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(±)-Anatoxin A fumarate

Nicotinic agonist CAS# 1219922-30-1

(±)-Anatoxin A fumarate

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Chemical structure

(±)-Anatoxin A fumarate

3D structure

Chemical Properties of (±)-Anatoxin A fumarate

Cas No. 1219922-30-1 SDF Download SDF
PubChem ID 45073416 Appearance Powder
Formula C14H19NO5 M.Wt 281.31
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 50 mM in water
Chemical Name 1-(9-azabicyclo[4.2.1]non-2-en-2-yl)ethanone;(E)-but-2-enedioic acid
SMILES CC(=O)C1=CCCC2CCC1N2.C(=CC(=O)O)C(=O)O
Standard InChIKey ZJSIFVODFDHYJU-WLHGVMLRSA-N
Standard InChI InChI=1S/C10H15NO.C4H4O4/c1-7(12)9-4-2-3-8-5-6-10(9)11-8;5-3(6)1-2-4(7)8/h4,8,10-11H,2-3,5-6H2,1H3;1-2H,(H,5,6)(H,7,8)/b;2-1+
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 (±)-Anatoxin A fumarate

DescriptionA potent nicotinic agonist (Ki values are 1.25 and 1840 nM for α4β2 and α7 nicotinic receptors respectively). Stimulates [3H]-dopamine release from rat striatal synaptosomes (EC50 = 136 nM).

(±)-Anatoxin A fumarate Dilution Calculator

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Preparing Stock Solutions of (±)-Anatoxin A fumarate

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.5548 mL 17.774 mL 35.548 mL 71.0959 mL 88.8699 mL
5 mM 0.711 mL 3.5548 mL 7.1096 mL 14.2192 mL 17.774 mL
10 mM 0.3555 mL 1.7774 mL 3.5548 mL 7.1096 mL 8.887 mL
50 mM 0.0711 mL 0.3555 mL 0.711 mL 1.4219 mL 1.7774 mL
100 mM 0.0355 mL 0.1777 mL 0.3555 mL 0.711 mL 0.8887 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 (±)-Anatoxin A fumarate

UB-165: a novel nicotinic agonist with subtype selectivity implicates the alpha4beta2* subtype in the modulation of dopamine release from rat striatal synaptosomes.[Pubmed:10751429]

J Neurosci. 2000 Apr 15;20(8):2783-91.

Presynaptic nicotinic acetylcholine receptors (nAChRs) on striatal synaptosomes stimulate dopamine release. Partial inhibition by the alpha3beta2-selective alpha-conotoxin-MII indicates heterogeneity of presynaptic nAChRs on dopamine terminals. We have used this alpha-conotoxin and UB-165, a novel hybrid of epibatidine and anatoxin-a, to address the hypothesis that the alpha-conotoxin-MII-insensitive subtype is composed of alpha4 and beta2 subunits. UB-165 shows intermediate potency, compared with the parent molecules, at alpha4beta2* and alpha3-containing binding sites, and resembles epibatidine in its high discrimination of these sites over alpha7-type and muscle binding sites. (+/-)-Epibatidine, (+/-)-anatoxin-a, and (+/-)-UB-165 stimulated [(3)H]-dopamine release from striatal synaptosomes with EC(50) values of 2.4, 134, and 88 nM, and relative efficacies of 1:0.4:0.2, respectively. alpha-Conotoxin-MII inhibited release evoked by these agonists by 48, 56, and 88%, respectively, suggesting that (+/-)-UB-165 is a very poor agonist at the alpha-conotoxin-MII-insensitive nAChR subtype. In assays of (86)Rb(+) efflux from thalamic synaptosomes, a model of an alpha4beta2* nAChR response, (+/-)-UB-165 was a very weak partial agonist; the low efficacy of (+/-)-UB-165 at alpha4beta2 nAChR was confirmed in Xenopus oocytes expressing various combinations of human nAChR subunits. In contrast, (+/-)-UB-165 and (+/-)-anatoxin-a were similarly efficacious and similarly sensitive to alpha-conotoxin-MII in increasing intracellular Ca(2+) in SH-SY5Y cells, a functional assay for native alpha3-containing nAChR. These data support the involvement of alpha4beta2* nAChR in the presynaptic modulation of striatal dopamine release and illustrate the utility of exploiting a novel partial agonist, together with a selective antagonist, to dissect the functional roles of nAChR subtypes in the brain.

(+)-Anatoxin-a is a potent agonist at neuronal nicotinic acetylcholine receptors.[Pubmed:8492133]

J Neurochem. 1993 Jun;60(6):2308-11.

The effects of the nicotinic agonist (+)-anatoxin-a have been examined in four different preparations, representing at least two classes of neuronal nicotinic receptors. (+)-Anatoxin-a was most potent (EC50 = 48 nM) in stimulating 86Rb+ influx into M10 cells, which express the nicotinic receptor subtype comprising alpha 4 and beta 2 subunits. A presynaptic nicotinic receptor mediating acetylcholine release from hippocampal synaptosomes was similarly sensitive to (+)-anatoxin-a (EC50 = 140 nM). alpha-Bungarotoxin-sensitive neuronal nicotinic receptors, studied using patch-clamp recording techniques, required slightly higher concentrations of this alkaloid for activation: Nicotinic currents in hippocampal neurons were activated by (+)-anatoxin-a with an EC50 of 3.9 microM, whereas alpha 7 homooligomers reconstituted in Xenopus oocytes yielded an EC50 value of 0.58 microM for (+)-anatoxin-a. In these diverse preparations, (+)-anatoxin-a was between three and 50 times more potent than (-)-nicotine and approximately 20 times more potent than acetylcholine, making it the most efficacious nicotinic agonist thus far described.

Induced release of acetylcholine from guinea pig ileum longitudinal muscle-myenteric plexus by anatoxin-a.[Pubmed:1469655]

J Pharmacol Exp Ther. 1992 Dec;263(3):997-1002.

Anatoxin-a (ANTX), a nicotinic agonist, has been shown to induce contraction of guinea pig ileum, which was abrogated by the muscarinic antagonist atropine and the nicotinic antagonists tubocurarine and hexamethonium. We showed here that the ganglionic nicotinic antagonist mecamylamine was a better inhibitor of the contraction of ileum induced by ANTX. The sodium channel blocker tetrodotoxin also abolished ANTX-induced contraction. In contrast, alpha-bungarotoxin, the muscle type nicotinic receptor blocker, had no effect on ANTX-induced contraction of guinea pig ileum. Longitudinal muscle-myenteric plexus prepared from guinea pig ileum, labeled with [3H]choline and then incubated with ANTX was shown for the first time to release [3H]acetylcholine (ACh) in a dose-dependent manner. Pretreatment of longitudinal muscle-myenteric plexus with tubocurarine, hexamethonium or mecamylamine blocked ANTX-induced release of [3H]ACh. In contrast, atropine was without effect. Mecamylamine was the most potent antagonist. As observed in ileum contraction, tetrodotoxin completely and potently blocked the release of [3H]ACh induced by ANTX. Neither alpha-bungarotoxin nor the neuromuscular junction blockers conotoxin G1 or M1 could inhibit the [3H]ACh release. Taken together, these results suggested that ANTX activated nicotinic receptors on ganglionic interneurons to trigger a release of ACh, which next stimulated muscarinic receptors and induced ileum contraction.

Behavioural effects of anatoxin, a potent nicotinic agonist, in rats.[Pubmed:1630597]

Neuropharmacology. 1992 Mar;31(3):311-4.

Preliminary behavioural studies with the nicotinic agonist (+)-anatoxin have been carried with procedures sensitive to (-)-nicotine. In experimentally naive rats, (+)-anatoxin decreased locomotor activity; this effect resembled that of (-)-nicotine, but it was not blocked by mecamylamine. In nicotine-tolerant rats, (+)-anatoxin differed from (-)-nicotine because it did not increase locomotion. However, in rats trained to discriminate nicotine from saline in an operant conditioning procedure, (+)-anatoxin produced a partial nicotine-like discriminative stimulus effect that was blocked by mecamylamine, and a decreased rate of responding that was insensitive to mecamylamine. The behavioural profile of (+)-anatoxin differs from that of (-)-nicotine and it can be used for further investigations of CNS nicotinic receptors.

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