MK-789
MK-789 is a competitive reversible inhibitor of dehydropeptidase I (DHP-I). MK-789 competitively blocks the entry of N-formimidoylthienamycin into proximal tubular cells, thereby inhibiting its renal metabolism. MK-789 shifts the renal excretion pathway of N-formimidoylthienamycin to glomerular filtration only, increasing its urinary recovery rate and renal clearance. MK-789 is applicable to studies on renal metabolism and pharmacokinetics.
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- CAS No.: 85394-14-5
- Formule: C14H23NO3
- Masse moléculaire:253.34
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
In Vitro
MK-789 and its oxidative metabolites inhibit purified dehydropeptidase I in spectrophotometric assays[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 85394-14-5
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Masse moléculaire 253.34
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Formule C14H23NO3
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SMILES
O=C(/C(NC(C1CC1(C)C)=O)=C\CCCCC)O
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Protocol for Pharmacokinetic Study
Pharmacokinetic studies quantify how an organism handles a drug over time through absorption, distribution, metabolism, and excretion, and the core experimental readout is the concentration-time profile of parent drug and, when relevant, metabolites in biological matrices such as plasma, whole blood, urine, bile, or tissue. Pharmacokinetic analysis links dose, route, exposure, clearance, half-life, distribution, bioavailability, and systemic exposure to drug efficacy and toxicity hypotheses rather than measuring a signaling pathway directly. The literature links pharmacokinetics to drug-development phenotypes by showing that drug metabolism and pharmacokinetics influence compound progression, exposure-response interpretation, safety margins, dosing strategy, and failure risk during discovery and development. DMPK science contributes to compound optimization by integrating physicochemical properties, in vitro metabolism, transporter behavior, in vivo exposure, and pharmacodynamic contex
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)