Side-by-side · Research reference
AdamaxvsIGF-1 LR3
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-REVIEWED10/58 cited
Adamax
ACTH(4-10) Analogue · Russian Nootropic
Intranasal · Research Use Only
IGF-1 LR3
IGF-1 Analogue · Research
3–10×Potency vs IGF-I
Low IGFBPBinding affinity
ResearchStatus
Research only · SQ typical in animal models
01Mechanism of Action
Parameter
Adamax
IGF-1 LR3
Primary target
Melanocortin receptors (MC-Rs) in hippocampus and cortex
IGF-1 receptor (IGF-1R)McTavish 2009
Pathway
ACTH(4-10) fragment → MC-R binding → BDNF/trkB upregulation → neurotrophic signaling
IGF-1R → IRS-1 → PI3K/Akt → Cell proliferation, protein synthesis, anti-apoptosisMuhlbradt 2009
Downstream effect
Increased hippocampal BDNF expression, trkB tyrosine phosphorylation, enhanced conditioned avoidance learning, circadian rhythm normalizationDolotov 2006Arushanian 2008
Enhanced cell proliferation, muscle anabolism, inhibition of apoptosis, increased telomerase activity
Feedback intact?
Non-endocrine — devoid of adrenal axis effectsvan 1978
No — exogenous IGF analogue bypasses GH-mediated regulation
Origin
ACTH(4-10) fragment with modified amino acid sequence at positions 8, 9, 10Teter 2001
Synthetic 83-AA analogue: 13-AA N-terminal extension + Arg substitution at position 3
Antibody development
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02Dosage Protocols
Parameter
Adamax
IGF-1 LR3
Animal dose (rat)
50 mcg/kg body weightDolotov 2006
Single intranasal application; produced maximal BDNF response.
—
Frequency
Single-dose or chronic administration protocols
Chronic dosing normalized circadian rhythms; single-dose produced acute BDNF elevation.
—
Human dose (exploratory)
Not established — limited human data
ACTH(4-10) and analogs dosed 30–60 mcg intranasally in early human studies.
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Evidence basis
Animal (rodent, rabbit) studies; minimal human RCT data
Animal / in vitro only
Timing
Variable — chronic administration for circadian effects
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Research dose (animal models)
—
Variable by protocol and species
In vivo murine atherosclerosis studies used sustained delivery.
In vitro typical concentration
—
10–1000 ng/mLThomas 2007
Dose-dependent effects on follicle growth and estradiol production.
Half-maximal stimulation
—
0.6 nM LR3 vs 1.5 nM native IGF-1Price 2004
2.5-fold greater potency in lung fibroblast proliferation.
Human use
—
Not FDA-approved; no published human trials
03Metabolic / Fat Loss Evidence
Parameter
Adamax
IGF-1 LR3
Mechanism
—
IGF-1R activation → lipolytic signaling; secondary to anabolic effects
Direct lipolytic evidence
—
Minimal — primarily anabolic/anti-apoptotic in literature
Atherosclerotic plaque effects
—
Reduced stenosis and core size in ApoE-KO micevon 2011
Plaque stabilization via vSMC phenotype modulation, not direct fat loss.
Human data
—
None published
04Side Effects & Safety
Parameter
Adamax
IGF-1 LR3
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.
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Behavioral suppression
Suppression of aggression, reduced orientation-cognition reactions in rabbitsTeter 2001
May reflect anxiolytic or stress-dampening profile.
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Long-term safety
Unknown — chronic human safety data lacking
—
Hypoglycemia risk
—
Theoretical — IGF-1 analogues can lower blood glucose
Excessive cell proliferation
—
Mitogenic signaling; theoretical tumor promotion risk
Telomerase activation
—
2–10-fold increase in prostate cancer cells (PC-3, DU-145, LAPC-4)Wetterau 2003
Critically involved in cancer cell immortalization.
Oocyte degeneration
—
Increased oocyte degeneration at high doses (≥1000 ng/mL) in bovine folliclesThomas 2007
Unregulated anabolism
—
Bypasses physiological GH/IGF-1 feedback; no pulsatility control
Unknown human safety profile
—
No published human trials; safety data absent
Absolute Contraindications
Adamax
- ·Pregnancy and lactation (precautionary; no data)
- ·Active cardiovascular instability (due to potential pressor effects)
IGF-1 LR3
- ·Active malignancy or history of cancer
- ·Not approved for human use
Relative Contraindications
Adamax
- ·Hypertension (monitor BP if using higher doses)
- ·Renal impairment (natriuretic effects may alter electrolyte balance)
IGF-1 LR3
- ·Diabetes or glucose intolerance
- ·Family history of cancer
05Administration Protocol
Parameter
Adamax
IGF-1 LR3
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.
IGF-1 LR3 is not FDA-approved for human use. All administration data derives from animal or in vitro studies.
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 or intraperitoneal injection in animal models. In vitro: added directly to culture medium at concentrations of 10–1000 ng/mL.Thomas 2007
3. Timing
Variable. Single-dose protocols for acute cognitive tasks; chronic daily dosing for circadian rhythm normalization and sustained neuroprotection.
Lyophilised powder reconstituted in sterile water or buffered saline per manufacturer protocol. Store at 2–8 °C after reconstitution.
4. Storage
Lyophilised: room temperature, light-protected. Reconstituted: refrigerate 2–8 °C, use within manufacturer-specified timeframe.
Enhanced stability vs native IGF-1 due to reduced IGFBP binding; exact half-life in vivo not fully characterized in humans.
06Stack Synergy
Adamax
+ Semax
ModerateBoth 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
IGF-1 LR3
+ GHRP-6
Multi-pathwayGHRP-6 stimulates endogenous GH release, which drives hepatic IGF-1 synthesis. IGF-1 LR3 provides exogenous, IGFBP-resistant IGF signaling. Combining upstream GH stimulation with downstream IGF receptor activation creates a dual-pathway anabolic effect. However, this bypasses natural feedback and carries compounded mitogenic risk.
- GHRP-6
- 100–200 mcg SQ · 2–3× daily
- IGF-1 LR3
- Research doses variable · post-workout typical in animal models
- Note
- Research context only — no human protocols exist
- Primary benefit
- Theoretical maximal anabolic signaling (GH + IGF axes)
+ Ipamorelin
Multi-pathwayIpamorelin (selective GHRP) stimulates pulsatile GH release without cortisol/prolactin elevation. IGF-1 LR3 directly activates IGF-1R independent of GH. This stack targets both upstream (GH secretion) and downstream (IGF receptor) nodes but eliminates physiological feedback, raising safety concerns around unchecked proliferation.
- Ipamorelin
- 200–300 mcg SQ · evening
- IGF-1 LR3
- Research doses only · timing variable
- Caution
- No human data; animal/in vitro only
- Primary benefit
- Dual-axis anabolic signaling (theoretical)