Table 2.

RAGE Inhibitors.

Inhibitors	Targeting of RAGE Domain	Effects	Ref.
TTP488	V	AGEs, HMGB1, CML, S100B, and Aβ-RAGE binding inhibition	[4,220,221]
4,6-disubstituted 2-amino pyrimidines	V	Aβ-RAGE binding inhibition	[223]
4-fluorophenoxy analog	V	Inhibition of amyloid plaques inside the brain	[224]
FPS-ZM1	V	Aβ-RAGE binding inhibition and low cytotoxicity in vitro and in vivo	[186]
GM-1111	VC1C2	CML, GMGB1, and S100B-RAGE binding inhibition	[226]
S100-derived peptide	VC1C2	Reduced RAGE-mediated activation of NF-κB, inflammation, tumor growth, and metastasis in various cancer cells	[227]
HMGB1-derived Peptide	VC1C2	Suppressed the formation of pulmonary metastasis and invasion in tumor cells	[228]
Alagebrium	AGE cross-link breaker	Reduced AGE accumulation and atherosclerotic plaque formation and lesions	[73]
DNA-aptamers		against the AGE-RAGE axis in diabetes-associated complications	[229]
Group of 13 compounds	cytoplasmic	Inhibition of ctRAGE interaction with mDia1	[14]
Aptamer-based antagonist	V	inhibit interaction between RAGE and S100B	[230]

AGEs: Advanced glycation end-products; HMGB1: High mobility group box-1 protein; CML: N_ɛ-carboxymethyl-lysine; ctRAGE: cytoplasmic domain of RAGE.