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Specimen Atlas of Research Peptides81 plates · MIT
Side-by-side · Research reference

AdamaxvsGHK-Cu

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-REVIEWED8/47 cited
Adamax
ACTH(4-10) Analogue · Russian Nootropic
1.4×BDNF protein ↑Dolotov 2006
BDNF mRNA (exon III)Dolotov 2006
1.6×trkB phosphorylationDolotov 2006
Intranasal · Research Use Only
GHK-Cu
Tripeptide · Skin / Hair / Wound Healing
1–2 mgSQ dosePickart 2018
HumanMechanisticPickart 2018Zink 2003
HoursHalf-life
SQ or topical · Local · Daily or 2-3×/week

01Mechanism of Action

Parameter
Adamax
GHK-Cu
Primary target
Melanocortin receptors (MC-Rs) in hippocampus and cortex
Copper-dependent enzymes (lysyl oxidase, SOD); regulator of >4000 human genesPickart 2018
Pathway
ACTH(4-10) fragment → MC-R binding → BDNF/trkB upregulation → neurotrophic signaling
Cu(II) delivery via GHK chelation → ↑collagen / elastin / GAG synthesis; ↓inflammatory cytokines; ↑hair follicle growth-factor signalingPickart 2018
Downstream effect
Increased hippocampal BDNF expression, trkB tyrosine phosphorylation, enhanced conditioned avoidance learning, circadian rhythm normalizationDolotov 2006Arushanian 2008
Skin firmness + texture improvement, accelerated wound healing, hair regrowth, anti-inflammatory actionPickart 2018Zink 2003
Feedback intact?
Non-endocrine — devoid of adrenal axis effectsvan 1978
Replaces declining endogenous levels
Origin
ACTH(4-10) fragment with modified amino acid sequence at positions 8, 9, 10Teter 2001
Endogenous tripeptide first isolated from human plasma; declines from ~200 ng/mL at age 20 to ~80 ng/mL at age 60Pickart 2018
Antibody development

02Dosage Protocols

Parameter
Adamax
GHK-Cu
Animal dose (rat)
50 mcg/kg body weightDolotov 2006
Single intranasal application; produced maximal BDNF response.
Route
Frequency
Single-dose or chronic administration protocols
Chronic dosing normalized circadian rhythms; single-dose produced acute BDNF elevation.
Daily or 2–3× per week (SQ)
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
Human-mechanistic + topical clinical studiesPickart 2018
Timing
Variable — chronic administration for circadian effects
No specific time; evening preferred for topicals
Standard SQ dose
1–2 mg / dayPickart 2018
Anecdotal injectable range; topical creams use 0.1–2% solutions.
Topical concentration
0.1–2.0% in serum / cream
Lower / starter dose
0.5 mg / day SQ
Duration
8–12 weeks for visible skin / hair effect
Reconstitution
Bacteriostatic water; light-protected
Half-life
Hours (estimated; rapid tissue uptake)

04Side Effects & Safety

Parameter
Adamax
GHK-Cu
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
Erythema, mild pruritus (common)
Topical irritation
Mild redness, transient stinging
Copper accumulation
Theoretical with very high chronic doses
Allergic reaction
Rare hypersensitivity to copper
Pregnancy / OB
Avoid topical and SQ — insufficient data
Wilson disease
Contraindicated
Absolute Contraindications
Adamax
  • ·Pregnancy and lactation (precautionary; no data)
  • ·Active cardiovascular instability (due to potential pressor effects)
GHK-Cu
  • ·Wilson disease (copper-overload disorder)
  • ·Pregnancy / breastfeeding
  • ·Known copper hypersensitivity
Relative Contraindications
Adamax
  • ·Hypertension (monitor BP if using higher doses)
  • ·Renal impairment (natriuretic effects may alter electrolyte balance)
GHK-Cu
  • ·Hemochromatosis (copper-iron crosstalk theoretical)
  • ·Concurrent copper-chelator therapy

05Administration Protocol

Parameter
Adamax
GHK-Cu
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 1–2 mL bacteriostatic water to a 50 mg vial → 25–50 mg/mL. Use within 30 days, refrigerated.
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
SQ — local to the area of interest (face, scalp) for skin / hair indications. Rotate sites.
3. Timing
Variable. Single-dose protocols for acute cognitive tasks; chronic daily dosing for circadian rhythm normalization and sustained neuroprotection.
Anytime; evening preferred. Topical: apply to clean dry skin.
4. Storage
Lyophilised: room temperature, light-protected. Reconstituted: refrigerate 2–8 °C, use within manufacturer-specified timeframe.
Lyophilised: room temp, light-protected. Reconstituted: refrigerate, light-protected, ≤30 days.
5. Needle
30–31G, short (4–6 mm) for shallow SQ. Topical: clean fingertips, no needle.

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
GHK-Cu
+ BPC-157
Moderate
View BPC-157

GHK-Cu drives ECM remodelling and copper-dependent enzymes; BPC-157 upregulates VEGFR2 angiogenesis and fibroblast migration. The pathways are non-overlapping and complementary — together they accelerate wound healing more than either alone in anecdotal protocols.

GHK-Cu
1–2 mg SQ · daily near wound
BPC-157
250–500 mcg SQ · daily near wound
Primary benefit
Combined ECM rebuilding + angiogenesis for tissue repair