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Plerixafor is a bicyclam molecule that antagonizes the binding of the chemokine stromal cell-derived factor-1 (SDF-1) to its cognate receptor CXCR4. The CXCR4 alpha-chemokine receptor and one of its ligands, SDF-1, are important in hematopoietic stem cell homing to the bone marrow and in hematopoietic stem cell quiescence. CXCR-4 antagonist Plerixafor is one of the most efficient bone marrow stem cell mobilizers. Plerixafor inhibits SDF-1 mediated GTP-binding, SDF-1 mediated calcium flux and SDF-1 stimulated chemotaxis with IC50 of 27 nM, 572 nM and 51 nM, respectively. Plerixafor results in the rapid and reversible mobilization of hematopoietic stem cells into the peripheral circulation and is synergistic when combined with G-CSF.
J Nanobiotechnology. 2024 May 3;22(1):219.
Migrasomes from adipose derived stem cells enrich CXCL12 to recruit stem cells via CXCR4/RhoA for a positive feedback loop mediating soft tissue regeneration
Plerixafor (AMD3100) purchased from AbMole
Biomaterials. 2023 Oct 17.
The genetic background determines material-induced bone formation through the macrophage-osteoclast axis
Plerixafor (AMD3100) purchased from AbMole
Plast Reconstr Surg. 2023 Jan 9.
Early angiogenesis dependent CXCL12 attracts Adipose-derived stem cells to promote the repair of fat grafting in a mice model
Plerixafor (AMD3100) purchased from AbMole
Front Pharmacol. 2022 Feb 1;792293.
Deletion of Wild-type p53 Facilitates Bone Metastatic Function by Blocking the AIP4 Mediated Ligand-Induced Degradation of CXCR4
Plerixafor (AMD3100) purchased from AbMole
. figure 4.jpg) |
Source | Tianjin Med J (2015). Figure 4. AMD3100 (Abmole Bioscience) |
| Method | Caspase-3 Assay | |
| Cell Lines | EPCs | |
| Concentrations | 25 μmol/L | |
| Incubation Time | 24、48、96 h | |
| Results | Compared with the control group, GLP-1 overexpression decreased Caspase-3 mRNA expression and Caspase-3 activity, both of which were significantly decreased after 48 h of GLP-1 treatment, and the most significant down-regulation trend was shown at 96 h (P<0.05). When the SDF-1/CXCR4 signaling pathway was blocked, the inhibitory effect of GLP-1 on Caspase-3 mRNA expression and Caspase-3 activity were significantly decreased (P <0.05). As shown in figure 4. |
. figure 3.jpg) |
Source | Tianjin Med J (2015). Figure 3. AMD3100 (Abmole Bioscience) |
| Method | MTT | |
| Cell Lines | EPCs | |
| Concentrations | 25 μmol/L | |
| Incubation Time | 24、48、96 h | |
| Results | Compared with the control group, GLP-1 overexpression significantly promoted cell proliferation (P<0.05). After blocking the SDF-1/CXCR4 signaling pathway with AMD3100 blocker, the proliferation effect of GLP-1 on EPCs was significantly decreased (P<0.05), as shown in Figure 3. |
. figure 2.jpg) |
Source | Tianjin Med J (2015). Figure 2. AMD3100 (Abmole Bioscience) |
| Method | qPCR | |
| Cell Lines | EPCs | |
| Concentrations | ||
| Incubation Time | 24、48、96 h | |
| Results | Compared with the control group, GLP-1 overexpression significantly increased the mRNA expressions of C/EBPα and PPARγ (P<0.05) in a time dependent manner. After the SDF-1/CXCR4 signaling pathway was blocked, GLP-1 significantly inhibited the mRNA expression of C/EBPα and PPARγ (P < 0.05), as shown in Figure 2. |
. figure 1.jpg) |
Source | Tianjin Med J (2015). Figure 1. AMD3100 (Abmole Bioscience) |
| Method | western blot | |
| Cell Lines | EPCs | |
| Concentrations | 0、5、15 and 25 μmol/L | |
| Incubation Time | 48h | |
| Results | Compared with the control group (0.465±0.085), CXCR4 protein expression was significantly decreased after treatment with different doses of AMD3100, and the effect of 25 μmol/L AMD3100 group (0.054±0.023) was the most significant (F=16.347, P < 0.05), see Figure 1. It was proved that 25 μmol/L AMD3100 had the best blocking effect and could be used for subsequent blocking experiments. |
| Cell Experiment | |
|---|---|
| Cell lines | OS cell lines (LM8 and Dunn) |
| Preparation method | MTT assay. The effects of CXCL12 and AMD3100 on the survival of two OS cell lines (LM8 and Dunn) were assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cells were seeded in 96-well plates at 2×10^3/well in DMEM-h. After overnight growth, the cells were cultured for 7 days in FBS-free medium in the presence of 0 or 100 ng/ml CXCL12, 30 μM AMD3100 alone or 100 ng/ml CXCL12 with 10, 20 or 30 μM AMD3100. The FBS-free cells without 100 ng/ml CXCL12 or AMD3100 served as the control group. After the 7 day incubation, 20 μl MTT (5 mg/ml) was added into each well and incubated for 4 h at 37°C. Culture medium was removed and 150 μl dimethylsulfoxide was added. The optical density (OD) was then measured using a model ELx800 microplate reader at 490 nm. The cell viability was calculated using the equation: Cell viability (%) = (OD490nm of treatment/OD490nm of control) ×100%. |
| Concentrations | 30 μM |
| Incubation time | 7 days |
| Animal Experiment | |
|---|---|
| Animal models | orthotopic animal model of OS in Ten 4-week-old female C3H mice |
| Formulation | PBS |
| Dosages | 5 mg/kg every 2 days |
| Administration | tail vein injection |
| Molecular Weight | 502.78 |
| Formula | C28H54N8 |
| CAS Number | 110078-46-1 |
| Solubility (25°C) | Ethanol 50 mg/mL Water < 1 mg/mL |
| Storage |
Powder -20°C 3 years ; 4°C 2 years In solvent -80°C 6 months ; -20°C 1 month |
| Related CXCR Products |
|---|
| WZ 811
WZ811 is a highly competitive CXCR4 antagonist with oral activity. WZ811 effectively inhibited CXCR4/SDF-1 (also known as CXCL12) -mediated regulation of cAMP level (EC50=1.2 nM) and SDF-1-induced matrix glue invasion (EC50=5.2 nM) in cells. |
| Navarixin
Navarixin (SCH 527123) is a novel, selective CXCR2 receptor antagonist with IC50 of 3 nM. Navarixin (SCH 527123) has Kd values of 41 nM for cynomolgus CXCR1 and 0.20 nM, 0.20 nM, 0.08 nM for mouse, rat and cynomolgus monkey CXCR2, respectivelly. |
| AMD3465 hexahydrobromide (AMD3465 )
AMD3465 hexahydrobromide（AMD3465 ) is an effective CXCR4 antagonist that inhibits 12G5 mAb in SupT1 cells. The IC50 values of CXCL12AF647 and CXCR4 were 0.75 nM and 18 nM, respectively. AMD 3465 also effectively inhibited X4 HIV replication (IC50, 1-10 nM), but not R5 HIV replication. |
| Plerixafor 8HCl
Plerixafor 8HCl (AMD3100 8HCl) is a chemokine receptor antagonist for CXCR4 and CXCL12-mediated chemotaxis with IC50 of 44 nM and 5.7 nM, respectively. |
| SB225002
SB225002 is a potent and selective non-peptide inhibitor of CXCR2 with IC50 of 22 nM and >150-fold selectivity over CXCR1 and four other 7-TMRs. |
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