How is daptomycin metabolized?

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Last updated: November 22, 2025View editorial policy

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Metabolism of Daptomycin

Daptomycin undergoes minimal to no hepatic metabolism and is excreted primarily unchanged by the kidneys, with approximately 52% of the administered dose recovered in urine as microbiologically active drug and only minor inactive oxidative metabolites detected. 1

Metabolic Pathway

  • Daptomycin is not metabolized by human liver microsomes in vitro studies, indicating negligible hepatic cytochrome P450 involvement 1

  • No metabolites are observed in plasma following administration of daptomycin 6 mg/kg to adult subjects on Day 1 of therapy 1

  • Minor amounts of three oxidative metabolites and one unidentified compound are detected only in urine, not in plasma, suggesting limited peripheral metabolism 1

  • The specific site of metabolism has not been identified, though it appears to occur outside the liver 1

Excretion and Elimination

  • Approximately 78% of the administered dose is recovered in urine based on total radioactivity (52% as microbiologically active drug), while only 5.7% is recovered in feces over 9 days 1

  • Renal excretion is the primary route of elimination, making daptomycin particularly susceptible to accumulation in patients with renal impairment 1, 2

  • The elimination half-life is approximately 9 hours in patients with normal renal function (creatinine clearance >80 mL/min), but increases to 14.7 hours in moderate renal impairment and further in severe renal dysfunction 1

Clinical Implications

  • Protein binding is 90-93% to serum albumin in a concentration-independent manner, which limits distribution (volume of distribution ~0.1 L/kg) 1, 2

  • Dosage adjustment is required for creatinine clearance <30 mL/min, as renal clearance decreases by 46% in severe renal impairment, leading to 2-3 fold higher AUC compared to normal renal function 1

  • Hepatic impairment does not affect daptomycin pharmacokinetics, as protein binding and clearance remain similar in patients with Child-Pugh Class B hepatic impairment compared to healthy subjects 1

References

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This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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