FPS-ZM1

FPS-ZM1 is a high-affinity, selective small molecule antagonist of the receptor for advanced glycation end products (RAGE; AGER), with a Ki of approximately 25 nM. It blocks amyloid-β (Aβ) binding to the V domain of RAGE, inhibiting Aβ40- and Aβ42-induced cellular stress and neuroinflammation in RAGE-expressing cells in vitro and in animal models in vivo. FPS-ZM1 rapidly crosses the blood-brain barrier and specifically targets RAGE in the brain, attenuating β-secretase activity, Aβ production, and microglial activation. In models of Alzheimer's disease, the compound reduces brain Aβ accumulation and normalizes cognitive performance and cerebral blood flow. FPS-ZM1 also demonstrates anti-inflammatory effects in other disease models by modulating JAK/STAT, NF-κB, and MAPK signaling and has been shown to reduce liver lipid deposition in diabetic mice by inhibiting SREBP-1c, NF-κB, and p38 MAPK signaling. FPS-ZM1 is at preclinical development status; it was initially developed by University of Rochester Medical Center and is supplied for research use by specialty reagent companies[1][3][4][5][6][7][8][9][10].

Other names

4-Chloro-N-cyclohexyl-N-(phenylmethyl)benzamide