A laboratory-made molecule that gathers inside mitochondria and appears to raise the energy they produce by reshaping their internal folds. Cells, worms and mice show more energy, less oxygen damage, and protected kidney, hearing and movement. No published study has measured a health outcome in a living person, and no usable material exists. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Resting lactate | 0.5–1.3 mmol/L | Primary readout of the mitochondrial deficit MA-5 targets |
| GDF-15 | Below 750 pg/mL | Fell with MA-5 in animals; tracks mitochondrial stress |
| Free and total carnitine | Free 25–50; total 30–70 µmol/L | Detects inhibition of the carrier MA-5 blocks in vitro |
| Acylcarnitine-to-free-carnitine ratio | Below 0.25 | Rises early when fatty-acid entry is impeded |
| Creatinine and eGFR | eGFR above 90 mL/min/1.73 m² | Organ with the clearest animal response and injury signal |
| BUN | 10–16 mg/dL | Second renal marker that moved in blinded mouse work |
| ALT and AST | Both below 25 U/L | Presumed clearance route, and that route is unpublished |
| Creatine kinase | 50–150 U/L | Muscle is a target tissue; detects damage from any cause |
| Pure-tone audiometry | No target; track change in decibels from own baseline at 4 and 8 kHz | Hearing is the endpoint the human trial was built around |
Cadence: No protocol validated. Were exposure to occur: baseline before starting; carnitine and lactate at 4 weeks; kidney and liver at 12 weeks; full set every 6-12 months with annual audiometry.