Tauro-α-muricholic acid (T-α-MCA) sodium is an FXR (Farnesoid X receptor) antagonist (IC50=28μM). Tauro-α-muricholic acid sodium is also an endogenously produced metabolite found in the cecum.

Physicochemical Properties

Molecular Formula	C26H44NNAO7S
Molecular Weight	537.68
Exact Mass	537.273
CAS #	2260905-08-4
Related CAS #	25613-05-2
PubChem CID	137700104
Appearance	White to off-white solid powder
Hydrogen Bond Donor Count	4
Hydrogen Bond Acceptor Count	7
Rotatable Bond Count	7
Heavy Atom Count	36
Complexity	897
Defined Atom Stereocenter Count	11
SMILES	C[C@H](CCC(=O)NCCS(=O)(=O)[O-])[C@H]1CC[C@@H]2[C@@]1(CC[C@H]3[C@H]2[C@@H]([C@H]([C@H]4[C@@]3(CC[C@H](C4)O)C)O)O)C.[Na+]
InChi Key	NYXROOLWUZIWRB-BAMGEBLESA-M
InChi Code	InChI=1S/C26H45NO7S.Na/c1-15(4-7-21(29)27-12-13-35(32,33)34)17-5-6-18-22-19(9-11-25(17,18)2)26(3)10-8-16(28)14-20(26)23(30)24(22)31;/h15-20,22-24,28,30-31H,4-14H2,1-3H3,(H,27,29)(H,32,33,34);/q;+1/p-1/t15-,16-,17-,18+,19+,20+,22+,23+,24+,25-,26-;/m1./s1
Chemical Name	sodium;2-[[(4R)-4-[(3R,5R,6S,7S,8S,9S,10R,13R,14S,17R)-3,6,7-trihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoyl]amino]ethanesulfonate
Synonyms	2260905-08-4; Tauro-alpha-muricholic acid sodium salt; 2-[[(3alpha,5beta,6beta,7alpha)-3,6,7-trihydroxy-24-oxocholan-24-yl]amino]-ethanesulfonicacid,monosodiumsalt; sodium;2-[[(4R)-4-[(3R,5R,6S,7S,8S,9S,10R,13R,14S,17R)-3,6,7-trihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoyl]amino]ethanesulfonate; Tauro-; A-muricholic acid (sodium); Tauro-a-muricholic Acid Sodium Salt; Tauro-?-muricholic acid sodium;
HS Tariff Code	2934.99.9001
Storage	Powder-20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.
Shipping Condition	Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Biological Activity

Targets	FXR/Farnesoid X receptor (IC50 = 28μM); Microbial Metabolite
ln Vitro	Tauro-α-muricholic acid (T-α-MCA) (IC50 = 28 μM) and tauro-β-muricholic acid (T-α-MCA) (IC50 = 28 μM) and tauro-β-muricholic acid (T-β-MCA)) (IC50 = 40 μM) are both known as efficient natural antagonists of FXR (Chiang and Ferrell, 2018). They can competitively inhibit the activation of FXR by other bile acids (Li et al., 2013). Next, we found that the sum of cecal T-α-MCA and T-β-MCA levels were significantly upregulated in the LD group compared with the NC group, and their levels were downregulated by NaB treatment. The change in sum of T-α-MCA and T-β-MCA levels in serum was contrary to change observed in the cecal contents (Fig. 4H) [2].
ln Vivo	NaB administration changed bile acid and cholesterol transporters in the liver and ileum in LD-fed mice [2] To determine the effect of the FXR signaling pathway on the CGS mouse model (Li et al., 2013), we detected the signaling molecules related to this pathway. In the current study, we examined the levels of liver Fxr (Nr1h4), Shp (Nr0b2) and Fgfr4 mRNA. We found that Fxr and Shp were downregulated in LD-fed mice and upregulated by NaB treatment, but the change was not significant. The mRNA expression of Fgfr4 was significantly reduced in the LD group and upregulated by NaB treatment. Next, we assessed the expression of several genes encoding catalytic enzymes for the synthesis of bile acids and regulated by the FXR-FGF-15/SHP-FGFR4 signaling pathway: cholesterol 7α-hydroxylase (Cyp7a1), sterol 12α-hydroxylase (Cyp8b1), sterol 27-hydroxylase (Cyp27a1) and oxysterol 7α-hydroxylase (Cyp7b1). We found that these genes were markedly decreased in LD-fed mice compared with NC mice and were further decreased by NaB treatment (Fig. 5A). It was suggested that the synthesis of primary bile acids was inhibited in LD-fed mice and that NaB treatment exacerbated this inhibition. Furthermore, we found that the mRNA expression of Fxr in the ileum was markedly decreased in LD-fed mice compared with NC mice and was significantly upregulated by NaB treatment. The mRNA expression of Fgf-15 and Shp was upregulated in LD-fed mice and significantly further upregulated with NaB treatment (Fig. 5B). The protein expression of FGF-15 in the ileum was assessed by immunofluorescence, and the results were consistent with the mRNA level (Fig. 5C). These results suggested that a high dosage of CA administered in the ileum could have led to ileum FXR activation in LD-fed mice (Chiang and Ferrell, 2018). However, the high contents of T-α-MCA and T-β-MCA in the LD group partially inhibited the activity of FXR. The inhibition of FXR was reduced, and the expression of ileum FXR was upregulated by NaB treatment, which may lead to full FXR activation. After sacrifice, liver and ileum samples were collected at postoperative week 20. The BA profiles are showed in Figure 4. The amount of GUDCA (1687.7 ± 2352.3 ng/ml vs. 16.8 ± 17.2 ng/ml, P = 0.049), T-α-MCA and T-β-MCA (1800.0 ± 1857.5 ng/ml vs. 15.5 ± 14.0 ng/ml, P = 0.011) in liver tissues in the IT group was more than that in the SH group, and the amount of α-MCA (26.8 ± 29.9 ng/ml vs. 535.1 ± 314.3 ng/ml, P < 0.001) was less than that in the SH group. In ileal tissue samples, the amount of GUDCA (12673.2 ± 7011.8 ng/ml vs. 62.2 ± 88.9 ng/ml, P < 0.001), T-α-MCA and T-β-MCA (15645.0 ± 17267.4 ng/ml vs. 111.0 ± 179.7 ng/ml, P = 0.016) in the IT group was more than that in the SH group (Figure 4) [1].
Animal Protocol	Bile acid profiles [1] To identify changes of BA profiles after IT, 17 kinds of BAs, such as α-muricholic acid (α-MCA), β-muricholic acid (β-MCA), cholic acid (CA), chenodeoxycholic acid (CDCA), deoxycholic acid (DCA), hyodeoxycholic acid (HDCA), glycocholic acid (GCA), glycochenodeoxycholic acid (GCDCA), glycodeoxycholic acid (GDCA), glycoursodeoxycholic acid (GUDCA), lithocholic acid (LCA), tauro-α-muricholic acid (T-α-MCA), tauro-β-muricholic acid (T-β-MCA), taurocholic acid (TCA), turoursodeoxycholic acid (TDCA), taurohyodeoxycholic acid (THDCA) and tauroursodeoxycholic acid (TUDCA) were measured in samples.
References	[1]. Farnesoid X receptor is inhibited after ileum transposition in diabetic rats: its hypoglycemic effect. Int J Med Sci. 2023 Apr 2;20(5):595-605. [2]. Sodium butyrate alleviates cholesterol gallstones by regulating bile acid metabolism. Eur J Pharmacol. 2021 Oct 5;908:174341.
Additional Infomation	Background: Aim to investigate bile acid profile changes and the Farnesoid X receptor (FXR) status after ileotransposition (IT), and reveal its possible hypoglycemic mechanism. Methods: Twenty male diabetic rats were randomly assigned into the IT group and the sham IT (SH) group. Bile acid profiles were measured using an ultra-performance liquid chromatography-tandem mass spectrometry. Glucose metabolism was monitored after oral administration of FXR inhibitor and agonist. And the expression of key FXR target genes were measured. Results: The levels of β-muricholic acid (P = 0.047), tauro-α-muricholic acid and tauro-β-muricholic acid (P < 0.001) in plasma in the IT group were higher than those in the SH group, and the levels of taurocholic acid (P = 0.049) and turoursodeoxycholic acid (P = 0.030) were lower than those in the SH group. After inhibition of intestinal FXR, the glucose metabolism in the SH group was improved. When FXR agonist was given, the blood glucose level was increased in both groups. After sacrifice, the levels of glycoursodeoxycholic acid, tauro-α-muricholic acid and tauro-β-muricholic acid in liver and ileum tissues were higher than those in the SH group (P < 0.05), the level of α- muricholic acid (P < 0.001) in liver tissues were lower than that in the SH group. Moreover, the expression of CYP7A1 mRNA (P < 0.001) and FGF15 mRNA (P = 0.001) in the IT group was significantly higher, and the expression of PEPCK mRNA (P = 0.004), SREPB1c mRNA (P = 0.005) and SRB1 mRNA (P = 0.001) were significantly lower than that in the SH group. Conclusions: We demonstrate a remarkable heterogeneity of BA profiles after IT, FXR activation might has a detrimental effect on glucose metabolism. [1] holesterol overloading and bile acid metabolic disorders play an important role in the onset of cholesterol gallstone (CGS). Short-chain fatty acids (SCFAs) can regulate bile acid metabolism by modulating the gut microbiota. However, the role and mechanism by which sodium butyrate (NaB) targets bile acids to attenuate CGS are still unknown. In this study, continuous administration of 12 mg/day for 8 weeks was decreased the incidence of gallstones induced by lithogenic diet (LD) from 100% to 25%. NaB modulated SCFAs and improved the gut microbiota. The remodeling of the gut microbiota changed the bile acid compositions and decreased cecal tauro-α-muricholic acid (T-α-MCA) and tauro-β-muricholic acid (T-β-MCA) which are effective farnesoid X receptor (FXR) antagonists. The quantitative real-time PCR examination showed that NaB significantly increased levels of ileal Fxr, fibroblast growth factor-15 (Fgf-15) and small heterodimer partner (Shp) mRNA and subsequently inhibited bile acid synthesis. In addition, NaB enhanced bile acid excretion by increasing the levels of hepatic multidrug resistance protein 2 (Mdr2) and bile salt export pump (Bsep) mRNA, and it enhanced bile acid reabsorption in the intestine by increasing the levels of ileal bile acid transporter (Ibat) mRNA. In addition, NaB reduced the absorption of cholesterol in the intestine and inhibited the excretion of cholesterol in the liver, which reduced the cholesterol concentration in serum and bile. Furthermore, the protective effects of NaB administration were abolished by FXR antagonists. Taken together, our results suggest that NaB mitigates CGS by modulating the gut microbiota to regulate the FXR-FGF-15/SHP signaling pathway.[2]

Solubility Data

Solubility (In Vitro)

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

Solubility (In Vivo)

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. Injection Formulations (e.g. IP/IV/IM/SC) 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). 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) Oral Formulations 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). 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 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.  (Please use freshly prepared in vivo formulations for optimal results.)

Preparing Stock Solutions		1 mg	5 mg	10 mg
	1 mM	1.8598 mL	9.2992 mL	18.5984 mL
	5 mM	0.3720 mL	1.8598 mL	3.7197 mL
	10 mM	0.1860 mL	0.9299 mL	1.8598 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.