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    Zidovudine (Azidothymidine)
    Zidovudine (Azidothymidine)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1823
    CAS #: 30516-87-1Purity ≥98%

    Description: Zidovudine (also known as ZDV, Azidothymidine; Retrovir; Zidovudinum, NSC 602670) is a nucleoside analogue reverse transcriptase inhibitor (NRTI) which used to treat and prevent HIV. Zidovudine is the first effective agent for the management of HIV-1 infection and is approved by FDA as a drug for AIDs in 1987. As a nucleoside analogue, zidovudine inhibits the activity of the reverse transcriptase with its triphosphate structure. It can also be used to prevent HIV transmission, such as from mother to child during the period of birth or after a needle stick injury. Used by itself in HIV-infected patients, AZT slows HIV replication in patients, but does not stop it entirely. 

    References: Clin Ther. 1996;18(6):1080-92; J Med Virol. 1999;58(2):165-73; Biochim Biophys Acta. 1996;1316(1):51-9.

    Related CAS#: 40093-94-5 (Torcitabine)

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    Molecular Weight (MW)267.24 
    FormulaC10H13N5O4 
    CAS No.30516-87-1 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 53 mg/mL (198.3 mM) 
    Water: 53 mg/mL (198.3 mM) 
    Ethanol: N/A
    Solubility (In vivo)18 mg/mL (67.4 mM) 
    SynonymsAzidothymidine, NSC-602670, NSC602670, NSC 602670, Zidovudinu; BW A509U; BWA 509U; BWA-509U; BWA509U; ZDV; AZT; Retrovir.


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    In Vitro

    In vitro activity: Zidovudine pretreatment has potent anti-HIV-1 activity in the newly infected T and monocytic cells but not in chronically infected cells. Inhibition of reverse transcription by Zidovudine decreases p24 antigen levels modestly, decreased HIV-1 gag by 19-fold, and inhibits detection of 2-LTR HIV-1 DNA. Zidovudine and dideoxynucleosides deplete wild-type mitochondrial DNA levels and increase deletedmitochondrial DNA levels in cultured Kearns-Sayre syndrome fibroblasts. Zidovudine (AZT, 0.1-50 mM) has a concentration dependent suppressive effect on the growth of granulocyte-monocyte colony forming unit (CFU-GM) derived colonies. Zidovudine exposure also induces a concentration dependent suppressive effect (35-90%) on GM-CSF receptor type alpha (GM-CSFR alpha) gene expression. Zidovudine causes a much lower decrease (15-22%) on the IL-3 receptor type alpha (IL-3R alpha) message level, and has an insignificant effect on glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and c-myc message levels. Zidovudine causes a concentration-dependent inhibition in the levels of the mRNA of Epo receptors and c-fos, whereas the level of c-myc mRNA is unaffected. Zidovudine also inhibits protein kinase C (PKC) activity in a concentration- and time-dependent manner, causing 50% inhibition at 10 mM within 3 hours. Zidovudine-induced down-regulation of Epo receptors and c-fos expression coupled with inhibition of Epo receptor-mediated signal transduction through PKC are significant contributory factors to AZT-induced erythroid toxicity.


    Cell Assay: Assays are performed in all cell types in the presence of titrating concentrations of ARV. 5,000 SVG, 2,500 PFA, 200,000 PBMC, or 50,000 MDM cells/well are seeded into triplicate wells of 96-well plates. Twenty-four hours later, the culture medium is removed and replaced with medium containing the ARV or DMSO (0.5% vol/vol), and equivalent TCID50 infectious units of luciferase reporter virus are added to the cells. After a 16 h incubation at 37°C, the initial viral inoculum is removed and replaced with culture medium containing the same antiretroviral drug (ARV) or DMSO (0.5% vol/vol) concentrations. At 72 h post infection, the medium is aspirated, the cells are lysed and HIV-1 infection measured using the Luciferase Assay System. Luminescence is measured using a FLUOStar Optima microplate reader. Inhibition curves and the 50% (EC50) and 90% (EC90) effective concentrations are determined by nonlinear regression analysis, using GraphPad Prism software.

    In VivoIntravitrous injection of the NRTIs Lamivudine (3TC), Zidovudine (AZT), or Abacavir (ABC) suppresses the laser-induced choroidal neovascularization (CNV) in wild-type mice compared to PBS vehicle. The mean level of VEGF-A in the RPE/choroid, which peaks on day 3 after laser injury, is significantly reduced in 3TC-, AZT- and ABC-treated eyes compared with control eyes in wild-type mice, but not inP2rx7-/- mice.
    Animal modelMice
    Formulation & DosageC57BL/6J (wild-type) and P2rx7-/- mice are used. The Nlrp3-/- mice are used. The NRTIs 3TC, AZT, and ABC or the P2X7 antagonist A438079 hydrochloride are dissolved in PBS. For CNV, each group of mice is injected once with 1 μL of NRTIs (3TC, 125 ng/μL; ABC, 183 ng/μL; AZT, 146 ng/μL), 1 μL of A438079 hydrochloride (3, 30, or 300 ng/μL), or the same volume of vehicle (PBS) into the vitreous humor using a 33-gauge needle immediately after laser injury. Another group of mice is injected with 3TC (125 ng) in combination with an anti-mouse VEGF polyclonal antibody (10 ng). Goat whole IgG (10 ng) is used as a biological control for the anti-mouse VEGF antibody. .
    ReferencesClin Ther. 1996 Nov-Dec;18(6):1080-92; J Med Virol. 1999 Jun;58(2):165-73; Biochim Biophys Acta. 1996 May 24;1316(1):51-9. 


    These protocols are for reference only. InvivoChem does not independently validate these methods.

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