5-HT₃ Receptor ( IC50 = 2.09 μM ); mAChR

When applied alone to oocytes expressing 5-HT₃ receptors, Scopolamine does not elicit a response. However, when 2 μM 5-HT is also applied concurrently, the response is concentration-dependently inhibited. With a Hill Slope of 1.06 ± 0.05, the pIC50 value for Scopolamine is 5.68±0.05 (IC50=2.09 μM, n=6). As a result, 3.23 μM was the K_b. Applying Scopolamine concurrently with the 5-HT application results in the same concentration-dependent effect. In order to investigate the possibility of a competitive binding at the 5-HT₃ receptor, [³H]granisetron, a well-known high-affinity competitive antagonist at these receptors, is used to measure the competition of unlabelled Scopolamine. A concentration-dependent competition is seen with 0.6 nM [³H]granisetron (~K_d) for scopopolamine, resulting in an average pKi of 5.17±0.24 (Ki=6.76 μM, n=3)[1].

The histology of the brain shows no discernible changes in the histopathology study. 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 hippocampus[2]. When compared to the normal group's 3.06±0.296 activity, the administration of Scopolamine alone significantly increases the activity of the Acetylcholinesterase enzyme (AchE) (7.98±0.065; P<0.001). In comparison to the normal group (12.82±2.86), the animals treated with Scopolamine report significantly higher levels of malondialdehyde (MDA) (34.61±4.85; P<0.01). In comparison to the normal group (0.3906±0.02), the scopolamine-treated group exhibits a significant decrease in reduced glutathione (GSH) levels (P<0.001; 0.1504±0.03). The concentration of β amyloid (Aβ_1-42) 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].

In order to measure saturation binding (8 point) curves, 0.5 mL incubations containing 10 mM HEPES buffer (pH 7.4), 0.1-1 nM [³H]granisetron or 1-10 nM [³H]N-methylScopolamine are incubated with either crude extracts of HEK 293 cells stably expressing 5-HT₃ receptors or Guinea pig membrane preparations. The same receptor preparations are incubated in 0.5 mL HEPES buffer containing either 0.6 nM [³H]granisetron or 0.6 nM [³H]N-methylScopolamine, as well as varying concentrations of competing ligands, in order to determine competition binding (10 point). One can measure non-specific binding using quipazine at 1 mM or Scopolamine at 10 μM, respectively. Filtration onto Whatman GF/B filters wetted with HEPES buffer + 0.3% polyethyleneimine is used to end the incubations. This is followed by two quick washes with ice-cold HEPES buffer. Using standards for bovine serum albumin, a Lowry protein assay is used to determine the protein concentration. Tri-Carb 2100 TR scintillation counters are used to measure radioactivity[1].

Mice: After the mice are weighed, labeled, and divided into seven groups of five animals each, 3 mg/kg of Scopolamine is pre-injected intraperitoneally into each group. For three days in a row, groups 1-3 receive 0.2 mL equivalent doses of 4 mg/kg, 6 mg/kg, and 8 mg/kg of the Morinda lucida extract, groups 4-6 receive the same doses of Peltophorum pterocarpum extract, and group 7 receives 0.2 mL of distilled water (negative control).
Rats: In this work, healthy male Wistar rats, 12 months of age, weighing 180–200 g, are employed. Group I comprises of six rats; Group II is for disease control (Scopolamine hydrobromide 3 mg/kg, i.p. ); Group III is for Scopolamine+Quercetin (25 mg/kg, p.o. ); Group IV is for standard treatment (Scopolamine+Donepezil hydrochloride 3 mg/kg, p.o. ); and Group V is for Scopolamine+Quercetin (25 mg/kg, p.o.)+Donepezil (3 mg/kg, p.o.). For a period of 14 days, the rats in groups III, IV, and V receive their prescribed doses of medication every 24 hours. The 14^th day is dedicated to the acquisition trail for the Morris water maze, elevated plus maze, and passive avoidance paradigm. Following the acquisition trail, all groups—aside from the normal control group—receive an injection of scopolamine (3 mg/kg, i.p.) on the same day, which causes cognitive impairment in rats. The fifteenth day is dedicated to testing memory retention; on the same day, rats are killed and brain tissues are removed in order to measure the levels of the enzyme acetylcholinesterase (AchE) and markers of brain oxidative stress, such as reduced glutathione (GSH) and lipid peroxidase (LPO). To estimate the level of β amyloid (Aβ_1-42), an ELISA kit is utilized. Rat brains are used to dissect the hippocampus and examine any histopathological abnormalities.

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 of 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. 2192

[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 capable of crossing 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.

C17H22CLNO4

339.81388

339.123

C, 60.09; H, 6.53; Cl, 10.43; N, 4.12; O, 18.83

55-16-3

Scopolamine; 51-34-3; Scopolamine hydrobromide; 114-49-8; Scopolamine butylbromide; 149-64-4; Scopolamine hydrobromide trihydrate; 6533-68-2

6852406

Solid powder

460.3ºC at 760mmHg

232.2ºC

1.658

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.Cl

KXPXJGYSEPEXMF-WYHSTMEOSA-N

InChI=1S/C17H21NO4.ClH/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;hydrochloride

Hyoscine hydrochloride; Hyoscine HCl; 55-16-3; Scopolamine HCl; Scopolamine, hydrochloride; Chlorhydrate de scopolamine; Q2P66EIP1F; DTXSID6044692; Chlorhydrate de scopolamine [French]; Scopolamine hydrochloride

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

DMSO: ~250 mg/mL (~650.6 mM)
H2O: ≥ 100 mg/mL (~260.2 mM)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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