AMD 3465 hexahydrobromide, CXCR4 antagonist
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(5 Publications)
MW 410.6 Da, Purity >97%. Potent and selective CXCR4 antagonist. Shows 8-fold greater affinity than AMD 3100 (ab120718). Potent HIV entry inhibitor (IC50 = ~10 nM). Additionally mobilizes stem cells in vivo.
View Alternative Names
C-X-C chemokine receptor type 4, CD184, CD184 antigen, CXCR4_HUMAN, Chemokine (C X C motif) receptor 4, Chemokine CXC Motif Receptor 4, D2S201E, FB22, Fusin, HM89, HSY3RR, LCR1, LESTR, Leukocyte-derived seven transmembrane domain receptor, Lipopolysaccharide associated protein 3, NPY3R, NPYR, NPYRL, NPYY3, NPYY3R, Neuropeptide Y receptor Y3, Probable G protein coupled receptor lcr1 homolog, SDF-1 receptor, SEVEN-TRANSMEMBRANE-SEGMENT RECEPTOR, Stromal cell-derived factor 1 receptor, WHIM, WHIMS
- Chemical Structure
Lab
Chemical Structure - AMD 3465 hexahydrobromide, CXCR4 antagonist (AB120809)
2D chemical structure image of ab120809, AMD 3465 hexahydrobromide, CXCR4 antagonist
Properties and storage information
Shipped at conditions
Appropriate short-term storage conditions
Appropriate long-term storage conditions
Storage information
Supplementary information
This supplementary information is collated from multiple sources and compiled automatically.
Biological function summary
CXCR4 plays an important role in the immune system hematopoiesis and angiogenesis. It does not function alone and is often part of a larger protein complex where it recruits and activates other G proteins. The receptor mediates chemotactic responses directing cells to sites of inflammation or injury. Its interaction with CXCL12 is critical for maintaining immune surveillance aiding in the movement and positioning of immune cells.
Pathways
CXCR4 integrates into significant cellular signaling pathways such as the PI3K/AKT pathway and the MAPK pathway. It collaborates closely with signaling proteins like AKT1 and MAPK1 impacting cell survival and growth. These pathways are essential for various cellular functions including cell cycle progression and apoptosis regulation. The cross-talk between CXCR4 and these pathways underlines its influence on cell fate decisions.
Publications (5)
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Frontiers in physiology 15:1349119 PubMed38370015
2024
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Oncotarget 8:2261-2274 PubMed27903985
2016
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Biochemical pharmacology 78:993-1000 PubMed19540208
2009
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The American journal of pathology 169:424-32 PubMed16877345
2006
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Biochemical pharmacology 70:752-61 PubMed16011832
2005
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Product promise
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