预约演示
更新于：2025-05-16
Iguratimod
艾拉莫德
更新于：2025-05-16
概要
基本信息
原研机构 |
非在研机构- |
权益机构- |
最高研发阶段批准上市 |
首次获批日期 中国 (2011-08-23), |
最高研发阶段(中国)批准上市 |
特殊审评- |
登录后查看时间轴
结构/序列
分子式C17H14N2O6S |
InChIKeyANMATWQYLIFGOK-UHFFFAOYSA-N |
CAS号123663-49-0 |
关联
96
项与 艾拉莫德 相关的临床试验NCT06945666
A Multicenter Prospective Study of Iguratimod in Combination With Tofacitinib in Patients With Rheumatoid Arthritis With Poor Response to Conventional or Biological DMARDs
CTR20250496
艾拉莫德片人体生物等效性试验
CTR20250109
艾拉莫德片在中国健康人群中单次给药的人体生物等效性临床试验
100 项与 艾拉莫德 相关的临床结果
登录后查看更多信息
100 项与 艾拉莫德 相关的转化医学
登录后查看更多信息
100 项与 艾拉莫德 相关的专利（医药）
登录后查看更多信息
373
项与 艾拉莫德 相关的文献（医药）2025-08-01TISSUE & CELL
Iguratimod modulates osteoclast differentiation in rheumatoid arthritis: Insights into AMPK/HIF-1α signaling pathway regulation
Article
作者: Long, Li ; Peiting, Li ; Jun, Liu ; Jiashun, Zeng ; Ying, Huang ; Xin, Yue ; Xingyi, Li
BACKGROUND:
Rheumatoid arthritis (RA) leads to joint deformities and diminishes quality of life if not managed promptly. Investigating Iguratimod effects on osteoclast differentiation in RA patients could provide insights into disease management.
METHODS:
Peripheral blood mononuclear cells (PBMCs) were extracted from blood samples taken from RA patients. TRAP staining confirmed the ability of these cells to differentiate into osteoclasts. Those cells were treated with Iguratimod, AMPK agonist (AICAR), and HIF-1α interference (PX-478) during osteoclast induction. CCK8, flow cytometry, ELISA, qPCR, and WB were used to detect changes after exposure in each group.
RESULTS:
Iguratimod, AICAR and PX-478 reduced osteoclast formation and viability while promoting apoptosis. ELISA results showed that exposure with Iguratimod, AICAR and PX-478 significantly reduced the levels of CXCL8, CCL20, TNF-α, IL-1, IL-6, IL-17 and TPRA secreted by PBMCs from RA patients. In addition, the results demonstrate that Iguratimod, along with AICAR, PX-478, and Leflunomide, significantly suppresses the expression of osteoclast-specific markers (HIF-1α, TRAP, CTSK, CTR, MMP9, and RANK) at both mRNA and protein levels. Notably, Iguratimod, AICAR, and Leflunomide increase the expression of AMPK and p-AMPK, while PX-478 decreases their expression.
CONCLUSIONS:
Iguratimod potentially modulates AMPK/HIF-1α pathway, thereby suppressing release of inflammatory factors and influencing differentiation of peripheral blood osteoclasts in RA patients. These findings suggest promising therapeutic strategies for exposure of joint deformities associated with RA.
2025-06-01EUROPEAN JOURNAL OF PHARMACOLOGY
Iguratimod, a promising therapeutic agent for COVID-19 that attenuates excessive inflammation in mouse models
Article
作者: Hosoya, Tadashi ; Iwai, Hideyuki ; Oba, Seiya ; Suzuki, Tadaki ; Komiya, Yoji ; Ainai, Akira ; Kawata, Daisuke ; Hasegawa, Hideki ; Miyamoto, Sho ; Yasuda, Shinsuke ; Kanno, Takayuki ; Koike, Ryuji
In severe COVID-19 patients, excessive inflammation can lead to multiorgan dysfunction. Current anti-inflammatory treatments like glucocorticoids partially improve the outcomes, while immune systems are compromised. We have identified that SARS-CoV-2-infected obese mice were a good model of the cytokine storm seen in COVID-19. Here, we revealed that iguratimod (IGU), an approved agent for rheumatoid arthritis, improved survival by attenuating inflammation with minimal immune suppression. In this study, C57BL/6 mice were fed a high-fat diet (HFD) or a normal-fat diet (NFD) for ten weeks before being infected with a mouse-adapted SARS-CoV-2. IGU significantly improved survival rates and reduced lung inflammation in HFD-fed mice, with minimal impact on interferon-induced genes and viral load. Meanwhile, dexamethasone (DEX) did not improve survival, while it suppressed various immune reactions with different mechanisms to IGU. Interestingly, IGU-treated mice had fewer SARS-CoV-2 positive cells in the lung, although viral replication was comparable to the control mice. Neither IGU nor DEX inhibited the SARS-CoV-2 infection in Vero-E6 cells, unlike the antiviral agent, remdesivir. Of note, IGU was effective prophylactically and therapeutically in HFD mice, and showed beneficial effects in NFD-fed mice with a lethal dose exposure of SARS-CoV-2. We demonstrated that IGU could be a promising treatment for severe COVID-19, especially in obese patients, by fine-tuning inflammation without compromising antiviral immunity. This study supports the possibility of drug repositioning for IGU COVID-19 beyond autoimmune diseases.
2025-01-01JOURNAL OF ORAL PATHOLOGY & MEDICINE
The Mechanism of Immune Intervention by Iguratimod in Oral Lichen Planus Patients: An In Vitro Experimental Study
Article
作者: Cheng, Juehua ; Geng, Yanlin ; Zhu, Yuchi ; Yang, Liqun ; Zhang, Mengna ; Fan, Yuan ; Liu, Jia
ABSTRACT:
Background:
Oral lichen planus (OLP) is a T cell‐mediated immune disease. Iguratimod (IGU) is a novel immunomodulatory agent for rheumatoid arthritis. No studies have been reported on the mechanism of IGU in the treatment of OLP, which deserves investigation.
Methods:
Samples were collected from two batches of non‐erosive OLP, erosive OLP (EOLP) patients and healthy control subjects. In the first batch, the effects of IGU or the same volume of dimethyl sulfoxide (DMSO) on proliferation, apoptosis and migration of peripheral blood T lymphocytes (PBL T) were examined by CCK‐8, flow cytometry and transwell assay respectively. The levels of IL‐6, IL‐17, TNF‐α, TGF‐β and IL‐10 were measured by enzyme‐linked immunosorbent assay. In the second batch, the percentages of Th17 and Treg cells were determined by flow cytometry in peripheral blood mononuclear cells after IGU or DMSO stimulation.
Results:
Compared with the control, IGU promoted apoptosis and inhibited migration, but had no significant effect on the proliferation of PBL T in OLP. IL‐6, IL‐17 and TNF‐α were decreased in OLP. TGF‐β and IL‐10 showed an upward trend in the IGU‐treated EOLP. IGU decreased Th17 in OLP and reduced Th17/Treg ratio in EOLP. The percentage of Treg cells showed an upregulated trend but the difference was not statistically significant.
Conclusion:
IGU may intervene in the immune response of OLP by affecting functions of PBL T, improving the balance of Th17/Treg and regulating related cytokines.
100 项与 艾拉莫德 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 |
|---|---|---|---|
| 类风湿关节炎 | 中国 | 2011-08-23 | |
| 类风湿关节炎 | 中国 | 2011-08-23 |
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 |
|---|---|---|---|---|
| 原发性干燥综合征 | 临床2期 | 中国 | 2021-03-22 |
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4期 | 911 | 遞積憲鬱醖顧選壓襯觸(鏇築顧遞鏇範觸憲壓鹹) = 窪蓋顧蓋觸遞鹽蓋廠膚 醖鏇襯糧齋顧範願鑰鹹 (積鏇糧壓蓋範構範淵淵 ) | 积极 | 2024-07-26 | |||
遞積憲鬱醖顧選壓襯觸(鏇築顧遞鏇範觸憲壓鹹) = 簾齋範蓋鏇顧簾窪廠築 醖鏇襯糧齋顧範願鑰鹹 (積鏇糧壓蓋範構範淵淵 ) | |||||||
临床2期 | 71 | 鏇製膚遞簾壓簾網築壓(顧鑰窪築範廠繭醖構選): odds ratio = 1.82 (95% CI, 1.22 ~ 2.7), P-Value = 0.003 | - | 2023-12-10 | |||
临床4期 | 类风湿关节炎 一线 | 246 | IGU combination with csDMARDs | 餘衊艱膚窪壓糧願蓋構(製簾繭夢鹹觸鹽簾觸製) = 構醖顧繭艱蓋製鏇鬱窪 鬱簾糧願觸廠廠範遞範 (鹽製遞衊積鏇鹽觸選鬱 ) 更多 | - | 2023-05-31 | |
N/A | 302 | NSAIDs only | 願製淵壓製夢憲餘選醖(網糧網齋觸襯鹽構築網) = 膚醖網夢憲範蓋蓋鹹鑰 鹽艱構艱範積構遞衊夢 (鹽窪顧廠艱鹽鹹範蓋襯 ) | 积极 | 2023-05-31 | ||
NSAIDs combined with SSZ | 願製淵壓製夢憲餘選醖(網糧網齋觸襯鹽構築網) = 鬱襯願糧顧壓憲膚繭夢 鹽艱構艱範積構遞衊夢 (鹽窪顧廠艱鹽鹹範蓋襯 ) | ||||||
N/A | - | 壓餘窪壓淵夢餘壓糧醖(顧願膚鏇觸衊顧憲觸鬱) = 夢獵廠選廠襯選製窪廠 願蓋餘積衊蓋網網願顧 (艱鏇憲糧築鬱窪廠構淵 ) 更多 | - | 2023-05-31 | |||
N/A | - | 網繭夢積蓋餘膚顧糧齋(簾築窪淵醖鑰鬱衊獵餘) = 築獵窪餘願範觸構選製 壓憲襯艱醖鹽鏇夢蓋壓 (餘蓋築構夢壓艱憲夢窪 ) 更多 | 积极 | 2021-11-09 | |||
Placebo | 網繭夢積蓋餘膚顧糧齋(簾築窪淵醖鑰鬱衊獵餘) = 壓獵鏇艱製獵網廠鹹鏇 壓憲襯艱醖鹽鏇夢蓋壓 (餘蓋築構夢壓艱憲夢窪 ) 更多 | ||||||
临床4期 | 313 | IGU monotherapy | 鏇淵願獵襯蓋遞築膚製(蓋衊夢齋齋衊襯齋窪鹹) = 廠築憲選鑰膚構顧艱壓 遞獵鬱憲鬱簾鏇積觸獵 (網鏇蓋獵網願蓋遞醖選 ) 更多 | 积极 | 2021-06-02 | ||
Combination therapies with methotrexate, hydroxychloroquine, and prednisone | 鏇淵願獵襯蓋遞築膚製(蓋衊夢齋齋衊襯齋窪鹹) = 餘膚夢觸鹽膚獵顧衊壓 遞獵鬱憲鬱簾鏇積觸獵 (網鏇蓋獵網願蓋遞醖選 ) 更多 | ||||||
N/A | 类风湿关节炎 Bio | 107 | IGU therapy | 窪襯觸範憲壓鑰鏇簾製(獵選願餘繭獵築淵鹽選) = 選鑰艱淵衊鏇鬱鏇醖鑰 糧齋選簾範構簾餘憲壓 (鹽壓襯壓製構齋鹹鑰衊 ) 更多 | 积极 | 2020-06-03 | |
N/A | 类风湿关节炎 一线 | - | 餘願壓觸蓋憲憲選構鹹(憲齋鹽憲願齋遞淵淵鏇) = 糧憲餘願積構鑰蓋艱壓 鏇淵簾膚糧鬱膚構繭遞 (網積範範膚網獵窪願廠 ) 更多 | 积极 | 2020-06-03 | ||
餘願壓觸蓋憲憲選構鹹(憲齋鹽憲願齋遞淵淵鏇) = 廠廠繭艱窪鑰窪顧構鹹 鏇淵簾膚糧鬱膚構繭遞 (網積範範膚網獵窪願廠 ) 更多 | |||||||
N/A | - | Iguratimod 25 mg twice per day | 艱鏇淵餘壓願壓鬱構淵(憲觸繭築餘醖廠醖觸齋) = one had severe adverse event 淵鏇齋鏇膚襯觸齋顧鹽 (鬱衊鹽遞鬱鹹積願鏇衊 ) | - | 2019-11-12 |
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
Eureka LS:
全新生物医药AI Agent 覆盖科研全链路，让突破性发现快人一步
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