A bacterial protein-cutting enzyme, once a Japanese prescription medicine, now sold mostly as a supplement. Its clearest measured effect is less swelling and stiffness after surgery or injury. Claims about clearing arterial deposits and bacterial films rest on laboratory work, not human trials. The evidence base is small, old, and mostly produced by parties with a stake in it. (Full Review)
| Marker | Target | Why |
|---|---|---|
| High-sensitivity C-reactive protein | < 1.0 mg/L | Tracks the systemic inflammation the enzyme is taken to reduce |
| Absolute eosinophil count | < 300 cells/µL | Earliest detectable signal of the lung and skin hypersensitivity reactions |
| Erythrocyte sedimentation rate | < 10 mm/hour | Corroborates the inflammation signal with a slower-moving marker |
| Fibrinogen | 200–300 mg/dL | Fibrinogen is the substrate the enzyme's fibrinolytic action targets, and an acute-phase marker in its own right |
| International normalised ratio with prothrombin time | 0.9–1.1 when not anticoagulated; on-target for the indication when anticoagulated | Detects any additive effect on clotting from combining the enzyme with antithrombotic drugs |
| Alanine aminotransferase | 10–26 U/L in men, 7–20 U/L in women | Screens for liver stress from any long-term oral supplement, including excipients and coatings |
Cadence: Baseline before starting, then complete blood count with differential and inflammatory markers at 4 weeks, again at 12 weeks, then every 6 months beyond a single course. Clotting studies repeat within one week of starting or stopping whenever an antithrombotic agent is co-administered; any new cough, breathlessness or fever triggers immediate testing.