Side-by-side · Research reference

AOD-9604vsGLP-1 (7-37)

Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.

APhase 2HUMAN-REVIEWED10/47 cited

BHuman-MechanisticHUMAN-REVIEWED16/43 cited

AOD-9604

HGH 176-191 · β3-AR Lipolytic

250–300 mcgDaily doseHeffernan 2001

Phase 2Evidence levelHeffernan 2001 Ng 2000

~30 minHalf-life

SQ · Abdomen · Daily fasted

GLP-1 (7-37)

Incretin Hormone · Native Peptide

~2 minHalf-lifeAlavi 2021 Ding 2017

3297.7 DaMolecular weightAlavi 2021

1922Discovery year

Research use only · IV/SC in experimental settings

01Mechanism of Action

Parameter

AOD-9604

GLP-1 (7-37)

Primary target

β3-adrenergic receptor (proposed)Ng 2000

GLP-1 receptor (class B GPCR)Koole 2015

Pathway

β3-AR activation → cAMP → hormone-sensitive lipase activation → triglyceride breakdown to FFA + glycerolNg 2000

GLP-1R activation → cAMP production → PKA signaling → insulin secretion (pancreatic β-cells)Lu 2025 Koole 2015

Downstream effect

Lipolysis of adipose tissue triglycerides; FFA release for oxidation; minimal IGF-1 / insulin impactHeffernan 2001

Glucose-dependent insulin release, glucagon suppression, delayed gastric emptying, reduced food intakeLu 2025 Ding 2017

Feedback intact?

No GH-axis or IGF-1 feedback

Yes — physiological secretion and degradation preserved

Origin

Synthetic modified C-terminal hexadecapeptide fragment of human GH (176-191) with N-terminal Tyr substitutionNg 2000

Endogenous peptide cleaved from proglucagon in intestinal L cells; secreted postprandially

Antibody development

—

02Dosage Protocols

Parameter

AOD-9604

GLP-1 (7-37)

Standard dose

250–300 mcg / dayHeffernan 2001

Anecdotal SQ range. Phase 2 trial dose 1 mg/day oral.

—

Frequency

Once daily, fasted

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Lower / starter dose

150 mcg / day

—

Evidence basis

Phase 2 trials + animal-strongHeffernan 2001 Ng 2000

—

Duration

8–12 weeks per cycle

—

Reconstitution

Bacteriostatic water, 1 mL per 2 mg vial → 2 mg/mL

—

Timing

Morning fasted preferred (pre-cardio)

Aligns with circadian lipolysis.

—

Half-life

~30 min plasma

~2 minutes (plasma)Alavi 2021 Ding 2017

Requires continuous infusion for sustained effect.

Clinical use

—

None — native GLP-1 not used therapeutically

Engineered analogues (semaglutide, liraglutide) used clinically.Friedman 2024

Research dosing

—

Variable — 0.1–10 nmol/kg in animal models

Used as reference standard for analogue comparison.

Modified analogues

—

t½ extended to 13 h (liraglutide), 165 h (semaglutide)

Via DPP-4 resistance + fatty acid acylation.

03Metabolic / Fat Loss Evidence

Parameter

AOD-9604

GLP-1 (7-37)

Mechanism

—

GLP-1R activation in hypothalamic satiety centers (arcuate nucleus) reduces food intakeLu 2025

Effect demonstrated with long-acting analogues (liraglutide).Lu 2025

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

AOD-9604

GLP-1 (7-37)

Injection site reaction

Mild erythema

—

GI symptoms

Rare mild nausea

—

Cardiovascular

Possible mild HR increase via β3-AR (theoretical β1 cross-reactivity)

—

IGF-1 elevation

None — designed to lack GH-axis activityHeffernan 2001

—

Insulin sensitivity

Neutral — no glucose impairmentHeffernan 2001

—

Cancer risk

No GH/IGF-1 axis activity → lower theoretical risk vs HGH

—

Pregnancy / OB

Avoid

—

Native GLP-1

—

Well-tolerated in research settings; no prolonged exposure data

Hypoglycemia risk

—

Low — insulin secretion is glucose-dependent

Analogue side effects

—

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

AOD-9604

·Pregnancy / breastfeeding
·Severe cardiovascular disease (caution with β-receptor agonists)

GLP-1 (7-37)

—

Relative Contraindications

AOD-9604

·Concurrent β-blocker therapy (theoretical antagonism)
·Pheochromocytoma

GLP-1 (7-37)

—

05Administration Protocol

Parameter

AOD-9604

GLP-1 (7-37)

1. Reconstitution

Add 1 mL bacteriostatic water to 2 mg vial → 2 mg/mL = 200 mcg per 0.1 mL.

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. Injection site

SQ — abdomen preferred. Rotate sites.

Lyophilised peptide stored at -20°C or below. Reconstituted solutions should be prepared fresh and used immediately due to rapid degradation.

3. Timing

Morning, fasted, ideally pre-cardio for amplified fat oxidation.

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 temp, light-protected. Reconstituted: refrigerate, ≤30 days.

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5. Needle

29–31G, 4–8 mm insulin syringe.

—

06Stack Synergy

AOD-9604

+ MOTS-c

Moderate

View MOTS-c →

AOD-9604 mobilises FFAs from adipose via β3-AR; MOTS-c upregulates AMPK / PGC-1α / FAO machinery so that mobilised FFAs are efficiently oxidised. The pathways are sequential — supply (AOD) plus demand (MOTS-c) — and produce more durable lipolytic effects than either alone in anecdotal protocols.

AOD-9604: 250–300 mcg SQ · morning fasted (daily)
MOTS-c: 5 mg SQ · 2–3× per week (pre-workout)
Primary benefit: Fat mobilisation + mitochondrial oxidation, no IGF-1 concern

GLP-1 (7-37)

— no documented stacks