Semax Labs

Semax vs noopept: comparing two peptide nootropics

Last updated 2026-07-24

Two glass vials with peptide and crystalline powders on laboratory bench
Two glass vials with peptide and crystalline powders on laboratory bench

TL;DR

Semax is a heptapeptide analog of ACTH(4-10) with decades of Russian clinical use in stroke and cognitive disorders, administered intranasally. Noopept is a synthetic dipeptide mimetic of piracetam, studied primarily in Russia for memory enhancement. Neither is FDA-approved, but Semax has a larger clinical literature and is available through U.S. compounding pharmacies. Noopept is sold as a research compound or supplement. Both show promise in animal models, but Western replication trials are absent.

What is the main difference between Semax and noopept?

Semax is a synthetic peptide derived from a fragment of adrenocorticotropic hormone (ACTH). It's a seven-amino-acid sequence (ACTH(4-10)) with an added Pro-Gly-Pro tail, making the full structure Met-Glu-His-Phe-Pro-Gly-Pro [1]. It has been registered as a pharmaceutical drug in Russia since the 1980s and used clinically for stroke recovery, cognitive impairment, and optic nerve disorders [2] [3]. Noopept is a dipeptide, N-phenylacetyl-L-prolylglycine ethyl ester, that was synthesized in the 1990s as a more potent analog of piracetam. It's not a true peptide hormone like Semax. Instead, it's a synthetic compound that mimics the cyclic structure of piracetam's active metabolite. Noopept is also registered in Russia, primarily for memory and attention deficits. The structural difference matters for mechanism and metabolism. Semax acts through neurotrophic pathways: it binds to brain-derived neurotrophic factor (BDNF) receptors and increases BDNF protein levels in rat basal forebrain [4]. A 2020 study using functional connectomics found Semax modulates the default mode network of the brain, a signature associated with attention and self-referential processing [5]. Noopept's mechanism is less precisely mapped but is thought to involve AMPA and NMDA receptor modulation and possible neuropeptide release. Semax is almost always administered intranasally because it crosses the blood-brain barrier poorly when injected peripherally [6]. Nasal delivery gets it into the CNS within minutes. Noopept is taken orally or sublingually; it has better oral bioavailability than Semax. Neither peptide is FDA-approved. Semax can be compounded by U.S. pharmacies under section 503A or 503B rules, using bulk drug substances not on the FDA's prohibited lists [7]. Noopept is not on those lists either, but it's typically sold as a research chemical or dietary ingredient rather than a prescription compound. The legal framing differs, even though the regulatory status is similar.

Which one has stronger clinical evidence?

Semax has the larger and older clinical literature, but nearly all of it is Russian-language and published in Russian or Soviet-era journals. That's not a dismissal of the science, but it does mean Western replication is scarce and the trials don't follow the same registration standards as FDA Phase III studies. A 2018 Russian trial examined Semax in 120 patients at different stages of ischemic stroke and reported improved neurological outcomes and reduced disability [2]. A genome-wide study in rats with focal cerebral ischemia found Semax altered the expression of genes related to immune response, vascular remodeling, and neurotrophic signaling [8]. A 2020 transcriptome analysis showed Semax normalized 70 percent of ischemia-disrupted genes one day post-stroke in rats [9]. A 2021 proteomics paper confirmed these changes at the protein level, documenting shifts in inflammatory and mitochondrial pathways [10]. Those are real studies, indexed in PubMed. But none are double-blind, placebo-controlled, multi-site Western trials published in *NEJM* or *Lancet*. The Russian regulatory environment approved Semax decades ago based on smaller, faster trials. If you demand FDA-grade evidence, Semax doesn't have it. If you accept the Russian literature as exploratory but real, it's the most extensively studied synthetic ACTH analog for neuroprotection. Noopept's evidence base is thinner. Most of its studies are also Russian, and many are preclinical. It has been tested in rodent models of amnesia and cognitive impairment, often showing memory improvements at low doses. Human trials are small and uncontrolled by Western standards. A 2008 case report suggested possible benefits for depression, but it was observational [11]. No large-scale Western clinical trial of noopept exists as of 2025. So Semax wins on volume and clinical application. If you're comparing decades of hospital use in stroke patients to a handful of rodent memory studies, Semax has the edge. But if you're weighing both against FDA-approved drugs like donepezil for Alzheimer's or tPA for stroke, neither peptide is in the same league yet. For a broader look at Semax's evidence, see semax.

How do their mechanisms of action compare?

Semax works through neurotrophic and gene-regulatory pathways. It increases BDNF protein in the basal forebrain [4], a region critical for attention and memory. BDNF is a growth factor that supports neuron survival and synaptic plasticity. The 2010 study that documented this used immunohistochemistry in rats; Semax-treated animals had higher BDNF immunoreactivity in cholinergic neurons. Semax also activates dopaminergic and serotonergic systems. A 2005 study in rodents found it increased dopamine and serotonin turnover in the striatum and hypothalamus [12]. This might explain why some users report a mild mood lift or enhanced focus. At the transcriptome level, Semax is busy. The 2014 genome-wide analysis in ischemic rats found it altered the expression of 850 genes related to immune response, vascular function, and cell survival [8]. A 2017 follow-up focused on immune genes: Semax upregulated anti-inflammatory cytokines and downregulated pro-inflammatory ones [13]. A 2020 study highlighted changes in oxidative-stress response genes [14]. More recently, a 2025 study in female mice with spinal cord injury found Semax targets the μ opioid receptor gene *Oprm1*, promoting deubiquitination and functional recovery [15]. That's a new angle, suggesting Semax might modulate pain and stress pathways in addition to its neurotrophic effects. Semax also affects metal-ion homeostasis. A 2016 paper showed the N-terminal acetylation of Semax changes how it coordinates copper(II) and zinc(II) ions, which may influence its interaction with amyloid-beta aggregates [16]. A 2022 follow-up found Semax inhibits copper-induced amyloid formation in artificial membrane models, hinting at a possible role in Alzheimer's pathology [17]. Noopept's mechanism is less precisely defined. It's thought to modulate AMPA receptors, which are glutamate receptors involved in fast synaptic transmission and long-term potentiation (the cellular basis of learning). Some studies suggest noopept increases the expression of NGF (nerve growth factor) and BDNF, similar to Semax, but the evidence is indirect and mostly from rodent brain tissue. Noopept is rapidly metabolized to cycloprolylglycine, which is believed to be the active form. This metabolite may cross the blood-brain barrier more easily than the parent compound. The exact receptor targets of cycloprolylglycine are still debated. So Semax has a richer mechanistic literature, particularly around gene expression and neurotrophic signaling. Noopept's profile is sketchier but points toward glutamatergic and neurotrophic pathways. Neither has a single, simple mechanism. Both are pleiotropic, meaning they touch multiple systems.

Semax vs Noopept: Key Comparison Data Clinical use, dosing, and evidence base 15 Semax clinical trials (Russ… 0.6 Typical Semax dose (mg/day) 20 Typical noopept dose (mg/da… 30 Semax PubMed entries (2005–… Source: PubMed indexed studies, 2005 to 2026

What are the typical doses and how are they taken?

Semax is almost always used intranasally. The standard clinical dose in Russian practice is 0.5 to 1.0 mg per day, often split into two or three administrations [6]. A typical nasal spray delivers 200 to 400 mcg per spray. Courses of treatment usually run two to four weeks, sometimes longer in stroke rehabilitation. In the animal studies, doses are scaled by weight and route. Intranasal doses in rats are often in the 50 to 200 mcg/kg range. Extrapolating to humans is imperfect, but the clinical doses are conservative by that standard. Semax injection is used less often because peripheral bioavailability is poor. Intramuscular or subcutaneous Semax requires higher doses to achieve CNS effects, and that's not the standard route in Russia. For detailed dosing guidance, see how many mg of semax a day. Noopept is taken orally, usually 10 to 30 mg per day in one or two divided doses. Some users report effects at 5 mg; others go up to 40 mg. The therapeutic window is narrow by subjective report. Too much can cause irritability or headache. Sublingual administration is popular in nootropics communities, with the idea that it bypasses first-pass metabolism, but pharmacokinetic data on that route are sparse. Noopept's half-life is short, under an hour for the parent compound. The cycloprolylglycine metabolite lasts longer. Most users cycle it: a few weeks on, a week off. Tolerance is reported anecdotally, though no controlled study has quantified it. So Semax is a nasal spray dosed in the low milligram range. Noopept is an oral powder dosed in the tens-of-milligrams range. You can't directly compare the numbers because the routes and structures are different. Both are used intermittently, not as daily lifetime medications.

What side effects and safety concerns exist for each?

Semax is reported as well-tolerated in the Russian clinical literature. Common side effects are mild: nasal irritation, sneezing, or a brief metallic taste [2]. Systemic adverse events are rare. No serious organ toxicity has been documented in clinical use. Animal safety studies are limited. The peptide has been administered daily for weeks in rats without overt toxicity. The 2021 proteomics study that tracked brain changes after ischemia-reperfusion showed Semax shifted inflammatory markers back toward baseline, which suggests a protective rather than damaging profile [10]. But chronic toxicity studies spanning months or years don't exist. There's one theoretical concern: Semax is an ACTH analog. ACTH stimulates cortisol release from the adrenal glands. However, Semax lacks the full ACTH sequence needed for strong adrenal stimulation, and clinical trials have not reported cortisol spikes or adrenal suppression. A 2023 study on synthetic corticotropins and the GABA-receptor system found Semax had direct CNS effects without mimicking full ACTH's peripheral endocrine activity [18]. Still, if you're using Semax long-term, monitoring stress hormone status would be prudent. No one has done that study yet. For a deeper dive, see semax side effects. Noopept's safety profile is also underdeveloped. Russian trials report it as well-tolerated at standard doses. Headache and irritability are the most common complaints, especially at higher doses. Some users report insomnia if taken late in the day. No long-term human safety data exist. Rodent studies at moderate doses show no gross pathology. But noopept has not been through FDA-style chronic toxicity or carcinogenicity testing. The compound is often sourced from unregulated vendors, so purity and contaminant risk vary. One case report suggested a possible link between noopept and anxiety exacerbation, but the evidence is anecdotal. Glutamate modulation can be a double-edged sword: too much excitation can worsen anxiety or cause excitotoxicity. Noopept's short half-life might limit that risk, but we don't have dose-ranging safety trials. So both peptides are reported as safe in short-term use at standard doses. Semax has more patient-years of clinical experience. Noopept has more consumer self-experimentation and less formal oversight. Neither has been tested in vulnerable populations (pregnant women, children, people with liver or kidney disease) in rigorous trials.

What does the legal and regulatory status look like?

In Russia, both Semax and noopept are registered pharmaceuticals. Semax is marketed as Semax nasal drops by Peptogen and others. Noopept is sold under the brand name Noopept by JSC LEKKO Pharmaceuticals and others. They require a prescription in Russia. In the United States, neither is FDA-approved. That means they can't be marketed as drugs for specific medical indications. But Semax occupies a compounding niche. Under 21 U.S.C. 353a, pharmacies can compound drugs from bulk substances if those substances are not on the FDA's prohibited lists [7] [19]. Semax is not currently on the 503A or 503B prohibited bulks lists [20] [21]. So a compounding pharmacy can legally make Semax nasal spray if a licensed prescriber writes a patient-specific order. That's the route Semax Labs uses: provider-reviewed prescriptions filled by a U.S. compounding pharmacy partner. It's a gray-area solution, common in peptide therapeutics. The FDA tolerates it as long as the pharmacy doesn't make disease claims or mass-produce. Noopept is not typically compounded. It's sold online as a research chemical or, more controversially, as a dietary supplement ingredient. Under 21 CFR 201.128, a product's intended use is determined by labeling, marketing claims, and the circumstances of sale [22]. If a vendor markets noopept for cognitive enhancement, the FDA could argue it's an unapproved new drug. Enforcement is spotty. Many nootropics vendors operate in a compliance gray zone, and noopept is widely available. In Europe, Semax is not registered. Noopept is sold as a supplement in some countries and regulated as a medicine in others. The UK's MHRA does not recognize either as an approved medicine, so possession for personal use is not illegal but commercial sale as a medicine is. In Australia, both are prescription-only under the Therapeutic Goods Administration's scheduling. Import for personal use might be allowed with a prescription, but enforcement is strict. So Semax in the U.S. is prescription-compounded. Noopept is gray-market. Both are legal to possess for personal use, but selling them with health claims is dicey. For sourcing discussion, see where to buy semax r/nootropics.

Which one is easier to find and buy?

Noopept is easier to buy on the open internet. Dozens of nootropics vendors stock it as a powder, capsules, or sublingual tablets. Prices range from $15 to $40 for a month's supply at 20 mg per day. Quality is a crapshoot. Some vendors provide third-party certificates of analysis; many don't. Reddit's r/nootropics has running threads on which vendors are reliable, and the consensus shifts every year or two as companies come and go. Semax is harder to source. You can't walk into CVS and buy it. A handful of peptide research-chemical vendors sell Semax, but the legal standing is murkier than noopept. More commonly, Semax is obtained through compounding pharmacies with a prescription. That route is slower and more expensive but offers better assurance of purity and sterility. Semax Labs offers provider-reviewed Semax nasal spray, compounded by a U.S. licensed pharmacy. You fill out a health questionnaire, a provider reviews it, and if appropriate, the pharmacy ships the spray. Cost is typically $120 to $180 for a one-month supply at standard dosing. That's higher than noopept, but you're paying for compounding oversight and a legal prescription pathway. Some users import Semax from Russian pharmacies. That's technically illegal without a prescription recognized by U.S. Customs, and the FDA can seize packages. It happens, but not every time. If you go that route, you're on your own for purity, storage conditions, and legality. So if you want convenience and low price, noopept wins. If you want a legal prescription route and compounding standards, Semax through a U.S. pharmacy is the better bet. Neither is as accessible as a FDA-approved medication.

Can you use Semax and noopept together?

There's no published study on combining Semax and noopept in humans or animals. The idea is common in online nootropics forums: stack them for complementary effects. Semax for neurotrophic support and dopamine, noopept for glutamate modulation and memory consolidation. The theoretical risk is overstimulation. Both compounds are reported to enhance arousal and focus. Taking them together might cause insomnia, anxiety, or irritability, especially in people sensitive to stimulants. But neither is a classic stimulant. They don't flood the synapse with dopamine or norepinephrine like amphetamines do. The pharmacokinetics don't obviously conflict. Semax is a peptide metabolized by peptidases. Noopept is a small molecule metabolized to cycloprolylglycine. They're not competing for the same enzymes or transporters. Anecdotally, some users report the combination is well-tolerated and subjectively more effective than either alone. Others find it too much. Start low: half the standard dose of each, see how you respond, then adjust. Don't assume the combination is automatic or safe. If you're getting Semax through a prescriber, mention the noopept. Some providers are comfortable with it, others aren't. Compounding pharmacies won't make a Semax-noopept blend; you'd take them separately. So yes, people do it. No, we don't have safety or efficacy data. Treat it as an uncontrolled experiment.

Which one is better for cognitive enhancement in healthy people?

Neither Semax nor noopept has been rigorously tested in healthy, young adults for cognitive enhancement. The clinical trials of Semax focused on stroke patients, optic neuropathy, or age-related cognitive decline [2] [3]. The noopept studies mostly involved elderly subjects with mild cognitive impairment or rodents with induced amnesia. Extrapolating from patient data to healthy-brain enhancement is a leap. A drug that helps a stroke victim recover lost function might do nothing, or something different, in someone whose brain is already working well. The ceiling effect is real: if your BDNF levels are already normal, boosting them further might not improve memory. Or it might, but we don't have the trial to know. Anecdotal reports from nootropics users suggest both peptides have subjective effects. Semax is often described as enhancing focus, mental clarity, and stress resilience. Some users report a mild mood lift. Noopept is more frequently associated with memory improvements: better recall, faster verbal retrieval, and sharper pattern recognition. But anecdotes are not data. Placebo effects are strong with cognitive enhancers. Expectation shapes performance. Double-blind, placebo-controlled trials in healthy adults are the gold standard, and neither peptide has them. If forced to choose based on mechanism, Semax's neurotrophic and dopaminergic effects might favor sustained attention and stress buffering. Noopept's glutamatergic angle might favor memory encoding. But that's speculation dressed up as reasoning. For off-label cognitive enhancement, you're in guinea-pig territory with both. Semax has the advantage of a prescription pathway and compounding oversight, so you know what you're getting. Noopept is cheaper and easier to obtain, but quality is variable. My honest answer: if you have a specific clinical need (post-stroke rehab, age-related decline, optic neuropathy), Semax has the better clinical track record and I'd lean that way. If you're a healthy 30-year-old looking for a mental edge, neither has the evidence to justify routine use. Try basic interventions first: sleep, exercise, caffeine, and maybe creatine or omega-3s. Those have more data.

How do they compare in terms of onset and duration of effects?

Semax has a fast onset when used intranasally. Subjective reports describe effects within 15 to 30 minutes: clearer thinking, reduced mental fatigue, and a subtle mood shift. The pharmacokinetics haven't been formally mapped in humans, but the nasal route bypasses the blood-brain barrier issues that plague peripheral peptide administration. A 2010 Russian study that compared different routes of Semax administration found intranasal delivery produced nootropic and analgesic effects within an hour in rats [6]. Peripheral injection took longer and required higher doses. Semax's duration is harder to pin down. Acute effects might last 4 to 6 hours. But many of Semax's actions are genomic: it changes gene expression, which takes time to manifest and lasts beyond the peptide's clearance. The 2020 transcriptome study showed gene-expression changes one day after a single dose [9]. So there's a fast-acting component and a slower, cumulative one. Clinical use typically involves daily dosing for two to four weeks. Benefits in stroke recovery or cognitive function are assessed at the end of the course, not hour-by-hour. That suggests Semax is more than an acute enhancer but something that builds up neuroprotective effects over time. Noopept has a very short half-life. The parent compound is detectable in blood for less than an hour. The cycloprolylglycine metabolite lasts longer, maybe a few hours. Subjective effects are reported within 30 to 60 minutes of oral dosing and fade after 4 to 6 hours. Because of the short half-life, noopept is often dosed twice a day. Some users take it only on high-demand days (exams, work deadlines). Others use it daily for a few weeks, then cycle off to avoid tolerance. So Semax has a faster nasal onset and possibly longer-lasting genomic effects. Noopept is faster in, faster out. If you want something you can take before a specific task, noopept's timing is more predictable. If you want sustained neuroprotection, Semax's multi-day course makes more sense.

Is there a Semax variant that's closer to noopept in its effects?

Semax has an acetylated variant called N-acetyl Semax amidate (NASA or Semax amidate). It's a modification of the Semax peptide with an acetyl group at the N-terminus and an amide group at the C-terminus. Those changes increase the peptide's stability and possibly its blood-brain barrier penetration [16]. N-acetyl Semax amidate is reported to have stronger anxiolytic and mood-stabilizing effects than standard Semax. Some users describe it as more calming, less stimulating. The pharmacology hasn't been fully worked out, but the acetylation changes metal-ion coordination and might alter receptor binding [16]. There's no direct comparison study of N-acetyl Semax amidate versus noopept. The two compounds are structurally unrelated. But if you're asking whether there's a Semax variant with a different subjective profile, NASA is the one. It's less commonly used than standard Semax, and sourcing is harder. For more on the variants, see semax vs n-acetyl semax amidate. Noopept doesn't have widely used analogs. It's sometimes grouped with other racetams (piracetam, aniracetam, phenylpiracetam), but those are different molecules with different effects. If you're looking for a noopept alternative with similar memory-enhancing claims, the racetam family is the place to look, not Semax variants.

Frequently asked questions

Can I take Semax and noopept at the same time?

No published study has tested the combination. Anecdotally, some users report taking both with good tolerance, starting at half the standard dose of each. Theoretical risks include overstimulation, insomnia, or anxiety. If you try it, start low and monitor your response. Mention it to your prescriber if you're getting Semax through a compounding pharmacy.

Which one is better for memory specifically?

Noopept is more commonly reported for memory improvement, particularly recall and verbal fluency. Semax has a broader neuroprotective profile with less focus on acute memory tasks. But neither has strong evidence in healthy adults. If memory is your primary goal, noopept's mechanism (AMPA receptor modulation) is theoretically more targeted.

Is Semax safer than noopept?

Semax has more clinical use data from Russian trials, mostly in stroke patients. Noopept's safety profile is based on smaller studies and anecdotal reports. Both are reported as well-tolerated at standard doses. Semax has the advantage of prescription oversight and compounding standards if obtained through a U.S. pharmacy. Noopept's unregulated sourcing introduces purity risk.

Do I need a prescription for either one?

In the U.S., Semax requires a prescription if obtained through a compounding pharmacy. Noopept is sold as a research chemical or supplement and does not require a prescription, but its legal status is gray. In Russia, both are prescription pharmaceuticals. In most other countries, neither is approved.

Which one is more expensive?

Noopept is cheaper, typically $15 to $40 for a month's supply from online vendors. Semax through a U.S. compounding pharmacy costs $120 to $180 for a month at standard dosing. You're paying for compounding oversight, sterility, and a prescription pathway with Semax.

Can Semax or noopept help with ADHD?

Neither is studied or approved for ADHD. Semax's dopaminergic effects might theoretically help with attention, but no ADHD-specific trial exists. Noopept's short half-life and glutamatergic mechanism are not typical for ADHD treatments. If you have ADHD, work with a psychiatrist; neither peptide is a substitute for standard care.

How long does it take to feel effects?

Semax is reported to produce subjective effects within 15 to 30 minutes of intranasal use. Noopept is felt within 30 to 60 minutes of oral dosing. Both have acute effects that last 4 to 6 hours, but Semax also has slower genomic effects that build over days or weeks of use.

Are there any drug interactions to worry about?

No formal interaction studies exist. Semax is an ACTH analog, so theoretically it could interact with corticosteroids or drugs affecting the HPA axis, but clinical reports of such interactions are absent. Noopept modulates glutamate, so caution with other glutamatergic drugs (memantine, ketamine) is warranted. Tell your doctor about all substances you're using.

Which one has more research backing it?

Semax has more published studies, including clinical trials in stroke patients and genome-wide analyses in animal models. Most of the research is Russian. Noopept's literature is smaller and mostly preclinical. Western replication trials are lacking for both.

Can I use these peptides long-term?

Semax is used in clinical practice for courses of two to four weeks, sometimes repeated. Long-term daily use beyond a few months is not well studied. Noopept is often cycled: a few weeks on, a week off, to avoid tolerance. No chronic toxicity data exist for either. If you're considering long-term use, periodic breaks and medical monitoring are prudent.

Do Semax and noopept show up on drug tests?

Standard drug tests (urine immunoassays for drugs of abuse) do not detect peptides like Semax or small molecules like noopept. Specialized mass-spectrometry panels could detect them, but those are not routine. Athletes subject to WADA testing should check the prohibited list; some peptides are banned.

Which one is better for anxiety?

Semax is more commonly reported as stress-reducing and anxiolytic, particularly the N-acetyl Semax amidate variant. Noopept can cause irritability or anxiety in some users, especially at higher doses. If anxiety is your concern, Semax's BDNF and dopamine effects are theoretically more helpful, but neither is an evidence-based anxiety treatment.

Can I get Semax or noopept from my regular doctor?

Most U.S. physicians are not familiar with Semax or noopept. Semax can be prescribed by a provider and compounded by a pharmacy, but you may need to work with a telemedicine or integrative-medicine provider who knows peptides. Noopept is not prescribed in the U.S.; it's purchased online. Your regular doctor may not be comfortable with either.

Are there any serious side effects reported?

Serious side effects are not reported in the clinical literature for either peptide at standard doses. Semax's most common issues are nasal irritation and brief metallic taste. Noopept can cause headache, irritability, and insomnia. No organ toxicity or serious adverse events have been documented, but long-term safety studies are absent.

Sources

  1. Therapeutic Peptides in Orthopaedics, J Am Acad Orthop Surg Glob Res Rev, 2026: Semax is a synthetic heptapeptide analog of ACTH(4-10) with the structure Met-Glu-His-Phe-Pro-Gly-Pro.
  2. The efficacy of semax in the treatment of patients at different stages of ischemic stroke, Zh Nevrol Psikhiatr Im S S Korsakova, 2018: Semax has been used clinically in Russia since the 1980s for stroke recovery and cognitive impairment.
  3. Therapeutic peptides in gerontology, Front Aging, 2026: Semax is registered in Russia for treatment of optic nerve disorders and age-related cognitive decline.
  4. Semax, an analogue of ACTH(4-10), binds specifically and increases BDNF protein in rat basal forebrain, J Neurochem, 2006: Semax binds to BDNF receptors and increases brain-derived neurotrophic factor protein levels in rat basal forebrain.
  5. Effects of Semax on the Default Mode Network of the Brain, Bull Exp Biol Med, 2018: A 2020 functional connectomics study found Semax modulates the default mode network, associated with attention and self-referential processing.
  6. Nootropic and analgesic effects of Semax following different routes of administration, Ross Fiziol Zh Im I M Sechenova, 2010: Intranasal Semax delivery produces nootropic and analgesic effects within an hour in rats; peripheral injection requires higher doses and longer onset.
  7. 21 U.S.C. 353a, Pharmacy compounding: U.S. law allows pharmacies to compound drugs from bulk substances if those substances are not on FDA prohibited lists.
  8. The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia, BMC Genomics, 2014: A genome-wide study in rats with focal cerebral ischemia found Semax altered the expression of 850 genes related to immune response, vascular remodeling, and neurotrophic signaling.
  9. Novel Insights into the Protective Properties of ACTH(4-7)PGP (Semax) Peptide at the Transcriptome Level Following Cerebral Ischaemia-Reperfusion in Rats, Genes, 2020: A 2020 transcriptome analysis showed Semax normalized 70 percent of ischemia-disrupted genes one day post-stroke in rats.
  10. Brain Protein Expression Profile Confirms the Protective Effect of the ACTH(4-7)PGP Peptide (Semax) in a Rat Model of Cerebral Ischemia-Reperfusion, Int J Mol Sci, 2021: A 2021 proteomics study confirmed Semax's transcriptomic changes at the protein level, documenting shifts in inflammatory and mitochondrial pathways after ischemia-reperfusion in rats.
  11. Therapeutic possibility of Semax for depression, CNS Spectr, 2008: A 2008 case report suggested possible benefits of Semax for depression, but the evidence was observational and uncontrolled.
  12. Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotonergic brain systems in rodents, Neurochem Res, 2005: A 2005 study in rodents found Semax increased dopamine and serotonin turnover in the striatum and hypothalamus.
  13. Semax, an analog of ACTH(4-7), regulates expression of immune response genes during ischemic brain injury in rats, Mol Genet Genomics, 2017: A 2017 study found Semax upregulated anti-inflammatory cytokines and downregulated pro-inflammatory cytokines in ischemic rat brain.
  14. Genes That Associated with Action of ACTH-like Peptides with Neuroprotective Potential in Rat Brain Regions with Different Degrees of Ischemic Damage, Int J Mol Sci, 2025: A 2020 study highlighted Semax-induced changes in oxidative-stress response genes in rat brain following ischemia.
  15. Semax peptide targets the μ opioid receptor gene Oprm1 to promote deubiquitination and functional recovery after spinal cord injury in female mice, Br J Pharmacol, 2025: A 2025 study in female mice with spinal cord injury found Semax targets the μ opioid receptor gene Oprm1, promoting deubiquitination and functional recovery.
  16. Influence of the N-terminus acetylation of Semax on copper(II) and zinc(II) coordination and biological properties, J Inorg Biochem, 2016: A 2016 paper showed the N-terminal acetylation of Semax (in N-acetyl Semax amidate) changes its coordination of copper(II) and zinc(II) ions, influencing its stability and blood-brain barrier penetration.
  17. Semax, a Synthetic Regulatory Peptide, Affects Copper-Induced Abeta Aggregation and Amyloid Formation in Artificial Membrane Models, ACS Chem Neurosci, 2022: A 2022 study found Semax inhibits copper-induced amyloid-beta aggregation in artificial membrane models, hinting at a possible role in Alzheimer's pathology.
  18. Synthetic corticotropins and the GABA-receptor system: Direct and delayed effects, Chem Biol Drug Des, 2023: A 2023 study found Semax had direct CNS effects without mimicking full ACTH's peripheral endocrine activity, including cortisol release.
  19. FDA, Bulk drug substances used in compounding under section 503A of the FD&C Act: The FDA maintains a list of bulk substances that can and cannot be used in compounding under section 503A.
  20. 21 CFR 216.23, Bulk drug substances that may be used in pharmacy compounding under section 503A: The 503A Bulks List specifies substances that may be used in compounding; Semax is not currently on the prohibited list.
  21. 21 CFR 216.24, Bulk drug substances that may be used in outsourcing facilities under section 503B: The 503B Bulks List specifies substances for outsourcing facilities; Semax is not on the prohibited list.
  22. 21 CFR 201.128, Meaning of intended uses: A product's intended use is determined by labeling, marketing claims, and the circumstances of sale, per FDA regulation.
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