FPS-ZM1

Cas No.:	945714-67-0
Chemical Name:	Fps-ZM1
Synonyms:	N-benzyl-4-chloro-N-cyclohexylbenzamide;FPS-ZM1;FPS ZM1;4-Chloro-N-cyclohexyl-N-(phenylmethyl)benzamide;BCP16845;s8185;BDBM50249567;N-Benzyl-N-cyclohexyl-4-chlorobenzamide;AK474177;FPS ZM1;FPSZM1; FPS-ZM 1; FPS ZM-1; FPSZM 1
SMILES:	ClC1C([H])=C([H])C(=C([H])C=1[H])C(N(C([H])([H])C1C([H])=C([H])C([H])=C([H])C=1[H])C1([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C1([H])[H])=O
Formula:	C20H22ClNO
M.Wt:	327.8478
Sotrage:	2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

Description:	FPS-ZM1 is a high-affinity RAGE inhibitor with a Ki of 25 nM.
In Vivo:	FPS-ZM1 is nontoxic to mice and readily crossed the blood-brain barrier. In aged APPsw/0 mice overexpressing human Aβ-precursor protein, a transgenic mouse model of AD with established Aβ pathology, FPS-ZM1 inhibits RAGE-mediated influx of circulating Aβ40 and Aβ42 into the brain. In brain, FPS-ZM1 binds exclusively to RAGE, which inhibits β-secretase activity and Aβ production and suppresses microglia activation and the neuro-inflammatory response[1]. FPS-ZM1 treatment reduces the level of Aβ1-40 and Aβ1-42 in AGEs Rats. It Inhibits AGEs-mediated increase of Aβ-metabolism-related proteins and downregulates AGEs-mediated increase of pro-inflammatory cytokines in the hippocampus. FPS-ZM1 up-Regulates anti-oxidant defense system and attenuated AGEs induced memory impairment in AGEs rats[2].
In Vitro:	FPS-ZM1 inhibits Aβ/RAGE binding in CHO cells with approximately 2-fold greater affinity than its parent molecule, FPS2. FPS-ZM1 inhibits binding of other known RAGE ligands to sRAGE, including S100 calcium-binding protein B and amphoterin. FPS-ZM1 is more effective than FPS2 in reducing Aβ40-induced increases inBACE1 mRNA and protein levels and the generation of sAPPβ, an APP cleavage product of BACE1 indicative of BACE1 activity[1].