid Ester (Experimental Nootropic)

PRL-8-53 is a non-peptide small-molecule aminoalkyl benzoic acid ester (methyl 3-[2-[benzyl(methyl)amino]ethyl]benzoate hydrochloride, CAS 51352-87-5) originally described in 1974 animal pharmacology as a spasmolytic and CNS-active agent. The only located human study is a 1978 double-blind trial (Hansl & Mead, Psychopharmacology) testing oral PRL-8-53 on verbal learning acquisition and retention, which reported statistically significant retention improvement (P<0.01) and no significant effects on visual reaction time or motor control. No mechanism of action has been validated in peer-reviewed literature, and no receptor-binding or target-identification studies were found. PRL-8-53 has never been approved as a drug by any regulatory agency and is currently sold only by research-chemical suppliers labeled “for research use only.”

Fatty Acid Synthase Inhibitor (Fisetin-Derived Neuroprotective)

CMS121 is a synthetic small-molecule quinoline derived from the flavonoid fisetin, designed to inhibit fatty acid synthase (FASN) and reduce lipid peroxidation—a mechanism implicated in neurodegeneration. Discovered via phenotypic screening for compounds blocking ferroptosis-related nerve cell death, CMS121 was validated by DARTS proteomics to bind FASN in neuronal and HeLa cells. In a transgenic mouse model of Alzheimer’s disease (APPswe/PS1dE9), dietary CMS121 normalized hippocampal lipid-peroxidation markers and reversed cognitive deficits in Morris water maze testing. A completed Phase 1 trial in ~100 healthy volunteers tested single doses up to 1800 mg and repeat doses up to 900 mg/day, reporting generally mild adverse events and dose-proportional pharmacokinetics with significant age and food effects. No human efficacy data exist; the compound remains investigational with no approved indication.

GABA-B Receptor Agonist (Anxiolytic-Nootropic)

Phenibut (β-phenyl-GABA) is a non-peptide GABA analogue acting primarily as a GABA-B receptor agonist — markedly weaker than baclofen (~92 μM vs ~6 μM at GABA-B) — with secondary GABA-A activity and α2-δ calcium-channel binding. Approved in Russia/Latvia since the 1960s for anxiety, sleep, and vestibular disorders, it is not FDA-approved and not a lawful US dietary ingredient; FDA has issued warning letters to sellers. No registered clinical trials exist in ClinicalTrials.gov. Human data consists of case reports documenting dependence (average 13.6 g/day in case series), severe withdrawal (anxiety, tremor, delirium, seizures), and baclofen-assisted tapering. Widely sold as an unregulated “nootropic” supplement despite regulatory action. Research-only compound with well-documented abuse and withdrawal risk.

Isoquinoline Alkaloid (Mixed Dopamine Receptor Antagonist)

L-Tetrahydropalmatine (L-THP) is a non-peptide isoquinoline alkaloid extracted from Corydalis yanhusuo and Stephania rotunda, acting as a mixed dopamine receptor antagonist (D1, D2, D3) with additional affinity for serotonin 5-HT1A and alpha-1 adrenergic receptors. Preclinical studies in rats and mice demonstrated dose-dependent reductions in methamphetamine, cocaine, and ethanol self-administration, implicating postsynaptic dopamine receptor antagonism in drug-reward pathways. The sole human randomized controlled trial (63 adults, 60 mg/day adjunctive treatment for schizophrenia) found no significant improvement in psychiatric symptoms and unexpectedly increased inflammatory markers (sICAM-1, CRP) versus placebo, contrary to animal data. L-THP is well absorbed orally with a ~10-hour human half-life but has no validated human dose for any indication outside the failed schizophrenia trial. Sold by gray-market vendors as a research chemical.

3-Hydroxypyridine Antioxidant (Membrane-Protective Agent)

Emoxypine succinate (Mexidol) is a non-peptide 3-hydroxypyridine derivative marketed as a prescription drug in Russia since the 1990s but not approved by the FDA or EMA. Proposed mechanisms include free-radical scavenging in phospholipid membranes, upregulation of antioxidant enzymes (catalase, glutathione peroxidase), allosteric modulation of GABA-benzodiazepine receptors, and succinate-driven mitochondrial complex II support under hypoxic stress. Human data derive from Russia-conducted trials, including a 333-child double-blind RCT in ADHD; independent non-Russian replication is limited. In vitro work shows inhibition of ABCB1 (P-glycoprotein) and SLCO1B1 (OATP1B1) drug transporters. A 2024 review notes pharmacological similarity to WADA-banned metabolic modulators meldonium and trimetazidine, flags it for future prohibited-list consideration, and documents past use by Russian athletes—though it is not currently WADA-prohibited. Sold in the US/EU only as an unregulated research chemical.

5-HT3 Antagonist & α7 Nicotinic Receptor Partial Agonist

Tropisetron is a non-peptide small-molecule 5-HT3 receptor antagonist and α7 nicotinic acetylcholine receptor partial agonist approved in 1992 as a prescription antiemetic (Navoban) outside the United States. Human RCT data exist for fibromyalgia (418-patient multicenter trial, 5–15 mg/day) and schizophrenia-associated cognitive/sensory-gating deficits (40-patient add-on trial, 10 mg/day), but NO validated human dosing exists for cognitive enhancement in healthy adults. Preclinical studies in rodents and aged primates show low-nanomolar tropisetron sensitizes α7-containing receptors to acetylcholine and improves memory-related task performance. Sold by gray-market vendors for research use only; all human safety data derive from clinical-trial patient populations at specific studied doses, not from healthy cognitive-enhancement users.

High-Affinity Choline Uptake Enhancer (Racetam-Family Nootropic)

Coluracetam is a non-peptide racetam-family nootropic that enhances high-affinity choline uptake (HACU) by increasing trafficking of the choline transporter CHT1 to synaptic membranes—the rate-limiting step in acetylcholine synthesis. In AF64A-lesioned rodent models, oral coluracetam (1–10 mg/kg) improved learning and memory deficits without the cholinergic side effects (tremor, salivation, hypothermia) seen with tacrine. One completed Phase 2 trial (NCT00621270, 115 participants, MDD with anxiety, 80 mg once or three times daily vs. placebo) has no posted results; no peer-reviewed human efficacy or safety data exist. Originally developed as MKC-231 (Mitsubishi Tanabe) for Alzheimer's and later as BCI-540 (BrainCells Inc.) for depression, coluracetam is not FDA-approved and is sold only as an unregulated research chemical.

Metabotropic Glutamate Receptor Activator (Racetam-Class Nootropic)

Fasoracetam is a non-peptide racetam-class small molecule (pyrrolidinone derivative) that acts as a metabotropic glutamate receptor (mGluR) activator and modulates acetylcholine release and GABA-B signaling. One completed Phase 1 trial in 30 adolescents (age 12–17) with ADHD and mGluR-network gene variants (NCT02286817, Elia et al. 2018) demonstrated significant improvement in CGI-I and CGI-S scores from baseline to week 5, with headache (63.3%) and fatigue (36.7%) as the most common adverse events. Broader ADHD development was discontinued, and fasoracetam has never been approved as a drug in any jurisdiction. It is sold only as an unregulated research chemical/nootropic by gray-market vendors.

Piperazine Derivative (Putative NMDA-Glycine-Site Modulator)

Sunifiram (DM-235, CAS 314728-85-3) is a synthetic non-peptide benzoylpiperazine derivative sold online as a cognitive enhancer, often mislabeled as an “ampakine.” Preclinical mouse and rat studies show it potentiates hippocampal long-term potentiation and reverses amnesia via activation of the glycine-binding site of the NMDA receptor, triggering a PKCα/CaMKII cascade that increases AMPA receptor phosphorylation—an indirect mechanism, not direct AMPA agonism. Sunifiram displayed antiamnesic potency roughly four orders of magnitude greater than piracetam in rodent models and increased acetylcholine release from rat cortex in vitro. No human trials or toxicology studies exist; it remains unapproved for any use worldwide and is sold without clinical vetting.

Synthetic Eugeroic (Wakefulness-Promoting Prodrug)

Adrafinil is a synthetic eugeroic (wakefulness-promoting) compound and prodrug of modafinil, metabolized in the liver to its active form. Historically approved in France (1984–2011) for narcolepsy, it was voluntarily withdrawn due to hepatotoxicity concerns. Adrafinil is pharmacologically inactive or weakly active itself; modafinil, its metabolite, acts as a weak atypical dopamine transporter (DAT) inhibitor in rodent studies. No validated human dosing regimen from a regulatory-approved label exists. It is not FDA-approved and is classified as an unapproved new drug in the US. Adrafinil is prohibited in competitive sport under WADA’s S6.a Non-Specified Stimulants category. Research is limited to historical French approval data, one forensic self-administration case (n=1), and preclinical studies in aged dogs and rats.

Cytidine Nucleotide-Choline Conjugate (Cholinergic Phospholipid Precursor)

CDP-choline (citicoline) is a non-peptide cytidine nucleotide–choline conjugate and intermediate in the Kennedy pathway for phosphatidylcholine biosynthesis. Orally administered citicoline is hydrolyzed into cytidine and choline, which cross the blood–brain barrier separately and are re-synthesized into CDP-choline within cells to support membrane phospholipid synthesis. It is approved as a prescription drug for stroke and cognitive indications in Japan and parts of Europe but sold only as a dietary supplement in the US. Small placebo-controlled trials in healthy and older adults report modest verbal/episodic memory improvements at 500–1,000 mg/day, but the largest phase 3 RCT (COBRIT, n=1,213 traumatic brain injury patients) found no functional or cognitive benefit over placebo.

Neurogenic Benzylpiperazine-Aminopyridine (Investigational Antidepressant)

NSI-189 (INN: amdiglurax; ALTO-100) is a non-peptide benzylpiperazine-aminopyridine small molecule discovered via phenotypic screening for compounds that stimulate human hippocampal neural progenitor cell proliferation and neurogenic differentiation. Its proposed antidepressant mechanism involves hippocampal neurogenesis and downstream neuroplasticity/BDNF pathways, independent of serotonin/dopamine/norepinephrine reuptake. Human trials include a Phase 1B study (n=24 MDD patients, 28-day dosing) and a Phase 2 double-blind trial (n=220, 12 weeks) that missed primary MADRS endpoints at both 40 mg and 80 mg daily, though some secondary patient-reported outcomes favored 40 mg. A 2024 Phase 2b trial (~300 adults) under the ALTO-100 designation also failed its primary endpoint. NSI-189 has never received FDA approval and remains investigational; no validated therapeutic human dose exists outside controlled research settings.

α7 Nicotinic Acetylcholine Receptor Agonist (Cinnamamide Alkaloid)

Lemairamin (WGX-50, GX-50) is a non-peptide cinnamamide alkaloid reported in preclinical rodent and cell-culture work as an α7 nicotinic acetylcholine receptor agonist. Mouse studies show it disassembles amyloid-β oligomers, reduces cortical Aβ accumulation, inhibits Aβ-induced neuronal apoptosis, and improves Morris water maze performance in transgenic Alzheimer’s models. Rodent pain models link spinal α7 nAChR activation to IL-10 and β-endorphin release, producing antinociceptive effects without evident tolerance. Microglial cultures demonstrate JAK2/STAT3 and PI3K/AKT signaling suppression of pro-inflammatory cytokines. No human clinical trials, pharmacokinetic data, or safety studies exist. Sold only as an unregulated ‘research chemical’ labeled ‘not for human consumption.’

Atypical Dopamine Transporter Inhibitor (Modafinil Analog)

(S)-CE-123 is a non-peptide atypical dopamine transporter (DAT) inhibitor structurally derived from modafinil. Unlike amphetamine-class releasers, it blocks dopamine reuptake without triggering transporter-mediated dopamine efflux. In vitro, it inhibits human DAT with EC₅₀ = 2.76 µM, showing ~30-fold selectivity over NET and >400-fold over SERT. Preclinical rodent studies report improved effort-based responding, attentional set-shifting, and spatial memory, alongside increased extracellular dopamine in the nucleus accumbens and ~5-fold greater unbound brain penetration than R-modafinil. No human clinical trials, approved indications, or validated human doses exist. Authors explicitly call for abuse-liability characterization before therapeutic development. Sold by research-chemical vendors labeled “for research use only.”

Ampakine-like Cognition Enhancer (Pyrrolopyrazinone Sulfonamide)

Unifiram (DM-232, CAS 272786-64-8) is a synthetic pyrrolopyrazinone sulfonamide derivative investigated in early-2000s Italian academic research as a cognition enhancer. Preclinical rodent studies showed it facilitated AMPA-receptor-mediated neurotransmission and increased acetylcholine release, reversing scopolamine- and NBQX-induced amnesia in mouse passive-avoidance and rat Morris water-maze tests at doses reported as ~1,000-fold lower than piracetam. Radioligand binding assays found no affinity for major central receptors, leaving the precise molecular target unidentified. Unifiram has never entered human trials, is not approved or investigational in any jurisdiction, and remains available only as an unregulated research chemical. No human pharmacokinetic, safety, or efficacy data exist.

Ladasten (Adamantane Actoprotector)

Bromantane (brand name Ladasten in Russia) is a non-peptide adamantane derivative studied as an “actoprotector” — a compound intended to sustain physical and mental performance under stress — with a combined mild stimulant and anxiolytic profile. Preclinical rat and in-vitro work attributes its effects to dopaminergic action, including regulation of tyrosine hydroxylase and an epigenetic increase in dopamine-synthesis gene transcription. Human evidence is limited to a single Russian open-label trial in asthenic disorder; no blinded, placebo-controlled trial exists, and it is not approved outside Russia. It is a WADA S6 prohibited stimulant with a historical Olympic doping scandal (Atlanta 1996), and gray-market powder is unregulated with no independent purity verification.

PE 22-28

PE-22-28 is a 7-amino-acid synthetic analog of spadin, a peptide fragment (residues 22-28) of the 44-aa propeptide (PE) released during post-translational maturation of sortilin (the neurotensin receptor-3). It is studied in preclinical models as a fast-acting antidepressant that works by selectively blocking the TREK-1 two-pore potassium channel. There is no established use for hair growth — that is a separate compound and the two should not be confused.

FPF-1070

Cerebrolysin is not a single peptide but a complex biologic produced by enzymatic hydrolysis of purified porcine brain tissue, containing low-molecular-weight peptides (<10 kDa) and free amino acids. Manufactured by EVER Pharma (Austria), it is registered in 50+ countries (Europe, Asia, Russia, Latin America) for ischemic stroke, traumatic brain injury, and dementia, but is NOT FDA-approved in the United States.

HN

Humanin is a mitochondrial-derived peptide encoded within the 16S ribosomal RNA gene. It was discovered through its ability to protect neurons from Alzheimer's disease-related toxicity and is studied for neuroprotection, metabolic regulation, and anti-aging applications.

EDR

Pinealon is a synthetic tripeptide (Glu-Asp-Arg) from the Khavinson bioregulator series, studied for its potential role in regulating pineal gland function and neuroprotective signaling pathways in preclinical models.

Semax/Selank

Pre-mixed blend of Semax (an ACTH(4-10) analog) and Selank (a heptapeptide tuftsin analog), both developed at the Russian Institute of Molecular Genetics. The individual compounds are registered as prescription drugs in Russia (intranasal); neither is FDA- or EMA-approved. The blend itself is NOT clinically validated — no controlled trial has tested Semax and Selank co-administered.

N-acetyl Semax amidate adamantylated

Adamax is a grey-market nootropic peptide developed and sold by the Mexico-based vendor Ceretropic. It is marketed as a Semax derivative: N-acetyl Semax amide (Ac-MEHFPGP-NH2) with an adamantane (adamantyl-glycine) moiety appended at the C-terminus, reportedly intended to improve metabolic stability and blood-brain-barrier penetration. It is NOT an ADNP / NAP / davunetide analog despite some online descriptions conflating it with those compounds. Adamax has no indexed peer-reviewed literature of its own; all claimed effects are extrapolated from Semax data plus anecdotal user reports.

P021

P21 (also P021) is a small peptidergic compound — the tetrapeptide core Asp-Gly-Gly-Leu with an N-terminal acetyl and a C-terminal adamantylated glycine amide (Ac-DGGL(A)G-NH2) — derived from an active region (residues ~148–151) of human ciliary neurotrophic factor (CNTF). It was designed and characterized in the Khalid Iqbal laboratory at the New York State Institute for Basic Research in Developmental Disabilities (NYS IBR). It is an experimental, preclinical compound — NOT FDA-approved and NOT tested in humans in published trials. Distinct from the cyclin-dependent kinase inhibitor protein p21/CDKN1A/WAF1 (a completely different gene product; the two share only the name).