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Arecaidine propargyl ester tosylate

Muscarinic agonist CAS# 147202-94-6

Arecaidine propargyl ester tosylate

Catalog No. BCC6628----Order now to get a substantial discount!

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Chemical structure

Arecaidine propargyl ester tosylate

3D structure

Chemical Properties of Arecaidine propargyl ester tosylate

Cas No. 147202-94-6 SDF Download SDF
PubChem ID 6604936 Appearance Powder
Formula C17H21NO5S M.Wt 351.42
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in water
Chemical Name 4-methylbenzenesulfonic acid;prop-2-ynyl 1-methyl-3,6-dihydro-2H-pyridine-5-carboxylate
SMILES CC1=CC=C(C=C1)S(=O)(=O)O.CN1CCC=C(C1)C(=O)OCC#C
Standard InChIKey LYHWIOMAWPVTPI-UHFFFAOYSA-N
Standard InChI InChI=1S/C10H13NO2.C7H8O3S/c1-3-7-13-10(12)9-5-4-6-11(2)8-9;1-6-2-4-7(5-3-6)11(8,9)10/h1,5H,4,6-8H2,2H3;2-5H,1H3,(H,8,9,10)
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Arecaidine propargyl ester tosylate

DescriptionA potent muscarinic receptor agonist. Shows some selectivity for cardiac versus ileal M2 receptors.

Arecaidine propargyl ester tosylate Dilution Calculator

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Arecaidine propargyl ester tosylate Molarity Calculator

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Preparing Stock Solutions of Arecaidine propargyl ester tosylate

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.8456 mL 14.228 mL 28.456 mL 56.912 mL 71.1399 mL
5 mM 0.5691 mL 2.8456 mL 5.6912 mL 11.3824 mL 14.228 mL
10 mM 0.2846 mL 1.4228 mL 2.8456 mL 5.6912 mL 7.114 mL
50 mM 0.0569 mL 0.2846 mL 0.5691 mL 1.1382 mL 1.4228 mL
100 mM 0.0285 mL 0.1423 mL 0.2846 mL 0.5691 mL 0.7114 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Arecaidine propargyl ester tosylate

Striatal muscarinic receptors promote activity dependence of dopamine transmission via distinct receptor subtypes on cholinergic interneurons in ventral versus dorsal striatum.[Pubmed:20203199]

J Neurosci. 2010 Mar 3;30(9):3398-408.

Striatal dopamine (DA) and acetylcholine (ACh) regulate motivated behaviors and striatal plasticity. Interactions between these neurotransmitters may be important, through synchronous changes in parent neuron activities and reciprocal presynaptic regulation of release. How DA signaling is regulated by striatal muscarinic receptors (mAChRs) is unresolved; contradictory reports indicate suppression or facilitation, implicating several mAChR subtypes on various neurons. We investigated whether mAChR regulation of DA signaling varies with presynaptic activity and identified the mAChRs responsible in sensorimotor- versus limbic-associated striatum. We detected DA in real time at carbon fiber microelectrodes in mouse striatal slices. Broad-spectrum mAChR agonists [oxotremorine-M, APET (Arecaidine propargyl ester tosylate)] decreased DA release evoked by low-frequency stimuli (1-10 Hz, four pulses) but increased the sensitivity of DA release to presynaptic activity, even enhancing release by high frequencies (e.g., >25 Hz for four pulses). These bidirectional effects depended on ACh input to striatal nicotinic receptors (nAChRs) on DA axons but not GABA or glutamate input. In caudate-putamen (CPu), knock-out of M(2)- or M(4)-mAChRs (not M(5)) prevented mAChR control of DA, indicating that M(2)- and M(4)-mAChRs are required. In nucleus accumbens (NAc) core or shell, mAChR function was prevented in M(4)-knock-outs, but not M(2)- or M(5)-knock-outs. These data indicate that striatal mAChRs, by inhibiting ACh release from cholinergic interneurons and thus modifying nAChR activity, offer variable control of DA release probability that promotes how DA release reflects activation of dopaminergic axons. Furthermore, different coupling of striatal M(2)/M(4)-mAChRs to the control of DA release in CPu versus NAc suggests targets to influence DA/ACh function differentially between striatal domains.

The relative potencies of some agonists at M2 muscarinic receptors in guinea-pig ileum, atria and bronchi.[Pubmed:3896364]

Br J Pharmacol. 1985 Jun;85(2):437-40.

The effects of some agonists on isolated preparations of guinea-pig ileum, atria and bronchial muscle have been compared with those of carbachol. The concentrations producing comparable responses were used to estimate the equipotent molar ratio relative to carbachol. Arecaidine propargyl ester was 4 to 5 times as active as carbachol on the ileum but more than 10 times as active as carbachol on atrial rate or atrial force, so the results confirm that this compound has a 2 to 3 fold selectivity for receptors in atria. Ethoxyethyltrimethylammonium iodide was one-quarter to one-third as active as carbachol on ileum but only one-tenth as active as carbachol on atrial rate or atrial force and so shows a 3 to 4 fold selectivity for receptors in ileum. The other compounds tested, which included acetylcholine, methacholine, n-pentyltrimethyl-ammonium iodide and bethanechol showed less selectivity. There were no obvious differences between effects on atrial rate and effects on atrial force, though with esters it was often difficult to obtain effects on atrial rate in the absence of an inhibitor of cholinesterase. Activity on bronchial muscle was generally similar to activity on ileum.

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