JMS-17-2
产品说明书
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同义名 : | - |
| CAS号 : | 1380392-05-1 | |
| 货号 : | A278381 | |
| 分子式 : | C25H26ClN3O | |
| 纯度 : | 97% | |
| 分子量 : | 419.946 | |
| MDL号 : | MFCD30489012 | |
| 存储条件： |
Pure form Sealed in dry,Room Temperature In solvent -20°C:3-6个月-80°C:12个月 |
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| 溶解度 : |
DMSO: 25 mg/mL(59.53 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO |
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| 动物实验配方： |
| 生物活性 | |||
|---|---|---|---|
| 描述 | One signaling pathway through which neurons and microglia communicate is the neuronal cytokine CX3CL1 (fractalkine) and its microglial receptor (CX3CR1). CX3CL1 is expressed by neurons either as a membrane-bound or a secreted ligand. The binding of CX3CL1 to CX3CR1 maintains microglia in an “off” state, thereby inhibiting the release of pro-inflammatory cytokines. In contrast, deficiency of CX3CL1 or CX3CR1 leads to an increased production of pro-inflammatory molecules[1]. JMS-17-2 is a potent and selective CX3CR1 antagonist with an IC50 value of 0.32 nM. The favorable potency shown by JMS-17-2 is combined with significant selectivity for CX3CR1 over other chemokine receptors, such as CXCR2 and CXCR1[2]. Interestingly, the two concentrations of JMS-17-2 most effective in blocking FKN-induced ERK phosphorylation also significantly reduced the migration of breast cancer cells in vitro[2]. Pharmacokinetic evaluation of JMS-17-2 administered to mice at a dose of 10 mg/kg (i.p.) produced drug levels of 89 ng/mL (210 nM) in blood measured one hour after dosing, which corresponds to a 20-fold increase over the lowest fully effective dose of this compound in vitro[2]. JMS-17-2 (10 mg/kg; administered i.p.; twice a day for three weeks) caused a dramatic reduction of tumors in both skeleton and visceral organs in SCID mice with MDA-231 xenograft[2]. | ||
| 实验方案 | |||
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| 1mg | 5mg | 10mg | |
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1 mM 5 mM 10 mM |
2.38mL 0.48mL 0.24mL |
11.91mL 2.38mL 1.19mL |
23.81mL 4.76mL 2.38mL |
| 参考文献 |
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