Arecaidine propargyl ester hydrobromide ape

Manufactured by Merck Group

Sourced in Italy

Arecaidine Propargyl Ester hydrobromide (APE) is a chemical compound used in various laboratory applications. It serves as a precursor or intermediate in the synthesis of other compounds. The core function of APE is to provide a specific chemical structure and properties that may be leveraged in research and development processes. Further details on the intended use of this product are not available.

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Lab products found in correlation

Pirenzepine, by Merck Group (2 mentions) 4 damp, by Merck Group (2 mentions) α bungarotoxin, by Bio-Techne (1 mentions) Methoctramine, by Merck Group (1 mentions)

4 protocols using arecaidine propargyl ester hydrobromide ape

Anoxic Culture of Glioblastoma Cells

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For reproducing the anoxic environment, we used a hypoxic/anaerobic chamber (BBLTM GasPakTM, Franklin Lakes, NJ, USA). The system was set up at 37 °C in 5% CO₂, 95% N₂. Cells were transferred into the humidified chamber and incubated with the appropriate media for 24 h. The cells were then detached and analyzed according to the experimental plan. Control cells were incubated under normoxic conditions.
Arecaidine Propargyl Ester hydrobromide (Ape, Sigma-Aldrich, Milan, Italy) is a synthetic alkaloid obtained from modification of areca nut arecaidine. Its ability to selectively bind M2 muscarinic subtype has been largely demonstrated by pharmacological binding and M2 knockdown experiments [17 (link),18 (link)]. Cells were treated with 100 µM Ape, considering that this concentration was able to negatively control cell growth both in GBM cell lines and in GSCs, as previously demonstrated [18 (link)].

Cristofaro I., Limongi C., Piscopo P., Crestini A., Guerriero C., Fiore M., Conti L., Confaloni A, & Tata A.M. (2020). M2 Receptor Activation Counteracts the Glioblastoma Cancer Stem Cell Response to Hypoxia Condition. International Journal of Molecular Sciences, 21(5), 1700.

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Selective Activation of α7 nAChR

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The compound 3-methoxy-1-oxa-2,7-diaza-7,10-ethanospirodec- 2-ene sesquifumarate (ICH3) was used to selectively activate the α7 nAChR.^{41-44 (link)} ICH3 was used at the final concentration of 10 μM. α-Bungarotoxin (Tocris Bioscience, Bristol, UK), an α7 nicotinic receptor antagonist, was used at final concentration of 100 nM and it was added 2 h before ICH3 treatment. The M2 muscarinic receptor selective agonist arecaidine propargyl ester hydrobromide (APE, Sigma-Aldrich, Milan, Italy) was used at the final concentration of 100 μM.^{32 (link),45 (link)} Controls were obtained maintaining the cells in normal growth medium. Technical and experimental triplicates were performed for all experiments.

Pernarella M., Piovesana R., Matera C., Faroni A., Fiore M., Dini L., Reid A.J., Dallanoce C, & Tata A.M. (2020). Effects mediated by the α7 nicotinic acetylcholine receptor on cell proliferation and migration in rat adipose-derived stem cells. European Journal of Histochemistry : EJH, 64(Suppl 2), 3159.

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Selective M2 mAChR Agonist Assay

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M2 mAChR agonist, arecaidine propargyl ester hydrobromide (APE; Sigma-Aldrich), was used at different concentrations (from 25 to 100 µM). The APE selectivity for M2 receptor was confirmed by pharmacological binding experiments using different mAChR antagonists. 15, (link)20 (link) mAChR antagonists were used at the final concentration of 10 -6 M for Gallamine (M2 antagonist; CliniSciences), 10 -7 M for Pirenzepine (M1 antagonist; Sigma-Aldrich), and 10 -8 M for 4-DAMP (M3-M5 antagonist; Sigma-Aldrich). 15 (link) The cells were preincubated for 2 h with the antagonists before APE treatment. Cell lines were also treated with Muscarine chloride hydrate (Sigma-Aldrich) an agonist of all mAChRs, at the final concentration of 100 µM, according to previous studies. 21 (link)

Taggi M., Kovacevic A., Capponi C., Falcinelli M., Cacciamani V., Vicini E., Canipari R, & Tata A.M. (2022). The activation of M2 muscarinic receptor inhibits cell growth and survival in human epithelial ovarian carcinoma. Journal of cellular biochemistry, 123(9).

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M2 Receptor Activation and Muscarinic Antagonism

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The cells were treated with M2 muscarinic receptor agonist, Arecaidine Propargyl Ester hydrobromide (APE, Sigma-Aldrich, St. Louis, MO, USA) at the final concentration of 100µM.
The APE selectivity for M2 receptors was largely confirmed by siRNA transfection for M2 receptors and by pharmacological binding experiments (Alessandrini et al, 2015) . According previous experiments, muscarinic antagonists were used at the final concentration of 10 -7 M for Methoctramine (M2 antagonist, Sigma-Aldrich, St. Louis, MO, USA), 10 -7 M for Pirenzepine (M1 antagonist Sigma-Aldrich, St. Louis, MO, USA) and 10 -8 M for 4-DAMP (M3 antagonist Sigma-Aldrich, St. Louis, MO, USA), (Ferretti et al, 2013 , Alessandrini et al, 2015) . The cells were treated with muscarinic receptor antagonist 2h before APE treatment.

Piovesana R., Melfi S., Fiore M., Magnaghi V, & Tata A.M. (2018). M2 muscarinic receptor activation inhibits cell proliferation and migration of rat adipose-mesenchymal stem cells. Journal of cellular physiology, 233(7).

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