Enhancing placental insulin-like growth factor(IGF) availability appears an attractive strategy for improving outcomes in fetal growth restriction(FGR). Our approach was the use of [Leu²⁷]IGFII, a human IGF-II analogue that binds the IGF-II clearance receptor, IGF2R, in FGR mice. We hypothesised that the impact of [Leu²⁷]IGFII infusion in C57BL/6J(wild-type,WT) and endothelial nitric oxide synthase knockout(eNOS^-/-,FGR) mice would be to enhance fetal growth and investigated this from mid to late gestation. 1mg/kg/day [Leu²⁷]IGFII was delivered via a subcutaneous mini-osmotic pump from E12.5-E18.5. Fetal and placental weights, recorded at E18.5, were used to generate frequency distribution curves; fetuses <5^th centile were deemed growth-restricted. Placentas were harvested for immunohistochemical analysis of the IGF system, and maternal serum collected for measurement of exogenously administered IGF-II. In WT pregnancies, [Leu²⁷]IGFII treatment halved the number of FGR fetuses, reduced fetal(p=0.028) and placental weight variations(p=0.0032), and increased numbers of pups close to the mean fetal weight(131vs112 pups within 1 SD). Mixed-models analysis confirmed litter size to be negatively correlated with fetal and placental weight, and showed that Leu²⁷[IGFII] preferentially improved fetal weight in the largest litters, as defined by number. Unidirectional ^14CMeAIB transfer per g placenta(System A amino acid transporter activity) was inversely correlated with fetal weight in Leu²⁷IGFII-treated WT animals(p<0.01). In eNOS^-/- mice, [Leu²⁷]IGFII reduced the number of FGR fetuses(1vs5 in the untreated group). The observed reduction in FGR pup numbers in both C57 and eNOS^-/- litters suggests the use of this analogue as a means of standardising and rescuing fetal growth, preferentially in the smallest offspring.