AMD 3465 also potently inhibits the replication of X4 HIV strains (IC50: 1-10 nM). However, it has no effect on CCR5-using (R5) viruses. AMD 3465 (GENZ-644494) is a potent antagonist of CXCR4, inhibits binding of 12G5 mAb and CXCL12AF647 to CXCR4, with IC

AMD 3465 is a potent antagonist of CXCR4, inhibits binding of 12G5 mAb and CXCL12AF647 to CXCR4, with IC50s of 0.75 nM and 18 nM in SupT1 cells and it is cytotoxic to the X4 HIV-1 strains IIIB, NL4.3, RF and HE with an IC50 ranging from 6 to 12 nM. AMD 3465 inhibits CXCL-12-induced growth in U87 and Daoy cells. AMD 3465 treatment stimulates the phosphorylation of Erk1/2 in U87 and Daoy cells[2]. AMD 3465 (50 nM) totally blocks CXCL12-induced calcium mobilization, with an IC50 of 17 nM. However, it shows no effect on the intracellular calcium fluxes elicited by the CCR5 ligands RANTES, LD78β and MIP-1β in U87.CD4.CCR5 cells. AMD 3465 also potently inhibits the replication of X4 HIV strains (IC50: 1-10 nM), but has no effect on CCR5-using (R5) viruses. The IC50 for suppression of the HIV-2 strains ROD and EHO is 12.3 nM[1].

AMD 3465, administered subcutaneously at a dosage of 2.5 mg/kg/day for five weeks, significantly inhibits the growth of U87 glioblastoma multiforme (GBM) and Daoy xenograft tumors.