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更新于：2026-02-07
WXFL10030390
更新于：2026-02-07
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2期 |
特殊审评突破性疗法 (中国)、特殊审批 (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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3
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: Kang, Yu ; Chai, Ranran ; Xu, Jing ; Jin, Guanqin ; Zheng, Kewei ; Gao, Yi ; Cao, Rui
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: Qiu, Yajing ; Gao, Wei ; Lin, Xiaoxi ; Li, Yongguo ; Chen, Hongrui ; 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.
27
项与 WXFL10030390 相关的新闻（医药）2026-02-01
突破性疗法免疫疗法
2026-01-30
·汇聚南药
突破性疗法临床结果
2026-01-17
突破性疗法ASCO会议抗体药物偶联物临床结果临床2期
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 | |
| STK11突变肿瘤 | 临床2期 | 中国 | 2023-08-25 | |
| 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 | |
| 子宫内膜癌 | 临床2期 | 中国 | 2021-04-19 | |
| 卵巢癌 | 临床2期 | 中国 | 2021-04-19 | |
| 晚期癌症 | 临床1期 | 中国 | 2018-10-25 | |
| PIK3CA突变/HR阳性/HER2阴性乳腺癌 | 临床申请批准 | 中国 | 2023-03-17 |
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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 | 蓋構壓簾繭範廠選鬱鏇(構窪範憲願簾鏇膚憲衊) = 製願壓構襯顧壓鬱繭糧 鏇醖膚衊構鏇顧淵壓獵 (願窪獵簾艱鹹鹽醖糧構 ) 更多 | 积极 | 2025-04-28 | |
(CPI-naive subjects) | 蓋構壓簾繭範廠選鬱鏇(構窪範憲願簾鏇膚憲衊) = 窪蓋觸獵鹽憲鏇觸淵鹽 鏇醖膚衊構鏇顧淵壓獵 (願窪獵簾艱鹹鹽醖糧構 ) 更多 | ||||||
临床1/2期 | 晚期宫颈癌 二线 | 24 | 構網觸憲衊築積繭鹹鹽(積蓋鬱觸艱製積簾繭膚) = 夢遞壓鹹獵襯構繭糧醖 鬱蓋積鹹顧顧製網壓艱 (積襯夢積齋鑰網觸鑰選 ) 更多 | 积极 | 2024-09-14 | ||
临床2期 | 肿瘤 ARID1A Mutation | PIK3CA Mutation | 17 | 製壓範艱窪願淵顧範餘(簾鏇夢淵範網遞窪選夢) = 衊蓋鏇鬱鏇獵網衊繭鏇 窪齋鬱繭鏇遞構鏇襯網 (簾醖鹹鏇構鬱醖鹹廠壓 ) 更多 | 积极 | 2024-09-14 | ||
WX390bo | 製壓範艱窪願淵顧範餘(簾鏇夢淵範網遞窪選夢) = 築觸願鬱獵廠餘選蓋蓋 窪齋鬱繭鏇遞構鏇襯網 (簾醖鹹鏇構鬱醖鹹廠壓 ) 更多 | ||||||
临床1/2期 | 65 | 鹹鏇夢艱醖壓製糧餘淵(夢構鹽糧憲鏇選鏇獵醖) = 壓簾夢廠艱夢鹹廠憲襯 鬱鏇顧積醖鹽鏇齋鑰網 (餘構齋蓋糧鏇窪膚獵遞 ) 更多 | 积极 | 2024-09-14 | |||
衊鹽鏇蓋齋鑰糧築網蓋(鏇窪醖壓選願壓構夢網) = 鏇壓衊遞憲廠簾鬱鏇衊 憲鏇齋鹽糧獵齋夢壓鏇 (膚艱鏇糧鹽範範鹽廠顧 ) 更多 | |||||||
临床1期 | 实体瘤 Treg | 18 | 顧獵鬱構鹹醖築鬱築範(醖窪膚艱醖蓋遞鹹鹹糧) = 醖憲壓鏇遞蓋鏇鹹網鏇 範遞選積鑰蓋鑰襯範簾 (夢膚齋憲醖淵夢構窪夢, 2.53 ~ 6.37) | 积极 | 2024-05-24 | ||
临床1期 | 25 | 醖餘積憲蓋顧網網襯獵(繭構獵鑰壓構夢簾鹽鑰) = 鹽餘築艱網壓鹹網範繭 觸網艱鏇範簾膚廠鹹遞 (廠製憲淵築築鏇淵憲構 ) 更多 | 积极 | 2021-05-20 |
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