SML2841
(R)-(-)-2-氟-α-甲基-4-联苯乙酸
≥98% (HPLC)
别名:
(R)-2-氟比洛芬, 氟比洛芬
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关于此项目
线性分子式:
C6H5C6H3(F)CH(CH3)CO2H
化学文摘社编号:
分子量:
244.26
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
InChI
1S/C15H13FO2/c1-10(15(17)18)12-7-8-13(14(16)9-12)11-5-3-2-4-6-11/h2-10H,1H3,(H,17,18)/t10-/m1/s1
SMILES string
C[C@@H](C(O)=O)c1ccc(c(F)c1)-c2ccccc2
InChI key
SYTBZMRGLBWNTM-SNVBAGLBSA-N
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
Quality Level
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Biochem/physiol Actions
Tarenflurbil (or R-flurbiprofen) is an R enantiomer of racemic NSAID flurbiprofen that does not inhibit either cyclooxygenase 1 (COX-1) or cyclooxygenase 2 (COX-2). Tarenflurbil potently reduces levels of beta amyloid in human cells through direct inhibition of γ-secretase.
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 3 Dermal - Acute Tox. 3 Oral - Repr. 2 - Skin Sens. 1B
存储类别
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Jason L Eriksen et al.
The Journal of clinical investigation, 112(3), 440-449 (2003-08-05)
Epidemiologic studies demonstrate that long-term use of NSAIDs is associated with a reduced risk for the development of Alzheimer disease (AD). In this study, 20 commonly used NSAIDs, dapsone, and enantiomers of flurbiprofen were analyzed for their ability to lower
T Morihara et al.
Journal of neurochemistry, 83(4), 1009-1012 (2002-11-08)
Non-steroidal anti-inflammatory drugs (NSAIDs) have been associated with reduced risk for Alzheimer's disease (AD) and selected NSAIDs racemates suppress beta-amyloid (Abeta) accumulation in vivo and Abeta42 production in vitro. Clinical use of NSAIDs for preventing or treating AD has been
Ling Rong Wong et al.
The Journal of pharmacy and pharmacology, 70(1), 59-69 (2017-10-17)
R-flurbiprofen (R-FP) was found to offer neuroprotective effects by inhibiting mitochondrial calcium overload induced by β-amyloid peptide toxicity in Alzheimer's disease (AD). However, poor brain penetration after oral administration posed a challenge to its further development for AD treatment. In
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