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Peptides for PTSD & Trauma (Emerging Research)

Post-traumatic stress disorder affects roughly [6% of American adults](https://www.ptsd.va.gov/professional/treat/essentials/epidemiology.asp) at some point in their lives, and among combat veterans, that number climbs to 15-29% depending on the era of service.

Post-traumatic stress disorder affects roughly 6% of American adults at some point in their lives, and among combat veterans, that number climbs to 15-29% depending on the era of service. The two FDA-approved medications for PTSD --- sertraline (Zoloft) and paroxetine (Paxil) --- produce full remission in only 20-30% of patients. Response rates hover around 50-60%, meaning nearly half of people who try these drugs get little meaningful relief.

That gap between what exists and what's needed has pushed researchers toward a different class of molecules: peptides. From neuropeptides already circulating in your brain to synthetic compounds designed in the lab, multiple peptide-based approaches are now in various stages of research for trauma-related conditions.

This guide covers what the science actually says --- what's promising, what's preliminary, and what remains unproven.

Table of Contents

Why Current PTSD Treatments Fall Short {#why-current-ptsd-treatments-fall-short}

The pharmacological toolkit for PTSD is thin. Sertraline and paroxetine --- both selective serotonin reuptake inhibitors (SSRIs) --- remain the only FDA-approved medications, along with venlafaxine (an SNRI) as an off-label first-line option. These drugs work by increasing serotonin availability in the brain, but PTSD involves far more than serotonin.

Here's the problem: SSRIs were developed for depression and anxiety, not specifically for the neurobiological changes that trauma produces. Their efficacy in PTSD is modest at best [1]. In clinical trials, response rates range from 50-62%, but remission --- actually getting rid of the disorder --- happens in only 20-30% of patients. The re-experiencing symptom cluster (flashbacks, intrusive memories) shows the least improvement of all PTSD symptom domains [2].

For veterans, outcomes are even worse. Combat-related PTSD is harder to treat than civilian PTSD, with lower response rates and higher dropout from treatment. About 30% of patients quit SSRIs before finishing a trial course, often due to side effects like sexual dysfunction, weight gain, and emotional blunting [3].

Gold-standard psychotherapies --- Prolonged Exposure (PE), Cognitive Processing Therapy (CPT), and EMDR --- work better than medication for many people, but roughly one-third of patients drop out of these treatments too. And some people don't respond to either pills or therapy.

The field needs new approaches that target the specific biology of trauma. That's where peptides enter the picture.

How Trauma Changes Brain Chemistry {#how-trauma-changes-brain-chemistry}

To understand why peptides might help, you need to understand what PTSD does to the brain.

When you experience a life-threatening event, your brain activates a cascade of stress responses. The hypothalamic-pituitary-adrenal (HPA) axis floods your body with cortisol. Your amygdala --- the brain's threat detector --- goes into overdrive. Norepinephrine surges. This is all normal and adaptive in the moment.

In PTSD, these systems don't properly reset. The result is a brain stuck in threat mode:

  • Overactive amygdala: The fear center fires too easily, triggering fight-or-flight responses to non-threatening stimuli (a car backfiring, a crowded room).
  • Underactive prefrontal cortex: The brain region responsible for rational thought and emotional regulation can't properly suppress the amygdala's alarm signals.
  • Disrupted hippocampus: The memory center --- responsible for contextualizing experiences as past or present --- shrinks and malfunctions, which is why traumatic memories feel like they're happening right now.
  • Dysregulated neuropeptide systems: Levels of stress-buffering neuropeptides like Neuropeptide Y drop, while stress-activating peptides like corticotropin-releasing factor (CRF) remain elevated [4].

A 2023 study from the University of Wisconsin mapped over 600 neuropeptides involved in the trauma stress response --- many from peptide families already targeted by existing drugs for other conditions. This discovery suggests that peptide-based interventions could open entirely new treatment pathways.

Neuropeptide Y: The Resilience Molecule {#neuropeptide-y-the-resilience-molecule}

Neuropeptide Y (NPY) is a 36-amino-acid peptide found throughout the brain, particularly concentrated in the amygdala, hippocampus, and prefrontal cortex --- the exact regions disrupted in PTSD. It's one of the most abundant neuropeptides in the human brain, and mounting evidence points to it as a key factor in stress resilience.

The NPY-PTSD Connection

The relationship between NPY and PTSD is well-documented:

  • Studies of Special Forces soldiers --- among the most stress-resilient people on earth --- found they have significantly higher baseline NPY levels than regular military personnel [5].
  • People with PTSD consistently show lower NPY levels in both blood plasma and cerebrospinal fluid compared to trauma-exposed individuals who didn't develop PTSD.
  • NPY levels predict recovery: higher NPY after trauma exposure is associated with fewer PTSD symptoms over time.

In animal models, supplementing NPY after traumatic stress exposure prevents the development of PTSD-like behaviors, including anxiety, hyperarousal, and fear conditioning [6].

Clinical Trial Results

A randomized dose-ranging study (NCT01533519) at Mount Sinai tested intranasal NPY in PTSD patients. The results showed that:

  • Single doses up to 9.6 mg were well tolerated with no serious adverse effects.
  • Higher doses produced greater anxiety reduction on the Beck Anxiety Inventory (P = 0.038).
  • The intranasal route appears to deliver NPY directly to the central nervous system without significant peripheral side effects [7].

Intranasal delivery is important because systemic NPY can cause unwanted effects on blood pressure, inflammation, and fat metabolism. Going through the nose bypasses those problems.

Where It Stands

NPY is arguably the most biologically validated peptide target for PTSD, but clinical development has been slow. The existing trial was small and exploratory. Larger, definitive trials are needed before NPY could become a treatment option. One major challenge: NPY is rapidly degraded in the body, making delivery and dosing difficult [8].

Oxytocin: Rewiring Fear Memories {#oxytocin-rewiring-fear-memories}

Oxytocin is best known as the "bonding hormone," but its role in PTSD research goes far beyond social attachment. Oxytocin appears to modulate fear memory processing --- the core dysfunction in PTSD.

How Oxytocin Relates to Trauma

People with PTSD tend to have lower circulating oxytocin levels than trauma-exposed controls without PTSD. This deficit may contribute to several hallmark symptoms: social withdrawal, difficulty trusting others, and impaired fear extinction (the process by which your brain learns that a previously threatening stimulus is now safe) [9].

In animal models, oxytocin administered after trauma exposure rescues both behavioral and neurological changes associated with PTSD. A 2020 study in Translational Psychiatry found that oxytocin-enhanced emotional processing durably reversed trauma-induced behavioral deficits and brain structural changes in rats.

Active Clinical Trials

Multiple randomized controlled trials are currently testing intranasal oxytocin for PTSD:

Enhancing Prolonged Exposure Therapy (UCSF/VA, NCT04228289): This is the first adequately powered trial examining intranasal oxytocin combined with PE therapy in veterans with PTSD. Participants self-administer 40 IU of oxytocin (or placebo) 30 minutes before each weekly PE session. The rationale: oxytocin may improve the fear extinction learning that PE relies on, while also reducing dropout rates [10].

Prevention After Acute Trauma: An RCT of 107 recently trauma-exposed individuals found that an eight-day course of intranasal oxytocin didn't reduce PTSD symptoms overall --- but it did significantly reduce symptoms in people with high acute stress levels, suggesting it may work as a targeted early intervention [11].

Couples Therapy Augmentation (UCSD, NCT06194851): Veterans receive 40 IU of intranasal oxytocin before each of 8 cognitive-behavioral couples therapy sessions. This trial recognizes that PTSD damages relationships, and that relationship repair can help treat PTSD.

Where It Stands

Oxytocin is further along in clinical testing than most peptide candidates for PTSD. The evidence suggests it works best as an add-on to psychotherapy rather than a standalone treatment --- boosting the brain's capacity for fear extinction during therapy sessions. Results from the large UCSF/VA trial should provide clearer answers about efficacy.

BPC-157: Neuroprotection After Brain Trauma {#bpc-157-neuroprotection-after-brain-trauma}

BPC-157 (Body Protection Compound-157) is a 15-amino-acid peptide derived from human gastric juice. It's been extensively studied for tissue healing, but a growing body of preclinical research suggests neuroprotective properties that could be relevant to trauma.

What the Brain Research Shows

BPC-157 has not been studied directly for PTSD. However, its effects on brain injury and neurotransmitter systems are worth examining:

Traumatic brain injury (TBI): In mice with induced TBI, BPC-157 significantly reduced brain damage severity --- less hemorrhage, less brain swelling, less tissue destruction, and lower mortality [12]. Given that TBI and PTSD frequently co-occur (especially in military populations), this overlap is relevant.

Hippocampal protection: BPC-157 protected against hippocampal ischemia-reperfusion injury in rats, preserving memory and coordination function. The hippocampus is one of the brain structures most affected by chronic PTSD [13].

Neurotransmitter modulation: BPC-157 interacts with both serotonergic and dopaminergic systems --- the same pathways targeted by SSRIs and other psychiatric medications. It has shown benefits in animal models of depression, anxiety, and behavioral disturbances caused by neurotransmitter system damage [14].

Antioxidant and anti-inflammatory effects: BPC-157 appears to reduce oxidative stress and neuroinflammation in the brain, both of which are elevated in PTSD [15].

Where It Stands

There's an important distinction to make: protecting neurons from physical damage (what BPC-157 does in TBI models) is not the same as treating the learned fear responses and emotional dysregulation of PTSD. These are related but different problems. Neuroinflammation, hippocampal damage, and neurotransmitter imbalance are all features of PTSD, and BPC-157 addresses all three in animal models --- but all current evidence is preclinical. No human trials exist for any neurological or psychiatric indication, and much more research is needed.

Selank: The Anxiolytic Peptide {#selank-the-anxiolytic-peptide}

Selank is a synthetic heptapeptide developed at the Institute of Molecular Genetics (Russian Academy of Sciences) as a modified version of the naturally occurring immunomodulatory peptide tuftsin. It's approved in Russia as an anxiolytic medication and has been studied for generalized anxiety disorder (GAD) --- a condition that shares substantial symptom overlap with PTSD.

Mechanism of Action

Selank's anti-anxiety effects appear to work through multiple pathways:

  • GABA modulation: Selank binds to GABA-A receptors and allosterically enhances their activity, similar to benzodiazepines but without the sedation, dependence, or cognitive impairment [16].
  • Serotonin and dopamine: Selank modulates both serotonergic and dopaminergic activity, which may explain its combined anxiolytic and motivational effects.
  • Enkephalin metabolism: Both Selank and Semax inhibit enzymes that degrade enkephalins (the body's natural painkillers and mood regulators).

Clinical Evidence

In a study of 62 patients with GAD and neurasthenia, Selank produced anxiolytic effects comparable to medazepam (a benzodiazepine), but with additional antiasthenic and psychostimulant effects that benzodiazepines don't provide [17]. Unlike benzodiazepines, Selank didn't cause sedation or dependence.

A separate study showed Selank enhanced the anxiolytic effects of diazepam in chronically stressed rats, suggesting potential as an adjunct therapy [18].

Relevance to PTSD

Selank has not been tested directly in PTSD clinical trials. However, its pharmacological profile --- GABA enhancement without sedation, serotonin/dopamine modulation, no dependence potential --- addresses several unmet needs in PTSD treatment. The hyperarousal and anxiety symptoms of PTSD are often treated with benzodiazepines despite guideline warnings against their use (benzodiazepines can actually worsen PTSD outcomes). A non-addictive alternative with anxiolytic properties would fill a real clinical gap.

Where It Stands

The evidence base for Selank is predominantly from Russian research institutions, with limited international replication. It is not FDA-approved and is not available as a prescribed medication in most countries outside Russia. International clinical trials would be needed to validate its therapeutic potential.

GLP-1 Receptor Agonists and Mental Health {#glp-1-receptor-agonists-and-mental-health}

This might seem like an unexpected entry in a PTSD article, but emerging data on semaglutide and other GLP-1 receptor agonists suggests these metabolic peptides may have neuropsychiatric effects beyond blood sugar and weight control.

What the Research Shows

A Mendelian randomization study published in BMC Psychiatry (2025) used genetic data to investigate causal relationships between GLP-1 receptor activation and psychiatric conditions. The analysis suggested GLP-1 receptor agonists may decrease the risk of several conditions including PTSD, anxiety disorders, bipolar disorder, and schizophrenia.

Anecdotal reports from patients taking semaglutide for weight loss describe significant mental health improvements. A mixed-methods analysis of social media posts found users reporting reduced anxiety, improved mood, and decreased compulsive behaviors --- with some describing the effect as "what people SAY antidepressants are supposed to feel like."

A propensity-score matched cohort study published in eClinicalMedicine found semaglutide was not associated with higher neuropsychiatric risk compared to other diabetes medications, with potential beneficial associations for cognitive function and nicotine dependence.

Important Caveats

The picture isn't uniformly positive. Other studies have flagged potential psychiatric risks:

  • A pharmacovigilance analysis found signals for depressed mood and suicidality with semaglutide, though these were not seen in randomized controlled trials [19].
  • The JAMA Internal Medicine post-hoc analysis of STEP trials assessed psychiatric safety in people without major psychopathology and did not find increased risk.

The mechanisms linking GLP-1 receptor agonists to mental health remain under investigation. Possible pathways include modulation of neuroinflammation, effects on brain glucose metabolism, and interactions with serotonergic and GABAergic signaling.

Where It Stands

No clinical trial has specifically tested a GLP-1 receptor agonist for PTSD. The evidence is genetic (Mendelian randomization), observational, and anecdotal. This is a hypothesis-generating area, not a treatment recommendation. But given the millions of people already taking these drugs, researchers will likely have answers relatively soon.

Other Peptides Under Investigation {#other-peptides-under-investigation}

Several additional peptide-based approaches are in earlier stages of research:

TAT-GRpep: Blocking Fear Memory Formation

Researchers at the Centre for Addiction and Mental Health (CAMH) in Toronto discovered that the protein complex between the glucocorticoid receptor (GR) and FKBP51 is elevated in PTSD patients. They created a peptide called TAT-GRpep that disrupts this complex.

In animal models, administering TAT-GRpep after a distressing event prevented both the consolidation and recall of fear memories [20]. If this translates to humans, it could form the basis of a post-trauma intervention that prevents PTSD from developing. CAMH has filed a patent, and further testing is underway.

CAQK: Protecting the Injured Brain

A four-amino-acid peptide called CAQK showed powerful brain-protective effects in animal models of traumatic brain injury (December 2025). Delivered intravenously, CAQK homes in on injured brain tissue, reducing inflammation and cell death. Researchers are preparing for early human trials. While designed for TBI rather than PTSD, the overlap between these conditions makes it relevant.

PACAP and CRF

Researchers at McLean Hospital are studying how pituitary adenylate cyclase-activating polypeptide (PACAP) interacts with corticotropin-releasing factor (CRF) to hard-wire traumatic memories. Understanding these neuropeptides could lead to interventions that prevent trauma memories from becoming pathologically persistent [21].

LCGA-17

The peptide LCGA-17 acts on voltage-gated calcium channels with putative synergy with GABA-A receptors. In rodent models of PTSD and chronic stress, it showed anxiolytic and antidepressant effects [22]. It remains in early preclinical stages.

PeptidePrimary MechanismResearch StageKey EvidencePTSD-Specific Data
Neuropeptide Y (NPY)Stress buffering, amygdala regulationPhase I clinical trial (intranasal)Anxiolytic effects at higher doses in humansYes --- direct PTSD trials
OxytocinFear extinction, social bondingPhase II/III clinical trialsBenefits as therapy adjunct; mixed as standaloneYes --- multiple active RCTs
BPC-157Neuroprotection, neurotransmitter modulationPreclinical onlyReduced TBI damage, hippocampal protection in rodentsNo --- indirect relevance
SelankGABA-A modulation, serotonin/dopamineApproved in Russia for GADComparable to benzodiazepines without sedationTheoretical only
GLP-1 RAs (Semaglutide)Neuroinflammation, brain metabolismObservational/genetic studiesMendelian randomization suggests lower PTSD riskNo direct trials
TAT-GRpepBlocks GR-FKBP51 fear memory complexPreclinicalPrevented fear memory consolidation in miceYes --- designed for PTSD prevention
CAQKTargets injured brain tissuePreclinical (moving to Phase I)Reduced TBI damage in mice and pigsNo --- TBI focus

Limitations and Safety Considerations {#limitations-and-safety-considerations}

Before you get too excited, some perspective is needed:

Most of this research is preclinical. Animal models of PTSD --- like predator odor exposure or inescapable shock in rodents --- capture some features of the human disorder but not all of it. Many promising animal findings don't translate to people.

No peptide is approved for PTSD treatment anywhere in the world. Not in the U.S., not in Europe, not anywhere. Sertraline and paroxetine remain the only FDA-approved medications, alongside psychotherapy.

Self-administration of research peptides carries real risks. Peptides sold by research chemical companies are not pharmaceutical-grade. Purity, dosing, stability, and sterility are all concerns. The potential for contamination, degradation, or misidentification is significant.

Peptide research for PTSD is underfunded. Compared to the billions invested in metabolic peptides like semaglutide and tirzepatide, psychiatric peptide research receives a fraction of the funding. This limits the pace of clinical translation.

PTSD is a complex disorder. No single molecule is likely to be a complete solution. Some practitioners have speculated about growth hormone secretagogues like CJC-1295 for PTSD-related sleep disruption and HPA axis dysfunction, but no clinical data supports this use. The most promising approaches --- like oxytocin-enhanced psychotherapy --- combine peptide pharmacology with behavioral treatment. If peptides become part of PTSD care, they'll most likely work alongside therapy, not replace it.

If you're dealing with PTSD, the most evidence-backed treatments available right now are trauma-focused psychotherapies (PE, CPT, EMDR) and FDA-approved medications. Talk to your healthcare provider about options that are currently available while keeping an eye on what the research pipeline may deliver.

Frequently Asked Questions {#frequently-asked-questions}

Are any peptides currently FDA-approved for PTSD?

No. As of early 2026, no peptide is FDA-approved for PTSD. The only approved medications are the SSRIs sertraline (Zoloft) and paroxetine (Paxil). All peptide research for PTSD is either preclinical or in early clinical trials.

What is the most promising peptide for PTSD based on current evidence?

Neuropeptide Y (NPY) and oxytocin have the strongest evidence bases. NPY has direct biological plausibility as a resilience factor and early positive clinical trial data. Oxytocin has multiple active Phase II/III trials testing it as a psychotherapy enhancer in veterans with PTSD.

Can BPC-157 help with PTSD?

There is no direct evidence that BPC-157 treats PTSD. BPC-157 has shown neuroprotective effects in animal models of traumatic brain injury and modulates serotonin and dopamine systems, which gives it theoretical relevance. But all data is preclinical, and no human PTSD studies exist. See our full BPC-157 guide for more detail.

Does semaglutide affect mental health?

The evidence is mixed. Genetic studies and some observational data suggest GLP-1 receptor agonists might lower the risk of certain psychiatric conditions including PTSD. However, pharmacovigilance databases have also flagged potential signals for depressive symptoms. No randomized controlled trial has specifically tested semaglutide for any psychiatric indication. See our semaglutide guide for more.

How does oxytocin work for PTSD?

Oxytocin appears to improve fear extinction --- the process by which your brain learns that previously threatening stimuli are now safe. In PTSD, fear extinction is impaired, which is why traumatic memories remain vivid and triggering. Intranasal oxytocin given before therapy sessions may help the brain "rewrite" fear associations more effectively during exposure-based treatments.

Is intranasal neuropeptide Y safe?

In the published dose-ranging clinical trial, intranasal NPY was well tolerated at doses up to 9.6 mg with no serious adverse effects. However, this was a small, single-dose study. Long-term safety data in PTSD populations doesn't exist yet.

What about peptides for anxiety and stress more broadly?

Several peptides show anxiolytic potential. Selank has been approved in Russia for generalized anxiety disorder. Semax shows cognitive and stress-modulating properties. DSIP is studied for sleep and stress regulation. For a broader overview, see our guide on best peptides for anxiety and stress.

The Bottom Line {#the-bottom-line}

PTSD treatment is overdue for new options. SSRIs help some people, but the remission rate of 20-30% leaves the majority still struggling. Peptide research offers multiple plausible paths forward --- from NPY's resilience-boosting properties to oxytocin's ability to enhance fear extinction therapy.

But "plausible" and "proven" are different things. Most of the peptide approaches discussed here are years from clinical availability, if they make it at all. The most advanced candidates (oxytocin, NPY) are in clinical trials with results expected in the coming years. Others (BPC-157, Selank, GLP-1 agonists for mental health) have suggestive but preliminary data.

What we know for certain: the biology of PTSD involves neuropeptide systems in fundamental ways. Over 600 neuropeptides participate in the brain's stress response. The question isn't whether peptides are relevant to PTSD --- it's which ones, at what doses, delivered how, and for which patients. Those are the questions that clinical trials are now working to answer.

References {#references}

  1. Clinician's Guide to Medications for PTSD. National Center for PTSD, U.S. Department of Veterans Affairs. https://www.ptsd.va.gov/professional/treat/txessentials/clinician_guide_meds.asp

  2. Stein DJ, et al. "Comparative Efficacy and Acceptability of Pharmaceutical Management for Adults With Post-Traumatic Stress Disorder." Frontiers in Pharmacology. 2020;11:559. https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2020.00559/full

  3. Stein DJ, et al. "Pharmacotherapy for Post-traumatic Stress Disorder in Combat Veterans." Psychiatric Clinics. 2009. https://pmc.ncbi.nlm.nih.gov/articles/PMC3278188/

  4. Sah R, Geracioti TD. "Neuropeptide Y and posttraumatic stress disorder." Molecular Psychiatry. 2013;18(6):646-55. https://pmc.ncbi.nlm.nih.gov/articles/PMC8375392/

  5. Morgan CA, et al. "Neuropeptide-Y, cortisol, and subjective distress in humans exposed to acute stress." Biological Psychiatry. 2000;47(10):902-909.

  6. Sabban EL, et al. "Single intranasal neuropeptide Y infusion attenuates development of PTSD-like symptoms to traumatic stress in rats." Neuropeptides. 2015;52:43-50. https://pubmed.ncbi.nlm.nih.gov/23376740/

  7. Sayed S, et al. "A Randomized Dose-Ranging Study of Neuropeptide Y in Patients with Posttraumatic Stress Disorder." International Journal of Neuropsychopharmacology. 2018;21(1):3-11. https://pmc.ncbi.nlm.nih.gov/articles/PMC5795352/

  8. Sabban EL, Serova LI. "Potential of neuropeptide Y for preventing or treating post-traumatic stress disorder." Neuropeptides. 2018;68:57-65. https://www.sciencedirect.com/science/article/am/pii/S0143417915001195

  9. Sippel LM, et al. "Oxytocin and Stress-related Disorders." Frontiers in Psychology. 2021. https://www.frontiersin.org/journals/psychology/articles/10.3389/fpsyg.2021.612338/full

  10. Tuerk PW, et al. "Enhancing Prolonged Exposure Therapy for PTSD among Veterans with Oxytocin: Design of a Multisite Randomized Controlled Trial." Contemporary Clinical Trials. 2020;96:106099. https://pmc.ncbi.nlm.nih.gov/articles/PMC7484278/

  11. van Zuiden M, et al. "Preventing PTSD with oxytocin." European Neuropsychopharmacology. 2017. https://pmc.ncbi.nlm.nih.gov/articles/PMC5400019/

  12. Tudor M, et al. "Traumatic brain injury in mice and pentadecapeptide BPC 157 effect." Regulatory Peptides. 2010;160(1-3):26-32. https://pubmed.ncbi.nlm.nih.gov/19931318/

  13. Vukojevic J, et al. "The effect of pentadecapeptide BPC 157 on hippocampal ischemia/reperfusion injuries in rats." Brain and Behavior. 2020;10(8):e01726. https://onlinelibrary.wiley.com/doi/full/10.1002/brb3.1726

  14. Sikiric P, et al. "Pentadecapeptide BPC 157 and the central nervous system." Neural Regeneration Research. 2022;17(3):482-487. https://pmc.ncbi.nlm.nih.gov/articles/PMC8504390/

  15. Sikiric P, et al. "Brain-gut Axis and Pentadecapeptide BPC 157: Theoretical and Practical Implications." Current Neuropharmacology. 2016;14(8):857-865. https://pmc.ncbi.nlm.nih.gov/articles/PMC5333585/

  16. Skrebitsky VG, et al. "Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission." Frontiers in Pharmacology. 2016;7:31. https://pmc.ncbi.nlm.nih.gov/articles/PMC4757669/

  17. Zozulya AA, et al. "Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia." Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova. 2008;108(4):38-48. https://pubmed.ncbi.nlm.nih.gov/18454096/

  18. Narkevich VB, et al. "Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats." Bulletin of Experimental Biology and Medicine. 2017;162(4):464-467. https://pmc.ncbi.nlm.nih.gov/articles/PMC5322660/

  19. Psychopharmacological adverse effects associated with GLP-1 RAs. Clinical Nutrition. 2025. https://www.sciencedirect.com/science/article/pii/S0261561425001657

  20. Study finds potential new treatment for preventing PTSD. Centre for Addiction and Mental Health (CAMH). https://www.camh.ca/en/camh-news-and-stories/study-finds-potential-new-treatment-for-preventing-ptsd

  21. Two Researchers Brought Together by One Goal: Identifying Treatment of Anxiety and PTSD. McLean Hospital. https://www.mcleanhospital.org/news/two-researchers-brought-together-one-goal-identifying-treatment-anxiety-and-ptsd

  22. Sviridov SI, et al. "Peptide LCGA-17 Attenuates Behavioral and Neurochemical Deficits in Rodent Models of PTSD and Depression." Pharmaceuticals. 2022;15(4):462. https://www.mdpi.com/1424-8247/15/4/462