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Azoramide
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Azoramide图片
CAS NO:932986-18-0
规格:≥98%
包装与价格:
包装价格(元)
5mg电议
10mg电议
25mg电议
50mg电议
100mg电议
250mg电议
500mg电议

产品介绍
理化性质和储存条件
Molecular Weight (MW) 308.83
Formula C15H17ClN2OS
CAS No. 932986-18-0
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)DMSO:>61 mg/mL (197.5 mM)
Water: < 1 mg/mL
Ethanol: >61 mg/mL (197.5 mM)
Chemical Name N-[2-[2-(4-chlorophenyl)-4-thiazolyl]ethyl]-butanamide
Synonyms Azoramide
SMILES Code CCCC(NCCC1=CSC(C2=CC=C(Cl)C=C2)=N1)=O
实验参考方法
In Vitro

In vitro activity: Azoramide may have the protective effects of enhancing chaperone expression and reducing protein synthesis without inducing cytotoxicity and apoptosis. Azoramide may require the presence of intact IRE1 and PERK branches of the UPR to fully increase chaperone capacity. Azoramide is found to be a kind of compound with the dual property of not only boosting ER folding acutely but also activating ER chaperone capacity chronically to promote ER homeostasis. Its treatment potently protects cells against chemically-induced ER stress conditions. Azoramide preserves beta cell function and survival during metabolic ER stress. Azoramide pretreatment does not impair ER function as part of its initial action. Azoramide treatment leads to increased SERCA expression, resulting in enhanced retention of Ca+2 within the ER. Azoramide interacts with UPR pathways to promote resolution of ER stress and improve ER function.


Kinase Assay: Cells cultured under the different conditions were washed with ice-cold PBS and lysed in RIPA buffer containing a protease inhibitor cocktail (Roche, Mannheim, Germany). Protein concentrations were determined using the BCA assay kit. Total protein of 50 μg was separated on 12% SDS-polyacrylamide gels and transferred to nitrocellulose membrane, and the membrane was blocked with 5% nonfat milk in Tris-buffered saline (TBS). The membrane was then incubated with the appropriate primary antibodies in TBS at 4 °C overnight. Antibodies for Runx2, PPARγ, Fabp4, β-catenin, and phospho-β-catenin were from Cell Signaling Technology (Beverly, MA, USA). GLP-1R antibody was from Ruiying Biological, and antibodies against PKAc and β-actin were from Sangon. Secondary antibodies conjugated to IRDye 800 were detected using an Odyssey infrared imaging system. All Western blots were independently replicated at least three times and the intensities of the bands were quantified using ImageJ software.


Cell Assay: C3H10T1/2 cells were seeded on coverslips. After different treatment, cells were fixed with 4% paraformaldehyde for 15 min and permeabilized with 0.1% Triton X-100 in TBS for 15 min. After being blocked in 5% FBS in PBS for 30 min, cells were incubated with anti-β-catenin (Cell Signaling Technology) overnight at 4 °C. After washing three times with PBS, cells were incubated with DyLight(TM) 594-conjugated secondary antibodies (Thermo Scientific) for 60 min at room temperature and then stained with 4′,6-diamidino-2-phenylindole (DAPI; Sigma-Aldrich) for 10 min. Slides were then washed three times and mounted. Immunofluorescence was detected using an Olympus inverted fluorescence microscope.

In VivoC57BL/6 mice were housed at the animal care facility at 22 °C with 12-h light/dark cycles. In vivo analysis of azoramide responses by BMP2 calvarial injection was conducted as described below. Briefly, 14-day-old mice were injected with recombinant BMP2 (10 mg/ml) 30 μl per injection, three times a day for 5 days, into the periosteal tissue overlying the right parietal bone; saline vehicle control was injected into the left parietal bone. Meanwhile, azoramide compound (20 mg/ml, 30 μl per injection) was administered via intraperitoneal injection once a day for 14 consecutive days. Animals were then sacrificed after the last injection to analyze bone formation.
Animal modelC57BL/6 mice
Formulation & Dosage i.p. injection; azoramide compound (20 mg/ml, 30 μl per injection) was administered via intraperitoneal injection once a day for 14 consecutive days.
References Stem Cell Res Ther. 2018; 9: 57.