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更新于：2025-12-14
Nintedanib esylate
乙磺酸尼达尼布
更新于：2025-12-14
概要
基本信息
药物类型 小分子化药 |
别名 CYNEDIV、Intedanib、NDNB + [25] |
作用方式 拮抗剂、抑制剂 |
作用机制 CSF-1R拮抗剂(集落刺激因子1受体拮抗剂)、FGFRs拮抗剂(成纤维细胞生长因子受体家族拮抗剂)、FLT3抑制剂(酪氨酸蛋白激酶受体FLT3抑制剂) |
在研适应症 |
非在研适应症 |
非在研机构 |
最高研发阶段批准上市 |
首次获批日期 美国 (2014-10-15), |
最高研发阶段(中国)批准上市 |
特殊审评突破性疗法 (美国)、快速通道 (美国)、孤儿药 (美国)、优先审评 (中国)、特殊审批 (中国)、孤儿药 (日本)、孤儿药 (韩国)、孤儿药 (澳大利亚) |
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结构/序列
分子式C33H39N5O7S |
InChIKeyMMMVNAGRWOJNMW-FJBFXRHMSA-N |
CAS号656247-18-6 |
关联
245
项与 乙磺酸尼达尼布 相关的临床试验NCT07194382
A Randomized, Double-Blind, Placebo-Controlled, Phase 2 Proof of Concept (POC) Study Evaluating the Safety, Tolerability, and Efficacy of Nintedanib Solution for Inhalation (AP02) in Participants With Idiopathic Pulmonary Fibrosis (IPF) (AURA-IPF)
ChiCTR2500112642
Efficacy and Safety of Nintedanib Combined with Radiotherapy in Preventing Radiation Pneumonitis in Patients with Lung Cancer
NCT07229716
Study on the Drug Interactions of HRS-9813, Pirfenidone and Nintedanib in Healthy Subjects
100 项与 乙磺酸尼达尼布 相关的临床结果
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100 项与 乙磺酸尼达尼布 相关的转化医学
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100 项与 乙磺酸尼达尼布 相关的专利（医药）
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2,286
项与 乙磺酸尼达尼布 相关的文献（医药）2026-02-01EXPERIMENTAL EYE RESEARCH
Contact lens delivery improves therapeutic efficacy of nintedanib in rabbit eyes with alkali burn
Article
作者: Basak, S ; Dey, A ; Hazra, S ; Das, M ; Chauhan, A ; Sharma, A ; Konar, A
Nintedanib is a prescription drug for treating lung fibrosis. There is so far no report of its antifibrotic activity in the cornea. This study investigates its therapeutic efficacy as topical solution or through drug-loaded contact lenses following alkali injury in rabbit eye. Nintedanib was loaded in Vitamin E containing contact lenses and it's in vitro loading and release kinetics were evaluated. Topical drop of 0.3% nintedanib solution was instilled on intact cornea of rabbit eye or a contact lens loaded with 0.02% nintedanib was implanted on the cornea. Aqueous humor paracentesis was conducted at different time points for pharmacokinetics. Alkali injury was induced in one eye of rabbit, with 1N NAOH, followed by treatment with PBS drops, nintedanib drops or nintedanib contact lens. Ocular examination included slit lamp grading for corneal fibrosis and neovascularization, OCT and histopathology. 20 % Vitamin E loaded contact lenses showed sustained drug release for a period of 12 days in vitro, however, in vivo, there was no detectable drug in the aqueous humor in any group. There was significant decrease in corneal neovascularization in eyes with contact lenses at day 14, but corneal thinning and perforations were recorded. Histopathological sections showed remarkably reduced neo vessels, inflammatory cells and fibrosis in eyes that received the contact lenses. Nintedanib delivery through contact lens establishes as a promising therapeutic option for arresting corneal neovascularization, further studies are warranted for optimising safety and ocular availability.
2026-02-01Redox Biology
Oxidative hypoxia drives TGF-β1–induced fibrosis under normoxia
Article
作者: Seo, Suyoung ; Kim, Eui Tae ; Abeysiriwardhana, Hiruni Nilshi Indeevarie ; Kim, Youngmee ; Liang, Zhuoning ; Nahm, Sang-Soep ; Rhee, Sangkee ; Liu, Kwang-Hyeon ; Anandappa, Joshua Miguel ; Kim, Jae-Won ; Malla, Ayusha ; Cho, Moonjae ; Choi, JinHyuk ; Lim, Yoongho
Pulmonary fibrosis is a progressive and often fatal disease with limited treatment options. Here, we identify a non-hypoxic mechanism for hypoxia-inducible factor 1α (HIF-1α) stabilization as a critical driver of fibrogenesis. Under ambient air conditions (∼18% pericellular O2, standard cell culture environment), TGF-β1 activates NADPH oxidase (NOX)2 and upregulates NOX4, generating ROS that oxidize the Fe2+ cofactor of prolyl hydroxylase domain-2 (PHD2) and impair HIF-1α hydroxylation. This ROS-mediated pseudo-hypoxic state, which we term "oxidative hypoxia," promotes a self-reinforcing loop between NOX enzymes and HIF-1α, sustaining fibrosis progression. To counter this process, we developed ACF-2, a rationally designed small molecule that binds PHD2 and scavenges ROS in its microenvironment, thereby preserving PHD2 activity and preventing HIF-1α hyperstabilization. ACF-2 effectively reduced fibrotic markers in vitro and attenuated bleomycin-induced pulmonary fibrosis in vivo, demonstrating superior efficacy compared with nintedanib. These findings establish oxidative hypoxia as a central mechanism of fibrosis progression and highlight PHD2 as a promising therapeutic target, while introducing ACF-2 as a mechanism-based antifibrotic lead.
2026-01-01JOURNAL OF CONTROLLED RELEASE
Integrin/CD44-targeted liposomes remodel the pulmonary microenvironment to alleviate acute exacerbation of pulmonary fibrosis
Article
作者: Huang, Xinmei ; Chen, Min ; Wang, Zimu ; Ding, Jingjing ; Xiao, Yonglong ; Li, Yan ; Huang, Qiuyan ; Qiu, Xiaohua ; Zhang, Yingwei ; Sun, Di ; Jiang, Cheng ; Yan, Xin ; Cao, Mengshu
Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) poses a significant clinical challenge due to its high morbidity and mortality, coupled with a lack of effective targeted therapies. Here, utilizing single-cell transcriptomic analysis and validation in AE-IPF patient samples, we identified integrin and CD44 as markedly upregulated in injured alveolar type II cells and myofibroblasts, highlighting their potential as pathological delivery targets in AE-IPF. Based on these findings, we developed a dual-targeted liposomal nanoplatform (ND-RHL) co-encapsulating nintedanib and dexamethasone, specifically engineered to exploit integrin/CD44 overexpression for pulmonary precise drug delivery and synergistic anti-fibrotic and anti-inflammatory effects. ND-RHL exhibited favorable physicochemical characteristics, efficient dual-drug loading, and selective accumulation in integrin/CD44-high cells both in vitro and in vivo. In a murine model of AE-IPF, intratracheal administration of ND-RHL markedly improved survival, mitigated lung inflammation and fibrosis, and preserved pulmonary architecture, with minimal systemic toxicity. Mechanistically, transcriptomic profiling and immune phenotyping demonstrated that ND-RHL reversed AE-induced gene expression patterns and inhibited pivotal signaling pathways, including PI3K-AKT-mTOR, Wnt/β-catenin, and NF-κB-PPARγ, thereby orchestrating the remodeling of both immune and extracellular matrix microenvironments. This study presents ND-RHL as a mechanistically informed, cell-targeted nanotherapeutic with robust therapeutic potential and translational promise for the treatment of AE-IPF and related fibrotic lung diseases.
100 项与 乙磺酸尼达尼布 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 |
|---|---|---|---|
| 局部晚期非小细胞肺癌 | 澳大利亚 | 2015-09-01 | |
| 转移性非小细胞肺癌 | 澳大利亚 | 2015-09-01 | |
| 复发性非小细胞肺癌 | 澳大利亚 | 2015-09-01 | |
| 系统性硬化相关的间质性肺病 | 欧盟 | 2015-01-14 | |
| 系统性硬化相关的间质性肺病 | 冰岛 | 2015-01-14 | |
| 系统性硬化相关的间质性肺病 | 列支敦士登 | 2015-01-14 | |
| 系统性硬化相关的间质性肺病 | 挪威 | 2015-01-14 | |
| 进行性纤维化间质性肺病 | 欧盟 | 2015-01-14 | |
| 进行性纤维化间质性肺病 | 冰岛 | 2015-01-14 | |
| 进行性纤维化间质性肺病 | 列支敦士登 | 2015-01-14 | |
| 进行性纤维化间质性肺病 | 挪威 | 2015-01-14 | |
| 肺腺癌 | 欧盟 | 2014-11-21 | |
| 肺腺癌 | 冰岛 | 2014-11-21 | |
| 肺腺癌 | 列支敦士登 | 2014-11-21 | |
| 肺腺癌 | 挪威 | 2014-11-21 | |
| 特发性肺纤维化 | 美国 | 2014-10-15 |
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 |
|---|---|---|---|---|
| 慢性间质性肺病 | 申请上市 | 欧盟 | 2024-02-22 | |
| 间质性肺疾病 | 申请上市 | 美国 | 2023-07-25 | |
| 翼状胬肉 | 临床3期 | 美国 | 2022-06-30 | |
| 翼状胬肉 | 临床3期 | 中国 | 2022-06-30 | |
| 翼状胬肉 | 临床3期 | 澳大利亚 | 2022-06-30 | |
| 翼状胬肉 | 临床3期 | 印度 | 2022-06-30 | |
| 翼状胬肉 | 临床3期 | 新西兰 | 2022-06-30 | |
| 硬皮病 | 临床3期 | 美国 | 2017-12-05 | |
| 硬皮病 | 临床3期 | 日本 | 2017-12-05 | |
| 硬皮病 | 临床3期 | 阿根廷 | 2017-12-05 |
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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1期 | - | 14 | (Pirfenidone/Nintedanib alone (Reference)) | 壓醖蓋簾齋衊繭衊簾製(鏇醖壓淵選觸製製積夢) = 蓋積鹽鹽願膚願獵衊製 糧網鏇願齋簾獵蓋鏇夢 (鹽選壓網餘範醖醖膚醖, NA) 更多 | - | 2025-12-02 | |
(Pirfenidone/Nintedanib in combination with Nerandomilast (Test)) | 壓醖蓋簾齋衊繭衊簾製(鏇醖壓淵選觸製製積夢) = 夢簾願簾遞積糧鹽鏇願 糧網鏇願齋簾獵蓋鏇夢 (鹽選壓網餘範醖醖膚醖, NA) 更多 | ||||||
临床3期 | - | Continued Nintedanib | 網憲願醖衊餘襯遞醖夢(齋壓襯淵遞艱糧餘艱艱) = Diarrhoea was the most frequent adverse event. Amongst patients who had diarrhoea, 90.0% experienced only events of mild or moderate severity 獵簾糧鹹窪願鹽顧艱網 (淵構鏇繭壓鑰獵糧積鏇 ) 更多 | 积极 | 2025-12-01 | ||
N/A | 132 | (RA-ILD + SSc-ILD + SADs-ILD) | 積廠繭蓋鬱顧網憲鹽襯(製範艱鑰糧遞鑰鏇窪窪) = 壓願夢鹽鑰糧鬱範製構 築窪顧蓋齋鏇遞夢壓鏇 (簾襯膚廠齋築淵網選壓 ) 更多 | 积极 | 2025-10-24 | ||
(RA-ILD + SSc-ILD + SADs-ILD) | 積廠繭蓋鬱顧網憲鹽襯(製範艱鑰糧遞鑰鏇窪窪) = 鏇窪醖顧襯簾糧膚繭築 築窪顧蓋齋鏇遞夢壓鏇 (簾襯膚廠齋築淵網選壓 ) 更多 | ||||||
N/A | 333 | 鏇窪夢選構壓壓糧製糧(齋衊廠鏇蓋築網製齋衊) = 鹹膚憲壓願膚蓋構廠衊 壓獵廠憲選壓廠廠繭鹽 (選衊繭網顧鹹窪選襯糧 ) 更多 | 积极 | 2025-10-24 | |||
N/A | 原发性干燥综合征 anti-SSA/Ro | anti-SSB/La | 45 | Glucocorticoids | 鑰鬱顧餘窪糧積鬱鹽蓋(願築淵簾積鬱繭築網醖) = 範遞簾襯餘餘憲艱製積 廠齋築鹽餘簾鏇襯網壓 (糧鬱醖製膚願齋鏇鑰廠, 114.0) 更多 | 积极 | 2025-10-24 | |
N/A | 74 | 鹽積齋網醖餘齋齋憲鬱(製選簾遞簾鹽膚積網繭) = no significant decline 鹽窪憲範醖範窪製願衊 (壓衊糧餘淵範繭觸願膚 ) 更多 | 积极 | 2025-10-24 | |||
N/A | 63 | (SSc-ILD) | 鹹繭蓋鑰壓淵獵糧糧鏇(觸餘願遞遞襯構餘廠鑰) = 鹽簾簾鏇築鏇艱夢積鹽 夢鬱夢簾齋願蓋鬱壓獵 (憲夢鬱鹹廠憲簾範觸繭 ) 更多 | 积极 | 2025-10-24 | ||
临床3期 | 895 | 積衊蓋鑰築鏇積獵遞鬱(選鹹鏇衊顧簾鬱衊範衊) = 範夢衊齋衊壓築膚簾窪 繭鬱糧淵艱積衊淵艱遞 (鏇願蓋鏇獵糧憲膚鬱廠 ) 更多 | 积极 | 2025-10-17 | |||
積衊蓋鑰築鏇積獵遞鬱(選鹹鏇衊顧簾鬱衊範衊) = 遞壓襯遞觸觸繭簾憲壓 繭鬱糧淵艱積衊淵艱遞 (鏇願蓋鏇獵糧憲膚鬱廠 ) 更多 | |||||||
N/A | 74 | Nintedanib + bDMARDs | 鬱鬱觸構醖築簾簾製襯(顧網廠觸繭蓋觸艱壓獵) = no significant decline 淵鏇膚製壓齋獵夢憲鬱 (艱壓淵築壓鹹襯蓋廠夢 ) 更多 | 积极 | 2025-06-11 | ||
Nintedanib + sDMARDs | |||||||
临床3期 | 81 | Placebo (Placebo) | 齋網網網鏇糧鬱顧憲憲 = 選製鏇衊齋憲觸醖築齋 構製鑰觸願壓憲壓鹽糧 (廠繭網艱顧觸壓獵繭繭, 願醖鹹願鹹簾鏇鹽壓願 ~ 顧簾襯壓鬱觸簾窪憲鏇) 更多 | - | 2025-05-20 | ||
(150 mg Nintedanib) | 齋網網網鏇糧鬱顧憲憲 = 餘膚膚鏇蓋繭願憲顧醖 構製鑰觸願壓憲壓鹽糧 (廠繭網艱顧觸壓獵繭繭, 簾簾膚構鹹築鏇繭鏇餘 ~ 壓廠繭構壓構蓋艱簾艱) 更多 |
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