Glycocholic acid hydrate
Based on 4 publication(s) in Google Scholar
Glycocholic acid hydrate is a bile acid derivative. Glycocholic acid hydrate downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Glycocholic acid hydrate inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Glycocholic acid hydrate modulates related bile acid receptor signaling. Glycocholic acid hydrate suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Glycocholic acid hydrate can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA).
연구목적의 판매만을 진행합니다. 환자를 대상으로 한 판매는 하지 않습니다.
- Purity : 99.85%
- CAS No.: 1192657-83-2
- 화학식: C26H43NO6.xH2O
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보관:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biological Activity
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Chemical Information
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용액&용해도
- Protocol
- 순도&문서
- References
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Help & FAQs
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HY-N0324R
Cholic acid (Standard)Endogenous Metabolite -
HY-B0172
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HY-B0172R
Lithocholic acid (Standard)Autophagy Inducer -
HY-13771R
Ursodeoxycholic acid (Standard)GPCR19 Agonist /FXR Antagonist -
HY-N0324
Cholic acidEndogenous Metabolite -
HY-13771
Ursodeoxycholic acidGPCR19 Agonist /FXR Antagonist
Publications Citing Use of MedChemExpress (MCE) Glycocholic acid hydrate
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Customer Validation & Images
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RT-PCR
All Endogenous Metabolite Isoforms
MoreAll Caspase Isoforms
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Biological Activity
제품 설명
IC50 & Target
[1]|
Caspase 3 |
Caspase-9 |
Bax |
Bcl-2 |
S1PR2 |
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. Further protocols information, click here.
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Cell Line:human colon adenocarcinoma Caco-2 cells
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Concentration:0 μM, 100 μM, 250 μM, 300 μM, 400 μM, 500 μM
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Incubation Time:0 h, 24 h, 48 h, 72 h
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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.
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Cell Line:human colon adenocarcinoma Caco-2 cells
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Concentration:250 μM (in combination with Epirubicin (HY-13624))
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Incubation Time:72 h
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Result:Reduced the mean IC50 value of epirubicin to 8.08 μg/mL, which was significantly lower than the IC50 value for epirubicin alone.
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Cell Line:human colon adenocarcinoma Caco-2 cells
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Concentration:250 μM
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Incubation Time:72 h
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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.
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Cell Line:human colon adenocarcinoma Caco-2 cells
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Concentration:250 μM
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Incubation Time:72 h
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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%).
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Cell Line:SNU-245 cholangiocarcinoma (CCA) cell line
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Concentration:1.6 μM
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Incubation Time:48 h
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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.
Chemical Information
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CAS No. 1192657-83-2
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Appearance Solid
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화학식 C26H43NO6.xH2O
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Color White to off-white
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SMILES
O=C(O)CNC(CC[C@@H](C)[C@H]1CC[C@@]2([H])[C@]3([H])[C@H](O)C[C@]4([H])C[C@H](O)CC[C@]4(C)[C@@]3([H])C[C@H](O)[C@]12C)=O.[x H2O]
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Structure Classification
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Initial Source
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Publications (4)
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Journal Impact Factor
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Most Recent
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Nature
2025 Jul;643(8070):192-200. PMID: 39695227 -
Nat Commun
2024 Sep 19;15(1):8221. PMID: 39300135 -
Adv Sci (Weinh)
Targeting FDFT1 Reduces Cholesterol and Bile Acid Production and Delays Hepatocellular Carcinoma Progression Through the HNF4A/ALDOB/AKT1 Axis. [Abstract]2025 Mar;12(12):e2411719. PMID: 39899681
Glycocholic acid hydrate purchased from MedChemExpress. Usage Cited in: Adv Sci (Weinh). 2025 Mar;12(12):e2411719. [Abstract]
The mRNA levels of ALDOB in Huh7 or HCCLM3 cells treated with various bile acids (100 μM, 24 h). All data are presented as mean ± SD. Data were analyzed by one-way ANOVA with Bonferroni multiple-comparison correction. CA, cholic acid; TCA, taurocholic acid; GCA, glycocholic acid; TCDCA, taurochenodeoxycholic acid; GCDCA, glycochenodeoxycholic acid; LCA, lithocholic acid; TLCA, taurolithocholic acid; GLCA, glycolithocholic acid; DCA, deoxycholic acid; TDCA, taurodeoxycholic acid; GDCA, glycodeoxycholic acid; UDCA, ursodeoxycholic acid; TUDCA, tauroursodeoxycholic acid; GUDCA, glycoursodeoxycholic acid.
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용액&용해도
In Vitro:
DMSO : 250 mg/mL (Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- 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.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.08 mg/mL; Clear solution
This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.08 mg/mL; Clear solution
This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocol
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
순도&문서
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Data Sheet (284 KB)
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SDS (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Lo YL, et al. Inhibit multidrug resistance and induce apoptosis by using glycocholic acid and epirubicin. Eur J Pharm Sci. 2008;35(1-2):52-67. [Content Brief]
[2]. Song WS, et al. Discovery of glycocholic acid and taurochenodeoxycholic acid as phenotypic biomarkers in cholangiocarcinoma. Sci Rep. 2018;8(1):11088. Published 2018 Jul 23. [Content Brief]
[3]. Piscon B, et al. The Effect of glycocholic acid on the growth, membrane permeability, conjugation and antibiotic susceptibility of Enterobacteriaceae. Front Cell Infect Microbiol. 2025;15:1550545. Published 2025 Mar 20. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Glycocholic acid hydrate Related Classifications
HY-N1423B Related Classifications
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