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MEDICAL DISCLAIMER: Educational research guidelines only. Lyophilized peptides are investigational chemical compounds and are NOT approved for human consumption, diagnosis, or therapy. Consult a licensed physician before any research application.

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N-Acetyl Semax Amidate Dosage Chart, Schedule & Reconstitution Protocol

Nootropic PeptideVial Size: 10 mg
Typical dose300-600 mcg/day intranasal (up to 900)
FrequencyRefer to guidelines
Concentration5 mg/mL
Reconstitute2 mL BAC water
Vial size10 mg

Quickstart Highlights

N-Acetyl Semax Amidate (NA-Semax, Semax amidate) is a doubly stabilized analog of the Russian nootropic neuropeptide Semax, derived from the ACTH(4-10) fragment with a Pro-Gly-Pro tail. An N-terminal acetyl group and a C-terminal amide block the peptidases that rapidly degrade native Semax, so it is engineered to act longer and more potently per microgram. Its core mechanism is upregulation of BDNF and its TrkB receptor plus modulation of dopaminergic and serotonergic signaling, effects tied to attention, memory, and neuroprotection (PMID 16996037; PMID 16362768). The clinical and practical route is an intranasal spray; the subcutaneous reconstitution numbers here are an educational measurement reference only. Typical research dosing is about 300-600 mcg per day, sometimes up to 900 mcg, often split into morning doses and cycled. It is not approved by the FDA or EMA and is sold for research and educational use only.

  • Reconstitute: Add 2 mL bacteriostatic water → 5 mg/mL concentration.

  • Typical dose: 300-600 mcg/day intranasal (up to 900)

  • Easy measuring: At 5 mg/mL, 1 unit = 0.01 mL = 0.0500 mg (50 mcg) on a U-100 insulin syringe.

  • Storage: Lyophilized powder stored frozen at −20 °C and protected from light. Once reconstituted, refrigerate at 2-8 °C and use within roughly 3-4 weeks. Commercial intranasal sprays are kept refrigerated and protected from light.

  • Half-life: Native Semax plasma half-life is only minutes; intranasal CNS uptake peaks ~30 min with functional effects lasting 12-24 h. The acetyl/amide caps are intended to extend this, but human PK for the analog is unpublished.

  • Route: Intranasal metered spray (clinical/practical route). The subcutaneous vial-and-bac-water protocol shown here is an educational measurement reference, not a validated injection method.

  • Status: Not FDA- or EMA-approved. Parent Semax is registered only in Russia; the amidate analog is sold strictly for research and educational use.

About N-Acetyl Semax Amidate

N-Acetyl Semax Amidate (NA-Semax, Semax amidate) is a stabilized analog of the heptapeptide Semax, an ACTH(4-10)-derived neuropeptide developed in Russia. Adding an N-terminal acetyl cap and a C-terminal amide blocks the aminopeptidases and carboxypeptidases that rapidly clear native Semax, so the molecule is engineered to survive longer and engage the BDNF/TrkB system that underlies its cognitive and neuroprotective effects [1][2].\n\nImportant route note: clinically and in practice, Semax and its analogs are administered INTRANASALLY as a metered spray, not by injection. The subcutaneous vial-and-bacteriostatic-water figures below are an educational reconstitution reference that mirrors how this site models every compound; they are not a recommendation to inject N-Acetyl Semax Amidate.\n\nThis guide models a 10 mg vial reconstituted with 2 mL of bacteriostatic water (5 mg/mL, 50 mcg per insulin-syringe unit) so research doses map cleanly onto a U-100 syringe: 300 mcg ≈ 6 units, 600 mcg ≈ 12 units, and 900 mcg ≈ 18 units. Most protocols start near 300 mcg/day to gauge tolerance, then settle around 600 mcg/day; intranasal users typically split this into a morning (and sometimes midday) dose and run short 10-14 day cycles with rest periods.\n\nFrequency: Once daily in this educational model (intranasally, the daily total is usually split into one to two morning doses). N-Acetyl Semax Amidate is not FDA- or EMA-approved and is presented here for educational, research-only purposes.

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Quick Protocol Navigation

Reconstitution Instruction & Mixing Step-by-Step

Lyophilized powder must be reconstituted carefully. Agitating peptide chains can shear disulfide bonds and render the peptide biologically inert.

1

Draw 2 mL of bacteriostatic water into a sterile syringe.

2

Inject the water slowly down the inner glass wall of the 10 mg N-Acetyl Semax Amidate vial; do not spray it directly onto the powder and do not shake.

3

Swirl gently until the solution is completely clear; this yields a 5 mg/mL concentration (50 mcg per U-100 insulin-syringe unit).

4

Store refrigerated at 2-8 °C and draw the prescribed units per dose: 300 mcg ≈ 6 units, 600 mcg ≈ 12 units, 900 mcg ≈ 18 units.

5

Educational note: N-Acetyl Semax Amidate is clinically administered INTRANASALLY as a metered spray; these subcutaneous reconstitution figures are a measurement reference only and are not a validated injection protocol.

Visual Reconstitution Planner

Interactive N-Acetyl Semax Amidate Syringe Calculator

Currently visualizing the 10 mg vial reconstituted with 2 mL bacteriostatic water. Adjust the target dose to dynamically render syringe units.

Pre-selected Dosages
Peptide Vial Size 10 mg10 mg
Bacteriostatic Water Added 2.0 mL2 mL
Target Research Dose 250 mcg250 mcg
Concentration
5.00mg/mL
Injection Volume
0.050mL
U-100 Syringe Pull
5.0Units

Reconstitution Calculation: 10mg dry powder in 2mL water yields 5.00 mg/mL. To evaluate a 250mcg dose, pull to 5.0 units (5 syringe ticks).

Active Visualizer

U-100 Syringe Representation

Syringe drawn to 0.0 of 100 unitsINSULIN · U-10001020304050607080901000.0IU
Syringe SizeStandard insulin syringe — 100 units = 1 mL

Educational reference visual. Assumes standard U-100 insulin syringe where 1.0 mL volume = 100 units.

Titration & Dose Escalation Schedules

PhaseDose per injectionUnits (per injection)
Starter (days 1-3)300 mcg6 units (0.06 mL)
Standard daily600 mcg12 units (0.12 mL)
High / extended focus (advanced)900 mcg18 units (0.18 mL)

Administration guidelines: Refer to guidelines | 2 mL Reconstitution

Research Supplies Quantity Planner

Scientific mathematical planning of syringes, bacteriostatic water and dry vials needed for extended research blocks using the 10 mg vial.

Peptide Vials (N-Acetyl Semax Amidate, 10 mg each):

  • checkAt a standard 600 mcg/day, one 10 mg vial lasts about 16 days of continuous use.
  • check8-week course (continuous): about 3-4 vials; 12-week: about 5 vials; 16-week: about 7 vials.
  • checkIntranasal practice usually cycles 10-14 days on with rest periods, which lowers real vial consumption well below the continuous estimates.

Insulin Syringes (U-100):

  • checkOne 0.3 mL (30-unit) U-100 syringe per administration in this once-daily educational model.
  • checkRoughly 56 syringes for 8 weeks, 84 for 12 weeks, and 112 for 16 weeks of continuous use.
  • checkA standard box of 100 covers about a 14-week continuous course.

Bacteriostatic Water (10 mL or 30 mL bottles): Use 2 mL per vial for reconstitution.

  • checkEach reconstituted 10 mg vial uses 2 mL, so about 8 mL over 8 weeks, 10 mL over 12 weeks, and 14 mL over 16 weeks.
  • checkA single 30 mL bottle comfortably covers a full 16-week course with margin.
  • checkDiscard any opened bottle after roughly 28 days per common bacteriostatic-water labeling.

Alcohol Swabs: Wipe the vial septum and, in the educational subcutaneous model, the injection site before each use.

  • checkBudget about 2 swabs per administration (vial top plus site).
  • checkRoughly 112 swabs for 8 weeks, 168 for 12 weeks, and 224 for 16 weeks.
  • checkA 200-count box covers most courses.

Mechanism of Action (MOA)

N-Acetyl Semax Amidate is a synthetic heptapeptide built on the Semax scaffold Met-Glu-His-Phe-Pro-Gly-Pro, an analog of the adrenocorticotropic hormone fragment ACTH(4-10) fused to the C-terminal tripeptide Pro-Gly-Pro (PGP). The "N-acetyl" and "amidate" descriptors denote two terminal modifications, acetylation of the N-terminus and amidation of the C-terminus (Ac-Met-Glu-His-Phe-Pro-Gly-Pro-NH2). These caps block the aminopeptidases and carboxypeptidases that otherwise degrade native Semax within minutes, which is the basis for the common claim that NA-Semax Amidate is more stable, longer-acting, and more potent per microgram than the parent peptide.\n\nThe best-characterized molecular action of the Semax family is upregulation of neurotrophins. A single intranasal dose of Semax raises brain-derived neurotrophic factor (BDNF) protein and increases phosphorylation of its receptor TrkB in the rat hippocampus, with parallel increases in BDNF and TrkB mRNA [1]. Semax also binds specifically in the basal forebrain and elevates BDNF there [8], and both Semax and its PGP metabolite drive transcription of neurotrophins (BDNF, NGF) and their receptors after cerebral ischemia [2]. Beyond neurotrophins, Semax activates dopaminergic and serotonergic systems in rodent brain [5] and inhibits enkephalin-degrading enzymes, prolonging the activity of endogenous regulatory peptides [6]. Together these actions are proposed to enhance selective attention, memory consolidation, and resistance to ischemic and oxidative stress.\n\nPharmacokinetics: the defining feature of this peptide class is a very short systemic half-life paired with a much longer functional effect. Native Semax is cleared from plasma within minutes by peptidases, yet intranasal delivery routes peptide directly to the brain along olfactory and trigeminal pathways; radiolabeled studies show peak brain concentrations within roughly 30 minutes and detectable CNS levels persisting for many hours, with the PGP fragment dominating in tissue [7]. Downstream BDNF/NGF and behavioral effects can last about 12-24 hours, which is why once- or twice-daily intranasal dosing is used. The acetyl and amide caps on NA-Semax Amidate are intended to lengthen this window further, although formal human pharmacokinetic data for the modified analog have not been published and the longer half-life remains an inference from its chemistry rather than a measured value.\n\nRoute and regulatory status: the clinically validated and practical route is intranasal spray; the subcutaneous reconstitution scheme shown here is an educational measurement convention used across this site, not a delivery method that has been studied for this compound. The parent Semax is registered only in Russia (for ischemic stroke, optic neuropathy, and cognitive indications). N-Acetyl Semax Amidate is not approved by the FDA, EMA, or other Western regulators and is sold strictly for research and educational use [3][6].

Clinical Trial Efficacy Highlights

  • starDolotov and colleagues (2006, Brain Research) showed that a single intranasal dose of Semax (50 mcg/kg) produced a maximal ~1.4-fold rise in hippocampal BDNF protein and a ~1.6-fold increase in TrkB tyrosine phosphorylation, with roughly 3-fold and 2-fold increases in exon III BDNF and TrkB mRNA, providing the molecular basis for the cognitive effects of the Semax family [1].
  • starIn a companion study (Dolotov et al., 2006, Journal of Neurochemistry), radiolabeled Semax bound specifically in the rat basal forebrain and increased BDNF protein levels there, supporting a direct, receptor-associated neurotrophic mechanism rather than a purely nonspecific effect [8].
  • starShadrina and colleagues (2010, Cellular and Molecular Neurobiology) demonstrated that both Semax and its PGP metabolite activate transcription of neurotrophins (BDNF, NGF) and their receptor genes in rat cortex after permanent middle cerebral artery occlusion, linking the peptide to a genomic neuroprotective response in ischemia [2].
  • starGusev, Skvortsova and colleagues evaluated intranasal Semax in the acute period of hemispheric ischemic stroke; the most effective daily doses were about 12 mg for moderate strokes and 18 mg for severe strokes over 5-10 day courses, and Semax accelerated regression of cerebral and focal, especially motor, deficits while being well tolerated [3].
  • starA later Russian clinical analysis of Semax across different stages of ischemic stroke reported continued neurological benefit and good tolerability when the peptide was added to standard intensive therapy, reinforcing the stroke-recovery signal seen in earlier trials [4].
  • starEremin and colleagues (2005, Neurochemical Research) found that Semax activates dopaminergic and serotonergic systems in rodent brain, a mechanism consistent with its reported effects on mood, motivation, and attention [5].
  • starA 2024 rodent study reported antidepressant-like and antistress effects of the ACTH(4-10) analog Semax in a model of chronic unpredictable stress, extending the behavioral evidence beyond cognition into stress resilience [9].
  • starImportant evidence caveat: nearly all controlled data are for native Semax, and the high-microgram cognitive and milligram-level stroke doses studied differ from the lower research doses used for the more potent N-Acetyl Semax Amidate; no published randomized human trials specifically test the doubly modified amidate analog [6].

Side Effects & Tolerability Profile

Clinical subjects transiently report mild side effects. Slowly escalating the titration dose represents the single most effective intervention to limit side effects.

  • warningThe Semax family is generally well tolerated in published trials; in stroke studies at 12-18 mg/day intranasal, no significant adverse events were reported [3].
  • warningRoute-specific (intranasal) effects include local nasal irritation, dryness, sneezing, congestion, and an unpleasant taste or sore throat from the metered spray.
  • warningStimulant-like over-activation can occur, including anxiety, irritability, restlessness, or insomnia if dosed late in the day; because NA-Semax Amidate is more potent than native Semax, starting low (around 300 mcg) reduces the chance of overshooting.
  • warningHeadache and lightheadedness are occasionally reported, usually transient.
  • warningBecause Semax modulates dopaminergic and serotonergic signaling, theoretical caution applies when combining it with antidepressants, MAO inhibitors, or stimulants; formal interaction data do not exist [5].
  • warningSafety has not been established in pregnancy, breastfeeding, or pediatric use in Western practice, and long-term human safety of the modified analog is unknown; it should be avoided in these populations.
  • warningThe subcutaneous route modeled on this page has not been studied for this compound; injecting any non-sterile research peptide carries infection, contamination, and dosing-error risks that are not part of any validated protocol.
  • warningRegulatory/research status: N-Acetyl Semax Amidate is NOT approved by the FDA or EMA; the parent Semax is registered only in Russia, and the amidate analog is sold for laboratory research and educational use only.

Subcutaneous Injection Technique

Most research peptides require subcutaneous injection into fatty tissue. Never inject directly into a blood vessel or deep muscle tissue unless clinically detailed.

1. Site Selection

Common locations include the abdomen (2 inches from navel), outer upper arms, or thighs.

2. Sanitization

Thoroughly clean the selected site, stopper and vial top using 70% isopropyl alcohol prep swabs.

3. Angle & Push

Pinch the skin and insert the needle at a 45 to 90-degree angle. Depress plunger smoothly.

4. Site Rotation

Rotate injection sites continuously to avoid lipodystrophy or tissue scarring.

Frequently Asked Questions

What is the typical N-Acetyl Semax Amidate dosage?expand_more

In research and practical use the typical N-Acetyl Semax Amidate dosage is about 300-600 mcg per day intranasally, sometimes increased to 900 mcg and frequently split into a morning and midday dose. Because the acetyl and amide caps make it more potent than native Semax, most protocols start near 300 mcg/day and run short 10-14 day cycles with rest periods. The 50 mcg-per-unit subcutaneous figures on this page are an educational measurement reference, not the clinical route.

Is N-Acetyl Semax Amidate FDA approved?expand_more

No. N-Acetyl Semax Amidate is not approved by the FDA, the EMA, or any other Western regulator for any indication. The parent peptide Semax is registered only in Russia, where it is used for ischemic stroke, optic neuropathy, and cognitive disorders. In the United States and Europe the amidate analog is sold strictly for laboratory research and educational purposes and is not a dietary supplement or medicine.

How do you reconstitute N-Acetyl Semax Amidate?expand_more

Clinically the compound is an intranasal spray and is not reconstituted for injection. For this site's educational measurement model, a 10 mg vial is mixed with 2 mL of bacteriostatic water to give 5 mg/mL, or 50 mcg per U-100 insulin-syringe unit. Add the water slowly down the vial wall, swirl gently without shaking until clear, and refrigerate. At that concentration 300 mcg is about 6 units and 600 mcg is about 12 units.

What is the half-life of N-Acetyl Semax Amidate?expand_more

Native Semax has a very short plasma half-life of only a few minutes because peptidases clear it quickly, but intranasal delivery sends peptide directly to the brain, where peak levels appear within roughly 30 minutes and downstream BDNF and behavioral effects can last 12-24 hours. The N-acetyl and C-amide modifications are designed to slow enzymatic breakdown and extend this window, though formal human pharmacokinetic data for the modified analog have not been published.

Can N-Acetyl Semax Amidate be stacked with Selank or other nootropics?expand_more

Users frequently pair NA-Semax Amidate with the anxiolytic peptide Selank, and anecdotally with cholinergics or racetams, but there are no controlled human trials evaluating these combinations for safety or added benefit. Because Semax modulates dopamine and serotonin, combining it with antidepressants, MAO inhibitors, or stimulants is a theoretical interaction concern. Any stacking is experimental and outside validated medical use.

Related Guides & Tools

Step-by-step references for reconstituting, measuring, and storing N-Acetyl Semax Amidate, plus the universal dosing calculator.

Academic References & Study Citations

[1]

Dolotov OV, et al. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Research. 2006;1117(1):54-60. View Scientific Paper →

[2]

Shadrina M, et al. Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia. Cellular and Molecular Neurobiology. 2010;30(1):71-79. View Scientific Paper →

[3]

Gusev EI, Skvortsova VI, et al. [Effectiveness of semax in acute period of hemispheric ischemic stroke (a clinical and electrophysiological study)]. Zhurnal Nevrologii i Psikhiatrii im. S.S. Korsakova. 1997. View Scientific Paper →

[4]

[The efficacy of semax in the treatment of patients at different stages of ischemic stroke]. Zhurnal Nevrologii i Psikhiatrii im. S.S. Korsakova. 2018. View Scientific Paper →

[5]

Eremin KO, et al. Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents. Neurochemical Research. 2005;30(12):1493-1500. View Scientific Paper →

[6]

Tsai SJ. Semax, an analogue of adrenocorticotropin (4-10), is a potential agent for the treatment of attention-deficit hyperactivity disorder and Rett syndrome. Medical Hypotheses. 2007;68(5):1144-1146. View Scientific Paper →

[7]

Eremin KO, et al. Kinetics of Semax penetration into the brain and blood of rats after its intranasal administration. Russian Journal of Bioorganic Chemistry. 2006;32(1):52-57. View Scientific Paper →

[8]

Dolotov OV, et al. Semax, an analogue of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain. Journal of Neurochemistry. 2006;97 Suppl 1:82-86. View Scientific Paper →

[9]

Antidepressant-like and antistress effects of the ACTH(4-10) synthetic analogs Semax and Melanotan II on male rats in a model of chronic unpredictable stress. 2024. View Scientific Paper →

[10]

Ashmarin IP, et al. [A nootropic adrenocorticotropin analog 4-10-semax (15 years experience in its design and study)]. Zhurnal Vysshei Nervnoi Deyatelnosti im. I.P. Pavlova. 1997;47(2):420-430. View Scientific Paper →