BAY MKH 6562 [flucarbazone-sodium (proposed)], an acetolactate synthase (ALS)-inhibiting herbicide of the sulfonylaminocarbonyltriazolinone family, provides postemergence wild oat control in wheat. Whole-plant dose responses and in vitro ALS sensitivity assays were used to evaluate the magnitude and nature of cross-resistance to BAY MKH 6562 in a wild oat accession (AR1) with metabolism-based resistance to imazamethabenz, an ALS inhibitor of the imidazolinone family. An imazamethabenz-susceptible wild oat accession (AHS2), five BAY MKH 6562-resistant wild oat accessions, AN104, AN205, AN307, AN406, and ASB11, and wheat were also evaluated. AHS2 and AR1 dose responses to BAY MKH 6562 indicated a resistant/susceptible (R/S) herbicide dose required to cause 50% growth reduction (GR50) ratio of 200. Inhibition of ALS from the AHS2 and AR1 wild oat by BAY MKH 6562 was similar, with a concentration of herbicide required to cause 50% inhibition of enzymatic activity (I50) of 0.007 µmoles, indicating that cross-resistance was not due to an altered ALS enzyme. The GR50 for BAY MKH 6562 for the AN104, AN205, AN307, AN406, and ASB11 wild oat accessions was 0.23, 0.07, 0.23, 0.22, and 0.12 kg ai/ha, respectively, and the R/S ratio to the GR50 value for the AHS2 accession was 230, 70, 230, 220, and 120, respectively. Studies on ALS sensitivity to BAY MKH 6562 indicated that the I50 for the AN104, AN205, AN307, AN406, and ASB11 wild oat accessions was 5.2, 0.003, 0.008, 9.8, and 0.007 µmoles, respectively, and the R/S ratio to the I50 value for the AHS2 accession was 759, 0.5, 1, 1,444, and 1, respectively. Of the five wild oat accessions resistant to BAY MKH 6562, accessions AN104 and AN406 had high R/S I50 ratios indicative of an altered target site and accessions AN205, AN307, and AR1 had low R/S I50 ratios indicative of resistance based on metabolic degradation. Hard red spring wheat (2371) was 800-fold tolerant to BAY MKH 6562 and inhibition of ALS from wheat by BAY MKH 6562 was similar to that of ALS from the susceptible accession AHS2.