Anisodine hydrobromideCAS# 76822-34-9 |
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| Cas No. | 76822-34-9 | SDF | Download SDF |
| PubChem ID | 134688123 | Appearance | White powder |
| Formula | C17H22BrNO5 | M.Wt | 400.3 |
| Type of Compound | Nitrogen-containing Compounds | Storage | Desiccate at -20°C |
| Synonyms | Daturamine hydrobromide; α-Hydroxyscopolamine hydrobromide | ||
| Solubility | Soluble in methanol and water | ||
| Chemical Name | [(1R,2R,4S,5S)-9-methyl-3-oxa-9-azatricyclo[3.3.1.02,4]nonan-7-yl] 2,3-dihydroxy-2-phenylpropanoate;hydrobromide | ||
| SMILES | CN1C2CC(CC1C3C2O3)OC(=O)C(CO)(C4=CC=CC=C4)O.Br | ||
| Standard InChIKey | GJPDCORRBGIJOP-BVNVJSNWSA-N | ||
| Standard InChI | InChI=1S/C17H21NO5.BrH/c1-18-12-7-11(8-13(18)15-14(12)23-15)22-16(20)17(21,9-19)10-5-3-2-4-6-10;/h2-6,11-15,19,21H,7-9H2,1H3;1H/t11?,12-,13+,14-,15+,17?; | ||
| 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. |
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| 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. |
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| 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. | ||
Anisodine hydrobromide Dilution Calculator
Anisodine hydrobromide Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.4981 mL | 12.4906 mL | 24.9813 mL | 49.9625 mL | 62.4532 mL |
| 5 mM | 0.4996 mL | 2.4981 mL | 4.9963 mL | 9.9925 mL | 12.4906 mL |
| 10 mM | 0.2498 mL | 1.2491 mL | 2.4981 mL | 4.9963 mL | 6.2453 mL |
| 50 mM | 0.05 mL | 0.2498 mL | 0.4996 mL | 0.9993 mL | 1.2491 mL |
| 100 mM | 0.025 mL | 0.1249 mL | 0.2498 mL | 0.4996 mL | 0.6245 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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Effects of Anisodine Hydrobromide on the Cardiovascular and Respiratory Functions in Conscious Dogs.[Pubmed:33116414]
Drug Des Devel Ther. 2020 Oct 13;14:4263-4276.
Purpose: Anisodine hydrobromide (Ani) is isolated from the medicinal plant Anisodus tanguticus (Maxim.) Pascher for clinical use. Although considerable research regarding Ani has been reported, the safety profiles of Ani are currently unknown. This study investigated the cardiorespiratory effects of Ani in conscious dogs to provide clinicians a detailed safety profile of Ani on the cardiorespiratory system. Materials and Methods: Using the Latin square design, the study was divided into six phases, where in each phase, six telemetered beagle dogs received one dose of normal saline or sotalol hydrochloride or Ani (0.1, 0.4, 1.6, or 6.4 mg/kg). Electrocardiogram, blood pressure (BP) and respiratory parameters were collected before and after administration for 24 hours. Statistical comparisons were performed at scheduled time-points. Results: The heart rate was significantly increased, PR and QTCV intervals were significantly shortened in Ani 0.4, 1.6, 6.4 mg/kg treatment group after drug administration. Compared with the saline group, a significant increase in heart rate and shortening of PR, QTCV intervals were observed in the Ani 1.6, 6.4 mg/kg treatment groups from 5 min to 4 h time-points. Diastolic and mean BP were significantly increased in Ani 1.6, 6.4 mg/kg from 1 h to 2 h time-points compared to those of the saline control. Accelerated breathing was observed in the first 20 min after Ani 0.4, 1.6, and 6.4 mg/kg treatment, although not statistically significant. Furthermore, no significant differences were observed in any of the corresponding indexes of Ani 0.1 mg/kg treatment group at different time-points compared to those of the saline group. Conclusion: Ani may have adverse effects on the cardio-respiratory systems of dogs at doses above 0.4 mg/kg, whereas Ani 0.1 mg/kg was devoid of potentially deleterious effects on cardiorespiratory function.
Low Dose of Anisodine Hydrobromide Induced Neuroprotective Effects in Chronic Cerebral Hypoperfusion Rats.[Pubmed:29076436]
CNS Neurol Disord Drug Targets. 2017;16(10):1111-1119.
BACKGROUND: Chronic cerebral hypoperfusion is a common pathophysiological state in various cerebrovascular diseases. Anisodine has been reported to exert neuroprotective effects in cerebral ischemia/reperfusion (I/R) animal model. However, it is unclear whether Anisodine hydrobromide, the hydrobromide format of anisodine, one of the tropic alkanes alkaloids, exhibits the same neuroprotective effect on chronic cerebral hypoperfusion(CCH) rats. Herein, we tried to unravel these issues. METHODS: CCH model in adult male Sprague-Dawley rats was established by permanent ligation of the bilateral common carotid arteries [two-vessel occlusion (2-VO)] surgery. Rats were randomly divided into six groups: sham, 2-VO, 2-VO + Butyl phthalide and sodium chloride injection (NBP, as positive control group), 2-VO + Anisodine hydrobromide (AH)1.2mg/kg, 2-VO +AH0.6mg/kg, 2-VO +AH0.3mg/kg. Cognitive behavior was examined by Morris Water Maze Test. Neuronal survival and apoptosis were evaluated by Nissl staining and Terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL staining). The relative monoamine neurotransmitter (5-hydroxytryptamine (5-HT), norepinephrine (NA)), the content of Ach, the activity of acetylcholin esterase (AchE) were measured in cholinergic system, and the protein expressions of Bcl-2, Bax, p-Akt and p-GSK-3betawere detected by Western blot assay. RESULTS: The results showed that there is significant memory impairment and a remarkable neuron necrosis and apoptosis, along with the dysfunction of the neurotransmitter systems and central cholinergic system in CCH rats. AH treatment could significantly improve cognitive deficits, while reducing neuron necrosis and apoptosis, apart from increasing the content of 5-HT and decreasing the activity of AchE markedly. Further study revealed that AH could promote the protein expression of Bcl-2, phosphorylation of Akt and GSK-3beta, and downregulate the protein of Bax. CONCLUSION: AH was demonstrated to ameliorate memory deficits by revising the imbalance of the monoamine neurotransmitter and cholinergic dysfunction. Moreover, AH can attenuate neuronal cell death and apoptosis by activating the Akt/GSK-3betasignaling pathway.
