MedChemExpress - Model Azeliragon - 603148-36-3
Azeliragon (TTP488) is an orally bioavailable inhibitor of the receptor for advanced glycation end products (RAGE) in development as a potential treatment to slow disease progression in patients with mild Alzheimer’s disease (AD)[1]. Azeliragon also can cross the blood-brain barrier (BBB)[2].MCE products for research use only. We do not sell to patients.
Azeliragon
MCE China：Azeliragon
Brand：MedChemExpress (MCE)
Cat. No.HY-50682
CAS：603148-36-3
Synonyms：TTP488; PF-04494700
Purity：99.37%
Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Shipping：Room temperature in continental US; may vary elsewhere.
Description：Azeliragon (TTP488) is an orally bioavailable inhibitor of the receptor for advanced glycation end products (RAGE) in development as a potential treatment to slow disease progression in patients with mild Alzheimer’s disease (AD). Azeliragon also can cross the blood-brain barrier (BBB).
In Vitro：Azeliragon (4 nM; 16 hours; T cells) treatment inhibits of wild type mice (WT) but not the deletion of the receptor (RAGE-/- mice) T cells and significant reduction in the production of IFN-γ[3].
In Vivo：Azeliragon (100 mcg/d; intraperitoneal injection; every day) treatment reduces syngeneic islet graft and islet allograft in NOD and B6 mice (Islets were isolated from young prediabetic NOD/LtJ mice and transplanted into NOD mice with spontaneous diabetes; islets were isolated from WT BALB/c mice and transplanted into B6 mice with diabetes)[3].
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References：
[1]. Burstein AH, et al. Assessment of Azeliragon QTc Liability Through Integrated, Model-Based Concentration QTc Analysis. Clin Pharmacol Drug Dev. 2019 May;8(4):426-435. [Content Brief]
[2]. Bongarzone S, et al. Targeting the Receptor for Advanced Glycation Endproducts (RAGE): A Medicinal Chemistry Perspective. J Med Chem. 2017 Sep 14;60(17):7213-7232. [Content Brief]
[3]. Chen Y, et al. RAGE ligation affects T cell activation and controls T cell differentiation. J Immunol. 2008 Sep 15;181(6):4272-8. [Content Brief]
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