2. Membrane Transporter/Ion Channel Metabolic Enzyme/Protease
  3. Apical Sodium-Dependent Bile Acid Transporter Cytochrome P450
  4. Cholestyramine

Cholestyramine  (Synonyms: Cholestyramine resin; Colestyramine)

Cat. No.: HY-104081
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Cholestyramine (Cholestyramine resin) is an orally active bile acid sequestrant. Cholestyramine upregulates the expression of intestinal Apical sodium-dependent bile acid transporter and hepatic Cholesterol 7α-hydroxylase. Cholestyramine induces the expression of intestinal and hepatic cholesterol synthesis genes as well as hepatic lipogenesis genes, and promotes bile acid- and neutral sterol-mediated reverse cholesterol transport. Cholestyramine reduces intestinal cholesterol absorption and induces cholesterol efflux. Cholestyramine is applicable to research related to coronary artery disease, atherosclerotic cardiovascular disease and atherosclerosis.

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Cholestyramine

Cholestyramine Chemical Structure

CAS No. : 11041-12-6

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Based on 8 publication(s) in Google Scholar

Cholestyramine Related Antibodies

Top Publications Citing Use of Products

View All Cytochrome P450 Isoform Specific Products:

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CYP1 CYP2 CYP3 CYP4 CYP11 CYP17 Aromatase/CYP19A1 CYP26 CYP51 CYP1A2 CYP2D6 CYP2C9 CYP2C19 CYP3A CYP3A4 CYP17A1

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Description

Cholestyramine (Cholestyramine resin) is an orally active bile acid sequestrant. Cholestyramine upregulates the expression of intestinal Apical sodium-dependent bile acid transporter and hepatic Cholesterol 7α-hydroxylase. Cholestyramine induces the expression of intestinal and hepatic cholesterol synthesis genes as well as hepatic lipogenesis genes, and promotes bile acid- and neutral sterol-mediated reverse cholesterol transport. Cholestyramine reduces intestinal cholesterol absorption and induces cholesterol efflux. Cholestyramine is applicable to research related to coronary artery disease, atherosclerotic cardiovascular disease and atherosclerosis[1][2][3].

In Vitro

Cholestyramine (0.1-50 μg/mL; 48 h) dose-dependently enhances cholesterol efflux from HMEC-1 immortalized human microvascular endothelial cells, with a 66% reduction in cholesterol load at 50 μg/mL after 48-hour incubation[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cholestyramine Related Antibodies
In Vivo

Supplementation with cholestyramine (2%; administered orally via diet; ad libitum access; 4 weeks) in normolipidemic male C57BL/6 mice alters the expression of genes related to bile acid, cholesterol and triglyceride homeostasis in the intestine and liver, reduces serum levels of bile acids, triglycerides and non-esterified fatty acids, increases fecal excretion of bile acids, lipids and non-esterified fatty acids, and does not affect body weight or liver enzyme levels[1].
Co-administration of cholestyramine (2%; oral via diet; ad libitum access; 4 weeks) and GSPE (250 mg/kg; oral; single dose) in normolipidemic male C57BL/6 mice synergistically enhances the expression of hepatic bile acid synthesis genes, attenuates the cholestyramine-induced upregulation of hepatic cholesterol and lipogenesis gene expression, and reduces serum triglyceride levels more significantly than cholestyramine alone[1].
Cholestyramine (2% (w/w); administered orally via diet; daily; for 14 days) increases the level of macrophage-to-feces reverse cholesterol transport in wild-type C57BL/6J mice by 3.6-fold within 24-48 h by enhancing fecal excretion of bile acids and neutral sterols; no additive effect is observed when it is used in combination with rHDL[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6 (male, 8 weeks old)[1]
Dosage: 2%
Administration: dietary supplementation; ad libitum; 4 weeks
Result: Showed no significant difference in body weight relative to control at any weekly time point over 4 weeks.
Robustly induced apical sodium-dependent bile acid transporter (Asbt) expression relative to control.
Significantly reduced ileal bile acid binding protein (Ibabp) and fibroblast growth factor 15 (Fgf15) expression relative to control.
Significantly increased expression of intestinal cholesterol synthesis genes 3-hydroxy-3-methylglutaryl-CoA synthase 1 (Hmgcs1) and 3-hydroxy-3-methylglutaryl-CoA reductase (Hmgcr), as well as scavenger receptor class b, member 1 (Scarb1) and low density lipoprotein receptor (Ldlr) relative to control.
Induced cholesterol 7α-hydroxylase (Cyp7a1) expression 8-fold relative to control.
Increased sterol 12α-hydroxylase (Cyp8b1) expression relative to control.
Decreased oxysterol 7α-hydroxylase (Cyp7b1) expression relative to control.
Significantly increased expression of hepatic cholesterol synthesis genes Hmgcs1 and Hmgcr, as well as sterol regulatory element binding protein 1c (Srebf1c) and its lipogenic target genes acetyl CoA carboxylase 1 (Acc1), fatty acid synthase (Fasn), and stearoyl CoA desaturase (Scd1) relative to control.
Reduced serum bile acid levels relative to control.
Reduced serum triglyceride levels by 56% relative to control.
Reduced serum non-esterified fatty acid levels relative to control.
Showed no change in serum cholesterol, alanine aminotransferase (ALT), or aspartate aminotransferase (AST) levels relative to control.
Increased fecal bile acid excretion relative to control.
Increased total fecal lipid excretion relative to control.
Increased fecal non-esterified fatty acid excretion relative to control.
Showed no change in fecal cholesterol excretion relative to control.
Animal Model: C57BL/6 (male, 8 weeks old)[1]
Dosage: 2% (cholestyramine); 250 mg/kg (GSPE)
Administration: dietary supplementation; ad libitum; 4 weeks (cholestyramine); p.o.; single dose (GSPE)
Result: Robustly induced Asbt expression relative to control.
Significantly reduced Ibabp and Fgf15 expression relative to control.
Significantly increased expression of intestinal cholesterol synthesis genes Hmgcs1 and Hmgcr, as well as Acat2, Mttp, Scarb1, and Ldlr relative to control.
Induced Cyp7a1 expression nearly 13-fold relative to control.
Increased Cyp8b1 and sterol 27-hydroxylase (Cyp27a1) expression relative to control.
Showed no change in Cyp7b1 expression relative to control.
Attenuated the cholestyramine-induced increases in hepatic Hmgcs1, Hmgcr, Srebf1c, Acc1, Fasn, and Scd1 expression relative to cholestyramine alone.
Reduced serum bile acid levels to a greater extent than cholestyramine alone relative to control.
Reduced serum triglyceride levels by 66.7% relative to control (a 25% additional decrease compared to cholestyramine alone).
Reduced serum non-esterified fatty acid levels relative to control.
Showed no change in serum cholesterol, ALT, or AST levels relative to control.
Increased fecal bile acid excretion relative to control.
Increased total fecal lipid excretion relative to control.
Increased fecal non-esterified fatty acid excretion relative to control.
Showed no change in fecal cholesterol excretion relative to control.
Animal Model: C57BL/6J mice[2]
Dosage: 2% (w/w)
Administration: p.o.; daily; 14 days
Result: Decreased intestinal cholesterol absorption by 24%.
Increased fecal bile acid excretion several fold.
Increased fecal neutral sterol excretion at 0-4 h, 4-24 h, and 24-48 h.
Increased overall macrophage-to-feces RCT by 2.2-fold (4-24 h) and 3.6-fold (24-48 h).
Increased fecal tracer excretion within bile acids by 3.9-fold (4-24 h) and 3.2-fold (24-48 h).
Increased fecal tracer excretion within neutral sterols at 4-24 h and 24-48 h.
Did not change baseline plasma free or total cholesterol or triglyceride levels.
Caused a decrease in plasma free cholesterol levels at 4 h and an increase at 24 h and 48 h when combined with a single dose of rHDL (100 mg/kg apoA-I-POPC).
Showed no additive effect on RCT when combined with rHDL.
Clinical Trial
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

C[N+](C)(C)CC1=CC=C(C(CC(C)C2=CC=CC=C2)CC)C=C1.CC(CC)C.[Cl-].[n]
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

1 M HCl : < 1 mg/mL (insoluble)

DMSO : < 1 mg/mL (insoluble or slightly soluble)

H2O : < 0.1 mg/mL (insoluble)

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In Vivo:

For the following dissolution methods, please prepare the working solution directly. It is recommended to prepare fresh solutions and use them promptly within a short period of time.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

  • Protocol 1

    Add each solvent one by one:  0.5% CMC-Na/saline water

    Solubility: 60 mg/mL; Suspended solution; Need ultrasonic

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Purity & Documentation

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COA (246 KB)

Handling Instructions (2659 KB)
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Cholestyramine Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Cholestyramine11041-12-6Cholestyramine resin ColestyramineApical Sodium-Dependent Bile Acid TransporterCytochrome P450ASBTIleal Bile Acid TransporterIBATSLC10A2CYPsatherosclerosisC57BL/6 miceendothelial cellsatherosclerotic cardiovascular diseaseHMEC-1 immortalized human microvascular endothelial cellscoronary artery diseasemacrophage-to-feces reverse cholesterol transportcholesterol 7α-hydroxylaseapical sodium-dependent bile acid transporterC57BL/6J miceInhibitorinhibitorinhibit

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