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IdentificationBack Directory
[MDL Number]

MFCD30742957
Chemical PropertiesBack 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 InformationBack 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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