Finerenone
(Synonyms: 非奈利酮,BAY 94-8862) 目录号 : GC60842
非奈利酮（Finerenone；BAY 94-8862）是第三代选择性、具有口服活性的、非甾体类盐皮质激素受体 （MR）拮抗剂，IC50为18 nM。
Cas No.:1050477-31-0
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Finerenone (BAY 94-8862) is a third-generation selective, orally active, nonsteroidal mineralocorticoid receptor (MR) antagonist with an IC50 of 18 nM[1]. Finerenone is more selective for MR than for glucocorticoid receptor (GR), androgen receptor (AR), and progesterone receptor (AR) (>500-fold)[2]. Finerenone is mainly used in the study of cardiorenal diseases, such as type 2 diabetes and chronic kidney disease[3].
In vitro, treatment of neonatal rat cardiomyocytes (NRCM) with finerenone (20 nM) reduced apoptosis stimulated by high glucose and high fatty acids, improved cardiomyocyte metabolism and reduced ROS generation via the PPARγ/CD36 pathway[4].
In vivo, oral treatment of chronic kidney disease model (MWF) and wild-type rats with finerenone (10mg/kg) significantly reduced albuminuria in MWF rats, increased endothelial nitric oxide utilization, and significantly improved endothelial function in MWF rats[5]. Finerenone (5mg/kg) was intraperitoneally injected into mice with induced retinopathy (OIR), which reduced retinal systolic pressure, gliosis, vascular leakage, and microglia/macrophage density[6]. Finerenone (10 mg/kg) was orally administered into mice with cardiac/renal inflammation model, which significantly improved the upregulation of infiltrating renal RORγt γδ-positive T cells induced by deoxycorticosterone acetate (DOCA) salt exposure and prevented cardiac and renal damage[7].
References:
[1] Liu L C Y, Schutte E, Gansevoort R T, et al. Finerenone: third-generation mineralocorticoid receptor antagonist for the treatment of heart failure and diabetic kidney disease[J]. Expert opinion on investigational drugs, 2015, 24(8): 1123-1135.
[2] Bădilă E. The expanding class of mineralocorticoid receptor modulators: New ligands for kidney, cardiac, vascular, systemic and behavioral selective actions[J]. Acta Endocrinologica (Bucharest), 2020, 16(4): 487.
[3] Agarwal R, Filippatos G, Pitt B, et al. Cardiovascular and kidney outcomes with finerenone in patients with type 2 diabetes and chronic kidney disease: the FIDELITY pooled analysis[J]. European heart journal, 2022, 43(6): 474-484.
[4] Jin T, Fu X, Liu M, et al. Finerenone attenuates myocardial apoptosis, metabolic disturbance and myocardial fibrosis in type 2 diabetes mellitus[J]. Diabetology & Metabolic Syndrome, 2023, 15(1): 87.
[5] González-Blázquez R, Somoza B, Gil-Ortega M, et al. Finerenone attenuates endothelial dysfunction and albuminuria in a chronic kidney disease model by a reduction in oxidative stress[J]. Frontiers in Pharmacology, 2018, 9: 1131.
[6] Jerome J R, Deliyanti D, Suphapimol V, et al. Finerenone, a non-steroidal mineralocorticoid receptor antagonist, reduces vascular injury and increases regulatory T-cells: Studies in rodents with diabetic and neovascular retinopathy[J]. International Journal of Molecular Sciences, 2023, 24(3): 2334.
[7] Luettges K, Bode M, Diemer J N, et al. Finerenone reduces renal RORγt γδ T cells and protects against cardiorenal damage[J]. American Journal of Nephrology, 2022, 53(7): 552-564.
非奈利酮（Finerenone；BAY 94-8862）是第三代选择性、具有口服活性的、非甾体类盐皮质激素受体 （MR）拮抗剂，IC50为18 nM[1]。Finerenone对MR的选择性高于糖皮质激素受体（GR）、雄激素受体（AR）和孕酮受体（AR）（>500-fold）[2]。Finerenone 主要用于心肾疾病研究，如2型糖尿病和慢性肾脏疾病[3]。
在体外，Finerenone（20nM）处理新生大鼠心肌细胞（NRCM），可降低高糖和高脂肪酸刺激的细胞凋亡，通过PPARγ/CD36通路改善心肌细胞代谢并减少ROS生成[4]。
在体内，Finerenone（10mg/kg）通过口服治疗慢性肾病模型（MWF）和野生型大鼠，显著减少MWF大鼠中白蛋白尿量，增加内皮一氧化氮的利用率从而显著改善MWF大鼠的内皮功能[5]。Finerenone（5mg/kg）通过腹腔注射治疗诱导性视网膜病变（OIR）小鼠，降低了视网膜收缩压，减少了神经胶质增生、血管渗漏和小胶质细胞/巨噬细胞密度[6]。Finerenone（10mg/kg）通过口服治疗心脏/肾脏炎症模型小鼠，显著改善了由醋酸脱氧皮质酮（DOCA）盐暴露引起的浸润肾RORγt γδ阳性T细胞上调，防止心肾损伤[7]。
| Cell experiment [1]: | |
Cell lines | Neonatal rat cardiomyocytes |
Preparation Method | Neonatal rat cardiomyocytes (NRCMs) were extracted for cell culture, and the medium used was DMEM) medium. Hyperlipidemia or hyperglycemia regulation was mimicked by incubation with high concentrations of common saturated FFA (sodium palmitate, 16:0, 0.3 mM) or glucose (D-glucose, 33 mM). Palmitate was previously conjugated with BSA in a 3:1 molar ratio. In control cells, BSA was added as described but in the absence of palmitate. Finerenone (20nM) was added 1 h before stimulation. |
Reaction Conditions | 20nM; 1 h |
Applications | Finerenone reduces the apoptosis of cardiomyocytes stimulated by high glucose and high fatty acid. Finerenone improves cardiomyocyte metabolism and reduces ROS generation through PPARγ/CD36 pathway. |
| Animal experiment [2]: | |
Animal models | Male Wistar and MWF rats |
Preparation Method | Twelve-week-old male Wistar and MWF rats were housed in groups of two under controlled dark-light cycles, temperature conditions and with food and water available ad libitum. Animals were randomly grouped to receive finerenone (10mg/kg/day in 10% EtOH, 40% PEG400, 50% water; W-FIN; MWF-FIN) or vehicle (10% EtOH, 40% PEG400, 50% water; W-C; MWF-C) during 4 weeks by once daily oral gavage. Last oral administration of FIN was performed the day before sacrifice. |
Dosage form | 10mg/kg; p.o. |
Applications | Finerenone lead to a significant reduction (>40%) in albuminuria in the MWF mode, while normoalbuminuria was not affected in Wistar rats. |
References: [1] Jin T, Fu X, Liu M, et al. Finerenone attenuates myocardial apoptosis, metabolic disturbance and myocardial fibrosis in type 2 diabetes mellitus[J]. Diabetology & Metabolic Syndrome, 2023, 15(1): 87. [2] González-Blázquez R, Somoza B, Gil-Ortega M, et al. Finerenone attenuates endothelial dysfunction and albuminuria in a chronic kidney disease model by a reduction in oxidative stress[J]. Frontiers in Pharmacology, 2018, 9: 1131. | |
| Cas No. | 1050477-31-0 | SDF | |
| 别名 | 非奈利酮,BAY 94-8862 | ||
| Canonical SMILES | O=C(C1=C(C)NC2=C(C(OCC)=NC=C2C)[C@@H]1C3=CC=C(C#N)C=C3OC)N | ||
| 分子式 | C21H22N4O3 | 分子量 | 378.42 |
| 溶解度 | DMSO : 100 mg/mL (DMSO moisture absorption will reduce the solubility of the compound, please use a new DMSO; Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.6426 mL | 13.2128 mL | 26.4257 mL |
| 5 mM | 0.5285 mL | 2.6426 mL | 5.2851 mL |
| 10 mM | 0.2643 mL | 1.3213 mL | 2.6426 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet