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Canagliflozin

Canagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor medication used to manage type 2 diabetes.
It works by reducing the reabsorption of glucose in the kidneys, thereby increasing urinary glucose excretion and lowering blood glucose levels.
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Most cited protocols related to «Canagliflozin»

1
Canagliflozin vs Sitagliptin for Type 2 Diabetes
Cited 9 times
During the placebo run-in period, participants received single-blind placebo capsules matching study drug once daily. Participants were randomised to receive canagliflozin 100 mg or 300 mg, sitagliptin 100 mg or placebo (2:2:2:1) once daily for 26 weeks. The canagliflozin 100 mg and 300 mg once-daily doses were selected based on findings from a dose-ranging, Phase 2 study in patients with type 2 diabetes on background metformin [5 (link)]; a 300 mg twice-daily regimen provided only incremental benefits vs the once-daily regimen and was therefore not selected for further development. The use of placebo as a control for the 26 week core treatment period was done in accordance with US Food and Drug Administration and European Medicines Agency regulatory guidelines [15 , 16 ]. The computer-generated randomisation schedule was prepared by the sponsor before the study. Randomisation was balanced using permuted blocks of seven and stratified by whether a participant was on metformin monotherapy or metformin plus sulfonylurea at screening. After randomisation, HbA1c and FPG values were masked to the study centres unless they met glycaemic rescue criteria. After completion of period I, the database was locked and the study was unblinded by the sponsor for regulatory filing; the participants and the study centre and local sponsor personnel remained blinded throughout period II.
Participants who completed period I then entered period II, during which those randomised to canagliflozin (100 or 300 mg) or sitagliptin 100 mg continued on those treatments while those randomised to placebo switched to sitagliptin 100 mg in a blinded fashion. During the double-blind treatment period, glycaemic rescue therapy with glimepiride (added to study drug and background metformin) was initiated if FPG >15.0 mmol/l after day 1 to week 6, >13.3 mmol/l after week 6 to week 12, and >11.1 mmol/l after week 12 to week 26. Glimepiride therapy was also started if HbA1c >8.0% (64 mmol/mol) after week 26.
Lavalle-González F.J., Januszewicz A., Davidson J., Tong C., Qiu R., Canovatchel W, & Meininger G. (2013). Efficacy and safety of canagliflozin compared with placebo and sitagliptin in patients with type 2 diabetes on background metformin monotherapy: a randomised trial. Diabetologia, 56(12), 2582-2592.
Publication 2013
Canagliflozin Capsule Diabetes Mellitus, Non-Insulin-Dependent Europeans glimepiride Metformin Patients Placebos Sitagliptin Sulfonylurea Compounds Therapeutics Treatment Protocols
2
Canagliflozin vs. Sitagliptin for T2DM
Cited 8 times
The primary hypothesis for this study was that canagliflozin 300 mg was noninferior to sitagliptin 100 mg in reducing A1C from baseline to week 52. The primary analysis was based on the modified intent-to-treat population (all randomized subjects who received one or more doses of study drug) with a last observation carried forward approach to impute missing data at the end point. Assuming no difference between canagliflozin and sitagliptin in A1C-lowering efficacy and a common SD of 1.0% with respect to change in A1C, it was estimated that 234 subjects per treatment group would provide ∼90% power to demonstrate the noninferiority of canagliflozin compared with sitagliptin. In addition, per-protocol analysis (subjects completing the 52-week study and without protocol deviations that could impact efficacy assessment) was conducted to further support the noninferiority assessment. To provide 90% power for the per-protocol analysis, assuming a discontinuation rate of 35% over 52 weeks, the sample size was increased to 360 subjects per treatment group.
Safety analyses and the primary efficacy analysis were conducted using the modified intent-to-treat population. The last observation carried forward approach was used for the primary analysis of efficacy data. All statistical tests were interpreted at a two-sided significance level of 5%, and all CIs were interpreted at a two-sided confidence level of 95%. Primary and continuous secondary end points were assessed using an ANCOVA model, including treatment and stratification factors as fixed effects and the corresponding baseline value as a covariate. The least squares (LS) mean differences and two-sided 95% CIs were estimated for the comparisons of canagliflozin versus sitagliptin. Noninferiority of canagliflozin to sitagliptin was assessed based on a prespecified margin of 0.3% for the upper limit of the two-sided 95% CI for the comparison in the primary last observation carried forward analysis. If noninferiority was demonstrated, then superiority was assessed, as determined by an upper bound of the 95% CI around the between-group difference (canagliflozin minus sitagliptin) of <0.0%. A prespecified hierarchical testing sequence was implemented to strongly control overall type I error attributable to multiplicity; P values are reported for prespecified comparisons only.
For subgroup analysis, descriptive statistics and 95% CIs for the change from baseline in A1C were provided for subgroups of subjects with baseline A1C of <8.0% (64 mmol/mol), ≥8.0% (64 mmol/mol) to <9.0% (75 mmol/mol), and ≥9.0% (75 mmol/mol). For indices of βCF, descriptive statistics and 95% CIs for the changes from baseline were provided; comparisons of canagliflozin with sitagliptin for changes from baseline at week 52 were assessed using an ANCOVA model with treatment and stratification factors as fixed effects and the corresponding baseline value as a covariate.
Schernthaner G., Gross J.L., Rosenstock J., Guarisco M., Fu M., Yee J., Kawaguchi M., Canovatchel W, & Meininger G. (2013). Canagliflozin Compared With Sitagliptin for Patients With Type 2 Diabetes Who Do Not Have Adequate Glycemic Control With Metformin Plus Sulfonylurea: A 52-week randomized trial. Diabetes Care, 36(9), 2508-2515.
Publication 2013
Canagliflozin Safety Sitagliptin
3
Cardiovascular Risk in SGLT2 Inhibitor Users
Cited 5 times
We used TriNetX, a global federated research network providing access to statistics on EMR (diagnoses, procedures, medications, laboratory values, genomic information). The analytics subset allowed the analysis of approximately 38 million patients in 35 large Health Care Organizations predominately in the United States. As a federated network, TriNetX received a waiver from Western IRB, since only aggregated counts, statistical summaries of de-identified information, and no protected health information is received. In addition, no study-specific activities are performed in retrospective analyses. Details of the network have been described elsewhere[6 -8 ]. All analyses were done in the TriNetX “Analytics” network using the browser-based real-time analytics features. At the time of the analysis in June 2018, we analyzed the EMR of 46909 patients in the network who had an instance of any SGLT2 inhibitor (empagliflozin, dapagliflozin or canagliflozin) any time within the past ten years in their electronic medical record. As a comparison group, we chose patients who had taken dipeptidyl peptidase (DPP) 4 inhibitors (linagliptin, alogliptin, sitagliptin or saxagliptin) during the same time, and found 189120 patients. Using a Bayesian statistical approach[9 ] on demographics and pre-existing (baseline) comorbidities of the two groups, we identified five potential confounding factors and built strata with the following criteria: age ≥ 60 years, presence of hypertension [International Classification of Diseases (ICD)10 code I10], presence of CKD (ICD10 code N18), co-medication with insulin, and co-medication with metformin. Separately analyzing strata allowed us to address potential bias in the federated data model without direct access to the individual data sets on the patient level.
Cardiovascular events were counted by selecting any stroke (ICD10 code I63) or myocardial infarction (ICD10 code I21) occurring during a three-year observation period after the first instance of the above mentioned medications in the patients’ records.
The risks of experiencing an event in each stratum were calculated by dividing the number of patients with an event (numerator) by the total number of patients with the respective medication in each stratum (denominator). The risk ratios for SGLT2 inhibitors vs the comparison group were calculated by dividing the risk for each SGLT2 stratum by the risk in each corresponding DPP4 stratum.
, & Stapff M.P. (2018). Using real world data to assess cardiovascular outcomes of two antidiabetic treatment classes. World Journal of Diabetes, 9(12), 252-257.
Publication 2018
alogliptin Canagliflozin Cardiovascular System Cerebrovascular Accident dapagliflozin Diagnosis Dipeptidyl-Peptidase IV Inhibitors DPP4 protein, human empagliflozin Genome High Blood Pressures Insulin Linagliptin Metformin Myocardial Infarction Patients Pharmaceutical Preparations saxagliptin Sitagliptin SLC5A2 protein, human Sodium-Glucose Transporter 2 Inhibitors
4
Propensity Score Matching for Comparative Effectiveness of Canagliflozin
Cited 5 times
Baseline characteristics were cross tabulated by each pair of canagliflozin or its comparator. To control for imbalances in patient characteristics between cohorts, we calculated exposure propensity scores as the predicted probability of receiving the treatment of interest (ie, canagliflozin v each comparator) conditional upon the subjects’ baseline covariates using three separate multivariable logistic regression models.18 (link) All variables were included and no further selection was conducted. We 1:1 matched cohorts on their propensity score using a caliper width equal to 0.2 of the standard deviation of the logit of the propensity score.19 (link) Covariate balance between the cohorts before and after propensity score matching was assessed using standardized differences; meaningful imbalances were defined as a standardized difference greater than 0.1.20 (link) For each comparison and for all outcomes, we calculated unadjusted and propensity score matched number of events, incidence rates, and hazard ratios with 95% confidence intervals. We assessed the proportional hazards assumption by testing the significance of the interaction term between exposure and time, and confirmed that it was not violated.21 (link)
We conducted several sensitivity analyses to test the robustness of our primary findings. First, among the patients with baseline HbA1c levels available (approximately one third of the total population depending on the cohort), we re-estimated the propensity score adding HbA1c level in addition to the other baseline covariates to further account for underlying glucose control. Second, to address the potential for unmeasured confounding associated with the high risk for recurrence, we restricted to patients who had not been admitted to hospital for heart failure, acute coronary, or cerebrovascular events during the 60 day period before entry to the cohort. Third, to address potential informative censoring, we carried forward the exposure to the initiated drug for 365 days without considering drug discontinuation or switching, to mimic an intention to treat approach.22 (link)
In addition, we conducted subgroup analyses stratified by presence of heart failure or cardiovascular disease at baseline for the primary outcomes of heart failure admission to hospital or the composite cardiovascular endpoint respectively (see web appendix 3 for the definition of subgroups).
All analyses were performed using SAS 9.3 Statistical Software (SAS Institute Inc, Cary, NC).
Patorno E., Goldfine A.B., Schneeweiss S., Everett B.M., Glynn R.J., Liu J, & Kim S.C. (2018). Cardiovascular outcomes associated with canagliflozin versus other non-gliflozin antidiabetic drugs: population based cohort study. The BMJ, 360, k119.
Publication 2018
Canagliflozin Cardiovascular Diseases Cardiovascular System Congestive Heart Failure Glucose Heart Hypersensitivity Patients Pharmaceutical Preparations Recurrence
5
Canagliflozin vs Placebo and Sitagliptin in T2DM
Cited 5 times
The primary hypothesis was that canagliflozin 300 mg is statistically superior to placebo in reducing HbA1c from baseline to week 26. Key secondary hypotheses were statistical superiority of canagliflozin 100 mg to placebo in HbA1c- lowering effect at week 26 and non-inferiority of canagliflozin 300 mg or both canagliflozin doses to sitagliptin 100 mg in reducing HbA1c from baseline to week 52. Primary efficacy analysis was performed in the modified intent-to-treat (mITT) population (randomised participants who received ≥1 dose of study drug) using a last observation carried forward (LOCF) approach. Assuming a group difference of 0.5% (5.5 mmol/mol) between canagliflozin and placebo and a common SD of 1.0% (10.9 mmol/mol) for change in HbA1c, and using a two-sample, two-sided t test with a type I error rate of 0.05, an estimated 86 participants per group were required to achieve 90% power to demonstrate statistical superiority of canagliflozin to placebo. To support superiority and non-inferiority objectives for the primary endpoint in the mITT population and for supportive analysis in the per-protocol population (mITT participants who completed the study, did not receive rescue therapy and had no major protocol violations), an estimated 360 randomised participants were needed for each active treatment group and 180 for the placebo group, assuming a 35% discontinuation rate at week 52 and with a 2:2:2:1 randomisation ratio for canagliflozin 100 mg, canagliflozin 300 mg, sitagliptin 100 mg and placebo.
Primary efficacy analyses were performed in the mITT population according to randomised treatment assignment using LOCF to impute missing data; for participants who received rescue therapy, the last post-baseline value before rescue was used. Safety analyses were performed in the same population according to the predominant treatment received; in this study, the mITT and safety populations were identical. Only data from participants randomised to sitagliptin 100 mg on day 1 (i.e. not including participants who switched from placebo to sitagliptin at week 26) were included in efficacy comparisons at week 52. Safety analyses over 52 weeks included participants who received canagliflozin 100 mg or 300 mg or sitagliptin and those who switched from placebo to sitagliptin after 26 weeks (placebo/sitagliptin group).
An analysis of covariance (ANCOVA) model with treatment and stratification factor as fixed effects and corresponding baseline value as a covariate was used to assess primary and continuous secondary endpoints. Least squares (LS) mean differences between groups and two-sided 95% CIs were estimated. The categorical secondary endpoint was analysed with a logistic model with treatment and stratification factor as fixed effects and baseline HbA1c as a covariate. Assessment of non-inferiority of canagliflozin to sitagliptin was based on a pre-specified margin of 0.3% for the upper limit of the two-sided 95% CI for the comparison. If non-inferiority was demonstrated, then superiority was assessed based on an upper bound of the 95% CI around the between-group differences of <0.0%.
Comparisons were performed for canagliflozin vs placebo at week 26 and vs sitagliptin at week 52 based on pre-specified hierarchical testing sequences implemented to strongly control overall type I error due to multiplicity. At week 26, statistical tests were interpreted at a two-sided significance level of 5% for all endpoints except change in systolic BP, HDL-cholesterol and triacylglycerol. These were grouped together into two separate families (one each for canagliflozin 100 mg and 300 mg) and each family was tested using the Hochberg procedure at the 2.5% significance level. Comparisons of canagliflozin with sitagliptin at week 52 were initiated after statistical superiority of canagliflozin 100 mg and 300 mg to placebo in HbA1c lowering at week 26 was established; statistical tests at week 52 were interpreted at a two-sided significance level of 5% for all endpoints. The p values are reported for pre-specified comparisons only.
Lavalle-González F.J., Januszewicz A., Davidson J., Tong C., Qiu R., Canovatchel W, & Meininger G. (2013). Efficacy and safety of canagliflozin compared with placebo and sitagliptin in patients with type 2 diabetes on background metformin monotherapy: a randomised trial. Diabetologia, 56(12), 2582-2592.
Publication 2013
Canagliflozin High Density Lipoprotein Cholesterol Placebos Safety Sitagliptin Systolic Pressure Triglycerides

Most recents protocols related to «Canagliflozin»

1
Comparative Effectiveness of SGLT2i and DPP-4i in T2D
The study population included patients 18 years and older who initiated treatment with a SGLT2i (canagliflozin, dapagliflozin, empagliflozin, or ertugliflozin) or a DPP-4i (alogliptin, saxagliptin, linagliptin, or sitagliptin) between April 1, 2013 (consistent with the US Food and Drug Administration [FDA] approval of the first SGLT2i), and June 30, 2021. Treatment with DPP-4i was selected as the comparator because these medications are also frequently used as second-line therapy for T2D, have similar out-of-pocket costs as SGLT2i but a different mechanism of action, which does not involve inhibition of kidney glucose reabsorption and osmotic diuresis, and have shown no association with atherosclerotic cardiovascular outcomes. Cohort entry was the day of the first filled prescription of either SGLT2i or DPP-4i, with no use in the previous 6 months. Study eligibility was limited to patients with at least 6 months of continuous health plan enrollment, a recorded T2D diagnosis before cohort entry, and at least 1 HbA1c laboratory result recorded within 3 months before cohort entry. We excluded patients with records of type 1, secondary, or gestational diabetes; malignant neoplasms; end-stage kidney disease; kidney replacement therapy; no laboratory results for creatinine; or nursing home residence within 6 months preceding cohort entry (eFigure 1 and eTable 2 in Supplement 1). Based on the most recent HbA1c baseline value, we identified 3 different subcohorts which comprised patients with controlled (HbA1c <7.5%), above-target (HbA1c 7.5%-9%), or elevated (HbA1c >9%) glycemia, respectively (to convert percentage of total hemoglobin to proportion of total hemoglobin, multiply by 0.01). The cutoffs for HbA1c stratification were chosen by both inspecting terciles of the HbA1c distribution among SGLT2i treatment initiators and considering the thresholds currently recommended to define controlled vs uncontrolled hyperglycemia.12 (link),13 (link)
D’Andrea E., Wexler D.J., Kim S.C., Paik J.M., Alt E, & Patorno E. (2023). Comparing Effectiveness and Safety of SGLT2 Inhibitors vs DPP-4 Inhibitors in Patients With Type 2 Diabetes and Varying Baseline HbA1c Levels. JAMA Internal Medicine, 183(3), 242-254.
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Publication 2023
alogliptin Canagliflozin Cardiovascular System Creatinine dapagliflozin Diagnosis Dietary Supplements Diuretics, Osmotic Drug Kinetics Eligibility Determination empagliflozin ertugliflozin Food Gestational Diabetes Glucose Health Planning Hemoglobin Hyperglycemia Kidney Failure, Chronic Linagliptin Malignant Neoplasms Patients Pharmaceutical Preparations Psychological Inhibition Renal Reabsorption Renal Replacement Therapy saxagliptin Sitagliptin
2
Real-World Comparative Effectiveness of Antidiabetic Drugs
This was a retrospective cohort study based on administrative data in three East Asian countries: Japan, South Korea, and Taiwan12. Patients with type 2 diabetes newly initiating treatment with empagliflozin, any SGLT2i (canagliflozin, dapagliflozin, or empagliflozin), or any DPP‐4i were analyzed separately in each country. After the country‐level analyses, meta‐analyses were performed. Main analyses used an ‘as‐treated’ approach comparing empagliflozin use with DPP‐4i use. A similar approach compared any SGLT2i use with DPP‐4i use. Sensitivity analyses of empagliflozin vs DPP‐4i used (i) an intention‐to‐treat (ITT) approach and, analyzed (ii) sub‐populations of patients with and without cardiovascular history, and (iii) patients who initiated empagliflozin 10 mg.
Kim D.J., Sheu W.H., Chung W., Yabe D., Ha K.H., Nangaku M., Tan E.C., Node K., Yasui A., Lei W., Lee S., Saarelainen L., Deruaz‐Luyet A., Kyaw M.H, & Seino Y. (2023). Empagliflozin is associated with lower risk of cardiovascular events and all‐cause mortality in routine care in East Asia: Results from the EMPRISE study. Journal of Diabetes Investigation, 14(3), 417-428.
Publication 2023
Canagliflozin Cardiovascular System dapagliflozin Diabetes Mellitus, Non-Insulin-Dependent East Asian People empagliflozin Hypersensitivity Patients Population Group
3
Detailed Protocols for Mouse Aging Study
All the mouse samples were prepared at the University of Michigan in a specific pathogen-free colony kindly supplied by Dr. R. Miller. Genetic background and husbandry conditions for the Snell dwarf and GHRKO mice were described previously19 (link). Mice used for Rapamycin (encapsulated, used at 14 ppm), Canagliflozin (180 ppm), 17α-estradiol (17aE2) (14.4 ppm), Acarbose (1000 ppm), and Calorie-Restricted samples were of the UM-HET3 stock, produced as the offspring of CByB6F1/J mothers and C3D2F1/J fathers, as described in this article20 (link). The base diet was Purina 5LG6. To monitor specific-pathogen status, sentinel mice were exposed to spent bedding for two weeks prior to testing and all tests were negative for the entire aging colony during the experimental period. The protocols were reviewed and approved by the University of Michigan’s Institutional Animal Care and Use Committee. The metadata of the mouse liver, kidney, gastrocnemius muscle tissues, and plasma samples are provided in Supplementary Table 1.
Midha M.K., Kapil C., Maes M., Baxter D.H., Morrone S.R., Prokop T.J, & Moritz R.L. (2023). Vacuum Insulated Probe Heated ElectroSpray Ionization source (VIP-HESI) enhances micro flow rate chromatography signals in the Bruker timsTOF mass spectrometer. bioRxiv.
Publication Preprint 2023
Acarbose Canagliflozin Diet Dwarfism Estradiol Fathers Genetic Background Institutional Animal Care and Use Committees Kidney Liver Mice, House Mothers Muscle, Gastrocnemius pathogenesis Plasma Sirolimus Specific Pathogen Free
4
Comparative Analysis of SGLT2i and DPP4i Drugs on AKI Risk
SGLT2i (dapagliflozin, empagliflozin, and canagliflozin) and DPP4i (alogliptin, linagliptin, sitagliptin, saxagliptin, and vildagliptin) were analyzed for drug type, quantity, dose, dispensing date, and days of drug supply. The primary outcomes were the incidences of AKI and AKI-D in the propensity score–matched cohort. AKI diagnosis was based on ICD-9-CM and ICD-10-CM diagnostic codes (eTable 1 in Supplement 1), while AKI-D diagnosis also required dialysis treatment during the same hospitalization. The dialysis treatment procedure codes are shown in eTable 1 in Supplement 1. The codes used to identify AKI were validated in our database, with a positive predictive value of 98.5% and a negative predictive value of 74.0%.14 (link) The accuracy of acute dialysis procedure coding has also been validated, with a positive predictive value of 98%,15 (link) as accurate procedure codes are necessary for reimbursement in Taiwan.
Different diseases interact with AKI and possibly aggravate it. Likewise, AKI can induce injury in these distant organs. These are grouped as AKI with heart disease, sepsis, respiratory failure, and shock. These 4 diseases were chosen because they are the most common contributors to AKI.16 (link) These diseases were diagnosed based on ICD-9-CM and ICD-10-CM diagnostic codes (eTable 1 in Supplement 1) during the AKI hospitalization. AKI prognosis was also analyzed. We considered advanced CKD (defined as CKD stages 4 and 5 by ICD-10-CM diagnostic codes), ESKD (confirmed by the registry of catastrophic illness), or death that occurred within 90 days of AKI hospitalization.
Chung M.C., Hung P.H., Hsiao P.J., Wu L.Y., Chang C.H., Hsiao K.Y., Wu M.J., Shieh J.J., Huang Y.C, & Chung C.J. (2023). Sodium-Glucose Transport Protein 2 Inhibitor Use for Type 2 Diabetes and the Incidence of Acute Kidney Injury in Taiwan. JAMA Network Open, 6(2), e230453.
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Publication 2023
alogliptin Canagliflozin Catastrophic Illness dapagliflozin Diagnosis Dialysis Dietary Supplements empagliflozin Heart Diseases Hospitalization Injuries Involuntary Treatment Linagliptin Pharmaceutical Preparations Prognosis Respiratory Failure saxagliptin Septicemia Shock Sitagliptin Vildagliptin
5
Evaluating SGLT2i Impact on AKI Risk
We performed propensity score matching to construct a comparative cohort for SGLT2i users from the study population. Propensity scores (PS) were calculated as a probability dependent on a vector of observed covariates associated with receipt of treatment with SGLT2i. We conducted a logistic regression analysis for estimating PS with adjustment for age, sex, comorbidities, and related clinical medications. A 1:1 PS-matched cohort was constructed using greedy nearest neighbor matching, and the caliper width was within 0.2.17 (link) Moreover, standardized mean differences with a cutoff value of 0.10 were used to observe the fitness of covariate comparisons between the propensity score–matched groups.18 (link),19 (link) Continuous variables are presented as mean and SD and categorical variables as numbers and frequencies. Age was stratified into 10-year groups of younger than 25 years, 25 to 34 years, 35 to 44 years, and so on. All participants were followed up from the index date until AKI diagnosis, death, or the study end date (December 31, 2018), whichever occurred first. Kaplan-Meier survival curves were expressed and compared for the risk of AKI or AKI-D incidence using log-rank tests. We used conditional Cox proportional hazard regressions to determine the crude and adjusted hazard ratios (HRs) and 95% CIs for risk of AKI or AKI-D after SGLT2i administration. SGLT2is, including dapagliflozin, empagliflozin, and canagliflozin, were evaluated separately for AKI or AKI-D risk using stratification analysis. We then added a multiplicative interaction term to the regression models to calculate the interactions between comorbidities and the use of SGLT2i on AKI risk. Finally, we analyzed the associations between SGLT2i use and concomitant diseases with AKI using conditional Cox proportional hazard regression analysis. The prognostic outcomes of AKI, including advanced CKD, ESKD, and death, were compared using χ2 tests. All hypothesis tests were 2-sided. Significance was defined as α = 0.05. Statistical analysis was performed using the SAS statistical software version 9.4 (SAS Institute). Data analysis was conducted from October 15, 2021, to January 30, 2022.
Chung M.C., Hung P.H., Hsiao P.J., Wu L.Y., Chang C.H., Hsiao K.Y., Wu M.J., Shieh J.J., Huang Y.C, & Chung C.J. (2023). Sodium-Glucose Transport Protein 2 Inhibitor Use for Type 2 Diabetes and the Incidence of Acute Kidney Injury in Taiwan. JAMA Network Open, 6(2), e230453.
Full text: Click here
Publication 2023
Canagliflozin Cloning Vectors concomitant disease dapagliflozin Diagnosis empagliflozin Pharmaceutical Preparations

Top products related to «Canagliflozin»

1
Canagliflozin by Selleck Chemicals
Sourced in United States, Germany
Canagliflozin is a laboratory chemical compound that functions as a sodium-glucose cotransporter 2 (SGLT2) inhibitor. It is used in research applications.
2
Canagliflozin by Mitsubishi
Sourced in Japan
Canagliflozin is a sodium-glucose co-transporter 2 (SGLT2) inhibitor, a type of laboratory equipment used in research and clinical settings. Its core function is to inhibit the reabsorption of glucose in the kidneys, thereby increasing urinary glucose excretion.
3
Dapagliflozin by Selleck Chemicals
Sourced in United States, Germany
Dapagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor, a class of pharmaceutical compounds used to lower blood glucose levels in individuals with type 2 diabetes. It functions by reducing the reabsorption of glucose in the kidneys, leading to increased urinary glucose excretion.
4
Empagliflozin by Selleck Chemicals
Sourced in Germany
Empagliflozin is a laboratory reagent used in research applications. It is a sodium-glucose cotransporter 2 (SGLT2) inhibitor. The core function of Empagliflozin is to inhibit SGLT2, which is responsible for the reabsorption of glucose in the kidneys.
5
Canagliflozin by Merck Group
Sourced in United States
Canagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor, a class of medications used to lower blood glucose levels in individuals with type 2 diabetes. It works by inhibiting the SGLT2 protein in the kidneys, which is responsible for reabsorbing glucose from the urine, leading to increased excretion of glucose through the urine.
6
Fetal bovine serum (fbs) by Thermo Fisher Scientific
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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Nicotinamide by Merck Group
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Nicotinamide is a form of vitamin B3 that serves as a precursor for the coenzyme nicotinamide adenine dinucleotide (NAD) in biological systems. NAD is essential for various metabolic processes within cells, including energy production and DNA repair.
8
Penicillin by Merck Group
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Penicillin is a type of antibacterial drug that is widely used in medical and laboratory settings. It is a naturally occurring substance produced by certain fungi, and it is effective against a variety of bacterial infections. Penicillin works by inhibiting the growth and reproduction of bacteria, making it a valuable tool for researchers and medical professionals.
9
Streptomycin by Merck Group
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Streptomycin is a laboratory product manufactured by Merck Group. It is an antibiotic used in research applications.
10
Sucrose by Merck Group
Sourced in United States, Germany, United Kingdom, France, Switzerland, Sao Tome and Principe, China, Macao, Italy, Poland, Canada, Spain, India, Australia, Belgium, Japan, Sweden, Israel, Denmark, Austria, Singapore, Ireland, Mexico, Greece, Brazil
Sucrose is a disaccharide composed of glucose and fructose. It is commonly used as a laboratory reagent for various applications, serving as a standard reference substance and control material in analytical procedures.

More about "Canagliflozin"

Canagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor medication used to manage type 2 diabetes.
It works by reducing the reabsorption of glucose in the kidneys, thereby increasing urinary glucose excretion and lowering blood glucose levels.
This novel antidiabetic drug is part of the SGLT2 inhibitor class, which also includes other medications like dapagliflozin and empagliflozin.
Canagliflozin's mechanism of action involves inhibiting the SGLT2 transporter, which is responsible for the majority of glucose reabsorption in the renal proximal tubules.
By blocking this transporter, canagliflozin enhances the excretion of glucose through urine, leading to a reduction in blood glucose levels.
This unique approach to diabetes management has shown promising results in improving glycemic control, reducing the risk of cardiovascular events, and potentially offering additional benefits such as weight loss and renal protection.
Alongside canagliflozin, other important substances in diabetes research include the fasting blood sugar (FBS) test, which is a common diagnostic tool for assessing glucose levels, and compounds like nicotinamide, penicillin, and streptomycin, which have been studied for their potential roles in diabetes management or as research tools.
Sucrose, a common dietary sugar, is also relevant in the context of diabetes and its impact on blood glucose levels.
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