Zidovudine-d₄

Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs^[1].
Zidovudine inhibits SVG, Primary human fetal astrocytes (PFA), peripheral blood mononuclear cells (PBMC), and monocyte-derived macrophages (MDM) with EC₅₀ of 17, 1311, 8, and 5 nM, respectively. Zidovudine inhibits SVG, PFA, PBMC, and MDM with EC₉₀ of 0.205 μM, 44.157 μM, 0.481 μM, and 0.219 μM, respectively^[2]. Genome editing via CRISPR/Cas9 has become an efficient and reliable way to make precise, targeted changes to the genome of living cells. CXCR4 is a co-receptor for the human immunodeficiency virus type 1 (HIV-1) infection and has been considered as an important therapeutic target for AIDS. CXCR4 mediates viral entry into human CD4⁺ cells by binding to envelope protein, gp120. Human CXCR4 gene is efficiently disrupted by CRISPR/Cas9-mediated genome editing, leading to HIV-1 resistance of human primary CD4⁺ T cells. The Cas9-mediated ablation of CXCR4 demonstrated high specificity and negligible off-target effects without affecting cell division and propagation^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.