Mode of Action
- Invokana is an SGLT2 inhibitor1
- SGLT2 is a sodium-glucose co-transporter expressed in the proximal renal tubules, and is responsible for 90% of glucose reabsorption1,2
- SGLT2 inhibitors act independently of β-cell function or insulin sensitivity – removing excess blood glucose by increasing urinary glucose excretion3
- This also results in a loss of excess calories and water – which is why Invokana may also reduce weight and blood pressure4,5
Weight loss and blood pressure reduction are
additional benefits only and not licensed indications.
An insulin independent approach to achieve glycaemic control
T2DM without Invokana
T2DM with Invokana
- SGLT2s are responsible for 90% of glucose reabsorption, making it an attractive target for inhibition.6
- SGLT2 inhibitors act independently of β-cell function or insulin sensitivity – removing excess blood glucose by increasing urinary glucose excretion.3 This also results in a loss of excess calories and water – which is why Invokana may also reduce both weight and blood pressure.4,5
- Invokana increases estimated urinary glucose excretion ranging from 77–119 g per day. This translates to an equivalent loss of 308-476 kcal/day.1 [Results from Phase I studies of urinary glucose excretion in patients with type 2 diabetes]
This leads to:
- Improved glycaemic control and a reduction in HbA1c1
- A loss of calories and therefore a reduction in body weight1
- A mild osmotic diuresis, with the diuretic effect leading to a reduction in systolic blood pressure1
Weight loss and blood pressure reduction are additional benefits only and not licensed indications.
How Invokana delivers renal benefits
- In type 2 diabetes, SGLT2 is overexpressed – contributing to glomerular hyperfiltration. Inhibiting SGLT2 may, therefore, reduce hyperfiltration and lead to decreases in intraglomerular pressure.7,8
HbA1c: Haemoglobin A1c; SGLT2: Sodium-Glucose Co-Transporter 2; SGLT2i: Sodium-Glucose Co-transporter 2 inhibitor; T2DM: Type 2 Diabetes Mellitus.
- Invokana Summary of Product Characteristics. Napp Pharmaceuticals Limited. Available at: https://www.medicines.org.uk/emc/product/8855/smpc and https://www.medicines.org.uk/emc/medicine/28400#gref [Accessed December 2021].
- Bays H. From victim to ally: the kidney as an emerging target for the treatment of diabetes mellitus. Curr Med Res Opin. 2009;25(3):671-681. doi:10.1185/03007990802710422.
- Bailey C, et al. Dapagliflozin add-on to metformin in type 2 diabetes inadequately controlled with metformin: a randomized, double-blind, placebo-controlled 102-week trial. BMC Med. 2013;11(1). doi:10.1186/1741-7015-11-43.
- Rothenberg PL, et al. European Association for the Study of Diabetes (EASD) Annual Meeting. Stockholm, Sweden 2016. Abstract No. 876 (poster).
- Lavalle-González F, et al. Efficacy and safety of canagliflozin compared with placebo and sitagliptin in patients with type 2 diabetes on background metformin monotherapy: a randomised trial. Diabetologia. 2013;56(12):2582-2592. doi:10.1007/s00125-013-3039-1.
- Dokken B. The Kidney as a Treatment Target for Type 2 Diabetes. Diabetes Spectrum. 2012;25(1):29-36. doi:10.2337/diaspect.25.1.29.
- Rahmoune H, et al. Glucose Transporters in Human Renal Proximal Tubular Cells Isolated From the Urine of Patients With Non-Insulin-Dependent Diabetes. Diabetes. 2005;54(12):3427-3434. doi:10.2337/diabetes.54.12.3427.
- Fioretto P, Zambon A, Rossato M, Busetto L, Vettor R. SGLT2 Inhibitors and the Diabetic Kidney. Diabetes Care. 2016;39(Supplement 2):S165-S171. doi:10.2337/dcs15-3006