A plant pigment sold as a supplement on the strength of one mouse survival finding that the largest independent animal aging program did not reproduce. Human data are small and short: inflammation, blood sugar and body weight improved, mostly in people with illness or excess weight. Cheap, apparently well tolerated, unproven in people — a bet on a mechanism. (Full Review)
| Marker | Target | Why |
|---|---|---|
| hs-CRP | < 1.0 mg/L | Primary inflammation marker moved in the human trials |
| Interleukin-6 | < 2.0 pg/mL | Second inflammatory signal that fell with fisetin |
| suPAR | < 3.5 ng/mL | Primary endpoint of the ongoing low-dose fisetin trial |
| Fasting insulin | 2–6 µIU/mL | Insulin resistance improved in both obesity trials |
| HOMA-IR | < 1.5 | The composite index that actually moved |
| Fasting glucose | 75–86 mg/dL | Fell in every active trial arm |
| HbA1c | 4.8–5.3% | Confirms that fasting changes reflect real glycaemic change |
| LDL cholesterol | < 80 mg/dL | Lipids shifted in the combined training arm |
| ALT | 10–26 U/L (women), 10–30 U/L (men) | Detects liver effects no trial was long enough to exclude |
| eGFR | > 90 mL/min/1.73 m² | Kidney clearance safety check |
| Platelet count | 175–250 ×10⁹/L | Baseline for the theoretical antiplatelet effect |
| Seated blood pressure | 110–120 / 70–80 mmHg | Catches additive vasodilation |
| Epigenetic age | No established target — track the change from the individual's own baseline | The outcome the only human aging pilot measured |
Cadence: Baseline panel before the first dose; on an intermittent monthly schedule, repeat the inflammation and metabolic markers at 8–12 weeks and then every 6 months; liver and kidney panels once at 3 months and annually thereafter; home blood pressure daily through the first two cycles for anyone already on antihypertensive medication