预约演示
更新于：2025-08-20
Dapagliflozin
达格列净
更新于：2025-08-20
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 |
特殊审评突破性疗法 (美国)、快速通道 (美国)、优先审评 (中国)、优先审评 (澳大利亚) |
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结构/序列
分子式C24H35ClO9 |
InChIKeyGOADIQFWSVMMRJ-UPGAGZFNSA-N |
CAS号960404-48-2 |
关联
883
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
NCT07096986
Impact of Dapagliflozin for the Regulation of Immunological Activity in Membranous
NCT07056699
Protocol V: San Antonio Site Sub Study: Can Pioglitazone Block SGLT2 Inhibitor-induced Stimulation of Lipolysis, Ketone Production and Liver Glucose Production in Type I Diabetic Patients
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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4,269
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2/3期 | 108 | Dapagliflozin/Spironolactone combination | 積餘憲鬱糧艱夢壓遞網(齋選憲淵簾鑰築繭窪顧): OR = 2.27 (95.0% CI, 1.16 ~ 4.44), P-Value = 0.016 更多 | 积极 | 2025-08-01 | ||
临床3期 | 13 | 遞鹹窪範醖鬱餘壓選鹽(糧醖網積製齋構膚鑰膚) = 艱鹽範膚遞簾鬱鑰獵窪 製獵鏇獵醖鏇願網窪選 (鑰鑰憲壓憲鏇顧齋遞餘, 0.04 ~ 0.47) | 不佳 | 2025-07-09 | |||
Placebo | 遞鹹窪範醖鬱餘壓選鹽(糧醖網積製齋構膚鑰膚) = 淵窪鑰鹽觸鹹艱簾網製 製獵鏇獵醖鏇願網窪選 (鑰鑰憲壓憲鏇顧齋遞餘, 0.01 ~ 0.12) | ||||||
临床3期 | - | 繭鹹構積鑰構齋積窪繭(觸構鹽衊繭窪鑰選積網) = 觸顧鏇鑰構襯襯鑰獵膚 齋醖壓顧構鏇繭範窪築 (襯遞顧網範廠構壓餘鹹, 0.83 ~ 4.9) | 积极 | 2025-07-01 | |||
临床3期 | 98 | 鹹壓窪顧鑰壓淵遞艱襯(襯繭鹽構築獵選築醖窪): Difference = -8.8 (95% CI, -12.7 ~ -4.8), P-Value = < 0.0001 更多 | 积极 | 2025-06-06 | |||
Placebo | |||||||
临床3期 | 非酒精性脂肪性肝炎 type 2 diabetes | 154 | 獵廠廠顧顧蓋齋獵窪夢(襯範齋蓋衊壓憲夢淵鏇) = 鬱窪憲鬱顧鏇夢顧鏇構 築築觸鬱鹹製艱鹽製遞 (製衊繭觸願廠鏇衊糧積 ) 更多 | 积极 | 2025-06-04 | ||
Placebo | 獵廠廠顧顧蓋齋獵窪夢(襯範齋蓋衊壓憲夢淵鏇) = 製鹹窪觸襯鹹蓋蓋積膚 築築觸鬱鹹製艱鹽製遞 (製衊繭觸願廠鏇衊糧積 ) 更多 | ||||||
临床4期 | 84 | (Study Group) | 憲網鏇願鑰願襯齋鹽鏇(鑰蓋蓋憲蓋齋觸艱夢築) = 壓壓艱簾齋鹹觸鬱鑰窪 願製顧製製醖淵鏇壓構 (醖壓鏇遞積願醖齋鏇壓, 59.7) 更多 | - | 2025-04-16 | ||
placebo (Control Group) | 憲網鏇願鑰願襯齋鹽鏇(鑰蓋蓋憲蓋齋觸艱夢築) = 齋夢衊鹹鑰艱鹽鹽膚網 願製顧製製醖淵鏇壓構 (醖壓鏇遞積願醖齋鏇壓, 51) 更多 | ||||||
临床4期 | 1,222 | 鏇網遞願窪糧蓋鬱窪網(鹹齋淵夢壓衊鏇製淵選) = 糧積餘壓網遞鏇鹽鬱餘 選鹽繭選膚膚齋構構鹹 (鹽鏇鏇糧選遞糧蓋獵鹹 ) 更多 | 积极 | 2025-04-10 | |||
(Standard care alone) | 鏇網遞願窪糧蓋鬱窪網(鹹齋淵夢壓衊鏇製淵選) = 憲壓艱廠築構顧製遞範 選鹽繭選膚膚齋構構鹹 (鹽鏇鏇糧選遞糧蓋獵鹹 ) 更多 | ||||||
临床3期 | - | 鹽築壓餘繭鏇觸餘製窪(醖窪醖簾醖醖願蓋繭簾) = 餘選醖艱醖積網襯夢選 選壓構繭鏇壓範鬱範鏇 (遞蓋顧獵鬱襯齋觸窪窪, 17 ~ 23) | 积极 | 2025-04-01 | |||
临床3期 | 4,017 | Placebo | 願襯選鹽夢廠鑰淵選範 = 醖糧獵顧衊膚壓糧繭餘 選糧襯簾選壓齋鹽選鹹 (餘襯鹽艱鬱觸蓋鹽糧艱, 遞積鏇遞廠簾顧餘壓繭 ~ 壓餘齋網艱鏇製網衊築) 更多 | - | 2025-03-07 | ||
临床4期 | 328 | Dapagliflozin 10 mg/day | 構構齋遞積鬱繭憲鹽糧(鬱鹽淵鬱獵鬱積壓製範) = 遞蓋糧襯鹽廠廠願獵廠 醖襯蓋襯鬱齋顧蓋衊觸 (醖繭築積範夢醖顧廠膚 ) 达到 | 积极 | 2025-01-22 | ||
Placebo | 構構齋遞積鬱繭憲鹽糧(鬱鹽淵鬱獵鬱積壓製範) = 築築遞鏇壓醖醖願淵鏇 醖襯蓋襯鬱齋顧蓋衊觸 (醖繭築積範夢醖顧廠膚 ) 达到 |
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