| Chemical Properties | Back Directory | [Boiling point ]
1608.4±65.0 °C(Predicted) | [density ]
1.223±0.06 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
Soluble in DMSO | [form ]
Solid | [pka]
4.43±0.10(Predicted) | [color ]
White to off-white | [Water Solubility ]
Soluble to 1 mg/ml in water | [Sequence]
Ac-Glu-Leu-Lys-Val-Leu-Met-Glu-Lys-Glu-Leu-NH2 |
| Hazard Information | Back Directory | [Uses]
RAGE antagonist peptide is an advanced glycation end products (RAGE) antagonist. RAGE antagonist peptide prevents RAGE from binding with several of its most important ligands, including HMGB-1, S100P, and S100A4. RAGE antagonist peptide (RAP) possesses anti-tumor and anti-inflammatory activities[1][2]. | [in vivo]
RAGE antagonist peptide (RAP, 100 μg) inhibits RAGE-mediated Basal NFκB Activity in PDAC cells in vivo[1].
RAGE antagonist peptide (RAP) reduces the growth and metastasis of pancreatic tumors and also inhibited glioma tumor growth[1].
In mice bearing asthma, RAGE antagonist peptide (RAP; 4 mg/kg; i.p.) blunts airway reactivity, airway inflammation and goblet cell metaplasia, and decreases release of Th2 cytokines. RAGE antagonist peptide also reduces total, cytoplasmic and nuclear levels of β-catenin, enhanced 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]. | Animal Model: | Cancer cells expressing the NFκB-luc reporter implanted into immune-deficient mice[1]. | | Dosage: | 100 μg. | | Administration: | Intratumoral delivery (or intraperitoneally). | | Result: | Systemic administration caused a substantial reduction (p<0.05) in the NFκB signal 5 h after injection. |
| [storage]
Store at -20°C | [References]
[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. DOI:10.1158/1078-0432.CCR-12-0221
[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. DOI:10.1111/bph.13539 |
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