Ertugliflozin 15mg tablets
Requires a prescription from a doctor or prescriber
Ertugliflozin is a sodium-dependent glucose cotransporter-2 (SGLT2) inhibitor used to treat type II diabetes mellitus.
Official documents, adverse reaction reporting, and safety monitoring
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Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Ertugliflozin
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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Suspected adverse reactions reported for Ertugliflozin
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1 branded products available
MHRA licensed products
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Steglatro 15mg tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
10 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(2)
Ertugliflozin as monotherapy or with metformin for treating type 2 diabetes (TA572)
Ertugliflozin with metformin and a dipeptidyl peptidase-4 inhibitor for treating type 2 diabetes (TA583)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Supply & safety information
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 27 · Randomised trials: 14 · 2017–2026
Showing the 50 most relevant studies, sorted by most relevant.
D. Cherney, B. Charbonnel, F. Cosentino, et al.
Diabetologia, 2021
Bhalraam U, Veerni RB, Paddock S, et al.
2026
- Neoplasms
- Heart Failure
- Cancer Survivors
AimsSodium-glucose cotransporter-2 inhibitors (SGLT2i) are recognized for their cardiovascular benefits. This systematic review and meta-analysis evaluated the impact of SGLT2i on heart failure (HF) outcomes in cancer patients and survivors, focusing on HF hospitalization and new HF diagnoses.Methods and resultsA comprehensive search of PubMed, MEDLINE, and Embase via Ovid, and the Cochrane Library was conducted up to 5 June 2024, focusing on studies involving cancer patients and survivors treated with SGLT2i. The search criterion used was [(SGLT2) OR (Sodium glucose cotransporter 2 inhibitors) OR (canagliflozin) OR (dapagliflozin) OR (empagliflozin) OR (ertugliflozin) AND (cancer)]. The primary outcomes assessed were HF hospitalization and new HF diagnoses. The search yielded 1880 studies, from which 13 studies encompassing 88 273 patients were included. SGLT2i use reduced HF hospitalizations by 51% (RR 0.49, 95% CI 0.36-0.66, I² = 28%, P ConclusionSGLT2i significantly lower the risk of HF hospitalization and new HF diagnoses among cancer patients and survivors, with particularly pronounced benefits in breast cancer patients receiving anthracycline-based chemotherapy. These findings support the need for prospective trials to further investigate the integration of SGLT2i into cancer patient management to enhance cardiovascular outcomes.
Abstract licence: CC BY-NC
R. Pratley, R. Eldor, Annaswamy Raji, et al.
Diabetes, Obesity & Metabolism, 2018
Qian Cheng, Shupeng Zou, Chengyang Feng, et al.
Medicine, 2023
J.B. Lee, M.Z. Sabran, K.Y. Rubismo, et al.
Journal of Hypertension, 2023
Dăniluc L, Dăniluc R, Benea A, et al.
2026
Background: Type 2 diabetes mellitus (T2DM) is associated with subclinical myocardial dysfunction, which may occur despite preserved left ventricular ejection fraction. Left ventricular global longitudinal strain (LV GLS) is a sensitive marker of early systolic impairment and may detect subtle changes in myocardial function before conventional echocardiographic parameters become abnormal. The effect of sodium-glucose cotransporter-2 inhibitors (SGLT2i) on LV GLS in adults with T2DM remains incompletely defined. Objective: To synthesize the available evidence on the effects of SGLT2i therapy on LV GLS or LV strain in adults with T2DM. Methods: Original full-text human studies evaluating SGLT2i therapy in adults with T2DM and reporting LV GLS or LV strain were included. LV GLS was assessed primarily by speckle-tracking echocardiography, while one study used cardiac magnetic resonance feature-tracking. Reviews, conference abstracts, protocols, animal-only studies, and studies without LV strain assessment were excluded. Risk of bias was assessed using RoB 2 for randomized studies and ROBINS-I for non-randomized studies. Results: Twenty-six studies involving more than 2300 participants were included. The studies evaluated dapagliflozin, empagliflozin, ertugliflozin, canagliflozin, or mixed SGLT2i regimens across heterogeneous clinical populations, including patients with preserved ejection fraction, pre-heart failure, diabetes-related cardiomyopathy, chronic heart failure, coronary artery disease, hypertension, non-alcoholic fatty liver disease, and cardio-oncology risk. Most observational and before-after studies reported favorable changes in LV GLS after SGLT2i therapy, whereas randomized and controlled studies showed more variable findings. Several studies also reported improvements in LV remodeling, diastolic function, left atrial function, myocardial work indices, NT-proBNP, cardiometabolic parameters, or epicardial adipose tissue thickness. However, the certainty of evidence was limited by methodological heterogeneity, differences in comparator groups, variable follow-up duration, non-standardized imaging protocols, and risk of bias, particularly in non-randomized and single-arm studies. Conclusions: SGLT2i therapy may be associated with favorable changes in LV GLS in adults with T2DM, suggesting a potential beneficial effect on subclinical left ventricular systolic function. However, current evidence does not definitively establish a consistent treatment effect across all populations. Larger randomized controlled trials with standardized strain imaging protocols, predefined LV GLS endpoints, and clinically relevant follow-up are needed to determine whether SGLT2i-related improvements in LV GLS reflect true myocardial benefit and translate into improved cardiovascular outcomes.
Abstract licence: CC BY
Joher I, Singla S, Shakeel Ahmed U, et al.
2025
Sodium-glucose cotransporter-2 (SGLT2) inhibitors have emerged as a transformative therapy in type 2 diabetes mellitus (T2DM), offering benefits that extend beyond glycemic control. We conducted a meta-analysis of six large randomized controlled trials (RCTs), enrolling more than 47,000 patients with T2DM and varying risks of cardiovascular disease (CVD) and chronic kidney disease (CKD), to evaluate the effect of SGLT2 inhibitors on hospitalization for heart failure (HHF). Across a mean follow-up ranging from 1.3 to 4.2 years, SGLT2 inhibitors were associated with a 28% relative risk reduction in HHF compared with placebo or standard care. This benefit was consistent across most agents, including empagliflozin, canagliflozin, dapagliflozin, and sotagliflozin, while ertugliflozin showed a nonsignificant trend in the same direction. Subgroup analyses confirmed benefits in patients with established atherosclerotic CVD as well as those with CKD, underscoring the broad applicability of this therapy. The results demonstrate that SGLT2 inhibitors confer clinically meaningful cardiorenal protection that is recognized to occur through mechanisms largely independent of glucose lowering, reinforcing their role as cornerstone agents in the management of T2DM. These findings highlight the importance of prioritizing SGLT2 inhibitors in contemporary diabetes care to reduce the global burden of heart failure (HF).
Abstract licence: CC BY
Abdelfadil Elgazzar R, Ramadan M
2026
Sodium-glucose cotransporter 2 (SGLT2) inhibitors were initially developed as glucose-lowering agents for type 2 diabetes mellitus (T2DM) by reducing proximal tubular glucose reabsorption and promoting glucosuria. Subsequent cardiovascular and renal outcome trials established that these agents provide clinically meaningful benefits that extend beyond glycemic control, including reductions in heart failure (HF) events and slowing of chronic kidney disease (CKD) progression in patients with and without diabetes. We conducted a narrative literature review using PubMed and Google Scholar to identify English-language studies published between January 2019 and December 2025 evaluating SGLT2 inhibitors (empagliflozin, dapagliflozin, canagliflozin, ertugliflozin) across cardiovascular and renal outcomes. Eligible evidence included randomized controlled trials, large observational studies, systematic reviews/meta-analyses, guidelines, post‑hoc exploratory analyses, secondary analyses, and mechanistic/preclinical studies. Mechanistic data support benefits through natriuresis and osmotic diuresis with favorable ventricular loading, restoration of tubuloglomerular feedback and reduced intraglomerular pressure, improved myocardial energetics, and attenuation of oxidative stress and inflammation. Clinically, SGLT2 inhibitors consistently reduce HF hospitalizations and composite cardiorenal endpoints in diabetic and non-diabetic populations across CKD stages studied and heart conditions, with a generally favorable safety profile; genital mycotic infections are most common, while diabetic ketoacidosis and volume depletion are uncommon with appropriate patient selection and counselling. Evidence gaps remain for stage 5 CKD and dialysis populations and for defining outcomes in lower-risk post-myocardial infarction cohorts. Overall, current data support SGLT2 inhibitors as foundational therapy for eligible patients with HF and/or CKD irrespective of diabetes status.
Abstract licence: CC BY
Galih Indra Permana, Ervi Audina Munthe, I. Irfan
Devotion : Journal of Research and Community Service, 2025
Felix Bratosin
2024
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
26 found
Half-life
11 to 17 hours
Mechanism
Kidneys play an integral role in glucose homeostasis.
Food interactions
2 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
5 mg
Half-life
11 to 17 hours
[A31583]
…
Protein binding
93.6%
Volume of distribution
215.3 L
Metabolism
12%
Elimination
40.9%
Clearance
178.7 mL/min
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Ertugliflozin was first approved by the FDA in December 2017.[A261951][L1132] It was also approved by the European Commission in March 2018.[L48621]
[L48466]
It is also available in combination with either [metformin] or [sitagliptin].
[L1134][L1135]
Ertugliflozin is not recommended for use to improve glycemic control in patients with type 1 diabetes mellitus.
[L48466]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 634 interactions
[L48471]
There are limited clinical experiences of ertugliflozin overdose. It is recommended to initiate supportive measures in the event of drug overdosage. Removal of ertugliflozin by hemodialysis has not been studied.
[L48466]
Ertugliflozin is an inhibitor of SGLT2 that reduces renal reabsorption of filtered glucose and lowers the renal threshold for glucose, thereby increasing urinary glucose excretion.[L48466]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L48466]
Following administration of a 15 mg dose, the Cmax was 268 ng/mL and the AUC was 1193 ng h/mL.
[L1136]
The absolute oral bioavailability of ertugliflozin following administration of a 15 mg dose was approximately 100%,[L48466] though it is reported to range from 70% to 90%.
[A31583]
Administration of ertugliflozin with a high-fat and high-calorie meal decreases ertugliflozin Cmax by 29%. It prolongs Tmax by one hour but does not alter AUC compared to the fasted state.
The observed effect of food on ertugliflozin pharmacokinetics is not considered clinically relevant, and ertugliflozin may be administered with or without food.
[L48466]
[A31583]
The mean elimination half-life in T2DM patients with normal renal function was estimated to be 16.6 hours based on the population pharmacokinetic analysis.
[L48466]
[L48466]
[L1136]
The mean steady-state volume of distribution of ertugliflozin following an intravenous dose is 85.5 L.
[L48466]
[L48466]
Several metabolites have been found in plasma, feces, and urine. In plasma, the unchanged form of ertugliflozin was found to be the major component of the administered dose.
[A31583]
[L48466]
[L1136]
In another study, the mean systemic plasma clearance following an intravenous 100 µg dose was 11.2 L/hr.
[L48466]
Proteins and enzymes this drug interacts with in the body
PMID:20980548 PMID:28592437 PMID:34880493 PMID:37217492 PMID:38057552
Transporter activity is driven by a transmembrane Na(+) electrochemical gradient set by the Na(+)/K(+) pump .
PMID:20980548 PMID:28592437 PMID:34880493
Unlike SLC5A1/SGLT1, requires the auxiliary protein PDZK1IP1/MAP17 for full transporter activity .
PMID:37217492
Has a primary role in D-glucose reabsorption from glomerular filtrate across the brush border of the early proximal tubules of the kidney (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
ATC A10BD23
ATC A10BK04
ATC A10BD24
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Ertugliflozin
Additional database identifiers
Drugs Product Database (DPD)
22949
ChemSpider
26340533
BindingDB
50342885
ZINC
ZINC000068197809
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11037
GeneCards
SLC5A2
Guide to Pharmacology
916
UniProt Accession
SC5A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12541
GeneCards
UGT1A9
GenBank Gene Database
S55985
GenBank Protein Database
7690346
UniProt Accession
UD19_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12554
GeneCards
UGT2B7
GenBank Gene Database
J05428
GenBank Protein Database
340080
UniProt Accession
UD2B7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12530
GeneCards
UGT1A1
GenBank Gene Database
M57899
GenBank Protein Database
184473
Guide to Pharmacology
2990
UniProt Accession
UD11_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12536
GeneCards
UGT1A4
GenBank Gene Database
M57951
GenBank Protein Database
184475
UniProt Accession
UD14_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72