Glycochenodeoxycholic acid metabolite;

GCDC3-glucuronide is synthesized by UDP-glucuronyl transferase in the liver, and elevated levels were reported in T2DM patients. Increased levels of GCDC3-glucuronide might have links to dysfunctional liver metabolism in men [1].

[1]. Postprandial Metabolism is Impaired in Overweight Normoglycemic Young Adults without Family History of Diabetes. Sci Rep. 2020;10(1):353. Published 2020 Jan 15.

[2]. Untargeted plasma metabolomics for risk prediction of hepatocellular carcinoma: A prospective study in two Chinese cohorts[J]. International Journal of Cancer, 2022, 151(12): 2144-2154.

Glycinecholic acid-3-glucuronide is a steroidal glycosidic acid. While risk factors for type 2 diabetes mellitus (T2DM) are known, early predictive biomarkers for the transition from a normal state to a prediabetic state have not been identified. We investigated basal metabolism and metabolic responses after a mixed dietary challenge in 110 healthy subjects aged 18 to 40 years (male-to-female ratio 1:1); subjects were divided into four groups: first-degree relatives of T2DM patients (n = 30), those with a body mass index >23 kg/m² but <30 kg/m² (n = 30), prediabetic patients (n = 20), and normal controls (n = 30). We performed untargeted metabolomics analysis of plasma and correlated it with clinical and biochemical parameters, inflammatory markers, and insulin sensitivity. Similar to prediabetic patients, overweight subjects exhibited insulin resistance, significantly elevated levels of C-peptide, adiponectin, and glucagon, and decreased levels of ghrelin. The levels of metabolites such as MG (22:2(13Z, 16Z)/0:0/0:0) and lysophosphatidylcholine (15:0) were decreased in overweight and prediabetic subjects. Men had significantly lower insulin sensitivity than women. Men had elevated levels of fasting uric acid, xanthine, and glycocholic acid-3-glucuronide. However, women had higher levels of lysophosphatidylcholine and antioxidant defense metabolites. The impaired postprandial metabolism and decreased insulin sensitivity in overweight but normal-glucose young adults suggest a risk of hyperglycemia. Our results also suggest that young men have a higher risk of developing diabetes. [1]

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Characterization of metabolic disorders before the onset of hepatocellular carcinoma (HCC) helps to deepen the understanding of pathogenic pathways and identify novel biomarkers for early prevention. We conducted two 1:1 paired nested case-control studies (108 and 55 pairs, respectively) to investigate the association between plasma metabolomics (analyzed using liquid chromatography-mass spectrometry (LC-MS)) and HCC risk in two prospective cohort studies in China. Paired t-tests and orthogonal partial least squares discriminant analysis (OPLS-DA) were used to identify differentially expressed metabolites. Weighted gene co-expression network analysis (WGCNA) was performed to classify metabolites into modules to identify biological pathways involved in hepatocellular carcinoma development. We used a multivariate logistic regression model to assess the predictive value of metabolites. Among the 612 named metabolites, 44 differentially expressed metabolites were identified between the case and control groups, including 12 androgen/progesterone steroid hormones, 8 bile acids, 10 amino acids, 6 phospholipids, and 8 other metabolites. Multivariate logistic regression analysis showed that these metabolites were associated with hepatocellular carcinoma (HCC) with odds ratios ranging from 0.19 (95% confidence interval [CI]: 0.11–0.35) to 5.09 (95% CI: 2.73–9.50). Weighted co-expression network analysis (WGCNA) of these 612 metabolites showed that there were 8 significant modules associated with HCC risk, including modules representing androgen and progesterone metabolism pathways, primary and secondary bile acid and amino acid metabolism pathways. A combination of 18 metabolites with independent effects showed the potential to predict the risk of hepatocellular carcinoma, with AUCs of 0.87 (95% CI: 0.82–0.92) and 0.86 (95% CI: 0.80–0.93) on the training and validation sets, respectively. In summary, we identified a group of plasma metabolites that may be associated with the occurrence of hepatocellular carcinoma and have the potential to predict the risk of hepatocellular carcinoma. [2]

C32H51NO11

625.75

625.346

79254-98-1

44263370

Typically exists as solid at room temperature

1.4±0.1 g/cm3

856.1±65.0 °C at 760 mmHg

471.6±34.3 °C

0.0±0.6 mmHg at 25°C

1.597

1.51

7

11

9

44

1090

15

C[C@H](CCC(=O)NCC(=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@H]5[C@@H]([C@H]([C@@H]([C@H](O5)C(=O)O)O)O)O)C)O)C

ABFZMYIIUREPLL-ASWJIRIHSA-N

InChI=1S/C32H51NO11/c1-15(4-7-22(35)33-14-23(36)37)18-5-6-19-24-20(9-11-32(18,19)3)31(2)10-8-17(12-16(31)13-21(24)34)43-30-27(40)25(38)26(39)28(44-30)29(41)42/h15-21,24-28,30,34,38-40H,4-14H2,1-3H3,(H,33,35)(H,36,37)(H,41,42)/t15-,16+,17-,18-,19+,20+,21-,24+,25+,26+,27-,28+,30-,31+,32-/m1/s1

(2S,3S,4S,5R,6R)-6-[[(3R,5R,7R,8R,9S,10S,13R,14S,17R)-17-[(2R)-5-(carboxymethylamino)-5-oxopentan-2-yl]-7-hydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-3-yl]oxy]-3,4,5-trihydroxyoxane-2-carboxylic acid

Glycochenodeoxycholic acid 3-glucuronide; 79254-98-1; N-(3alpha,7alpha-dihydroxy-5beta-cholan-24-oyl)-glycine 3-D-glucuronide; (2S,3S,4S,5R,6R)-6-[[(3R,5R,7R,8R,9S,10S,13R,14S,17R)-17-[(2R)-5-(carboxymethylamino)-5-oxopentan-2-yl]-7-hydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-3-yl]oxy]-3,4,5-trihydroxyoxane-2-carboxylic acid; CHEBI:166729; DTXSID701274667; Glycochenodeoxycholate 3-glucuronide;

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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