This page shows what was measured, who it was measured in, and what that does not settle.
What Fluvastatin Sodium does in the body
High cholesterol, and reducing the chance of needing a stent or a bypass in people who already have coronary disease
Fluvastatin blocks the enzyme the liver uses to make cholesterol, so the liver cell puts out more receptors and pulls LDL particles from the bloodstream instead. Two things set it apart. It is entirely man-made — an indole ring designed to mimic what the fungal statins do, rather than a mould product tinkered with afterwards. And it is broken down mostly by a different liver enzyme, CYP2C9, which is why the drugs it interferes with are warfarin, phenytoin and glyburide rather than the antifungals and antibiotics that collide with the rest of the class.
What happened in people
LDL cholesterol lowered 32% in ALERT and 37% at the time of angioplasty in FLARE
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
The recorded finding that sits closest to something a person would notice. Written into the record, not signed off, and it carries no population or interval.
That fluvastatin reduces myocardial infarction or death — neither is in its licensed indication, and its only positive primary endpoint was a composite containing reintervention
Where it acts
Hepatocyte cytoplasm — cleared mainly by CYP2C9 rather than by CYP3A4, which gives this statin an interaction profile that looks nothing like the rest of the class
Kind of result
A number that stands in for health
Supervision
Professional supervision is normally required. A regulator classifies this substance in a way that restricts how it is supplied.
What the registries record it as
The substance registry classes this as chemical.
FDA substance registry · PYF7O1FV7F · read 2026-08-29
Where each sentence above came from
No recorded sentence describes the change this makes in a way that stands on its own. The page opens with what it is taken for instead, and the recorded explanation follows below.
Shown as the opening line on this page.
A limit recorded against this substance. Not signed off as a reviewed claim.
The four opening statements run to 130 words.
Words this page uses
Four words worth knowing first
Chosen from what this page shows, with each one explained before the word it depends on.
Stand-in result
A stand-in result is a number measured because the real result takes too long.
A picture of it, and where the picture fails
It is like judging a journey by the speedometer rather than by arriving.
Where that stops being true. Speed does predict arrival. Many stand-in results do not predict the real one.
What people get wrong. A stand-in result is often reported as the result itself.
A surrogate endpoint substituted for a clinical endpoint, valid only where the substitution has been shown to hold.
Randomisation
Randomisation means chance decides who gets which treatment.
A picture of it, and where the picture fails
It is like a coin toss deciding the groups.
Where that stops being true. A coin toss is fair once. Fairness here comes from doing it for everyone.
What people get wrong. It is thought to make groups identical. It makes them similar on average, including on things nobody measured.
Allocation of participants to arms by a chance process, so that unmeasured factors are balanced in expectation.
Confidence interval
A confidence interval is the range the true answer is likely to sit in.
A picture of it, and where the picture fails
It is like a weather forecast giving a range rather than one number.
Where that stops being true. A forecast range covers tomorrow. This one covers what the study could resolve.
What people get wrong. The middle number is read as the answer. A range crossing zero means no change is still possible.
An interval estimate that would contain the true parameter in a stated proportion of repeated studies.
Pathway
A pathway is a chain of steps inside a cell, each one setting off the next.
A picture of it, and where the picture fails
A pathway is like a row of dominoes.
Where that stops being true. Dominoes fall one way. Pathways loop back and can switch themselves off.
What people get wrong. Changing one step is read as changing the outcome. Other steps often absorb it.
An ordered series of molecular interactions producing a defined cellular change.
What happened in people◇Read from sources, not yet reviewed
What was measured, goal by goal
One row for each goal a registered study measured something for. One column for each kind of thing that could be measured.
Registered studies list 22 outcome measures that RNAWiki could read. A registered study says what someone planned to measure. It does not say what they found. 0 of the matched studies tested this substance, and 0 posted a result.
There is no single score. A strong test result and a weak life result are different facts.
Goals down the side, kinds of measurement across the top. Each cell says what kind of thing was registered, not what was found.
Goal
Life outcome
What a body can do
How a person feels
A test result
A step in the body
Harms
How long
Who was studied
Cholesterol
∅Nothing in the sources checkedNo registered study lists a life outcome for this goal.
∅Nothing in the sources checkedNo registered study lists a performance measure for this goal.
∅Nothing in the sources checkedNo registered study lists a symptom measure for this goal.
△Only a number moved5 registered test measure.
∅Nothing in the sources checkedNo registered study lists a body-step measure for this goal.
—Not recordedHarms were not a registered measure for this goal.
—Not recordedNo finished study window is recorded.
…Waiting for a reviewerWho was studied is listed further down the page.
Blood sugar
∅Nothing in the sources checkedNo registered study lists a life outcome for this goal.
∅Nothing in the sources checkedNo registered study lists a performance measure for this goal.
∅Nothing in the sources checkedNo registered study lists a symptom measure for this goal.
∅Nothing in the sources checkedNo registered study lists a test result for this goal.
∅Nothing in the sources checkedNo registered study lists a body-step measure for this goal.
—Not recordedHarms were not a registered measure for this goal.
—Not recordedNo finished study window is recorded.
…Waiting for a reviewerWho was studied is listed further down the page.
Which registered measures put each goal on this table
Cholesterol
low density lipoprotein cholesterol after 12 weeks; fasting plasma low density lipoprotein cholesterol; reduction in low density lipoprotein cholesterol; ldl c from baseline at study endpoint week 12; low density lipoprotein cholesterol
Blood sugar
incident type 2 diabetes
Sorted by fixed word lists, version v1. A name the rules do not recognise stays unsorted rather than moving to the nearest column.
What each mark on this table means
∅ Nothing in the sources checked
No registered study lists a life outcome for this goal.
△ Only a number moved
5 registered test measure.
— Not recorded
Harms were not a registered measure for this goal.
… Waiting for a reviewer
Who was studied is listed further down the page.
What happened in people◇Read from sources, not yet reviewed
What happened in people
Each card is one study: the exact question it asked, who was in it, and whether it showed what it set out to show.
Survival time free of major adverse cardiac events — cardiac death, non-fatal myocardial infarction or reintervention — after a first successful percutaneous coronary intervention
✓ The study showed what it set out to show
Who was studied
LIPS — Lescol Intervention Prevention Study (JAMA 2002;287:3215-3222)
181 of 844 (21.4%) against 222 of 833 (26.7%); relative risk 0.78 (95% CI 0.64 to 0.95), p=0.01, over a median 3.9 years
Repeated elsewhere
Unreplicated
What this does not prove. Meeting one endpoint in one population does not carry to other goals or other people.
The limits of this study, and where it came from
Main limit. The composite includes reintervention, which is a decision as much as an event and is not blinded to the treating cardiologist in the same way a death is. The diabetes and multivessel-disease subgroup results are exploratory. There were no creatine kinase elevations above ten times normal and no rhabdomyolysis in the fluvastatin arm.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral extended-release tablet at 80 mg once daily; formerly also an immediate-release capsule at 20 and 40 mg
Interval reported. 95% CI 0
Written into the record, not signed off as a reviewed claim.
Fluvastatin sodium extended-release tablets United States prescribing information — Indications 1, Contraindications 4, Warnings and Precautions 5.1 to 5.3, … · a recorded source, not a stored snapshot
Major adverse cardiac event — cardiac death, non-fatal myocardial infarction or coronary intervention procedure — in renal transplant recipients over five to six years
✗ The study did not show it
Who was studied
ALERT — Assessment of Lescol in Renal Transplantation (Lancet 2003;361:2024-2031)
Risk ratio 0.83 (95% CI 0.64 to 1.06), p=0.139, over a mean 5.1 years, with LDL cholesterol lowered 32%
Repeated elsewhere
Failed to Replicate
What this does not prove. A study that did not show an effect does not show that no effect exists anywhere.
The limits of this study, and where it came from
Main limit. The secondary combination of cardiac death or non-fatal myocardial infarction was 70 against 104, risk ratio 0.65 (95% CI 0.48 to 0.88), p=0.005 — and it is the number usually quoted from this trial. Coronary intervention procedures and all other secondary endpoints, including all-cause mortality and graft loss, did not differ. Because the primary endpoint was not met, the prespecified subgroup analyses could not be interpreted.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral extended-release tablet at 80 mg once daily; formerly also an immediate-release capsule at 20 and 40 mg
Interval reported. 95% CI 0
Written into the record, not signed off as a reviewed claim.
Fluvastatin sodium extended-release tablets United States prescribing information — Indications 1, Contraindications 4, Warnings and Precautions 5.1 to 5.3, … · a recorded source, not a stored snapshot
Angiographic restenosis measured as loss in minimal luminal diameter at 26 weeks after successful balloon angioplasty without a stent
0.23 ± 0.49 mm on fluvastatin against 0.23 ± 0.52 mm on placebo, p=0.95; restenosis rate 28% against 31%, p=0.42; composite clinical endpoint at 40 weeks 22.4% against 23.3%, p=0.74
Repeated elsewhere
Failed to Replicate
What this does not prove. A study that did not show an effect does not show that no effect exists anywhere.
The limits of this study, and where it came from
Main limit. A post-hoc lower incidence of death and myocardial infarction — six (1.4%) against 17 (4.0%), log-rank p=0.025 — was described by the authors as not previously reported with statin therapy, and they called for a trial designed a priori to test it. That trial was LIPS. Only 836 of the 1,054 randomised patients entered the intention-to-treat analysis, because entry required a successful angioplasty after at least two weeks of pre-treatment.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral extended-release tablet at 80 mg once daily; formerly also an immediate-release capsule at 20 and 40 mg
Interval reported. Not recorded in this summary
Written into the record, not signed off as a reviewed claim.
Fluvastatin sodium extended-release tablets United States prescribing information — Indications 1, Contraindications 4, Warnings and Precautions 5.1 to 5.3, … · a recorded source, not a stored snapshot
What we know
RNAWiki holds 3 written-up human studies for this substance, each with the question it asked.
How we know it
Each card names the study, the number of people and what the study set out to measure.
What this does not prove
These summaries were written by a person and have not been signed off as reviewed claims.
Why it matters
A study that failed is as informative as one that worked, and both are here.
What we still do not know
No reviewed claim exists, so no exact population, effect size or interval is published yet.
What happened in people◇Read from sources, not yet reviewed
How close this is to real life
The top step is something a person would feel or care about. The bottom is a guess from software. Filled steps are where evidence exists for this substance.
■Living longer, or avoiding a major eventEvidence recorded. Death, a heart attack, a stroke, a hospital stay.1 registered measure of this kind. 1 written-up study measured this and did not show a benefit.
□What a body can do day to dayNo evidence recorded. Walking, dressing, breathing, recovering.No registered study measures this.
□Measured performanceNo evidence recorded. How much was lifted, how far was run, how fast.No registered study measures this.
□Symptoms and quality of lifeNo evidence recorded. Pain, tiredness, mood, sleep, as the person rated it.No registered study measures this.
■A number that stands in for healthEvidence recorded. Cholesterol, blood sugar, bone density. A stand-in, not the thing itself.7 registered measures of this kind.
■A step measured inside a personEvidence recorded. Something measured in human tissue or human cells.A human record sits on the stored organism ladder.
■AnimalsEvidence recorded. Mice, rats, dogs. Useful for ideas, not proof about people.Stored records in Mouse, Rat. A result in animals says what to test next. It does not say what happens in people.
■Cells in a dishEvidence recorded. Cells or chemistry on a bench, far from a whole body.Stored mechanism abstracts describe steps measured in cells or tissue.
□A guess from softwareNo evidence recorded. Nobody measured it. RNAWiki never publishes one as a finding.RNAWiki stores no prediction for this record. Software can suggest a link. RNAWiki does not publish one as a finding.
Higher on these steps means closer to something a person would feel. It does not mean better done.
What it changes in the body◇Read from sources, not yet reviewed
The path through the body
From what a person takes to what changes. A solid line is a step measured in people. A dashed line is a step nobody has measured that way.
Start
Fluvastatin Sodium
What a person takes: Oral extended-release tablet at 80 mg once daily; formerly also an immediate-release capsule at 20 and 40 mg.
The measurement behind this step
The extended-release tablet reaches peak concentration at about three hours fasting and has a mean relative bioavailability of approximately 29%, with a wide range of 9% to 66%, compared with the immediate-release capsule taken fasting. A high-fat meal delays absorption to a peak at six hours and raises bioavailability by about 50%, though the peak concentration still stays below that of the immediate-release forms. Elimination half-life is about three hours. Around 90% of a dose is excreted in the faeces as metabolites with under 2% unchanged, and about 5% is recovered in urine. Plasma levels do not differ significantly in patients over 65.
Getting in
Designed, not harvested
Every earlier statin came from a mould. This one was drawn on paper: a synthetic indole built to do the same job as the fungal molecules.
╌╌Described, with no measurement named. No measurement is named for this step, so it is drawn as an unconfirmed link.
The measurement behind this step
A 3-(4-fluorophenyl)-1-isopropylindole carrying an E-vinyl bridge to a 3,5-dihydroxyheptenoic acid, given as the sodium salt. It has two enantiomers, and the label states both are metabolised in a similar manner.
The liver enzyme that disposes of it is a different one from the enzyme that handles most statins, which is why its list of clashing drugs looks unfamiliar.
╌╌Described, with no measurement named. No measurement is named for this step, so it is drawn as an unconfirmed link.
The measurement behind this step
Metabolism proceeds by hydroxylation of the indole ring at the 5- and 6-positions with N-dealkylation and side-chain β-oxidation. CYP2C9 accounts for approximately 75%, CYP3A4 about 20% and CYP2C8 about 5%. Half-life is about three hours; about 90% of a dose leaves in the faeces.
Inside the liver cell it occupies the site the enzyme uses to build cholesterol, and the pathway stalls.
╌╌Described, with no measurement named. No measurement is named for this step, so it is drawn as an unconfirmed link.
The measurement behind this step
Competitive inhibition of HMG-CoA reductase, the rate-limiting enzyme converting HMG-CoA to mevalonate. Given in the active acid form, so no metabolic activation step is required.
The liver responds by putting more receptors on its surface and pulling LDL particles out of the blood, reaching full effect after about a month.
╌╌Described, with no measurement named. No measurement is named for this step, so it is drawn as an unconfirmed link.
The measurement behind this step
The label states that inhibition of HMG-CoA reductase accelerates expression of LDL receptors, followed by uptake of LDL-C from blood to the liver, and that sustained inhibition also decreases VLDL. Maximum LDL reduction is usually achieved by four weeks and maintained. LDL fell 32% in ALERT and 37% at the time of angioplasty in FLARE.
The one trial in which the drug met its main goal was in people who had just had a first successful angioplasty.
╌╌Described, with no measurement named. No measurement is named for this step, so it is drawn as an unconfirmed link.
The measurement behind this step
LIPS: major adverse cardiac events in 181 of 844 (21.4%) against 222 of 833 (26.7%), relative risk 0.78 (95% CI 0.64 to 0.95), p=0.01, over a median 3.9 years, with no rhabdomyolysis and no creatine kinase elevation above ten times normal in the treated arm.
It did not stop arteries re-narrowing after angioplasty, and it did not reach significance on its main measure in kidney transplant patients.
╌╌Described, with no measurement named. No measurement is named for this step, so it is drawn as an unconfirmed link.
The measurement behind this step
FLARE: loss in minimal luminal diameter 0.23 mm against 0.23 mm, p=0.95; restenosis 28% against 31%, p=0.42. ALERT: major adverse cardiac events risk ratio 0.83 (95% CI 0.64 to 1.06), p=0.139, over a mean 5.1 years in 2,102 renal transplant recipients.
No suggested links are held for this record, so nothing is hidden from this path.
What we know
The record describes 6 steps from taking it to an effect in a person.
How we know it
Each step names the study behind it in the technical detail beside it.
What this does not prove
A change inside the body is a reason to look. It is not a result in a person.
Why it matters
A reader can see exactly where the chain stops being measured in people.
What we still do not know
No reviewed claim binds any of these steps to a named population.
What it would be like to take◇Read from sources, not yet reviewed
Felt, measured, or meaningful
Three different things that get called the same word. Registered studies measured all three, and mixing them is how a blood test becomes a health claim.
Felt
Things a person could notice without a test.
No registered study measured anything of this kind.
Measured
Things only a test, a scale or a device shows.
low density lipoprotein cholesterol after 12 weeks
circulating marker of inflammation after 5 weeks
serum inflammatory markers after 52 weeks
fasting plasma low density lipoprotein cholesterol
reduction in low density lipoprotein cholesterol
ldl c from baseline at study endpoint week 12
low density lipoprotein cholesterol
Meaningful
Things that change how a life goes, not only a number.
recurrent stroke
A registered study says what someone planned to measure. It does not say what they found. A number moving is not the same as a life going better. The two are shown apart here.
Felt, but not shown to help. A person notices a change. No study showed it leads anywhere good.
Measured, but not felt. A number moves. The person notices nothing. Both can be true.
Measured, but not shown to matter. A number moves in the good direction. Nobody showed that lives went better.
Matters, but takes years. The result that counts may take longer than anyone would keep watching.
Names that fit none of the three (14)
progression of calcified aortic stenosis measured by
transthoracic echocardiography
catheterization
cardivasculary events
penile blood flow after 8 weeks of treatment
viral load reduction liver test changes
sustained viral response
metabolic syndrome
general cardiovascular risk profile framingham heart study
30 day maces after pci
carotid imt
incident type 2 diabetes
hospitalized for acute kidney injury
genetic profile shift in melanoma transcriptome
These are harms, study-process measures, or names the rules did not recognise. They are shown rather than dropped.
What it would be like to take◇Read from sources, not yet reviewed
How long anything takes
Nine different lengths of time that get confused with each other. None of them is worked out from another.
Before anything is noticed.RNAWiki does not store this separately, and never works it out from another figure on this page.
Before a test result moves.RNAWiki does not store this separately, and never works it out from another figure on this page.
Before performance moves.RNAWiki does not store this separately, and never works it out from another figure on this page.
How long the result was watched.No finished study window is recorded for a study that tested this substance.
How long people took it.How long people actually took it is not stored. The study window is not the same thing.
How long people were followed.Follow-up length is not stored separately. It is never read off the study window, which would be a different thing.
How fast the body clears it. 3 hours hours
Read from the label, which states: “The elimination half-life (t 1/2 ) of fluvastatin is approximately 3 hours.”
How long effects linger.RNAWiki does not store this separately, and never works it out from another figure on this page.
Beyond the studies. Nothing is recorded about the long term.
The longest finished study sets the edge of what anyone measured.
A study window is not how long people took it, and neither is how long they were followed. Where RNAWiki holds only one of the three, it shows one.
What is missing or unclear◇Read from sources, not yet reviewed
Were people like you studied?
RNAWiki cannot tell whether a study fits you. It can show who was in it, and where the result stops carrying.
Who was studied
People similar to this profile were included.
Adults with coronary disease and high cholesterol, adults and children from ten with familial hypercholesterolaemia, and — historically — patients on drug regimens where the CYP3A4 statins were unusable.
Who is missing from the studies
Which groups were under-represented in the studies has not been recorded for this substance. Pregnancy, breastfeeding, children, older adults, and people with liver or kidney conditions are commonly excluded from trials; nothing here says whether they were.
What the label states about particular groups
On pediatric, the label states: “The safety and effectiveness of fluvastatin sodium extended-release tablets have not been established in pediatric patients younger than 10 years of age with HeFH or in pediatric patients with other types of hyperlipidemia (other than HeFH).”
US prescribing information · 5ab4296c-87c2-4c64-b218-d620eef51310 · read 2026-08-30
On older people, the label states: “Fluvastatin exposures were not significantly different between the nonelderly and elderly populations (age ≥ 65 years) [see Clinical Pharmacology ( 12.3 )] .”
US prescribing information · 5ab4296c-87c2-4c64-b218-d620eef51310 · read 2026-08-30
On people who are pregnant, the label states: “Risk Summary Discontinue fluvastatin sodium extended-release tablets when pregnancy is recognized.”
US prescribing information · 5ab4296c-87c2-4c64-b218-d620eef51310 · read 2026-08-30
On people who are breastfeeding, the label states: “Risk Summary There is no information about the presence of fluvastatin in human milk, the effects of the drug on the breastfed infant or the effects of the drug on milk production.”
US prescribing information · 5ab4296c-87c2-4c64-b218-d620eef51310 · read 2026-08-30
On people with reduced liver function, the label states: “Fluvastatin sodium extended-release tablets are contraindicated in patients with acute liver failure or decompensated cirrhosis [see Contraindications ( 4 ), Warnings and Precautions ( 5.3 )].”
US prescribing information · 5ab4296c-87c2-4c64-b218-d620eef51310 · read 2026-08-30
On people with reduced kidney function, the label states: “is a risk factor for myopathy and rhabdomyolysis.”
US prescribing information · 5ab4296c-87c2-4c64-b218-d620eef51310 · read 2026-08-30
Where the result stopped carrying
FLARE: no effect at all on restenosis, the endpoint the whole trial was designed around
ALERT: primary endpoint not met at p=0.139 after five years in the largest fluvastatin population studied
The antiproliferative mechanism claimed to distinguish fluvastatin from other statins did not produce a clinical effect when tested directly
The licence, written from what was actually measured, claims neither infarction reduction nor mortality reduction
This is a scope explorer, not a diagnosis engine.
It shows who was studied so you can see whether people similar to you were included.
RNAWiki cannot tell whether a study fits you. It can show who was in it.
What it would be like to take◇Read from sources, not yet reviewed
Why it might seem to do nothing
A real effect and a noticed effect are different things. These are the recorded reasons the two come apart.
It was studied for a different goal
The studies measured something else entirely.
On this record: Some registered studies measured things that match no goal on this page.
It was studied in different people
The people in the studies were not much like the reader.
On this record: Which groups were under-represented in the studies has not been recorded for this substance. Pregnancy, breastfeeding, children, older adults, and people with liver or kidney conditions are commonly excluded from trials; nothing here says whether they were.
The evidence may simply be wrong
Small early studies often do not hold up.
On this record: RNAWiki has not yet published a reviewed conclusion for this use.
Other reasons RNAWiki checked and found nothing for (10)
A different form was studied
The studied form is not the form on the shelf. Nothing in this record points to this reason.
There was nothing to correct
Where a level is already normal, topping it up may change nothing. Nothing in this record points to this reason.
Something else had to happen too
In the studies it was paired with training, a diet or another treatment. Nothing in this record points to this reason.
The change is too small to feel
A real change can still sit below what a person notices. Nothing in this record points to this reason.
Day-to-day swing hides it
Sleep, food, stress and time of day move most numbers more than this would. Nothing in this record points to this reason.
Not enough time yet
The studies ran longer than the person has waited. Nothing in this record points to this reason.
It was not taken as studied
Missed days change the result, and studies count them. Nothing in this record points to this reason.
Something else changed at the same time
Two changes at once cannot be told apart afterwards. Nothing in this record points to this reason.
The product may not be what it says
Contents of a sold product are not always what the label states. Nothing in this record points to this reason.
No recorded reason
RNAWiki has nothing stored that would explain it. Nothing in this record points to this reason.
None of these is a reason to take more. Taking more is not a step this page ever suggests.
What it would be like to take◇Read from sources, not yet reviewed
What taking it involves
The recorded facts about getting hold of it and using it. Nothing here is a suggestion about what you should do.
How it is supplied
Prescription only
❝ Quoted from a source
Where this came from
Copied from a source RNAWiki stored, with the source named.
Read from the recorded approval status.
No source is stored against this line.
Form and route
Oral extended-release tablet at 80 mg once daily; formerly also an immediate-release capsule at 20 and 40 mg
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
The form and route recorded on this substance.
No source is stored against this line.
Who oversees it
Professional supervision is normally required. A regulator classifies this substance in a way that restricts how it is supplied.
❝ Quoted from a source
Where this came from
Copied from a source RNAWiki stored, with the source named.
Suppression classes recorded: S3.
No source is stored against this line.
What is in the pack
The extended-release tablet reaches peak concentration at about three hours fasting and has a mean relative bioavailability of approximately 29%, with a wide range of 9% to 66%, compared with the immediate-release capsule taken fasting.
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
Recorded notes on how this is sold. The rest of the recorded wording: A high-fat meal delays absorption to a peak at six hours and raises bioavailability by about 50%, though the peak concentration still stays below that of the immediate-release forms. Elimination half-life is about three hours. Around 90% of a dose is excreted in the faeces as metabolites with under 2% unchanged, and about 5% is recovered in urine. Plasma levels do not differ significantly in patients over 65.
No source is stored against this line.
Where it is registered
Regulatory records are listed in the technical disclosure at the foot of this page.
# Counted from records
Where this came from
A count of rows RNAWiki holds. It describes our records, not your body.
Register entries are stored per jurisdiction and shown with their dates.
No source is stored against this line.
Why people stop
Not recorded.
∅ Nothing recorded
Where this came from
RNAWiki holds nothing here and says so rather than guessing.
No record of why people stopped taking it is stored for this substance.
No source is stored against this line.
What it would be like to take◇Read from sources, not yet reviewed
What can go wrong
Sorted by where each line came from. A regulator's label and a report somebody sent in are not the same kind of fact.
·Worth asking a clinician aboutWritten into the record from the studies named on this page
Contraindicated in acute liver failure or decompensated cirrhosis and in hypersensitivity, with anaphylaxis, angioedema and Stevens-Johnson syndrome reported. Myopathy with creatine kinase above ten times the upper limit of normal occurred in under 0.1% of the programme; risk factors are age 65 and over, uncontrolled hypothyroidism, renal impairment and concomitant interacting drugs. Rhabdomyolysis with acute kidney injury and rare fatalities has occurred with statins including this one. Immune-mediated necrotising myopathy has been reported rarely and persists after discontinuation. Transaminase increases occur, some persistent, with rare reports of fatal and non-fatal hepatic failure. Avoid gemfibrozil, ciclosporin and fluconazole. Warfarin requires INR monitoring on starting and stopping; phenytoin levels and, in patients on glyburide, blood glucose should be monitored when fluvastatin is initiated.
Nobody counted how many people took this and were fine, so this cannot be turned into a rate.
Over a long time. No completed tested study window is recorded, so long-term effects are not established by the registry record.
Groups the studies covered thinly. Which groups were under-represented in the studies has not been recorded for this substance. Pregnancy, breastfeeding, children, older adults, and people with liver or kidney conditions are commonly excluded from trials; nothing here says whether they were.
What is missing or unclear◇Read from sources, not yet reviewed
Does the exact form matter?
Evidence belongs to the exact thing that was tested. A different salt, a different mixture or a different preparation is a different question.
The form that was studied
Oral extended-release tablet at 80 mg once daily; formerly also an immediate-release capsule at 20 and 40 mg
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
The form used in the studies cited on this page.
No source is stored against this line.
What is sold
A high-fat meal delays absorption to a peak at six hours and raises bioavailability by about 50%, though the peak concentration still stays below that of the immediate-release forms. Elimination half-life is about three hours. Around 90% of a dose is excreted in the faeces as metabolites with under 2% unchanged, and about 5% is recovered in urine. Plasma levels do not differ significantly in patients over 65.
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
Recorded notes on which forms are sold and how they compare.
No source is stored against this line.
What is recorded as being sold
21 products list this as an active ingredient in the United States drug directory. 21 of them contain it and nothing else.
FDA National Drug Code directory · 11712-396 · read 2026-08-29
They are sold as capsule, powder, tablet, extended release and tablet, film coated, extended release, taken oral.
FDA National Drug Code directory · 11712-396 · read 2026-08-29
The regulator's established pharmacologic class for it is hmg-coa reductase inhibitor [epc] and hydroxymethylglutaryl-coa reductase inhibitors [moa].
FDA National Drug Code directory · 11712-396 · read 2026-08-29
11 published labels name it as an active ingredient. 11 of them describe this substance alone, which is where its own label text on this page comes from.
US prescribing information · 5ab4296c-87c2-4c64-b218-d620eef51310 · read 2026-08-29
Those labels are classed as human prescription drug.
US prescribing information · 5ab4296c-87c2-4c64-b218-d620eef51310 · read 2026-08-29
FLUVASTATIN SODIUM ER is oral at 3 DOSAGE FORMS AND STRENGTHS Extended-release tablets: 80 mg of fluvastatin: yellow, round, slightly biconvex film-coated tablets with beveled edges debossed with “LESCOL XL” on one side and “80” on the other., recorded as fda label in effect 2024-01-31 in the United States.
US prescribing information · 5ab4296c-87c2-4c64-b218-d620eef51310 · read 2026-08-30
Recorded price in US: 2.71783–2.85812 USD per one unit as the pricing file counts it — a tablet, capsule, patch or single item, across 8 priced products whose strengths and pack forms differ, as of 2026-08-26, paid by retail pharmacies buying the product, as surveyed by the Centers for Medicare & Medicaid Services. It is not a list price, an insurance price, or what anyone pays at a counter..
Recorded source · 2026-08-26 · read 2026-08-28
Evidence carries across two names for one substance. It does not carry across a salt, a mirror form or a mixture.
What it would be like to take◇Read from sources, not yet reviewed
What you could measure
This one is decided with a clinician, so this section holds questions to ask rather than a plan to run.
Self-experiment planning is not offered for a prescription or clinician-supervised medicine. The questions below are for a clinician or pharmacist.
Questions worth asking
Which of the trials of Fluvastatin Sodium studied people like me?
What was measured, and for how long?
Was the result a laboratory value or a health outcome?
What would we watch for, and when would we stop?
Tracking can show whether something changed for you. It cannot show what caused it.
RNAWiki records evidence. It does not say whether this substance is right for you.
What is missing or unclear◇Read from sources, not yet reviewed
Claims that go past the evidence
Things said about this substance that sound reasonable, and the exact step that is missing between the evidence and the claim.
✗Goes past the evidence
That fluvastatin reduces myocardial infarction or death — neither is in its licensed indication, and its only positive primary endpoint was a composite containing reintervention
Why it sounds right. It follows from something real on this page: a body step, an animal result or a related finding.
The missing step. Nobody measured this in people for this use, or the study that did measure it did not show it.
What would change this
A study in people, for this exact use, measuring this exact thing, that a reviewer signs off.
RNAWiki has not yet published a reviewed conclusion for this use.
✗Goes past the evidence
That the ALERT secondary result of cardiac death or non-fatal infarction stands on its own, when the trial missed its primary endpoint and could not interpret its subgroups
Why it sounds right. It follows from something real on this page: a body step, an animal result or a related finding.
The missing step. Nobody measured this in people for this use, or the study that did measure it did not show it.
What would change this
A study in people, for this exact use, measuring this exact thing, that a reviewer signs off.
RNAWiki has not yet published a reviewed conclusion for this use.
✗Goes past the evidence
That fluvastatin inhibits vascular smooth muscle proliferation to clinically useful effect — the hypothesis FLARE was built on and disproved
Why it sounds right. It follows from something real on this page: a body step, an animal result or a related finding.
The missing step. Nobody measured this in people for this use, or the study that did measure it did not show it.
What would change this
A study in people, for this exact use, measuring this exact thing, that a reviewer signs off.
RNAWiki has not yet published a reviewed conclusion for this use.
✗Goes past the evidence
That its price reflects any measured advantage; on potency, licence breadth and outcome evidence it is behind every cheaper statin in the class
Why it sounds right. It follows from something real on this page: a body step, an animal result or a related finding.
The missing step. Nobody measured this in people for this use, or the study that did measure it did not show it.
What would change this
A study in people, for this exact use, measuring this exact thing, that a reviewer signs off.
RNAWiki has not yet published a reviewed conclusion for this use.
What is missing or unclear◇Read from sources, not yet reviewed
What nobody knows yet
Open questions, each with why it is open and what would close it.
Missing populations
Which groups were under-represented in the studies has not been recorded.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
Missing long-term data
No completed tested study window is recorded.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
No reviewed conclusion
RNAWiki has not yet published a reviewed conclusion for this use.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
Missing interaction studies
No interaction was found in the registers checked. Not finding one is not the same as showing there is none.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
Formulation uncertainty
Several salts, forms or products of Fluvastatin Sodium are recorded. Results from one form may not transfer to another.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
Mechanism not reviewed
No reviewed mechanism story exists for this substance.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
What happened in people◇Read from sources, not yet reviewed
Check any of this yourself
Every line above traced back to the study it came from. This is the technical layer, and the vocabulary changes here.
Every line above can be traced to the study named beside it. Follow the link and read it.
The licence claims revascularisations, not heart attacks and not death
In plain words
Read the indication. Fluvastatin is licensed to reduce the chance of needing a stent or a bypass and to slow the disease on an angiogram. It is not licensed to reduce heart attacks, and it is not licensed to reduce death.
What was measured
That fluvastatin carries the class-wide claim of preventing infarction and death, when its own licence claims neither
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
The fluvastatin extended-release indication reads: to reduce the risk of undergoing coronary revascularisation procedures and slow the progression of coronary atherosclerosis in adults with clinically evident coronary heart disease; and, as an adjunct to diet, to reduce LDL cholesterol in primary hyperlipidaemia and in heterozygous familial hypercholesterolaemia. Set that beside the siblings. Simvastatin: to reduce the risk of total mortality by reducing coronary heart disease death, non-fatal myocardial infarction and stroke. Pravastatin: to reduce the risk of total mortality by reducing coronary death. Lovastatin: to reduce myocardial infarction, unstable angina and revascularisation. Fluvastatin claims the least of the four, and the reason is visible in its trial record — one positive composite in a post-angioplasty population, and two trials that missed their primary endpoints. A regulator writes an indication from what was measured, and this indication is what fluvastatin measured.
Source
Fluvastatin sodium extended-release tablets United States prescribing information, section 1
Role in the trial
Not matched to a registered study
Identity check
no open identity hold
Audit mark
caution
Review state
Written into the record, not signed off as a reviewed claim
LIPS: the one primary endpoint fluvastatin met
In plain words
In 1,677 people who had just had a successful first angioplasty, major cardiac events over four years fell from 26.7% to 21.4%.
What was measured
Major adverse cardiac events over a median 3.9 years after a first successful percutaneous coronary intervention
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
LIPS randomised 1,677 patients aged 18 to 80 with stable or unstable angina or silent ischaemia after a first successful percutaneous coronary intervention, with total cholesterol 135 to 270 mg/dL, to fluvastatin 80 mg daily (n=844) or placebo (n=833), started a median two days after the procedure, with median follow-up 3.9 years. At least one major adverse cardiac event — cardiac death, non-fatal myocardial infarction or reintervention — occurred in 181 (21.4%) against 222 (26.7%): relative risk 0.78 (95% CI 0.64 to 0.95), p=0.01. The result was independent of baseline cholesterol above or below the median. There were no creatine kinase elevations of ten times the upper limit of normal and no rhabdomyolysis in the fluvastatin arm. Two subgroup findings — diabetes, RR 0.53 in 202 patients, and multivessel disease, RR 0.66 in 614 — are hypothesis-generating rather than established.
Written into the record, not signed off as a reviewed claim
ALERT missed its primary endpoint in 2,102 transplant recipients
In plain words
The largest fluvastatin trial ran for five years in kidney transplant patients and did not reach significance on what it set out to measure. A secondary measure did separate, and that is what gets quoted.
What was measured
Major adverse cardiac events over a mean 5.1 years in renal transplant recipients (risk ratio 0.83, 95% CI 0.64 to 1.06, p=0.139)
Effect estimate
No reviewed effect estimate exists for this record.
Limits
This entry records a failure.
From the source
ALERT randomised 2,102 renal transplant recipients with total cholesterol 4.0 to 9.0 mmol/L to fluvastatin (n=1,050) or placebo (n=1,052), with follow-up of five to six years and a mean of 5.1. Fluvastatin lowered LDL cholesterol by 32%. The primary endpoint — a major adverse cardiac event, defined as cardiac death, non-fatal myocardial infarction or coronary intervention — gave a risk ratio of 0.83 (95% CI 0.64 to 1.06), p=0.139. Not significant. The secondary combination of cardiac death or non-fatal myocardial infarction was 70 events against 104, risk ratio 0.65 (95% CI 0.48 to 0.88), p=0.005. Coronary intervention procedures and the other secondary endpoints did not differ. The authors’ own interpretation is careful: although cardiac deaths and non-fatal myocardial infarction seemed to be reduced, fluvastatin did not generally reduce rates of coronary intervention procedures or mortality. A secondary endpoint in a trial that missed its primary is a hypothesis, and the trial’s prespecified subgroup analyses were themselves precluded by the primary result.
Written into the record, not signed off as a reviewed claim
FLARE: no effect on the thing it was designed to measure
In plain words
Fluvastatin was given before and after balloon angioplasty to stop the artery re-narrowing. It did not. The re-narrowing was identical to two decimal places.
What was measured
Loss in minimal luminal diameter at 26 weeks after balloon angioplasty: 0.23 mm on fluvastatin against 0.23 mm on placebo, p=0.95
Effect estimate
No reviewed effect estimate exists for this record.
Limits
This entry records a failure.
From the source
FLARE randomised 1,054 patients to fluvastatin 40 mg twice daily or placebo, starting two to four weeks before planned balloon angioplasty and continuing to follow-up angiography at 26 weeks. The rationale was a laboratory claim that fluvastatin inhibits proliferating vascular myocytes more than other statins independently of lipid lowering. The primary endpoint — loss in minimal luminal diameter — was 0.23 ± 0.49 mm on fluvastatin against 0.23 ± 0.52 mm on placebo, p=0.95. Angiographic restenosis was 28% against 31%, p=0.42. The composite clinical endpoint at 40 weeks was 22.4% against 23.3%, p=0.74. Everything the trial was built to detect came back flat, and the authors state plainly that fluvastatin did not affect the process of restenosis and is not indicated for that purpose. A post-hoc observation of lower death and myocardial infarction — six patients (1.4%) against 17 (4.0%), log-rank p=0.025 — is included here because the authors themselves called it unprecedented and called for a priori investigation. That investigation became LIPS.
Written into the record, not signed off as a reviewed claim
A different enzyme, and therefore a different list of collisions
In plain words
Most statins are cleared by CYP3A4, so they clash with antifungals and antibiotics. This one is cleared mostly by CYP2C9, so it clashes with warfarin, phenytoin and a diabetes tablet instead.
What was measured
Fraction of fluvastatin metabolism attributable to each cytochrome P450 isoenzyme, and the resulting interaction directions
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
The label states that CYP2C9 is primarily involved in fluvastatin metabolism, at approximately 75%, with CYP3A4 at about 20% and CYP2C8 at about 5%. The interaction section follows directly from that: obtain an INR before starting warfarin-treated patients and monitor after initiation or discontinuation; monitor plasma phenytoin when fluvastatin is started; monitor blood glucose when it is started in patients on glyburide. Gemfibrozil, ciclosporin and fluconazole are to be avoided. The clinically important consequence is that a prescriber who has learned the statin interaction table from simvastatin will get this molecule wrong in both directions — expecting collisions that do not happen, and missing the anticoagulation one that does.
Source
Fluvastatin sodium extended-release tablets United States prescribing information, sections 7.1, 7.2 and 12.3
Role in the trial
Not matched to a registered study
Identity check
no open identity hold
Audit mark
verified
Review state
Written into the record, not signed off as a reviewed claim
Ninety times the price of simvastatin, for less
In plain words
A fluvastatin tablet costs a pharmacy about two dollars eighty. A simvastatin tablet costs about three cents. Both are generic, both block the same enzyme, and only one of them has trials measuring survival.
What was measured
Pharmacy acquisition cost per unit across the statin class, from a single survey date
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
From the same CMS National Average Drug Acquisition Cost survey effective 19 August 2026: fluvastatin US$2.82 per unit across 15 listed products; simvastatin US$0.0314 across 90; atorvastatin US$0.0281 across 278; rosuvastatin US$0.0449 across 179; pravastatin US$0.0620 across 93. Fluvastatin is roughly ninety times simvastatin, sixty times rosuvastatin and a hundred times atorvastatin. It is also the weakest of the five on LDL reduction and carries the narrowest cardiovascular indication. The proximate explanation for the price is the product count: 15 listed generics against 90 to 278 for the others, and a market that thin does not compete a price down. What that means for a reader is specific — a fluvastatin prescription is almost always a decision worth asking about, because the properties that would justify it are held by cheaper molecules.
Source
CMS National Average Drug Acquisition Cost (NADAC) survey, effective 19 August 2026, medians across listed products for fluvastatin, simvastatin, atorvastatin, rosuvastatin and pravastatin
Role in the trial
Not matched to a registered study
Identity check
no open identity hold
Audit mark
caution
Review state
Written into the record, not signed off as a reviewed claim
How many documents were read
11 documents were read for this substance.
RNAWiki source record
11 of them state the same halfLife, and they agree.
RNAWiki source record
11 of them state the same tMax, and they agree.
RNAWiki source record
11 of them state the same volumeOfDistribution, and they agree.
RNAWiki source record
Where else this substance is registered
FDA substance identifier (UNII)
PYF7O1FV7F
RxNorm concept
310405
Checks this page had to pass
✓ Passed
Identity resolved
no open identity hold
✓ Passed
No unresolved merge across substance families
no quarantine open
✓ Passed
Every public sentence names a source
The opening statement carries the origin: Written into the record, not signed off.
✗ Not passed
Trial roles classified for highlighted evidence
No registered study is classified as testing this substance.
✓ Passed
No internal keys in reader text
enforced by the copy-contract test over the rendered page
✓ Passed
Safety mode resolved
Suppression classes recorded: S3.
✓ Passed
Canonical metadata present
slug and display name present
What is missing or unclear◇Read from sources, not yet reviewed
How this medicine reached us
Kept near the foot of the page. A historical event moves up only when it changes something about this substance today.
What the approval register records
8 approved applications cover products containing this substance. The earliest was NDA020261, approved 19931231 to NOVARTIS.
This order is fixed in code and does not count clicks or time on the page.
What is not here
3 questions this page could not answer
These sections were prepared and left out because there was nothing to put in them. They are listed rather than hidden, so the gaps in this record are visible.
What it may clash with — found nothing in the sources checked.
Other ways to the same goal — found nothing in the sources checked.
What changed on this page — found nothing in the sources checked.
The record as stored
The full record, for auditing
Everything above is built from what is below. This layer keeps the technical vocabulary, record identifiers and every stored row, so a reader who wants to check the page can.
The older medicine-wide conclusion held in this record
Written for a clinical reader, and about the medicine as a whole rather than about one indication, population and set of trials. RNAWiki does not treat it as a programme conclusion and no reviewer has signed it off in that form. It is here word for word because it is what the record holds.
The first fully synthetic statin, licensed only to reduce coronary revascularisations and slow atherosclerotic progression — never to prevent infarction or death — which met its primary endpoint in LIPS (major adverse cardiac events 21.4% against 26.7%, RR 0.78, p=0.01) and missed it in both ALERT (RR 0.83, p=0.139) and FLARE (p=0.95), and which costs about ninety times as much per tablet as simvastatin.
Recorded evidence blocks (11)
Q2
What did Fluvastatin Sodium's largest trial (2067639 people) and its longest (11 years) measure?
2067639 people in Fluvastatin Sodium's largest registered study, 11 years in its longest registered window, measuring To study changes in CRP (mg/dL) concentration at the end of the study (12 months). ClinicalTrials.gov · 2026-09-01
19 phase4, 10 phase3, 9 phase2, 3 na or unstated, 1 early phase1, 1 na; NCT00404287; 2018-01. Last human test completed 2022, NCT03510884.
Interpretation These counts include studies where Fluvastatin Sodium was a comparison treatment, a background treatment or an exposure in an observational study, and the longest window may be a planned end date. Trial roles have not yet been classified for this record.
Show the evidence
phase4
19
phase3
10
phase2
9
na or unstated
3
early phase1
1
na
1
1 more recorded row
Last recorded human testNCT03510884
2022-08-05
recorded 2026-09-01 · last checked 2026-09-04
Q3
From mouse to human: where has Fluvastatin Sodium shown lifespan?
2 recorded entries; human; also "Fluvastatin 80 mg", "Fluvastatin 20 MG"
Show the evidence
human
NCT01715714
Fluvastatin 80 mg
NCT04029584
Fluvastatin 20 MG
recorded 2026-09-01 · last checked 2026-09-04
Q6
Fluvastatin Sodium's half-life is 3 hours — which schedules were studied?
3 hours, the half-life Fluvastatin Sodium's label states. openfda-label · ccd6bbe1-e293-4e1c-9ec4-e6c217612e77 · 2026-08-30
bioavailability 29% %.
Show the evidence
half life
3 hours hours; The elimination half-life (t 1/2 ) of fluvastatin is approximately 3 hours.
tmax
At steady state, administration of fluvastatin with the evening meal results in a 50% decrease in C max , an 11% decrease in AUC, and a more than two-fold increase in t max as compared to administration 4 hours after the evening meal.
bioavailability
29% %; The mean relative bioavailability of the extended-release tablet is approximately 29% (range, 9% to 66%) compared to that of the fluvastatin immediate-release capsule administered under fasting conditions.
metabolism
After single or multiple doses above 20 mg, fluvastatin exhibits saturable first-pass metabolism resulting in more than dose proportional plasma fluvastatin concentrations.
recorded 2026-08-30 · last checked 2026-09-04
Q7
Which of 30 day maces after pci, cardivasculary events and carotid imt did Fluvastatin Sodium's trials measure?
30 day maces after pci, cardivasculary events and carotid imt lead 22 outcome terms across Fluvastatin Sodium's trials. ClinicalTrials.gov · 2026-09-01
progression of calcified aortic stenosis measured by, transthoracic echocardiography, catheterization, cardivasculary events, penile blood flow after 8 weeks of treatment and viral load reduction liver test changes follow.
Show the evidence
low density lipoprotein cholesterol after 12 weeks
1
circulating marker of inflammation after 5 weeks
1
serum inflammatory markers after 52 weeks
1
progression of calcified aortic stenosis measured by
1
transthoracic echocardiography
1
catheterization
1
14 more recorded rows
cardivasculary events
1
penile blood flow after 8 weeks of treatment
1
viral load reduction liver test changes
1
sustained viral response
1
fasting plasma low density lipoprotein cholesterol
1
metabolic syndrome
1
general cardiovascular risk profile framingham heart study
1
reduction in low density lipoprotein cholesterol
1
30 day maces after pci
1
ldl c from baseline at study endpoint week 12
1
recurrent stroke
1
carotid imt
1
low density lipoprotein cholesterol
1
incident type 2 diabetes
1
recorded 2026-09-01 · last checked 2026-09-04
Q8
Which 20 trials of Fluvastatin Sodium posted no result?
Posted no result
20 of 20 completed trials
Registrations
NCT00171236, NCT00125125, NCT00138528, NCT00136799, NCT00821574 and NCT00171262, and 14 more
Completion dates
oldest 2005-03; newest 2021-03-31
Show the evidence
Trial
NCT00171236
2005-03
NCT00125125
2005-12
NCT00138528
2006-02
NCT00136799
2006-04
NCT00821574
2007-03
NCT00171262
2007-06
14 further recorded trials
NCT00441493
2007-09
NCT00814723
2007-09
NCT00199927
2008-03
NCT00718796
2009-10
NCT00549926
2010-02
NCT00487318
2010-10
NCT00416403
2011-06
NCT01293097
2011-10
NCT02518516
2013-01
NCT02518503
2013-02
NCT01992042
2016-12
NCT03189511
2018-02-19
NCT01715714
2020-09-27
NCT01563731
2021-03-31
Q9
At the median, Fluvastatin Sodium's trials enrolled 142 people — anything larger?
Median enrolment
142
Largest enrolment
2067639
Registered trials counted
42
Q10
Fluvastatin Sodium and CYP2C8, CYP2C9 and CYP3A4: shared by which compounds?
CYP2C8, CYP2C9 and CYP3A4 appear in Fluvastatin Sodium's recorded interaction sentences, 3 in all. openfda-label+europepmc · 2026-08-30
Interpretation pharmacokinetics
Show the evidence
CYP2C8pharmacokinetics
CYP2C9 isoenzyme is primarily involved in the metabolism of fluvastatin (approximately 75%), while CYP2C8 and CYP3A4 isoenzymes are involved to a much less extent, i.e., approximately 5% and approximately 20%, respectively.
CYP2C9pharmacokinetics
CYP2C9 isoenzyme is primarily involved in the metabolism of fluvastatin (approximately 75%), while CYP2C8 and CYP3A4 isoenzymes are involved to a much less extent, i.e., approximately 5% and approximately 20%, respectively.
CYP3A4pharmacokinetics
CYP2C9 isoenzyme is primarily involved in the metabolism of fluvastatin (approximately 75%), while CYP2C8 and CYP3A4 isoenzymes are involved to a much less extent, i.e., approximately 5% and approximately 20%, respectively.
recorded 2026-08-30 · last checked 2026-09-04
Q11
Was Fluvastatin Sodium studied with fasting and exercise?
fasting and exercise are named in Fluvastatin Sodium's label sentences: "In a randomized three-phase crossover study, 11 healthy volunteers ingested a single 20-mg dose of fluvastatin with green tea extract (GTE), containing 150 mg of EGCG, along with water (300 mL), brewed green tea (300 mL), or water (300 mL) after overnight fasting." openfda-label+europepmc · 2026-08-30
2 recorded statements; fasting, exercise
Show the evidence
fasting
In a randomized three-phase crossover study, 11 healthy volunteers ingested a single 20-mg dose of fluvastatin with green tea extract (GTE), containing 150 mg of EGCG, along with water (300 mL), brewed green tea (300 mL), or water (300 mL) after overnight fasting.
exercise
This 12-month, randomized, double-blind placebo-controlled study investigated the effect of statin (fluvastatin) treatment on ambulatory blood pressure (ABP), exercise blood pressure (EBP), myocardial structure, endothelial function and insulin resistance in 50 hypertensive patients.
recorded 2026-08-30 · last checked 2026-09-04
Q12
What is recorded about Fluvastatin Sodium and autophagy?
"Fluvastatin inhibits tumour progression and induces the autophagy of breast cancer cells; however, the role of autophagy in fluvastatin-induced inhibition of breast cancer metastasis is unknown." — where Fluvastatin Sodium and autophagy appear together. Europe PMC · pathway abstract search · 2024-05-27
"Fluvastatin inhibits tumour progression and induces the autophagy of breast cancer cells; however, the role of autophagy in fluvastatin-induced inhibition of breast cancer metastasis is unknown."
PMID 38123008
"We found that fluvastatin administration effectively prevented the migration/invasion of triple-negative breast cancer cells, an effect that was largely dependent on the induction of autophagy."
PMID 38123008
"Administration of the autophagy inhibitor chloroquine prevented the fluvastatin-induced suppression of lung metastasis in the nude mouse model."
mTOR
PMID 38123008
"Furthermore, fluvastatin increased Ras homolog family member B (RhoB) expression, and the autophagy and anti-metastatic activity induced by fluvastatin were predominantly dependent on the regulation of RhoB through the protein kinase B-mammalian target of rapamycin (Akt-mTOR) signaling pathway."
PMID 38123008
"These results suggest that fluvastatin inhibits the metastasis of triple-negative breast cancer cells by modulating autophagy via the up regulation of RhoB through the AKT-mTOR signaling pathway."
sirtuin
PMID 38801625
"The results showed that fluvastatin sodium may possess inhibitory activity against SIRT2."
PMID 38801625
"Subsequently, fluvastatin sodium was subjected to molecular docking experiments with various SIRT isoforms, and the combined results from Western blotting experiments indicated its potential as a SIRT2 inhibitor."
PMID 38801625
"Overall, this study provides a systematic virtual screening workflow for the discovery of SIRT2 activity inhibitors, identifies the potential inhibitory effect of fluvastatin sodium as a lead compound on SIRT2, and opens up a new direction for developing highly active and selectively targeted SIRT2 inhibitors."
mTORPMID 31675763
"The HMG-CoA reductase inhibitor fluvastatin reportedly activates the mTOR inhibitor AMP-activated protein kinase (AMPK), and we thought that it would potentiate vorinostat's anticancer activity in renal cancer cells."
AMPK
PMID 31675763
"The HMG-CoA reductase inhibitor fluvastatin reportedly activates the mTOR inhibitor AMP-activated protein kinase (AMPK), and we thought that it would potentiate vorinostat's anticancer activity in renal cancer cells."
PMID 31675763
"Vorinostat activated the mTOR pathway, as evidenced by the phosphorylation of ribosomal protein S6, and fluvastatin inhibited this phosphorylation by activating AMPK."
PMID 33793833
"Although fluvastatin inhibited prenylation in neuronal cells, the protective effects of fluvastatin against H2O2-induced neuronal cytotoxicity are not associated with prenylation inhibition or AMPK activation."
IGF-1
PMID 19254730
"We investigated the effects of fluvastatin on IGF-1-induced activation of intracellular signal pathways and MC proliferation, and examined the inhibitory mechanisms of fluvastatin."
PMID 19254730
"Fluvastatin or PD98059, an MEK1 inhibitor, completely abolished IGF-1-induced MEK1/2 and ERK1/2 phosphorylation and MC proliferation, whereas inhibition of Akt had no effect on MC proliferation."
PMID 19254730
"Mevalonic acid prevented fluvastatin inhibition of IGF-1-induced MEK1/2 and ERK1/2 phosphorylation, cyclin D1 expression, and MC proliferation."
recorded 2024-05-27 · last checked 2026-09-04
Where it is registeredIdentifiers, relations and other names
ClinicalTrials.gov — US Government work · Europe PMC — metadata only, under the recorded legal gate · derived from this page's own recorded fields; no external licence · mixed register set; per-register licences in docs/specs/corpus-20k-sources.md · openFDA / DailyMed — US Government work
✗ required summary fields resolved: 4 required field(s) not terminal: Why people use it, Best-supported result, Biggest unanswered question, Human evidence
✓ public claims reviewed: 0 reviewed claim(s); drafts are never rendered
✓ source coverage passed: 10 source rows
✓ no critical contamination: no quarantine open
✓ canonical metadata passed: slug and display name present
✓ no raw internal fields: enforced by the copy-contract test over the rendered page
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