On this page
Quick Reference
Overview and Recommendations
Key Facts
- •Empagliflozin functions as a selective inhibitor of the (SGLT2) located in the S1 segment of the proximal convoluted tubule. By blocking the reabsorption of approximately 90% of filtered glucose, it promotes the excretion of 64–78 g of glucose per day in the urine, effectively lowering plasma glucose levels without increasing the risk of hyperinsulinemia or weight gain.
- •The therapeutic paradigm for empagliflozin shifted from simple glycemic control to comprehensive organ protection following the landmark trial (2015). This trial demonstrated a 38% relative risk reduction in cardiovascular death among patients with type 2 diabetes and established cardiovascular disease, establishing the drug as a primary agent for reducing major adverse cardiovascular events (MACE).
- •Renal protection is achieved through the restoration of tubuloglomerular feedback, a mechanism often impaired in diabetes. By increasing sodium delivery to the macula densa, empagliflozin triggers afferent arteriolar vasoconstriction, which reduces intraglomerular hypertension and hyperfiltration, thereby preserving long-term nephron integrity as evidenced in the trial.
- •Cardioprotective benefits extend across the entire spectrum of heart failure, including both reduced (HFrEF) and preserved (HFpEF) ejection fractions. Landmark trials such as and confirmed that empagliflozin reduces the combined risk of cardiovascular death or hospitalization for heart failure by approximately 21–25%, regardless of the patient's diabetic status.
- •Metabolic and cellular effects include a shift in myocardial fuel utilization toward ketone bodies, which are more oxygen-efficient than fatty acids, and the activation of the pathway. These shifts promote cellular autophagy, reduce oxidative stress, and mitigate iron-dependent cell death ( ), providing a multi-layered defense against progressive ventricular remodeling and diabetic cardiomyopathy.
Clinical Use
- •Assess renal function via (eGFR) and evaluate volume status prior to initiation. In patients with clinical evidence of volume depletion, such as those on high-dose or the elderly, volume status must be corrected before the first dose to minimize the risk of symptomatic hypotension or acute kidney injury.
- •Initiate therapy for at a starting dose of 10 mg orally once daily, taken in the morning with or without food. If additional glycemic control is required and the 10 mg dose is well-tolerated, the dosage may be increased to a maximum of 25 mg once daily in both adults and pediatric patients aged 10 years and older.
- •Administer a fixed dose of 10 mg once daily for the management of (HFrEF or HFpEF) and (CKD). While the glucose-lowering efficacy of empagliflozin diminishes as renal function declines, its cardiorenal protective benefits persist; it is currently indicated for initiation in CKD patients with an eGFR as low as 20 mL/min/1.73 m².
- •Anticipate an acute, transient "dip" in eGFR of approximately 2–4 mL/min/1.73 m² within the first 4 weeks of therapy. This shift is hemodynamically mediated, reflecting the desired reduction in intraglomerular pressure, and is not indicative of structural kidney injury; long-term therapy eventually stabilizes the eGFR slope compared to placebo.
- •Monitor for when adding empagliflozin to regimens containing or insulin secretagogues like . Clinicians should consider a preemptive dose reduction of the background insulin-stimulating agent to maintain glycemic safety while the SGLT2 inhibitor is titrated.
- •Withhold empagliflozin for at least 3 days prior to major elective surgery or any procedure requiring prolonged fasting. This "surgical pause" is essential to mitigate the risk of SGLT2-inhibitor-associated , which can occur even with near-normal blood glucose levels (euglycemic DKA).
- •Resume therapy only after the patient is hemodynamically stable, has resumed normal oral intake, and the risk of metabolic stress has subsided. Glucosuria can persist for several days after the last dose, so monitoring for delayed DKA symptoms is prudent in the postoperative period.
Safety
- •Counsel patients regarding the increased risk of genital mycotic infections, such as in women and balanitis in men, which occur in approximately 5–6% of patients. These infections are typically mild and can be managed with standard antifungal treatments without requiring the permanent discontinuation of empagliflozin.
- •Maintain a high index of suspicion for euglycemic (DKA), characterized by metabolic acidosis with blood glucose levels typically below 250 mg/dL. Patients presenting with nausea, vomiting, or abdominal pain should be screened for ketones in the blood or urine regardless of their blood sugar reading.
- •Monitor for symptomatic and volume depletion, particularly in patients aged 75 years or older, those with a baseline eGFR < 60 mL/min/1.73 m², or those using . The drug's mild diuretic effect can lead to orthostatic changes and transient increases in serum creatinine if volume status is not carefully managed.
- •Educate patients on the rare but severe risk of (necrotizing fasciitis of the perineum). Any report of perineal pain, tenderness, erythema, or swelling accompanied by fever or malaise requires immediate drug cessation and urgent surgical evaluation.
- •Avoid the use of empagliflozin during the second and third trimesters of pregnancy and during lactation. Animal models indicate that exposure during periods of renal maturation can cause permanent structural damage to the fetal kidneys, including pelvic and tubule dilatations.
- •Monitor serum levels closely during initiation and titration, as SGLT2 inhibitors may increase renal lithium clearance and lead to subtherapeutic lithium concentrations. Dose adjustments of lithium may be necessary to maintain psychiatric stability.
- •Advise patients that empagliflozin will cause a positive urine glucose test due to its primary mechanism of action. Alternative methods, such as or fingerstick glucose monitoring, should be used to assess glycemic control rather than urine-based assays.
Board Review — High Yield
- •Mechanism — Inhibits SGLT2 in the proximal tubule, causing glucosuria and natriuresis.
- •eGFR Dip — A transient 2-4 mL/min/1.73 m² decline upon initiation is hemodynamic and protective, not toxic.
- •Euglycemic DKA — Metabolic acidosis occurring with blood glucose < 250 mg/dL; requires high clinical suspicion.
- •Fournier's Gangrene — Rare but life-threatening necrotizing fasciitis of the perineum associated with SGLT2 inhibitors.
- •EMPA-REG OUTCOME — Landmark trial showing reduced CV death in T2DM patients with established CV disease.
- •Surgical Pause — Must stop the drug 3 days before major surgery to prevent perioperative DKA.
- •Tubuloglomerular Feedback — Restored by SGLT2i, leading to afferent arteriolar vasoconstriction and reduced glomerular pressure.
Deep Dive — Evidence Details
Introduction and Chemical Structure
- ▸Empagliflozin is a selective SGLT2 inhibitor indicated for glycemic control in type 2 diabetes, heart failure risk reduction, and chronic kidney disease management [label].
- ▸The drug functions via an insulin-independent mechanism, promoting urinary glucose excretion by lowering the renal glucose threshold [label].
Empagliflozin is a potent, highly selective inhibitor of the sodium-glucose cotransporter 2 (SGLT2) that has transformed the of metabolic and cardiorenal diseases [label]. By blocking glucose reabsorption in the proximal convoluted tubule, it lowers the renal threshold for glucose and promotes osmotic diuresis and natriuresis [label]. This mechanism provides a unique, insulin-independent pathway for glycemic control while simultaneously exerting profound protective effects on the heart and kidneys [6]A1b[7]A1a.
Mechanism of Action
- ▸Inhibits SGLT2 in the proximal tubule to increase urinary glucose excretion (64–78 g/day) and lower the renal glucose threshold.
- ▸Restores tubuloglomerular feedback to reduce intraglomerular pressure, providing direct nephroprotection.
Selective inhibition of the sodium-glucose cotransporter 2 (SGLT2) in the proximal convoluted tubule serves as the primary pharmacological action of this agent [label]. SGLT2 is the predominant transporter responsible for reabsorbing approximately 90% of filtered glucose from the glomerular filtrate back into the systemic circulation [label]. By blocking this pathway, the drug lowers the renal threshold for glucose and induces significant urinary glucose excretion (UGE) [label].
Pharmacokinetics (LADME)
- ▸The 12.4-hour half-life and dose-proportional pharmacokinetics support once-daily dosing without regard to food.
- ▸Metabolism is primarily mediated by UGT enzymes; the absence of major CYP450 metabolism minimizes the risk of common drug-drug interactions.
Peak plasma concentrations occur approximately 1.5 hours after oral administration, reflecting rapid systemic absorption [label]. While a high-fat, high-calorie meal reduces the maximum plasma concentration ($C_{max}$) by 37% and the area under the curve (AUC) by 16%, these changes are not clinically significant; therefore, the medication may be administered with or without food [label, 28]. Systemic exposure increases in a dose-proportional manner across the therapeutic range of 10 mg to 25 mg [label, 26].
Pharmacodynamics
- ▸Urinary glucose excretion increases immediately and dose-dependently, averaging 64–78 g/day in patients with diabetes.
- ▸An acute, reversible eGFR 'dip' of 2–4 mL/min/1.73 m² occurs upon initiation due to reduced intraglomerular pressure via tubuloglomerular feedback.
Urinary glucose excretion (UGE) increases immediately following the first dose, driven by a reduction in the renal threshold for glucose reabsorption [label]. In patients with type 2 diabetes, 10 mg and 25 mg doses result in mean UGE of 64 g/day and 78 g/day, respectively [label]. This effect is maintained over chronic treatment but returns to baseline within 3 days of drug cessation [label].
Indications and Clinical Use
- ▸Indicated for glycemic control in T2DM (adults and children ≥10 years), heart failure (all ejection fractions), and chronic kidney disease progression.
- ▸Provides significant cardiovascular mortality reduction in patients with T2DM and established cardiovascular disease.
Therapeutic utility extends across the metabolic, cardiovascular, and renal continuums, positioning the agent as a foundational therapy for multi-organ protection. Clinical application is primarily driven by its ability to decouple glycemic control from systemic organ preservation, particularly in patients with high cardiovascular or renal risk profiles. ### Glycemic Control in Type 2 Diabetes of type 2 diabetes mellitus (T2DM) involves use as an adjunct to diet and exercise to improve glycemic control in adults and pediatric patients aged 10 years and older [label].
Dose and Administration
- ▸The standard dose is 10 mg daily for heart failure and CKD, with titration to 25 mg permitted only for glycemic control in T2DM.
- ▸Therapy must be discontinued at least 3 days prior to scheduled surgery to minimize the risk of euglycemic ketoacidosis.
Standard administration involves a 10 mg oral dose once daily in the morning, taken with or without food [label]. While this 10 mg dose is the fixed therapeutic target for reducing cardiovascular death and hospitalizations in or slowing progression in (CKD), the regimen for glycemic control in (T2DM) allows for titration [label]. In adults and pediatric patients aged 10 years and older with T2DM, clinicians may increase the dose to 25 mg once daily if the 10 mg dose is well-tolerated but additional glycemic control is required [label].
Dose Modification
- ▸Empagliflozin is not recommended for glycemic control when eGFR is below 30 mL/min/1.73 m², though it maintains cardiovascular and renal benefits.
- ▸A mandatory 3-day treatment interruption is required prior to major surgery to prevent euglycemic ketoacidosis.
Renal function serves as the primary determinant for dose adjustments and therapeutic viability [label]. While empagliflozin provides cardiovascular and renal protection down to lower eGFR levels, it is not recommended for glycemic control in patients with an eGFR < 30 mL/min/1.73 m² due to diminished glucose-lowering efficacy [label]. Clinicians must assess renal function prior to initiation and monitor periodically thereafter [label].
Adverse Effects and Toxicity
- ▸Genital mycotic infections are the most common adverse effect, occurring in approximately 6% of female patients.
- ▸An initial 'eGFR dip' of 2–4 mL/min/1.73 m² is a normal hemodynamic response and predicts long-term renal preservation.
Genital mycotic infections occur in 5.4% to 6.4% of women treated with empagliflozin, representing the most frequent adverse reaction observed in clinical trials [label]. These infections, which include and mycotic vulvovaginitis, are significantly more common than in placebo groups (1.5%) and are driven by the drug's primary mechanism of increasing urinary glucose concentration [label], [65]A1a. In men, the incidence is lower but still elevated compared to placebo, ranging from 1.6% to 3.1% [label].
Drug Interactions
- ▸No clinically relevant pharmacokinetic interaction was observed between empagliflozin and metformin.[90]
- ▸No clinically relevant interaction was identified with verapamil, ramipril, or digoxin in healthy volunteers.[83]
- ▸Simvastatin did not materially alter empagliflozin exposure, and empagliflozin caused only minor changes in simvastatin exposure.[86]
- ▸Pioglitazone exposure increased with empagliflozin in a healthy-volunteer study; the supplied abstract does not provide the magnitude or clinical significance.[31]
- ▸No relevant pharmacokinetic interaction was reported for empagliflozin and lobeglitazone.[89]
- ▸Diuretic combinations require attention to volume status because empagliflozin has been studied in patients receiving hydrochlorothiazide, torasemide, and loop diuretics.[32][71][72]
- ▸Empagliflozin effects were similar with and without background mineralocorticoid receptor antagonist therapy in EMPEROR-Reduced.[75]
- ▸Gemfibrozil, rifampicin, and probenecid were investigated as transporter or enzyme modifiers, but the supplied abstract does not provide complete quantitative results.[82]
Overview
Empagliflozin has been evaluated with several antidiabetic, cardiovascular, diuretic, lipid-lowering, hormonal, and transporter-modifying medicines. Available evidence consists mainly of small, open-label pharmacokinetic studies in healthy volunteers, with additional clinical analyses in patients with diabetes, heart failure, or chronic kidney disease.[31]A1b[32]A1b[71]C4[72]A1b[75]A1b[81][82][83][84][86][89][90][91]C Pharmacokinetic findings from healthy-volunteer studies may not fully predict effects in people with renal impairment, heart failure, volume depletion, or polypharmacy.[32]A1b[71]C4[72]A1b[75]A1b[81][82]
Antidiabetic medicines
Coadministration with pioglitazone was investigated in healthy volunteers. Pioglitazone exposure, measured by maximum concentration and area under the concentration–time curve, increased when administered with empagliflozin, although the supplied study abstract does not provide the magnitude or clinical significance of this increase.[31]A1b A 24-week randomized trial in people with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease evaluated pioglitazone 15 mg, empagliflozin 10 mg, and their combination; the study was designed to assess complementary therapeutic effects rather than a pharmacokinetic interaction.[74]A1b
No relevant pharmacokinetic interaction was reported between empagliflozin and lobeglitazone in a randomized crossover study of 30 healthy subjects receiving empagliflozin 25 mg, lobeglitazone 0.5 mg, or both once daily for 5 days.[89]
Empagliflozin has also been studied with dipeptidyl peptidase-4 inhibitors. Coadministration with linagliptin was evaluated in a randomized crossover study in healthy male volunteers, with the rationale that the drugs have complementary glucose-lowering mechanisms.[84] Empagliflozin was likewise evaluated with evogliptin in a randomized multiple-dose crossover study, and with sitagliptin in an earlier randomized crossover study.[22]B2b[73]A1b These studies assessed pharmacokinetic and, for evogliptin, pharmacodynamic interactions; the supplied abstracts do not report clinically important interaction findings for these combinations.[22]B2b[73]A1b[84]
Metformin had no clinically relevant effect on empagliflozin exposure: the geometric mean ratios were 96.9% for steady-state area under the curve and 100.5% for steady-state maximum concentration.[90] Empagliflozin also had no clinically relevant effect on metformin pharmacokinetics in the same study.[90] A later bioequivalence study evaluated fixed-dose metformin/empagliflozin 1000 mg/5 mg tablets under fasting and fed conditions in 56 healthy Chinese subjects; it compared tablet formulations rather than testing a new pharmacologic interaction.[68]A1b
Diuretics, mineralocorticoid receptor antagonists, and volume status
Empagliflozin was studied with hydrochlorothiazide 25 mg and torasemide 5 mg in patients with type 2 diabetes. The randomized crossover design specifically assessed potential pharmacokinetic interactions between empagliflozin and these thiazide or loop diuretics.[32]A1b In heart failure with reduced ejection fraction, the EMPEROR-Reduced trial examined empagliflozin in patients with and without recent volume overload; approximately 40% had experienced volume overload within the preceding 4 weeks.[72]A1b These data support consideration of the combined diuretic and volume-depleting effects when empagliflozin is used with diuretics, particularly in patients with fluid retention or changing volume status.[72]A1b
In a secondary EMPEROR-Reduced analysis, 71% of participants were receiving a mineralocorticoid receptor antagonist at randomization. Empagliflozin’s effects on efficacy endpoints and safety were similar in patients receiving and not receiving a mineralocorticoid receptor antagonist, with no evidence of treatment interaction reported in the supplied abstract.[75]A1b A secondary analysis of the CONFIDENCE trial evaluated empagliflozin with finerenone in people with chronic kidney disease and type 2 diabetes, focusing on blood-pressure lowering and albuminuria-related outcomes; the supplied abstract describes combination therapy as a studied strategy but does not provide complete numerical results.[81] A small exploratory study in 15 patients with type 2 diabetes and heart failure with reduced ejection fraction found a significant interaction between loop-diuretic use and the effect of empagliflozin on cardiorespiratory fitness, although the study was not powered to establish a definitive clinical interaction.[71]C4
Transporter, enzyme, and cardiovascular medicines
Potential interactions with transporter or enzyme inhibitors were investigated using gemfibrozil, rifampicin, and probenecid. Gemfibrozil inhibits OATP1B1/OATP1B3 and OAT3; rifampicin inhibits OATP1B1/OATP1B3; and probenecid inhibits OAT3 and uridine diphosphate glucuronosyltransferase. These agents were evaluated in randomized crossover studies in healthy subjects to characterize their effects on empagliflozin pharmacokinetics.[82] The supplied abstract does not provide the complete quantitative results; therefore, these findings should not be used to infer a required dose adjustment from the available information.[82]
No clinically relevant drug–drug interaction was identified in healthy-volunteer studies of empagliflozin with verapamil, ramipril, or digoxin.[83] Simvastatin had no meaningful effect on empagliflozin exposure: the area-under-the-curve geometric mean ratio was 102.05% and the maximum-concentration ratio was 109.49%; empagliflozin produced only minor changes in simvastatin exposure.[86]
Hormonal contraceptives and food
Empagliflozin 25 mg once daily was studied with ethinylestradiol 30 micrograms plus levonorgestrel 150 micrograms at steady state in healthy female volunteers to assess effects on oral-contraceptive pharmacokinetics.[91]C The supplied abstract does not provide the complete numerical results, so a definitive interaction conclusion cannot be drawn from the information provided.[91]C
Food affects empagliflozin pharmacokinetics, and a high-fat meal was specifically evaluated in a randomized crossover study.[87] A later study examined high-fat-diet effects on empagliflozin pharmacokinetics, renal-function parameters, and renin–angiotensin–aldosterone-system-related parameters after a 10-mg dose in healthy Chinese adults.[88] Separate studies assessed bioequivalence of empagliflozin tablets under fasting and fed conditions.[85] These findings concern absorption and pharmacodynamic assessment rather than a drug–drug interaction.[85][87][88]
Practical interpretation
The strongest available evidence supports no clinically relevant pharmacokinetic interaction with metformin, simvastatin, verapamil, ramipril, or digoxin, while evidence with pioglitazone and transporter-modifying drugs requires interpretation from the individual study results.[31]A1b[82][83][86][90] When empagliflozin is combined with diuretics or mineralocorticoid receptor antagonists, monitor volume status, blood pressure, and renal function according to the patient’s clinical context because overlapping renal and diuretic effects may be clinically important even when pharmacokinetic interaction is absent.[32]A1b[72]A1b[75]A1b[81]
| Medicine or class | Evidence from supplied references | Practical interpretation |
|---|---|---|
| Metformin | No clinically relevant effect in either direction; empagliflozin AUC GMR 96.9% and Cmax GMR 100.5%.[90] | No pharmacokinetic interaction identified. |
| Simvastatin | No meaningful effect on empagliflozin; only minor changes in simvastatin exposure.[86] | No clinically relevant interaction identified. |
| Verapamil, ramipril, digoxin | No clinically relevant interaction reported in healthy volunteers.[83] | No interaction identified in the studied settings. |
| Pioglitazone | Pioglitazone Cmax and AUC increased with empagliflozin; quantitative results are incomplete in the supplied abstract.[31]A1b | Interpret clinically and monitor combined therapy. |
| Lobeglitazone | No relevant pharmacokinetic interaction reported.[89] | No interaction identified in the study. |
| Hydrochlorothiazide, torasemide, loop diuretics | Pharmacokinetic and clinical interaction studies were performed; empagliflozin’s volume effects are relevant in heart failure.[32]A1b[71]C4[72]A1b | Monitor volume status, blood pressure, and renal function. |
| Mineralocorticoid receptor antagonists and finerenone | Empagliflozin efficacy and safety were similar with or without MRAs; finerenone combination was evaluated in CKD and type 2 diabetes.[75]A1b[81] | Combination is clinically studied; monitor according to disease status. |
| Gemfibrozil, rifampicin, probenecid | Transporter/enzyme interaction studies were conducted, but complete quantitative results are not supplied.[82] | Avoid assuming a dose adjustment from the available abstract alone. |
| Oral contraceptives | Ethinylestradiol/levonorgestrel pharmacokinetics were assessed with empagliflozin 25 mg; complete results are not supplied.[91]C | No definitive conclusion from the supplied abstract. |
Special Populations and Contraindications
- ▸Contraindicated in the second and third trimesters of pregnancy due to risks of fetal renal pelvic and tubule dilatation.
- ▸Approved for pediatric patients ≥10 years with type 2 diabetes at a starting dose of 10 mg daily.
Hypersensitivity reactions, including and , represent absolute contraindications to treatment [label]. While the drug provides significant metabolic and cardiovascular benefits, its use is restricted in specific clinical contexts to ensure safety and avoid developmental or hemodynamic complications. ### Pregnancy and Lactation Avoidance of therapy is recommended during the second and third trimesters of pregnancy due to potential risks to fetal renal development [label].
References
- [1]
Kongmalai T, Hadnorntun P, Leelahavarong P et al.. “Comparative cardiovascular benefits of individual SGLT2 inhibitors in type 2 diabetes and heart failure: a systematic review and network meta-analysis of randomized controlled trials.” Frontiers in endocrinology (2023). PMID: 38179304 ↗
L1SR_MA_RCTCited in: Introduction and Chemical Structure - [2]
Bonilha I, Yoshinaga MY, Chaves-Filho AB et al.. “LDL subspecies and lipidome change by evolocumab add-on therapy to empagliflozin in patients with type 2 diabetes: A prespecified secondary analysis of a randomized clinical trial.” Atherosclerosis (2026). PMID: 41806515 ↗
L1RCTCited in: Introduction and Chemical Structure, Indications and Clinical Use, Adverse Effects and Toxicity - [3]
Murugavel S, Retnakaran R, Feig DS et al.. “Empagliflozin for the preservation of beta-cell function in women with recent gestational diabetes: A randomized placebo-controlled trial.” Diabetes, obesity & metabolism (2025). PMID: 40964955 ↗
L1RCTCited in: Introduction and Chemical Structure, Special Populations and Contraindications - [4]
Bauer KI, Baker D, Lerner R et al.. “Effect of Empagliflozin on the plasma lipidome in patients with type 2 diabetes mellitus: results from the EmDia clinical trial.” Cardiovascular diabetology (2025). PMID: 40922034 ↗
L1RCTCited in: Introduction and Chemical Structure, Adverse Effects and Toxicity - [5]
Agarwal R, Green JB, Heerspink HJL et al.. “COmbinatioN effect of FInerenone anD EmpaglifloziN in participants with chronic kidney disease and type 2 diabetes using a UACR Endpoint (CONFIDENCE) trial: baseline clinical characteristics.” Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association (2025). PMID: 39916475 ↗
L5RCTCited in: Introduction and Chemical Structure - [6]
Packer M, Ferreira JP, Butler J et al.. “Reaffirmation of Mechanistic Proteomic Signatures Accompanying SGLT2 Inhibition in Patients With Heart Failure: A Validation Cohort of the EMPEROR Program.” Journal of the American College of Cardiology (2024). PMID: 39217550 ↗
L1RCTCited in: Introduction and Chemical Structure - [7]
Yankah RK, Anku EK, Eligar V. “Sodium-Glucose Cotransporter-2 Inhibitors and Cardiovascular Protection Among Patients With Type 2 Diabetes Mellitus: A Systematic Review.” Journal of diabetes research (2024). PMID: 38766320 ↗
L1SR_OBSCited in: Introduction and Chemical Structure - [8]
Kim NH, Lim S, Jeong IK et al.. “Study Design and Protocol for a Randomized Controlled Trial of Enavogliflozin to Evaluate Cardiorenal Outcomes in Type 2 Diabetes (ENVELOP).” Diabetes & metabolism journal (2025). PMID: 39756817 ↗
L5TRIAL_NONRANDOMCited in: Introduction and Chemical Structure - [9]
Nowak-Szwed A, Eyileten C, Wicik Z et al.. “Sirtuins and regulatory miRNAs as epigenetic determinants of empagliflozin-mediated recovery after acute myocardial infarction.” Cardiovascular diabetology (2025). PMID: 41462250 ↗
L5RCTCited in: Mechanism of Action, Indications and Clinical Use, Adverse Effects and Toxicity - [10]
Molaei A, Molaei E, Sadeghnia H et al.. “LKB1: An emerging therapeutic target for cardiovascular diseases.” Life sciences (2022). PMID: 35907495 ↗
L5REVIEW_NARRATIVECited in: Mechanism of Action - [11]
Luo H, Zhang N, Liu Y et al.. “Roles of Empagliflozin in Diabetic Cardiomyopathy: A Review.” Current vascular pharmacology (2025). PMID: 41601174 ↗
L5REVIEW_NARRATIVECited in: Mechanism of Action - [12]
Li YC, Chai HT, Ko SF et al.. “Combined Empagliflozin and Sacubitril/Valsartan Therapy Additively Improves Cardiorenal Function Through AMPK Activation and Angiotensin II Type 1 Receptor Signaling Attenuation in a Rat Model of Cardiorenal Syndrome.” FASEB journal : official publication of the Federation of American Societies for Experimental Biology (2026). PMID: 41854484 ↗
L5OTHERCited in: Mechanism of Action - [13]
Shi X, Zou W, Li X et al.. “SGLT2 inhibition attenuates diabetic tubulopathy by suppressing SGK1-mediated pyroptosis.” Frontiers in endocrinology (2025). PMID: 41030847 ↗
L5OTHERCited in: Mechanism of Action - [14]
Cui M, Zhang J, Wang Z et al.. “Empagliflozin Attenuates Diabetic Cardiomyopathy via Inhibiting Cardiomyocyte Ferroptosis Through the USP7/NRF2 Signaling Pathway.” Antioxidants & redox signaling (2026). PMID: 41002023 ↗
L5OTHERCited in: Mechanism of Action - [15]
Zhang P, Mao C, Sun A et al.. “Real-world observations of GLP-1 receptor agonists and SGLT-2 inhibitors as potential treatments for Alzheimer's disease.” Alzheimer's & dementia : the journal of the Alzheimer's Association (2025). PMID: 40898408 ↗
L3OTHERCited in: Mechanism of Action - [16]
Hoehlschen J, Gosset É, Hofreither D et al.. “Heart saver: Comprehensive investigation of (redox-) proteomic and thiol metabolite changes induced by Cana-, Dapa-, Empagliflozin treatment in 2D and 3D heart cell models reveals increased mitochondrial activity and glutathione redox defense and involvement of redox signaling.” Life sciences (2025). PMID: 40840617 ↗
L5OTHERCited in: Mechanism of Action - [17]
Hu X, Li D, Chen W et al.. “Sodium Glucose Transporter 2 Inhibitor Protects Against Heart Failure With Preserved Ejection Fraction: Preclinical "2-Hit" Model Reveals Autophagy Enhancement Via AMP-Activated Protein Kinase/Mammalian Target of Rapamycin Complex 1 Pathway.” Journal of the American Heart Association (2025). PMID: 40767292 ↗
L5OTHERCited in: Mechanism of Action - [18]
Han Z, Han S, Fang X et al.. “Acetyl-CoA carboxylase activation disrupts iron homeostasis to drive ferroptosis.” Free radical biology & medicine (2025). PMID: 40449808 ↗
L5OTHERCited in: Mechanism of Action - [19]
Heo YJ, Park J, Lee N et al.. “Empagliflozin Alleviates Hepatic Steatosis and Oxidative Stress via the NRF1 Pathway in High-Fat Diet-Induced Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease.” International journal of molecular sciences (2025). PMID: 40362294 ↗
L5OTHERCited in: Mechanism of Action - [20]
Herwig M, Sieme M, Kovács A et al.. “Diabetes mellitus aggravates myocardial inflammation and oxidative stress in aortic stenosis: a mechanistic link to HFpEF features.” Cardiovascular diabetology (2025). PMID: 40361188 ↗
L4OTHERCited in: Mechanism of Action - [21]
Ferrannini E, Baldi S, Frascerra S et al.. “Shift to Fatty Substrate Utilization in Response to Sodium-Glucose Cotransporter 2 Inhibition in Subjects Without Diabetes and Patients With Type 2 Diabetes.” Diabetes (2016). PMID: 26861783 ↗
L2RCTCited in: Pharmacokinetics (LADME) - [22]
Brand T, Macha S, Mattheus M et al.. “Pharmacokinetics of empagliflozin, a sodium glucose cotransporter-2 (SGLT-2) inhibitor, coadministered with sitagliptin in healthy volunteers.” Advances in therapy (2012). PMID: 23054692 ↗
L2RCTCited in: Pharmacokinetics (LADME), Drug Interactions - [23]
Ferrannini E, Muscelli E, Frascerra S et al.. “Metabolic response to sodium-glucose cotransporter 2 inhibition in type 2 diabetic patients.” The Journal of clinical investigation (2014). PMID: 24463454 ↗
L2TRIAL_NONRANDOMCited in: Pharmacokinetics (LADME) - [24]
Macha S, Rose P, Mattheus M et al.. “Pharmacokinetics, safety and tolerability of empagliflozin, a sodium glucose cotransporter 2 inhibitor, in patients with hepatic impairment.” Diabetes, obesity & metabolism (2014). PMID: 23859534 ↗
L2TRIAL_NONRANDOMCited in: Pharmacokinetics (LADME) - [25]
Macha S, Mattheus M, Halabi A et al.. “Pharmacokinetics, pharmacodynamics and safety of empagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, in subjects with renal impairment.” Diabetes, obesity & metabolism (2014). PMID: 23859488 ↗
L2TRIAL_NONRANDOMCited in: Pharmacokinetics (LADME) - [26]
Sarashina A, Koiwai K, Seman LJ et al.. “Safety, tolerability, pharmacokinetics and pharmacodynamics of single doses of empagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, in healthy Japanese subjects.” Drug metabolism and pharmacokinetics (2013). PMID: 23149871 ↗
L1RCTCited in: Pharmacokinetics (LADME) - [27]
Rascher J, Cheng S, Johnston C et al.. “Pharmacokinetics and pharmacodynamics of empagliflozin in paediatric patients aged 10-17 years with type 2 diabetes mellitus.” British journal of clinical pharmacology (2025). PMID: 40390307 ↗
L2RCTCited in: Pharmacokinetics (LADME), Dose and Administration, Special Populations and Contraindications - [28]
Chen G, Zhang D, Du A et al.. “Pharmacokinetics, Safety, and Bioequivalence of Two Empagliflozin Formulations after Single Oral Administration under Fasting and Fed Conditions in Healthy Chinese Subjects: An Open-label Randomized Single-dose Two-sequence, Two-treatment, Two-period Crossover Study.” Pharmacotherapy (2020). PMID: 32498113 ↗
L1RCTCited in: Pharmacokinetics (LADME) - [29]
Macha S, Brand T, Meinicke T et al.. “Pharmacokinetics and Pharmacodynamics of Twice Daily and Once Daily Regimens of Empagliflozin in Healthy Subjects.” Clinical therapeutics (2015). PMID: 26138865 ↗
L1RCTCited in: Pharmacokinetics (LADME) - [30]
Zhao X, Cui Y, Zhao S et al.. “Pharmacokinetic and Pharmacodynamic Properties and Tolerability of Single- and multiple-dose Once-daily Empagliflozin, a Sodium Glucose Cotransporter 2 Inhibitor, in Chinese Patients With Type 2 Diabetes Mellitus.” Clinical therapeutics (2015). PMID: 26101175 ↗
L1RCTCited in: Pharmacokinetics (LADME) - [31]
Macha S, Mattheus M, Pinnetti S et al.. “Pharmacokinetics of Empagliflozin and Pioglitazone After Coadministration in Healthy Volunteers.” Clinical therapeutics (2015). PMID: 26051874 ↗
L1RCTCited in: Pharmacokinetics (LADME), Drug Interactions - [32]
Heise T, Mattheus M, Woerle HJ et al.. “Assessing pharmacokinetic interactions between the sodium glucose cotransporter 2 inhibitor empagliflozin and hydrochlorothiazide or torasemide in patients with type 2 diabetes mellitus: a randomized, open-label, crossover study.” Clinical therapeutics (2015). PMID: 25636696 ↗
L1RCTCited in: Pharmacokinetics (LADME), Drug Interactions - [33]
AlHussaini KI. “Efficacy of empagliflozin in patients with metabolic dysfunction-associated steatotic liver disease with or without diabetes: a systematic review and meta-analysis of randomized controlled trials.” Frontiers in medicine (2025). PMID: 41717349 ↗
L1SR_MA_RCTCited in: Pharmacodynamics - [34]
Lin R, Hsu CL, Shih MC et al.. “Comparison of the renal outcomes of novel antidiabetic agents in patients with type 2 diabetes with chronic kidney disease: A systematic review and network meta-analysis of randomized controlled trials.” Diabetes, obesity & metabolism (2026). PMID: 41147324 ↗
L1SR_MA_RCTCited in: Pharmacodynamics, Indications and Clinical Use - [35]
Lim S, Kim TN, Mok JO et al.. “Efficacy and Safety of Fixed-Dose Combinations of Sitagliptin and Empagliflozin as Add-On to Metformin in Korean Patients With Type 2 Diabetes: A Randomised, Double-Blind, Multi-Centre, Placebo-Controlled, Phase III Trial.” Diabetes, obesity & metabolism (2026). PMID: 41883295 ↗
L1RCTCited in: Pharmacodynamics, Indications and Clinical Use, Adverse Effects and Toxicity - [36]
Gashaw IA, Tuttle KR, Monroy Kuhn M et al.. “Pharmacodynamics of vicadrostat for aldosterone synthase inhibition in patients with CKD.” European journal of endocrinology (2026). PMID: 41436034 ↗
L1RCTCited in: Pharmacodynamics, Indications and Clinical Use, Dose and Administration, Dose Modification - [37]
Lee SH, Han KA, Hong EG et al.. “Efficacy and safety of combining empagliflozin in people with type 2 diabetes mellitus uncontrolled with metformin and sitagliptin: A randomised, double-blind, multicentre, therapeutic confirmatory phase 3 clinical trial.” Diabetes, obesity & metabolism (2026). PMID: 41417560 ↗
L1RCTCited in: Pharmacodynamics, Indications and Clinical Use, Adverse Effects and Toxicity - [38]
Seo DH, Min KW, Sohn HS et al.. “Lobeglitazone improves glycaemic control as add-on therapy to empagliflozin plus metformin in patients with type 2 diabetes mellitus: A double-blind, randomised, placebo-controlled trial.” Diabetes, obesity & metabolism (2026). PMID: 41236870 ↗
L1RCTCited in: Pharmacodynamics, Adverse Effects and Toxicity - [39]
Hassan Waseem M, Abideen ZU, Shoaib A et al.. “Comparing Efficacy and Safety of Different Aldosterone Synthase Inhibitors for Hypertension: A Systematic Review and Network Meta-analysis of Randomized Controlled Trials.” Clinical Medicine Insights. Cardiology (2026). PMID: 41993949 ↗
L1SR_MA_RCTCited in: Pharmacodynamics - [40]
Okita S, Kitahara H, Shoji M et al.. “Evaluation of the efficacy of empagliflozin in patients with preserved left ventricular ejection fraction undergoing transcatheter aortic valve implantation for aortic stenosis: protocol for a randomised, open-label, controlled study.” BMJ open (2026). PMID: 42082222 ↗
L5TRIAL_NONRANDOMCited in: Pharmacodynamics - [41]
Delic D, Gashaw I, Duran-Fernandez I et al.. “Urine Extracellular Vesicle miRNA Changes Induced by Vicadrostat with/Without Empagliflozin in Patients with Chronic Kidney Disease.” International journal of molecular sciences (2025). PMID: 41303298 ↗
L2TRIAL_NONRANDOMCited in: Pharmacodynamics - [42]
Zhu X, Wang X, Zhang P et al.. “Efficacy and safety of novel antidiabetic drugs in patients with type 2 diabetes and chronic kidney disease: a network meta-analysis.” Frontiers in endocrinology (2026). PMID: 41987895 ↗
L1SR_OBSCited in: Pharmacodynamics - [43]
Su AY, Csere MM, Shan R et al.. “Comparative efficacy and safety of SGLT2 inhibitor class members in patients with heart failure and type 2 diabetes: A systematic review and network meta-analysis of randomized controlled trials.” Diabetes research and clinical practice (2025). PMID: 40324721 ↗
L1SR_MA_RCTCited in: Indications and Clinical Use - [44]
Wong SY, Chan SC, Mo YF et al.. “Effects of Empagliflozin and Lifestyle Intervention on Improving Body Weight and Other Metabolic Parameters in Atypical Antipsychotics-treated Patients with Schizophrenia Spectrum Disorders-A Double-blind Randomized Placebo-controlled Trial.” Schizophrenia bulletin (2026). PMID: 42104798 ↗
L1RCTCited in: Indications and Clinical Use, Adverse Effects and Toxicity - [45]
Nesti L, Santoni L, Baldi S et al.. “Exercise Metabolic Flexibility in Type 2 Diabetes Treated With Empagliflozin: An Exploratory Analysis of the Randomised Trial EMPA-HEART.” Diabetes, obesity & metabolism (2026). PMID: 41918256 ↗
L2RCTCited in: Indications and Clinical Use - [46]
Cliff CL, Shah MU, Ward JK et al.. “Timing-dependent anti-inflammatory effects of empagliflozin in monocyte-derived macrophages from post-myocardial infarct patients with type 2 diabetes.” Cardiovascular diabetology (2026). PMID: 41680826 ↗
L2RCTCited in: Indications and Clinical Use, Dose and Administration, Adverse Effects and Toxicity - [47]
Makino H, Kasahara M, Takashima R et al.. “Effect of empagliflozin on urinary albumin excretion and hypoxic biomarkers in early diabetic kidney disease: A randomised double-blind, placebo-controlled trial.” Diabetes, obesity & metabolism (2026). PMID: 41582689 ↗
L1RCTCited in: Indications and Clinical Use - [48]
Calvigioni M, Biancalana E, Rossi C et al.. “Effect of SGLT2 Inhibitors + DPP-4 Inhibitors on Urine Microbiota in Type 2 Diabetes.” Diabetes/metabolism research and reviews (2026). PMID: 41566786 ↗
L1RCTCited in: Indications and Clinical Use - [49]
Ferreira JP, Packer M, Butler J et al.. “Serum Magnesium, Outcomes, and the Effect of Empagliflozin in Heart Failure With Mildly Reduced and Preserved Ejection Fraction: Findings From EMPEROR-Preserved.” JACC. Heart failure (2026). PMID: 41493412 ↗
L2RCTCited in: Indications and Clinical Use - [50]
Agarwal R, Green JB, Heerspink HJL et al.. “Risk of Hyperkalemia With Empagliflozin, Finerenone, or Both: Secondary Analysis of the CONFIDENCE Randomized Trial.” Journal of the American College of Cardiology (2026). PMID: 41493296 ↗
L2RCTCited in: Indications and Clinical Use, Adverse Effects and Toxicity - [51]
Yu D, Zou M, Cheng B et al.. “Effects of 5:2 intermittent fasting meal replacement on body composition and abdominal fat distribution in overweight and obese adults with early type 2 diabetes.” Clinical nutrition (Edinburgh, Scotland) (2026). PMID: 41485450 ↗
L1RCTCited in: Indications and Clinical Use - [52]
Refardt J, Imber C, Sailer CO et al.. “A Randomized Trial of Empagliflozin to Increase Plasma Sodium Levels in Patients with the Syndrome of Inappropriate Antidiuresis.” Journal of the American Society of Nephrology : JASN (2020). PMID: 32019783 ↗
L1RCTCited in: Dose and Administration - [53]
Wanner C, Heerspink HJL, Zinman B et al.. “Empagliflozin and Kidney Function Decline in Patients with Type 2 Diabetes: A Slope Analysis from the EMPA-REG OUTCOME Trial.” Journal of the American Society of Nephrology : JASN (2018). PMID: 30314978 ↗
L1RCTCited in: Dose and Administration - [54]
Yoshikawa F, Kumashiro N, Shigiyama F et al.. “Efficacy of intermittent empagliflozin supplementation on dietary self-management and glycaemic control in patients with poorly controlled type 2 diabetes: A 24-week randomized controlled trial.” Diabetes, obesity & metabolism (2019). PMID: 30187632 ↗
L1RCTCited in: Dose and Administration - [55]
DeFronzo RA, Lee C, Kohler S. “Safety and Tolerability of Combinations of Empagliflozin and Linagliptin in Patients with Type 2 Diabetes: Pooled Data from Two Randomized Controlled Trials.” Advances in therapy (2018). PMID: 29949041 ↗
L1RCTCited in: Dose and Administration - [56]
Shimada A, Hanafusa T, Yasui A et al.. “Empagliflozin as adjunct to insulin in Japanese participants with type 1 diabetes: Results of a 4-week, double-blind, randomized, placebo-controlled phase 2 trial.” Diabetes, obesity & metabolism (2018). PMID: 29766633 ↗
L1RCTCited in: Dose and Administration, Dose Modification - [57]
Laffel LMB, Tamborlane WV, Yver A et al.. “Pharmacokinetic and pharmacodynamic profile of the sodium-glucose co-transporter-2 inhibitor empagliflozin in young people with Type 2 diabetes: a randomized trial.” Diabetic medicine : a journal of the British Diabetic Association (2018). PMID: 29655290 ↗
L1RCTCited in: Dose and Administration, Dose Modification, Special Populations and Contraindications - [58]
Inzucchi SE, Zinman B, Fitchett D et al.. “How Does Empagliflozin Reduce Cardiovascular Mortality? Insights From a Mediation Analysis of the EMPA-REG OUTCOME Trial.” Diabetes care (2018). PMID: 29203583 ↗
L1RCTCited in: Dose and Administration - [59]
Uster A, Desai N, Navaneethan SD et al.. “Empagliflozin Reduces Risk of Hospitalization in Patients With Chronic Kidney Disease in the EMPA-KIDNEY Trial.” Clinical therapeutics (2025). PMID: 41047325 ↗
L1RCTCited in: Dose Modification, Adverse Effects and Toxicity - [60]
Mancia G, Cannon CP, Tikkanen I et al.. “Impact of Empagliflozin on Blood Pressure in Patients With Type 2 Diabetes Mellitus and Hypertension by Background Antihypertensive Medication.” Hypertension (Dallas, Tex. : 1979) (2016). PMID: 27977392 ↗
L1RCTCited in: Dose Modification - [61]
Hadjadj S, Rosenstock J, Meinicke T et al.. “Initial Combination of Empagliflozin and Metformin in Patients With Type 2 Diabetes.” Diabetes care (2016). PMID: 27493136 ↗
L1RCTCited in: Dose Modification - [62]
Yoon KH, Nishimura R, Lee J et al.. “Efficacy and safety of empagliflozin in patients with type 2 diabetes from Asian countries: pooled data from four phase III trials.” Diabetes, obesity & metabolism (2016). PMID: 27265507 ↗
L1RCTCited in: Dose Modification - [63]
Chilton R, Tikkanen I, Cannon CP et al.. “Effects of empagliflozin on blood pressure and markers of arterial stiffness and vascular resistance in patients with type 2 diabetes.” Diabetes, obesity & metabolism (2015). PMID: 26343814 ↗
L1RCTCited in: Dose Modification - [64]
Kovacs CS, Seshiah V, Merker L et al.. “Empagliflozin as Add-on Therapy to Pioglitazone With or Without Metformin in Patients With Type 2 Diabetes Mellitus.” Clinical therapeutics (2015). PMID: 26138864 ↗
L2RCTCited in: Dose Modification - [65]
Kohler S, Zeller C, Iliev H et al.. “Safety and Tolerability of Empagliflozin in Patients with Type 2 Diabetes: Pooled Analysis of Phase I-III Clinical Trials.” Advances in therapy (2017). PMID: 28631216 ↗
L1TRIAL_NONRANDOMCited in: Dose Modification - [66]
Mottl A, Scott C, Green JB et al.. “Baseline Kidney Function, Albuminuria, and Urine Albumin-Creatinine Ratio Reduction with Finerenone, Empagliflozin, or Both: Post Hoc Analyses of CONFIDENCE Trial.” Journal of the American Society of Nephrology : JASN (2026). PMID: 41196655 ↗
L1RCTCited in: Adverse Effects and Toxicity - [67]
Agarwal R, Green JB, Heerspink HJL et al.. “Impact of Baseline GLP-1 Receptor Agonist Use on Albuminuria Reduction and Safety With Simultaneous Initiation of Finerenone and Empagliflozin in Type 2 Diabetes and Chronic Kidney Disease (CONFIDENCE Trial).” Diabetes care (2025). PMID: 40968755 ↗
L1RCTCited in: Adverse Effects and Toxicity - [68]
Lei Y, Yi Q, Ji S et al.. “Bioequivalence Evaluation of Two Metformin/Empagliflozin Fixed-Dose Combination Tablets in Healthy Chinese Subjects Under Fasting and Fed Conditions: A Randomized, Open-Label, Crossover Study.” Clinical pharmacology in drug development (2026). PMID: 41578725 ↗
L1RCTCited in: Adverse Effects and Toxicity - [69]
Lim S, Park CY, Jeong IK et al.. “Empagliflozin versus metformin for glucose variability and metabolic outcomes in drug-naïve type 2 diabetes: The EMPA-FIT study.” Journal of diabetes and its complications (2026). PMID: 41223492 ↗
L1RCTCited in: Adverse Effects and Toxicity - [70]
Yee KM, Sagim E, Leong CW et al.. “Pharmacokinetics and Bioequivalence of two Empagliflozin Tablet Formulations: Results From a Randomized, Open-Label, Crossover Study in Fasting Healthy Volunteers.” Clinical pharmacology in drug development (2026). PMID: 41077870 ↗
L1RCTCited in: Adverse Effects and Toxicity - [71]
Carbone S, Canada JM, Billingsley HE et al.. “Effects of empagliflozin on cardiorespiratory fitness and significant interaction of loop diuretics.” Diabetes, obesity & metabolism (2018). PMID: 29603546 ↗
L4TRIAL_NONRANDOMCited in: Drug Interactions - [72]
Packer M, Anker SD, Butler J et al.. “Empagliflozin in Patients With Heart Failure, Reduced Ejection Fraction, and Volume Overload: EMPEROR-Reduced Trial.” Journal of the American College of Cardiology (2021). PMID: 33736819 ↗
L1RCTCited in: Drug Interactions - [73]
Kim D, Choi M, Jin BH et al.. “Pharmacokinetic and pharmacodynamic drug-drug interactions between evogliptin and empagliflozin or dapagliflozin in healthy male volunteers.” Clinical and translational science (2023). PMID: 37282359 ↗
L1RCTCited in: Drug Interactions - [74]
Lee M, Hong S, Cho Y et al.. “Synergistic benefit of thiazolidinedione and sodium-glucose cotransporter 2 inhibitor for metabolic dysfunction-associated steatotic liver disease in type 2 diabetes: a 24-week, open-label, randomized controlled trial.” BMC medicine (2025). PMID: 40336058 ↗
L1RCTCited in: Drug Interactions - [75]
Ferreira JP, Zannad F, Pocock SJ et al.. “Interplay of Mineralocorticoid Receptor Antagonists and Empagliflozin in Heart Failure: EMPEROR-Reduced.” Journal of the American College of Cardiology (2021). PMID: 33736821 ↗
L1RCTCited in: Drug Interactions - [76]
Lava SAG, Laurence C, Di Deo A et al.. “Dapagliflozin and Empagliflozin in Paediatric Indications: A Systematic Review.” Paediatric drugs (2024). PMID: 38635113 ↗
L1SR_OBSCited in: Special Populations and Contraindications - [77]
Laffel LM, Danne T, Klingensmith GJ et al.. “Efficacy and safety of the SGLT2 inhibitor empagliflozin versus placebo and the DPP-4 inhibitor linagliptin versus placebo in young people with type 2 diabetes (DINAMO): a multicentre, randomised, double-blind, parallel group, phase 3 trial.” The lancet. Diabetes & endocrinology (2023). PMID: 36738751 ↗
L1RCTCited in: Special Populations and Contraindications - [78]
Furth SL. “Trials and Tribulations - The Challenges of Clinical Trials in Children.” NEJM evidence (2023). PMID: 38320507 ↗
L5TRIAL_NONRANDOMCited in: Special Populations and Contraindications - [79]
Gross O, Boeckhaus J, Weber LT et al.. “Protocol and rationale for a randomized controlled SGLT2 inhibitor trial in paediatric and young adult populations with chronic kidney disease: DOUBLE PRO-TECT Alport.” Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association (2025). PMID: 39122650 ↗
L5TRIAL_NONRANDOMCited in: Special Populations and Contraindications - [80]
Sailer MO, Neubacher D, Johnston C et al.. “Pharmacometrics-Enhanced Bayesian Borrowing for Pediatric Extrapolation - A Case Study of the DINAMO Trial.” Therapeutic innovation & regulatory science (2025). PMID: 39373938 ↗
L2RCTCited in: Special Populations and Contraindications - [81]
Agarwal R, Correa-Rotter R, Navaneethan SD et al.. “Safety and Synergy of Finerenone and Empagliflozin in Lowering Blood Pressure.” Hypertension (Dallas, Tex. : 1979) (2026). PMID: 42244376 ↗
L1bCited in: Drug Interactions - [82]
Macha S, Koenen R, Sennewald R et al.. “Effect of gemfibrozil, rifampicin, or probenecid on the pharmacokinetics of the SGLT2 inhibitor empagliflozin in healthy volunteers.” Clinical therapeutics (2014). PMID: 24491572 ↗
L1bCited in: Drug Interactions - [83]
Macha S, Sennewald R, Rose P et al.. “Lack of clinically relevant drug-drug interaction between empagliflozin, a sodium glucose cotransporter 2 inhibitor, and verapamil, ramipril, or digoxin in healthy volunteers.” Clinical therapeutics (2013). PMID: 23497760 ↗
L1bCited in: Drug Interactions - [84]
Friedrich C, Metzmann K, Rose P et al.. “A randomized, open-label, crossover study to evaluate the pharmacokinetics of empagliflozin and linagliptin after coadministration in healthy male volunteers.” Clinical therapeutics (2013). PMID: 23328275 ↗
L1bCited in: Drug Interactions - [85]
Lei Y, Liu Y, Gao L et al.. “Bioequivalence Study of Two Empagliflozin Tablets in Healthy Chinese Subjects Under Fasting and Fed Conditions.” Clinical pharmacology in drug development (2025). PMID: 40277386 ↗
L1bCited in: Drug Interactions - [86]
Macha S, Lang B, Pinnetti S et al.. “Pharmacokinetics of empagliflozin, a sodium glucose cotransporter 2 inhibitor, and simvastatin following co-administration in healthy volunteers.” International journal of clinical pharmacology and therapeutics (2014). PMID: 25161155 ↗
L1bCited in: Drug Interactions - [87]
Macha S, Jungnik A, Hohl K et al.. “Effect of food on the pharmacokinetics of empagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, and assessment of dose proportionality in healthy volunteers.” International journal of clinical pharmacology and therapeutics (2013). PMID: 24152604 ↗
L1bCited in: Drug Interactions - [88]
Jin Y, Zhao W, Li Q et al.. “To investigate the effect of a high-fat diet on pharmacokinetics/renal function/RAAS-related parameters after a single dose of empagliflozin in healthy Chinese adults.” BMC pharmacology & toxicology (2026). PMID: 41656305 ↗
L2bCited in: Drug Interactions - [89]
Kim YK, Hwang JG, Park MK. “No Relevant Pharmacokinetic Drug-Drug Interaction Between the Sodium-Glucose Co-Transporter-2 Inhibitor Empagliflozin and Lobeglitazone, a Peroxisome Proliferator-Activated Receptor-γ Agonist, in Healthy Subjects.” Drug design, development and therapy (2021). PMID: 33953542 ↗
L1bCited in: Drug Interactions - [90]
Macha S, Dieterich S, Mattheus M et al.. “Pharmacokinetics of empagliflozin, a sodium glucose cotransporter-2 (SGLT2) inhibitor, and metformin following co-administration in healthy volunteers.” International journal of clinical pharmacology and therapeutics (2013). PMID: 23253948 ↗
L2bCited in: Drug Interactions - [91]
Macha S, Mattheus M, Pinnetti S et al.. “Effect of empagliflozin on the steady-state pharmacokinetics of ethinylestradiol and levonorgestrel in healthy female volunteers.” Clinical drug investigation (2013). PMID: 23512637 ↗
L4Cited in: Drug Interactions