In the fruit fly, Drosophila melanogaster, the decision by females to mate or not is an important factor for mating success. However, little is known about the molecular and neuronal mechanisms regulating the sexual receptivity in virgin females. Previously, we found that genetic ablation of insulin-producing cells (IPCs) and suppression of neurosecretion from IPCs enhance female sexual receptivity. These result suggest that insulin signaling regulates female sexual receptivity in Drosophila. In this current study, we examined whether lack of Drosophila Insulin-like peptides affect female sexual receptivity. In Drosophila, Insulin-like peptide 2, 3 and 5 (Ilp2, Ilp3 and Ilp5) are co-expressed in the IPCs and these three genes are under individual transcriptional control. The mating success rates of female homozygous for Ilp2-, Ilp3- or Ilp5-knockout (KO) and females heterozygous for triple KO (Ilp2 Ilp3 Ilp5/+) were higher than those of wild-type females. In addition, targeted expression of Ilp2 RNAi in IPCs phenocopied the phenotype of Ilp2-KO females. Thus, our results suggest that Ilp2, Ilp3 and Ilp5 are required for regulation of female seual receptivity. In Drosophila, insulin signaling pathways are implicated not only in growth or lifespan but also in behaviors. Examples include the ablation of IPCs and mutations of Insulin-like receptor (InR) abolishing sexual dimorphism in locomotor activity; the impairment of IPC function leading to increased adult ethanol sensitivity; and the mutations of Ilps in IPCs and conditional expression of a dominant-negative transgene of InR affecting feeding preference toward nutritive sugars. Thus, insulin secretion from IPCs may affect the Drosophila central nervous system to modify the above-mentioned behaviors or female sexual receptivity.