| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| Targets |
t-AUCB targets soluble epoxide hydrolase (sEH), an enzyme that converts epoxides to their corresponding diols. By inhibiting sEH, t-AUCB increases the ratio of epoxyeicosatrienoic acids (EETs) to dihydroxyeicosatrienoic acids (DHETs). This modulates inflammation, pain, and vascular tone. It also activates NF-κB-p65 in glioblastoma cells.
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| ln Vitro |
In a mimic-dependent manner, trans-AUCB (t-AUCB; 25-300 μM; 48 hours) suppresses the proliferation of U251 and U87 cells [1]. In U251 and U87 cells, trans-AUCB (200 μM; 48 or 96 hours) causes cell cycle progression to G0/G1 phase lysis [1]. The phosphorylation level of p65 can be increased by trans-AUCB (200 μM; 10 min-4 hours) after 10 minutes, reaching its peak after 30 minutes, and being elevated for at least two hours [1]. Through the activation of NF-jB-p65, trans-AUCB (200 μM; 48 hours) suppresses the development of U251 and U87 cells[1]. An effective 30 minutes of trans-AUCB (10 μM) suppresses human cell blast tumor cell lines (U251,
In vitro, t-AUCB is a potent sEH inhibitor with IC50 values of 1.3 nM (human), 8 nM (mouse), and 8 nM (rat). It suppresses human glioblastoma cell growth by activating NF-κB-p65. It has been shown to reduce cortical infarct volume in stroke models. |
| ln Vivo |
In a dose-dependent manner, trans-AUCB (t-AUCB; sidewall 0.1, 0.5, 1 mg/kg) ameliorates LPS-induced hypoglycemia [2]. trans-AUCB (sidewall 0.1, 0.5, 1 mg/kg) with Cmax values of 30, 100, and 150 nmol/L po at 0.1, 0.5, and 1 mg/kg and t1/2 values of 20, 30, and 15 minutes[ 2]. Trans-AUCB (sc; 1, 3, 10 mg/kg) had Cmax values of 245, 2700, and 3600 nM for 1, 3, and 10 mg/kg, and t1/2 values of 60, 85, and 75 minutes[2]. The trans-AUCB (iv; 0.1 mg/kg) t1/2 values for the distribution (alpha) and elimination (beta) phases are 70 minutes and 10 hours, respectively. Trans-AUCB has a CL of 0.7 L/h kg and a Vdss of 17 L/kg[2].
In vivo, t-AUCB is orally active. It significantly reduces cortical infarct volume by 35% in stroke models. It elevates the cumulative EET-to-DHET ratio in brain cortex by twofold and improves functional outcomes. It has anticancer activity in glioblastoma models. |
| Enzyme Assay |
In vitro enzyme assays for t-AUCB measure its inhibition of sEH activity. The enzyme is incubated with its substrate and varying concentrations of the compound. Epoxide hydrolase activity is measured by quantifying the conversion of epoxide substrates to diols. IC50 values of 1.3 nM (human), 8 nM (mouse), and 8 nM (rat) are determined.
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| Cell Assay |
Cell Viability Assay[1]
Cell Types: U251, U87 cells Tested Concentrations: 25, 50, 100, 200, or 300 μM Incubation Duration: 48 hrs (hours) Experimental Results: Inhibited growth of U251 and U87 cells in a dose-dependent manner. Cell cycle analysis[1] Cell Types: U251, U87 Cell Tested Concentrations: 200 μM Incubation Duration: 48 or 96 hrs (hours) Experimental Results: Induced in U251 and U87 cells Arrest in the G0/G1 phase of the cell cycle. Western Blot Analysis[1] Cell Types: U251, U87 Cell Tested Concentrations: 200 μM Incubation Duration: 10 minutes, 30 minutes, 1 hour, 2 hrs (hours) or 4 hrs (hours) Experimental Results: p65 phosphorylation after 10 minutes Levels increase, peaking 30 minutes later and lasting for at least 2 hrs (hours). In vitro cell-based assays for t-AUCB use human glioblastoma cell lines to assess inhibition of cell growth. Cells are treated with serial dilutions of the compound, and cell viability is measured using MTT or other assays. NF-κB-p65 activation is assessed by Western blotting or reporter assays. |
| Animal Protocol |
Animal/Disease Models: Mouse (male CFW strain, 7 weeks old, 24-30 g; male C57BL/6 strain, 8 weeks old, 22-25 g) [2]
Doses: 0.1, 0.5, 1 mg/kg Route of Administration: Oral Experimental Results: Improved LPS-induced hypotension in a dose-dependent manner. Animal/Disease Models: Mouse (male CFW strain, 7 weeks old, 24-30g; male C57BL/6 strain, 8 weeks old, 22-25g) [2] Doses: 0.1, 0.5, 1mg/kg (pharmacokinetic/PK/PK analysis ) ) Route of Administration: PO Experimental Results: For 0.1, 0.5, and 1 mg/kg PO, the t1/2 values were 20, 30, and 15 minutes respectively, and the Cmax values were 30, 100, and 150 nmol/L respectively. In vivo animal models for t-AUCB include rat and mouse models of stroke. The compound is administered orally, and infarct volume is measured. EET-to-DHET ratios in brain cortex are quantified by LC-MS/MS. Functional outcomes are assessed using behavioral tests. Glioblastoma models are used to evaluate anticancer activity. |
| ADME/Pharmacokinetics |
t-AUCB has a molecular weight of 371.43 g/mol and a molecular formula of C₂₂H₂₉NO₄. It is orally active. The compound is soluble in DMSO and is stored at -20°C. It is also known as trans-AUCB. Pharmacokinetic parameters including oral bioavailability are documented in research publications.
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| Toxicity/Toxicokinetics |
The toxicity profile of t-AUCB is characterized in preclinical safety studies. As a soluble epoxide hydrolase inhibitor, the compound is generally well-tolerated at therapeutic doses. It is for research use only and is not approved for clinical use. Appropriate safety precautions should be taken during handling.
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| References |
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| Additional Infomation |
Structure in the first source
t-AUCB (trans-AUCB) is a potent, orally active, and selective soluble epoxide hydrolase (sEH) inhibitor with IC50 values of 1.3 nM, 8 nM, and 8 nM for human, mouse, and rat sEH, respectively. It suppresses human glioblastoma cell growth by activating NF-κB-p65. t-AUCB reduces cortical infarct volume in stroke models. It is also known as trans-AUCB. |
| Molecular Formula |
C24H32N2O4
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|---|---|
| Molecular Weight |
412.53
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| Exact Mass |
412.236
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| CAS # |
885012-33-9
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| PubChem CID |
16038368
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| Appearance |
White to off-white solid powder
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| Density |
1.3±0.1 g/cm3
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| Boiling Point |
641.3±48.0 °C at 760 mmHg
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| Flash Point |
341.7±29.6 °C
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| Vapour Pressure |
0.0±2.0 mmHg at 25°C
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| Index of Refraction |
1.612
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| LogP |
4.78
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
30
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| Complexity |
608
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| Defined Atom Stereocenter Count |
0
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| SMILES |
C1CC(CCC1NC(=O)NC23CC4CC(C2)CC(C4)C3)OC5=CC=C(C=C5)C(=O)O
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| InChi Key |
KNBWKJBQDAQARU-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C24H32N2O4/c27-22(28)18-1-5-20(6-2-18)30-21-7-3-19(4-8-21)25-23(29)26-24-12-15-9-16(13-24)11-17(10-15)14-24/h1-2,5-6,15-17,19,21H,3-4,7-14H2,(H,27,28)(H2,25,26,29)
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| Chemical Name |
4-[4-(1-adamantylcarbamoylamino)cyclohexyl]oxybenzoic acid
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| Synonyms |
t AUCB tAUCB t-AUCB
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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 |
| 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) |
DMSO : ~100 mg/mL (~242.41 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (5.04 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 20.8 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: ≥ 2.08 mg/mL (5.04 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 20.8 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: ≥ 2.08 mg/mL (5.04 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.4241 mL | 12.1203 mL | 24.2407 mL | |
| 5 mM | 0.4848 mL | 2.4241 mL | 4.8481 mL | |
| 10 mM | 0.2424 mL | 1.2120 mL | 2.4241 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.
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