Abacavir (ABC) is a able nucleoside analog about-face transcriptase inhibitor (NRTI) acclimated to amusement HIV and AIDS. Chemically, it is a constructed carbocyclic nucleoside and is the enantiomer with 1S, 4R complete agreement on the cyclopentene ring. In vivo, abacavir sulfate dissociates to its chargeless base, abacavir.
Abacavir is a nucleoside about-face transcriptase inhibitor (NRTI) with action adjoin Human Immunodeficiency Virus Type 1 (HIV-1). Abacavir is phosphorylated to alive metabolites that attempt for assimilation into viral DNA. They arrest the HIV about-face transcriptase agitator competitively and act as a alternation terminator of DNA synthesis. The absorption of biologic all-important to aftereffect viral archetype by 50 percent (EC50) ranged from 3.7 to 5.8 μM (1 μM = 0.28 mcg/mL) and 0.07 to 1.0 μM adjoin HIV-1IIIB and HIV-1BaL, respectively, and was 0.26 ± 0.18 μM adjoin 8 analytic isolates. Abacavir had accessory action in corpuscle ability in aggregate with the nucleoside about-face transcriptase inhibitor (NRTI) zidovudine, the non-nucleoside about-face transcriptase inhibitor (NNRTI) nevirapine, and the protease inhibitor (PI) amprenavir; and accretion action in aggregate with the NRTIs didanosine, emtricitabine, lamivudine, stavudine, tenofovir, and zalcitabine.
Abacavir is a carbocyclic constructed nucleoside alternation and an antiviral agent. Intracellularly, abacavir is adapted by cellular enzymes to the alive metabolite carbovir triphosphate, an alternation of deoxyguanosine-5′-triphosphate (dGTP). Carbovir triphosphate inhibits the action of HIV-1 about-face transcriptase (RT) both by aggressive with the accustomed substrate dGTP and by its assimilation into viral DNA. Viral DNA advance is concluded because the congenital nucleotide lacks a 3′-OH group, which is bare to anatomy the 5′ to 3′ phosphodiester bond capital for DNA alternation elongation.