Semax Peptide Guide

Semax is a synthetic seven-amino-acid peptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP). Its name derives from the Russian abbreviation for “seven amino acids” (СЕМь АминоКиСлот). The first four residues (Met-Glu-His-Phe) replicate the ACTH(4-7) fragment of adrenocorticotropic hormone, the portion responsible for ACTH’s neurotrophic activity. The final three residues (Pro-Gly-Pro) form a stabilising C-terminal tail that shields the peptide from rapid enzymatic degradation and extends its biological half-life to a therapeutically useful duration.

The Pro-Gly-Pro tripeptide is not pharmacologically inert. Research by the Semax development team at the Institute of Molecular Genetics demonstrated that this fragment carries independent anti-inflammatory and immunomodulatory activity, meaning Semax’s effects are not simply a stabilised version of ACTH(4-7) but a hybrid of the ACTH fragment’s neurotrophic properties and the PGP tail’s own signalling profile.

A critical pharmacological distinction: while Semax retains the neurotrophic effects of its parent ACTH fragment, it lacks full-length ACTH’s hormonal activity. It does not stimulate cortisol release from the adrenal glands. This separation of neurotrophic from endocrine function is what makes Semax pharmacologically distinct from ACTH itself and from other melanocortin-related compounds.

Property	Detail
Full name	Semax (СЕМАКС)
Sequence	Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP)
Parent fragment	ACTH(4-10) with C-terminal Pro-Gly-Pro extension
PubChem CID	68816
Route of administration	Intranasal (primary); subcutaneous (research)
Formulations (Russia)	0.1% solution (cognitive/general), 1% solution (acute neurological)
Developer	Institute of Molecular Genetics, Russian Academy of Sciences (Moscow)
Lead researchers	I.P. Ashmarin and N.F. Myasoedov
Manufacturer	Peptogen JSC (founded 2005, Moscow)

The bottom line: Semax is a well-characterised synthetic heptapeptide that retains the neurotrophic properties of its ACTH parent fragment while lacking the hormonal cortisol-stimulating activity, delivered intranasally for direct CNS access.

Semax was created in 1982 at the Institute of Molecular Genetics of the Russian Academy of Sciences in Moscow, under the supervision of Academician Igor Petrovich Ashmarin and Professor Nikolay Fedorovich Myasoedov. The programme built on earlier Soviet-era research demonstrating that fragments of the ACTH molecule – specifically the (4-7) and (4-10) sequences – possessed neurotrophic and nootropic properties entirely independent of ACTH’s adrenocortical hormone function.

The key design challenge was that the native ACTH(4-10) fragment degraded too rapidly for clinical use. Ashmarin and Myasoedov’s solution was appending the Pro-Gly-Pro tripeptide, which provided enzymatic protection without introducing D-amino acids or hydrophobic radicals that might have altered the pharmacological profile. Their 1995 paper in Neuroscience Research Communications (Ashmarin, Nezavibat’ko, Levitskaya et al.) documented this design rationale.

After more than a decade of preclinical and clinical testing, Semax was approved by the Russian Ministry of Health in the 1990s for cerebrovascular indications. It was added to the Russian List of Vital and Essential Drugs (VED list) by government decree on December 7, 2011, a designation reserved for medications considered critical to the national healthcare system. The commercial product is manufactured by Peptogen JSC, a Moscow-based company founded in 2005 with participation from the Institute of Molecular Genetics.

In Russian clinical practice, Semax is prescribed for ischemic stroke recovery, transient ischaemic attacks, traumatic brain injury, cognitive decline, optic nerve disease, and peptic ulcers. It has accumulated over three decades of clinical use in Russian hospitals, including in paediatric populations. Outside Russia and a small number of CIS countries, Semax has no regulatory approval from any Western agency.

The bottom line: Semax has a uniquely long clinical track record for a research peptide, with over 40 years from initial design to an active pharmaceutical product used in Russian hospitals, but that record exists almost entirely within one country’s regulatory framework.

Semax operates through multiple overlapping neurobiological mechanisms. No single receptor or pathway fully explains its effects, which is characteristic of neuropeptide pharmacology but also makes mechanistic claims harder to verify than for single-target drugs.

BDNF and Neurotrophin Upregulation

The most extensively documented mechanism is Semax’s upregulation of brain-derived neurotrophic factor (BDNF) and its receptor trkB. In a landmark 2006 study by Dolotov, Karpenko, and colleagues at the Institute of Molecular Genetics (Brain Research, vol 1117), a single intranasal dose of Semax at 50 mcg/kg in rats produced a 1.4-fold increase in BDNF protein levels, a 1.6-fold increase in trkB tyrosine phosphorylation, a 3-fold increase in exon III BDNF mRNA, and a 2-fold increase in trkB mRNA in the hippocampus. The same study confirmed improved conditioned avoidance learning in treated animals.

Separate work from the same laboratory (Dolotov et al., Journal of Neurochemistry 2006) demonstrated that Semax also increases BDNF protein in the basal forebrain, a region critical for cholinergic projections involved in attention and memory. BDNF is a potent modulator of synaptic plasticity – it promotes neuronal survival, strengthens synaptic connections, and supports long-term memory consolidation. Low BDNF levels are associated with depression, cognitive decline, and neurodegenerative disease.

Dopaminergic and Serotonergic Modulation

Eremin, Kudrin, and colleagues (Neurochemical Research, 2005) showed that Semax activates both dopaminergic and serotonergic systems in the rodent brain. These neurotransmitter effects are thought to underlie the subjective experiences of improved alertness, motivation, and task engagement reported in clinical use. The dopaminergic sensitisation distinguishes Semax from its sister compound Selank, which acts primarily through GABAergic and enkephalinergic pathways.

Neuroprotective Gene Expression

Genome-wide transcriptome analysis by Medvedeva, Dmitrieva, and colleagues at the Institute of Molecular Genetics (BMC Genomics, 2014) revealed that Semax predominantly enhances the expression of genes related to immune response and vascular function after experimental focal ischaemia in rats. At 24 hours after permanent middle cerebral artery occlusion, Semax treatment increased the expression of chemokine and immunoglobulin genes and enhanced immune cell mobilisation to the injury site.

A follow-up study by Filippenkov, Dergunova, and colleagues (Genes, 2020) extended this work using the transient MCAO model, demonstrating that Semax suppressed inflammatory gene expression while activating neurotransmitter genes at the transcriptome level. A 2021 protein expression study by Sudarkina and Filippenkov (International Journal of Molecular Sciences) confirmed these transcriptomic findings at the protein level, showing suppressed MMP-9 (matrix metalloproteinase-9) and activated anti-inflammatory markers.

The bottom line: Semax acts through BDNF/trkB upregulation, dopamine and serotonin system activation, and broad anti-inflammatory gene expression changes – a multi-target profile that is well-documented at the preclinical level but makes the compound harder to evaluate by Western single-endpoint trial design.

The Metabolite Cascade (Synacton Hypothesis)

One aspect of Semax pharmacology that is almost entirely absent from English-language peptide content is the synacton hypothesis, developed by Vyunova, Andreeva, Shevchenko, and Myasoedov at the Institute of Molecular Genetics. The central claim is that Semax does not act as a single molecule. When it enters the body, endogenous peptidases progressively cleave it from the N-terminus: the heptapeptide MEHFPGP degrades first to the pentapeptide HFPGP, then to the tetrapeptide FPGP, and finally to the tripeptide PGP. Each of these metabolites has its own distinct biological activity, its own binding affinity, and its own receptor targets on neuronal plasma membranes.

Tritium-labelling studies using [(3)H-Pro]MEHFPGP, [(3)H-Pro]HFPGP, and [(3)H-Pro]PGP revealed that the pentapeptide HFPGP is the major intermediate metabolite in the brain and shows the highest competitive activity for Semax’s own binding sites. However, the binding sites for HFPGP are not identical to those for Semax – they differ in affinity and regional distribution across the forebrain, hippocampus, and cerebellum. The tripeptide PGP binds at sites that are strongly inhibited by modulators of cannabinoid, adrenergic, vanilloid, nicotinic, and NMDA receptors, suggesting it interacts with a broader set of neuronal targets than the parent molecule.

Myasoedov’s group named this system a “synacton” – a complex of bioregulators acting in a defined sequence and in interaction. In this framework, the Pro-Gly-Pro tail is not simply a stability modification that delays degradation. It is itself a pharmacologically active metabolite that extends and diversifies Semax’s regulatory reach after the parent molecule has been cleaved. The synacton model proposes that the clinically observed effects of Semax are the aggregate product of the entire degradation cascade, not just the intact heptapeptide.

This has practical implications for understanding Semax pharmacology. PGP independently activates neurotrophic gene transcription after cerebral ischaemia (Dmitrieva and colleagues, Cellular and Molecular Neurobiology, 2010), increases proliferation of neuroglia and progenitor cells in the subventricular zone (Stavchansky and colleagues, Journal of Molecular Neuroscience, 2011), and has gastroprotective and anticoagulant properties documented in separate Russian studies. The gastroprotection data is particularly striking: PGP at equimolar concentrations to Semax showed consistent anti-ulcer effects across three different ulceration models (ethanol, stress, and indomethacin), while its constituent amino acids (proline and glycine alone) did not.

The PGP Matrikine Connection

In a line of Western research entirely independent of the Russian neuropeptide programme, the same tripeptide Pro-Gly-Pro has been extensively studied as a collagen-derived matrikine – a bioactive fragment of extracellular matrix with its own signalling properties. This work, led primarily by Blalock, Gaggar, and colleagues at the University of Alabama at Birmingham, identified PGP as a neutrophil chemoattractant that mimics the structure of CXC chemokines and binds to CXCR1 and CXCR2 receptors on immune cells.

In the lungs, PGP is generated when matrix metalloproteinases (MMP-8 and MMP-9) and prolyl endopeptidase sequentially cleave collagen. The resulting PGP recruits neutrophils, which release more MMP-9, which cleaves more collagen into more PGP – creating a self-propagating inflammatory cycle. Elevated PGP has been documented in patients with chronic obstructive pulmonary disease, cystic fibrosis, neutrophilic asthma, and bronchiolitis obliterans syndrome after lung transplantation. The acetylated form (Ac-PGP) is more potent and resistant to degradation by leukotriene A4 hydrolase, the enzyme that normally clears PGP from tissues.

The irony is that the same molecule is being studied by two research communities for essentially opposite purposes: as a driver of chronic inflammation in Western pulmonary medicine, and as a neuroprotective stabilisation tail in Russian neuropharmacology. Both findings may be valid simultaneously. PGP’s effects appear to be context-dependent, with its role in the brain differing from its role in peripheral tissue inflammation. But the fact that Semax’s C-terminal metabolite is a known CXCR1/2 ligand with documented immune-cell-recruiting activity adds a layer of complexity to the synacton model that the Russian research has not fully addressed.

The bottom line: Semax is not pharmacologically simple. Its metabolite cascade means that administering one peptide produces a sequential series of bioactive fragments, each with distinct receptor targets – and the final fragment in that cascade is a molecule with an entirely separate research literature in Western medicine as a collagen-derived immune signalling peptide.

Semax has a larger body of published research than most peptides in the nootropic category, but nearly all of it originates from Russian institutions with direct ties to the development programme. This concentration of evidence in one research ecosystem is both Semax’s strength (depth and consistency) and its limitation (no independent Western replication of the key clinical findings).

Ischemic Stroke Recovery (Human Data)

The most substantial human study was conducted by Gusev, Martynov, Kostenko, Petrova, and Bobyreva at Pirogov Russian National Research Medical University and the Moscow Centre for Research and Practice in Medical Rehabilitation. Published in Zhurnal Nevrologii i Psikhiatrii im. S.S. Korsakova (2017/2018), this non-randomised trial enrolled 110 ischaemic stroke patients (43 men, 67 women, mean age 58.0 +/- 9.7 years).

Patients were divided into early rehabilitation (89 +/- 9 days post-stroke) and late rehabilitation (214 +/- 22 days post-stroke) groups, each subdivided into Semax-treated and control subgroups. The Semax regimen consisted of two 10-day courses at 6,000 mcg/day intranasally, separated by a 20-day interval. Semax treatment elevated plasma BDNF levels regardless of rehabilitation timing, and patients with higher BDNF levels showed faster improvement on the Barthel Index (a standard measure of daily living ability) and MRC motor-scale scores. Early rehabilitation combined with Semax produced the best functional recovery outcomes.

An earlier study by Gusev, Skvortsova, and Myasoedov (Zhurnal Nevrologii i Psikhiatrii, 2001) tested Semax in 30 acute ischaemic stroke patients against 80 conventional-therapy controls. Using clinical rating scales and EEG monitoring with somatosensory evoked potentials, the study reported that adding Semax to standard intensive therapy accelerated the regression of general cerebral and focal motor deficits.

Cognitive Enhancement (Human Data)

A 1996 study by Kaplan, Kochetova, Nezavibathko, Rjasina, and Ashmarin (Neuroscience Research Communications) documented nootropic effects in healthy human subjects, reporting improvements in attention and cognitive processing speed after intranasal Semax administration. Smaller Russian studies have tested Semax in ADHD-spectrum children and adults with stress-related cognitive complaints, with favourable reported outcomes and minimal side effects. None of these meet Western Phase III evidence standards.

Optic Nerve Disease

Semax is approved in Russia for optic nerve atrophy. The proposed mechanism involves BDNF-mediated neuroprotection of retinal ganglion cells. Polunin and colleagues published clinical data in 2000 demonstrating therapeutic benefit. Evidence is limited to small Russian trials, and no independent Western replication exists for this indication.

Preclinical Neuroprotection

The preclinical neuroprotection data is considerably stronger. Studies using the transient and permanent middle cerebral artery occlusion models in rats consistently show that Semax reduces infarct volume, modulates inflammatory gene expression, enhances neurotransmitter gene transcription, and improves behavioural outcomes. The BMC Genomics 2014 and Genes 2020 transcriptome studies provide molecular-level evidence for these effects across hundreds of genes. A 2023 review by Dergunova, Filippenkov, Limborska, and Myasoedov (Genes, vol 14, no 953) synthesised the neuroprotection evidence and discussed potential new strategies for ischaemic stroke drug discovery based on the Semax transcriptomic data.

Separately, a recent study tested the ACTH(4-7)PGP peptide (Semax) in mouse models of mucopolysaccharidosis types IIIA and IIIC – a lysosomal storage disease affecting the CNS. Daily intranasal administration rescued synaptic transmission defects in hippocampal neurons, reduced hyperactivity, improved working and spatial memory, delayed neuroinflammation and axonal demyelination, and increased lifespan. This work, while early-stage, suggests Semax’s neuroprotective properties may extend beyond ischaemic injury.

The most recent mechanistic study (Kolbaev, Sharonova, and Skrebitsky; Bulletin of Experimental Biology and Medicine, 2025) used calcium imaging on hippocampal slices to test Semax’s effects on spontaneous intracellular calcium oscillations. At 1 micromolar, Semax significantly increased the frequency of spontaneous calcium fluctuations in pyramidal neurons of the hippocampal CA1 field – the region most directly associated with memory consolidation. Critically, it had no significant effect on proton-stimulated calcium entry in cerebellar granule cells, suggesting Semax’s cellular targets are localised to hippocampal networks rather than acting on a generic ion channel mechanism. This is the first study to provide real-time electrophysiological data on where in the brain Semax exerts its initial cellular effects.

Study / Finding	Evidence Tier	Key Result
Gusev 2017 stroke rehabilitation (n=110)	Human, non-randomised	Elevated plasma BDNF, improved Barthel Index and motor scores
Gusev 2001 acute stroke (n=30 vs n=80)	Human, non-randomised	Faster regression of cerebral and focal motor deficits
Kaplan 1996 healthy volunteers	Human, small	Improved attention and cognitive processing speed
Dolotov 2006 BDNF (rats)	Preclinical (rodent)	1.4x BDNF protein, 3x BDNF mRNA, 1.6x trkB phosphorylation
Medvedeva 2014 transcriptome (rats, pMCAO)	Preclinical (rodent)	Immune and vascular gene expression enhancement post-ischaemia
Filippenkov 2020 transcriptome (rats, tMCAO)	Preclinical (rodent)	Inflammatory gene suppression, neurotransmitter gene activation
Sudarkina/Filippenkov 2021 proteomics (rats)	Preclinical (rodent)	MMP-9 suppression, anti-inflammatory protein activation confirmed
MPS IIIA/IIIC models (mice)	Preclinical (rodent)	Rescued synaptic transmission, improved cognition, increased lifespan
Kolbaev 2025 calcium dynamics (rat hippocampus)	Preclinical (ex vivo)	Increased Ca2+ oscillation frequency in CA1 neurons, no effect in cerebellum
Vyunova/Andreeva synacton binding (rat brain)	Preclinical (in vitro)	Metabolites HFPGP and PGP have distinct binding sites from parent Semax

The bottom line: Semax has more published evidence than most research peptides, including human stroke rehabilitation data from the largest published clinical trial, but all major clinical findings originate from Russian research groups affiliated with the development programme, and no Western-standard randomised controlled trial has been published.

Semax exists in two regulatory worlds: an approved pharmaceutical in Russia and an unregulated research compound everywhere else. The PCAC review scheduled for July 24, 2026 represents the first serious opportunity for Semax to enter a Western regulatory framework through the 503A compounding pathway.

Jurisdiction	Status	Detail
Russia	Approved	VED list since December 7, 2011. Prescription medication for stroke, cognitive decline, optic nerve disease
United States (FDA)	Not approved	Removed from Category 2 April 15, 2026. PCAC review July 24, 2026 for cerebral ischaemia, migraine, trigeminal neuralgia. Docket FDA-2025-N-6895
United Kingdom (MHRA)	Not licensed	Not a controlled substance under the Misuse of Drugs Act. Not covered by the Psychoactive Substances Act 2016 (peptides generally exempt)
Australia (TGA)	Not approved	Not scheduled under the Poisons Standard. Not TGA-registered
WADA	Not listed	Not individually named on the 2024 Prohibited List. No direct ergogenic classification

The PCAC will evaluate Semax in both free base and acetate salt forms. Both forms were previously placed on Category 2 in September 2023 as part of the FDA’s broader peptide compounding restrictions. Their removal and referral to PCAC followed the April 15, 2026 reclassification of 12 peptides under Docket No. FDA-2025-N-6895. The PCAC’s recommendation is advisory – the FDA makes the final determination on whether to add Semax to the 503A Bulks List through a subsequent rulemaking process.

A critical variable for the PCAC outcome: how the committee handles non-English clinical data. Semax has decades of Russian-language clinical literature, but Western regulatory committees typically require English-language publications meeting specific trial design standards. For how individual countries regulate peptides more broadly, see our guides to peptide legality in the US, the UK and Australia.

The bottom line: Semax is an approved prescription drug in Russia and a regulatory unknown everywhere else, with its first opportunity for Western legitimacy arriving at the July 24, 2026 PCAC hearing under three nominated indications.

Semax has one of the cleaner safety profiles among research peptides, based on decades of pharmaceutical use in Russia across adult, paediatric, and stroke-patient populations. The Russian clinical record reports no major adverse effects, no addictive potential, and no withdrawal syndrome.

Reported side effects are typically mild and transient: nasal irritation or mild burning during or immediately after intranasal administration (the most common complaint), mild headache in a small percentage of users, and mild insomnia or overstimulation if administered late in the day. Because Semax modulates dopaminergic neurotransmission, it can be mildly activating in a way that interferes with sleep onset if timing is not managed.

A less commonly discussed finding: a 1996 study by Ashmarin’s group reported an anxiogenic component in some research subjects, suggesting Semax can amplify anxiety in individuals who are already highly anxious. This is consistent with its dopaminergic activation profile and is the opposite of what its sister compound Selank does.

The Alzheimer’s Drug Discovery Foundation (ADDF) Cognitive Vitality report on Semax notes that it may raise blood glucose levels in people with diabetes, and lists pregnancy and lactation as contraindications based on insufficient safety data. Because Semax affects neurotransmitter systems including serotonin, it has the potential to interact with SSRIs, MAOIs, and stimulant medications.

The bottom line: Semax has a favourable safety profile across three decades of Russian clinical use with no major adverse events reported, but the safety data has not been independently evaluated by any Western regulatory authority.

Nearly all Semax research originates from the Institute of Molecular Genetics of the Russian Academy of Sciences or institutions with direct collaborative ties to the development team. The lead author on the molecular work, Nikolay F. Myasoedov, is one of the original developers. The lead author on the clinical stroke studies, Evgeny I. Gusev, leads the neurology department at Pirogov Russian National Research Medical University. The manufacturer, Peptogen JSC, was co-founded by the Institute.

This is not unusual for early-stage pharmaceutical development, but it means that the entire evidence base for Semax lacks the independent replication that Western regulatory systems consider essential for establishing a compound’s safety and efficacy. The transcriptome studies, while published in Western peer-reviewed journals (BMC Genomics, Genes, International Journal of Molecular Sciences), are still conducted by the same laboratory.

One partial exception: the 2023 mucopolysaccharidosis study involved collaboration with researchers outside the core Semax programme, suggesting some broadening of the research base. But for the primary clinical indications under PCAC review, the evidence remains concentrated in Russian institutions with direct programme involvement.

The bottom line: Semax’s evidence is deep but narrow – extensive preclinical and clinical data from one research ecosystem, with no independent Western replication of the key clinical findings.

Selank is Semax’s sister compound, developed at the same Institute of Molecular Genetics using the same Pro-Gly-Pro stabilisation strategy but built on a completely different parent molecule (tuftsin, an immune tetrapeptide from IgG) rather than ACTH. Where Semax is activating and cognitively stimulating through BDNF and dopamine, Selank is calming and anxiolytic through GABA modulation and enkephalin stabilisation. The two are frequently used together in Russian clinical practice and in the research community. A detailed head-to-head comparison is covered in our Semax vs Selank comparison (forthcoming).

N-Acetyl Semax and N-Acetyl Semax Amidate are acetylated variants that appear in the research compound market. The N-terminal acetylation is designed to extend metabolic stability and potentially enhance blood-brain barrier penetration. These variants have no independent clinical data and no Russian regulatory approval – they exist in the grey market only.

For how Semax fits within the broader landscape of cognitive-enhancing peptides, see our Nootropic and Neuropeptide Compounds hub page.

What does Semax stand for?

The name derives from the Russian abbreviation for “seven amino acids” – СЕМь АминоКиСлот (SEM’ AminoKiSlot), contracted to СЕМАКС (SEMAKS). The peptide contains exactly seven amino acid residues: Met-Glu-His-Phe-Pro-Gly-Pro.

Is Semax the same as ACTH?

No. Semax is derived from the ACTH(4-10) fragment but is pharmacologically distinct from full-length ACTH. It retains ACTH’s neurotrophic effects on brain tissue but does not stimulate cortisol release from the adrenal glands. This separation of neurotrophic from hormonal activity is the foundation of Semax’s clinical utility.

Who developed Semax?

Semax was developed from 1982 onwards at the Institute of Molecular Genetics of the Russian Academy of Sciences in Moscow, under the supervision of Academician I.P. Ashmarin and Professor N.F. Myasoedov. The commercial product is manufactured by Peptogen JSC, a company founded in 2005 with participation from the Institute.

What is the PCAC reviewing Semax for?

The Pharmacy Compounding Advisory Committee will evaluate Semax (free base and acetate) on July 24, 2026 for potential inclusion on the Section 503A Bulk Drug Substances List for three indications: cerebral ischaemia, migraine, and trigeminal neuralgia. The review falls under the relevant FDA docket established during the April 2026 reclassification. A positive recommendation would allow licensed compounding pharmacies to legally prepare Semax with a valid prescription.

Is Semax safe?

The Russian pharmaceutical record includes over three decades of clinical use with a mild side-effect profile (nasal irritation, occasional headache, mild insomnia if dosed late). No major adverse events, addictive potential, or withdrawal syndrome have been reported. However, this safety record has not been independently evaluated by the FDA, EMA, MHRA, or TGA. It may raise blood glucose in diabetics and can amplify anxiety in highly anxious individuals.

How is Semax different from Selank?

Both were developed at the same Institute using the same Pro-Gly-Pro stabilisation design, but they are built on different parent molecules and work through different mechanisms. Semax is derived from ACTH and acts primarily through BDNF upregulation and dopaminergic stimulation – it is activating and cognitively enhancing. Selank is derived from tuftsin (an IgG fragment) and acts through GABA modulation and enkephalin stabilisation – it is calming and anxiolytic. The two are often used together as complementary compounds.

Can Semax be used with a certificate of analysis?

A COA verifies the identity and purity of a peptide sample but does not make it legal for human use. Where Semax is available as a research compound, a valid COA from a third-party analytical laboratory is the minimum verification that the product contains what the label claims. Look for HPLC purity above 98% and mass spectrometry confirmation of the correct molecular weight.