Dapagliflozina, el primer inhibidor SGLT 2 en el tratamiento de la diabetes tipo 2 / Dapagliflozin, the first SGLT-2 inhibitor in the treatment of type 2 diabetes

Dapagliflozina es el primer inhibidor selectivo del cotransportador de sodio-glucosa 2 (SGLT2) aprobado por la European Medicines Agency (Agencia Europea del Medicamento, EMA) para el tratamiento de la diabetes tipo 2. Dapagliflozina bloquea la reabsorción renal de glucosa, al inhibir el cotransportador SGLT2, produciendo un aumento de la excreción renal de glucosa y una reducción de los valores plasmáticos de glucosa. Su mecanismo de acción es independiente de la función de la célula β o de la modulación de la sensibilidad a la insulina. En los estudios fase III, dapagliflozina a dosis de 5 o 10 mg/día en monoterapia en pacientes no tratados previamente, o añadida a otros antidiabéticos como metformina, glimepirida, pioglitazona o insulina, reduce significativamente los valores de HbA1c y la glucemia en ayunas frente a placebo a las 24 semanas. Además, en el estudio comparativo frente a glipizida, dapagliflozina no fue inferior en el control de la glucosa a las 52 semanas cuando se utiliza como terapia añadida en pacientes diabéticos no controlados con metformina. En la mayoría de los ensayos clínicos dapagliflozina redujo el peso. La combinación de ambos efectos (mejoría del control glucémico y reducción ponderal) se alcanza en mayor grado en los tratamientos que combinan dapaglifozina. En los estudios de extensión, el efecto sobre el control glucémico y sobre la reducción ponderal se mantiene a los 2 y a los 4 años. Dapagliflozina fue bien tolerada. Las infecciones urinarias y genitales fueron más frecuentes en los pacientes que recibieron dapagliflozina que con placebo. Los episodios de hipoglucemia son escasos con dapagliflozina. En conclusión, dapagliflozina es una nueva opción terapéutica para el manejo de la diabetes tipo 2, sobre todo cuando se utiliza como terapia añadida a otros antidiabéticos (AU)

Dapagliflozin is the first novel sodium-glucose co-transporter-2 (SGLT2) inhibitor approved by the European Medicines Agency (EMA) for the treatment of type 2 diabetes. By inhibiting SGLT2, dapagliflozin blocks reabsorption of filtered glucose in the kidney, increasing urinary glucose excretion and reducing blood glucose levels. Its mechanism of action is independent of pancreatic β cell function and modulation of insulin sensitivity. The results of phase III clinical trials showed that dapagliflozin, at a dose of 5 or 10 mg/day for 24 weeks as monotherapy in previously untreated patients, or as add-on combination therapy with metformin, glimepiride, pioglitazone or insulin-based therapy, significantly reduced both HbA1c and fasting plasma glucose levels compared with placebo. In addition, dapagliflozin was noninferior to glipizide, in terms of glycemic control after 52 weeks, when used as add-on therapy in patients with type 2 diabetes inadequately controlled with metformin. In most clinical trials, dapagliflozin reduced body weight. The combination of both effects (improved glycemic control and weight loss) is achieved to a greater extent in treatments that include dapaglifozin. Longer-term extension studies indicated that the efficacy of dapagliflozin on the glycemic control and weight reducción is maintained for up to 2 and 4 years. Dapagliflozin was well tolerated. Genital infections and urinary tract infections were more frequent in patients who received dapagliflozin than in placebo recipients. Hypoglycemic episodes were scarce with dapagliflozin. In conclusion, dapagliflozin is a novel option for the management of type 2 diabetes, particularly when used as add-on therapy (AU)

[Dapagliflozin, the first SGLT-2 inhibitor in the treatment of type 2 diabetes]. / Dapagliflozina, el primer inhibidor SGLT 2 en el tratamiento de la diabetes tipo 2.

Dapagliflozin is the first novel sodium-glucose co-transporter-2 (SGLT2) inhibitor approved by the European Medicines Agency (EMA) for the treatment of type 2 diabetes. By inhibiting SGLT2, dapagliflozin blocks reabsorption of filtered glucose in the kidney, increasing urinary glucose excretion and reducing blood glucose levels. Its mechanism of action is independent of pancreatic ß cell function and modulation of insulin sensitivity. The results of phase III clinical trials showed that dapagliflozin, at a dose of 5 or 10mg/day for 24 weeks as monotherapy in previously untreated patients, or as add-on combination therapy with metformin, glimepiride, pioglitazone or insulin-based therapy, significantly reduced both HbA1c and fasting plasma glucose levels compared with placebo. In addition, dapagliflozin was noninferior to glipizide, in terms of glycemic control after 52 weeks, when used as add-on therapy in patients with type 2 diabetes inadequately controlled with metformin. In most clinical trials, dapagliflozin reduced body weight. The combination of both effects (improved glycemic control and weight loss) is achieved to a greater extent in treatments that include dapaglifozin. Longer-term extension studies indicated that the efficacy of dapagliflozin on the glycemic control and weight reducción is maintained for up to 2 and 4 years. Dapagliflozin was well tolerated. Genital infections and urinary tract infections were more frequent in patients who received dapagliflozin than in placebo recipients. Hypoglycemic episodes were scarce with dapagliflozin. In conclusion, dapagliflozin is a novel option for the management of type 2 diabetes, particularly when used as add-on therapy.