DT-109 is a three-part amino acid chain built to deliver glycine more efficiently than glycine itself. In mice and monkeys it reduced liver fat, liver injury, arterial plaque and arterial calcium. It has never been administered to a human in a published study, the animal record contradicts itself, and every finding comes from one group. (Full Review)
| Marker | Target | Why |
|---|---|---|
| ALT | 10–26 U/L (men), 8–22 U/L (women) | Liver cell injury; the endpoint DT-109 lowered in animals |
| AST | 10–26 U/L | Second liver enzyme; confirms an ALT signal |
| GGT | <20 U/L (men), <15 U/L (women) | Oxidative stress and bile duct strain; tracks glutathione demand |
| Liver fat fraction | <5% by MRI-PDFF; CAP <248 dB/m | Direct measure of the primary animal endpoint |
| HbA1c | 4.8–5.3% | Three-month average blood sugar; the compound's original target |
| Fasting insulin and HOMA-IR | Insulin 2–5 µIU/mL; HOMA-IR <1.0 | Detects insulin resistance earlier than glucose alone |
| ApoB and triglycerides | ApoB <80 mg/dL; triglycerides <80 mg/dL | The lipid claim is the most contested one in the animal record |
| hs-CRP | <0.5 mg/L | Cheapest proxy for the anti-inflammatory claim |
| eGFR and serum creatinine | eGFR >90 mL/min/1.73 m² | Kidney filtration, the organ exposed to the oxalate load |
| 24-hour urinary oxalate | <25 mg/24 h | Tracks the specific mechanistic stone risk of a glycine load |
| Plasma ammonia | 15–45 µmol/L | Tests the gut-liver mechanism and the nitrogen-load safety question |
| Whole-blood glutathione | No established target exists; the change from the individual's own baseline is what can be tracked | The proposed proximate mechanism of every claimed benefit |
Cadence: Baseline before any exposure, then four weeks, twelve weeks, then every three to six months, with kidney markers repeated sooner if any stone symptom appears.