Jardiance vs Invokana
Both are SGLT2 inhibitors. Here is how Jardiance and Invokana compare on class, mechanism, dosing, approval and supply.
At a glance
Key differences
- Same class. Both Jardiance and Invokana are SGLT2 inhibitors, so they work through the same broad mechanism. Differences between them tend to be about dosing, route, how selective they are, and side effects rather than what they target.
- How they are taken. Both are given by the oral route.
- Time on the market. Jardiance was first approved by the FDA in 2014, Invokana in 2013.
- Who markets them. Jardiance is marketed by Boehringer Ingelheim; Invokana by Janssen (Johnson & Johnson).
What each one treats
JARDIANCE is indicated: to reduce the risk of cardiovascular death and hospitalization for heart failure in adults with heart failure. to reduce the risk of cardiovascular death in adults with type 2 diabetes mellitus and established cardiovascular disease. as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. JARDIANCE is a sodium-glucose co-transporter 2 (SGLT2) inhibitor indicated: To reduce the risk of cardiovascular death and hospitalization for heart failure in adults with heart failure. ( 1 ) To reduce the risk of cardiovascular death in adults with type 2 diabetes mellitus and established cardiovascular disease. ( 1 ) As an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. ( 1 ) Limitations of Use: Not recommended in patients with type 1 diabetes mellitus. It may increase the risk o…
INVOKANA (canagliflozin) is indicated: • 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. • to reduce the risk of major adverse cardiovascular events (cardiovascular death, nonfatal myocardial infarction and nonfatal stroke) in adults with type 2 diabetes mellitus and established cardiovascular disease (CVD). • to reduce the risk of end-stage kidney disease (ESKD), doubling of serum creatinine, cardiovascular (CV) death, and hospitalization for heart failure in adults with type 2 diabetes mellitus and diabetic nephropathy with albuminuria greater than 300 mg/day. INVOKANA is a sodium-glucose co-transporter 2 (SGLT2) inhibitor indicated: • 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 …
How each one works
12.1 Mechanism of Action Empagliflozin is an inhibitor of the sodium-glucose co-transporter 2 (SGLT2), the predominant transporter responsible for reabsorption of glucose from the glomerular filtrate back into the circulation. By inhibiting SGLT2, empagliflozin reduces renal reabsorption of filtered glucose and lowers the renal threshold for glucose, and thereby increases urinary glucose excretion. Empagliflozin also reduces sodium reabsorption and increases the delivery of sodium to the distal tubule. This may influence several physiological functions such as lowering both pre-and afterload of the heart and downregulating sympathetic activity.
12.1 Mechanism of Action SGLT2, expressed in the proximal renal tubules, is responsible for the majority of the reabsorption of filtered glucose from the tubular lumen. Canagliflozin is an inhibitor of SGLT2. By inhibiting SGLT2, canagliflozin reduces reabsorption of filtered glucose and lowers the renal threshold for glucose (RT G ), and thereby increases urinary glucose excretion (UGE). Canagliflozin increases the delivery of sodium to the distal tubule by blocking SGLT2-dependent glucose and sodium reabsorption. This is believed to increase tubuloglomerular feedback and reduce intraglomerular pressure.
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Which medicine is right for a given person depends on their diagnosis, other conditions, other medicines, kidney and liver function, pregnancy, and cost or reimbursement — none of which this page knows. Two drugs in the same class are not automatically interchangeable. Never start, stop or switch a prescription medicine on the basis of a web page; that decision belongs to you and your clinician or pharmacist.
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.
- FDA Drug Label (openFDA) ↗ Indications, mechanism of action and pharmacologic class
- Drugs@FDA ↗ First FDA approval date and the company holding the application
- FDA Drug Shortage Database ↗ Current US supply / shortage status
Plain-English summaries and drug-class explainers are written and reviewed 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 9 Oct 2026. How every register is built: methodology · fixes we have made: corrections log.