A once-yearly infusion that binds to bone mineral and shuts down the cells that dissolve bone. It prevents broken bones, produces lasting remission in a disorder of runaway bone rebuilding, and reduces skeletal damage from cancer spread to bone. Signals of fewer cancers, heart attacks and deaths remain far less certain. Harms are mostly rare and mostly preventable. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Estimated glomerular filtration rate (eGFR) | Above 60 mL/min/1.73 m² | Determines whether the drug can be given at all |
| Albumin-corrected serum calcium | 9.2–10.0 mg/dL | Detects the post-infusion nadir before symptoms |
| 25-hydroxyvitamin D | 30–50 ng/mL | Strongest predictor of avoidable hypocalcaemia |
| Intact parathyroid hormone (PTH) | 15–40 pg/mL | Flags compensatory rise from falling calcium; unmasks primary hyperparathyroidism |
| Serum C-terminal telopeptide (CTX) | 0.2–0.4 ng/mL on treatment | Confirms the drug is working and when the effect fades |
| Procollagen type 1 N-terminal propeptide (P1NP) | 25–45 µg/L on treatment | Reads the formation arm of remodelling, which CTX misses |
| Serum magnesium | 2.0–2.4 mg/dL | Low magnesium blocks PTH release and deepens hypocalcaemia |
| Serum phosphate | 3.0–4.0 mg/dL | Falls alongside calcium after infusion |
| Bone mineral density T-score, total hip and lumbar spine | Improvement or stability from own baseline | The endpoint treatment is actually aimed at |
Cadence: Albumin-corrected calcium and kidney function 10 to 14 days after the first infusion, then before each subsequent one; 25-hydroxyvitamin D every 6 to 12 months; a bone turnover marker at 3 months and again when the next interval is decided; bone density scan every 2 to 3 years