FARXIGA mechanism of action
FARXIGA mechanism of action: Evidence supports cardiac, renal, and metabolic effects of SGLT2i1
*Includes feedback effects on other systems.
- Sodium-glucose cotransporter 2, 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 believed to be mediated by increased tubuloglomerular feedback
- Resultant outcomes include:
- An improvement in glycemic control in adults with T2D
- A reduction in the risk of sustained eGFR decline, ESKD, CV death, and hospitalization for heart failure in adults with CKD at risk of progression
- A reduction in the risk of hospitalization for heart failure in adults with T2D and either multiple CV risk factors or eCVD
- A reduction in the risk of CV death and hospitalization for heart failure in adults with HFrEF
CKD=chronic kidney disease; CV=cardiovascular; eCVD=established cardiovascular disease; eGFR=estimated glomerular filtration rate; ESKD=end-stage kidney disease; HFrEF=heart failure with reduced ejection fraction; hHF=hospitalization for heart failure; SGLT2=sodium-glucose cotransporter 2; SGLT2i=sodium-glucose cotransporter 2 inhibitor; T2D=type 2 diabetes.
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