Finerenone 10mg tablets
Requires a prescription from a doctor or prescriber
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Safety monitoring data
Yellow Card reports
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
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Suspected adverse reactions reported for Finerenone
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1 branded products available
MHRA licensed products
View all licensed products for Finerenone on the MHRA register
Kerendia 10mg tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
20 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(3)
Finerenone for treating chronic kidney disease in type 2 diabetes (TA877)
Finerenone for treating chronic heart failure with preserved or mildly reduced ejection fraction (TA1182)
Chronic kidney disease: assessment and management (NG203)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Codes for healthcare professionals and prescribing systems
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NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 20 · Randomised trials: 25 · 2020–2026
Showing the 50 most relevant studies, sorted by most relevant.
M. Vaduganathan, G. Filippatos, B. Claggett, et al.
Nature Medicine, 2024
J. C. Rivera-Martinez, Michael Sabina, Aqeel Khanani, et al.
Cardiovascular Drugs and Therapy, 2025
Jingyi Guo, Maoying Wei, Wenhua Zhang, et al.
Frontiers in Pharmacology, 2025
Objective To investigate the safety and clinical efficacy of sodium-glucose cotransporter protein-2 (SGLT-2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists and Finerenone in treating patients with type 2 diabetes mellitus (T2DM) combined with non-dialysis chronic kidney disease (CKD). Methods Cochrane Library, PubMed, EMBASE, Web of Science, CNKI, CQVIP database, and WanFang from their inception up to November 2023 were searched to compare the efficacy and safety of SGLT-2 inhibitors, GLP-1 RA receptor agonists and Finerenone in the treatment of T2DM patients with non-dialysis CKD. To assess the methodological quality and risk of bias in the included studies, we utilized the Cochrane Risk of Bias Assessment tool (RoB 2.0). The confidence of evidence was examined using Confidence in Network Meta-Analysis (CINeMA). Traditional meta-analysis of variables was conducted using Stata 17.0 software with a random-effects model. We assessed publication bias using funnel plots and explored potential sources of heterogeneity through subgroup analysis. Results A total of 39 studies (99,599 patients) were included. Compared to Placebo (PBO), SGLT-2 inhibitors demonstrated superior efficacy in reducing glycosylated hemoglobin (HbA1c) (MD = −0.33; 95%CI: from −0.52 to −0.15), systolic blood pressure (SBP) (MD from −5.52 to −1.50; 95%CI from −8.80 to −0.23), body weight (MD from −3.81 to −1.29; 95%CI from −6.34 to −0.84) and diastolic blood pressure (DBP) (MD = −1.86; 95%CI: −3.18, −40.54). The efficacy of Liraglutide in reducing Low-Density Lipoprotein Cholesterol (LDL-C) surpassed that of other agents (MD from −1.58 to −1.41; 95%CI from −2.05 to −0.81). Finerenone significantly reduced SBP (MD = −1.65; 95%CI: −2.48, −0.81) compared to PBO. According to the SUCRA based relative ranking of treatments, Empagliflozin was the most effective in reducing HbA1c and DBP. Semaglutide was the least harmful to estimated glomerular filtration rate. Liraglutide was the most effective in reducing LDL-C. Bexagliflozin, Canagliflozin were the most effective in reducing SBP and body weight. Finerenone had the lowest incidence of urinary tract infection, Hypoglycemia was the lowest in the Luseogliflozin group. Ertugliflozin was the least likely to cause acute kidney injury. Canagliflozin had the lowest probability of any adverse event. Conclusion The safety of these drugs has been confirmed, except for some special drugs. SGLT-2 inhibitors had a preferential glucose-lowering and weight-loss function, GLP-1 receptor agonists had a preferential lowering of LDL-C and blood glucose, and Finereone significantly reduced SBP compared with PBO. Systematic Review Registration: PROSPERO, CRD42024571544.
Abstract licence: CC BY
Wanqian Yu, F. Luo, Jingan Rao, et al.
Frontiers in Cardiovascular Medicine, 2025
Background Finerenone has been shown to improve outcomes in patients with heart failure (HF), encompassing those with reduced (HFrEF), mildly reduced (HFmrEF), or preserved ejection fraction (HFpEF). However, its clinical use is accompanied by notable adverse effects. This study aimed to evaluate the relative risks of adverse events associated with finerenone across HF phenotypes. Methods A systematic search of PubMed, Embase, and Web of Science identified six randomized controlled trials involving 8,527 HF patients. The analysis considered hyperkalemia, hypotension, treatment-emergent adverse events (TEAEs), treatment-emergent serious adverse events (TESAEs), and treatment discontinuation due to adverse events. Results Finerenone significantly increased the risk of hyperkalemia (RR = 2.07, 95% CI 1.77-2.44, P < 0.00001) and hypotension (RR = 1.49, 95% CI 1.31-1.68, P < 0.00001) compared to placebo, irrespective of HF phenotype. No significant differences were observed between finerenone and placebo in terms of TEAEs, TESAEs, or treatment discontinuation when analyzing the overall heart failure population. Compared to eplerenone, finerenone was associated with a lower risk of TEAEs (RR = 0.93, 95% CI: 0.89-0.98) and TESAEs (RR = 0.74, 95% CI: 0.66-0.84), with similar discontinuation rates. Additionally, one included study suggested that finerenone may have a lower risk of TEAEs (RR = 0.64, 95% CI 0.56-0.74), treatment discontinuation (RR = 0.37, 95% CI 0.25-0.54) and hyperkalemia (RR = 0.41, 95% CI 0.21-0.79) compared to spironolactone, with similar rates of hypotension (RR = 0.61, 95% CI 0.29-1.30) in HFrEF. Conclusion Finerenone (10-25 mg) showed a similar safety profile to placebo, with no significant differences in TEAEs, TESAEs, or treatment discontinuation. Compared to eplerenone, finerenone was associated with fewer TEAEs and TESAEs, with comparable discontinuation rates. Moreover, in patients with HFrEF, finerenone may offer lower risks of TEAEs, treatment discontinuation, and hyperkalemia than spironolactone, with similar rates of hypotension.
Abstract licence: CC BY
Zixuan Zhang, Fan Zhang, Yan Bai, et al.
Frontiers in Medicine, 2025
Background Although current guidelines have recommended finerenone as a first-line agent for patients with diabetic kidney disease (DKD), it is unclear what effect finerenone has on all-cause and cardiovascular mortality. This study aimed to assess the impact of finerenone on the prognosis and safety of patients with DKD. Methods A systematic search was performed in PubMed, Embase, Scopus, and Web of Science. We included randomized controlled trials involving patients diagnosed with DKD that had finerenone versus placebo. The number of deaths, including any cause and cardiovascular causes, hyperkalemia, and adverse events, were collected for the finerenone and placebo groups. Data were summarized as risk ratio (RR) with 95% confidence interval (95% CI). Results Four trials (13,943 participants) were included in the meta-analysis. Results of the restricted maximum likelihood-adjusted random-effects model showed that finerenone was associated with a reduced risk of all-cause (RR: 0.894; 95% CI 0.802–0.998) and cardiovascular mortalities (RR: 0.824; 95% CI 0.685–0.990) in DKD patients. Finerenone predisposed to hyperkalemia compared with placebo (RR: 2.280; 95% CI 1.937–2.682). Conclusion This meta-analysis provides key information on the prognosis and safety of finerenone in DKD patients. These results help to supplement the clinical evidence for finerenone. Systematic review registration https://www.crd.york.ac.uk/PROSPERO/, CRD42023463227.
Abstract licence: CC BY
Xiaoyue Wang, Yunfeng Yu, Yixin Xiang, et al.
BMJ Open, 2025
Bmc Nephrology, S. Abbas, U. Tahir, et al.
BMC Nephrology, 2025
S. Solomon, J. McMurray, M. Vaduganathan, et al.
The New England journal of medicine, 2024
Wanqian Yu, Fan Luo, Jingan Rao, et al.
Frontiers in Cardiovascular Medicine, 2025
Chen-Fu Wen, Min-Hsiang Chuang, Vin-Cent Wu, et al.
Frontiers in Pharmacology, 2026
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
17.4 hours
Mechanism
Finerenone is a non-steroidal selective mineralocorticoid receptor (MR) antagoni…
Food interactions
2 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
10 mg
Half-life
10 mg
Protein binding
92%
[L34739]
Volume of distribution
52.6L
[L34739]
Metabolism
90%
[A236519][L34739]
…
Elimination
47.8%
Clearance
25 L/h
[L34739]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Finerenone was granted FDA approval on 9 July 2021,[L34739] followed by the EMA approval on 11 March 2022.[L41449]
[L34739]
Finerenone has also been approved for reducing the risks of cardiovascular death, hospitalization for heart failure, and urgent heart failure visits in adult patients with heart failure with left ventricular ejection fraction≥ 40%.
[L43095]
In Europe, finerenone is indicated for the treatment of chronic kidney disease (stage 3 and 4 with albuminuria) associated with type 2 diabetes in adults.
[L41444]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1232 interactions
[L34739]
In the even of an overdose, immediately stop taking finerenone.
[L34739]
Treat patients with symptomatic and supportive treatment, including treatment for hyperkalemia if it develops.
[L34739]
Hemodialysis is not expected to remove finerenone from the blood due to its high plasma protein binding.
[L34739]
Aldosterone is a mineralocorticoid hormone involved in the regulation of blood pressure, sodium reabsorption, and potassium excretion.[A236524] In 1943, agonism of the MR along with increased salt was shown to be associated with malignant hypertension, which could progress to inflammation and fibrosis of organs.[A236524]
Binding of aldosterone, an MR agonist, to the MR causes a conformational change, which dissociates the receptor from inactivating chaperone proteins.[A236539] The active MR translocates to the nucleus along with a complex of other coactivators to induce transcription of a number of genes.[A236539]
Finerenone's binding to the MR prevents binding of MR coactivators, which in turn prevents pro-inflammatory and pro-fibrotic gene transcription.[A236524][A236529]
Clinical trial data shows that blocking the mineralocorticoid receptor reduces mortality and morbidity in patients with chronic severe congestive heart failure with an ejection fraction ≤35%.[A236534] Patients taking finerenone developed new onset atrial fibrillation or flutter (AFF) with a hazard ratio of 0.71.[A236529] Finerenone lowered the risk of first onset of kidney failure, a sustained eGFR decrease of ≥40%, or death from a renal cause to a hazard ratio of 0.82.[A236529] Cardiovascular outcomes including cardiovascular death, nonfatal heart attacks, nonfatal strokes, and hospitalization for heart failure in patients taking finerenone had a hazard ratio of 0.86 in patients with a history of AFF and 0.85 in patients without a history of AFF.[A236529]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A236519]
The same dose of finerenone reaches a Cmax of 226 µg/L, with a Tmax of 1.5 hours, and an AUC of 1840 µg\*h/L in whole blood.
[A236519]
Regular doses of 20 mg of finerenone reach a geometric mean steady state Cmax of 160 µg/L with an AUC of 686 µg\*h/L.
[L34739]
[A236519]
The terminal half life of finerenone is approximately 2-3 hours.
[L34739]
[L34739]
[L34739]
[A236519][L34739]
There is a minor contribution to metabolism by CYP1A1.
[A236519]
Finerenone has no active metabolites.
[A236524]
Finerenone is aromatized to the M1 metabolite by CYP3A4 and CYP2C8, which is further hydroxylated by CYP3A4 to the M2 metabolite, and finally oxidized bye CYP3A4 to the M3 metabolite.
[A236519]
Alternatively, finerenone can undergo epoxidation and possibly hydrolysis by CYP3A4 and CYP2C8 to form the M4 metabolite, which is hydroxylated again by CYP3A4 to the M5 metabolite, and oxidized to the M8 metabolite.
[A236519]
Finerenone can also be hydroxylated by CYP2C8 to the M7 metabolite, and further oxidized to the M9 metabolite.
[A236519]
The M10 metabolite is formed by the demethylation, oxidation, and ring opening of finerenone.
[A236519]
The M13 metabolite is formed through de-ethylation of finerenone by CYP1A1, and the M14 metabolite is formed through an undefined multi-step process involving CYP2C8 and CYP3A4.
[A236519]
[A236519]
The majority of the dose recovered in the feces was as the M5 metabolite, with only 0.2% eliminated as the unchanged parent compound.
[A236519]
The M1 metabolite made up <1.5% of the recovered dose in urine and feces.
[A236519]
Finerenone is not expected to be metabolized by the intestinal microflora.
[A236519]
[L34739]
Proteins and enzymes this drug interacts with in the body
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
ATC C03DA05
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Finerenone
Additional database identifiers
Drugs Product Database (DPD)
23792
ChemSpider
28669387
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7979
GenAtlas
NR3C2
GeneCards
NR3C2
GenBank Gene Database
M16801
GenBank Protein Database
307166
Guide to Pharmacology
626
UniProt Accession
MCR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2595
GeneCards
CYP1A1
GenBank Gene Database
K03191
GenBank Protein Database
181276
Guide to Pharmacology
1318
UniProt Accession
CP1A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72