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ATI 2341 trifluoroacetate salt, N-(1-Ohexadecyl)-L-methionylglycyl-L-tyrosyl-L-glutaminyl-L-lysyl-L-lysyl-L-leucyl-L-arginyl-L-seryl-L-methionyl-L-threonyl-L-α-aspartyl-L-lysyl-L-tyrosyl-L-arginyl- L-leucine, Pal-MGYQKKLRSMTDKYRL, Pal-Met-Gly-Tyr-Gln-Lys-Lys-Leu-Arg-Ser-Met-Thr-Asp-Lys-Tyr-Arg-Leu
C104H178N26O25S2 · xC2HF3O2
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Biochem/physiol Actions
ATI-2341 is a potent and selective allosteric agonist of chemokine CXC-type receptor 4 (CXCR4) that functions as a biased ligand, favoring Gαi activation over Gα13. ATI-2341 does not promote β-arrestin recruitment. ATI-2341 promotes the mobilization of PMNs and HSPCs in the peripheral circulation of both mice and monkeys.
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
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Proceedings of the National Academy of Sciences of the United States of America, 110(52), E5088-E5097 (2013-12-07)
Short lipidated peptide sequences derived from various intracellular loop regions of G protein-coupled receptors (GPCRs) are named pepducins and act as allosteric modulators of a number of GPCRs. Recently, a pepducin selectively targeting the C-X-C chemokine receptor type 4 (CXCR4)
Journal of molecular graphics & modelling, 60, 1-14 (2015-06-17)
Several examples of allosteric modulators of GPCRs have been reported recently in the literature, but understanding their molecular mechanism presents a new challenge for medicinal chemistry. For the specific case of the cellular receptor CXCR4, it is known that pepducins
Proceedings of the National Academy of Sciences of the United States of America, 107(51), 22255-22259 (2010-12-09)
The G protein-coupled receptor (GPCR), chemokine CXC-type receptor 4 (CXCR4), and its ligand, CXCL12, mediate the retention of polymorphonuclear neutrophils (PMNs) and hematopoietic stem and progenitor cells (HSPCs) in the bone marrow. Agents that disrupt CXCL12-mediated chemoattraction of CXCR4-expressing cells
Nature communications, 10(1), 5784-5784 (2019-12-21)
G-protein coupled receptors (GPCRs) are versatile cellular sensors for chemical stimuli, but also serve as mechanosensors involved in various (patho)physiological settings like vascular regulation, cardiac hypertrophy and preeclampsia. However, the molecular mechanisms underlying mechanically induced GPCR activation have remained elusive.
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