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1. Ac 2993
2. Ac 2993 Lar
3. Bydureon
4. Byetta
5. Ex4 Peptide
6. Exenatide
7. Exendin 4
8. Exendin-4
9. Itca 650
10. Peptide, Ex4
1. Exenatide
2. Exendin-4
3. Exendin 4
4. 141758-74-9
5. Chebi:64073
6. Heloderma Suspectum Gila Monster Exendin-4
7. H-his-gly-glu-gly-xithr-phe-xithr-ser-asp-leu-ser-lys-gln-met-glu-glu-glu-ala-val-arg-leu-phe-xiile-glu-trp-leu-lys-asn-gly-gly-pro-ser-ser-gly-ala-pro-pro-pro-ser-nh2
8. 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
| Molecular Weight | 4187 g/mol |
|---|---|
| Molecular Formula | C184H282N50O60S |
| XLogP3 | -21 |
| Hydrogen Bond Donor Count | 58 |
| Hydrogen Bond Acceptor Count | 66 |
| Rotatable Bond Count | 135 |
| Exact Mass | 4185.0306624 g/mol |
| Monoisotopic Mass | 4184.0273075 g/mol |
| Topological Polar Surface Area | 1780 Ų |
| Heavy Atom Count | 295 |
| Formal Charge | 0 |
| Complexity | 10300 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 34 |
| Undefined Atom Stereocenter Count | 3 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Hypoglycemic Agents
National Library of Medicine's Medical Subject Headings. Exenatide. Online file (MeSH, 2014). Available from, as of April 30 2014: https://www.nlm.nih.gov/mesh/2014/mesh_browser/MBrowser.html
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/
NIH; DailyMed. Current Medication Information for Byetta (Exenatide) Injection (Revised: February 2013). Available from, as of July 18, 2014: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=751747da-7c1f-41ad-b1a6-a6d920f70599
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/
NIH; DailyMed. Current Medication Information for Bydureon (Exenatide Extended-release for Injectable Suspension) (Revised: May 2014). Available from, as of July 18, 2014: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=a1c8ee2a-6a76-435e-ad38-8a9c99046ad9
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.
NIH; DailyMed. Current Medication Information for Bydureon (Exenatide Extended-release for Injectable Suspension) (Revised: May 2014). Available from, as of July 18, 2014: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=a1c8ee2a-6a76-435e-ad38-8a9c99046ad9
For more Therapeutic Uses (Complete) data for Exenatide (8 total), please visit the HSDB record page.
/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.
NIH; DailyMed. Current Medication Information for Bydureon (Exenatide Extended-release for Injectable Suspension) (Revised: May 2014). Available from, as of July 18, 2014: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=a1c8ee2a-6a76-435e-ad38-8a9c99046ad9
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.
American Society of Health-System Pharmacists 2014; Drug Information 2014. Bethesda, MD. 2014, p. 3214
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.
American Society of Health-System Pharmacists 2014; Drug Information 2014. Bethesda, MD. 2014, p. 3214
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.
American Society of Health-System Pharmacists 2014; Drug Information 2014. Bethesda, MD. 2014, p. 3214
For more Drug Warnings (Complete) data for Exenatide (15 total), please visit the HSDB record page.
Exenatide is indicated for improving glycemic control in adults with type 2 diabetes mellitus along with diet and exercise.
FDA Label
Byetta is indicated for treatment of type-2 diabetes mellitus in combination with:
- metformin;
- sulphonylureas;
- thiazolidinediones;
- metformin and a sulphonylurea;
- metformin and a thiazolidinedione;
in adults who have not achieved adequate glycaemic control on maximally tolerated doses of these oral therapies. Byetta is also indicated as adjunctive therapy to basal insulin with or without metformin and / or pioglitazone in adults who have not achieved adequate glycaemic control with these agents.
Bydureon is indicated in adults 18 years and older with type 2 diabetes mellitus to improve glycaemic control in combination with other glucose lowering medicinal products when the therapy in use, together with diet and exercise, does not provide adequate glycaemic control (see section 4. 4, 4. 5 and 5. 1 for available data on different combinations).
Bydureon is indicated for treatment of type 2 diabetes mellitus in combination with:
MetforminSulphonylureaThiazolidinedioneMetformin and sulphonylureaMetformin and thiazolidinedionein adults who have not achieved adequate glycaemic control on maximally tolerated doses of these oral therapies.
Treatment of type II diabetes mellitus
Treatment of type II diabetes mellitus
Treatment of type II diabetes mellitus
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.
Anti-Obesity Agents
Agents that increase energy expenditure and weight loss by neural and metabolic regulation. (See all compounds classified as Anti-Obesity Agents.)
Hypoglycemic Agents
Substances which lower blood glucose levels. (See all compounds classified as Hypoglycemic Agents.)
Incretins
Peptides which stimulate INSULIN release from the PANCREATIC BETA CELLS following oral nutrient ingestion, or postprandially. (See all compounds classified as Incretins.)
A10BJ01
A10BJ01
A - Alimentary tract and metabolism
A10 - Drugs used in diabetes
A10B - Blood glucose lowering drugs, excl. insulins
A10BJ - Glucagon-like peptide-1 (glp-1) analogues
A10BJ01 - Exenatide
Absorption
Exenatide reaches a peak plasma concentration in 2.1 hours. Because exenatide is administerd subcutaneously, the bioavailability is 1.
Route of Elimination
Exenatide is mainly eliminated by glomerular filtration followed by proteolysis before finally being eliminated in the urine.
Volume of Distribution
28.3L.
Clearance
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.
NIH; DailyMed. Current Medication Information for Bydureon (Exenatide Extended-release for Injectable Suspension) (Revised: May 2014). Available from, as of July 18, 2014: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=a1c8ee2a-6a76-435e-ad38-8a9c99046ad9
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.
NIH; DailyMed. Current Medication Information for Byetta (Exenatide) Injection (Revised: February 2013). Available from, as of July 21, 2014: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=751747da-7c1f-41ad-b1a6-a6d920f70599
The mean apparent volume of distribution of exenatide following SC administration of a single dose of Byetta is 28.3 L.
NIH; DailyMed. Current Medication Information for Byetta (Exenatide) Injection (Revised: February 2013). Available from, as of July 21, 2014: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=751747da-7c1f-41ad-b1a6-a6d920f70599
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.
NIH; DailyMed. Current Medication Information for Byetta (Exenatide) Injection (Revised: February 2013). Available from, as of July 21, 2014: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=751747da-7c1f-41ad-b1a6-a6d920f70599
For more Absorption, Distribution and Excretion (Complete) data for Exenatide (6 total), please visit the HSDB record page.
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.
2.4 hours
Terminal half life varied from 18 minutes in mice up to 114 minutes in rats.
European Medicines Agency (EMA), Committee for Medicinal Products for Human Use (CHMP), European Public Assessment Report (EPAR): Byetta (Exenatide), Scientific Discussion p.7 (2006). Available from, as of July 22, 2014: https://www.ema.europa.eu/docs/en_GB/document_library/EPAR_-_Scientific_Discussion/human/000698/WC500051842.pdf
Mean terminal half-life /in humans/ is 2.4 hr
NIH; DailyMed. Current Medication Information for Byetta (Exenatide) Injection (Revised: February 2013). Available from, as of July 21, 2014: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=751747da-7c1f-41ad-b1a6-a6d920f70599
Exenatide is a human glucacon-like peptide-1(GLP-1) receptor agonist. By activating this receptor, insulin secretion is increased and glucagon secretion is decreased in a glucose dependant manner. Exenatide also slows gastric emptying and decreases food intake. These effects work synergistically to improve glycemic control by reducing the likelihood of hyper and hypoglycemia.
Islet amyloid, formed by aggregation of human islet amyloid polypeptide (hIAPP), is associated with beta cell death in type 2 diabetes as well as in cultured and transplanted human islets. Impaired prohIAPP processing due to beta cell dysfunction is implicated in hIAPP aggregation. We examined whether the glucagon-like peptide-1 receptor (GLP-1R) agonist exenatide can restore impaired prohIAPP processing and reduce hIAPP aggregation in cultured human islets and preserve beta cell function/mass during culture conditions used in clinical islet transplantation. METHODS: Isolated human islets (n = 10 donors) were cultured with or without exenatide in normal or elevated glucose for 2 or 7 days. Beta cell apoptosis, proliferation, mass, function, cJUN N-terminal kinase (JNK) and protein kinase B (PKB) activation and amyloid formation were assessed. ProhIAPP, its intermediates and mature hIAPP were detected. Exenatide-treated islets had markedly lower JNK and caspase-3 activation and beta cell apoptosis, resulting in higher beta/alpha cell ratio and beta cell area than non-treated cultured islets. Exenatide improved beta cell function, manifested as higher insulin response to glucose and insulin content, compared with non-treated cultured islets. Phospho-PKB immunoreactivity was detectable in exenatide-treated but not untreated cultured islets. Islet culture caused impaired prohIAPP processing with decreased mature hIAPP and increased NH(2)-terminally unprocessed prohIAPP levels resulting in higher release of immature hIAPP. Exenatide restored prohIAPP processing and reduced hIAPP aggregation in cultured islets. Exenatide treatment enhances survival and function of cultured human islets and restores impaired prohIAPP processing in normal and elevated glucose conditions thereby reducing hIAPP aggregation. GLP-1R agonists may preserve beta cells in conditions associated with islet amyloid formation.
PMID:23262664 Park YJ et al; Diabetologia 56 (3): 508-19 (2013)
Incretins, such as glucagon-like peptide-1 (GLP-1), enhance glucose-dependent insulin secretion and exhibit other antihyperglycemic actions following their release into the circulation from the gut. Byetta is a GLP-1 receptor agonist that enhances glucose-dependent insulin secretion by the pancreatic beta-cell, suppresses inappropriately elevated glucagon secretion, and slows gastric emptying. The amino acid sequence of exenatide partially overlaps that of human GLP-1. Exenatide has been shown to bind and activate the human GLP-1 receptor in vitro. This leads to an increase in both glucose-dependent synthesis of insulin, and in vivo secretion of insulin from pancreatic beta cells, by mechanisms involving cyclic AMP and/or other intracellular signaling pathways.
NIH; DailyMed. Current Medication Information for Byetta (Exenatide) Injection (Revised: February 2013). Available from, as of July 21, 2014: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=751747da-7c1f-41ad-b1a6-a6d920f70599
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. /The aim of this study is/ 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 sulfide (H2S). ... The vasoactive effect of exenatide on isolated thoracic aortic rings of adult rats /was determined/. 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. 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. Exenatide induces vasodilation in rat thoracic aorta with the contribution of all three gasotransmitters. /This provides/ in vitro evidence for the potential ability of exenatide to lower central (aortic) blood pressure, which could have relevant clinical importance.
PMID:24693878 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3976540 Selley E et al; Cardiovasc Diabetol. 2014 Apr 2;13:69. doi: 10.1186/1475-2840-13-69
Glucagon-like peptide-1 receptor (GLP-1R) activation in the nucleus accumbens (NAc) core is pharmacologically and physiologically relevant for regulating palatable food intake. /An assessment was made/ whether GLP-1R signaling in the NAc core of rats modulates GABAergic medium spiny neurons (MSNs) through presynaptic-glutamatergic and/or presynaptic-dopaminergic signaling to control feeding. First, ex vivo fast-scan cyclic voltammetry showed that the GLP-1R agonist exendin-4 (Ex-4) does not alter dopamine release in the NAc core. Instead, support for a glutamatergic mechanism was provided by ex vivo electrophysiological analyses showing that Ex-4 activates presynaptic GLP-1Rs in the NAc core to increase the activity of MSNs via a glutamatergic, AMPA/kainate receptor-mediated mechanism, indicated by increased mEPSC frequency and decreased paired pulse ratio in core MSNs. Only a small, direct excitatory effect on MSNs by Ex-4 was observed, suggesting that the contribution of postsynaptic GLP-1R to MSN activity is minimal. The behavioral relevance of the electrophysiological data was confirmed by the finding that intracore injection of the AMPA/kainate receptor antagonist CNQX attenuated the ability of NAc core GLP-1R activation by Ex-4 microinjection to suppress food intake and body weight gain; in contrast, intracore NMDA receptor blockade by AP-5 did not inhibit the energy balance effects of NAc core Ex-4. Together, these data provide evidence for a novel glutamatergic, but not dopaminergic, mechanism by which NAc core GLP-1Rs promote negative energy balance.
PMID:24828651 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019807 Mietlicki-Baase EG et al; J Neurosci 34 (20): 6985-92 (2014)
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