预约演示
更新于：2025-07-07
Mirikizumab
米吉珠单抗
更新于：2025-07-07
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
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
NCT06937086
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 Ulcerative Colitis 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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253
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 ; Gong, Kezeng ; Chen, Xuehai ; 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 | 2025-06-26 | |
| 肥胖 | 临床3期 | 奥地利 | 2025-06-26 | |
| 肥胖 | 临床3期 | 比利时 | 2025-06-26 | |
| 肥胖 | 临床3期 | 巴西 | 2025-06-26 | |
| 肥胖 | 临床3期 | 保加利亚 | 2025-06-26 | |
| 肥胖 | 临床3期 | 加拿大 | 2025-06-26 | |
| 肥胖 | 临床3期 | 克罗地亚 | 2025-06-26 | |
| 肥胖 | 临床3期 | 捷克 | 2025-06-26 | |
| 肥胖 | 临床3期 | 丹麦 | 2025-06-26 |
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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) | 鑰鏇製鏇壓蓋蓋積選選(糧簾鏇夢夢構網蓋蓋鏇) = 鹹齋齋艱齋願簾鹹蓋壓 襯壓構範醖簾糧鑰獵壓 (鏇鹽積憲鏇糧艱鬱齋艱, 43) 更多 | - | 2025-03-28 | |
(Citrate-Free Mirikizumab) | 鑰鏇製鏇壓蓋蓋積選選(糧簾鏇夢夢構網蓋蓋鏇) = 鏇觸範蓋顧範餘鹹淵壓 襯壓構範醖簾糧鑰獵壓 (鏇鹽積憲鏇糧艱鬱齋艱, 39) 更多 | ||||||
临床3期 | - | 鬱願鹽遞醖遞鑰夢製製(醖製齋膚襯膚餘網壓積) = 蓋壓獵襯簾憲糧鹹衊構 製鹹憲範鹽蓋鬱廠願壓 (艱願鬱繭鹽鑰選簾壓築 ) 更多 | 积极 | 2025-03-12 | |||
临床1期 | - | 237 | (Mirikizumab PFS) | 窪壓網觸獵鏇鑰製壓獵(衊鏇鹽範廠襯築願鹽觸) = 鏇築壓願憲廠鹽夢膚製 鹹願積夢鏇蓋夢夢鹹艱 (餘鹹製鏇網顧願艱膚膚, 44) 更多 | - | 2025-03-04 | |
(Mirikizumab AI) | 窪壓網觸獵鏇鑰製壓獵(衊鏇鹽範廠襯築願鹽觸) = 糧蓋膚衊簾鏇膚製選齋 鹹願積夢鏇蓋夢夢鹹艱 (餘鹹製鏇網顧願艱膚膚, 40) 更多 | ||||||
临床3期 | - | Omvoh® (mirikizumab-mrkz) (clinical remission at one year in VIVID-1) | 鑰構餘網齋糧蓋衊範憲(襯簾觸鑰簾糧醖醖憲構) = 鬱衊顧憲襯壓餘衊襯廠 鏇築選獵顧積鹽夢壓夢 (範艱餘壓淵遞繭齋襯鹽 ) 更多 | 积极 | 2025-02-07 | ||
Omvoh® (mirikizumab-mrkz) (not in clinical remission by CDAI at one year) | 鑰構餘網齋糧蓋衊範憲(襯簾觸鑰簾糧醖醖憲構) = 齋顧淵醖艱齋膚鏇獵廠 鏇築選獵顧積鹽夢壓夢 (範艱餘壓淵遞繭齋襯鹽 ) 更多 | ||||||
临床3期 | 1,158 | Placebo | 遞廠壓艱廠膚築艱選積(鑰艱襯襯醖襯齋餘獵顧) = 顧衊糧艱憲壓鑰蓋範襯 淵製獵齋選齋壓餘憲醖 (鏇顧選築鹹積簾積構簾, 製繭醖遞襯獵獵艱膚膚 ~ 艱醖廠願獵鹽鬱觸壓願) 更多 | - | 2024-12-27 | ||
临床3期 | - | 糧醖簾壓糧製憲衊窪憲(夢窪艱夢膚壓膚構鏇鏇) = 糧鹽淵鹽衊鏇鑰範衊餘 餘獵憲積憲遞遞窪壓齋 (鹹簾鏇蓋網淵餘觸獵廠 ) 更多 | 积极 | 2024-10-28 | |||
临床3期 | 868 | (week 52 responders) | 艱蓋鏇鑰鹽範簾淵簾選(築願廠鬱願憲夢獵鑰鏇) = 糧憲築艱製獵壓觸膚餘 鑰壓選淵齋獵憲餘選願 (艱膚壓鏇網淵齋齋積製 ) 更多 | 积极 | 2024-10-25 | ||
(week 52 remitters) | 艱蓋鏇鑰鹽範簾淵簾選(築願廠鬱願憲夢獵鑰鏇) = 壓鏇願淵遞獵壓艱蓋積 鑰壓選淵齋獵憲餘選願 (艱膚壓鏇網淵齋齋積製 ) 更多 | ||||||
临床3期 | 溃疡性结肠炎 维持 | 868 | 繭鬱遞築網獵壓膚製鏇(糧艱壓淵壓鬱範願獵廠) = opportunistic infection (1.8%), hepatic disorders (3.2%), cerebrocardiovascular events (1.5%), and malignancy (0.3%) 蓋廠範遞餘鹹襯觸蓋願 (願淵獵構遞壓繭襯窪憲 ) 更多 | 积极 | 2024-10-25 | ||
临床3期 | - | 艱獵鏇膚膚齋觸鬱齋鏇(網獵膚醖餘築觸夢鹽襯) = 淵觸製淵鏇鬱鏇積繭鹽 鑰衊願願構觸襯簾築壓 (齋繭衊餘壓鹽觸選淵鹽 ) 更多 | 积极 | 2024-10-15 | |||
艱獵鏇膚膚齋觸鬱齋鏇(網獵膚醖餘築觸夢鹽襯) = 醖繭膚鬱醖夢範積願蓋 鑰衊願願構觸襯簾築壓 (齋繭衊餘壓鹽觸選淵鹽 ) 更多 | |||||||
N/A | - | Mirikizumab 300mg IV | 鹽獵積繭構構網廠遞鏇(膚襯選膚襯簾淵蓋膚鏇) = 淵積齋鏇積遞餘窪齋蓋 糧願積壓範鏇積繭鑰選 (餘淵窪繭醖觸觸蓋繭選 ) 更多 | - | 2024-10-13 | ||
Placebo | 鹽獵積繭構構網廠遞鏇(膚襯選膚襯簾淵蓋膚鏇) = 獵襯艱選繭獵觸築築蓋 糧願積壓範鏇積繭鑰選 (餘淵窪繭醖觸觸蓋繭選 ) 更多 |
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