2. Apoptosis Membrane Transporter/Ion Channel Anti-infection Metabolic Enzyme/Protease GPCR/G Protein
  3. Bacterial Bcl-2 Family LPL Receptor FXR P-glycoprotein MDM-2/p53 Endogenous Metabolite Caspase Apoptosis G protein-coupled Bile Acid Receptor 1
  4. Sodium glycocholate hydrate, 98%

Sodium glycocholate hydrate, 98%  (Synonyms: N-Cholylglycine sodium salt, 98%)

Cat. No.: HY-W013105 Purity: 99.91%
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Sodium glycocholate hydrate, 98% is a bile acid derivative. Sodium glycocholate hydrate, 98% downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Sodium glycocholate hydrate, 98% inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Sodium glycocholate hydrate, 98% modulates related bile acid receptor signaling. Sodium glycocholate hydrate, 98% suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Sodium glycocholate hydrate, 98% can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA).

For research use only. We do not sell to patients.

Sodium glycocholate hydrate, 98%

Sodium glycocholate hydrate, 98% Chemical Structure

CAS No. : 338950-81-5

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Based on 1 publication(s) in Google Scholar

Other Forms of Sodium glycocholate hydrate, 98%:

Sodium glycocholate hydrate, 98% Related Antibodies

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Description

Sodium glycocholate hydrate, 98% is a bile acid derivative. Sodium glycocholate hydrate, 98% downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Sodium glycocholate hydrate, 98% inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Sodium glycocholate hydrate, 98% modulates related bile acid receptor signaling. Sodium glycocholate hydrate, 98% suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Sodium glycocholate hydrate, 98% can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA)[1][2][3].

IC50 & Target

Microbial Metabolite

 

In Vitro

Glycocholic acid (0-500 μM; 0, 24, 48, 72 h) hydrate reduces the viability of human colon adenocarcinoma Caco-2 cells in a time- and concentration-dependent manner[1].
Glycocholic acid (250 μM; 72 h) hydrate at 250 μM significantly increases the chemosensitivity of human colon adenocarcinoma Caco-2 cells to Epirubicin (HY-13624)[1].
Glycocholic acid (250 μM; 72 h) hydrate alters the expression of multidrug resistance and apoptosis-related genes in human colon adenocarcinoma Caco-2 cells, downregulating MDR1, MRP1, MRP2, and Bcl-2 while upregulating Bax, caspase-3, caspase-9, and p53, and increasing the Bax-to-Bcl-2 ratio[1].
Glycocholic acid (250 μM; 72 h) hydrate reduces hMDR1 promoter activity in human colon adenocarcinoma Caco-2 cells[1].
Glycocholic acid (250 μM; 72 h) hydrate induces chromatin condensation, a marker of apoptosis, in human colon adenocarcinoma Caco-2 cells[1].
Glycocholic acid (250 μM; 72 h) hydrate increases the sub-G1 DNA content population, indicating apoptosis, in human colon adenocarcinoma Caco-2 cells[1].
Glycocholic acid (GCA) (1.6 μM; 48 h) hydrate modulates bile acid receptor gene expression in SNU-245 cholangiocarcinoma cells, reducing FXR expression and increasing TGR5 and S1PR2 expression[2].
Glycocholic acid hydrate inhibits late logarithmic phase growth of E. coli K1037, clinical UTI E. coli, Klebsiella pneumoniae, Klebsiella oxytoca, Salmonella Typhimurium, Raoultella ornithinolytica, and Citrobacter freundii in liquid LB culture, but not on solid LB agar medium[3].
Glycocholic acid hydrate reduces the MIC of ampicillin for E. coli K1037 by 2-fold and the MIC of chloramphenicol for Raoultella ornithinolytica and Citrobacter freundii by 2-fold, resulting in additive antimicrobial interactions (FIC index 0.625-0.75)[3].
Glycocholic acid (0.125-2%; 6 h) hydrate reduces conjugation frequency of multiple Enterobacteriaceae conjugative plasmids by 70 to 97% in a dose-dependent manner, with no prominent reduction in donor strain viability[3].
Glycocholic acid (0.2-2%; 16 h) hydrate significantly reduces E. coli K1037 motility on soft LB agar by downregulating fliC gene expression[3].
Glycocholic acid (0.125-2%) hydrate increases membrane permeability and compromises membrane integrity of E. coli K1037, as shown by increased NPN/EtBr uptake and cytoplasmic DnaK leakage[3].

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

Sodium glycocholate hydrate, 98% Related Antibodies

Cell Viability Assay[1]

Cell Line: human colon adenocarcinoma Caco-2 cells
Concentration: 0 μM, 100 μM, 250 μM, 300 μM, 400 μM, 500 μM
Incubation Time: 0 h, 24 h, 48 h, 72 h
Result: Reduced cell viability in a time-dependent manner, with the most profound effects seen after 72 h.
Decreased cell viability to 80% after 72 h incubation with 250 μM.
Caused further significant decreases in viability after 72 h at concentrations of 300, 400, 500 μM compared to lower concentrations.
Maintained cell viability at 96% and 90% after 24 h and 48 h incubation with 250 μM, respectively.

Cell Viability Assay[1]

Cell Line: human colon adenocarcinoma Caco-2 cells
Concentration: 250 μM (in combination with Epirubicin (HY-13624))
Incubation Time: 72 h
Result: Reduced the mean IC50 value of epirubicin to 8.08 μg/mL, which was significantly lower than the IC50 value for epirubicin alone.

Real Time qPCR[1]

Cell Line: human colon adenocarcinoma Caco-2 cells
Concentration: 250 μM
Incubation Time: 72 h
Result: Significantly downregulated mRNA expression of MDR1 (P-gp), MRP1, MRP2, and Bcl-2.
Significantly upregulated mRNA expression of Bax, caspase-3, caspase-9, and p53 compared to untreated controls.
Significantly increased the Bax-to-Bcl-2 ratio.
Showed no significant effect on caspase-8 expression.

Apoptosis Analysis[1]

Cell Line: human colon adenocarcinoma Caco-2 cells
Concentration: 250 μM
Incubation Time: 72 h
Result: Increased the percentage of cells in the sub-G1 phase (apoptotic cells) to 26.8% after treatment, which was significantly higher than the control (1.3%) and epirubicin alone (20.6%).

Real Time qPCR[1]

Cell Line: human colon adenocarcinoma Caco-2 cells
Concentration: 1.6 μM
Incubation Time: 48 h
Result: Reduced FXR gene expression to 0.17-fold of untreated control levels.
Increased TGR5 gene expression to 8.55-fold of untreated control levels, which was significantly higher than both control and taurochenodeoxycholic acid-treated cells.
Increased S1PR2 gene expression to 3.4-fold of untreated control levels and 3.9-fold of taurochenodeoxycholic acid-treated cell levels.
Formula

C26H43NO6.xH2O.Na
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

O[C@H]1[C@@]2([H])[C@@]3([H])[C@@]([C@@](CC3)([H])[C@H](C)CCC(NCC(O[Na])=O)=O)([C@H](C[C@]2([H])[C@@]4([C@](C[C@@H](CC4)O)([H])C1)C)O)C.O.[x]
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Solvent & Solubility
In Vitro: 

DMSO : 50 mg/mL (Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

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Sodium glycocholate hydrate, 98% Related Classifications

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Keywords:

Sodium glycocholate hydrate, 98%338950-81-5N-Cholylglycine sodium salt, 98%BacterialBcl-2 FamilyLPL ReceptorFXRP-glycoproteinMDM-2/p53Endogenous MetaboliteCaspaseApoptosisG protein-coupled Bile Acid Receptor 1Lysophospholipid ReceptorNR1H4P-gpPgpMultidrug resistance protein 1MDR1ATP-binding cassette sub-family B member 1ABCB1Cluster of differentiation 243CD243G-protein coupled receptor 19GPCR19TGR5GPBAR1Inhibitorinhibitorinhibit

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