S-Acetyl-L-glutathione is a derivative of glutathione .1 It increases intracellular GSH levels in primary fibroblasts derived from patients with glutathione synthetase deficiency when used at a concentration of 50 μM. S-Acetyl-L-glutathione (5 mM) induces apoptosis in Daudi, Raji, and Jurkat lymphoma cells.2 It inhibits the replication of herpes simplex virus 1 (HSV-1) in human foreskin fibroblasts when used at concentrations of 5 and 10 mM.3 S-Acetyl-L-glutathione (6.25 μg/g per day) increases survival in a mouse model of HSV-1 infection.
GSK812397 is a potent entry inhibitor of X4-tropic strains of HIV-1, as demonstrated in multiple in vitro cellular assays. GSK812397 is a noncompetitive antagonist of the CXCR4 receptor, with GSK812397 producing a concentration-dependent decrease in both an SDF-1-mediated chemotaxis and intracellular calcium release (IC50s were 0.34+ -0.01 nM and 2.41+ -0.50 nM, respectively). GSK812397 is effective against a broad range of X4- and X4R5-utilizing clinical isolates. The potency and efficacy of GSK812397 are dependent on the individual isolate, with complete inhibition of infection observed with 24 of 30 isolates. GSK812397 does not show any detectable in vitro cytotoxicity and was highly selective for CXCR4. GSK812397 shows acceptable pharmacokinetic properties and bioavailability across species. GSK812397 has antiviral activity against a broad range of X4-utilizing strains of HIV-1 via a noncompetitive antagonism of the CXCR4 receptor.
ent-Abacavir is an enatiomer of Abacavir. Abacavir is a carbocyclic 2'-deoxyguanosine nucleoside reverse transcriptase inhibitor and an anti-HIV drug used to treat HIV infection. Intracellular enzymes convert Abacavir to its active form, carbovir-triphosphate (CBV-TP), which then selectively inhibits HIV reverse transcriptase by incorporating into viral DNA. Abacavir is metabolized in the liver by uridine diphosphate glucuronyltransferase and alcohol dehydrogenase resulting in inactive glucuronide and carboxylate metabolites, respectively.