Cognitive Performance

Research compounds studied for BDNF upregulation, anxiety reduction, synaptic plasticity, and neuroprotection. Primarily intranasal peptides with fast onset.

Most researched for Cognitive Performance

Semax

The most accessible and well-documented cognitive peptide in this category. Developed at the Russian Institute of Molecular Genetics and approved pharmaceutically in Russia. Research shows BDNF and NGF upregulation, dopaminergic activity enhancement, and neuroprotective effects. Fast onset via intranasal administration with a strong research base behind it.

NAD+

aka Nicotinamide adenine dinucleotide, Coenzyme I

PopularPreclinical

NAD+ is a coenzyme present in all living cells that carries electrons in the redox reactions of energy metabolism and serves as a substrate for enzymes such as sirtuins and PARPs that influence DNA repair. It is not a peptide and is not approved as a drug. Cellular NAD+ declines with age, which has driven interest in supplementation and infusion, but human clinical evidence that raising NAD+ improves outcomes remains limited.

How it works: It serves as an electron-carrying coenzyme in metabolism and as a substrate for sirtuins and PARPs involved in DNA repair.

Longevity research; metabolic support; cellular energy research; wellness infusions

Administration

IV

Timing

IV sessions require 2-8 hours in clinical setting; oral NR/NMN typically taken in the morning

Cycle length

4-8 week loading phase IV; ongoing for oral precursors

Common side effects: Nausea; flushing; chest discomfort during rapid infusion; lightheadedness

Half-life
Not established in humans
Storage
Dry: Lyophilized powder at -20C; reconstituted solution use within 24 hours
Reconstitution
Normal saline (0.9% NaCl) 250-500 mL for IV
Contraindications
Active malignancy under treatment (theoretical concern that NAD+ may support can; Known hypersensitivity to NAD+ or any formulation excipients; Severe hepatic impairment (altered NAD+ metabolism and precursor handling)Freque; Chemotherapy agents: NAD+ may theoretically enhance cancer cell DNA repair via P
Legal status
Investigational
Research evidence
Human trials - early or small
Indications
Anti-aging and longevity research; Neurodegenerative disease research (Alzheimer's, Parkinson's); Metabolic health and mitochondrial dysfunction studies; Cellular repair and DNA damage response research; Addiction and substance use disorder clinical trials
Chemical data
CAS 53-84-9 · C21H27N7O14P2 · 663.43 Da
Amino acids
138 aa

Carnosine

aka L-carnosine, beta-alanyl-L-histidine

PopularPhase 2

Carnosine is an endogenous dipeptide composed of beta-alanine and L-histidine, found naturally in muscle and brain tissue and sold as an oral supplement. Laboratory studies describe antioxidant, metal-chelating, anti-glycation, and pH-buffering activities. It has been investigated as a possible protective agent in aging, although human clinical outcomes remain mixed and preliminary.

How it works: It acts in laboratory studies as an antioxidant and free-radical scavenger, chelates metal ions, buffers pH, and limits glycation.

Antioxidant supplement; geroprotection research; muscle pH buffering; metabolic research

Administration

Oral

Timing

Take as oral capsules (typically two 500 mg capsules daily). No specific timing requirements; most studies used dosing with meals.

Cycle length

12-14 weeks

Common side effects: Not established

Half-life
Not established
Contraindications
No absolute contraindications established for carnosine at standard supplementat; Caution in individuals with very low blood pressure due to potential blood-press; Pregnancy and lactation: insufficient safety data; not recommended during pregna; Histidine metabolism disorders: theoretical concern in rare inherited conditions
Legal status
Investigational
Research evidence
Human trials - early or small
Indications
Anti-aging and longevity support; Glycemic control in prediabetes and type 2 diabetes; Cognitive function support in elderly populations; Exercise performance via intracellular pH buffering; Neuroprotection and brain health
Chemical data
CAS 305-84-0 · C9H14N4O3 · 226.23 Da
Amino acids
12 aa

Cortexin

ModerateInvestigational

Cortexin is a mixture of low-molecular-weight polypeptides extracted from the cerebral cortex of cattle, developed and marketed in Russia as a neuroprotective drug. It is approved and used in Russia and some neighboring countries but has no FDA approval and is considered investigational in the United States. Published research covers ischemic brain injury and cognitive and developmental disorders, mostly in small Russian studies.

How it works: It is thought to promote neuron survival and modulate glutamate and GABA signaling, though the mechanism is not fully defined.

Ischemic brain injury; cognitive disorders; developmental delay; neuroprotection

Research dose

10-20 mg, Once daily ×10 day course

Real-world (reported)

10 mg IM daily ×10 days; 2–4 cycles/year.

Administration

IM

Timing

Morning

Cycle length

10 days; 2–4×/year

Real-world figures are community-reported, not medical advice.

Common side effects: Hypersensitivity reactions; injection site discomfort; allergic reaction

Community take: [ANECDOTAL] More widely used Russia/CIS than West. Similar to Cerebrolysin. 10-day IM course standard.

Onset
Cognitive improvements 2–4 wks
Half-life
Not established
Storage
Dry: Fridge 2–8°C; never freeze; protect from light · Reconstituted: Never freeze; use each ampoule immediately
Reconstitution
Pre-filled — no reconstitution
Rare side effects
Allergic (porcine/bovine); rare seizure threshold effects
Contraindications
Pork/beef allergy; seizure disorder; pregnancy
Drug interactions
Anti-epileptics; CNS-active compounds
Recommended bloodwork
Cognitive assessments; CBC; renal function
Stacks well with
Semax: BDNF complement. Cerebrolysin: alternative — choose one.
Secondary uses
Memory; neuroplasticity; vascular dementia
Legal status
US: Not FDA-approved; research use; Rx in Eastern Europe · UK: Legal to import for research · Canada: Legal to import for research · Australia: Schedule 4 · EU: Approved Russia/CIS; research chemical most EU
Typical price
$30–$100 / ampoule pack
Research evidence
Human trials - early or small

Key risk: Serious allergic or hypersensitivity reactions are the main documented risk.

Oveporexton

aka TAK-861

ModeratePhase 3

Oveporexton is an investigational oral small molecule that selectively activates the orexin receptor 2. It is being developed for narcolepsy type 1, a disorder caused by loss of orexin-producing neurons. Two pivotal phase 3 trials reported improvements across wakefulness, daytime sleepiness, and cataplexy measures versus placebo. It is not approved; a new drug application is under FDA priority review.

How it works: It is a selective orexin receptor 2 agonist that restores deficient orexin signaling in narcolepsy type 1 to promote wakefulness.

Narcolepsy type 1; excessive daytime sleepiness; cataplexy; disturbed nighttime sleep

Administration

Oral

Timing

Taken as oral tablets twice daily (morning and evening); onset of clinical improvement observed within the first weeks of treatment

Cycle length

12 weeks (Phase 3)

Common side effects: Insomnia; urinary urgency; urinary frequency

Half-life
Not established
Contraindications
No specific contraindications have been formally established as oveporexton is i; Patients with severe hepatic impairment should be evaluated individually (althou; Caution in patients with pre-existing insomnia or sleep-onset difficulty, as ove; Orexin receptor antagonists (suvorexant, lemborexant): C
Legal status
Investigational
Research evidence
Human trials - phase 2 or 3
Indications
Narcolepsy type 1 (excessive daytime sleepiness and cataplexy); Narcolepsy type 2 (under investigation)
Chemical data
CAS 2460722-04-5 · C23H25F5N2O4S · 520.52 Da
Amino acids
170 aa

Selank

aka TP-7

ModerateApproved

Selank, also identified as TP-7, is a synthetic heptapeptide developed in Russia as an analog of the natural immune peptide tuftsin, with an added tripeptide that improves its stability. It is thought to act on the GABA system, monoamine neurotransmitters, and brain derived neurotrophic factor, and it may also modulate immune signaling. It has been studied mainly as an anxiolytic and nootropic, and it is not approved outside of Russia.

How it works: It is thought to modulate GABAergic signaling, monoamine neurotransmitters, and brain derived neurotrophic factor to reduce anxiety.

Anxiety research; cognitive function; stress resilience; immune modulation

Research dose

250-750 mcg, 1–3×/day

Real-world (reported)

Stable; strong niche in nootropic/anxiolytic community

Administration

Intranasal (most common) / SubQ

Timing

Morning and/or midday; can use afternoon (non-stimulant)

Cycle length

4–8 wks cyclical; or 10-day Russian intensive

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: [ANECDOTAL] 500–750 mcg intranasal 1–2×/day. Pairs well with Semax 250–500 mcg AM.

Onset
Anxiolytic 30–60 min; cumulative effects weeks
Half-life
Not established in humans
Storage
Dry: Nasal spray: refrigerate 30 days in-use. Lyophilized: fridge/freeze. · Reconstituted: Nasal spray: cloudiness, smell. Injectable: standard flags.
Reconstitution
Injectable: add 1 mL BAC water to 1 mg vial = 1 mg/mL
Rare side effects
Severe depression requiring Rx treatment (consult physician); pregnancy
Contraindications
CNS depressants (additive); anxiolytics (additive); Pregnancy and lactation (no human safety data available); Active bleeding disorders or concurrent anticoagulant/antiplatelet therapy (Sela; Known hypersensitivity to tuftsin-derived peptidesFrequency distribution of repo; Benzodiazepines and CNS depressants: Selank modulates GABAergic signaling and ma
Drug interactions
No standard BW; baseline anxiety assessment
Recommended bloodwork
Semax: complementary (Selank anxiolysis + Semax focus). DSIP: sleep/recovery synergy.
Stacks well with
[ANECDOTAL – r/Nootropics, Longecity] 'Liquid calm.' No dependence reported. Popular for social anxiety, public speaking.
Secondary uses
Immunomodulation; antidepressant-like; PTSD support; memory enhancement
Legal status
Approved
Typical price
~$0.75–$2.25 / 500 mcg dose
Research evidence
Human trials - early or small
Indications
Anxiety and generalized anxiety disorder research; Nootropic and cognitive enhancement studies; Immunomodulation research; Neurotransmitter system modulation studies
Chemical data
CAS 129954-34-3 · C33H57N11O9 · 751.9 Da
Amino acids
7 aa

Cerebrolysin

aka FPF-1070

ModerateApproved

Cerebrolysin is a preparation of low-molecular-weight peptides and amino acids derived from purified pig brain protein, marketed in Russia, China, and parts of Europe and Asia for stroke, dementia, and traumatic brain injury. It is not approved by the FDA and remains investigational in the United States. Many randomized trials exist, but a Cochrane review found the evidence for acute ischemic stroke inconclusive.

How it works: It is believed to mimic endogenous neurotrophic factors and support neuron survival and repair, though the mechanism stays uncertain.

Ischemic stroke; vascular dementia; Alzheimer disease; traumatic brain injury

Research dose

5-30 mL, Once daily (IM/IV) ×10–20 day course

Real-world (reported)

10–20 mL IM daily ×10–20 days. 2–4 cycles per year. IV administration in clinical settings only.

Administration

IM (most practical); IV (clinical hospital)

Timing

Once daily (morning or afternoon)

Cycle length

10–20 day intensive cycles; 2–4×/year

Real-world figures are community-reported, not medical advice.

Common side effects: Nausea; dizziness; headache; sweating; injection site reactions

Community take: [ANECDOTAL – Longecity, r/Nootropics] Strong reputation in longevity and biohacker community. 10 mL IM daily ×10 days described as 'most noticeable cognitive enhancement I've experienced.' Popular in Eastern European clinics.

Onset
Acute neuroprotective effects within days; cognitive improvement 2–6 wks
Half-life
Not established
Storage
Dry: Fridge 2–8°C; never freeze; protect from light; discard any unused portion · Reconstituted: Never freeze (damages the solution); use each ampoule immediately once opened
Reconstitution
Pre-filled ampoules — no reconstitution; ready-to-inject solution
Rare side effects
Allergic reactions (porcine-derived — rare but possible); seizure threshold lowering at very high doses
Contraindications
Pork/porcine allergy; active seizure disorder; pregnancy; renal failure (high doses); Epilepsy or seizure disorder; Severe renal impairment; Hypersensitivity to porcine proteinsFrequency distribution of reported side effe; Antidepressants (MAOIs)
Drug interactions
Anticoagulants (caution with IV); anti-epileptics
Recommended bloodwork
Cognitive assessments (MMSE, MoCA) pre/post cycle; CBC; renal function baseline
Stacks well with
Semax: additive BDNF stimulation. Selank: anxiolytic complement. Epitalon: longevity stack.
Secondary uses
Depression; vascular dementia; neurological rehabilitation
Legal status
Approved
Typical price
$50–$150 / 10 mL ampoule pack
Research evidence
Human trials - phase 2 or 3
Indications
Acute ischemic stroke treatment; Alzheimer's disease therapy; Traumatic brain injury recovery; Vascular dementia treatment
Chemical data
CAS 12656-61-0 · Complex mixture · RangePharmacological RoleLow-MW neuropeptides~25%<10 kDa
Amino acids
87 aa

Key risk: The main documented concern is a hypersensitivity reaction, with caution advised in people who have epilepsy or severe kidney disease.

Substance P

aka SP, Tachykinin

AdvancedPreclinical

Substance P is an endogenous eleven amino acid neuropeptide of the tachykinin family, expressed in the nervous system and immune cells. It signals mainly through the neurokinin-1 receptor and contributes to pain transmission, neurogenic inflammation, vasodilation, and immune modulation. It is used as a research tool; approved drugs in this pathway are neurokinin-1 antagonists rather than Substance P itself.

How it works: It is a tachykinin neuropeptide that activates the neurokinin-1 receptor, driving pain signaling and neurogenic inflammation.

Pain signaling research; neurogenic inflammation; NK1 receptor pharmacology; immune modulation

Research dose

10-250 nmol/kg

Administration

Intravenous injection; intracerebral infusion

Common side effects: Not established

Half-life
Not established in humans
Rare side effects
Stevens–Johnson syndrome, neutropenia, angioedema, QT prolongation (with NK antagonists)
Secondary uses
Colitis, dental pain, anxiety disorders, stress response
Research evidence
Animal studies only
Chemical data
CAS 11035-08-8 · C63H98N18O13S · 1347.6

Humanin

aka Oral / Nasal, Oral Humanin, Nasal Humanin

AdvancedPreclinical

This entry is an oral or nasal presentation of Humanin, a mitochondrial-derived micropeptide encoded within the MT-RNR2 region. It is the same peptide as the existing Humanin row and is not a distinct compound. Reported cytoprotective, anti-inflammatory, and neuroprotective activity has been studied in models of Alzheimer disease, ischemia, and metabolic stress.

How it works: It acts through cell-surface receptors and interacts with apoptotic regulators to reduce cell death in preclinical models.

Longevity research; neuroprotection; metabolic research

Research dose

1-3 mg, Daily (intranasal) or every other day (oral)

Real-world (reported)

1–2 mg intranasal daily — very experimental.

Administration

Intranasal / Oral

Timing

Any time

Cycle length

4–8 weeks cyclical

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: [ANECDOTAL] Very limited. Intranasal route theoretically superior for CNS effects. Essentially no community data.

Onset
CNS effects 1–4 wks (intranasal); systemic weeks
Half-life
Not established
Storage
Dry: Fridge; protect from light · Reconstituted: Refrigerate; use within 14–21 days
Reconstitution
Intranasal: add 1 mL BAC water; nasal spray bottle
Rare side effects
Same as SubQ Humanin but route-specific bioavailability concerns
Contraindications
Same as Humanin; active malignancy; pregnancy
Drug interactions
Insulin; metabolic compounds
Recommended bloodwork
Cognitive assessments; fasting glucose
Stacks well with
HNG: more potent alternative. SS-31: mitochondrial complement.
Secondary uses
Alzheimer's; cognitive protection; convenience vs injection
Legal status
US: Research use only · UK: Legal for research · Canada: Legal research chemical · Australia: Schedule 4 · EU: Unregulated
Typical price
$80–$200 / 5 mg (same as SubQ)
Research evidence
Animal studies only

Nemifitide

aka INN-00835, Netamiftide

AdvancedPhase 3

Nemifitide is a synthetic pentapeptide antidepressant candidate structurally related to the neuropeptide melanocyte-inhibiting factor. It was given by subcutaneous injection and evaluated in phase 1 and phase 2 trials for major depression, where early data suggested antidepressant activity. Its precise mechanism is not fully defined, development did not reach approval, and it remains investigational.

How it works: It is a peptide related to melanocyte-inhibiting factor with proposed central antidepressant activity through an incompletely defined mechanism.

Major depressive disorder; treatment-resistant depression; pharmacokinetic research

Administration

SC

Timing

Daily subcutaneous injection for 5 consecutive days; extended protocols use 10 consecutive days

Cycle length

5-10 days

Common side effects: Injection site reactions; injection site irritation

Half-life
Not established in humans
Contraindications
Not approved for human use by any regulatory agency; Known hypersensitivity to nemifitide or formulation components; Caution in patients with serotonergic medication interactionsFrequency distribut; Theoretical interaction with serotonergic medications (SSRIs, SNRIs, MAOIs) due
Legal status
Withdrawn From Market
Research evidence
Human trials - early or small
Indications
Major depressive disorder (investigational); Treatment-resistant depression (investigational); Rapid-onset antidepressant research
Chemical data
CAS 204992-09-6 · C33H43FN10O6 · 694.76 Da
Amino acids
238 aa

Key risk: No boxed warning applies; human safety data are limited to small early trials.

Adamax

AdvancedPhase 1

BPC-157 peptide comprehensive research guide. Covers mechanism of action (VEGF, nitric oxide, tendon healing), gut protection, musculoskeletal repair, oral vs injectable research, 2026 FDA reclassification status, safety profile, and clinical trial evidence for this gastric-derived healing peptide.

How it works: Its mechanism is not established in published research; vendors propose Semax-like effects on neurotrophic signaling.

Nootropic research; neuroprotection research; cognitive research

Research dose

250-1000 mcg, Once daily

Real-world (reported)

Median: 600–1000 mcg; Most common: 200–400 mcg (per PeptIQ community data)

Administration

SubQ injection; Intranasal (documented for parent compound)

Timing

Morning fasted or near injury site

Cycle length

4-12 weeks

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: Community reports (24 PeptIQ users) show 98% positive sentiment with reported benefits in energy and cognition; however, all effects are anecdotal with no human clinical evidence.

Half-life
Not established
Storage
Dry: -20°C for long-term; 2-8°C for short-term · Reconstituted: 2-8°C (refrigerated), protected from light; use within 28-30 days
Reconstitution
Add 3.0 mL bacteriostatic water slowly down vial wall to avoid foaming; swirl gently until dissolved (30-60 seconds); do not shake
Contraindications
Pregnancy and breastfeeding (no safety data); Active cancer (theoretical concerns about growth factors); Autoimmune conditions (potential immune modulation); Children and adolescents (no pediatric data)Frequency distribution of reported s
Secondary uses
Athletic performance support, memory enhancement, focus improvement
Legal status
Preclinical Research
Typical price
$50–$150 per 10mg vial (varies by vendor)
Research evidence
Minimal published research
Indications
Gastrointestinal healing and protection (preclinical); Tendon and ligament repair research (preclinical); Musculoskeletal injury recovery (preclinical); Wound healing and tissue repair (preclinical); Neuroprotection and spinal cord injury (preclinical)
Chemical data
CAS 137525-51-0 · C62H98N16O22 · 1419.53 Da
Amino acids
59 aa

N-Acetyl Semax

AdvancedPreclinical

N-Acetyl Semax is a chemically modified form of Semax, a synthetic analog of the adrenocorticotropic hormone fragment studied for nootropic and neuroprotective effects. Adding an acetyl group is a common strategy intended to reduce enzymatic degradation and extend duration of action. Direct published research on this specific acetylated variant is minimal, and most available evidence concerns unmodified Semax.

How it works: Parent Semax rapidly raises BDNF and TrkB expression in the hippocampus, while acetylation is intended to improve stability.

Cognitive research; neuroprotection research; focus research; stroke research

Research dose

200-600 mcg, 1–2×/day

Real-world (reported)

200–400 mcg intranasal morning; some use 1×/day only vs Semax 2×/day.

Administration

Intranasal / SubQ

Timing

Morning; avoid late day

Cycle length

4–8 weeks cyclical

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: [ANECDOTAL – r/Nootropics] Community reports N-Acetyl Semax as more potent and smoother than standard Semax. 'Cleaner and stronger.' Growing preference over standard form.

Onset
Cognitive effects 30–60 min
Half-life
Not established in humans
Storage
Dry: Fridge or freeze; light sensitive · Reconstituted: Refrigerate; use within 21 days
Reconstitution
Intranasal: use as supplied. Injectable: add 1 mL BAC water to 1 mg vial.
Rare side effects
Same concerns as Semax; less data on long-term safety
Contraindications
Same as Semax
Drug interactions
Same as Semax
Recommended bloodwork
No standard BW; optional BDNF (research)
Stacks well with
Selank: anxiolytic pairing. Cerebrolysin: additive neuroprotection.
Secondary uses
Greater BDNF elevation; longer duration of action than Semax
Legal status
US: Research use only · UK: Legal for research · Canada: Legal research chemical · Australia: Schedule 4 · EU: Unregulated
Typical price
$35–$75 / nasal spray vial
Research evidence
Minimal published research
Chemical data
CAS 2920938-90-3 · C39H54N10O10S · 855.0

Semax Amidate

AdvancedPreclinical

Semax Amidate is a chemically modified form of Semax, the synthetic ACTH fragment analog studied for nootropic and neuroprotective effects. Amidation of the peptide terminus is a standard modification intended to reduce enzymatic degradation and improve stability. Published research on this specific amidated variant is minimal, and most available evidence concerns unmodified Semax.

How it works: Parent Semax rapidly raises BDNF and TrkB expression in the hippocampus, while amidation is intended to improve stability.

Cognitive research; neuroprotection research; focus research; stroke research

Research dose

200-600 mcg, 1–2×/day

Real-world (reported)

200–400 mcg intranasal morning; 1×/day preferred by many.

Administration

Intranasal / SubQ

Timing

Morning; avoid late day

Cycle length

4–8 wks cyclical

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: [ANECDOTAL] Community split between N-Acetyl Semax and Semax Amidate. Both considered improvements. 'Smoother and longer.'

Onset
30–60 min cognitive effects
Half-life
Not established in humans
Storage
Dry: Fridge or freeze; light sensitive · Reconstituted: Refrigerate; use within 21 days
Reconstitution
Intranasal: use as supplied. Injectable: add 1 mL BAC water.
Rare side effects
Same as Semax; limited additional data
Contraindications
Same as Semax
Drug interactions
Same as Semax
Recommended bloodwork
No standard BW
Stacks well with
Selank/Selank Amidate: anxiolytic pairing. N-Acetyl Semax: comparison (different modification).
Secondary uses
Longer duration; greater BDNF; enhanced BBB penetration
Legal status
US: Research use only · UK: Legal for research · Canada: Legal research chemical · Australia: Schedule 4 · EU: Unregulated
Typical price
$35–$75 / nasal spray vial
Research evidence
Minimal published research

FGL

aka NCAM FG loop peptide, FG loop peptide

AdvancedPreclinical

FGL is a synthetic peptide derived from a binding region of the neural cell adhesion molecule. In rodent and laboratory studies it has promoted synapse formation, enhanced synaptic plasticity, and facilitated memory, and it has been explored in models of aging, stroke, and cognitive impairment. It remains a preclinical research peptide with no human clinical development.

How it works: It is an NCAM-derived peptide that engages fibroblast growth factor receptor signaling to promote synaptic plasticity and neuronal survival.

Synaptic plasticity research; memory research; neuroprotection; stroke recovery research

Research dose

2-8 mg, Once daily

Real-world (reported)

2–5 mg SubQ daily — extremely limited protocols.

Administration

SubQ / Intranasal

Timing

Any time

Cycle length

4–8 wks cyclical

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: [ANECDOTAL] Essentially no significant gray-market experience. Preclinical interesting. Extreme biohacker niche only.

Onset
Cognitive changes 2–4 wks
Half-life
Not established
Storage
Dry: Fridge 2–8°C; freeze · Reconstituted: Refrigerate; use within 21 days
Reconstitution
Add 1 mL BAC water to 5 mg vial
Rare side effects
No human trial safety data
Contraindications
Active neurological disease; pregnancy
Drug interactions
Other FGFR-modulating compounds
Recommended bloodwork
Cognitive assessments; optional BDNF
Stacks well with
Semax: BDNF complement. Dihexa: advanced nootropic combination.
Secondary uses
Neuroprotection; memory consolidation; neural repair
Legal status
US: Research use only · UK: Legal for research · Canada: Legal research chemical · Australia: Schedule 4 · EU: Unregulated
Typical price
$50–$200 / 5 mg vial
Research evidence
Animal studies only

Neuropeptide Y

aka NPY

AdvancedApproved

Neuropeptide Y is an abundant 36 amino acid neuropeptide widely expressed in the central and peripheral nervous systems. It is among the most potent physiological stimulants of food intake and also contributes to energy balance, stress and anxiety responses, and cardiovascular regulation. As an endogenous molecule it serves as a research and drug-target focus rather than a therapeutic product.

How it works: It is an endogenous agonist at Y-family receptors, modulating appetite, energy homeostasis, and stress and cardiovascular signaling.

Appetite research; stress and mood research; energy metabolism; cardiovascular research

Administration

Intranasal

Timing

Delivered via nasal atomizer device; intranasal route bypasses blood-brain barrier for direct CNS delivery

Cycle length

Single administration

Common side effects: Not established

Half-life
Not established
Contraindications
Not approved for human use by any regulatory agency; Caution in individuals with cardiovascular disease (NPY causes vasoconstriction; Caution in individuals with eating disorders or obesity (NPY stimulates appetite; Potential interaction with antihypertensive medications (NPY causes vasoconstric
Legal status
Investigational
Research evidence
Animal studies only
Indications
PTSD and stress resilience research; Depression treatment research; Appetite and energy homeostasis studies; Anxiety and mood regulation research
Chemical data
CAS 82785-45-3 · C190H287N55O57 · 4253.72 Da
Amino acids
240 aa

P021

aka P21, Peptide 6, CNTF mimetic

AdvancedPreclinical

P021 is a small CNTF-derived peptidergic compound developed as a neurotrophic and neurogenic agent for neurodegeneration research. In triple-transgenic Alzheimer mouse models, chronic oral treatment increased brain-derived neurotrophic factor, reduced tau hyperphosphorylation and soluble amyloid-beta, and restored deficits in neurogenesis and cognition. Research to date is preclinical, and these effects have not been established in humans.

How it works: It increases BDNF and decreases GSK-3 beta activity, promoting neurogenesis and reducing tau hyperphosphorylation in animal models.

Alzheimer research; neurodegeneration research; neurogenesis research; cognitive research

Research dose

100-500 mcg, [ANECDOTAL] Once daily

Real-world (reported)

SubQ: 100–500 mcg daily; Intranasal: 500 mcg–4 mg daily depending on protocol

Administration

SubQ: 100-500 mcg daily x 4-6 weeks; Intranasally: 500 mcg-1mg daily, increased to 2-4mg for acute effects

Timing

[ANECDOTAL] Morning administration is preferred as P21 may have stimulating effects that could interfere with sleep if taken later in the day.

Cycle length

[ANECDOTAL] 4–6 weeks (SubQ); up to 18 months tolerated in animal studies

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: Studies in 3xTg-AD mice suggest that chronic treatment with P021 restores cognitive function, increases neurogenesis and synaptic markers, and reduces Aβ and tau. Community consensus emphasizes preclinical efficacy but acknowledges lack of human trial data.

Onset
[ANECDOTAL] P21 effects typically become noticeable within 1-2 weeks of consistent use, with peak cognitive benefits often observed after 4-6 weeks of regular administration.
Half-life
Not established
Storage
Dry: Lyophilized P21 should be stored frozen at minus 20 degrees Celsius for long-term storage. · Reconstituted: After reconstitution with bacteriostatic water, store refrigerated at 2 to 8 degrees Celsius and use within 2 to 4 weeks.
Rare side effects
Mild gastrointestinal disturbance with oral use, occasional headache or fatigue
Contraindications
Safety in humans has not been assessed.
Secondary uses
Synaptic plasticity enhancement, tau pathology reduction, BDNF upregulation
Legal status
US: Not approved by the U.S. Food and Drug Administration (FDA), European Medicines Agency (EMA), or any other major regulatory authority for human therapeutic use. The compound is classified as an investigational new drug and is legally available only for research purposes.
Typical price
[ANECDOTAL] $40–$152 per vial (vendor-dependent, research chemical pricing)
Research evidence
Animal studies only
Chemical data
CAS 1246751-68-7 · C24H40N8O10 · 600.62 g/mol
Amino acids
4 aa

TLQP-21

aka VGF-derived peptide, VGF556-576

AdvancedPreclinical

TLQP-21 is a peptide derived from the VGF precursor protein, named for its N-terminal residues. In rodent studies it modulates energy metabolism, feeding, lipolysis, stress responses, and pain and inflammatory signaling. It is reported to act mainly through the complement C3a receptor. It is an experimental research peptide with no human clinical data and no approved use.

How it works: It is a VGF-derived peptide acting largely at the complement C3a receptor, influencing metabolic, stress, and immune signaling.

Energy metabolism research; obesity research; stress and depression models; neuroimmune research

Research dose

2-32 nmol, Research dosing varies; chronic dosing studied via osmotic pump and daily injections

Administration

Intracerebroventricular injection (i.c.v.); intravenous (i.v.); intraperitoneal (i.p.)

Common side effects: Not established

Onset
Acute effects measurable within hours; chronic effects over weeks to 28 days
Half-life
Not established
Rare side effects
Application of exogenous TLQP-21 induced dose-dependent thermal hyperalgesia, which was inhibited by p38 MAPK inhibitors and COX/lipoxygenase inhibitors
Secondary uses
Prevention or reduction of motor neuron death in neurodegenerative diseases; protection of cerebellar granule cells from apoptosis
Research evidence
Animal studies only
Chemical data
CAS 869988-94-3 · C107H170N40O26 · 2432.7

Selank Amidate

AdvancedPreclinical

Selank Amidate is a chemically modified form of Selank, the synthetic tuftsin-derived heptapeptide investigated for anxiolytic and cognitive activity. Converting the peptide terminus to an amide is an established method intended to resist enzymatic degradation and better mimic native peptides. Published data on this specific amidated variant are minimal, and nearly all reliable evidence describes unmodified Selank.

How it works: Parent Selank modulates GABA receptor binding and raises hippocampal BDNF, while amidation is intended to resist enzymatic breakdown.

Anxiety research; cognitive research; neuroprotection research; stress research

Research dose

200-500 mcg, 1–2×/day

Real-world (reported)

250–400 mcg intranasal 1–2×/day.

Administration

Intranasal / SubQ

Timing

Any time (non-stimulant)

Cycle length

4–8 wks cyclical

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: [ANECDOTAL] Reported as slightly stronger than standard Selank by some users.

Onset
Anxiolytic 30–60 min
Half-life
Not established in humans
Storage
Dry: Fridge or freeze; light sensitive · Reconstituted: Refrigerate; 21 days
Reconstitution
As supplied or add 1 mL BAC water
Rare side effects
Same as Selank; even less data
Contraindications
Same as Selank
Drug interactions
Same as Selank
Recommended bloodwork
No standard BW
Stacks well with
N-Acetyl Semax: focus complement. Standard Selank: compare directly.
Secondary uses
Greater stability; longer duration than standard Selank
Legal status
US: Research use only · UK: Legal for research · Canada: Legal research chemical · Australia: Schedule 4 · EU: Unregulated
Typical price
$40–$80 / nasal spray vial
Research evidence
Minimal published research

Thymosin Beta-4

aka Tb4, TB-4, RGN-259

AdvancedInvestigational

Thymosin beta-4 is a naturally occurring 43 amino acid protein that binds and sequesters actin, influencing cell migration, tissue repair, blood vessel formation, and inflammation. Laboratory and animal studies describe roles in wound healing and tissue regeneration, and a synthetic ophthalmic formulation has been evaluated for dry eye and neurotrophic keratopathy. It is the full-length protein, distinct from the TB-500 fragment, and it is not approved.

How it works: It binds and sequesters actin to regulate the cytoskeleton, supporting cell migration, tissue repair, and blood vessel growth.

Tissue and wound repair; ophthalmic surface healing; tissue regeneration research

Research dose

1-5 mg, 2×/week

Real-world (reported)

2–5 mg SubQ 2×/week. Same protocols as TB-500 community.

Administration

Topical (eye drops)

Timing

Any time

Cycle length

4–8 weeks

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: Peer-reviewed preclinical research demonstrates adjunctive Tβ4 + ciprofloxacin restores corneal nerve integrity and visual function in bacterial keratitis, with combination therapy outperforming monotherapy approaches.

Onset
Wound/tissue healing 2–4 wks
Half-life
Not established in humans
Storage
Dry: Freeze –20°C; fridge ≤12 mo; light sensitive · Reconstituted: Refrigerate; use within 28 days
Reconstitution
Add 2 mL BAC water to 5 mg vial = 2.5 mg/mL
Rare side effects
Theoretical tumor progression (angiogenic); very high cost vs LKKTETQ fragment
Contraindications
Active malignancy; pregnancy
Drug interactions
No well-documented interactions
Recommended bloodwork
CBC; CMP baseline
Stacks well with
Ciprofloxacin (antibiotic; combination therapy significantly outperformed either agent alone)
Secondary uses
Hair growth; anti-inflammatory; corneal repair
Legal status
US: Research use only · UK: Legal for research · Canada: Legal research chemical · Australia: Schedule 4 · EU: Unregulated
Typical price
$100–$400 / 5 mg vial
Research evidence
Human trials - early or small
Chemical data
CAS 77591-33-4 · C212H350N56O78S · 4963

Pinealon

aka EDR, Glu-Asp-Arg

AdvancedPreclinical

Pinealon is a synthetic tripeptide of glutamate, aspartate, and arginine, also called EDR, from the Khavinson family of short peptide bioregulators. Research suggests it may enter cells and bind DNA promoter regions, influencing expression of genes tied to neuronal survival and oxidative stress. It has been studied in cell and animal models mainly for neuroprotection, cognitive function, and cellular aging processes.

How it works: It is thought to enter cells and bind DNA promoter regions, modulating expression of genes involved in neuronal survival and oxidative stress.

Neuroprotection research; cognitive function; oxidative stress; cellular aging

Research dose

5-10 mg, Daily ×10 day course

Real-world (reported)

5–10 mg SC daily ×10 days; 2 cycles/year.

Administration

SC / Intranasal

Timing

AM preferred

Cycle length

10 days; 2× per year

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: [ANECDOTAL] Positive reports of improved mental clarity, memory, sleep during course. Small enthusiast community.

Onset
Subjective cognitive improvement 1–2 wks of course
Half-life
Not established
Storage
Dry: Fridge 2–8°C; freeze long-term · Reconstituted: Refrigerate; use within 28 days
Reconstitution
Add 1 mL BAC water to 10 mg vial = 10 mg/mL
Rare side effects
Very limited Western safety data
Contraindications
Active malignancy; pregnancy; Pregnancy and lactation: no human safety data; epigenetic DNA/histone interactio; Active or recent cancer: preclinical signals of anti-apoptotic and proliferative; Immunocompromised individuals: Pinealon reduces neutrophil ROS/respiratory burst
Drug interactions
No significant documented interactions
Recommended bloodwork
Cognitive assessments; optional BDNF
Stacks well with
Epitalon: anti-aging stack. Cortagen: brain + heart Khavinson protocol.
Secondary uses
Brain anti-aging; memory preservation; anti-Alzheimer's (preclinical)
Legal status
Preclinical Research
Typical price
$30–$70 / 10 mg vial
Research evidence
Animal studies only
Indications
Neuroprotection and cognitive function research; Peptide bioregulation studies; Epigenetic modulation investigations; Aging and neurodegeneration research
Chemical data
CAS 175175-23-2 · C15H24N4O9 · 404.37 Da
Amino acids
17 aa

Klotho

aka Alpha-Klotho, Soluble Klotho, s-Klotho

AdvancedPreclinical

Klotho, also called alpha-Klotho, is a protein made mainly in the kidney and brain that acts as a co-receptor for FGF23 and circulates in a soluble form linked to aging. In animal studies, higher Klotho extends lifespan and protects the kidneys, blood vessels, and brain, while low levels track with age-related disease. It is an endogenous protein under investigation with no approved therapeutic form, and most human evidence is observational.

How it works: It acts as an FGF23 co-receptor and, in soluble form, regulates phosphate handling and inhibits IGF-1, Wnt, and TGF-beta signaling.

Longevity research; kidney protection; cognitive aging; vascular health

Real-world (reported)

NO ESTABLISHED HUMAN PROTOCOL

Administration

IV (clinical research)

Timing

Research only

Cycle length

Research only

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: [ANECDOTAL] Bryan Johnson and similar self-experimenters referenced. Dramatic primate cognition data drives extreme interest. Very limited human experience.

Onset
Research only
Half-life
Not established in humans
Storage
Dry: Freeze –20°C; extremely fragile · Reconstituted: On ice; use immediately; never refreeze
Reconstitution
Sterile water; fragile protein
Rare side effects
Immunogenicity; unknown effects; very fragile compound
Contraindications
ALL until Phase 1/2 safety established; malignancy; pregnancy; No formal contraindications established as klotho peptides have not entered huma; Theoretical concern with TGF-beta inhibitors in patients with active wounds or i; Theoretical concern with Wnt inhibitors in patients with osteoporosis or bone di; TGF-beta pathway therapeutics
Drug interactions
None established — research only
Recommended bloodwork
Klotho serum (ELISA); FGF23; phosphate; cognitive assessments
Stacks well with
SS-31 + MOTS-c: mitochondrial longevity protocol.
Secondary uses
Cardiovascular protection; phosphate metabolism; longevity
Legal status
Preclinical Research
Typical price
$500–$5000+ / mg (research grade)
Research evidence
Animal studies only
Indications
Anti-fibrotic therapy for chronic kidney disease (preclinical); Diabetic kidney disease treatment (preclinical); Cognitive enhancement and neuroprotection (preclinical, full protein); Anti-aging research; Vascular calcification prevention in CKD (preclinical)
Chemical data
C149H203N39O43 · 3228.42 Da
Amino acids
74 aa

Dihexa

aka PNB-0408, N-hexanoic-Tyr-Ile-(6)-aminohexanoic amide

AdvancedPreclinical

Dihexa is a small orally active compound derived from angiotensin IV and studied as a candidate for cognitive disorders including Alzheimer disease. In cell and rodent studies it promotes formation of new synaptic connections and improves learning and memory, effects shown to depend on the hepatocyte growth factor and its c-Met receptor system. No human clinical trials have been published, and it remains a research compound.

How it works: It augments the hepatocyte growth factor and c-Met receptor system, promoting formation of new synaptic connections.

Cognitive research; Alzheimer research; synaptogenesis studies

Research dose

4-20 mg, Once daily

Real-world (reported)

8–16 mg oral daily. Very potent — start low. 2–4 week cycles with extended breaks.

Administration

Oral / SubQ

Timing

Morning

Cycle length

2–4 weeks on; 4+ weeks off (limited human data requires caution)

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: [ANECDOTAL – Longecity, advanced nootropic users] 'Most potent nootropic I've tried.' Reports of significant memory/learning improvements. Long washout effects (weeks). Small community, limited experience.

Onset
Cognitive effects may take 1–2 wks to fully manifest
Half-life
Not established in humans
Storage
Dry: Room temperature (oral); fridge (injectable) · Reconstituted: Refrigerate; use within 28 days
Reconstitution
Oral: no reconstitution. Injectable: add 1 mL BAC water.
Rare side effects
Limited long-term human safety data; tumor growth concern (HGF/MET promotes cell proliferation); theoretical cancer risk
Contraindications
Active malignancy or cancer history (HGF/MET pathway is pro-proliferative); pregnancy; Not approved for human use; no established contraindications from clinical data; Theoretical contraindication in individuals with active cancer or precancerous c; Pregnancy and breastfeeding (no reproductive toxicity data available)Frequency d; No drug interaction studies have been conducted in humans or animals
Drug interactions
Other nootropics affecting BDNF/TrkB pathway
Recommended bloodwork
No standard BW; neurological baseline recommended
Stacks well with
Semax/N-Acetyl Semax: additive BDNF effects. Selank: anxiolytic complement.
Secondary uses
Synaptogenesis; neuroprotection; depression (emerging)
Legal status
Preclinical Research
Typical price
$40–$100 / 50 mg
Research evidence
Animal studies only
Indications
Cognitive enhancement research (preclinical); Alzheimer's disease modeling; Neurotrophic factor signaling studies
Chemical data
CAS 1401708-83-5 · C27H44N4O5 · 504.66 Da
Amino acids
42 aa

Key risk: Because it activates the HGF and c-Met pathway implicated in tumor growth, there is a theoretical cancer-promotion concern, and it is untested for safety in humans.

PE-22-28

aka Spadin analog, TREK-1 blocker

AdvancedPreclinical

PE-22-28 is a synthetic seven amino acid peptide derived from spadin, a fragment of the sortilin propeptide. In rodent and laboratory studies it blocks the TREK-1 potassium channel with high potency and produced antidepressant-like effects along with signs of increased hippocampal neurogenesis. It has not been tested in humans and remains an investigational research compound.

How it works: It inhibits the TREK-1 potassium channel, an action linked in animal models to antidepressant effects and enhanced neurogenesis.

Depression research; neurogenesis research; TREK-1 studies

Research dose

50-200 mcg, Once or twice daily

Real-world (reported)

100 mcg intranasal or SubQ 1–2×/day — no established protocol.

Administration

SubQ / Intranasal

Timing

Any time

Cycle length

4–8 weeks

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: [ANECDOTAL – very limited] Essentially no significant gray-market community experience. Extreme biohacker niche only.

Onset
Mood effects 1–4 wks
Half-life
Not established in humans
Storage
Dry: Fridge 2–8°C; freeze long-term; light sensitive · Reconstituted: Refrigerate; use within 21 days
Reconstitution
Add 1 mL BAC water to 1 mg vial
Rare side effects
No human clinical trial safety data; unknown long-term effects
Contraindications
Active psychiatric conditions requiring prescription medication; bipolar disorder; pregnancy; Not approved for human use by any regulatory agency; Theoretical concern with cerebrovascular disease (TREK-1 provides neuroprotectio; Known hypersensitivity to PE-22-28 or any formulation componentFrequency distrib; Theoretical interaction with other potassium channel modulators
Drug interactions
Serotonergic antidepressants (theoretical TREK-1 + serotonin interaction)
Recommended bloodwork
No standard BW; neurological baseline recommended
Stacks well with
Semax: additive BDNF. Selank: anxiolytic complement.
Secondary uses
Neuroprotection; anxiolytic; potential neuroplasticity
Legal status
Preclinical Research
Typical price
$100–$500 / 1 mg
Research evidence
Animal studies only
Indications
Antidepressant research; Neurogenesis studies; TREK-1 channel pharmacology; Cognitive enhancement research
Chemical data
CAS 1801959-12-5 · C35H55N11O9 · 773.89 Da
Amino acids
7 aa

Rapastinel

aka GLYX-13, BV-102

AdvancedPhase 2

Rapastinel is a synthetic tetrapeptide that modulates the NMDA receptor, acting at the glycine co-agonist site, and was developed as a rapid-acting antidepressant. It advanced to phase 3 as an add-on treatment for major depression under Allergan. In 2019 the pivotal phase 3 program failed to separate from placebo, and development for depression was halted.

How it works: It is an NMDA receptor modulator acting as a partial agonist at the glycine co-agonist site, influencing glutamatergic plasticity.

Major depressive disorder; adjunctive antidepressant research; NMDA-based rapid antidepressant research

Administration

IV

Timing

Administered as IV infusion in clinical trial setting only. Effects onset within 2 hours and lasted up to 7 days from a single dose in phase 2.

Cycle length

Single dose to repeated weekly dosing

Common side effects: Not established

Half-life
Not established in humans
Contraindications
Not approved for any therapeutic use (clinical development discontinued); Known hypersensitivity to rapastinel or any excipientFrequency distribution of r; Concomitant antidepressants: Phase 3 trials evaluated rapastinel as adjunctive t; Other NMDA receptor modulators (ketamine, memantine): Theoretical pharmacodynami
Legal status
Withdrawn From Market
Research evidence
Human trials - phase 2 or 3
Indications
Adjunctive treatment of treatment-resistant depression (discontinued); NMDA receptor modulation research; Rapid-acting antidepressant mechanism studies
Chemical data
CAS 117928-94-6 · C18H31N5O6 · 413.47 Da
Amino acids
219 aa

Key risk: No boxed warning applies; the pivotal phase 3 program failed its endpoints and depression development was discontinued.

N-Acetyl Selank

AdvancedPreclinical

N-Acetyl Selank is a chemically modified form of Selank, a synthetic heptapeptide analog of the immune peptide tuftsin studied mainly for anxiolytic and cognitive effects. Attaching an acetyl group to the peptide is a standard approach intended to slow enzymatic breakdown and prolong activity. Published research on this specific acetylated version is minimal, and almost all reliable evidence describes unmodified Selank.

How it works: Parent Selank modulates GABA receptor binding and raises hippocampal BDNF, while acetylation is intended to slow enzymatic breakdown.

Anxiety research; cognitive research; neuroprotection research; stress research

Research dose

200-500 mcg, 1–2×/day

Real-world (reported)

200–400 mcg intranasal 1–2×/day.

Administration

Intranasal / SubQ

Timing

Morning or as needed for anxiety; afternoon OK (non-stimulant)

Cycle length

4–8 weeks cyclical

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: [ANECDOTAL] Preferred by some over standard Selank for stronger effect at lower dose.

Onset
Anxiolytic effects 30–60 min
Half-life
Not established in humans
Storage
Dry: Fridge or freeze; light sensitive · Reconstituted: Refrigerate; use within 21 days
Reconstitution
Intranasal: use as supplied. Injectable: add 1 mL BAC water to 1 mg vial.
Rare side effects
Same concerns as Selank
Contraindications
Same as Selank
Drug interactions
Same as Selank
Recommended bloodwork
No standard BW
Stacks well with
N-Acetyl Semax: complementary pairing. Semax/NA Semax for focus + NA Selank for calm.
Secondary uses
Stronger BDNF effect; longer duration than standard Selank
Legal status
US: Research use only · UK: Legal for research · Canada: Legal research chemical · Australia: Schedule 4 · EU: Unregulated
Typical price
$35–$75 / nasal spray vial
Research evidence
Minimal published research
Chemical data
C35H59N11O10 · 793.9

Conantokin G

aka Con-G, CGX-1007

AdvancedInvestigational

Conantokin G is a small peptide isolated from the venom of the fish-hunting cone snail Conus geographus. It acts as an NR2B-selective antagonist of NMDA-type glutamate receptors. It has been examined mainly as a research tool and in early development for epilepsy, neuropathic pain, and protection against excitotoxic brain injury. It is not an approved therapeutic.

How it works: It is an NR2B-selective antagonist of NMDA-type glutamate receptors, a venom-derived peptide rich in gamma-carboxyglutamate.

NMDA receptor research; epilepsy research; neuropathic pain; neuroprotection

Research dose

1-100 mcg

Administration

Administered directly into the central nervous system, most preferably intrathecally.

Common side effects: Not established

Half-life
Not established
Secondary uses
Ischemic stroke neuroprotection, anti-apoptotic effects
Research evidence
Animal studies only
Chemical data
CAS 93438-65-4 · C88H138N26O44 · 2264.2 Da

Key risk: Human safety is not established, and NMDA receptor antagonism may carry neurological and cognitive effects.

Davunetide

aka NAP, AL-108, CP201

AdvancedPhase 2

Davunetide is an eight amino acid peptide derived from activity-dependent neuroprotective protein that is thought to stabilize neuronal microtubules. It has been tested by nasal spray and by injection in progressive supranuclear palsy, schizophrenia, and mild cognitive impairment, and as CP201 in the rare ADNP syndrome, for which it holds orphan-drug designation. A pivotal trial missed its endpoints and it remains investigational.

How it works: It is an ADNP-derived peptide believed to stabilize neuronal microtubules and support neuronal survival.

Progressive supranuclear palsy; schizophrenia cognition; mild cognitive impairment; ADNP syndrome

Administration

Intranasal

Timing

Administered as a nasal spray solution. Intranasal delivery provides direct CNS access via olfactory and trigeminal nerve pathways.

Cycle length

52 weeks

Common side effects: Headache; nasal or sinus irritation

Half-life
Not established
Contraindications
Not approved for any therapeutic use; Known hypersensitivity to davunetide or formulation excipientsFrequency distribu; No significant drug interactions identified in clinical trials; Theoretical interaction with other microtubule-targeting agents (taxanes, vinca
Legal status
Withdrawn From Market
Research evidence
Human trials - phase 2 or 3
Indications
Neuroprotection research in tauopathies; ADNP syndrome therapeutic development; Microtubule stabilization studies
Chemical data
CAS 211439-12-2 · C36H60N10O12 · 824.93 Da
Amino acids
42 aa

Key risk: No boxed warning applies; it was generally well tolerated in trials, though efficacy was not established.

Humanin G

aka HNG, S14G-Humanin, Gly14-Humanin

AdvancedPreclinical

Humanin G is a synthetic single-substitution analog of humanin in which serine at position 14 is replaced by glycine. It is reported in laboratory assays to be substantially more potent than native humanin, and it has been used as a research tool in models of Alzheimer disease, ischemia, and tissue injury. It is a distinct engineered molecule rather than a route presentation of humanin.

How it works: It is an engineered humanin variant that engages the same cytoprotective and anti-apoptotic pathways with markedly greater reported potency.

Neuroprotection research; Alzheimer models; ischemia research; tissue protection

Research dose

0.2-2 mg, Once daily or every other day

Real-world (reported)

0.5–1 mg SubQ daily — very experimental.

Administration

SubQ

Timing

Any time

Cycle length

4–8 weeks

Real-world figures are community-reported, not medical advice.

Common side effects: Not established

Community take: [ANECDOTAL] Higher potency than Humanin drives interest. Essentially no community experience.

Onset
Neuroprotective biomarker 2–4 wks
Half-life
Not established
Storage
Dry: Freeze –20°C; protect from light · Reconstituted: Refrigerate; use within 21 days
Reconstitution
Add 1 mL BAC water to 2 mg vial
Rare side effects
No human trial data; 1000× potency amplifies unknown risks
Contraindications
Active malignancy; pregnancy; insulin-sensitive conditions
Drug interactions
Insulin; metabolic compounds
Recommended bloodwork
Fasting glucose; cognitive assessments; CBC
Stacks well with
SS-31: mitochondrial stack. MOTS-c: mitokine complement.
Secondary uses
Cardiovascular protection; insulin sensitivity; retinal protection
Legal status
US: Research use only · UK: Legal for research · Canada: Legal research chemical · Australia: Schedule 4 · EU: Unregulated
Typical price
$100–$500 / 2 mg vial
Research evidence
Animal studies only

Example stacks

Beginner

Cognitive - Beginner

Semax intranasally is the most accessible and well-studied starting point. Fast-acting, easy to dose, well-tolerated. Short cycles prevent tolerance.

Primary
Semax300 mcg/day - Morning intranasal
  • • Take in the morning - stimulating effect impacts sleep if taken late
  • • Use a clean dropper, tilt head back slightly
  • • Cycle 2-4 weeks on, 2 weeks off
Intermediate

Cognitive - Intermediate

Semax drives cognitive performance while Selank addresses anxiety-driven cognitive impairment. Together they produce a focused-but-calm state.

Primary
Semax300 mcg - Morning intranasal
Support
Selank250 mcg - Morning intranasal
  • • Alternate nostrils or allow 5 minutes between each
  • • Selank is especially effective on high-stress days
  • • Use before cognitively demanding tasks

Community outcome data

Collected from users researching this goal. Not a clinical database - for general reference only.

Share your experience

Your experience helps others research this goal. All submissions are anonymous.

Poor
Excellent

Ready to actually use this research?

FREE

Two tools that turn this research into something you can actually use - no signup needed.

For educational and research purposes only. Not medical advice. Always consult a qualified healthcare provider before using any research compound.