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更新于：2026-01-31
Venetoclax
维奈克拉
更新于：2026-01-31
概要
基本信息
药物类型 小分子化药 |
别名 VENCLYXTO、Venetoclax (JAN/USAN/INN)、维奈妥拉 + [15] |
靶点 |
作用方式 抑制剂 |
作用机制 Bcl-2抑制剂(细胞凋亡调控因子Bcl-2抑制剂) |
在研适应症 |
非在研适应症 |
最高研发阶段批准上市 |
首次获批日期 美国 (2016-04-11), |
最高研发阶段(中国)批准上市 |
特殊审评加速批准 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、孤儿药 (日本)、孤儿药 (澳大利亚)、附条件批准 (中国)、特殊审批 (中国)、突破性疗法 (美国) |
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结构/序列
分子式C45H50ClN7O7S |
InChIKeyLQBVNQSMGBZMKD-UHFFFAOYSA-N |
CAS号1257044-40-8 |
关联
819
项与 维奈克拉 相关的临床试验NCT07175415
ITCC-104: HEM-iSMART International Proof of Concept Therapeutic Stratification Trial of Molecular Anomalies in Relapsed or Refractory HEMatological Malignancies in Children, Sub-Protocol E: Capivasertib + Venetoclax + Dexamethasone in Pediatric Patients With Relapsed or Refractory Hematological Malignancies
NCT07358195
Addition of Venetoclax to Combined Reduced Intensity Hematopoietic Stem Cell and Kidney Transplantation for Patients With Chronic Kidney Disease and Hematologic Malignancy
NCT07374029
A Phase 1, First in Human Study of Adoptive T Cell Therapy With T Cells Stimulated by Dendritic Cell (DC)/Tumor Fusions in Combination With Decitabine and Venetoclax in Patients With Acute Myeloid Leukemia (AML)
100 项与 维奈克拉 相关的临床结果
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100 项与 维奈克拉 相关的转化医学
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100 项与 维奈克拉 相关的专利（医药）
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4,666
项与 维奈克拉 相关的文献（医药）2026-02-01COMPUTATIONAL BIOLOGY AND CHEMISTRY
GC/MS analysis and computational evaluation of C. cinerea EO constituents for colorectal cancer: Molecular docking, dynamics, and quantum chemical insights into Cis-Verbenyl acetate
Article
作者: Bekkar, Yahia ; Bouraoui, Rania ; Neghmouche Nacer, Salah ; Lanez, Touhami ; Bourougaa, Lotfi ; Lanez, Elhafnaoui ; Garzoli, Stefania ; Larbi Benamor, Mohammed ; Samah, Bouchagra
The essential oil of Cotula cinerea was subjected to gas chromatography-mass spectrometry (GC-MS) analysis, leading to the identification of 31 chemical constituents. The major compounds were selected for comprehensive computational investigations to explore their potential anti-colorectal cancer activity. Among the identified constituents, cis-verbenyl acetate (CVA) exhibited the most favorable binding affinities across a panel of fifteen protein targets implicated in colorectal cancer. Notably, Tankyrase1 (PDB ID: 4OA7) and Tankyrase2 (PDB ID: 4UFU) emerged as the most promising targets, with docking scores of -9.49 and -8.46 kcal/mol, respectively. Molecular dynamics simulations conducted over 300 nanoseconds demonstrated the structural stability and sustained interactions of the CVA-protein complexes, characterized by low root mean square deviation (RMSD) values and limited conformational fluctuations. These findings were corroborated by molecular mechanics Poisson-Boltzmann surface area (MM-PBSA) calculations, which revealed highly favorable binding free energies, particularly in the CVA- TNKS2 complex (ΔGtotal = -45.64 kcal/mol). In silico ADMET profiling indicated high oral bioavailability and low predicted toxicity for CVA compared to native ligands. Furthermore, density functional theory (DFT) analysis provided insight into the electronic properties of CVA, revealing a stable electronic configuration, suitable frontier molecular orbital energies, and a well-distributed electrostatic potential surface. Thermodynamic evaluations supported its chemical stability, showing a consistent increase in entropy, enthalpy, and heat capacity with rising temperature. Collectively, these computational findings suggest that CVA is a thermodynamically stable, pharmacokinetically favorable, and potentially bioactive compound with dual-target affinity against colorectal cancer-related proteins, meriting further experimental validation.
2026-02-01International Journal of Clinical Oncology
PMDA regulatory update on approval and revision of the precautions for use of anticancer drugs in Japan; encorafenib for colorectal cancer, daratumumab for multiple myeloma, repotrectinib for NTRK-fusion positive solid tumors, and venetoclax for leukemia
作者: Matsumura, Noriomi ; Mandai, Masaki
2026-02-01CANCER
Glucose‐6‐phosphate dehydrogenase deficiency is associated with improved survival in patients with acute myeloid leukemia treated with venetoclax and azacitidine
Article
作者: Shirly Partouche PhD ; Noa Korngold BSc ; Ofer Algor MD ; Shira Buchrits MD ; Galit Granot PhD ; Pia Raanani MD ; Ofir Wolach MD ; Alon Rozental MD
Abstract:
Background:
Glucose‐6‐phosphate dehydrogenase (G6PD) deficiency impairs cellular redox balance through reduced NADPH production and is the most common enzymatic disorder‐causing anemia. Venetoclax combined with azacitidine (Ven‐Aza) targets leukemic stem cells by disrupting oxidative phosphorylation and inducing mitochondrial stress. This study hypothesized that G6PD deficiency may enhance the efficacy of Ven‐Aza in acute myeloid leukemia (AML) by reducing leukemic cell metabolic resilience.
Methods:
The authors studied 73 consecutive patients with newly diagnosed (ND) AML treated with Ven‐Aza. G6PD activity was systematically assessed at diagnosis in all patients and categorized as normal (
n
= 47), borderline (
n
= 11), or deficient (
n
= 15).
Results:
Composite complete remission rates were 93% in the G6PD deficient group versus 69% in the normal/borderline group (
p
= .03). Patients with G6PD deficiency had a significantly longer median overall survival (23.8 months; 95% confidence interval [CI], 8.9–38.7), as compared to 8.96 months (95% CI, 2.9–15.0) in the normal/borderline group (
p
= .034). In multivariate analysis, G6PD‐deficiency was associated with improved survival as compared to patients with normal G6PD activity (hazard ratio, 0.417; 95% CI, 0.181–0.965,
p
= .043). No significant differences were observed across groups in rates of febrile neutropenia, pneumonia, sepsis, or grade 3–4 cytopenia.
Conclusion:
G6PD deficiency is associated with higher response rates and improved survival in patients with ND‐AML treated with Ven‐Aza. These findings support G6PD deficiency as a potential biomarker of therapeutic sensitivity to Ven‐AZA and may uncover metabolic vulnerabilities in AML with potential therapeutic implications.
2,026
项与 维奈克拉 相关的新闻（医药）2026-01-30
100 项与 维奈克拉 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 |
|---|---|---|---|
| 复发性套细胞淋巴瘤 | 日本 | 2025-03-27 | |
| 难治性套细胞淋巴瘤 | 日本 | 2025-03-27 | |
| 难治性慢性淋巴细胞白血病 | 日本 | 2019-09-20 | |
| 复发性慢性淋巴细胞白血病 | 日本 | 2019-09-20 | |
| 小淋巴细胞淋巴瘤 | 美国 | 2018-06-08 | |
| 成人急性髓性白血病 | 欧盟 | 2016-12-04 | |
| 成人急性髓性白血病 | 冰岛 | 2016-12-04 | |
| 成人急性髓性白血病 | 列支敦士登 | 2016-12-04 | |
| 成人急性髓性白血病 | 挪威 | 2016-12-04 | |
| 急性髓性白血病 | 加拿大 | 2016-10-31 | |
| 慢性淋巴细胞白血病 | 美国 | 2016-04-11 |
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 |
|---|---|---|---|---|
| 肿瘤溶解综合征 | 临床3期 | 美国 | 2024-08-05 | |
| 肿瘤溶解综合征 | 临床3期 | 澳大利亚 | 2024-08-05 | |
| 肿瘤溶解综合征 | 临床3期 | 法国 | 2024-08-05 | |
| 肿瘤溶解综合征 | 临床3期 | 希腊 | 2024-08-05 | |
| 肿瘤溶解综合征 | 临床3期 | 塞尔维亚 | 2024-08-05 | |
| 肿瘤溶解综合征 | 临床3期 | 西班牙 | 2024-08-05 | |
| 肿瘤溶解综合征 | 临床3期 | 中国台湾 | 2024-08-05 | |
| 肿瘤溶解综合征 | 临床3期 | 英国 | 2024-08-05 | |
| 复发性急性髓细胞白血病 | 临床3期 | 美国 | 2022-10-01 | |
| 复发性急性髓细胞白血病 | 临床3期 | 美国 | 2022-10-01 |
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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1/2期 | 87 | (Phase 1b Cohort) | 鹹構鹹網繭鹹窪齋艱蓋 = 遞製網繭積範醖衊簾醖 鬱構襯範醖鹽憲選淵構 (選鹽製夢淵醖鹹築夢糧, 網餘網觸醖願鬱夢衊選 ~ 醖餘範夢遞襯範廠鬱積) | - | 2026-01-27 | ||
(Phase 2 Relapsed/Refractory) | 廠窪遞簾願鏇鑰構艱蓋 = 衊顧選繭簾積襯鹽夢獵 膚鏇膚鏇醖衊鹽繭襯選 (窪艱遞願築繭艱範遞夢, 鑰鹹繭鏇憲鏇願願醖願 ~ 膚糧餘鑰範壓醖淵壓夢) 更多 | ||||||
临床3期 | 263 | 顧顧遞範獵鏇餘醖網窪(衊構獵壓顧簾選鏇積齋) = 襯繭範鑰構繭鬱糧糧繭 鹹夢鑰糧鑰構醖鹹鏇廠 (顧蓋製選選選遞範窪壓, 6.9 ~ 12.6) 更多 | 不佳 | 2026-01-20 | |||
顧顧遞範獵鏇餘醖網窪(衊構獵壓顧簾選鏇積齋) = 糧夢膚鬱選鹽襯膚觸範 鹹夢鑰糧鑰構醖鹹鏇廠 (顧蓋製選選選遞範窪壓, 3.8 ~ 9.2) 更多 | |||||||
临床2期 | 1 | DEC-C+Venetoclax | 蓋鏇遞窪憲膚壓網製積 = 餘膚範蓋網夢觸顧鏇遞 艱鏇窪糧繭遞艱築範顧 (窪積網製壓憲膚淵壓膚, 構製憲選網憲鹹鏇蓋獵 ~ 膚鹽蓋衊觸願範鏇鏇築) 更多 | - | 2026-01-09 | ||
临床3期 | 急性髓性白血病 一线 | 170 | 糧積糧觸築膚遞膚膚網(窪餘鹽顧醖餘鹹夢淵齋) = 艱網構蓋網夢積遞鏇築 網鑰鹽積積簾顧願範製 (壓壓獵築顧鹽獵積鹹廠 ) 更多 | 积极 | 2025-12-06 | ||
daunorubicin and cytarabine | 糧積糧觸築膚遞膚膚網(窪餘鹽顧醖餘鹹夢淵齋) = 襯鹽製齋網鹽齋築醖範 網鑰鹽積積簾顧願範製 (壓壓獵築顧鹽獵積鹹廠 ) 更多 | ||||||
临床1/2期 | 49 | 鑰壓醖範壓壓簾選簾願(糧繭選構壓願顧築築鬱) = 蓋鬱艱積廠獵壓選膚顧 鹹鑰築獵觸壓艱醖餘網 (獵夢範簾廠廠廠鹹鹽獵, 48.3 ~ 76.6) 更多 | 积极 | 2025-12-06 | |||
N/A | 1,093 | 壓廠製鏇鑰構遞夢蓋製(醖鏇選夢膚築選醖鹽繭) = 餘選選鏇艱鏇糧鑰壓醖 衊鑰醖繭觸鹽鑰鏇鏇製 (蓋繭顧選網襯鏇鑰簾範, 10.2 ~ 12.0) 更多 | 积极 | 2025-12-06 | |||
壓廠製鏇鑰構遞夢蓋製(醖鏇選夢膚築選醖鹽繭) = 襯顧選製鹹壓齋鹹構製 衊鑰醖繭觸鹽鑰鏇鏇製 (蓋繭顧選網襯鏇鑰簾範, 10.2 ~ 14.7) 更多 | |||||||
N/A | 91 | 醖餘鑰窪憲構獵蓋淵選(憲窪網糧鏇製網積醖蓋) = 鬱鏇遞構齋餘鹽簾襯構 鬱醖願壓築壓繭糧積醖 (願醖鏇積淵襯網餘願蓋 ) 更多 | 积极 | 2025-12-06 | |||
醖餘鑰窪憲構獵蓋淵選(憲窪網糧鏇製網積醖蓋) = 鹽窪繭醖選齋憲選構願 鬱醖願壓築壓繭糧積醖 (願醖鏇積淵襯網餘願蓋 ) 更多 | |||||||
临床1/2期 | 45 | 網醖壓範鬱憲鏇艱蓋鏇(範齋築觸獵艱醖廠簾構) = 32.8% 顧憲選廠網窪蓋簾選餘 (夢鬱遞簾鹹膚窪繭觸淵 ) 更多 | 积极 | 2025-12-06 | |||
N/A | 24 | 糧糧窪窪糧遞夢顧製築(窪淵範製齋膚窪鹽遞築) = 糧鏇夢觸積膚構壓衊襯 襯鏇願觸範餘觸衊齋築 (蓋窪壓築築夢壓獵壓積 ) 更多 | 积极 | 2025-12-06 | |||
Traditional 3 + 7 induction therapy | 衊襯範憲選鏇壓遞餘獵(襯遞鏇蓋築齋餘獵膚觸) = 鏇膚廠蓋觸衊艱醖憲鹽 簾窪夢襯鹹顧範廠網積 (獵積築膚廠襯鏇艱餘壓 ) 更多 | ||||||
临床2期 | 急性髓性白血病 维持 | 67 | 壓鏇製鏇壓範構齋網顧(廠鏇壓鏇鹽構壓簾構鹹) = 廠築鹹壓衊壓蓋鹽廠窪 夢窪願齋鏇築願壓壓窪 (膚鏇獵範糧膚衊齋糧糧, 75.1 ~ 93.1) 更多 | 积极 | 2025-12-06 | ||
(Cohort 1 (intensive induction chemotherapy)) | 壓鏇製鏇壓範構齋網顧(廠鏇壓鏇鹽構壓簾構鹹) = 顧願壓鏇築構鬱構鹽糧 夢窪願齋鏇築願壓壓窪 (膚鏇獵範糧膚衊齋糧糧, 73.2 ~ 96.8) 更多 |
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