Basal insulin reduces basal hyperglycemia (BHG) but HbA_1c may remain high due to persisting postprandial hyperglycemia (PPHG). Lixisenatide (LIXI), a GLP-1 receptor agonist in development for the treatment of Type 2 diabetes mellitus (T2DM), can reduce PPHG and HbA_1c with no weight gain, or with weight loss, and thus has properties complementary to those of basal insulin. Patient-level data were pooled from three randomized Phase III studies of once-daily LIXI + standard of care (SOC; basal insulin ± oral agents) vs placebo (PBO) + SOC to quantify the effects of LIXI on BHG and PPHG exposures. BHG (24-hr area above 5.6 mmol/L and under the fasting level) and incremental PPHG (area above fasting and under self-monitored 7-point plasma glucose profiles [AUC_24h]) exposures were calculated by a previously reported method. The 753 eligible patients had a mean age 57 years, BMI 29.8 kg/m², diabetes duration 11.5 years, HbA_1c 8.15% and fasting glucose 7.5 mmol/L. At baseline, mean daytime BHG and PPHG exposures were 49.2 and 55.1 mmol/L*h, respectively. Mean BHG and PPHG contributions to hyperglycemia were 42% and 58%, respectively. At Week 24, adjusted LS mean HbA_1cchange was –0.77% with LIXI + SOC and –0.29% with PBO + SOC (p<0.0001). The BHG exposure values for LIXI + SOC and PBO + SOC were similar (adjusted LS mean change for AUC_24h –13 mmol/L*h vs –11 mmol/L*h [NS]), but PPHG exposure was reduced more with LIXI + SOC compared with PBO + SOC (adjusted LS mean change –21 mmol/L*h vs –10 mmol/L*h, p<0.0001). The mean BHG and PPHG contributions to hyperglycemia were 46% vs 54% with LIXI + SOC and 39% vs 61% with PBO + SOC. In conclusion, this analysis suggests that once-daily LIXI complements the effects of basal insulin on glycemic control in T2DM, decreasing HbA_1cmainly by reducing PPHG.