- Muscarinic acetylcholine receptors [1]
- 5-HT3 receptors (pKi = 6.3) [1]

When applied alone, scopolane does not elicit a response from oocytes expressing 5-HT3 receptors. However, when 2 μM 5-HT is also applied concurrently, the reaction is concentration-dependently inhibited. Scopolamine's pIC50 value is 5.68±0.05 (IC50=2.09 μM, n=6), and its hill slope is 1.06 ± 0.05. The resulting Kb was 3.23 μM. When Scopolamine is delivered during the 5-HT administration, the same concentration-dependent impact is observed. The competitiveness of unlabeled Scopolamine is evaluated with [3H]granisetron, a proven high-affinity competitive antagonist at these receptors, in order to further investigate a potential competitive binding to the 5-HT3 receptor. With 0.6 nM [3H]granisetron (~ Kd), scopolamine exhibits concentration-dependent competition, resulting in an average pKi of 5.17±0.24 (Ki=6.76 μM, n=3)[1].

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Antagonism at 5-HT3 receptors: Scopolamine acts as a competitive antagonist at 5-HT3 receptors. In radioligand binding assays with [3H]granisetron, it inhibits binding to 5-HT3 receptors in a concentration-dependent manner. In functional assays using cells expressing human 5-HT3A receptors, it antagonizes 5-HT-induced inward currents, with the antagonism being surmountable, indicating competitive interaction [1]

The histology of the brain has not changed much in the histopathology investigation. On the other hand, it is noted that the control mice given Scopolamine and given only distilled water showed a decrease in cell density in their hippocampal regions[2]. When compared to the normal group (3.06±0.296), the administration of Scopolamine alone significantly enhances the activity of the Acetylcholinesterase enzyme (AchE) (7.98±0.065; P<0.001). Malondialdehyde (MDA) levels in the Scopolamine-treated rats are significantly higher (34.61±4.85; P<0.01) than in the control group (12.82±2.86). Compared to the normal group (0.3906±0.02), the scopolamine-treated group exhibits a significant drop in reduced glutathione (GSH) levels (P<0.001; 0.1504±0.03). The concentration of β amyloid (Aβ1-42) in the rats treated with Scopolamine is significantly higher (P<0.001; 146.2±1.74) than in the control group (43.21±3.46)[3].

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- Inducing amnesia: Administration of Scopolamine (1 mg/kg, i.p.) to mice induces amnesia, as evidenced by impaired performance in the Y-maze test (reduced spontaneous alternation behavior) and the elevated plus maze test (decreased transfer latency). This amnesic effect is associated with cholinergic dysfunction [2]
- Impairing memory in rats: Scopolamine (1 mg/kg, i.p.) administration to rats impairs memory, as shown by decreased performance in the Morris water maze test (increased escape latency and reduced time spent in the target quadrant) and the elevated plus maze test (increased transfer latency). The memory impairment is linked to reduced acetylcholine levels in the brain [3]

- Radioligand binding assay for 5-HT3 receptors: Membranes from cells expressing 5-HT3 receptors are incubated with [3H]granisetron in the presence of various concentrations of Scopolamine. After incubation, the mixture is filtered to separate bound and free ligand, and the radioactivity of the bound ligand is measured. The data are used to determine the inhibition constant (pKi) [1]
- Functional assay for 5-HT3 receptor antagonism: Cells expressing human 5-HT3A receptors are voltage-clamped using patch-clamp techniques. 5-HT is applied to induce inward currents, and the effect of Scopolamine on these currents is evaluated by co-applying Scopolamine with different concentrations of 5-HT. The concentration-response curves are analyzed to determine the nature of antagonism [1]

- Amnesia induction in mice: Mice are divided into groups, with one group receiving Scopolamine (1 mg/kg, i.p.) 30 minutes before behavioral tests. The Y-maze test is conducted to assess spontaneous alternation behavior, where mice are allowed to explore the maze for 5 minutes, and the alternation percentage is calculated. The elevated plus maze test is performed by placing mice on the open arm and measuring the transfer latency to move to the closed arm [2]
- Memory impairment in rats: Rats are administered Scopolamine (1 mg/kg, i.p.) 30 minutes prior to behavioral tests. The Morris water maze test is used, where rats are trained to find a hidden platform, and escape latency is recorded. On the probe day, the platform is removed, and the time spent in the target quadrant is measured. The elevated plus maze test is conducted by placing rats on the open arm, and transfer latency is recorded [3]

Absorption, Distribution and Excretion
The pharmacokinetics of scopolamine differ significantly across routes of administration. In healthy volunteers, after oral administration of 0.5 mg scopolamine, the peak plasma concentration (Cmax) was 0.54 ± 0.1 ng/mL, the time to peak concentration (tmax) was 23.5 ± 8.2 min, and the area under the curve (AUC) was 50.8 ± 1.76 ngmin/mL; the absolute bioavailability was low, only 13 ± 1%, likely due to first-pass metabolism. In contrast, after intravenous infusion of 0.5 mg scopolamine, 15 minutes later, the peak plasma concentration (Cmax) was 5.00 ± 0.43 ng/mL, the time to peak concentration (tmax) was 5.0 min, and the AUC was 369.4 ± 2.2 ngmin/mL. Other dosage forms have also been tested. Following subcutaneous injection of 0.4 mg scopolamine, the peak plasma concentration (Cmax) was 3.27 ng/mL, the time to peak concentration (tmax) was 14.6 min, and the area under the curve (AUC) was 158.2 ngmin/mL. Following intramuscular injection of 0.5 mg scopolamine, the peak plasma concentration (Cmax) was 0.96 ± 0.17 ng/mL, the time to peak concentration (tmax) was 18.5 ± 4.7 min, and the AUC was 81.3 ± 11.2 ngmin/mL. Intranasal administration resulted in rapid absorption; after 0.4 mg scopolamine, the peak plasma concentration (Cmax) was 1.68 ± 0.23 ng/mL, the time to peak concentration (tmax) was 2.2 ± 3 min, and the AUC was 167 ± 20 ngmin/mL. The bioavailability of scopolamine administered intranasally was also higher than that of oral scopolamine, at 83 ± 10%. Due to dose-dependent adverse reactions, a transdermal patch was developed to achieve therapeutic plasma concentrations over a longer period. Following patch application, scopolamine was detectable within 4 hours and reached peak concentration (tmax) within 24 hours. The mean plasma concentration was 87 pg/mL, and the total concentration of free and bound scopolamine reached 354 pg/mL. Following oral administration, approximately 2.6% of the unchanged scopolamine was excreted in the urine. In contrast, using the transdermal patch system, less than 10% of the total dose excreted in the urine over 108 hours (including unchanged scopolamine and its metabolites) was excreted. The amount of unchanged drug excreted was less than 5%. The volume of distribution of scopolamine has not been adequately characterized. The volume of distribution of 0.5 mg scopolamine administered intravenously was 141.3 ± 1.6 L 15 minutes later. The clearance rate of 0.5 mg scopolamine administered intravenously was 81.2 ± 1.55 L/h, while the clearance rate after subcutaneous injection was lower, at 0.14–0.17 L/h. Scopolamine hydrobromide is rapidly absorbed after intramuscular or subcutaneous injection. The drug is well absorbed in the gastrointestinal tract, primarily via the upper small intestine. Scopolamine can also be absorbed transdermally. After transdermal administration, scopolamine can be detected in plasma within 4 hours after applying a transdermal patch behind the ear, reaching peak concentrations on average within 24 hours. In a study of healthy individuals, the mean plasma concentrations of free and total (free plus bound) scopolamine were 87 pg/mL and 354 pg/mL, respectively, within 24 hours following a single topical application of the transdermal patch (releasing approximately 1 mg over 72 hours). /Scolophonamine hydrobromide/
In one subject, a peak concentration of approximately 2 ng/mL was reached within 1 hour after oral administration of 0.906 mg of scopolamine. Although commercially available transdermal patches contain 1.5 mg of scopolamine, this membrane-controlled diffusion system is designed to deliver approximately 1 mg of the drug into systemic circulation at a nearly constant rate over 72 hours. The initial dose of 0.14 mg of scopolamine is released from the system's adhesive layer at a controlled, gradually decreasing rate over 6 hours; subsequently, the remaining dose is released at a rate of approximately 5 μg/hour until the end of the system's remaining 66-hour effective duration. The manufacturer states that the initial starting dose saturates binding sites on the skin and rapidly brings plasma concentrations to steady state. A crossover study comparing urinary excretion rates of scopolamine in healthy subjects over multiple 12-hour collection intervals showed no difference in drug excretion rates between constant-rate intravenous infusion (3.7–6 μg/h) and transdermal administration at steady state (24–72 hours). Transdermal delivery systems appear to deliver the drug into systemic circulation at the same rate as constant-rate intravenous infusion; however, the relatively long collection intervals (12 hours) make precise interpretation of the data difficult. Scopolamine excretion rates via transdermal systems were higher than those via constant-rate intravenous infusion within 12–24 hours and 72 hours post-administration. The distribution of scopolamine is not fully understood. The drug appears to bind reversibly to plasma proteins. Given its central nervous system effects, scopolamine is apparently capable of crossing the blood-brain barrier. The drug has been reported to cross the placenta and distribute into breast milk. Although the metabolic and excretory pathways of scopolamine are not fully understood, it is believed that the drug is almost entirely metabolized in the liver (primarily through conjugation) and excreted in the urine. In one study, only a small amount (approximately 4-5%) of a single oral dose of scopolamine was excreted unchanged in the urine within 50 hours; the urinary clearance of the unchanged drug was approximately 120 ml/min. In another study, 3.4% and less than 1% of a single dose, administered subcutaneously or orally, were excreted unchanged in the urine within 72 hours, respectively. In healthy individuals, after a single application of transdermal scopolamine (releasing approximately 1 mg within 72 hours), the urinary excretion rates of free scopolamine and total scopolamine (free and conjugated forms) were approximately 0.7 μg/h and 3.8 μg/h, respectively. Following removal of the transdermal patch, the consumption of scopolamine bound to skin receptors at the patch site led to a logarithmic linear decrease in plasma scopolamine concentration. Within 108 hours, less than 10% of the total dose was excreted in the urine as unchanged drug and its metabolites.

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Metabolism/Metabolites
Although multiple metabolites have been detected in animal studies, little is known about the metabolism of scopolamine in humans. Generally, scopolamine is primarily metabolized in the liver, with the main metabolites being various glucuronides and sulfide conjugates. Although the enzymes responsible for scopolamine metabolism are not fully understood, in vitro studies have shown that oxidative demethylation is associated with CYP3A subfamily activity, and the pharmacokinetics of scopolamine are significantly altered when co-administered with grapefruit juice, suggesting that CYP3A4 is at least partially involved in oxidative demethylation.
Although the metabolic and excretion pathways of scopolamine are not fully understood, the drug is believed to be almost entirely metabolized in the liver (primarily through conjugation) and excreted in the urine.
Biological Half-Life
The half-life of scopolamine varies depending on the route of administration. The half-lives for intravenous, oral, and intramuscular administration are 68.7 ± 1.0 min, 63.7 ± 1.3 min, and 69.1 ± 8.0 min, respectively, and are similar. The half-life for subcutaneous administration is longer, at 213 min. After removal of the transdermal patch, plasma concentrations of scopolamine decrease logarithmically, with a half-life of 9.5 hours.
The mean elimination half-life of the drug after a single administration of the transdermal scopolamine system (releasing approximately 1 mg every 72 hours) is 9.5 hours.

Effects During Pregnancy and Lactation
◉ Overview of Use During Lactation
There is currently no information regarding the use of scopolamine during lactation. Use of scopolamine during labor appears to have an adverse effect on the newborn's breastfeeding behavior. Prolonged use of scopolamine may reduce milk production or the milk ejection reflex, but a single systemic or ocular dose is unlikely to interfere with breastfeeding. During prolonged use, observe for signs of reduced milk production (e.g., dissatisfaction, poor weight gain). To significantly reduce the amount of medication entering breast milk after using eye drops, press the tear duct at the corner of the eye for at least 1 minute, then wipe away any excess medication with absorbent tissue.
◉ Effects on Breastfed Infants
As of the revision date, no relevant published information was found.
◉ Effects on Lactation and Breast Milk
Anticholinergic drugs can inhibit lactation in animals, possibly by inhibiting the secretion of growth hormone and oxytocin. Anticholinergic drugs can also lower serum prolactin levels in non-lactating women. Prolactin levels in established lactating mothers may not affect their breastfeeding ability. A retrospective case-control study conducted in two hospitals in central Iran compared breastfeeding behavior in the first two hours postpartum in four groups of infants born to healthy, full-term, singleton vaginal deliveries. Groups included: no medication received during delivery, oxytocin combined with scopolamine, oxytocin combined with meperidine, and oxytocin, scopolamine, and meperidine. Infants in the no-medication group performed better than in all other groups, while the oxytocin combined with scopolamine group performed better than the meperidine group. Protein Binding: Scopolamine reversibly binds to human plasma proteins. In rats, the plasma protein binding rate of scopolamine is relatively low, at 30 ± 10%.

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Drug Interactions
Scholes should be used with caution in patients taking other medications that may cause central nervous system effects (e.g., sedatives, tranquilizers, or alcohol). Particular attention should be paid to potential interactions with medications that have anticholinergic properties; for example, other belladonna alkaloids, antihistamines (including meclomethasone), tricyclic antidepressants, and muscle relaxants.
Concomitant use of scopolamine may reduce the absorption of oral medications due to decreased gastric motility and delayed gastric emptying.
Concomitant use of anticholinergic drugs and corticosteroids may lead to increased intraocular pressure. /Anticholinergic Drugs/Antispasmodics/
Concomitant use of antacids may reduce the absorption of some oral anticholinergic drugs. Therefore, oral anticholinergic drugs should be taken at least 1 hour before taking antacids. Taking anticholinergic drugs before meals can prolong the effect of postprandial antacids. However, controlled studies failed to confirm a significant difference in gastric pH between the combined use of anticholinergic drugs and antacids and the use of antacids alone. /Antimuscarinic Drugs/Antispasmodics/
For more complete data on interactions of scopolamine (8 types), please visit the HSDB record page.

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Toxicity Overview
Due to the sustained-release nature of transdermal scopolamine formulations, the incidence of toxicity is low. Dosage data on the toxicity of tablet scopolamine are scattered. There are reports of death in children from daily doses of 10 mg. No deaths have been observed in adults from daily doses exceeding 100 mg. Another concerning poisoning syndrome caused by scopolamine overdose is anticholinergic syndrome, which can lead to tachycardia, hallucinations, high fever, and dry mucous membranes. In severe cases, intravenous administration of 1 to 4 mg of physostigmine can be used as an antidote. However, with transdermal administration, the most common side effects are only mild.

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Adverse Reactions
The most common side effects of scopolamine patches are blurred vision, dilated pupils, and dry mouth. Visual disturbances are usually due to inadequate handwashing after application. Less common side effects are associated with anticholinergic toxicity syndrome: flushing, tachycardia, agitation, and confusion. These side effects are usually mild and subside rapidly after removing the patch. If necessary, clinicians may use antagonists such as physostigmine if side effects persist.

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Drug Interactions
Scottamine should be used with caution in patients taking other medications that may cause central nervous system reactions (e.g., sedatives, tranquilizers, or alcohol). Special attention should be paid to potential interactions with medications that have anticholinergic properties; for example, other belladonna alkaloids, antihistamines (including meclomethasone), tricyclic antidepressants, and muscle relaxants.
Concomitant use of scopolamine may reduce the absorption of oral medications due to decreased gastric motility and delayed gastric emptying.
Concurrent use of anticholinergic drugs and corticosteroids may lead to increased intraocular pressure. /Anticholinergic drugs/Antispasmodics/
Concurrent use of antacids may reduce the absorption of some oral anticholinergic drugs. Therefore, oral anticholinergic drugs should be taken at least 1 hour before taking antacids. Taking anticholinergic drugs before meals can prolong the effect of postprandial antacids. However, controlled studies have failed to confirm a significant difference in gastric pH between combined use of anticholinergic drugs and antacids and use of antacids alone. /Antimuscarinic drugs/Antispasmodics/

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Antidotes and First Aid Measures
First Aid and Support Measures: Maintain an open airway and provide assisted ventilation if necessary. Treatment should be given for high fever, coma, rhabdomyolysis, and seizures. /Anticholinergic drugs/
Specific Drugs and Antidotes: For patients with severe poisoning (e.g., high fever, severe delirium, or tachycardia), a small dose of physostigmine may be administered. Note: Physostigmine can cause atrioventricular block, cardiac arrest, and seizures, especially in patients who have overdosed on tricyclic antidepressants. Neostigmine, a peripherally acting cholinesterase inhibitor, can be used to treat intestinal obstruction caused by anticholinergic drugs. /Anticholinergic Drugs/
Decontamination: Activated charcoal can be administered orally if available. Gastric lavage is unnecessary after small to moderate doses if activated charcoal is administered promptly. Intestinal cleansing procedures may be helpful even in patients who present late due to slowed gastrointestinal motility. /Anticholinergic Drugs/
Enhanced Clearance: Hemodialysis, hemoperfusion, peritoneal dialysis, and repeated administration of activated charcoal are not effective at clearing anticholinergic drugs. /Anticholinergic Drugs/

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Human Toxicity Summary
/Human Exposure Studies/ Cognitive and motor dysfunction caused by scopolamine has been widely confirmed in animals and humans, but the role of acetylcholine in working memory is not fully understood. This study used the Groton Maze Learning Test (GMLT) to investigate the role of acetylcholine neurotransmission in visuospatial short-term memory and working memory. The GMLT is a computerized hidden maze learning test used to measure cognitive processes such as spatial memory, working memory, and visuomotor function, as well as their integration in trial-and-error problem-solving. Healthy older adults received scopolamine (0.3 mg subcutaneously), donepezil (5 mg orally), scopolamine combined with donepezil, or placebo. Compared with placebo, low-dose scopolamine resulted in a decrease in scores on all GMLT indices. The decrease in scores caused by scopolamine was the most significant, especially in errors reflecting working memory processes (e.g., repetitive errors d = -2.98 and rule violations d = -2.49), and these impairments persisted even when the statistical model accounted for the scopolamine-induced slowing of visuomotor speed. Combined use of donepezil partially improves scopolamine-induced damage, and this improvement is more effective in working memory metrics than in short-term memory metrics. Donepezil alone slightly improves visuomotor function. These results indicate that scopolamine interferes with processes required for rule maintenance and behavioral monitoring, accompanied by visuomotor slowing and sequential position learning impairment. PMID:18514746
/Signs and Symptoms/ High doses of scopolamine produce central nervous system effects similar to those produced by toxic doses of other anticholinergic drugs (e.g., agitation, disorientation, irritability, hallucinations).
/Signs and Symptoms/ Scopolamine poisoning is usually caused by adulterated products or ingestion of plants containing scopolamine, producing typical anticholinergic syndrome. Central anticholinergic syndrome with hallucinations and urinary incontinence has been observed in both adults and children following a single transdermal patch treatment.
/Signs and Symptoms/ Occasionally, dizziness, nausea, vomiting, headache, and balance disturbances may occur after discontinuation of transdermal scopolamine patches after more than 3 days of use.

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Non-human Toxicity Excerpt
/Experimental Animals: Chronic Exposure or Carcinogenicity/ ... Conclusion: In these 2-year gavage studies, no carcinogenic activity was found in scopolamine hydrobromide trihydrate administered at doses of 1, 5, or 25 mg/kg to male or female F344/N rats or B6C3F1 mice. /Scolophonamine Hydrobromide/ Toxicology and Carcinogenicity Studies of Scopolamine Hydrobromide in F344/N Rats and B6C3F1 Mice (Gavage Studies). Technical Report Series 445 (1997) NIH Publication No. 97-3361, U.S. Department of Health and Human Services, National Institutes of Health. /Experimental Animals: Developmental or Reproductive Toxicity/ Reproductive studies in rats and rabbits using intravenously administered doses of scopolamine hydrobromide showed mild embryotoxicity in rabbits; no teratogenicity was observed in rats. This dose produced plasma drug concentrations 100 times higher than those achieved in humans after transdermal administration. /Scolophonamine Hydrobromide/
/Experimental Animals: Developmental or Reproductive Toxicity/ Teratogenicity studies were conducted in pregnant rats and rabbits with daily intravenous administration of scopolamine hydrobromide. No adverse reactions were recorded in rats. In rabbits, daily intravenous administration of scopolamine hydrobromide to plasma concentrations approximately 100 times higher than those achieved in humans after transdermal administration showed mild embryotoxicity. /Sconimus hydrobromide/
/Experimental Animals: Developmental or Reproductive Toxicity/ Fertility studies were conducted in female rats, and results showed that daily subcutaneous injection of scopolamine hydrobromide did not result in impaired fertility or fetal damage. The highest dose group (plasma concentrations approximately 500 times higher than human plasma concentrations after transdermal administration) showed a decrease in body weight in the mothers. /Sconimus hydrobromide/Thomson Health Care Inc.; Physician's Desk Reference, 62nd ed., Montville, NJ, 2008, p. 101. 2192

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6603108tratLD50toralt1270 mg/kgtArchives Internationales de Pharmacodynamie et de Therapie., 180(155), 1969 [PMID:5357002]
6603108tratLD50tsubcutaneoust296 mg/kgtUS Patent Document., #3380887
6603108tratLD50tintraduodenalt670 mg/kgtArchives Internationales de Pharmacodynamie et de Therapie., 180(155), 1969 [PMID:5357002]
6603108tmousetLD50toralt1880 mg/kgtArzneimittel-Forschung. Drug Research., 18(1132), 1968 [PMID:5755927]
6603108tmousetLD50tintraperitonealt650 mg/kgt New Drug LD50 Compilation.

[1]. The muscarinic antagonists Scopolamine and atropine are competitive antagonists at 5-HT3 receptors. Neuropharmacology. 2016 Sep;108:220-8.

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

Scopolamine is a muscarinic acetylcholine receptor antagonist that can cross the blood-brain barrier. It is frequently used in preclinical studies to induce memory impairment, mimicking the cholinergic dysfunction observed in Alzheimer's disease. Its ability to antagonize 5-HT3 receptors suggests a possible interaction with the serotonergic system, which may contribute to its pharmacological effects. Scopolamine hydrobromide is a colorless crystal, white powder, or solid, odorless. A 5% solution has a pH of 4-5.5. It effloresces slightly in dry air. It has a bitter taste. (NTP, 1992) Anhydrous scopolamine hydrobromide is the hydrobromide salt prepared by reacting scopolamine with hydrogen bromide. It is a muscarinic receptor antagonist. It contains scopolamine (1+). Scopolamine hydrobromide is the hydrobromide form of scopolamine, a tropane alkaloid derived from plants in the Solanaceae family, particularly Hyoscyamus niger and Atropa belladonna. It possesses anticholinergic, antiemetic, and antivertigo effects. Scopolamine's structure is similar to acetylcholine, antagonizing acetylcholine activity mediated by muscarinic receptors on structures innervated by postganglionic cholinergic nerves and on smooth muscle that responds to acetylcholine but lacks cholinergic innervation. This drug is used to induce mydriasis, ciliary muscle paralysis, control salivation and gastric acid secretion, slow intestinal motility, and prevent vomiting. It is an alkaloid derived from plants in the Solanaceae family, particularly those in the genera Datura and Scopolia. Scopolamine and its quaternary ammonium derivatives have anticholinergic effects similar to atropine, but may have a stronger effect on the central nervous system. They have a wide range of uses, including as a pre-anesthetic medication, for treating urinary incontinence and motion sickness, as an antispasmodic, mydriatic, and cycloplegic agent.

C17H21NO4.HBR

384.26

383.073

C, 53.14; H, 5.77; Br, 20.79; N, 3.65; O, 16.65

114-49-8

Scopolamine;51-34-3;Scopolamine butylbromide;149-64-4;Scopolamine hydrobromide trihydrate;6533-68-2;Scopolamine hydrochloride;55-16-3

6603108

White to off-white solid powder

460.3ºC at 760 mmHg

195-199 °C (dry matter)(lit.)

2.51E-10mmHg at 25°C

1.814

2

5

5

23

418

5

CN1[C@@H]2CC(C[C@H]1[C@H]3[C@@H]2O3)OC(=O)[C@H](CO)C4=CC=CC=C4.Br

WTGQALLALWYDJH-WYHSTMEOSA-N

InChI=1S/C17H21NO4.BrH/c1-18-13-7-11(8-14(18)16-15(13)22-16)21-17(20)12(9-19)10-5-3-2-4-6-10;/h2-6,11-16,19H,7-9H2,1H3;1H/t11?,12-,13-,14+,15-,16+;/m1./s1

[(1S,2S,4R,5R)-9-methyl-3-oxa-9-azatricyclo[3.3.1.02,4]nonan-7-yl] (2S)-3-hydroxy-2-phenylpropanoate;hydrobromide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 2.08 mg/mL (5.41 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (5.41 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (5.41 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)