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Medchemexpress/Plerixafor(Synonyms: AMD3100; JM3100)/HY-10046/50mg
Description |
Plerixafor is a selective CXCR4 antagonist with IC50 of 44 nM. |
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IC50 & Target |
IC50: 44 nM (CXCR4)[1] |
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[1]. Plerixafor (10 μM)-treated cells show a moderate reduction in cell proliferation compared to CXCL12-stimulated cells, which do not reach statistical significance[2]. |
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[3]. Both perivascular and interstitial fibrosis are significantly reduced by the CXCR4 antagonist, Plerixafor (AMD3100) at 8 weeks[4]. LD50, mouse, SC: 16.3 mg/kg; LD50, rat, SC: >50 mg/kg; LD50, mouse and rat, IV injection: 5.2 mg/kg. |
Clinical Trial |
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References |
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Cell Assay
[2] |
Plerixafor is dissolved in DMSO and then diluted with appropriate medium[2]. U87MG 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]. MCE has not independently confirmed the accuracy of these methods. They are for reference only. |
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Animal Administration
[3][4] |
Plerixafor is prepared in PBS (Mice)[3]. Mice[3] |
References |
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Molecular Weight |
502.78 |
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Formula |
C₂₈H₅₄N₈ |
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CAS No. |
110078-46-1 |
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Storage |
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Shipping | Room temperature in continental US; may vary elsewhere |
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Solvent & Solubility |
Ethanol Plerixafor (AMD3100) is prepared in vehicle (normal saline)[5]. * "<1 mg/ml"="" means="" slightly="" soluble="" or="" insoluble.="" "≥"="" means="" soluble,="" but="" saturation="">1> |
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References |
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Purity: >98.0%
COA (92 KB) HNMR (209 KB)
Handling Instructions (1252 KB)-
[1]. Zabel BA, et al. Elucidation of CXCR7-mediated signaling events and inhibition of CXCR4-mediated tumor cell transendothelial migration by CXCR7 ligands. J Immunol. 2009 Sep 1;183(5):3204-11.
[2]. Mercurio L, et al. Targeting CXCR4 by a selective peptide antagonist modulates tumor microenvironment and microglia reactivity in a human glioblastoma model. J Exp Clin Cancer Res. 2016 Mar 25;35:55.
[3]. Yang J, et al. Continuous AMD3100 Treatment Worsens Renal Fibrosis through Regulation of Bone Marrow Derived Pro-Angiogenic Cells Homing and T-Cell-Related Inflammation. PLoS One. 2016 Feb 22;11(2):e0149926.
[4]. Chu PY, et al. CXCR4 Antagonism Attenuates the Development of Diabetic Cardiac Fibrosis. PLoS One. 2015 Jul 27;10(7):e0133616.
[5]. He G, et al. SDF-1 in Mammary Fibroblasts of Bovine with Mastitis Induces EMT and Inflammatory Response of Epithelial Cells. Int J Biol Sci. 2017 May 5;13(5):604-614.