Zidovudine

Reverse transcriptase inhibitor CAS# 30516-87-1

Zidovudine

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Quality Control of Zidovudine

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Chemical structure

Zidovudine

3D structure

Chemical Properties of Zidovudine

Cas No. 30516-87-1 SDF Download SDF
PubChem ID 35370 Appearance Powder
Formula C10H13N5O4 M.Wt 267.24
Type of Compound N/A Storage Desiccate at -20°C
Synonyms Azidothymidine; AZT; ZDV
Solubility DMSO : ≥ 100 mg/mL (374.20 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name 1-[(2R,4S,5S)-4-azido-5-(hydroxymethyl)oxolan-2-yl]-5-methylpyrimidine-2,4-dione
SMILES CC1=CN(C(=O)NC1=O)C2CC(C(O2)CO)N=[N+]=[N-]
Standard InChIKey HBOMLICNUCNMMY-XLPZGREQSA-N
Standard InChI InChI=1S/C10H13N5O4/c1-5-3-15(10(18)12-9(5)17)8-2-6(13-14-11)7(4-16)19-8/h3,6-8,16H,2,4H2,1H3,(H,12,17,18)/t6-,7+,8+/m0/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Zidovudine

DescriptionSelective reverse transcriptase inhibitor. Exhibits 100-fold selectivity for HIV reverse transcriptase over DNA polymerase α. Suppresses HIV-1 replication and enhances cell viability in HIV-1 infected T cells. Attenuates growth of multiple myeloma (MM) cells in vitro and reduces growth of MM tumor xenografts in mice. Orally bioavailable and brain penetrant. Antiretroviral agent. Also decreases CRISPR-mediated homology directed repair (HDR) efficiency.

Zidovudine Dilution Calculator

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Preparing Stock Solutions of Zidovudine

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.742 mL 18.7098 mL 37.4195 mL 74.8391 mL 93.5489 mL
5 mM 0.7484 mL 3.742 mL 7.4839 mL 14.9678 mL 18.7098 mL
10 mM 0.3742 mL 1.871 mL 3.742 mL 7.4839 mL 9.3549 mL
50 mM 0.0748 mL 0.3742 mL 0.7484 mL 1.4968 mL 1.871 mL
100 mM 0.0374 mL 0.1871 mL 0.3742 mL 0.7484 mL 0.9355 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Zidovudine

Zidovudine is an inhibitor of the reverse transcriptase of HIV-1[1].

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. In the in vitro studies, zidovudine shows strong inhibition of HIV-1 replication and the cytopathic effect of the virus. The addition of 5μM and 10μM zidovudine completely protects TM3 cells (a normal IL-2-dependent helper/inducer T-cell clone) and ATH8 cells against the cytopathic effect of HIV. It exhibits complete inhibition of reverse transcriptase at concentration up to 0.5μM. However, the resistance of zidovudine has been found in vitro and in vivo since 1989 [1, 2].

References:
[1] Mitsuya H, Weinhold K J, Furman P A, et al. 3'-Azido-3'-deoxythymidine (BW A509U): an antiviral agent that inhibits the infectivity and cytopathic effect of human T-lymphotropic virus type III/lymphadenopathy-associated virus in vitro. Proceedings of the National Academy of Sciences, 1985, 82(20): 7096-7100.
[2] McLeod G X, Hammer S M. Zidovudine: five years later. Annals of internal medicine, 1992, 117(6): 487-501.

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References on Zidovudine

Metabolic syndrome in patients on first-line antiretroviral therapy containing zidovudine or tenofovir in rural Lesotho, Southern Africa.[Pubmed:28342180]

Trop Med Int Health. 2017 Jun;22(6):725-733.

OBJECTIVE: To assess the prevalence of metabolic syndrome (MetS) among patients in rural Lesotho who are taking first-line antiretroviral therapy (ART) containing either Zidovudine or tenofovir disoproxil. METHODS: Cross-sectional survey in 10 facilities in Lesotho among adult (>/=16 years) patients on non-nucleoside reverse transcriptase inhibitor (NNRTI)-based first-line ART for >/=6 months. MetS was defined according to the International Diabetes Federation criteria. RESULTS: Among 1166 patients (65.8% female), 22.2% (95% CI: 19.3-25.3) of women and 6.3% (4.1-9.1) of men met the IDF definition of MetS (P < 0.001). In both sexes, there was no significant difference in MetS prevalence between NNRTIs. However, in women taking Zidovudine as nucleoside reverse transcriptase inhibitor (NRTI), MetS prevalence was 27.9%, vs. 18.8% in those taking tenofovir. In the multivariate logistic regression allowing for socio-demographic and clinical covariates, ART containing Zidovudine was associated with MetS in women (aOR 2.17 (1.46-3.22), P < 0.001) but not in men. CONCLUSION: In this study, taking ART containing Zidovudine instead of tenofovir disoproxil was an independent predictor of MetS in women but not in men. This finding endorses WHO's recommendation of tenofovir as preferred NRTI.

Placental Mitochondrial Toxicity, Oxidative Stress, Apoptosis, and Adverse Perinatal Outcomes in HIV Pregnancies Under Antiretroviral Treatment Containing Zidovudine.[Pubmed:28234688]

J Acquir Immune Defic Syndr. 2017 Aug 1;75(4):e113-e119.

OBJECTIVE: To determine whether mitochondrial, oxidative, and apoptotic abnormalities in placenta derived from HIV and combined antiretroviral therapy (cART) containing Zidovudine (AZT) could be associated with adverse perinatal outcome. DESIGN: Cross-sectional, controlled, observational study. METHODS: We studied obstetric results and mitochondrial, oxidative, and apoptotic state in placenta of 24 treated HIV-infected and 32 -uninfected pregnant women. We measured mitochondrial DNA (mtDNA) content by quantitative reverse transcriptase-polymerase chain reaction (mtND2/n18SrRNA), oxidative stress by the spectrophotometric quantification of lipid peroxidation and apoptosis by Western blot analysis of active caspase-3 respect to beta-actin content and analysis of the terminal deoxynucleotidyl transferase dUTP nick end labeling. RESULTS: Global adverse perinatal outcome (defined as preterm delivery or/and small newborns for gestational age) was significantly increased in HIV pregnancies [or 6.7 (1.3-33.2); P < 0.05]. mtDNA content in HIV-infected women was significantly depleted (39.20% +/- 2.78%) with respect to controls (0.59 +/- 0.03 vs. 0.97 +/- 0.07; P < 0.001). A significant 29.50% +/- 9.14% increase in oxidative stress was found in placentas of HIV-infected women (23.23 +/- 1.64 vs. 17.94 +/- 1.03; P < 0.01). A trend toward 41.18% +/- 29.41% increased apoptosis active caspase-3/beta-actin was found in HIV patients (0.48 +/- 0.10 vs. 0.34 +/- 0.05; P = not significant), confirmed by transferase dUTP nick end labeling assay. Adverse perinatal outcome did not correlate mitochondrial, oxidative, or apoptotic findings. CONCLUSIONS: Placentas of HIV-infected pregnant women under AZT cART showed evidence of mtDNA depletion, increased oxidative stress levels, and apoptosis suggestive of secondary mitochondrial failure, potential base of associated adverse perinatal outcome. Despite the fact that further demonstration of causality would need new approaches and bigger sample sizes, AZT-sparing cART should be considered in the context of pregnancy.

Zidovudine continuous infusion in an HIV-infected pregnant woman with a phobia of swallowing pills.[Pubmed:28367828]

Antivir Ther. 2017;22(8):727-729.

The authors report the difficulties of preventing mother-to-child transmission in a pregnant HIV-infected woman with a phobia of swallowing pills. After multiple attempts and just as many failures, the authors ended up with cART consisting of small tablets of nevirapine, lamivudine and a continuous intravenous infusion of Zidovudine given via an elastomeric pump at home. This case demonstrates the difficulties that HIV physicians can encounter in pregnant women who have difficulties in swallowing tablets. In exceptional circumstances, continuous infusion of Zidovudine may be an option, even in an outpatient setting.

Small molecules enhance CRISPR genome editing in pluripotent stem cells.[Pubmed:25658371]

Cell Stem Cell. 2015 Feb 5;16(2):142-7.

The bacterial CRISPR-Cas9 system has emerged as an effective tool for sequence-specific gene knockout through non-homologous end joining (NHEJ), but it remains inefficient for precise editing of genome sequences. Here we develop a reporter-based screening approach for high-throughput identification of chemical compounds that can modulate precise genome editing through homology-directed repair (HDR). Using our screening method, we have identified small molecules that can enhance CRISPR-mediated HDR efficiency, 3-fold for large fragment insertions and 9-fold for point mutations. Interestingly, we have also observed that a small molecule that inhibits HDR can enhance frame shift insertion and deletion (indel) mutations mediated by NHEJ. The identified small molecules function robustly in diverse cell types with minimal toxicity. The use of small molecules provides a simple and effective strategy to enhance precise genome engineering applications and facilitates the study of DNA repair mechanisms in mammalian cells.

Azidothymidine is effective against human multiple myeloma: a new use for an old drug?[Pubmed:22931421]

Anticancer Agents Med Chem. 2013 Jan;13(1):186-92.

Azidothymidine (AZT) is an antiretroviral drug that affects cell proliferation, apoptosis, and the NF-kappaB pathway. As multiple myeloma (MM) presents with constitutive activation of NF-kappaB, we analyzed the effect of AZT on human MM cell lines. We evaluated the cytotoxic effect of AZT in human MM cell lines sensitive (8226/S) or resistant to doxorubicin (8226/DX5) and human T cell lymphoblast-like cells, uterine sarcoma cells, and HUVEC using MTT assay. Cytotoxicity was also evaluated in vivo in nude mice xenografted with 8226/S tumor. The effect of AZT on the expression of genes involved in cell proliferation, apoptosis, angiogenesis, and the NF-kappaB pathway was analyzed in the xenografts using real-time polymerase chain reaction. AZT was effective against both 8226/S and 8226/DX5 cells in a dose and time-dependent manner (p = 0.02) in vitro and promoted cell cycle arrest in S phase in these cells. The tumor volume was lower in mice treated with AZT compared to untreated mice (p = 0.0003). AZT down-regulated the pro-proliferative genes encoding AKT1, MYC, STAT1, MAPK8, MAPK9, CCL-3, Bcl-3, and cyclin D2; pro-angiogenenic genes encoding VEGF and IL8; and genes involved in cell adhesion (ICAM1 and FN1) and the NF-kappaB pathway. AZT up-regulated the expression of tumor suppressor gene FOXP1 and the pro-apoptotic genes encoding BID, Bcl-10, and caspase-8. Thus, we demonstrated the cytotoxic effect of AZT in human MM cell lines for the first time. Our data may provide the rationale for future clinical trials of AZT for treating MM.

The development of antiretroviral therapy and its impact on the HIV-1/AIDS pandemic.[Pubmed:20018391]

Antiviral Res. 2010 Jan;85(1):1-18.

In the last 25 years, HIV-1, the retrovirus responsible for the acquired immunodeficiency syndrome (AIDS), has gone from being an "inherently untreatable" infectious agent to one eminently susceptible to a range of approved therapies. During a five-year period, starting in the mid-1980s, my group at the National Cancer Institute played a role in the discovery and development of the first generation of antiretroviral agents, starting in 1985 with Retrovir (Zidovudine, AZT) in a collaboration with scientists at the Burroughs-Wellcome Company (now GlaxoSmithKline). We focused on AZT and related congeners in the dideoxynucleoside family of nucleoside reverse transcriptase inhibitors (NRTIs), taking them from the laboratory to the clinic in response to the pandemic of AIDS, then a terrifying and lethal disease. These drugs proved, above all else, that HIV-1 infection is treatable, and such proof provided momentum for new therapies from many sources, directed at a range of viral targets, at a pace that has rarely if ever been matched in modern drug development. Antiretroviral therapy has brought about a substantial decrease in the death rate due to HIV-1 infection, changing it from a rapidly lethal disease into a chronic manageable condition, compatible with very long survival. This has special implications within the classic boundaries of public health around the world, but at the same time in certain regions may also affect a cycle of economic and civil instability in which HIV-1/AIDS is both cause and consequence. Many challenges remain, including (1) the life-long duration of therapy; (2) the ultimate role of pre-exposure prophylaxis (PrEP); (3) the cardiometabolic side-effects or other toxicities of long-term therapy; (4) the emergence of drug-resistance and viral genetic diversity (non-B subtypes); (5) the specter of new cross-species transmissions from established retroviral reservoirs in apes and Old World monkeys; and (6) the continued pace of new HIV-1 infections in many parts of the world. All of these factors make refining current therapies and developing new therapeutic paradigms essential priorities, topics covered in articles within this special issue of Antiviral Research. Fortunately, there are exciting new insights into the biology of HIV-1, its interaction with cellular resistance factors, and novel points of attack for future therapies. Moreover, it is a short journey from basic research to public health benefit around the world. The current science will lead to new therapeutic strategies with far-reaching implications in the HIV-1/AIDS pandemic. This article forms part of a special issue of Antiviral Research marking the 25th anniversary of antiretroviral drug discovery and development, Vol. 85, issue 1, 2010.

Phosphorylation of 3'-azido-3'-deoxythymidine and selective interaction of the 5'-triphosphate with human immunodeficiency virus reverse transcriptase.[Pubmed:2430286]

Proc Natl Acad Sci U S A. 1986 Nov;83(21):8333-7.

The thymidine analog 3'-azido-3'-deoxythymidine (BW A509U, azidothymidine) can inhibit human immunodeficiency virus (HIV) replication effectively in the 50-500 nM range [Mitsuya, H., Weinhold, K. J., Furman, P. A., St. Clair, M. H., Nusinoff-Lehrman, S., Gallo, R. C., Bolognesi, D., Barry, D. W. & Broder, S. (1985) Proc. Natl. Acad. Sci. USA 82, 7096-7100]. In contrast, inhibition of the growth of uninfected human fibroblasts and lymphocytes has been observed only at concentrations above 1 mM. The nature of this selectivity was investigated. Azidothymidine anabolism to the 5'-mono-, di-, and -triphosphate derivatives was similar in uninfected and HIV-infected cells. The level of azidothymidine monophosphate was high, whereas the levels of the di- and triphosphate were low (less than or equal to 5 microM and less than or equal to 2 microM, respectively). Cytosolic thymidine kinase (EC 2.7.1.21) was responsible for phosphorylation of azidothymidine to its monophosphate. Purified thymidine kinase catalyzed the phosphorylations of thymidine and azidothymidine with apparent Km values of 2.9 microM and 3.0 microM. The maximal rate of phosphorylation with azidothymidine was equal to 60% of the rate with thymidine. Phosphorylation of azidothymidine monophosphate to the diphosphate also appeared to be catalyzed by a host-cell enzyme, thymidylate kinase (EC 2.7.4.9). The apparent Km value for azidothymidine monophosphate was 2-fold greater than the value for dTMP (8.6 microM vs. 4.1 microM), but the maximal phosphorylation rate was only 0.3% of the dTMP rate. These kinetic constants were consistent with the anabolism results and indicated that azidothymidine monophosphate is an alternative-substrate inhibitor of thymidylate kinase. This conclusion was reflected in the observation that cells incubated with azidothymidine had reduced intracellular levels of dTTP. IC50 (concentration of inhibitor that inhibits enzyme activity 50%) values were determined for azidothymidine triphosphate with HIV reverse transcriptase and with immortalized human lymphocyte (H9 cell) DNA polymerase alpha. Azidothymidine triphosphate competed about 100-fold better for the HIV reverse transcriptase than for the cellular DNA polymerase alpha. The results reported here suggest that azidothymidine is nonselectively phosphorylated but that the triphosphate derivative efficiently and selectively binds to the HIV reverse transcriptase. Incorporation of azidothymidylate into a growing DNA strand should terminate DNA elongation and thus inhibit DNA synthesis.

3'-Azido-3'-deoxythymidine (BW A509U): an antiviral agent that inhibits the infectivity and cytopathic effect of human T-lymphotropic virus type III/lymphadenopathy-associated virus in vitro.[Pubmed:2413459]

Proc Natl Acad Sci U S A. 1985 Oct;82(20):7096-100.

The acquired immune deficiency syndrome (AIDS) is thought to result from infection of T cells by a pathogenic human retrovirus, human T-lymphotropic virus type III (HTLV-III) or lymphadenopathy-associated virus (LAV). In this report, we describe the antiviral effects of a thymidine analogue,3'-azido-3'-deoxythymidine (BW A509U), which, as a triphosphate, inhibits the reverse transcriptase of HTLV-III/LAV. This agent blocks the expression of the p24 gag protein of HTLV-III/LAV in H9 cells following exposure to virus. The drug also inhibits the cytopathic effect of HTLV-IIIB (a virus derived from a pool of American patients) and HTLV-III/RF-II (an isolate obtained from a Haitian patient that differs by about 20% in the amino acid sequence of the envelope gene from several isolates of HTLV-III/LAV, including HTLV-IIIB, analyzed so far). 3'-Azido-3'-deoxythymidine also completely blocks viral replication as assessed by reverse transcriptase production in normal human peripheral blood mononuclear cells exposed to HTLV-IIIB. Finally, at concentrations of 3'-azido-3'-deoxythymidine that block the in vitro infectivity and cytopathic effect of HTLV-IIIB, the in vitro immune functions of normal T cells remain basically intact.

Description

Zidovudine is a nucleoside reverse transcriptase inhibitor (NRTI), widely used to treat HIV infection. Zidovudine increases CRISPR/Cas9-mediated editing frequency.

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