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Comparison Table: Research Peptides for Cellular Senescence Research
NMN (Nicotinamide Mononucleotide) NAD+ precursor; bypasses NAMPT rate-limiting step Metabolic senescence; CD38-driven NAD+ depletion 100–500 μM (in vitro); 250–500 mg/kg (in vivo) High. Multiple RCTs, published in Science, Cell Metabolism Best choice for metab
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- NMN (Nicotinamide Mononucleotide)
- NAD+ precursor; bypasses NAMPT rate-limiting step
- Metabolic senescence; CD38-driven NAD+ depletion
- 100–500 μM (in vitro); 250–500 mg/kg (in vivo)
- High. Multiple RCTs, published in Science, Cell Metabolism
- Best choice for metabolic senescence models and NAD+-dependent pathways; does not clear senescent cells
- SS-31 (Elamipretide)
- Mitochondrial membrane stabilization via cardiolipin binding; reduces ROS
- Mitochondrial dysfunction; cGAS-STING-driven SASP
- 1–10 μM (in vitro); 3–5 mg/kg (in vivo)
- Moderate. Phase 2 clinical trials in heart failure; limited senescence-specific data
- Reduces SASP intensity without clearing cells; ideal for paracrine senescence models
- MOTS-c
- AMPK activation; inhibits mTOR; mitochondrial biogenesis
- Metabolic stress-induced senescence; mTOR-driven SASP
- 5–50 μM (in vitro); 5–15 mg/kg (in vivo)
- Moderate. Published in Cell Metabolism; primarily aging studies, not senescence-specific endpoints
- Strong tool for metabolic rescue in aged tissue; less effective in replicative senescence
- FoxO4-DRI (experimental)
- Disrupts p53-FOXO4 interaction in senescent cells; induces apoptosis
- Direct senolytic. Targets anti-apoptotic pathway upregulation
- 5–25 μM (in vitro); dosing in vivo highly variable
- Low-Moderate. One landmark Cell publication; limited replication
- Only peptide with documented senolytic activity; inconsistent results across models