In Vivo (Add solvents to the product individually and in order.)
Homogeneous suspension
CMC-NA
≥5mg/ml
Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
Clear solution
5%DMSO
40%PEG300
5%Tween80
50%ddH2O
Validated by Selleck labs. Should you need adjustments to this formulation, contact our sales team for custom testing.
3.250mg/ml
(9.93mM)
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.
Clear solution
5% DMSO
95% Corn oil
Validated by Selleck labs. Should you need adjustments to this formulation, contact our sales team for custom testing.
1.600mg/ml
(4.89mM)
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.
* <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.)
Preparing Stock Solutions
Biological Activity
Description
3BDO, a butyrolactone derivative, could target FKBP1A and activate the mTOR signalling pathway. It inhibits autophagy in HUVECs. This compound inhibits oxLDL-induced apoptosis.
Targets
FKBP1A (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 (tumour protein p53), TP53 nuclear translocation and reactive oxygen species overproduction. This compound activates MTOR by targeting FKBP1A (FK506-binding protein 1A, 12 kDa). It 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 this compound-decreased FLJ11812 level. It inhibits excessive Aβ (25 to 35) peptide-induced autophagy in PC12 neuronal cells and increased the phosphorylation of RPS6KB1. This chemical could inhibit human umbilical vein EC (HUVEC) apoptosis and senescence induced by deprivation of serum and basic fibroblast growth factor 2. It selectively protects vascular ECs (VECs) and inhibits vascular smooth muscle cell (VSMC) proliferation and migration. It (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.
In Vivo
In vivo experiments showed that 3BDO had a good safety profile. This compound treatment could significantly reduce the number of autophagosomes and improve neuronal function in App and Psen1 transgenic mice. It 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. This chemical protects VECs by activating mTOR and thus stabilised atherosclerotic lesions in apoE-/- mice.
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 this compound. HUVECs were treated with DMSO or 60 µM of this chemical for 24 h, then total RNA was extracted with use of Trizol reagent. The cDNA microarray assay in response to this compound treatment was performed.
3BDO inhibits the proliferation, epithelial-mesenchymal transition (EMT), and stemness via suppressing survivin in human glioblastoma cells
[ J Cancer, 2022, 13(4):1203-1213]
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]
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]
Nanoparticle ferritin-bound erastin and rapamycin: a nanodrug combining autophagy and ferroptosis for anticancer therapy.
[ Biomater Sci, 2019, 7(9):3779-3787]
RETURN POLICY
Selleck Chemical’s Unconditional Return Policy ensures a smooth online shopping experience for our customers. If you are in any way unsatisfied with your purchase, you may return any item(s) within 7 days of receiving it. In the event of product quality issues, either protocol related or product related problems, you may return any item(s) within 365 days from the original purchase date. Please follow the instructions below when returning products.
SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.
NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.
