阿昔洛韦作用机制 - Medchemexpress - MCE中国

1、Product Data SheetAcyclovirCat. No.: HY-17422CAS No.: 59277-89-3分式: CHNO分量: 225.2作靶点: HSV; Apoptosis; Bacterial作通路: Anti-infection; Apoptosis储存式: Powder -20°C 3 years4°C 2 yearsIn solvent -80°C 6 months-20°C 1 month溶解性数据体外实验 DMSO : 50 mg/mL (222.02 mM)* "" means soluble

2、, but saturation unknown.SolventMass1 mg 5 mg 10 mgConcentration制备储备液1 mM 4.4405 mL 22.2025 mL 44.4050 mL5 mM 0.8881 mL 4.4405 mL 8.8810 mL10 mM 0.4440 mL 2.2202 mL 4.4405 mL请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；旦配成溶液，请分装保存，避免反复冻融造成的产品失效。储备液的保存式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6

3、 个内使，-20°C 储存时，请在 1 个内使。体内实验请根据您的实验动物和给药式选择适当的溶解案。以下溶解案都请先按照 In Vitro 式配制澄清的储备液，再依次添加助溶剂：为保证实验结果的可靠性，澄 的储备液可以根据储存条件，适当保存；体内实验的作液，建议您现现配，当天使； 以下溶剂前显的百分 指该溶剂在您配制终溶液中的体积占；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的式助溶1. 请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% salineSolubility: 2.5 mg/mL (11.10 mM); Clear

4、 solution此案可获得 2.5 mg/mL (11.10 mM，饱和度未知) 的澄清溶液。以 1 mL 作液为例，取 100 L 25.0 mg/mL 的澄 DMSO 储备液加到 400 L PEG300 中，混合均匀；向上述体系中加50 L Tween-80，混合均匀；然后继续加 450 L 理盐定容 1 mL。2. 请依序添加每种溶剂： 10% DMSO 90% corn oilSolubility: 2.5 mg/mL (11.10 mM); Clear solutionPage 1 of 2 www.MedChemE此案可获得 2.5 mg/mL (11.10 mM，饱和度未知)

5、 的澄 溶液，此案不适于实验周 期在半个以上的实验。以 1 mL 作液为例，取 100 L 25.0 mg/mL 的澄 DMSO 储备液加到 900 L 油中，混合均匀。BIOLOGICAL ACTIVITY物活性 Acyclovir (Aciclovir) 种鸟嘌呤类似物和种服活性的抗病毒剂。Acyclovir 具有抗 HSV-1 (IC50 为 0.85 M)，HSV-2 (IC50 为 0.85 M) 和痘带状疱疹病毒的活性。Acyclovir 可被病毒胸苷激酶 (TK) 磷酸化，三磷酸 Acyclovir 通过鸟苷三磷酸的竞争性抑制和强制性链终来扰病毒 DNA 聚合。Acyclovir

6、 可预防急性病的诱导疗法中的细菌感染。IC & Target IC50: 0.85 M (HSV-1); 0.86 M (HSV-2)2体外研究 Acyclovir (3-100 µM; 24-72 hours; Jurkat, U937, and K562 leukemia cells) treatment shows a dose- and time-dependent reduction of cell viability3.Acyclovir (10-100 µM; 24-72 hours; Jurkat cells) treatment shows a d

7、elay/block in S phase and an increase of the sub-G1 peak3.Acyclovir (10-100 µM; 24-72 hours; Jurkat cells) treatment activates caspase-3 and presences nuclear DNAfragmentation, thereby indicating apoptotic cell death3.In HSV-infected cells, HSV thymidine kinase (HSV-TK) specifically phosphoryla

8、te Acyclovir to its monophosphate, andthis activation confers a high degree of selectivity of the drugs. Thereafter, the monophosphate is furtherphosphorylated to the diphosphate (Acyclovir -DP) and triphosphate (Acyclovir -TP) by cellular kinases. Thetriphosphate is the fully activated metabolite t

9、hat is toxic to the virus4.Cell Viability Assay3Cell Line: Jurkat, U937, and K562 leukemia cellsConcentration: 3 µM, 10 µM, 30 µM, 100 µMIncubation Time: 24 hours, 48 hours, and 72 hoursResult: Showed a dose- and time-dependent reduction of cell viability.Cell Cycle Analysis3Cell

10、 Line: Jurkat cellsConcentration: 10 µM, 100 µMIncubation Time: 24 hours, 48 hours, and 72 hoursResult: Revealed a dose-dependent accumulation of cells in S phase after 24 and 48 h.Showed a dose-dependent increase of the sub-G1 hypodiploid peak after 72 h.Apoptosis Analysis3Cell Line: Jurk

11、at cellsConcentration: 10 µM, 100 µMIncubation Time: 24 hours, 48 hours, and 72 hoursResult: Induced cell apoptosis.Page 2 of 3 www.MedChemE体内研究 Acyclovir (20 mg/kg; oral administration; three times daily; for 10 days; BALB/c mice) treatment in infected micesuppresses the development of sk

12、in lesions and results in a dissociation between DTH response and antibody production1.Animal Model: Specific-pathogen-free BALB/c mice (7-week-old) infected with HSV-11Dosage: 20 mg/kgAdministration: Oral administration; three times daily; for 10 daysResult: Suppressed the development of skin lesio

13、ns and resulted in a dissociation betweenDTH response and antibody production.REFERENCES1. Li Z, et al. Acyclovir treatment of skin lesions results in immune deviation in mice infected cutaneously with herpes simplex virus. Antivir ChemChemother. 1999 Sep;10(5):251-7.2. Suzuki M, et al. Synergistic

14、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 cytoto

15、xicity. LifeSci. 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):1056-67.5. Lönnqvist B, et al. Oral acyclovir as prophylaxis for bacterial infections during induction therapy for acute leukaemia in adults. The Leukemia Group ofMiddle Sweden. Support Care Cancer. 1993 May;1(