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

AdamaxvsFollistatin-344

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
BHuman-MechanisticHUMAN-REVIEWED4/58 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
Follistatin-344
Myostatin/Activin Antagonist · Research Use
15–25%FST/MSTN ratio ↑
344 AACirculating isoform
ResearchPhase status
Research · No approved protocol

01Mechanism of Action

Parameter
Adamax
Follistatin-344
Primary target
Melanocortin receptors (MC-Rs) in hippocampus and cortex
Myostatin (MSTN/GDF-8) and Activin A
Pathway
ACTH(4-10) fragment → MC-R binding → BDNF/trkB upregulation → neurotrophic signaling
FST-344 binds MSTN/Activin → prevents ActRIIB receptor engagement → disinhibits muscle anabolism
Downstream effect
Increased hippocampal BDNF expression, trkB tyrosine phosphorylation, enhanced conditioned avoidance learning, circadian rhythm normalizationDolotov 2006Arushanian 2008
Elevated follistatin/myostatin ratio, increased muscle protein synthesis, attenuated muscle atrophy signalingJeong 2026
Feedback intact?
Non-endocrine — devoid of adrenal axis effectsvan 1978
Yes — indirect antagonist, preserves endogenous regulation
Origin
ACTH(4-10) fragment with modified amino acid sequence at positions 8, 9, 10Teter 2001
Endogenous glycoprotein, 344-AA isoform lacking heparin-binding domain (vs FST-315)
Antibody development
Not documented in available trials (endogenous protein)

02Dosage Protocols

Parameter
Adamax
Follistatin-344
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.
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
Human observational / biomarker studies
Timing
Variable — chronic administration for circadian effects
Clinical protocol
None — no approved dosing regimen
Follistatin-344 measured as endogenous biomarker, not administered exogenously in cited trials.
Research context
Endogenous modulation via exercise + nutrition
Resistance training + EAA intake elevated FST/MSTN ratio by 15–25% in 12-week RCT (older women).
Half-life
Not established
Circulating isoform; lacks tissue-binding domain of FST-315.

03Metabolic / Fat Loss Evidence

Parameter
Adamax
Follistatin-344
Primary target
Muscle mass preservation, not direct lipolysis
Indirect fat effect
Increased lean mass → elevated resting metabolic rate
Not primary mechanism. Muscle-sparing during deficit.
Clinical evidence
Lorcaserin trial (6 mo) showed no MAFI axis changes during fat lossRamirez-Cisneros 2026
Suggests follistatin not primary driver of fat loss in weight-reduction interventions.
GLP-1RA studies
Liraglutide (35 days) — no significant MAFI axis modulation despite fat/lean changes

04Side Effects & Safety

Parameter
Adamax
Follistatin-344
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
Clinical safety data
None — no human exogenous administration trials in literature
Theoretical risks
Excessive myostatin inhibition → muscle overgrowth, impaired glucose tolerance
Based on myostatin-null animal models and clinical myostatin inhibitor trials.
Endogenous elevation (exercise)
No adverse effects reported in 12-week resistance + EAA trials
Cancer risk (theoretical)
Myostatin inhibition may promote tumor growth in malignancy (preclinical data)
Regulatory status
Not approved for human use — research peptide only
Absolute Contraindications
Adamax
  • ·Pregnancy and lactation (precautionary; no data)
  • ·Active cardiovascular instability (due to potential pressor effects)
Follistatin-344
  • ·Active malignancy
  • ·No approved protocol — research use only
Relative Contraindications
Adamax
  • ·Hypertension (monitor BP if using higher doses)
  • ·Renal impairment (natriuretic effects may alter electrolyte balance)
Follistatin-344
  • ·Insulin resistance / Type 2 diabetes (monitor glucose)
  • ·Pregnancy / lactation (unknown safety profile)

05Administration Protocol

Parameter
Adamax
Follistatin-344
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.
Follistatin-344 is not approved for human administration. All cited studies measure endogenous serum follistatin as a biomarker, not as an exogenous therapeutic agent.
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
Resistance exercise combined with essential amino acid (EAA) supplementation elevated the follistatin/myostatin ratio by 15–25% in 12-week randomized trials. Protein intake (1.2–1.5 g/kg/day) synergizes with training to upregulate endogenous follistatin.
3. Timing
Variable. Single-dose protocols for acute cognitive tasks; chronic daily dosing for circadian rhythm normalization and sustained neuroprotection.
Serum follistatin and follistatin/myostatin ratio are used diagnostically in sarcopenia screening and as biomarkers of muscle anabolic balance in clinical trials.
4. Storage
Lyophilised: room temperature, light-protected. Reconstituted: refrigerate 2–8 °C, use within manufacturer-specified timeframe.
Gene therapy and recombinant follistatin delivery are under preclinical investigation for muscular dystrophy and sarcopenia. No human safety or efficacy data for exogenous FST-344 administration.

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
Follistatin-344
+ BPC-157
Multi-pathway
View BPC-157

Follistatin-344 (myostatin antagonist) and BPC-157 (tissue repair peptide) address complementary pathways in muscle recovery. FST-344 promotes muscle protein synthesis by disinhibiting myostatin signaling, while BPC-157 accelerates healing of tendons, ligaments, and microtears via angiogenesis and collagen synthesis. Combined, they may support both hypertrophy and structural repair during high-volume training or injury recovery.

Follistatin-344
No approved protocol — endogenous modulation via resistance exercise + EAA
BPC-157
250–500 mcg SQ · twice daily · near injury site or systemic
Duration
4–8 weeks
Primary benefit
Muscle hypertrophy + accelerated soft tissue repair
+ TB-500
Moderate
View TB-500

TB-500 (thymosin beta-4 fragment) promotes cell migration, angiogenesis, and anti-inflammatory signaling in muscle and connective tissue. Follistatin-344's anabolic signaling may synergize with TB-500's regenerative effects during muscle damage or overtraining, particularly in older adults where both myostatin inhibition and tissue repair are rate-limiting.

Follistatin-344
Endogenous upregulation (resistance training + protein)
TB-500
2–5 mg SQ · twice weekly · loading phase 4 weeks, then maintenance
Frequency
Twice weekly TB-500, daily training stimulus for FST
Primary benefit
Enhanced recovery, reduced inflammation, muscle growth support