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Finerenone

  • Prescription medicine
  • Prescription only
  • Identity checked
  • Sources last checked 2026-09-04

This page shows what was measured, who it was measured in, and what that does not settle.

What Finerenone does in the body

Used for diabetic kidney disease and one form of heart failure.

Aldosterone tells the kidney to hold salt and drives scarring in the heart and kidney. Finerenone blocks the receptor it acts on, but it is not built from a steroid skeleton, so it does not also block the male hormone receptor and it distributes evenly between heart and kidney instead of concentrating in the kidney. Less scarring, less protein leaking into the urine, and fewer heart failure admissions.

What happened in people

Added to standard treatment, finerenone modestly reduced worsening kidney disease and heart-failure admissions.

Reviewed first-read answer

Where this came from

A person wrote this and a reviewer approved it against this exact record. It carries no effect size.

A reviewer approved this against this record. The reviewed-claim record carrying the exact population and effect size does not exist yet.

No source is stored against this line.

The limit that matters most

No large study has shown that finerenone helps people live longer.

Where it acts
Mineralocorticoid receptors in kidney tubule, cardiac fibroblasts and vascular tissue
Kind of result
The kind of result is not recorded
Supervision
RNAWiki has not recorded a supervision or regulatory status for this substance.

What the registries record it as

  • The substance registry classes this as chemical.

    FDA substance registry · DE2O63YV8R · read 2026-08-29

  • Its recorded molecular formula is C21H22N4O3, weighing 378.43 g/mol.

    US prescribing information · fc726765-5d5a-4d6e-b037-b847bda9fb7c · read 2026-08-30

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.

The limit a reviewer approved as the one that matters most here.

The four opening statements run to 94 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 peopleRead 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 26 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.
GoalLife outcomeWhat a body can doHow a person feelsA test resultA step in the bodyHarmsHow longWho was studied
Blood sugarNothing 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
Blood sugar
progression of non proliferative diabetic retinopathy

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.
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 peopleRead 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.

Composite of kidney failure, sustained decrease of at least 40% in eGFR, or death from renal causes

The study showed what it set out to show

Who was studied
FIDELIO-DKD (NCT02540993)
How many people
5674
Study design
Randomised double-blind placebo-controlled trial, median 2.6 years
Compared against
A dummy treatment
Kind of result
Living longer, or avoiding a major event
What was found
HR 0.82 (95% CI 0.73-0.93), P = 0.001
Repeated elsewhere
Replicated

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 is dominated by a laboratory threshold (40% eGFR decline) rather than by kidney failure itself. Hyperkalaemia-related discontinuation was 2.3% against 0.9%.

How far it carries. This study is recorded from the curated record, not from the registry match.

Form and route. Oral tablet in two strengths

Interval reported. 95% CI 0

Written into the record, not signed off as a reviewed claim.

Composite of cardiovascular death, non-fatal myocardial infarction, non-fatal stroke or hospitalisation for heart failure

The study showed what it set out to show

Who was studied
FIGARO-DKD (NCT02545049)
How many people
7437
Study design
Randomised double-blind placebo-controlled trial, median 3.4 years
Compared against
A dummy treatment
Kind of result
Living longer, or avoiding a major event
What was found
HR 0.87 (95% CI 0.76-0.98), P = 0.03
Repeated elsewhere
Replicated

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 paper states the benefit was driven primarily by heart failure hospitalisation (HR 0.71). The kidney secondary composite gave 0.87 with an interval reaching 1.01.

How far it carries. This study is recorded from the curated record, not from the registry match.

Form and route. Oral tablet in two strengths

Interval reported. 95% CI 0

Written into the record, not signed off as a reviewed claim.

Composite of total worsening heart failure events and death from cardiovascular causes, ejection fraction ≥40%

The study showed what it set out to show

Who was studied
FINEARTS-HF (NCT04435626)
How many people
6001
Study design
Randomised double-blind placebo-controlled trial, median 32 months
Compared against
A dummy treatment
Kind of result
Living longer, or avoiding a major event
What was found
Rate ratio 0.84 (95% CI 0.74-0.95), P = 0.007
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. Cardiovascular death alone was 8.1% against 8.7%, HR 0.93 (0.78-1.11). The endpoint counted total recurrent events rather than time to first, which increases power and weights repeat admitters more heavily.

How far it carries. This study is recorded from the curated record, not from the registry match.

Form and route. Oral tablet in two strengths

Interval reported. 95% CI 0

Written into the record, not signed off as a reviewed claim.

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 peopleRead 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.

  1. Living longer, or avoiding a major event No evidence recorded. Death, a heart attack, a stroke, a hospital stay.No registered study measures this.
  2. What a body can do day to day No evidence recorded. Walking, dressing, breathing, recovering.No registered study measures this.
  3. Measured performance No evidence recorded. How much was lifted, how far was run, how fast.No registered study measures this.
  4. Symptoms and quality of life No evidence recorded. Pain, tiredness, mood, sleep, as the person rated it.No registered study measures this.
  5. A number that stands in for health Evidence recorded. Cholesterol, blood sugar, bone density. A stand-in, not the thing itself.5 registered measures of this kind.
  6. A step measured inside a person Evidence recorded. Something measured in human tissue or human cells.A human record sits on the stored organism ladder.
  7. Animals Evidence recorded. Mice, rats, dogs. Useful for ideas, not proof about people.Stored records in Mouse. A result in animals says what to test next. It does not say what happens in people.
  8. Cells in a dish Evidence recorded. Cells or chemistry on a bench, far from a whole body.Stored mechanism abstracts describe steps measured in cells or tissue.
  9. A guess from software No 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 bodyRead 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.

  1. Start

    Finerenone

    What a person takes: Oral tablet in two strengths.

    The measurement behind this step

    Once daily with or without food. The half-life is only 2 to 3 hours, so the effect depends on receptor occupancy rather than on sustained plasma concentration. Clearance is dominated by CYP3A4, and strong inhibitors of that enzyme are contraindicated while strong inducers are to be avoided.

  2. Getting in

    Absorbed completely and cleared by one liver enzyme

    Essentially all of the tablet is absorbed, and a single liver enzyme removes it. Drugs that block that enzyme raise levels substantially.

    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

    Oral bioavailability is about 44% after first-pass metabolism, with essentially complete absorption. Clearance is dominated by CYP3A4 with a minor CYP2C8 contribution, and the half-life is 2 to 3 hours — short, so the sustained effect depends on receptor occupancy rather than on drug persistence. Strong CYP3A4 inhibitors are contraindicated in the label.

  3. Reaching the cell

    It distributes evenly between heart and kidney rather than concentrating in kidney

    Steroidal blockers pile up in the kidney. This one spreads roughly evenly between kidney and heart tissue, which is the argument for why it affects cardiac scarring at doses that do not maximally block the kidney.

    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

    Being non-steroidal and lacking the steroid transport characteristics of spironolactone and its metabolites, finerenone shows an approximately balanced tissue distribution between cardiac and renal tissue in preclinical work, whereas the steroidal antagonists concentrate in kidney. Its target, the mineralocorticoid receptor, is a cytoplasmic nuclear-receptor-family transcription factor present in tubular epithelium, cardiac fibroblasts and myocytes, and vascular smooth muscle.

  4. What it acts on

    It jams the receptor open in a shape that cannot recruit its partners

    Rather than simply competing for the pocket, its bulky shape holds the receptor in a form that cannot assemble the machinery it needs to switch genes on.

    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 bulky dihydronaphthyridine scaffold binds the ligand-binding domain and destabilises the receptor-coactivator interface, protruding into helix 12 and preventing the agonist conformation required for coactivator recruitment. Because it shares no skeleton with aldosterone, affinity for androgen, progesterone and glucocorticoid receptors is negligible, which removes the endocrine off-target effects that limit spironolactone.

  5. The change it makes

    Sodium retention and pro-fibrotic gene programmes both fall

    The kidney holds less salt and keeps more potassium, and in the heart and kidney the genes driving inflammation and scarring are turned down.

    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

    Reduced mineralocorticoid receptor signalling lowers transcription of the epithelial sodium channel subunits and serum and glucocorticoid-regulated kinase 1, producing natriuresis and potassium retention. In cardiac fibroblasts and renal cells it reduces transcription of connective tissue growth factor, transforming growth factor beta targets, plasminogen activator inhibitor-1 and inflammatory mediators, which is the proposed basis for reduced albuminuria and slowed eGFR decline rather than for the diuretic effect.

  6. What that does for a person

    Kidney decline slows and heart failure admissions fall; death does not change

    Across three large trials the consistent findings are slower kidney deterioration and fewer heart failure hospitalisations. Cardiovascular deaths were not reduced in any of them.

    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

    FIDELIO-DKD: kidney composite 17.8% against 21.1%, hazard ratio 0.82. FIGARO-DKD: cardiovascular composite 12.4% against 14.2%, hazard ratio 0.87, driven by heart failure hospitalisation at 0.71. FINEARTS-HF: total heart failure events plus cardiovascular death, rate ratio 0.84, with cardiovascular death alone at 0.93 (0.78 to 1.11).

No suggested links are held for this record, so nothing is hidden from this path.

What we know
The record describes 5 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 takeRead 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.

  • urinary albumin to creatinine
  • kidney function
  • urine albumin to creatinine
  • systolic blood pressure
  • urine albumin to creatinine uacr

Meaningful

Things that change how a life goes, not only a number.

No registered study measured anything of this kind.

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 (21)
  • progression of non proliferative diabetic retinopathy
  • treatment emergent adverse event
  • serious adverse events
  • clinical benefit
  • egfr slope
  • mace + hhf
  • treatment adherence
  • 24h systolic bp drop value
  • treatment emergent adverse events
  • estimated glomerular filtration rate
  • chronic egfr slope
  • left ventricular mass indexed to baseline body surface area
  • albuminuria
  • adverse events
  • on study retention rate at 6 months
  • sustained decline in egfr 30
  • uacr
  • markers of renal health
  • markes of cardio health
  • incidence of treatment emergent adverse events

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 takeRead 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.

  1. Before anything is noticed. RNAWiki does not store this separately, and never works it out from another figure on this page.

  2. Before a test result moves. RNAWiki does not store this separately, and never works it out from another figure on this page.

  3. Before performance moves. RNAWiki does not store this separately, and never works it out from another figure on this page.

  4. How long the result was watched. No finished study window is recorded for a study that tested this substance.

  5. How long people took it. How long people actually took it is not stored. The study window is not the same thing.

  6. 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.

  7. How fast the body clears it. 2 to 3 hours hours

    Read from the label, which states: “Elimination The terminal half-life of finerenone is about 2 to 3 hours, and the systemic blood clearance is about 25 L/h.”

  8. How long effects linger. RNAWiki does not store this separately, and never works it out from another figure on this page.

  9. 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 unclearRead 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.

  • People with chronic kidney disease and type 2 diabetes already on maximum tolerated renin-angiotensin blockade, and people with heart failure and an ejection fraction of 40% or above. Increasingly used alongside an SGLT2 inhibitor rather than instead of one.

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 efficacy of Kerendia have not been established in patients below 18 years of age.”

    US prescribing information · fc726765-5d5a-4d6e-b037-b847bda9fb7c · read 2026-08-30

  • On older people, the label states: “Of the 6510 patients who received Kerendia in the FIDELIO-DKD and FIGARO-DKD studies, 55% of patients were 65 years and older, and 14% were 75 years and older.”

    US prescribing information · fc726765-5d5a-4d6e-b037-b847bda9fb7c · read 2026-08-30

  • On people who are pregnant, the label states: “Risk Summary There are no available data on Kerendia use in pregnancy to evaluate for a drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes.”

    US prescribing information · fc726765-5d5a-4d6e-b037-b847bda9fb7c · read 2026-08-30

  • On people who are breastfeeding, the label states: “Risk Summary There are no data on the presence of finerenone or its metabolite in human milk, the effects on the breastfed infant or the effects of the drug on milk production.”

    US prescribing information · fc726765-5d5a-4d6e-b037-b847bda9fb7c · read 2026-08-30

  • On people with reduced liver function, the label states: “Avoid use of Kerendia in patients with severe hepatic impairment (Child Pugh C).”

    US prescribing information · fc726765-5d5a-4d6e-b037-b847bda9fb7c · read 2026-08-30

Where the result stopped carrying

  • The kidney secondary composite in FIGARO-DKD gave a hazard ratio of 0.87 with a confidence interval reaching 1.01
  • Cardiovascular death alone was not significantly reduced in FINEARTS-HF
  • Spironolactone, the cheap steroidal predecessor, missed in the same preserved-ejection-fraction territory that FINEARTS-HF was designed to address, and no trial has compared the two
  • 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 takeRead 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 takeRead 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 tablet in two strengths

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

RNAWiki has not recorded a supervision or regulatory status for this substance.

Quoted from a source

Where this came from

Copied from a source RNAWiki stored, with the source named.

No register row and no identity class settled the question.

No source is stored against this line.

What is in the pack

Once daily with or without food. The half-life is only 2 to 3 hours, so the effect depends on receptor occupancy rather than on sustained plasma concentration. Clearance is dominated by CYP3A4, and strong inhibitors of that enzyme are contraindicated while strong inducers are to be avoided.

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 and what that means for what is in the pack.

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 takeRead 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

Hyperkalaemia is the defining risk and the reason potassium is checked before starting and periodically after: hyperkalaemia-related discontinuation was 2.3% against 0.9% on placebo in FIDELIO-DKD and 1.2% against 0.4% in FIGARO-DKD. It is contraindicated with strong CYP3A4 inhibitors and in adrenal insufficiency. Because it is not a steroid, it does not cause the gynaecomastia, breast pain or menstrual irregularity associated with spironolactone. All trials required maximised renin-angiotensin blockade at baseline, which itself raises potassium.

Nobody counted how many people took this and were fine, so this cannot be turned into a rate.

Where this came from

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 unclearRead 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 tablet in two strengths

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

The half-life is only 2 to 3 hours, so the effect depends on receptor occupancy rather than on sustained plasma concentration. Clearance is dominated by CYP3A4, and strong inhibitors of that enzyme are contraindicated while strong inducers are to be avoided.

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

  • 15 products list this as an active ingredient in the United States drug directory. 15 of them contain it and nothing else.

    FDA National Drug Code directory · 70600-059 · read 2026-08-29

  • They are sold as powder, tablet and tablet, film coated, taken oral.

    FDA National Drug Code directory · 70600-059 · read 2026-08-29

  • The regulator's established pharmacologic class for it is mineralocorticoid receptor antagonists [moa] and nonsteroidal mineralocorticoid-receptor antagonist [epc].

    FDA National Drug Code directory · 70600-059 · read 2026-08-29

  • 1 published label names it as an active ingredient. 1 of them describe this substance alone, which is where its own label text on this page comes from.

    US prescribing information · fc726765-5d5a-4d6e-b037-b847bda9fb7c · read 2026-08-29

  • Those labels are classed as human prescription drug.

    US prescribing information · fc726765-5d5a-4d6e-b037-b847bda9fb7c · read 2026-08-29

  • Kerendia is oral at 3 DOSAGE FORMS AND STRENGTHS Kerendia is available as film-coated, oblong tablets in three strengths. 10 mg: pink, with "FI" on one side, "10" on the other side. 20 mg: yellow, with "FI" on one side, "20" on the other s…, recorded as fda label in effect 2025-08-28 in the United States.

    US prescribing information · fc726765-5d5a-4d6e-b037-b847bda9fb7c · read 2026-08-30

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 takeRead 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.

RNAWiki could not confidently classify this substance, so no self-experiment plan is offered.

Questions worth asking

  • Which of the trials of Finerenone 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 unclearRead 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 finerenone reduces cardiovascular death — the hazard ratio was 0.93 (0.78 to 1.11) in FINEARTS-HF and cardiovascular death was never separately significant in the kidney trials

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 finerenone is superior to spironolactone — no head-to-head trial exists, and spironolactone holds the only mortality result 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.

Goes past the evidence

That the FIDELIO-DKD result represents prevented kidney failure — the composite is dominated by a 40% eGFR decline threshold rather than by dialysis or transplantation

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 balanced cardiac and renal tissue distribution explains the clinical difference from spironolactone — a mechanistic argument, not a tested one

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 unclearRead 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 Finerenone 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 peopleRead 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.

FIDELIO-DKD: kidney progression fell 17.8% against 21.1%
In plain words
In more than five and a half thousand patients with diabetic kidney disease already on maximum standard therapy, finerenone reduced the combined kidney endpoint by about a sixth relative.
What was measured
Composite of kidney failure, sustained 40% eGFR decline or renal death over a median 2.6 years
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
FIDELIO-DKD randomised patients with chronic kidney disease and type 2 diabetes 1:1 to finerenone or placebo. Eligibility required either a urinary albumin-to-creatinine ratio of 30 to under 300 with eGFR 25 to under 60 and diabetic retinopathy, or a ratio of 300 to 5,000 with eGFR 25 to under 75. All patients were on renin-angiotensin blockade titrated before randomisation to the maximum labelled dose that did not cause unacceptable side effects. Over a median 2.6 years the primary composite of kidney failure, a sustained decrease of at least 40% in eGFR, or death from renal causes occurred in 504 of 2,833 (17.8%) against 600 of 2,841 (21.1%): hazard ratio 0.82 (95% CI 0.73 to 0.93), p=0.001. The key secondary composite of cardiovascular death, non-fatal infarction, non-fatal stroke or heart failure hospitalisation occurred in 367 (13.0%) against 420 (14.8%): hazard ratio 0.86 (0.75 to 0.99), p=0.03. Adverse event frequency was similar overall; hyperkalaemia-related discontinuation was 2.3% against 0.9%.
Source
Bakris GL et al., FIDELIO-DKD, N Engl J Med 2020;383:2219-2229 (NCT02540993)
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
FIGARO-DKD: the cardiovascular composite fell, driven by heart failure admissions
In plain words
A second trial of more than seven thousand patients measured cardiovascular events as its main endpoint. It fell, and the paper states the benefit came mainly from fewer heart failure hospitalisations.
What was measured
Composite of cardiovascular death, non-fatal infarction, non-fatal stroke or heart failure hospitalisation over a median 3.4 years
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
FIGARO-DKD randomised 7,437 patients with type 2 diabetes and either stage 2 to 4 chronic kidney disease with moderately elevated albuminuria or stage 1 or 2 with severely elevated albuminuria, all on maximum tolerated renin-angiotensin blockade. Over a median 3.4 years the primary composite of cardiovascular death, non-fatal myocardial infarction, non-fatal stroke or hospitalisation for heart failure occurred in 458 of 3,686 (12.4%) against 519 of 3,666 (14.2%): hazard ratio 0.87 (95% CI 0.76 to 0.98), p=0.03, with the paper stating the benefit was driven primarily by a lower incidence of heart failure hospitalisation (hazard ratio 0.71, 0.56 to 0.90). The first secondary composite of kidney failure, sustained 40% eGFR decline or renal death occurred in 350 (9.5%) against 395 (10.8%): hazard ratio 0.87 (0.76 to 1.01) — an interval that includes no effect. Hyperkalaemia-related discontinuation was 1.2% against 0.4%.
Source
Pitt B et al., FIGARO-DKD, N Engl J Med 2021;385:2252-2263 (NCT02545049)
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
FINEARTS-HF: succeeded where spironolactone missed, on a total-events endpoint
In plain words
In six thousand patients with heart failure and a normal or near-normal pumping fraction, the combined endpoint fell by about a sixth. Cardiovascular deaths were 8.1% against 8.7%, which is not a demonstrated difference.
What was measured
Total worsening heart failure events plus cardiovascular death, as a rate ratio over a median 32 months
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
FINEARTS-HF randomised patients with heart failure and left ventricular ejection fraction of 40% or greater 1:1 to finerenone at a maximum of 20 or 40 mg once daily, or placebo, on top of usual therapy. Over a median 32 months there were 1,083 primary-outcome events in 624 of 3,003 patients on finerenone against 1,283 events in 719 of 2,998 on placebo: rate ratio 0.84 (95% CI 0.74 to 0.95), p=0.007. Total worsening heart failure events were 842 against 1,024: rate ratio 0.82 (0.71 to 0.94), p=0.006. Cardiovascular death occurred in 8.1% against 8.7%: hazard ratio 0.93 (0.78 to 1.11) — an interval including no effect. Finerenone was associated with increased hyperkalaemia and reduced hypokalaemia. The primary endpoint counted total recurrent events rather than time to first, a design choice that increases statistical power and weights patients with multiple admissions more heavily.
Source
Solomon SD et al., FINEARTS-HF, N Engl J Med 2024;391:1475-1485 (NCT04435626)
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
Every composite was carried by its softest component, and no trial changed mortality
In plain words
Across three large trials the endpoints that moved were kidney function decline and heart failure admissions. Cardiovascular death never moved, and total death was never shown to.
What was measured
That finerenone reduces cardiovascular death or mortality — the cardiovascular death hazard ratios were 0.93 in FINEARTS-HF and never separately significant in the kidney trials
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
FIDELIO-DKD: the primary composite is dominated by sustained 40% eGFR decline, a laboratory-defined event rather than kidney failure itself. FIGARO-DKD: the paper states the cardiovascular benefit was driven primarily by heart failure hospitalisation (hazard ratio 0.71), and its kidney secondary composite gave 0.87 with an interval reaching 1.01. FINEARTS-HF: the primary was total worsening heart failure events plus cardiovascular death, and cardiovascular death alone gave 0.93 (0.78 to 1.11). Hospitalisation is a clinician decision as well as a patient event, and a 40% eGFR decline is a threshold crossing on a blood test. None of this makes the results less real — slowing kidney decline and keeping people out of hospital are worth doing in their own right. It does mean that a summary describing finerenone as reducing cardiovascular death or mortality is describing something none of the three trials demonstrated.
Source
Bakris GL et al., N Engl J Med 2020;383:2219-2229; Pitt B et al., N Engl J Med 2021;385:2252-2263; Solomon SD et al., N Engl J Med 2024;391:1475-1485
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
Finerenone has never been compared with spironolactone, which costs a fraction as much
In plain words
The two block the same receptor. One is a brand-only drug with three modern trials; the other is a generic costing cents with a mortality result the newer drug has never matched. No trial has compared them.
What was measured
That finerenone is superior to spironolactone — no head-to-head randomised trial exists, and spironolactone holds the only mortality result in the class
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Every finerenone trial used placebo on a background of maximised renin-angiotensin blockade. None used spironolactone or eplerenone as a comparator, so the entire case for the non-steroidal class over the steroidal one rests on indirect comparison plus receptor-selectivity and tissue-distribution arguments. The available indirect facts point in both directions: spironolactone reduced all-cause death from 46% to 35% in severe heart failure with reduced ejection fraction, which finerenone has never demonstrated in any population; and spironolactone missed its primary endpoint in preserved ejection fraction in TOPCAT (p=0.14) and after myocardial infarction in CLEAR SYNERGY, where finerenone succeeded in the first of those. The selectivity difference is real and measurable at the receptor — no androgen antagonism, therefore no gynaecomastia — and the hyperkalaemia rates in the finerenone trials are lower than the doubling seen in TOPCAT, though across different populations and monitoring protocols. What none of this is, is a randomised comparison.
Source
Bakris GL et al., N Engl J Med 2020;383:2219-2229; Pitt B et al., RALES, N Engl J Med 1999;341:709-717; Pitt B et al., TOPCAT, N Engl J Med 2014;370:1383-1392
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
Hyperkalaemia is lower than with the steroidal antagonists and is still the limiting effect
In plain words
About one in forty patients stopped finerenone because of high potassium in the kidney trials, against about one in a hundred on placebo. That is a smaller problem than with spironolactone, and it is the same problem.
What was measured
Hyperkalaemia-related discontinuation rates against placebo across two randomised trials
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Hyperkalaemia-related discontinuation of trial regimen occurred in 2.3% on finerenone against 0.9% on placebo in FIDELIO-DKD, and 1.2% against 0.4% in FIGARO-DKD; overall adverse event frequency did not differ substantially in either. FINEARTS-HF reported increased hyperkalaemia and reduced hypokalaemia. For comparison, TOPCAT recorded hyperkalaemia in 18.7% on spironolactone against 9.1% on placebo — a different measure in a different population with a different monitoring schedule, so the comparison is indicative rather than quantitative. All the finerenone trials required maximised renin-angiotensin blockade at baseline, which itself raises potassium, and all excluded patients whose baseline potassium exceeded a threshold. The spironolactone page records what happened when a mineralocorticoid antagonist result was rolled out into practice without those safeguards: hyperkalaemia hospitalisations in one Canadian province rose from 2.4 to 11.0 per 1,000 eligible patients.
Source
Bakris GL et al., N Engl J Med 2020;383:2219-2229; Pitt B et al., N Engl J Med 2021;385:2252-2263; Juurlink DN et al., N Engl J Med 2004;351:543-551
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

Where else this substance is registered

FDA substance identifier (UNII)
DE2O63YV8R
RxNorm concept
2562816

Checks this page had to pass

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    No registered study is classified as testing this substance.

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    Canonical metadata present

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What is missing or unclearRead 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

  • 1 approved application covers products containing this substance. The earliest was NDA215341, approved 20210709 to BAYER HLTHCARE.

    Drugs@FDA application register · NDA215341 · read 2026-08-29

  • Marketing status on the register: prescription.

    Drugs@FDA application register · NDA215341 · read 2026-08-29

  • The earliest marketing start date recorded for a listed product is 20210701.

    FDA National Drug Code directory · 70600-059 · read 2026-08-29

What is missing or unclearRead from sources, not yet reviewed

What to learn next

Ordered by what would most change how you read this page, starting with what is easiest to misunderstand.

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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.

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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.

A non-steroidal aldosterone blocker with three positive large trials and no demonstrated mortality benefit in any of them: the kidney composite fell 17.8% against 21.1% in 5,674 patients, the cardiovascular composite 12.4% against 14.2% in 7,352 driven mainly by heart failure hospitalisation, and the heart failure composite by a rate ratio of 0.84 in 6,001 with cardiovascular death unchanged at 8.1% against 8.7%.

Recorded evidence blocks (13)

What did Finerenone's largest trial (150000 people) and its longest (6 years) measure?


150000 people in Finerenone's largest registered study, 6 years in its longest registered window, measuring Cardiovascular Mortality and Heart Failure Hospitalization. ClinicalTrials.gov · 2026-09-01

23 phase4, 19 phase3, 16 na or unstated, 10 phase2, 6 na, 3 phase1; NCT05457283; 2028-11-07; no ageing endpoint recorded. Last human test completed 2026, NCT06835322.

Interpretation These counts include studies where Finerenone 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
    23
  • phase3
    19
  • na or unstated
    16
  • phase2
    10
  • na
    6
  • phase1
    3
1 more recorded row
  • Last recorded human test NCT06835322
    2026-04-01

recorded 2026-09-01 · last checked 2026-09-04

From mouse to human: where has Finerenone shown lifespan?


mouse: mechanism-only and human: lifespan (77): the rungs where Finerenone has a recorded finding. Europe PMC and ClinicalTrials.gov · organism ladder · 2026-09-01

Interpretation Cardiovascular Mortality and Heart Failure Hospitalization — the recorded outcome words.

Yeast C. elegans Drosophila Mouse mechanism-onlyRat Dog Non-human primate Human lifespan
Show the evidence
  • mouse
    mechanism-only
  • human NCT07351864
    lifespan; Cardiovascular Mortality and Heart Failure Hospitalization; 77

recorded 2026-09-01 · last checked 2026-09-04

Why did Finerenone's trial NCT06818305 stop?


1 recorded trial of Finerenone stopped. ClinicalTrials.gov · 2026-09-01

"The patient enrollment rate is proceeding too slowly"; 1 of 77 registered studies

Show the evidence
  • Trial NCT06818305
    terminated; "The patient enrollment rate is proceeding too slowly"

recorded 2026-09-01 · last checked 2026-09-04

Human studies of Finerenone used Finerenone (BAY94-8862): 20 mg intact tablet — over how long?


Human studies of Finerenone used "Finerenone (BAY94-8862): 20 mg intact tablet". ClinicalTrials.gov · 2026-09-01

7 recorded entries; human; tablet; also "Finerenone (BAY94-8862): 20 mg crushed and resuspended tablet", "Finerenone (BAY94-8862): 20 mg suspension", "Finerenone (BAY94-8862 ) 10 mg"

Show the evidence

human

  • NCT02957396
    tablet; Finerenone (BAY94-8862): 20 mg intact tablet
  • NCT02957396
    tablet; Finerenone (BAY94-8862): 20 mg crushed and resuspended tablet
  • NCT02957396
    Finerenone (BAY94-8862): 20 mg suspension
  • NCT05254002
    Finerenone (BAY94-8862 ) 10 mg
  • NCT05254002
    Finerenone (BAY94-8862 ) 20 mg
  • NCT06244758
    Finerenone 20 MG Oral Tablet
1 more recorded row
  • human NCT07155694
    Finerenone 10 MG

recorded 2026-09-01 · last checked 2026-09-04

Finerenone's half-life is 2 to 3 hours — which schedules were studied?


2 to 3 hours, the half-life Finerenone's label states. openfda-label · fc726765-5d5a-4d6e-b037-b847bda9fb7c · 2026-08-30

bioavailability 44% %.

Show the evidence
  • half life
    2 to 3 hours hours; Elimination The terminal half-life of finerenone is about 2 to 3 hours, and the systemic blood clearance is about 25 L/h.
  • bioavailability
    44% %; Absorption Finerenone is completely absorbed after oral administration but undergoes metabolism resulting in absolute bioavailability of 44%.
  • metabolism
    Absorption Finerenone is completely absorbed after oral administration but undergoes metabolism resulting in absolute bioavailability of 44%.

recorded 2026-08-30 · last checked 2026-09-04

Could one person measure Finerenone's effect on urinary albumin to creatinine?


Urinary albumin to creatinine: measured in Finerenone's trials.

Interpretation urinary albumin to creatinine is the recorded endpoint.

Show the evidence

biomarkers

  • urinary albumin to creatinine; 2026-09-01
  • progression of non proliferative diabetic retinopathy; 2026-09-01
  • treatment emergent adverse event; 2026-09-01
  • serious adverse events; 2026-09-01
  • clinical benefit; 2026-09-01
  • egfr slope; 2026-09-01
14 more recorded rows
  • biomarkers
    mace + hhf; 2026-09-01
  • biomarkers
    treatment adherence; 2026-09-01
  • biomarkers
    24h systolic bp drop value; 2026-09-01
  • biomarkers
    kidney function; 2026-09-01
  • biomarkers
    urine albumin to creatinine; 2026-09-01
  • biomarkers
    treatment emergent adverse events; 2026-09-01
  • biomarkers
    systolic blood pressure; 2026-09-01
  • biomarkers
    estimated glomerular filtration rate; 2026-09-01
  • biomarkers
    chronic egfr slope; 2026-09-01
  • biomarkers
    left ventricular mass indexed to baseline body surface area; 2026-09-01
  • biomarkers
    albuminuria; 2026-09-01
  • biomarkers
    adverse events; 2026-09-01
  • biomarkers
    urine albumin to creatinine uacr; 2026-09-01
  • biomarkers
    on study retention rate at 6 months; 2026-09-01
  • half life
    2026-09-04; halfLife; hours; 2 to 3 hours; 2026-08-30
  • human trials at or under30
    6
  • smallest human trial
    10; NCT06818305; PHASE2; the smallest recorded human enrolment at or below 30; the registry states no direction of its result; TERMINATED

Which of 24h systolic bp drop value, adherence to study drug and adverse events did Finerenone's trials measure?


24h systolic bp drop value, adherence to study drug and adverse events lead 26 outcome terms across Finerenone's trials. ClinicalTrials.gov · 2026-09-01

serious adverse events, clinical benefit, egfr slope, mace + hhf, treatment adherence and 24h systolic bp drop value follow.

Show the evidence
  • urinary albumin to creatinine
    1
  • progression of non proliferative diabetic retinopathy
    1
  • treatment emergent adverse event
    1
  • serious adverse events
    1
  • clinical benefit
    1
  • egfr slope
    1
14 more recorded rows
  • mace + hhf
    1
  • treatment adherence
    1
  • 24h systolic bp drop value
    1
  • kidney function
    1
  • urine albumin to creatinine
    1
  • treatment emergent adverse events
    1
  • systolic blood pressure
    1
  • estimated glomerular filtration rate
    1
  • chronic egfr slope
    1
  • left ventricular mass indexed to baseline body surface area
    1
  • albuminuria
    1
  • adverse events
    1
  • urine albumin to creatinine uacr
    1
  • on study retention rate at 6 months
    1

recorded 2026-09-01 · last checked 2026-09-04

Which of Finerenone's 45 ongoing trials reports first?


45 registered trials of Finerenone are open; earliest completion 2026-05-21. ClinicalTrials.gov · 2026-09-01

Percent change in Urinary protein-to-creatinine ratio (UPCR) reduction from baseline to day 180+/-7; Descriptive analysis of clinical characteristics of participants with chronic kidney disease (CKD) and with type 2 diabetes(T2D).; latest 2031-12-31

Show the evidence

Trial

  • NCT05196035
    "A Study to Learn More About How Well the Study Treatment Finerenone Works, How Safe it is, How it Moves Into, Through, and Out of the Body, and the Effects it Has on the Body When Taken With an ACE Inhibitor or Angiotensin Receptor Blocker in Children With Chronic Kidney Disease and Proteinuria"; n 219; "Percent change in Urinary protein-to-creatinine ratio (UPCR) reduction from baseline to day 180+/-7"; 2027-05-10
  • NCT05348733
    "A Study Called FINE-REAL to Learn More About the Use of the Drug Finerenone in a Routine Medical Care Setting"; n 4613; "Descriptive analysis of clinical characteristics of participants with chronic kidney disease (CKD) and with type 2 diabetes(T2D)."; 2026-12-22
  • NCT05457283
    "A Study to Learn More About How Safe the Study Treatment Finerenone is in Long-term Use When Taken With an ACE Inhibitor or Angiotensin Receptor Blocker Over 18 Months of Use in Children and Young Adults From 1 to 18 Years of Age With Chronic Kidney Disease and Proteinuria"; n 100; "Number of participants with treatment emergent adverse event (TEAEs)"; 2028-11-07
  • NCT06008197
    "A Study to Determine the Efficacy and Safety of Finerenone on Morbidity and Mortality Among Hospitalized Heart Failure Patients"; n 5200; "Composite of total HF events and cardiovascular (CV) death."; 2027-12
  • NCT06024746
    "A Study to Determine the Efficacy and Safety of Finerenone and SGLT2i in Combination in Hospitalized Patients With Heart Failure (CONFIRMATION-HF)"; n 1500; "Clinical benefit"; 2027-11
  • NCT06033950
    "A Study to Evaluate Finerenone on Clinical Efficacy and Safety in Patients With Heart Failure Who Are Intolerant or Not Eligible for Treatment With Steroidal Mineralocorticoid Receptor Antagonists"; n 2600; "Time to first occurrence of cardiovascular (CV) death or HF event."; 2028-01
14 further recorded trials
  • NCT06058585
    "The Chronic Kidney Disease Adaptive Platform Trial Investigating Various Agents for Therapeutic Effect"; n 1000; "eGFR slope"; 2029-03-31
  • NCT06059664
    "The EFfect of FinErenone in Kidney TransplantiOn Recipients: The EFFEKTOR Study"; n 100; "Feasibility of recruitment to the main clinical trial: Total number of participants who were eligible and enrolled in the main clinical trial"; 2027-12-31
  • NCT06082063
    "Multifactorial Intervention to Reduce Cardiovascular Disease in Type 1 Diabetes"; n 2000; "MACE + HHF"; 2029-07-01
  • NCT06278207
    "An Observational Study Called FINEROD to Learn More About the Use of the Treatment Finerenone Including How Safe it is and How Well it Works Under Real-world Conditions"; n 50000; "Participants' characteristics at baseline in a cohort of participants with CKD and T2D who initiate finerenone."; 2026-09-30
  • NCT06580288
    "Effect of Finerenone in IgA Nephropathy"; n 120; "change in uACR between the two groups"; 2026-10-08
  • NCT06608212
    "An Observational Study to Learn More About How Safe Finerenone is and How Well it Works in People With Chronic Kidney Disease and Type 2 Diabetes in Routine Medical Care in the United States"; n 150000; "Time to the first occurrence of composite cardiovascular outcome"; 2026-06-30
  • NCT06727409
    "Use of Clinical-trials and Simulation Models to Estimate Cost-effectiveness of Non-steroidal Mineralocorticoid Antagonists, RASi and SGLT2i as Triple Therapy With Type 2 Diabetes and Chronic Kidney Disease"; n 82; "Change in urine albumin creatinine ratio (uACR)"; 2026-12-31
  • NCT06763146
    "An Observational Study to Learn More About How Safe Finerenone is and How Well it Works in Indian People With Chronic Kidney Disease and Type 2 Diabetes in Routine Medical Practice"; n 1200; "Descriptive summary of specialty of prescribing physician"; 2026-09-30
  • NCT06838416
    "Evaluation of the Effect of Finerenone on Renal Function in Patients With Type 2 Diabetes and Chronic Kidney Disease"; n 300; "Change in Urine Albumin-to-Creatinine Ratio (UACR)"; 2026-12-31
  • NCT06906081
    "Finerenone Treatment for Diabetic Cardiovascular Autonomic Neuropathy: the FibroCAN Study"; n 100; "Between-group (finerenone vs. placebo) difference in changes on the CART E/I ratio"; 2028-01
  • NCT06954090
    "Urinary Proteomics to Guide Early Intervention to Prevent Complications in Type 2 Diabetes - a Feasibility Study"; n 50; "Proteomic feasibility"; 2027-05-31
  • NCT07026539
    "Effect of Treatment With Finerenone on Cardio-Renal Target Organ Damage in Patients With Type 2 Diabetes."; n 80; "Change in left ventricular mass measured by non-contrast cardiac MRI of the heart"; 2028-04-30
  • NCT07056595
    "Finerenone in Patients With IgA-nephropathy: Prospective Interventional Trial"; n 30; "Median change in albuminuria from baseline"; 2026-05-21
  • NCT07155694
    "Role of Finerenone in African American Veterans With Diabetic Kidney Disease"; n 30; "Urine Exosome Assay"; 2027-08

recorded 2026-09-01 · last checked 2026-09-04

Which running trial of Finerenone could settle lifespan?


NCT07351864 measures Cardiovascular Mortality and Heart Failure Hospitalization, reading out 2026-07-31.

2 open trials; n 60; "Finerenone Plus SGLT2 Inhibitors in Heart Failure"

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Trial

  • NCT07351864
    "Finerenone Plus SGLT2 Inhibitors in Heart Failure"; n 60; "Cardiovascular Mortality and Heart Failure Hospitalization"; 2026-07-31
  • NCT07575672
    "Finerenone in Patients Undergoing Transcatheter Aortic Valve Implantation With Heart Failure"; n 2832; "A composite of all-cause mortality or worsening of heart failure (hospitalization for HF or urgent HF visit), any of the first occurrence during the follow-up."; 2029-12-31

Which 9 trials of Finerenone posted no result?


Posted no result
9 of 9 completed trials
Registrations
NCT04908436, NCT01968668, NCT04881994, NCT02957396, NCT04477707 and NCT04795726, and 3 more
Completion dates
oldest 2012-01-27; newest 2024-03-31
Show the evidence

Trial

  • NCT04908436
    2012-01-27
  • NCT01968668
    2014-11-07
  • NCT04881994
    2014-12-08
  • NCT02957396
    2017-03-01
  • NCT04477707
    2021-06-25
  • NCT04795726
    2021-06-30
3 further recorded trials
  • NCT05640180
    2023-12-20
  • NCT05924620
    2024-03-12
  • NCT06460987
    2024-03-31

At the median, Finerenone's trials enrolled 160 people — anything larger?


Median enrolment
160
Largest enrolment
150000
Registered trials counted
77

Finerenone and CYP3A4, CYP2C8 and BCRP: shared by which compounds?


CYP3A4, CYP2C8 and BCRP appear in Finerenone's recorded interaction sentences, 11 in all. openfda-label+europepmc · 2026-08-30

Interpretation pharmacokinetics

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CYP2C8

  • pharmacokinetics
    Metabolism Finerenone is primarily metabolized by CYP3A4 (90%) and to a lesser extent by CYP2C8 (10%) to inactive metabolites.
  • pharmacokinetics
    There was no clinically significant difference in finerenone pharmacokinetics when used concomitantly with gemfibrozil (strong CYP2C8 inhibitor).
  • pharmacokinetics
    CYP2C8 Substrates: Concomitant use of multiple finerenone 40 mg doses once daily with repaglinide (sensitive CYP2C8 substrate) increased the mean AUC and C max of repaglinide by 59% and 30%, respectively.
  • CYP2C9 pharmacokinetics
    Other Drugs : No clinically significant differences in the pharmacokinetics of the following drugs were observed or predicted when used concomitantly with finerenone: S-warfarin (CYP2C9 substrate), digoxin (P-gp substrate), and rosuvastatin (BCRP and OATP substrate).

CYP3A4

  • pharmacokinetics
    Metabolism Finerenone is primarily metabolized by CYP3A4 (90%) and to a lesser extent by CYP2C8 (10%) to inactive metabolites.
  • pharmacokinetics
    CYP3A4 Substrates: Concomitant use of multiple finerenone 40 mg doses once daily with midazolam (sensitive CYP3A4 substrate) increased the mean AUC by 31% with no effect on C max .
  • pharmacokinetics
    Strong or Moderate CYP3A Inducers : Concomitant use of efavirenz (moderate CYP3A4 inducer) and rifampicin (strong CYP3A4 inducer) was predicted to decrease finerenone AUC by 80% and 90%, respectively.
  • pharmacokinetics
    Drug Interaction Studies Clinical Studies and Model-Informed Approaches Strong CYP3A Inhibitors : Concomitant use of itraconazole (strong CYP3A4 inhibitor) was predicted to increase finerenone AUC by >400%.
  • pharmacokinetics
    Moderate CYP3A Inhibitors : Concomitant use of erythromycin (moderate CYP3A4 inhibitor) increased finerenone mean AUC and C max by 248% and 88%, respectively.
  • pharmacokinetics
    Concomitant use of verapamil (moderate CYP3A4 inhibitor) increased finerenone mean AUC and C max by 170% and 122%, respectively.
1 more recorded row
  • CYP3A4 pharmacokinetics
    Weak CYP3A Inhibitors : Concomitant use of amiodarone (weak CYP3A4 inhibitor) increased finerenone AUC by 21%.

recorded 2026-08-30 · last checked 2026-09-04

What is recorded about Finerenone and AMPK?


"Finerenone inhibits and antagonizes excessive MR activation, enhanced AMP-activated protein kinase (AMPK) phosphorylation, and downregulated sterol regulatory element-binding protein 1 (SREBP1) and fatty acid synthase (FASN), thereby inhibiting de novo lipogenesis." — where Finerenone and AMPK appear together. Europe PMC · pathway abstract search · 2026-06-12

AMPK, autophagy, mTOR; PMID 42264075, 42209198, 42285992, 41101220

Show the evidence

AMPK

  • PMID 42264075
    "Finerenone inhibits and antagonizes excessive MR activation, enhanced AMP-activated protein kinase (AMPK) phosphorylation, and downregulated sterol regulatory element-binding protein 1 (SREBP1) and fatty acid synthase (FASN), thereby inhibiting de novo lipogenesis."
  • PMID 42264075
    "Conversely, aldosterone reversed the lipid-lowering effects of finerenone through the AMPK/SREBP1/FASN pathway."
  • PMID 42264075
    "In conclusion, finerenone alleviates hepatic lipid accumulation in MASLD, at least in part, by inhibiting MR signaling and modulating the AMPK/SREBP1/FASN pathway."

autophagy

  • PMID 42209198
    "Moreover, Atg5 knockdown counteracted Finerenone-mediated suppression of fibrosis-related proteins, confirming that Finerenone's anti-fibrotic effects depend on Atg5-mediated autophagy activation."
  • PMID 42285992
    "Finerenone significantly improved the viability of cardiomyocytes and endothelial cells subjected to OGD, reduced autophagosome accumulation by enhancing autophagosome degradation, inhibited apoptosis, and promoted endothelial cell migration and tube formation capacity."
  • PMID 42285992
    "Finerenone confers significant cardioprotection by inhibiting autophagy, apoptosis, and enhancing angiogenesis in both cardiomyocytes and vascular endothelial cells."
  • mTOR PMID 41101220
    "The combined administration of finerenone and exenatide demonstrated potent nephroprotective effects in DN by attenuating inflammation and oxidative damage via modulation of NF-κB, PI3K/Akt/mTOR, and NRF2 pathways."

recorded 2026-06-12 · last checked 2026-09-04

Where it is registered
Identifiers, relations and other names

The exact record

ChEMBL id
CHEMBL2181927
PubChem CID
59349636
CAS number
1050477-30-9
RxCUI
2562816
InChIKey
BTBHLEZXCOBLCY-QGZVFWFLSA-N
Development code
BAY 94-8862
Also called
Bay94-8862, Finerenona, bay948862, Finerenone [INN], Finerenone [JAN], Finerenone [MI], Finerenone [ORANGE BOOK], Finerenone [USAN], Finerenone [WHO-DD]
Trade name
Kerendia
Sources (9)

Sources

3 more sources
  • openfda-label fc726765-5d5a-4d6e-b037-b847bda9fb7c ·
  • openfda-label+europepmc K1:DE2O63YV8R ·
  • national registers US, EU, CA ·

ChEMBL ATC CC BY-SA · 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

How these records are assembled · Which registers were checked

Index-quality checks
  • identity passed: no open identity hold
  • 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: 9 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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