Starter candidate — MOTS-c evidence-backed seed framing.
The MOTS-c starter candidate, framed against published evidence so the seed is grounded before any generation.
MOTS-c is a literature-backed seed for metabolic-resilience discovery.
DiscoveryLab treats MOTS-c as a starting scaffold for research programs: an endogenous mitochondrial peptide with strong preclinical metabolic signals, exercise-induced human expression data, and explicit human efficacy gaps.
Prioritize as DL-SEED-MOTS-C for scaffold analog generation, evidence-gated triage, and wet-lab assay planning. Not positioned as a validated injectable therapy.
- Seed
- MOTS-c
- Human sequence
- MRWQEMGYIFYPRKLR
- Class
- 16-amino-acid mitochondrial-derived peptide
- Encoded by
- mtDNA 12S rRNA / MT-RNR1 region
- Program lens
- metabolic resilience, insulin sensitivity, age-related physical decline
Metabolic homeostasis
Identified MOTS-c as a mitochondrial-encoded 16-aa peptide; mouse treatment prevented age-dependent and high-fat-diet-induced insulin resistance and diet-induced obesity, with AMPK pathway involvement.
Stress-response transcription
Showed metabolic stress can drive AMPK-dependent MOTS-c nuclear translocation, chromatin binding, and regulation of nuclear gene expression including antioxidant response element programs.
Exercise and old-mouse performance
Reported acute exercise-induced endogenous MOTS-c in human skeletal muscle and circulation; old mice treated with MOTS-c ran 2.0x longer and 2.16x farther on treadmill testing.
Mouse metabolic and performance data are compelling enough to seed a program.
Acute exercise increased endogenous MOTS-c in a small human cohort.
Exogenous MOTS-c has not been proven to double performance or treat obesity in humans.