This randomized, rater-blind, multicenter clinical trial will evaluate whether a personalized pharmaco-lifestyle intervention improves mental functioning in adults with severe mental illness, including schizophrenia, bipolar disorder, or major depressive disorder. Participants will be randomized to either a modular individualized intervention program or a structured psychoeducation control condition. The individualized intervention may include physical exercise, an anti-inflammatory diet, sleep intervention, social prescribing, semaglutide for eligible participants with overweight or obesity, and optional closed-loop transcranial alternating current stimulation for participants with prominent depressive symptoms. The primary outcome is change in the SF-36 Mental Component Summary score from baseline to Month 3.

开始日期2028-10-01

申办/合作机构

Ludwig-Maximilians-Universität München

NCT07430332

/ Not yet recruiting临床2期IIT

Leveraging Semaglutide for Preservation of Beta Cell Function and Restoration of Alpha Cell Function

This study seeks to evaluate the hormone responses of insulin, c-peptide, glucagon, and incretins to semaglutide, a GLP-1 receptor agonist therapy, in individuals with stage 1 type 1 diabetes. The goal of this study is to see if semaglutide can protect beta cell function in this group of people and delay the progression to stage 2 type 1 diabetes.

开始日期2027-09-01

申办/合作机构

Children's Hospital & Medical Center

NCT07797036

/ Not yet recruiting临床2/3期IIT

Postpartum Semaglutide to Reduce Cardiometabolic Risk After Gestational Diabetes: An Effectiveness-Implementation Hybrid Type 1 Randomized Trial

This is an effectiveness-implementation Hybrid Type 1 study using a randomized clinical trial design to evaluate the effectiveness and potential real-world integration of immediate postpartum semaglutide following a pregnancy complicated by gestational diabetes mellitus (GDM). A total of 226 postpartum individuals with recent GDM will be randomized 1:1 to semaglutide or standard postpartum care for a 6-month active treatment phase. The primary effectiveness outcome, development of metabolic syndrome, will be assessed at 6 months postpartum. Participants will subsequently enter a 6-month maintenance phase, during which semaglutide continuation, discontinuation, or initiation will reflect patient preferences, clinical decision-making, medication access, and insurance coverage.

开始日期2027-09-01

申办/合作机构

UMass Chan Medical School

100 项与司美格鲁肽 (诺和诺德) 相关的临床结果

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393

项与司美格鲁肽 (诺和诺德) 相关的文献（医药）

2026-11-01·JOURNAL OF CONTROLLED RELEASE

Dual-transporter-targeted oral semaglutide nanomicelles enable enhanced intestinal absorption and metabolic reprogramming in obesity and diabetes

Article

作者: Kim, Eunbin ; Phuyal, Susmita ; Cho, Seung-Sik ; Bamjan, Arjun Dhwoj ; Subedi, Laxman ; Kim, Ki-Taek ; Park, Jin Woo ; Shim, Jung-Hyun ; Sapkota, Binaya ; Seo, Jong Bae

Obesity is a chronic, relapsing metabolic disorder associated with insulin resistance, dyslipidemia, and related complications. Although glucagon-like peptide-1 receptor agonists (GLP-1 RAs), particularly semaglutide (SEMA), exhibit robust therapeutic efficacy, their clinical application is limited by low oral bioavailability. Here, we report a dual-transporter-targeted oral nanomicellar platform (SGT-M) designed to overcome these limitations. SEMA was electrostatically complexed with glucosamine and taurolithocholate to enable transporter-mediated recognition, followed by incorporation into an n-dodecyl-β-D-maltoside-based nanomicelle. The optimized SGT-M had a particle size of 64.7 ± 1.27 nm and near-complete drug incorporation. In vitro, SGT-M enhanced apparent permeability by 28.8-fold in Caco-2/HT-29-MTX-E12 monolayers, while in situ intestinal perfusion demonstrated a 12.6-fold increase in effective permeability. Oral administration achieved a relative bioavailability of 4.62%. Mechanistic studies revealed a multivalent absorption pathway involving dual targeting of the apical sodium-dependent bile acid transporter (ASBT) and glucose transporter 2 (GLUT2), together with clathrin- and caveolae/lipid-mediated endocytosis. In a high-fat-diet-induced obese mouse model, daily oral administration of SGT-M produced dose-dependent therapeutic effects; at 5 mg/kg, it reduced body weight by 30.3% and fasting glucose by 65.6%, while improving HbA1c and HOMA-IR and decreasing adipose tissue mass. Notably, the highest oral dose of SGT-M produced therapeutically meaningful outcomes that approached those observed with subcutaneous SEMA (0.5 mg/kg) under the experimental conditions used. Collectively, SGT-M represents an engineered oral SEMA delivery system that enables effective systemic exposure and therapeutic efficacy, offering a promising strategy to transform injectable peptide therapies into clinically viable oral formulations.

2026-11-01·TOXICOLOGY AND APPLIED PHARMACOLOGY

Reprogramming NAD+ homeostasis and FOXO3a–Nrf2 signaling mitigates bleomycin-driven pulmonary fibrosis

Article

作者: Amer, Ahmed E ; Saber, Sameh ; El-Kashef, Hassan A ; Mo'men, Maha

Pulmonary fibrosis arises from intertwined oxidative, inflammatory, and profibrotic processes, whereas current therapies target only parts of this network. Here, we evaluated an adjunctive strategy in which nicotinic acid (NA), a NAD⁺-supporting supplement/adjuvant, was added to semaglutide (SEMA), a GLP-1 receptor agonist. The prespecified objective was to determine whether adding NA to SEMA provides greater protection than SEMA alone in bleomycin (BLM)-induced pulmonary fibrosis. Rats were challenged with BLM and treated with SEMA, NA, or SEMA+NA for 21 days. Biochemical, molecular, histological, and western blot endpoints were assessed, and the fixed-dose Highest Single Agent (HSA) and Bliss independence models were used as exploratory interaction metrics. BLM induced oxidative stress, inflammatory cytokine elevation, NAD⁺ and SIRT1 depletion, FOXO3a suppression, TGF-β/SMAD activation, and collagen deposition. Compared with SEMA alone, SEMA+NA produced broader protection, restoring NAD⁺/SIRT1-FOXO3a-Nrf2 pathway-associated readouts and suppressing NF-κB/TGF-β-linked inflammatory and fibrotic markers. Exploratory HSA and Bliss analyses suggested enhanced fixed-dose effects across several endpoints but were interpreted descriptively, not as definitive pharmacological synergy. These findings indicate that NA-driven NAD⁺ metabolic support can amplify the protective profile of SEMA in experimental pulmonary fibrosis. Dose-response matrices, pathway-inhibition studies, temporal profiling, and lung-function testing remain required to establish definitive synergy, mechanism, and translational relevance.

2026-11-01·Current Opinion in HIV and AIDS

Weight gain, adipose tissue remodeling and cardiometabolic disease in people with HIV

Review

作者: Lagathu, Claire ; Gorwood, Jennifer ; Béréziat, Véronique ; Capeau, Jacqueline

Purpose of review:

Weight gain and associated adipose tissue remodeling have been partly linked to HIV infection and to some current antiretroviral therapy (ART) regimens in ART-naive and ART-controlled people with HIV (PWH). This review addresses recent findings on adipose tissue distribution and remodeling in PWH, receiving dolutegravir, bictegravir and/or tenofovir alafenamide (TAF), highlighting how visceral adiposity contributes to cardiometabolic comorbidities.

Recent findings:

Preclinical models exposed to dolutegravir, bictegravir, tenofovir disoproxil fumarate (TDF) and/or TAF demonstrate alterations in adipose tissue, including mitochondrial dysfunction, fibrosis, inhibited beiging, and insulin resistance. Transcriptomic studies of abdominal subcutaneous fat from ART-controlled PWH further revealed elevated inflammation, fibrosis and insulin resistance. Increased visceral adiposity raises the risk of cardiometabolic disorders such as insulin resistance and diabetes, metabolic-dysfunction-associated steatotic liver disease and cardiovascular diseases. Reversing weight gain linked to ART, by switching regimens or adding antiobesity medications like the GLP-1 receptor agonist semaglutide, has shown potential in reducing adipose tissue remodeling, visceral adiposity and cardiometabolic risk factors.

Summary:

Weight gain and increased visceral adiposity partly driven by some ARTs are associated with higher cardiometabolic risk. HIV and ART can either activate or suppress the fat beiging/browning phenotype. Reversing weight gain and visceral adiposity in at-risk PWH is a critical clinical goal.

19,088

项与司美格鲁肽 (诺和诺德) 相关的新闻（医药）

2026-10-16

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吃减重药的人那么多，为什么你的肠道反应格外大？

一项顶刊研究指向罕见但真实的胃肠风险，脑肠轴敏感的人如何守住日常防线。过去这一年，GLP-1减重药在全球开出了数亿张处方，“减肥神药”这几个字，几乎人人都听过。但2023年秋天，一组在《JAMA》上发表的真实世界数据，给这股热潮泼了盆冷水：肠梗阻风险升高4倍多，胃轻瘫风险升高近3.7倍。不少人一看到就慌了，也有人一查发生几率不算高，转头就把这事当成了科普段子。其实这两种反应，都没抓住重点。再少见的副作用风险，我们也得知道；日常出现的肠道波动，我们也得关注。 01 《JAMA》真实世界研究，减重药的胃肠风险，罕见但真实当GLP-1受体激动剂被数亿人当成“减肥神药”之后，不列颠哥伦比亚大学Mahyar Etminan团队开展了一项研究。他们专门盯着非糖尿病人群——因为糖尿病本身就和胃肠病纠缠不清，在糖友身上看到的副作用，分不清是药还是病。此前随机对照试验虽然证实了减重效果，但样本量和随访时间都不够捕捉罕见事件。研究设计挺巧妙：把新用司美格鲁肽或利拉鲁肽的人，和新用安非他酮-纳曲酮（非GLP-1类减重药）的人做对比。他们筛掉所有有糖尿病记录的人，最终锁定4144名利拉鲁肽使用者、613名司美格鲁肽使用者、654名对照使用者，追踪了肠梗阻、胃轻瘫、胰腺炎及胆道疾病四种副作用。肠梗阻在利拉鲁肽组为每1000人年8.1例，对照组1.7例；胃轻瘫在司美格鲁肽组为9.1例，利拉鲁肽组7.3例，对照组3.1例。与对照组相比，肠梗阻风险增加4倍多，胃轻瘫接近3.7倍。胰腺炎和胆道疾病也有信号，但发生率更低，不如肠道这两项突出。虽然换算一下绝对发生率不算高，约等于每两百个人用药一年，还不到一个人会遇到这类问题。但客观问题是，用药的人太多了，低概率乘上亿级基数，还是需要重视起来。图1 · 减重用GLP-1的真实世界研究，设计、对照与四类胃肠道结局的风险读数图：Sodhi 2023（JAMA）研究设计与风险读数示意图；数据来源PharMetrics Plus数据库。 02 《Scientific Reports》动物研究，乳酸菌素片或可打破肠易激“脑肠失调”恶性循环在看完减重药的罕见副作用外，我们回来看看减重用药期的常见副作用。腹痛、腹胀、排便不规律，这些症状和一种常见的功能性肠病——肠易激综合征（irritable bowel syndrome，简称IBS）——症状高度相关。在全球范围内，肠易激综合征的患病率约为4%，腹痛、排便异常反复纠缠，还常与焦虑、抑郁绑定。近日，来自现代化国家重点实验室（江中药业）的刘文俊团队与李琼团队在Scientific Reports上发表了一项研究，为破解这一困境提供了一种新思路。研究团队以江中乳酸菌素片为工具，发现其不仅能显著降低大鼠的内脏高敏感和肠道动力紊乱，还能改善其焦虑抑郁样行为，背后的机制与调节肠道菌群和抑制肠道炎症密切相关。研究者先用醋酸灌肠加束缚应激把大鼠造成肠易激模型，再连续两周给乳酸菌素片，每天0.84克每公斤。结果，模型大鼠肠道对扩张刺激的敏感阈值回升，过快的推进率也降下来了——核心症状改善很明确。行为学上更有意思：模型大鼠活动减少、对糖水兴趣下降，给药后探索欲和偏好都回来了。不管是肠道还是情绪，都轻松了不少。肠壁层面也有变化。黏蛋白2（MUC2）表达上调，紧密连接蛋白claudin-1和occludin回升，结肠组织损伤减轻。菌群层面，造模让丰富度和均匀度下降，厚壁菌门与拟杆菌门比值升高；给药后这些指标往回走。具体菌属里，产丁酸的毛螺菌科NK4A136群丰度回升，气球菌属、肠球菌属、葡萄球菌属三类条件致病菌下降。结肠转录组显示，Ccl4、Il17c、Il12rb2等炎症相关基因表达下调。这构筑了一条清晰的逻辑链：乳酸菌素片通过调节肠道菌群，进而抑制了肠道的异常免疫激活和炎症反应，最终保护了肠道屏障——外周的炎症信号轻了，中枢的情绪行为也可能跟着放松。这项研究首次系统性地揭示了乳酸菌素片作为一种后生元，在改善IBS方面的多重药效及潜在机制。图2 · 肠易激模型中，乳酸菌素片养菌、紧屏障、降炎症、松脑肠图：设计基于 Fan 2025（Sci Rep）数据原创绘制；机制数据来自动物实验，人体验证仍待补充。图3 · 乳酸菌素片两周干预，把内脏敏感与肠推进率往回拉论文原图：Fan 2025，Figure 1，AWR 容量阈值（A）与肠推进率（B）；Control 对照、IBS 模型、IBS+LH 干预；动物模型线索，尚待人体研究验证。 03 罕见风险要认得，日常肠道要管住对正在用减重药的人来说，第一篇研究提醒你：肠梗阻、胃轻瘫这类事件虽然绝对发生率不高，但用药基数大，如果出现了持续腹痛、反复呕吐、排便习惯突然改变——别犹豫，马上联系医生。第二篇研究则给出了另一个角度的提示：乳酸菌素片可以通过“养菌”帮助肠道菌群恢复平衡、修复肠道屏障，从而改善肠道和情绪状态。按现行说明书，乳酸菌素片改善肠道环境是通过保护促进有益菌生长，并在肠道形成保护层，阻止有害菌的侵袭。总的来说，用药期间的肠道日常调理，可以分三步：第一，顺着胃肠节奏养护菌群。GLP-1类药物会延缓胃排空、减慢肠道推进，菌群的环境也会跟着变。用药期间要时刻关注肠道反应，像便秘这类日常范围内的小幅波动，不要等它拖成明显紊乱再处理。可以适当补充乳酸菌素片，通过保护和促进有益菌生长，帮助菌群在肠道节律变慢的情况下也不容易紊乱、失衡。第二，修复屏障，帮助肠黏膜抗住刺激。减重用药期间，肠道副作用会打乱原有的节律，黏膜受力不均匀，屏障就容易变松，细菌和毒素更容易往里钻。乳酸菌素片能在肠道表面形成一层保护膜，减少病原菌和病毒对肠壁的直接刺激；同时选择性抑制致病菌，给有益菌腾出生存空间，帮助菌群恢复平衡；还会刺激肠道分泌抗体，增强局部免疫力。再加上它调节肠黏膜电解质和水分平衡、促进胃液分泌，减重药引起的腹胀、排便异常也会跟着减轻。第三，症状要分个轻重。像排便偏慢、肚子偶尔胀这种时好时坏的情况，记下来，边调整边观察就行；但如果是持续腹痛、反复呕吐这种信号，就别犹豫，直接联系医生。说到底，减重靠的是药物、饮食、肠道状态一起使劲。《JAMA》披露的罕见事件是减重路上必须知道的底线风险，虽然不常见，但你要能认出来；江中乳酸菌素片则是日常可以发力的地方。排便和肠道的日常波动，靠日常管理慢慢调。体重管理这场长跑，肠道就是跑道。但如果出现这些情况，别自己硬扛：症状持续加重，或者明显脱水；肚子剧烈或持续地疼；头晕乏力、尿量明显变少；便血、黑便，或者症状突然变重。只要出现任何一种，马上联系医生，或者直接去医院，交给专业的人来判断，不能自己随便停药或改剂量。本文仅用于医学科普，不替代医生诊断和个体化用药建议。具体用药请以药品说明书及医生、药师指导为准。参考文献 [1] Sodhi M, Rezaeianzadeh R, Kezouh A, Etminan M. Risk of gastrointestinal adverse events associated with glucagon-like peptide-1 receptor agonists for weight loss. JAMA. 2023;330(18):1795-1797. PMID:37796527. doi:10.1001/jama.2023.19574。 [2] Fan H, Zhan Y, Cheng X, et al. Lacidophilin tablets relieve irritable bowel syndrome in rats by regulating gut microbiota dysbiosis and intestinal inflammation. Sci Rep. 2025;15:8151. PMID:40059226. doi:10.1038/s41598-025-91883-3。审校：Yuki 排版：Zelda 执行：Zelda 本平台旨在为医疗卫生专业人士传递更多医学信息。本平台发布的内容，不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议。如该等信息被用于了解医学信息以外的目的，本平台不承担相关责任。本平台对发布的内容，并不代表同意其描述和观点。若涉及版权问题，烦请权利人与我们联系，我们将尽快处理。

2026-10-16

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15 亿美元！阿斯利康掉头重寻疾病靶点

正文共：3000字预计阅读时间：8分钟 “外面全是竞品，我们快速推进管线啊！” 阿斯利康：“推不了。” “为什么？股东，投资者，同行们都在盯着呢？” 阿斯利康：“要稳，宁可慢一点，也不能坏了规矩。” “你不怕别人项目快速上市，抢占市场吗？” 阿斯利康：“怕，但更怕推得太快，没效果，怕账算不清。” “你还是一如既往的稳，跟着你干不烧心！” 2026年10月15日，阿斯利康与AI制药公司Insitro达成研发合作，聚焦MASH和心肌病两大疾病领域。 Insitro将运用其Virtual Human™（虚拟人类）平台解析疾病致病生物学，识别高置信度靶点；阿斯利康将负责候选靶点后续全部临床开发、监管申报与商业化工作。作为回报，Insitro将获得4000万美元首付款，最高约14.6亿美元的里程碑付款，以及个位数百分比的销售分成。在这笔交易中，最关键的并非是账面金额，而是阿斯利康愿意花15亿美元用AI去找疾病靶点这件事本身。 MASH和心肌病早不是空白赛道。 MASH领域，Madrigal的Rezdiffra于2024年获FDA批准，成为首个获批的MASH疗法；诺和诺德的司美格鲁肽（Wegovy）随后于2025年获批用于MASH伴中度至重度肝纤维化。此后GLP-1药物蜂拥涌入，MASH成为必争之地。心肌病领域，辉瑞的氯苯唑酸（Vyndaqel/Vyndamax）于2019年获批用于ATTR-CM，BMS的玛伐凯泰（Camzyos）于2022年获批用于梗阻性肥厚型心肌病，赛诺菲的阿夫凯泰（Aficamten）于2025年获FDA批准。后来者更是有Braveheart、恒瑞等选手紧追不舍。阿斯利康若在这两大领域从零开始，实属不智。实际上，阿斯利康在这两大领域早有涉足，只是跌了跟头。2025年11月，阿斯利康与Ionis合作开发的MASH候选药物AZD2693，因Ⅱ期试验未达预期被终止；而此前与Ionis共同开发的Wainua（依普特森），在2023年获批治疗遗传性转甲状腺素蛋白淀粉样变性多发性神经病（hATTR-PN）后，冲刺ATTR-CM适应症的Ⅲ期试验，最终以风险比1.14、心血管死亡与复发事件发生率反而高出对照组14%的成绩宣告失败。目前，阿斯利康仍保留MASH方向Ⅰ期抗纤维化资产AZD2389，心肌病领域R14del型扩张型心肌病候选药AZD4063。但接连的临床失利，让阿斯利康意识到：新药研发，找对疾病机制远比加速推进分子更重要。恰好，这正与Daphne Koller近年来最核心的主张高度契合。作为Insitro创始人兼CEO，斯坦福大学计算机科学系教授（26岁任职）、麦克阿瑟“天才奖”得主（36岁）、美国工程院及美国艺术与科学院双院士、Coursera联合创始人、连续创业者。 Daphne Koller个人光环众多。2018年，她投身AI制药，创立Insitro。公司累计融资超7.5亿美元，成为AI制药赛道融资最高的公司之一。她在近期的一个专栏采访中表示，AI在药物研发中的最大价值，不在于更快地制造分子，而在于帮助人们发现正确的疾病机制。在她看来，当前AI制药的四种主流叙事（超级智能万能论、AI分子设计工具、虚拟细胞、AI自主实验室）均存在关键陷阱，它们共同建立在一个被证伪的假设之上：我们对人类生物学已经了解得足够透彻。好像，只要有一个足够聪明的推理者，就能在已有知识库中找到治愈一切的答案。但事实却是，现代医学对大多数人类疾病的理解，用“盲人摸象”来概括最为贴切。 Daphne Koller给出具体数据，超过90%的药物在进入临床试验后失败，且这个数字几十年来几乎没有改善；在绝大多数失败案例中，分子设计本身没有问题，问题出在它所靶向的机制是错的。 "我们制造钥匙的技术相当不错，但这些钥匙通常打不开正确的锁。" 她认为，AI 即便能以更快的速度造出更好的钥匙，也无法提高我们识别正确锁的能力。而这，正是阿斯利康目前所需要的：不是更快的分子设计工具，而是对疾病机制的更深刻理解。 Insitro做的，就是用人类数据证明因果关系。 Insitro的Virtual Human平台，定位是“遗传锚定的因果AI引擎”。其逻辑并不算复杂：从UK Biobank等大型队列的人群遗传与影像数据中锁定候选基因，再用 iPSC分化的人源肝细胞、心肌细胞、神经元做实验，通过CRISPR敲低、高内涵成像等手段观察表型变化，从而把 "相关" 推进为 "因果"。这类整合人类遗传锚点、人源细胞表型、基因扰动因果证据、多组学对齐的数据集，构建门槛极高。不是网上爬文献能拼出来的，也不是买几张芯片就能补上的。目前，这条技术路径，已在Insitro自研管线中呈现初步结果： MASH方向，他们从480个肝脂肪相关遗传信号中筛出IRS1，发现其与纤维化的关联，在排除肝脂肪影响后依然存在：即IRS1可能不仅是“降脂靶点”，还可能独立抗纤维化。候选分子CTRO-1013（肝靶向siRNA沉默IRS1）已在小鼠模型中显示降脂与降纤维化标志物的双重信号。肥胖方向，Insitro从UK Biobank近7万人的MRI影像中提取棕色脂肪表型，通过GWAS找到新位点。小鼠实验中敲低该靶点4周，体重下降15%、脂肪量下降25%，且不掉肌肉、不影响进食。关键是，该靶点通过外周产热发挥作用，作用机制与GLP-1减重通路完全正交。这些项目的共同特点，是都经过了“人类遗传证据→人类细胞验证→体内功能确认”的闭环。这种机遇，也并非只有阿斯利康看重。 2019年，Insitro与吉利德达成肝病药物合作（1500万美元首付+10亿美元里程碑）；2020年，又与BMS达成ALS和额颞叶痴呆相关合作（5000万美元首付，总金额超21亿美元），且多年来续签并扩大合作范围；2024年，礼来也与其达成合作，合作把TuneLab ADMET模型开放给整个生物技术社区。 2026年9月，麦肯锡发布了一份让AI制药行业报告，回答了一个核心问题：钱投去了哪？ 2025年，全球AI药物发现领域的融资达到84.0亿美元，较2023年的41.0亿美元翻了一倍，年复合增长率43.0%。但钱的流向，比钱的规模更值得细看。大部分流向了数据最成熟、工具最完善的分子设计领域，而最难、最关键的靶点识别和临床前转化环节几乎无人问津。麦肯锡把这称为“资本-科学悖论”：资本追随技术的确定性，但生物学的困难度被留在了原地。为什么钱扎堆在分子设计？因为该环节成熟度最高，有结构化数据和快速实验反馈。三个研发环节的 AI 成熟度差异：分子设计最高，临床前转化最低（图源：麦肯锡报告，BioTender 制图）反观，生物学与靶点发现属于中成熟度环节。不仅周期长，AI靶点模型还很难区分“因果关系”和“统计相关性”，容易把观察到的相关误判为疾病驱动因素。方向错了，分子优化得再好也只是在加速失败。麦肯锡报告揭示的“资本-科学悖论”，恰恰回答了阿斯利康这笔交易的核心。这既是Insitro的价值，用人类数据把“靶点为什么成立”讲清楚。这条路比分子设计更难、更慢、反馈循环更长，但一旦走通，带来的临床获益也更大。参考资料： 1.AstraZeneca bulks up MASH, cardio work in up to $1.5B AI partnership with insitro（BioSpace） 2.AstraZeneca inks $1.5B insitro deal for AI-enabled target discovery of liver, heart disease drugs（Fierce Pharma） 3.麦肯锡：AI 制药的 84 亿美元，投错了地方（BioTender） 4.重磅！AI制药独角兽创始人反思：行业该醒醒了，真正瓶颈不在“造分子”！（药智网） 5.Insitro AI制药路线深度剖析：因果生物学重写靶点发现，英矽智能走在国内前面（研究僧随笔） 6.AI 制药指南：算法、实验能力与产业兑现（招财小黄鸭） 7.其他公开资料图片来源：即梦AI 超20亿美元！又一家MNC入股AI，探寻渐冻症新靶点 2025-10-16 制药巨子BMS牵手机器学习新贵Insitro，双方将碰撞出怎样的火花？ 2020-10-31 1.5亿美元！吉利德大手笔！与AI明星公司Insitro强强联手主攻NASH！ 2019-04-17 版权声明/免责声明本文为原创文章。本文仅作信息交流之目的，不提供任何商用、医用、投资用建议。文中图片、视频、字体、音乐等素材或为药时代购买的授权正版作品，或来自微信公共图片库，或取自公司官网/网络，部分素材根据CC0协议使用，版权归拥有者，药时代尽力注明来源。如有任何问题，请与我们联系。衷心感谢! 药时代官方网站:www.drugtimes.cn 联系方式: 电话:13651980212 微信:27674131 邮箱:contact@drugtimes.cn 点击查看更多精彩内容！

2026-10-16

·Firstwordpharma

Lilly's weight-loss pill Foundayo gets backing from EU regulator

Eli Lilly's Foundayo (orforglipron) looks set to be the second oral GLP-1 receptor agonist cleared in the EU after the EMA's Committee for Medicinal Products for Human Use (CHMP) recommended approval for weight management and the treatment of type 2 diabetes in adults.In July, the pill version of Novo Nordisk's Wegovy (semaglutide) became the first oral GLP-1 receptor agonist approved in the EU, gaining authorisation for the treatment of adults with obesity or overweight with at least one weight-related comorbidity. And the availability of an oral option has been strongly welcomed by doctors in the region; see — Physician Views Results: If Novo navigates access, the European appetite for Wegovy pill is significant.Lilly will also be hoping it can tap into this enthusiasm, especially as the launch of Foundayo in the US following its FDA approval in April has been somewhat muted. Second-quarter sales of the oral weight loss drug reached $98 million, below analysts forecasts of around $105.6 million, although the company has pointed to signs of an inflection.On Friday, the EMA announced the CHMP's positive decision for Foundayo, which for weight management is based on two studies involving more than 4740 adults with obesity or overweight. Results showed that after 72 weeks, participants treated with Foundayo lost around 5% to 11% of their body weight, depending on the dose they took, compared with around 2% to 2.5% in those on placebo.The CHMP's recommendation in weight management covers the use of Foundayo alongside a healthy diet and physical activity in adults with obesity or overweight who have at least one weight-related health problem. Meanwhile, for type 2 diabetes, Foundayo is to be used alongside a healthy diet and physical activity in adults with type 2 diabetes whose blood glucose levels are not sufficiently controlled.The CHMP's decision in type 2 diabetes was based on four studies involving 3765 adults whose blood glucose was not adequately controlled with diet and physical activity alone or with other diabetes medicines. Across the trials, Foundayo reduced HbA1c by around 1.2 to 1.9 percentage points, depending on the dose received.

临床结果上市批准

100 项与司美格鲁肽 (诺和诺德) 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D10025	司美格鲁肽 (诺和诺德)	A10BJ06	DB13928

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
心脏病	英国	Novo Nordisk A/S	2026-04-01
肝纤维化	美国	Novo Nordisk, Inc.	2025-12-22
肺纤维化	加拿大	Novo Nordisk Canada, Inc.	2025-12-21
代谢功能障碍相关脂肪性肝炎	美国	Novo Nordisk A/S	2025-08-15
代谢功能障碍相关脂肪性肝炎	美国	Novo Nordisk, Inc.	2025-08-15
慢性肾病	美国	Novo Nordisk A/S	2025-01-28
慢性肾病	美国	Novo Nordisk, Inc.	2025-01-28
脑卒中	澳大利亚	Novo Nordisk Pharmaceuticals Pty Ltd.	2024-12-16
心肌梗塞	加拿大	Novo Nordisk Canada, Inc.	2024-11-27
心血管疾病	美国	Novo Nordisk, Inc.	2024-03-08
肥胖	美国	Novo Nordisk, Inc.	2021-06-04
超重	美国	Novo Nordisk, Inc.	2021-06-04
2型糖尿病	美国	Novo Nordisk, Inc.	2017-12-05

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
白蛋白尿	临床3期	加拿大	Novo Nordisk A/S	2022-03-14
白蛋白尿	临床3期	德国	Novo Nordisk A/S	2022-03-14
白蛋白尿	临床3期	荷兰	Novo Nordisk A/S	2022-03-14
白蛋白尿	临床3期	西班牙	Novo Nordisk A/S	2022-03-14
膝关节炎	临床3期	美国	Novo Nordisk A/S	2021-10-01
膝关节炎	临床3期	加拿大	Novo Nordisk A/S	2021-10-01
膝关节炎	临床3期	哥伦比亚	Novo Nordisk A/S	2021-10-01
膝关节炎	临床3期	丹麦	Novo Nordisk A/S	2021-10-01
膝关节炎	临床3期	法国	Novo Nordisk A/S	2021-10-01
膝关节炎	临床3期	挪威	Novo Nordisk A/S	2021-10-01

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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


NCT06041217 (STEP 12, Pubmed \| Lancet Diabetes Endocrinol)	临床3期	超重 \| 肥胖	242	Semaglutide 2.4 mg	積醖憲醖鑰衊鑰壓衊夢(網簾齋夢膚簾壓構願範) = 糧艱蓋願窪構餘鑰構襯膚衊艱範構夢衊醖積鑰 (膚壓衊鏇願鹽願壓願醖 )	积极	2026-10-01
				Placebo	積醖憲醖鑰衊鑰壓衊夢(網簾齋夢膚簾壓構願範) = 廠構醖鹹顧構廠鑰網鏇膚衊艱範構夢衊醖積鑰 (膚壓衊鏇願鹽願壓願醖 )
REVEAL-1 (EASD2026)	N/A	肥胖	231,442	GLP-1RA-naïve initiators	襯糧獵糧鏇遞糧獵鑰衊(獵鏇構範選遞膚蓋廠製) = 網糧襯簾繭蓋夢願選淵獵製獵構繭窪鬱選觸鑰 (選糧壓願廠鹹網艱鬱壓 ) 更多	积极	2026-09-28
EASD2026	N/A	2型糖尿病	5,326	Semaglutide users	-	积极	2026-09-28
				Non-semaglutide users	鑰鏇淵築簾醖積齋壓壓(窪壓壓願糧觸窪醖鹽壓) = 製淵鏇壓膚鹹襯襯鑰構構糧鏇積鹹衊獵鏇鏇遞 (網鑰顧鹽淵顧憲觸膚襯 )
OCTANE (EASD2026)	N/A	超重 \| 肥胖	194	oral semaglutide	範窪夢餘艱壓範鏇夢範(積繭醖積膚鑰製範壓鬱) = 夢艱繭淵鹹膚簾鬱廠淵網膚獵遞衊壓簾窪齋鏇 (糧壓鹹淵淵齋構構觸膚, 1.4) 更多	积极	2026-09-28
SUSTAIN FORTE (EASD2026)	临床3期	2型糖尿病	961	Semaglutide 2.0 mg	遞衊膚構醖遞選鑰構構(觸遞鬱壓廠膚餘醖衊鬱) = 繭齋餘膚願鏇襯鏇構鏇構淵網襯夢衊願鹹膚壓 (醖廠鹽顧遞艱艱獵製鏇 ) 更多	积极	2026-09-28
				Semaglutide 1.0 mg	遞衊膚構醖遞選鑰構構(觸遞鬱壓廠膚餘醖衊鬱) = 鑰築顧積簾鏇襯顧夢範構淵網襯夢衊願鹹膚壓 (醖廠鹽顧遞艱艱獵製鏇 ) 更多
EASD2026	N/A	2型糖尿病	636,525	escalating to semaglutide 2.0 mg	獵鑰鹹簾齋膚網醖獵獵(醖醖積窪餘顧顧鬱餘範): HR = 1.06 (95.0% CI, 1.04 ~ 1.08), P-Value = 0.005 更多	不佳	2026-09-28
				switching to tirzepatide
EASD2026	N/A	2型糖尿病	6,616	Semaglutide (Adherers)	艱獵鏇選憲壓艱獵遞鹽(艱蓋簾顧鑰範簾壓膚襯) = Gastrointestinal disorders were the most frequent safety events, with higher rates observed in early discontinuers (semaglutide 23.5/100 PY; dulaglutide 26.1/100 PY) than adherers (semaglutide 13.8/100 PY; dulaglutide 10.6/100 PY). 鑰製鬱蓋淵夢觸鏇製繭 (鏇鏇簾鹹鹽醖壓鬱膚齋 ) 更多	积极	2026-09-28
				Dulaglutide (Adherers)
NCT06299098 (COURAGE, EASD2026)	临床2期	肥胖	975	Trevogrumab 25 mgSemaglutide + Trevogrumab 25 mgSemaglutide 25 mg	鏇簾獵獵淵鏇壓鏇衊衊(遞鏇淵襯膚鹽願糧壓鏇) = 廠獵遞鏇鏇鑰積鬱願夢餘鹽襯醖夢蓋膚築鏇廠 (鑰範遞獵壓鏇製壓餘夢, 0.71)	积极	2026-09-28
				Trevogrumab 75 mgSemaglutide + Trevogrumab 75 mgSemaglutide 75 mg	鏇簾獵獵淵鏇壓鏇衊衊(遞鏇淵襯膚鹽願糧壓鏇) = 範壓壓襯簾網衊壓壓襯餘鹽襯醖夢蓋膚築鏇廠 (鑰範遞獵壓鏇製壓餘夢, 0.74)
STEP UP (EASD2026)	临床3期	肥胖	1,407	Semaglutide 7.2 mg	簾糧醖繭願簾範範餘遞(觸積鬱簾鬱選網鏇憲鹹) = 糧構築鬱構壓艱醖鏇網鏇廠衊壓夢繭夢衊構膚 (鏇鑰衊鹽獵夢淵範積齋 )	积极	2026-09-28
				Semaglutide 2.4 mg	簾糧醖繭願簾範範餘遞(觸積鬱簾鬱選網鏇憲鹹) = 觸網餘網齋觸淵夢淵範鏇廠衊壓夢繭夢衊構膚 (鏇鑰衊鹽獵夢淵範積齋 )
NCT06351748 (SCHOLAR, Pubmed \| Diabetes Ther)	N/A	2型糖尿病	11,361	Semaglutide+SGLT2i	窪餘醖窪繭衊鹽衊廠廠(遞鏇遞窪醖夢窪艱襯觸) = Gastrointestinal adverse events were most frequent. 鑰窪憲餘遞鬱餘憲製鹹 (網遞願網願顧膚顧築廠 )	积极	2026-09-28