Molecular Formula | C28H54N8 |
Molar Mass | 502.78 |
Melting Point | 188 - 193°C (dec.) |
Boling Point | 657.5℃ at 760mmHg |
Solubility | DMSO <1 mg/mL Water 100 mg/mL Ethanol <1 mg/mL |
Appearance | Form solid, color White |
Color | White |
Storage Condition | Sealed in dry,Store in freezer, under -20°C |
Stability | Stable for 1 year from date of purchase as supplied. Solutions in distilled water may be stored at -20°C for up to 2 months. |
Physical and Chemical Properties | Bioactive Plerixafor (AMD3100, JM 3100) 8HCl is a Plerixafor hydrochloride and a CXCR4 chemokine receptor antagonist that acts on CXCR4 and CXCL12 mediated chemotaxis with IC50 of 44 nM and 5.7 nM respectively. Plerixafor can be used as anti-HIV drugs. |
Use | Uses Proxafu hydrochloride is an immunostimulant used to mobilize hematopoietic stem cells in cancer patients. It is a hematopoietic stem cell (HSC) mobilization agent that inhibits the CXCR4 chemokine receptor and blocks the binding of its ligand, stromal cell-derived factor-1-α (SDF-1-α). |
In vitro study | Plerixafor 8HCl (amd31008hcl) inhibits cxcl12-mediated chemotaxis with slightly higher affinity than for CXCR4. Plerixafor 8HCl (AMD3100 8HCl) also inhibited SDF-1/CXCL12 ligand binding with an IC50 of 651 nM. Plerixafor 8HCl (AMD3100 8HCl) inhibited SDF-1 regulated GTP binding, SDF-1 regulated calcium flux, and SDF-1 regulated chemotaxis with IC50 of 27 nM, 572 nM, and 51 nM, respectively. Plerixafor acts on cells expressing CXCR3, CCR1, CCR2b, CCR4, CCR5 or CCR7 and does not inhibit calcium flux when stimulated by their cognate ligands. Plerixafor 8HCl (amd31008hcl) also did not inhibit the receptor binding of ltb4. Plerixafor 8HCl (AMD3100 8HCl) acts on CCRF-CEM cells that express a variety of GPCRs, including CXCR4,CCR4 and CCR7, without calcium flux. Plerixafor 8HCl (amd31008hcl) inhibits cxcl12-mediated chemotaxis with slightly higher affinity than for CXCR4. Plerixafor 8HCl (AMD3100 8HCl) also inhibited SDF-1/CXCL12 ligand binding with an IC50 of 651 nM. Plerixafor 8HCl (AMD3100 8HCl) inhibited SDF-1 regulated GTP binding, SDF-1 regulated calcium flux, and SDF-1 regulated chemotaxis with IC50 of 27 nM, 572 nM, and 51 nM, respectively. Plerixafor acts on cells expressing CXCR3, CCR1, CCR2b, CCR4, CCR5 or CCR7 and does not inhibit calcium flux when stimulated by their cognate ligands. Plerixafor 8HCl (amd31008hcl) also did not inhibit the receptor binding of ltb4. Plerixafor 8HCl (AMD3100 8HCl) acts on CCRF-CEM cells that express a variety of GPCRs, including CXCR4,CCR4 and CCR7, without calcium flux. |
In vivo study | Plerixafor is locally treated alone, by increasing cytokine production, mobilizing bone marrow EPCs, and enhancing the activity of fibroblasts and monocytes/macrophages, thereby increasing angiogenesis, and promote wound healing in diabetic mice. Plerixafor alone is locally treated to enhance angiogenesis by increasing cytokine production, mobilizing bone marrow EPCs, and enhancing fibroblast and monocyte/macrophage activity, and promote wound healing in diabetic mice. |
Safety Description | S22 - Do not breathe dust. S24/25 - Avoid contact with skin and eyes. |
WGK Germany | 3 |
Target
Target Value
CXCL12
(Cell-free assay) 5.7 nM
CXCR4
(Cell-free assay) 44 nM
in vitro studies
Plerixafor 8HCl (AMD3100 8HCl) inhibits the chemotaxis regulated by CXCL12, which is slightly higher than the affinity for CXCR4. Plerixafor 8HCl (AMD3100 8HCl) also inhibits SDF-1/CXCL12 ligand binding with an IC50 of 651 nM. Plerixafor 8HCl (AMD3100 8HCl) inhibits SDF-1-regulated GTP binding, SDF-1-regulated calcium flow, and SDF-1-regulated chemotaxis, IC50 is 27 nM, 572 nM, and 51 nM, respectively. Plerixafor act on cells expressing CXCR3, CCR1, CCR2b, CCR4, CCR5 or CCR7 and do not inhibit calcium flow when stimulated by their homologous ligands. Plerixafor 8HCl (AMD3100 8HCl) also did not inhibit receptor binding of LTB4. Plerixafor 8HCl (AMD3100 8HCl) acts on CCRF-CEM cells expressing a variety of GPCRs, including CXCR4,CCR4 and CCR7, without calcium flow.
In vivo studies
Plerixafor alone, local treatment can promote wound healing in diabetic mice by increasing cytokine production, mobilizing bone marrow EPCs, and enhancing the activity of fibroblasts and monocytes/macrophages, thus improving angiogenesis.
use | proxafu hydrochloride is an immunostimulant used to mobilize hematopoietic stem cells in cancer patients. It is a hematopoietic stem cell (HSC) mobilization agent that inhibits the CXCR4 chemokine receptor and blocks the binding of its ligand, stromal cell-derived factor-1-α (SDF-1-α). |
biological activity | Plerixafor 8HCl (AMD3100 8HCl) is a Plerixafor hydrochloride, a CXCR4 chemokine receptor antagonist, which acts on CXCR4 and CXCL12-regulated chemotaxis, IC50 is 44 nM and 5.7 nM respectively. Plerixafor (AMD3100, JM 3100) 8HCl is Plerixafor hydrochloride and CXCR4 chemokine receptor antagonist, which acts on CXCR4 and CXCL12 to mediate chemotaxis. IC50 is 44 nM and 5.7 nM respectively. Plerixafor can be used as anti-HIV drugs. |
In vitro study | Plerixafor 8HCl (AMD3100 8HCl) inhibits the chemotaxis regulated by CXCL12, which is slightly higher than the affinity for CXCR4. Plerixafor 8HCl (AMD3100 8HCl) also inhibits SDF-1/CXCL12 ligand binding with an IC50 of 651 nM. Plerixafor 8HCl (AMD3100 8HCl) inhibits SDF-1-regulated GTP binding, SDF-1-regulated calcium flow, and SDF-1-regulated chemotaxis, IC50 is 27 nM, 572 nM, and 51 nM, respectively. Plerixafor act on cells expressing CXCR3, CCR1, CCR2b, CCR4, CCR5 or CCR7 and do not inhibit calcium flow when stimulated by their homologous ligands. Plerixafor 8HCl (AMD3100 8HCl) also did not inhibit receptor binding of LTB4. Plerixafor 8HCl (AMD3100 8HCl) acts on CCRF-CEM cells expressing a variety of GPCRs, including CXCR4,CCR4 and CCR7, without calcium flow. Plerixafor 8HCl (AMD3100 8HCl) inhibits the chemotaxis regulated by CXCL12 and has slightly higher affinity than acting on CXCR4. Plerixafor 8HCl (AMD3100 8HCl) also inhibits SDF-1/CXCL12 ligand binding with an IC50 of 651 nM. Plerixafor 8HCl (AMD3100 8HCl) inhibits SDF-1-regulated GTP binding, SDF-1-regulated calcium flow, and SDF-1-regulated chemotaxis, IC50 is 27 nM, 572 nM, and 51 nM, respectively. Plerixafor act on cells expressing CXCR3, CCR1, CCR2b, CCR4, CCR5 or CCR7 and do not inhibit calcium flow when stimulated by their homologous ligands. Plerixafor 8HCl (AMD3100 8HCl) also did not inhibit receptor binding of LTB4. Plerixafor 8HCl (AMD3100 8HCl) acts on CCRF-CEM cells expressing a variety of GPCRs, including CXCR4,CCR4 and CCR7, without calcium flow. |
in vivo studies | Plerixafor separate local treatment, by increasing cytokine production, mobilizing bone marrow EPCs, and enhancing the activity of fibroblasts and monocytes/macrophages, thus improving angiogenesis and promoting wound healing in diabetic mice. Plerixafor alone, local treatment can improve angiogenesis and promote wound healing in diabetic mice by increasing cytokine production, mobilizing bone marrow EPCs, and enhancing the activity of fibroblasts and monocytes/macrophages. |
target | TargetValue CXCL12 (Cell-free assay) 5.7 nM CXCR4 (Cell-free assay) 44 nM |
Target | Value |
CXCL12 (Cell-free assay) | 5.7 nM |
CXCR4 (Cell-free assay) | 44 nM |