3BDO - CAS 890405-51-3
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C18H17NO5
Molecular Weight:
327.33
COA:
Inquire
Targets:
Autophagy
Description:
3BDO, a cell-permeable, orally bioavailable, non-toxic butyrolactone derivative, could target FKBP1A and activate the mTOR signaling pathway, which inhibits autophagyin HUVECs. 3BDO inhibits autophagy in human umbilical vein endothelial cells (HUVECs) and neuronal cells.
Brife Description:
Inhibits autophagy in human umbilical vein endothelial cells (HUVECs) and neuronal cells
Purity:
99.15 %
Appearance:
White to light pink powder
Synonyms:
3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one
Solubility:
DMSO Solubility: 65 mg/mL (198.57 mM)
Storage:
Store in a cool and dry place (or refer to the Certificate of Analysis).
MSDS:
Inquire
Boiling Point:
540.0±20.0 °C | Condition: Press: 760 Torr
Density:
1.279±0.06 g/cm3
InChIKey:
AXPZIVKEZRHGAS-UHFFFAOYSA-N
InChI:
1S/C18H17NO5/c20-18-14(10-13-6-2-1-3-7-13)11-15(24-18)12-23-17-9-5-4-8-16(17)19(21)22/h1-9,14-15H,10-12H2
Canonical SMILES:
C1C(C(=O)OC1COC2=CC=CC=C2[N+](=O)[O-])CC3=CC=CC=C3
1.Protective effects of a synthesized butyrolactone derivative against chloroquine-induced autophagic vesicle accumulation and the disturbance of mitochondrial membrane potential and Na+,K+-ATPase activity in vascular endothelial cells.
Huang B;Meng N;Zhao B;Zhao J;Zhang Y;Zhang S;Miao J Chem Res Toxicol. 2009 Mar 16;22(3):471-5. doi: 10.1021/tx8002824.
We previously found a butyrolactone derivative, 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one (3BDO), could inhibit vascular endothelial cell (VEC) apoptosis and senescence induced by a deprivation of serum and FGF-2. In this study, we aimed to investigate its actions in VEC autophagy induced by chloroquine (CQ). The measurement on the volume of acidic compartments (VAC) and autophagy analysis by acridine orange (AO) staining and microtubule-associated protein 1 light chain 3 (MAP1LC3) process revealed that 3BDO was an effective inhibitor of autophagic vesicle accumulation (vacuolation) induced by CQ in VECs. 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolylcarbocyanine iodide (JC-1) was used for mitochondrial membrane potential (MMP) measurement. The results showed that CQ elevated MMP significantly and that 3BDO could significantly inhibit CQ-induced MMP increase. Na+,K+-ATPase activity assay showed that CQ inhibited this enzyme activity significantly and that 3BDO attenuated the alteration of Na+,K+-ATPase activity caused by CQ. We concluded that 3BDO was a promising inhibitor of CQ-induced accumulation of autophagic vesicles in VECs and could weaken the alterations of MMP and Na+,K+-ATPase activity induced by CQ.
2.Identification of a novel MTOR activator and discovery of a competing endogenous RNA regulating autophagy in vascular endothelial cells.
Ge D;Han L;Huang S;Peng N;Wang P;Jiang Z;Zhao J;Su L;Zhang S;Zhang Y;Kung H;Zhao B;Miao J Autophagy. 2014 Jun;10(6):957-71. doi: 10.4161/auto.28363.
MTOR, a central regulator of autophagy, is involved in cancer and cardiovascular and neurological diseases. Modulating the MTOR signaling balance could be of great significance for numerous diseases. No chemical activators of MTOR have been found, and the urgent challenge is to find novel MTOR downstream components. In previous studies, we found a chemical small molecule, 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one (3BDO), that inhibited autophagy in human umbilical vein endothelial cells (HUVECs) and neuronal cells. Here, we found that 3BDO activated MTOR by targeting FKBP1A (FK506-binding protein 1A, 12 kDa). We next used 3BDO to detect novel factors downstream of the MTOR signaling pathway. Activation of MTOR by 3BDO increased the phosphorylation of TIA1 (TIA1 cytotoxic granule-associated RNA binding protein/T-cell-restricted intracellular antigen-1). Finally, we used gene microarray, RNA interference, RNA-ChIP assay, bioinformatics, luciferase reporter assay, and other assays and found that 3BDO greatly decreased the level of a long noncoding RNA (lncRNA) derived from the 3' untranslated region (3'UTR) of TGFB2, known as FLJ11812. TIA1 was responsible for processing FLJ11812.
3.A new microRNA signal pathway regulated by long noncoding RNA TGFB2-OT1 in autophagy and inflammation of vascular endothelial cells.
Huang S;Lu W;Ge D;Meng N;Li Y;Su L;Zhang S;Zhang Y;Zhao B;Miao J Autophagy. 2015;11(12):2172-83. doi: 10.1080/15548627.2015.1106663.
TGFB2-OT1 (TGFB2 overlapping transcript 1) is a newly discovered long noncoding RNA (lncRNA) derived from the 3'UTR of TGFB2. It can regulate autophagy in vascular endothelial cells (VECs). However, the mechanisms of TGFB2-OT1 action are unclear, and whether it is involved in VECs dysfunction needs investigation. Here, the level of TGFB2-OT1 was markedly increased by lipopolysaccharide and oxidized low-density lipoprotein, 2 VECs inflammation triggers. A chemical small molecule, 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one (3BDO) significantly decreased TGFB2-OT1 levels and inhibited the effect of LPS and oxLDL. The NUPR1 level was upregulated by the 2 inflammation inducers and modulated the TGFB2-OT1 level by promoting the expression of TIA1, responsible for TGFB2-OT1 processing. We focused on how TGFB2-OT1 regulated autophagy and inflammation. Use of miRNA chip assay, TGFB2-OT1 overexpression technology and 3BDO revealed that TGFB2-OT1 regulated the levels of 3 microRNAs, MIR3960, MIR4488 and MIR4459. Further studies confirmed that TGFB2-OT1 acted as a competing endogenous RNA, bound to MIR3960, MIR4488 and MIR4459, then regulated the expression of the miRNA targets CERS1 (ceramide synthase 1), NAT8L (N-acetyltransferase 8-like [GCN5-related, putative]), and LARP1 (La ribonucleoprotein domain family, member 1).
Molecular Weight Calculator Molarity Calculator Solution Dilution Calculator

Related Autophagy Products


CAS 890405-51-3 3BDO

3BDO
(CAS: 890405-51-3)

3BDO, a cell-permeable, orally bioavailable, non-toxic butyrolactone derivative, could target FKBP1A and activate the mTOR signaling pathway, which inhibits aut...

CAS 1644443-47-9 Autophinib

Autophinib
(CAS: 1644443-47-9)

Autophinib is a novel potent autophagy inhibitor, which can inhibit autophagy induced by starvation or rapamycin with IC50 values of 0.04 µM and 0.09 µM, respec...

CAS 307538-42-7 SMER28

SMER28
(CAS: 307538-42-7)

SMER28 is a small molecule modulator of autophagy that increases autophagosome synthesis and enhances clearance of aggregate-prone substrates, including those r...

CAS 1884220-36-3 SBI0206965

SBI0206965
(CAS: 1884220-36-3)

SBI-0206965 is a novel selective inhibitor of the autophagy-initiating kinase ULK1 (IC50 = 108 nM) that is less effective against ULK2 (IC50 = 711 nM). SBI02069...

Chemical Structure

CAS 890405-51-3 3BDO

Quick Inquiry

Verification code

Featured Items