yingweiwo

Exenatide (Exendin-4)

Alias: DA 3091; ITCA 650; LY 2148568; LY2148568; Byetta; Exenatide; Exendin-4; 141758-74-9; Exendin 4 (Heloderma suspectum); PT302; AC 2993; Exenatide; AC 2993A; AC-2993; Exendin-4; AC002993; AC2993; AC2993A; Bydureon
Cat No.:V32928 Purity: =98.36%
Exenatide (Exendin-4), a bioactive peptide composed of 39 amino acids, is antidiabetic medication acting as a long-acting glucagon-like peptide-1 receptor agonist with an IC50 of 3.22 nM.
Exenatide (Exendin-4)
Exenatide (Exendin-4) Chemical Structure CAS No.: 141758-74-9
Product category: GCGR
This product is for research use only, not for human use. We do not sell to patients.
Size Price Stock Qty
1mg
5mg
10mg
25mg
50mg
100mg
250mg
500mg
Other Sizes

Other Forms of Exenatide (Exendin-4):

  • Exendin-4 Acetate
Official Supplier of:
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Top Publications Citing lnvivochem Products
Purity & Quality Control Documentation

Purity: =98.36%

Product Description

Exenatide (Exendin-4), a bioactive peptide composed of 39 amino acids, is antidiabetic medication acting as a long-acting glucagon-like peptide-1 receptor agonist with an IC50 of 3.22 nM. Exenatide, a synthetic version of endogenous glucagon-like peptide-1, suppresses hunger, inhibits the release of glucagon, increases insulin secretion, and slows stomach emptying. It is therefore utilized as supplemental therapy for diabetes mellitus.

Biological Activity I Assay Protocols (From Reference)
Targets
glucagon-like peptide-1 receptor ( IC50 = 3.22 nM )
ln Vitro
Exendin-4 dramatically and dose-dependently raises NO production, phosphorylation of endothelial NO synthase (eNOS), and GTP cyclohydrolase 1 (GTPCH1) in human umbilical vein endothelial cells[2]. MCF-7 breast cancer cells exhibit cytotoxic effects from exendin-4, with an IC50 of 5 μM after 48 hours[3].
Exendin-4 is a GLP-1 analog used for the treatment of type 2 diabetes mellitus in its synthetic form. As women with diabetes have higher breast cancer incidence and mortality, we examined the effect of the incretin drug exendin-4 on breast cancer cells. The aim of the study is to investigate anticancer mechanism of exendin-4 in MCF-7 breast cancer cells. Cytotoxic effects of exendin-4 were determined by XTT assay. IC50 dose in MCF-7 cells were detected as 5 μM at 48th hour. Gene messenger RNA (mRNA) expressions were evaluated by real-time PCR. According to results, caspase-9, Akt, and MMP2 expression was reduced in dose group cells, compared with the control group cells. p53, caspase-3, caspase-8, caspase-10, BID, DR4, DR5, FADD, TRADD, PARP, PTEN, PUMA, NOXA, APAF, TIMP1, and TIMP2 expression was increased in dose group cells, compared with the control group cells. Effects of exendin-4 on cell invasion, colony formation, and cell migration were detected by Matrigel chamber, colony formation assay, and wound-healing assay, respectively. To conclude, it is thought that exendin-4 demonstrates anticarcinogenesis activity by effecting apoptosis, invasion, migration, and colony formation in MCF-7 cells. Exendin-4 may be a therapeutic agent for treatment of breast cancer as single or in combination with other agents. More detailed researches are required to define the pathways of GLP-1 effect on breast cancer cells because of the molecular biology of breast cancer that involves a complex network of interconnected signaling pathways that have role in cell growth, survival, and cell invasion[3].
ln Vivo
Exendin-4 treatment, at both low and high doses, improves serum ALT and lowers serum glucose levels in ob/ob mice as well as computes HOMA scores in comparison to control. In the last four weeks of the study, the net weight gain of the ob/ob mice treated with extendin-4 is significantly reduced[4]. The Exendin-4-treated animals weigh a great deal less than the control rats and exhibit increased pyknotic nuclei and pancreatic acinar inflammation. Rats treated with extendin-4 have lower HOMA values and lower levels of leptin[5]. The rat thoracic aorta relaxes in response to exenatide in a dose-dependent manner. This relaxation is mediated primarily by H2S but also by NO and CO, and it is evoked through the GLP-1 receptor[6].
Nonalcoholic fatty liver disease (NAFLD) represents a burgeoning problem in hepatology, and is associated with insulin resistance. Exendin-4 is a peptide agonist of the glucagon-like peptide (GLP) receptor that promotes insulin secretion. The aim of this study was to determine whether administration of Exendin-4 would reverse hepatic steatosis in ob/ob mice. Ob/ob mice, or their lean littermates, were treated with Exendin-4 [10 microg/kg or 20 microg/kg] for 60 days. Serum was collected for measurement of insulin, adiponectin, fasting glucose, lipids, and aminotransferase concentrations. Liver tissue was procured for histological examination, real-time RT-PCR analysis and assay for oxidative stress. Rat hepatocytes were isolated and treated with GLP-1. Ob/ob mice sustained a reduction in the net weight gained during Exendin-4 treatment. Serum glucose and hepatic steatosis was significantly reduced in Exendin-4 treated ob/ob mice. Exendin-4 improved insulin sensitivity in ob/ob mice, as calculated by the homeostasis model assessment. The measurement of thiobarbituric reactive substances as a marker of oxidative stress was significantly reduced in ob/ob-treated mice with Exendin-4. Finally, GLP-1-treated hepatocytes resulted in a significant increase in cAMP production as well as reduction in mRNA expression of stearoyl-CoA desaturase 1 and genes associated with fatty acid synthesis; the converse was true for genes associated with fatty acid oxidation. In conclusion, Exendin-4 appears to effectively reverse hepatic steatosis in ob/ob mice by improving insulin sensitivity. Our data suggest that GLP-1 proteins in liver have a novel direct effect on hepatocyte fat metabolism.[4]
Aims/hypothesis: Exendin-4 is a 39 amino acid agonist of the glucagon-like peptide receptor and has been approved for treatment of type 2 diabetes. Many reports describe an increased incidence of acute pancreatitis in humans treated with exendin-4 (exenatide). Previous studies have evaluated the effect of exendin-4 on beta cells and beta cell function. We evaluated the histological and biochemical effects of exendin-4 on the pancreas in rats. Methods: We studied 20 Sprague-Dawley male rats, ten of which were treated with exendin-4 and ten of which were used as controls. The study period was 75 days. Serum and pancreatic tissue were removed for biochemical and histological study. Blood glucose, amylase, lipase, insulin and adipocytokines were compared between the two groups. Results: Animals treated with exendin-4 had more pancreatic acinar inflammation, more pyknotic nuclei and weighed significantly less than control rats. They also had higher serum lipase than control animals. Exendin-4 treatment was associated with lower insulin and leptin levels as well as lower HOMA values than in the untreated control group. Conclusions/interpretation: Although the use of exendin-4 in rats is associated with decreased weight gain, lower insulin resistance and lower leptin levels than in control animals, extended use of exendin-4 in rats leads to pancreatic acinar inflammation and pyknosis. This raises important concerns about the likelihood of inducing acute pancreatitis in humans receiving incretin mimetic therapy.[5]
Background: It has been reported that GLP-1 agonist exenatide (exendin-4) decreases blood pressure. The dose-dependent vasodilator effect of exendin-4 has previously been demonstrated, although the precise mechanism is not thoroughly described. Here we have aimed to provide in vitro evidence for the hypothesis that exenatide may decrease central (aortic) blood pressure involving three gasotransmitters, namely nitric oxide (NO) carbon monoxide (CO), and hydrogen sulphide (H2S). Methods: We determined the vasoactive effect of exenatide on isolated thoracic aortic rings of adult rats. Two millimetre-long vessel segments were placed in a wire myograph and preincubated with inhibitors of the enzymes producing the three gasotransmitters, with inhibitors of reactive oxygen species formation, prostaglandin synthesis, inhibitors of protein kinases, potassium channels or with an inhibitor of the Na+/Ca2+-exchanger. Results: Exenatide caused dose-dependent relaxation of rat thoracic aorta, which was evoked via the GLP-1 receptor and was mediated mainly by H2S but also by NO and CO. Prostaglandins and superoxide free radical also play a part in the relaxation. Inhibition of soluble guanylyl cyclase significantly diminished vasorelaxation. We found that ATP-sensitive-, voltage-gated- and calcium-activated large-conductance potassium channels are also involved in the vasodilation, but that seemingly the inhibition of the KCNQ-type voltage-gated potassium channels resulted in the most remarkable decrease in the rate of vasorelaxation. Inhibition of the Na+/Ca2+-exchanger abolished most of the vasodilation. Conclusions: Exenatide induces vasodilation in rat thoracic aorta with the contribution of all three gasotransmitters. We provide in vitro evidence for the potential ability of exenatide to lower central (aortic) blood pressure, which could have relevant clinical importance[6].
Enzyme Assay
Competitive binding of peptides to GLP-1 receptor in intact cells [1]
Binding studies were performed as described by Montrose-Rafizadeh et al. Briefly, CHO/GLP-1R cells were grown to confluency on 12-well plates and washed with serum-free ham F-12 medium for 2 h before the experiment. After two washes in 0.5 ml binding buffer, cells were incubated overnight at 4 °C with 0.5 ml buffer containing 2% bovine serum albumin, 50 μm DPP-IV inhibitor, 400 kallikrein inactivator units (KIU) aprotinin, 10 mM glucose, 1–1000 nM GLP-1 or other peptides and 30,000 cpm [125I]GLP-1. At the end of the incubation, the supernatant was discarded and the cells were washed three times with ice-cold phosphate-buffered saline (PBS) and incubated at room temperature with 0.5 ml of 0.5 M NaOH and 0.1% sodium dodecylsulfate for 10 min. Radioactivity in cell lysates was measured in an ICN Apec-Series γ-counter. Specific binding was determined as total binding minus the radioactivity associated with cells incubated in the presence of a large excess of unlabeled GLP-1 (1 μM).
Exendin-4, a 39-amino acid (AA) peptide, is a long-acting agonist at the glucagon-like peptide-1 (GLP-1) receptor. Consequently, it may be preferable to GLP-1 as a long-term treatment for type 2 diabetes mellitus. Exendin-4 (Ex-4), unlike GLP-1, is not degraded by dipeptidyl peptidase IV (DPP IV), is less susceptible to degradation by neutral endopeptidase, and possesses a nine-AA C-terminal sequence absent from GLP-1. Here we examine the importance of these nine AAs for biological activity of Ex-4, a sequence of truncated Ex-4 analogs, and native GLP-1 and GLP-1 analogs to which all or parts of the C-terminal sequence have been added. We found that removing these AAs from Ex-4 to produce Ex (1-30) reduced the affinity for the GLP-1 receptor (GLP-1R) relative to Ex-4 (IC50: Ex-4, 3.22+/-0.9 nM; Ex (1-30), 32+/-5.8 nM) but made it comparable to that of GLP-1 (IC50: 44.9+/-3.2 nM). The addition of this nine-AA sequence to GLP-1 improved the affinity of both GLP-1 and the DPP IV resistant analog GLP-1 8-glycine for the GLP-1 receptor (IC50: GLP-1 Gly8 [GG], 220+/-23 nM; GLP-1 Gly8 Ex (31-39), 74+/-11 nM). Observations of the cAMP response in an insulinoma cell line show a similar trend for biological activity [1].
Cell Assay
Cytotoxicity assay [3]
Cytotoxicity assays and determination of IC50 dose of Exenatide (Exendin-4) in MCF-7 cells were performed by using trypan blue dye exclusion test and XTT assay as indicated in the manufacturers’ instruction.
Wound-healing assay [3]
The control and dose group cells were plated at 106 cells per well of 60 × 15 mm xstyle cell culture dishes and grown overnight at 37 °C with 5 % CO2. The 80 % confluent control group and dose group cells were treated with 5 μM Exenatide (Exendin-4) after a straight line scratch was made on a confluent monolayer of cells using a sterile 200-μl plastic pipette tip. To remove debris and smooth the edge of the scratch, the cells were washed with 2 ml serum-free DMEM. Images of the MCF-7 cell proliferation were taken at 0 16, 24, and 48 h after the scratch. The scratch assay was performed in triplicate.
Animal Protocol
Rats: 20 Sprague-Dawley male rats, ten of which are treated with exendin-4 (10 μg/kg) and ten of which are used as controls. There are 75 days in the study period. Pancreatic tissue and serum are extracted for histological and biochemical analysis. The two groups' levels of blood glucose, lipase, amylase, and adipocytokines are compared[5].
Mice: For the first 14 days, 10 μg/kg is administered to the exendin-4 treatment groups every 24 hours. This therapy is the initiating stage. Every 24 hours, the corresponding control mice (lean and ob/ob) are given saline. Exendin-4-treated mice are split into two groups at random after 14 days: the first group is given a high dose of exendin-4 (20 μg/kg) every 12 hours, while the second group is given a low dose of exendin-4 (10 μg/kg) every 12 hours. Every twelve hours, saline is still given to the control mice. Every day for the duration of the 60-day treatment, the mice are weighed[4].
Use of ob/ob Mouse Model and Treatment With Exenatide (Exendin-4) [4]
Obese male (ob/ob) 6-week-old mice and their lean littermates were used. For both ob/ob mice and their lean littermates the we followed the same treatment strategy. All animals were treated for 60 days. The Exenatide (Exendin-4) treatment groups were treated with 10 μg/kg every 24 hours for the first 14 days. This treatment was the induction phase. Respective control mice (lean and ob/ob) received saline every 24 hours. After 14 days Exendin-4–treated mice were randomly divided into two groups: one group received high dose Exendin-4 (20 μg/kg) every 12 hours, while the second group continued with low dose Exendin-4 (10 μg/kg) every 12 hours.
Exenatide (Exendin-4) administration and tissue removal [5]
Highly purified drug (Exenatide (Exendin-4)) was stored at −70°C and dosages prepared as needed. In line with previous publications on exendin-4 in rats and in order to better elucidate the effect of exendin-4 on the pancreas, it was decided to use a dose of 10 μg/kg [7]. This dosage was administered subcutaneously to the treated group each day immediately before the 12 h dark cycle when rats are known to feed. Animal weights were recorded weekly and doses adjusted according to weight. The ten exendin-treated rats and ten control animals were killed after 75 days of treatment. Serum was obtained from each animal and necropsy tissue collection specimens were fixed in 10% formalin.
Vasoreactivity experiments [6]
After all vessel segments had reached a stable contraction plateau, increasing doses of Exenatide (Exendin-4) were administered to the organ baths, and relaxant responses were assessed. The dose of exenatide that was applied to relax the aorta correlated with the dose of epinephrine we used to preconstrict the vessels. Plasma epinephrine level is approximately 30 pM at rest, while in our experiments we used 100 nM, which is a 3000 times higher concentration. The plasma exenatide level was found to be 70 pM, while in our experiments we used a 4500 times higher concentration.
In order to identify the extracellular and intracellular mediators of the vasodilator effect of Exenatide (Exendin-4) we performed a series of experiments. Prior to contracting the vessels with epinephrine we preincubated the vessels (n = 5 of each experiment) with different materials. To determine whether the vasodilation due to exenatide evoked via the GLP-1R, we preincubated vessels with GLP-1R antagonist exendin(9–39) (32 μM, 30 min). Because the affinity of exendin(9–39) to bind GLP-1R is smaller than that of exenatide, we applied a ten times higher concentration of the receptor antagonist than the highest dose of exenatide.
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Exenatide reaches a peak plasma concentration in 2.1 hours. Because exenatide is administerd subcutaneously, the bioavailability is 1.
Exenatide is mainly eliminated by glomerular filtration followed by proteolysis before finally being eliminated in the urine.
28.3L.
9.1 L/hour.
Following a single dose of Bydureon, exenatide is released from the microspheres over approximately 10 weeks. There is an initial period of release of surface-bound exenatide followed by a gradual release of exenatide from the microspheres, which results in two subsequent peaks of exenatide in plasma at around week 2 and week 6 to 7, respectively, representing the hydration and erosion of the microspheres. Following initiation of once every 7 days (weekly) administration of 2 mg Bydureon, gradual increase in the plasma exenatide concentration is observed over 6 to 7 weeks. After 6 to 7 weeks, mean exenatide concentrations of approximately 300 pg/mL were maintained over once every 7 days (weekly) dosing intervals indicating that steady state was achieved.
Nonclinical studies have shown that exenatide is predominantly eliminated by glomerular filtration with subsequent proteolytic degradation. The mean apparent clearance of exenatide in humans is 9.1 L/hr and the mean terminal half-life is 2.4 hr. These pharmacokinetic characteristics of exenatide are independent of the dose. In most individuals, exenatide concentrations are measurable for approximately 10 hr post-dose.
The mean apparent volume of distribution of exenatide following SC administration of a single dose of Byetta is 28.3 L.
Following SC administration to patients with type 2 diabetes, exenatide reaches median peak plasma concentrations in 2.1 hr. The mean peak exenatide concentration (Cmax) was 211 pg/mL and overall mean area under the time-concentration curve (AUC0-inf) was 1036 pg hr/mL following SC administration of a 10 ug dose of Byetta. Exenatide exposure (AUC) increased proportionally over the therapeutic dose range of 5 ug to 10 ug. The Cmax values increased less than proportionally over the same range. Similar exposure is achieved with SC administration of Byetta in the abdomen, thigh, or upper arm.
For more Absorption, Distribution and Excretion (Complete) data for Exenatide (6 total), please visit the HSDB record page.
Metabolism / Metabolites
Exenatide is filtered through the glomerulus before being degraded to smaller peptides and amino acids by dipeptidyl peptidase-4, metalloproteases, endopeptidase 24-11, amino proteases, and serine proteases. It is currently believed that the metalloproteases are responsible for most of the degradation of exenatide. Exenatide is metabolised to small peptides <3 amino acids in length by enzymes in the kidney.
Biological Half-Life
2.4 hours
Terminal half life varied from 18 minutes in mice up to 114 minutes in rats.
Mean terminal half-life /in humans/ is 2.4 hr
Toxicity/Toxicokinetics
Toxicity Summary
IDENTIFICATION AND USE: Exenatide is a white to off-white powder formulated into solution for subcutaneous use. Exenatide is available in both a twice daily formulation and an extended-release formulation that is administered weekly. Exenatide is a synthetic, long-acting human glucagon-like peptide-1 (GLP-1) receptor agonist (incretin mimetic). It is used as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. HUMAN EXPOSURE AND TOXICITY: Overdose of exenatide has been reported in a clinical study. Effects have included severe nausea, severe vomiting, and rapidly declining blood glucose concentrations. Post marketing reports also include acute pancreatitis, including fatal and nonfatal hemorrhagic or necrotizing pancreatitis requiring hospitalization and serious hypersensitivity reactions (e.g. anaphylaxis and angioedema). Deterioration of renal function (e.g., increased serum creatinine concentrations, renal impairment/insufficiency, and chronic renal failure, acute renal failure sometimes requiring hemodialysis or kidney transplantation) has also been reported with the use of exenatide. Exenatide extended-release also caused thyroid C-cell tumors at clinically relevant exposures in rats. It is unknown whether the drug causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as human relevance could not be determined by clinical or nonclinical studies. Therefore, exenatide extended release is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2. ANIMAL STUDIES: Exenatide had no adverse effects on fertility when given to male mice at doses up to 760 ug/kg/day. However, exenatide did cause developmental toxicity in rats, mice and rabbits. Fetuses from pregnant rats given subcutaneous doses of exenatide extended-release at 0.3, 1, or 3 mg/kg on gestation days 6, 9, 12, and 15 demonstrated reduced fetal growth at all doses and produced skeletal ossification deficits at 1 and 3 mg/kg in association with maternal effects (decreased food intake and decreased body weight gain). In pregnant mice given sc doses of 6, 68, 460, or 760 ug/kg/day from gestation day 6 through 15 (organogenesis), cleft palate (some with holes) and irregular fetal skeletal ossification of rib and skull bones were observed at 6 ug/kg/day. In pregnant rabbits given sc doses of 0.2, 2, 22, 156, or 260 ug/kg/day from gestation day 6 through 18 (organogenesis), irregular fetal skeletal ossifications were observed at 2 ug/kg/day. Studies for the carcinogenicity potential of exenatide were also conducted in rats. Benign thyroid C-adenomas were observed in female rats given extenatide by sc injection at doses of 18, 70, or 250 ug/kg/day. In another carcinogenicity study with exenatide extended-release male and female rats were administrated doses of 0.3, 1.0, and 3.0 mg/kg by subcutaneous injection every other week. A statistically significant increase in thyroid C-cell tumor incidence was observed in both males and females. The incidence of C-cell adenomas was statistically significantly increased at all doses (27%-31%) in females and at 1.0 and 3.0 mg/kg (46% and 47%, respectively) in males compared with the control group (13% for males and 7% for females). A statistically significantly higher incidence of C-cell carcinomas occurred in the high-dose group females (6%), while numerically higher incidences of 3%, 7%, and 4% (nonstatistically significant versus controls) were noted in the low-, mid-, and high-dose group males compared with the control group (0% for both males and females). An increase in benign fibromas was seen in the skin subcutis at injection sites of males given 3 mg/kg. No treatment-related injection-site fibrosarcomas were observed at any dose. Exenatide was not mutagenic or clastogenic, with or without metabolic activation, in the Ames bacterial mutagenicity assay or chromosomal aberration assay in Chinese hamster ovary cells. Exenatide was negative in the in vivo mouse micronucleus assay
Hepatotoxicity
Liver injury due to exenatide must be rare, if it occurs at all. In large clinical trials, serum enzyme elevations were no more common with exenatide therapy than with placebo or comparator agents, and no instances of clinically apparent liver injury were reported. Since licensure, there have been no published case reports of hepatotoxicity due to exenatide and the product label does not list liver injury as an adverse event. Exenatide has been linked to rare instances of acute pancreatitis, but even this complication is usually not associated with elevations in serum bilirubin and aminotransferase levels.
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
No information is available on the clinical use of exenatide during breastfeeding. Because exenatide is a large peptide molecule with a molecular weight of 4187 daltons, the amount in milk is likely to be very low and absorption is unlikely because it is probably partially destroyed in the infant's gastrointestinal tract. It has a short half-life, which might make it a better choice among drugs in this class for nursing mothers. If exenatide is required by the mother, it is not a reason to discontinue breastfeeding. However, until more data become available, exenatide should be used with caution during breastfeeding, especially while nursing a newborn or preterm infant.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.
Protein Binding
Protein binding of exenatide has not been determined.
Interactions
Increases in international normalized ratio (INR), sometimes associated with bleeding, have been reported during postmarketing experience with concomitant use of exenatide and warfarin. In a drug interaction study, no clinically important changes in warfarin (S- or R-enantiomer) AUC, peak plasma concentrations, or therapeutic response (as indicated by INR) were observed when warfarin sodium (single 25-mg dose) was administered 35 minutes after exenatide (5 ug subcutaneously twice daily for 2 days, then 10 ug twice daily for 7 days); however, the time to peak warfarin concentration was delayed by approximately 2 hours. In patients receiving warfarin, prothrombin time should be monitored more frequently after initiating or altering exenatide therapy; once a stable prothrombin time has been achieved, prothrombin times may be monitored at intervals usually recommended for patients receiving warfarin therapy.
In healthy women, repeated daily administration of a fixed-combination oral contraceptive (30 ug of ethinyl estradiol and 150 ug of levonorgestrel) 30 minutes after subcutaneous injection of exenatide (10 ug twice daily) decreased the peak plasma concentrations of ethinyl estradiol and levonorgestrel by 45 and 27%, respectively, and delayed the time to peak plasma concentrations of ethinyl estradiol and levonorgestrel by 3 and 3.5 hours, respectively. Repeated daily administration of the fixed-combination oral contraceptive 1 hour prior to administration of exenatide decreased the mean peak plasma concentration of ethinyl estradiol by 15%; however, the mean peak plasma concentration of levonorgestrel was not substantially changed. Exenatide did not alter the mean trough concentrations of levonorgestrel following repeated daily administration of the fixed-combination oral contraceptive for both regimens; however, the mean trough concentration of ethinyl estradiol increased by 20% when the fixed-combination oral contraceptive was administered 30 minutes after exenatide injection. In this study, the effect of exenatide on the pharmacokinetics of oral contraceptives was confounded by the possible effect of food on oral contraceptives. Therefore, oral contraceptives should be administered at least 1 hour prior to exenatide administration.
Administration of exenatide (10 ug subcutaneously twice daily) 30 minutes before lovastatin (single 40-mg oral dose) decreased the lovastatin AUC and peak plasma concentration by approximately 40 and 28%, respectively, and delayed the time to peak plasma concentration of lovastatin by 4 hours. In clinical trials, the use of exenatide in patients already receiving HMG-CoA reductase inhibitors (statins) was not associated with consistent changes in lipid profiles compared to baseline.
In patients with mild to moderate hypertension receiving stable dosages of lisinopril (5-20 mg daily), exenatide (10 ug subcutaneously twice daily) did not alter the steady-state AUC or peak plasma concentration of lisinopril or the 24-hour mean systolic and diastolic blood pressure. However, the steady-state time to peak plasma concentration of lisinopril was delayed by 2 hours.
For more Interactions (Complete) data for Exenatide (10 total), please visit the HSDB record page.
References

[1]. The importance of the nine-amino acid C-terminal sequence of exendin-4 for binding to the GLP-1 receptor and for biological activity. Regul Pept. 2003 Jul 15;114(2-3):153-8.

[2]. Exenatide exerts direct protective effects on endothelial cells through the AMPK/Akt/eNOS pathway in a GLP-1 receptor-dependent manner. Am J Physiol Endocrinol Metab. 2016 Jun 1;310(11):E947-57.

[3]. Antidiabetic exendin-4 activates apoptotic pathway and inhibits growth of breast cancer cells. Tumour Biol. 2016 Feb;37(2):2647-53.

[4]. Exendin-4, a glucagon-like protein-1 (GLP-1) receptor agonist, reverses hepatic steatosis in ob/obmice. Hepatology. 2006 Jan;43(1):173-81.

[5]. Biochemical and histological effects of exendin-4 (exenatide) on the rat pancreas. Diabetologia. 2010 Jan;53(1):153-9.

[6]. Exenatide induces aortic vasodilation increasing hydrogen sulphide, carbon monoxide and nitric oxide production. Cardiovasc Diabetol. 2014 Apr 2;13:69.

Additional Infomation
Therapeutic Uses
Hypoglycemic Agents
Byetta is a glucagon-like peptide-1 (GLP-1) receptor agonist indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus /Included in US product label/
Bydureon is a glucagon-like peptide-1 (GLP-1) receptor agonist indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. Bydureon is an extended-release formulation of exenatide. Do not coadminister with Byetta. /Included in US product label/
Prior treatment with Byetta is not required when initiating Bydureon therapy. If the decision is made to start Bydureon in an appropriate patient already taking Byetta, Byetta should be discontinued. Patients changing from Byetta to Bydureon may experience transient (approximately 2 weeks) elevations in blood glucose concentrations.
For more Therapeutic Uses (Complete) data for Exenatide (8 total), please visit the HSDB record page.
Drug Warnings
/BOXED WARNING/ WARNING: RISK OF THYROID C-CELL TUMORS. Exenatide extended-release causes thyroid C-cell tumors at clinically relevant exposures in rats. It is unknown whether Bydureon causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as human relevance could not be determined by clinical or nonclinical studies. Bydureon is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2.
Acute pancreatitis, including fatal and nonfatal hemorrhagic or necrotizing pancreatitis requiring hospitalization, has been reported during postmarketing experience with exenatide. Persistent, severe abdominal pain, which may be accompanied by vomiting, is the hallmark symptom of acute pancreatitis. Most patients who have developed pancreatitis have had at least one other risk factor for acute pancreatitis (e.g., gallstones, severe hypertriglyceridemia, alcohol use) and have required hospitalization. Some patients have developed serious complications including dehydration and renal failure, suspected ileus, phlegmon, and ascites. Acute or worsening pancreatitis has been associated temporally with an increase in exenatide dosage from 5 ug to 10 ug twice daily, the maximum recommended dosage, in some patients. Symptoms of acute pancreatitis (e.g., nausea, vomiting, abdominal pain) recurred upon rechallenge with the drug in several patients; abdominal pain abated after permanent discontinuance of the drug in one patient. Most patients have improved upon discontinuance of exenatide.
The US Food and Drug Administration (FDA) is evaluating unpublished findings suggesting an increased risk of pancreatitis and precancerous cellular changes (pancreatic duct metaplasia) in patients with type 2 diabetes mellitus receiving incretin mimetics (exenatide, liraglutide, sitagliptin, saxagliptin, alogliptin, or linagliptin). These findings are based on examination of a small number of pancreatic tissue specimens taken from patients who died from unspecified causes while receiving an incretin mimetic. FDA has not yet reached any new conclusions about safety risks with incretin mimetics. FDA will notify healthcare professionals of its conclusions and recommendations when the review is complete, or when the agency has additional information to report. FDA states that at this time clinicians should continue to follow the recommendations in the prescribing information for incretin mimetics. The manufacturer states that after initiation of exenatide, and after increases in dosage, patients should be observed carefully for signs and symptoms of acute pancreatitis (e.g., unexplained, persistent severe abdominal pain that may radiate to the back; nausea; vomiting; elevated serum amylase or lipase concentrations). If pancreatitis is suspected, therapy with exenatide and other potentially suspect drugs should be promptly discontinued, confirmatory tests performed (e.g., serum amylase or lipase concentrations, radiologic imaging), and appropriate therapy initiated. Exenatide should not be resumed if pancreatitis is confirmed. Exenatide has not been studied in patients with a history of pancreatitis; other antidiabetic therapies should be considered in such patients.
Deterioration of renal function (e.g., increased serum creatinine concentrations, renal impairment/insufficiency, worsened chronic renal failure, acute renal failure sometimes requiring hemodialysis or kidney transplantation) has been reported rarely with exenatide. Some of these events occurred in patients experiencing nausea, vomiting, and/or diarrhea with or without dehydration; these adverse effects may have contributed to development of altered renal function in these patients. Some of these events also occurred in patients receiving exenatide in combination with other agents known to affect renal function or hydration status (e.g., angiotensin-converting enzyme inhibitors, nonsteroidal anti-inflammatory agents, diuretics). Exenatide has not been found to be directly nephrotoxic in preclinical or clinical studies. Renal effects usually have been reversible with supportive treatment and discontinuance of potentially causative agents, including exenatide. Altered renal function may be a consequence of diabetes mellitus, independent of any risk associated with exenatide therapy. Clinicians should closely monitor patients receiving exenatide for signs and symptoms of renal dysfunction and consider discontinuance of the drug if renal dysfunction is suspected and cannot be explained by other causes.
For more Drug Warnings (Complete) data for Exenatide (15 total), please visit the HSDB record page.
Pharmacodynamics
When patients take exenatide the body's natural response to glucose is modulated. More insulin and less glucagon are released in response to glucose, though in cases of hypoglycemia a normal amount of glucagon is released. Exenatide also slows gastric emptying, leading to a slower and prolonged release of glucose into the systemic circulation. Together these effects prevent hyper and hypoglycemia.
Glucagon-like peptide-1 (GLP-1) may have direct favorable effects on cardiovascular system. The aim of this study was to investigate the effects of the GLP-1 analog exenatide on improving coronary endothelial function in patients with type 2 diabetes and to investigate the underlying mechanisms. The newly diagnosed type 2 diabetic subjects were enrolled and given either lifestyle intervention or lifestyle intervention plus exenatide treatment. After 12-wk treatment, coronary flow velocity reserve (CFVR), an important indicator of coronary endothelial function, was improved significantly, and serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were remarkably decreased in the exenatide treatment group compared with the baseline and the control group. Notably, CFVR was correlated inversely with hemoglobin A1c (Hb A1c) and positively with high-density lipoprotein cholesterol (HDL-C). In human umbilical vein endothelial cells, exendin-4 (a form of exenatide) significantly increased NO production, endothelial NO synthase (eNOS) phosphorylation, and GTP cyclohydrolase 1 (GTPCH1) level in a dose-dependent manner. The GLP-1 receptor (GLP-1R) antagonist exendin (9-39) or GLP-1R siRNA, adenylyl cyclase inhibitor SQ-22536, AMPK inhibitor compound C, and PI3K inhibitor LY-294002 abolished the effects of exendin-4. Furthermore, exendin-4 reversed homocysteine-induced endothelial dysfunction by decreasing sICAM-1 and reactive oxygen species (ROS) levels and upregulating NO production and eNOS phosphorylation. Likewise, exendin (9-39) diminished the protective effects of exendin-4 on the homocysteine-induced endothelial dysfunction. In conclusion, exenatide significantly improves coronary endothelial function in patients with newly diagnosed type 2 diabetes. The effect may be mediated through activation of AMPK/PI3K-Akt/eNOS pathway via a GLP-1R/cAMP-dependent mechanism.[2]
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C₁₈₄H₂₈₂N₅₀O₆₀S
Molecular Weight
4186.57
Exact Mass
4184.03
Elemental Analysis
C, 52.79; H, 6.79; N, 16.73; O, 22.93; S, 0.77
CAS #
141758-74-9
Related CAS #
Exendin-4 acetate; 914454-01-6
PubChem CID
53396299
Sequence
His-Gly-Glu-Gly-Thr-Phe-Thr-Ser-Asp-Leu-Ser-Lys-Gln-Met-Glu-Glu-Glu-Ala-Val-Arg-Leu-Phe-Ile-Glu-Trp-Leu-Lys-Asn-Gly-Gly-Pro-Ser-Ser-Gly-Ala-Pro-Pro-Pro-Ser-NH2
SequenceShortening
HGEGTFTSDLSKQMEEEAVRLFIEWLKNGGPSSGAPPPS-NH2
Appearance
White to off-white solid powder
LogP
-21
Hydrogen Bond Donor Count
58
Hydrogen Bond Acceptor Count
66
Rotatable Bond Count
135
Heavy Atom Count
295
Complexity
10300
Defined Atom Stereocenter Count
0
SMILES
[HGEGTFTSDLSKQMEEEAVRLFIEWLKNGGPSSGAPPPS-NH2]
InChi Key
HTQBXNHDCUEHJF-XWLPCZSASA-N
InChi Code
InChI=1S/C184H282N50O60S/c1-16-94(10)147(178(289)213-114(52-58-144(257)258)163(274)218-121(73-101-77-195-105-39-24-23-38-103(101)105)168(279)215-116(68-90(2)3)165(276)205-107(41-26-28-61-186)158(269)219-122(75-134(189)243)154(265)198-79-135(244)196-83-139(248)231-63-30-43-129(231)175(286)225-127(87-238)174(285)223-125(85-236)155(266)200-80-136(245)202-96(12)181(292)233-65-32-45-131(233)183(294)234-66-33-46-132(234)182(293)232-64-31-44-130(232)176(287)222-124(84-235)150(190)261)229-170(281)119(71-99-34-19-17-20-35-99)217-166(277)117(69-91(4)5)214-159(270)108(42-29-62-194-184(191)192)212-177(288)146(93(8)9)228-151(262)95(11)203-156(267)111(49-55-141(251)252)208-161(272)112(50-56-142(253)254)209-162(273)113(51-57-143(255)256)210-164(275)115(59-67-295-15)211-160(271)110(47-53-133(188)242)207-157(268)106(40-25-27-60-185)206-172(283)126(86-237)224-167(278)118(70-92(6)7)216-169(280)123(76-145(259)260)220-173(284)128(88-239)226-180(291)149(98(14)241)230-171(282)120(72-100-36-21-18-22-37-100)221-179(290)148(97(13)240)227-138(247)82-199-153(264)109(48-54-140(249)250)204-137(246)81-197-152(263)104(187)74-102-78-193-89-201-102/h17-24,34-39,77-78,89-98,104,106-132,146-149,195,235-241H,16,25-33,40-76,79-88,185-187H2,1-15H3,(H2,188,242)(H2,189,243)(H2,190,261)(H,193,201)(H,196,244)(H,197,263)(H,198,265)(H,199,264)(H,200,266)(H,202,245)(H,203,267)(H,204,246)(H,205,276)(H,206,283)(H,207,268)(H,208,272)(H,209,273)(H,210,275)(H,211,271)(H,212,288)(H,213,289)(H,214,270)(H,215,279)(H,216,280)(H,217,277)(H,218,274)(H,219,269)(H,220,284)(H,221,290)(H,222,287)(H,223,285)(H,224,278)(H,225,286)(H,226,291)(H,227,247)(H,228,262)(H,229,281)(H,230,282)(H,249,250)(H,251,252)(H,253,254)(H,255,256)(H,257,258)(H,259,260)(H4,191,192,194)/t94-,95-,96-,97+,98+,104-,106-,107-,108-,109-,110-,111-,112-,113-,114-,115-,116-,117-,118-,119-,120-,121-,122-,123-,124-,125-,126-,127-,128-,129-,130-,131-,132-,146-,147-,148-,149-/m0/s1
Chemical Name
(4S)-5-[[2-[[(2S,3R)-1-[[(2S)-1-[[(2S,3R)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S,3S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-4-amino-1-[[2-[[2-[(2S)-2-[[(2S)-1-[[(2S)-1-[[2-[[(2S)-1-[(2S)-2-[(2S)-2-[(2S)-2-[[(2S)-1-amino-3-hydroxy-1-oxopropan-2-yl]carbamoyl]pyrrolidine-1-carbonyl]pyrrolidine-1-carbonyl]pyrrolidin-1-yl]-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]carbamoyl]pyrrolidin-1-yl]-2-oxoethyl]amino]-2-oxoethyl]amino]-1,4-dioxobutan-2-yl]amino]-1-oxohexan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxopropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-carboxy-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-2-oxoethyl]amino]-4-[[2-[[(2S)-2-amino-3-(1H-imidazol-4-yl)propanoyl]amino]acetyl]amino]-5-oxopentanoic acid
Synonyms
DA 3091; ITCA 650; LY 2148568; LY2148568; Byetta; Exenatide; Exendin-4; 141758-74-9; Exendin 4 (Heloderma suspectum); PT302; AC 2993; Exenatide; AC 2993A; AC-2993; Exendin-4; AC002993; AC2993; AC2993A; Bydureon
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.
Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
H2O: ~33.3 mg/mL (~8.0 mM)
DMSO: ≥ 32 mg/mL (~7.6 mM)
Ethanol: < 1 mg/mL
Solubility (In Vivo)

Note: Please refer to the "Guidelines for Dissolving Peptides" section in the 4th page of the "Instructions for use" file (upper-right section of this webpage) for how to dissolve peptides.
Solubility in Formulation 1: ≥ 2.5 mg/mL (0.60 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.5 mg/mL (0.60 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

View More

Solubility in Formulation 3: ≥ 2.5 mg/mL (0.60 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


Solubility in Formulation 4: 100 mg/mL (23.89 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication (<60°C).

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 0.2389 mL 1.1943 mL 2.3886 mL
5 mM 0.0478 mL 0.2389 mL 0.4777 mL
10 mM 0.0239 mL 0.1194 mL 0.2389 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

Calculator

Molarity Calculator allows you to calculate the mass, volume, and/or concentration required for a solution, as detailed below:

  • Calculate the Mass of a compound required to prepare a solution of known volume and concentration
  • Calculate the Volume of solution required to dissolve a compound of known mass to a desired concentration
  • Calculate the Concentration of a solution resulting from a known mass of compound in a specific volume
An example of molarity calculation using the molarity calculator is shown below:
What is the mass of compound required to make a 10 mM stock solution in 5 ml of DMSO given that the molecular weight of the compound is 350.26 g/mol?
  • Enter 350.26 in the Molecular Weight (MW) box
  • Enter 10 in the Concentration box and choose the correct unit (mM)
  • Enter 5 in the Volume box and choose the correct unit (mL)
  • Click the “Calculate” button
  • The answer of 17.513 mg appears in the Mass box. In a similar way, you may calculate the volume and concentration.

Dilution Calculator allows you to calculate how to dilute a stock solution of known concentrations. For example, you may Enter C1, C2 & V2 to calculate V1, as detailed below:

What volume of a given 10 mM stock solution is required to make 25 ml of a 25 μM solution?
Using the equation C1V1 = C2V2, where C1=10 mM, C2=25 μM, V2=25 ml and V1 is the unknown:
  • Enter 10 into the Concentration (Start) box and choose the correct unit (mM)
  • Enter 25 into the Concentration (End) box and select the correct unit (mM)
  • Enter 25 into the Volume (End) box and choose the correct unit (mL)
  • Click the “Calculate” button
  • The answer of 62.5 μL (0.1 ml) appears in the Volume (Start) box
g/mol

Molecular Weight Calculator allows you to calculate the molar mass and elemental composition of a compound, as detailed below:

Note: Chemical formula is case sensitive: C12H18N3O4  c12h18n3o4
Instructions to calculate molar mass (molecular weight) of a chemical compound:
  • To calculate molar mass of a chemical compound, please enter the chemical/molecular formula and click the “Calculate’ button.
Definitions of molecular mass, molecular weight, molar mass and molar weight:
  • Molecular mass (or molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
  • Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.
/

Reconstitution Calculator allows you to calculate the volume of solvent required to reconstitute your vial.

  • Enter the mass of the reagent and the desired reconstitution concentration as well as the correct units
  • Click the “Calculate” button
  • The answer appears in the Volume (to add to vial) box
In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
Step 2: Enter in vivo formulation (This is only a calculator, not the exact formulation for a specific product. Please contact us first if there is no in vivo formulation in the solubility section.)
+
+
+

Calculation results

Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
             (2) Be sure to add the solvent(s) in order.

Clinical Trial Information
A Pan-European Post-Authorisation Safety Study: Risk of Pancreatic Cancer Among Type 2 Diabetes Patients Who Initiated Exenatide as Compared With Those Who Initiated Other Non-Glucagon-Like Peptide 1 Receptor Agonists Based Glucose Lowering Drugs
CTID: NCT05663515
Phase:    Status: Recruiting
Date: 2024-11-01
Comparison of Type 2 Diabetes Pharmacotherapy Regimens
CTID: NCT05073692
Phase:    Status: Recruiting
Date: 2024-10-24
GLP-1 and Hyperoxia for Organ Protection in Heart Surgery
CTID: NCT02673931
Phase: N/A    Status: Active, not recruiting
Date: 2024-08-28
Exenatide For Reducing the Reinforcing Effects of Cocaine
CTID: NCT06252623
Phase: Phase 1    Status: Recruiting
Date: 2024-08-06
Diabetes Islet Preservation Immune Treatment
CTID: NCT02586831
Phase: Phase 1/Phase 2    Status: Withdrawn
Date: 2024-06-06
View More

Brain Activation and Satiety in Children 2
CTID: NCT04520490
Phase: Phase 3    Status: Active, not recruiting
Date: 2024-05-14


Exenatide-test for Diagnosing Endogenous Hyperinsulinemic Hypoglycemia
CTID: NCT04909333
Phase: N/A    Status: Completed
Date: 2024-05-08
Haemodynamic Effects of GLP-1 and Glucagon in Healthy Male Volunteers
CTID: NCT03835013
Phase: N/A    Status: Completed
Date: 2024-04-03
Exenatide Pharmacokinetics and Pharmacodynamics in Gestational Diabetes
CTID: NCT05482789
Phase: Phase 4    Status: Recruiting
Date: 2024-03-08
FLuctuATion Reduction With inSULin and Glp-1 Added togetheR (FLAT-SUGAR)
CTID: NCT01524705
Phase: Phase 4    Status: Completed
Date: 2023-12-29
Can Exenatide Prevent Increase in EGP in Response to Dapagliflozin-induced Increase in Glucosuria
CTID: NCT03331289
Phase: Phase 4    Status: Completed
Date: 2023-07-24
Effect of Chronic Exenatide Therapy on Beta Cell Function and Insulin Sensitivity in T2DM
CTID: NCT02981069
Phase: Phase 4    Status: Completed
Date: 2023-07-20
Impact of Exenatide on Cardiovascular Exercise Performance in Type 2 Diabetes
CTID: NCT01364584
Phase: N/A    Status: Completed
Date: 2023-07-12
Extended Release Exenatide Versus Placebo In Diabetic Patients With Type 4 Cardiorenal Syndrome
CTID: NCT02251431
Phase: Phase 3    Status: Completed
Date: 2023-05-17
Impact of Exenatide on Sleep Duration
CTID: NCT01416649
Phase:    Status: Completed
Date: 2023-04-26
Effects on Re-endothelialisation With Bydureon Treatment in Type 2 Diabetes Subjects
CTID: NCT02621489
Phase: Phase 4    Status: Completed
Date: 2023-04-20
Pharmacogenomics of GLP1 Receptor Agonists
CTID: NCT05762744
Phase: Phase 1    Status: Terminated
Date: 2023-03-10
The Effect of GLP-1 Receptor Agonist on Cerebral Blood Flow Velocity in Stroke
CTID: NCT02829502
Phase: Phase 2    Status: Recruiting
Date: 2023-03-03
GLP-1 Agonism for Blocking Cocaine Euphoria and Self-Administration
CTID: NCT02302976
Phase: Phase 1    Status: Completed
Date: 2023-02-16
Exeantide in Type 2 Diabetes on Insulin
CTID: NCT01154933
Phase: Phase 2    Status: Completed
Date: 2022-10-06
Effects of Exenatide on Motor Function and the Brain
CTID: NCT03456687
Phase: Phase 1    Status: Completed
Date: 2022-09-16
Exenatide Treatment in Parkinson's Disease
CTID: NCT04305002
Phase: Phase 2    Status: Unknown status
Date: 2022-09-13
Exenatide for Treating Cocaine Use Disorder
CTID: NCT04941521
Phase: Phase 1/Phase 2    Status: Completed
Date: 2022-06-27
Effect of Exenatide, Sitagliptin or Glimepiride on Functional ß -Cell Mass
CTID: NCT00775684
Phase: N/A    Status: Completed
Date: 2022-06-07
Double-blinded, 6 Months Study With Bydureon® or Placebo in Adolescents With Obesity to Explore Changes in BMI
CTID: NCT02794402
Phase: Phase 2    Status: Completed
Date: 2022-05-18
Energy Balance & Weight Loss in Craniopharyngioma-related or Other Hypothalamic Tumors in Hypothalamic Obesity
CTID: NCT02664441
Phase: Phase 3    Status: Completed
Date: 2022-05-05
Effects of Combined Dapagliflozin and Exenatide Versus Dapagliflozin and Placebo on Ectopic Lipids in Patients With Uncontrolled Type 2 Diabetes Mellitus.
CTID: NCT03007329
Phase: Phase 4    Status: Completed
Date: 2022-04-15
Effects of GLP-1 Analogue Combined With Metformin and Metformin on Gonadal and Metabolic Profiles in Chinese Overweight/Obese PCOS Patients With Hyperandrogenemia.
CTID: NCT04969627
Phase: Phase 4    Status: Completed
Date: 2022-04-14
GLP Analogs for Diabetes in Wolfram Syndrome Patients
CTID: NCT01302327
Phase: N/A    Status: Withdrawn
Date: 2022-03-29
Efficacy and Safety of the Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC) Versus GLP-1 Receptor Agonist in Patients With Type 2 Diabetes, With a FRC Extension Period
CTID: NCT02787551
Phase: Phase 3    Status: Completed
Date: 2022-03-25
The Effects of Exenatide, a GLP-1 Agonist, on Alcohol Self-Administration in Heavy Drinkers
CTID: NCT03645408
Phase: Phase 1    Status: Terminated
Date: 2022-02-09
Exenatide Weekly Injections as an Adjunctive Treatment in Patients With Schizophrenia
CTID: NCT02417142
Phase: Phase 4    Status: Completed
Date: 2022-01-14
Trial of EXenatide in Acute Ischaemic Stroke
CTID: NCT03287076
Phase: Phase 2    Status: Unknown status
Date: 2021-09-14
Effectiveness of Exenatide Plus Dapagliflozin on 24 Hour Glucose Variability Measured by CGM. A Proof of Concept.
CTID: NCT03970044
Phase: Phase 4    Status: Completed
Date: 2021-08-30
Long-acting Exenatide and Cognitive Decline in Dysglycemic Patients
CTID: NCT02847403
Phase: Phase 3    Status: Unknown status
Date: 2021-08-17
New Onset Type 1 Diabetes: Role of Exenatide
CTID: NCT01269034
Phase: Phase 4    Status: Completed
Date: 2021-08-04
Weight Loss With Exenatide Treatment
CTID: NCT01590433
Phase: Phase 4    Status: Completed
Date: 2021-06-23
DECREASE: Dapagliflozin Plus Exenatide on Central REgulation of Appetite in diabeteS typE 2
CTID: NCT03361098
Phase: Phase 4    Status: Completed
Date: 2021-06-11
Does Treatment With GLP-1 Reduce Alcohol Intake in Patients With Alcohol Dependence?
CTID: NCT03232112
Phase: Phase 2    Status: Completed
Date: 2021-06-04
Bexagliflozin Drug/Drug Interaction Study With Exenatide Injection
CTID: NCT03167411
Phase: Phase 1    Status: Completed
Date: 2021-05-28
Evaluating Exenatide for the Treatment of Postprandial Hyperinsulinemic Hypoglycemia
CTID: NCT02685852
Phase: Phase 1    Status: Completed
Date: 2021-05-06
Effects of GLP-1 RAs on Weight and Metabolic Indicators in Obese Patients
CTID: NCT03671733
Phase: Phase 3    Status: Unknown status
Date: 2021-04-09
Impact of Perioperative Exenatide Infusion on Quality of Life in Cardiac Surgery Patients
CTID: NCT02432976
Phase: Phase 2/Phase 3    Status: Completed
Date: 2021-03-09
Exenatide Once Weekly for Smoking Cessation
CTID: NCT02975297
Phase: Phase 1/Phase 2    Status: Completed
Date: 2021-01-28
Safety and Efficacy of Exenatide as Monotherapy and Adjunctive Therapy to Oral Antidiabetic Agents in Adolescents With Type 2 Diabetes
CTID: NCT00658021
Phase: Phase 3    Status: Completed
Date: 2020-12-01
COMBinAtion Therapy in Myocardial Infarction: The COMBAT-MI Trial
CTID: NCT02404376
Phase: Phase 3    Status: Completed
Date: 2020-11-03
A Study Comparing the Effect of Albiglutide With Exenatide on Regional Brain Activity Related to Nausea in Healthy Subjects
CTID: NCT02802514
Phase: Phase 4    Status: Terminated
Date: 2020-10-30
An Exploratory Study on the Effects of Repeat Doses of Albiglutide Compared to Exenatide on Gastric Myoelectrical Activity and Gastric Emptying in Type 2 Diabetes Mellitus Subjects
CTID: NCT02793154
Phase: Phase 4    Status: Terminated
Date: 2020-10-30
Evaluating the Use of Exenatide in People With Type 2 Diabetes and Diastolic Heart Failure
CTID: NCT00799435
Phase: Phase 4    Status: Terminated
Date: 2020-09-04
Gut Derived Hormones, Body Composition and Metabolism in Prader-Willi Syndrome
CTID: NCT00551343
Phase: N/A    Status: Completed
Date: 2020-07-07
The Potential of Dapagliflozin Plus Exenatide in Obese Insulin-resistant Patients
CTID: NCT03419624
Phase: Phase 3    Status: Terminated
Date: 2020-03-31
A Phase II Trial to Examine the Effect of Subcutaneous Exenatide (Bydureon®) on Glucose Control in Patients With Type I Diabetes
CTID: NCT01928329
Phase: Phase 2    Status: Completed
Date: 2020-03-19
Effect of Exenatide on 24h-UAER in Patients With Diabetic Nephropathy
CTID: NCT02690883
Phase: Phase 4    Status: Completed
Date: 2020-03-09
Gut Hormones in Obesity, Nicotine and Alcohol Dependence
CTID: NCT02690987
PhaseEarly Phase 1    Status: Unknown status
Date: 2020-02-13
Effects of Exenatide on Hypothalamic Obesity
CTID: NCT01061775
Phase: Phase 1/Phase 2    Status: Completed
Date: 2019-10-08
Research of Exenatide for Overweight/Obese PCOS Patients With IGR
CTID: NCT03352869
Phase: Phase 4    Status: Completed
Date: 2019-09-11
Exenatide Compared With Insulin Glargine to Change Liver Fat Content in Type 2 Diabetes
CTID: NCT02303730
Phase: Phase 4    Status: Completed
Date: 2019-08-28
Metformin vs Metformin Combined With GLP-1RA (Glucagon-like Peptide 1 Receptor Agonist) on Overweight/Obese PCOS Patients
CTID: NCT04029272
Phase: Phase 4    Status: Unknown status
Date: 2019-07-23
Meal-time Administration of Exenatide for Glycaemic Control in Type 1 Diabetic Cases
CTID: NCT03017352
Phase: Phase 2    Status: Completed
Date: 2019-07-10
Exenatide Inpatient Trial: A Randomized Controlled Pilot Trial on the Safety and Efficacy of Exenatide (Byetta®) Therapy for the Inpatient Management of Patients With Type 2 Diabetes
CTID: NCT02455076
Phase: Phase 4    Status: Completed
Date: 2019-06-20
Efficacy and Safety of Semaglutide Once-weekly Versus Exenatide ER 2.0 mg Once-weekly as add-on to 1-2 Oral Antidiabetic Drugs (OADs) in Subjects With Type 2 Diabetes
CTID: NCT01885208
Phase: Phase 3    Status: Completed
Date: 2019-06-13
The Effects of Exenatide (Byetta ) on Energy Expenditure and Weight Loss in Nondiabetic Obese Subjects
CTID: NCT00856609
Phase: Phase 3    Status: Completed
Date: 2019-06-04
A 12/24-weeks, Open, Multi-centre, Phase IV Study on Safety and Efficacy of 2mg Exenatide Once Weekly (Bydureon) in T2DM Patients.
CTID: NCT02533453
Phase: Phase 4    Status: Completed
Date: 2019-05-31
Role of Exenatide in Type 1 Diabetes
CTID: NCT00456300
Phase: Phase 2    Status: Completed
Date: 2019-02-26
Phase III Study to Evaluate Safety and Efficacy of Added Exenatide Versus Placebo to Titrated Basal Insulin Glargine in Inadequately Controlled Patients With Type II Diabetes Mellitus
CTID: NCT02229383
Phase: Phase 3    Status: Completed
Date: 2019-01-08
The Efficacy of Insulin Degludec/Liraglutide in Controlling Glycaemia in Adults With Type 2 Diabetes Inadequately Controlled on GLP-1 Receptor Agonist and OAD Therapy
CTID: NCT01676116
Phase: Phase 3    Status: Completed
Date: 2019-01-03
Efficacy and Safety of Basal Insulin Glargine Combination With Exenatide Bid vs Aspart30 in T2DM
CTID: NCT02467920
Phase: Phase 4    Status: Completed
Date: 2018-11-14
Comparison of Exenatide vs. Biphasic Insulin Aspart 30 on Glucose Variability in Type 2 Diabetes
CTID: NCT02449603
Phase: Phase 4    Status: Completed
Date: 2018-11-14
Efficacy and Safety of Exenatide in the Treatment of Hypothalamic Obesity After Craniopharyngioma Therapy
CTID: NCT02860923
Phase: Phase 3    Status: Completed
Date: 2018-10-16
Impact of Exenatide on Sleep in Type 2 Diabetes
CTID: NCT01136798
Phase: N/A    Status: Completed
Date: 2018-09-12
Intravenous Exenatide in Patients With Acute Brain Injury
CTID: NCT02058940
Phase: Phase 4    Status: Completed
Date: 2018-07-12
Effects of Antidiabetic Medications on the Postprandial State in Prediabetes
CTID: NCT02104739
Phase: Phase 4    Status: Completed
Date: 2018-07-03
Effect of Bydureon on Carotid Atherosclerosis Progression in Type 2 Diabetes Mellitus
CTID: NCT02162550
Phase: Phase 4    Status: Unknown status
Date: 2018-06-14
Effect of Exenatide on Cortisol Secretion
CTID: NCT03160261
Phase: Phase 4    Status: Completed
Date: 2018-05-03
Exenatide for the Treatment of Weight Gain Associated With Olanzapine in Obese Adults
CTID: NCT00845507
Phase: Phase 4    Status: Completed
Date: 2018-04-20
Exenatide and Impaired Hypoglycaemic Awareness in Type 1 Diabetes
CTID: NCT02735031
Phase: Phase 2/Phase 3    Status: Completed
Date: 2018-04-12
Use of Exenatide and Pramlintide to Decrease Post-prandial Hyperglycemia
CTID: NCT01269047
Phase: Phase 4    Status: Completed
Date: 2018-04-12
Study Looking at Cardiovascular Effects of Exenatide, Its Blood Pressure Lowering Effect and Its Mechanisms
CTID: NCT01046721
Phase: N/A    Status: Completed
Date: 2018-03-06
Safety Evaluation of Adverse Reactions in Diabetes
CTID: NCT02092597
Phase: Phase 4    Status: Completed
Date: 2018-02-07
Effect of Pioglitazone and Exenatide on Body Weight and Beta Cell Function
CTID: NCT00845182
Phase: Phase 4    Status: Completed
Date: 2018-01-18
The Effect of Exenatide Compared to Lantus Insulin on Vascular Function in Type 2 Diabetes
CTID: NCT00353834
Phase: Phase 4    Status: Completed
Date: 2018-01-09
Research of Intensive Metabolic Intervention Before Pregnancy in PCOS
CTID: NCT03383068
Phase: Phase 4    Status: Unknown status
Date: 2017-12-26
Acute Effect of Exenatide on Brain Glucose Metabolism
CTID: NCT01588418
Phase: Phase 4    Status: Completed
Date: 2017-11-24
Effects of the GLP-1 Exenatide on Satiety in Lean and Obese Women
CTID: NCT01501084
Phase: Phase 1    Status: Completed
Date: 2017-11-07
Feasibility Study of Exenatide by Continuous Subcutaneous Infusion
CTID: NCT01857895
Phase: Phase 1    Status: Completed
Date: 2017-10-19
Exenatide for Stress Hyperglycemia
CTID: NCT01969149
Phase: Phase 2/Phase 3    Status: Completed
Date: 2017-10-06
Pharmacology of Exenatide in Pediatric Sepsis
CTID: NCT01573806
Phase: Phase 1/Phase 2    Status: Withdrawn
Date: 2017-10-05
GLP-1 Analogs for Neuroprotection After Cardiac Arrest
CTID: NCT02442791
Phase: N/A    Status: Completed
Date: 2017-09-28
The Effect of Exenatide on Weight and Hunger in Obese, Healthy Women
CTID: NCT00456885
Phase: Phase 4    Status: Completed
Date: 2017-09-11
Effects Of Exenatide On Liver Biochemistry, Liver Histology And Lipid Metabolism In Patients With Fatty Liver Disease
CTID: NCT00529204
Phase: Phase 2    Status: Terminated
Date: 2017-06-20
Changes in Bone Turnover With Exposure to a GLP-1 Receptor Agonist
CTID: NCT01381926
Phase: Phase 4    Status: Terminated
Date: 2017-06-14
Continuous Glucose Monitoring Evaluation of Exenatide Twice Daily Versus Insulin Glargine
CTID: NCT01089569
Phase: N/A    Status: Completed
Date: 2017-05-23
The Effect of Byetta and Symlin on Post-meal Meal Blood Sugar Levels in Children With Type 2 Diabetes
CTID: NCT00950677
Phase: Phase 4    Status: Completed
Date: 2017-04-24
Role of Exenatide in NASH-a Pilot Study
CTID: NCT00650546
Phase: Phase 2/Phase 3    Status: Completed
Date: 2017-04-11
Effect of Liraglutide or Exenatide Added to an Ongoing Treatment on Blood Glucose Control in Subjects With Type 2 Diabetes
CTID: NCT00518882
Phase: Phase 3    Status: Completed
Date: 2017-03-08
Weight Loss Study for Patients With Obesity Due to Craniopharyngioma or Other Brain Tumor
CTID: NCT01484873
Phase: Phase 2    Status: Completed
Date: 2017-03-03
Evaluation of Exenatide in Patients With Diabetic Neuropathy
CTID: NCT00855439
Phase: N/A    Status: Completed
Date: 2017-03-01
Clinical Trial for PB-119 in Subjects With Type 2 Diabetes Mellitus
CTID: NCT03059719
Phase: Phase 1    Status: Completed
Date: 2017-02-23
A Comparison of Exenatide and Insulin Glargine
CTID: NCT02325960
Phase: Phase 4    Status: Completed
Date: 2017-02-23
The Effect of GLP-1 Receptor Agonist on Cerebral Blood Flow Velocity in Non-stroke Volunteers
CTID: NCT02838589
Phase: Phase 2    Status: Completed
Date: 2017-02-07
Roflumilast Plus Alogliptin Proof-of-Mechanism Study in Type2 Diabetes
CTID: NCT01664624
Phase: Phase 1    Status: Completed
Date: 2017-02-01
Study to Evaluate the Effect of BYDUREON on 24-hour Glucose Control in Metformin Treated Patients With Type 2 Diabetes.
CTID: NCT02288273
Phase: Phase 4    Status: Completed
Date: 2017-01-27
Study of the Effects of Intravenous Exenatide on Cardiac Repolarization
CTID: NCT02650479
Phase: Phase 1    Status: Completed
Date: 2017-01-27
GLP-1 Agonism Stimulates Browning of Subcutaneous White Adipose Tissue in Obesity Men
CTID: NCT02170324
Phase: Phase 4    Status: Completed
Date: 2017-01-18
A Study of the Effect of Glucagon-like Peptide 1(GLP-1) Receptor Agonist in Combination With Metformin Therapy on Diabetes Remission in Subjects With Newly Diagnosed Type 2 Diabetes Who Are Overweight or Obese
CTID: NCT03018665
Phase: Phase 4    Status: Unknown status
Date: 2017-01-12
Effects of Biphasic Insulin Aspart 70/30 vs. Exenatide in Type 2 Diabetes Patients Not Reaching Blood Glucose Targets on Metformin and a Sulfonylurea.
CTID: NCT00313001
Phase: Phase 3    Status: Completed
Date: 2017-01-06
Exenatide and Brown Adipose Tissue
CTID: NCT03002675
Phase: Phase 4    Status: Unknown status
Date: 2016-12-26
GLP-1 Receptor Agonist Lixisenatide Versus Exenatide in Patients With Type 2 Diabetes for Glycemic Control and Safety Evaluation, on Top of Metformin
CTID: NCT00707031
Phase: Phase 3    Status: Completed
Date: 2016-12-02
Exploratory Study to Investigate the Effect of Dapagliflozin and Exenatide Combined on Body Weight
CTID: NCT02313220
Phase: Phase 2    Status: Completed
Date: 2016-11-17
Trial of Exenatide for Parkinson's Disease
CTID: NCT01971242
Phase: Phase 2    Status: Completed
Date: 2016-11-17
A Study of Taspoglutide Versus Exenatide for the Treatment of Patients With Type 2 Diabetes Mellitus Inadequately Controlled With Metformin, Thiazolidinedione or a Combination of Both.
CTID: NCT00717457
Phase: Phase 3    Status: Completed
Date: 2016-11-02
Addition Of Exenatide To Insulin Glargine In Type 2 Diabetes Mellitus
CTID: NCT00765817
Phase: Phase 3    Status: Completed
Date: 2016-10-24
Effects of Exenatide on Overweight Adolescents With Prader-Willi Syndrome
CTID: NCT01444898
Phase: N/A    Status: Completed
Date: 2016-09-29
Adding Exenatide to Insulin Therapy for Patients With Type 2 Diabetes and Non-Alcoholic Fatty Liver Disease
CTID: NCT01006889
Phase: Phase 4    Status: Completed
Date: 2016-09-28
Effects of Exenatide on Glycemic Control and Weight in Continuous Subcutaneous Insulin Infusion (CSII) Type 2 Treated Patients With Type 2 Diabetes
CTID: NCT01140893
Phase: Phase 2/Phase 3    Status: Unknown status
Date: 2016-08-23
Effect of Exenatide in Obese Patients With Accelerated Gastric Emptying
CTID: NCT02160990
Phase: Phase 4    Status: Completed
Date: 2016-08-09
Exenatide for Myocardial Protection During Reperfusion Study
CTID: NCT01938235
Phase: Phase 2    Status: Unknown status
Date: 2016-08-05
Comparison Between GLP 1 Analogues and DPP 4 Inhibitors in Type 1 Diabetes Mellitus
CTID: NCT01235819
Phase: Phase 4    Status: Completed
Date: 2016-07-27
Study of the Acute Metabolic Effect of Exenatide in Type 1 Diabetes
CTID: NC
Effect of Exenatide on disease progression in early Parkinson's disease.
CTID: null
Phase: Phase 2    Status: Ongoing
Date: 2019-10-23
A randomised, double blind, parallel group, placebo controlled, Phase 3 trial of exenatide once weekly over 2 years as a potential disease modifying treatment for Parkinson's disease.
CTID: null
Phase: Phase 3    Status: GB - no longer in EU/EEA
Date: 2019-09-04
A multicentre, randomised controlled Trial of Exenatide versus standard care in Acute Ischemic Stroke (TEXAIS)
CTID: null
Phase: Phase 2    Status: Completed
Date: 2019-03-11
iPAVE – imaging Pituitary ActiVation by Exendin
CTID: null
Phase: Phase 2    Status: Ongoing
Date: 2019-01-02
Comparison of the beta cell mass during and shortly after the honeymoon phase of type 1 diabetes using Ga-68-exendin PET
CTID: null
Phase: Phase 2    Status: Ongoing
Date: 2018-10-15
EXenatide onCe weekly or sitAgliptin as add on to basaL Insulin: effects on novel markers of endothelial fnction/dysfunction and on metaBolic control in T2DM sUbjects tRial: the EXCALIBUR Trial
CTID: null
Phase: Phase 4    Status: Ongoing
Date: 2018-07-27
An open-label randomised cross-over study to evaluate the albuminuria lowering effect of dapagliflozin, exenatide and their combination in patients with type 2 diabetes
CTID: null
Phase: Phase 3    Status: Ongoing
Date: 2018-04-24
A 28-week, multi-center randomized, double-blind, placebo-controlled study to evaluate the potential of Dapagliflozin plus Exenatide in combination with high-dose intensive insulin therapy compared to Placebo in obese insulin-resistant patients with Type 2 Diabetes mellitus (Proof-of-concept study)
CTID: null
Phase: Phase 3    Status: Prematurely Ended
Date: 2017-12-28
Combined effects of SGLT2 inhibition and GLP-1 receptor agonism on food intake, body weight and central satiety and reward circuits in obese T2DM patients
CTID: null
Phase: Phase 4    Status: Ongoing
Date: 2017-08-14
A randomized, non-blinded, 24-week pilot study to evaluate the effect of dapagliflozin (10 mg once daily) plus exenatide (2.0 mg once weekly) on type 2 diabetic patients awaiting for bariatric surgery. DEXBASU study
CTID: null
Phase: Phase 2    Status: Ongoing
Date: 2017-08-07
Beta cell imaging in type 1 diabetes with stable near-normal and unstable glucose control using PET
CTID: null
Phase: Phase 2    Status: Prematurely Ended
Date: 2017-07-27
A Phase 3b, Randomized, Active Comparator, Open-label, Multicenter Study to Compare the Efficacy, Safety, and Tolerability of ITCA 650 to Empagliflozin and to Glimepiride as Add-on Therapy to Metformin in Patients with Type 2 Diabetes
CTID: null
Phase: Phase 3    Status: Completed, Prematurely Ended
Date: 2017-06-22
Effect of exenatide on cortisol secretion
CTID: null
Phase: Phase 4    Status: Ongoing
Date: 2017-06-12
Does Glucagon-like Peptide 1 (GLP-1) receptor stimulation reduce alcohol intake in patients with alcohol dependence?
CTID: null
Phase: Phase 2    Status: Prematurely Ended
Date: 2017-04-12
Effect of the GLP-1 receptor agonist exenatide on impaired hypoglycaemic awareness in type 1 diabetes
CTID: null
Phase: Phase 2    Status: Completed
Date: 2017-01-04
Visualizing beta cells in morbid obese patients with T2D before and after bariatric surgery
CTID: null
Phase: Phase 4    Status: Ongoing
Date: 2016-12-07
Meal-time Administration of exenatide for Glycaemic control in type 1 diabetic Cases: A randomised, placebo-controlled trial
CTID: null
Phase: Phase 2    Status: Completed
Date: 2016-10-10
RESILIENT: RandomisEd, controlled, double blind Study to assess mechanistic effects of combination therapy of dapagliflozin with Exenatide QW versus dapagliflozin alone in obese (BMI>30 kg/m2) patients with Type 2 diabetes mellitus
CTID: null
Phase: Phase 4    Status: GB - no longer in EU/EEA
Date: 2016-10-03
A 24 week monocentric prospective randomized, placebo-controlled trial to evaluate Efficacy of combination of Exenatide and Dapagliflozin compared to Dapagliflozin and Placebo and its effects on hepatic, myocardial and pancreatic fat distribution in patients with uncontrolled type 2 diabetes mellitus.
CTID: null
Phase: Phase 4    Status: Completed
Date: 2016-08-31
Visualizing beta cells in patients with a history of gestational diabetes
CTID: null
Phase: Phase 2    Status: Ongoing
Date: 2016-08-30
The effect of Exenatide on brown adipose tissue activity and energy expenditure in healthy young men
CTID: null
Phase: Phase 4    Status: Completed
Date: 2016-08-09
Effect of glucagon-like peptide 1 (GLP-1) based diabetes medication on
CTID: null
Phase: Phase 2    Status: Completed
Date: 2016-06-17
A 26-Week Randomized, Open-label, Active Controlled, Parallel-group, Study Assessing the Efficacy and Safety of the Insulin Glargine/Lixisenatide Fixed Ratio Combination in Adults with Type 2 Diabetes Inadequately Controlled on GLP-1 Receptor Agonist and Metformin (alone or with Pioglitazone and/or SGLT2 inhibitors), Followed by a Fixed Ratio Combination Single-arm 26-Week Extension Period
CTID: null
Phase: Phase 3    Status: Completed
Date: 2016-06-17
Effect of glucagon-like peptide 1 (GLP-1) based diabetes medication on blood flow velocity in ischemic stroke patients
CTID: null
Phase: Phase 2    Status: Prematurely Ended
Date: 2016-06-17
A Phase 3, Double-Blind, Placebo-Controlled, Randomized, Multi-Center Study to Assess the Safety and Efficacy of Exenatide Once Weekly in Adolescents with Type 2 Diabetes
CTID: null
Phase: Phase 3    Status: Completed
Date: 2016-04-13
Multicenter double-blind randomized clinical trial assessing efficacy and safety of exenatide in the treatment of hypothalamic obesity after craniopharyngioma therapy.
CTID: null
Phase: Phase 3    Status: Completed
Date: 2016-03-15
Efficacy of GLP-1 agonists and restrictive vs. liberal FiO2 in patients undergoing coronary artery bypass grafting or aortic valve replacement – a 2-by-2 factorial designed, randomized clinical study
CTID: null
Phase: Phase 3    Status: Ongoing
Date: 2015-11-10
The physiology of glucagon-like peptide-1 receptor expression in patients with endogenous hyperinsulinism: correlation with histopathology
CTID: null
Phase: Phase 2    Status: Not Authorised
Date: 2015-10-29
Visualizing beta cells after Intrahepatic Islet of Langerhans Transplantation
CTID: null
Phase: Phase 1, Phase 2    Status: Prematurely Ended
Date: 2015-09-22
Long-acting exenatide: a tool to stop cognitive decline in patients with mild cognitive impairment with or without dysglycemia?
CTID: null
Phase: Phase 2    Status: Completed
Date: 2015-09-11
Visualizing beta cells in patients with postprandial hyperinsulinemic hypoglycemia after bariatric surgery
CTID: null
Phase: Phase 4    Status: Ongoing
Date: 2015-08-06
Effects on re-endothelialisation with Bydureon treatment add on to Insulin versus Insulin alone, both in combination with Metformin in type 2 diabetic subjects (Rebuild Study).
CTID: null
Phase: Phase 3    Status: Ongoing
Date: 2015-07-24
COMBinAtion Therapy in Myocardial Infarction:
CTID: null
Phase: Phase 3    Status: Completed
Date: 2015-07-09
Visualizing beta cells in patients with remission of T2DM after bariatric surgery
CTID: null
Phase: Phase 2    Status: Ongoing
Date: 2015-02-25
Effect of Gelofusine on 111In-DTPA-AHX-Lys40-Exendin 4 uptake in the kidney
CTID: null
Phase: Phase 2    Status: Ongoing
Dat e.querySelector("font strong").innerText = 'View More' } else if(up_display === 'none' || up_display === '') { icon_angle_down.style.display = 'none';

Biological Data
  • Exendin-4 (Ex-4; a form of exenatide) increases nitric oxide (NO) production, endothial nitric oxide synthase (eNOS) phosphorylation, and GTP cyclohydrolase 1 (GTPCH1) level in human umbilical vein endothelial cells (HUVECs). Am J Physiol Endocrinol Metab . 2016 Jun 1;310(11):E947-57.
  • The effect of Exendin-4 administration on the rate of net weight gain in ob/ob and their lean littermates. Hepatology . 2006 Jan;43(1):173-81.
  • Assessment of lipid content and hepatic histology in the liver of ob/ob mice and their lean littermates after Exendin-4 treatment. Hepatology . 2006 Jan;43(1):173-81.
  • TBAR measurements following Exendin-4 treatment reveals that high-dose therapy resulted in significant reduction in oxidative stress. Hepatology . 2006 Jan;43(1):173-81.
  • Effect of exenatide on the vasoactivity of rat thoracic aorta. Cardiovasc Diabetol . 2014 Apr 2:13:69.
  • Role of GLP-1 receptor and endothelial denudation in the vasodilatation due to exenatide. Cardiovasc Diabetol . 2014 Apr 2:13:69.
Contact Us