- ￥3560.61
- SIGMA
- 美国
- A2385-1g
- 2026年07月01日
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- 文献和实验
- 技术资料
- 保存条件：
−20°C
- 保质期：
见瓶身
- 英文名：
≥98% (HPLC), powder, DNA methyltransferase inhibitor
- 库存：
现货
- 供应商：
麦飞生物
- CAS号：
320-67-2
- 规格：
A2385-1g
说明
General description
5-氮杂胞苷是胞苷的化学类似物。它起低甲基化剂 （hypomethylating agent）的作用。5-氮杂胞苷用于治疗骨髓增生异常综合征（MDS）。
化学结构:核苷
Application
5-氮杂胞苷已被用于：
细胞诱导
研究其对牛胚胎间充质干细胞（bfMSC）的影响
研究其对人骨髓基质细胞（hBMSC）的影响
研究其对DNA甲基转移酶1（DNMT1）和Ras蛋白样激活剂 1（RASAL1）表达的影响
干扰DNA甲基化和组蛋白乙酰化
确定其对对照成纤维细胞转化的影响
用于光学相干断层扫描（OCT）和荧光素血管造影（FA)
重新激活Sal-like蛋白（SALL）3的表达
Biochem/physiol Actions
5-氮杂胞苷（Aza-CR）有望成为急性骨髓性白血病的化疗方案。[1]该药物具有选择性增加γ-球蛋白合成的能力。 因此，5-氮杂胞苷可用于治疗重度β-地中海贫血。Aza-CR可用作强效的抑菌、抗肿瘤和诱变剂。此外，它还表现出各种生物学活性，如免疫抑制、抗有丝分裂、辐射防护和抑制病毒作用。
一种强效生长抑制剂及细胞毒素剂，抑制 DNA 甲基转移酶，一种基因表达、基因激活和沉默的重要调节机制。
导致DNA去甲基化或半去甲基化，形成一个开口，使转录因子与DNA结合，并重新激活肿瘤抑制基因。
强效生长抑制剂及细胞毒素剂，抑制 DNA 甲基转移酶。
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文献和实验Pharmacological boosting of azacitidine/venetoclax in acute myeloid leukemia.
In Blood Neoplasia on 1 May 2026 by Westra, N., Cerro, E. R., et al.
Azacitidine/venetoclax is the standard treatment for patients with acute myeloid leukemia (AML) unfit for intensive chemotherapy. Cytochrome P450 3A4 (CYP3A4) is the major metabolizing enzyme for venetoclax, and its inhibition can boost venetoclax. In the HOVON 171 phase 2 trial, patients with AML were treated with azacitidine/venetoclax/cobicistat. This 2-stage, open-label, multicenter phase 2 trial included a crossover run-in phase followed by an ongoing extension phase. In cycle 1, patients received standard-dose azacitidine/venetoclax. In cycle 2, cobicistat was added, and venetoclax was reduced to 50 mg. The primary end point was pharmacokinetic equivalence, defined as 90% confidence interval (CI) of geometric mean ratios (GMRs) >0.8 for area under the curve over 24 hours (AUC0-24h) and maximum plasma concentration (Cmax). Polymorphisms in genes encoding for CYP enzymes were determined. In vitro assays were performed to assess cobicistat's impact on the antileukemic effect of azacitidine/venetoclax in AML cell lines. In 13 evaluable patients, cobicistat-boosted venetoclax at 50 mg achieved higher exposure than standard 400-mg dosing. GMRs were 2.0 (90% CI, 1.4-2.8) for AUC0-24h and 1.4 (90% CI, 1.0-2.0) for Cmax. In the intention-to-treat population, 65% achieved complete remission (CR) or CR with incomplete hematologic recovery. Interpatient variability in venetoclax exposure because of CYP3A4 polymorphisms was reduced by cobicistat. No unexpected toxicities were observed. In in vitro, cobicistat enhanced azacitidine/venetoclax antileukemic effects. In conclusion, cobicistat enhances and optimizes venetoclax exposure, enabling an eightfold dose reduction while maintaining efficacy. The potentiated antileukemic activity positions cobicistat as a promising complementary agent in AML therapy. This trial was registered at www.clinicaltrials.gov as NCT06014489.
© 2026 American Society of Hematology. Published by Elsevier Inc. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution. All other rights reserved.
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