3BDO

Catalog No.S8317 Batch:S831701

Technical Data

Formula	C₁₈H₁₇NO₅
Molecular Weight	327.33	CAS No.	890405-51-3
Solubility (25°C)*	In vitro	DMSO	65 mg/mL (198.57 mM)
		Ethanol	19.7 mg/mL (60.18 mM)
		Water	Insoluble
* <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. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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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.

Targets

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].

Protocol (from reference)

Cell Assay:^{^[1]}	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.
Animal Study:^{^[2]}	Animal Models Male apoE-/- mice (8 weeks old; C57BL/6J-knockout) Dosages 50 mg/kg/d OR 100 mg/kg/d Administration i.p.

Cell Assay:^{^[1]}

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.

Animal Study:^{^[2]}

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

References

Selleck's 3BDO has been cited by 10 publications

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

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