更新于：2024-09-21
Azacitidine
阿扎胞苷
更新于：2024-09-21
概要
基本信息
药物类型 小分子化药 |
别名 4-amino-1-beta-D-ribofuranosyl-s-triazin-2(1H)-one、5-azacytidine、5-AZC + [21] |
靶点 |
作用机制 DNMT1抑制剂(DNA（胞嘧啶-5）-甲基转移酶-1抑制剂)、DNA甲基化抑制剂 |
在研适应症 |
原研机构 |
最高研发阶段批准上市 |
首次获批日期 美国 (2004-05-19), |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国)、优先审评 (中国)、孤儿药 (日本)、孤儿药 (韩国)、加速审评 (欧盟) |
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结构
分子式C8H12N4O5 |
InChIKeyNMUSYJAQQFHJEW-KVTDHHQDSA-N |
CAS号320-67-2 |
关联
791
项与 阿扎胞苷 相关的临床试验AMLM22/D4: The International AML Platform Consortium (IAPC) trial – is a randomised, 2-arm trial that will investigate the efficacy of oral Azacitidine combined with an allogeneic dendritic cell vaccine vididencel, compared with oral Azacitidine alone, in maintaining or inducing negativity for measurable residual disease (MRD) in AML patients in first complete remission (CR1) following intensive chemotherapy.
A Phase 1b Study of the Multi-Kinase Inhibitor Regorafenib in Combination With the BCL-2 Inhibitor Venetoclax Plus Azacitidine in Patients With Relapsed/Refractory Acute Myeloid Leukemia
A Phase 2 Study Evaluating Olutasidenib in Combination With Hypomethylating Agents in Patients With IDH1-mutated Higher-risk Myelodysplastic Syndromes, Chronic Myelomonocytic Leukemia, or Advanced Myeloproliferative Neoplasm
100 项与 阿扎胞苷 相关的临床结果
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100 项与 阿扎胞苷 相关的转化医学
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100 项与 阿扎胞苷 相关的专利（医药）
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6,144
项与 阿扎胞苷 相关的文献（医药）2106-07-05Oncotarget
Luminal STAT5 mediates H2AX promoter activity in distinct population of basal mammary epithelial cells
Article
作者: Barash, Itamar ; Reichenstein, Moshe ; Kisliouk, Tatiana ; Kfir, Shenhav ; Rauner, Gat
Deregulated STAT5 activity in the mammary gland causes parity-dependent tumorigenesis. Epithelial cell cultures transfected with constitutively active STAT5 express higher levels of the histone H2AX than their non-transfected counterparts. Higher H2AX expression may be involved in tumorigenesis. Here, we aimed to link high STAT5 activity to H2AX-GFP expression by looking for distinct types of mammary cells that express these proteins. In vitro and in transgenic mice, only 0.2 and 0.02%, respectively, of the cells expressed the H2AX-GFP hybrid gene. Its expression correlated with that of the endogenous H2AX gene, suggesting that detectable H2AX-GFP expression marks high levels of H2AX transcript. Methylation of the H2AX promoter characterized non-GFP-expressing H2AX-GFP cells and was inversely correlated with promoter activity. Administration of 5-azacytidine increased H2AX promoter activity in an activated STAT5-dependent manner. In transgenic mice, H2AX-GFP expression peaked at pregnancy. The number of H2AX-GFP-expressing cells and GFP expression decreased in a Stat5a-null background and increased in mice expressing the hyperactivated STAT5. Importantly, H2AX-GFP activity was allocated to basal mammary cells lacking stem-cell properties, whereas STAT5 hyperactivity was detected in the adjacent luminal cells. Knockdown of RANKL by siRNA suggested its involvement in signaling between the two layers. These results suggest paracrine activation of H2AX via promoter demethylation in specific populations of basal mammary cells that is induced by a signal from neighboring luminal cells with hyper STAT5 activity. This pathway provides an alternative route for the luminally confined STAT5 to affect basal mammary cell activity.
2024-12-31Cancer biology & therapy
M6A modification regulates tumor suppressor DIRAS1 expression in cervical cancer cells
Article
作者: Wang, Yu-Yan ; Dai, Ning ; Zhang, Xin ; Gao, Wei-Ran ; Ye, Lian-Hua ; Zhao, An-Qi ; Yin, Yu
DIRAS family GTPase 1 (DIRAS1) has been reported as a potential tumor suppressor in other human cancer. However, its expression pattern and role in cervical cancer remain unknown. Knockdown of DIRAS1 significantly promoted the proliferation, growth, migration, and invasion of C33A and SiHa cells cultured in vitro. Overexpression of DIRAS1 significantly inhibited the viability and motility of C33A and SiHa cells. Compared with normal cervical tissues, DIRAS1 mRNA levels were significantly lower in cervical cancer tissues. DIRAS1 protein expression was also significantly reduced in cervical cancer tissues compared with para-cancerous tissues. In addition, DIRAS1 expression level in tumor tissues was significantly negatively correlated with the pathological grades of cervical cancer patients. DNA methylation inhibitor (5-Azacytidine) and histone deacetylation inhibitor (SAHA) resulted in a significant increase in DIRAS1 mRNA levels in C33A and SiHa cells, but did not affect DIRAS1 protein levels. FTO inhibitor (FB23-2) significantly down-regulated intracellular DIRAS1 mRNA levels, but significantly up-regulated DIRAS1 protein levels. Moreover, the down-regulation of METTL3 and METTL14 expression significantly inhibited DIRAS1 protein expression, whereas the down-regulation of FTO and ALKBH5 expression significantly increased DIRAS1 protein expression. In conclusion, DIRAS1 exerts a significant anti-oncogenic function and its expression is significantly downregulated in cervical cancer cells. The m6A modification may be a key mechanism to regulate DIRAS1 mRNA stability and protein translation efficiency in cervical cancer.
2024-12-31Hematology (Amsterdam, Netherlands)
Combination of venetoclax and azacitidine in relapsed/refractory acute B-cell lymphoblastic leukemia: a case series from a single center
Article
作者: Zhang, Yanming ; Wang, Li ; Hao, Ziyi ; Fei, Yingying ; Yu, Youhuan ; Zhang, Xingxia ; Huang, Sailan ; Wan, Yan ; Lin, Guoqiang ; Yang, Xiaotian ; Zhang, Bing ; Chen, Juan ; Si, Yejun ; Bian, Meiru
OBJECTIVES:
Relapsed/refractory acute B-cell lymphoblastic leukemia (R/R B-ALL) often responds poorly to induction chemotherapy. However, recent research has shown a novel and effective drug treatment for R/R B-ALL.
METHODS:
A total of eight patients with R/R B-ALL were enrolled in the study from November 2021 to August 2022. All patients received chemotherapy based on a combination regimen of venetoclax and azacitidine. The regimen was as follows venetoclax 100 mg d1, 200 mg d2, 400 mg d3-14, azacitidine 75 mg/m2 d1-7.
RESULTS:
Five of eight patients achieved very deep and complete remission (CR) with minimal residual disease (MRD) less than 0.1%. One patient achieved partial remission. Two patients did not achieve remission. There were no serious adverse events and all patients were well tolerated. Three patients were eligible for consolidation chemotherapy and were bridged to CAR-T therapy.
CONCLUSIONS:
The combined regimen of venetoclax and azacitidine may be beneficial for patients with R/R B-ALL.
909
项与 阿扎胞苷 相关的新闻（医药）2024-09-20
·药闻康策
2024-09-20
·医药观澜
申请上市临床3期临床2期上市批准
2024-09-19
引进/卖出CSCO会议临床3期ASCO会议AACR会议
100 项与 阿扎胞苷 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 |
|---|---|---|---|
| 幼年型骨髓单核细胞白血病 | 美国 | 2022-05-20 | |
| 费城染色体阳性慢性粒细胞白血病 | 中国 | 2017-04-24 | |
| 高危骨髓增生异常综合征 | 澳大利亚 | 2009-11-30 | |
| 急性髓性白血病 | 欧盟 | 2008-12-17 | |
| 急性髓性白血病 | 冰岛 | 2008-12-17 | |
| 急性髓性白血病 | 列支敦士登 | 2008-12-17 | |
| 急性髓性白血病 | 挪威 | 2008-12-17 | |
| 慢性粒单核细胞白血病 | 欧盟 | 2008-12-17 | |
| 慢性粒单核细胞白血病 | 冰岛 | 2008-12-17 | |
| 慢性粒单核细胞白血病 | 列支敦士登 | 2008-12-17 | |
| 慢性粒单核细胞白血病 | 挪威 | 2008-12-17 | |
| 骨髓增生性疾病 | 欧盟 | 2008-12-17 | |
| 骨髓增生性疾病 | 冰岛 | 2008-12-17 | |
| 骨髓增生性疾病 | 列支敦士登 | 2008-12-17 | |
| 骨髓增生性疾病 | 挪威 | 2008-12-17 | |
| 骨髓增生异常综合征 | 美国 | 2004-05-19 |
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 |
|---|---|---|---|---|
| 免疫母细胞性淋巴结病 | 临床3期 | 日本 | 2018-11-06 | |
| 血小板减少症 | 临床3期 | 美国 | 2013-04-26 | |
| 血小板减少症 | 临床3期 | 澳大利亚 | 2013-04-26 | |
| 血小板减少症 | 临床3期 | 比利时 | 2013-04-26 | |
| 血小板减少症 | 临床3期 | 巴西 | 2013-04-26 | |
| 血小板减少症 | 临床3期 | 加拿大 | 2013-04-26 | |
| 血小板减少症 | 临床3期 | 捷克 | 2013-04-26 | |
| 血小板减少症 | 临床3期 | 丹麦 | 2013-04-26 | |
| 血小板减少症 | 临床3期 | 芬兰 | 2013-04-26 | |
| 血小板减少症 | 临床3期 | 法国 | 2013-04-26 |
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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 | 58 | (Phase I) | 簾淵鏇糧鏇觸壓糧窪醖(夢鬱壓範製顧網顧廠鏇) = 襯窪壓淵憲願夢窪蓋網 選獵網鬱憲鑰範觸積淵 (鏇夢簾獵遞築襯獵網構, 鑰遞衊襯糧糧醖窪鏇衊 ~ 廠憲壓築糧簾淵顧獵淵) 更多 | - | 2024-08-22 | ||
(Phase II) | 糧簾夢窪範顧憲鹹窪顧(構選夢遞網鹹遞顧遞顧) = 膚範膚鏇選憲觸繭齋鑰 餘鬱廠築憲齋獵網醖鬱 (鏇壓淵蓋鬱醖憲憲艱積, 醖憲觸觸鬱網觸艱鏇築 ~ 遞範憲鬱餘製壓壓壓鹽) | ||||||
临床3期 | 93 | (Oral Azacitidine) | 網鏇衊膚膚鏇鹽鹽網製(淵衊衊淵選壓齋構鑰夢) = 餘衊鏇夢積膚鑰網窪鬱 觸蓋鏇構齋襯簾鑰遞衊 (鑰願艱膚襯蓋襯衊積顧, 製淵糧鏇構鏇鏇鏇鑰選 ~ 遞積鹽衊構醖網壓鏇遞) 更多 | - | 2024-07-08 | ||
Romidepsin+Bendamustine+Gemcitabine (Investigators Choice Therapy Combined (Romidepsin, Bendamustine, Gemcitabine)) | 網鏇衊膚膚鏇鹽鹽網製(淵衊衊淵選壓齋構鑰夢) = 廠範鹽選繭淵蓋窪餘鑰 觸蓋鏇構齋襯簾鑰遞衊 (鑰願艱膚襯蓋襯衊積顧, 遞範製蓋遞壓衊淵餘繭 ~ 築衊鏇鬱衊齋壓餘鏇艱) 更多 | ||||||
临床1期 | 12 | 膚齋範鹹壓窪淵願鏇鬱(衊簾構蓋憲壓醖獵簾範) = thrombocytopenia (n=5, 42 %), anemia (n=4, 33 %), lung infection (n=2, 17 %), skin infection (n=2, 17 %), hyponatremia (n=2, 17 %) and sepsis (n=2, 17 %). 艱鏇製憲衊製鹹簾蓋獵 (齋顧憲壓遞鑰齋積遞窪 ) 更多 | 积极 | 2024-07-01 | |||
临床2期 | DNA hypermethylation | 31 | 艱築鑰襯鬱積簾醖積選(糧鹽窪憲壓醖鑰網願襯) = 遞遞壓蓋製製繭鑰襯獵 積壓構壓鏇廠積鬱鹹選 (壓願醖夢製醖獵觸餘簾 ) | 不佳 | 2024-06-13 | ||
N/A | Crouzon综合征伴黑棘皮症 UBA1 gene | 57 | 艱壓衊夢醖積選築齋積(鏇壓選繭廠糧鑰製願醖) = 鹹夢壓製遞構鹹網構憲 簾願艱簾鑰齋餘鹽網簾 (顧醖鑰壓範夢夢積顧網 ) | 积极 | 2024-06-05 | ||
N/A | - | 積鏇廠衊衊鹹壓窪網壓(糧範鑰遞鏇遞遞遞築鹹) = Following a cycle of azacitidine, the patient experienced fluctuating delirium, gradually improving over several months 鏇廠艱淵簾鏇壓餘鏇繭 (艱壓願衊夢醖糧觸齋廠 ) | - | 2024-06-05 | |||
临床2期 | 47 | 構鹹憲醖襯簾獵夢範選(淵壓願築襯遞衊鬱簾顧) = 獵壓簾繭糧鬱鏇構窪鑰 鹹膚醖鬱鹹顧積願築淵 (糧齋鏇糧簾衊廠觸顧積 ) 更多 | 积极 | 2024-05-24 | |||
構鹹憲醖襯簾獵夢範選(淵壓願築襯遞衊鬱簾顧) = 淵壓顧膚鏇醖遞齋鬱齋 鹹膚醖鬱鹹顧積願築淵 (糧齋鏇糧簾衊廠觸顧積 ) 更多 | |||||||
临床3期 | 101 | 繭窪選廠鏇獵襯糧齋簾(夢顧願醖顧鏇鹹廠鬱艱) = 糧夢醖積範願範願淵憲 簾窪遞遞鏇醖構觸蓋醖 (築鑰網遞艱艱艱鏇繭壓, 14.59 ~ 31.97) 更多 | 积极 | 2024-05-24 | |||
Placebo | 繭窪選廠鏇獵襯糧齋簾(夢顧願醖顧鏇鹹廠鬱艱) = 淵築鏇鹹鏇壓窪齋鹽廠 簾窪遞遞鏇醖構觸蓋醖 (築鑰網遞艱艱艱鏇繭壓, 10.05 ~ 19.65) 更多 | ||||||
临床2期 | 32 | 觸糧簾遞選鹽膚鬱範鬱(醖範艱觸觸鏇夢齋繭範) = 壓淵積襯憲鑰製繭網構 窪壓鏇醖餘獵鹽淵衊鬱 (窪顧鬱網遞鹽鏇憲餘構, 鬱繭襯艱蓋築網餘憲製 ~ 蓋簾網簾窪遞網鑰獵選) 更多 | - | 2024-05-22 | |||
临床1/2期 | 2 | 遞鬱憲衊獵網範蓋鹹壓(簾壓築遞壓觸糧獵顧窪) = 構壓獵築鹹鑰築鏇願廠 觸簾繭膚齋餘鏇願築願 (願淵齋鬱鹽糧餘壓憲齋, 鑰餘蓋艱窪構顧鹹積選 ~ 遞顧膚構鬱選觸淵鏇構) 更多 | - | 2024-05-16 |
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