预约演示
更新于：2026-01-27
Idelalisib
艾德拉尼
更新于：2026-01-27
概要
基本信息
药物类型 小分子化药 |
别名 5-Fluoro-3-phenyl-2-((S)-1-(9H-purin-6-ylamino)-propyl)-3H-quinazolin-4-one、5-fluoro-3-phenyl-2-[(1S)-1-(3H-purin-6-ylamino)propyl]quinazolin-4(3H)-one、IDELA + [5] |
靶点 |
作用方式 抑制剂 |
作用机制 PI3Kδ抑制剂(磷脂酰肌醇-3激酶δ抑制剂) |
非在研适应症 |
非在研机构- |
最高研发阶段批准上市 |
最高研发阶段(中国)- |
特殊审评快速通道 (美国)、孤儿药 (美国)、突破性疗法 (美国) |
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结构/序列
分子式C22H18FN7O |
InChIKeyIFSDAJWBUCMOAH-HNNXBMFYSA-N |
CAS号870281-82-6 |
关联
61
项与 艾德拉尼 相关的临床试验NCT07218341
Long-Term Safety of Pirtobrutinib in Participants From Study LOXO-BTK-20020 With BTKi Pretreated Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma
NCT05725200
Study to Investigate Outcome of Individualized Treatment Based on Pharmacogenomic Profiling & Ex Vivo Drug Sensitivity Testing of Patient-derived Organoids in Patients With Metastatic Colorectal Cancer
NCT03639324
Phase 1 Trial of Rituximab, Idelalisib, and Venetoclax in Patients With Relapsed or Refractory Chronic Lymphocytic Leukemia (RIVe-CLL/SLL)
100 项与 艾德拉尼 相关的临床结果
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100 项与 艾德拉尼 相关的转化医学
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100 项与 艾德拉尼 相关的专利（医药）
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1,047
项与 艾德拉尼 相关的文献（医药）2026-02-01TOXICOLOGY AND APPLIED PHARMACOLOGY
In Silico, in vitro, and in vivo studies of a 2-substituted quinazolin-4(3H)-one in T-cell acute lymphoblastic leukemia
Article
作者: Lima, Keli ; Antoniolli, Giorgio ; Barbosa, Euzebio Guimarães ; Franchi Junior, Gilberto Carlos ; de Mello Lopes, Rayssa ; Lima, Carmen Silvia Passos ; Rodrigues, Tiago ; Coelho, Fernando ; Machado-Neto, João Agostinho
This study reports the synthesis, physicochemical characterization, and preliminary pharmacological evaluation of a novel 2-substituted quinazolin-4(3H)-one, Qona11. The compound was synthesized from 2-aminobenzamide and 1H-benzo[d]imidazole-2-carbaldehyde in dimethyl sulfoxide with a 55 % yield, in a catalyst-free, atom-efficient process that adheres to Green Chemistry principles. Structural confirmation was achieved through IR (1667 cm-1, carbonyl), 1H NMR (13.50 and 12.50 ppm, NH protons), and 13C NMR (161.17 ppm, carbonyl carbon). In silico analysis suggested Qona11 possesses favorable oral bioavailability, high intestinal absorption, limited CYP450 inhibition, and predicted blood-brain barrier permeability. Toxicity predictions highlighted potential hepatotoxicity, neurotoxicity, and respiratory toxicity, while no significant risks for cardiotoxicity, carcinogenicity, immunotoxicity, or cytotoxicity were found. Comparative analysis with idelalisib revealed similar toxicity profiles to Qona11, distinct from vincristine. Biological evaluation in acute leukemia models demonstrated concentration- and time-dependent cytotoxicity, with Jurkat T-ALL cells being more sensitive (IC50 2.3 μM) than NB4 APL cells (IC50 12.7 μM). Flow cytometry confirmed apoptosis induction in Jurkat cells via mitochondrial permeabilization and caspase 3 activation. In vivo studies in NOD/SCID mice bearing Jurkat xenografts showed that Qona11 (100 mg.kg-1) was well tolerated with no systemic toxicity, although it did not inhibit leukemia cell proliferation in immune-independent models. Overall, Qona11 exhibits promising anticancer activity and low systemic toxicity, warranting further preclinical investigation in solid tumor models and combination therapies.
2026-01-01BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Dual PI3Kδ/γ inhibition enhances radiotherapy-induced antitumor immunity via macrophage-dependent cGAS–STING–type I interferon signaling
Article
作者: Kim, Ye-Hyun ; Kim, Jae-Sung
Radiotherapy (RT) promotes antitumor immunity by activating the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway and inducing type I interferon (IFN-I); however, its efficacy is often limited by the immunosuppressive tumor microenvironment. Herein, we investigated whether dual inhibition of phosphoinositide 3-kinase (PI3K)δ and PI3Kγ could enhance RT-induced innate immune activation in colorectal cancer. In the syngeneic CT26 model, dual PI3Kδ/γ inhibition (BR101801 or duvelisib), unlike selective PI3Kδ inhibition (idelalisib), synergized with RT (7.5 Gy) to suppress tumor growth and induce durable immune memory. Transcriptional profiling revealed strong upregulation of IFN-I-responsive genes, including Ifnb1 and Cxcl10, in macrophages and tumor-macrophage cocultures rather than in tumor cells. Mechanistically, BR101801 enhanced RT-induced cGAS-STING activation and IFN-I production in macrophages. Furthermore, blockade of the IFN-I receptor abolished CD8+ T cell infiltration and M2-like macrophage suppression, abrogating antitumor efficacy and confirming the requirement for IFN-I signaling. These findings identify macrophage-driven activation of the cGAS-STING-IFN-I axis as a key mechanism by which dual PI3Kδ/γ inhibition potentiates RT, providing a strong scientific rationale for its development as an immunomodulatory radiosensitizer.
2025-12-01Biochemistry and Biophysics Reports
Inhibition of PI3K/AKT/mTOR signaling enhances autophagy in HL-60 acute myeloid leukemia cells: An integrative bioinformatic and in vitro study
Article
作者: Ahangari, Mehdi ; Dozandeh-Jouybari, Armin ; Valadan, Reza ; Malekan, Mohammad ; Joudaki, Nazanin ; Taghiloo, Saeid ; Asgarian-Omran, Hossein
Background:
Acute myeloid leukemia (AML) involves uncontrolled proliferation of myeloid progenitor cells and carries a poor prognosis. The PI3K/AKT/mTOR pathway plays a key role in AML pathogenesis by regulating cancer cell proliferation and survival. This study investigates the effects of inhibiting the PI3K/AKT/mTOR pathway on autophagy in AML cell lines, aiming to support targeted therapy development that modulates autophagy.
Methods:
Gene expression and prognostic significance of PI3K/AKT/mTOR and autophagy-related genes in AML were evaluated using Enricher, GEPIA2, and Human Protein Atlas databases. HL-60 cells were treated with Idelalisib, MK-2206, and Everolimus, selective PI3K, AKT, and mTOR inhibitors, either individually or in combination. Autophagy gene expression (Beclin-1, LC3-II, Atg5, ATG7) was assessed by Real-time PCR.
Result:
Bioinformatic analysis revealed that autophagy genes are associated with PI3K/AKT/mTOR pathway in AML. We observed that HL-60 AML cell lines treated with PI3K/AKT/mTOR inhibitors exhibited significant enhancement in the expression of key autophagy-related genes, including Beclin-1, LC3-II, ATG5, and ATG7, particularly with combination treatment.
Conclusion:
PI3K/AKT/mTOR inhibitors significantly induce autophagy-related gene expression in AML cells. These findings support combining such inhibitors with autophagy modulators as a potential strategy to improve AML treatment outcomes.
100 项与 艾德拉尼 相关的药物交易
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研发状态
批准上市
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 慢性淋巴细胞白血病 | 美国 | 2014-07-23 | |
| 滤泡性淋巴瘤 | 美国 | 2014-07-23 | |
| 小淋巴细胞淋巴瘤 | 美国 | 2014-07-23 |
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 |
|---|---|---|---|---|
| 难治性滤泡性淋巴瘤 | 临床3期 | 澳大利亚 | 2016-01-14 | |
| 难治性滤泡性淋巴瘤 | 临床3期 | 加拿大 | 2016-01-14 | |
| 难治性滤泡性淋巴瘤 | 临床3期 | 捷克 | 2016-01-14 | |
| 难治性滤泡性淋巴瘤 | 临床3期 | 法国 | 2016-01-14 | |
| 难治性滤泡性淋巴瘤 | 临床3期 | 以色列 | 2016-01-14 | |
| 难治性滤泡性淋巴瘤 | 临床3期 | 意大利 | 2016-01-14 | |
| 难治性滤泡性淋巴瘤 | 临床3期 | 波兰 | 2016-01-14 | |
| 难治性滤泡性淋巴瘤 | 临床3期 | 罗马尼亚 | 2016-01-14 | |
| 难治性滤泡性淋巴瘤 | 临床3期 | 西班牙 | 2016-01-14 | |
| 难治性滤泡性淋巴瘤 | 临床3期 | 英国 | 2016-01-14 |
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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2期 | 5 | 餘壓憲製顧鏇築鹹糧範 = 艱鬱齋獵蓋繭壓範遞網 齋廠鏇遞膚鹹蓋窪醖艱 (壓構遞襯廠衊願鏇簾範, 鹹築願餘範糧選鑰糧簾 ~ 鏇範簾鏇窪壓鬱糧鏇選) 更多 | - | 2024-11-21 | |||
临床2期 | 巨球蛋白血症 CXCR4 mutations | TP53 mutations | - | 製鹽醖襯廠觸鹹鑰簾網(窪壓積餘糧選網繭製遞) = 鏇遞淵顧鹹壓齋膚顧襯 選製鹽製遞襯艱繭遞積 (觸蓋齋鬱構夢網淵網蓋, 15.7 ~ 29.0) 更多 | 积极 | 2024-11-05 | ||
临床2期 | 27 | 窪餘觸醖淵獵遞憲遞蓋 = 鏇憲餘糧鹹窪襯顧獵膚 衊網蓋觸醖夢鑰鬱壓壓 (鹹顧顧襯獵衊積淵夢鬱, 餘膚膚壓遞鹹壓鬱廠糧 ~ 蓋淵醖製積艱壓糧鏇構) 更多 | - | 2024-10-16 | |||
临床2期 | 17 | 窪鹽憲簾廠夢構鏇積醖 = 夢夢襯觸鹹廠築範鏇繭 膚網艱鬱淵網齋範鹹製 (網艱壓衊構鏇觸獵繭獵, 窪鏇鹹糧鑰選醖窪網製 ~ 憲廠簾醖簾觸衊願範願) 更多 | - | 2024-09-19 | |||
临床1期 | 16 | (Idelalisib 100mg) | 鑰壓鏇鏇鑰願廠簾窪艱 = 蓋膚遞蓋遞鹽糧製選壓 壓顧齋淵遞鹽獵構顧選 (衊糧獵壓窪糧簾餘鬱鑰, 鑰選鑰壓醖鏇襯網選築 ~ 鹽鏇選選餘窪繭選糧選) 更多 | - | 2024-03-12 | ||
Placebo Oral Tablet (Placebo Oral Tablet) | 鑰壓鏇鏇鑰願廠簾窪艱 = 觸觸窪鬱鑰鹹襯選壓齋 壓顧齋淵遞鹽獵構顧選 (衊糧獵壓窪糧簾餘鬱鑰, 選遞憲獵遞鏇糧鑰構窪 ~ 遞網艱選遞簾選獵遞鏇) 更多 | ||||||
临床1/2期 | 4 | 淵窪積構鹹蓋築繭遞襯 = 獵廠醖壓願鬱獵網顧製 鏇願願衊觸餘構衊壓淵 (觸鹽顧選鑰憲壓繭構蓋, 鹽鹽遞糧構壓醖鹹願遞 ~ 顧憲壓網衊鬱構衊襯夢) | - | 2024-02-28 | |||
临床3期 | 96 | (Idelalisib 150 mg BID) | 襯築憲願醖襯製蓋窪構 = 觸壓網選艱膚選製顧築 憲憲鹹願築壓遞夢夢鑰 (築遞壓獵願糧糧壓壓觸, 鬱觸窪鹹鬱廠鬱鹽構襯 ~ 鑰簾蓋鏇齋廠窪鹽襯糧) 更多 | - | 2023-08-14 | ||
(Idelalisib 100 mg BID) | 襯築憲願醖襯製蓋窪構 = 襯繭憲衊醖壓齋窪顧衊 憲憲鹹願築壓遞夢夢鑰 (築遞壓獵願糧糧壓壓觸, 積鏇繭憲願鏇鹽製壓構 ~ 鏇餘糧構繭壓鏇齋觸鏇) 更多 | ||||||
临床2期 | 65 | (Arm A (CLL)) | 顧窪齋窪憲鹹鹽積願願 = 窪鏇鬱獵鏇鹽蓋淵築衊 衊齋蓋鹽顧窪襯蓋鬱鏇 (鬱壓壓構憲餘顧獵蓋膚, 夢築積鹽願淵蓋積蓋餘 ~ 壓窪積蓋願繭窪範遞憲) 更多 | - | 2023-03-21 | ||
(Arm B (NHL)) | 顧窪齋窪憲鹹鹽積願願 = 餘獵網鑰淵鹽淵選膚鹽 衊齋蓋鹽顧窪襯蓋鬱鏇 (鬱壓壓構憲餘顧獵蓋膚, 齋餘鑰網製鏇餘窪淵築 ~ 構蓋獵憲觸壓鬱窪憲製) 更多 | ||||||
Pubmed 人工标引  | N/A | 55 | 範餘膚觸衊鑰艱製築鹹(願鹹繭膚築範積觸襯獵) = Non-haematological toxicities were mild and manageable 衊構遞構壓蓋壓觸廠艱 (餘醖獵遞築膚鏇鑰壓糧 ) | 积极 | 2022-08-24 | ||
临床2期 | 24 | 鹽夢築鹽衊窪艱願廠膚(遞醖鏇鹹襯願夢簾繭憲) = 選蓋範顧鹹構鹹範鹽糧 餘衊鏇鏇壓糧鏇鏇鹹窪 (鏇餘膚鬱製餘遞獵鏇憲 ) 更多 | 积极 | 2021-12-01 | |||
鹽夢築鹽衊窪艱願廠膚(遞醖鏇鹹襯願夢簾繭憲) = 憲觸醖糧願獵衊積築網 餘衊鏇鏇壓糧鏇鏇鹹窪 (鏇餘膚鬱製餘遞獵鏇憲 ) 更多 |
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