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Peptide Atlas
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Peptides Studied for Mental Clarity and Long-Term Brain Health

Researchers have studied several peptides for their effects on memory, attention and the growth signals that keep neurons alive. The strongest human evidence sits with older-brain and injury populations rather than healthy people seeking sharper focus, and much of the work is preclinical or from Russian and Eastern European clinics. No compound here is an approved brain-boosting treatment in the United States for everyday cognitive enhancement.

The biology of this goal

Your brain runs on nerve cells that need constant maintenance to survive, connect and communicate. Special proteins called growth factors — the best known is BDNF (brain-derived neurotrophic factor) — act like fertilizer that keeps neurons healthy and helps them form new connections. Attention and motivation depend on chemical messengers such as dopamine, while the enzyme systems that produce energy inside cells keep the whole network running. Many of the peptides here are studied because they are thought to raise these growth signals, protect cells from damage, or steady the chemical messengers behind focus.

What the research supports

9 of 16 compounds considered

Cerebrolysin

Tier 1 · Human trials

Human trials and meta-analyses report modest cognitive benefits in dementia and injury populations, but no study has tested whether it helps healthy adults or prevents decline.

Cerebrolysin is a liquid made from pig brain tissue, broken down into free amino acids and small peptides. These pieces are thought to act like the body's own nerve-growth signals, helping brain cells survive and form connections. It is given by injection and is used in some countries for stroke, brain injury and dementia.

  • A meta-analysis of six randomized controlled trials (597 participants) found a beneficial effect on general cognition (MMSE weighted mean difference 1.10; 95% CI 0.37 to 1.82) and on ADAS-cog+ (WMD -4.01; 95% CI -5.36 to -2.66) in vascular dementia of mild to moderate severity.2

  • In a randomized controlled trial in infants with severe perinatal brain insult, the Cerebrolysin group showed large increases from baseline in social, speech, symbolic and total communication scores after three months (p<0.001 for all).1

  • It is approved in many European and Asian countries for stroke, traumatic brain injury and dementia but not in the United States; it improved cognition and memory in schizophrenia patients, though its effect on memory was lower than currently approved Alzheimer's drugs, and one positive result in healthy elderly people could have been placebo.3

What this doesn't establish

The evidence does not establish that Cerebrolysin improves clarity or protects the brain in healthy people; it remains unknown whether it prevents dementia or slows cognitive decline.

Cortexin

Tier 1 · Human trials

Human trials report cognitive improvements in children and in post-Covid patients, though these come from Russian clinical settings and independent reviewers judge the evidence base weak.

Cortexin is a mixture of small peptides extracted from the brain cortex of cattle and pigs, given by injection. It is proposed to protect neurons broadly and to help balance brain chemicals, including dopamine. It is used clinically in Russia and neighbouring countries for cognitive and developmental problems.

  • A multicenter study reported a reliable effect on cognitive impairment across 635 children aged 3–7 in four clinical groups, with ability to modulate brain dopamine shown in experimental studies.4

  • In post-Covid cognitive impairment, Cortexin at 10 mg intramuscularly for 20 days improved concentration and executive control (p<0.05) and auditory-verbal memory (p=0.002), with no adverse events in the treatment group.5

  • In rat models of developmental delay, Cortexin decreased structural changes in brain tissue.6

What this doesn't establish

The evidence does not establish a benefit for mental clarity in healthy adults, and the trials lack the independent replication and rigour expected for firm conclusions.

Semax

Tier 2 · Preclinical

Animal and laboratory studies suggest nootropic and neuroprotective effects, with limited human data reporting improved operative memory in healthy volunteers.

Semax is a lab-made peptide based on a fragment of the hormone ACTH, but without the hormonal effect on the adrenal glands. In animals it raises brain growth factors like BDNF and nudges dopamine and serotonin. It has mainly been studied for stroke recovery and for improving short-term memory and attention.

  • Semax increases expression of neurotrophins such as BDNF and TrkB in the hippocampus and ischemic brain tissue and has progressed to clinical use as a nootropic and neuroprotective agent in cerebrovascular and stress-related conditions.7

  • In healthy volunteers, intranasal Semax improved operative memory.7

  • In mouse models Semax and a derivative improved cognitive function across open field, novel object recognition and Barnes maze tests, and in rats it normalized brain biogenic amine levels and reduced anxiety-like behaviour after early-life fluvoxamine exposure.8,9

What this doesn't establish

The evidence does not include rigorous controlled human trials for cognitive enhancement in healthy people; most mechanistic support is preclinical.

Noopept

Tier 2 · Preclinical

Human clinical studies in patients with mild cognitive disorders report improvements in memory and attention, though the trials are small and largely from Russian settings.

Noopept is a synthetic dipeptide related to piracetam and based on a natural brain peptide. It is broken down quickly in the body and works largely by converting into a metabolite thought to carry its longer-lasting effects. Animal studies link it to higher levels of growth factors and better acetylcholine signalling, and Russian clinical studies report improved memory and attention.

  • Noopept is a synthetic dipeptide that raises the neurotrophic factors BDNF and NGF, penetrates the blood-brain barrier when taken orally, and is used in Europe for mild cognitive decline.10

  • In a clinical trial in patients with psychoorganic disorders, Noopept improved memory and attention, with the most marked improvement in attention (distribution, stability and volume) and short visual memory, and produced EEG changes typical of nootropic drugs.11

  • Its metabolite cycloprolylglycine has nootropic potential on its own when injected, though to a lesser degree than Noopept.12

What this doesn't establish

The evidence does not establish benefit in healthy people seeking sharper focus, and the human data come from patients with existing brain pathology rather than controlled enhancement studies.

P21

Tier 3 · Reported use

Animal and laboratory studies suggest it promotes neurogenesis and rescues cognitive deficits in Alzheimer's-model mice, but there are no completed human clinical trials.

P21 is a tiny, chemically stabilized fragment of a natural growth factor called CNTF, designed to be small enough to reach the brain and survive digestion. In animals it raises BDNF, encourages the birth of new neurons, and reduces the tau tangling linked to Alzheimer's. All of the findings so far come from animals — there is no human trial data.

  • In transgenic mouse models of Alzheimer's disease, oral P21 prevented and rescued cognitive deficits, reduced tau pathology, and promoted neurogenesis with increased spine density and synaptic markers.13

  • A 2014 study reported chronic oral P21 reduced abnormal tau hyperphosphorylation and improved cognition in triple-transgenic Alzheimer's-model mice, and a 2017 paper reported it rescued dendritic and synaptic deficits.15

  • P21 enhances synaptic density and glutamate receptor expression, with an adamantane modification aiding blood-brain barrier penetration.14

What this doesn't establish

The evidence does not establish any effect in humans; there is no validated human dose, no regulatory approval and no human safety data.

Selank

Tier 2 · Preclinical

Human trials report anxiolytic effects comparable to benzodiazepines in anxiety disorders, with additional animal evidence for stress and cytokine modulation.

Selank is a lab-made peptide based on a natural immune fragment, studied mainly for its calming (anti-anxiety) effect alongside memory support. Animal studies report it fine-tunes the brain's calming GABA system and nudges serotonin, dopamine and growth factors like BDNF. Reviews note its calming profile without the amnesia or dependence seen with tranquilizers.

  • In patients with generalized anxiety disorder and neurasthenia, Selank showed anxiolytic effects similar to medazepam.16

  • In rats, individual Selank was most effective at reducing elevated anxiety, and combining diazepam with Selank was most effective under chronic mild stress.17

  • Under social stress conditions in rats, Selank reduced the concentrations of the inflammatory cytokines IL-1β, IL-6 and TNF-α toward control values.18

What this doesn't establish

The evidence for direct cognitive enhancement is limited; the strongest human data concern anxiety rather than mental clarity, and its BDNF and neurotrophic effects in humans are not directly demonstrated for this goal.

Pinealon

Tier 3 · Reported use

Community and vendor reports describe cognitive and neuroprotective effects, but there are no PubMed-indexed human trials and the animal evidence has not been independently replicated.

Pinealon is a synthetic three-amino-acid peptide from the Russian 'peptide bioregulator' tradition. Vendors and reviewers propose it enters cells and interacts with DNA to influence which genes are active, particularly those tied to neuron protection and antioxidant defence. Much of this is theoretical, and sources caution its brain penetration has not been confirmed.

  • Vendor sources describe a 72-patient study of post-traumatic cerebrasthenia reporting improved memory, reduced headache and better emotional stability, and cite improvement in 59.4% of subjects with traumatic brain injury.19

  • Independent review notes zero PubMed-indexed human studies and zero RCTs, with the fundamental question of blood-brain barrier penetration for the tripeptide remaining unanswered.20

  • In a separate line of work, arginine-enriched peptides reversed learning and memory impairment in d-galactose-induced brain aging in mice on Morris water maze and step-down tests.21

What this doesn't establish

The evidence does not establish that Pinealon reaches the brain in meaningful amounts or improves cognition in humans; its safety profile is essentially unknown.

Epithalon

Tier 3 · Reported use

Community reports and preclinical work describe antioxidant, circadian and neurogenic effects, but there are no human studies for cognition or neuroprotection.

Epithalon is a synthetic four-amino-acid peptide modeled on a pineal gland extract. It is studied mostly for switching on telomerase (an enzyme that maintains chromosome caps) and for restoring nighttime melatonin and body-clock rhythms. There are no human studies of its effects on thinking or brain protection.

  • There are no human studies on cognition or neuroprotection; preclinically it may have antioxidant activity in the brain, increase melatonin, and cross the blood-brain barrier to stimulate cortical neurons and raise phospho-CREB, a DNA-binding protein important in learning and memory.22

  • AEDG peptide regulates pineal, retinal and brain function and epigenetically stimulated neuronal differentiation gene expression in human stem cells, increasing key markers by 1.6–1.8 times.23

  • It has a plasma half-life of about 30 minutes and is cleared from circulation within 24 to 48 hours.24

What this doesn't establish

The evidence does not establish any cognitive or neuroprotective benefit in humans; the neurogenic findings come from cell cultures and animals.

SS-31

Tier 2 · Preclinical

Animal studies suggest it protects cognition and supports BDNF signalling, but no human trial demonstrates prevention of decline or improved cognition, and its human trials to date have been in muscle and cardiac disease.

SS-31 (elamipretide) is a small peptide that targets the mitochondria — the power plants inside cells. It binds a special fat called cardiolipin to keep the energy-producing machinery organized and to reduce harmful free radicals at their source. In brain-injury models it also supported growth-factor signalling, but it has not been tested for cognition in humans.

  • In mice, elamipretide ameliorated LPS-induced learning and memory impairment and facilitated BDNF signalling, reversing synaptic-signaling proteins and increasing synaptic structural complexity.26

  • In models of cognitive impairment SS-31 improved cognitive function by promoting mitochondrial and synaptic health and decreasing inflammation, and protected cognition in aged mice exposed to anesthesia — but no human clinical trials demonstrate prevention of dementia or improved cognition.25

  • In a post hoc analysis of the MMPOWER-3 trial, exposure-response analysis showed a weak positive correlation between plasma elamipretide concentration and six-minute walk test improvement in the nuclear-DNA cohort.27

What this doesn't establish

The evidence does not establish any cognitive benefit in humans; the one high-tier human finding concerns walking distance in mitochondrial myopathy, not brain function.

How they work together

Check this stack

Cerebrolysin and Cortexin are the closest pair here — both are enzymatically digested animal-brain peptide mixtures acting as broad neurotrophic mimics, so running both together is largely redundant and makes it impossible to tell which is responsible for any effect; most people would pick one. Pinealon and Epithalon are also same-class Khavinson 'bioregulators' proposed to act on gene expression, and are likewise overlapping rather than additive. By contrast, several pairings are described as complementary because they hit brain protection from different angles: Cortexin's anti-excitotoxic protection alongside Noopept's or Semax's BDNF/TrkB neurotrophic signalling; SS-31's mitochondrial protection alongside any of the neurotrophic compounds; and Selank's calming GABAergic effect balancing the stimulating, attention-oriented Semax. Noopept and Semax, and Semax and Selank, are widely used real-world nootropic pairings that converge on BDNF signalling from different starting points. Importantly, nearly all of these combination claims are preclinical or anecdotal — human data for stacking any of these together are lacking.

  • Cortexin + Cerebrolysin

    Worth caution — see why below

    Both are enzymatically-digested animal-brain peptide mixtures (bovine/porcine cortex) working as broad neurotrophic-factor mimics — anti-apoptotic, anti-excitotoxic, anti-inflammatory, and pro-neuroplasticity. Because they occupy almost the same conceptual niche, running both together is largely redundant rather than additive, and it becomes impossible to tell which product is responsible for any benefit or side effect. Most users should pick one crude neurotrophic mixture rather than stack the two.

    Not fully established

    The mechanism descriptions clearly establish substantial overlap in the shared dimensions claimed. Both peptides are enzymatically-processed animal-brain extracts (bovine cortex for Cortexin, porcine brain for Cerebrolysin) containing small peptides and amino acids under ~10,000 Da. The four shared dimensions are all explicitly supported: (1) anti_inflammatory—both list anti-inflammatory effects and pathways; (2) neurogenesis—both explicitly target neurogenesis and neuroplasticity; (3) dopaminergic_system—both include dopaminergic modulation in their approved tags and pathways; (4) BDNF_signaling—both explicitly list BDNF_signaling as an approved tag and describe neurotrophic-factor mimicry. Both also share anti-apoptotic and anti-excitotoxic mechanisms. The explanation's characterization of them as 'broad neurotrophic-factor mimics' with overlapping neuroprotective profiles is directly supported by the parallel targeting of neurotrophic pathways (BDNF, neurotrophic factors), anti-inflammatory effects, and neurogenesis. The claim that they occupy a similar conceptual niche is justified by the mechanism material.

  • Pinealon + P21

    Worth caution — see why below

    Both report enhanced dendritic arborization, synaptic plasticity and neurogenesis. P21 drives BDNF/TrkB and PI3K/Akt–GSK-3β signaling, while Pinealon is proposed to reach similar endpoints via gene-expression/ERK modulation. The distinct mechanisms pointing at the same plasticity outcome make them complementary in principle, with only preclinical/anecdotal support for combining.

    Not fully established

    Both peptides' mechanisms clearly support the claimed shared dimension of neurogenesis and dendritic arborization. Pinealon reports dendritic arborization/neuroplasticity (src-26, src-47) and MAPK/ERK modulation (src-18, src-8, src-22, src-32, src-47). P21 reports enhanced dendritic arborization and dendritic spine density, stimulation of adult hippocampal neurogenesis, and BDNF/TrkB and PI3K/Akt signaling. Both mechanisms converge on neuroplasticity outcomes through distinct pathways (ERK-based vs. BDNF/TrkB/PI3K-Akt-GSK-3β). The 'complementary' relationship type is justified: they target overlapping functional endpoints (neurogenesis, dendritic plasticity, synaptic enhancement) via mechanistically distinct routes, which is the definition of complementarity. The explanation accurately reflects the mechanism material provided—different signaling cascades achieving similar neuroprotective/neuroplastic effects. The caveat about preclinical/anecdotal support is appropriate given the evidence levels cited.

  • Pinealon + Epithalon

    Worth caution — see why below

    Both are short Khavinson-school 'peptide bioregulators' proposed to act by binding DNA/histones and switching gene expression rather than a membrane receptor, and both are pitched as neuroprotective/neurogenic with effects on circadian and melatonin biology. Because they share the same class and proposed mechanism, running them together is largely redundant rather than additive — pick one for your goal rather than stacking two overlapping bioregulators.

    Not fully established

    While both peptides are synthetic short peptides proposed to interact with DNA/histones, the mechanism material does not establish they share the same mechanism. Epithalon's mechanisms are explicitly centered on telomerase/hTERT upregulation, telomere elongation, and senescence pathway modulation (p16/p21), with circadian/melatonin effects as secondary outcomes. Pinealon's mechanisms focus on MAPK/ERK signaling, caspase-3/p53 apoptotic pathways, and antioxidant enzyme expression (SOD2, GPX1), with circadian/melatonin effects only 'proposed' and 'theoretical.' The DNA/histone binding is proposed for both, but the downstream pathways and primary therapeutic targets differ substantially. Neurogenesis is tagged for Pinealon only; Epithalon's neurogenic effects are mentioned but not mechanistically detailed in the same way. The claim of redundancy due to 'same class and proposed mechanism' overgeneralizes from shared structural features (short peptides, DNA-binding hypothesis) without demonstrating convergent pathway activation. The mechanisms do not support that these peptides operate via the same molecular logic.

  • Cortexin + Noopept

    May be complementary

    Cortexin modulates AMPA/glutamate signaling and protects neurons from excitotoxicity, while Noopept positively modulates AMPA receptors and raises BDNF/NGF via its cycloprolylglycine metabolite. They act on overlapping glutamatergic/neurotrophic machinery through distinct entry points, making them a plausible complementary nootropic pairing.

    Not fully established

    Both peptides' mechanisms clearly establish the two shared dimensions claimed: (1) Anti-inflammatory: Cortexin explicitly lists 'Anti-inflammatory (central and systemic)' with neuroinflammatory pathway involvement; Noopept lists 'Antioxidant and anti-inflammatory action (animal/in vitro)' with anti_inflammatory tag. (2) BDNF_signaling: Cortexin explicitly includes 'BDNF-like / NGF-like neurotrophic signaling' and BDNF_signaling tag; Noopept lists 'BDNF / NGF neurotrophin signaling' and BDNF_signaling tag. The explanation's claim of complementary action through distinct entry points on overlapping glutamatergic/neurotrophic machinery is also supported: Cortexin targets AMPA/kainate/mGluR receptors directly; Noopept positively modulates AMPA receptors via cycloprolylglycine metabolite and activates TrkB (neurotrophin receptor). Both converge on neuroprotection against excitotoxicity and neurotrophic support through mechanistically distinct pathways, justifying the 'complementary' relationship type.

  • Cortexin + Semax

    May be complementary

    Cortexin supports neuronal survival through anti-excitotoxic, anti-apoptotic and neurotrophic actions, while Semax (an ACTH fragment) drives BDNF/NGF-TrkB signaling and cognitive enhancement by a distinct mechanism. Both converge on neuroprotection, neurogenesis and improved memory/attention, so they can complement each other rather than overlap.

    Not fully established

    Both peptides' mechanisms clearly establish the four claimed shared dimensions: (1) dopaminergic_system—Cortexin explicitly modulates dopaminergic balance; Semax explicitly modulates serotonergic and dopaminergic systems; (2) anti_inflammatory—both mechanisms list anti-inflammatory effects as primary; (3) neurogenesis—both approved tags include neurogenesis, supported by Cortexin's neurotrophic support and Semax's BDNF/NGF upregulation; (4) BDNF_signaling—Cortexin engages BDNF-like/NGF-like neurotrophic signaling; Semax explicitly targets BDNF/NGF-TrkB signaling. The explanation correctly identifies that they achieve neuroprotection and cognitive enhancement through distinct mechanisms (Cortexin via glutamatergic/GABAergic/caspase modulation; Semax via TrkB/CREB/enkephalinase pathways), making them complementary rather than redundant. The mechanisms support convergence on shared functional outcomes without direct target overlap.

  • Cortexin + SS-31

    May be complementary

    SS-31 protects neurons at the mitochondrial level (cardiolipin/ETC stabilization, reduced mitochondrial ROS), while Cortexin provides receptor-level anti-excitotoxic, antioxidant and anti-apoptotic protection. Two different arms of neuroprotection (energy metabolism vs. glutamate/apoptosis) that plausibly complement one another.

    Not fully established

    Both peptides' mechanisms explicitly support the claimed shared dimensions: (1) anti_inflammatory is documented for both (Cortexin: 'Anti-inflammatory (central and systemic)' and 'Neuroinflammatory pathways'; SS-31: 'Inflammation/pyroptosis modulation' and approved tag 'anti_inflammatory'), and (2) BDNF_signaling is documented for both (Cortexin: 'BDNF-like / NGF-like neurotrophic signaling' and approved tag 'BDNF_signaling'; SS-31: 'BDNF synaptic signaling' and approved tag 'BDNF_signaling'). The explanation correctly identifies distinct mechanistic pathways: Cortexin operates via glutamatergic/GABAergic receptor modulation, caspase inhibition, and antioxidant effects, while SS-31 operates via mitochondrial cardiolipin stabilization, ETC coupling, and mitochondrial ROS reduction. These represent complementary neuroprotective mechanisms at different cellular levels (receptor/cytoplasmic vs. mitochondrial), justifying the 'complementary' relationship type.

  • Cortexin + P21

    May be complementary

    P21 is a CNTF fragment that strongly upregulates BDNF and hippocampal neurogenesis while reducing tau phosphorylation, whereas Cortexin provides broad neurotrophic and anti-excitotoxic protection. Different upstream mechanisms both feeding neuroplasticity and neuronal survival, so the two are complementary.

    Not fully established

    Both peptides' mechanisms clearly support the claimed shared dimensions. Cortexin explicitly targets BDNF-like/NGF-like neurotrophic signaling and has approved tags for neurogenesis and BDNF_signaling. P21 directly upregulates BDNF expression via TrkB and stimulates adult hippocampal neurogenesis with approved tags matching these dimensions. The proposed relationship as 'complementary' is justified: P21 acts through BDNF/TrkB and GSK-3beta pathways to enhance neurogenesis and synaptic plasticity, while Cortexin provides broader neuroprotection through multiple mechanisms (glutamatergic modulation, caspase-8 inhibition, antioxidant effects, and neurotrophic support). These represent distinct upstream mechanisms converging on shared neuroplasticity and neuronal survival outcomes, fitting the complementary characterization.

  • Cortexin + Selank

    May be complementary

    Both influence GABAergic tone and neurotransmitter balance and support BDNF signaling, but by different routes — Cortexin protects against glutamate excitotoxicity and Selank adds anxiolytic GABA-A/serotonergic modulation plus enkephalinase inhibition. Together they cover both the neuroprotective and the calm/anxiolytic side of brain function.

    Not fully established

    The mechanisms clearly establish the four shared dimensions: (1) GABA_signaling—both target GABA-A receptor (Cortexin: direct modulation via multiple glutamate receptors and GABAergic effects; Selank: allosteric modulation); (2) BDNF_signaling—both explicitly list BDNF-like/NGF-like neurotrophic signaling and BDNF signaling in their pathways; (3) dopaminergic_system—both include dopaminergic neurotransmitter balance/modulation in their mechanisms; (4) anti_inflammatory—both have anti-inflammatory effects listed. The complementary relationship is justified: Cortexin acts primarily through glutamate receptor modulation, caspase inhibition, and antioxidant/neuroprotective mechanisms, while Selank acts through serotonergic (5-HT1A/2A) and enkephalinergic pathways with allosteric GABA-A modulation. The explanation accurately reflects that they converge on shared neurotransmitter systems (GABA, dopamine, BDNF) but via distinct mechanistic routes—one emphasizing excitotoxicity protection and the other anxiolytic/serotonergic modulation—making them genuinely complementary rather than redundant.

  • Noopept + Semax

    May be complementary

    Both are cognitive-enhancing peptides that raise BDNF/NGF and act through the TrkB neurotrophin pathway, but by different upstream routes — Noopept via its cycloprolylglycine metabolite modulating AMPA/TrkB, and Semax via ACTH-fragment neurotrophin signaling. They converge on the same goals (memory, attention, neuroprotection, anxiolysis) and are commonly used together in nootropic practice, making the pairing potentially additive rather than redundant.

    Not fully established

    The mechanism descriptions clearly establish both shared dimensions: (1) anti_inflammatory — both peptides have documented anti-inflammatory effects (Noopept: 'Antioxidant and anti-inflammatory action'; Semax: 'Anti-inflammatory / immune modulation'); (2) BDNF_signaling — both explicitly target BDNF/NGF neurotrophin pathways via TrkB receptor activation (Noopept: 'BDNF / NGF neurotrophin signaling' and 'TrkB receptor (neuroprotection via activation)'; Semax: 'BDNF/NGF-TrkB neurotrophin signaling' and 'TrkB receptor'). The explanation correctly identifies convergent endpoints (memory, attention, neuroprotection, anxiolysis) achieved through distinct upstream mechanisms (Noopept via AMPA/cycloprolylglycine; Semax via ACTH-fragment/enkephalinase inhibition), which justifies the 'complementary' relationship type as additive rather than redundant. The mechanisms support this characterization.

  • Noopept + P21

    May be complementary

    Both peptides ultimately drive the BDNF/TrkB neurotrophin cascade and promote synaptic plasticity and memory — P21 as a CNTF-derived fragment that upregulates BDNF, Noopept via its metabolite acting on TrkB and AMPA. They reach the same downstream output (enhanced BDNF signaling and neuroprotection) from different upstream starting points, which is generally synergistic but worth noting as overlapping rather than independent.

    Not fully established

    Both peptides' mechanisms clearly establish BDNF/TrkB pathway engagement as a shared downstream output. Noopept's mechanism explicitly lists 'BDNF / NGF neurotrophin signaling' as a pathway and 'BDNF_signaling' as an approved tag, with TrkB receptor activation documented. P21's mechanism explicitly states 'Upregulation of BDNF expression and secretion' and 'BDNF/TrkB' as a primary pathway with 'BDNF_signaling' as an approved tag. Both mechanisms converge on enhanced synaptic plasticity and neuroprotection through this shared cascade, despite different upstream mechanisms (Noopept via metabolite/TrkB/AMPA; P21 via CNTF-derived BDNF upregulation). The 'same_downstream' relationship type and BDNF_signaling shared dimension are directly supported by the provided mechanism material.

  • Noopept + Selank

    May be complementary

    Selank and Noopept both engage BDNF signaling and both report anxiolytic plus nootropic effects, but through distinct mechanisms — Selank via GABAergic/serotonergic modulation and enkephalinase inhibition, Noopept via AMPA/TrkB neurotrophic pathways. Their overlapping calming-plus-cognitive profiles are complementary and this combination is a well-known real-world nootropic pairing.

    Not fully established

    The mechanism descriptions clearly establish both shared dimensions: (1) BDNF_signaling is explicitly listed in approved tags for both peptides, and both pathways sections reference BDNF/NGF neurotrophin signaling; (2) anti_inflammatory is explicitly approved for both. The explanation correctly identifies distinct mechanistic routes—Selank via GABAergic/serotonergic/enkephalinase pathways versus Noopept via AMPA/TrkB/HIF-1 pathways—that converge on overlapping anxiolytic and nootropic effects. This constitutes a valid complementary relationship: shared functional outcomes (anxiety reduction, cognitive support) achieved through non-overlapping molecular mechanisms, with both engaging the claimed shared dimensions. The distinction between mechanisms supports rather than undermines complementarity.

  • Noopept + Cerebrolysin

    May be complementary

    Noopept raises BDNF/NGF, activates TrkB, and provides antioxidant/anti-inflammatory neuroprotection, echoing Cerebrolysin's neurotrophic and mitochondrial-support actions through a distinct dipeptide mechanism. The two can reinforce cognitive and neuroprotective signaling; combination evidence is anecdotal.

    Not fully established

    The mechanism descriptions clearly establish the three claimed shared dimensions: (1) mitochondrial_function—both peptides are tagged with this and show antioxidant/anti-inflammatory actions supporting mitochondrial health; (2) anti_inflammatory—both explicitly target anti-inflammatory pathways (Cerebrolysin via TNF-α downregulation and microglia modulation; Noopept via antioxidant and anti-inflammatory action); (3) BDNF_signaling—both are tagged with this and their mechanisms confirm it (Cerebrolysin upregulates BDNF; Noopept activates BDNF/NGF signaling via TrkB). The explanation correctly identifies distinct mechanisms (Cerebrolysin's multi-target neurotrophic approach vs. Noopept's HIF-1/TrkB pathway) that converge on overlapping neuroprotective and cognitive outcomes, which justifies the 'complementary' relationship type. The claim that they can reinforce each other through these shared dimensions is supported by the parallel but mechanistically distinct pathways described.

  • Semax + P21

    May be complementary

    P21 raises BDNF that then activates TrkB; Semax also upregulates BDNF/NGF and signals through TrkB and CREB. Both end up driving the same BDNF/TrkB neurotrophic and neurogenic output through different starting points, so they are potentially additive for memory and neuroprotection rather than redundant. Monitor for over-stimulation, since both also touch CREB and plasticity pathways.

    Not fully established

    Both peptides' mechanisms clearly converge on BDNF/TrkB signaling and neurogenesis. P21 upregulates BDNF expression which activates TrkB, and Semax directly upregulates BDNF/NGF and signals through TrkB. Both activate CREB and drive neurogenesis through overlapping downstream pathways (PI3K/Akt and BDNF/TrkB for P21; BDNF/NGF-TrkB and CREB for Semax). The proposed relationship accurately identifies that despite different mechanisms of action (P21 as CNTF mimetic, Semax as ACTH-derived peptide), they converge on the same neurogenic and BDNF-signaling outputs, making them potentially additive rather than redundant. The shared dimensions of neurogenesis and BDNF_signaling are explicitly supported by both mechanisms.

  • Semax + Selank

    May be complementary

    Selank and Semax are sister Russian regulatory peptides that both raise BDNF/NGF and both inhibit enkephalinase (extending your own opioid peptides), yet they push in different directions: Selank is calming/anxiolytic while Semax is stimulating and pro-attention. Stacked, one tends to smooth out the over-activation of the other, which is why they are a widely used nootropic pairing.

    Not fully established

    The mechanism descriptions clearly establish all three claimed shared dimensions: (1) dopaminergic_system—both peptides explicitly modulate serotonergic and dopaminergic pathways; (2) anti_inflammatory—both are tagged anti_inflammatory and target immune/cytokine signaling (Selank via Th1-Th2 and interferon, Semax via interferon and antigen-presentation); (3) BDNF_signaling—both are tagged BDNF_signaling and upregulate BDNF/NGF (Selank via BDNF/NGF signaling, Semax via BDNF/NGF-TrkB neurotrophin signaling). The proposed complementarity is also mechanistically justified: Selank targets GABA-A (allosteric, anxiolytic) and 5-HT1A/2A (calming), while Semax targets TrkB and melanocortin receptors with attention/stimulation effects. Both inhibit enkephalinase, supporting the shared opioid-peptide extension claim. The sister-peptide pairing and opposing functional profiles (calming vs. stimulating) while sharing core neurotrophin and immune pathways align with the complementary relationship type.

  • Semax + Cerebrolysin

    May be complementary

    Both upregulate BDNF and act via TrkB, reduce neuroinflammation, and modulate dopaminergic tone, but Semax (an ACTH fragment) adds enkephalinase inhibition and its own neurotrophin induction. Different upstream triggers converging on the same neuroprotective/nootropic output make them a plausible complementary nootropic pair. Human combination data are lacking.

    Not fully established

    The mechanism descriptions clearly establish all four claimed shared dimensions: (1) BDNF_signaling—both explicitly upregulate BDNF and target TrkB receptor; (2) dopaminergic_system—Cerebrolysin lists kinase inhibition affecting dopaminergic system and dopaminergic_system tag; Semax lists dopaminergic modulation and dopaminergic_system tag; (3) anti_inflammatory—both reduce neuroinflammation (Cerebrolysin via microglia modulation and TNF-α downregulation; Semax via immune modulation and NF-κB modulation); (4) neurogenesis—both have neurogenesis tags and mechanisms supporting it. The explanation correctly identifies convergence on neuroprotective/nootropic outcomes via different upstream mechanisms (Cerebrolysin via TrkA/TrkB/GFRα1 and multiple kinase pathways; Semax via μ-opioid receptor, melanocortin receptors, and enkephalinase inhibition). The claim that Semax adds enkephalinase inhibition (distinct from Cerebrolysin's endorphinergic effects via peptide fragments) is supported by the mechanisms. The 'complementary' relationship type is justified by the shared dimensions combined with mechanistically distinct upstream triggers converging on similar outputs, which is the hallmark of complementarity.

  • SS-31 + Cerebrolysin

    May be complementary

    SS-31 protects mitochondrial energy production and reduces oxidative stress at the cardiolipin level, while Cerebrolysin improves neuronal energy metabolism and provides neurotrophic support. Pairing a targeted mitochondrial protector with a neurotrophic mixture addresses neuroprotection from two angles. Combination evidence is anecdotal.

    Not fully established

    Both peptides' mechanisms clearly establish the three claimed shared dimensions: (1) mitochondrial_function—SS-31 directly targets cardiolipin and ETC supercomplexes to improve ATP synthesis and mitochondrial structure; Cerebrolysin improves neuronal energy metabolism and is tagged with mitochondrial_function. (2) anti_inflammatory—SS-31 modulates inflammation/pyroptosis; Cerebrolysin explicitly includes anti-inflammatory modulation of microglia and TNF-α downregulation. (3) BDNF_signaling—both are explicitly tagged with BDNF_signaling, and SS-31's mechanisms include BDNF synaptic signaling while Cerebrolysin upregulates BDNF. The proposed 'complementary' relationship is justified: SS-31 provides targeted mitochondrial protection at the cardiolipin/ETC level, while Cerebrolysin provides broader neurotrophic and neuroprotective effects including energy metabolism support. These mechanisms operate on overlapping but distinct targets and pathways, supporting a complementary rather than redundant pairing. The explanation accurately reflects both mechanisms.

  • P21 + Cerebrolysin

    May be complementary

    Cerebrolysin stimulates BDNF and signals through TrkB and PI3K/Akt survival pathways, while P21 (a CNTF fragment) drives BDNF expression that also feeds TrkB and neurogenesis. They reach the same BDNF/TrkB neuroplasticity endpoint from different starting points, so they can reinforce each other's neurotrophic and pro-neurogenic effects. Evidence for the specific combination is anecdotal.

    Not fully established

    Both peptides' mechanisms clearly establish the three claimed shared dimensions. Cerebrolysin targets TrkB, upregulates BDNF/VEGF/IGF-1, activates PI3K/AKT survival signaling, and promotes neurogenesis (approved tags: BDNF_signaling, mTOR_PI3K, neurogenesis). P21 induces BDNF expression, signals via TrkB, activates PI3K/Akt and Akt–GSK-3beta pathways, and stimulates adult hippocampal neurogenesis (approved tags: BDNF_signaling, mTOR_PI3K, neurogenesis). The explanation correctly identifies that both converge on BDNF/TrkB and PI3K/Akt pathways despite different mechanisms of action (Cerebrolysin as a multi-target neuroprotective mixture; P21 as a CNTF-mimetic fragment). The 'complementary' relationship type is justified: they operate through overlapping downstream pathways (BDNF/TrkB, PI3K/Akt, neurogenesis) but via distinct upstream mechanisms, supporting potential synergistic or reinforcing effects. The caveat about anecdotal evidence for the specific combination does not undermine the mechanistic justification for the relationship itself.

  • Noopept + SS-31

    No known conflict in the research

    SS-31 protects neurons by stabilizing mitochondria and cutting oxidative stress, while Noopept provides neurotrophic (BDNF) and anti-excitotoxic support. Both share mitochondrial, anti-inflammatory and BDNF-related tags but act through different targets, so they can converge on neuroprotection from complementary angles.

    Not fully established

    Both peptides' mechanisms explicitly support the three claimed shared dimensions. Noopept lists approved tags: mitochondrial_function, anti_inflammatory, BDNF_signaling. SS-31 lists identical approved tags: mitochondrial_function, anti_inflammatory, BDNF_signaling. The mechanisms confirm distinct targets and pathways: SS-31 acts directly on cardiolipin, mPTP, and ETC complexes to stabilize mitochondria and reduce ROS; Noopept acts via AMPA/TrkB receptors, HIF-1 stabilization, and cholinergic signaling to provide neuroprotection and BDNF signaling. Both demonstrate anti-inflammatory effects through different mechanisms (SS-31 via ferroptosis/pyroptosis suppression; Noopept via stress kinase repression and antioxidant action). The explanation accurately characterizes them as converging on neuroprotection through complementary but distinct mechanistic pathways, which is justified by the provided material.

  • Semax + SS-31

    No known conflict in the research

    SS-31 protects neurons by stabilizing mitochondria and reducing ROS, while Semax protects them through neurotrophin (BDNF/TrkB) signaling. The mitochondrial-protection plus neurotrophic-signaling combination targets different arms of neuroprotection, making them potentially complementary.

    Not fully established

    Both peptides' mechanisms explicitly support the claimed shared dimensions. Semax directly targets BDNF/NGF-TrkB neurotrophin signaling and produces anti-inflammatory effects through NF-kB modulation and interferon signaling. SS-31 explicitly lists BDNF synaptic signaling and inflammation/pyroptosis modulation in its pathways, plus anti-inflammatory in approved tags. The explanation correctly identifies that they operate through distinct mechanistic routes (Semax via neurotrophin signaling and dopaminergic/serotonergic modulation; SS-31 via mitochondrial stabilization and ROS reduction) that converge on shared outcomes (neuroprotection, anti-inflammation, BDNF signaling). This represents genuine complementarity—different upstream mechanisms producing overlapping protective effects—which is well-justified by the provided mechanism material.

  • Semax + Pinealon

    No known conflict in the research

    Both support neuroprotection and neurogenesis but by completely different mechanisms — Semax via BDNF/TrkB neurotrophin signaling and Pinealon via proposed direct gene/DNA regulation and antioxidant enzyme upregulation. Different upstream targets converging on neuronal survival make this a plausibly complementary neuroprotective pairing.

    Not fully established

    Both peptides' mechanisms explicitly support neurogenesis and neuroprotection through distinct pathways: Semax via BDNF/NGF-TrkB neurotrophin signaling and CREB activation; Pinealon via MAPK/ERK modulation, antioxidant enzyme expression (SOD2, GPX1), and caspase-3/p53 apoptotic pathway inhibition. The proposed relationship correctly identifies that they converge on neuronal survival and neurogenesis through different upstream mechanisms (growth factor signaling vs. gene regulation/antioxidant defense), which is the definition of complementarity. The shared dimension of neurogenesis is explicitly tagged for both peptides, and the explanation accurately reflects the mechanistic divergence described in both mechanism profiles.

  • Semax + Epithalon

    No known conflict in the research

    Semax drives BDNF/NGF neurotrophin signaling for cognitive and neuroprotective effects, a mechanism distinct from Epithalon's antioxidant/senescence and circadian actions. The two hit neurogenesis and brain protection through separate pathways and may be complementary.

    Not fully established

    Both peptides' mechanisms explicitly support neurogenesis as a shared dimension through distinct pathways: Epithalon lists 'neurogenesis' as an approved tag and describes 'neuroprotective and neurogenic effects' via antioxidant/senescence pathways and circadian regulation; Semax lists 'neurogenesis' as an approved tag and achieves neuroprotection through BDNF/NGF-TrkB neurotrophin signaling. The proposed relationship correctly identifies that they target neurogenesis through mechanistically separate pathways (Epithalon via telomerase/senescence/circadian mechanisms; Semax via BDNF/TrkB signaling), making them complementary rather than redundant. This aligns with the mechanism descriptions provided.

  • SS-31 + Epithalon

    No known conflict in the research

    SS-31 stabilizes cardiolipin and cuts mitochondrial ROS at the source, whereas Epithalon's reported benefits run through telomerase and general antioxidant/senescence pathways. Both reduce oxidative/mitochondrial aging burden via unrelated mechanisms, making them plausibly complementary.

    Not fully established

    Both peptides' mechanisms establish mitochondrial_function as a shared dimension through distinct pathways: SS-31 directly targets cardiolipin, mPTP, and ETC supercomplexes to reduce mitochondrial ROS production and preserve mitochondrial structure; Epithalon activates telomerase and antioxidant pathways while modulating mitochondrial ROS. The proposed relationship as 'complementary' is justified—they address mitochondrial aging burden through unrelated mechanisms (direct mitochondrial targeting vs. telomerase/antioxidant upregulation), making them mechanistically non-overlapping yet synergistic for the shared dimension of mitochondrial function. Both peptides' approved tags include 'mitochondrial_function,' confirming this shared dimension is recognized in their mechanism profiles.

  • Pinealon + Cerebrolysin

    No known conflict in the research

    Pinealon is a short bioregulator peptide reported to reduce neuronal oxidative stress and apoptosis and support dendritic/neuroplastic changes, overlapping with Cerebrolysin's neurogenic and neuroprotective goal via a different (proposed gene-regulatory) mechanism. Combination is anecdotal.

    Not fully established

    Both peptides' mechanisms describe effects supporting neurogenesis and neuroprotection through distinct pathways. Cerebrolysin achieves this via neurotrophic factor mimicry (TrkA/TrkB, BDNF/VEGF/IGF-1 upregulation, PI3K/AKT signaling, anti-apoptotic pathways). Pinealon achieves similar neuroprotective outcomes through proposed gene-regulatory mechanisms (DNA/promoter binding affecting CASP3, GAP43, antioxidant enzyme expression, MAPK/ERK, PI3K/Akt, caspase-3 inhibition, ROS reduction). Both are tagged with neurogenesis and both reduce apoptosis and oxidative stress. The mechanisms justify the claim of complementary action on a shared dimension (neurogenesis/neuroprotection) via mechanistically distinct routes—one primarily via growth factor signaling, the other via transcriptional/gene-regulatory pathways. The explanation accurately reflects the provided mechanism material.

  • P21 + Selank

    No known conflict in the research

    Selank supports BDNF (and NGF) signaling alongside its anxiolytic/nootropic actions, overlapping with the BDNF/TrkB pathway P21 activates. Coming from different upstream mechanisms and converging on BDNF-mediated plasticity, they are plausibly complementary for cognition and mood support.

    Not fully established

    Both peptides' mechanisms explicitly include BDNF signaling as a pathway. P21 directly targets TrkB receptor via induced BDNF and lists BDNF/TrkB as a core pathway with approved tag BDNF_signaling. Selank lists BDNF signaling as an explicit pathway and carries the same BDNF_signaling approved tag. The proposed relationship correctly identifies that despite different upstream mechanisms (P21 via CNTF-mimicry and TrkB activation; Selank via GABAergic, serotonergic, and enkephalinase pathways), both converge on BDNF-mediated signaling. The explanation accurately characterizes this as downstream convergence on a shared dimension (BDNF signaling) that supports neuroplasticity-related effects. The mechanism descriptions fully justify the same_downstream relationship type and the BDNF_signaling shared dimension claim.

  • Selank + Cerebrolysin

    No known conflict in the research

    Selank supports BDNF signaling, modulates monoamines and adds GABAergic anxiolytic tone plus immunomodulation, complementing Cerebrolysin's neurotrophic and anti-inflammatory profile. A reasonable nootropic/anxiolytic pairing, though only anecdotally documented together.

    Not fully established

    The mechanism descriptions clearly establish all three claimed shared dimensions: (1) dopaminergic_system—both peptides modulate dopamine (Cerebrolysin via kinase inhibition affecting dopaminergic system; Selank via dopamine receptor modulation and monoamine metabolism); (2) anti_inflammatory—both are tagged with anti_inflammatory effects (Cerebrolysin via TNF-α downregulation and microglia modulation; Selank via immunomodulatory and cytokine signaling); (3) BDNF_signaling—both explicitly upregulate or support BDNF (Cerebrolysin via BDNF upregulation pathway; Selank via BDNF signaling pathway). The explanation correctly identifies complementary mechanisms: Cerebrolysin provides broad neurotrophic/neuroprotective effects while Selank adds GABAergic anxiolytic tone and enkephalinase inhibition. The proposed relationship type (complementary) is justified by the distinct but non-overlapping primary mechanisms (Cerebrolysin's TrkA/TrkB targeting vs. Selank's GABA-A modulation) combined with shared downstream effects on the three dimensions. The caveat about anecdotal documentation does not undermine the mechanistic support.

  • Epithalon + Cerebrolysin

    No known conflict in the research

    Epithalon contributes antioxidant, geroprotective and neurogenic effects with mitochondrial ROS modulation, complementing Cerebrolysin's neurotrophic and energy-metabolism support. Different mechanisms converging on neuronal health; combination evidence is anecdotal.

    Not fully established

    Both peptides' mechanisms clearly support the claimed shared dimensions. For mitochondrial_function: Cerebrolysin explicitly includes 'mitochondrial_function' tag and 'Improved neuronal energy metabolism' effect; Epithalon includes 'mitochondrial_function' tag and 'Antioxidant / mitochondrial ROS modulation' pathway. For neurogenesis: both peptides explicitly list 'neurogenesis' in their approved tags and describe neurogenic effects (Cerebrolysin: 'neurogenesis and synaptogenesis'; Epithalon: 'Neuroprotective and neurogenic effects'). The explanation accurately characterizes their mechanisms as complementary—Epithalon targets cellular senescence and oxidative stress at the mitochondrial level while Cerebrolysin provides neurotrophic support and metabolic enhancement—representing different but convergent approaches to neuronal health. The mechanisms do not contradict this relationship; they support it.

  • Cortexin + Pinealon

    No documented interaction in our data — that is not a safety clearance.

  • Cortexin + Epithalon

    No documented interaction in our data — that is not a safety clearance.

  • Noopept + Pinealon

    No documented interaction in our data — that is not a safety clearance.

  • Noopept + Epithalon

    No documented interaction in our data — that is not a safety clearance.

  • SS-31 + Pinealon

    No documented interaction in our data — that is not a safety clearance.

  • SS-31 + P21

    No documented interaction in our data — that is not a safety clearance.

  • SS-31 + Selank

    No documented interaction in our data — that is not a safety clearance.

  • Pinealon + Selank

    No documented interaction in our data — that is not a safety clearance.

  • P21 + Epithalon

    No documented interaction in our data — that is not a safety clearance.

  • Selank + Epithalon

    No documented interaction in our data — that is not a safety clearance.

Compounds we looked at and left out

These share some biology with this goal, so you may have seen them recommended for it. Here is what our own research says about each.

  • Argirelinematched on acetylcholine pathway

    Argireline is linked to acetylcholine pathway, but in this compound that activity is about reducing facial muscle contractions to soften expression lines.

    “By imitating this fragment, it is proposed to interfere with the machinery nerves use to release the chemical messenger (acetylcholine) that tells facial muscles to contract. The idea is that reducing these contractions softens the repeated creasing that forms expression lines, giving it a marketing reputation as a topical, needle-free alternative to Botox.”— from its own profile
  • Leuphasylmatched on acetylcholine pathway

    Leuphasyl is linked to acetylcholine pathway, but in this compound that activity is about wrinkle reduction and skin relaxation.

    “it is reported to bind enkephalin/opioid receptors on the nerve side of the neuromuscular junction and dampen the release of acetylcholine, the signal that makes facial muscles contract”— from its own profile
  • SYN-AKEmatched on acetylcholine pathway

    SYN-AKE is linked to acetylcholine pathway, but in this compound that activity is about cosmetic wrinkle reduction and facial muscle relaxation.

    “Vendor and reference sources describe SYN-AKE as a small synthetic peptide designed to mimic Waglerin-1, a component of Temple Viper venom, in order to relax facial muscles and soften the appearance of expression wrinkles while still allowing normal expressions.”— from its own profile
  • SNAP-8matched on acetylcholine pathway

    SNAP-8 is linked to acetylcholine pathway, but in this compound that activity is about reducing facial wrinkles and expression lines.

    “SNAP-8 is a lab-made cosmetic peptide, an extended version of Argireline, designed to relax the small facial muscles that create expression lines.”— from its own profile
  • Oxytocinmatched on dopamine system

    Oxytocin is linked to dopamine system, but in this compound that activity is about social bonding and stress reduction.

    “Beyond the uterus, reviews describe oxytocin acting in the brain as a 'prosocial' signaling molecule linked to social recognition, bonding, trust, empathy, stress responses and anxiety, though human behavioral findings are mixed and often fail to confirm effects seen in animals.”— from its own profile
  • Bremelanotidematched on dopamine system

    Bremelanotide is linked to dopamine system, but in this compound that activity is about sexual desire and arousal.

    “It switches on melanocortin receptors (mainly MC4R, and also MC3R) in the hypothalamus, tuning brain circuits involved in sexual desire and arousal.”— from its own profile
  • Melanotan IImatched on dopamine system

    Melanotan II is linked to dopamine system, but in this compound that activity is about sexual arousal and tanning.

    “Because it also hits receptors in the brain, it can trigger erections and sexual desire, suppress appetite, and affect glands — effects that cannot be separated from the tanning effect because the peptide is non-selective.”— from its own profile

Sources

Ordered as cited above.

  1. :: JCN :: Journal of Clinical Neurology(opens in a new tab)
    Tier 1Web · thejcn.com
  2. Cerebrolysin for vascular dementia.(opens in a new tab)
    Tier 1PubMed · pubmed.ncbi.nlm.nih.gov
  3. Cerebrolysin & Your Brain | Cognitive Vitality | Alzheimer's Drug Discovery Foundation(opens in a new tab)
    Tier 1Web · alzdiscovery.org
  4. Results of a multicenter study on the efficacy of cortexin in treatment of cognitive dysfunction in children - MedCrave online(opens in a new tab)
    Tier 1Web · medcraveonline.com
  5. [Neuprotection of post-acute COVID-19 cognitive impairment].(opens in a new tab)
    Tier 1PubMed · pubmed.ncbi.nlm.nih.gov
  6. Neurotropic Effects of Cortexin on Models of Mental and ...(opens in a new tab)
    Tier 1Web · pmc.ncbi.nlm.nih.gov
  7. Semax and N Acetyl Semax-Amide: discovery, actions, safety, animal data, and development(opens in a new tab)
    Tier 2Web · hvm.bioflux.com.ro
  8. The Potential of the Peptide Drug Semax and Its Derivative for ...(opens in a new tab)
    Tier 2Web · pmc.ncbi.nlm.nih.gov
  9. Semax, synthetic ACTH(4-10) analogue, attenuates behavioural and neurochemical alterations following early-life fluvoxamine exposure in white rats.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov
  10. Comparative studies of Noopept and piracetam in the ...(opens in a new tab)
    Tier 1Web · researchgate.net
  11. PII: S0924-977X(05)80441-9(opens in a new tab)
    Tier 1Web · pillbuys.com
  12. N-Phenylacetyl-L-prolylglycine ethyl ester(opens in a new tab)
    Tier 2Web · examine.com
  13. P21 (CNTF-Derived Peptide): Research Evidence & Safety Profile | PeptideInsight(opens in a new tab)
    Tier 2Web · peptideinsight.com
  14. P21 — Molecular Specifications & Research Monograph | Peptide Biologix(opens in a new tab)
    Tier 2Web · peptidebiologix.com
  15. P21 Peptide (P021): CNTF Mimetic Research Guide | PeptideStat(opens in a new tab)
    Tier 2Web · peptidestat.com
  16. Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia(opens in a new tab)
    Tier 1Web · researchgate.net
  17. Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov
  18. The Influence of Selank on the Level of Cytokines Under the Conditions of "Social" Stress.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov
  19. Pinealon | Peptide | Peptide Mind(opens in a new tab)
    Tier 3Web · peptidemind.com
  20. Pinealon: Mechanism, Benefits, Evidence & Safety | Peptide Treatments(opens in a new tab)
    Tier 3Web · peptidetreatments.com
  21. Effect of seabuckthorn seed protein and its arginine-enriched peptides on combating memory impairment in mice.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov
  22. Epithalamin/Epithalon(opens in a new tab)
    Tier 3Web · alzdiscovery.org
  23. AEDG Peptide (Epitalon) Stimulates Gene Expression and Protein Synthesis during Neurogenesis: Possible Epigenetic Mechanism.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov
  24. How Long Epithalon Stays in System — Half-Life and(opens in a new tab)
    Tier 3Web · realpeptides.co
  25. SS-31 (also known as Elamipretide®, Bendavia®, and ...(opens in a new tab)
    Tier 3Web · alzdiscovery.org
  26. Elamipretide (SS-31) improves mitochondrial dysfunction, synaptic and memory impairment induced by lipopolysaccharide in mice.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov
  27. Genotype-specific effects of elamipretide in patients with primary mitochondrial myopathy: a post hoc analysis of the MMPOWER-3 trial.(opens in a new tab)
    Tier 1PubMed · pubmed.ncbi.nlm.nih.gov

This brief reports what published research says about these compounds. It is information, not medical advice, and not a recommendation to use anything described here. Evidence quality varies by compound and is labelled throughout. Talk to a qualified clinician before acting on any of it.