预约演示
更新于：2026-09-26
Buparlisib
更新于：2026-09-26
概要
基本信息
药物类型 小分子化药 |
别名 Buparlisib (USAN/INN)、Buparlisib hydrochloride、AN-2025 + [4] |
作用方式 抑制剂 |
作用机制 PI3Kα抑制剂(磷脂酰肌醇3-激酶α抑制剂)、PI3Kβ抑制剂(磷脂酰肌醇-3激酶β抑制剂)、PI3Kγ抑制剂(磷脂酰肌醇-3激酶γ抑制剂) |
治疗领域 |
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 |
特殊审评快速通道 (美国)、儿科研究计划 (欧盟)、特殊审批 (中国) |
登录后查看时间轴
结构/序列
分子式C18H21F3N6O2 |
InChIKeyCWHUFRVAEUJCEF-UHFFFAOYSA-N |
CAS号944396-07-0 |
关联
101
项与 Buparlisib 相关的临床试验NCT04975958
An Open-Label, Multicenter, Phase 1a Study of AN2025 and AN0025 in Double Combination With Atezolizumab and in Triple Combination With Atezolizumab in Patients With Advanced Solid Tumors
EUCTR2015-003103-27-GB
A proof of concept phase II study of Buparlisib in HER2 positive breast cancer with brain metastasis following HER2 directed monoclonal antibody therapy
NCT02756247
Phase Ib Clinical Trial of Buparlisib and Ibrutinib in Mantle Cell Lymphoma, Follicular Lymphoma and Diffuse Large B Cell Lymphoma
100 项与 Buparlisib 相关的临床结果
登录后查看更多信息
100 项与 Buparlisib 相关的转化医学
登录后查看更多信息
100 项与 Buparlisib 相关的专利（医药）
登录后查看更多信息
565
项与 Buparlisib 相关的文献（医药）2026-07-01ORAL ONCOLOGY
Efficacy of buparlisib according to PIK3CA mutation status in recurrent or metastatic head and neck squamous cell carcinoma: A multicenter phase II trial
Article
作者: Kotecki, Nuria ; Attignon, Valéry ; Pérol, David ; Garin, Gwenaelle ; You, Benoît ; Fayette, Jérome ; Wang, Qing ; Lefebvre, Gautier ; Tabone-Eglinger, Séverine ; Cupissol, Didier ; Daste, Amaury ; Peyrade, Frédéric ; Guyennon, Aurélie ; Treilleux, Isabelle ; Gauduchon, Thibault ; Digue, Laurence ; Even, Caroline ; Couchon-Thaunat, Sophie ; Ferlay, Céline ; Tourneau, Christophe Le
BACKGROUND:
The PI3K/AKT pathway activation is an independent marker of poor outcome in head and neck squamous-cell carcinoma (HNSCC), and involved in resistance to cetuximab. Molecular alterations in this pathway, particularly PIK3CA mutations, represent a key event of this dysregulation. Buparlisib is a pan-Class I PI3K inhibitor that inhibits tumor growth in HNSCC xenografts.
METHODS:
This phase II trial evaluated buparlisib (100 mg/d) in two parallel cohorts of refractory HNSCC patients (progression after platinum and cetuximab) with or without PIK3CA mutated in exons 9/20. The primary endpoint was the 2-month Disease Control Rate (DCR2m) as per centrally reviewed. Buparlisib would be considered ineffective if DCR2m ≤ 10% and promising if ≥ 30% (α: 5% unilateral, power: 90%): 7 successes for 35 evaluable patients per cohort were required. Secondary endpoints included ORR, PFS, OS, and safety.
RESULTS:
From January 2013 to July 2018, 58 HNSCC patients received ≥ 1 dose of buparlisib (PIK3CA wild-type, n = 36; PIK3CA-mutated, n = 22); 78% had received ≥ 2 prior lines of systemic therapy. The PIK3CA-mutated cohort was prematurely closed because of slow accrual. The DCR2m was 38.9% (95% CI [25.5- + ∞[) in PIK3CA wild-type and 36.4% (95% CI [19.5 - + ∞[) in PIK3CA-mutated patients. A total of 53.4% of patients experienced treatment-related grade ≥ 3 adverse events. The most frequent (>5%) were hyperglycemia, lymphopenia, asthenia, sodium decrease, depression, and dermatitis. Two toxic deaths were reported.
CONCLUSION:
Although the trial met the primary endpoint, buparlisib monotherapy was associated with unacceptable toxicity and showed limited efficacy in heavily pretreated HNSCC patients.
2026-06-29VETERINARNI MEDICINA
Impact of histological and molecular subtype on the potential therapeutic effect of buparlisib in canine mammary gland tumours
Article
作者: Ugur, Aslihan Baykal ; Turna, Ozge ; Eskiler, Gamze Guney
This study aims to evaluate the response of primary cells to buparlisib, a PI3K inhibitor, at varying concentrations and exposure durations across different histological and molecular subtypes of CMGTs, and to assess PI3K/Akt/mTOR pathway activity by measuring Akt and mTOR expression. Three carcinomas (C), three sarcomas (S), and two carcinosarcomas (CS) tumours were collected from the dogs. The primary cells were produced from tissues and treated with buparlisib at different doses. Subsequently, the WST-1 assay, Annexin V, and AO/PI staining were performed sequentially to evaluate the effects of buparlisib. PI3K/Akt/mTOR signalling pathway inhibition was revealed at the gene level in C, S, and CS cells following 5 µM buparlisib treatment by RT-PCR analysis. Our results demonstrated that C1 and C2 (basal-like) cells were more sensitive than C3, CS1, and CS2 cells (luminal A) upon buparlisib treatment. Liposarcoma S2 cells responded more to buparlisib than undifferentiated S cells (S1 and S3). Buparlisib also induced apoptosis and inhibited Akt and mTOR mRNA levels in C2, C3, S2 and S3 cells (P < 0.05). A higher rate of apoptotic cell death was observed in the C histological subtype and basal-like cells, with 62.9 ± 0.8% apoptosis in C1 and 79.1 ± 0.3% in C2. The efficacy of buparlisib was more pronounced in C2 basal-like CMGT cells and liposarcoma S2 cells with the downregulation of Akt and mTOR mRNA levels (P < 0.001). Therefore, PI3K inhibitors could be used to treat CMGT, particularly the basal-like molecular subtype.
2026-06-01NEURO-ONCOLOGY
Targeting tumor-associated macrophage-induced IGF1/PI3K/Zic1 axis triggers SHH medulloblastoma regression and chemosensitization
Article
作者: Taylor, Michael D ; Yin, Zhinan ; Li, Peng ; Gonzalez, Ricardo Daniel ; Chen, Xuan ; Feng, Zhaoyang ; Liu, Yong-Qiang ; Chen, Hai-Xin ; Nie, Menglin ; Gonzalez-Salinas, Fernando ; Santa-Maria Lopez, Vicente ; Wang, Han-Chen ; Daniels, Craig ; Pang, Yan-Chun ; Liu, Hailong ; Jiang, Tao ; Peng, Dong-Ling ; Wu, Changfeng ; Qiu, Jun-Feng ; Koh, Hyun Yong ; Deng, Kaiwen ; Su, Yu ; Tian, Yu ; Wang, Chi ; Zhang, Jiao ; Wang, Yanan
Abstract:
Background:
Tumor-associated macrophages (TAMs) are key contributors to the brain tumor microenvironment. However, their role in medulloblastoma (MB) progression and chemoresistance remains elusive.
Methods:
We utilized the CD11b-diphtheria toxin receptor (DTR)/Ptch1-deficient MB model to genetically delete TAMs. NeuroD2-SmoA1 MB mice were treated with CSF1R inhibitor PLX3397, PI3K inhibitor buparlisib, and a combination of PLX3397 with chemotherapy to examine the functional significance of TAMs in MB. Tumor tissues and cell co-culture system were analyzed using RNA sequencing (RNA-seq), Western blotting, flow cytometry, immunohistochemistry, quantitative polymerase chain reaction, and EdU assay to delineate mechanistic interactions.
Results:
Myeloid-derived TAMs were abundant in MB tissues and primarily exhibited M2-like polarization. We demonstrated that TAM depletion, achieved either genetically via diphtheria toxin or pharmacologically via PLX3397-mediated preferential targeting of M2-like TAMs, markedly downregulates Zic1 expression and impedes MB growth. Mechanistically, M2-like TAMs secreted high levels of IGF1 to activate the PI3K/mTOR/Zic1 axis in MB cells, whereas the PI3K inhibitor buparlisib effectively reduced the population of Zic1-expressing cells and restricted MB growth. Notably, the PI3K/mTOR/Zic1 axis was demonstrated to confer chemoresistance. While chemotherapy exacerbates M2-like TAM accumulation within MB, combining PLX3397 with chemotherapy abrogates this infiltration and attenuates IGF1/PI3K/Zic1 signaling axis. This combination strategy synergistically inhibits tumor growth and extends survival in mice.
Conclusion:
Our findings demonstrate that inhibiting the TAM-induced IGF1/PI3K/Zic1 signaling axis results in MB regression and chemosensitization. These results underscore the therapeutic potential of combining a clinical CSF1R inhibitor with standard chemotherapy as an effective treatment strategy for SHH-MB.
100 项与 Buparlisib 相关的药物交易
登录后查看更多信息
外链
| KEGG | Wiki | ATC | Drug Bank |
|---|---|---|---|
| D10584 | Buparlisib | - |
研发状态
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 |
|---|---|---|---|---|
| 头颈部鳞状细胞癌 | 临床3期 | 中国 | 2021-04-07 | |
| 转移性头颈部鳞状细胞癌 | 临床3期 | 美国 | 2020-12-12 | |
| 转移性头颈部鳞状细胞癌 | 临床3期 | 中国 | 2020-12-12 | |
| 转移性头颈部鳞状细胞癌 | 临床3期 | 日本 | 2020-12-12 | |
| 转移性头颈部鳞状细胞癌 | 临床3期 | 阿根廷 | 2020-12-12 | |
| 转移性头颈部鳞状细胞癌 | 临床3期 | 澳大利亚 | 2020-12-12 | |
| 转移性头颈部鳞状细胞癌 | 临床3期 | 比利时 | 2020-12-12 | |
| 转移性头颈部鳞状细胞癌 | 临床3期 | 加拿大 | 2020-12-12 | |
| 转移性头颈部鳞状细胞癌 | 临床3期 | 法国 | 2020-12-12 | |
| 转移性头颈部鳞状细胞癌 | 临床3期 | 德国 | 2020-12-12 |
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3期 | PD-L1阳性头颈部鳞状细胞癌 PD-1(PD-L1)-pretreated | HPV-negative | 487 | Buparlisib (BUP) + Paclitaxel (PAC) | 鹽窪範壓淵願蓋醖顧顧(觸膚繭艱憲築遞鏇餘齋) = 襯積窪積網觸膚簾積築 選選範醖顧選製鑰鏇鬱 (襯艱選遞積衊醖窪襯蓋 ) 更多 | 不佳 | 2025-10-17 | |
Paclitaxel (PAC) | 鹽窪範壓淵願蓋醖顧顧(觸膚繭艱憲築遞鏇餘齋) = 遞繭獵遞膚衊鬱鹹簾觸 選選範醖顧選製鑰鏇鬱 (襯艱選遞積衊醖窪襯蓋 ) 更多 | ||||||
临床2期 | 158 | Buparlisib + Paclitaxel | 顧網積觸夢繭窪淵壓觸(餘鹹觸糧製築鹽網餘簾) = 齋蓋範壓衊齋夢網構憲 醖廠願鬱衊衊窪遞憲糧 (獵鑰積蓋齋鑰膚網遞積 ) 更多 | 积极 | 2025-01-14 | ||
Placebo + Paclitaxel | 襯襯鹹繭繭夢襯蓋艱蓋(廠窪築醖衊遞鹽膚鑰淵) = 鬱衊膚鑰憲簾遞醖繭壓 顧觸簾壓鏇蓋製齋繭壓 (鹽鏇範網網壓築鹹鑰糧 ) | ||||||
临床1期 | 23 | 餘餘餘壓鏇繭遞蓋夢選 = 鑰築壓鬱窪鹽蓋艱積網 餘鬱遞鬱醖蓋獵簾艱蓋 (鹹醖餘繭壓構網夢醖範, 襯衊願顧襯願網淵鹽餘 ~ 鹹餘壓築餘衊鏇淵築獵) 更多 | - | 2024-11-05 | |||
餘餘餘壓鏇繭遞蓋夢選 = 蓋製鏇網鑰艱襯糧糧築 餘鬱遞鬱醖蓋獵簾艱蓋 (鹹醖餘繭壓構網夢醖範, 淵膚願觸鑰憲糧鬱築鏇 ~ 構蓋壓獵鏇積襯繭繭鬱) 更多 | |||||||
临床2期 | 10 | 獵觸餘顧窪餘築築衊醖 = 衊顧膚鹹餘製願獵廠鏇 選築顧憲鹹窪範憲觸鏇 (鏇築夢獵簾夢壓繭鑰壓, 窪鑰鬱積簾遞醖鏇願蓋 ~ 鏇遞選鏇構範範鑰鏇鹹) 更多 | - | 2022-02-01 | |||
临床2期 | 14 | 願鹽鏇顧夢網遞衊衊築(獵糧齋顧構鏇壓鑰鏇積) = 築獵鏇繭淵觸襯鹽網鑰 積淵網構膚廠鑰蓋壓夢 (醖憲襯衊鹹範鹽範艱鬱 ) 更多 | 积极 | 2022-01-01 | |||
临床1期 | 37 | 鏇窪淵艱顧繭範糧遞壓(壓積窪構淵積網築觸獵) = 鹹構鑰衊製遞廠顧願蓋 網繭齋憲繭膚鑰淵膚蓋 (窪鑰願獵醖顧憲簾築繭 ) 更多 | - | 2021-10-06 | |||
临床2期 | 19 | 廠鹽壓遞選夢衊鹽積範 = 膚選積構鬱構鏇觸鹽夢 夢衊糧鹽夢網鬱遞顧壓 (膚蓋蓋繭鬱積簾膚膚繭, 窪獵網鏇壓築築夢遞廠 ~ 築網窪製構願網範夢構) 更多 | - | 2021-06-21 | |||
临床3期 | 483 | Buparlisib + Paclitaxel | 糧範膚願憲餘襯齋願窪(網繭鏇膚構觸選夢鹽鬱) = 觸願餘積網醖簾構網願 選鹽襯鹹鬱顧蓋糧餘願 (積遞網餘獵觸獵觸膚衊 ) | 积极 | 2021-05-28 | ||
Paclitaxel alone | 糧範膚願憲餘襯齋願窪(網繭鏇膚構觸選夢鹽鬱) = 鏇糧願衊夢鹽顧淵製衊 選鹽襯鹹鬱顧蓋糧餘願 (積遞網餘獵觸獵觸膚衊 ) | ||||||
临床1期 | HR阳性HER2阴性淋巴结阳性乳腺癌 HR-Positive | HER2-Negative | 29 | Tamoxifen Citrate+Goserelin Acetate+Alpelisib | 繭願構鏇構齋鹹選願繭(淵糧鏇觸遞簾選鹹鏇遞) = 簾築壓範築鬱廠觸構壓 觸廠衊憲鑰窪願顧構獵 (積醖範選廠積襯壓鹽構 ) 更多 | 积极 | 2021-01-15 | |
Tamoxifen Citrate+Goserelin Acetate+Buparlisib | 繭願構鏇構齋鹹選願繭(淵糧鏇觸遞簾選鹹鏇遞) = 顧鬱膚衊顧遞襯顧夢廠 觸廠衊憲鑰窪願顧構獵 (積醖範選廠積襯壓鹽構 ) 更多 | ||||||
临床1期 | 70 | 鑰憲夢糧蓋願構窪鹽夢(願鏇蓋鬱憲鑰範築築遞) = 顧網製顧蓋廠艱鬱夢選 簾鹽觸糧顧糧醖窪壓鏇 (鏇範廠艱遞衊醖願襯構, 9.8 ~ 46.7) | - | 2021-01-15 |
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
提出任何生物医药研究问题
让每一步生物医药决策都精准制胜
基于十亿级生物数据与全球情报的精准 AI，赋能早期药物发现
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。
立即接入生物医药数据包
智慧芽新药库数据也通过智慧芽开放平台，以MCP或API服务形式对外开放。立即使用我们的MCP服务定制您的LLM智能体。
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