Fusarium graminearum is an economically important fungus causing Fusarium head blight (FHB), which has become an increasing threat to the security of global cereal production. The use of genetically resistant cultivars is a critical tool for managing FHB; however, modern elite wheat germplasm lacks genetic diversity, and only a limited number of known resistance genes are currently available. The germplasm of wild species is a diverse and underutilized source of novel alleles associated with many important traits, including disease resistance. Approximately a third of known FHB resistance genes originated from a wild species. Aegilops tauschii is the donor of the D-genome in wheat and only a limited amount of Ae. tauschii germplasm is represented in modern wheat germplasm. Four accessions of Aegilops tauschii, that showed FHB resistance in a prior screening have been used to develop 607 BC1F5 derived introgression lines (ILs) in the background of adapted cultivars. In this study, we aimed to identify resistant ILs and map underlying resistance genes. ILs were grown in Kansas State University’s Fusarium head blight screening nursery for two seasons and phenotyped pre- and post-harvest for disease traits. 30 ILs either never headed or headed extremely late missing the disease outbreak, resulting in only 577 ILs being analyzed. 203 ILs were found to exhibit lower disease scores in all phenotyped traits compared to the recurrent winter wheat accession. For FHB incidence ratings,146 of these lines were moderately resistance, while 57 lines were resistant. 93 ILs had mycotoxin content levels of 6.12 ppm or lower, which were approximately at least half of the recurrent accession’s mycotoxin content levels. The primary mycotoxin present was deoxynivalenol. Plant height was found to have negative moderate correlation with all disease traits but deoxynivalenol content. Based on phenotypic data, genetic resistance present in Ae. tauschii accessions was introgressed into wheat. ILs were genotyped using low-pass whole genome sequencing, while parental lines were whole-genome sequenced. Variant calling is currently in progress, which will be followed by SNP imputation to identify and correct missing regions in the sequenced introgression lines. Due to equipment failure and a late disease outbreak, phenotypic data from the second field trial replication cannot be used. Field trials will be replicated for a third time in the coming spring. A genome-wide association study using the r package GAPIT v3 will be conducted to map resistance associated chromosomal regions. KASP markers for resistant regions will be developed.