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 substantially between different dosage routes. Oral administration of 0.5 mg scopolamine in healthy volunteers produced a Cmax of 0.54 ± 0.1 ng/mL, a tmax of 23.5 ± 8.2 min, and an AUC of 50.8 ± 1.76 ng\*min/mL; the absolute bioavailability is low at 13 ± 1%, presumably because of first-pass metabolism. By comparison, IV infusion of 0.5 mg scopolamine over 15 minutes resulted in a Cmax of 5.00 ± 0.43 ng/mL, a tmax of 5.0 min, and an AUC of 369.4 ± 2.2 ng\*min/mL. Other dose forms have also been tested. Subcutaneous administration of 0.4 mg scopolamine resulted in a Cmax of 3.27 ng/mL, a tmax of 14.6 min, and an AUC of 158.2 ng\*min/mL. Intramuscular administration of 0.5 scopolamine resulted in a Cmax of 0.96 ± 0.17 ng/mL, a tmax of 18.5 ± 4.7 min, and an AUC of 81.3 ± 11.2 ng\*min/mL. Absorption following intranasal administration was found to be rapid, whereby 0.4 mg of scopolamine resulted in a Cmax of 1.68 ± 0.23 ng/mL, a tmax of 2.2 ± 3 min, and an AUC of 167 ± 20 ng\*min/mL; intranasal scopolamine also had a higher bioavailability than that of oral scopolamine at 83 ± 10%. Due to dose-dependent adverse effects, the transdermal patch was developed to obtain therapeutic plasma concentrations over a longer period of time. Following patch application, scopolamine becomes detectable within four hours and reaches a peak concentration (tmax) within 24 hours. The average plasma concentration is 87 pg/mL, and the total levels of free and conjugated scopolamine reach 354 pg/mL.
Following oral administration, approximately 2.6% of unchanged scopolamine is recovered in urine. Compared to this, using the transdermal patch system, less than 10% of the total dose, both as unchanged scopolamine and metabolites, is recovered in urine over 108 hours. Less than 5% of the total dose is recovered unchanged.
The volume of distribution of scopolamine is not well characterized. IV infusion of 0.5 mg scopolamine over 15 minutes resulted in a volume of distribution of 141.3 ± 1.6 L.
IV infusion of 0.5 mg scopolamine resulted in a clearance of 81.2 ± 1.55 L/h, while subcutaneous administration resulted in a lower clearance of 0.14-0.17 L/h.
Scopolamine hydrobromide is rapidly absorbed following IM or subcutaneous injection. The drug is well absorbed from the GI tract, principally from the upper small intestine. Scopolamine also is well absorbed percutaneously. Following topical application behind the ear of a transdermal system, scopolamine is detected in plasma within 4 hours, with peak concentrations occurring within an average of 24 hours. In one study in healthy individuals, mean free and total (free plus conjugated) plasma scopolamine concentrations of 87 and 354 pg/mL, respectively, have been reported within 24 hours following topical application of a single transdermal scopolamine system that delivered approximately 1 mg/72 hours. /Scopolamine hydrobromide/
Following oral administration of a 0.906-mg dose of scopolamine in one individual, a peak concentration of about 2 ng/mL was reached within 1 hour. Although the commercially available transdermal system contains 1.5 mg of scopolamine, the membrane-controlled diffusion system is designed to deliver approximately 1 mg of the drug to systemic circulation at an approximately constant rate over a 72-hour period. An initial priming dose of 0.14 mg of scopolamine is released from the adhesive layer of the system at a controlled, asymptotically declining rate over 6 hours; then, the remainder of the dose is released at an approximate rate of 5 ug/hour for the remaining 66-hour functional lifetime of the system. The manufacturer states that the initial priming dose saturates binding sites on the skin and rapidly brings the plasma concentration to steady-state. In a crossover study comparing urinary excretion rates of scopolamine during multiple 12-hour collection intervals in healthy individuals, there was no difference between the rates of excretion of drug during steady-state (24-72 hours) for constant-rate IV infusion (3.7-6 mcg/hour) and transdermal administration. The transdermal system appeared to deliver the drug to systemic circulation at the same rate as the constant-rate IV infusion; however, relatively long collection intervals (12 hours) make it difficult to interpret the data precisely. During the 12- to 24-hour period of administration and after 72 hours, the rate of excretion of scopolamine was higher with the transdermal system than with the constant-rate IV infusion.
The distribution of scopolamine has not been fully characterized. The drug appears to be reversibly bound to plasma proteins. Scopolamine apparently crosses the blood-brain barrier since the drug causes CNS effects. The drug also reportedly crosses the placenta and is distributed into milk..
Although the metabolic and excretory fate of scopolamine has not been fully determined, the drug is thought to be almost completely metabolized (principally by conjugation) in the liver and excreted in urine. Following oral administration of a single dose of scopolamine in one study, only small amounts of the dose (about 4-5%) were excreted unchanged in urine within 50 hours; urinary clearance of unchanged drug was about 120 mL/minute. In another study, 3.4% or less than 1% of a single dose was excreted unchanged in urine within 72 hours following subcutaneous injection or oral administration of the drug, respectively. Following application of a single transdermal scopolamine system that delivered approximately 1 mg/72 hours in healthy individuals, the urinary excretion rate of free and total (free plus conjugated) scopolamine was about 0.7 and 3.8 ug/hour, respectively. Following removal of the transdermal system of scopolamine, depletion of scopolamine bound to skin receptors at the site of the application of the transdermal system results in a log-linear decrease in plasma scopolamine concentrations. Less than 10% of the total dose is excreted in urine as unchanged drug and its metabolites over 108 hours.

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Metabolism / Metabolites
Little is known about the metabolism of scopolamine in humans, although many metabolites have been detected in animal studies. In general, scopolamine is primarily metabolized in the liver, and the primary metabolites are various glucuronide and sulphide conjugates. Although the enzymes responsible for scopolamine metabolism are unknown, _in vitro_ studies have demonstrated oxidative demethylation linked to CYP3A subfamily activity, and scopolamine pharmacokinetics were significantly altered by coadministration with grapefruit juice, suggesting that CYP3A4 is responsible for at least some of the oxidative demethylation.
Although the metabolic and excretory fate of scopolamine has not been fully determined, the drug is thought to be almost completely metabolized (principally by conjugation) in the liver and excreted in urine.

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Biological Half-Life
The half-life of scopolamine differs depending on the route. Intravenous, oral, and intramuscular administration have similar half-lives of 68.7 ± 1.0, 63.7 ± 1.3, and 69.1 ±8/0 min, respectively. The half-life is greater with subcutaneous administration at 213 min. Following removal of the transdermal patch system, scopolamine plasma concentrations decrease in a log-linear fashion with a half-life of 9.5 hours.
Following application of a single transdermal scopolamine system that delivered approximately 1 mg/72 hours, the average elimination half-life of the drug was 9.5 hours.

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
No information is available on the use of scopolamine during breastfeeding. Use during labor appears to have a detrimental effect on newborn infants' nursing behavior. Long-term use of scopolamine might reduce milk production or milk letdown, but a single systemic or ophthalmic dose is not likely to interfere with breastfeeding. During long-term use, observe for signs of decreased lactation (e.g., insatiety, poor weight gain). To substantially diminish the amount of drug that reaches the breastmilk after using eye drops, place pressure over the tear duct by the corner of the eye for 1 minute or more, then remove the excess solution with an absorbent tissue.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Anticholinergics can inhibit lactation in animals, apparently by inhibiting growth hormone and oxytocin secretion. Anticholinergic drugs can also reduce serum prolactin in nonnursing women. The prolactin level in a mother with established lactation may not affect her ability to breastfeed.
A retrospective case-control study conducted in two hospitals in central Iran compared breastfeeding behaviors in the first 2 hours postdelivery by infants of 4 groups of primiparous women with healthy, full-term singleton births who had vaginal deliveries. The groups were those who received no medications during labor, those who received oxytocin plus scopolamine, those who received oxytocin plus meperidine, and those who received oxytocin, scopolamine and meperidine. The infants in the no medication group performed better than those in all other groups, and the oxytocin plus scopolamine group performed better than the groups that had received meperidine.

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Protein Binding
Scopolamine may reversibly bind plasma proteins in humans. In rats, scopolamine exhibits relatively low plasma protein binding of 30 ± 10%.

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Interactions
Scopolamine should be used with care in patients taking other drugs that are capable of causing CNS effects such as sedatives, tranquilizers, or alcohol. Special attention should be paid to potential interactions with drugs having anticholinergic properties; e.g., other belladonna alkaloids, antihistamines (including meclizine), tricyclic antidepressants, and muscle relaxants.
The absorption of oral medications may be decreased during the concurrent use of scopolamine because of decreased gastric motility and delayed gastric emptying.
Concomitant administration of antimuscarinics and corticosteroids may result in increased intraocular pressure. /Antimuscarinics/Antispasmodics/
Antacids may decrease the extent of absorption of some oral antimuscarinics when these drugs are administered simultaneously. Therefore, oral antimuscarinics should be administered at least 1 hour before antacids. Antimuscarinics may be administered before meals to prolong the effects of postprandial antacid therapy. However, controlled studies have failed to demonstrate a substantial difference in gastric pH when combined antimuscarinic and antacid therapy was compared with antacid therapy alone. /Antimuscarinics/Antispasmodics/
For more Interactions (Complete) data for SCOPOLAMINE (8 total), please visit the HSDB record page.

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Toxicity Summary
Toxicity does not happen as frequently with the transdermal form of scopolamine due to its extended-release nature. Data on the toxic dose of scopolamine in the tablet form is scattered. Reports exist that 10 mg a day can be lethal for children. In adults, consumption of more than 100 mg a day did not result in death. The other feared toxidrome of scopolamine overdose is an anticholinergic syndrome resulting in tachycardia, hallucinations, hyperthermia, and dry membranes. Physostigmine 1 to 4 mg IV can serve as an antidote in such severe cases. However, with the transdermal application, only minor side effects are most commonly observed.

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Adverse Effects
The most commonly reported side effects of scopolamine patch use are blurred vision, dilated pupils, and dry mouth. The vision disturbances are most often due to inadequate handwashing techniques after the application of the patch. Less frequently reported side effects are related to anticholinergic toxidrome: flushed skin, tachycardia, agitation, and confusion. These side effects are usually mild and quick to resolve after patch removal. If needed, the clinician can administer a reversal agent like physostigmine if a side effect persists.

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Interactions
Scopolamine should be used with care in patients taking other drugs that are capable of causing CNS effects such as sedatives, tranquilizers, or alcohol. Special attention should be paid to potential interactions with drugs having anticholinergic properties; e.g., other belladonna alkaloids, antihistamines (including meclizine), tricyclic antidepressants, and muscle relaxants.
The absorption of oral medications may be decreased during the concurrent use of scopolamine because of decreased gastric motility and delayed gastric emptying.
Concomitant administration of antimuscarinics and corticosteroids may result in increased intraocular pressure. /Antimuscarinics/Antispasmodics/
Antacids may decrease the extent of absorption of some oral antimuscarinics when these drugs are administered simultaneously. Therefore, oral antimuscarinics should be administered at least 1 hour before antacids. Antimuscarinics may be administered before meals to prolong the effects of postprandial antacid therapy. However, controlled studies have failed to demonstrate a substantial difference in gastric pH when combined antimuscarinic and antacid therapy was compared with antacid therapy alone. /Antimuscarinics/Antispasmodics/

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Antidote and Emergency Treatment
Emergency and supportive measures: Maintain an open airway and assist ventilation if needed. Treat hyperthermia, coma, rhabdomyolysis, and seizures if they occur. /Anticholinergics/
Specific drugs and antidotes: A small dose of physostigmine .... can be given to patients with severe toxicity (e.g., hyperthermia, severe delirium, or tachycardia). Caution: Physostigmine can cause AV block, asystole, and seizures, especially in patients with tricyclic antidepressant overdose. Neostigmine, a peripherally acting cholinesterase inhibitor, may be useful in treating anticholinergic-induced ileus. /Anticholinergics/
Decontamination: Administer activated charcoal orally if conditions are appropriate. Gastric lavage is not necessary after small to moderate ingestions if activated charcoal can be given promptly. Because of slowed gastrointestinal motility, gut decontamination procedures may be helpful even in late-presenting patients. /Anticholinergics/
Enhanced elimination: Hemodialysis, hemoperfusion, peritoneal dialysis, and repeat-dose charcoal are not effective in removing anticholinergic agents. /Anticholinergics/

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Human Toxicity Excerpts
/HUMAN EXPOSURE STUDIES/ Scopolamine-induced deficits in cognitive and motor processes have been widely demonstrated in animals and humans, although the role of acetylcholine in working memory is not as well understood. This study examined the role of acetylcholine neurotransmission in visuospatial short term and working memory using the Groton Maze Learning Test (GMLT). The GMLT is a computerized hidden maze learning test that yields measures of component 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 were administered scopolamine (0.3 mg subcutaneous), the acetlycholinesterase inhibitor donepezil (5 mg oral), scopolamine with donepezil, or placebo. Compared to placebo, low-dose scopolamine led to performance deficits on all measures of the GMLT. The greatest scopolamine-induced deficits were observed in errors reflecting working memory processes (e.g., perseverative errors d=-2.98, and rule-break errors d=-2.49) and these impairments remained robust when statistical models accounted for scopolamine-related slowing in visuomotor speed. Co-administration of donepezil partially ameliorated scopolamine-related impairments and this effect was greatest for measures of working memory than short-term memory. By itself, donepezil was associated with a small improvement in visuomotor function. These results suggest that scopolamine disrupts processes required for rule maintenance and performance monitoring, in combination with visuomotor slowing and sequential location learning. PMID:18514746

/SIGNS AND SYMPTOMS/ High doses of scopolamine produce CNS effects (e.g., restlessness, disorientation, irritability, hallucinations) similar to those produced by toxic doses of other antimuscarinics.
/SIGNS AND SYMPTOMS/ Scopolamine toxicity usually arises from adulterated products or ingestion of scopolamine-containing plants, producing classic anticholinergic syndrome. Adults as well as children have developed central anticholinergic syndrome with hallucinations and incontinence after being treated with a single transdermal patch.
/SIGNS AND SYMPTOMS/ When transdermal scopolamine has been used for longer than 3 days, withdrawal of its use has occasionally been followed by dizziness, nausea, vomiting, headache, and disturbance of equilibrium.

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Non-Human Toxicity Excerpts
/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ ... CONCLUSIONS: Under the conditions of these 2 year gavage studies, there was no evidence of carcinogenic activity of scopolamine hydrobromide trihydrate in male or female F344/N rats or B6C3F1 mice administered l, 5, or 25 mg/kg. /Scopolamine hydrobromide/ Toxicology & Carcinogenesis Studies of Scopolamine Hydrobromide in F344/N Rats and B6C3F1 Mice (Gavage Studies). Technical Report Series No. 445 (1997) NIH Publication No. 97-3361 U.S. Department of Health and Human Services, National
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Reproductive studies in rats and rabbits using IV scopolamine hydrobromide at dosages producing plasma concentrations of the drug 100 times greater than those achievable after application of the transdermal system in humans have shown a marginal embryotoxic effect in rabbits; no teratogenic effects were observed in rats. /Scopolamine hydrobromide/
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Teratogenic studies were performed in pregnant rats and rabbits with scopolamine hydrobromide administered by daily intravenous injection. No adverse effects were recorded in rats. Scopolamine hydrobromide has been shown to have a marginal embryotoxic effect in rabbits when administered by daily intravenous injection at doses producing plasma levels approximately 100 times the level achieved in humans using a transdermal system. /Scopolamine hydrobromide/
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Fertility studies were performed in female rats and revealed no evidence of impaired fertility or harm to the fetus due to scopolamine hydrobromide administered by daily subcutaneous injection. Maternal body weights were reduced in the highest-dose group (plasma level approximately 500 times the level achieved in humans using a transdermal system). /Scopolamine hydrobromide/ Thomson Health Care Inc.; Physicians' Desk Reference 62 ed., Montvale, 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 that crosses the blood-brain barrier. It is commonly 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 potential interactions with serotonergic systems, 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.)