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].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

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].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

1386.58

C₅₉H₁₀₂F₃N₁₃O₁₉S

Ac-ELKVLMEKEL-NH2

Room temperature in continental US; may vary elsewhere.

Sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

H₂O : 25 mg/mL (18.03 mM; Need ultrasonic)

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

• [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.

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].

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

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

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].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

1272.56

C₅₇H₁₀₁N₁₃O₁₇S

1092460-91-7

Ac-ELKVLMEKEL-NH2

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [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.

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].

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

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

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].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

1272.56

C₅₇H₁₀₁N₁₃O₁₇S

1092460-91-7

Ac-ELKVLMEKEL-NH2

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [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.

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].

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

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

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].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

1272.56

C₅₇H₁₀₁N₁₃O₁₇S

1092460-91-7

Ac-ELKVLMEKEL-NH2

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [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.