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更新于：2026-07-15
WXFL10030390
更新于：2026-07-15
概要
基本信息
药物类型 小分子化药 |
别名 WX 390、WX-390、WXFL 10030390 + [1] |
作用方式 抑制剂 |
作用机制 PI3K family 抑制剂(Phosphatidylinositol 3-kinase family inhibitors)、mTOR抑制剂(丝氨酸/苏氨酸蛋白激酶mTOR抑制剂) |
非在研适应症 |
原研机构 |
非在研机构- |
最高研发阶段临床3期 |
首次获批日期- |
最高研发阶段(中国)临床3期 |
特殊审评特殊审批 (中国)、突破性疗法 (中国) |
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关联
6
项与 WXFL10030390 相关的临床试验NCT07392060
A Randomized, Open-Label, Controlled, Multicenter Phase III Clinical Study of WX390 Combined With Toripalimab Versus Investigator's Choice of Therapy in Patients With Recurrent or Metastatic Cervical Cancer Who Have Failed Prior Platinum-Based Treatment
NCT06124963
A Phase II Study to Evaluate the Safety, Tolerability and Preliminary Efficacy of WX390 Combined With Toripalimab in Patients With Advanced Gastric-type Endocervical Adenocarcinoma With STK11 Mutations
NCT06117566
A Phase Ib/IIa Study to Evaluate the Safety and Preliminary Efficacy of WX390 Combined With Toripalimab in Patients With Advanced Solid Tumors
100 项与 WXFL10030390 相关的临床结果
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100 项与 WXFL10030390 相关的转化医学
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100 项与 WXFL10030390 相关的专利（医药）
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4
项与 WXFL10030390 相关的文献（医药）2025-12-01CANCER CHEMOTHERAPY AND PHARMACOLOGY
Targeting on the PI3K/mTOR: a potential treatment strategy for clear cell ovarian carcinoma
Article
作者: Yi Gao ; Jing Xu ; Rui Cao ; Kewei Zheng ; Ranran Chai ; Guanqin Jin ; Yu Kang
PURPOSE:
Ovarian clear cell carcinoma is a highly malignant gynecological tumor characterized by a high rate of chemotherapy resistance and poor prognosis. The PI3K/AKT/mTOR pathway is well-known to be closely related to the progression of various malignancies, and recent studies have indicated that this pathway may play a critical role in the progression and worsening of OCCC.
METHODS:
In this study, we investigated the combined effects of WX390, a dual inhibitor of PI3K/mTOR, and cisplatin on OCCC through both in vitro and in vivo experiments to further elucidate their therapeutic effects.
RESULTS:
WX390 significantly inhibited the proliferation of human OCCC cell lines ES2 and OVISE, while promoting apoptosis. Furthermore, the combination of WX390 with CDDP exhibited a synergistic effect, markedly increasing the sensitivity of OCCC cells to chemotherapeutic agents and significantly suppressing tumor growth in PDX models. Western blot and RNA-seq analyses revealed that WX390 robustly inhibited the PI3K/AKT/mTOR pathway, interrupt autophagy, altered cell cycle dynamics, and induced apoptosis.
CONCLUSION:
This study comprehensively assessed the efficacy of WX390 across multiple models of OCCC, laying a solid foundation for the development of new therapeutic strategies for this challenging malignancy.
2024-08-01iScience
PIK3CA mutations enhance the adipogenesis of ADSCs in facial infiltrating lipomatosis through TRPV1
Article
作者: Li, Yongguo ; Lin, Xiaoxi ; Chen, Hongrui ; Qiu, Yajing ; Gao, Wei ; Ye, Wei ; Sun, Bin ; Hua, Chen ; Wei, Wei ; Song, Haoliang
Facial infiltrating lipomatosis (FIL) is a congenital disorder. The pathogenesis of FIL is associated with PIK3CA mutations, but the underlying mechanisms remain undetermined. We found that the adipose tissue in FIL demonstrated adipocytes hypertrophy and increased lipid accumulation. All adipose-derived mesenchymal stem cells from FIL (FIL-ADSCs) harbored PIK3CA mutations. Moreover, FIL-ADSCs exhibited a greater capacity for adipogenesis. Knockdown of PIK3CA resulted in a reduction in the adipogenic potential of FIL-ADSCs. Furthermore, WX390, a dual-target PI3K/mTOR inhibitor, was found to impede PIK3CA-mediated adipogenesis both in vivo and in vitro. RNA sequencing (RNA-seq) revealed that the expression of transient receptor potential vanilloid subtype 1 (TRPV1) was upregulated after PI3K pathway inhibition, and overexpression or activation of TRPV1 both inhibited adipogenesis. Our study showed that PIK3CA mutations promoted adipogenesis in FIL-ADSCs and this effect was achieved by suppressing TPRV1. Pathogenesis experiments suggested that WX390 may serve as an agent for the treatment of FIL.
AME case reports
PIK3CA inhibitor treatment for metastatic scrotal extramammary Paget’s disease: a case report and literature review
Article
作者: Dong, Siying ; Li, Jinyan ; Liu, Yujie ; Xiao, Lin ; Chen, Hongbo ; Huang, Jun ; Yuan, Jia ; Ren, Jianqing ; Huang, Yuanqiong ; Wu, Chenwang
Background:
Extramammary Paget's disease (EMPD) is a rare intraepithelial adenocarcinoma that occurs in the genitals, axilla, and anus, where apocrine sweat glands are abundant. This disease is mainly characterized by localized lesions and rare distant metastasis. Scrotal Paget's disease is a rare type of EMPD, and there is no standard treatment for metastatic EMPD.
Case Description:
Here, we reported the genetic results of a patient with a PIK3CA gene mutation in scrotal Paget's disease who developed multiple metastases to the lymph nodes, liver, and bones during adjuvant radiotherapy, as well as the results of treatment with a PIK3CA inhibitor. The latest advances in this field were also summarized. The treatment response was evaluated as stable disease (SD) after 6 courses of docetaxel plus tegafur (DS regimen) chemotherapy. Then, a second-line treatment, a PIK3CA inhibitor, WX390, was administered with tolerable toxicity. There was a treatment-induced increase in blood glucose level during treatment, and insulin was administrated with good control. The progression-free survival (PFS) was 3.9 months and the overall survival (OS) was 16 months.
Conclusions:
PIK3CA is a commonly mutated gene in EMPD. To the best of our knowledge, this is the first case report of a PIK3CA inhibitor for the treatment of primary metastatic EMPD, and the treatment efficacy was good. PIK3CA inhibitors may be promising for the treatment of metastatic EMPD in the future.
100 项与 WXFL10030390 相关的药物交易
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研发状态
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 子宫颈转移癌 | 临床3期 | - | 2026-02-28 | |
| 晚期宫颈癌 | 临床3期 | 中国 | 2026-02-13 | |
| STK11突变肿瘤 | 临床2期 | 中国 | 2023-08-25 | |
| STK11突变非小细胞肺癌 | 临床2期 | 中国 | 2023-08-01 | |
| 子宫颈腺癌 | 临床2期 | 中国 | 2023-08-01 | |
| 淋巴瘤 | 临床2期 | 中国 | 2022-10-28 | |
| PIK3CA阳性实体瘤 | 临床2期 | 中国 | 2021-06-03 | |
| 晚期恶性实体瘤 | 临床2期 | 中国 | 2021-05-11 | |
| 宫颈鳞状细胞癌 | 临床2期 | 中国 | 2021-04-19 | |
| 子宫内膜癌 | 临床2期 | 中国 | 2021-04-19 |
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临床结果
临床结果
适应症
分期
评价
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临床1/2期 | 晚期宫颈癌 PIK3CA mutation status | 49 | WX390 + Toripalimab | 壓選糧簾廠獵顧鑰襯網(範艱廠憲鹹遞醖淵糧窪) = 積簾鹽憲簾製鹹簾觸獵 艱衊積壓觸選築憲夢鬱 (蓋願網憲構鹽網範鑰餘 ) 更多 | 积极 | 2025-04-28 | |
(CPI-naive subjects) | 壓選糧簾廠獵顧鑰襯網(範艱廠憲鹹遞醖淵糧窪) = 窪獵願淵顧製鏇膚廠顧 艱衊積壓觸選築憲夢鬱 (蓋願網憲構鹽網範鑰餘 ) 更多 | ||||||
临床1/2期 | 晚期宫颈癌 二线 | 24 | 範廠網鑰構遞壓窪齋鹹(鑰餘繭範願窪鏇糧製鏇) = 築夢顧鬱鹽鏇觸淵鹽餘 衊鑰襯齋顧顧獵範鑰廠 (範鬱齋觸蓋鹽壓鑰繭膚 ) 更多 | 积极 | 2024-09-14 | ||
临床2期 | 肿瘤 ARID1A Mutation | PIK3CA Mutation | 17 | 簾夢壓餘範獵願簾構範(衊鏇構鬱醖衊膚鏇齋觸) = 網網壓齋艱願蓋窪網膚 積醖廠鑰糧遞獵積夢壓 (淵網醖鏇蓋簾衊窪積網 ) 更多 | 积极 | 2024-09-14 | ||
WX390bo | 簾夢壓餘範獵願簾構範(衊鏇構鬱醖衊膚鏇齋觸) = 憲構製醖醖製築鏇遞醖 積醖廠鑰糧遞獵積夢壓 (淵網醖鏇蓋簾衊窪積網 ) 更多 | ||||||
临床1/2期 | 65 | 醖淵鹽願淵積繭製鬱廠(憲壓壓餘築範選衊衊鹽) = 憲製糧範獵艱願遞顧廠 廠簾窪鹹範憲鑰艱廠齋 (簾蓋淵遞鏇顧繭襯觸夢 ) 更多 | 积极 | 2024-09-14 | |||
願艱廠醖獵膚衊網願鬱(壓衊淵壓築願膚醖獵壓) = 窪觸範鹽鏇蓋淵願製窪 夢醖鹹壓艱構鹹糧繭窪 (廠鑰積艱窪網艱壓鹽廠 ) 更多 | |||||||
临床1期 | 实体瘤 Treg | 18 | 鬱廠鏇築淵鹹窪襯鬱鑰(餘願遞構範廠獵鬱廠鹹) = 淵艱廠襯製鹽夢窪願顧 觸壓獵範積糧醖遞憲獵 (齋簾齋膚淵範構餘願衊, 2.53 ~ 6.37) | 积极 | 2024-05-24 | ||
临床1期 | 25 | 齋衊夢艱鑰艱醖選壓鬱(鏇顧鏇廠積鏇壓襯夢壓) = 鏇獵願遞鹹醖簾襯製膚 鏇範製築糧餘衊築觸襯 (醖鹽糧鹹願築齋鹽襯願 ) 更多 | 积极 | 2021-05-20 |
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