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4-IPP

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Chemical Structure| 41270-96-6 同义名 : 4-Iodo-6-phenylpyrimidine
CAS号 : 41270-96-6
货号 : A888571
分子式 : C10H7IN2
纯度 : 99%+
分子量 : 282.08
MDL号 : MFCD00234609
存储条件：

粉末 Keep in dark place,Inert atmosphere,Store in freezer, under -20°C

液体 -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 105 mg/mL(372.23 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
动物实验配方：
生物活性
描述 Migration inhibitory factor (MIF) is a pleiotropic inflammatory mediator that inhibits macrophage migration in innate and adaptive immunologic responses. 4-IPP is an irreversible MIF inhibitor that binds covalently to MIF to inhibit its activity. It inhibited the viability of bone marrow macrophages (BMMs) with an IC50 value of 104.3µM at 72h. 4-IPP at 5-20µM suppressed the formation of TRAP-positive multinucleated osteoclasts in a dose-dependent manner. 4-IPP treatment at a dose of 20µM also significantly downregulated the expression of genes involved in BMM precursor fusion (i.e. DC-STAMP), osteoclast maturation (i.e. c-Fos and NFATc1), and bone resorption (i.e. TRAP and CTSK) in BMM-derived osteoclasts. Osteoclasts-treated with 20µM 4-IPP resorbed 3.73±1.24% of the bone discs, whereas the untreated cells resorbed >40% of the total bone area. Incubation of BMMs with 20µM 4-IPP inhibited RANKL-induced NF-κB activation, resulting in the suppression of NFATc1 induction. Treatment with 20µM 4-IPP for 5 days suppressed the formation of TRAP-positive multinucleated osteoclasts in BMMs extracted from wild-type mice but not MIF knockout BMMs. Subcutaneous injection of 4-IPP at a dose of 1 or 5mg/kg every 2 days for 2 weeks reduced the extent of Ti particle-induced bone destruction in mice. Administration of 4-IPP at 1 or 5mg/kg also alleviated the bone loss associated with estrogen deficiency in a mouse model of ovariectomy-induced osteoporosis[1].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

3.55mL

0.71mL

0.35mL

17.73mL

3.55mL

1.77mL

35.45mL

7.09mL

3.55mL
参考文献

[1]Zheng L, Gao J, Jin K, et al. Macrophage migration inhibitory factor (MIF) inhibitor 4-IPP suppresses osteoclast formation and promotes osteoblast differentiation through the inhibition of the NF-κB signaling pathway. FASEB J. 2019;33(6):7667-7683. doi:10.1096/fj.201802364RR