Finerenone

Last updated on: 16.11.2025

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DefinitionThis section has been translated automatically.

Finerenone belongs to the group of diuretics and is a selective, non-steroidal mineralocorticoid receptor antagonist (MRA) that blocks the effect of aldosterone (non-steroidal aldosterone antagonist).

Finerenone is used in the treatment of CKD in combination with type 2 DM and has been shown to reduce cardio-renal risk (CKD progression, terminal renal failure, cardiovascular risk, in particular hospital admissions due to progression of HI)

Finerenone is a third-generation MRA, acts with higher selectivity only at the MR receptor and therefore has less risk of steroid-related side effects (e.g. gynecomastia) and a comparatively lower risk of hyperkalemia than steroidal MRAs of earlier generations such as spironolactone and eplerenone.

Furthermore, due to the positive cardiovascular results and additional clinical studies in HF with EF ≥40%, the aim is to extend the approval for the treatment of certain forms of HI (HFmrEF, HFpEF).

Pharmacodynamics (Effect)This section has been translated automatically.

Mechanism of action: Finerenone is a non-steroidal, selective antagonist of the mineralocorticoid receptor (MR), which is activated by aldosterone and cortisol and also regulates the gene transcription of proinflammatory and profibrotic mechanisms.

Inhibition of the aldosterone effect inhibits the reabsorption of sodium and water (diuresis) and reduces the excretion of potassium.

The reduction in blood pressure by finerenone is also directly mediated via the renin-angiotensin-aldosterone system (RAAS). By blocking the aldosterone effect, finerenone also generally counteracts the consequences of RAAS overactivation.

It is also thought to have a direct effect on the heart (remodeling).

Its binding to the MR creates a specific receptor-ligand complex that blocks the recruitment of transcriptional coactivators, which are involved in the expression of proinflammatory and profibrotic mediators, particularly in the case of overactivation, which are inhibited as a result (anti-inflammatory effect).

Phase III clinical safety and efficacy studies in adult patients with CKD and TYP2DM on renal and cardiovascular (CV) endpoints:

Short studies in patients with CKD showed that finerenone can reduce albuminuria.

FIDELIO-DKD RCT; study primarily focused on efficacy with regard to worsening renal disease and secondarily investigated cardiovascular outcome: 5734 patients with CKD and TYP2DM; UACR 30-300; eGFR 25-60 ml/min, diabetic retinopathy or UACR 300-5000; eGFR 25-75 ml/min. Background therapy: RAAS blockade with max. tolerated dose. Primary combined endpoint (time-to-effent): renal failure, persistent eGFR reduction of at least 40%, death of renal cause, mean follow-up 2.6 years. Results: renal failure, eGFR deterioration, death of renal cause. 17.8% patients with finerenone versus 21.1% patients with placebo group (HR 0.82; 95% CI, 0.73 to 0.93; P=0.001). Secondary composite endpoint: death from cardiovascular event, MI, stroke, hospitalization for HI. 13.0% finerenone versus 14.8% (HR 0.86; 95% CI, 0.75 to 0.99; P=0.03). Equivalent safety and tolerability as placebo, but increased rate of hyperkalemia with finerenone (2.3% versus 0.9%). Improved prognosis in CKD (stage 3 and 4 albuminuria), reduced risk of progression and death in CKD. Improvement in cardiovascular risk. (Bakris GL et al 2020).

FIGARO-DKD RCT: Study primarily focused on cardiovascular outcome in all stages of CKD in TYP2DM and secondarily on nephrological outcome. 7437 patients with CKD (all stages) and TYP2DM; UACR 30 to 300; eGFR 25 to 90 ml/min (stage 2 to 4 CKD) or UACR of 300 to 5000 and eGFR of at least 60 ml/min (stage 1 or 2 CKD). Background therapy: RAAS blockade with max. tolerated dose. Primary combined endpoint (time-to-event) death from cardiovascular causes, MI, stroke, hospitalization due to HI. Secondary combined endpoint of renal failure, persistent deterioration of eGFR at least 40%, death of renal causes, mean follow-up 3.4 years. Results: cardiovascular events Events 12.4% finerenone vs. 14.2% placebo (HR 0.87; 95%, CI 0.76 to 0.98, P=0.03) mainly due to less hospitalization for HI (HR 0.71; 95% CI, 0.56 to 0.90); renal endpoints: (9.5%) finerenone (10.8%) placebo (HR 0.87; 95% CI, 0.76 to 1.01). Same safety and tolerability as placebo, increased rate of hyperkalemia with finerenone (1.2%) versus placebo (0.4%) (Pitt B et al 2021). Improved prognosis in CKD (all stages 2-4), reduced risk of progression and death from CKD. Improvement in cardiovascular risk.

FINEARTS-HF RCT: Study primarily investigating cardiovascular outcome in patients with HFpEF and HFmrEF (EF≥40%). Finerenone 20mg or 40 mg plus standard therapy versus placebo. Primary combined endpoint all cardiovascular events (worsening HF with unplanned hospitalization or emergency treatment) and death of cardiovascular cause; 32 months median follow-up. Results: 1083 primary-outcome events in 624 of 3003 patients on finerenone; 1283 primary-outcome events in 719 of 2998 patients on placebo (rate ratio, 0.84; 95% CI, 0.74 to 0.95; P=0.007). Total number of events due to worsening HF: 842 with finerenone and 1024 with placebo (rate ratio, 0.82; 95% CI, 0.71 to 0.94; P=0.006). Death from cardiovascular causes: 8.1% finerenone versus 8.7% placebo (hazard ratio, 0.93; 95% CI, 0.78 to 1.11). Safety: higher risk of hyperkalemia and lower risk of hypokalemia with finerenone. I.e. significantly lower rate of events (esp. hospitalization) due to deterioration in patients with HFpEV and HFmrEF on finerenone (Solomon SD et al 2024). (This improvement also in addition to treatment with SGLT2 inhibitors (standard therapy for HF)). Extension of approval for this patient group (HFpEF, HFmrEF) has been applied for.

PharmacokineticsThis section has been translated automatically.

Absorption: rapid and almost complete absorption; maximum plasma concentrations (Cmax) 0.5 to 1.25 hours after fasting; absolute bioavailability is 43.5 % due to first-pass metabolism in the intestinal wall and liver; finerenone is a substrate of the efflux transporter P-glycoprotein in vitro, but probably not relevant for absorption in vivo due to high diffusibility of finerenone.

Distribution: Volume of distribution at steady state (Vss) 52.6 l. Plasma protein binding in humans is 91.7 % in vitro, primary binding protein is serum albumin.

Biotransformation/metabolism: by CYP3A4 approx. 90% and CYP2C8 approx. 10%; four main metabolites in serum; all are pharmacologically inactive.

Elimination: rapid elimination with elimination half-life (t½) of approx. 2 to 3 hours; systemic clearance from the blood is approx. 25 l/h; excretion via urine approx. 80 % and via feces approx. 20 % via feces; almost exclusively in the form of metabolites; only insignificantly low excretion of unchanged finerenone (< 1 % of the dose via urine due to glomerular filtration, < 0.2 % via feces).

Linear pharmacokinetics in the dose range from 1.25 mg to 80 mg, as a single oral dose.

 

IndicationThis section has been translated automatically.

Treatment of chronic kidney disease CKD (with albuminuria) in conjunction with type 2 diabetes in adults.

Pregnancy/nursing periodThis section has been translated automatically.

Important: Before treatment, women of childbearing age must be informed about contraindications during pregnancy and breastfeeding and adequate contraception must be ensured during treatment!

Pregnancy: Do not use during pregnancy! Animal studies show reproductive toxicity.

Reliable contraception is required for women of childbearing age! If pregnancy occurs unintentionally, information about the risks is absolutely necessary!

Lactation: Do not use during lactation or do not breastfeed during treatment! In animal studies, finerenone and metabolites pass into breast milk and young animals show toxicity. A risk for the infant cannot be excluded. Women should be informed about these risks and a decision should be made taking into account all aspects for or against breastfeeding versus for or against treatment with finerenone.

Dosage and method of useThis section has been translated automatically.

Recommended dose: 20 mg once a day; maximum dose: 20 mg once a day, orally, independent of food, not together with grapefruit or grapefruit juice! Forgotten dose: make up as soon as possible, but only on the same day; do not take a double dose!

Before starting treatment: it is mandatory to determine potassium and eGFR.

Decision to start treatment: only if potassium ≤4 .8 mmol/l.

if serum potassium ≥ 4.8- 5.0 mmol/l treatment may be considered taking into account the clinical situation and additional monitoring of the potassium level over 4 weeks.

Do not start treatment if potassium ≥5 mmol/l!

Monitoring: regular determination of eGFR and potassium obligatory during treatment! and, if necessary, additionally on the basis of patient characteristics.

Suspend ongoing treatmentif potassium 5.5 mmol/l! Follow guidelines for the treatment of hyperkalemia,

if potassium 5 mmol/l treatment can be continued under close monitoring, reduce dose if necessary.

Dose determination (starting dose) based on eGFR:


eGFR (ml/min/1.73 m2) Starting dose (once daily)
≥ 60 20 mg
≥ 25 to < 60 10 mg
< 25 Treatment with finerenone not recommended

Continuation of treatment in case of worsening of renal function impairment: at eGFR of ≥ 15 ml/min, treatment can be continued with dose adjustment according to potassium value and patient characteristics (dose regimens according to specialist information).

Current finerenone dose (once daily)
10 mg 20 mg
Current
potassium value
(mmol/l)≤ 4.8 increase to 20 mg once a day* maintain 20 mg once a day

> 4.8 to 5.5 Maintain 10 mg once a day Maintain 20 mg once a day

> 5.5 Discontinue finerenone Discontinue finerenone

If necessary, consider restarting with 10 mg once a day
if potassium ≤ 5.0 mmol/l.

(* Maintain 10 mg once daily if eGFR falls by > 30 % compared to the previous measurement)

In case of progression to terminal renal failure (eGFR < 15 ml/min/1.73 m2), discontinue treatment (insufficient clinical data).

Liver function impairment:

mild and moderate: no initial dose adjustment necessary; monitoring esp. serum potassium according to patient characteristics.

severe hepatic impairment: no use (no data available).

with concomitant medication that can lead to hyperkalemia : dose adjustment may also be necessary here! Close monitoring of potassium levels is also mandatory in this case!

Consider risk factors for increased risk of hyperkalemia: low eGFR, elevated serum potassium levels and previous episodes of hyperkalemia.

 

Undesirable effectsThis section has been translated automatically.

Very common: Hyperkalemia

Frequent: hyponatremia, hyperuricemia, hypotension, decreased eGFR, pruritus

Occasional: decreased hemoglobin

Overdose/toxicity: Hyperkalemia is most likely to occur and should be treated with the usual treatment methods.

Since plasma protein binding ≥90%, dialysis is not effective in case of overdose.

InteractionsThis section has been translated automatically.

The elimination of finerenone occurs almost exclusively via cytochrome P450(CYP) mediated oxidative metabolism, predominantly by CYP3A4(90 %) and to a lesser extent by CYP2C8(10 %).

contraindicated: concomitant use of strong CYP3A4inhibitors: itraconazole, clarithromycin, ketoconazole, ritonavir, nelfinavir, cobicistat, telithromycin or nefazodone, etc.
a considerable increase in finerenone exposure is to be expected!

not recommended: concomitant use of strong and moderate CYP3A4 inducers: rifampicin, carbamazepine, phenytoin, phenobarbital, St. John's wort, efavirenz, etc.
considerable decrease in plasma concentration and weakening of the therapeutic effect is expected!

Grapefruit: Ingredients CYP3A4 inhibitors, thereforeno consumption of grapefruit or grapefruit juice during treatment with finerenone! Increase in finerenone exposure!

 

Beware of hyperkalemia due to concomitant medication, simultaneous use not recommended for:

  • potassium-sparing diuretics (e.g. amiloride, triamterene)
  • other mineralocorticoid receptor antagonists (MRA), e.g. eplerenone, esaxerenone, spironolactone and canrenone

Increased monitoring of potassium levels with simultaneous use of:

  • Potassium supplements
  • Trimethoprim or trimethoprim/sulfmethoxazole (temporarily suspend finerenone if necessary!)

Take particular care with the following risk factors that increase the risk of hyperkalemia: low eGFR, elevated potassium levels and previous episodes of hyperkalemia.

Caution with simultaneous treatment with several antihypertensives; increased risk of hypotension (blood pressure should be monitored closely!)

ContraindicationThis section has been translated automatically.

  • Hypersensitivity to the active substance or any of the other ingredients.
  • Concomitant treatment with strong CYP3A4 inhibitors such as: Itraconazole, ketoconazole, ritonavir, nelfinavir, cobicistat, clarithromycin, telithromycin, nefazodone
  • Addison's disease.
  • Hyperkalemia ≥ 5 mmol/l (caution and close monitoring of values from 4.8.mmol/l; caution with low eGFR and history of hyperkalemia; caution with concomitant use of medications that can increase potassium, including potassium-sparing diuretics).
  • severe liver dysfunction (significant increase in exposure is expected).
  • Do not use in children and adolescents ≤18 years of age (no data available; no approval to date).
  • Patients with the rare hereditary galactose intolerance, complete lactase deficiency or glucose-galactose malabsorption should not use this medicinal product (contains lactose).

PreparationsThis section has been translated automatically.

Kerendia® (Bayer) 10mg/20mg Finerenone

LiteratureThis section has been translated automatically.

Bakris GL, Agarwal R, Anker SD et. al. for the FIDELIO-DK Investigators (2020). Effect of Finerenone on Chronic Kidney Disease Outcomes in Type 2 Diabetes. N Engl J Med 383:2219-2229. doi/10.1056/NEJMoa2025845

Pitt B, Filippatos G, Agarwal R et. al.for the FIGARO-DKD Investigators (2021). Cardiovascular Events with Finerenone in Kidney Disease and Type 2 Diabetes. N Engl J Med 385:2252-2263. doi/full/10.1056/NEJMoa2110956

Solomon SD, McMurray JJV, Vaduganathan M et. al. for the FINEARTS-HF Committees and Investigators (2024). Finerenone in Heart Failure with Mildly Reduced or Preserved Ejection Fraction. N Engl J Med 391:1475-1485. doi/full/10.1056/NEJMoa2407107

Specialist information Finerenone: Kerendia® 10mg/20mg (Bayer Healthcare)

Figure credits: Palanisamy S, Hernandez MF, Chang TI, Mahaffey KW (2022). Cardiovascular and Renal Outcomes with Finerenone, a Selective Mineralocorticoid Receptor Antagonist. Cardiol Ther (2022) 11:337-354 doi.org/10.1007/s40119-022-00269-3

Last updated on: 16.11.2025