Cotadutide(Cotadutide) - 药物靶点：GCGR x GLP-1R_专利_临床

概要

基本信息

药物类型

合成多肽

别名

Cotadutide (USAN)、MEDI 0382、MEDI-0382

靶点

GCGR x GLP-1R

作用方式

激动剂

作用机制

GCGR激动剂(胰高血糖素受体激动剂)、GLP-1R激动剂(胰高血糖素样肽-1激动剂)

治疗领域

消化系统疾病其他疾病内分泌与代谢疾病

在研适应症-

非在研适应症

2型糖尿病肝纤维化代谢功能障碍相关脂肪性肝炎+ [2]

原研机构

MedImmune LLC

在研机构-

非在研机构

AstraZeneca AB

AstraZeneca PLC

MedImmune LLC

+ [1]

权益机构-

最高研发阶段终止临床2/3期

首次获批日期-

最高研发阶段(中国)终止

特殊审评-

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结构/序列

分子式C167H252N42O55

InChIKeyYEKUUBPJRPXMBM-PTCFZACGSA-N

CAS号1686108-82-6

Sequence Code 9614849

来源: *****

关联

24

项与 Cotadutide 相关的临床试验

NCT05668936

/ Terminated临床1期

A Thorough QTc Evaluation of the Effect of Cotadutide on Cardiac Repolarization in Healthy Participants: A Randomized, Double-blind, Placebo-controlled, 3-arm Parallel Study With a Nested Crossover Design for Positive Control With Moxifloxacin Administration

This study will investigate the effect of multiple doses of cotadutide on the cardiac activity (QTc interval) of healthy participants.

开始日期2023-01-03

申办/合作机构

AstraZeneca PLC

NCT05517226

/ Terminated临床1期

A Phase I, Parallel-group, Multi-center, Open-label, Investigation of the Pharmacokinetics, Safety and Tolerability of a Single Subcutaneous Injection of Cotadutide in Participants With Mild, Moderate or Severe Hepatic Impairment Compared to Participants With Normal Hepatic Function

This study will assess the pharmacokinetics (PK), safety, and tolerability of a single subcutaneous injection of cotadutide in participants with mild, moderate or severe hepatic impairment compared to participants with normal hepatic function.

开始日期2022-09-06

申办/合作机构

AstraZeneca PLC

[+1]

NCT05364931

/ Completed临床2期

A Phase II Randomized, Double-blind, Placebo-controlled, Proof-of-Concept Study to Evaluate the Safety and Efficacy of Cotadutide in Participants With Non-cirrhotic Non-alcoholic Steatohepatitis With Fibrosis

The purpose of this study is to evaluate the safety and efficacy of cotadutide in participants with non-cirrhotic NASH with fibrosis.

开始日期2022-07-14

申办/合作机构

AstraZeneca PLC

100 项与 Cotadutide 相关的临床结果

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100 项与 Cotadutide 相关的转化医学

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100 项与 Cotadutide 相关的专利（医药）

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51

项与 Cotadutide 相关的文献（医药）

2026-06-01·DIABETES OBESITY & METABOLISM

Relative Efficacy of Next‐Generation Incretin Therapies for Cardio‐Renal Protection in Type 2 Diabetes: Evidence From a Network Meta‐Analysis

Review

作者: Pham, Thanh‐Huong ; Le, Thi‐Thuy‐Duong ; Nguyen, The‐Anh ; Ha, Hai‐Anh ; Tran, Thanh‐Thien ; Dao, Tien‐Phat ; Ngo, Ngoc‐Phuoc ; Huynh, Dang‐Mai‐Linh ; Vo, Thi‐Minh‐Nhat ; Pham, Thi‐Phuong‐Thao

ABSTRACT:

Background:

Type 2 diabetes (T2D) management has shifted towards integrated cardiometabolic and renal risk reduction. Although glucagon‐like peptide‐1 receptor agonists (GLP‐1RAs) and newer dual agonists show promising benefits, comparative evidence across agents and outcomes remains limited.

Objectives:

To compare the cardiovascular and renal effects of modern GLP‐1RAs (dulaglutide, semaglutide, lixisenatide), tirzepatide and cotadutide in high‐risk T2D populations, and to explore multivariate relationships among clinical outcomes.

Methods:

A systematic review and network meta‐analysis was conducted following PRISMA and Cochrane guidance (PROSPERO: CRD42024592825). Randomised controlled trials published between 2014 and 2025 with ≥ 6 months follow‐up were included. Outcomes were cardiovascular death, myocardial infarction (MI), stroke, total major adverse cardiovascular events (MACE), eGFR and UACR. Random‐ and common‐effects models were applied using netmeta (R). Treatment rankings were estimated using p ‐scores. Inconsistency, heterogeneity and small‐study effects were evaluated. Correlation networks and principal component analysis (PCA) were performed to characterise interrelationships among clinical variables.

Results:

Thirty‐four trials were included, predominantly multinational CVOTs and CKD‐focused studies. Semaglutide regimens showed the most consistent reduction in MACE and MI versus placebo, with the strongest effect observed for semaglutide combined with SGLT2 inhibition. Dulaglutide 1.5 mg and tirzepatide 15 mg significantly reduced stroke risk. Cardiovascular death estimates were largely imprecise with evidence of small‐study effects. Renal effects differed by endpoint: eGFR changes were generally modest, whereas UACR showed marked reductions, particularly with dulaglutide plus dapagliflozin, DPP‐4 inhibitors and semaglutide 1 mg. PCA confirmed strong cardiometabolic‐renal interdependence.

Conclusions:

Cardiovascular and renal benefits of GLP‐1‐based therapies are outcome‐specific. Semaglutide favoured MACE/MI reduction, dulaglutide and tirzepatide supported stroke prevention, and albuminuria outcomes were more responsive than eGFR. Further long‐term head‐to‐head trials are needed.

2026-04-01·CLINICAL PHARMACOKINETICS

Systemic Pharmacokinetic Principles of Therapeutic Peptides

Article

作者: Gennemark, Peter ; Nordell, Pär ; Jansson-Löfmark, Rasmus

INTRODUCTION:

Peptide-based therapeutics represent a rapidly expanding class of drugs. Endogenous peptides typically exhibit short elimination half-lives due to proteolytic cleavage and renal filtration. However, modifications such as amino acid substitutions and fatty-acid conjugation can significantly prolong their half-lives, enabling, for example, once weekly dosing. This study revisits the systemic pharmacokinetics of peptide drugs using classical pharmacokinetic principles and elucidates the scaling of peptide pharmacokinetics across species.

METHODS:

Preclinical and clinical pharmacokinetic data were collected from published literature and AstraZeneca internal sources, covering four unconjugated peptides (teduglutide, apraglutide, pramlintide, and exenatide) and five fatty-acid conjugated peptides (tirzepatide, cotadutide, liraglutide, semaglutide and pemvidutide). Algebraic equations for clearance, volume of distribution, and plasma half-life were derived.

RESULTS:

Theoretical predictions from these models were broadly consistent with collected data; however, there was a tendency to overpredict the volume of distribution. Furthermore, for each peptide drug, these pharmacokinetic parameters were well described by inter-species allometric relationships. The allometric exponents for apparent clearance ranged from 0.58 to 0.88 (geometric mean: 0.72; n = 9; R² ≥ 0.93), while those for apparent volume of distribution ranged from 0.89 to 1.1 (geometric mean: 0.98; n = 8; R² ≥ 0.88). Notably, there were no differences in scaling exponents between unconjugated and fatty-acid conjugated peptides.

CONCLUSION:

In summary, our results underscore that the systemic pharmacokinetics of peptide drugs generally follow size-related physiological scaling patterns and provide quantitative tools to facilitate translational assessments in the drug discovery process.

2026-04-01·Diabetes Therapy

Renal Outcomes of GLP-1 Receptor Agonists and Tirzepatide Across CKD Stages and Metabolic Phenotypes (Type 2 Diabetes and/or Overweight/Obesity): A Scoping Review

Review

作者: Rico-Fontalvo, Jorge ; Lorca-Herrera, Eduardo ; Sánchez-Polo, Vicente ; Builes-Montaño, Carlos E ; Elbert, Alicia ; de Moraes, Thyago Proença ; Daza-Arnedo, Rodrigo ; Dina-Batlle, Eliana ; Correa-Rotter, Ricardo

INTRODUCTION:

Diabetes mellitus is the leading global cause of chronic kidney disease (CKD) and end-stage renal disease. Although cardiovascular outcomes have improved substantially, renal risk remains high. Glucagon-like peptide 1 (GLP-1) receptor agonists and the dual GLP-1/GIP agonist tirzepatide have demonstrated potential cardiorenal benefits, but renal evidence has not been systematically mapped across CKD stages and metabolic phenotypes. This scoping review aimed to identify and describe clinical evidence on renal outcomes associated with GLP-1-based therapies in adults with type 2 diabetes and/or overweight/obesity, with or without CKD.

METHODS:

Following the Joanna Briggs Institute framework and PRISMA-ScR guidelines (protocol: OSF.IO/SZ87J), we searched PubMed, Embase, and CENTRAL from inception to October 2025. Eligible studies included phase 2-4 randomized controlled trials (RCTs), post hoc RCT analyses, and comparative observational studies reporting kidney outcomes. Data were charted using a structured extraction form with AI-assisted screening and manual validation. Risk of bias and certainty were appraised using RoB 2, ROBINS-I, and GRADE frameworks.

RESULTS:

Of 607 records identified, 35 studies met inclusion criteria. Randomized evidence supports renal benefits for semaglutide, dulaglutide, and liraglutide, including reductions in composite kidney outcomes and slower eGFR decline. Tirzepatide demonstrated consistent albuminuria reductions and attenuation of eGFR decline compared with insulin glargine. Efpeglenatide, cotadutide, exenatide, and lixisenatide showed class-consistent antiproteinuric effects. Observational data extended findings to real-world and advanced CKD populations. Across agents, renal benefits were partly independent of glycemic and weight effects.

CONCLUSION:

GLP-1-based therapies demonstrate consistent renoprotective signals across CKD stages and metabolic phenotypes, particularly in type 2 diabetes. Evidence is strongest for semaglutide and dulaglutide, with emerging data for tirzepatide and other incretin-based agents. These findings provide a structured evidence map to inform future consensus and clinical decision-making.

81

项与 Cotadutide 相关的新闻（医药）

2026-09-02

·简书

模生物为该研究提供了Xiap-KO和Ascl2flox/flox; villin-cre小鼠

胰高血糖素样肽-1 受体（glucagon-like peptide-1 receptor，GLP-1R）与胰高血糖素受体（glucagon receptor，GCGR）是能量代谢调控中的两个重要靶点。近年来，同时激动 GLP-1R 与 GCGR 的双靶点候选药物（如 Cotadutide）在减重、改善血糖与肝脏代谢方面受到关注。这类候选药物针对的是人源靶点，在普通小鼠体内因种属差异难以有效评价其活性，需要在表达人源靶点的人源化小鼠上进行体内药效验证，人源化小鼠模型已成为这类双靶点药物研发中常用的小鼠模型。该品系由hGCGR 人源化小鼠与 hGLP1R 人源化小鼠杂交获得，在两个基因位点上同时表达人源 GCGR 与人源 GLP-1R。 Fig.1 Body weight change of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.2 Food intakechange of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide Fig.3 Fat mass and lean mass changes of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide Fig.4 Liver triglyceride and cholesterol content of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.5 Blood glucose levels of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.6 Serum insulin levels of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.7 White adipose tissue weight of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.8 Brown adipose tissue weight of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.9 Muscle weights of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.10 Oxygen consumption of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.11 Carbon dioxide production of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.12 Respiratory exchange ratio of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.13 Heat production of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. 官网产品页以Cotadutide 为工具药物，在高脂饮食诱导的肥胖模型上验证了该品系的体内药效响应。结果显示，Cotadutide 处理可显著降低肥胖小鼠的体重（图1）与摄食量（图2）；在身体组成方面，脂肪与瘦体重均出现下降，而瘦体重占体重的比例有所升高（图3）。肝脏指标方面，肝脏总胆固醇显著下降，肝脏甘油三酯在各组间无显著差异（图4）。代谢指标方面，Cotadutide 处理可显著降低血糖并改善糖耐量（图5），同时降低血清胰岛素水平（图6）。脂肪组织方面，附睾、腹股沟与肠系膜白色脂肪组织的重量均降低（图7），棕色脂肪组织重量亦降低（图8）；而胫骨前肌与腓肠肌的重量占体重比例则有所升高（图9）。能量代谢方面，Cotadutide 处理可显著升高耗氧量（图10）、二氧化碳产生量（图11）、呼吸交换率（图12）与产热（图13）。上述数据表明，该品系能够对同时作用于GLP-1R 与 GCGR 的候选药物产生相应的体内药效响应，可用于此类双靶点候选药物的减重、血糖与代谢改善效果的体内评价。

2026-09-02

·搜狐新闻

hGCGR/hGLP1R人源化小鼠-Cotadutide肥胖模型药效验证-减重降糖双靶点评价

胰高血糖素样肽-1 受体（glucagon-like peptide-1 receptor，GLP-1R）与胰高血糖素受体（glucagon receptor，GCGR）是能量代谢调控中的两个重要靶点。近年来，同时激动 GLP-1R 与 GCGR 的双靶点候选药物（如 Cotadutide）在减重、改善血糖与肝脏代谢方面受到关注。这类候选药物针对的是人源靶点，在普通小鼠体内因种属差异难以有效评价其活性，需要在表达人源靶点的人源化小鼠上进行体内药效验证，人源化小鼠模型已成为这类双靶点药物研发中常用的小鼠模型。该品系由hGCGR 人源化小鼠与 hGLP1R 人源化小鼠杂交获得，在两个基因位点上同时表达人源 GCGR 与人源 GLP-1R。 Fig.1 Body weight change of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.2 Food intakechange of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide Fig.3 Fat mass and lean mass changes of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide Fig.4 Liver triglyceride and cholesterol content of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.5 Blood glucose levels of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.6 Serum insulin levels of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.7 White adipose tissue weight of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.8 Brown adipose tissue weight of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.9 Muscle weights of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.10 Oxygen consumption of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.11 Carbon dioxide production of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.12 Respiratory exchange ratio of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. Fig.13 Heat production of HFD-induced hGCGR/hGLP1R obese mice treated with Cotadutide. 官网产品页以Cotadutide 为工具药物，在高脂饮食诱导的肥胖模型上验证了该品系的体内药效响应。结果显示，Cotadutide 处理可显著降低肥胖小鼠的体重（图1）与摄食量（图2）；在身体组成方面，脂肪与瘦体重均出现下降，而瘦体重占体重的比例有所升高（图3）。肝脏指标方面，肝脏总胆固醇显著下降，肝脏甘油三酯在各组间无显著差异（图4）。代谢指标方面，Cotadutide 处理可显著降低血糖并改善糖耐量（图5），同时降低血清胰岛素水平（图6）。脂肪组织方面，附睾、腹股沟与肠系膜白色脂肪组织的重量均降低（图7），棕色脂肪组织重量亦降低（图8）；而胫骨前肌与腓肠肌的重量占体重比例则有所升高（图9）。能量代谢方面，Cotadutide 处理可显著升高耗氧量（图10）、二氧化碳产生量（图11）、呼吸交换率（图12）与产热（图13）。上述数据表明，该品系能够对同时作用于GLP-1R 与 GCGR 的候选药物产生相应的体内药效响应，可用于此类双靶点候选药物的减重、血糖与代谢改善效果的体内评价。返回搜狐，查看更多

2026-09-01

·今日头条

陆军军医大学郑宏庭、郑怡、瞿华Science Advances！新发现：不止 GLP‑1，GCGR 可调控溶酶体功能，干预糖尿病肾病肾小管损伤

慢性肾脏病已经成为全球公共卫生重大难题，糖尿病是诱发该类疾病最主要的危险因素。相关统计显示，约三分之一至四成糖尿病患者最终会进展为慢性肾脏病，自1990到2017年，由2型糖尿病引发的肾病新增病例涨幅达到74%，疾病带来的社会负担持续加重。现有干预手段虽能够改善蛋白尿表现，延缓肾小球滤过率下降速度，但人群层面终末期肾病的发病态势并未得到有效遏制，美国公开数据显示2002‑2022年间终末期肾病新增病例数上涨超三成。当前双重GLP‑1R/GCGR激动剂在临床试验中展现出肾脏保护效果，mazdutide、cotadutide两类药物可降低患者尿白蛋白肌酐比值，科研界由此推测GCGR激活参与肾脏获益过程。但肾小管GCGR信号能否直接保护肾脏、具体分子通路尚不清晰，同时肾小管区域磷脂代谢紊乱介导的脂毒性损伤逐渐被学界重视，溶酶体磷脂沉积是肾病损伤的标志性现象，调控该稳态的上游信号有待进一步挖掘。在这项研究中，研究人员依托肾小管特异性GCGR敲除与过表达小鼠模型，结合人源肾脏临床样本开展系列实验，探究GCGR在糖尿病肾病中的生物学作用。实验观察到，糖尿病肾病状态下人和小鼠肾脏的肾小管GCGR表达水平下降，该现象和肾功能恶化、肾脏组织损伤程度存在相关性；将小鼠肾小管GCGR基因敲除后，糖尿病肾病病理改变明显加重，同时细胞内部体积增大的溶酶体出现磷脂大量蓄积。团队进一步解析分子机制，GCGR能够结合V‑ATPase复合物的V1A亚基ATP6V1A，当GCGR缺失时二者相互作用被破坏，V1‑V0亚单位组装受阻，直接造成溶酶体酸化功能缺陷。溶酶体酸化不足会抑制磷脂水解过程，阻碍蛋白酶成熟，阻断细胞自噬流程，最终诱发肾小管上皮细胞损伤。动物回补实验证实，体内上调ATP6V1A可以逆转GCGR缺失带来的溶酶体异常，减缓肾病进展；借助AAV9载体重新恢复肾小管GCGR表达，也可以修复溶酶体功能，减少磷脂堆积，减轻肾脏病理损伤。该研究通过多组遗传学证据，证实肾小管GCGR具备直接的肾脏保护能力，完整勾勒出GCGR‑ATP6V1A‑溶酶体这一全新的肾小管保护信号轴，对既往双重受体激动剂肾脏保护效应的观察做出机制层面补充。过往研究大多聚焦GLP‑1通路的肾脏获益，本成果提示GCGR本身即可作用于肾小管，依靠调控溶酶体装配、维持磷脂稳态来对抗脂毒性损伤，拓展了糖尿病肾病的病理理解角度。从转化意义来看，该通路为糖尿病肾病提供潜在干预靶点，说明除现有肾小球靶向策略外，修复肾小管溶酶体功能可以作为疾病防控思路。不过本研究主要基于动物模型与人组织样本开展，药物开发、靶点临床转化仍需要更多研究验证。该成果也解释了双重GLP‑1R/GCGR激动剂的肾脏获益可能部分来自GCGR本身对肾小管的调控，为后续肾病药物研发、临床用药评估提供新的理论参考。仅作科研人员学术交流。本文内容若存在版权问题，请联系我们及时处理。

100 项与 Cotadutide 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11304	Cotadutide	-	DB15194

研发状态

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
肝纤维化	临床3期	美国	AstraZeneca AB	2022-07-12
肝纤维化	临床3期	日本	AstraZeneca AB	2022-07-12
肝纤维化	临床3期	阿根廷	AstraZeneca AB	2022-07-12
肝纤维化	临床3期	澳大利亚	AstraZeneca AB	2022-07-12
肝纤维化	临床3期	奥地利	AstraZeneca AB	2022-07-12
肝纤维化	临床3期	巴西	AstraZeneca AB	2022-07-12
肝纤维化	临床3期	加拿大	AstraZeneca AB	2022-07-12
肝纤维化	临床3期	哥伦比亚	AstraZeneca AB	2022-07-12
肝纤维化	临床3期	法国	AstraZeneca AB	2022-07-12
肝纤维化	临床3期	德国	AstraZeneca AB	2022-07-12

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临床结果

适应症

分期

评价

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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


NCT05364931 (PROXYMO-ADV, CTgov)	临床2期	代谢功能障碍相关脂肪性肝炎	54	Cotadutide (Cotadutide 300 ug)	獵襯鬱膚淵齋憲鏇鑰蓋 = 艱鏇構夢簾選鑰衊簾襯鬱觸願鏇簾膚廠築衊膚 (選襯願壓壓膚鹹艱憲蓋, 繭襯鹽願糧選鏇鹹築繭 ~ 積夢簾繭顧繭積顧衊鑰) 更多	-	2025-09-03
				Cotadutide (Cotadutide 600 ug)	獵襯鬱膚淵齋憲鏇鑰蓋 = 艱襯範鹽繭艱糧願鹽範鬱觸願鏇簾膚廠築衊膚 (選襯願壓壓膚鹹艱憲蓋, 選衊餘鑰築膚鹹鬱壓構 ~ 糧艱廠鹽憲簾醖齋選壓) 更多
NCT04515849 (CTgov)	临床2期	2型糖尿病	248	Cotadutide (Cotadutide 100 ug)	鏇網製積鬱願獵積壓遞(夢獵網構鬱選鹹繭膚網) = 壓淵獵膚遞醖構鑰範願壓鏇顧窪醖醖願鏇淵獵 (鏇繭糧艱夢齋鹽選蓋鹽, 鹹製衊衊簾壓襯網顧衊 ~ 餘獵襯遞餘選鬱範製襯) 更多	-	2025-01-17
				Cotadutide (Cotadutide 300 µg)	鏇網製積鬱願獵積壓遞(夢獵網構鬱選鹹繭膚網) = 壓積願艱顧遞築齋鑰夢壓鏇顧窪醖醖願鏇淵獵 (鏇繭糧艱夢齋鹽選蓋鹽, 鬱選膚網糧糧齋鏇簾築 ~ 襯觸壓獵築遞糧鑰襯鹹) 更多
NCT04515849 (Pubmed) 人工标引	临床2期	2型糖尿病 \| 糖尿病肾病	248	CotadutideCotadutide 300 μg	獵築淵鏇醖齋鏇廠觸築(廠膚壓憲餘範選選窪夢) = 範簾獵窪膚壓醖蓋觸膚壓鹹憲鹽壓鬱積憲鑰願 (鬱積襯餘壓膚窪製艱齋 )	积极	2025-01-13
				Cotadutide 600 μg	獵築淵鏇醖齋鏇廠觸築(廠膚壓憲餘範選選窪夢) = 範簾鹽構顧淵鹽獵製鬱壓鹹憲鹽壓鬱積憲鑰願 (鬱積襯餘壓膚窪製艱齋 )
phase 2b trial (Pubmed \| Kidney Int)	临床2期	糖尿病肾病 type 2 diabetes \| chronic kidney disease	248	Cotadutide 300 μg	獵憲選選餘網襯淵醖窪(製鹽膚獵簾齋膚簾廠構) = 壓築窪餘廠鬱廠艱簾積積糧醖構簾艱築鏇繭網 (廠壓觸膚廠淵積夢淵蓋, -54.7 ~ -30.6)	积极	2024-12-01
				Cotadutide 600 μg	獵憲選選餘網襯淵醖窪(製鹽膚獵簾齋膚簾廠構) = 壓鹽艱繭鏇壓襯憲簾糧積糧醖構簾艱築鏇繭網 (廠壓觸膚廠淵積夢淵蓋, -59.3 ~ -38.4)
NCT03555994 (CTgov)	临床2期	2型糖尿病 \| 肥胖	51	Placebo (Placebo (Part A))	壓壓簾觸襯糧遞鑰積簾(構鹽醖醖鬱夢鑰糧齋壓) = 夢齋窪範窪壓蓋遞醖壓鏇膚鑰獵糧糧夢構鑰壓 (構獵廠積鹹鬱鹽遞構構, 糧築簾繭鑰鬱齋糧襯繭 ~ 獵簾鬱壓糧鬱窪簾艱齋) 更多	-	2024-11-12
				MEDI0382 (MEDI0382 (Part A))	壓壓簾觸襯糧遞鑰積簾(構鹽醖醖鬱夢鑰糧齋壓) = 範齋遞餘襯構壓顧觸壓鏇膚鑰獵糧糧夢構鑰壓 (構獵廠積鹹鬱鹽遞構構, 繭選衊獵積選鏇艱鹽淵 ~ 製願糧醖鹹壓繭夢鹽衊) 更多
NCT03596177 (Pubmed \| Diabetes Obes Metab)	临床2期	2型糖尿病	24	cotadutide (Type 2 diabetes + Obesity)	鹹築齋願鑰網鏇繭網繭(觸衊夢願範淵醖廠壓襯): P-Value = 0.011 更多	积极	2024-07-01
				Placebo (Type 2 diabetes + Obesity)
NCT04019561 (PROXYMO, Pubmed) 人工标引	临床2期	代谢功能障碍相关脂肪性肝炎 \| 代谢功能障碍相关的脂肪肝病	74	Cotadutide 600 μg	獵鑰憲獵遞窪簾願積鏇(襯窪餘衊獵獵範鹽鹽糧) = 襯衊鬱範鹹鏇廠襯構遞淵遞願齋餘鬱範膚鹽遞 (憲窪窪蓋餘網鏇襯鏇衊 ) 更多	积极	2024-05-09
				Cotadutide 300 μg	廠憲獵鑰衊遞繭鏇壓憲(鏇網醖繭憲衊網積窪願) = 窪網衊壓鹹餘鏇範鏇顧糧繭餘憲餘構鹹遞鏇淵 (繭遞襯鏇膚構醖夢淵夢 ) 更多
NCT04515849 (EASD2023)	临床2期	糖尿病肾病	-	Cotadutide 100 µg	壓餘網網選獵製憲積壓(簾獵鏇廠繭範簾顧夢願) = 窪鏇膚蓋蓋簾遞襯繭窪網齋鬱齋網蓋糧選蓋鏇 (簾廠製糧願鏇齋範獵鹹, -52.5 ~ -23.9) 更多	积极	2023-10-03
				Cotadutide 300 µg	獵製製壓膚鑰鏇觸鬱獵(憲鬱構膚繭積築鬱廠夢) = 淵築鹹觸壓艱繭襯顧獵鬱製鑰鏇鑰廠選蓋夢顧 (糧憲艱膚獵窪蓋製鬱壓 ) 更多
NAASO2022	临床2期	肥胖	18	Cotadutide	夢壓鹹艱鹹夢獵構艱遞(繭鹽願蓋觸範膚膚構顧) = 夢構簾選製淵繭餘窪簾壓鏇襯蓋網顧餘醖廠範 (簾範艱積艱鏇鏇艱鏇齋 ) 更多	-	2022-11-21
				Placebo	夢壓鹹艱鹹夢獵構艱遞(繭鹽願蓋觸範膚膚構顧) = 鹽築遞製淵製願範壓淵壓鏇襯蓋網顧餘醖廠範 (簾範艱積艱鏇鏇艱鏇齋 ) 更多