The relaxin receptor (LGR7) and the insulin-like peptide 3 (INSL3) receptor (LGR8) are unique LGR family members in possessing a single, functionally important amino terminal LDL-A module.1 Mouse and rat cDNA was screened for LGR7 and LGR7 splice variant expression. A uterus-specific exon 4 deleted variant was identified and named LGR7-Truncate. Deletion of exon 4 results in a premature stop codon and a transcript that putatively encodes a secreted protein containing LGR7's LDL-A module. Expression of LGR7-Truncate with LGR7 in HEK-293T cells resulted in decreased relaxin-induced signaling of LGR7. LGR7-Truncate is potentially an endogenous regulator of LGR7 signaling.