FLUVASTATIN SODIUM

Clinical safety rating: avoid

Contraindicated (not allowed)

How it works

Competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme in cholesterol biosynthesis, leading to decreased intracellular cholesterol levels and upregulation of LDL receptors.

What the body does with it

Metabolism	Hepatic via CYP2C9; minor contributions from CYP3A4 and CYP2D6.
Excretion	Fluvastatin sodium is primarily eliminated via biliary/fecal excretion (approximately 90%), with renal excretion accounting for less than 6% of the administered dose.
Half-life	The terminal elimination half-life is 2.3 hours (range 1.4–3.1 hours). Due to its short half-life, it is dosed once daily for sustained HMG-CoA reductase inhibition; however, pharmacodynamic effects (LDL reduction) persist beyond plasma clearance.
Protein binding	Fluvastatin is highly protein-bound (>99%), primarily to albumin.
Volume of Distribution	Volume of distribution (Vd) is approximately 0.35 L/kg, indicating distribution mainly into extracellular fluid and minimal tissue binding.
Bioavailability	Oral bioavailability is 24% (range 19–29%) due to extensive first-pass metabolism; absorption is rapid (Tmax 0.5–1 hour).
Onset of Action	Oral administration: Onset of lipid-lowering effect is observed within 1–2 weeks, with maximal effect at 4 weeks.
Duration of Action	Duration of lipid-lowering effect: After discontinuation, the effect persists for several days; LDL-C levels return to baseline within about 6 weeks. The duration of clinical benefit requires continuous dosing.

Classification & Brands

Dosing & administration

20 to 80 mg orally once daily in the evening; immediate-release: 20-40 mg once daily; extended-release: 80 mg once daily.

Dosage form	TABLET, EXTENDED RELEASE
Renal impairment	No dose adjustment required for mild to moderate renal impairment (eGFR ≥30 mL/min/1.73 m²). Not recommended in severe renal impairment (eGFR <30 mL/min/1.73 m²) due to lack of data.
Liver impairment	Contraindicated in active liver disease or unexplained persistent transaminase elevations. Child-Pugh Class A: use with caution; Class B or C: not recommended.
Pediatric use	For heterozygous familial hypercholesterolemia: 20 mg orally once daily initially, may increase up to 80 mg once daily (immediate-release) based on response. Limited data for children <10 years.
Geriatric use	No specific dose adjustment; consider increased risk of myopathy and rhabdomyolysis, especially with higher doses or concurrent interacting medications. Use lowest effective dose.

Use during pregnancy

1st trimester	Consult provider
2nd trimester	Consult provider
3rd trimester	Consult provider

Clinical note

Can increase the effects of warfarin and other drugs metabolized by CYP2C9 Can cause myopathy and rhabdomyolysis.

Breastfeeding	Excretion into human milk unknown; animal studies indicate presence. M/P ratio not available. Due to potential for adverse effects on infant lipid metabolism, discontinue breastfeeding or avoid use.
Teratogenic Risk	Fluvastatin is contraindicated in pregnancy. First trimester: Case reports suggest teratogenic potential, including skeletal and CNS defects; risk not quantified. Second and third trimesters: Theoretical risk of fetal toxicity from cholesterol synthesis inhibition; no human data. Absolute contraindication due to risk of embryotoxicity.

Warnings & precautions

■ FDA Black Box Warning

Not applicable.

Side Effect Profile

Common Effects	Headache
Serious Effects

Absolute Contraindications

["Active liver disease","Unexplained persistent elevations of serum transaminases","Pregnancy","Lactation","Hypersensitivity to fluvastatin"]

Clinical Precautions

Precautions

["Myopathy/rhabdomyolysis risk increased with concomitant use of gemfibrozil, cyclosporine, or high-dose niacin","Hepatic enzyme elevations","Increased risk of diabetes mellitus","Use caution in patients with risk factors for myopathy","Avoid in pregnancy"]

Clinical Tips & Counseling

Drug interactions

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