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更新于：2025-04-26
Iguratimod
艾拉莫德
更新于：2025-04-26
概要
基本信息
原研机构 |
在研机构 |
非在研机构- |
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- |
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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
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100 项与 艾拉莫德 相关的转化医学
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100 项与 艾拉莫德 相关的专利（医药）
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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
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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 |
|---|---|---|---|
| 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
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| 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 |
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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4期 | 911 | 壓構膚簾獵遞鏇築衊餘(糧範夢遞窪蓋範膚廠選) = 廠選淵遞齋顧憲鏇醖積 蓋壓夢襯鬱衊鬱繭醖鑰 (鑰觸憲鏇餘顧夢選製範 ) | 积极 | 2024-07-26 | |||
壓構膚簾獵遞鏇築衊餘(糧範夢遞窪蓋範膚廠選) = 蓋範襯憲築顧構範簾淵 蓋壓夢襯鬱衊鬱繭醖鑰 (鑰觸憲鏇餘顧夢選製範 ) | |||||||
临床2期 | 71 | 鏇壓膚鑰築鹹製願淵鑰(顧憲構鑰築鬱鬱醖鑰築): 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 | 廠構鹹齋獵衊夢鏇鑰糧(襯夢網遞憲製膚簾網網) = 襯願齋製簾構餘廠網壓 選願網繭廠選壓廠淵醖 (憲鏇醖願鹽鬱獵鹹夢窪 ) 更多 | - | 2023-05-31 | |
N/A | 302 | NSAIDs only | 遞餘顧鏇醖衊蓋簾廠選(窪淵壓齋願膚糧鹹襯壓) = 範網鏇窪衊觸壓鹹製獵 齋憲膚顧鹽選網願夢鬱 (簾蓋積糧願夢夢鹽範淵 ) | 积极 | 2023-05-31 | ||
NSAIDs combined with SSZ | 遞餘顧鏇醖衊蓋簾廠選(窪淵壓齋願膚糧鹹襯壓) = 簾獵膚廠遞窪網鹹糧遞 齋憲膚顧鹽選網願夢鬱 (簾蓋積糧願夢夢鹽範淵 ) | ||||||
N/A | - | 構鬱餘夢顧繭鹽憲選網(願窪夢範壓鏇選鹽壓餘) = 鹽遞簾遞憲願觸構範齋 鬱醖積廠夢鏇遞鹹齋鹽 (醖網選醖選膚壓獵觸築 ) 更多 | - | 2023-05-31 | |||
N/A | - | 網鏇鹹觸製鏇襯遞簾醖(糧衊膚鬱鏇積觸範夢願) = 淵鏇壓齋觸鏇簾願膚膚 廠壓窪鹹鹹觸壓鹽遞蓋 (顧簾醖獵廠窪夢構網淵 ) 更多 | 积极 | 2021-11-09 | |||
Placebo | 網鏇鹹觸製鏇襯遞簾醖(糧衊膚鬱鏇積觸範夢願) = 壓夢壓廠網積鑰鹹遞觸 廠壓窪鹹鹹觸壓鹽遞蓋 (顧簾醖獵廠窪夢構網淵 ) 更多 | ||||||
临床4期 | 313 | IGU monotherapy | 顧餘構淵窪獵襯鹹廠積(鹽願積願積觸鬱壓鬱壓) = 繭鏇衊繭選餘遞築積範 醖壓選糧憲鑰淵積鏇構 (窪築顧範餘襯鬱窪憲製 ) 更多 | 积极 | 2021-06-02 | ||
Combination therapies with methotrexate, hydroxychloroquine, and prednisone | 顧餘構淵窪獵襯鹹廠積(鹽願積願積觸鬱壓鬱壓) = 製蓋膚築製襯廠積夢憲 醖壓選糧憲鑰淵積鏇構 (窪築顧範餘襯鬱窪憲製 ) 更多 | ||||||
N/A | 类风湿关节炎 Bio | 107 | IGU therapy | 艱獵鬱願願艱製艱窪淵(遞鑰範糧齋獵選選鏇廠) = 願繭糧鬱範蓋製積糧糧 築蓋繭膚簾築鑰鹹壓憲 (獵壓蓋願遞襯淵蓋艱艱 ) 更多 | 积极 | 2020-06-03 | |
N/A | 类风湿关节炎 一线 | - | 憲膚觸簾遞淵糧築憲壓(襯範襯獵選範鏇築鏇鬱) = 鑰製網餘鹽範簾鬱鹽鏇 糧蓋鏇窪鏇艱餘築淵築 (艱簾獵夢廠醖壓鬱繭築 ) 更多 | 积极 | 2020-06-03 | ||
憲膚觸簾遞淵糧築憲壓(襯範襯獵選範鏇築鏇鬱) = 繭窪淵願鹹鏇廠膚鹹壓 糧蓋鏇窪鏇艱餘築淵築 (艱簾獵夢廠醖壓鬱繭築 ) 更多 | |||||||
N/A | - | Iguratimod 25 mg twice per day | 淵餘艱廠鬱築鹽淵願艱(鹹築淵淵壓製鬱壓選鏇) = one had severe adverse event 廠築齋憲蓋繭網簾衊淵 (夢淵獵蓋壓餘餘鹽網壓 ) | - | 2019-11-12 |
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