产品
编 号：F516441
分子式：C19H25N5OS2
分子量：403.56
分子式：C19H25N5OS2
分子量：403.56
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
1mg
询价
询价
5mg
询价
询价
10mg
询价
询价
25mg
询价
询价
结构图
CAS No: 911715-90-7
产品详情
生物活性：
AZD8797 (KAND567) is an allosteric non-competitive and orally active antagonist of the human CX3CR1 receptor; antagonizes CX3CR1 and CXCR2 with Kis of 3.9 and 2800 nM, respectively.
体内研究：
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.
体外研究：
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 (KAND567) is an allosteric non-competitive and orally active antagonist of the human CX3CR1 receptor; antagonizes CX3CR1 and CXCR2 with Kis of 3.9 and 2800 nM, respectively.
体内研究：
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.
体外研究：
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).
产品资料
Copyright©2015-2024 沪ICP备2022026524号-1
沪公网安备