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Sophoridine
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Sophoridine图片
CAS NO:6882-68-4
包装与价格:
包装价格(元)
5mg电议
10mg电议
20mg电议

产品介绍
Sophoridine 是一种从豆科植物槐豆斜生植物的叶子中分离出来的喹喔啉生物碱。Sophoridine 诱导细胞凋亡 (apoptosis)。Sophoridine 有可能成为胰腺癌的有效,选择性和耐受性良好的候选药物。
Cas No.6882-68-4
别名槐定碱
Canonical SMILESO=C1CCC[C@]2([H])[C@@]3([H])CCCN4[C@@]3([H])[C@@](CCC4)([H])CN21
分子式C15H24N2O
分子量248.36
溶解度DMSO: 50 mg/mL (201.32 mM)
储存条件Store at -20°C
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

Sophoridine is a quinolizidine alkaloid isolated from leafs of Leguminous plant Sophora alopecuroides.L. Sophoridine induces apoptosis. Sophoridine has the potential to be a novel, potent and selective antitumor drug candidate for pancreatic cancer with well-tolerated toxicity[1].

Sophoridine (0-500 μM; 48 hours) exhibits remarkable inhibition effects to the growth of human pancreatic, gastric, liver, colon, gallbladder, and prostate carcinoma cells with IC50 values of about 20 μM to 200 μM[1].Sophoridine (0-20 μM; 48 hours) increases S phase cell population from 26.23% (control) to 38.67% in Miapaca-2 cells and from 29.56% (control) to 39.16% in PANC-1 cells, about a 1.5-fold and a 1.3-fold increase, respectively[1].Sophoridine (0-20 μM; 48 hours) significantly increases bad and bax levels, and decreases bcl-2 and bcl-xl levels in contrast, with a significant increase in Bax/Bcl-2 ratio[1]. Cell Viability Assay[1] Cell Line: Normal cells: IOSE144, HL-7702 and LO2, BEAS-2B, GES-1, HEK 293 T, HPDE, FHC, Human cancer cells: PANC-1, Mapaca-1, hepG2, SGC-7901, CBC-SD,SGC-996,PC-3,MKN-45,MGC-803,Hela and HCT116 cells

Sophoridine (intraperitoneal injection; 20 or 40 mg/kg; 21 days) can inhibit the growth of xenograft pancreatic tumors[1]. Animal Model: BALB/c homozygous (nu/nu) nude mice[1]

[1]. Xu Z, et al. Sophoridine induces apoptosis and S phase arrest via ROS-dependent JNK and ERK activation in human pancreatic cancer cells. J Exp Clin Cancer Res. 2017 Sep 11;36(1):124.