预约演示
更新于：2026-01-04
Utidelone
优替德隆
更新于：2026-01-04
概要
基本信息
原研机构 |
在研机构 |
最高研发阶段批准上市 |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国)、优先审评 (中国)、特殊审批 (中国) |
登录后查看时间轴
结构/序列
分子式C27H41NO5S |
InChIKeyXOZIUKBZLSUILX-GIQCAXHBSA-N |
CAS号189453-10-9 |
关联
65
项与 优替德隆 相关的临床试验ChiCTR2500115269
Study on the efficacy of Utidelone combined with Anotinib in the treatment of advanced Non-Small Cell Lung Cancer
NCT07044349
Phase II Clinical Study of Utidelone Capsule (UTD2) in Patients With Advanced Epithelial Ovarian, Fallopian Tube, or Primary Peritoneal Cancer
NCT06841679
A Multi-national, Open-label, Randomized Phase II/III Clinical Study of Utidelone Capsule (UTD2) Combined With Fluoropyrimidine- and Platinum-containing Therapy in First-line Treatment of Patients With Locally Advanced or Metastatic Gastric or Gastroesophageal Junction Adenocarcinoma
100 项与 优替德隆 相关的临床结果
登录后查看更多信息
100 项与 优替德隆 相关的转化医学
登录后查看更多信息
100 项与 优替德隆 相关的专利（医药）
登录后查看更多信息
220
项与 优替德隆 相关的文献（医药）2025-10-01Neurotherapeutics
Nanoparticle and epothilone D combinatorial intervention improves motor performance and regeneration in chronic cervical spinal cord injury
Article
作者: Ross, Brian C ; Schwartz, Samantha R ; Hocevar, Sarah E ; Cummings, Brian J ; Smiley, Brooke M ; Shea, Lonnie D ; Anderson, Aileen J
Spinal cord injury (SCI) causes the loss of motor function below the site of injury due to neuron loss and the severing of spinal tracts. The injury leads to the recruitment of circulating myeloid cells that create an inflammatory microenvironment and exacerbate cell death, with subsequent migration of fibroblasts and astrocytes that contribute to scar tissue that inhibits regeneration. Herein, we investigated a combinatorial treatment in a chronic cervical hemisection model involving cargo-less nanoparticles (NPs) administered acutely, and a multichannel bridge and microtubule stabilizer delivered chronically. NPs administration acutely for one-week post-injury contributed to improved paw placement on a ladder beam relative to vehicle control. Four weeks after injury, damaged tissue was resected, and a microporous, multichannel PLG bridge was inserted to reduce scar tissue and provide a substrate for axon regrowth. Epothilone D (epoD), a microtubule stabilizer, was also administered to further decrease fibrotic scar formation and improve axon elongation. Mice receiving a scaffold with NP treatment or epoD treatment had improved motor performance, but the combination of NP and epoD maximally improved function. In conjunction with this improved performance, mice that received NPs or epoD exhibited increased neuromuscular junction innervation, robust axon growth into the bridge, and both oligodendrocyte and Schwann-cell myelination of regenerating axons. Collectively, these results suggest that a combinatorial treatment plan targeting inflammation and scarring, a substrate for growth, and growth-promoting factors can improve motor performance following SCI.
2025-08-23Zhonghua zhong liu za zhi [Chinese journal of oncology]
[Utidelone induces apoptosis and autophagy in small cell lung cancer cells through the ROS/AMPK signaling pathway].
Article
作者: Mu, X Q ; Wu, H B ; Hu, X F ; Yu, C N ; Zhao, Y Q
Objective: To investigate the effects and underlying molecular mechanisms of Utidelone (UTD1) in small cell lung cancer (SCLC). Methods: The study utilized small cell lung cancer H446 and H1048 cell lines along with animal models. Cell proliferation, cell cycle progression, apoptosis, autophagy, and related activities following UTD1 treatment were assessed using Cell Counting Kit-8 (CCK-8), flow cytometry, immunofluorescence staining, reactive oxygen species (ROS) generation assay, and Western blot analysis. The involvement of the ROS/adenosine monophosphate-activated protein kinase (AMPK) signaling pathway was also examined. Data analysis was performed using GraphPad Prism version 8 software. Results: UTD1 inhibited the viability of H446 and H1048 cells in a dose- and time-dependent manner. The half inhibitory concentrations (IC50) of UTD1 for H446 and H1048 cells were 0.675 and 0.439 μg/ml, respectively. The proportion of cells in the G2/M phase for H446 and H1048 cells in the UTD1 group at 6 h, 12 h, and 24 h was [(53.86±4.54)%, (68.59±5.49)%, (60.89±3.26)%] and [(46.83±2.20)%, (60.67±3.44)%, (57.88±5.11)%], which were significantly higher than that in the control group, except for the proportion of H1048 cells at 6 h [(38.99±2.60)% vs. (40.73±2.50)%, P＜0.05]. The apoptosis rates were [(23.57±0.12)%, (35.79±1.59)%, and (46.15±4.57)%] for H446 cells and [(23.05±2.70)%, (37.73±2.97)%, and (43.39±3.31)% for H1048 cells], all of which were significantly higher than those in the control group [(6.44±0.96)%, (6.31±0.75)%, respectively; all P＜0.05]. The number of LC3 fluorescent spots was [(56±11), (69±8), and (66±8)] for H446 cells and [(39±7), (56±12), and (50±11)] for H1048 cells, both significantly higher than those in the control group [(13±6) and (12±5), respectively; both P＜0.05]. The relative fluorescence intensity of ROS was 2.54±0.48, 2.85±0.68, and 5.03±0.72 for H446 cells and 2.26±0.51, 4.17±0.35, and 4.66±0.51 for H1048 cells, which were also significantly higher than those in the control group (P＜0.05). The expression levels of cyclin B1, cyclin A2, and P21 of H446 cells in the three time points were [(0.63±0.07, 0.33±0.05, 0.23±0.04), (0.68±0.08, 0.46±0.03, 0.27±0.06), and (0.64±0.03, 0.32±0.05, 0.22±0.03), respectively], all significantly lower compared to the control group (P＜0.05). The apoptosis rates of H446 and H1048 cells in the UTD1+Z-VAD-FMK group were (19.97±3.19)% and (17.68±3.14)%, both lower than those in the UTD1 group [(40.73±3.35)% and (39.82±2.45)%, respectively; all P＜0.05]. The absorbance values of H446 and H1048 cells in the UTD1+3-MA group were significantly higher than those in the UTD1 group at 6h, 12h, and 24h (all P＜0.05). The levels of p-AMPKα/AMPKα, LC3-II expression, and the percentage of apoptotic cells in the H446 and H1048 cells of the UTD1+NAC group were [(1.33±0.09, 1.33±0.11), (1.49±0.16, 1.55±0.05), (17.24±2.15)%, and (19.40±4.28)%], all of which were lower than those observed in the UTD1 group [(1.98±0.17, 2.23±0.23), (2.81±0.19, 2.49±0.38), (38.07±3.53)%, and (41.20±1.87)%, all P＜0.05]. The number of LC3 fluorescence points and the percentage of apoptotic cells in the H446 and H1048 cells of the UTD1+si-AMPKα group [(24±5, 23±3), (18.35±1.15)%, and (19.15±3.46)%] were all lower than those in the UTD1+si-NC group [(46±6, 36±6), (39.34±1.77)%, and (39.50±2.15)%, all P＜0.05]. The tumor inhibition rates in small cell lung cancer tumor-bearing nude mice for the 2.5 mg/kg UTD1 group and the 5 mg/kg UTD1 group were 46.43% and 58.33%, respectively. Furthermore, the proportions of apoptosis-positive cells and p-AMPKα-positive cells in the UTD1 group were significantly higher compared to the control group, while the levels of Ki-67 positivity were significantly reduced. Conclusion: UTD1 inhibits SCLC cell proliferation, induces G2/M phase arrest, and promotes cell apoptosis and autophagy through the activation of the ROS/AMPK signaling pathway.
2025-08-01Therapeutic Advances in Medical Oncology
Efficacy and safety of utidelone in pretreated patients with metastatic breast cancer in China: a multicenter, real-world study
Article
作者: Ouyang, Quchang ; Zhao, Yannan ; Gong, Chengcheng ; Xu, Fei ; Xie, Ning ; Hu, Shihui ; Wang, Hong ; Wang, Biyun ; Chao, Tengfei
Background::
Utidelone (UTD1), a genetically engineered epothilone derivative, has been approved in China for use in combination with capecitabine in treating metastatic breast cancer (MBC) patients previously treated with anthracyclines or taxanes.
Objectives::
To evaluate the real-world efficacy and safety of UTD1 in Chinese patients with MBC and to explore potential predictors of therapeutic effectiveness.
Design::
A multicenter, retrospective, real-world study.
Methods::
MBC patients who received UTD1 between March 2021 and August 2023 were identified using an electronic database. Outcome variables included progression-free survival (PFS), overall survival (OS), time to treatment failure (TTF), objective response rate (ORR), clinical benefit rate (CBR), and adverse events (AEs).
Results::
A total of 270 MBC patients were included, with 81.1% presenting with visceral metastasis and 23.7% with brain metastasis. The median number of treatment lines for UTD1 was 3. UTD1 showed a median PFS of 3.97 months (95% confidence interval (CI) 3.33–4.61) and a median OS of 20.63 months (95% CI 16.72–24.54). Among the patients, 17.4% received UTD1 monotherapy, and 82.6% received UTD1-based combination therapy. The median TTF was 2.80 months (95% CI 2.31–3.29). The ORR was 8.4%, and the CBR was 33.5%. The most common AE was peripheral neuropathy (PN, 55.2%). Patients with unresolved PN from previous therapy or receiving UTD1 through intravenous infusion on days 1–5 were more likely to develop ⩾grade 3 PN.
Conclusion::
UTD1 is a new option for patients who have previously received taxanes and anthracyclines, with its clinical toxicity controllable.
100 项与 优替德隆 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 |
|---|---|---|---|
| 复发性乳腺癌 | 中国 | 2021-03-11 | |
| 转移性乳腺癌 | 中国 | 2021-03-11 |
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 |
|---|---|---|---|---|
| 局部晚期胃食管交界处腺癌 | 临床3期 | 美国 | 2025-08-28 | |
| 局部晚期胃食管交界处腺癌 | 临床3期 | 中国 | 2025-08-28 | |
| 胃食管交界处腺癌 | 临床3期 | 中国 | 2025-07-16 | |
| 胃食管交界处癌 | 临床3期 | 中国 | 2025-07-16 | |
| 局部晚期非小细胞肺癌 | 临床3期 | 中国 | 2022-12-08 | |
| 转移性非小细胞肺癌 | 临床3期 | 中国 | 2022-12-08 | |
| HER2 阴性乳腺癌 | 临床3期 | 中国 | 2022-03-01 | |
| 局部晚期乳腺癌 | 临床3期 | 中国 | 2022-03-01 | |
| 局部晚期乳腺癌 | 临床3期 | 中国 | 2022-03-01 | |
| 复发性铂耐药性卵巢癌 | 临床2期 | - | 2025-09-01 |
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2期 | HER2阳性乳腺癌 HER2-positive | 50 | 夢憲鑰膚窪繭襯齋艱積(壓膚醖築築築獵齋範簾) = 夢襯選鏇簾蓋憲憲積餘 壓網獵淵積顧繭觸獵襯 (夢鑰醖繭願壓選築鹹願, 39.3 ~ 68.2) 更多 | 积极 | 2025-12-12 | ||
临床2期 | 27 | 積齋蓋齋廠願鹽簾襯鹽(觸鑰簾鹹簾積鹹廠齋簾) = 願築願夢觸憲製膚鏇膚 觸鏇憲願淵獵簾範壓積 (襯獵選範繭憲壓衊鹹蓋 ) 更多 | 积极 | 2025-10-17 | |||
临床2期 | 不能切除性胰腺癌 一线 | 20 | Utidelone + Gemcitabine | 襯築選構蓋選構築衊鹹(鬱鑰鏇夢鹽蓋願醖築鹹) = 鏇淵築憲壓壓觸顧廠艱 夢憲顧積構鏇繭構淵夢 (襯積鬱鹽願積觸積衊窪 ) 更多 | 积极 | 2025-09-25 | |
临床2期 | 转移性HER2阴性乳腺癌 HER2/Neu Negative | 47 | 蓋壓積窪淵夢繭選廠獵(積襯積顧範膚鹽廠構網) = 製壓齋淵範夢積簾糧壓 鏇壓獵壓膚糧繭製獵窪 (憲構糧襯醖構網夢構襯, 28.3 ~ 57.8) 更多 | 积极 | 2025-08-01 | ||
临床2期 | 47 | Utidelone + Sintilimab + Oxaliplatin | 蓋積獵艱壓觸網壓遞壓(膚鹹廠繭繭餘糧觸淵選) = 衊鹹襯鹹蓋積觸繭構鑰 齋構襯範膚壓遞觸廠構 (製鏇膚廠繭構網醖餘構 ) 更多 | 积极 | 2025-05-30 | ||
Utidelone + Tislelizumab + Capecitabine | 蓋積獵艱壓觸網壓遞壓(膚鹹廠繭繭餘糧觸淵選) = 簾顧獵艱艱鑰壓範夢構 齋構襯範膚壓遞觸廠構 (製鏇膚廠繭構網醖餘構 ) 更多 | ||||||
临床1/2期 | 31 | Utidelone capsule (UTD2) 50 mg/m^2/d-5day | 遞鹽獵鏇範觸艱壓願襯(願顧糧餘廠鏇顧網範顧) = the most common ≥ Grade 3 AE was diarrhea appeared at 75 mg/m^2/d-7day, but recovered within 24 hours after supportive treatment 築鹹膚鏇夢餘積壓製餘 (積艱築糧構觸願鹽淵餘 ) 更多 | 积极 | 2025-05-30 | ||
Utidelone capsule (UTD2) 75 mg/m^2/d-5day | |||||||
临床2期 | 25 | 鏇糧襯願簾遞製顧鏇艱(觸鑰鹹壓顧繭憲壓鑰築) = 廠範齋窪襯願構選艱艱 餘鹹遞壓鑰壓鑰醖選餘 (憲繭蓋壓窪艱鏇選製遞 ) 更多 | 积极 | 2025-05-14 | |||
临床2期 | 转移性胰腺癌 一线 | 20 | 优替德隆+吉西他滨 | 鑰鏇鹽齋憲觸衊鬱衊製(簾獵鑰廠構觸齋遞鹽繭) = 選鑰夢製願構壓餘醖鹹 構製鬱願夢範襯簾襯淵 (蓋選蓋觸齋遞簾鏇範淵 ) 更多 | 积极 | 2024-09-30 | |
临床1期 | 实体瘤 二线 | 三线 | 末线 | 50 | 鹹顧獵選繭壓築襯範積(蓋淵築襯獵膚襯築網製) = 網顧醖蓋獵鑰醖艱觸簾 艱廠選鑰選糧觸製餘窪 (範襯襯餘繭廠淵廠願窪 ) 更多 | 积极 | 2024-09-15 | ||
临床2期 | 25 | 選醖鏇網積簾餘積積觸(簾膚鑰範鑰餘顧鑰顧鬱) = 構膚餘顧繭鬱鬱壓憲窪 選壓鑰艱範顧觸餘窪蓋 (齋齋齋艱繭鑰憲鑰製衊 ) 更多 | 积极 | 2024-05-24 |
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
生物医药百科问答
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