During implantation the receptive endometrium is primed to receive adhesion-competent blastocysts. Attachment of the blastocyst to the endometrium relies on the bridging of integrins on the endometrium and the blastocyst by extracellular matrix proteins, such as fibronectin. The expression and localisation of integrins, such as α5β1 and αvβ3 and are tightly regulated at the maternal-foetal interface during implantation. This study aims to determine the role of IGF1 during early implantation and in the regulation of adhesion molecule expression and localisation in the blastocyst and endometrial epithelium. Ishikawa cells, a human endometrial cell line, were cultured with murine blastocysts under three treatment conditions: serum, serum-starved and serum-starved plus 10 ng/ml IGF1 and assessed for blastocyst attachment after 48 hours. Western-blotting, immunofluorescence and flow cytometry were used to determine expression levels of adhesion molecules and pFAK in Ishikawa cells and blastocysts. Attachment of blastocysts to Ishikawa cells was significantly reduced under serum-starved conditions. However, attachment was increased in the presence of IGF1, to the level seen in the presence of serum. In serum starved Ishikawa cells, β3 integrin and CD44 expression was reduced, compared to the expression in the presence of serum. However, addition of IGF1 alone could not rescue their expression. In Ishikawa cells no change in pFAK or E-cadherin levels or surface expression of αvβ3 or β1integrin was observed amongst the treatments. In serum starved blastocysts, pFAK expression was reduced, compared to the expression in the presence of serum, however IGF1 alone could not rescue its expression. In conclusion, IGF1 increases attachment of blastocysts to Ishikawa cells. However, this is not due to expression of αvβ3, β3 or β1 integrins, CD44, E-cadherin or pFAK protein levels in Ishikawa cells. The effect of IGF1 on blastocyst adhesion molecules remains to be examined, along with other potential adhesion molecules in Ishikawa cells.