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

AdamaxvsHGH 191AA

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
BFDA-ApprovedHUMAN-REVIEWED0/75 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
HGH 191AA
Recombinant hGH · FDA-Approved
0.024–0.034 mg/kg/dayPediatric GHD dose
2–4 hoursPlasma half-life
191 AASequence length
SQ · Daily · Evening preferred

01Mechanism of Action

Parameter
Adamax
HGH 191AA
Primary target
Melanocortin receptors (MC-Rs) in hippocampus and cortex
Growth hormone receptor (GHR) — JAK2/STAT5 pathway
Pathway
ACTH(4-10) fragment → MC-R binding → BDNF/trkB upregulation → neurotrophic signaling
GHR activation → JAK2/STAT5 → liver IGF-1 synthesis + direct metabolic effects
Downstream effect
Increased hippocampal BDNF expression, trkB tyrosine phosphorylation, enhanced conditioned avoidance learning, circadian rhythm normalizationDolotov 2006Arushanian 2008
Linear growth, lipolysis, protein synthesis, nitrogen retention, carbohydrate metabolism modulation
Feedback intact?
Non-endocrine — devoid of adrenal axis effectsvan 1978
No — exogenous GH bypasses hypothalamic-pituitary axis, suppresses endogenous pulsatility
Origin
ACTH(4-10) fragment with modified amino acid sequence at positions 8, 9, 10Teter 2001
Recombinant DNA technology — 191 AA, identical to pituitary hGH, no methionyl residue
Antibody development
Rare — <2% develop binding antibodies, typically non-neutralizing

02Dosage Protocols

Parameter
Adamax
HGH 191AA
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.
Once daily, typically evening
Evening administration mimics physiological GH pulse.
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
FDA-approved / decades of RCT data
Timing
Variable — chronic administration for circadian effects
Pediatric GHD
0.024–0.034 mg/kg/day SQ
6–7× per week dosing typical. Brand-specific ranges.
Adult GHD
0.004–0.016 mg/kg/day SQ
Start low, titrate based on IGF-1 levels.
Turner syndrome
0.045–0.050 mg/kg/day SQ
Idiopathic short stature
0.037 mg/kg/day SQ
AIDS wasting
0.1 mg/kg/day SQ (high-dose)
Short-term indication. Monitor glucose.
Monitoring
IGF-1, glucose, thyroid function, bone age (children)
Duration
Years (children until epiphyseal closure); indefinite (adult GHD)

03Metabolic / Fat Loss Evidence

Parameter
Adamax
HGH 191AA
Primary fat target
Visceral and subcutaneous adipose tissue
Mechanism
Lipolysis via hormone-sensitive lipase activation, FFA oxidation
Effect on lean mass
Significant lean mass increase (protein synthesis, nitrogen retention)
Insulin sensitivity
Acute insulin resistance (anti-insulin effect); chronic neutral-to-improved via fat loss
IGF-1 elevation
Dose-dependent, significant — primary anabolic mediator
Glucose metabolism
Hyperglycemia risk, especially high doses (AIDS wasting)
Body composition
↓ fat mass, ↑ lean mass, ↑ bone mineral density (children)
Clinical context
FDA-approved for AIDS wasting (cachexia). Off-label use for body recomposition lacks long-term safety data.

04Side Effects & Safety

Parameter
Adamax
HGH 191AA
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
Lipohypertrophy, lipoatrophy, erythema (rotate sites)
Fluid retention / Edema
Peripheral edema, arthralgia, carpal tunnel syndrome (dose-dependent)
Glucose intolerance
Hyperglycemia, new-onset diabetes (anti-insulin effect)
Intracranial hypertension
Benign intracranial hypertension (pseudotumor cerebri) — headache, visual changes, papilledema
Slipped capital femoral epiphysis
SCFE risk in children — limp, hip/knee pain (requires surgery)
Scoliosis progression
Rapid growth may unmask/progress scoliosis (monitor spine in children)
Hypothyroidism
Central hypothyroidism unmasking or worsening (monitor TSH, free T4)
Cancer risk
Contraindicated in active malignancy. Theoretical risk in cancer survivors (controversial).
Antibody formation
Rare (<2%), typically non-neutralizing. Loss of efficacy if neutralizing antibodies develop.
Pancreatitis
Rare. Higher risk in children with certain syndromes (Prader-Willi).
Gynecomastia
Adolescent males (physiological during puberty, may be exacerbated)
Absolute Contraindications
Adamax
  • ·Pregnancy and lactation (precautionary; no data)
  • ·Active cardiovascular instability (due to potential pressor effects)
HGH 191AA
  • ·Active malignancy or history of cancer (especially childhood cancer survivors with risk factors)
  • ·Acute critical illness (post-cardiac surgery, trauma, acute respiratory failure)
  • ·Diabetic retinopathy (active proliferative or severe non-proliferative)
  • ·Prader-Willi syndrome with severe obesity, sleep apnea, or respiratory impairment
  • ·Closed epiphyses (for growth indications)
Relative Contraindications
Adamax
  • ·Hypertension (monitor BP if using higher doses)
  • ·Renal impairment (natriuretic effects may alter electrolyte balance)
HGH 191AA
  • ·Diabetes mellitus (monitor closely, may require insulin adjustment)
  • ·Intracranial lesions or history of intracranial hypertension
  • ·Scoliosis (monitor curve progression)
  • ·Untreated hypothyroidism (treat before GH initiation)
  • ·Severe obesity (assess OSA risk, cardiovascular status)

05Administration Protocol

Parameter
Adamax
HGH 191AA
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 diluent (sterile water or bacteriostatic water per manufacturer) to vial. Swirl gently — do not shake. Solution should be clear, colorless. Concentration varies by brand (e.g., 5 mg or 10 mg per vial).
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
Subcutaneous — rotate sites: abdomen, thigh, buttocks, upper arm. Avoid same site within 1 cm for 2 weeks to prevent lipodystrophy.
3. Timing
Variable. Single-dose protocols for acute cognitive tasks; chronic daily dosing for circadian rhythm normalization and sustained neuroprotection.
Once daily, evening preferred (6–8 PM or pre-sleep). Mimics physiological nocturnal GH secretion. Consistency is critical.
4. Storage
Lyophilised: room temperature, light-protected. Reconstituted: refrigerate 2–8 °C, use within manufacturer-specified timeframe.
Unreconstituted: refrigerate 2–8 °C, protect from light. Reconstituted: refrigerate, use within 14–28 days (brand-specific). Do not freeze.
5. Needle
27–31G, 4–8 mm insulin syringe or pen device. Pinch skin, 45–90° angle depending on subcutaneous thickness.
6. Monitoring
Baseline and periodic: IGF-1 (target age/sex-adjusted midrange), fasting glucose, HbA1c, thyroid function (TSH, free T4), bone age (children), lipid panel. Fundoscopy if headache/visual symptoms.

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
HGH 191AA
+ Ipamorelin
Moderate
View Ipamorelin

Ipamorelin (GHRP) stimulates endogenous GH release, which is redundant when exogenous rhGH is administered. However, ipamorelin may still amplify pulsatility of remaining endogenous secretion in partial GHD or during GH dose titration. Not typically combined in standard clinical practice; more common in experimental or off-label protocols. Limited evidence for additive benefit.

HGH 191AA
Standard dose per indication
Ipamorelin
100–200 mcg SQ · morning (if used)
Note
Monitor IGF-1 closely; avoid supraphysiological levels
Primary benefit
Theoretical enhancement of pulsatility; limited clinical rationale
+ Tesamorelin
Weak
View Tesamorelin

Tesamorelin (GHRH analogue) stimulates endogenous GH secretion, which is unnecessary when exogenous rhGH is already provided. Combining both offers no mechanistic advantage and increases cost, side effects, and IGF-1 elevation risk. Not recommended in clinical practice.

Note
Combination not recommended — choose one GH modality
Primary benefit
None — redundant mechanisms