Side-by-side · Research reference
AdamaxvsGLP-1 (7-37)
Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.
AAnimal-StrongHUMAN-REVIEWED20/47 cited
BHuman-MechanisticHUMAN-REVIEWED16/43 cited
Adamax
ACTH(4-10) Analogue · Russian Nootropic
Intranasal · Research Use Only
GLP-1 (7-37)
Incretin Hormone · Native Peptide
Research use only · IV/SC in experimental settings
01Mechanism of Action
Parameter
Adamax
GLP-1 (7-37)
Primary target
Melanocortin receptors (MC-Rs) in hippocampus and cortex
GLP-1 receptor (class B GPCR)Koole 2015
Pathway
ACTH(4-10) fragment → MC-R binding → BDNF/trkB upregulation → neurotrophic signaling
GLP-1R activation → cAMP production → PKA signaling → insulin secretion (pancreatic β-cells)Lu 2025Koole 2015
Downstream effect
Increased hippocampal BDNF expression, trkB tyrosine phosphorylation, enhanced conditioned avoidance learning, circadian rhythm normalizationDolotov 2006Arushanian 2008
Feedback intact?
Non-endocrine — devoid of adrenal axis effectsvan 1978
Yes — physiological secretion and degradation preserved
Origin
ACTH(4-10) fragment with modified amino acid sequence at positions 8, 9, 10Teter 2001
Endogenous peptide cleaved from proglucagon in intestinal L cells; secreted postprandially
Antibody development
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02Dosage Protocols
Parameter
Adamax
GLP-1 (7-37)
Animal dose (rat)
50 mcg/kg body weightDolotov 2006
Single intranasal application; produced maximal BDNF response.
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Frequency
Single-dose or chronic administration protocols
Chronic dosing normalized circadian rhythms; single-dose produced acute BDNF elevation.
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Human dose (exploratory)
Not established — limited human data
ACTH(4-10) and analogs dosed 30–60 mcg intranasally in early human studies.
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Evidence basis
Animal (rodent, rabbit) studies; minimal human RCT data
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Timing
Variable — chronic administration for circadian effects
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Clinical use
—
None — native GLP-1 not used therapeutically
Engineered analogues (semaglutide, liraglutide) used clinically.Friedman 2024
Research dosing
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Variable — 0.1–10 nmol/kg in animal models
Used as reference standard for analogue comparison.
Modified analogues
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t½ extended to 13 h (liraglutide), 165 h (semaglutide)
Via DPP-4 resistance + fatty acid acylation.
03Metabolic / Fat Loss Evidence
Parameter
Adamax
GLP-1 (7-37)
Mechanism
—
Native GLP-1 efficacy
—
Minimal — rapid degradation prevents sustained appetite suppression
Gastric emptying
—
Delayed in animal models, contributing to satiety
Body weight impact
—
Not observed with native GLP-1 — requires analogue formulations
04Side Effects & Safety
Parameter
Adamax
GLP-1 (7-37)
Cardiovascular effects
ACTH(4-10) fragments may have pressor and cardioaccelerator actions at high dosesGruber 1984
Effects attenuated by α/β-receptor antagonists; observed at 30–1000 nmol/kg IV in rats.
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Behavioral suppression
Suppression of aggression, reduced orientation-cognition reactions in rabbitsTeter 2001
May reflect anxiolytic or stress-dampening profile.
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Long-term safety
Unknown — chronic human safety data lacking
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Native GLP-1
—
Well-tolerated in research settings; no prolonged exposure data
Hypoglycemia risk
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Low — insulin secretion is glucose-dependent
Analogue side effects
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Nausea, vomiting, diarrhea (GLP-1R agonists)
Not applicable to native GLP-1 due to non-therapeutic use.
GLP-1 resistance
—
High glucose-induced PKCβ overexpression may reduce GLP-1 responsiveness in endothelial cellsPujadas 2016
Absolute Contraindications
Adamax
- ·Pregnancy and lactation (precautionary; no data)
- ·Active cardiovascular instability (due to potential pressor effects)
GLP-1 (7-37)
—Relative Contraindications
Adamax
- ·Hypertension (monitor BP if using higher doses)
- ·Renal impairment (natriuretic effects may alter electrolyte balance)
GLP-1 (7-37)
—05Administration Protocol
Parameter
Adamax
GLP-1 (7-37)
1. Reconstitution (if lyophilised)
Add sterile water or bacteriostatic water to lyophilised vial per manufacturer guidance. Roll gently — do not shake. Ensure clarity before use.
Native GLP-1(7-37) is not formulated for therapeutic use. Administered IV or SC in experimental protocols to study GLP-1R pharmacology and as reference standard for analogue development.
2. Route
Intranasal administration is the primary route in animal and exploratory human studies. Delivered via nasal spray or dropper to ensure mucosal absorption.Dolotov 2006Smolnik 2000
Lyophilised peptide stored at -20°C or below. Reconstituted solutions should be prepared fresh and used immediately due to rapid degradation.
3. Timing
Variable. Single-dose protocols for acute cognitive tasks; chronic daily dosing for circadian rhythm normalization and sustained neuroprotection.
For therapeutic GLP-1R activation, use FDA-approved long-acting analogues: semaglutide (once weekly), liraglutide (once daily), dulaglutide (once weekly), or exenatide (twice daily or once weekly).
4. Storage
Lyophilised: room temperature, light-protected. Reconstituted: refrigerate 2–8 °C, use within manufacturer-specified timeframe.
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06Stack Synergy
Adamax
+ Semax
ModerateBoth Adamax and Semax are ACTH(4-10)-derived nootropics acting via melanocortin receptors and BDNF upregulation. Adamax has distinct amino acid modifications at positions 8-10, potentially offering complementary receptor binding profiles or metabolic stability. Stacking may amplify neurotrophic signaling and cognitive enhancement, though direct synergy studies are absent. Theoretical multi-pathway benefit.
- Adamax
- Research dose intranasal
- Semax
- 300–600 mcg intranasal
- Frequency
- Once daily, morning or pre-cognitive task
- Primary benefit
- Enhanced BDNF upregulation, cognitive performance, neuroprotection
GLP-1 (7-37)
— no documented stacks