Mavorixafor (AMD-070) is an effective and selective antagonist of CXCR4, with an IC50 value of 13 nM against CXCR4 125I-SDF binding. Mavorixafor inhibits the replication of T-tropic HIV-1 (NL4.3 strain) in MT-4 cells (IC50 = 1 nM) and PBMCs (IC50 = 9 nM).

HIV-1 (NL4.3 strain):1 nM (in MT-4 cells), HIV-1 (NL4.3 strain):9 nM (in PBMCs), HIV-1 (NL4.3 strain):3 nM (in MT-4 cells), HIV-1 (NL4.3 strain):26 nM (IC90, in PBMCs), [125I]-SDF-CXCR4:13 nM

Mavorixafor (6.6 µM) significantly decreases the anchorage-dependent growth, migration, and matrigel invasion of the B88-SDF-1 cells [1]. Mavorixafor shows no effect on other chemokine receptors (CCR1, CCR2b, CCR4, CCR5, CXCR1, and CXCR2) [2].

AMD-070 (2 mg/kg, p.o.) markedly decreases the quantity of metastatic lung nodules in mice and reduces human Alu DNA expression without causing weight loss [1].

Cells are seeded on a 96-well plate at 5 × 10^3 cells/well in DMEM containing 10% FCS. Twenty-four hours later, the cells are treated with or without 2 µM AMD3100 or 6.6 µM AMD-070. After 24 or 48 h, the number of cells is quantified by an assay using MTT [2].

BALB/c nude mice are maintained under pathogen-free conditions. The experiments are initiated when the mice are 8 weeks of age. Briefly, the cells are inoculated into the blood vessels of nude mice (1× 10^6). These mice are sacrificed at day 49. The presence or absence of distant metastases is confirmed by hematoxylin and eosin (H&E) staining. For experimental chemotherapy, the mice are treated by the daily oral administration of 0.2 mL of saline for a vehicle or the same volume of AMD-070 (2 mg/kg) [2].