To explore cardiometabolic risk profiles, the probability of sustainable control, and the effectiveness of treatment with sodium-glucose co-transporter-2 (SGLT2) inhibitors in black and white adults in the United States with type 2 diabetes.Using nationally representative US electronic medical records, 72 690 white and 10 004 black adults diagnosed with type 2 diabetes initiating SGLT2 inhibitors during the period 2013 to 2018, continuing it for ≥6 months, and with follow-up of ≥12 months, were identified. Glycated haemoglobin (HbA1c), body weight, systolic blood pressure (SBP) and lipid changes at 6 months, and sustainability of control over 18 months post SGLT2 inhibitor initiation were explored, separately in those with and without atherosclerotic cardiovascular disease (ASCVD).The white group was older (58 years) with lower mean HbA1c (8.5%), compared to the black group (age 54 years, HbA1c 9.0%). Body mass index distribution was similar. The proportions of people with uncontrolled SBP, LDL cholesterol, non-HDL cholesterol and triglyceride levels were 24%, 42%, 51% and 62%, respectively, in white patients, and 31%, 51%, 49% and 32%, respectively, in black patients. At 6-month follow-up white and black patients had similar adjusted reductions in HbA1c (1.1%), SBP (8-10 mmHg), LDL cholesterol (0.26 - 0.34 mmol / L) and body weight (1.1-1.4 kg). However, over 18 months' follow-up, compared to white patients, black patients were significantly less likely to achieve sustainable control in HbA1c (odds ratio [OR] 0.67, 95% confidence interval [CI] 0.63-0.72), body weight (OR 0.81, 95% CI 0.72-0.91), SBP (OR 0.67, 95% CI 0.61-0.74) and LDL cholesterol (OR 0.77, 95% CI 0.67-0.89). Triglyceride control was significantly better among black patients. Black patients had a significantly higher risk factor burden, irrespective of ASCVD status.While the effectiveness of SGLT2 inhibitors was similar among black and white patients, irrespective of ASCVD status, black patients continued to have worse cardiometabolic risk factor burden after SGLT2 inhibitor initiation.