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Sitagliptin

Sitagliptin is a dipeptidyl peptidase-4 (DPP-4) inhibitor used in the treatment of type 2 diabetes.
It works by increasing the levels of incretins, hormones that stimulate insulin release and suppress glucagon secretion.
Sitagliptin has been shown to improve glycemic control and reduce the risk of cardiovascular events in patients with type 2 diabetes.
It is typically taken orally, either alone or in combination with other antidiabetic medications.
Reasearch on the optimal use of Sitagliptin, including dosing, safety, and efficacy, is an active area of study.

Most cited protocols related to «Sitagliptin»

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.
Publication 2013
Canagliflozin Capsule Diabetes Mellitus, Non-Insulin-Dependent Europeans glimepiride Metformin Patients Placebos Sitagliptin Sulfonylurea Compounds Therapeutics Treatment Protocols
In order to analyze biofilm inhibition, the method of Sakar et al. [27 (link)] was followed with some modification. The biofilm of the tested strain of S. marcescens was formed on glass slides placed in polystyrene petri plates in the presence and absence of 1 mg/ml of sitagliptin. The plates were incubated for 24 hr at 28°C; the slides were washed with water three times and stained with crystal violet (1%) for 20 min. The slides were examined after staining under the light microscope at a 100X magnification.
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Publication 2020
Biofilms Light Microscopy Polystyrenes Psychological Inhibition Sitagliptin Strains Violet, Gentian
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.
Publication 2013
Canagliflozin Safety Sitagliptin
In order to determine the protease inhibitory activity of sitagliptin, the skim milk agar method was used [30 (link)]. S. marcescens treated with sitagliptin sub-MIC or untreated overnight cultures in LB broth were adjusted to OD600 of 0.4, centrifuged at 10,000 rpm for 15 min and the protease activities were measured by adding the supernatants in 100 μl aliquots to the wells made in skim milk agar plates (5%). The plates were incubated overnight at 37°C and the diameters of the clear zones surrounding the growth were measured. The experiment was made in triplicate and the clear zones obtained by protease produced by sitagliptin treated S. marcescens cultures were expressed as mean ± standard error of percentage change from the protease inducing clear zones obtained by untreated S. marcescens control on skim milk agar plates. The percentage of protease inhibition was calculated using the following formula:
[ClearzonediameterofcontrolClearzonediameterinpresenceofsitagliptin]/Clearzonediameterofcontrol
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Publication 2020
Agar Endopeptidases Milk, Cow's Psychological Inhibition Serratia marcescens Sitagliptin
The effect of sub-inhibitory concentration of sitagliptin on the growth of the tested strain of S. marcescens was detected according to Nalca et al. [25 (link)]. Overnight culture from S. marcescens was prepared in LB broth and adjusted to 0.5 McFarland Standard. The prepared suspension was used to inoculate LB broth containing 1 mg/ml of sitagliptin and control LB broth without sitagliptin so that the final inoculum is approximately 1×108 CFU/ml. After overnight incubation at 37°C, the optical densities of both cultures were measured at 600 nm by using Biotek Spectrofluorimeter (Biotek, USA). The experiment was performed in triplicate and data are presented as the mean ± standard error. A P value < 0.05 was considered statistically significant using Student's t-test with (Graphpad Prism 5 software).
Sub-inhibitory concentration of sitagliptin was used to investigate its anti-virulence and anti-quorum sensing activities on S. marcescens. The reason for the use of this concentration is to avoid any effect on the growth of the tested bacterial strain. The OD600 of sitagliptin sub-MIC-treated (1 mg/ml) and untreated cultures of S. marcescens were compared to show that the growth was not affected by sitagliptin treatment. For normalizing the results in all the next experiments, the sitagliptin treated or untreated bacterial cultures were adjusted to the growth density OD600 of 0.4 (1×108 CFU/ ml).
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Publication 2020
Bacteria prisma Psychological Inhibition Sitagliptin Strains Virulence Vision

Most recents protocols related to «Sitagliptin»

For GTTs, mice received a glucose bolus i.p. (2 g/kg body weight, Braun) after 6 h of fasting. Blood glucose was measured after 0, 15, 30, 60, 90 and 120 min using a freestyle lite glucometer (Cat#7091870, Abbott). Blood was collected at time points 0, 15 and 30 min for insulin measurements.
For ITTs, mice were fasted 3 h and injected with 1U/kg body weight insulin (Actrapid Penfill Insulin 100 IU/mL, Novo Nordisk). Glucose levels were measured at 0, 15, 30, 60, 90, and 120 min after injection.
For GLP-1 measurements, mice were i.p. injected with 25 mg/kg body weight Sitagliptin (Cat# sc-364620, Santa Cruz) 30 min prior to oral glucose administration and blood collected in diprotein A (Cat# I9759, Bachem). To block GLP-1 signaling, synthetic exendin (9–39) 25 nM/kg body weight (Cat# H-8740, Bachem) was injected i.p. 1 min prior to GTT.
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Publication 2023
Actrapid insulin Administration, Oral BLOOD Blood Glucose Body Weight Cardiac Arrest Glucagon-Like Peptide 1 Glucose Glucose Tolerance Test Insulin Mice, House Sitagliptin
The transgenic motor neuron green fluorescent strain zebrafish (NBT, 270) aged 5 days (dpf) were randomly selected and feed in a beaker containing 50 ml water (30 zebrafish in each group). The hyperglycemic zebrafish model was established as described in section “2.8.1. Determination of maximum detection concentration,” following by the treatment with 1,000, 1,500, and 2,000 μg/ml E70 PRA extract at 28°C for 7.5 h/day. After 2 days treatment, 10 zebrafish in each group were randomly selected and photographed with AZ100 fluorescence microscope (Nikon, Japan). The fluorescence intensity (S) of peripheral motor nerve in the area of two segments above the ventral pores of zebrafish was analyzed by NIS-Elements D 3.20. Sitagliptin (STGP, 350 μg/ml) was used as positive control, the protective effect on peripheral nerve was calculated as follows:
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Publication 2023
Animals, Transgenic Fluorescence Microscopy, Fluorescence Motor Neurons Peripheral Nerves Sitagliptin Strains Zebrafish
Dried PRA was purchased from Anqing Chunyuan Pharmacy (Anhui, China). Pioglitazone hydrochloride tablets were bought from Deyuan Pharmaceutical Co., Ltd. (Jiangsu, China). Glucose, gallic acid, quercetin, and ethanol were from Aladdin Biotechnology Technology (Shanghai, China). Acarbose, 1-diphenyl-2-picrylhydrazyl (DPPH⋅), 4′-nitrophenyl-beta-D-glucopyranoside (pNPG), 2,2-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS⋅+), and α-glucosidase were purchased from Sigma-Aldrich (St. Louis, MO, USA). HepG2 cell and Dulbecco’s modified Eagle’s medium (DMEM) with high sugar medium were from Beina Biology (Beijing, China). Amino guanidine was from Bio-Rad Laboratories Ltd. (Shanghai, China). Sitagliptin was bought from Macklin (Shanghai, China). All other chemicals were analytical grade and purchased from Sinopharm Chemical Reagent Co., Ltd. (Shanghai, China).
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Publication 2023
2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 4-nitrophenyl 4-nitrophenylgalactoside Acarbose alpha Glucosidase Carbohydrates diphenyl Eagle Ethanol Gallic Acid Glucose Guanidine Hep G2 Cells Pharmaceutical Preparations Pioglitazone Hydrochloride Quercetin Sitagliptin Sulfonic Acids
Propensity score (PS) matching was used to control for confounding. The PS for initiating SGLT2i vs DPP-4i therapy was calculated within each HbA1c subcohort separately through a logistic regression model with 128 prespecified covariates. Laboratory data, except for HbA1c and eGFRCr, were not included in the model because of the substantial proportion of missing information. Initiators of SGLT2i therapy were 1:1 matched to initiators of DPP-4i therapy on their estimated PS within each HbA1c subcohort using the nearest neighbor approach with a caliper width of 0.01 on the PS scale. Covariate balance was assessed with standardized differences, with meaningful imbalances set at values higher than 10%.29 (link),30 (link) We also reviewed the balance in laboratory test results not included in the PS model, to evaluate potential residual confounding after PS matching.
We tabulated numbers of events, incidence rates (IRs), and rate differences (RDs) per 1000 person-years. Hazard ratios (HRs) and 95% CIs were estimated by Cox proportional hazard models. We used Kaplan-Meier methods to plot cumulative incidence of primary outcomes and log-rank tests to compare hazard rates between drug classes. Two-sided P values for homogeneity were obtained by performing Wald tests and values <.05 were considered indicative of treatment heterogeneity.
We inspected the robustness of the main findings through sensitivity analyses (see eMethods in Supplement 1), addressing potential informative censoring, time-lag bias,31 (link) unmeasured confounding for high risk for recurrence, and DPP-4i effects on HHF (since saxagliptin and alogliptin showed an increased HHF rate in CVOTs,32 (link),33 (link) which resulted in an FDA warning,34 we conducted a sensitivity analysis for the HHF outcome redefining the comparator group as sitagliptin only).
All analyses were implemented using Aetion Evidence Platform (Aetion Inc) and Stata statistical software, version 15.1 (StataCorp LLC).
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Publication 2023
alogliptin Dietary Supplements Genetic Heterogeneity Hypersensitivity Pharmaceutical Preparations Recurrence saxagliptin Sitagliptin
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)
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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

Top products related to «Sitagliptin»

Sourced in United States, China, United Kingdom, Israel
Sitagliptin is a pharmaceutical product developed by Merck Group. It is a dipeptidyl peptidase-4 (DPP-4) inhibitor, which functions by inhibiting the enzyme DPP-4 to regulate blood glucose levels.
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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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STZ is a laboratory equipment product manufactured by Merck Group. It is designed for use in scientific research and experiments. The core function of STZ is to serve as a tool for carrying out specific tasks or procedures in a laboratory setting. No further details or interpretation of its intended use are provided.
Sourced in United States
Sitagliptin is a small-molecule inhibitor of the enzyme dipeptidyl peptidase-4 (DPP-4). It is a pharmaceutical product used for the treatment of type 2 diabetes.
Sourced in United States, Germany, United Kingdom, China, Italy, Sao Tome and Principe, France, Macao, India, Canada, Switzerland, Japan, Australia, Spain, Poland, Belgium, Brazil, Czechia, Portugal, Austria, Denmark, Israel, Sweden, Ireland, Hungary, Mexico, Netherlands, Singapore, Indonesia, Slovakia, Cameroon, Norway, Thailand, Chile, Finland, Malaysia, Latvia, New Zealand, Hong Kong, Pakistan, Uruguay, Bangladesh
DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
Sourced in United States
The DPPIV-Glo™ Protease Assay is a bioluminescent assay designed to quantify the activity of the protease enzyme dipeptidyl peptidase-IV (DPPIV). The assay utilizes a proluciferin substrate that is cleaved by DPPIV, resulting in the release of luciferin which is then detected by a luciferase reaction, producing luminescence. The intensity of the luminescent signal is proportional to DPPIV activity.
Sourced in United States, Estonia
The DPP-IV inhibitor screening assay kit is a laboratory tool designed to measure the inhibitory activity of compounds against the enzyme dipeptidyl peptidase-IV (DPP-IV). DPP-IV is an enzyme that plays a role in regulating various physiological processes. The kit provides a standardized method for screening and evaluating the potency of potential DPP-IV inhibitors.
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SAS 9.4 is an integrated software suite for advanced analytics, data management, and business intelligence. It provides a comprehensive platform for data analysis, modeling, and reporting. SAS 9.4 offers a wide range of capabilities, including data manipulation, statistical analysis, predictive modeling, and visual data exploration.
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The LSRFortessa is a flow cytometer designed for multiparameter analysis of cells and other particles. It features a compact design and offers a range of configurations to meet various research needs. The LSRFortessa provides high-resolution data acquisition and analysis capabilities.
Sourced in United States, United Kingdom, Japan, Germany, Switzerland, Spain, China
The FlexStation 3 is a multimode microplate reader that measures various assays, including fluorescence, luminescence, and absorbance. It is designed to provide consistent and reliable results for a wide range of applications in life science research and drug discovery.

More about "Sitagliptin"

Sitagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, is a widely used medication for the treatment of type 2 diabetes.
It works by increasing the levels of incretins, hormones that stimulate insulin release and suppress glucagon secretion, thereby improving glycemic control and reducing the risk of cardiovascular events in patients with type 2 diabetes.
Sitagliptin can be taken orally, either alone or in combination with other antidiabetic medications.
Research on the optimal use of Sitagliptin, including dosing, safety, and efficacy, is an active area of study.
Researchers often utilize a variety of tools and techniques to investigate Sitagliptin, such as the DPPIV-Glo™ Protease Assay, a DPP-IV inhibitor screening assay kit, as well as statistical software like SAS 9.4 and laboratory equipment like the LSRFortessa and FlexStation 3.
Understanding the mechanisms of action and the potential benefits of Sitagliptin is crucial for healthcare professionals and researchers working in the field of type 2 diabetes management.
PubCompare.ai's AI-driven protocol comparison tool can help optimize Sitagliptin research by allowing users to easily locate and identify the best protocols and products from literature, pre-prints, and patents.
This can enhance reproducibility and drive Sitagliptin research forward, ultimately benefiting patients with type 2 diabetes.