Side-by-side · Research reference

AdamaxvsGHRP-2

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-REVIEWED15/42 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

GHRP-2

Hexapeptide GHRP · Phase 2 (clinical diagnostic)

100–300 mcgPer doseBowers 1990

Phase 2Evidence levelBowers 1990 Sigalos 2018

~30 minHalf-lifeMalagón 1999

SQ · Multiple sites · 1–3×/day

01Mechanism of Action

Parameter

Adamax

GHRP-2

Primary target

Melanocortin receptors (MC-Rs) in hippocampus and cortex

Ghrelin receptor (GHS-R1a) on anterior pituitaryBowers 1990

Pathway

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

GHS-R1a → Gαq → Ca²⁺ → GH vesicle exocytosisBowers 2002

Downstream effect

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

Strong GH pulse + IGF-1 elevation; appetite increase via ghrelin agonismBowers 2002

Feedback intact?

Non-endocrine — devoid of adrenal axis effectsvan 1978

Yes, with somatostatin feedback active

Origin

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

Synthetic hexapeptide; developed by Bowers/Tulane group in the 1980sBowers 1990

Antibody development

—

02Dosage Protocols

Parameter

Adamax

GHRP-2

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.

1–3× per day

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 + clinical diagnostic useBowers 1990

Timing

Variable — chronic administration for circadian effects

Pre-sleep + fasted preferred

Standard dose

—

100–300 mcg per injectionBowers 1990

Lower / starter dose

—

50 mcg per dose

Duration

—

8–12 weeks on / 4 off (anecdotal)

Reconstitution

—

Bacteriostatic water

Half-life

—

~30 minMalagón 1999

04Side Effects & Safety

Parameter

Adamax

GHRP-2

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

—

Cortisol elevation

—

Mild but measurableBowers 1990

Prolactin elevation

—

Mild but measurable

Hunger

—

Strong appetite increase

Injection site reaction

—

Mild erythema

IGF-1 elevation

—

Strong; monitor with chronic high-dose use

Cancer risk

—

Contraindicated in active malignancy

Pregnancy / OB

—

Avoid

Absolute Contraindications

Adamax

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

GHRP-2

·Active malignancy
·Pregnancy / breastfeeding

Relative Contraindications

Adamax

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

GHRP-2

·Untreated diabetes

05Administration Protocol

Parameter

Adamax

GHRP-2

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 2 mL bacteriostatic water to 5 mg vial → 2.5 mg/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 or thigh. Rotate sites.

3. Timing

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

Pre-sleep + fasted preferred.

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

GHRP-2

+ CJC-1295 (no DAC)

Strong

View CJC-1295 (no DAC) →

GHRP-2 + CJC-1295-no-DAC is a higher-amplitude alternative to the ipamorelin + CJC-1295 stack. GHRP-2 produces a stronger pulse but with cortisol + prolactin signal — choose when maximum GH amplitude is the goal and the side-effect tolerance is acceptable.

GHRP-2: 100–200 mcg SQ · pre-sleep
CJC-1295 (no DAC): 100 mcg SQ · same injection
Primary benefit: High-amplitude GH pulse, body composition

Bowers 1990 Teichman 2006