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Purity: ≥98%
Sodium Tauroursodeoxycholate (TUDC) is a water soluble bile salt, which is used for the treatment of gallstones and liver cirrhosis. Tauroursodeoxycholate exhibits protective and reversing effects in vitro against the impairment of the cVA-of-CLF brought on by 17βEG. Tauroursodeoxycholate reduces cell growth in Mz-ChA-1 cholangiocarcinoma cells through pathways that depend on Ca2+-, PKC, and MAPK. Tauroursodeoxycholate inhibits bile acid-induced apoptosis in isolated rat hepatocytes by causing the formation of cAMP through the β1-integrin.
Targets |
Human Endogenous Metabolite; ERK; Caspase-3/12;
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ln Vitro |
Tauroursodeoxycholate (TUDCA) reduces the viability and migration of vascular smooth muscle cells (VSMCs) by inhibiting the phosphorylation of ERK and by inducing mitogen-activated protein kinase phosphatase-1 (MKP-1) via PKCα. By blocking ERK through Ca2+-dependent PKC translocation, tauroursodeoxycholate prevents the VSMCs from proliferating and migrating. Platelet-derived growth factor (PDGF) and MMP-9 expression brought on by vascular injury are both prevented by tauroursodeoxycholate. Tauroursodeoxycholate (200 μM) reduced VSMC viability, which suggests that Tauroursodeoxycholate's ability to inhibit cell proliferation depended on MKP-1 expression[1]. MKP-1 expression can be reduced by using specific si-RNA to knock it down.
Tauroursodeoxycholate (TUDCA) activates mitogen-activated phosphophosphatase 1 (MKP-1) through PKCα and suppresses ERK phosphorylation, ultimately decreasing the survival and migration of vascular smooth muscle cells (VSMC). Tauroursodeoxycholate suppresses ERK through Ca2+-induced PKCα translocation Tauroursodeoxycholate (200 μM) can restore VSMC decreased by Tauroursodeoxycholate (200 μM), consequently limiting the proliferation and migration of VSMC. activity, which implies that the anti-stress impact of Tauroursodeoxycholate depends on the expression of MKP-1 [1]. Transporters of TUDCA uptake in human VSMCs (hVSMCs) were analysed by RT-PCR and western blot. A knock-down experiment using specific si-RNA revealed that TUDCA was incorporated into hVSMCs via organic anion transporter 2 (OATP2). TUDCA reduced the viability of hVSMCs, which were mediated by inhibition of extracellular signal-regulated kinase (ERK) by induction of mitogen-activated protein kinase phosphatase-1 (MKP-1) via protein kinase Cα (PKCα). The anti-proliferative effect of TUDCA was reversed by treatment with 7-hydroxystaurosporine, an inhibitor of PKC, and by the knock-down of MKP-1. In addition, TUDCA suppressed hVSMC migration, which was mediated by reduced matrix metalloproteinase-9 (MMP-9) expression by ERK inhibition, as well as reduced viability of hVSMCs. The uptake of TUDCA was mediated by OATP2 in hVSMCs. TUDCA suppresses both viability and migration of VSMCs through inhibition of ERK phosphorylation, by induction of MKP-1 via PKCα. TUDCA suppressed the PDGF-mediated proliferation and migration of VSMCs. [1] |
ln Vivo |
Immunohistochemistry is used to examine the impact of tauroursodeoxycholate (TUDCA) on the proliferation and apoptosis of VSMCs in vivo. Tauroursodeoxycholate (10, 50, and 100 mg/kg) increases the caspase 3 activity of injured tissues in a dose-dependent manner, suggesting that it causes VSMCs in the neointima to undergo apoptosis. At one week after injury, additional testing and comparison of the phosphorylation level of ERK and MMP-9 expression is done using the injured tissues in comparison to normal controls. Both ERK phosphorylation and MMP-9 expression were upregulated in the tissues after balloon injury. Tauroursodeoxycholate (10, 50, and 100 mg/kg) inhibits the expression of MMP-9 and ERK in a dose-dependent manner[1]. Tauroursodeoxycholate (TUDCA) is a hydrophilic bile acid. By lowering ER stress and apoptosis, tauroursodeoxycholate, a cytoprotective agent, enhances liver function and can prevent hepatocellular carcinoma. In Ang II-induced ApoE-/- mice, tauroursodeoxycholate significantly decreases expression of apoptosis molecules like caspase-3, caspase-12, C/EBP homologous protein, c-Jun N-terminal kinase (JNK), activating transcription factor 4 (ATF4), X-box binding protein (XBP), and eukaryotic initiation factor 2α (eIF2; p<0.05). In ApoE-/- mice, tauroursodeoxycholate prevents the development of abdominal aortic aneurysms (AAAs) brought on by Ang II. Tauroursodeoxycholate is administered to ApoE-/- mice (ER stress inhibitor group) at a dose of 0.5 g/kg/day. Total cholesterol levels (663.6±88.7 mg/dL vs 655.7±65.4 mg/dL; p>0 .05) and systolic blood pressure (141.3±5.6 mmHg vs 145.98.9 mmHg; p>0.05) were comparable between the AAA model group and the Tauroursodeoxycholate group. Additionally, when compared to the AAA model group, the Tauroursodeoxycholate group's maximum aortic diameter was significantly lower (0.95±0.03 mm vs 1.79±0.04 mm; p<0.05). The AAA lesion areas in the Tauroursodeoxycholate group are also smaller than those in the AAA model group (0.37±0.03 mm2 vs 1.51±0.06 mm2; p<0.05)[2].
Reduction in neointimal hyperplasia by TUDCA in vivo [1] The in vitro results suggest that TUDCA could inhibit neointima formation after vessel injury through ERK inhibition via PKCα. The rat carotid artery injury model was used to analyse the effects of TUDCA on neointima formation. After balloon injury, the oral administration of TUDCA for 2 weeks significantly suppressed neointima formation in a dose-dependent manner (I/M ratio; 50 mg/kg, 1.48 ± 0.11; 100 mg/kg, 1.17 ± 0.16 vs. control, 1.86 ± 0.17, n= 8, P< 0.05) (Figure 4A and B). In addition, neointimal area (vehicle, 100 ± 12.9%; TUDCA 10 mg/kg, 80.0 ± 19.7%; TUDCA 50 mg/kg, 75.5 ± 6.8%; TUDCA 100 mg/kg, 56.9 ± 20%, n= 8 in each group) and neointimal thickness (vehicle, 133.5 ± 26.7 μm; TUDCA 10 mg/kg, 92.1 ± 23.3 μm; TUDCA 50 mg/kg, 78.5 ± 15.7 μm; TUDCA 100 mg/kg, 61.8 ± 16.3 μm, n= 8 in each group) were significantly reduced by administration of TUDCA (Figure 4C and D), whereas TUDCA increased the lumen area in a dose-dependent manner (normal, 100 ± 5.6%;vehicle, 63.3 ± 7.1%; TUDCA 10 mg/kg, 73.1 ± 11.1%; TUDCA 50 mg/kg, 78.7 ± 5.8%; TUDCA 100 mg/kg, 91.2 ± 8.2%, n= 8 in each group) proportional to the decrease in neointimal area (Figure 4E). In addition, the medial area and medial cell number were not affected (Supplementary material online, Figure S5A and B). |
Enzyme Assay |
FITC-TUDCA uptake assay [1]
Human VSMCs (hVSMCs) were cultured in Smooth Muscle Cell Growth Medium 2. Cells between passages 4 and 7, from four donors, were used for this study. hVSMCs (1 × 104) were seeded onto a 96-well plate and cultured. Each indicated concentration of FITC-TUDCA was added and washed with cold phosphate-buffered saline. The FITC signal was evaluated by counting the absorbance at 488 nm. For the competition assay, 100 μM of FITC-TUDCA was mixed with the indicated concentration of non-labelled TUDCA, and then treated to hVSMCs for 15 min. The detailed methods were described in Supplementary material online. Zymography [1] Cells were incubated with TUDCA for 24 h. Then, the supernatants were harvested and loaded onto SDS–PAGE containing 1 mg/mL gelatin. After electrophoresis, the gel was incubated in the reaction buffer for 24 h, and then subsequently stained with 0.15% Coomassie Brilliant Blue R250. The detailed methods were described in Supplementary material online. |
Cell Assay |
Ez-Cytox is used to assess the viability and growth of cells. Smooth Muscle Cell Growth Medium 2 (SMCGM2) is used to seed and cultivate VSMCs (5×103 cells) on 96-well plates. After serum starvation, Tauroursodeoxycholate (0, 50, 100, and 200 μM) is added to the hVSMCs, with or without 1,2-bis(o-aminophenoxy) ethane-N,N,N′,N′-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA, 10 μM) and 7-hydroxystaurosporine (H7, 10 μM) and cultured for 24 h. HVSMCs are seeded onto 96-well plates and cultured to determine the impact of tauroursodeoxycholate on the PDGF-stimulated hVSMC proliferation. Tauroursodeoxycholate (0, 50, 100, and 200 μM) is added to the hVSMCs after serum starvation, with or without PDGF-BB (50 ng/mL), and the cells are then cultured. The optical density at 450 nm is used to assess cell viability after the addition of 10 μL of Ez-Cytox into each well[1].
The scratch-wound assay [1] Migration of hVSMCs was evaluated using the scratch-wound model, as described previously.24 hVSMCs (1 × 106) were seeded onto 60 mm dishes and cultured until the cells reached confluence. Each indicated concentration of TUDCA was added to the hVSMCs for 1 h, and the confluent monolayers were scraped, through the middle of the dish, using a modified yellow tip. After wounding, the monolayers were washed with serum-free SMCGM2 and were cultured with TUDCA for 36 h. The hVSMCs that migrated from the wound edge were counted by three separate investigators. Flow cytometry [1] Apoptosis of the hVSMCs by TUDCA were evaluated by flow cytometry. After serum starvation for 24 h, TUDCA in increasing concentrations (i.e. 0, 50, 100, and 200 μM) was added to the hVSMCs. Cells were harvested and fixed and then the DNA content was analysed by flow cytometry. The detailed methods were described in Supplementary material online. |
Animal Protocol |
Rats: Ketamine (70 mg/kg) and Xylazine (7 mg/kg) are combined to anesthetize Sprague-Dawley rats. For two weeks, tauroursodeoxycholate is given orally once daily at various concentrations (e.g., vehicle, 10, 50, and 100 mg/kg). The carotid arteries are preserved by perfusion with 4% formaldehyde, followed by paraffin embedding and H&E staining of sections (8 μm)[1].
Mice: Thirty C57BL/6 male ApoE-/- mice are divided into three groups at random, each with ten mice, and they are eight weeks old. (i) ApoE-/- mice are implanted with mini-osmotic pumps to release Ang II (1000 ng/kg/min) over the course of 28 days (AAA model group); (ii) AAA model mice are treated with Tauroursodeoxycholate daily for 4 weeks at a dosage of 0.5 g/kg/day in drinking water (Tauroursodeoxycholate group). Following a 28-day Ang II infusion, mice are sacrificed[2]. Rat carotid artery balloon injury [1] The rats were anaesthetized with a combined anaesthetic (ketamine, 70 mg/kg; xylazine, 7 mg/kg ip). Noxious stimuli were applied to a limb occasionally throughout the experiments, while monitoring changes in the end-tidal carbon dioxide, heart rate, blood pressure, and cardiac rhythm, in order to ascertain the level of anaesthesia. After the left external carotid artery was exposed, a 2 F Fogarty embolectomy catheter was introduced through an external carotid arteriotomy incision, advanced to the common carotid artery, inflated with 0.2 mL of saline, and withdrawn 10 times, with rotation.TUDCA was then administered orally once a day, in different concentrations (i.e. vehicle, 10, 50, and 100 mg/kg) for 2 weeks. The carotid arteries were fixed by perfusion with 4% formaldehyde, then the tissues were embedded in paraffin, and sections (8 μm) were stained with H&E. The detailed methods were described in Supplementary material online. Ang II induced AAA model in mice [2] Thirty ApoE−/− C57BL/6 male mice aged 8 weeks were randomly divided into three groups (n = 10 in each group): (i) sham operated and injected with physiologic (0.9%) saline as vehicle (“normal: group); (ii) mini-osmotic pumps were implanted subcutaneously into the right flank of ApoE−/− mice to release Ang II (1000 ng/kg/min) over the course of 28 days (“AAA model” group); (iii) AAA model mice treated with ER stress inhibitor (TUDCA) daily for 4 weeks at a dosage of 0.5 g/kg/day in drinking water (“ER stress inhibitor” group). Mice were sacrificed after 28 days of Ang II infusion. As described previously,22 systolic blood pressure was obtained 1 week before the implantation of the mini-osmotic pumps in mice and after 28 days of infusion, by use of a non-invasive tail cuff system. Blood was collected from the retro-orbital sinus under isoflurane anaesthesia. Serum total cholesterol levels were measured using an enzymatic method. |
ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
There is evidence that tauroursodeoxycholic acid crosses the blood brain barrier in humans. Metabolism / Metabolites There is little biotransformation of tauroursodeoxycholic acid. It is partially deconjugated by intestinal microflora to form unconjugated bile acids. |
Toxicity/Toxicokinetics |
9848818 rat LD50 oral >5 gm/kg Japanese Kokai Tokyo Koho Patents., #92-235918
9848818 rat LD50 intravenous 300 mg/kg Japanese Kokai Tokyo Koho Patents., #92-235918 9848818 mouse LD50 oral >6 gm/kg Japanese Kokai Tokyo Koho Patents., #92-235918 9848818 mouse LD50 intravenous 350 mg/kg Japanese Kokai Tokyo Koho Patents., #92-235918 |
References |
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Additional Infomation |
Tauroursodeoxycholic acid is a bile acid taurine conjugate derived from ursoodeoxycholic acid. It has a role as a human metabolite, an anti-inflammatory agent, a neuroprotective agent, an apoptosis inhibitor, a cardioprotective agent and a bone density conservation agent. It is functionally related to an ursodeoxycholic acid. It is a conjugate acid of a tauroursodeoxycholate.
Tauroursodeoxycholic acid, also known as ursodoxicoltaurine, is a highly hydrophilic tertiary bile acid that is produced in humans at a low concentration. It is a taurine conjugate of [ursodeoxycholic acid] with comparable therapeutic efficacy and safety, but a much higher hydrophilicity. Normally, hydrophilic bile acids regulates hydrophobic bile acids and their cytotoxic effects. Tauroursodeoxycholic acid can reduce the absorption of cholesterol in the small intestine, thereby reducing the body's intake of dietary cholesterol and the body cholesterol content. Tauroursodeoxycholic acid is currently used in Europe to treat and prevent gallstones as a bile acid derivative. Due to a range of its molecular properties - namely its anti-apoptotic effects - tauroursodeoxycholic acid has been examined in inflammatory metabolic diseases and neurodegenerative diseases. Tauroursodeoxycholic acid has been reported in Homo sapiens with data available. Drug Indication Tauroursodeoxycholic acid is used to prevent and treat gallstone formation. Tauroursodeoxycholic acid is used in combination with [phenylbutyric acid] to treat amyotrophic lateral sclerosis (ALS) in adults. Mechanism of Action About 90% of gallstones are formed by cholesterol, which may be caused by altered gut microbiota from a high-fat diet and other factors. The gut microbiota regulates bile acid metabolism; thus, altered composition in gut microbiota may significantly change the bile acid pool and alter cholesterol secretion. While the exact mechanism of action of tauroursodeoxycholic acid in reducing and preventing gallstone formation is unclear, tauroursodeoxycholic acid may achieve this effect in a number of ways. A recent mouse study suggests that tauroursodeoxycholic acid inhibits intestinal cholesterol absorption and lowers liver cholesterol levels by upregulating the bile acid excretion from the liver to the gallbladder. Tauroursodeoxycholic acid lowers the bile cholesterol saturation in the gallbladder, thereby increasing the solubility of cholesterol in bile. It can also maintain a specific gut microbiota composition to promote the synthesis of bile acids and reduce liver inflammation caused by the lipopolysaccharide in the blood. Ultimately, tauroursodeoxycholic acid enhances the synthesis of bile acids in the liver and reduces cholesterol in the serum and liver. Tauroursodeoxycholic acid inhibits cell apoptosis by disrupting the mitochondrial pathway of cell death. It works by inhibiting oxygen-radical production, ameliorating endoplasmic reticulum (ER) stress, and stabilizing the unfolded protein response. Other anti-apoptotic processes mediated by tauroursodeoxycholic acid include cytochrome c release, caspase activation, DNA and nuclear fragmentation, and inhibition of p53 transactivation. It is believed that tauroursodeoxycholic acid works on multiple cellular targets to inhibit apoptosis and upregulate survival pathways. TAURURSODIOL is a small molecule drug with a maximum clinical trial phase of IV (across all indications) that was first approved in 2022 and has 2 investigational indications. Aims: Hyperplasia of vascular smooth muscle cells (VSMCs) after blood vessel injury is one of the major pathophysiological mechanisms associated with neointima. Tauroursodeoxycholate (TUDCA) is a cytoprotective agent in a variety of cells including hepatocytes as well as an inducer of apoptosis in cancer cells. In this study, we investigated whether TUDCA could prevent neointimal hyperplasia by suppressing the growth and migration of VSMCs. Methods and results: Transporters of TUDCA uptake in human VSMCs (hVSMCs) were analysed by RT-PCR and western blot. A knock-down experiment using specific si-RNA revealed that TUDCA was incorporated into hVSMCs via organic anion transporter 2 (OATP2). TUDCA reduced the viability of hVSMCs, which were mediated by inhibition of extracellular signal-regulated kinase (ERK) by induction of mitogen-activated protein kinase phosphatase-1 (MKP-1) via protein kinase Cα (PKCα). The anti-proliferative effect of TUDCA was reversed by treatment with 7-hydroxystaurosporine, an inhibitor of PKC, and by the knock-down of MKP-1. In addition, TUDCA suppressed hVSMC migration, which was mediated by reduced matrix metalloproteinase-9 (MMP-9) expression by ERK inhibition, as well as reduced viability of hVSMCs. Rats with carotid artery balloon injury received oral administration of TUDCA; this reduced the increase in ERK and MMP-9 caused by balloon injury. TUDCA significantly decreased the ratio of intima to media by reducing proliferation and inducing apoptosis of the VSMCs. Conclusion: TUDCA inhibits neointimal hyperplasia by reducing proliferation and inducing apoptosis of smooth muscle cells by suppression of ERK via PKCα-mediated MKP-1 induction. [1] Objective/background: Abdominal aortic aneurysm (AAA) is characterised by the infiltration of smooth muscle cell (SMC) apoptosis, inflammatory cells, neovascularisation, and degradation of the extracellular matrix. Previous work has shown that endoplasmic reticulum (ER) stress and SMC apoptosis were increased both in a mouse model and human thoracic aortic aneurysm. However, whether the ER stress is activated in AAA formation and whether suppressing ER stress attenuates AAA is unknown. Methods: Human AAA and control aorta samples were collected. Expression of ER stress chaperones glucose-regulated protein (GRP)-78 and GRP-94 was detected by immunohistochemical staining. The effect of ER stress inhibitor tauroursodeoxycholic acid (TUDCA) on AAA formation in angiotensin (Ang) II induced apolipoprotein E-/- mice was explored. Elastin staining was used to observe the rupture of elastic fragmentation. Immunohistochemistry and Western blot analysis were performed, to detect the protein expression of ER stress chaperones and apoptosis molecules. Results: There was significant upregulation of GRP-78 and GRP-94 in aneurysmal areas of human AAA and Ang II induced ApoE-/- mice (p < .05). TUDCA significantly attenuated the maximum diameters of abdominal aortas in Ang II induced ApoE-/- mice (p < .05). TUDCA significantly reduced expression of ER stress chaperones and the apoptotic cell numbers (p < .05). Furthermore, TUDCA significantly reduced expression of apoptosis molecules, such as caspase-3, caspase-12, C/EBP homologous protein, c-Jun N-terminal kinase activating transcription factor 4, X-box binding protein, and eukaryotic initiation factor 2α in Ang II induced ApoE-/- mice (p < .05). Conclusion: The results suggest that ER stress is involved in human and Ang II induced AAA formation in ApoE-/- mice. TUDCA attenuates Ang II induced AAA formation in ApoE-/- mice by inhibiting ER stress mediated apoptosis. [2] |
Molecular Formula |
C26H44NNAO6S
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Molecular Weight |
521.69
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Exact Mass |
521.278
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Elemental Analysis |
C, 59.86; H, 8.50; N, 2.68; Na, 4.41; O, 18.40; S, 6.15
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CAS # |
35807-85-3
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Related CAS # |
Tauroursodeoxycholate;14605-22-2;Tauroursodeoxycholate-d4 sodium;2410279-95-5;Tauroursodeoxycholate dihydrate;117609-50-4
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PubChem CID |
46782978
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Appearance |
White to off-white solid powder
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LogP |
4.526
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Hydrogen Bond Donor Count |
3
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Hydrogen Bond Acceptor Count |
6
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Rotatable Bond Count |
7
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Heavy Atom Count |
35
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Complexity |
864
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Defined Atom Stereocenter Count |
10
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SMILES |
S(C([H])([H])C([H])([H])N([H])C(C([H])([H])C([H])([H])[C@@]([H])(C([H])([H])[H])[C@@]1([H])C([H])([H])C([H])([H])[C@@]2([H])[C@]3([H])[C@]([H])(C([H])([H])[C@]4([H])C([H])([H])[C@@]([H])(C([H])([H])C([H])([H])[C@]4(C([H])([H])[H])[C@]3([H])C([H])([H])C([H])([H])[C@@]21C([H])([H])[H])O[H])O[H])=O)(=O)(=O)[O-].[Na+]
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InChi Key |
IYPNVUSIMGAJFC-JUWYWQLMSA-M
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InChi Code |
InChI=1S/C26H45NO6S.Na/c1-16(4-7-23(30)27-12-13-34(31,32)33)19-5-6-20-24-21(9-11-26(19,20)3)25(2)10-8-18(28)14-17(25)15-22(24)29;/h16-22,24,28-29H,4-15H2,1-3H3,(H,27,30)(H,31,32,33);/q;+1/p-1/t16-,17+,18-,19-,20+,21+,22+,24+,25+,26-;/m1./s1
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Chemical Name |
sodium;2-[[(4R)-4-[(3R,5S,7S,8R,9S,10S,13R,14S,17R)-3,7-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]pentanoyl]amino]ethanesulfonate
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Synonyms |
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HS Tariff Code |
2934.99.9001
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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. |
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Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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Solubility (In Vitro) |
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Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (4.79 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% 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 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 (4.79 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 (4.79 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 100 mg/mL (191.68 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 1.9168 mL | 9.5842 mL | 19.1685 mL | |
5 mM | 0.3834 mL | 1.9168 mL | 3.8337 mL | |
10 mM | 0.1917 mL | 0.9584 mL | 1.9168 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.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
NCT00771901 | Completed | Drug: tauroursodeoxycholic acid Other: placebo |
Insulin Resistance Diabetes |
Washington University School of Medicine |
February 2008 | Not Applicable |