Side-by-side · Research reference

AOD-9604vsHGH Fragment 176-191

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

BAnimal-StrongHUMAN-REVIEWED28/59 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

HGH Fragment 176-191

GH Fragment · Pre-Clinical

50%Weight gain reductionNg 2000

~26 minHalf-life (est.)

No IGF-1 ↑GH axis impact

SQ · IP (animal) · Oral (tested)

01Mechanism of Action

Parameter

AOD-9604

HGH Fragment 176-191

Primary target

β3-adrenergic receptor (proposed)Ng 2000

Beta-3 adrenergic receptors on adipocytesHeffernan 2001

Pathway

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

Fragment → β3-AR upregulation → Enhanced lipolytic sensitivityHeffernan 2001

Downstream effect

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

Increased lipolysis and beta-3 AR mRNA expression without IGF-1 axis activation

Feedback intact?

No GH-axis or IGF-1 feedback

N/A — does not interact with GH/IGF-1 axis

Origin

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

Synthetic peptide derived from hGH residues 176-191; AOD9604 includes N-terminal tyrosine (177-191)Cox 2015

Antibody development

—

Not reported in available studies

02Dosage Protocols

Parameter

AOD-9604

HGH Fragment 176-191

Standard dose

250–300 mcg / dayHeffernan 2001

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

—

Frequency

Once daily, fasted

Once daily (animal models)

Lower / starter dose

150 mcg / day

—

Evidence basis

Phase 2 trials + animal-strongHeffernan 2001 Ng 2000

Animal studies only

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

—

Animal dose (oral)

—

500 mcg/kg body weightNg 2000

Obese Zucker rats, 19 days.

Animal dose (IP)

—

Not specified (14-day chronic administration)Heffernan 2001

Obese mice, daily IP injection.

Human equivalent dose

—

Not established — no published human RCTs

Duration tested

—

14–19 daysHeffernan 2001 Ng 2000

Detection window

—

50 pg/mL LOD in urine; stable metabolite extends detectionCox 2015

WADA-banned; anti-doping testing available.

Oral bioavailability

—

Demonstrated efficacy in animal oral administrationNg 2000

Potential for oral therapeutic development.

03Metabolic / Fat Loss Evidence

Parameter

AOD-9604

HGH Fragment 176-191

Primary fat target

—

Adipose tissue (general) — beta-3 AR mediated lipolysisHeffernan 2001

Weight gain reduction

—

50% reduction vs control (15.8 ± 0.6 g vs 35.6 ± 0.8 g)Ng 2000

Obese Zucker rats, 19 days oral administration.

Body fat reduction

—

Significant decrease in body weight and body fat in obese mice (14 days)Heffernan 2001

Lipolytic activity

—

Increased adipose tissue lipolytic activityNg 2000

Direct measurement in treated animals.

Beta-3 AR expression

—

Upregulated β3-AR mRNA in obese mice to lean-comparable levelsHeffernan 2001

Insulin sensitivity

—

No adverse effect — euglycemic clamp confirmedNg 2000

Contrasts with intact hGH diabetogenic effects.

IGF-1 impact

—

No elevation — fragment does not activate GH/IGF-1 axis

Beta-3 AR dependency

—

Effect abolished in β3-AR knockout miceHeffernan 2001

Confirms β3-AR as primary mechanism.

Route of administration

—

Efficacy demonstrated via oral and IP routesNg 2000 Heffernan 2001

Human evidence

—

None published — pre-clinical only

04Side Effects & Safety

Parameter

AOD-9604

HGH Fragment 176-191

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

No adverse effects observed in euglycemic clamp (animal)Ng 2000

Cancer risk

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

—

Pregnancy / OB

Avoid

—

GH/IGF-1 axis

—

No activation — avoids diabetogenic effects of full GHNg 2000

Human safety data

—

Not available — no published human trials

WADA status

—

Banned as performance-enhancing drugCox 2015

Metabolic profile

—

Six metabolites identified; CRSVEGSCG most stableCox 2015

Detection window implications for doping control.

Absolute Contraindications

AOD-9604

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

HGH Fragment 176-191

·Competitive athletes (WADA-banned)Cox 2015

Relative Contraindications

AOD-9604

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

HGH Fragment 176-191

·Absence of human safety data — experimental use only

05Administration Protocol

Parameter

AOD-9604

HGH Fragment 176-191

1. Reconstitution

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

Subcutaneous injection primary route in research context. Oral administration demonstrated efficacy in animal models at 500 mcg/kg.

2. Injection site

SQ — abdomen preferred. Rotate sites.

Once daily dosing used in animal studies. Timing not specified; GH-independent mechanism suggests flexibility.

3. Timing

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

Animal protocols: 14–19 days. Human duration not established — no published trials.

4. Storage

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

Lyophilized peptide storage per standard peptide protocols. Metabolite stability suggests refrigerated reconstituted solution viable.

5. Needle

29–31G, 4–8 mm insulin syringe.

Detectable in urine via SPE-LC-MS at 50 pg/mL LOD. Extended detection window via stable metabolite CRSVEGSCG.Cox 2015

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

HGH Fragment 176-191

— no documented stacks