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Cinacalcet

Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.

IDDRUG-CINACALCET
TypeDrug
Aliases
MimparaSensiparЦинакалцет
Statusreviewed 2026-07-11 | pending_clinical_signoff
DiseasesDIS-PARATHYROID-CARCINOMA
SourcesSRC-NCCN-THYROID-2025

Drug Facts

ClassCalcimimetic (calcium-sensing receptor allosteric agonist)
MechanismAllosterically increases the sensitivity of the parathyroid calcium-sensing receptor (CaSR) to extracellular calcium, suppressing PTH secretion and lowering serum calcium. Acts on the biochemical consequence of the disease (PTH-driven hypercalcemia) rather than the tumor itself — no direct antitumor / cytotoxic effect.
Typical dosingInitiate 30 mg PO BID. Titrate no more frequently than every 2-4 weeks through sequential doses of 30 mg BID → 60 mg BID → 90 mg BID → 90 mg TID → 90 mg QID (maximum labeled dose) to normalize serum calcium. Take with food (improves bioavailability). Check serum calcium within 1 week of initiation or any dose change. FDA-approved specifically for hypercalcemia of parathyroid carcinoma (also approved for secondary hyperparathyroidism in dialysis-dependent CKD and severe hypercalcemia in primary hyperparathyroidism when parathyroidectomy is not appropriate).
Ukraine registeredFalse
NSZU reimbursedFalse
Ukraine last verified2026-07-11

Notes

STUB pending clinical co-lead signoff (CHARTER §6.1 — dev-mode- exempted draft content, not published/verified clinical advice). Cinacalcet is the only FDA-approved medical therapy specifically labeled for hypercalcemia of parathyroid carcinoma. It has no cytostatic/cytotoxic effect on the tumor — it controls the biochemical consequence (PTH-driven hypercalcemia) in unresectable, recurrent, or metastatic disease. Distinct from bisphosphonates (DRUG-ZOLEDRONATE) / denosumab (DRUG-DENOSUMAB) — already in the KB — which act on osteoclast-mediated bone turnover to prevent skeletal-related events from bone metastases rather than suppressing PTH secretion; the two mechanisms are complementary and may be used concurrently in refractory hypercalcemia, per the parent Disease entity's narrative (DIS-PARATHYROID-CARCINOMA).

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