Tauroursodeoxycholic Acid (TUDCA)

Catalog No.S3654 Batch:S365407

Technical Data

Formula	C₂₆H₄₅NO₆S
Molecular Weight	499.70	CAS No.	14605-22-2
Solubility (25°C)*	In vitro	DMSO	100 mg/mL (200.12 mM)
		Ethanol	100 mg/mL (200.12 mM)
		Water	13 mg/mL (26.01 mM)
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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Biological Activity

Description	Tauroursodeoxycholic acid (TUDCA) is the taurine conjugate of ursodeoxycholic acid (UDCA) and acts as a mitochondrial stabilizer and anti-apoptotic agent in several models of neurodegenerative diseases, including AD, Parkinson's diseases (PD), and Huntington's diseases (HD).
In vitro	Tauroursodeoxycholic acid (TUDCA) is an endogenous hydrophilic tertiary bile acid produces in humans at a low level. In ER stress conditions, TUDCA treatment of MSCs (mesenchymal stem cells) reduces the activation of ER stress-associated proteins, including GRP78, PERK, eIF2α, ATF4, IRE1α, JNK, p38, and CHOP, and inhibits the dissociation between GRP78 and PERK, resulting in reduced ER stress-mediated cell death. TUDCA treatment increases PrP^C (Cellular prion protein) expression. TUDCA regulates stem cell differentiation into various lineages such as adipogenic and osteogenic lineages. TUDCA attenuates ER stress, prevents unfolded protein response dysfunction, and stabilizes mitochondria. Under ER stress, treatment with TUDCA significantly increases the expression of BCL-2 and significantly decreases the expression of Bax, cleaved caspase-3, and cleaved PARP-1, compared with that of untreated cells^[1].
In vivo	TUDCA is effective for treating cholestatic liver diseases. It also has an ameliorating effect on several diseases, including neurodegenerative diseases, osteoarthritis, vascular diseases, and diabetes. In a murine hindlimb ischemia model, TUDCA-treated mesenchymal stem cells (MSCs) transplantation augments the blood perfusion ratio, vessel formation, and transplanted cell survival more than untreated MSC transplantation does. Augmented functional recovery following MSC transplantation is blocked by PrP^C downregulation^[1]. Several studies in animals have shown that TUDCA, an endogenous ambiphilic bile acid, can inhibit unfolded protein response dysfunction and ameliorate ER stress. TUDCA administration attenuates HDM-induced ER stress, airway inflammation, mucus metaplasia, airway remodeling, and methacholine-induced AHR^[2].

Protocol (from reference)

Cell Assay:^{^[1]}	Cell lines Mesenchymal stem cells (MSCs) Concentrations 100 μM Incubation Time 30 min Method MSCs are washed twice with phosphate buffer saline (PBS), and fresh α-MEM supplemented with 10% FBS is added. To investigate the apoptosis signaling pathway, MSCs are pretreated with TUDCA (100 μM) at 37 °C for 30 min and then treated with H2O2 (200 μM) for various times (0, 2, 4, 6, or 8 h). To assess another cell signaling pathway, MSCs are treated with an Akt inhibitor (10⁻⁶ M) for 30 min at 37 °C before treatment with TUDCA.
Animal Study:^{^[2]}	Animal Models House dust mite-induced allergic airway disease mouse model (background: C57BL/6 NJ mice) Dosages 0.5, 1, and 5 mg/kg body wt Administration via the nasopharynx

Cell Assay:^{^[1]}

Cell lines
Mesenchymal stem cells (MSCs)
Concentrations
100 μM
Incubation Time
30 min
Method
MSCs are washed twice with phosphate buffer saline (PBS), and fresh α-MEM supplemented with 10% FBS is added. To investigate the apoptosis signaling pathway, MSCs are pretreated with TUDCA (100 μM) at 37 °C for 30 min and then treated with H2O2 (200 μM) for various times (0, 2, 4, 6, or 8 h). To assess another cell signaling pathway, MSCs are treated with an Akt inhibitor (10⁻⁶ M) for 30 min at 37 °C before treatment with TUDCA.

Animal Study:^{^[2]}

Animal Models
House dust mite-induced allergic airway disease mouse model (background: C57BL/6 NJ mice)
Dosages
0.5, 1, and 5 mg/kg body wt
Administration
via the nasopharynx

References

Selleck's Tauroursodeoxycholic Acid (TUDCA) has been cited by 31 publications

Advanced oxidation protein products induce Paneth cells defects by endoplasmic reticulum stress in Crohn's disease [ iScience, 2023, 26(8):107312]	PubMed: 37539032
Routes of Albumin Overload Toxicity in Renal Tubular Epithelial Cells [ Int J Mol Sci, 2023, 24(11)9640]	PubMed: 37298591
Tauroursodeoxycholic Acid Supplementation in In Vitro Culture of Indicine Bovine Embryos: Molecular and Cellular Effects on the In Vitro Cryotolerance [ Int J Mol Sci, 2023, 24(18)14060]	PubMed: 37762363
Tauroursodeoxycholic acid protects Schwann cells from high glucose-induced cytotoxicity by targeting NLRP3 to regulate cell migration and pyroptosis [ Biotechnol Appl Biochem, 2023, 10.1002/bab.2518]	PubMed: 37749820
Very-low-density lipoprotein receptor-enhanced lipid metabolism in pancreatic stellate cells promotes pancreatic fibrosis [ Immunity, 2022, 55(7):1185-1199.e8]	PubMed: 35738281
Mitochondrial fission links ECM mechanotransduction to metabolic redox homeostasis and metastatic chemotherapy resistance [ Nat Cell Biol, 2022, 24(2):168-180]	PubMed: 35165418
Tauroursodeoxycholic acid functions as a critical effector mediating insulin sensitization of metformin in obese mice [ Redox Biol, 2022, 57:102481]	PubMed: 36148770
Tripartite motif 25 ameliorates doxorubicin-induced cardiotoxicity by degrading p85α [ Cell Death Dis, 2022, 13(7):643]	PubMed: 35871160
Endoplasmic reticulum stress contributes to cisplatin-induced chronic kidney disease via the PERK-PKCδ pathway [ Cell Mol Life Sci, 2022, 79(8):452]	PubMed: 35895146
S1PR2/RhoA/ROCK1 pathway promotes inflammatory bowel disease by inducing intestinal vascular endothelial barrier damage and M1 macrophage polarization [ Biochem Pharmacol, 2022, 201:115077]	PubMed: 35537530

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SHIPPING AND STORAGE
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