预约演示
更新于：2025-01-17
Mirikizumab
米吉珠单抗
更新于：2025-01-17
概要
基本信息
原研机构 |
非在研机构- |
最高研发阶段批准上市 |
首次获批日期 日本 (2023-03-27), |
最高研发阶段(中国)申请上市 |
特殊审评突破性疗法 (中国) |
登录后查看时间轴
结构/序列
Sequence Code 9007H
来源: *****
Sequence Code 9009L
来源: *****
关联
44
项与 米吉珠单抗 相关的临床试验NCT06598943
An Adaptive, Dose-Ranging, Phase 2 Study of Eltrekibart Given Alone or in Combination With Mirikizumab for the Treatment of Adult Patients With Moderately to Severely Active Ulcerative Colitis
NCT06626165
Mirikizumab Therapy is Effective for Patients with Moderate to Severe Ulcerative Colitis Patients Whose Geboes Score Grade is ≥3.2) on Endoscopic Biopsy
NCT06475729
A Bioequivalence Study of Subcutaneous Injections of Citrate-Free Mirikizumab Solution Using a 1-mL Autoinjector and an Investigational 2-mL Autoinjector in Healthy Participants
100 项与 米吉珠单抗 相关的临床结果
登录后查看更多信息
100 项与 米吉珠单抗 相关的转化医学
登录后查看更多信息
100 项与 米吉珠单抗 相关的专利（医药）
登录后查看更多信息
237
项与 米吉珠单抗 相关的文献（医药）2025-04-01COLLOIDS AND SURFACES B-BIOINTERFACES
Platelet-mimicking nanoparticles loaded with diallyl trisulfide for Mitigating Myocardial Ischemia‐Reperfusion Injury in rats
Article
作者: Gao, Tang ; Xu, Lingling ; Fu, Wenpei ; Xu, Chunyan ; Wu, Wenqian ; Xie, Mingxing ; Dong, Xiaoqiu ; Bai, Ying ; Jin, Qiaofeng ; Wang, Jing ; Zhang, Li ; Chen, Yihan ; Lv, Qing ; Yang, Yali ; Lin, Ling ; Huang, Tian
Hydrogen sulfide (H2S) shows promise in treating myocardial ischemia-reperfusion injury (MIRI), but the challenge of controlled and sustained release hinders its clinical utility. In this study, we developed a platelet membrane-encapsulated mesoporous silica nanoparticle loaded with the H2S donor diallyl trisulfide (PM-MSN-DATS). PM-MSN-DATS demonstrated optimal encapsulation efficiency and drug-loading content. Comprehensive in vitro and in vivo assessments confirmed the biosafety of PM-MSN-DATS. In vitro, PM-MSN-DATS adhered to inflammation-activated endothelial cells and exhibited targeted accumulation in MIRI rat hearts. In vivo experiments revealed significant reductions in reactive oxygen species (ROS) and myocardial fibrosis area, improving cardiac function. Our findings highlight successfully creating a targeted H2S delivery system through platelet membrane-coated MSN nanoparticles. This well-designed drug delivery platform holds significant promise for advancing MIRI treatment strategies.
2025-01-01JOURNAL OF ETHNOPHARMACOLOGY
Dehydrocorydaline attenuates myocardial ischemia-reperfusion injury via the FoXO signalling pathway: A multimodal study based on network pharmacology, molecular docking, and experimental study
Article
作者: Chen, Keji ; Renfeng, Li ; Keji, Chen ; Zucheng, Shang ; Hua, Qu ; Lin, Guosheng ; Li, Mengfan ; Daxin, Chen ; Zhi, Guo ; Zikai, Yu ; Wenwen, Yang ; Qu, Hua ; Li, Renfeng ; Shen, Aling ; Meizhu, Wu ; Guosheng, Lin ; Guo, Zhi ; Mengfan, Li ; Chen, Daxin ; Hongzheng, Li ; Yang, Wenwen ; Aling, Shen ; Shang, Zucheng ; Yingdong, Lu ; Wu, Meizhu ; Li, Hongzheng ; Lu, Yingdong ; Fu, Changgeng ; Yu, Zikai ; Changgeng, Fu
ETHNOPHARMACOLOGICAL RELEVANCE:
Dehydrocorydaline (DHC), an active component of Corydalis yanhusuo (Y.H. Chou & Chun C. Hsu) W.T. Wang ex Z.Y. Su & C.Y. Wu (Papaveraceae), exhibits protective and pain-relieving effects on coronary heart disease, but the underlying mechanism still remains unknown.
AIM OF THE STUDY:
Network pharmacology and experimental validation both in vivo and in vitro were applied to assess whether DHC can treat myocardial ischemia-reperfusion injury (MIRI) by regulating the forkhead box O (FoxO) signalling pathway to inhibit apoptosis.
MATERIALS AND METHODS:
DHC and MIRI targets were retrieved from various databases. Molecular docking and microscale thermophoresis (MST) determined potential binding affinity. An in vivo mouse model of MIRI was established by ligating the left anterior descending coronary artery. C57BL/6N mice were divided into sham, MIRI, and DHC (intraperitoneal injection of 5 mg/kg DHC) groups. Haematoxylin and eosin, Masson, and immunohistochemical stainings verified DHC treatment effects and the involved signalling pathways. In vitro, H9c2 cells were incubated with DHC and underwent hypoxia/reoxygenation. TUNEL, JC-1, and reactive oxygen species stainings and western blots were used to explore the protective effects of DHC and the underlying mechanisms.
RESULTS:
Venny analysis identified 120 common targets from 121 DHC and 23,354 MIRI targets. DHC exhibited high affinity for CCND1, CDK2, and MDM2 (<-7 kcal/mol). In vivo, DHC attenuated decreases in left ventricular ejection fraction and fractional shortening, reduced infarct sizes, and decreased cTnI and lactate dehydrogenase levels. In vitro, DHC alleviated apoptosis and oxidative stress in the hypoxia/reoxygenation model by attenuating ΔΨm disruption; reducing the production of reactive oxygen species; upregulating Bax and CCND1 via the FoxO signalling pathway, as well as cleaved-caspase 8; downregulating the apoptosis-associated proteins Bcl-2, Bid, cleaved-caspase 3, and cleaved-caspase 9; and promoting the phosphorylation of FOXO1A and MDM2.
CONCLUSION:
By upregulating the FoxO signaling pathway to inhibit apoptosis, DHC exerts a cardioprotective effect, which could serve as a potential therapeutic option for MIRI.
2025-01-01LANCET
Guselkumab in patients with moderately to severely active ulcerative colitis (QUASAR): phase 3 double-blind, randomised, placebo-controlled induction and maintenance studies
Article
BACKGROUND:
Interleukin-23 inhibition is effective in treating ulcerative colitis. Guselkumab is a dual-acting, human IgG1, interleukin-23p19 subunit inhibitor that potently neutralises interleukin-23 and can bind to CD64. We aimed to evaluate the efficacy and safety of guselkumab as induction and maintenance therapy in patients with ulcerative colitis.
METHODS:
The primary populations of these two phase 3, randomised, double-blind, placebo-controlled studies (QUASAR phase 3 induction and maintenance) included randomised and treated adults with moderately to severely active ulcerative colitis (induction baseline modified Mayo score from 5 to 9) with inadequate response or intolerance to conventional or advanced ulcerative colitis therapy. Patients were randomly assigned (3:2) to receive guselkumab 200 mg given intravenously or placebo at weeks 0, 4, and 8 (phase 3 induction study). All patients were randomly assigned using web-based interactive response technology. Patients in clinical response 12 weeks after guselkumab induction given intravenously (from QUASAR phase 2b and phase 3 induction studies) were randomly assigned (1:1:1) at maintenance week 0 to guselkumab 200 mg given subcutaneously every 4 weeks or 100 mg every 8 weeks or placebo for 44 weeks (maintenance). Primary endpoints were clinical remission at induction week 12 and maintenance week 44. This study is registered with ClinicalTrials.gov, NCT04033445.
FINDINGS:
The induction study primary population included 701 patients (guselkumab 200 mg given intravenously 60% [421 patients]; placebo 40% [280 patients]). The maintenance study primary population included 568 guselkumab induction responders randomly assigned to receive guselkumab 200 mg given subcutaneously every 4 weeks (190 [33%] patients) or 100 mg every 8 weeks (188 [33%] patients) or placebo (guselkumab withdrawal 190 [33%] patients). A significantly greater proportion of patients treated with guselkumab given intravenously had clinical remission at induction week 12 (23% [95 of 421 patients]) than did placebo-treated patients (8% [22 of 280 patients]; adjusted treatment difference 15%, 95% CI 10-20; p<0·0001). Clinical remission at maintenance week 44 was achieved by a significantly greater proportion of patients treated with guselkumab 200 mg given subcutaneously every 4 weeks (50% [95 of 190 patients]; adjusted treatment difference 30%, 95% CI 21-38; p<0·0001) and 100 mg every 8 weeks (45% [85 of 188 patients]; adjusted treatment difference 25%, 16-34; p<0·0001) than with placebo (19% [36 of 190 patients]). The overall safety profile was favourable and consistent with that of guselkumab in approved indications. In the induction study, adverse events were reported by 49% of patients in both groups (208 of 421 guselkumab-treated patients and 138 of 280 placebo-treated patients), serious adverse events were reported by 3% (12 of 421) of guselkumab-treated patients and 7% (20 of 280) of placebo-treated patients, and adverse events leading to treatment discontinuation were reported by 2% (seven of 421) of guselkumab-treated patients and 4% (11 of 280) of placebo-treated patients. In the maintenance study, adverse event rates were similar among groups, and the most frequently reported adverse events in all groups were ulcerative colitis, COVID-19, and arthralgia. No active tuberculosis, anaphylaxis, serum sickness, or clinically important hepatic disorders were reported in either study.
INTERPRETATION:
Guselkumab was effective and safe as induction and maintenance therapy in patients with moderately to severely active ulcerative colitis.
FUNDING:
Janssen Research and Development.
253
项与 米吉珠单抗 相关的新闻（医药）2025-01-17
·抗体圈
免疫疗法疫苗细胞疗法核酸药物基因疗法
2025-01-16
并购抗体药物偶联物免疫疗法细胞疗法疫苗
2025-01-16
·贝壳社
并购疫苗细胞疗法免疫疗法抗体药物偶联物
100 项与 米吉珠单抗 相关的药物交易
登录后查看更多信息
研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
登录
| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 活动性中度克罗恩病 | 美国 | 2025-01-15 | |
| 活动性重度克罗恩病 | 美国 | 2025-01-15 | |
| 活动性中度溃疡性结肠炎 | 欧盟 | 2023-05-26 | |
| 活动性中度溃疡性结肠炎 | 冰岛 | 2023-05-26 | |
| 活动性中度溃疡性结肠炎 | 列支敦士登 | 2023-05-26 | |
| 活动性中度溃疡性结肠炎 | 挪威 | 2023-05-26 | |
| 活动性重度溃疡性结肠炎 | 欧盟 | 2023-05-26 | |
| 活动性重度溃疡性结肠炎 | 冰岛 | 2023-05-26 | |
| 活动性重度溃疡性结肠炎 | 列支敦士登 | 2023-05-26 | |
| 活动性重度溃疡性结肠炎 | 挪威 | 2023-05-26 | |
| 溃疡性结肠炎 | 日本 | 2023-03-27 |
未上市
10 条进展最快的记录, 后查看更多信息
登录
| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 克罗恩病 | 申请上市 | 美国 | 2024-04-30 | |
| 小儿克罗恩病 | 临床3期 | 美国 | 2024-03-13 | |
| 小儿克罗恩病 | 临床3期 | 日本 | 2024-03-13 | |
| 小儿克罗恩病 | 临床3期 | 奥地利 | 2024-03-13 | |
| 小儿克罗恩病 | 临床3期 | 比利时 | 2024-03-13 | |
| 小儿克罗恩病 | 临床3期 | 巴西 | 2024-03-13 | |
| 小儿克罗恩病 | 临床3期 | 加拿大 | 2024-03-13 | |
| 小儿克罗恩病 | 临床3期 | 法国 | 2024-03-13 | |
| 小儿克罗恩病 | 临床3期 | 以色列 | 2024-03-13 | |
| 小儿克罗恩病 | 临床3期 | 意大利 | 2024-03-13 |
登录后查看更多信息
临床结果
临床结果
适应症
分期
评价
查看全部结果
临床3期 | 1,158 | Placebo | 築壓鏇憲憲觸網築夢膚(憲衊選鬱繭鹹製鹽膚製) = 醖構繭選獵選簾鹹艱膚 憲鏇鹹鹹繭繭鹽衊鹽憲 (糧積製網積願繭選鏇獵, 艱選壓廠蓋簾遞獵鹹獵 ~ 網遞簾艱鏇夢築繭範顧) 更多 | - | 2024-12-27 | ||
临床3期 | - | 構夢窪顧鹽餘蓋觸遞廠(鬱鏇鹽鹽窪廠簾觸糧醖) = 憲範獵鏇糧糧鑰範艱蓋 網衊蓋獵鏇糧鏇壓醖醖 (艱襯鹽夢構齋醖鹽襯簾 ) 更多 | 积极 | 2024-10-28 | |||
临床3期 | 868 | (week 52 responders) | 遞構淵窪願淵網顧鏇鹽(獵淵顧鹹鬱淵選觸艱選) = 醖簾淵鏇糧鏇簾醖築襯 憲齋範選構壓鑰積衊網 (鑰鑰淵遞構顧廠繭夢願 ) 更多 | 积极 | 2024-10-25 | ||
(week 52 remitters) | 遞構淵窪願淵網顧鏇鹽(獵淵顧鹹鬱淵選觸艱選) = 觸鑰夢簾窪鑰築襯願鏇 憲齋範選構壓鑰積衊網 (鑰鑰淵遞構顧廠繭夢願 ) 更多 | ||||||
临床3期 | 溃疡性结肠炎 维持 | 868 | 餘齋夢衊淵簾構願觸遞(鹽淵範遞餘願願餘網網) = opportunistic infection (1.8%), hepatic disorders (3.2%), cerebrocardiovascular events (1.5%), and malignancy (0.3%) 衊壓築範網艱積醖繭蓋 (構窪鬱淵蓋選遞窪憲顧 ) 更多 | 积极 | 2024-10-25 | ||
临床3期 | - | 膚製鏇積製艱艱築顧醖(鹽糧鏇範壓鑰鹹鏇選醖) = 顧構繭製蓋鹹鬱蓋鑰範 構鑰齋鑰憲網鏇構觸襯 (窪鬱觸憲範鬱齋獵鏇範 ) 更多 | 积极 | 2024-10-15 | |||
Stelara (ustekinumab) | 膚製鏇積製艱艱築顧醖(鹽糧鏇範壓鑰鹹鏇選醖) = 積積醖鬱淵願壓觸襯構 構鑰齋鑰憲網鏇構觸襯 (窪鬱觸憲範鬱齋獵鏇範 ) 更多 | ||||||
N/A | - | Mirikizumab 300mg IV | 簾醖網蓋鏇築獵淵夢艱(範遞網鏇觸觸繭窪簾憲) = 窪觸齋壓構憲遞繭衊襯 廠餘網壓鬱襯廠鏇鹹壓 (膚築願醖淵膚膚糧餘範 ) 更多 | - | 2024-10-13 | ||
Placebo | 簾醖網蓋鏇築獵淵夢艱(範遞網鏇觸觸繭窪簾憲) = 獵衊鏇獵鬱繭遞鏇襯淵 廠餘網壓鬱襯廠鏇鹹壓 (膚築願醖淵膚膚糧餘範 ) 更多 | ||||||
N/A | - | Mirikizumab 300mg IV | 鑰艱鏇觸遞鏇淵淵糧構(觸蓋窪淵淵糧鹽遞衊膚) = 艱築鹹鑰壓夢糧繭繭醖 夢鑰糧繭鏇廠製衊範鬱 (膚願艱顧鹽積夢淵鏇鹹, 2.4) 更多 | - | 2024-10-13 | ||
N/A | - | 艱鑰窪齋遞醖窪網積廠(鏇廠構艱蓋獵鏇蓋齋窪) = 艱襯憲膚醖鹹壓餘製築 淵顧築醖襯衊範鬱窪襯 (選窪膚築醖窪鑰鑰鏇襯 ) 更多 | - | 2024-10-13 | |||
Placebo | 艱鑰窪齋遞醖窪網積廠(鏇廠構艱蓋獵鏇蓋齋窪) = 衊繭鑰齋餘夢願選構醖 淵顧築醖襯衊範鬱窪襯 (選窪膚築醖窪鑰鑰鏇襯 ) 更多 | ||||||
N/A | - | 積糧範襯衊範鏇襯範願(襯積構製構網膚願選獵) = The most common treatment-emergent adverse events (TEAEs) during induction period in miri-treated patients were COVID-19, anaemia and headache 夢鹹窪積積網廠構範鬱 (壓蓋鏇簾衊艱顧窪積範 ) 更多 | - | 2024-10-13 | |||
Placebo | |||||||
N/A | - | 積夢獵範願膚築齋獵築(糧簾築淵選醖廠顧餘餘) = 鬱築餘衊製壓襯鬱鏇網 簾範廠糧鹽積觸鹽網繭 (鹽廠衊襯壓積夢製繭蓋 ) 更多 | - | 2024-10-13 |
登录后查看更多信息
转化医学
使用我们的转化医学数据加速您的研究。
登录
或
药物交易
使用我们的药物交易数据加速您的研究。
登录
或
核心专利
使用我们的核心专利数据促进您的研究。
登录
或
临床分析
紧跟全球注册中心的最新临床试验。
登录
或
批准
利用最新的监管批准信息加速您的研究。
登录
或
特殊审评
只需点击几下即可了解关键药物信息。
登录
或
来和芽仔聊天吧
立即开始免费试用!
智慧芽新药情报库是智慧芽专为生命科学人士构建的基于AI的创新药情报平台，助您全方位提升您的研发与决策效率。
立即开始数据试用!
智慧芽新药库数据也通过智慧芽数据服务平台，以API或者数据包形式对外开放，助您更加充分利用智慧芽新药情报信息。
生物序列数据库
生物药研发创新
免费使用
化学结构数据库
小分子化药研发创新
免费使用