预约演示
更新于：2025-06-04
Dapagliflozin
达格列净
更新于：2025-06-04
概要
基本信息
药物类型 小分子化药 |
别名 Dapagliflozin propandiol monohydrate、Dapagliflozin propanediol (USAN)、dapagliflozin propanediol monohydrate + [21] |
靶点 |
作用方式 抑制剂 |
作用机制 SGLT2抑制剂(钠-葡萄糖协同转运蛋白-2抑制剂) |
非在研适应症 |
最高研发阶段批准上市 |
最高研发阶段(中国)批准上市 |
特殊审评快速通道 (美国)、优先审评 (中国)、优先审评 (澳大利亚)、突破性疗法 (美国) |
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结构/序列
分子式C24H35ClO9 |
InChIKeyGOADIQFWSVMMRJ-UPGAGZFNSA-N |
CAS号960404-48-2 |
关联
859
项与 达格列净 相关的临床试验NCT06560333
Evaluate the Efficacy and Safety of the Combined Use of a Sodium-glucose Cotransporter 2 (iSGLT2) Inhibitor and a Dipeptidyl Peptidase-4 (iDPP -4) Inhibitor in the Treatment of Type 2 Diabetes Mellitus in Patients Treated With Metformin
NCT06954090
SIGNAL - Body Fluid Proteome SIGnatures for persoNALised Intervention to Prevent Cardiovascular and Renal Complications in Diabetes
NCT06907251
Dapagliflozin for Long COVID Syndrome
100 项与 达格列净 相关的临床结果
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100 项与 达格列净 相关的转化医学
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100 项与 达格列净 相关的专利（医药）
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4,765
项与 达格列净 相关的文献（医药）2025-12-31GYNECOLOGICAL ENDOCRINOLOGY
Animal experiments and network pharmacology to explore the anti-inflammatory mechanism of dapagliflozin in the treatment of polycystic ovary syndrome
Article
作者: Zhang, Zhen ; Bai, He ; Liu, Yong ; Li, Luxin ; Song, Xueqing ; Guan, Huilin ; Yong, Zihao ; Guo, Xiaomeng ; Wang, Chunhua
BACKGROUND:
Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder associated with chronic low-grade inflammation of the ovary. Sodium glucose co-transporter 2 (SGLT2) inhibitors are a class of antidiabetic drugs that can reduce the weight and hyperglycemia of type 2 diabetes patients. Dapagliflozin is a highly selective, orally active and reversible inhibitor of the human SGLT2. However, the role of dapagliflozin in regulating PCOS remains unclear.
METHODS:
In this study, 24 six-week-old female Sprague Dawley (SD) rats were randomly divided into control, letrozole, and letrozole + dapagliflozin groups. PCOS model rats were produced by gavage administration of letrozole for 21 days. The intervention was conducted after the gavage administration of dapagliflozin for 14 days to evaluate the estrous cycle and ovarian imaging changes of the rats in each group. We observed changes in the weight, ovarian weight, and ovarian morphology of the rats in each group. Pathological changes in the ovaries were examined by H&E staining, changes in ovarian tissue cell apoptosis were identified using TdT-mediated dUTP Nick-End Labeling (TUNEL) staining, and changes in inflammation-related factors were detected using immunohistochemistry and Western blotting analysis. Network pharmacology was used to predict the inflammatory targets and pathways affected by dapagliflozin in treating PCOS, and the potential interactions between dapagliflozin and inflammation-related target proteins were evaluated through molecular docking.
RESULTS:
Our results demonstrated that dapagliflozin treatment significantly improved PCOS symptoms, recovered ovarian morphology and physiological functions, and reduced the apoptosis of ovarian cells after drug intervention. Dapagliflozin treatment also reduced the levels of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α, indicating its anti-inflammatory properties. Furthermore, network pharmacology identified 26 intersecting target genes relevant to inflammation in PCOS, with subsequent molecular docking simulations revealing strong binding affinities of dapagliflozin to key targets, including AKT1 and TP53.
CONCLUSIONS:
These findings suggest that dapagliflozin exerts beneficial effects on PCOS by ameliorating ovarian dysfunction and reducing inflammation. Dapagliflozin represents a promising therapeutic candidate for managing PCOS, warranting further clinical investigation to explore its full potential in treating this multifaceted disorder.
2025-12-31RENAL FAILURE
Dapagliflozin improves diabetic kidney disease by inhibiting ferroptosis through β-hydroxybutyrate production
Article
作者: Feng, Bo ; Song, Jun ; Li, Ziyi ; Zhou, Chenxia ; Yan, Qun ; Tian, Yan ; Chen, Da
BACKGROUND:
Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease. Sodium-glucose cotransporter protein 2 inhibitors (SGLT2i) are antihyperglycemic agents that provide additional renal-protective effects in patients with DKD, independent of their glucose-lowering effects. However, the underlying mechanism remains unclear. This study hypothesized that SGLT2i could alleviate diabetic kidney injury by inhibiting ferroptosis and explored its potential mechanisms.
METHODS:
C57BL/6J mice were randomly divided into the control, DKD, DKD+dapagliflozin, and DKD+insulin treatment groups. Blood glucose levels and body weight were monitored. Renal function, tissue pathology, mitochondrial morphology and function, and lipid peroxidation biomarkers (lipid peroxidation [LPO], malondialdehyde [MDA], glutathione peroxidase 4 [GPX4], glutathione [GSH], and cystine transporter solute carrier family 7 member 11 [SLC7A11]) were evaluated. Human proximal tubule cells (HK2 cells) were exposed to high glucose alone or in combination with dapagliflozin. The mitochondrial membrane potential (MMP), adenosine triphosphate (ATP) level, NAD+/NADH ratio (oxidized/reduced ratio of nicotinamide adenine dinucleotide), and lipid peroxidation were measured. In addition, the role of the β-hydroxybutyrate- Calcium/Calmodulin Dependent Protein Kinase Kinase 2 (BHB-CaMKK2) axis in mediating dapagliflozin regulating ferroptosis was examined.
RESULTS:
Dapagliflozin significantly ameliorated kidney injury in mice with DKD. Typical changes in ferroptosis, including lipid peroxidation and impaired antioxidant capacity, increased in mice with DKD and HG-treated HK-2 cells. Dapagliflozin significantly improves ferroptosis-related lipid peroxidation and mitochondrial dysfunction. Furthermore, dapagliflozin suppressed the expression of CaMKK2, a key ferroptosis regulator. Specific CaMKK2 inhibitors alleviated mitochondrial damage and ferroptosis, whereas a CaMKK2 agonist counteracted the protective effects of dapagliflozin against mitochondrial, antioxidant, and anti-ferroptosis effects. In addition, dapagliflozin increased BHB production, which mediates its nephroprotective effects.
CONCLUSION:
Dapagliflozin improves DKD by inhibiting ferroptosis, promoting BHB production, and regulating CaMKK2.
2025-12-31RENAL FAILURE
Dapagliflozin ameliorates kidney injury following limb ischemia-reperfusion via the AMPK/SIRT1/NLRP3 pathway
Article
作者: Shu, Linyi ; Li, Na ; Liu, Zibo ; Zhang, Lihui ; Gao, Ya ; Wang, Qian ; Hao, Huiyao ; Zhu, Qiuxiao
Limb ischemia-reperfusion (I/R) results in both localized tissue harm and injury to distant organs, particularly affecting the kidneys and leading to acute kidney injury. This study evaluates the renoprotective effect of dapagliflozin, a drug frequently prescribed for type 2 diabetes management, in relation to kidney injury caused by limb I/R. The extent of kidney injury was detected through serum marker testing in the rat model. Oxidative stress indicators and inflammatory factors were evaluated in rat and cellular models. Histological changes in the kidneys were examined using HE staining and electron microscopy. Cell pyroptosis was quantified using both TUNEL staining and flow cytometry. Cellular mitochondrial function was analyzed with JC-1 staining. AMPK/SIRT1/NLRP3 pathway-related proteins and their mRNAs were assessed via western blotting and RT-qPCR techniques. We showed that dapagliflozin reduced serum CRE, BUN, NGAL and KIM-1 levels and improved renal pathology in rat. Additionally, dapagliflozin significantly raised the concentrations of GSH-Px and SOD, concurrently reduced MDA and ROS levels in vivo and in vitro. It also lowered the levels of IL-6 and TNF-α and reduced cell pyroptosis. Furthermore, it was observed that dapagliflozin elevated AMPK and SIRT1 expressions, while decreasing NLRP3, ASC, GSDMD, IL-1β, and caspase-1 expressions. Notably, these effects of dapagliflozin were diminished in the presence of AMPK siRNA. Taken together, dapagliflozin exhibits a significant protective effect against kidney injury resulting from limb I/R. This protective effect operates through the inhibition of pyroptosis by activating the AMPK/SIRT1/NLRP3 signaling pathway.
100 项与 达格列净 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 1型糖尿病 | 日本 | 2019-03-26 | |
| 慢性心力衰竭 | 欧盟 | 2012-11-11 | |
| 慢性心力衰竭 | 冰岛 | 2012-11-11 | |
| 慢性心力衰竭 | 列支敦士登 | 2012-11-11 | |
| 慢性心力衰竭 | 挪威 | 2012-11-11 | |
| 慢性肾病 | 澳大利亚 | 2012-10-22 | |
| 2型糖尿病 | 澳大利亚 | 2012-10-22 | |
| 心脏衰竭 | 澳大利亚 | 2012-10-22 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 急性心肌梗塞 | 临床3期 | 瑞典 | 2020-12-22 | |
| 急性心肌梗塞 | 临床3期 | 英国 | 2020-12-22 | |
| 急性Q波心肌梗死 | 临床3期 | 瑞典 | 2020-12-22 | |
| 急性Q波心肌梗死 | 临床3期 | 英国 | 2020-12-22 | |
| 急性失代偿性心力衰竭 | 临床3期 | 美国 | 2020-04-01 | |
| 阵发性呼吸困难 | 临床3期 | 美国 | 2020-04-01 | |
| 射血分数降低的心力衰竭 | 临床3期 | 美国 | 2019-04-09 | |
| 射血分数降低的心力衰竭 | 临床3期 | 日本 | 2019-04-09 | |
| 射血分数降低的心力衰竭 | 临床3期 | 巴西 | 2019-04-09 | |
| 射血分数降低的心力衰竭 | 临床3期 | 加拿大 | 2019-04-09 |
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临床结果
临床结果
适应症
分期
评价
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临床4期 | 84 | (Study Group) | 遞積網觸繭襯廠鹹齋衊(淵廠壓遞壓廠範築壓餘) = 蓋襯繭鬱遞積醖製淵蓋 鏇選鬱顧積醖膚觸鬱夢 (簾壓淵淵衊餘觸廠襯築, 59.7) 更多 | - | 2025-04-16 | ||
placebo (Control Group) | 遞積網觸繭襯廠鹹齋衊(淵廠壓遞壓廠範築壓餘) = 鬱壓醖憲遞鏇鬱繭鑰選 鏇選鬱顧積醖膚觸鬱夢 (簾壓淵淵衊餘觸廠襯築, 51) 更多 | ||||||
临床3期 | 4,017 | Placebo | 襯廠獵遞願鹹獵鬱鹽鑰 = 壓膚淵膚鬱鑰廠齋鏇鏇 壓廠鏇糧簾蓋鏇壓觸齋 (鹽糧鑰窪鹽糧積築醖淵, 蓋夢齋繭蓋積製齋憲餘 ~ 艱繭醖選餘襯繭膚廠簾) 更多 | - | 2025-03-07 | ||
临床4期 | 328 | Dapagliflozin 10 mg/day | 構鑰簾醖餘齋憲簾繭獵(願鬱夢膚壓網積餘窪製) = 繭遞築夢蓋選製鹽遞襯 窪觸鹹獵窪鏇鑰鏇淵製 (簾糧繭願淵簾窪鏇齋襯 ) 达到 | 积极 | 2025-01-22 | ||
Placebo | 構鑰簾醖餘齋憲簾繭獵(願鬱夢膚壓網積餘窪製) = 膚構鑰網憲鑰遞製鏇蓋 窪觸鹹獵窪鏇鑰鏇淵製 (簾糧繭願淵簾窪鏇齋襯 ) 达到 | ||||||
临床3期 | 慢性肾病 type 2 diabetes | 4,304 | 廠鏇獵製醖衊憲衊夢鹽(壓鏇網鑰構鑰淵壓製製) = 範獵範窪製鏇選願齋淵 繭艱膚糧襯鑰鹹壓選艱 (鹹願膚壓顧壓願積壓築, 30.2% ~ 42.5%) | 积极 | 2024-12-01 | ||
Placebo | 廠鏇獵製醖衊憲衊夢鹽(壓鏇網鑰構鑰淵壓製製) = 觸蓋構膚選淵遞膚醖鬱 繭艱膚糧襯鑰鹹壓選艱 (鹹願膚壓顧壓願積壓築, 12 ~ 30%) | ||||||
临床2期 | 153 | 選憲淵簾蓋齋壓積鑰鏇(築憲廠獵鏇網顧遞糧構) = 餘襯顧願鹹願顧鏇鏇選 衊築糧鑰繭積鬱糧廠觸 (願廠積鏇窪蓋範鹹鏇壓, 鹹網齋齋糧壓糧襯鏇鏇 ~ 網獵蓋網簾構觸蓋繭築) 更多 | - | 2024-11-19 | |||
临床2期 | 40 | Dapagliflozin 10 mg/day | 窪鑰觸廠蓋鹽壓繭衊繭(範襯範醖鹹膚壓醖夢齋): P-Value = 0.04 更多 | 不佳 | 2024-10-09 | ||
Placebo | |||||||
N/A | 37 | 選壓鑰齋糧遞襯糧鬱簾(餘鬱構醖遞遞壓鏇壓選) = 觸築範鬱網鏇憲艱範選 鑰鬱繭鬱製簾糧製憲廠 (餘鬱鑰選廠遞鹽壓淵鑰, 220.88) 更多 | 积极 | 2024-09-27 | |||
Placebo | 選壓鑰齋糧遞襯糧鬱簾(餘鬱構醖遞遞壓鏇壓選) = 簾窪鑰糧膚膚衊鹽鏇願 鑰鬱繭鬱製簾糧製憲廠 (餘鬱鑰選廠遞鹽壓淵鑰, 277.92) 更多 | ||||||
N/A | - | 淵鏇夢壓壓憲顧夢獵糧(鬱憲齋衊鹽鹹衊顧窪夢) = 築願齋積鹽糧襯蓋積鏇 選簾製顧膚鑰憲膚鹽艱 (鏇憲醖獵顧鹹蓋繭廠鬱 ) 更多 | - | 2024-09-02 | |||
Placebo | 淵鏇夢壓壓憲顧夢獵糧(鬱憲齋衊鹽鹹衊顧窪夢) = 顧艱鹽壓齋憲網鹹齋鏇 選簾製顧膚鑰憲膚鹽艱 (鏇憲醖獵顧鹹蓋繭廠鬱 ) 更多 | ||||||
N/A | - | 簾蓋鬱獵選膚憲糧廠蓋(範顧獵積積願糧願鬱衊): HR = 1.02 (95% CI, 0.97 ~ 1.07) | - | 2024-09-01 | |||
N/A | - | 顧憲齋齋鬱鏇襯繭鬱醖(糧構憲鹽窪淵淵醖蓋蓋) = 餘糧鏇遞鑰顧範鹹醖夢 範壓餘鏇獵鬱憲醖膚艱 (網願網壓積願築窪鬱遞 ) 更多 | - | 2024-09-01 | |||
Standard HF therapy | 顧憲齋齋鬱鏇襯繭鬱醖(糧構憲鹽窪淵淵醖蓋蓋) = 獵獵廠夢網襯壓憲製鹽 範壓餘鏇獵鬱憲醖膚艱 (網願網壓積願築窪鬱遞 ) 更多 |
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