The investigators recently demonstrated that blockade of Glucagon-Like Peptide-1's (GLP-1) receptor (GLP1R) results in changes in islet function without changes in circulating GLP-1. These effects are more pronounced in people with early type 2 diabetes (T2DM) in keeping with increased expression of PC-1/3 and GLP-1 that is observed in diabetic islets. However, its regulation is at present unknown. Common genetic variation in the TCF7L2 locus (T-allele at rs7903146) arguably confers the greatest genetic risk of T2DM. It is associated with α- and β-cell dysfunction. TCF7L2 (the product of TCF7L2) was first described as the transcription factor necessary for proglucagon expression in intestinal L-cells (which secrete GLP-1). This led to speculation that TCF7L2 confers risk of diabetes via changes in circulating GLP-1. This has turned out to not be the case. This raises the possibility that these diabetogenic effects are mediated via an inability of islet GLP-1 to adapt to rising glycemia. Therefore, this experiment will determine the contribution of islet GLP-1 to the functional abnormalities of the islet associated with the TCF7L2 locus.

开始日期2026-10-01

申办/合作机构

Mayo Clinic

NCT07373236

/ RecruitingN/AIIT

Examining the Effect of Endogenous Glucagon-like Peptide-1 on Glucagon Secretion in Type 1 Diabetes

Type 1 diabetes is a serious and burdensome disease that carries the risk of severe complications and premature death, partly due to low blood sugar, also called hypoglycaemia. This is a constant threat, as individuals with type 1 diabetes lack the body's natural safeguard against low blood sugar: the hormone glucagon, which is normally released from the pancreas.
Recent research in mice suggests that this missing safeguard may be due to an imbalance in the hormones released from different cells in the pancreas. More specifically, glucagon-like peptide-1 (GLP-1) appears to play a role in the lack of glucagon secretion. By blocking this hormone using the substance exendin(9-39)NH₂, normalization of glucagon release during low blood sugar has been observed in mice with type 1 diabetes.
The present study aims to investigate whether the same mechanism applies in humans with type 1 diabetes. If confirmed, this finding could form the basis for a novel adjunct treatment to insulin therapy and thereby potentially reduce the risk of hypoglycaemia in this patient group.

开始日期2026-01-23

申办/合作机构-

NCT06967558

/ Recruiting临床2期IIT

The Role of Islet GLP-1 in the Pathogenesis of Prediabetes

We recently demonstrated that blockade of Glucagon-Like Peptide-1's (GLP-1) receptor (GLP1R) results in changes in islet function without changes in circulating GLP-1. These effects are more pronounced in people with early type 2 diabetes (T2DM) in keeping with increased expression of PC-1/3 and GLP-1 that is observed in diabetic islets. However, its regulation is at present unknown. At present it is unknown if these abnormalities develop in prediabetes and whether they contribute to the phenotypes observed. In this experiment we will use blockade of GLP1R to probe the contribution of endogenous GLP-1 secretion to the regulation of fasting glucose and islet function in prediabetes.

开始日期2025-11-01

申办/合作机构

Mayo Clinic

100 项与 Avexitide 相关的临床结果

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100 项与 Avexitide 相关的转化医学

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100 项与 Avexitide 相关的专利（医药）

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项与 Avexitide 相关的文献（医药）

2026-02-01·Neural Regeneration Research

Topical administration of GLP-1 eyedrops improves retinal ganglion cell function by facilitating presynaptic GABA release in early experimental diabetes

Article

作者: Zhang, Ti-Hui ; Weng, Shi-Jun ; Wang, Lu ; Wang, Yong-Chen ; Ruan, Hang-Ze ; Shao, Yu-Qi ; Zhong, Yong-Mei ; Liu, Yun-Feng ; Yang, Xiong-Li

JOURNAL/nrgr/04.03/01300535-202602000-00048/figure1/v/2025-05-17T081902Z/r/image-tiff Diabetic retinopathy is a prominent cause of blindness in adults, with early retinal ganglion cell loss contributing to visual dysfunction or blindness. In the brain, defects in γ-aminobutyric acid synaptic transmission are associated with pathophysiological and neurodegenerative disorders, whereas glucagon-like peptide-1 has demonstrated neuroprotective effects. However, it is not yet clear whether diabetes causes alterations in inhibitory input to retinal ganglion cells and whether and how glucagon-like peptide-1 protects against neurodegeneration in the diabetic retina through regulating inhibitory synaptic transmission to retinal ganglion cells. In the present study, we used the patch-clamp technique to record γ-aminobutyric acid subtype A receptor–mediated miniature inhibitory postsynaptic currents in retinal ganglion cells from streptozotocin-induced diabetes model rats. We found that early diabetes (4 weeks of hyperglycemia) decreased the frequency of GABAergic miniature inhibitory postsynaptic currents in retinal ganglion cells without altering their amplitude, suggesting a reduction in the spontaneous release of γ-aminobutyric acid to retinal ganglion cells. Topical administration of glucagon-like peptide-1 eyedrops over a period of 2 weeks effectively countered the hyperglycemia-induced downregulation of GABAergic mIPSC frequency, subsequently enhancing the survival of retinal ganglion cells. Concurrently, the protective effects of glucagon-like peptide-1 on retinal ganglion cells in diabetic rats were eliminated by topical administration of exendin-9-39, a specific glucagon-like peptide-1 receptor antagonist, or SR95531, a specific antagonist of the γ-aminobutyric acid subtype A receptor. Furthermore, extracellular perfusion of glucagon-like peptide-1 was found to elevate the frequencies of GABAergic miniature inhibitory postsynaptic currents in both ON- and OFF-type retinal ganglion cells. This elevation was shown to be mediated by activation of the phosphatidylinositol-phospholipase C/inositol 1,4,5-trisphosphate receptor/Ca2+/protein kinase C signaling pathway downstream of glucagon-like peptide-1 receptor activation. Moreover, multielectrode array recordings revealed that glucagon-like peptide-1 functionally augmented the photoresponses of ON-type retinal ganglion cells. Optomotor response tests demonstrated that diabetic rats exhibited reductions in visual acuity and contrast sensitivity that were significantly ameliorated by topical administration of glucagon-like peptide-1. These results suggest that glucagon-like peptide-1 facilitates the release of γ-aminobutyric acid onto retinal ganglion cells through the activation of glucagon-like peptide-1 receptor, leading to the de-excitation of retinal ganglion cell circuits and the inhibition of excitotoxic processes associated with diabetic retinopathy. Collectively, our findings indicate that the γ-aminobutyric acid system has potential as a therapeutic target for mitigating early-stage diabetic retinopathy. Furthermore, the topical administration of glucagon-like peptide-1 eyedrops represents a non-invasive and effective treatment approach for managing early-stage diabetic retinopathy.

2025-12-01·JOURNAL OF CLINICAL INVESTIGATION

Fatty acid transport protein 2 inhibition enhances glucose tolerance through α cell–mediated GLP-1 secretion

Article

作者: Li, Vincent ; Khan, Shenaz ; Samuels, Ivy ; Son, Jinsook ; Garvin, Jeffrey L ; Gaivin, Robert J ; Schelling, Jeffrey R ; Accili, Domenico ; Osei-Owusu, Patrick ; Liu, Zhiyu

Type 2 diabetes affects more than 38 million people in the United States, and a major complication is kidney disease. During the analysis of lipotoxicity in diabetic kidney disease, global fatty acid transport protein 2 (FATP2) gene deletion was noted to markedly reduce plasma glucose in db/db mice due to sustained insulin secretion. To identify the mechanism, we observed that islet FATP2 expression was restricted to α cells and that α cell FATP2 was functional. Basal glucagon and alanine-stimulated gluconeogenesis were reduced in FATP2-KO db/db mice compared with db/db mice. Direct evidence of FATP2-KO-induced α cell-mediated glucagon-like peptide 1 (GLP-1) secretion included increased GLP-1+ α cell mass in FATP2-KO db/db mice, small-molecule FATP2 inhibitor enhancement of GLP-1 secretion in αTC1-6 cells and human islets, and exendin[9-39]-inhibitable insulin secretion in FATP2 inhibitor-treated human islets. FATP2-dependent enteroendocrine GLP-1 secretion was excluded by demonstration of similar glucose tolerance and plasma GLP-1 concentrations in db/db FATP2-KO mice following oral versus i.p. glucose loading, nonoverlapping FATP2 and preproglucagon mRNA expression, and lack of FATP2 and GLP-1 coimmunolocalization in the intestines. We conclude that FATP2 deletion or inhibition exerts glucose-lowering effects through α cell-mediated GLP-1 secretion and paracrine β cell insulin release.

2025-12-01·Alzheimers & Dementia

Risk of Alzheimer's Disease and Alzheimer's Disease‐Related Dementias with liraglutide compared to semaglutide and dulaglutide in veterans with type 2 diabetes: An emulated clinical trial observational study

Article

作者: Sarwal, Amara ; Wei, Guo ; Katkam, Niharika ; Nevers, McKenna R ; Hartsell, Sydney E ; Shen, Jincheng ; Takyi, Augustine ; Singh, Ravinder ; Chakravartula, Akhil R ; Beddhu, Srinivasan

Abstract:

Background:

Liraglutide, semaglutide and dulaglutide are non‐exendin based GLP‐1RA that are widely used in type 2 diabetes (T2D) management. GLP‐1RA use may be associated with lower risk of dementia, however, intra‐class effects of GLP‐1RA on AD/ADRD risk need to be further elucidated.

Method:

We followed the active comparator, new user design to emulate a trial comparing the effect of initiating liraglutide, semaglutide or dulaglutide. Veterans with T2D on metformin who initiated any one of these three agents between 01/01/2018 to 12/31/2021 and did not have baseline dementia, as identified by ICD 9 or 10 codes, were included ( N = 21,173). Previous use of GLP‐1RA, SGLT2i or insulin glargine was an exclusion criterion. Administrative censor date was 03/31/2023. Generalized propensity score based inverse probability weighting (IPW) was employed to control confounding in the observational data and facilitate comparisons among the three agents. In IPW Cox models with adjustment for baseline covariates, the study drug classes were related to the risk of AD/ADRD, death and composite of AD/ADRD/death.

Result:

Of the 21,173 veterans, 25% were initiated on liraglutide, 50% on semaglutide, and 25% on dulaglutide. The mean age was 63 ± 11 years, with 9% female and 17% African American. There were 679 AD/ADRD events over 62,724 person‐years of follow up and 1,428 deaths over 63,579 person‐years of follow‐up. Semaglutide had the highest unweighted event rate of AD/ADRD compared to liraglutide and dulaglutide. In IPW Cox regression models, liraglutide had a lower risk of AD/ADRD compared to semaglutide (HR 0.68, 95% CI 0.55, 0.83), and similar risk compared to dulaglutide (Table). Semaglutide had a higher risk of AD/ADRD than dulaglutide (HR 1.32, 95% CI 1.08, 1.62). In addition, liraglutide had the lowest risk of death as well as composite AD/ADRD/death compared to both semaglutide and dulaglutide.

Conclusion:

Liraglutide had a lower risk of AD/ADRD compared to semaglutide as well as a lower risk of death compared to other commonly used GLP‐1RA. Dulaglutide had similar risk of AD/ADRD to liraglutide, however death benefit was not seen.

项与 Avexitide 相关的新闻（医药）

2026-01-30

·中肽生化

行业研究 | 2026年值得关注的中美多肽药物关键临床一览

｜中肽生化内容团队编辑在经历了跌宕起伏的2025年后，多肽药物开发在2026年又将迎来一批后期临床的“到彼岸”。本文选取在clinicaltrials.gov上注册，在中国或美国进行的3，4期多肽药物的临床试验，它们将于2026年实现主要终点的完成。所涉适应症涵盖遗传性生长障碍、代谢与肥胖相关疾病、肿瘤辅助或免疫治疗、内分泌功能紊乱、炎症与自身免疫疾病，以及分子影像诊断等多个彼此独立的临床场景。多肽药物：Vosoritide 开发商：BioMarin 适应症：Hypochondroplasia (轻型软骨发育不全) 临床：NCT06455059 ，（CANOPY-HCH-3 ）3期 Primary Completion: 2026-08-01 这项 III 期临床研究（NCT06455059）聚焦于轻型软骨发育不全（Hypochondroplasia）这一由 FGFR3 激活突变驱动的遗传性骨骼发育障碍，评估 Vosoritide 作为疾病干预手段的疗效与安全性。Vosoritide 是一种 C 型利钠肽（CNP）类似物，通过激活 NPR-B（NPR2）–cGMP 信号通路，在生长板软骨细胞中功能性对冲 FGFR3 过度信号，从而改善内软骨成骨过程；这一机制已在同一通路相关的骨骼发育障碍中建立了明确的生物学合理性。此前的 II 期研究显示，在经基因检测确诊的 HCH 儿童中，vosoritide 治疗可带来相较基线具有一致方向性的年化生长速度（AGV）改善，且整体安全性特征与其既往在 FGFR3 相关疾病中的经验相符，为进入确证性研究奠定了基础。在此背景下，CANOPY-HCH-3 采用随机、分层、安慰剂对照、双盲、多中心设计，对从既往研究滚入的儿童患者进行 52 周每日皮下注射治疗，以 AGV 作为主要终点，系统验证该机制导向的多肽治疗能否在 HCH 人群中转化为稳定、可重复的临床获益。研究由 BioMarin Pharmaceutical赞助，代表其在 FGFR3 相关罕见骨骼发育障碍领域对既有平台的进一步拓展。多肽药物： GLSI-100（GP2 + GM-CSF）开发商： Greenwich LifeSciences, Inc. 适应症： HER2/Neu 阳性乳腺癌（高复发风险、完成新辅助及辅助治疗后人群）临床阶段： III 期（FLAMINGO-01，NCT05232916） Primary Completion： 2026-12 这项 III 期临床研究（FLAMINGO-01，NCT05232916）评估 GLSI-100 在 HER2/Neu 阳性乳腺癌高复发风险人群中的疗效与安全性。GLSI-100 是一种多肽肿瘤疫苗型免疫治疗，由 HER2/Neu 衍生肽 GP2 联合 GM-CSF 佐剂构成，其靶点为 HER2 蛋白跨膜区表位，设计目标是在完成新辅助治疗及术后辅助曲妥珠单抗为基础标准治疗后，通过诱导HER2 特异性 CD8⁺ T 细胞免疫反应，降低残余病灶或高复发风险患者的复发概率。既往 II 期研究在 HLA-A*02 阳性、HER2 阳性乳腺癌患者中显示，GLSI-100 可诱导持久的抗原特异性免疫应答，并在部分亚组中观察到无病生存期（DFS）改善趋势，且安全性良好，主要不良反应为注射部位反应和轻度全身免疫相关症状。在此基础上，FLAMINGO-01 采用前瞻性、随机、双盲、安慰剂对照、多中心设计，计划入组约 750 例 HER2 阳性受试者，主要研究人群为 HLA-A*02 阳性患者，同时设置第三个开放标签队列探索非 HLA-A*02 阳性人群的免疫治疗潜力。研究旨在系统验证该 HER2 靶向多肽疫苗策略是否能够在高复发风险人群中转化为具有临床意义的长期结局改善。多肽药物： PJ009 开发商： Chongqing Peg-Bio Biopharm Co., Ltd.（重庆派金生物科技）适应症： Short Bowel Syndrome（短肠综合征）；临床阶段： III 期（NCT06512584，CQPJ-PJ009-III） Primary Completion： 2026-03-30 这项 III 期临床研究（NCT06512584）评估 PJ009 在短肠综合征（Short Bowel Syndrome，SBS）且需长期肠外营养支持患者中的疗效与安全性。治疗方案为按体重每日皮下注射，核心评估围绕肠外营养依赖程度的变化及整体安全性展开，验证 PJ009 是否能够在 SBS 人群中带来具有临床意义的营养支持负担改善。多肽药物： 68Ga-PSMA-11 开发商： Telix Pharmaceuticals (Innovations) Pty Limited 适应症：前列腺癌（Prostate Cancer，影像学检测）临床阶段： III 期（NCT07052214） Primary Completion： 2026-06 这项 III 期研究评估 68Ga-PSMA-11 PSMA PET 联合 MRI (磁共振成像) 相较标准诊疗路径在前列腺癌检测中的诊断价值。研究以 PSMA 靶向多肽放射性配体成像为核心，通过与 MRI 结果联合指导系统性及靶向活检，旨在提高临床显著性前列腺癌的检出率并减少不必要的活检。多肽药物： Avexitide 开发商： Amylyx Pharmaceuticals Inc. 适应症： Post-Bariatric Hypoglycemia（术后低血糖，Roux-en-Y 胃旁路术后）临床阶段： III 期（NCT06747468，LUCIDITY / AVX-001） Primary Completion： 2026-03 这项 III 期临床研究（LUCIDITY，NCT06747468）评估 Avexitide 在减重手术后低血糖（Post-Bariatric Hypoglycemia，PBH）患者中的疗效与安全性。PBH 常见于 Roux-en-Y 胃旁路术（RYGB）后，其核心病理与术后 GLP-1 信号异常增强、继发高胰岛素反应密切相关。Avexitide 为一款 GLP-1 受体拮抗多肽，通过抑制过度的 GLP-1 介导信号，减少餐后胰岛素峰值，从而降低低血糖事件发生频率。该研究由 Amylyx Pharmaceuticals Inc. 赞助，验证这一机制导向的多肽拮抗策略是否能够为 PBH 提供稳定、可长期使用的药物治疗方案。多肽药物： iGlarLixi（insulin glargine + lixisenatide）开发商： Sanofi 适应症： 2 型糖尿病（T2D，口服降糖药控制不佳的中国初治胰岛素人群）临床阶段： IV 期（NCT06671587，China Soli-CGM / LPS18034） Primary Completion： 2026-09-18 这项 IV 期、多中心、随机、开放标签研究（China Soli-CGM，NCT06671587）比较 iGlarLixi 与胰岛素甘精 U100（Gla-100）在中国口服降糖药治疗失败的 2 型糖尿病患者中的血糖控制效果。研究以连续血糖监测（CGM）测得的血糖达标时间（TIR）变化为主要终点，评估在真实世界治疗路径中，将基础胰岛素与 GLP-1 受体激动剂（lixisenatide）组合是否能够在不增加治疗复杂度的前提下，带来更优的整体血糖稳定性。研究结果将为固定复方注射制剂在中国 T2D 人群中的临床定位与使用策略提供循证依据。多肽药物： CagriSema（cagrilintide + semaglutide）开发商： Novo Nordisk A/S 适应症： 2 型糖尿病（T2D，已使用二甲双胍和/或 SGLT2 抑制剂但控制不佳）临床阶段： III 期（NCT06534411，REIMAGINE 5） Primary Completion： 2026-06-02 这项 III 期随机对照研究（REIMAGINE 5）比较 CagriSema 与 Tirzepatide 在 2 型糖尿病患者中的降糖与减重效果。CagriSema 为 cagrilintide（胰淀素类似物）与 semaglutide（GLP-1 受体激动剂）的联合给药方案，研究采用每周一次皮下注射，评估其在标准口服降糖治疗基础上的血糖控制和体重改善潜力。该研究计划定位于与双/多靶点肠促胰素类药物的头对头比较，为 CagriSema 在 T2D 治疗中的临床价值提供直接对照证据。多肽药物： CagriSema（cagrilintide + semaglutide）开发商： Novo Nordisk A/S 适应症： 2 型糖尿病（T2D，二甲双胍治疗后控制不佳，可合并或不合并 SGLT2 抑制剂）临床阶段： III 期（NCT06221969） Primary Completion： 2026-02-20 这项 III 期随机对照研究（NCT06221969）比较 CagriSema（cagrilintide + semaglutide，2.4 mg/2.4 mg，每周一次皮下注射）与 Tirzepatide（15 mg，每周一次）在 2 型糖尿病患者中的降糖与减重效果。研究入组约 1,000 例在二甲双胍基础治疗下血糖控制不佳的患者，允许合并或不合并 SGLT2 抑制剂，核心在于通过胰淀素通路（cagrilintide）与 GLP-1 通路（semaglutide）的联合调控，评估其相较多靶点肠促胰素药物的临床获益幅度，为 CagriSema 在 T2D 治疗中的定位提供直接头对头证据。多肽药物： Tirzepatide 开发商： Eli Lilly 适应症： 2 型糖尿病（T2D，斋月禁食期间用药管理）临床阶段： IV 期（NCT06635057） Primary Completion： 2026-04 这项 IV 期、多中心、多国家、开放标签、单臂研究（T-RAM，NCT06635057）评估 Tirzepatide 在斋月禁食背景下启动并按说明书用药的有效性与安全性。研究关注在禁食—进食节律显著改变的情境中，每周一次给药的 GLP-1/GIP 双受体激动多肽是否能够维持稳定的血糖控制并避免低血糖风险，为穆斯林 T2D 人群在斋月期间的真实世界用药策略提供循证依据。多肽药物： Tirzepatide 开发商： Eli Lilly 适应症：青少年肥胖或超重（伴至少一种体重相关合并症）临床阶段： III 期（NCT06075667） Primary Completion： 2026-05 这项 III 期随机、双盲、安慰剂对照研究（NCT06075667）评估 Tirzepatide 在青少年肥胖或超重合并症人群中的疗效、安全性与药代动力学。研究采用每周一次给药方案，在生活方式干预基础上比较其相较安慰剂的体重改善效果，并设置长期延伸治疗以评估持续用药的安全性与维持效应，为 GLP-1/GIP 双受体激动多肽在青少年体重管理中的临床应用提供确证性证据。多肽药物： Tirzepatide 开发商： Eli Lilly 适应症：肥胖或超重（伴体重相关合并症，体重减轻后的维持治疗）临床阶段： III 期（Phase 3b）（NCT06047548） Primary Completion： 2026-05 这项 III 期（Phase 3b）随机对照研究（SURMOUNT-MAINTAIN，NCT06047548）评估 Tirzepatide 在完成初始体重下降后的体重维持阶段的疗效与安全性。研究设计为先进行 60 周开放标签减重期，在达到随机条件后进入 52 周双盲维持期，比较固定低剂量（5 mg）或最大耐受剂量（MTD）的 tirzepatide 与安慰剂在维持既有体重减轻效果方面的差异。该研究重点回答 GLP-1/GIP 双受体激动多肽是否能够在长期治疗中稳定维持减重获益，为肥胖的慢病化、长期管理策略提供循证依据。多肽药物： Retatrutide 开发商： Eli Lilly 适应症：肥胖症临床阶段： III 期（NCT06662383） Primary Completion： 2026-12 这项 III 期随机、双盲研究（NCT06662383）头对头比较 Retatrutide 与 Tirzepatide 在成人肥胖人群中的疗效与安全性。Retatrutide 为 GLP-1/GIP/胰高血糖素三受体激动多肽，在 GLP-1/GIP 双通路基础上引入胰高血糖素通路调控，旨在进一步增强能量消耗与体重下降幅度；Tirzepatide 则作为已建立临床基准的 GLP-1/GIP 双受体激动多肽作为直接对照。研究计划入组约 800 例受试者，治疗随访约 89 周，定位于评估三重肠促胰素策略是否能够在肥胖治疗中实现相较现有双靶点方案的增量获益。多肽药物： Inpegsomatropin 开发商： Xiamen Amoytop Biotech Co., Ltd. 适应症：特发性矮小（Idiopathic Short Stature，ISS）临床阶段： III 期（NCT06927310，PEGPESEN-4-2-001） Primary Completion： 2026-03 这项 III 期、多中心、随机、开放标签、阳性对照研究（NCT06927310）比较 Inpegsomatropin 与重组人生长激素（rhGH）在特发性矮小（ISS）儿童中的疗效与安全性。Inpegsomatropin为经 PEG 修饰的人生长激素多肽，采用每周一次皮下注射给药方案，研究以 52 周治疗期为核心，评估其在促进线性生长方面是否能够达到或接近每日给药 rhGH 的疗效，同时验证长效给药在依从性与长期安全性方面的潜在优势。多肽药物： JNJ-77242113 (Icotrokinra) 开发商：J&J 适应症：中重度斑块型银屑病（Plaque Psoriasis）临床阶段： III 期（NCT06934226，ICONIC-ASCEND） Primary Completion： 2026-03-30 这项 III 期、多中心、随机、双盲研究（ICONIC-ASCEND，NCT06934226）比较 JNJ-77242113 (Icotrokinra) 与安慰剂及 Ustekinumab 在中重度斑块型银屑病患者中的疗效与安全性。JNJ-77242113 是一款口服 IL-23 受体拮抗多肽，通过阻断 IL-23/IL-23R 通路抑制 Th17 相关炎症反应；Ustekinumab 作为 IL-12/IL-23 单抗提供成熟生物制剂对照。研究旨在验证口服多肽直接拮抗受体的策略，是否能够在保持生物学疗效的同时，提供不同于注射抗体的给药便利性与长期管理潜力。多肽药物： Cyclosporine（眼用凝胶）赞助商： Zhaoke (Guangzhou) Ophthalmology Pharmaceutical Ltd. 适应症：中至重度干眼病（Dry Eye Disease）临床阶段： III 期（NCT06766357） Primary Completion： 2026-02 这项 III 期、多中心、随机、双盲、载体对照研究（NCT06766357）评估环孢素（Cyclosporine）眼用凝胶在中至重度干眼病患者中的疗效与安全性。Cyclosporine 是一款环状十一肽免疫抑制剂，通过抑制钙调神经磷酸酶（calcineurin），下调 T 细胞介导的炎症反应，从而改善干眼相关的炎症病理。研究以 84 天双盲治疗期作为主要疗效分析阶段，随后进入开放用药的安全性观察期，旨在验证局部多肽免疫调节策略在中重度干眼治疗中的临床价值与耐受性。

临床3期临床2期疫苗免疫疗法临床终止

2026-01-09

·中肽生化

行业研究 | 2025年美国多肽临床研究回顾：探索与应用的多样化

｜中肽生化内容团队编辑近年来，多肽药物在不同治疗领域中的临床应用持续扩展，其研发形态也逐渐呈现出明显分化。从代谢相关疾病到肿瘤，再到炎症与免疫适应症，多肽不再以单一技术路径出现，而是被纳入到具体的临床开发路径之中，承担不同的治疗或技术功能。回到已经注册的临床试验，可以更清楚地观察这一变化。2025 年在clinicaltrials.gov上注册，临床地点在美国的一系列多肽相关临床研究，覆盖了从早期探索到后期验证的不同阶段，涉及新抗原肽疫苗、放射性标记多肽、GLP-1 及相关代谢通路，以及口服环肽等多种形式。这些项目所体现的多肽在不同疾病领域和开发阶段中的最新具体应用方式（表1）。需要指出的是，本文基于 ClinicalTrials.gov 数据库中 2025 年登记的多肽相关临床研究。所纳入的研究均满足以下条件：试验在美国开展，研究类型为干预性研究（interventional study），赞助方为产业方（industry sponsor），覆盖 I 期至 IV 期临床阶段。统计对象以单个临床试验登记为单位，不限于多肽新药。表1. Clnicaltrials.gov上注册的2025年多肽临床研究（美国）一览表 1. 多肽疫苗在肿瘤中的应用 2025 年在美国注册的多肽疫苗相关临床试验，数量并不算多，但适应症选择高度集中，且每一个项目的设计逻辑都与所面对的肿瘤类型紧密相关。这些研究围绕不同肿瘤的生物学特征和既有治疗瓶颈，设定了相对明确的验证目标。胆道癌 NCT06564623（mBTCvax，I 期）选择的适应症是晚期胆道癌。这一选择本身具有指向性。胆道癌总体突变负荷不高，对免疫检查点抑制剂的反应率有限，即便在联合免疫方案中，疗效提升空间也较为受限。在这一背景下，引入多肽疫苗的核心目的，并不是增强已有免疫治疗的强度，而是尝试解决一个更基础的问题：免疫系统是否能够被明确指向肿瘤特异的突变信息。 mBTCvax 采用来源于肿瘤驱动基因突变所产生的突变肽。这类抗原在正常组织中不存在，理论上能够降低免疫耐受带来的干扰。试验设计中将该疫苗与 PD-L1 抑制剂 durvalumab 及 CTLA-4 抑制剂 tremelimumab联合使用，意味着研究者默认单一免疫解除手段不足以支撑突变肽发挥作用。从试验阶段和联合方案来看，该项目的重点并不在于临床缓解率，而在于突变肽在高度调节过的免疫环境中，是否能够诱导稳定、可检测的特异性免疫应答。这一设计更接近免疫生物学层面的验证，而非疗效竞争。低级别胶质瘤与胆道癌不同，NCT05609994（PEPIDH1M，I 期）所针对的低级别胶质瘤，在分子层面具有高度一致的特征。IDH1 突变在这一人群中高度富集，且突变位点相对固定，为突变肽疫苗提供了清晰的抗原来源。该研究将 IDH1 突变肽疫苗与 IDH1/2 双重抑制剂vorasidenib 联合使用，其临床逻辑并非简单叠加两种作用机制，而是围绕肿瘤演化过程中的两个不同层面展开。一方面，小分子抑制剂直接作用于突变酶活性，抑制肿瘤代谢异常；另一方面，突变肽疫苗尝试在相对低度免疫抑制的脑肿瘤环境中，引入针对特定突变的免疫识别。在这一适应症中，多肽疫苗的作用并非补救既有免疫治疗失败，而是作为分子分型明确背景下的探索性工具，用于评估突变特异免疫应答在中枢神经系统肿瘤中的可行性。这也是该项目选择 I 期、并将安全性与免疫反应作为主要观察重点的原因。胰腺癌与结直肠癌围绕 KRAS 突变展开的多肽疫苗研究，是 2025 年肿瘤多肽疫苗中最成体系的一组。 SPL mKRASvax（NCT06411691，I b 期）以及 NCT06782932（I/II 期）均将结直肠癌和胰腺导管腺癌作为主要适应症。这两类肿瘤的共同特征在于 KRAS 驱动突变高度常见，同时肿瘤微环境免疫抑制显著，传统免疫治疗效果有限。在这些研究中，突变 KRAS 肽疫苗并未被放置在单一免疫检查点抑制剂背景下，而是与 PD-1 抗体 balstilimab 及共刺激通路抗体（如AGEN2373 或 botensilimab）联合使用。这样的组合反映出一个现实判断：在 KRAS 突变相关肿瘤中，仅依靠解除免疫抑制不足以放大突变肽信号，还需要通过共刺激途径增强 T 细胞活化。 NCT06782932 进一步引入了对照设计，将突变 KRAS 肽疫苗与 GVAX 全细胞疫苗分别用于新辅助或辅助治疗阶段。这一比较试图回答一个更具体的问题：在相同免疫调节框架下，基于单一突变信息的肽疫苗，与包含多种抗原的全细胞疫苗，在免疫应答质量和可控性上是否存在差异。膀胱癌 NCT06529822 临床研究针对的是肌层浸润性膀胱癌，采用的是个体化定制的合成新抗原长肽疫苗。该项目处于 I 期，适应症选择和疫苗形式共同指向一个相对谨慎的应用场景：围绕肿瘤特异新抗原，在疾病负荷相对可控的阶段探索免疫应答。与前述 KRAS 或 IDH1 项目不同，该研究并未聚焦单一驱动突变，而是基于个体肿瘤测序结果，筛选多个潜在新抗原并合成长肽形式。这种策略更强调覆盖面和个体化，而非靶点一致性。选择膀胱癌这一免疫治疗已有一定基础的适应症，也降低了探索性研究的系统风险。 2. 放射性配体多肽与多肽疫苗主要围绕免疫应答展开不同，2025 年在美国注册的放射性配体多肽项目，临床关注点高度集中在药物本体的靶向能力、体内分布特征以及成像可解释性。在这一领域，多肽并不承担治疗功能，而是作为放射性示踪剂或先导配体，被用于验证靶点与疾病之间是否存在稳定、可重复的关联。 Evuzamitide：淀粉样蛋白沉积成像放射性多肽在淀粉样蛋白相关疾病中，最具代表性的项目是 ¹²⁴I-Evuzamitide。该药物是一种能够特异性结合淀粉样蛋白的多肽，通过 ¹²⁴I 放射性标记后，用于 PET/CT 成像。在 2025 年注册的 II 期研究中，Evuzamitide 被用于评估既往存在腰椎管狭窄或腕管综合征患者的心脏及心外淀粉样蛋白沉积情况。腕管综合征和腰椎管狭窄被认为是系统性淀粉样变性（尤其是 ATTR）可能出现的早期临床信号。将 Evuzamitide 用于这一人群，研究重点在于其是否能够在临床症状尚不典型的阶段，提供清晰、可量化的影像学证据。在这一应用场景中，多肽的价值体现在其分子量较小、组织穿透性较强以及对淀粉样蛋白构象的选择性结合能力。与抗体类成像探针相比，Evuzamitide 更有利于降低背景信号干扰，并在心肌等致密组织中获得更高的信噪比。这也是该项目能够从早期探索推进至 II 期的关键原因。 LY4257496：靶向 GRPR 的实体瘤放射性配体多肽在肿瘤相关放射性配体多肽中，礼来推进的 LY4257496 是 2025 年最具代表性的项目之一。该药物是一种靶向 Gastrin-Releasing Peptide Receptor（GRPR）的放射性配体多肽，目前处于 1a/b 期临床阶段，适应症覆盖乳腺癌、结直肠癌、前列腺癌和子宫内膜癌。 LY4257496 的临床设计横跨多个实体瘤适应症，这一策略本身就揭示了该项目的真实目标：系统性评估 GRPR 在不同肿瘤中的表达一致性与成像可行性。研究重点包括配体在体内的分布特征、肿瘤与背景组织的对比度，以及不同剂量条件下的安全性与成像质量。在这一阶段，LY4257496功能定位是成像与靶点验证。这种循序推进的路径，反映出放射性配体开发中的一种理性策略：只有在靶点表达模式和体内行为被充分验证之后，才具备进入治疗性放射性配体（RLT）开发的基础。多肽在这一项目中的优势，同样体现在快速血液清除、较低非特异性背景信号以及成像时间窗口可控等工程属性上。这些特征对于早期靶点验证尤为关键。 3. 代谢相关适应症 2025 年美国多肽临床试验中，代谢相关适应症占据了最明显的比重。这是因为以 GLP-1 为代表的一类多肽，已经完成了从机制探索到临床路径标准化的转变，开始被用于回答更复杂、更细分的临床问题。 VK2735 Viking Therapeutics 推进的 VK2735 是这一组项目中临床阶段最为靠前的代表之一。2025 年，该药物分别启动了针对肥胖症（NCT07104500）和2 型糖尿病（NCT07104383）的 III 期临床试验。将肥胖与 2 型糖尿病作为两个独立 III 期适应症推进，反映的是临床对这两类患者需求的区分：前者关注的是体重控制、代谢改善及长期耐受性，后者则需要在降糖效果之外，平衡低血糖风险与合并用药背景。 Tirzepatide 礼来的 tirzepatide 在 2025 年并未出现在探索性创新的位置，而是作为一个已经被广泛验证的多肽，进入了更细分的人群与更真实的临床场景。值得注意的是，tirzepatide 被用于肥胖或超重合并 1 型糖尿病的人群（NCT06962280、NCT06914895），这本身就是一个高度谨慎的适应症选择。1 型糖尿病患者在胰岛素治疗背景下使用 GLP-1/GIP 双激动剂，对低血糖风险、剂量调整和代谢波动的要求远高于 2 型糖尿病人群。将 tirzepatide 推进到这一领域，意味着其安全性边界已经被认为足以支持更复杂的代谢干预。此外，NCT06864026 进一步将 tirzepatide放入真实世界背景：在接受 IL-17A 单抗 ixekizumab 治疗的银屑病关节炎合并超重或肥胖患者中，评估其体重和代谢改善效果。这类研究关注在免疫疾病合并代谢异常的真实人群中，多肽治疗是否具备可操作性与可持续性。这些试验共同体现出一个趋势：tirzepatide 已经被当作可跨疾病使用的代谢调节工具，而不仅限于传统意义上的降糖或减重药物。 Retatrutide 在代谢功能障碍相关脂肪性肝病（MASLD）领域，礼来选择推进的是 retatrutide 与 tirzepatide 的组合路径（NCT07165028）。MASLD 本身并不是一个单纯的体重问题，而是涉及胰岛素抵抗、脂质代谢异常和肝脏炎症等多个层面的系统性代谢紊乱。将 GLP-1/GIP 相关多肽引入这一适应症，意味着研发重点已经从体重控制延伸至代谢网络整体重塑。在这一场景中，多肽的价值并不取决于短期体重下降幅度，而在于其是否能够在长期给药中改善肝脏代谢指标，并与现有生活方式干预形成可叠加的治疗策略。 MET097 Metsera 推进的 MET097 处于 II 期临床阶段（NCT06897202），适应症为肥胖或超重合并 2 型糖尿病。这一定位介于VK2735 的 III 期注册路径与早期探索项目之间。选择这一人群，意味着 MET097 的研发重点仍然集中在剂量探索、代谢指标变化以及耐受性评估上。相较于单纯肥胖或单纯糖尿病，合并人群对多肽治疗的耐受性与风险管理提出了更高要求，也为 II 期阶段提供了更具信息量的数据。 Avexitide 在多肽药物的代谢适应症相关的临床项目中，avexitide（NCT06747468）具有明显的差异性。该药物是一种exendin-4 类似物，但其临床用途并非激活 GLP-1 通路，而是用于胃旁路术术后低血糖（PBH）这一特殊适应症。这一项目已经进入 III 期，说明该路径在前期研究中已经获得了较为明确的信号。PBH 的发生机制与 GLP-1 过度刺激密切相关，在这一背景下，GLP-1拮抗或调节策略成为一种针对病因的干预方式。avexitide 的存在本身提醒人们：随着 GLP-1 类多肽的广泛使用，其反向调节在特定临床场景中同样具有不可替代的价值。 Eloralintide 礼来在 2025 年启动的 eloralintide（NCT06916065）是一项 I 期研究，属于胰淀素类似物路径。相较于GLP-1 轴线，这一机制在临床上的成熟度明显较低。将 eloralintide 放在肥胖适应症中进行早期探索，反映的是对多激素协同调节的持续兴趣。该阶段的研究重点在于明确其药代特征、安全性以及是否具备与现有代谢药物联合使用的潜力。 4. 炎症与自身免疫适应症在 2025 年美国启动的多肽相关临床研究中，炎症与自身免疫适应症并未形成规模化扩张，但进入临床的项目具有高度聚焦的技术取向。这些研究围绕两个更为现实的问题展开：一是多肽是否能够突破长期依赖注射给药的限制，二是在慢性自身免疫疾病中，是否存在比广泛免疫抑制更精细的调节方式。 JNJ-77242113 JNJ-77242113 是一款靶向 IL-23 通路的口服环肽，目前已进入中重度银屑病的 III 期临床阶段。作为银屑病治疗中的成熟通路，IL-23 已经被多款注射型生物制剂反复验证，其在疾病控制中的作用边界相对清晰。在这一背景下，JNJ-77242113 的研发核心转向了另一个层面：多肽是否能够在口服给药条件下，实现稳定、可预测的系统暴露，并支撑长期治疗需求。环肽结构的引入，本质上是为了解决传统线性多肽在胃肠道环境中稳定性不足的问题，通过构象约束提升分子耐受性，从而为口服途径提供工程基础。进入 III 期临床，意味着该药物在早期研究中已经展示出可接受的安全性特征和相对一致的药代行为。在银屑病这样的慢性炎症性疾病中，治疗往往需要持续多年，给药依从性和患者负担成为影响真实疗效的重要因素。JNJ-77242113 所验证的，正是多肽在这一现实治疗场景中是否能够提供新的可行选项。 OPT101 与 JNJ-77242113 面向成熟炎症适应症不同，OPT101切入的是自身免疫疾病中更早期、也更基础的免疫调节问题。OPT101 是一款靶向 CD40L（CD154）通路的免疫调节多肽，目前正在 1 型糖尿病患者中开展 II 期临床研究。 1 型糖尿病的治疗长期以来以胰岛素替代为核心，针对免疫病因本身的干预手段相对有限。OPT101 的开发目标并非恢复已经丧失的β细胞功能，而是尝试在疾病进展过程中，通过调节免疫反应强度，延缓自身免疫攻击对残余β细胞的进一步破坏。 CD40–CD154 通路在 T 细胞与抗原呈递细胞的相互作用中发挥关键作用，是多种自身免疫反应放大的重要节点。OPT101 选择以多肽形式作用于这一通路，体现的是一种相对克制的干预思路：并不追求完全阻断免疫信号，而是通过调节实现免疫反应的重新平衡。这种策略在理论上有助于降低长期免疫抑制带来的系统性风险。从临床设计来看，该 II 期研究重点关注安全性、耐受性和药代特征，并探索其对残余β细胞功能的早期影响。 5. 总结基于 2025 年在clinicaltrials.gov注册，在美国展开的多肽相关临床试验，可以观察到多肽类药物在不同疾病领域中的应用呈现出明确分层。肿瘤相关研究主要集中于新抗原肽疫苗与放射性配体两条路径，分别用于免疫应答诱导与靶点表达及分布的成像验证；代谢相关适应症中的多肽项目已进入系统化开发阶段，多项研究推进至 III–IV 期，覆盖肥胖、糖尿病及其复杂合并人群；炎症与自身免疫领域的多肽研究则以给药方式和免疫调节精细化为重点，在既有治疗框架内开展验证。

疫苗临床1期免疫疗法

2026-01-08

·gubra.dk

Amylyx Pharmaceuticals announces nomination of AMX0318 as a novel, long-acting GLP-1 receptor antagonist development candidate, identified in collaboration with Gubra

AMX0318 selected as development candidate after meeting key criteria, demonstrating a robust chemical stability profile, strong in vitro potency, evidence of in vivo efficacy and tolerability, high solubility, and a favorable pharmacokinetic profile consistent with a long-acting peptide IND-enabling studies expected to initiate in 2026 with an IND targeted for 2027, pending successful completion of IND-enabling studies CAMBRIDGE, Mass. January 8, 2026 – Amylyx Pharmaceuticals, Inc. (NASDAQ: AMLX) (“Amylyx” or the “Company”) today announced the selection of AMX0318, a long-acting glucagon-like peptide-1 (GLP-1) receptor antagonist, as a development candidate for post-bariatric hypoglycemia (PBH) and other rare diseases. AMX0318 was identified through a research collaboration with Gubra A/S (“Gubra”), a company specializing in peptide-based drug discovery and preclinical contract research services. “We are very pleased to nominate AMX0318 as a development candidate and were highly impressed by Gubra’s proprietary and innovative process, which identified a peptide that surpassed our research target profile for a long-acting GLP-1 receptor antagonist. AMX0318 has thus far shown robust preclinical and chemical properties, including a pharmacokinetic profile that may support long-acting administration,” said Camille L. Bedrosian, MD, Chief Medical Officer at Amylyx. “We are excited about the opportunity to develop additional therapeutic possibilities for people who may benefit from inhibiting GLP-1 receptor activity, including people with PBH and other rare diseases. The GLP-1 receptor is a well-characterized biological target and one of the key regulators of glucose-insulin homeostasis.” Dr. Bedrosian continued, “We have strong conviction that inhibiting GLP-1 receptor activity represents an important therapeutic approach given the statistically significant data that avexitide, our investigational, first-in-class GLP-1 receptor antagonist, has generated to date. We continue to expect completion of recruitment in our pivotal Phase 3 LUCIDITY trial of avexitide in Q1 2026, with topline data expected in Q3 2026.” AMX0318 has completed extensive preclinical evaluation, including stability, solubility, potency, in vivo pharmacokinetics and pharmacodynamics, and in vivo tolerability studies. Amylyx expects the program to advance into investigational new drug (IND)-enabling studies later this year, with an IND targeted for 2027, pending successful completion of IND-enabling studies. “We are pleased to see AMX0318 advance as a development candidate, a milestone that reflects both the strong collaboration between the Gubra and Amylyx teams and the capabilities of Gubra’s proprietary peptide drug discovery platform,” said Louise S. Dalbøge, Chief Science Officer at Gubra. “Our AI-driven streaMLine platform enables multi-parameter optimization of peptide candidates, and we are excited to see this applied successfully to AMX0318 in close collaboration with Amylyx.” Under the terms of the research collaboration, Gubra is eligible to receive more than $50 million in success-based development and commercialization milestones plus mid-single digit royalties on worldwide net sales. The selection and handover of the development candidate will provide milestone payments of $4 million to Gubra. About Gubra Gubra, founded in 2008 in Denmark and listed on NASDAQ Copenhagen, is a disease-agnostic techbio company specialized in peptide-based drug discovery and preclinical contract research services. Gubra’s activities are focused on the early stages of drug development and are organized in two main business units – Biotech (D&P) and CRO services. The two business areas are highly synergistic and create a unique entity capable of generating a steady cash flow from the CRO business while investing in high-impact biotech R&D projects with significant value inflection potential through partnerships. Gubra has around 300 employees and had revenue of DKK 2.6 billion (around EUR 350 million) in the first 9 months of 2025. See www.gubra.dk for more information. About Amylyx Pharmaceuticals At Amylyx, our mission is to usher in a new era of treating diseases with high unmet needs. Where others see challenges, we see opportunities that we pursue with urgency, rigorous science, and unwavering commitment to the communities we serve. We are currently focused on four investigational therapies across several neurodegenerative and endocrine diseases in which we believe they can make the greatest impact. For more information, visit amylyx.com and follow us on LinkedIn and X. For investors, please visit investors.amylyx.com. Amylyx 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, as amended. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Such statements include, but are not limited to, Amylyx’ expectations regarding: the therapeutic potential for AMX0318, the expected timeline for the IND-enabling studies and IND submission for AMX0318, the payments and royalties to be received by Gubra, and the expected timeline for certain development, regulatory, and commercial milestones. Any forward-looking statements in this press release are based on management’s current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. Risks that contribute to the uncertain nature of the forward-looking statements include: the success, cost, and timing of Amylyx’ program development activities; Amylyx’ ability to execute on its regulatory development plans and expectations regarding the timing of results from its planned data announcements and initiation of clinical studies; the risk that early-stage results may not reflect later-stage results; Amylyx’ ability to fund operations, and the impact that global macroeconomic uncertainty, geopolitical instability, and public health events will have on Amylyx’ operations, as well as the risks and uncertainties set forth in Amylyx’ United States Securities and Exchange Commission (SEC) filings, including Amylyx’ Annual Report on Form 10-K for the year ended December 31, 2024 and subsequent filings with the SEC. All forward-looking statements contained in this press release speak only as of the date on which they were made. Amylyx undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made, except as required by law. Gubra Media Sofia Pitt Boserup +45 4188 9586 sbo@gubra.dk Gubra Investors Kristian Borbos +45 3080 8035 kbo@gubra.dk Emma Jappe Lange +45 5361 6755 ejl@gubra.dk Amylyx Media Amylyx Media Team (857) 320-6191 amylyxmediateam@amylyx.com Amylyx Investors Lindsey Allen (857) 320-6244 Investors@amylyx.com

引进/卖出临床3期多肽偶联药物

100 项与 Avexitide 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11418	-	-	DB14806

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
低血糖	临床3期	美国	Amylyx Pharmaceuticals, Inc.	2025-04-29
高血糖	临床3期	美国	Mayo Clinic	2022-10-17
2型糖尿病	临床3期	美国	Mayo Clinic	2021-04-15
糖尿病前期	临床2期	美国	Mayo Clinic	2025-11-01
先天性高胰岛素血症	临床2期	美国	The Children's Hospital of Philadelphia	2009-05-01
胃肠道疾病	临床1期	美国	Mayo Clinic	2014-05-01
肥胖	临床1期	美国	Mayo Clinic	2014-05-01

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临床结果

适应症

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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


NCT03373435 (PREVENT, Company_Website) 人工标引	临床2期	低血糖	-	avexitide	壓範遞壓蓋齋繭膚範醖(獵糧繭鏇襯簾鹽觸衊醖) = 窪淵衊鑰選鹹鑰觸繭壓選選鏇鹽夢願鏇鑰鹹窪 (遞築糧鏇願鬱觸遞醖鹹 )	积极	2025-07-13
NCT02844907 (CTgov)	临床4期	-	6	Hyperglycemic Clamp+Exendin (9-39)	選窪網製觸製鬱膚遞繭(蓋選積蓋構築築顧範鬱) = 顧築觸淵齋餘夢淵憲選廠衊壓糧夢築糧夢製鬱 (襯鏇獵衊夢窪願遞鏇網, 1984) 更多	-	2024-12-12
NCT03373435 (PREVENT, Biospace) 人工标引	临床2期	低血糖	-	AvexitideAvexitide 30 mg BID	壓鬱齋淵鹹醖襯蓋鑰襯(齋願觸築簾窪艱構獵壓) = 蓋廠窪壓鹽選齋製觸廠鹽蓋夢壓蓋顧鏇選蓋願 (憲積顧觸壓廠顧鬱壓簾 ) 更多	积极	2024-07-10
				AvexitideAvexitide 60 mg QD	壓鬱齋淵鹹醖襯蓋鑰襯(齋願觸築簾窪艱構獵壓) = 觸膚獵網積壓觸鏇簾膚鹽蓋夢壓蓋顧鏇選蓋願 (憲積顧觸壓廠顧鬱壓簾 ) 更多
NCT04459338 (CTgov)	临床3期	-	11	glucagon (Insulin Secretion During the Saline Study)	艱襯顧壓壓衊蓋鬱鬱壓(製遞顧鏇獵淵網鹹築鹽) = 願憲艱蓋獵築蓋鏇糧網廠獵構夢壓糧艱鹹鬱夢 (鹹壓顧製膚鹽餘齋獵遞, 23)	-	2023-06-09
				Exendin-9,39 (Insulin Secretion During the Exendin-9,39 Study)	艱襯顧壓壓衊蓋鬱鬱壓(製遞顧鏇獵淵網鹹築鹽) = 鹹鑰觸襯艱選獵襯醖鏇廠獵構夢壓糧艱鹹鬱夢 (鹹壓顧製膚鹽餘齋獵遞, 19)
NCT04652479 (PREVENT, ENDO2022)	临床2期	低血糖 GLP-1	8	Avexitide 45mg BID	顧鬱蓋糧願顧襯襯製選(窪糧鹽鬱築鑰壓餘網積) = 憲繭積餘選網築網繭製製壓醖願壓餘鏇鬱積襯 (網鬱鹹願製淵鏇艱艱簾 ) 更多	积极	2022-11-01
				Avexitide 90mg QD	顧鬱蓋糧願顧襯襯製選(窪糧鹽鬱築鑰壓餘網積) = 積簾獵醖構膚積築網夢製壓醖願壓餘鏇鬱積襯 (網鬱鹹願製淵鏇艱艱簾 ) 更多
NCT03101930 (CTgov)	临床4期	糖尿病前期 \| 肥胖	329	Placebos+Exendin (9-39)+Liraglutide (Liraglutide)	觸齋膚選蓋簾淵鑰艱餘(壓構糧築積憲淵獵網襯) = 範糧夢餘獵觸顧鏇繭繭廠製鹹遞膚鹽廠鹽窪顧 (鹹鑰餘壓襯選觸夢製衊, 4.82) 更多	-	2022-08-16
				Placebos+Sitagliptin+Exendin (9-39) (Sitagliptin)	觸齋膚選蓋簾淵鑰艱餘(壓構糧築積憲淵獵網襯) = 範憲醖獵齋憲鏇餘獵廠廠製鹹遞膚鹽廠鹽窪顧 (鹹鑰餘壓襯選觸夢製衊, 6.42) 更多
NCT03373435 (PREVENT, CTgov)	临床2期	低血糖	18	Avexitide (Avexitide 30 mg BID)	憲廠網獵窪艱鏇齋蓋憲(選窪網鹽觸齋憲鏇夢願) = 餘艱淵鏇製鏇製鏇齋糧齋鑰蓋鑰襯製窪淵餘鏇 (憲選糧願窪構蓋餘淵壓, 16.5) 更多	-	2022-06-28
				Avexitide (Avexitide 60 mg QD)	憲廠網獵窪艱鏇齋蓋憲(選窪網鹽觸齋憲鏇夢願) = 築觸餘鏇窪願鬱選淵窪齋鑰蓋鑰襯製窪淵餘鏇 (憲選糧願窪構蓋餘淵壓, 16.1) 更多
NCT02762708 (Microbiome, CTgov)	临床2期	2型糖尿病 \| 肥胖	12	Roux-en-Y Gastric Bypass (RYGB) (Roux-en-Y Gastric Bypass (RYGB))	淵築製艱壓憲鏇窪鏇築(糧夢齋衊夢壓鏇憲襯範) = 窪鑰築衊製選遞鹽構構製積簾鹽齋積鏇衊範觸 (淵網淵夢鬱觸選遞廠鬱, 0.88) 更多	-	2022-05-03
				Caloric Restriction (Caloric Restriction)	淵築製艱壓憲鏇窪鏇築(糧夢齋衊夢壓鏇憲襯範) = 糧鹽餘憲膚鏇艱憲膚窪製積簾鹽齋積鏇衊範觸 (淵網淵夢鬱觸選遞廠鬱, 0.98) 更多
NCT03373435 (PREVENT, Pubmed \| J Clin Endocrinol Metab)	临床2期	低血糖	18	Avexitide 30 mg BID	遞遞膚鹹鑰廠膚範夢簾(選蓋製積構鹽顧艱壓夢) = 膚衊鹽網觸獵衊網顧製網鬱窪鏇願鹹構鬱遞積 (憲夢願構壓構築襯鹹繭 ) 更多	积极	2021-02-22
				Avexitide 60 mg QD	遞遞膚鹹鑰廠膚範夢簾(選蓋製積構鹽顧艱壓夢) = 繭網鑰願餘觸窪繭憲憲網鬱窪鏇願鹹構鬱遞積 (憲夢願構壓構築襯鹹繭 ) 更多
NCT02771574 (CTgov)	临床2期	低血糖	19	Lyo avexitide (Part A: Lyo Avexitide 0.15 mg/kg)	範蓋選選餘鹹繭獵艱壓(鏇壓齋醖淵醖餘範顧餘) = 糧獵觸壓鏇齋窪壓膚觸餘築範鏇醖願鬱壓鬱鹹 (廠顧獵繭餘淵糧齋願膚, 7) 更多	-	2020-08-14
				Lyo avexitide (Part A: Lyo Avexitide 0.35 mg/kg)	範蓋選選餘鹹繭獵艱壓(鏇壓齋醖淵醖餘範顧餘) = 鹽遞遞憲範構蓋艱淵蓋餘築範鏇醖願鬱壓鬱鹹 (廠顧獵繭餘淵糧齋願膚, 7) 更多