Potent synthetic glucocorticoids like dexamethasone are administered to pregnant women at risk of delivering preterm to reduce neonatal morbidity and mortality. In experimental models, chronically high antenatal glucocorticoid exposure adversely affects placental efficiency and offspring cardiovascular function. However, placental and fetal vulnerability to synthetic glucocorticoid exposure may depend on gestational stage. We hypothesised that dexamethasone exposure prior to, or coincident with, the normal rise in fetal endogenous glucocorticoids will differentially impact placental and cardiovascular function. C57BL/6 mice were time-mated and the day of plug designated E0.5. Dams were injected IP with vehicle or dexamethasone (500μg/kg) at E13.5 or E16.5 (n=5-7/group). In vivo pulsed-wave Doppler ultrasound scanning was conducted 24h post-injection (E14.5 or E17.5, respectively) to measure umbilical artery (UA) blood flow and fetal cardiac function. Immediately after scanning, tissues were collected. Data were analysed by 2-way ANOVA with post-hoc Bonferroni’s test. Dexamethasone treatment reduced fetal weight at E14.5 (p=0.002) and placental weight at E17.5 (p=0.009). UA pulsatility index and velocity time integral remained unchanged at E14.5 and E17.5. An interaction effect was observed at E17.5 in UA resistance index (p=0.027) and systolic/diastolic ratio (p=0.025). At E14.5, dexamethasone reduced fetal heart rate (p=0.004) and increased isovolumetric relaxation time (p=0.007), ejection time (p=0.003) and mitral deceleration index (p=0.037). In contrast, at E17.5, dexamethasone had no significant effect on fetal cardiac function, though a strong trend (p=0.052) for increased myocardial performance index was evident. Fetal, but not placental, tissues appear sensitive to precocious dexamethasone exposure at E14.5, with reduced fetal growth and altered cardiac parameters suggesting impaired cardiovascular function. However, at peak fetal endogenous glucocorticoid synthesis (E16.5-17.5) when the fetus is no longer naive to glucocorticoids, fetal growth and cardiac function were preserved following dexamethasone exposure. This preservation at E17.5 was despite impaired placental capacity, alluding to protective fetal mechanisms.