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My CartCAS：59277-89-3
Molecular Formula：C8H11N5O3
Molecular Weight：225.2
Storage：Powder:2-8℃，2 years;Insolvent(Mother Liquid):-20℃，6 months;-80℃，1 year
Purity：HPLC≥98%
Appearance：White to off-white Solid
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| CAS | 59277-89-3 |
| Name | Acyclovir |
| Molecular Formula | C8H11N5O3 |
| Molecular Weight | 225.2 |
| Solubility | Soluble in DMSO ≥2mg/mL(Need ultrasonic) |
| Purity | HPLC≥98% |
| Appearance | White to off-white Solid |
| Storage | Powder:2-8℃，2 years;Insolvent(Mother Liquid):-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 |
| Target Point | HSV |
| Passage | Anti-infection |
| Background | It is a class of thymidine kinase that can inhibit the herpes virus. |
| Biological Activity | 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]. |
| In Vivo | 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]. |
| Data Literature Source | [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. |
| Unit | Bottle |
| Specification | 20mg 10mM*1mL in DMSO 50mg |
是一类能够抑制疱疹病毒的胸苷激酶。
Remark：These protocols are for reference only. Solarbio does not independently validate these methods.
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BMS-265246,a Cyclin-Dependent Kinase Inhibitor,Inhibits the Infection of Herpes Simplex Virus Type 1
Click to check >>Author：Lefang Jiang, Yang Yu, Zhuogang Li, Yarou Gao, Haonan Zhang, Mingxin Zhang, Weihua Cao, Qun Peng, Xulin Chen
IF：4.7000
Publish_to：Viruses-Basel
PMID：37631985
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