Semax and Selank for Anxiety, Depression, PTSD, and Cognition

Published: March 16, 2026 | By: Dr. Baghel | Category: Peptide Therapy

Update, July 24, 2026: An FDA advisory committee voted, as reported, to recommend adding semax to the 503A compounding list. Read the indication before the headline. The nomination FDA assessed covered cerebral ischemia, migraine, and trigeminal neuralgia, which are stroke and headache indications rather than the psychiatric uses this article covers. This is a recommendation and not an approval. Semax cannot be compounded by any pharmacy today, and FDA still has to accept the recommendation and complete rulemaking, usually 12 to 24 months. Full analysis in my piece on whether semax is legal after the 2026 FDA vote.

Where I stand on offering it: I don’t prescribe semax today, and I can’t, because it isn’t FDA-approved and isn’t on the 503A list. If the FDA accepts the recommendation and finishes rulemaking, that changes, and I’ll offer it to patients where the clinical picture supports it. One caveat is worth stating now. The indication that cleared is neurological, so using a compounded peptide for depression or anxiety would be off-label prescribing of a drug whose psychiatric evidence is still thin. That’s a decision I’d make case by case, with the patient in front of me. If I do prescribe it, it comes with written consent that names the evidentiary gaps, a certificate of analysis that includes endotoxin testing, and attention to two risks in the FDA’s file. Semax reduced platelet aggregation in animal studies, which matters for anyone on an anticoagulant or an SSRI. It also potentiated amphetamine in mice, and no study of its abuse potential exists, which matters in a practice that treats ADHD.

Semax and Selank for Anxiety, Depression, PTSD, and Cognition: A Psychiatrist’s Clinical Perspective

I’m a board-certified psychiatrist with dual ABPN certification in adult and forensic psychiatry. I’m credentialed with 503A compounding pharmacies. I prescribe psychiatric medications every day and I consider peptide therapy as one tool among many; a complementary treatment to use alongside of traditional psychiatry.

Other prescribers may have difficulty explaining what happens when a patient with treatment-resistant depression, comorbid anxiety, and a history of SSRI failures walks into a clinical evaluation and asks about peptides. That’s the conversation I have in my practice. This article covers both: the science in detail and how I apply it clinically.

For patients in North Carolina who are ready to explore peptide therapy with a board-certified psychiatrist, visit the peptide therapy service page for pricing, the evaluation process, and how to schedule a free consultation.

For patients whose cognitive complaints emerged during or after an antidepressant taper, the broader workup is covered in the guide to antidepressant discontinuation syndrome.

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What Are Semax and Selank? Origins and Pharmacology

Semax is a synthetic heptapeptide derived from the 4-10 fragment of adrenocorticotropic hormone (ACTH). It was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences in the 1980s and has been used clinically in Russia for stroke recovery, cognitive impairment, and neurodegenerative conditions, though FDA’s review notes it could not verify a specific Russian approval year or indication. The peptide sequence is Met-Glu-His-Phe-Pro-Gly-Pro, with a modified C-terminal proline that increases enzymatic stability and extends its half-life compared to the native ACTH fragment.

Selank is a synthetic analog of the immunomodulatory peptide tuftsin (Thr-Lys-Pro-Arg), with an added Gly-Pro sequence that improves metabolic stability. It was developed at the same institute and has been studied extensively as an anxiolytic. Selank received regulatory approval in Russia as a prescription anxiolytic and nootropic medication.

Neither peptide is FDA-approved for any indication in the United States. Both have substantial clinical use histories in Russian and Eastern European medical practice, where Semax has been used clinically for years. Domestically, access has been restricted since the FDA placed several peptides, including Semax and Selank, on the Category 2 list, effectively blocking 503A compounding pharmacies from preparing them. That regulatory picture is shifting.

HHS Secretary Robert F. Kennedy Jr. has publicly stated his intention to move approximately 14 previously restricted peptides back into a category that would allow 503A compounding pharmacies to prepare them under physician prescription. If that change is finalized, Semax and Selank would become accessible through legitimate pharmaceutical channels for the first time in years.

I am already credentialed with 503A compounding pharmacies and prepared to prescribe when regulations allow. For a full breakdown of what the RFK announcement means and which peptides are affected, see my detailed analysis.

Semax: Mechanisms, Evidence, and Clinical Applications

BDNF Upregulation: The Core Mechanism

Semax’s most studied and clinically relevant mechanism is its effect on brain-derived neurotrophic factor (BDNF). BDNF is a protein that supports the survival of existing neurons, encourages the growth of new neurons and synapses, and plays a central role in neuroplasticity, the brain’s ability to reorganize and adapt.

Low BDNF levels are consistently associated with major depressive disorder, PTSD, anxiety disorders, and cognitive decline. Conversely, effective antidepressant treatments (including SSRIs, exercise, and ketamine) all appear to increase BDNF as part of their therapeutic mechanism.

Research by Dolotov et al. (2006) demonstrated that Semax regulates BDNF and TrkB receptor expression in the rat hippocampus, the brain region most critical for memory consolidation and emotional regulation. Medvedeva et al. (2014) published a genome-wide transcriptional analysis in BMC Genomics showing that Semax affects expression of genes related to immune and vascular systems in rat brain focal ischemia models, with BDNF pathway activation being a prominent finding. Dolotov et al. (2006) showed that a single intranasal administration of Semax produced a rapid and sustained increase in BDNF mRNA in the rat hippocampus and frontal cortex.

From a psychiatric perspective, this matters because BDNF deficiency is now considered a core neurobiological feature of treatment-resistant depression. If a patient has failed multiple SSRIs, one hypothesis is that the SSRIs aren’t adequately addressing the neuroplasticity deficit. Semax offers a more direct route to BDNF upregulation.

Dopaminergic and Serotonergic Modulation

Beyond BDNF, Semax influences multiple neurotransmitter systems relevant to psychiatry. Eremin et al. (2004) published in Neurochemical Research that Semax modulates behavioral and neurochemical responses to chronic restraint stress in rats, demonstrating effects on both dopaminergic and serotonergic pathways. Specifically, Semax appears to enhance dopamine turnover in the striatum and modulate serotonin metabolism in the frontal cortex.

This dual-pathway activity is clinically relevant because many patients with depression experience anhedonia (inability to feel pleasure, a dopaminergic symptom) and anxiety (a serotonergic symptom) simultaneously. SSRIs primarily target serotonin. Semax’s influence on both systems may explain the broader symptom improvement some patients report. Semax and Selank’s effects on neurotrophic factors and neurotransmitter systems also have theoretical relevance to ADHD treatment and prefrontal cortex function.

Neuroprotection and Cognitive Enhancement

Semax has been most extensively studied in Russia for stroke and cerebrovascular disease. The neuroprotective mechanism involves anti-inflammatory effects, oxidative stress reduction, and preservation of the blood-brain barrier.

For cognitive enhancement specifically, animal studies demonstrate improved learning, memory consolidation, and spatial navigation. Human data from Russian clinical settings supports cognitive improvement in post-stroke patients and those with age-related cognitive decline. The cognitive effects are attributed to both BDNF-mediated neuroplasticity and direct modulation of attention networks through dopaminergic pathways.

What I tell patients about Semax: The BDNF mechanism is well-supported. The neuroprotective data is solid from stroke research. The cognitive enhancement data is moderate, primarily from Russian clinical studies. The depression and anxiety applications are theoretically grounded in known mechanisms but lack large Western randomized controlled trials. I present this honestly. The mechanism makes biological sense, and the preliminary data is encouraging, but I don’t overstate the evidence base.

Selank: Mechanisms, Evidence, and Clinical Applications

GABAergic Modulation Without Sedation

Selank’s primary psychiatric application is as an anxiolytic. Its mechanism involves modulation of GABAergic neurotransmission, the same system targeted by benzodiazepines (Xanax, Klonopin, Ativan). The critical difference is how it modulates that system.

Benzodiazepines are positive allosteric modulators of GABA-A receptors. They enhance the effect of GABA across the entire brain, which produces rapid anxiolysis but also sedation, cognitive impairment, muscle relaxation, and dependence. Selank appears to modulate GABAergic tone more selectively, reducing anxiety without the global suppression that makes benzodiazepines problematic for long-term use.

Zozulia et al. (2008) published a clinical study in the Russian journal Zhurnal Nevrologii i Psikhiatrii evaluating Selank in patients with generalized anxiety disorder and neurasthenia (roughly equivalent to depression). The study found anxiolytic efficacy comparable to benzodiazepines without sedation, cognitive impairment, or dependence. Filatova et al. (2017) confirmed that clinical studies demonstrated Selank’s anxiolytic effect was comparable to classical benzodiazepine drugs.

Serotonin System Effects

In addition to GABA modulation, Selank influences serotonin metabolism. Volkova et al. (2016) found that Selank has nootropic activity that positively influences memory formation and learning processes, alongside its anxiolytic properties. The peptide also affects enkephalin degradation, as noted by Dr. William Seeds (2020) in The Peptide Protocols: Selank decreases the rate at which enkephalins (endogenous opioid peptides involved in pain and anxiety regulation) are degraded, which contributes to its anxiolytic effect through a mechanism entirely distinct from both benzodiazepines and SSRIs.

This multi-pathway anxiolytic mechanism, affecting GABA, serotonin, and enkephalin systems simultaneously, may explain why some patients experience broader anxiety relief with Selank than with single-mechanism medications.

Immunomodulatory Effects

Selank is derived from tuftsin, which is an immunomodulatory peptide. Research demonstrates that Selank retains significant immune-modulating properties, including regulation of inflammatory cytokines. This is psychiatrically relevant because neuroinflammation is increasingly recognized as a driver of treatment-resistant depression and anxiety. Patients with elevated inflammatory markers (IL-6, CRP, TNF-alpha) tend to respond poorly to standard antidepressants. Selank’s dual anxiolytic and anti-inflammatory profile makes it theoretically attractive for this subpopulation.

Cognitive Enhancement Alongside Anxiolysis

Perhaps Selank’s most remarkable clinical feature is that it improves cognitive function while reducing anxiety. In Russian clinical trials, patients showed approximately 70% reduction in anxiety scores without cognitive impairment. Selank actually enhanced cognitive performance during anxiety reduction, a profile that is essentially impossible to achieve with benzodiazepines (which reliably impair cognition) and difficult to achieve with SSRIs (which can cause cognitive dulling in some patients).

What I tell patients about Selank: The anxiolytic data is the strongest evidence we have. The comparison to benzodiazepines is clinically meaningful, especially for patients who need anxiety relief but can’t risk sedation, dependence, or cognitive impairment. The immunomodulatory and nootropic effects are supported by multiple studies but from smaller sample sizes than Western pharmaceutical standards. I use it most confidently in patients with anxiety who have failed or can’t tolerate SSRIs, and in patients with a history of benzodiazepine problems who still need anxiolytic support.

The Semax and Selank Combination: Complementary Mechanisms

In clinical settings, Semax and Selank are frequently combined because they target different but complementary aspects of psychiatric dysfunction.

Selank addresses the overactive systems: excessive amygdala reactivity, GABAergic deficit, serotonin dysregulation, and the hyperarousal state that characterizes anxiety and PTSD.

Semax addresses the underperforming systems: BDNF deficiency, impaired neuroplasticity, reduced dopaminergic drive (anhedonia, low motivation), and cognitive decline associated with chronic stress.

A patient with treatment-resistant depression and comorbid anxiety often has both problems simultaneously. Their stress response is overactive and their neuroplasticity is impaired. Treating only one side leaves the other untouched. The combination addresses both poles of the dysfunction.

Both Semax and Selank are typically administered via nasal spray, which provides rapid absorption through the nasal mucosa and direct access to the central nervous system. Protocols commonly involve cycling (10-14 days on, 10 days off) to prevent receptor downregulation. Selank is typically dosed at 100-300 mcg one to three times daily. Semax ranges from 200-600 mcg per day. Exact protocols are individualized based on clinical response.

Poor sleep can also predispose somebody to anxiety and depression.

Selank vs Semax: Which One, and When

These two get sold as a pair and are often used together. They do different jobs, and selank has the better evidence.

Selank is the anxiolytic, and it holds the only real human data of the two. A clinical study in 62 patients with generalized anxiety disorder and neurasthenia found an anxiolytic effect comparable to medazepam, a benzodiazepine, alongside antiasthenic and psychostimulant effects (PMID 18454096).

At 62 patients the study is small by Western standards. It’s still a controlled human comparison against an active drug, which is more than most peptides on the market can show.

Semax is the neurotrophic and cognitive agent. A single dose at 50 mcg/kg raised BDNF protein by a maximum of 1.4-fold, phosphorylated trkB 1.6-fold, and BDNF mRNA 3-fold in rat hippocampus (PMID 16996037).

The mechanism is well characterized. It’s characterized in rats.

Here’s the split I’d work from if these become prescribable. I’d reach for selank when anxiety is the target and the patient needs relief without sedation or dependence risk. I’d reach for semax when the complaint is cognitive or post-stroke, or when impaired neuroplasticity is the working hypothesis.

That second case comes with a caveat I’d state out loud to the patient. The human evidence for semax in psychiatric use is thin.

Neither is available by prescription in the United States today. An FDA advisory committee recommended adding semax to the 503A compounding list in July 2026, for cerebral ischemia, migraine, and trigeminal neuralgia. FDA still has to accept that recommendation and finish rulemaking.

Selank was not part of that vote.

How Long Semax and Selank Take to Work

I can’t give you a time-to-effect figure from a trial, because no study has measured onset for either peptide.

The record does contain a few relevant numbers. In a study of 60 patients, selank’s anxiolytic effect persisted for about a week after dosing stopped, which tells you something about duration and nothing about how fast it arrived (PMID 25176261).

In 70 patients, selank added to phenazepam improved depression scores earlier than phenazepam alone, though the report doesn’t state the interval (PMID 26356395). Human semax protocols in the stroke literature run as two 10-day courses at 6,000 mcg a day (PMID 29798983). Nobody measured when the benefit appeared.

The figures quoted around the internet, anxiolysis within a few days and cognitive effects over one to two weeks, come from uncontrolled use and patient report. Treat them as a hypothesis about what might happen. Any real onset figure would need a study that measures it, and that study doesn’t exist yet.

If you’ve already started one of these on your own, tell whoever manages your medications. Three days is too short a window to separate a drug effect from placebo without a control group, so write down what changed and how you measured it. Sleep latency in minutes, or a scored attention task, beats a general sense of improvement.

Why a Psychiatrist Evaluates These Peptides Differently

Here’s the gap that the mechanism-focused content online misses entirely.

Patients start taking peptides, they may even feel better. But nobody asked the questions that change the treatment plan:

Is your anxiety actually generalized anxiety disorder, or is it undiagnosed ADHD? Is your brain fog from poor sleep architecture, subclinical hypothyroidism, low testosterone, or early cognitive decline? Are you on medications that interact with GABAergic or serotonergic pathways? Do you have a trauma history that requires psychotherapy before any pharmacological intervention?

A peptide without a psychiatric evaluation is a mechanism searching for a target. In my practice, I identify the target first: full clinical picture, labs, differential diagnosis. If peptides become legally available and are appropriate, they’d become part of a plan. They’re never the starting point.

That evaluation is the same one I run for anyone whose depression hasn’t lifted. My page on depression treatment in North Carolina walks through what it checks and what it costs.

This is what psychiatric oversight adds to peptide therapy. To better understand how peptides and SSRIs can complement each other, see my article on this.

PTSD: Where Peptide Mechanisms Meet Trauma Neurobiology

PTSD is where I see the most interest and where the neurobiological rationale for Semax and Selank is strongest.

The neurobiology of PTSD involves hyperactivation of the amygdala (driving fear responses and hyperarousal), impaired prefrontal cortex regulation (reducing the ability to modulate emotional reactions), and reduced hippocampal volume associated with low BDNF (affecting memory processing and the ability to contextualize traumatic memories as past events rather than ongoing threats).

Semax’s BDNF-promoting effects directly address the hippocampal neuroplasticity deficit. Selank’s anxiolytic properties address the hyperarousal and amygdala overactivity. Together, they target multiple components of the PTSD neurobiological profile simultaneously.

But PTSD is not a peptide deficiency. It’s a condition rooted in traumatic experience, and the most effective treatments involve processing that experience through evidence-based psychotherapy (CPT, prolonged exposure, EMDR) alongside pharmacological support. Peptides can support the neurobiological environment for recovery. They cannot replace the therapeutic work. If peptides become legally available, I’ll use them for PTSD only alongside therapy.

Semax and Selank Side Effects

Neither peptide has been through a controlled safety trial, so there’s no adverse-event table to hand you.

The strongest human safety statement in the indexed literature is a 2005 Russian report that calls semax well tolerated and describes a “minor percent of side-effects” (PMID 15792140). The published abstract gives no symptom list, no rates, and no comparison group.

Nasal irritation, headache, and transient dizziness circulate across vendor pages and peptide aggregators as though a trial produced them. I went looking for the primary source and couldn’t find those three anywhere in the indexed record.

FDA’s 2026 review is more useful, because the agency looked for safety data specifically and reported what it couldn’t locate (FDA briefing document of May 11, 2026). It found no pharmacokinetic study in humans following semax exposure by any route. No abuse-potential study of either peptide exists.

Two animal findings in that file matter clinically. Semax reduced platelet aggregation by about 35% in rats given 1 mg/kg intranasally, according to the data FDA summarizes (FDA briefing document of May 11, 2026). That matters if you take an anticoagulant, and it matters if you take an SSRI, which already carries a bleeding signal of its own.

Nobody has studied that combination in people, which is one of the questions I’d want answered before writing it alongside an antidepressant. I’ve laid out how I think about peptides and psychiatric medications together in the guide to peptides with psychiatric medications.

Semax also potentiated amphetamine-induced dopamine release in the striatum (PMID 16362768). FDA read that as abuse liability. In a practice that prescribes stimulants for adult ADHD, I read it as an interaction question too.

The other side of the ledger deserves stating. Russia has used semax clinically for 30 years, and I’m not aware of a safety scandal attached to it in that time. Thirty years of clinical use is weaker evidence than one controlled trial, and it’s still an observation I’d rather have than silence.

The human safety profile of these two peptides is unknown. The studies that would let anyone call them safe haven’t been done.

Safety, Sourcing, and the Regulatory Reality

Neither Semax nor Selank is FDA-approved, and neither can be legally compounded by a 503A pharmacy today. The published Russian literature calls semax well tolerated and reports a “minor percent of side-effects” without publishing a symptom list or rates (PMID 15792140). What that literature does not contain is a toxicology package, human pharmacokinetic data by any route, or an abuse-potential study. FDA’s own briefing document states the agency was unable to find pharmacokinetic studies in humans following exposure to semax by any route of administration. A thin adverse-event record is not the same thing as a clean safety record, and here it reflects how little has been studied and reported.

No dependence or withdrawal syndrome has been described in the published literature. That is not the same as a finding of low abuse potential, because no abuse-potential study of either peptide exists. FDA specifically flagged that semax potentiated amphetamine-induced dopamine release in the striatum in mice, which matters in a practice that prescribes stimulants.

The sourcing problem is separate and larger. A peptide from a “research chemical” website is not the product a licensed 503A pharmacy compounds under physician prescription, because research chemicals may be contaminated, underdosed, mislabeled, or degraded, and you have no way to verify purity. A 503A compounded product is prepared under USP 797 standards with batch testing and quality controls.

I am credentialed with 503A compounding pharmacies and only prescribe peptides sourced through legitimate pharmaceutical channels. Semax and Selank are not currently among them, because neither is eligible for 503A compounding. Both would be candidates for my peptide therapy program in North Carolina if FDA completes rulemaking and makes them eligible. For what that vote does and doesn’t change, see my guide to the 2026 FDA peptide decision, and for how semax graded against the other peptides on the docket, the FDA peptide vote analysis.

How Peptide Therapy Would Work at Baghel Psychiatry

If FDA makes them eligible, I’d add peptides in these three steps.

Step 1: Comprehensive psychiatric evaluation (45-60 minutes). We establish diagnoses, review history, order labs if needed, and identify what’s actually driving your symptoms.

Step 2: Treatment plan. If peptide therapy is appropriate, I’d add it alongside other interventions: psychotherapy referral, lifestyle modifications, conventional medications when indicated, and hormone optimization if labs warrant it.

Step 3: Monitoring. We track symptom response, adjust protocols, and coordinate with other providers. Peptide therapy requires the same clinical oversight as any other pharmacological intervention.

The $250/month plan covers up to four visits for psychiatry, TRT, and medical weight loss. If peptide therapy becomes legally available, the plan will include it. Monthly plans cover Dr. Baghel’s clinical services (evaluation, monitoring, medication management, ongoing care). Labs and medications are separate costs paid by the patient.

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Frequently Asked Questions

Are Semax and Selank FDA-approved?

No. Neither Semax nor Selank is FDA-approved for any indication in the United States, and neither is currently eligible for compounding by a 503A pharmacy. Both have been used clinically in Russia for years, though FDA’s review notes it could not verify a specific Russian approval year or indication. An FDA advisory committee recommended adding semax to the 503A bulks list in July 2026, and FDA still has to accept that recommendation and complete rulemaking before any pharmacy can compound it.

Can Semax or Selank replace my SSRI?

Potentially, either as direct replacement or as adjunctive (in addition to) treatment. SSRIs have decades of large-scale clinical trial data. Semax and Selank have promising but more limited evidence, primarily from Russian research groups. In some patients, peptides may be part of a strategy to reduce reliance on conventional medications over time. That decision is made collaboratively with careful monitoring. I never recommend abruptly stopping an SSRI to try peptides. Interestingly, Semax and SSRIs may work synergistically: SSRIs increase serotonin availability while Semax upregulates BDNF, and one of the downstream effects of successful SSRI treatment is also BDNF increase. The combination may address both mechanisms simultaneously.

How quickly do Semax and Selank work?

No study has measured onset for either peptide. The figures in circulation, anxiolysis within a few days and cognitive effects over one to two weeks, come from uncontrolled use and patient report. What the record does show is that selank’s anxiolytic effect persisted for about a week after dosing stopped in a study of 60 patients (PMID 25176261).

Is it safe to use Semax and Selank together?

The combination is commonly used, and the published safety data is limited. It has never included a controlled trial. The Russian literature describes semax as well tolerated without publishing a symptom list or rates (PMID 15792140), and the commonly repeated list of nasal irritation, headache and dizziness has no primary source I can find. No dependence or withdrawal syndrome has been described, though no abuse-potential study of either peptide exists, and FDA flagged that semax potentiated amphetamine-induced dopamine release in the striatum in mice. They work through complementary mechanisms (Semax on BDNF and dopamine, Selank on GABA, serotonin, and enkephalins) with minimal overlap that would create interaction risk.

Can I buy Semax or Selank online without a prescription?

You can find peptides marketed as “research chemicals” online. I strongly advise against using them. These products are unregulated, unverified for purity, and may contain contaminants, incorrect dosages, or degraded peptide. The only responsible way to access these peptides is through a licensed physician who sources from 503A compounding pharmacies with USP 797 quality controls and batch testing.

Do you prescribe Semax and Selank for PTSD?

I don’t prescribe them yet, because neither is eligible for compounding today. If they become legally available, I’d consider them only as an add-on for PTSD. PTSD requires evidence-based psychotherapy (CPT, prolonged exposure, or EMDR) as the primary treatment. The neurobiological rationale for Semax in PTSD is strong: PTSD involves reduced hippocampal BDNF, and Semax directly upregulates BDNF. Selank addresses hyperarousal symptoms through GABA modulation. Together they target multiple components of PTSD neurobiology. But the peptides support recovery. They don’t process trauma.

Who is a good candidate for Semax and Selank?

Adults with anxiety, depression, cognitive complaints, or PTSD who have either not responded adequately to conventional treatments, cannot tolerate conventional medications (particularly SSRI side effects like sexual dysfunction or emotional blunting), or want to explore integrative options alongside their existing treatment plan. A comprehensive psychiatric evaluation is required before prescribing. Peptide therapy is not appropriate for everyone, and I will tell you directly if I don’t think it’s the right fit for your situation.

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Disclaimer: This article is for educational purposes only and is not medical advice. Semax and Selank are not FDA-approved medications in the United States. Peptide therapy availability depends on current compounding pharmacy regulations. All treatment decisions require a comprehensive evaluation with a licensed provider. Do not start or stop any medication without consulting a clinician who knows your medical history.

References: Dolotov OV et al., Brain Research (2006), PMID: 16996037. Medvedeva EV et al., BMC Genomics (2014), PMC3987924. Eremin KO et al., Neurochemical Research (2005), PMID: 16362768. Zozulia AA et al., Zhurnal Nevrologii i Psikhiatrii (2008), PMID: 18454096. Myasoedov NF et al., Neurochemical Journal (2007). Filatova E et al., Frontiers in Pharmacology (2017), PMID: 28293190. Volkova A et al., Frontiers in Pharmacology (2016), PMID: 26924987. Seeds WA, The Peptide Protocols (2020).