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- 详细信息
- 文献和实验
- 技术资料
- 保存条件:
Powder:2-8℃,2 years;Insolvent(母液):-20℃,6 months;-80℃,1 year
- 保质期:
Powder:2-8℃,2 years;Insolvent(母液):-20℃,6 months;-80℃,1 year
- 英文名:
Acyclovir
- 库存:
现询
- 供应商:
北京索莱宝科技有限公司
- CAS号:
59277-89-3
- 规格:
100mg/50mg/20mg/10mM*1mL in DMSO
| 规格: | 100mg | 产品价格: | ¥870.0 |
|---|---|---|---|
| 规格: | 50mg | 产品价格: | ¥540.0 |
| 规格: | 20mg | 产品价格: | ¥360.0 |
| 规格: | 10mM*1mL in DMSO | 产品价格: | ¥380.0 |
是一类能够抑制疱疹病毒的胸苷激酶。
【本资料源自公开渠道,如需(此处)屏蔽,请联系删除】
标题:BMS-265246,a Cyclin-Dependent Kinase Inhibitor,Inhibits the Infection of Herpes Simplex Virus Type 1
成员:Lefang Jiang, Yang Yu, Zhuogang Li, Yarou Gao, Haonan Zhang, Mingxin Zhang, Weihua Cao, Qun Peng, Xulin Chen
论文因子:4.7 发表期刊:Viruses-Basel pmid:37631985
| 基本信息 | |
| CAS | No.59277-89-3 |
| 中文名称 | 阿昔洛韦 |
| 英文名称 | Acyclovir |
| 别名 | Acycloguanosine |
| 分子式 | C8H11N5O3 |
| 分子量 | 225.2 |
| 溶解性 | Soluble in DMSO ≥2mg/mL(Need ultrasonic) |
| 纯度 | HPLC≥98% |
| 外观(性状) | White to off-white Solid |
| 储存条件 | Powder:2-8℃,2 years;Insolvent(母液):-20℃,6 months;-80℃,1 year |
| EC | EINECS 261-685-1 |
| MDL | MFCD00057880 |
| SMILES | O=C1NC(N)=NC2=C1N=CN2COCCO |
| InChIKey | MKUXAQIIEYXACX-UHFFFAOYSA-N |
| InChI | InChI=1S/C8H11N5O3/c9-8-11-6-5(7(15)12-8)10-3-13(6)4-16-2-1-14/h3,14H,1-2,4H2,(H3,9,11,12,15) |
| PubChem CID | 135398513 |
| 靶点 | HSV |
| 通路 | Anti-infection |
| 背景说明 | 是一类能够抑制疱疹病毒的胸苷激酶。 |
| 生物活性 | Acyclovir prevents bacterial infections during induction therapy for acute leukaemia. Acyclovir (Aciclovir) is a guanosine analogue and an orally active antiviral agent. Acyclovir inhibits HSV-1 (IC50 of 0.85 μM), HSV-2 (IC50 of 0.86 μM) and varicella-zoster virus. Acyclovir can be phosphorylated by viral thymidine kinase (TK), and Acyclovir triphosphate interferes with viral DNA polymerization through competitive inhibition with guanosine triphosphate and obligatory chain termination[1-4]. |
| In Vitro | Acyclovir(3-100 μM; 24-72 hours; Jurkat,U937,and K562 leukemia cells)treatment shows a dose- and time-dependent reduction of cell viability.Acyclovir(10-100 μM; 24-72 hours; Jurkat cells)treatment shows a delay/block in S phase and an increase of the sub-G1 peak.Acyclovir(10-100 μM; 24-72 hours; Jurkat cells)treatment activates caspase-3 and presences nuclear DNA fragmentation,thereby indicating apoptotic cell death[3].In HSV-infected cells,HSV thymidine kinase(HSV-TK)specifically phosphorylate Acyclovir to its monophosphate,and this activation confers a high degree of selectivity of the drugs. Thereafter,the monophosphate is further phosphorylated to the diphosphate(Acyclovir -DP)and triphosphate(Acyclovir -TP)by cellular kinases. The triphosphate is the fully activated metabolite that is toxic to the virus[4]. |
| 细胞实验 | Acyclovir(20 mg/kg; oral administration; three times daily; for 10 days; BALB/c mice)treatment in infected mice suppresses the development of skin lesions and results in a dissociation between DTH response and antibody production[1]. |
| 数据来源文献 | [1]. Li Z, et al. Acyclovir treatment of skin lesions results in immune deviation in mice infected cutaneously with herpes simplex virus. Antivir Chem Chemother. 1999 Sep;10(5):251-7. [2]. Suzuki M, et al. Synergistic antiviral activity of acyclovir and vidarabine against herpes simplex virus types 1 and 2 and varicella-zoster virus. Antiviral Res. 2006 Nov;72(2):157-61. [3]. Benedetti S, et al. Acyclovir induces cell cycle perturbation and apoptosis in Jurkat leukemia cells, and enhances chemotherapeutic drug cytotoxicity. Life Sci. 2018 Dec 15;215:80-85. [4]. Hayashi K, et al. The role of a HSV thymidine kinase stimulating substance, scopadulciol, in improving the efficacy of cancer gene therapy. J Gene Med. 2006 Aug;8(8):1056-67. |
| 单位 | 瓶 |
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文献和实验【本资料源自公开渠道,如需(此处)屏蔽,请联系删除】
标题:BMS-265246,a Cyclin-Dependent Kinase Inhibitor,Inhibits the Infection of Herpes Simplex Virus Type 1
成员:Lefang Jiang, Yang Yu, Zhuogang Li, Yarou Gao, Haonan Zhang, Mingxin Zhang, Weihua Cao, Qun Peng, Xulin Chen
论文因子:4.7 发表期刊:Viruses-Basel pmid:37631985
侵袭性真菌感染(Invasive Fungal Infection, IFI)是接受联合化疗及 造血干细胞 移植(Hematopoietic stem cell transplantation, HSCT)患者的严重并发症,其中侵袭性曲霉菌病(Invasive Aspergillosis , IA)是较为常见的一种,且发生率逐年上升,1在血液病和HSCT患者中病死率高达50%-90%。2造成高病死率的主要原因是IA 早期诊断困难,使得治疗延迟。3 以往常用的诊断IA
细菌感染和增强免疫调节的作用。其中白细胞介素2还可使患者淋巴细胞数增加,改善人体免疫功能。近年来,重组人生长激素在促进生长、营养支持、代谢调理方面的显著效果使其在AIDS治疗中倍受关注。此外已建立的免疫功能抑制的动物模型证明生长激素在免疫力增强和T细胞之间相互调节中也有一定作用,故其在AIDS治疗领域有着广阔的研究应用价值。 3 抗机会性感染药 临床上抗AIDS辅助用药的抗感染药主要分为4类: 第1类用于卡氏肺孢子虫肺炎,主要药物为复方磺胺甲恶唑和戊双咪,二者单用或复用均有一定疗效。 第2类
细胞起约束作用。 (一)Mφ、T、B细胞相互作用过程中的MHC约束性 Rosenthal和Shevach(1973)首先在豚鼠中观察到T细胞只能被具有相同MHc I区基因(Ⅱ类基因)的抗原提呈细胞所激活(表6-13)。同年Katz等人也发现Th与B细胞相互作用时,只有在两者MHc I区(Ⅱ类基因)相同的条件才会出现协作应(表6-14)。 表6-13 豚鼠T细胞对胸腺信赖抗原的免疫应答中Mφ提呈抗原与Ia抗原的关系 OVA预处理T细胞 OVA加Mφ DNA合成的增加
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