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Farxiga

Dapagliflozin · also sold as Farxiga / Forxiga

An oral therapy for diabetes, heart failure and chronic kidney disease.

Reviewed by the Priya Life Science Editorial Team, led by Sreepriya Prasannan
MSc Digital Transformation of Life Sciences (Innopharma Education / Griffith College); MSc & BSc Botany HSE Spark Ignite 2026 — Top 14 finalist
Compiled from official FDA data · Last verified · Editorial standards
Generic name
Dapagliflozin
Brand names
Farxiga / Forxiga
Route
Oral
Marketed by
AstraZeneca
First FDA approval
8 Jan 2014

What Farxiga is used for

FARXIGA (dapagliflozin) is indicated: • To reduce the risk of sustained eGFR decline, end-stage kidney disease, cardiovascular (CV) death, and hospitalization for heart failure in adults with chronic kidney disease at risk of progression. • To reduce the risk of CV death, hospitalization for heart failure, and urgent heart failure visit in adults with heart failure. • To reduce the risk of hospitalization for heart failure in adults with type 2 diabetes mellitus and either established CV disease or multiple CV risk factors. • As an adjunct to diet and exercise to improve glycemic control in adults and pediatric patients aged 10 years and older with type 2 diabetes mellitus. Limitations of Use • FARXIGA is not recommended for use to improve glycemic control in patients with type 1 diabetes mellitus [see Warnings and Precautions (5.1) ] . • FARXIGA is not recommended for use to improve gl…

How it works

12.1 Mechanism of Action Sodium-glucose cotransporter 2 (SGLT2), expressed in the proximal renal tubules, is responsible for the majority of the reabsorption of filtered glucose from the tubular lumen. Dapagliflozin is an inhibitor of SGLT2. By inhibiting SGLT2, dapagliflozin reduces reabsorption of filtered glucose and thereby promotes urinary glucose excretion. Dapagliflozin also reduces sodium reabsorption and increases the delivery of sodium to the distal tubule. This may influence several physiological functions including, but not restricted to, lowering both pre- and afterload of the heart and downregulation of sympathetic activity, and decreased intraglomerular pressure which is beli…

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How this page is built

The facts on this page are pulled directly from official U.S. FDA datasets — they are not written from memory. Each field below names the dataset it came from, so you can check it yourself.

Plain-English summaries and drug-class explainers are written and reviewed by the Priya Life Science editorial team, led by Sreepriya Prasannan (MSc Digital Transformation of Life Sciences (Innopharma Education / Griffith College); MSc & BSc Botany). Data is retrieved automatically from the sources above and cross-checked with AI-assisted verification (Anthropic's Claude) — brand and generic names are matched against the exact FDA product record so that a combination product or a different formulation cannot be mistaken for the drug on this page. An editor reviews the result before publication. We describe this in full in our editorial standards and corrections policy. The FDA data on this page was last retrieved on 6 Aug 2026.

Please verify before you rely on this. This page is general information for life-science and pharmaceutical professionals. It is not medical advice, and it has not been reviewed by a clinician — our editorial team holds life-science qualifications, not clinical ones. It is not exhaustive and may not reflect the most recent label change. Always check the official prescribing information (US Prescribing Information or EU SmPC) and speak to your doctor or pharmacist before acting on anything here. Drugs in the same class are not automatically interchangeable, and approvals, brand names and indications differ between the US, the EU/Ireland (EMA/HPRA) and other regions. Spotted an error? Tell us — we correct promptly and log it.