Onco Wiki / Drogue

Cinacalcet

Vue déterministe de l'entité source de la LJAM. L'autorité clinique demeure avec les ID de la source cités et l'état d'approbation de l ́examinateur.

IDDRUG-CINACALCET
TypeMédicament
Alias
MimparaSensibleЦинакалцет
Étatreviewed 2026-07-11 | pending_clinical_signoff
MaladiesDIS-PARATHYROID-CARCINOMA
SourcesSRC-NCCN-THYROID-2025

Faits sur les drogues

CatégorieCalcimimétique (agoniste des récepteurs allostériques sensibles au calcium)
MécanismeAllosterically 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.
Dose typiqueInitiate 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 enregistréeFaux
NSZU rembourséFaux
Ukraine vérifiée pour la dernière fois2026-07-11

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).

Utilisé par

Maladie

Protocole thérapeutique