3'-Deoxythymidine - CAS 3416-05-5
Category:
Nucleosides
Product Name:
3'-Deoxythymidine
Catalog Number:
3416-05-5
CAS Number:
3416-05-5
Molecular Weight:
226.23
Molecular Formula:
C10H14N2O4
COA:
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MSDS:
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Structure\Application:
2',3'-Dideoxy-Nucleosides
Chemical Structure
CAS 3416-05-5 3'-Deoxythymidine

Related 2',3'-Dideoxy-Nucleosides Products


Reference Reading


1.Genetic requirements for sensitivity of bacteriophage t7 to dideoxythymidine.
Tran NQ1, Tabor S1, Richardson CC2. J Bacteriol. 2014 Aug;196(15):2842-50. doi: 10.1128/JB.01718-14. Epub 2014 May 23.
We previously reported that the presence of dideoxythymidine (ddT) in the growth medium selectively inhibits the ability of bacteriophage T7 to infect Escherichia coli by inhibiting phage DNA synthese (N. Q. Tran, L. F. Rezende, U. Qimron, C. C. Richardson, and S. Tabor, Proc. Natl. Acad. Sci. U. S. A. 105:9373-9378, 2008, doi:10.1073/pnas.0804164105). In the presence of T7 gene 1.7 protein, ddT is taken up into the E. coli cell and converted to ddTTP. ddTTP is incorporated into DNA as ddTMP by the T7 DNA polymerase, resulting in chain termination. We have identified the pathway by which exogenous ddT is converted to ddTTP. The pathway consists of ddT transport by host nucleoside permeases and phosphorylation to ddTMP by the host thymidine kinase. T7 gene 1.7 protein phosphorylates ddTMP and ddTDP, resulting in ddTTP. A 74-residue peptide of the gene 1.7 protein confers ddT sensitivity to the same extent as the 196-residue wild-type gene 1.
2.Myristoylated derivatives of 2',3'-didehydro-2',3'-dideoxythymidine (stavudine) bi-functional prodrugs with potent anti-HIV-1 activity and low cytotoxicity.
Singh RK1, Miazga A, Dąbrowska A, Lipniacki A, Piasek A, Kulikowski T, Shugar D. Antivir Chem Chemother. 2014 Dec 16;23(6):231-5. doi: 10.3851/IMP2679.
BACKGROUND: To improve in vitro antiviral activity and selectivity of stavudine (d4T), a range of its bi-functional prodrugs, 5'-O-myristoylated derivatives, have been synthesized.
3.Synthesis of β-triphosphotriester pronucleotides.
Beni Y1, Dash C2, Parang K3. Tetrahedron Lett. 2015 Apr 22;56(17):2247-2250. Epub 2015 Mar 16.
Dinucleoside phosphorochloridite were synthesized from phosphorus trichloride and three nucleoside analogues, 3'-fluoro-2',3'-dideoxythymidine (FLT), 2',3'-dideoxy-5-fluoro-3'-thiacytidine (FTC), and 2',3'-dideoxy-3'-thiacytidine (3TC), in a multistep synthesis. Polymer-bound N-Boc p-acetoxybenzyl 5'-O-2'-deoxythymidine was reacted with dinucleoside phosphorochloridite in the presence of 2,6-lutidine, followed by the reaction with dodecyl alcohol and 5-(ethylthio)-1H-tetrazole, oxidation with tert-butyl hydroperoxide, and acidic cleavage, respectively, to afford the β-triphosphotriester derivatives containing three different nucleosides.
4.Zidovudine induces downregulation of mitochondrial deoxynucleoside kinases: implications for mitochondrial toxicity of antiviral nucleoside analogs.
Sun R1, Eriksson S1, Wang L2. Antimicrob Agents Chemother. 2014 Nov;58(11):6758-66. doi: 10.1128/AAC.03613-14. Epub 2014 Sep 2.
Mitochondrial thymidine kinase 2 (TK2) and deoxyguanosine kinase (dGK) catalyze the initial phosphorylation of deoxynucleosides in the synthesis of the DNA precursors required for mitochondrial DNA (mtDNA) replication and are essential for mitochondrial function. Antiviral nucleosides are known to cause toxic mitochondrial side effects. Here, we examined the effects of 3'-azido-2',3'-dideoxythymidine (AZT) (zidovudine) on mitochondrial TK2 and dGK levels and found that AZT treatment led to downregulation of mitochondrial TK2 and dGK in U2OS cells, whereas cytosolic deoxycytidine kinase (dCK) and thymidine kinase 1 (TK1) levels were not affected. The AZT effects on mitochondrial TK2 and dGK were similar to those of oxidants (e.g., hydrogen peroxide); therefore, we examined the oxidative effects of AZT. We found a modest increase in cellular reactive oxygen species (ROS) levels in the AZT-treated cells. The addition of uridine to AZT-treated cells reduced ROS levels and protein oxidation and prevented the degradation of mitochondrial TK2 and dGK.