Factory Supply High Quality Scopolamine 99% Solid CAS 51-34-3

Bioactivity of scopolamine
Description Scopolamine is a high-affinity (nM level) muscarinic antagonist. Scopolamine reversibly inhibited 5-HT3 receptor response with IC50 of 2.09 μM.
Related category
Signaling Pathway >> G protein-coupled receptors /G proteins >> 5-HT receptors
Signaling Pathways >> Neural Signaling Pathways >> 5-HT receptors
Signaling Pathway >> G Protein-coupled receptors /G proteins >> mAChR
Signaling Pathways >> Neural Signaling Pathways >> mAChR
Natural Products >> Alkaloids
Research Areas >> Neurological diseases
Target point
5-HT3 Receptor:2.09 μM (IC50)

mAChR

In vitro studies of the application of scopolamine to oocytes expressing 5-HT3 receptors did not cause a response when administered alone, but caused a concentration-dependent inhibition of response during co-administration of 2μM5-HT. The pIC50 value of scopolamine was 5.68±0.05(IC50 =2.09μM,n = 6), and the Hill slope was 1.06±0.05. This gives a Kb of 3.23μM. The same concentration-dependent effect was observed when scopolamine was administered during 5-HT application. To further test the competitive binding of 5-HT3 receptors, competition of unlabeled scopolamine was measured with [3H] granisetron, an established high-affinity competitive antagonist on these receptors. Scopolamine showed dose-dependent competition with 0.6 nM [3H] granisetron (~Kd), with a mean pKi of 5.17±0.24(Ki =6.76μM,n = 3)[1].
In vivo studies In histopathological studies, there are no significant changes in the histology of the brain. However, a decrease in hippocampal cell density was observed in control mice pretreated with scopolamine only in distilled water [2]. Compared with the normal group (3.06±0.296), the acetyl cholinesterase (AchE) activity was significantly increased by using scopolamine alone (7.98±0.065; P <0.001). Animals treated with scopolamine reported a significant increase in malondialdehyde (MDA) levels compared to the normal group (12.82±2.86) (34.61±4.85; P <0.01). Compared with the normal group (0.3906±0.02), the level of reduced glutathione (GSH) in the scopolamine treated group was significantly decreased (P <0.001; 0.1504±0.03). Compared with the normal group (43.21±3.46), scopolamine treated rats showed significantly increased concentrations of amyloid beta (Aβ1-42) (P <0.001; 146.2±1.74)[3].
The kinase assay measured the saturation binding (8-point) curve by incubating a crude extract or guinea pig membrane formulation of HEK 293 cells with a stable expression of the 5-HT3 receptor in a 0.5mL culture containing a 10 mm HEPES buffer (pH7.4) and 0.1 to 1nM. 3H] granisetron or 1-10nM [3H] n-methyl-cyclopropylamine. Competitive binding was determined by incubating the same receptor formulation in 0.5mL HEPES buffer containing 0.6nM [3H] granisetron or 0.6nM [3H] N-methylcyclopropylamine and different concentrations of competing ligand (10 points). Nonspecific binding was determined with 1mM quinoperidine or 10μM scopolamine, respectively. Incubation was terminated by filtration to a Whatman GF/B filter moistened with HEPES buffer + 0.3% polyvinylimide, and then washed quickly twice with cold HEPES buffer. The protein concentration was calculated using the Lowry protein assay with bovine serum albumin standard. Radioactivity was measured using the Tri-Carb 2100 TR scintillation counter [1].
Animal experimental mice [2] were weighed, labeled, and divided into 7 groups with 5 animals in each group. After that, all the animals were injected with 3mg/kg scopolamine in advance peritoneum. Groups 1-3 were given 0.2mL equivalent doses of 4mg/kg, 6mg/kg and 8mg/kg of Morinda officinalis extract, while groups 4-6 were given the same dose of ustilago officinalis extract and group 7 was given 0.2. Distilled water for 3 consecutive days (negative control). Rats [3] Healthy male Wistar rats weighing 180-200g (12 months old) were used in this study. The rats were divided into 5 groups (n = 6 / group). Group I- normal control, group II- disease control (scopolamine hydrobromide 3mg/kg, ip), group III- scopolamine + quercetin (25mg/kg, po), group IV- standard treatment (scopolamine + Donepezil hydrochloride 3mg/kg, po) and V-scopolamine + quercetin (25mg/kg, Po) Oral) + Donepezil (3mg/kg orally). Rats in groups III, IV, and V were given their respective drugs at 24 hour intervals for 14 consecutive days. The collection routes of Morris water maze, elevated maze, and passive avoidance paradigms were performed on day 14, and scopolamine (3 mg/kg, ip) was administered on day 14 after collection to all groups causing cognitive impairment in rats except normal controls. Memory retention was tested on day 15, and on the same day, the rats were killed and brain tissue was isolated to estimate acetylcholinesterase (AchE) and brain oxidative stress markers such as lipid peroxidase (LPO), glutathione (GSH) (reduced)). ELISA kits are used to estimate amyloid beta (Aβ1-42) levels. The hippocampus of rats was dissected and its histopathological changes were studied.
reference
[1]. Lochner M, et al. The muscarinic antagonists Scopolamine and atropine are competitive antagonists at 5-HT3 receptors. Neuropharmacology. 2016 Sep; 108:220-8.

[2]. O ET, et al. COGNITIVE-ENHANCING PROPERTIES OF MORINDA LUCIDA (RUBIACEAE) AND PELTOPHORUM PTEROCARPUM (FABACEAE) IN SCOPOLAMINE-INDUCED AMNESIC MICE. Afr J Tradit Complement Altern Med. 2017 Mar 1; 14 (3) : 136-141.

[3]. Pattanashetti LA, et al. Evaluation of neuroprotective effect of Quercetin with Donepezil in Scopolamine-induced amnesia in rats. Indian J Pharmacol. 2017 Jan-Feb; 49 (1) : 60-64.

Physical and chemical properties of scopolamine
Density 1.3± 0.1g /cm3
Boiling point 460.3±45.0 °C at 760 mmHg
Melting point 59ºC
Molecular formula C17H21NO4
Molecular weight 303.353
Flash point 232.2±28.7 °C
Accurate mass 303.147064
PSA 62.30000
LogP 0.76
Vapor pressure 0.0±1.2 mmHg at 25°C
Refractive index 1.614
Storage conditions Warehouse low temperature, ventilation, dry