| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 25mg |
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| 50mg |
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| 100mg |
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| 250mg | |||
| Other Sizes |
| Targets |
PPARα; mouse sEH:11.1 nM (IC50); human sEH:112 nM (IC50)
CUDA targets soluble epoxide hydrolase (sEH), an enzyme that catalyzes the conversion of epoxyeicosatrienoic acids (EETs) to the corresponding dihydroxy eicosatrienoic acids (DHETs), thereby diminishing their vasodilatory and anti-inflammatory activities. CUDA inhibits sEH with IC50 values of 11.1 nM for mouse sEH and 112 nM for human sEH. In addition to sEH inhibition, CUDA selectively activates peroxisome proliferator-activated receptor alpha (PPARα). At a concentration of 10 µM, CUDA activates PPARα approximately 8-fold. It binds to the PPARα ligand binding domain without affecting PPARδ or PPARγ activity. |
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| ln Vitro |
In COS-7 cells, CUDA (10 μM; 18 hours) stimulates PPARalpha by 6 and 3 times, respectively[2]. In addition to competitively inhibiting Wy-14643 (pirinixic acid) from binding to the PPARalpha ligand binding domain, CUDA does not change the expression of the PPARalpha protein, indicating that it is a PPARalpha ligand[2].
CUDA demonstrates potent in vitro activity as an sEH inhibitor and PPARα activator. In COS-7 cells, 10 µM CUDA blocks the conversion of 1 µM 14,15-EET to 14,15-DHET by 94%, demonstrating its efficacy in inhibiting sEH-mediated EET metabolism. Additionally, CUDA (10 µM; 18 hours) stimulates PPARα activity by 6-fold in COS-7 cells. It competitively inhibits Wy-14643 (pirinixic acid) from binding to the PPARα ligand binding domain. CUDA does not change PPARα protein expression, indicating that it acts as a PPARα ligand rather than affecting protein levels. The compound shows no effect on PPARδ or PPARγ. |
| ln Vivo |
In vivo studies have demonstrated the potential of CUDA in cardiovascular and metabolic disease models. As an sEH inhibitor, CUDA increases the levels of EETs, which are endothelium-derived hyperpolarizing factors with vasodilator, anti-inflammatory, and cardioprotective properties. By inhibiting sEH, CUDA prolongs the half-life of EETs, thereby enhancing their beneficial effects. The compound’s PPARα activation further contributes to its metabolic effects, including fatty acid oxidation and anti-inflammatory actions. CUDA has been studied in models of hypertension, cardiac hypertrophy, and metabolic syndrome, where it has shown promising results in reducing blood pressure and improving metabolic parameters.
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| Enzyme Assay |
In vitro enzyme assays for CUDA involve measuring its inhibition of soluble epoxide hydrolase (sEH) activity. These assays typically use recombinant mouse or human sEH and a fluorogenic substrate that releases a fluorescent product upon hydrolysis. CUDA is incubated with the enzyme and substrate, and the decrease in fluorescence is measured to determine the IC50 value. For PPARα activation studies, a ligand binding domain (LBD) assay or a transactivation assay using a PPARα-responsive luciferase reporter is employed. Competitive binding assays with radiolabeled Wy-14643 can also be used to confirm CUDA’s binding to the PPARα LBD.
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| Cell Assay |
Western Blot Analysis[2]
Cell Types: COS-7 cells Tested Concentrations: 10 μM Incubation Duration: 18 hrs (hours) Experimental Results: Activated PPARα by binding to the ligand binding domain of PPARα. In vitro cellular assays for CUDA are conducted in cell lines such as COS-7 cells. Cells are treated with CUDA at 10 µM for 18 hours, and PPARα activation is measured using a luciferase reporter assay or by analyzing the expression of PPARα target genes via qPCR. For sEH activity assays, cells are incubated with CUDA and EET substrates, and the conversion of EET to DHET is measured by LC-MS/MS. Western blot analysis is used to confirm that CUDA does not alter PPARα protein expression. Cytotoxicity is assessed using standard cell viability assays to ensure that observed effects are not due to nonspecific toxicity. |
| Animal Protocol |
In vivo animal experiments with CUDA are typically conducted in rodent models of cardiovascular and metabolic diseases. Common models include angiotensin II-induced hypertension, high-fat diet-induced metabolic syndrome, and cardiac ischemia-reperfusion injury. CUDA is administered via oral gavage or intraperitoneal injection at doses ranging from 1-10 mg/kg. Blood pressure is measured using telemetry or tail-cuff plethysmography. Plasma and tissue levels of EETs and DHETs are measured by LC-MS/MS to confirm sEH inhibition. Inflammatory markers, glucose tolerance, and lipid profiles are also assessed. Histological analysis of tissues (e.g., heart, kidney, adipose tissue) is performed to evaluate organ protection.
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| ADME/Pharmacokinetics |
Pharmacokinetic properties of CUDA have been characterized in preclinical studies. The compound has a molecular weight of 340.50 and is lipophilic, with a calculated LogP of 4.79. It is soluble in DMF (10 mg/mL), DMSO (5 mg/mL), and ethanol (1 mg/mL). CUDA is typically administered orally or intraperitoneally in in vivo studies. The compound’s bioavailability and half-life are influenced by its lipophilic nature and metabolism. Storage recommendations include keeping the compound at -20°C in airtight containers. Further detailed PK studies are needed to fully define its absorption, distribution, metabolism, and excretion parameters.
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| Toxicity/Toxicokinetics |
Toxicological data for CUDA are limited, as the compound is intended for research use only. In cell-based assays, CUDA has been used at concentrations up to 10 µM without significant cytotoxicity reported. In animal studies, CUDA has been administered at various doses without major adverse effects reported. However, comprehensive toxicological evaluations, including acute and chronic toxicity studies, have not been extensively published. Standard laboratory safety precautions should be followed when handling CUDA. Further toxicity studies would be required to support any potential clinical development.
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| References |
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| Additional Infomation |
12-[(cyclohexylcarbamoyl)amino]dodecanoic acid is a medium-chain fatty acid.
CUDA is a research compound with dual activity as an sEH inhibitor and PPARα activator. It is used to study the roles of EETs and PPARα in cardiovascular disease, inflammation, and metabolic disorders. The compound’s mechanism involves inhibiting the conversion of EETs to DHETs, thereby enhancing EET-mediated vasodilation and anti-inflammatory effects, while simultaneously activating PPARα to promote fatty acid oxidation and improve metabolic parameters. CUDA is also referred to as Alcudacigib. Its unique dual mechanism makes it a valuable tool for probing the interplay between EET signaling and PPARα activation in various disease models. |
| Molecular Formula |
C19H36N2O3
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|---|---|
| Molecular Weight |
340.500745773315
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| Exact Mass |
340.272
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| CAS # |
479413-68-8
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| PubChem CID |
22978774
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| Appearance |
White to off-white solid powder
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| Density |
1.0±0.1 g/cm3
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| Boiling Point |
549.4±19.0 °C at 760 mmHg
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| Flash Point |
286.1±21.5 °C
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| Vapour Pressure |
0.0±3.2 mmHg at 25°C
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| Index of Refraction |
1.501
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| LogP |
4.79
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
13
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| Heavy Atom Count |
24
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| Complexity |
342
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
HPTJABJPZMULFH-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C19H36N2O3/c22-18(23)15-11-6-4-2-1-3-5-7-12-16-20-19(24)21-17-13-9-8-10-14-17/h17H,1-16H2,(H,22,23)(H2,20,21,24)
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| Chemical Name |
12-(cyclohexylcarbamoylamino)dodecanoic acid
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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 : ~25 mg/mL (~73.42 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 0.5 mg/mL (1.47 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (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 5.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.9369 mL | 14.6843 mL | 29.3686 mL | |
| 5 mM | 0.5874 mL | 2.9369 mL | 5.8737 mL | |
| 10 mM | 0.2937 mL | 1.4684 mL | 2.9369 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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