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LBA-3, a selective and orally active inhibitor of the sodium-coupled citrate transporter SLC13A5, exhibits an IC50 of 67 nM. This compound effectively reduces triglyceride and total cholesterol levels in both oleic and palmitic acid (OPA)-stimulated AML12 cells and PCN-stimulated primary mouse hepatocytes, as well as in mouse models, without showing detectable toxicity. Additionally, LBA-3 is permeable to the blood-brain barrier [1].

| Pack Size | Price | USA Warehouse | Global Warehouse | Quantity |
|---|---|---|---|---|
| 10 mg | Inquiry | 10-14 weeks | 10-14 weeks | |
| 50 mg | Inquiry | 10-14 weeks | 10-14 weeks |
| Description | LBA-3, a selective and orally active inhibitor of the sodium-coupled citrate transporter SLC13A5, exhibits an IC50 of 67 nM. This compound effectively reduces triglyceride and total cholesterol levels in both oleic and palmitic acid (OPA)-stimulated AML12 cells and PCN-stimulated primary mouse hepatocytes, as well as in mouse models, without showing detectable toxicity. Additionally, LBA-3 is permeable to the blood-brain barrier [1]. |
| In vivo | In Sprague Dawley rats, the pharmacokinetic profile of LBA-3 (50 mg/kg, oral, single dose) shows a peak plasma concentration (C max) of 288262.00 μg/L, an AUC of 704570.43 h/μg–1·L, and an oral bioavailability of 48.67% [1]. |
| Molecular Weight | 314.33 |
| Formula | C18H18O5 |
| Cas No. | 2918263-09-7 |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
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