Plerixafor octahydrochloride (JM3100 octahydrochloride) blocks the binding of stromal cell-derived factor (SDF-1alpha) to the cellular receptor CXCR4, resulting in hematopoietic stem cell (HSC) release from bone marrow and HSC movement into the peripheral circulation. Plerixafor is a bicyclam with hematopoietic stem cell-mobilizing activity.

CXCL12:5.7 nM, CXCR4:44 nM

AMD 3100 can inhibit the replication of low-passage clinical HIV-1 isolates (K31, D370, K6/-2, HEM, and JRCSF) in primary T4 lymphocytes (EC50s: 0.16-1.5 ng/ml; EC90s: 0.36-4.7 ng/ml). In primary monocytes, AMD 3100 was active against HIV-1 (K31 and SF-162) at EC50s of 0.28-7.2 ng/mL and EC90s of 0.68-12 ng/mL.

Serum drug levels in rabbits given AMD 3100 (10 mg/kg) by the subcutaneous route were determined by a bioassay based on the EC50 of the compound required to inhibit HIV-1 cytopathicity in MT-4 cells.

Plerixafor is dissolved in DMSO and then diluted with appropriate medium[2]. U87 mg cells are seeded in 96-well plates at the density of 6×103 cells in 200 μL/well and treated with CXCL12, Plerixafor or with peptide R, as described in the previous "Treatments" section. MTT (5 μg/mL) is added at each time point (24, 48, 72 h) during the final 2 h of treatment. After removing cell medium, 100 μL DMSO are added and optical densities measured at 595 nm with a LT-4000MS Microplate Reader. Measurements are made in triplicates from three independent experiments[2].