PeptideJournal
Guides19 min read

Peptides for TBI & Concussion Recovery

Every year, roughly 214,000 Americans are hospitalized for traumatic brain injuries, and another 69,000 die from them [1]. Those numbers only capture the severe cases.

Every year, roughly 214,000 Americans are hospitalized for traumatic brain injuries, and another 69,000 die from them [1]. Those numbers only capture the severe cases. When you include concussions treated in urgent care clinics, doctor's offices, and the millions that go unreported entirely, estimates put annual TBI incidence at nearly 10 million in the United States alone [2].

And here is the uncomfortable truth about treating brain injuries: there are no FDA-approved drugs that stop the damage. Emergency care focuses on managing intracranial pressure, maintaining blood flow, and preventing secondary complications. Once the initial injury happens, clinicians have almost nothing to directly protect or regenerate the damaged brain tissue. Rehabilitation can help the brain rewire around damage, but the process is slow, incomplete, and highly variable between patients.

This gap has pushed researchers toward peptides -- small protein fragments that can cross the blood-brain barrier, reduce neuroinflammation, promote neuronal survival, and in some cases stimulate the growth of entirely new neural connections. None of these compounds are approved for TBI treatment yet, but the preclinical evidence for several of them is substantial, and a few have human data worth examining closely.

Table of Contents

What Happens to the Brain After TBI

Traumatic brain injury is not a single event. It unfolds in two phases, and the second phase is where most of the treatable damage occurs.

Primary injury -- torn axons, ruptured blood vessels, bruised tissue -- happens at the moment of impact and is largely irreversible by the time medical care begins.

Secondary injury is the cascade that follows over hours, days, and weeks, and is where most treatable damage occurs:

  • Neuroinflammation: Microglia and astrocytes flood the injury site with TNF-alpha, IL-1-beta, and IL-6, amplifying damage far beyond the original impact zone
  • Excitotoxicity: Excessive glutamate release overstimulates NMDA receptors, triggering calcium overload and cell death
  • Oxidative stress: Mitochondrial damage produces reactive oxygen species that attack cell membranes, proteins, and DNA
  • Blood-brain barrier breakdown: The protective barrier becomes leaky, allowing inflammatory molecules to enter brain tissue
  • Cerebral edema: Swelling increases intracranial pressure, compressing healthy tissue

Every peptide in this guide targets one or more of these secondary mechanisms.

Why Peptides for Brain Injury Recovery?

The brain presents unique drug development challenges. The blood-brain barrier blocks most large molecules. Neural tissue regenerates slowly. And the secondary injury cascade involves dozens of overlapping pathways, making single-target drugs less effective.

Peptides fit this problem for several reasons:

  • Blood-brain barrier penetration: Many small peptides cross the BBB, and some (like the CAQK tetrapeptide) accumulate preferentially in injured brain tissue
  • Multi-target activity: Peptides often modulate multiple pathways simultaneously -- anti-inflammatory, anti-apoptotic, pro-angiogenic -- matching the cascade's complexity
  • Neurotrophic factor stimulation: Several peptides upregulate BDNF, NGF, and other growth factors supporting neuronal survival
  • Low systemic toxicity: Natural origins and rapid metabolism generally produce fewer off-target effects

Most TBI peptide research is preclinical. But a few compounds have advanced to human studies with encouraging results.

The Top Peptides for TBI Research

BPC-157: Reducing Hemorrhage and Edema

BPC-157 is best known for musculoskeletal repair, but its neuroprotective properties in TBI models are striking. The foundational study, published by Tudor et al. in Regulatory Peptides (2010), used a falling-weight TBI model in mice and found that BPC-157 markedly reduced brain damage across multiple measures [3].

What the research shows:

Mice given BPC-157 (10 micrograms/kg or 10 nanograms/kg, injected intraperitoneally) after TBI had smaller brain lesions, less cell death, and lower levels of inflammatory markers compared to untreated controls. The hemorrhagic damage -- subarachnoid bleeding, intraventricular hemorrhage, and brain lacerations -- was less severe. Brain edema, which drives much of the secondary damage in TBI, was significantly reduced [3].

When given as a preventive treatment 30 minutes before injury, BPC-157 improved the ratio of conscious to unconscious animals across multiple impact forces. Even against the maximal force tested (0.159 N·s), the higher dose maintained a protective effect [3].

Beyond TBI specifically, BPC-157 has shown neuroprotective effects in spinal cord injury models (improving functional recovery and reducing cyst formation), peripheral nerve transection (accelerating regeneration), and various encephalopathy models [4].

How it works:

BPC-157's neuroprotection appears to operate through several overlapping mechanisms. It upregulates Egr1 and Vegfr2, promoting vascularization in injured tissue. It modulates the nitric oxide system in a pattern that is neuroprotective -- upregulating NOS-3 (endothelial, protective) and NOS-1 (neuronal) while suppressing NOS-2 (inducible, inflammatory). It also modulates serotonergic and dopaminergic neurotransmitter systems, which may explain its effects on behavioral recovery [4].

Evidence level: Animal studies only. No human TBI trials. But the preclinical data is consistent and the mechanisms are well-characterized.

TB-500 (Thymosin Beta-4): Dual Neuroprotection and Neurorestoration

TB-500 is the synthetic version of thymosin beta-4 (Tbeta4), a naturally occurring protein with an unusually broad set of biological activities -- cell migration, anti-inflammation, anti-apoptosis, angiogenesis, and stem cell differentiation. For TBI, it offers something most compounds cannot: both neuroprotection (limiting acute damage) and neurorestoration (promoting long-term recovery).

What the research shows:

A series of studies from Xiong, Mahmood, Chopp and colleagues tested Tbeta4 in rat TBI models with different treatment timing:

When administered 6 hours after injury, Tbeta4 reduced cortical lesion volume, preserved hippocampal neurons, and improved functional recovery on motor and cognitive tests. This early treatment window is clinically relevant because most TBI patients reach medical care within this timeframe [5].

When treatment was delayed to 24 hours post-injury, Tbeta4 no longer reduced lesion size but still significantly improved functional outcomes. The mechanism shifted: rather than preventing acute damage, delayed treatment promoted angiogenesis, neurogenesis, and oligodendrogenesis (new myelin-producing cells) in the surviving tissue [6].

Tbeta4 treatment also changed the brain's microRNA profile after severe TBI, significantly increasing miR-200a-3p and miR-200b-3p -- both associated with neuroprotective signaling [7].

How it works:

Tbeta4 is the major G-actin-sequestering molecule in cells, which gives it fundamental control over cell shape, migration, and division. In the brain, it promotes new blood vessel growth into damaged areas, stimulates neural stem cell proliferation and differentiation, supports oligodendrocyte generation for remyelination, and reduces neuronal apoptosis. The distinction between early (neuroprotective) and late (neurorestorative) effects makes it potentially useful across the full TBI recovery timeline [5, 6].

Evidence level: Multiple rat TBI studies with consistent results. No human TBI trials published, though Tbeta4 has been tested in humans for other indications (corneal and cardiac repair) with a good safety profile.

Cerebrolysin: The Neuropeptide Preparation With Clinical Trials

Cerebrolysin stands apart from the other peptides in this guide because it has actual randomized controlled trial data in TBI patients. It is a preparation of low-molecular-weight neuropeptides and free amino acids derived from porcine brain proteins, and it is used clinically in over 50 countries -- though not approved in the United States.

What the research shows:

The CAPTAIN trial series includes two phase IIIb/IV randomized, double-blind, placebo-controlled trials in moderate-to-severe TBI. A prospective meta-analysis of 185 patients found that Cerebrolysin (50 mL/day for 10 days, followed by two 10 mL/day cycles) added to standard care improved overall outcomes compared to placebo [8].

A separate double-blind, placebo-controlled trial in mild TBI found that Cerebrolysin-treated patients had significantly greater cognitive improvement at 12 weeks. Drawing function improved by week 4, and both drawing and long-term memory were significantly better by week 12. The cognitive assessment score difference was 21.0 points for Cerebrolysin versus 7.6 for placebo (p = 0.0461) [9].

A multi-center retrospective study found dose-dependent improvement: patients receiving either 20 mL/day or 30 mL/day of Cerebrolysin showed better Glasgow Outcome Scale and Modified Rankin Disability scores at 10 and 30 days post-TBI compared to standard care alone [10].

For severe TBI specifically, a study of 87 patients found that those receiving Cerebrolysin had stronger improvement in Glasgow Coma Scale and Glasgow Outcome Scale scores, along with shorter hospital stays [11].

How it works:

Cerebrolysin is not a single peptide but a standardized mixture of neuropeptides that collectively promote neuroplasticity, neurogenesis, and neuroprotection. Its composition mimics several endogenous neurotrophic factors. The multi-component nature may actually be an advantage for TBI, where the secondary injury cascade involves many simultaneous pathways [8].

Evidence level: The strongest human evidence of any compound in this guide. Multiple RCTs and meta-analyses. However, Cerebrolysin is not approved in the U.S., Canada, or Australia, and some reviewers have noted inconsistent results across studies.

Semax: BDNF Upregulation and Stroke Recovery

Semax is a synthetic heptapeptide analog of ACTH(4-10) that has been approved in Russia for ischemic stroke treatment. While stroke and TBI are different injuries, they share the same secondary damage pathways -- neuroinflammation, oxidative stress, excitotoxicity -- making Semax's stroke data relevant to TBI research.

What the research shows:

A single intranasal dose of Semax (50 micrograms/kg) increased BDNF protein levels 1.4-fold in the rat hippocampus, accompanied by a 1.6-fold increase in TrkB receptor activation and a 3-fold increase in BDNF mRNA [12]. This is significant because BDNF is one of the most important proteins for neuronal survival and synapse formation after brain injury.

In a clinical stroke rehabilitation study of 110 patients, Semax (6,000 mcg/day for 10-day courses) increased plasma BDNF levels that remained elevated throughout the study period. The Semax groups showed faster functional recovery and better motor performance outcomes, with the greatest benefit seen in patients who started rehabilitation early [13].

In cerebral ischemia models, Semax suppressed inflammatory gene expression while simultaneously activating genes related to neurotransmission -- essentially reversing the gene expression pattern caused by ischemia-reperfusion injury [14].

How it works:

Semax upregulates the transcription of BDNF, NGF, and their high-affinity receptors in multiple brain regions. It modulates GABA neurotransmission (producing anxiolytic effects comparable to benzodiazepines without dependence risk), inhibits enkephalin-degrading enzymes, and has anti-inflammatory properties through cytokine modulation. Its PGP (Pro-Gly-Pro) tripeptide fragment improves blood-brain barrier penetration [12, 13, 14].

Evidence level: Approved for stroke in Russia. Clinical data in stroke patients. No published human TBI trials, but mechanism overlap with TBI secondary injury is substantial.

Dihexa: The Synapse Builder

Dihexa is a synthetic derivative of angiotensin IV that was designed at Washington State University specifically to promote synaptogenesis -- the formation of new connections between neurons. For TBI recovery, where cognitive deficits often persist because neural circuits have been disrupted, a compound that rebuilds synaptic connections could change the recovery calculus.

What the research shows:

In APP/PS1 mice (an Alzheimer's model), oral Dihexa restored spatial learning and memory, increased neuronal cell counts, and boosted synaptophysin (SYP) protein expression -- a marker of synapse density. It also decreased microglial and astrocyte activation, reduced pro-inflammatory cytokines IL-1-beta and TNF-alpha, and increased the anti-inflammatory cytokine IL-10 [15].

Across nine studies testing angiotensin IV and its analogs (including Dihexa), eight found improved performance on spatial working memory and passive avoidance tasks. Orally delivered Dihexa reversed cognitive deficits induced by scopolamine, demonstrating that it crosses the blood-brain barrier and reaches relevant brain regions [16].

How it works:

Dihexa binds with high affinity to hepatocyte growth factor (HGF), augmenting HGF-dependent activation of the c-Met receptor. The HGF/c-Met system drives synaptogenesis, neuronal survival, and neurite outgrowth. Dihexa also activates the PI3K/AKT signaling pathway, which is central to neuronal survival and anti-apoptosis. Binding sites for angiotensin IV are concentrated in the hippocampus, neocortex, and basal nucleus of Meynert -- brain regions critical for learning, memory, and executive function [15, 16].

Evidence level: Preclinical only. No human trials for TBI or any other indication. Safety concerns exist regarding the HGF/c-Met pathway's involvement in cancer biology. Long-term data is absent.

MOTS-c and Humanin: Mitochondrial-Derived Neuroprotectors

Mitochondrial damage is one of the earliest and most destructive events after TBI. Two peptides encoded directly in mitochondrial DNA -- MOTS-c and Humanin -- target this problem from different angles.

MOTS-c can cross the blood-brain barrier and activate the Nrf2/Keap1 antioxidant pathway while inhibiting NF-kB inflammation and promoting mitochondrial biogenesis through AMPK signaling [17, 18]. A 2024 TBI mouse study found MOTS-c improved memory, learning, and motor function after injury. It simultaneously reduces oxidative damage to injured neurons and builds new mitochondria to restore their energy supply.

Humanin was discovered in 2001 from surviving neurons in Alzheimer's disease brains. In intracerebral hemorrhage models, it improved recovery by promoting mitochondrial transfer from astrocytes to microglia, shifting microglia from a destructive inflammatory state to a reparative phagocytic phenotype [19]. Humanin activates three major survival pathways simultaneously through the GP130/IL6ST receptor: PI3K/AKT, ERK1/2, and STAT3 [20]. Novel analogs are being developed for improved clinical potential [21].

Evidence level: MOTS-c has preclinical TBI data (2024). Humanin has preclinical hemorrhagic brain injury data. Neither has human TBI trials.

Selank: Anxiety Reduction and Cognitive Recovery

Selank is a synthetic analog of the immunomodulatory peptide tuftsin, developed primarily as an anxiolytic. Its effects on BDNF expression and cognitive function make it relevant to the anxiety, depression, and cognitive impairment that commonly follow TBI.

What the research shows:

In rats exposed to chronic ethanol (a model of brain injury), Selank (0.3 mg/kg/day for 7 days) prevented memory and attention disturbances while modulating BDNF levels in the hippocampus and frontal cortex [22]. In clinical studies, Selank produced anxiolytic effects comparable to benzodiazepines without tolerance, dependence, or cognitive impairment [23] -- an important distinction because benzodiazepines are generally avoided after brain injury.

How it works:

Selank's PGP tail improves blood-brain barrier penetration. In the brain, it upregulates BDNF and NGF, modulates GABA-A receptor function, normalizes serotonin and dopamine levels, and suppresses pro-inflammatory cytokines. This multi-target profile addresses several common post-TBI symptoms simultaneously [22, 23].

Evidence level: Clinical anxiety data (Russian approval). Animal data for cognitive protection. No human TBI trials.

CJC-1295 and Ipamorelin: Growth Hormone Support for Brain Repair

Growth hormone (GH) deficiency affects an estimated 20-40% of TBI survivors. GH and its downstream mediator IGF-1 play significant roles in neurogenesis, synaptogenesis, and cognitive recovery -- not just muscle and metabolism.

CJC-1295 and Ipamorelin stimulate the pituitary to release GH naturally. CJC-1295 produced dose-dependent GH increases (2- to 10-fold) lasting 6+ days and IGF-1 increases (1.5- to 3-fold) lasting 9-11 days in healthy adults [24]. Combined with Ipamorelin, the GH pulses are stronger and more physiological, without cortisol or prolactin elevation [25].

By restoring GH/IGF-1 levels in deficient TBI patients, these secretagogues may support the brain's repair mechanisms. CJC-1295 also improves REM sleep duration [25] -- relevant because sleep disturbance is among the most common post-concussion complaints, and sleep quality directly affects neuroplasticity.

Evidence level: Well-characterized human pharmacokinetics. GH deficiency post-TBI is well-documented. No dedicated TBI trials with these secretagogues.

Peptide Comparison Table

PeptidePrimary TBI MechanismEvidence LevelTreatment WindowKey Advantage
BPC-157Anti-edema, anti-hemorrhage, NO modulationAnimal TBI studiesAcute (pre- and post-injury)Reduces brain swelling and bleeding
TB-500Neuroprotection + neurorestorationRat TBI studies6-24 hours post-injuryBoth acute protection and long-term repair
CerebrolysinNeuroplasticity, neurogenesisHuman RCTsAcute to subacuteStrongest human evidence
SemaxBDNF upregulation, anti-inflammatoryHuman stroke trialsAcute to chronicApproved for stroke in Russia
DihexaSynaptogenesis via HGF/c-MetAnimal cognitive studiesChronic recovery phasePotent synapse formation
MOTS-cMitochondrial protection, antioxidantAnimal TBI study (2024)AcuteTargets mitochondrial energy failure
HumaninMitochondrial transfer, anti-apoptosisBrain hemorrhage modelsAcute to subacuteShifts microglia to reparative state
SelankBDNF, anxiolytic, anti-inflammatoryClinical anxiety dataPost-acute to chronicAddresses post-concussion anxiety
CJC-1295 + IpamorelinGH/IGF-1 neurorestorationHuman PK dataChronic recoveryRestores GH axis for brain repair

The Secondary Injury Cascade: Where Peptides Intervene

These peptides map onto different phases of the TBI timeline:

PhaseTimeframePeptidesTarget
AcuteMinutes to hoursBPC-157, MOTS-c, Humanin, TB-500 (early)Hemorrhage, edema, mitochondrial collapse, lesion size
SubacuteHours to daysTB-500, Cerebrolysin, SemaxAngiogenesis, neuroplasticity, BDNF upregulation
Early recoveryDays to weeksCJC-1295/Ipamorelin, Dihexa, SelankGH/IGF-1 restoration, synaptogenesis, anxiety
Chronic recoveryWeeks to monthsSemax, Dihexa, GH secretagoguesOngoing neuroplasticity, synapse building, IGF-1

This timeline is conceptual and based on preclinical data. Clinical protocols for TBI peptide therapy do not yet exist in standardized form.

Current Limitations and Research Gaps

The peptide research for TBI is promising but must be evaluated honestly:

Cerebrolysin has the strongest human evidence but is not available in the U.S., and effect sizes vary across trials. BPC-157 and TB-500 have consistent preclinical data but no human TBI trials, and most BPC-157 brain research comes from a single laboratory group. Semax has human stroke data and Russian approval, but Western validation is limited. Dihexa raises safety questions because the HGF/c-Met pathway is also involved in tumor growth. MOTS-c and Humanin are new to TBI research and need replication.

The fundamental gap: No peptide has completed a phase III randomized controlled trial for TBI. The FDA has not approved any neuroprotective drug for TBI despite decades of attempts. This reflects TBI's complexity, not a specific failure of peptides.

Frequently Asked Questions

Can peptides help with concussion symptoms like brain fog and memory problems?

Several peptides target the mechanisms behind post-concussion cognitive symptoms. Semax and Selank upregulate BDNF, which is central to memory formation and cognitive flexibility. Dihexa promotes new synapse formation. CJC-1295/Ipamorelin restore GH/IGF-1 levels that support neurogenesis. However, none of these have been tested in formal concussion recovery trials. See our guide on best peptides for cognitive enhancement for more on the cognitive mechanisms.

When should peptides be started after a brain injury?

The preclinical data suggests timing matters and varies by peptide. BPC-157 and MOTS-c may be most useful in the acute phase (first hours), while TB-500 showed benefit even when started 24 hours post-injury. Growth hormone secretagogues and synaptogenesis-promoting peptides like Dihexa are more relevant during the recovery phase (weeks to months). Any treatment decisions after TBI should involve a neurologist or brain injury specialist.

Are peptides safe to combine with standard TBI medications?

No dedicated interaction studies exist between these peptides and standard TBI medications (anticonvulsants, osmotic agents, sedatives). Peptides generally have low systemic toxicity, but the absence of interaction data means caution is warranted. Never combine experimental peptides with prescribed medications without physician oversight.

Which peptide has the most evidence for brain injury?

Cerebrolysin, by a significant margin. It has multiple randomized controlled trials in TBI showing improved cognitive and functional outcomes. Among the non-mixture peptides, TB-500 (thymosin beta-4) has the most consistent TBI-specific preclinical data, with consistent results across multiple dosing timepoints and endpoints.

Is there anything specifically for sports-related concussions?

Sports concussions are typically mild TBI, and the research for peptides in mild TBI is thinner than for moderate-severe cases. The Cerebrolysin mild TBI trial showed cognitive benefits. Semax's BDNF-boosting effects are theoretically relevant to the neuroplasticity needed for concussion recovery. CJC-1295/Ipamorelin may help if GH deficiency develops post-concussion. But no peptide protocol has been validated specifically for sports concussion recovery.

What about the new CAQK peptide I've seen in the news?

CAQK is a four-amino-acid peptide that made headlines in late 2025 when research showed it accumulates in injured brain tissue after IV administration and has intrinsic neuroprotective properties -- reducing lesion size, cell death, and inflammation in both mouse and pig TBI models [26]. The researchers are preparing for early human clinical trials. If successful, CAQK could become the first non-invasive drug specifically approved for acute TBI treatment. It is still in the early stages, but the data is genuinely exciting.

The Bottom Line

The brain has limited options for self-repair after trauma, and medicine has had little to offer beyond supportive care. Peptides represent the most promising class of compounds for changing that equation.

Cerebrolysin already has clinical trial data showing cognitive improvement after both mild and moderate-severe TBI. TB-500 and BPC-157 show consistent preclinical neuroprotection and neurorestoration. Semax has human stroke data and BDNF-boosting effects directly relevant to brain repair. Mitochondrial peptides like MOTS-c and Humanin target the energy failure that kills neurons in the hours after injury. And growth hormone secretagogues address the GH deficiency that silently impairs recovery in a large fraction of TBI survivors.

None of this means peptides are ready for routine TBI treatment. The research is still working its way toward human validation, the regulatory picture is unsettled, and combining multiple experimental compounds without clinical guidance carries real risk. But the trajectory of the science is clear, and for patients and families frustrated by the current lack of treatment options, these compounds represent the most active frontier in TBI therapeutics.

If you or someone you know is recovering from a brain injury, the next step is a conversation with a neurologist who is familiar with both standard TBI rehabilitation and the emerging peptide research. For more on peptides that support nervous system recovery, see our guides on best peptides for nerve regeneration and best peptides for cognitive enhancement.

References

  1. CDC. Facts About TBI. Traumatic Brain Injury & Concussion. https://www.cdc.gov/traumatic-brain-injury/data-research/facts-stats/index.html

  2. Prevalence of traumatic brain injury among adults and children. ScienceDirect. 2025. https://www.sciencedirect.com/science/article/abs/pii/S1047279725000316

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

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

  5. Xiong Y, et al. Neuroprotective and neurorestorative effects of thymosin beta4 treatment initiated 6 hours post injury following traumatic brain injury in rats. Journal of Neurosurgery. 2012;116(5):1081-1092. PMC3392183. https://pmc.ncbi.nlm.nih.gov/articles/PMC3392183/

  6. Xiong Y, et al. Treatment of traumatic brain injury with thymosin beta4 in rats. Journal of Neurosurgery. 2011;114(1):102-115. PMC2962722. https://pmc.ncbi.nlm.nih.gov/articles/PMC2962722/

  7. Morris DC, et al. Thymosin beta 4 induces significant changes in the plasma miRNA profile following severe traumatic brain injury in the rat lateral fluid percussion injury model. Expert Opinion on Biological Therapy. 2018;18(sup1):159-165. PMID: 29873258. https://pubmed.ncbi.nlm.nih.gov/29873258/

  8. Muresanu DF, et al. Cerebrolysin after moderate to severe traumatic brain injury: prospective meta-analysis of the CAPTAIN trial series. Neurological Sciences. 2021;42:735-746. PMID: 33620612. https://pubmed.ncbi.nlm.nih.gov/33620612/

  9. Chen CC, et al. Cerebrolysin enhances cognitive recovery of mild traumatic brain injury patients: double-blind, placebo-controlled, randomized study. British Journal of Neurosurgery. 2013;27(6):803-7. PMID: 23656173. https://pubmed.ncbi.nlm.nih.gov/23656173/

  10. Alvarez XA, et al. A retrospective, multi-center cohort study evaluating the severity-related effects of cerebrolysin treatment on clinical outcomes in traumatic brain injury. CNS Neuroscience & Therapeutics. 2015;21(9):727-35. PMID: 25924999. https://pubmed.ncbi.nlm.nih.gov/25924999/

  11. Effect of Cerebrolysin in severe traumatic brain injury: A multi-center, retrospective cohort study. Neuroscience Letters. 2022. https://www.sciencedirect.com/science/article/abs/pii/S030384672200097X

  12. Dolotov OV, et al. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Research. 2006;1117(1):54-60. PMID: 16996037. https://pubmed.ncbi.nlm.nih.gov/16996037/

  13. Gusev EI, et al. The efficacy of Semax in the treatment of patients at different stages of ischemic stroke. Zhurnal Nevrologii i Psikhiatrii. 2018. PMID: 29798983. https://pubmed.ncbi.nlm.nih.gov/29798983/

  14. Dergunova LV, et al. Semax and Pro-Gly-Pro Activate the Transcription of Neurotrophins and Their Receptor Genes after Cerebral Ischemia. Cells. 2024;13(20):1696. PMC11498467. https://pmc.ncbi.nlm.nih.gov/articles/PMC11498467/

  15. Gao Z, et al. AngIV-Analog Dihexa Rescues Cognitive Impairment and Recovers Memory in the APP/PS1 Mouse via the PI3K/AKT Signaling Pathway. Brain Sciences. 2021;11(11):1487. PMC8615599. https://pmc.ncbi.nlm.nih.gov/articles/PMC8615599/

  16. Wright JW, Harding JW. The Procognitive and Synaptogenic Effects of Angiotensin IV-Derived Peptides Are Dependent on Activation of the Hepatocyte Growth Factor/c-Met System. Journal of Pharmacology and Experimental Therapeutics. 2015;352(2):344-9. PMC4201273. https://pmc.ncbi.nlm.nih.gov/articles/PMC4201273/

  17. Li J, et al. Neuroprotective mechanism of MOTS-c in TBI mice through integrated transcriptomic and metabolomic analyses. 2024. Referenced in MOTS-c literature reviews.

  18. Yin X, et al. Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging. Journal of Translational Medicine. 2023;21:36. PMC9854231. https://pmc.ncbi.nlm.nih.gov/articles/PMC9854231/

  19. Cai R, et al. The Mitochondria-Derived Peptide Humanin Improves Recovery from Intracerebral Hemorrhage: Implication of Mitochondria Transfer and Microglia Phenotype Change. Journal of Neuroscience. 2020;40(10):2154-2167. https://www.jneurosci.org/content/40/10/2154

  20. Kim SJ, et al. The mitochondrial-derived peptide humanin activates the ERK1/2, AKT, and STAT3 signaling pathways and has age-dependent signaling differences in the hippocampus. Oncotarget. 2016;7(30):46899-46912. https://www.oncotarget.com/article/10380/text/

  21. Yen K, et al. Novel humanin analogs confer neuroprotection and myoprotection to neuronal and myoblast cell cultures exposed to ischemia-like and doxorubicin-induced cell death insults. Peptides. 2020;134:170412. https://www.sciencedirect.com/science/article/abs/pii/S0196978120301480

  22. Inozemtseva LS, et al. Selank, Peptide Analogue of Tuftsin, Protects Against Ethanol-Induced Memory Impairment by Regulating of BDNF Content in the Hippocampus and Prefrontal Cortex in Rats. Bulletin of Experimental Biology and Medicine. 2019;167(5):641-644. PMID: 31625062. https://pubmed.ncbi.nlm.nih.gov/31625062/

  23. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Frontiers in Pharmacology. 2016. PMC4757669. https://pmc.ncbi.nlm.nih.gov/articles/PMC4757669/

  24. Teichman SL, et al. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. Journal of Clinical Endocrinology & Metabolism. 2006;91(3):799-805. PMID: 16352683. https://pubmed.ncbi.nlm.nih.gov/16352683/

  25. CJC-1295 and Ipamorelin combination pharmacology. Referenced in clinical practice reviews and pharmacological summaries.

  26. Mann AP, et al. A neuroprotective tetrapeptide for treatment of acute traumatic brain injury. EMBO Molecular Medicine. 2025. PMC12603041. https://pmc.ncbi.nlm.nih.gov/articles/PMC12603041/