Side-by-side · Research reference

AdamaxvsHumanin

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

BAnimal-StrongHUMAN-REVIEWED14/52 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

Humanin

Mitochondrial-Derived Peptide · Cytoprotective

24-AAPeptide lengthZhu 2022

mtDNAEncoded originZhu 2022 Shahzaib 2026

Bax/BimPrimary targetZhu 2022 Morris 2021

SQ · Experimental

01Mechanism of Action

Parameter

Adamax

Humanin

Primary target

Melanocortin receptors (MC-Rs) in hippocampus and cortex

Intracellular: Bax, Bim, tBid (pro-apoptotic Bcl-2 family). Extracellular: FPRL1/2 G-protein-coupled receptorsZhu 2022 Lue 2021

Pathway

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

Humanin binds Bax/Bim → inhibits mitochondrial outer membrane permeabilization (MOMP) → blocks cytochrome c release → prevents caspase activation → cell survival

Downstream effect

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

Suppression of apoptosis, mitochondrial stabilization, reduced oxidative stress, preservation of germ cells and neurons under stressZhu 2022 Lue 2021 Velentza 2024

Feedback intact?

Non-endocrine — devoid of adrenal axis effectsvan 1978

Not applicable — peptide acts as anti-apoptotic signal, not hormonal axis

Origin

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

Encoded by short open reading frame in mitochondrial 16S rRNA gene (MTRNR2). 24-28 amino acids. 13 homologous variants (MTRNR2L1-L13) identified.Zhu 2022 Shahzaib 2026

Antibody development

—

Not reported in animal models

02Dosage Protocols

Parameter

Adamax

Humanin

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.

Daily (IP)

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

Animal models (rat, mouse)Huang 2025 El 2022 Velentza 2024

Timing

Variable — chronic administration for circadian effects

—

Standard experimental dose (HNG)

—

4 mg/kg IP (rat)

Most common dose in rodent models.

Ex vivo bone culture

—

1 µg/mL

Protective against venetoclax-induced bone growth retardation.

Duration

—

8–12 weeks in animal studies

Human data

—

None — no clinical trials reported

Analog (HNG)

—

Gly[14]-humanin — more potent variant

Substitution at position 14 enhances cytoprotective activity.

03Metabolic / Fat Loss Evidence

Parameter

Adamax

Humanin

Direct fat loss evidence

—

None

Mechanism overlap

—

Mitochondrial health may indirectly influence metabolic efficiency, but no quantified effect

04Side Effects & Safety

Parameter

Adamax

Humanin

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

—

Animal model safety

—

Well-tolerated in rat and mouse studies at 4 mg/kg for 8–12 weeks

Human safety data

—

None — no clinical trials

Theoretical fibrillation risk

—

Induces amyloid-like fibrillation of Bax/BID. Long-term sequelae unknown.

Injection site reaction

—

Not reported in animal studies (IP route)

Reproductive safety

—

Protective in POI model (cyclophosphamide-induced), no adverse effects on fertility notedHuang 2025

Absolute Contraindications

Adamax

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

Humanin

·Unknown — no human data

Relative Contraindications

Adamax

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

Humanin

·Active malignancy (theoretical risk of anti-apoptotic effect on tumour cells)

05Administration Protocol

Parameter

Adamax

Humanin

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.

Intraperitoneal (IP) in animal models. Subcutaneous route untested. No human protocols exist.

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

Synthetic peptide reconstituted in sterile saline or PBS. No commercial formulation available.

3. Timing

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

Daily administration in animal studies. Optimal timing not characterized.

4. Storage

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

Lyophilised powder: -20 °C. Reconstituted: 4 °C, use within 7 days. Avoid freeze-thaw cycles.

5. Human use

—

No FDA approval, no IND, no clinical trials. Experimental research tool only.

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

Humanin

+ MOTS-c

Multi-pathway

View MOTS-c →

Both are mitochondrial-derived peptides. MOTS-c enhances metabolic efficiency and insulin sensitivity via AMPK activation, while humanin prevents mitochondrial apoptosis. Combined, they address mitochondrial function (MOTS-c) and survival signaling (humanin), supporting cellular resilience under metabolic and oxidative stress.

Humanin: 4 mg/kg IP · daily (animal model)
MOTS-c: 5 mg/kg IP · daily (animal model)
Frequency: Once daily
Primary benefit: Mitochondrial health, metabolic efficiency, anti-apoptotic signaling