Thyroid hormone is essential for normal human fetal development and prior to the 12th week of pregnancy the fetus is dependent on placental delivery of maternal thyroid hormone. Human placenta expresses several thyroid hormone transporters however, the very high levels of inactivating deiodinase type 3 present in placenta suggest that only limited placental transfer of thyroid hormone can occur unless the deiodinase type 3 enzyme is inhibited . Despite this, we know that transfer of maternal thyroid hormone occurs throughout pregnancy. We have previously demonstrated that placental homogenates express the thyroid hormone binding protein transthyretin and binding to transthyretin protects thyroid hormone from deiodination [2, 3]. The human placenta also secretes and endocytoses transthyretin suggesting that it may play a role in transplacental transfer of thyroid hormone. Using Ligand Capture technology (CaptiRec TriCEPS v 3.0) we have identified a putative placental receptor for transthyretin. When the receptor expression was knocked down to 22 ± 11% of control levels using esiRNA, uptake of Alexa-labelled transthyretin was reduced by >50% over 24 hours. Further study is required to determine the contribution that receptor mediated uptake of transthyretin bound thyroid hormone plays in overall transplacental transfer of thyroid hormone and how uptake is modified in placental pathologies such as gestational diabetes and preeclampsia.