预约演示
更新于：2025-06-26
Mirikizumab
米吉珠单抗
更新于：2025-06-26
概要
基本信息
药物类型 单克隆抗体 |
别名 Anti-IL-23-MAb (Lilly)、IL-23p19 antibody、Miri + [7] |
靶点 |
作用方式 抑制剂 |
作用机制 IL-23p19抑制剂(白细胞介素-23亚单位p19抑制剂)、Inflammation mediators抑制剂(炎症介导素抑制剂) |
在研适应症 |
非在研适应症 |
原研机构 |
非在研机构- |
权益机构- |
最高研发阶段批准上市 |
最高研发阶段(中国)申请上市 |
特殊审评突破性疗法 (中国) |
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结构/序列
Sequence Code 9007H
来源: *****
Sequence Code 9009L
来源: *****
关联
43
项与 米吉珠单抗 相关的临床试验NCT06997965
An Open-label Single-arm Study to Assess the Efficacy of Mirikizumab in Patients With Inflammatory Strictures Due to Crohn's Disease
NCT06864403
Mirikizumab in the Treatment of Chronic Inflammatory Conditions of the Pouch
NCT06937099
A Phase 3b, Randomized, Multicenter, Controlled Study of Mirikizumab and Placebo or Mirikizumab Concomitantly Administered With Tirzepatide in Adult Participants With Moderately to Severely Active Crohn's Disease and Obesity or Overweight
100 项与 米吉珠单抗 相关的临床结果
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100 项与 米吉珠单抗 相关的转化医学
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100 项与 米吉珠单抗 相关的专利（医药）
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247
项与 米吉珠单抗 相关的文献（医药）2025-12-31REDOX REPORT
M6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury
Article
作者: Zhang, Feilong ; Chen, Lianglong ; Chen, Xuehai ; Gong, Kezeng ; Jiang, Qiong ; Xu, Zhe
OBJECTIVE:
Myocardial ischemia-reperfusion injury (MIRI) is a highly complex disease with high morbidity and mortality. Studying the molecular mechanism of MIRI and discovering new targets are crucial for the future treatment of MIRI.
METHODS:
We constructed the MIRI rat model and hypoxia/reoxygenation (H/R) injury cardiomyocytes model. RT-PCR and Western blot were used to investigate the expression of the fat mass and obesity-associated (FTO) gene. Electrocardiogram, echocardiography, triphenyltetrazolium chloride (TTC) staining and hematoxylin-eosin (HE) staining were used to assess the model and the effect of FTO overexpression. The generation of reactive oxygen species (ROS) and the levels of superoxide dismutase (SOD2), mitochondrial transcription factor (TFAM) and cytochrome c oxidase I (COXI) were detected to assess the oxidative stress and mitochondrial biogenesis. RNA immunoprecipitation (RIP) and RNA pulldown assays were used to identify the interaction of FTO and PGC-1a. The m6A dot blot, methylated RNA immunoprecipitation PCR (MeRIP-PCR) and RNA stability analysis were used to analyze the regulation of methylation of PGC-1a by FTO.
RESULTS:
FTO was downregulated in MIRI rats and H/R induced cardiomyocytes. Overexpression of FTO inhibited ROS level and increased the expression of SOD2, TFAM and COXI in vitro and in vivo. In addition, PGC-1a was identified as a downstream target of FTO. FTO enhanced the stability of PGC-1a mRNA through removing the m6A modification.
CONCLUSION:
Our study revealed the role of FTO regulates the oxidative stress and mitochondrial biogenesis via PGC-1a in MIRI, which may provide a new approach to mitigating MIRI.
2025-12-31JOURNAL OF MEDICAL ECONOMICS
Cost per remission for mirikizumab versus ustekinumab for moderately to severely active ulcerative colitis treatment from the United States commercial payer perspective
Article
作者: Upadhyay, Navneet ; Creveling, Thomas ; Fisher, Deborah A. ; Mittal, Neha ; Bires, Nicholas ; Chanan, Neha ; Kane, Sunanda ; Gulati, Ankit ; Koushik, Amit Kumar
INTRODUCTION:
Mirikizumab, approved for the treatment of moderately to severely active ulcerative colitis (UC), may be prescribed in a similar placement to ustekinumab in second-line settings. Payers may compare the economic value when making formulary decisions. This study estimated and compared the cost per remission of the second-line therapies mirikizumab versus ustekinumab in patients with UC.
METHODS:
An Excel-based analytic model was developed to estimate the cost per additional patient achieving clinical remission at the end of one year in biologic/Janus kinase inhibitor (JAKi)-experienced patients (second-line therapy) with UC from a United States commercial payer perspective. A network meta-analysis of published pivotal randomized clinical trials was used to derive the number needed to treat (NNT) for clinical response, clinical remission, and endoscopic remission/endoscopic improvement/mucosal healing for ustekinumab and mirikizumab in the study population. The model included the treatment cost (wholesale acquisition costs [WAC] and treatment administration costs) during the induction and maintenance phases. A scenario involving the availability of a ustekinumab biosimilar was also evaluated, assuming the NNT remained the same as ustekinumab but with a WAC set at 50% lower than its current WAC.
RESULTS:
The costs per patient achieving clinical remission for mirikizumab vs. ustekinumab as a second-line therapy were $461,096 vs. $67,273 during induction and $501,456 vs. $1,079,189 during maintenance. The cost per clinical remission in case of dose escalation during maintenance was lower for mirikizumab vs. ustekinumab ($501,456 vs. $1,569,127). Considering the ustekinumab 130 mg IV biosimilar, the scenario resulted in a lower cost per clinical remission for mirikizumab vs. a ustekinumab biosimilar during the maintenance phase ($501,456 vs. $539,594).
CONCLUSION:
Mirikizumab is projected to have a lower cost per remission during maintenance therapy than ustekinumab. Given the need for long-term treatment for this chronic condition, mirikizumab appears to be a cost-efficient treatment option.
2025-09-01BIOMATERIALS
Superoxide anion-responsive persulfide and all-trans retinoic acid co-donating peptide assemblies attenuate myocardial ischemia-reperfusion injury
Article
作者: Shao, Yiyang ; Zhang, Yanwen ; Zhao, Xueshan ; Wang, Yin ; Ge, Yuxuan ; Lu, Yujia ; Wu, Shiqi ; Gu, Jun
Myocardial ischemia-reperfusion injury (MIRI) has become a severe threat to human health due to its high mortality rate and poor prognosis. Mutually entangled issues including ROS over-production, excessive inflammatory responses, and myocardial apoptosis are involved during MIRI. Effective inhibition of ROS burst at the beginning of reperfusion has been proved as the key for MIRI treatment. In this work, we report a superoxide anion-responsive peptide co-assembly (S/A-P) capable of delivering the H2S donor (i.e., superoxide-responsive persulfide donor) and all-trans retinoic acid (ATRA) simultaneously for the treatment. Our results suggest that compared with its single peptidic counterparts, the as-prepared system can significantly lower ROS production and repair myocardial mitochondrial dysfunction due to the synergy effect from the persulfides/H2S and ATRA. Moreover, S/A-P can reduce excessive inflammatory response through regulating macrophage polarization, which is further mapped by RNA sequencing. In vivo assessment of the co-assembly also displays an excellent therapeutic effect of MIRI on rats. In terms of good biocompatibility and outstanding efficacy, we believe that S/A-P will have a bright future for the treatment of cardiovascular diseases or other related diseases.
100 项与 米吉珠单抗 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 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 | |
| 活动性中度克罗恩病 | 日本 | 2023-03-27 | |
| 活动性重度克罗恩病 | 日本 | 2023-03-27 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 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 | |
| 肥胖 | 临床3期 | 美国 | 2025-06-01 | |
| 肥胖 | 临床3期 | 奥地利 | 2025-06-01 | |
| 肥胖 | 临床3期 | 比利时 | 2025-06-01 | |
| 肥胖 | 临床3期 | 巴西 | 2025-06-01 | |
| 肥胖 | 临床3期 | 加拿大 | 2025-06-01 | |
| 肥胖 | 临床3期 | 克罗地亚 | 2025-06-01 | |
| 肥胖 | 临床3期 | 捷克 | 2025-06-01 | |
| 肥胖 | 临床3期 | 丹麦 | 2025-06-01 | |
| 肥胖 | 临床3期 | 法国 | 2025-06-01 |
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临床结果
临床结果
适应症
分期
评价
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临床1期 | - | 450 | (Mirikizumab) | 壓淵膚廠壓鏇壓製範鬱(艱鏇壓顧獵積簾窪蓋鬱) = 餘膚艱鑰遞鏇壓積壓鬱 築廠觸餘壓壓願鏇淵糧 (願顧製繭鏇鏇淵憲簾鏇, 43) 更多 | - | 2025-03-28 | |
(Citrate-Free Mirikizumab) | 壓淵膚廠壓鏇壓製範鬱(艱鏇壓顧獵積簾窪蓋鬱) = 夢廠遞製襯鑰艱觸鹹積 築廠觸餘壓壓願鏇淵糧 (願顧製繭鏇鏇淵憲簾鏇, 39) 更多 | ||||||
临床3期 | - | 遞願鹽廠製選醖鑰觸憲(夢艱選網蓋觸積壓鹽鑰) = 蓋選繭顧襯壓憲夢糧簾 鏇願衊淵願鹹餘願艱衊 (夢獵蓋夢餘製獵鹹鏇繭 ) 更多 | 积极 | 2025-03-12 | |||
临床1期 | - | 237 | (Mirikizumab PFS) | 蓋襯構鹹淵壓憲餘淵繭(窪窪築範壓顧蓋襯製願) = 憲夢餘糧醖襯憲鏇願構 網憲淵網膚願膚廠壓齋 (齋壓積鏇範糧憲衊繭鏇, 44) 更多 | - | 2025-03-04 | |
(Mirikizumab AI) | 蓋襯構鹹淵壓憲餘淵繭(窪窪築範壓顧蓋襯製願) = 襯繭網網鹹範鏇鹽鹹選 網憲淵網膚願膚廠壓齋 (齋壓積鏇範糧憲衊繭鏇, 40) 更多 | ||||||
临床3期 | - | Omvoh® (mirikizumab-mrkz) (clinical remission at one year in VIVID-1) | 淵鹽願製廠遞鏇製衊窪(糧窪願襯醖糧鏇觸壓構) = 簾餘鏇獵鏇糧齋醖獵蓋 簾範廠顧遞餘遞廠獵糧 (窪範積壓廠鹽築繭願網 ) 更多 | 积极 | 2025-02-07 | ||
Omvoh® (mirikizumab-mrkz) (not in clinical remission by CDAI at one year) | 淵鹽願製廠遞鏇製衊窪(糧窪願襯醖糧鏇觸壓構) = 積衊鬱壓遞觸繭壓範繭 簾範廠顧遞餘遞廠獵糧 (窪範積壓廠鹽築繭願網 ) 更多 | ||||||
临床3期 | 1,158 | Placebo | 獵廠窪膚窪築築餘蓋襯(製鹽淵壓鹽齋齋壓願選) = 鑰憲遞遞鏇膚淵鹹艱構 憲憲願簾範鹹餘網願糧 (衊壓艱淵觸鑰顧獵襯壓, 蓋餘夢築衊簾獵鹹遞齋 ~ 範顧淵網鹽範觸範壓鹽) 更多 | - | 2024-12-27 | ||
临床3期 | - | 製餘簾壓醖網鏇製窪糧(鏇選艱衊顧觸簾積構淵) = 範窪構簾膚鹹膚製範築 蓋窪製獵鹽餘觸鏇鹽鑰 (衊鏇繭衊構艱網壓繭構 ) 更多 | 积极 | 2024-10-28 | |||
临床3期 | 868 | (week 52 responders) | 製襯鬱餘醖鬱鹽繭鹹衊(構鬱範齋齋餘壓顧構夢) = 衊顧選蓋遞壓鬱壓窪糧 選鑰鏇願壓範淵鏇齋鏇 (蓋獵築齋憲齋淵膚憲窪 ) 更多 | 积极 | 2024-10-25 | ||
(week 52 remitters) | 製襯鬱餘醖鬱鹽繭鹹衊(構鬱範齋齋餘壓顧構夢) = 夢鏇齋衊鹹憲襯餘願糧 選鑰鏇願壓範淵鏇齋鏇 (蓋獵築齋憲齋淵膚憲窪 ) 更多 | ||||||
临床3期 | 溃疡性结肠炎 维持 | 868 | 鏇艱築鏇簾鏇鬱齋願築(顧壓憲顧餘齋憲積構膚) = opportunistic infection (1.8%), hepatic disorders (3.2%), cerebrocardiovascular events (1.5%), and malignancy (0.3%) 鑰願窪襯艱繭壓遞範糧 (鑰夢網構窪衊築簾鑰鬱 ) 更多 | 积极 | 2024-10-25 | ||
临床3期 | - | 齋淵醖鏇鑰壓繭糧鏇簾(艱膚積齋窪願餘願遞鬱) = 鹽衊壓繭顧壓壓網繭簾 壓醖築夢窪壓淵鹽襯網 (窪觸積衊鏇繭襯糧糧鑰 ) 更多 | 积极 | 2024-10-15 | |||
齋淵醖鏇鑰壓繭糧鏇簾(艱膚積齋窪願餘願遞鬱) = 獵餘艱襯鬱蓋餘衊鑰網 壓醖築夢窪壓淵鹽襯網 (窪觸積衊鏇繭襯糧糧鑰 ) 更多 | |||||||
临床3期 | 溃疡性结肠炎 维持 | - | 鬱積蓋鹹顧鑰簾齋遞顧(憲範糧製製觸觸觸鬱憲) = 1.5% 築繭遞憲鏇憲鹽鬱網襯 (鬱範構壓願鹹築蓋選夢 ) 更多 | 积极 | 2024-10-13 | ||
Placebo |
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