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

AOD-9604vsFollistatin-344

Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.

APhase 2HUMAN-REVIEWED10/47 cited
BHuman-MechanisticHUMAN-REVIEWED4/58 cited
AOD-9604
HGH 176-191 · β3-AR Lipolytic
250–300 mcgDaily doseHeffernan 2001
Phase 2Evidence levelHeffernan 2001Ng 2000
~30 minHalf-life
SQ · Abdomen · Daily fasted
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
AOD-9604
Follistatin-344
Primary target
β3-adrenergic receptor (proposed)Ng 2000
Myostatin (MSTN/GDF-8) and Activin A
Pathway
β3-AR activation → cAMP → hormone-sensitive lipase activation → triglyceride breakdown to FFA + glycerolNg 2000
FST-344 binds MSTN/Activin → prevents ActRIIB receptor engagement → disinhibits muscle anabolism
Downstream effect
Lipolysis of adipose tissue triglycerides; FFA release for oxidation; minimal IGF-1 / insulin impactHeffernan 2001
Elevated follistatin/myostatin ratio, increased muscle protein synthesis, attenuated muscle atrophy signalingJeong 2026
Feedback intact?
No GH-axis or IGF-1 feedback
Yes — indirect antagonist, preserves endogenous regulation
Origin
Synthetic modified C-terminal hexadecapeptide fragment of human GH (176-191) with N-terminal Tyr substitutionNg 2000
Endogenous glycoprotein, 344-AA isoform lacking heparin-binding domain (vs FST-315)
Antibody development
Not documented in available trials (endogenous protein)

02Dosage Protocols

Parameter
AOD-9604
Follistatin-344
Standard dose
250–300 mcg / dayHeffernan 2001
Anecdotal SQ range. Phase 2 trial dose 1 mg/day oral.
Frequency
Once daily, fasted
Lower / starter dose
150 mcg / day
Evidence basis
Phase 2 trials + animal-strongHeffernan 2001Ng 2000
Human observational / biomarker studies
Duration
8–12 weeks per cycle
Reconstitution
Bacteriostatic water, 1 mL per 2 mg vial → 2 mg/mL
Timing
Morning fasted preferred (pre-cardio)
Aligns with circadian lipolysis.
Half-life
~30 min plasma
Not established
Circulating isoform; lacks tissue-binding domain of FST-315.
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).

03Metabolic / Fat Loss Evidence

Parameter
AOD-9604
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
AOD-9604
Follistatin-344
Injection site reaction
Mild erythema
GI symptoms
Rare mild nausea
Cardiovascular
Possible mild HR increase via β3-AR (theoretical β1 cross-reactivity)
IGF-1 elevation
None — designed to lack GH-axis activityHeffernan 2001
Insulin sensitivity
Neutral — no glucose impairmentHeffernan 2001
Cancer risk
No GH/IGF-1 axis activity → lower theoretical risk vs HGH
Pregnancy / OB
Avoid
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
AOD-9604
  • ·Pregnancy / breastfeeding
  • ·Severe cardiovascular disease (caution with β-receptor agonists)
Follistatin-344
  • ·Active malignancy
  • ·No approved protocol — research use only
Relative Contraindications
AOD-9604
  • ·Concurrent β-blocker therapy (theoretical antagonism)
  • ·Pheochromocytoma
Follistatin-344
  • ·Insulin resistance / Type 2 diabetes (monitor glucose)
  • ·Pregnancy / lactation (unknown safety profile)

05Administration Protocol

Parameter
AOD-9604
Follistatin-344
1. Reconstitution
Add 1 mL bacteriostatic water to 2 mg vial → 2 mg/mL = 200 mcg per 0.1 mL.
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. Injection site
SQ — abdomen preferred. Rotate sites.
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
Morning, fasted, ideally pre-cardio for amplified fat oxidation.
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 temp, light-protected. Reconstituted: refrigerate, ≤30 days.
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.
5. Needle
29–31G, 4–8 mm insulin syringe.

06Stack Synergy

AOD-9604
+ MOTS-c
Moderate
View MOTS-c

AOD-9604 mobilises FFAs from adipose via β3-AR; MOTS-c upregulates AMPK / PGC-1α / FAO machinery so that mobilised FFAs are efficiently oxidised. The pathways are sequential — supply (AOD) plus demand (MOTS-c) — and produce more durable lipolytic effects than either alone in anecdotal protocols.

AOD-9604
250–300 mcg SQ · morning fasted (daily)
MOTS-c
5 mg SQ · 2–3× per week (pre-workout)
Primary benefit
Fat mobilisation + mitochondrial oxidation, no IGF-1 concern
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