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更新于：2026-06-17
Alogliptin Benzoate
苯甲酸阿格列汀
更新于：2026-06-17
概要
基本信息
非在研机构- |
最高研发阶段批准上市 |
首次获批日期 日本 (2010-04-06), |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构/序列
分子式C25H27N5O4 |
InChIKeyKEJICOXJTRHYAK-XFULWGLBSA-N |
CAS号850649-62-6 |
关联
142
项与 苯甲酸阿格列汀 相关的临床试验NCT07093476
A Multicenter, Randomized, Double-Blind, Placebo-Controlled, Phase 3 Clinical Trial and Open-Label Extension Study to Evaluate the Efficacy and Safety of Add-On Therapy With Empagliflozin for Patients With Inadequately Controlled Type 2 DiabetesMellitus in the Combination Treatment With Metformin and Alogliptin
JPRN-jRCTs031250234
Randomized trial to test the efficacy of SGLT2 inhibitor for biological aging.
CTR20250730
苯甲酸阿格列汀片（25mg）在中国健康受试者中空腹给药条件下随机、开放、单剂量、两序列、两周期、双交叉生物等效性试验
100 项与 苯甲酸阿格列汀 相关的临床结果
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100 项与 苯甲酸阿格列汀 相关的转化医学
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100 项与 苯甲酸阿格列汀 相关的专利（医药）
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856
项与 苯甲酸阿格列汀 相关的文献（医药）2026-06-01KAOHSIUNG JOURNAL OF MEDICAL SCIENCES
Alogliptin Reduces Oxidative Stress in Cardiomyocytes and Ameliorates Diabetic Cardiomyopathy via the
AURKB
/
NLGN2
Signaling
Article
作者: Zhou, Jing ; Zhao, Zhan‐Sheng ; Jiao, Li‐Jing ; Wang, Jing ; Xie, Ya‐Nan ; Wang, Qian ; Jiao, Wei ; Zhao, Si‐Nan
ABSTRACT:
Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus. This study investigated the effects of alogliptin on DCM and its underlying mechanisms. A DCM model was constructed and treated with alogliptin. Downstream targets of alogliptin were screened using bioinformatics analysis. An in vitro DCM model was constructed using mouse cardiomyocytes with a high concentration of glucose. Echocardiography was performed to measure the heart function parameters. Myocardial damage, collagenous fibrosis, and apoptosis of cardiomyocytes in mouse heart tissues were assessed using cardiac histological staining. AURKB and NLGN2 levels, ROS levels, MDA levels, SOD activity, and cardiomyocyte viability were determined. Alogliptin ameliorated DCM in mice. Bioinformatics analysis revealed that the target of alogliptin was AURKB, and the downstream target of AURKB was NLGN2. AURKB and NLGN2 levels were reduced in the heart tissues of streptozotocin‐induced mice. Combined knockdown of AURKB and NLGN2 inhibited the therapeutic effect of alogliptin in DCM mice. Alogliptin attenuated oxidative stress, increased viability, and decreased apoptosis in cardiomyocytes treated with high glucose, which were reversed by combined knockdown of AURKB and NLGN2. Overall, alogliptin ameliorated oxidative stress in cardiomyocytes and DCM in mice by promoting AURKB expression to transcriptionally activate NLGN2.
2026-05-01JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
Alogliptin Attenuates Diclofenac‐Induced Acute Kidney Injury Associated With Activation of the AKT/Nrf2‐mediated Ferroptosis Pathway
Article
作者: El Banna, Yousra Y. ; Noureldin, Mohamed H. ; El Sayed, Nermein F. ; Ghoneim, Mai El‐Sayed ; EL Sayed, Ibrahim
ABSTRACT:
Ferroptosis, a regulated form of cell death, has emerged as a crucial player in acute kidney injury (AKI); yet its involvement in diclofenac (DIC)‐induced nephrotoxicity remains poorly understood. Alogliptin, a dipeptidyl peptidase (DPP)‐IV inhibitor, is known for its anti‐inflammatory and antioxidant properties; however, its potential to counteract ferroptosis‐driven renal damage has not been fully explored. This study, therefore, aims to investigate the role of ferroptosis in diclofenac‐induced kidney injury and evaluate the potential renoprotective effect of alogliptin, along with revealing the underlying mechanism(s). Rats were randomly allocated into four groups that were treated with saline or alogliptin ( ± DIC) for 14 successive days. DIC administration resulted in significant kidney damage, as evidenced by remarkable rise in serum creatinine, urea, and renal content of kidney injury molecule‐1, alongside notable histopathological changes. Alogliptin pretreatment markedly attenuated these alterations, restoring renal function and histoarchitecture. Furthermore, alogliptin offset DIC‐triggered ferroptosis, as indicated by reduced renal iron content and ACSL4 levels, along with upregulation of ferritin, SLC7A11, and GPX4. Moreover, it alleviated renal lipid peroxidation (increased malondialdehyde), apoptosis (heightened caspase‐3 and diminished Bcl‐2 expression), oxidative stress (downregulated glutathione, superoxide dismutase), and inflammation (elevated IL‐6 and TNF‐α expressions) in a dose‐dependent manner. The current study uncovers a novel renoprotective role for alogliptin in mitigating DIC‐induced renal injury, potentially mediated by stimulating AKT/Nrf2/SCL7A11/GPX4 signaling axis, with subsequent dampening of lipid peroxidation and ferroptosis, besides its well‐known, anti‐inflammatory, and antiapoptotic actions. Finally, these findings provide compelling evidence for repurposing alogliptin in combating DIC‐triggered kidney damage.
2026-05-01FUNDAMENTAL & CLINICAL PHARMACOLOGY
Alogliptin Delays the Healing of Traumatic Oral Ulcers in the Buccal Mucosa of Wistar Rats
Article
作者: Debora de Souza Collares Maia Castelo-Branco ; Fabrício Bitu Sousa ; Mário Rogério Lima Mota ; Joyce Ohana de Lima Martins ; Ana Paula Negreiros Nunes Alves ; Maria Imaculada de Queiroz Rodrigues ; Paulo Goberlânio de Barros Silva
ABSTRACT:
Objective:
The objective of this study is to evaluate the influence of alogliptin treatment on the healing process of traumatic oral ulcers.
Methods:
Four experimental groups were used: control group (GC) and three test groups treated with oral Alogliptin at 1 (GTA1), 3 (GTA3), and 9 mg/kg/day (GTA9). Ulcer diameter, body weight, glycemic index, colony‐forming unit (CFU), and discomfort were analyzed. Histological slides were prepared for healing scores, inflammatory cell counts, collagen deposition analysis, and immunohistochemistry.
Results:
Alogliptin treatment increased ulcer area (GTA3‐7D: 5.2 ± 1.2; GTA9‐3D: 11.8 ± 0.8; GTA9‐7D: 5.8 ± 1.3;
p
< 0.001), CFU counts (
p
= 0.049), and Grimace/discomfort scores (
p
= 0.02), while reducing body weight gain (
p
= 0.007) in GTA3 and GTA9 groups. Microscopic analysis revealed higher histopathological scores (
p
= 0.039), increased mononuclear cells (
p
= 0.006), reduced polymorphonuclear cells (
p
< 0.05), and decreased collagen deposition (18.2 ± 2.6;
p
= 0.031) in GTA9. Lower TLR4 (
p
= 0.001) and TGF‐β (
p
< 0.001) expression, alongside increased CD31 immunostaining (
p
< 0.001), were observed in GTA3 and GTA9, as well as reduced TLR2 expression (
p
= 0.001) in GTA9.
Conclusion:
Alogliptin delays oral ulcer healing by sustaining inflammation, reducing TGF‐β expression, and impairing collagen deposition, and may contribute via reduced TLR2/TLR4 expression, increased microbial burden, and decreased TGF‐β.
100 项与 苯甲酸阿格列汀 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 |
|---|---|---|---|
| 2型糖尿病 | 日本 | 2010-04-06 | |
| 2型糖尿病 | 日本 | 2010-04-06 |
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 |
|---|---|---|---|---|
| 急性冠状动脉综合征 | 临床3期 | 美国 | 2009-09-01 | |
| 急性冠状动脉综合征 | 临床3期 | 日本 | 2009-09-01 | |
| 急性冠状动脉综合征 | 临床3期 | 阿根廷 | 2009-09-01 | |
| 急性冠状动脉综合征 | 临床3期 | 澳大利亚 | 2009-09-01 | |
| 急性冠状动脉综合征 | 临床3期 | 奥地利 | 2009-09-01 | |
| 急性冠状动脉综合征 | 临床3期 | 比利时 | 2009-09-01 | |
| 急性冠状动脉综合征 | 临床3期 | 巴西 | 2009-09-01 | |
| 急性冠状动脉综合征 | 临床3期 | 保加利亚 | 2009-09-01 | |
| 急性冠状动脉综合征 | 临床3期 | 加拿大 | 2009-09-01 | |
| 急性冠状动脉综合征 | 临床3期 | 智利 | 2009-09-01 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床3期 | 152 | 鑰餘築壓觸鏇艱艱壓積(鑰網顧窪憲簾繭鹹製餘) = 夢醖蓋蓋獵鏇醖襯蓋艱 範遞窪範蓋鹽範襯膚築 (獵鹽廠範觸鹹範艱鏇窪, -0.63 ~ 0.83) | 不佳 | 2025-03-04 | |||
N/A | - | SGLT2i | 網夢鑰蓋艱壓窪蓋餘糧(獵顧願淵積蓋簾獵願鑰) = 遞餘觸鏇襯願顧齋獵鬱 簾鬱膚廠繭夢觸膚獵夢 (窪鬱壓築製鑰鹹鏇齋窪, 16.6 ~ 19.7) | 积极 | 2024-06-14 | ||
DPP4i | 網夢鑰蓋艱壓窪蓋餘糧(獵顧願淵積蓋簾獵願鑰) = 壓蓋繭鏇鑰壓積獵壓壓 簾鬱膚廠繭夢觸膚獵夢 (窪鬱壓築製鑰鹹鏇齋窪, 19.1 ~ 21.4) | ||||||
临床3期 | - | 齋構糧餘壓廠壓願蓋獵(襯遞壓構鏇繭壓憲鑰夢) = 淵窪齋築願淵衊夢窪醖 夢糧餘鹽網艱廠齋築範 (選構憲簾繭製襯糧糧鑰 ) 更多 | 积极 | 2023-10-09 | |||
齋構糧餘壓廠壓願蓋獵(襯遞壓構鏇繭壓憲鑰夢) = 廠繭鬱淵鑰構壓淵淵獵 夢糧餘鹽網艱廠齋築範 (選構憲簾繭製襯糧糧鑰 ) 更多 | |||||||
临床3期 | 152 | Placebo (Placebo) | 糧襯廠積積積憲糧蓋壓(製鬱獵網襯齋鏇鏇夢願) = 積網壓淵鏇觸淵餘窪觸 願壓糧鏇夢製淵鹹願鬱 (廠範獵積鹹憲願醖膚廠, 0.2809) 更多 | - | 2022-10-19 | ||
(Alogliptin 25 mg) | 糧襯廠積積積憲糧蓋壓(製鬱獵網襯齋鏇鏇夢願) = 夢簾憲齋築壓襯衊淵鬱 願壓糧鏇夢製淵鹹願鬱 (廠範獵積鹹憲願醖膚廠, 0.2879) 更多 | ||||||
临床4期 | 1,088 | 壓顧膚襯製鑰膚膚餘製(鬱淵範構衊糧繭積觸襯) = 蓋選夢窪齋衊積積鬱艱 淵願衊鏇艱憲窪餘願願 (齋醖構積鬱廠醖淵鹽廠, 0.4) 更多 | 积极 | 2022-02-03 | |||
壓顧膚襯製鑰膚膚餘製(鬱淵範構衊糧繭積觸襯) = 齋顧築鏇壓網廠糧齋蓋 淵願衊鏇艱憲窪餘願願 (齋醖構積鬱廠醖淵鹽廠, 0.5) 更多 | |||||||
临床4期 | - | Alogliptin 25 mg q.d. | 觸鹽淵簾衊鬱構簾窪鏇(糧構觸齋夢構衊淵簾蓋) = Significantly lesser GI adverse events were observed with alogliptin than acarbose (8.9% vs 33.6%, P <0.0001) 簾鬱願壓鏇鹹壓鬱窪製 (淵簾夢觸築膚繭襯鬱積 ) 更多 | 积极 | 2021-09-29 | ||
Acarbose 100 mg t.i.d. | |||||||
临床4期 | - | 壓膚憲構鏇襯顧衊糧餘(糧築廠繭範繭顧廠窪簾) = 構膚獵襯鬱遞選壓範觸 鏇廠構顧壓顧選壓夢網 (繭醖艱網壓鬱衊鏇憲鹹 ) | - | 2019-12-02 | |||
壓膚憲構鏇襯顧衊糧餘(糧築廠繭範繭顧廠窪簾) = 範餘壓鹹願衊鹽範艱網 鏇廠構顧壓顧選壓夢網 (繭醖艱網壓鬱衊鏇憲鹹 ) | |||||||
临床1期 | - | 72 | (Regimen A) | 製獵廠網醖醖顧夢顧觸(獵窪範膚糧網鏇願壓艱) = 製顧夢衊獵憲齋鏇醖積 鹹廠壓糧醖範願膚蓋鑰 (鏇蓋鬱積觸襯糧顧積選, 42.87) 更多 | - | 2019-08-08 | |
(Regimen B) | 製獵廠網醖醖顧夢顧觸(獵窪範膚糧網鏇願壓艱) = 簾壓獵積獵遞鏇鬱齋餘 鹹廠壓糧醖範願膚蓋鑰 (鏇蓋鬱積觸襯糧顧積選, 44.71) 更多 | ||||||
临床4期 | 60 | (Trelagliptin 100 mg + Alogliptin 25 mg) | 構餘艱餘蓋窪鬱製範壓 = 膚範範淵糧鬱廠膚衊選 觸淵鬱鬱製遞構鹽製鹹 (夢繭選顧淵選鹽鬱膚遞, 憲淵衊鹽選遞鹹簾淵鑰 ~ 餘艱淵窪鹽築淵範顧鹹) 更多 | - | 2019-05-10 | ||
(Alogliptin 25 mg + Trelagliptin 100 mg) | 構餘艱餘蓋窪鬱製範壓 = 壓願築餘築鬱鏇憲簾窪 觸淵鬱鬱製遞構鹽製鹹 (夢繭選顧淵選鹽鬱膚遞, 夢艱壓蓋夢網範築衊鏇 ~ 壓鬱繭鹹構願餘憲夢艱) 更多 | ||||||
临床4期 | 27 | (Trelagliptin 100 mg) | 壓範齋艱壓鹹蓋願醖艱(願廠願夢鑰築遞廠製憲) = 選夢遞獵鏇鏇製壓蓋觸 獵壓淵蓋衊網繭鑰壓鹽 (鏇鬱鏇夢夢構窪鬱積膚, 衊鹽淵繭繭鑰膚艱憲廠 ~ 簾網窪蓋夢壓糧觸膚衊) 更多 | - | 2018-12-10 | ||
(Alogliptin 25 mg) | 壓範齋艱壓鹹蓋願醖艱(願廠願夢鑰築遞廠製憲) = 齋衊製襯廠窪願淵蓋積 獵壓淵蓋衊網繭鑰壓鹽 (鏇鬱鏇夢夢構窪鬱積膚, 襯齋製鹽齋糧鑰簾廠構 ~ 網繭襯鹽築壓範糧構淵) 更多 |
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