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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

The antiviral activity, mechanism of action, clinical significance and resistance of abacavir in the treatment of pediatric AIDS.

The novel carbocyclic nucleoside, abacavir, is metabolized in cells to carbovir triphosphate which is a potent inhibitor of HIV reverse transcriptase (K(i) 0.021 microM with calf thymus DNA template primer). Abacavir exhibits potent in vitro antiviral activity against wild-type HIV-1 (IC(50) 4.0 microM, MT-4 cells) but this activity is lower than the activity of AZT (IC(50) 0.040 microM, MT-4 cells). However, there is no significant difference between the levels of activity of abacavir (IC(50) 0.26 microM) and AZT (IC(50) 0.23 microM) against clinical isolates of HIV-1. The in vitro toxicity data (CC(50)) of abacavir were: 160 microM (CEM cells); 140 microM (CD4+ CEM cells) and 110 microM (normal bone progenitor cells, BFU-E). Abacavir has been approved in the United States for the treatment of pediatric and adult HIV infection and current recommendations consist of combination therapy in children with HIV infection. Resistance to abacavir develops relatively slowly, with most of the mutations conferring minimal resistance. The M184V mutation appears to be the cornerstone of higher level resistance in regimens containing abacavir, imparting a 2-4 fold reduction in the susceptibility of HIV to abacavir.[1]

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