Plerixafor (AMD3100)

製品コードS8030 バッチS803003

印刷

化学情報

Synonyms

JM 3100, SID791

Storage
(From the date of receipt)

3 years -20°C powder
1 years -80°C in solvent

化学式

C₂₈H₅₄N₈

分子量

502.78

CAS No.

110078-46-1

Solubility (25°C)*

体外

Ethanol

100 mg/mL (198.89 mM)

DMSO

Insoluble

Water

Insoluble

体内（毎回新しく調製した物を用意してください）

Clear solution

5%absolute ethyl alcohol 1 40% PEG 300 2 5%Tween80 3 50%ddH2O

この製剤はselleckのラボで検証済みです。上記の溶解方法がご要望を満たさない場合、selleckの営業担当までお問い合わせ頂ければ、個別の試験を行います。

1.100mg/ml (2.19mM)

Taking the 1 mL working solution as an example, add 50 μL of 22 mg/ml absolute ethyl alcohol stock solution to 400 μL of PEG300, mix evenly to clarify it; add 50 μL of Tween80 to the above system, mix evenly to clarify; then continue to add 500 μL of ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results.

* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

溶剤液（一定の濃度）を調合する

生物活性

製品説明	Plerixafor (AMD3100, JM 3100, SID791) is a chemokine receptor antagonist for CXCR4 and CXCL12-mediated chemotaxis with IC50 of 44 nM and 5.7 nM in cell-free assays, respectively. Plerixafor inhibits human immunodeficiency virus (HIV) replication.
in vitro	Plerixafor (AMD3100) inhibits CXCL12-mediated chemotaxis with a potency lightly better than its affinity for CXCR4. ^[1] It also antagonizes SDF-1/CXCL12 ligand binding with an IC50 of 651 nM. This compound 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 does not inhibit calcium flux against cells expressing CXCR3, CCR1, CCR2b, CCR4, CCR5 or CCR7 when stimulated with their cognate ligands, nor does it inhibit receptor binding of LTB4. On its own, it does not induce a calcium flux in the CCRF–CEM cells, which express multiple GPCRs including CXCR4, CCR4 and CCR7. ^[2]
in vivo	In diabetic mice, a single topical application of Plerixafor (AMD3100) promotes wound healing by increasing cytokine production, mobilizing bone marrow EPCs, and enhancing the activity of fibroblasts and monocytes/macrophages, thereby increasing both angiogenesis and vasculogenesis. ^[3] Cohorts of mice are administered with PBS, IGF1, PDGF, SCF, or VEGF for five consecutive days and this compound on the 5th day. The number and size of the colonies are highest in IGF1 plus it injected mice compared to PDGF, SCF and VEGF treated groups, in combination with Plerixafor. ^[4]

製品説明

Plerixafor (AMD3100, JM 3100, SID791) is a chemokine receptor antagonist for CXCR4 and CXCL12-mediated chemotaxis with IC50 of 44 nM and 5.7 nM in cell-free assays, respectively. Plerixafor inhibits human immunodeficiency virus (HIV) replication.

in vitro

Plerixafor (AMD3100) inhibits CXCL12-mediated chemotaxis with a potency lightly better than its affinity for CXCR4. ^[1]

It also antagonizes SDF-1/CXCL12 ligand binding with an IC50 of 651 nM. This compound 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 does not inhibit calcium flux against cells expressing CXCR3, CCR1, CCR2b, CCR4, CCR5 or CCR7 when stimulated with their cognate ligands, nor does it inhibit receptor binding of LTB4. On its own, it does not induce a calcium flux in the CCRF–CEM cells, which express multiple GPCRs including CXCR4, CCR4 and CCR7. ^[2]

in vivo

In diabetic mice, a single topical application of Plerixafor (AMD3100) promotes wound healing by increasing cytokine production, mobilizing bone marrow EPCs, and enhancing the activity of fibroblasts and monocytes/macrophages, thereby increasing both angiogenesis and vasculogenesis. ^[3]

Cohorts of mice are administered with PBS, IGF1, PDGF, SCF, or VEGF for five consecutive days and this compound on the 5th day. The number and size of the colonies are highest in IGF1 plus it injected mice compared to PDGF, SCF and VEGF treated groups, in combination with Plerixafor. ^[4]

プロトコル(参考用のみ)

キナーゼアッセイ	Receptor binding assays
キナーゼアッセイ	For the competition binding studies against CXCR4, a concentration range of Plerixafor (AMD3100) is incubated for 3 hours at 4 °C in binding buffer (PBS containing 5 mM MgCl₂, 1 mM Ca Cl₂, 0.25% BSA, pH 7.4) with 5 × 10⁵ CCRF–CEM cells and 100 pM ¹²⁵I-SDF-1α (2200 Ci/mmol) in Milipore Durapore^TM filter plates. Unbound ¹²⁵I-SDF-1α is removed by washing with cold 50 mM HEPES, 0.5 M NaCl pH 7.4. The competition binding assay against BLT1 is performed on membranes from CHO-S cells expressing recombinant BLT1. The membranes are prepared by mechanical cell lysis followed by high speed centrifugation, re-suspended in 50 mm HEPES, 5 mM MgCl₂ buffer and flash frozen. This compound is incubated with the membrane preparation for 1 hour at room temperature in an assay mixture containing 50 mM Tris, pH 7.4, 10 mM MgCl₂, 10 mM CaCl₂, 4 nM LTB₄ mixed with 1 nM ³H-LTB₄ (195.0 Ci/mmol) and 8 μg membrane. The unbound ³H-LTB₄ is separated by filtration on Millipore Type GF-C filter plates.
細胞アッセイ	細胞株	Cell-free assays
	濃度	44 and 5.7 nM for CXCR4 and CXCL12
	反応時間
	実験の流れ
動物実験	動物モデル	Twelve-week-old C57BL/6 mice with segmental bone defect
	投薬量	5 mg/kg
	投与方法	Administered via i.p.

参考

https://pubmed.ncbi.nlm.nih.gov/19641136/
https://pubmed.ncbi.nlm.nih.gov/16815309/
https://pubmed.ncbi.nlm.nih.gov/22048734/

https://pubmed.ncbi.nlm.nih.gov/22342795/

+ 展开

カスタマーフィードバック

: Data from [Data independently produced by Blood, 2014, 123(21), 3296-304]

: Data from [Data independently produced by , , J Clin Invest, 2015, 125(8): 3226-40]

: Data from [Data independently produced by , , Angiogenesis, 2016, 19(3):359-71]

Selleckの高級品が、幾つかの出版された研究調査結果（以下を含む）で使われた：

Endothelial cell-derived SDF-1α elicits stemness traits of glioblastoma via dual-regulation of GLI1 [ Theranostics, 2025, 15(18):9819-9837]	PubMed: 41041071
CXCL12/CXCR4 modulates macrophage efferocytosis to induce glomerular crescent formation and fibrosis via ELMO1/DOCK180/RAC1 signaling in ANCA-associated glomerulonephritis [ Cell Mol Life Sci, 2025, 82(1):280]	PubMed: 40682610
Exosomal Galectin-3 promotes peritoneal metastases in gastric adenocarcinoma via microenvironment alterations [ iScience, 2025, 28(1):111564]	PubMed: 39811647
Physical and functional interactions between LDLR family members and CXCR4 in breast cancer [ FEBS J, 2025, NONE]	PubMed: 40022442
Anti-Inflammatory Resveratrol Protects Mice From Early Mortality After Haematopoietic Stem Cell Transplantation [ J Cell Mol Med, 2025, 29(3):e70395]	PubMed: 39900564
Transcriptional signature of rapidly responding NK cells reveals S1P5 and CXCR4 as anti-tumor response disruptors [ Sci Rep, 2025, 15(1):10769]	PubMed: 40155684
Investigating the mechanism of Gentiopicroside in rheumatoid arthritis through network pharmacology, molecular docking, and experimental validation [ Sci Rep, 2025, 15(1):19871]	PubMed: 40473698
BMP9 regulates the endothelial secretome to drive pulmonary hypertension [ bioRxiv, 2025, 2025.08.29.673113]	PubMed: 40950088
CXCR4-LASP1-G9a-SNAIL axis drives NEPC transdifferentiation via induction of EMT and downregulation of REST [ Cell Genom, 2025, S2666-979X(25)00172-7]	PubMed: 40499539
PAMD-Ch17, a Polymeric Analog of Plerixafor, Induces Mitochondrial Dysfunction in T-ALL Cells Independent of CXCR4 [ bioRxiv, 2025, 2025.05.28.656643]	PubMed: 40501752

長期の保管のために-20°Cの下で製品を保ってください。

人間や獣医の診断であるか治療的な使用のためにでない。

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