Molecular Formula | C20H22ClNO |
Molar Mass | 327.85 |
Density | 1.18±0.1 g/cm3(Predicted) |
Boling Point | 497.6±38.0 °C(Predicted) |
Solubility | Soluble in DMSO (up to 35 mg/ml) or in Ethanol (up to 20 mg/ml) |
Appearance | solid |
Color | Off-white |
pKa | -1.54±0.20(Predicted) |
Storage Condition | 2-8°C |
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. |
In vitro study | FPS-ZM1 prevents Aβ from binding to the V region of RAGE and inhibits Aβ40-and Aβ42-induced cellular stress in RAGE-expressing cells. It also inhibits the binding of other ligands to RAGE, such as S100B,AGE, and HMGB1, which may be involved in RAGE-mediated long-term tissue damage (in diabetic models), immune/inflammatory diseases, Alzheimer's disease, etc. |
In vivo study | FPS-ZM1 is not toxic to mice and can pass the blood brain barrier. It inhibits RAGE in the brain and the blood-brain barrier in 17-month-old APPsw/0 mice with Aβ and amyloid lesions, effectively controls Aβ-mediated brain disease, related neurovascular and Cognitive Disorder progression. |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 3.05 ml | 15.251 ml | 30.502 ml |
5 mM | 0.61 ml | 3.05 ml | 6.1 ml |
10 mM | 0.305 ml | 1.525 ml | 3.05 ml |
5 mM | 0.061 ml | 0.305 ml | 0.61 ml |
Biological activity | FPS-ZM1 is a non-toxic, tertiary amide compound that can penetrate the blood and brain barrier. It is a specific inhibitor of RAGE and inhibits the binding of Aβ to the V region of RAGE. |
target | TargetValue RAGE |
Target | Value |
In vitro study | FPS-ZM1 prevent Aβ from binding to the V region of RAGE, and inhibit Aβ40-and Aβ42-induced cell stress in RAGE-expressing cells. It also inhibits the binding of other ligands to RAGE, such as S100B,AGE and HMGB1. These ligands bind to RAGE and may be involved in RAGE-mediated long-term tissue damage (in diabetes models), immune/inflammatory diseases, Alzheimer's disease, etc. |
in vivo research | FPS-ZM1 is non-toxic to mice and can pass through the blood-brain barrier. It can effectively control the development of Aβ-mediated brain diseases, related neurovascular and cognitive disorders by inhibiting RAGE in the brain and blood-brain barrier in 17-month-old APPsw/0 mice with Aβ and amyloid lesions. |