3BDO

製品コードS8317 バッチS831702

印刷

化学情報

Chemical Structure Synonyms 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one Storage
(From the date of receipt)		 3 years -20°C powder
1 years -80°C in solvent
化学式

C18H17NO5
分子量 327.33 CAS No. 890405-51-3
Solubility (25°C)* 体外 DMSO 65 mg/mL (198.57 mM)
Ethanol 32 mg/mL (97.76 mM)
Water Insoluble
体内 （毎回新しく調製した物を用意してください）
Clear solution
5% DMSO 95% Corn oil
1.6mg/ml Taking the 1 mL working solution as an example, add 50 μL of 32 mg/ml clear DMSO stock solution to 950 μL of corn oil and mix evenly. The mixed solution should be used immediately for optimal results. 
Clear solution
5%DMSO 40%PEG300 5%Tween80 50%ddH2O
3.25mg/ml Taking the 1 mL working solution as an example, add 50 μL of 65 mg/ml clarified DMSO stock solution to 400 μL of PEG300, mix evenly to clarify it; add 50 μL of Tween80 to the above system, mix evenly to clarify; then continue to add 500 μL of ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results. 
* <1 mg/ml means slightly soluble or 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.

溶剤液（一定の濃度）を調合する

生物活性

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

プロトコル(参考用のみ)

細胞アッセイ 細胞株 HUVECs
濃度 60 μM
反応時間 24 h
実験の流れ

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.
動物実験 動物モデル Male apoE-/- mice (8 weeks old; C57BL/6J-knockout)
投薬量 50 mg/kg/d OR 100 mg/kg/d
投与方法 i.p.

Selleckの高級品が、幾つかの出版された研究調査結果（以下を含む）で使われた：

Malic Enzyme 1 as a Novel Anti-Ferroptotic Regulator in Hepatic Ischemia/Reperfusion Injury [ Adv Sci (Weinh), 2023, 10(13):e2205436] PubMed: 36840630
Impaired Arginine Metabolism in Hair Follicles: A Potential Mechanism in Androgenetic Alopecia [ Research Square, 2023, 10.21203/rs.3.rs-3629594/v1] PubMed: none
3BDO inhibits the proliferation, epithelial-mesenchymal transition (EMT), and stemness via suppressing survivin in human glioblastoma cells [ J Cancer, 2022, 13(4):1203-1213] PubMed: 35281871
Rapamycin Promotes ROS-Mediated Cell Death via Functional Inhibition of xCT Expression in Melanoma Under γ-Irradiation [ Front Oncol, 2021, 11:665420] PubMed: 33959512
Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway [ Mol Med Rep, 2021, 24(2)592] PubMed: 34165172
Metformin prevents PFKFB3-related aerobic glycolysis from enhancing collagen synthesis in lung fibroblasts by regulating AMPK/mTOR pathway [ Exp Ther Med, 2021, 21(6):581] PubMed: 33850553
PDK1 Regulates the Maintenance of Cell Body and the Development of Dendrites of Purkinje Cells by pS6 and PKCγ [ J Neurosci, 2020, 40(29):5531-5548] PubMed: 32487697
Rapamycin-Induced Autophagy Promotes the Chondrogenic Differentiation of Synovium-Derived Mesenchymal Stem Cells in the Temporomandibular Joint in Response to IL-1β [ Biomed Res Int, 2020, 2020:4035306] PubMed: 33145347
Nanoparticle ferritin-bound erastin and rapamycin: a nanodrug combining autophagy and ferroptosis for anticancer therapy. [ Biomater Sci, 2019, 7(9):3779-3787] PubMed: 31211307
High-Frequency Repetitive Transcranial Magnetic Stimulation Mediates Autophagy Flux in Human Bone Mesenchymal Stromal Cells via NMDA Receptor-Ca2+-Extracellular Signal-Regulated Kinase-Mammalian Target of Rapamycin Signaling. [ Front Neurosci, 2019, 13:1225] PubMed: 31798406

長期の保管のために-20°Cの下で製品を保ってください。

人間や獣医の診断であるか治療的な使用のためにでない。

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