Taurocholic acid | CAS:81-24-3 | Manufacturer ChemFaces

Taurocholic acid

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Description:

Taurocholic acid feeding shows cytoprotective effects on the biliary tree after adrenergic denervation of the liver; taurocholic acid feeding prevents tumor necrosis factor-alpha-induced damage of cholangiocytes by a PI3K-mediated pathway. Rectal administration of taurocholic acid can stimulate glucagon-like peptide-1 and peptide YY by TGR5 receptor activation, which may have potential for the management of type 2 diabetes and obesity.

Targets:

TNF-α | PI3K | Akt | p38MAPK | Caspase | TGR5

In vivo:

Diabetes Obes Metab. 2013 May;15(5):474-7.

Effects of rectal administration of taurocholic acid on glucagon-like peptide-1 and peptide YY secretion in healthy humans.[Pubmed: 23181598 ]

Glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), secreted by enteroendocrine L-cells located most densely in the colon and rectum, are of fundamental importance in blood glucose and appetite regulation. In animal models, colonic administration of bile acids can stimulate GLP-1 and PYY by TGR5 receptor activation.
METHODS AND RESULTS:
We evaluated the effects of Taurocholic acid (TCA), administered as an enema, on plasma GLP-1 and PYY, as well as gastrointestinal sensations in 10 healthy male subjects, and observed that rectal administration of TCA promptly stimulated secretion of both GLP-1 and PYY, and increased fullness, in a dose-dependent manner.
CONCLUSIONS:
These observations confirm that topical application of bile acids to the distal gut may have potential for the management of type 2 diabetes and obesity.

Liver Int. 2007 May;27(4):558-68.

Cytoprotective effects of taurocholic acid feeding on the biliary tree after adrenergic denervation of the liver.[Pubmed: 17403196 ]

Cholangiopathies impair the balance between proliferation and apoptosis of cholangiocytes leading to the disappearance of bile ducts and liver failure. Taurocholic acid (TC) is essential for cholangiocyte proliferative and functional response to cholestasis. Bile acids and neurotransmitters co-operatively regulate the biological response of the biliary epithelium to cholestasis. Adrenergic denervation of the liver during cholestasis results in the damage of bile ducts. To verify whether TC feeding prevents the damage of the biliary tree induced by adrenergic denervation in the course of cholestasis.
METHODS AND RESULTS:
Rats subjected to bile duct ligation (BDL) and to adrenergic denervation were fed a TC-enriched diet, in the absence or presence of daily administration of the phosphatidyl-inositol-3-kinase (PI3K) inhibitor wortmannin for 1 week. TC prevented the induction of cholangiocyte apoptosis induced by adrenergic denervation. TC also restored cholangiocyte proliferation and functional activity, reduced after adrenergic denervation. TC prevented AKT dephosphorylation induced by adrenergic denervation. The cytoprotective effects of TC were abolished by the simultaneous administration of wortmannin.
CONCLUSIONS:
TC administration prevents the damage of the biliary tree induced by the adrenergic denervation of the liver. These novel findings open novel perspectives in the understanding of the potential of bile acids especially in post-transplant liver disease.

Taurocholic acid Description

Source:	From snake bile.
Solvent:	Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Storage:	Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C). Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour. Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com
After receiving:	The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.

Kinase Assay:

Placenta. 2014 Jul;35(7):496-500.

High concentraction of taurocholic acid induced apoptosis in HTR-8/SVneo cells via overexpression of ERp29 and activation of p38.[Pubmed: 24780196 ]

Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific disease associated with a significant risk of fetal complications. Our previous study using an iTRAQ-based proteomics approach showed that ERp29 was overexpressed in the placenta tissue of ICP patients, which was an apoptosis-related protein and has not been investigated in the pathogenesis of ICP. The aim of this study was to explore the role of ERp29 in the mechanism of apoptosis in the placenta of ICP.
METHODS AND RESULTS:
HTR-8/SVneo cells were cultured and treated with different concentrations of Taurocholic acid (TCA) (0, 10, 50 and 100 μM). The apoptotic index and cell cycle were detected by flow cytometry; furthermore, the expression levels of ERp29 and p-p38 were detected by western blot. The ERp29-siRNA was also used to confirm the role of ERp29 in TCA induced-apoptosis. ERp29 expression and the apoptotic index were significantly increased in HTR-8/SVneo cells exposed to 100 μM TCA; so were p-p38 and caspase-3 activity, compared with the 50 μM, 10 μM TCA groups and negative control group (P < 0.05, respectively). The induction of apoptosis by TCA and the expression of p-p38 were reduced in HTR-8/SVneo cells after treatment with ERp29-siRNA, compared with controls (P < 0.05, respectively).
CONCLUSIONS:
This study suggested that overexpression of ERp29 may play a key role in TCA-induced apoptosis in HTR-8/SVneo cells via activation of p38, which may participate in the pathogenesis of ICP and may represent a novel target for ICP treatment.

Animal Research:

Exp Biol Med (Maywood). 2007 Jul;232(7):942-9.

Taurocholic acid feeding prevents tumor necrosis factor-alpha-induced damage of cholangiocytes by a PI3K-mediated pathway.[Pubmed: 17609511]

Cholangiopathies, such as primary biliary cirrhosis and primary sclerosis cholangitis, are characterized at the end stage by ductopenia due to increased cholangiocyte apoptosis and decreased cholangiocyte proliferation. Although cholangiocyte proliferation is associated with an increased number of intra-hepatic bile ducts and secretin-stimulated ductal secretion, ductopenia is coupled with decreased ductal mass and secretin-induced ductal secretory activity.
METHODS AND RESULTS:
We have shown that a single injection of actinomycin D + tumor necrosis factor-alpha (TNF-alpha ) to bile duct-ligated (BDL) rats induces cholangiocyte injury, which is characterized by loss of cholangiocyte proliferation, and secretory activity and by an increase in cholangiocyte apoptosis. We also have shown that Taurocholic acid both in vivo and in vitro stimulates cholangiocyte proliferation. We hypothesize that Taurocholic acid feeding protects cholangiocytes against TNF-alpha -induced apoptosis through a phosphatidylinositol-3-kinase (PI3K)-dependent pathway. Immediately after BDL, rats were fed Taurocholic acid or control diet in the absence/presence of daily injections of wortmannin for 1 week. Seven days later, control-fed or Taurocholic acid-fed rats were treated with a single intraperitoneal injection of actinomycin D + TNF-alpha . Twenty-four hours later we evaluated: (i) cholangiocyte apoptosis and proliferation in liver sections and (ii) basal and secretin-stimulated bile and bicarbonate secretion in bile fistula rats.
CONCLUSIONS:
Taurocholic acid feeding prevented TNF-alpha -induced increases in cholangiocyte apoptosis and decreases in growth and secretin-stimulated bile and bicarbonate secretion, changes that were blocked by PI3K inhibition. The PI3K survival pathway is important in bile acid protection against immune-mediated cholangiocyte injury in cholestatic liver diseases.

Product Name	Taurocholic acid
Price:
CAS No.:	81-24-3
Catalog No.:	CFN96646
Molecular Formula:	C₂₆H₄₅NO₇S
Molecular Weight:	515.70 g/mol
Purity:	>=98%
Type of Compound:	Steroids
Physical Desc.:	Powder
Source:	From snake bile.
Solvent:	Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download:	COA MSDS
Similar structural:	Comparison (Web) (SDF)
Guestbook:

Size /Price /Stock	10 mM * 100 uL in DMSO / Inquiry / In-stock 10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries	Hepatoprotective Compound Library Pro-apoptotic Compound Library Anti-diabetic Compound Library Anti-obesity Compound Library Cytoprotective Compound Library Steroids Compound Library TNF-α Inhibitor Library PI3K Inhibitor Library p38MAPK Inhibitor Library Caspase Inhibitor Library Akt Inhibitor Library

	1 mg	5 mg	10 mg	20 mg	25 mg
1 mM	1.9391 mL	9.6956 mL	19.3911 mL	38.7822 mL	48.4778 mL
5 mM	0.3878 mL	1.9391 mL	3.8782 mL	7.7564 mL	9.6956 mL
10 mM	0.1939 mL	0.9696 mL	1.9391 mL	3.8782 mL	4.8478 mL
50 mM	0.0388 mL	0.1939 mL	0.3878 mL	0.7756 mL	0.9696 mL
100 mM	0.0194 mL	0.097 mL	0.1939 mL	0.3878 mL	0.4848 mL

CFN96646	Taurocholic acid	81-24-3	515.70	C₂₆H₄₅NO₇S
CFN96645	Tauroursodeoxycholic acid	14605-22-2	499.70	C₂₆H₄₅NO₆S
CFN80241	Sodium taurochenodeoxycholate	6009-98-9	521.68	C₂₆H₄₄NNaO₆S
CFN96464	Ursodeoxycholic acid	128-13-2	392.58	C₂₄H₄₀O₄
CFN90478	Chenodeoxycholic acid	474-25-9	392.57	C₂₄H₄₀O₄
CFN99796	Cholic acid	81-25-4	408.57	C₂₂H₄₀O₅
CFN91626	Hyocholic acid	547-75-1	408.6	C₂₄H₄₀O₅
CFN99798	Deoxycholic acid	83-44-3	392.57	C₂₄H₄₀O₄
CFN89170	Lithocholic acid	434-13-9	376.58	C₂₄H₄₀O₃
CFN96673	Sodium cholate	361-09-1	430.55	C₂₄H₃₉NaO₅