For research use only.

Catalog No.S8317 Synonyms: 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one

6 publications

3BDO Chemical Structure

CAS No. 890405-51-3

3BDO, a butyrolactone derivative, could target FKBP1A and activate the mTOR signaling pathway. It inhibits autophagy in HUVECs. 3BDO inhibits oxLDL-induced apoptosis.

Selleck's 3BDO has been cited by 6 publications

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Biological Activity

Description 3BDO, a butyrolactone derivative, could target FKBP1A and activate the mTOR signaling pathway. It inhibits autophagy in HUVECs. 3BDO inhibits oxLDL-induced apoptosis.
FKBP1A [1]
(Cell-free assay)
In vitro

3BDO inhibits autophagy in human umbilical vein endothelial cells (HUVECs) and neuronal cells. It suppresses lipopolysaccharide-induced HUVEC autophagic injury by downregulating the protein levels of NUPR1 (nuclear protein, transcriptional regulator) and TP53 (tumor protein p53), TP53 nuclear translocation and reactive oxygen species overproduction. 3BDO activates MTOR by targeting FKBP1A (FK506-binding protein 1A, 12 kDa). 3BDO greatly decreases the level of a long noncoding RNA (lncRNA) derived from the 3′ untranslated region (3′UTR) of TGFB2, known as FLJ11812, but does not affect TGFB2 expression. ATG13 protein level is decreased along with 3BDO-decreased FLJ11812 level. 3BDO inhibits excessive Aβ (25 to 35) peptide-induced autophagy in PC12 neuronal cells and increased the phosphorylation of RPS6KB1[1]. 3BDO could inhibit human umbilical vein EC (HUVEC) apoptosis and senescence induced by deprivation of serum and basic fibroblast growth factor 2. iT selectively protecteS vascular ECs (VECs) and inhibitS vascular smooth muscle cell (VSMC) proliferation and migration[2]. 3BDO (20-60 μg/ml) could inhibit VEC apoptosis and suppress integrin β4 expression, but it could not depress the ROS level induced by deprivation of serum and FGF-2[3].

In vivo In vivo experiments showed that 3BDO had a good safety profile. 3BDO treatment could significantly reduce the number of autophagosomes and improve neuronal function in App and Psen1 transgenic mice[1]. 3BDO activated mTOR in vivo and decreased the protein level of ATG13 in the plaque endothelium of apoE-/- mice. It does not affect the activity of mTOR and autophagy in macrophage cell line RAW246.7 and vascular smooth muscle cells of apoE-/- mice, but suppressed plaque endothelial cell death and restricted atherosclerosis development in the mice. 3BDO protecteS VECs by activating mTOR and thus stabilized atherosclerotic lesions in apoE-/- mice[2].


Cell Research:


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  • Cell lines: HUVECs
  • Concentrations: 60 μM
  • Incubation Time: 24 h
  • Method:

    HUVECs are cultured in M199 medium with 20% (v/v) fetal bovine serum and 10 IU/mL fibroblast growth factor 2 (FGF2) in a humidified incubator at 37 °C with 5% CO2. When HUVECs were grown to 80% confluency, cells were treated with or without 3BDO. HUVECs were treated with DMSO or 60 µM 3BDO for 24 h, then total RNA was extracted with use of Trizol reagent. The cDNA microarray assay in response to 3BDO treatment was performed.

    (Only for Reference)
Animal Research:


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  • Animal Models: Male apoE-/- mice (8 weeks old; C57BL/6J-knockout)
  • Dosages: 50 mg/kg/d OR 100 mg/kg/d
  • Administration: i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 65 mg/mL (198.57 mM)
Ethanol 49 mg/mL (149.69 mM)
Water Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 327.33


CAS No. 890405-51-3
Storage powder
in solvent
Synonyms 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one
Smiles C1C(C(=O)OC1COC2=CC=CC=C2[N+](=O)[O-])CC3=CC=CC=C3

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID