Mavorixafor 是一种有效的特异性 CXCR4 拮抗剂，对 CXCR4 125I-SDF 结合的 IC50 值为 13 nM。 Mavorixafor 在 MT-4 细胞 (IC50 = 1 nM) 和 PBMC (IC50 = 9 nM) 中抑制 T-tropic HIV-1 (NL4.3 株) 的复制。

Mavorixafor 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).

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.) significantly reduces the number of metastatic lung nodules in mice, and lowers the expression of human Alu DNA in mice, without body 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].

558447-26-0

C21H27N5

349.47

AMD-070;Mavorixafor

Ethanol:44 mg/mL (125.9 mM)
DMSO:17 mg/mL (48.64 mM)
H2O:7 mg/mL (20.03 mM),warming
Powder: -20°C for 3 years
In solvent: -80°C for 2 years