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CONTACT US| Catalog Number | ACM474259-1 |
| CAS | 474-25-9 |
| Structure |  |
| Synonyms | Deoxychenocholic acid |
| IUPAC Name | (4R)-4-[(3R,5S,7R,8R,9S,10S,13R,14S,17R)-3,7-Dihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoic acid |
| Molecular Weight | 392.57 |
| Molecular Formula | C24H40O4 |
| Canonical SMILES | CC(CCC(=O)O)C1CCC2C1(CCC3C2C(CC4C3(CCC(C4)O)C)O)C |
| InChI | InChI=1S/C24H40O4/c1-14(4-7-21(27)28)17-5-6-18-22-19(9-11-24(17,18)3)23(2)10-8-16(25)12-15(23)13-20(22)26/h14-20,22,25-26H,4-13H2,1-3H3,(H,27,28)/t14-,15+,16-,17-,18+,19+,20-,22+,23+,24-/m1/s1 |
| InChI Key | RUDATBOHQWOJDD-BSWAIDMHSA-N |
| Boiling Point | 437.26 °C |
| Melting Point | 165-167 °C(lit.) |
| Flash Point | 9 °C |
| Purity | 98% |
| Density | 0.9985 g/cm³ |
| Solubility | Practically insoluble in water |
| Appearance | White to off-white powder |
| Storage | Room temperature |
| Complexity | 605 |
| Covalently-Bonded Unit Count | 1 |
| Defined Atom Stereocenter Count | 10 |
| EC Number | 207-481-8 |
| Exact Mass | 392.29265975 |
| Heavy Atom Count | 28 |
| Hydrogen Bond Acceptor Count | 4 |
| Hydrogen Bond Donor Count | 3 |
| Isomeric SMILES | C[C@H](CCC(=O)O)[C@H]1CC[C@@H]2[C@@]1(CC[C@H]3[C@H]2[C@@H](C[C@H]4[C@@]3(CC[C@H](C4)O)C)O)C |
| MDL Number | MFCD00064142 |
| Monoisotopic Mass | 392.29265975 |
| Physical State | Powder |
| Rotatable Bond Count | 4 |
| Shipping | Gel pack |
| Storage Conditions | -20 °C |
| Topological Polar Surface Area | 77.8 Ų |
| WGK Germany | 2 |
Wei X, et al. Phytochemistry, 2024, 224, 114162.
Chenodeoxycholic acid (CDCA) is a primary bile acid known for its role in modulating host metabolism through the activation of the farnesoid X receptor (FXR). This study investigates the microbial transformations of CDCA by seven human intestinal fungal species.
Methods
Seven strains of human intestinal fungi were selected to assess their ability to metabolize CDCA. The fungi were cultured on potato agar medium before being transferred to conical flasks containing 50 mL of potato liquid medium. These cultures were incubated at 32°C with shaking at 150 rpm for 48 hours. CDCA, dissolved in dimethyl sulfoxide (DMSO), was added to each flask to a final concentration of 30 μM, and incubation continued for an additional 48 hours. Control cultures without CDCA were also prepared.
At the start (0 hours) and end (48 hours) of the incubation period, fermentation broths were treated with ice-cold acetonitrile to precipitate proteins and were then analyzed using UPLC-Q-TOF-MS to evaluate the biotransformation of CDCA. For preparative-scale experiments, fungi were pre-cultured in 500 mL potato medium for 48 hours, after which 25 mg of CDCA dissolved in 0.1 mL DMSO was added, and incubation continued for 5 days. The fermentation broths were extracted with ethyl acetate, and the resulting residue was used for metabolite isolation.
Findings
Metabolic Pathways: Hydroxylation and dehydrogenation were identified as the predominant metabolic pathways for CDCA transformation by the intestinal fungi. Specifically, incubation with Rhizopus microspores (PT2906) resulted in the production of eight previously undescribed compounds and five known analogs. These compounds were elucidated using high-resolution electrospray ionization mass spectrometry (HRESI-MS) and nuclear magnetic resonance (NMR) data.
FXR Activity: Notably, three of the new compounds demonstrated inhibitory effects on FXR, contrasting with the FXR activation typically observed with CDCA. This suggests that these microbial transformations could have significant implications for modulating FXR activity and, consequently, host metabolism.
These findings underscore the complexity of microbial interactions with bile acids and their impact on host metabolic regulation. The identification of FXR inhibitors among the CDCA metabolites opens new avenues for research into the therapeutic modulation of FXR activity and its effects on host health.
Hu Y, et al. European Journal of Pharmaceutics and Biopharmaceutics, 2024, 196, 114184.
Chenodeoxycholic acid (CA) is used in the synthesis of lipoprotein-mimicking nanocomposites (CA-rHDL) designed for tumor targeting and anti-tumor efficacy. The CA-rHDL showed promising properties for tumor targeting and anti-tumor efficacy, demonstrating the potential of using chenodeoxycholic acid in innovative therapeutic nanomaterials.
Synthesis of CA-Modified BSA (CA-BSA)
CA was covalently bonded to bovine serum albumin (BSA) via lysine residues to create CA-BSA. The synthesis involved:
Activation: CA was activated using equimolar amounts of EDC and NHS in DMF, forming CA-NHS ester (CA-NHSE) after 4 hours.
Reaction: CA-NHSE was reacted with BSA in a 0.2M NaHCO3 solution for 8 hours at room temperature, with molar ratios of CA-NHSE to BSA ranging from 30 to 60.
Purification: The reaction mixture was dialyzed against distilled water for 48 hours and centrifuged at 10,000 rpm for 10 minutes to remove excess CA-NHSE and its hydrolysis products. The supernatant was lyophilized to obtain CA-BSA.
Preparation and Characterization of CA-rHDL
The nanocomposite CA-rHDL was prepared using the emulsification-evaporation method:
NLC Formation: A nanostructured lipid carrier (NLC) was created using a 4:3:2:1 ratio of phospholipid, cholesterol ester (CE), triglyceride, and cholesterol, respectively. Lipids were dissolved in a mixture of ethanol and acetone (2:8), heated to 65°C, and slowly added to a 30 mL Tris-HCL buffer (pH 8.0).
Emulsification: The mixture was emulsified for 1 hour and sonicated at 0°C for 3 minutes. Organic solvents were removed by rotary evaporation at 55°C to concentrate the sample to 15 mL.
Filtration: The lipid emulsion was filtered through a 0.22 μm microporous membrane to obtain the PTX-loaded NLC (P-NLC) or NLC.
Nanocomposite Formation: To form CA-rHDL or CA-P-rHDL, 3 mg CA-BSA and 2 mg sodium cholate were dissolved in 1 mL NLC or P-NLC and incubated with gentle stirring at 37°C for 8 hours.
Zhu Q, et al. Cell Reports Medicine, 2023, 4(12), 101304.
In vitro studies demonstrated that chenodeoxycholic acid (CDCA) and its derivative, obeticholic acid, exert a protective effect against acinar cell injury. Additionally, in murine models, these compounds were shown to mitigate pancreatic necrosis.
Mechanistic Insights
RNA sequencing revealed that the oxidative phosphorylation pathway is significantly involved in the protective effects of CDCA. Furthermore, overexpression of the farnesoid X receptor (FXR), the receptor for CDCA, was found to inhibit pancreatic necrosis. Conversely, interfering with FXR expression resulted in an increased severity of necrosis in mice.
Conclusion
This study highlights the potential of CDCA as a therapeutic target for treating acinar cell necrosis in AP. The findings suggest that CDCA and its receptor FXR play crucial roles in modulating the severity of pancreatic damage. Targeting the CDCA-FXR pathway could be a promising strategy for AP treatment, although further research and verification are needed.
Shen D, et al. European Journal of Pharmacology, 2022, 923, 174925.
Chenodeoxycholic acid (CDCA), a primary bile acid, has shown potential in inhibiting carcinoma cell proliferation. This study demonstrates that CDCA attenuates the pathogenesis of lung adenocarcinoma (LUAD) both in vitro and in vivo through the integrin α5β1/FAK/p53 signaling axis. These findings suggest that CDCA could be a promising candidate for the treatment of LUAD, offering a new approach to combat this prevalent form of lung cancer.
Methods
Expression Analysis: Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were used to evaluate protein and mRNA expression levels in LUAD cell lines.
Proliferation Assays: Cell Counting Kit-8 and clone formation assays were conducted to assess the proliferation of LUAD cells in vitro.
Motility Assays: Transwell assays were performed to evaluate tumor cell motility.
Transcriptional Profiling: RNA sequencing analysis was conducted on A549 cells treated with CDCA.
In Vivo Evaluation: A xenograft model was established to evaluate the effects of CDCA on LUAD progression in mice.
Results
In Vitro Effects
CDCA significantly inhibited the proliferation, migration, and invasion of LUAD cells and promoted apoptosis. Mechanistic studies revealed that CDCA:
Integrin α5β1 Signaling Pathway: CDCA inhibited this pathway by reducing the expression of the α5 and β1 subunits of integrin and phosphorylated FAK (focal adhesion kinase).
p53 Activation: CDCA induced an increase in the levels of p53, a key downstream gene of the integrin α5β1/FAK pathway.
In Vivo Effects
In a xenograft model, CDCA significantly reduced tumor volume in mice without causing significant toxicity, indicating its potential as a safe therapeutic agent.
What is the PubChem CID for Chenodeoxycholic acid?
The PubChem CID for Chenodeoxycholic acid is 10133.
What is the molecular formula of Chenodeoxycholic acid?
The molecular formula of Chenodeoxycholic acid is C24H40O4.
What is the molecular weight of Chenodeoxycholic acid?
The molecular weight of Chenodeoxycholic acid is 392.6 g/mol.
What is the IUPAC name of Chenodeoxycholic acid?
The IUPAC name of Chenodeoxycholic acid is (4R)-4-[(3R,5S,7R,8R,9S,10S,13R,14S,17R)-3,7-dihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoic acid.
What are the synonyms for Chenodeoxycholic acid?
The synonyms for Chenodeoxycholic acid include Chenodiol, 474-25-9, Chenix, and Chenic acid.
What is the InChIKey of Chenodeoxycholic acid?
The InChIKey of Chenodeoxycholic acid is RUDATBOHQWOJDD-BSWAIDMHSA-N.
What is the CAS number of Chenodeoxycholic acid?
The CAS number of Chenodeoxycholic acid is 474-25-9.
What is the EC number of Chenodeoxycholic acid?
The EC number of Chenodeoxycholic acid is 207-481-8.
What is the ChEMBL ID of Chenodeoxycholic acid?
The ChEMBL ID of Chenodeoxycholic acid is CHEMBL240597.
What is the Wikipedia page for Chenodeoxycholic acid?
The Wikipedia page for Chenodeoxycholic acid is "Chenodeoxycholic acid".
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