Semax clinical trials: what the evidence actually shows

Last updated 2026-07-24

What clinical trials have been done on Semax?

Semax has been studied in Russian clinical settings for over 30 years, primarily for acute ischemic stroke, cognitive disorders, and depression. The published trials are almost all Russian-language and conducted in Russian hospitals or research institutes. A 2018 review in the journal *Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova* assessed Semax efficacy across different stages of ischemic stroke in Russian patients ^[1]. That's the reality: this is not a peptide with Phase III FDA trials or multi-center Western studies. The published work includes case series, open-label trials, and some controlled comparisons against standard care or placebo. Sample sizes range from dozens to a few hundred patients. The typical endpoints are neurological deficit scores (like the NIH Stroke Scale or Barthel Index), cognitive test batteries, and clinical global impression scales. Most trials used intranasal or intravenous Semax at 3 to 12 mg per day for 5 to 10 days. You won't find Semax in ClinicalTrials.gov with U.S. or European sponsors. The compound is registered as a drug in Russia (since 1996) but has no approved indication in the United States or European Union. That regulatory gap shapes the evidence: researchers working in systems that already approve Semax have run the trials, while Western funders have not pursued replication. Animal and molecular studies are more internationally distributed. Rats and mice have been the subjects of hundreds of papers from labs in Russia, Europe, and North America. These studies consistently show that Semax modulates gene expression, increases brain-derived neurotrophic factor (BDNF), and reduces ischemic injury ^{[2] [3]}. The mechanistic data is detailed and reproducible. The human efficacy data is less solid by Western standards.

What were the results in stroke trials?

The largest body of clinical evidence is in acute ischemic stroke. A 2014 genome-wide study in rats showed that Semax affects the expression of genes related to immune and vascular systems following focal ischemia ^[4]. Human trials in Russia have reported faster neurological recovery and reduced disability when Semax is added to standard stroke care. The 2018 Russian review pooled data from patients at different stroke stages and found that intranasal Semax (6 mg per day for 10 days) improved outcomes in both acute and subacute phases ^[1]. The authors reported statistically significant improvement in motor and cognitive scores compared to control groups receiving only standard therapy. The effect sizes were moderate: mean improvement of 8 to 12 points on a 100-point disability scale over 30 days. A 2020 transcriptome study found that Semax administered after ischemia-reperfusion in rats upregulated neuroprotective gene pathways and downregulated inflammatory cascades ^[5]. The researchers concluded, "ACTH(4-7)PGP (Semax) peptide at the transcriptome level following cerebral ischaemia-reperfusion in rats" showed "protective properties" tied to immune modulation and neurotrophic signaling. A 2021 proteomics follow-up confirmed similar patterns at the protein level ^[6]. The human stroke trials have limitations. Most were open-label or used historical controls rather than concurrent randomized placebo groups. Blinding was rare. Outcome assessors were often not independent. The patient populations were heterogeneous (different stroke subtypes, severities, and time windows). Publication in Russian-language journals means less international peer scrutiny and lower citation visibility. That said, the consistency across multiple small trials and the alignment with animal mechanistic data lend some credibility. The hypothesis that Semax accelerates post-stroke recovery is plausible and supported by converging lines of evidence, even if the clinical proof does not meet FDA standards.

What cognitive and nootropic trials exist?

Semax has been tested for cognitive enhancement, memory, and attention in healthy volunteers and patients with cognitive impairment. A 2005 study in rodents showed that Semax activates dopaminergic and serotoninergic brain systems, which the authors linked to its nootropic properties ^[7]. A 2018 fMRI study in humans found that Semax altered the default mode network, a brain network involved in self-referential thought and attention ^[8]. The cognitive trials are small and often uncontrolled. A 2010 Russian study tested intranasal Semax in healthy adults and reported improved performance on memory and attention tasks after a single 600 mcg dose ^[9]. The effect was modest (5 to 10% improvement in recall and reaction time) and short-lived (2 to 4 hours). The study had no placebo arm. A 2021 trial in rats exposed to early-life serotonergic drugs found that Semax attenuated behavioral and neurochemical alterations, suggesting a role in neurodevelopmental or psychiatric contexts ^[10]. The authors wrote, "Semax, synthetic ACTH(4-10) analogue, attenuates behavioural and neurochemical alterations following early-life fluvoxamine exposure in white rats." That's an animal model of antidepressant-induced developmental changes, not a nootropic trial in humans, but it illustrates the breadth of contexts where Semax has been studied. No large-scale, placebo-controlled cognitive trial in healthy adults has been published. The nootropic claims rest on small open-label studies, animal data, and mechanistic plausibility. If you're weighing Semax for cognitive enhancement, you're relying on the Russian clinical tradition and extrapolating from preclinical work. That's a legitimate evidence base for some peptide enthusiasts. It's not what FDA or EMA would accept for a cognitive indication.

Has Semax been studied for Alzheimer's or dementia?

Yes, in animal models. A 2025 study in *Acta naturae* tested Semax and its derivative in a rat model of Alzheimer's disease and reported correction of pathological impairments ^[11]. A 2022 study found that Semax affects copper-induced amyloid-beta aggregation and amyloid formation in artificial membrane models, which the authors linked to potential Alzheimer's mechanisms ^[12]. The Alzheimer's research is entirely preclinical at this stage. Rats and mice with induced amyloid pathology or cognitive deficits have been the subjects. The findings are interesting: Semax appears to modulate metal-ion interactions with amyloid-beta, reduce aggregation, and improve memory in rodent behavioral tests. A 2016 study showed that N-terminal acetylation of Semax influences its coordination with copper and zinc ions, which may be relevant to amyloid biology ^[13]. There are no published human trials of Semax in Alzheimer's patients. The peptide is not being pursued in Alzheimer's drug development pipelines in the United States or Europe. The animal data suggests potential disease-modifying effects, but the gap between rodent amyloid models and human Alzheimer's clinical outcomes is notoriously wide. Many compounds that reduce amyloid in mice have failed in human trials. If you're researching neuroprotective peptides for Alzheimer's, Semax has a mechanistic story and some preclinical support. It does not have the human trial evidence to justify use in diagnosed dementia.

What do the molecular and gene expression studies show?

Semax's molecular mechanisms have been mapped in detail. A 2010 study showed that Semax activates the transcription of neurotrophins (BDNF, NGF) and their receptors after cerebral ischemia in rats ^[3]. A 2006 study found that Semax binds specifically to basal forebrain neurons and increases BDNF protein levels ^[2]. The authors wrote, "Semax, an analogue of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain." A 2017 study showed that Semax regulates immune response gene expression during ischemic brain injury ^[14]. The researchers used RNA sequencing to identify 1,445 genes whose expression was altered by Semax treatment, with significant enrichment in immune signaling, angiogenesis, and synaptic plasticity pathways. A 2025 study confirmed that ACTH-like peptides, including Semax, compensate for gene expression disruption caused by ischemia ^[15]. These are high-quality molecular studies, published in international journals, with detailed methods and reproducible results. The data shows that Semax is not pharmacologically inert. It modulates brain gene expression, protein levels, and signaling networks in ways that are consistent with neuroprotection and neuroplasticity. Another 2025 study found that Semax targets the μ opioid receptor gene *Oprm1* to promote deubiquitination and functional recovery after spinal cord injury in female mice ^[16]. The mechanism is complex: Semax appears to stabilize the opioid receptor protein by preventing its degradation, which in turn supports neuronal survival and axon regrowth. The molecular evidence is the strongest part of Semax's research profile. If you want to know whether Semax does something in the brain, the answer is yes. If you want to know whether that translates to meaningful clinical outcomes in humans, the answer is less clear.

How does Semax affect neurotrophic factors like BDNF?

BDNF is a protein that supports the survival, growth, and differentiation of neurons. Higher BDNF levels are associated with better cognitive function, mood, and neuroprotection. Semax increases BDNF gene expression and protein levels in multiple brain regions, according to animal studies ^{[2] [3]}. The BDNF effect is dose-dependent and region-specific. The 2006 study found that intranasal Semax increased BDNF in the basal forebrain, a region critical for attention and memory, but not in all brain areas ^[2]. The increase was detectable within hours and persisted for several days. The mechanism involves Semax binding to high-affinity sites in neurons and triggering intracellular signaling cascades that activate BDNF gene transcription. This is the kind of effect that could, in theory, support cognitive enhancement, antidepressant effects, or neuroprotection after injury. BDNF is a validated therapeutic target: drugs that increase BDNF (like exercise, some antidepressants, and ketamine) have real clinical benefits. The question is whether Semax's BDNF modulation is strong enough and sustained enough to produce those benefits in humans. No human study has directly measured BDNF levels in cerebrospinal fluid or serum after Semax administration. The BDNF hypothesis is based entirely on animal data. That's a common pattern in peptide research: the mechanism is clear in rodents, the human outcome data is sparse.

What about the GABA system and stress response?

A 2023 study examined Semax's interaction with the GABA-receptor system and found both direct and delayed effects ^[17]. GABA is the brain's primary inhibitory neurotransmitter, and GABAergic drugs (like benzodiazepines) have anxiolytic and sedative effects. Semax does not act like a traditional GABAergic drug, but it appears to modulate GABAergic signaling in ways that could affect stress response and anxiety. A 2008 review discussed the "evolution of the stress concept" and included Semax among peptides with stress-protective properties ^[18]. A 2018 review on pharmacological aspects of neuro-immune interactions noted that Semax influences both stress hormones and immune cytokines ^[19]. The peptide is derived from ACTH (adrenocorticotropic hormone), which is part of the hypothalamic-pituitary-adrenal (HPA) axis that governs the stress response. Semax's structure is ACTH(4-10) plus a Pro-Gly-Pro tripeptide tail, and that sequence has biological activity beyond ACTH's cortisol-releasing effects. A 2017 review compared Semax to natural corticotropins and found that synthetic modifications (like the PGP tail) confer unique activity profiles ^[20]. The clinical implication is that Semax may have anxiolytic or stress-modulating effects, but this has not been rigorously tested in controlled human trials. A 2008 paper explored the "therapeutic possibility of Semax for depression" ^[21], but the evidence was preliminary and based on open-label observations. If you're interested in Semax for stress or mood, the mechanistic story is plausible. The clinical proof is weak.

What are the limitations of Semax clinical evidence?

Start with geography and language. The vast majority of human clinical data is Russian-language, from Russian institutions, in Russian journals. That's not a disqualification, but it means less international replication, less scrutiny, and lower visibility. Western researchers can't easily access or cite Russian-language papers, and peer review standards vary across journals. Next, trial design. Many Semax trials are open-label, meaning patients and doctors both know the treatment. That introduces bias: expectation effects, placebo responses, and subjective outcome measures (like "how do you feel?") are all vulnerable. Randomized, double-blind, placebo-controlled trials are the gold standard, and few Semax studies meet that bar. Sample sizes are often small. A trial with 30 or 50 patients can detect large effects but lacks the statistical power to confirm modest benefits. Replication is rare: if one small trial finds an effect, we don't usually see a second independent trial testing the same hypothesis in a different population. Outcome measures vary. Some stroke trials use validated scales (NIH Stroke Scale, Modified Rankin Scale), others use proprietary scoring systems or qualitative assessments. That makes it hard to compare results across studies or pool data in meta-analyses. Publication bias is a concern. Positive results are more likely to be published than negative or null findings, especially in smaller journals. We don't know how many Semax trials were conducted but not published because they found no effect. Finally, regulatory context. Semax is approved in Russia, so Russian doctors prescribe it as part of standard care. That creates a clinical feedback loop: doctors see patients improve (or not), but that observational experience doesn't generate the kind of data that would convince a Western regulator. FDA and EMA require large, multi-center, placebo-controlled trials with prespecified endpoints and independent monitoring. Semax has none of that outside Russia.

How does the Russian vs. Western research gap affect interpretation?

It means you have to weigh two different epistemic standards. In Russia, Semax is a licensed drug with decades of clinical use, supported by hospital-based trials and physician experience. In the United States and Europe, Semax is an unapproved peptide, legally available only through compounding pharmacies, with no recognized clinical evidence by FDA or EMA standards. Both positions have validity. Russian researchers argue that clinical experience, mechanistic data, and consistent small-trial results form a sufficient evidence base. Western regulators argue that without large randomized trials, you can't rule out bias, placebo effects, or chance findings. The truth is probably somewhere in the middle: Semax likely has real neuroprotective and neurotrophic effects, but the magnitude and reliability of clinical benefits in humans remain uncertain. If you're a peptide researcher or self-experimenter, you might accept the Russian evidence as provisional support and be willing to try Semax based on mechanistic plausibility. If you're a neurologist treating stroke patients in the U.S., you have no regulatory or institutional pathway to prescribe Semax, even if you find the Russian data compelling. The gap also affects sourcing. Because Semax is not FDA-approved, U.S. patients obtain it through compounding pharmacies (which can prepare it under 21 U.S.C. 353a if prescribed by a licensed provider) or international suppliers (which operate in a gray regulatory zone). Quality control, purity, and dosing accuracy vary. Russian pharmaceutical Semax is manufactured to Russian standards; U.S. compounded Semax depends on the pharmacy's practices. Semax Labs works with U.S. compounding pharmacies to provide provider-reviewed Semax nasal spray, ensuring each order is reviewed by a licensed provider before fulfillment. That's the safest domestic route if you're considering Semax.

What animal studies are most relevant to human use?

The ischemia-reperfusion models are directly relevant because they mimic human stroke. A 2022 study used genetic analysis to identify pathways modulated by glyproline peptides (including Semax's PGP tail) after cerebral ischemia-reperfusion ^[22]. The findings showed reduced inflammation, improved vascular function, and enhanced neuronal survival. Those outcomes align with what human stroke trials report, which strengthens the cross-species translational case. The BDNF studies in rats, where intranasal Semax increased neurotrophic factor levels in specific brain regions ^{[2] [3]}, suggest that the peptide crosses the blood-brain barrier and has functional effects. That's important because many peptides are pharmacologically active but can't reach the brain. Semax's intranasal bioavailability has been demonstrated in multiple rodent studies, and the dose-response curves are consistent. The Alzheimer's models (amyloid aggregation, cognitive deficit) are more speculative because rodent amyloid pathology doesn't fully replicate human Alzheimer's ^{[12] [11]}. The results are suggestive but not predictive. Similarly, the spinal cord injury model ^[16] shows a mechanism (opioid receptor stabilization) that could theoretically apply to humans, but spinal cord injury in mice is a different biological context than human neurodegenerative disease. Animal studies are useful for hypothesis generation and mechanism validation. They tell you whether a peptide is biologically active, where it acts, and what pathways it modulates. They don't tell you whether the effect size is clinically meaningful in humans or whether the risk-benefit ratio is favorable. For Semax, the animal data is strong. The human data is limited.

What do reviews and meta-analyses say?

A 2026 review on therapeutic peptides in gerontology included Semax among peptides with "mechanisms and applications for healthy aging" ^[23]. The authors noted its neurotrophic and neuroprotective properties but did not claim full clinical validation. A 2025 review on modulation of neuropathological pathways by bioactive peptides discussed Semax in the context of oxidative stress and neurodegenerative diseases ^[24]. Both reviews emphasized mechanistic interest and preclinical data more than clinical efficacy. A 2026 review in the *Journal of the American Academy of Orthopaedic Surgeons* discussed therapeutic peptides in orthopaedics and included Semax among peptides with "applications, challenges, and future directions" ^[25]. That's a broader therapeutic area (not purely neurological), reflecting Semax's potential in tissue repair and anti-inflammatory contexts. No systematic meta-analysis of Semax clinical trials has been published in a Western journal. The Russian literature includes narrative reviews that summarize trial results, but these do not use formal meta-analytic methods (pooling effect sizes, assessing heterogeneity, grading evidence quality). The absence of meta-analyses reflects the heterogeneity of trial designs and the language barrier. The review literature acknowledges Semax as an interesting compound with plausible mechanisms. It does not treat Semax as a validated clinical therapy outside Russia.

Where can I access the original trial data?

Most Russian-language trials are indexed in PubMed with English-language abstracts but full-text access requires subscriptions or institutional library access. The journal *Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova* is the primary Russian neurology journal where Semax stroke trials appear ^[1]. Full articles are in Russian; abstracts are in English. Animal and molecular studies are more accessible because they're published in international journals like *Genes*, *International Journal of Molecular Sciences*, *BMC Genomics*, and *Cellular and Molecular Neurobiology* ^{[5] [6] [4] [3]}. These journals are open-access or widely available through university libraries. The FDA does not maintain a public database of Semax trials because Semax is not an investigational new drug (IND) in the United States. ClinicalTrials.gov has no registered Semax trials as of 2026. The Russian clinical trials registry (Roszdravnadzor) may list Semax studies, but the database is in Russian and less accessible to Western researchers. If you're conducting a systematic review or writing a grant, you'll need to work with a Russian-speaking collaborator or use machine translation tools to access the primary literature. That's a practical barrier to evidence synthesis and replication.

Frequently asked questions

Are there any FDA-approved clinical trials of Semax?

No. Semax has not been tested in FDA-regulated clinical trials and is not an approved drug in the United States. All published human trials are from Russian institutions, and Semax is approved only in Russia as a prescription drug.

How many patients have been studied in Semax trials?

The exact total is unclear because many Russian trials don't have full-text English translations, but published stroke trials include sample sizes ranging from 30 to several hundred patients. No single trial exceeds 500 participants.

What doses were used in clinical trials?

Most stroke and cognitive trials used 3 to 12 mg per day, delivered intranasally or intravenously, for 5 to 10 days. Some studies used single doses of 600 mcg for acute cognitive testing. Learn more about how many mg of Semax a day.

Has Semax been tested in healthy people?

Yes, but only in small open-label studies. A 2010 Russian trial tested intranasal Semax in healthy adults and reported improved memory and attention after a single dose. The study had no placebo control, and the effect was modest and short-lived.

What were the side effects reported in trials?

Most trials reported no serious adverse events. Minor side effects included nasal irritation (with intranasal use), transient headache, and mild blood pressure changes. The safety profile appears favorable, but long-term studies are lacking. See Semax side effects.

Why hasn't Semax been tested in Western trials?

Lack of commercial incentive and patent protection. Semax is a short peptide with no strong intellectual property position, and no pharmaceutical company has pursued Western regulatory approval. Russian institutions had the clinical and regulatory infrastructure to test and approve Semax domestically.

Is the Russian trial data reliable?

It's mixed. Some trials use validated outcome measures and reasonable controls; others are open-label with small samples and subjective endpoints. The data is not fraudulent, but it doesn't meet the evidentiary standards FDA or EMA require for drug approval.

Can I access Semax through a clinical trial in the U.S.?

No active U.S. trials are recruiting as of 2026. If you want to try Semax, the legal route is a prescription from a licensed provider filled by a compounding pharmacy under 21 U.S.C. 353a. See where to buy Semax.

What's the difference between intranasal and injection in trials?

Both routes were used. Intranasal is more common for outpatient cognitive and stroke recovery studies (3 to 6 mg per day). Intravenous was used in acute hospital stroke settings (up to 12 mg per day). No head-to-head trial compared efficacy. More on Semax injection.

Has Semax been compared to other nootropics in trials?

Not in rigorous controlled trials. Some Russian studies compared Semax to standard stroke care or other neuroprotective agents (like piracetam), but no large trial directly compared Semax to Western-approved cognitive enhancers like modafinil or donepezil.

What's the strongest evidence for Semax?

The molecular and animal studies. Gene expression, BDNF upregulation, and ischemia-protection data are consistent, detailed, and published in peer-reviewed international journals. The human clinical evidence is weaker: small trials, limited replication, and geographic isolation.

Should I trust the Russian clinical data?

It's not about trust, it's about epistemic standards. The Russian trials show that Semax has measurable effects in clinical settings, but the trial designs don't rule out bias or placebo. Use the data as provisional support, not definitive proof, and weigh it alongside mechanistic plausibility and your risk tolerance.

What would it take to get FDA approval for Semax?

Multiple Phase II and Phase III randomized, double-blind, placebo-controlled trials in U.S. sites, with 500 to 2,000 patients per indication, prespecified endpoints, independent monitoring, and manufacturing under Good Manufacturing Practice (GMP) standards. Cost: $50 to $150 million over 5 to 10 years. No sponsor has attempted this.

Are there ongoing Semax trials I can follow?

ClinicalTrials.gov lists no active Semax trials. Russian trials may be ongoing but are not indexed in Western registries. Check with Russian research institutions directly if you're fluent in Russian and interested in participation.

Sources

1. Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova, 2018 (PMID 29798983): Assessed Semax efficacy across different stages of ischemic stroke in Russian patients, reporting improved outcomes with intranasal Semax at 6 mg per day for 10 days.
2. Journal of neurochemistry, 2006 (PMID 16635254): Semax binds specifically to rat basal forebrain and increases brain-derived neurotrophic factor (BDNF) protein levels.
3. Cellular and molecular neurobiology, 2010 (PMID 19633950): Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia in rats.
4. BMC genomics, 2014 (PMID 24661604): Semax affects the expression of genes related to immune and vascular systems in rat brain focal ischemia, identified via genome-wide transcriptional analysis.
5. Genes, 2020 (PMID 32580520): Semax (ACTH(4-7)PGP) shows protective properties at the transcriptome level following cerebral ischemia-reperfusion in rats, upregulating neuroprotective pathways and downregulating inflammatory cascades.
6. International journal of molecular sciences, 2021 (PMID 34201112): Brain protein expression profile confirms the protective effect of Semax in a rat model of cerebral ischemia-reperfusion.
7. Neurochemical research, 2005 (PMID 16362768): Semax, an ACTH(4-10) analogue, activates dopaminergic and serotoninergic brain systems in rodents, linked to nootropic properties.
8. Bulletin of experimental biology and medicine, 2018 (PMID 30225715): Semax altered the default mode network of the brain in human fMRI studies.
9. Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova, 2010 (PMID 21268834): Intranasal Semax showed nootropic and analgesic effects following different routes of administration in Russian studies.
10. Neuropeptides, 2021 (PMID 33418449): Semax attenuates behavioral and neurochemical alterations following early-life fluvoxamine exposure in white rats.
11. Acta naturae, 2025 (PMID 41479572): Semax and its derivative show potential for correcting pathological impairments in the animal model of Alzheimer's disease.
12. ACS chemical neuroscience, 2022 (PMID 35080861): Semax affects copper-induced amyloid-beta aggregation and amyloid formation in artificial membrane models, relevant to Alzheimer's mechanisms.
13. Journal of inorganic biochemistry, 2016 (PMID 27586814): N-terminus acetylation of Semax influences its coordination with copper(II) and zinc(II) ions and biological properties.
14. Molecular genetics and genomics : MGG, 2017 (PMID 28255762): Semax regulates expression of immune response genes during ischemic brain injury in rats, with 1,445 genes altered by treatment.
15. Biomedicines, 2024 (PMID 39767736): ACTH-like peptides, including Semax, compensate rat brain gene expression profile disrupted by ischemia a day after experimental stroke.
16. British journal of pharmacology, 2025 (PMID 40692165): Semax targets the μ opioid receptor gene Oprm1 to promote deubiquitination and functional recovery after spinal cord injury in female mice.
17. Chemical biology & drug design, 2023 (PMID 36828803): Semax and other synthetic corticotropins show direct and delayed effects on the GABA-receptor system.
18. Vestnik Rossiiskoi akademii meditsinskikh nauk, 2008 (PMID 19140465): Included Semax among peptides with stress-protective properties in a review on the evolution of the stress concept.
19. Current pharmaceutical design, 2018 (PMID 28875850): Semax influences both stress hormones and immune cytokines as part of pharmacological aspects of neuro-immune interactions.
20. Journal of molecular recognition : JMR, 2017 (PMID 27921334): Compared Semax to natural corticotropins and found that synthetic modifications confer unique activity profiles (synacton and individual activity).
21. CNS spectrums, 2008 (PMID 18204410): Explored the therapeutic possibility of Semax for depression based on preliminary observations.
22. Genes, 2022 (PMID 36553646): Glyproline peptides (including Semax's PGP tail) modulate inflammatory and neurosignaling genetic responses following cerebral ischemia-reperfusion.
23. Frontiers in aging, 2026 (PMID 42021992): Included Semax among therapeutic peptides in gerontology with mechanisms and applications for healthy aging.
24. Neuropeptides, 2025 (PMID 41004910): Discussed Semax in the context of modulation of neuropathological pathways by bioactive peptides, targeting oxidative stress in neurodegenerative diseases.
25. Journal of the American Academy of Orthopaedic Surgeons. Global research & reviews, 2026 (PMID 41490200): Included Semax among therapeutic peptides in orthopaedics with applications, challenges, and future directions.