Cognitive Peptide Dosage Protocols
Cognitive and neurotropic peptides modulate neurotrophin expression and synaptic plasticity. Selank, Semax, Cerebrolysin, and the Khavinson short-chain peptides (Pinealon, Adamax, PE-22-28) sit in this directory.
18 protocols indexed
Noopept
Noopept (development code GVS-111; international nonproprietary name Omberacetam) is a synthetic proline-containing dipeptide nootropic, chemically N-phenylacetyl-L-prolylglycine ethyl ester, designed at Russia's Zakusov Institute of Pharmacology to reproduce the activity of the pyrrolidone nootropic piracetam in a far more potent, peptide-like scaffold [1][8]. It behaves as a prodrug: in the brain it is rapidly hydrolyzed and cyclized to cycloprolylglycine (cPG), an endogenous AMPA-receptor-modulating dipeptide, and it raises hippocampal expression of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) while blunting the neurotoxic "triad" of excess intracellular calcium, glutamate excitotoxicity and free radicals [1][2][3]. The standard Noopept dosage in Russian clinical practice is 10 mg twice daily (20 mg/day total), within a usual range of 10-30 mg/day taken orally or sublingually over courses of roughly 1.5 to 3 months [5]. Because the parent molecule has a very short plasma half-life (on the order of minutes) while the cPG metabolite persists longer, divided twice-daily dosing sustains the effect [6][7]. Noopept is sold over the counter as a medicine in Russia and some neighbouring countries but is NOT approved by the FDA or EMA; in the United States it is an unapproved drug available only for research. The subcutaneous reconstitution figures below are an educational reference, not medical advice.
Open Protocolarrow_forwardNootropic Mitochondrial EnhancerMethylene Blue
Methylene Blue (methylthioninium chloride) is a synthetic phenothiazine dye and small-molecule mitochondrial/metabolic enhancer first synthesized in 1876, now used at low doses as a nootropic and at higher intravenous doses as an established antidote. It is a redox-active electron cycler: at low concentrations it accepts electrons from NADH and donates them to cytochrome c, bypassing complexes I-III to raise brain cytochrome c oxidase activity, cerebral oxygen consumption, and ATP output; at high concentrations it flips to a pro-oxidant, producing the classic hormetic, inverted-U dose-response. The most-studied Methylene Blue dosage for cognition is a single low oral dose of roughly 0.5-4 mg/kg (about 260-280 mg in controlled human fMRI and fear-extinction trials), while daily low-dose nootropic users typically take far less, on the order of 5-30 mg. It also potently inhibits monoamine oxidase-A and reduces methemoglobin back to functional hemoglobin. Regulatory status: Methylene Blue is FDA-approved as an intravenous drug (Provayblue, 2016) for acquired methemoglobinemia at 1 mg/kg IV; low-dose oral nootropic use is off-label and not FDA-approved. The subcutaneous reconstitution figures on this page are an educational measurement reference only, because the real-world route is oral (or hospital IV). Only pharmaceutical USP-grade material is appropriate for human reference.
Open Protocolarrow_forwardNootropic PeptidomimeticDihexa
Dihexa (PNB-0408; N-hexanoic-Tyr-Ile-(6)-aminohexanoic amide) is a synthetic, orally active peptidomimetic in the angiotensin IV-derived hepatocyte growth factor (HGF)/c-Met nootropic class, engineered at Washington State University to be metabolically stable and blood-brain-barrier permeable. In rodents it was reported to potentiate HGF signaling, drive synaptogenesis at picomolar concentrations, and reverse chemically induced memory deficits. There is no validated human Dihexa dosage. Published preclinical work used oral gavage at about 1.25-2 mg/kg, while nootropic communities self-report 5-20 mg once daily by mouth or applied topically in a DMSO carrier. The closest human data come not from Dihexa itself but from fosgonimeton (ATH-1017), a related HGF/MET prodrug that cleared Phase 1 but failed its Phase 2 and Phase 2/3 Alzheimer's trials in 2024. Critically, several foundational Dihexa mechanism papers were retracted in 2025 for fabricated data, so its proposed mechanism should be treated as unproven. Dihexa is not approved by the FDA or EMA and is sold only as a research chemical. The subcutaneous reconstitution figures below are an educational reference, since the real-world route is oral or topical, not injection.
Open Protocolarrow_forwardNootropic PeptideN-Acetyl Semax Amidate
N-Acetyl Semax Amidate (NA-Semax, Semax amidate) is a doubly modified analog of the Russian nootropic neuropeptide Semax, which is itself derived from the adrenocorticotropic hormone fragment ACTH(4-10) fused to the C-terminal tripeptide Pro-Gly-Pro. Its sequence, Ac-Met-Glu-His-Phe-Pro-Gly-Pro-NH2, adds an N-terminal acetyl group and a C-terminal amide to the parent Semax heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro), blocking aminopeptidase and carboxypeptidase cleavage so the molecule resists enzymatic breakdown and is thought to act longer and more potently per microgram. Mechanistically it upregulates brain-derived neurotrophic factor (BDNF) and its TrkB receptor, modulates dopaminergic and serotonergic tone, and inhibits enkephalin-degrading enzymes, effects linked to attention, memory consolidation, and neuroprotection. The headline N-Acetyl Semax Amidate dosage studied and used in practice is roughly 300-600 mcg per day intranasally, sometimes up to 900 mcg and frequently split into morning doses, delivered as a metered nasal spray. As a member of the regulatory-peptide / nootropic class, it is not approved by the FDA or EMA; the parent Semax is registered only in Russia for ischemic stroke and cognitive disorders, and NA-Semax Amidate is sold in Western markets strictly for research and educational use. The subcutaneous reconstitution figures on this page are an educational measurement reference only; the real-world route is intranasal.
Open Protocolarrow_forwardNootropic Anxiolytic PeptideN-Acetyl Selank Amidate
N-Acetyl Selank Amidate (NA-Selank, Selank amidate) is a second-generation synthetic analog of the heptapeptide anxiolytic Selank, which is itself derived from the endogenous immunomodulatory tetrapeptide tuftsin (Thr-Lys-Pro-Arg) extended with a Pro-Gly-Pro tail. The "amidate" form adds N-terminal acetylation and C-terminal amidation, two modifications that cap the alpha-amino and carboxyl termini, block aminopeptidase and carboxypeptidase cleavage, and are expected to extend metabolic stability relative to native Selank [2][8]. Like its parent, it is studied as a non-benzodiazepine positive allosteric modulator of GABAergic tone and an upregulator of brain-derived neurotrophic factor (BDNF), producing anxiolytic and nootropic effects without the sedation, tolerance, or dependence seen with benzodiazepines in the parent compound's Russian clinical trials [1][3][8]. The headline N-Acetyl Selank Amidate dosage used in research and nootropic practice is 600-900 mcg per day administered intranasally, divided across 2-3 doses of roughly 300 mcg each, typically run in 14-day cycles with a washout period. No dedicated human trials of the amidate itself exist; its profile is inferred from the substantial Selank literature plus the known pharmacology of terminal peptide modification. N-Acetyl Selank Amidate has no FDA, EMA, or MHRA approval; only the parent Selank is registered as a prescription nasal solution in Russia. Outside Russia it is a research and educational compound only. This page presents an educational subcutaneous reconstitution reference, although the real-world route is intranasal.
Open Protocolarrow_forwardNeuroprotective PolypeptideCortexin
Cortexin is a low-molecular-weight polypeptide complex extracted from mammalian (bovine, sometimes porcine) cerebral cortex and classed as a nootropic, neuroprotective neuropeptide preparation. Each batch contains a mixture of acidic and neutral water-soluble polypeptides of roughly 1,000-10,000 daltons together with the stabilizing amino acid glycine [1]. Marketed by the Russian manufacturer Geropharm and approved for prescription use in Russia and several CIS countries, but not by the FDA or EMA, it is injected intramuscularly for stroke recovery, traumatic brain injury, epilepsy, encephalopathy, and cognitive or developmental disorders in children. The standard adult Cortexin dosage is 10 mg once daily as a 10-day course; the 5 mg formulation is used in children under 20 kg at about 0.5 mg/kg, and acute ischemic-stroke protocols give 10 mg twice daily [3][4]. Mechanistically, its peptides modulate glutamatergic (AMPA, kainate, mGluR) and GABAergic transmission, act as antioxidants and anti-inflammatories, inhibit brain caspase-8-mediated apoptosis, and bind neuron-specific partners such as beta-tubulin, creatine kinase B and 14-3-3 proteins, while crossing the blood-brain barrier in animal models [2][5]. Most supporting evidence comes from Russian clinical studies and rodent ischemia models rather than large international trials. As an unapproved compound in the US and EU, this polypeptide complex is presented here for educational purposes only, not as medical advice.
Open Protocolarrow_forwardCNS Peptide BioregulatorCerluten
Cerluten (also sold as CNS Cytomax A-5) is a peptide bioregulator from Vladimir Khavinson's Russian school of bioregulation. It is not a single defined molecule but a low-molecular-weight polypeptide complex (peptides up to roughly 10 kDa) extracted from the cerebral cortex of young calves and formulated as 10 mg oral capsules for central-nervous-system support [1][2]. The proposed mechanism is tissue-specific epigenetic regulation of gene expression in neural cells, in the same conceptual framework as the injectable cortical extract Cortexin and the synthetic Khavinson short peptides [2][3]. The most commonly published Cerluten dosage is 1-2 capsules (10-20 mg) one to two times daily with food, delivering 10-40 mg of the A-5 complex per day, taken as a one-month course one or two times per year [5][7]. Because Cerluten is an undefined biological extract, no human pharmacokinetic studies have been published, so its half-life is not formally characterized; the real-world route is oral, and the subcutaneous reconstitution figures on this page are an educational measurement convention used across this site rather than a validated delivery method. Cerluten is marketed as a dietary supplement in Russia and is NOT approved by the FDA, EMA, or any Western regulatory agency; published evidence is largely preclinical and class-level rather than from Cerluten-specific randomized trials. This page is an educational reference only and is not medical advice.
Open Protocolarrow_forwardCNTF-Derived Nootropic PeptideP21
P21 (also written P021; aliases include the CNTF-derived peptide and GLXC-21260) is a small synthetic peptidergic compound modeled on the active region of human ciliary neurotrophic factor (CNTF). Its sequence is Ac-DGGL(A)G-NH2, an N-acetylated, C-amidated tetra/hexapeptide carrying an adamantylated glycine that confers oral bioavailability, metabolic stability, and blood-brain-barrier penetration. Developed by Khalid Iqbal and colleagues at the New York State Institute for Basic Research, P21 enhances dentate gyrus neurogenesis and dendritic/synaptic plasticity by competitively inhibiting leukemia inhibitory factor (LIF) signaling and increasing brain-derived neurotrophic factor (BDNF) expression, which lowers GSK-3β activity and abnormal tau phosphorylation [1][3]. Critically, all efficacy data come from rodent Alzheimer's, aging, and neurodevelopmental models; there are no published human clinical trials. In studies the compound was given orally (in the diet) rather than by injection. Because no validated human protocol exists, the P21 dosage figures presented here are an educational subcutaneous reconstitution reference rather than a clinically established regimen; community use trends toward roughly 0.5–1 mg per day by oral or intranasal routes. Plasma half-life in rodents exceeds three hours (versus minutes for native CNTF). P21 is not approved by the FDA, EMA, or any regulator and is sold strictly as a research chemical. This monograph summarizes its mechanism, preclinical evidence, and a measurable reconstitution model for educational purposes only; it is not medical advice.
Open Protocolarrow_forwardNootropic & NeuropeptideSelank
Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) is a synthetic heptapeptide anxiolytic derived from the endogenous immunomodulator tuftsin, developed at the Russian Academy of Sciences' Institute of Molecular Genetics. It acts as a non-benzodiazepine GABA-A modulator and upregulates brain-derived neurotrophic factor (BDNF), producing anxiolysis without sedation, dependence, or withdrawal [1][2]. In a controlled trial of generalized anxiety disorder, Selank produced anxiolytic efficacy equivalent to medazepam while improving rather than impairing attention and working memory [3]. Intranasal dosing of 250–750 mcg per administration two to three times daily (total 900–1350 mcg) is the standard Russian clinical regimen across 14-day courses. Selank is registered as a prescription pharmaceutical in Russia (Peptogen, 0.15% nasal solution) for anxiety and asthenic disorders but has no FDA, EMA, or MHRA approval; in the United States it remains a research compound only. Its safety record across two decades of clinical use is favorable, with no reported abuse liability.
Open Protocolarrow_forwardResearch PeptideAdamax
Adamax (Ac-MEHFPGP-AG-NH2) is a synthetic nonapeptide derivative of Semax with an N-terminal acetyl group and a C-terminal Ala-Gly amide tail engineered to confer greater enzymatic stability and lipophilicity than the parent ACTH(4-10) analogue [1]. It belongs to the broader family of melanocortin-derived nootropic peptides developed within the Russian Academy of Sciences' neuropeptide program. Like Semax, Adamax is investigated for melanocortin receptor activity, BDNF/TrkB upregulation, and protection against ischemic and oxidative neuronal injury, with the modified backbone giving it longer in vivo half-life and stronger blood-brain barrier penetration on a per-dose basis [2]. Research dosing is typically 100–600 mcg intranasally one to two times daily, well below the equivalent Semax dose range, with cycle lengths of 2–6 weeks. Adamax is not FDA approved, has no EMA authorization, and is not registered as a pharmaceutical in any jurisdiction; it remains a research-only compound with no published human clinical trials.
Open Protocolarrow_forwardResearch PeptideCerebrolysin
Cerebrolysin is a porcine brain-derived peptide and amino acid concentrate produced by enzymatic hydrolysis of purified porcine brain proteins, yielding a complex mixture of low-molecular-weight neuropeptides (under 10 kDa) with neurotrophic activity analogous to BDNF, NGF, GDNF, and CNTF. It is registered as a prescription neurotrophic drug in over 50 countries (including Austria, Germany, Russia, China, and across Eastern Europe) for stroke, traumatic brain injury, vascular dementia, and Alzheimer disease [1][2]. The pivotal CASTA and CARS randomized trials demonstrated improved neurological recovery at 30 mL intravenous daily for 10–21 days in acute ischemic stroke [3][4], and the CONSCIOUS observational program documented arousal improvements in minimally conscious state at 10 mL/day for 20+ days. Cerebrolysin is not FDA approved and is unavailable in the United States. Typical adult dosing ranges from 5 to 30 mL daily by slow IV infusion or intramuscular injection, with 10-day to 4-week cycles repeated 1–4 times yearly depending on indication.
Open Protocolarrow_forwardNootropic & NeuropeptideDSIP
DSIP (Delta Sleep-Inducing Peptide) is a naturally occurring nonapeptide (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) first isolated by Schoenenberger and Monnier in 1977 from the cerebral venous dialysate of rabbits undergoing slow-wave sleep induced by intralaminar thalamic stimulation [1][2]. Synthetic DSIP enhances delta and spindle EEG activity, modulates the hypothalamic-pituitary axis, and exerts measurable effects on circadian rhythm, cortisol release, and growth hormone secretion in rodents and small human cohorts, with EEG delta activity rising approximately 35 percent in cortex of recipient rabbits [3][4]. The peptide does not bind GABA-A, melatonin, or adenosine receptors with high affinity; its mechanism appears to involve indirect modulation of CRH tone, GHRH pulses, and central noradrenergic activity. In a controlled clinical study of chronic insomniacs, intravenous DSIP at 25 nmol/kg increased total sleep time, improved subjective sleep quality, and slightly increased REM sleep without daytime sedation or hangover effect [5]. DSIP is not approved by the FDA, EMA, or other Western regulators and is used in research contexts only. Typical research dosing is 100 to 500 mcg subcutaneously or intramuscularly approximately 30 to 60 minutes before sleep onset, cycled 5 to 14 nights per month rather than continuously.
Open Protocolarrow_forwardBioregulator PeptideCortagen
Cortagen is a synthetic tetrapeptide (Ala-Glu-Asp-Pro, AEDP) developed by Vladimir Khavinson and colleagues at the St. Petersburg Institute of Bioregulation and Gerontology, derived by directed synthesis from the amino-acid composition of the polypeptide preparation Cortexin (a bovine cerebral cortex hydrolysate used in Russian neurology since the 1980s) [1][2]. Cortagen is classified as a peptide bioregulator targeting the cerebral cortex and is investigated for neuroprotection, cognitive support, nerve regeneration, and modulation of neurogenic and immune gene programs. Preclinical work shows Cortagen activates interleukin-2 mRNA synthesis, corrects metabolic disturbances in models of chronic cerebral ischemia, and supports peripheral and central nerve regeneration after injury [3]. Research dosing is empirical: typically 100–400 mcg/day subcutaneously or 1–3 mg/day orally across 10–20 day cycles, repeated 2–4 times yearly. Cortagen is registered as a dietary peptide product in Russia under bioregulator legislation but has no FDA, EMA, or MHRA approval. Human safety data are limited to Russian observational use.
Open Protocolarrow_forwardResearch PeptideOxytocin
Oxytocin is a nine-amino-acid cyclic neuropeptide (Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-Gly-NH2) synthesized in the paraventricular and supraoptic nuclei of the hypothalamus and released from the posterior pituitary, acting through the oxytocin receptor (OXTR), a Gq-coupled GPCR, to mediate uterine contraction during labor, milk ejection during lactation, and a broad range of central effects on social bonding, stress regulation, fear extinction, and pair-bonding behavior across mammalian species [1][2]. Synthetic oxytocin (Pitocin) has been FDA approved since 1962 for medical induction or augmentation of labor, control of postpartum hemorrhage, and management of incomplete or inevitable abortion, with ACOG-standardized titration protocols based on uterine contraction adequacy [3]. Research applications outside obstetrics use intranasal or sublingual formulations to study social cognition, autism spectrum disorder, post-traumatic stress disorder, and alcohol use disorder, with typical doses of 12 to 40 IU intranasally given 30 to 45 minutes before behavioral or psychophysiological testing [4][5]. Off-label and research dosing varies widely by formulation and indication; the obstetric route remains intravenous infusion only, while behavioral neuroscience studies use intranasal delivery designed to reach the brain via olfactory and trigeminal pathways.
Open Protocolarrow_forwardResearch PeptidePE-22-28
PE-22-28 is a 7-amino-acid synthetic peptide derived as a truncated analogue of spadin, the 17-residue sortilin-derived peptide first described by Mazella and colleagues in PLoS Biology 2010 as a selective TREK-1 potassium channel blocker with antidepressant-like activity [1]. PE-22-28 was developed by Djillani and colleagues in 2017 as a shortened analog with dramatically improved potency (IC50 ~0.12 nM vs. 40–60 nM for spadin), in vivo stability, and action duration of up to 23 hours [2]. By inhibiting the two-pore-domain potassium channel TREK-1, PE-22-28 produces fast-onset antidepressant effects in rodent models without the cardiovascular, gastrointestinal, or pro-seizure side effects associated with TREK-1 knockout phenotypes. PE-22-28 has no human clinical trial data, no FDA or EMA approval, and is not registered as a pharmaceutical in any jurisdiction. It remains a research-only compound used preclinically at typical doses of 100–500 mcg/kg subcutaneously or intranasally; equivalent human research dosing is empirical and unvalidated.
Open Protocolarrow_forwardBioregulator PeptidePinealon
Pinealon is a synthetic tripeptide (Glu-Asp-Arg, EDR) designed by Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology as a short-peptide bioregulator targeting the pineal gland and broader neuroendocrine system [1][2]. It belongs to the Khavinson cytogen family of short peptides that, according to Khavinson and colleagues, penetrate plasma and nuclear membranes to bind specific DNA sequences and modulate tissue-specific gene programs. Preclinical work documents neuroprotection against hypoxia and oxidative stress, modulation of PCNA and p21 expression in neuronal cultures, and protection of induced neurons from age-related changes [3][4]. Research dosing varies widely: published rodent protocols use 10–100 mcg subcutaneously or intranasally, while outpatient Russian peptide-bioregulator practice uses 1–20 mg orally per day in 10–30 day cycles repeated 2–4 times per year. Pinealon is registered in Russia under dietary peptide-bioregulator legislation but has no FDA, EMA, or MHRA approval. Human safety data are limited to observational use.
Open Protocolarrow_forwardNootropic & NeuropeptideSemax
Semax (Met-Glu-His-Phe-Pro-Gly-Pro, MEHFPGP) is a synthetic heptapeptide analogue of adrenocorticotropic hormone fragment ACTH(4-10), with a stabilizing Pro-Gly-Pro tail added to confer resistance to proteolysis. Developed at the M. M. Shemyakin and Yu. A. Ovchinnikov Institute of Bioorganic Chemistry by Kaplan, Ashmarin and colleagues, Semax exerts nootropic, neuroprotective, and antidepressant-like effects through melanocortin receptor signaling and robust BDNF/trkB upregulation in the hippocampus [1][2]. Russian clinical trials in acute ischemic stroke (Gusev group) showed reduced infarct progression and improved neurological recovery at intranasal doses of 12–18 mg/day [3]. Semax is on the Russian Federation List of Vital and Essential Drugs and has been registered since 1994 for stroke, optic nerve disease, and cognitive disorders. Typical research dosing in healthy adults is 600–1500 mcg intranasally per day. Semax is not FDA or EMA approved; it remains an investigational compound outside Russia and is scheduled for FDA Pharmacy Compounding Advisory Committee review.
Open Protocolarrow_forwardTherapeutic BlendNeuroxelin
Neuroxelin is a research-only neuropeptide blend formulated in the broader category of compounded neuroprotective peptide preparations used in exploratory cognitive and neurodegenerative research, with no single defined structure, no FDA or EMA approval, and no published randomized controlled trials specific to the branded combination [1][2]. The composition of branded Neuroxelin preparations varies by source and typically includes selank, semax, cerebrolysin-derived fragments, or other neurotrophic peptides aimed at modulating BDNF expression, monoaminergic tone, and neuroinflammatory signaling [3][4]. Research applications draw on the much larger published evidence base for the individual constituent peptides (selank for anxiolysis, semax for attention and stroke recovery, cerebrolysin for vascular dementia and ischemic stroke), without specific data on the blend itself [5][6]. Typical research dosing in the underlying selank/semax literature uses 250 to 900 mcg intranasally per day, divided into two or three doses; injectable formulations and dose ranges depend on which specific peptides constitute a given Neuroxelin product.
Open Protocolarrow_forward