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Identification
- Summary
Finerenone is a nonsteroidal mineralocorticoid receptor antagonist indicated to lower the risk of eGFR decline, end stage kidney disease, cardiovascular death, heart attack, and hospitalization for heart failure in chronic kidney disease associated with type 2 diabetes.
- Brand Names
- Kerendia
- Generic Name
- Finerenone
- DrugBank Accession Number
- DB16165
- Background
Finerenone, or BAY 94-8862, is a mineralocorticoid receptor antagonist indicated to reduce the risk of sustained decline in glomerular filtration rate, end stage kidney disease, cardiovascular death, heart attacks, and hospitalization due to heart failure in adults with chronic kidney disease associated with type II diabetes mellitus.1,7 Patients with kidney disease, would originally be given spironolactone or eplerenone to antagonize the mineraclocorticoid receptor.6 Spironolactone has low selectivity and affinity for the receptor; it dissociates quickly and can also have effects at the androgen, progesterone, and glucocorticoid receptors.6 Eplerenone is more selective and has longer lasting effects.6 More selective nonsteroidal mineralocorticoid antagonists such as apararenone, esaxerenone, and finerenone were later developed.6 So far, finerenone is the only nonsteroidal mineralocorticoid receptor antagonist to be FDA approved.6,7
Finerenone was granted FDA approval on 9 July 2021,7 followed by the EMA approval on 11 March 2022.9
- Type
- Small Molecule
- Groups
- Approved, Investigational
- Structure
Structure for Finerenone (DB16165)
- Weight
- Average: 378.432
Monoisotopic: 378.169190584 - Chemical Formula
- C21H22N4O3
- Synonyms
- Finerenone
- External IDs
- BAY 94-8862
- BAY-94-8862
Pharmacology
- Indication
In the US, finerenone is indicated to reduce the risk of sustained decline in glomerular filtration rate, end stage kidney disease, cardiovascular death, heart attacks, and hospitalization due to heart failure in adults with chronic kidney disease associated with type II diabetes mellitus.7
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.8
Reduce drug development failure ratesBuild, train, & validate machine-learning modelswith evidence-based and structured datasets.Build, train, & validate predictive machine-learning models with structured datasets.- Associated Conditions
Indication Type Indication Combined Product Details Approval Level Age Group Patient Characteristics Dose Form Prophylaxis of Cardiovascular mortality •••••••••••• ••••• •••• • •••••••• ••••••••• ••••••• •••••• ••••••• ••••• •••••• Management of Chronic kidney disease, stage 3 (moderate) •••••••••••• ••••• ••••••••••• •••••• Prophylaxis of End-stage kidney disease •••••••••••• ••••• •••• • •••••••• ••••••••• ••••••• •••••• ••••••• ••••• •••••• Prophylaxis of Hospitalizations •••••••••••• ••••• •••• • •••••••• ••••••••• ••••••• •••••• ••••••• ••••• •••••• Management of Stage 4 chronic kidney disease •••••••••••• ••••• ••••••••••• •••••• - Contraindications & Blackbox Warnings
Prevent Adverse Drug Events TodayTap into our Clinical API for life-saving information on contraindications & blackbox warnings, population restrictions, harmful risks, & more.Avoid life-threatening adverse drug events with our Clinical API- Pharmacodynamics
Finerenone is a non-steroidal mineralocorticoid receptor antagonist indicated to reduce the risk of sustained decline in glomerular filtration rate, end stage kidney disease, cardiovascular death, heart attacks, and hospitalization due to heart failure in adults with chronic kidney disease associated with type II diabetes mellitus.7 It has a moderate duration of action as it is taken once daily, and a wide therapeutic window as patients were given doses from 1.25 mg to 80 mg in clinical trials.7 Patients should be counselled regarding the risk of hyperkalemia.7
- Mechanism of action
Finerenone is a non-steroidal selective mineralocorticoid receptor (MR) antagonist with no significant affinity or activity at androgen, progesterone, estrogen, and glucocorticoid receptors.2,7 Animal studies have shown that finerenone binding to the MR reduces inflammation and fibrosis, and phase 2 clinical trials showed a reduction in albuminuria.2,3
Aldosterone is a mineralocorticoid hormone involved in the regulation of blood pressure, sodium reabsorption, and potassium excretion.2 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.2
Binding of aldosterone, an MR agonist, to the MR causes a conformational change, which dissociates the receptor from inactivating chaperone proteins.5 The active MR translocates to the nucleus along with a complex of other coactivators to induce transcription of a number of genes.5
Finerenone's binding to the MR prevents binding of MR coactivators, which in turn prevents pro-inflammatory and pro-fibrotic gene transcription.2,3
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%.4 Patients taking finerenone developed new onset atrial fibrillation or flutter (AFF) with a hazard ratio of 0.71.3 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 0.82.3 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.3
Target Actions Organism AMineralocorticoid receptor antagonistHumans - Absorption
A 10 mg oral dose of finerenone reaches a Cmax of 351 µg/L, with a Tmax of 1.5 hours, and an AUC of 2820 µg*h/L in plasma.1 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.1
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.7
- Volume of distribution
The volume of distribution of finerenone as steady state is 52.6L.7
- Protein binding
Finerenone is 92% protein bound in plasma; predominantly to serum albumin.7
- Metabolism
Finerenone is approximately 90% metabolized by CYP3A4, and 10% metabolized by CYP2C8.1,7 There is a minor contribution to metabolism by CYP1A1.1 Finerenone has no active metabolites.2
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.1 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.1 Finerenone can also be hydroxylated by CYP2C8 to the M7 metabolite, and further oxidized to the M9 metabolite.1
The M10 metabolite is formed by the demethylation, oxidation, and ring opening of finerenone.1 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 CYP3A4.1
Hover over products below to view reaction partners
- Route of elimination
The majority of the dose recovered in urine was in the form of the M2, M3 (47.8%), and M4 metabolites; <1.3% of the dose recovered in the urine was as the unchanged parent compound.1 The majority of the dose recovered in the feces was as the M5 metabolite, with only 0.2% eliminated as the unchanged parent compound.1 The M1 metabolite made up <1.5% of the recovered dose in urine and feces.1
Finerenone is not expected to be metabolized by the intestinal microflora.1
- Half-life
The half life of a 10 mg dose of finerenone in 4 healthy men was 17.4 hours in plasma and 12.3 hours in whole blood.1 The terminal half life of finerenone is approximately 2-3 hours.7
- Clearance
The systemic clearance of finerenone is approximately 25 L/h.7
- Adverse Effects
Improve decision support & research outcomesWith structured adverse effects data, including: blackbox warnings, adverse reactions, warning & precautions, & incidence rates. View sample adverse effects data in our new Data Library!Improve decision support & research outcomes with our structured adverse effects data.- Toxicity
Patients experiencing an overdose of finerenone may experience hyperkalemia.7 In the even of an overdose, immediately stop taking finerenone.7 Treat patients with symptomatic and supportive treatment, including treatment for hyperkalemia if it develops.7 Hemodialysis is not expected to remove finerenone from the blood due to its high plasma protein binding.7
- Pathways
- Not Available
- Pharmacogenomic Effects/ADRs
- Not Available
Interactions
- Drug Interactions
- This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
Drug Interaction Integrate drug-drug
interactions in your softwareAbacavir Finerenone may increase the excretion rate of Abacavir which could result in a lower serum level and potentially a reduction in efficacy. Abametapir The serum concentration of Finerenone can be increased when it is combined with Abametapir. Abatacept The metabolism of Finerenone can be increased when combined with Abatacept. Abiraterone The metabolism of Finerenone can be decreased when combined with Abiraterone. Acalabrutinib The serum concentration of Finerenone can be increased when it is combined with Acalabrutinib. - Food Interactions
- Avoid grapefruit products. Grapefruit products may increase exposure to finerenone, increasing the risk and severity of adverse effects.
- Take with or without food. Food does not have a clinically significant effect on area under the curve.
Products
Drug product information from 10+ global regionsOur datasets provide approved product information including:dosage, form, labeller, route of administration, and marketing period.Access drug product information from over 10 global regions.- International/Other Brands
- Kerendia (Bayer)
- Brand Name Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Kerendia Tablet 10 mg Oral Bayer Ag 2022-11-22 Not applicable Canada 
Kerendia Tablet, film coated 20 mg Oral Bayer Ag 2022-05-04 Not applicable EU 
Kerendia Tablet, film coated 10 mg Oral Bayer Ag 2022-05-04 Not applicable EU Kerendia Tablet, film coated 20 mg/1 Oral Bayer HealthCare Pharmaceuticals Inc. 2021-07-09 Not applicable US 
Kerendia Tablet, film coated 20 mg Oral Bayer Ag 2022-05-04 Not applicable EU
Categories
- ATC Codes
- C03DA05 — Finerenone
- Drug Categories
- Classification
- Not classified
- Affected organisms
- Humans
Chemical Identifiers
- UNII
- DE2O63YV8R
- CAS number
- 1050477-31-0
- InChI Key
- BTBHLEZXCOBLCY-QGZVFWFLSA-N
- InChI
- InChI=1S/C21H22N4O3/c1-5-28-21-18-17(14-7-6-13(9-22)8-15(14)27-4)16(20(23)26)12(3)25-19(18)11(2)10-24-21/h6-8,10,17,25H,5H2,1-4H3,(H2,23,26)/t17-/m1/s1
- IUPAC Name
- (4S)-4-(4-cyano-2-methoxyphenyl)-5-ethoxy-2,8-dimethyl-1,4-dihydro-1,6-naphthyridine-3-carboxamide
- SMILES
- CCOC1=NC=C(C)C2=C1[C@H](C1=CC=C(C=C1OC)C#N)C(C(N)=O)=C(C)N2
References
- General References
- Gerisch M, Heinig R, Engelen A, Lang D, Kolkhof P, Radtke M, Platzek J, Lovis K, Rohde G, Schwarz T: Biotransformation of Finerenone, a Novel Nonsteroidal Mineralocorticoid Receptor Antagonist, in Dogs, Rats, and Humans, In Vivo and In Vitro. Drug Metab Dispos. 2018 Nov;46(11):1546-1555. doi: 10.1124/dmd.118.083337. Epub 2018 Aug 31. [Article]
- Epstein M: Aldosterone and Mineralocorticoid Receptor Signaling as Determinants of Cardiovascular and Renal Injury: From Hans Selye to the Present. Am J Nephrol. 2021;52(3):209-216. doi: 10.1159/000515622. Epub 2021 Apr 15. [Article]
- Filippatos G, Bakris GL, Pitt B, Agarwal R, Rossing P, Ruilope LM, Butler J, Lam CSP, Kolkhof P, Roberts L, Tasto C, Joseph A, Anker SD: Finerenone Reduces New-Onset Atrial Fibrillation in Patients With Chronic Kidney Disease and Type 2 Diabetes. J Am Coll Cardiol. 2021 Jul 13;78(2):142-152. doi: 10.1016/j.jacc.2021.04.079. Epub 2021 May 17. [Article]
- Li Z, Zhao H, Wang J: Metabolism and Chronic Inflammation: The Links Between Chronic Heart Failure and Comorbidities. Front Cardiovasc Med. 2021 May 5;8:650278. doi: 10.3389/fcvm.2021.650278. eCollection 2021. [Article]
- Yang J, Young MJ: The mineralocorticoid receptor and its coregulators. J Mol Endocrinol. 2009 Aug;43(2):53-64. doi: 10.1677/JME-09-0031. [Article]
- Vodosek Hojs N, Bevc S, Ekart R, Piko N, Petreski T, Hojs R: Mineralocorticoid Receptor Antagonists in Diabetic Kidney Disease. Pharmaceuticals (Basel). 2021 Jun 11;14(6). pii: ph14060561. doi: 10.3390/ph14060561. [Article]
- FDA Approved Drug Products: Kerendia (Finerenone) Oral Tablet [Link]
- EMA Approved Drug Products: Kerendia (finerenone) Oral Tablets [Link]
- European Medicines Agency Medicines: Kerendia (finerenone) [Link]
- External Links
- ChemSpider
- 28669387
- 2562811
- ChEMBL
- CHEMBL2181927
- Wikipedia
- Finerenone
Clinical Trials
- Clinical Trials
Clinical Trial & Rare Diseases Add-on Data Package
Explore 4,000+ rare diseases, orphan drugs & condition pairs, clinical trial why stopped data, & more. Preview package Phase Status Purpose Conditions Count Start Date Why Stopped 100+ additional columns Unlock 175K+ rows when you subscribe.View sample dataNot Available Completed Not Available Chronic Kidney Disease (CKD) / Type 2 Diabetes Mellitus 3 somestatus stop reason just information to hide Not Available Completed Not Available Diabetic Retinopathy (DR) 1 somestatus stop reason just information to hide Not Available Completed Not Available Finerenone / Immunoglobulin A Nephropathy / Proteinuria / Safety Issues 1 somestatus stop reason just information to hide Not Available Completed Other Diabetic Retinopathy (DR) 1 somestatus stop reason just information to hide Not Available Not Yet Recruiting Not Available Chronic Kidney Disease (CKD) / Type 2 Diabetes Mellitus 1 somestatus stop reason just information to hide
Pharmacoeconomics
- Manufacturers
- Not Available
- Packagers
- Not Available
- Dosage Forms
Form Route Strength Tablet Oral 10.000 mg Tablet Oral 10 mg Tablet Oral 20 mg Tablet, film coated Oral 10 mg/1 Tablet, film coated Oral 20 mg/1 Tablet, film coated Oral 10 mg Tablet, film coated Oral 20 mg - Prices
- Not Available
- Patents
Patent Number Pediatric Extension Approved Expires (estimated) Region US8436180 No 2013-05-07 2029-04-12 US USRE49826 No 2015-07-29 2035-07-29 US
Properties
- State
- Solid
- Experimental Properties
- Not Available
- Predicted Properties
Property Value Source Water Solubility 0.0354 mg/mL ALOGPS logP 2.21 ALOGPS logP 1.85 Chemaxon logS -4 ALOGPS pKa (Strongest Acidic) 14.87 Chemaxon pKa (Strongest Basic) 6.06 Chemaxon Physiological Charge 0 Chemaxon Hydrogen Acceptor Count 6 Chemaxon Hydrogen Donor Count 2 Chemaxon Polar Surface Area 110.26 Å2 Chemaxon Rotatable Bond Count 5 Chemaxon Refractivity 109.13 m3·mol-1 Chemaxon Polarizability 39.66 Å3 Chemaxon Number of Rings 3 Chemaxon Bioavailability 1 Chemaxon Rule of Five Yes Chemaxon Ghose Filter Yes Chemaxon Veber's Rule No Chemaxon MDDR-like Rule No Chemaxon - Predicted ADMET Features
- Not Available
Spectra
- Mass Spec (NIST)
- Not Available
- Spectra
Spectrum Spectrum Type Splash Key Predicted MS/MS Spectrum - 10V, Positive (Annotated) Predicted LC-MS/MS splash10-004i-0009000000-fd01ad01cb20e65a0659 Predicted MS/MS Spectrum - 10V, Negative (Annotated) Predicted LC-MS/MS splash10-0a4i-0009000000-29282602ee7e486ec1c4 Predicted MS/MS Spectrum - 20V, Positive (Annotated) Predicted LC-MS/MS splash10-01t9-0009000000-16ab2c3e3fe4bc2b83e4 Predicted MS/MS Spectrum - 20V, Negative (Annotated) Predicted LC-MS/MS splash10-004i-1009000000-c4256969f4e8e6d3c786 Predicted MS/MS Spectrum - 40V, Positive (Annotated) Predicted LC-MS/MS splash10-004i-0798000000-74a1bf3b3175728c74d8 Predicted MS/MS Spectrum - 40V, Negative (Annotated) Predicted LC-MS/MS splash10-0uyi-1039000000-916e263e2a4014db7cbd Predicted 1H NMR Spectrum 1D NMR Not Applicable Predicted 13C NMR Spectrum 1D NMR Not Applicable - Chromatographic Properties
Collision Cross Sections (CCS)
Adduct CCS Value (Å2) Source type Source [M-H]- 205.2665676 predictedDarkChem Lite v0.1.0 [M+H]+ 205.9463676 predictedDarkChem Lite v0.1.0 [M+Na]+ 205.4491676 predictedDarkChem Lite v0.1.0
Targets
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Antagonist
- General Function
- Receptor for both mineralocorticoids (MC) such as aldosterone and glucocorticoids (GC) such as corticosterone or cortisol. Binds to mineralocorticoid response elements (MRE) and transactivates target genes. The effect of MC is to increase ion and water transport and thus raise extracellular fluid volume and blood pressure and lower potassium levels
- Specific Function
- DNA-binding transcription factor activity
- Gene Name
- NR3C2
- Uniprot ID
- P08235
- Uniprot Name
- Mineralocorticoid receptor
- Molecular Weight
- 107080.615 Da
References
- Trujillo H, Caravaca-Fontan F, Caro J, Morales E, Praga M: The Forgotten Antiproteinuric Properties of Diuretics. Am J Nephrol. 2021 Jul 7:1-15. doi: 10.1159/000517020. [Article]
- Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]
- FDA Approved Drug Products: Kerendia (Finerenone) Oral Tablet [Link]
Enzymes
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Substrate
- General Function
- A cytochrome P450 monooxygenase involved in the metabolism of sterols, steroid hormones, retinoids and fatty acids (PubMed:10681376, PubMed:11093772, PubMed:11555828, PubMed:12865317, PubMed:14559847, PubMed:15373842, PubMed:15764715, PubMed:19965576, PubMed:20702771, PubMed:21490593, PubMed:21576599). Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate, and reducing the second into a water molecule, with two electrons provided by NADPH via cytochrome P450 reductase (NADPH--hemoprotein reductase). Catalyzes the hydroxylation of carbon-hydrogen bonds (PubMed:12865317, PubMed:14559847, PubMed:15373842, PubMed:15764715, PubMed:21490593, PubMed:21576599, PubMed:2732228). Exhibits high catalytic activity for the formation of hydroxyestrogens from estrone (E1) and 17beta-estradiol (E2), namely 2-hydroxy E1 and E2, as well as D-ring hydroxylated E1 and E2 at the C-16 position (PubMed:11555828, PubMed:12865317, PubMed:14559847). Plays a role in the metabolism of androgens, particularly in oxidative deactivation of testosterone (PubMed:15373842, PubMed:15764715, PubMed:22773874, PubMed:2732228). Metabolizes testosterone to less biologically active 2beta- and 6beta-hydroxytestosterones (PubMed:15373842, PubMed:15764715, PubMed:2732228). Contributes to the formation of hydroxycholesterols (oxysterols), particularly A-ring hydroxylated cholesterol at the C-4beta position, and side chain hydroxylated cholesterol at the C-25 position, likely contributing to cholesterol degradation and bile acid biosynthesis (PubMed:21576599). Catalyzes bisallylic hydroxylation of polyunsaturated fatty acids (PUFA) (PubMed:9435160). Catalyzes the epoxidation of double bonds of PUFA with a preference for the last double bond (PubMed:19965576). Metabolizes endocannabinoid arachidonoylethanolamide (anandamide) to 8,9-, 11,12-, and 14,15-epoxyeicosatrienoic acid ethanolamides (EpETrE-EAs), potentially modulating endocannabinoid system signaling (PubMed:20702771). Plays a role in the metabolism of retinoids. Displays high catalytic activity for oxidation of all-trans-retinol to all-trans-retinal, a rate-limiting step for the biosynthesis of all-trans-retinoic acid (atRA) (PubMed:10681376). Further metabolizes atRA toward 4-hydroxyretinoate and may play a role in hepatic atRA clearance (PubMed:11093772). Responsible for oxidative metabolism of xenobiotics. Acts as a 2-exo-monooxygenase for plant lipid 1,8-cineole (eucalyptol) (PubMed:11159812). Metabolizes the majority of the administered drugs. Catalyzes sulfoxidation of the anthelmintics albendazole and fenbendazole (PubMed:10759686). Hydroxylates antimalarial drug quinine (PubMed:8968357). Acts as a 1,4-cineole 2-exo-monooxygenase (PubMed:11695850). Also involved in vitamin D catabolism and calcium homeostasis. Catalyzes the inactivation of the active hormone calcitriol (1-alpha,25-dihydroxyvitamin D(3)) (PubMed:29461981)
- Specific Function
- 1,8-cineole 2-exo-monooxygenase activity
- Gene Name
- CYP3A4
- Uniprot ID
- P08684
- Uniprot Name
- Cytochrome P450 3A4
- Molecular Weight
- 57342.67 Da
References
- Heinig R, Gerisch M, Bairlein M, Nagelschmitz J, Loewen S: Results from Drug-Drug Interaction Studies In Vitro and In Vivo Investigating the Effect of Finerenone on the Pharmacokinetics of Comedications. Eur J Drug Metab Pharmacokinet. 2020 Aug;45(4):433-444. doi: 10.1007/s13318-020-00610-y. [Article]
- Heinig R, Gerisch M, Engelen A, Nagelschmitz J, Loewen S: Pharmacokinetics of the Novel, Selective, Non-steroidal Mineralocorticoid Receptor Antagonist Finerenone in Healthy Volunteers: Results from an Absolute Bioavailability Study and Drug-Drug Interaction Studies In Vitro and In Vivo. Eur J Drug Metab Pharmacokinet. 2018 Dec;43(6):715-727. doi: 10.1007/s13318-018-0483-9. [Article]
- Gerisch M, Heinig R, Engelen A, Lang D, Kolkhof P, Radtke M, Platzek J, Lovis K, Rohde G, Schwarz T: Biotransformation of Finerenone, a Novel Nonsteroidal Mineralocorticoid Receptor Antagonist, in Dogs, Rats, and Humans, In Vivo and In Vitro. Drug Metab Dispos. 2018 Nov;46(11):1546-1555. doi: 10.1124/dmd.118.083337. Epub 2018 Aug 31. [Article]
- FDA Approved Drug Products: Kerendia (Finerenone) Oral Tablet [Link]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Substrate
- General Function
- A cytochrome P450 monooxygenase involved in the metabolism of various endogenous substrates, including fatty acids, steroid hormones and vitamins (PubMed:11093772, PubMed:14559847, PubMed:15766564, PubMed:19965576, PubMed:7574697). Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate, and reducing the second into a water molecule, with two electrons provided by NADPH via cytochrome P450 reductase (NADPH--hemoprotein reductase) (PubMed:11093772, PubMed:14559847, PubMed:15766564, PubMed:19965576, PubMed:7574697). Primarily catalyzes the epoxidation of double bonds of polyunsaturated fatty acids (PUFA) with a preference for the last double bond (PubMed:15766564, PubMed:19965576, PubMed:7574697). Catalyzes the hydroxylation of carbon-hydrogen bonds. Metabolizes all trans-retinoic acid toward its 4-hydroxylated form (PubMed:11093772). Displays 16-alpha hydroxylase activity toward estrogen steroid hormones, 17beta-estradiol (E2) and estrone (E1) (PubMed:14559847). Plays a role in the oxidative metabolism of xenobiotics. It is the principal enzyme responsible for the metabolism of the anti-cancer drug paclitaxel (taxol) (PubMed:26427316)
- Specific Function
- arachidonic acid epoxygenase activity
- Gene Name
- CYP2C8
- Uniprot ID
- P10632
- Uniprot Name
- Cytochrome P450 2C8
- Molecular Weight
- 55824.275 Da
References
- Heinig R, Gerisch M, Bairlein M, Nagelschmitz J, Loewen S: Results from Drug-Drug Interaction Studies In Vitro and In Vivo Investigating the Effect of Finerenone on the Pharmacokinetics of Comedications. Eur J Drug Metab Pharmacokinet. 2020 Aug;45(4):433-444. doi: 10.1007/s13318-020-00610-y. [Article]
- Heinig R, Gerisch M, Engelen A, Nagelschmitz J, Loewen S: Pharmacokinetics of the Novel, Selective, Non-steroidal Mineralocorticoid Receptor Antagonist Finerenone in Healthy Volunteers: Results from an Absolute Bioavailability Study and Drug-Drug Interaction Studies In Vitro and In Vivo. Eur J Drug Metab Pharmacokinet. 2018 Dec;43(6):715-727. doi: 10.1007/s13318-018-0483-9. [Article]
- Gerisch M, Heinig R, Engelen A, Lang D, Kolkhof P, Radtke M, Platzek J, Lovis K, Rohde G, Schwarz T: Biotransformation of Finerenone, a Novel Nonsteroidal Mineralocorticoid Receptor Antagonist, in Dogs, Rats, and Humans, In Vivo and In Vitro. Drug Metab Dispos. 2018 Nov;46(11):1546-1555. doi: 10.1124/dmd.118.083337. Epub 2018 Aug 31. [Article]
- FDA Approved Drug Products: Kerendia (Finerenone) Oral Tablet [Link]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Substrate
- General Function
- A cytochrome P450 monooxygenase involved in the metabolism of various endogenous substrates, including fatty acids, steroid hormones and vitamins (PubMed:10681376, PubMed:11555828, PubMed:12865317, PubMed:14559847, PubMed:15041462, PubMed:15805301, PubMed:18577768, PubMed:19965576, PubMed:20972997). Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate, and reducing the second into a water molecule, with two electrons provided by NADPH via cytochrome P450 reductase (NADPH--hemoprotein reductase) (PubMed:10681376, PubMed:11555828, PubMed:12865317, PubMed:14559847, PubMed:15041462, PubMed:15805301, PubMed:18577768, PubMed:19965576, PubMed:20972997). Catalyzes the hydroxylation of carbon-hydrogen bonds. Exhibits high catalytic activity for the formation of hydroxyestrogens from estrone (E1) and 17beta-estradiol (E2), namely 2-hydroxy E1 and E2, as well as D-ring hydroxylated E1 and E2 at the C15-alpha and C16-alpha positions (PubMed:11555828, PubMed:12865317, PubMed:14559847, PubMed:15805301). Displays different regioselectivities for polyunsaturated fatty acids (PUFA) hydroxylation (PubMed:15041462, PubMed:18577768). Catalyzes the epoxidation of double bonds of certain PUFA (PubMed:15041462, PubMed:19965576, PubMed:20972997). Converts arachidonic acid toward epoxyeicosatrienoic acid (EET) regioisomers, 8,9-, 11,12-, and 14,15-EET, that function as lipid mediators in the vascular system (PubMed:20972997). Displays an absolute stereoselectivity in the epoxidation of eicosapentaenoic acid (EPA) producing the 17(R),18(S) enantiomer (PubMed:15041462). May play an important role in all-trans retinoic acid biosynthesis in extrahepatic tissues. Catalyzes two successive oxidative transformation of all-trans retinol to all-trans retinal and then to the active form all-trans retinoic acid (PubMed:10681376). May also participate in eicosanoids metabolism by converting hydroperoxide species into oxo metabolites (lipoxygenase-like reaction, NADPH-independent) (PubMed:21068195)
- Specific Function
- arachidonic acid monooxygenase activity
- Gene Name
- CYP1A1
- Uniprot ID
- P04798
- Uniprot Name
- Cytochrome P450 1A1
- Molecular Weight
- 58164.815 Da
References
- Gerisch M, Heinig R, Engelen A, Lang D, Kolkhof P, Radtke M, Platzek J, Lovis K, Rohde G, Schwarz T: Biotransformation of Finerenone, a Novel Nonsteroidal Mineralocorticoid Receptor Antagonist, in Dogs, Rats, and Humans, In Vivo and In Vitro. Drug Metab Dispos. 2018 Nov;46(11):1546-1555. doi: 10.1124/dmd.118.083337. Epub 2018 Aug 31. [Article]
Carriers
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Binder
- General Function
- Binds water, Ca(2+), Na(+), K(+), fatty acids, hormones, bilirubin and drugs (Probable). Its main function is the regulation of the colloidal osmotic pressure of blood (Probable). Major zinc transporter in plasma, typically binds about 80% of all plasma zinc (PubMed: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 (PubMed:6234017). Does not prevent iron uptake by the bacterial siderophore aerobactin (PubMed:6234017)
- Specific Function
- antioxidant activity
- Gene Name
- ALB
- Uniprot ID
- P02768
- Uniprot Name
- Albumin
- Molecular Weight
- 69365.94 Da
References
- FDA Approved Drug Products: Kerendia (Finerenone) Oral Tablet [Link]
Drug created at December 15, 2020 18:14 / Updated at April 10, 2022 18:50