Finerenone Oral

Kidney and Cardiovascular Disease Risk Reduction in Patients with Type 2 Diabetes

Finerenone is used to reduce the risk of sustained estimated glomerular filtration rate (eGFR) decline, end-stage kidney disease, cardiovascular death, nonfatal myocardial infarction, and hospitalization for heart failure in adult patients with chronic kidney disease (CKD) associated with type 2 diabetes.^[1] Efficacy of finerenone for this use was established in 2 randomized, double-blind, phase 3 trials (FIDELIO-DKD and FIGARO-DKD).^[1][2][3] Guidelines from the American Diabetes Association (ADA) and Kidney Disease: Improving Global Outcomes (KDIGO) recommend the use offinerenone for patients with type 2 diabetes and CKD at high risk for CKD progression and cardiovascular events despite use of recommended therapies.^[5][6]

Clinical Experience

Efficacy of finerenone for reduction in decline of eGFR, kidney failure, or renal death in adult patients with CKD associated with type 2 diabetes was evaluated in the FIDELIO-DKD trial: a phase 3, randomized, double-blind trial.^[1][2] In FIDELIO-DKD, 5674 patients were randomized to treatment (1:1 ratio) with either finerenone or placebo and followed for a median of 2.6 years.^[1][2] The starting dose of finerenone was based on eGFR and titrated to a target of 20 mg daily.^[1] The primary outcomewas a composite of kidney failure (defined as chronic dialysis, kidney transplantation, or a sustained decrease in eGFR to <15 mL/min/1.73m²), a sustained decrease of >=40% in eGFR from baseline over at least 4 weeks, or death from renal causes.^[1][2] The key secondary outcome was a composite of death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure.^[1][2]

Enrolled patients had a mean age of 66 years, 70% were male, 63% were white, and 5% were Black (24% in the United States cohort).^{[1] [2]} The mean eGFR at baseline was 44 mL/min/1.73m²; 55% of patients had an eGFR <45 mL/min/1.73m².^[1][2]

The primary outcome occurred in 17.8% or 21.1% of finerenone- or placebo-treated patients, respectively.^[2] Finerenone resulted in an event rate of 7.6 per 100 patient-years for the primary renal composite outcome compared to 9.1 events per 100 patient-years with placebo.^[1] For the secondary composite cardiovascular outcome, use of finerenone resulted in a reduction of events (13% for finerenone vs. 14.8% for placebo), with an event rate of 5.1 per 100 patient-years in patients treated with finerenone and 5.9 events per 100 patient-years for placebo.^[1][2]

Efficacy of finerenone in the reduction of risk of cardiovascular events (cardiovascular death, nonfatal myocardial infarction, and hospitalization for heart failure) in patients with type 2 diabetes and CKD was evaluated in the FIGARO-DKD study: a phase 3, randomized, double-blind trial.^[1][3] In FIGARO-DKD, 7352 patients were randomized to treatment (1:1 ratio) with either finerenone or placebo and followed for a median of 3.4 years.^[1][3] The starting dose of finerenone was based on eGFR and titrated to a target of 20 mg daily.^[1] The primary outcomewas a composite of death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure.^[1][3] The secondary outcomewas a composite of time to kidney failure (defined as end-stage renal disease or a sustained decrease in eGFR to <15 mL/min/1.73m²over a period of >=4 weeks), a sustained decline in eGFR of >=40% compared to baseline over at least 4 weeks, or renal death.^[1][3]

Enrolled patients had a mean age of 64 years, 69.4% were male, 71.8% were white, and 3.5% were Black.^[3] The mean eGFR at baseline was 67.8 mL/min/1.73m²; 62% of patients had an eGFR >=60 mL/min/1.73m².^[3]

The primary outcome occurred in 12.4% or 14.2% of finerenone- or placebo-treated patients, respectively.^[3] Finerenone resulted in an event rate of 3.9 per 100 patient-years for the primary cardiovascular event composite outcome compared to 4.5 events per 100 patient-years with placebo.^[1] For the secondary composite renal event outcome, use of finerenone resulted in a reduction of events (9.5% for finerenone vs. 10.8% for placebo), with an event rate of 3.2 per 100 patient-years in patients treated with finerenone and 3.6 events per 100 patient-years for placebo.^[1][3]

Clinical Perspective

Chronic kidney disease occurs in approximately 40% of adult patients with type 2 diabetes and is defined as persistentlyelevated urinary albumin excretion (>30 mg/g) and/or persistentlyreduced eGFR (<60 mL/min/1.73m²) for >3 months.^[4][5] Albuminuria, regardless of eGFR, is associated with an increased risk of cardiovascular disease, CKDprogression, and mortality.^[6] Current recommendations from Kidney Disease: Improving Global Outcomes (KDIGO) for treatment of patients with diabetes and CKD include a comprehensive approach, with lifestyle management (e.g., weight loss, smoking cessation, diet, exercise) and drug therapy for glycemic control, lipid management, and blood pressure control to provide both renal and cardiovascular protection.^[5] First-line drug therapies include a sodium-glucose cotransporter-2 inhibitor (SGLT2i), metformin, a renin-angiotensin system (RAS) inhibitor, and moderate- to high-intensity statins.^[5] Additional risk-based therapies include glucagon-like peptide-1 (GLP-1) receptor agonists, dihydropyridine calcium channel blockers and/or diuretics, antiplatelet agents, and additional lipid-lowering agents such as ezetimibe.^[5] The KDIGO guidelines recommend use offinerenone for patients with type 2 diabetes and an eGFR >=25 mL/min/1.73m², a normal serum potassium concentration, and albuminuria >=30 mg/g, who are at high risk for CKD progression and cardiovascular events, despite a maximally tolerated dose of a RAS inhibitor.^[5]

Recommendations from the American Diabetes Association (ADA) for the treatment of patients with diabetes and CKD are similar to those of KDIGO and include an SGLT2i and a RAS inhibitor (for patients with hypertension and albuminuria), with a goal of glucose and blood pressure control to reduce CKD progression as well as cardiovascular risks.^[6] For patients withCKD and albuminuriaat risk for CKD progression or cardiovascular events, use offinerenone is recommended.^[6]

General

Pretreatment Screening

Measure serum potassium levels and estimated glomerular filtration rate (eGFR) prior to initiating treatment with finerenone.^[1] Do not initiate if serum potassium is >5 mEq/L.^[1]

Patient Monitoring

Measure serum potassium levels 4 weeks after treatment initiation, 4 weeks after any dose adjustment, upon initiation or dosage adjustment of moderate or weak cytochrome P450 (CYP) isoenzyme 3A4 inhibitors, and periodically throughout treatment.^[1] More frequent monitoring is warranted in patients receiving concomitant treatment with drugs or supplements that increase potassium levels.^[1]Monitor eGFR periodically throughout treatment.^[1]

Administration

Finerenone is available as atablet administered orally once daily with or without food.^[1] For patients unable to swallow whole tablets, finerenone can be crushed and mixed with water or soft foods (e.g., applesauce) immediately prior to use.^[1]

A missed dose should be taken as soon as possible,but onlyon the same day.^[1] If not taken on the same day, skip the dose and resume with the next scheduled dose as prescribed.^[1]

Store tablets at 20-25°C (excursions permitted to 15-30°C).^[1]

Dosage

Adults

Kidney and Cardiovascular Disease Risk Reduction in Patients with Type 2 Diabetes

The recommended starting dosage for finerenone is based on eGFR.^[1] For patients with an eGFR >=60 mL/min/1.73m², startingdosage is20 mg once daily.^[1] For patients with an eGFR >=25 to <60 mL/min/1.73m², startingdosage is10 mg once daily.^[1] Initiation of finerenone is not recommended for patients with an eGFR <25 mL/min/1.73m².^[1]

The target dose of finerenone is 20 mg once daily.^[1] Measure serum potassium 4 weeks after initiating treatment and adjust the dose based on the potassium level (See Table 1).^[1] Monitor serum potassium 4 weeks after any dosage adjustment and throughout treatment, and adjust the dose further as needed.^[1]

If eGFR hasdecreased by >30% compared to previous measurement, maintain 10 mg dose.\[1 \]

Special Populations

Hepatic Impairment

No dosage adjustment is required in patients with mild to moderate hepatic impairment (Child Pugh A and B).^[1] Consider additional serum potassium monitoring in patients with moderate hepatic impairment (Child Pugh B).^[1] Avoid use in patients with severe hepatic impairment (Child Pugh C).^[1]

Renal Impairment

Renal function is used to guide starting dosage.^[1] Initiation of finerenone is not recommended in patients with an eGFR <25 mL/min/1.73m².^[1]

Geriatric Use

No dosage adjustment is required in geriatric patients.^[1]

Contraindications

Concomitant treatment with strong cytochrome P450 (CYP) isoenzyme 3A4 inhibitors.^[1]Adrenal insufficiency.^[1]

Warnings/Precautions

Hyperkalemia

Finerenone can cause hyperkalemia.^[1] The risk for developing hyperkalemia increases with declining renal function and is greater in patients with higher potassium levels at baseline or other risk factors for hyperkalemia.^[1]

Measure serum potassium and estimated glomerular filtration rate (eGFR) in all patients prior to initiation and periodically throughout treatment and adjustdose accordingly.^[1] Do not initiate finerenone if the serum potassium is >5 mEq/L.^[1] More frequent monitoring may be necessary for patients at risk for hyperkalemia, including those on concomitant medications that impair potassium excretion or increase serum potassium.^[1]

Specific Populations

Pregnancy

There are no available data on finerenone use in pregnancy to evaluate for a drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes.^[1] Animal studies have shown developmental toxicity at exposures about 4 times those expected in humans.^[1]

Lactation

There are no data on the presence of finerenone in human milk, the effects on the breast-fed infant, or the effect on milk production.^[1] Ina pre- and postnatal developmental toxicity study in rats, increased pup mortality and lower pup weight were observed at approximately 4 times the area under the concentration-time curve (AUC)_unbound expected in humans.^[1] These findings suggest that finerenone is present in rat milk.^[1] When a drug is present in animal milk, it is likely that it is present in human milk.^[1]

Due to the potential risk to breast-fed infants from exposure to finerenone, avoid breastfeeding during treatment and for 1 day after treatment.^[1]

Pediatric Use

Safety and efficacy of finerenone have not been established in patients <18 years of age.^[1]

Geriatric Use

Of the 6510 patients who received finerenone in clinical studies, 55% were >=65 years of age and 14% were >=75 years of age.^[1] No overall differences in safety or efficacy were observed between these patients and younger patients.^[1]

Renal Impairment

There were no clinically relevant differences in AUC or maximum plasma concentrations in patients with aneGFR 15 to <90 mL/min/1.73m² compared to aneGFR >=90 mL/min/1.73m².^[1]

Hepatic Impairment

No clinically significant effect on finerenone exposure observed in patients with mild hepatic impairment (Child Pugh A).^[1] The mean AUC was increased by 38% and no change in maximum plasma concentration was observed in cirrhoticpatients with moderate hepatic impairment (Child Pugh B) compared to healthy controls.^[1] The effect of severe hepatic impairment (Child Pugh C) on finerenone pharmacokinetics has not been studied.^[1]

Common Adverse Effects

Adverse effects that occurred in >=1% of patients on finerenone and more frequently than placebo in clinical trials include hyperkalemia, hypotension, and hyponatremia.^[1]

Finerenone is a cytochrome P450 (CYP) isoenzyme 3A4 substrate.^[1]

Drugs Affecting or Metabolized by Hepatic Microsomal Enzymes

CYP Inhibitors

Use of finerenone is contraindicated in patients receiving concomitant treatment with strong CYP3A4 inhibitors; concomitant use with these drugs increases exposure to finerenone, increasing the risk of adverse reactions.^[1] Concomitant use of itraconazole (a strong CYP3A4 inhibitor) increased finerenone area under the concentration-time curve (AUC) by >400%.^[1] Avoid concomitant intake of grapefruit or grapefruit juice.^[1]

Concomitant use of finerenone with weak or moderate CYP3A4 inhibitors increases exposure to finerenone and may increase the risk of adverse reactions.^[1] Concomitant use of erythromycin (amoderate CYP3A4 inhibitor) increased finerenone AUC by 248% and maximum serum concentration (C_max) by 88%.^[1] Concomitant use of amiodarone (aweak CYP3A4 inhibitor) increased finerenone AUC by 21%.^[1] If used concomitantly, monitor serum potassium during drug initiation or dosage adjustment of finerenone or moderate/weak CYP3A4 inhibitors, and adjust the finerenone dosage as appropriate.^[1]

No clinically significant difference in finerenone pharmacokinetics was seen when used concomitantly with gemfibrozil (astrong CYP2C8 inhibitor).^[1]

CYP Inducers

Concomitant use of finerenone with a moderate or strong CYP3A4 inducer decreases exposure to finerenone and may reduce its efficacy.^[1] Concomitant use of rifampin (astrong CYP3A4 inducer) decreased finerenone AUC by 90%.^[1] Concomitant use of efavirenz (amoderate CYP3A4 inducer) decreased finerenone AUC by 80%.^[1] Avoid concomitant use of finerenone with strong or moderate CYP3A4 inducers.^[1]

CYP Substrates

Drug interaction studies have not shown finerenone to impact the pharmacokinetics of warfarin (a CYP2C9 substrate), midazolam (a CYP3A4 substrate), or repaglinide (a CYP2C8 substrate).^[1]

Drugs Affecting or Affected by Transport Proteins

Concomitant use of finerenone with digoxin (a P-glycoprotein [P-gp] substrate) or rosuvastatin (a breast cancer resistance protein [BCRP] and organic anion transport protein [OATP] substrate) has not been shown to have clinically significant effects on the pharmacokinetics of either agent.^[1]

Drugs Affecting Gastric Acidity

No clinically significant difference in finerenone pharmacokinetics was seen when used concomitantly with omeprazole (aproton pump inhibitor) or an aluminum hydroxide and magnesium hydroxide antacid.^[1]

Drugs Affecting Serum Potassium

More frequent serum potassium monitoring is warranted in patients receiving concomitant therapy with drugs or supplements that increase serum potassium.^[1]

Finerenone is a nonsteroidal, selective antagonist of the mineralocorticoid receptor (MR); the MR is activated by aldosterone and cortisol and regulates gene transcription.^[1] Finerenone prevents sodium reabsorpotion via MR antagonism and prevents overactivation of MR in epithelial and nonepithelial tissues.^[1] Overactivation of the MR is thought to contribute to fibrosis and inflammation.^[1] Finerenone has a high potency and selectivity for the MR and does not have relevant affinity for androgen, progesterone, estrogen, and glucocorticoid receptors.^[1]

Finerenone exposure increased proportionally over a dose range of 1.25-80 mg (0.06-4 times the maximum approved dosage).^[1] After oral administration, finerenone is completely absorbed but undergoes metabolism resulting in an absolute bioavailability of 44%.^[1] The maximum plasma concentrations are achieved in approximately 0.5 to 1.25 hours following a dose, with steady-state concentrations achieved after 2 days of dosing.^[1] No significant impact on pharmacokinetics was observed following administration of a high fat, high calorie food.^[1] Finerenone is 92% protein-bound, primarily to albumin.^[1] The terminal half-life of finerenone is 2-3 hours.^[1] Metabolism primarilyoccurs by cytochrome P450 (CYP) isoenzyme 3A4 (90%) and to a lesser extent by CYP2C8 (10%) to inactive metabolites.^[1] About 80% of the administered dose is excreted in urine (<1% as unchanged) and approximately 20% in feces (<0.2% as unchanged).^[1] Age (18-79 years), sex, race/ethnicity (white, Asian, Black, and Hispanic), or weight (58-121 kg) do not have a clinically significant effect on the pharmacokinetics of finerenone.^[1]

Advise patients of the need for periodic monitoring of serum potassium levels.^[1] Advise patients to consult with their clinician before using potassium supplements or salt substitutes containing potassium.^[1] Advise patients to avoid strong or moderate cytochrome P450 (CYP) isoenzyme 3A4 inducers and to find alternative medicinal products with no or weak potential to induce CYP3A4.^[1] Advise patients to avoid concomitant intake of grapefruit or grapefruit juice as it is expected to increase finerenone concentrations.^[1]Advise women to inform their clinician if they are or plan to become pregnant or plan to breast-feed.^[1] Advise women that breast-feeding is not recommended during treatment with finerenone and for 1 day after treatment.^[1]Advise patients to inform their clinician of existing or contemplated concomitant therapy, including prescription and OTC drugs and dietary or herbal supplements, as well as any concomitant illnesses.^[1]Inform patients of other important precautionary information.^[1]

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

AHFS Drug Information®. © Copyright, 1959-2024, Selected Revisions November 27, 2023. American Society of Health-System Pharmacists®, 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

This AHFS Drug Information Database is copyrighted by the American Society of Health-System Pharmacists, Inc. (C) 2025, ASHP, Bethesda, Maryland 20814. All Rights Reserved. Duplication must be expressly authorized by ASHP, unless such duplication consists of printing or downloading portions of the data inherent in the program for non-commercial use.

The American Society of Health-System Pharmacists, Inc. represents that the database provided hereunder as formulated with a reasonable standard of care, and in conformity with professional standards in the field. The American Society of Health-System Pharmacists, Inc. makes no representations or warranties, express or implied, including, but not limited to, any implied warranty or merchantability and/or fitness for a particular purpose, with respect to such database and specifically disclaims all such warranties and representations. Users are advised that decisions regarding drug therapy are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and the database if provided for informational purposes only. The entire monograph for a drug should be reviewed for a throrough understanding of the drug's actions, uses and side effects. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug in the database. The information contained in the database is not a substitute for medical care or treatment by a licensed health care provider.