Children affected by prenatal stress (PS) might show alterations of the fetal ANS and HPA axis. Subjects were recruited from a cohort of pregnant women attending the “Klinikum rechts der Isar” of the Technical University of Munich (TUM). Pregnant women were screened for stress exposure using Cohen Perceived Stress Scale and were classified into stressed group (SG, PSS-10≥19, n= 55) and control group (CG, PSS-10<19, n=55). Fetal electrocardiograms were recorded by taECG. Coupling between mHR and fHR was analyzed resulting in fetal stress index (FSI). Upon delivery, hair strands were collected for cortisol measurements and newborn’s cord blood and saliva samples were collected. DNA was extracted from saliva samples (n=114) and DNA methylation was measured using EPIC Bead-Chip array. To identify associations between cortisol/FSI and methylation, linear regression models adjusting for confounders (sex, age, smoking and cell-types) were run. FSI was significantly higher in fetuses of SG when compared to CG. No difference in methylation levels were found in PS newborns. The top hit of the regression analysis is cg15652683 (p = 2.16e-06), a CpG annotated to VIPR2 gene (Chr 7q36.3) coding for Vasoactive Intestinal Peptide Receptor 2. VIP is a small peptide with important neuroendocrine functions. Our work is ongoing and aims to develop an electrophysiological and epigenetic biomarker panel as an early non-invasive measure of the neurodevelopmental outcome of PS-exposed infants.