Abacavir - CAS 136470-78-5
Not Intended for Therapeutic Use. For research use only.
Category:
Inhibitor
Product Name:
Abacavir
Catalog Number:
136470-78-5
Synonyms:
Ziagen
CAS Number:
136470-78-5
Description:
Abacavir sulfate is a Nucleoside analog reverse transcriptase inhibitor (NRTI); guanosine analog used to treat HIV and AIDS.
Molecular Weight:
286.33
Molecular Formula:
C14H18N6O
COA:
Inquire
MSDS:
Inquire
Targets:
HIV
Chemical Structure
CAS 136470-78-5 Abacavir

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Reference Reading


1. Syntheses and anti-HIV activities of (±)-norcarbovir and (±)-norabacavir
Weiqiang Huang, Marvin J. Miller,* Erik De Clercqc and Jan Balzarini. Org. Biomol. Chem., 2007, 5, 1164–1166
Inspired by the fact that both aristeromycin and 5’-noraristeromycin are inhibitors of S-adenosyl-L-homocysteine hydrolase (AdoHcy hydrolase), which likely accounts for their wide spectrum of antiviral activity, we considered the syntheses of norcarbovir (1) and norabacavir (2) with the anticipation that these two desmethylene derivatives might have anti-HIV activity similar to carbovir and abacavir. Besides the possible changes in biological activity, including cytotoxicity, the removal of the 5’-methylene group would also greatly shorten synthetic routes. To date, only the syntheses of phosphate analogs of 1 have been reported, but not the parent compound 1 itself. The synthesis and biological studies of norabacavir (2) surprisingly have not been previously described. We herein report highly efficient syntheses of 1 and 2, along with their biological activities.
2. Highly efficient inhibition of human immunodeficiency virus type 1 reverse transcriptase by aptamers functionalized gold nanoparticles
Yen-Chun Shiang, Chung-Mao Ou, Huan-Tsung Chang*. Nanoscale, 2013, 5, 2756–2764
We further compare the Apt–Au NP-based inhibitors with a commercial anti-HIV drug (nucleoside RT inhibitors; abacavir) in lentivirus infectivity assays (Fig. 4). The dosage dependence of infectivity revealed that the 40Aptpol-T45–Au NPs and 40AptRH-T45–Au NPs relative to abacavir provided much higher inhibition abilities. For example, the infectivity using 40AptRH-T45–Au NPs (7.5 nM; [AptRH] ¼ 300 nM) was 40.2%, while it was 72.5% when using abacavir (10 mM). Synergistic effects of 40AptRH-T45–Au NPs/Aptpol and 40Aptpol-T45–Au NPs/AptRH were not taken into account, because of low cellular uptake of the free aptamers. 40Aptpol-T45–Au NPs/40AptRH-T45–Au NPs showed little decrease in inhibiting efficiency, mainly because of molecular crowding effect; the 40Aptpol-T45–Au NPs/40AptRH-T45–Au NPs could not easily bind to HIV-1 RT at the same time in crowdedmedia of cell plasma (Fig. 4B). As a result, the synergistic effect was weakened. Since fatal hypersensitivity reactions have been associated with therapy with abacavir, the highly effective 40AptRH-T45–Au NPs/Aptpol inhibitors hold great potential for HIV therapy.
3. Towards the development of mechanism-based biomarkers to diagnose drug hypersensitivity
N. Duran-Figueroa, J. A. Badillo-Corona, D. J. Naisbitt and J. L. Castrejon-Flores*. Toxicol. Res.,2015, 4, 777–795
As discussed above, T-cells can be activated via a processing-independent mechanism by a direct interaction between the drug, TCR and MHC membrane receptors or by the modification of self-MHC presented peptides by drugs. Neither of these binding interactions fully explains the mechanism of T-cell activation by Abacavir. Independent studies recently proposed that Abacavir binds to the F-pocket of endogenous HLA-B*57:01, altering the repertoire of self-peptides that bind and are subsequently displayed on the cell surface. Mass spectrometric analysis, X-ray crystallography and docking studies demonstrated that the drug interacts non-covalently with amino acid residues found in the F-pocket site and particularly with Ser-116 expressed exclusively in HLA-B*57:01 and no other closely related alleles (HLA-B*57:02, HLA-B*57:03, HLA-B*57:11 or HLA-B*58:01). As a result of the Abacavir–Ser-116 interaction, the peptide repertoire presented by HLA-B*57:01 is modified with peptides containing less bulky amino acids at the anchor position being preferentially presented. The presence of Abacavir during protein processing leads to a 25% shift in the peptides presented by antigen presenting cells. Analysis of HLA-B*57:01 eluted peptides showed a peak with 287.1615 mass (MH+) corresponding to Abacavir, although no trace of the metabolite bound irreversibly to peptides was detected. Importantly, only 55% of the HLA-B*57:01+ patients suffer hypersensitivity reaction to this drug suggesting that TCR clonality, metabolism or the disease itself might represent additional susceptibility factors.