CAS |
155148-31-5 |
Chinese Name |
盐酸普瑞克沙因 |
English Name |
Plerixafor 8Hydrochloride |
Synonyms |
AMD3100辛基盐酸盐 |
Molecular Formula |
C28H54N8·8HCl |
Molecular Weight |
794.47 |
Solubility |
Soluble in Water ≥5mg/mL |
Purity |
≥98% |
Appearance |
White to yellow Solid |
Storage |
Powder:-20℃,2 years;Insolvent(Mother Liquid):-20℃,6 months;-80℃,1 year |
EC |
EINECS 828-184-5 |
MDL |
MFCD04974488 |
SMILES |
[H]Cl.[H]Cl.[H]Cl.[H]Cl.[H]Cl.[H]Cl.[H]Cl.[H]Cl.N1(CCCNCCNCCCNCC1)CC2=CC=C(C=C2)CN3CCCNCCNCCCNCC3 |
InChIKey |
UEUPDYPUTTUXLJ-UHFFFAOYSA-N |
InChI |
InChI=1S/C28H54N8.8ClH/c1-9-29-15-17-31-13-3-21-35(23-19-33-11-1)25-27-5-7-28(8-6-27)26-36-22-4-14-32-18-16-30-10-2-12-34-20-24-36;;;;;;;;/h5-8,29-34H,1-4,9-26H2;8*1H |
PubChem CID |
65014 |
Target Point |
CXCR |
Passage |
Immunology & Inflammation;GPCR & G Protein |
Background |
Plerixafor 8Hydrochloride is a selective CXCR4 antagonist. |
Biological Activity |
Plerixafor octahydrochloride是一种选择性的 CXCR4 拮抗剂, IC50 为 44 nM。[1-4] |
In Vitro |
CXCR4抑制剂Plerixafor(AMD3100)是CXCL12介导的趋化性(IC50,5.7 nM)的有效抑制剂,其效力略好于其对CXCR4的亲和力。用CCX771或CXCL11处理细胞对CXCL12介导的MOLT-4或U937 TEM没有影响。相比之下,10μMPlerixafor抑制两种细胞系中CXCL12介导的TEM [1]。与CXCL12刺激的细胞相比,Plerixafor(10μM)处理的细胞显示出细胞增殖的适度减少,这些细胞没有达到统计学意义[2]。 |
In Vivo |
向UUO小鼠施用Plerixafor(2mg / kg)会加重肾间质T细胞浸润,导致促炎细胞因子IL-6和IFN-γ的产生增加,并且抗炎细胞因子IL-10的表达降低[3]。 。血管周围和间质纤维化在8周时被CXCR4拮抗剂Plerixafor(AMD3100)显著降低[4]。 LD50,小鼠,SC:16.3mg / kg; LD50,大鼠,SC:> 50mg / kg; LD50,小鼠和大鼠,IV注射:5.2mg / kg。 |
Cell Experiment |
将U87MG细胞以200μL/孔的密度接种于96孔板中,密度为6×103细胞,并用CXCL12,Plerixafor或肽R处理,如先前“处理”部分所述。在最后2小时的治疗期间的每个时间点(24,48,72小时)加入MTT(5μg/ mL)。除去细胞培养基后,加入100μLDMSO,用LT-4000MS微孔板读数仪在595nm处测量光密度。通过三次独立实验一式三份进行测量[2]。 |
Animal Experiment |
小鼠[3]使用雄性C57bl / 6小鼠(6-7周龄,体重20g)。这些动物适应住房环境,即SPF,温度为22°C,12h / 12h光照/黑暗周期持续一周。然后,将它们随机分成以下实验组,每组8只小鼠:正常(无特异性干预),UUO + AMD3100(小鼠接受UUO手术和2mg / kg AMD3100)和UUO + PBS(小鼠接受UUO手术)和相同体积的PBS)。每天通过腹膜内注射给予AMD3100和PBS直至处死。大鼠[4]将CXCR4拮抗剂AMD3100溶解于H2O中,以2mg / kg /天的剂量在2型糖尿病沙鼠模型中递送,持续8周。在补充研究中,检查了CXCR4拮抗作用(AMD3100 6mg / kg / d)对调节性T细胞数量的影响。对于这些研究,AMD3100或车辆通过微型泵输送一周。 |
Data Literature Source |
[1]. Zabel BA,et al. Elucidation of CXCR7-mediated signaling events and inhibition of CXCR4-mediated tumor cell transendothelial migration by CXCR7 ligands. J Immunol. 2009 Sep 1;183(5):3204-11. [2]. Mercurio L,et al. Targeting CXCR4 by a selective peptide antagonist modulates tumor microenvironment and microglia reactivity in a human glioblastoma model. J Exp Clin Cancer Res. 2016 Mar 25;35:55. [3]. Yang J,et al. Continuous AMD3100 Treatment Worsens Renal Fibrosis through Regulation of Bone Marrow Derived Pro-Angiogenic Cells Homing and T-Cell-Related Inflammation. PLoS One. 2016 Feb 22;11(2):e0149926. [4]. Chu PY,et al. CXCR4 Antagonism Attenuates the Development of Diabetic Cardiac Fibrosis. PLoS One. 2015 Jul 27;10(7):e0133616 |
Unit |
Bottle |
Specification |
5mg 10mg |