The signature compound in poplar bee resin, it switches off a central inflammatory control system in laboratory cells. No controlled human study has ever given the isolated compound to people; the human data come from whole bee-resin extracts. Skin and lip allergy is the clearest documented harm, and resin origin decides content. (Full Review)
| Marker | Target | Why |
|---|---|---|
| High-sensitivity C-reactive protein | Below 0.5 mg/L | Primary target; the marker with the largest pooled propolis effect |
| Interleukin-6 | Below 1.5 pg/mL | Upstream driver of C-reactive protein; moved most in pooled trials |
| Fasting glucose | 75–90 mg/dL | Detects the glycemic effect seen in pooled propolis trials |
| Glycated hemoglobin | 4.9–5.4% | Averages blood sugar over roughly three months, so less noisy than single readings |
| Low-density lipoprotein cholesterol | Below 100 mg/dL, below 70 mg/dL with vascular disease | Tracks the lipid change reported in pooled trials |
| Uric acid | 3.5–5.5 mg/dL | CAPE inhibits the enzyme that makes urate; guards against over-suppression |
| Alanine aminotransferase | Below 25 U/L in men, below 20 U/L in women | Safety marker for a compound with uncharacterized human hepatic clearance |
| Creatinine with estimated filtration rate | Filtration rate above 90 mL/min/1.73 m² | Safety marker, and relevant to clearing any contaminant load |
| Eosinophil count | Below 300 cells/µL | Screens for the hypersensitivity response that is this compound's documented harm |
| Home systolic blood pressure | Below 120 mmHg | Captures the small pressure effect reported in pooled propolis trials |
Cadence: Baseline, then inflammation, glucose and lipid markers at 8 to 12 weeks, then at 6 months, then every 6 to 12 months if stable; liver enzymes and kidney markers at the same visits; clotting weekly for the first month on warfarin.