Objective — to evaluate the role of interactions between genes of energy metabolism, the folate cycle regulators, components of the hemostatic system, blood pressure regulators and receptors of estrogen in the formation of a hereditary risk of developing fetal growth retardation syndrome development. Material and methods. Two groups of women were included in the study. The main group consisted of 76 pregnant women with an established diagnosis fetal growth retardation syndrome development II—III degree. The control group consisted of 82 somatically healthy women with physiological pregnancy. Was conducted for molecular genetic testing of allelic polymorphisms in 26 genes (PPARA 2498 G>C, PPARD-87 C>T, PPARG P12A C>G, PPARGC 1A S482G G>A, PPARGC 1B A203P G>C, AMPD Q12X G>A, FGB 455 G>A, F2 20210 G>A, F5 1691 G>A, PAI-1 5G>4G, ITGA2 807 C>T, ITGB3 1565 T>C, F7 10976 G>A, F13A1 G>T, MTR 2756 A>G, MTRR 66 A>G, MTHFR 677 C>T, MTHFR 1298 A>C, AGT 704 T>C, AGT 521 C>T, AGTR1 1166 A>C, AGTR2 1675 G>A, NOS 786 T>C, NOS 894 G>T, ESR 397 T>C, ESR 351 A>G). Univariate analysis was carried out and step-by-step logistic regression analysis was used. Results. Developed a mathematical model for prediction of individual risk of the formation of the fetal growth retardation syndrome development, which includes a combination of six allelic genotypes of the polymorphisms of genes: PPARA 2498 G>C, PPARGC A203P1 G>C, MTRR 66 A>G, AGT 704 T>C, AGT 521 T>C and NOS 894 G>T. Conclusions. The use of the prognosis model for the formation of fetal growth retardation syndrome in high-risk patients will allow to prevent the development of placental insufficiency from early gestation, it can contribute to the improvement of perinatal outcomes.