Endogenous Metabolite; Microbial Metabolite

The cell line MGC803, generated by 100 μM of deoxycholic acid (DCA) is able to withstand acidified bile acids and exhibits enhanced ischemia and burst activity when bile acids are present [2]. Deoxycholic acid (DCA, 100 μM) caused morphological alterations in MGC803 cells, markedly raised telomerase activity, improved cell viability, and decreased inflammation [2].

---

Generation of MGC803 cells resistant to acidified bile acids [2]
To simulate chronic local recurrent disease in vitro, the gastric cancer cell line MGC803 was exposed to acidified medium (pH 5.5) containing 100 μmol/L DCA and CDCA. An untreated log‐growth MGC803 cell line was generated to be used as a control in normal pH media. After daily 10‐min exposure to the acidified bile acids for 60 weeks, MGC803‐resistant cells were able to survive and proliferate after 120‐min exposure.

---

Bile acids (BAs), well-defined signaling molecules with diverse metabolic functions, play important roles in cellular processes associated with many cancers. As one of the most common BAs, Deoxycholic Acid (DCA) is originally synthesized in the liver, stored in the gallbladder, and processed in the gut. Deoxycholic Acid (DCA) plays crucial roles in various tumors; however, functions and molecular mechanisms of DCA in gallbladder cancer (GBC) still remain poorly characterized. Here, we analyzed human GBC samples and found that DCA was significantly downregulated in GBC, and reduced levels of DCA was associated with poor clinical outcome in patients with GBC. DCA treatment impeded tumor progression by halting cell proliferation. DCA decreased miR-92b-3p expression in an m6A-dependent posttranscriptional modification manner by facilitating dissociation of METTL3 from METTL3–METTL14–WTAP complex, which increased the protein level of the phosphatase and tensin homolog, a newly identified target of miR-92b-3p, and subsequently inactivated the PI3K/AKT signaling pathway. Our findings revealed that DCA might function as a tumor suppressive factor in GBC at least by interfering with miR-92b-3p maturation, and suggested that DCA treatment could provide a new therapeutic strategy for GBC[3].

Klb–/– mice show a modified BA composition. [1]
Given the key role of FGF21/FGFR1c/β-klotho signaling in fat oxidation, glucose uptake, and energy homeostasis, the resistance of Klb–/– mice to DIO was an unexpected observation. Further, these findings raised the question of the underlying mechanism(s). Since β-klotho is known to participate in a negative feedback loop that represses hepatic BA synthesis, we investigated whether Klb deficiency could also qualitatively impact BA homeostasis. Cyp7a1, the rate-limiting enzyme in BA synthesis, was highly overexpressed in the liver of Klb–/– mice (Figure 3A), as previously reported. Cyp8b1 (encoding sterol 12-α-hydroxylase) was also upregulated, while Cyp7b1 and Cyp27a1 (driving the alternative [acidic] BA synthesis) were underexpressed compared with WT mice (Figure 3B). This specific transcriptional pattern of BA enzymes led us to investigate differences in hepatic primary BA production and the circulating BA composition. Primary BAs are directly synthesized by the liver and converted into secondary BAs by bacterial action in the colon. In the liver, tauro-β-muricholic acid (T-βMCA) levels were decreased in Klb–/– mice (Figure 3C), confirming the downregulation of the alternative pathway. Plasma levels of both primary taurocholic acid (T-CA) and its secondary derivative deoxycholic acid (conjugated [T-DCA] and unconjugated [Deoxycholic Acid (DCA)] forms) were dramatically increased in Klb–/– mice (Figure 3, D and E). The global composition of circulating BAs was substantially modified between genotypes, with a predominance of T-CA and T-DCA in Klb–/– mice (Figure 3F).

---

Resistance of Klb–/– mice to DIO is Deoxycholic Acid (DCA) driven and microbiota dependent. [1]
The massive increase of Deoxycholic Acid (DCA) and T-DCA levels in Klb–/– mice led us to investigate the specific contribution of this secondary BA to the increase in energy expenditure on HFD. To this end, we treated orally (0.5 g/l in drinking water) both Klb–/– and WT mice with vancomycin (VCM) 1 week before initiation and during the entire period of HFD consumption. VCM is a poorly absorbed antibiotic preferentially targeting Gram-positive bacteria, including Clostridium species classically described as responsible for the conversion of primary BAs into secondary BAs (such as 7α-dehydroxylation of CA into Deoxycholic Acid (DCA)). VCM treatment similarly reshapes the gut microbiota of Klb–/– and WT mice, massively decreasing both intestinal Bacteroidetes and Firmicutes content in both genotypes on HFD (Figure 7A). In contrast, Proteobacteria content was not impacted by VCM in WT and showed an increasing trend in Klb–/– mice (Figure 7A). Notably, the reshaped microbiota presents drastically reduced 7α-dehydroxylation activity, leading to residual circulating levels of DCA and T-DCA (Figure 7, B and C). Instead, the circulating BA pool is mainly composed of T-βMCA and T-CA in WT mice and of T-CA in Klb–/– mice on HFD+VCM (Figure 7D). The specific pattern of primary BA synthesis due to Klb deficiency was not affected by VCM treatment, since HFD-fed Klb–/– mice presented again higher levels of Cyp7a1 and Cyp8b1 and lower levels of Cyp7b1 compared with HFD-fed WT mice (Supplemental Figure 2A). Importantly, following VCM administration, Klb–/– mice lose their resistance to DIO. Indeed, they gain similar weight (Figure 7E) and exhibit similar fat proportion and content to that of WT (Figure 7F and Supplemental Figure 2B), despite a still lighter eWAT (Figure 7G); no major change was observed in adipose-targeted gene expression (Supplemental Figure 2, C and D), glucose tolerance (Figure 7H), or stool energy content (Figure 7I). Consistently, BAT weight (Figure 8A) and morphology (Figure 8B) were indistinguishable between Klb–/– and WT mice on HFD+VCM. VO2 (Figure 8, C and D), VCO2 (Supplemental Figure 2, E and F), and RER (Figure 8E) were also similar between Klb–/– and WT mice on HFD+VCM. Gene expression analysis in this tissue confirmed the abrogation of thermogenesis induction in Klb–/– mice on HFD+VCM, with a trend towards lower Ucp1, Dio2, and Elovl3 expression levels and significantly lower Pgc1a and Cidea expression levels (Figure 8F). We also observed a massive increase in liver weight (Figure 8G), indicating a preferential storage of fat in the liver rather than in the WAT of Klb–/– mice in the absence of Deoxycholic Acid (DCA)-driven BAT overactivity (Figure 8, H and I). This observation is also corroborated by increased hepatic expression of the scavenger receptor (fatty acid translocase, Cd36) involved in lipid accumulation under excessive fat supply (Figure 8J). Finally, hepatic gene expression of cholesterogenesis enzymes (Figure 8K) and proinflammatory cytokines (Figure 8L) remained elevated in Klb–/– mice on HFD+VCM.

---

Deoxycholic Acid (DCA) suppresses GBC tumor growth by downregulating miR-92b-3p expression [3]
To further explore the critical role of miR-92b-3p in GBC, we subcutaneously inoculated ectopically expressed miR-92b-3p or the empty vector as a control in NOZ cells into nude mice, which were then fed food containing Deoxycholic Acid (DCA) or equal amount of vehicle. Compared with the empty vector, overexpression of miR-92b-3p significantly increased the cell proliferation, whereas DCA treatment could significantly attenuated miR-92b-3p-mediated tumor growth (Fig. 7a). Consistently, the tumors excised from mice with miR-92b-3p-overexpressing cells increased weights compared with those excised from mice inoculated with the empty vector, even when treated with DCA (Fig. 7b, c). Similarly, immunohistochemical measurement of Ki-67 as well as p-AKT (Ser473), p-70S6K (Thr389), and p-eIF4EBP1 (phospho T37) showed remarkably lower proliferation rates coupled with significantly decreased levels of AKT signaling pathway after treatment with DCA; miR-92b-3p overexpression partially rescued the DCA-induced growth inhibition by targeting PTEN in GBC tumors (Fig. 7d).

Drug affinity responsive targets stability (DARTS) [3]
DARTS was performed to determine the potential targets of Deoxycholic Acid (DCA). Briefly, 50 × 106 cells were lysed with M-PER supplemented with protease/phosphatase inhibitor cocktail. TNC buffer (50 mM Tris-HCL pH8.0, 50 mM NaCl, and 10 mM CaCl2) was added to the lysates. The supernatants were incubated with increasing concentration of Deoxycholic Acid (DCA) or EtOH (vehicle) for 1 h at room temperature following digestion with Pronase (1:3000) for 30 min. The digestion was terminated with protease inhibitor cocktail following ice incubation immediately. The immunoblotting signals were detected by the ECL Kit. The experiments were performed with three biological replicates.

---

Cellular thermal shift assay (CETSA) [3]
Cells were pretreated with 50 μM Deoxycholic Acid (DCA) for 24 h prior to subject to the CETSA protocol. Cells were washed with PBS containing protease inhibitor cocktail and transferred into PCR tubes. The cells were subjected to heat shocked with indicated temperature for 5 min to denature proteins, then were immediately cooled down at room temperature for 5 min. All the samples were next undergone three freeze-thaw cycles to lyse cells. The supernatant was subjected to immunoblotting and the band density was detected. The experiments were performed with three biological replicates.

---

miRNA expression analysis (NGS) [3]
For miRNAs-seq, total RNA of two pairs NOZ cells treated with vehicle or Deoxycholic Acid (DCA) were extracted using the miRNeasy Micro Kit. RNA-seq libraries were obtained by using the NEBnext Multiplex Small RNA Library Prep Set, following the manufacturer’s instructions. Sequencing was performed on Illumina Hi-Seq4000 platform with 50 bp single end reads using Illumina reagents according to the manufacturer’s instructions.

Cell lines and cell culture conditions [2]
MGC803 cells were cultured in Roswell Park Memorial Institute media supplemented with 10% fetal calf serum and 100 U/mL penicillin and 100 mg/mL streptomycin. To generate MGC803‐resistant cells, we adjusted the pH value of the MGC803 culture medium to the experimental conditions using the hydrochloric acid (A). The bile acids GCDA and Deoxycholic Acid (DCA) were diluted to optimal working concentrations of 100 μmol/L (B) with culture medium, and the overall pH (A + B) was adjusted to pH 5.5, simulating the gastric environment. Initially, MGC803 cells were chronically exposed to acidified medium with bile acids (A + B) for 10 min every 24 h. The experimental time and conditions were optimized in our preliminary experiments, which showed that 10 min was enough and did not result in cell damage. This procedure was repeated and it took 60 weeks for the MGC803 cells to survive and proliferate under the exposure of A + B for 120 min 12, 13. Control untreated cells were cultured in neutral RPMI medium at pH 7.4 in parallel to the resistant cells for 60 weeks. The morphological changes in MGC803 cells exposed to acidified bile acids (A+B) were documented at 30 and 60 weeks.

---

Cell proliferation assays [3]
Cells were seeded in 96-well plates (2000 cells per well) treated with indicated concentration of Deoxycholic Acid (DCA) (50 μM) or vehicle and after a certain time of culturation, cell growth rate was measured using CCK-8 assays, followed by detection of the absorbance at 450 nm through Synergy 2 microplate reader.. Each experiment with three replicates was repeated three times.

---

Cytotoxic assays in vitro [3]
Cells were seeded in 96-well plates (2000 cells per well) then treated with increasing concentrations of Deoxycholic Acid (DCA) for indicated times. Cell viability was assessed by the Cell Counting Kit-8 assay. The absorbance at 450 nm was measured thorough a Synergy 2 microplate reader. Each experiment with three replicates was repeated three times.

---

Colony formation assay [3]
Cells were seeded in 6-well plates (1000 cells per well) for 10 days until colonies were visible, and then treated with 50 μM Deoxycholic Acid (DCA) or vehicle for 48 h. The colonies were fixed with 4% paraformaldehyde and followed by staining with 0.1% crystal violet.

For xenograft tumor model experiments, 2 × 106 cells GBC-SD or NOZ cells were resuspended with 100 μl of 1 × PBS and subcutaneously into the flanks of BALB/c nude mice (male, 4–6-week old). Six days after injection, mice were randomly allocated to control and treatment groups. All mice were sacrificed and tumors were embedded in paraffin for tissue staining. [3]

Absorption, Distribution and Excretion
Deoxycholic acid is rapidly absorbed after subcutaneous administration. After maximum recommended single treatment dose, 100mg, the post-treatment plasma levels returned to endogenous levels within 24 hours. With the proposed treatment guideline, no accumulation is expected.
The exogenous deoxycholic acid joins the endogenous bile acid pool in the enterohepatic circulation and is excreted unchanged in feces along with endogenous deoxycholic acid.
LIVER NORMALLY SECRETES APPROX 24 G OF BILE SALTS IN 700 TO 1000 ML OF BILE IN 24 HR. MOST OF BILE SALTS ARE REABSORBED IN LOWER SMALL INTESTINE & AGAIN BECOME AVAILABLE FOR SECRETION. ... POOL OF BILE SALTS IS APPROX 2 TO 5 G. /BILE SALTS/

---

Metabolism / Metabolites
Deoxycholic acid is not metabolized to any significant extent under normal conditions.

Protein Binding
98%

---

Interactions
...COMPETITION FOR EXTRAVASCULAR BINDING SITES BY DEOXYCHOLIC ACID MAY EXPLAIN REDUCED VOL OF DISTRIBUTION OF BROMSULFOPHTHALEIN IN PRESENCE OF BILE ACID.
COMPD INCL DEOXYCHOLATE POTENTIATED ANTISTAPHYLOCOCCI ACTIVITY OF GENTAMYCIN, MONOMYCIN, KANAMYCIN, & NEOMYCIN.
Deoxycholic acid was tested alone and as a promoter of N-nitrosobis(2-hydroxypropyl)amine induced carcinogenesis in the hamster. Three groups of 5 to 6-wk-old male Syrian hamsters (SYR)/NI were used and 10 animals per group were given subcutaneous injections of 0.9% NaCl, once per week for 5 weeks. Group 1 received no further treatment; groups 2 and 3 received 0.1% and 0.5% DCA in their feed for 30 weeks, respectively. Animals were autopsied at week 35. There was no significant difference in body wt. between groups 1 and 2, whereas there was a significant decrease in body weight for group 3 (P<0.005). There were no liver tumors, bile duct proliferation, gallbladder lesions or polyps, pancreatic lesions, or pancreatic duct hyperplasia in these 3 groups. In the promoter study, three groups of 5 to 6-wk-old hamsters (number not stated) were given a subcutaneous injection of 500 mg/kg body wt. N-nitrosobis(2-hydroxypropyl)amine per week for 5 weeks. Group 4 received no further treatment and the N-nitrosobis(2-hydroxypropyl)amine treatment was followed by 0.1% DCA (group 5) , or 0.5% DCA (group 6) in the feed for 30 weeks. There was a significant body weight loss (P<0.005) for groups 5 and 6 compared to group 4. DCA significantly increased the induction of cholangiocarcinomas 10/19 in group 5 (P<0.006); 9/25 in group 6 (P<0.05) compared to group 4 which had 1/15. Pancreatic carcinomas were significantly increased in group 5 (14/19, P<0.03). Therefore, under the conditions of this experiment, DCA was not carcinogenic when given alone but was an effective promoter of N-nitrosobis(2-hydroxypropyl)amine-induced hepatic and pancreatic carcinogenesis in hamsters.

---

222528 rat LD50 oral 1 gm/kg BEHAVIORAL: FOOD INTAKE (ANIMAL) Nara Igaku Zasshi. Journal of the Nara Medical Association., 33(71), 1982
222528 mouse LD50 oral 1 gm/kg Nara Igaku Zasshi. Journal of the Nara Medical Association., 33(71), 1982
222528 mouse LD50 intravenous 130 mg/kg Arzneimittel-Forschung. Drug Research., 20(323), 1970 [PMID:5467505]
222528 rabbit LDLo intravenous 2 gm/kg Zeitschrift fuer die Gesamte Experimentelle Medizin., 52(779), 1926

[1]. β-Klotho deficiency protects against obesity through a crosstalk between liver, microbiota, and brown adipose tissue. JCI Insight. 2017 Apr 20;2(8). pii: 91809.

[2]. Acidified bile acids enhance tumor progression and telomerase activity of gastric cancer in micedependent on c-Myc expression. Cancer Med. 2017 Apr;6(4):788-797.

[3]. Deoxycholic acid modulates the progression of gallbladder cancer through N6-methyladenosine-dependent microRNA maturation. Oncogene. 2020 Jun 8;39(26):4983–5000.

Therapeutic Uses
Cholagogues and Choleretics; Detergents
The useful effects of exogenous bile acids result from their capacity to decrease the cholesterol content of the bile and promote dissolution of cholesterol gallstones. /Bile acids/
VET USE: TO INCR VOL OF BILE WITHOUT SIGNIFICANTLY ALTERING PROPORTIONS OF ITS CONSTITUENTS. MOST EFFECTIVE BILE ACID IN AIDING ABSORPTION OF FATS & FAT-SOLUABLE VITAMINS.

---

Deoxycholic acid is a bile acid that is 5beta-cholan-24-oic acid substituted by hydroxy groups at positions 3 and 12 respectively. It has a role as a human blood serum metabolite. It is a bile acid, a dihydroxy-5beta-cholanic acid and a C24-steroid. It is a conjugate acid of a deoxycholate.
Deoxycholic acid is a a bile acid which emulsifies and solubilizes dietary fats in the intestine, and when injected subcutaneously, it disrupts cell membranes in adipocytes and destroys fat cells in that tissue. In April 2015, deoxycholic acid was approved by the FDA for the treatment submental fat to improve aesthetic appearance and reduce facial fullness or convexity. It is marketed under the brand name Kybella by Kythera Biopharma and is the first pharmacological agent available for submental fat reduction, allowing for a safer and less invasive alternative than surgical procedures.

ATX-101 (medical), sodium deoxycholate for subcutaneous injection, is being evaluated as a treatment for the reduction of localized fat deposits. This includes treatment of superficial lipomas (benign tumors of soft tissue composed of mature fat cells), fat deposits in the submental region of the face/neck, and localized fat deposits in other parts of the body. Deoxycholic acid is a naturally occurring bile acid produced by the liver as one of several end products of cholesterol metabolism. As a naturally occurring component of the human body, deoxycholate is considered a ‘biocompatible’ detergent that solubilizes fat in the small intestine. ATX-101 demonstrates a relative selectivity for fat over other tissues.

Deoxycholic acid is a metabolite found in or produced by Escherichia coli (strain K12, MG1655). E. coli Metabolome Database (ECMDB) Deoxycholic acid is a Cytolytic Agent. The physiologic effect of deoxycholic acid is by means of Decreased Cell Membrane Integrity.

Deoxycholic acid has been reported in Homo sapiens and Pseudomonas syringae with data available. LOTUS - the natural products occurrence database Deoxycholic Acid is a steroidal acid that is a secondary bile acid, with cytolytic activity. Upon subcutaneous administration, deoxycholic acid causes lysis of adipocytes and improves the appearance of fullness associated with submental fat. Also, it may potentially be able to reduce fat in other subcutaneous fatty tissues. Deoxycholic acid, naturally produced by the metabolism of cholic acid by intestinal bacteria, is involved in the emulsification of dietary fats in the intestine.

DEOXYCHOLIC ACID is a small molecule drug with a maximum clinical trial phase of IV (across all indications) that was first approved in 2015 and has 4 investigational indications.
Deoxycholic acid is a bile acid formed by bacterial action from cholate. It is usually conjugated with glycine or taurine. Deoxycholic acid acts as a detergent to solubilize fats for intestinal absorption, is reabsorbed itself, and is used as a choleretic and detergent. Bile acids are steroid acids found predominantly in bile of mammals. The distinction between different bile acids is minute, depends only on presence or absence of hydroxyl groups on positions 3, 7, and 12. Bile acids are physiological detergents that facilitate excretion, absorption, and transport of fats and sterols in the intestine and liver. Bile acids are also steroidal amphipathic molecules derived from the catabolism of cholesterol. They modulate bile flow and lipid secretion, are essential for the absorption of dietary fats and vitamins, and have been implicated in the regulation of all the key enzymes involved in cholesterol homeostasis. Bile acids recirculate through the liver, bile ducts, small intestine and portal vein to form an enterohepatic circuit. They exist as anions at physiological pH and, consequently, require a carrier for transport across the membranes of the enterohepatic tissues. The unique detergent properties of bile acids are essential for the digestion and intestinal absorption of hydrophobic nutrients. Bile acids have potent toxic properties (e.g., membrane disruption) and there are a plethora of mechanisms to limit their accumulation in blood and tissues. (A3407, A3408, A3409, A3410). A3407: St-Pierre MV, Kullak-Ublick GA, Hagenbuch B, Meier PJ: Transport of bile acids in hepatic and non-hepatic tissues. J Exp Biol. 2001 May;204(Pt 10):1673-86. PMID:11316487 A3408: Claudel T, Staels B, Kuipers F: The Farnesoid X receptor: a molecular link between bile acid and lipid and glucose metabolism. Arterioscler Thromb Vasc Biol. 2005 Oct;25(10):2020-30. Epub 2005 Jul 21. PMID:16037564 A3409: Chiang JY: Bile acid regulation of hepatic physiology: III. Bile acids and nuclear receptors. Am J Physiol Gastrointest Liver Physiol. 2003 Mar;284(3):G349-56. PMID:12576301 A3410: Davis RA, Miyake JH, Hui TY, Spann NJ: Regulation of cholesterol-7alpha-hydroxylase: BAREly missing a SHP. J Lipid Res. 2002 Apr;43(4):533-43. PMID:11907135

A bile acid formed by bacterial action from cholate. It is usually conjugated with glycine or taurine. Deoxycholic acid acts as a detergent to solubilize fats for intestinal absorption, is reabsorbed itself, and is used as a choleretic and detergent.

---

β-Klotho (encoded by Klb) is the obligate coreceptor mediating FGF21 and FGF15/19 signaling. Klb-/- mice are refractory to beneficial action of pharmacological FGF21 treatment including stimulation of glucose utilization and thermogenesis. Here, we investigated the energy homeostasis in Klb-/- mice on high-fat diet in order to better understand the consequences of abrogating both endogenous FGF15/19 and FGF21 signaling during caloric overload. Surprisingly, Klb-/- mice are resistant to diet-induced obesity (DIO) owing to enhanced energy expenditure and BAT activity. Klb-/- mice exhibited not only an increase but also a shift in bile acid (BA) composition featured by activation of the classical (neutral) BA synthesis pathway at the expense of the alternative (acidic) pathway. High hepatic production of cholic acid (CA) results in a large excess of microbiota-derived deoxycholic acid (DCA). DCA is specifically responsible for activating the TGR5 receptor that stimulates BAT thermogenic activity. In fact, combined gene deletion of Klb and Tgr5 or antibiotic treatment abrogating bacterial conversion of CA into DCA both abolish DIO resistance in Klb-/- mice. These results suggested that DIO resistance in Klb-/- mice is caused by high levels of DCA, signaling through the TGR5 receptor. These data also demonstrated that gut microbiota can regulate host thermogenesis via conversion of primary into secondary BA. Pharmacologic or nutritional approaches to selectively modulate BA composition may be a promising target for treating metabolic disorders.[1]

---

c-Myc overexpression has been implicated in several malignancies including gastric cancer. Here, we report that acidified bile acids enhance tumor progression and telomerase activity in gastric cancer via c-Myc activation both in vivo and in vitro. c-Myc mRNA and protein levels were assessed in ten primary and five local recurrent gastric cancer samples by quantitative real-time polymerase chain reaction and western blotting analysis. The gastric cancer cell line MGC803 was exposed to bile salts (100 μmol/L glycochenodeoxycholic acid and deoxycholic acid) in an acid medium (pH 5.5) for 10 min daily for 60 weeks to develop an MGC803-resistant cell line. Control MGC803 cells were grown without acids or bile salts for 60 weeks as a control. Cell morphology, proliferation, colony formation and apoptosis of MGC803-resistant cells were analyzed after 60 weeks. To determine the involvement of c-Myc in tumor progression and telomere aging in MGC803-resistant cells, we generated xenografts in nude mice and measured xenograft volume and in vivo telomerase activity. The c-Myc and hTERT protein and mRNA levels were significantly higher in local recurrent gastric cancer samples than in primary gastric cancer samples. MGC803-resistant cells showed a marked phenotypic change under normal growth conditions with more clusters and acini, and exhibited increased cell viability and colony formation and decreased apoptosis in vitro. These phenotypic changes were found to be dependent on c-Myc activation using the c-Myc inhibitor 10058-F4. MGC803-resistant cells also showed a c-Myc-dependent increase in xenograft growth and telomerase activity in vivo. In conclusion, these observations support the hypothesis that acidified bile acids enhance tumor progression and telomerase activity in gastric cancer and that these effects are dependent on c-Myc activity. These findings suggest that acidified bile acids play an important role in the malignant progression of local recurrent gastric cancer.[2]

C24H40O4

392.572

392.292

C, 73.43; H, 10.27; O, 16.30

83-44-3

Deoxycholic acid sodium salt;302-95-4;Deoxycholic acid-d4;112076-61-6;Deoxycholic acid-d5;52840-14-9;Deoxycholic acid-13C;52886-37-0;Deoxycholic acid sodium hydrate;145224-92-6;Deoxycholic acid-d6

222528

White to off-white solid powder

1.1±0.1 g/cm3

547.1±35.0 °C at 760 mmHg

171-174 °C(lit.)

298.8±22.4 °C

0.0±3.3 mmHg at 25°C

1.543

4.66

3

4

4

28

605

10

C[C@@]12[C@@H]([C@H](C)CCC(=O)O)CC[C@H]1[C@@H]1CC[C@@H]3C[C@@H](CC[C@]3(C)[C@H]1C[C@@H]2O)O

KXGVEGMKQFWNSR-LLQZFEROSA-N

InChI=1S/C24H40O4/c1-14(4-9-22(27)28)18-7-8-19-17-6-5-15-12-16(25)10-11-23(15,2)20(17)13-21(26)24(18,19)3/h14-21,25-26H,4-13H2,1-3H3,(H,27,28)/t14-,15-,16-,17+,18-,19+,20+,21+,23+,24-/m1/s1

(4R)-4-[(3R,5R,8R,9S,10S,12S,13R,14S,17R)-3,12-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

Deoxycholic acid; DEOXYCHOLIC ACID; 83-44-3; Desoxycholic acid; deoxycholate; Cholerebic; Cholorebic; Choleic acid; Degalol; cholanoic acid; deoxycholate

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)

DMSO : ≥ 100 mg/mL (~254.73 mM)
H2O : < 0.1 mg/mL

Solubility in Formulation 1: 2.5 mg/mL (6.37 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

---

Solubility in Formulation 2: ≥ 2.5 mg/mL (6.37 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

---

View More

Solubility in Formulation 3: ≥ 2.5 mg/mL (6.37 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

---

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