Plerixafor octahydrochloride

Research use only, not for human use.

Plerixafor?octahydrochloride (JM-3100, AMD-3100, SID-791) is a potent, selective CXCR4 inhibitor (IC50=44 nM) that inhibits the replication of various HIV-1 and HIV-2 strains in various cell lines with EC50 of 10ng/ml.

Plerixafor?octahydrochloride (JM-3100, AMD-3100, SID-791) is a potent, selective CXCR4 inhibitor (IC50=44 nM) that inhibits the replication of various HIV-1 and HIV-2 strains in various cell lines with EC50 of 10ng/ml; can produce mesenchymal stem cells and endothelial progenitor cells in mice in combination with VEGF; also is an allosteric agonist of CXCR7.Multiple Sclerosis Preclinical(In Vitro):The CXCR4 inhibitor Plerixafor (AMD3100) is a potent inhibitor of CXCL12-mediated chemotaxis (IC50, 5.7 nM) with a potency slightly better than its affinity for CXCR4. Treating the cells with CCX771 or CXCL11 has no effect on CXCL12-mediated MOLT-4 or U937 TEM. In contrast, 10 μM Plerixafor inhibits CXCL12-mediated TEM in both cells lines. Plerixafor (10 μM)-treated cells show a moderate reduction in cell proliferation compared to CXCL12-stimulated cells, which do not reach statistical significance. (In Vivo):Plerixafor (2 mg/kg) administration to UUO mice exacerbates renal interstitial T cell infiltration, resulting in increased production of the pro-inflammatory cytokines IL-6 and IFN-γ and decreased expression of the anti-inflammatory cytokine IL-10. Both perivascular and interstitial fibrosis are significantly reduced by the CXCR4 antagonist, Plerixafor (AMD3100) at 8 weeks. LD50, mouse, SC: 16.3 mg/kg; LD50, rat, SC: >50 mg/kg; LD50, mouse and rat, IV injection: 5.2 mg/kg.

The CXCR4 inhibitor Plerixafor (AMD3100) is a potent inhibitor of CXCL12-mediated chemotaxis (IC50, 5.7 nM) with a potency slightly better than its affinity for CXCR4. Treating the cells with CCX771 or CXCL11 has no effect on CXCL12-mediated MOLT-4 or U937 TEM. In contrast, 10 μM Plerixafor inhibits CXCL12-mediated TEM in both cells lines. Plerixafor (10 μM)-treated cells show a moderate reduction in cell proliferation compared to CXCL12-stimulated cells, which do not reach statistical significance.

Plerixafor (2 mg/kg) administration to UUO mice exacerbates renal interstitial T cell infiltration, resulting in increased production of the pro-inflammatory cytokines IL-6 and IFN-γ and decreased expression of the anti-inflammatory cytokine IL-10. Both perivascular and interstitial fibrosis are significantly reduced by the CXCR4 antagonist, Plerixafor (AMD3100) at 8 weeks. LD50, mouse, SC: 16.3 mg/kg; LD50, rat, SC: >50 mg/kg; LD50, mouse and rat, IV injection: 5.2 mg/kg.

AMD-3100 octahydrochloride | JM-3100 octahydrochloride | SID-791 octahydrochloride

GPCR/G Protein

Chemokine Receptor

CXCL12|CXCR4

Inflammation/Immunology

Multiple Sclerosis

155148-31-5

794.4695

C28H62Cl8N8

>98% (HPLC)

H2O: ≥ 42 mg/mL

C1CNCCNCCCN(CCNC1)CC2=CC=C(C=C2)CN3CCCNCCNCCCNCC3.Cl.Cl.Cl.Cl.Cl.Cl.Cl.Cl

1,4,8,11-Tetraazacyclotetradecane, 1,1'-[1,4-phenylenebis(methylene)]bis-, hydrochloride (1:8)

(-20℃)

With Ice Pack

≥ 2 years