| Identification | Back Directory | [Name]
N-benzyl-4-chloro-N-cyclohexylbenzaMide | [CAS]
945714-67-0 | [Synonyms]
FPS-ZM1
CS-2304
N-benzyl-4-chloro-N-cyclohexylbenzaMide
4-Chloro-N-cyclohexyl-N-(phenylmethyl)benzamide
Benzamide, 4-chloro-N-cyclohexyl-N-(phenylmethyl)- | [Molecular Formula]
C20H22ClNO | [MDL Number]
MFCD22378757 | [MOL File]
945714-67-0.mol | [Molecular Weight]
327.85 |
| Chemical Properties | Back Directory | [Boiling point ]
497.6±38.0 °C(Predicted) | [density ]
1.18±0.1 g/cm3(Predicted) | [storage temp. ]
Sealed in dry,2-8°C | [solubility ]
Soluble in DMSO (up to 35 mg/ml) or in Ethanol (up to 20 mg/ml) | [form ]
solid | [pka]
-1.54±0.20(Predicted) | [color ]
Off-white | [Stability:]
Stable for 1 year from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20°C for up to 3 months. |
| Hazard Information | Back Directory | [Description]
FPS-ZM1 (945714-67-0) is a high-affinity RAGE (Receptor for Advanced Glycation End products) receptor antagonist (IC50?= 0.6 μM). It lowers levels of Aβ via binding to the V domain of RAGE and can block multiple mechanisms of Aβ40- and Aβ42-induced cellular stress in RAGE-expressing brain endothelium, neurons and microglia?in vitro?and?in vivo.1,2? Can cross the BBB.? In a rat model of intracerebral hemorrhage, FPS-ZM1 was able to attenuate blood-brain barrier and white matter fiber damage.3?FPS-ZM1 antagonism of RAGE was able to ameliorate inflammatory damage after acute intracerebral hemorrhage via downstream blockade of high mobility box-1(HMGB1) signaling.4? FPS-ZM1 has also been shown to impair breast cancer cell invasion and metastasis.5 | [Uses]
FPS-ZM1 is a blood-brain-barrier permeant blocker of RAGE V domain-mediated ligand binding (Ki?= 25, 148, & 230 nM, respectively, against Aβ40, HMGB1 & S100B, binding to sRAGE). | [in vitro]
fps-zm1 was identified as a high-affinity inhibitor of the receptor for advanced glycation end products. fps-zm1 could block the binding of amyloid β (aβ) protein to rage and inhibit aβ40- and aβ42-induced cellular stress in rage-expressing cells [1]. | [in vivo]
animal study found that fps-zm1 was nontoxic to mice and readily crossed the blood-brain barrier (bbb). in aged appsw/0 mice overexpressing human aβ-precursor protein, fps-zm1 could inhibit rage-mediated influx of circulating aβ40 and aβ42 into the brain. fps-zm1 bound exclusively to rage in brain, which inhibited β-secretase activity and aβ production and suppressed microglia activation and the neuroinflammatory response. moreover, the blockade of rage actions at the bbb and in the brain could reduce aβ40 and aβ42 levels in brain in aged appsw/0 mice [1]. | [storage]
Store at -20°C | [References]
1) Deane?et al.?(2012),?A multimodal RAGE-specific inhibitor reduces amyloid β-mediated brain disorder in a mouse model of Alzheimer disease; J. Clin. Invest.?122?1377
2) Hong?et al.?(2016),?Effects of RAGE-Specific Inhibitor FPS-ZM1 on Amyloid-β Metabolism and AGEs-Induced Inflammation and Oxidative Stress in Rat Hippocampus?; Neurochem. Res.?41?1192
3) Yang?et al.?(2015),?Receptor for advanced glycation end-product antagonist reduces blood-brain barrier damage after intracerebral hemorrhage; Stroke?46?1328
4) Li?et al. (2015),?Blockade of high mobility box-1 signaling via the receptor for advanced end-products ameliorates inflammatory damage after acute intracerebral hemorrhage; Neurosci. Lett.?609?109
5) Kwak?et al.?(2017),?Targeting of RAGE-ligand signaling impairs breast cancer cell invasion and metastasis;?Oncogene?36?155 |
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