After 24 hours of treatment, cholestyramine (0.1–50 μg/mL) caused the most noticeable effects; efflux was 65% higher than in control cells. As an anion exchange resin, cholestyramine is water insoluble. ether, chloroform, and ethanol. Choleestyramine was first moistened with a tiny amount of DMSO and then diluted with medium for the experiment. Dimethyl sulfoxide (DMSO) was used to generate a blank sample devoid of cholestyramine, which did not differ from the control sample [3].

The bile acid-binding resin cholestyramine prevents the absorption of bile acid in the digestive tract, which can result in? boosts the production of cholesterol via bile acid [1]. According to the findings, cholestyramine alone had a different regulatory effect on the metabolism of TG, BA, and cholesterol than did GSPE therapy alone or in combination with it. Interestingly, cholestyramine markedly increased the expression of the sodium-dependent bile acid transporter (Asbt) gene at the intestinal apex, while GSPE considerably decreased it. as GSPE or cholestyramine were administered alone or in combination, they dramatically increased the expression of genes involved in hepatic BA biosynthesis, particularly cholesterol 7α-hydroxylase (Cyp7a1), as compared to the control. The induction of intestinal and hepatic cholesterol-generating gene expression was seen upon cholestyramine treatment; however, the induction of liver cholesterol-generating gene expression was not affected by coadministration of GSPE. Hepatic lipogenic gene expression is also induced by cholestyramine and can be reduced by co-administration with GSPE [2].

Absorption, Distribution and Excretion
Previous studies performed on excised gastric tissue and in healthy volunteers revealed that the ion exchange resin, cholestyramine, exhibits mucoadherent behaviour. This study was designed to elucidate whether surface charge affected this behaviour. Gamma scintigraphy was performed on fasted normal subjects following oral administration of cholestyramine or the cationic exchanger Amberlite(R) IRP-69, either uncoated or polymer-coated to mask their charge. Subjects were fed after 4 h. The initial gastric emptying of all formulations was similar (T(50) values (mean+/-S.E.M.): cholestyramine=85.86+/-9.16 min; IRP-69=76.09+/-9.23 min; polymer-coated cholestyramine=72.0+/-12.64 min; polymer-coated IRP-69=70.25+/-10.57 min: P=0.724). However, after 3 h the emptying pattern of cholestyramine was slower than that of IRP-69. This resulted in greater retention times than IRP-69 (AUC(0-6) values (relative units)=15,200+/-1093 versus 9452+/-811; cholestyramine versus IRP-69: P=0.0004). This effect was reduced by polymer-coating the cholestyramine. Serial images showed that cholestyramine was trapped in the oropharyngeal region and subsequently displaced by the meal, resulting in higher levels of activity remaining at 6 h. Thus, cholestyramine exhibited prolonged gastric residence via mucoadhesion and was distributed throughout the stomach. The surface charge of the resin was found to have a contributory role. These materials may have potential for the delivery of drugs in the topical treatment of the gastric mucosa, for example in the eradication of Helicobacter pylori.
Not absorbed from the gastrointestinal tract.

Interactions
Concurrent use /of oral thiazide diuretics, oral penicillin G, phenylbutazone, oral propranolol, oral tetracyclines/ with cholestyramine may result in binding of these medications, thus decreasing their absorption; an interval of several hours between administration of cholestyramine and any of these medications is recommended.
Cholestyramine may reduce the half-life of these medications /digitalis glycosides, especially digitoxin/ by decreasing intestinal reabsorption and enterohepatic circulation; caution is recommended, especially when cholestyramine is withdrawn from a patient who was stabilized on the digitalis glycoside while receiving cholestyramine, because of the potential for serious toxicity; some clinicians recommend administration of cholestyramine approximately 8 hours after the digitalis glycoside.
Effect may be decreased when chenodiol or ursodiol is used concurrently with cholestyramine, which binds these medications and decrease their absorption and also tends to increase cholesterol saturation of bile.
Concurrent use may significantly increase the anticoagulant effects as a result of depletion of vitamin K, but cholestyramine may also bind with oral anticoagulants in the gastrointestinal tract and reduce their effects; administration at least 6 hours before cholestyramine and adjustment of anticoagulant dosage based on frequent prothrombin-time determinations are recommended.
For more Interactions (Complete) data for CHOLESTYRAMINE RESIN (8 total), please visit the HSDB record page.

[1]. rHDL administration increases reverse cholesterol transport in mice, but is not additive on top of ezetimibe or cholestyramine treatment. Atherosclerosis. 2013 Jul;229(1):94-101.

[2]. Grape Seed Procyanidins and Cholestyramine Differentially Alter Bile Acid and Cholesterol Homeostatic Gene Expression in Mouse Intestine and Liver. PLoS One. 2016; 11(4): e0154305.

[3]. Use of a human microvascular endothelial cell line as a model system to evaluate cholesterol uptake. Pathobiology. 1993;61(5-6):283-7.

A strongly basic anion exchange resin whose main constituent is polystyrene trimethylbenzylammonium Cl(-) anion.
See also: Cholestyramine (annotation moved to).

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Mechanism of Action
Cholestyramine binds with bile acids in the intestine, preventing their reabsorption and producing an insoluble complex, which is excreted in the feces.

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Therapeutic Uses
Ion exchange resin (bile salts); antihyperlipoproteinemic
Cholestyramine is indicated for use in patients with primary hypercholesterolemia (type IIa hyperlipidemia) and a significant risk of coronary artery disease who have not responded to diet and other measures alone. Cholestyramine reduces plasma total cholesterol and low density lipoprotein (LDL) concentrations, but causes no change or a slight increase in serum triglyceride concentrations, and so is not useful in patients with elevated triglyceride concentrations alone. Its use is limited in other types of hyperlipidemia (including type IIb) because it may cause further elevation of triglycerides. /Included in US product labeling/
Cholestyramine is indicated to reduce the risks of atherosclerotic heart disease and myocardial infarctions. /Included in US product labeling/
Cholestyramine is indicated for the relief of pruritus associated with partial biliary obstruction (including primary biliary cirrhosis and various other forms of bile stasis). It is not useful in patients with complete biliary obstruction or the pruritus due to other causes. /Included in US product labeling/
For more Therapeutic Uses (Complete) data for CHOLESTYRAMINE RESIN (8 total), please visit the HSDB record page.

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Drug Warnings
The most common adverse effects of cholestyramine involved the GI tract, especially after high doses (more than 24 g daily) and in patients older than 60 years of age. The most frequent adverse effect of cholestyramine resin is constipation, which occurs in about 20% of patients receiving the drug; cholestyramine resin may also increase the severity of preexisting constipation. Fecal impaction and/or hemorrhoids with or without bleeding have been reported rarely in association with constipation, most often when high dose of cholestyramine have been used in children and in the elderly.
Other less common adverse GI effects of cholestyramine are abdominal pain and distention, bloating, flatulence, nausea, vomiting, diarrhea, anorexia, dyspepsia, heartburn, biliary colic, and indigestion. Bloating and flatulence often disappear with continued therapy. Other reported adverse Gi effects include dysphagia, hiccups, ulcer attack, rectal bleeding, black stools, sour taste, pancreatitis, bleeding from know duodenal ulcer, rectal pain, and diverticulitis; however, a direct relationship of these effects to drug therapy has not been established.
Large quantities of chloride, which are liberated from cholestyramine resin, may be absorbed in place of intestinal bicarbonate and can lead to hyperchloremic acidosis and increased urinary calcium excretion. This effect is prevalent mainly with high dose of usual dose in small patients or children and may be partially offset by decreasing chloride intake.
Adverse dermatologic effects of cholestyramine have included rash and irritation of the skin, tongue, and perianal area.
For more Drug Warnings (Complete) data for CHOLESTYRAMINE RESIN (14 total), please visit the HSDB record page.

C27H47N

385.66878

331.206

11041-12-6

137699107

White to off-white solid powder

1

2

8

30

329

0

POJQWPZVKOFVHS-UHFFFAOYSA-M

InChI=1S/C22H32N.C5H12.ClH.H3N/c1-6-20(16-18(2)21-10-8-7-9-11-21)22-14-12-19(13-15-22)17-23(3,4)5;1-4-5(2)3;;/h7-15,18,20H,6,16-17H2,1-5H3;5H,4H2,1-3H3;1H;1H3/q+1;;;/p-1

azane;2-methylbutane;trimethyl-[[4-(5-phenylhexan-3-yl)phenyl]methyl]azanium;chloride

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 : ~1 mg/mL
H2O : ~0.1 mg/mL
1M HCl :< 1 mg/mL

Solubility in Formulation 1: 60 mg/mL (Infinity mM) in 0.5% CMC-Na/saline water (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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