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RAGE antagonist peptide TFA
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。
包装与价格:
包装价格(元)
1mg电议
5mg电议

产品介绍
RAGE antagonist peptide TFA 是一种晚期糖基化终产物 (RAGE) 拮抗剂。RAGE antagonist peptide TFA 可阻断 RAGE 和几个重要配体 HMGB-1,S100P,S100A4 的结合。RAGE antagonist peptide TFA 具有抗肿瘤和抗炎活性。
分子式C59H102F3N13O19S
分子量1386.58
溶解度Water : 25 mg/mL (18.03 mM; Need ultrasonic)
储存条件-20°C, away from moisture
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

RAGE antagonist peptide TFA is an advanced glycation end products (RAGE) antagonist. RAGE antagonist peptide TFA prevents RAGE from binding with several of its most important ligands, including HMGB-1, S100P, and S100A4. RAGE antagonist peptide TFA possesses anti-tumor and anti-inflammatory activities[1][2].

RAGE antagonist peptide TFA (RAP) reduces the ability of the ligands to stimulate RAGE activation of NFκB in cancer cells in vitro[1].

RAGE antagonist peptide TFA (RAP, 100 µg) inhibits RAGE-mediated Basal NFκB Activity in PDAC cells in vivo[1].RAGE antagonist peptide TFA (RAP) reduces the growth and metastasis of pancreatic tumors and also inhibited glioma tumor growth[1].In mice bearing asthma, RAGE antagonist peptide TFA (RAP; 4 mg/kg; i.p.) blunts airway reactivity, airway inflammation and goblet cell metaplasia, and decreases release of Th2 cytokines. RAGE antagonist peptide TFA also reduces total, cytoplasmic and nuclear levels of β-catenin, enhances β-catenin phosphorylation at Ser33/37/Thr41, which triggers ubiquitination, down-regulated expression of β-catenin targeted genes, and tends to keep β-catenin at the cytomembrane, shifting β-catenin from a signalling active pattern to an adhesive function[2].

[1]. Thiruvengadam Arumugam, et al. S100P-derived RAGE antagonistic peptide reduces tumor growth and metastasis. Clin Cancer Res. 2012 Aug 15;18(16):4356-64.
[2]. Lihong Yao, et al. The receptor for advanced glycation end products is required for β-catenin stabilization in a chemical-induced asthma model. Br J Pharmacol. 2016 Sep;173(17):2600-13.