Side-by-side · Research reference

AdamaxvsARA 290

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-REVIEWED17/59 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

ARA 290

EPO-Derived Peptide · Innate Repair Receptor Agonist

4 mgDaily doseBrines 2015 Culver 2017

28 daysPhase 2 durationCulver 2017

Non-erythropoieticSafety profileBrines 2015 Liu 2014

SQ · DailyBrines 2015 Culver 2017

01Mechanism of Action

Parameter

Adamax

ARA 290

Primary target

Melanocortin receptors (MC-Rs) in hippocampus and cortex

Innate repair receptor (EPO receptor / CD131 heterodimer)

Pathway

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

EPO/CD131 → JAK2 activation → PI3K/AKT, MAPK signaling → anti-inflammatory, anti-apoptotic cascades

Downstream effect

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

Tissue protection, nerve fiber regeneration, suppression of inflammatory macrophage activation, altered T-cell differentiation (↑Treg, ↑Th2, ↓Th1)Liu 2014 Culver 2017

Feedback intact?

Non-endocrine — devoid of adrenal axis effectsvan 1978

N/A — does not interact with hematopoietic EPO receptorLiu 2014

Origin

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

11-amino-acid sequence from EPO helix B, engineered to eliminate hematopoietic activity while retaining tissue-protective properties

Antibody development

—

Not reported in clinical trials

02Dosage Protocols

Parameter

Adamax

ARA 290

Animal dose (rat)

50 mcg/kg body weightDolotov 2006

Single intranasal application; produced maximal BDNF response.

—

Route

IntranasalDolotov 2006 Smolnik 2000

SubcutaneousBrines 2015

Frequency

Single-dose or chronic administration protocols

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

Once daily

Self-administered subcutaneously.

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 RCTsCulver 2017 Brines 2015

64-subject sarcoidosis trial, type 2 diabetes trial.

Timing

Variable — chronic administration for circadian effects

Any time of day

No circadian dependence reported.

Standard dose (Phase 2)

—

4 mg / dayBrines 2015 Culver 2017

Sarcoidosis SFN and diabetic neuropathy trials.

Duration

—

28 days (Phase 2)Culver 2017

Corneal nerve improvements observed by day 28.

03Metabolic / Fat Loss Evidence

Parameter

Adamax

ARA 290

Primary effect

—

Improved metabolic control (HbA1c, fasting glucose)Brines 2015

Secondary to neuropathy treatment; direct lipolytic effects not established.

HbA1c

—

Significant reduction vs placebo

Observed in type 2 diabetes + neuropathy trial.

Fasting glucose

—

Improved in ARA 290 group

Body composition

—

Not directly quantified

Fat loss not a primary endpoint; metabolic improvements may reflect insulin sensitivity.

04Side Effects & Safety

Parameter

Adamax

ARA 290

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, transient

Hematopoiesis

—

None — non-erythropoietic

Distinguishes ARA 290 from native EPO.

Cardiovascular

—

No thrombotic events or hypertension reported

Immunogenicity

—

No antibody formation reported

Tolerability

—

Well-tolerated in Phase 2 trialsCulver 2017 Brines 2015

Absolute Contraindications

Adamax

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

ARA 290

·Hypersensitivity to ARA 290

Relative Contraindications

Adamax

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

ARA 290

·Active malignancy (theoretical EPO-axis concern; not observed in trials)

05Administration Protocol

Parameter

Adamax

ARA 290

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.

Reconstitute lyophilised powder per manufacturer instructions. Use sterile technique.

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

Subcutaneous — abdomen, thigh, or upper arm. Rotate sites to avoid lipohypertrophy.

3. Timing

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

Once daily, any time of day. Self-administered in Phase 2 trials.Brines 2015

4. Storage

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

4 mg daily for 28 days (Phase 2 protocol). Duration for chronic use not established.Culver 2017

5. Storage

—

Lyophilised: store at controlled room temperature. Reconstituted: refrigerate, use within specified timeframe.

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

ARA 290

+ BPC-157

Moderate

View BPC-157 →

ARA 290 targets the innate repair receptor (EPO/CD131) for nerve regeneration and anti-inflammatory signaling, while BPC-157 promotes angiogenesis and tissue repair through distinct mechanisms (likely involving VEGF, growth hormone receptor pathways). Combined, they may address both neuroinflammation and structural tissue repair in neuropathy or injury models. No direct clinical data; mechanistic overlap in tissue protection.

ARA 290: 4 mg SQ · daily
BPC-157: 250–500 mcg SQ · daily
Frequency: Once daily, same or separate injections
Primary benefit: Nerve regeneration, pain reduction, tissue healing