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Merck

SML1687

Sigma-Aldrich

3BDO

≥98% (HPLC)

Sinónimos:

3-Benzyl-5-((2-nitrophenoxy)methyl)-dihydrofuran-2(3H)-one

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About This Item

Fórmula empírica (notación de Hill):
C18H17NO5
Número de CAS:
Peso molecular:
327.33
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.32

Quality Level

assay

≥98% (HPLC)

form

oil

color

colorless to light brown

storage temp.

2-8°C

SMILES string

O=C1OC(COC2=C([N+]([O-])=O)C=CC=C2)CC1CC3=CC=CC=C3

Application

3BDO has been used to investigate the potential effects of metformin on inflammatory lung injury.

Biochem/physiol Actions

3BDO is a cell-permeable, orally bioavailable, non-toxic butyrolactone derivative that is shown to competitively bind FKBP1A (FK506-binding protein 1A, 12 kDa) in a reversible manner, and suppress autophagy via the mTOR pathway. 3BDO inhibits both LPS- and oxLDL-induced autophagy in HUVECs, increases TIA1 phosphorylation, and reduces autophagosomes number. It is reported to be brain permeant, and significantly decreases atherosclerosis development in apoE-/- mice (100 mg/kg, q.d., p.o.). 3BDO increases IDE and neprilysin levels, lowers amyloid-β deposition in an AβPP/PS1 transgenic mouse model of Alzheimer′s disease, and alleviates memory deficits.
An orally bioavailable, brain-permeant suppressor of mTOR-mediated autophagy; reduces Aβ levels and prevents cognitive deficits in AβPP/PS1 mouse model.
3-benzyl-5-[(2-nitrophenoxy) methyl]-dihydrofuran-2 (3H)-one (3BDO) blocks rise in LC3-II stimulated by uric acid (UA). It protects the capability of Rheb1-deficient macrophages to perform phagocytosis. 3BDO also prevents the inhibitory effects of EX-527 on eukaryotic translation initiation factor-binding protein 1(4E-BP1) phosphorylation.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Yu-Lan Sheng et al.
Experimental neurology, 297, 138-147 (2017-08-20)
Serum urate levels are reported to be significantly lowered in patients with Parkinson's disease (PD) and inversely correlated to the risk and progression of PD. However, the mechanism by which urate affects PD is poorly understood. Here we showed that
The SIRT1 inhibitor EX-527 suppresses mTOR activation and alleviates acute lung injury in mice with endotoxiemia.
Huang J, et al.
Innate Immunity, 23(8), 678-686 (2017)
Metformin alleviated endotoxemia-induced acute lung injury via restoring AMPK-dependent suppression of mTOR.
Wu K, et al.
Chemico-Biological Interactions, 291, 1-6 (2018)
Rheb1-mTORC1 maintains macrophage differentiation and phagocytosis in mice.
Wang X, et al.
Experimental Cell Research, 344(2), 219-228 (2016)

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