Batch 001 - Live Allocation

Next Release: Aug 2026

Vivre Labs

Institutional Longevity

Catalogue
Single-vial Blends · one injection
Clinical Details

- Peptides -

- Single-vial Blends -

- Goals -

- Clinical Reference -

- Guides -

- Integrity -

◇ Compound Reference

FOCUS & MOODLimited EvidencePopularPopular · Cognitive

Semax

ACTH Analog · 10mg

Status

Limited Evidence

Route

Intranasal / SubQ

Half-life

~2-5 minutes plasma

Class

ACTH-fragment peptide

MechanismBDNF Upregulation

Cohort94 active prescriptions

Educational reference only - not a prescription or dosing recommendation. Some compounds are investigational or used off-label; suitability, dose, and monitoring are determined by your supervising physician. See Informed Consent & Disclaimer.

V-Series Member

$75 USD/vial

À-la-carte: $85 USD/vial · Save 12%

Vials per allocation

Member total (1×)$75

À-la-carte total$85

Flat per-vial pricing. Quantity is allocated and dispensed within your physician-supervised protocol - not a direct sale.

What this is

Heptapeptide derived from ACTH. Drives brain-derived neurotrophic factor expression and supports cognitive performance under load.

ACTH Analog · 10mg per vial · dispensed after a physician review.

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Janoshik Verified

HPLC + MS purity, every batch

Independent third-party lab

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COA Per Batch

Lot-level certificates published

Labeled vs actual mg disclosed

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Protocol Reviewed

Used in V-Series clinical stacks

Phase 1 supervision onboarding

Used inV-Series

V-02

Focus - Memory & Mental Clarity

Semax · Focus & mood

◆ Certificate of Analysis · Semax

JANOSHIK ANALYTICALHPLC + MS · Independent third-party

Lot-specific COAs for Semax are published with each batch release. Sample certificates available on request via partnerships@vivrelabs.com.

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Clinical Overview

Semax

Semax is a 7-amino-acid synthetic peptide derived from the N-terminal fragment of adrenocorticotropic hormone (ACTH 4-10). Developed in Russia and approved for clinical use there for cognitive disorders.

Demonstrates broad neuroprotective and neurotrophic activity.

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Neurotrophic Signaling

Drives BDNF and NGF expression (Russian-origin neuropeptide).

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Neuromodulation

Modulates serotonergic and dopaminergic systems.

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Evidence Status

Mechanistic data stronger than Western human-outcome evidence.

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Mechanism

How It Works

Drives BDNF (brain-derived neurotrophic factor) and NGF (nerve growth factor) expression. Modulates serotonergic and dopaminergic systems.

Demonstrated neuroprotection in ischemic models.

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Patient Bloodwork Guide

Bloodwork for Cognitive & Neuro Protocols

Nootropic / neuro - Semax, Selank, DSIP, Oxytocin, PT-141, Kisspeptin

These protocols target cognition, mood, stress regulation, and sleep. Their effects are mostly subjective and behavioral, so monitoring leans on functional and stress-axis markers more than a classic blood panel - the aim is to confirm benefit without disrupting your stress hormones or sleep architecture.

Incremental approach. These are low-dose, often short-course or as-needed protocols. Vivre tracks how you actually feel and function alongside a light marker panel, rather than chasing numbers - the subjective response is the primary signal here.

Stress axis & recovery

Cortisol rhythm (AM/PM)Confirms the protocol is calming the stress axis, not over-stimulating it. The key safety/efficacy marker for this group.

HRV (heart-rate variability)A non-blood measure of nervous-system balance and recovery - rises as stress regulation improves.

Brain & vascular health

HomocysteineElevated levels are linked to cognitive risk; a useful baseline to optimize.

BDNFA marker tied to neuroplasticity - context for neuro-supportive protocols (where testing is available).

Routine safety

CBC & CMPStandard blood count, liver, and kidney panels.

When the tests happen

BaselineCortisol rhythm, HRV, homocysteine, plus how you rate mood/focus/sleep.

Month 1HRV and a subjective check-in - is it helping, any over-stimulation?

Month 3Repeat cortisol rhythm and HRV to confirm a sustained, healthy direction.

Educational only - not medical advice or a dosing instruction. Your physician orders the tests, sets your dose, interprets results, and decides if a protocol is right for you. See the Informed Consent & Disclaimer for full terms.

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Technical Profile

Measurable Properties

Class	Synthetic ACTH(4–10) analogue heptapeptide
Studied mechanism	Neuromodulatory; BDNF-related signalling studied (largely Russian clinical/preclinical literature)
Human pharmacokinetics	Short peptide half-life; intranasal use studied
Evidence base	Moderate within regional literature; limited Western controlled trials
Form	Lyophilized powder / intranasal, under clinical protocol
Regulatory status	Not an approved therapy in most markets; physician-supervised use only

Certificate of Analysis (per batch)

Analytical method: UHPLC-MS. Batch COA available on request - link to be populated per shipment.

COA link - pending per batch

Evidence base partly regional and not extensively replicated in Western trials. Educational only.

Clinical Literature

Peer-Reviewed References

Peptide Pharmaceutical Drugs Based on Synthetic Analogues of Adrenocorticotropic Hormone Fragments

Kolomin T, Shadrina M, Slominsky P, Limborska S, Myasoedov N · 2013 · Current Pharmaceutical Design 2013;19(34):6051–6060

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Findings

Review covering Semax as an ACTH(4-10) analogue developed at the Russian Academy of Sciences. Describes preclinical mechanism (binding in basal forebrain, BDNF/NGF upregulation, monoamine modulation) and summarises Russian clinical use for stroke, dyscirculatory encephalopathy, and Parkinson's. Important methodology notes: most primary Russian clinical studies referenced are abstract-only or Russian-language and are not independently replicated in Western peer-reviewed RCTs. The Alzheimer's Drug Discovery Foundation Cognitive Vitality report (2018, public) summarises the evidence as "well-conducted studies lacking" for cognitive applications in healthy adults.

View on publisher ↗

Default Mode Network functional connectivity following Semax administration in healthy volunteers

Lebedeva IS, Panikratova YR, Sokolov OY, et al. · 2018 · Frontiers in Pharmacology / pilot study

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Findings

Small pilot study (n=24) showing that intranasal Semax (1.2 mg) altered resting-state fMRI signal in the default mode network rostral subcomponent versus placebo. Single-session, small cohort, surrogate-endpoint design - establishes mechanistic plausibility of acute CNS engagement but does not constitute outcome evidence for cognitive applications.

View on publisher ↗

Semax in prevention of disease progress and development of exacerbations in patients with cerebrovascular insufficiency

Gusev EI, Skvortsova VI, Chukanova EI · 2005 · Zh Nevrol Psikhiatr Im S S Korsakova 2005;105(2):35–40

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Findings

Open-label clinical evaluation in 187 patients with cerebrovascular insufficiency (CI) examining tolerability, clinical efficacy, and disease-course outcomes. Authors reported clinical stabilisation and reduced incidence of transient ischemic attacks under Semax treatment, with low side-effect rate including in older patients. Important methodology notes: published in Russian (Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova); single-group design without modern Western RCT controls; the abstract documents the indication and outcomes but not blinding or randomisation procedures. Cited as part of the Russian clinical-use record for Semax in cerebrovascular indications - not as Western-standard RCT evidence.

View on publisher ↗

Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia

Medvedeva EV, Dmitrieva VG, Povarova OV, Limborska SA, Skvortsova VI, Myasoedov NF, Dergunova LV · 2009 · Cellular and Molecular Neurobiology 2009;30(1):71–79

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Findings

Preclinical mechanism paper in adult rats subjected to permanent middle cerebral artery occlusion (pMCAO). Demonstrated for the first time that Semax (and its C-terminal Pro-Gly-Pro fragment) selectively activated cortical transcription of Bdnf, Ngf, and the receptor genes TrkA, TrkB, TrkC at 3 and 24 hours post-occlusion, while PGP alone showed broadly non-specific effects. Establishes the neurotrophin-upregulation mechanism that anchors the cognitive-recovery hypothesis. A subsequent 2014 genome-wide transcriptome study (Medvedeva et al., BMC Genomics) extended this finding - Semax modulated >50% of expression-changed genes toward immune and vascular-system pathways in the same pMCAO model.

View on publisher ↗

Semax has a real Russian clinical-use history (stroke, dyscirculatory encephalopathy) but is not approved in Western jurisdictions. The Alzheimer's Drug Discovery Foundation review explicitly concludes that "published literature of well-conducted studies is lacking" for cognitive applications in healthy adults, and "there is no evidence for Alzheimer's disease." Vivre presents Semax honestly: real mechanism (neurotrophin / BDNF upregulation demonstrated in pMCAO rat models), real Russian clinical use (cerebrovascular indications, n=187 cohort), but evidence base for the cognitive applications most commonly marketed by retailers is weak. Allocation requires physician supervision with explicit consent that addresses the evidence-class limitations.

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Clinical Applications

Indications

Cognitive performance under load
Stroke recovery and neuroprotection (clinical use in Russia)
ADHD adjunct (research-grade)
Component of nootropic protocols

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Pharmacokinetics

Half-Life & Duration of Action

Half-life is how long a compound stays at active plasma concentration in your body. Most peptides in this catalogue have short plasma half-lives - they clear from your bloodstream within hours, sometimes minutes. The long-half-life compounds in this catalogue are the approved-class incretins (Tirzepatide, Semaglutide, Retatrutide), which are designed for once-weekly dosing - that's the molecular engineering choice that makes weekly dosing work.

Plasma Half-Life

~2-5 minutes plasma (parent peptide). Downstream effects via the active metabolite Pro-Gly-Pro, BDNF/NGF mRNA upregulation, and enkephalinase inhibition persist for hours after the parent peptide is cleared.

Why this matters for you

If you don't tolerate a compound or need to discontinue a protocol, short-half-life peptides are out of your bloodstream within hours - not days or weeks. That said, the biological effects they initiate (tissue repair signalling, mitochondrial signalling, gene expression changes) often persist longer than the peptide itself, through downstream cellular cascades. This is normal peptide pharmacology and is important context - the molecule clears fast, but the biology takes longer to wind down.

Evidence Base

Approved in Russia. Limited Western clinical literature but growing research interest.

Dosing protocols, administration frequency, and titration schedules are physician-determined at consultation - not published on these public pages. Vivre maintains a separate internal clinical reference for treating physicians.

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Featured In

V-Series Protocols Including Semax

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Commonly Paired

Compounds Often Prescribed With Semax

Clinical co-allocation patterns observed in Vivre's allocation history. Pairings are not prescriptions - the physician determines suitability per patient at consultation.

Anxiolytic Peptide

Selank

Tuftsin Analog · 10mg

◆ cognitive pair

Semax (BDNF stimulation) paired with Selank (HPA axis modulation) - neuroplasticity plus stress-axis regulation. The core pairing in Vivre's V-02 cognitive protocol.

View Selank detail →

Metabolic Coenzyme

NAD+

High-Dose IV · 500mg

◆ cellular substrate

NAD+ provides the mitochondrial energy substrate that supports the neuroplastic effects of Semax. Both compounds appear together in V-02.

View NAD+ detail →

READY TO PROCEED

Start with the Biological Audit

Semax is verified and lot-tested, dispensed following a Biological Audit. The Audit is complimentary for the Batch 001 cohort.

$75 USD/vial

Semax · Member rate