Side-by-side · Research reference
AdamaxvsTB-500
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-REVIEWED8/46 cited
Adamax
ACTH(4-10) Analogue · Russian Nootropic
Intranasal · Research Use Only
TB-500
Thymosin β4 fragment · Healing
SQ or IM · Multiple sites · 2–3×/week
01Mechanism of Action
Parameter
Adamax
TB-500
Primary target
Melanocortin receptors (MC-Rs) in hippocampus and cortex
G-actin (sequestering) + cell-surface integrinsGoldstein 2012
Pathway
ACTH(4-10) fragment → MC-R binding → BDNF/trkB upregulation → neurotrophic signaling
Actin remodelling → cell migration; integrin-linked signaling → angiogenesis; anti-inflammatory cytokine modulationGoldstein 2012Malinda 1999
Downstream effect
Increased hippocampal BDNF expression, trkB tyrosine phosphorylation, enhanced conditioned avoidance learning, circadian rhythm normalizationDolotov 2006Arushanian 2008
Accelerated wound healing, endothelial migration, hair follicle regeneration, cardiac repair (preclinical)Goldstein 2012
Feedback intact?
Non-endocrine — devoid of adrenal axis effectsvan 1978
Endogenous protein at baseline; supplementation amplifies
Origin
ACTH(4-10) fragment with modified amino acid sequence at positions 8, 9, 10Teter 2001
17-AA active fragment of endogenous 43-AA thymosin β4 (TMSB4X gene)Goldstein 2012
Antibody development
—
—
02Dosage Protocols
Parameter
Adamax
TB-500
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.
2× per week (loading); then 1× per week (maintenance)
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-strong + Phase 2 dermal/ocular trialsGoldstein 2012
Timing
Variable — chronic administration for circadian effects
Evening or pre-rest preferred (anecdotal)
Standard dose
—
2 mg per injectionGoldstein 2012
Anecdotal community range; clinical Phase 2 trials used 70–840 mcg/kg IV.
Lower / starter dose
—
1 mg per injection
Duration
—
4–8 weeks loading; longer maintenance for chronic injury
Reconstitution
—
Bacteriostatic water, 1–2 mL per 5 mg vial
Half-life
—
~2 hours (estimated; tissue uptake longer)
04Side Effects & Safety
Parameter
Adamax
TB-500
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.
—
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
Unknown beyond Phase 2
Injection site reaction
—
Mild erythema, transient pain
GI symptoms
—
Rare nausea (anecdotal)
Cancer risk
—
Theoretical via angiogenesis pathway
Lethargy / fatigue
—
Reported anecdotally during loading phase
Antibody formation
—
No data (no long-term human trials)
Pregnancy / OB
—
Avoid
Absolute Contraindications
Adamax
- ·Pregnancy and lactation (precautionary; no data)
- ·Active cardiovascular instability (due to potential pressor effects)
TB-500
- ·Active malignancy (theoretical angiogenesis concern)
- ·Pregnancy / breastfeeding
Relative Contraindications
Adamax
- ·Hypertension (monitor BP if using higher doses)
- ·Renal impairment (natriuretic effects may alter electrolyte balance)
TB-500
- ·Cancer history
- ·Concurrent VEGF inhibitor therapy
05Administration Protocol
Parameter
Adamax
TB-500
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 5 mg vial → 2.5–5 mg/mL. Roll gently.
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 near injury site (preferred), or systemic SQ (abdomen). Rotate sites.
3. Timing
Variable. Single-dose protocols for acute cognitive tasks; chronic daily dosing for circadian rhythm normalization and sustained neuroprotection.
Evening or pre-sleep is most common anecdotal timing.
4. Storage
Lyophilised: room temperature, light-protected. Reconstituted: refrigerate 2–8 °C, use within manufacturer-specified timeframe.
Lyophilised: room temp, light-protected. Reconstituted: refrigerate, ≤30 days.
5. Needle
—
27–31G, 4–8 mm insulin syringe.
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
TB-500
+ BPC-157
StrongTB-500 and BPC-157 cover complementary halves of tissue repair: BPC-157 upregulates VEGFR2-driven angiogenesis and fibroblast outgrowth; TB-500 sequesters G-actin to enable endothelial / epithelial migration. The anecdotal canonical "healing stack" — pairs especially well for tendon and ligament injuries.
- TB-500
- 2 mg SQ · 2× per week
- BPC-157
- 250–500 mcg SQ · daily
- Primary benefit
- Combined angiogenesis + cell migration for tendon/ligament/muscle repair