Novo’s Victoza beats SGLT2 inhibitors in lowering blood sugar

by | 2nd Dec 2015 | News

New data show that treatment with Novo Nordisk’s Victoza provides a greater HbA1c reduction and an improved likelihood of reaching glycaemic goals compared to sodium-glucose co-transporter 2 inhibitors in people with type II diabetes unable to hit targets with other treatments.

New data show that treatment with Novo Nordisk’s Victoza provides a greater HbA1c reduction and an improved likelihood of reaching glycaemic goals compared to sodium-glucose co-transporter 2 inhibitors in people with type II diabetes unable to hit targets with other treatments.

The network meta-analysis, presented at the World Diabetes Congress, assessed the relative efficacy of the human glucagon-like peptide-1 (GLP-1) analogue against SGLT-2 inhibitors such as Johnson & Johnson’s Invokana (canagliflozin), Lilly/Boehringer’s Jardiance (empagliflozin) and AstraZeneca’s Farxiga (dapagliflozin) across 17 randomised controlled trials.

Victoza (liraglutide) demonstrated greater reductions in mean HbA1c compared to all SGLT-2 inhibitors, with a placebo-adjusted mean change of -1.01%/-1.18% for Victoza, -0.64%/-0.79% for Invokaka, -0.32%/-0.38% for Farxiga, and -0.59%/-0.62% for Jardiance, Novo said.

“In the absence of head-to-head trials, this analysis provides valuable insight into the comparative outcomes with liraglutide versus SGLT-2 inhibitiors in people with type 2 diabetes uncontrolled on oral antidiabetic treatments,” said Maria Lorenzi, MSc, lead author and research manager, Redwood Outcomes.

Victoza was launched in the European Union in 2009 for adults with type II diabetes to achieve glycaemic control in combination with oral glucose-lowering medicinal products and/or basal insulin when these, together with diet and exercise, do not provide adequate control.

GLP-1 agonists like Victoza mimic the functions of natural incretin hormones in the body that help lower post-meal blood sugar levels by: stimulating the release of insulin by the pancreas after eating; inhibiting the release of glucagon by the pancreas; and slowing glucose absorption into the bloodstream by reducing the speed at which the stomach empties after eating.

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