Rosuvastatin (cancer chemoprevention context; statin class proxy)
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| ID | DRUG-ROSUVASTATIN-CHEMOPREVENTION |
|---|---|
| Тип | Препарат |
| Синоніми | CrestorMertenilRosuvastatin (cancer chemoprevention)RoxeraStatin (rosuvastatin proxy)Розувастатин (хіміопрофілактика раку; представник статинів) |
| Статус | переглянуто 2026-05-18 | очікує клінічного підпису |
| Хвороби | Не вказано |
| Джерела | SRC-NCCN-BCELL-2025 SRC-WCRF-AICR-CUP-2018 |
Дані про препарат
| Клас | HMG-CoA reductase inhibitor (statin) — hydrophilic, high-potency |
|---|---|
| Механізм дії | Hydrophilic, third-generation statin that competitively inhibits HMG-CoA reductase, the rate-limiting enzyme in mevalonate / cholesterol biosynthesis. Higher LDL-lowering potency than atorvastatin at equivalent doses. Cancer-prevention rationale: shared statin pleiotropic effects (decreased isoprenoid prenylation of Ras/Rho, anti-inflammatory, antiproliferative, pro-apoptotic), with observational meta-analyses suggesting modest reductions in CRC, hepatocellular, esophageal, and prostate cancer incidence. Rosuvastatin is hydrophilic and minimally CYP3A4-metabolized — different interaction profile than lipophilic statins (atorvastatin, simvastatin). Primary regulatory indication is cardiovascular risk reduction; cancer-prevention RCT-level evidence is ABSENT. |
| Типове дозування | Cardiovascular-prevention dosing range: 5-40 mg PO once daily (with or without food). Typical starting dose 10-20 mg/day; titrate per LDL target. No specific oncology-prevention dose. Asian ancestry / mild- moderate renal impairment: start at 5 mg. CrCl <30: max 10 mg/day. Hepatic monitoring (baseline LFTs); CK only if symptomatic. |
| Зареєстровано в Україні | True |
| Відшкодовується НСЗУ | True |
| Остання перевірка для України | 2026-05-18 |
Нотатки
STUB — v0.2 chemoprevention-workstream authoring (batch 3); pending two- Clinical-Co-Lead signoff per CHARTER §6.1 dev-mode. STATIN CLASS-DETAIL entity (alongside DRUG-ATORVASTATIN-CHEMOPREVENTION) for cancer- chemoprevention discussions. Primary clinical use remains cardiovascular. Cancer-incidence signals from observational meta-analyses are modest (~5-15% relative reductions in select sites) and have NOT translated to RCT-level cancer-prevention recommendations from USPSTF, NCCN, or ESMO. Engine should NOT recommend statin initiation for cancer prevention; appropriate when CV indications justify use. Class-vs-molecule effect debated — rosuvastatin is hydrophilic (vs lipophilic atorvastatin/ simvastatin), interaction profile minimally CYP-dependent (mostly OATP1B1).
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