LPS was purchased from Santa Cruz Biotechnology, nigericin, and vildagliptin and Ac-YVAD-CMK from the Cayman Chemical Company, PMA and sitagliptin from Sigma, Ala-Pro-AFC from Bachem, saxagliptin from Toronto Research Chemicals, and Z-VAD-FMK and etoposide from Enzo Life Sciences. Val-boroPro45 (link), 1G24424 (link), FP-biotin15 (link), L-allo-Ile-isoindoline14 (link), and L-allo-Ile-thiazolidine14 (link) were synthesized according to previously published protocols. For cell culture experiments, Val-boroPro was resuspended in DMSO containing 0.1% TFA to prevent compound cyclization. Antibodies used include: human caspase-1 (#2225, Cell Signaling Technology), mouse caspase-1 (clone Casper-1, Adipogen), caspase-3 (clone 8G10, Cell Signaling Technology), human caspase-4 (clone 4B9, Santa Cruz), human caspase-5 (clone D3G4W, Cell Signaling Technology), caspase-7 (clone D2Q3L, Cell Signaling Technology), human IL-1β (Clone 2805, R&D Systems), mouse IL-1β (clone D4T2D, Cell Signaling Technology), IL-1α (#AF-200, R&D Systems), IL-18 (#AF2548, R&D Systems), GAPDH (clone 14C10, Cell Signaling Technology), DPP7 (Clone 398024, R&D Systems), DPP8 (ab42076, Abcam), DPP9 (ab42080, Abcam), PARP (#9542, Cell Signaling Technology), GSDMD (NBP2-33422, Novus Biologicals), DPP4 (#11D7, GeneTex), FAP (ABT11, Millipore), and SCPEP1 (SAB2700267, Sigma).
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Vildagliptin
Vildagliptin
Vildagliptin is a dipeptidyl peptidase-4 (DPP-4) inhibitor used to treat type 2 diabetes.
It works by increasing levels of incretins, hormones that stimulate insulin production and reduce glucagon secretion.
Vildagliptin has been shown to improve glycemic control and reduce the risk of hypoglycemia in patients with type 2 diabetes.
Reseach on Vildagliptin's efficacy, safety, and optimal use is an area of active investigation.
It works by increasing levels of incretins, hormones that stimulate insulin production and reduce glucagon secretion.
Vildagliptin has been shown to improve glycemic control and reduce the risk of hypoglycemia in patients with type 2 diabetes.
Reseach on Vildagliptin's efficacy, safety, and optimal use is an area of active investigation.
Most cited protocols related to «Vildagliptin»
alanylproline
Alloisoleucine
Antibodies
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
Biological Factors
Caimans
Casp1 protein, mouse
CASP4 protein, human
CASP5 protein, human
Caspase-7
Caspase 1
Caspase 3
Cell Culture Techniques
Clone Cells
Cyclization
DPP4 protein, human
DPP9 protein, human
Etoposide
GAPDH protein, human
Homo sapiens
Interleukin-1 beta
interleukin 18 protein, human
Mus
N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone
Nigericin
Novus
saxagliptin
Sitagliptin
Sulfoxide, Dimethyl
Vildagliptin
The present trial (clinicaltrials.gov identifier: NCT02145611) will be randomized, open label, parallel assignment, controlled by drug. It was designed to assess the effect of vildagliptin (100 mg/day b.i.d.) on endothelial function in patients with T2DM and hypertension compared to glibenclamide (5–20 mg/day depending on glycemic control). The Research Ethics Committee of the institution approved the study protocol according to national and international guidelines. All patients will give their informed consent. Twenty-five individuals with T2DM and hypertension will be evaluated in the vildagliptin plus metformin group compared to 25 diabetic and hypertensive subjects in the glibenclamide plus metformin group. Figure 1 shows a flow chart of participant selection and interventions. The inclusion and exclusion criteria are presented in Table 1 .![]()
Flowchart of Study
Inclusion and exclusion criteria
| Inclusion criteria | Exclusion criteria |
|---|---|
| Patients aged ≥35 years | Use of NPH or regular insulin, pioglitazone, GLP-1 receptor agonist, DPP-4 inhibitor or acarbose |
| History of DM and mild hypertension (blood pressure <160/100 mmHg) no longer than 15 years | Intolerance to metformin |
| Body mass index <35 kg/m2 | Use of three or more anti-hypertensive drugs, which characterizes resistant hypertension |
| Glycated hemoglobin (HbA1c) between 7.0 and 10.5 % | Smoking within the previous 6 months |
| Pregnancy or breastfeeding | |
| Creatinine clearance <45 mL/min (MDRD) | |
| Serum alanine aminotransferase or aspartate aminotransferase level of more than three times the upper limit of the normal range | |
| Subjects with ischemic heart disease, cerebrovascular disease, other atherosclerotic disease, cancer, or heart failure in functional classes II, III and IV | |
| Treadmill stress test with typical chest pain or with ST segment depression ≥1 mm, or with a horizontal or descending trace on the electrocardiogram for a duration of 0.08 s after the J point | |
| Presence of coronary heart disease diagnosed by treadmill stress test, myocardial scintigraphy or coronary angiography | |
| Inability to give informed consent |
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Alanine Transaminase
Antihypertensive Agents
Aspartate Transaminase
Blood Pressure
Cerebrovascular Disorders
Chest Pain
Congestive Heart Failure
Dipeptidyl-Peptidase IV Inhibitors
Electrocardiography
Endothelium
Ethics Committees, Research
Exercise Tests
Glucagon-Like Peptide-1 Receptor
Glyburide
Glyburide-metformin
Glycemic Control
Heart
Heart Disease, Coronary
Hemoglobin
High Blood Pressures
Insulin
Malignant Neoplasms
Metformin
Myocardial Ischemia
Myocardial Scintigraphy
Patients
Pioglitazone
Serum
Vildagliptin
After the 4 weeks of vildagliptin administration with or without infusions of incretin receptor blockers, the systolic blood pressure (SBP) and pulse rate were measured using indirect tail-cuff equipment. Blood samples were collected after a 6-hour fast. Plasma levels of glucose, total cholesterol, high-density lipoprotein (HDL) cholesterol, triglyceride, and nonesterified fatty acids (NEFA) were measured by enzymatic methods. Non-HDL cholesterol was calculated by subtracting HDL cholesterol from total cholesterol. HbA1c was measured by the quick test (A1CNow+ ® 20test-kits; Bayer Yakuhin, Osaka, Japan). Plasma levels of active GLP-1, total GLP-1, total GIP, and insulin were determined by an enzyme-linked immunosorbent assay (ELISA Kit, Millipore, MA; Ultra Sensitive “PLUS” Mouse Insulin ELISA Kit, Morinaga, Yokohama, Japan). Only total GIP was measured, as no test kit for measuring active GIP was commercially available. The plasma levels of total GIP in the Pro3-infused animals remained undetermined, as the test kit for total GIP was cross-reacted with Pro3. Oral glucose tolerance tests were performed on nondiabetic Apoe−/− mice with or without vildagliptin treatment after a 6-h fast. Glucose (1.5 mg/g body weight) was administered orally through a gavage tube, and blood glucose levels were measured by the glucose oxidase method using the Glucose Monitor System (Sanwa Kagaku, Nagoya, Japan).
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Aftercare
Animals
Apolipoproteins E
BLOOD
Blood Glucose
Body Weight
Cholesterol
Enzyme-Linked Immunosorbent Assay
Enzymes
Glucagon-Like Peptide 1
Glucose
High Density Lipoprotein Cholesterol
Incretins
Insulin
Mice, House
Nonesterified Fatty Acids
Oral Glucose Tolerance Test
Oxidase, Glucose
Plasma
Pulse Rate
Systolic Pressure
Tail
Test, Quick
Triglycerides
Tube Feeding
Vildagliptin
After approval from the Mayo Clinic Institutional Review Board, 14 subjects with type 2 diabetes gave written informed consent to participate in the study. All subjects were in good health and at a stable weight and did not engage in regular vigorous exercise. Subjects were not taking medication known to alter gastric emptying such as narcotics or calcium channel blockers. None of the subjects had a history of microvascular complications of diabetes. All subjects were instructed to follow a weight-maintenance diet containing 55% carbohydrate, 30% fat, and 15% protein for the period of study. All oral agents used for the treatment of diabetes were discontinued 3 weeks before the study.
We used a randomized, double-blind, placebo-controlled crossover design. Subjects received either 50 mg vildagliptin or placebo taken before breakfast and the evening meal over a 10-day treatment period with the two treatment intervals being separated by at least a 2-week washout period. The order of treatment was random.
Subjects were admitted to the General Clinical Research Center on the evening of the 6th day of the treatment period. Gastric accommodation was measured on the 7th day of the treatment period. The maximum tolerated volumes of caloric or noncaloric liquids were measured on the 8th and 10th day of the treatment period to examine the effect of DPP-4 inhibition on satiety and postprandial gastrointestinal symptoms. Glucose turnover and gastric emptying were measured simultaneously on the 9th day of the treatment period; those results have been reported previously (6 (link)). Glucose, insulin, and C-peptide concentrations measured before and after ingestion of a mixed meal on day 9 and analyzed using the oral and C-peptide minimal models are the subject of the current report.
In brief, after an 8-h fast, a forearm vein was cannulated with an 18-gauge needle to allow infusions to be performed. An 18-gauge cannula was inserted retrogradely into a vein of the dorsum of the contralateral hand. This was placed in a heated Plexiglas box maintained at 55°C to allow sampling of arterialized venous blood. At −180 min a primed continuous infusion of [6,6-2H2]glucose was initiated. Subjects received the morning dose (50 mg vildagliptin or placebo) at −30 min. At time 0 subjects consumed a meal consisting of two scrambled eggs labeled with 0.75 mCi 99mTc-sulfur colloid, 55g of Canadian bacon, 240 ml of water, and Jell-O containing 75 g glucose labeled with [1-13C]glucose (4% enrichment). This provided 510 kcal (61% carbohydrate, 19% protein, and 21% fat). An infusion of [6-3H]glucose was started at this time, and the infusion rate varied to mimic the anticipated glucose appearance of the meal [1-13C]glucose as described previously (15 (link)). At the same time, the rate of infusion of the [6,6-2H2]glucose was altered to approximate the anticipated pattern of fall in endogenous glucose production (15 (link)). Blood was collected at frequent intervals. To allow a model-independent assessment of the effect of vildagliptin on insulin action, 5 hours after the study start (300 min) subjects received 0.02 unit/kg body weight of insulin intravenously (over a 5-min period).
We used a randomized, double-blind, placebo-controlled crossover design. Subjects received either 50 mg vildagliptin or placebo taken before breakfast and the evening meal over a 10-day treatment period with the two treatment intervals being separated by at least a 2-week washout period. The order of treatment was random.
Subjects were admitted to the General Clinical Research Center on the evening of the 6th day of the treatment period. Gastric accommodation was measured on the 7th day of the treatment period. The maximum tolerated volumes of caloric or noncaloric liquids were measured on the 8th and 10th day of the treatment period to examine the effect of DPP-4 inhibition on satiety and postprandial gastrointestinal symptoms. Glucose turnover and gastric emptying were measured simultaneously on the 9th day of the treatment period; those results have been reported previously (6 (link)). Glucose, insulin, and C-peptide concentrations measured before and after ingestion of a mixed meal on day 9 and analyzed using the oral and C-peptide minimal models are the subject of the current report.
In brief, after an 8-h fast, a forearm vein was cannulated with an 18-gauge needle to allow infusions to be performed. An 18-gauge cannula was inserted retrogradely into a vein of the dorsum of the contralateral hand. This was placed in a heated Plexiglas box maintained at 55°C to allow sampling of arterialized venous blood. At −180 min a primed continuous infusion of [6,6-2H2]glucose was initiated. Subjects received the morning dose (50 mg vildagliptin or placebo) at −30 min. At time 0 subjects consumed a meal consisting of two scrambled eggs labeled with 0.75 mCi 99mTc-sulfur colloid, 55g of Canadian bacon, 240 ml of water, and Jell-O containing 75 g glucose labeled with [1-13C]glucose (4% enrichment). This provided 510 kcal (61% carbohydrate, 19% protein, and 21% fat). An infusion of [6-3H]glucose was started at this time, and the infusion rate varied to mimic the anticipated glucose appearance of the meal [1-13C]glucose as described previously (15 (link)). At the same time, the rate of infusion of the [6,6-2H2]glucose was altered to approximate the anticipated pattern of fall in endogenous glucose production (15 (link)). Blood was collected at frequent intervals. To allow a model-independent assessment of the effect of vildagliptin on insulin action, 5 hours after the study start (300 min) subjects received 0.02 unit/kg body weight of insulin intravenously (over a 5-min period).
BACON protocol
BLOOD
Body Weight
C-Peptide
Calcium Channel Blockers
Cannula
Carbohydrates
Colloids
Complications of Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus, Non-Insulin-Dependent
Eggs
Ethics Committees, Research
Forearm
Gels
Glucose
Insulin
Narcotics
Needles
Ocular Accommodation
Pharmaceutical Preparations
Placebos
Plexiglas
Proteins
Psychological Inhibition
Satiation
Stomach
Sulfur
Therapy, Diet
Veins
Vildagliptin
For the molecular docking analysis, the crystal structure of DPP-IV in complex with vildagliptin (Protein Data Bank ID: 6B1E) was selected as the acceptor, and it was optimized by hydrogenation and CHARMm force field calculations. The binding site was defined by the ligand atoms, and the radius range was automatically generated. The CHARMm force field and annealing simulation algorithm were used to optimize the energy of the complexes of ligands with the protein, combining them in different conformations. Parameters were set at their default values. After each compound was docked, the 10 best conformations were obtained. The compounds were screened by comprehensively considering their interaction energy and binding free energy. The analysis of the binding mode (3D or 2D ligand–receptor interaction simulation map) of each selected compound was also conducted using CDOCKER.
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Binding Sites
DPP4 protein, human
Hydrogenation
Ligands
Proteins
Radius
Vildagliptin
Most recents protocols related to «Vildagliptin»
The cost of DPP4 inhibitors for the treatment of T2DM began to be reimbursed by NHI in March, 2009 and the prescriptions included sitagliptin, vildagliptin, saxagliptin, alogliptin, and linagliptin. The anatomical Therapeutic Chemical (ATC) code in the patients’ post-T2DM-diagnosis prescription records, oral antiviral drug use, and insulin use are shown in Supplementary Table S1 . Chronic HBV or HCV infection, and the comorbidities of cirrhosis were identified using International Classification of Diseases, Ninth Revision or Tenth Revision (ICD-9 or ICD-10, respectively) codes (Supplementary Table S2 ).
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alogliptin
Antiviral Agents
Diagnosis
Dipeptidyl-Peptidase IV Inhibitors
Hepatitis C
Insulin
Linagliptin
Liver Cirrhosis
Patients
saxagliptin
Sitagliptin
Therapeutics
Vildagliptin
T0901317, 9-cis-retinoic acid, phorbol 12-myristate 13-acetate (PMA), GLP-1 (7–37), and exendin-(9–39) were purchased from Sigma (St Louis, MO, USA). Endotoxin, fatty-acid-free bovine serum albumin (BSA), and the PKA inhibitor 14–22 amide were purchased from Calbiochem (Merck KGaA, Darmstadt, Germany). Sitagliptin phosphate and vildagliptin were purchased from Toronto Research Chemicals Inc. (Toronto, ON, Canada).
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Alitretinoin
Amides
Endotoxins
Fatty Acids
Glucagon-Like Peptide 1
PKA inhibitor
Serum Albumin, Bovine
Sitagliptin Phosphate
T0901317
Tetradecanoylphorbol Acetate
Vildagliptin
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 inSupplement 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.
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
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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
Among patients with T2D who had undergone PAD revascularization, 2,455 and 8,695 had received first prescriptions for SGLT2i and DPP4i, respectively, between May 1, 2016, and December 31, 2019. The SGLT2i agents were dapagliflozin, empagliflozin, and canagliflozin and were prescribed to 997 (40.61%), 1305 (53.16%), and 153 (6.23%) patients, respectively. The DPP4i agents were sitagliptin, vildagliptin, linagliptin, saxagliptin, and alogliptin and were prescribed to 1,875 (21.56%), 1,780 (20.47%), 4,436 (51.02%), 562 (6.46%), and 42 (0.48%) patients, respectively. Before PSM, we observed that compared with the DPP4i group, the SGLT2i group was younger; had a male predominance; had a lower prevalence of chronic kidney disease (CKD), hypertension, and malignancy; had a higher prevalence of dyslipidemia, ischemic heart disease, and history of percutaneous coronary intervention; and had a higher rate of prescriptions for metformin, sulfonylurea, acarbose, glitazones, antiplatelet agents, angiotensin-converting enzyme inhibitors/angiotensin II receptor antagonists (ACEIs/ARBs), beta blockers, statins, direct oral anticoagulants, mineralocorticoid receptor antagonists, and angiotensin receptor–neprilysin inhibitors (ASMD > 0.1). After PSM, the two study groups were well balanced in all baseline characteristics (ASMD < 0.1; Table 1
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Acarbose
Adrenergic beta-Antagonists
alogliptin
Angiotensin-Converting Enzyme Inhibitors
Angiotensin II Type 2 Receptor Blockers
Angiotensin Receptor
Anterior segment mesenchymal dysgenesis
Anticoagulants
Antiplatelet Agents
Canagliflozin
Chronic Kidney Diseases
Coronary Arteriosclerosis
dapagliflozin
Dyslipidemias
empagliflozin
High Blood Pressures
Hydroxymethylglutaryl-CoA Reductase Inhibitors
inhibitors
Linagliptin
Males
Malignant Neoplasms
Metformin
Mineralocorticoid Receptor Antagonists
Neprilysin
Patients
Percutaneous Coronary Intervention
Prescriptions
saxagliptin
Sitagliptin
Sulfonylurea Compounds
Thiazolidinediones
Vildagliptin
Youth
This nationwide retrospective cohort study enrolled patients from the Taiwan National Health Insurance Research Database (NHIRD), which contains health-care information for more than 23 million (> 99%) residents of Taiwan [14 ]. From a cohort of 2,826,059 patients with T2D—diagnosed using International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) code 250 (between 2010 and 2015) or International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM) codes E11 and E13 (between 2016 and 2019)—we identified 43,568 patients who had undergone PAD revascularization. Of the identified patients, 17,975 had been treated with SGLT2i (n = 3,389) or DPP4i (n = 15,726). After excluding patients who had used these study agents before the index date of PAD revascularization, we identified a total of 2,455 and 8,695 patients who had received first prescriptions for SGLT2i (empagliflozin, dapagliflozin, or canagliflozin) and DPP4i (saxagliptin, vildagliptin, sitagliptin, linagliptin, or alogliptin) during the study period, respectively. Notably, according to Taiwan’s National Health Insurance regulations, patients with T2D cannot use SGLT2i and DPP4i simultaneously. The index date for each study group was defined as the date of the first prescription for SGLT2i or DPP4i after PAD revascularization. The follow-up period was defined as the time from the index date to the independent occurrence of any study outcome, discontinuation of the index drug, or the end of the study period (December 31, 2020), whichever occurred first. The patient enrollment flowchart is illustrated in Fig. 1 ( 201801427B0) . Informed consent was waived because the original identification number of each patient in the NHIRD had been encrypted and deidentified to protect their privacy.![]()
Enrollment of patients with T2D who were treated with SGLT2i or DPP4i after PAD revascularization. DPP4i dipeptidyl peptidase-4 inhibitors, PAD peripheral artery disease, SGLT2i sodium–glucose cotransporter-2 inhibitors, T2D type 2 diabetes
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alogliptin
Canagliflozin
dapagliflozin
Diabetes Mellitus, Non-Insulin-Dependent
Dipeptidyl-Peptidase IV Inhibitors
empagliflozin
Ethics Committees, Research
inhibitors
Linagliptin
National Health Insurance
Patients
Peripheral Arterial Diseases
Pharmaceutical Preparations
saxagliptin
Sitagliptin
SLC5A2 protein, human
Vildagliptin
Top products related to «Vildagliptin»
Sourced in Switzerland
Vildagliptin is a dipeptidyl peptidase-4 (DPP-4) inhibitor. It is a pharmaceutical compound used in the treatment of type 2 diabetes.
Sourced in United States
Vildagliptin is a pharmaceutical compound developed by Merck Group. It is a dipeptidyl peptidase-4 (DPP-4) inhibitor, which works by increasing the levels of incretin hormones in the body. Incretins help regulate blood glucose levels by stimulating insulin release and suppressing glucagon secretion. Vildagliptin is used in the treatment of type 2 diabetes mellitus.
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.
Sourced in United States
The OneTouch Select is a blood glucose meter designed to measure blood glucose levels. It provides a simple and convenient way for individuals to monitor their blood sugar levels.
Sourced in United States, Germany, China, Sao Tome and Principe, United Kingdom, India, Japan, Macao, Canada, France, Italy, Switzerland, Egypt, Poland, Hungary, Denmark, Indonesia, Singapore, Sweden, Belgium, Malaysia, Israel, Spain, Czechia
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, Germany, Japan, United Kingdom
The EGLP-35K is a laboratory equipment product manufactured by the Merck Group. It is designed for general laboratory use. The core function of the EGLP-35K is to perform laboratory tasks, but a detailed description is not available while maintaining an unbiased and factual approach.
Sourced in Germany, United States
Linagliptin is a dipeptidyl peptidase-4 (DPP-4) inhibitor. It is a medication used to control blood sugar levels in adults with type 2 diabetes.
Sourced in United Kingdom
The GLP-1 (Active) ELISA Kit (EGLP-35K) is a laboratory equipment product manufactured by Merck Group. The kit is designed to detect and quantify the levels of active glucagon-like peptide-1 (GLP-1) in biological samples using the enzyme-linked immunosorbent assay (ELISA) technique.
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.
Sourced in United States
Vildagliptin is a laboratory chemical compound used in research and development. It is a dipeptidyl peptidase-4 (DPP-4) inhibitor, which is a class of drugs used in the treatment of type 2 diabetes. Vildagliptin functions by inhibiting the DPP-4 enzyme, which is responsible for the breakdown of certain hormones that regulate blood sugar levels.
More about "Vildagliptin"
Vildagliptin is a powerful dipeptidyl peptidase-4 (DPP-4) inhibitor, a class of medications used to treat type 2 diabetes.
It works by increasing levels of incretins, hormones that stimulate insulin production and reduce glucagon secretion.
This leads to improved glycemic control and a reduced risk of hypoglycemia (low blood sugar) in patients with type 2 diabetes.
Vildagliptin is closely related to other DPP-4 inhibitors like sitagliptin, which share similar mechanisms of action and therapeutic benefits.
Research on vildagliptin's efficacy, safety, and optimal use is an active area of investigation, with researchers exploring its potential in combination with other diabetes medications like metformin or GLP-1 agonists.
To optimize your vildagliptin research, consider using tools like PubCompare.ai, which can help you identify the most reproducible and accurate protocols from literature, preprints, and patents.
This can be especially useful when working with related compounds like STZ (streptozotocin, a chemical used to induce diabetes in animal models) or EGLP-35K (a GLP-1 ELISA kit).
By incorporating insights from the latest research and leveraging smart tools like PubCompare.ai, you can ensure your vildagliptin studies are efficient, accurate, and aligned with the latest scientific advancements in diabetes management.
Whether you're exploring vildagliptin's mechanisms, efficacy, or safety profile, a comprehensive understanding of this DPP-4 inhibitor and related compounds can lead to breakthroughs in type 2 diabetes treatment.
It works by increasing levels of incretins, hormones that stimulate insulin production and reduce glucagon secretion.
This leads to improved glycemic control and a reduced risk of hypoglycemia (low blood sugar) in patients with type 2 diabetes.
Vildagliptin is closely related to other DPP-4 inhibitors like sitagliptin, which share similar mechanisms of action and therapeutic benefits.
Research on vildagliptin's efficacy, safety, and optimal use is an active area of investigation, with researchers exploring its potential in combination with other diabetes medications like metformin or GLP-1 agonists.
To optimize your vildagliptin research, consider using tools like PubCompare.ai, which can help you identify the most reproducible and accurate protocols from literature, preprints, and patents.
This can be especially useful when working with related compounds like STZ (streptozotocin, a chemical used to induce diabetes in animal models) or EGLP-35K (a GLP-1 ELISA kit).
By incorporating insights from the latest research and leveraging smart tools like PubCompare.ai, you can ensure your vildagliptin studies are efficient, accurate, and aligned with the latest scientific advancements in diabetes management.
Whether you're exploring vildagliptin's mechanisms, efficacy, or safety profile, a comprehensive understanding of this DPP-4 inhibitor and related compounds can lead to breakthroughs in type 2 diabetes treatment.