SML2106
Roflupram
≥98% (HPLC)
Sinónimos:
1-[4-(Difluoromethoxy)-3-[(tetrahydro-3-furanyl)oxy]phenyl]-3-methyl-1-butanone, FFPM, ZL-n-91
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About This Item
Productos recomendados
assay
≥98% (HPLC)
form
oil
color
colorless to light brown
Storage temp.
2-8°C
SMILES string
O=C(CC(C)C)C1=CC=C(OC(F)F)C(OC2CCOC2)=C1
Biochem/physiol Actions
Roflupram (FFPM) is a potent anti-inflammatory phosphodiesterase 4 (PDE4) inhibitor that was found to suppress inflammasome activation in microglial cells by enhancing autophagy. In microglial BV-2 cells roflupram enhanced the level of microtubule-associated protein 1 light chain 3 II (LC3-II) and decreased the autophagy receptor ubiquitin-binding protein p62 (SQSTM1), enhancing autophagy, reducing the activation of inflammasome and suppressing the production of IL-1β. Roflupram (FFPM) was found to reverse learning and memory deficits in APP/PS1 transgenic mice.
Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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ACS chemical neuroscience, 8(11), 2381-2392 (2017-06-13)
Inhibition of phosphodiesterase 4 (PDE4) suppressed the inflammatory responses in the brain. However, the underlying mechanisms are poorly understood. Roflupram (ROF) is a novel PDE4 inhibitor. In the present study, we found that ROF enhanced the level of microtubule-associated protein
Journal of medicinal chemistry, 51(24), 7673-7688 (2008-12-04)
Phosphodiesterase 4 catalyzes the hydrolysis of cyclic AMP and is a target for the development of anti-inflammatory agents. We have designed and synthesized a series of phenyl alkyl ketones as PDE4 inhibitors. Among them, 13 compounds were identified as having
Neuropharmacology, 116, 260-269 (2017-01-10)
Thus far, phosphodiesterase-4 (PDE4) inhibitors have not been approved for application in Alzheimer's disease (AD) in a clinical setting due to severe side effects, such as nausea and vomiting. In this study, we investigated the effect of FFPM, a novel
International immunopharmacology, 10(4), 406-411 (2010-01-16)
In the present study, we investigated the effect of classic PDE4 inhibitor rolipram and novel PDE4 inhibitor ZL-n-91 on LPS-induced acute lung injury (ALI) in mice and its mechanism. ALI was induced in ICR mice by instilling intratracheally with LPS
International immunopharmacology, 90, 107176-107176 (2020-11-28)
Roflupram (ROF) is a novel phosphodiesterase 4 inhibitor. We previously found that ROF suppressed the production of pro-inflammatory factors in microglial cells; however, the underlying mechanisms are largely unknown. The present study aimed to elucidate the underlying molecular mechanisms of
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