Arecaidine-propargyl ester
Arecaidine-propargyl ester is a selective M2 muscarinic receptor agonist with blood-brain barrier permeability, with a pKi of 5.91 for hm1, 7.06 for hm2, 6.07 for hm3, 6.01 for hm4, and 6.03 for hm5. Arecaidine-propargyl ester stimulates central and peripheral muscarinic receptors. Arecaidine-propargyl ester increases intracellular ROS, induces DNA damage and Apoptosis, and upregulates the expression of MnSOD and SIRT1. Arecaidine-propargyl ester reduces sympathetic nerve outflow, induces dose-dependent hypotension, and triggers negative chronotropic effects at high peripheral doses. Arecaidine-propargyl ester can be used in research related to Alzheimer's disease and glioblastoma.
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- CAS. Nr.: 35516-99-5
- Formel: C10H13NO2
- Molecular Weight:179.22
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
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mAChR1 5.91 (pKi) |
mAChR2 7.06 (pKi) |
mAChR3 6.07 (pKi) |
mAChR4 6.01 (pKi) |
mAChR5 6.03 (pKi) |
SIRT1 |
Arecaidine-propargyl ester (0.01-1000 mM; 120 min) binds to cloned hm1, hm2, hm3, hm4, and hm5 muscarinic receptors expressed in CHO cells, with pKi values ranging from 5.91 to 7.06[2].
Arecaidine-propargyl ester (25-100 μM; 2 h) induces significant intracellular ROS production in glioblastoma cell lines U251MG and U87MG, and this effect is completely blocked by the ROS scavenger NAC[3].
Arecaidine-propargyl ester (100 μM; 72 h) induces significant apoptosis and reduces cell numbers in human glioblastoma cell lines U251MG and U87MG, with a stronger apoptotic effect on U251MG cells. Both of these effects are abrogated by the ROS scavenger NAC[3].
Arecaidine-propargyl ester (100 μM; 24-48 h) significantly upregulates the expression of SIRT1 protein in glioblastoma U251MG and U87MG cells in a time-dependent manner in vitro[3].
Arecaidine-propargyl ester (100 μM; 24-48 h) significantly upregulates the expression of MnSOD protein in U251MG and U87MG glioblastoma cells in a time-dependent manner[3].
Arecaidine-propargyl ester (100 μM; 24-48 h) significantly upregulates the mRNA expression level of Gadd45α in glioblastoma cell lines U251MG and U87MG[3].
Arecaidine-propargyl ester (100 μM; 24 h) increases total glutathione levels by 50% in U251MG glioblastoma cells, whereas no significant metabolic changes are detected in U87MG cells[3].
Arecaidine-propargyl ester (100 μM; 24-48 h) induces DNA double-strand breaks (detected by γ-H2AX positive rate) in glioblastoma cell lines U251MG and U87MG, and this effect depends on the activation of M2 muscarinic receptors in U251MG cells[3].
Arecaidine-propargyl ester (50-100 μM; 24 h) induces significant chromosomal aberrations in glioblastoma U251MG and U87MG cells; among them, U251MG cells exhibit higher sensitivity at 50 μM, and only U251MG cells show a significant increase in sister chromatid exchange levels at 50 μM[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:U251MG, U87MG human glioblastoma cell lines
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Concentration:100 μM
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Incubation Time:72 h
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Result:Increased the apoptotic index in U87MG cells and U251MG cells.
Significantly reduced the apoptotic index in both cell lines, returning levels near control values when co-treated with 5 μM NAC.
Caused a significant decrease in cell number in both lines, an effect reversed by co-treatment with NAC.
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Cell Line:U251MG, U87MG human glioblastoma cell lines
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Concentration:100 μM
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Incubation Time:24 h, 30 h, 48 h
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Result:Caused a significant increase in Gadd45α mRNA expression in both cell lines.
Increased Gadd45α/18S ratios in U87MG cells.
Increased Gadd45α/18S ratios in U251MG cells.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:either sex, weight 2-4 kg (anaesthetized for cardiovascular function monitoring)[1]
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Dosage:1.0 × 10-9 moles/kg (vertebral artery); 1.4 × 10-9 moles/kg (femoral vein)
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Administration:left vertebral artery; femoral vein
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Result:Caused dose-dependent reduction in mean arterial pressure (intravenous), which was blocked by intravenous methylatropine (300 μg/kg) but not centrally administered atropine (30 μg/kg) or D-benzethimide (10 μg/kg).
Caused dose-dependent reduction in mean arterial pressure (vertebral artery), which was not blocked by intravenous methylatropine (300 μg/kg) but was blocked by vertebral artery-administered atropine (50 μg/kg) or D-benzethimide (10 μg/kg).
Did not alter heart rate with central administration; only relatively high intravenous doses caused a decrease in cardiac frequency.
Exhibited ED-25 of 1.0 × 10-9 moles/kg via vertebral artery and 1.4 × 10-9 moles/kg via femoral vein.
Chemical Information
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CAS. Nr. 35516-99-5
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Molecular Weight 179.22
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Formel C10H13NO2
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SMILES
O=C(C1=CCCN(C1)C)OCC#C
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[1]. Porsius AJ, et al. Central action of some cholinergic drugs (arecaidine esters) and nicotine on blood pressure and heart rate of cats. Prog Brain Res. 1977;47:131-5. [Content Brief]
[2]. Scapecchi S, et al. Highly chiral muscarinic ligands: the discovery of (2S,2'R,3'S,5'R)-1-methyl-2-(2-methyl-1,3-oxathiolan-5-yl)pyrrolidine 3-sulfoxide methyl iodide, a potent, functionally selective, M2 partial agonist. J Med Chem. 2006 Mar 23;49(6):1925-31. [Content Brief]
[3]. Di Bari M, et al. Cytotoxic and genotoxic effects mediated by M2 muscarinic receptor activation in human glioblastoma cells. Neurochem Int. 2015;90:261-270. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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