Side-by-side · Research reference

AdamaxvsAOD-9604

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

BPhase 2HUMAN-REVIEWED10/47 cited

Adamax

ACTH(4-10) Analogue · Russian Nootropic

1.4×BDNF protein ↑Dolotov 2006

3×BDNF mRNA (exon III)Dolotov 2006

1.6×trkB phosphorylationDolotov 2006

Intranasal · Research Use Only

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

01Mechanism of Action

Parameter

Adamax

AOD-9604

Primary target

Melanocortin receptors (MC-Rs) in hippocampus and cortex

β3-adrenergic receptor (proposed)Ng 2000

Pathway

ACTH(4-10) fragment → MC-R binding → BDNF/trkB upregulation → neurotrophic signaling

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

Downstream effect

Increased hippocampal BDNF expression, trkB tyrosine phosphorylation, enhanced conditioned avoidance learning, circadian rhythm normalizationDolotov 2006 Arushanian 2008

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

Feedback intact?

Non-endocrine — devoid of adrenal axis effectsvan 1978

No GH-axis or IGF-1 feedback

Origin

ACTH(4-10) fragment with modified amino acid sequence at positions 8, 9, 10Teter 2001

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

Antibody development

—

02Dosage Protocols

Parameter

Adamax

AOD-9604

Animal dose (rat)

50 mcg/kg body weightDolotov 2006

Single intranasal application; produced maximal BDNF response.

—

Route

IntranasalDolotov 2006 Smolnik 2000

—

Frequency

Single-dose or chronic administration protocols

Chronic dosing normalized circadian rhythms; single-dose produced acute BDNF elevation.

Once daily, fasted

Human dose (exploratory)

Not established — limited human data

ACTH(4-10) and analogs dosed 30–60 mcg intranasally in early human studies.

—

Evidence basis

Animal (rodent, rabbit) studies; minimal human RCT data

Phase 2 trials + animal-strongHeffernan 2001 Ng 2000

Timing

Variable — chronic administration for circadian effects

Morning fasted preferred (pre-cardio)

Aligns with circadian lipolysis.

Standard dose

—

250–300 mcg / dayHeffernan 2001

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

Lower / starter dose

—

150 mcg / day

Duration

—

8–12 weeks per cycle

Reconstitution

—

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

Half-life

—

~30 min plasma

04Side Effects & Safety

Parameter

Adamax

AOD-9604

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.

—

Natriuretic effect

ACTH(4-10) exhibited natriuretic activity at lower doses (7 nmol/kg)Gruber 1984

—

Behavioral suppression

Suppression of aggression, reduced orientation-cognition reactions in rabbitsTeter 2001

May reflect anxiolytic or stress-dampening profile.

—

Long-term safety

Unknown — chronic human safety data lacking

—

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

Absolute Contraindications

Adamax

·Pregnancy and lactation (precautionary; no data)
·Active cardiovascular instability (due to potential pressor effects)

AOD-9604

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

Relative Contraindications

Adamax

·Hypertension (monitor BP if using higher doses)
·Renal impairment (natriuretic effects may alter electrolyte balance)

AOD-9604

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

05Administration Protocol

Parameter

Adamax

AOD-9604

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.

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

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 2006 Smolnik 2000

SQ — abdomen preferred. Rotate sites.

3. Timing

Variable. Single-dose protocols for acute cognitive tasks; chronic daily dosing for circadian rhythm normalization and sustained neuroprotection.

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

4. Storage

Lyophilised: room temperature, light-protected. Reconstituted: refrigerate 2–8 °C, use within manufacturer-specified timeframe.

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

5. Needle

—

29–31G, 4–8 mm insulin syringe.

06Stack Synergy

Adamax

+ Semax

Moderate

View Semax →

Both 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

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