格列本脲(Glyburide) - 药物靶点：BSEP x Kir6.2 x SUR1_在研适应症：6q24暂时性新生儿糖尿病，新生儿糖尿病，糖尿病_专利_临床

概要

基本信息

药物类型

小分子化药

别名

1-((p-(2-(5-chloro-o-anisamido)ethyl)phenyl)sulfonyl)-3-cyclohexylurea、1-(p-(2-(5-chloro-2-methoxybenzamido)ethyl)benzenesulfonyl)-3-cyclohexylurea、5-chloro-N-(2-(4-((((cyclohexylamino)carbonyl)amino)sulfonyl)phenyl)ethyl)-2-methoxybenzamide

+ [23]

靶点

BSEP x Kir6.2 x SUR1

作用方式

抑制剂、激动剂

作用机制

BSEP inhibitors(ATP binding cassette subfamily B member 11 inhibitors)、Kir6.2激动剂(potassium inwardly rectifying channel subfamily J member 11 agonists)、SUR1抑制剂(磺酰脲类受体1抑制剂)

治疗领域

内分泌与代谢疾病其他疾病肿瘤+ [1]

在研适应症

6q24暂时性新生儿糖尿病新生儿糖尿病糖尿病+ [2]

非在研适应症

脑震荡脑挫伤脑水肿+ [5]

原研机构

Pfizer Inc.

在研机构

Sanofi-Aventis U.S. LLC

Pfizer Inc.Ammtek Ltd.

+ [3]

非在研机构

Remedy Pharmaceuticals, Inc.

Biogen, Inc.

江苏奥赛康药业有限公司

+ [1]

权益机构

Biogen, Inc.

Eton Pharmaceuticals, Inc.

Remedy Pharmaceuticals, Inc.

+ [1]

最高研发阶段批准上市

首次获批日期

日本 (1971-03-02),

2型糖尿病

最高研发阶段(中国)批准上市

特殊审评孤儿药 (欧盟)、优先审评 (中国)

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结构/序列

分子式C23H28ClN3O5S

InChIKeyZNNLBTZKUZBEKO-UHFFFAOYSA-N

CAS号10238-21-8

关联

90

项与格列本脲相关的临床试验

NCT06589141

/ Not yet recruitingN/AIIT

Comparison Between Metformin and Glyburide in the Management of Gestational Diabetes: a Randomized Controlled Trial (GDM-MERGE Trial)

This study aims to compare the maternal, fetal, and neonatal outcomes associated with the use of metformin versus glyburide for managing gestational diabetes.
The objective is to assess the safety and effectiveness profiles of both medications as potential alternatives to initiating insulin therapy.

开始日期2025-01-01

申办/合作机构

Assiut University

CTRI/2023/12/060716

/ RecruitingN/AIIT

Role of Sulphonylurea-receptor1(SUR1) inhibition in Traumatic Brain injury (TBI): A randomized controlled trial to assess efficacy and safety of Glibenclamide in moderate to severe TBI - STRATEGY

开始日期2024-01-01

申办/合作机构

Indian Council of Medical Research

NCT05687500

/ Recruiting临床2期IIT

Oral Glibenclamide in Preterm Infants with Hyperglycaemia (GALOP)

The purpose of this study is to confirm hypothesis that Glibenclamide can be administered orally and is an alternative to insulin therapy in treating transient hyperglycemia of premature newborns.

开始日期2023-05-20

申办/合作机构

Assistance Publique des Hôpitaux de Paris SA

100 项与格列本脲相关的临床结果

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100 项与格列本脲相关的转化医学

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100 项与格列本脲相关的专利（医药）

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16,030

项与格列本脲相关的文献（医药）

2025-08-01·Microbial Pathogenesis

A new target for drug repositioning: CEBPα elicits LL-37 expression in a vitamin D-independent manner promoting Mtb clearance

Article

作者: González-Muñiz, Óscar E ; Félix-Arellano, Camelia ; Santos-Mena, Alan ; Navarro-Tovar, Gabriela ; Rodríguez-Carlos, Adrián ; Rivas-Santiago, Bruno ; Jacobo-Delgado, Yolanda M

Tuberculosis is an infectious disease caused by Mycobacterium tuberculosis (Mtb) and is a growing public health problem worldwide. Within the innate immune response, we highlight the secretion of the antimicrobial peptide LL-37, which is crucial for Mtb elimination in infected cells. Previous reports have shown that CEBPα activation induces LL-37 independently of its main inducer, vitamin D, under endoplasmic reticulum (ER) stress. In this study, we report that infection with Mtb causes ER stress in pulmonary epithelial cells and macrophages. The stress induces the activation of CEBPα, which in turn promotes the LL-37 expression. Furthermore, the participation of CEBPα is necessary for the correct clearance of Mtb in an in vitro infection model. We identify candidate drugs (mycophenolic acid, indapamide, and glibenclamide) capable of activating CEBPα and promoting LL-37 through in silico assays. The effect of the drugs was corroborated by gene and protein expression analysis. Finally, we observed that treatment with these drugs improves bacterial clearance in infected cells. Our results lead us to suggest CEBPα as a potential therapeutic target as an adjuvant in the standard treatment of tuberculosis, seeking a reduction in treatment time, and thus a lower appearance of drug resistance.

2025-07-01·Archives of Biochemistry and Biophysics

A glibenclamide analog lacking the cyclohexylurea portion fails to block ischemic preconditioning-induced mitochondrial and cardiac protection against ischemia/reperfusion injury

Article

作者: de Freitas Soares, Geovanna Carvalho ; Palácio, Plínio Bezerra ; Facundo, Heberty Tarso

Despite significant research, there are no definitive therapies to prevent ischemia/reperfusion injury. During reperfusion, mitochondrial reactive oxygen species (ROS) cause cell damage. Ischemic preconditioning (IP), characterized by brief cycles of ischemia and reperfusion, activates mitochondrial ATP-sensitive potassium channels (mitoKATP) and provides cardioprotection. The aim of the present study is to investigate the impact of a truncated glibenclamide (lacking the cyclohexylurea portion - IMP-A) in ischemic preconditioning (IP)-mediated cardioprotection. Our study shows that IMP-A (2-5 μM) does not inhibit the protective effects of IP against ischemia/reperfusion damage in isolated rat hearts. In this context, IP hearts (with or without IMP-A) exhibited preserved cardiac function, as indicated by stable left ventricular developed pressure, maximal and minimal first derivatives, and rate-pressure product, along with a reduced infarct size following ischemia/reperfusion injury. Conversely, glibenclamide (2 μM - a well-characterized mitoKATP inhibitor) abolished the protective effects of IP against ischemia/reperfusion damage. Mitochondria isolated from reperfused IP hearts (treated or not with IMP-A) produced significantly lower levels of mitochondrial ROS and had lower susceptibility to Ca²⁺-induced swelling secondary to mitochondrial permeability transition pore (mPTP) opening. Additionally, IP hearts (treated or not with IMP-A) had preserved protein sulfhydryls. Glibenclamide elevated mitochondrial ROS production and negatively impacted mPTP and the sulfhydryl protection seen in IP hearts. Importantly, mitochondrial O₂ consumption was preserved in IP hearts (treated or not with IMP-A), and this preservation was disrupted by glibenclamide but not by IMP-A. These findings suggest that the cyclohexylurea group of glibenclamide is essential for its ability to block IP-mediated cardioprotection, providing valuable insights for developing novel therapeutic strategies.

2025-06-01·European Journal of Pharmacology

The sodium-glucose cotransporter 2 inhibitor tofogliflozin induces vasodilation of rabbit femoral artery by activating Kv channels, the SERCA pump, and the sGC/cGMP pathway

Article

作者: Kim, Hye Ryung ; An, Jin Ryeol ; Jung, Won-Kyo ; Seo, Mi Seon ; Jeong, Junsu ; Park, Minju ; Park, Hongzoo ; Jang, YeEun ; Park, Won Sun ; Zhuang, Wenwen ; Choi, Il-Whan

Tofogliflozin is a sodium-glucose cotransporter 2 inhibitor widely used to treat type 2 diabetes mellitus, but it also exhibits cardio-protective effects. This study investigated the vasodilatory action of tofogliflozin using rabbit femoral artery rings pre-contracted with phenylephrine (1 μM). The results showed the concentration-dependent induction of vasodilation by tofogliflozin, a response that remained unchanged following endothelial removal, pretreatment with the nitric oxide synthase inhibitor L-NAME (100 μM), or the inhibition of low- and intermediate-conductance Ca²⁺-activated K⁺ channels using apamin (1 μM) in combination with TRAM-34 (1 μM). Furthermore, pretreatment with the voltage-dependent K⁺ (Kv) channel inhibitor 4-AP (3 mM) reduced the vasodilatory effects of tofogliflozin whereas pretreatment with the ATP-sensitive K⁺ channel inhibitor glibenclamide (10 μM) or the large-conductance Ca²⁺-activated K⁺ channel inhibitor paxilline (1 μM) did not. Notably, our findings indicated that Kv7.X, rather than Kv1.5 or Kv2.1, is the primary Kv subtype involved in tofogliflozin-induced vasodilation. The vasodilatory effects of tofogliflozin were also significantly inhibited in femoral arterial rings pretreated with the sarco/endoplasmic reticulum Ca²⁺-ATPase (SERCA) pump inhibitors thapsigargin (1 μM) and cyclopiazonic acid (10 μM). Tofogliflozin-induced vasodilation was unaltered in arterial rings exposed to the adenylyl cyclase inhibitor SQ 22536 (50 μM), the protein kinase A (PKA) inhibitor KT 5720 (1 μM), and the protein kinase G inhibitor KT 5823 (1 μM) whereas it was effectively reduced by the soluble guanylyl cyclase (sGC) inhibitor ODQ (10 μM). These findings suggest that tofogliflozin-induced vasodilation is mediated by the activation of the SERCA pump, the sGC/cGMP pathway, and Kv channels.

77

项与格列本脲相关的新闻（医药）

2025-04-28

·GlobeNewswire-Health Care

Eton Pharmaceuticals Announces Submission of NDA for ET-600 (Desmopressin Oral Solution)

- NDA submitted for the treatment of central diabetes insipidus -- Expected 10-month review; commercial preparations underway for a potential Q1 2026 launch – DEER PARK, Ill., April 28, 2025 (GLOBE NEWSWIRE) -- Eton Pharmaceuticals, Inc (“Eton” or the “Company”) (Nasdaq: ETON), an innovative pharmaceutical company focused on developing and commercializing treatments for rare diseases, today announced the submission of a New Drug Application (NDA) to the U.S. Food and Drug Administration (FDA) for ET-600, Eton’s proprietary, patented oral solution of desmopressin under development for the treatment of central diabetes insipidus. The Company expects the application to be assigned a 10-month FDA review, allowing for potential approval and launch in the first quarter of 2026. “The NDA submission for ET-600 is another important milestone for Eton, and for the thousands of children impacted by diabetes insipidus. If approved, ET-600 will be the only FDA-approved oral liquid formulation of desmopressin, providing the small, precise, and titratable doses required to treat pediatric patients,” said Sean Brynjelsen, CEO of Eton Pharmaceuticals. “Leading pediatric endocrinologists have long expressed a need for this product, and we’re pleased to be one step closer to bringing it to patients. Pre-launch commercial activities are already underway as we plan for a potential approval in the first quarter of 2026.” Eton has been issued a patent by the U.S. Patent and Trademark Office on ET-600, which expires in 2044 and has additional patent applications under review. In a bioequivalence study conducted in 75 human subjects, ET-600 demonstrated pharmacokinetic equivalence to the FDA-approved reference product of the same active ingredient. The company estimates that central diabetes insipidus impacts approximately 3,000 pediatric patients in the United States. About Eton Pharmaceuticals Eton is an innovative pharmaceutical company focused on developing and commercializing treatments for rare diseases. The Company currently has seven commercial rare disease products: INCRELEX®, ALKINDI SPRINKLE®, GALZIN®, PKU GOLIKE®, Carglumic Acid, Betaine Anhydrous, and Nitisinone. The Company has six additional product candidates in late-stage development: ET-400, ET-600, Amglidia®, ET-700, ET-800 and ZENEO® hydrocortisone autoinjector. For more information, please visit our website at www.etonpharma.com. Forward-Looking Statements Statements contained in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, including statements associated with the expected ability of Eton to undertake certain activities and accomplish certain goals and objectives. These statements include but are not limited to statements regarding Eton’s business strategy, Eton’s plans to develop and commercialize its product candidates, the safety and efficacy of Eton’s product candidates, Eton’s plans and expected timing with respect to regulatory filings and approvals, and the size and growth potential of the markets for Eton’s product candidates. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Words such as “believes,” “anticipates,” “plans,” “expects,” “intends,” “will,” “goal,” “potential” and similar expressions are intended to identify forward-looking statements. These forward-looking statements are based upon Eton’s current expectations and involve assumptions that may never materialize or may prove to be incorrect. Actual results and the timing of events could differ materially from those anticipated in such forward-looking statements as a result of various risks and uncertainties, which include, without limitation, risks associated with the process of discovering, developing and commercializing drugs that are safe and effective for use as human therapeutics, and in the endeavor of building a business around such drugs. These and other risks concerning Eton’s development programs and financial position are described in additional detail in Eton’s filings with the Securities and Exchange Commission. All forward-looking statements contained in this press release speak only as of the date on which they were made. Eton undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made. Investor Relations:Lisa M. Wilson, In-Site Communications, Inc.T: 212-452-2793E: lwilson@insitecony.com Source: Eton Pharmaceuticals, Inc.

申请上市

2025-04-28

·ir.etonpharma.com

Eton Pharmaceuticals Announces Submission of NDA for ET-600 (Desmopressin Oral Solution) | Eton Pharmaceuticals, Inc.

News Release Details « Back to news Eton Pharmaceuticals Announces Submission of NDA for ET-600 (Desmopressin Oral Solution) - NDA submitted for the treatment of central diabetes insipidus - - Expected 10-month review; commercial preparations underway for a potential Q1 2026 launch – DEER PARK, Ill., April 28, 2025 (GLOBE NEWSWIRE) -- Eton Pharmaceuticals, Inc (“Eton” or the “Company”) (Nasdaq: ETON), an innovative pharmaceutical company focused on developing and commercializing treatments for rare diseases, today announced the submission of a New Drug Application (NDA) to the U.S. Food and Drug Administration (FDA) for ET-600, Eton’s proprietary, patented oral solution of desmopressin under development for the treatment of central diabetes insipidus. The Company expects the application to be assigned a 10-month FDA review, allowing for potential approval and launch in the first quarter of 2026. “The NDA submission for ET-600 is another important milestone for Eton, and for the thousands of children impacted by diabetes insipidus. If approved, ET-600 will be the only FDA-approved oral liquid formulation of desmopressin, providing the small, precise, and titratable doses required to treat pediatric patients,” said Sean Brynjelsen, CEO of Eton Pharmaceuticals. “Leading pediatric endocrinologists have long expressed a need for this product, and we’re pleased to be one step closer to bringing it to patients. Pre-launch commercial activities are already underway as we plan for a potential approval in the first quarter of 2026.” Eton has been issued a patent by the U.S. Patent and Trademark Office on ET-600, which expires in 2044 and has additional patent applications under review. In a bioequivalence study conducted in 75 human subjects, ET-600 demonstrated pharmacokinetic equivalence to the FDA-approved reference product of the same active ingredient. The company estimates that central diabetes insipidus impacts approximately 3,000 pediatric patients in the United States. About Eton Pharmaceuticals Eton is an innovative pharmaceutical company focused on developing and commercializing treatments for rare diseases. The Company currently has seven commercial rare disease products: INCRELEX®, ALKINDI SPRINKLE®, GALZIN®, PKU GOLIKE®, Carglumic Acid, Betaine Anhydrous, and Nitisinone. The Company has six additional product candidates in late-stage development: ET-400, ET-600, Amglidia®, ET-700, ET-800 and ZENEO® hydrocortisone autoinjector. For more information, please visit our website at www.etonpharma.com. Forward-Looking Statements Statements contained in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, including statements associated with the expected ability of Eton to undertake certain activities and accomplish certain goals and objectives. These statements include but are not limited to statements regarding Eton’s business strategy, Eton’s plans to develop and commercialize its product candidates, the safety and efficacy of Eton’s product candidates, Eton’s plans and expected timing with respect to regulatory filings and approvals, and the size and growth potential of the markets for Eton’s product candidates. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Words such as “believes,” “anticipates,” “plans,” “expects,” “intends,” “will,” “goal,” “potential” and similar expressions are intended to identify forward-looking statements. These forward-looking statements are based upon Eton’s current expectations and involve assumptions that may never materialize or may prove to be incorrect. Actual results and the timing of events could differ materially from those anticipated in such forward-looking statements as a result of various risks and uncertainties, which include, without limitation, risks associated with the process of discovering, developing and commercializing drugs that are safe and effective for use as human therapeutics, and in the endeavor of building a business around such drugs. These and other risks concerning Eton’s development programs and financial position are described in additional detail in Eton’s filings with the Securities and Exchange Commission. All forward-looking statements contained in this press release speak only as of the date on which they were made. Eton undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made. Investor Relations: Lisa M. Wilson, In-Site Communications, Inc. T: 212-452-2793 E: lwilson@insitecony.com Source: Eton Pharmaceuticals, Inc. Source: Eton Pharmaceuticals

申请上市

2025-04-25

·石药集团

石药集团1类创新药普卢格列汀上市会隆重召开，引领多重用药安全变革

4月20日，石药集团普卢格列汀片（商标名：善泽平®）上市会在湖南长沙隆重召开，业内多位权威专家及学者展开专业探讨，会议现场吸引了众多临床一线工作者的广泛参与。上市会伊始，石药集团执行总裁王振国先生发表致辞，对莅临上市会的各位专家学者及临床医务工作者表示热烈欢迎和诚挚问候。他表示，普卢格列汀是石药集团在糖尿病领域上市的第一个1类创新药；未来，石药集团将以普卢格列汀为起点，全面布局糖尿病产品管线。作为我国自主研发的新一代DPP-4抑制剂，普卢格列汀在化学结构中引入氟原子，显著提高活性与选择性，从而实现对DPP-4表现出高选择性和强抑制性1。在中国开展的两项多中心III期临床试验（普卢格列汀单药III期试验、普卢格列汀联合二甲双胍III期试验）均取得积极结果，充分展现了普卢格列汀优异的降糖疗效和良好的安全性2,3，尤其在T2DM患者多重用药管理中具有独特优势。普卢格列汀在中国的成功上市为糖尿病治疗领域注入全新动力，也标志着国内广大T2DM患者迎来了有效、安全的治疗新选择，普卢格列汀临床应用前景可期！普卢格列汀如何破解多重用药困局T2DM管理调挑战升级：多重用药显著增加药物相互作用风险（DDI）中国糖尿病患病率仍在持续攀升，预计2050年中国患病人群将达到1.68亿4。从治疗现状来看，糖尿病的生理机制复杂，不论是“早期联合”还是“阶梯治疗”，采用不同作用机制的药物联合治疗已成为血糖控制的必经之路。然而，目前更为棘手的是，作为糖尿病的高发人群，老年患者往往多病共存，多重用药现象日益普遍。除多种降糖药外，许多患者还需要接受降压药、调脂药、抗血小板药等治疗5-8。据统计，64%的老年T2DM患者需同时使用5种以上药物9。北京协和医院肖新华教授强调，多重用药致使DDI风险显著增加，这给T2DM综合管理带来新的挑战，因为DDI不仅对血糖控制产生不利影响，还可能增加患者住院甚至死亡风险，进一步加重患者负担10-12。DPP4抑制剂新成员——普卢格列汀：多重用药患者的安全新选择面对这一严峻的临床挑战，新型DPP-4抑制剂普卢格列汀通过优化代谢途径，提供了有效解决方案。DPP-4抑制剂具有低血糖发生率低、体重影响中性、胃肠道反应少等特点，已成为老年糖尿病患者的一线用药13。目前国内已有多种DPP-4抑制剂类药物上市，虽然机制相同，但不同药物的代谢途径并不相同。CYP450酶、P糖蛋白（P-pg）是介导代谢性DDI发生的两大主要途径14，普卢格列汀的优势之一在于其不经过CYP450酶代谢，且非P-pg底物，因此DDI风险更小1。并且，普卢格列汀不与格列本脲及临床常用心血管药物（包括缬沙坦、辛伐他汀、华法林、地高辛）发生相互作用，联用时普卢格列汀及上述药物均不需要调整剂量1。因此，普卢格列汀的上市为多重用药患者提供了一种安全、便捷的治疗新选择。从降糖效果来看，由北京大学第一医院郭晓蕙教授牵头的普卢格列汀单药治疗未经治疗的T2DM患者的III期研究显示，普卢格列汀100mg QD治疗24周后，糖化血红蛋白（HbA1c）水平显著降低，降幅达0.61%（去除安慰剂效应，p<0.001)，48%的患者血糖达标（HbA1c≤7%），患者空腹血糖（FPG）和餐后2h血糖（2h-PPG）也实现有效改善2。图1.T2DM患者应用善泽平100mg QD治疗24周后HbA1c的变化另一项普卢格列汀联合二甲双胍治疗T2DM患者的III期研究由北京协和医院肖新华教授牵头，在中国30个中心进行。结果显示，普卢格列汀100mg QD+二甲双胍治疗24周后，HbA1c水平降幅达0.63%（去除安慰剂效应，p<0.001)， 50.0%的患者血糖达标（HbA1c≤7%）， FPG和2h-PPG也均明显降低3。图2.T2DM患者应用善泽平100mg QD+二甲双胍治疗24周后HbA1c的变化普卢格列汀降糖疗效确切，低血糖发生率低2,3，能够满足患者长期用药需求，尤其有助于多重用药患者实现更佳的治疗体验。结语普卢格列汀作为国家“重大新药创制”专项成果，其上市不仅是中国糖尿病创新药物研发的又一里程碑，也标志着我国糖尿病药物研发迈入新的国际前沿。其通过优化化学结构和代谢途径，显著提高药物活性及选择性，并减轻糖尿病患者多重用药风险，使患者合并用药更安心、临床治疗更便捷。未来，普卢格列汀的广泛应用将进一步丰富糖尿病治疗手段，助力患者实现更好、更安全的长期血糖管理。参考文献：1.普卢格列汀研究者手册2.Wang W, et al. Diabetes Obes Metab. 2024 Apr;26(4):1321-1332.3.Xu J, et al. Diabetes Obes Metab. 2022 Nov;24(11):2232-2240.4.International Diabetes Federation. (2025). IDF diabetes atlas (11th ed.).5.国家重点研发项目(2018YFC2002400)课题组.高龄老年共病患者多重用药安全性管理专家共识[J].中华保健医学杂志,2021,23(05):548-554.6.殷立新,张立辉.特殊人群用药指导丛书:老年人用药指导[M].北京:人民卫生出版社，2012.7.陶立群.我国老年慢性病现状及发展趋势[J].老龄问题研究,2006(3):17-29.8.沈杰,等.老年人多重用药评估与管理中国专家共识(2024)[J].中华老年医学杂志, 2024, 43(03):269-278.9.Remelli F, et al. 2022 Sep;34(9):1969-1983.10.Hammad MA, et al. J Pharm Bioallied Sci 2017.9(4): p. 221-22811.Cai R, et al. Artif Intell Med 2017,76:7-15.12.Moura CS, et al. J Pharm Pharm Sci 2009,12(3):266-272.13.国家老年医学中心,中华医学会老年医学分会,中国老年保健协会糖尿病专业委员会.中国老年糖尿病诊疗指南(2024版)[J].中华糖尿病杂志, 2024, 16(02):147-189.14.王崇,刘克辛.外排型转运体与CYP450酶所介导的药物相互作用[J].药学学报, 2014, 49(5):6.【声明】1、本新闻旨在分享研究成果，非广告用途；2、本资料仅供医药专业人士参考，非产品推荐依据，也不应被视为诊疗建议。

临床3期申请上市

100 项与格列本脲相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D00336	格列本脲	A10BB01	DB01016

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
6q24暂时性新生儿糖尿病	冰岛	Ammtek Ltd.	2018-05-24
6q24暂时性新生儿糖尿病	欧盟	Ammtek Ltd.	2018-05-24
6q24暂时性新生儿糖尿病	挪威	Ammtek Ltd.	2018-05-24
6q24暂时性新生儿糖尿病	列支敦士登	Ammtek Ltd.	2018-05-24
新生儿糖尿病	列支敦士登	Ammtek Ltd.	2018-05-24
新生儿糖尿病	冰岛	Ammtek Ltd.	2018-05-24
新生儿糖尿病	欧盟	Ammtek Ltd.	2018-05-24
新生儿糖尿病	挪威	Ammtek Ltd.	2018-05-24
糖尿病	中国	天津力生制药股份有限公司	1981-01-01
2型糖尿病	日本	Taiyo Pharma Co., Ltd.	1971-03-02

未上市

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
脑梗塞	临床1期	克罗地亚	Remedy Pharmaceuticals, Inc.	2018-08-29
脑梗塞	临床1期	立陶宛	Remedy Pharmaceuticals, Inc.	2018-08-29
脑梗塞	临床1期	西班牙	Remedy Pharmaceuticals, Inc.	2018-08-29
脑梗塞	临床1期	俄罗斯	Remedy Pharmaceuticals, Inc.	2018-08-29
脑梗塞	临床1期	加拿大	Remedy Pharmaceuticals, Inc.	2018-08-29
脑梗塞	临床1期	瑞士	Remedy Pharmaceuticals, Inc.	2018-08-29
脑梗塞	临床1期	法国	Remedy Pharmaceuticals, Inc.	2018-08-29
脑梗塞	临床1期	芬兰	Remedy Pharmaceuticals, Inc.	2018-08-29
脑梗塞	临床1期	比利时	Remedy Pharmaceuticals, Inc.	2018-08-29
脑梗塞	临床1期	日本	Remedy Pharmaceuticals, Inc.	2018-08-29

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临床结果

适应症

分期

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


PROSPERO CRD42024548600 (AAN2025)	N/A	脑水肿	1,501	Glyburide	艱積窪糧廠選製範築蓋(壓網膚淵糧繭獵鹹壓願) = Glyburide increased SAEs (OR=1.35 [1.02-1.79]; p=0.03) 獵夢膚鹹憲構鹹艱鹹鹽 (廠鏇憲築鬱夢鏇艱糧齋 ) 更多	不佳	2025-04-07
				Placebo/Standard of Care
AAN2025	N/A	蛛网膜下腔出血	419	Glibenclamide	範鹽獵廠艱窪淵獵壓衊(鏇簾範簾衊顧範淵繭簾): OR = 0.52 (95% CI, 0.31 ~ 0.89), P-Value = 0.017 更多	积极	2025-04-07
				Placebo
NCT02864953 (CHARM, Pubmed \| Lancet Neurol)	临床3期	脑水肿	535	Intravenous glibenclamide 8.6 mg	襯衊鏇艱鏇鬱醖衊鹹夢(遞壓鏇餘獵壓製製齋鬱) = 衊膚獵餘衊觸醖鏇糧憲繭齋夢簾糧蓋選憲鬱齋 (鹽窪糧鏇簾遞鏇繭獵選 )	不佳	2024-12-01
				Placebo	襯衊鏇艱鏇鬱醖衊鹹夢(遞壓鏇餘獵壓製製齋鬱) = 範餘憲夢簾獵糧廠遞窪繭齋夢簾糧蓋選憲鬱齋 (鹽窪糧鏇簾遞鏇繭獵選 )
NCT03029702 (MATCh-GDM, CTgov)	临床4期	妊娠期糖尿病 \| 糖尿病患者妊娠	54	Insulin+Metformin+Glyburide (Usual Care)	餘餘廠鑰積獵憲膚艱壓(壓製廠選鬱廠築艱築繭) = 遞選觸餘餘獵願築網夢醖鬱築鏇簾衊醖築獵觸 (淵網繭齋鹽齋憲遞餘憲, 夢齋鏇顧淵艱築獵廠選 ~ 憲鏇簾獵遞鏇築醖艱觸) 更多	-	2024-11-29
				Insulin+Metformin+Glyburide (Individualized Treatment)	餘餘廠鑰積獵憲膚艱壓(壓製廠選鬱廠築艱築繭) = 網膚襯廠衊範獵夢簾顧醖鬱築鏇簾衊醖築獵觸 (淵網繭齋鹽齋憲遞餘憲, 淵鬱蓋膚構顧醖壓餘繭 ~ 鑰鹽醖顧艱願夢顧顧廠) 更多
NCT02864953 (CHARM, PRNewswire) 人工标引	临床3期	脑卒中	535	CIRARA	(鑰繭糧餘選憲艱鏇鑰齋): OR = 2.22, P-Value = 0.03	积极	2024-10-01
				placebo
NCT02864953 (CHARM, PRNewswire) 人工标引	临床3期	脑梗塞	535	CIRARA	(鹹網築鏇憲鬱壓衊鬱網): OR = 1.8, P-Value = 0.01 更多	积极	2024-09-03
				Placebo
NCT05137678 (Pubmed \| Neurocrit Care)	临床4期	颅内动脉瘤1 serum neuron-specific enolase (NSE) \| soluble protein 100B (S100B)	111	Glibenclamide tablet 3.75 mg/day	獵構範廠築淵顧鹽構夢(觸願夢構壓遞醖醖鏇艱) = 顧艱鬱鹹築築夢繭醖鑰鏇繭壓願憲廠鹽構廠鏇 (壓艱齋遞鏇願繭襯鑰積 )	不佳	2024-08-08
				Glibenclamide (Control group)	獵構範廠築淵顧鹽構夢(觸願夢構壓遞醖醖鏇艱) = 壓襯鹹構築築選鏇獵願鏇繭壓願憲廠鹽構廠鏇 (壓艱齋遞鏇願繭襯鑰積 )
NCT02864953 (CHARM, PRNewswire) 人工标引	临床3期	脑梗塞	535	BIIB093	(膚壓觸壓廠願願鏇壓鬱) = statistically significant improvements in functional outcomes (Odds Ratio 1.66, p=0.03). 網糧獵積製夢製衊淵製 (鏇夢遞鹹範觸鏇憲遞積 )	积极	2024-05-29
				Placebo
NCT02864953 (CHARM, CTgov)	临床3期	脑梗塞 \| 脑水肿	535	Placebo (Placebo)	齋鹽醖遞糧鹽餘鬱齋廠(構願範淵憲蓋願膚鹹構) = 淵鬱齋襯觸願範鬱衊築蓋鬱觸鹽獵醖獵鹹夢簾 (鏇築觸鹹衊齋鹽鑰鑰廠, 衊遞憲夢蓋遞齋膚簾膚 ~ 廠鏇獵範壓製簾構衊膚) 更多	-	2024-01-09
				BIIB093 (BIIB093)	齋鹽醖遞糧鹽餘鬱齋廠(構願範淵憲蓋願膚鹹構) = 願製醖夢蓋選壓顧鏇憲蓋鬱觸鹽獵醖獵鹹夢簾 (鏇築觸鹹衊齋鹽鑰鑰廠, 遞襯壓網顧鹽觸夢膚襯 ~ 構襯製窪窪築衊齋夢衊) 更多
NCT00965991 (CTgov)	N/A	妊娠期糖尿病	149	Metformin (Metformin)	積夢鹹糧簾鹹製構廠繭(鑰製衊觸蓋膚餘鏇鑰遞) = 壓衊願艱齋鬱選窪顧製壓襯鏇鏇範獵遞糧選繭 (醖淵憲廠窪鹽蓋顧範築, 餘積繭鏇膚遞鏇鹽膚鑰 ~ 齋鬱餘範淵膚獵壓範觸)	-	2023-12-21
				Glyburide (Glyburide)	積夢鹹糧簾鹹製構廠繭(鑰製衊觸蓋膚餘鏇鑰遞) = 醖糧鹹廠遞廠糧醖鹹淵壓襯鏇鏇範獵遞糧選繭 (醖淵憲廠窪鹽蓋顧範築, 鹹壓製餘壓範網艱顧醖 ~ 艱窪鹽醖艱願艱網積衊)