These oral medications block the body's main brake on clot dissolution. Longevity interest rests on a family that makes half the normal amount from birth and lives longer, plus mouse work. Human results are narrow: two small cancer studies and one ageing study, all without comparison groups, almost all from the compound's owners. None is approved anywhere. (Full Review)
| Marker | Target | Why |
|---|---|---|
| PAI-1 activity | Below 10 IU/mL | Direct target engagement |
| PAI-1 antigen | Below 20 ng/mL | Total protein pool, active plus latent |
| Platelet count and haemoglobin | Platelets 150–400 × 10⁹/L; haemoglobin mid-reference for sex | Detects bleeding before it is visible |
| Prothrombin time with INR, and activated partial thromboplastin time | Within laboratory reference range | Baseline clotting competence |
| D-dimer | Below 0.5 mg/L fibrinogen-equivalent units | Rises when clot breakdown accelerates |
| Fibrinogen | 200–300 mg/dL | Falling values suggest excessive fibrinolysis |
| Alanine and aspartate aminotransferase, bilirubin | Alanine aminotransferase below 25 U/L in men and 20 U/L in women | Detects the one adverse event attributed to this drug class |
| Fasting insulin and HOMA-IR | Insulin below 5 µIU/mL; HOMA-IR below 1.5 | The metabolic axis linked to low PAI-1 in carriers |
| High-sensitivity C-reactive protein | Below 1.0 mg/L | Inflammation is the main upstream driver of PAI-1 |
| eGFR | Above 90 mL/min/1.73 m² | Clearance route is unpublished, so kidney function is tracked as a precaution |
Cadence: Baseline, one week, four weeks, eight weeks, then every three months while treatment continues; tightening to weekly if any bleeding symptom or liver enzyme rise appears.