SLCO2B1 Knockout Huh-7 Cell Line

The choice depends on whether you are studying SLCO2B1 (OATP2B1)'s role in intestinal and hepatic drug absorption or its contributions to drug-drug interactions in pharmacokinetics. The Knockout line is the standard tool for asking whether SLCO2B1 is required for cellular uptake of its substrates — including statins (atorvastatin, rosuvastatin) and various drugs subject to food-drug interactions. Overexpression is useful for studying transport kinetics in defined backgrounds and for assessing inhibitor specificity. For pharmacokinetics research, the EDITGENE SLCO2B1 Knockout in Huh-7 is highly relevant — Huh-7 is a widely used hepatocellular carcinoma line for drug transporter studies. SLCO2B1 is the principal hepatic and intestinal OATP for many drugs. Rescue with wild-type or transport-deficient SLCO2B1 enables structure-function and inhibitor specificity studies (e.g., grapefruit juice-mediated SLCO2B1 inhibition).

Primary applications: • Statin uptake: ³H-atorvastatin, ³H-rosuvastatin, or LC-MS-based statin uptake assays to assess SLCO2B1-dependent hepatic statin clearance. • Food-drug interaction: SLCO2B1 inhibition assays with grapefruit juice components (naringin) and apple juice components, relevant to clinical food-drug interactions. • Substrate scope analysis: testing OATP2B1 transport of estrone-3-sulfate, DHEA-S, prostaglandins, and other reported substrates. • Inhibitor pharmacology: critical genetic control for SLCO2B1-targeted compound development. EDITGENE recommends this model for researchers investigating OATP2B1 biology, hepatic and intestinal drug uptake, and clinical food-drug interaction mechanisms.

Yes. SLCO2B1 rescue experiments are well-established in pharmacology research: • Construct design: use a codon-modified SLCO2B1 sequence with a small C-terminal tag (FLAG, HA). The 12 transmembrane topology and N-terminal extracellular loops must be preserved. • Surface expression validation: confirm plasma membrane localization by cell surface staining or biotinylation before transport assays. • Transport-deficient rescue: mutations in the substrate-binding pocket enable functional dissection. • Functional readout: rescue should restore statin uptake (³H-atorvastatin or LC-MS detection) and other OATP2B1 substrate transport activity. Huh-7 transduces efficiently with lentivirus and is a standard hepatocyte-derived background for drug transporter rescue studies.