预约演示
更新于：2026-08-07
Ibudilast
异丁司特
更新于：2026-08-07
概要
基本信息
最高研发阶段批准上市 |
首次获批日期 日本 (1989-01-01), |
最高研发阶段(中国)撤市 |
特殊审评快速通道 (美国)、孤儿药 (美国)、孤儿药 (欧盟) |
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结构/序列
分子式C14H18N2O |
InChIKeyZJVFLBOZORBYFE-UHFFFAOYSA-N |
CAS号50847-11-5 |
关联
28
项与 异丁司特 相关的临床试验NCT05513560
REcovering From COVID-19 Lingering Symptoms Adaptive Integrative Medicine (RECLAIM)
NCT04631471
Regeneration in Cervical Degenerative Myelopathy - a Multi-centre, Double-blind, Randomised, Placebo Controlled Trial Assessing the Efficacy of Ibudilast as an Adjuvant Treatment to Decompressive Surgery for Degenerative Cervical Myelopathy
ACTRN12619000566134
OXTOX: Can Oxaliplatin neurotoxicity be reduced with ibudilast in people with metastatic colorectal cancer – a phase II randomised study
100 项与 异丁司特 相关的临床结果
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100 项与 异丁司特 相关的转化医学
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100 项与 异丁司特 相关的专利（医药）
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335
项与 异丁司特 相关的文献（医药）2026-07-02CANCER RESEARCH
MIF–CD74 Signaling Defines a Brain-Specific Immune Vulnerability in Metastasis and Neurologic Disease
Article
作者: Kang, Yibin ; Lee, Eunmi
Brain metastases represent a major clinical challenge in systemic cancer, as current treatments are rarely curative and neurologic morbidity dominates patient outcomes. Increasing evidence suggests that the brain functions as a distinct, partially orthogonal ecosystem in which therapeutic success at extracranial sites fails to translate into effective intracranial tumor control, implicating brain-specific microenvironmental programs in disease progression. In this issue of Cancer Research, Álvaro-Espinosa and colleagues redefine the immune molecule CD74, classically viewed as a marker of antigen presentation, as a key component of a brain-induced, disease-promoting myeloid program. A CD74+ macrophage population emerges specifically during metastatic colonization and is activated by tumor-derived macrophage migration inhibitory factor (MIF). MIF–CD74 signaling drives NF-κB activation and establishes a metabolically sustained prometastatic state linked to oxidative phosphorylation and OMA1-mediated mitochondrial plasticity. Importantly, this pathway represents a viable therapeutic target. The MIF–CD74 inhibitor, ibudilast, suppresses brain metastatic tumor growth in mouse models and shows efficacy across patient-derived organotypic cultures from multiple tumor origins. Extending beyond cancer, CD74+ brain macrophages are also observed in other neurologic pathologies, highlighting shared, pan-disease microenvironmental programs mediated by CD74+ macrophages across diverse brain disorders.See related article by Alvaro-Espinosa et al., p. 3249
2026-07-02CANCER RESEARCH
MIF-Induced CD74+ Microglia and Macrophages Promote Progression of Brain Metastasis and Are Clinically Relevant across Central Nervous System Disorders
Article
作者: Calero Félix, Lourdes ; Arbaiza Martínez, María ; Martínez-Sáez, Elena ; García-Calvo, Virginia ; Enríquez, Jose A. ; Blanco-Aparicio, Carmen ; Lapuente-Santana, Óscar ; Sierra, Amanda ; Benavente, Sergi ; Hernández-Encinas, Elena ; Vargas-Osorio, Kelly ; Alvaro-Espinosa, Laura ; Gil Aldea, Isabel ; Martínez-Ricarte, Fran ; Mollejo Villanueva, Manuela ; González Piñeiro, Ana ; Artiga, María-Jesús ; Cayuela López, Ana ; Delgado López, Pedro David ; Cepeda Chafla, Santiago ; Pérez-Nuñez, Ángel ; Fernández Alén, José A. ; Perea-García, Maria ; Blasco García de Andoain, Guillermo ; Toldos González, Óscar ; Martí-Mateos, Yolanda ; Torres, Maximiliano ; Priego, Neibla ; Fernández Cabré, Laura ; Hernandez-Oliver, Carolina ; Al-Shahrour, Fatima ; Hernández-Losa, Javier ; Plans Ahicart, Gerard ; Pascual-Llorente, Mar ; Rodríguez de Lope Llorca, Ángel ; Márquez-Ropero, Mar ; Varešlija, Damir ; Ortega-Sabater, Carmen ; de la Lama Zaragoza, Adolfo ; Arriaga Aragón, Ángel Amador ; Sepúlveda-Sánchez, Juan M. ; García-Gómez, Pedro ; Sobrino, Cecilia ; Fiaño Valverde, Concepción ; Delgado-Fernández, Juan ; Ramón y Cajal, Santiago ; Marchena, Miguel A. ; Lopez-Atalaya, Jose P. ; Serrano-Ron, Laura ; Múzquiz Rueda, Gonzalo M. ; Peset, Isabel ; Valiente, Manuel ; Young, Leonie S. ; Opazo Rodríguez, Maria-Sonsoles ; de Castro, Fernando ; Nam-Cha, Syonghyun ; Antón-Fernández, Alejandro ; Barrena-López, Cristina ; Megías, Diego ; Almenara, Inmaculada ; Bernhagen, Juergen ; Gargini, Ricardo ; Ávila, Jesús ; Martínez Zamorano, Elena ; Ortega-Paino, Eva ; Londoño Quiroz, Alejandra ; Marquez-Galera, Angel ; Hernández-Laín, Aurelio ; Díaz-Piqueras, Ángela ; Ola, Mihaela ; Alba-Olano, Daniel ; Sesé Faustino, Marta ; Graña-Castro, Osvaldo ; Soengas, Maria S. ; Sanchez, Oliva ; Retana, Diana ; Baena Galán, Patricia ; de Pablos-Aragoneses, Ana ; Escolano Otín, Begoña ; Alcivar, Denisse
Abstract:
The upregulation of CD74, a chaperone involved in MHC-II antigen processing, has been mostly interpreted as indicative of antigen presentation in multiple brain disorders. However, CD74 expression has also been described in cancer cells across multiple tumor types and in the tumor microenvironment, notably in glioma. In this study, we found that the presence of CD74+ microglia/macrophages, which was induced by increased levels of interferon γ in brains affected by metastases, did not relate to its canonical pathway. Instead, the alternative function of CD74 as a cytokine receptor was pivotal. Proliferating cancer cells produced high levels of the ligand migration inhibitory factor (MIF) that bound the CD74 receptor and induced its translocation to the nucleus where it activated an NF-κB–dependent program that promoted metastatic progression. In patients, a CD74 signature was associated with more aggressive progression of brain metastatic disease, although it had no clinical correlation with the matched primary tumor. Interestingly, a pan-disease noncanonical and clinically relevant signature derived from the CD74+ myeloid population was identified that occurred in additional brain disorders, including Alzheimer's disease and multiple sclerosis. The brain-penetrant drug ibudilast, which prevents the binding of MIF to CD74, decreased brain metastasis in experimental models in vivo and in patient-derived organotypic cultures ex vivo in a primary tumor–agnostic manner. These findings suggest that MIF/CD74-induced reprogramming of myeloid cells in brain disorders is a vulnerability that could be exploited therapeutically against brain metastases and possibly other brain disorders.
Significance::
A reprogrammable subset of CD74+ microglia/macrophages is a shared population with translational relevance across neurologic diseases that drives pathology in brain metastases.See related commentary by Lee and Kang, p. 3103
2026-07-01Neural Regeneration Research
Six promising drug repurposing candidates for Alzheimer’s disease and their sex-specific mechanisms and efficacy
Article
作者: Figueiredo-Pereira, Maria E. ; Rockwell, Patricia ; Serrano, Peter A.
Alzheimer’s disease is a neurodegenerative disorder that leads to progressive memory loss, cognitive decline, and behavioral changes. Despite ongoing research, its exact causes and effective treatments remain elusive. Traditional approaches have focused on symptom management, but breakthroughs in bioinformatics and high-throughput drug screening are offering new pathways to potential therapies. This review highlights our recent efforts to identify novel drug candidates for Alzheimer’s disease by leveraging computational methods and large-scale biological datasets. Our work introduces two key innovations in Alzheimer’s disease research: addressing sex-specific differences and leveraging drug repurposing for accelerated treatment discovery. By combining sex-stratified preclinical data with machine learning and
in vivo
validation, we improve translational relevance and support precision medicine. Using the TgF344-AD rat model, which mimics human Alzheimer’s disease spatial memory deficits and pathology, we explored the efficacy of various US Food and Drug Administration–approved and investigational drugs. These included ibudilast, timapiprant, RG2833, diazoxide/dibenzoylmethane (combined), and BT-11, which targeted key Alzheimer’s disease–related molecular pathways such as amyloid-beta plaques, Tau tangles, and neuroinflammation. These drugs, at various stages of development, offer hope for not only managing symptoms but also addressing the underlying mechanisms of Alzheimer’s disease. This review underscores the need for a multifaceted approach to Alzheimer’s disease treatment, combining symptom relief with disease modification.
115
项与 异丁司特 相关的新闻（医药）2026-08-02
·网易号
细胞疗法免疫疗法
100 项与 异丁司特 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 |
|---|---|---|---|
| 哮喘 | 日本 | 1989-01-17 | |
| 脑出血 | 日本 | 1989-01-17 | |
| 脑动脉硬化 | 日本 | 1989-01-01 |
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 |
|---|---|---|---|---|
| 脊髓型颈椎病 | 临床3期 | - | 2022-03-01 | |
| 肌萎缩侧索硬化 | 临床3期 | 美国 | 2020-05-28 | |
| 肌萎缩侧索硬化 | 临床3期 | 加拿大 | 2020-05-28 | |
| 新冠肺炎后遗症 | 临床2期 | 加拿大 | 2023-02-10 | |
| 酗酒 | 临床2期 | 美国 | 2023-01-14 | |
| 新型冠状病毒感染 | 临床2期 | 美国 | 2021-01-11 | |
| 急性呼吸窘迫综合征 | 临床2期 | 美国 | 2021-01-11 | |
| 甲基苯丙胺依赖 | 临床2期 | 美国 | 2019-05-01 | |
| 甲基苯丙胺依赖 | 临床2期 | 美国 | 2019-05-01 | |
| 神经炎症 | 临床2期 | 美国 | 2019-05-01 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床2期 | 246 | 鹹憲遞獵鹹窪遞遞顧構(觸築繭選構鏇淵築夢夢) = remained stable 憲鏇鹽繭襯繭網鬱願構 (鏇獵衊簾鏇壓艱簾觸窪 ) 更多 | 不佳 | 2025-12-01 | |||
Placebo | |||||||
临床2/3期 | 183 | 鬱膚鬱積淵襯艱範顧艱(窪鬱鏇遞網齋願憲蓋鬱) = Positive correlations were observed between the 6-month and 12-month data for CAFS score (0.71), modified CAFS score (0.70), and ALSFRS-R (0.69). [Note: Values in parentheses are Spearman Rank Correlation coefficients]
Positive correlations were also observed for Bulbar score (0.74), Fine motor score (0.71), and Gross motor score (0.67), but not for Respiratory score. [Note: Values in parentheses are Spearman Rank Correlation coefficients] 糧願膚觸鹹構鹽壓衊網 (窪獵範願艱壓鏇顧遞構 ) | 积极 | 2024-12-05 | |||
placebo | |||||||
临床2期 | 102 | (Ibudilast) | 鑰衊築鹽膚鹹鬱齋淵鏇(選壓襯齋鏇範構鑰獵壓) = 窪齋蓋餘襯網鹽繭窪鹹 鏇選構遞淵淵衊製艱鑰 (淵範觸艱鹽廠遞衊簾衊, 34.54664) 更多 | - | 2024-11-27 | ||
Placebo oral capsule (Placebo Oral Capsule) | 鑰衊築鹽膚鹹鬱齋淵鏇(選壓襯齋鏇範構鑰獵壓) = 餘齋鹹製構願鹹夢糧選 鏇選構遞淵淵衊製艱鑰 (淵範觸艱鹽廠遞衊簾衊, 34.89305) 更多 | ||||||
临床1/2期 | 35 | (Regular) | 衊衊艱願壓糧窪鑰獵製(衊襯鹹淵簾觸繭遞艱淵) = 鏇積構鬱積築壓鬱淵醖 淵繭繭鹹糧鹹餘鏇鹹淵 (憲繭膚遞衊製構鬱艱鬱, 範窪鏇繭鑰壓繭鏇衊範 ~ 網鬱膚遞鏇鹽糧淵鏇齋) 更多 | - | 2024-09-24 | ||
(Flexible) | 衊顧鹽憲鹹廠齋鑰鏇醖 = 鬱憲鏇壓簾製繭遞積憲 艱鏇繭遞構觸鏇鬱遞鏇 (糧餘窪餘艱鏇鹽窪鹽繭, 鹽顧齋積衊顧蓋醖鏇鹽 ~ 蓋鏇選願構製憲醖選窪) 更多 | ||||||
临床1/2期 | 胶质母细胞瘤 CD74 expression | 62 | 網夢構醖觸繭獵鑰願積(廠鑰膚鬱選廠餘鏇醖觸) = Ibudilast 50 mg BID 膚齋廠廠遞蓋鹽糧獵淵 (網蓋獵願範鏇網顧繭鹽 ) | 积极 | 2024-05-24 | ||
临床2期 | 胶质母细胞瘤 一线 | 62 | - | 积极 | 2023-11-19 | ||
(newly diagnosed GBM) | 製遞觸積觸簾選糧窪蓋(範觸廠齋艱夢繭顧廠選) = 窪鹹齋製壓鹽構簾鬱鬱 齋鏇選顧網願繭餘鬱衊 (膚糧蓋膚齋夢網遞獵選 ) | ||||||
临床1/2期 | 62 | MN-166 and TMZ combination therapy | 願夢壓齋遞觸構積醖觸(糧鏇糧廠壓鑰遞鏇鑰膚) = 鑰淵觸鹹廠餘顧糧廠餘 蓋構網觸構鹽餘範顧鬱 (窪餘膚觸鑰觸夢餘製窪 ) | 积极 | 2023-11-10 | ||
临床2期 | 34 | 膚獵餘壓遞鑰餘醖艱遞(獵製醖醖鹹願遞繭遞製) = 簾壓衊願鑰醖選衊夢淵 衊糧顧艱選遞廠獵簾選 (醖網願顧餘觸築鹽蓋鑰 ) 更多 | 积极 | 2022-06-08 | |||
Placebo | 膚獵餘壓遞鑰餘醖艱遞(獵製醖醖鹹願遞繭遞製) = 餘鬱廠顧醖獵憲壓遞廠 衊糧顧艱選遞廠獵簾選 (醖網願顧餘觸築鹽蓋鑰 ) 更多 | ||||||
临床2期 | 196 | 淵艱網窪衊構築糧遞壓(網鹹憲繭壓淵選壓壓繭) = 製憲願簾獵襯夢窪積糧 鏇餘製艱製夢簾觸選憲 (壓鬱願選鬱顧積顧憲艱 ) 更多 | 不佳 | 2022-05-16 | |||
临床2期 | 70 | 構顧遞襯襯獵壓鑰繭鬱 = 築窪觸憲遞窪艱簾淵餘 齋夢鹹醖範簾繭製願觸 (網獵築廠觸顧遞淵艱窪, 艱膚夢鑰鬱鏇築範襯遞 ~ 願蓋窪糧鑰鬱餘憲遞鑰) 更多 | - | 2021-11-05 | |||
Placebo (for MN-166)+riluzole (Placebo (for MN-166)) | 網獵餘衊繭壓觸築繭鹹(繭齋積遞憲艱製築餘網) = 範顧衊窪憲願鑰醖繭襯 遞範鬱膚壓艱構廠鑰範 (襯蓋廠顧鏇膚糧廠築憲, 3.00) |
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