Phosphorus is a necessary component of all living organisms. This nutrient is mainly transported from the maternal blood to the fetus via the placenta, and insufficient phosphorus availability via the placenta disturbs the normal development of the fetus, especially fetal bone formation in late gestation. Key proteins (phosphate transporters and exporters) that are responsible for the maintenance of placental‐fetal phosphorus homeostasis have been identified. A deficiency in the phosphate transporter Pit2 has been shown to result in placental calcification and the retardation of fetal development in mice. What roles does XPR1 (the only known phosphate exporter) play in maintaining placental‐fetal phosphorus homeostasis? In this study, we found that Xpr1 expression is strong in the murine placenta and increases with age during gestation. We generated a global Xpr1 knockout mouse and found that heterozygous (Xpr1^+/−) and homozygous (Xpr1^−/−) fetuses have lower inorganic phosphate (Pi) levels in amniotic fluid and serum and a decreased skeletal mineral content. Xpr1 ‐deficient placentas show abnormal Pi exchange during gestation. Therefore, Xpr1 deficiency in the placenta disrupts placental‐fetal Pi homeostasis. We also discovered that the placentas of the Xpr1^+/− and Xpr1^−/− embryos are severely calcified. Mendelian inheritance statistics for offspring outcomes indicated that Xpr1 ‐deficient embryos are significantly reduced in late gestation. In addition, Xpr1^−/− mice die perinatally and a small proportion of Xpr1^+/− mice die neonatally. RNA sequence (RNA‐Seq) analysis of placental mRNA revealed that many of the transcripts are significantly differentially expressed due to Xpr1 deficiency and are linked to dysfunction of the placenta. This study is the first to reveal that XPR1 plays an important role in maintaining placental‐fetal Pi homeostasis, disruption of which causes severe placental calcification, delays normal placental function, and restricts fetal growth.