Glyburide and fetal safety; transplacental pharmacokinetic considerations

Reprod Toxicol. 2001 May-Jun;15(3):227-9. doi: 10.1016/s0890-6238(01)00122-8.

Abstract

Oral hypoglycemics have been avoided in pregnancy due to their potential to cause fetal hyperinsulinemia/hypoglycemia. A recent human study has shown glyburide to minimally cross the placenta, allowing a safe new treatment for gestational diabetes. The mechanisms for the minimal placental passage of this small molecule are not clear. In this presentation, the role of pKa, molecular weight, lipid solubility, and protein binding is considered. Out of these physical and pharmacologic characteristics, the very extensive plasma protein binding and short elimination half-life of glyburide appear to be major determinants of its minimal transplacental transfer.

Publication types

  • Review

MeSH terms

  • Adult
  • Female
  • Fetal Diseases / chemically induced
  • Fetus / drug effects
  • Fetus / metabolism*
  • Glyburide / adverse effects
  • Glyburide / pharmacokinetics*
  • Humans
  • Hypoglycemic Agents / adverse effects
  • Hypoglycemic Agents / pharmacokinetics*
  • Ions
  • Maternal-Fetal Exchange*
  • Molecular Weight
  • Placenta / drug effects
  • Placenta / metabolism*
  • Pregnancy
  • Pregnancy Outcome
  • Protein Binding
  • Randomized Controlled Trials as Topic

Substances

  • Hypoglycemic Agents
  • Ions
  • Glyburide