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AZD8797

  Cat. No.:  DC10202   Featured
Chemical Structure
911715-90-7
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More than 5000 active chemicals with high quality for research!
Field of application
AZD8797 is an allosteric non-competitive modulator of the human CX3CR1 receptor; antagonizes CX3CL1 with IC50 values of 6 and 300 nM in B-lymphocyte cell line and human whole blood, respectively.
Cas No.: 911715-90-7
Chemical Name: AZD8797
Synonyms: 1-Pentanol, 2-[[2-amino-5-[[(1s)-1-phenylethyl]thio]thiazolo[4,5-d]pyrimidin-7-yl]amino]-4-methyl-, (2r)-;AZD 8797;AZD-8797;AZD8797;2(R)-[2-Amino-5-(1(S)-phenyl-ethylsulfanyl)-thiazolo[4,5-d]pyrimidin-7-ylamino]-4-methyl-pentan-1-ol;CX3CR1 antagonist 18a;BCP25433;BDBM50432452;J3.660.752A;(2R)-2-[[2-amino-5-[(1S)-1-phenylethyl]sulfanyl-[1,3]thiazolo[4,5-d]pyrimidin-7-yl]amino]-4-methylpentan-1-;(2R)-2-[[2-Amino-5-[[(1S)-1-phenylethyl]thio]thiazolo[4,5-d]pyrimidin-7-yl]amino]-4-methyl-1-pentanol (ACI)
SMILES: N(C1N=C(S[C@H](C2C=CC=CC=2)C)N=C2N=C(SC=12)N)[C@@H](CO)CC(C)C
Formula: C19H25N5Os2
M.Wt: 403.564700841904
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: In a flow adhesion assay, AZD8797 antagonizes the natural ligand, fractalkine (CX3CL1), in both human whole blood (hWB) and in a B-lymphocyte cell line with IC50 values of 300 and 6 nM respectively. AZD8797 also prevents G-protein activation in a [35S]GTPγS accumulation assay. AZD8797 positively modulates the CX3CL1 response at sub-micromolar concentrations in a β-arrestin recruitment assay. In equilibrium saturation binding experiments, AZD8797 reduces the maximal binding of 125I-CX3CL1 without affecting Kd. AZD8797 binds selectively with high affinity to human and rat CX3CR1 (Ki of hCX3CR1, 4 nM; Ki of rCX3CR1, 7 nM, respectively). The equilibrium dissociation constant, KB, demonstrates that AZD8797 is a very potent inhibitor for human CX3CR1 (10 nM). The potency is threefold lower for rat CX3CR1 (29 nM) and decreases even further at mouse CX3CR1 (54 nM).AZD8797 treatment in Dark Agouti rats with myelin oligodendrocyte glycoprotein-induced EAE results in reduced paralysis, CNS pathology, and incidence of relapses. The compound is effective when starting treatment before onset, as well as after the acute phase.
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