Source comparison
AOD-9604 MOTS-C Protocol: Research Design Comparison
Primary Mechanism Beta-3 adrenergic lipolysis via HSL activation AMPK activation, mitochondrial biogenesis, ACC inhibition Sequential lipolysis + oxidation pathway targeting Dual-peptide model addresses both substrate release and utilization. Single-peptide pr
This comparison does not assign a generated winner or score.
- Primary Mechanism
- Beta-3 adrenergic lipolysis via HSL activation
- AMPK activation, mitochondrial biogenesis, ACC inhibition
- Sequential lipolysis + oxidation pathway targeting
- Dual-peptide model addresses both substrate release and utilization. Single-peptide protocols leave one pathway unaddressed
- Dosing Range (Subcutaneous)
- 250–1000 mcg daily
- 5–15 mg daily or 3× weekly
- 500 mcg AOD + 10 mg MOTS-C with 45-min offset
- Offset timing critical. Simultaneous dosing reduces efficacy because oxidation pathways need mobilized lipids to act on
- Fasted-State Requirement
- Mandatory (insulin blocks HSL)
- Optional (AMPK activation insulin-independent)
- Mandatory for AOD component
- Fasting increases FFA release 3–5×. Fed-state protocols show minimal lipolytic response
- Metabolic Outcome Measured
- Visceral fat reduction, circulating FFA elevation
- Improved insulin sensitivity, increased fat oxidation rate
- Fat mass reduction + substrate utilization shift
- Published dual-peptide trials show 18–22% greater fat loss vs monotherapy at equivalent caloric deficit
- Reconstitution Stability
- 28 days refrigerated, <10% potency loss
- 28 days refrigerated, degrades faster if temp >8°C
- Both require cold chain, multi-dose vials need aseptic handling
- Temperature excursion during shipping is most common potency failure. Request verification of cold-chain delivery
- Contraindications
- Active malignancy (theoretical growth promotion risk)
- None established in human trials to date
- Same as AOD monotherapy
- AOD-9604 does not activate IGF-1 receptors, but precautionary exclusion of cancer patients standard in trials