Compounds > exenatide
Page last updated: 2024-11-12

exenatide

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth

Description

Exenatide: A synthetic form of exendin-4, a 39-amino acid peptide isolated from the venom of the Gila monster lizard (Heloderma suspectum). Exenatide increases CYCLIC AMP levels in pancreatic acinar cells and acts as a GLUCAGON-LIKE PEPTIDE-1 RECEPTOR (GLP-1) agonist and incretin mimetic, enhancing insulin secretion in response to increased glucose levels; it also suppresses inappropriate glucagon secretion and slows gastric emptying. It is used an anti-diabetic and anti-obesity agent. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID45588096
SCHEMBL ID14634818
MeSH IDM0199975
PubMed CID16157882
MeSH IDM0199975

Synonyms (34)

Synonym
bydureon
itca 650
exendin-4 ,
exenatide
exendin 4
ac 2993a
ac 2993
exendin 3 (heloderma horridum), 2-glycine-3-l-glutamic acid-
ac002993
ac2993a
bydureon pen
pt302
hsdb 7789
exenatide [usan:inn:ban:jan]
ly 2148568
9p1872d4ol ,
da 3091
unii-9p1872d4ol
AKOS015994651
HS-2012
Y-100006
exenatide; exendin-4
SCHEMBL14634818
c184h282n50o60s
(ser-39 = c-terminal amide)
HB3157
hgegtftsdlskqmeeeavrlfiewlknggpssgappps
itca-650
ac-2993lar
ac-002993
ac-2993a
da-3091
ly-2148568
exenatide free base

Research Excerpts

Toxicity

Exenatide treatment was generally well-tolerated and the incidence of severe adverse event was rare. The most frequent adverse events with exen atide and sitagliptin were nausea and diarrhoea.

ExcerptReferenceRelevance
" There were no serious adverse events and no patient withdrawals related to treatment."( Pharmacokinetics, pharmacodynamics, and safety of exenatide in patients with type 2 diabetes mellitus.
Baron, AD; Fineman, MS; Kim, DD; Kolterman, OG; Nielsen, LL; Ruggles, JA; Shen, L, 2005)		0.33
" Careful postmarketing surveillance for adverse effects, especially among the DPP4 inhibitors, and continued evaluation in longer-term studies and in clinical practice are required to determine the role of this new class among current pharmacotherapies for type 2 diabetes."( Efficacy and safety of incretin therapy in type 2 diabetes: systematic review and meta-analysis.
Amori, RE; Lau, J; Pittas, AG, 2007)		0.34
" This article reviews the profile of adverse effects for these agents in relation to their current (exenatide) and anticipated (liraglutide) role in the management of Type 2 diabetes."( Safety and adverse effects associated with GLP-1 analogues.
Bain, SC; Stephens, JW, 2007)		0.34
" This was offset, however, by an exenatide discontinuation rate of 36%, primarily due to adverse gastrointestinal effects."( Safety and efficacy of exenatide in combination with insulin in patients with type 2 diabetes mellitus.
Abelseth, JM; Bakst, G; Busch, RS; Hamilton, RA; Kane, MP; Sheffield, CA, 2008)		0.35
" Nausea, generally mild-to-moderate, was the most common adverse event with exenatide (25% vs."( Efficacy and safety of exenatide in patients of Asian descent with type 2 diabetes inadequately controlled with metformin or metformin and a sulphonylurea.
Brodows, R; Chuang, LM; Gao, Y; Jang, HC; Johns, D; Mohan, V; Ning, G; Northrup, J; Shah, S; Wu, TJ; Yoon, KH, 2009)		0.35
" All adverse events were mild or moderate in severity."( Pharmacokinetics, pharmacodynamics, tolerability, and safety of exenatide in Japanese patients with type 2 diabetes mellitus.
de la Peña, A; Fineman, M; Irie, S; Isaka, Y; Kothare, PA; Linnebjerg, H; Mace, K; Sakata, Y; Shigeta, H; Teng, CH; Uenaka, K; Yamamura, A; Yeo, KP, 2008)		0.35
" Treatment-emergent adverse events (TEAEs) at any time during the study were observed in 40 and 47% of patients with positive and negative treatment-emergent antibodies, respectively."( The effect of exenatide re-exposure on safety and efficacy.
Braun, DK; Brodows, R; Burger, J; Faludi, P; Ivanyi, T, 2009)		0.35
" No serious adverse events (AEs) were reported and no AEs led to study discontinuation in any group."( Safety, tolerability, pharmacokinetics, and pharmacodynamics of exenatide once weekly in Japanese patients with type 2 diabetes.
Iwamoto, K; Kothare, PA; Linnebjerg, H; Mace, K; Nasu, R; Wolka, AM; Yamamura, A, 2009)		0.35
" Nausea was the most common adverse event in placebo- and active-controlled trials."( Exenatide efficacy and safety: a systematic review.
Chan, BK; Lee, N; Norris, SL; Thakurta, S, 2009)		0.35
"The objective was to investigate whether varying administration time of exenatide affects the magnitude of satiety responses, blood glucose, and adverse events in healthy volunteers."( Effect of administration time of exenatide on satiety responses, blood glucose, and adverse events in healthy volunteers.
Abouhassan, A; Ayar, C; Clarke, AW; Commissaris, RL; Jaber, LA; Jaber, NA; Jantz, A; Pinelli, NR; Smith, Z, 2011)		0.37
" The most frequent adverse events with exenatide and sitagliptin were nausea (n=38, 24%, and n=16, 10%, respectively) and diarrhoea (n=29, 18%, and n=16, 10%, respectively); upper-respiratory-tract infection (n=17, 10%) and peripheral oedema (n=13, 8%) were the most frequent events with pioglitazone."( Efficacy and safety of exenatide once weekly versus sitagliptin or pioglitazone as an adjunct to metformin for treatment of type 2 diabetes (DURATION-2): a randomised trial.
Bergenstal, RM; Macconell, L; Malloy, J; Malone, J; Porter, LE; Walsh, B; Wilhelm, K; Wysham, C; Yan, P, 2010)		0.36
" No hypoglycemia or serious adverse events were reported, and exenatide was generally well tolerated in both age groups."( Exenatide - pharmacokinetics, pharmacodynamics, safety and tolerability in patients ≥ 75 years of age with Type 2 diabetes.
Kothare, PA; Linnebjerg, H; Mitchell, MI; Seger, M; Wolka, AM, 2011)		0.37
" HbA1c and weight changes, exenatide discontinuation, adverse events and treatment satisfaction were compared between non-insulin and insulin-treated patients."( Safety, efficacy and tolerability of exenatide in combination with insulin in the Association of British Clinical Diabetologists nationwide exenatide audit*.
Cull, ML; Jose, B; Mills, AP; Rigby, AS; Ryder, RE; Sathyapalan, T; Shafiq, W; Sukumar, N; Thong, KY; Walton, C, 2011)		0.37
" Adverse events were statistically but probably not clinically significantly higher, but combination treatment was less well tolerated."( Safety, efficacy and tolerability of exenatide in combination with insulin in the Association of British Clinical Diabetologists nationwide exenatide audit*.
Cull, ML; Jose, B; Mills, AP; Rigby, AS; Ryder, RE; Sathyapalan, T; Shafiq, W; Sukumar, N; Thong, KY; Walton, C, 2011)		0.37
" Customized primary major adverse CV events (MACE) included stroke, myocardial infarction, cardiac mortality, acute coronary syndrome, and revascularization procedures."( Cardiovascular safety of exenatide BID: an integrated analysis from controlled clinical trials in participants with type 2 diabetes.
Han, J; Hoogwerf, BJ; Nicewarner, D; Ratner, R; Shen, L; Yushmanova, I, 2011)		0.37
" Exenatide once-weekly was generally well tolerated and adverse events were predominantly mild or moderate in intensity."( DURATION-2: efficacy and safety of switching from maximum daily sitagliptin or pioglitazone to once-weekly exenatide.
Bergenstal, R; Malloy, J; Malone, J; Taylor, K; Walsh, B; Wysham, C; Yan, P, 2011)		0.37
"Therapeutic proteins/peptides can produce immunogenic responses that may increase the risk of adverse events or reduce efficacy."( Liraglutide treatment is associated with a low frequency and magnitude of antibody formation with no apparent impact on glycemic response or increased frequency of adverse events: results from the Liraglutide Effect and Action in Diabetes (LEAD) trials.
Brett, JH; Buse, JB; Garber, A; Holst, J; Nauck, M; Rosenstock, J; Schmidt, WE; Videbæk, N, 2011)		0.37
" Conversely, decreasing human IAPP release with diazoxide or somatostatin limited amyloid formation and its toxic effects."( Exendin-4 increases islet amyloid deposition but offsets the resultant beta cell toxicity in human islet amyloid polypeptide transgenic mouse islets.
Aston-Mourney, K; Hull, RL; Kahn, SE; Subramanian, SL; Udayasankar, J; Zraika, S, 2011)		0.37
"IAPP release is necessary for islet amyloid formation and its toxic effects."( Exendin-4 increases islet amyloid deposition but offsets the resultant beta cell toxicity in human islet amyloid polypeptide transgenic mouse islets.
Aston-Mourney, K; Hull, RL; Kahn, SE; Subramanian, SL; Udayasankar, J; Zraika, S, 2011)		0.37
"Although several classes of pharmacotherapy are available for type 2 diabetes, glycaemic control is often hampered by medication-related adverse effects and contraindications such as renal impairment."( The safety and tolerability of GLP-1 receptor agonists in the treatment of type 2 diabetes: a review.
Aroda, VR; Ratner, R, 2011)		0.37
" They provide lesser effect on PPG, similar reduction in body weight, and result in a potentially favorable adverse event profile compared with exenatide twice daily."( Efficacy and safety of long-acting glucagon-like peptide-1 receptor agonists compared with exenatide twice daily and sitagliptin in type 2 diabetes mellitus: a systematic review and meta-analysis.
Hurren, KM; Pinelli, NR, 2011)		0.37
" Common adverse events were as follows: EQW, nausea (11."( Efficacy and safety of exenatide once weekly versus metformin, pioglitazone, and sitagliptin used as monotherapy in drug-naive patients with type 2 diabetes (DURATION-4): a 26-week double-blind study.
Boardman, MK; Chan, M; Cuddihy, RM; González, JG; Hanefeld, M; Kumar, A; Russell-Jones, D; Wolka, AM, 2012)		0.38
" GLP-1 agonists have been well tolerated, with the most common adverse effects being gastrointestinal related, which occurred early in therapy but typically resolved after 4-8 weeks."( Clinical efficacy and safety of once-weekly glucagon-like peptide-1 agonists in development for treatment of type 2 diabetes mellitus in adults.
Brackett, A; Harris, K; Tzefos, M, 2012)		0.38
" Other than injection-site reactions, adverse event rates in antibody-positive and antibody-negative patients were similar."( Clinical relevance of anti-exenatide antibodies: safety, efficacy and cross-reactivity with long-term treatment.
Booker Porter, TK; Cirincione, BB; Darsow, T; Diamant, M; Fineman, MS; Kinninger, LA; Mace, KF; Trautmann, ME, 2012)		0.38
" No serious adverse event was observed."( Effects of intravenous exenatide in type 2 diabetic patients with congestive heart failure: a double-blind, randomised controlled clinical trial of efficacy and safety.
Frick, M; Hedman, A; Löfström, U; Nathanson, D; Nyström, T; Sjöholm, A; Ullman, B, 2012)		0.38
" Gastrointestinal adverse effects and injection site reactions are common, but rarely lead to drug discontinuation."( Review of the safety and efficacy of exenatide once weekly for the treatment of type 2 diabetes mellitus.
Murphy, CE, 2012)		0.38
" Between-group differences in adverse event (AE) and hypoglycaemia incidences were calculated."( Comparison of safety and tolerability with continuous (exenatide once weekly) or intermittent (exenatide twice daily) GLP-1 receptor agonism in patients with type 2 diabetes.
Han, J; MacConell, L; Moretto, T; Pencek, R; Porter, L; Ridge, T; Schulteis, C, 2012)		0.38
"Both exenatide formulations were generally safe and well-tolerated, with ExQW associated with less nausea and vomiting but more injection-site AEs."( Comparison of safety and tolerability with continuous (exenatide once weekly) or intermittent (exenatide twice daily) GLP-1 receptor agonism in patients with type 2 diabetes.
Han, J; MacConell, L; Moretto, T; Pencek, R; Porter, L; Ridge, T; Schulteis, C, 2012)		0.38
" The most common adverse events overall were nausea (38."( Exenatide twice daily: analysis of effectiveness and safety data stratified by age, sex, race, duration of diabetes, and body mass index.
Anderson, PW; Blickensderfer, A; Brunell, SC; Li, Y; Pencek, R, 2012)		0.38
" Gastrointestinal events were the most common adverse events."( Exenatide twice daily: analysis of effectiveness and safety data stratified by age, sex, race, duration of diabetes, and body mass index.
Anderson, PW; Blickensderfer, A; Brunell, SC; Li, Y; Pencek, R, 2012)		0.38
" This meta-analysis was aimed at evaluating the risk of those serious adverse events associated with GLP-1 agonists in patients with type 2 diabetes."( A meta-analysis of serious adverse events reported with exenatide and liraglutide: acute pancreatitis and cancer.
Alves, C; Batel-Marques, F; Macedo, AF, 2012)		0.38
" These rare and long-term adverse events deserve properly monitoring in future studies evaluating GLP-1 agonists."( A meta-analysis of serious adverse events reported with exenatide and liraglutide: acute pancreatitis and cancer.
Alves, C; Batel-Marques, F; Macedo, AF, 2012)		0.38
" The adverse event (AE) profile and effects on glycemic control have not been assessed for the glucagon-like peptide-1 receptor agonist exenatide once weekly in combination with a thiazolidinedione (TZD) with or without metformin."( Safety of exenatide once weekly in patients with type 2 diabetes mellitus treated with a thiazolidinedione alone or in combination with metformin for 2 years.
Boardman, MK; Haber, H; Liutkus, JF; Norwood, P; Pintilei, E; Trautmann, ME, 2012)		0.38
" Gastrointestinal-related and injection site-related adverse events occurred more frequently with EQW than with detemir."( Once-weekly exenatide versus once- or twice-daily insulin detemir: randomized, open-label, clinical trial of efficacy and safety in patients with type 2 diabetes treated with metformin alone or in combination with sulfonylureas.
Adetunji, O; Davies, M; Heller, S; Sapin, H; Sreenan, S; Tahbaz, A; Vora, J, 2013)		0.39
" was generally well tolerated, and the majority of adverse events reported were mild in severity."( Pharmacokinetics, safety, and tolerability of single- and multiple-dose exenatide once weekly in Chinese patients with type 2 diabetes mellitus.
Cui, YM; Guo, XH; Linnebjerg, H; Mace, K; Tang, CC; Tham, LS; Zhang, DM, 2013)		0.39
" has a pharmacokinetic profile in this patient population similar to that observed in other ethnic and racial populations, and appears to be safe and generally well tolerated, with the potential to improve glycemic control and decrease body weight without increasing the risk of hypoglycemia."( Pharmacokinetics, safety, and tolerability of single- and multiple-dose exenatide once weekly in Chinese patients with type 2 diabetes mellitus.
Cui, YM; Guo, XH; Linnebjerg, H; Mace, K; Tang, CC; Tham, LS; Zhang, DM, 2013)		0.39
"5%) placebo-treated patients reported one or more treatment-emergent adverse events; nausea was the most frequently reported side effect (exenatide, 4 [15."( Safety and efficacy of twice-daily exenatide in Taiwanese patients with inadequately controlled type 2 diabetes mellitus.
Chuang, LM; Lu, CH; Ni, E; Reed, V; Sheu, WH; Shih, KC; Wu, TJ; Yu, M, 2013)		0.39
" Transient, mild-to-moderate gastrointestinal treatment-emergent adverse events and injection-site treatment-emergent adverse events were reported most frequently, but were seldom treatment limiting."( Efficacy, safety, and tolerability of exenatide once weekly in patients with type 2 diabetes mellitus: an integrated analysis of the DURATION trials.
Dong, H; Griffin, P; Grimm, M; Han, J; Malloy, J; Schulteis, CT; Weaver, C, 2013)		0.39
"Drugs are designed for therapy, but medication-related adverse events are common, and risk/benefit analysis is critical for determining clinical use."( Systems pharmacology of adverse event mitigation by drug combinations.
Azeloglu, EU; Badimon, JJ; Benard, L; Chen, Y; Giannarelli, C; Goldfarb, J; Gottesman, O; Hajjar, RJ; Iyengar, R; Nishimura, T; Zafar, MU; Zhao, S, 2013)		0.39
" The most common gastrointestinal adverse events for dulaglutide were nausea, vomiting, and diarrhea."( Efficacy and safety of dulaglutide added onto pioglitazone and metformin versus exenatide in type 2 diabetes in a randomized controlled trial (AWARD-1).
Arakaki, R; Atisso, C; Blevins, T; Colon, G; Garcia, P; Kuhstoss, D; Lakshmanan, M; Wysham, C, 2014)		0.4
"Available evidence about safety, tolerability and potential adverse events relative to GLP-1Rx agonists presently used."( Potential side effects to GLP-1 agonists: understanding their safety and tolerability.
Consoli, A; Formoso, G, 2015)		0.42
" Long-term safety data included adverse events, liver and renal function, and heart rate."( Five-year efficacy and safety data of exenatide once weekly: long-term results from the DURATION-1 randomized clinical trial.
Griffin, PS; MacConell, LA; Maggs, DG; Trautmann, ME; Wysham, CH; Zhou, M, 2015)		0.42
" The main adverse effects of treatment included gastrointestinal and injection site reactions."( Efficacy and safety of once-weekly glucagon-like peptide 1 receptor agonists for the management of type 2 diabetes: a systematic review and meta-analysis of randomized controlled trials.
Athanasiadou, E; Bekiari, E; Boura, P; Karagiannis, T; Liakos, A; Mainou, M; Matthews, DR; Paschos, P; Rika, M; Tsapas, A; Vasilakou, D, 2015)		0.42
"Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are increasingly being used for the treatment of type 2 diabetes mellitus, but consideration of benefits and potential adverse events is required."( Glucagon-Like Peptide-1 Receptor Agonists for Type 2 Diabetes: A Clinical Update of Safety and Efficacy.
Drab, SR, 2016)		0.43
" This meta-analysis revealed the use of dulaglutide as a monotherapy or an add-on to OAM and lispro appeared to be effective and safe for adults with T2DM."( Efficacy and safety of dulaglutide in patients with type 2 diabetes: a meta-analysis and systematic review.
Tong, N; Zhang, L; Zhang, M; Zhang, Y, 2016)		0.43
"Exenatide, metformin (MET), and biphasic insulin aspart 30 (BIA30) have been widely used in the treatment of patients with type 2 diabetes mellitus (T2DM); however, each of these medications has significant adverse effects, which limit their utilization."( Phase III Study on Efficacy and Safety of Triple Combination (Exenatide/Metformin/Biphasic Insulin Aspart) Therapy for Type 2 Diabetes Mellitus.
Bai, Y; Ji, Z; Liu, Y; Lv, C; Su, K; Wang, H; Wang, Y, )		0.13
"7%) were the most common adverse events."( Efficacy and Safety of Multiple Doses of Exenatide Once-Monthly Suspension in Patients With Type 2 Diabetes: A Phase II Randomized Clinical Trial.
Hardy, E; MacConell, L; Wysham, CH, 2016)		0.43
" Our main end-points were control of glycaemia, body weight, hypoglycaemia and gastrointestinal adverse events (AEs)."( Efficacy and safety of once-weekly glucagon-like peptide-1 receptor agonists compared with exenatide and liraglutide in type 2 diabetes: a systemic review of randomised controlled trials.
Liu, F; Ren, Z; Xue, X; Yang, Q; Zhang, A; Zhang, W, 2016)		0.43
" The aim of this study was to assess the risk of adverse events (AEs) with GLP-1 RAs and their relation to dose, background medication and duration of action."( Occurrence of nausea, vomiting and diarrhoea reported as adverse events in clinical trials studying glucagon-like peptide-1 receptor agonists: A systematic analysis of published clinical trials.
Abd El Aziz, MS; Bettge, K; Kahle, M; Meier, JJ; Nauck, MA, 2017)		0.46
"The RCTs in the present analysis show that all GLP-1RAs improve glycaemic control, reduce body weight and increase the risk of adverse gastrointestinal symptoms compared with placebo."( Efficacy and safety of glucagon-like peptide-1 receptor agonists in type 2 diabetes: A systematic review and mixed-treatment comparison analysis.
Davies, MJ; Htike, ZZ; Khunti, K; Papamargaritis, D; Webb, DR; Zaccardi, F, 2017)		0.46
"To characterize gastrointestinal adverse events (AEs) with different glucagon-like peptide-1 receptor agonists (GLP-1RAs)."( Upper and/or lower gastrointestinal adverse events with glucagon-like peptide-1 receptor agonists: Incidence and consequences.
Aroda, VR; Han, J; Hardy, E; Horowitz, M; Rayner, CK, 2017)		0.46
" The most common adverse events with exenatide QWS-AI were gastrointestinal events and injection-site reactions."( Efficacy and safety of autoinjected exenatide once-weekly suspension versus sitagliptin or placebo with metformin in patients with type 2 diabetes: The DURATION-NEO-2 randomized clinical study.
Gadde, KM; Hardy, E; Iqbal, N; Öhman, P; Vetter, ML, 2017)		0.46
" Adverse events and adverse drug reactions were estimated in patients who were treated with exenatide at least once and for whom follow-up for safety has been completed."( Effectiveness and safety of exenatide in Korean patients with type 2 diabetes inadequately controlled with oral hypoglycemic agents: an observational study in a real clinical practice.
Cho, JH; Hwang, YC; Jo, E; Kim, A; Lee, BW; Yang, Y, 2017)		0.46
" In terms of safety profile, exenatide treatment was generally well-tolerated and the incidence of severe adverse event was rare (0."( Effectiveness and safety of exenatide in Korean patients with type 2 diabetes inadequately controlled with oral hypoglycemic agents: an observational study in a real clinical practice.
Cho, JH; Hwang, YC; Jo, E; Kim, A; Lee, BW; Yang, Y, 2017)		0.46
"Lipotoxicity cardiomyopathy is the result of excessive accumulation and oxidation of toxic lipids in the heart."( Glucagon-like peptide-1 ameliorates cardiac lipotoxicity in diabetic cardiomyopathy via the PPARα pathway.
Liu, L; Wang, DW; Wang, K; Wang, P; Wang, W; Wen, Z; Wu, L, 2018)		0.48
" However, there are key differences within this class of drugs in macrovascular, microvascular, gastrointestinal and injection-site reaction adverse events, and these should be considered when healthcare providers are prescribing therapy."( Safety of Once-weekly Glucagon-like Peptide-1 Receptor Agonists in Patients with Type 2 Diabetes.
Frias, JP, 2018)		0.48
" Gastrointestinal adverse events (e."( Glycemic Efficacy, Weight Effects, and Safety of Once-Weekly Glucagon-Like Peptide-1 Receptor Agonists.
Cannon, A; Handelsman, Y; Schneider, D; Shannon, M; Wyne, K, 2018)		0.48
" Following determination of the significant toxic doses of glucose and fructose, the cells were treated with various doses of exenatide (10-250 nM) in the presence or absence of glucose and fructose."( The investigation of protective effects of glucagon-like peptide-1 (GLP-1) analogue exenatide against glucose and fructose-induced neurotoxicity.
Khalilnezhad, A; Taskiran, D, 2019)		0.51
" Expert opinion: Exenatide QW is an efficacious and safe treatment for T2D."( The efficacy and safety of exenatide once weekly in patients with type 2 diabetes.
Brønden, A; Dejgaard, TF; Heimbürger, SM; Johansen, NJ; Knop, FK; Vilsbøll, T, 2019)		0.51
" There was no serious adverse event related to the study drug."( Efficacy and safety of once-weekly exenatide after switching from twice-daily exenatide in patients with type 2 diabetes.
Imai, T; Inaishi, J; Irie, J; Itoh, H; Kanazawa, Y; Kou, K; Masaoka, T; Meguro, S; Murakami, R; Okubo, Y; Saisho, Y; Sasaki, H; Tokui, M; Tsuchiya, T; Watanabe, Y; Yamauchi, A, 2020)		0.56
" Except for the 5-µg and 10-µg groups, the safety and tolerability tests showed no adverse reactions in the 2-µg to 50-µg groups."( Safety, Tolerability and Pharmacokinetics of Single Dose Polyethylene Glycolated Exenatide Injection (PB-119) in Healthy Volunteers.
Cui, H; Li, Y; Liu, Y; Lv, Y; Tian, JH; Wei, MJ; Xia, YH; Zhang, P; Zhao, CY; Zhu, Y, 2020)		0.56
"The administration of polyethylene glycolated exenatide injection at a single dose of 2-200 µg is safe and tolerable for healthy volunteers."( Safety, Tolerability and Pharmacokinetics of Single Dose Polyethylene Glycolated Exenatide Injection (PB-119) in Healthy Volunteers.
Cui, H; Li, Y; Liu, Y; Lv, Y; Tian, JH; Wei, MJ; Xia, YH; Zhang, P; Zhao, CY; Zhu, Y, 2020)		0.56
" The incidence of adverse events, including the incidence of hypoglycemia (18."( Efficacy and safety of generic exenatide injection in Chinese patients with type 2 diabetes: a multicenter, randomized, controlled, non-inferiority trial.
Gao, Y; Guo, L; Hong, T; Li, Q; Tian, Q; Xiao, W; Yang, J; Zhong, L, 2020)		0.56
" All long-acting GLP-1RAs have, at minimum, been shown to be safe and not increase cardiovascular (CV) risk and most (liraglutide, semaglutide injectable, dulaglutide, albiglutide) have been shown in CV outcomes trials (CVOTs) to significantly reduce the risk of major cardiac adverse events."( Long-acting GLP-1RAs: An overview of efficacy, safety, and their role in type 2 diabetes management.
Butts, A; Chun, JH, 2020)		0.56
" Extracted safety data included gastrointestinal (GI) adverse events (AEs), hypoglycaemia, injection-site reactions, pancreatitis, neoplasms, gallbladder events, and diabetic retinopathy (DR) and/or its complications (DRCs)."( Safety and tolerability of once-weekly GLP-1 receptor agonists in type 2 diabetes.
Trujillo, J, 2020)		0.56
" However, GLP-1RAs treatments had more gastrointestinal adverse events (such as nausea and vomiting) than placebo and Met."( The Antiobesity Effect and Safety of GLP-1 Receptor Agonist in Overweight/Obese Patients Without Diabetes: A Systematic Review and Meta-Analysis.
Gong, F; Guo, X; Lyu, X; Pan, H; Wang, L; Xu, H; Yang, H; Zhou, Z; Zhu, H, 2022)		0.72
" There were no significant differences between treatments in the incidence of adverse events, except that liraglutide+metformin had significant adverse effect such as abdominal pain."( Comparative efficacy and safety of glucose-lowering drugs in children and adolescents with type 2 diabetes: A systematic review and network meta-analysis.
Feng, Y; Ge, Y; He, Y; Hou, L; Huo, M; Ji, Y; Li, H; Liu, X; Liu, Y; Luo, Q; Qian, F; Wang, J; Wei, Y; Wu, S; Wu, Y; Xue, F; Yu, Y, 2022)		0.72
" Randomized clinical trials (RCTs) comparing pharmacological interventions in children with obesity are scarce; therefore, we aimed to analyze the relative efficacy and adverse reactions of these drugs and compare the effects of each drug on body mass index (BMI)."( Comparison of weight loss and adverse events of obesity drugs in children and adolescents: a systematic review and meta-analysis.
Liu, H; Wu, F; Xie, Y; Yin, S; Zhang, Q; Zhao, G, 2022)		0.72
" However, it was most associated with drug withdrawal due to adverse events while topiramate was least."( Comparison of weight loss and adverse events of obesity drugs in children and adolescents: a systematic review and meta-analysis.
Liu, H; Wu, F; Xie, Y; Yin, S; Zhang, Q; Zhao, G, 2022)		0.72
"The study aimed to determine whether GLP-1RAs are associated with increased detection of pancreatic carcinoma based on the FDA Adverse Events Reporting System and clarify its potential mechanisms through keyword co-occurrence analysis from literature database."( Glucagon-like peptide 1 receptor agonists and the potential risk of pancreatic carcinoma: a pharmacovigilance study using the FDA Adverse Event Reporting System and literature visualization analysis.
Cao, M; Pan, C; Tian, Y; Wang, L; Zhao, Z; Zhu, B, 2023)		0.91

Pharmacokinetics

The pharmacokinetics of polyethylene glycolated exenatide was studied in 36 subjects. It showed slow absorption, a mean peak time of 20-40 h, and a mean elimination half-life of 51-64 h. The aim of the present analysis was to develop a core population pharmacokinetic model.

ExcerptReferenceRelevance
"The purpose of this study is to ascertain the pharmacodynamic properties of exendin-4, a glucose-dependent insulinotropic agent, from plasma glucose and insulin concentration-time profiles following a 60-min intravenous infusion in healthy and type 2 diabetic subjects."( Exendin-4 pharmacodynamics: insights from the hyperglycemic clamp technique.
Abernethy, DR; Egan, JM; Elahi, D; Mager, DE, 2004)		0.32
"In both studies, plasma exenatide pharmacokinetic profiles appeared dose proportional."( Pharmacokinetics, pharmacodynamics, and safety of exenatide in patients with type 2 diabetes mellitus.
Baron, AD; Fineman, MS; Kim, DD; Kolterman, OG; Nielsen, LL; Ruggles, JA; Shen, L, 2005)		0.33
" injection resulted in dose-proportional exenatide pharmacokinetics and antidiabetic pharmacodynamic activity."( Pharmacokinetics, pharmacodynamics, and safety of exenatide in patients with type 2 diabetes mellitus.
Baron, AD; Fineman, MS; Kim, DD; Kolterman, OG; Nielsen, LL; Ruggles, JA; Shen, L, 2005)		0.33
" Digoxin urinary pharmacokinetic parameters were not altered."( Effect of exenatide on the steady-state pharmacokinetics of digoxin.
Chan, C; Kothare, PA; Lim, M; Linnebjerg, H; Mace, KF; Park, S; Soon, DK; Wise, SD; Yeo, A, 2005)		0.33
"Despite observed changes in lovastatin bioavailability in the pharmacokinetic drug interaction study, exenatide did not negatively affect long-term lipid profiles or statin dosage in patients with concurrent statin therapy."( Exenatide effects on statin pharmacokinetics and lipid response.
Fineman, M; Han, J; Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, M; Pena, A; Reddy, S; Skrivanek, Z, 2007)		0.34
"Exenatide, 5 microg and 10 microg, was rapidly absorbed with a median tmax of 1 h after single and multiple doses."( Exenatide pharmacokinetics in healthy Chinese subjects.
Cui, YM; Kothare, P; Linnebjerg, H; Mace, K; Soon, D; Teng, LL; Tham, LS; Yeo, KP; Zhang, HL; Zhao, X; Zhou, Y, 2008)		0.35
"Exenatide was rapidly absorbed, with similar pharmacokinetic properties following single and multiple doses."( Exenatide pharmacokinetics in healthy Chinese subjects.
Cui, YM; Kothare, P; Linnebjerg, H; Mace, K; Soon, D; Teng, LL; Tham, LS; Yeo, KP; Zhang, HL; Zhao, X; Zhou, Y, 2008)		0.35
" For the evaluable pharmacokinetic population, geometric mean (90% confidence interval) steady-state plasma concentrations (pg/mL) were 81."( Safety, tolerability, pharmacokinetics, and pharmacodynamics of exenatide once weekly in Japanese patients with type 2 diabetes.
Iwamoto, K; Kothare, PA; Linnebjerg, H; Mace, K; Nasu, R; Wolka, AM; Yamamura, A, 2009)		0.35
" The primary pharmacodynamic parameters were baseline-adjusted 24-hour mean systolic and diastolic blood pressure."( The effect of exenatide on lisinopril pharmacodynamics and pharmacokinetics in patients with hypertension.
Kothare, P; Linnebjerg, H; Mace, K; Mitchell, M; Park, S, 2009)		0.35
" The aim of this work is to estimate the population pharmacokinetics of liraglutide and make a comparison to the pharmacokinetic profile of exenatide."( Population pharmacokinetics of liraglutide, a once-daily human glucagon-like peptide-1 analog, in healthy volunteers and subjects with type 2 diabetes, and comparison to twice-daily exenatide.
Ingwersen, SH; Jacobsen, LV; Jonker, DM; Watson, E, 2010)		0.36
" These molecules, called CovX-Bodies, maintain both the pharmacologic properties of a given peptide and the pharmacokinetic properties of a monoclonal antibody."( Combined use of immunoassay and two-dimensional liquid chromatography mass spectrometry for the detection and identification of metabolites from biotherapeutic pharmacokinetic samples.
Del Rosario, J; Kinhikar, AG; Levin, N; Murphy, RE; Preston, R; Shields, MJ; Ward, GH, 2010)		0.36
" The pharmacokinetic and safety effects of single-dose subcutaneous administration of exenatide ER (2."( Pharmacokinetics and pharmacodynamics of exenatide extended-release after single and multiple dosing.
Aisporna, M; Cirincione, B; Diamant, M; Fineman, M; Flanagan, S; Kothare, P; Li, WI; MacConell, L; Mace, KF; Shen, LZ; Taylor, K; Walsh, B, 2011)		0.37
" Pharmacokinetic parameters for exenatide after subcutaneous administration of a single dose of 5-10 μg were as follows: Cmax=77."( Pharmacokinetics, pharmacodynamics, and tolerability of a generic formulation of exenatide: a randomized, open-label, single- and multiple-dose study in healthy Chinese volunteers.
Li, Z; Liu, Y; Shi, S; Wu, J; Zeng, F; Zhou, X, 2012)		0.38
" Single- (Day 8) and multiple-dose (Day 22) pharmacokinetic profiles were assessed for each treatment period."( Effect of exenatide on the pharmacokinetics of a combination oral contraceptive in healthy women: an open-label, randomised, crossover trial.
Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, MI; Northrup, J; Seger, ME, 2012)		0.38
" Single-dose oral contraceptive administration 30 minutes after exenatide resulted in mean (90% CI) Cmax reductions of 46% (42-51%) and 41% (35-47%) for EE and LV, respectively."( Effect of exenatide on the pharmacokinetics of a combination oral contraceptive in healthy women: an open-label, randomised, crossover trial.
Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, MI; Northrup, J; Seger, ME, 2012)		0.38
"The observed reduction in Cmax is likely of limited importance given the unaltered oral contraceptive bioavailability and trough concentrations; however, for oral medications that are dependent on threshold concentrations for efficacy, such as contraceptives and antibiotics, patients should be advised to take those drugs at least 1 hour before exenatide injection."( Effect of exenatide on the pharmacokinetics of a combination oral contraceptive in healthy women: an open-label, randomised, crossover trial.
Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, MI; Northrup, J; Seger, ME, 2012)		0.38
"45 h(-1), and the two-compartment model well described its pharmacokinetic profile."( Pharmacokinetic/pharmacodynamic studies on exenatide in diabetic rats.
Chen, Y; Li, L; Li, XG; Lu, W; Ren, YP; Zhou, TY; Zhou, X, 2012)		0.38
" After obtained the conjugate we confirmed its glucose-lowering activity in normal mice and determined its half-life in SD rats."( A site-specific PEGylated analog of exendin-4 with improved pharmacokinetics and pharmacodynamics in vivo.
Gao, M; Gao, X; Jin, Y; Tian, H; Tong, Y; Yao, W, 2012)		0.38
" In SD rats its half-life was prolonged to 27."( A site-specific PEGylated analog of exendin-4 with improved pharmacokinetics and pharmacodynamics in vivo.
Gao, M; Gao, X; Jin, Y; Tian, H; Tong, Y; Yao, W, 2012)		0.38
" The GLP-1-RA are administered subcutaneously and differ substantially in pharmacokinetic profiles."( GLP-1 agonists for type 2 diabetes: pharmacokinetic and toxicological considerations.
Christensen, M; Jespersen, MJ; Knop, FK, 2013)		0.39
" The difference in chemical structure have strong implications for key pharmacokinetic parameters such as absorption and clearance, and eventually the safety and efficacy of the individual GLP-1-RA."( GLP-1 agonists for type 2 diabetes: pharmacokinetic and toxicological considerations.
Christensen, M; Jespersen, MJ; Knop, FK, 2013)		0.39
" Human pharmacokinetic profiles following IV and SC administration were simulated using the final model structure and parameter estimates and compared to clinical data."( Interspecies modeling and prediction of human exenatide pharmacokinetics.
Chen, T; Kagan, L; Mager, DE, 2013)		0.39
" Pharmacokinetic parameters of exenatide, fasting plasma glucose (FPG), HbA1c, and body weight were summarized using descriptive statistics."( Pharmacokinetics, safety, and tolerability of single- and multiple-dose exenatide once weekly in Chinese patients with type 2 diabetes mellitus.
Cui, YM; Guo, XH; Linnebjerg, H; Mace, K; Tang, CC; Tham, LS; Zhang, DM, 2013)		0.39
" has a pharmacokinetic profile in this patient population similar to that observed in other ethnic and racial populations, and appears to be safe and generally well tolerated, with the potential to improve glycemic control and decrease body weight without increasing the risk of hypoglycemia."( Pharmacokinetics, safety, and tolerability of single- and multiple-dose exenatide once weekly in Chinese patients with type 2 diabetes mellitus.
Cui, YM; Guo, XH; Linnebjerg, H; Mace, K; Tang, CC; Tham, LS; Zhang, DM, 2013)		0.39
"The purpose of this study is to investigate the effect of exenatide on glycemic control following two administration routes in a streptozotocin/nicotinamide (STZ/NA)-induced diabetic rat model, and to develop a pharmacodynamic model to better understand the disease progression and the action of exenatide in this experimental system."( Population pharmacodynamic modeling of exenatide after 2-week treatment in STZ/NA diabetic rats.
Chen, T; Kagan, L; Mager, DE, 2013)		0.39
"The aim of this study was to evaluate the pharmacokinetic properties, pharmacodynamic properties, and tolerability of PT302 after a single subcutaneous injection in healthy individuals."( Pharmacokinetic properties and effects of PT302 after repeated oral glucose loading tests in a dose-escalating study.
Cho, SH; Gu, N; Jang, IJ; Kim, J; Lee, H; Lim, KS; Seol, E; Shin, D; Shin, SG; Yu, KS, 2014)		0.4
" Noncompartmental analysis was performed to assess the pharmacokinetic characteristics of PT302."( Pharmacokinetic properties and effects of PT302 after repeated oral glucose loading tests in a dose-escalating study.
Cho, SH; Gu, N; Jang, IJ; Kim, J; Lee, H; Lim, KS; Seol, E; Shin, D; Shin, SG; Yu, KS, 2014)		0.4
"PT302 exhibits a biphasic pharmacokinetic profile, with the initial peak occurring 2 hours after administration."( Pharmacokinetic properties and effects of PT302 after repeated oral glucose loading tests in a dose-escalating study.
Cho, SH; Gu, N; Jang, IJ; Kim, J; Lee, H; Lim, KS; Seol, E; Shin, D; Shin, SG; Yu, KS, 2014)		0.4
"The pharmacokinetic characteristics of PT302 were biphasic and dose proportional."( Pharmacokinetic properties and effects of PT302 after repeated oral glucose loading tests in a dose-escalating study.
Cho, SH; Gu, N; Jang, IJ; Kim, J; Lee, H; Lim, KS; Seol, E; Shin, D; Shin, SG; Yu, KS, 2014)		0.4
" Using hybrid PK/PD model, simulations were done to explore the potential dosing regimens which could achieve likelihood of more pharmacodynamic exposure with respect to FPG and HbA1c over a much shorter period compared with the currently used treatment protocol."( Target-mediated pharmacokinetic/pharmacodynamic model based meta-analysis and dosing regimen optimization of a long-acting release formulation of exenatide in patients with type 2 diabetes mellitus.
Fan, X; Li, H; Xu, J, 2015)		0.42
"Our work identifies sources of potential pharmacokinetic variability relating to the method of delivery and the drug's formulation that will be valuable to investigators contemplating the delivery of peptides via insulin infusion pumps."( Pharmacokinetics and Tolerability of Exenatide Delivered by 7-Day Continuous Subcutaneous Infusion in Healthy Volunteers.
Chism, JP; Gruenloh, CJ; Johnson, SL; Lin, J; Nunez, DJ; Vlasakakis, G; Yao, X, 2015)		0.42
" The purpose of this study was to examine pharmacodynamic outcomes with exenatide once weekly and to determine whether changes are secondary to weight loss and thus delayed by the sequential nature of responses."( Early Pharmacodynamic Effects of Exenatide Once Weekly in Type 2 Diabetes Are Independent of Weight Loss: A Pooled Analysis of Patient-level Data.
Han, J; Ruggles, J; Trautmann, ME, 2016)		0.43
" There were no clinically meaningful correlations between weight loss and improvements in pharmacodynamic outcomes at weeks 2, 4, or 24."( Early Pharmacodynamic Effects of Exenatide Once Weekly in Type 2 Diabetes Are Independent of Weight Loss: A Pooled Analysis of Patient-level Data.
Han, J; Ruggles, J; Trautmann, ME, 2016)		0.43
"Improvements in pharmacodynamic end points occurred early in treatment with exenatide once weekly, before steady-state plasma concentrations."( Early Pharmacodynamic Effects of Exenatide Once Weekly in Type 2 Diabetes Are Independent of Weight Loss: A Pooled Analysis of Patient-level Data.
Han, J; Ruggles, J; Trautmann, ME, 2016)		0.43
"The aim of the present analysis was to develop a core population pharmacokinetic model for the pharmacokinetic properties of immediate-release (IR) exenatide, which can be used in subsequent analyses of novel sustained-release formulations."( Population pharmacokinetics of exenatide.
Cirincione, B; Mager, DE, 2017)		0.46
"The present analysis provides a comprehensive population pharmacokinetic model for exenatide, expanding the elimination process to include both linear and nonlinear components, providing a suitable platform for a broad range of concentrations and patient conditions that can be leveraged in future modelling efforts of sustained-release exenatide formulations."( Population pharmacokinetics of exenatide.
Cirincione, B; Mager, DE, 2017)		0.46
" The goal of this analysis was to develop a pharmacokinetic model for the ER formulation following single and once-weekly multiple-dose administration."( Population Pharmacokinetics of an Extended-Release Formulation of Exenatide Following Single- and Multiple-Dose Administration.
Cirincione, B; Edwards, J; Mager, DE, 2017)		0.46
" We evaluated pharmacokinetic parameters of rE-4 and exenatide, fasting plasma glucose (FPG), 2-h postprandial blood glucose (PG2 h), glycosylated hemoglobin (HbA1c) and body weight at designated time points."( Pharmacokinetics and Preliminary Pharmacodynamics of Single- and Multiple-dose Lyophilized Recombinant Glucagon-like Peptide-1 Receptor Agonist (rE-4) in Chinese Patients with Type 2 Diabetes Mellitus.
Chen, Y; Cui, Y; Fang, Y; Guo, X; Ji, L; Lou, K; Wang, Q; Wang, Y; Xu, B; Xu, L; Zhao, X; Zhu, L, 2017)		0.46
"rE-4 twice a day has a pharmacokinetic profile similar to exenatide and rE-4 with metformin after single and multiple doses in Chinese patients with T2DM."( Pharmacokinetics and Preliminary Pharmacodynamics of Single- and Multiple-dose Lyophilized Recombinant Glucagon-like Peptide-1 Receptor Agonist (rE-4) in Chinese Patients with Type 2 Diabetes Mellitus.
Chen, Y; Cui, Y; Fang, Y; Guo, X; Ji, L; Lou, K; Wang, Q; Wang, Y; Xu, B; Xu, L; Zhao, X; Zhu, L, 2017)		0.46
" Exenatide release from PT320 exhibited a triphasic pharmacokinetic profile."( Pharmacokinetics of Exenatide in nonhuman primates following its administration in the form of sustained-release PT320 and Bydureon.
Choi, HI; Greig, NH; Jung, J; Kim, DS; Kim, HK; Li, Y; Mattison, JA; Tweedie, D; Vaughan, KL, 2019)		0.51
" Our study aimed to evaluate the safety, tolerability and pharmacokinetic characteristics of polyethylene glycolated exenatide as a single subcutaneous injection in healthy volunteers."( Safety, Tolerability and Pharmacokinetics of Single Dose Polyethylene Glycolated Exenatide Injection (PB-119) in Healthy Volunteers.
Cui, H; Li, Y; Liu, Y; Lv, Y; Tian, JH; Wei, MJ; Xia, YH; Zhang, P; Zhao, CY; Zhu, Y, 2020)		0.56
" The pharmacokinetic test was carried out in the 25- to 400-µg groups, and plasma samples were collected to determine the pharmacokinetics of polyethylene glycolated exenatide."( Safety, Tolerability and Pharmacokinetics of Single Dose Polyethylene Glycolated Exenatide Injection (PB-119) in Healthy Volunteers.
Cui, H; Li, Y; Liu, Y; Lv, Y; Tian, JH; Wei, MJ; Xia, YH; Zhang, P; Zhao, CY; Zhu, Y, 2020)		0.56
" The pharmacokinetics of polyethylene glycolated exenatide was studied in 36 subjects, which showed slow absorption, a mean peak time of 20-40 h, and a mean elimination half-life of 51-64 h."( Safety, Tolerability and Pharmacokinetics of Single Dose Polyethylene Glycolated Exenatide Injection (PB-119) in Healthy Volunteers.
Cui, H; Li, Y; Liu, Y; Lv, Y; Tian, JH; Wei, MJ; Xia, YH; Zhang, P; Zhao, CY; Zhu, Y, 2020)		0.56
"This pilot study provides validation for the value of a frequently sampled intravenous glucose tolerance test (including minimal model analysis) to provide primary data for our ongoing pharmacogenomic study of pharmacodynamic effects of semaglutide (NCT05071898)."( Acute pharmacodynamic responses to exenatide: Drug-induced increases in insulin secretion and glucose effectiveness.
Beitelshees, AL; Fan, H; Mitchell, BD; Montasser, ME; Muniyappa, R; Shuldiner, AR; Streeten, EA; Taylor, SI; Whitlatch, HB; Yazdi, ZS; Yuen, AH, 2023)		0.91

Compound-Compound Interactions

Exenatide can improve metabolic and endocrine markers, and the diversity and abundance of gut microbiota in patients with obesity with PCOS. The adverse event (AE) profile and effects on glycemic control have not been assessed for the glucagon-like peptide-1 receptor agonist.

ExcerptReferenceRelevance
"This 16-week study explored the safety of substituting exenatide for insulin in patients with type 2 diabetes using insulin in combination with oral antidiabetes agents."( Exploring the substitution of exenatide for insulin in patients with type 2 diabetes treated with insulin in combination with oral antidiabetes agents.
Brodows, RG; Davis, SN; Johns, D; Maggs, D; Northrup, JH; Xu, H, 2007)		0.34
"To evaluate the 1-year efficacy and safety of treatment with exenatide in combination with insulin (a use not approved by the US Food and Drug Administration)."( Safety and efficacy of exenatide in combination with insulin in patients with type 2 diabetes mellitus.
Abelseth, JM; Bakst, G; Busch, RS; Hamilton, RA; Kane, MP; Sheffield, CA, 2008)		0.35
"We identified 134 patients with T2DM initiating exenatide therapy in combination with insulin between April 2005 and April 2006."( Safety and efficacy of exenatide in combination with insulin in patients with type 2 diabetes mellitus.
Abelseth, JM; Bakst, G; Busch, RS; Hamilton, RA; Kane, MP; Sheffield, CA, 2008)		0.35
"Exenatide in combination with insulin in patients with T2DM was associated with significant reductions in A1C and weight after 1 year of therapy."( Safety and efficacy of exenatide in combination with insulin in patients with type 2 diabetes mellitus.
Abelseth, JM; Bakst, G; Busch, RS; Hamilton, RA; Kane, MP; Sheffield, CA, 2008)		0.35
" Under these circumstances sub-chronic administration of exendin-4 alone or particularly when combined with N-AcGIP significantly (P<0."( Antidiabetic effects of sub-chronic activation of the GIP receptor alone and in combination with background exendin-4 therapy in high fat fed mice.
Flatt, PR; Frizzell, N; Hunter, K; Irwin, N, 2009)		0.35
"When combined with lifestyle modification, exenatide treatment led to significant weight loss, improved glycemic control, and decreased blood pressure compared with lifestyle modification alone in overweight or obese participants with type 2 diabetes on metformin and/or sulfonylurea treatment."( Effects of exenatide combined with lifestyle modification in patients with type 2 diabetes.
Apovian, CM; Bergenstal, RM; Cuddihy, RM; Glass, LC; Lenox, S; Lewis, MS; Qu, Y, 2010)		0.36
"Exenatide added to TZDs alone or in combination with metformin significantly improved glycaemic control as determined by significant improvement in HbA(1c) without associated hypoglycaemia."( A placebo-controlled trial of exenatide twice-daily added to thiazolidinediones alone or in combination with metformin.
Cao, D; Liutkus, J; Northrup, J; Norwood, P; Pop, L; Rosas Guzman, J; Trautmann, M, 2010)		0.36
" Herein, the results of clinical trials assessing the efficacy, safety and tolerability of liraglutide when used in combination with either one or two oral antidiabetic therapies are summarised, then contrasted with the effects of exenatide and dipeptidyl peptidase (DPP-4) inhibitors."( Liraglutide in oral antidiabetic drug combination therapy.
Garber, AJ, 2012)		0.38
" Recent findings suggest that amylin is able to restore leptin sensitivity and when used in combination with leptin enhances body weight loss in obese rodents and humans."( Restoration of leptin responsiveness in diet-induced obese mice using an optimized leptin analog in combination with exendin-4 or FGF21.
Axelrod, DW; DeGuzman, MJ; DiMarchi, R; Grant, E; Habegger, K; Hembree, J; Holland, J; Kabra, D; Kraynov, VS; Krishna, R; Müller, TD; Ottaway, N; Perez-Tilve, D; Pfluger, PT; Pinkstaff, JK; Siladi, ME; Sullivan, LM; Tschöp, MH; Yi, CX, 2012)		0.38
" The adverse event (AE) profile and effects on glycemic control have not been assessed for the glucagon-like peptide-1 receptor agonist exenatide once weekly in combination with a thiazolidinedione (TZD) with or without metformin."( Safety of exenatide once weekly in patients with type 2 diabetes mellitus treated with a thiazolidinedione alone or in combination with metformin for 2 years.
Boardman, MK; Haber, H; Liutkus, JF; Norwood, P; Pintilei, E; Trautmann, ME, 2012)		0.38
" In FAERS, rosiglitazone usage is associated with increased occurrence of MI, but its combination with exenatide significantly reduces rosiglitazone-associated MI."( Systems pharmacology of adverse event mitigation by drug combinations.
Azeloglu, EU; Badimon, JJ; Benard, L; Chen, Y; Giannarelli, C; Goldfarb, J; Gottesman, O; Hajjar, RJ; Iyengar, R; Nishimura, T; Zafar, MU; Zhao, S, 2013)		0.39
"The effects of the dipeptidyl peptidase-4 (DPP-4) inhibitor, linagliptin, alone and in combination with voglibose or exendin-4, on glycaemic control and body weight were assessed in an animal model of type 2 diabetes."( Effect of linagliptin, alone and in combination with voglibose or exendin-4, on glucose control in male ZDF rats.
Cheetham, SC; Headland, KR; Jones, RB; Klein, T; Mark, M; Vickers, SP, 2014)		0.4
"To evaluate the cost-effectiveness of metformin combined with liraglutide or exenatide in Chinese patient with T2DM."( Long-Term Effectiveness and Cost-Effectiveness of Metformin Combined with Liraglutide or Exenatide for Type 2 Diabetes Mellitus Based on the CORE Diabetes Model Study.
Li, Y; Liu, G; Liu, S; Tian, M; Wang, Y; Zhang, X, 2016)		0.43
"Patients with T2DM from the Third Hospital of Hebei Medical University were treated with oral metformin combined with liraglutide (0."( Long-Term Effectiveness and Cost-Effectiveness of Metformin Combined with Liraglutide or Exenatide for Type 2 Diabetes Mellitus Based on the CORE Diabetes Model Study.
Li, Y; Liu, G; Liu, S; Tian, M; Wang, Y; Zhang, X, 2016)		0.43
" We investigated the effects of Ex-4 in combination with human adipose tissue-derived stem cells (ADSCs) on diabetic wound healing in a diabetic animal model."( Exendin-4 in combination with adipose-derived stem cells promotes angiogenesis and improves diabetic wound healing.
Choi, W; Hong, IS; Jun, HS; Jun, JB; Lim, JS; Seo, E, 2017)		0.46
" In this study, we evaluated metabolic properties of oral nutritional supplement epigallocatechin gallate (EGCG) in combination with GLP-1 agonist exendin-4 in a mouse model of dietary-induced diabetes and obesity."( Beneficial metabolic effects of dietary epigallocatechin gallate alone and in combination with exendin-4 in high fat diabetic mice.
Flatt, PR; Gault, VA; Millar, PJB; Pathak, NM; Pathak, V, 2018)		0.48
"EGCG alone and particularly in combination with exendin-4 exerts positive metabolic properties in HF mice."( Beneficial metabolic effects of dietary epigallocatechin gallate alone and in combination with exendin-4 in high fat diabetic mice.
Flatt, PR; Gault, VA; Millar, PJB; Pathak, NM; Pathak, V, 2018)		0.48
"Both exenatide combined with metformin and metformin monotherapy can improve metabolic and endocrine markers, and the diversity and abundance of gut microbiota in patients with obesity with PCOS."( Metagenomics study on taxonomic and functional change of gut microbiota in patients with obesity with PCOS treated with exenatide combination with metformin or metformin alone.
Chen, J; Deng, Y; Ding, XS; Gan, J; Ma, RL; Sun, AJ; Zhu, SY, 2023)		0.91
" In this meta-analysis, we aimed to compare the effectiveness and safety of exenatide alone or in combination with metformin versus metformin in patients suffering from PCOS."( Comparison of exenatide alone or combined with metformin versus metformin in the treatment of polycystic ovaries: a systematic review and meta-analysis.
Guo, Y; Hamiti, S; Hu, Y; Ma, Y; Song, X; Wang, X; Yusufu, M; Zhang, K, 2023)		0.91
" Exenatide combined with metformin was more effective in improving SHBG (MD 10."( Comparison of exenatide alone or combined with metformin versus metformin in the treatment of polycystic ovaries: a systematic review and meta-analysis.
Guo, Y; Hamiti, S; Hu, Y; Ma, Y; Song, X; Wang, X; Yusufu, M; Zhang, K, 2023)		0.91
"Exenatide alone or in combination with metformin is more effective than metformin for women with PCOS."( Comparison of exenatide alone or combined with metformin versus metformin in the treatment of polycystic ovaries: a systematic review and meta-analysis.
Guo, Y; Hamiti, S; Hu, Y; Ma, Y; Song, X; Wang, X; Yusufu, M; Zhang, K, 2023)		0.91

Bioavailability

Exenatide was well absorbed with a median t(max) of 1. It did not negatively affect long-term lipid profiles or statin dosage in patients with concurrent statin therapy.

ExcerptReferenceRelevance
"The goal of this study was to determine the relative bioavailability of exenatide injected subcutaneously into the abdomen, arm, or thigh."( A randomized, open-label, crossover study examining the effect of injection site on bioavailability of exenatide (synthetic exendin-4).
Calara, F; Carr, EM; Fineman, M; Han, J; Taylor, K; Wintle, M; Zabala, E, 2005)		0.33
"Patients with type 2 DM were randomized in an open-label, crossover study to assess relative bioavailability of exenatide (10 microg) injected into the arm and thigh versus injection into the abdomen."( A randomized, open-label, crossover study examining the effect of injection site on bioavailability of exenatide (synthetic exendin-4).
Calara, F; Carr, EM; Fineman, M; Han, J; Taylor, K; Wintle, M; Zabala, E, 2005)		0.33
" Based on animal studies, the bioavailability of exenatide after subcutaneous injection has been estimated to be between 65% and 75%."( Exenatide.
Bray, GM, 2006)		0.33
" Exenatide slows gastric emptying, which may alter the absorption rate of co-administered oral medications."( Exenatide effects on statin pharmacokinetics and lipid response.
Fineman, M; Han, J; Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, M; Pena, A; Reddy, S; Skrivanek, Z, 2007)		0.34
"Despite observed changes in lovastatin bioavailability in the pharmacokinetic drug interaction study, exenatide did not negatively affect long-term lipid profiles or statin dosage in patients with concurrent statin therapy."( Exenatide effects on statin pharmacokinetics and lipid response.
Fineman, M; Han, J; Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, M; Pena, A; Reddy, S; Skrivanek, Z, 2007)		0.34
" Bioavailability (versus intravenous administration) and C(max) per unit dose differed markedly."( Pharmacokinetics and pharmacodynamics of exenatide following alternate routes of administration.
Bhavsar, S; Chen, K; Gedulin, BR; Jodka, CM; Nielsen, LL; Parkes, DG; Smith, PA; Young, AA, 2008)		0.35
" The absolute bioavailability (BA (%)) values depend on the physichochemical characters of drugs, stereoisomer character of penetratin, and site of administration."( Efficiency of cell-penetrating peptides on the nasal and intestinal absorption of therapeutic peptides and proteins.
Eda, Y; Ikeno, Y; Kamei, N; Khafagy, el-S; Morishita, M; Takayama, K, 2009)		0.35
" This dose showed systemic bioavailability (0."( 3-Iodothyronamine: a modulator of the hypothalamus-pancreas-thyroid axes in mice.
Bigagli, E; Chiellini, G; Cinci, L; De Siena, G; Dicembrini, I; Lodovici, M; Manni, ME; Marchini, M; Raimondi, L; Saba, A; Zucchi, R, 2012)		0.38
" The absorption rate constant (k(a)) decreased with increasing doses in all three species."( Target-mediated pharmacokinetic and pharmacodynamic model of exendin-4 in rats, monkeys, and humans.
Gao, W; Jusko, WJ, 2012)		0.38
"Consistent with its effect on gastric emptying, exenatide, an injectable treatment for type 2 diabetes, may slow the absorption rate of concomitantly administered oral drugs resulting in a decrease in maximum concentration (Cmax)."( Effect of exenatide on the pharmacokinetics of a combination oral contraceptive in healthy women: an open-label, randomised, crossover trial.
Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, MI; Northrup, J; Seger, ME, 2012)		0.38
"Exenatide did not alter the bioavailability nor decrease daily trough concentrations for either oral contraceptive component."( Effect of exenatide on the pharmacokinetics of a combination oral contraceptive in healthy women: an open-label, randomised, crossover trial.
Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, MI; Northrup, J; Seger, ME, 2012)		0.38
"The observed reduction in Cmax is likely of limited importance given the unaltered oral contraceptive bioavailability and trough concentrations; however, for oral medications that are dependent on threshold concentrations for efficacy, such as contraceptives and antibiotics, patients should be advised to take those drugs at least 1 hour before exenatide injection."( Effect of exenatide on the pharmacokinetics of a combination oral contraceptive in healthy women: an open-label, randomised, crossover trial.
Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, MI; Northrup, J; Seger, ME, 2012)		0.38
" The bioavailability of the exenatide-loaded microspheres, relative to subcutaneous injection of exenatide, reached 10."( Oral delivery of exenatide via microspheres prepared by cross-linking of alginate and hyaluronate.
Chen, Y; Fan, Y; He, D; Liu, N; Zhang, B, 2014)		0.4
" Orally bioavailable orthosteric small-molecule agonists are unlikely to be developed, whereas positive allosteric modulators (PAMs) may offer an improved therapeutic profile."( A Duplexed High-Throughput Screen to Identify Allosteric Modulators of the Glucagon-Like Peptide 1 and Glucagon Receptors.
Days, EL; Lindsley, CW; Mi, D; Morris, LC; Niswender, KD; Turney, M; Weaver, CD, 2014)		0.4
" Although several limited studies demonstrated non-invasive means of protein delivery, major hurdles for commercial success such as short half-life, enzymatic degradation and low bioavailability still remain to overcome."( Thermo-reversible injectable gel based on enzymatically-chopped low molecular weight methylcellulose for exenatide and FGF 21 delivery to treat types 1 and 2 diabetes.
Cha, YH; Kim, JK; Kim, YH; Yoo, C, 2014)		0.4
" Our results demonstrate that such a system indeed improves the relative oral bioavailability of exenatide to a level of about 77% compared to subcutaneous injection due to the presence of dextran in the coating wall of the NPs which apparently promotes the lymphatic uptake in the enterocytes."( Improved oral absorption of exenatide using an original nanoencapsulation and microencapsulation approach.
Benita, S; Naraykin, N; Nassar, T; Soudry-Kochavi, L, 2015)		0.42
" In-vivo administration of the devices provided significant enhancement of drug absorption with 13- and 80-fold enhancement of relative bioavailability for insulin and exenatide compared to intestinal injections with significant increase in half-lives, thus resulting in prolonged blood glucose reduction."( Delivery of Exenatide and Insulin Using Mucoadhesive Intestinal Devices.
Anselmo, AC; Banerjee, A; Doshi, N; Gupta, V; Hwang, BH; Mitragotri, S, 2016)		0.43
" Cocaine acts by altering DA bioavailability by targeting the DAT."( Glucagon-like peptide 1 receptor activation regulates cocaine actions and dopamine homeostasis in the lateral septum by decreasing arachidonic acid levels.
Bering, T; Bluett, RJ; Erreger, K; Fink-Jensen, A; Galli, A; Graham, D; Hackett, TA; Osses, N; Patel, S; Pino, JA; Reddy, IA; Reyes, JG; Stanwood, GD; Sørensen, G; Torres, GE; Valle, C; Weikop, P; Wortwein, G, 2016)		0.43
" The mean bioavailability was 20% relative to subcutaneous administration, even though it fell short of 1% when exendin-4 alone was administered nasally."( Biocompatible Polymers Modified with d-Octaarginine as an Absorption Enhancer for Nasal Peptide Delivery.
Fujii, K; Higashitarumi, S; Hiwatari, KI; Ishizaki, S; Kobayashi, H; Kumagai, H; Miyata, K; Mohri, K; Ochiai, K; Sakuma, S; Shigeno, K; Tanishita, S; Tobita, E; Tsubaki, K; Ukawa, M; Yamada, M, 2018)		0.48
" While MCTs are edible oils present in many foods, including foodstuffs containing coconut and palm kernel oils, limited information is available regarding the oral and subcutaneous bioavailability of MCTs as well as safety following subcutaneous injection."( Nonclinical safety and pharmacokinetics of Miglyol 812: A medium chain triglyceride in exenatide once weekly suspension.
Baughman, T; Buss, N; Dixit, R; Gordon, C; Patterson, C; Roy, D; Ryan, P, 2018)		0.48
"Exenatide preconditioning attenuated the oxidative stress injury and promoted the myocardial function in I/R-induced myocardial injury, while the application of block copolymer PLL-PEG-PLL as a potential exenatide nanocarrier with sustained release significantly enhanced the bioavailability of exenatide."( Pharmacological Signatures of the Exenatide Nanoparticles Complex Against Myocardial Ischemia Reperfusion Injury.
Hu, B; Jin, L; Qian, P; Shen, R; Shen, X; Shen, Y; Xu, G; Zhang, X; Zhang, Y; Zhou, H, 2018)		0.48
" In rat models, a single oral dose (200 μg/kg) of EL-CSG showed a relative oral bioavailability of 19."( Long-term oral administration of Exendin-4 to control type 2 diabetes in a rat model.
Bae, YH; Kim, KS; Suzuki, K, 2019)		0.51
" This strategy increases the endogenous secretion of GLP-1 and the oral bioavailability of the GLP-1 analogue exenatide (4% bioavailability with our nanosystem)."( Novel strategy for oral peptide delivery in incretin-based diabetes treatment.
Beloqui, A; Cani, PD; Préat, V; Suriano, F; Van Hul, M; Xu, Y, 2020)		0.56
"We developed a novel nanosystem compatible with human use that synergizes its own biological effect with the effects of increasing the bioavailability of a GLP-1 analogue."( Novel strategy for oral peptide delivery in incretin-based diabetes treatment.
Beloqui, A; Cani, PD; Préat, V; Suriano, F; Van Hul, M; Xu, Y, 2020)		0.56
"Our previous mouse studies demonstrated that mean bioavailability of exendin-4, which is an injectable glucagon-like peptide-1 (GLP-1) analogue whose molecular weight (Mw) and isoelectric point (pI) are ca."( Nasal absorption enhancement of protein drugs independent to their chemical properties in the presence of hyaluronic acid modified with tetraglycine-L-octaarginine.
Igi, R; Ishizaki, S; Kobayashi, H; Kumagai, H; Miwa, T; Miyata, K; Nonomura, M; Sakuma, S; Tobita, E; Tomono, T; Ukawa, M; Yagi, H, 2020)		0.56
" When this product was administered subcutaneously to rats, it produced a comparatively constant plasma exenatide concentration that lasted for 24 days and superior bioavailability than the exenatide microspheres (EXT-MS)."( The Modified Exenatide Microspheres: PLGA-PEG-PLGA Gel and Zinc-Exenatide Complex Synergistically Reduce Burst Release and Shorten Platform Stage.
Chen, Y; Gao, X; Jiang, W; Li, D; Wang, Q; Yang, X; Zhang, X, 2023)		0.91

Dosage Studied

differences may be due to dosing device differences for exenatide QW and liraglutide, which allows the opportunity for daily self-titration dosing. It is an attractive option because it is dosed once-weekly, provides A1C lowering similar to liragsutide.

ExcerptRelevanceReference
" Exenatide administration does not cause any changes in digoxin steady-state pharmacokinetics that would be expected to have clinical sequelae; thus, dosage adjustment does not appear warranted, based on pharmacokinetic considerations."( Effect of exenatide on the steady-state pharmacokinetics of digoxin.
Chan, C; Kothare, PA; Lim, M; Linnebjerg, H; Mace, KF; Park, S; Soon, DK; Wise, SD; Yeo, A, 2005)		0.33
"The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, drug interactions, and dosage and administration of exenatide are discussed."( Exenatide.
Bray, GM, 2006)		0.33
" The recommended starting dosage is 5 microg subcutaneously twice daily within one hour before the morning and evening meals."( Exenatide.
Bray, GM, 2006)		0.33
"05 for all treatments), while post-meal dosing groups exhibited a trend towards higher insulin peaks compared with placebo."( Exenatide: effect of injection time on postprandial glucose in patients with Type 2 diabetes.
Atkins, M; de la Peña, A; Ernest, CS; Kothare, PA; Linnebjerg, H; Skrivanek, Z; Trautmann, ME, 2006)		0.33
" These data support flexible dosing of exenatide at any time within 60 min before a meal."( Exenatide: effect of injection time on postprandial glucose in patients with Type 2 diabetes.
Atkins, M; de la Peña, A; Ernest, CS; Kothare, PA; Linnebjerg, H; Skrivanek, Z; Trautmann, ME, 2006)		0.33
" The recommended dosage is 5 mug to 10 mug twice daily subcutaneously before breakfast and dinner."( Exenatide: a novel incretin mimetic agent for treating type 2 diabetes mellitus.
Lam, S; See, S, )		0.13
"This article reviews available information on the clinical pharmacology, comparative efficacy, tolerability, drug interactions, contraindications and precautions, dosage and administration, availability and storage, and cost of exenatide."( Exenatide: an incretin mimetic for the treatment of type 2 diabetes mellitus.
Baker, DE; Iltz, JL; Keith Campbell, R; Setter, SM, 2006)		0.33
" Outcome measures were the model-based beta-cell function parameters dose-response relating insulin secretion to glucose concentration, rate sensitivity, and potentiation."( Mathematical modeling shows exenatide improved beta-cell function in patients with type 2 diabetes treated with metformin or metformin and a sulfonylurea.
DeFronzo, RA; Ferrannini, E; Halseth, A; Mari, A; Nanayakkara, N; Nielsen, LL, 2006)		0.33
" In a second clinical setting, changes in lipid profiles and statin dosage over 30 weeks in patients with type 2 diabetes were retrospectively compared (n = 180 exenatide 10 microg twice daily (BID), n = 168 placebo BID) in a combined analysis of three placebo-controlled, randomized exenatide Phase 3 trials."( Exenatide effects on statin pharmacokinetics and lipid response.
Fineman, M; Han, J; Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, M; Pena, A; Reddy, S; Skrivanek, Z, 2007)		0.34
" In the exenatide Phase 3 trials, 30-week changes from baseline for low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol, triglycerides and statin dosage were not significantly different between the exenatide and placebo groups treated with statins."( Exenatide effects on statin pharmacokinetics and lipid response.
Fineman, M; Han, J; Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, M; Pena, A; Reddy, S; Skrivanek, Z, 2007)		0.34
"Despite observed changes in lovastatin bioavailability in the pharmacokinetic drug interaction study, exenatide did not negatively affect long-term lipid profiles or statin dosage in patients with concurrent statin therapy."( Exenatide effects on statin pharmacokinetics and lipid response.
Fineman, M; Han, J; Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, M; Pena, A; Reddy, S; Skrivanek, Z, 2007)		0.34
"Since tolerability and PK changes were considered clinically acceptable in patients with mild to moderate RI, it would be appropriate to administer exenatide to these patients without dosage adjustment."( Effect of renal impairment on the pharmacokinetics of exenatide.
Kothare, PA; Linnebjerg, H; Lins, R; Mace, K; Mitchell, M; Park, S; Reddy, S, 2007)		0.34
" Insulin dosage requirements were assessed."( Exenatide therapy in obese patients with type 2 diabetes mellitus treated with insulin.
Al-Atrash, F; Bhatia, R; Chaudhuri, A; Dandona, P; Mohanty, P; Viswanathan, P, 2007)		0.34
"007), and the insulin dosage requirement decreased for rapid-acting and mixed insulins (P<."( Exenatide therapy in obese patients with type 2 diabetes mellitus treated with insulin.
Al-Atrash, F; Bhatia, R; Chaudhuri, A; Dandona, P; Mohanty, P; Viswanathan, P, 2007)		0.34
" Additionally, these treatment modalities are often limited by inconvenient dosage regimens and safety and tolerability issues, the latter including hypoglycemia, bodyweight gain, edema, and gastrointestinal intolerance."( Long-acting GLP-1 analogs for the treatment of type 2 diabetes mellitus.
Knop, FK; Vilsbøll, T, 2008)		0.35
" Exenatide Cmax and AUCtau,ss were (geometric mean (90% CI)) 145 (119 - 176) pg/ml and 370 (297 - 460) pg x h/ml, respectively, after multiple dosing with 5 microg."( Exenatide pharmacokinetics in healthy Chinese subjects.
Cui, YM; Kothare, P; Linnebjerg, H; Mace, K; Soon, D; Teng, LL; Tham, LS; Yeo, KP; Zhang, HL; Zhao, X; Zhou, Y, 2008)		0.35
" The current formulation of exenatide requires twice-daily dosing (exenatide BID), and an extended-release formulation of exenatide is now in development for use as a once-weekly injection (exenatide QW)."( Exenatide once weekly for the treatment of type 2 diabetes.
Kendall, DM; Malone, J; Taylor, K; Trautmann, M; Wilhelm, K, 2009)		0.35
"To develop an improved sustained-release (SR) formulation of exenatide (a therapy for patients with type 2 diabetes mellitus) in a biweekly dosage form with therapeutic efficacy comparable to that achieved with twice-daily injections of the drug."( Pharmacokinetics and efficacy of a biweekly dosage formulation of exenatide in Zucker diabetic fatty (ZDF) rats.
Hwang, S; Kang, SH; Kim, TH; Kim, YJ; Kwak, HH; Lee, GI; Shim, CK; Shim, WS; Son, MK; Yoon, ZH; Youn, HJ, 2009)		0.35
"DA-3091 has the potential to be used safely and efficaciously in a biweekly dosing regimen."( Pharmacokinetics and efficacy of a biweekly dosage formulation of exenatide in Zucker diabetic fatty (ZDF) rats.
Hwang, S; Kang, SH; Kim, TH; Kim, YJ; Kwak, HH; Lee, GI; Shim, CK; Shim, WS; Son, MK; Yoon, ZH; Youn, HJ, 2009)		0.35
" Advances in GLP-1 receptor agonist therapy include development of agents with longer durations of activity allowing for more convenient dosing of therapies for patients with type 2 diabetes, which should lead to better patient compliance, adherence, and overall clinical outcomes."( Beyond glycemic control: treating the entire type 2 diabetes disorder.
Brunton, S, 2009)		0.35
" Exenatide delayed the time to attain maximum lisinopril concentration (tmax,ss) by 2 hours but did not significantly alter maximum lisinopril concentration (Cmax,ss) or area under the concentration-time profile (AUCtau,ss) over the 24-hour steady-state dosing interval."( The effect of exenatide on lisinopril pharmacodynamics and pharmacokinetics in patients with hypertension.
Kothare, P; Linnebjerg, H; Mace, K; Mitchell, M; Park, S, 2009)		0.35
" It was concluded that pharmacokinetic profiles estimated by modeling showed that liraglutide has pharmacokinetic properties consistent with once-daily dosing in humans and provides better pharmacokinetic coverage in comparison with twice-daily exenatide."( Population pharmacokinetics of liraglutide, a once-daily human glucagon-like peptide-1 analog, in healthy volunteers and subjects with type 2 diabetes, and comparison to twice-daily exenatide.
Ingwersen, SH; Jacobsen, LV; Jonker, DM; Watson, E, 2010)		0.36
" The HA - exendin 4 conjugates will be investigated further as a twice a week injection dosage form for clinical applications."( Long acting hyaluronate--exendin 4 conjugate for the treatment of type 2 diabetes.
Chae, SY; Hahn, SK; Kong, JH; Lee, KC; Oh, EJ, 2010)		0.36
" After reduction of the metformin dosage (500 mg twice daily) and discontinuance of exenatide as well as a reduction of his physical activity (because of joint pain) for six months, the glucose control worsened."( [Sequential treatment with insulin glargine and metformin, and exenatide in a patient with newly diagnosed type-2 diabetes].
Kress, S, 2010)		0.36
" Our aim here was to identify a dosing strategy for intraperitoneal (IP) infusion of GLP-1 homologue exendin-4 alone and with PYY(3-36) that produces a sustained reduction in daily food intake and body weight in diet-induced obese (DIO) rats."( Effects of exendin-4 alone and with peptide YY(3-36) on food intake and body weight in diet-induced obese rats.
Anders, KL; Apenteng, BA; Haver, AC; Reidelberger, RD; Steenson, SM, 2011)		0.37
"To use time trade-off (TTO) to compare patient preferences for profiles of two glucagon-like peptide (GLP-1) products for the treatment of type 2 diabetes (liraglutide and exenatide) that vary on four key attributes - efficacy (as measured by hemoglobin A(1C)), incidence of nausea, incidence of hypoglycemia, and dosing frequency (QD vs."( A comparison of preferences for two GLP-1 products--liraglutide and exenatide--for the treatment of type 2 diabetes.
Conner, C; Hammer, M; McDonald, S; Polster, M; Zanutto, E, 2010)		0.36
" Estimated preference scores from the conjoint analysis revealed that efficacy measured by hemoglobin A(1C) is the most important attribute, followed by nausea, hypoglycemia, and dosing schedule."( A comparison of preferences for two GLP-1 products--liraglutide and exenatide--for the treatment of type 2 diabetes.
Conner, C; Hammer, M; McDonald, S; Polster, M; Zanutto, E, 2010)		0.36
" To date, GLP-1 analogs are only available as injectable dosage forms, and its oral delivery is expected to provide physiological portal/peripheral concentration ratios while fostering patient compliance and adherence."( Novel glucagon-like peptide-1 analog delivered orally reduces postprandial glucose excursions in porcine and canine models.
Arbit, E; Eldor, R; Greenberg-Shushlav, Y; Kidron, M, 2010)		0.36
" Further development of this drug class in an oral dosage form is expected to enhance diabetes control and patient compliance."( Novel glucagon-like peptide-1 analog delivered orally reduces postprandial glucose excursions in porcine and canine models.
Arbit, E; Eldor, R; Greenberg-Shushlav, Y; Kidron, M, 2010)		0.36
" Average increases in insulin dosage with exenatide and placebo were 13 U/d and 20 U/d."( Use of twice-daily exenatide in Basal insulin-treated patients with type 2 diabetes: a randomized, controlled trial.
Bergenstal, RM; Buse, JB; Glass, LC; Heilmann, CR; Hoogwerf, BJ; Kwan, AY; Lewis, MS; Rosenstock, J, 2011)		0.37
" Weekly dosing resulted in steady-state plasma exenatide concentrations after 6-7 weeks."( Pharmacokinetics and pharmacodynamics of exenatide extended-release after single and multiple dosing.
Aisporna, M; Cirincione, B; Diamant, M; Fineman, M; Flanagan, S; Kothare, P; Li, WI; MacConell, L; Mace, KF; Shen, LZ; Taylor, K; Walsh, B, 2011)		0.37
" Longer-acting GLP-1 agonists are dosed less frequently, appear to be associated with less nausea, and may be associated with better rates of adherence than shorter-acting agents."( Optimizing outcomes for GLP-1 agonists.
Freeman, JS, 2011)		0.37
" To address the need to directly compare the food intake- and body weight-suppressive effects of these two GLP-1R ligands, acute and chronic dosing experiments were performed."( Comparative effects of the long-acting GLP-1 receptor ligands, liraglutide and exendin-4, on food intake and body weight suppression in rats.
Alhadeff, AL; Grill, HJ; Hayes, MR; Kanoski, SE, 2011)		0.37
" Finally, the action of GLP-1 on β-cell mass expansion is abolished in both transgenic mice and cultured β-cells with increased dosage of SirT1."( Glucagon-like peptide 1 inhibits the sirtuin deacetylase SirT1 to stimulate pancreatic β-cell mass expansion.
Bastien-Dionne, PO; Buteau, J; Gu, W; Kon, N; Valenti, L, 2011)		0.37
" Statistically significant reductions in the use or dosage of either oral glucose-lowering medications or insulin after initiating exenatide treatment were found in every observational study that assessed medication changes, including reductions in dosage of up to 75% in sulphonylureas dosages, 22% in metformin, 66% in thiazolidinediones (TZD) or TZD combination therapy and 75% in prandial insulin."( The effects of exenatide bid on metabolic control, medication use and hospitalization in patients with type 2 diabetes mellitus in clinical practice: a systematic review.
Best, JH; DeYoung, MB; Garrison, LP; Lavillotti, K, 2012)		0.38
" GLP-1R agonists-which can be dosed to pharmacologic levels-act directly upon the GLP-1R."( The pharmacologic basis for clinical differences among GLP-1 receptor agonists and DPP-4 inhibitors.
Morales, J, 2011)		0.37
" However, short-term treatment (14 weeks) with liraglutide increased b-cell maximal response capacity in a dose-response fashion."( [Protective effects of glucagon-like peptide-1 on beta-cells: preclinical and clinical data].
Consoli, A; Di Biagio, R, 2011)		0.37
" After the acute test, rats were dosed bi-daily for 14 days in which period food intake and body weight was monitored."( Liraglutide: short-lived effect on gastric emptying -- long lasting effects on body weight.
Hansen, G; Jelsing, J; Knudsen, LB; Raun, K; Tang-Christensen, M; Vrang, N, 2012)		0.38
"While both compounds exerted robust acute reductions in GE, the effect was markedly diminished following 14 days of dosing with liraglutide."( Liraglutide: short-lived effect on gastric emptying -- long lasting effects on body weight.
Hansen, G; Jelsing, J; Knudsen, LB; Raun, K; Tang-Christensen, M; Vrang, N, 2012)		0.38
" These agents allow for less-frequent dosing schedules, improved glycemic control throughout the day, and improved treatment satisfaction compared to some available agents."( Clinical efficacy and safety of once-weekly glucagon-like peptide-1 agonists in development for treatment of type 2 diabetes mellitus in adults.
Brackett, A; Harris, K; Tzefos, M, 2012)		0.38
"Once-weekly GLP-1 agonists provide similar glycemic control with weight reduction, as well as overall higher treatment satisfaction for patients because of their ease of use and need for less-frequent dosing compared to some available agents."( Clinical efficacy and safety of once-weekly glucagon-like peptide-1 agonists in development for treatment of type 2 diabetes mellitus in adults.
Brackett, A; Harris, K; Tzefos, M, 2012)		0.38
" Because of its short t1/2, Css, min could not be detected in any plasma samples prior to daily dosing on days 3-5."( Pharmacokinetics, pharmacodynamics, and tolerability of a generic formulation of exenatide: a randomized, open-label, single- and multiple-dose study in healthy Chinese volunteers.
Li, Z; Liu, Y; Shi, S; Wu, J; Zeng, F; Zhou, X, 2012)		0.38
" Using slow-cleaving linkers, the latter may provide a generic format for once-a-month dosage forms of potent drugs."( Predictable and tunable half-life extension of therapeutic agents by controlled chemical release from macromolecular conjugates.
Ashley, GW; Reid, R; Robinson, L; Santi, DV; Schneider, EL, 2012)		0.38
" Male and female ZDF rats were dosed for 13 wk with liraglutide (0."( The effects of 13 wk of liraglutide treatment on endocrine and exocrine pancreas in male and female ZDF rats: a quantitative and qualitative analysis revealing no evidence of drug-induced pancreatitis.
Jelsing, J; Jensen, AE; Knudsen, LB; Simonsen, L; Søeborg, H; Thorup, I; Vrang, N, 2012)		0.38
" Sitagliptin 100 mg daily was substituted, and glipizide was later added and its dosage adjusted over the next several months."( Combination exenatide-sitagliptin therapy used with glipizide in a patient with type 2 diabetes mellitus.
Edgerton, LP; Elmore, LK; Patel, MB; Whalin, LM, 2012)		0.38
" The future may hold interesting developments in terms of reduced dosing frequency, oral formulations and alternative therapeutic uses."( A comparison of currently available GLP-1 receptor agonists for the treatment of type 2 diabetes.
Montanya, E, 2012)		0.38
" Patients were on a stable dosage of TZD (rosiglitazone or pioglitazone) and, if applicable, metformin."( Safety of exenatide once weekly in patients with type 2 diabetes mellitus treated with a thiazolidinedione alone or in combination with metformin for 2 years.
Boardman, MK; Haber, H; Liutkus, JF; Norwood, P; Pintilei, E; Trautmann, ME, 2012)		0.38
"Peptide or protein degradation often occurs when water flows into the dosage form."( Effect of water on exenatide acylation in poly(lactide-co-glycolide) microspheres.
Li, X; Li, Y; Liang, R; Liu, W; Shi, Y; Sun, K; Wang, A, 2013)		0.39
" Many researchers have attempted to prolong the acting time of exenatide by preparing sustained-release dosage forms, modifying its structure, gene therapies, and other means."( Long-acting preparations of exenatide.
Cai, Y; Huang, X; Liu, Z; Ma, L; Tao, A; Wei, L; Yuan, W, 2013)		0.39
" Compound 10's terminal half-life of ~27 h should translate favorably to weekly dosing in humans."( Bifunctional PEGylated exenatide-amylinomimetic hybrids to treat metabolic disorders: an example of long-acting dual hormonal therapeutics.
Forood, B; Ghosh, SS; Griffin, P; Jodka, CM; Neravetla, S; Parkes, DG; Sun, C; Trevaskis, JL; Wang, Y; Xu, K, 2013)		0.39
" After dosing for 4 weeks, exenatide, dapagliflozin and exenatide + dapagliflozin similarly decreased haemoglobin A1c (HbA1c)."( Combined antidiabetic benefits of exenatide and dapagliflozin in diabetic mice.
D'Souza, LJ; Janssen, S; Parkes, DG; Polizzi, C; Tatarkiewicz, K; Villescaz, C; Wang, Y, 2014)		0.4
" Furthermore, during light-phase restricted feeding, repeated dosing of exendin-4 at the beginning of the dark phase profoundly influenced both the food intake and daily rhythms of clock gene expression in peripheral tissues."( Indirect effects of glucagon-like peptide-1 receptor agonist exendin-4 on the peripheral circadian clocks in mice.
Ando, H; Fujimura, A; Ushijima, K, 2013)		0.39
" The plasma concentrations of exenatide in serial blood samples were quantified for 56 days after dosing with an exendin-4 fluorescent immunoassay kit."( Pharmacokinetic properties and effects of PT302 after repeated oral glucose loading tests in a dose-escalating study.
Cho, SH; Gu, N; Jang, IJ; Kim, J; Lee, H; Lim, KS; Seol, E; Shin, D; Shin, SG; Yu, KS, 2014)		0.4
"5-mg, 1-mg, 2-mg, and 4-mg dosage groups of PT302, respectively."( Pharmacokinetic properties and effects of PT302 after repeated oral glucose loading tests in a dose-escalating study.
Cho, SH; Gu, N; Jang, IJ; Kim, J; Lee, H; Lim, KS; Seol, E; Shin, D; Shin, SG; Yu, KS, 2014)		0.4
" Therefore, we examined 3-mo dosing of exenatide in mice lacking a functional GLP-1R (Glp1r(-/-))."( Long-term metabolic benefits of exenatide in mice are mediated solely via the known glucagon-like peptide 1 receptor.
Parkes, DG; Polizzi, CJ; Sablan, EJ; Tatarkiewicz, K; Villescaz, C, 2014)		0.4
" Twice-weekly subcutaneously dosed [Leu(14)]exenatide-ABD displayed superior glucose lowering and weight loss in diabetic mice when compared to continuously infused exenatide at the same total weekly dose."( Novel exenatide analogs with peptidic albumin binding domains: potent anti-diabetic agents with extended duration of action.
D'Souza, LJ; Ghosh, SS; Jin, LJ; Jodka, CM; Levy, OE; Mamedova, L; Parkes, DG; Ren, SS; Samant, M; Sharma, A; Soares, CJ; Tatarkiewicz, K; Yuskin, DR, 2014)		0.4
" Male Zucker Diabetic Fatty (ZDF) rats were dosed for 3 days, fasted overnight and a sucrose/glucose tolerance test was performed."( Effect of linagliptin, alone and in combination with voglibose or exendin-4, on glucose control in male ZDF rats.
Cheetham, SC; Headland, KR; Jones, RB; Klein, T; Mark, M; Vickers, SP, 2014)		0.4
"A new formulation of exenatide has become available recently that is the first antidiabetic medication for type 2 diabetes mellitus (T2DM) dosed on a weekly schedule."( Pathophysiological and pharmacological rationale for the use of exenatide once weekly in patients with type 2 diabetes.
Grossman, SS, 2014)		0.4
"Experiment 1 examined the dose-response effects of exendin-4 (0."( Behavioural profile of exendin-4/naltrexone dose combinations in male rats during tests of palatable food consumption.
Rodgers, RJ; Wright, FL, 2014)		0.4
" It is an attractive option because it is dosed once-weekly, provides A1C lowering similar to liraglutide, weight reduction similar to exenatide, and has an adverse effect profile similar to exenatide and liraglutide."( Dulaglutide: the newest GLP-1 receptor agonist for the management of type 2 diabetes.
Thompson, AM; Trujillo, JM, 2015)		0.42
" Using hybrid PK/PD model, simulations were done to explore the potential dosing regimens which could achieve likelihood of more pharmacodynamic exposure with respect to FPG and HbA1c over a much shorter period compared with the currently used treatment protocol."( Target-mediated pharmacokinetic/pharmacodynamic model based meta-analysis and dosing regimen optimization of a long-acting release formulation of exenatide in patients with type 2 diabetes mellitus.
Fan, X; Li, H; Xu, J, 2015)		0.42
" We found that exendin-4 exerts its effect on failing human islet grafts in a bell-shaped dose-response curve."( The effects of exendin-4 treatment on graft failure: an animal study using a novel re-vascularized minimal human islet transplant model.
Abadpour, S; Foss, A; Gorman, T; Hoeyem, M; Johansson, L; Korsgren, O; Sahraoui, A; Scholz, H; Skrtic, S; Smith, DM; Winzell, MS, 2015)		0.42
"These data show that d-Ala(8) GLP-1(Lys(37) ) pentasaccharide exerts significant antidiabetic actions and has a projected pharmacokinetic/pharmacodynamic profile that merits further evaluation in humans for a possible once-weekly dosing regimen."( Pharmacological characterization and antidiabetic activity of a long-acting glucagon-like peptide-1 analogue conjugated to an antithrombin III-binding pentasaccharide.
Bos, ES; de Kort, M; Dokter, WH; Flatt, PR; Irwin, N; Miltenburg, AM; Moffett, RC; Patterson, S, 2015)		0.42
"We conducted a systematic review and meta-analysis of randomized controlled trials comparing any GLP-1 RA licensed for once-weekly dosing (albiglutide, dulaglutide or exenatide extended release) with placebo or other antidiabetic agents."( Efficacy and safety of once-weekly glucagon-like peptide 1 receptor agonists for the management of type 2 diabetes: a systematic review and meta-analysis of randomized controlled trials.
Athanasiadou, E; Bekiari, E; Boura, P; Karagiannis, T; Liakos, A; Mainou, M; Matthews, DR; Paschos, P; Rika, M; Tsapas, A; Vasilakou, D, 2015)		0.42
"Given their dosing scheme and overall efficacy and safety profile, once-weekly GLP-1 RAs are a convenient therapeutic option for use as add-on to metformin."( Efficacy and safety of once-weekly glucagon-like peptide 1 receptor agonists for the management of type 2 diabetes: a systematic review and meta-analysis of randomized controlled trials.
Athanasiadou, E; Bekiari, E; Boura, P; Karagiannis, T; Liakos, A; Mainou, M; Matthews, DR; Paschos, P; Rika, M; Tsapas, A; Vasilakou, D, 2015)		0.42
" Differences may be due to dosing device differences for exenatide QW and liraglutide, which, in the case of liraglutide, allows the opportunity for daily self-titration dosing."( Liraglutide Versus Exenatide Once Weekly: Persistence, Adherence, and Early Discontinuation.
Fernandez Lando, L; Kabul, S; Swindle, RW; Xie, J; Yu, M, 2016)		0.43
" Pharmacokinetic simulations indicate that the hydrogel-exenatide microspheres should support weekly or biweekly subcutaneous dosing in humans."( Hydrogel Drug Delivery System Using Self-Cleaving Covalent Linkers for Once-a-Week Administration of Exenatide.
Ashley, GW; Henise, J; Reid, R; Santi, DV; Schneider, EL, 2016)		0.43
" Exenatide was given using standard diabetes dosing without dietary modifications."( Effects of exenatide on weight and appetite in overweight adolescents and young adults with Prader-Willi syndrome.
Azen, CG; Geffner, ME; Hsu, I; Jeandron, D; Mittelman, SD; Salehi, P, 2017)		0.46
"After run-in on metformin and basal-bolus insulin (BBI), 102 participants continued metformin and basal insulin and were randomized to exenatide dosing before the two largest meals (glucacon-like peptide-1 receptor agonist and insulin [GLIPULIN group]) or continuation of rapid-acting insulin analogs (BBI group)."( Glucose Variability in a 26-Week Randomized Comparison of Mealtime Treatment With Rapid-Acting Insulin Versus GLP-1 Agonist in Participants With Type 2 Diabetes at High Cardiovascular Risk.
, 2016)		0.43
"0001), regardless of dosage and population, was achieved by the obese or overweight patients in exenatide group."( Exenatide in obese or overweight patients without diabetes: A systematic review and meta-analyses of randomized controlled trials.
Du, H; Kwong, JS; Li, J; Li, L; Li, Q; Li, S; Li, Y; Ren, K; Su, N; Sun, X; Tian, H; Xu, T, 2016)		0.43
" In addition, GCMs had a longer interval between dosing (two weeks) and a lower dosage(2."( Effects of Pluronic F127-PEG multi-gel-core on the release profile and pharmacodynamics of Exenatide loaded in PLGA microspheres.
Cai, C; Gong, H; Gou, J; Ren, T; Tang, X; Wang, P; Wang, Q; Zhang, Y, 2016)		0.43
"Forty clean NOD mice were randomly divided into four groups (in each group, n = 10): One is blank control group D which is intervened with normal saline, and the other three groups were divided into low-dose group A, middle-dose group B, and high-dose group C according to the different exendin-4 dosage 2, 4, and 8 μg/kg·d."( Influence and significance of intervening diabetes microRNA expression profile of NOD mice with exendin-4.
Fang, YL; He, JS; Lian, CW; Wu, JZ; Ye, XL; Zhu, SB, 2016)		0.43
" The effects of exenatide were examined on the following prespecified covariates within the first 6 hours from study drug initiation: lactate level, blood glucose level, heart rate, mean arterial pressure, and combined dosage of norepinephrine and dopamine."( The Glucagon-Like Peptide-1 Analog Exenatide Increases Blood Glucose Clearance, Lactate Clearance, and Heart Rate in Comatose Patients After Out-of-Hospital Cardiac Arrest.
Engstrøm, T; Frydland, M; Hassager, C; Høfsten, DE; Kjaergaard, J; Køber, L; Lindholm, MG; Møller, JE; Schmidt, H; Thomsen, JH; Wiberg, S; Winther-Jensen, M, 2018)		0.48
" This pharmacokinetic disadvantage has largely restricted the development of noninvasive dosage forms of biologics that deliver into systemic circulation."( Biocompatible Polymers Modified with d-Octaarginine as an Absorption Enhancer for Nasal Peptide Delivery.
Fujii, K; Higashitarumi, S; Hiwatari, KI; Ishizaki, S; Kobayashi, H; Kumagai, H; Miyata, K; Mohri, K; Ochiai, K; Sakuma, S; Shigeno, K; Tanishita, S; Tobita, E; Tsubaki, K; Ukawa, M; Yamada, M, 2018)		0.48
" The favorable safety profiles of OW GLP-1 RAs, added to their efficacy and the favorable weekly dosing regimen, make these agents appropriate options for patients with T2D."( Safety of Once-weekly Glucagon-like Peptide-1 Receptor Agonists in Patients with Type 2 Diabetes.
Frias, JP, 2018)		0.48
" An optimal exendin-4 treatment dosing regimen was identified, where four high doses (0."( Neuroprotective exendin-4 enhances hypothermia therapy in a model of hypoxic-ischaemic encephalopathy.
Carlsson, Y; Hagberg, H; Jonsdotter, A; Leverin, AL; Nair, S; Poupon, L; Rahim, AA; Rocha-Ferreira, E; Thornton, C; Zelco, A, 2018)		0.48
" In contrast, treatment with comparable dosing of des-acyl ghrelin failed to significantly impact metabolic activity."( Exendin-4 antagonizes the metabolic action of acylated ghrelinergic signaling in the hypothalamic paraventricular nucleus.
Abtahi, S; Bastacky, JMR; Currie, PJ; Dunn, DP; Howell, E; Salvucci, JT, 2019)		0.51
" This convenient single, sustained-release dosing regimen also has application for other neurological disorders, such as Alzheimer's disease, Parkinson's disease, multiple system atrophy and multiple sclerosis where prior preclinical studies, likewise, have demonstrated positive Exenatide actions."( Pharmacokinetics and efficacy of PT302, a sustained-release Exenatide formulation, in a murine model of mild traumatic brain injury.
Bader, M; Choi, HI; Glotfelty, E; Greig, NH; Hoffer, BJ; Kim, DS; Kim, HK; Lecca, D; Li, Y; Pick, CG; Rachmany, L; Rubovitch, V; Tweedie, D, 2019)		0.51
"c dosing with the combination of PYY(3-36) (200 μg/kg) and Ex4 (2."( PYY(3-36) and exendin-4 reduce food intake and activate neuronal circuits in a synergistic manner in mice.
Kjaergaard, M; Raun, K; Rehfeld, JF; Salinas, CBG; Secher, A; Wulff, BS, 2019)		0.51
" The results showed that acute pharmacological dosage of GLP-1RA (Liraglutide or Exenatide) could significantly influence food intake."( Comparative study on anorexigenic effect of glucagon-like peptide-1 receptor agonists in rats.
Gong, M; Jin, JL; Nguyen, T; Wang, CX; Wen, S; Xiao, WZ; Zhou, LG, 2019)		0.51
" GLP-1 RA dosing varies from once weekly to twice daily, and the class is well tolerated in patients with type 2 diabetes."( Glucagon-like peptide 1 receptor agonists in type 1 diabetes mellitus.
Brooks, A; Guyton, J; Jeon, M, 2019)		0.51
" In a dose-response comparison, DA-CH5 was more effective than the GLP-1 receptor agonist exendin-4."( The Novel Dual GLP-1/GIP Receptor Agonist DA-CH5 Is Superior to Single GLP-1 Receptor Agonists in the MPTP Model of Parkinson's Disease.
Hölscher, C; Li, L; Li, Y; Melchiorsen, JU; Rosenkilde, M; Zhang, L, 2020)		0.56
"Seventy subjects were randomly assigned to 8 incremental dosage groups (2, 5, 10, 25, 50, 100, 200 and 400 µg)."( Safety, Tolerability and Pharmacokinetics of Single Dose Polyethylene Glycolated Exenatide Injection (PB-119) in Healthy Volunteers.
Cui, H; Li, Y; Liu, Y; Lv, Y; Tian, JH; Wei, MJ; Xia, YH; Zhang, P; Zhao, CY; Zhu, Y, 2020)		0.56
" Because Exendin-4 (Ex-4) displays similar functional properties to native GLP-1, we used this agonist to perform a dose-response study on progressive motility and cholesterol efflux, showing that 300 pM Ex-4 was the most effective treatment."( Human Sperm Express the Receptor for Glucagon-like Peptide-1 (GLP-1), Which Affects Sperm Function and Metabolism.
Andò, S; Aquila, S; D'Agata, R; De Rose, D; Malivindi, R; Panza, S; Rago, V; Santoro, M, 2020)		0.56
" Most recommendations for drug usage and dosage are based on collective clinical experience."( Ultrasonographic assessment of the effect of metoclopramide, erythromycin, and exenatide on solid-phase gastric emptying in healthy cats.
Fletcher, JM; Gaschen, FP; Gaschen, L; Husnik, R, 2020)		0.56
"A total of 30 trials were identified for inclusion; eight were head-to-head trials involving another GLP-1 RA; of these, six compared GLP-1 RAs with different dosing regimens (QW vs once-daily or twice-daily), and two were direct QW vs QW GLP-1 RA comparisons."( Safety and tolerability of once-weekly GLP-1 receptor agonists in type 2 diabetes.
Trujillo, J, 2020)		0.56
" Furthermore, chronic dosing of HEX15 significantly ameliorated the manifestations of diabetes in the db/db mice, including body weight, food intake, glycometabolism as well as hyperlipemia."( Albumin-binding tag derived Exendin-4 analogue for treating hyperglycemia and diabetic complications.
Fang, D; Li, H; Wang, F; Wang, Y; Xu, S, 2022)		0.72
"To establish the impact of sex, dosing route, fasting duration and acute habituation stress on glucose tolerance test (GTT) measurements used in the preclinical evaluation of potential glucose-modulating therapeutics."( The glucose tolerance test in mice: Sex, drugs and protocol.
Chapple, S; Kennard, MR; King, AJ; Nandi, M, 2022)		0.72
"As low-temperature storage and transportation of peptides require high costs, improving the dosage form of peptides can reduce costs."( Thermal stability of exenatide encapsulated in stratified dissolving microneedles during storage.
Cheng, A; Gao, Y; Liu, H; Meng, F; Wang, B; Xing, M; Xu, B; Yan, C; Yang, G; Zhang, S, 2023)		0.91
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Protein Targets (4)

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Glucagon-like peptide 1 receptorRattus norvegicus (Norway rat)IC50 (µMol)0.00010.00010.50011.0000AID475807
Glucagon-like peptide 1 receptorHomo sapiens (human)IC50 (µMol)0.00230.00010.00310.0140AID1708347; AID1874888; AID385217
Glucagon-like peptide 1 receptorHomo sapiens (human)Ki0.00010.00010.00270.0063AID1911939; AID1911940
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Glucagon-like peptide 1 receptorMus musculus (house mouse)EC50 (µMol)0.00000.00000.00000.0000AID1483062
Glucagon-like peptide 1 receptorHomo sapiens (human)EC50 (µMol)0.05260.00000.04170.7943AID1066039; AID1392277; AID1483054; AID1498065; AID1601241; AID1708340; AID1874889; AID1874890; AID1874891; AID1874892; AID1911919; AID1911921; AID1911922; AID1911934; AID1911936; AID385218; AID494632
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (13)

Processvia Protein(s)Taxonomy
cell surface receptor signaling pathwayGlucagon-like peptide 1 receptorHomo sapiens (human)
adenylate cyclase-activating G protein-coupled receptor signaling pathwayGlucagon-like peptide 1 receptorHomo sapiens (human)
activation of adenylate cyclase activityGlucagon-like peptide 1 receptorHomo sapiens (human)
positive regulation of cytosolic calcium ion concentrationGlucagon-like peptide 1 receptorHomo sapiens (human)
learning or memoryGlucagon-like peptide 1 receptorHomo sapiens (human)
regulation of heart contractionGlucagon-like peptide 1 receptorHomo sapiens (human)
cAMP-mediated signalingGlucagon-like peptide 1 receptorHomo sapiens (human)
post-translational protein targeting to membrane, translocationGlucagon-like peptide 1 receptorHomo sapiens (human)
negative regulation of blood pressureGlucagon-like peptide 1 receptorHomo sapiens (human)
hormone secretionGlucagon-like peptide 1 receptorHomo sapiens (human)
cellular response to glucagon stimulusGlucagon-like peptide 1 receptorHomo sapiens (human)
response to psychosocial stressGlucagon-like peptide 1 receptorHomo sapiens (human)
positive regulation of blood pressureGlucagon-like peptide 1 receptorHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (5)

Processvia Protein(s)Taxonomy
transmembrane signaling receptor activityGlucagon-like peptide 1 receptorHomo sapiens (human)
protein bindingGlucagon-like peptide 1 receptorHomo sapiens (human)
glucagon-like peptide 1 receptor activityGlucagon-like peptide 1 receptorHomo sapiens (human)
peptide hormone bindingGlucagon-like peptide 1 receptorHomo sapiens (human)
glucagon receptor activityGlucagon-like peptide 1 receptorHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (2)

Processvia Protein(s)Taxonomy
plasma membraneGlucagon-like peptide 1 receptorRattus norvegicus (Norway rat)
plasma membraneGlucagon-like peptide 1 receptorHomo sapiens (human)
membraneGlucagon-like peptide 1 receptorHomo sapiens (human)
plasma membraneGlucagon-like peptide 1 receptorHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (145)

Assay IDTitleYearJournalArticle
AID1068435Antioxidant activity in STZ-induced mouse model assessed as MDA level at 1 umol/kg, ip administered for 20 days measured on day 21 (Rvb = 12.49 +/- 1.35 nmol/ml)2014European journal of medicinal chemistry, Feb-12, Volume: 73Design, synthesis and biological evaluation of novel peptide MC62 analogues as potential antihyperglycemic agents.
AID1874897Agonist activity at human GLP-1R expressed in CHO cells coexpressing beta-arrestin-2 assessed as increase in beta arrestin-2 recruitment by measuring maximum efficacy incubated for 1 hr by chemiluminescence based pathHunter assay relative to GLP12022Journal of medicinal chemistry, 09-08, Volume: 65, Issue:17
Modifying a Hydroxyl Patch in Glucagon-like Peptide 1 Produces Biased Agonists with Unique Signaling Profiles.
AID475806Binding affinity to human serum albumin at 100 ug/mL in phosphate buffer saline after 2 hrs2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID1392281Hypoglycemic activity in STZ-induced diabetic Kunming mouse model assessed as time required to reduce blood glucose level of 8.35 nmol/L at 25 nmol/kg, ip administered as single dose2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Novel fatty acid chain modified GLP-1 derivatives with prolonged in vivo glucose-lowering ability and balanced glucoregulatory activity.
AID1874890Agonist activity at human GLP-1R expressed in CHO cells coexpressing beta-arrestin-2 assessed as stimulation intracellular calcium mobilization measured after 180 secs by Fluo-3-AM dye based fluorescence assay2022Journal of medicinal chemistry, 09-08, Volume: 65, Issue:17
Modifying a Hydroxyl Patch in Glucagon-like Peptide 1 Produces Biased Agonists with Unique Signaling Profiles.
AID1066035Antidiabetic activity in Sprague-Dawley rat assessed as increase of plasma insulin level at 25 nmol/kg, ip administered 0.5 hrs prior to glucose challenge measured at 45 mins by ELISA2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1068436Antioxidant activity in STZ-induced mouse model assessed as SOD level at 1 umol/kg, ip administered for 20 days measured on day 21 (Rvb = 41.58 +/- 2.89 U/ml)2014European journal of medicinal chemistry, Feb-12, Volume: 73Design, synthesis and biological evaluation of novel peptide MC62 analogues as potential antihyperglycemic agents.
AID447511Cmax in insulin-resistant ob/ob mouse at 1 nmol/kg, sc up to 24 hrs by LC-MS/MS analysis2009Journal of medicinal chemistry, Dec-10, Volume: 52, Issue:23
Eleven amino acid glucagon-like peptide-1 receptor agonists with antidiabetic activity.
AID1066040Antidiabetic activity in Sprague-Dawley rat assessed as increase of plasma insulin level at 25 nmol/kg, ip administered 0.5 hrs prior to glucose challenge measured at 15 mins by ELISA2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1066029Elimination half life in Sprague-Dawley rat at 15 nmol/kg, sc by LC-MS/MS analysis2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1498066Agonist activity at human glucagon receptor expressed in HEK293 cells assessed as cAMP accumulation after 30 mins by HTRF assay2018Journal of medicinal chemistry, 07-12, Volume: 61, Issue:13
Dual Glucagon-like Peptide 1 (GLP-1)/Glucagon Receptor Agonists Specifically Optimized for Multidose Formulations.
AID748318Potentiation of glucose-stimulated insulin secretion in human pancreatic islets at 1 uM2013ACS medicinal chemistry letters, Jun-13, Volume: 4, Issue:6
Discovery and Optimization of Potent GPR40 Full Agonists Containing Tricyclic Spirocycles.
AID1601241Agonist activity at human GLP1 receptor expressed in HEK293 cells assessed as induction of cAMP levels after 20 mins by time-resolved fluorescence analysis2019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID418684Antidiabetic activity in po dosed type 2 diabetes mellitus patient assessed as reduction in HbA1C level in pancreas2009Journal of medicinal chemistry, Apr-09, Volume: 52, Issue:7
Development of the renal glucose reabsorption inhibitors: a new mechanism for the pharmacotherapy of diabetes mellitus type 2.
AID1601242Half life in Sprague-Dawley rat plasma at 1000 ng/ml measured up to 72 hrs by UPLC-MS/MS analysis2019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID475811Insulinotropic activity in 16.7 mM glucose-stimulated Sprague-Dawley rat islets of langerhans assessed as insulin release per 20 islets at 10 nM treated for 2 hrs after glucose challenge measured after 2 hrs of glucose stimulation by EIA (Rvb = 58.32 +/- 2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID1601243Antidiabetic activity in STZ-induced diabetic Kunming mouse assessed as decrease in postprandial blood glucose level at 25 nmol/kg, ip pretreated with STZ for 5 consecutive days and measured up to 48 hrs post induction by glucometric analysis (Rvb > 16.7 2019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID475817Tmax in cannulated Sprague-Dawley rat at 10 nmol, sc by EIA2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID475828Antidiabetic activity in C57BL/6 db/db mouse assessed as decrease in glucose AUC at 15 nmol/kg, sc administered as single dose measured after 24 hrs by glucometry2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID1601253Hepatoprotective activity against STZ-induced diabetic Kunming mouse assessed as reduction in AST levels at 25 nmol/kg, ip qd administered for 3 weeks and measured at day 242019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID1639345Antiobesity activity in C57BL/6J mouse model of diet-induced obesity assessed as reduction in circulating leptin level at 25 nmol/kg, ip qd for 4 weeks2019Bioorganic & medicinal chemistry, 04-15, Volume: 27, Issue:8
Novel nonapeptide GLP (28-36) amide derivatives with improved hypoglycemic and body weight lowering effects.
AID1708352Suppression of cumulative food intake in lean Sprague-Dawley rat at 10 to 20 nmol/kg per dosed daily for 8 days2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID1708338Toxicity in lean Sprague-Dawley rat assessed as induction of emesis at 0.3 to 60 nmol/kg dosed daily for 2 days by kaolin consumption assay2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID385217Displacement of [125I]GLP1 from human GLP1R expressed in CHOK1 cells2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
Design and synthesis of conformationally constrained glucagon-like peptide-1 derivatives with increased plasma stability and prolonged in vivo activity.
AID1911935Agonist activity at human GLP-1R expressed in PathHunter CHO-K1 GLP1R beta-arrestin-1 cell assessed as induction of beta-arrestin 1 recruitment by measuring maximum efficacy incubated for 90 mins by pathHunter assay relative to control2022Journal of medicinal chemistry, 06-23, Volume: 65, Issue:12
A Small-Molecule Oral Agonist of the Human Glucagon-like Peptide-1 Receptor.
AID758130Toxicity in type 2 diabetes patient assessed as gastro-intestinal side effects at 10 ug, bid up to 104 weeks2013Bioorganic & medicinal chemistry letters, Jul-15, Volume: 23, Issue:14
Recent progress and future options in the development of GLP-1 receptor agonists for the treatment of diabesity.
AID475820Elimination half life in cannulated Sprague-Dawley rat at 10 nmol, sc by EIA2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID494632Agonist activity at human GLP-1 receptor expressed in CHO cells assessed as increase in cAMP production2010Bioorganic & medicinal chemistry letters, Aug-01, Volume: 20, Issue:15
Identification of glycosylated exendin-4 analogue with prolonged blood glucose-lowering activity through glycosylation scanning substitution.
AID475822Apparent oral clearance in cannulated Sprague-Dawley rat at 10 nmol, sc after 4 hrs by EIA2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID475819AUC in cannulated Sprague-Dawley rat at 10 nmol, sc after 4 hrs by EIA2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID1708347Displacement of GLP-1-red from human GLP-1R expressed in CHO-K1 cells by fluorescent competitive binding assay2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID294991Insulinotropic activity in RIN5F cells assessed as stimulation of glucose-dependent insulin secretion per ug of protein at 1 uM2007Bioorganic & medicinal chemistry, May-01, Volume: 15, Issue:9
Design, synthesis, and biological evaluation of substituted-N-(thieno[2,3-b]pyridin-3-yl)-guanidines, N-(1H-pyrrolo[2,3-b]pyridin-3-yl)-guanidines, and N-(1H-indol-3-yl)-guanidines.
AID1708350Half life in Sprague-Dawley rat liver microsomes at 30 uM in presence of NADPH by HPLC analysis2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID475808Displacement of [125I]exendin-4 from GLP1 receptor in rat RINm5F cells at 10 nM after 2 hrs by gamma counting2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID1639332Cytoprotective activity against H2O2-induced oxidative stress-mediated cell death in rat INS-1 cells assessed as reduction in apoptotic cells at 10 uM after 24 hrs by Annexin V/propidium iodide staining-based flow cytometric analysis2019Bioorganic & medicinal chemistry, 04-15, Volume: 27, Issue:8
Novel nonapeptide GLP (28-36) amide derivatives with improved hypoglycemic and body weight lowering effects.
AID1911940Displacement of [3H]PF-06883365 from FAP-tagged human GLP-1R expressed in CHO cells assessed as inhibition constant by radioligand binding assay2022Journal of medicinal chemistry, 06-23, Volume: 65, Issue:12
A Small-Molecule Oral Agonist of the Human Glucagon-like Peptide-1 Receptor.
AID1068431Inhibition of palmitate-induced apoptosis in mouse MIN6 cells assessed as reduction of apoptotic cells at 10 nM preincubated for 24 hrs followed by palmitate challenge measured after 1 hr by Hoechst 33342 staining-based microscopic analysis2014European journal of medicinal chemistry, Feb-12, Volume: 73Design, synthesis and biological evaluation of novel peptide MC62 analogues as potential antihyperglycemic agents.
AID1708349Stimulation of glucose stimulated insulin secretion in rat pancreatic islets at 50 nM in presence of 3 mM glucose incubated for 60 mins2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID1465192Agonist activity at GLP1 receptor in mouse BetaTC6 cells assessed as increase in insulin secretion at 10'-12 to 10'-5 M after 120 mins by sandwich ELISA2017Bioorganic & medicinal chemistry letters, 11-15, Volume: 27, Issue:22
Synthesis and in vitro biological evaluation of new pyrimidines as glucagon-like peptide-1 receptor agonists.
AID475825Antidiabetic activity in C57BL/6 db/db mouse assessed as normalization of blood glucose level at 15 nmol/kg, sc administered as single dose measured after 8 hrs by glucometry2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID447504Antidiabetic activity in insulin-resistant ob/ob mouse assessed as reduction in plasma glucose level at 1 nmol/kg, sc administered 30 mins before glucose infusion measured after 30 to 180 mins of glucose challenge by intraperitoneal glucose tolerance test2009Journal of medicinal chemistry, Dec-10, Volume: 52, Issue:23
Eleven amino acid glucagon-like peptide-1 receptor agonists with antidiabetic activity.
AID1066030AUC (0 to infinity) in Sprague-Dawley rat at 15 nmol/kg, sc by LC-MS/MS analysis2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID294992Insulinotropic activity in RIN5F cells assessed as stimulation of glucose-dependent insulin secretion per microgram of protein at 10 uM2007Bioorganic & medicinal chemistry, May-01, Volume: 15, Issue:9
Design, synthesis, and biological evaluation of substituted-N-(thieno[2,3-b]pyridin-3-yl)-guanidines, N-(1H-pyrrolo[2,3-b]pyridin-3-yl)-guanidines, and N-(1H-indol-3-yl)-guanidines.
AID475814Antidiabetic activity in overnight fasted db/db mouse assessed as blood glucose level at 10 nmol/kg, sc administered 30 mins prior to glucose challenge measured after 30 mins by IPGTT (Rvb = 20.96 +/- 2.20 nM)2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID447508Antidiabetic activity in insulin-resistant ob/ob mouse assessed as increase in plasma insulin level at 1 nmol/kg, sc administered 30 mins before glucose infusion measured after 30 mins of glucose challenge by intraperitoneal glucose tolerance test2009Journal of medicinal chemistry, Dec-10, Volume: 52, Issue:23
Eleven amino acid glucagon-like peptide-1 receptor agonists with antidiabetic activity.
AID1066038Half life in Sprague-Dawley rat plasma at 1000 ng/mL by LC-MS/MS analysis2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1066027Hypoglycemic activity in C57BL/6J-m+/+Leprdb (db/db) mouse assessed as reduction of plasma glucose level at 25 nmol/kg, ip administered 0.5 hrs prior to glucose challenge measured up to 5 hrs by IPGTT2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1911924Agonist activity at human GLP-1R expressed in CHO-K1 cells assessed as cAMP accumulation by measuring maximal efficacy at 20 uM incubated for 30 mins in absence of BETP by plate reader method relative to control2022Journal of medicinal chemistry, 06-23, Volume: 65, Issue:12
A Small-Molecule Oral Agonist of the Human Glucagon-like Peptide-1 Receptor.
AID1068446Antihyperglycemic activity in overnight fasted STZ-induced diabetic mouse model assessed as blood glucose level at 0.03 umol/kg, ip qd administered for 20 days measured after 20 days relative to control2014European journal of medicinal chemistry, Feb-12, Volume: 73Design, synthesis and biological evaluation of novel peptide MC62 analogues as potential antihyperglycemic agents.
AID475813Antidiabetic activity in overnight fasted db/db mouse assessed as increase in glucose tolerance at 10 nmol/kg, sc administered 30 mins prior to glucose challenge measured after 120 mins by IPGTT2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID475824Antidiabetic activity in C57BL/6 db/db mouse assessed as normalization of blood glucose level at 15 nmol/kg, sc administered as single dose measured after 6 hrs by glucometry2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID1392288Cytoprotective activity against H2O2-induced glucolipotoxicity in rat INS-1 cells assessed as reduction in apoptosis at 10 nM after 24 hrs by Annexin-V-FITC/propidium iodide staining based flow cytometric analysis2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Novel fatty acid chain modified GLP-1 derivatives with prolonged in vivo glucose-lowering ability and balanced glucoregulatory activity.
AID1874891Agonist activity at human GLP-1R assessed as increase in ERK1/2 phosphorylation at Thr202/Tyr204 residues incubated for 20 mins by AlphaLISA assay2022Journal of medicinal chemistry, 09-08, Volume: 65, Issue:17
Modifying a Hydroxyl Patch in Glucagon-like Peptide 1 Produces Biased Agonists with Unique Signaling Profiles.
AID1601255Anti-obesity activity in 12 hrs fasted diet-induced obese C57BL/6J mouse assessed as reduction in food intake at 25 nmol/kg, ip measured up to 360 mins2019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID758129Half life in human2013Bioorganic & medicinal chemistry letters, Jul-15, Volume: 23, Issue:14
Recent progress and future options in the development of GLP-1 receptor agonists for the treatment of diabesity.
AID1066028Mean residence time in Sprague-Dawley rat at 15 nmol/kg, sc by LC-MS/MS analysis2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID758122Antidiabetic activity in type 2 diabetes patient assessed as reduction of HbA1c at 10 ug, bid after 26 weeks relative to control2013Bioorganic & medicinal chemistry letters, Jul-15, Volume: 23, Issue:14
Recent progress and future options in the development of GLP-1 receptor agonists for the treatment of diabesity.
AID1392275Half life in Sprague-Dawley rat plasma by LC-MS/MS analysis2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Novel fatty acid chain modified GLP-1 derivatives with prolonged in vivo glucose-lowering ability and balanced glucoregulatory activity.
AID1601250Antidiabetic activity against STZ-induced diabetic Kunming mouse assessed as reduction in HbA1c level at 25 nmol/kg, ip qd administered for 3 weeks and measured after 24 days2019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID1639333Cytoprotective activity against STZ-mediated cell death in rat INS-1 cells assessed as reduction in apoptotic cells at 10 uM after 24 hrs by Annexin V/propidium iodide staining-based flow cytometric analysis2019Bioorganic & medicinal chemistry, 04-15, Volume: 27, Issue:8
Novel nonapeptide GLP (28-36) amide derivatives with improved hypoglycemic and body weight lowering effects.
AID1911936Agonist activity at human GLP-1R expressed in PathHunter CHO-K1 GLP1R beta-arrestin-2 cell assessed as induction of beta-arrestin 2 recruitment incubated for 90 mins by pathHunter assay2022Journal of medicinal chemistry, 06-23, Volume: 65, Issue:12
A Small-Molecule Oral Agonist of the Human Glucagon-like Peptide-1 Receptor.
AID1639342Antiobesity activity in C57BL/6J mouse model of diet-induced obesity assessed as reduction in body weight at 25 nmol/kg, ip qd for 4 weeks2019Bioorganic & medicinal chemistry, 04-15, Volume: 27, Issue:8
Novel nonapeptide GLP (28-36) amide derivatives with improved hypoglycemic and body weight lowering effects.
AID475807Displacement of [125I]exendin-4 from GLP1 receptor in rat RINm5F cells after 2 hrs by gamma counting2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID385218Agonist activity at human GLP1R expressed in CHO cells assessed as increase in cAMP level by cAMP-response element/luciferase activation assay2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
Design and synthesis of conformationally constrained glucagon-like peptide-1 derivatives with increased plasma stability and prolonged in vivo activity.
AID1662694Agonist activity at human GPR146 receptor expressed in HEK293 cells assessed as recruitment of beta-arrestin by Path Hunter assay2020Bioorganic & medicinal chemistry letters, 07-01, Volume: 30, Issue:13
Is GPR146 really the receptor for proinsulin C-peptide?
AID1392287Cytoprotective activity against STZ-induced oxidative stress in rat INS-1 cells assessed as reduction in apoptosis at 10 nM after 24 hrs by Annexin-V-FITC/propidium iodide staining based flow cytometric analysis2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Novel fatty acid chain modified GLP-1 derivatives with prolonged in vivo glucose-lowering ability and balanced glucoregulatory activity.
AID1392277Agonist activity at recombinant human GLP1 receptor expressed in HEK293 cells assessed as cAMP accumulation by TR-FRET assay2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Novel fatty acid chain modified GLP-1 derivatives with prolonged in vivo glucose-lowering ability and balanced glucoregulatory activity.
AID1483054Agonist activity at human GLP-1 receptor expressed in HEK293 cells assessed as cAMP accumulation after 30 mins by HTRF assay2017Journal of medicinal chemistry, 05-25, Volume: 60, Issue:10
Design of Novel Exendin-Based Dual Glucagon-like Peptide 1 (GLP-1)/Glucagon Receptor Agonists.
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID447509Antidiabetic activity in insulin-resistant ob/ob mouse assessed as increase in plasma insulin level at 1 nmol/kg, sc administered 30 mins before glucose infusion measured after 60 mins of glucose challenge by intraperitoneal glucose tolerance test2009Journal of medicinal chemistry, Dec-10, Volume: 52, Issue:23
Eleven amino acid glucagon-like peptide-1 receptor agonists with antidiabetic activity.
AID1392292Antidiabetic activity in C57BL/6 mouse assessed as reduction in blood glucose level at 25 nmol/kg, ip treated 30 mins prior to glucose challenge measured after 120 mins by IPGTT2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Novel fatty acid chain modified GLP-1 derivatives with prolonged in vivo glucose-lowering ability and balanced glucoregulatory activity.
AID1708348Stimulation of glucose stimulated insulin secretion in rat pancreatic islets at 50 nM in presence of 10 mM glucose incubated for 60 mins2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID1601248Antidiabetic activity against STZ-induced diabetic Kunming mouse assessed as reduction in cumulative water intake at 25 nmol/kg, ip qd administered for 3 weeks and measured every day2019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID475812Insulinotropic activity in 2.2 mM glucose-stimulated Sprague-Dawley rat islets of langerhans assessed as insulin release per 20 islets at 10 nM treated for 2 hrs after glucose challenge measured after 2 hrs of glucose stimulation by EIA2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID475821Apparent volume of distribution with respect to bioavailability in cannulated Sprague-Dawley rat at 10 nmol, sc after 4 hrs by EIA2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID1601258Antidiabetic activity in Sprague-Dawley rat assessed as decrease in glucose level at 25 nmol/kg, ip pretreated for 30 mins followed by glucose challenge and measured up to 180 mins by OGTT relative to control2019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID1911919Agonist activity at human GLP-1R expressed in CHO-K1 cells assessed as cAMP accumulation incubated for 30 mins in absence of BETP by plate reader method2022Journal of medicinal chemistry, 06-23, Volume: 65, Issue:12
A Small-Molecule Oral Agonist of the Human Glucagon-like Peptide-1 Receptor.
AID1708341Agonist activity at human NPY2R expressed in HEK293 cells assessed as inhibition of adenosine-induced stimulation of cAMP accumulation by FRET assay2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID1068438Antihyperglycemic activity in overnight fasted STZ-induced mouse model assessed as decrease in glycated haemoglobin level at 0.03 umol/kg, ip administered for 20 days measured on day 212014European journal of medicinal chemistry, Feb-12, Volume: 73Design, synthesis and biological evaluation of novel peptide MC62 analogues as potential antihyperglycemic agents.
AID1392274Binding affinity to human serum albumin after 3 hrs by LC-MS/MS analysis2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Novel fatty acid chain modified GLP-1 derivatives with prolonged in vivo glucose-lowering ability and balanced glucoregulatory activity.
AID1911937Agonist activity at human GLP-1R expressed in PathHunter CHO-K1 GLP1R beta-arrestin-2 cell assessed as induction of beta-arrestin 2 recruitment by measuring maximum efficacy incubated for 90 mins by pathHunter assay relative to control2022Journal of medicinal chemistry, 06-23, Volume: 65, Issue:12
A Small-Molecule Oral Agonist of the Human Glucagon-like Peptide-1 Receptor.
AID1066016Antidiabetic activity in C57BL/6J-m+/+Leprdb (db/db) mouse assessed as reduction of blood glucose AUC (0 to 48 hrs) at 25 nmol/kg, ip administered for 0.5 hrs2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1601252Hepatoprotective activity against STZ-induced diabetic Kunming mouse assessed as reduction in ALT levels at 25 nmol/kg, ip qd administered for 3 weeks and measured at day 242019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID1911922Agonist activity at GLP-1R (unknown origin) expressed in candidate selection CHO cells assessed as cAMP accumulation incubated for 30 mins by plate reader method2022Journal of medicinal chemistry, 06-23, Volume: 65, Issue:12
A Small-Molecule Oral Agonist of the Human Glucagon-like Peptide-1 Receptor.
AID1392278Antidiabetic activity in Sprague-Dawley rat assessed as blood glucose level at 25 nmol/kg, ip treated 30 mins prior to glucose challenge measured at 15 mins interval for 180 mins by OGTT (Rvb = 13.8 +/- 1.31 nmol/L)2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Novel fatty acid chain modified GLP-1 derivatives with prolonged in vivo glucose-lowering ability and balanced glucoregulatory activity.
AID1911939Displacement of [125I]GLP-1 from FAP-tagged human GLP-1R expressed in CHO cells assessed as inhibition constant by radioligand binding assay2022Journal of medicinal chemistry, 06-23, Volume: 65, Issue:12
A Small-Molecule Oral Agonist of the Human Glucagon-like Peptide-1 Receptor.
AID1911921Agonist activity at FAP-tagged human GLP-1R expressed in HEK293 cells assessed as receptor internalization2022Journal of medicinal chemistry, 06-23, Volume: 65, Issue:12
A Small-Molecule Oral Agonist of the Human Glucagon-like Peptide-1 Receptor.
AID1066031Cmax in Sprague-Dawley rat at 15 nmol/kg, sc by LC-MS/MS analysis2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1483063Agonist activity at mouse glucagon receptor expressed in HEK293 cells assessed as cAMP accumulation after 30 mins by HTRF assay2017Journal of medicinal chemistry, 05-25, Volume: 60, Issue:10
Design of Novel Exendin-Based Dual Glucagon-like Peptide 1 (GLP-1)/Glucagon Receptor Agonists.
AID1066026Hypoglycemic activity in C57BL/6J-m+/+Leprdb (db/db) mouse assessed as reduction of plasma glucose level at 25 nmol/kg, ip administered 0.5 hrs prior to glucose challenge measured after 6 to 9 hrs by IPGTT2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1483062Agonist activity at mouse GLP-1 receptor expressed in HEK293 cells assessed as cAMP accumulation after 30 mins by HTRF assay2017Journal of medicinal chemistry, 05-25, Volume: 60, Issue:10
Design of Novel Exendin-Based Dual Glucagon-like Peptide 1 (GLP-1)/Glucagon Receptor Agonists.
AID475818Cmax in cannulated Sprague-Dawley rat at 10 nmol, sc after 4 hrs by EIA2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID1392298Antidiabetic activity in STZ/diet-induced obese C57BL/6 mouse assessed as reduction in body weight gain at 25 nmol/kg, ip administered daily for 4 weeks measured daily during compound dosing2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Novel fatty acid chain modified GLP-1 derivatives with prolonged in vivo glucose-lowering ability and balanced glucoregulatory activity.
AID1483066Terminal half life in IGT patient at 10 ug, sc twice daily2017Journal of medicinal chemistry, 05-25, Volume: 60, Issue:10
Design of Novel Exendin-Based Dual Glucagon-like Peptide 1 (GLP-1)/Glucagon Receptor Agonists.
AID1465193Agonist activity at GLP1 receptor in mouse BetaTC6 cells assessed as increase in glucose-dependent insulin secretion at 10'-12 to 10'-5 M after 120 mins by sandwich ELISA2017Bioorganic & medicinal chemistry letters, 11-15, Volume: 27, Issue:22
Synthesis and in vitro biological evaluation of new pyrimidines as glucagon-like peptide-1 receptor agonists.
AID1601247Antidiabetic activity against STZ-induced diabetic Kunming mouse assessed as reduction in cumulative food intake at 25 nmol/kg, ip qd administered for 3 weeks and measured every day2019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID1365156Anorectic activity in overnight fasted Y2R-/- C57BL/6J mouse assessed as inhibition of food intake at 10 nmol/kg, sc followed by re-feeding post dose and measured for 2 hrs2017Bioorganic & medicinal chemistry, 10-15, Volume: 25, Issue:20
Highly potent antiobesity effect of a short-length peptide YY analog in mice.
AID1874892Agonist activity at human GLP-1R expressed in CHO cells coexpressing beta-arrestin-2 assessed as increase in beta arrestin-2 recruitment incubated for 1 hr by chemiluminescence based pathHunter assay2022Journal of medicinal chemistry, 09-08, Volume: 65, Issue:17
Modifying a Hydroxyl Patch in Glucagon-like Peptide 1 Produces Biased Agonists with Unique Signaling Profiles.
AID758128Antidiabetic activity in type 2 diabetes patient assessed as reduction of HbA1c at 2 mg, sc relative to control2013Bioorganic & medicinal chemistry letters, Jul-15, Volume: 23, Issue:14
Recent progress and future options in the development of GLP-1 receptor agonists for the treatment of diabesity.
AID1662686Agonist activity at human GPR146 expressed in CHO-K1 cells assessed as induction of dynamic mass redistribution response at 5 uM by DMR assay2020Bioorganic & medicinal chemistry letters, 07-01, Volume: 30, Issue:13
Is GPR146 really the receptor for proinsulin C-peptide?
AID1874895Agonist activity at human GLP-1R expressed in CHO cells coexpressing beta-arrestin-2 assessed as stimulation intracellular calcium mobilization by measuring maximum efficacy measured after 180 secs by Fluo-3-AM dye based fluorescence assay relative to GLP2022Journal of medicinal chemistry, 09-08, Volume: 65, Issue:17
Modifying a Hydroxyl Patch in Glucagon-like Peptide 1 Produces Biased Agonists with Unique Signaling Profiles.
AID1639334Cytoprotective activity against glucolipotoxicity-mediated cell death in rat INS-1 cells assessed as reduction in apoptotic cells at 10 uM after 24 hrs by Annexin V/propidium iodide staining-based flow cytometric analysis2019Bioorganic & medicinal chemistry, 04-15, Volume: 27, Issue:8
Novel nonapeptide GLP (28-36) amide derivatives with improved hypoglycemic and body weight lowering effects.
AID1483055Agonist activity at human glucagon receptor expressed in HEK293 cells assessed as cAMP accumulation after 30 mins by HTRF assay2017Journal of medicinal chemistry, 05-25, Volume: 60, Issue:10
Design of Novel Exendin-Based Dual Glucagon-like Peptide 1 (GLP-1)/Glucagon Receptor Agonists.
AID1874889Agonist activity at human GLP-1R expressed in CHO cells coexpressing beta-arrestin-2 assessed as reduction in cAMP accumulation incubated for 2 hrs under dark condition by LANCE cAMP assay2022Journal of medicinal chemistry, 09-08, Volume: 65, Issue:17
Modifying a Hydroxyl Patch in Glucagon-like Peptide 1 Produces Biased Agonists with Unique Signaling Profiles.
AID1365155Anorectic activity in overnight fasted C57BL/6J mouse assessed as inhibition of food intake at 10 nmol/kg, sc followed by re-feeding post dose and measured for 2 hrs2017Bioorganic & medicinal chemistry, 10-15, Volume: 25, Issue:20
Highly potent antiobesity effect of a short-length peptide YY analog in mice.
AID1662693Agonist activity at human GLP1R expressed in HEK293 cells assessed as recruitment of beta-arrestin by PathHunter assay2020Bioorganic & medicinal chemistry letters, 07-01, Volume: 30, Issue:13
Is GPR146 really the receptor for proinsulin C-peptide?
AID1639340Antiobesity activity in C57BL/6J mouse model of diet-induced obesity assessed as reduction in cumulative food intake at 25 nmol/kg, ip qd for 4 weeks relative to control2019Bioorganic & medicinal chemistry, 04-15, Volume: 27, Issue:8
Novel nonapeptide GLP (28-36) amide derivatives with improved hypoglycemic and body weight lowering effects.
AID1066033Antidiabetic activity in Sprague-Dawley rat assessed as reduction of plasma glucose level at 25 nmol/kg, ip administered 0.5 hrs prior to glucose challenge measured at 15 to 60 mins by OGTT2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1066032Tmax in Sprague-Dawley rat at 15 nmol/kg, sc by LC-MS/MS analysis2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1708343Agonist activity at rat glucagon receptor expressed in HEK293 cells assessed as stimulation of cAMP accumulation by FRET assay2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID1601254Antidiabetic activity against STZ-induced diabetic Kunming mouse assessed as increase in insulin positive cells at 25 nmol/kg,ip qd administered for 3 weeks and measured after 24 days by immunohistochemical analysis2019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID1066036Antidiabetic activity in Sprague-Dawley rat assessed as reduction of plasma glucose level at 25 nmol/kg, ip administered 0.5 hrs prior to glucose challenge by OGTT (Rvb = 13.32 +/- 1.84 mM)2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1911938Agonist activity at FAP-tagged human GLP-1R expressed in HEK293 cells assessed as receptor internalization by measuring maximal efficacy relative to control2022Journal of medicinal chemistry, 06-23, Volume: 65, Issue:12
A Small-Molecule Oral Agonist of the Human Glucagon-like Peptide-1 Receptor.
AID475815Antidiabetic activity in overnight fasted db/db mouse assessed as blood glucose level at 10 nmol/kg, sc administered 30 mins prior to glucose challenge measured after 120 mins by IPGTT (Rvb = 13.14 +/- 0.90 nM)2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID1601257Antidiabetic activity in STZ-induced diabetic Kunming mouse assessed as hypoglycemic time duration for glycemia under 8.35 mmol/L at 25 nmol/kg, ip pretreated with STZ for 5 consecutive days and measured up to 48 hrs2019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID1392280Antidiabetic activity in Sprague-Dawley rat assessed as time required to increase in plasma insulin level at 25 nmol/kg, ip treated 30 mins prior to glucose challenge by ELISA2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Novel fatty acid chain modified GLP-1 derivatives with prolonged in vivo glucose-lowering ability and balanced glucoregulatory activity.
AID1066039Activation of human GLP-1 receptor overexpressed in HEK293 cells assessed as cAMP accumulation after 20 mins by HTRF assay2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID758127Antidiabetic activity in type 2 diabetes patient assessed as reduction in body weight at 2 mg, sc2013Bioorganic & medicinal chemistry letters, Jul-15, Volume: 23, Issue:14
Recent progress and future options in the development of GLP-1 receptor agonists for the treatment of diabesity.
AID1874894Agonist activity at human GLP-1R expressed in CHO cells coexpressing beta-arrestin-2 assessed as reduction in cAMP accumulation by measuring maximum efficacy incubated for 2 hrs under dark condition by LANCE cAMP assay relative to GLP12022Journal of medicinal chemistry, 09-08, Volume: 65, Issue:17
Modifying a Hydroxyl Patch in Glucagon-like Peptide 1 Produces Biased Agonists with Unique Signaling Profiles.
AID1874888Binding affinity to human GLP-1R expressed in CHO cells coexpressing beta-arrestin-2 incubated for 1 hr by time-resolved fluorescence assay2022Journal of medicinal chemistry, 09-08, Volume: 65, Issue:17
Modifying a Hydroxyl Patch in Glucagon-like Peptide 1 Produces Biased Agonists with Unique Signaling Profiles.
AID294990Insulinotropic activity in RIN5F cells assessed as stimulation of glucose-dependent insulin secretion per ug of protein at 0.1 uM2007Bioorganic & medicinal chemistry, May-01, Volume: 15, Issue:9
Design, synthesis, and biological evaluation of substituted-N-(thieno[2,3-b]pyridin-3-yl)-guanidines, N-(1H-pyrrolo[2,3-b]pyridin-3-yl)-guanidines, and N-(1H-indol-3-yl)-guanidines.
AID1708340Agonist activity at human GLP-1R expressed in HEK293 cells assessed as stimulation of cAMP accumulation by FRET assay2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID1066018Hypoglycemic activity in C57BL/6J-m+/+Leprdb (db/db) mouse assessed as time required to reduce plasma glucose level below 8.35 mM at 25 nmol/kg, ip administered for 0.5 hrs2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1392279Antidiabetic activity in Sprague-Dawley rat assessed as reduction in blood glucose AUC at 25 nmol/kg, ip treated 30 mins prior to glucose challenge measured at 15 mins interval for 180 mins by OGTT2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Novel fatty acid chain modified GLP-1 derivatives with prolonged in vivo glucose-lowering ability and balanced glucoregulatory activity.
AID1708361Toxicity in musk shrew assessed as induction of emesis at 10 to 60 nmol/kg, ip measured after 120 mins2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID1601244Antidiabetic activity in Sprague-Dawley rat assessed as increase in insulin level at 25 nmol/kg, ip pretreated for 30 mins followed by glucose challenge and measured after 15 to 60 mins by ELISA method2019Bioorganic & medicinal chemistry, 10-15, Volume: 27, Issue:20
Novel lipid side chain modified exenatide analogs emerged prolonged glucoregulatory activity and potential body weight management properties.
AID475816Antidiabetic activity in overnight fasted db/db mouse assessed as decrease in glucose AUC at 10 nmol/kg, sc administered 30 mins prior to glucose challenge measured after 120 mins by IPGTT2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID1639353Antiobesity activity in C57BL/6J mouse model of diet-induced obesity assessed as reduction in circulating adiponectin level at 25 nmol/kg, ip qd for 4 weeks2019Bioorganic & medicinal chemistry, 04-15, Volume: 27, Issue:8
Novel nonapeptide GLP (28-36) amide derivatives with improved hypoglycemic and body weight lowering effects.
AID1874896Agonist activity at human GLP-1R assessed as increase in ERK1/2 phosphorylation by measuring maximum efficacy at Thr202/Tyr204 residues incubated for 20 mins by AlphaLISA assay relative to GLP12022Journal of medicinal chemistry, 09-08, Volume: 65, Issue:17
Modifying a Hydroxyl Patch in Glucagon-like Peptide 1 Produces Biased Agonists with Unique Signaling Profiles.
AID1662687Agonist activity at human GLP1R expressed in CHO-K1 cells assessed as induction of dynamic mass redistribution response at 5 uM by DMR assay2020Bioorganic & medicinal chemistry letters, 07-01, Volume: 30, Issue:13
Is GPR146 really the receptor for proinsulin C-peptide?
AID1708358Suppression of blood glucose level in prediabetic Sprague-Dawley rat model of DIO assessed as reduction in post-dextrose bolus blood glucose at 10 nmol/kg dosed daily for 5 days by IPGTT method2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID1068432Inhibition of H202-induced apoptosis in mouse MIN6 cells assessed as change in nuclear fragmentation at 10 nM preincubated for 24 hrs followed by H202 challenge measured after 1 hr by Hoechst 33342 staining-based microscopic analysis2014European journal of medicinal chemistry, Feb-12, Volume: 73Design, synthesis and biological evaluation of novel peptide MC62 analogues as potential antihyperglycemic agents.
AID1498065Agonist activity at human GLP1R expressed in HEK293 cells assessed as cAMP accumulation after 30 mins by HTRF assay2018Journal of medicinal chemistry, 07-12, Volume: 61, Issue:13
Dual Glucagon-like Peptide 1 (GLP-1)/Glucagon Receptor Agonists Specifically Optimized for Multidose Formulations.
AID475823Mean residence time in cannulated Sprague-Dawley rat at 10 nmol, sc after 4 hrs by EIA2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Preparation and structural, biochemical, and pharmaceutical characterizations of bile acid-modified long-acting exendin-4 derivatives.
AID1708351Intrinsic clearance in Sprague-Dawley rat liver microsomes at 30 uM in presence of NADPH by HPLC analysis2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID1639335Antidiabetic activity in STZ-induced diabetic ICR mouse model assessed as fasting blood glucose level at 25 nmol/kg, ip for 5 consecutive days by glucometery (Rvb = 17.7 +/- 1.1 mM)2019Bioorganic & medicinal chemistry, 04-15, Volume: 27, Issue:8
Novel nonapeptide GLP (28-36) amide derivatives with improved hypoglycemic and body weight lowering effects.
AID1066037Binding affinity to human serum albumin at 100 ug/mL after 3 hrs relative to control2013Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24
Design, synthesis, and biological activity of novel dicoumarol glucagon-like peptide 1 conjugates.
AID1911934Agonist activity at human GLP-1R expressed in PathHunter CHO-K1 GLP1R beta-arrestin-1 cell assessed as induction of beta-arrestin 1 recruitment incubated for 90 mins by pathHunter assay2022Journal of medicinal chemistry, 06-23, Volume: 65, Issue:12
A Small-Molecule Oral Agonist of the Human Glucagon-like Peptide-1 Receptor.
AID1708342Agonist activity at human NPY1R expressed in HEK293 cells assessed as inhibition of adenosine-induced stimulation of cAMP accumulation by FRET assay2021Journal of medicinal chemistry, 01-28, Volume: 64, Issue:2
Design and Evaluation of Peptide Dual-Agonists of GLP-1 and NPY2 Receptors for Glucoregulation and Weight Loss with Mitigated Nausea and Emesis.
AID1068433Antioxidant activity in STZ-induced mouse model assessed as GSH level at 1 umol/kg, ip administered for 20 days measured on day 21 (Rvb = 8.13 +/- 0.13 mg/ml)2014European journal of medicinal chemistry, Feb-12, Volume: 73Design, synthesis and biological evaluation of novel peptide MC62 analogues as potential antihyperglycemic agents.
AID1498067Agonist activity at human GIP receptor expressed in HEK293 cells assessed as cAMP accumulation after 30 mins by HTRF assay2018Journal of medicinal chemistry, 07-12, Volume: 61, Issue:13
Dual Glucagon-like Peptide 1 (GLP-1)/Glucagon Receptor Agonists Specifically Optimized for Multidose Formulations.
AID1068434Antioxidant activity in STZ-induced mouse model assessed as GSH-PX level at 1 umol/kg, ip administered for 20 days measured on day 21 (Rvb = 1449.23 +/- 49.42 U/ml)2014European journal of medicinal chemistry, Feb-12, Volume: 73Design, synthesis and biological evaluation of novel peptide MC62 analogues as potential antihyperglycemic agents.
AID1911923Agonist activity at GLP-1R (unknown origin) expressed in candidate selection CHO cells assessed as cAMP accumulation by measuring maximal efficacy at 20 uM incubated for 30 mins by plate reader method relative to control2022Journal of medicinal chemistry, 06-23, Volume: 65, Issue:12
A Small-Molecule Oral Agonist of the Human Glucagon-like Peptide-1 Receptor.
AID1392294Antidiabetic activity in STZ-induced diabetic Kunming mouse model assessed as increase in islet beta-cell area 25 nmol/kg, ip administered once daily for 3 weeks measured post last dose by hematoxylin and eosin staining based assay2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Novel fatty acid chain modified GLP-1 derivatives with prolonged in vivo glucose-lowering ability and balanced glucoregulatory activity.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (2,738)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's30 (1.10)18.2507
2000's534 (19.50)29.6817
2010's1748 (63.84)24.3611
2020's426 (15.56)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials383 (13.65%)5.53%
Trials0 (0.00%)5.53%
Reviews402 (14.33%)6.00%
Reviews3 (13.64%)6.00%
Case Studies72 (2.57%)4.05%
Case Studies0 (0.00%)4.05%
Observational22 (0.78%)0.25%
Observational0 (0.00%)0.25%
Other1,927 (68.67%)84.16%
Other19 (86.36%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (318)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
iPAVE - Imaging Pituitary ActiVation by Exendin [NCT03923114]20 participants (Anticipated)Interventional2019-05-23Recruiting
The Physiology of Glucagon-like-peptide-1 Espression in Patients With Endogenous Hyperinsulinism: Correlation With Histopathology [NCT03768518]40 participants (Anticipated)Observational2018-02-07Recruiting
Impact of Exenatide on Cardiovascular Exercise Performance in Type 2 Diabetes [NCT01364584]23 participants (Actual)Interventional2010-10-31Completed
The Effect of GLP-1 Receptor Activation on Central Reward and Satiety Circuits in Response to Food Stimuli in Obesity and Diabetes [NCT01281228]48 participants (Actual)Interventional2011-09-30Completed
Effects of Exenatide (Byetta®) on Biochemical and Histological Parameters of Liver Function in Patients With Nonalcoholic Steatohepatitis (NASH) [NCT01208649]Phase 413 participants (Actual)Interventional2008-07-31Completed
Intravenous Exenatide (Byetta) for the Treatment of Perioperative Hyperglycemia: Rollover Phase I/II Trial [NCT00882050]Phase 1/Phase 2104 participants (Actual)Interventional2009-03-31Completed
A Dose Block-randomized, Double-blind, Placebo-controlled, Dose-escalating, Phase I Study to Evaluate Safety and Pharmacokinetics/Pharmacodynamics of DA-3091 After Subcutaneous Injection in Healthy Male Subjects [NCT01156779]Phase 131 participants (Actual)Interventional2010-07-31Completed
A Pilot Study Evaluating Exenatide for the Treatment of Postprandial Hyperinsulinemic Hypoglycemia Post-RYGB [NCT02685852]Phase 111 participants (Actual)Interventional2016-02-29Completed
Incretin-based Drugs and the Risk of Heart Failure: A Multi-center Network Observational Study [NCT02456428]1,499,650 participants (Actual)Observational2014-03-31Completed
Visualizing Beta Cells in Patients With a History of Gestational Diabetes [NCT03182296]24 participants (Anticipated)Interventional2016-11-10Recruiting
Exenatide Weekly Injections as an Adjunctive Treatment in Patients With Schizophrenia [NCT02417142]Phase 470 participants (Actual)Interventional2014-09-30Completed
Evaluation of the Single-Use Pre-Filled Autoinjector [NCT02349802]Phase 13,052 participants (Actual)Interventional2013-02-28Completed
Enhancing Weight Loss Maintenance With GLP-1RA (BYDUREON™) in Adolescents With Severe Obesity [NCT02496611]Phase 2100 participants (Actual)Interventional2015-12-31Completed
A Phase 1, Open-label, Randomized, Two-period, Two-treatment, Crossover Study to Evaluate the Effect of Exenatide on the Pharmacokinetics and Pharmacodynamics of Bexagliflozin in Healthy Subjects [NCT03167411]Phase 120 participants (Actual)Interventional2017-05-24Completed
A Phase 1b, Exploratory, Randomized, Partially Single Blinded, Placebo and Open Label Controlled, Parallel Group Study to Assess the Effects of HM11260C and an Active Comparator on Gastric Emptying and Beta-Cell Response in Subjects With Type 2 Diabetes M [NCT02059564]Phase 144 participants (Anticipated)Interventional2013-12-31Recruiting
Effects of GLP-1 Receptor Agonist on Fat Redistribution and Inflammatory Status in Female Patients With Type 2 Diabetes and Obesity [NCT02118376]20 participants (Anticipated)Interventional2014-08-31Not yet recruiting
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 [NCT03060980]Phase 3245 participants (Actual)Interventional2017-03-03Terminated(stopped due to Decision by Sponsor)
Randomized Trial Investigating Exenatide for Diabetes Prevention in Obese, Insulin-Resistant Individuals With Prediabetes [NCT02084654]Phase 166 participants (Actual)Interventional2007-11-30Completed
Bioenergetic Alterations After Exenatide Administration [NCT00623545]Phase 428 participants (Actual)Interventional2008-01-31Completed
An Open Label, Single Site, 12 Month, Phase II, Randomised Controlled Trial Evaluating the Safety and Efficacy of Exendin-4 (Exenatide) in the Treatment of Patients With Moderate Severity Parkinson's Disease. [NCT01174810]Phase 240 participants (Anticipated)Interventional2010-07-31Active, not recruiting
An Evaluation of the Metabolic Effects of Exenatide, Rosiglitazone, and Exenatide Plus Rosiglitazone in Subjects With Type 2 Diabetes Mellitus Treated With Metformin [NCT00135330]Phase 3137 participants (Actual)Interventional2005-10-31Completed
A Phase 3, Randomized, Open Label, Comparator-Controlled, Parallel Group, Multicenter Study to Compare the Effects of Exenatide and Insulin Glargine on Beta Cell Function and Cardiovascular Risk Markers in Subjects With Type 2 Diabetes Treated With Metfor [NCT00097500]Phase 369 participants (Actual)Interventional2004-09-30Completed
Efficacy of Exenatide (AC2993, Synthetic Exendin-4, LY2148568) Compared With Twice-Daily Biphasic Insulin Aspart in Patients With Type 2 Diabetes Using Sulfonylurea and Metformin [NCT00082407]Phase 3505 participants (Actual)Interventional2003-11-30Completed
Safety and Efficacy of Exenatide Once Weekly Versus Liraglutide in Subjects With Type 2 Diabetes and Inadequate Glycemic Control Treated With Lifestyle Modification and Oral Antidiabetic Medications [NCT01029886]Phase 3912 participants (Actual)Interventional2010-01-31Completed
Effect of Additional Treatment With EXenatide in Patients With an Acute Myocardial Infarction (the EXAMI Trial) [NCT01254123]Phase 340 participants (Anticipated)Interventional2009-11-30Recruiting
The Use of Incretin-based Drugs and the Risk of Acute Pancreatitis in Patients With Type 2 Diabetes [NCT02476760]1,417,914 participants (Actual)Observational2014-03-31Completed
A Comparison of Exenatide and Insulin Glargine on Glycemic Variability in T2DM Patients Inadequately Controlled With Metformin Monotherapy [NCT02325960]Phase 444 participants (Actual)Interventional2015-01-31Completed
Does Glucagon-like Peptide (GLP-1) Receptor Agonist Stimulation Reduce Alcohol Intake in Patients With Alcohol Dependence? [NCT03232112]Phase 2152 participants (Actual)Interventional2017-08-07Completed
COMBinAtion Therapy in Myocardial Infarction: The COMBAT-MI Trial [NCT02404376]Phase 3378 participants (Actual)Interventional2016-03-31Completed
The Effects of Faecal Microbiota Transplantation on Beta Cell Preservation in Patients With Newly Diagnosed Type 1 Diabetes [NCT05622123]Phase 220 participants (Anticipated)Interventional2023-02-23Recruiting
A Randomized, Placebo-Controlled Comparison of the Effects of Two Doses of LY2189265 or Exenatide on Glycemic Control in Patients With Type 2 Diabetes on Stable Doses of Metformin and Pioglitazone (AWARD-1: Assessment of Weekly Administration of LY2189265 [NCT01064687]Phase 3978 participants (Actual)Interventional2010-02-28Completed
Effects of Exenatide on Postprandial Hyperlipidemia and Inflammation [NCT00974272]Phase 439 participants (Actual)Interventional2006-08-31Completed
Effects of GLP-1 RAs on Weight and Metabolic Indicators in Obese Patients [NCT03671733]Phase 3150 participants (Anticipated)Interventional2018-09-01Recruiting
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 (DUAL™ III -GLP-1 Switch) [NCT01676116]Phase 3438 participants (Actual)Interventional2012-08-29Completed
Effects of Exenatide on Hypothalamic Obesity [NCT01061775]Phase 1/Phase 219 participants (Actual)Interventional2010-01-31Completed
EBIRIOS - Exenatide and Basal Insulins Use in the Real Setting: an Italian Observational Study in Patients With Type 2 Diabetes and Secondary Failure of Oral Antihyperglycemic Treatment [NCT01060059]888 participants (Actual)Observational2010-04-30Completed
A Pilot Study on the Effect of Glucagon and Glucagon-like Peptide-1 Co-agonism on Cardiac Function and Metabolism in Overweight Participants With Type 2 Diabetes (COCONUT) [NCT04307797]Phase 416 participants (Anticipated)Interventional2022-01-18Recruiting
Effect of Bydureon on Carotid Atherosclerosis Progression in T2DM [NCT02162550]Phase 4148 participants (Anticipated)Interventional2014-06-30Active, not recruiting
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 [NCT03419624]Phase 313 participants (Actual)Interventional2018-02-19Terminated(stopped due to Delay in patient enrolment)
Post-Marketing Surveillance Study: 12 To 24 Weeks Study On The Treatment Emergent Adverse Events In Patients With Type 2 Diabetes Taking Exenatide In Korea [NCT02090673]1,711 participants (Actual)Observational2009-02-28Completed
Effect of Short-term Intensive Insulin Sequential Exenatide Therapy on Beta Cell Function and Glycaemic Control in Patients With Newly Diagnosed Type 2 Diabetes :a Multicenter Prospective Randomized Control Study [NCT02129985]Phase 4100 participants (Anticipated)Interventional2014-02-28Recruiting
Exenatide BID Compared With Insulin Glargine to Change Liver Fat Content in Non-alcoholic Fatty-liver Disease Patients With Type 2 Diabetes [NCT02303730]Phase 476 participants (Actual)Interventional2015-03-31Completed
[NCT02170324]Phase 420 participants (Actual)Interventional2014-06-30Completed
Effect of AC 2993 (Synthetic Exendin-4) - Administered Alone or in Combination With Daclizumab - on Islet Function in Patients With Type I Diabetes [NCT00064714]Phase 247 participants (Actual)Interventional2003-07-31Completed
SGLT2 INHIBITION AND STIMULATION OF ENDOGENOUS GLUCOSE PRODUCTION [EGP]: Can the Glucagon-like Peptide-1 [GLP-1] Receptor Agonist, Exenatide, Prevent the Increase in EGP in Response to Dapagliflozin-induced Increase in Glucosuria [NCT03331289]Phase 4107 participants (Actual)Interventional2018-02-28Completed
A 24-week, Single Centre, Randomized, Parallel-group, Double-blind, Placebo Controlled Phase II Study With an Optional 28-week Open-label Extension to Evaluate the Efficacy on Body Weight of Dapagliflozin 10 mg Once Daily in Combination With Exenatide 2 m [NCT02313220]Phase 250 participants (Actual)Interventional2014-12-31Completed
EXEnatide in Patients Undergoing Coronary Artery Bypass Grafting for Improved glUcose conTrol and hemodynamIc ValuEs [NCT01373216]Phase 338 participants (Actual)Interventional2011-06-30Completed
Effects of EXEnatide on Glycemic Control and Weight Over 26 Weeks in Continuous Subcutaneous Insulin Infusion (CSII) Treated Patients With Type 2 Diabetes : a Phase 2/3 Double Blind randoMized Placebo-controlled Trial. [NCT01140893]Phase 2/Phase 3110 participants (Anticipated)Interventional2010-11-30Recruiting
Effect of the Weekly Administration of Exenatide LAR or Dulaglutide on the Variability of Blood Pressure and Heart Rate of 24 Hours in Patients With Type 2 Diabetes Mellitus Without Pharmacological Treatment. [NCT03444142]Phase 430 participants (Anticipated)Interventional2017-11-17Recruiting
A Phase 2, Prospective, Randomized, Multicenter, Open-Label, Controlled Trial to Assess the Efficacy and Safety of Exenatide SR for the Prevention of Diabetes After Kidney Transplantation. [NCT03961256]Phase 29 participants (Actual)Interventional2019-05-09Completed
Comparison Between GLP 1 Analogues and DPP 4 Inhibitors in Type 1 Diabetes Mellitus [NCT01235819]Phase 420 participants (Actual)Interventional2010-11-30Completed
Pharmacogenomics of GLP1 Receptor Agonists [NCT05762744]Phase 178 participants (Actual)Interventional2016-06-01Terminated(stopped due to We concluded that it would not be possible to meet our recruitment targets within the available budget. The study was ended when the funding ended.)
The Effect of Exenatide on Insulin Requirement, Weight and Inflammation in Obese Type 2 Diabetic Subjects on Insulin [NCT01154933]Phase 224 participants (Actual)Interventional2008-04-30Completed
Research of Intensive Metabolic Intervention Before Pregnancy in Polycystic Ovary Syndrome [NCT03383068]Phase 4160 participants (Anticipated)Interventional2018-01-01Not yet recruiting
Effect of Chronic Exenatide Therapy on Beta Cell Function and Insulin Sensitivity in Type 2 Diabetes Mellitus (T2DM) [NCT02981069]Phase 490 participants (Actual)Interventional2017-12-15Completed
The Effect of Exenatide on Fasting Bile Acids in Newly Diagnosed Type 2 Diabetes Mellitus Patients, a Pilot Study [NCT04303819]38 participants (Actual)Observational2020-01-05Completed
A Randomized, Phase 1, Three-Period, Placebo- and Positive-Controlled, Double-Blind, Crossover Study to Assess the Electrophysiological Effects of Exenatide at Therapeutic and Supratherapeutic Concentrations on the 12-Lead Electrocardiogram QT Interval in [NCT01297062]Phase 194 participants (Actual)Interventional2011-02-28Completed
Efficacy of Once-Weekly Exenatide Versus Once or Twice Daily Insulin Detemir in Patients With Type 2 Diabetes Treated With Metformin Alone or in Combination With Sulphonylurea [NCT01003184]Phase 3222 participants (Actual)Interventional2009-10-31Completed
Effect of Exenatide on 24h-UAER in Patients With Diabetic Nephropathy: a 24- Week Study [NCT02690883]Phase 492 participants (Actual)Interventional2016-04-08Completed
A Pilot Study to Determine the Effects of a Single Dose of Exenatide (Byetta ®) on the Acute Metabolic Responses to a Mixed Meal or Intravenous Glucose Tolerance Test in Patients With Type 1 Diabetes [NCT01855490]Phase 117 participants (Actual)Interventional2012-01-31Completed
A New Treatment Strategy of Adding Exenatide to Insulin Therapy for Patients With Type 2 Diabetes and Non-Alcoholic Fatty Liver Disease (NAFLD) [NCT01006889]Phase 424 participants (Actual)Interventional2008-01-31Completed
The Effect of GLP-1 on Postprandial Glucagon Secretion During Prolonged and Intermittent Stimulation of the GLP-1 Receptor Independent of The Gastric Emptying Rate. A Randomized, Open-label Study in People With Type 1 Diabetes [NCT02584582]Phase 2/Phase 310 participants (Anticipated)Interventional2015-07-31Enrolling by invitation
The Effect of Glucagon-like Peptide 1 (GLP-1) Receptor Agonist on Cerebral Blood Flow Velocity in Stroke Patients [NCT02829502]Phase 230 participants (Anticipated)Interventional2016-08-31Recruiting
A Placebo- and Positive-Controlled Study of the Electrophysiological Effects of a Single 10 μg Dose of Exenatide on the 12-Lead Electrocardiogram QT Interval in Healthy Subjects [NCT00672399]Phase 170 participants (Actual)Interventional2008-04-30Completed
Safety and Efficacy of Exenatide as Monotherapy and Adjunctive Therapy to Oral Antidiabetic Agents in Adolescents With Type 2 Diabetes. [NCT00658021]Phase 3122 participants (Actual)Interventional2008-05-30Completed
An Open-Label Study Examining the Long-Term Safety of Exenatide Given Twice Daily to Patients With Type 2 Diabetes Mellitus [NCT01876849]Phase 3275 participants (Actual)Interventional2003-12-31Completed
Randomized, Active Controlled, Open Label Study to Compare Taspoglutide vs Exenatide as add-on Treatment to Metformin and/or Thiazolidinediones in Patients With Type 2 Diabetes Mellitus [NCT00717457]Phase 31,189 participants (Actual)Interventional2008-07-31Completed
Glucagon-Like Peptide-1 Agonist Effects on Energy Balance in Hypothalamic Obesity [NCT02664441]Phase 342 participants (Actual)Interventional2016-03-31Completed
Effect of Exenatide Once Weekly on Cardiovascular Risk Markers in Patients With Type-2 Diabetes [NCT02380521]Phase 460 participants (Actual)Interventional2015-01-31Completed
Research of Exenatide for Management of Reproductive and Metabolic Dysfunction in Overweight/Obese PCOS Patients With Impaired Glucose Regulation [NCT03352869]Phase 4183 participants (Actual)Interventional2017-11-28Completed
[NCT02092597]Phase 442 participants (Actual)Interventional2013-10-31Completed
Beijing Chao-Yang Hospital, Capital Medical University [NCT03297879]Phase 4230 participants (Actual)Interventional2013-01-01Completed
A Randomized, Open-Label, Long-Term, Parallel-Group, Comparator-Controlled, Multicenter Study to Compare the Glycemic Effects, Safety, and Tolerability of Exenatide Once Weekly Suspension to Exenatide Twice Daily in Subjects With Type 2 Diabetes Mellitus [NCT01652716]Phase 3377 participants (Actual)Interventional2013-01-31Completed
New Imaging Procedure for the Localisation of Insulinoma [NCT02127541]52 participants (Actual)Interventional2014-01-06Completed
The Differential Effects of Diabetes Therapy on Inflammation [NCT02150707]17 participants (Actual)Observational2014-05-31Completed
A Phase 1b, Randomized, Double-Blind, Active Comparator (Open-Label Exenatide) Controlled Study to Evaluate the Effect of Roflumilast Plus Alogliptin on Postprandial Active GLP-1 Level and 24-hour Glucose Level in Subjects With Type 2 Diabetes Who Are Ina [NCT01664624]Phase 140 participants (Actual)Interventional2012-07-31Completed
Effect of Exenatide on Disease Progression in Early Parkinson's Disease [NCT04305002]Phase 260 participants (Actual)Interventional2020-01-21Active, not recruiting
Effect of Gelofusine on 111In-DTPA-AHX-Lys40-Exendin 4 Uptake in the Kidney [NCT02541734]Phase 1/Phase 212 participants (Actual)Interventional2015-08-31Completed
6-Months Exenatide and Glucose Homeostasis Determinants in Type 2 Diabetic Patients [NCT00948168]Phase 434 participants (Actual)Interventional2008-07-31Completed
A 16-Week, Parallel-Group, Double-Blind, Randomized, Placebo-Controlled, Multicenter, Dose-Ranging Study to Evaluate the Efficacy, Safety, and Tolerability of Multiple Doses and Multiple Treatment Regimens of GSK716155, With Byetta as an Open Label Active [NCT00518115]Phase 2361 participants (Actual)Interventional2007-04-30Completed
Efficacy of a Glucagon-like-peptide-1 Agonist and Restrictive vs. Liberal Oxygen Supply in Patients Undergoing Coronary Artery Bypass Grafting or Aortic Valve Replacement - a 2-by-2 Factorial Designed, Randomized Clinical Study [NCT02673931]1,400 participants (Actual)Interventional2016-02-29Active, not recruiting
A Pilot, Safety and Feasibility Trial of Anti-Thymocyte Globulin (ATG), Low Dose Interleukin-2 (IL-2), Adalimumab and Exenatide in the Treatment of New-Onset Type 1 Diabetes [NCT02586831]Phase 1/Phase 245 participants (Anticipated)Interventional2024-06-01Not yet recruiting
Effect of AC2993 (Synthetic Exendin-4) Compared With Insulin Glargine in Patients With Type 2 Diabetes Also Using Combination Therapy With Sulfonylurea and Metformin [NCT00082381]Phase 3551 participants (Actual)Interventional2003-06-30Completed
A Dose Block-randomized, Double-blind, Placebo-controlled, Dose-escalating Study to Evaluate Safety and Pharmacokinetics/Pharmacodynamics of SR Exenatide (PT302) After Subcutaneous Injection in Healthy Male Volunteers [NCT00964262]Phase 134 participants (Actual)Interventional2009-08-31Completed
Effect of Pioglitazone With and Without Exenatide on Body Weight, Fat Topography, Beta Cell Function, and Glycemic Control in Type 2 Diabetic Patients [NCT00845182]Phase 443 participants (Actual)Interventional2007-06-30Completed
The Effect of the Glucagon Suppressors Pramlintide and Exenatide on Postprandial Glucose Metabolism in Children With Type 2 Diabetes Mellitus [NCT00950677]Phase 416 participants (Actual)Interventional2009-07-31Completed
A Comparator-Controlled Study to Examine the Effects of Exenatide Once-Weekly Injection on Glucose Control (HbA1c) and Safety in Asian Subjects With Type 2 Diabetes Mellitus Managed With Oral Antidiabetic Medications [NCT00917267]Phase 3691 participants (Actual)Interventional2009-07-31Completed
Do Appetitive Gut Hormones Reduce Addictive and Eating Behaviours in Obesity, and Nicotine and Alcohol Dependence? [NCT02690987]Early Phase 195 participants (Actual)Interventional2015-08-31Active, not recruiting
Two-Part, Randomized, Placebo and Active-Controlled, Double-Blind, Thorough QT Study Evaluating the Effects of Intravenous Exenatide on Cardiac Repolarization in Healthy Male and Female Volunteers [NCT02650479]Phase 182 participants (Actual)Interventional2016-01-31Completed
A Phase 1, Fixed-Sequence, Open-label Study in Healthy Subjects to Estimate the Effects of ITCA 650 on Gastric Emptying and on the Absorption Pharmacokinetics of Each of 4 Commonly Studied Drug/Drug Interaction (DDI) Probe Compounds [NCT02641899]Phase 133 participants (Actual)Interventional2015-12-31Completed
Multiple-Dose Study to Examine Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of LY2148568 Long-Acting Release in Japanese Patients With Type 2 Diabetes Mellitus [NCT00612794]Phase 130 participants (Actual)Interventional2007-09-30Completed
A Cohort Study of the Benefits of Bydureon in Customary Clinical Care in the United States - Additional Analyses [NCT02917057]6,024 participants (Actual)Observational2015-08-01Completed
Clinical Evaluation of 68Ga-NOTA-MAL-Cys39-exendin-4 Positron Emission Tomography in the Detection of Insulinoma [NCT04185350]Early Phase 160 participants (Anticipated)Interventional2019-05-05Recruiting
Acute Effect of a GLP-1-Analogue (Exenatide) and of a DPP-4-Inhibitor (Sitagliptin) in Subjects With Type 2 Diabetes Treated With Insulin Glargine Once Daily [NCT00971659]Phase 148 participants (Actual)Interventional2008-01-31Completed
A Randomized, Open-Label, Parallel-Group, Comparator-Controlled, Multicenter Study to Evaluate the Glycemic Effects, Safety, and Tolerability of Exenatide Once Weekly in Subjects With Type 2 Diabetes Mellitus [NCT00877890]Phase 3254 participants (Actual)Interventional2009-03-31Completed
An Open Label Study Comparing Exenatide With Basal Insulin in Achieving an HbA1c of ≤ 7.4% With Minimum Weight Gain, in Type 2 Diabetes Patients Who Are Not Achieving Adequate HbA1c Control on Oral Anti Diabetic Therapies Alone [NCT00360334]Phase 3235 participants (Actual)Interventional2006-06-30Completed
An Exploratory Study of the Effect of Treatment Interruption on Safety of Exenatide in Patients With Type 2 Diabetes [NCT00516048]Phase 358 participants (Actual)Interventional2007-08-31Completed
Effect of Liraglutide or Exenatide Added to a Background Treatment of Metformin, Sulphonylurea or a Combination of Both on Glycaemic Control in Subjects With Type 2 Diabetes [NCT00518882]Phase 3467 participants (Actual)Interventional2007-08-31Completed
A Study to Assess the Effect of Exenatide Treatment on Mean 24-Hour Heart Rate in Patients With Type 2 Diabetes [NCT00516074]Phase 354 participants (Actual)Interventional2007-09-30Completed
The Physiology of Glucagon-like-peptide-1 Receptor Expression in Patients With Endogenous Hyperinsulinism - Correlation With Histopathology [NCT00937079]30 participants (Actual)Observational2007-11-30Completed
A Pilot Study of Effects of Exenatide on Body Weight in Non-Diabetic, Obese Patients [NCT00500370]Phase 2163 participants (Actual)Interventional2007-06-30Completed
Investigation of the Cardiovascular Effects of Exenatide in Healthy Male Subjects [NCT01046721]8 participants (Actual)Interventional2009-09-30Completed
The Role of Exenatide in Type 1 Diabetes Mellitus [NCT00456300]Phase 211 participants (Actual)Interventional2007-03-31Completed
[NCT01302327]0 participants (Actual)Interventional2011-03-01Withdrawn(stopped due to Very rare disease, we were unable to recruit patients)
Exenatide (Byetta ®) Regulation of Intestinal and Hepatic Lipoprotein Particle Production in Humans. [NCT01056549]15 participants (Actual)Interventional2010-01-31Completed
A Randomized Clinical Trial to Study Glucose Dependent Insulin Secretion Methodologies in Healthy Lean Male Subjects [NCT00782418]Phase 127 participants (Actual)Interventional2008-09-30Completed
Safety and Efficacy of Exenatide in Patients With Type 2 Diabetes Using a Thiazolidinedione or a Thiazolidinedione and Metformin [NCT00603239]Phase 3165 participants (Actual)Interventional2008-01-31Completed
A Comparison of Adding Exenatide With Switching to Exenatide in Patients With Type 2 Diabetes Experiencing Inadequate Glycemic Control With Sitagliptin Plus Metformin [NCT00870194]Phase 4255 participants (Actual)Interventional2009-03-31Completed
MB001-067 A PROSPECTIVE, DOUBLE BLIND, PLACEBO CONTROLLED, PARALLEL GROUP, RANDOMIZED TRIAL OF EXTENDED RELEASE EXENATIDE VERSUS PLACEBO (COHORT A) AND A PROSPECTIVE, SINGLE GROUP, OPEN-LABEL, BLINDED OUTCOME TRIAL OF EXTENDED RELEASE EXENATIDE (COHORT B) [NCT02251431]Phase 357 participants (Actual)Interventional2015-11-30Completed
Safety of Exenatide Once Weekly in Patients With Type 2 Diabetes Mellitus Treated With Thiazolidinedione Alone or Thiazolidinedione in Combination With Metformin [NCT00753896]Phase 3134 participants (Actual)Interventional2008-10-31Completed
Comparison of the Effect of Exenatide vs. Sitagliptin on 24-hour Average Glucose in Patients With Type 2 Diabetes on Metformin or a Thiazolidinedione [NCT00729326]Phase 483 participants (Actual)Interventional2008-08-31Completed
Efficacy of Once-Weekly Exenatide Long-Acting Release and Once-Daily Insulin Glargine in Patients With Type 2 Diabetes Treated With Metformin Alone or in Combination With Sulfonylurea [NCT00641056]Phase 3467 participants (Actual)Interventional2008-04-30Completed
Assessment of Pancreatic Beta Cell Mass and Function With the Aid of Positron Emission Tomography Imaging in Human Diabetes Mellitus [NCT05662189]70 participants (Anticipated)Interventional2022-03-15Recruiting
The Effect of Exenatide Compared to Insulin Glargine on Cardiac Function and Metabolism in Type 2 Diabetic Patients With Congestive Heart Failure: a Randomized Comparator-controlled Trial [NCT00766857]Phase 427 participants (Actual)Interventional2009-05-31Completed
Efficacy and Safety of LY2148568 in Japanese Patients With Type 2 Diabetes Who Are Treated With Oral Antidiabetic(s) But Not Well Controlled [NCT00577824]Phase 3181 participants (Actual)Interventional2008-01-31Completed
Comparison of Type 2 Diabetes Pharmacotherapy Regimens Using Targeted Learning [NCT05073692]270,000 participants (Anticipated)Observational2021-07-01Recruiting
A Parallel, Double-blinded, Randomized, 6 Months, Two Arms Study With Lifestyle Intervention and Bydureon® or Lifestyle Intervention and Placebo in Adolescents With Obesity to Explore Differences With Regard to Change in BMI SDS [NCT02794402]Phase 244 participants (Actual)Interventional2015-09-30Completed
Efficacy of Exenatide-LAR Alone and in Combination With Dapagliflozin in Overweight/Obese, Insulin Treated Patients With Uncontrolled Type 2 Diabetes [NCT02811484]Phase 40 participants (Actual)Interventional2016-06-30Withdrawn(stopped due to Inability to enroll due to the widespread use of both classes of drugs in patients with T2DM, including those on concomitant insulin therapy.)
Phase 2 Study of ITCA 650 in Subjects With Type 2 Diabetes Mellitus [NCT00943917]Phase 2155 participants (Actual)Interventional2009-08-31Completed
The Effects of Exenatide (Byetta) on Energy Expenditure and Weight Loss in Non-Diabetic Obese Subjects [NCT00856609]Phase 3150 participants (Actual)Interventional2009-03-03Completed
A Single-center,Proof of Concept,Randomized,Controlled Parallel Group Clinical Trial of the Effects of Exenatide vs. a Long Acting Insulin Analog to Evaluate the Efficacy of Exenatide in Patients With Diabetic Neuropathy and Type 2 Diabetes [NCT00855439]46 participants (Actual)Interventional2008-06-30Completed
The Effects of Exenatide on Post-Prandial Glucose Excursions and Vascular Health in Obese/Pre-Diabetic Young Adults [NCT00845559]Phase 40 participants (Actual)Interventional2008-08-31Withdrawn
A Randomized, Multi-dose, Controlled Trial Investigating the Efficacy, Safety and Tolerability, and Pharmacokinetics of Exenatide Once Monthly Suspension. [NCT01104701]Phase 2121 participants (Actual)Interventional2010-05-31Completed
A Phase 1, Randomized, Double-blind, Placebo-Controlled, Crossover Study to Assess the Effect of ITCA 650 on the Pharmacokinetics and Pharmacodynamics of a Combination Oral Contraceptive in Healthy Premenopausal Female Subjects [NCT02641990]Phase 128 participants (Actual)Interventional2015-12-31Completed
Additional GLP-1 Analogue on CSII Treatment for Poorly Controlled Type 2 Diabetic Patients [NCT01473147]51 participants (Actual)Interventional2011-10-31Completed
Safety and Efficacy of Exenatide Once Weekly Injection Versus Metformin, Dipeptidyl Peptidase-4 Inhibitor, or Thiazolidinedione as Monotherapy in Drug-Naive Patients With Type 2 Diabetes [NCT00676338]Phase 3820 participants (Actual)Interventional2008-11-30Completed
Assessment of Hepatic Glucose and Fat Regulation in Overweight Adolescent Girls [NCT02157974]Phase 2/Phase 392 participants (Actual)Interventional2014-08-31Completed
A Pilot Study of the Effects of BYETTA® (Exenatide) on Weight Loss in Morbidly Obese Non Diabetic Patients Following Adjustable Gastric Banding [NCT00872378]Phase 2/Phase 328 participants (Anticipated)Interventional2009-02-28Recruiting
Prednisolone-induced Impairment of Glucose Metabolism and Beta-cell Dysfunction and the Protective Effects of Exenatide: a Single-center, Randomized, Double-blind, Placebo-controlled Crossover Study in Healthy Volunteers [NCT00744224]8 participants (Anticipated)Interventional2009-02-28Completed
A Randomized Trial Comparing Exenatide With Placebo in Subjects With Type 2 Diabetes on Insulin Glargine With or Without Oral Antihyperglycemic Medications [NCT00765817]Phase 3261 participants (Actual)Interventional2008-10-31Completed
The Effect of the GLP-1 Analogue Exenatide on Glucose Metabolism in the CNS and Heart During Hyperglycemia in Type-2 Diabetic Patients Assessed by PET [NCT00747968]Phase 2/Phase 38 participants (Actual)Interventional2010-02-28Completed
68Ga-NOTA-exendin-4 PET/CT for the Localization of Insulinoma and Diagnosis of Nesidioblastosis [NCT02560376]Early Phase 1100 participants (Anticipated)Interventional2014-02-28Recruiting
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 [NCT04232969]Phase 3194 participants (Actual)Interventional2020-01-20Active, not recruiting
Effect of the GLP-1 Receptor Agonist Exenatide on Impaired Hypoglycaemic Awareness in Type 1 Diabetes [NCT02735031]Phase 2/Phase 310 participants (Actual)Interventional2017-02-21Completed
A Real-world, Observational Study of GLP-1 Therapy Added to Basal Insulin in Patients With Type 2 Diabetes Mellitus [NCT02895672]150 participants (Actual)Observational2016-08-31Completed
[NCT02584075]Phase 4100 participants (Anticipated)Interventional2015-11-30Not yet recruiting
Contribution of a GLP-1 Agonist to Appetite Regulation, Metabolism and Body Composition in Subjects With Prader-Willi Syndrome. [NCT00551343]20 participants (Actual)Interventional2007-10-31Completed
Pharmacological Postconditioning to Reduce Infarct Size Following Primary PCI in Patients With STEMI [NCT00835848]Phase 4100 participants (Anticipated)Interventional2009-01-31Completed
CHOICE: CHanges to Treatment and Outcomes in Patients With Type 2 Diabetes Initiating InjeCtablE Therapy - A European Observational Study of Patients With Type 2 Diabetes Initiating Injectable Therapy to Determine Time to Treatment Change, Factors Associa [NCT00635492]2,515 participants (Actual)Observational2008-01-31Completed
A Phase 1, Open-Label Study to Evaluate Single and Multiple Dose Pharmacokinetics, Safety, and Tolerability of Exenatide Once-Weekly Suspension in Chinese Patients With Type 2 Diabetes Mellitus [NCT04001231]Phase 10 participants (Actual)Interventional2020-06-30Withdrawn(stopped due to The study is stopped based upon strategic considerations impacting the clinical development of exenatide once-weekly suspension in China)
A Randomized, Open-Label, Multicenter, Comparator-Controlled Study to Examine the Effects of Exenatide Long-Acting Release on Glucose Control (HbA1c) and Safety in Subjects With Type 2 Diabetes Mellitus Managed With Diet Modification and Exercise and/or O [NCT00308139]Phase 3303 participants (Actual)Interventional2006-04-30Completed
Effect of Exenatide Plus Metformin vs. Premixed Human Insulin Aspart Plus Metformin on Glycemic Control and Hypoglycemia in Patients With Inadequate Control of Type 2 Diabetes on Oral Antidiabetic Treatment [NCT00434954]Phase 3494 participants (Actual)Interventional2007-02-28Completed
Effect on Weight Loss of Exenatide Versus Placebo in Subjects With Type 2 Diabetes Participating in a Lifestyle Modification Program [NCT00375492]Phase 3196 participants (Actual)Interventional2006-09-30Completed
The Effect of Detemir Compared to Exenatide and/or the Combination of Detemir and Exenatide on Glycemic Control and Weight in Patients With Type 2 Diabetes Mellitus Who Have Failed Oral Hypoglycemic Agents [NCT01076842]Phase 475 participants (Anticipated)Interventional2008-04-30Completed
Long Term Treatment With Exenatide Versus Glimepiride in Patients With Type 2 Diabetes Pretreated With Metformin (EUREXA: European Exenatide Study) [NCT00359762]Phase 31,029 participants (Actual)Interventional2006-09-30Completed
Effectiveness of Once-weekly Exenatide (BCise) Plus Dapagliflozin on 24 Hour Glucose Variability Measured by CGM. A Proof of Concept. [NCT03970044]Phase 467 participants (Actual)Interventional2019-07-02Completed
Effects of KATP Channel Blockers on GLP-1 and Its Analogues' Mediated Microvascular Function [NCT01934816]2 participants (Actual)Interventional2013-06-30Terminated(stopped due to Technical Issues with intervention)
Exenatide for Myocardial Protection During Reperfusion Study: A Double-blind, Placebo-controlled Trial [NCT01938235]Phase 2198 participants (Anticipated)Interventional2014-02-28Recruiting
An Open-Label Extension Study of Protocol 2993-112 to Examine the Long-Term Effect on Glucose Control (HbA1c) and Safety and Tolerability of AC2993 Given Two Times a Day to Subjects Treated With Metformin Alone [NCT01789957]Phase 3225 participants (Actual)Interventional2002-09-30Completed
Intravenous Exenatide (Byetta®) Versus Insulin for Perioperative Glycemic Control in Cardiac Surgery: the Open-labeled Randomized Phase II/III ExStress Study [NCT01969149]Phase 2/Phase 3110 participants (Actual)Interventional2015-01-31Completed
A Randomised, Double Blind, Placebo Controlled, Single Centre, 60 Week Trial of Exenatide Once Weekly for the Treatment of Moderate Severity Parkinson's Disease [NCT01971242]Phase 260 participants (Actual)Interventional2014-06-30Completed
GLP-1's Influence on Intestinal Blood Flow [NCT01988545]8 participants (Anticipated)Interventional2013-11-30Recruiting
A Randomized Trial Comparing Two Therapies: Basal Insulin/Glargine, Exenatide and Metformin Therapy (BET) or Basal Insulin/Glargine, Bolus Insulin Lispro and Metformin Therapy (BBT) in Subjects With Type 2 Diabetes Who Were Previously Treated by Basal Ins [NCT00960661]Phase 31,036 participants (Actual)Interventional2009-09-30Completed
Brain Systems and Behaviors Underlying Response to Obesity Treatment in Children [NCT04520490]Phase 364 participants (Anticipated)Interventional2021-01-28Recruiting
FLAT-SUGAR: FLuctuATion Reduction With inSULin and Glp-1 Added togetheR [NCT01524705]Phase 4102 participants (Actual)Interventional2012-08-31Completed
A Retrospective Cohort Study of Acute Pancreatitis in Relation to Use of Byetta (Exenatide) and Other Antidiabetic Agents [NCT01077323]363,766 participants (Actual)Observational2004-09-30Completed
Effect of Exenatide in Obese Patients With Accelerated Gastric Emptying [NCT02160990]Phase 420 participants (Actual)Interventional2014-06-30Completed
Exenatide and Postprandial Endothelial Dysfunction: Effects and Mechanisms [NCT01181986]Phase 476 participants (Actual)Interventional2010-08-31Completed
EXCEED - 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 [NCT05663515]2,400 participants (Anticipated)Observational2024-01-01Not yet recruiting
The Clinical Application of 68Ga-NOTA-exendin-4 PET/CT in Detecting Insulinoma [NCT04979611]Phase 160 participants (Anticipated)Interventional2020-08-01Recruiting
Metformin, Exenatide, and Glargine Insulin in Combination for Treatment of Patients With Type 2 Diabetes [NCT00667732]Phase 441 participants (Actual)Interventional2007-03-31Completed
A Randomized, Open-label, Active-controlled, 2-arm Parallel-group, Multicenter 24-week Study Followed by an Extension Assessing the Efficacy and Safety of AVE0010 Versus Exenatide on Top of Metformin in Patients With Type 2 Diabetes Not Adequately Control [NCT00707031]Phase 3639 participants (Actual)Interventional2008-06-30Completed
A Randomized Controlled Trial of Exenatide as an Adjunct to Nicotine Patch for Smoking Cessation and Prevention of Post-Cessation Weight Gain [NCT05610800]Phase 2216 participants (Anticipated)Interventional2022-12-07Recruiting
A Randomized, Controlled Trial Comparing the Effect of Exenatide, Sitagliptin or Glimepiride on Functional ß -Cell Mass in Patients With Impaired Fasting Glucose or Early Type 2 Diabetes [NCT00775684]47 participants (Actual)Interventional2008-10-31Completed
An Open-Label Multi-Center Sub-Study to Evaluate the Efficacy, Safety and Tolerability of ITCA 650 in Patients With Type 2 Diabetes With High Baseline HbA1c [NCT01785771]Phase 3100 participants (Anticipated)Interventional2013-05-31Terminated(stopped due to Decision by Sponsor)
Efficacy and Durability of Glucagon Like Peptide 1 Receptor Agonists (GLP-1 RA)/Thiazolidinedione Versus Basal Bolus Insulin Therapy in Poorly Controlled Type 2 Diabetic Patients (T2DM) Patients on Sulfonylurea Plus Metformin [NCT02887625]410 participants (Anticipated)Interventional2015-02-28Recruiting
Multicentre Double-blind Randomized Clinical Trial Assessing Efficacy and Safety of Exenatide in the Treatment of Hypothalamic Obesity After Craniopharyngioma Therapy [NCT02860923]Phase 342 participants (Actual)Interventional2017-01-11Completed
A Two-Cohort, Single- and Repeat Dose Study to Examine the Pharmacokinetics, Tolerability, and Safety of Ready to Use Exenatide Once Weekly in Healthy Subjects and in Subjects With Type 2 Diabetes Mellitus [NCT00894322]Phase 1/Phase 265 participants (Actual)Interventional2009-04-30Completed
Durability of Early Initial Combination Therapy With Exenatide/Pioglitazone/Metformin vs Conventional Therapy in New Onset Type 2 Diabetes [NCT01107717]Phase 4521 participants (Actual)Interventional2009-01-31Active, not recruiting
Long-acting Exenatide: a Tool to Stop Cognitive Decline in Dysglycemic Patients With Mild Cognitive Impairment? [NCT02847403]Phase 340 participants (Anticipated)Interventional2016-02-29Active, not recruiting
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 Patie [NCT03007329]Phase 434 participants (Actual)Interventional2017-03-08Completed
The Effect of Glucagon-like Peptide 1 (GLP-1) Receptor Agonist on Cerebral Blood Flow Velocity in Non-Stroke Volunteers (EGRABINS1) [NCT02838589]Phase 230 participants (Actual)Interventional2016-08-31Completed
Impact of Exenatide on Sleep Duration and Quality in Type 2 Diabetes [NCT01416649]8 participants (Actual)Observational2011-02-01Completed
A Phase 2, Randomized, Triple-Blind, Placebo-Controlled, Multicenter Study to Examine the Effect of Exenatide Monotherapy on Glucose Control in Subjects With Type 2 Diabetes Mellitus [NCT00085969]Phase 299 participants (Actual)Interventional2003-09-30Completed
A Pilot Prospective Comparison of [68Ga]Ga-HBED-CC-exendin-4 and [68Ga]Ga-NOTA-exendin-4 PET/CT Imaging in the Same Group of Insulinoma Patients [NCT05034783]Early Phase 120 participants (Actual)Interventional2021-10-01Active, not recruiting
Parallel Group Study to Evaluate the Efficacy and Safety of Exenatide Once-Weekly Injection Compared to Once-Daily Insulin in Type 2 Diabetes Mellitus Treated With Oral Antidiabetic(s) [NCT00935532]Phase 3427 participants (Actual)Interventional2009-07-31Completed
An Open-Label Exploratory Study to Investigate the Feasibility of Administering Exenatide by Continuous Subcutaneous Infusion to Healthy Subjects [NCT01857895]Phase 110 participants (Actual)Interventional2013-05-16Completed
GLP-1 Analogue in Preventing Progression of Small Vessel Disease (GAPP-SVD) - A Pilot Study [NCT05356104]Phase 2110 participants (Anticipated)Interventional2022-05-25Recruiting
Visualizing Beta Cells in Patients With T2D Before and After Bariatric Surgery [NCT03182231]Phase 1/Phase 212 participants (Anticipated)Interventional2016-10-07Recruiting
A Phase II, 16-week, Double-blind, Placebo-controlled, Parallel-group, Randomised, Multicentre Trial to Assess Effect on Glycaemic Control of Three Doses of HM11260C in Subjects With Inadequately Controlled Type 2 Diabetes Receiving a Stable Dose of Metfo [NCT02081118]Phase 2209 participants (Actual)Interventional2014-02-28Completed
A Randomized, Double-Blind, Parallel-Group, Multicenter Study to Compare the Glycemic Effects, Safety, and Tolerability of Exenatide Long-Acting Release(Once Weekly) to Those of Sitagliptin and a Thiazolidinedione in Subjects With Type 2 Diabetes Mellitus [NCT00637273]Phase 3514 participants (Actual)Interventional2008-01-31Completed
A Multicentre, Randomised Controlled Trial of Exenatide Versus Standard Care in Acute Ischemic Stroke (TEXAIS) [NCT03287076]Phase 2350 participants (Actual)Interventional2017-11-23Active, not recruiting
Comparison of Dapagliflozin (DAPA) and Once-weekly Exenatide (EQW), Co-administered or Alone, DAPA/ Glucophage (DAPA/MET ER) and Phentermine/Topiramate (PHEN/TPM) ER on Metabolic Profiles and Body Composition in Obese PCOS Women [NCT02635386]Phase 3119 participants (Actual)Interventional2016-03-22Completed
A Comparison of the Haemodynamic and Metabolic Effects of Intravenous Glucagon-like Peptide-1, Glucagon and Glucagon-like Peptide-1:Glucagon Co-agonism in Healthy Male Participants [NCT03835013]20 participants (Anticipated)Interventional2019-02-11Recruiting
A Randomized, Double-Blind, Crossover Study to Compare the Effects of Exenatide and Sitagliptin on Postprandial Glucose in Subjects With Type 2 Diabetes Mellitus [NCT00477581]Phase 4102 participants (Actual)Interventional2007-05-31Completed
Randomized Clinical Trial to Evaluate The Effect of Metformin-GLP-1 Receptor Agonist Versus Oral Contraceptive (OC) Therapy on Reproductive Disorders and Cardiovascular Risks in Overweight Polycystic Ovarian Syndrome (PCOS) Patients [NCT03151005]Phase 470 participants (Actual)Interventional2017-07-01Completed
Cardioprotective Effects of Exenatide in Patients With ST-segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention ; Results of Exenatide Myocardial Protection In REvascularization (EMPIRE) Study [NCT01580514]Phase 4127 participants (Actual)Interventional2009-09-30Completed
A Study by Scintigraphy to Evaluate the Effect of Exenatide on Gastric Emptying in Subjects With Type 2 Diabetes [NCT00517283]Phase 117 participants (Actual)Interventional2005-01-31Completed
A Phase II, 12-week, Double-blind, Randomised, Parallel Group, Multi-centre, International Trial to Assess the Effect on Glycaemic Control of Five Doses of HM11260C Versus Placebo or Open-label Liraglutide in Subjects With Type 2 Diabetes [NCT02057172]Phase 2254 participants (Actual)Interventional2014-01-31Completed
Meal-time Administration of Exenatide for Glycaemic Control in Type 1 Diabetic Cases: A Randomised, Placebo-controlled Trial [NCT03017352]Phase 2108 participants (Actual)Interventional2016-12-31Completed
Safety and Efficacy of Exenatide as Monotherapy in Drug Naive Patients With Type 2 Diabetes [NCT00381342]Phase 3233 participants (Actual)Interventional2006-09-30Completed
An Investigation Into the Effect of Dapagliflozin on Ketogenesis in Type 1 Diabetes [NCT02962492]Phase 480 participants (Anticipated)Interventional2016-11-30Not yet recruiting
Effect of Exenatide on 24-Hour Blood Glucose Profile Compared With Placebo in Patients With Type 2 Diabetes Using Metformin or Metformin Plus a Thiazolidinedione [NCT00241423]Phase 230 participants (Actual)Interventional2005-10-31Completed
An Exploratory Study of the Safety of Substituting Exenatide for Insulin in Patients With Type 2 Diabetes Who Have Been Using Insulin in Combination With Oral Antidiabetic Therapy [NCT00099333]Phase 249 participants (Actual)Interventional2004-02-29Completed
A Phase 2, Randomized, Double-Blind, Placebo-Controlled, Multicenter Study to Examine Safety and Pharmacokinetics of Exenatide Long-Acting Release Administered Weekly in Subjects With Type 2 Diabetes Mellitus [NCT00103935]Phase 245 participants (Actual)Interventional2005-02-28Completed
A Randomized, Single-Blind, Dose-Rising, Placebo-Controlled, Crossover Study to Evaluate the Pharmacokinetics, Pharmacodynamics, and Tolerability of Exenatide in Adolescent Subjects With Type 2 Diabetes Mellitus [NCT00254254]Phase 213 participants (Actual)Interventional2006-02-28Completed
The Effect of Exenatide on Single and Multiple Doses Oral Contraceptive Pharmacokinetics in Healthy Female Subjects [NCT00254800]Phase 138 participants (Actual)Interventional2005-11-30Completed
An Open Label Study to Examine the Long Term Effect on Glucose Control (HbA1c) and Safety and Tolerability of Exenatide Given Two Times a Day to Subjects With Type 2 Diabetes Mellitus [NCT00111540]Phase 3456 participants (Actual)Interventional2002-11-30Completed
Identification and Clinical Relevance of an Oxytocin Deficient State: a Randomized, Crossover, Placebo-controlled, Proof-of-concept, Physiopathological Study (GLP1 Study) [NCT04897802]Phase 452 participants (Anticipated)Interventional2021-09-13Recruiting
A Double-Masked, Randomized, Placebo-Controlled, Multiple Ascending Dose Phase 2 Study to Determine the Tolerability, Pharmacokinetics, and Pharmacodynamics of the GLP 1 Agonist HM11260C in Adult Subjects With Type 2 Diabetes Mellitus on Stable Metformin [NCT01452451]Phase 272 participants (Actual)Interventional2011-12-31Completed
Comparison of the Effects of Monotherapy With Exenatide or Metformin to Combined Exenatide and Metformin Therapy on Menstrual Cyclicity in Overweight Women With Polycystic Ovary Syndrome [NCT00344851]Phase 260 participants (Actual)Interventional2006-06-30Completed
Safety and Efficacy of Exenatide in Patients With Type 2 Diabetes Using Thiazolidinediones or Thiazolidinediones and Metformin [NCT00099320]Phase 3182 participants (Actual)Interventional2004-05-31Completed
Effect of Short-Term Intensive Insulin Sequential Exenatide Therapy on β-cell Function and Glycemic Remission Rate in Newly Diagnosed Type 2 Diabetic Patients [NCT01776788]Phase 4156 participants (Actual)Interventional2012-08-31Completed
GLP-1 Therapy for Weight Loss and Improved Glucose Tolerance in Obese Children: A Randomized, Controlled, Pilot Study [NCT00886626]Phase 212 participants (Actual)Interventional2009-05-31Completed
Effects on Re-endothelialisation With Bydureon Treatment Add on to Insulin Versus Insulin Alone, Both in Combination With Metformin in Type 2 Diabetic Subjects [NCT02621489]Phase 438 participants (Actual)Interventional2015-12-31Completed
Exenatide Study of Cardiovascular Event Lowering Trial (EXSCEL). A Randomized, Placebo Controlled Clinical Trial to Evaluate Cardiovascular Outcomes After Treatment With Exenatide Once Weekly in Patients With Type 2 Diabetes Mellitus. [NCT01144338]Phase 314,752 participants (Actual)Interventional2010-06-18Completed
Treatment of Antipsychotic-associated Obesity With a GLP-1 Analogue [NCT01794429]Phase 345 participants (Actual)Interventional2013-02-28Completed
Pilot Study of Exenatide Pharmacokinetics and Pharmacodynamics in Gestational Diabetes [NCT00572689]Phase 40 participants (Actual)Interventional2013-08-31Withdrawn
A Pilot Study of Exendin-4 in Alzheimer s Disease [NCT01255163]Phase 257 participants (Actual)Interventional2010-11-21Terminated(stopped due to AstraZeneca withdrew support for the study.)
Study of Comparison the Treatment Effect Between Gastric Bypass and Exenatide in Type 2 Diabetes [NCT01435980]Phase 460 participants (Anticipated)Interventional2008-02-29Recruiting
Randomized, Placebo-Controlled, Single-Dose, Crossover Study to Evaluate the Safety, Pharmacokinetics, and Pharmacodynamics of BMS-686117 in Subjects With Type 2 Diabetes [NCT00508287]Phase 136 participants (Anticipated)Interventional2007-08-31Completed
Efficacy of Exenatide Compared With Insulin Glargine in Patients With Type 2 Diabetes Using Metformin or Sulfonylurea for Whom Insulin is the Next Appropriate Therapy [NCT00099619]Phase 3138 participants (Actual)Interventional2004-09-30Completed
Effect of Exenatide Treatment on Myocardial Fat Content, Left Ventricular Function, and Vascular Inflammation in Patients With Type 2 Diabetes Mellitus [NCT01951651]Phase 424 participants (Actual)Interventional2010-04-30Completed
A Phase 3, Randomized, Triple-Blind, Parallel-Group, Long-Term, Placebo-Controlled, Multicenter Study to Examine the Effect on Glucose Control (HbA1c) of AC2993 Given Two Times a Day in Subjects With Type 2 Diabetes Mellitus Treated With Metformin Alone [NCT00039013]Phase 3336 participants (Actual)Interventional2002-03-31Completed
An Open-Label Study to Examine the Long-Term Effect on Glucose Control (HbA1c) and Safety of AC2993 Given Two Times a Day to Subjects With Type 2 Diabetes Treated With Metformin, a Sulfonylurea, or Metformin and Sulfonylurea Combination [NCT00044668]Phase 3155 participants (Actual)Interventional2002-08-31Completed
Glucagon Like Peptide 1 Receptor (GLP1R) Expression and Beta-cell Mass in Patients With Type 2 Diabetes - the Role of Glucose Homeostasis on Uptake of Beta-cell Tracer Exendin-4 [NCT04733508]28 participants (Anticipated)Interventional2019-11-01Recruiting
A Cohort Study of the Benefits of Bydureon in Customary Clinical Care in the United States [NCT02974244]7,000 participants (Actual)Observational2014-10-28Completed
A Phase 3, Randomized, Triple-Blind, Parallel-Group, Long-Term, Placebo-Controlled, Multicenter Study to Examine the Effect on Glucose Control (HbA1c) of AC2993 Given Twice Daily in Subjects With Type 2 Diabetes Mellitus Treated With Metformin and a Sulfo [NCT00035984]Phase 3734 participants (Actual)Interventional2002-05-31Completed
Feasibility of Exenatide, a GLP-1R Agonist, for Treating Cocaine Use Disorder: A Case Series Study [NCT04941521]Phase 1/Phase 23 participants (Actual)Interventional2021-06-24Completed
A Phase 3, Randomized, Triple-Blind, Parallel-Group, Long-Term, Placebo-Controlled, Multicenter Study to Examine the Effect on Glucose Control (HbA1c) of AC2993 Given Two Times a Day in Subjects With Type 2 Diabetes Mellitus Treated With a Sulfonylurea Al [NCT00039026]Phase 3377 participants (Actual)Interventional2002-02-28Completed
A Phase 2, Randomized, Triple-Blind, Placebo-Controlled, Short-Term, Dose-Response Study to Examine the Effect on Glucose Control and Safety and Tolerability of AC2993 Given Two Times a Day in Subjects With Type 2 Diabetes Mellitus [NCT00044694]Phase 2156 participants (Actual)Interventional2002-08-31Completed
Comparative Effects of Antidiabetic Medications on Postprandial Hyperlipidemia, Free Fatty Acid Signaling, and Endothelial Dysfunction in Individuals With Prediabetes [NCT02104739]Phase 421 participants (Actual)Interventional2014-04-30Completed
Study on the Effect of Metformin vs Metformin Combined With GLP-1 RA (Exenatide) on Overweight/Obese Patients With Polycystic Ovary Syndrome (PCOS) [NCT04029272]Phase 480 participants (Anticipated)Interventional2019-07-20Recruiting
The Microvascular Function of GLP-1 and Its Analogues in Humans, in Vivo: the Role of DPP-IV Inhibition [NCT01677104]63 participants (Anticipated)Interventional2012-08-31Completed
Effect of Exenatide on Abdominal Fat Distribution in Patients With Type 2 Diabetes Pretreated With Metformin [NCT00701935]Phase 280 participants (Actual)Interventional2008-08-31Terminated(stopped due to Enrollment was much slower than anticipated, leading to a decision to terminate the study early for enrollment futility.)
Islet Transplantation in Type 1 Diabetic Patients Using the Edmonton Protocol of Steroid Free Immunosuppression [NCT00566813]Phase 1/Phase 210 participants (Actual)Interventional2004-11-30Completed
Comparative Effectiveness and Safety of Four Second Line Pharmacological Strategies in Type 2 Diabetes Study [NCT05220917]781,430 participants (Anticipated)Observational2021-08-01Active, not recruiting
The Effects of Short-Term Exenatide Therapy on the Beta-Cell Function and Long-term Glycemic Control in Newly Diagnosed Type 2 Diabetic Patients [NCT01270191]Phase 4160 participants (Anticipated)Interventional2010-11-30Recruiting
The Use of Incretin-based Drugs and the Risk of Pancreatic Cancer in Patients With Type 2 Diabetes [NCT02475499]886,172 participants (Actual)Observational2014-03-31Completed
Treatment With Glucagon-Like Peptide-1 Receptor, Exenatide, in Patients With Diabetes and Heart Failure With Normal Left Ventricular Ejection Fraction [NCT00799435]Phase 42 participants (Actual)Interventional2009-07-31Terminated(stopped due to Inability to recruit adequate Sample Size who met the entry criteria)
A Double-Blind Placebo-Controlled Study of Exenatide for the Treatment of Weight Gain Associated With Olanzapine in Obese Adults With Bipolar Disorder, Major Depressive Disorder, Schizophrenia or Schizoaffective Disorder [NCT00845507]Phase 454 participants (Actual)Interventional2008-12-31Completed
Acute Effects of a Glucagon-like Peptide 1 Analog, Exenatide, on Gastrointestinal Motor Function and Permeability in Patients With Short Bowel Syndrome on Home Parenteral Nutrition [NCT01818648]Phase 40 participants (Actual)Interventional2013-03-31Withdrawn(stopped due to Study was withdrawn by PI due to decision to study a different medication.)
Evaluation of Insulin Glargine and Exenatide: A Randomized Clinical Trial With Continuous Glucose Monitoring and Ambulatory Glucose Profile Analysis [NCT01089569]60 participants (Actual)Interventional2010-04-30Completed
Pilot Study of Exenatide Pharmacokinetics and Pharmacodynamics in Gestational Diabetes [NCT05482789]Phase 413 participants (Anticipated)Interventional2023-04-12Recruiting
A Randomized, Open-label, Placebo-controlled, Repeat-dose Study to Assess the Pharmacokinetics and Pharmacodynamics of 5 Micrograms Exenatide Administered Subcutaneously Twice Daily for 7 Days in Healthy Normal Volunteers and in Subjects With Type 2 Diabe [NCT00259896]Phase 130 participants Interventional2005-10-31Completed
Clinical and Histopathological Effect of GLP-1 Analogs on Psoriasis in Type 2 Diabetic Patients [NCT01687582]10 participants (Actual)Interventional2012-01-31Completed
Intensive Exenatide Therapy in Hyperglycemic Patients Admitted to the Coronary Intensive Care Unit [NCT00736229]Phase 440 participants (Actual)Interventional2008-08-31Completed
Safety and Efficacy of Exenatide in Patients With Type 2 Diabetes Using Metformin or Sulfonylureas and Metformin [NCT00324363]Phase 3466 participants (Actual)Interventional2006-01-31Completed
Effects of NovoLog® Mix 70/30 (Biphasic Insulin Aspart 70/30) BID and QD vs. Byetta™ Exenatide) BID on Glycemic Control: A Multicenter, 24-Week, Open-Label, Parallel Group Study in Patients With Type 2 Diabetes Mellitus Not Achieving Glycemic Targets With [NCT00313001]Phase 3373 participants (Actual)Interventional2006-04-30Completed
Effects of the GLP-1 Exenatide on Intrinsic Brain Activity in Lean and Obese Women [NCT01501084]Phase 134 participants (Actual)Interventional2011-12-31Completed
The Effect of Exenatide on Brown Adipose Tissue Activity and Energy Expenditure in Healthy Young Men [NCT03002675]Phase 424 participants (Anticipated)Interventional2016-08-31Recruiting
The Chronic and Acute Postprandial Vascular Effects of Exenatide vs. Metformin in Abdominally Obese Patients With Impaired Glucose Tolerance [NCT00546728]Phase 450 participants (Actual)Interventional2007-10-31Completed
A Phase II Trial to Examine the Effect of Subcutaneous Exenatide (Bydureon®) on Glucose Control in Patients With Type I Diabetes [NCT01928329]Phase 279 participants (Actual)Interventional2013-09-30Completed
Visualizing Beta Cells in Patients With Hyperinsulinemic Hypoglycemia After Bariatric Surgery [NCT03182192]Phase 112 participants (Anticipated)Interventional2016-04-01Recruiting
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 [NCT02787551]Phase 3514 participants (Actual)Interventional2016-07-06Completed
A Phase IV, Randomized, Double-blind, Placebo-controlled, Parallel-group Trial to Assess the Effect of 12-week Treatment With the Glucagon-like Peptide-1 Receptor Agonist (GLP-1RA) Liraglutide or Dipeptidyl Peptidase-4 Inhibitor (DPP-4i) Sitagliptin on th [NCT01744236]Phase 470 participants (Actual)Interventional2013-04-30Completed
Effects of Exenatide on Obesity and/or Diabetes Mellitus Due to Hypothalamic Damage [NCT01783717]10 participants (Anticipated)Interventional2012-12-31Recruiting
68Ga-NODAGA-exendin-4 PET/CT in Patients With AHH - a Prospective Comparative Evaluation of Preoperative Imaging [NCT03189953]Phase 1/Phase 256 participants (Anticipated)Interventional2015-04-30Completed
Effects of Exenatide on Motor Function and the Brain [NCT03456687]Phase 15 participants (Actual)Interventional2018-06-05Completed
A Phase 1, Randomized, Single-blind, Placebo-controlled, Multiple-dose, Two-sequence, Cross-over Study to Evaluate the Effect of Ranolazine on Glucagon Secretion in Subjects With Type 2 Diabetes Mellitus, Followed by An Open-label, Single Dose, Exenatide [NCT01843127]Phase 124 participants (Actual)Interventional2013-04-30Completed
Impact of Exenatide on Sleep and Circadian Function in Type 2 Diabetes: A Pilot Study [NCT01136798]18 participants (Actual)Interventional2010-06-01Completed
A Phase 3, Randomized, Active Comparator, Double-Blind, Multi-Center Study to Compare the Efficacy, Safety and Tolerability of ITCA 650 to Sitagliptin as Add-on Therapy to Metformin in Patients With Type 2 Diabetes [NCT01455909]Phase 30 participants (Actual)Interventional2013-02-28Withdrawn
Effect of Exenatide on Brain Glucose Uptake in Relations to Pancreatic, Adipose Tissue, and Hepatic Function [NCT01588418]Phase 415 participants (Actual)Interventional2010-07-31Completed
A Randomized Double-blind, Parallel-group Study to Evaluate the Effect of BYDUREON Compared With Placebo on 24-hour Glucose Control in Metformin-treated Patients With Type 2 Diabetes [NCT02288273]Phase 4239 participants (Actual)Interventional2014-12-31Completed
Exenatide Once Weekly for Smoking Cessation: A Randomized Clinical Trial [NCT02975297]Phase 1/Phase 284 participants (Actual)Interventional2016-07-31Completed
Safety and Efficacy of Exenatide Taken Before Lunch and Before Dinner Compared With Before Breakfast and Before Dinner in Patients With Type 2 Diabetes Using Oral Antidiabetic Therapy [NCT00359879]Phase 3377 participants (Actual)Interventional2006-09-30Completed
Changes in Bone Turnover With Exposure to a GLP-1 Receptor Agonist (UAB Core Center for Basic Skeletal Research) [NCT01381926]Phase 414 participants (Actual)Interventional2011-02-28Terminated(stopped due to unavailability of study drug and matching placebo)
A Dose Response Study to Assess the Effect on Glucose Control and Safety and Tolerability of LY2148568 in Japanese Patients With Type 2 Diabetes Who Are Treated With Oral Antidiabetic(s) But Not Well Controlled [NCT00382239]Phase 2153 participants (Actual)Interventional2006-09-30Completed
Evaluation of the Clinical and Economic Outcomes Associated With Exenatide Versus Basal Insulin in People With Type 2 Diabetes [NCT02987348]18,000 participants (Actual)Observational2015-06-30Completed
The Effects of Exenatide, a GLP-1 Agonist, on Alcohol Self-Administration in Heavy Drinkers [NCT03645408]Phase 18 participants (Actual)Interventional2019-05-02Terminated(stopped due to Due to COVID-19 hospital-wide policies halting recruitment)
Exenatide-test for Diagnosing Endogenous Hyperinsulinemic Hypoglycemia [NCT04909333]28 participants (Anticipated)Interventional2021-04-29Recruiting
Efficacy and Mechanism of Exenatide on Improving Heart Function in Type 2 Diabetes With Heart Failure Patients [NCT02344641]234 participants (Anticipated)Interventional2015-01-31Not yet recruiting
A Randomized,Active-controlled,Open-label Clinical Trial to Evaluate the Effect of GLP-1 Receptor Agonist (Exenatide Injection) in Combination With Metformin Therapy Compared to Premixed Insulin (BIAsp30) in Combination With Metformin Therapy on Diabetes [NCT03018665]Phase 4200 participants (Anticipated)Interventional2017-02-28Not yet recruiting
A Randomized, Multi-Center Study to Evaluate Cardiovascular Outcomes With ITCA 650 in Patients Treated With Standard of Care for Type 2 Diabetes [NCT01455896]Phase 34,156 participants (Actual)Interventional2013-03-31Completed
New Onset Type 1 Diabetes: Role of Exenatide [NCT01269034]Phase 413 participants (Actual)Interventional2010-12-31Completed
Comparison of Exenatide, Insulin or Pioglitazone on Glycaemic Control and β-cell Function in Drug-naïve Type 2 Diabetic Patients: A Multicentre Randomized Parallel-group Trial [NCT01147627]416 participants (Actual)Interventional2010-08-31Completed
Effect of Exenatide Treatment on Hepatic Fat Content and Plasma Adipocytokine Levels in Patients With Type 2 Diabetes Mellitus [NCT01432405]Phase 424 participants (Actual)Interventional2007-06-30Completed
Exenatide in Extreme Pediatric Obesity [NCT01237197]Phase 226 participants (Actual)Interventional2010-10-31Completed
A Phase 3, Randomized, Active Comparator, Double-Blind, Multi-Center Study to Compare the Efficacy, Safety and Tolerability of ITCA 650 to Glimepiride as Add-on Therapy to Metformin in Patients With Type 2 Diabetes [NCT01455883]Phase 30 participants (Actual)Interventional2013-02-28Withdrawn
Phase 3, Randomized, Double-Blind, Placebo-Controlled, Multi-Center Study to Evaluate the Efficacy, Safety and Tolerability of ITCA 650 in Patients With Type 2 Diabetes [NCT01455857]Phase 3460 participants (Actual)Interventional2013-03-31Completed
Effects of Exenatide on Obesity and Appetite in Overweight Patients With Prader-Willi Syndrome [NCT01444898]10 participants (Actual)Interventional2012-03-31Completed
Pilot Study of Extended-release Exenatide to Improve Glucose Control and Reduce Systemic Inflammation in Diabetic, HIV-infected Adults on Antiretroviral Therapy [NCT01791465]Phase 46 participants (Actual)Interventional2013-03-31Terminated(stopped due to This study was terminated after 6 patients due to loss of funding)
A Randomized, Open-label, Active-Controlled, Parallel-Group, Exploratory Study on the Effects of Repeated Doses of Albiglutide Compared to Exenatide on Gastric Myoelectrical Activity and Gastric Emptying in Subjects With Type 2 Diabetes Mellitus [NCT02793154]Phase 44 participants (Actual)Interventional2016-09-26Terminated(stopped due to Early termination due to insufficient enrollment.)
An Exploratory Randomized, 2-Part, Single-blind, 2-Period Crossover Study Comparing the Effect of Albiglutide With Exenatide on Regional Brain Activity Related to Nausea in Healthy Volunteers [NCT02802514]Phase 45 participants (Actual)Interventional2016-09-20Terminated
Phase 1-2 Study of the Pharmacology of Exenatide in Pediatric Sepsis [NCT01573806]Phase 1/Phase 20 participants (Actual)Interventional2012-10-31Withdrawn(stopped due to No funding)
DIabetes REsearCh on Patient sTratification (DIRECT): GLP-1R Agonists [NCT01575301]411 participants (Actual)Interventional2011-03-31Completed
A Phase 3, Randomized, Active Comparator, Double-Blind, Multi-Center Study to Compare the Efficacy, Safety and Tolerability of ITCA 650 to Sitagliptin as Add-on Therapy to Metformin in Patients With Type 2 Diabetes [NCT01455870]Phase 3535 participants (Actual)Interventional2013-05-31Completed
Impact of Intravenous Exenatide Versus Insulin on Quality of Life in Cardiac Surgery Patients: an Ancillary Study of the ExSTRESS Phase II/III Clinical Trial [NCT02432976]Phase 2/Phase 364 participants (Actual)Interventional2015-05-31Completed
A 12/24-weeks, Open, Multi-centre, Phase IV Study on Safety and Efficacy of 2mg Exenatide Once Weekly (Bydureon) in Patients With Type 2 Diabetes Mellitus [NCT02533453]Phase 4110 participants (Actual)Interventional2016-01-28Completed
Effects of GLP-1 Analogue Combined With Metformin and Metformin on Gonadal and Metabolic Profiles in Chinese Overweight/Obese PCOS Patients With Hyperandrogenemia. [NCT04969627]Phase 460 participants (Actual)Interventional2021-01-04Completed
GLP-1 Agonism for Blocking Cocaine Euphoria and Self-Administration [NCT02302976]Phase 113 participants (Actual)Interventional2014-11-30Completed
Pathophysiological Study of the Increase in Pancreatic Volume in Type 2 Diabetes Treatments. [NCT02244164]5 participants (Actual)Interventional2014-10-31Terminated(stopped due to Recruitment too slow)
Exendin PET/CT for Paragangliomas [NCT05418907]10 participants (Anticipated)Observational2022-06-01Recruiting
Effects of Exenatide on Body Weight in Patients With Hypothalamic Obesity [NCT01484873]Phase 210 participants (Actual)Interventional2012-06-30Completed
The Effect of Exenatide on Body Weight, Energy Expenditure and Hunger in Obese Women Without Diabetes Mellitus [NCT00456885]Phase 441 participants (Actual)Interventional2007-04-30Completed
The Pharmacokinetic Comparison and Bioequivalence Evaluation of Two 10-µg Recombinant Exendin-4 Formulations in Chinese Healthy Male Subjects [NCT03199261]Phase 124 participants (Actual)Interventional2016-12-23Completed
Comparison of Exenatide vs. Biphasic Insulin Aspart 30 on Glucose Variability in Type 2 Diabetes : a Randomised Open Parallel-controlled Study [NCT02449603]Phase 4150 participants (Actual)Interventional2015-11-30Completed
A Randomized, Open, Comparative to the Positive-Controlled, Parallel Group, Multiple Dose Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics of PB-119 to Subjects Newly Diagnosed as Type 2 Diabetes Mellitus [NCT03059719]Phase 136 participants (Actual)Interventional2015-04-08Completed
GLP-1 Analogs for Neuroprotection After Out-of-hospital Cardiac Arrest, a Randomized Clinical Trail [NCT02442791]120 participants (Actual)Interventional2014-06-30Completed
Intravenous Exenatide Infusion in Critically Ill Patients With Acute Brain Injury [NCT02058940]Phase 48 participants (Actual)Interventional2015-08-31Completed
Effect of Exenatide on Cortisol Secretion [NCT03160261]Phase 410 participants (Actual)Interventional2017-09-07Completed
The Effect of Exenatide Compared to Lantus Insulin on Vascular Function Before and After a Meal Tolerance Test in Patients With Type 2 Diabetes [NCT00353834]Phase 472 participants (Actual)Interventional2006-08-31Completed
A Phase 1 Study to Evaluate the Pharmacokinetics of ITCA 650 in Subjects With Mild and Moderate Renal Impairment Compared to the Pharmacokinetics of Subjects With Normal Renal Function [NCT02320045]Phase 138 participants (Actual)Interventional2014-11-30Completed
GLP-1 Receptor Agonist Therapy and Albuminuria in Patients With Type 2 Diabetes [NCT03029351]Phase 415 participants (Actual)Interventional2017-01-10Terminated(stopped due to termination by sponsor)
A Phase 3, Randomized, Active Comparator, Double-Blind, Multi-Center Study to Compare the Efficacy, Safety and Tolerability of ITCA 650 to Glimepiride as Add-on Therapy to Metformin in Patients With Type 2 Diabetes [NCT01455922]Phase 30 participants (Actual)Interventional2013-02-28Withdrawn
Islet Transplantation in Type 1 Diabetic Patients Using the UIC Protocol, Phase 3 [NCT00679042]Phase 321 participants (Actual)Interventional2007-09-05Active, not recruiting
Effects Of Exenatide (Byetta®) On Liver Biochemistry, Liver Histology And Lipid Metabolism In Patients With Non-Alcoholic Fatty Liver Disease [NCT00529204]Phase 21 participants (Actual)Interventional2007-10-31Terminated(stopped due to Lack of recruitment)
A Prospective Study of Patterns, Predictors, and Mechanisms of Weight Loss With Exenatide Treatment in Overweight and Obese Women Without Diabetes [NCT01590433]Phase 4249 participants (Actual)Interventional2012-03-31Completed
An Open Label, Single Site, 48 Week, Randomised Controlled Trial Evaluating the Safety and Efficacy of Exenatide Once-weekly in the Treatment of Patients With Multiple System Atrophy [NCT04431713]Phase 250 participants (Anticipated)Interventional2020-09-16Recruiting
A GLP-1 Receptor PET Imaging Substudy Within the VER-A-T1D Trial Investigating the Effects on Beta Cell Mass [NCT04615910]Phase 230 participants (Anticipated)Interventional2021-07-01Recruiting
Role of Exenatide in Treatment of NASH-a Pilot Study [NCT00650546]Phase 2/Phase 38 participants (Actual)Interventional2006-08-31Completed
Exenatide (Byetta) Vs Pramlintide (Symlin): Role in Post-prandial Hyperglycemia [NCT01269047]Phase 437 participants (Actual)Interventional2009-08-31Completed
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 (SUSTAIN™ 3 - vs. QW GLP-1) [NCT01885208]Phase 3813 participants (Actual)Interventional2013-12-02Completed
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 [NCT03361098]Phase 465 participants (Actual)Interventional2017-09-18Completed
The Effect of the GLP-1 Receptor Agonists on Blood Levels of Lipoprotein (a) [NCT02501850]Phase 440 participants (Anticipated)Interventional2014-10-31Recruiting
A Phase Ib, Randomized, Open-Label, Multi-Center, 4-Week Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of ITCA 650 in Subjects With Type 2 Diabetes Mellitus [NCT01798264]Phase 144 participants (Actual)Interventional2009-02-28Completed
Efficacy and Safety of Basal Insulin Glargine Combination With Exenatide Bid vs Switching Premix Human Insulin to Aspart30 in T2DM With Inadequate Glycaemic Control on Premixed Human Insulin and Metformin: a Randomized, Open, Parallel Trial [NCT02467920]Phase 4349 participants (Actual)Interventional2015-08-31Completed
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 [NCT01554618]Phase 384 participants (Actual)Interventional2011-12-02Completed
An Open-Label, Multi-Center, Randomized, Phase 3b Study to Evaluate the Safety and Tolerability of Switching to One of Two Dosing Strategies of ITCA 650 in Patients With Type 2 Diabetes Receiving Stable Doses of Liraglutide [NCT02638805]Phase 3136 participants (Actual)Interventional2015-12-31Completed
Exenatide Inpatient Trial: A Randomized Controlled Pilot Trial on the Safety and Efficacy of Exenatide (Byetta®) Therapy for the Inpatient Management of General Medicine and Surgery Patients With Type 2 Diabetes [NCT02455076]Phase 4150 participants (Actual)Interventional2015-09-30Completed
Preserving Beta-cell Function in Type 2 Diabetes With Exenatide and Insulin (PREVAIL) [NCT02194595]Phase 3105 participants (Actual)Interventional2014-09-30Completed
A PET/CT Study to Assess the Receptor Occupancy by SAR425899 After Repeat Dosing Using Radiolabelled Tracers for the Glucagon and GLP-1 Receptor in Overweight to Obese T2DM Patients [NCT03350191]Phase 113 participants (Actual)Interventional2017-12-20Completed
An Individualized treatMent aPproach for oldER patIents: A Randomized, Controlled stUdy in Type 2 Diabetes Mellitus (IMPERIUM) [NCT02072096]Phase 4192 participants (Actual)Interventional2014-02-28Terminated(stopped due to The trial was terminated per protocol because of lack of feasibility.)
A Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel Group, Phase 3 Trial to Evaluate the Safety and Efficacy of Once Weekly Exenatide Therapy Added to Titrated Basal Insulin Glargine Compared to Placebo Added to Titrated Basal Insulin Gl [NCT02229383]Phase 3464 participants (Actual)Interventional2014-09-06Completed
Safety, Tolerability, Pharmacokinetics, and Efficacy of LY3053102 With 12 Weeks of Treatment in Patients With Type 2 Diabetes Mellitus [NCT02020616]Phase 1/Phase 260 participants (Actual)Interventional2013-12-31Terminated(stopped due to Lack of Efficacy)
A Randomized, Parallel-Group Study to Assess the Safety, Tolerability, and Pharmacokinetics of NPM-119 (Exenatide Implant) in Patients With Type 2 Diabetes Mellitus [NCT05670379]Phase 116 participants (Anticipated)Interventional2024-03-31Not yet recruiting
A Randomized, Long-Term, Open-Label, 3-Arm, Multicenter Study to Compare the Glycemic Effects, Safety, and Tolerability of Exenatide Once Weekly Suspension to Sitagliptin and Placebo in Subjects With Type 2 Diabetes Mellitus [NCT01652729]Phase 3365 participants (Actual)Interventional2013-02-28Completed
Comparison of the Oxyntomodulin Analog, LY2944876, to Once-Weekly Exenatide and to Placebo in Patients With Type 2 Diabetes [NCT02119819]Phase 2420 participants (Actual)Interventional2014-04-30Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00082381 (7) [back to overview]Percentage of Patients With Hypoglycemic Events
NCT00082381 (7) [back to overview]Percentage of Patients Achieving HbA1c <=7%
NCT00082381 (7) [back to overview]Change in 7-point Self-monitored Blood Glucose (SMBG) Profile
NCT00082381 (7) [back to overview]Change in Rate of Hypoglycemic Events
NCT00082381 (7) [back to overview]Change in Glycosylated Hemoglobin (HbA1c)
NCT00082381 (7) [back to overview]Change in Fasting Serum Glucose
NCT00082381 (7) [back to overview]Change in Body Weight
NCT00082407 (7) [back to overview]Percentage of Patients Achieving HbA1c <=7%
NCT00082407 (7) [back to overview]Percentage of Patients With Hypoglycemic Events
NCT00082407 (7) [back to overview]Change in 7-point Self-monitored Blood Glucose (SMBG) Profile
NCT00082407 (7) [back to overview]Change in Body Weight
NCT00082407 (7) [back to overview]Change in Rate of Hypoglycemic Events
NCT00082407 (7) [back to overview]Change in Glcosylated Hemoglobin (HbA1c)
NCT00082407 (7) [back to overview]Change in Fasting Serum Glucose
NCT00097500 (9) [back to overview]Beta-cell Function 4 Weeks After Cessation of Therapy
NCT00097500 (9) [back to overview]Beta-cell Function After 52 Weeks of Therapy
NCT00097500 (9) [back to overview]Change in Body Weight
NCT00097500 (9) [back to overview]Change in Fasting Plasma Glucose
NCT00097500 (9) [back to overview]Change in Glycosylated Hemoglobin (HbA1c)
NCT00097500 (9) [back to overview]Change in First Phase C-peptide Release
NCT00097500 (9) [back to overview]Change in Second Phase C-peptide Release
NCT00097500 (9) [back to overview]M-value at Baseline, Week 52 and Week 56
NCT00097500 (9) [back to overview]Seven Point Self Monitored Blood Glucose (SMBG) Measurements
NCT00135330 (28) [back to overview]Change in Fasting HDL Cholesterol
NCT00135330 (28) [back to overview]Change in Waist-to-hip Ratio
NCT00135330 (28) [back to overview]Hypoglycemia Rate Per 30 Days Per Patient
NCT00135330 (28) [back to overview]Incidence of Hypoglycemia Events
NCT00135330 (28) [back to overview]Change in ASIiAUC During a Hyperglycemic Clamp Test.
NCT00135330 (28) [back to overview]Change in AUC for C-peptide During a Meal Challenge Test (MCT).
NCT00135330 (28) [back to overview]Change in AUC for Glucose During a Meal Challenge Test (MCT).
NCT00135330 (28) [back to overview]Change in Body Fat Mass During a Meal Challenge Test (MCT)
NCT00135330 (28) [back to overview]Change in Body Weight
NCT00135330 (28) [back to overview]Pedal Edema Score
NCT00135330 (28) [back to overview]Change in Fasting Insulin
NCT00135330 (28) [back to overview]Change in Fasting LDL Cholesterol
NCT00135330 (28) [back to overview]Change in Fasting Proinsulin
NCT00135330 (28) [back to overview]Change in Fasting Serum Glucose Concentration.
NCT00135330 (28) [back to overview]Change in Fasting Total Cholesterol.
NCT00135330 (28) [back to overview]Ratio (Value at Endpoint Divided by Value at Baseline) of AUC for Insulin During a Meal Challenge Test (MCT).
NCT00135330 (28) [back to overview]Change in HbA1c
NCT00135330 (28) [back to overview]Change in Hip Circumference
NCT00135330 (28) [back to overview]Change in Incremental for Postprandial C-peptide During Meal Challenge Test (MCT).
NCT00135330 (28) [back to overview]Change in Incremental for Postprandial Glucose During a Meal Challenge Test (MCT).
NCT00135330 (28) [back to overview]Change in Incremental for Postprandial Insulin During Meal Challenge Test (MCT).
NCT00135330 (28) [back to overview]Change in Fasting Triglycerides
NCT00135330 (28) [back to overview]Change in Insulin iAUC From Baseline to Endpoint.
NCT00135330 (28) [back to overview]Change in Insulin Sensitivity Index as Measured by M-value.
NCT00135330 (28) [back to overview]Change in Lean Body Mass During a Meal Challenge Test (MCT)
NCT00135330 (28) [back to overview]Change in Percent Body Fat During a Meal Challenge Test (MCT)
NCT00135330 (28) [back to overview]Change in Waist Circumference
NCT00135330 (28) [back to overview]Change in Insulin AUC in the First Stage From Baseline to Endpoint.
NCT00308139 (24) [back to overview]Change in HbA1c From Baseline to Week 30
NCT00308139 (24) [back to overview]Change in HbA1c From Baseline to Week 364
NCT00308139 (24) [back to overview]Change in High-density Lipoprotein Cholesterol (HDL-C) From Baseline to Week 30
NCT00308139 (24) [back to overview]Change in High-density Lipoprotein Cholesterol (HDL-C) From Baseline to Week 364
NCT00308139 (24) [back to overview]Change in Low-density Lipoprotein Cholesterol (LDL-C) From Baseline to Week 364
NCT00308139 (24) [back to overview]Change in Total Cholesterol From Baseline to Week 30
NCT00308139 (24) [back to overview]Change in Total Cholesterol From Baseline to Week 364
NCT00308139 (24) [back to overview]Exenatide LAR Steady State Concentration From Week 29 to Week 30
NCT00308139 (24) [back to overview]Percentage of Subjects Achieving HbA1c Target of <=6.0%
NCT00308139 (24) [back to overview]Percentage of Subjects Achieving HbA1c Target of <=6.5%
NCT00308139 (24) [back to overview]Percentage of Subjects Achieving HbA1c Target of <=6.5%
NCT00308139 (24) [back to overview]Ratio of Triglycerides at Week 364 to Baseline
NCT00308139 (24) [back to overview]Percentage of Subjects Achieving HbA1c Target of <7%
NCT00308139 (24) [back to overview]Percentage of Subjects Achieving HbA1c Target of <7%
NCT00308139 (24) [back to overview]Ratio of Triglycerides at Week 30 to Baseline
NCT00308139 (24) [back to overview]Change in Fasting Plasma Glucose From Baseline to Week 364
NCT00308139 (24) [back to overview]Change in Blood Pressure From Baseline to Week 364
NCT00308139 (24) [back to overview]Change in Blood Pressure From Baseline to Week 30
NCT00308139 (24) [back to overview]Assessment on Event Rate of Treatment-emergent Hypoglycemic Events With SU Use at Screening
NCT00308139 (24) [back to overview]Assessment on Event Rate of Treatment-emergent Hypoglycemic Events With Non-SU Use at Screening
NCT00308139 (24) [back to overview]Change in Body Weight From Baseline to Week 364
NCT00308139 (24) [back to overview]Change in 2 Hours (2h) Postprandial Glucose From Baseline to Week 14
NCT00308139 (24) [back to overview]Change in Body Weight From Baseline to Week 30
NCT00308139 (24) [back to overview]Change in Fasting Plasma Glucose From Baseline to Week 30
NCT00353834 (2) [back to overview]First Will be the Changes in TNG Stimulated Arterial Dilation (Endothelial-independent) in Subjects Treated With Exenatide Compared With Subjects Treated With Lantus at the End of the Study Compared to Baseline Measurements
NCT00353834 (2) [back to overview]The Primary Endpoint Was the Change in FMD at the End of the Study Compared to Baseline Measurements in Subjects Treated With Exenatide Compared to Subjects Treated With Lantus.
NCT00359762 (27) [back to overview]Number of Patients With Treatment Failure
NCT00359762 (27) [back to overview]Triglycerides at Year 3
NCT00359762 (27) [back to overview]Total Cholesterol at Year 3
NCT00359762 (27) [back to overview]Time to Treatment Failure
NCT00359762 (27) [back to overview]Systolic Blood Pressure at Year 3
NCT00359762 (27) [back to overview]Ratio of the 30 Minute Increment in Plasma Insulin Concentration and the 30 Minute Increment in Plasma Glucose During the Oral Glucose Tolerance Test (DI30/DG30 Ratio) at Year 3
NCT00359762 (27) [back to overview]High-density Lipoprotein (HDL) Cholesterol at Year 3
NCT00359762 (27) [back to overview]Change in HbA1c From Baseline to Year 2 for Patients Not Randomized at Entry in Period III
NCT00359762 (27) [back to overview]Heart Rate at Year 3
NCT00359762 (27) [back to overview]Fasting Proinsulin/Insulin Ratio at Year 3
NCT00359762 (27) [back to overview]Fasting Plasma Glucose at Year 3
NCT00359762 (27) [back to overview]Disposition Index at Year 3
NCT00359762 (27) [back to overview]Diastolic Blood Pressure at Year 3
NCT00359762 (27) [back to overview]Change in Postprandial (2 Hours) Plasma Glucose From Baseline to Endpoint
NCT00359762 (27) [back to overview]Change in HOMA-B From Baseline to Endpoint
NCT00359762 (27) [back to overview]Change in HbA1c From Baseline to Endpoint
NCT00359762 (27) [back to overview]Change in Fasting Proinsulin/Insulin Ratio From Baseline to Endpoint.
NCT00359762 (27) [back to overview]Change in Fasting Plasma Glucose From Baseline to Endpoint
NCT00359762 (27) [back to overview]Change in Disposition Index From Baseline to Endpoint
NCT00359762 (27) [back to overview]Change in DI30/DG30 Ratio From Baseline to Endpoint
NCT00359762 (27) [back to overview]Change in Body Weight From Baseline to Year 3
NCT00359762 (27) [back to overview]Change in HbA1c From Baseline to Year 3
NCT00359762 (27) [back to overview]Change in HbA1c From Baseline to Year 2 for Patients Randomized at Entry in Period III
NCT00359762 (27) [back to overview]Postprandial (2 Hours) Plasma Glucose at Year 3
NCT00359762 (27) [back to overview]Hypoglycemia Rate Per Year in Period III
NCT00359762 (27) [back to overview]Hypoglycemia Rate Per Year
NCT00359762 (27) [back to overview]Homeostasis Model Assessment of Beta-cell Function (HOMA-B) at Year 3
NCT00360334 (28) [back to overview]Percent of Patients Achieving HbA1c < 6.5%
NCT00360334 (28) [back to overview]Change in High Density Lipoprotein (HDL) Cholesterol
NCT00360334 (28) [back to overview]Percent of Patients Achieving 10% Weight Loss
NCT00360334 (28) [back to overview]Percent Change in Body Weight
NCT00360334 (28) [back to overview]Nocturnal Hypoglycemic Rate Per 30 Days
NCT00360334 (28) [back to overview]Incidence of Severe Hypoglycemic Episodes
NCT00360334 (28) [back to overview]Incidence of Nocturnal Hypoglycemic Episodes
NCT00360334 (28) [back to overview]Percent of Patients Achieving 5% Weight Loss
NCT00360334 (28) [back to overview]Incidence of Hypoglycemic Episodes
NCT00360334 (28) [back to overview]Change in Fasting Serum Triglycerides
NCT00360334 (28) [back to overview]Change in Fasting Serum Glucose
NCT00360334 (28) [back to overview]Percent of Patients Achieving HbA1c < 7%
NCT00360334 (28) [back to overview]Change in Apolipoprotein-B
NCT00360334 (28) [back to overview]Change in Low Density Lipoprotein (LDL) Cholesterol
NCT00360334 (28) [back to overview]Change in TC to HDL Cholesterol Ratio
NCT00360334 (28) [back to overview]Hypoglycemic Rate Per 30 Days
NCT00360334 (28) [back to overview]Change in Fasting Serum Total Cholesterol (TC)
NCT00360334 (28) [back to overview]Change in Waist-to-hip Ratio
NCT00360334 (28) [back to overview]Change in Waist Circumference
NCT00360334 (28) [back to overview]Change in Systolic Blood Pressure
NCT00360334 (28) [back to overview]Change in Diastolic Blood Pressure
NCT00360334 (28) [back to overview]Change in Body Weight
NCT00360334 (28) [back to overview]Change in Body Mass Index (BMI)
NCT00360334 (28) [back to overview]Change in 7 Point Self Monitored Blood Glucose Profile
NCT00360334 (28) [back to overview]Severe Hypoglycemic Rate Per 30 Days
NCT00360334 (28) [back to overview]Percent of Patients Who Achieved HbA1c ≤ 7.4% With Minimal Weight Gain (≤ 1kg)
NCT00360334 (28) [back to overview]Percent of Patients Who Achieved HbA1c ≤ 7.4% and Weight Gain ≤ 0.5kg
NCT00360334 (28) [back to overview]Percent of Patients Achieving HbA1c ≤ 7.4%
NCT00375492 (12) [back to overview]Change From Baseline in High Density Lipoprotein (HDL) Cholesterol at Week 24
NCT00375492 (12) [back to overview]Change From Baseline in Glycosylated Hemoglobin (HbA1c) at Week 24
NCT00375492 (12) [back to overview]Change From Baseline in Body Weight
NCT00375492 (12) [back to overview]Change From Baseline in 6-point Self Monitored Blood Glucose (SMBG) Profile at Week 24
NCT00375492 (12) [back to overview]Ratio of Triglycerides at Week 24 to Triglycerides at Baseline
NCT00375492 (12) [back to overview]Ratio of Homeostatic Model Assessment-Insulin Sensitivity (HOMA-S) at Week 24 to HOMA-S at Baseline
NCT00375492 (12) [back to overview]Ratio of Homeostatic Model Assessment-Beta Cell (HOMA-B) at Week 24 to HOMA-B at Baseline
NCT00375492 (12) [back to overview]Rate of Hypoglycemic Events
NCT00375492 (12) [back to overview]Number of Participants With Hypoglycemic Events During the Study
NCT00375492 (12) [back to overview]Change From Baseline in Low Density Lipoprotein (LDL) Cholesterol at Week 24
NCT00375492 (12) [back to overview]Change From Baseline in Waist Circumference at Week 24
NCT00375492 (12) [back to overview]Change From Baseline in Total Cholesterol at Week 24
NCT00434954 (12) [back to overview]Change in Body Weight
NCT00434954 (12) [back to overview]Change in Body Mass Index (BMI)
NCT00434954 (12) [back to overview]Change in Glycosylated Hemoglobin (HbA1c)
NCT00434954 (12) [back to overview]Incidence of Nocturnal Hypoglycemia (Percentage of Subjects Who Experienced at Least One Episode of Nocturnal Hypoglycemia During the 26 Week Treatment Period)
NCT00434954 (12) [back to overview]Percentage of Subjects Achieving HbA1c Target of < 6.5%
NCT00434954 (12) [back to overview]Percentage of Subjects Achieving HbA1c Target of < 7.0%
NCT00434954 (12) [back to overview]7 Point Self-monitored Blood Glucose (SMBG) Profiles
NCT00434954 (12) [back to overview]Blood Lipid Levels
NCT00434954 (12) [back to overview]Incidence of Hypoglycemia (Percentage of Participants With at Least One Hypoglycemic Episode)
NCT00434954 (12) [back to overview]Patient Reported Outcomes: Diabetes Treatment Satisfaction Questionnaire (DTSQ)
NCT00434954 (12) [back to overview]Patient Reported Outcomes: Quality of Life (SF-12)
NCT00434954 (12) [back to overview]Incidence of Hypoglycemic Episodes [Blood Glucose <= 3.0 mmol/L or Severe] (Percentage of Subjects Who Experienced at Least One Treatment-emergent Hypoglycemic Episode During the 26-week Treatment Period)
NCT00456300 (1) [back to overview]Mean Plasma Glucose Area Under the Curve (AUC) for Blood Glucose Concentration in the Exenatide 1.25 mcg or Exenatide 2.5 mcg Treated Groups Along With Insulin, Compared to Insulin Alone
NCT00456885 (13) [back to overview]Change in Two Hour Glucose
NCT00456885 (13) [back to overview]Change in Insulin
NCT00456885 (13) [back to overview]Change in Fasting Glucose
NCT00456885 (13) [back to overview]Change in Body Mass Index
NCT00456885 (13) [back to overview]Adiponectin
NCT00456885 (13) [back to overview]Changes in Body Composition
NCT00456885 (13) [back to overview]Change in Waist Circumference
NCT00456885 (13) [back to overview]Systolic Blood Pressure
NCT00456885 (13) [back to overview]REE
NCT00456885 (13) [back to overview]HOMA Score
NCT00456885 (13) [back to overview]Diastolic Blood Pressure
NCT00456885 (13) [back to overview]Changes in Leptin
NCT00456885 (13) [back to overview]Change in Weight
NCT00500370 (16) [back to overview]Change in Total Cholesterol
NCT00500370 (16) [back to overview]Change in Serum Glucose AUC Levels Following Oral Glucose Tolerance Test (OGTT)
NCT00500370 (16) [back to overview]Change in Waist-to-hip Ratio
NCT00500370 (16) [back to overview]Incidence of Patients That Demonstrate Normalization of Impaired Fasting Glucose (IFG) and/or Impaired Glucose Tolerance (IGT)
NCT00500370 (16) [back to overview]Incidence of Patients That Demonstrate Overt Signs of Diabetes Mellitus Diagnosis
NCT00500370 (16) [back to overview]Percentage of Patients Experiencing >=5% Weight Loss
NCT00500370 (16) [back to overview]Ratio of Endpoint (LOCF) to Baseline for Fasting Triglycerides (Logarithmically Transformed)
NCT00500370 (16) [back to overview]Ratio of Endpoint (LOCF) to Baseline for Homeostatic Model Assessment-Insulin Sensitivity (HOMA-S) (Logarithmically Transformed)
NCT00500370 (16) [back to overview]Ratio of Endpoint (LOCF) to Baseline for Homeostatic Model Assessment-Beta Cell (HOMA-B) (Logarithmically Transformed)
NCT00500370 (16) [back to overview]Change in Low Density Lipoprotein (LDL) Cholesterol
NCT00500370 (16) [back to overview]Change in High Sensitivity C-reactive Protein (hsCRP)
NCT00500370 (16) [back to overview]Change in High Density Lipoprotein (HDL) Cholesterol
NCT00500370 (16) [back to overview]Change in Glycosylated Hemoglobin (HbA1c)
NCT00500370 (16) [back to overview]Change in Fasting Serum Glucose
NCT00500370 (16) [back to overview]Change in Body Weight
NCT00500370 (16) [back to overview]Change in Body Mass Index (BMI)
NCT00516048 (3) [back to overview]Treatment-emergent Antibody Status (Maximum Titer Level Experienced)
NCT00516048 (3) [back to overview]Incidence of Potentially Immune-related Treatment-emergent Adverse Events
NCT00516048 (3) [back to overview]Change in Hemoglobin A1c (HbA1c) From Baseline to Endpoint
NCT00516074 (6) [back to overview]Change in Nighttime (2400-0600) Heart Rate From Baseline to Endpoint
NCT00516074 (6) [back to overview]Change in Mean 24-hour Heart Rate From Baseline to Endpoint
NCT00516074 (6) [back to overview]Change in Mean 24 Hour Systolic Blood Pressure From Baseline to Endpoint
NCT00516074 (6) [back to overview]Change in Mean 24 Hour Diastolic Blood Pressure From Baseline to Endpoint
NCT00516074 (6) [back to overview]Change in Hemoglobin A1c (HbA1c) From Baseline to Endpoint
NCT00516074 (6) [back to overview]Change in Daytime Heart Rate From Baseline to Endpoint
NCT00518115 (18) [back to overview]Number of Participants Who Achieved Target Values for HbA1c <6.5% and >=6.5% to <7% at Weeks 4, 5, 7, 8, 9, 12, 15, and 16
NCT00518115 (18) [back to overview]Change From Baseline in Fasting Insulin at Weeks 5, 8, 12, and 16
NCT00518115 (18) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG) at Weeks 4, 5, 7, 8, 9, 12, 15, and 16
NCT00518115 (18) [back to overview]Change From Baseline in Functional Living Index - Emesis (FLIE) Scores at Week 16
NCT00518115 (18) [back to overview]Percent Change From Baseline in Body Weight at Week 16
NCT00518115 (18) [back to overview]Change From Baseline in HbA1c at Weeks 4, 5, 7, 8, 9, 12, 15, and 16
NCT00518115 (18) [back to overview]Change From Baseline in Fasting C-peptide at Weeks 5, 8, 12, and 16
NCT00518115 (18) [back to overview]Change From Baseline in Fasting Fructosamine at Weeks 5, 8, 12, and 16
NCT00518115 (18) [back to overview]Mean Half-maximal Effective Concentration (EC50) of Albiglutide for HbA1c and FPG
NCT00518115 (18) [back to overview]Change From Baseline in Fasting Glucagon at Weeks 5, 8, 12, and 16
NCT00518115 (18) [back to overview]Number of Participants With the Indicated Response to Questions on the Hunger, Craving, and Fullness Questionnaire (HCFQ) at Week 16
NCT00518115 (18) [back to overview]Change From Baseline in Triglycerides, Free Fatty Acids, Total Cholesterol, Low-density Lipoprotein Cholesterol, and High-density Lipoprotein Cholesterol at Weeks 5, 8, 12, and 16
NCT00518115 (18) [back to overview]Mean Volume of Distribution of Albiglutide
NCT00518115 (18) [back to overview]Mean Clearance of Albiglutide
NCT00518115 (18) [back to overview]Mean Absorption Rate of Albiglutide
NCT00518115 (18) [back to overview]Change From Baseline in Waist Circumference at Week 16
NCT00518115 (18) [back to overview]Change From Baseline in Glycosylated Hemoglobin (HbA1c) at Week 16
NCT00518115 (18) [back to overview]Change From Baseline in Body Weight at Week 16
NCT00518882 (55) [back to overview]Change in High-density Lipoprotein-cholesterol at Week 26
NCT00518882 (55) [back to overview]Change in Glycosylated A1c (HbA1c), Weeks 26-78
NCT00518882 (55) [back to overview]Change in Glycosylated A1c (HbA1c) at Week 78
NCT00518882 (55) [back to overview]Change in Glycosylated A1c (HbA1c) at Week 26
NCT00518882 (55) [back to overview]Change in Free Fatty Acid, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Free Fatty Acid at Week 78
NCT00518882 (55) [back to overview]Change in Free Fatty Acid at Week 26
NCT00518882 (55) [back to overview]Change in Fasting Plasma Glucose, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Fasting Plasma Glucose at Week 78
NCT00518882 (55) [back to overview]Change in Fasting Plasma Glucose at Week 26
NCT00518882 (55) [back to overview]Change in Body Weight, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Low-density Lipoprotein-cholesterol at Week 78
NCT00518882 (55) [back to overview]Change in Body Weight at Week 26
NCT00518882 (55) [back to overview]Change in Beta-cell Function, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Beta-cell Function at Week 78
NCT00518882 (55) [back to overview]Change in Beta-cell Function at Week 26
NCT00518882 (55) [back to overview]Change in Total Cholesterol, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Apolipoprotein B, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Apolipoprotein B at Week 78
NCT00518882 (55) [back to overview]Change in Apolipoprotein B at Week 26
NCT00518882 (55) [back to overview]Change in Body Weight at Week 78
NCT00518882 (55) [back to overview]Change in Triglyceride at Week 78
NCT00518882 (55) [back to overview]Change in Triglyceride, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Total Cholesterol at Week 78
NCT00518882 (55) [back to overview]Change in Total Cholesterol at Week 26
NCT00518882 (55) [back to overview]Change in Mean Prandial Increment of Plasma Glucose After Lunch, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Mean Prandial Increment of Plasma Glucose After Lunch at Week 78
NCT00518882 (55) [back to overview]Change in Mean Prandial Increment of Plasma Glucose After Lunch at Week 26
NCT00518882 (55) [back to overview]Change in Mean Prandial Increment of Plasma Glucose After Dinner, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Mean Prandial Increment of Plasma Glucose After Dinner at Week 78
NCT00518882 (55) [back to overview]Change in Very Low-density Lipoprotein-cholesterol at Week 26
NCT00518882 (55) [back to overview]Change in Very Low-density Lipoprotein-cholesterol at Week 78
NCT00518882 (55) [back to overview]Change in Very Low-density Lipoprotein-cholesterol, Weeks 26-78
NCT00518882 (55) [back to overview]Hypoglycaemic Episodes at Week 26
NCT00518882 (55) [back to overview]Change in Triglyceride at Week 26
NCT00518882 (55) [back to overview]Hypoglyceamic Episodes, Weeks 26-78
NCT00518882 (55) [back to overview]Percentage of Subjects Achieving Treatment Target of Either HbA1c < 7.0% or =< 6.5% at Week 26
NCT00518882 (55) [back to overview]Percentage of Subjects Achieving Treatment Target of Either HbA1c < 7.0% or =< 6.5% at Week 78
NCT00518882 (55) [back to overview]Change in Mean Prandial Increment of Plasma Glucose After Dinner at Week 26
NCT00518882 (55) [back to overview]Change in Mean Prandial Increment of Plasma Glucose After Breakfast, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Mean Prandial Increment of Plasma Glucose After Breakfast at Week 78
NCT00518882 (55) [back to overview]Change in Mean Prandial Increment of Plasma Glucose After Breakfast at Week 26
NCT00518882 (55) [back to overview]Change in Mean Postprandial Increment of Plasma Glucose After Lunch, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Mean Postprandial Increment of Plasma Glucose After Lunch at Week 78
NCT00518882 (55) [back to overview]Change in Mean Postprandial Increment of Plasma Glucose After Lunch at Week 26
NCT00518882 (55) [back to overview]Change in Mean Postprandial Increment of Plasma Glucose After Dinner, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Mean Postprandial Increment of Plasma Glucose After Dinner at Week 78
NCT00518882 (55) [back to overview]Change in Mean Postprandial Increment of Plasma Glucose After Dinner at Week 26
NCT00518882 (55) [back to overview]Change in Mean Postprandial Increment of Plasma Glucose After Breakfast, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Mean Postprandial Increment of Plasma Glucose After Breakfast at Week 78
NCT00518882 (55) [back to overview]Change in Mean Postprandial Increment of Plasma Glucose After Breakfast at Week 26
NCT00518882 (55) [back to overview]Change in Low-density Lipoprotein-cholesterol, Weeks 26-78
NCT00518882 (55) [back to overview]Change in Low-density Lipoprotein-cholesterol at Week 26
NCT00518882 (55) [back to overview]Change in High-density Lipoprotein-cholesterol, Weeks 26-78
NCT00518882 (55) [back to overview]Change in High-density Lipoprotein-cholesterol at Week 78
NCT00529204 (3) [back to overview]Changes in Components of Liver Histology at Baseline and Week 24 Including Steatosis, Inflammation and Fibrosis
NCT00529204 (3) [back to overview]Safety of Exenatide in Patients With NAFLD and Type 2 Diabetes
NCT00529204 (3) [back to overview]Reduction in Serum ALT From Baseline to 24 Weeks of Exenatide Therapy
NCT00546728 (1) [back to overview]Change in Reactive Hyperemic Index Over the 3-month Treatment Period
NCT00566813 (3) [back to overview]Number of Participants With Adverse Events Including Laboratory Abnormalities at the End of Study Participation
NCT00566813 (3) [back to overview]Number of Participants With HbA1c Less Than or Equal to 6.5 & Free of Severe Hypoglycemic Events
NCT00566813 (3) [back to overview]Number of Participants With Insulin Independence at End of Study Participation
NCT00577824 (17) [back to overview]Change in 1,5-anhydroglucitol
NCT00577824 (17) [back to overview]Change in Fasting Blood Glucose
NCT00577824 (17) [back to overview]Change in Glycosylated Hemoglobin (HbA1c) From Baseline to Week 24
NCT00577824 (17) [back to overview]Change in High Density Lipoprotein Cholesterol (HDL-C)
NCT00577824 (17) [back to overview]Change in Homeostasis Model Assessment - Beta Cell Function (HOMA-B)
NCT00577824 (17) [back to overview]Change in Body Weight
NCT00577824 (17) [back to overview]Change in Homeostasis Model Assessment - Insulin Resistance (HOMA-R)
NCT00577824 (17) [back to overview]Change in Low Density Lipoprotein Cholesterol (LDL-C)
NCT00577824 (17) [back to overview]Change in Serum Insulin
NCT00577824 (17) [back to overview]7 Point Self-monitored Blood Glucose (SMBG) Profiles at Baseline and Week 24
NCT00577824 (17) [back to overview]Change in Waist Size
NCT00577824 (17) [back to overview]Change in C-peptide
NCT00577824 (17) [back to overview]Percentage of Patients Achieving HbA1c < 6.5%
NCT00577824 (17) [back to overview]Percentage of Patients Achieving HbA1c < 7.0%
NCT00577824 (17) [back to overview]Change in Triglycerides
NCT00577824 (17) [back to overview]Change in Total Cholesterol
NCT00577824 (17) [back to overview]Change in Waist-to-hip Ratio
NCT00603239 (11) [back to overview]Change in Impact of Weight on Quality of Life (IWQOL)-Lite Score
NCT00603239 (11) [back to overview]Change in Euroqol - 5 Domain Quality of Life (EQ-5D) Score
NCT00603239 (11) [back to overview]Percentage of Patients Achieving HbA1c <= 7%
NCT00603239 (11) [back to overview]Percentage of Patients Achieving HbA1c <= 6.5%
NCT00603239 (11) [back to overview]Number of Subjects Who Experienced an Episode of Minor Hypoglycemia
NCT00603239 (11) [back to overview]Change in Waist Circumference
NCT00603239 (11) [back to overview]Change in Insulin Sensitivity.
NCT00603239 (11) [back to overview]Change in Glycosylated Hemoglobin (HbA1c)
NCT00603239 (11) [back to overview]Change in Fasting Serum Glucose (FSG)
NCT00603239 (11) [back to overview]Change in Body Weight
NCT00603239 (11) [back to overview]Change in Beta-cell Function
NCT00623545 (2) [back to overview]Weight Loss After Administration of Exenatide.
NCT00623545 (2) [back to overview]Change in Energy Intake Measured Before Treatment and at the End of Treatment.
NCT00635492 (21) [back to overview]Percentage of Patients Achieving HbA1c Concentration <7.0% at Month 24
NCT00635492 (21) [back to overview]Diet and Exercise Advice in Diabetes Management Associated With Treatment Choice at Baseline
NCT00635492 (21) [back to overview]Changes in HbA1c From Baseline to Month 24
NCT00635492 (21) [back to overview]Reasons for Discontinuation of Baseline Regimen
NCT00635492 (21) [back to overview]Percentage of Patients Hospitalized Between Baseline and 24 Months
NCT00635492 (21) [back to overview]Percentage of Patients Contacting Health Care Providers Between Baseline and 24 Months
NCT00635492 (21) [back to overview]Number of Contacts With Health Care Providers Between Baseline and 24 Months
NCT00635492 (21) [back to overview]Factors Associated With Treatment Change in Insulin Cohort
NCT00635492 (21) [back to overview]Factors Associated With Treatment Change in Exenatide BID Cohort
NCT00635492 (21) [back to overview]Estimates of Probability to Remain on Initial Injectable Treatment at 12 and 24 Months.
NCT00635492 (21) [back to overview]Changes in Weight From Baseline to Month 24
NCT00635492 (21) [back to overview]Disinhibited Eating Associated With Treatment Choice at Baseline
NCT00635492 (21) [back to overview]Frequent Blood Glucose Self Monitoring Associated With Treatment Choice at Baseline
NCT00635492 (21) [back to overview]Higher Body Mass Index (BMI) Associated With Treatment Choice at Baseline
NCT00635492 (21) [back to overview]Higher Hemoglobin A1c (HbA1) Associated With Treatment Choice at Baseline
NCT00635492 (21) [back to overview]Higher Random Glucose Associated With Treatment Choice at Baseline
NCT00635492 (21) [back to overview]Higher Value of Low Density Lipoprotein Cholesterol Associated With Treatment Choice at Baseline
NCT00635492 (21) [back to overview]Incidence of Gastro Intestinal Symptoms Between Baseline and 24 Months
NCT00635492 (21) [back to overview]Incidence of Hypoglycemia Between Baseline and 24 Months
NCT00635492 (21) [back to overview]Older Age Associated With Treatment Choice at Baseline
NCT00635492 (21) [back to overview]Percentage of Patients Achieving HbA1c Concentration <6.5% at Month 24
NCT00637273 (12) [back to overview]Assessment on Event Rate of Treatment-emergent Hypoglycemic Events
NCT00637273 (12) [back to overview]Change in HbA1c From Baseline to Week 26
NCT00637273 (12) [back to overview]Change in Fasting Total Cholesterol From Baseline to Week 26
NCT00637273 (12) [back to overview]Change in Diastolic Blood Pressure From Baseline to Week 26
NCT00637273 (12) [back to overview]Change in Body Weight From Baseline to Week 26
NCT00637273 (12) [back to overview]Change in Fasting High-density Lipoprotein (HDL) From Baseline to Week 26
NCT00637273 (12) [back to overview]Change in Fasting Plasma Glucose From Baseline to Week 26
NCT00637273 (12) [back to overview]Ratio of Fasting Triglycerides at Week 26 to Baseline
NCT00637273 (12) [back to overview]Percentage of Subjects Achieving HbA1c Target of <7% at Week 26
NCT00637273 (12) [back to overview]Percentage of Subjects Achieving HbA1c Target of <=6.5% at Week 26
NCT00637273 (12) [back to overview]Percentage of Subjects Achieving HbA1c Target of <=6.0% at Week 26
NCT00637273 (12) [back to overview]Change in Systolic Blood Pressure From Baseline to Week 26
NCT00641056 (10) [back to overview]Change in Blood Pressure From Baseline to Week 26
NCT00641056 (10) [back to overview]Percentage of Patients Achieving HbA1c <=7.0% at Week 26
NCT00641056 (10) [back to overview]Change in Fasting Serum Glucose (FSG) From Baseline to Week 26
NCT00641056 (10) [back to overview]Change in HbA1c From Baseline to Week 26
NCT00641056 (10) [back to overview]Change in High-density Lipoprotein Cholesterol (HDL) From Baseline to Week 26
NCT00641056 (10) [back to overview]Change in Total Cholesterol From Baseline to Week 26
NCT00641056 (10) [back to overview]Change in Body Weight (BW) From Baseline to Week 26
NCT00641056 (10) [back to overview]Percentage of Patients Achieving HbA1c <=6.5% at Week 26
NCT00641056 (10) [back to overview]Ratio of Triglycerides at Week 26 to Baseline
NCT00641056 (10) [back to overview]Assessment on Event Rate of Treatment-emergent Hypoglycemic Episodes
NCT00650546 (2) [back to overview]Change in NAS
NCT00650546 (2) [back to overview]Number of Patients With Improvement in Liver Histology After Treatment With Exenatide
NCT00658021 (9) [back to overview]Percentage of Participants Achieving HbA1c Goals of < 7%, <= 6.5%, and < 6.5% Through Week 28
NCT00658021 (9) [back to overview]Percentage of Participants Discontinuing the Study Due to Failure to Maintain Glycemic Control Through Week 28
NCT00658021 (9) [back to overview]Adjusted Change From Baseline in Fasting Serum Insulin at Week 28
NCT00658021 (9) [back to overview]Adjusted Change From Baseline in Body Weight Through Week 28
NCT00658021 (9) [back to overview]Adjusted Change From Baseline in Fasting Serum Glucose (FSG) at Week 28
NCT00658021 (9) [back to overview]Adjusted Change From Baseline in Glycated Hemoglobin A1c (HbA1c) at Week 28
NCT00658021 (9) [back to overview]Adjusted Change From Baseline in Homeostasis Model Assessments - Beta-Cell Function (HOMA-B) and Insulin Sensitivity (HOMA-S) at Week 28
NCT00658021 (9) [back to overview]Number of Participants With Post-Treatment Adverse Events of Special Interest (AESI) During Safety Follow-up Period
NCT00658021 (9) [back to overview]Adjusted Change From Baseline in Self-Monitored Blood Glucose (SMBG) at Week 28
NCT00667732 (2) [back to overview]The Percentage of Per Protocol Participants Randomized and Treated in Each Arm Who Had Lab-measured A1c <6.5% at 24 Weeks of Treatment
NCT00667732 (2) [back to overview]The Percentage of Intent to Treat Participants Randomized and Treated in Each Arm Who Had Lab-measured A1c <6.5% at 24 Weeks of Treatment
NCT00676338 (11) [back to overview]Percentage of Patients Achieving HbA1c <=7% at Week 26
NCT00676338 (11) [back to overview]Change in Body Weight From Baseline to Week 26
NCT00676338 (11) [back to overview]Assessment on Event Rate of Treatment-emergent Major Hypoglycemic Events
NCT00676338 (11) [back to overview]Assessment on Event Rate of Treatment-Emergent Minor Hypoglycemic Events
NCT00676338 (11) [back to overview]Ratio of Fasting Triglycerides at Week 26 to Baseline
NCT00676338 (11) [back to overview]Change in Systolic Blood Pressure From Baseline to Week 26.
NCT00676338 (11) [back to overview]Change in HbA1c From Baseline to Week 26
NCT00676338 (11) [back to overview]Change in Fasting Total Cholesterol (TC) From Baseline to Week 26
NCT00676338 (11) [back to overview]Change in Fasting Serum Glucose (FSG) From Baseline to Week 26
NCT00676338 (11) [back to overview]Change in Fasting High-Density Lipoprotein (HDL) From Baseline to Week 26
NCT00676338 (11) [back to overview]Change in Diastolic Blood Pressure From Baseline to Week 26.
NCT00679042 (5) [back to overview]Treatment Emergent Adverse Events
NCT00679042 (5) [back to overview]Reduction in Hypoglycemic Severity Measured by %Reduction in HYPO Score
NCT00679042 (5) [back to overview]Number of Subjects Reaching the Efficacy Goal
NCT00679042 (5) [back to overview]Number of Patients Presenting With Insulin Independence at Day 365 Post First and Last Transplant
NCT00679042 (5) [back to overview]Hypoglycemic Episodes by HYPO Score
NCT00701935 (13) [back to overview]Change in Triglycerides From Baseline to 6 Months
NCT00701935 (13) [back to overview]Change in Weight From Baseline to 6 Months
NCT00701935 (13) [back to overview]Percentage Change in Abdominal Visceral Fat From Baseline to 6 Months
NCT00701935 (13) [back to overview]Percentage Change in Subcutaneous Abdominal Fat From Baseline to 6 Months
NCT00701935 (13) [back to overview]Percentage Change in Total Abdominal Fat From Baseline to 6 Months
NCT00701935 (13) [back to overview]Assessment of Event Rate of Treatment- Emergent Hypoglycemic Event
NCT00701935 (13) [back to overview]Change in Diastolic Blood Pressure From Baseline to 6 Months
NCT00701935 (13) [back to overview]Change in Fasting Plasma Glucose From Baseline to 6 Months
NCT00701935 (13) [back to overview]Percentage of Patients With HbA1c <=7.0% at 6 Months
NCT00701935 (13) [back to overview]Change in HbA1c From Baseline to 6 Months
NCT00701935 (13) [back to overview]Change in High-Density Lipoprotein (HDL) Cholesterol From Baseline to 6 Months
NCT00701935 (13) [back to overview]Change in Systolic Blood Pressure From Baseline to 6 Months
NCT00701935 (13) [back to overview]Change in Total Cholesterol From Baseline to 6 Months
NCT00707031 (9) [back to overview]Percentage of Patients With Glycosylated Hemoglobin (HbA1c) Level Less Than 7% at Week 24
NCT00707031 (9) [back to overview]Absolute Change From Baseline in Glycosylated Hemoglobin (HbA1c) at Week 24
NCT00707031 (9) [back to overview]Change From Baseline in Body Weight at Week 24
NCT00707031 (9) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG) at Week 24
NCT00707031 (9) [back to overview]Percentage of Patients Requiring Rescue Therapy During Main 24-Week Period
NCT00707031 (9) [back to overview]Percentage of Patients With at Least 5% Weight Loss From Baseline at Week 24
NCT00707031 (9) [back to overview]Percentage of Patients With Glycosylated Hemoglobin (HbA1c) Level Less Than or Equal to 6.5% at Week 24
NCT00707031 (9) [back to overview]Quality of Life: Change From Baseline in Patient's Satisfaction to Treatment (PAGI-QOL) at Week 24
NCT00707031 (9) [back to overview]Number of Patients With Symptomatic Hypoglycemia and Severe Symptomatic Hypoglycemia
NCT00729326 (19) [back to overview]Episodes of Hypoglycemia (Overall)
NCT00729326 (19) [back to overview]Episodes of Hypoglycemia (Week 4 to Week 8)
NCT00729326 (19) [back to overview]Percentage of Patients Experiencing Hypoglycemia (Week 4 to Week 8)
NCT00729326 (19) [back to overview]Change in Postprandial C-peptide AUC After the Morning Meal
NCT00729326 (19) [back to overview]Change in Postprandial C-peptide AUC Excursion After the Morning Meal
NCT00729326 (19) [back to overview]Change in Fasting Blood Glucose After the Morning Meal
NCT00729326 (19) [back to overview]Change in Postprandial Active GLP-1 AUC After the Morning Meal
NCT00729326 (19) [back to overview]Change in Postprandial Active GLP-1 AUC Excursion After the Monrning Meal
NCT00729326 (19) [back to overview]Change in Postprandial Glucagon Area Under the Concentration-time Curve (AUC) After the Morning Meal
NCT00729326 (19) [back to overview]Change in Postprandial Glucagon AUC Excursion After the Morning Meal
NCT00729326 (19) [back to overview]Change in Postprandial Insulin AUC After the Morning Meal
NCT00729326 (19) [back to overview]Change in Postprandial Insulin AUC Excursion After the Morning Meal
NCT00729326 (19) [back to overview]Change in Two-hour Postprandial Glucose After the Morning Meal
NCT00729326 (19) [back to overview]Change in Time-averaged Glucose During a 24 Hour Period
NCT00729326 (19) [back to overview]Change in Postprandial Triglyceride AUC Excursion After the Morning Meal
NCT00729326 (19) [back to overview]Change in Postprandial Triglyceride AUC After the Morning Meal
NCT00729326 (19) [back to overview]Percentage of Patients Experiencing Hypoglycemia (Baseline to Week 4)
NCT00729326 (19) [back to overview]Percentage of Patients Experiencing Hypoglycemia (Overall)
NCT00729326 (19) [back to overview]Episodes of Hypoglycemia (Baseline to Week 4)
NCT00736229 (4) [back to overview]Median Glucose Values From Steady State Through 48 Hours or Until Discharge.
NCT00736229 (4) [back to overview]Serious Adverse Events (Death, Non-fatal Myocardial Infarction, and Non-fatal Stroke Through 30 Days)
NCT00736229 (4) [back to overview]Time to Steady State
NCT00736229 (4) [back to overview]Rates of Hypoglycemia and Severe Hypoglycemia
NCT00753896 (11) [back to overview]Change in Body Weight From Baseline to Week 52
NCT00753896 (11) [back to overview]Change in Fasting Serum Glucose From Baseline to Week 52
NCT00753896 (11) [back to overview]Change in HbA1c From Baseline to Week 52
NCT00753896 (11) [back to overview]Change in Triglycerides From Baseline to Week 52
NCT00753896 (11) [back to overview]Assessment of Event Rate of Treatment-Emergent Hypoglycemic Events
NCT00753896 (11) [back to overview]Change in Blood Pressure From Baseline to Week 52
NCT00753896 (11) [back to overview]Percentage of Patients Experiencing Adverse Events
NCT00753896 (11) [back to overview]Percentage of Patients Achieving HbA1c <=7% at Week 52
NCT00753896 (11) [back to overview]Percentage of Patients Achieving HbA1c <=6.5% at Week 52
NCT00753896 (11) [back to overview]Change in Total Cholesterol From Baseline to Week 52
NCT00753896 (11) [back to overview]Change in High-density Lipoprotein (HDL) From Baseline to Week 52
NCT00765817 (17) [back to overview]Change in Triglycerides
NCT00765817 (17) [back to overview]Change in Total Cholesterol
NCT00765817 (17) [back to overview]Percentage of Subjects Experiencing Minor Hypoglycemia
NCT00765817 (17) [back to overview]Change in Fasting Serum Glucose
NCT00765817 (17) [back to overview]Change in High Density Lipoprotein (HDL) Cholesterol
NCT00765817 (17) [back to overview]Change in Systolic Blood Pressure (SBP)
NCT00765817 (17) [back to overview]Change in Glycosylated Hemoglobin (HbA1c)
NCT00765817 (17) [back to overview]Change in Body Weight
NCT00765817 (17) [back to overview]Change in Daily Insulin Dose
NCT00765817 (17) [back to overview]Change in 7-point Self-monitored Blood Glucose (SMBG) Profile
NCT00765817 (17) [back to overview]Change in Low Density Lipoprotein (LDL) Cholesterol
NCT00765817 (17) [back to overview]Change in Waist Circumference
NCT00765817 (17) [back to overview]Change in Daily Insulin Dose (on a Per Body Weight Basis)
NCT00765817 (17) [back to overview]Change in Diastolic Blood Pressure (DBP)
NCT00765817 (17) [back to overview]Percentage of Patients Achieving HbA1c <=7%
NCT00765817 (17) [back to overview]Percentage of Patients Achieving HbA1c <=6.5%
NCT00765817 (17) [back to overview]Minor Hypoglycemia Rate Per Year
NCT00775684 (5) [back to overview]Effect on Functional Beta-cell Mass as Determined by Change in ß-cell Secretory Capacity at 6 Months (μU/ml)
NCT00775684 (5) [back to overview]PG 50 (the Plasma Glucose Level at Which Half-maximal Insulin Secretion is Achieved During the Glucose-potentiated Arginine Test) at Baseline and 6 Months
NCT00775684 (5) [back to overview]Change in Acute Insulin Response to Arginine. (AIRarg)
NCT00775684 (5) [back to overview]Effect on Functional Beta-cell Mass as Determined by Change in ß-cell Secretory Capacity at 6 Months (pg/mL)
NCT00775684 (5) [back to overview]Insulin Sensitivity at Baseline and 6 Months
NCT00782418 (3) [back to overview]Change From Baseline in Insulin Concentration
NCT00782418 (3) [back to overview]Change From Baseline in Insulin Secretion Rate (ISR) Normalized to Ambient Plasma Glucose
NCT00782418 (3) [back to overview]Change From Baseline in C-peptide Concentration
NCT00799435 (1) [back to overview]Change in Aortic Stiffness, as Measured by the Change in the Mean Aortic Pulse Wave Velocity
NCT00845182 (2) [back to overview]HbA1c
NCT00845182 (2) [back to overview]Effect of Pioglitazone, Exenatide and Combined Pioglitazone and Exenatide on Body Weight
NCT00845507 (2) [back to overview]Change in Weight From Baseline to Endpoint.
NCT00845507 (2) [back to overview]Change in Body Mass Index (BMI) From Baseline to Endpoint.
NCT00855439 (4) [back to overview]Confirmed Clinical Neuropathy (CCN)
NCT00855439 (4) [back to overview]Cardiac Autonomic Neuropathy (CAN)
NCT00855439 (4) [back to overview]Cardiac Autonomic Neuropathy
NCT00855439 (4) [back to overview]Intra-epidermal Nerve Fiber Density
NCT00856609 (3) [back to overview]Energy Intake
NCT00856609 (3) [back to overview]Body Weight
NCT00856609 (3) [back to overview]Twenty-four-hour Energy Expenditure
NCT00870194 (17) [back to overview]Incidence of Hypoglycemia (Overall)
NCT00870194 (17) [back to overview]Change in Body Weight (kg)
NCT00870194 (17) [back to overview]Change in FSG (mmol/L)
NCT00870194 (17) [back to overview]Change in HbA1c (Percent)
NCT00870194 (17) [back to overview]Change in HDL (mmol/L)
NCT00870194 (17) [back to overview]Change in LDL (mmol/L)
NCT00870194 (17) [back to overview]Change in Total Cholesterol (mmol/L)
NCT00870194 (17) [back to overview]Change in Triglycerides (mmol/L)
NCT00870194 (17) [back to overview]Change in Waist Circumference (cm)
NCT00870194 (17) [back to overview]Incidence of Confirmed Hypoglycemia(Overall)
NCT00870194 (17) [back to overview]Incidence of Nocturnal Hypoglycemia (Overall)
NCT00870194 (17) [back to overview]Incidence of Severe Hypoglycemia(Overall)
NCT00870194 (17) [back to overview]Percentage of Patients Achieving HbA1c <=7.0%
NCT00870194 (17) [back to overview]Percentage of Patients Achieving HbA1c <7.0%
NCT00870194 (17) [back to overview]SMBG (mmol/L)
NCT00870194 (17) [back to overview]Waist-to-Hip Ratio
NCT00870194 (17) [back to overview]Percentage of Patients Achieving HbA1c <=6.5%
NCT00877890 (13) [back to overview]Ratio of Triglycerides at Week 24 to Baseline
NCT00877890 (13) [back to overview]Assessment on Event Rate of Treatment-emergent Minor Hypoglycemic Events
NCT00877890 (13) [back to overview]Change in Sitting Systolic Blood Pressure From Baseline to Week 24
NCT00877890 (13) [back to overview]Change in Body Weight From Baseline to Week 24
NCT00877890 (13) [back to overview]Change in Fasting Plasma Glucose From Baseline to Week 24
NCT00877890 (13) [back to overview]Change in HbA1c From Baseline to Week 24
NCT00877890 (13) [back to overview]Change in Sitting Diastolic Blood Pressure From Baseline to Week 24
NCT00877890 (13) [back to overview]Percentage of Subjects Achieving HbA1c Target of <7%
NCT00877890 (13) [back to overview]Percentage of Subjects Achieving HbA1c Target of <=6.5%
NCT00877890 (13) [back to overview]Percentage of Subjects Achieving Fasting Plasma Glucose Target of <=126 mg/dL
NCT00877890 (13) [back to overview]Change in Total Cholesterol From Baseline to Week 24
NCT00877890 (13) [back to overview]Change in High-density Lipoprotein (HDL) From Baseline to Week 24
NCT00877890 (13) [back to overview]Assessment on Event Rate of Treatment-emergent Major Hypoglycemic Events
NCT00882050 (1) [back to overview]The Primary Objective is to Determine the Ability of Intravenous Exenatide to: Maintain Intraoperative Euglycemia in Subjects With Initial Blood Glucose < 126 mg/dL in Surgical Subjects as Compared to Placebo,
NCT00886626 (1) [back to overview]Change in Body Mass Index (BMI)
NCT00894322 (19) [back to overview]Least Square Mean Change From Baseline in Hemoglobin A1c (HbA1c) to Week 12 in Participants With Diabetes (Cohort 2) in the ITT Population
NCT00894322 (19) [back to overview]Average Exenatide Concentration (Cave) of 10 mg Exenatide (Cohort 1) in Healthy Participants in the Pharmacokinetic Evaluable Population
NCT00894322 (19) [back to overview]AUC (0 Hour to 168 Hour) for 10 mg Exenatide (Cohort 1) in Healthy Participants in the Pharmacokinetic Evaluable Population
NCT00894322 (19) [back to overview]Time to Maximum Concentration (Tmax) of 2 mg Exenatide (Cohort 2) in Participants With Diabetes in Pharmacokinetic Evaluable Population
NCT00894322 (19) [back to overview]Time to Maximum Concentration (Tmax) for Single Dose of 10 mg Exenatide (Cohort 1) in Healthy Participants in the Pharmacokinetic Evaluable Population
NCT00894322 (19) [back to overview]Number of Participants With Treatment Emergent Adverse Events (TEAEs), Injection Site TEAEs, Serious Adverse Events (SAEs), Deaths, and Withdrawals Due to AEs in Cohort 1 and Cohort 2 in Intent to Treat (ITT) Population
NCT00894322 (19) [back to overview]Number of Participants With Hematology and Serum Chemistry Laboratory Values of Potential Clinical Importance in Cohorts 1 and 2 in ITT Population
NCT00894322 (19) [back to overview]Number of Participants Achieving HbA1c Less Than Equal to (<=) 6.5% and Less Than (<) 7% at Week 12 in Participants With Diabetes (Cohort 2) in the ITT Population
NCT00894322 (19) [back to overview]Mean Change From Baseline to End of Study in Sitting Diastolic and Systolic Blood Pressure in Cohorts 1 and 2 in ITT Population
NCT00894322 (19) [back to overview]Maximum Concentration (Cmax) for Single Dose of 10 mg Exenatide (Cohort 1) in Healthy Participants in the Pharmacokinetic Evaluable Population
NCT00894322 (19) [back to overview]Maximum Concentration (Cmax) for 2 mg Exenatide (Cohort 2) in Participants With Diabetes in the Pharmacokinetic Evaluable Population
NCT00894322 (19) [back to overview]Average Exenatide Concentration (Cave) of 2 mg Exenatide (Cohort 2) in Participants With Diabetes in the Pharmacokinetic Evaluable Population
NCT00894322 (19) [back to overview]Area Under the Curve (AUC) for Single Dose of 10 mg Exenatide (Cohort 1) in Healthy Participants in the Pharmacokinetic Evaluable Population
NCT00894322 (19) [back to overview]Area Under the Curve (AUC) for 2 mg Exenatide (Cohort 2) in Participants With Diabetes in the Pharmacokinetic Evaluable Population
NCT00894322 (19) [back to overview]Antibody Titers for Participants With Treatment Emergent Positive Antibodies to Exenatide in Participants Who Received Exenatide in Cohorts 1 and 2
NCT00894322 (19) [back to overview]Mean Change From Baseline to End of Study in Sitting Heart Rate in Cohorts 1 and 2 in ITT Population
NCT00894322 (19) [back to overview]Mean Change From Baseline at Week 12 in Fasting Plasma Glucose in Participants With Diabetes (Cohort 2) for the ITT Population
NCT00894322 (19) [back to overview]Mean Change From Baseline at Week 12 in Body Weight in Participants With Diabetes (Cohort 2) in the ITT Population
NCT00894322 (19) [back to overview]Number of Participants With Concomitant Medications in Cohort 1 and Cohort 2 in ITT Population
NCT00917267 (10) [back to overview]Change in Fasting Serum Glucose (FSG) From Baseline to Week 26
NCT00917267 (10) [back to overview]Change in HbA1c From Baseline to Week 26.
NCT00917267 (10) [back to overview]Change in High-Density Lipoprotein (HDL) From Baseline to Week 26
NCT00917267 (10) [back to overview]Change in Total Cholesterol (TC) From Baseline to Week 26
NCT00917267 (10) [back to overview]Change in Body Weight (BW) From Baseline to Week 26
NCT00917267 (10) [back to overview]Ratio of Triglycerides (TG) at Week 26 to Baseline
NCT00917267 (10) [back to overview]Assessment of Event Rate of Treatment-emergent Hypoglycemic Events
NCT00917267 (10) [back to overview]Change in Blood Pressure From Baseline to Week 26
NCT00917267 (10) [back to overview]Percentage of Patients Achieving HbA1c Targets <=7% at Week 26
NCT00917267 (10) [back to overview]Percentage of Patients Achieving HbA1c Targets <=6.5% at Week 26
NCT00935532 (11) [back to overview]Change in Body Weight From Baseline to Endpoint (Week 26)
NCT00935532 (11) [back to overview]Change in Fasting Serum Glucose (FSG) From Baseline to Endpoint (Week 26)
NCT00935532 (11) [back to overview]Change in HbA1c From Baseline to Endpoint (Week 26)
NCT00935532 (11) [back to overview]Change in High-density Lipoprotein Cholesterol (HDL-C) From Baseline to Endpoint (Week 26)
NCT00935532 (11) [back to overview]Change in Total Cholesterol From Baseline to Endpoint (Week 26)
NCT00935532 (11) [back to overview]Percentage of Subjects Achieving HbA1c<=6.5%
NCT00935532 (11) [back to overview]Percentage of Subjects Achieving HbA1c<=7%
NCT00935532 (11) [back to overview]Ratio of Fasting Triglycerides at Endpoint (Week 26) to Baseline
NCT00935532 (11) [back to overview]Change in Blood Pressure From Baseline to Endpoint (Week 26)
NCT00935532 (11) [back to overview]Assessment on Event Rate of Treatment-emergent Major Hypoglycemic Events
NCT00935532 (11) [back to overview]Assessment on Event Rate of Treatment-emergent Minor Hypoglycemic Events
NCT00943917 (6) [back to overview]Mean Change in HbA1c (Per Protocol)
NCT00943917 (6) [back to overview]Mean Change in HbA1c (Per Protocol)
NCT00943917 (6) [back to overview]Mean Change in HbA1c (Per Protocol)
NCT00943917 (6) [back to overview]Mean Change in HbA1c (ITT)
NCT00943917 (6) [back to overview]Mean Change in HbA1c (ITT)
NCT00943917 (6) [back to overview]Mean Change in HbA1c (ITT)
NCT00960661 (13) [back to overview]Change in Diastolic Blood Pressure (DBP) From Baseline to Week 30
NCT00960661 (13) [back to overview]Change in Systolic Blood Pressure (SBP) From Baseline to Week 30
NCT00960661 (13) [back to overview]Change in Body Weight From Baseline to Week 30.
NCT00960661 (13) [back to overview]Change in Low Density Lipoprotein (LDL) From Baseline to Week 30
NCT00960661 (13) [back to overview]Change in Total Cholesterol From Baseline to Week 30
NCT00960661 (13) [back to overview]Major Hypoglycemia Rate Per Year
NCT00960661 (13) [back to overview]Minor Hypoglycemia Rate Per Year
NCT00960661 (13) [back to overview]Percent of Participants Achieving HbA1c ≤ 6.5%.
NCT00960661 (13) [back to overview]Percentage of Participants Achieving HbA1C < 7.0%
NCT00960661 (13) [back to overview]Daily Insulin Glargine Dose at Baseline and at Week 30
NCT00960661 (13) [back to overview]Change in High Density Lipoprotein (HDL) From Baseline to Week 30
NCT00960661 (13) [back to overview]Change in Glycosylated Hemoglobin (HbA1c) From Baseline to Week 30
NCT00960661 (13) [back to overview]Change in Fasting Blood Glucose (FBG) From Baseline to Week 30.
NCT01003184 (14) [back to overview]Changes in Systolic Blood Pressure From Baseline to Week 26
NCT01003184 (14) [back to overview]Change in Triglycerides From Baseline to Endpoint (Week 26).
NCT01003184 (14) [back to overview]Percentage of Patients Achieving ≤6.5% at Endpoint
NCT01003184 (14) [back to overview]Percentage of Patients Who Have Achieved HbA1c ≤7.4% With Weight Loss (≥1.0 kg) at Endpoint (Week 26)
NCT01003184 (14) [back to overview]Change in Body Weight From Baseline to Week 26
NCT01003184 (14) [back to overview]Change in Diastolic Blood Pressure From Baseline to Week 26.
NCT01003184 (14) [back to overview]Change in Fasting Serum Glucose From Baseline to Endpoint (Week 26).
NCT01003184 (14) [back to overview]Change in HbA1c From Baseline to Week 26
NCT01003184 (14) [back to overview]Change in High-density Lipoprotein (HDL) Cholesterol From Baseline to Endpoint (Week 26).
NCT01003184 (14) [back to overview]Change in Total Cholesterol From Baseline to Endpoint (Week 26).
NCT01003184 (14) [back to overview]Hypoglycemia Rate Per Year
NCT01003184 (14) [back to overview]Percentage of Patients Achieving ≤7.0% at Endpoint
NCT01003184 (14) [back to overview]Percentage of Patients Achieving Glycosylated Hemoglobin (HbA1c) Concentration ≤7.0% With Weight Loss (≥1.0 kg) at Endpoint (Week 26)
NCT01003184 (14) [back to overview]Percentage of Patients Achieving HbA1c ≤7.4% at Endpoint
NCT01006889 (8) [back to overview]Change in Anthropometric Variables (BMI).
NCT01006889 (8) [back to overview]Lipid Profiles, Lipoprotein Analysis by NMR (LipoScience).
NCT01006889 (8) [back to overview]Insulin Secretion (Hyperglycemic Clamp)
NCT01006889 (8) [back to overview]Percent Change From Baseline in Glucose Infusion (M Value) During Hyperglycemic Clamp
NCT01006889 (8) [back to overview]Number of Severe Hypoglycemic (Glucose ≤40 mg/dL) Events.
NCT01006889 (8) [back to overview]Hepatic Steatosis
NCT01006889 (8) [back to overview]Change in Anthropometric Variables (Weight).
NCT01006889 (8) [back to overview]A1c
NCT01029886 (10) [back to overview]Change in Total Cholesterol From Baseline to Week 26
NCT01029886 (10) [back to overview]Change in High-Density Lipoprotein Cholesterol (HDL-C) From Baseline to Week 26
NCT01029886 (10) [back to overview]Change in HbA1c From Baseline to Week 26
NCT01029886 (10) [back to overview]Change in Body Weight From Baseline to Week 26
NCT01029886 (10) [back to overview]Change in Fasting Serum Glucose From Baseline to Week 26
NCT01029886 (10) [back to overview]Change in Systolic Blood Pressure (SBP) From Baseline to Week 26
NCT01029886 (10) [back to overview]Assessment of Event Rate of Treatment-emergent Hypoglycemic Events
NCT01029886 (10) [back to overview]Ratio of Fasting Triglycerides at Week 26 to Baseline
NCT01029886 (10) [back to overview]Percentage of Patients Achieving HbA1c <7.0% at Week 26
NCT01029886 (10) [back to overview]Change in Diastolic Blood Pressure (DBP) From Baseline to Week 26
NCT01060059 (23) [back to overview]Changes in Diastolic Blood Pressure Between Baseline and Month 12
NCT01060059 (23) [back to overview]Changes in Fasting Blood Glucose From Baseline to Month 12
NCT01060059 (23) [back to overview]Changes in Fasting HDL Between Baseline and Month 12
NCT01060059 (23) [back to overview]Changes in Fasting Total Cholesterol Between Baseline and Month 12
NCT01060059 (23) [back to overview]Changes in Fasting Triglycerides Between Baseline and Month 12
NCT01060059 (23) [back to overview]Changes in HbA1c From Baseline to Month 12
NCT01060059 (23) [back to overview]Changes in Systolic Blood Pressure Between Baseline and Month 12
NCT01060059 (23) [back to overview]Changes in Weight From Baseline to Month 12
NCT01060059 (23) [back to overview]Factor of 1 Percent (%) Higher Baseline HbA1c Associated With Treatment Choice at Baseline
NCT01060059 (23) [back to overview]Factor of Greater Height Associated With Treatment Choice at Baseline
NCT01060059 (23) [back to overview]Factor of Higher Body Mass Index (BMI) Associated With Treatment Choice at Baseline
NCT01060059 (23) [back to overview]Factor of Longer Duration of Diabetes Associated With Treatment Choice at Baseline
NCT01060059 (23) [back to overview]Factor of Older Age Associated With Treatment Choice at Baseline
NCT01060059 (23) [back to overview]Percentage of Patients Achieving a Weight Decrease >=3% Between Baseline and Month 12
NCT01060059 (23) [back to overview]Percentage of Patients Achieving a Weight Decrease >=5% Between Baseline and Month 12
NCT01060059 (23) [back to overview]Percentage of Patients Achieving HbA1c Concentration <=7.0% at Month 12
NCT01060059 (23) [back to overview]Percentage of Patients Achieving HbA1c Concentration <6.5% at Month 12
NCT01060059 (23) [back to overview]Percentage of Patients Who Achieved Glycemic Target of HbA1c ≤ 7.0% With Minimal Weight Gain (≤ 1 Kg) at Month 12.
NCT01060059 (23) [back to overview]Percentage of Patients With HbA1c Reduction From Baseline >= 1.0% at Month 12
NCT01060059 (23) [back to overview]Percentage of Patients With Hypoglycemia Episodes Between Baseline and Month 12
NCT01060059 (23) [back to overview]Factors of Gender, Baseline Presence of Medical Conditions, and Previous Gastrointestinal Symptoms Associated With Treatment Choice at Baseline
NCT01060059 (23) [back to overview]Factors of Higher Creatinine, Higher Fasting High Density Lipoprotein (HDL) Cholesterol, Higher Fasting Cholesterol, and Higher Fasting Triglycerides Which Were Associated With Treatment Choice at Baseline
NCT01060059 (23) [back to overview]Changes in Fasting LDL Between Baseline and Month 12
NCT01061775 (4) [back to overview]BMI Change
NCT01061775 (4) [back to overview]Waist to Height Ratio (WHtR)
NCT01061775 (4) [back to overview]Childhood Eating Behavior Questionnaire (CEBQ)
NCT01061775 (4) [back to overview]Calorie Intake Based on 3-day Diet Records
NCT01064687 (47) [back to overview]Percentage of Participants Attaining Glycosylated Hemoglobin (HbA1c) Less Than 7% and Less Than or Equal to 6.5% at 26 Weeks
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks on Pancreatic Enzymes
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks on Electrocardiogram Parameters, Fridericia Corrected QT (QTcF) Interval and PR Interval
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks on Blood Pressure
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks in Updated Homeostasis Model Assessment of Beta-cell Function (HOMA2-%B) and Updated Homeostasis Model Assessment of Insulin Sensitivity (HOMA2-%S)
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks in the EuroQol 5
NCT01064687 (47) [back to overview]Pharmacokinetics: Area Under the Concentration Curve (AUC) for LY2189265
NCT01064687 (47) [back to overview]Number of Participants With Treatment Emergent Adverse Events at 52 Weeks
NCT01064687 (47) [back to overview]Number of Participants With Treatment Emergent Adverse Events at 26 Weeks
NCT01064687 (47) [back to overview]Number of Participants With LY2189265 Antibodies at 26 Weeks
NCT01064687 (47) [back to overview]Number of Participants With Adjudicated Pancreatitis at 52 Weeks
NCT01064687 (47) [back to overview]Number of Participants With Adjudicated Pancreatitis at 26 Weeks
NCT01064687 (47) [back to overview]Number of Participants Requiring Rescue Therapy Due to Hyperglycemia at 52 Weeks
NCT01064687 (47) [back to overview]Number of Participants Requiring Rescue Therapy Due to Hyperglycemia at 26 Weeks
NCT01064687 (47) [back to overview]Change in Baseline to 52 Weeks on Pulse Rate
NCT01064687 (47) [back to overview]Change in Baseline to 26 Weeks on Pulse Rate
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks on the Impact of Weight on Self-Perception
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks in the EuroQol 5
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks on Body Mass Index (BMI)
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks in the Impact of Weight on Activities of Daily Living
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks in Hematological and Biochemical Lab Values
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks for Daily Mean Blood Glucose Values From the 8-point Self-monitored Plasma Glucose (SMPG) Profiles
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks for Body Weight
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks Endpoint in Glycosylated Hemoglobin (HbA1c)
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks on the Impact of Weight on Self-Perception
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks on Serum Calcitonin
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks on Body Mass Index (BMI)
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks in the Impact of Weight on Activities of Daily Living
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks in the Diabetes Treatment Satisfaction Questionnaire Status (DTSQs) Version
NCT01064687 (47) [back to overview]Number of Participants With LY2189265 Antibodies at 52 Weeks and 4 Weeks After Last Dose of Study Drug
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks in N Terminal Pro Brain Natriuretic Peptide (NT-proBNP)
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks in Hematological and Biochemical Lab Values
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks for Daily Mean Blood Glucose Values From the 8-point Self-monitored Plasma Glucose (SMPG) Profiles
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks for Body Weight
NCT01064687 (47) [back to overview]Change From Baseline to 26 Weeks Endpoint in Glycosylated Hemoglobin (HbA1c)
NCT01064687 (47) [back to overview]Rate of Self-reported Hypoglycemic Events at 52 Weeks
NCT01064687 (47) [back to overview]Rate of Self-reported Hypoglycemic Events at 26 Weeks
NCT01064687 (47) [back to overview]Percentage of Participants Attaining Glycosylated Hemoglobin (HbA1c) Less Than 7% and Less Than or Equal to 6.5% at 52 Weeks
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks on Serum Calcitonin
NCT01064687 (47) [back to overview]Number of Self-reported Hypoglycemic Events at 52 Weeks
NCT01064687 (47) [back to overview]Number of Self-reported Hypoglycemic Events at 26 Weeks
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks in the Diabetes Treatment Satisfaction Questionnaire Status (DTSQs) and Change (DTSQc) Versions
NCT01064687 (47) [back to overview]Number of Participants With Adjudicated Cardiovascular Events at 52 Weeks
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks on Pancreatic Enzymes
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks on Electrocardiogram Parameters, Fridericia Corrected QT (QTcF) Interval and PR Interval
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks on Blood Pressure
NCT01064687 (47) [back to overview]Change From Baseline to 52 Weeks in Updated Homeostasis Model Assessment of Beta-cell Function (HOMA2-%B) and Updated Homeostasis Model Assessment of Insulin Sensitivity (HOMA2-%S)
NCT01077323 (4) [back to overview]"Incidence Rates Per 100,000 Person-Years of Likely Acute Pancreatitis (Among Recent Use Period) - Time on Drug Analysis"
NCT01077323 (4) [back to overview]"Incidence Rates Per 100,000 Person-Years of Likely Acute Pancreatitis (During Current Use Period) - Time on Drug Analysis"
NCT01077323 (4) [back to overview]"Incidence Rates Per 100,000 Person-Years of Likely Acute Pancreatitis (During Past Use Period) - Time on Drug Analysis"
NCT01077323 (4) [back to overview]Incidence Rates Per 100,000 Person-Years of Likely Acute Pancreatitis Among Initiators of Exenatide, Diabetics Initiating Other Antidiabetic Drugs, and the Non-diabetes Cohort - Intent to Treat Analysis
NCT01089569 (7) [back to overview]HbA1c Change
NCT01089569 (7) [back to overview]Change From Baseline in Weight Changes
NCT01089569 (7) [back to overview]Change From Baseline in Incidence of Hypoglycemia (Frequency)
NCT01089569 (7) [back to overview]Change From Baseline in Incidence of Hypoglycemia (Degree)
NCT01089569 (7) [back to overview]Change From Baseline in Glucose Stability (Absolute Hourly Rate of Change in Median Curve)
NCT01089569 (7) [back to overview]Change From Baseline in Glucose Exposure (Area Under the Diurnal Median Curve or AUC)
NCT01089569 (7) [back to overview]Change From Baseline in CGM Glucose Variability
NCT01104701 (12) [back to overview]Participants Negative or Positive for Anti-exenatide Antibodies - ITT Population
NCT01104701 (12) [back to overview]Number of Participants With Treatment-Emergent Adverse Events (AEs), Serious AEs (SAEs), and AEs Leading to Discontinuation - ITT Population
NCT01104701 (12) [back to overview]Number of Chemistry Laboratory Values of Potential Clinical Importance Observed During Treatment Period - ITT Population
NCT01104701 (12) [back to overview]Number of Hematology Laboratory Values of Potential Clinical Importance Observed During Treatment Period - ITT Population
NCT01104701 (12) [back to overview]Percentage of Participants Achieving HbA1c Target Values at Week 20 - Evaluable Population
NCT01104701 (12) [back to overview]Mean Change From Baseline in Heart Rate at Week 20 - Intent to Treat (ITT) Population
NCT01104701 (12) [back to overview]Number of Participants With Injection Site Reaction Treatment Emergent Adverse Events - ITT Population
NCT01104701 (12) [back to overview]Mean Change From Baseline in Diastolic and Systolic Blood Pressure at Week 20 - Intent to Treat (ITT) Population
NCT01104701 (12) [back to overview]Mean Change in Body Weight From Baseline to Week 20 - Evaluable Population
NCT01104701 (12) [back to overview]Mean Change in Fasting Glucose From Baseline to Week 20 - Evaluable Population
NCT01104701 (12) [back to overview]Mean Change in HbA1c From Baseline to End of Treatment (Week 20) - Evaluable Population
NCT01104701 (12) [back to overview]Time Weighted Average Concentration and Peak to Trough of Exenatide From Week 12 Through Week 16 - Pharmacokinetic Evaluable - Steady State Population
NCT01136798 (5) [back to overview]Severity of Obstructive Sleep Apnea
NCT01136798 (5) [back to overview]Sleep Efficiency During Polysomnographic Recording
NCT01136798 (5) [back to overview]Mean 24-h Blood Glucose Levels
NCT01136798 (5) [back to overview]Minutes of Wake After Sleep Onset During Sleep Recording
NCT01136798 (5) [back to overview]Non-REM Slow Wave Sleep
NCT01147627 (1) [back to overview]the Comparison Between Treatment Groups of the Changes From Baseline in HbA1c at 48 Weeks
NCT01154933 (4) [back to overview]HbA1c
NCT01154933 (4) [back to overview]Fasting Insulin
NCT01154933 (4) [back to overview]Weight
NCT01154933 (4) [back to overview]Intranuclear NFκB Binding Activity
NCT01181986 (3) [back to overview]Reactive Hyperemia Index (RHI)
NCT01181986 (3) [back to overview]Plasma Triglycerides
NCT01181986 (3) [back to overview]Plasma Glucose
NCT01237197 (1) [back to overview]Percent Change From Baseline in Body Mass Index at 3-months
NCT01255163 (9) [back to overview]Mini Mental State Examination (MMSE)
NCT01255163 (9) [back to overview]Number of Participants With Incidence of Nausea
NCT01255163 (9) [back to overview]Cerebrospinal Fluid Amyloid-beta 42 (CSF Abeta42)
NCT01255163 (9) [back to overview]Body Mass Index (BMI)
NCT01255163 (9) [back to overview]Cerebrospinal Fluid (CSF) Total Tau
NCT01255163 (9) [back to overview]Cerebrospinal Fluid phospho181-tau (CSF p181-tau)
NCT01255163 (9) [back to overview]Clinical Dementia Rating (CDR) Global Score
NCT01255163 (9) [back to overview]Alzheimer's Disease Assessment Scale-cognitive Subscale (ADAS-cog70)
NCT01255163 (9) [back to overview]Clinical Dementia Rating (CDR) Sum of Boxes
NCT01269047 (2) [back to overview]Post-prandial Blood Glucose Concentration in Both Pramlintide and Exenatide Treated Groups in Acute and Chronic Setting, Compared to Insulin Monotherapy in Type 1 Diabetes Mellitus.
NCT01269047 (2) [back to overview]Difference in HbA1C Between the Treatment and the Control Groups
NCT01297062 (9) [back to overview]Assay Sensitivity of Moxifloxacin at 1200h (3 Hour Post-administration of Moxifloxacin) on Day 2
NCT01297062 (9) [back to overview]Plasma Exenatide Concentrations at Steady State on Day 1, 2 and 3
NCT01297062 (9) [back to overview]Number of Subjects With QTcP Interval >450msec at Any Timepoint on Any Day in Exenatide and Placebo
NCT01297062 (9) [back to overview]Number of Subjects With Increase of QTcP Interval From Baseline >30msec at Any Timepoint on Any Day in Exenatide and Placebo
NCT01297062 (9) [back to overview]Comparison of LS Mean Changes From Baseline in QTcP Intervals Between Exenatide and Placebo on Day 3 Averaged Over 1300h, 1400h, 1500h (Target Steady State Exenatide Concentration of 500 pg/mL)
NCT01297062 (9) [back to overview]Comparison of LS Mean Changes From Baseline in QTcP Intervals Between Exenatide and Placebo on Day 2 Averaged Over 1300h, 1400h, 1500h (Target Steady State Exenatide Concentration of 300 pg/mL)
NCT01297062 (9) [back to overview]Comparison of Least Squares (LS) Mean Changes From Baseline in Population-based Corrected QT Intervals (QTcP) Between Exenatide and Placebo on Day 1 Averaged Over 1300h, 1400h, 1500h (Target Steady State Exenatide Concentration of 200 pg/mL)
NCT01297062 (9) [back to overview]Assay Sensitivity of Moxifloxacin at 1100h (2 Hour Post-administration of Moxifloxacin) on Day 2
NCT01297062 (9) [back to overview]Assay Sensitivity of Moxifloxacin at 1000h (1 Hour Post-administration of Moxifloxacin) on Day 2
NCT01364584 (14) [back to overview]Echocardiographic Measures - Longitudinal Strain
NCT01364584 (14) [back to overview]Echocardiographic Measures - Lateral E'
NCT01364584 (14) [back to overview]Echocardiographic Measures - Circumferential Strain
NCT01364584 (14) [back to overview]Change From Baseline in Arterial Stiffness
NCT01364584 (14) [back to overview]Echocardiographic Measures - Mitral Valve Deceleration Time
NCT01364584 (14) [back to overview]Echocardiographic Measures - Septal E:E'
NCT01364584 (14) [back to overview]Echocardiographic Measures - Mitral Valve E Wave Velocity
NCT01364584 (14) [back to overview]Oxygen Uptake Kinetics Steady State Tau
NCT01364584 (14) [back to overview]Peak Oxygen Consumption (VO2 Peak)
NCT01364584 (14) [back to overview]Echocardiographic Measures - Mitral Valve E:A Wave Velocity
NCT01364584 (14) [back to overview]Echocardiographic Measures - Septal E'
NCT01364584 (14) [back to overview]Echocardiographic Measures - Lateral E:E'
NCT01364584 (14) [back to overview]Change From Baseline in Peak Dilation of Brachial Artery Diameter
NCT01364584 (14) [back to overview]Echocardiographic Measures - Stroke Volume
NCT01381926 (3) [back to overview]Determine Changes in Bone Resorption Markers During the Treatment With a GLP-1 Receptor Agonist (Exenatide) Compared to Placebo in Patients With T2DM.
NCT01381926 (3) [back to overview]Determine Changes in Bone Turnover Markers by Tartrate-Resistant Acid Phosphatase 5b (TRACP5b) During the Treatment With a GLP-1 Receptor Agonist (Exenatide) Compared to Placebo in Patients With T2DM.
NCT01381926 (3) [back to overview]Determine Changes in Bone Turnover Markers by Serum N-Telo Peptide During the Treatment With a GLP-1 Receptor Agonist (Exenatide) Compared to Placebo in Patients With T2DM.
NCT01432405 (2) [back to overview]Plasma Adipocytokines
NCT01432405 (2) [back to overview]Hepatic Fat
NCT01444898 (9) [back to overview]Change in Weight
NCT01444898 (9) [back to overview]Appetite Scores
NCT01444898 (9) [back to overview]% Change in Body Mass Index (BMI)
NCT01444898 (9) [back to overview]Change in Acy Ghr
NCT01444898 (9) [back to overview]Change in Insulin Levels
NCT01444898 (9) [back to overview]Change in Leptin
NCT01444898 (9) [back to overview]Change in Pancreatic Peptide (PP)
NCT01444898 (9) [back to overview]Change in BMI Z-Score
NCT01444898 (9) [back to overview]Change in HbA1c (%)
NCT01484873 (5) [back to overview]Resting Energy Expenditure (Kcals Per Day)
NCT01484873 (5) [back to overview]Insulin Secretion (Area Under the Curve)
NCT01484873 (5) [back to overview]Gastric Emptying Rate (13C-octanoic Acid Isotope Excretion Half Life)
NCT01484873 (5) [back to overview]Body Weight (kg)
NCT01484873 (5) [back to overview]Visual Analogue Scales for Post-meal Satiety
NCT01524705 (4) [back to overview]HbA1C Levels
NCT01524705 (4) [back to overview]Weight Change During Trial
NCT01524705 (4) [back to overview]Coefficient of Variation at 26 Weeks Minus Coefficient of Variation at Baseline
NCT01524705 (4) [back to overview]Number of Participants With Hypoglycemia
NCT01554618 (24) [back to overview]Change From Baseline in Glycosylated Hemoglobin A1c (HbA1c) to Week 24 (Controlled Assessment Period)
NCT01554618 (24) [back to overview]Change From Baseline in HbA1c to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)
NCT01554618 (24) [back to overview]Change From Baseline in Blood Pressure (Systolic and Diastolic) to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)
NCT01554618 (24) [back to overview]Change From Baseline in HOMA-B and HOMA-S to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)
NCT01554618 (24) [back to overview]Change From Baseline in Lipids Profiles to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)
NCT01554618 (24) [back to overview]Plasma Exenatide Concentrations to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)
NCT01554618 (24) [back to overview]Percentage of Patients Positive for Anti-Drug Antibodies (ADAs) to Exenatide up to Week 24
NCT01554618 (24) [back to overview]Percentage of Patients Reporting AEs of Injection Site Reactions up to Week 24 (Controlled Assessment Period)
NCT01554618 (24) [back to overview]Percentage of Patients Reporting AEs of Injection Site Reactions up to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)
NCT01554618 (24) [back to overview]Percentage of Patients With On-Treatment Adverse Events (AEs) up to Week 24 (Controlled Assessment Period)
NCT01554618 (24) [back to overview]Change From Baseline in Homeostasis Model Assessments - Beta-Cell Function (HOMA-B) and Insulin Sensitivity (HOMA-S) to Week 24 (Controlled Assessment Period)
NCT01554618 (24) [back to overview]Change From Baseline in Lipid Profiles to Week 24 (Controlled Assessment Period)
NCT01554618 (24) [back to overview]Change From Baseline in Body Weight to Week 24 (Controlled Assessment Period)
NCT01554618 (24) [back to overview]Change From Baseline in Body Weight to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)
NCT01554618 (24) [back to overview]Plasma Exenatide Concentrations to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)
NCT01554618 (24) [back to overview]Change From Baseline in Fasting Insulin to Week 24 (Controlled Assessment Period)
NCT01554618 (24) [back to overview]Change From Baseline in Fasting Insulin to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)
NCT01554618 (24) [back to overview]Change From Baseline in Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) to Week 24 (Controlled Assessment Period)
NCT01554618 (24) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG) Concentration to Week 24 (Controlled Assessment Period)
NCT01554618 (24) [back to overview]Change From Baseline in FPG Concentration to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)
NCT01554618 (24) [back to overview]Number of Patients Needing Rescue Medication Due to Failure to Maintain Glycemic Control up to Week 24 (Controlled Assessment Period)
NCT01554618 (24) [back to overview]Number of Patients Needing Rescue Medication Due to Failure to Maintain Glycemic Control up to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)
NCT01554618 (24) [back to overview]Percentage of Participants Achieving HbA1c Goals of < 6.5%, ≤ 6.5%, and < 7.0% to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)
NCT01554618 (24) [back to overview]Percentage of Patients Achieving HbA1c Goals of < 6.5%, ≤ 6.5%, and < 7.0% at Week 24 (Controlled Assessment Period)
NCT01588418 (1) [back to overview]Effect of Exenatide on Brain (Total Gray Matter) Glucose Metabolism
NCT01590433 (1) [back to overview]Change in Body Weight
NCT01652716 (5) [back to overview]Change in 2-hour Postprandial Glucose Concentrations From Baseline to Week 16
NCT01652716 (5) [back to overview]Change in Body Weight (kg) From Baseline to Week 28
NCT01652716 (5) [back to overview]Change in Fasting Plasma Glucose Concentrations From Baseline to Week 28
NCT01652716 (5) [back to overview]Change in HbA1c (Glycosylated Hemoglobin) From Baseline to Week 28
NCT01652716 (5) [back to overview]Percentage of Subjects Achieving HbA1c <7% at Week 28
NCT01652729 (5) [back to overview]Percentage of Subjects Achieving HbA1c <7% at Week 28
NCT01652729 (5) [back to overview]Change in 2-hour Postprandial Glucose Concentrations From Baseline to Week 16 (Visit 8)
NCT01652729 (5) [back to overview]Change in Body Weight (kg) From Baseline to Week 28
NCT01652729 (5) [back to overview]Change in Fasting Plasma Glucose Concentrations From Baseline to Week 28
NCT01652729 (5) [back to overview]Change in HbA1c (Glycosylated Hemoglobin) From Baseline to Week 28
NCT01664624 (6) [back to overview]Change From Baseline in Postprandial AUC(0-8) of Insulin
NCT01664624 (6) [back to overview]Change From Baseline to Day 11 in 24-hour Average Plasma Glucose
NCT01664624 (6) [back to overview]Change From Baseline to Day 11 in AUC(0-8) of Appetite Sensation
NCT01664624 (6) [back to overview]Change From Baseline in AUC(0-8) of Postprandial Plasma Glucose
NCT01664624 (6) [back to overview]Change From Baseline in Postprandial Area Under the Curve From Time 0 to 8 Hours (AUC[0-8]) for Active Glucagon-like Peptide-1
NCT01664624 (6) [back to overview]Change From Baseline in Postprandial AUC(0-8) of C-peptide
NCT01676116 (9) [back to overview]Responders Achieving Pre-defined Target: HbA1c Below or Equal to 6.5% (48 mmol/Mol)
NCT01676116 (9) [back to overview]Change in Glycosylated Haemoglobin (HbA1c) From Baseline (Randomisation, Visit 2)
NCT01676116 (9) [back to overview]Number of Adverse Events (AEs)
NCT01676116 (9) [back to overview]Change From Baseline in Patient Reported Outcomes (PROs) Based on the Treatment Related Impact Measure - Diabetes (TRIM-D)
NCT01676116 (9) [back to overview]Responders Achieving Pre-defined Target: HbA1c Below 7.0% (53 mmol/Mol)
NCT01676116 (9) [back to overview]Change From Baseline in Patient Reported Outcomes (PROs) Based on Diabetes Treatment Satisfaction Questionnaire (DTSQ).
NCT01676116 (9) [back to overview]Number of Severe or Minor Hypoglycaemic Episodes
NCT01676116 (9) [back to overview]Change From Baseline in Body Weight
NCT01676116 (9) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG)
NCT01791465 (21) [back to overview]Body Mass Index at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Body Weight at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Peripheral Endothelial Tonography, as Measured by the Non-invasive EndoPAT System Using the LnRHI (Natural Log of Reactive Hyperemia Index), at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum Adipokine Leptin Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum Hemoglobin A1c (HbA1c) Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum HDL Cholesterol Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum Highly-sensitive C-reactive Protein (hsCRP) Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum Interleukin 6 (IL-6) at Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Oral Glucose Insulin Sensitivity (OGIS) at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum Total Cholesterol Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Waist Circumference at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Waist to Hip Ratio at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Hip Circumference at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum Triglycerides Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum Macrophage Chemotactic Protein-1 (MCP-1) Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum Macrophage Inflammatory Protein 1 Alpha (MIP-1 Alpha) Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum LDL Cholesterol Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum Soluble CD14 Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum Soluble Tumor Necrosis Factor Alpha (TNF-α) Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum TNF-a Receptor 1 Levels at Baseline and 16 Weeks
NCT01791465 (21) [back to overview]Serum TNF-a Receptor 2 Levels at Baseline and 16 Weeks
NCT01798264 (4) [back to overview]To Characterize the Pharmacokinetic Profile of ITCA 650 in Subjects With Type 2 Diabetes Mellitus
NCT01798264 (4) [back to overview]Number of Subjects With Study Drug-Related Adverse Events
NCT01798264 (4) [back to overview]Change in Fasting Plasma Glucose (FPG) 4 Weeks From Baseline
NCT01798264 (4) [back to overview]Change in Weight From Baseline to 4 Weeks
NCT01885208 (5) [back to overview]Change From Baseline in Body Weight
NCT01885208 (5) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG)
NCT01885208 (5) [back to overview]Change From Baseline in HbA1c (Glycosylated Haemoglobin)
NCT01885208 (5) [back to overview]Change From Baseline in Patient Reported Outcome (PRO) Questionnaire Diabetes Treatment Satisfaction Questionnaire Status (DTSQs)
NCT01885208 (5) [back to overview]Change From Baseline in Systolic and Diastolic Blood Pressure
NCT01928329 (4) [back to overview]Major Hypoglycemic Event Rate Off Drug
NCT01928329 (4) [back to overview]Major Hypoglycemic Event Rate On Drug
NCT01928329 (4) [back to overview]Change From Baseline in HbA1c Levels
NCT01928329 (4) [back to overview]Change From Baseline in HbA1c Levels
NCT01951651 (4) [back to overview]Myocardial Fat Content
NCT01951651 (4) [back to overview]Monocyte Inflammatory Protein Nuclear Factor Kappa-B (NFkappaB) (%)
NCT01951651 (4) [back to overview]Left Ventricular Ejection Fraction (LVEF)(%).
NCT01951651 (4) [back to overview]Hepatic Fat Content
NCT02020616 (12) [back to overview]Change From Baseline in Bone Metabolism at 12-Week Endpoint (Beta-Crosslaps and Procollagen 1 N-Terminal Propeptide [P1NP])
NCT02020616 (12) [back to overview]Change From Baseline in Body Weight at 12-Week Endpoint
NCT02020616 (12) [back to overview]Change From Baseline in Hemoglobin A1c (HbA1c) at 12-Week Endpoint
NCT02020616 (12) [back to overview]Percentage of Participants That Require Rescue Therapy
NCT02020616 (12) [back to overview]Percentage of Participants With Anti-Drug Antibodies to LY3053102
NCT02020616 (12) [back to overview]Percentage of Participants With Hypoglycemia
NCT02020616 (12) [back to overview]Pharmacokinetics: Area Under the Concentration Versus Time Curve During One Dosing Interval at Steady State (AUC [τ,ss]) of LY3053102
NCT02020616 (12) [back to overview]Change From Baseline in 7-Point Blood Glucose Profile at 12-Week Endpoint
NCT02020616 (12) [back to overview]Change From Baseline in Bone Metabolism at 12-Week Endpoint (Osteocalcin and Bone-Specific Alkaline Phosphatase [Bone-Specific ALP])
NCT02020616 (12) [back to overview]Change From Baseline in Bone Mineral Density Markers at 12-Week Endpoint
NCT02020616 (12) [back to overview]Change From Baseline in Lipids at 12-Week Endpoint
NCT02020616 (12) [back to overview]Percentage of Participants Achieving HbA1c <7.0% or HbA1c ≤6.5% at 12-Week Endpoint
NCT02058940 (14) [back to overview]Median Intensive Care Unit Length of Stay
NCT02058940 (14) [back to overview]Median Insulin Use
NCT02058940 (14) [back to overview]Median Hospital Length of Stay
NCT02058940 (14) [back to overview]Median Glucose Concentration During Exenatide Infusion
NCT02058940 (14) [back to overview]Glycemic Variability
NCT02058940 (14) [back to overview]Correlation of Exenatide Concentrations With Creatinine Clearance
NCT02058940 (14) [back to overview]Median Time to Reach Glucose Measurements Within Goal Range (110-180 mg/dL)
NCT02058940 (14) [back to overview]Percentage of Critically Ill Patients With Acute Brain Injury Achieving Pre-specified Feasibility Criteria
NCT02058940 (14) [back to overview]Percentage of Patients With >1 Episode of Hypotensive Episode (SBP<100 mmHg)
NCT02058940 (14) [back to overview]Percentage of Hypotensive Episodes (SBP<100 mmHg)
NCT02058940 (14) [back to overview]Percentage of Patients With >1 Episode of Hypoglycemia (<80 mg/dL)
NCT02058940 (14) [back to overview]Percentage of Patients Requiring Rescue Insulin Infusion Protocol
NCT02058940 (14) [back to overview]Percentage of Hypoglycemic Episodes (<80 mg/dL)
NCT02058940 (14) [back to overview]Percentage of Glucose Measurements Within Goal Range
NCT02072096 (6) [back to overview]Change From Baseline in Body Mass Index (BMI)
NCT02072096 (6) [back to overview]Change From Baseline of Estimated Glomerular Filtration Rate (eGFR)
NCT02072096 (6) [back to overview]Change From Baseline of Urinary Albumin to Creatinine Ratio
NCT02072096 (6) [back to overview]Percentage of Participants Achieving and Maintaining Individualized Glycated Hemoglobin A1c (HbA1c) Targets Without Clinically Significant Hypoglycemia
NCT02072096 (6) [back to overview]Number of Participants With Total Hypoglycemia and Other Categories of Hypoglycemia
NCT02072096 (6) [back to overview]Percentage of Participants Requiring Alternative Treatment Due to Glycemic Failure of First Line Injectable Therapy
NCT02104739 (13) [back to overview]Triglycerides
NCT02104739 (13) [back to overview]Triglycerides
NCT02104739 (13) [back to overview]Triglycerides
NCT02104739 (13) [back to overview]Triglycerides
NCT02104739 (13) [back to overview]Free Fatty Acids
NCT02104739 (13) [back to overview]Free Fatty Acids
NCT02104739 (13) [back to overview]Free Fatty Acids
NCT02104739 (13) [back to overview]Free Fatty Acids
NCT02104739 (13) [back to overview]Monocyte NfkB Levels as Detected by Western Blotting
NCT02104739 (13) [back to overview]Monocyte NfkB Levels as Detected by Western Blotting
NCT02104739 (13) [back to overview]Peak Forearm Blood Flow
NCT02104739 (13) [back to overview]Peak Forearm Blood Flow
NCT02104739 (13) [back to overview]Peak Forearm Blood Flow
NCT02119819 (15) [back to overview]Change From Baseline in Glucagon Levels
NCT02119819 (15) [back to overview]Percent Change From Baseline in Body Weight
NCT02119819 (15) [back to overview]Change From Baseline in Fasting Fibroblast Growth Factor 21
NCT02119819 (15) [back to overview]Change From Baseline in Lipids
NCT02119819 (15) [back to overview]Percentage of Participants Developing Anti-Drug Antibodies to LY2944876
NCT02119819 (15) [back to overview]Pharmacokinetics: Area Under the Concentration Curve (AUC) of LY2944876
NCT02119819 (15) [back to overview]Percentage of Participants Requiring Rescue Therapy
NCT02119819 (15) [back to overview]Change From Baseline in HbA1c at Week 24
NCT02119819 (15) [back to overview]Change From Baseline in Insulin Levels
NCT02119819 (15) [back to overview]Change From Baseline in Fasting Blood Glucose
NCT02119819 (15) [back to overview]Change From Baseline in Hemoglobin A1c (HbA1c) at Week 12
NCT02119819 (15) [back to overview]Pharmacokinetics (PK): Maximum Concentration (Cmax) of LY2944876
NCT02119819 (15) [back to overview]Change From Baseline in Beta-Hydroxy Butyrate Levels
NCT02119819 (15) [back to overview]Change From Baseline in Adiponectin Levels
NCT02119819 (15) [back to overview]Change From Baseline in 7-point Self-Monitored Blood Glucose (SMBG) Values
NCT02160990 (7) [back to overview]Maximum Tolerated Volume
NCT02160990 (7) [back to overview]Aggregate Satiation Symptom Score
NCT02160990 (7) [back to overview]Satiation Expressed as Volume to Fullness
NCT02160990 (7) [back to overview]Gastric Emptying Half-time (T 1/2) of Solids
NCT02160990 (7) [back to overview]Change in Body Weight
NCT02160990 (7) [back to overview]Buffet Meal Intake (kcal)
NCT02160990 (7) [back to overview]Percentage of Gastric Contents Emptied at 1 Hour
NCT02229383 (7) [back to overview]Percentage of Participants Achieving HbA1c <7.0% at Week 28, No Weight Gain at Week 28, and No Major Hypoglycemia Over 28 Weeks
NCT02229383 (7) [back to overview]Change in Seated Systolic Blood Pressure From Baseline to Week 28
NCT02229383 (7) [back to overview]Percentage of Participants Achieving HbA1c <7.0% at Week 28
NCT02229383 (7) [back to overview]Change in HbA1c From Baseline to Week 28
NCT02229383 (7) [back to overview]Change in Body Weight From Baseline to Week 28
NCT02229383 (7) [back to overview]Change From Baseline to Week 28 in Daily Insulin Dose
NCT02229383 (7) [back to overview]Change From Baseline to Week 28 in 2-hour Postprandial Glucose After a Standard Meal Tolerance Test (MTT)
NCT02251431 (13) [back to overview]L-FABP
NCT02251431 (13) [back to overview]ST2
NCT02251431 (13) [back to overview]NGAL
NCT02251431 (13) [back to overview]Cystatin-C
NCT02251431 (13) [back to overview]Pi GST
NCT02251431 (13) [back to overview]Troponin I
NCT02251431 (13) [back to overview]ACR
NCT02251431 (13) [back to overview]Alpha GST
NCT02251431 (13) [back to overview]BNP
NCT02251431 (13) [back to overview]NAG
NCT02251431 (13) [back to overview]Galectin-3
NCT02251431 (13) [back to overview]IL-18
NCT02251431 (13) [back to overview]KIM-1
NCT02288273 (7) [back to overview]Average of Change in 24-hour Mean Weighted Glucose From Baseline to Week 4 and Baseline to Week 10
NCT02288273 (7) [back to overview]Change in 24-hour Mean Weighted Glucose Between Day 1 of Week 10 (Day 64/65) and Day 6 of Week 10 (Day 69/70) Within Each EQW-treated Patient
NCT02288273 (7) [back to overview]Change From Baseline (Day1) to Day 70 and Day 22 in FPG
NCT02288273 (7) [back to overview]Average of Change in 24-hour Mean Weighted Glucose From Baseline to Week 4 and Baseline to Week 10
NCT02288273 (7) [back to overview]Change in HbA1c From Baseline to Day 22 and Baseline to Day 70
NCT02288273 (7) [back to overview]Change in 24-hour Mean Weighted Glucose
NCT02288273 (7) [back to overview]Change From Baseline (Day -1) to Day 64 and Day 22 in 2- Hour Mean Weighted PPG (After the Breakfast Meal)
NCT02417142 (2) [back to overview]Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery (MCCB) Composite T-score
NCT02417142 (2) [back to overview]Negative Symptoms as Measured by the Scale for the Assessment of Negative Symptoms (SANS) Total Score
NCT02455076 (30) [back to overview]Number of Hospital Readmissions
NCT02455076 (30) [back to overview]Number of Acute Kidney Injury Events
NCT02455076 (30) [back to overview]Mean Premeal Blood Glucose Levels Inpatient
NCT02455076 (30) [back to overview]Mean Fasting Blood Glucose Levels Inpatient
NCT02455076 (30) [back to overview]Mean Daily Blood Glucose Concentration Inpatient
NCT02455076 (30) [back to overview]Mean Fasting Blood Glucose Levels During Outpatient Period
NCT02455076 (30) [back to overview]Mean Daily Blood Glucose Concentration During Outpatient Period
NCT02455076 (30) [back to overview]Incidence of the Need for ICU Care Inpatient
NCT02455076 (30) [back to overview]Incidence of Hypoglycemic Events Inpatient
NCT02455076 (30) [back to overview]Incidence of Hyperglycemic Events Inpatient
NCT02455076 (30) [back to overview]Incidence of Hospital Readmissions
NCT02455076 (30) [back to overview]Total Daily Dose of Insulin Inpatient
NCT02455076 (30) [back to overview]Number of Severe Gastrointestinal Adverse Events
NCT02455076 (30) [back to overview]Number of Patients With Severe Hypoglycemic Events Inpatient
NCT02455076 (30) [back to overview]Incidence of Gastrointestinal Adverse Events Inpatient
NCT02455076 (30) [back to overview]Number of Patients With Severe Hypoglycemic Events
NCT02455076 (30) [back to overview]Number of Patients Who Had Emergency Room Visits
NCT02455076 (30) [back to overview]The Number of Patients With Hypoglycemia Outpatient
NCT02455076 (30) [back to overview]Incidence of Acute Kidney Injury Inpatient
NCT02455076 (30) [back to overview]Hospital Mortality
NCT02455076 (30) [back to overview]Efficacy, Measured by HbA1c Levels and no Weight Gain
NCT02455076 (30) [back to overview]Efficacy, Measured by HbA1c Levels and no Hypoglycemia
NCT02455076 (30) [back to overview]Change in Systolic Blood Pressure
NCT02455076 (30) [back to overview]Change in Heart Rate
NCT02455076 (30) [back to overview]Change in HbA1c Concentration Inpatient
NCT02455076 (30) [back to overview]Change in Diastolic Blood Pressure
NCT02455076 (30) [back to overview]Change in Body Weight
NCT02455076 (30) [back to overview]Change in Body Mass Index
NCT02455076 (30) [back to overview]Average Number of Days of Hospital Stay
NCT02455076 (30) [back to overview]Hospital Complications
NCT02496611 (1) [back to overview]Body Mass Index
NCT02533453 (6) [back to overview]Change in Vital Sign
NCT02533453 (6) [back to overview]Change in HbA1c
NCT02533453 (6) [back to overview]Change in Fasting Plasma Gloucose
NCT02533453 (6) [back to overview]Change in Body Weight
NCT02533453 (6) [back to overview]Percentage of Participants With Adverse Events(AEs) and Serious Adverse Event(SAEs)
NCT02533453 (6) [back to overview]"Evaluation of Subjective Improvement of Main Indication"
NCT02635386 (23) [back to overview]Systolic Blood Pressure (SBP)
NCT02635386 (23) [back to overview]Total Body Fat (%) by DEXA
NCT02635386 (23) [back to overview]Total Cholesterol Levels
NCT02635386 (23) [back to overview]Total Fat Mass (kg) Evaluated by DEXA
NCT02635386 (23) [back to overview]Total Testosterone Concentrations
NCT02635386 (23) [back to overview]Triglyceride (TRG) Levels
NCT02635386 (23) [back to overview]Trunk/Leg Fat Ratio by DEXA
NCT02635386 (23) [back to overview]Waist-to-Height Ratio (WHtR)
NCT02635386 (23) [back to overview]Waist-to-Hip Ratio (WHR)
NCT02635386 (23) [back to overview]Dehydroepiandrosterone Sulfate (DHEA-S) Levels
NCT02635386 (23) [back to overview]Absolute Body Weight
NCT02635386 (23) [back to overview]Android-Gynoid Ratio (AGR) as Determined by DEXA
NCT02635386 (23) [back to overview]Body Mass Index (BMI)
NCT02635386 (23) [back to overview]Central Adiposity (Waist Circumference)
NCT02635386 (23) [back to overview]Change in Percent Body Weight
NCT02635386 (23) [back to overview]Corrected First Phase Insulin Secretion (IGI/HOMA-IR)
NCT02635386 (23) [back to overview]Diastolic Blood Pressure (DBP)
NCT02635386 (23) [back to overview]Fasting Blood Glucose
NCT02635386 (23) [back to overview]Fasting Insulin Sensitivity (HOMA-IR)
NCT02635386 (23) [back to overview]Free Androgen Index (FAI)
NCT02635386 (23) [back to overview]Matsuda Sensitivity Index Derived From the OGTT(SI OGTT)
NCT02635386 (23) [back to overview]OGTT Mean Blood Glucose (MBG)
NCT02635386 (23) [back to overview]Oral Disposition (Insulin Sensitivity-insulin Secretion) Index
NCT02664441 (11) [back to overview]Changes of Energy Intake Assessed by Automated Self-Administered 24-Hour Dietary Recall (ASA24-Kids)
NCT02664441 (11) [back to overview]Changes in HDL Cholesterol and Triglycerides Assessed by Fasting Lipids
NCT02664441 (11) [back to overview]Changes in Fat and Total Calorie Intake Assessed by Free Buffet Meal Analysis.
NCT02664441 (11) [back to overview]Percent Change of Body Mass Index (BMI) as Calculated by the Formula: Body Weight in kg Divided by Height in Meters².
NCT02664441 (11) [back to overview]Changes of Insulin Resistance Assessed by Homeostasis Model Assessment of Insulin Resistance (HOMA-IR)
NCT02664441 (11) [back to overview]Changes of Energy Expenditure Assessed by Doubly Labeled Water Analysis
NCT02664441 (11) [back to overview]Changes of Circulating Leptin Levels
NCT02664441 (11) [back to overview]Changes in Inflammation Assessed by C-reactive Protein (CRP)
NCT02664441 (11) [back to overview]Changes in Glucose 120 Minutes Following an Oral Glucose Tolerance Test
NCT02664441 (11) [back to overview]Changes in Fasting Glucose
NCT02664441 (11) [back to overview]Changes in Body Composition as Assessed by Body Fat Mass Using Dual Energy X-ray Absorptiometry (DEXA)
NCT02787551 (18) [back to overview]Percentage of Participants Reaching HbA1c <7 % or <=6.5% at Week 52: Single Arm Extension Period
NCT02787551 (18) [back to overview]Number of Documented Symptomatic Hypoglycemia Events Per Participant-Year: Single Arm Extension Period
NCT02787551 (18) [back to overview]Number of Documented Symptomatic Hypoglycemia Events Per Participant-Year: Core Period
NCT02787551 (18) [back to overview]Percentage of Participants Requiring Rescue Therapy During the 52 Week Treatment Period: Single Arm Extension Period
NCT02787551 (18) [back to overview]Percentage of Participants Requiring Rescue Therapy During the 26 Week Treatment Period: Core Period
NCT02787551 (18) [back to overview]Change From Baseline in the Daily Average of the 7-point Self-monitored Plasma Glucose (SMPG) to Week 52: Single Arm Extension Period
NCT02787551 (18) [back to overview]Change From Baseline in Glycated Hemoglobin (HbA1c) to Week 52: Single Arm Extension Period
NCT02787551 (18) [back to overview]Change From Baseline in Glycated Hemoglobin (HbA1c) to Week 26: Core Period
NCT02787551 (18) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG) to Week 52: Single Arm Extension Period
NCT02787551 (18) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG) to Week 26: Core Period
NCT02787551 (18) [back to overview]Change From Baseline in Body Weight to Week 52: Single Arm Extension Period
NCT02787551 (18) [back to overview]Percentage of Participants Reaching HbA1c <7% or <=6.5% at Week 26: Core Period
NCT02787551 (18) [back to overview]Change From Baseline in Body Weight at Week 26: Core Period
NCT02787551 (18) [back to overview]Change From Baseline in 2-Hour Postprandial Plasma Glucose (PPG) During Standardized Meal Test to Week 52: Single Arm Extension Period
NCT02787551 (18) [back to overview]Change From Baseline in 2-Hour Postprandial Plasma Glucose (PPG) During Standardized Meal Test to Week 26: Core Period
NCT02787551 (18) [back to overview]Change From Baseline in 2-Hour Blood Glucose Excursion During Standardized Meal Test to Week 52: Single Arm Extension Period
NCT02787551 (18) [back to overview]Change From Baseline in 2-Hour Blood Glucose Excursion During Standardized Meal Test to Week 26: Core Period
NCT02787551 (18) [back to overview]Change From Baseline in the Daily Average of the 7-point Self-monitored Plasma Glucose (SMPG) to Week 26: Core Period
NCT02793154 (29) [back to overview]Part A: Hematocrit Level at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: Hemoglobin Level at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: Number of Par. With Adverse Events (AEs) and Serious AEs (SAEs)
NCT02793154 (29) [back to overview]Part A: Number of Par. With Presence of Ketones, Occult Blood, Glucose, Nitrates and Leukocyte Esterase in Urine at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: Percentage of Time With the Dominant EGG Frequencies in the Four Frequency Ranges of Bradygastria, Normal, Tachygastria and Duodenal
NCT02793154 (29) [back to overview]Part A: Potential of Hydrogen (pH) of Urine at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: Presence RBC and WBC in Urine Assessed by Microscopy
NCT02793154 (29) [back to overview]Part A: Rate of [13]C Dose Excreted in Breath
NCT02793154 (29) [back to overview]Part A: Ratios of Average Power Post- WLT/Pre-WLT by Frequency Region
NCT02793154 (29) [back to overview]Part A: Red Blood Cell (RBC) Count at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: Specific Gravity of Urine at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: The Volume of Water Ingested During EGG
NCT02793154 (29) [back to overview]Part A: Time to Half-gastric Emptying
NCT02793154 (29) [back to overview]Part A: Total Protein, Albumin Levels at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: Number of Par. With Nausea AEs Presenting Outside the Timing of the WLT and GCSI-DD
NCT02793154 (29) [back to overview]Part A: Alanine Amino Transferase (ALT), Aspartate Amino Transferase (AST), Gamma Glutamyl Transferase (GGT) Levels at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: Albumin Level in Urine at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: Assessment of Heart Rate (HR) as a Measure of Safety
NCT02793154 (29) [back to overview]Part A: Assessment of Nausea by Visual Analogue Scale (VAS) Score
NCT02793154 (29) [back to overview]Part A: Assessment of Stomach Fullness, Hunger, Bloating and Abdominal Pain by VAS Score
NCT02793154 (29) [back to overview]Part A: Assessment of Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) as a Measure of Safety
NCT02793154 (29) [back to overview]Part A: Average Dominant Frequency
NCT02793154 (29) [back to overview]Part A: Basophils, Eosinophil, Lymphocytes, Monocytes, Platelet Count, Total Neutrophils, White Blood Cell (WBC) Level at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: Concentration of Creatinine in Urine at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: Creatinine, Direct Bilirubin, Total Bilirubin, Indirect Bilirubin Levels at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: Distribution of Average Power by Frequency Region
NCT02793154 (29) [back to overview]Part A: Estimated Glomerular Filtration Rate at Indicated Time Points
NCT02793154 (29) [back to overview]Part A: Gastroparesis Cardinal Symptom Index -Daily Diary (GCSI-DD) Score
NCT02793154 (29) [back to overview]Part A: Glucose, Calcium, Magnesium, Potassium, Sodium, Phosphorus Inorganic, Chloride, Urea/Blood Urea Nitrogen (BUN) Levels
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Urinalysis
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Heart Rate for Session 1
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Heart Rate for Session 1
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Heart Rate for Session 2
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Heart Rate for Session 2
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Heart Rate for Session 2
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) for Session 1
NCT02802514 (29) [back to overview]Number of Participants With Non-serious Adverse Events (AE) With Incidence > = 2 % and Serious AEs (SAE)
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) for Session 1
NCT02802514 (29) [back to overview]Number of Participants With Abnormal SBP and DBP for Session 2
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Heart Rate for Session 2
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) for Session 1
NCT02802514 (29) [back to overview]Number of Participants With Abnormal SBP and DBP for Session 2
NCT02802514 (29) [back to overview]Number of Participants With Abnormal SBP and DBP for Session 2
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) for Session 1
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Clinical Chemistry Parameters
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Glycemic Parameters
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Hematology Parameters
NCT02802514 (29) [back to overview]Number of Participants With Abnormal SBP and DBP for Session 2
NCT02802514 (29) [back to overview]Gastrointestinal (GI) Visual Analogue Scale (VAS) for Assessment of Nausea for Session 1
NCT02802514 (29) [back to overview]Gastrointestinal (GI) Visual Analogue Scale (VAS) for Assessment of Nausea for Session 1
NCT02802514 (29) [back to overview]GI VAS for Assessment of Nausea for Session 2
NCT02802514 (29) [back to overview]GI VAS for Assessment of Nausea for Session 2
NCT02802514 (29) [back to overview]Motion Sickness Assessment Questionnaire (MSAQ) for Assessment of Nausea for Session 1
NCT02802514 (29) [back to overview]Motion Sickness Assessment Questionnaire (MSAQ) for Assessment of Nausea for Session 1
NCT02802514 (29) [back to overview]MSAQ for Assessment of Nausea for Session 2
NCT02802514 (29) [back to overview]MSAQ for Assessment of Nausea for Session 2
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Heart Rate for Session 1
NCT02802514 (29) [back to overview]Number of Participants With Abnormal Heart Rate for Session 1
NCT02975297 (7) [back to overview]Post-quit Craving as Assessed by the Questionnaire of Smoking Urges
NCT02975297 (7) [back to overview]Post-quit Craving as Assessed by the Questionnaire of Smoking Urges
NCT02975297 (7) [back to overview]Post-quit Craving as Assessed by the Questionnaire of Smoking Urges
NCT02975297 (7) [back to overview]Withdrawal Symptoms as Assessed by the Wisconsin Smoking Withdrawal Scale
NCT02975297 (7) [back to overview]Number of Participants Who Self-Reported Abstinence and Who Were Biochemically Verified as Abstinent Via Expired CO Level of ≤ 5ppm
NCT02975297 (7) [back to overview]Number of Participants Who Self-Reported Abstinence and Who Were Biochemically Verified as Abstinent Via Expired CO Level of ≤ 5ppm
NCT02975297 (7) [back to overview]Number of Participants Who Self-Reported Abstinence and Who Were Biochemically Verified as Abstinent Via Expired CO Level of ≤ 5ppm
NCT02981069 (5) [back to overview]Change in Plasma Insulin Concentration
NCT02981069 (5) [back to overview]Change in Endogenous Glucose Production (EGP) After 16 Weeks of Treatment With Each Study Drug.
NCT02981069 (5) [back to overview]Change in Endogenous Glucose Production (EGP) After Acute Exposure to a Single Dose and Again After 16 Weeks of Treatment
NCT02981069 (5) [back to overview]Change in Fasting Plasma Glucose (FPG) Concentration
NCT02981069 (5) [back to overview]Change in Plasma Glucagon Concentration
NCT03151005 (5) [back to overview]Assessment of Reproductive Function
NCT03151005 (5) [back to overview]Assessment of Liver Function
NCT03151005 (5) [back to overview]Assessment of Blood Pressure
NCT03151005 (5) [back to overview]Basic Vital Signs
NCT03151005 (5) [back to overview]Assessment of Reproductive Functions
NCT03167411 (5) [back to overview]Tmax (Time of Maximum Observed Plasma Concentration)
NCT03167411 (5) [back to overview]T1/2 (Apparent Terminal Elimination Half-life)
NCT03167411 (5) [back to overview]Cmax (Maximum Observed Plasma Concentration)
NCT03167411 (5) [back to overview]AUC0-inf (Area Under the Plasma Concentration-time Curve From Time 0 to Infinity)
NCT03167411 (5) [back to overview]Urinary Glucose Excretion (UGE)
NCT03331289 (1) [back to overview]Change in EGP From Baseline to Post-oral Glucose Load.
NCT03645408 (1) [back to overview]Alcohol Consumption
NCT03961256 (8) [back to overview]Hemoglobin A1c
NCT03961256 (8) [back to overview]Incidence of Mesangial Expansion
NCT03961256 (8) [back to overview]Creatinine
NCT03961256 (8) [back to overview]Graft Loss
NCT03961256 (8) [back to overview]Incidence of Death
NCT03961256 (8) [back to overview]Progression From Prediabetes to Diabetes
NCT03961256 (8) [back to overview]Adverse Events for Exenatide SR Intervention
NCT03961256 (8) [back to overview]Progression From Prediabetes to Diabetes
NCT04941521 (13) [back to overview]Clinical Effect of Exenatide as Assessed by Number of Participants Who Self-reported Cocaine Use on 50% or More Days of the Week
NCT04941521 (13) [back to overview]Clinical Effect of Exenatide as Indicated by Number of Participants Who Had an Increase in Positive Affect Symptoms by Week 6 as Indicated on the Positive/Negative Affect Schedule
NCT04941521 (13) [back to overview]Clinical Effect of Exenatide as Assessed by Number of Participants Who Had a Decrease in Drug Demand by Week 6
NCT04941521 (13) [back to overview]Feasibility as Indicated by Overall Acceptability as Reported on the Satisfaction Survey
NCT04941521 (13) [back to overview]Clinical Effect of Exenatide as Assessed by Number of Participants Who Were Below the Clinical Range for Depression by Week 6 as Indicated by the Beck Depression Inventory
NCT04941521 (13) [back to overview]Clinical Effect of Exenatide as Indicated by Number of Participants Who Had a Decrease in Negative Affect Symptoms Indicated on the Positive/Negative Affect Schedule
NCT04941521 (13) [back to overview]Clinical Effect of Exenatide as Indicated by Number of Participants Who Reported a Reduction in Craving by Week 6 as Indicated by Cocaine Craving on the Brief Substance Craving Scale
NCT04941521 (13) [back to overview]Drug Safety as Assessed by Total Number of Adverse Events Reported During Treatment
NCT04941521 (13) [back to overview]Feasibility as Assessed by Number of Participants Enrolled
NCT04941521 (13) [back to overview]Feasibility as Assessed by Number of Participants Who Completed Treatment
NCT04941521 (13) [back to overview]Feasibility as Assessed by Number of Study Visits Attended
NCT04941521 (13) [back to overview]Feasibility as Assessed by Retention as Indicated by Total Number of Completed Study Visits
NCT04941521 (13) [back to overview]Clinical Effect of Exenatide as Assessed by Cocaine Use During Treatment as Indicated by Number of Participants With Cocaine-positive Urine Drug Screen Results

Percentage of Patients With Hypoglycemic Events

Percentage of patients who experienced at least one episode of hypoglycemia at any point during the 26 week Parent Study (incidence of hypoglycemia = number of patients who experienced at least one episode of hypoglycemia at any point during the 26 week Parent Study divided by the total number of patients who participated in the 26 week Parent Study (NCT00082381)
Timeframe: 26 weeks

Interventionpercentage of participants (Number)
Exenatide Arm55.32
Insulin Glargine Arm59.93

[back to top]

Percentage of Patients Achieving HbA1c <=7%

Percentage of patients in each arm who had HbA1c >7% at baseline and had HbA1c <=7% at week 26 (percentage = [number of subjects with HbA1c <=7% at week 26 divided by number of subjects with HbA1c >7% at baseline] * 100%). (NCT00082381)
Timeframe: 26 weeks

Interventionpercentage of participants (Number)
Exenatide Arm46.43
Insulin Glargine Arm48.03

[back to top]

Change in 7-point Self-monitored Blood Glucose (SMBG) Profile

Change in 7-point (pre-breakfast, 2 hour post breakfast, pre-lunch, 2 hour post lunch, pre-dinner, 2 hour post dinner, 0300 hours) SMBG profile from baseline to week 26 (NCT00082381)
Timeframe: Baseline, week 26

,
Interventionmmol/L (Least Squares Mean)
Pre-breakfast: Baseline SMBGPre-breakfast: Change in SMBG at week 262hr post breatfast: Baseline SMBG2hr post breakfast: Change in SMBG at week 26Pre-lunch: Baseline SMBGPre-lunch: Change in SMBG at week 262hr post lunch: Baseline SMBG2hr post lunch: Change in SMBG at week 26Pre-dinner: Baseline SMBGPre-dinner: Change in SMBG at week 262hr post dinner: Baseline SMBG2hr post dinner: Change in SMBG at week 263:00 AM: Baseline SMBG3:00 AM: Change in SMBG at week 26
Exenatide Arm9.47-1.2512.51-3.779.61-1.5011.15-1.689.46-1.1511.17-3.069.02-1.05
Insulin Glargine Arm9.50-2.5612.36-2.869.47-1.9310.96-1.699.35-1.7211.49-1.659.36-1.97

[back to top]

Change in Rate of Hypoglycemic Events

Change in rate of hypoglycemic events per 30 days per patient from baseline to week 26 (NCT00082381)
Timeframe: Baseline, week 26

,
Interventionevents per 30 days per patient (Least Squares Mean)
Baseline event rateChange in event rate at week 26
Exenatide Arm0.090.23
Insulin Glargine Arm0.110.29

[back to top]

Change in Glycosylated Hemoglobin (HbA1c)

Change in HbA1c from baseline to week 26 (NCT00082381)
Timeframe: Baseline, week 26

,
Interventionpercentage (Least Squares Mean)
Baseline HbA1cChange in HbA1c at week 26
Exenatide Arm8.13-1.00
Insulin Glargine Arm8.19-1.05

[back to top]

Change in Fasting Serum Glucose

Change in fasting serum glucose from baseline to week 26 (NCT00082381)
Timeframe: Baseline, week 26

,
Interventionmmol/L (Least Squares Mean)
Baseline fasting serum glucoseChange in fasting serum glucose at week 26
Exenatide Arm10.27-1.22
Insulin Glargine Arm10.46-2.86

[back to top]

Change in Body Weight

Change in body weight from baseline to week 26 (NCT00082381)
Timeframe: Baseline, week 26

,
Interventionkg (Least Squares Mean)
Baseline body weightChange in body weight at week 26
Exenatide Arm88.42-2.32
Insulin Glargine Arm89.251.75

[back to top]

Percentage of Patients Achieving HbA1c <=7%

Percentage of patients in each arm who had HbA1c >7% at baseline and had HbA1c <=7% at week 52 (percentage = [number of subjects with HbA1c <=7% at week 52 divided by number of subjects with HbA1c >7% at baseline] * 100%). (NCT00082407)
Timeframe: 52 weeks

Interventionpercentage of participants (Number)
Exenatide Arm31.7
Biphasic Insulin Aspart Arm24.1

[back to top]

Percentage of Patients With Hypoglycemic Events

Percentage of patients who experienced at least one episode of hypoglycemia at any point during the 52 week Parent Study (incidence of hypoglycemia = number of patients who experienced at least one episode of hypoglycemia at any point during the 52 week Parent Study divided by the total number of patients who particiapted in the 52 week Parent Study (NCT00082407)
Timeframe: 52 weeks

Interventionpercentage of participants (Number)
Exenatide Arm53.0
Biphasic Insulin Aspart Arm51.6

[back to top]

Change in 7-point Self-monitored Blood Glucose (SMBG) Profile

Change in 7-point (pre-breakfast, after breakfast, pre-lunch, after lunch, pre-dinner, after dinner, 0300 hours) SMBG profile from baseline to week 52 (NCT00082407)
Timeframe: baseline, week 52

,
Interventionmmol/L (Mean)
Pre-breakfast: Baseline SMBGPre-breakfast: Change in SMBG at week 52After breakfast: Baseline SMBGAfter breakfast: Change in SMBG at week 52Pre-lunch: Baseline SMBGPre-lunch: Change in SMBG at week 52After lunch: Baseline SMBGAfter lunch: Change in SMBG at week 52Pre-dinner: Baseline SMBGPre-dinner: Change in SMBG at week 52After dinner: Baseline SMBGAfter dinner: Change in SMBG at week 523:00 AM: Baseline SMBG3:00 AM: Change in SMBG at week 52
Biphasic Insulin Aspart Arm9.86-1.6812.71-3.069.86-2.4011.39-1.769.57-1.5211.68-2.449.58-1.95
Exenatide Arm9.57-1.1512.30-3.839.38-1.4711.18-1.729.35-1.0611.25-3.119.08-0.96

[back to top]

Change in Body Weight

Change in body weight from baseline to week 52. (NCT00082407)
Timeframe: baseline, week 52

,
Interventionkg (Least Squares Mean)
Baseline body weightChange in body weight at week 52
Biphasic Insulin Aspart Arm83.382.92
Exenatide Arm85.51-2.54

[back to top]

Change in Rate of Hypoglycemic Events

Change in rate of hypoglycemic events per 30 days per patient from baseline to week 52 (NCT00082407)
Timeframe: baseline, week 52

,
Interventionevents per 30 days per patient (Least Squares Mean)
Baseline event rateChange in event rate at week 52
Biphasic Insulin Aspart Arm0.180.26
Exenatide Arm0.220.19

[back to top]

Change in Glcosylated Hemoglobin (HbA1c)

Change in HbA1c from baseline to week 52 (NCT00082407)
Timeframe: baseline, week 52

,
Interventionpercentage (Least Squares Mean)
Baseline HbA1cChange in HbA1c at week 52
Biphasic Insulin Aspart Arm8.65-0.88
Exenatide Arm8.59-0.98

[back to top]

Change in Fasting Serum Glucose

Change in fasting serum glucose from baseline to week 52 (NCT00082407)
Timeframe: baseline, week 52

,
Interventionmmol/L (Least Squares Mean)
Baseline fasting serum glucoseChange in fasting serum glucose at week 52
Biphasic Insulin Aspart Arm11.30-1.64
Exenatide Arm11.00-1.75

[back to top]

Beta-cell Function 4 Weeks After Cessation of Therapy

Treatment effect on beta-cell function as measured by the ratio of Week 56 arginine-stimulated insulin secretion during a hyperglycemic clamp(specifically, the incremental AUC of insulin with respect to basal value over a 10 min period [i.e., clamp time 290 min to 300 min]) to that at baseline (i.e., the ratio is calculated as arginine-stimulated insulin secretion at week 56 divided by arginine-stimulated insulin secretion at baseline [week -2]). (NCT00097500)
Timeframe: Baseline (week -2) and 56 weeks

Interventionratio (Least Squares Mean)
Exenatide Arm1.02
Insulin Glargine Arm1.08

[back to top]

Beta-cell Function After 52 Weeks of Therapy

Treatment effect on beta-cell function as measured by the ratio of Week 52 arginine-stimulated insulin secretion during a hyperglycemic clamp(specifically, the incremental AUC of insulin with respect to basal value over a 10 min period [i.e., clamp time 290 min to 300 min]) to that at baseline (i.e., the ratio is calculated as arginine-stimulated insulin secretion at week 52 divided by arginine-stimulated insulin secretion at baseline [week -2]). (NCT00097500)
Timeframe: Baseline (week -2) and 52 weeks

Interventionratio (Least Squares Mean)
Exenatide Arm2.89
Insulin Glargine Arm1.15

[back to top]

Change in Body Weight

Change in body weight from week 0 to week 52 (i.e., body weight at week 52 minus body weight at week 0). (NCT00097500)
Timeframe: 0 weeks and 52 weeks

Interventionkg (Least Squares Mean)
Exenatide Arm-3.80
Insulin Glargine Arm0.75

[back to top]

Change in Fasting Plasma Glucose

Change in fasting plasma glucose from week 0 to week 52 (i.e., fasting plasma glucose at week 52 minus fasting plasma glucose at week 0). (NCT00097500)
Timeframe: 0 weeks and 52 weeks

Interventionmmol/L (Least Squares Mean)
Exenatide Arm-1.53
Insulin Glargine Arm-3.10

[back to top]

Change in Glycosylated Hemoglobin (HbA1c)

Change in HbA1c from week 0 to week 52 (i.e., HbA1c at week 52 minus HbA1c at week 0). (NCT00097500)
Timeframe: Week 0 and week 52

Interventionpercent (Least Squares Mean)
Exenatide Arm-0.97
Insulin Glargine Arm-0.87

[back to top]

Change in First Phase C-peptide Release

Ratio of first phase C-peptide response to glucose at 52 weeks (end of on-drug period) and 56 weeks (during off-drug period) compared to first phase C-peptide response to glucose at baseline (i.e., C-peptide response to glucose at week 52 or week 56 divided by C-peptide response to glucose at baseline [week -2]). C-peptide is measured as a surrogate marker of insulin secretion. First phase C-peptide/insulin release is measured during the first ten minutes of glucose infusion during a hyperglycemic clamp procedure. (NCT00097500)
Timeframe: baseline (week -2), 52 weeks, and 56 weeks

,
Interventionratio (Least Squares Mean)
52 weeks56 weeks
Exenatide Arm1.720.95
Insulin Glargine Arm1.131.06

[back to top]

Change in Second Phase C-peptide Release

Ratio of second phase C-peptide response to glucose at 52 weeks (end of on-drug period) and 56 weeks (during off-drug period) compared to second phase C-peptide response to glucose at baseline (i.e., C-peptide response to glucose at week 52 or week 56 divided by C-peptide response to glucose at baseline [week -2]). C-peptide is measured as a surrogate marker of insulin secretion. Second phase C-peptide/insulin release is measured from time=10 minutes to time=80 minutes of glucose infusion during a hyperglycemic clamp procedure. (NCT00097500)
Timeframe: baseline (-2 weeks), 52 weeks, and 56 weeks

,
Interventionratio (Least Squares Mean)
52 weeks56 weeks
Exenatide Arm2.881.00
Insulin Glargine Arm1.011.08

[back to top]

M-value at Baseline, Week 52 and Week 56

M-value at baseline (week -2), week 52 (end of on-drug period), and week 56 (during off-drug period). Insulin sensitivity was assessed during the euglycemic/hyperglycemic clamp test at baseline (week -2), week 52, and week 56. Insulin-mediated glucose uptake (M-value) was calculated as the mean glucose requirement during the 90-120 minute interval of the clamp. (NCT00097500)
Timeframe: baseline (week -2), 52 weeks, and 56 weeks

,
Interventionmg/min/kg (Mean)
baseline (week -2)week 52week 56
Exenatide Arm2.243.183.19
Insulin Glargine Arm2.793.852.81

[back to top]

Seven Point Self Monitored Blood Glucose (SMBG) Measurements

SMBG measured at 7 time points (before and after breakfast, before and after lunch, before and after dinner, at bedtime). (NCT00097500)
Timeframe: 0 weeks and 52 weeks

,
Interventionmmol/L (Mean)
Pre-breakfast measurement (week 0)Pre-breakfast measurement (week 52)2-hour post-breakfast measurement (week 0)2-hour post-breakfast measurement (week 52)Pre-lunch measurement (week 0)Pre-lunch measurement (week 52)2-hour post-lunch measurement (week 0)2-hour post-lunch measurement (week 52)Pre-dinner measurement (week 0)Pre-dinner measurement (week 52)2-hour post-dinner measurement (week 0)2-hour post-dinner measurement (week 52)Bedtime measurement (week 0)Bedtime measurement (week 52)
Exenatide Arm8.927.2711.006.988.146.529.907.978.387.5310.426.989.767.61
Insulin Glargine Arm8.385.6311.177.538.546.2410.528.158.076.9810.268.819.858.03

[back to top]

Change in Fasting HDL Cholesterol

Change in fasting high-density lipoprotein (HDL) cholesterol from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
Interventionmmol/L (Least Squares Mean)
Baseline HDLChange from baseline HDL at week 20
Exenatide1.130.022
Exenatide Plus Rosiglitazone1.170.046
Rosiglitazone1.170.055

[back to top]

Change in Waist-to-hip Ratio

Change in waist-to-hip ratio (waist circumference divided by hip circumference) from baseline to week 20 (NCT00135330)
Timeframe: 20 weeks

,,
Interventionratio (cm/cm) (Least Squares Mean)
Baseline waist-to-hip ratioChange in waist-to-hip ratio at week 20
Exenatide0.939-0.016
Exenatide Plus Rosiglitazone0.957-0.022
Rosiglitazone0.943-0.016

[back to top]

Hypoglycemia Rate Per 30 Days Per Patient

Average number of episodes of hypoglycemia per 30 days per patient (NCT00135330)
Timeframe: 20 weeks

Interventionhypoglycemia events / 30 days / patient (Mean)
Exenatide0.391
Exenatide Plus Rosiglitazone0.594
Rosiglitazone0.853

[back to top]

Incidence of Hypoglycemia Events

Number of subjects experiencing hypoglycemia at any point during the study (NCT00135330)
Timeframe: 20 weeks

Interventionparticipants (Number)
Exenatide8
Exenatide Plus Rosiglitazone9
Rosiglitazone6

[back to top]

Change in ASIiAUC During a Hyperglycemic Clamp Test.

Change in insulin incremental area under the concentration-time curve (ASIiAUC) from baseline to week 20. ASIiAUC is a measure of beta-cell function. (NCT00135330)
Timeframe: 20 weeks

,,
InterventionuIU-min/ml (Least Squares Mean)
Baseline ASIiAUCChange in ASIiAUC at week 20
Exenatide643.40747.26
Exenatide Plus Rosiglitazone686.41194.68
Rosiglitazone786.12-99.85

[back to top]

Change in AUC for C-peptide During a Meal Challenge Test (MCT).

Ratio (value at endpoint divided by value at baseline) of AUC(15-180 min) for C-peptide (nmol-min/L) during a MCT from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
Interventionnmol-min/L (Geometric Mean)
Baseline C-peptide during a MCTRatio(endpoint/baseline) of C-peptide during a MCT
Exenatide319.770.908
Exenatide Plus Rosiglitazone310.510.804
Rosiglitazone325.650.854

[back to top]

Change in AUC for Glucose During a Meal Challenge Test (MCT).

Change in AUC(15-180 min) for glucose during a MCT baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
Interventionmmol-min/L (Least Squares Mean)
Baseline glucose AUC during MCTChange in glucose AUC during MCT at week 20
Exenatide1782.86-560.12
Exenatide Plus Rosiglitazone1799.68-635.24
Rosiglitazone1741.87-425.59

[back to top]

Change in Body Fat Mass During a Meal Challenge Test (MCT)

Change in body fat mass form baseline to week 20, as assessed during an MCT (NCT00135330)
Timeframe: 20 weeks

,,
Interventionkg (Least Squares Mean)
Baseline body fat massChange in body fat mass at week 20
Exenatide32.05-2.76
Exenatide Plus Rosiglitazone32.55-1.06
Rosiglitazone30.54-1.99

[back to top]

Change in Body Weight

Change in body weight from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
Interventionkg (Least Squares Mean)
Baseline body weightChange in body weight at week 20
Exenatide93.05-2.82
Exenatide Plus Rosiglitazone93.76-1.21
Rosiglitazone91.781.48

[back to top]

Pedal Edema Score

"Pedal edema scores experienced by each patient throughout the study (1+ indicates a patient experienced a pedal edema score of 1 , 2, or 3; 2+ indicates a patient experienced a pedal edema score of 2 or 3, etc.)~Scale:~Slight pitting, no visible distortion, disappears rapidly~A somewhat deeper pit than in 1+, but again no readily detectable distortion, and it disappears in 10 - 15 seconds~The pit is noticeably deep and may last more than a minute; the dependent extremity looks fuller and swollen~The pit is very deep, lasts as long as 2 - 5 minutes, and the dependent extremity is grossly distorted" (NCT00135330)
Timeframe: 20 weeks

,,
Interventionparticipants (Number)
No edemaEdema score: 1+Edema score: 2+Edema score: 3+
Exenatide37710
Exenatide Plus Rosiglitazone341130
Rosiglitazone301461

[back to top]

Change in Fasting Insulin

Change in fasting insulin from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
InterventionuIU/ml (Geometric Mean)
Baseline fasting insulinRatio (wk20/baseline)of fasting insulin
Exenatide12.840.980
Exenatide Plus Rosiglitazone10.960.599
Rosiglitazone12.770.755

[back to top]

Change in Fasting LDL Cholesterol

Change in fasting low-density lipoprotein (LDL) cholesterol from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
Interventionmmol/L (Least Squares Mean)
Baseline LDLChange from baseline LDL at week 20
Exenatide2.59-0.049
Exenatide Plus Rosiglitazone2.570.096
Rosiglitazone2.710.334

[back to top]

Change in Fasting Proinsulin

Ratio (endpoint value divided by baseline value) for fasting proinsulin, comparing endpoint (week 20) to baseline (NCT00135330)
Timeframe: Week 20

,,
Interventionpmol/L (Geometric Mean)
Baseline fasting proinsulinRatio(wk20/baseline)of fasting proinsulin
Exenatide4.320.663
Exenatide Plus Rosiglitazone3.800.538
Rosiglitazone3.560.623

[back to top]

Change in Fasting Serum Glucose Concentration.

Change in fasting serum glucose concentration from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
Interventionmmol/L (Least Squares Mean)
Baseline fasting serum glucoseChange fr baseline fasting serum glucose at wk 20
Exenatide8.42-1.46
Exenatide Plus Rosiglitazone8.43-1.60
Rosiglitazone8.48-1.80

[back to top]

Change in Fasting Total Cholesterol.

Change in fasting total cholestrol from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
Interventionmmol/L (Least Squares Mean)
Baseline total cholesterolChange fr baseline total cholesterol at week 20
Exenatide4.42-0.128
Exenatide Plus Rosiglitazone4.410.258
Rosiglitazone4.620.438

[back to top]

Ratio (Value at Endpoint Divided by Value at Baseline) of AUC for Insulin During a Meal Challenge Test (MCT).

Ratio (value at endpoint divided by value at baseline) of AUC (15-180 min) for insulin (uIU-min/ml) during MCT. (NCT00135330)
Timeframe: Week 20

,,
InterventionuIU-min/ml (Geometric Mean)
Baseline AUC for insulin during MCTRatio(endpoint/baseline) of insulin AUC during MCT
Exenatide5171.400.806
Exenatide Plus Rosiglitazone4324.130.664
Rosiglitazone5816.830.722

[back to top]

Change in HbA1c

Change in HbA1c from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
InterventionPercentage (Least Squares Mean)
Baseline HbA1cChange from baseline HbA1c at week 20
Exenatide7.79-0.908
Exenatide Plus Rosiglitazone7.84-1.31
Rosiglitazone7.92-0.968

[back to top]

Change in Hip Circumference

Change in hip circumference form baseline to week 20 (NCT00135330)
Timeframe: 20 weeks

,,
Interventioncm (Least Squares Mean)
Baseline hip circumferenceChange in hip circumference at week 20
Exenatide113.29-1.28
Exenatide Plus Rosiglitazone112.120.147
Rosiglitazone111.901.51

[back to top]

Change in Incremental for Postprandial C-peptide During Meal Challenge Test (MCT).

Change in incremental for postprandial C-peptide (mmol/L) during MCT from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
Interventionmmol/L (Least Squares Mean)
Baseline C-peptide at 15 minChange fr baseline C-peptide at 15 min at week 20Baseline C-peptide at 30 minChange fr baseline C-peptide at 30 min at week 20Baseline C-peptide at 60 minChange fr baseline C-peptide at 60 min at week 20Baseline C-peptide at 90 minChange fr baseline C-peptide at 90 min at week 20Baseline C-peptide at 120 minChange fr baseline C-peptide at 120 min at week 20Baseline C-peptide at 150 minChange fr baseline C-peptide at 150 min at week 20Baseline C-peptide at 180 minChange fr baseline C-peptide at 180 min at week 20
Exenatide0.238-0.0060.521-0.0710.818-0.1480.895-0.1850.817-0.2590.843-0.2510.610-0.075
Exenatide Plus Rosiglitazone0.2590.0160.517-0.0360.871-0.0250.953-0.1170.828-0.1340.651-0.2540.482-0.238
Rosiglitazone0.2060.0870.5600.0990.8810.0541.03-0.0520.972-0.0160.813-0.0930.619-0.092

[back to top]

Change in Incremental for Postprandial Glucose During a Meal Challenge Test (MCT).

Change in incremental for postprandial glucose (mmol/L) during a MCT from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
Interventionmmol/L (Least Squares Mean)
Baseline glucose at 15 minChange fr baseline glucose at 15 min at wk 20Baseline glucose at 30 minChange fr baseline glucose at 30 min at wk 20Baseline glucose at 60 minutesChange fr baseline glucose at 60 min at wk 20Baseline glucose at 90 minutesChange fr baseline glucose at 90 min at wk 20Baseline glucose at 120 minutesChange fr baseline glucose at 120 min at wk 20Baseline glucose at 150 minutesChange fr baseline glucose at 150 min at wk 20Baseline glucose at 180 minutesChange fr baseline glucose at 180 min at wk 20
Exenatide0.950-0.6512.39-1.463.59-2.563.24-2.872.49-2.241.62-1.420.461-0.583
Exenatide Plus Rosiglitazone1.12-0.2862.54-1.063.88-2.463.36-2.912.24-2.521.14-1.950.036-0.995
Rosiglitazone0.8280.1502.23-0.0663.48-0.7203.48-0.9522.31-0.9121.25-0.8300.279-0.481

[back to top]

Change in Incremental for Postprandial Insulin During Meal Challenge Test (MCT).

Change in incremental for postprandial insulin (mmol/L) during meal challenge test (MCT) from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
Interventionmmol/L (Least Squares Mean)
Baseline insulin at 15 minChange fr baseline insulin at 15 min at wk 20Baseline insulin at 30 minChange fr baseline insulin at 30 min at wk 20Baseline insulin at 60 minChange fr baseline insulin at 60 min at wk 20Baseline insulin at 90 minChange fr baseline insulin at 90 min at wk 20Baseline insulin at 120 minChange fr baseline insulin at 120 min at wk 20Baseline insulin at 150 minChange fr baseline insulin at 150 min at wk 20Baseline insulin at 180 minChange fr baseline insulin at 180 min at wk 20
Exenatide9.97-1.7119.81-3.0027.92-11.0426.06-9.4219.56-11.2615.67-7.4810.580.031
Exenatide Plus Rosiglitazone8.09-1.8414.79-2.6327.67-7.4721.85-9.2717.52-8.6912.74-8.138.18-5.26
Rosiglitazone7.53-0.45518.83-1.0432.09-7.4232.25-6.1925.47-6.4318.11-5.5710.74-4.04

[back to top]

Change in Fasting Triglycerides

Ratio (endpint value divided by baseline value) of fasting triglycerides from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
Interventionmmol/L (Geometric Mean)
Baseline triglycerideRatio (endpoint/baseline) for triglycerides
Exenatide1.560.861
Exenatide Plus Rosiglitazone1.670.977
Rosiglitazone1.760.992

[back to top]

Change in Insulin iAUC From Baseline to Endpoint.

"Change in insulin iAUC in the first stage(uIU-min/ml) from baseline to week 20. First stage represents the first 10 minutes after reaching a steady state during a hyperglycemic clamp test." (NCT00135330)
Timeframe: Week 20

,,
InterventionuIU-min/ml (Least Squares Mean)
Baseline insulin iAUCChange from baseline insulin iAUC at week 20
Exenatide5.9899.08
Exenatide Plus Rosiglitazone-9.9253.71
Rosiglitazone23.0911.51

[back to top]

Change in Insulin Sensitivity Index as Measured by M-value.

Change of M-Value (mg/kg-min) during hyperinsulinemic euglycemic clamp test from baseline to week 20. (NCT00135330)
Timeframe: Week 20

,,
Interventionmg/kg-min (Least Squares Mean)
M-Value at baselineChange in M-Value from baseline at week 20
Exenatide3.890.477
Exenatide Plus Rosiglitazone2.492.07
Rosiglitazone4.021.42

[back to top]

Change in Lean Body Mass During a Meal Challenge Test (MCT)

Change in lean body mass from baseline to week 20, as assessed during an MCT (NCT00135330)
Timeframe: 20 weeks

,,
Interventionkg (Least Squares Mean)
Baseline lean body massChange in lean body mass at week 20
Exenatide64.62-2.99
Exenatide Plus Rosiglitazone60.940.532
Rosiglitazone61.091.23

[back to top]

Change in Percent Body Fat During a Meal Challenge Test (MCT)

Change in percent body fat from baseline to week 20, as assessed during an MCT (NCT00135330)
Timeframe: 20 weeks

,,
Interventionpercentage (Least Squares Mean)
Baseline percent body fatChange in percent body fat at week 20
Exenatide33.42-1.40
Exenatide Plus Rosiglitazone34.07-0.347
Rosiglitazone32.50-1.18

[back to top]

Change in Waist Circumference

Change in waist circumference from baseline to week 20 (NCT00135330)
Timeframe: 20 weeks

,,
Interventioncm (Least Squares Mean)
Baseline waist circumferenceChange in waist circumference at Week 20
Exenatide105.98-2.95
Exenatide Plus Rosiglitazone106.85-2.38
Rosiglitazone105.34-0.225

[back to top]

Change in Insulin AUC in the First Stage From Baseline to Endpoint.

"Change in insulin AUC in the first stage(uIU-min/ml) from baseline to week 20. First stage represents the first 10 minutes after reaching a steady state during a hyperglycemic clamp test." (NCT00135330)
Timeframe: Week 20

,,
InterventionuIU-min/ml (Least Squares Mean)
Baseline insulin AUCChange from baseline insulin AUC at week 20
Exenatide200.50134.88
Exenatide Plus Rosiglitazone136.8432.12
Rosiglitazone157.49-50.81

[back to top]

Change in HbA1c From Baseline to Week 30

Absolute change in HbA1c from Baseline (Day -3) to Week 30 [Week 30 - Baseline] (NCT00308139)
Timeframe: Day -3, Week 30

Interventionpercentage of total hemoglobin (Least Squares Mean)
Exenatide Once Weekly-1.87
Exenatide Twice Daily-1.54

[back to top]

Change in HbA1c From Baseline to Week 364

Absolute change in HbA1c from Baseline (Day -3) to Week 364 (NCT00308139)
Timeframe: Day -3, Week 364

Interventionpercentage of total hemoglobin (Least Squares Mean)
Exenatide Once Weekly -> Exenatide Once Weekly-1.49
Exenatide Twice Daily -> Exenatide Once Weekly-1.57
All Treatment-1.53

[back to top]

Change in High-density Lipoprotein Cholesterol (HDL-C) From Baseline to Week 30

Change in high-density lipoprotein cholesterol (HDL-C) from baseline (Day -3) to Week 30. (NCT00308139)
Timeframe: Day -3, Week 30

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-0.9
Exenatide Twice Daily-1.3

[back to top]

Change in High-density Lipoprotein Cholesterol (HDL-C) From Baseline to Week 364

Change in high-density lipoprotein cholesterol (HDL-C) from baseline (Day -3) to Week 364. (NCT00308139)
Timeframe: Day -3, Week 364

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly -> Exenatide Once Weekly2.2
Exenatide Twice Daily -> Exenatide Once Weekly3.4
All Treatment2.8

[back to top]

Change in Low-density Lipoprotein Cholesterol (LDL-C) From Baseline to Week 364

Change in low-density lipoprotein cholesterol (LDL-C) from baseline (Day -3) to Week 364. (NCT00308139)
Timeframe: Day -3, Week 364

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly -> Exenatide Once Weekly-13.6
Exenatide Twice Daily -> Exenatide Once Weekly-7.5
All Treatment-10.4

[back to top]

Change in Total Cholesterol From Baseline to Week 30

Change in total cholesterol from baseline (Day -3) to Week 30. (NCT00308139)
Timeframe: Day -3, Week 30

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-11.9
Exenatide Twice Daily-3.8

[back to top]

Change in Total Cholesterol From Baseline to Week 364

Change in total cholesterol from baseline (Day -3) to Week 364. (NCT00308139)
Timeframe: Day -3, Week 364

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly -> Exenatide Once Weekly-15.0
Exenatide Twice Daily -> Exenatide Once Weekly-4.8
All Treatment-9.6

[back to top]

Exenatide LAR Steady State Concentration From Week 29 to Week 30

Steady-state plasma exenatide concentration over the dosing interval of Week 29 to Week 30 (0-168 hours) was evaluated. Geometric mean for the average steady-state concentration and its 10th and 90th percentiles were reported. (NCT00308139)
Timeframe: Week 29 to Week 30

Interventionpg/mL (Geometric Mean)
Exenatide Once Weekly300.23

[back to top]

Percentage of Subjects Achieving HbA1c Target of <=6.0%

Percentage of subjects achieving HbA1c target values of <=6.0% at Week 30. (NCT00308139)
Timeframe: Week 30

Interventionpercentage of subjects (Number)
Exenatide Once Weekly23.0
Exenatide Twice Daily16.3

[back to top]

Percentage of Subjects Achieving HbA1c Target of <=6.5%

Percentages of subjects achieving HbA1c target values of <=6.5% at Week 30. (NCT00308139)
Timeframe: Week 30

Interventionpercentage of subjects (Number)
Exenatide Once Weekly3.0
Exenatide Twice Daily16.3

[back to top]

Percentage of Subjects Achieving HbA1c Target of <=6.5%

Percentages of subjects achieving HbA1c target values of <=6.5% at Week 364 (NCT00308139)
Timeframe: Week 364

Interventionpercentage of subjects (Number)
Exenatide Once Weekly -> Exenatide Once Weekly22.4
Exenatide Twice Daily -> Exenatide Once Weekly37.5
All Treatmeat30.3

[back to top]

Ratio of Triglycerides at Week 364 to Baseline

Ratio of triglycerides (measured in mg/dL) at Week 364 to baseline (Day -3). Log (Postbaseline Triglycerides) - log (Baseline Triglycerides); change from baseline to endpoint is presented as ratio of endpoint to baseline. (NCT00308139)
Timeframe: Day -3, Week 364

Interventionratio (Least Squares Mean)
Exenatide Once Weekly -> Exenatide Once Weekly0.91
Exenatide Twice Daily -> Exenatide Once Weekly0.94
All Treatment0.93

[back to top]

Percentage of Subjects Achieving HbA1c Target of <7%

Percentage of subjects achieving HbA1c target value of <7% at Week 30. (NCT00308139)
Timeframe: Week 30

Interventionpercentage of subjects (Number)
Exenatide Once Weekly70.9
Exenatide Twice Daily51.0

[back to top]

Percentage of Subjects Achieving HbA1c Target of <7%

Percentages of subjects achieving HbA1c target value of <7% at Week 364 (NCT00308139)
Timeframe: Week 364

Interventionpercentage of subjects (Number)
Exenatide Once Weekly -> Exenatide Once Weekly41.4
Exenatide Twice Daily -> Exenatide Once Weekly50.0
All Treatment45.9

[back to top]

Ratio of Triglycerides at Week 30 to Baseline

Ratio of triglycerides (measured in mg/dL) at Week 30 to baseline (Day -3). Log (Postbaseline Triglycerides) - log (Baseline Triglycerides); change from baseline to endpoint is presented as ratio of endpoint to baseline. (NCT00308139)
Timeframe: Day -3, Week 30

Interventionratio (Least Squares Mean)
Exenatide Once Weekly0.85
Exenatide Twice Daily0.89

[back to top]

Change in Fasting Plasma Glucose From Baseline to Week 364

Change in fasting plasma glucose from baseline (Day -3) to Week 364. (NCT00308139)
Timeframe: Day -3, Week 364

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly -> Exenatide Once Weekly-18.3
Exenatide Twice Daily -> Exenatide Once Weekly-27.7
All Treatment-23.6

[back to top]

Change in Blood Pressure From Baseline to Week 364

Change in Sitting Diastolic Blood Pressure and Sitting Systolic Blood Pressure from baseline to Week 364 (NCT00308139)
Timeframe: Day -3, Week 364

,,
InterventionmmHg (Mean)
Sitting Systolic Blood PressureSitting Diastolic Blood Pressure
All Treatment1.2-2.7
Exenatide Once Weekly -> Exenatide Once Weekly1.3-1.7
Exenatide Twice Daily -> Exenatide Once WeeklyEdit1.0-3.6

[back to top]

Change in Blood Pressure From Baseline to Week 30

Change in Sitting Diastolic Blood Pressure and Sitting Systolic Blood Pressure from baseline to Week 30 (NCT00308139)
Timeframe: Day -3, Week 30

,
InterventionmmHg (Mean)
Sitting Systolic Blood PressureSitting Diastolic Blood Pressure
Exenatide Once Weekly-4.4-1.1
Exenatide Twice Daily-3.8-2.3

[back to top]

Assessment on Event Rate of Treatment-emergent Hypoglycemic Events With SU Use at Screening

The major hypoglycemia category included events that, in the judgment of the investigator or physician, resulted in loss of consciousness, seizure, coma, or other change in mental status consistent with neuroglycopenia, in which symptoms resolved after administration of intramuscular glucagon or intravenous glucose, required third-party assistance, and was accompanied by a blood glucose concentration of less than 54 mg/dL prior to treatment, whether or not symptoms of hypoglycemia were perceived by the subject. The minor hypoglycemia were accompanied by a blood glucose concentration of less than 54 mg/dL prior to treatment and not classified as major hypoglycemia. (NCT00308139)
Timeframe: Day 1 to Week 364

,,,
Interventionevents per subject-year (Mean)
Major hypoglycemic eventsMinor hypoglycemic events
Exenatide Once Weekly -> Exenatide Once Weekly With SU0.000.49
Exenatide Once Weekly With SU0.000.000.570.36
Exenatide Twice Daily -> Exenatide Once Weekly With SU0.000.22
Exenatide Twice Daily With SU0.000.38

[back to top]

Assessment on Event Rate of Treatment-emergent Hypoglycemic Events With Non-SU Use at Screening

The major hypoglycemia category included events that, in the judgment of the investigator or physician, resulted in loss of consciousness, seizure, coma, or other change in mental status consistent with neuroglycopenia, in which symptoms resolved after administration of intramuscular glucagon or intravenous glucose, required third-party assistance, and was accompanied by a blood glucose concentration of less than 54 mg/dL prior to treatment, whether or not symptoms of hypoglycemia were perceived by the subject. The minor hypoglycemia were accompanied by a blood glucose concentration of less than 54 mg/dL prior to treatment and not classified as major hypoglycemia. (NCT00308139)
Timeframe: Day 1 to Week 364

,,,
Interventionevents per subject-year (Mean)
Major hypoglycemic eventsMinor hypoglycemic events
Exenatide Once Weekly -> Exenatide Once Weekly With Non-SU0.000.03
Exenatide Once Weekly With Non-SU0.000.000.000.04
Exenatide Twice Daily -> Exenatide Once Weekly With Non-SU0.000.06
Exenatide Twice Daily With Non-SU0.000.02

[back to top]

Change in Body Weight From Baseline to Week 364

Change in body weight from baseline (Day -3) to Week 364 (NCT00308139)
Timeframe: Day -3, Week 364

Interventionkg (Least Squares Mean)
Exenatide Once Weekly -> Exenatide Once Weekly-5.25
Exenatide Twice Daily -> Exenatide Once Weekly-2.71
All Treatment-3.87

[back to top]

Change in 2 Hours (2h) Postprandial Glucose From Baseline to Week 14

Change in 2h Postprandial Glucose from baseline (Day -3) to Week 14 (NCT00308139)
Timeframe: Day -3, Week 14

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-95.88
Exenatide Twice Daily-125.96

[back to top]

Change in Body Weight From Baseline to Week 30

Change in body weight from baseline (Day -3) to Week 30 (NCT00308139)
Timeframe: Day -3, Week 30

Interventionkg (Least Squares Mean)
Exenatide Once Weekly-3.67
Exenatide Twice Daily-3.59

[back to top]

Change in Fasting Plasma Glucose From Baseline to Week 30

Change in fasting plasma glucose from baseline (Day -3) to Week 30. (NCT00308139)
Timeframe: Day -3, Week 30

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-41.5
Exenatide Twice Daily-24.6

[back to top]

First Will be the Changes in TNG Stimulated Arterial Dilation (Endothelial-independent) in Subjects Treated With Exenatide Compared With Subjects Treated With Lantus at the End of the Study Compared to Baseline Measurements

Trinitroglycerin (TNG) response evaluates endothelium independent vasodilation. The brachial artery was scanned before and 5 minutes after sublingual administration of 400 ug of trinitroglycerin. This was performed only at 4 hours following the test meal and fifteen minutes after completion of the FMD study to allow for the brachial artery to return to baseline. This was performed at both the baseline and 3 month visits. (NCT00353834)
Timeframe: Baseline and end of study

InterventionPercentage dilation (Mean)
Glargine Insulin10.7
Exenatide11.3

[back to top]

The Primary Endpoint Was the Change in FMD at the End of the Study Compared to Baseline Measurements in Subjects Treated With Exenatide Compared to Subjects Treated With Lantus.

Flow mediated dilation (FMD) of the brachial artery was measured at rest and during reactive hyperemia using a high-resolution 10.0 MHz linear array transducer and an HOI Ultramark 9 system. Reactive hyperemia was produced by inflating a pneumatic tourniquet on the forearm distal to the brachial artery to 50 mmHg above the systolic BP for 5 minutes, then deflating it . Brachial artery diameter was measured before inflation of the cuff and 1-2 minutes after cuff deflation and expressed as the percentage change. This protocol is described in detail elsewhere. This was performed fasting, 2, and 4 hours after the meal challenge at baseline and 3 months. (NCT00353834)
Timeframe: Baseline and End of Study

InterventionPercentage dilation (Mean)
Glargine Insulin5.0
Exenatide4.7

[back to top]

Number of Patients With Treatment Failure

Treatment failure is defined as one of the following:1. HbA1c exceeding 9% at any visit after the initial 3 months of treatment (i.e., earliest at Month 6), on the maximally tolerated dose of antidiabetic agents. 2. HbA1c exceeding 7% at 2 consecutive visits 3 months apart, after the initial 6 months of treatment (i.e., earliest at Month 9), on the maximally tolerated dose of antidiabetic agents. (NCT00359762)
Timeframe: Baseline to end of Period II (up to 4.5 years)

,
Interventionnumber of patients (Number)
Number of patients with treatment failureNumber of patients censored
Exen + Met203287
Glim + Met262225

[back to top]

Triglycerides at Year 3

Triglycerides at Year 3. (NCT00359762)
Timeframe: Year 3 in Period II

Interventionmmol/L (Least Squares Mean)
Exen + Met1.69
Glim + Met1.95

[back to top]

Total Cholesterol at Year 3

Total Cholesterol at Year 3. (NCT00359762)
Timeframe: Year 3 in Period II

Interventionmmol/L (Least Squares Mean)
Exen + Met4.77
Glim + Met4.75

[back to top]

Time to Treatment Failure

Treatment failure is defined as one of the following:1. HbA1c exceeding 9% at any visit after the initial 3 months of treatment (i.e., earliest at Month 6), on the maximally tolerated dose of antidiabetic agents. 2. HbA1c exceeding 7% at 2 consecutive visits 3 months apart, after the initial 6 months of treatment (i.e., earliest at Month 9), on the maximally tolerated dose of antidiabetic agents. (NCT00359762)
Timeframe: Baseline to end of Period II (up to 4.5 years)

Interventionweek (Median)
Exen + Met180.0
Glim + Met142.1

[back to top]

Systolic Blood Pressure at Year 3

Systolic Blood pressure at Year 3. (NCT00359762)
Timeframe: Year 3 in Period II

InterventionmmHg (Least Squares Mean)
Exen + Met130.58
Glim + Met135.78

[back to top]

Ratio of the 30 Minute Increment in Plasma Insulin Concentration and the 30 Minute Increment in Plasma Glucose During the Oral Glucose Tolerance Test (DI30/DG30 Ratio) at Year 3

DI30/DG30 at Year 3. DI30/DG30 ratio was calculated as (30 minute post prandial insulin - fasting insulin) (measured in pmol/L)/(30 minute post prandial glucose - fasting glucose) (measured in mmol/L). (NCT00359762)
Timeframe: Year 3 in Period II

Interventionratio (Least Squares Mean)
Exen + Met25.81
Glim + Met26.38

[back to top]

High-density Lipoprotein (HDL) Cholesterol at Year 3

HDL Cholesterol at Year 3. (NCT00359762)
Timeframe: Year 3 in Period II

Interventionmmol/L (Least Squares Mean)
Exen + Met1.31
Glim + Met1.25

[back to top]

Change in HbA1c From Baseline to Year 2 for Patients Not Randomized at Entry in Period III

Change in HbA1c from baseline to Year 2. (NCT00359762)
Timeframe: Baseline in Period III, Year 2 in Period III

Interventionpercentage of total hemoglobin (Mean)
Glim + Met + Exen - Not Randomized-0.47

[back to top]

Heart Rate at Year 3

Heart rate at Year 3. (NCT00359762)
Timeframe: Year 3 in Period II

Interventionbeats per minute (Least Squares Mean)
Exen + Met73.51
Glim + Met74.23

[back to top]

Fasting Proinsulin/Insulin Ratio at Year 3

Fasting proinsulin (measured in pmol/L)/insulin (measured in pmol/L) ratio at Year 3. (NCT00359762)
Timeframe: Year 3 in Period II

Interventionratio (Least Squares Mean)
Exen + Met0.22
Glim + Met0.23

[back to top]

Fasting Plasma Glucose at Year 3

Fasting plasma glucose at Year 3. (NCT00359762)
Timeframe: Year 3 in Period II

Interventionmmol/L (Least Squares Mean)
Exen + Met7.27
Glim + Met7.96

[back to top]

Disposition Index at Year 3

Disposition Index at Year 3. Disposition index was calculated as (DI30/DG30 ratio)/(HOMA index for insulin resistance (HOMA-IR)); where HOMA-IR=(fasting insulin (measured in pmol/L) x fasting glucose (measured in mmol/L))/(22.5 x 7.175). (NCT00359762)
Timeframe: Year 3 in Period II

Interventionratio (Least Squares Mean)
Exen + Met12.56
Glim + Met7.89

[back to top]

Diastolic Blood Pressure at Year 3

Diastolic Blood pressure at Year 3. (NCT00359762)
Timeframe: Year 3 in Period II

InterventionmmHg (Least Squares Mean)
Exen + Met77.45
Glim + Met79.16

[back to top]

Change in Postprandial (2 Hours) Plasma Glucose From Baseline to Endpoint

Change from baseline in postprandial (2 hours) plasma glucose to endpoint. (NCT00359762)
Timeframe: Baseline, end of Period II (up to 4.5 years)

Interventionmmol/L (Least Squares Mean)
Exen + Met-2.72
Glim + Met-0.53

[back to top]

Change in HOMA-B From Baseline to Endpoint

Change in HOMA-B from baseline to endpoint. (NCT00359762)
Timeframe: Baseline, end of Period II (up to 4.5 years)

Interventionratio (Least Squares Mean)
Exen + Met5.56
Glim + Met19.92

[back to top]

Change in HbA1c From Baseline to Endpoint

Change in HbA1c from baseline to endpoint. Endpoint for HbA1c was defined as the HbA1c measured at the treatment failure for patients reaching primary endpoint and was the last observation in study period II for other patients (either followed until the end of the study period II or discontinuing the study). (NCT00359762)
Timeframe: Baseline, end of Period II (up to 4.5 years)

Interventionpercentage of total hemoglobin (Least Squares Mean)
Exen + Met-0.36
Glim + Met-0.21

[back to top]

Change in Fasting Proinsulin/Insulin Ratio From Baseline to Endpoint.

Change in fasting proinsulin (measured in pmol/L)/insulin (measured in pmol/L) ratio from baseline to endpoint. (NCT00359762)
Timeframe: Baseline, end of Period II (up to 4.5 years)

Interventionratio (Least Squares Mean)
Exen + Met0.03
Glim + Met0.05

[back to top]

Change in Fasting Plasma Glucose From Baseline to Endpoint

Change in fasting plasma glucose from baseline to endpoint. (NCT00359762)
Timeframe: Baseline, end of Period II (up to 4.5 years)

Interventionmmol/L (Least Squares Mean)
Exen + Met-0.87
Glim + Met-0.41

[back to top]

Change in Disposition Index From Baseline to Endpoint

Change in disposition index from baseline to endpoint. (NCT00359762)
Timeframe: Baseline, end of Period II (up to 4.5 years)

Interventionratio (Least Squares Mean)
Exen + Met9.15
Glim + Met1.82

[back to top]

Change in DI30/DG30 Ratio From Baseline to Endpoint

Change in DI30/DG30 ratio from baseline to endpoint. (NCT00359762)
Timeframe: Baseline, end of Period II (up to 4.5 years)

Interventionratio (Least Squares Mean)
Exen + Met12.10
Glim + Met0.91

[back to top]

Change in Body Weight From Baseline to Year 3

Change in Body weight from baseline to Year 3. (NCT00359762)
Timeframe: Baseline, Year 3 in Period II

Interventionkg (Least Squares Mean)
Exen + Met-3.92
Glim + Met1.47

[back to top]

Change in HbA1c From Baseline to Year 3

Change in HbA1c from baseline to Year 3. (NCT00359762)
Timeframe: Baseline, Year 3 in Period II

Interventionpercentage of total hemoglobin (Least Squares Mean)
Exen + Met-0.30
Glim + Met-0.12

[back to top]

Change in HbA1c From Baseline to Year 2 for Patients Randomized at Entry in Period III

Change in HbA1c from baseline to Year 2. (NCT00359762)
Timeframe: Baseline in Period III, Year 2 in Period III

Interventionpercentage of total hemoglobin (Least Squares Mean)
Exen + Met + Glim - Randomized-0.19
Exen + Met + Pio or Rosi - Randomized-0.47

[back to top]

Postprandial (2 Hours) Plasma Glucose at Year 3

Postprandial (2 hours) plasma glucose at Year 3. (NCT00359762)
Timeframe: Year 3 in Period II

Interventionmmol/L (Least Squares Mean)
Exen + Met12.65
Glim + Met15.45

[back to top]

Hypoglycemia Rate Per Year in Period III

All hypoglycemia episodes were taken into account. Severe hypoglycemia: event requiring assistance of another person to administer carbohydrate, glucagons, or other resuscitative actions; Documented symptomatic hypoglycemia: event with typical symptoms accompanied by a measured plasma glucose concentration <=70 mg/dL; Asymptomatic hypoglycemia: event not accompanied by typical symptoms but with a measured plasma glucose concentration <=70 mg/dL; Probable symptomatic hypoglycemia: event with symptoms not accompanied by a plasma glucose determination. (NCT00359762)
Timeframe: Start of Period III to end of study

Interventionevents per subject-year (Mean)
Exen + Metformin + Glim - Randomized2.78
Exen + Met + Pio or Rosi - Randomized0.60
Glim + Met + Exen - Not Randomized4.62

[back to top]

Hypoglycemia Rate Per Year

All hypoglycemia episodes were taken into account. Severe hypoglycemia: event requiring assistance of another person to administer carbohydrate, glucagons, or other resuscitative actions; Documented symptomatic hypoglycemia: event with typical symptoms accompanied by a measured plasma glucose concentration <=70 mg/dL; Asymptomatic hypoglycemia: event not accompanied by typical symptoms but with a measured plasma glucose concentration <=70 mg/dL; Probable symptomatic hypoglycemia: event with symptoms not accompanied by a plasma glucose determination. (NCT00359762)
Timeframe: Baseline to end of Period II (up to 4.5 years)

Interventionevents per subject-year (Least Squares Mean)
Exen + Met1.52
Glim + Met5.32

[back to top]

Homeostasis Model Assessment of Beta-cell Function (HOMA-B) at Year 3

HOMA-B at Year 3. HOMA-B is an index of beta-cell function and was calculated as: HOMA-B = (20 x fasting insulin (measured in pmol/L))/((fasting glucose (measured in mmol/L) - 3.5) x 7.175). (NCT00359762)
Timeframe: Year 3 in Period II

Interventionratio (Least Squares Mean)
Exen + Met66.86
Glim + Met68.52

[back to top]

Percent of Patients Achieving HbA1c < 6.5%

Percent of patients achieving specified HbA1c target at endpoint (NCT00360334)
Timeframe: 26 weeks

InterventionPercentage of participants (Number)
Exenatide15.3
Insulin Glargine11.2

[back to top]

Change in High Density Lipoprotein (HDL) Cholesterol

Change in HDL cholesterol from baseline to endpoint (NCT00360334)
Timeframe: 26 weeks

Interventionmmol/L (Least Squares Mean)
Exenatide0.01
Insulin Glargine0.02

[back to top]

Percent of Patients Achieving 10% Weight Loss

Percent of patients who lost at least 10% of baseline body weight at endpoint (NCT00360334)
Timeframe: 26 weeks

InterventionPercentage of participants (Number)
Exenatide4.2
Insulin Glargine0.0

[back to top]

Percent Change in Body Weight

Percent change in baseline body weight at endpoint (NCT00360334)
Timeframe: 26 Weeks

InterventionPercentage (Least Squares Mean)
Exenatide-2.8
Insulin Glargine3.1

[back to top]

Nocturnal Hypoglycemic Rate Per 30 Days

Number of nocturnal hypoglycemic episodes per patient adjusted per 30 days (NCT00360334)
Timeframe: 26 weeks

InterventionNumber of episodes per 30 days (Median)
Exenatide0.000
Insulin Glargine0.000

[back to top]

Incidence of Severe Hypoglycemic Episodes

Percent of total patients in each arm experiencing severe hypoglycemia at any point during the 26 week study (NCT00360334)
Timeframe: 26 weeks

Interventionpercent (Number)
Exenatide4.2
Insulin Glargine5.3

[back to top]

Incidence of Nocturnal Hypoglycemic Episodes

Percent of total patients in each arm experiencing nocturnal hypoglycemia at any point in the 26 week study (NCT00360334)
Timeframe: 26 weeks

Interventionpercent (Number)
Exenatide11.9
Insulin Glargine29.8

[back to top]

Percent of Patients Achieving 5% Weight Loss

Percent of patients who lost at least 5% of baseline body weight at endpoint (NCT00360334)
Timeframe: 26 weeks

InterventionPercentage of participants (Number)
Exenatide19.5
Insulin Glargine0.9

[back to top]

Incidence of Hypoglycemic Episodes

Percent of total patients in each arm experiencing hypoglycemia at any point in the 26 week study (NCT00360334)
Timeframe: 26 weeks

Interventionpercent (Number)
Exenatide50.0
Insulin Glargine59.6

[back to top]

Change in Fasting Serum Triglycerides

Change in fasting serum triglycerides from baseline to endpoint (NCT00360334)
Timeframe: 26 weeks

Interventionmmol/L (Least Squares Mean)
Exenatide-0.33
Insulin Glargine-0.38

[back to top]

Change in Fasting Serum Glucose

Change in fasting serum glucose from baseline (week 0) to endpoint (week 26) (NCT00360334)
Timeframe: 26 weeks

Interventionmmol/L (Least Squares Mean)
Exenatide-2.12
Insulin Glargine-3.61

[back to top]

Percent of Patients Achieving HbA1c < 7%

Percent of patients achieving specified HbA1c target at endpoint (NCT00360334)
Timeframe: 26 weeks

InterventionPercentage of participants (Number)
Exenatide34.7
Insulin Glargine43.1

[back to top]

Change in Apolipoprotein-B

Change in apolipoprotein-B from baseline to endpoint (NCT00360334)
Timeframe: 26 weeks

Interventiong/L (Least Squares Mean)
Exenatide-0.09
Insulin Glargine-0.08

[back to top]

Change in Low Density Lipoprotein (LDL) Cholesterol

Change in LDL cholesterol from baseline to endpoint (NCT00360334)
Timeframe: 26 weeks

Interventionmmol/L (Least Squares Mean)
Exenatide-0.25
Insulin Glargine-0.07

[back to top]

Change in TC to HDL Cholesterol Ratio

Change in TC to HDL cholesterol ratio from baseline to endpoint (NCT00360334)
Timeframe: 26 weeks

InterventionRatio (Least Squares Mean)
Exenatide-0.40
Insulin Glargine-0.34

[back to top]

Hypoglycemic Rate Per 30 Days

Number of hypoglycemic episodes per patient adjusted per 30 days (NCT00360334)
Timeframe: 26 weeks

InterventionNumber of episodes per 30 days (Median)
Exenatide0.069
Insulin Glargine0.164

[back to top]

Change in Fasting Serum Total Cholesterol (TC)

Change in TC from baseline to endpoint (NCT00360334)
Timeframe: 26 weeks

Interventionmmol/L (Least Squares Mean)
Exenatide-0.36
Insulin Glargine-0.21

[back to top]

Change in Waist-to-hip Ratio

Change in waist-to-hip ratio from baseline to endpoint (NCT00360334)
Timeframe: 26 weeks

,
InterventionRatio (Least Squares Mean)
Baseline (Week 0)Change at endpoint (Week 26)
Exenatide0.99-0.02
Insulin Glargine0.980.01

[back to top]

Change in Waist Circumference

Change in waist circumference from baseline to endpoint (NCT00360334)
Timeframe: 26 Weeks

,
Interventioncm (Least Squares Mean)
Baseline (Week 0)Change at endpoint (Week 26)
Exenatide112.07-2.19
Insulin Glargine110.641.97

[back to top]

Change in Systolic Blood Pressure

Change in systolic blood pressure from baseline to endpoint (NCT00360334)
Timeframe: 26 weeks

,
InterventionmmHg (Least Squares Mean)
Baseline (Week 0)Change at endpoint (Week 26)
Exenatide134.0-3.6
Insulin Glargine134.70.6

[back to top]

Change in Diastolic Blood Pressure

Change in diastolic blood pressure from baseline to endpoint (NCT00360334)
Timeframe: 26 weeks

,
InterventionmmHg (Least Squares Mean)
Baseline (Week 0)Change at endpoint (Week 26)
Exenatide79.6-0.8
Insulin Glargine79.70.9

[back to top]

Change in Body Weight

Change in body weight from baseline to endpoint (NCT00360334)
Timeframe: 26 weeks

,
Interventionkg (Least Squares Mean)
Baseline (Week 0)Change at endpoint (Week 26)
Exenatide101.19-2.73
Insulin Glargine97.932.98

[back to top]

Change in Body Mass Index (BMI)

Change in BMI from baseline to endpoint (NCT00360334)
Timeframe: 26 weeks

,
Interventionkg/m^2 (Least Squares Mean)
Baseline (Week 0)Change at endpoint (Week 26)
Exenatide34.49-0.95
Insulin Glargine33.711.01

[back to top]

Change in 7 Point Self Monitored Blood Glucose Profile

Change from baseline to endpoint in self monitored blood glucose levels measured at 7 time points during the day (NCT00360334)
Timeframe: 26 weeks

,
Interventionmmol/L (Mean)
Pre-breakfast: Baseline (Week 0)Pre-breakfast: Change at endpoint (Week 26)2 hrs after breakfast: Baseline (Week 0)2 hrs after breakfast: Change at endpt (Week 26)Pre-lunch: Baseline (Week 0)Pre-lunch: Change at endpoint (Week 26)2 hrs after lunch: Baseline (Week 0)2 hrs after lunch: Change at endpoint (Week 26)Pre-dinner: Baseline (Week 0)Pre-dinner: Change at endpoint (Week 26)2 hrs after dinner: Baseline (Week 0)2 hrs after dinner: Change at endpoint (Week 26)Bedtime: Baseline (Week 0)Bedtime: Change at endpoint (Week 26)
Exenatide9.98-2.0113.53-5.099.95-2.2112.07-3.209.95-2.1312.59-4.5911.63-3.56
Insulin Glargine9.88-3.9913.33-3.959.54-2.5911.15-2.489.37-1.4611.80-2.0611.24-2.20

[back to top]

Severe Hypoglycemic Rate Per 30 Days

Number of severe hypoglycemic episodes per patient adjusted per 30 days (NCT00360334)
Timeframe: 26 weeks

InterventionNumber of episodes per 30 days (Median)
Exenatide0.000
Insulin Glargine0.000

[back to top]

Percent of Patients Who Achieved HbA1c ≤ 7.4% With Minimal Weight Gain (≤ 1kg)

Composite endpoint evaluating effect of treatment on glycemic control and weight (NCT00360334)
Timeframe: 26 weeks

Interventionpercentage of participants (Number)
Exenatide53.4
Insulin Glargine19.8

[back to top]

Percent of Patients Who Achieved HbA1c ≤ 7.4% and Weight Gain ≤ 0.5kg

Composite endpoint evaluating effect of treatment on glycemic control and weight (NCT00360334)
Timeframe: 26 weeks

InterventionPercentage of participants (Number)
Exenatide52.5
Insulin Glargine16.4

[back to top]

Percent of Patients Achieving HbA1c ≤ 7.4%

Percent of patients achieving specified HbA1c target at endpoint (NCT00360334)
Timeframe: 26 weeks

InterventionPercentage of participants (Number)
Exenatide54.2
Insulin Glargine61.2

[back to top]

Change From Baseline in High Density Lipoprotein (HDL) Cholesterol at Week 24

Change in HDL cholesterol from baseline after 24 weeks of treatment (i.e., HDL cholesterol at week 24 minus HDL cholesterol at week 0). HDL measured as mmol/L. (NCT00375492)
Timeframe: baseline, Week 24

Interventionmmol/L (Least Squares Mean)
Group A (Exenatide)0.02
Group B (Placebo)0.02

[back to top]

Change From Baseline in Glycosylated Hemoglobin (HbA1c) at Week 24

Change in HbA1c from baseline (Week 0) after 24 weeks of treatment (i.e., HbA1c at week 24 minus HbA1c at week 0). HbA1c is measured as percent (%) of hemoglobin. (NCT00375492)
Timeframe: baseline, Week 24

Interventionpercent hemoglobin (Least Squares Mean)
Group A (Exenatide)-1.21
Group B (Placebo)-0.73

[back to top]

Change From Baseline in Body Weight

Change in body weight from baseline (Week 0) after 24 weeks of treatment (i.e., weight at week 24 minus weight at week 0). Body weight measured in kilograms (k). (NCT00375492)
Timeframe: Baseline, Week 24

Interventionkg (Least Squares Mean)
Group A (Exenatide)-6.16
Group B (Placebo)-3.97

[back to top]

Change From Baseline in 6-point Self Monitored Blood Glucose (SMBG) Profile at Week 24

Change in SMBG at each of 6 time points throughout a day (blood glucose measurements before and 2 hours after the start of the morning, mid-day, and evening meals); week 24 compared to week 0 (i.e., SMBG at week 24 minus SMBG at week 0). Fasting Glucose measured in millimoles per liter (mmol/L). (NCT00375492)
Timeframe: baseline, Week 24

,
Interventionmmol/L (Least Squares Mean)
Morning Pre-Meal2 Hours Post Morning MealMidday Pre-Meal2 Hours Post Midday MealEvening Pre-Meal2 Hours Post Evening Meal
Group A (Exenatide)-1.87-2.67-1.40-2.12-1.57-3.09
Group B (Placebo)-1.20-1.92-1.37-1.51-1.32-2.28

[back to top]

Ratio of Triglycerides at Week 24 to Triglycerides at Baseline

Ratio of triglyceride levels at Week 24 to triglyceride levels at baseline, Week 0 (ie., triglycerides at Week 24 divided by triglycerides at baseline, Week 0). Triglycerides measured in mmol/L. (NCT00375492)
Timeframe: baseline, Week 24

InterventionRatio (Geometric Mean)
Group A (Exenatide)0.83
Group B (Placebo)0.92

[back to top]

Ratio of Homeostatic Model Assessment-Insulin Sensitivity (HOMA-S) at Week 24 to HOMA-S at Baseline

Ratio of HOMA-S at Week 24 to HOMA-S at baseline, week 0. HOMA-S is a computer solved model used to predict the homeostatic concentrations which arise from varying degrees of insulin sensitivity. HOMA-S allows a quantitative assessment of the contributions of insulin sensitivity to the fasting hyperglycemia. HOMA-S is measured as a percent of the normal population (normal insulin sensitivity = 100%, which is used as a reference in the calculation). The higher the percent the better for the participant. (NCT00375492)
Timeframe: baseline, Week 24

InterventionRatio (Geometric Mean)
Group A (Exenatide)1.08
Group B (Placebo)0.97

[back to top]

Ratio of Homeostatic Model Assessment-Beta Cell (HOMA-B) at Week 24 to HOMA-B at Baseline

Ratio of HOMA-B at Week 24 to HOMA-B at baseline (Week 0). HOMA-B is a computer solved model used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency. HOMA-B allows a quantitative assessment of the contributions of deficient beta cell function to the fasting hyperglycemia. HOMA-B is measured as a percent of the normal population (normal beta cell function = 100%, which is used as a reference in the calculation). The higher the percent the better for the participant. (NCT00375492)
Timeframe: baseline, Week 24

InterventionRatio (Geometric Mean)
Group A (Exenatide)1.46
Group B (Placebo)1.29

[back to top]

Rate of Hypoglycemic Events

Overall rate of hypoglycemia, adjusted for 1 year (ie., events of hypoglycemia per participant per year). (NCT00375492)
Timeframe: 24 weeks

Interventionevents per patient per year (Least Squares Mean)
Group A (Exenatide)7.14
Group B (Placebo)4.58

[back to top]

Number of Participants With Hypoglycemic Events During the Study

Number of participants experiencing one or more events of hypoglycemia at any point in the study (NCT00375492)
Timeframe: Baseline to 24 weeks

Interventionparticipants (Number)
Group A (Exenatide)33
Group B (Placebo)30

[back to top]

Change From Baseline in Low Density Lipoprotein (LDL) Cholesterol at Week 24

Change in LDL cholesterol from baseline (Week 0) after 24 weeks of treatment (ie., LDL cholesterol at week 24 minus LDL cholesterol at week 0). LDL cholesterol measured in mmol/L (NCT00375492)
Timeframe: baseline, Week 24

Interventionmmol/L (Least Squares Mean)
Group A (Exenatide)-0.06
Group B (Placebo)-0.04

[back to top]

Change From Baseline in Waist Circumference at Week 24

Change in waist circumference from baseline after 24 weeks of treatment (i.e., waist circumference at week 24 minus waist circumference at week 0). Waist measured in centimeters (cm). (NCT00375492)
Timeframe: baseline, Week 24

Interventioncm (Least Squares Mean)
Group A (Exenatide)-5.33
Group B (Placebo)-4.18

[back to top]

Change From Baseline in Total Cholesterol at Week 24

Change in total cholesterol from baseline after 24 weeks of treatment (i.e., total cholesterol at week 24 minus total cholesterol at week 0). Total cholesterol measured in mmol/L. (NCT00375492)
Timeframe: baseline, week 24

Interventionmmol/L (Least Squares Mean)
Group A (Exenatide)-0.16
Group B (Placebo)-0.03

[back to top]

Change in Body Weight

Change in body weight from baseline after 26 weeks of treatment (i.e., body weight at week 26 minus body weight at week 0) (NCT00434954)
Timeframe: Baseline and 26 weeks

Interventionkg (Least Squares Mean)
Exenatide Twice Daily-4.10
Premixed Insulin Aspart Twice Daily1.02

[back to top]

Change in Body Mass Index (BMI)

Change in BMI from baseline after 26 weeks of treatment (i.e., BMI at week 26 minus BMI at week 0) (NCT00434954)
Timeframe: Baseline and 26 weeks

Interventionkg/m^2 (Least Squares Mean)
Exenatide Twice Daily-1.39
Premixed Insulin Aspart Twice Daily0.32

[back to top]

Change in Glycosylated Hemoglobin (HbA1c)

Change in HbA1c from baseline after 26 weeks of treatment (i.e., HbA1c at week 26 minus HbA1c at week 0) (NCT00434954)
Timeframe: Baseline and 26 weeks

InterventionPercentage of glycosylated hemoglobin (Least Squares Mean)
Exenatide Twice Daily-1.00
Premixed Insulin Aspart Twice Daily-1.14

[back to top]

Incidence of Nocturnal Hypoglycemia (Percentage of Subjects Who Experienced at Least One Episode of Nocturnal Hypoglycemia During the 26 Week Treatment Period)

Risk for first nocturnal (night-time) hypoglycemic episode to occur up to week 26 (percentage of subjects who experienced at least one episode of nocturnal hypoglycemia during the 26 week treatment period) [i.e., number of subjects who experienced nocturnal hypoglycemia divided by total number of subjects times 100%]. (NCT00434954)
Timeframe: 26 weeks

InterventionPercentage of participants (Number)
Exenatide Twice Daily3.9
Premixed Insulin Aspart Twice Daily7.0

[back to top]

Percentage of Subjects Achieving HbA1c Target of < 6.5%

Percentage of subjects achieving HbA1c target of < 6.5% at the end of study (week 26) [i.e., number of subjects who achieved HbA1c < 6.5% divided by total number of subjects times 100%]. (NCT00434954)
Timeframe: 26 weeks

InterventionPercentage of participants (Number)
Exenatide Twice Daily27.6
Premixed Insulin Aspart Twice Daily24.9

[back to top]

Percentage of Subjects Achieving HbA1c Target of < 7.0%

Percentage of subjects achieving HbA1c target of < 7.0% at the end of study (week 26) [i.e., number of subjects who achieved HbA1c < 7.0% divided by total number of subjects times 100%]. (NCT00434954)
Timeframe: 26 weeks

InterventionPercentage of participants (Number)
Exenatide Twice Daily49.2
Premixed Insulin Aspart Twice Daily56.6

[back to top]

7 Point Self-monitored Blood Glucose (SMBG) Profiles

7-point self-monitored blood glucose profiles at baseline and the end of the study, measured at 7 times during the day (pre-breakfast, 2 hours post-breakfast, pre-lunch, 2 hours post-lunch, pre-dinner, 2 hours post-dinner, and 3:00am). (NCT00434954)
Timeframe: Baseline and 26 weeks

,
Interventionmg/dL (Mean)
Pre-breakfast at baseline (week 0)Pre-breakfast at endpoint (week 26)2 hrs post-breakfast at baseline (week 0)2 hrs post-breakfast at endpoint (week 26)Pre-lunch at baseline (week 0)Pre-lunch at endpoint (week 26)2 hrs post-lunch at baseline (week 0)2 hrs post-lunch at endpoint (week 26)Pre-dinner at baseline (week 0)Pre-dinner at endpoint (week 26)2 hrs post-dinner at baseline (week 0)2 hrs post-dinner at endpoint (week 26)3:00 am at baseline (week 0)3:00 am at endpoint (week 26)
Exenatide Twice Daily8.9337.77410.8218.0148.4437.5069.6988.5138.6847.61610.2417.7278.3237.518
Premixed Insulin Aspart Twice Daily9.0057.29310.9028.3048.3576.6569.8998.2168.7597.19410.2598.1438.4756.999

[back to top]

Blood Lipid Levels

Total cholesterol, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol (calculated), and triglyceride levels at baseline (week 0) and the end of the study (week 26) (NCT00434954)
Timeframe: Baseline and 26 weeks

,
Interventionmmol/L (Mean)
Total cholesterol at baseline (week 0)Total cholesterol at endpoint (week 26)HDL cholesterol at baseline (week 0)HDL cholesterol at endpoint (week 26)LDL cholesterol (calculated) at baseline (week 0)LDL cholesterol (calculated) at endpoint (week 26)Triglycerides at baseline (week 0)Triglycerides at endpoint (week 26)
Exenatide Twice Daily5.1474.9711.2341.2442.8452.7382.3912.234
Premixed Insulin Aspart Twice Daily5.0845.0501.2551.3192.7682.8522.4102.006

[back to top]

Incidence of Hypoglycemia (Percentage of Participants With at Least One Hypoglycemic Episode)

Risk for first hypoglycemic episode (blood glucose <=3.9 mmol/L or severe episode) to occur up to week 26 (NCT00434954)
Timeframe: 26 weeks

InterventionPercentage of participants (Number)
Exenatide Twice Daily8.0
Premixed Insulin Aspart Twice Daily20.5

[back to top]

Patient Reported Outcomes: Diabetes Treatment Satisfaction Questionnaire (DTSQ)

Total DTSQ treatment satisfaction score at baseline (week 0) and after 26 weeks of treatment (LOCF). Total DTSQ treatment satisfaction score is derived as sum score of the individual components 1 and 4-8 of the DTSQ questionnaire. Each component is scored on a scale of 0 (worst case) to 6 (best case). Higher values represent higher treatment satisfaction. (NCT00434954)
Timeframe: Baseline and 26 weeks

,
Interventionscores on DTSQ scale (Mean)
DTSQ score at baseline (week 0)DTSQ score at endpoint (week 26)
Exenatide Twice Daily29.530.6
Premixed Insulin Aspart Twice Daily29.729.3

[back to top]

Patient Reported Outcomes: Quality of Life (SF-12)

SF-12 Physical and Mental Component Summary Scores at baseline (week 0) and after 26 weeks of treatment (LOCF). SF-12 Physical and Mental Component Summary Scores are normalized scores ranging from 0 (worst case) to 100 (best case), and are derived from responses to 12 questions. Scores > 50 indicate an above-average health status. (NCT00434954)
Timeframe: Baseline and 26 weeks

,
Interventionscores on SF-12 scale (Mean)
Physical Component at baseline (week 0)Physical Component at endpoint (week 26)Mental Component at baseline (week 0)Mental Component at endpoint (week 26)
Exenatide Twice Daily35.539.131.331.1
Premixed Insulin Aspart Twice Daily36.337.728.329.6

[back to top]

Incidence of Hypoglycemic Episodes [Blood Glucose <= 3.0 mmol/L or Severe] (Percentage of Subjects Who Experienced at Least One Treatment-emergent Hypoglycemic Episode During the 26-week Treatment Period)

Risk for the first hypoglycemic episode to occur up to Week 26 (percentage of subjects who experienced at least one treatment-emergent hypoglycemic episode during the 26-week treatment period)[ i.e., number of subjects experiencing at least one hypoglycemic episode divided by total number of subjects times 100%] (NCT00434954)
Timeframe: 26 weeks

InterventionPercentage of participants (Number)
Exenatide Twice Daily1.8
Premixed Insulin Aspart Twice Daily6.3

[back to top]

Mean Plasma Glucose Area Under the Curve (AUC) for Blood Glucose Concentration in the Exenatide 1.25 mcg or Exenatide 2.5 mcg Treated Groups Along With Insulin, Compared to Insulin Alone

Post-prandial blood glucose concentration in terms of mean AUC (0-120 min) was determined in subjects treated with either Exenatide 1.25 mcg or Exenatide 2.5 along with insulin, compared to insulin alone, given as a single subcutaneous injection (NCT00456300)
Timeframe: 0-120 minutes post-dose

Interventionmmol*L/min (Mean)
Exenatide 1.25 mcg + Insulin49
Exenatide 2.5 mcg + Insulin44
Insulin Monotherapy379

[back to top]

Change in Two Hour Glucose

(NCT00456885)
Timeframe: 16 weeks from the start of each treatment period.

Interventionmg/dl (Mean)
Exenatide-10
Placebo-0.5

[back to top]

Change in Insulin

(NCT00456885)
Timeframe: 16 weeks from the start of each treatment period.

Interventionmicrounits per liter (Mean)
Exenatide1.1
Placebo0.4

[back to top]

Change in Fasting Glucose

(NCT00456885)
Timeframe: 16 weeks from the start of each treatment period.

Interventionmg/dl (Mean)
Exenatide0.5
Placebo3.1

[back to top]

Change in Body Mass Index

(NCT00456885)
Timeframe: 16 weeks from the start of each treatment period.

InterventionKg/m^2 (Mean)
Exenatide-0.93
Placebo0.18

[back to top]

Adiponectin

(NCT00456885)
Timeframe: 16 weeks after the beginning of each treatment

Interventionmicrogram per ml (Mean)
Exenatide0.4
Placebo0.07

[back to top]

Changes in Body Composition

Per cent body body fat was assessed using bio-electrical impedance with a BIA; RJL System Quantum II Bioelectrical Body Composition Analyzer. The data is reported as per cent body fat. (NCT00456885)
Timeframe: 16 weeks after the beginning of each treatment

Interventionper cent (Mean)
Exenatide-0.4
Placebo-0.7

[back to top]

Change in Waist Circumference

(NCT00456885)
Timeframe: 16 weeks from the start of each treatment period.

Interventioncentimeters (Mean)
Exenatide-1.68
Placebo0.94

[back to top]

Systolic Blood Pressure

Blood pressure was measured using a Dynamap automated monitoring device. The change is reported as the blood pressure measured at the beginning of the treatment group and after 16 weeks. We are reporting the change in the systolic blood presssure recorded. (NCT00456885)
Timeframe: 16 weeks after the beginning of each treatment

Interventionmm of mercury (Mean)
Exenatide-2.5
Placebo-1.3

[back to top]

REE

Resting Energy Expenditure (NCT00456885)
Timeframe: 16 weeks from the start of each treatment period.

InterventionKilocalories (Mean)
Exenatide-13.7
Placebo6.5

[back to top]

HOMA Score

(NCT00456885)
Timeframe: 16 weeks from the start of each treatment period.

InterventionRatio fasting glucose to insulin (Mean)
Exenatide0.2
Placebo0.2

[back to top]

Diastolic Blood Pressure

(NCT00456885)
Timeframe: 16 weeks after the beginning of each treatment

Interventionmm of mercury (Mean)
Exenatide-1.2
Placebo-0.4

[back to top]

Changes in Leptin

(NCT00456885)
Timeframe: 16 weeks from the start of each treatment period.

Interventionng/ml (Mean)
Exenatide-3.7
Placebo-0.2

[back to top]

Change in Weight

Change in weight at the end of each treatment period. (NCT00456885)
Timeframe: 16 weeks after the beginning of each treatment

Interventionkilograms (Mean)
Exenatide-2.49
Placebo0.43

[back to top]

Change in Total Cholesterol

Change in total cholesterol from baseline after 24 weeks of treatment (i.e., total cholesterol at week 24 minus total cholesterol at week 0) (NCT00500370)
Timeframe: 24 weeks

,
Interventionmmol/L (Least Squares Mean)
Baseline (Week 0)Change at Endpoint (Week 24)
Group A (Exenatide)4.870.19
Group B (Placebo)4.880.33

[back to top]

Change in Serum Glucose AUC Levels Following Oral Glucose Tolerance Test (OGTT)

Change in serum glucose AUC following OGTT (week 24 compared to week 0) (i.e., serum glucose AUC at week 24 minus serum glucose AUC at week 0) (NCT00500370)
Timeframe: 24 weeks

,
Intervention(mmol*hr)/L (Least Squares Mean)
Baseline (Week 0)Change at Endpoint (Week 24)
Group A (Exenatide)15.73-0.47
Group B (Placebo)15.19-0.01

[back to top]

Change in Waist-to-hip Ratio

Waist-to-hip ratio at week 24 compared to waist-to-hip ratio at week 0 (i.e., waist-to-hip ratio at week 24 minus waist-to-hip ratio at week 0). Waist-to-hip ratio equals waist circumference at given time point divided by hip circumference at given timepoint. (NCT00500370)
Timeframe: 24 weeks

,
InterventionRatio (Least Squares Mean)
Baseline (Week 0)Change at Endpoint (Week 24)
Group A (Exenatide)0.90-0.001
Group B (Placebo)0.900.002

[back to top]

Incidence of Patients That Demonstrate Normalization of Impaired Fasting Glucose (IFG) and/or Impaired Glucose Tolerance (IGT)

Number of patients in each treatment group that demonstrate normalization of IFG and/or IGT by week 24 (NCT00500370)
Timeframe: 24 weeks

InterventionParticipants (Number)
Group A (Exenatide)13
Group B (Placebo)9

[back to top]

Incidence of Patients That Demonstrate Overt Signs of Diabetes Mellitus Diagnosis

Number of patients in each treatment group that demonstrate overt signs of diabetes mellitus diagnosis by week 24 (NCT00500370)
Timeframe: 24 weeks

InterventionParticipants (Number)
Group A (Exenatide)3
Group B (Placebo)2

[back to top]

Percentage of Patients Experiencing >=5% Weight Loss

Percentage of exenatide and placebo treated patients experiencing >=5% weight loss after 24 weeks of treatment (i.e., [weight at week 0 minus weight at week 24] divided by weight at week 0 times 100% >=5%) (NCT00500370)
Timeframe: 24 weeks

Interventionpercentage of patients (Number)
Group A (Exenatide)31.5
Group B (Placebo)16.5

[back to top]

Ratio of Endpoint (LOCF) to Baseline for Fasting Triglycerides (Logarithmically Transformed)

Ratio of triglycerides at week 24 compared to triglycerides at week 0 (i.e., triglycerides at week 24 divided by triglycerides at week 0) (NCT00500370)
Timeframe: 24 weeks

InterventionRatio (Least Squares Mean)
Group A (Exenatide)0.99
Group B (Placebo)0.96

[back to top]

Ratio of Endpoint (LOCF) to Baseline for Homeostatic Model Assessment-Insulin Sensitivity (HOMA-S) (Logarithmically Transformed)

Ratio of HOMA-S at week 24 to HOMA-S at week 0 (i.e., HOMA-S at week 24 divided by HOMA-S at week 0). HOMA-S is a measure of insulin sensitivity. (NCT00500370)
Timeframe: 24 weeks

InterventionRatio (Least Squares Mean)
Group A (Exenatide)0.92
Group B (Placebo)0.91

[back to top]

Ratio of Endpoint (LOCF) to Baseline for Homeostatic Model Assessment-Beta Cell (HOMA-B) (Logarithmically Transformed)

Ratio of HOMA-B at week 24 to HOMA-B at week 0 (i.e., HOMA-B at week 24 divided by HOMA-B at week 0). HOMA-B is a measure of beta cell function. (NCT00500370)
Timeframe: 24 weeks

InterventionRatio (Least Squares Mean)
Group A (Exenatide)1.06
Group B (Placebo)1.08

[back to top]

Change in Low Density Lipoprotein (LDL) Cholesterol

Change in LDL cholesterol from baseline following 24 weeks of treatment (i.e., LDL cholesterol at week 24 minus LDL cholesterol at week 0) (NCT00500370)
Timeframe: 24 weeks

,
Interventionmmol/L (Least Squares Mean)
Baseline (Week 0)Change at Endpoint (Week 24)
Group A (Exenatide)2.860.20
Group B (Placebo)2.790.34

[back to top]

Change in High Sensitivity C-reactive Protein (hsCRP)

Change in hsCRP levels from baseline following 24 weeks of treatment (i.e., hsCRP at week 24 minus hsCRP at week 0) (NCT00500370)
Timeframe: 24 weeks

,
Interventionpmol/L (Least Squares Mean)
Baseline (Week 0)Change at Endpoint (Week 24)
Group A (Exenatide)8.61-1.31
Group B (Placebo)8.03-0.44

[back to top]

Change in High Density Lipoprotein (HDL) Cholesterol

Change in HDL cholesterol from baseline after 24 weeks of treatment (i.e., HDL cholesterol at week 24 minus HDL cholesterol at week 0) (NCT00500370)
Timeframe: 24 weeks

,
Interventionmmol/L (Least Squares Mean)
Baseline (Week 0)Change at Endpoint (Week 24)
Group A (Exenatide)1.270.004
Group B (Placebo)1.360.06

[back to top]

Change in Glycosylated Hemoglobin (HbA1c)

Change in HbA1c from baseline following 24 weeks of treatment (i.e., HbA1c at week 24 minus HbA1c at week 0) (NCT00500370)
Timeframe: 24 weeks

,
Interventionpercent (Least Squares Mean)
Baseline (Week 0)Change at Endpoint (Week 24)
Group A (Exenatide)5.61-0.003
Group B (Placebo)5.580.09

[back to top]

Change in Fasting Serum Glucose

Change in fasting serum glucose from baseline following 24 weeks of treatment (i.e., fasting serum glucose at week 24 minus fasting serum glucose at week 0) (NCT00500370)
Timeframe: 24 weeks

,
Interventionmmol/L (Least Squares Mean)
Baseline (Week 0)Change at Endpoint (Week 24)
Group A (Exenatide)5.370.000
Group B (Placebo)5.37-0.02

[back to top]

Change in Body Weight

Change in body weight from baseline after 24 weeks of treatment (i.e., body weight at week 24 minus body weight at week 0) (NCT00500370)
Timeframe: 24 weeks

,
Interventionkg (Least Squares Mean)
Baseline (Week 0)Change at Endpoint (Week 24)
Group A (Exenatide)109.48-5.06
Group B (Placebo)107.64-1.61

[back to top]

Change in Body Mass Index (BMI)

Change in BMI from baseline after 24 weeks of treatment (i.e., BMI at week 24 minus BMI at week 0) (NCT00500370)
Timeframe: 24 weeks

,
Interventionkg/m^2 (Least Squares Mean)
Baseline (Week 0)Change at Endpoint (Week 24)
Group A (Exenatide)39.64-1.83
Group B (Placebo)39.39-0.58

[back to top]

Treatment-emergent Antibody Status (Maximum Titer Level Experienced)

Patients who experienced specified treatment-emergent antibody status at any point during the study (grouped by maximum titer level experienced) (NCT00516048)
Timeframe: 24 weeks

,,
InterventionParticipants (Number)
Antibody negativeLow titer antibodiesHigher titer antibodies
Enrolled But Withdrew Before Receiving Treatment000
Exenatide: Treatment-Emergent Antibody Positive02517
Exenatide:Treatment-Emergent Antibody Negative1500

[back to top] [back to top]

Change in Hemoglobin A1c (HbA1c) From Baseline to Endpoint

Change in HbA1c from baseline (Week 0) to endpoint (Week 24) by treatment-emergent antibody status (NCT00516048)
Timeframe: 24 weeks

,,
Interventionpercent (Mean)
Baseline HbA1c (Week 0)Change in HbA1c at endpoint (Week 24)
Enrolled But Withdrew Before Receiving Treatment00
Exenatide: Treatment-Emergent Antibody Positive8.05-0.30
Exenatide:Treatment-Emergent Antibody Negative8.13-1.03

[back to top]

Change in Nighttime (2400-0600) Heart Rate From Baseline to Endpoint

Change from baseline to endpoint in nighttime (2400-0600) heart rate as measured by an ambulatory blood pressure monitor (NCT00516074)
Timeframe: 12 weeks

,
Interventionbeats per minute (Least Squares Mean)
Baseline (Week 0)Change at endpoint (Week 12)
Exenatide BID71.541.43
Placebo71.77-0.28

[back to top]

Change in Mean 24-hour Heart Rate From Baseline to Endpoint

Change from baseline to endpoint in average heart rate measured over 24 hours by an ambulatory blood pressure monitor. (NCT00516074)
Timeframe: 12 weeks

,
Interventionbeats per minute (Least Squares Mean)
Baseline (Week 0)Change at endpoint (Week 12)
Exenatide BID74.832.14
Placebo74.47-0.71

[back to top]

Change in Mean 24 Hour Systolic Blood Pressure From Baseline to Endpoint

Change from baseline to endpoint in average systolic blood pressure measured over 24 hours by an ambulatory blood pressure monitor (NCT00516074)
Timeframe: 12 weeks

,
InterventionmmHg (Least Squares Mean)
Baseline (Week 0)Change at endpoint (Week 12)
Exenatide BID126.61-0.81
Placebo119.93-0.34

[back to top]

Change in Mean 24 Hour Diastolic Blood Pressure From Baseline to Endpoint

Change from baseline to endpoint in average diastolic blood pressure measured over 24 hours by an ambulatory blood pressure monitor (NCT00516074)
Timeframe: 12 weeks

,
InterventionmmHg (Least Squares Mean)
Baseline (Week 0)Change at endpoint (Week 12)
Exenatide BID75.70-0.60
Placebo70.54-2.34

[back to top]

Change in Hemoglobin A1c (HbA1c) From Baseline to Endpoint

Change from baseline to endpoint in HbA1c (NCT00516074)
Timeframe: 12 weeks

,
Interventionpercent (Least Squares Mean)
Baseline (Week 0)Change at endpoint (Week 12)
Exenatide BID7.50-0.15
Placebo7.110.12

[back to top]

Change in Daytime Heart Rate From Baseline to Endpoint

Change from baseline to endpoint in daytime heart rate as measured by an ambulatory blood pressure monitor (NCT00516074)
Timeframe: 12 weeks

,
Interventionbeats per minute (Least Squares Mean)
Baseline (Week 0)Change at endpoint (Week 12)
Exenatide BID75.972.35
Placebo75.37-0.87

[back to top]

Number of Participants Who Achieved Target Values for HbA1c <6.5% and >=6.5% to <7% at Weeks 4, 5, 7, 8, 9, 12, 15, and 16

The number of participants who achieved target values for HbA1c (i.e., HbA1c <6.5% and >=6.5% to <7%) were assessed. The last observation carried forward (LOCF) method was used to impute missing data, in which the last valid observation recorded on treatment (scheduled or unscheduled) was used to impute the missing measurement. For participants who had missing observations before their last observation on treatment, the closest previous non-missing on-treatment observation was carried forward to missing visits. If a participant had missing observation(s) immediately after Baseline, the Baseline observation was not carried forward and was left as missing. (NCT00518115)
Timeframe: Weeks (W) 4, 5, 7, 8, 9, 12, 15, and 16

,,,,,,,,,
InterventionParticipants (Number)
W4: <6.5%, n=47,34,33,34,28,29,31,34,34,30W4: >=6.5% to <7%, n=47,34,33,34,28,29,31,34,34,30W5: <6.5%, n=49,34,34,34,29,30,32,34,35,31W5: >=6.5% to <7%, n=49,34,34,34,29,30,32,34,35,31W7: <6.5%, n=50,34,34,34,29,30,32,34,35,32W7: >=6.5% to <7%, n=50,34,34,34,29,30,32,34,35,32W8: <6.5%, n=50,34,34,34,29,30,32,34,35,32W8: >=6.5% to <7%, n=50,34,34,34,29,30,32,34,35,32W9: <6.5%, n=50,34,34,34,29,30,32,34,35,32W9: >=6.5% to <7%, n=50,34,34,34,29,30,32,34,35,32W12: <6.5%, n=50,34,34,34,29,30,32,34,35,33W12:>=6.5% to <7%, n=50,34,34,34,29,30,32,34,35,33W15: <6.5%, n=50,34,34,34,29,30,32,34,35,33W15:>=6.5% to <7%, n=50,34,34,34,29,30,32,34,35,33W16: <6.5%, n=50,34,34,34,29,30,32,34,35,33W16:>=6.5% to <7%, n=50,34,34,34,29,30,32,34,35,33
Albiglutide 100 mg Every 4 Weeks364125851198789788
Albiglutide 15 mg Bi-weekly06151919110374753
Albiglutide 15 mg Weekly1827444867584848
Albiglutide 30 mg Bi-weekly081931141231131368412
Albiglutide 30 mg Weekly484885688511587105
Albiglutide 4 mg Weekly0515141625242533
Albiglutide 50 mg Bi-weekly3521169710710811109108
Albiglutide 50 mg Every 4 Weeks1617282429293835
Exenatide BID0507192729384648
Placebo18241911039373828

[back to top]

Change From Baseline in Fasting Insulin at Weeks 5, 8, 12, and 16

Fasting insulin levels were measured after the participant had not eaten (fasted) for at least eight hours prior to the sampling. The Baseline insulin value is the last non-missing value before the start of treatment. Change from Baseline in insulin was calculated as the post-Baseline value minus the Baseline value. The LOCF method was used to impute missing data, in which the last valid observation recorded on treatment (scheduled or unscheduled) was used to impute the missing measurement. For participants who had missing observations before their last observation on treatment, the closest previous non-missing on-treatment observation was carried forward to missing visits. If a participant had missing observation(s) immediately after Baseline, the Baseline observation was not carried forward and was left as missing. (NCT00518115)
Timeframe: Baseline and Weeks 5, 8, 12, and 16

,,,,,,,,,
InterventionPicomoles per liter (pmol/L) (Mean)
Week 5, n=47,31,32,33,27,28,31,30,33,30Week 8, n=49,32,33,34,28,29,32,31,33,31Week 12, n=49,32,33,34,28,29,32,31,33,33Week 16, n=49,32,33,34,28,29,32,31,33,33
Albiglutide 100 mg Every 4 Weeks36.26.611.618.4
Albiglutide 15 mg Bi-weekly28.518.617.821.9
Albiglutide 15 mg Weekly-16.4-8.5-7.9-19.9
Albiglutide 30 mg Bi-weekly-38.3-14.4-26.1-24.0
Albiglutide 30 mg Weekly0.42.4-1.125.1
Albiglutide 4 mg Weekly-12.4-16.5-12.42.9
Albiglutide 50 mg Bi-weekly-8.4-16.80.2-17.4
Albiglutide 50 mg Every 4 Weeks11.112.938.012.9
Exenatide BID29.65.418.017.4
Placebo5.19.28.8-5.8

[back to top]

Change From Baseline in Fasting Plasma Glucose (FPG) at Weeks 4, 5, 7, 8, 9, 12, 15, and 16

The FPG test measures blood sugar levels after the participant has not eaten (fasted) for at least eight hours prior to the sampling. The Baseline FPG value is the last non-missing value before the start of treatment. Change from Baseline in FPG was calculated as the post-Baseline value minus the Baseline value. The LOCF method was used to impute missing data, in which the last valid observation recorded on treatment (scheduled or unscheduled) was used to impute the missing measurement. For participants who had missing observations before their last observation on treatment, the closest previous non-missing on-treatment observation was carried forward to missing visits. If a participant had missing observation(s) immediately after Baseline, the Baseline observation was not carried forward and was left as missing. (NCT00518115)
Timeframe: Baseline and Weeks 4, 5, 7, 8, 9, 12, 15, and 16

,,,,,,,,,
InterventionMillimoles per liter (mmol/L) (Mean)
Week 4, n=47,33,32,32,29,28,32,32,34,32Week 5, n=47,33,32,32,29,28,32,32,34,32Week 7, n=47,33,32,32,29,28,32,32,34,33Week 8, n=47,33,32,32,29,28,32,32,34,33Week 9, n=47,33,32,32,29,28,32,32,34,33Week 12, n=47,33,32,32,29,28,32,32,34,33Week 15, n=47,33,32,32,29,28,32,32,34,33Week 16, n=47,33,32,32,29,28,32,32,34,33
Albiglutide 100 mg Every 4 Weeks-0.61-2.12-1.07-1.29-2.25-1.50-1.27-1.22
Albiglutide 15 mg Bi-weekly-1.06-1.41-1.16-1.29-1.29-1.11-1.45-1.28
Albiglutide 15 mg Weekly-0.58-1.05-0.13-0.80-0.71-0.70-0.70-0.72
Albiglutide 30 mg Bi-weekly-0.97-1.72-1.51-1.27-1.64-1.57-1.71-1.58
Albiglutide 30 mg Weekly-1.39-1.53-1.54-1.60-1.49-1.85-1.54-1.44
Albiglutide 4 mg Weekly-0.99-1.02-0.80-1.22-1.13-1.04-0.67-0.47
Albiglutide 50 mg Bi-weekly-1.35-2.17-1.87-1.29-1.68-1.49-1.66-1.32
Albiglutide 50 mg Every 4 Weeks-0.14-1.55-0.41-0.66-1.48-0.49-0.79-0.72
Exenatide BID-1.11-1.06-1.25-1.43-1.54-1.32-1.27-0.80
Placebo-0.40-0.40-0.19-0.44-0.25-0.27-0.44-0.10

[back to top]

Change From Baseline in Functional Living Index - Emesis (FLIE) Scores at Week 16

The FLIE questionnaire is used to record the participant's feelings/opinions concerning the effects of nausea/vomiting on their quality of life during the past five days. Participants completed the questionnaire by responding to 18 questions. The first set of 9 questions refer to nausea, and the second set of 9 questions refer to vomiting. Each question is scored on a seven-point visual analog scale (1 to 7). On this scale, a score of 1 corresponds to 0 millimeters (mm), and a score of 7 correspond to 100 mm. Anything in between is marked at the appropriate point on the scale and is measured in mm. Data are reported in mm in this table. In FLIE questions (FLIEQ) 1, 2, 4, 5, 7, 8, 9, 10, 12, 13, 14, 16, and 17, a score of 1 indicates no effect on the quality of life, and a score of 7 indicates a great effect on the quality of life. In FLIEQ 3, 6, 11, 15, and 18, a score of 1 indicates a great effect on the quality of life, and a score of 7 indicates no effect on the quality of life. (NCT00518115)
Timeframe: Baseline and Week 16

,,,,,,,,,
InterventionScore on a scale (Mean)
FLIEQ1FLIEQ2FLIEQ3FLIEQ4FLIEQ5FLIEQ6FLIEQ7FLIEQ8FLIEQ9FLIEQ10FLIEQ11FLIEQ12FLIEQ13FLIEQ14FLIEQ15FLIEQ16FLIEQ17FLIEQ18
Albiglutide 100 mg Every 4 Weeks-2.8-0.27.3-1.8-1.43.9-1.9-2.3-3.2-2.04.0-0.8-2.1-2.14.0-1.5-0.66.9
Albiglutide 15 mg Bi-weekly8.65.910.35.60.210.25.710.15.64.57.95.39.85.35.68.24.510.1
Albiglutide 15 mg Weekly1.02.6-4.0-2.8-1.8-0.51.5-1.0-0.5-1.6-0.5-0.8-2.2-1.4-4.9-1.4-1.2-3.2
Albiglutide 30 mg Bi-weekly-1.0-0.83.9-1.6-1.34.2-1.0-0.7-0.7-0.33.6-0.2-0.3-0.13.5-0.1-0.27.1
Albiglutide 30 mg Weekly4.63.018.61.52.920.00.22.62.3-0.121.91.81.01.819.7-0.5-1.214.9
Albiglutide 4 mg Weekly5.75.510.36.46.49.45.75.75.35.813.86.46.36.414.26.36.314.2
Albiglutide 50 mg Bi-weekly8.24.718.25.94.518.04.96.24.04.318.34.44.34.318.44.54.318.5
Albiglutide 50 mg Every 4 Weeks-0.3-0.64.5-1.91.55.6-0.1-0.4-0.10.27.2-0.40.0-0.11.50.9-1.15.7
Exenatide BID-4.4-3.57.8-3.5-4.03.6-3.1-3.5-3.4-4.93.3-3.1-4.0-4.17.0-3.8-4.16.9
Placebo-0.10.215.60.4-0.311.20.4-0.6-0.1-0.315.30.10.1-0.315.5-0.40.118.1

[back to top]

Percent Change From Baseline in Body Weight at Week 16

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline in body weight was calculated as the value at Week 16 minus the value at Baseline. Percent change from Baseline was calculated as the ([value at Week 16 minus the Baseline value] divided by the Baseline value) multiplied by 100. The LOCF method was used to impute missing data, in which the last valid observation recorded on treatment (scheduled or unscheduled) was used to impute the missing measurement. For participants who had missing observations before their last observation on treatment, the closest previous non-missing on-treatment observation was carried forward to missing visits. If a participant had missing observation(s) immediately after Baseline, the Baseline observation was not carried forward and was left as missing. (NCT00518115)
Timeframe: Baseline and Week 16

InterventionPercent change (Mean)
Placebo-0.72
Exenatide BID-2.53
Albiglutide 4 mg Weekly-0.94
Albiglutide 15 mg Weekly-1.04
Albiglutide 30 mg Weekly-1.59
Albiglutide 15 mg Bi-weekly-1.97
Albiglutide 30 mg Bi-weekly-1.69
Albiglutide 50 mg Bi-weekly-1.32
Albiglutide 50 mg Every 4 Weeks-1.37
Albiglutide 100 mg Every 4 Weeks-1.89

[back to top]

Change From Baseline in HbA1c at Weeks 4, 5, 7, 8, 9, 12, 15, and 16

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over a 2- to 3-month period. The Baseline HbA1c value is defined as the last non-missing value before the start of treatment. Change from Baseline in HbA1c was calculated as the post-Baseline value minus the value at Baseline. The last observation carried forward (LOCF) method was used to impute missing data, in which the last valid observation recorded on treatment (scheduled or unscheduled) was used to impute the missing measurement. For participants who had missing observations before their last observation on treatment, the closest previous non-missing on-treatment observation was carried forward to missing visits. If a participant had missing observation(s) immediately after Baseline, the Baseline observation was not carried forward and was left as missing. (NCT00518115)
Timeframe: Baseline and Weeks 4, 5, 7, 8, 9, 12, 15, and 16

,,,,,,,,,
InterventionPercentage of HbA1c in the blood (Mean)
Week 4, n=47,34,33,34,28,29,31,34,34,30Week 5, n=49,34,34,34,29,30,32,34,35,31Week 7, n=50,34,34,34,29,30,32,34,35,32Week 8, n=50,34,34,34,29,30,32,34,35,32Week 9, n=50,34,34,34,29,30,32,34,35,32Week 12, n=50,34,34,34,29,30,32,34,35,33Week 15, n=50,34,34,34,29,30,32,34,35,33Week 16, n=50,34,34,34,29,30,32,34,35,33
Albiglutide 100 mg Every 4 Weeks-0.42-0.65-0.63-0.68-0.82-0.84-0.88-0.87
Albiglutide 15 mg Bi-weekly-0.35-0.42-0.52-0.54-0.56-0.59-0.61-0.56
Albiglutide 15 mg Weekly-0.33-0.39-0.44-0.50-0.55-0.58-0.49-0.49
Albiglutide 30 mg Bi-weekly-0.34-0.510.64-0.67-0.71-0.71-0.79-0.79
Albiglutide 30 mg Weekly-0.56-0.62-0.79-0.77-0.85-0.96-0.86-0.87
Albiglutide 4 mg Weekly-0.12-0.16-0.19-0.24-0.19-0.18-0.19-0.11
Albiglutide 50 mg Bi-weekly-0.45-0.58-0.68-0.71-0.77-0.79-0.80-0.79
Albiglutide 50 mg Every 4 Weeks-0.41-0.47-0.45-0.41-0.54-0.51-0.58-0.55
Exenatide BID-0.23-0.32-0.36-0.45-0.51-0.56-0.53-0.54
Placebo-0.14-0.09-0.15-0.17-0.21-0.19-0.27-0.17

[back to top]

Change From Baseline in Fasting C-peptide at Weeks 5, 8, 12, and 16

Fasting C-peptide levels were measured after the participant had not eaten (fasted) for at least eight hours prior to the sampling. The Baseline C-peptide value is the last non-missing value before the start of treatment. Change from Baseline in C-peptide was calculated as the post-Baseline value minus the Baseline value. The LOCF method was used to impute missing data, in which the last valid observation recorded on treatment (scheduled or unscheduled) was used to impute the missing measurement. For participants who had missing observations before their last observation on treatment, the closest previous non-missing on-treatment observation was carried forward to missing visits. If a participant had missing observation(s) immediately after Baseline, the Baseline observation was not carried forward and was left as missing. (NCT00518115)
Timeframe: Baseline and Weeks 5, 8, 12, and 16

,,,,,,,,,
InterventionNanomoles per liter (nmol/L) (Mean)
Week 5, n=48,33,32,33,27,28,32,33,35,30Week 8, n=50,34,33,34,28,29,32,33,35,31Week 12, n=50,34,33,34,28,29,32,33,35,33Week 16, n=50,34,33,34,28,29,32,33,35,33
Albiglutide 100 mg Every 4 Weeks0.2300.0070.062-0.005
Albiglutide 15 mg Bi-weekly0.015-0.038-0.098-0.059
Albiglutide 15 mg Weekly-0.034-0.026-0.046-0.075
Albiglutide 30 mg Bi-weekly-0.128-0.015-0.153-0.137
Albiglutide 30 mg Weekly0.0890.0950.0230.171
Albiglutide 4 mg Weekly-0.020-0.073-0.044-0.051
Albiglutide 50 mg Bi-weekly0.004-0.062-0.076-0.066
Albiglutide 50 mg Every 4 Weeks0.0720.0310.1550.076
Exenatide BID0.2740.1040.1740.216
Placebo0.004-0.019-0.092-0.091

[back to top]

Change From Baseline in Fasting Fructosamine at Weeks 5, 8, 12, and 16

Fasting fructosamine levels were measured after the participant had not eaten (fasted) for at least eight hours prior to the sampling. The Baseline fructosamine value is the last non-missing value before the start of treatment. Change from Baseline in fructosamine was calculated as the post-Baseline value minus the Baseline value. The LOCF method was used to impute missing data, in which the last valid observation recorded on treatment (scheduled or unscheduled) was used to impute the missing measurement. For participants who had missing observations before their last observation on treatment, the closest previous non-missing on-treatment observation was carried forward to missing visits. If a participant had missing observation(s) immediately after Baseline, the Baseline observation was not carried forward and was left as missing. (NCT00518115)
Timeframe: Baseline and Weeks 5, 8, 12, and 16

,,,,,,,,,
InterventionMicromoles per liter (µmol/L) (Mean)
Week 5, n=48,34,32,33,28,29,32,34,35,29Week 8, n=50,34,33,34,28,29,32,34,35,31Week 12, n=50,34,33,34,28,29,32,34,35,33Week 16, n=50,34,33,34,28,29,32,34,35,33
Albiglutide 100 mg Every 4 Weeks-32.5-29.5-31.1-24.9
Albiglutide 15 mg Bi-weekly-21.3-28.9-25.2-23.0
Albiglutide 15 mg Weekly-23.8-25.7-26.7-18.2
Albiglutide 30 mg Bi-weekly-34.4-40.9-40.2-38.1
Albiglutide 30 mg Weekly-30.7-35.5-31.8-30.8
Albiglutide 4 mg Weekly-11.9-13.1-12.5-7.8
Albiglutide 50 mg Bi-weekly-30.1-32.7-32.7-29.4
Albiglutide 50 mg Every 4 Weeks-29.2-24.9-26.4-26.5
Exenatide BID-24.7-30.6-30.1-24.6
Placebo-8.3-10.1-11.2-3.2

[back to top]

Mean Half-maximal Effective Concentration (EC50) of Albiglutide for HbA1c and FPG

EC50 is defined as the concentration of albiglutide that give a half-maximal HbA1c and FPG response. Samples were collected prior to the administration of study medication on dosing days (Weeks 0, 4, 5, 7, 8, 9, 12, 15) and on the day of the clinic visit at Weeks 16, 17, 18, 20, 23, and 27. The Week 5, 8, and 12 post-dose (PK sampling was performed within 6 days of drug administration. EC50 estimates used PK data as well as HbA1c and FPG efficacy data. EC50 was estimated from an inhibitory Emax (maximal possible effect of albiglutide) model. (NCT00518115)
Timeframe: Weeks 0, 4, 5, 7, 8, 9, 12, 15, 16, 17 18, 20, 23, and 27

Interventionnanograms per milliliter (Mean)
HbA1c, Treatment-naïve groupHbA1c, Prior monotherapy groupFPG
All Participants Receiving Any Dose of Albiglutide114012301970

[back to top]

Change From Baseline in Fasting Glucagon at Weeks 5, 8, 12, and 16

Fasting glucagon levels were measured after the participant had not eaten (fasted) for at least eight hours prior to the sampling. The Baseline glucagon value is the last non-missing value before the start of treatment. Change from Baseline in glucagon was calculated as the post-Baseline value minus the Baseline value. The LOCF method was used to impute missing data, in which the last valid observation recorded on treatment (scheduled or unscheduled) was used to impute the missing measurement. For participants who had missing observations before their last observation on treatment, the closest previous non-missing on-treatment observation was carried forward to missing visits. If a participant had missing observation(s) immediately after Baseline, the Baseline observation was not carried forward and was left as missing. (NCT00518115)
Timeframe: Baseline and Weeks 5, 8, 12, and 16

,,,,,,,,,
InterventionNanograms per liter (ng/L) (Mean)
Week 5, n=48,33,33,33,27,28,32,34,35,30Week 8, n=50,34,34,34,28,29,32,34,35,31Week 12, n=50,34,34,34,28,29,32,34,35,33Week 16, n=50,34,34,34,28,29,32,34,35,33
Albiglutide 100 mg Every 4 Weeks1.90.5-2.1-4.7
Albiglutide 15 mg Bi-weekly-6.0-12.4-11.1-7.1
Albiglutide 15 mg Weekly-13.9-15.6-20.1-20.5
Albiglutide 30 mg Bi-weekly-7.6-3.10.2-5.0
Albiglutide 30 mg Weekly-3.6-2.4-4.5-2.6
Albiglutide 4 mg Weekly-3.2-5.6-8.6-3.9
Albiglutide 50 mg Bi-weekly-11.6-10.7-3.3-10.9
Albiglutide 50 mg Every 4 Weeks-9.3-0.3-3.7-11.5
Exenatide BID-3.9-14.8-5.5-4.5
Placebo3.86.90.1-2.1

[back to top]

Number of Participants With the Indicated Response to Questions on the Hunger, Craving, and Fullness Questionnaire (HCFQ) at Week 16

"The HCFQ questionnaire is used to record how often participants have felt hungry or craved food, and how full participants felt after finishing meals, on average, in the past week. Participants answered the following seven questions with the response that best described their feelings of hunger, craving, and fullness: Q1, In the past week I was hungry; Q2, In the past week I thought about food; Q3, In the past week I wanted to eat; Q4, In the past week I ate more than I should have; Q5, In the past week, I craved specific food; Q6, In the past week when finished meals I felt full; Q7, In the past week when finished meals I felt satisfied." (NCT00518115)
Timeframe: Week 16

,,,,,,,,,
InterventionParticipants (Number)
Q1: AlwaysQ1: OftenQ1: SometimesQ1: RarelyQ1: NeverQ2: AlwaysQ2: OftenQ2: SometimesQ2: RarelyQ2: NeverQ3: AlwaysQ3: OftenQ3: SometimesQ3: RarelyQ3: NeverQ4: Yes, definitelyQ4: Yes, probablyQ4: I don't knowQ4: Probably notQ4: Definitely notQ5: AlwaysQ5: OftenQ5: SometimesQ5: RarelyQ5: NeverQ6: Much too fullQ6: Very fullQ6: Comfortably fullQ6: Slightly hungryQ6: Very hungryQ7: Extremely satisfiedQ7: SatisfiedQ7: Neither satisfied nor dissatisfiedQ7: DissatisfiedQ7: Extremely dissatisfied
Albiglutide 100 mg Every 4 Weeks16122126112109111131224103883121720114520
Albiglutide 15 mg Bi-weekly238601310411410402924201783041320015310
Albiglutide 15 mg Weekly07144007135014182029194041344151720117520
Albiglutide 30 mg Bi-weekly251701361501441610212443261520142000222100
Albiglutide 30 mg Weekly06142007114017131029173211450031810119110
Albiglutide 4 mg Weekly021531021450041610082101025113031800117300
Albiglutide 50 mg Bi-weekly221142239433212222525703963121800115500
Albiglutide 50 mg Every 4 Weeks262020361641361740792102051195271821223410
Exenatide BID051771151941052050185124121584022800027300
Placebo152841142851372630415107312191610102630327900

[back to top]

Change From Baseline in Triglycerides, Free Fatty Acids, Total Cholesterol, Low-density Lipoprotein Cholesterol, and High-density Lipoprotein Cholesterol at Weeks 5, 8, 12, and 16

Serum lipid components, including triglycerides (TG), free fatty acids (FFA), total cholesterol (CL), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C), were measured at Baseline and Weeks 5, 8, 12, and 16. The Baseline value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. The LOCF method was used to impute missing data, in which the last valid observation recorded on treatment (scheduled or unscheduled) was used to impute the missing measurement. For participants who had missing observations before their last observation on treatment, the closest previous non-missing on-treatment observation was carried forward to missing visits. If a participant had missing observation(s) immediately after Baseline, the Baseline observation was not carried forward and was left as missing. (NCT00518115)
Timeframe: Baseline and Weeks 5, 8, 12, and 16

,,,,,,,,,
Interventionmmol/L (Mean)
TG, Week 5, n=45,31,34,31,27,29,31,34,35,30TG, Week 8, n=50,33,34,34,27,30,32,34,35,31TG, Week 12, n=50,34,34,34,28,30,32,34,35,33TG, Week 16, n=50,34,34,34,28,30,32,34,35,33FFA, Week 5, n=48,33,32,33,27,28,32,34,35,29FFA, Week 8, n=50,34,33,34,28,29,32,34,35,31FFA, Week 12, n=50,34,33,34,28,29,32,34,35,33FFA, Week 16, n=50,34,33,34,28,29,32,34,35,33Total CL, Week 5, n=45,31,34,31,27,29,31,34,35,30Total CL, Week 8, n=50,33,34,34,27,30,32,34,35,31Total CL, Week 12, n=50,34,34,34,28,30,32,34,35,33Total CL, Week 16, n=50,34,34,34,28,30,32,34,35,33LDL-C, Week 5, n=41,29,31,29,26,28,29,27,32,29LDL-C, Week 8, n=45,32,32,32,26,30,31,28,32,30LDL-C, Week 12, n=45,33,32,32,28,30,31,28,32,32LDL-C, Week 16, n=46,33,32,32,28,30,31,28,32,32HDL-C, Week 5, n=45,31,34,31,27,29,31,34,35,30HDL-C, Week 8, n=50,33,34,34,27,30,32,34,35,31HDL-C, Week 12, n=50,34,34,34,28,30,32,34,35,33HDL-C, Week 16, n=50,34,34,34,28,30,32,34,35,33
Albiglutide 100 mg Every 4 Weeks-0.184-0.0280.070-0.1140.0060.1750.1230.094-0.2450.0600.0150.018-0.0910.0540.0100.054-0.053-0.016-0.045-0.048
Albiglutide 15 mg Bi-weekly-0.266-0.219-0.380-0.2580.0250.0170.0100.034-0.372-0.172-0.190-0.225-0.285-0.160-0.034-0.123-0.038-0.018-0.018-0.015
Albiglutide 15 mg Weekly-0.376-0.408-0.341-0.296-0.008-0.048-0.0130.016-0.139-0.162-0.140-0.037-0.155-0.157-0.152-0.045-0.0100.019-0.019-0.010
Albiglutide 30 mg Bi-weekly-0.147-0.150-0.269-0.331-0.028-0.027-0.051-0.005-0.140-0.094-0.092-0.178-0.082-0.052-0.004-0.062-0.045-0.030-0.041-0.031
Albiglutide 30 mg Weekly0.112-0.0090.1060.0990.0140.0460.0430.050-0.1130.002-0.0200.009-0.0680.0890.0040.003-0.063-0.061-0.061-0.046
Albiglutide 4 mg Weekly0.3030.1780.2210.122-0.0320.0330.0220.020-0.153-0.060-0.025-0.032-0.294-0.132-0.096-0.1090.0010.0060.004-0.007
Albiglutide 50 mg Bi-weekly-1.423-1.494-1.539-1.469-0.012-0.0040.0110.025-0.451-0.418-0.338-0.4470.0260.0530.1560.059-0.076-0.050-0.029-0.065
Albiglutide 50 mg Every 4 Weeks-0.725-0.175-0.362-0.426-0.0010.055-0.0300.012-0.407-0.183-0.134-0.217-0.106-0.087-0.061-0.088-0.047-0.054-0.033-0.033
Exenatide BID-0.068-0.2380.094-0.149-0.038-0.045-0.007-0.031-0.239-0.1820.054-0.031-0.153-0.0140.1050.096-0.047-0.058-0.003-0.025
Placebo-0.225-0.222-0.329-0.3770.0290.0340.0750.078-0.023-0.0500.0450.0950.0660.0660.1380.190-0.020-0.005-0.011-0.002

[back to top]

Mean Volume of Distribution of Albiglutide

Volume of distribution is defined as the apparent volume in which albiglutide is distributed. Samples were collected prior to the administration of study medication on dosing days (Weeks 0, 4, 5, 7, 8, 9, 12, 15) and on the day of the clinic visit at Weeks 16, 17, 18, 20, 23, and 27. The Week 5, 8, and 12 post-dose (PK sampling was performed within 6 days of drug administration. (NCT00518115)
Timeframe: Weeks 0, 4, 5, 7, 8, 9, 12, 15, 16, 17 18, 20, 23, and 27

InterventionLiters (Mean)
All Participants Receiving Any Dose of Albiglutide16400

[back to top]

Mean Clearance of Albiglutide

Clearance is defined as the volume of plasma cleared of albiglutide per unit time. Samples were collected prior to the administration of study medication on dosing days (Weeks 0, 4, 5, 7, 8, 9, 12, 15) and on the day of the clinic visit at Weeks 16, 17, 18, 20, 23, and 27. The Week 5, 8, and 12 post-dose pharmacokinetic (PK) sampling was performed within 6 days of drug administration. (NCT00518115)
Timeframe: Weeks 0, 4, 5, 7, 8, 9, 12, 15, 16, 17 18, 20, 23, and 27

Interventionmilliliters per hour (Mean)
All Participants Receiving Any Dose of Albiglutide94.2

[back to top]

Mean Absorption Rate of Albiglutide

Absorption rate is defined as the rate at which albiglutide enters the blood circulation. Samples were collected prior to the administration of study medication on dosing days (Weeks 0, 4, 5, 7, 8, 9, 12, 15) and on the day of the clinic visit at Weeks 16, 17, 18, 20, 23, and 27. The Week 5, 8, and 12 post-dose (PK sampling was performed within 6 days of drug administration. (NCT00518115)
Timeframe: Weeks 0, 4, 5, 7, 8, 9, 12, 15, 16, 17 18, 20, 23, and 27

Interventionhour^-1 (Mean)
All Participants Receiving Any Dose of Albiglutide0.0193

[back to top]

Change From Baseline in Waist Circumference at Week 16

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline in waist circumference was calculated as the value at Week 16 minus the value at Baseline. The last observation carried forward (LOCF) method was used to impute missing data, in which the last valid observation recorded on treatment (scheduled or unscheduled) was used to impute the missing measurement. For participants who had missing observations before their last observation on treatment, the closest previous non-missing on-treatment observation was carried forward to missing visits. If a participant had missing observation(s) immediately after Baseline, the Baseline observation was not carried forward and was left as missing. (NCT00518115)
Timeframe: Baseline and Week 16

InterventionCentimeters (Mean)
Placebo-0.51
Exenatide BID-3.53
Albiglutide 4 mg Weekly-1.50
Albiglutide 15 mg Weekly-3.16
Albiglutide 30 mg Weekly-1.14
Albiglutide 15 mg Bi-weekly-1.83
Albiglutide 30 mg Bi-weekly-0.47
Albiglutide 50 mg Bi-weekly-2.00
Albiglutide 50 mg Every 4 Weeks-0.88
Albiglutide 100 mg Every 4 Weeks-0.77

[back to top]

Change From Baseline in Glycosylated Hemoglobin (HbA1c) at Week 16

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over a 2- to 3-month period. The Baseline HbA1c value is defined as the last non-missing value before the start of treatment. Change from Baseline in HbA1c was calculated as the value at Week 16 minus the value at Baseline. Based on ANCOVA: Change = treatment + Baseline HbA1c + prior therapy + gender + region. The last observation carried forward (LOCF) method was used to impute missing data, in which the last valid observation recorded on treatment (scheduled or unscheduled) was used to impute the missing measurement. For participants who had missing observations before their last observation on treatment, the closest previous non-missing on-treatment observation was carried forward to missing visits. If a participant had missing observation(s) immediately after Baseline, the Baseline observation was not carried forward and was left as missing. (NCT00518115)
Timeframe: Baseline and Week 16

InterventionPercentage of HbA1c in the blood (Least Squares Mean)
Placebo-0.46
Albiglutide 4 mg Weekly-0.25
Albiglutide 15 mg Weekly-0.71
Albiglutide 30 mg Weekly-1.08
Albiglutide 15 mg Bi-weekly-0.68
Albiglutide 30 mg Bi-weekly-1.01
Albiglutide 50 mg Bi-weekly-1.03
Albiglutide 50 mg Every 4 Weeks-0.80
Albiglutide 100 mg Every 4 Weeks-1.06

[back to top]

Change From Baseline in Body Weight at Week 16

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline in body weight was calculated as the value at Week 16 minus the value at Baseline. The last observation carried forward (LOCF) method was used to impute missing data, in which the last valid observation recorded on treatment (scheduled or unscheduled) was used to impute the missing measurement. For participants who had missing observations before their last observation on treatment, the closest previous non-missing on-treatment observation was carried forward to missing visits. If a participant had missing observation(s) immediately after Baseline, the Baseline observation was not carried forward and was left as missing. (NCT00518115)
Timeframe: Baseline and Week 16

InterventionKilograms (Kg) (Mean)
Placebo-0.71
Exenatide BID-2.41
Albiglutide 4 mg Weekly-0.91
Albiglutide 15 mg Weekly-0.90
Albiglutide 30 mg Weekly-1.43
Albiglutide 15 mg Bi-weekly-1.76
Albiglutide 30 mg Bi-weekly-1.59
Albiglutide 50 mg Bi-weekly-1.14
Albiglutide 50 mg Every 4 Weeks-1.08
Albiglutide 100 mg Every 4 Weeks-1.65

[back to top]

Change in High-density Lipoprotein-cholesterol at Week 26

Change in High-density Lipoprotein-cholesterol (HDL-C) from baseline (week 0) to 26 weeks (end of randomisation) (NCT00518882)
Timeframe: week 0, week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.04
Exenatide -> Liraglutide -> Liraglutide-0.05

[back to top]

Change in Glycosylated A1c (HbA1c), Weeks 26-78

Percentage point change in glycosylated A1c (HbA1c) from Week 26 (end of randomisation) to Week 78 (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group) (NCT00518882)
Timeframe: week 26, week 78

Interventionpercentage point of total HbA1c (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.25
Exenatide -> Liraglutide -> Liraglutide-0.00

[back to top]

Change in Glycosylated A1c (HbA1c) at Week 78

Percentage point change in glycosylated A1c (HbA1c) from baseline (week 0) to 78 weeks (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group) (NCT00518882)
Timeframe: week 0, week 78

Interventionpercentage point of total HbA1c (Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.98
Exenatide -> Liraglutide -> Liraglutide-0.85

[back to top]

Change in Glycosylated A1c (HbA1c) at Week 26

Percentage point change in glycosylated A1c (HbA1c) from baseline (week 0) to 26 weeks (end of randomisation) (NCT00518882)
Timeframe: week 0, week 26

Interventionpercentage point of total HbA1c (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-1.12
Exenatide -> Liraglutide -> Liraglutide-0.79

[back to top]

Change in Free Fatty Acid, Weeks 26-78

Change in Free Fatty Acid (FFA) from Week 26 (end of randomisation) to Week 78 (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.06
Exenatide -> Liraglutide -> Liraglutide0.01

[back to top]

Change in Free Fatty Acid at Week 78

Change in Free Fatty Acid (FFA) from baseline (week 0) to 78 weeks (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.10
Exenatide -> Liraglutide -> Liraglutide-0.07

[back to top]

Change in Free Fatty Acid at Week 26

Change in Free Fatty Acid (FFA) from baseline (week 0) to 26 weeks (end of randomisation) (NCT00518882)
Timeframe: week 0, week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.17
Exenatide -> Liraglutide -> Liraglutide-0.10

[back to top]

Change in Fasting Plasma Glucose, Weeks 26-78

Change in fasting plasma glucose from Week 26 (end of randomisation) to Week 78 (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group) (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.7
Exenatide -> Liraglutide -> Liraglutide-0.1

[back to top]

Change in Fasting Plasma Glucose at Week 78

Change in fasting plasma glucose from baseline (week 0) to 78 weeks (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group) (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-1.3
Exenatide -> Liraglutide -> Liraglutide-0.8

[back to top]

Change in Fasting Plasma Glucose at Week 26

Change in fasting plasma glucose (FPG) from baseline (week 0) to 26 weeks (end of randomisation) (NCT00518882)
Timeframe: week 0, week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-1.61
Exenatide -> Liraglutide -> Liraglutide-0.60

[back to top]

Change in Body Weight, Weeks 26-78

Change in body weight from Week 26 (end of randomisation) to Week 78 (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group) (NCT00518882)
Timeframe: week 26, week 78

Interventionkg (Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.4
Exenatide -> Liraglutide -> Liraglutide-0.7

[back to top]

Change in Low-density Lipoprotein-cholesterol at Week 78

Change in Low-density Lipoprotein-cholesterol (LDL-C) from baseline (week 0) to 78 weeks (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.30
Exenatide -> Liraglutide -> Liraglutide-0.21

[back to top]

Change in Body Weight at Week 26

Change in body weight from baseline (week 0) to 26 weeks (end of randomisation) (NCT00518882)
Timeframe: week 0, week 26

Interventionkg (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-3.24
Exenatide -> Liraglutide -> Liraglutide-2.87

[back to top]

Change in Beta-cell Function, Weeks 26-78

"Change in Beta-cell function from Week 26 (end of randomisation) to Week 78 (end of treatment). Beta-cell function was derived from fasting plasma glucose (FPG) and fasting insulin concentrations using the homeostasic model assessment (HOMA) method which uses the assumption that normal-weight normal subjects aged under 35 years have a 100% beta-cell function (HOMA-B).~Beta-cell function: HOMA-B (%) = 20∙fasting insulin[uU/mL] divided by (FPG mmol/L]-3.5)." (NCT00518882)
Timeframe: week 26, week 78

Interventionpercentage point (%point) (Mean)
Liraglutide -> Liraglutide -> Liraglutide-18.18
Exenatide -> Liraglutide -> Liraglutide2.29

[back to top]

Change in Beta-cell Function at Week 78

"Change in Beta-cell function from baseline (week 0) to 78 weeks (end of treatment). Beta-cell function was derived from fasting plasma glucose (FPG) and fasting insulin concentrations using the homeostasic model assessment (HOMA) method which uses the assumption that normal-weight normal subjects aged under 35 years have a 100% beta-cell function (HOMA-B).~Beta-cell function: HOMA-B (%) = 20∙fasting insulin[uU/mL] divided by (FPG mmol/L]-3.5)." (NCT00518882)
Timeframe: week 0, week 78

Interventionpercentage point (%point) (Mean)
Liraglutide -> Liraglutide -> Liraglutide24.86
Exenatide -> Liraglutide -> Liraglutide11.13

[back to top]

Change in Beta-cell Function at Week 26

"Change in Beta-cell function from baseline (week 0) to 26 weeks (end of randomisation). Beta-cell function was derived from fasting plasma glucose (FPG) and fasting insulin concentrations using the homeostasic model assessment (HOMA) method which uses the assumption that normal-weight normal subjects aged under 35 years have a 100% beta-cell function (HOMA-B).~Beta-cell function: HOMA-B (%) = 20∙fasting insulin[uU/mL] divided by (FPG mmol/L]-3.5)." (NCT00518882)
Timeframe: week 0, week 26

Interventionpercentage point (%point) (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide32.12
Exenatide -> Liraglutide -> Liraglutide2.74

[back to top]

Change in Total Cholesterol, Weeks 26-78

Change in total cholesterol (TC) from Week 26 (end of randomisation) to Week 78 (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.11
Exenatide -> Liraglutide -> Liraglutide0.12

[back to top]

Change in Apolipoprotein B, Weeks 26-78

Change in apolipoprotein B (ApoB) from Week 26 (end of randomisation) to Week 78 (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 26, week 78

Interventiong/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.02
Exenatide -> Liraglutide -> Liraglutide-0.03

[back to top]

Change in Apolipoprotein B at Week 78

Change in apolipoprotein B (ApoB) from baseline (week 0) to 78 weeks (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 0, week 78

Interventiong/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.08
Exenatide -> Liraglutide -> Liraglutide-0.07

[back to top]

Change in Apolipoprotein B at Week 26

Change in apolipoprotein B (ApoB) from baseline (week 0) to 26 weeks (end of randomisation) (NCT00518882)
Timeframe: week 0, week 26

Interventiong/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.06
Exenatide -> Liraglutide -> Liraglutide-0.03

[back to top]

Change in Body Weight at Week 78

Change in body weight from baseline (Week 0) to 78 weeks (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group) (NCT00518882)
Timeframe: week 0, week 78

Interventionkg (Mean)
Liraglutide -> Liraglutide -> Liraglutide-3.3
Exenatide -> Liraglutide -> Liraglutide-3.2

[back to top]

Change in Triglyceride at Week 78

Change in triglyceride (TG) from baseline (week 0) to 78 weeks (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.3
Exenatide -> Liraglutide -> Liraglutide-0.1

[back to top]

Change in Triglyceride, Weeks 26-78

Change in Triglyceride (TG) from Week 26 (end of randomisation) to Week 78 (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.1
Exenatide -> Liraglutide -> Liraglutide-0.0

[back to top]

Change in Total Cholesterol at Week 78

Change in total cholesterol (TC) from baseline (week 0) to 78 weeks (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.07
Exenatide -> Liraglutide -> Liraglutide0.09

[back to top]

Change in Total Cholesterol at Week 26

Change in total cholesterol (TC) from baseline (week 0) to 26 weeks (end of randomisation) (NCT00518882)
Timeframe: week 0, week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.20
Exenatide -> Liraglutide -> Liraglutide-0.09

[back to top]

Change in Mean Prandial Increment of Plasma Glucose After Lunch, Weeks 26-78

Change in mean prandial increment of plasma glucose after lunch from Week 26 (end of randomisation) to Week 78 (end of treatment). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after a lunch. (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.05
Exenatide -> Liraglutide -> Liraglutide-0.09

[back to top]

Change in Mean Prandial Increment of Plasma Glucose After Lunch at Week 78

Change in mean prandial increment of plasma glucose after lunch from baseline (week 0) to 78 weeks (end of treatment). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after lunch. (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.26
Exenatide -> Liraglutide -> Liraglutide-0.37

[back to top]

Change in Mean Prandial Increment of Plasma Glucose After Lunch at Week 26

Change in mean prandial increment of plasma glucose after lunch from baseline (week 0) to 26 weeks (end of randomisation). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after lunch. (NCT00518882)
Timeframe: week 0, week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide0.06
Exenatide -> Liraglutide -> Liraglutide0.06

[back to top]

Change in Mean Prandial Increment of Plasma Glucose After Dinner, Weeks 26-78

Change in mean prandial increment of plasma glucose after dinner from Week 26 (end of randomisation) to Week 78 (end of treatment). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after dinner. (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.22
Exenatide -> Liraglutide -> Liraglutide1.07

[back to top]

Change in Mean Prandial Increment of Plasma Glucose After Dinner at Week 78

Change in mean prandial increment of plasma glucose after dinner from baseline (week 0) to 78 weeks (end of treatment). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after dinner. (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.35
Exenatide -> Liraglutide -> Liraglutide-0.95

[back to top]

Change in Very Low-density Lipoprotein-cholesterol at Week 26

Change in very low-density lipoprotein-cholesterol (VLDL-C) from baseline (week 0) to 26 weeks (end of randomisation) (NCT00518882)
Timeframe: week 0, week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide0.20
Exenatide -> Liraglutide -> Liraglutide0.27

[back to top]

Change in Very Low-density Lipoprotein-cholesterol at Week 78

Change in Very Low-density Lipoprotein-cholesterol (VLDL-C) from baseline (week 0) to 78 weeks (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.27
Exenatide -> Liraglutide -> Liraglutide0.31

[back to top]

Change in Very Low-density Lipoprotein-cholesterol, Weeks 26-78

Change in Very Low-density Lipoprotein-cholesterol (VLDL-C) from Week 26 (end of randomisation) to Week 78 (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.06
Exenatide -> Liraglutide -> Liraglutide0.03

[back to top]

Hypoglycaemic Episodes at Week 26

Total number of hypoglycaemic episodes occurring after baseline (week 0) and until week 26 (end of randomisation). Hypoglycaemic episodes were defined as major, minor, or symptoms only. Major if the subject was unable to treat her/himself. Minor if subject was able to treat her/himself and plasma glucose was below 3.1 mmol/L. Symptoms only if subject was able to treat her/himself and with no plasma glucose measurement or plasma glucose higher than or equal to 3.1 mmol/L. (NCT00518882)
Timeframe: weeks 0-26

,
Interventionepisodes (Number)
MajorMinorSymptoms only
Exenatide -> Liraglutide -> Liraglutide226493
Liraglutide -> Liraglutide -> Liraglutide020879

[back to top]

Change in Triglyceride at Week 26

Change in triglyceride (TG) from from baseline (week 0) to 26 weeks (end of randomisation) (NCT00518882)
Timeframe: week 0, week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.41
Exenatide -> Liraglutide -> Liraglutide-0.23

[back to top]

Hypoglyceamic Episodes, Weeks 26-78

Total number of hypoglycaemic episodes occurring after end of randomisation (week 26) and until week 78 (end of treatment). Hypoglycaemic episodes were defined as major, minor, or symptoms only. Major if the subject was unable to treat her/himself. Minor if subject was able to treat her/himself and plasma glucose was below 3.1 mmol/L. Symptoms only if subject was able to treat her/himself and with no plasma glucose measurement or plasma glucose higher than or equal to 3.1 mmol/L. (NCT00518882)
Timeframe: weeks 26-78

,
Interventionepisodes (Number)
MajorMinorSymptoms only
Exenatide -> Liraglutide -> Liraglutide017232
Liraglutide -> Liraglutide -> Liraglutide114037

[back to top]

Percentage of Subjects Achieving Treatment Target of Either HbA1c < 7.0% or =< 6.5% at Week 26

Percentage of subjects achieving treatment target of HbA1c less than 7.0% or less than or equal to 6.5% at Week 26 (end of randomisation) (NCT00518882)
Timeframe: week 0, week 26

,
Interventionpercentage (%) of subjects (Number)
Treatment target HbA1c < 7%Treatment target HbA1c =< 6.5%
Exenatide -> Liraglutide -> Liraglutide4220
Liraglutide -> Liraglutide -> Liraglutide5334

[back to top]

Percentage of Subjects Achieving Treatment Target of Either HbA1c < 7.0% or =< 6.5% at Week 78

Percentage of subjects achieving treatment target of HbA1c less than 7.0% or less than or equal to 6.5% at Week 78 (end of treatment) (NCT00518882)
Timeframe: week 0, week 78

,
Interventionpercentage (%) of subjects (Number)
Treatment target HbA1c < 7%Treatment target HbA1c =< 6.5%
Exenatide -> Liraglutide -> Liraglutide4835
Liraglutide -> Liraglutide -> Liraglutide4731

[back to top]

Change in Mean Prandial Increment of Plasma Glucose After Dinner at Week 26

Change in mean prandial increment of plasma glucose after dinner from baseline (week 0) to 26 weeks (end of randomisation). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after dinner. (NCT00518882)
Timeframe: week 0, week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-1.10
Exenatide -> Liraglutide -> Liraglutide-2.11

[back to top]

Change in Mean Prandial Increment of Plasma Glucose After Breakfast, Weeks 26-78

Change in mean prandial increment of plasma glucose after breakfast from Week 26 (end of randomisation) to Week 78 (end of treatment). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after breakfast. (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.22
Exenatide -> Liraglutide -> Liraglutide1.15

[back to top]

Change in Mean Prandial Increment of Plasma Glucose After Breakfast at Week 78

Change in mean prandial increment of plasma glucose after breakfast from baseline (week 0) to 78 weeks (end of treatment). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after breakfast. (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-1.08
Exenatide -> Liraglutide -> Liraglutide-0.99

[back to top]

Change in Mean Prandial Increment of Plasma Glucose After Breakfast at Week 26

Change in mean prandial increment of plasma glucose after breakfast from baseline (week 0) to 26 weeks (end of randomisation). Prandial increments of plasma glucose were calculated as the difference between glucose values measured before and after breakfast. (NCT00518882)
Timeframe: week 0, week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.83
Exenatide -> Liraglutide -> Liraglutide-2.16

[back to top]

Change in Mean Postprandial Increment of Plasma Glucose After Lunch, Weeks 26-78

Change in mean postprandial increment of plasma glucose after lunch from Week 26 (end of randomisation) to Week 78 (end of treatment). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after lunch. (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.67
Exenatide -> Liraglutide -> Liraglutide-0.09

[back to top]

Change in Mean Postprandial Increment of Plasma Glucose After Lunch at Week 78

Change in mean postprandial increment of plasma glucose after lunch from baseline (week 0) to 78 weeks (end of treatment). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after lunch. (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-1.93
Exenatide -> Liraglutide -> Liraglutide-2.17

[back to top]

Change in Mean Postprandial Increment of Plasma Glucose After Lunch at Week 26

Change in mean postprandial increment of plasma glucose after lunch from baseline (week 0) to 26 weeks (end of randomisation). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after lunch. (NCT00518882)
Timeframe: week 0. week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-2.74
Exenatide -> Liraglutide -> Liraglutide-2.35

[back to top]

Change in Mean Postprandial Increment of Plasma Glucose After Dinner, Weeks 26-78

Change in mean postprandial increment of plasma glucose after dinner from Week 26 (end of randomisation) to Week 78 (end of treatment). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after dinner. (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.32
Exenatide -> Liraglutide -> Liraglutide0.58

[back to top]

Change in Mean Postprandial Increment of Plasma Glucose After Dinner at Week 78

Change in mean postprandial increment of plasma glucose after dinner from baseline (week 0) to 78 weeks (end of treatment). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after dinner. (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-2.21
Exenatide -> Liraglutide -> Liraglutide-2.55

[back to top]

Change in Mean Postprandial Increment of Plasma Glucose After Dinner at Week 26

Change in mean postprandial increment of plasma glucose after dinner from baseline (week 0) to 26 weeks (end of randomisation). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after dinner. (NCT00518882)
Timeframe: week 0, week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-3.05
Exenatide -> Liraglutide -> Liraglutide-3.59

[back to top]

Change in Mean Postprandial Increment of Plasma Glucose After Breakfast, Weeks 26-78

Change in mean postprandial increment of plasma glucose after breakfast from Week 26 (end of randomisation) to Week 78 (end of treatment). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after breakfast. (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.06
Exenatide -> Liraglutide -> Liraglutide0.72

[back to top]

Change in Mean Postprandial Increment of Plasma Glucose After Breakfast at Week 78

Change in mean postprandial increment of plasma glucose after breakfast from baseline (week 0) to 78 weeks (end of treatment). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after breakfast. (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-3.31
Exenatide -> Liraglutide -> Liraglutide-3.13

[back to top]

Change in Mean Postprandial Increment of Plasma Glucose After Breakfast at Week 26

Change in mean postprandial increment of plasma glucose after breakfast from baseline (week 0) to 26 weeks (end of randomisation). Prandial increments of plasma glucose were calculated as the difference between plasma glucose values measured before and after breakfast. (NCT00518882)
Timeframe: week 0, week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-3.20
Exenatide -> Liraglutide -> Liraglutide-3.93

[back to top]

Change in Low-density Lipoprotein-cholesterol, Weeks 26-78

Change in low-density lipoprotein-cholesterol (LDL-C) from Week 26 (end of randomisation) to Week 78 (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide0.03
Exenatide -> Liraglutide -> Liraglutide0.08

[back to top]

Change in Low-density Lipoprotein-cholesterol at Week 26

Change in Low-density Lipoprotein-cholesterol (LDL-C) from baseline (week 0) to 26 weeks (end of randomisation) (NCT00518882)
Timeframe: week 0, week 26

Interventionmmol/L (Least Squares Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.44
Exenatide -> Liraglutide -> Liraglutide-0.40

[back to top]

Change in High-density Lipoprotein-cholesterol, Weeks 26-78

Change in High-density Lipoprotein-cholesterol (HDL-C) from Week 26 (end of randomisation) to Week 78 (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 26, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.01
Exenatide -> Liraglutide -> Liraglutide0.00

[back to top]

Change in High-density Lipoprotein-cholesterol at Week 78

Change in High-density Lipoprotein-cholesterol (HDL-C) from baseline (week 0) to 78 weeks (end of treatment) within each treatment group (the liraglutide -> liraglutide group and the exenatide -> liraglutide group). (NCT00518882)
Timeframe: week 0, week 78

Interventionmmol/L (Mean)
Liraglutide -> Liraglutide -> Liraglutide-0.03
Exenatide -> Liraglutide -> Liraglutide-0.02

[back to top]

Changes in Components of Liver Histology at Baseline and Week 24 Including Steatosis, Inflammation and Fibrosis

"Steatosis was grades on a scale of 0 (< 5%); 1 (5%- 33%); 2 (> 33% - 66%); and 3 (> 66%).~Inflammation was graded on a scale of 0 (No foci); 1 (< 2 foci per 200 X field); 2 (2-4 foci per 200 X field); and 3 (>4 foci per 200 X field) Fibrosis was graded on a scale of 0 (None); 1 (Mild periportal or perisinusoidal); 2 (Moderate periportal or perisinusoidal); 3 (Bridging fibrosis); and 4 (cirrhosis)" (NCT00529204)
Timeframe: 24 weeks

Interventionunits on a scale (Number)
steatosisinflammationfibrosis
Exenatide-1-10

[back to top]

Safety of Exenatide in Patients With NAFLD and Type 2 Diabetes

(NCT00529204)
Timeframe: 24 weeks

Interventionadverse events (Number)
Exenatide0

[back to top]

Reduction in Serum ALT From Baseline to 24 Weeks of Exenatide Therapy

(NCT00529204)
Timeframe: 24 weeks

InterventionIU (Number)
Exenatide61

[back to top]

Change in Reactive Hyperemic Index Over the 3-month Treatment Period

Change in reactive hyperemic index over the 3-month treatment period, which is a measure of endothelial (inner lining of blood vessels) function. This is measured as a ratio of post-occlusion blood flow volume versus baseline blood flow volume in fingertips. Higher ratio values are considered indicative of better arterial health. (NCT00546728)
Timeframe: Change from baseline to 3 months

Interventionratio (Mean)
Exenatide0.01
Metformin-0.17

[back to top]

Number of Participants With Adverse Events Including Laboratory Abnormalities at the End of Study Participation

"Frequency of adverse events including laboratory abnormalities~HbA1C (less than 6.1% is considered normal)~Glucose control and absence of hypoglycemic coma/unawareness, as evidenced by no further requirement for third-party assistance or hospital attendance resulting from a severe hypoglycemic episode~Renal function, measured both by serum creatinine and calculated GFR using the Cockroft & Gault~Lipid profiles for cholesterol, triglycerides, low density lipoprotein (LDL) and high density lipoprotein (HDL)~PRA~Doppler ultrasound to exclude or document portal vein thrombosis~Immunosuppressive drug trough levels~Renal clearance (GFR)~Liver function tests~Diagnosis of opportunistic infections, e.g., CMV" (NCT00566813)
Timeframe: 15 months after the last transplant

Interventionparticipants (Number)
Islet Cells4
Islet Cells + Etanercept + Exenatide5

[back to top]

Number of Participants With HbA1c Less Than or Equal to 6.5 & Free of Severe Hypoglycemic Events

HbA1c less than or equal to 6.5 at end of 15 month study participation, and lack of or free from severe hypoglycemic events, defined as an event with symptoms compatible with hypoglycemia in which the subject required the assistance of another person and which was associated with either a blood glucose level < 50 mg/dl (2.8 mmol/L) or prompt recovery after oral carbohydrate, intravenous glucose, or glucagon administration. (NCT00566813)
Timeframe: At end of 15 month study participation

Interventionparticipants (Number)
Islet Cells4
Islet Cells + Etanercept + Exenatide5

[back to top]

Number of Participants With Insulin Independence at End of Study Participation

Primary efficacy outcome: independence from insulin injections with adequate control of blood glucose in subjects with Type 1 diabetes. Transplant is considered a success when 2 weeks after their last transplant, subjects are not using insulin, and fasting glucose levels do not exceed 7.8 mmol/L (140 mg/dL) more than 3 times/week, and two-hour post-prandial glucose values do not exceed 10 mmol/L (180 mg/dL) more than 4 times/week. During the 15 months after last transplant, a subject will be considered a success if an illness or other event (e.g., high tacrolimus level) causes need for insulin not exceeding 14 days providing evidence of graft rejection is not apparent. The proportion of subjects who are insulin independent and meet criteria for glucose control will be determined at 2 weeks and 1, 3, 6, 12, and 15 months following their final islet transplant. (NCT00566813)
Timeframe: End of 15 Month Study Participation/Follow-up

Interventionparticipants (Number)
Islet Cells4
Islet Cells + Etanercept + Exenatide5

[back to top]

Change in 1,5-anhydroglucitol

Change in 1,5-anhydroglucitol from baseline to endpoint (i.e., 1,5-anhydroglucitol at week 24 minus 1,5-anhydroglucitol at week 0) (NCT00577824)
Timeframe: baseline, week 24

Interventionmcg/mL (Mean)
5mcg Exenatide BID5.29
10mcg Exenatide BID4.52
Placebo BID0.66

[back to top]

Change in Fasting Blood Glucose

Change in fasting blood glucose from baseline to endpoint (i.e., fasting blood glucose at week 24 minus fasting blood glucose at week 0) (NCT00577824)
Timeframe: baseline, week 24

Interventionmg/dL (Least Squares Mean)
5mcg Exenatide BID-25.1
10mcg Exenatide BID-29.0
Placebo BID-7.6

[back to top]

Change in Glycosylated Hemoglobin (HbA1c) From Baseline to Week 24

Change in HbA1c from baseline following 24 weeks of treatment (i.e., HbA1c at week 24 minus HbA1c at week 0) (NCT00577824)
Timeframe: baseline, 24 weeks

InterventionPercentage of hemoglobin (Least Squares Mean)
5mcg Exenatide BID-1.34
10mcg Exenatide BID-1.62
Placebo BID-0.28

[back to top]

Change in High Density Lipoprotein Cholesterol (HDL-C)

Change in HDL-C from baseline to endpoint (i.e., HDL-C at week 24 minus HDL-C at week 0) (NCT00577824)
Timeframe: baseline, week 24

Interventionmg/dL (Mean)
5mcg Exenatide BID-4.63
10mcg Exenatide BID-4.22
Placebo BID-0.97

[back to top]

Change in Homeostasis Model Assessment - Beta Cell Function (HOMA-B)

Change in HOMA-B from baseline to endpoint (i.e., HOMA-B at week 24 minus HOMA-B at week 0). HOMA-B is a measurement of beta cell function. (NCT00577824)
Timeframe: baseline, week 24

Interventionratio (Mean)
5mcg Exenatide BID2.475
10mcg Exenatide BID6.836
Placebo BID-0.707

[back to top]

Change in Body Weight

Change in body weight form baseline to endpoint (i.e., body weight at week 24 minus body weight at week 0) (NCT00577824)
Timeframe: baseline, week 24

Interventionkg (Least Squares Mean)
5mcg Exenatide BID-0.39
10mcg Exenatide BID-1.54
Placebo BID-0.47

[back to top]

Change in Homeostasis Model Assessment - Insulin Resistance (HOMA-R)

Change in HOMA-R from baseline to endpoint (i.e., HOMA-R at week 24 minus HOMA-R at week 0). HOMA-R is a measurement of insulin resistance. (NCT00577824)
Timeframe: baseline, week 24

Interventionratio (Mean)
5mcg Exenatide BID-0.541
10mcg Exenatide BID-0.366
Placebo BID-0.375

[back to top]

Change in Low Density Lipoprotein Cholesterol (LDL-C)

Change in LDL-C from baseline to endpoint (i.e., LDL-C at week 24 minus LDL-C at week 0) (NCT00577824)
Timeframe: baseline, week 24

Interventionmg/dL (Mean)
5mcg Exenatide BID-8.89
10mcg Exenatide BID-5.03
Placebo BID-2.66

[back to top]

Change in Serum Insulin

Change in serum insulin from baseline to endpoint (i.e., serum insulin at week 24 minus serum insulin at week 0) (NCT00577824)
Timeframe: baseline, week 24

InterventionmcU/mL (Mean)
5mcg Exenatide BID-0.2
10mcg Exenatide BID0.2
Placebo BID-0.7

[back to top]

7 Point Self-monitored Blood Glucose (SMBG) Profiles at Baseline and Week 24

Self-monitored blood glucose at 7 different time points during the day (glucose measurements before and 2 hours after the start of the morning, midday, and evening meals, and at bedtime). (NCT00577824)
Timeframe: baseline, week 24

,,
Interventionmg/dL (Mean)
30 minutes prior to breakfast SMBG at week 030 minutes prior to breakfast SMBG at week 242hr post-breakfast SMBG at week 02hr post-breakfast SMBG at week 2430 minutes prior to lunch SMBG at week 030 minutes prior to lunch SMBG at week 242hr post-lunch SMBG at week 02hr post-lunch SMBG at week 2430 minutes prior to dinner SMBG at week 030 minutes prior to dinner SMBG at week 242hr post-dinner SMBG at week 02hr post-dinner SMBG at week 24bedtime SMBG at week 0bedtime SMBG at week 24
10mcg Exenatide BID175140263149189152268195176140247141225151
5mcg Exenatide BID169150261178179155263213166149246160216170
Placebo BID170167254257179182264254173181239247206212

[back to top]

Change in Waist Size

Change in waist size from baseline to endpoint (i.e., waist size at week 24 minus waist size at week 0) (NCT00577824)
Timeframe: baseline, week 24

Interventioncm (Mean)
5mcg Exenatide BID-0.17
10mcg Exenatide BID-1.81
Placebo BID0.41

[back to top]

Change in C-peptide

Change in C-peptide from baseline to endpoint (i.e., C-peptide at week 24 minus C-peptide at week 0) (NCT00577824)
Timeframe: baseline, week 24

Interventionng/mL (Mean)
5mcg Exenatide BID0.05
10mcg Exenatide BID0.07
Placebo BID-0.08

[back to top]

Percentage of Patients Achieving HbA1c < 6.5%

Percentage of subjects whose HbA1c was >=6.5% at baseline who achieved an HbA1c < 6.5% at endpoint (i.e., number of eligible subjects who achieved HbA1c < 6.5% divided by total number of eligible subjects times 100) (NCT00577824)
Timeframe: 24 weeks

Interventionpercentage of participants (Number)
5mcg Exenatide BID36.6
10mcg Exenatide BID47.2
Placebo BID8.6

[back to top]

Percentage of Patients Achieving HbA1c < 7.0%

Percentage of subjects whose HbA1c was >=7.0% at baseline who achieved an HbA1c < 7.0% at endpoint (i.e., number of eligible subjects who achieved HbA1c < 7.0% divided by total number of eligible subjects times 100) (NCT00577824)
Timeframe: 24 weeks

Interventionpercentage of participants (Number)
5mcg Exenatide BID67.1
10mcg Exenatide BID71.0
Placebo BID15.2

[back to top]

Change in Triglycerides

Change in triglycerides from baseline to endpoint (i.e., triglycerides at week 24 minus triglycerides at week 0) (NCT00577824)
Timeframe: baseline, week 24

Interventionmg/dL (Mean)
5mcg Exenatide BID4.00
10mcg Exenatide BID4.13
Placebo BID-4.60

[back to top]

Change in Total Cholesterol

Change in total cholesterol from baseline to endpoint (i.e., total cholesterol at week 24 minus total cholesterol at week 0) (NCT00577824)
Timeframe: baseline, week 24

Interventionmg/dL (Mean)
5mcg Exenatide BID-14.45
10mcg Exenatide BID-7.01
Placebo BID-4.80

[back to top]

Change in Waist-to-hip Ratio

Change in waist-to-hip ratio from baseline to endpoint (i.e., waist-to-hip ratio at week 24 minus waist-to-hip ratio at week 0). Waist-to-hip ratio is waist circumference divided by hip circumference. (NCT00577824)
Timeframe: baseline, week 24

Interventionratio (cm/cm) (Mean)
5mcg Exenatide BID0.0016
10mcg Exenatide BID-0.0108
Placebo BID-0.0007

[back to top]

Change in Impact of Weight on Quality of Life (IWQOL)-Lite Score

"IWQOL-Lite analysis of change from baseline to endpoint (26 weeks). IWQOL-Lite is a 31-item questionnaire, assessing the domains of physical function, self-esteem, sexual life, public distress, and work. Response categories for each item range from 1 = never true to 5 = always true." (NCT00603239)
Timeframe: baseline and 26 weeks

,
Interventionunits on a scale (Least Squares Mean)
Change in Total ScoreChange in Physical Function componentChange in Self-Esteem componentChange in Sexual Life componentChange in Public Distress componentChange in Work component
Exenatide Twice Daily (BID)-1.56-3.840.200.12-0.48-0.91
Placebo0.11-1.05-0.545.01-0.280.08

[back to top]

Change in Euroqol - 5 Domain Quality of Life (EQ-5D) Score

EQ-5D Score - change from baseline to endpoint (26 weeks). EQ-5D is a 5-item questionnaire used to characterize current health states. The tool and accompanying visual analog scale (VAS) assess 5 domains of quality of life, including mobility, self-care, usual activity, pain, and anxiety/depression. Weights are used to score the responses to the 5 domains, with 3 options possible in each domain: extreme problems, some/moderate problems, or no problems. Scores range from 0 to 1, with a score of 1 representing a perfect health state. (NCT00603239)
Timeframe: baseline and 26 weeks

,
Interventionunits on a scale (Least Squares Mean)
Change in Health State ScoreChange in Mobility componentChange in Self Care componentChange Usual Activities componentChange in Pain/Discomfort componentChange in Anxiety/Depression component
Exenatide Twice Daily (BID)0.790.140.080.170.29-0.10
Placebo-2.940.150.030.190.23-0.26

[back to top]

Percentage of Patients Achieving HbA1c <= 7%

Percentage of intent-to-treat (ITT) patients who had HbA1c > 7% at baseline that decreased to <= 7% at endpoint (Week 26 or early discontinuation) (NCT00603239)
Timeframe: 26 weeks

Interventionpercentage of participants (Number)
Exenatide Twice Daily (BID)49.0
Placebo36.5

[back to top]

Percentage of Patients Achieving HbA1c <= 6.5%

Percentage of ITT patients who had achieved HbA1c <= 6.5% at endpoint (Week 26 or early discontinuation) (NCT00603239)
Timeframe: 26 weeks

Interventionpercentage of participants (Number)
Exenatide Twice Daily (BID)33.6
Placebo13.0

[back to top]

Number of Subjects Who Experienced an Episode of Minor Hypoglycemia

Overall number of subjects who experienced an episode of minor hypoglycemia. (NCT00603239)
Timeframe: 26 weeks

InterventionParticipants (Number)
Exenatide Twice Daily (BID)4
Placebo1

[back to top]

Change in Waist Circumference

Change in waist circumference from baseline to endpoint (26 weeks) (NCT00603239)
Timeframe: baseline and 26 weeks

Interventioncm (Mean)
Exenatide Twice Daily (BID)-2.26
Placebo-1.85

[back to top]

Change in Insulin Sensitivity.

Change in homeostatic model assessment-insulin sensitivity (HOMA-S) from baseline to endpoint (26 weeks) (outcome measure is presented as the ratio of endpoint HOMA-S divided by baseline HOMA-S). (NCT00603239)
Timeframe: baseline and 26 weeks

Interventionratio (Least Squares Mean)
Exenatide Twice Daily (BID)1.09
Placebo1.07

[back to top]

Change in Glycosylated Hemoglobin (HbA1c)

Change in HbA1c from baseline to endpoint after 26 weeks of treatment (i.e., HbA1c at endpoint minus HbA1c at baseline) (NCT00603239)
Timeframe: baseline and 26 weeks

InterventionPercentage (Least Squares Mean)
Exenatide Twice Daily (BID)-0.84
Placebo-0.10

[back to top]

Change in Fasting Serum Glucose (FSG)

Change in FSG from baseline to endpoint (26 weeks) (NCT00603239)
Timeframe: baseline and 26 weeks

Interventionmmol/L (Least Squares Mean)
Exenatide Twice Daily (BID)-0.65
Placebo0.37

[back to top]

Change in Body Weight

Change in body weight from baseline to endpoint (26 weeks) (NCT00603239)
Timeframe: baseline and 26 weeks

Interventionkg (Least Squares Mean)
Exenatide Twice Daily (BID)-1.43
Placebo-0.75

[back to top]

Change in Beta-cell Function

Change in homeostatic model assessment-beta cell (HOMA-B) from baseline to endpoint (Week 26) (outcome measure is presented as the ratio of endpoint HOMA-B divided by baseline HOMA-B). HOMA-B is a measure of pancreatic beta-cell function. (NCT00603239)
Timeframe: baseline and 26 weeks

Interventionratio (Geometric Mean)
Exenatide Twice Daily (BID)1.08
Placebo0.84

[back to top]

Weight Loss After Administration of Exenatide.

Body weight after overnight fast in light clothing (NCT00623545)
Timeframe: 3 months

Interventionkg (Mean)
Exenitide Treatment-2.0

[back to top]

Change in Energy Intake Measured Before Treatment and at the End of Treatment.

Energy intake is as calculated from energy expenditure as measured by doubly labeled water and change in body energy stores before and at the end of treatment. Units are kcal/d. (NCT00623545)
Timeframe: 3 months

Interventionkcal/d (Mean)
Exenitide Treatment-167

[back to top]

Percentage of Patients Achieving HbA1c Concentration <7.0% at Month 24

Percentage of Patients Achieving HbA1c Concentration <7.0% at Month 24. Only patients with baseline HbA1c >= 7.0 % were included in this analysis (NCT00635492)
Timeframe: Month 24

Interventionpercentage of patients (Number)
Exenatide BID26.9
Insulin28.5

[back to top]

Diet and Exercise Advice in Diabetes Management Associated With Treatment Choice at Baseline

Receipt of diet and exercise advice was one of the Factors evaluated for association with treatment choice at baseline. The number of participants who checked yes or no during the baseline visit for prior receipt of diet/exercise advice in his/her Diabetes management is provided below and the statistical analysis provides the 2 arms odds ratio. Participants were assigned to the exenatide BID or insulin cohort based the injectable treatment started at baseline; analyses were conducted irrespective of later treatment changes. Baseline was Visit T1 (prior to start of treatment). (NCT00635492)
Timeframe: Baseline

,
Interventionparticipants (Number)
MissingNoYesUnknown
Exenatide BID12131910124
Insulin1237905172

[back to top]

Changes in HbA1c From Baseline to Month 24

Changes in HbA1c From Baseline to Month 24 (NCT00635492)
Timeframe: Baseline, Month 24

Interventionpercentage of total hemoglobin (Mean)
Exenatide BID-1.03
Insulin-1.71

[back to top]

Reasons for Discontinuation of Baseline Regimen

Reasons for Discontinuation of Baseline Regimen (NCT00635492)
Timeframe: Baseline to Month 24

,
Interventionnumber of patients (Number)
Inadequate responseAdverse eventPatient decisionNon complianceCannot afford medicationOther
Exenatide BID17091699450
Insulin8711153138

[back to top]

Percentage of Patients Hospitalized Between Baseline and 24 Months

Percentage of Patients Hospitalized Between Baseline and 24 Months (NCT00635492)
Timeframe: Baseline to Month 24

,
Interventionpercentage of patients (Number)
Last 6 months prior to baselineBaseline to 24 months
Exenatide BID4.74.3
Insulin6.47.8

[back to top]

Percentage of Patients Contacting Health Care Providers Between Baseline and 24 Months

Percentage of Patients Contacting Health Care Providers Between Baseline and 24 Months (NCT00635492)
Timeframe: Baseline to Month 24

,
Interventionpercentage of patients (Number)
Last 6 months prior to baselineBaseline to 24 months
Exenatide BID94.490.4
Insulin94.192.3

[back to top]

Number of Contacts With Health Care Providers Between Baseline and 24 Months

Number of contacts with Health Care Providers Between Baseline and 24 Months (NCT00635492)
Timeframe: Baseline to Month 24

,
Interventionnumber of contacts (Mean)
Last 6 months prior to baselineBaseline to 24 months
Exenatide BID7.1719.00
Insulin7.6424.58

[back to top]

Factors Associated With Treatment Change in Insulin Cohort

Hazards ratios from Backward Cox Regression Model for time to significant treatment change in Insulin cohort (NCT00635492)
Timeframe: Baseline to Month 24

Interventionhazard ratio (Number)
HbA1c (%) at baselineDHP barriers to activity subscale at baselineGastrointestinal symptoms: yes vs. no at baselineInsulin regimen: basal/bolus vs. long-acting onlyInsulin regimen: mixtures vs. long-acting onlyInsulin regimen: other vs. long-acting onlyInsulin regimen: short-acting only vs. long-actin
Insulin Cohort1.1180.9602.5320.4370.6760.5492.164

[back to top]

Factors Associated With Treatment Change in Exenatide BID Cohort

Hazards ratios from Backward Cox Regression Model for time to significant treatment change in Exenatide BID cohort. EQ-5D (Health Questionnaire Copyright @ Euro QoL Group 1998). (NCT00635492)
Timeframe: Baseline to Month 24

Interventionhazard ratio (Number)
Gastro intestinal symptoms: yes vs no at baselineEQ-5D index value at baseline
Exenatide BID1.4630.601

[back to top]

Estimates of Probability to Remain on Initial Injectable Treatment at 12 and 24 Months.

"The primary objective of this study is to estimate the time spent on initial treatment regime before significant treatment change for patients with type 2 diabetes initiating therapy with either insulin or exenatide for the first time.~Initial treatment regime is defined as the treatment regime prescribed when the patient is enrolled in the study.~Significant treatment change for patients initiated on insulin or exenatide is defined as at least one of the following:~Insulin:~Addition of a new medication for the treatment of type 2 diabetes~A change in the number of times insulin is administered per day~Discontinuation of any insulin initiated at baseline~Substitution of a human insulin for an analogue insulin or vice-versa.~Switching between brands of the same class/type of insulin is not included in the definition of significant treatment change.~Exenatide:~Addition of a new medication for the treatment of type 2 diabetes~Discontinuation of exenatide." (NCT00635492)
Timeframe: Month 24

,
Interventionprobability (%) (Number)
Estimate at 24 monthsEstimate at 12 months
Exenatide BID53.967.8
Insulin60.670.6

[back to top]

Changes in Weight From Baseline to Month 24

Changes in Weight From Baseline to Month 24 (NCT00635492)
Timeframe: Baseline, Month 24

Interventionkg (Mean)
Exenatide BID-3.22
Insulin2.16

[back to top]

Disinhibited Eating Associated With Treatment Choice at Baseline

Diabetes Health Profile (DHP-18) - consists of 18 items across 3 domains (psychological distress, barriers to activity, and disinhibited eating), with each item standardized score rated from 0-100; 0=no dysfunction, higher numbers=greater dysfunction. The subscale of disinhibited eating was one of the Factors evaluated for association with treatment choice at baseline. The number of participants with disinhibited eating at baseline is provided below and the statistical analysis provides the 2 arms odds ratio for disinhibited eating. Participants were assigned to the exenatide BID or insulin cohort based the injectable treatment started at baseline; analyses were conducted irrespective of later treatment changes. Baseline was Visit T1 (prior to start of treatment). (NCT00635492)
Timeframe: Baseline

Interventionunits on a scale (Mean)
Exenatide BID43.52
Insulin34.38

[back to top]

Frequent Blood Glucose Self Monitoring Associated With Treatment Choice at Baseline

Frequent glucose self-testing (1 test/week more) was one of the Factors evaluated for association with treatment choice at baseline. The mean number of self monitoring blood glucose tests per week over the last 4 weeks prior to baseline was determined at baseline and is provided below. The statistical analysis provides the 2 arms odds ratio. Participants were assigned to the exenatide BID or insulin cohort based the injectable treatment started at baseline; analyses were conducted irrespective of later treatment changes. Baseline was Visit T1 (prior to start of treatment). (NCT00635492)
Timeframe: 4 weeks prior to Baseline

Interventiontests/week (Mean)
Exenatide BID9.28
Insulin9.91

[back to top]

Higher Body Mass Index (BMI) Associated With Treatment Choice at Baseline

Higher BMI was one of the Factors evaluated for association with treatment choice at baseline. BMI was calculated as body weight in kilograms (kg) divided by height in meters (m) squared (kg/m^2). The mean BMI at baseline is provided below and the statistical analysis provides the 2 arms odds ratio for BMI=1 kg/m^2 higher. Participants were assigned to the exenatide BID or insulin cohort based the injectable treatment started at baseline; analyses were conducted irrespective of later treatment changes. Baseline was Visit T1 (prior to start of treatment). (NCT00635492)
Timeframe: Baseline

Interventionkg/m^2 (Mean)
Exenatide BID35.3
Insulin29.7

[back to top]

Higher Hemoglobin A1c (HbA1) Associated With Treatment Choice at Baseline

Higher HbA1c was one of the Factors evaluated for association with treatment choice at baseline.HbA1c was reported in percent of hemoglobin. The mean HbA1c at baseline is provided below and the statistical analysis provides the 2 arms odds ratio for HbA1c=1% higher. (NCT00635492)
Timeframe: Baseline

Interventionpercent of hemoglobin (Mean)
Exenatide BID8.4
Insulin9.2

[back to top]

Higher Random Glucose Associated With Treatment Choice at Baseline

Random Glucose 1 millimole per liter (mmol/L) higher was one of the Factors evaluated for association with treatment choice at baseline. Random glucose is a glucose within the last 6 months prior to baseline. The mean is provided below and the statistical analysis provides the 2 arms odds ratio for the glucose 1 mmol/L higher. Participants were assigned to the exenatide BID or insulin cohort based the injectable treatment started at baseline; analyses were conducted irrespective of later treatment changes. Baseline was Visit T1 (prior to start of treatment). (NCT00635492)
Timeframe: 6 months prior to Baseline

Interventionmmol/L (Mean)
Exenatide BID10.37
Insulin12.13

[back to top]

Higher Value of Low Density Lipoprotein Cholesterol Associated With Treatment Choice at Baseline

Higher (1 mmol/L higher) LDL cholesterol was one of the Factors evaluated for association with treatment choice at baseline. The mean LDL cholesterol at baseline is provided below and the statistical analysis provides the 2 arms odds ratio for 1 mmol/L higher at baseline. Participants were assigned to the exenatide BID or insulin cohort based the injectable treatment started at baseline; analyses were conducted irrespective of later treatment changes. Baseline was Visit T1 (prior to start of treatment). (NCT00635492)
Timeframe: Baseline

Interventionmmol/L (Mean)
Exenatide BID2.82
Insulin3.00

[back to top]

Incidence of Gastro Intestinal Symptoms Between Baseline and 24 Months

Incidence of Gastro Intestinal Symptoms between Baseline and 24 Months (NCT00635492)
Timeframe: Baseline to Month 24

Interventionpercentage of patients (Number)
Exenatide BID29.4
Insulin5.0

[back to top]

Incidence of Hypoglycemia Between Baseline and 24 Months

Incidence of Hypoglycemia between Baseline and 24 Months (NCT00635492)
Timeframe: Baseline to Month 24

Interventionpercentage of patients (Number)
Exenatide BID17.5
Insulin35.2

[back to top]

Older Age Associated With Treatment Choice at Baseline

Older age (1 year older) was one of the Factors evaluated for association with treatment choice at baseline. The mean age at baseline is provided below and the statistical analysis provides the 2 arms odds ratio for age 1 year older. Participants were assigned to the exenatide BID or insulin cohort based the injectable treatment started at baseline; analyses were conducted irrespective of later treatment changes. Baseline was Visit T1 (prior to start of treatment). (NCT00635492)
Timeframe: Baseline

Interventionyears (Mean)
Exenatide BID58.1
Insulin63.7

[back to top]

Percentage of Patients Achieving HbA1c Concentration <6.5% at Month 24

Percentage of Patients Achieving HbA1c Concentration <6.5% at Month 24. Note: Only patients with baseline HbA1c >=6.5% were included in this analysis. (NCT00635492)
Timeframe: Month 24

Interventionpercentage of patients (Number)
Exenatide BID12.5
Insulin10.7

[back to top]

Assessment on Event Rate of Treatment-emergent Hypoglycemic Events

Major hypoglycemia: events that, in the judgment of the investigator or physician, resulted in loss of consciousness, seizure, coma, or other change in mental status consistent with neuroglycopenia, in which symptoms resolved after administration of intramuscular glucagon or intravenous glucose, required third-party assistance, and was accompanied by a blood glucose concentration < 54 mg/dL prior to treatment. Minor hypoglycemia: symptoms consistent with hypoglycemia and blood glucose concentration < 54 mg/dL prior to treatment and not classified as major hypoglycemia. (NCT00637273)
Timeframe: Day 1 to Week 26

,,
Interventionrate per subject-year (Mean)
Treatment-Emergent Major HypoglycemiaTreatment-Emergent Minor Hypoglycemia
Exenatide Once Weekly0.000.03
Pioglitazone0.000.01
Sitagliptin0.000.12

[back to top]

Change in HbA1c From Baseline to Week 26

Absolute change in HbA1c from baseline (Day 1) to Week 26 [Week 26 - Baseline]. (NCT00637273)
Timeframe: Day 1, Week 26

Interventionpercentage of total hemoglobin (Least Squares Mean)
Exenatide Once Weekly-1.55
Sitagliptin-0.92
Pioglitazone-1.23

[back to top]

Change in Fasting Total Cholesterol From Baseline to Week 26

Change in fasting total cholesterol from baseline (Day 1) to Week 26. (NCT00637273)
Timeframe: Day 1, Week 26

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-0.6
Sitagliptin3.1
Pioglitazone6.2

[back to top]

Change in Diastolic Blood Pressure From Baseline to Week 26

Change in diastolic blood pressure from baseline (Day 1) to Week 26. (NCT00637273)
Timeframe: Day 1, Week 26

InterventionmmHg (Least Squares Mean)
Exenatide Once Weekly-1.4
Sitagliptin-0.4
Pioglitazone-2.5

[back to top]

Change in Body Weight From Baseline to Week 26

Change in body weight from baseline (Day 1) to Week 26. (NCT00637273)
Timeframe: Day 1, Week 26

Interventionkg (Least Squares Mean)
Exenatide Once Weekly-2.31
Sitagliptin-0.77
Pioglitazone2.79

[back to top]

Change in Fasting High-density Lipoprotein (HDL) From Baseline to Week 26

Change in fasting HDL from baseline (Day 1) to Week 26. (NCT00637273)
Timeframe: Day 1, Week 26

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly2.0
Sitagliptin2.0
Pioglitazone6.2

[back to top]

Change in Fasting Plasma Glucose From Baseline to Week 26

Change in fasting plasma glucose from baseline (Day 1) to Week 26. (NCT00637273)
Timeframe: Day 1, Week 26

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-31.8
Sitagliptin-16.3
Pioglitazone-27.3

[back to top]

Ratio of Fasting Triglycerides at Week 26 to Baseline

Ratio of triglycerides (measured in mg/dL) at Week 26 to baseline (Day 1). Log (Postbaseline Triglycerides) - log (Baseline Triglycerides); change from baseline to endpoint is presented as ratio of endpoint to baseline. (NCT00637273)
Timeframe: Day 1, Week 26

Interventionratio (Least Squares Mean)
Exenatide Once Weekly0.95
Sitagliptin0.95
Pioglitazone0.84

[back to top]

Percentage of Subjects Achieving HbA1c Target of <7% at Week 26

Percentages of subjects achieving HbA1c target values of <7% at Week 26. (NCT00637273)
Timeframe: Week 26

Interventionpercentage of subjects (Number)
Exenatide Once Weekly58.8
Sitagliptin30.7
Pioglitazone43.6

[back to top]

Percentage of Subjects Achieving HbA1c Target of <=6.5% at Week 26

Percentages of subjects achieving HbA1c target values of <=6.5% at Week 26. (NCT00637273)
Timeframe: Week 26

Interventionpercentage of subjects (Number)
Exenatide Once Weekly38.8
Sitagliptin15.7
Pioglitazone26.7

[back to top]

Percentage of Subjects Achieving HbA1c Target of <=6.0% at Week 26

Percentages of subjects achieving HbA1c target values of <=6.0% at Week 26. (NCT00637273)
Timeframe: Week 26

Interventionpercentage of subjects (Number)
Exenatide Once Weekly13.8
Sitagliptin9.0
Pioglitazone4.8

[back to top]

Change in Systolic Blood Pressure From Baseline to Week 26

Change in systolic blood pressure from baseline (Day 1) to Week 26. (NCT00637273)
Timeframe: Day 1, Week 26

InterventionmmHg (Least Squares Mean)
Exenatide Once Weekly-3.6
Sitagliptin0.2
Pioglitazone-1.6

[back to top]

Change in Blood Pressure From Baseline to Week 26

Change in Systolic Blood Pressure (mmHg) and Diastolic Blood Pressure (mmHg) from Baseline to Week 26 (NCT00641056)
Timeframe: Baseline, Week 26

,
InterventionmmHg (Mean)
Systolic Blood PressureDiastolic Blood Pressure
Exenatide Once Weekly-3.03-1.15
Insulin Glargine-0.63-0.72

[back to top]

Percentage of Patients Achieving HbA1c <=7.0% at Week 26

Percentage of patients achieving HbA1c <=7.0% at Week 26 (for patients with HbA1c >7% at baseline) (NCT00641056)
Timeframe: Baseline, Week 26

Interventionpercentage of patients (Number)
Exenatide Once Weekly62.2
Insulin Glargine54.1

[back to top]

Change in Fasting Serum Glucose (FSG) From Baseline to Week 26

Change in FSG (mmol/L) from Baseline to Week 26 (NCT00641056)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly-2.13
Insulin Glargine-2.76

[back to top]

Change in HbA1c From Baseline to Week 26

Change in HbA1c from baseline to Week 26 (NCT00641056)
Timeframe: Baseline, Week 26

Interventionpercentage of total hemoglobin (Least Squares Mean)
Exenatide Once Weekly-1.47
Insulin Glargine-1.31

[back to top]

Change in High-density Lipoprotein Cholesterol (HDL) From Baseline to Week 26

Change in HDL (mmol/L) from Baseline to Week 26 (NCT00641056)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly-0.00
Insulin Glargine0.01

[back to top]

Change in Total Cholesterol From Baseline to Week 26

Change in Total Cholesterol (mmol/L) from Baseline to Week 26 (NCT00641056)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly-0.12
Insulin Glargine-0.04

[back to top]

Change in Body Weight (BW) From Baseline to Week 26

Change in BW (kg) from Baseline to Week 26 (NCT00641056)
Timeframe: Baseline, Week 26

Interventionkg (Least Squares Mean)
Exenatide Once Weekly-2.63
Insulin Glargine1.42

[back to top]

Percentage of Patients Achieving HbA1c <=6.5% at Week 26

Percentage of patients achieving HbA1c <=6.5% at Week 26 (for patients with HbA1c >6.5% at baseline) (NCT00641056)
Timeframe: Baseline, Week 26

Interventionpercentage of patients (Number)
Exenatide Once Weekly43.2
Insulin Glargine28.4

[back to top]

Ratio of Triglycerides at Week 26 to Baseline

Ratio of Triglycerides (measured in mmol/L) at Week 26 to Baseline. Log (Postbaseline Triglycerides) - log (Baseline Triglycerides); change from baseline to endpoint is presented as ratio of endpoint to baseline. (NCT00641056)
Timeframe: Baseline, Week 26

Interventionratio (Least Squares Mean)
Exenatide Once Weekly0.96
Insulin Glargine0.89

[back to top]

Assessment on Event Rate of Treatment-emergent Hypoglycemic Episodes

Major hypoglycemia: any episode with symptoms consistent with hypoglycemia that resulted in loss of consciousness or seizure with prompt recovery in response to administration of glucagon or glucose or documented hypoglycemia (blood glucose <3.0 mmol/L [54 mg/dL]) and required the assistance of another person. Minor hypoglycemia: any time a patient felt that he or she was experiencing a sign or symptom of hypoglycemia that was self-treated or resolved on its own and had a blood glucose level <3.0 mmol/L (54 mg/dL) and not classified as major hypoglycemia. (NCT00641056)
Timeframe: Baseline to Week 26

,,,
Interventionrate per subject-year (Mean)
Major HypoglycemiaMinor Hypoglycemia
Exenatide Once Weekly No SU0.010.10
Exenatide Once Weekly With SU0.001.14
Insulin Glargine No SU0.010.63
Insulin Glargine With SU0.032.66

[back to top]

Change in NAS

The NAFLD Activity Score (NAS) is an underweight sum of steatosis (score 0-3), inflammation (score 0-3), ballooning scores (0-2). The NAS can range from 0-8 with the higher score indicating more aggressive disease. (NCT00650546)
Timeframe: Between baseline and 28 weeks of treatment with exenatide, sub q, 5-10 mcq.

Interventionunits on a scale (Mean)
Individuals Who Recieved Treatment With Exenatide-1.5

[back to top]

Number of Patients With Improvement in Liver Histology After Treatment With Exenatide

Number of patients with liver histology improved with exenatide. The improvement of liver histology was defined as (1) no worsening of the fibrosis score, (11) improved score by at least one point in hepatocyte ballooning, and (111) either (a) improvement in NAS (NAFLD Activity Score) by two points spread across as least two of the three NAS components, or by (B)post-treatment NAS<3. (NCT00650546)
Timeframe: between baseline and 24-28 weeks after initiating treatment

Interventionparticipants (Number)
Treatment With Exenatide8

[back to top]

Percentage of Participants Achieving HbA1c Goals of < 7%, <= 6.5%, and < 6.5% Through Week 28

The percentage of participants achieving HbA1c goals of < 7%, <= 6.5%, and < 6.5% through Week 28 were compared between treatments using the Cochran-Mantel-Haenszel (CMH) procedure, in which screening HbA1c strata and background diabetes therapy strata served as the stratification factors. The CMH analysis excluded measurements after initiation of rescue medication and study drug discontinuation with missing data treated as non-responder. (NCT00658021)
Timeframe: Weeks 0, 4, 12, 20 and 28

,
Interventionpercentage of participants (Number)
HbA1c < 7%: Week 0HbA1c < 7%: Week 4HbA1c < 7%: Week 12HbA1c < 7%: Week 20HbA1c < 7%: Week 28HbA1c <=6.5%: Week 0HbA1c <=6.5%: Week 4HbA1c <=6.5%: Week 12HbA1c <=6.5%: Week 20HbA1c <=6.5%: Week 28HbA1c <6.5%: Week 0HbA1c <6.5%: Week 4HbA1c <6.5%: Week 12HbA1c <6.5%: Week 20HbA1c <6.5%: Week 28
Placebo38.142.933.335.728.616.723.823.819.019.07.121.419.019.014.3
Total Exenatide Twice Daily (EBID)37.244.943.635.933.317.929.533.324.423.115.426.930.821.823.1

[back to top]

Percentage of Participants Discontinuing the Study Due to Failure to Maintain Glycemic Control Through Week 28

"Participants were discontinued from the study due to failure to maintain glycemic control if either discontinuation reason on summary case report form was Loss of glucose control or AE with lower level Medical Dictionary for Regulatory Activities (MedDRA) term Loss of control of blood sugar or Hyperglycaemia leading to study drug discontinuation, using MedDRA Version 23.0." (NCT00658021)
Timeframe: Weeks 2, 4, 8, 12, 16, 20, 24 and 28

,
Interventionpercentage of participants (Number)
Week 2Week 4Week 8Week 12Week 16Week 20Week 24Week 28
Placebo02.405.0014.76.90
Total Exenatide Twice Daily (EBID)0001.41.4001.6

[back to top]

Adjusted Change From Baseline in Fasting Serum Insulin at Week 28

Change from baseline in fasting serum insulin is reported as adjusted LS mean values at Week 28. Baseline is defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of study medication. An ANCOVA analysis was performed, excluding measurements after initiation of rescue medication and study drug discontinuation. (NCT00658021)
Timeframe: Baseline (Day 1) and Week 28

Interventionpicomoles per liter (Least Squares Mean)
Total Exenatide Twice Daily (EBID)1.67
Placebo12.49

[back to top]

Adjusted Change From Baseline in Body Weight Through Week 28

Change from baseline in body weight is reported as adjusted LS mean values at Weeks 4, 12, 20 and 28. Baseline is defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of study medication. A MMRM analysis was performed, excluding measurements after initiation of rescue medication and study drug discontinuation. (NCT00658021)
Timeframe: Baseline (Day 1) up to Week 28

,
Interventionkilogram (Least Squares Mean)
Week 4Week 12Week 20Week 28
Placebo0.04-0.42-0.33-0.36
Total Exenatide Twice Daily (EBID)-0.89-1.09-0.71-0.81

[back to top]

Adjusted Change From Baseline in Fasting Serum Glucose (FSG) at Week 28

Change from baseline in FSG is reported as adjusted LS mean values at Week 28. Baseline is defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of study medication. An analysis of covariance (ANCOVA) analysis was performed, excluding measurements after initiation of rescue medication and study drug discontinuation. (NCT00658021)
Timeframe: Baseline (Day 1) and Week 28

Interventionmillimoles per liter (mmol/L) (Least Squares Mean)
Total Exenatide Twice Daily (EBID)0.791
Placebo1.072

[back to top]

Adjusted Change From Baseline in Glycated Hemoglobin A1c (HbA1c) at Week 28

Change from baseline in HbA1c is reported as adjusted least square (LS) mean values at Week 28. Baseline is defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of study medication. A mixed model with repeated measures (MMRM) analysis was performed, excluding measurements after initiation of rescue medication and study drug discontinuation. (NCT00658021)
Timeframe: Baseline (Day 1) and Week 28

Interventionpercentage (%HbA1c) (Least Squares Mean)
Total Exenatide Twice Daily (EBID)0.11
Placebo0.38

[back to top]

Adjusted Change From Baseline in Homeostasis Model Assessments - Beta-Cell Function (HOMA-B) and Insulin Sensitivity (HOMA-S) at Week 28

Change from baseline in HOMA-B and HOMA-S are reported as adjusted LS mean values at Week 28. Baseline is defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of study medication. An ANCOVA analysis was performed, excluding measurements after initiation of rescue medication and study drug discontinuation. (NCT00658021)
Timeframe: Baseline (Day 1) and Week 28

,
Interventionpercentage (%HOMA-B and %HOMA-S) (Least Squares Mean)
HOMA-BHOMA-S
Placebo-22.10-2.90
Total Exenatide Twice Daily (EBID)-25.93-3.18

[back to top]

Number of Participants With Post-Treatment Adverse Events of Special Interest (AESI) During Safety Follow-up Period

Post-treatment adverse events (AEs) were defined as AEs that started or worsened during the off-treatment period (Safety Follow-up Period), which was defined as the day after the Week 28/early discontinuation (ED) visit to the date of completion of the Safety Follow-up Period. The AESIs recorded were as follows: hematological malignancies, thyroid neoplasms, pancreas neoplasms, aplastic anemia, pancreatitis, pregnancy and pregnancy outcomes (including congenital anomalies). (NCT00658021)
Timeframe: From 1 day after the Week 28/ED visit to 3 years after Week 28/ED visit.

InterventionParticipants (Count of Participants)
Exenatide 5 mcg0
Exenatide 10 mcg0
Placebo0

[back to top]

Adjusted Change From Baseline in Self-Monitored Blood Glucose (SMBG) at Week 28

Change from baseline in SMBG measurements are reported as adjusted LS mean values at Week 28. SMBG measurements were taken before (pre-prandial) and 2 hours after (post-prandial) the 2 main meals of the day on 3 separate days during the week before baseline (Day 1) and Week 28. Post-prandial excursions were calculated as the difference between the pre-prandial and post-prandial blood glucose concentrations (post-prandial - pre-prandial) and averaged (mean) over the 2 main meals over the 3 separate days in each period. Baseline is defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of study medication. An ANCOVA analysis was performed, excluding measurements after initiation of rescue medication and study drug discontinuation. (NCT00658021)
Timeframe: Pre-meal and 2 hours post-meal on Baseline (Day 1) and Week 28

,
Interventionmmol/L (Least Squares Mean)
Pre-meal SMBGPost-meal SMBGPost-prandial excursion SMBGOverall SMBG
Placebo-0.888-1.542-0.391-1.193
Total Exenatide Twice Daily (EBID)-0.699-1.029-0.181-0.877

[back to top]

The Percentage of Per Protocol Participants Randomized and Treated in Each Arm Who Had Lab-measured A1c <6.5% at 24 Weeks of Treatment

efficacy criteria, 50% of per protocol participants reached A1c target of <6.5% (NCT00667732)
Timeframe: After 24 weeks of randomized treatment

Interventionpercentage of participants (Number)
Exenatide Group50
Placebo Group12

[back to top]

The Percentage of Intent to Treat Participants Randomized and Treated in Each Arm Who Had Lab-measured A1c <6.5% at 24 Weeks of Treatment

(NCT00667732)
Timeframe: After 24 weeks of randomized treatment

Interventionpercentage of participants (Number)
Exenatide Group47
Placebo Group12

[back to top]

Percentage of Patients Achieving HbA1c <=7% at Week 26

Percentage of patients achieving HbA1c <=7% at Week 26 (for patients with baseline HbA1c >7%). (NCT00676338)
Timeframe: Baseline, Week 26

Interventionpercentage of patients (Number)
Exenatide Once Weekly64.2
Metformin57.3
Pioglitazone63.3
Sitagliptin45.5

[back to top]

Change in Body Weight From Baseline to Week 26

Change in Body Weight from baseline to Week 26. (NCT00676338)
Timeframe: Baseline, Week 26

Interventionkg (Least Squares Mean)
Exenatide Once Weekly-2.04
Metformin-2.00
Pioglitazone1.52
Sitagliptin-0.76

[back to top]

Assessment on Event Rate of Treatment-emergent Major Hypoglycemic Events

Major hypoglycemia is defined as any event that has symptoms consistent with hypoglycemia resulting in loss of consciousness or seizure that shows prompt recovery in response to administration of glucagon or glucose, or documented hypoglycemia (blood glucose <3.0 mmol/L [54 mg/dL]) requiring the assistance of another person because of severe impairment in consciousness or behavior (whether or not symptoms of hypoglycemia are detected by the patient). Mean event rate = total number of events for all subjects in a treatment regimen / the total number of subject years of exposure for all subjects in that treatment. Standard error = square root of (total number of events / (subject years of exposure)**2). (NCT00676338)
Timeframe: Baseline to Week 26

Interventionevents per subject-year (Mean)
Exenatide Once Weekly0.00
Metformin0.00
Pioglitazone0.00
Sitagliptin0.00

[back to top]

Assessment on Event Rate of Treatment-Emergent Minor Hypoglycemic Events

Minor hypoglycemia is defined as a sign or symptom associated with hypoglycemia that is either self-treated by the patient or resolves on its own AND has a concurrent finger stick blood glucose <3.0 mmol/L (54 mg/dL) and not classified as major hypoglycemia. Mean event rate = total number of events for all subjects in a treatment regimen / the total number of subject years of exposure for all subjects in that treatment. Standard error = square root of (total number of events / (subject years of exposure)**2). (NCT00676338)
Timeframe: Baseline to Week 26

Interventionevents per subject-year (Mean)
Exenatide Once Weekly0.05
Metformin0.00
Pioglitazone0.00
Sitagliptin0.00

[back to top]

Ratio of Fasting Triglycerides at Week 26 to Baseline

Ratio of Fasting Triglycerides (measured in mmol/L) at Week 26 to baseline. Log(Post-baseline Triglycerides) - log(Baseline Triglycerides); change from baseline to Week 26 is presented as ratio of endpoint to baseline. (NCT00676338)
Timeframe: Baseline, Week 26

Interventionratio (Least Squares Mean)
Exenatide Once Weekly0.98
Metformin0.96
Pioglitazone0.85
Sitagliptin0.94

[back to top]

Change in Systolic Blood Pressure From Baseline to Week 26.

Change in Systolic Blood Pressure from baseline to Week 26. (NCT00676338)
Timeframe: Baseline, Week 26

InterventionmmHg (Least Squares Mean)
Exenatide Once Weekly-1.25
Metformin0.14
Pioglitazone-1.74
Sitagliptin-1.81

[back to top]

Change in HbA1c From Baseline to Week 26

Change in HbA1c from baseline to Week 26. (NCT00676338)
Timeframe: Baseline, Week 26

Interventionpercentage of total hemoglobin (Least Squares Mean)
Exenatide Once Weekly-1.53
Metformin-1.48
Pioglitazone-1.63
Sitagliptin-1.15

[back to top]

Change in Fasting Total Cholesterol (TC) From Baseline to Week 26

Change in Fasting TC from baseline to Week 26. (NCT00676338)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly-0.24
Metformin-0.22
Pioglitazone0.09
Sitagliptin-0.01

[back to top]

Change in Fasting Serum Glucose (FSG) From Baseline to Week 26

Change in FSG from baseline to Week 26. (NCT00676338)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly-2.25
Metformin-1.98
Pioglitazone-2.57
Sitagliptin-1.13

[back to top]

Change in Fasting High-Density Lipoprotein (HDL) From Baseline to Week 26

Change in Fasting HDL from baseline to Week 26. (NCT00676338)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly0.01
Metformin0.07
Pioglitazone0.17
Sitagliptin0.04

[back to top]

Change in Diastolic Blood Pressure From Baseline to Week 26.

Change in Diastolic Blood Pressure from baseline to Week 26. (NCT00676338)
Timeframe: Baseline, Week 26

InterventionmmHg (Least Squares Mean)
Exenatide Once Weekly-0.50
Metformin-0.86
Pioglitazone-2.50
Sitagliptin-0.45

[back to top]

Treatment Emergent Adverse Events

Safety endpoints: Incidence and severity of events related to islet infusion, immunosuppression, and islet preparations (NCT00679042)
Timeframe: From first islet transplant through one year after last transplant (maximum 3 infusions possible), an average of 1 year

InterventionParticipants (Count of Participants)
TEAESerious TEAETEAEs rated as severe or beyondTEAEs leading to death or discontinuation
Treatment2111160

[back to top]

Reduction in Hypoglycemic Severity Measured by %Reduction in HYPO Score

%reduction in Ryan HYPO Score [%(baseline score - 1-year post transplant score)/baseline] at time of evaluation. (NCT00679042)
Timeframe: One year after the first and last transplant

Interventionpercentage of HYPO baseline (Mean)
% Reduction from baseline to first tx day 365% Reduction from baseline to last tx day 365
Treatment66.190.1

[back to top]

Number of Subjects Reaching the Efficacy Goal

"A successful primary endpoint was defined as HbA1c ≤ 6.5% at the one-year follow-up visit and absence of severe hypoglycemic events (SHE) from Day 28 post-first transplant to 1 year after first and last transplant.~The primary analysis was to estimate the true rate of the composite favorable outcome at 1 year following first and last transplant in patients in the ITT population." (NCT00679042)
Timeframe: One year after islet transplant

InterventionParticipants (Count of Participants)
Success at 1 yr post first transplantSuccess at 1 yr post last transplant
Treatment811

[back to top]

Number of Patients Presenting With Insulin Independence at Day 365 Post First and Last Transplant

"Number of patients presenting with insulin independence, including:~Absence of exogenous insulin injection reported at Day 365.~Fasting capillary glucose level not exceeding 140 mg/dL (7.8 mmol/L) more than 3 times in a week (based on measuring capillary glucose levels a minimum of 7 times in a 7-day period) at Day 365 ± 28 days.~Fasting plasma glucose level ≤ 126 mg/dL (7.0 mmol/L) at Day 365 ± 28 days (if the fasting plasma glucose level is > 126 mg/dL [7.0 mmol/L], it must have been confirmed in an additional 1 out of 2 measurements).~Two-hour post-prandial capillary glucose not exceeding 180 mg/dL (10.0 mmol/L) more than 1 out of every 7 times in a week (based on measuring capillary glucose levels a minimum of 7 times in a 7-day period) at Day 365 ± 28 days.~Evidence of endogenous insulin production defined as fasting or stimulated C-peptide levels ≥ 0.5 ng/mL (0.16 nmol/L) at Day 365 ± 28 days" (NCT00679042)
Timeframe: 1 year after islet infusion

InterventionParticipants (Count of Participants)
First Tx Day 365 Absence of exogenous insulinLast Tx Day 365 Absence of exogenous insulinFirst Tx Day 365 Fasting capillary glucose in a week not exceeding 140 mg/dL more than 3XLast Tx Day 365 Fasting capillary glucose in a week not exceeding 140 mg/dL more than 3XFirst Tx Day 365 Fasting plasma glucose ≤126 mg/dLLast Tx Day 365 Fasting plasma glucose ≤126 mg/dLFirst Tx Day 365 Post-prandial capillary glucose in a week: Not exceeding 180 mg/dL more than 1X/7XLast Tx Day 365 Post-prandial capillary glucose in a week: Not exceeding 180 mg/dL more than 1X/7XFirst Tx Day 365 C-peptide (fasting or stimulated) ≥0.5 ng/mLLast Tx Day 365 C-peptide (fasting or stimulated) ≥0.5 ng/mL
Treatment1012741011531010

[back to top]

Hypoglycemic Episodes by HYPO Score

"Hypoglycemic episodes will be measured by the Ryan hypoglycemic (HYPO) Score derived from the number and severity of hypoglycemic episodes recorded throughout the follow-up phase from Day 28 to Day 365.~(From Ryan et al., 2004) A HYPO score was generated based on a combination of scores from the 4 weeks of readings and the patients' self-reported episodes over the previous year using the scoring system found in online appendix 2 (available at http://diabetes.diabetesjournals.org). The record sheets returned by the patients were analyzed for the number of episodes of glucose values recorded as <2.5 mmol/l and between 2.5 and 2.9 mmol/l. Points were awarded if symptoms were absent or were neuroglycopenic rather than autonomic... Thus the more severe the problem with hypoglycemia, the higher the score. A Ryan score ranges from 0 (no event) to a cumulative sum of episode points of total events reported during the 4 weeks then multiplied by 13 to provide a 1-year value." (NCT00679042)
Timeframe: One year after the last transplant

Interventionscore on a scale (Median)
Baseline (pre-Tx)First Tx Day 365Last Tx Day 365
Treatment26640.618.7

[back to top]

Change in Triglycerides From Baseline to 6 Months

Change in triglycerides (NCT00701935)
Timeframe: baseline, 6 months

Interventionmmol/L (Least Squares Mean)
Exenatide BID-0.17
Placebo0.06

[back to top]

Change in Weight From Baseline to 6 Months

Change in weight (NCT00701935)
Timeframe: baseline, 6 months

Interventionkg (Least Squares Mean)
Exenatide BID-2.54
Placebo-0.33

[back to top]

Percentage Change in Abdominal Visceral Fat From Baseline to 6 Months

Percentage change in abdominal visceral fat (NCT00701935)
Timeframe: baseline, 6 months

Intervention% change (Least Squares Mean)
Exenatide BID-5.28
Placebo-4.30

[back to top]

Percentage Change in Subcutaneous Abdominal Fat From Baseline to 6 Months

Percentage change in subcutaneous abdominal fat (NCT00701935)
Timeframe: baseline, 6 months

Intervention% change (Least Squares Mean)
Exenatide BID-7.27
Placebo-3.56

[back to top]

Percentage Change in Total Abdominal Fat From Baseline to 6 Months

Percentage change in total abdominal fat (NCT00701935)
Timeframe: baseline, 6 months

Intervention% change (Least Squares Mean)
Exenatide BID-5.81
Placebo-3.74

[back to top]

Assessment of Event Rate of Treatment- Emergent Hypoglycemic Event

All hypoglycemia episodes defined as major (results in loss of consciousness, seizure or coma resolving after administration of glucagon or glucose OR needing third-party assistance to resolve due to severe impairment in consciousness and associated with glucose concentration < 2.8 mol/L.) or minor (non-major event with symptoms consistent with hypoglycemia and glucose value < 2.8 mmol/L prior to treating) or symptoms of hypoglycemia (does not meet the criteria for a major or minor event). (NCT00701935)
Timeframe: baseline, 6 months

Interventionhypoglycemia rate/year (Mean)
Exenatide BID0.41
Placebo0.12

[back to top]

Change in Diastolic Blood Pressure From Baseline to 6 Months

Change in Diastolic blood pressure (NCT00701935)
Timeframe: baseline, 6 months

InterventionmmHg (Mean)
Exenatide BID-2.86
Placebo-0.18

[back to top]

Change in Fasting Plasma Glucose From Baseline to 6 Months

Change in Fasting plasma glucose (NCT00701935)
Timeframe: baseline, 6 months

Interventionmmol/L (Least Squares Mean)
Exenatide BID-1.47
Placebo-0.08

[back to top]

Percentage of Patients With HbA1c <=7.0% at 6 Months

Percentage of patients with HbA1c values <= 7.0% measured at 6 months. HbA1c is a measurement of the amount of hemogobin that is glycosylated. (NCT00701935)
Timeframe: 6 months

InterventionPercentage of patients (Number)
Exenatide BID60.7
Placebo21.4

[back to top]

Change in HbA1c From Baseline to 6 Months

Change in HbA1c from baseline to 6 months. HbA1c is a measurement of the amount of hemogobin that is glycosylated. (NCT00701935)
Timeframe: baseline, 6 months

Intervention% change (Least Squares Mean)
Exenatide BID-0.69
Placebo0.19

[back to top]

Change in High-Density Lipoprotein (HDL) Cholesterol From Baseline to 6 Months

Change in HDL cholesterol (NCT00701935)
Timeframe: baseline, 6 months

Interventionmmol/L (Least Squares Mean)
Exenatide BID0.06
Placebo0.04

[back to top]

Change in Systolic Blood Pressure From Baseline to 6 Months

Change in Systolic blood pressure (NCT00701935)
Timeframe: baseline, 6 months

InterventionmmHg (Mean)
Exenatide BID-7.48
Placebo1.79

[back to top]

Change in Total Cholesterol From Baseline to 6 Months

Change in total cholesterol (NCT00701935)
Timeframe: baseline, 6 months

Interventionmmol/L (Least Squares Mean)
Exenatide BID-0.06
Placebo0.14

[back to top]

Percentage of Patients With Glycosylated Hemoglobin (HbA1c) Level Less Than 7% at Week 24

The on-treatment period for this efficacy variable is time from the first dose of study drug and up to 3 days after the last dose of study drug, on or before Visit 11 (Week 24) or Day 169 if Visit 11 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00707031)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Lixisenatide48.5
Exenatide49.8

[back to top]

Absolute Change From Baseline in Glycosylated Hemoglobin (HbA1c) at Week 24

Absolute Change = HbA1c value at Week 24 minus HbA1c value at baseline. The on-treatment period for this efficacy variable is time from the first dose of study drug and up to 3 days after the last dose of study drug, on or before Visit 11 (Week 24) or Day 169 if Visit 11 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00707031)
Timeframe: Baseline, Week 24

Interventionpercentage of hemoglobin (Least Squares Mean)
Lixisenatide-0.79
Exenatide-0.96

[back to top]

Change From Baseline in Body Weight at Week 24

Change was calculated by subtracting baseline value from Week 24 value. The on-treatment period for this efficacy variable is time from the first dose of study drug and up to 3 days after the last dose of study drug, on or before Visit 11 (Week 24) or Day 169 if Visit 11 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00707031)
Timeframe: Baseline, Week 24

Interventionkilogram (Least Squares Mean)
Lixisenatide-2.96
Exenatide-3.98

[back to top]

Change From Baseline in Fasting Plasma Glucose (FPG) at Week 24

Change was calculated by subtracting baseline value from Week 24 value. The on-treatment period for this efficacy variable is time from the first dose of study drug and up to 1 day after the last dose of study drug, on or before Visit 11 (Week 24) or Day 169 if Visit 11 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00707031)
Timeframe: Baseline, Week 24

Interventionmmol/L (Least Squares Mean)
Lixisenatide-1.22
Exenatide-1.45

[back to top]

Percentage of Patients Requiring Rescue Therapy During Main 24-Week Period

Routine fasting self-monitored plasma glucose (SMPG) and central laboratory FPG (and HbA1c after week 12) values were used to determine the requirement of rescue medication. If fasting SMPG value exceeded the specified limit for 3 consecutive days, the central laboratory FPG (and HbA1c after week 12) were performed. Threshold values - from baseline to Week 8: fasting SMPG/FPG >270 milligram/deciliter (mg/dL) (15.0 mmol/L), from Week 8 to Week 12: fasting SMPG/FPG >240 mg/dL (13.3 mmol/L), and from Week 12 to Week 24: fasting SMPG/FPG >200 mg/dL (11.1 mmol/L) or HbA1c > 8.5%. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00707031)
Timeframe: Baseline up to Week 24

Interventionpercentage of participants (Number)
Lixisenatide2.2
Exenatide3.8

[back to top]

Percentage of Patients With at Least 5% Weight Loss From Baseline at Week 24

The on-treatment period for this efficacy variable is time from the first dose of study drug and up to 3 days after the last dose of study drug, on or before Visit 11 (Week 24) or Day 169 if Visit 11 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00707031)
Timeframe: Baseline, Week 24

Interventionpercentage of participants (Number)
Lixisenatide25.1
Exenatide31.4

[back to top]

Percentage of Patients With Glycosylated Hemoglobin (HbA1c) Level Less Than or Equal to 6.5% at Week 24

The on-treatment period for this efficacy variable is time from the first dose of study drug and up to 3 days after the last dose of study drug, on or before Visit 11 (Week 24) or Day 169 if Visit 11 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00707031)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Lixisenatide28.5
Exenatide35.4

[back to top]

Quality of Life: Change From Baseline in Patient's Satisfaction to Treatment (PAGI-QOL) at Week 24

PAGI-QOL: a 30-item self-administered questionnaire to measure health related QOL of patients with upper gastrointestinal disorders during past 2 weeks. Consists of 5 sub-scales. Each item rated on a 0-5 point Likert scale (0 [none of the time] to 5 [all the time]). Sub-scale score calculated by dividing sum of all items of subscale by number of items in the sub-scale. Total score calculated by taking mean of sub-scale scores. Sub-scale score and total score ranges from 0=none of the time (lowest score) to 5=all of the time (highest score) with lower scores indicating better QOL. The on-treatment period for this variable is time from the first dose of study drug and up to 3 days after the last dose of study drug, on or before Visit 11 (Week 24) or Day 169 if Visit 11 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00707031)
Timeframe: Baseline, Week 24

Interventionunits on a scale (Least Squares Mean)
Lixisenatide-0.09
Exenatide-0.06

[back to top]

Number of Patients With Symptomatic Hypoglycemia and Severe Symptomatic Hypoglycemia

Symptomatic hypoglycemia was an event with clinical symptoms that were considered to result from a hypoglycemic episode with an accompanying plasma glucose less than 60 mg/dL (3.3 mmol/L) or associated with prompt recovery after oral carbohydrate, intravenous glucose, or glucagon administration if no plasma glucose measurement was available. Severe symptomatic hypoglycemia was an event with clinical symptoms that were considered to result from hypoglycemia in which the patient required the assistance of another person and was associated with either a plasma glucose level below 36 mg/dL (2.0 mmol/L) or prompt recovery after oral carbohydrate, intravenous glucose, or glucagon administration, if no plasma glucose measurement was available. (NCT00707031)
Timeframe: First dose of study drug up to 3 days after the last dose administration, for up to 116 weeks

,
Interventionparticipants (Number)
Symptomatic HypoglycemiaSevere Symptomatic Hypoglycemia
Exenatide460
Lixisenatide160

[back to top]

Episodes of Hypoglycemia (Overall)

Number of episodes of hypoglycemia experienced overall during the study (NCT00729326)
Timeframe: 4 weeks and 8 weeks

Interventionepisodes of hypoglycemia (Number)
Exenatide3
Sitagliptin1

[back to top]

Episodes of Hypoglycemia (Week 4 to Week 8)

Number of episodes of hypoglycemia experienced between week 4 and week 8 of the study (NCT00729326)
Timeframe: 8 weeks

Interventionepisodes of hypoglycemia (Number)
Exenatide2
Sitagliptin0

[back to top]

Percentage of Patients Experiencing Hypoglycemia (Week 4 to Week 8)

Percentage of patients experiencing minor hypoglycemia with a confirmed glucose <54mg/dL (NCT00729326)
Timeframe: 8 weeks

InterventionPercentage of patients (Number)
Exenatide5.7
Sitagliptin0.0

[back to top]

Change in Postprandial C-peptide AUC After the Morning Meal

Change in postprandial C-peptide AUC after the morning meal (t=0 to 4 hours) (i.e., postprandial C-peptide AUC after the morning meal at baseline minus postprandial C-peptide AUC after the morning meal at endpoint) (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionnmol*hours/L (Least Squares Mean)
Exenatide-1.78
Sitagliptin0.25

[back to top]

Change in Postprandial C-peptide AUC Excursion After the Morning Meal

Change in Postprandial C-peptide AUC excursion after the morning meal (t=0 to 4 hours) (i.e., postprandial C-peptide AUC excursion after the morning meal at baseline minus postprandial C-peptide AUC excursion after the morning meal at endpoint) (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionnmol*hours/L (Least Squares Mean)
Exenatide-2.83
Sitagliptin0.14

[back to top]

Change in Fasting Blood Glucose After the Morning Meal

Change in fasting blood glucose after the morning meal from baseline to endpoint (i.e., fasting blood glucose after the morning meal at baseline minus fasting blood glucose after the morning meal at endpoint) (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionmg/dL (Least Squares Mean)
Exenatide-28.93
Sitagliptin-28.22

[back to top]

Change in Postprandial Active GLP-1 AUC After the Morning Meal

Change in Postprandial active GLP-1 AUC after the morning meal (t=0 to 4 hours) (i.e., postprandial active GLP-1 AUC after the morning meal at baseline minus postprandial active GLP-1 AUC after the morning meal at endpoint) (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionpmol*hours/L (Least Squares Mean)
Exenatide-14.28
Sitagliptin47.37

[back to top]

Change in Postprandial Active GLP-1 AUC Excursion After the Monrning Meal

Change in Postprandial active GLP-1 AUC excursion after the morning meal (t=0 to 4 hours) (i.e., postprandial active GLP-1 AUC excursion after the morning meal at baseline minus postprandial active GLP-1 AUC excursion after the morning meals at endpoint) (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionpmol*hours/L (Least Squares Mean)
Exenatide-14.04
Sitagliptin23.53

[back to top]

Change in Postprandial Glucagon Area Under the Concentration-time Curve (AUC) After the Morning Meal

Change in Postprandial Glucagon AUC after the morning meal (t=0 to 4 hours) (i.e., Glucagon AUC over the first 4 hours following the morning meal at baseline minus glucagon AUC over the first 4 hours following the morning meal at endpoint) (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionpmol*hours/L (Least Squares Mean)
Exenatide-29.60
Sitagliptin-16.91

[back to top]

Change in Postprandial Glucagon AUC Excursion After the Morning Meal

Change in postprandial glucagon AUC excursion after the morning meal (t=0 to 4 hours) (i.e., glucagon AUC excursion for 4 hours following the morning meal at baseline minus glucagon AUC excursion for 4 hours following the morning meal at endpoint) (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionpmol*hours/L (Least Squares Mean)
Exenatide-30.94
Sitagliptin-14.93

[back to top]

Change in Postprandial Insulin AUC After the Morning Meal

Change in postprandial insulin AUC after the morning meal (t=0 to 4 hours) (i.e., postprandial insulin AUC after the morning meal at baseline minus postprandial insulin AUC after the morning meal at endpoint) (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionpmol*hours/L (Least Squares Mean)
Exenatide-396.12
Sitagliptin-8.79

[back to top]

Change in Postprandial Insulin AUC Excursion After the Morning Meal

Change in Postprandial insulin AUC excursion after the morning meal (t=0 to 4 hours) (i.e., postprandial insulin AUC excursion after the morning meal at baseline minus postprandial insulin AUC excursion after the morning meal at endpoint) (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionpmol*hours/L (Least Squares Mean)
Exenatide-525.01
Sitagliptin-34.83

[back to top]

Change in Two-hour Postprandial Glucose After the Morning Meal

Change in 2 hour post-prandial glucose after the morning meal from baseline to endpoint (i.e., glucose level 2 hours after the morning meal at baseline minus glucose level 2 hours after the morning meal at endpoint) (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionmg/dL (Least Squares Mean)
Exenatide-108.35
Sitagliptin-44.43

[back to top]

Change in Time-averaged Glucose During a 24 Hour Period

Change in time-averaged glucose during a 24-hour period from baseline to endpoint (i.e., time-averaged glucose over 24 hours at endpoint minus time-averaged glucose over 24 hours at baseline). (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionmg/dL (Least Squares Mean)
Exenatide-41.65
Sitagliptin-29.56

[back to top]

Change in Postprandial Triglyceride AUC Excursion After the Morning Meal

Change in postprandial triglyceride AUC excursion after the morning meal (t=0 to 4 hours) (i.e., postprandial triglyceride AUC excursion after the morning meal at baseline minus postprandial triglyceride AUC excursion after the morning meal at endpoint) (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionmg*hours/dL (Least Squares Mean)
Exenatide-108.16
Sitagliptin-41.39

[back to top]

Change in Postprandial Triglyceride AUC After the Morning Meal

Change in postprandial triglyceride AUC after the morning meal (t=0 to 4 hours) (i.e., postprandial triglyceride AUC after the morning meal at baseline minus postprandial triglyceride AUC after the morning meal at endpoint) (NCT00729326)
Timeframe: baseline and 8 Weeks

Interventionmg*hours/dL (Least Squares Mean)
Exenatide0.83
Sitagliptin0.87

[back to top]

Percentage of Patients Experiencing Hypoglycemia (Baseline to Week 4)

Percentage of patients experiencing minor hypoglycemia with a confirmed glucose <54mg/dL (NCT00729326)
Timeframe: 4 Weeks

InterventionPercentage of patients (Number)
Exenatide2.9
Sitagliptin2.7

[back to top]

Percentage of Patients Experiencing Hypoglycemia (Overall)

Percentage of patients experiencing minor hypoglycemia with a confirmed glucose <54mg/dL (NCT00729326)
Timeframe: 4 weeks and 8 weeks

InterventionPercentage of patients (Number)
Exenatide4.3
Sitagliptin1.4

[back to top]

Episodes of Hypoglycemia (Baseline to Week 4)

Number of episodes of hypoglycemia experienced during the first 4 weeks of the study (NCT00729326)
Timeframe: 4 weeks

Interventionepisodes of hypoglycemia (Number)
Exenatide1
Sitagliptin1

[back to top]

Median Glucose Values From Steady State Through 48 Hours or Until Discharge.

Time to steady state was defined as the time from the initiation of drug infusion to first glucose value that is ≤140 mg/dl. Median glucose values were then calculated for each patient from the start of steady state through 48 hours or until discharge. (NCT00736229)
Timeframe: 1-48 hours

Interventionmg/dL (Median)
Exenatide132
Moderate127
Intensive105

[back to top]

Serious Adverse Events (Death, Non-fatal Myocardial Infarction, and Non-fatal Stroke Through 30 Days)

(NCT00736229)
Timeframe: 30 days

Interventionparticipants (Number)
Exenatide4

[back to top]

Time to Steady State

Time to steady state was defined as the time from the initiation of drug infusion (Exenatide or Insulin) to first glucose value that is ≤140 mg/dl. (NCT00736229)
Timeframe: Start of infusion through 48 hours or until discharge

Interventionhours (Median)
Exenatide2.0
Moderate12.0
Intensive3.0

[back to top]

Rates of Hypoglycemia and Severe Hypoglycemia

Total number of patients having at least one hypoglycemic episode (blood glucose less than 70 mg/dl), including episodes classified as severe (blood glucose less than 50 mg/dl) (NCT00736229)
Timeframe: 1-48 hours

,,
Interventionparticipants (Number)
Patients with at least one hypoglycemic episodePatients with at least one severe episode
Exenatide40
Intensive221
Moderate142

[back to top]

Change in Body Weight From Baseline to Week 52

Change in body weight from baseline to endpoint (NCT00753896)
Timeframe: Baseline, Week 52

Interventionkg (Mean)
Exenatide Once Weekly-1.50

[back to top]

Change in Fasting Serum Glucose From Baseline to Week 52

Change in fasting serum glucose from baseline to endpoint (NCT00753896)
Timeframe: Baseline, Week 52

Interventionmmol/L (Mean)
Exenatide Once Weekly-1.59

[back to top]

Change in HbA1c From Baseline to Week 52

Change in HbA1c from baseline to endpoint (NCT00753896)
Timeframe: Baseline, Week 52

Interventionpercentage of total hemoglobin (Mean)
Exenatide Once Weekly-0.78

[back to top]

Change in Triglycerides From Baseline to Week 52

Change in Triglycerides from baseline to endpoint (NCT00753896)
Timeframe: Baseline, Week 52

Interventionmmol/L (Mean)
Exenatide Once Weekly-0.19

[back to top]

Assessment of Event Rate of Treatment-Emergent Hypoglycemic Events

Major hypoglycemia: any episode with symptoms consistent with hypoglycemia that resulted in loss of consciousness or seizure with prompt recovery in response to administration of glucagon or glucose OR documented hypoglycemia (blood glucose <3.0 mmol/L [54 mg/dL]) and required the assistance of another person. Minor hypoglycemia: any sign or symptom associated with hypoglycemia that is either self-treated by the patient or resolves on its own AND has a concurrent finger stick blood glucose <3.0 mmol/L (54 mg/dL) and not classified as major hypoglycemia. Mean event rate = total number of events for all subjects in a treatment regimen / the total number of subject years of exposure for all subjects in that treatment. Standard error = square root of (total number of events / (subject years of exposure)**2). (NCT00753896)
Timeframe: Baseline to Week 52

Interventionevents per subject-year (Mean)
Major HypoglycemiaMinor Hypoglycemia
Exenatide Once Weekly0.000.02

[back to top]

Change in Blood Pressure From Baseline to Week 52

Change in Systolic and Diastolic Blood Pressure from baseline to endpoint (NCT00753896)
Timeframe: Baseline, Week 52

InterventionmmHg (Mean)
Systolic Blood PressureDiastolic Blood Pressure
Exenatide Once Weekly-1.69-0.19

[back to top]

Percentage of Patients Experiencing Adverse Events

Percentage of patients experiencing treatment-emergent adverse events over 52 weeks (NCT00753896)
Timeframe: Baseline to Week 52

Interventionpercentage of patients (Number)
Exenatide Once Weekly73.1

[back to top]

Percentage of Patients Achieving HbA1c <=7% at Week 52

Percentage of patients achieving HbA1c <=7% at endpoint (for patients with HbA1c >7% at baseline) (NCT00753896)
Timeframe: Baseline, Week 52

Interventionpercentage of patients (Number)
Exenatide Once Weekly68.8

[back to top]

Percentage of Patients Achieving HbA1c <=6.5% at Week 52

Percentage of patients achieving HbA1c <=6.5% at endpoint (for patients with HbA1c >6.5% at baseline) (NCT00753896)
Timeframe: Baseline, Week 52

Interventionpercentage of patients (Number)
Exenatide Once Weekly54.2

[back to top]

Change in Total Cholesterol From Baseline to Week 52

Change in Total Cholesterol from baseline to endpoint (NCT00753896)
Timeframe: Baseline, Week 52

Interventionmmol/L (Mean)
Exenatide Once Weekly-0.18

[back to top]

Change in High-density Lipoprotein (HDL) From Baseline to Week 52

Change in HDL from baseline to endpoint (NCT00753896)
Timeframe: Baseline, Week 52

Interventionmmol/L (Mean)
Exenatide Once Weekly0.04

[back to top]

Change in Triglycerides

Change in triglycerides following 30 weeks of therapy (i.e., triglycerides at week 30 minus triglycerides at baseline) (NCT00765817)
Timeframe: baseline and 30 weeks

Interventionmmol/L (Least Squares Mean)
Exenatide Arm-0.02
Placebo Arm-0.03

[back to top]

Change in Total Cholesterol

Change in total cholesterol following 30 weeks of therapy (i.e., total cholesterol at week 30 minus total cholesterol at baseline) (NCT00765817)
Timeframe: baseline and 30 weeks

Interventionmmol/L (Least Squares Mean)
Exenatide Arm-0.16
Placebo Arm-0.02

[back to top]

Percentage of Subjects Experiencing Minor Hypoglycemia

Percentage of subjects in each arm experiencing at least one episode of minor hypoglycemia at any point during the study. Minor hypoglycemia was defined as any time a subject felt he or she was experiencing a sign or symptom associated with hypoglycemia that was either self-treated by the subject or resolved on its own and had a concurrent finger stick blood glucose <3.0 mmol/L (54 mg/dL). (NCT00765817)
Timeframe: baseline and weeks 2, 4, 6, 8, 10, 14, 18, 22, 26, and 30

Interventionpercentage (Number)
Exenatide Arm24.8
Placebo Arm28.7

[back to top]

Change in Fasting Serum Glucose

Change in fasting serum glucose following 30 weeks of therapy (i.e., fasting serum glucose at week 30 minus fasting serum glucose at baseline) (NCT00765817)
Timeframe: baseline and 30 weeks

Interventionmmol/L (Least Squares Mean)
Exenatide Arm-1.28
Placebo Arm-0.87

[back to top]

Change in High Density Lipoprotein (HDL) Cholesterol

Change in HDL cholesterol following 30 weeks of therapy (i.e., HDL cholesterol at week 30 minus HDL cholesterol at baseline) (NCT00765817)
Timeframe: baseline and 30 weeks

Interventionmmol/L (Least Squares Mean)
Exenatide Arm0.01
Placebo Arm0.00

[back to top]

Change in Systolic Blood Pressure (SBP)

Change in SBP following 30 weeks of therapy (i.e., SBP at week 30 minus SBP at baseline) (NCT00765817)
Timeframe: baseline and 30 weeks

InterventionmmHg (Least Squares Mean)
Exenatide Arm-2.74
Placebo Arm1.71

[back to top]

Change in Glycosylated Hemoglobin (HbA1c)

Change in HbA1c from baseline following 30 weeks of therapy (i.e., HbA1c at week 30 minus HbA1c at baseline). Unit of measure is percent of hemoglobin that is glycosylated. (NCT00765817)
Timeframe: baseline and 30 weeks

Interventionpercentage of hemoglobin (Least Squares Mean)
Exenatide Arm-1.71
Placebo Arm-1.00

[back to top]

Change in Body Weight

Change in body weight following 30 weeks of therapy (i.e., body weight at week 30 minus body weight at baseline) (NCT00765817)
Timeframe: baseline and 30 weeks

Interventionkg (Least Squares Mean)
Exenatide Arm-1.78
Placebo Arm0.96

[back to top]

Change in Daily Insulin Dose

Change in daily insulin dose following 30 weeks of therapy (i.e., daily insulin dose at week 30 minus daily insulin dose at baseline) (NCT00765817)
Timeframe: baseline and 30 weeks

Interventioninsulin units (U) (Least Squares Mean)
Exenatide Arm13.19
Placebo Arm19.71

[back to top]

Change in 7-point Self-monitored Blood Glucose (SMBG) Profile

Change in 7-point (pre-breakfast, 2 hour post-breakfast, pre-lunch, 2 hour post-lunch, pre-dinner, 2 hour post-dinner, 0300 hours) SMBG profile from baseline to week 30 (change = blood glucose value at week 30 minus blood glucose value at baseline) (NCT00765817)
Timeframe: baseline and 30 weeks

,
Interventionmmol/L (Least Squares Mean)
Pre-breakfast: baselinePre-breakfast: change at week 302 hour post-breakfast: baseline2 hour post-breakfast: change at week 30Pre-lunch: baselinePre-lunch: change at week 302 hour post-lunch: baseline2 hour post-lunch: change at week 30Pre-dinner: baselinePre-dinner: change at week 302 hour post-dinner: baseline2 hour post-dinner: change at week 300300: baseline0300: change at week 30
Exenatide Arm7.89-1.5810.89-3.568.95-2.2311.35-2.749.85-2.2512.03-3.878.95-2.27
Placebo Arm8.27-1.4811.82-1.729.77-1.1511.70-1.389.99-1.3311.86-1.349.20-1.48

[back to top]

Change in Low Density Lipoprotein (LDL) Cholesterol

Change in LDL cholesterol following 30 weeks of therapy (i.e., LDL cholesterol at week 30 minus LDL cholesterol at baseline) (NCT00765817)
Timeframe: baseline and 30 weeks

Interventionmmol/L (Least Squares Mean)
Exenatide Arm-0.19
Placebo Arm-0.00

[back to top]

Change in Waist Circumference

Change in waist circumference following 30 weeks of therapy (i.e., waist circumference at week 30 minus waist circumference at baseline) (NCT00765817)
Timeframe: baseline and 30 weeks

Interventioncm (Least Squares Mean)
Exenatide Arm-1.08
Placebo Arm-0.25

[back to top]

Change in Daily Insulin Dose (on a Per Body Weight Basis)

Change in daily insulin dose per kilogram (kg) following 30 weeks of therapy (i.e., daily insulin dose per kg at week 30 minus daily insulin dose per kg at baseline) (NCT00765817)
Timeframe: baseline and 30 weeks

Interventioninsulin units per kg (U/kg) (Least Squares Mean)
Exenatide Arm0.15
Placebo Arm0.20

[back to top]

Change in Diastolic Blood Pressure (DBP)

Change in DBP following 30 weeks of therapy (i.e., DBP at week 30 minus DBP at baseline) (NCT00765817)
Timeframe: baseline and 30 weeks

InterventionmmHg (Least Squares Mean)
Exenatide Arm-1.73
Placebo Arm1.69

[back to top]

Percentage of Patients Achieving HbA1c <=7%

Percentage of patients in each arm who had HbA1c >7% at baseline and had HbA1c <=7% at week 30 (percentage = [number of subjects with HbA1c <=7% at week 30 divided by number of subjects with HbA1c >7% at baseline] * 100%). (NCT00765817)
Timeframe: baseline and 30 weeks

Interventionpercentage (Number)
Exenatide Arm58.3
Placebo Arm31.1

[back to top]

Percentage of Patients Achieving HbA1c <=6.5%

Percentage of patients in each arm who had HbA1c >6.5% at baseline and had HbA1c <=6.5% at week 30 (percentage = [number of subjects with HbA1c <=6.5% at week 30 divided by number of subjects with HbA1c >6.5% at baseline] * 100%). (NCT00765817)
Timeframe: baseline and 30 weeks

Interventionpercentage (Number)
Exenatide Arm42.0
Placebo Arm13.3

[back to top]

Minor Hypoglycemia Rate Per Year

Number of minor hypoglycemia events experienced per subject per year. Minor hypoglycemia was defined as any time a subject felt he or she was experiencing a sign or symptom associated with hypoglycemia that was either self-treated by the subject or resolved on its own and had a concurrent finger stick blood glucose <3.0 mmol/L (54 mg/dL). (NCT00765817)
Timeframe: baseline and weeks 2, 4, 6, 8, 10, 14, 18, 22, 26, and 30

Interventionevents per subject per year (Mean)
Exenatide Arm1.61
Placebo Arm1.55

[back to top]

Effect on Functional Beta-cell Mass as Determined by Change in ß-cell Secretory Capacity at 6 Months (μU/ml)

The acute insulin response to arginine (AIRarg) performed during the 340mg/dl glucose clamp allows for estimation of the the beta-cell secretory capacity (AIRmax) or functional beta-cell mass. Changes from baseline to 6 months of AIRmax were compared across groups (NCT00775684)
Timeframe: Baseline and 6 months

,,
InterventionμU/ml (Mean)
Acute Insulin Response (AIRmax)BaselineAcute Insulin Response (AIRmax) 6 Months
Exenatide214188.5
Glimepiride133202.5
Sitagliptin149158.3

[back to top]

PG 50 (the Plasma Glucose Level at Which Half-maximal Insulin Secretion is Achieved During the Glucose-potentiated Arginine Test) at Baseline and 6 Months

Between ∼60 and 250 mg/dL, the magnitude of AIRarg is a linear function of the plasma glucose level, so the difference in AIRarg at fasting and 230 mg/dL glucose levels divided by the difference in plasma glucose (ΔAIRarg/ΔPG) gives the glucose-potentiation slope (GPS) (8,24-26). Using the y-intercept (b) from the line created by these two points, the plasma glucose level at which half-maximal insulin secretion is achieved (PG50) is derived from solving the equation 1/2 (AIRmax) = (GPS · PG50) + b, and provides a measure of β-cell sensitivity to glucose The mean difference after 6 months in PG 50 were compared. Listed below are the PG50 values at baseline and 6 months. (NCT00775684)
Timeframe: Baseline and 6 months

,,
Interventionmg/dL (Mean)
PG50 BaselinePG50 6 Months
P50 Exenatide175190
P50 Glimepiride168182
P50 Sitagliptin226209

[back to top]

Change in Acute Insulin Response to Arginine. (AIRarg)

The changes in B-cell insulin secretion, Acute Insulin Response to arginine (AIRarg) after 6 months were compared to baseline AIRarg for each group. Listed below are AIRarg at baseline and 6 months for each group. (NCT00775684)
Timeframe: Baseline and 6 months

,,
InterventionuU/mL (Mean)
Acute Insulin Response (AIRarg) BaselineAcute Insulin Response (AIRarg) 6 Months
AIRarg Exenatide5252
AIRarg Glimepiride4442
AIRarg Sitagliptin3534

[back to top]

Effect on Functional Beta-cell Mass as Determined by Change in ß-cell Secretory Capacity at 6 Months (pg/mL)

AGRmin is performed during the 340mg/dl glucose clamp allows for estimation of the minimum alpha-cell glucagon secretion. Changes from baseline to 6 months of AGRmin were compared across groups. (NCT00775684)
Timeframe: Baseline and 6 months

,,
Interventionpg/mL (Mean)
Acute Glucose Response (AGRmin) BaselineAcute Glucose Response (AGRmin) 6 Months
Exenatide5152
Glimepiride3759
Sitagliptin5559

[back to top]

Insulin Sensitivity at Baseline and 6 Months

Insulin sensitivity (M/I) was determined by dividing the mean glucose infusion rate required during the 230 mg/dL glucose clamp (M) by the mean prestimulus insulin level (I) between 40 and 45 min of the glucose infusion The mean difference after 6 months in insulin sensitivity (M/I) were compared (NCT00775684)
Timeframe: Baseline and 6 months

,,
Intervention((mg/kg) /min) /uU/mL (Mean)
M/I BaselineM/I 6 Months
M/I Exenatide0.30.3
M/I Glimepiride0.30.3
M/I Sitagliptin0.30.3

[back to top]

Change From Baseline in Insulin Concentration

(NCT00782418)
Timeframe: Pre and Post glucose infusion

InterventionμIU(insulin)/mL (Least Squares Mean)
HGC - Exenatide 5 μg592
HGC - Exenatide 1.5 μg293
HGC - Placebo46.5

[back to top]

Change From Baseline in Insulin Secretion Rate (ISR) Normalized to Ambient Plasma Glucose

"Comparison of Glucose Dependent Insulin Secretion (GDIS) measured after HGC at steady-state to GDIS measured after GGI at the highest glucose infusion rate.~Insulin Secretion Rate (ISR)/ Blood Glucose (BG)" (NCT00782418)
Timeframe: Steady-state of HGC: 90 - 120 minutes post dose; highest glucose infusion rate of GGI: 120 - 160 minutes post dose

Intervention(ng/min) / (mg/dL) (Geometric Mean)
HGC - Exenatide 5 μg2.14
HGC - Exenatide 1.5 μg1.49
HGC - Placebo0.53
GGI - Exenatide 5 μg2.95
GGI - Exenatide 1.5 μg2.07
GGI - Placebo0.71

[back to top]

Change From Baseline in C-peptide Concentration

(NCT00782418)
Timeframe: Pre and Post glucose infusion

Interventionng/mL (Least Squares Mean)
HGC - Exenatide 5 μg29.3
HGC - Exenatide 1.5 μg22.6
HGC - Placebo6.24

[back to top]

Change in Aortic Stiffness, as Measured by the Change in the Mean Aortic Pulse Wave Velocity

(NCT00799435)
Timeframe: Measured at Week 12

,
Interventionm/sec (Mean)
Baseline Pulse Wave VelocityFollow-up Pulse Wave Velocity
Exenatide9.310.2
Usual Care11.4NA

[back to top]

HbA1c

change in HbA1c was measured before and after treatment in three groups (NCT00845182)
Timeframe: baseline and 6 months

Interventionpercent point decrease from baseline (Mean)
Pioglitazone1.37
Exenatide1.09
Drug Pioglitazone and Drug Exentatide1.91

[back to top]

Effect of Pioglitazone, Exenatide and Combined Pioglitazone and Exenatide on Body Weight

Effect of Pioglitazone, Exenatide and combined Pioglitazone and Exenatide on body weight and beta cell function (NCT00845182)
Timeframe: baseline and 6 months

Interventionkg (Mean)
PIOGLITAZONE5.5
EXENATIDE2.4
PIOGLITAZONE and EXNATIDE2.7

[back to top]

Change in Weight From Baseline to Endpoint.

Change in weight from baseline to endpoint in the intent-to-treat (ITT) population (all subjects who took at least one dose of study medication and had one post-baseline evaluation). (NCT00845507)
Timeframe: 16 Weeks

InterventionPounds (Mean)
Exenatide Group-1.1
Placebo Group5.9

[back to top]

Change in Body Mass Index (BMI) From Baseline to Endpoint.

Secondary outcome measures included change in body mass index (BMI). (NCT00845507)
Timeframe: 16 Weeks

InterventionKgs/meter squared (Mean)
Exenatide Group-0.2
Placebo Group1.0

[back to top]

Confirmed Clinical Neuropathy (CCN)

CCN was defined by a composite score comprised of at least two positive responses among symptoms, sensory signs, or absent or hypoactive reflexes consistent with a distal symmetrical polyneuropathy (16), and at least one abnormal nerve conduction study result in two anatomically distinct nerves, e.g. the sural sensory and peroneal motor nerves (defined as a amplitude < 5 μV and a conduction velocity < 40 m/sec for the sural nerve and an amplitude < 2.5 μV and a conduction velocity < 40 m/sec for the peroneal nerve). (NCT00855439)
Timeframe: 18 Months

Interventionparticipants (Number)
Exenatide14
Glargine18

[back to top]

Cardiac Autonomic Neuropathy (CAN)

Group differences in E/I ratio, a measure of cardiac autonomic function. (NCT00855439)
Timeframe: 18 months

Interventionunit-less measure (Mean)
Exenatide1.1
Glargine1.1

[back to top]

Cardiac Autonomic Neuropathy

resting heart rate as marker of autonomic function at rest (NCT00855439)
Timeframe: 18 month

Interventionbeats per minute (Mean)
Exenatide70
Glargine77

[back to top]

Intra-epidermal Nerve Fiber Density

Exploratory endpoint: Regeneration of intra-epidermal nerve fibers after denervation by capsiacin. (NCT00855439)
Timeframe: 12 months

Interventionnerve fibers per mm of skin (Mean)
Exenatide2.1
Glargine4.6

[back to top]

Energy Intake

Mean of 3-day food intake change between 3 days (Day 6-7-8) at baseline assessment and 3 days (Day 12-13-14) during the intervention period between the exenatide and placebo groups (NCT00856609)
Timeframe: Day 6-7-8 (at baseline) and Day 12-13-14 (3 days after starting study intervention)

Interventionkcal/day (Mean)
Exenatide1016.1
Placebo245.1

[back to top]

Body Weight

Mean decrease between pre- and post-randomization in 5 Weeks between the exenatide and placebo groups. (NCT00856609)
Timeframe: 5 weeks

Interventionkg (Mean)
Exenatide1.6
Placebo0.27

[back to top]

Twenty-four-hour Energy Expenditure

Change of twenty-four-hour energy expenditure between at Day 5 at baseline assessment and at Day 11 two days after starting study medication between the exenatide and placebo groups (NCT00856609)
Timeframe: Day 5 and Day 11

Interventionkcal/day (Mean)
Exenatide51.6
Placebo28.9

[back to top]

Incidence of Hypoglycemia (Overall)

Incidence of hypoglycemic episodes experienced overall during the study (NCT00870194)
Timeframe: Baseline to 20 Weeks

InterventionParticipants (Number)
Exenatide + Placebo5
Exenatide + Sitagliptin10

[back to top]

Change in Body Weight (kg)

Change in body weight from baseline to endpoint (Week 20) (NCT00870194)
Timeframe: Baseline to 20 Weeks

Interventionkg (Least Squares Mean)
Exenatide + Placebo-2.58
Exenatide + Sitagliptin-2.20

[back to top]

Change in FSG (mmol/L)

Change in fasting serum glucose (FSG) from baseline to endpoint (Week 20) (NCT00870194)
Timeframe: Baseline to 20 Weeks

Interventionmmol/L (Least Squares Mean)
Exenatide + Placebo0.06
Exenatide + Sitagliptin-0.55

[back to top]

Change in HbA1c (Percent)

Change in HbA1c from baseline to endpoint (Week 20); difference of base percent values [X% - Y%] (NCT00870194)
Timeframe: Baseline to 20 Weeks

InterventionPercent HbA1c (Least Squares Mean)
Exenatide + Placebo-0.38
Exenatide + Sitagliptin-0.68

[back to top]

Change in HDL (mmol/L)

Change in high-density lipoprotein (HDL) cholesterol from baseline to endpoint (Week 20) (NCT00870194)
Timeframe: Baseline to 20 Weeks

Interventionmmol/L (Least Squares Mean)
Exenatide + Placebo-0.03
Exenatide + Sitagliptin-0.01

[back to top]

Change in LDL (mmol/L)

Change in low-density lipoprotein (LDL) cholesterol from baseline to endpoint (Week 20) (NCT00870194)
Timeframe: Baseline to 20 Weeks

Interventionmmol/L (Least Squares Mean)
Exenatide + Placebo0.06
Exenatide + Sitagliptin0.10

[back to top]

Change in Total Cholesterol (mmol/L)

Change in total cholesterol from baseline to endpoint (Week 20) (NCT00870194)
Timeframe: Baseline to 20 Weeks

Interventionmmol/L (Least Squares Mean)
Exenatide + Placebo0.09
Exenatide + Sitagliptin0.08

[back to top]

Change in Triglycerides (mmol/L)

Change in triglycerides from baseline to endpoint (Week 20) (NCT00870194)
Timeframe: Baseline to 20 Weeks

Interventionmmol/L (Least Squares Mean)
Exenatide + Placebo0.17
Exenatide + Sitagliptin-0.07

[back to top]

Change in Waist Circumference (cm)

Change in waist circumference from baseline to endpoint (Week 20) (NCT00870194)
Timeframe: Baseline to 20 Weeks

Interventioncm (Least Squares Mean)
Exenatide + Placebo-3.25
Exenatide + Sitagliptin-2.36

[back to top]

Incidence of Confirmed Hypoglycemia(Overall)

Incidence of confirmed hypoglycemia experienced overall during the study (NCT00870194)
Timeframe: Baseline to 20 Weeks

InterventionParticipants (Number)
Exenatide + Placebo1
Exenatide + Sitagliptin2

[back to top]

Incidence of Nocturnal Hypoglycemia (Overall)

Incidence of nocturnal hypoglycemia experienced overall during the study (NCT00870194)
Timeframe: Baseline to 20 Weeks

InterventionParticipants (Number)
Exenatide + Placebo0
Exenatide + Sitagliptin3

[back to top]

Incidence of Severe Hypoglycemia(Overall)

Incidence of severe hypoglycemia experienced overall during the study (NCT00870194)
Timeframe: Baseline to 20 Weeks

InterventionParticipants (Number)
Exenatide + Placebo1
Exenatide + Sitagliptin0

[back to top]

Percentage of Patients Achieving HbA1c <=7.0%

Percentage of patients whose baseline HbA1c was > 7.0% achieving HbA1c <=7.0% at endpoint (Week 20) (NCT00870194)
Timeframe: Baseline to 20 Weeks

InterventionPercentage (Number)
Exenatide + Placebo29.5
Exenatide + Sitagliptin44.3

[back to top]

Percentage of Patients Achieving HbA1c <7.0%

Percentage of patients whose baseline HbA1c was >=7.0% achieving HbA1c <7.0% at endpoint (Week 20) (NCT00870194)
Timeframe: Baseline to 20 Weeks

InterventionPercentage (Number)
Exenatide + Placebo26.6
Exenatide + Sitagliptin41.7

[back to top]

SMBG (mmol/L)

7 point Self Monitored Blood Glucose Profiles - daily mean value (Week 20) (NCT00870194)
Timeframe: Baseline to 20 Weeks

Interventionmmol/L (Least Squares Mean)
Exenatide + Placebo8.57
Exenatide + Sitagliptin8.16

[back to top]

Waist-to-Hip Ratio

Change in waist-to-hip ratio from baseline to endpoint (Week20) (NCT00870194)
Timeframe: Baseline to 20 Weeks

InterventionRatio (Least Squares Mean)
Exenatide + Placebo-0.01
Exenatide + Sitagliptin-0.00

[back to top]

Percentage of Patients Achieving HbA1c <=6.5%

Percentage of patients whose baseline HbA1c was > 6.5% achieving HbA1c <=6.5% at endpoint (Week 20) (NCT00870194)
Timeframe: Baseline to 20 Weeks

InterventionPercentage (Number)
Exenatide + Placebo16.5
Exenatide + Sitagliptin20.7

[back to top]

Ratio of Triglycerides at Week 24 to Baseline

Ratio of triglycerides (measured in mg/dL) at Week 24 to baseline (Day 1). Log (Postbaseline Triglycerides) - log (Baseline Triglycerides); change from baseline to endpoint is presented as ratio of endpoint to baseline. (NCT00877890)
Timeframe: Day 1, Week 24

Interventionratio (Least Squares Mean)
Exenatide Once Weekly0.94
Exenatide Twice Daily0.99

[back to top]

Assessment on Event Rate of Treatment-emergent Minor Hypoglycemic Events

The minor hypoglycemia category included events in which symptoms consistent with hypoglycemia were accompanied by a blood glucose concentration of less than 54 mg/dL prior to treatment and not classified as major hypoglycemia. (NCT00877890)
Timeframe: Day 1 to Week 24

Interventionrate per subject-year (Mean)
Exenatide Once Weekly With SU0.75
Exenatide Twice Daily With SU0.31
Exenatide Once Weekly No SU0.00
Exenatide Twice Daily No SU0.00

[back to top]

Change in Sitting Systolic Blood Pressure From Baseline to Week 24

Change in systolic blood pressure from baseline (Day 1) to Week 24. (NCT00877890)
Timeframe: Day 1, Week 24

InterventionmmHg (Least Squares Mean)
Exenatide Once Weekly-2.9
Exenatide Twice Daily-1.2

[back to top]

Change in Body Weight From Baseline to Week 24

Change in body weight from baseline (Day 1) to Week 24. (NCT00877890)
Timeframe: Day 1, Week 24

Interventionkg (Least Squares Mean)
Exenatide Once Weekly-2.33
Exenatide Twice Daily-1.37

[back to top]

Change in Fasting Plasma Glucose From Baseline to Week 24

Change in fasting plasma glucose from baseline (Day 1) to Week 24. (NCT00877890)
Timeframe: Day 1, Week 24

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-25.1
Exenatide Twice Daily-4.6

[back to top]

Change in HbA1c From Baseline to Week 24

Change in HbA1c from baseline (Day 1) to Week 24 [Week 24 - Baseline]. (NCT00877890)
Timeframe: Day 1, Week 24

Interventionpercentage of total hemoglobin (Least Squares Mean)
Exenatide Once Weekly-1.57
Exenatide Twice Daily-0.90

[back to top]

Change in Sitting Diastolic Blood Pressure From Baseline to Week 24

Change in diastolic blood pressure from baseline (Day 1) to Week 24. (NCT00877890)
Timeframe: Day 1, Week 24

InterventionmmHg (Least Squares Mean)
Exenatide Once Weekly0.2
Exenatide Twice Daily-0.1

[back to top]

Percentage of Subjects Achieving HbA1c Target of <7%

Percentages of subjects achieving HbA1c target value of <7% at Week 24. (NCT00877890)
Timeframe: Week 24

Interventionpercentage of subjects (Number)
Exenatide Once Weekly58.1
Exenatide Twice Daily30.1

[back to top]

Percentage of Subjects Achieving HbA1c Target of <=6.5%

Percentages of subjects achieving HbA1c target values of <=6.5% at Week 24. (NCT00877890)
Timeframe: Week 24

Interventionpercentage of subjects (Number)
Exenatide Once Weekly41.1
Exenatide Twice Daily16.3

[back to top]

Percentage of Subjects Achieving Fasting Plasma Glucose Target of <=126 mg/dL

Percentages of subjects achieving fasting plasma glucose target of <=126 mg/dL at Week 24. (NCT00877890)
Timeframe: Week 24

Interventionpercentage of subjects (Number)
Exenatide Once Weekly50.4
Exenatide Twice Daily30.9

[back to top]

Change in Total Cholesterol From Baseline to Week 24

Change in total cholesterol from baseline (Day 1) to Week 24. (NCT00877890)
Timeframe: Day 1, Week 24

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-15.4
Exenatide Twice Daily0.6

[back to top]

Change in High-density Lipoprotein (HDL) From Baseline to Week 24

Change in HDL from baseline (Day 1) to Week 24. (NCT00877890)
Timeframe: Day 1, Week 24

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly0.0
Exenatide Twice Daily1.3

[back to top]

Assessment on Event Rate of Treatment-emergent Major Hypoglycemic Events

The major hypoglycemia category included events that, in the judgment of the investigator or physician, resulted in loss of consciousness, seizure, coma, or other change in mental status consistent with neuroglycopenia, in which symptoms resolved after administration of intramuscular glucagon or intravenous glucose, required third-party assistance, and was accompanied by a blood glucose concentration of less than 54 mg/dL prior to treatment, whether or not symptoms of hypoglycemia were perceived by the subject. (NCT00877890)
Timeframe: Day 1 to Week 24

Interventionrate per subject-year (Mean)
Exenatide Once Weekly With SU0.00
Exenatide Twice Daily With SU0.00
Exenatide Once Weekly No SU0.00
Exenatide Twice Daily No SU0.00

[back to top]

The Primary Objective is to Determine the Ability of Intravenous Exenatide to: Maintain Intraoperative Euglycemia in Subjects With Initial Blood Glucose < 126 mg/dL in Surgical Subjects as Compared to Placebo,

Logistic regression analysis will be utizlized to determine maintenance of euglycemia (yes v no) for our primary analysis. A standard area under the curve (AUC) analysis will be performed for each time point to map out drug deposition. Assuming a standard 2 compartment model, 10 subjects per group is sufficient to accurately predict mean AUC. Our primary analysis should provide ample statistical power. (NCT00882050)
Timeframe: Baseline and 90 minutes after starting infusion;

,,
Interventionmlg/dL (Mean)
Pre glucose levelsat 90 minutes post infusion glucose levels
Exenatide 0.41ng/kg/Min108.1125.0
Exentatide 0.27 ng/kg/Min112.3120.3
Placebo IV NSS110.4120.8

[back to top]

Change in Body Mass Index (BMI)

Change in body mass index (BMI) over three months (NCT00886626)
Timeframe: 3-month

Interventionchange in kg/m^2 (Mean)
Exenatide-0.9
Control0.84

[back to top]

Least Square Mean Change From Baseline in Hemoglobin A1c (HbA1c) to Week 12 in Participants With Diabetes (Cohort 2) in the ITT Population

HbA1c was measured as a percent of hemoglobin at screening, Day 1, Weeks 4, 8, 12 or early termination. Last observation carried forward (LOCF) was applied to estimate missing values at post baseline timepoints. Baseline=Day 1, last measurement prior to first dose of study drug. (NCT00894322)
Timeframe: Day 1 to Week 12

InterventionPercent of hemoglobin (Least Squares Mean)
Cohort 2 Exenatide 2 mg-0.87
Cohort 2 Placebo0.08

[back to top]

Average Exenatide Concentration (Cave) of 10 mg Exenatide (Cohort 1) in Healthy Participants in the Pharmacokinetic Evaluable Population

Cohort 1: Blood samples for the assessment of plasma exenatide were collected at time = -15, 60, 90, 120, 180, 240, 360, and 480 minutes relative to study medication injection at time = 0 on Day 1. At all visits following the single dose, a single blood sample was collected for assessment of exenatide concentrations. Cave(0-168h) was the time-weighted mean concentration over the sampling period from time x to time y corresponding to AUC (0-168h) and was measured in picograms per milliliter (pg/mL). Exenatide concentration was measured using a validated enzyme-linked immunosorbent assay (ELISA). PK evaluable population consisted of all ITT participants who had at least 4 detectable plasma exenatide measurements [not less than (<) lower limits of quantification (LLOQ)] from Day 1 to Week 12 and had reliable PK data. (NCT00894322)
Timeframe: Day 1 to Week 1

Interventionpg/mL (Geometric Mean)
Cohort 1 Exenatide 10 mg32.5

[back to top]

AUC (0 Hour to 168 Hour) for 10 mg Exenatide (Cohort 1) in Healthy Participants in the Pharmacokinetic Evaluable Population

Cohort 1: Blood samples for the assessment of plasma exenatide were collected at time = -15, 60, 90, 120, 180, 240, 360, and 480 minutes relative to study medication injection at time = 0 on Day 1. At all visits following the single injection, a single blood sample was collected for assessment of exenatide concentrations. AUC (0-168 h) data represents average concentration rather than maximum concentration. Exenatide concentration was measured using a validated enzyme-linked immunosorbent assay (ELISA). AUC calculated using linear trapezoidal method from time x to time y and measured in pg*h/mL. PK evaluable population consisted of all ITT participants who had at least 4 detectable plasma exenatide measurements (not < LLOQ) from Day 1 to Week 12 and had reliable PK data. (NCT00894322)
Timeframe: Day 1 to Week 1

Interventionpg*h/mL (Geometric Mean)
Cohort 1 Exenatide 10 mg3269.6

[back to top]

Time to Maximum Concentration (Tmax) of 2 mg Exenatide (Cohort 2) in Participants With Diabetes in Pharmacokinetic Evaluable Population

Cohort 2: Blood samples for the assessment of plasma exenatide were collected on Day 1, Weeks 2, 4, 6, 8, and 10. At Week 10, blood samples were collected at time = -15, 60, 90, 120, 180, 240, and 360 minutes relative to study medication injection at time = 0. Tmax was measured in hours (h). Exenatide was measured using a validated ELISA. Tmax summarized at 0-6 h at Week 10, 0-168 h at Weeks 10-11, and 0-tlast at Weeks 10-12. PK evaluable population consisted of all ITT participants who had at least 4 detectable plasma exenatide measurements (not < LLOQ) from Day 1 to Week 12 and had reliable PK data. (NCT00894322)
Timeframe: Week 10, Weeks 10-11, Weeks 10-12

Interventionhours (Geometric Mean)
Tmax 0-6 h Week; n=18Tmax 0-168 h Weeks 10-11; n=18Tmax 0-tlast Weeks 10-12; n=17
Cohort 2 Exenatide 2 mg1.434.360.0

[back to top]

Time to Maximum Concentration (Tmax) for Single Dose of 10 mg Exenatide (Cohort 1) in Healthy Participants in the Pharmacokinetic Evaluable Population

Cohort 1: Blood samples for the assessment of plasma exenatide were collected at time(t) = -15, 60, 90, 120, 180, 240, 360, and 480 minutes relative to study medication injection at time = 0 on Day 1 an the mean is presented below. At all visits following the single injection, a single blood sample was collected for assessment of exenatide concentrations. Tmax was measured in hours and Tmax (0-8h) and (0-tlast) are presented below. Exenatide concentration was measured using a validated enzyme-linked immunosorbent assay (ELISA). PK evaluable population consisted of all ITT participants who had at least 4 detectable plasma exenatide measurements [not less than (<) lower limits of quantification (LLOQ)] and had reliable PK data. (NCT00894322)
Timeframe: Day 1, Week 12

Interventionhours (Geometric Mean)
Tmax (0 to 8 hours), n=27Tmax (0 hour to Week 12), n=30
Cohort 1 Exenatide 10 mg7.0998.1

[back to top]

Number of Participants With Treatment Emergent Adverse Events (TEAEs), Injection Site TEAEs, Serious Adverse Events (SAEs), Deaths, and Withdrawals Due to AEs in Cohort 1 and Cohort 2 in Intent to Treat (ITT) Population

Treatment emergent (TE)=occurs during or after treatment with study drug. Adverse Event (AE)=any new unfavorable symptom, sign, or disease or worsening of a preexisting condition that may not have a causal relationship with treatment. SAE=a medical event that at any dose results in death, persistent or significant disability/incapacity, or drug dependency/abuse; is life-threatening, an important medical event, or a congenital anomaly/birth defect; or requires or prolongs hospitalization. Participants experiencing multiple episodes of a given AE are counted once. Injection site AEs: adverse events that existed prior to Day 1 and worsened after the first administration at Day 1, or occurred after the first administration at Day 1 through Week 12, or after Study Termination if considered by investigator to be clinically significant. (NCT00894322)
Timeframe: Day 1 to Week12

,,
Interventionparticipants (Number)
TEAEInjection Site TEAEsWithdrawal due to AESAEDeath
Cohort 1 Exenatide 10 mg2616000
Cohort 2 Exenatide 2 mg2218000
Cohort 2 Placebo97010

[back to top]

Number of Participants With Hematology and Serum Chemistry Laboratory Values of Potential Clinical Importance in Cohorts 1 and 2 in ITT Population

Abbreviations: Upper Limit of Normal (ULN); milligram per deciliter (mg/dL); units per liter (U/L); micro liters (µL); creatine kinase (CK); gamma-glutamyltransferase (G-GT). Normal ranges = Hematocrit: 40.6-52.3% (male), 35.3-47.0 (female); Platelets 155-361*10^3/µL(male/female); Calcium: 8.6-10.4 mg/dL (male/female); CK: 43-350 U/L (male), 28-207 U/L (female); G-GT: 7-62 U/L (male/female); Glucose 73-105 mg/dL (male/female); Lipase 14-70 U/L (male/female); Uric acid: 3.5-7.8 mg/dL (male), 2.3-5.9 mg/dL (female). Blood samples for laboratories were collected at screening, Day 1, Weeks 4, 8, 12 or early termination. Value for potential clinical importance is presented in each category presented below. (NCT00894322)
Timeframe: Day 1 to Week 12

,,
Interventionparticipants (Number)
Hematocrit low <36%Platelets high <75 to >500*10^3/µ/LCalcium high <8 to >11 mg/dLCK high >3*ULNG-GT high >3*ULN in U/LGlucose low <50 to > 450 mg/dLLipase high >3*ULN in U/LUric Acid high >8.0 mg/dL
Cohort 1 Exenatide 10 mg00010100
Cohort 2 Exenatide 2 mg01100001
Cohort 2 Placebo10001010

[back to top]

Number of Participants Achieving HbA1c Less Than Equal to (<=) 6.5% and Less Than (<) 7% at Week 12 in Participants With Diabetes (Cohort 2) in the ITT Population

HbA1c was measured as a percent of hemoglobin at screening, Day 1, Weeks 4, 8, 12 or early termination. LOCF was applied to estimate missing values at post baseline timepoints. Baseline=Day 1, last measurement prior to first dose of study drug. (NCT00894322)
Timeframe: Week 12

,
Interventionparticipants (Number)
Baseline HbA1c >= 7%Week 12 HbA1c <= 6.5%Week 12 HbA1c <7%
Cohort 2 Exenatide 2 mg22914
Cohort 2 Placebo1212

[back to top]

Mean Change From Baseline to End of Study in Sitting Diastolic and Systolic Blood Pressure in Cohorts 1 and 2 in ITT Population

In Cohort 1, sitting blood pressures were obtained at Screening (Visit 1), Day 1 (Visit 2), Weeks 1-11 (Visits 3-13), Week 12 (Visit 14), and at early termination. Blood pressures (diastolic and systolic) were measured in millimeters of mercury (mmHg). In Cohort 2, sitting blood pressures were obtained at Screening (Visit 1), Day 1 (Visit 2), Weeks 1-10 (Visits 3-12), Week 11 (Visit 15), Week 12 (Visit 16) and at early termination. Baseline was defined as last measurement prior to first injection of study drug. (NCT00894322)
Timeframe: Day 1 to Week 12

,,
InterventionmmHg (Mean)
Diastolic Blood PressureSystolic Blood Pressure
Cohort 1 Exenatide 10 mg6.2-1.4
Cohort 2 Exenatide 2 mg4.6-8.4
Cohort 2 Placebo6.8-1.7

[back to top]

Maximum Concentration (Cmax) for Single Dose of 10 mg Exenatide (Cohort 1) in Healthy Participants in the Pharmacokinetic Evaluable Population

Cohort 1: Blood samples for the assessment of plasma exenatide were collected at time = -15, 60, 90, 120, 180, 240, 360, and 480 minutes relative to study medication injection at time = 0 on Day 1 and the mean is presented below. At all visits following the single injection, a single blood sample was collected for assessment of exenatide concentrations. Cmax was measured in picograms per milliliter (pg/mL). Exenatide concentration was measured using a validated enzyme-linked immunosorbent assay (ELISA). PK evaluable population consisted of all ITT participants who had at least 4 detectable plasma exenatide measurements [not less than (<) lower limits of quantification (LLOQ)] from Day 1 to Week 12 for the evaluation of the PK characteristics of plasma exenatide and had reliable PK data. Cmax (0-8h) and (0-tlast) are presented below. (NCT00894322)
Timeframe: Day 1, Week 12

Interventionpg/mL (Geometric Mean)
Cmax 0 hour to 8 hoursCmax 0 hour to Week 12
Cohort 1 Exenatide 10 mg34.9331.2

[back to top]

Maximum Concentration (Cmax) for 2 mg Exenatide (Cohort 2) in Participants With Diabetes in the Pharmacokinetic Evaluable Population

Cohort 2: Blood samples for the assessment of plasma exenatide were collected on Day 1, Weeks 2, 4, 6, 8, and 10. At Week 10, blood samples were collected at time = -15, 60, 90, 120, 180, 240, and 360 minutes relative to study medication injection at time = 0. Cmax was measured in pg/mL. Exenatide was measured using a validated enzyme-linked immunosorbent assay (ELISA). Cmax summarized at 0-6 h at Week 10, 0-168 h at Weeks 10-11, and 0-tlast at Weeks 10-12. PK evaluable population consisted of all ITT participants who had at least 4 detectable plasma exenatide measurements (not < LLOQ) from Day 1 to Week 12 and had reliable PK data. (NCT00894322)
Timeframe: Week 10, Weeks 10-11, Weeks 10-12

Interventionpg/mL (Geometric Mean)
Cmax at 0-6 h Week 10; n=18Cmax at 0-168 h Weeks 10=11; n=18Cmax at 0-tlast Weeks 10-12; n=17
Cohort 2 Exenatide 2 mg304.9362.6410.5

[back to top]

Average Exenatide Concentration (Cave) of 2 mg Exenatide (Cohort 2) in Participants With Diabetes in the Pharmacokinetic Evaluable Population

Cohort 2: Blood samples for the assessment of plasma exenatide were collected on Day 1, Weeks 2, 4, 6, 8, and 10. At Week 10, blood samples were collected at time = -15, 60, 90, 120, 180, 240, and 360 minutes relative to study medication injection at time = 0. At all visits following the single injection, a single blood sample was collected for assessment of exenatide concentrations. Cave(0-168h) and Cave(0-tlast) was the time-weighted mean concentration over the sampling period from time x to time y corresponding to AUC (0-168h), and AUC (0-tlast), respectively. Cave was measured in picograms per milliliter (pg/mL). Exenatide concentration was measured using a validated enzyme-linked immunosorbent assay (ELISA). PK evaluable population consisted of all ITT participants who had at least 4 detectable plasma exenatide measurements (not < LLOQ) from Day 1 to Week 12 and had reliable PK data. (NCT00894322)
Timeframe: Week 10 - Week 11; Week 10 - Week 12

Interventionpg/mL (Geometric Mean)
Cave at Weeks 10-11; n=18Cave at Weeks 10-12; n=17
Cohort 2 Exenatide 2 mg292.7302.4

[back to top]

Area Under the Curve (AUC) for Single Dose of 10 mg Exenatide (Cohort 1) in Healthy Participants in the Pharmacokinetic Evaluable Population

Cohort 1: Blood samples for the assessment of plasma exenatide were collected at time = -15, 60, 90, 120, 180, 240, 360, and 480 minutes relative to study medication injection at time = 0 on Day 1 and the mean is presented below. At all visits following the single injection, a single blood sample was collected for assessment of exenatide concentrations. AUC was measured in picograms * hours per milliliter (pg*hr/mL). Exenatide was measured using a validated enzyme-linked immunosorbent assay (ELISA). AUC calculated using linear trapezoidal method from time x to time y; AUC (0-8h) and (0-tlast) are presented below. Pharmacokinetic (PK) evaluable population consisted of all ITT participants who had at least 4 detectable plasma exenatide measurements [not less than (<) lower limits of quantification (LLOQ)] from Day 1 to Week 12 and had reliable PK data. (NCT00894322)
Timeframe: Day 1, Week 12

Interventionpg*h/mL (Geometric Mean)
AUC (0-8h), n=30AUC (0-Week 12), n=30
Cohort 1 Exenatide 10 mg125.6147220.2

[back to top]

Area Under the Curve (AUC) for 2 mg Exenatide (Cohort 2) in Participants With Diabetes in the Pharmacokinetic Evaluable Population

Cohort 2: Blood samples for the assessment of plasma exenatide were collected on Day 1, Weeks 2, 4, 6, 8, and 10. At Week 10, blood samples were collected at time = -15, 60, 90, 120, 180, 240, and 360 minutes relative to study medication injection at time = 0. AUC was measured in picograms * hours per milliliter (pg*hr/mL). Exenatide was measured using a validated enzyme-linked immunosorbent assay (ELISA). AUC calculated using linear trapezoidal method from time x to time y; AUC (0-6h) measured at Week 10, AUC (0-168h) steady state measured between Weeks 10 and 11, and AUC (0-tlast) for time interval between Weeks 10 and 12 (approximately336 hours) are presented below. PK evaluable population consisted of all ITT participants who had at least 4 detectable plasma exenatide measurements (not < LLOQ) from Day 1 to Week 12 and had reliable PK data. (NCT00894322)
Timeframe: Week 10-11; Weeks 10 - 12

Interventionpg*hr/mL (Geometric Mean)
AUC (0-6h) at Week 10, n=18AUC (0-168h) at Weeks 10-11, n=18AUC (0-tlast) at Weeks 10-12, n=17
Cohort 2 Exenatide 2 mg1535.349100.2101615.0

[back to top]

Antibody Titers for Participants With Treatment Emergent Positive Antibodies to Exenatide in Participants Who Received Exenatide in Cohorts 1 and 2

Serum titers of antibodies to exenatide were evaluated using a validated enzyme-linked immunosorbent assay (Covance Method No. ELISA-0308). Positive antibody to exenatide titer: observed at the indicated visit following a negative or missing titer at baseline, or a positive titer that has increased by at least 3 dilutions at the indicated visit from a detectable baseline. Baseline=Day 1. Negative titers were assigned a value of 1 in order to calculate geometric mean. Geometric mean of reportable titers, by study week, are presented below. (NCT00894322)
Timeframe: Day 1 to Week 12

,
InterventionReportable Titers (Geometric Mean)
Week 2, N=30, 23; n=4, 1Week 4, N=30, 23; n=14, 10Week 6, N=30, 23; n=0, 15Week 8, N=29, 23; n=22,15Week 10, N=29, 23; n=0,15Last visit, N=30, 23; n=20, 15
Cohort 1 Exenatide 10 mg25.0394.6NA300.7NA202.6
Cohort 2 Exenatide 2 mg25.0202.6295.9561.4453.0625.0

[back to top]

Mean Change From Baseline to End of Study in Sitting Heart Rate in Cohorts 1 and 2 in ITT Population

In Cohort 1, sitting heart rates were obtained at Screening (Visit 1), Day 1 (Visit 2), Weeks 1-11 (Visits 3-13), Week 12 (Visit 14), and at early termination. Heart rate was measured in beats per minute (bpm). In Cohort 2, sitting heart rates were obtained at Screening (Visit 1), Day 1 (Visit 2), Weeks 1-10 (Visits 3-12), Week 11 (Visit 15), Week 12 (Visit 16) and at early termination. Baseline was defined as last measurement prior to first injection of study drug. (NCT00894322)
Timeframe: Day 1 to Week 12

Interventionbpm (Mean)
Cohort 1 Exenatide 10 mg-7.5
Cohort 2 Exenatide 2 mg-5.4
Cohort 2 Placebo-9.1

[back to top]

Mean Change From Baseline at Week 12 in Fasting Plasma Glucose in Participants With Diabetes (Cohort 2) for the ITT Population

Baseline was the last measurement at the screening visit. Fasting plasma glucose (FPG) was measured at screening, Day 1, Weeks 2, 4, 6, 8, 12, or early termination and reported in milligrams per deciliter (mg/dL). (NCT00894322)
Timeframe: Baseline, Week 12

Interventionmg/dL (Least Squares Mean)
Cohort 2 Exenatide 2 mg-32
Cohort 2 Placebo8

[back to top]

Mean Change From Baseline at Week 12 in Body Weight in Participants With Diabetes (Cohort 2) in the ITT Population

Body weight was measured in kilograms (kg). Baseline was Day 1, last measurement prior to first dose of study drug. Body weight was measured at screening, Day 1, Weeks 4, 8, 12 or early termination and the LOCF approach was applied to estimate missing value at each post baseline timepoint. (NCT00894322)
Timeframe: Baseline, Week 12

Interventionkg (Least Squares Mean)
Cohort 2 Exenatide 2 mg-1.41
Cohort 2 Placebo-0.39

[back to top]

Number of Participants With Concomitant Medications in Cohort 1 and Cohort 2 in ITT Population

Concomitant medications are defined as those medications received on or after the date of the first injection on Day 1, including prior medications that continued past Day 1 and new concomitant medications. Participants may be counted in more than one medication class and no more than once in each class. Categories by Anatomical Therapeutic Chemical (ATC) classification using the World Health Organization (WHO) Drug Dictionary version C1, 01 March 2009. As per protocol, all participants in Cohort 1 could receive up to 2 anti-emetic medications approximately 30 minutes prior to the exenatide. (NCT00894322)
Timeframe: Day 1 to 12 weeks

Interventionparticipants (Number)
Cohort 1 Exenatide 10 mg30
Cohort 2 Exenatide 2 mg21
Cohort 2 Placebo11

[back to top]

Change in Fasting Serum Glucose (FSG) From Baseline to Week 26

Change in FSG from baseline to Week 26. (NCT00917267)
Timeframe: Baseline, Week 26

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-40.57
Exenatide Twice Daily-23.90

[back to top]

Change in HbA1c From Baseline to Week 26.

Change in HbA1c from baseline to Week 26. (NCT00917267)
Timeframe: Baseline, Week 26

Interventionpercentage of total hemoglobin (Least Squares Mean)
Exenatide Once Weekly-1.43
Exenatide Twice Daily-1.12

[back to top]

Change in High-Density Lipoprotein (HDL) From Baseline to Week 26

Change in HDL from baseline to Week 26. (NCT00917267)
Timeframe: Baseline, Week 26

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-0.11
Exenatide Twice Daily-0.48

[back to top]

Change in Total Cholesterol (TC) From Baseline to Week 26

Change in TC from baseline to Week 26. (NCT00917267)
Timeframe: Baseline, Week 26

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-9.41
Exenatide Twice Daily-8.10

[back to top]

Change in Body Weight (BW) From Baseline to Week 26

Change in BW from baseline to Week 26. (NCT00917267)
Timeframe: Baseline, Week 26

Interventionkg (Least Squares Mean)
Exenatide Once Weekly-1.63
Exenatide Twice Daily-2.45

[back to top]

Ratio of Triglycerides (TG) at Week 26 to Baseline

Ratio of TG (measured in mg/dL) at Week 26 to baseline. Log(Post-baseline TG) - log(Baseline TG); change from baseline to Week 26 is presented as ratio of Week 26 to baseline. (NCT00917267)
Timeframe: Baseline, Week 26

Interventionratio (Least Squares Mean)
Exenatide Once Weekly0.97
Exenatide Twice Daily0.97

[back to top]

Assessment of Event Rate of Treatment-emergent Hypoglycemic Events

Major hypoglycemia: any episode with symptoms consistent with hypoglycemia that resulted in loss of consciousness or seizure with prompt recovery in response to administration of glucagon or glucose OR documented hypoglycemia (blood glucose <3.0 mmol/L [54 mg/dL]) and required the assistance of another person. Minor hypoglycemia: any sign or symptom associated with hypoglycemia that is either self-treated by the patient or resolves on its own AND has a concurrent finger stick blood glucose <3.0 mmol/L (54 mg/dL) and not classified as major hypoglycemia. Event rate per subject year was calculated for each subject: (number of events observed from a subject/exposure from a subject)*365.25 where exposure = last post-baseline visit date - baseline visit date. Mean and Standard Error were then derived from ITT. (NCT00917267)
Timeframe: Baseline to Week 26

,,,
Interventionevents per subject-year (Mean)
Major HypoglycemiaMinor Hypoglycemia
Exenatide Once Weekly With SU Use at Screening0.000.24
Exenatide Once Weekly Without SU Use at Screening0.000.03
Exenatide Twice Daily With SU Use at Screening0.010.59
Exenatide Twice Daily Without SU Use at Screening0.000.11

[back to top]

Change in Blood Pressure From Baseline to Week 26

Change in systolic blood pressure and diastolic blood pressure from baseline to Week 26. (NCT00917267)
Timeframe: Baseline, Week 26

,
InterventionmmHg (Mean)
Systolic Blood PressureDiastolic Blood Pressure
Exenatide Once Weekly-5.33-1.47
Exenatide Twice Daily-5.22-2.24

[back to top]

Percentage of Patients Achieving HbA1c Targets <=7% at Week 26

Percentage of patients achieving HbA1c <=7% at Week 26 (for patients with HbA1c >7% at baseline). (NCT00917267)
Timeframe: Baseline, Week 26

Interventionpercentage of patients (Number)
Exenatide Once Weekly46.7
Exenatide Twice Daily35.7

[back to top]

Percentage of Patients Achieving HbA1c Targets <=6.5% at Week 26

Percentage of patients achieving HbA1c <=6.5% at Week 26 (for patients with HbA1c >6.5% at baseline). (NCT00917267)
Timeframe: Baseline, Week 26

Interventionpercentage of patients (Number)
Exenatide Once Weekly26.0
Exenatide Twice Daily15.5

[back to top]

Change in Body Weight From Baseline to Endpoint (Week 26)

Change in Body Weight from baseline to endpoint (Week 26) (NCT00935532)
Timeframe: Baseline, Week 26

Interventionkg (Least Squares Mean)
Exenatide Once Weekly-1.67
Insulin Glargine0.34

[back to top]

Change in Fasting Serum Glucose (FSG) From Baseline to Endpoint (Week 26)

Change in FSG (centralized measurement) from baseline to endpoint (Week 26) (NCT00935532)
Timeframe: Baseline, Week 26

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-46.09
Insulin Glargine-40.82

[back to top]

Change in HbA1c From Baseline to Endpoint (Week 26)

Change in HbA1c from baseline to endpoint (Week 26). (NCT00935532)
Timeframe: Baseline, Week 26

Interventionpercentage of total hemoglobin (Least Squares Mean)
Exenatide Once Weekly-1.11
Insulin Glargine-0.68

[back to top]

Change in High-density Lipoprotein Cholesterol (HDL-C) From Baseline to Endpoint (Week 26)

Change in HDL-C from baseline to endpoint (Week 26) (NCT00935532)
Timeframe: Baseline, Week 26

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-0.99
Insulin Glargine-0.71

[back to top]

Change in Total Cholesterol From Baseline to Endpoint (Week 26)

Change in Total Cholesterol from baseline to endpoint (Week 26) (NCT00935532)
Timeframe: Baseline, Week 26

Interventionmg/dL (Least Squares Mean)
Exenatide Once Weekly-14.21
Insulin Glargine-6.32

[back to top]

Percentage of Subjects Achieving HbA1c<=6.5%

Percentage of subjects achieving HbA1c <=6.5% (for subjects with HbA1c >6.5% at baseline) (NCT00935532)
Timeframe: Baseline, Week 26

Interventionpercentage of subjects (Number)
Exenatide Once Weekly20.6
Insulin Glargine4.2

[back to top]

Percentage of Subjects Achieving HbA1c<=7%

Percentage of subjects achieving HbA1c <=7.0% (for subjects with HbA1c >7% at baseline) (NCT00935532)
Timeframe: Baseline, Week 26

Interventionpercentage of subjects (Number)
Exenatide Once Weekly42.2
Insulin Glargine21.0

[back to top]

Ratio of Fasting Triglycerides at Endpoint (Week 26) to Baseline

Ratio of Triglycerides (measured in mg/dL) at endpoint (Week 26) to Baseline. Log(Postbaseline Triglycerides) - log(Baseline Triglycerides); change from baseline to endpoint is presented as ratio of endpoint to baseline. (NCT00935532)
Timeframe: Baseline, Week 26

Interventionratio (Least Squares Mean)
Exenatide Once Weekly1.00
Insulin Glargine1.00

[back to top]

Change in Blood Pressure From Baseline to Endpoint (Week 26)

Change in Blood Pressure from baseline to endpoint (Week 26) (NCT00935532)
Timeframe: Baseline, Week 26

,
InterventionmmHg (Mean)
Systolic Blood PressureDiastolic Blood Pressure
Exenatide Once Weekly-4.5-1.1
Insulin Glargine-2.6-2.5

[back to top]

Assessment on Event Rate of Treatment-emergent Major Hypoglycemic Events

Major confirmed hypoglycemia was defined as (1) any event accompanying symptoms consistent with hypoglycemia that resulted in loss of consciousness or seizure but resolved promptly in response to administration of glucagon or (2) glucose, or documented hypoglycemia (blood glucose <3.0 mmol/L [54 mg/dL]) requiring assistance because of severe impairment in consciousness or motor activity whether or not symptoms of hypoglycemia were felt by the patient. Event rate per subject year was calculated for each subject: (number of events observed from a subject/exposure from a subject)*365.25 where exposure = last postbaseline visit date - baseline visit date. Mean and SE were then derived from FAS. (NCT00935532)
Timeframe: Baseline to Week 26

Interventionevents per subject-year (Mean)
Exenatide Once Weekly0.00
Insulin Glargine0.00

[back to top]

Assessment on Event Rate of Treatment-emergent Minor Hypoglycemic Events

Minor confirmed hypoglycemia was defined as any event a patient felt that he or she was experiencing a sign or symptom associated with hypoglycemia that resolved by self-treatment or on its own, and a concurrent self-monitoring fingerstick blood glucose <3.0 mmol/L (54 mg/dL) and not classified as major hypoglycemia. Event rate per subject year was calculated for each subject: (number of events observed from a subject/exposure from a subject)*365.25 where exposure = last postbaseline visit date - baseline visit date. Mean and SE were then derived from FAS. (NCT00935532)
Timeframe: Baseline to Week 26

Interventionevents per subject-year (Mean)
Exenatide Once Weekly0.01
Insulin Glargine0.16

[back to top]

Mean Change in HbA1c (Per Protocol)

Mean change in HbA1c through Week 48 (NCT00943917)
Timeframe: Day 0 to Week 48

Interventionpercent change (Mean)
ITCA 650 20/20-1.00
ITCA 650 20/60-1.23
ITCA 650 40/40-0.69
ITCA 650 40/80-1.37
Ex Inj/ITCA 650 40-1.45
Ex Inj/ITCA 650 60-1.88

[back to top]

Mean Change in HbA1c (Per Protocol)

Mean change in HbA1c through Week 24 (NCT00943917)
Timeframe: Day 0 to Week 24

Interventionpercent change (Mean)
ITCA 650 20/20-.89
ITCA 650 20/60-1.26
ITCA 650 40/40-0.67
ITCA 650 40/80-1.36
Ex Inj/ITCA 650 40-1.01
Ex Inj/ITCA 650 60-1.51

[back to top]

Mean Change in HbA1c (Per Protocol)

Mean change in HbA1c over first 12 weeks (Stage I) (NCT00943917)
Timeframe: Day 0 and Week 12

Interventionpercent change (Mean)
ITCA 650 20 mcg/Day - STAGE I-0.96
ITCA 650 40 mcg/Day - STAGE I-1.04
Exenatide Injection - STAGE I-0.82

[back to top]

Mean Change in HbA1c (ITT)

Mean change in HbA1c through Week 48 (NCT00943917)
Timeframe: Day 0 to Week 48

Interventionpercent change (Mean)
ITCA 650 20/20-1.13
ITCA 650 20/60-1.25
ITCA 650 40/40-0.48
ITCA 650 40/80-1.40
Ex Inj/ITCA 650 40-1.16
Ex Inj/ITCA 650 60-1.84

[back to top]

Mean Change in HbA1c (ITT)

Mean change in HbA1c through Week 24 (NCT00943917)
Timeframe: Day 0 to Week 24

Interventionpercent change (Mean)
ITCA 650 20/20-0.89
ITCA 650 20/60-1.26
ITCA 650 40/40-0.70
ITCA 650 40/80-1.36
Ex Inj/ITCA 650 40-1.01
Ex Inj/ITCA 650 60-1.51

[back to top]

Mean Change in HbA1c (ITT)

Mean change in HbA1c through Week 12 (NCT00943917)
Timeframe: Day 0 to Week 12

Interventionpercent change (Mean)
ITCA 650 20 mcg/Day - STAGE I-.93
ITCA 650 40 mcg/Day - STAGE I-0.96
Exenatide Injection - STAGE I-0.75

[back to top]

Change in Diastolic Blood Pressure (DBP) From Baseline to Week 30

Change in Diastolic Blood Pressure (DBP) from baseline to Week 30 using MMRM model.The model included the respective baseline outcome as covariate, treatment, country, prior use of SUs, week of visit, and treatment-by-week interaction as fixed effects and patient and error as random effects. (NCT00960661)
Timeframe: baseline, Week 30

InterventionmmHg (Least Squares Mean)
Exenatide (BET)-0.64
Insulin Lispro (BBT)-0.14

[back to top]

Change in Systolic Blood Pressure (SBP) From Baseline to Week 30

Change in Systolic Blood Pressure (SBP) from baseline to Week 30 using MMRM model.The model included the respective baseline outcome as covariate, treatment, country, prior use of SUs, week of visit, and treatment-by-week interaction as fixed effects and patient and error as random effects. (NCT00960661)
Timeframe: Baseline, Week 30

InterventionmmHg (Least Squares Mean)
Exenatide (BET)-4.13
Insulin Lispro (BBT)0.37

[back to top]

Change in Body Weight From Baseline to Week 30.

Change in body weight from baseline to Week 30 using MMRM model.The model included the respective baseline outcome as covariate, treatment, country, prior use of SUs, week of visit, and treatment-by-week interaction as fixed effects and patient and error as random effects. (NCT00960661)
Timeframe: baseline, week 30

Interventionkg (Least Squares Mean)
Exenatide (BET)-2.45
Insulin Lispro (BBT)2.11

[back to top]

Change in Low Density Lipoprotein (LDL) From Baseline to Week 30

Change in Low Density Lipoprotein (LDL) from baseline to week 30 using ANCOVA model.The model included the respective secondary outcome as dependent variable, country, prior use of SU's and treatment groups as factors, and the respective outcomes baseline value as a covariate. (NCT00960661)
Timeframe: Baseline, Week 30

Interventionmmol/L (Least Squares Mean)
Exenatide (BET)-0.12
Insulin Lispro (BBT)-0.03

[back to top]

Change in Total Cholesterol From Baseline to Week 30

Change in total cholesterol from baseline to Week 30 using ANCOVA model. The model included the respective secondary outcome as dependent variable, country, prior use of SU's and treatment groups as factors, and the respective outcomes baseline value as a covariate. (NCT00960661)
Timeframe: Baseline, week 30

Interventionmmol/L (Least Squares Mean)
Exenatide (BET)-0.14
Insulin Lispro (BBT)-0.03

[back to top]

Major Hypoglycemia Rate Per Year

Mean (standard deviation) of major hyperglycemia episodes experienced per year. Rates per year were calculated for each individual as the number of episodes divided by the total number of days in the study (from randomization to last visit date), then multiplied by 365.25. Major hypoglycemia was defined as any symptoms consistent with hypoglycemia resulting in loss of consciousness or seizure that shows prompt recovery in response to administration of glucagon or glucose OR documented hypoglycemia (blood glucose <3.0 mmol/L [54 mg/dL]) and requiring the assistance of another person because of severe impairment in consciousness or behavior. (NCT00960661)
Timeframe: 30 weeks

Interventionrate per year (Mean)
Exenatide (BET)0.0
Insulin Lispro (BBT)0.1

[back to top]

Minor Hypoglycemia Rate Per Year

Mean (standard deviation) of minor hyperglycemia episodes experienced per year. Rates per year were calculated for each individual as the number of episodes divided by the total number of days in the study (from randomization to last visit date), then multiplied by 365.25. Minor hypoglycemia was defined as any time a participant feels that he or she is experiencing a sign or symptom associated with hypoglycemia that is either self-treated by the participant or resolves on its own AND has a concurrent finger stick blood glucose <3.0 mmol/L (54 mg/dL) (NCT00960661)
Timeframe: 30 weeks

Interventionrate per year (Mean)
Exenatide (BET)2.1
Insulin Lispro (BBT)5.0

[back to top]

Percent of Participants Achieving HbA1c ≤ 6.5%.

Percent of participants achieving HbA1c ≤ 6.5%. (NCT00960661)
Timeframe: Week 30

Interventionpercentage of participants (Number)
Exenatide (BET)26.2
Insulin Lispro (BBT)25.5

[back to top]

Percentage of Participants Achieving HbA1C < 7.0%

Percentage of participants achieving HbA1C < 7.0% (NCT00960661)
Timeframe: Week 30

InterventionPercentage of participants (Number)
Exenatide (BET)46.7
Insulin Lispro (BBT)42.6

[back to top]

Daily Insulin Glargine Dose at Baseline and at Week 30

Daily Insulin Glargine Dose at baseline and at Week 30 (NCT00960661)
Timeframe: Baseline, week 30

,
InterventionIU/day (Mean)
BaselineWeek 30
Exenatide (BET)61.556.9
Insulin Lispro (BBT)61.151.5

[back to top]

Change in High Density Lipoprotein (HDL) From Baseline to Week 30

Change in High Density Lipoprotein (HDL) from baseline to Week 30 using ANCOVA model.The model included the respective secondary outcome as dependent variable, country, prior use of SU's and treatment groups as factors, and the respective outcomes baseline value as a covariate. (NCT00960661)
Timeframe: Baseline, week 30

Interventionmmol/L (Least Squares Mean)
Exenatide (BET)-0.04
Insulin Lispro (BBT)0.03

[back to top]

Change in Glycosylated Hemoglobin (HbA1c) From Baseline to Week 30

Change in HbA1c from baseline following 30 weeks of therapy (i.e. HbA1c at week 30 minus HbA1c at baseline). (NCT00960661)
Timeframe: Baseline, 30 weeks

Interventionpercent of hemoglobin (Least Squares Mean)
Exenatide (BET)-1.13
Insulin Lispro (BBT)-1.10

[back to top]

Change in Fasting Blood Glucose (FBG) From Baseline to Week 30.

Change in fasting blood glucose (FBG) from Baseline to Week 30 using MMRM model. The model included the respective baseline outcome as covariate, treatment, country, prior use of SUs, week of visit, and treatment-by-week interaction as fixed effects and patient and error as random effects. (NCT00960661)
Timeframe: Baseline, Week 30

Interventionmmol/L (Least Squares Mean)
Exenatide (BET)-0.46
Insulin Lispro (BBT)0.18

[back to top]

Changes in Systolic Blood Pressure From Baseline to Week 26

Change in systolic blood pressure from baseline to Week 26 (NCT01003184)
Timeframe: Baseline, Week 26

InterventionmmHg (Least Squares Mean)
Exenatide Once Weekly-7.37
Insulin Detemir-2.65

[back to top]

Change in Triglycerides From Baseline to Endpoint (Week 26).

Change in triglycerides from baseline to endpoint (week 26). (NCT01003184)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly-0.01
Insulin Detemir-0.08

[back to top]

Percentage of Patients Achieving ≤6.5% at Endpoint

Percentage of patients achieving HbA1c ≤6.5% at endpoint (NCT01003184)
Timeframe: Week 26

InterventionPercentage (Number)
Exenatide Once Weekly27.9
Insulin Detemir7.6

[back to top]

Percentage of Patients Who Have Achieved HbA1c ≤7.4% With Weight Loss (≥1.0 kg) at Endpoint (Week 26)

Percentage of patients who have achieved HbA1c ≤7.4% with weight loss (≥1.0 kg) at endpoint (Week 26) (NCT01003184)
Timeframe: Baseline, Week 26

InterventionPercentage (Number)
Exenatide Once Weekly58.9
Insulin Detemir17.8

[back to top]

Change in Body Weight From Baseline to Week 26

Change in body weight from baseline to week 26 (NCT01003184)
Timeframe: Baseline, Week 26

Interventionkilograms (Least Squares Mean)
Exenatide Once Weekly-2.79
Insulin Detemir0.88

[back to top]

Change in Diastolic Blood Pressure From Baseline to Week 26.

Change in diastolic blood pressure from baseline to week 26. (NCT01003184)
Timeframe: Baseline, Week 26

InterventionmmHg (Least Squares Mean)
Exenatide Once Weekly-0.79
Insulin Detemir-0.34

[back to top]

Change in Fasting Serum Glucose From Baseline to Endpoint (Week 26).

Change in fasting serum glucose from baseline to endpoint (Week 26). (NCT01003184)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly-2.33
Insulin Detemir-2.43

[back to top]

Change in HbA1c From Baseline to Week 26

Change in HbA1c from baseline to week 26 (NCT01003184)
Timeframe: Baseline, Week 26

InterventionPercentage of total hemoglobin (Least Squares Mean)
Exenatide Once Weekly-1.32
Insulin Detemir-0.91

[back to top]

Change in High-density Lipoprotein (HDL) Cholesterol From Baseline to Endpoint (Week 26).

Change in High-density lipoprotein (HDL) cholesterol from baseline to endpoint (week 26). (NCT01003184)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly0.02
Insulin Detemir0.04

[back to top]

Change in Total Cholesterol From Baseline to Endpoint (Week 26).

Change in total cholesterol from baseline to endpoint (week 26). (NCT01003184)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly-0.09
Insulin Detemir0.06

[back to top]

Hypoglycemia Rate Per Year

All confirmed hypoglycemia episodes defined as either minor (any time a patient feels that he or she is experiencing a sign or symptom associated with hypoglycaemia and blood glucose (BG) <3.0 mmol/L (54 mg/dL)) or major (any hypoglycaemic episode with symptoms consistent with hypoglycaemia, resulting in loss of consciousness or seizure, and shows prompt recovery in response to administration of glucagon or glucose, or BG measurement < 3.0mmol/L is available and the patient is not capable of self-treating were taken into account. (NCT01003184)
Timeframe: Baseline, Week 26

Interventionevents per subject-year (Number)
Exenatide Once Weekly0.06
Insulin Detemir0.10

[back to top]

Percentage of Patients Achieving ≤7.0% at Endpoint

Percentage of patients achieving ≤7.0% at endpoint. (NCT01003184)
Timeframe: Week 26

InterventionPercentage (Number)
Exenatide Once Weekly51.4
Insulin Detemir34.3

[back to top]

Percentage of Patients Achieving Glycosylated Hemoglobin (HbA1c) Concentration ≤7.0% With Weight Loss (≥1.0 kg) at Endpoint (Week 26)

The primary endpoint is the percentage of patients achieving HbA1c concentration ≤7.0% with weight loss (≥1.0 kg) at endpoint. The last post-baseline measurement set of both non-missing HbA1c concentration and weight (measured at the same time point, i.e. visit) is used as endpoint value. Patients who do not have a baseline weight measurement, have a protocol violation of baseline HbA1c <=7.0%, and/or have missing post-baseline measurements for HbA1c concentration and/or weight, are included in the analysis as non-responders regarding the primary objective. (NCT01003184)
Timeframe: Baseline, Week 26

InterventionPercentage (Number)
Exenatide Once Weekly44.1
Insulin Detemir11.4

[back to top]

Percentage of Patients Achieving HbA1c ≤7.4% at Endpoint

Percentage of patients who have achieved HbA1c ≤.7.4% at endpoint (NCT01003184)
Timeframe: Week 26

InterventionPercentage (Number)
Exenatide Once Weekly66.7
Insulin Detemir54.3

[back to top]

Change in Anthropometric Variables (BMI).

(NCT01006889)
Timeframe: 6 months

InterventionKg/m2 (Mean)
Exenatide (Twice Daily)-1.5

[back to top]

Lipid Profiles, Lipoprotein Analysis by NMR (LipoScience).

Change in lipid levels vs. pretreatment. (NCT01006889)
Timeframe: 6 months

Interventionmg/dl (Mean)
CholesterolTriglycerideLDL-CHDL-C
Exenatide (Twice Daily)-421-8-1

[back to top]

Insulin Secretion (Hyperglycemic Clamp)

Change in C-peptide levels vs. pretreatment in the first and second phase. (NCT01006889)
Timeframe: 6 months

Interventionng/ml (Mean)
Delta first phase insulin secretionDelta second phase insulin secretion
Exenatide (Twice Daily)-0.11.1

[back to top]

Percent Change From Baseline in Glucose Infusion (M Value) During Hyperglycemic Clamp

M value represents glucose infusion change (NCT01006889)
Timeframe: 6 months

Interventionpercentage change vs pretreatment (Mean)
Exenatide (Twice Daily)30

[back to top]

Number of Severe Hypoglycemic (Glucose ≤40 mg/dL) Events.

(NCT01006889)
Timeframe: 6 months

Interventionnumber of events (Number)
Exenatide (Twice Daily)0

[back to top]

Hepatic Steatosis

Hepatic steatosis was assessed non-invasively by MRS. (NCT01006889)
Timeframe: 6 months

InterventionPercentage of liver fat (Mean)
Exenatide (Twice Daily)4.0

[back to top]

Change in Anthropometric Variables (Weight).

(NCT01006889)
Timeframe: 6 months

InterventionKg (Mean)
Exenatide (Twice Daily)-4.7

[back to top]

A1c

Patients with controlled T2DM with bedtime insulin alone (n=5) or bedtime insulin and premeal rapid-acting insulin novolog (n=15) had eventide given twice daily for 6 months (if on premeal insulin it was stopped). The goal is to assess if adding SQ exenatide is effective to maintain optimal glycemic control in this population. (NCT01006889)
Timeframe: 6 months

Interventionpercentage of A1c (Mean)
Exenatide (Twice Daily)6.8

[back to top]

Change in Total Cholesterol From Baseline to Week 26

Change in total cholesterol from baseline to the treatment endpoint at Week 26. (NCT01029886)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly-0.06
Liraglutide Once Daily-0.15

[back to top]

Change in High-Density Lipoprotein Cholesterol (HDL-C) From Baseline to Week 26

Change in HDL-C from baseline to the treatment endpoint at Week 26. (NCT01029886)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly0.02
Liraglutide Once Daily0.02

[back to top]

Change in HbA1c From Baseline to Week 26

Change in HbA1c from baseline to the treatment endpoint at Week 26. (NCT01029886)
Timeframe: Baseline, Week 26

Interventionpercentage of total hemoglobin (Least Squares Mean)
Exenatide Once Weekly-1.28
Liraglutide Once Daily-1.48

[back to top]

Change in Body Weight From Baseline to Week 26

Change in body weight from baseline to the treatment endpoint at Week 26. (NCT01029886)
Timeframe: Baseline, Week 26

Interventionkg (Least Squares Mean)
Exenatide Once Weekly-2.68
Liraglutide Once Daily-3.57

[back to top]

Change in Fasting Serum Glucose From Baseline to Week 26

Change in fasting serum glucose from baseline to the treatment endpoint at Week 26. (NCT01029886)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Exenatide Once Weekly-1.76
Liraglutide Once Daily-2.12

[back to top]

Change in Systolic Blood Pressure (SBP) From Baseline to Week 26

Change in SBP from baseline to the treatment endpoint at Week 26. (NCT01029886)
Timeframe: Baseline, Week 26

InterventionmmHg (Least Squares Mean)
Exenatide Once Weekly-2.48
Liraglutide Once Daily-3.45

[back to top]

Assessment of Event Rate of Treatment-emergent Hypoglycemic Events

Major hypoglycemia: any episode with symptoms consistent with hypoglycemia that resulted in loss of consciousness or seizure with prompt recovery in response to administration of glucagon or glucose OR documented hypoglycemia (blood glucose <3.0 mmol/L [54 mg/dL]) and required the assistance of another person. Minor hypoglycemia: any sign or symptom associated with hypoglycemia that is either self-treated by the patient or resolves on its own AND has a concurrent finger stick blood glucose <3.0 mmol/L (54 mg/dL) and not classified as major hypoglycemia. Event rate per subject year was calculated for each subject: (number of events observed from a subject/exposure from a subject)*365.25 where exposure = last post-baseline visit date - baseline visit date. Mean and Standard Error were then derived from ITT. (NCT01029886)
Timeframe: Baseline to Week 26

,,,
Interventionevents per subject-year (Mean)
Major HypoglycemiaMinor Hypoglycemia
Exenatide Once Weekly With SU Use at Screening0.000.76
Exenatide Once Weekly Without SU Use at Screening0.000.67
Liraglutide Once Daily With SU Use at Screening0.000.55
Liraglutide Once Daily Without SU Use at Screening0.000.05

[back to top]

Ratio of Fasting Triglycerides at Week 26 to Baseline

Ratio of fasting triglycerides (measured in mmol/L) treatment endpoint at Week 26 to baseline. Log(Postbaseline fasting triglycerides) - log(Baseline fasting triglycerides); change from baseline to the treatment endpoint at Week 26 is presented as ratio of Week 26 to baseline. (NCT01029886)
Timeframe: Baseline, Week 26

Interventionratio (Least Squares Mean)
Exenatide Once Weekly0.97
Liraglutide Once Daily0.89

[back to top]

Percentage of Patients Achieving HbA1c <7.0% at Week 26

Percentage of patients achieving HbA1c <7.0% at treatment endpoint at Week 26. (NCT01029886)
Timeframe: Baseline, Week 26

Interventionpercentage of patients (Number)
Exenatide Once Weekly52.7
Liraglutide Once Daily60.2

[back to top]

Change in Diastolic Blood Pressure (DBP) From Baseline to Week 26

Change in DBP from baseline to the treatment endpoint at Week 26. (NCT01029886)
Timeframe: Baseline, Week 26

InterventionmmHg (Least Squares Mean)
Exenatide Once Weekly-0.49
Liraglutide Once Daily-0.51

[back to top]

Changes in Diastolic Blood Pressure Between Baseline and Month 12

Changes in Diastolic Blood Pressure Between Baseline and Month 12 (NCT01060059)
Timeframe: Baseline, Month 12

InterventionmmHg (Mean)
Exenatide-2.4
Basal Insulin0.2

[back to top]

Changes in Fasting Blood Glucose From Baseline to Month 12

Changes in Fasting Blood Glucose From Baseline to Month 12 (NCT01060059)
Timeframe: Baseline, Month 12

Interventionmg/dL (Mean)
Exenatide-26.7
Basal Insulin-51.4

[back to top]

Changes in Fasting HDL Between Baseline and Month 12

Changes in Fasting HDL Between Baseline and Month 12 (NCT01060059)
Timeframe: Baseline, Month 12

Interventionmg/dL (Mean)
Exenatide1.3
Basal Insulin0.2

[back to top]

Changes in Fasting Total Cholesterol Between Baseline and Month 12

Changes in Fasting Total Cholesterol Between Baseline and Month 12 (NCT01060059)
Timeframe: Baseline, Month 12

Interventionmg/dL (Mean)
Exenatide-6.0
Basal Insulin-7.5

[back to top]

Changes in Fasting Triglycerides Between Baseline and Month 12

Changes in Fasting Triglycerides Between Baseline and Month 12 (NCT01060059)
Timeframe: Baseline, Month 12

Interventionmg/dL (Mean)
Exenatide-16.5
Basal Insulin-30.2

[back to top]

Changes in HbA1c From Baseline to Month 12

Changes in HbA1c from Baseline to Month 12 (NCT01060059)
Timeframe: Baseline, Month 12

Interventionpercent (Mean)
Exenatide-1.1
Basal Insulin-1.4

[back to top]

Changes in Systolic Blood Pressure Between Baseline and Month 12

Changes in Systolic Blood Pressure Between Baseline and Month 12 (NCT01060059)
Timeframe: Baseline, Month 12

InterventionmmHg (Mean)
Exenatide-4.6
Basal Insulin-1.0

[back to top]

Changes in Weight From Baseline to Month 12

Changes in Weight From Baseline to Month 12 (NCT01060059)
Timeframe: Baseline, Month 12

Interventionkg (Mean)
Exenatide-3.9
Basal Insulin0.2

[back to top]

Factor of 1 Percent (%) Higher Baseline HbA1c Associated With Treatment Choice at Baseline

Factor of 1% higher baseline HbA1c (from most recent HbA1c) was analyzed for association with treatment choice at baseline. A total of 12 factors were evaluated. A multivariate logistic regression model using the full analysis set (FAS) population was performed for each of the factors to determine if exenatide treatment was more likely to be initiated in the presence of the specific factor. HbA1c was measured as a percent of normal (%). (NCT01060059)
Timeframe: baseline

InterventionPercentage of normal (Mean)
Exenatide8.7
Basal Insulin9.2

[back to top]

Factor of Greater Height Associated With Treatment Choice at Baseline

Factor of greater height (1 centimeter higher) was analyzed for association with treatment choice at baseline. A total of 12 factors were evaluated. A multivariate logistic regression model using the full analysis set (FAS) population was performed for each of the factors to determine if exenatide treatment was more likely to be initiated in the presence of the specific factor. Height was measured in centimeters (cm) . (NCT01060059)
Timeframe: baseline

Interventioncm (Mean)
Exenatide165.8
Basal Insulin164.4

[back to top]

Factor of Higher Body Mass Index (BMI) Associated With Treatment Choice at Baseline

Factor of higher body mass index (BMI) (1 kilogram per meter squared (kg/m^2) higher) was analyzed for association with treatment choice at baseline. A total of 12 factors were evaluated. A multivariate logistic regression model using the full analysis set (FAS) population was performed for each of the factors to determine if exenatide treatment was more likely to be initiated in the presence of the specific factor. BMI measured as kg/m^2. (NCT01060059)
Timeframe: baseline

Interventionkg/m^2 (Mean)
Exenatide35.4
Basal Insulin29.4

[back to top]

Factor of Longer Duration of Diabetes Associated With Treatment Choice at Baseline

The Factor of longer duration of diabetes at baseline (diagnosed 1 year longer) was analyzed for association with treatment choice at baseline. A total of 12 factors were evaluated. A multivariate logistic regression model using the full analysis set (FAS) population was performed for each of the factors to determine if exenatide treatment was more likely to be initiated in the presence of the specific factor. Duration of diabetes was measured in years since the date of diabetes diagnosis. (NCT01060059)
Timeframe: baseline

Interventionyears (Mean)
Exenatide9.0
Basal Insulin12.4

[back to top]

Factor of Older Age Associated With Treatment Choice at Baseline

Older age (1 year older) was analyzed for association with treatment choice at baseline. A total of 12 factors were evaluated. A multivariate logistic regression model using the full analysis set (FAS) population was performed for each of the factors to determine if exenatide treatment was more likely to be initiated in the presence of the specific factor. Age was measured in years. (NCT01060059)
Timeframe: baseline

Interventionyears (Mean)
Exenatide59.2
Basal Insulin65.9

[back to top]

Percentage of Patients Achieving a Weight Decrease >=3% Between Baseline and Month 12

Percentage of Patients Achieving a Weight Decrease >=3% between Baseline and Month 12 (NCT01060059)
Timeframe: Baseline, Month 12

Interventionpercentage of patients (Number)
Exenatide43.0
Basal Insulin17.6

[back to top]

Percentage of Patients Achieving a Weight Decrease >=5% Between Baseline and Month 12

Percentage of Patients Achieving a Weight Decrease >=5% between Baseline and Month 12 (NCT01060059)
Timeframe: Baseline, Month 12

Interventionpercentage of patients (Number)
Exenatide29.7
Basal Insulin10.7

[back to top]

Percentage of Patients Achieving HbA1c Concentration <=7.0% at Month 12

Percentage of Patients Achieving HbA1c Concentration <=7.0% at Month 12 (NCT01060059)
Timeframe: Month 12

Interventionpercentage of patients (Number)
Exenatide39.0
Basal Insulin22.2

[back to top]

Percentage of Patients Achieving HbA1c Concentration <6.5% at Month 12

Percentage of Patients Achieving HbA1c Concentration <6.5% at Month 12 (NCT01060059)
Timeframe: Month 12

Interventionpercentage of patients (Number)
Exenatide13.1
Basal Insulin4.9

[back to top]

Percentage of Patients Who Achieved Glycemic Target of HbA1c ≤ 7.0% With Minimal Weight Gain (≤ 1 Kg) at Month 12.

Percentage of patients who achieved glycemic target of HbA1c ≤ 7.0% with minimal weight gain (≤ 1 Kg) at month 12. (NCT01060059)
Timeframe: Baseline, Month 12

Interventionpercentage of patients (Number)
Exenatide35.0
Basal Insulin15.8

[back to top]

Percentage of Patients With HbA1c Reduction From Baseline >= 1.0% at Month 12

Percentage of Patients with HbA1c Reduction from Baseline >= 1.0% at Month 12 (NCT01060059)
Timeframe: Baseline, Month 12

Interventionpercentage of patients (Number)
Exenatide49.4
Basal Insulin51.1

[back to top]

Percentage of Patients With Hypoglycemia Episodes Between Baseline and Month 12

"Percentage of patients with Hypoglycemia Episodes Between Baseline and Month 12.~All episodes consistent with hypoglycemia with or without a confirmatory blood glucose reading were collected." (NCT01060059)
Timeframe: Baseline to Month 12

Interventionpercentage of patients (Number)
Exenatide3.6
Basal Insulin8.2

[back to top] [back to top]

Factors of Higher Creatinine, Higher Fasting High Density Lipoprotein (HDL) Cholesterol, Higher Fasting Cholesterol, and Higher Fasting Triglycerides Which Were Associated With Treatment Choice at Baseline

Factors of higher creatinine: 1 milligram per deciliter higher (mg/dL) and higher fasting lipids (HDL cholesterol: 1 mg/dL higher; total cholesterol: 1 mg/dL higher; triglycerides: 1 mg/dL higher) were analyzed for association with treatment choice at baseline. A total of 12 factors were evaluated. A multivariate logistic regression model using the full analysis set (FAS) population was performed for each of the factors to determine if exenatide treatment was more likely to be initiated in the presence of the specific factor. Creatinine and fasting lipids were measured in milligrams per deciliter (mg/dL). (NCT01060059)
Timeframe: baseline

,
Interventionmg/dL (Mean)
Creatinine (N=324, 333)HDL (N=335, 326)Total Cholesterol (N=368, 355)Triglycerides (N=364, 360)
Basal Insulin1.046.9182.7173.6
Exenatide0.944.7181.1177.5

[back to top]

Changes in Fasting LDL Between Baseline and Month 12

Changes in Fasting LDL Between Baseline and Month 12 (NCT01060059)
Timeframe: Baseline, Month 12

Interventionmg/dL (Mean)
Exenatide-4.6
Basal Insulin-4.5

[back to top]

BMI Change

BMI was collected at baseline and 24 weeks (NCT01061775)
Timeframe: 24 weeks

Interventionkg/m^2 (Mean)
Exenatide-0.77

[back to top]

Waist to Height Ratio (WHtR)

Waist circumference was measured at the natural waist level (midway between the lowest rib margin and the iliac crest) at baseline and 24 weeks (NCT01061775)
Timeframe: 24 weeks

Interventionpercentage (Mean)
Exenatide-2.06

[back to top]

Childhood Eating Behavior Questionnaire (CEBQ)

The Child Eating Behaviour Questionnaire (CEBQ) was designed as parent-report measure comprised of 35 items, each rated on a five-point likert scale that ranges from never to always. We utilized the CEBQ as a self-report measure during this study; it has not been validated for such use. For the purposes of this study, we looked at the Satiety Responsiveness Subscale Scores (5 questions; total scores could range from 5-25 with lower scores denoting a lower level of satiety). The results reported show the change between baseline and week 24 scores. (NCT01061775)
Timeframe: 24 weeks

Interventionunits on a scale (Mean)
Exenatide14

[back to top]

Calorie Intake Based on 3-day Diet Records

Dietary data were collected via 3-day diet records (Crawford et al. 1994) twice during the study, at baseline and week 24. Three-day diet records were collected on consecutive days including one weekend day. A registered dietitian (RD) instructed subjects on dietary data collection at baseline appointment. Depending on the age and capacity of the subject, the patient, parent or a collaboration of both recorded dietary intake. A RD entered dietary data into Nutritionist Pro software (First DataBank, SanBruno, CA) and the mean difference was analyzed. (NCT01061775)
Timeframe: 24 weeks

Interventionkcals (Mean)
Exenatide406.700

[back to top]

Percentage of Participants Attaining Glycosylated Hemoglobin (HbA1c) Less Than 7% and Less Than or Equal to 6.5% at 26 Weeks

The percentage of participants achieving HbA1c level less than 7.0% and less than or equal to 6.5% was analyzed with a logistic regression model with baseline, country, and treatment as factors included in the model. (NCT01064687)
Timeframe: Baseline, 26 weeks

,,,
Interventionpercentage of participants (Number)
HbA1c Less Than 7%HbA1c Less Than or Equal to 6.5%
0.75 mg LY218926565.853.2
1.5 mg LY218926578.262.7
Exenatide52.338.0
Placebo42.924.4

[back to top]

Change From Baseline to 26 Weeks on Pancreatic Enzymes

Amylase (total and pancreas-derived) and lipase concentrations were measured. (NCT01064687)
Timeframe: Baseline, 26 weeks

,,,
Interventionunits per liter (Median)
Amylase, Total (n=253, 253, 254, 127)Amylase, Pancreas-derived (n=237, 247, 246, 122)Lipase (n=198, 203, 222, 114)
0.75 mg LY21892653.2810.340.00
1.5 mg LY218926512.5014.8110.34
Exenatide5.565.563.94
Placebo-3.33-3.77-9.53

[back to top]

Change From Baseline to 26 Weeks on Electrocardiogram Parameters, Fridericia Corrected QT (QTcF) Interval and PR Interval

The QT interval is a measure of the time between the start of the Q wave and the end of the T wave and was calculated from electrocardiogram (ECG) data using Fridericia's formula: QTc = QT/RR^0.33. Corrected QT (QTc) is the QT interval corrected for heart rate and RR, which is the interval between two R waves. PR is the interval between the P wave and the QRS complex. Least Squares (LS) means of change from baseline were calculated using a mixed-effects model for repeated measures (MMRM) with treatment, country, visit, and treatment-by-visit interaction as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 26 weeks

,,,
Interventionmilliseconds (msec) (Least Squares Mean)
QTcF Interval (n=253, 260, 250, 120)PR Interval (n=252, 259, 246, 116)
0.75 mg LY21892650.910.93
1.5 mg LY2189265-1.112.35
Exenatide1.211.01
Placebo1.32-1.83

[back to top]

Change From Baseline to 26 Weeks on Blood Pressure

Seated systolic blood pressure (SBP) and seated diastolic blood pressure (DBP) were measured. Least Squares (LS) means of change from baseline were calculated using a mixed-effects model for repeated measures (MMRM) with treatment, country, visit, and treatment-by-visit interaction as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 26 weeks

,,,
Interventionmillimeters of mercury (mmHg) (Least Squares Mean)
Seated SBP (n=263, 266, 259, 127)Seated DBP (n=263, 266, 259, 127)
0.75 mg LY2189265-0.360.56
1.5 mg LY21892650.110.76
Exenatide0.06-0.11
Placebo3.401.25

[back to top]

Change From Baseline to 26 Weeks in Updated Homeostasis Model Assessment of Beta-cell Function (HOMA2-%B) and Updated Homeostasis Model Assessment of Insulin Sensitivity (HOMA2-%S)

The homeostatic model assessment (HOMA) quantifies insulin resistance and beta-cell function. HOMA2-B is a computer model that uses fasting plasma insulin and glucose concentrations to estimate steady-state beta cell function (%B) as a percentage of a normal reference population (normal young adults). HOMA2-S is a computer model that uses fasting plasma insulin and glucose concentrations to estimate insulin sensitivity (%S) as percentages of a normal reference population (normal young adults). The normal reference populations were set at 100%. Least Squares (LS) means of change from baseline were calculated using a mixed-effects model for repeated measures (MMRM) with treatment, country, visit, and treatment-by-visit interaction as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 26 weeks

,,,
Interventionpercentage of HOMA2 (Least Squares Mean)
HOMA2-%BHOMA2-%S
0.75 mg LY218926523.611.16
1.5 mg LY218926536.14-3.14
Exenatide15.02-1.59
Placebo0.932.56

[back to top]

Change From Baseline to 26 Weeks in the EuroQol 5

The European Quality of Life - 5 dimensions (EQ-5D) questionnaire is a generic, multidimensional, health-related, quality-of-life instrument. It consists of 2 parts: the first part assesses 5 dimensions (mobility, self-care, usual activities, pain/discomfort, and anxiety/depression) that have 3 possible levels of response (no problem, some problem, or extreme problem). These dimensions are converted into a weighted health-state Index Score. The EQ-5D United Kingdom (UK) score ranges from -0.59 to 1.0, where a score of 1.0 indicates perfect health and negative values are valued as worse than dead. The second part of the questionnaire consists of a visual analog scale (VAS) on which the participants rated their perceived health state on that day from 0 (worst imaginable health state) to 100 (best imaginable health). Least Squares (LS) means of change from baseline were calculated using analysis of covariance (ANCOVA) and adjusted by treatment, country, and baseline. (NCT01064687)
Timeframe: Baseline, 26 weeks

,,,
Interventionunits on a scale (Least Squares Mean)
VAS Health State Score (n=270, 267, 264, 119)EQ-5D UK (n=270, 266, 264, 119)
0.75 mg LY21892652.410.01
1.5 mg LY21892654.500.01
Exenatide3.940.00
Placebo0.71-0.00

[back to top]

Pharmacokinetics: Area Under the Concentration Curve (AUC) for LY2189265

Evaluable pharmacokinetic concentrations from the 4-week, 13-week, 26-week, and 52-week timepoints were combined and utilized in a population approach to determine the population mean estimate and standard deviation at steady-state. (NCT01064687)
Timeframe: 4 weeks, 13 weeks, 26 weeks, and 52 weeks

Interventionnanogram hours per milliliter (ng*hr/mL) (Mean)
1.5 mg LY218926512383
0.75 mg LY21892656627

[back to top]

Number of Participants With Treatment Emergent Adverse Events at 52 Weeks

A treatment-emergent adverse event (TEAE) was defined as an event that first occurs or worsens (increases in severity) after baseline regardless of causality or severity. The number of participants with one or more TEAE is summarized cumulatively at 52 weeks, with the exception of the Placebo/1.5 mg LY2189265 and Placebo/0.75 mg LY2189265 treatment groups, which include only TEAEs that occurred during treatment with LY2189265 (26 weeks through 52 weeks). A summary of serious and other non-serious adverse events regardless of causality is located in the Reported Adverse Events module. (NCT01064687)
Timeframe: Baseline through 52 weeks

Interventionparticipants (Number)
1.5 mg LY2189265226
0.75 mg LY2189265220
Exenatide221
Placebo/1.5 mg LY218926547
Placebo/0.75 mg LY218926541

[back to top]

Number of Participants With Treatment Emergent Adverse Events at 26 Weeks

A treatment-emergent adverse event (TEAE) was defined as an event that first occurs or worsens (increases in severity) after baseline regardless of causality or severity. The number of participants with one or more TEAE is summarized cumulatively at 26 weeks. A summary of serious and other non-serious adverse events regardless of causality is located in the Reported Adverse Events module. (NCT01064687)
Timeframe: Baseline through 26 weeks

Interventionparticipants (Number)
1.5 mg LY2189265215
0.75 mg LY2189265199
Exenatide198
Placebo104

[back to top]

Number of Participants With LY2189265 Antibodies at 26 Weeks

LY2189265 (Dulaglutide) anti-drug antibodies (ADA) were assessed. The number of participants with initial postbaseline detection of treatment emergent (defined as a 4-fold increase in the ADA titer from baseline) LY2189265 ADA were summarized. (NCT01064687)
Timeframe: Baseline through 26 weeks

Interventionparticipants (Number)
0.75 mg LY2189265 or 1.5 mg LY21892656
Exenatide12
Placebo2

[back to top]

Number of Participants With Adjudicated Pancreatitis at 52 Weeks

The number of participants with pancreatitis confirmed by adjudication is summarized cumulatively at 52 weeks, with the exception of the Placebo/1.5 mg LY2189265 and Placebo/0.75 mg LY2189265 treatment groups, which include only participants with confirmed pancreatitis during treatment with LY2189265 (26 weeks through 52 weeks). A summary of serious and other non-serious adverse events regardless of causality is located in the Reported Adverse Events module. (NCT01064687)
Timeframe: Baseline through 52 weeks

Interventionparticipants (Number)
1.5 mg LY21892651
0.75 mg LY21892650
Exenatide0
Placebo/1.5 mg LY21892650
Placebo/0.75 mg LY21892650

[back to top]

Number of Participants With Adjudicated Pancreatitis at 26 Weeks

The number of participants with pancreatitis confirmed by adjudication is summarized cumulatively at 26 weeks. A summary of serious and other non-serious adverse events regardless of causality is located in the Reported Adverse Events module. (NCT01064687)
Timeframe: Baseline through 26 weeks

Interventionparticipants (Number)
1.5 mg LY21892650
0.75 mg LY21892650
Exenatide0
Placebo0

[back to top]

Number of Participants Requiring Rescue Therapy Due to Hyperglycemia at 52 Weeks

"Rescue therapy was defined as any additional therapeutic intervention in participants who developed persistent, severe hyperglycemia despite full compliance with the assigned therapeutic regimen, or initiation of an alternative antihyperglycemic medication following study drug discontinuation. Participants who had no rescue therapy within specified study period were considered as censored observations at the last available contact date up to specified study period. Time to start first new glucose-lowering intervention due to hyperglycemia (rescue therapy) was analyzed between the groups using the semi-parametric proportional hazard regression model with treatment group and country as fixed effects and baseline glycosylated hemoglobin (HbA1c) as a covariate." (NCT01064687)
Timeframe: Baseline through 52 weeks

Interventionparticipants (Number)
1.5 mg LY218926510
0.75 mg LY218926527
Exenatide31

[back to top]

Number of Participants Requiring Rescue Therapy Due to Hyperglycemia at 26 Weeks

"Rescue therapy was defined as any additional therapeutic intervention in participants who developed persistent, severe hyperglycemia despite full compliance with the assigned therapeutic regimen, or initiation of an alternative antihyperglycemic medication following study drug discontinuation. Participants who had no rescue therapy within specified study period were considered as censored observations at the last available contact date up to specified study period. Time to start first new glucose-lowering intervention due to hyperglycemia (rescue therapy) was analyzed between the groups using the semi-parametric proportional hazard regression model with treatment group and country as fixed effects and baseline glycosylated hemoglobin (HbA1c) as a covariate." (NCT01064687)
Timeframe: Baseline through 26 weeks

Interventionparticipants (Number)
1.5 mg LY21892654
0.75 mg LY218926514
Exenatide13
Placebo22

[back to top]

Change in Baseline to 52 Weeks on Pulse Rate

Seated pulse rate was measured. Least Squares (LS) means of change from baseline were calculated using a mixed-effects model for repeated measures (MMRM) with treatment, country, visit, and treatment-by-visit interaction as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 52 weeks

Interventionbeats per minute (bpm) (Least Squares Mean)
1.5 mg LY21892651.68
0.75 mg LY21892651.56
Exenatide1.15

[back to top]

Change in Baseline to 26 Weeks on Pulse Rate

Seated pulse rate was measured. Least Squares (LS) means of change from baseline were calculated using a mixed-effects model for repeated measures (MMRM) with treatment, country, visit, and treatment-by-visit interaction as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 26 weeks

Interventionbeats per minute (bpm) (Least Squares Mean)
1.5 mg LY21892652.80
0.75 mg LY21892652.80
Exenatide1.18
Placebo0.61

[back to top]

Change From Baseline to 52 Weeks on the Impact of Weight on Self-Perception

The Impact of Weight on Self-Perception (IW-SP) questionnaire contains 3 items that assess how often the participants' body weight affects how happy they are with their appearance and how often they feel self-conscious when out in public. Items are scored on a 5-point numeric rating scale where 5 = never and 1 = always. A single total score is calculated by summing the scores for all 3 items. Total score ranges between 3 and 15, where a higher score is indicative of better self-perception. Least Squares (LS) means of change from baseline were calculated using analysis of covariance (ANCOVA) with country and treatment as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
1.5 mg LY21892650.50
0.75 mg LY21892650.47
Exenatide0.64

[back to top]

Change From Baseline to 52 Weeks in the EuroQol 5

The European Quality of Life - 5 dimensions (EQ-5D) questionnaire is a generic, multidimensional, health-related, quality-of-life instrument. It consists of 2 parts: the first part assesses 5 dimensions (mobility, self-care, usual activities, pain/discomfort, and anxiety/depression) that have 3 possible levels of response (no problem, some problem, or extreme problem). These dimensions are converted into a weighted health-state Index Score. The EQ-5D United Kingdom (UK) score ranges from -0.59 to 1.0, where a score of 1.0 indicates perfect health and negative values are valued as worse than dead. The second part of the questionnaire consists of a visual analog scale (VAS) on which the participants rated their perceived health state on that day from 0 (worst imaginable health state) to 100 (best imaginable health). Least Squares (LS) means of change from baseline were calculated using analysis of covariance (ANCOVA) and adjusted by treatment, country, and baseline. (NCT01064687)
Timeframe: Baseline, 52 weeks

,,
Interventionunits on a scale (Least Squares Mean)
VAS Health State Score (n=270, 267, 264)EQ-5D UK (n=270, 266, 264)
0.75 mg LY21892653.520.01
1.5 mg LY21892655.150.02
Exenatide3.51-0.00

[back to top]

Change From Baseline to 52 Weeks on Body Mass Index (BMI)

Least Squares (LS) means of change from baseline were calculated using a mixed-effects model for repeated measures (MMRM) with treatment, country, visit, and treatment-by-visit interaction as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 52 weeks

Interventionkilograms per meter squared (kg/m^2) (Least Squares Mean)
1.5 mg LY2189265-0.37
0.75 mg LY21892650.18
Exenatide-0.28

[back to top]

Change From Baseline to 52 Weeks in the Impact of Weight on Activities of Daily Living

"The Impact of Weight on Activities of Daily Living (renamed the Ability to Perform Physical Activities of Daily Living [APPADL]) questionnaire contains 7 items that assess how difficult it is for participants to engage in certain activities considered to be integral to normal daily life, such as walking, standing and climbing stairs. Items are scored on a 5-point numeric rating scale where 5 = not at all difficult and 1 = unable to do. The individual scores from all 7 items are summed and a single total score is calculated and may range between 7 and 35. A higher score indicates better ability to perform activities of daily living. Least Squares (LS) means of change from baseline were calculated using analysis of covariance (ANCOVA) with country and treatment as fixed effects and baseline as a covariate." (NCT01064687)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
1.5 mg LY21892650.18
0.75 mg LY2189265-0.18
Exenatide0.35

[back to top]

Change From Baseline to 52 Weeks in Hematological and Biochemical Lab Values

(NCT01064687)
Timeframe: Baseline, 52 weeks

Intervention (Least Squares Mean)
1.5 mg LY2189265NA
0.75 mg LY2189265NA
ExenatideNA

[back to top]

Change From Baseline to 52 Weeks for Daily Mean Blood Glucose Values From the 8-point Self-monitored Plasma Glucose (SMPG) Profiles

The SMPG data were collected at the following 8 time points: pre-morning meal; 2 hours post-morning meal; pre-midday meal; 2 hours post-midday meal; pre-evening; 2 hours post-evening meal; bedtime; and 3AM or 5 hours after bedtime. Least squares (LS) means of the mean of the 8 time points (daily mean) were calculated using a mixed-effects model for repeated measures (MMRM) analysis with treatment, country, visit, and treatment-by-visit as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 52 weeks

Interventionmilligrams per deciliter (mg/dL) (Least Squares Mean)
1.5 mg LY2189265-43.84
0.75 mg LY2189265-40.62
Exenatide-36.16

[back to top]

Change From Baseline to 52 Weeks for Body Weight

Least squares (LS) means of change from baseline were calculated using a mixed-effects model for repeated measures (MMRM) analysis with treatment, country, visit, and treatment-by-visit as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 52 weeks

Interventionkilograms (kg) (Least Squares Mean)
1.5 mg LY2189265-1.08
0.75 mg LY21892650.49
Exenatide-0.76

[back to top]

Change From Baseline to 52 Weeks Endpoint in Glycosylated Hemoglobin (HbA1c)

Least squares (LS) means were calculated using analysis of covariance (ANCOVA) with country and treatment as fixed effects and baseline HbA1c as a covariate. (NCT01064687)
Timeframe: Baseline, 52 weeks

Interventionpercentage of glycosylated hemoglobin (Least Squares Mean)
1.5 mg LY2189265-1.36
0.75 mg LY2189265-1.07
Exenatide-0.80

[back to top]

Change From Baseline to 26 Weeks on the Impact of Weight on Self-Perception

The Impact of Weight on Self-Perception (IW-SP) questionnaire contains 3 items that assess how often the participants' body weight affects how happy they are with their appearance and how often they feel self-conscious when out in public. Items are scored on a 5-point numeric rating scale where 5 = never and 1 = always. A single total score is calculated by summing the scores for all 3 items. Total score ranges between 3 and 15, where a higher score is indicative of better self-perception. Least Squares (LS) means of change from baseline were calculated using analysis of covariance (ANCOVA) with country and treatment as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 26 weeks

Interventionunits on a scale (Least Squares Mean)
1.5 mg LY21892650.56
0.75 mg LY21892650.47
Exenatide0.46
Placebo0.45

[back to top]

Change From Baseline to 26 Weeks on Serum Calcitonin

(NCT01064687)
Timeframe: Baseline, 26 weeks

Interventionpicograms per milliliter (pg/mL) (Mean)
1.5 mg LY21892650.20
0.75 mg LY21892650.22
Exenatide0.05
Placebo0.05

[back to top]

Change From Baseline to 26 Weeks on Body Mass Index (BMI)

Least Squares (LS) means of change from baseline were calculated using a mixed-effects model for repeated measures (MMRM) with treatment, country, visit, and treatment-by-visit interaction as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 26 weeks

Interventionkilograms per meter squared (kg/m^2) (Least Squares Mean)
1.5 mg LY2189265-0.48
0.75 mg LY21892650.07
Exenatide-0.41
Placebo0.49

[back to top]

Change From Baseline to 26 Weeks in the Impact of Weight on Activities of Daily Living

"The Impact of Weight on Activities of Daily Living (renamed the Ability to Perform Physical Activities of Daily Living [APPADL]) questionnaire contains 7 items that assess how difficult it is for participants to engage in certain activities considered to be integral to normal daily life, such as walking, standing and climbing stairs. Items are scored on a 5-point numeric rating scale where 5 = not at all difficult and 1 = unable to do. The individual scores from all 7 items are summed and a single total score is calculated and may range between 7 and 35. A higher score indicates better ability to perform activities of daily living. Least Squares (LS) means of change from baseline were calculated using analysis of covariance (ANCOVA) with country and treatment as fixed effects and baseline as a covariate." (NCT01064687)
Timeframe: Baseline, 26 weeks

Interventionunits on a scale (Least Squares Mean)
1.5 mg LY21892650.18
0.75 mg LY21892650.12
Exenatide0.47
Placebo0.03

[back to top]

Change From Baseline to 26 Weeks in the Diabetes Treatment Satisfaction Questionnaire Status (DTSQs) Version

The Diabetes Treatment Satisfaction Questionnaire status version (DTSQs) is used to assess participant treatment satisfaction at each study visit. The questionnaire consists of 8 items, 6 of which (1, and 4 through 8) assess treatment satisfaction. Each item is rated on a 7-point Likert scale. Scores from the 6 treatment satisfaction items are summed to a Total Treatment Satisfaction Score, which ranges from 0 (very dissatisfied) to 36 (very satisfied). The DTSQ change version (DTSQc) was not collected at 26 weeks. Least Squares (LS) means of change from baseline were calculated using analysis of covariance (ANCOVA) with country and treatment as fixed effects and baseline score as a covariate. (NCT01064687)
Timeframe: Baseline, 26 weeks

Interventionunits on a scale (Least Squares Mean)
1.5 mg LY21892652.40
0.75 mg LY21892652.56
Exenatide0.85
Placebo0.49

[back to top]

Number of Participants With LY2189265 Antibodies at 52 Weeks and 4 Weeks After Last Dose of Study Drug

LY2189265 (Dulaglutide) anti-drug antibodies (ADA) were assessed. The number of participants with initial postbaseline detection of treatment emergent (defined as a 4-fold increase in the ADA titer from baseline) LY2189265 ADA were summarized. (NCT01064687)
Timeframe: 26 weeks through 52 weeks and 53 weeks through 4 weeks after last dose

,,
Interventionparticipants (Number)
52 weeks4 weeks after last study dose
0.75 mg LY2189265 or 1.5 mg LY218926531
Exenatide20
Placebo/0.75 mg LY2189265 or 1.5 mg LY218926521

[back to top]

Change From Baseline to 26 Weeks in N Terminal Pro Brain Natriuretic Peptide (NT-proBNP)

(NCT01064687)
Timeframe: Baseline, 26 weeks

Interventionpicograms per milliliter (pg/mL) (Median)
1.5 mg LY2189265-6.77
0.75 mg LY2189265-2.96
Exenatide-3.38
Placebo-0.85

[back to top]

Change From Baseline to 26 Weeks in Hematological and Biochemical Lab Values

(NCT01064687)
Timeframe: Baseline, 26 weeks

Intervention (Least Squares Mean)
1.5 mg LY2189265NA
0.75 mg LY2189265NA
ExenatideNA
PlaceboNA

[back to top]

Change From Baseline to 26 Weeks for Daily Mean Blood Glucose Values From the 8-point Self-monitored Plasma Glucose (SMPG) Profiles

The SMPG data were collected at the following 8 time points: pre-morning meal; 2 hours post-morning meal; pre-midday meal; 2 hours post-midday meal; pre-evening; 2 hours post-evening meal; bedtime; and 3AM or 5 hours after bedtime. Least squares (LS) means of the mean of the 8 time points (daily mean) were calculated using a mixed-effects model for repeated measures (MMRM) analysis with treatment, country, visit, and treatment-by-visit as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 26 weeks

Interventionmilligrams per deciliter (mg/dL) (Least Squares Mean)
1.5 mg LY2189265-46.82
0.75 mg LY2189265-42.09
Exenatide-37.48
Placebo-18.07

[back to top]

Change From Baseline to 26 Weeks for Body Weight

Least squares (LS) means of change from baseline were calculated using a mixed-effects model for repeated measures (MMRM) analysis with treatment, country, visit, and treatment-by-visit as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 26 weeks

Interventionkilograms (kg) (Least Squares Mean)
1.5 mg LY2189265-1.34
0.75 mg LY21892650.18
Exenatide-1.14
Placebo1.37

[back to top]

Change From Baseline to 26 Weeks Endpoint in Glycosylated Hemoglobin (HbA1c)

Least squares (LS) means were calculated using analysis of covariance (ANCOVA) with country and treatment as fixed effects and baseline HbA1c as a covariate. (NCT01064687)
Timeframe: Baseline, 26 weeks

Interventionpercentage of glycosylated hemoglobin (Least Squares Mean)
1.5 mg LY2189265-1.51
0.75 mg LY2189265-1.30
Exenatide-0.99
Placebo-0.46

[back to top]

Rate of Self-reported Hypoglycemic Events at 52 Weeks

Hypoglycemic events (HE) were classified as severe (defined as episodes requiring the assistance of another person to actively administer resuscitative actions), documented symptomatic (defined as any time a participant feels that he/she is experiencing symptoms and/or signs associated with hypoglycemia, and has a plasma glucose level of equal to or less than millimoles/liter [mmol/L]), asymptomatic (defined as events not accompanied by typical symptoms of hypoglycemia but with a measured plasma glucose of equal to or less than 3.9 mmol/L), nocturnal (defined as any hypoglycemic event that occurred between bedtime and waking), or probable symptomatic (defined as events during which symptoms of hypoglycemia were not accompanied by a plasma glucose determination). The 1-year adjusted rate of hypoglycemic events is summarized cumulatively at 52 weeks. A summary of serious and other non-serious adverse events regardless of causality is located in the Reported Adverse Events module. (NCT01064687)
Timeframe: Baseline through 52 weeks

,,
Interventionevents per participant per year (Mean)
Severe HEDocumented symptomatic HEAsymptomatic HENocturnal HEProbable symptomatic HE
0.75 mg LY21892650.000.140.560.190.21
1.5 mg LY21892650.000.190.170.070.03
Exenatide0.010.760.370.210.02

[back to top]

Rate of Self-reported Hypoglycemic Events at 26 Weeks

Hypoglycemic events (HE) were classified as severe (defined as episodes requiring the assistance of another person to actively administer resuscitative actions), documented symptomatic (defined as any time a participant feels that he/she is experiencing symptoms and/or signs associated with hypoglycemia, and has a plasma glucose level of equal to or less than 3.9 millimoles/liter [mmol/L]), asymptomatic (defined as events not accompanied by typical symptoms of hypoglycemia but with a measured plasma glucose of equal to or less than 3.9 mmol/L), nocturnal (defined as any hypoglycemic event that occurred between bedtime and waking), or probable symptomatic (defined as events during which symptoms of hypoglycemia were not accompanied by a plasma glucose determination). The 1-year adjusted rate of hypoglycemic events is summarized cumulatively at 26 weeks. A summary of serious and other non-serious adverse events regardless of causality is located in the Reported Adverse Events module. (NCT01064687)
Timeframe: Baseline through 26 weeks

,,,
Interventionevents per participant per year (Mean)
Severe HEDocumented symptomatic HEAsymptomatic HENocturnal HEProbable symptomatic HE
0.75 mg LY21892650.000.180.690.190.24
1.5 mg LY21892650.000.220.190.060.04
Exenatide0.011.070.380.230.02
Placebo0.000.060.270.270.04

[back to top]

Percentage of Participants Attaining Glycosylated Hemoglobin (HbA1c) Less Than 7% and Less Than or Equal to 6.5% at 52 Weeks

The percentage of participants achieving HbA1c level less than 7.0% and less than or equal to 6.5% was analyzed with a logistic regression model with baseline, country, and treatment as factors included in the model. (NCT01064687)
Timeframe: Baseline, 52 weeks

,,
Interventionpercentage of participants (Number)
HbA1c Less Than 7.0%HbA1c Less Than or Equal to 6.5%
0.75 mg LY218926559.148.3
1.5 mg LY218926570.857.2
Exenatide49.234.6

[back to top]

Change From Baseline to 52 Weeks on Serum Calcitonin

(NCT01064687)
Timeframe: Baseline, 52 weeks

Interventionpicograms per milliliter (pg/mL) (Mean)
1.5 mg LY21892650.21
0.75 mg LY21892650.05
Exenatide0.10

[back to top]

Number of Self-reported Hypoglycemic Events at 52 Weeks

Hypoglycemic events (HE) were classified as severe (defined as episodes requiring the assistance of another person to actively administer resuscitative actions), documented symptomatic (defined as any time a participant feels that he/she is experiencing symptoms and/or signs associated with hypoglycemia, and has a plasma glucose level of less than or equal to 3.9 millimoles/liter [mmol/L]), asymptomatic (defined as events not accompanied by typical symptoms of hypoglycemia but with a measured plasma glucose of less than or equal to 3.9 mmol/L), nocturnal (defined as any hypoglycemic event that occurred between bedtime and waking), or probable symptomatic (defined as events during which symptoms of hypoglycemia were not accompanied by a plasma glucose determination). The number of self-reported hypoglycemic events is summarized cumulatively at 52 weeks. A summary of serious and other non-serious adverse events regardless of causality is located in the Reported Adverse Events module. (NCT01064687)
Timeframe: Baseline through 52 weeks

,,
Interventionevents (Number)
Severe HEDocumented Symptomatic HEAsymptomatic HENocturnal HEProbable Symptomatic HE
0.75 mg LY21892650391572922
1.5 mg LY218926505347208
Exenatide220598574

[back to top]

Number of Self-reported Hypoglycemic Events at 26 Weeks

Hypoglycemic events (HE) were classified as severe (defined as episodes requiring the assistance of another person to actively administer resuscitative actions), documented symptomatic (defined as any time a participant feels that he/she is experiencing symptoms and/or signs associated with hypoglycemia, and has a plasma glucose level of less than or equal to 3.9 millimoles/liter [mmol/L]), asymptomatic (defined as events not accompanied by typical symptoms of hypoglycemia but with a measured plasma glucose of less than or equal to 3.9 mmol/L), nocturnal (defined as any hypoglycemic event that occurred between bedtime and waking), or probable symptomatic (defined as events during which symptoms of hypoglycemia were not accompanied by a plasma glucose determination). The number of self-reported hypoglycemic events is summarized cumulatively at 26 weeks. A summary of serious and other non-serious adverse events regardless of causality is located in the Reported Adverse Events module. (NCT01064687)
Timeframe: Baseline through 26 weeks

,,,
Interventionevents (Number)
Severe HEDocumented Symptomatic HEAsymptomatic HENocturnal HEProbable Symptomatic HE
0.75 mg LY2189265025951516
1.5 mg LY21892650312695
Exenatide114651313
Placebo04563

[back to top]

Change From Baseline to 52 Weeks in the Diabetes Treatment Satisfaction Questionnaire Status (DTSQs) and Change (DTSQc) Versions

The Diabetes Treatment Satisfaction Questionnaire status (DTSQs) and change (DTSQc) versions are used to assess participant treatment satisfaction at each study visit and relative change in satisfaction from baseline, respectively. Both questionnaires consist of 8 items, 6 of which (1, and 4 through 8) assess treatment satisfaction. Each item is rated on a 7-point Likert scale. The change version has the same 8 items as the status version with a small alteration of the wording of Item 7. Scores from the 6 treatment satisfaction items are summed to a Total Treatment Satisfaction Score, which ranges from 0 (very dissatisfied) to 36 (very satisfied) for the DTSQs and from -18 (much less satisfied) to +18 (much more satisfied) for the DTSQc. Least Squares (LS) means of change from baseline were calculated using analysis of covariance (ANCOVA) with country and treatment as fixed effects and baseline score as a covariate. (NCT01064687)
Timeframe: Baseline, 52 weeks

,,
Interventionunits on a scale (Least Squares Mean)
DTSQs Treatment Satisfaction (n=270, 268, 266)DTSQc Treatment Satisfaction (n=249, 237, 226)
0.75 mg LY21892652.1115.46
1.5 mg LY21892652.0515.36
Exenatide0.6914.01

[back to top]

Number of Participants With Adjudicated Cardiovascular Events at 52 Weeks

Information on cardiovascular (CV) risk factors was collected at baseline. Data on any new CV event was prospectively collected using a CV event electronic case report form. At prespecified visits, participants were asked about any new CV event since the previous inquiry. Deaths and nonfatal cardiovascular adverse events (AEs) were adjudicated by an external committee of physicians with cardiology expertise. Nonfatal cardiovascular AEs to be adjudicated included myocardial infarction, hospitalization for unstable angina, hospitalization for heart failure, coronary interventions, and cerebrovascular events, including cerebrovascular accident (stroke) and transient ischemic attack. The number of participants with CV events confirmed by adjudication is summarized cumulatively at 52 weeks. Serious and all other non-serious adverse events regardless of causality are summarized in the Reported Adverse Events module. (NCT01064687)
Timeframe: Baseline through 52 weeks

,,
Interventionparticipants (Number)
Any CV EventAny Fatal EventAny Non-fatal CV Event
0.75 mg LY2189265202
1.5 mg LY2189265313
Exenatide202

[back to top]

Change From Baseline to 52 Weeks on Pancreatic Enzymes

Amylase (total and pancreas-derived) and lipase concentrations were measured. (NCT01064687)
Timeframe: Baseline, 52 weeks

,,
Interventionunits per liter (Median)
Amylase, Total (n=255, 263, 261)Amylase, Pancreas-derived (n=236, 253, 246)Lipase (n=201, 205, 221)
0.75 mg LY21892652.787.690.00
1.5 mg LY21892659.2116.675.45
Exenatide2.387.853.57

[back to top]

Change From Baseline to 52 Weeks on Electrocardiogram Parameters, Fridericia Corrected QT (QTcF) Interval and PR Interval

The QT interval is a measure of the time between the start of the Q wave and the end of the T wave and was calculated from electrocardiogram (ECG) data using Fridericia's formula: QTc = QT/RR^0.33. Corrected QT (QTc) is the QT interval corrected for heart rate and RR, which is the interval between two R waves. PR is the interval between the P wave and the QRS complex. Least Squares (LS) means of change from baseline were calculated using a mixed-effects model for repeated measures (MMRM) with treatment, country, visit, and treatment-by-visit interaction as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 52 weeks

,,
Interventionmilliseconds (msec) (Least Squares Mean)
QTcF Interval (n=239, 243, 226)PR Interval (n=237, 243, 220)
0.75 mg LY21892652.300.69
1.5 mg LY21892651.282.57
Exenatide2.52-0.82

[back to top]

Change From Baseline to 52 Weeks on Blood Pressure

Seated systolic blood pressure (SBP) and seated diastolic blood pressure (DBP) were measured. Least Squares (LS) means of change from baseline were calculated using a mixed-effects model for repeated measures (MMRM) with treatment, country, visit, and treatment-by-visit interaction as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 52 weeks

,,
Interventionmillimeters of mercury (mmHg) (Mean)
Seated SBP (n=248, 256, 238)Seated DBP (n=248, 256, 238)
0.75 mg LY21892651.620.76
1.5 mg LY21892650.830.89
Exenatide0.020.02

[back to top]

Change From Baseline to 52 Weeks in Updated Homeostasis Model Assessment of Beta-cell Function (HOMA2-%B) and Updated Homeostasis Model Assessment of Insulin Sensitivity (HOMA2-%S)

The homeostatic model assessment (HOMA) quantifies insulin resistance and beta-cell function. HOMA2-B is a computer model that uses fasting plasma insulin and glucose concentrations to estimate steady-state beta cell function (%B) as a percentage of a normal reference population (normal young adults). HOMA2-S is a computer model that uses fasting plasma insulin and glucose concentrations to estimate insulin sensitivity (%S) as percentages of a normal reference population (normal young adults). The normal reference populations were set at 100%. Least Squares (LS) means of change from baseline were calculated using a mixed-effects model for repeated measures (MMRM) with treatment, country, visit, and treatment-by-visit interaction as fixed effects and baseline as a covariate. (NCT01064687)
Timeframe: Baseline, 52 weeks

,,
Interventionpercentage of HOMA2 (Least Squares Mean)
HOMA2-%BHOMA2-%S
0.75 mg LY218926525.69-5.49
1.5 mg LY218926535.21-7.48
Exenatide13.57-3.75

[back to top]

"Incidence Rates Per 100,000 Person-Years of Likely Acute Pancreatitis (Among Recent Use Period) - Time on Drug Analysis"

"Crude time-on-drug incidence rate per 100,000 person-years of likely acute pancreatitis in initiators of exenatide, initiators of other antidiabetic drugs and the non-diabetes cohort. Analysis period is the recent use period, described as time following current use plus an additional 31 days excluding subsequent current use." (NCT01077323)
Timeframe: 43 months

InterventionCases per 100,000 person-years (Number)
Exenatide Initiators321.4
Other Antidiabetic Drug (OADs) Initiators325.5
Non-Diabetes Cohort56.2

[back to top]

"Incidence Rates Per 100,000 Person-Years of Likely Acute Pancreatitis (During Current Use Period) - Time on Drug Analysis"

"Crude time-on-drug incidence rate per 100,000 person-years of likely acute pancreatitis in initiators of exenatide, initiators of other antidiabetic drugs and the non-diabetes cohort. Analysis period is current use period, described as time during current day's supply plus 31 days." (NCT01077323)
Timeframe: 43 months

InterventionCases per 100,000 person-years (Number)
Exenatide Initiators219.7
Other Antidiabetic Drug (OADs) Initiators226.7
Non-Diabetes Cohort56.2

[back to top]

"Incidence Rates Per 100,000 Person-Years of Likely Acute Pancreatitis (During Past Use Period) - Time on Drug Analysis"

"Crude time-on-drug incidence rate per 100,000 person-years of likely acute pancreatitis in initiators of exenatide, initiators of other antidiabetic drugs and the non-diabetes cohort. Analysis period is past use period, described as time following recent use excluding subsequent current or recent use." (NCT01077323)
Timeframe: 43 months

InterventionCases per 100,000 person-years (Number)
Exenatide Initiators354.5
Other Antidiabetic Drug (OADs) Initiators218.1
Non-Diabetes Cohort56.2

[back to top]

Incidence Rates Per 100,000 Person-Years of Likely Acute Pancreatitis Among Initiators of Exenatide, Diabetics Initiating Other Antidiabetic Drugs, and the Non-diabetes Cohort - Intent to Treat Analysis

Crude intent-to-treat incidence rate per 100,000 person-years of likely acute pancreatitis in initiators of exenatide, initiators of other antidiabetic drugs and the non-diabetes cohort. (NCT01077323)
Timeframe: 43 months

InterventionCases per 100,000 person-years (Number)
Exenatide Initiators272.7
Other Antidiabetic Drug (OADs) Initiators227.6
Non-Diabetes Cohort56.2

[back to top]

HbA1c Change

"Measure the changes in HbA1C attributable to exenatide, insulin glargine and their combination.~Employ CGM with AGP analysis to determine if there is an incremental benefit for subjects who do not reach target to add exenatide to insulin glargine or insulin glargine to exenatide in patients taking metformin." (NCT01089569)
Timeframe: baseline to final visit (32 weeks)

,,
Intervention%HbA1c (Mean)
BaselineFinal - Week 32
Exenatide6.47.8
Exenatide + Insulin Glargine6.27.6
Insulin Glargine6.47.6

[back to top]

Change From Baseline in Weight Changes

"Measure the changes in weight attributable to exenatide, insulin glargine and their combinations.~Employ CGM with AGP analysis to determine if there is an incremental benefit for subjects who do not reach target to add exenatide to insulin glargine or insulin glargine to exenatide in patients taking metformin.~Change from baseline was calculated as weight in pounds at baseline minus weight in pounds at final visit (32 weeks)." (NCT01089569)
Timeframe: baseline - final visit (32 weeks)

Interventionlbs (pounds) (Mean)
Exenatide-13.5
Insulin Glargine-0.5
Exenatide + Insulin Glargine-10.3

[back to top]

Change From Baseline in Incidence of Hypoglycemia (Frequency)

"Employ Continuous Glucose Monitoring (CGM) with Ambulatory Glucose Profile (AGP) analysis to characterize the diurnal patterns produced by oral medications (metformin) used in the treatment of type 2 diabetes.~Employ CGM to measure the effect of exenatide, insulin glargine and exenatide plus insulin glargine in terms of underlying physiological defects and alter medications in a manner that improves- iv. Incidence of hypoglycemia (frequency)~Change from baseline was calculated as mean incidence rate at baseline minus mean incidence rate at final visit (32 weeks)" (NCT01089569)
Timeframe: baseline to final visit (32 weeks)

Interventionepisodes/day (Mean)
Exenatide.7
Insulin Glargine.8
Exenatide + Insulin Glargine.6

[back to top]

Change From Baseline in Incidence of Hypoglycemia (Degree)

"Employ Continuous Glucose Monitoring (CGM) with Ambulatory Glucose Profile (AGP) analysis to characterize the diurnal patterns produced by oral medications (metformin) used in the treatment of type 2 diabetes.~Employ CGM to measure the effect of exenatide, insulin glargine and exenatide plus insulin glargine in terms of underlying physiological defects and alter medications in a manner that improves- iv. Incidence of hypoglycemia (degree) Change from baseline was calculated as mean incidence percentage at baseline minus mean incidence percentage at final visit (32 weeks)" (NCT01089569)
Timeframe: baseline to final visit (32 weeks)

Interventionpercentage of measures under 70 mg/dL (Mean)
Exenatide1.7
Insulin Glargine1.7
Exenatide + Insulin Glargine1.3

[back to top]

Change From Baseline in Glucose Stability (Absolute Hourly Rate of Change in Median Curve)

"Employ Continuous Glucose Monitoring (CGM) with Ambulatory Glucose Profile (AGP) analysis to characterize the diurnal patterns produced by oral medications (metformin) used in the treatment of type 2 diabetes.~Employ CGM to measure the effect of exenatide, insulin glargine and exenatide plus insulin glargine in terms of underlying physiological defects and alter medications in a manner that improves iii. Glucose stability (absolute hourly rate of change in median curve)~Change from baseline was calculated as mean absolute hourly rate of change in median curve at baseline minus rate at final visit (32 weeks). Mean absolute hourly rate of change in the smoothed median curve is calculated as delta subscript MC = ( (NCT01089569)
Timeframe: p subscript 50 zero - p subscript 50 23

Interventionp subscript 50 zero - p subscript 50 23 (+Sum superscript 23 subscript i = 1)
Exenatide p subscript 50i - p subscript 50 i-1
Insulin Glargine p subscript 50i - p subscript 50 i-1
Exenatide + Insulin Glargine p subscript 50i - p subscript 50 i-1

[back to top]

Change From Baseline in Glucose Exposure (Area Under the Diurnal Median Curve or AUC)

"Employ Continuous Glucose Monitoring (CGM) with Ambulatory Glucose Profile (AGP) analysis to characterize the diurnal patterns produced by oral medications (metformin) used in the treatment of type 2 diabetes.~Employ CGM to measure the effect of exenatide, insulin glargine and exenatide plus insulin glargine in terms of underlying physiological defects and alter medications in a manner that improves- i. Glucose exposure (area under the diurnal median curve) Change from baseline was calculated as area under the diurnal median curve at baseline minus AUC value at final visit (32 weeks).~AUC is calculated using modified rectangle method AUC = sum of superscript 23, subscript i=0 P subscript 50i I = hour of day P subscript 50i = smoother 50th percentile value for ith hour of day" (NCT01089569)
Timeframe: baseline - final visit (32 weeks)

Interventionmg/dL*24hr (Mean)
Exenatide-1207.1
Insulin Glargine-1476.2
Exenatide + Insulin Glargine-1315

[back to top]

Change From Baseline in CGM Glucose Variability

"Employ Continuous Glucose Monitoring (CGM) with Ambulatory Glucose Profile (AGP) analysis to characterize the diurnal patterns produced by oral medications (metformin) used in the treatment of type 2 diabetes.~Employ CGM to measure the effect of exenatide, insulin glargine and exenatide plus insulin glargine in terms of underlying physiological defects and alter medications in a manner that improves- ii. Glucose variability (inter-quartile range)~IQR is the difference between the 75th and 25th percentiles. Change from baseline was calculated as IQR at baseline minus IQR value at final visit (32 weeks)." (NCT01089569)
Timeframe: baseline to final visit (32 weeks)

Interventionmg/dL (Mean)
Exenatide-9
Insulin Glargine-7.7
Exenatide + Insulin Glargine-12.1

[back to top]

Participants Negative or Positive for Anti-exenatide Antibodies - ITT Population

Serum titers of antibodies to exenatide were evaluated using a validated enzyme-linked immunosorbent assay (Covance Method No. ELISA-0308). Positive antibody to exenatide titer: observed at the indicated visit following a negative or missing titer at baseline, or a positive titer that has increased by at least 3 dilutions at the indicated visit from a detectable baseline. Baseline=Day 1. (NCT01104701)
Timeframe: Day 1 to Study Termination (24 weeks) or early termination

,,,
Interventionparticipants (Number)
Week 2 Negative (n=30,30,30,30)Week 2 Low Titer (<625)(n=30,30,30,30)Week 2 High Titer (≥625)(n=30,30,30,30)Week 20 Negative (n=30,26,29,28)Week 20 Low Titer (<625)(n=30,26,29,28)Week 20 High Titer (≥625)(n=30,26,29,28)
11 mg Exenatide Monthly29109154
2 mg Exenatide Weekly27307158
5 mg Exenatide Monthly30008108
8 mg Exenatide Monthly30009155

[back to top]

Number of Participants With Treatment-Emergent Adverse Events (AEs), Serious AEs (SAEs), and AEs Leading to Discontinuation - ITT Population

AE=any new unfavorable symptom, sign, or disease or worsening of a preexisting condition that may not have a causal relationship with treatment. SAE=a medical event that at any dose results in death, persistent or significant disability/incapacity, or drug dependency/abuse; is life-threatening, an important medical event, or a congenital anomaly/birth defect; or requires or prolongs hospitalization. All participants who received at least one dose of study drug were included in the ITT analysis. Treatment-emergent (TE) adverse events were defined as those with onset at or after initiation of study medication on Day 1 through study termination or early termination. (NCT01104701)
Timeframe: Day 1 to Study Termination (24 Weeks) or early Termination

,,,
Interventionparticipants (Number)
Treatment-Emergent AESTreatment-Emergent SAEsTreatment-Emergent AEs Leading to Discontinuation
11 mg Exenatide Monthly2401
2 mg Exenatide Weekly2700
5 mg Exenatide Monthly2520
8 mg Exenatide Monthly2000

[back to top]

Number of Chemistry Laboratory Values of Potential Clinical Importance Observed During Treatment Period - ITT Population

Potential clinical importance (PCI): triacylglycerol lipase high values were > 3* upper limit of normal (ULN); creatinine high values in males >1.6 mg/dL, females >1.4 mg/dL; gamma glutamyl transferase (GGT) high value >3* ULN; bilirubin high value > 2 mg/dL; Urate high values > 10 (males), >8 (females) mg/dL; potassium low value < 3 milliequivalents per liter (mEq/L), high value >5.5 mEq/L; calcium low value < 8 mg/dL and high value > 11 mg/dL. Laboratory samples were obtained at baseline (Day 1 or if unavailable, last measurement prior to first study drug dose), Weeks 6, 12, 20, and at study termination (Week 24) or early termination. Number of laboratory values of potential clinical importance (values could be either low or high) are presented for Weeks 6 - Week 24 or early termination. Note: those tests with no values meeting the PCI criteria, ie, 0 values observed across all treatment arms, are not presented. (NCT01104701)
Timeframe: Day 1 to Study Termination (Week24) or early termination

,,,
Interventionlaboratory values (Number)
triacylglycerol lipase Week 12 (n=30,29,29,28)triacylglycerol lipase Week 20 (n=30,27,29,28)Creatinine Week 6 (n=30,30,30,30)Creatinine Week 12 (n=30,29,30,28)Creatinine Week 20 (n=30,26,28,28)Creatinine at study termination (n=30,26,29,28)GGT Week 6 (n=30,30,30,30)GGT Week 20 (n=30,26,28,28)GGT study termination (n=30,26,29,28)Bilirubin Week 6 (n=30,30,30,30)Bilirubin Week 12 (n=30,29,30,28)Urate Week 6 (n=30,30,30,30)Urate Week 12 (n=30,29,30,28)Urate Week 20 (n=30,26,28,28)Urate Study termination (n=30,26,29,28)Potassium Week 6 (n=30,30,30,30)Calcium Week 6 (n=30,30,30,30)
11 mg Exenatide Monthly01000000000222000
2 mg Exenatide Weekly11010021100100111
5 mg Exenatide Monthly10101000011131000
8 mg Exenatide Monthly00000101100212000

[back to top]

Number of Hematology Laboratory Values of Potential Clinical Importance Observed During Treatment Period - ITT Population

Potential clinical importance are the following: Hematocrit values for males less than (<) 36%, females < 30%; hemoglobin for males <12 grams per deciliter (g/dL), females < 10 g/dL; low platelet values <75,000/micro liter (µL), high values greater than (>) 500,000 µL. Laboratory samples were obtained at baseline (Day 1 or if unavailable, last measurement prior to first study drug dose), Weeks 6, 12, 20, and at study termination (Week 24) or early termination. Number of laboratory values of potential clinical importance presented for Weeks 6 - Week 24 or early termination. (NCT01104701)
Timeframe: Day 1 to study termination (24 weeks) or early termination

,,,
Interventionlaboratory values (Number)
Week 6 Hematocrit (n=30,30,30,30)Hematocrit at study termination (n=30,27,29,28)Week 12 Platelets (n=30, 29, 30, 28)
11 mg Exenatide Monthly000
2 mg Exenatide Weekly000
5 mg Exenatide Monthly111
8 mg Exenatide Monthly000

[back to top]

Percentage of Participants Achieving HbA1c Target Values at Week 20 - Evaluable Population

HbA1c was measured as a percent (%) of total hemoglobin. The Target values for HbA1c were <7% and ≤ 6.5% at Week 20. Evaluable population was defined as participants who completed study procedures in compliance with the protocol and had adequate exposure to the study drug. (NCT01104701)
Timeframe: Week 20

,,,
Interventionpercentage of Participants (Number)
< 7.0% HbA1c≤ 6.5% HbA1c
11 mg Exenatide Monthly70.448.1
2 mg Exenatide Weekly48.344.8
5 mg Exenatide Monthly50.026.9
8 mg Exenatide Monthly57.139.3

[back to top]

Mean Change From Baseline in Heart Rate at Week 20 - Intent to Treat (ITT) Population

Baseline was Day 1, or last measurement prior to first dose of study drug. Heart rate was measured after the participant had rested for approximately 5 minutes and with the participant in a sitting position. Measurement was recorded in beats per minute (bpm). The measurement was repeated after at least 30 seconds and the average of the two readings recorded. ITT population was defined as all participants who received at least one dose of the study drug. (NCT01104701)
Timeframe: Baseline (Day 1), Week 20

Interventionbpm (Mean)
2 mg Exenatide Weekly2.8
5 mg Exenatide Monthly3.9
8 mg Exenatide Monthly5.6
11 mg Exenatide Monthly-0.3

[back to top]

Number of Participants With Injection Site Reaction Treatment Emergent Adverse Events - ITT Population

"AE is any new unfavorable symptom, sign, or disease or worsening of a preexisting condition that may not have a causal relationship with treatment. Injection site related adverse events were defined as the adverse events with 'injection site' phrase in preferred term excluding 'injection site nodule'. The following events were Injection Site Reaction AEs: erythema, hematoma, hemorrhage, site pain, site papule, site pruritus, site warmth.~Participants receiving study drug monthly received 5 injections with last injection at Week 16; Participants receiving study drug weekly received 20 injections with last injection at Week 19.~." (NCT01104701)
Timeframe: Day 1 through study termination (Week 24) or early termination.

Interventionparticipants (Number)
2 mg Exenatide Weekly6
5 mg Exenatide Monthly8
8 mg Exenatide Monthly3
11 mg Exenatide Monthly6

[back to top]

Mean Change From Baseline in Diastolic and Systolic Blood Pressure at Week 20 - Intent to Treat (ITT) Population

Baseline was Day 1, or last measurement prior to first dose of study drug. Vital signs were measured after the participant had rested for approximately 5 minutes and with the participant in a sitting position. Measurement was recorded in millimeters of mercury (mmHg). The blood pressure measurement was repeated after at least 30 seconds and the average of the two readings recorded. ITT population was defined as all participants who received at least one dose of the study drug. (NCT01104701)
Timeframe: Baseline (Day 1), Week 20

,,,
InterventionmmHg (Mean)
Diastolic Blood PressureSystolic Blood Pressure
11 mg Exenatide Monthly1.95.0
2 mg Exenatide Weekly-1.7-2.3
5 mg Exenatide Monthly3.44.4
8 mg Exenatide Monthly1.80.5

[back to top]

Mean Change in Body Weight From Baseline to Week 20 - Evaluable Population

Body weight was measured in kilograms (kg) at Baseline, and during treatment at Weeks 2, 4, 6, 8, 9-11, 12, 13, 14, 15, 16, 17-19, and 20. Baseline was Day 1, or last measurement prior to first dose of study drug. Evaluable population was defined as all participants who completed study procedures in compliance with the protocol and had adequate exposure to the study drug. (NCT01104701)
Timeframe: Baseline (Day 1) to Week 20

,,,
Interventionkg (Mean)
Change from baseline to Week 2 (n=29,26,28,27)Change from baseline to Week 4 (n=29,26,28,27)Change from baseline to Week 6 (n=29,26,28,27)Change from baseline to Week 8 (n=28,26,28,27)Change from baseline to Weeks 9-11 (n=29,26,28,27)Change from baseline to Week 12 (n=28,26,28,27)Change from baseline to Week 13 (n=29,26,28,27)Change from baseline to Week 14 (n=29,26,28,27)Change from baseline to Week 15 (n=29,26,28,26)Change from baseline to Week 16 (n=29,26,28,27)Change from baseline to Weeks 17-19(n=29,26,28,27)Change from baseline to Week 20 (n=29,26,28,27)
11 mg Exenatide Monthly0.350.03-0.74-0.70-0.83-0.76-0.97-0.81-1.24-1.02-1.72-1.14
2 mg Exenatide Weekly-0.31-0.66-1.26-1.36-1.73-1.49-1.96-1.91-1.84-1.85-1.63-1.36
5 mg Exenatide Monthly0.32-0.04-0.74-0.85-0.57-0.91-1.20-0.96-1.34-1.33-1.17-1.10
8 mg Exenatide Monthly0.310.32-0.45-0.33-0.49-0.33-0.56-0.76-0.80-0.26-0.58-0.41

[back to top]

Mean Change in Fasting Glucose From Baseline to Week 20 - Evaluable Population

Fasting glucose was measured in milligrams per deciliter (mg/dL) at screening, Baseline, and during treatment at Weeks 2, 4, 6, 8, 9-11, 12, 13, 14, 15, 16, 17-19, and 20. Baseline was Day 1, or last measurement prior to first dose of study drug. Evaluable population was defined as all participants who completed study procedures in compliance with the protocol and had adequate exposure to the study drug. (NCT01104701)
Timeframe: Baseline (Day 1) to Week 20

,,,
Interventionmg/dL (Mean)
Change from baseline to Week 2 (n=29, 26, 28,27)Change from baseline to Week 4 (n=29, 25, 28,27)Change from baseline to Week 6 (n=28, 26, 28,27)Change from baseline to Week 8 (n=28, 26, 28,27)Change from baseline to Weeks 9-11 (n=29,26,27,27)Change from baseline to Weeks 12 (n=29,26,27,27)Change from baseline to Weeks 13 (n=29,26,28,27)Change from baseline to Weeks 14 (n=29,26,28,27)Change from baseline to Weeks 15 (n=29,26,28,26)Change from baseline to Weeks 16 (n=29,26,28,27)Change from baseline to Weeks17-19 (n=29,26,28,27)Change from baseline to Week 20 (n=29,26,28,27)
11 mg Exenatide Monthly-23.5-23.1-48.8-44.0-48.1-44.9-45.7-51.6-53.1-46.3-55.1-48.9
2 mg Exenatide Weekly-1.16-21.7-32.8-40.8-32.8-44.8-42.0-36.3-38.0-34.5-33.3-34.2
5 mg Exenatide Monthly-12.9-18.0-42.6-45.7-40.2-37.4-38.0-37.3-37.3-31.6-42.4-25.1
8 mg Exenatide Monthly-14.6-14.2-39.5-36.8-44.3-45.4-48.6-47.5-46.9-43.3-34.6-29.8

[back to top]

Mean Change in HbA1c From Baseline to End of Treatment (Week 20) - Evaluable Population

HbA1c was measured as a percent of total hemoglobin at screening, Baseline, and during treatment on Weeks 4, 8, 12, 16, and 20. Baseline was Day 1, or last measurement prior to first dose of study drug. The Evaluable population was defined as participants who completed study procedures in compliance with the protocol and had adequate exposure to the study drug. (NCT01104701)
Timeframe: Baseline (Day 1) to 20 weeks

,,,
InterventionPercent of Hemoglobin (Mean)
Change from baseline at Week 4 (n=29, 26, 28, 27)Change from baseline at Week 8 (n=25, 22, 25, 27)Change from baseline at Week 12 (n=29, 26, 28, 27)Change from baseline at Week 16 (n=29, 26, 28, 27)Change from baseline at Week 20 (n=29, 26, 28, 27)
11 mg Exenatide Monthly-0.34-0.91-1.26-1.43-1.45
2 mg Exenatide Weekly-0.52-1.15-1.43-1.58-1.54
5 mg Exenatide Monthly-0.33-0.89-1.30-1.40-1.29
8 mg Exenatide Monthly-0.24-1.03-1.19-1.41-1.31

[back to top]

Time Weighted Average Concentration and Peak to Trough of Exenatide From Week 12 Through Week 16 - Pharmacokinetic Evaluable - Steady State Population

All participants received an initial blood draw prior to the first dose and a single blood sample was collected at all other subsequent visits, for plasma exenatide assessments and the characterization of pharmacokinetic (PK) parameters following multiple monthly doses over the study period. Exenatide was measured using a validated enzyme-linked immunosorbent assay (ELISA). Time weighted average concentration (Cave (2016-2688 h) and Peak to Trough were measured in picograms per milliliter (pg/mL). (NCT01104701)
Timeframe: Day 1 to Week 20

,,,
Interventionpg/mL (Geometric Mean)
Cave(2016-2688h) pg/mLPeak-Trough (2016-2688h) pg/mL
11 mg Exenatide Monthly218.07328.52
2 mg Exenatide Weekly262.92171.27
5 mg Exenatide Monthly127.13198.06
8 mg Exenatide Monthly247.38424.47

[back to top]

Severity of Obstructive Sleep Apnea

The apnea-hypopnea index (AHI) will be calculated from polysomnographic recordings. The minimum score for AHI is 0 (zero), corresponding to total absence of apnea or hypopnea. There is no theoretical maximum score although scores above 100 are very rarely observed. The lower the AHI value, the better. Higher AHI values correspond to greater severity of sleep apnea, a worse outcome. There are no subscales. We use continuous AHI values to measure severity of obstructive sleep apnea. (NCT01136798)
Timeframe: baseline and after 6 weeks of treatment

,
Interventionunits on a scale (Mean)
BaselineAt 6 week
Usual T2 DM Med Regimen15.916.5
Usual T2 DM Med Regimen Plus Exenatide16.410.9

[back to top]

Sleep Efficiency During Polysomnographic Recording

Sleep efficiency will be calculated as total sleep time over total recording time. (NCT01136798)
Timeframe: baseline and after 6 weeks of treatment

,
Interventionpercentage of total recording time (Mean)
BaselineAt 6 week
Usual T2 DM Med Regimen84.383.8
Usual T2 DM Med Regimen Plus Exenatide85.389.4

[back to top]

Mean 24-h Blood Glucose Levels

Mean plasma levels of glucose will be calculated from samples collected across the 24-h cycle. (NCT01136798)
Timeframe: baseline and after 6 weeks of treatment

,
Interventionmg/dl (Mean)
BaselineAt 6 week
Usual T2 DM Med Regimen134.4141.3
Usual T2 DM Med Regimen Plus Exenatide142.2136.1

[back to top]

Minutes of Wake After Sleep Onset During Sleep Recording

total amount of time spent awake after sleep onset and before morning awakening will be calculated (NCT01136798)
Timeframe: baseline and after 6 weeks of treatment

,
Interventionminutes (Mean)
BaselineAt 6 week
Usual T2 DM Med Regimen70.452.3
Usual T2 DM Med Regimen Plus Exenatide56.636.6

[back to top]

Non-REM Slow Wave Sleep

Total minutes of non-REM sleep was measured (NCT01136798)
Timeframe: baseline and after 6 weeks of treatment

,
Interventionminutes (Mean)
BaselineAt 6 week
Usual T2 DM Med Regimen47.357.3
Usual T2 DM Med Regimen Plus Exenatide34.341.4

[back to top]

the Comparison Between Treatment Groups of the Changes From Baseline in HbA1c at 48 Weeks

(NCT01147627)
Timeframe: 48 weeks

Interventionpercentage of HbA1c (Mean)
Exenatide-1.8
Premixed Insulin Analog-1.74
Thiazolidinedione-1.47

[back to top]

HbA1c

To compare the HbA1c at the end of 12 weeks in patients on exenatide subcutaneously twice daily (5 or 10 mcg/injection) as compared to controls in insulin treated obese type 2 diabetic patients. (NCT01154933)
Timeframe: value at 12 weeks minus value at baseline

Interventionpercent (Mean)
Exenatide 10 mcg-1.2
Placebo-0.5

[back to top]

Fasting Insulin

To compare the fasting insulin level at the end of 12 weeks in patients on exenatide subcutaneously twice daily (5 or 10 mcg/injection) as compared to controls in insulin treated obese type 2 diabetic patients. (NCT01154933)
Timeframe: after 24 hours fast at baseline and 12 weeks

,
InterventionμU/mL (Mean)
At BaselineAt 12 weeks
Exenatide 10 mcg12.716.4
Placebo13.113.9

[back to top]

Weight

To compare the body weight at the end of 12 weeks in patients on exenatide subcutaneously twice daily (5 or 10 mcg/injection) as compared to controls in insulin treated obese type 2 diabetic patients (NCT01154933)
Timeframe: value at 12 weeks minus value at baseline

Interventionlbs (Mean)
Exenatide 10 mcg0
Placebo3

[back to top]

Intranuclear NFκB Binding Activity

Measured by a gel shift assay showing the NFKB and Oct-1 binding to the doublestranded oligonucleotide containing the NFKB DNA binding site in Exenatide group and placebo group (NCT01154933)
Timeframe: measured after 6 hours of a single dose of placebo or exenatide treatment for value measured at 12 weeks minus baseline

Intervention% ratio of NFKB/Oct-1 (Mean)
Exenatide 10 mcg26
Placebo0

[back to top]

Reactive Hyperemia Index (RHI)

Greater RHI reflects greater endothelial function. It is calculated as average post-ischemia pulse magnitude divided by average pre-ischemia pulse magnitude. Results are expressed as least-square means of ANCOVA models. (NCT01181986)
Timeframe: 0, 2, 4, 6 and 8 hours on Day 11 (Sub-study 1); 0 and 120 minutes on test Days 1, 2 & 3 (Sub-study 2)

Interventionratio (Least Squares Mean)
Exenatide (Subs-study 1)1.90
Placebo (Sub-study 1)1.79
Saline+Exenatide (Sub-study 2)2.24
Saline+Placebo (Sub-study 2)1.95
Exendin-9+Exenatide (Sub-study 2)1.99

[back to top]

Plasma Triglycerides

Triglycerides concentrations were measured before and 2, 4, 6 and 8 hours following study drug. Results are expressed as least-square means of ANCOVA models adjusted for sampling time and intervention sequence. (NCT01181986)
Timeframe: 0, 2, 4, 6 and 8 hours post-study drug on day 11

Interventionmg/dl (Least Squares Mean)
Exenatide (Sub-study 1)175
Placebo (Sub-study 1)230

[back to top]

Plasma Glucose

Plasma glucose was measured before and 2, 4, 6 and 8 hours following study drug administration. Results are expressed as least-square means of ANCOVA models adjusted for sampling time and intervention sequence. (NCT01181986)
Timeframe: 0, 2, 4, 6, and 8 hours post-study drug on day 11

Interventionmg/dl (Least Squares Mean)
Exenatide (Sub-study 1)115
Placebo (Sub-study 1)136

[back to top]

Percent Change From Baseline in Body Mass Index at 3-months

As results are measured by BMI reduction, percent change (reduction) in BMI is primary outcome measure. (NCT01237197)
Timeframe: Baseline and 3-months

Interventionpercentage of change in BMI (Mean)
Exenatide-2.9
Placebo Injection-0.15

[back to top]

Mini Mental State Examination (MMSE)

Scale range: 0 - 30 points (higher is better) (NCT01255163)
Timeframe: 18 months

Interventionunits on a scale (Mean)
Exendin-423.11
Placebo23.11

[back to top]

Number of Participants With Incidence of Nausea

Tolerability of exenatide (nausea is the most common expected adverse event of exenatide) (NCT01255163)
Timeframe: 18 months

InterventionParticipants (Count of Participants)
Exendin-45
Placebo0

[back to top]

Cerebrospinal Fluid Amyloid-beta 42 (CSF Abeta42)

Abeta42 peptide measured in CSF using Luminex xMAP technology and INNO-BIA Alz Bio3 kits (Research Use Only) provided by Fujirebio (NCT01255163)
Timeframe: 18 months

Interventionpg/dl (Mean)
Exendin-4177.43
Placebo176.38

[back to top]

Body Mass Index (BMI)

Body Mass Index defined as a person's weight in kilograms (kg) divided by his or her height in meters squared. (NCT01255163)
Timeframe: 18 months

Interventionkg/m^2 (Mean)
Exendin-425.867
Placebo25.789

[back to top]

Cerebrospinal Fluid (CSF) Total Tau

Total Tau measured in CSF using Luminex xMAP technology and INNO-BIA Alz Bio3 kits (Research Use Only) provided by Fujirebio (NCT01255163)
Timeframe: 18 months

Interventionpg/dl (Mean)
Exendin-486.57
Placebo70.75

[back to top]

Cerebrospinal Fluid phospho181-tau (CSF p181-tau)

p-181-Tau measured in CSF using Luminex xMAP technology and INNO-BIA Alz Bio3 kits (Research Use Only) provided by Fujirebio (NCT01255163)
Timeframe: 18 months

Interventionpg/dl (Mean)
Exendin-454.57
Placebo44.25

[back to top]

Clinical Dementia Rating (CDR) Global Score

Clinical Dementia Rating global score range: 0 (no dementia); 0.5 (Mild Cognitive Impairment); 1 (mild dementia); 2 (moderate dementia); 3 (severe dementia). Higher is worse. (NCT01255163)
Timeframe: 18 months

Interventionunits on a scale (Mean)
Exendin-40.889
Placebo0.833

[back to top]

Alzheimer's Disease Assessment Scale-cognitive Subscale (ADAS-cog70)

Alzheimer's dementia scale cognitive sub-scale range: 0 - 70 points (higher is worse) (NCT01255163)
Timeframe: 18 months

Interventionunits on a scale (Mean)
Exendin-416
Placebo17.78

[back to top]

Clinical Dementia Rating (CDR) Sum of Boxes

"Sum of the Clinical Dementia Rating boxes (memory, orientation, judgment and problem solving, community affairs, home and hobbies, personal care). Each box is rated as 0, 0.5, 1, 2 or 3. Range for the sum of boxes is 0 - 18. Higher scores reflect a greater severity of dementia." (NCT01255163)
Timeframe: 18 months

Interventionunits on a scale (Mean)
Exendin-44.778
Placebo4.5

[back to top]

Post-prandial Blood Glucose Concentration in Both Pramlintide and Exenatide Treated Groups in Acute and Chronic Setting, Compared to Insulin Monotherapy in Type 1 Diabetes Mellitus.

We measured post-prandial blood sugars in both pramlintide and exenatide treated groups in acute and chronic setting, when compared to insulin monotherapy in subjects with Type 1 Diabetes Mellitus (NCT01269047)
Timeframe: 6 months

Interventionmmol/L (Mean)
Acute Pramlintide + Insulin Group9.03
Acute Exenatide + Insulin Group8.4
Chronic Pramlintide + Insulin Group8.0
Chronic Exenatide + Insulin Group10.2
Insulin Monotherapy10.8

[back to top]

Difference in HbA1C Between the Treatment and the Control Groups

(NCT01269047)
Timeframe: 6 months

Interventionpercentage of HbA1C values (Mean)
Acute Pramlintide + Insulin Group0.30
Acute Exenatide + Insulin Group0.60
Chronic Pramlintide + Insulin Group0.23
Chronic Exenatide + Insulin Group0.40
Insulin Monotherapy-0.40

[back to top]

Assay Sensitivity of Moxifloxacin at 1200h (3 Hour Post-administration of Moxifloxacin) on Day 2

Change from baseline in QTcP was analyzed by a MMRM between moxifloxacin and placebo. (NCT01297062)
Timeframe: Baseline, Day 2

Interventionmsec (Least Squares Mean)
Moxifloxacin12.47
Placebo1.56

[back to top]

Plasma Exenatide Concentrations at Steady State on Day 1, 2 and 3

The plasma exenatide concentration at steady state was descriptively summarized by geometric mean, standard error, and its effect on placebo-adjusted change from baseline in QTcP was assessed. (NCT01297062)
Timeframe: Baseline, Day 1, 2, and 3

Interventionpg/mL (Geometric Mean)
Day 1Day 2Day 3
Exenatide252.74399.14626.65

[back to top]

Number of Subjects With QTcP Interval >450msec at Any Timepoint on Any Day in Exenatide and Placebo

Number of subjects with QTcP > 450 msec at any timepoint on any day was summarized by frequency for exenatide and placebo. (NCT01297062)
Timeframe: Day 1, 2, or 3

Interventionparticipants (Number)
Exenatide0
Placebo0

[back to top]

Number of Subjects With Increase of QTcP Interval From Baseline >30msec at Any Timepoint on Any Day in Exenatide and Placebo

Number of subjects with increase of QTcP interval from baseline >30 msec at any timepoint on any day was summarized by frequency for exenatide and placebo. (NCT01297062)
Timeframe: Baseline, Day 1, 2, or 3

Interventionparticpants (Number)
Exenatide0
Placebo0

[back to top]

Comparison of LS Mean Changes From Baseline in QTcP Intervals Between Exenatide and Placebo on Day 3 Averaged Over 1300h, 1400h, 1500h (Target Steady State Exenatide Concentration of 500 pg/mL)

Factors in QT correction formulas were first estimated using pre-therapy data. The most appropriate correction method (QTcP) minimized the mean squared individual QTc/RR regression slope with on-exenatide data. Adequacy of correction was validated with on-placebo data. Change from baseline in QTcP was analyzed by a MMRM between exenatide and placebo. (NCT01297062)
Timeframe: Baseline, Day 3

Interventionmsec (Least Squares Mean)
Exenatide-3.54
Placebo-2.41

[back to top]

Comparison of LS Mean Changes From Baseline in QTcP Intervals Between Exenatide and Placebo on Day 2 Averaged Over 1300h, 1400h, 1500h (Target Steady State Exenatide Concentration of 300 pg/mL)

Factors in QT correction formulas were first estimated using pre-therapy data. The most appropriate correction method (QTcP) minimized the mean squared individual QTc/RR regression slope with on-exenatide data. Adequacy of correction was validated with on-placebo data. Change from baseline in QTcP was analyzed by a MMRM between exenatide and placebo. (NCT01297062)
Timeframe: Baseline, Day 2

Interventionmsec (Least Squares Mean)
Exenatide-2.58
Placebo-0.56

[back to top]

Comparison of Least Squares (LS) Mean Changes From Baseline in Population-based Corrected QT Intervals (QTcP) Between Exenatide and Placebo on Day 1 Averaged Over 1300h, 1400h, 1500h (Target Steady State Exenatide Concentration of 200 pg/mL)

Factors in QT correction formulas were first estimated using pre-therapy data. The most appropriate correction method (QTcP) minimized the mean squared individual QTc/RR regression slope with on-exenatide data. Adequacy of correction was validated with on-placebo data. Change from baseline in QTcP was analyzed by a mixed-effects model for repeated measures (MMRM) between exenatide and placebo. (NCT01297062)
Timeframe: Baseline, Day 1

Interventionmsec (Least Squares Mean)
Exenatide-2.25
Placebo-0.89

[back to top]

Assay Sensitivity of Moxifloxacin at 1100h (2 Hour Post-administration of Moxifloxacin) on Day 2

Change from baseline in QTcP was analyzed by a MMRM between moxifloxacin and placebo. (NCT01297062)
Timeframe: Baseline, Day 2

Interventionmsec (Least Squares Mean)
Moxifloxacin9.75
Placebo-0.81

[back to top]

Assay Sensitivity of Moxifloxacin at 1000h (1 Hour Post-administration of Moxifloxacin) on Day 2

Change from baseline in QTcP was analyzed by a MMRM between moxifloxacin and placebo. (NCT01297062)
Timeframe: Baseline, Day 2

Interventionmsec (Least Squares Mean)
Moxifloxacin1.91
Placebo-3.56

[back to top]

Echocardiographic Measures - Longitudinal Strain

Potential change in cardiac function will be assessed by echocardiography before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

Intervention% difference in lengths (Mean)
Exenatide-18.5
Placebo-18.3

[back to top]

Echocardiographic Measures - Lateral E'

Potential change in cardiac function will be assessed by echocardiography before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

Interventioncentimeters/second (Mean)
Exenatide0.09
Placebo0.09

[back to top]

Echocardiographic Measures - Circumferential Strain

Potential change in cardiac function will be assessed by echocardiography before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

Intervention% difference in circumferences (Mean)
Exenatide-25.6
Placebo-22.6

[back to top]

Change From Baseline in Arterial Stiffness

Pulse wave velocity will be measured via sphygmocor before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

Interventionmeters/second (Mean)
Exenatide-1.23
Placebo0.37

[back to top]

Echocardiographic Measures - Mitral Valve Deceleration Time

Potential change in cardiac function will be assessed by echocardiography before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

Interventionmilliseconds (Mean)
Exenatide234.6
Placebo239.8

[back to top]

Echocardiographic Measures - Septal E:E'

Potential change in cardiac function will be assessed by echocardiography before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

Interventionratio (Mean)
Exenatide8.3
Placebo12.6

[back to top]

Echocardiographic Measures - Mitral Valve E Wave Velocity

Potential change in cardiac function will be assessed by echocardiography before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

Interventioncentimeters/second (Mean)
Exenatide0.61
Placebo0.78

[back to top]

Oxygen Uptake Kinetics Steady State Tau

Time to steady state oxygen consumption will be assessed in subject before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

Interventionseconds (Mean)
Exenatide71.4
Placebo67.2

[back to top]

Peak Oxygen Consumption (VO2 Peak)

Subjects' peak oxygen consumption (VO2 peak) will be tested on a stationary bike before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

Interventionmilliliters per kilogram per minute (Mean)
Exenatide16.6
Placebo16.1

[back to top]

Echocardiographic Measures - Mitral Valve E:A Wave Velocity

Potential change in cardiac function will be assessed by echocardiography before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

Interventioncentimeters/second (Mean)
Exenatide0.85
Placebo0.82

[back to top]

Echocardiographic Measures - Septal E'

Potential change in cardiac function will be assessed by echocardiography before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

Interventioncentimeters/second (Mean)
Exenatide0.08
Placebo0.07

[back to top]

Echocardiographic Measures - Lateral E:E'

Potential change in cardiac function will be assessed by echocardiography before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

Interventionratio (Mean)
Exenatide6.7
Placebo8.4

[back to top]

Change From Baseline in Peak Dilation of Brachial Artery Diameter

Change in the response of the brachial artery to hyperemia will be assessed before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

,
Interventionmillimeters (Mean)
Pre-Intervention (Baseline)Post-Intervention (3 months)
Exenatide0.1930.226
Placebo0.1920.151

[back to top]

Echocardiographic Measures - Stroke Volume

Potential change in cardiac function will be assessed by echocardiography before and after 3 months of study medication or placebo. (NCT01364584)
Timeframe: Baseline and 3 months

InterventionmL/beat (Mean)
Exenatide93.3
Placebo80.7

[back to top]

Determine Changes in Bone Resorption Markers During the Treatment With a GLP-1 Receptor Agonist (Exenatide) Compared to Placebo in Patients With T2DM.

Bone reabsorption by bone-specific alkaline phosphatase (BAP) was assessed. Distribution of the Difference between EX/PBO Low/High Dose and Baseline Levels were calculated. (NCT01381926)
Timeframe: Baseline to 20 weeks

Interventionmg/L (Mean)
Exenatide 1st Then Placebo1.925
Placebo 1st Then Exenatide-0.20

[back to top]

Determine Changes in Bone Turnover Markers by Tartrate-Resistant Acid Phosphatase 5b (TRACP5b) During the Treatment With a GLP-1 Receptor Agonist (Exenatide) Compared to Placebo in Patients With T2DM.

Bone turnover by Tartrate-Resistant Acid Phosphatase 5b (TRACP5b) was assessed. Distribution of the Difference between EX/PBO Low/High Dose and Baseline Levels were calculated. (NCT01381926)
Timeframe: Baseline to 20 weeks

InterventionU/L (Mean)
Exenatide 1st Then Placebo0.05
Placebo 1st Then Exenatide0.325

[back to top]

Determine Changes in Bone Turnover Markers by Serum N-Telo Peptide During the Treatment With a GLP-1 Receptor Agonist (Exenatide) Compared to Placebo in Patients With T2DM.

Bone turnover by Serum N-Telo peptide (NTX) was assessed. Distribution of the Difference between EX/PBO Low/High Dose and Baseline Levels were calculated (NCT01381926)
Timeframe: Baseline to 20 weeks

InterventionnMBCE/L (Mean)
Exenatide Then Placebo-0.8
Placebo Then Exenatide1.725

[back to top]

Plasma Adipocytokines

the effect of the intervention on plasma adiponectin levels. (NCT01432405)
Timeframe: one year

Interventionmicrogram per ml (Mean)
Pioglitazone and Exenatide23.2
Pioglitazone15.8

[back to top]

Hepatic Fat

The effect of exenatide and pioglitazone on liver fat content after one year of treatment in patients with type 2 diabetes. (NCT01432405)
Timeframe: one year

Interventionpercent of liver fat (Mean)
Pioglitazone and Exenatide4.7
Pioglitazone6.5

[back to top]

Change in Weight

Change in weight (kg) after 6 months of treatment with study drug. Described as mean +/- SD (NCT01444898)
Timeframe: 6 months

Interventionkg (Mean)
Exenatide-.5

[back to top]

Appetite Scores

"Appetite scores using a syndrome-validated hyperphagia questionnaire~11 item questionnaire divided into subcategories of behavior (5 questions), drive (4 questions), severity (2 questions). Tallied and analyzed as total and subcategory scores. Each question scored 1-5 with higher scores correlating with worse hyperphagia.~Possible ranges: Total 11-55, behavior 5-25, drive 4-20, severity 2-10" (NCT01444898)
Timeframe: 6 months

Interventionunits on a scale (Mean)
Total Appetite Score BaselineTotal Appetite Score 6 monthBehavior Score BaselineBehavior Score 6 monthsDrive Score BaselineDrive Score 6 monthsSeverity Score BaselineSeverity Score 6 months
Exenatide32.225.414.510.612.610.45.14.4

[back to top]

% Change in Body Mass Index (BMI)

Prior to analysis, distributions were evaluated for normality and natural log transformation was performed to analyse data not normally distributed. Data are presented as mean ±SD unless not normally distributed, in which case they are presented as median with intra-quartile ranges (25th and 75th percentiles). Within-subject changes between visits were analysed by mixed model repeated measures. When the overall F-test for difference among visits was significant, Dunnett-adjusted pairwise comparisons were made between baseline and each subsequent visit. (NCT01444898)
Timeframe: 6 months

Intervention% change in BMI (Mean)
Exenatide1.3

[back to top]

Change in Acy Ghr

(NCT01444898)
Timeframe: 6 months

Interventionpg ml^-1 (Mean)
Exenatide263

[back to top]

Change in Insulin Levels

(NCT01444898)
Timeframe: 6 months

Interventionu/U ml^-1 (Mean)
Exenatide3

[back to top]

Change in Leptin

(NCT01444898)
Timeframe: 6 months

Interventionng ml^-1 (Mean)
Exenatide-7.4

[back to top]

Change in Pancreatic Peptide (PP)

(NCT01444898)
Timeframe: 6 months

Interventionpg ml^-1 (Mean)
Exenatide15

[back to top]

Change in BMI Z-Score

(NCT01444898)
Timeframe: 6 months

Interventionunits on a scale (Mean)
Exenatide.1

[back to top]

Change in HbA1c (%)

(NCT01444898)
Timeframe: 6 months

Interventionpercentage (Mean)
Exenatide-.3

[back to top]

Resting Energy Expenditure (Kcals Per Day)

Change in resting energy expenditure from baseline to 50 weeks (NCT01484873)
Timeframe: baseline, 50 weeks

Interventionkcal/day (Mean)
Exenatide-157.7

[back to top]

Insulin Secretion (Area Under the Curve)

Change in insulin secretion from baseline (NCT01484873)
Timeframe: baseline, 50 weeks

Intervention120 min*uU/mL x (Mean)
Exenatide-89.3

[back to top]

Gastric Emptying Rate (13C-octanoic Acid Isotope Excretion Half Life)

Change in the isotope excretion half life during a gastric emptying test at baseline and at 50 weeks (NCT01484873)
Timeframe: baseline, 50 weeks

Interventionminutes (Mean)
Exenatide12.9

[back to top]

Body Weight (kg)

Change in body weight from baseline to end of study (NCT01484873)
Timeframe: baseline, 50 weeks

Interventionkg (Mean)
Exenatide-1.4

[back to top]

Visual Analogue Scales for Post-meal Satiety

Change in visual analogue scales scores from baseline to 50 weeks. Higher score indicates greater satiety (minimum 0, maximum 100). (NCT01484873)
Timeframe: baseline, 50 weeks

Interventionmm (Mean)
Exenatide-2.5

[back to top]

HbA1C Levels

% of glycosylated hemoglobin in whole blood at 26 weeks (NCT01524705)
Timeframe: Baseline vs 26 weeks

Intervention% of HbA1C (Mean)
Insulin Glargine, Metformin, Exenatide7.1
Insulin Glargine, Metformin, Prandial Insulin7.2

[back to top]

Weight Change During Trial

Weight in kg at 26 weeks minus weight at baseline. (NCT01524705)
Timeframe: Baseline vs 26 weeks

Interventionkg (Mean)
Insulin Glargine, Metformin, Exenatide-4.8
Insulin Glargine, Metformin, Prandial Insulin0.7

[back to top]

Coefficient of Variation at 26 Weeks Minus Coefficient of Variation at Baseline

The change in the coefficient of variation (CV) of continuous glucose readings, as assessed by Continuous Glucose Monitoring (CGM) (NCT01524705)
Timeframe: At baseline, 6 months of intervention

Interventionpercentage (Mean)
Insulin Glargine, Metformin, Exenatide-2.43
Insulin Glargine, Metformin, Prandial Insulin0.44

[back to top]

Number of Participants With Hypoglycemia

Severe hypoglycemia-documented glucose <50mg/dl (participant journal), and hypoglycemic attacks requiring hospitalization, or treatment by emergency personnel. (NCT01524705)
Timeframe: 26 weeks

InterventionParticipants (Count of Participants)
Insulin Glargine, Metformin, Exenatide0
Insulin Glargine, Metformin, Prandial Insulin0

[back to top]

Change From Baseline in Glycosylated Hemoglobin A1c (HbA1c) to Week 24 (Controlled Assessment Period)

Change from baseline in HbA1c (%) to Week 24 during the controlled assessment period is reported as adjusted least square (LS) mean values. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. A mixed model with repeated measures (MMRM) analysis was performed, excluding data collected after initiation of rescue medication or premature discontinuation of study medication. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 24

Interventionpercentage (% HbA1c) (Least Squares Mean)
Controlled Assessment Period - Exenatide-0.36
Controlled Assessment Period - Placebo0.49

[back to top]

Change From Baseline in HbA1c to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)

Change from baseline in HbA1c (%) to Week 52 among patients who received open-label exenatide during the treatment period is reported as mean values. The treatment period was defined as the controlled assessment period and extension period combined. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. Data collected after initiation of rescue medication or after premature discontinuation of study medication were excluded. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 52

Interventionpercentage (% HbA1c) (Mean)
Treatment Period - Exenatide-0.10
Treatment Period - Placebo Then Exenatide0.53

[back to top]

Change From Baseline in Blood Pressure (Systolic and Diastolic) to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)

Change from baseline in SBP and DBP to Week 52 among patients who received open-label exenatide during the treatment period is reported as mean values. The treatment period was defined as the controlled assessment period and extension period combined. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. Data collected after initiation of rescue medication or after premature discontinuation of study medication were excluded. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 52

,
InterventionmmHg (Mean)
SBPDBP
Treatment Period - Exenatide-0.71.1
Treatment Period - Placebo Then Exenatide-0.6-2.5

[back to top]

Change From Baseline in HOMA-B and HOMA-S to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)

Change from baseline in HOMA-B and HOMA-S to Week 52 among patients who received open-label exenatide during the treatment period is reported as mean values. The treatment period was defined as the controlled assessment period and extension period combined. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. Data collected after initiation of rescue medication or after premature discontinuation of study medication were excluded. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 52

,
Interventionpercentage (%HOMA-B and %HOMA-S) (Mean)
HOMA-BHOMA-S
Treatment Period - Exenatide-2.589.85
Treatment Period - Placebo Then Exenatide42.022.36

[back to top]

Change From Baseline in Lipids Profiles to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)

Change from baseline in lipid profiles to Week 52 among patients who received open-label exenatide during the treatment period is reported as mean values (SI units). The treatment period was defined as the controlled assessment period and extension period combined. The following lipids were assessed: total cholesterol, HDL-C, LDL-C, and triglycerides. All lipids presented were taken in a fasted state. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. Data collected after initiation of rescue medication or after premature discontinuation of study medication were excluded. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 52

,
Interventionmmol/L (Mean)
Total CholesterolHDL-CLDL-CTriglycerides
Treatment Period - Exenatide-0.1880.004-0.175-0.155
Treatment Period - Placebo Then Exenatide-0.255-0.076-0.152-0.043

[back to top]

Plasma Exenatide Concentrations to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)

Geometric mean plasma exenatide concentrations up to Week 52 during the treatment period are reported (for the placebo then exenatide treatment group, only Weeks 24 and 52 were applicable). The treatment period was defined as the controlled assessment period and extension period combined. Data collected after initiation of rescue medication were included. Data collected after discontinuation of study medication were excluded. (NCT01554618)
Timeframe: Samples were collected on Day 1 (Week 0), Week 4, Week 8, Week 12, Week 24 and Week 52

Interventionpicograms per milliliter (Geometric Mean)
BaselineWeek 4Week 8Week 12Week 24Week 52
Treatment Period - ExenatideNA41.51130.60163.58140.8188.88

[back to top]

Percentage of Patients Positive for Anti-Drug Antibodies (ADAs) to Exenatide up to Week 24

Percentage of patients positive for ADAs up to Week 24 for the exenatide treatment group is reported. Baseline was the antibody measurement at Week 0 (Day 1). A negative or missing antibody measurement was considered negative at baseline. High positive = antibody titers ≥ 625, including baseline assessment. Low positive = antibody titers < 625, including baseline assessment. A patient was said to have treatment-emergent ADA positive at a visit if the antibody test was positive after the first dose of exenatide following a negative or missing antibody measurement, or the titer increased by at least 1 titration category from a detectable measurement prior to first dose of randomized study medication. (NCT01554618)
Timeframe: Samples were collected on Day 1 (Week 0), Week 4, Week 8, Week 12 and Week 24

Interventionpercentage of participants (Number)
Week 4: High PositiveWeek 4: Low PositiveWeek 4: Treatment-Emergent ADA PositiveWeek 8: High PositiveWeek 8: Low PositiveWeek 8: Treatment-Emergent ADA PositiveWeek 12: High PositiveWeek 12: Low PositiveWeek 12: Treatment-Emergent ADA PositiveWeek 24: High PositiveWeek 24: Low PositiveWeek 24: Treatment-Emergent ADA Positive
Treatment Period - Exenatide17.030.245.353.838.592.360.038.098.040.855.195.9

[back to top]

Percentage of Patients Reporting AEs of Injection Site Reactions up to Week 24 (Controlled Assessment Period)

"Percentage of patients reporting injection site reactions at Week 24 and at each intermediate visit during the controlled assessment period is reported. Injection site reactions were presented from the AE case report form (CRF), based on the Injection site reactions higher level term. A controlled assessment period AE was defined as an AE starting on or after day of first dose of study medication up to but not including Week 24 for patients entering the extension period. For patients not entering the extension period, the period was defined up to and including last dose of study medication + 7 days (+ 90 days for SAEs and other clinically significant or related AEs)." (NCT01554618)
Timeframe: At Week 4, Week 8, Week 12, Week 18 and Week 24

,
Interventionpercentage of participants (Number)
Week 4Week 8Week 12Week 18Week 24
Controlled Assessment Period - Exenatide8.53.51.900
Controlled Assessment Period - Placebo8.74.3000

[back to top]

Percentage of Patients Reporting AEs of Injection Site Reactions up to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)

"Percentage of patients reporting injection site reactions at Week 52 and at each intermediate visit among patients who received open-label exenatide during the treatment period is reported. The treatment period was defined as the controlled assessment period and extension period combined. Injection site reactions were presented from the AE CRF, based on the Injection site reactions higher level term. An Extension Period AE was defined as an AE starting on or after day of first dose of open-label exenatide to last dose + 7 days (+ 90 days for SAEs and other clinically significant or related AEs)." (NCT01554618)
Timeframe: At Week 4, Week 8, Week 12, Week 18, Week 24, Week 28, Week 40 and Week 52

,
Interventionpercentage of participants (Number)
Week 4Week 8Week 12Week 18Week 24Week 28Week 40Week 52
Treatment Period - Exenatide10.04.02.0004.000
Treatment Period - Placebo Then Exenatide9.14.5000000

[back to top]

Percentage of Patients With On-Treatment Adverse Events (AEs) up to Week 24 (Controlled Assessment Period)

A controlled assessment period AE was defined as an AE starting on or after day of first dose of study medication up to but not including Week 24 for patients entering the extension period. For patients not entering the extension period, the period was defined up to and including last dose of study medication + 7 days (+ 90 days for serious AEs [SAEs] and other clinically significant or related AEs). The Investigator assessed AEs for causal relationship to study drug medication. (NCT01554618)
Timeframe: Day 1 (Week 0) up to Week 24, plus up to a maximum of 90 days follow up

,
Interventionpercentage of participants (Number)
Any AEAny AE with outcome of deathAny SAEAny AE leading to discontinuation of treatmentAny AE leading to discontinuation from studyAny AE related to treatment
Controlled Assessment Period - Exenatide61.003.40025.4
Controlled Assessment Period - Placebo73.904.30021.7

[back to top]

Change From Baseline in Homeostasis Model Assessments - Beta-Cell Function (HOMA-B) and Insulin Sensitivity (HOMA-S) to Week 24 (Controlled Assessment Period)

Change from baseline in HOMA-B and HOMA-S in patients who were not taking insulin to Week 24 during the controlled assessment period is reported as adjusted LS mean values. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. A MMRM analysis was performed, excluding data collected after initiation of rescue medication or after premature discontinuation of study medication. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 24

,
Interventionpercentage (%HOMA-B and %HOMA-S) (Least Squares Mean)
HOMA-BHOMA-S
Controlled Assessment Period - Exenatide63.980.62
Controlled Assessment Period - Placebo-26.397.37

[back to top]

Change From Baseline in Lipid Profiles to Week 24 (Controlled Assessment Period)

Change from baseline in lipid profiles to Week 24 during the controlled assessment period is reported as mean values (Standard International [SI] units). The following lipids were assessed: total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides. All lipids presented were taken in a fasted state. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. Data collected after initiation of rescue medication or after premature discontinuation of study medication were excluded. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 24

,
Interventionmillimoles per liter (mmol/L) (Mean)
Total CholesterolHDL-CLDL-CTriglycerides
Controlled Assessment Period - Exenatide-0.117-0.035-0.050-0.122
Controlled Assessment Period - Placebo-0.114-0.047-0.1100.094

[back to top]

Change From Baseline in Body Weight to Week 24 (Controlled Assessment Period)

Change from baseline in body weight to Week 24 during the controlled assessment period is reported as adjusted LS mean values. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. A MMRM analysis was performed, excluding data collected after initiation of rescue medication or after premature discontinuation of study medication. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 24

Interventionkilogram (kg) (Least Squares Mean)
Controlled Assessment Period - Exenatide-0.59
Controlled Assessment Period - Placebo0.63

[back to top]

Change From Baseline in Body Weight to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)

Change from baseline in body weight to Week 52 among patients who received open-label exenatide during the treatment period is reported as mean values. The treatment period was defined as the controlled assessment period and extension period combined. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. Data collected after initiation of rescue medication or after premature discontinuation of study medication were excluded. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 52

Interventionkg (Mean)
Treatment Period - Exenatide0.04
Treatment Period - Placebo Then Exenatide-0.04

[back to top]

Plasma Exenatide Concentrations to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)

Geometric mean plasma exenatide concentrations up to Week 52 during the treatment period are reported (for the placebo then exenatide treatment group, only Weeks 24 and 52 were applicable). The treatment period was defined as the controlled assessment period and extension period combined. Data collected after initiation of rescue medication were included. Data collected after discontinuation of study medication were excluded. (NCT01554618)
Timeframe: Samples were collected on Day 1 (Week 0), Week 4, Week 8, Week 12, Week 24 and Week 52

Interventionpicograms per milliliter (Geometric Mean)
Week 24Week 52
Treatment Period - Placebo Then ExenatideNA105.56

[back to top]

Change From Baseline in Fasting Insulin to Week 24 (Controlled Assessment Period)

Change from baseline in fasting insulin to Week 24 during the controlled assessment period is reported as adjusted LS mean values. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. A MMRM analysis was performed, excluding data collected after initiation of rescue medication or after premature discontinuation of study medication. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 24

Interventionpicomoles per liter (pmol/L) (Least Squares Mean)
Controlled Assessment Period - Exenatide79.6
Controlled Assessment Period - Placebo-15.3

[back to top]

Change From Baseline in Fasting Insulin to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)

Change from baseline in fasting insulin to Week 52 among patients who received open-label exenatide during the treatment period is reported as mean values. The treatment period was defined as the controlled assessment period and extension period combined. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. Data collected after initiation of rescue medication or after premature discontinuation of study medication were excluded. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 52

Interventionpmol/L (Mean)
Treatment Period - Exenatide-32.4
Treatment Period - Placebo Then Exenatide121.5

[back to top]

Change From Baseline in Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) to Week 24 (Controlled Assessment Period)

Change from baseline in SBP and DBP to Week 24 during the controlled assessment period is reported as adjusted LS mean values. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. A MMRM analysis was performed, excluding data collected after initiation of rescue medication or after premature discontinuation of study medication. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 24

,
Interventionmillimeters mercury (mmHg) (Least Squares Mean)
SBPDBP
Controlled Assessment Period - Exenatide-0.70.2
Controlled Assessment Period - Placebo2.2-1.3

[back to top]

Change From Baseline in Fasting Plasma Glucose (FPG) Concentration to Week 24 (Controlled Assessment Period)

Change from baseline in FPG to Week 24 during the controlled assessment period is reported as adjusted LS mean values. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. A MMRM analysis was performed, excluding data collected after initiation of rescue medication or after premature discontinuation of study medication. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 24

Interventionmilligrams per deciliter (mg/dL) (Least Squares Mean)
Controlled Assessment Period - Exenatide-5.2
Controlled Assessment Period - Placebo16.5

[back to top]

Change From Baseline in FPG Concentration to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)

Change from baseline in FPG to Week 52 among patients who received open-label exenatide during the treatment period is reported as mean values. The treatment period was defined as the controlled assessment period and extension period combined. Baseline was defined as the last non-missing assessment (scheduled or unscheduled) on or prior to the first dose of randomized study medication. Data collected after initiation of rescue medication or after premature discontinuation of study medication were excluded. (NCT01554618)
Timeframe: Baseline (Week 0) and Week 52

Interventionmg/dL (Mean)
Treatment Period - Exenatide-1.8
Treatment Period - Placebo Then Exenatide10.6

[back to top]

Number of Patients Needing Rescue Medication Due to Failure to Maintain Glycemic Control up to Week 24 (Controlled Assessment Period)

Number of patients needing rescue medication at Week 24 and at each intermediate visit during the controlled assessment period is reported. Patients with a loss of glycemic control, defined as either an increase from baseline in HbA1c values by ≥ 1.0% at 2 consecutive clinic visits that were at least 1 month apart, or a fasting plasma glucose value ≥ 250 mg/dL or random blood glucose value > 300 mg/dL for 4 days during a 7 day period, received rescue medication. Data collected after premature discontinuation of study medication were excluded. (NCT01554618)
Timeframe: At Week 4, Week 8, Week 12, Week 18 and Week 24

,
InterventionParticipants (Count of Participants)
Week 4Week 8Week 12Week 18Week 24
Controlled Assessment Period - Exenatide00010
Controlled Assessment Period - Placebo00000

[back to top]

Number of Patients Needing Rescue Medication Due to Failure to Maintain Glycemic Control up to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)

Number of patients needing rescue medication at Week 52 and at each intermediate visit during the treatment period is reported. The treatment period was defined as the controlled assessment period and extension period combined. Patients with a loss of glycemic control, defined as either an increase from baseline in HbA1c values by ≥ 1.0% at 2 consecutive clinic visits that were at least 1 month apart, or a fasting plasma glucose value ≥ 250 mg/dL or random blood glucose value > 300 mg/dL for 4 days during a 7 day period, received rescue medication. Data collected after premature discontinuation of study medication were excluded. (NCT01554618)
Timeframe: At Week 4, Week 8, Week 12, Week 18, Week 24, Week 28, Week 40 and Week 52

,
InterventionParticipants (Count of Participants)
Week 4Week 8Week 12Week 18Week 24Week 28Week 40Week 52
Treatment Period - Exenatide00010220
Treatment Period - Placebo Then Exenatide00000100

[back to top]

Percentage of Participants Achieving HbA1c Goals of < 6.5%, ≤ 6.5%, and < 7.0% to Week 52 Among Patients Who Received Open-Label Exenatide (Treatment Period)

The percentage of patients achieving HbA1c goals of < 6.5%, ≤ 6.5%, and < 7.0% at Week 52 among patients who received open-label exenatide during the treatment period is reported. The treatment period was defined as the controlled assessment period and extension period combined. Data collected after initiation of rescue medication or after premature discontinuation of study medication were excluded. (NCT01554618)
Timeframe: At Week 52

,
Interventionpercentage of participants (Number)
HbA1c < 6.5%HbA1c ≤ 6.5%HbA1c < 7.0%
Treatment Period - Exenatide30.830.835.9
Treatment Period - Placebo Then Exenatide23.523.529.4

[back to top]

Percentage of Patients Achieving HbA1c Goals of < 6.5%, ≤ 6.5%, and < 7.0% at Week 24 (Controlled Assessment Period)

The percentage of patients achieving HbA1c goals of < 6.5%, ≤ 6.5%, and < 7.0% at Week 24 during the controlled assessment period is reported. A Cochran-Mantel-Haenszel (CMH) analysis was performed with missing data treated as non-responder, and excluding data collected after initiation of rescue medication or after premature discontinuation of study medication. (NCT01554618)
Timeframe: At Week 24

,
Interventionpercentage of participants (Number)
HbA1c <6 .5%HbA1c ≤ 6.5%HbA1c < 7.0%
Controlled Assessment Period - Exenatide19.019.031.0
Controlled Assessment Period - Placebo4.24.28.3

[back to top]

Effect of Exenatide on Brain (Total Gray Matter) Glucose Metabolism

To study the acute effect of exenatide on brain glucose metabolism after the glucose load. Brain glucose uptake will be determined from serial FDG PET-imaging, by using graphical methods to quantify both global and regional results. The results obtained after Exenatide injection will be compared with the ones obtained after injection of placebo in the same subject. (NCT01588418)
Timeframe: 120 minutes after exenatide or placebo injection

Interventionμmol/(ml*min) (Mean)
total gray matter CMRglu after Exenatidetotal gray matter CMRglu after Placebo
Effect of Exenatide or Placebo on CMRglu0.140.10

[back to top]

Change in Body Weight

Change in body weight after 12 weeks of treatment with exenatide or placebo twice daily injections. This outcome compares baseline and 12 week body weight. (NCT01590433)
Timeframe: 12 weeks

Interventionpercentage weight loss (Mean)
Exenatide6.5
Placebo7.5

[back to top]

Change in 2-hour Postprandial Glucose Concentrations From Baseline to Week 16

Change in 2-hour postprandial glucose concentrations from baseline to Week 16. (NCT01652716)
Timeframe: Baseline to Week 16

Interventionmg/dL (Least Squares Mean)
Experimental: Exenatide QWS Suspension-87.00
Active Comparator: Exenatide BID-113.74

[back to top]

Change in Body Weight (kg) From Baseline to Week 28

Change in body weight (kg) from baseline to Week 28/Study Termination. (NCT01652716)
Timeframe: Baseline to Week 28

Interventionkg (Least Squares Mean)
Experimental: Exenatide QWS Suspension-1.49
Active Comparator: Exenatide BID-1.89

[back to top]

Change in Fasting Plasma Glucose Concentrations From Baseline to Week 28

Change in fasting plasma glucose concentrations from baseline to Week 28/Study Termination (NCT01652716)
Timeframe: Baseline to Week 28

Interventionmg/dL (Least Squares Mean)
Experimental: Exenatide QWS Suspension-32.7
Active Comparator: Exenatide BID-22.5

[back to top]

Change in HbA1c (Glycosylated Hemoglobin) From Baseline to Week 28

The primary objective of this study was to compare the effect on glycemic control (HbA1c) of exenatide suspension administered once weekly to that achieved by exenatide administered twice daily for 28 weeks in subjects with type 2 diabetes mellitus. (NCT01652716)
Timeframe: Baseline to Week 28

InterventionPercentage of total hemoglobin (Least Squares Mean)
Experimental: Exenatide QWS Suspension-1.39
Active Comparator: Exenatide BID-1.02

[back to top]

Percentage of Subjects Achieving HbA1c <7% at Week 28

Percentage of subjects achieving HbA1c <7% at Week 28/Study Termination (NCT01652716)
Timeframe: Baseline to Week 28

,
InterventionPercentage of subjects (Number)
Baseline YesBaseline NoWeek 28 YesWeek 28 NoBaseline missing
Active Comparator: Exenatide BID1.498.643.256.80
Experimental: Exenatide QWS Suspension3.995.249.349.80.9

[back to top]

Percentage of Subjects Achieving HbA1c <7% at Week 28

Percentage of subjects achieving HbA1c target values of < 7.0% at Week 28/Study Termination. (NCT01652729)
Timeframe: Baseline to Week 28

,,
Interventionpercentage of subjects (Number)
Baseline YesBaseline NoWeek 28 YesWeek 28 No
Active Comparator: Sitagliptin1.698.432.068.0
Experimental: Exenatide3.396.743.156.9
Placebo Comparator: Placebo3.396.724.675.4

[back to top]

Change in 2-hour Postprandial Glucose Concentrations From Baseline to Week 16 (Visit 8)

The change in 2-hour postprandial plasma glucose from baseline (Day 1) to Visit 8 (Week 16) was analyzed using a general linear model including treatment, and baseline HbA1c stratum (< 9% or ≥ 9%) as fixed factors, and the baseline 2-hour postprandial plasma glucose concentrations as a covariate. (NCT01652729)
Timeframe: Baseline to Week 16

Interventionmg/dL (Least Squares Mean)
Experimental: Exenatide-59.57
Active Comparator: Sitagliptin-23.61
Placebo Comparator: Placebo-38.68

[back to top]

Change in Body Weight (kg) From Baseline to Week 28

The change in body weight (kg) from baseline (Day 1) to Week 28/Study Termination. (NCT01652729)
Timeframe: Baseline to Week 28

Interventionkg (Least Squares Mean)
Experimental: Exenatide-1.12
Active Comparator: Sitagliptin-1.19
Placebo Comparator: Placebo0.15

[back to top]

Change in Fasting Plasma Glucose Concentrations From Baseline to Week 28

The change in fasting plasma glucose concentrations from baseline (Day 1) to Week 28/Study Termination. (NCT01652729)
Timeframe: Baseline to Week 28

Interventionmg/dL (Least Squares Mean)
Experimental: Exenatide-21.3
Active Comparator: Sitagliptin-11.3
Placebo Comparator: Placebo9.6

[back to top]

Change in HbA1c (Glycosylated Hemoglobin) From Baseline to Week 28

Absolute change in HbA1c from baseline (Day 1, Visit 3) to Week 28/Study Termination (Visit 11). Hypothesis testing on the primary endpoint followed a serial gated procedure with all tests carried out at a 2-sided significance level of 0.05 to protect the family-wise error rate. These tests were conducted sequentially, and are presented in the statistical analysis section below in the order in which they were performed; each test was the gatekeeper of later tests. (NCT01652729)
Timeframe: Baseline to Week 28

Interventionpercentage of total hemoglobin (Least Squares Mean)
Experimental: Exenatide-1.13
Active Comparator: Sitagliptin-0.75
Placebo Comparator: Placebo-0.40

[back to top]

Change From Baseline in Postprandial AUC(0-8) of Insulin

The concentration of insulin in blood before and up to 8 hours after eating was plotted and the area under the curve calculated using the linear trapezoidal rule at Baseline and on Day 11. Least squares means of the change from Baseline to Day 11 were obtained using an ANCOVA model with treatment as fixed effect, and Baseline postprandial AUC (0-8) of insulin as a continuous covariate. (NCT01664624)
Timeframe: Baseline and Day 11; samples were taken at -15 min and -5 min (pre-meal), and 15 min, 30 min, and 1, 2, 3, 4, 6, and 8 hours (post-meal).

Interventionpmol/L*hr (Least Squares Mean)
Roflumilast + Alogliptin-49.5
Alogliptin Alone107.8
Roflumilast Alone26.9
Exenatide-136.4

[back to top]

Change From Baseline to Day 11 in 24-hour Average Plasma Glucose

Plasma glucose was measured by Continuous Glucose Monitoring System (CGMS). CGMS measures glucose every 5 minutes, starting in the fasting state 8 hour prior to the standardized breakfast (12 AM) until 16 hours after the breakfast. The average 24-hour plasma glucose concentration was calculated. Least squares means were obtained using an ANCOVA model with treatment as fixed effect, and Baseline 24-hour Glucose Measured by CGMS as a continuous covariate. (NCT01664624)
Timeframe: Baseline (Day -1) and Day 11, from 12 AM through 24 hours.

Interventionmg/dL (Least Squares Mean)
Roflumilast + Alogliptin-25.4
Alogliptin Alone-17.5
Roflumilast Alone-14.5
Exenatide-34.9

[back to top]

Change From Baseline to Day 11 in AUC(0-8) of Appetite Sensation

"Appetite sensations were measured using a visual analog scale (VAS) questionnaire. Participants were asked to indicate their level of fullness, hunger, satiety, and prospective consumption (how much do you think you can eat?) on a 100 mm line ranging from Not at all (0 mm) to extremely (100 mm). Appetite sensation scores before and up to 8 hours after eating were plotted and the area under the curve calculated using the linear trapezoidal rule at Baseline and on Day 11. Least squares means of the change from Baseline to Day 11 were obtained using an ANCOVA model with treatment as fixed effect, and Baseline postprandial AUC (0-8) of appetite sensation VAS score as a continuous covariate." (NCT01664624)
Timeframe: At Baseline and Day 11, every 30 minutes, starting 1 hour before eating until 8 hour after the meal.

,,,
Interventionmm*hr (Least Squares Mean)
FullnessHungerProspective consumptionSatiety
Alogliptin Alone62.03.1-14.9-3.2
Exenatide116.8-122.5-124.3-127.7
Roflumilast + Alogliptin70.5-103.6-97.1-82.7
Roflumilast Alone136.0-132.7-169.5-139.2

[back to top]

Change From Baseline in AUC(0-8) of Postprandial Plasma Glucose

The concentration of glucose in blood before and up to 8 hours after eating (postprandial) was plotted and the area under the curve calculated using the linear trapezoidal rule at Baseline and on Day 11. Least squares means of the change from Baseline to Day 11 were obtained using an ANCOVA model with treatment as fixed effect, and baseline postprandial AUC (0-8) of plasma glucose as a continuous covariate. (NCT01664624)
Timeframe: Baseline and Day 11 at -15 min and -5 min (pre-meal), and 15 min, 30 min, and 1, 2, 3, 4, 6, and 8 hours (post-meal).

Interventionmmol/L*hr (Least Squares Mean)
Roflumilast + Alogliptin-13.4
Alogliptin Alone-9.8
Roflumilast Alone-9.0
Exenatide-18.5

[back to top]

Change From Baseline in Postprandial Area Under the Curve From Time 0 to 8 Hours (AUC[0-8]) for Active Glucagon-like Peptide-1

The concentration of glucagon-like peptide-1 (GLP-1) in blood before and up to 8 hours after eating (postprandial) was plotted and the area under the curve calculated using the linear trapezoidal rule at Baseline and on Day 11. Least squares means of the change from Baseline to Day 11 were obtained using an analysis of covariance (ANCOVA) model with treatment as fixed effect, and Baseline postprandial AUC (0-8) of active GLP-1 as a continuous covariate. (NCT01664624)
Timeframe: Baseline and Day 11; samples were taken at -15 min and -5 min (pre-meal), and 15 min, 30 min, and 1, 2, 3, 4, 6, and 8 hours (post-meal).

Interventionpmol/L*hr (Least Squares Mean)
Roflumilast + Alogliptin26.5
Alogliptin Alone31.6
Roflumilast Alone3.8
Exenatide-2.3

[back to top]

Change From Baseline in Postprandial AUC(0-8) of C-peptide

The concentration of C-peptide in blood before and up to 8 hours after eating (postprandial) was plotted and the area under the curve calculated using the linear trapezoidal rule at Baseline and on Day 11. Least squares means of the change from Baseline to Day 11 were obtained using an ANCOVA model with treatment as fixed effect, and Baseline postprandial AUC (0-8) of C-peptide as a continuous covariate. (NCT01664624)
Timeframe: Baseline and Day 11; samples were taken at -15 min and -5 min (pre-meal), and 15 min, 30 min, and 1, 2, 3, 4, 6, and 8 hours (post-meal).

Interventionng/mL*hr (Least Squares Mean)
Roflumilast + Alogliptin1.0
Alogliptin Alone1.4
Roflumilast Alone-0.7
Exenatide0.0

[back to top]

Responders Achieving Pre-defined Target: HbA1c Below or Equal to 6.5% (48 mmol/Mol)

Percentage of responders achieving pre-defined target for HbA1c - HbA1c ≤ 6.5% (48 mmol/mol). (NCT01676116)
Timeframe: Week 26

InterventionPercentage (Number)
Insulin Degludec/Liraglutide + Oral Anti Diabetic Drugs (OADs)63
Liraglutide or Exenatide + OADs22.6

[back to top]

Change in Glycosylated Haemoglobin (HbA1c) From Baseline (Randomisation, Visit 2)

(NCT01676116)
Timeframe: Week 0, week 26

Interventionpercentage of glycosylated haemoglobin (Least Squares Mean)
Insulin Degludec/Liraglutide + Oral Anti Diabetic Drugs (OADs)-1.32
Liraglutide or Exenatide + OADs-0.37

[back to top]

Number of Adverse Events (AEs)

Rate (events per 100 exposure years) of treatment-emergent adverse events (an event that had onset date (or an increase in severity) on or after the first day of exposure to randomised treatment and no later than 7 days after the last day of randomised treatment) which occurred during the 26 weeks of treatment. (NCT01676116)
Timeframe: After 26 weeks of treatment

Interventionevents per 100 exposure years (Number)
Insulin Degludec/Liraglutide + Oral Anti Diabetic Drugs (OADs)410.1
Liraglutide or Exenatide + OADs364.3

[back to top]

Change From Baseline in Patient Reported Outcomes (PROs) Based on the Treatment Related Impact Measure - Diabetes (TRIM-D)

The patient related outcome is calculated based on TRIM-D questionnaire. The TRIM-D questionnaire consists of 5 sub-domains (treatment burden, daily life, diabetes management, compliance and psychological health), where each question is scored to a 1-5-point scale with a higher score indicating a better health state (less negative impact). Mean TRIM-D individual sub-domain scores and total score are later transformed to a 0-100 scale for analysis. The mean change in scores from baseline to 26 weeks for all the individual sub domains and total scores are presented here. (NCT01676116)
Timeframe: Week 0, week 26

,
InterventionScores on a scale (Mean)
TRIM-D Treatment Burden ScoreTRIM-D Daily Life ScoreTRIM-D Diabetes Management ScoreTRIM-D Compliance ScoreTRIM-D Psychological Health ScoreTRIM-D Total Score
Insulin Degludec/Liraglutide + Oral Anti Diabetic Drugs (OADs)10.86.310.98.97.38.7
Liraglutide or Exenatide + OADs5.70.84.14.31.43.1

[back to top]

Responders Achieving Pre-defined Target: HbA1c Below 7.0% (53 mmol/Mol)

Percentage of subjects achieving HbA1c below 7.0% after 26 weeks of treatment. (NCT01676116)
Timeframe: Week 26

InterventionPercentage (Number)
Insulin Degludec/Liraglutide + Oral Anti Diabetic Drugs (OADs)75.3
Liraglutide or Exenatide + OADs35.6

[back to top]

Change From Baseline in Patient Reported Outcomes (PROs) Based on Diabetes Treatment Satisfaction Questionnaire (DTSQ).

Mean change in diabetes treatment satisfaction questionnaire (DTSQs) scores from baseline. The scores ranged from 0 to 6. Higher total score on a 0-6 point scale indicates a general higher treatment satisfaction, whereas higher score on perceived frequency of hyperglycaemia and perceived frequency of hypoglycaemia indicate that blood glucose levels are out of the target range. (NCT01676116)
Timeframe: Week 0, week 26

,
InterventionScores on a scale (Mean)
Treatment satisfaction scale totalHyperglycaemiaHypoglycaemia
Insulin Degludec/Liraglutide + Oral Anti Diabetic Drugs (OADs)3.1-1.80.2
Liraglutide or Exenatide + OADs1.1-0.6-0.1

[back to top]

Number of Severe or Minor Hypoglycaemic Episodes

Rate (events per 100 patient years of exposure) of treatment-emergent confirmed hypoglycaemic episodes. The pool of severe and minor hypoglycaemic episodes was referred to as confirmed hypoglycaemic episodes. Severe hypoglycaemia was categorised as an episode requiring assistance of another person to actively administer carbohydrate, glucagon, or other resuscitative actions. Minor hypoglycaemic episodes were defined as an episode with symptoms consistent with hypoglycaemia with confirmation by blood glucose <2.8 mmol/L (50 mg/dL) or PG <3.1 mmol/L (56 mg/dL), and which was handled by the subject himself/herself, or any asymptomatic blood glucose value <2.8 mmol/L (50 mg/dL) or PG value <3.1 mmol/L (56 mg/dL). (NCT01676116)
Timeframe: After 26 weeks of treatment

Interventionevents per 100 patient years of exposure (Number)
Insulin Degludec/Liraglutide + Oral Anti Diabetic Drugs (OADs)281.7
Liraglutide or Exenatide + OADs12.1

[back to top]

Change From Baseline in Body Weight

Mean change in body weight after 26 weeks of treatment. (NCT01676116)
Timeframe: Week 0, week 26

Interventionkg (Mean)
Insulin Degludec/Liraglutide + Oral Anti Diabetic Drugs (OADs)2
Liraglutide or Exenatide + OADs-0.8

[back to top]

Change From Baseline in Fasting Plasma Glucose (FPG)

Mean change in fasting plasma glucose from baseline, after 26 weeks of treatment. (NCT01676116)
Timeframe: Week 0, week 26

Interventionmmol/L (Mean)
Insulin Degludec/Liraglutide + Oral Anti Diabetic Drugs (OADs)-2.98
Liraglutide or Exenatide + OADs-0.6

[back to top]

Body Mass Index at Baseline and 16 Weeks

(NCT01791465)
Timeframe: 16 weeks

Interventionkg/m2 (Mean)
baseline16 weeks
Bydureon Treatment32.631.3

[back to top]

Body Weight at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionkilograms (Mean)
baseline16 weeks
Bydureon Treatment10096

[back to top]

Peripheral Endothelial Tonography, as Measured by the Non-invasive EndoPAT System Using the LnRHI (Natural Log of Reactive Hyperemia Index), at Baseline and 16 Weeks

Normal: LnRHI > 0.51 Abnormal: LnRHI ≤ 0.51 (NCT01791465)
Timeframe: baseline and 16 weeks

Interventionunits on a scale (Mean)
baseline16 weeks
Bydureon Treatment0.710.62

[back to top]

Serum Adipokine Leptin Levels at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionng/ml (Mean)
baseline16 weeks
Bydureon Treatment17.414.3

[back to top]

Serum Hemoglobin A1c (HbA1c) Levels at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionpercentage of glycated haemoglobin (Mean)
baseline16 weeks
Bydureon Treatment7.66.3

[back to top]

Serum HDL Cholesterol Levels at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionmg/dL (Mean)
baseline16 weeks
Bydureon Treatment3934

[back to top]

Serum Highly-sensitive C-reactive Protein (hsCRP) Levels at Baseline and 16 Weeks

The primary outcome will be the change in hsCRP levels from baseline (pre-treatment) to 16 weeks of Bydureon treatment. (NCT01791465)
Timeframe: baseline and 16 weeks

Interventionmg/dl (Median)
baseline16 weeks
Bydureon Treatment4.05.6

[back to top]

Serum Interleukin 6 (IL-6) at Levels at Baseline and 16 Weeks

The primary outcome will be the change in serum IL-6 levels from baseline (pre-treatment) to 16 weeks of Bydureon treatment. (NCT01791465)
Timeframe: baseline and 16 weeks

Interventionmg/dl (Median)
baselineweek 16
Bydureon Treatment1.071.27

[back to top]

Oral Glucose Insulin Sensitivity (OGIS) at Baseline and 16 Weeks

The Oral Glucose Insulin Sensitivity (OGIS) is a method for the assessment of insulin sensitivity from the oral glucose tolerance test. OGIS provides an index which is analogous to the index of insulin sensitivity obtained from the glucose clamp. OGIS values for glucose clearance are reported in units of ml/min per square meter of body surface area. Lower values indicate slower glucose clearance and higher insulin resistance. (NCT01791465)
Timeframe: baseline and 16 weeks

Interventionml/min/m^2 BSA (Mean)
baseline16 weeks
Bydureon Treatment310399

[back to top]

Serum Total Cholesterol Levels at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionmg/dL (Mean)
baseline16 weeks
Bydureon Treatment192176

[back to top]

Waist Circumference at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventioncentimeters (Mean)
baseline16 weeks
Bydureon Treatment113113

[back to top]

Waist to Hip Ratio at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionratio (Mean)
baseline16 weeks
Bydureon Treatment1.061.06

[back to top]

Hip Circumference at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventioncentimeters (Mean)
baseline16 weeks
Bydureon Treatment107103

[back to top]

Serum Triglycerides Levels at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionmg/dL (Mean)
baseline16 weeks
Bydureon Treatment172118

[back to top]

Serum Macrophage Chemotactic Protein-1 (MCP-1) Levels at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionpg/ml (Mean)
baseline16 weeks
Bydureon Treatment5.734.78

[back to top]

Serum Macrophage Inflammatory Protein 1 Alpha (MIP-1 Alpha) Levels at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionpg/ml (Mean)
baseline16 weeks
Bydureon Treatment0.0880.081

[back to top]

Serum LDL Cholesterol Levels at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionmg/dL (Mean)
baseline16 weeks
Bydureon Treatment127109

[back to top]

Serum Soluble CD14 Levels at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionpg/ml (Mean)
baseline16 weeks
Bydureon Treatment598671

[back to top]

Serum Soluble Tumor Necrosis Factor Alpha (TNF-α) Levels at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionpg/ml (Mean)
baseline16 weeks
Bydureon Treatment2.442.82

[back to top]

Serum TNF-a Receptor 1 Levels at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionpg/ml (Mean)
baseline16 weeks
Bydureon Treatment392399

[back to top]

Serum TNF-a Receptor 2 Levels at Baseline and 16 Weeks

(NCT01791465)
Timeframe: baseline and 16 weeks

Interventionpg/ml (Mean)
baseline16 weeks
Bydureon Treatment598671

[back to top]

To Characterize the Pharmacokinetic Profile of ITCA 650 in Subjects With Type 2 Diabetes Mellitus

Change in HbA1c from baseline (NCT01798264)
Timeframe: 4 weeks

Interventionpercentage (Mean)
10 Mcg/Day-0.5
20 Mcg/Day-0.6
40 Mcg/Day-0.5
80 Mcg/Day-0.7

[back to top] [back to top]

Change in Fasting Plasma Glucose (FPG) 4 Weeks From Baseline

(NCT01798264)
Timeframe: 4 weeks

Interventionmg/dL (Mean)
10 Mcg/Day-5.6
20 Mcg/Day-31.2
40 Mcg/Day-42.0
80 Mcg/Day-28.8

[back to top]

Change in Weight From Baseline to 4 Weeks

(NCT01798264)
Timeframe: 4 weeks

Interventionkg (Mean)
10 Mcg/Day-0.3
20 Mcg/Day-0.3
40 Mcg/Day-1.1
80 Mcg/Day-3.1

[back to top]

Change From Baseline in Body Weight

Mean change in body weight from baseline to week 56. (NCT01885208)
Timeframe: Week 0, week 56

Interventionkilograms (Least Squares Mean)
Semaglutide 1.0 mg-5.63
Exenatide ER 2.0 mg-1.85

[back to top]

Change From Baseline in Fasting Plasma Glucose (FPG)

Mean change in FPG from baseline to week 56. (NCT01885208)
Timeframe: Week 0, week 56

Interventionmg/dL (Least Squares Mean)
Semaglutide 1.0 mg-51.22
Exenatide ER 2.0 mg-36.1

[back to top]

Change From Baseline in HbA1c (Glycosylated Haemoglobin)

Mean change in HbA1c from baseline to week 56. (NCT01885208)
Timeframe: Week 0, week 56

Interventionpercentage of glycosylated haemoglobin (Least Squares Mean)
Semaglutide 1.0 mg-1.54
Exenatide ER 2.0 mg-0.92

[back to top]

Change From Baseline in Patient Reported Outcome (PRO) Questionnaire Diabetes Treatment Satisfaction Questionnaire Status (DTSQs)

The Diabetes Treatment Satisfaction Questionnaire (DTSQs) was used to assess a subject's treatment satisfaction. This questionnaire contained 8 components and measures the treatment for diabetes (including insulin, tablets and/or diet) in terms of convenience, flexibility and general feelings regarding treatment. The value presented is the 'Treatment Satisfaction' summary score, which is the sum of 6 of the 8 items of the DTSQs questionnaire. Response options range from 6 (best case) to 0 (worst case). Total scores for treatment satisfaction range from 0-36. Higher scores indicate higher satisfaction. (NCT01885208)
Timeframe: Week 0, week 56

InterventionUnits on a scale (Least Squares Mean)
Semaglutide 1.0 mg4.98
Exenatide ER 2.0 mg3.96

[back to top]

Change From Baseline in Systolic and Diastolic Blood Pressure

Mean changes in systolic and diastolic blood pressure from baseline to week 56. (NCT01885208)
Timeframe: Week 0, week 56

,
Interventionmm Hg (Least Squares Mean)
Systolic blood pressureDiastolic blood pressure
Exenatide ER 2.0 mg-2.23-0.1
Semaglutide 1.0 mg-4.6-1.0

[back to top]

Major Hypoglycemic Event Rate Off Drug

The hypoglycemic event rate was calculated for patients while on and off study drug. The event rate is calculated using the number of events divided by the number of months either on or off study drug. Major hypoglycemic events are categorized as an event with a blood glucose level < 55 mg/dL. (NCT01928329)
Timeframe: Up to 12 months

Interventionevents per month (Median)
Exenatide (Bydureon)0.33
Placebo0.50

[back to top]

Major Hypoglycemic Event Rate On Drug

The hypoglycemic event rate was calculated for patients while on and off study drug. The event rate is calculated using the number of events divided by the number of months either on or off study drug. Major hypoglycemic events are categorized as an event with a blood glucose level < 55 mg/dL. (NCT01928329)
Timeframe: Up to 6 months

Interventionevents per month (Median)
Exenatide (Bydureon)0.67
Placebo0.80

[back to top]

Change From Baseline in HbA1c Levels

(NCT01928329)
Timeframe: 12 months

Interventionmmol/mol (Least Squares Mean)
Exenatide (Bydureon)0.08
Placebo0.10

[back to top]

Change From Baseline in HbA1c Levels

(NCT01928329)
Timeframe: 6 months

Interventionmmol/mol (Least Squares Mean)
Exenatide (Bydureon)-0.12
Placebo0.11

[back to top]

Myocardial Fat Content

Myocardial fat content following intervention as measured by magnetic resonance imaging and spectroscopy (MRS) in patients with type 2 diabetes. (NCT01951651)
Timeframe: 6 months

Interventionpercentage of myocardium content (Mean)
Exenatide1.7
Glipizide1.1

[back to top]

Monocyte Inflammatory Protein Nuclear Factor Kappa-B (NFkappaB) (%)

The percentage change in monocyte inflammatory proteins NFkappaB (%) from baseline. (NCT01951651)
Timeframe: 6 months

Interventionpercentage change from baseline (Mean)
Exenatide-65.0
Glipizide0.0

[back to top]

Left Ventricular Ejection Fraction (LVEF)(%).

Left Ventricular Ejection Fraction following intervention as measured by magnetic resonance imaging in patients with type 2 diabetes. (NCT01951651)
Timeframe: 6 months

Interventionpercent of Left ventricular function (Mean)
Exenatide60
Glipizide56

[back to top]

Hepatic Fat Content

Hepatic fat content following intervention in patients with type 2 diabetes (NCT01951651)
Timeframe: 6 months

Interventionpercent of hepatic fat (Mean)
Exenatide10.9
Glipizide13.1

[back to top]

Change From Baseline in Bone Metabolism at 12-Week Endpoint (Beta-Crosslaps and Procollagen 1 N-Terminal Propeptide [P1NP])

LS means were calculated using MMRM analysis adjusting for metformin use, washout of second OAM, baseline HbA1c category, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline as a covariate, and participant as a random effect (excludes data after rescue therapy). (NCT02020616)
Timeframe: Baseline, Week 12

,,,,,,
Interventionnanogram/milliliter (ng/mL) (Least Squares Mean)
Beta-CrosslapsP1NP
100 mg LY30531020.004-6.8
15 mg LY3053102-0.0230.9
2 mg Exenatide ER-0.0102.3
200 mg LY30531020.031-0.2
50 mg LY30531020.0011.9
7 mg LY3053102-0.033-0.3
Placebo-0.0385.0

[back to top]

Change From Baseline in Body Weight at 12-Week Endpoint

LS means were calculated using MMRM analysis adjusting for baseline HbA1c category, metformin use, washout of second OAM, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline as a covariate, and participant as a random effect (excludes data after rescue therapy). (NCT02020616)
Timeframe: Baseline, Week 12

Interventionkilogram (kg) (Least Squares Mean)
Placebo0.7
7 mg LY30531021.5
15 mg LY30531020.0
50 mg LY30531020.4
100 mg LY3053102-1.7
200 mg LY3053102-2.0
2 mg Exenatide ER-0.1

[back to top]

Change From Baseline in Hemoglobin A1c (HbA1c) at 12-Week Endpoint

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over prolonged periods of time. Least Squares (LS) means were calculated using mixed model repeated measures (MMRM) analysis adjusting for metformin use, washout of second oral anti-hyperglycemic medication (OAM), treatment, visit, and treatment-by-visit interaction as fixed effects, baseline as a covariate, and participant as a random effect. (NCT02020616)
Timeframe: Baseline, Week 12

InterventionPercent of HbA1c (Least Squares Mean)
Placebo-0.49
7 mg LY3053102-0.70
15 mg LY3053102-0.75
50 mg LY3053102-0.22
100 mg LY3053102-0.48
200 mg LY3053102-0.52
2 mg Exenatide ER-1.43

[back to top]

Percentage of Participants That Require Rescue Therapy

Percentage of participants that required >=1 rescue (blood glucose lowering) medications. (NCT02020616)
Timeframe: Baseline through Week 12

InterventionPercentage of Participants (Number)
Placebo0.0
7 mg LY30531020.0
15 mg LY305310212.5
50 mg LY305310214.3
100 mg LY30531020.0
200 mg LY30531020.0
2 mg Exenatide ER0.0

[back to top]

Percentage of Participants With Anti-Drug Antibodies to LY3053102

Percentage of participants with anti-LY3053102 antibody titre changes from baseline to the maximum postbaseline value. (NCT02020616)
Timeframe: Baseline through Study Completion (Up to 6 Months)

InterventionPercentage of Participants (Number)
Placebo0
7 mg LY30531021
15 mg LY30531021
50 mg LY30531020
100 mg LY30531022
200 mg LY30531022
2 mg Exenatide ER2

[back to top]

Percentage of Participants With Hypoglycemia

Hypoglycemia was defined as any event meeting the criteria for documented symptomatic hypoglycemia, asymptomatic hypoglycemia, or probable symptomatic hypoglycemia. (NCT02020616)
Timeframe: Baseline through Week 12

InterventionPercentage of Participants (Number)
Placebo10.0
7 mg LY305310212.5
15 mg LY30531020.0
50 mg LY30531020.0
100 mg LY305310212.5
200 mg LY305310212.5
2 mg Exenatide ER20.0

[back to top]

Pharmacokinetics: Area Under the Concentration Versus Time Curve During One Dosing Interval at Steady State (AUC [τ,ss]) of LY3053102

AUC (τ,ss) = area under the concentration versus time curve during one dosing interval at steady state, where the dosing interval (τ) = 168 hours. (NCT02020616)
Timeframe: Predose, 0, 1, 2, 3, 4, 6, 8, 12, 24, 48, 72, 96, 168 hours post-dose

Interventionmicrogram•hour/milliliter (µg•h/mL) (Geometric Mean)
7 mg LY305310222.6
15 mg LY305310276.8
50 mg LY3053102190.0
100 mg LY3053102350.0
200 mg LY3053102917.0

[back to top]

Change From Baseline in 7-Point Blood Glucose Profile at 12-Week Endpoint

7-Point Self-Monitored Blood Glucose profiles are measures of blood glucose concentration taken 7 times a day at morning pre-prandial, morning 2 hours postprandial, midday pre-prandial, midday 2 hours postprandial, evening pre-prandial, evening 2 hour postprandial, and bedtime. LS means were calculated using MMRM analysis adjusting for baseline HbA1c category, metformin use, washout of second OAM, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline as a covariate, and participant as a random effect (excludes data after rescue therapy). (NCT02020616)
Timeframe: Baseline, Week 12

,,,,,,
Interventionmilligram/deciliter (mg/dL) (Least Squares Mean)
Morning Meal (Post- minus Pre-prandial)Midday Meal (Post- minus Pre-prandial)Evening Meal (Post- minus Pre-prandial)Bedtime
100 mg LY30531024.72.5-39.04.9
15 mg LY3053102-57.7-55.0-46.5-44.5
2 mg Exenatide ER-47.9-31.3-4.9-53.6
200 mg LY3053102-26.8-24.6-61.3-13.0
50 mg LY3053102-34.9-24.7-25.9-10.1
7 mg LY3053102-18.7-31.3-11.118.8
Placebo-23.4-1.1-18.83.9

[back to top]

Change From Baseline in Bone Metabolism at 12-Week Endpoint (Osteocalcin and Bone-Specific Alkaline Phosphatase [Bone-Specific ALP])

LS means were calculated using MMRM analysis adjusting for metformin use, washout of second OAM, baseline HbA1c category, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline as a covariate, and participant as a random effect (excludes data after rescue therapy). (NCT02020616)
Timeframe: Baseline, Week 12

,,,,,,
Interventionmicrogram/liter (ug/L) (Least Squares Mean)
OsteocalcinBone-Specific ALP
100 mg LY3053102-2.6-1.9
15 mg LY3053102-1.7-0.2
2 mg Exenatide ER0.3-2.3
200 mg LY3053102-0.2-0.3
50 mg LY30531020.0-1.9
7 mg LY3053102-0.7-0.1
Placebo1.20.4

[back to top]

Change From Baseline in Bone Mineral Density Markers at 12-Week Endpoint

LS means were calculated using MMRM analysis adjusting for metformin use, washout of second OAM, baseline HbA1c category, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline as a covariate, and participant as a random effect (excludes data after rescue therapy). (NCT02020616)
Timeframe: Baseline, Week 12

,,,,,,
Interventionmilligram/square centimeter (mg/cm2) (Least Squares Mean)
L1-L4 Intervertebral SpaceNeck of FemurTotal Hip
100 mg LY30531022.0-0.30.1
15 mg LY30531021.2-0.4-0.7
2 mg Exenatide ER1.8-2.1-1.0
200 mg LY30531021.6-1.2-0.7
50 mg LY30531021.0-0.8-1.0
7 mg LY3053102-0.4-0.6-0.6
Placebo1.40.20.2

[back to top]

Change From Baseline in Lipids at 12-Week Endpoint

Lipids includes: High Density Lipoprotein-Cholesterol (HDL-C), Low Density Lipoprotein-Cholesterol (LDL-C), Triglycerides, and Cholesterol. LS means were calculated using MMRM analysis adjusting for metformin use, washout of second OAM, baseline HbA1c category, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline as a covariate, and participant as a random effect (excludes data after rescue therapy). (NCT02020616)
Timeframe: Baseline, Week 12

,,,,,,
Interventionmg/dL (Least Squares Mean)
HDL-CLDL-C
100 mg LY30531026.0-2.2
15 mg LY30531029.3-25.6
2 mg Exenatide ER-2.3-19.9
200 mg LY305310211.4-7.3
50 mg LY30531026.4-6.5
7 mg LY30531026.06.8
Placebo1.012.1

[back to top]

Percentage of Participants Achieving HbA1c <7.0% or HbA1c ≤6.5% at 12-Week Endpoint

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over prolonged periods of time. (NCT02020616)
Timeframe: Week 12

,,,,,,
InterventionPercentage of Participants (Number)
HbA1c <7.0%HbA1c ≤6.5%
100 mg LY30531020.00.0
15 mg LY305310240.00.0
2 mg Exenatide ER83.366.7
200 mg LY30531020.00.0
50 mg LY305310220.00.0
7 mg LY305310214.30.0
Placebo0.00.0

[back to top]

Median Intensive Care Unit Length of Stay

Defined as the number of days admitted to the Intensive Care Unit (NCT02058940)
Timeframe: From enrollment to 30 days post study drug discontinuation

Interventiondays (Median)
Exenatide9.0

[back to top]

Median Insulin Use

Calculated from number of insulin units administered over 48 hours starting at infusion initiation (NCT02058940)
Timeframe: Over 48 hours from infusion initiation

Interventionunits/kg (Median)
Exenatide0.03

[back to top]

Median Hospital Length of Stay

Defined as the number of days admitted to the hospital (NCT02058940)
Timeframe: From enrollment to 30 days post study drug discontinuation

Interventiondays (Median)
Exenatide12.5

[back to top]

Median Glucose Concentration During Exenatide Infusion

Calculated from hourly blood glucose samples starting at infusion initiation over 48 hours (NCT02058940)
Timeframe: Over 48 hours from infusion initiation

Interventionmg/dL (Median)
Exenatide137.0

[back to top]

Glycemic Variability

Glycemic variability is defined as the standard deviation of glucose calculated from hourly glucose measurements starting at infusion initiation over 48 hours (NCT02058940)
Timeframe: Over 48 hours from infusion initiation

Interventionmg/dL (Median)
Exenatide22.2

[back to top]

Correlation of Exenatide Concentrations With Creatinine Clearance

Spearman's correlation coefficient calculated from exenatide concentrations and urine creatinine measurements collected for all patients during the study period. A correlation coefficient is a numerical measure of some type of correlation, meaning a statistical relationship between two variables. Spearman's correlation coefficient assumes values in the range from -1 to +1, where +1 indicates the strongest possible agreement and -1 the strongest possible disagreement. (NCT02058940)
Timeframe: Over 48 hours from infusion initiation

Interventioncorrelation coefficient (Number)
Exenatide-0.2

[back to top]

Median Time to Reach Glucose Measurements Within Goal Range (110-180 mg/dL)

Calculated from hourly blood glucose samples starting at infusion initiation over 48 hours (NCT02058940)
Timeframe: Over 48 hours from infusion initiation

Interventionminutes (Median)
Exenatide200.0

[back to top]

Percentage of Critically Ill Patients With Acute Brain Injury Achieving Pre-specified Feasibility Criteria

Feasibility is defined as the percentage of patients 1) experiencing severe hypoglycemia (<40 mg/dL); 2) achieving glucose measurements within goal (110-180 mg/dL); and 3) experiencing nausea requiring discontinuation of exenatide therapy. The pre-specified criteria for determining feasibility includes the following: 1) at least 75% of patients achieving glucose measurements within goal (110-180 mg/dL) and 2) no more than 25% of patients experiencing severe hypoglycemia (<40 mg/dL) or nausea requiring exenatide discontinuation. (NCT02058940)
Timeframe: Over 48 hours from infusion initiation

Interventionpercentage of patients (Number)
Percentage Experiencing Severe HypoglycemiaPercentage Achieving Glucose within GoalPercentage with Nausea Requiring Discontinuation
Exenatide087.50

[back to top]

Percentage of Patients With >1 Episode of Hypotensive Episode (SBP<100 mmHg)

Calculated from blood pressure measurements starting at infusion initiation over 48 hours (NCT02058940)
Timeframe: Over 48 hours from infusion initiation

Interventionpercentage of patients (Number)
Exenatide12.5

[back to top]

Percentage of Hypotensive Episodes (SBP<100 mmHg)

Defined as the number of hypotensive episodes (SBP<100 mmHg)for all patients/total number of blood pressure measurements collected for all patients. (NCT02058940)
Timeframe: Over 48 hours from infusion initiation

Interventionpercentage of measurements (Number)
Exenatide1.2

[back to top]

Percentage of Patients With >1 Episode of Hypoglycemia (<80 mg/dL)

Calculated from hourly blood glucose samples starting at infusion initiation over 48 hours (NCT02058940)
Timeframe: Over 48 hours from infusion initiation

Interventionpercentage of patients (Number)
Exenatide12.5

[back to top]

Percentage of Patients Requiring Rescue Insulin Infusion Protocol

Defined as the percentage of patients requiring an insulin infusion to control glucose concentrations during exenatide treatment (NCT02058940)
Timeframe: Over 48 hours from infusion initiation

Interventionpercentage of patients (Number)
Exenatide0

[back to top]

Percentage of Hypoglycemic Episodes (<80 mg/dL)

Percentage of hypoglycemic episodes is calculated as the total number of glucose measurements <80 mg/dL for all patients/total number of glucose measurements collected for all patients. (NCT02058940)
Timeframe: Over 48 hours from infusion initiation

Interventionpercentage of measurements (Number)
Exenatide1.2

[back to top]

Percentage of Glucose Measurements Within Goal Range

Percentage of glucose measurements within goal range is calculated as the number of glucose measurements within goal range (110-180 mg/dL) for all patients/total number of glucose measurements collected for all patients. (NCT02058940)
Timeframe: Over 48 hours from infusion initiation

Interventionpercentage of measurements (Number)
Exenatide69.6

[back to top]

Change From Baseline in Body Mass Index (BMI)

(NCT02072096)
Timeframe: Baseline, Week 72

Interventionkilogram per square meter (kg/m^2) (Mean)
Strategy A (Glucose-Dependent)-0.47
Strategy B (Reference)0.20

[back to top]

Change From Baseline of Estimated Glomerular Filtration Rate (eGFR)

The eGFR is used in addition to the Urinary Albumin to Creatinine Ratio to measure the incidence and progression of diabetic kidney disease. (NCT02072096)
Timeframe: Baseline, Week 72

Interventionmilliliter per minute/1.73 square meter (Mean)
Strategy A (Glucose-Dependent)-5.00
Strategy B (Reference)-5.88

[back to top]

Change From Baseline of Urinary Albumin to Creatinine Ratio

The Urinary Albumin to Creatinine Ratio is used in addition to Estimated Glomerular Filtration Rate (eGFR) to measure the incidence and progression of diabetic kidney disease. (NCT02072096)
Timeframe: Baseline, Week 72

Interventionmilligram per millimole (mg/mmol) (Mean)
Strategy A (Glucose-Dependent)1.85
Strategy B (Reference)1.85

[back to top]

Percentage of Participants Achieving and Maintaining Individualized Glycated Hemoglobin A1c (HbA1c) Targets Without Clinically Significant Hypoglycemia

Failed to reach and maintain HbA1c target, without clinically significant hypoglycemia, is defined as having 2 consecutive HbA1c > upper limit of HbA1c target over 12 weeks starting from Week 24 for participants with HbA1c data beyond Week 24, or Week 24 HbA1c > upper limit of HbA1c target for participants without HbA1c data beyond Week 24. Clinically significant hypoglycemia is defined as any severe hypoglycemia or repeated hypoglycemia interrupting participants activities or sleep and associated with blood glucose ≤3.9 millimole per liter (mmol/L), or repeated asymptomatic hypoglycemia associated with blood glucose <3.0 mmol/L. Success is defined as lacking of failure. (NCT02072096)
Timeframe: Baseline to last participant visit (up to 72 weeks)

Interventionpercentage of participants (Number)
Strategy A (Glucose-Dependent)64.5
Strategy B (Reference)54.9

[back to top]

Number of Participants With Total Hypoglycemia and Other Categories of Hypoglycemia

(NCT02072096)
Timeframe: Baseline to last participant visit (up to 72 weeks)

,
InterventionParticipants (Number)
Total HypoglycemiaSevere HypoglycemiaClinically Significant HypoglycemiaSymptomatic HypoglycemiaAsymptomatic HypoglycemiaProbable Symptomatic HypoglycemiaUnspecified HypoglycemiaRelative HypoglycemiaNocturnal Hypoglycemia
Strategy A (Glucose-Dependent)1000580214
Strategy B (Reference)5001343077610

[back to top]

Percentage of Participants Requiring Alternative Treatment Due to Glycemic Failure of First Line Injectable Therapy

(NCT02072096)
Timeframe: Baseline to last participant visit (up to 72 weeks)

Interventionpercentage of participants (Number)
Strategy A (Glucose-Dependent)21
Strategy B (Reference)13

[back to top]

Triglycerides

triglycerides (NCT02104739)
Timeframe: 2 hours after ingestion of meal

Interventionmilligrams per deciliter (Mean)
Exenatide119
Saxagliptin130
Placebo163
Exenatide Extended-release (ER)168

[back to top]

Triglycerides

triglycerides (NCT02104739)
Timeframe: 4 hours after ingestion of meal

Interventionmilligrams per deciliter (Mean)
Exenatide124
Saxagliptin153
Placebo206

[back to top]

Triglycerides

triglycerides (NCT02104739)
Timeframe: 6 hours after ingestion of meal

Interventionmilligrams per deciliter (Mean)
Exenatide161
Saxagliptin179
Placebo200

[back to top]

Triglycerides

triglycerides (NCT02104739)
Timeframe: baseline

Interventionmilligrams per deciliter (Mean)
Exenatide108
Saxagliptin101
Placebo102
Exenatide Extended-release (ER)106

[back to top]

Free Fatty Acids

Free Fatty Acids (NCT02104739)
Timeframe: 2 hours after meal

Interventionmillimoles per liter (Mean)
Exenatide0.35
Saxagliptin0.18
Placebo0.17
Exenatide Extended-release (ER)0.19

[back to top]

Free Fatty Acids

Free Fatty Acids (NCT02104739)
Timeframe: 4 hours after meal

Interventionmillimoles per liter (Mean)
Exenatide0.43
Saxagliptin0.24
Placebo0.23

[back to top]

Free Fatty Acids

Free Fatty Acids (NCT02104739)
Timeframe: 6 hours after meal

Interventionmillimoles per liter (Mean)
Exenatide0.29
Saxagliptin0.31
Placebo0.33

[back to top]

Free Fatty Acids

Free Fatty Acids (NCT02104739)
Timeframe: baseline

Interventionmillimoles per liter (Mean)
Exenatide0.45
Saxagliptin0.49
Placebo0.51
Exenatide Extended-release (ER)0.65

[back to top]

Monocyte NfkB Levels as Detected by Western Blotting

Monocyte NfkB p65 arbitrary units are quantified by densitometric analysis of the Western blots. (NCT02104739)
Timeframe: 2 hours after ingestion of meal

InterventionNfkB p65 arbitrary units (Mean)
Exenatide67.39
Saxagliptin68.39
Placebo71.37
Exenatide Extended-release (ER)93.47

[back to top]

Monocyte NfkB Levels as Detected by Western Blotting

Monocyte NfkB p65 arbitrary units are quantified by densitometric analysis of the Western blots. (NCT02104739)
Timeframe: baseline

InterventionNfkB p65 arbitrary units (Mean)
Exenatide62.79
Saxagliptin72.03
Placebo67.68
Exenatide Extended-release (ER)84.19

[back to top]

Peak Forearm Blood Flow

Peak forearm blood flow via strain gauge venous occlusion plethysmography (NCT02104739)
Timeframe: 3 hours after meal

InterventionmL per minute per 100mL of tissue (Mean)
Exenatide13.18
Saxagliptin13.25
Placebo15.11
Exenatide Extended-release (ER)16.54

[back to top]

Peak Forearm Blood Flow

Peak forearm blood flow via strain gauge venous occlusion plethysmography (NCT02104739)
Timeframe: 6 hours after meal

InterventionmL per minute per 100mL of tissue (Mean)
Exenatide14.25
Saxagliptin15.87
Placebo13.45

[back to top]

Peak Forearm Blood Flow

Peak forearm blood flow via strain gauge venous occlusion plethysmography (NCT02104739)
Timeframe: baseline

InterventionmL per minute per 100mL of tissue (Mean)
Exenatide12.65
Saxagliptin12.79
Placebo12.18
Exenatide Extended-release (ER)16.18

[back to top]

Change From Baseline in Glucagon Levels

LSM are calculated from MMRM analysis using REML with metformin use, baseline BMI category, baseline HbA1c category, country, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline parameter result as a covariate, and participant as a random effect. (NCT02119819)
Timeframe: Baseline, Week 12; Baseline, Week 24

,,,,,
Interventionpicomol per liter (pmol/L) (Least Squares Mean)
Week 12Week 24
10 mg LY2944876-1.26-2.30
15 mg LY2944876-2.65-2.25
30 mg LY2944876-5.14-4.40
50 mg LY2944876-6.21-4.93
Exenatide Extended-release-1.58-0.19
Placebo-0.040.66

[back to top]

Percent Change From Baseline in Body Weight

(NCT02119819)
Timeframe: Baseline, Week 12; Baseline, Week 24

,,,,,
InterventionPercentage change (Mean)
Week 12Week 24
10 mg LY2944876-1.09-1.57
15 mg LY2944876-1.86-2.13
30 mg LY2944876-2.01-1.98
50 mg LY2944876-3.23-3.41
Exenatide Extended-release-2.04-2.18
Placebo-1.22-1.70

[back to top]

Change From Baseline in Fasting Fibroblast Growth Factor 21

LSM was calculated from MMRM analysis using REML with metformin use, baseline BMI category, baseline HbA1c category, country, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline parameter result as a covariate, and participant as a random effect. (NCT02119819)
Timeframe: Baseline, Week 12; Baseline, Week 24

,,,,,
Interventionmicrogram per liter (µg/L) (Least Squares Mean)
Week 12Week 24
10 mg LY2944876-0.070.06
15 mg LY29448760.06-0.04
30 mg LY2944876-0.03-0.07
50 mg LY2944876-0.14-0.12
Exenatide Extended-release-0.09-0.06
Placebo-0.11-0.09

[back to top]

Change From Baseline in Lipids

Change from baseline in high-density lipoprotein cholesterol (HDL-C), total cholesterol, triglycerides, and low-density lipoprotein cholesterol (LDL-C). LSM was calculated from MMRM analysis using REML with metformin use, baseline BMI category, baseline HbA1c category, country, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline parameter result as a covariate, and participant an a random effect. (NCT02119819)
Timeframe: Baseline, Week 24

,,,,,
Interventionmg/dL (Least Squares Mean)
HDL-CTotal CholesterolTriglyceridesLDL-C
10 mg LY29448761.56-1.26-14.63-1.37
15 mg LY29448760.92-1.12-13.32-0.40
30 mg LY29448760.90-1.46-15.40-0.24
50 mg LY29448761.04-5.11-20.96-0.04
Exenatide Extended-release2.35-0.12-11.830.37
Placebo2.177.3210.614.55

[back to top]

Percentage of Participants Developing Anti-Drug Antibodies to LY2944876

Percentage of participants developing anti-drug antibodies to LY2944876. (NCT02119819)
Timeframe: Week 12 and Week 24

,,,,,
Interventionpercentage of participants (Number)
Week 12Week 24
10 mg LY29448761.71.8
15 mg LY29448761.40
30 mg LY29448761.51.5
50 mg LY294487600
Exenatide Extended-release1.60
Placebo00

[back to top]

Pharmacokinetics: Area Under the Concentration Curve (AUC) of LY2944876

Evaluable pharmacokinetic concentrations from the specified timepoints were combined and utilized in a population approach to determine the population mean estimate and standard deviation at steady-state. (NCT02119819)
Timeframe: Baseline, Week 8, Week 12, Week 16, Week 20, Week 24

Interventionnanograms*hour per milliliter (ng*h/mL) (Mean)
10 mg LY294487688100
15 mg LY2944876117000
30 mg LY2944876247000
50 mg LY2944876381000

[back to top]

Percentage of Participants Requiring Rescue Therapy

Participants who received rescue medication with non-study antihyperglycemic medications or change their stable dose of metformin. (NCT02119819)
Timeframe: Baseline through Therapy Completion (Week 24)

Interventionpercentage of participants (Number)
10 mg LY29448766.1
15 mg LY29448762.8
30 mg LY29448762.7
50 mg LY29448764.3
Exenatide Extended-release2.9
Placebo11.3

[back to top]

Change From Baseline in HbA1c at Week 24

HbA1c is the glycosylated fraction of hemoglobin A. HbA1c is measured to identify average plasma glucose concentration over prolonged periods of time. (NCT02119819)
Timeframe: Baseline, Week 24

Interventionpercentage of HbA1c (Mean)
10 mg LY2944876-0.85
15 mg LY2944876-1.14
30 mg LY2944876-1.37
50 mg LY2944876-1.29
Exenatide Extended-release-1.48
Placebo-0.38

[back to top]

Change From Baseline in Insulin Levels

LSM are calculated from MMRM analysis using REML with metformin use, baseline BMI category, baseline HbA1c category, country, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline parameter result as a covariate, and participant as a random effect. (NCT02119819)
Timeframe: Baseline, Week 12; Baseline, Week 24

,,,,,
Interventionmicro-international units/milliliter (Least Squares Mean)
Week 12Week 24
10 mg LY29448760.30-1.44
15 mg LY29448760.970.68
30 mg LY29448760.030.58
50 mg LY29448760.960.34
Exenatide Extended-release2.781.97
Placebo-0.851.45

[back to top]

Change From Baseline in Fasting Blood Glucose

Least square means (LSM) was calculated from mixed-effects model with repeated measures (MMRM) analysis using restricted maximum likelihood (REML) with metformin use, baseline body mass index (BMI) category, baseline HbA1c category, country, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline fasting blood glucose as a covariate, and participant as a random effect. (NCT02119819)
Timeframe: Baseline, Week 12; Baseline, Week 24

,,,,,
Interventionmilligrams per deciliter (mg/dL) (Least Squares Mean)
Week 12Week 24
10 mg LY2944876-20.881-21.497
15 mg LY2944876-21.991-30.186
30 mg LY2944876-31.309-29.875
50 mg LY2944876-28.405-31.390
Exenatide Extended-release-39.074-40.328
Placebo-1.5880.124

[back to top]

Change From Baseline in Hemoglobin A1c (HbA1c) at Week 12

HbA1c is the glycosylated fraction of hemoglobin A. HbA1c is measured to identify average plasma glucose concentration over prolonged periods of time. (NCT02119819)
Timeframe: Baseline, Week 12

Interventionpercentage of HbA1c (Mean)
10 mg LY2944876-1.07
15 mg LY2944876-1.09
30 mg LY2944876-1.44
50 mg LY2944876-1.33
Exenatide Extended-release-1.42
Placebo-0.29

[back to top]

Pharmacokinetics (PK): Maximum Concentration (Cmax) of LY2944876

Evaluable pharmacokinetic concentrations from the specified timepoints were combined and utilized in a population approach to determine the population mean estimate and standard deviation at steady-state. (NCT02119819)
Timeframe: Baseline, Week 8, Week 12, Week 16, Week 20, Week 24

Interventionnanogram per milliliter (ng/mL) (Mean)
10 mg LY2944876607
15 mg LY2944876799
30 mg LY29448761690
50 mg LY29448762570

[back to top]

Change From Baseline in Beta-Hydroxy Butyrate Levels

LSM are calculated from MMRM analysis using REML with metformin use, baseline BMI category, baseline HbA1c category, country, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline parameter result as a covariate, and participant as a random effect. (NCT02119819)
Timeframe: Baseline, Week 12; Baseline, Week 24

,,,,,
Interventionmg/dL (Least Squares Mean)
Week 12Week 24
10 mg LY2944876-0.27-0.33
15 mg LY2944876-0.28-0.39
30 mg LY2944876-0.13-0.34
50 mg LY2944876-0.31-0.33
Exenatide Extended-release-0.29-0.19
Placebo-0.23-0.37

[back to top]

Change From Baseline in Adiponectin Levels

LSM are calculated from MMRM analysis using REML with metformin use, baseline BMI category, baseline HbA1c category, country, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline parameter result as a covariate, and participant as a random effect. (NCT02119819)
Timeframe: Baseline, Week 12; Baseline, Week 24

,,,,,
Interventionµg/L (Least Squares Mean)
Week 12Week 24
10 mg LY29448760.140.03
15 mg LY29448760.030.30
30 mg LY2944876-0.100.28
50 mg LY29448760.120.58
Exenatide Extended-release0.040.14
Placebo0.030.25

[back to top]

Change From Baseline in 7-point Self-Monitored Blood Glucose (SMBG) Values

SMBG 7-point profiles were measured at morning pre-meal, morning 2 hours post-meal, mid-day pre-meal, mid-day 2 hours post-meal, evening pre-meal, evening 2 hours post-meal, and at bedtime. LSM were calculated from MMRM analysis using REML with metformin use, baseline BMI category, baseline HbA1c category, country, treatment, visit, and treatment-by-visit interaction as fixed effects, baseline fasting blood glucose as a covariate, and participant as a random effect. (NCT02119819)
Timeframe: Baseline, Week (Wk) 12; Baseline, Week 24

,,,,,
Interventionmg/dL (Least Squares Mean)
Morning pre-meal (Week 12)Morning pre-meal (Week 24)Morning 2 hours post-meal (Week 12)Morning 2 hours post-meal (Week 24)Mid-day pre-meal (Week 12)Mid-day pre-meal (Week 24)Mid-day 2 hours post-meal (Week 12)Mid-day 2 hours post-meal (Week 24)Evening pre-meal (Week 12)Evening pre-meal (Week 24)Evening 2 hours post-meal (Week 12)Evening 2 hours post-meal (Week 24)Bedtime (Week 12)Bedtime (Week 24)
10 mg LY2944876-26.8-23.5-27.9-29.9-17.1-16.3-17.1-12.2-24.1-24.9-25.1-30.2-19.3-28.9
15 mg LY2944876-28.4-29.1-34.2-35.9-19.6-23.4-20.7-26.6-24.8-24.3-26.5-27.9-33.5-25.4
30 mg LY2944876-34.3-29.6-36.0-37.1-26.1-22.4-24.6-21.9-28.5-33.0-33.4-26.0-33.2-32.3
50 mg LY2944876-34.8-34.2-26.4-42.8-24.2-23.5-22.2-33.4-30.1-29.6-32.8-37.2-36.2-38.5
Exenatide Extended-release-38.7-36.8-43.5-42.7-23.5-23.9-27.4-37.2-24.7-36.4-33.5-36.9-41.6-42.9
Placebo-7.4-14.4-1.5-6.3-2.3-4.0-8.9-8.5-1.5-5.74.01.15.6-6.9

[back to top]

Maximum Tolerated Volume

In the last 5 days of medication administration, subjects did a satiation/nutrient drink test. Participants recorded their sensations every 5 minutes using a visual analog scale (VAS) from 0-5, with level 0 being no symptoms, level 3 corresponding to fullness sensation after a typical meal, and level 5 corresponding to the maximal tolerated volume (maximum or unbearable fullness/satiation). This measure was the volume consumed when the fullness sensation reached level 5. (NCT02160990)
Timeframe: Visit 3, approximately 30 minutes after liquid meal

InterventionmL (Median)
Exenatide1244
Placebo1052

[back to top]

Aggregate Satiation Symptom Score

"Postprandial fullness, nausea, bloating, and pain were measured 30 minutes after the liquid meal using 100 mm horizontal visual analog scales (VAS). The subscale scores could each range from none(0) to worst ever (100) at the left and right ends of the lines for each symptom. These satiation symptom scores (postprandial fullness, nausea, bloating, and pain) were combined to generate a total scale score with a different total scale range (0 - 400 mm) with 0 mm indicating none and 400 indicating worst ever." (NCT02160990)
Timeframe: Visit 3, approximately 30 min after ingestion of nutrient drink test

Interventionmm (Median)
Exenatide145
Placebo172

[back to top]

Satiation Expressed as Volume to Fullness

In the last 5 days of medication administration, subjects did a satiation/nutrient drink test. Participants recorded their sensations every 5 minutes using a visual analog scale (VAS) from 0-5, with level 0 being no symptoms, level 3 corresponding to fullness sensation after a typical meal, and level 5 corresponding to the maximal tolerated volume (maximum or unbearable fullness/satiation). This measure was the volume consumed when the fullness sensation reached level 3. (NCT02160990)
Timeframe: Visit 3, approximately 30 minutes after liquid meal

InterventionmL (Median)
Exenatide705
Placebo675

[back to top]

Gastric Emptying Half-time (T 1/2) of Solids

Gastric emptying of solids half-time is defined as the time for half of the ingested solids to leave the stomach. Subjects were given a scrambled egg breakfast with toast and a glass of milk. The eggs contained a small amount of a radioactive substance. Anterior and posterior gamma camera images were obtain immediately after radiolabeled meal ingestion, every 15 minutes for the first 2 hours, then 30 minutes for the next 2 hours (total 4 hours after the radiolabeled meal). (NCT02160990)
Timeframe: time frame is 30 days after the initiation of dose.

Interventionminutes (Median)
Exenatide187
Placebo86

[back to top]

Change in Body Weight

(NCT02160990)
Timeframe: baseline, day 30

Interventionkg (Median)
Exenatide-0.95
Placebo-0.55

[back to top]

Buffet Meal Intake (kcal)

"Five hours after the standard egg meal ingested to measure gastric emptying, subjects were invited to eat, over a 30 minute period, a standard all you can eat meal. This meal consisted of either meat or vegetable lasagna, vanilla pudding, and skim milk. Personnel from the study team weighed the food servings post-meal and reported the amount of food left from single portions partially consumed. The total kcal of the food consumed was analyzed by using validated software." (NCT02160990)
Timeframe: "Visit 4, approximately 30 minutes after start of all you can eat meal"

Interventionkcal (Median)
Exenatide977
Placebo1110

[back to top]

Percentage of Gastric Contents Emptied at 1 Hour

Subjects were given a scrambled egg breakfast with toast and a glass of milk. The eggs contained a small amount of a radioactive substance. At the completion of the meal, subjects stood in front of a special camera and pictures were taken at specific intervals. This outcome measure is the proportion of the radiolabeled meal emptied at 1 hour. (NCT02160990)
Timeframe: Visit 4, approximately 1 hours after radiolabeled meal was ingested

Interventionpercentage of meal emptied (Median)
Exenatide12.4
Placebo38.2

[back to top]

Percentage of Participants Achieving HbA1c <7.0% at Week 28, No Weight Gain at Week 28, and No Major Hypoglycemia Over 28 Weeks

To compare the percentage of participants achieving HbA1c <7.0% at Week 28, no weight gain at Week 28, and no major hypoglycemia over 28 weeks between EQW added to titrated basal insulin glargine to placebo added to titrated basal insulin glargine, with or without metformin. (NCT02229383)
Timeframe: Baseline to Week 28

InterventionPercentage of participants (Number)
Exenatide22.2
Placebo2.2

[back to top]

Change in Seated Systolic Blood Pressure From Baseline to Week 28

To compare the change from baseline in seated systolic blood pressure achieved with EQW added to titrated basal insulin glargine to placebo added to titrated basal insulin glargine, with or without metformin, after 28 weeks of double-blind treatment. (NCT02229383)
Timeframe: Baseline to Week 28

Interventionmillimeter of mercury (Least Squares Mean)
Exenatide-2.5
Placebo-0.7

[back to top]

Percentage of Participants Achieving HbA1c <7.0% at Week 28

To compare the percentage of participants achieving HbA1c <7.0% between EQW added to titrated basal insulin glargine to placebo added to titrated basal insulin glargine, with or without metformin, after 28 weeks of double-blind treatment. (NCT02229383)
Timeframe: Baseline to Week 28

InterventionPercentage of participants (Number)
Exenatide32.6
Placebo7.0

[back to top]

Change in HbA1c From Baseline to Week 28

To compare the change from baseline in HbA1c achieved with exenatide once weekly (EQW) added to titrated basal insulin glargine to placebo added to titrated basal insulin glargine, with or without metformin, after 28 weeks of double-blind treatment. SU= sulfonylurea. (NCT02229383)
Timeframe: Baseline to Week 28

InterventionPercentage of HbA1c (Least Squares Mean)
Exenatide-0.96
Placebo-0.22

[back to top]

Change in Body Weight From Baseline to Week 28

To compare the change from baseline in body weight achieved with EQW added to titrated basal insulin glargine to placebo added to titrated basal insulin glargine, with or without metformin, after 28 weeks of double-blind treatment. (NCT02229383)
Timeframe: Baseline to Week 28

Interventionkilogram (Least Squares Mean)
Exenatide-1.04
Placebo0.48

[back to top]

Change From Baseline to Week 28 in Daily Insulin Dose

To compare the change from baseline in daily insulin dose achieved with EQW added to titrated basal insulin glargine to placebo added to titrated basal insulin glargine, with or without metformin, after 28 weeks of double-blind treatment. (NCT02229383)
Timeframe: Baseline to Week 28

InterventionUnits (Least Squares Mean)
Exenatide1.6
Placebo3.5

[back to top]

Change From Baseline to Week 28 in 2-hour Postprandial Glucose After a Standard Meal Tolerance Test (MTT)

To compare the change from baseline in 2-hour postprandial glucose after a standard MTT achieved with EQW added to titrated basal insulin glargine to placebo added to titrated basal insulin glargine, with or without metformin, after 28 weeks of double-blind treatment. (NCT02229383)
Timeframe: Baseline to Week 28

Interventionmilligram per deciliter (Least Squares Mean)
Exenatide-28.73
Placebo-0.96

[back to top]

L-FABP

Mean change in urine L-type fatty acid binding protein:Cr ratio (NCT02251431)
Timeframe: 38 weeks

,
Interventionng/mmol Creat (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release2.612.05
Placebo3.243

[back to top]

ST2

Mean change in plasma ST2 (pg/ml) (NCT02251431)
Timeframe: 38 weeks

,
Interventionpg/ml (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release635.2524.68
Placebo443.18534.53

[back to top]

NGAL

Mean change in urine neutrophil gelatinase associated lipocalin (NGAL):creatinine (Cr) ratio (NCT02251431)
Timeframe: 38 weeks

,
Interventionng/mmol Creat (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release17.3514.01
Placebo18.4424.39

[back to top]

Cystatin-C

Mean paired change in urine cystatin-C:Cr ratio (uCysC:Cr) (NCT02251431)
Timeframe: 38 weeks

,
Interventionng/mmol Creat (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release2.071.47
Placebo1.841.57

[back to top]

Pi GST

Mean change in pi glutathione S-transferase (piGST):Cr ratio (NCT02251431)
Timeframe: 38 weeks

,
Interventionng/mmol Creat (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release2.23.03
Placebo3.994.27

[back to top]

Troponin I

Mean change in plasma ultrasensitive troponin I (pg/ml) (NCT02251431)
Timeframe: 38 weeks

,
Interventionpg/ml (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release230.85238.53
Placebo415.65504.48

[back to top]

ACR

Mean change in urine albumin:Cr ratio (ACR) (NCT02251431)
Timeframe: 38 weeks

,
Interventionng/mmol Creat (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release6678.233963.49
Placebo9713.659825.2

[back to top]

Alpha GST

Mean change in urine alpha glutathione S-transferase (αGST):Cr ratio (NCT02251431)
Timeframe: 38 weeks

,
Interventionng/mmol Creat (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release0.060.05
Placebo0.670.27

[back to top]

BNP

Mean change in plasma B-type natriuretic peptide BNP (pg/ml) (NCT02251431)
Timeframe: 38 weeks

,
Interventionpg/ml (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release4.875.59
Placebo9.8814.02

[back to top]

NAG

Mean change in urine N-acetyl-β-D-glucosaminidase (NAG):Cr ratio (NCT02251431)
Timeframe: 38 weeks

,
Interventionng/mmol Creat (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release17.3514.01
Placebo18.4424.39

[back to top]

Galectin-3

Mean change in plasma galectin-3 (pg/ml) (NCT02251431)
Timeframe: 38 weeks

,
Interventionpg/ml (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release9570.919539.21
Placebo9266.78098.78

[back to top]

IL-18

Mean change in urine interleukin-18:Cr ratio (NCT02251431)
Timeframe: 38 weeks

,
Interventionpg/mmol Creat (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release1.681.96
Placebo3.482.68

[back to top]

KIM-1

Mean change in urine kidney injury molecule-1 (KIM-1):Cr ratio (NCT02251431)
Timeframe: 38 weeks

,
Interventionng/mmol Creat (Mean)
BaselineEnd of study (38th week)
Exenatide-extended Release0.10.13
Placebo0.130.1

[back to top]

Average of Change in 24-hour Mean Weighted Glucose From Baseline to Week 4 and Baseline to Week 10

(NCT02288273)
Timeframe: Week 4 and Week 10

,
Intervention% times patients had specific CGM/24-hr (Least Squares Mean)
Change in times(%): PG<70 baseline to Week 4Change in times (%): PG <70 baseline to Week 10Change in %: 70 Change in %: 70 Change in times (%): PG >180 baseline to Week 4Change in times (%): PG >180 baseline to Week 10
EQW + Met0.50.515.821.4-16.2-22.0
Placebo + Met0.20.14.11.3-4.3-1.4

[back to top]

Change in 24-hour Mean Weighted Glucose Between Day 1 of Week 10 (Day 64/65) and Day 6 of Week 10 (Day 69/70) Within Each EQW-treated Patient

(NCT02288273)
Timeframe: Day 64/65

Interventionmg/dL (Least Squares Mean)
EQW + Met5.2
Placebo + Met-6.9

[back to top]

Change From Baseline (Day1) to Day 70 and Day 22 in FPG

(NCT02288273)
Timeframe: Day 22/Day70

,
Interventionmg/dL (Least Squares Mean)
Baseline to Day 22Baseline to Day 70
EQW + Met-29.6-41.9
Placebo + Met-1.9-5.0

[back to top]

Average of Change in 24-hour Mean Weighted Glucose From Baseline to Week 4 and Baseline to Week 10

(NCT02288273)
Timeframe: Week 4 and Week 10

,
Interventionmg/dL (Least Squares Mean)
Change in mean weighted glucose baseline to Week 4Change in mean weighted glucose baseline - Week 10Change in MAGE (mg/dL) from baseline to Week 4Change in MAGE (mg/dL) from baseline to Week 10
EQW + Met-4.5-6.3-8.2-15.2
Placebo + Met-1.80.7-3.82.9

[back to top]

Change in HbA1c From Baseline to Day 22 and Baseline to Day 70

(NCT02288273)
Timeframe: Day 22 and Day 70

,
Intervention% Alc (Least Squares Mean)
Change from baseline to Day 22Change from baseline to Day 70
EQW + Met-0.30-0.92
Placebo + Met-0.10-0.20

[back to top]

Change in 24-hour Mean Weighted Glucose

Change in 24-hour mean weighted glucose from baseline (Day -1/1) to Day 6 of Week 4 (Day 27/28) and to Day 6 of Week 10 (Day 69/70). (NCT02288273)
Timeframe: Day 27/28

,
Intervention(mg/dL) (Mean)
Baseline (Day -1/1)Day 27/28Change from Baseline to Day 27/28Change from Baseline to Day 69/70
EQW + Met185.7158.3-26.0-30.8
Placebo + Met183.8176.9-5.3-3.0

[back to top]

Change From Baseline (Day -1) to Day 64 and Day 22 in 2- Hour Mean Weighted PPG (After the Breakfast Meal)

(NCT02288273)
Timeframe: Day 22 and Day 64

,
Interventionmg/dL (Least Squares Mean)
Baseline to Day 22Baseline to Day 64
EQW + Met-32.1-44.4
Placebo + Met-2.0-6.0

[back to top]

Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery (MCCB) Composite T-score

The MATRICS Consensus Cognitive Battery (MCCB) measures cognition relevant to schizophrenia and related disorders. The MCCB consists of ten individually administered tests that measure cognitive performance in seven domains including speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition. The raw scores from the ten tests are entered in the MCCB Computer Scoring Program software, which provides an age and gender-corrected T-score and percentile on the seven cognitive domains. A T-score of 50 +/- 10 represents a normative mean performance in each test. Accordingly, the criterion for assignment to cognitively normal-range group require an overall composite T-score from 40 to 60. These data points from baseline visit to week 24 will measure changes in cognition in addition overall cognitive ability compared to healthy individuals. (NCT02417142)
Timeframe: Baseline, Week 6, Week 12, Week 18, and Week 24.

,
Interventionscore on a scale (Mean)
BaselineWeek 6Week 12Week 18Week 24
Experimental26.927.328.428.731.2
Placebo24.727.228.132.233.9

[back to top]

Negative Symptoms as Measured by the Scale for the Assessment of Negative Symptoms (SANS) Total Score

SANS measures negative symptoms on a 25-item, six point scale each (0-5; none-severe). Items are listed under five domains including affective flattening or blunting, alogia, avolition/apathy, anhedonia/asociality, and attention. The total possible score ranges from 0 to 125. (NCT02417142)
Timeframe: Baseline, Week 6, Week 12, Week 18 and Week 24

,
Interventionscore on a scale (Mean)
BaselineWeek 6Week 12Week 18Week 24
Experimental33.134.135.836.135.2
Placebo34.132.834.535.235.0

[back to top]

Number of Hospital Readmissions

Number of hospital readmissions during 12 weeks after discharge will be recorded (NCT02455076)
Timeframe: 12 weeks after discharge

Interventionnumber of readmissions (Number)
Exenatide Outpatient12
Insulin Only Outpatient14

[back to top]

Number of Acute Kidney Injury Events

Number of Acute Kidney Injury events will be recorded (NCT02455076)
Timeframe: 12 weeks from discharge.

Interventionnumber of events (Number)
Exenatide Outpatient1
Insulin Only Outpatient1

[back to top]

Mean Premeal Blood Glucose Levels Inpatient

The blood glucose levels prior to each meal will using a glucose meter. (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days

Interventionmg/dL (Mean)
Exenatide178.7
Exenatide Plus Glargine Insulin153.4
Basal Bolus Regimen161.8

[back to top]

Mean Fasting Blood Glucose Levels Inpatient

The blood glucose levels prior to the patient's first meal of the day will be assessed using a glucose meter. (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days.

Interventionmg/dL (Mean)
Exenatide177.1
Exenatide Plus Glargine Insulin146.8
Basal Bolus Regimen157.7

[back to top]

Mean Daily Blood Glucose Concentration Inpatient

The levels of blood glucose (BG) will be measured before each meal and at bedtime using a glucose meter. Blood glucose will be measured at baseline and during the hospital stay (up to 10 days). (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days.

Interventionmg/dL (Mean)
Exenatide177.1
Exenatide Plus Glargine Insulin154.1
Basal Bolus Regimen166.1

[back to top]

Mean Fasting Blood Glucose Levels During Outpatient Period

Fasting Blood Glucose Levels were measured using blood test (NCT02455076)
Timeframe: 12 weeks after discharge

Interventionmg/dL (Mean)
Exenatide Outpatient146.5
Insulin Only Outpatient133.2

[back to top]

Mean Daily Blood Glucose Concentration During Outpatient Period

Mean Daily Blood Glucose Concentration will be calculated and recorded. (NCT02455076)
Timeframe: 12 weeks after discharge

Interventionmg/dL (Mean)
Exenatide Outpatient155.1
Insulin Only Outpatient144.7

[back to top]

Incidence of the Need for ICU Care Inpatient

The total number of patients who require transfer to the ICU will be recorded. (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days

InterventionParticipants (Count of Participants)
Exenatide2
Exenatide Plus Glargine Insulin3
Basal Bolus Regimen0

[back to top]

Incidence of Hypoglycemic Events Inpatient

The number of patients with hypoglycemia (blood glucose levels < 70 mg/dL) will be recorded. (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days

InterventionParticipants (Count of Participants)
Exenatide0
Exenatide Plus Glargine Insulin3
Basal Bolus Regimen6

[back to top]

Incidence of Hyperglycemic Events Inpatient

Percent of readings with hyperglycemia (blood glucose levels > 240 mg/dL) (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days

Interventionpercentage of readings (Mean)
Exenatide10.4
Exenatide Plus Glargine Insulin5.1
Basal Bolus Regimen11.2

[back to top]

Incidence of Hospital Readmissions

The number of patients who require readmission to the hospital from the time of discharge to 12 weeks after discharge will be recorded. (NCT02455076)
Timeframe: 12 weeks after discharge

InterventionParticipants (Count of Participants)
Exenatide4
Exenatide Plus Glargine Insulin16
Basal Bolus Regimen6

[back to top]

Total Daily Dose of Insulin Inpatient

The total daily dose of insulin needed for glycemic control from baseline through the patient's hospital stay will be recorded. (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days

Interventionunits/day (Mean)
Exenatide8.1
Exenatide Plus Glargine Insulin17.7
Basal Bolus Regimen28

[back to top]

Number of Severe Gastrointestinal Adverse Events

Number of Severe (require hospitalization) Gastrointestinal Adverse Events (NCT02455076)
Timeframe: 12 weeks from discharge.

Interventionnumber of events (Number)
Exenatide Outpatient1
Insulin Only Outpatient1

[back to top]

Number of Patients With Severe Hypoglycemic Events Inpatient

Occurrences of hypoglycemia (blood glucose levels < 40 mg/dL) will be recorded. (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days

InterventionParticipants (Count of Participants)
Exenatide0
Exenatide Plus Glargine Insulin0
Basal Bolus Regimen0

[back to top]

Incidence of Gastrointestinal Adverse Events Inpatient

The number of subjects who experience gastrointestinal side effects including nausea, vomiting and diarrhea will be recorded. (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days

InterventionParticipants (Count of Participants)
Exenatide5
Exenatide Plus Glargine Insulin5
Basal Bolus Regimen1

[back to top]

Number of Patients With Severe Hypoglycemic Events

Occurrences of hypoglycemia (blood glucose levels < 40 mg/dL) will be detected by blood test (NCT02455076)
Timeframe: 12 weeks after discharge

InterventionParticipants (Count of Participants)
Exenatide Outpatient1
Insulin Only Outpatient4

[back to top]

Number of Patients Who Had Emergency Room Visits

The number of patients who had emergency room visits from the time of discharge to 12 weeks after discharge will be recorded. (NCT02455076)
Timeframe: 12 weeks after discharge

Interventionparticipants (Number)
Exenatide Outpatient4
Insulin Only Outpatient12

[back to top]

The Number of Patients With Hypoglycemia Outpatient

Occurrence of hypoglycemia (blood glucose levels < 70 mg) will be identified by blood test (NCT02455076)
Timeframe: 12 weeks after discharge

InterventionParticipants (Count of Participants)
Exenatide Outpatient7
Insulin Only Outpatient7

[back to top]

Incidence of Acute Kidney Injury Inpatient

The number of patients who experience acute kidney injury diagnosed by an increment in serum creatinine >0.5 mg/dL from admission value or 50% of baseline value will be recorded. (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days

InterventionParticipants (Count of Participants)
Exenatide3
Exenatide Plus Glargine Insulin6
Basal Bolus Regimen3

[back to top]

Hospital Mortality

The total number of subject deaths during hospital stay will be recorded. (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days

InterventionParticipants (Count of Participants)
Exenatide0
Exenatide Plus Glargine Insulin0
Basal Bolus Regimen0

[back to top]

Efficacy, Measured by HbA1c Levels and no Weight Gain

Number of patients who have an HbA1c <7.0% and no weight gain at 12 weeks from discharge will be recorded. (NCT02455076)
Timeframe: 12 weeks from discharge.

InterventionParticipants (Count of Participants)
Exenatide Outpatient8
Insulin Only Outpatient5

[back to top]

Efficacy, Measured by HbA1c Levels and no Hypoglycemia

Number of patients who have an HbA1c <7.0% and no hypoglycemia at 12 weeks from discharge will be recorded. (NCT02455076)
Timeframe: 12 weeks from discharge.

InterventionParticipants (Count of Participants)
Exenatide Outpatient11
Insulin Only Outpatient8

[back to top]

Change in Systolic Blood Pressure

Change in Systolic Blood Pressure from the time of discharge to 12 weeks after discharge will be recorded (NCT02455076)
Timeframe: Discharge (after day 10 or hospital stay), 12 weeks after discharge

InterventionmmHg (Mean)
Exenatide Outpatient3.2
Insulin Only Outpatient1.8

[back to top]

Change in Heart Rate

Change in heart rate from the time of discharge to 12 weeks after discharge will be recorded (NCT02455076)
Timeframe: Discharge (after day 10 or hospital stay), 12 weeks after discharge

Interventionheart beats/min (Mean)
Exenatide Outpatient-3.1
Insulin Only Outpatient0.2

[back to top]

Change in HbA1c Concentration Inpatient

The difference in the levels of HbA1c at discharge and at 12 weeks from discharge will be measured. The A1C test result is reported as a percentage. The higher the percentage, the higher a person's blood glucose levels have been. A normal A1C level is below 5.7 percent. (NCT02455076)
Timeframe: 12 weeks from discharge.

Interventionpercentage of HbA1c (Mean)
Exenatide-1.3
Exenatide Plus Glargine Insulin-1.1
Basal Bolus Regimen-1.4

[back to top]

Change in Diastolic Blood Pressure

Change in Diastolic Blood Pressure from the time of discharge to 12 weeks after discharge will be recorded (NCT02455076)
Timeframe: Discharge (after day 10 or hospital stay), 12 weeks after discharge

InterventionmmHg (Mean)
Exenatide Outpatient4.2
Insulin Only Outpatient-1.0

[back to top]

Change in Body Weight

The change in Body Weight from discharge to 12 weeks after discharge will be recorded (NCT02455076)
Timeframe: Time of discharge, 12 weeks after discharge

Interventionpounds (Mean)
Exenatide Outpatient-2.3
Insulin Only Outpatient-1.2

[back to top]

Change in Body Mass Index

The change in BMI from discharge to 12 weeks after discharge will be calculated (NCT02455076)
Timeframe: Discharge (after day 10 or hospital stay), 12 weeks after discharge 12 weeks after discharge

Interventionkg/m2 (Mean)
Exenatide Outpatient-0.8
Insulin Only Outpatient-0.7

[back to top]

Average Number of Days of Hospital Stay

The average number of days in the hospital for subjects will be calculated. (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days

Interventiondays (Median)
Exenatide4
Exenatide Plus Glargine Insulin5
Basal Bolus Regimen4

[back to top]

Hospital Complications

The total number of subjects who experience hospital complications like nosocomial pneumonia, bacteremia, respiratory failure, acute renal failure, and wound infections (surgery patients) will be recorded. Nosocomial infections will be diagnosed based on standardized Centers for Disease Control (CDC) criteria. (NCT02455076)
Timeframe: Duration of hospital stay, an expected average of 10 days

InterventionParticipants (Count of Participants)
Exenatide4
Exenatide Plus Glargine Insulin6
Basal Bolus Regimen3

[back to top]

Body Mass Index

Percentage of body mass index change from Randomization to Week 52 (NCT02496611)
Timeframe: 52 weeks

Interventionpercentage (body mass index) (Mean)
Weight Loss Maintenance Without Pharmacotherapy10.1
Weight Loss Maintenance With Pharmacotherapy4.6

[back to top]

Change in Vital Sign

Change in vital sign at 12 and 24 weeks from start of the treatment(24 weeks just for patients allocated in long-term treatment) (NCT02533453)
Timeframe: baseline and 12/24 weeks

InterventionmmHg (Mean)
SBPDBP
12/24 Weeks Treatment-3.35-0.15

[back to top]

Change in HbA1c

Change in HbA1c at 12 and 24 weeks from start of the treatment(24 weeks just for patients allocated in long-term treatment) (NCT02533453)
Timeframe: baseline and 12/24 weeks

Interventionpercentage of Hba1c (Mean)
12/24 Weeks Treatment-1.21

[back to top]

Change in Fasting Plasma Gloucose

Change in Fasting plasma gloucose at 12 and 24 weeks from start of the treatment(24 weeks just for patients allocated in long-term treatment) (NCT02533453)
Timeframe: baseline and 12/24 weeks

Interventionmg/dL (Mean)
12/24 Weeks Treatment-34.2

[back to top]

Change in Body Weight

Change in body weight at 12 and 24 weeks from start of the treatment(24 weeks just for patients allocated in long-term treatment) (NCT02533453)
Timeframe: baseline and 12/24 weeks

Interventionkg (Mean)
12/24 Weeks Treatment-0.95

[back to top]

Percentage of Participants With Adverse Events(AEs) and Serious Adverse Event(SAEs)

was to estimate the incidence rates of adverse events (AEs) and serious adverse events (SAEs) in patients who are treated with 2 mg exenatide once weekly for type 2 diabetes mellitus in the normal clinical practice setting over a period of 12/24 weeks for long-term surveillance. (NCT02533453)
Timeframe: baseline and 12/24 weeks

Interventionpercentage of participants (Number)
rate of all AEsrate of all SAEs
12/24 Weeks Treatment52.93.8

[back to top]

"Evaluation of Subjective Improvement of Main Indication"

"Subjective improvement of main indication will be assessed as improved, slightly improved, unchanged, aggravated, or unable to evaluate." (NCT02533453)
Timeframe: baseline and 12/24 weeks

Interventionparticipants (Number)
ImprovedSlightly improvedUnchangedAggravatedunable to evaluate
12/24 Weeks Treatment8411611

[back to top]

Systolic Blood Pressure (SBP)

Treatment effect on SBP after 24 weeks of treatment (NCT02635386)
Timeframe: 24 weeks treatment

InterventionmmHg (Mean)
Exenatide Once Weekly (EQW )123.6
Dapagliflozin (DAPA)123
EQW Plus DAPA122
Dapagliflozin Plus Glucophage (MET ER)128
Phentermine /Topiramate (PHEN/ TPM) ER124

[back to top]

Total Body Fat (%) by DEXA

Treatment impact on percent total body fat by DEXA (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionpercent fat mass (Mean)
Exenatide Once Weekly (EQW )46.1
Dapagliflozin (DAPA)46.4
EQW Plus DAPA45.8
Dapagliflozin Plus Glucophage (MET ER)46.1
Phentermine /Topiramate (PHEN/ TPM) ER45.2

[back to top]

Total Cholesterol Levels

Treatment effect on blood concentrations of total cholesterol (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionmg/dL (Mean)
Exenatide Once Weekly (EQW )189
Dapagliflozin (DAPA)186
EQW Plus DAPA185
Dapagliflozin Plus Glucophage (MET ER)192
Phentermine /Topiramate (PHEN/ TPM) ER178

[back to top]

Total Fat Mass (kg) Evaluated by DEXA

Treatment impact on total fat mass by DEXA (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionkilogram (Mean)
Exenatide Once Weekly (EQW )47.6
Dapagliflozin (DAPA)47.8
EQW Plus DAPA45.9
Dapagliflozin Plus Glucophage (MET ER)48
Phentermine /Topiramate (PHEN/ TPM) ER44.5

[back to top]

Total Testosterone Concentrations

Treatment effect on blood concentrations of total testosterone (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionng/dL (Mean)
Exenatide Once Weekly (EQW )38.8
Dapagliflozin (DAPA)35
EQW Plus DAPA42.6
Dapagliflozin Plus Glucophage (MET ER)39.5
Phentermine /Topiramate (PHEN/ TPM) ER45.5

[back to top]

Triglyceride (TRG) Levels

Treatment effect on blood concentrations of triglycerides (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionmg/dL (Mean)
Exenatide Once Weekly (EQW )130
Dapagliflozin (DAPA)132
EQW Plus DAPA112
Dapagliflozin Plus Glucophage (MET ER)105
Phentermine /Topiramate (PHEN/ TPM) ER110

[back to top]

Trunk/Leg Fat Ratio by DEXA

Treatment impact on trunk/limb ratio (measure of central adiposity) by DEXA (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionratio (Mean)
Exenatide Once Weekly (EQW )1.03
Dapagliflozin (DAPA).95
EQW Plus DAPA.93
Dapagliflozin Plus Glucophage (MET ER).98
Phentermine /Topiramate (PHEN/ TPM) ER.99

[back to top]

Waist-to-Height Ratio (WHtR)

Treatment impact on WHtR which is a measure of central adiposity (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionratio (Mean)
Exenatide Once Weekly (EQW ).64
Dapagliflozin (DAPA).61
EQW Plus DAPA.65
Dapagliflozin Plus Glucophage (MET ER).61
Phentermine /Topiramate (PHEN/ TPM) ER.59

[back to top]

Waist-to-Hip Ratio (WHR)

Treatment impact on central adiposity after 24 weeks (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionratio (Mean)
Exenatide Once Weekly (EQW ).83
Dapagliflozin (DAPA).79
EQW Plus DAPA.86
Dapagliflozin Plus Glucophage (MET ER).83
Phentermine /Topiramate (PHEN/ TPM) ER.81

[back to top]

Dehydroepiandrosterone Sulfate (DHEA-S) Levels

Treatment effect on blood concentrations of DHEA-S (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionmcg/dL (Mean)
Exenatide Once Weekly (EQW )165
Dapagliflozin (DAPA)187
EQW Plus DAPA169
Dapagliflozin Plus Glucophage (MET ER)189
Phentermine /Topiramate (PHEN/ TPM) ER201

[back to top]

Absolute Body Weight

Treatment effect on body weight at 24 weeks of treatment (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionkilogram (Mean)
Exenatide Once Weekly (EQW )100.4
Dapagliflozin (DAPA)102.6
EQW Plus DAPA99
Dapagliflozin Plus Glucophage (MET ER)101.2
Phentermine /Topiramate (PHEN/ TPM) ER97

[back to top]

Android-Gynoid Ratio (AGR) as Determined by DEXA

treatment impact on measure of central adiposity as determined by android/gynoid ratio (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionratio (Mean)
Exenatide Once Weekly (EQW )1.07
Dapagliflozin (DAPA)1.02
EQW Plus DAPA1.04
Dapagliflozin Plus Glucophage (MET ER)1.04
Phentermine /Topiramate (PHEN/ TPM) ER1.03

[back to top]

Body Mass Index (BMI)

Treatment efficacy in reducing body mass at 24 weeks of treatment (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionkilogram/meter squared (Mean)
Exenatide Once Weekly (EQW )37.3
Dapagliflozin (DAPA)37.4
EQW Plus DAPA36.7
Dapagliflozin Plus Glucophage (MET ER)37
Phentermine /Topiramate (PHEN/ TPM) ER35.3

[back to top]

Central Adiposity (Waist Circumference)

Treatment effect on loss of central adiposity after 24 weeks (NCT02635386)
Timeframe: 24 weeks of treatment

Interventioncentimeters (Mean)
Exenatide Once Weekly (EQW )104
Dapagliflozin (DAPA)101
EQW Plus DAPA106
Dapagliflozin Plus Glucophage (MET ER)101.3
Phentermine /Topiramate (PHEN/ TPM) ER97

[back to top]

Change in Percent Body Weight

Treatment effect on change in percent body weight from baseline (NCT02635386)
Timeframe: Change from baseline (time 0) to study end (24 weeks)

Interventionpercentage change in body weight (Mean)
Exenatide Once Weekly (EQW )3.8
Dapagliflozin (DAPA)1.5
EQW Plus DAPA6.9
Dapagliflozin Plus Glucophage (MET ER)1.7
Phentermine /Topiramate (PHEN/ TPM) ER8.1

[back to top]

Corrected First Phase Insulin Secretion (IGI/HOMA-IR)

Treatment effect on insulin secretion from 0 to 30 minutes after glucose load corrected for by fasting insulin sensitivity. A higher score shows improved first phase insulin secretion in response to glucose (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionindex score (Mean)
Exenatide Once Weekly (EQW )1.03
Dapagliflozin (DAPA)0.6
EQW Plus DAPA0.91
Dapagliflozin Plus Glucophage (MET ER)0.7
Phentermine /Topiramate (PHEN/ TPM) ER1.1

[back to top]

Diastolic Blood Pressure (DBP)

Treatment effect on DBP after 24 weeks (NCT02635386)
Timeframe: 24 weeks of treatment

InterventionmmHg (Mean)
Exenatide Once Weekly (EQW )81
Dapagliflozin (DAPA)79.8
EQW Plus DAPA76
Dapagliflozin Plus Glucophage (MET ER)82
Phentermine /Topiramate (PHEN/ TPM) ER83.6

[back to top]

Fasting Blood Glucose

Treatment impact on fasting concentration of glucose in the blood (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionmg/dL (Mean)
Exenatide Once Weekly (EQW )91
Dapagliflozin (DAPA)93
EQW Plus DAPA86.5
Dapagliflozin Plus Glucophage (MET ER)89
Phentermine /Topiramate (PHEN/ TPM ER91.4

[back to top]

Fasting Insulin Sensitivity (HOMA-IR)

Treatment effect on the ratio HOMA-IR which is insulin resistance measure derived from fasting blood glucose and insulin and is calculated by insulin (mU/ml)*glucose (mmol/L)/22,5. The higher thenumber the more insulin resistant. (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionindex score (Mean)
Exenatide Once Weekly (EQW )3.7
Dapagliflozin (DAPA)3.6
EQW Plus DAPA2.6
Dapagliflozin Plus Glucophage (MET ER)3.3
Phentermine /Topiramate (PHEN/ TPM) ER3.4

[back to top]

Free Androgen Index (FAI)

Treatment effect on FAI calculated from total testosterone divided by sex hormone binding globulin (SHBG) levels. A higher score indicates a worse outcome. (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionindex score (Mean)
Exenatide Once Weekly (EQW )5.3
Dapagliflozin (DAPA)4.7
EQW Plus DAPA5.2
Dapagliflozin Plus Glucophage (MET ER)5.7
Phentermine /Topiramate (PHEN/ TPM) ER5

[back to top]

Matsuda Sensitivity Index Derived From the OGTT(SI OGTT)

The SI IOGTT is a measure of peripheral insulin sensitivity derived from the values of Insulin (microunits per milliliter) and Glucose (milligrams per deciliter) obtained from the OGTT and the corresponding fasting values. SI (OGTT) = 10,000/ [(G fasting x I fasting) x (G OGTTmean x I OGTTmean)], where fasting glucose and insulin data are taken from time 0 of the OGTT and mean data represent the average glucose and insulin values obtained during the entire OGTT. The square root is used to correct for nonlinear distribution of insulin, and 10,000 is a scaling factor in the equation. The higher value, the more sensitive to insulin. (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionindex score (Mean)
Exenatide Once Weekly (EQW )3.1
Dapagliflozin (DAPA)3.6
EQW Plus DAPA3.9
Dapagliflozin Plus Glucophage (MET ER)4.8
Phentermine /Topiramate (PHEN/ TPM) ER4.7

[back to top]

OGTT Mean Blood Glucose (MBG)

Treatment effect on MBG measured during the oral glucose tolerance test (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionmg/dL (Mean)
Exenatide Once Weekly (EQW )118
Dapagliflozin (DAPA)126.4
EQW Plus DAPA112
Dapagliflozin Plus Glucophage (MET ER)119
Phentermine /Topiramate (PHEN/ TPM ER113

[back to top]

Oral Disposition (Insulin Sensitivity-insulin Secretion) Index

An estimation of β-cell compensatory function, the insulin secretion-sensitivity index (IS-SI) will be derived by applying the concept of the oral disposition index to measurements obtained during the 2-h OGTT and calculated as the index of insulin secretion factored by insulin sensitivity (ΔINS/ΔPG 30 x Matsuda SIOGTT) from the OGTT. A higher score shows improved pancreatic insulin responsiveness relative to resistance. (NCT02635386)
Timeframe: 24 weeks of treatment

Interventionindex score (Mean)
Exenatide Once Weekly (EQW )471
Dapagliflozin (DAPA)311
EQW Plus DAPA503
Dapagliflozin Plus Glucophage (MET ER)395
Phentermine /Topiramate (PHEN/ TPM) ER545

[back to top]

Changes of Energy Intake Assessed by Automated Self-Administered 24-Hour Dietary Recall (ASA24-Kids)

Self-reported daily energy intake was assessed by Automated Self-Administered 24-Hour Dietary Recall (ASA24-Kids, http://appliedresearch.cancer.gov/tools/instruments/asa24/), a web-based diet assessment tool that allows 24-hour diet recall using branded food items. (NCT02664441)
Timeframe: Baseline and 36 weeks

Interventionkcals (Mean)
Exenatide Once Weekly Extended-release-62
Matching Placebo-210

[back to top]

Changes in HDL Cholesterol and Triglycerides Assessed by Fasting Lipids

Change in fasting HDL cholesterol and triglycerides between baseline and the end of the 36-week randomized drug treatment phase. (NCT02664441)
Timeframe: From baseline to 36 weeks

,
Interventionmg/dL (Mean)
HDL CholesterolTriglycerides
Exenatide Once Weekly Extended-release0.7-0.6
Matching Placebo0.64.2

[back to top]

Changes in Fat and Total Calorie Intake Assessed by Free Buffet Meal Analysis.

"Changes in fat and total calorie intake during free buffet meals assessed at baseline and after 36-weeks of study drug treatment.~The buffet meal is an objective measure of satiety as it assesses food intake and choice after a caloric preload. A standardized test meal preload provided 20% of estimated daily caloric requirements,based on the Schofield-HW equation. The purpose of the test meal is to ensure that study participants are in an equally fed state. Ninety minutes later, an ad libitum buffet meal was served consisting of a wide variety of food items and more than the child's estimated daily calorie requirements will be offered (5,000 kcal). Children had access to the buffet for 30 min, after which calorie intake and composition of consumed foods was measured by weighing back uneaten food." (NCT02664441)
Timeframe: From baseline to 36 weeks

,
Interventiongrams (Mean)
Fat IntakeTotal Calorie Intake
Exenatide Once Weekly Extended-release-9.5-287
Matching Placebo14.5224

[back to top]

Percent Change of Body Mass Index (BMI) as Calculated by the Formula: Body Weight in kg Divided by Height in Meters².

Percent change of body mass index (BMI), as calculated by the formula: body weight in kg divided by height in meters², between baseline and the end of the 36-week randomized drug treatment phase. (NCT02664441)
Timeframe: From baseline to 36 weeks

Interventionpercent change from baseline (Mean)
Exenatide Once Weekly Extended-release1.7
Matching Placebo3.5

[back to top]

Changes of Insulin Resistance Assessed by Homeostasis Model Assessment of Insulin Resistance (HOMA-IR)

Changes of insulin resistance estimated by the homeostasis model assessment of insulin resistance (HOMA-IR) using the formula HOMA-IR = insulin [mU/l] x glucose [mmol/l]) / 22.5 where both insulin and glucose values are obtained from a fasting blood sample. (NCT02664441)
Timeframe: From baseline to 36 weeks

InterventionHOMA-IR score (Mean)
Exenatide Once Weekly Extended-release3.5
Matching Placebo2.2

[back to top]

Changes of Energy Expenditure Assessed by Doubly Labeled Water Analysis

Total energy expenditure in the free-living environment was measured using doubly labeled water which estimates carbon dioxide production by measuring the elimination of the tracers deuterium (²H) and oxygen-18 (¹⁸O) from the body. These measures are used to determine the average daily rate of carbon dioxide production which is then used to calculate total energy expenditure using an equation from Weir and an assumed food quotient (0.85). (NCT02664441)
Timeframe: Baseline and 36 weeks

Interventionkcals/day (Mean)
Exenatide Once Weekly Extended-release-17.8
Matching Placebo146.3

[back to top]

Changes of Circulating Leptin Levels

Change in circulating leptin between baseline and the end of the 36-week randomized drug treatment phase. (NCT02664441)
Timeframe: From baseline to 36 weeks

Interventionng/mL (Mean)
Exenatide Once Weekly Extended-release1.4
Matching Placebo11.8

[back to top]

Changes in Inflammation Assessed by C-reactive Protein (CRP)

Change in C-reactive protein (CRP) between baseline and the end of the 36-week randomized drug treatment phase. (NCT02664441)
Timeframe: From baseline to 36 weeks

Interventionmg/dL (Mean)
Exenatide Once Weekly Extended-release0.00
Matching Placebo0.18

[back to top]

Changes in Glucose 120 Minutes Following an Oral Glucose Tolerance Test

Change in blood glucose measures 120 minutes post-glucose bolus during an oral glucose tolerance test between baseline and the end of the 36-week randomized drug treatment phase. (NCT02664441)
Timeframe: From baseline to 36 weeks

Interventionmg/dL (Mean)
Exenatide Once Weekly Extended-release-12.4
Matching Placebo-3.4

[back to top]

Changes in Fasting Glucose

Change in fasting blood glucose between baseline and the end of the 36-week randomized drug treatment phase. (NCT02664441)
Timeframe: From baseline to 36 weeks

Interventionmg/dL (Mean)
Exenatide Once Weekly Extended-release7.4
Matching Placebo3.7

[back to top]

Changes in Body Composition as Assessed by Body Fat Mass Using Dual Energy X-ray Absorptiometry (DEXA)

Body composition change between baseline and the end of the 36-week randomized drug treatment phase assessed by dual energy x-ray absorptiometry (DEXA) and expressed as the change in adipose tissue mass. (NCT02664441)
Timeframe: At baseline and 36 weeks

Interventionkilograms (Mean)
Exenatide Once Weekly Extended-release1.5
Matching Placebo4.6

[back to top]

Percentage of Participants Reaching HbA1c <7 % or <=6.5% at Week 52: Single Arm Extension Period

Participants without any available HbA1c assessment at Week 52 were considered as non-responders. (NCT02787551)
Timeframe: Week 52

Interventionpercentage of participants (Number)
HbA1c <7%HbA1c <=6.5%
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)64.142.7

[back to top]

Number of Documented Symptomatic Hypoglycemia Events Per Participant-Year: Single Arm Extension Period

Documented symptomatic hypoglycemia was an event during which symptoms of hypoglycemia were accompanied by a measured plasma glucose concentration of <=3.9 mmol/L (70 mg/dL). Hypoglycemic episodes with plasma glucose of <3.0 mmol/L (54 mg/dL) were also analyzed. (NCT02787551)
Timeframe: From Baseline to Week 52

Interventionevents per participant-year (Number)
Documented symptomatic hypoglycemia(<=3.9 mmol/L)Documented symptomatic hypoglycemia (<3.0 mmol/L)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)1.590.24

[back to top]

Number of Documented Symptomatic Hypoglycemia Events Per Participant-Year: Core Period

Documented symptomatic hypoglycemia was an event during which symptoms of hypoglycemia were accompanied by a measured plasma glucose concentration of <=3.9 mmol/L (70 mg/dL). Hypoglycemic episodes with plasma glucose of <3.0 mmol/L (54 mg/dL) were also analyzed. (NCT02787551)
Timeframe: From Baseline to Week 26

,
Interventionevents per participant-year (Number)
Documented symptomatic hypoglycemia(<=3.9 mmol/L)Documented symptomatic hypoglycemia (<3.0 mmol/L)
GLP-1 Receptor Agonist0.080.01
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)1.540.25

[back to top]

Percentage of Participants Requiring Rescue Therapy During the 52 Week Treatment Period: Single Arm Extension Period

Routine HbA1c value was used to determine the requirement of rescue medication. Threshold values at Week 12 or later on Week 12: HbA1c >8%. (NCT02787551)
Timeframe: From Week 26 to Week 52

Interventionpercentage of participants (Number)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)1.5

[back to top]

Percentage of Participants Requiring Rescue Therapy During the 26 Week Treatment Period: Core Period

Routine HbA1c value was used to determine the requirement of rescue medication. Threshold values at Week 12 or later on Week 12: HbA1c >8%. (NCT02787551)
Timeframe: From Baseline to Week 26

Interventionpercentage of participants (Number)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)4.8
GLP-1 Receptor Agonist15.0

[back to top]

Change From Baseline in the Daily Average of the 7-point Self-monitored Plasma Glucose (SMPG) to Week 52: Single Arm Extension Period

The 7-point SMPG profile was measured at the following 7 points: pre-prandial and 2 hours postprandial for breakfast, lunch, dinner and at bedtime. Two hours postprandial (breakfast, lunch and dinner) was defined as 2 hours after the start of the meal. (NCT02787551)
Timeframe: Baseline, Week 52

Interventionmmol/L (Mean)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)-1.68

[back to top]

Change From Baseline in Glycated Hemoglobin (HbA1c) to Week 52: Single Arm Extension Period

Change in HbA1c was calculated by subtracting baseline value from Week 52 value. (NCT02787551)
Timeframe: Baseline, Week 52

Interventionpercentage of HbA1c (Mean)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)-1.01

[back to top]

Change From Baseline in Glycated Hemoglobin (HbA1c) to Week 26: Core Period

Change in HbA1c was calculated by subtracting baseline value from Week 26 value. Adjusted least squares (LS) mean and standard error (SE) were obtained from Mixed-effect model with repeated measures (MMRM) to account for missing data using all available post baseline data during the 26 week treatment period. (NCT02787551)
Timeframe: Baseline, Week 26

Interventionpercentage of HbA1c (Least Squares Mean)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)-1.02
GLP-1 Receptor Agonist-0.38

[back to top]

Change From Baseline in Fasting Plasma Glucose (FPG) to Week 52: Single Arm Extension Period

Change in FPG was calculated by subtracting baseline value from Week 52 value. (NCT02787551)
Timeframe: Baseline, Week 52

Interventionmmol/L (Mean)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)-2.27

[back to top]

Change From Baseline in Fasting Plasma Glucose (FPG) to Week 26: Core Period

Change in FPG was calculated by subtracting baseline value from Week 26 value. Adjusted LS means and SE were obtained from MMRM to account for missing data using all available post baseline data during the 26 week treatment period. (NCT02787551)
Timeframe: Baseline, Week 26

Interventionmillimoles per litre (mmol/L) (Least Squares Mean)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)-2.28
GLP-1 Receptor Agonist-0.60

[back to top]

Change From Baseline in Body Weight to Week 52: Single Arm Extension Period

Change in body weight was calculated by subtracting baseline value from Week 52 value. (NCT02787551)
Timeframe: Baseline, Week 52

Interventionkg (Mean)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)2.78

[back to top]

Percentage of Participants Reaching HbA1c <7% or <=6.5% at Week 26: Core Period

Participants without any available HbA1c assessment at Week 26 were considered as non-responders. (NCT02787551)
Timeframe: Week 26

,
Interventionpercentage of participants (Number)
HbA1c <7%HbA1c <=6.5%
GLP-1 Receptor Agonist25.79.9
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)61.940.5

[back to top]

Change From Baseline in Body Weight at Week 26: Core Period

Change in body weight was calculated by subtracting baseline value from Week 26 value. (NCT02787551)
Timeframe: Baseline, Week 26

Interventionkilogram (kg) (Least Squares Mean)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)1.89
GLP-1 Receptor Agonist-1.14

[back to top]

Change From Baseline in 2-Hour Postprandial Plasma Glucose (PPG) During Standardized Meal Test to Week 52: Single Arm Extension Period

The 2-hour PPG test measured blood glucose 2 hours after eating a liquid standardized breakfast meal. Change in PPG was calculated by subtracting baseline value from Week 52 value. Missing data was imputed using LOCF. (NCT02787551)
Timeframe: Baseline, Week 52

Interventionmmol/L (Mean)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)-4.30

[back to top]

Change From Baseline in 2-Hour Postprandial Plasma Glucose (PPG) During Standardized Meal Test to Week 26: Core Period

The 2-hour PPG test measured blood glucose 2 hours after eating a liquid standardized breakfast meal. Change in PPG was calculated by subtracting baseline value from Week 26 value. Missing data was imputed using last observation carried forward (LOCF). (NCT02787551)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)-3.96
GLP-1 Receptor Agonist-1.11

[back to top]

Change From Baseline in 2-Hour Blood Glucose Excursion During Standardized Meal Test to Week 52: Single Arm Extension Period

2-hour plasma glucose excursion = 2-hour PPG value minus plasma glucose value obtained 30 minutes prior to the start of meal and before IMP administration if IMP was injected before breakfast. Change in plasma glucose excursions were calculated by subtracting baseline value from Week 52 value. Missing data was imputed using LOCF. (NCT02787551)
Timeframe: Baseline, Week 52

Interventionmmol/L (Mean)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)-1.85

[back to top]

Change From Baseline in 2-Hour Blood Glucose Excursion During Standardized Meal Test to Week 26: Core Period

2-hour plasma glucose excursion = 2-hour PPG value minus plasma glucose value obtained 30 minutes prior to the start of meal and before investigational medicinal product (IMP) administration if IMP was injected before breakfast. Change in plasma glucose excursions were calculated by subtracting baseline value from Week 26 value. Missing data was imputed using LOCF. (NCT02787551)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)-1.51
GLP-1 Receptor Agonist-0.52

[back to top]

Change From Baseline in the Daily Average of the 7-point Self-monitored Plasma Glucose (SMPG) to Week 26: Core Period

The 7-point SMPG profile was measured at the following 7 points: pre-prandial and 2 hours postprandial for breakfast, lunch, dinner and at bedtime. Two hours postprandial (breakfast, lunch and dinner) was defined as 2 hours after the start of the meal. Adjusted LS means and SE were obtained from MMRM to account for missing data using all available post baseline data during the 26 week treatment period. (NCT02787551)
Timeframe: Baseline, Week 26

Interventionmmol/L (Least Squares Mean)
Insulin Glargine/Lixisenatide Fixed Ratio Combination (FRC)-1.69
GLP-1 Receptor Agonist-0.67

[back to top]

Part A: Hematocrit Level at Indicated Time Points

Blood samples were collected for analysis of hematocrit level. Individual Par. data at indicated time points has been presented. (NCT02793154)
Timeframe: Day 5

InterventionProportion of RBC in blood (Number)
Par. 1Par. 2Par. 3Par. 4
Part A: Exenatide SC Injection0.3990.4260.4660.462

[back to top]

Part A: Hemoglobin Level at Indicated Time Points

Blood samples were collected for analysis of hemoglobin level. Individual Par. data at indicated time point has been presented. (NCT02793154)
Timeframe: Day 5

InterventionGrams per liter (Number)
Par. 1Par. 2Par. 3Par. 4
Part A: Exenatide SC Injection125133149156

[back to top]

Part A: Number of Par. With Adverse Events (AEs) and Serious AEs (SAEs)

An AE is any untoward medical occurrence in a clinical investigation Par. temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. SAE is defined as any untoward medical occurrence that, at any dose results in death, is life-threatening, requires hospitalization or prolongation of existing hospitalization, results in disability, is a congenital anomaly/ birth effect, other situations and is associated with liver injury or impaired liver function. Number of Par. with AEs and SAEs have been presented. (NCT02793154)
Timeframe: Up to 12 days

InterventionParticipants (Number)
Any AEAny SAE
Part A: Exenatide SC Injection10

[back to top]

Part A: Number of Par. With Presence of Ketones, Occult Blood, Glucose, Nitrates and Leukocyte Esterase in Urine at Indicated Time Points

Urine samples were collected to analyze presence of ketones, occult blood, glucose, nitrates and leukocyte esterase in urine. The dipstick test gives results in a semi-quantitative manner. NA represents data was not available due to lab data transfer error. Individual Par. data at indicated time point has been presented. (NCT02793154)
Timeframe: Day 5

InterventionParticipants (Number)
Par. 1; Ketones; NegativePar 1; Occult blood; TracePar 1; GlucosePar 1; NitratesPar 1; Leukocyte esterasePar. 2; Ketones; NegativePar. 2; Occult blood; NegativePar. 2; GlucosePar 2; NitratesPar 2; Leukocyte esterasePar. 3; Ketones; NegativePar. 3; Occult blood; NegativePar. 3; GlucosePar 3; NitratesPar 3; Leukocyte esterasePar. 4; Ketones; NegativePar. 4; Occult blood; NegativePar. 4; GlucosePar 4; NitratesPar 4; Leukocyte esterase
Part A: Exenatide SC Injection11NANANA11NANANA11NANANA11NANANA

[back to top]

Part A: Percentage of Time With the Dominant EGG Frequencies in the Four Frequency Ranges of Bradygastria, Normal, Tachygastria and Duodenal

The effect of exenatide on gastric myoelectrical activity was assessed by EGG using WLT. EGG with WLT is a standardized test to induce gastric distention and measure myoelectrical responses. The gastric myoelectrical activity is generated by the pacemaker interstitial cells at a normal frequency of 3 cycles per minute. The shift of frequency from normal gastric myoelectrical activity to a slower rhythm is bradygastria or faster rhythm is tachygastria. Individual Par. data for dominant EGG frequencies including bradygastria, normal, tachygastria and duodenal at pre-WL and after treatment with exenatide at pre-WL and 10, 20, 30 minutes post-WL has been presented. (NCT02793154)
Timeframe: Up to Day 4

InterventionPercentage of time (Number)
Par. 1; Day 1; Pre-WL; BradygastriaPar. 1; Day 1; Pre-WL; NormalPar. 1; Day 1; Pre-WL; TachygastriaPar. 1; Day 1; Pre-WL; DuodenalPar. 1; Day 1; 10 minutes Post-WL; BradygastriaPar. 1; Day 1; 10 minutes Post-WL; NormalPar. 1; Day 1; 10 minutes Post-WL; TachygastriaPar. 1; Day 1; 10 minutes Post-WL; DuodenalPar. 1; Day 1; 20 minutes Post-WL; BradygastriaPar. 1; Day 1; 20 minutes Post-WL; NormalPar. 1; Day 1; 20 minutes Post-WL; TachygastriaPar. 1; Day 1; 20 minutes Post-WL; DuodenalPar. 1; Day 1; 30 minutes Post-WL; BradygastriaPar. 1; Day 1; 30 minutes Post-WL; NormalPar. 1; Day 1; 30 minutes Post-WL; TachygastriaPar. 1; Day 1; 30 minutes Post-WL; DuodenalPar. 1; Day 4; Pre-WL; BradygastriaPar. 1; Day 4; Pre-WL; NormalPar. 1; Day 4; Pre-WL; TachygastriaPar. 1; Day 4; Pre-WL; DuodenalPar. 1; Day 4; 10 minutes Post-WL; BradygastriaPar. 1; Day 4; 10 minutes Post-WL; NormalPar. 1; Day 4; 10 minutes Post-WL; TachygastriaPar. 1; Day 4; 10 minutes Post-WL; DuodenalPar. 1; Day 4; 20 minutes Post-WL; BradygastriaPar. 1; Day 4; 20 minutes Post-WL; NormalPar. 1; Day 4; 20 minutes Post-WL; TachygastriaPar. 1; Day 4; 20 minutes Post-WL; DuodenalPar. 1; Day 4; 30 minutes Post-WL; BradygastriaPar. 1; Day 4; 30 minutes Post-WL; NormalPar. 1; Day 4; 30 minutes Post-WL; TachygastriaPar. 1; Day 4; 30 minutes Post-WL; DuodenalPar. 2; Day 1; Pre-WL; BradygastriaPar. 2; Day 1; Pre-WL; NormalPar. 2; Day 1; Pre-WL; TachygastriaPar. 2; Day 1; Pre-WL; DuodenalPar. 2; Day 1; 10 minutes Post-WL; BradygastriaPar. 2; Day 1; 10 minutes Post-WL; NormalPar. 2; Day 1; 10 minutes Post-WL; TachygastriaPar. 2; Day 1; 10 minutes Post-WL; DuodenalPar. 2; Day 1; 20 minutes Post-WL; BradygastriaPar. 2; Day 1; 20 minutes Post-WL; NormalPar. 2; Day 1; 20 minutes Post-WL; TachygastriaPar. 2; Day 1; 20 minutes Post-WL; DuodenalPar. 2; Day 1; 30 minutes Post-WL; BradygastriaPar. 2; Day 1; 30 minutes Post-WL; NormalPar. 2; Day 1; 30 minutes Post-WL; TachygastriaPar. 2; Day 1; 30 minutes Post-WL; DuodenalPar. 2; Day 4; Pre-WL; BradygastriaPar. 2; Day 4; Pre-WL; NormalPar. 2; Day 4; Pre-WL; TachygastriaPar. 2; Day 4; Pre-WL; DuodenalPar. 2; Day 4; 10 minutes Post-WL; BradygastriaPar. 2; Day 4; 10 minutes Post-WL; NormalPar. 2; Day 4; 10 minutes Post-WL; TachygastriaPar. 2; Day 4; 10 minutes Post-WL; DuodenalPar. 2; Day 4; 20 minutes Post-WL; BradygastriaPar. 2; Day 4; 20 minutes Post-WL; NormalPar. 2; Day 4; 20 minutes Post-WL; TachygastriaPar. 2; Day 4; 20 minutes Post-WL; DuodenalPar. 2; Day 4; 30 minutes Post-WL; BradygastriaPar. 2; Day 4; 30 minutes Post-WL; NormalPar. 2; Day 4; 30 minutes Post-WL; TachygastriaPar. 2; Day 4; 30 minutes Post-WL; DuodenalPar. 3; Day 1; Pre-WL; BradygastriaPar. 3; Day 1; Pre-WL; NormalPar. 3; Day 1; Pre-WL; TachygastriaPar. 3; Day 1; Pre-WL; DuodenalPar. 3; Day 1; 10 minutes Post-WL; BradygastriaPar. 3; Day 1; 10 minutes Post-WL; NormalPar. 3; Day 1; 10 minutes Post-WL; TachygastriaPar. 3; Day 1; 10 minutes Post-WL; DuodenalPar. 3; Day 1; 20 minutes Post-WL; BradygastriaPar. 3; Day 1; 20 minutes Post-WL; NormalPar. 3; Day 1; 20 minutes Post-WL; TachygastriaPar. 3; Day 1; 20 minutes Post-WL; DuodenalPar. 3; Day 1; 30 minutes Post-WL; BradygastriaPar. 3; Day 1; 30 minutes Post-WL; NormalPar. 3; Day 1; 30 minutes Post-WL; TachygastriaPar. 3; Day 1; 30 minutes Post-WL; DuodenalPar. 3; Day 4; Pre-WL; BradygastriaPar. 3; Day 4; Pre-WL; NormalPar. 3; Day 4; Pre-WL; TachygastriaPar. 3; Day 4; Pre-WL; DuodenalPar. 3; Day 4; 10 minutes Post-WL; BradygastriaPar. 3; Day 4; 10 minutes Post-WL; NormalPar. 3; Day 4; 10 minutes Post-WL; TachygastriaPar. 3; Day 4; 10 minutes Post-WL; DuodenalPar. 3; Day 4; 20 minutes Post-WL; BradygastriaPar. 3; Day 4; 20 minutes Post-WL; NormalPar. 3; Day 4; 20 minutes Post-WL; TachygastriaPar. 3; Day 4; 20 minutes Post-WL; DuodenalPar. 3; Day 4; 30 minutes Post-WL; BradygastriaPar. 3; Day 4; 30 minutes Post-WL; NormalPar. 3; Day 4; 30 minutes Post-WL; TachygastriaPar. 3; Day 4; 30 minutes Post-WL; DuodenalPar. 4; Day 1; Pre-WL; BradygastriaPar. 4; Day 1; Pre-WL; NormalPar. 4; Day 1; Pre-WL; TachygastriaPar. 4; Day 1; Pre-WL; DuodenalPar. 4; Day 1; 10 minutes Post-WL; BradygastriaPar. 4; Day 1; 10 minutes Post-WL; NormalPar. 4; Day 1; 10 minutes Post-WL; TachygastriaPar. 4; Day 1; 10 minutes Post-WL; DuodenalPar. 4; Day 1; 20 minutes Post-WL; BradygastriaPar. 4; Day 1; 20 minutes Post-WL; NormalPar. 4; Day 1; 20 minutes Post-WL; TachygastriaPar. 4; Day 1; 20 minutes Post-WL; DuodenalPar. 4; Day 1; 30 minutes Post-WL; BradygastriaPar. 4; Day 1; 30 minutes Post-WL; NormalPar. 4; Day 1; 30 minutes Post-WL; TachygastriaPar. 4; Day 1; 30 minutes Post-WL; DuodenalPar. 4; Day 4; Pre-WL; BradygastriaPar. 4; Day 4; Pre-WL; NormalPar. 4; Day 4; Pre-WL; TachygastriaPar. 4; Day 4; Pre-WL; DuodenalPar. 4; Day 4; 10 minutes Post-WL; BradygastriaPar. 4; Day 4; 10 minutes Post-WL; NormalPar. 4; Day 4; 10 minutes Post-WL; TachygastriaPar. 4; Day 4; 10 minutes Post-WL; DuodenalPar. 4; Day 4; 20 minutes Post-WL; BradygastriaPar. 4; Day 4; 20 minutes Post-WL; NormalPar. 4; Day 4; 20 minutes Post-WL; TachygastriaPar. 4; Day 4; 20 minutes Post-WL; DuodenalPar. 4; Day 4; 30 minutes Post-WL; BradygastriaPar. 4; Day 4; 30 minutes Post-WL; NormalPar. 4; Day 4; 30 minutes Post-WL; TachygastriaPar. 4; Day 4; 30 minutes Post-WL; Duodenal
Part A: Exenatide SC Injection802000100000100000505000100000100000100000505000100000100000100000100000100000100000100000505000100000100000010000050500100000100000100000100000100000100000100000100000100000100000100000080200

[back to top]

Part A: Potential of Hydrogen (pH) of Urine at Indicated Time Points

Urine Samples were collected to analyze pH. pH is a measure of hydrogen ion concentration and used to determine the acidity or alkalinity of urine. pH scale ranges from 0 to 14. A neutral pH is 7.0. The higher number indicates the more basic (alkaline) nature of urine and lower the number indicates the more acidic urine.Individual Par. data at indicated time point has been presented. (NCT02793154)
Timeframe: Day 5

InterventionPoints on a scale (Number)
Par. 1Par. 2Par. 3Par. 4
Part A: Exenatide SC Injection55.565

[back to top]

Part A: Presence RBC and WBC in Urine Assessed by Microscopy

"Samples were collected to analyze the presence of RBC and WBC in urine by microscopy. Individual Par. data at indicated time point has been presented. NA indicates data was not available as RBC and WBC count would only available if blood or protein were abnormal. The RBC and WBC values of 1 for participant 1 actually reflect 0-1." (NCT02793154)
Timeframe: Day 5

InterventionHigh Power field (Number)
Par.1; RBCPar. 1; WBCPar. 2; RBCPar. 2; WBCPar. 3; RBCPart. 3; WBCPart 4; RBCPart. 4; WBC
Part A: Exenatide SC Injection11NANANANANANA

[back to top]

Part A: Rate of [13]C Dose Excreted in Breath

The effect of exenatide on gastric emptying was be assessed by calculating the percent dose excreted of 13C in breath multiplied by 1000 (kPCD). Breath samples were collected at the indicated time points. Individual Par. data at pre-meal and 45, 90, 120, 150, 180 and 240 minutes post-meal has been presented. (NCT02793154)
Timeframe: Day 5

InterventionkPCD per minute (Number)
Par. 1; Day 5; Pre-MealPar. 1; Day 5; 45 Minutes Post-MealPar. 1; Day 5; 90 Minutes Post-MealPar. 1; Day 5; 120 Minutes Post-MealPar. 1; Day 5; 150 Minutes Post-MealPar. 1; Day 5; 180 Minutes Post-MealPar. 1; Day 5; 240 Minutes Post-MealPar. 2; Day 5; Pre-MealPar. 2; Day 5; 45 Minutes Post-MealPar. 2; Day 5; 90 Minutes Post-MealPar. 2; Day 5; 120 Minutes Post-MealPar. 2; Day 5; 150 Minutes Post-MealPar. 2; Day 5; 180 Minutes Post-MealPar. 2; Day 5; 240 Minutes Post-MealPar. 3; Day 5; Pre-MealPar. 3; Day 5; 45 Minutes Post-MealPar. 3; Day 5; 90 Minutes Post-MealPar. 3; Day 5; 120 Minutes Post-MealPar. 3; Day 5; 150 Minutes Post-MealPar. 3; Day 5; 180 Minutes Post-MealPar. 3; Day 5; 240 Minutes Post-MealPar. 4; Day 5; Pre-MealPar. 4; Day 5; 45 Minutes Post-MealPar. 4; Day 5; 90 Minutes Post-MealPar. 4; Day 5; 120 Minutes Post-MealPar. 4; Day 5; 150 Minutes Post-MealPar. 4; Day 5; 180 Minutes Post-MealPar. 4; Day 5; 240 Minutes Post-Meal
Part A: Exenatide SC Injection01.83.33.13.37.421.1022.242.566.582.384.775.8012.36.516.428.256.3011.327.839.651.159.861.6

[back to top]

Part A: Ratios of Average Power Post- WLT/Pre-WLT by Frequency Region

The effect of exenatide on gastric myoelectrical activity was assessed by EGG using WLT. EGG with WLT is a standardized test to induce gastric distention and measure myoelectrical responses. The gastric myoelectrical activity is generated by the pacemaker interstitial cells at a normal frequency of 3 cycles per minute. The shift of frequency from normal gastric myoelectrical activity to a slower rhythm is bradygastria or faster rhythm is tachygastria. Individual Par. data for ratios of average power post- WLT/pre-WLT in the bradygastria, normal, tachygastria and duodenal range after treatment with exenatide at 10, 20, and 30 minutes post-WL has been presented. (NCT02793154)
Timeframe: Up to Day 4

InterventionRatio (Number)
Par. 1; Day 1; 10 minutes Post-WL; BradygastriaPar. 1; Day 1; 10 minutes Post-WL; NormalPar. 1; Day 1; 10 minutes Post-WL; TachygastriaPar. 1; Day 1; 10 minutes Post-WL; DuodenalPar. 1; Day 1; 20 minutes Post-WL; BradygastriaPar. 1; Day 1; 20 minutes Post-WL; NormalPar. 1; Day 1; 20 minutes Post-WL; TachygastriaPar. 1; Day 1; 20 minutes Post-WL; DuodenalPar. 1; Day 1; 30 minutes Post-WL; BradygastriaPar. 1; Day 1; 30 minutes Post-WL; NormalPar. 1; Day 1; 30 minutes Post-WL; TachygastriaPar. 1; Day 1; 30 minutes Post-WL; DuodenalPar. 1; Day 4; 10 minutes Post-WL; BradygastriaPar. 1; Day 4; 10 minutes Post-WL; NormalPar. 1; Day 4; 10 minutes Post-WL; TachygastriaPar. 1; Day 4; 10 minutes Post-WL; DuodenalPar. 1; Day 4; 20 minutes Post-WL; BradygastriaPar. 1; Day 4; 20 minutes Post-WL; NormalPar. 1; Day 4; 20 minutes Post-WL; TachygastriaPar. 1; Day 4; 20 minutes Post-WL; DuodenalPar. 1; Day 4; 30 minutes Post-WL; BradygastriaPar. 1; Day 4; 30 minutes Post-WL; NormalPar. 1; Day 4; 30 minutes Post-WL; TachygastriaPar. 1; Day 4; 30 minutes Post-WL; DuodenalPar. 2; Day 1; 10 minutes Post-WL; BradygastriaPar. 2; Day 1; 10 minutes Post-WL; NormalPar. 2; Day 1; 10 minutes Post-WL; TachygastriaPar. 2; Day 1; 10 minutes Post-WL; DuodenalPar. 2; Day 1; 20 minutes Post-WL; BradygastriaPar. 2; Day 1; 20 minutes Post-WL; NormalPar. 2; Day 1; 20 minutes Post-WL; TachygastriaPar. 2; Day 1; 20 minutes Post-WL; DuodenalPar. 2; Day 1; 30 minutes Post-WL; BradygastriaPar. 2; Day 1; 30 minutes Post-WL; NormalPar. 2; Day 1; 30 minutes Post-WL; TachygastriaPar. 2; Day 1; 30 minutes Post-WL; DuodenalPar. 2; Day 4; 10 minutes Post-WL; BradygastriaPar. 2; Day 4; 10 minutes Post-WL; NormalPar. 2; Day 4; 10 minutes Post-WL; TachygastriaPar. 2; Day 4; 10 minutes Post-WL; DuodenalPar. 2; Day 4; 20 minutes Post-WL; BradygastriaPar. 2; Day 4; 20 minutes Post-WL; NormalPar. 2; Day 4; 20 minutes Post-WL; TachygastriaPar. 2; Day 4; 20 minutes Post-WL; DuodenalPar. 2; Day 4; 30 minutes Post-WL; BradygastriaPar. 2; Day 4; 30 minutes Post-WL; NormalPar. 2; Day 4; 30 minutes Post-WL; TachygastriaPar. 2; Day 4; 30 minutes Post-WL; DuodenalPar. 3; Day 1; 10 minutes Post-WL; BradygastriaPar. 3; Day 1; 10 minutes Post-WL; NormalPar. 3; Day 1; 10 minutes Post-WL; TachygastriaPar. 3; Day 1; 10 minutes Post-WL; DuodenalPar. 3; Day 1; 20 minutes Post-WL; BradygastriaPar. 3; Day 1; 20 minutes Post-WL; NormalPar. 3; Day 1; 20 minutes Post-WL; TachygastriaPar. 3; Day 1; 20 minutes Post-WL; DuodenalPar. 3; Day 1; 30 minutes Post-WL; BradygastriaPar. 3; Day 1; 30 minutes Post-WL; NormalPar. 3; Day 1; 30 minutes Post-WL; TachygastriaPar. 3; Day 1; 30 minutes Post-WL; DuodenalPar. 3; Day 4; 10 minutes Post-WL; BradygastriaPar. 3; Day 4; 10 minutes Post-WL; NormalPar. 3; Day 4; 10 minutes Post-WL; TachygastriaPar. 3; Day 4; 10 minutes Post-WL; DuodenalPar. 3; Day 4; 20 minutes Post-WL; BradygastriaPar. 3; Day 4; 20 minutes Post-WL; NormalPar. 3; Day 4; 20 minutes Post-WL; TachygastriaPar. 3; Day 4; 20 minutes Post-WL; DuodenalPar. 3; Day 4; 30 minutes Post-WL; BradygastriaPar. 3; Day 4; 30 minutes Post-WL; NormalPar. 3; Day 4; 30 minutes Post-WL; TachygastriaPar. 3; Day 4; 30 minutes Post-WL; DuodenalPar. 4; Day 1; 10 minutes Post-WL; BradygastriaPar. 4; Day 1; 10 minutes Post-WL; NormalPar. 4; Day 1; 10 minutes Post-WL; TachygastriaPar. 4; Day 1; 10 minutes Post-WL; DuodenalPar. 4; Day 1; 20 minutes Post-WL; BradygastriaPar. 4; Day 1; 20 minutes Post-WL; NormalPar. 4; Day 1; 20 minutes Post-WL; TachygastriaPar. 4; Day 1; 20 minutes Post-WL; DuodenalPar. 4; Day 1; 30 minutes Post-WL; BradygastriaPar. 4; Day 1; 30 minutes Post-WL; NormalPar. 4; Day 1; 30 minutes Post-WL; TachygastriaPar. 4; Day 1; 30 minutes Post-WL; DuodenalPar. 4; Day 4; 10 minutes Post-WL; BradygastriaPar. 4; Day 4; 10 minutes Post-WL; NormalPar. 4; Day 4; 10 minutes Post-WL; TachygastriaPar. 4; Day 4; 10 minutes Post-WL; DuodenalPar. 4; Day 4; 20 minutes Post-WL; BradygastriaPar. 4; Day 4; 20 minutes Post-WL; NormalPar. 4; Day 4; 20 minutes Post-WL; TachygastriaPar. 4; Day 4; 20 minutes Post-WL; DuodenalPar. 4; Day 4; 30 minutes Post-WL; BradygastriaPar. 4; Day 4; 30 minutes Post-WL; NormalPar. 4; Day 4; 30 minutes Post-WL; TachygastriaPar. 4; Day 4; 30 minutes Post-WL; Duodenal
Part A: Exenatide SC Injection0000000000000000000000000.010000.040.04000.010.02000.030000.030.020.0100.220.110.050.010.130.290.520.20.20.990.70.330.151.381.360.40.160.080.130.090.20.10.110.070.160.080.190.192.62.213.880.760.892.242.522.761.543.292.441.474.70.741.440.9710.242.282.981.553.411.63.51.74

[back to top]

Part A: Red Blood Cell (RBC) Count at Indicated Time Points

Blood samples were collected for analysis of RBC count. Individual Par. data at indicated time point has been presented. (NCT02793154)
Timeframe: Day 5

InterventionTetra unit per liter (Number)
Par. 1Par. 2Par. 3Par. 4
Part A: Exenatide SC Injection4.74.854.9

[back to top]

Part A: Specific Gravity of Urine at Indicated Time Points

Urine samples were collected to analyze specific gravity of urine. Specific gravity, is a measure of urine concentration and is measured using a chemical test. Specific gravity measurements provide a comparison of the amount of substances dissolved in urine as compared to pure water. If there were no solutes present, the specific gravity of urine would be 1.000 the same as pure water. Specific gravity between 1.002 and 1.035 could be considered as normal. Individual Par. data at indicated time point has been presented. (NCT02793154)
Timeframe: Day 5

InterventionKilograms per meter^3 (Number)
Par. 1Par. 2Par. 3Par. 4
Part A: Exenatide SC Injection1.0211.0191.0231.027

[back to top]

Part A: The Volume of Water Ingested During EGG

The volume of water consumed by Par. at indicated time points after treatment with exenatide during EGG with WLT was determined. An EGG with WLT is a standardized test to induce gastric distention. Individual Par. data has been presented. (NCT02793154)
Timeframe: Up to Day 4

InterventionMilliliter (Number)
Par. 1; Day 1Par. 1; Day 4Par. 2; Day 1Par. 2; Day 4Par. 3; Day 1Par. 3; Day 4Par. 4; Day 1Par. 4; Day 4
Part A: Exenatide SC Injection43036021601980900108010001000

[back to top]

Part A: Time to Half-gastric Emptying

Breath samples were collected to assess the time to half gastric emptying using gastric emptying breath test (GEBT) containing 13 Carbon (13C)-Spirulina pre-meal and post GEBT meal. The GEBT method was used to measure GE of solid food. The time to half gastric emptying for individual Par. has been presented. (NCT02793154)
Timeframe: Up to Day 5

InterventionMinutes (Number)
Par. 1; Day -1Par. 1; Day 5Par. 2; Day -1Par. 2; Day 5Par. 3; Day -1Par. 3; Day 5Par. 4; Day -1Par. 4; Day 5
Part A: Exenatide SC Injection87.2226.573.075.557.6174.052.9103.8

[back to top]

Part A: Total Protein, Albumin Levels at Indicated Time Points

Blood samples were collected for analysis of clinical chemistry parameters including total protein and albumin levels. Individual Par. data at indicated time point has been presented. (NCT02793154)
Timeframe: Day 5

InterventionGrams per liter (Number)
Par. 1; Total ProteinPar. 1; Albumin levelsPar. 2; Total ProteinPar. 2; Albumin levelsPar. 3; Total ProteinPar. 3; Albumin levelsPar. 4; Total ProteinPar. 4; Albumin levels
Part A: Exenatide SC Injection7743754671447446

[back to top]

Part A: Number of Par. With Nausea AEs Presenting Outside the Timing of the WLT and GCSI-DD

GCSI-DD is a questionnaire of gastroparesis symptom severity covering the following domains: nausea/vomiting, fullness/early satiety, and bloating. The effect of exenatide on gastric myoelectrical activity was assessed by EGG using WLT. (NCT02793154)
Timeframe: Up to 12 days

InterventionParticipants (Number)
Part A: Exenatide SC Injection0

[back to top]

Part A: Alanine Amino Transferase (ALT), Aspartate Amino Transferase (AST), Gamma Glutamyl Transferase (GGT) Levels at Indicated Time Points

Blood samples were collected for analysis of clinical chemistry parameters including ALT, AST and GGT. Individual Par. data at indicated time point has been presented. (NCT02793154)
Timeframe: Day 5

InterventionInternational unit per liter (Number)
Par. 1; ALTPar. 1; ASTPar. 1; GGTPar. 2; ALTPar. 2; ASTPar. 2; GGTPar. 3; ALTPar. 3; ASTPar. 3; GGTPar. 4; ALTPar. 4; ASTPar. 4; GGT
Part A: Exenatide SC Injection212046251876111219172030

[back to top]

Part A: Albumin Level in Urine at Indicated Time Points

Samples were collected to analyze albumin level in urine. Individual Par. data at indicated time point has been collected. (NCT02793154)
Timeframe: Day 5

InterventionMilligrams per liter (Number)
Par. 1Par. 2Par. 3Par. 4
Part A: Exenatide SC Injection353555

[back to top]

Part A: Assessment of Heart Rate (HR) as a Measure of Safety

HR was measured either in a semi-recumbent or seated position after at least a 5-minute rest period. Individual Par. data for HR up to follow-up (up to 12 days) has been presented. (NCT02793154)
Timeframe: Up to 12 days

InterventionBeats per minute (Number)
Par. 1; Day -1Par. 1; Day 1Par. 1; Day 4Par. 1; Day 5Par. 1; Follow-upPar. 2; Day -1Par. 2; Day 1Par. 2; Day 4Par. 2; Day 5Par. 2; Follow-upPar. 3; Day -1Par. 3; Day 1Par. 3; Day 4Par. 3; Day 5Par. 3; Follow-upPar. 4; Day -1Par. 4; Day 1Par. 4; Day 4Par. 4; Day 5Par. 4; Follow-up
Part A: Exenatide SC Injection6965668468576462825872747882787889778272

[back to top]

Part A: Assessment of Nausea by Visual Analogue Scale (VAS) Score

The effect of exenatide on gastric myoelectrical activity was evaluated using EGG with WLT. An EGG with WLT is a standardized test to induce gastric distention and collect VAS of upper gastrointestinal symptoms. The gastric distention produced by the WL induces nausea in Par. allowing the assessment of gastric myoelectrical activity during the episodes of nausea. The intensity of upper gastrointestinal symptom of nausea was measured using VAS ranging from 0 (no nausea) to 100 (severe nausea) immediately before (pre-WL) and 10, 20, 30 minutes post-WL. Individual Par. responses to VAS score scale has been presented. (NCT02793154)
Timeframe: Day 4

InterventionScores on a scale (Number)
Par. 1; Day 4; Pre-WLPar. 1; Day 4; 10 minutes Post-WLPar. 1; Day 4; 20 minutes Post-WLPar. 1; Day 4; 30 minutes Post-WLPar. 2; Day 4; Pre-WLPar. 2; Day 4; 10 minutes Post-WLPar. 2; Day 4; 20 minutes Post-WLPar. 2; Day 4; 30 minutes Post-WLPar. 3; Day 4; Pre-WLPar. 3; Day 4; 10 minutes Post-WLPar. 3; Day 4; 20 minutes Post-WLPar. 3; Day 4; 30 minutes Post-WLPar. 4; Day 4; Pre-WLPar. 4; Day 4; 10 minutes Post-WLPar. 4; Day 4; 20 minutes Post-WLPar. 4; Day 4; 30 minutes Post-WL
Part A: Exenatide SC Injection42433442410004534

[back to top]

Part A: Assessment of Stomach Fullness, Hunger, Bloating and Abdominal Pain by VAS Score

The effect of exenatide on gastric myoelectrical activity was evaluated using EGG with WLT. An EGG with WLT is a standardized test to induce gastric distention and collect VAS of upper gastrointestinal symptoms. The gastric distention produced by the WL induces upper gastrointestinal symptoms including stomach fullness, hunger, bloating and abdominal pain in Par. allowing the assessment of gastric myoelectrical activity. The intensity of upper gastrointestinal symptoms was measured using VAS scores ranging from stomach empty (0) to stomach full (100), hunger (0) to satiety (100) and no bloating (0) to severe bloating (100). Individual Par. responses to VAS has been presented. (NCT02793154)
Timeframe: Day 4

InterventionScores on VAS scale (Number)
Par. 1; Day 4; Pre-WL; Stomach fullnessPar. 1; Day 4; 10 minutes Post-WL;Stomach fullnessPar. 1; Stomach fullness;Day 4; 20 minutes Post-WLPar. 1; Day 4; 30 minutes Post-WL;Stomach fullnessPar. 2; Day 4; Pre-WL;Stomach fullnessPar. 2; Day 4; 10 minutes Post-WL;Stomach fullnessPar. 2; Day 4; 20 minutes Post-WL;Stomach fullnessPar. 2; Day 4; 30 minutes Post-WL;Stomach fullnessPar. 3; Day 4; Pre-WL; Stomach fullnessPar. 3; Day 4; 10 minutes Post-WL;Stomach fullnessPar. 3; Day 4; 20 minutes Post-WL;Stomach fullnessPar. 3; Day 4; 30 minutes Post-WL;Stomach fullnessPar. 4; Day 4; Pre-WL;Stomach fullnessPar. 4; Day 4; 10 minutes Post-WL;Stomach fullnessPar. 4; Day 4; 20 minutes Post-WL;Stomach fullnessPar. 4; Day 4; 30 minutes Post-WL;Stomach fullnessPar. 1; Day 4; Pre-WL; BloatingPar. 1; Day 4; 10 minutes Post-WL;BloatingPar. 1; Day 4; 20 minutes Post-WL;BloatingPar. 1; Day 4; 30 minutes Post-WL; BloatingPar. 2; Day 4; Pre-WL;BloatingPar. 2; Day 4; 10 minutes Post-WL;BloatingPar. 2; Day 4; 20 minutes Post-WL;BloatingPar. 2; Day 4; 30 minutes Post-WL;BloatingPar. 3; Bloating; Day 4; Pre-WL;BloatingPar. 3; Day 4; 10 minutes Post-WL;BloatingPar. 3; Day 4; 20 minutes Post-WL;BloatingPar. 3; Day 4; 30 minutes Post-WL;BloatingPar. 4; Day 4; Pre-WL; BloatingPar. 4; Day 4; 10 minutes Post-WL;BloatingPar. 4; Day 4; 20 minutes Post-WL; BloatingPar. 4; Bloating; Day 4; 30 minutes Post-WLPar. 1; Day 4; Pre-WL; Abdominal painPar. 1; Day 4; 10 minutes Post-WL; Abdominal painPar. 1; Day 4; 20 minutes Post-WL; Abdominal painPar. 1; Day 4; 30 minutes Post-WL;Abdominal painPar. 2; Day 4; Pre-WL; Abdominal painPar. 2; Day 4; 10 minutes Post-WL; Abdominal painPar. 2; Day 4; 20 minutes Post-WL; Abdominal painPar. 2; Day 4; 30 minutes Post-WL;Abdominal painPar. 3; Day 4; Pre-WL; Abdominal painPar. 3;Day 4; 10 minutes Post-WL; Abdominal painPar. 3; Day 4; 20 minutes Post-WL; Abdominal painPar. 3; Day 4; 30 minutes Post-WL; Abdominal painPar. 4; Day 4; Pre-WL; Abdominal painPar. 4; Day 4; 10 minutes Post-WL;Abdominal painPar. 4; Day 4; 20 minutes Post-WL; Abdominal painPar. 4; Day 4; 30 minutes Post-WL; Abdominal painPar. 1; Day 4; Pre-WL; HungerPar. 1; Day 4; 10 minutes Post-WL; HungerPar. 1; Day 4; 20 minutes Post-WL;HungerPar. 1;Day 4; 30 minutes Post-WL;HungerPar. 2; Day 4; Pre-WL;HungerPar. 2; Day 4; 10 minutes Post-WL; HungerPar. 2; Day 4; 20 minutes Post-WL; HungerPar. 2; Day 4; 30 minutes Post-WL; HungerPar. 3; Day 4; Pre-WL; HungerPar. 3; Day 4; 10 minutes Post-WL; HungerPar. 3; Day 4; 20 minutes Post-WL; HungerPar. 3; Day 4; 30 minutes Post-WL;HungerPar. 4; Day 4; Pre-WL;HungerPar. 4; Day 4; 10 minutes Post-WL; HungerPar. 4; Day 4; 20 minutes Post-WL; HungerPar. 4; Day 4; 30 minutes Post-WL;Hunger
Part A: Exenatide SC Injection343509119492851089827528343835427464535626100132242353433447600004455887985843216192721361719162937

[back to top]

Part A: Assessment of Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) as a Measure of Safety

SBP and DBP was measured either in a semi-recumbent or seated position after at least a 5-minute rest period. Individual Par. data for SBP and DBP up to follow-up (up to 12 days) has been presented. (NCT02793154)
Timeframe: Up to 12 days

InterventionMillimeter of mercury (Number)
Par. 1; Day -1; SBPPar. 1; Day 1; SBPPar. 1; Day 4; SBPPar. 1; Day 5; SBPPar. 1; Follow-up; SBPPar. 1; Day -1; DBPPar. 1; Day 1; DBPPar. 1; Day 4; DBPPar. 1; Day 5; DBPPar. 1; Follow-up; DBPPar. 2; Day -1; SBPPar. 2; Day 1; SBPPar. 2; Day 4; SBPPar. 2; Day 5; SBPPar. 2; Follow-up; SBPPar. 2; Day -1; DBPPar. 2; Day 1; DBPPar. 2; Day 4; DBPPar. 2; Day 5; DBPPar. 2; Follow-up; DBPPar. 3; Day -1; SBPPar. 3; Day 1; SBPPar. 3; Day 4; SBPPar. 3; Day 5; SBPPar. 3; Follow-up; SBPPar. 3; Day -1; DBPPar. 3; Day 1; DBPPar. 3; Day 4; DBPPar. 3; Day 5; DBPPar. 3; Follow-up; DBPPar. 4; Day -1; SBPPar. 4; Day 1; SBPPar. 4; Day 4; SBPPar. 4; Day 5; SBPPar. 4; Follow-up; SBPPar. 4; Day -1; DBPPar. 4; Day 1; DBPPar. 4; Day 4; DBPPar. 4; Day 5; DBPPar. 4; Follow-up; DBP
Part A: Exenatide SC Injection1261211241121257161696772105109119121124616871687513113113211212686828776871381391271231608390838186

[back to top]

Part A: Average Dominant Frequency

The effect of exenatide on gastric myoelectrical activity was assessed by EGG using WLT. An EGG with WLT is a standardized test to induce gastric distention and measure myoelectrical responses. The gastric myoelectrical activity is generated by the pacemaker interstitial cells at a normal frequency of 3 cycles per minute. The shift of frequency from normal gastric myoelectrical activity to a slower rhythm is bradygastria or faster rhythm is tachygastria. Individual Par. data for average dominant frequency in the bradygastria, normal, tachygastria and duodenal range after treatment with exenatide at Pre-WL and 10, 20, 30 minutes post-WL has been presented. (NCT02793154)
Timeframe: Up to Day 4

InterventionCycles per minute (Number)
Par. 1; Day 1; Pre-WL; BradygastriaPar. 1; Day 1; 10 minutes Post-WL; BradygastriaPar. 1; Day 1; 20 minutes Post-WL; BradygastriaPar. 1; Day 1; 30 minutes Post-WL; BradygastriaPar. 1; Day 4; Pre-WL; BradygastriaPar. 1; Day 4; 10 minutes Post-WL; BradygastriaPar. 1; Day 4; 20 minutes Post-WL; BradygastriaPar. 1; Day 4; 30 minutes Post-WL; BradygastriaPar. 2; Day 1; Pre-WL; BradygastriaPar. 2; Day 1; 10 minutes Post-WL; BradygastriaPar. 2; Day 1; 20 minutes Post-WL; BradygastriaPar. 2; Day 1; 30 minutes Post-WL; BradygastriaPar. 2; Day 4; Pre-WL; BradygastriaPar. 2; Day 4; 10 minutes Post-WL; BradygastriaPar. 2; Day 4; 20 minutes Post-WL; BradygastriaPar. 2; Day 4; 30 minutes Post-WL; BradygastriaPar. 3; Day 1; Pre-WL; BradygastriaPar. 3; Day 1; 10 minutes Post-WL; BradygastriaPar. 3; Day 1; 20 minutes Post-WL; NormalPar. 3; Day 1; 30 minutes Post-WL; TachygastriaPar. 3; Day 4; Pre-WL; BradygastriaPar. 3; Day 4; 10 minutes Post-WL; BradygastriaPar. 3; Day 4; 20 minutes Post-WL; BradygastriaPar. 3; Day 4; 30 minutes Post-WL; BradygastriaPar. 4; Day 1; Pre-WL; BradygastriaPar. 4; Day 1; 10 minutes Post-WL; BradygastriaPar. 4; Day 1; 20 minutes Post-WL; BradygastriaPar. 4; Day 1; 30 minutes Post-WL; BradygastriaPar. 4; Day 4; Pre-WL; BradygastriaPar. 4; Day 4; 10 minutes Post-WL; BradygastriaPar. 4; Day 4; 20 minutes Post-WL; BradygastriaPar. 4; Day 4; 30 minutes Post-WL; Normal
Part A: Exenatide SC Injection1.50.751.252.191.050.961.252.38111.51.750.751.3812.420.961.8334.131.21.50.941.50.861.881.71.191.20.941.292.9

[back to top]

Part A: Basophils, Eosinophil, Lymphocytes, Monocytes, Platelet Count, Total Neutrophils, White Blood Cell (WBC) Level at Indicated Time Points

Blood samples were collected for analysis of hematology parameters including basophils, eosinophil, lymphocytes, monocytes, platelet count, total neutrophils, and WBC. Individual Par. data at indicated time point has been presented. (NCT02793154)
Timeframe: Day 5

InterventionGiga unit per liter (Number)
Par.1; BasophilsPar.1; EosinophilsPar.1; LymphocytesPar.1; MonocytesPar.1; Platelet countPar.1; Total NeutrophilsPar.1; WBCPar.2; BasophilsPar.2; EosinophilsPar.2; LymphocytesPar.2; MonocytesPar.2; Platelet countPar.2; Total NeutrophilsPar.2; WBCPar.3; BasophilsPar.3; EosinophilsPar.3; LymphocytesPar.3; MonocytesPar.3; Platelet countPar.3; Total NeutrophilsPar.3; WBCPar.4; BasophilsPar.4; EosinophilsPar.4; LymphocytesPar.4; MonocytesPar.4; Platelet countPar.4; Total NeutrophilsPar.4; WBC
Part A: Exenatide SC Injection0.020.111.570.352686.338.40.020.041.390.252172.544.20.030.211.770.582025.097.70.040.233.060.892301.25.4

[back to top]

Part A: Concentration of Creatinine in Urine at Indicated Time Points

Samples were collected to analyze concentration of creatinine in urine. Individual Par. at indicated time point has been presented at indicated time points. (NCT02793154)
Timeframe: Day 5

InterventionMicromoles per liter (Number)
Par. 1Par. 2Par. 3Par. 4
Part A: Exenatide SC Injection12450162401330022020

[back to top]

Part A: Creatinine, Direct Bilirubin, Total Bilirubin, Indirect Bilirubin Levels at Indicated Time Points

Blood samples were collected for analysis of clinical chemistry parameters including creatinine, direct bilirubin, total bilirubin, indirect bilirubin levels. Individual Par. data at indicated time points has been presented. (NCT02793154)
Timeframe: Day 5

InterventionMicromoles per liter (Number)
Par. 1; CreatininePar. 1; Direct BilirubinPar. 1; Total BilirubinPar. 1; Indirect BilirubinPar. 2; CreatininePar. 2; Direct BilirubinPar. 2; Total BilirubinPar. 2; Indirect BilirubinPar. 3; CreatininePar. 3; Direct BilirubinPar. 3; Total BilirubinPar. 3; Indirect BilirubinPar. 4; CreatininePar. 4; Direct BilirubinPar. 4; Total BilirubinPar. 4; Indirect Bilirubin
Part A: Exenatide SC Injection67.22108105.226476.94161283.1264

[back to top]

Part A: Distribution of Average Power by Frequency Region

The effect of exenatide on gastric myoelectrical activity was assessed by electrogastrogram (EGG) using water load test (WLT). EGG with WLT is a standardized test to induce gastric distention and measure myoelectrical responses. The gastric myoelectrical activity is generated by the pacemaker interstitial cells at a normal frequency of 3 cycles per minute. The shift of frequency from normal gastric myoelectrical activity to a slower rhythm is bradygastria or faster rhythm is tachygastria. Individual Par. data for distribution of average power in the bradygastria, normal, tachygastria and duodenal range during pre-WL and 10, 20 and 30 minutes post-WL after treatment with exenatide has been presented. The analysis was performed on Pharmacodynamic Population, which included all Par. who received at least one dose of study medication and had valid data. (NCT02793154)
Timeframe: Up to Day 4

InterventionPercentage of power (Number)
Par. 1; Day 1; Pre-WL; BradygastriaPar. 1; Day 1; Pre-WL; NormalPar. 1; Day 1; Pre-WL; TachygastriaPar. 1; Day 1; Pre-WL; DuodenalPar. 1; Day 1; 10 minutes Post-WL; BradygastriaPar. 1; Day 1; 10 minutes Post-WL; NormalPar. 1; Day 1; 10 minutes Post-WL; TachygastriaPar. 1; Day 1; 10 minutes Post-WL; DuodenalPar. 1; Day 1; 20 minutes Post-WL; BradygastriaPar. 1; Day 1; 20 minutes Post-WL; NormalPar. 1; Day 1; 20 minutes Post-WL; TachygastriaPar. 1; Day 1; 20 minutes Post-WL; DuodenalPar. 1; Day 1; 30 minutes Post-WL; BradygastriaPar. 1; Day 1; 30 minutes Post-WL; NormalPar. 1; Day 1; 30 minutes Post-WL; TachygastriaPar. 1; Day 1; 30 minutes Post-WL; DuodenalPar. 1; Day 4; Pre-WL; BradygastriaPar. 1; Day 4; Pre-WL; NormalPar. 1; Day 4; Pre-WL; TachygastriaPar. 1; Day 4; Pre-WL; DuodenalPar. 1; Day 4; 10 minutes Post-WL; BradygastriaPar. 1; Day 4; 10 minutes Post-WL; NormalPar. 1; Day 4; 10 minutes Post-WL; TachygastriaPar. 1; Day 4; 10 minutes Post-WL; DuodenalPar. 1; Day 4; 20 minutes Post-WL; BradygastriaPar. 1; Day 4; 20 minutes Post-WL; NormalPar. 1; Day 4; 20 minutes Post-WL; TachygastriaPar. 1; Day 4; 20 minutes Post-WL; DuodenalPar. 1; Day 4; 30 minutes Post-WL; BradygastriaPar. 1; Day 4; 30 minutes Post-WL; NormalPar. 1; Day 4; 30 minutes Post-WL; TachygastriaPar. 1; Day 4; 30 minutes Post-WL; DuodenalPar. 2; Day 1; Pre-WL; BradygastriaPar. 2; Day 1; Pre-WL; NormalPar. 2; Day 1; Pre-WL; TachygastriaPar. 2; Day 1; Pre-WL; DuodenalPar. 2; Day 1; 10 minutes Post-WL; BradygastriaPar. 2; Day 1; 10 minutes Post-WL; NormalPar. 2; Day 1; 10 minutes Post-WL; TachygastriaPar. 2; Day 1; 10 minutes Post-WL; DuodenalPar. 2; Day 1; 20 minutes Post-WL; BradygastriaPar. 2; Day 1; 20 minutes Post-WL; NormalPar. 2; Day 1; 20 minutes Post-WL; TachygastriaPar. 2; Day 1; 20 minutes Post-WL; DuodenalPar. 2; Day 1; 30 minutes Post-WL; BradygastriaPar. 2; Day 1; 30 minutes Post-WL; NormalPar. 2; Day 1; 30 minutes Post-WL; TachygastriaPar. 2; Day 1; 30 minutes Post-WL; DuodenalPar. 2; Day 4; Pre-WL; BradygastriaPar. 2; Day 4; Pre-WL; NormalPar. 2; Day 4; Pre-WL; TachygastriaPar. 2; Day 4; Pre-WL; DuodenalPar. 2; Day 4; 10 minutes Post-WL; BradygastriaPar. 2; Day 4; 10 minutes Post-WL; NormalPar. 2; Day 4; 10 minutes Post-WL; TachygastriaPar. 2; Day 4; 10 minutes Post-WL; DuodenalPar. 2; Day 4; 20 minutes Post-WL; BradygastriaPar. 2; Day 4; 20 minutes Post-WL; NormalPar. 2; Day 4; 20 minutes Post-WL; TachygastriaPar. 2; Day 4; 20 minutes Post-WL; DuodenalPar. 2; Day 4; 30 minutes Post-WL; BradygastriaPar. 2; Day 4; 30 minutes Post-WL; NormalPar. 2; Day 4; 30 minutes Post-WL; TachygastriaPar. 2; Day 4; 30 minutes Post-WL; DuodenalPar. 3; Day 1; Pre-WL; BradygastriaPar. 3; Day 1; Pre-WL; NormalPar. 3; Day 1; Pre-WL; TachygastriaPar. 3; Day 1; Pre-WL; DuodenalPar. 3; Day 1; 10 minutes Post-WL; BradygastriaPar. 3; Day 1; 10 minutes Post-WL; NormalPar. 3; Day 1; 10 minutes Post-WL; TachygastriaPar. 3; Day 1; 10 minutes Post-WL; DuodenalPar. 3; Day 1; 20 minutes Post-WL; BradygastriaPar. 3; Day 1; 20 minutes Post-WL; NormalPar. 3; Day 1; 20 minutes Post-WL; TachygastriaPar. 3; Day 1; 20 minutes Post-WL; DuodenalPar. 3; Day 1; 30 minutes Post-WL; BradygastriaPar. 3; Day 1; 30 minutes Post-WL; NormalPar. 3; Day 1; 30 minutes Post-WL; TachygastriaPar. 3; Day 1; 30 minutes Post-WL; DuodenalPar. 3; Day 4; Pre-WL; BradygastriaPar. 3; Day 4; Pre-WL; NormalPar. 3; Day 4; Pre-WL; TachygastriaPar. 3; Day 4; Pre-WL; DuodenalPar. 3; Day 4; 10 minutes Post-WL; BradygastriaPar. 3; Day 4; 10 minutes Post-WL; NormalPar. 3; Day 4; 10 minutes Post-WL; TachygastriaPar. 3; Day 4; 10 minutes Post-WL; DuodenalPar. 3; Day 4; 20 minutes Post-WL; BradygastriaPar. 3; Day 4; 20 minutes Post-WL; NormalPar. 3; Day 4; 20 minutes Post-WL; TachygastriaPar. 3; Day 4; 20 minutes Post-WL; DuodenalPar. 3; Day 4; 30 minutes Post-WL; BradygastriaPar. 3; Day 4; 30 minutes Post-WL; NormalPar. 3; Day 4; 30 minutes Post-WL; TachygastriaPar. 3; Day 4; 30 minutes Post-WL; DuodenalPar. 4; Day 1; Pre-WL; BradygastriaPar. 4; Day 1; Pre-WL; NormalPar. 4; Day 1; Pre-WL; TachygastriaPar. 4; Day 1; Pre-WL; DuodenalPar. 4; Day 1; 10 minutes Post-WL; BradygastriaPar. 4; Day 1; 10 minutes Post-WL; NormalPar. 4; Day 1; 10 minutes Post-WL; TachygastriaPar. 4; Day 1; 10 minutes Post-WL; DuodenalPar. 4; Day 1; 20 minutes Post-WL; BradygastriaPar. 4; Day 1; 20 minutes Post-WL; NormalPar. 4; Day 1; 20 minutes Post-WL; TachygastriaPar. 4; Day 1; 20 minutes Post-WL; DuodenalPar. 4; Day 1; 30 minutes Post-WL; BradygastriaPar. 4; Day 1; 30 minutes Post-WL; NormalPar. 4; Day 1; 30 minutes Post-WL; TachygastriaPar. 4; Day 1; 30 minutes Post-WL; DuodenalPar. 4; Day 4; Pre-WL; BradygastriaPar. 4; Day 4; Pre-WL; NormalPar. 4; Day 4; Pre-WL; TachygastriaPar. 4; Day 4; Pre-WL; DuodenalPar. 4; Day 4; 10 minutes Post-WL; BradygastriaPar. 4; Day 4; 10 minutes Post-WL; NormalPar. 4; Day 4; 10 minutes Post-WL; TachygastriaPar. 4; Day 4; 10 minutes Post-WL; DuodenalPar. 4; Day 4; 20 minutes Post-WL; BradygastriaPar. 4; Day 4; 20 minutes Post-WL; NormalPar. 4; Day 4; 20 minutes Post-WL; TachygastriaPar. 4; Day 4; 20 minutes Post-WL; DuodenalPar. 4; Day 4; 30 minutes Post-WL; BradygastriaPar. 4; Day 4; 30 minutes Post-WL; NormalPar. 4; Day 4; 30 minutes Post-WL; TachygastriaPar. 4; Day 4; 30 minutes Post-WL; Duodenal
Part A: Exenatide SC Injection56.1523.49173.3593.972.92.40.7357.1323.2913.176.4143.4436.1617.782.6271.94139.515.5543.9912.9428.3314.7473.8710.978.776.3948.8716.6623.1611.3167.4410.6717.24.6894.052.462.830.6785.6411.722.430.2277.3415.576.230.8643.3223.8218.7114.1484.237.936.811.0266.3219.4311.72.5573.0519.646.470.8459.669.0522.398.9132.7311.0348.777.4729.9422.8439.727.516.3222.4854.776.4352.8516.6413.2117.2964.2710.3713.2612.171.6611.119.527.7253.978.6116.1221.382.476.667.863.0181.895.611.630.8862.9612.8417.047.1773.6412.711.12.5654.9817.622.974.4583.74.210.691.482.965.9210.11.0239.0142.6116.771.62

[back to top]

Part A: Estimated Glomerular Filtration Rate at Indicated Time Points

"Estimated glomerular filtration rate was calculated using the modification of diet in renal disease (MDRD) formula by multiplying 175 with serum creatinine^-1.154 multiplied by age^-0.203 multiplied by 0.742 (if female) multiplied by 1.212 (if African American Par.). Individual Par. data at indicated time point has been presented." (NCT02793154)
Timeframe: Day 5

InterventionMilliliter per second per 1.73 meter ^2 (Number)
Part. 1Part. 2Part. 3Part. 4
Part A: Exenatide SC Injection1.30261.28591.51971.6533

[back to top]

Part A: Gastroparesis Cardinal Symptom Index -Daily Diary (GCSI-DD) Score

GCSI-DD is a questionnaire of gastroparesis symptom severity covering the following domains: episodes (epi) of vomiting, epi of retching, nausea/vomiting, fullness/early satiety, and bloating. GCSI-DD contains two symptom severity items upper abdominal pain and overall rating of gastroparesis symptoms. Par. rate each symptom on a 6-point scale from 0 (none), 1 (very mild), 2 (mild), 3 (moderate), 4 (severe),to 5 (very severe). Individual Par. data has been presented. All Subjects Population was used which consisted of all Par. who received at least one dose of study medication. (NCT02793154)
Timeframe: Up to Day 5

InterventionScores on GCSI-DD scale (Number)
Par. 1; Day-1; Epi of vomitingPar. 1; Day 1; Epi of vomitingPar. 1; Day 4; Epi of vomitingPar. 1; Day 5; Epi of vomitingPar. 1; Day -1; Epi of retchingPar. 1; Day 1; Epi of retchingPar. 1; Day 4; Epi of retchingPar. 1; Day 5; Epi of retchingPar 1; Day -1; NauseaPar 1; Day 1; NauseaPar 1; Day 4; NauseaPar 1; Day 5; NauseaPar 1; Day -1; Excessively full after mealsPar 1; Day 1; Excessively full after mealsPar 1; Day 4; Excessively full after mealsPar 1; Day 5; Excessively full after mealsPar 1; Day -1; BloatingPar 1; Day 1; BloatingPar 1; Day 4; BloatingPar 1; Day 5; BloatingPar 1; Day -1; Unable to finish normal-sized mealPar 1; Day 1; Unable to finish normal-sized mealPar 1; Day 4; Unable to finish normal-sized mealPar 1; Day 5; Unable to finish normal-sized mealPar 1; Day -1; RetchingPar 1; Day 1; RetchingPar 1; Day 4; RetchingPar 1; Day 5; RetchingPar 1; Day -1; VomitingPar 1; Day 1; VomitingPar 1; Day 4; VomitingPar 1; Day 5; VomitingPar 1; Day -1; Stomach or belly visibly largerPar 1; Day 1; Stomach or belly visibly largerPar 1; Day 4; Stomach or belly visibly largerPar 1; Day 5; Stomach or belly visibly largerPar 1; Day -1; Stomach fullnessPar 1; Day 1; Stomach fullnessPar 1; Day 4; Stomach fullnessPar 1; Day 5; Stomach fullnessPar 1; Day -1; Loss of appetitePar 1; Day 1; Loss of appetitePar 1; Day 4; Loss of appetitePar 1; Day 5; Loss of appetitePar 1; Day -1; Upper abdominal painPar 1; Day 1; Upper abdominal painPar 1; Day 4; Upper abdominal painPar 1; Day 5; Upper abdominal painPar 1; Day -1; Upper abdominal discomfortPar 1; Day 1; Upper abdominal discomfortPar 1; Day 4; Upper abdominal discomfortPar 1; Day 5; Upper abdominal discomfortPar 1; Day -1; Overall severity of gastroparesisPar 1; Day 1; Overall severity of gastroparesisPar 1; Day 4; Overall severity of gastroparesisPar 1; Day 5; Overall severity of gastroparesisPar. 2; Day -1; Epi of vomitingPar. 2; Day 1; Epi of vomitingPar. 2; Day 4; Epi of vomitingPar. 2; Day 5; Epi of vomitingPar. 2; Day -1; Epi of retchingPar. 2; Day 1; Epi of retchingPar. 2; Day 4; Epi of retchingPar. 2; Day 5; Epi of retchingPar. 2; Day -1; NauseaPar. 2 Day 1; NauseaPar. 2; Day 4; NauseaPar. 2; Day 5; NauseaPar. 2; Day -1; Excessively full after mealsPar. 2; Day 1; Excessively full after mealsPar. 2; Day 4; Excessively full after mealsPar. 2; Day 5; Excessively full after mealsPar. 2; Day -1; BloatingPar. 2; Day 1; BloatingPar. 2; Day 4; BloatingPar. 2; Day 5; BloatingPar. 2; Day -1; Unable to finish normal-sized mealPar. 2; Day 1; Unable to finish normal-sized mealPar. 2; Day 4; Unable to finish normal-sized mealPar. 2; Day 5; Unable to finish normal-sized mealPar. 2; Day -1; RetchingPar. 2; Day 1; RetchingPar. 2; Day 4; RetchingPar. 2; Day 5; RetchingPar. 2; Day -1; VomitingPar. 2; Day 1; VomitingPar. 2; Day 4; VomitingPar. 2; Day 5; VomitingPar. 2; Day -1; Stomach or belly visibly largerPar. 2; Day 1; Stomach or belly visibly largerPar. 2; Day 4; Stomach or belly visibly largerPar. 2; Day 5; Stomach or belly visibly largerPar. 2; Day -1; Stomach fullnessPar. 2; Day 1; Stomach fullnessPar. 2; Day 4; Stomach fullnessPar. 2; Day 5; Stomach fullnessPar. 2; Day -1; Loss of appetitePar. 2; Day 1; Loss of appetitePar. 2; Day 4; Loss of appetitePar. 2; Day 5; Loss of appetitePar. 2; Day -1; Upper abdominal painPar. 2; Day 1; Upper abdominal painPar. 2; Day 4; Upper abdominal painPar. 2; Day 5; Upper abdominal painPar. 2; Day -1; Upper abdominal discomfortPar. 2; Day 1; Upper abdominal discomfortPar. 2; Day 4; Upper abdominal discomfortPar. 2; Day 5; Upper abdominal discomfortPar. 2; Day -1; Overall severity of gastroparesisPar. 2; Day 1; Overall severity of gastroparesisPar. 2; Day 4; Overall severity of gastroparesisPar. 2; Day 5; Overall severity of gastroparesisPar. 3; Day -1; Epi of vomitingPar. 3; Day 1; Epi of vomitingPar. 3; Day 4; Epi of vomitingPar. 3; Day 5; Epi of vomitingPar. 3; Day -1; Epi of retchingPar. 3; Day 1; Epi of retchingPar. 3; Day 4; Epi of retchingPar. 3; Day 5; Epi of retchingPar. 3; Day -1; NauseaPar. 3; Day 1; NauseaPar. 3; Day 4; NauseaPar. 3; Day 5; NauseaPar. 3; Day -1; Excessively full after mealsPar. 3; Day 1; Excessively full after mealsPar. 3; Day 4; Excessively full after mealsPar. 3; Day 5; Excessively full after mealsPar. 3; Day -1; BloatingPar. 3; Day 1; BloatingPar. 3; Day 4; BloatingPar. 3; Day 5; BloatingPar. 3; Day -1; Unable to finish normal-sized mealPar. 3; Day 1; Unable to finish normal-sized mealPar. 3; Day 4; Unable to finish normal-sized mealPar. 3; Day 5; Unable to finish normal-sized mealPar. 3; Day -1; RetchingPar. 3; Day 1; RetchingPar. 3; Day 4; RetchingPar. 3; Day 5; RetchingPar. 3; Day -1; VomitingPar. 3; Day 1; VomitingPar. 3; Day 4; VomitingPar. 3; Day 5; VomitingPar. 3; Day -1; Stomach or belly visibly largerPar. 3; Day 1; Stomach or belly visibly largerPar. 3; Day 4; Stomach or belly visibly largerPar. 3; Day 5; Stomach or belly visibly largerPar. 3; Day -1; Stomach fullnessPar. 3; Day 1; Stomach fullnessPar. 3; Day 4; Stomach fullnessPar. 3; Day 5; Stomach fullnessPar. 3; Day -1; Loss of appetitePar. 3; Day 1; Loss of appetitePar. 3; Day 4; Loss of appetitePar. 3; Day 5; Loss of appetitePar. 3; Day -1; Upper abdominal painPar. 3; Day 1; Upper abdominal painPar. 3; Day 4; Upper abdominal painPar. 3; Day 5; Upper abdominal painPar. 3; Day -1; Upper abdominal discomfortPar. 3; Day 1; Upper abdominal discomfortPar. 3; Day 4; Upper abdominal discomfortPar. 3; Day 5; Upper abdominal discomfortPar. 3; Day -1; Overall severity of gastroparesisPar. 3; Day 1; Overall severity of gastroparesisPar. 3; Day 4; Overall severity of gastroparesisPar. 3; Day 5; Overall severity of gastroparesisPar. 4; Day -1; Epi of vomitingPar. 4; Day 1; Epi of vomitingPar. 4; Day 4; Epi of vomitingPar. 4; Day 5; Epi of vomitingPar. 4; Day -1; Epi of retchingPar. 4; Day 1; Epi of retchingPar. 4; Day 4; Epi of retchingPar. 4; Day 5; Epi of retchingPar. 4; Day -1; NauseaPar. 4; Day 1; NauseaPar. 4; Day 4; NauseaPar. 4; Day 5; NauseaPar. 4; Day -1; Excessively full after mealsPar. 4; Day 1; Excessively full after mealsPar. 4; Day 4; Excessively full after mealsPar. 4; Day 5; Excessively full after mealsPar. 4; Day -1; BloatingPar. 4; Day 1; BloatingPar. 4; Day 4; BloatingPar. 4; Day 5; BloatingPar.4; Day -1; Unable to finish normal-sized mealPar.4; Day 1; Unable to finish normal-sized mealPar.4; Day 4; Unable to finish normal-sized mealPar.4; Day 5; Unable to finish normal-sized mealPar. 4; Day -1; RetchingPar. 4; Day 1; RetchingPar. 4; Day 4; RetchingPar. 4; Day 5; RetchingPar. 4; Day -1; VomitingPar. 4; Day 1; VomitingPar. 4; Day 4; VomitingPar. 4; Day 5; VomitingPar. 4; Day -1; Stomach or belly visibly largerPar. 4; Day 1; Stomach or belly visibly largerPar. 4; Day 4; Stomach or belly visibly largerPar. 4; Day 5; Stomach or belly visibly largerPar. 4; Day -1; Stomach fullnessPar. 4; Day 1; Stomach fullnessPar. 4; Day 4; Stomach fullnessPar. 4; Day 5; Stomach fullnessPar. 4; Day -1; Loss of appetitePar. 4; Day 1; Loss of appetitePar. 4; Day 4; Loss of appetitePar. 4; Day 5; Loss of appetitePar. 4; Day -1; Upper abdominal painPar. 4; Day 1; Upper abdominal painPar. 4; Day 4; Upper abdominal painPar. 4; Day 5; Upper abdominal painPar. 4; Day -1; Upper abdominal discomfortPar. 4; Day 1; Upper abdominal discomfortPar. 4; Day 4; Upper abdominal discomfortPar. 4; Day 5; Upper abdominal discomfortPar. 4; Day -1; Overall severity of gastroparesisPar. 4; Day 1; Overall severity of gastroparesisPar. 4; Day 4; Overall severity of gastroparesisPar. 4; Day 5; Overall severity of gastroparesis
Part A: Exenatide SC Injection00000000002122520005225200210000000022552202000300030004000000000000000000000000000000000000001000000000000000000000000000000000000000000000000000000000000000000000000000000000000001100100000000000000000001100000000000000110

[back to top]

Part A: Glucose, Calcium, Magnesium, Potassium, Sodium, Phosphorus Inorganic, Chloride, Urea/Blood Urea Nitrogen (BUN) Levels

Blood samples were collected for analysis of glucose, calcium, magnesium, potassium, sodium, phosphorus inorganic, chloride, and urea/BUN levels. Individual Par. data at indicated time point has been presented. (NCT02793154)
Timeframe: Day 5

InterventionMillimoles per liter (Number)
Par. 1; GlucosePar. 1; CalciumPar. 1; MagnesiumPar. 1; PotassiumPar. 1; SodiumPar. 1; Phosphorus inorganicPar. 1; ChloridePar. 1; Urea/BUNPar. 2; GlucosePar. 2; CalciumPar. 2; MagnesiumPar. 2; PotassiumPar. 2; SodiumPar. 2; Phosphorus inorganicPar. 2; ChloridePar. 2; Urea/BUNPar. 3; GlucosePar. 3; CalciumPar. 3; MagnesiumPar. 3; PotassiumPar. 3; SodiumPar. 3; Phosphorus inorganicPar. 3; ChloridePar. 3; Urea/BUNPar. 4; GlucosePar. 4; CalciumPar. 4; MagnesiumPar. 4; PotassiumPar. 4; SodiumPar. 4; Phosphorus inorganicPar. 4; ChloridePar. 4; Urea/BUN
Part A: Exenatide SC Injection9.22.440.865.61391.51057.57.52.440.95.11391.251056.59.12.380.84.21401.210377.92.40.84.31381.151014.5

[back to top]

Number of Participants With Abnormal Urinalysis

Urinalysis parameters included assessment of specific gravity, microscopic analysis, and potential of hydrogen (pH), glucose, protein, blood and ketones by dipstick method. (NCT02802514)
Timeframe: Up to Week 11

InterventionParticipants (Count of Participants)
Albiglutide 50 mg0
Exenatide 10 µg0

[back to top]

Number of Participants With Abnormal Heart Rate for Session 1

Data of participants with abnormal heart rate (measured during site visits by sphygmomanometer) were reported. Participants with low and high heart rate has been presented. Potential clinical concern value for heart rate is < 50 beats per minute to > 120 beats per minute. Safety Population comprised of all participants who received at least one dose of the study treatment. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: -2 hour pre-MRI, 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
Day 5, high, n=0, 0, 0, 2Day 5, low, n=0, 0, 0, 2
Off-therapy Visit00

[back to top]

Number of Participants With Abnormal Heart Rate for Session 1

Data of participants with abnormal heart rate (measured during site visits by sphygmomanometer) were reported. Participants with low and high heart rate has been presented. Potential clinical concern value for heart rate is < 50 beats per minute to > 120 beats per minute. Safety Population comprised of all participants who received at least one dose of the study treatment. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: -2 hour pre-MRI, 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
Day 1, Pre MRI, high, n=0, 0, 2, 0Day 1, Pre MRI, low, n=0, 0, 2, 0Day 1, Post MRI 0.5 hr, high, n=0, 0, 2, 0Day 1, Post MRI 0.5 hr, low, n=0, 0, 2, 0
Off-therapy MRI Arm0000

[back to top]

Number of Participants With Abnormal Heart Rate for Session 2

Data of participants with abnormal heart rate (measured during site visits by sphygmomanometer) were reported. Participants with low and high heart rate has been presented. Potential clinical concern value for heart rate is < 50 beats per minute to > 120 beats per minute. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: -2 hour pre-MRI, 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
Day 4, -2 hr pre-MRI, high, n=1, 1,0, 0Day 4, -2 hr pre-MRI, low, n=1, 1, 0, 0Day 4, Post MRI 0.5 hr, high, n=1, 1, 0, 0Day 4, 0.5 hr Post MRI, low, n=1, 1, 0, 0Day 4, 1 hr Post MRI, high, n=1, 1, 0, 0Day 4, 1 hr Post MRI, low, n=1, 1, 0, 0Day 8, -2 hr pre-MRI, high, n=1, 1, 0, 0Day 8, -2 hr pre-MRI, low, n=1, 1, 0, 0Day 8, 0.5 hr Post MRI, high, n=1, 1, 0, 0Day 8, 0.5 hr Post MRI, low, n=1, 1, 0, 0
Albiglutide 50 mg0000000000

[back to top]

Number of Participants With Abnormal Heart Rate for Session 2

Data of participants with abnormal heart rate (measured during site visits by sphygmomanometer) were reported. Participants with low and high heart rate has been presented. Potential clinical concern value for heart rate is < 50 beats per minute to > 120 beats per minute. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: -2 hour pre-MRI, 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
Day 4, -2 hr pre-MRI, high, n=1, 1,0, 0Day 4, -2 hr pre-MRI, low, n=1, 1, 0, 0Day 4, Post MRI 0.5 hr, high, n=1, 1, 0, 0Day 4, 0.5 hr Post MRI, low, n=1, 1, 0, 0Day 4, 1 hr Post MRI, high, n=1, 1, 0, 0Day 4, 1 hr Post MRI, low, n=1, 1, 0, 0Day 8, -2 hr pre-MRI, high, n=1, 1, 0, 0Day 8, -2 hr pre-MRI, low, n=1, 1, 0, 0Day 8, 0.5 hr Post MRI, high, n=1, 1, 0, 0Day 8, 0.5 hr Post MRI, low, n=1, 1, 0, 0Day 8, 1 hr Post MRI, high, n=0, 1, 0, 0Day 8, 1 hr Post MRI, low, n=0, 1, 0, 0
Exenatide 10 µg000000000000

[back to top]

Number of Participants With Abnormal Heart Rate for Session 2

Data of participants with abnormal heart rate (measured during site visits by sphygmomanometer) were reported. Participants with low and high heart rate has been presented. Potential clinical concern value for heart rate is < 50 beats per minute to > 120 beats per minute. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: -2 hour pre-MRI, 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
Day 5, high, n=0, 0, 0, 2Day 5, low, n=0, 0, 0, 2
Off-therapy Visit00

[back to top]

Number of Participants With Abnormal Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) for Session 1

SBP and DBP were measured in supine position after 5 minutes rest. Data for Session 1 and 2 and for Pre and Post MRI has been presented. Potential clinical concern value for SBP is <100 millimeters of mercury (mmHg) and >170 mmHg. Potential clinical concern value for DBP is <50 mmHg and >110 mmHg. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
SBP, Day 4,-2 hr pre-MRI, high, n=1,1, 0, 0SBP, Day 4,-2 hr pre-MRI, low, n=1,1, 0, 0SBP, Day 4,0.5 hr post MRI , high, n=1,1, 0, 0SBP, Day 4,0.5 hr post MRI, low, n=1,1, 0, 0SBP, Day 4,1 hr post MRI , high, n=1,1, 0, 0SBP, Day 4,1 hr post MRI , low, n=1,1, 0, 0SBP, Day 8,0.5 hr Post MRI, high, n=1,1, 0, 0SBP, Day 8,0.5 hr Post MRI, low, n=1,1, 0, 0DBP, Day 4,-2 hr pre-MRI, high, n=1,1, 0, 0DBP, Day 4,-2 hr pre-MRI, low, n=1,1, 0, 0DBP, Day 4,0.5 hr Post MRI, high,n= 1,1, 0, 0DBP, Day 4,0.5 hr Post MRI, low,n= 1,1, 0, 0DBP, Day 4,1 hr post MRI, high,n= 1,1, 0, 0DBP, Day 4,1 hr post MRI , low,n= 1,1, 0, 0DBP, Day 8, 0.5 hr post MRI ,high, n=1,1,0, 0DBP, Day 8, 0.5 hr post MRI, low, n= 1,1, 0, 0
Albiglutide 50 mg0000000000000000

[back to top]

Number of Participants With Non-serious Adverse Events (AE) With Incidence > = 2 % and Serious AEs (SAE)

An AE is any untoward medical occurrence in a clinical investigation participant, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. Any untoward event resulting in death, life threatening, requires hospitalization or prolongation of existing hospitalization; results in disability/incapacity, congenital anomaly/birth defect or any other situation according to medical or scientific judgment were categorized as SAE. Data of participants with non-serious AEs ( with incidence >= 2%) and SAEs has been presented. Placebo was included to maintain the single blind only; similar to double dummy. (NCT02802514)
Timeframe: Up to Week 13

,,,
InterventionParticipants (Count of Participants)
Non-serious AEsSAE
Albiglutide 50 mg10
Albiglutide Matching Placebo00
Exenatide 10 µg00
Exenatide Matching Placebo00

[back to top]

Number of Participants With Abnormal Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) for Session 1

SBP and DBP were measured in supine position after 5 minutes rest. Data for Session 1 and 2 and for Pre and Post MRI has been presented. Potential clinical concern value for SBP is <100 millimeters of mercury (mmHg) and >170 mmHg. Potential clinical concern value for DBP is <50 mmHg and >110 mmHg. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
SBP, Day 1, Pre-MRI, high, n=0, 0, 2, 0SBP, Day 1, Pre-MRI, low, n=0, 0, 2, 0SBP, Day 1, 0.5 hr post MRI, high, n=0, 0, 2, 0SBP, Day 1,0.5 hr post MRI , low, n=0, 0, 2, 0DBP, Day 1, Pre MRI, high,n= 0,0, 2, 0DBP, Day 1, Pre MRI, low,n= 0, 0, 2, 0DBP, Day 1,0.5 hr post MRI, high,n= 0, 0, 2, 0DBP, Day 1,0.5 hr post MRI, low,n= 0, 0, 2, 0
Off-therapy MRI Arm00000000

[back to top]

Number of Participants With Abnormal SBP and DBP for Session 2

SBP and DBP were measured in supine position after 5 minutes rest. Data for Session 1 and 2 and for Pre and Post MRI has been presented. Potential clinical concern value for SBP is <100 millimeters of mercury (mmHg) and >170 mmHg. Potential clinical concern value for DBP is <50 mmHg and >110 mmHg. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
SBP, Day 5, high, n=0, 0, 0, 2SBP, Day 5, low, n=0, 0, 0, 2DBP, Day 5, high, n= 0,0,0,2DBP, Day 5, low, n= 0,0,0,2
Off-therapy Visit0000

[back to top]

Number of Participants With Abnormal Heart Rate for Session 2

Data of participants with abnormal heart rate (measured during site visits by sphygmomanometer) were reported. Participants with low and high heart rate has been presented. Potential clinical concern value for heart rate is < 50 beats per minute to > 120 beats per minute. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: -2 hour pre-MRI, 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
Day 1, Pre MRI, high, n=0, 0, 2, 0Day 1, Pre MRI, low, n=0, 0, 2, 0Day 1, Post MRI 0.5 hr, high, n=0, 0, 2, 0Day 1, Post MRI 0.5 hr, low, n=0, 0, 2, 0
Off-therapy MRI Arm0000

[back to top]

Number of Participants With Abnormal Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) for Session 1

SBP and DBP were measured in supine position after 5 minutes rest. Data for Session 1 and 2 and for Pre and Post MRI has been presented. Potential clinical concern value for SBP is <100 millimeters of mercury (mmHg) and >170 mmHg. Potential clinical concern value for DBP is <50 mmHg and >110 mmHg. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
SBP, Day 4,-2 hr pre-MRI, high, n=1,1, 0, 0SBP, Day 4,-2 hr pre-MRI, low, n=1,1, 0, 0SBP, Day 4,0.5 hr post MRI , high, n=1,1, 0, 0SBP, Day 4,0.5 hr post MRI, low, n=1,1, 0, 0SBP, Day 4,1 hr post MRI , high, n=1,1, 0, 0SBP, Day 4,1 hr post MRI , low, n=1,1, 0, 0SBP, Day 8,0.5 hr Post MRI, high, n=1,1, 0, 0SBP, Day 8,0.5 hr Post MRI, low, n=1,1, 0, 0SBP, Day 8,1 hr Post MRI, high, n= 0,1, 0, 0SBP, Day 8,1 hr post MRI , low, n= 0,1, 0, 0DBP, Day 4,-2 hr pre-MRI, high, n=1,1, 0, 0DBP, Day 4,-2 hr pre-MRI, low, n=1,1, 0, 0DBP, Day 4,0.5 hr Post MRI, high,n= 1,1, 0, 0DBP, Day 4,0.5 hr Post MRI, low,n= 1,1, 0, 0DBP, Day 4,1 hr post MRI, high,n= 1,1, 0, 0DBP, Day 4,1 hr post MRI , low,n= 1,1, 0, 0DBP, Day 8, 0.5 hr post MRI ,high, n=1,1,0, 0DBP, Day 8, 0.5 hr post MRI, low, n= 1,1, 0, 0DBP, Day 8, 1 hr post MRI, high, n=0,1, 0, 0DBP, Day 8, 1 hr post MRI, low, n=0,1, 0, 0
Exenatide 10 µg00000000000000000000

[back to top]

Number of Participants With Abnormal SBP and DBP for Session 2

SBP and DBP were measured in supine position after 5 minutes rest. Data for Session 1 and 2 and for Pre and Post MRI has been presented. Potential clinical concern value for SBP is <100 millimeters of mercury (mmHg) and >170 mmHg. Potential clinical concern value for DBP is <50 mmHg and >110 mmHg. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
SBP, Day 4,-2 hr pre-MRI, high, n=1,1, 0, 0SBP, Day 4,-2 hr pre-MRI, low, n=1,1, 0, 0SBP, Day 4,0.5 hr post MRI , high, n=1,1, 0, 0SBP, Day 4,0.5 hr post MRI, low, n=1,1, 0, 0SBP, Day 4,1 hr post MRI , high, n=1,1, 0, 0SBP, Day 4,1 hr post MRI , low, n=1,1, 0, 0SBP, Day 8,0.5 hr Post MRI, high, n=1,1, 0, 0SBP, Day 8,0.5 hr Post MRI, low, n=1,1, 0, 0DBP, Day 4,-2 hr pre-MRI, high, n=1,1, 0, 0DBP, Day 4,-2 hr pre-MRI, low, n=1,1, 0, 0DBP, Day 4,0.5 hr Post MRI, high,n= 1,1, 0, 0DBP, Day 4,0.5 hr Post MRI, low,n= 1,1, 0, 0DBP, Day 4,1 hr post MRI, high,n= 1,1, 0, 0DBP, Day 4,1 hr post MRI , low,n= 1,1, 0, 0DBP, Day 8, 0.5 hr post MRI ,high, n=1,1,0, 0DBP, Day 8, 0.5 hr post MRI, low, n= 1,1, 0, 0
Albiglutide 50 mg0000000000000000

[back to top]

Number of Participants With Abnormal SBP and DBP for Session 2

SBP and DBP were measured in supine position after 5 minutes rest. Data for Session 1 and 2 and for Pre and Post MRI has been presented. Potential clinical concern value for SBP is <100 millimeters of mercury (mmHg) and >170 mmHg. Potential clinical concern value for DBP is <50 mmHg and >110 mmHg. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
SBP, Day 4,-2 hr pre-MRI, high, n=1,1, 0, 0SBP, Day 4,-2 hr pre-MRI, low, n=1,1, 0, 0SBP, Day 4,0.5 hr post MRI , high, n=1,1, 0, 0SBP, Day 4,0.5 hr post MRI, low, n=1,1, 0, 0SBP, Day 4,1 hr post MRI , high, n=1,1, 0, 0SBP, Day 4,1 hr post MRI , low, n=1,1, 0, 0SBP, Day 8,0.5 hr Post MRI, high, n=1,1, 0, 0SBP, Day 8,0.5 hr Post MRI, low, n=1,1, 0, 0SBP, Day 8,1 hr Post MRI, high, n= 0,1, 0, 0SBP, Day 8,1 hr post MRI , low, n= 0,1, 0, 0DBP, Day 4,-2 hr pre-MRI, high, n=1,1, 0, 0DBP, Day 4,-2 hr pre-MRI, low, n=1,1, 0, 0DBP, Day 4,0.5 hr Post MRI, high,n= 1,1, 0, 0DBP, Day 4,0.5 hr Post MRI, low,n= 1,1, 0, 0DBP, Day 4,1 hr post MRI, high,n= 1,1, 0, 0DBP, Day 4,1 hr post MRI , low,n= 1,1, 0, 0DBP, Day 8, 0.5 hr post MRI ,high, n=1,1,0, 0DBP, Day 8, 0.5 hr post MRI, low, n= 1,1, 0, 0DBP, Day 8, 1 hr post MRI, high, n=0,1, 0, 0DBP, Day 8, 1 hr post MRI, low, n=0,1, 0, 0
Exenatide 10 µg00000000000000000000

[back to top]

Number of Participants With Abnormal Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) for Session 1

SBP and DBP were measured in supine position after 5 minutes rest. Data for Session 1 and 2 and for Pre and Post MRI has been presented. Potential clinical concern value for SBP is <100 millimeters of mercury (mmHg) and >170 mmHg. Potential clinical concern value for DBP is <50 mmHg and >110 mmHg. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
SBP, Day 5, high, n=0, 0, 0, 2SBP, Day 5, low, n=0, 0, 0, 2DBP, Day 5, high, n= 0,0,0,2DBP, Day 5, low, n= 0,0,0,2
Off-therapy Visit0000

[back to top]

Number of Participants With Abnormal Clinical Chemistry Parameters

Clinical chemistry parameters included assessment of blood urea nitrogen (BUN), creatinine, epidermal growth factor receptor (eGRF), potassium, sodium, calcium, Aspartate transaminase (AST), Alanine transaminase (AST), Alkaline phosphatase, total and direct bilirubin, total protein and albumin. (NCT02802514)
Timeframe: Up to Week 11

InterventionParticipants (Count of Participants)
Albiglutide 50 mg0
Exenatide 10 µg0

[back to top]

Number of Participants With Abnormal Glycemic Parameters

Glycemic parameters included assessment of capillary blood glucose and fasting plasma glucose. (NCT02802514)
Timeframe: Up to Week 11

InterventionParticipants (Count of Participants)
Albiglutide 50 mg0
Exenatide 10 µg0

[back to top]

Number of Participants With Abnormal Hematology Parameters

Hematology parameters included assessment of platelet count, red blood cell (RBC) count, hemoglobin, hemotocrit, RBC indices including mean corpuscular volume and mean corpuscular hemoglobin (MCH), and White blood cells (WBC) count with differential count including, neutrophils, lymphocytes, monocytes, eosinophils and basophils. (NCT02802514)
Timeframe: Up to Week 11

InterventionParticipants (Count of Participants)
Albiglutide 50 mg0
Exenatide 10 µg0

[back to top]

Number of Participants With Abnormal SBP and DBP for Session 2

SBP and DBP were measured in supine position after 5 minutes rest. Data for Session 1 and 2 and for Pre and Post MRI has been presented. Potential clinical concern value for SBP is <100 millimeters of mercury (mmHg) and >170 mmHg. Potential clinical concern value for DBP is <50 mmHg and >110 mmHg. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
SBP, Day 1, Pre-MRI, high, n=0, 0, 2, 0SBP, Day 1, Pre-MRI, low, n=0, 0, 2, 0SBP, Day 1, 0.5 hr post MRI, high, n=0, 0, 2, 0SBP, Day 1,0.5 hr post MRI , low, n=0, 0, 2, 0DBP, Day 1, Pre MRI, high,n= 0, 0, 2, 0DBP, Day 1, Pre MRI, low,n= 0, 0, 2, 0DBP, Day 1,0.5 hr post MRI, high,n= 0, 0, 2, 0DBP, Day 1,0.5 hr post MRI, low,n= 0, 0, 2, 0
Off-therapy MRI00000010

[back to top]

Gastrointestinal (GI) Visual Analogue Scale (VAS) for Assessment of Nausea for Session 1

Participant completed VAS to record their perception of stomach fullness, hunger, nausea, bloating and abdominal pain. The VAS was represented by lines, 100 millimeter in length, anchored with words describing the most negative rating on the left and the most positive rating on the right. Scores ranged from 0 mm to 100 mm. Scores of 0 mm are worst (most negative rating on the left) and scores of 100 mm are best (most positive rating on the right). NA indicates that data were not available as standard deviation could not be calculated due to low number of participants. (NCT02802514)
Timeframe: Day 1 (Pre-MRI and 0.5 hour post-MRI); Day 4 (Pre-MRI and 0.5 hour post-MRI); and Day 8 (Pre-MRI and 0.5 hour post-MRI)

InterventionScores on scale (Mean)
Hunger, Day1, pre-MRI,n=0,0,2Hunger, Day1, 0.5 hour post-MRI,n=0,0,2Stomach fullness, Day1, pre-MRI,n=0,0,2Stomach fullness, Day1, 0.5 hour post-MRI,n=0,0,2Nausea, Day1, pre- MRI,n=0,0,2Nausea, Day1,0.5 hour post-MRI,n=0,0,2Bloating, Day1, pre-MRI,n=0,0,2Bloating, Day1, 0.5 hour post-MRI,n=0,0,2Abdominal pain, Day1, pre-MRI,n=0,0,2Abdominal pain, Day1,0.5 hour post-MRI,n=0,0,2
Off-therapy MRI29.055.09.00.51.019.01.51.02.01.5

[back to top]

Gastrointestinal (GI) Visual Analogue Scale (VAS) for Assessment of Nausea for Session 1

Participant completed VAS to record their perception of stomach fullness, hunger, nausea, bloating and abdominal pain. The VAS was represented by lines, 100 millimeter in length, anchored with words describing the most negative rating on the left and the most positive rating on the right. Scores ranged from 0 mm to 100 mm. Scores of 0 mm are worst (most negative rating on the left) and scores of 100 mm are best (most positive rating on the right). NA indicates that data were not available as standard deviation could not be calculated due to low number of participants. (NCT02802514)
Timeframe: Day 1 (Pre-MRI and 0.5 hour post-MRI); Day 4 (Pre-MRI and 0.5 hour post-MRI); and Day 8 (Pre-MRI and 0.5 hour post-MRI)

,
InterventionScores on scale (Mean)
Hunger, Day4, pre-MRI,n=1,1,0Hunger, Day4, 0.5 hour post-MRI,n=1,1,0Hunger, Day8, pre-MRI,n=1,1,0Hunger, Day8, 0.5 hour post-MRI,n=1,1,0Stomach fullness, Day4,pre-MRI,n=1,1,0Stomach fullness, Day4, 0.5 hour post-MRI,n=1,1,0Stomach fullness, Day8, pre-MRI,n=1,1,0Stomach fullness, Day8, 0.5 hour post- MRI,n=1,1,0Nausea, Day4, pre-MRI,n=1,1,0Nausea, Day4, 0.5 hour post-MRI,n=1,1,0Nausea, Day8, pre-MRI,n=1,1,0Nausea, Day8,0.5 hour post-MRI,n=1,1,0Bloating, Day4, pre-MRI,n=1,1,0Bloating, Day4, 0.5 hour post-MRI,n=1,1,0Bloating, Day8, pre-MRI,n=1,1,0Bloating, Day8, 0.5 hour post-MRI,n=1,1,0Abdominal pain, Day4, pre-MRI,n=1,1,0Abdominal pain, Day4, 0.5 hour post-MRI,n=1,1,0Abdominal pain, Day8, pre-MRI,n=1,1,0Abdominal pain, Day8, 0.5 hour post-MRI,n=1,1,0
Exenatide 10 µg40.050.025.026.01.02.01.01.01.01.00.01.03.01.00.01.00.01.01.01.0
Albiglutide 50 mg65.066.01.031.03.06.00.00.03.024.00.00.02.04.00.00.03.05.00.00.0

[back to top]

GI VAS for Assessment of Nausea for Session 2

Participant completed VAS to record their perception of stomach fullness, hunger, nausea, bloating and abdominal pain. The VAS was represented by lines, 100 millimeter in length, anchored with words describing the most negative rating on the left and the most positive rating on the right. Scores ranged from 0 mm to 100 mm. Scores of 0 mm are worst (most negative rating on the left) and scores of 100 mm are best (most positive rating on the right). NA indicates that data were not available as standard deviation could not be calculated due to low number of participants. (NCT02802514)
Timeframe: Day 1 (Pre-MRI and 0.5 hour post-MRI); Day 4 (Pre-MRI and 0.5 hour post-MRI); and Day 8 (Pre-MRI and 0.5 hour post-MRI)

InterventionScores on scale (Mean)
Hunger, Day1, pre-MRI,n=0,0,2Hunger, Day1,0.5 hour post-MRI,n=0,0,2Stomach fullness, Day1, pre-MRI,n=0,0,2Stomach fullness, Day1, 0.5 hour post-MRI,n=0,0,2Nausea, Day1, pre-MRI,n=0,0,2Nausea, Day1, 0.5 hour post-MRI,n=0,0,2Bloating, Day1, pre-MRI,n=0, 0, 2Bloating, Day1, 0.5 hour post-MRI,n=0,0,2Abdominal pain, Day1, pre-MRI,n=0,0,2Abdominal pain, Day1, 0.5 hour post-MRI,n=0,0,2
Off-therapy MRI54.567.511.57.023.517.56.04.07.54.0

[back to top]

GI VAS for Assessment of Nausea for Session 2

Participant completed VAS to record their perception of stomach fullness, hunger, nausea, bloating and abdominal pain. The VAS was represented by lines, 100 millimeter in length, anchored with words describing the most negative rating on the left and the most positive rating on the right. Scores ranged from 0 mm to 100 mm. Scores of 0 mm are worst (most negative rating on the left) and scores of 100 mm are best (most positive rating on the right). NA indicates that data were not available as standard deviation could not be calculated due to low number of participants. (NCT02802514)
Timeframe: Day 1 (Pre-MRI and 0.5 hour post-MRI); Day 4 (Pre-MRI and 0.5 hour post-MRI); and Day 8 (Pre-MRI and 0.5 hour post-MRI)

,
InterventionScores on scale (Mean)
Hunger, Day4, pre-MRI,n=1,1,0Hunger, Day4,0.5 hour post-MRI,n=1,1,0Hunger, Day8, pre-MRI,n=1,1,0Hunger, Day8, 0.5 hour post-MRI,n=1,1,0Stomach fullness, Day4, pre-MRI,n=1,1,0Stomach fullness, Day4,0.5 hour post-MRI,n=1,1,0Stomach fullness, Day8, pre-MRI,n=1,1,0Stomach fullness, Day8,0.5 hour post-MRI,n=1,1,0Nausea, Day4, pre-MRI,n=1,1,0Nausea, Day4,0.5 hour post-MRI,n=1,1,0Nausea, Day8, pre-MRI,n=1,1,0Nausea, Day8, 0.5 hour post-MRI,n=1,1,0Bloating, Day4, pre-MRI,n=1,1,0Bloating, Day4,0.5 hour post-MRI,n=1,1,0Bloating, Day8, pre-MRI,n=1,1,0Bloating, Day8, 0.5 hour post-MRI,n=1,1,0Abdominal pain, Day4, pre-MRI,n=1,1,0Abdominal pain, Day4, 0.5 hour post-MRI,n=1,1,0Abdominal pain, Day8, pre-MRI,n=1,1,0Abdominal pain, Day8, 0.5 hour post-MRI,n=1,1,0
Albiglutide 50 mg2.057.038.053.02.01.011.03.01.00.02.02.02.01.01.02.01.01.01.02.0
Exenatide 10 µg53.066.077.073.00.00.010.013.00.00.048.038.00.00.06.06.00.00.07.06.0

[back to top]

Motion Sickness Assessment Questionnaire (MSAQ) for Assessment of Nausea for Session 1

Participant completed MSAQ to quantify the severity of different dimensions of nausea induced by motion sickness. There were total 16 items: 4 related to gastro-intestinal (GI), 5 related to central (C), 3 related to peripheral (P) and 4 related to sopite-related (SR). All items were scored individually on a scale of 1-9 where 1 means 'not at all severe' and 9 means 'severe', with higher score indicates more severity. Individual 16 items with their scores are presented. NA indicates that data were not available as standard deviation could not be calculated due to low number of participants. (NCT02802514)
Timeframe: Day 1 0.5 hour post-MRI; Day 4 0.5 hour post-MRI; and Day 8 0.5 hour post-MRI

InterventionScores on scale (Mean)
C, Felt faint like, Day1,0.5 hr,Post MRI,n=0,0,2C, Felt lightheaded, Day1,0.5 hr,Post MRI,n=0,0,2C, Felt disoriented, Day1,0.5 hr,Post MRI,n=0,0,2C, Felt dizzy, Day1,0.5 hr,Post MRI,n=0,0,2C, Felt spinning, Day1,0.5 hr,Post MRI,n=0,0,2GI, stomach sick, Day1,0.5hr,Post MRI,n=0,0,2GI, felt queasy, Day1,0.5hr,Post MRI,n=0,0,2GI, nauseated, Day1, 0.5hr,Post MRI,n=0,0,2GI, may vomit, Day1,0.5hr,Post MRI,n=0,0,2P, sweaty, Day1,0.5hr,Post MRI,n=0,0,2P, clammy/cold sweat,Day1,0.5hr,Post MRI,n=0,0,2P, hot/warm, Day1,0.5hr,Post MRI,n=0, 0, 2SR,annoyed/irritated,Day1,0.5hr,Post MRI,n=0,0,2SR, drowsy, Day1,0.5hr,Post MRI,n=0,0,2SR, tired/fatigued, Day1,0.5hr,Post MRI,n=0,0,2SR, uneasy, Day1,0.5hr,Post MRI,n=0,0,2
Off-therapy MRI4.05.54.58.05.55.06.56.56.54.54.52.55.01.01.58.0

[back to top]

Motion Sickness Assessment Questionnaire (MSAQ) for Assessment of Nausea for Session 1

Participant completed MSAQ to quantify the severity of different dimensions of nausea induced by motion sickness. There were total 16 items: 4 related to gastro-intestinal (GI), 5 related to central (C), 3 related to peripheral (P) and 4 related to sopite-related (SR). All items were scored individually on a scale of 1-9 where 1 means 'not at all severe' and 9 means 'severe', with higher score indicates more severity. Individual 16 items with their scores are presented. NA indicates that data were not available as standard deviation could not be calculated due to low number of participants. (NCT02802514)
Timeframe: Day 1 0.5 hour post-MRI; Day 4 0.5 hour post-MRI; and Day 8 0.5 hour post-MRI

,
InterventionScores on scale (Mean)
C, Felt faint like, Day4,0.5 hr,Post MRI,n=1,1,0C, Felt faint like, Day8, 0.5 hr,Post MRI,n=1,1,0C, Felt lightheaded, Day4,0.5 hr,Post MRI,n=1,1,0C, Felt lightheaded, Day8, 0.5 hr,Post MRI,n=1,1,0C, Felt disoriented, Day4, 0.5 hr,Post MRI,n=1,1,0C, Felt disoriented, Day8, 0.5 hr,Post MRI,n=1,1,0C, Felt dizzy, Day4,0.5 hr,Post MRI,n=1,1,0C, Felt dizzy, Day8,0.5 hr,Post MRI,n=1,1,0C, Felt spinning, Day4,0.5 hr,Post MRI,n=1,1,0C, Felt spinning, Day8, 0.5 hr,Post MRI,n=1,1,0GI, stomach sick, Day4,0.5hr,Post MRI,n=1,1,0GI, stomach sick, Day8,0.5hr,Post MRI,n=1,1,0GI, felt queasy, Day4,0.5hr,Post MRI,n=1,1,0GI, felt queasy, Day8,0.5hr,Post MRI,n=1,1,0GI, nauseated, Day4,0.5hr,Post MRI,n=1,1,0GI, nauseated, Day8,0.5hr,Post MRI,n=1,1,0GI, may vomit, Day4,0.5hr,Post MRI,n=1,1,0GI, may vomit, Day8,0.5hr,Post MRI,n=1,1,0P, sweaty, Day4,0.5 hr,Post MRI,n=1,1,0P, sweaty, Day8, 0.5 hr,Post MRI,n=1,1,0P,clammy/cold sweat,Day4,0.5 hr,Post MRI,n=1,1,0P, clammy/cold sweat,Day8,0.5 hr,Post MRI,n=1,1,0P, hot/warm, Day4,0.5 hr,Post MRI,n=1,1,0P, hot/warm, Day8, 0.5 hr,Post MRI,n=1,1,0SR,annoyed/irritated,Day4,0.5 hr,Post MRI,n=1,1,0SR,annoyed/irritated,Day8, 0.5 hr,Post MRI,n=1,1,0SR, drowsy, Day4, 0.5 hr,Post MRI,n=1,1,0SR, drowsy, Day8, 0.5 hr,Post MRI,n=1,1,0SR, tired/fatigued, Day4,0.5 hr,Post MRI,n=1,1,0SR, tired/fatigued, Day8,0.5 hr,Post MRI,n=1,1,0SR, uneasy, Day4, 0.5 hr,Post MRI,n=1,1,0SR, uneasy, Day8,0.5 hr,Post MRI,n=1,1,0
Albiglutide 50 mg1.02.02.01.03.01.02.01.01.01.01.01.04.01.03.01.01.01.02.02.03.02.01.01.01.01.05.01.04.01.02.01.0
Exenatide 10 µg1.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.02.02.01.02.02.01.01.0

[back to top]

MSAQ for Assessment of Nausea for Session 2

Participant completed MSAQ to quantify the severity of different dimensions of nausea induced by motion sickness. There were total 16 items: 4 related to gastro-intestinal (GI), 5 related to central (C), 3 related to peripheral (P) and 4 related to sopite-related (SR). All items were scored individually on a scale of 1-9 where 1 means 'not at all severe' and 9 means 'severe', with higher score indicates more severity. Individual 16 items with their scores are presented. NA indicates that data were not available as standard deviation could not be calculated due to low number of participants. (NCT02802514)
Timeframe: Day 1 0.5 hour post-MRI; Day 4 0.5 hour post-MRI; and Day 8 0.5 hour post-MRI

InterventionScores on scale (Mean)
C, Felt faint like, Day1,0.5 hr Post MRI ,n=0,0,2C, Felt lightheaded, Day1,0.5 hr Post MRI,n=0,0,2C, Felt disoriented, Day1,0.5 hr, Post MRI,n=0,0,2C, Felt dizzy, Day1, 0.5 hr,Post MRI,n=0,0,2C, Felt spinning, Day1,0.5 hr,Post MRI,n=0,0,2GI, stomach sick, Day1,0.5hr,Post MRI, n=0,0,2GI, felt queasy, Day1, 0.5hr post-MRI,n=0,0,2GI, nauseated, Day1,0.5hr,Post MRI,n=0,0,2GI, may vomit, Day1,0.5hr,Post MRI,n=0,0,2P, sweaty, Day1,0.5 hr,Post MRI,n=0,0,2P,clammy/cold sweat,Day1,0.5hr,post-MRI,n=0,0,2P, hot/warm, Day1,0.5 hr, Post-MRI,n=0,0,2SR,annoyed/irritated,Day1,0.5hr, Post-MRI,n=0,0,2SR, drowsy, Day1, 0.5 hr,Post-MRI,n=0,0,2SR, tired/fatigued, Day1,0.5 hr,Post MRI,n=0,0,2SR, uneasy, Day1, 0.5 hr,Post-MRI,n=0,0,2
Off-therapy MRI3.02.02.02.04.05.04.56.02.01.52.01.01.54.04.54.0

[back to top]

MSAQ for Assessment of Nausea for Session 2

Participant completed MSAQ to quantify the severity of different dimensions of nausea induced by motion sickness. There were total 16 items: 4 related to gastro-intestinal (GI), 5 related to central (C), 3 related to peripheral (P) and 4 related to sopite-related (SR). All items were scored individually on a scale of 1-9 where 1 means 'not at all severe' and 9 means 'severe', with higher score indicates more severity. Individual 16 items with their scores are presented. NA indicates that data were not available as standard deviation could not be calculated due to low number of participants. (NCT02802514)
Timeframe: Day 1 0.5 hour post-MRI; Day 4 0.5 hour post-MRI; and Day 8 0.5 hour post-MRI

,
InterventionScores on scale (Mean)
C, Felt faint like, Day4,0.5 hr Post MRI ,n=1,1,0C, Felt faint like, Day8,0.5 hr,Post MRI,n=1,1,0C, Felt lightheaded, Day4, 0.5 hr Post MRI,n=1,1,0C, Felt lightheaded, Day8, 0.5 hr,Post MRI,n=1,1,0C, Felt disoriented, Day4,0.5 hr Post MRI,n=1,1,0C, Felt disoriented, Day8,0.5 hr,Post MRI,n=1,1,0C, Felt dizzy, Day4,0.5 hr,Post MRI,n=1,1,0C, Felt dizzy, Day8,0.5 hr,Post MRI,n=1,1,0C, Felt spinning, Day4,0.5 hr,Post MRI,n=1,1,0C, Felt spinning, Day8,0.5 hr,Post MRI,n=1,1,0GI, stomach sick, Day4, 0.5hr post-MRI,n=1,1,0GI, stomach sick, Day8,0.5hr,Post MRI,n=1,1,0GI, felt queasy, Day4,0.5hr,Post MRI,n=1,1,0GI, felt queasy, Day8, 0.5h,Post MRI,n=1,1,0GI, nauseated, Day4,0.5hr,Post MRI,n=1,1,0GI, nauseated, Day8,0.5hr,Post MRI, n=1,1,0GI, may vomit, Day4,0.5hr,Post MRI,n=1,1,0GI, may vomit, Day8,0.5 hr,Post MRI,n=1,1,0P, sweaty, Day4, 0.5 hr,Post MRI,n=1,1,0P, sweaty, Day8,0.5 hr,Post MRI,n=1,1,0P, clammy/cold sweat, Day4,0.5 hr,Post MRI,n=1,1,0P,clammy/cold sweat,Day8,0.5hr,Post-MRI,n=1,1,0P, hot/warm, Day4, 0.5 hr,Post-MRI,n=1,1,0P, hot/warm,Day8, 0.5 hr Post-MRI,n=1,1,0SR,annoyed/irritated,Day4,0.5hr,Post-MRI,n=1,1,0SR,annoyed/irritated,Day8,0.5hr,Post MRI,n=1,1,0SR, drowsy, Day4, 0.5 hr,Post-MRI,n=1,1,0SR, drowsy, Day8, 0.5 hr, Post-MRI,n=1,1,0SR, tired/fatigued, Day4,0.5 hr,Post MRI,n=1,1,0SR, tired/fatigued, Day8,0.5 hr,Post MRI,n=1,1,0SR, uneasy, Day4, 0.5 hr,Post MRI,n=1,1,0SR, uneasy, Day8, 0.5 hr,Post MRI,n=1,1,0
Albiglutide 50 mg1.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.01.05.01.04.03.01.01.0
Exenatide 10 µg2.01.02.02.01.01.01.01.01.01.01.01.01.02.01.03.01.01.03.01.03.01.01.01.01.01.01.05.01.03.01.01.0

[back to top]

Number of Participants With Abnormal Heart Rate for Session 1

Data of participants with abnormal heart rate (measured during site visits by sphygmomanometer) were reported. Participants with low and high heart rate has been presented. Potential clinical concern value for heart rate is < 50 beats per minute to > 120 beats per minute. Safety Population comprised of all participants who received at least one dose of the study treatment. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: -2 hour pre-MRI, 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
Day 4, -2 hr pre-MRI, high, n=1, 1, 0, 0Day 4, -2 hr pre-MRI, low, n=1, 1, 0, 0Day 4, Post MRI 0.5 hr, high, n=1, 1, 0, 0Day 4, 0.5 hr Post MRI, low, n=1, 1, 0, 0Day 4, 1 hr Post MRI, high, n=1, 1, 0, 0Day 4, 1 hr Post MRI, low, n=1, 1, 0, 0Day 8, -2 hr pre-MRI, high, n=1, 1, 0, 0Day 8, -2 hr pre-MRI, low, n=1, 1, 0, 0Day 8, 0.5 hr Post MRI, high, n=1, 1, 0, 0Day 8, 0.5 hr Post MRI, low, n=1, 1, 0, 0
Albiglutide 50 mg0000000000

[back to top]

Number of Participants With Abnormal Heart Rate for Session 1

Data of participants with abnormal heart rate (measured during site visits by sphygmomanometer) were reported. Participants with low and high heart rate has been presented. Potential clinical concern value for heart rate is < 50 beats per minute to > 120 beats per minute. Safety Population comprised of all participants who received at least one dose of the study treatment. (NCT02802514)
Timeframe: Day 1: pre-MRI, 0.5 hour post-MRI; Day 4: -2 hours pre-MRI, 0.5 and 1 hour post MRI; Day 5; Day 8: -2 hour pre-MRI, 0.5 and 1 hour post-MRI

InterventionParticipants (Count of Participants)
Day 4, -2 hr pre-MRI, high, n=1, 1, 0, 0Day 4, -2 hr pre-MRI, low, n=1, 1, 0, 0Day 4, Post MRI 0.5 hr, high, n=1, 1, 0, 0Day 4, 0.5 hr Post MRI, low, n=1, 1, 0, 0Day 4, 1 hr Post MRI, high, n=1, 1, 0, 0Day 4, 1 hr Post MRI, low, n=1, 1, 0, 0Day 8, -2 hr pre-MRI, high, n=1, 1, 0, 0Day 8, -2 hr pre-MRI, low, n=1, 1, 0, 0Day 8, 0.5 hr Post MRI, high, n=1, 1, 0, 0Day 8, 0.5 hr Post MRI, low, n=1, 1, 0, 0Day 8, 1 hr Post MRI, high, n=0, 1, 0, 0Day 8, 1 hr Post MRI, low, n=0, 1, 0, 0
Exenatide 10 µg000000000000

[back to top]

Post-quit Craving as Assessed by the Questionnaire of Smoking Urges

Questionnaire of Smoking Urges (QSU) is a 10-item scale (total score range = 10-70, a lower score indicates lower cravings for cigarettes) that evaluates the intention and desire to smoke and anticipation of relief from withdrawal-associated negative affect. (NCT02975297)
Timeframe: 10 weeks (4 weeks after end of treatment)

Interventionscore on a scale (Mean)
Exenatide Plus NRT Plus Counseling11.5
Placebo Plus NRT Plus Counseling11.2

[back to top]

Post-quit Craving as Assessed by the Questionnaire of Smoking Urges

Questionnaire of Smoking Urges (QSU) is a 10-item scale (total score range = 10-70, a lower score indicates lower cravings for cigarettes) that evaluates the intention and desire to smoke and anticipation of relief from withdrawal-associated negative affect. (NCT02975297)
Timeframe: 6 weeks

Interventionscore on a scale (Mean)
Exenatide Plus NRT Plus Counseling17.2
Placebo Plus NRT Plus Counseling16.9

[back to top]

Post-quit Craving as Assessed by the Questionnaire of Smoking Urges

Questionnaire of Smoking Urges (QSU) is a 10-item scale (total score range = 10-70, a lower score indicates lower cravings for cigarettes) that evaluates the intention and desire to smoke and anticipation of relief from withdrawal-associated negative affect. (NCT02975297)
Timeframe: 7 weeks (1 week after end of treatment)

Interventionscore on a scale (Mean)
Exenatide Plus NRT Plus Counseling13.3
Placebo Plus NRT Plus Counseling14.2

[back to top]

Withdrawal Symptoms as Assessed by the Wisconsin Smoking Withdrawal Scale

The Wisconsin Smoking Withdrawal Scale is a 28-item questionnaire designed to assess different aspects of the smoking withdrawal syndrome. Participants rate each item on a Likert scale from zero (strongly disagree) to four (strongly agree). Total score ranges from 0 to 112, with a higher score indicating greater withdrawal. (NCT02975297)
Timeframe: 6 weeks

Interventionscore on a scale (Mean)
Exenatide Plus NRT Plus Counseling40.5
Placebo Plus NRT Plus Counseling44.5

[back to top]

Number of Participants Who Self-Reported Abstinence and Who Were Biochemically Verified as Abstinent Via Expired CO Level of ≤ 5ppm

(NCT02975297)
Timeframe: 7 weeks (1 week after end of treatment)

InterventionParticipants (Count of Participants)
Exenatide Plus NRT Plus Counseling15
Placebo Plus NRT Plus Counseling7

[back to top]

Number of Participants Who Self-Reported Abstinence and Who Were Biochemically Verified as Abstinent Via Expired CO Level of ≤ 5ppm

(NCT02975297)
Timeframe: 6 weeks

InterventionParticipants (Count of Participants)
Exenatide Plus NRT Plus Counseling19
Placebo Plus NRT Plus Counseling11

[back to top]

Number of Participants Who Self-Reported Abstinence and Who Were Biochemically Verified as Abstinent Via Expired CO Level of ≤ 5ppm

(NCT02975297)
Timeframe: 10 weeks (4 weeks after end of treatment)

InterventionParticipants (Count of Participants)
Exenatide Plus NRT Plus Counseling9
Placebo Plus NRT Plus Counseling4

[back to top]

Change in Plasma Insulin Concentration

Measurement of change in plasma insulin concentration from baseline to 16 weeks following treatment with each study drug(s). Placebo arm was not included in this 16 week portion of the study, since subjects are diabetic. Only 3 arms of the study were conducted: (i) Byetta/Bydureon, (ii) Dapagliflozin (iii) Byetta/Bydureon plus Dapagliflozin. (NCT02981069)
Timeframe: Baseline to 16 weeks

InterventionmicroUnits/ml (Mean)
Dapa+Exe-2
Dapa-2
Exenatide3

[back to top]

Change in Endogenous Glucose Production (EGP) After 16 Weeks of Treatment With Each Study Drug.

"After screening, eligible subjects will receive a measurement of endogenous glucose production (EGP) with a prime-continuous infusion of 3-3H-glucose. The EGP measurement will be performed in the morning after a 10-12 hour overnight fast and will last 8.5 hours (from 6 AM to 2:30 PM). After a 3.5-hour tracer equilibration period, subjects (20 per group) will receive one of the following medications: (i) exenatide 5 ug subcutaneously; (ii) dapagliflozin (10 mg); and (iii) dapagliflozin 10 mg + exenatide 5 ug. Only three groups will be followed for 16 weeks since subjects are diabetic and placebo is not appropriate to use for this period. Again, subjects will be randomized to treatment with either exenatide, dapagliflozin or both drugs in combination. Repeat EGP will be measured again at 16 weeks as described above and data will be compared to respective acute studies." (NCT02981069)
Timeframe: 16 weeks

Interventionmg/kg.min (Mean)
EXENATIDE-0.23
Dapagliflozin0.20
Exenatide Plus Dapagliflozin-0.12

[back to top]

Change in Endogenous Glucose Production (EGP) After Acute Exposure to a Single Dose and Again After 16 Weeks of Treatment

After screening, eligible subjects will receive a measurement of endogenous glucose production (EGP) with a prime-continuous infusion of 3-3H-glucose. The EGP measurement will be performed in the morning after a 10-12 hour overnight fast and will last 8.5 hours (from 6 AM to 2:30 PM). After a 3.5-hour tracer equilibration period, subjects (20 per group) will receive one of the following medications: (i) placebo; (ii) exenatide 5 ug subcutaneously; (iii) dapagliflozin (10 mg); and (iv) dapagliflozin 10 mg + exenatide 5 ug [ACUTE STUDY]. (NCT02981069)
Timeframe: ACUTE [after a single dose of each study drug or placebo]

Interventionmg/kg.min (Mean)
EXENATIDE-0.18
Dapagliflozin0.14
Exenatide Plus Dapagliflozin-0.08
Placebo-0.03

[back to top]

Change in Fasting Plasma Glucose (FPG) Concentration

The change in (FPG) above baseline following administration of study interventions after 16 weeks of treatment with each study drug(s) compared to data obtained during the acute exposure. Placebo arm was not included in this 16 week portion of the study, since subjects are diabetic. Only 3 arms of the study were conducted: (i) Byetta/Bydureon, (ii) Dapagliflozin (iii) Byetta/Bydureon plus Dapagliflozin. (NCT02981069)
Timeframe: 16 weeks

Interventionmg/dl (Mean)
Byetta / Bydureon42
Dapagliflozin72
Byetta/Bydureon Plus Dapagliflozin11

[back to top]

Change in Plasma Glucagon Concentration

Measurement of change in plasma glucagon concentration after 16 weeks of treatment with each study drug(s) compared to acute exposure at baseline. Placebo arm was not included in this 16 week portion of the study, since subjects are diabetic. Only 3 arms of the study were conducted: (i) Byetta/Bydureon, (ii) Dapagliflozin (iii) Byetta/Bydureon plus Dapagliflozin. (NCT02981069)
Timeframe: Baseline to 16 weeks

Interventionpg/ml (Mean)
Dapa+Exe4
Dapa5
Exenatide-6

[back to top]

Assessment of Reproductive Function

Changes in testosterone levels were measured (NCT03151005)
Timeframe: 12 weeks

Interventionnmol/L (Mean)
Metformin-GLP-1 Receptor Agonist1.82
Metformin-Oral Contraceptive(OC)2.14

[back to top]

Assessment of Liver Function

Alanine transaminase was measured in IU/L. (NCT03151005)
Timeframe: 12 weeks

InterventionIU/L (Mean)
Metformin-GLP-1 Receptor Agonist39.09
Metformin-Oral Contraceptive(OC)36.73

[back to top]

Assessment of Blood Pressure

Systolic blood pressure was measured in mmHg. (NCT03151005)
Timeframe: 12 weeks

InterventionmmHg (Mean)
Metformin-GLP-1 Receptor Agonist122.83
Metformin-Oral Contraceptive(OC)122.40

[back to top]

Basic Vital Signs

Weight and height will be combined to report BMI in kg/m^2. (NCT03151005)
Timeframe: 12 weeks

Interventionkg/m^2 (Mean)
Metformin-GLP-1 Receptor Agonist26.26
Metformin-Oral Contraceptive(OC)27.12

[back to top]

Assessment of Reproductive Functions

Concentration of LH was measured in mIU/ml. (NCT03151005)
Timeframe: 12 weeks

InterventionmIU/ml (Mean)
Metformin-GLP-1 Receptor Agonist5.52
Metformin-Oral Contraceptive(OC)5.33

[back to top]

Tmax (Time of Maximum Observed Plasma Concentration)

Whole venous blood samples of 3 mL was collected from peripheral vein at each period at pre-dose and at 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 24, 36 and 48 h post-dose of bexagliflozin. A non-compartmental pharmacokinetic analysis was used to calculate the PK parameters. Tmax was obtained directly from experimental observations. (NCT03167411)
Timeframe: Up to 48 hrs

Interventionhours (Median)
Bexagliflozin2.00
Bexagliflozin With Exenatide5.00

[back to top]

T1/2 (Apparent Terminal Elimination Half-life)

Whole venous blood samples of 3 mL was collected from peripheral vein at each period at pre-dose and at 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 24, 36 and 48 h post-dose of bexagliflozin. A non-compartmental pharmacokinetic analysis was used to calculate the PK parameters. T1/2 was calculated as the natural log of 2 divided by the terminal phase rate constant. (NCT03167411)
Timeframe: Up to 48 hrs

Interventionhours (Geometric Mean)
Bexagliflozin12.1
Bexagliflozin With Exenatide8.8

[back to top]

Cmax (Maximum Observed Plasma Concentration)

Whole venous blood samples of 3 mL was collected from peripheral vein at each period at pre-dose and at 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 24, 36 and 48 h post-dose of bexagliflozin. A non-compartmental pharmacokinetic analysis was used to calculate the PK parameters. Cmax was obtained directly from experimental observations. (NCT03167411)
Timeframe: Up to 48 hrs

Interventionng/mL (Geometric Mean)
Bexagliflozin95.9
Bexagliflozin With Exenatide121.6

[back to top]

AUC0-inf (Area Under the Plasma Concentration-time Curve From Time 0 to Infinity)

Whole venous blood samples of 3 mL was collected from peripheral vein at each period at pre-dose and at 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 24, 36 and 48 h post-dose of bexagliflozin. A non-compartmental pharmacokinetic analysis was used to calculate the PK parameters. AUC0-inf was calculated using the linear trapezoidal rule, using actual elapsed time values. If the actual time of sample collection was not available, the nominal time was used for the purpose of parameter estimation. (NCT03167411)
Timeframe: Up to 48 hrs

Interventionhr*ng/mL (Geometric Mean)
Bexagliflozin776.0
Bexagliflozin With Exenatide1085.3

[back to top]

Urinary Glucose Excretion (UGE)

Post-dose urine was collected without preservative in four batches: 0 to 12 h, 12 to 24 h, 24 to 36 h, and 36 to 48 h collections. After collection, the total volume of each batch and collection time was recorded. UGE, including UGE(t1-t2) and total 0-24 h and 0-48 h UGE were calculated. UGE(t1-t2) was derived from urine volume (Vt1-t2) multiplied by glucose concentration divided by 100. (NCT03167411)
Timeframe: 0-48 hours

,
Interventiong (Mean)
Pre-dose (-12 to 0 hours)0 - 12 hours12 - 24 hours24 - 36 hours36 - 48 hours0 - 24 hours0 - 48 hours
Bexagliflozin0.0738.3226.8921.939.5665.2196.70
Bexagliflozin With Exenatide0.0526.3828.9522.169.2155.6588.11

[back to top]

Change in EGP From Baseline to Post-oral Glucose Load.

The difference in rate of EGP during the last hour of the study (from 240-300 minutes) between drug-treatment and placebo treatment studies represents the effect of drug treatment on EGP, which will be compared among the 3 acute drug treatments (exenatide; dapagliflozin; exenatide plus dapagliflozin this data includes change in EGP above baseline following dapagliflozin alone vs dapagliflozin/exenatide) with ANOVA. (NCT03331289)
Timeframe: From baseline [-35 to 0min] to the last hour post-glucose load [240-300 minutes]

Interventionmg/kg.min (Mean)
Placebo-0.03
Exenatide-0.18
Dapagliflozin0.14
Exenatide and Dapagliflozin-0.08

[back to top]

Alcohol Consumption

Alcohol consumption was measured by using a graduated cylinder to determine the amount of alcohol given to the subject that was not consumed. The amount not consumed was then subtracted from the total amount of alcohol served to the subject in order to calculate the amount consumed. This outcome was measured in standard drink units (SDUs). A standard drink contains approximately 0.6 fluid ounces of pure alcohol. (NCT03645408)
Timeframe: 2 hours

Interventionstandard drink units (SDUs) (Mean)
Exenatide Injection0.93
Sham Injection (Placebo)2.78

[back to top]

Hemoglobin A1c

Hemoglobin is a protein within red blood cells. As glucose enters the bloodstream, it binds to hemoglobin, or glycates. The more glucose that enters the bloodstream, the higher the amount of glycated hemoglobin. An A1C level below 5.7 percent is considered normal. (NCT03961256)
Timeframe: 12 and 24 months after kidney transplantation

,
Interventionpercentage of glycated hemoglobin (Median)
12 months24 months
Exenatide SR Intervention Group5.65.65
Standard of Care5.855.75

[back to top]

Incidence of Mesangial Expansion

Number of subjects to experience mesangial expansion >20%. Mesangial expansion occurs due to increased deposition of extracellular matrix proteins, for example fibronectin, into the mesangium. Accumulation of extracellular matrix proteins then occurs due to insufficient degradation by matrix metalloproteinases. (NCT03961256)
Timeframe: 12 and 24 months after kidney transplantation

,
InterventionParticipants (Count of Participants)
12 months24 months
Exenatide SR Intervention Group00
Standard of Care00

[back to top]

Creatinine

A creatinine blood test measures the level of creatinine in the blood. Creatinine is a waste product that forms when creatine, which is found in the muscle, breaks down. Creatinine levels in the blood can provide the doctors with information about how well the kidneys are working. As measured in mg/dL units. (NCT03961256)
Timeframe: From enrollment, up to 20 months post-enrollment

Interventionmg/dL (Median)
Exenatide SR Intervention Group1.7
Standard of Care1.4

[back to top]

Graft Loss

The number of subjects to experience graft loss. Primary graft failure is defined as no evidence of engraftment or hematological recovery of donor cells, within the first month after transplant, without evidence of disease relapse. Secondary graft failure refers to the loss of a previously functioning graft, resulting in cytopenia involving at least two blood cell lineages. (NCT03961256)
Timeframe: From enrollment, up to 20 months post-enrollment

InterventionParticipants (Count of Participants)
Exenatide SR Intervention Group0

[back to top]

Incidence of Death

Number of subjects to experience death by any cause (NCT03961256)
Timeframe: From enrollment, up to 20 months post-enrollment

InterventionParticipants (Count of Participants)
Exenatide SR Intervention Group0

[back to top]

Progression From Prediabetes to Diabetes

Number of subjects to have an increase in HbA1C or fasting blood sugar to diabetic range based on the American Diabetes Association (ADA) criteria after kidney transplantation (NCT03961256)
Timeframe: 12 months after transplantation

InterventionParticipants (Count of Participants)
Exenatide SR Intervention Group0
Standard of Care1

[back to top]

Adverse Events for Exenatide SR Intervention

Total number of adverse events reported by the subjects that received the Exenatide SR Intervention (NCT03961256)
Timeframe: 12 months

InterventionAdverse Events (Number)
Exenatide SR Intervention Group10

[back to top]

Progression From Prediabetes to Diabetes

Number of subjects to have an increase in HbA1C or fasting blood sugar to diabetic range based on the American Diabetes Association (ADA) criteria after kidney transplantation (NCT03961256)
Timeframe: 24 months after transplantation

InterventionParticipants (Count of Participants)
Exenatide SR Intervention Group1
Standard of Care1

[back to top]

Clinical Effect of Exenatide as Assessed by Number of Participants Who Self-reported Cocaine Use on 50% or More Days of the Week

Timeline Followback (TLFB) administered once weekly. (NCT04941521)
Timeframe: From Week 1 to Week 6

InterventionParticipants (Count of Participants)
week 1week 2week 3week 4week 5week 6
Exenatide and Drug Counseling221212

[back to top]

Clinical Effect of Exenatide as Indicated by Number of Participants Who Had an Increase in Positive Affect Symptoms by Week 6 as Indicated on the Positive/Negative Affect Schedule

The Positive/Negative Affect Schedule is a 20-item questionnaire divided into 10 positive affect items and 10 negative affect items. The score for the positive affect items ranges from 10 to 50, with a higher score indicating higher levels of positive affect. The scores from each timepoint will be plotted as a trend line. (NCT04941521)
Timeframe: From Week 0 to Week 6

InterventionParticipants (Count of Participants)
Exenatide and Drug Counseling1

[back to top]

Clinical Effect of Exenatide as Assessed by Number of Participants Who Had a Decrease in Drug Demand by Week 6

Drug demand will be measured by the computerized Cocaine Purchasing Task (CPT). The CPT asks participants how much cocaine they would purchase at the beginning of a hypothetical day as the cost of cocaine increases from $0 to $1,000. The CPT simulates changes in price and consumption of drug in order to assess demand curves associated with drug consumption. The CPT will assess both cocaine reward value as well as motivation to consume cocaine. (NCT04941521)
Timeframe: From Week 0 to Week 6

InterventionParticipants (Count of Participants)
Exenatide and Drug Counseling1

[back to top]

Feasibility as Indicated by Overall Acceptability as Reported on the Satisfaction Survey

The Satisfaction Survey includes a 9-point likert scale that ranges from 1 to 9, with a higher score indicating greater acceptability. (NCT04941521)
Timeframe: Week 6

Interventionscore on a scale (Mean)
treatment helpfulnesstreatment usefulnesslikelihood of treatment recommendationdesire to continue treatment
Exenatide and Drug Counseling7.666.007.337.33

[back to top]

Clinical Effect of Exenatide as Assessed by Number of Participants Who Were Below the Clinical Range for Depression by Week 6 as Indicated by the Beck Depression Inventory

The Beck Depression Inventory score ranges from 0 to 63, with a higher score indicating greater depressive symptoms. The scores from each timepoint will be plotted as a trend line. (NCT04941521)
Timeframe: Week 6

InterventionParticipants (Count of Participants)
Exenatide and Drug Counseling3

[back to top]

Clinical Effect of Exenatide as Indicated by Number of Participants Who Had a Decrease in Negative Affect Symptoms Indicated on the Positive/Negative Affect Schedule

The Positive/Negative Affect Schedule is a 20-item questionnaire divided into 10 positive affect items and 10 negative affect items. The score for the negative affect items ranges from 10 to 50, with a lower score indicating lower levels of negative affect. The scores from each timepoint will be plotted as a trend line. (NCT04941521)
Timeframe: From Week 0 to Week 6

InterventionParticipants (Count of Participants)
Exenatide and Drug Counseling1

[back to top]

Clinical Effect of Exenatide as Indicated by Number of Participants Who Reported a Reduction in Craving by Week 6 as Indicated by Cocaine Craving on the Brief Substance Craving Scale

The brief substance craving scale (BSCS) is a 16-item, self-report instrument that assesses craving for cocaine and other substances of abuse over a 24 hour period. The domains of intensity, frequency, and duration are recorded on a five-point Likert scale. The range of scores for each domain is 0 to 4, and the total score is the sum of all three domains. The total score range is 0 to 12, and higher scores indicate higher craving (worse outcome.) (NCT04941521)
Timeframe: From Week 0 to Week 6

InterventionParticipants (Count of Participants)
Exenatide and Drug Counseling2

[back to top]

Drug Safety as Assessed by Total Number of Adverse Events Reported During Treatment

Adverse events (AEs) will be reported to study nurse during the course of treatment. (NCT04941521)
Timeframe: From Week 1 to Week 6

Interventionadverse events (Number)
Exenatide and Drug Counseling7

[back to top]

Feasibility as Assessed by Number of Participants Enrolled

Enrollment will be assessed by the number of participants signing the informed consent. (NCT04941521)
Timeframe: Week 0

InterventionParticipants (Count of Participants)
Exenatide and Drug Counseling3

[back to top]

Feasibility as Assessed by Number of Participants Who Completed Treatment

Treatment completion will be assessed by attendance at the end-of-treatment timepoint. (NCT04941521)
Timeframe: Week 6

InterventionParticipants (Count of Participants)
Exenatide and Drug Counseling3

[back to top]

Feasibility as Assessed by Number of Study Visits Attended

There were 6 study visits planned. (NCT04941521)
Timeframe: From Week 1 to Week 6

Interventionstudy visits (Mean)
Exenatide and Drug Counseling6

[back to top]

Feasibility as Assessed by Retention as Indicated by Total Number of Completed Study Visits

Retention will be assessed by the total number of completed study visits. A completed study visit is a visit in which the participant attended and received the study treatment. (NCT04941521)
Timeframe: From Week 1 to Week 6

Interventioncompleted study visits (Mean)
Exenatide and Drug Counseling6

[back to top]

Clinical Effect of Exenatide as Assessed by Cocaine Use During Treatment as Indicated by Number of Participants With Cocaine-positive Urine Drug Screen Results

Urine drug screens were performed weekly. For a cocaine-negative urine drug screen result, benzoylecgonine levels must be under 300 ng/mL. (NCT04941521)
Timeframe: From Week 1 to Week 6

InterventionParticipants (Count of Participants)
week 1week 2week 3week 4week 5week 6
Exenatide and Drug Counseling333222

[back to top]
SubstanceRelationship StrengthStudiesTrialsClassesRoles
phosphoserine
Phosphoserine: The phosphoric acid ester of serine.		2.1110non-proteinogenic alpha-amino acid;
O-phosphoamino acid;
serine derivative		human metabolite
gamma-aminobutyric acid
gamma-Aminobutyric Acid: The most common inhibitory neurotransmitter in the central nervous system.. gamma-aminobutyric acid : A gamma-amino acid that is butanoic acid with the amino substituent located at C-4.		3.790amino acid zwitterion;
gamma-amino acid;
monocarboxylic acid		human metabolite;
neurotransmitter;
Saccharomyces cerevisiae metabolite;
signalling molecule
5-hydroxytryptophan
5-Hydroxytryptophan: The immediate precursor in the biosynthesis of SEROTONIN from tryptophan. It is used as an antiepileptic and antidepressant.. 5-hydroxytryptophan : A tryptophan derivative that is tryptophan substituted by a hydroxy group at position 5.		3.3510hydroxytryptophanhuman metabolite;
neurotransmitter
acetic acid
Acetic Acid: Product of the oxidation of ethanol and of the destructive distillation of wood. It is used locally, occasionally internally, as a counterirritant and also as a reagent. (Stedman, 26th ed). acetic acid : A simple monocarboxylic acid containing two carbons.		2.110monocarboxylic acidantimicrobial food preservative;
Daphnia magna metabolite;
food acidity regulator;
protic solvent
adenine
[no description available]		3.07406-aminopurines;
purine nucleobase		Daphnia magna metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
butyric acid
Butyric Acid: A four carbon acid, CH3CH2CH2COOH, with an unpleasant odor that occurs in butter and animal fat as the glycerol ester.. butyrate : A short-chain fatty acid anion that is the conjugate base of butyric acid, obtained by deprotonation of the carboxy group.. butyric acid : A straight-chain saturated fatty acid that is butane in which one of the terminal methyl groups has been oxidised to a carboxy group.		2.2510fatty acid 4:0;
straight-chain saturated fatty acid		human urinary metabolite;
Mycoplasma genitalium metabolite
carbamates
[no description available]		4.7930amino-acid anion
carbon monoxide
Carbon Monoxide: Carbon monoxide (CO). A poisonous colorless, odorless, tasteless gas. It combines with hemoglobin to form carboxyhemoglobin, which has no oxygen carrying capacity. The resultant oxygen deprivation causes headache, dizziness, decreased pulse and respiratory rates, unconsciousness, and death. (From Merck Index, 11th ed). carbon monoxide : A one-carbon compound in which the carbon is joined only to a single oxygen. It is a colourless, odourless, tasteless, toxic gas.		7.110carbon oxide;
gas molecular entity;
one-carbon compound		biomarker;
EC 1.9.3.1 (cytochrome c oxidase) inhibitor;
human metabolite;
ligand;
metabolite;
mitochondrial respiratory-chain inhibitor;
mouse metabolite;
neurotoxin;
neurotransmitter;
P450 inhibitor;
probe;
signalling molecule;
vasodilator agent
carnitine
[no description available]		2.5520amino-acid betainehuman metabolite;
mouse metabolite
choline
[no description available]		2.0210cholinesallergen;
Daphnia magna metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
neurotransmitter;
nutrient;
plant metabolite;
Saccharomyces cerevisiae metabolite
chlorine
chloride : A halide anion formed when chlorine picks up an electron to form an an anion.		2.1510halide anion;
monoatomic chlorine		cofactor;
Escherichia coli metabolite;
human metabolite
hydrochloric acid
Hydrochloric Acid: A strong corrosive acid that is commonly used as a laboratory reagent. It is formed by dissolving hydrogen chloride in water. GASTRIC ACID is the hydrochloric acid component of GASTRIC JUICE.. hydrogen chloride : A mononuclear parent hydride consisting of covalently bonded hydrogen and chlorine atoms.		2.1110chlorine molecular entity;
gas molecular entity;
hydrogen halide;
mononuclear parent hydride		mouse metabolite
coumarin
2H-chromen-2-one: coumarin derivative		2.110coumarinsfluorescent dye;
human metabolite;
plant metabolite
hydrogen sulfide
Hydrogen Sulfide: A flammable, poisonous gas with a characteristic odor of rotten eggs. It is used in the manufacture of chemicals, in metallurgy, and as an analytical reagent. (From Merck Index, 11th ed). hydrogen sulfide : A sulfur hydride consisting of a single sulfur atom bonded to two hydrogen atoms. A highly poisonous, flammable gas with a characteristic odour of rotten eggs, it is often produced by bacterial decomposition of organic matter in the absence of oxygen.. thiol : An organosulfur compound in which a thiol group, -SH, is attached to a carbon atom of any aliphatic or aromatic moiety.		2.110gas molecular entity;
hydracid;
mononuclear parent hydride;
sulfur hydride		Escherichia coli metabolite;
genotoxin;
metabolite;
signalling molecule;
toxin;
vasodilator agent
3-hydroxybutyric acid
3-Hydroxybutyric Acid: BUTYRIC ACID substituted in the beta or 3 position. It is one of the ketone bodies produced in the liver.. 3-hydroxybutyric acid : A straight-chain 3-hydroxy monocarboxylic acid comprising a butyric acid core with a single hydroxy substituent in the 3- position; a ketone body whose levels are raised during ketosis, used as an energy source by the brain during fasting in humans. Also used to synthesise biodegradable plastics.		3.4811(omega-1)-hydroxy fatty acid;
3-hydroxy monocarboxylic acid;
hydroxybutyric acid		human metabolite
bupropion
Bupropion: A propiophenone-derived antidepressant and antismoking agent that inhibits the uptake of DOPAMINE.. bupropion : An aromatic ketone that is propiophenone carrying a tert-butylamino group at position 2 and a chloro substituent at position 3 on the phenyl ring.		2.0610aromatic ketone;
monochlorobenzenes;
secondary amino compound		antidepressant;
environmental contaminant;
xenobiotic
n(g),n(g')-dimethyl-l-arginine
N,N-dimethylarginine: asymmetric dimethylarginine; do not confuse with N,N'-dimethylarginine		2.5820alpha-amino acid
trimetaphosphoric acid
trimetaphosphoric acid: RN given refers to parent cpd; structure. cyclotriphosphoric acid : The cyclic anhydride of triphosphoric acid.		2.1110cyclic phosphorus acid anhydride;
inorganic heterocyclic compound;
phosphorus oxoacid
3,4-dihydroxyphenylacetic acid
3,4-Dihydroxyphenylacetic Acid: A deaminated metabolite of LEVODOPA.. (3,4-dihydroxyphenyl)acetic acid : A dihydroxyphenylacetic acid having the two hydroxy substituents located at the 3- and 4-positions. It is a metabolite of dopamine.. dihydroxyphenylacetic acid : A dihydroxy monocarboxylic acid consisting of phenylacetic acid having two phenolic hydroxy substituents.		2.5920catechols;
dihydroxyphenylacetic acid		human metabolite
creatine
[no description available]		2.2110glycine derivative;
guanidines;
zwitterion		geroprotector;
human metabolite;
mouse metabolite;
neuroprotective agent;
nutraceutical
lactic acid
Lactic Acid: A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed). 2-hydroxypropanoic acid : A 2-hydroxy monocarboxylic acid that is propanoic acid in which one of the alpha-hydrogens is replaced by a hydroxy group.		8.122612-hydroxy monocarboxylic acidalgal metabolite;
Daphnia magna metabolite
dimethyl sulfoxide
Dimethyl Sulfoxide: A highly polar organic liquid, that is used widely as a chemical solvent. Because of its ability to penetrate biological membranes, it is used as a vehicle for topical application of pharmaceuticals. It is also used to protect tissue during CRYOPRESERVATION. Dimethyl sulfoxide shows a range of pharmacological activity including analgesia and anti-inflammation.. dimethyl sulfoxide : A 2-carbon sulfoxide in which the sulfur atom has two methyl substituents.		2.0810sulfoxide;
volatile organic compound		alkylating agent;
antidote;
Escherichia coli metabolite;
geroprotector;
MRI contrast agent;
non-narcotic analgesic;
polar aprotic solvent;
radical scavenger
formaldehyde
paraform: polymerized formaldehyde; RN given refers to parent cpd; used in root canal therapy		2.110aldehyde;
one-carbon compound		allergen;
carcinogenic agent;
disinfectant;
EC 3.5.1.4 (amidase) inhibitor;
environmental contaminant;
Escherichia coli metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
glycine
[no description available]		3.8230alpha-amino acid;
amino acid zwitterion;
proteinogenic amino acid;
serine family amino acid		EC 2.1.2.1 (glycine hydroxymethyltransferase) inhibitor;
fundamental metabolite;
hepatoprotective agent;
micronutrient;
neurotransmitter;
NMDA receptor agonist;
nutraceutical
glycerol
Moon: The natural satellite of the planet Earth. It includes the lunar cycles or phases, the lunar month, lunar landscapes, geography, and soil.		7.5720alditol;
triol		algal metabolite;
detergent;
Escherichia coli metabolite;
geroprotector;
human metabolite;
mouse metabolite;
osmolyte;
Saccharomyces cerevisiae metabolite;
solvent
glycolic acid
glycolic acid: RN given refers to parent cpd. glycolic acid : A 2-hydroxy monocarboxylic acid that is acetic acid where the methyl group has been hydroxylated.		7.1102-hydroxy monocarboxylic acid;
primary alcohol		keratolytic drug;
metabolite
hydrogen carbonate
Bicarbonates: Inorganic salts that contain the -HCO3 radical. They are an important factor in determining the pH of the blood and the concentration of bicarbonate ions is regulated by the kidney. Levels in the blood are an index of the alkali reserve or buffering capacity.. hydrogencarbonate : The carbon oxoanion resulting from the removal of a proton from carbonic acid.		2.0610carbon oxoanioncofactor;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
histamine
[no description available]		1.9810aralkylamino compound;
imidazoles		human metabolite;
mouse metabolite;
neurotransmitter
pyruvaldehyde
Pyruvaldehyde: An organic compound used often as a reagent in organic synthesis, as a flavoring agent, and in tanning. It has been demonstrated as an intermediate in the metabolism of acetone and its derivatives in isolated cell preparations, in various culture media, and in vivo in certain animals.. methylglyoxal : A 2-oxo aldehyde derived from propanal.		2.86302-oxo aldehyde;
propanals		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
inositol
Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction.. inositol : Any cyclohexane-1,2,3,4,5,6-hexol.. 1D-chiro-inositol : Belonging to the inositol family of compounds, D-chiro-inositol (DCI) is an isomer of glucose. It is an important secondary messenger in insulin signal transduction.. muco-inositol : An inositol that is cyclohexane-1,2,3,4,5,6-hexol having a (1R,2R,3r,4R,5S,6r)-configuration.		2.110cyclitol;
hexol
melatonin
[no description available]		3.8930acetamides;
tryptamines		anticonvulsant;
central nervous system depressant;
geroprotector;
hormone;
human metabolite;
immunological adjuvant;
mouse metabolite;
radical scavenger
niacinamide
nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.		4.96110pyridine alkaloid;
pyridinecarboxamide;
vitamin B3		anti-inflammatory agent;
antioxidant;
cofactor;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor;
EC 3.5.1.98 (histone deacetylase) inhibitor;
Escherichia coli metabolite;
geroprotector;
human urinary metabolite;
metabolite;
mouse metabolite;
neuroprotective agent;
Saccharomyces cerevisiae metabolite;
Sir2 inhibitor
nitrites
Nitrites: Salts of nitrous acid or compounds containing the group NO2-. The inorganic nitrites of the type MNO2 (where M=metal) are all insoluble, except the alkali nitrites. The organic nitrites may be isomeric, but not identical with the corresponding nitro compounds. (Grant & Hackh's Chemical Dictionary, 5th ed)		2.0810monovalent inorganic anion;
nitrogen oxoanion;
reactive nitrogen species		human metabolite
triphosphoric acid
triphosphoric acid: used as water softener, peptizing agent, emulsifier & dispersing agent; ingredient of cleansers; meat preservative; RN given refers to parent cpd; structure		2.110acyclic phosphorus acid anhydride;
phosphorus oxoacid
palmitic acid
Palmitic Acid: A common saturated fatty acid found in fats and waxes including olive oil, palm oil, and body lipids.. hexadecanoic acid : A straight-chain, sixteen-carbon, saturated long-chain fatty acid.		4.18150long-chain fatty acid;
straight-chain saturated fatty acid		algal metabolite;
Daphnia magna metabolite;
EC 1.1.1.189 (prostaglandin-E2 9-reductase) inhibitor;
plant metabolite
phosphorylcholine
Phosphorylcholine: Calcium and magnesium salts used therapeutically in hepatobiliary dysfunction.. phosphocholine : The phosphate of choline; and the parent compound of the phosphocholine family.		2.4420phosphocholinesallergen;
epitope;
hapten;
human metabolite;
mouse metabolite
propylene glycol
Propylene Glycol: A clear, colorless, viscous organic solvent and diluent used in pharmaceutical preparations.. propane-1,2-diol : The simplest member of the class of propane-1,2-diols, consisting of propane in which a hydrogen at position 1 and a hydrogen at position 2 are substituted by hydroxy groups. A colourless, viscous, hygroscopic, low-melting (-59degreeC) and high-boiling (188degreeC) liquid with low toxicity, it is used as a solvent, emulsifying agent, and antifreeze.		2.2510glycol;
propane-1,2-diols		allergen;
human xenobiotic metabolite;
mouse metabolite;
protic solvent
pyridoxine
4,5-bis(hydroxymethyl)-2-methylpyridin-3-ol: structure in first source. vitamin B6 : Any member of the group of pyridines that exhibit biological activity against vitamin B6 deficiency. Vitamin B6 deficiency is associated with microcytic anemia, electroencephalographic abnormalities, dermatitis with cheilosis (scaling on the lips and cracks at the corners of the mouth) and glossitis (swollen tongue), depression and confusion, and weakened immune function. Vitamin B6 consists of the vitamers pyridoxine, pyridoxal, and pyridoxamine and their respective 5'-phosphate esters (and includes their corresponding ionized and salt forms).		2.9510hydroxymethylpyridine;
methylpyridines;
monohydroxypyridine;
vitamin B6		cofactor;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
pyrogallol
benzenetriol : A triol in which three hydroxy groups are substituted onto a benzene ring.		2.1110benzenetriol;
phenolic donor		plant metabolite
taurine
[no description available]		2.4620amino sulfonic acid;
zwitterion		antioxidant;
Escherichia coli metabolite;
glycine receptor agonist;
human metabolite;
mouse metabolite;
nutrient;
radical scavenger;
Saccharomyces cerevisiae metabolite
uracil
2,4-dihydroxypyrimidine: a urinary biomarker for bipolar disorder		6.5590pyrimidine nucleobase;
pyrimidone		allergen;
Daphnia magna metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
prodrug;
Saccharomyces cerevisiae metabolite
uric acid
Uric Acid: An oxidation product, via XANTHINE OXIDASE, of oxypurines such as XANTHINE and HYPOXANTHINE. It is the final oxidation product of purine catabolism in humans and primates, whereas in most other mammals URATE OXIDASE further oxidizes it to ALLANTOIN.. uric acid : An oxopurine that is the final oxidation product of purine metabolism.. 6-hydroxy-1H-purine-2,8(7H,9H)-dione : A tautomer of uric acid having oxo groups at C-2 and C-8 and a hydroxy group at C-6.. 7,9-dihydro-1H-purine-2,6,8(3H)-trione : An oxopurine in which the purine ring is substituted by oxo groups at positions 2, 6, and 8.		2.1510uric acidEscherichia coli metabolite;
human metabolite;
mouse metabolite
urea
pseudourea: clinical use; structure. isourea : A carboximidic acid that is the imidic acid tautomer of urea, H2NC(=NH)OH, and its hydrocarbyl derivatives.		2.5120isourea;
monocarboxylic acid amide;
one-carbon compound		Daphnia magna metabolite;
Escherichia coli metabolite;
fertilizer;
flour treatment agent;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
2-amino-5-phosphonovalerate
2-Amino-5-phosphonovalerate: The D-enantiomer is a potent and specific antagonist of NMDA glutamate receptors (RECEPTORS, N-METHYL-D-ASPARTATE). The L form is inactive at NMDA receptors but may affect the AP4 (2-amino-4-phosphonobutyrate; APB) excitatory amino acid receptors.		2.1110non-proteinogenic alpha-amino acidNMDA receptor antagonist
sk&f 82958
[no description available]		2.1110benzazepine
ibotenic acid
Ibotenic Acid: A neurotoxic isoxazole (similar to KAINIC ACID and MUSCIMOL) found in AMANITA mushrooms. It causes motor depression, ataxia, and changes in mood, perceptions and feelings, and is a potent excitatory amino acid agonist.		3.3620non-proteinogenic alpha-amino acidneurotoxin
1,2-dimethylhydrazine
1,2-Dimethylhydrazine: A DNA alkylating agent that has been shown to be a potent carcinogen and is widely used to induce colon tumors in experimental animals.. 1,2-dimethylhydrazine : A member of the class of hydrazines that is hydrazine in which one of the hydrogens attached to each nitrogen is replaced by a methyl group. A powerful DNA alkylating agent and carcinogen, it is used to induce colon cancer in laboratory rats and mice.		7.520hydrazinesalkylating agent;
carcinogenic agent
1-anilino-8-naphthalenesulfonate
1-anilino-8-naphthalenesulfonate: RN given refers to parent cpd. 8-anilinonaphthalene-1-sulfonic acid : A naphthalenesulfonic acid that is naphthalene-1-sulfonic acid substituted by a phenylamino group at position 8.		3.8100aminonaphthalene;
naphthalenesulfonic acid		fluorescent probe
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine: A dopaminergic neurotoxic compound which produces irreversible clinical, chemical, and pathological alterations that mimic those found in Parkinson disease.. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine : A tetrahydropyridine that is 1,2,3,6-tetrahydropyridine substituted by a methyl group at position 1 and a phenyl group at position 4.		2.7930methylpyridines;
phenylpyridine;
tetrahydropyridine		neurotoxin
mercaptoethanol
Mercaptoethanol: A water-soluble thiol derived from hydrogen sulfide and ethanol. It is used as a reducing agent for disulfide bonds and to protect sulfhydryl groups from oxidation.		2.5120alkanethiol;
primary alcohol		geroprotector
5-hydroxydecanoate
5-hydroxydecanoic acid: Potassium Channel Blocker; RN refers to parent cpd		2.0810medium-chain fatty acid
tacrine
Tacrine: A cholinesterase inhibitor that crosses the blood-brain barrier. Tacrine has been used to counter the effects of muscle relaxants, as a respiratory stimulant, and in the treatment of Alzheimer's disease and other central nervous system disorders.. tacrine : A member of the class of acridines that is 1,2,3,4-tetrahydroacridine substituted by an amino group at position 9. It is used in the treatment of Alzheimer's disease.		2.2510acridines;
aromatic amine		EC 3.1.1.7 (acetylcholinesterase) inhibitor
acetaminophen
Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.. paracetamol : A member of the class of phenols that is 4-aminophenol in which one of the hydrogens attached to the amino group has been replaced by an acetyl group.		11.563acetamides;
phenols		antipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
cyclooxygenase 3 inhibitor;
environmental contaminant;
ferroptosis inducer;
geroprotector;
hepatotoxic agent;
human blood serum metabolite;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
alprazolam
Alprazolam: A triazolobenzodiazepine compound with antianxiety and sedative-hypnotic actions, that is efficacious in the treatment of PANIC DISORDERS, with or without AGORAPHOBIA, and in generalized ANXIETY DISORDERS. (From AMA Drug Evaluations Annual, 1994, p238). alprazolam : A member of the class of triazolobenzodiazepines that is 4H-[1,2,4]triazolo[4,3-a][1,4]benzodiazepine carrying methyl, phenyl and chloro substituents at positions 1, 6 and 8 respectively. Alprazolam is only found in individuals that have taken this drug.		2.0210organochlorine compound;
triazolobenzodiazepine		anticonvulsant;
anxiolytic drug;
GABA agonist;
muscle relaxant;
sedative;
xenobiotic
am 251
AM 251: an analog of SR141716A; structure given in first source. AM-251 : A carbohydrazide obtained by formal condensation of the carboxy group of 1-(2,4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-1H-pyrazole-3-carboxylic acid with the amino group of 1-aminopiperidine. An antagonist at the CB1 cannabinoid receptor.		2.4820amidopiperidine;
carbohydrazide;
dichlorobenzene;
organoiodine compound;
pyrazoles		antidepressant;
antineoplastic agent;
apoptosis inducer;
CB1 receptor antagonist
pimagedine
pimagedine: diamine oxidase & nitric oxide synthase inhibitor; an advanced glycosylation end product inhibitor; used in the treatment of diabetic complications; structure. aminoguanidine : A one-carbon compound whose unique structure renders it capable of acting as a derivative of hydrazine, guanidine or formamide.		3.2110guanidines;
one-carbon compound		EC 1.14.13.39 (nitric oxide synthase) inhibitor;
EC 1.4.3.4 (monoamine oxidase) inhibitor
azathioprine
Azathioprine: An immunosuppressive agent used in combination with cyclophosphamide and hydroxychloroquine in the treatment of rheumatoid arthritis. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance has been listed as a known carcinogen. (Merck Index, 11th ed). azathioprine : A thiopurine that is 6-mercaptopurine in which the mercapto hydrogen is replaced by a 1-methyl-4-nitroimidazol-5-yl group. It is a prodrug for mercaptopurine and is used as an immunosuppressant, prescribed for the treatment of inflammatory conditions and after organ transplantation and also for treatment of Crohn's didease and MS.		3.1710aryl sulfide;
C-nitro compound;
imidazoles;
thiopurine		antimetabolite;
antineoplastic agent;
carcinogenic agent;
DNA synthesis inhibitor;
hepatotoxic agent;
immunosuppressive agent;
prodrug
caffeine
[no description available]		210purine alkaloid;
trimethylxanthine		adenosine A2A receptor antagonist;
adenosine receptor antagonist;
adjuvant;
central nervous system stimulant;
diuretic;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
environmental contaminant;
food additive;
fungal metabolite;
geroprotector;
human blood serum metabolite;
mouse metabolite;
mutagen;
plant metabolite;
psychotropic drug;
ryanodine receptor agonist;
xenobiotic
chlorpromazine
Chlorpromazine: The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking DOPAMINE RECEPTORS. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup.. chlorpromazine : A substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropanamine moiety.		2.0810organochlorine compound;
phenothiazines;
tertiary amine		anticoronaviral agent;
antiemetic;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
phenothiazine antipsychotic drug
cilostazol
[no description available]		2.0810lactam;
tetrazoles		anticoagulant;
bronchodilator agent;
EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor;
fibrin modulating drug;
neuroprotective agent;
platelet aggregation inhibitor;
vasodilator agent
decanoic acid
decanoate : A fatty acid anion 10:0 that is the conjugate base of decanoic acid.. decanoic acid : A C10, straight-chain saturated fatty acid.		2.8230medium-chain fatty acid;
straight-chain saturated fatty acid		algal metabolite;
anti-inflammatory agent;
antibacterial agent;
human metabolite;
plant metabolite;
volatile oil component
deferoxamine
Deferoxamine: Natural product isolated from Streptomyces pilosus. It forms iron complexes and is used as a chelating agent, particularly in the mesylate form.. desferrioxamine B : An acyclic desferrioxamine that is butanedioic acid in which one of the carboxy groups undergoes formal condensation with the primary amino group of N-(5-aminopentyl)-N-hydroxyacetamide and the second carboxy group undergoes formal condensation with the hydroxyamino group of N(1)-(5-aminopentyl)-N(1)-hydroxy-N(4)-[5-(hydroxyamino)pentyl]butanediamide. It is a siderophore native to Streptomyces pilosus biosynthesised by the DesABCD enzyme cluster as a high affinity Fe(III) chelator.		2.1110acyclic desferrioxaminebacterial metabolite;
ferroptosis inhibitor;
iron chelator;
siderophore
amphetamine
Amphetamine: A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is DEXTROAMPHETAMINE.. 1-phenylpropan-2-amine : A primary amine that is isopropylamine in which a hydrogen attached to one of the methyl groups has been replaced by a phenyl group.. amphetamine : A racemate comprising equimolar amounts of (R)-amphetamine (also known as levamphetamine or levoamphetamine) and (S)-amphetamine (also known as dexamfetamine or dextroamphetamine.		2.7830primary amine
diazepam
Diazepam: A benzodiazepine with anticonvulsant, anxiolytic, sedative, muscle relaxant, and amnesic properties and a long duration of action. Its actions are mediated by enhancement of GAMMA-AMINOBUTYRIC ACID activity.. diazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a chloro group at position 7, a methyl group at position 1 and a phenyl group at position 5.		2.11101,4-benzodiazepinone;
organochlorine compound		anticonvulsant;
anxiolytic drug;
environmental contaminant;
sedative;
xenobiotic
diazoxide
Diazoxide: A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group.. diazoxide : A benzothiadiazine that is the S,S-dioxide of 2H-1,2,4-benzothiadiazine which is substituted at position 3 by a methyl group and at position 7 by chlorine. A peripheral vasodilator, it increases the concentration of glucose in the plasma and inhibits the secretion of insulin by the beta- cells of the pancreas. It is used orally in the management of intractable hypoglycaemia and intravenously in the management of hypertensive emergencies.		2.4820benzothiadiazine;
organochlorine compound;
sulfone		antihypertensive agent;
beta-adrenergic agonist;
bronchodilator agent;
cardiotonic drug;
diuretic;
K-ATP channel agonist;
sodium channel blocker;
sympathomimetic agent;
vasodilator agent
pentetic acid
Pentetic Acid: An iron chelating agent with properties like EDETIC ACID. DTPA has also been used as a chelator for other metals, such as plutonium.		5.2841pentacarboxylic acidcopper chelator
thiorphan
Thiorphan: A potent inhibitor of membrane metalloendopeptidase (ENKEPHALINASE). Thiorphan potentiates morphine-induced ANALGESIA and attenuates naloxone-precipitated withdrawal symptoms.		1.9910N-acyl-amino acid
dsp 4
DSP 4: RN given refers to parent cpd		2.0710
fenofibrate
Pharmavit: a polyvitamin product, comprising vitamins A, D2, B1, B2, B6, C, E, nicotinamide, & calcium pantothene; may be a promising agent for application to human populations exposed to carcinogenic and genetic hazards of ionizing radiation; RN from CHEMLINE		2.0810aromatic ether;
chlorobenzophenone;
isopropyl ester;
monochlorobenzenes		antilipemic drug;
environmental contaminant;
geroprotector;
xenobiotic
fentanyl
Fentanyl: A potent narcotic analgesic, abuse of which leads to habituation or addiction. It is primarily a mu-opioid agonist. Fentanyl is also used as an adjunct to general anesthetics, and as an anesthetic for induction and maintenance. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1078). fentanyl : A monocarboxylic acid amide resulting from the formal condensation of the aryl amino group of N-phenyl-1-(2-phenylethyl)piperidin-4-amine with propanoic acid.		2.3110anilide;
monocarboxylic acid amide;
piperidines		adjuvant;
anaesthesia adjuvant;
anaesthetic;
intravenous anaesthetic;
mu-opioid receptor agonist;
opioid analgesic
fluorouracil
Fluorouracil: A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.. 5-fluorouracil : A nucleobase analogue that is uracil in which the hydrogen at position 5 is replaced by fluorine. It is an antineoplastic agent which acts as an antimetabolite - following conversion to the active deoxynucleotide, it inhibits DNA synthesis (by blocking the conversion of deoxyuridylic acid to thymidylic acid by the cellular enzyme thymidylate synthetase) and so slows tumour growth.		3.6120nucleobase analogue;
organofluorine compound		antimetabolite;
antineoplastic agent;
environmental contaminant;
immunosuppressive agent;
radiosensitizing agent;
xenobiotic
furosemide
Furosemide: A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.. furosemide : A chlorobenzoic acid that is 4-chlorobenzoic acid substituted by a (furan-2-ylmethyl)amino and a sulfamoyl group at position 2 and 5 respectively. It is a diuretic used in the treatment of congestive heart failure.		2.0710chlorobenzoic acid;
furans;
sulfonamide		environmental contaminant;
loop diuretic;
xenobiotic
gliclazide
Gliclazide: An oral sulfonylurea hypoglycemic agent which stimulates insulin secretion.		4.1640N-sulfonylureahypoglycemic agent;
insulin secretagogue;
radical scavenger
glimepiride
glimepiride: structure given in first source		12.48248sulfonamide
glipizide
Glipizide: An oral hypoglycemic agent which is rapidly absorbed and completely metabolized.. glipizide : An N-sulfonylurea that is glyburide in which the (5-chloro-2-methoxybenzoyl group is replaced by a (5-methylpyrazin-2-yl)carbonyl group. An oral hypoglycemic agent, it is used in the treatment of type 2 diabetes mellitus.		10.7151aromatic amide;
monocarboxylic acid amide;
N-sulfonylurea;
pyrazines		EC 2.7.1.33 (pantothenate kinase) inhibitor;
hypoglycemic agent;
insulin secretagogue
glutaral
Glutaral: One of the protein CROSS-LINKING REAGENTS that is used as a disinfectant for sterilization of heat-sensitive equipment and as a laboratory reagent, especially as a fixative.. glutaraldehyde : A dialdehyde comprised of pentane with aldehyde functions at C-1 and C-5.		2.110dialdehydecross-linking reagent;
disinfectant;
fixative
glyburide
Glyburide: An antidiabetic sulfonylurea derivative with actions like those of chlorpropamide. glyburide : An N-sulfonylurea that is acetohexamide in which the acetyl group is replaced by a 2-(5-chloro-2-methoxybenzamido)ethyl group.		12.5382monochlorobenzenes;
N-sulfonylurea		anti-arrhythmia drug;
EC 2.7.1.33 (pantothenate kinase) inhibitor;
EC 3.6.3.49 (channel-conductance-controlling ATPase) inhibitor;
hypoglycemic agent
guaifenesin
Guaifenesin: An expectorant that also has some muscle relaxing action. It is used in many cough preparations.		2.7730methoxybenzenes
guanethidine
Guanethidine: An antihypertensive agent that acts by inhibiting selectively transmission in post-ganglionic adrenergic nerves. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues.. guanethidine : A member of the class of guanidines in which one of the hydrogens of the amino group has been replaced by a 2-azocan-1-ylethyl group.. guanethidine sulfate : A organic sulfate salt composed of two molecules of guanethidine and one of sulfuric acid.		2.110azocanes;
guanidines		adrenergic antagonist;
antihypertensive agent;
sympatholytic agent
1-(5-isoquinolinesulfonyl)-2-methylpiperazine
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine: A specific protein kinase C inhibitor, which inhibits superoxide release from human neutrophils (PMN) stimulated with phorbol myristate acetate or synthetic diacylglycerol.. 1-(5-isoquinolinesulfonyl)-2-methylpiperazine : A member of the class of N-sulfonylpiperazines that is 2-methylpiperazine substituted at position 1 by a 5-isoquinolinesulfonyl group.		2.0210isoquinolines;
N-sulfonylpiperazine		EC 2.7.11.13 (protein kinase C) inhibitor
haloperidol
Haloperidol: A phenyl-piperidinyl-butyrophenone that is used primarily to treat SCHIZOPHRENIA and other PSYCHOSES. It is also used in schizoaffective disorder, DELUSIONAL DISORDERS, ballism, and TOURETTE SYNDROME (a drug of choice) and occasionally as adjunctive therapy in INTELLECTUAL DISABILITY and the chorea of HUNTINGTON DISEASE. It is a potent antiemetic and is used in the treatment of intractable HICCUPS. (From AMA Drug Evaluations Annual, 1994, p279). haloperidol : A compound composed of a central piperidine structure with hydroxy and p-chlorophenyl substituents at position 4 and an N-linked p-fluorobutyrophenone moiety.		2.110aromatic ketone;
hydroxypiperidine;
monochlorobenzenes;
organofluorine compound;
tertiary alcohol		antidyskinesia agent;
antiemetic;
dopaminergic antagonist;
first generation antipsychotic;
serotonergic antagonist
hydralazine
Hydralazine: A direct-acting vasodilator that is used as an antihypertensive agent.. hydralazine : The 1-hydrazino derivative of phthalazine; a direct-acting vasodilator that is used as an antihypertensive agent.		2.0310azaarene;
hydrazines;
ortho-fused heteroarene;
phthalazines		antihypertensive agent;
vasodilator agent
1-methyl-3-isobutylxanthine
1-Methyl-3-isobutylxanthine: A potent cyclic nucleotide phosphodiesterase inhibitor; due to this action, the compound increases cyclic AMP and cyclic GMP in tissue and thereby activates CYCLIC NUCLEOTIDE-REGULATED PROTEIN KINASES. 3-isobutyl-1-methylxanthine : An oxopurine that is xanthine which is substituted at positions 1 and 3 by methyl and isobutyl groups, respectively.		2.05103-isobutyl-1-methylxanthine
isoflurane
Isoflurane: A stable, non-explosive inhalation anesthetic, relatively free from significant side effects.		2.1110organofluorine compoundinhalation anaesthetic
isoproterenol
Isoproterenol: Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.. isoprenaline : A secondary amino compound that is noradrenaline in which one of the hydrogens attached to the nitrogen is replaced by an isopropyl group. A sympathomimetic acting almost exclusively on beta-adrenergic receptors, it is used (mainly as the hydrochloride salt) as a bronghodilator and heart stimulant for the management of a variety of cardiac disorders.		2.1710catechols;
secondary alcohol;
secondary amino compound		beta-adrenergic agonist;
bronchodilator agent;
cardiotonic drug;
sympathomimetic agent
2-(4-morpholinyl)-8-phenyl-4h-1-benzopyran-4-one
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one: specific inhibitor of phosphatidylinositol 3-kinase; structure in first source		3.4970chromones;
morpholines;
organochlorine compound		autophagy inhibitor;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor;
geroprotector
metformin
Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289). metformin : A member of the class of guanidines that is biguanide the carrying two methyl substituents at position 1.		21.57214100guanidinesenvironmental contaminant;
geroprotector;
hypoglycemic agent;
xenobiotic
metoclopramide
Metoclopramide: A dopamine D2 antagonist that is used as an antiemetic.. metoclopramide : A member of the class of benzamides resulting from the formal condensation of 4-amino-5-chloro-2-methoxybenzoic acid with the primary amino group of N,N-diethylethane-1,2-diamine.		8.6411benzamides;
monochlorobenzenes;
substituted aniline;
tertiary amino compound		antiemetic;
dopaminergic antagonist;
environmental contaminant;
gastrointestinal drug;
xenobiotic
metoprolol
Metoprolol: A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.. metoprolol : A propanolamine that is 1-(propan-2-ylamino)propan-2-ol substituted by a 4-(2-methoxyethyl)phenoxy group at position 1.		3.3110aromatic ether;
propanolamine;
secondary alcohol;
secondary amino compound		antihypertensive agent;
beta-adrenergic antagonist;
environmental contaminant;
geroprotector;
xenobiotic
clorgyline
Clorgyline: An antidepressive agent and monoamine oxidase inhibitor related to PARGYLINE.. clorgyline : An aromatic ether that is the 2,4-dichlorophenyl ether of 3-aminopropan-1-ol in which the nitrogen is substituted by a methyl group and a prop-1-yn-3-yl group. A monoamine oxidase inhibitor, it was formerly used as an antidepressant.		2.0710aromatic ether;
dichlorobenzene;
terminal acetylenic compound;
tertiary amino compound		antidepressant;
EC 1.4.3.4 (monoamine oxidase) inhibitor
activins
Activins: Activins are produced in the pituitary, gonads, and other tissues. By acting locally, they stimulate pituitary FSH secretion and have diverse effects on cell differentiation and embryonic development. Activins are glycoproteins that are hetero- or homodimers of INHIBIN-BETA SUBUNITS.		3.3360
nifedipine
Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.		2.1110C-nitro compound;
dihydropyridine;
methyl ester		calcium channel blocker;
human metabolite;
tocolytic agent;
vasodilator agent
nitroglycerin
Nitroglycerin: A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.. nitroglycerol : A nitrate ester that is glycerol in which nitro group(s) replace the hydrogen(s) attached to one or more of the hydroxy groups.. nitroglycerin : A nitroglycerol that is glycerol in which the hydrogen atoms of all three hydroxy groups are replaced by nitro groups. It acts as a prodrug, releasing nitric oxide to open blood vessels and so alleviate heart pain.		2.1110nitroglycerolexplosive;
muscle relaxant;
nitric oxide donor;
prodrug;
tocolytic agent;
vasodilator agent;
xenobiotic
ofloxacin
Ofloxacin: A synthetic fluoroquinolone antibacterial agent that inhibits the supercoiling activity of bacterial DNA GYRASE, halting DNA REPLICATION.. 9-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid : An oxazinoquinoline that is 2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinolin-7-one substituted by methyl, carboxy, fluoro, and 4-methylpiperazin-1-yl groups at positions 3, 6, 9, and 10, respectively.. ofloxacin : A racemate comprising equimolar amounts of levofloxacin and dextrofloxacin. It is a synthetic fluoroquinolone antibacterial agent which inhibits the supercoiling activity of bacterial DNA gyrase, halting DNA replication.		2.07103-oxo monocarboxylic acid;
N-arylpiperazine;
N-methylpiperazine;
organofluorine compound;
oxazinoquinoline
omeprazole
Omeprazole: A 4-methoxy-3,5-dimethylpyridyl, 5-methoxybenzimidazole derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits an H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.. omeprazole : A racemate comprising equimolar amounts of (R)- and (S)-omeprazole.. 5-methoxy-2-{[(4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl}-1H-benzimidazole : A member of the class of benzimidazoles that is 1H-benzimidazole which is substituted by a [4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl group at position 2 and a methoxy group at position 5.		2.4920aromatic ether;
benzimidazoles;
pyridines;
sulfoxide
ondansetron
Ondansetron: A competitive serotonin type 3 receptor antagonist. It is effective in the treatment of nausea and vomiting caused by cytotoxic chemotherapy drugs, including cisplatin, and has reported anxiolytic and neuroleptic properties.		2.110carbazoles
oxidopamine
Oxidopamine: A neurotransmitter analogue that depletes noradrenergic stores in nerve endings and induces a reduction of dopamine levels in the brain. Its mechanism of action is related to the production of cytolytic free-radicals.. oxidopamine : A benzenetriol that is phenethylamine in which the hydrogens at positions 2, 4, and 5 on the phenyl ring are replaced by hydroxy groups. It occurs naturally in human urine, but is also produced as a metabolite of the drug DOPA (used for the treatment of Parkinson's disease).		3.4770benzenetriol;
catecholamine;
primary amino compound		drug metabolite;
human metabolite;
neurotoxin
oxybutynin
oxybutynin: RN given refers to parent cpd. oxybutynin : A racemate comprising equimolar amounts of (R)-oxybutynin and esoxybutynin. An antispasmodic used for the treatment of overactive bladder.		2.110acetylenic compound;
carboxylic ester;
racemate;
tertiary alcohol;
tertiary amino compound		antispasmodic drug;
calcium channel blocker;
local anaesthetic;
muscarinic antagonist;
muscle relaxant;
parasympatholytic
fenclonine
Fenclonine: A selective and irreversible inhibitor of tryptophan hydroxylase, a rate-limiting enzyme in the biosynthesis of serotonin (5-HYDROXYTRYPTAMINE). Fenclonine acts pharmacologically to deplete endogenous levels of serotonin.		2.1510phenylalanine derivative
papaverine
Papaverine: An alkaloid found in opium but not closely related to the other opium alkaloids in its structure or pharmacological actions. It is a direct-acting smooth muscle relaxant used in the treatment of impotence and as a vasodilator, especially for cerebral vasodilation. The mechanism of its pharmacological actions is not clear, but it apparently can inhibit phosphodiesterases and it may have direct actions on calcium channels.. papaverine : A benzylisoquinoline alkaloid that is isoquinoline substituted by methoxy groups at positions 6 and 7 and a 3,4-dimethoxybenzyl group at position 1. It has been isolated from Papaver somniferum.		2.1110benzylisoquinoline alkaloid;
dimethoxybenzene;
isoquinolines		antispasmodic drug;
vasodilator agent
pd 98059
2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one: inhibits MAP kinase kinase (MEK) activity, p42 MAPK and p44 MAPK; structure in first source. 2-(2-amino-3-methoxyphenyl)chromen-4-one : A member of the class of monomethoxyflavones that is 3'-methoxyflavone bearing an additional amino substituent at position 2'.		2.7330aromatic amine;
monomethoxyflavone		EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
geroprotector
pentoxifylline
[no description available]		2.0310oxopurine
phenobarbital
Phenobarbital: A barbituric acid derivative that acts as a nonselective central nervous system depressant. It potentiates GAMMA-AMINOBUTYRIC ACID action on GABA-A RECEPTORS, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations.. phenobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by ethyl and phenyl groups.		2.1110barbituratesanticonvulsant;
drug allergen;
excitatory amino acid antagonist;
sedative
phentermine
Phentermine: A central nervous system stimulant and sympathomimetic with actions and uses similar to those of DEXTROAMPHETAMINE. It has been used most frequently in the treatment of obesity.		9.6211primary amineadrenergic agent;
appetite depressant;
central nervous system drug;
central nervous system stimulant;
dopaminergic agent;
sympathomimetic agent
pioglitazone
Pioglitazone: A thiazolidinedione and PPAR GAMMA agonist that is used in the treatment of TYPE 2 DIABETES MELLITUS.. pioglitazone : A member of the class of thiazolidenediones that is 1,3-thiazolidine-2,4-dione substituted by a benzyl group at position 5 which in turn is substituted by a 2-(5-ethylpyridin-2-yl)ethoxy group at position 4 of the phenyl ring. It exhibits hypoglycemic activity.		16.325425aromatic ether;
pyridines;
thiazolidinediones		antidepressant;
cardioprotective agent;
EC 2.7.1.33 (pantothenate kinase) inhibitor;
EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
geroprotector;
hypoglycemic agent;
insulin-sensitizing drug;
PPARgamma agonist;
xenobiotic
potassium chloride
Potassium Chloride: A white crystal or crystalline powder used in BUFFERS; FERTILIZERS; and EXPLOSIVES. It can be used to replenish ELECTROLYTES and restore WATER-ELECTROLYTE BALANCE in treating HYPOKALEMIA.. potassium chloride : A metal chloride salt with a K(+) counterion.		2.0610inorganic chloride;
inorganic potassium salt;
potassium salt		fertilizer
propranolol
Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.. propranolol : A propanolamine that is propan-2-ol substituted by a propan-2-ylamino group at position 1 and a naphthalen-1-yloxy group at position 3.		2.0410naphthalenes;
propanolamine;
secondary amine		anti-arrhythmia drug;
antihypertensive agent;
anxiolytic drug;
beta-adrenergic antagonist;
environmental contaminant;
human blood serum metabolite;
vasodilator agent;
xenobiotic
ro 31-8220
Ro 31-8220: a protein kinase C inhibitor		2.7130imidothiocarbamic ester;
indoles;
maleimides		EC 2.7.11.13 (protein kinase C) inhibitor
ropinirole
[no description available]		2.0310indolones;
tertiary amine		antidyskinesia agent;
antiparkinson drug;
central nervous system drug;
dopamine agonist
saccharin
Saccharin: Flavoring agent and non-nutritive sweetener.. saccharin : A 1,2-benzisothiazole having a keto-group at the 3-position and two oxo substituents at the 1-position. It is used as an artificial sweetening agent.		2.11101,2-benzisothiazole;
N-sulfonylcarboxamide		environmental contaminant;
sweetening agent;
xenobiotic
sibutramine
sibutramine: serotonin and norepinephrine transporter inhibitor; Meridia is tradename for sibutramine hydrochloride		4.0520organochlorine compound;
tertiary amino compound		anti-obesity agent;
serotonin uptake inhibitor
2,4-thiazolidinedione
thiazolidine-2,4-dione: structure in first source. 1,3-thiazolidine-2,4-dione : A thiazolidenedione carrying oxo substituents at positions 2 and 4.		8.2562thiazolidenedione
tolbutamide
Tolbutamide: A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290). tolbutamide : An N-sulfonylurea that consists of 1-butylurea having a tosyl group attached at the 3-position.		2.7730N-sulfonylureahuman metabolite;
hypoglycemic agent;
insulin secretagogue;
potassium channel blocker
trimethoprim
Trimethoprim: A pyrimidine inhibitor of dihydrofolate reductase, it is an antibacterial related to PYRIMETHAMINE. It is potentiated by SULFONAMIDES and the TRIMETHOPRIM, SULFAMETHOXAZOLE DRUG COMBINATION is the form most often used. It is sometimes used alone as an antimalarial. TRIMETHOPRIM RESISTANCE has been reported.. trimethoprim : An aminopyrimidine antibiotic whose structure consists of pyrimidine 2,4-diamine and 1,2,3-trimethoxybenzene moieties linked by a methylene bridge.		3.3110aminopyrimidine;
methoxybenzenes		antibacterial drug;
diuretic;
drug allergen;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
environmental contaminant;
xenobiotic
troglitazone
Troglitazone: A chroman and thiazolidinedione derivative that acts as a PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS (PPAR) agonist. It was formerly used in the treatment of TYPE 2 DIABETES MELLITUS, but has been withdrawn due to hepatotoxicity.		2.0210chromanes;
thiazolidinone		anticoagulant;
anticonvulsant;
antineoplastic agent;
antioxidant;
EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
hypoglycemic agent;
platelet aggregation inhibitor;
vasodilator agent
zardaverine
zardaverine: structure given in first source. zardaverine : A pyridazinone derivative in which pyridazin-3(2H)-one is substituted at C-6 with a 4-(difluoromethoxy)-3-methoxyphenyl group. It is a phosphodiesterase inhibitor, selective for PDE3 and 4.		2.1310organofluorine compound;
pyridazinone		anti-asthmatic drug;
bronchodilator agent;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
peripheral nervous system drug
zopiclone
zopiclone: S(+)-enantiomer of racemic zopiclone; azabicyclo(4.3.0)nonane; a nonbenzodiazepine; one of the so-called of Z drugs (zopiclone, eszopiclone, zolpidem, and zaleplon) for which there is some correlation with tumors; was term of zopiclone 2004-2007. zopiclone : A pyrrolo[3,4-b]pyrazine compound having a 4-methylpiperazine-1-carboxyl group at the 5-position, a 5-chloropyridin-2-yl group at the 6-position and an oxo-substituent at the 7-position.		2.4320monochloropyridine;
pyrrolopyrazine		central nervous system depressant;
sedative
corticosterone
[no description available]		5.1510111beta-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
C21-steroid;
glucocorticoid;
primary alpha-hydroxy ketone		human metabolite;
mouse metabolite
reserpine
Reserpine: An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria. Reserpine inhibits the uptake of norepinephrine into storage vesicles resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals. It has been used as an antihypertensive and an antipsychotic as well as a research tool, but its adverse effects limit its clinical use.. reserpine : An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria.		2.0810alkaloid ester;
methyl ester;
yohimban alkaloid		adrenergic uptake inhibitor;
antihypertensive agent;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
environmental contaminant;
first generation antipsychotic;
plant metabolite;
xenobiotic
phentolamine
Phentolamine: A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of RAYNAUD DISEASE and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease.. phentolamine : A substituted aniline that is 3-aminophenol in which the hydrogens of the amino group are replaced by 4-methylphenyl and 4,5-dihydro-1H-imidazol-2-ylmethyl groups respectively. An alpha-adrenergic antagonist, it is used for the treatment of hypertension.		2.0410imidazoles;
phenols;
substituted aniline;
tertiary amino compound		alpha-adrenergic antagonist;
vasodilator agent
alloxan
Alloxan: Acidic compound formed by oxidation of URIC ACID. It is isolated as an efflorescent crystalline hydrate.. alloxan : A member of the class of pyrimidones, the structure of which is that of perhydropyrimidine substituted at C-2, -4, -5 and -6 by oxo groups.		2.1310pyrimidonehyperglycemic agent;
metabolite
hydroxyproline
Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ASCORBIC ACID can result in impaired hydroxyproline formation.. hydroxyproline : A proline derivative that is proline substituted by at least one hydroxy group.		2.31104-hydroxyproline;
L-alpha-amino acid zwitterion		human metabolite;
mouse metabolite;
plant metabolite
dextroamphetamine
Dextroamphetamine: The d-form of AMPHETAMINE. It is a central nervous system stimulant and a sympathomimetic. It has also been used in the treatment of narcolepsy and of attention deficit disorders and hyperactivity in children. Dextroamphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulating release of monamines, and inhibiting monoamine oxidase. It is also a drug of abuse and a psychotomimetic.. (S)-amphetamine : A 1-phenylpropan-2-amine that has S configuration.		2.41101-phenylpropan-2-amineadrenergic agent;
adrenergic uptake inhibitor;
dopamine uptake inhibitor;
dopaminergic agent;
neurotoxin;
sympathomimetic agent
carbachol
Carbachol: A slowly hydrolyzed CHOLINERGIC AGONIST that acts at both MUSCARINIC RECEPTORS and NICOTINIC RECEPTORS.		2.7530ammonium salt;
carbamate ester		cardiotonic drug;
miotic;
muscarinic agonist;
nicotinic acetylcholine receptor agonist;
non-narcotic analgesic
spironolactone
Spironolactone: A potassium sparing diuretic that acts by antagonism of aldosterone in the distal renal tubules. It is used mainly in the treatment of refractory edema in patients with congestive heart failure, nephrotic syndrome, or hepatic cirrhosis. Its effects on the endocrine system are utilized in the treatments of hirsutism and acne but they can lead to adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p827). spironolactone : A steroid lactone that is 17alpha-pregn-4-ene-21,17-carbolactone substituted by an oxo group at position 3 and an alpha-acetylsulfanyl group at position 7.		3.21103-oxo-Delta(4) steroid;
oxaspiro compound;
steroid lactone;
thioester		aldosterone antagonist;
antihypertensive agent;
diuretic;
environmental contaminant;
xenobiotic
aldosterone
[no description available]		2.743011beta-hydroxy steroid;
18-oxo steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
C21-steroid hormone;
mineralocorticoid;
primary alpha-hydroxy ketone;
steroid aldehyde		human metabolite;
mouse metabolite
prednisone
Prednisone: A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.. prednisone : A synthetic glucocorticoid drug that is particularly effective as an immunosuppressant, and affects virtually all of the immune system. Prednisone is a prodrug that is converted by the liver into prednisolone (a beta-hydroxy group instead of the oxo group at position 11), which is the active drug and also a steroid.		4.371111-oxo steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
C21-steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		adrenergic agent;
anti-inflammatory drug;
antineoplastic agent;
immunosuppressive agent;
prodrug
dehydroepiandrosterone
Dehydroepiandrosterone: A major C19 steroid produced by the ADRENAL CORTEX. It is also produced in small quantities in the TESTIS and the OVARY. Dehydroepiandrosterone (DHEA) can be converted to TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE. Most of DHEA is sulfated (DEHYDROEPIANDROSTERONE SULFATE) before secretion.. dehydroepiandrosterone : An androstanoid that is androst-5-ene substituted by a beta-hydroxy group at position 3 and an oxo group at position 17. It is a naturally occurring steroid hormone produced by the adrenal glands.		2.522017-oxo steroid;
3beta-hydroxy-Delta(5)-steroid;
androstanoid		androgen;
human metabolite;
mouse metabolite
triiodothyronine
Triiodothyronine: A T3 thyroid hormone normally synthesized and secreted by the thyroid gland in much smaller quantities than thyroxine (T4). Most T3 is derived from peripheral monodeiodination of T4 at the 5' position of the outer ring of the iodothyronine nucleus. The hormone finally delivered and used by the tissues is mainly T3.. 3,3',5-triiodo-L-thyronine : An iodothyronine compound having iodo substituents at the 3-, 3'- and 5-positions. Although some is produced in the thyroid, most of the 3,3',5-triiodo-L-thyronine in the body is generated by mono-deiodination of L-thyroxine in the peripheral tissues. Its metabolic activity is about 3 to 5 times that of L-thyroxine. The sodium salt is used in the treatment of hypothyroidism.		5.16312-halophenol;
amino acid zwitterion;
iodophenol;
iodothyronine		human metabolite;
mouse metabolite;
thyroid hormone
biguanides
Biguanides: Derivatives of biguanide (the structure formula HN(C(NH)NH2)2) that are primarily used as oral HYPOGLYCEMIC AGENTS for the treatment of DIABETES MELLITUS, TYPE 2 and PREDIABETES.. biguanides : A class of oral hypoglycemic drugs used for diabetes mellitus or prediabetes treatment. They have a structure based on the 2-carbamimidoylguanidine skeleton.		5.8540guanidines
alanine
Alanine: A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases IMMUNITY, and provides energy for muscle tissue, BRAIN, and the CENTRAL NERVOUS SYSTEM.. alanine : An alpha-amino acid that consists of propionic acid bearing an amino substituent at position 2.		2.0510alanine zwitterion;
alanine;
L-alpha-amino acid;
proteinogenic amino acid;
pyruvate family amino acid		EC 4.3.1.15 (diaminopropionate ammonia-lyase) inhibitor;
fundamental metabolite
serine
Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from GLYCINE or THREONINE. It is involved in the biosynthesis of PURINES; PYRIMIDINES; and other amino acids.. serine : An alpha-amino acid that is alanine substituted at position 3 by a hydroxy group.		2.4620L-alpha-amino acid;
proteinogenic amino acid;
serine family amino acid;
serine zwitterion;
serine		algal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
aspartic acid
Aspartic Acid: One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter.. aspartic acid : An alpha-amino acid that consists of succinic acid bearing a single alpha-amino substituent. L-aspartic acid : The L-enantiomer of aspartic acid.		4.651aspartate family amino acid;
aspartic acid;
L-alpha-amino acid;
proteinogenic amino acid		Escherichia coli metabolite;
mouse metabolite;
neurotransmitter
lysine
Lysine: An essential amino acid. It is often added to animal feed.. lysine : A diamino acid that is caproic (hexanoic) acid bearing two amino substituents at positions 2 and 6.. L-lysine : An L-alpha-amino acid; the L-isomer of lysine.		2.9740aspartate family amino acid;
L-alpha-amino acid zwitterion;
L-alpha-amino acid;
lysine;
organic molecular entity;
proteinogenic amino acid		algal metabolite;
anticonvulsant;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
sucrose
Saccharum: A plant genus of the family POACEAE widely cultivated in the tropics for the sweet cane that is processed into sugar.		4.4270glycosyl glycosidealgal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
osmolyte;
Saccharomyces cerevisiae metabolite;
sweetening agent
ethinyl estradiol
Ethinyl Estradiol: A semisynthetic alkylated ESTRADIOL with a 17-alpha-ethinyl substitution. It has high estrogenic potency when administered orally, and is often used as the estrogenic component in ORAL CONTRACEPTIVES.. 17alpha-ethynylestradiol : A 3-hydroxy steroid that is estradiol substituted by a ethynyl group at position 17. It is a xenoestrogen synthesized from estradiol and has been shown to exhibit high estrogenic potency on oral administration.		4.371117-hydroxy steroid;
3-hydroxy steroid;
terminal acetylenic compound		xenoestrogen
apomorphine
Apomorphine: A derivative of morphine that is a dopamine D2 agonist. It is a powerful emetic and has been used for that effect in acute poisoning. It has also been used in the diagnosis and treatment of parkinsonism, but its adverse effects limit its use.		2.0410aporphine alkaloidalpha-adrenergic drug;
antidyskinesia agent;
antiparkinson drug;
dopamine agonist;
emetic;
serotonergic drug
aminopyrine
Aminopyrine: A pyrazolone with analgesic, anti-inflammatory, and antipyretic properties but has risk of AGRANULOCYTOSIS. A breath test with 13C-labeled aminopyrine has been used as a non-invasive measure of CYTOCHROME P-450 metabolic activity in LIVER FUNCTION TESTS.. aminophenazone : A pyrazolone that is 1,2-dihydro-3H-pyrazol-3-one substituted by a dimethylamino group at position 4, methyl groups at positions 1 and 5 and a phenyl group at position 2. It exhibits analgesic, anti-inflammatory, and antipyretic properties.		2.3920pyrazolone;
tertiary amino compound		antipyretic;
environmental contaminant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
tetrabenazine
9,10-dimethoxy-3-isobutyl-1,3,4,6,7,11b-hexahydro-2H-pyrido[2,1-a]isoquinolin-2-one : A benzoquinolizine that is 1,2,3,4,4a,9,10,10a-octahydrophenanthrene in which the carbon at position 10a is replaced by a nitrogen and which is substituted by an isobutyl group at position 2, an oxo group at position 3, and methoxy groups at positions 6 and 7.		3.3510benzoquinolizine;
cyclic ketone;
tertiary amino compound
bromodeoxyuridine
Bromodeoxyuridine: A nucleoside that substitutes for thymidine in DNA and thus acts as an antimetabolite. It causes breaks in chromosomes and has been proposed as an antiviral and antineoplastic agent. It has been given orphan drug status for use in the treatment of primary brain tumors.		3.1450pyrimidine 2'-deoxyribonucleosideantimetabolite;
antineoplastic agent
galactose
galactopyranose : The pyranose form of galactose.		3.711D-galactose;
galactopyranose		Escherichia coli metabolite;
mouse metabolite
levodopa
Levodopa: The naturally occurring form of DIHYDROXYPHENYLALANINE and the immediate precursor of DOPAMINE. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to DOPAMINE. It is used for the treatment of PARKINSONIAN DISORDERS and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system.. L-dopa : An optically active form of dopa having L-configuration. Used to treat the stiffness, tremors, spasms, and poor muscle control of Parkinson's disease		2.7830amino acid zwitterion;
dopa;
L-tyrosine derivative;
non-proteinogenic L-alpha-amino acid		allelochemical;
antidyskinesia agent;
antiparkinson drug;
dopaminergic agent;
hapten;
human metabolite;
mouse metabolite;
neurotoxin;
plant growth retardant;
plant metabolite;
prodrug
edetic acid
Edetic Acid: A chelating agent that sequesters a variety of polyvalent cations such as CALCIUM. It is used in pharmaceutical manufacturing and as a food additive.		2.0710ethylenediamine derivative;
polyamino carboxylic acid;
tetracarboxylic acid		anticoagulant;
antidote;
chelator;
copper chelator;
geroprotector
tyrosine
Tyrosine: A non-essential amino acid. In animals it is synthesized from PHENYLALANINE. It is also the precursor of EPINEPHRINE; THYROID HORMONES; and melanin.. tyrosine : An alpha-amino acid that is phenylalanine bearing a hydroxy substituent at position 4 on the phenyl ring.		2.9440amino acid zwitterion;
erythrose 4-phosphate/phosphoenolpyruvate family amino acid;
L-alpha-amino acid;
proteinogenic amino acid;
tyrosine		EC 1.3.1.43 (arogenate dehydrogenase) inhibitor;
fundamental metabolite;
micronutrient;
nutraceutical
cysteamine
Cysteamine: A mercaptoethylamine compound that is endogenously derived from the COENZYME A degradative pathway. The fact that cysteamine is readily transported into LYSOSOMES where it reacts with CYSTINE to form cysteine-cysteamine disulfide and CYSTEINE has led to its use in CYSTINE DEPLETING AGENTS for the treatment of CYSTINOSIS.. cysteamine : An amine that consists of an ethane skeleton substituted with a thiol group at C-1 and an amino group at C-2.		2.4220amine;
thiol		geroprotector;
human metabolite;
mouse metabolite;
radiation protective agent
methionine
Methionine: A sulfur-containing essential L-amino acid that is important in many body functions.. methionine : A sulfur-containing amino acid that is butyric acid bearing an amino substituent at position 2 and a methylthio substituent at position 4.		2.4620aspartate family amino acid;
L-alpha-amino acid;
methionine zwitterion;
methionine;
proteinogenic amino acid		antidote to paracetamol poisoning;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical
phenylalanine
Phenylalanine: An essential aromatic amino acid that is a precursor of MELANIN; DOPAMINE; noradrenalin (NOREPINEPHRINE), and THYROXINE.. L-phenylalanine : The L-enantiomer of phenylalanine.. phenylalanine : An aromatic amino acid that is alanine in which one of the methyl hydrogens is substituted by a phenyl group.		2.5220amino acid zwitterion;
erythrose 4-phosphate/phosphoenolpyruvate family amino acid;
L-alpha-amino acid;
phenylalanine;
proteinogenic amino acid		algal metabolite;
EC 3.1.3.1 (alkaline phosphatase) inhibitor;
Escherichia coli metabolite;
human xenobiotic metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
desoxycorticosterone
Desoxycorticosterone: A steroid metabolite that is the 11-deoxy derivative of CORTICOSTERONE and the 21-hydroxy derivative of PROGESTERONE		2.071020-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
mineralocorticoid;
primary alpha-hydroxy ketone		human metabolite;
mouse metabolite
cycloheximide
Cycloheximide: Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.. cycloheximide : A dicarboximide that is 4-(2-hydroxyethyl)piperidine-2,6-dione in which one of the hydrogens attached to the carbon bearing the hydroxy group is replaced by a 3,5-dimethyl-2-oxocyclohexyl group. It is an antibiotic produced by the bacterium Streptomyces griseus.		2.0110antibiotic fungicide;
cyclic ketone;
dicarboximide;
piperidine antibiotic;
piperidones;
secondary alcohol		anticoronaviral agent;
bacterial metabolite;
ferroptosis inhibitor;
neuroprotective agent;
protein synthesis inhibitor
asparagine
Asparagine: A non-essential amino acid that is involved in the metabolic control of cell functions in nerve and brain tissue. It is biosynthesized from ASPARTIC ACID and AMMONIA by asparagine synthetase. (From Concise Encyclopedia Biochemistry and Molecular Biology, 3rd ed). asparagine : An alpha-amino acid in which one of the hydrogens attached to the alpha-carbon of glycine is substituted by a 2-amino-2-oxoethyl group.		2.1310amino acid zwitterion;
asparagine;
aspartate family amino acid;
L-alpha-amino acid;
proteinogenic amino acid		Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
valine
Valine: A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway.. valine : A branched-chain amino acid that consists of glycine in which one of the hydrogens attached to the alpha-carbon is substituted by an isopropyl group.. L-valine : The L-enantiomer of valine.		2.4620L-alpha-amino acid zwitterion;
L-alpha-amino acid;
proteinogenic amino acid;
pyruvate family amino acid;
valine		algal metabolite;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
Saccharomyces cerevisiae metabolite
threonine
Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins.. threonine : An alpha-amino acid in which one of the hydrogens attached to the alpha-carbon of glycine is substituted by a 1-hydroxyethyl group.		2.0510amino acid zwitterion;
aspartate family amino acid;
L-alpha-amino acid;
proteinogenic amino acid;
threonine		algal metabolite;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
tryptophan
Tryptophan: An essential amino acid that is necessary for normal growth in infants and for NITROGEN balance in adults. It is a precursor of INDOLE ALKALOIDS in plants. It is a precursor of SEROTONIN (hence its use as an antidepressant and sleep aid). It can be a precursor to NIACIN, albeit inefficiently, in mammals.. tryptophan : An alpha-amino acid that is alanine bearing an indol-3-yl substituent at position 3.		2.7130erythrose 4-phosphate/phosphoenolpyruvate family amino acid;
L-alpha-amino acid zwitterion;
L-alpha-amino acid;
proteinogenic amino acid;
tryptophan zwitterion;
tryptophan		antidepressant;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
isoleucine
Isoleucine: An essential branched-chain aliphatic amino acid found in many proteins. It is an isomer of LEUCINE. It is important in hemoglobin synthesis and regulation of blood sugar and energy levels.. isoleucine : A 2-amino-3-methylpentanoic acid having either (2R,3R)- or (2S,3S)-configuration.. L-isoleucine : The L-enantiomer of isoleucine.		2.0510aspartate family amino acid;
isoleucine;
L-alpha-amino acid zwitterion;
L-alpha-amino acid;
proteinogenic amino acid		algal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
plant metabolite;
Saccharomyces cerevisiae metabolite
arginine
Arginine: An essential amino acid that is physiologically active in the L-form.. arginine : An alpha-amino acid that is glycine in which the alpha-is substituted by a 3-guanidinopropyl group.		7.17123arginine;
glutamine family amino acid;
L-alpha-amino acid;
proteinogenic amino acid		biomarker;
Escherichia coli metabolite;
micronutrient;
mouse metabolite;
nutraceutical
trifluoroethanol
Trifluoroethanol: A non-aqueous co-solvent that serves as tool to study protein folding. It is also used in various pharmaceutical, chemical and engineering applications.		210fluoroalcohol
tert-butylhydroperoxide
tert-Butylhydroperoxide: A direct-acting oxidative stress-inducing agent used to examine the effects of oxidant stress on Ca(2+)-dependent signal transduction in vascular endothelial cells. It is also used as a catalyst in polymerization reactions and to introduce peroxy groups into organic molecules.. tert-butyl hydroperoxide : An alkyl hydroperoxide in which the alkyl group is tert-butyl. It is widely used in a variety of oxidation processes.		3.0140alkyl hydroperoxideantibacterial agent;
oxidising agent
divinyl sulfone
divinyl sulfone: cross-linking reagent for agarose gels. divinyl sulfone : A sulfone compound having two S-vinyl substituents.		2.0510sulfonecross-linking reagent
tromethamine
Tromethamine: An organic amine proton acceptor. It is used in the synthesis of surface-active agents and pharmaceuticals; as an emulsifying agent for cosmetic creams and lotions, mineral oil and paraffin wax emulsions, as a biological buffer, and used as an alkalizer. (From Merck, 11th ed; Martindale, The Extra Pharmacopoeia, 30th ed, p1424)		2.1510primary amino compound;
triol		buffer
acrylic acid
acrylic acid: RN given refers to parent cpd. acrylic acid : A alpha,beta-unsaturated monocarboxylic acid that is ethene substituted by a carboxy group.		7.110alpha,beta-unsaturated monocarboxylic acidmetabolite
bisphenol a
4,4'-isopropylidene diphenol: stimulates proliferative responses and cytokine productions of murine spleen cells and thymus cells in vitro. bisphenol : By usage, the methylenediphenols, HOC6H4CH2C6H4OH, commonly p,p-methylenediphenol, and their substitution products (generally derived from condensation of two equivalent amounts of a phenol with an aldehyde or ketone). The term also includes analogues in the the methylene (or substituted methylene) group has been replaced by a heteroatom.. bisphenol A : A bisphenol that is 4,4'-methanediyldiphenol in which the methylene hydrogens are replaced by two methyl groups.		2.0810bisphenolendocrine disruptor;
environmental contaminant;
xenobiotic;
xenoestrogen
taurocholic acid
Taurocholic Acid: The product of conjugation of cholic acid with taurine. Its sodium salt is the chief ingredient of the bile of carnivorous animals. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as a cholagogue and cholerectic.. taurocholate : An organosulfonate oxoanion that is the conjugate base of taurocholic acid.. taurocholic acid : A bile acid taurine conjugate of cholic acid that usually occurs as the sodium salt of bile in mammals.		2.2510amino sulfonic acid;
bile acid taurine conjugate		human metabolite
methylprednisolone
Methylprednisolone: A PREDNISOLONE derivative with similar anti-inflammatory action.. 6alpha-methylprednisolone : The 6alpha-stereoisomer of 6-methylprednisolone.		2.1106-methylprednisolone;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		adrenergic agent;
anti-inflammatory drug;
antiemetic;
environmental contaminant;
neuroprotective agent;
xenobiotic
rotenone
Derris: A plant genus of the family FABACEAE. The root is a source of rotenoids (ROTENONE) and flavonoids. Some species of Pongamia have been reclassified to this genus and some to MILLETTIA. Some species of Deguelia have been reclassified to this genus.. rotenoid : Members of the class of tetrahydrochromenochromene that consists of a cis-fused tetrahydrochromeno[3,4-b]chromene skeleton and its substituted derivatives. The term was originally restricted to natural products, but is now also used to describe semi-synthetic and fully synthetic compounds.		7.1510organic heteropentacyclic compound;
rotenones		antineoplastic agent;
metabolite;
mitochondrial NADH:ubiquinone reductase inhibitor;
phytogenic insecticide;
piscicide;
toxin
isosorbide dinitrate
Isosorbide Dinitrate: A vasodilator used in the treatment of ANGINA PECTORIS. Its actions are similar to NITROGLYCERIN but with a slower onset of action.		2.0310glucitol derivative;
nitrate ester		nitric oxide donor;
vasodilator agent
quinoxalines
quinoxaline : A naphthyridine in which the nitrogens are at positions 1 and 4.		2.7730mancude organic heterobicyclic parent;
naphthyridine;
ortho-fused heteroarene
quinuclidines
Quinuclidines: A class of organic compounds which contain two rings that share a pair of bridgehead carbon atoms and contains an amine group.		2.0310quinuclidines;
saturated organic heterobicyclic parent
dimethyl succinate
dimethyl succinate: potent insulin secretagogue		210fatty acid methyl ester
allylamine
Allylamine: Possesses an unusual and selective cytotoxicity for VASCULAR SMOOTH MUSCLE cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation.		3.5720alkylamine
pyrroles
1H-pyrrole : A tautomer of pyrrole that has the double bonds at positions 2 and 4.. pyrrole : A five-membered monocyclic heteroarene comprising one NH and four CH units which forms the parent compound of the pyrrole group of compounds. Its five-membered ring structure has three tautomers. A 'closed class'.. azole : Any monocyclic heteroarene consisting of a five-membered ring containing nitrogen. Azoles can also contain one or more other non-carbon atoms, such as nitrogen, sulfur or oxygen.		2.7230pyrrole;
secondary amine
catechin
Catechin: An antioxidant flavonoid, occurring especially in woody plants as both (+)-catechin and (-)-epicatechin (cis) forms.. catechin : Members of the class of hydroxyflavan that have a flavan-3-ol skeleton and its substituted derivatives.. rac-catechin : A racemate comprising equimolar amounts of (+)- and (-)-catechin. (+)-catechin : The (+)-enantiomer of catechin and a polyphenolic antioxidant plant metabolite.		2.1710catechinantioxidant;
plant metabolite
quinazolines
Quinazolines: A group of aromatic heterocyclic compounds that contain a bicyclic structure with two fused six-membered aromatic rings, a benzene ring and a pyrimidine ring.. quinazoline : A mancude organic heterobicyclic parent that is naphthalene in which the carbon atoms at positions 1 and 3 have been replaced by nitrogen atoms.. quinazolines : Any organic heterobicyclic compound based on a quinazoline skeleton and its substituted derivatives.		5.2660azaarene;
mancude organic heterobicyclic parent;
ortho-fused heteroarene;
quinazolines
adamantane
Adamantane: A tricyclo bridged hydrocarbon.		14.43612adamantanes;
polycyclic alkane
isoxazoles
Isoxazoles: Azoles with an OXYGEN and a NITROGEN next to each other at the 1,2 positions, in contrast to OXAZOLES that have nitrogens at the 1,3 positions.. isoxazole : A monocyclic heteroarene with a structure consisting of a 5-membered ring containing three carbon atoms and an oxygen and nitrogen atom adjacent to each other. It is the parent of the class of isoxazoles.. isoxazoles : Oxazoles in which the N and O atoms are adjacent.		2.4920isoxazoles;
mancude organic heteromonocyclic parent;
monocyclic heteroarene
oxazoles
Oxazoles: Five-membered heterocyclic ring structures containing an oxygen in the 1-position and a nitrogen in the 3-position, in distinction from ISOXAZOLES where they are at the 1,2 positions.. 1,3-oxazole : A five-membered monocyclic heteroarene that is an analogue of cyclopentadiene with O in place of CH2 at position 1 and N in place of CH at position 3.. oxazole : An azole based on a five-membered heterocyclic aromatic skeleton containing one N and one O atom.		3.13101,3-oxazoles;
mancude organic heteromonocyclic parent;
monocyclic heteroarene
thiazoles
[no description available]		2.95401,3-thiazoles;
mancude organic heteromonocyclic parent;
monocyclic heteroarene
pyrazines
Pyrazines: A heterocyclic aromatic organic compound with the chemical formula C4H4N2.. pyrazine : A diazine that is benzene in which the carbon atoms at positions 1 and 4 have been replaced by nitrogen atoms.		18.7813122diazine;
pyrazines		Daphnia magna metabolite
calcium gluconate
[no description available]		2.4110calcium saltnutraceutical
hydrazine
diamine : Any polyamine that contains two amino groups.		2.0810azane;
hydrazines		EC 4.3.1.10 (serine-sulfate ammonia-lyase) inhibitor
evans blue
Evans Blue: An azo dye used in blood volume and cardiac output measurement by the dye dilution method. It is very soluble, strongly bound to plasma albumin, and disappears very slowly.. Evans blue : An organic sodium salt that is the tetrasodium salt of 6,6'-{(3,3'-dimethyl[1,1'-biphenyl]-4,4'-diyl)bis[diazene-2,1-diyl]}bis(4-amino-5-hydroxynaphthalene-1,3-disulfonate). It is sometimes used as a counterstain, especially in fluorescent methods to suppress background autofluorescence.		2.8430organic sodium saltfluorochrome;
histological dye;
sodium channel blocker;
teratogenic agent
monocrotaline
Monocrotaline: A pyrrolizidine alkaloid and a toxic plant constituent that poisons livestock and humans through the ingestion of contaminated grains and other foods. The alkaloid causes pulmonary artery hypertension, right ventricular hypertrophy, and pathological changes in the pulmonary vasculature. Significant attenuation of the cardiopulmonary changes are noted after oral magnesium treatment.		2.1710pyrrolizidine alkaloid
aminophylline
Aminophylline: A drug combination that contains THEOPHYLLINE and ethylenediamine. It is more soluble in water than theophylline but has similar pharmacologic actions. It's most common use is in bronchial asthma, but it has been investigated for several other applications.. aminophylline : A mixture comprising of theophylline and ethylenediamine in a 2:1 ratio.		2.1110mixturebronchodilator agent;
cardiotonic drug
aminoimidazole carboxamide
Aminoimidazole Carboxamide: An imidazole derivative which is a metabolite of the antineoplastic agents BIC and DIC. By itself, or as the ribonucleotide, it is used as a condensation agent in the preparation of nucleosides and nucleotides. Compounded with orotic acid, it is used to treat liver diseases.. 5-aminoimidazole-4-carboxamide : An aminoimidazole in which the amino group is at C-5 with a carboxamido group at C-4.		2.5120aminoimidazole;
monocarboxylic acid amide		mouse metabolite
lithocholic acid
Lithocholic Acid: A bile acid formed from chenodeoxycholate by bacterial action, usually conjugated with glycine or taurine. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as cholagogue and choleretic.. lithocholic acid : A monohydroxy-5beta-cholanic acid with a alpha-hydroxy substituent at position 3. It is a bile acid obtained from chenodeoxycholic acid by bacterial action.. lithocholate : A bile acid anion that is the conjugate base of lithocholic acid.		2.7630bile acid;
C24-steroid;
monohydroxy-5beta-cholanic acid		geroprotector;
human metabolite;
mouse metabolite
glycocholic acid
Glycocholic Acid: The glycine conjugate of CHOLIC ACID. It acts as a detergent to solubilize fats for absorption and is itself absorbed.. glycocholic acid : A bile acid glycine conjugate having cholic acid as the bile acid component.. glycocholate : A cholanic acid conjugate anion that is the conjugate base of glycocholic acid, obtained by deprotonation of the carboxy group; major species at pH 7.3.		2.3110bile acid glycine conjugatehuman metabolite
alpha-aminopyridine
alpha-aminopyridine: RN given refers to parent cpd; structure in Merck Index, 9th ed, #485. aminopyridine : Compounds containing a pyridine skeleton substituted by one or more amine groups.		2.1510
thiazolidines
Thiazolidines: Reduced (protonated) form of THIAZOLES. They can be oxidized to THIAZOLIDINEDIONES.		2.9940thiazolidine
maleimide
[no description available]		3.2150dicarboximide;
maleimides		EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
malondialdehyde
Malondialdehyde: The dialdehyde of malonic acid.. malonaldehyde : A dialdehyde that is propane substituted by two oxo groups at the terminal carbon atoms respectively. A biomarker of oxidative damage to lipids caused by smoking, it exists in vivo mainly in the enol form.		6.44141dialdehydebiomarker
docusate
Dioctyl Sulfosuccinic Acid: All-purpose surfactant, wetting agent, and solubilizer used in the drug, cosmetics, and food industries. It has also been used in laxatives and as cerumenolytics. It is usually administered as either the calcium, potassium, or sodium salt.		2.2510diester;
organosulfonic acid
acetylcysteine
N-acetyl-L-cysteine : An N-acetyl-L-amino acid that is the N-acetylated derivative of the natural amino acid L-cysteine.		3.8730acetylcysteine;
L-cysteine derivative;
N-acetyl-L-amino acid		antidote to paracetamol poisoning;
antiinfective agent;
antioxidant;
antiviral drug;
ferroptosis inhibitor;
geroprotector;
human metabolite;
mucolytic;
radical scavenger;
vulnerary
c.i. 42510
Rosaniline Dyes: Compounds that contain the triphenylmethane aniline structure found in rosaniline. Many of them have a characteristic magenta color and are used as COLORING AGENTS.. basic fuchsin : A four-component mixture of chemically related dyes comprising pararosanilin, rosanilin, magenta II and new fuchsin in varying amounts. rosanilin : A hydrochloride that is the monohydrochloride of 4-[(4-aminophenyl)(4-iminocyclohexa-2,5-dien-1-ylidene)methyl]-2-methylaniline. One of the major constituents of Basic fuchsin, together with pararosanilin, magenta II and new fuchsin.		2.3110
erythromycin
Erythromycin: A bacteriostatic antibiotic macrolide produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.. erythromycin : Any of several wide-spectrum macrolide antibiotics obtained from actinomycete Saccharopolyspora erythraea (formerly known as Streptomyces erythraeus).. erythromycin A : An erythromycin that consists of erythronolide A having 2,6-dideoxy-3-C-methyl-3-O-methyl-alpha-L-ribo-hexopyranosyl and 3,4,6-trideoxy-3-(dimethylamino)-beta-D-xylo-hexopyranosyl residues attahced at positions 4 and 6 respectively.		4.7532cyclic ketone;
erythromycin
2-piperidone
2-piperidone: structure given in first source. piperidin-2-one : A delta-lactam that is piperidine which is substituted by an oxo group at position 2.		2.1310delta-lactam;
piperidones		EC 1.2.1.88 (L-glutamate gamma-semialdehyde dehydrogenase) inhibitor
levonorgestrel
Levonorgestrel: A synthetic progestational hormone with actions similar to those of PROGESTERONE and about twice as potent as its racemic or (+-)-isomer (NORGESTREL). It is used for contraception, control of menstrual disorders, and treatment of endometriosis.		4.371117beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
terminal acetylenic compound		contraceptive drug;
female contraceptive drug;
progestin;
synthetic oral contraceptive
durapatite
Durapatite: The mineral component of bones and teeth; it has been used therapeutically as a prosthetic aid and in the prevention and treatment of osteoporosis.. hydroxylapatite : A phosphate mineral with the formula Ca5(PO4)3(OH).		2.3110
nitrofen
nitrofen: structure		2.0810organic molecular entityEC 1.3.3.4 (protoporphyrinogen oxidase) inhibitor;
herbicide
ethyldimethylaminopropyl carbodiimide
Ethyldimethylaminopropyl Carbodiimide: Carbodiimide cross-linking reagent.		2.0610
s,n,n'-tripropylthiocarbamate
Reward: An object or a situation that can serve to reinforce a response, to satisfy a motive, or to afford pleasure.. vernolate : A monounsaturated fatty acid anion that is the conjugate base of vernolic acid, obtained by deprotonation of the carboxy group; major species at pH 7.3.		8.98164tertiary amine
amiloride
Amiloride: A pyrazine compound inhibiting SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS. This inhibition creates a negative potential in the luminal membranes of principal cells, located in the distal convoluted tubule and collecting duct. Negative potential reduces secretion of potassium and hydrogen ions. Amiloride is used in conjunction with DIURETICS to spare POTASSIUM loss. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p705). amiloride : A member of the class of pyrazines resulting from the formal monoacylation of guanidine with the carboxy group of 3,5-diamino-6-chloropyrazine-2-carboxylic acid.		2.520aromatic amine;
guanidines;
organochlorine compound;
pyrazines		diuretic;
sodium channel blocker
fluorescein-5-isothiocyanate
Fluorescein-5-isothiocyanate: Fluorescent probe capable of being conjugated to tissue and proteins. It is used as a label in fluorescent antibody staining procedures as well as protein- and amino acid-binding techniques.. fluorescein 5-isothiocyanate : The 5-isomer of fluorescein isothiocyanate. Acts as a fluorescent probe capable of being conjugated to tissue and proteins; used as a label in fluorescent antibody staining procedures as well as protein- and amino acid-binding techniques.		2.1110fluorescein isothiocyanate
mannose
mannopyranose : The pyranose form of mannose.		2.0510D-aldohexose;
D-mannose;
mannopyranose		metabolite
carbonates
Carbonates: Salts or ions of the theoretical carbonic acid, containing the radical CO2(3-). Carbonates are readily decomposed by acids. The carbonates of the alkali metals are water-soluble; all others are insoluble. (From Grant & Hackh's Chemical Dictionary, 5th ed). carbonates : Organooxygen compounds that are salts or esters of carbonic acid, H2CO3.		2.0710carbon oxoanion
dideoxyadenosine
Dideoxyadenosine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is an inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal side effect is nephrotoxicity. In vivo, dideoxyadenosine is rapidly metabolized to DIDANOSINE (ddI) by enzymatic deamination; ddI is then converted to dideoxyinosine monophosphate and ultimately to dideoxyadenosine triphosphate, the putative active metabolite.		2.5820adenosines;
purine 2',3'-dideoxyribonucleoside		EC 3.5.4.4 (adenosine deaminase) inhibitor;
EC 4.6.1.1 (adenylate cyclase) inhibitor
fructosamine
Fructosamine: An amino sugar formed when glucose non-enzymatically reacts with the N-terminal amino group of proteins. The fructose moiety is derived from glucose by the classical Amadori rearrangement.		3.411
hepes
[no description available]		2.4110HEPES;
organosulfonic acid
lutetium
Lutetium: An element of the rare earth family of metals. It has the atomic symbol Lu, atomic number 71, and atomic weight 175.		2.1510d-block element atom;
lanthanoid atom
mercury
Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to MERCURY POISONING. Because of its toxicity, the clinical use of mercury and mercurials is diminishing.. mercury(0) : Elemental mercury of oxidation state zero.		2.4110elemental mercury;
zinc group element atom		neurotoxin
technetium
Technetium: The first artificially produced element and a radioactive fission product of URANIUM. Technetium has the atomic symbol Tc, and atomic number 43. All technetium isotopes are radioactive. Technetium 99m (m=metastable) which is the decay product of Molybdenum 99, has a half-life of about 6 hours and is used diagnostically as a radioactive imaging agent. Technetium 99 which is a decay product of technetium 99m, has a half-life of 210,000 years.		3.6820manganese group element atom
europium
Europium: An element of the rare earth family of metals. It has the atomic symbol Eu, atomic number 63, and atomic weight 152. Europium is used in the form of its salts as coatings for cathode ray tubes and in the form of its organic derivatives as shift reagents in NMR spectroscopy.		2.3110f-block element atom;
lanthanoid atom
gadolinium
Gadolinium: An element of the rare earth family of metals. It has the atomic symbol Gd, atomic number 64, and atomic weight 157.25. Its oxide is used in the control rods of some nuclear reactors.		2.2510f-block element atom;
lanthanoid atom
zirconium
Zirconium: A rather rare metallic element with atomic number 40, atomic weight 91.224, and symbol Zr.		2.1110titanium group element atom
galactosamine
2-amino-2-deoxy-D-galactopyranose : The pyranose form of D-galactosamine.. D-galactosamine : The D-stereoisomer of galactosamine.		2.0310D-galactosamine;
primary amino compound		toxin
tungstate
[no description available]		2.0210divalent inorganic anion;
tungsten oxoanion
vasotocin
Vasotocin: A nonapeptide that contains the ring of OXYTOCIN and the side chain of ARG-VASOPRESSIN with the latter determining the specific recognition of hormone receptors. Vasotocin is the non-mammalian vasopressin-like hormone or antidiuretic hormone regulating water and salt metabolism.. vasotocin : A heterodetic cyclic peptide that is homologous to oxytocin and vasopressin. It is a pituitary hormone that acts as an endocrine regulator for water balance, osmotic homoeostasis and is involved in social and sexual behavior in non-mammalian vertebrates.		2.1310
sodium selenite
disodium selenite : An inorganic sodium salt composed of sodium and selenite ions in a 2:1 ratio.		2.0710inorganic sodium salt;
selenite salt		nutraceutical
clodronic acid
Clodronic Acid: A diphosphonate which affects calcium metabolism. It inhibits bone resorption and soft tissue calcification.. clodronic acid : An organochlorine compound that is methylene chloride in which both hydrogens are replaced by phosphonic acid groups. It inhibits bone resorption and soft tissue calcification, and is used (often as the disodium salt tetrahydrate) as an adjunct in the treatment of severe hypercalcaemia associated with malignancy, and in the management of osteolytic lesions and bone pain associated with skeletal metastases.		2.17101,1-bis(phosphonic acid);
one-carbon compound;
organochlorine compound		antineoplastic agent;
bone density conservation agent
tetradecanoylphorbol acetate
Tetradecanoylphorbol Acetate: A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.. phorbol ester : Esters of phorbol, originally found in croton oil (from Croton tiglium, of the family Euphorbiaceae). A number of phorbol esters possess activity as tumour promoters and activate the mechanisms associated with cell growth. Some of these are used in experiments as activators of protein kinase C.. phorbol 13-acetate 12-myristate : A phorbol ester that is phorbol in which the hydroxy groups at the cyclopropane ring juction (position 13) and the adjacent carbon (position 12) have been converted into the corresponding acetate and myristate esters. It is a major active constituent of the seed oil of Croton tiglium. It has been used as a tumour promoting agent for skin carcinogenesis in rodents and is associated with increased cell proliferation of malignant cells. However its function is controversial since a decrease in cell proliferation has also been observed in several cancer cell types.		2.110acetate ester;
diester;
phorbol ester;
tertiary alpha-hydroxy ketone;
tetradecanoate ester		antineoplastic agent;
apoptosis inducer;
carcinogenic agent;
mitogen;
plant metabolite;
protein kinase C agonist;
reactive oxygen species generator
phenyl acetate
phenyl acetate: The ester formed between phenol and acetic acid. Don't confuse with phenylacetic acid derivatives listed under PHENYLACETATES.. phenyl acetate : An acetate ester obtained by the formal condensation of phenol with acetic acid.		3.4460benzenes;
phenyl acetates
propionic anhydride
[no description available]		2.0210
ursodeoxycholic acid
Ursodeoxycholic Acid: An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic.. ursodeoxycholic acid : A bile acid found in the bile of bears (Ursidae) as a conjugate with taurine. Used therapeutically, it prevents the synthesis and absorption of cholesterol and can lead to the dissolution of gallstones.. ursodeoxycholate : A bile acid anion that is the conjugate base of ursodeoxycholic acid, obtained by deprotonation of the carboxy group; major species at pH 7.3.		7.5220bile acid;
C24-steroid;
dihydroxy-5beta-cholanic acid		human metabolite;
mouse metabolite
transferrin
Transferrin: An iron-binding beta1-globulin that is synthesized in the LIVER and secreted into the blood. It plays a central role in the transport of IRON throughout the circulation. A variety of transferrin isoforms exist in humans, including some that are considered markers for specific disease states.		2.520
glutamic acid
Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.. glutamic acid : An alpha-amino acid that is glutaric acid bearing a single amino substituent at position 2.		4.7100glutamic acid;
glutamine family amino acid;
L-alpha-amino acid;
proteinogenic amino acid		Escherichia coli metabolite;
ferroptosis inducer;
micronutrient;
mouse metabolite;
neurotransmitter;
nutraceutical
azides
Azides: Organic or inorganic compounds that contain the -N3 group.. azide : Any nitrogen molecular entity containing the group -N3.		2.1510pseudohalide anionmitochondrial respiratory-chain inhibitor
s-adenosylmethionine
acylcarnitine: structure in first source. S-adenosyl-L-methioninate : A sulfonium betaine that is a conjugate base of S-adenosyl-L-methionine obtained by the deprotonation of the carboxy group.		3.710sulfonium betainehuman metabolite
substance p
[no description available]		2.110peptideneurokinin-1 receptor agonist;
neurotransmitter;
vasodilator agent
ribavirin
Rebetron: Rebetron is tradename		2.05101-ribosyltriazole;
aromatic amide;
monocarboxylic acid amide;
primary carboxamide		anticoronaviral agent;
antiinfective agent;
antimetabolite;
antiviral agent;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
ng-nitroarginine methyl ester
NG-Nitroarginine Methyl Ester: A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.		3.1550alpha-amino acid ester;
L-arginine derivative;
methyl ester;
N-nitro compound		EC 1.14.13.39 (nitric oxide synthase) inhibitor
decamethrin
decamethrin: pyrethroid insecticide; RN given refers to cpd without isomeric designation; structure		2.0310aromatic ether;
cyclopropanecarboxylate ester;
nitrile;
organobromine compound		agrochemical;
antifeedant;
calcium channel agonist;
EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor;
pyrethroid ester insecticide
meglitinide
meglitinide: structure given in first source & in Negwer, 5th ed, #6436		4.0520
captopril
Captopril: A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.. captopril : A L-proline derivative in which L-proline is substituted on nitrogen with a (2S)-2-methyl-3-sulfanylpropanoyl group. It is used as an anti-hypertensive ACE inhibitor drug.		2.0510alkanethiol;
L-proline derivative;
N-acylpyrrolidine;
pyrrolidinemonocarboxylic acid		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
colforsin
Colforsin: Potent activator of the adenylate cyclase system and the biosynthesis of cyclic AMP. From the plant COLEUS FORSKOHLII. Has antihypertensive, positive inotropic, platelet aggregation inhibitory, and smooth muscle relaxant activities; also lowers intraocular pressure and promotes release of hormones from the pituitary gland.		4.98140acetate ester;
cyclic ketone;
labdane diterpenoid;
organic heterotricyclic compound;
tertiary alpha-hydroxy ketone;
triol		adenylate cyclase agonist;
anti-HIV agent;
antihypertensive agent;
plant metabolite;
platelet aggregation inhibitor;
protein kinase A agonist
lovastatin
Lovastatin: A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.. lovastatin : A fatty acid ester that is mevastatin carrying an additional methyl group on the carbobicyclic skeleton. It is used in as an anticholesteremic drug and has been found in fungal species such as Aspergillus terreus and Pleurotus ostreatus (oyster mushroom).		3.4211delta-lactone;
fatty acid ester;
hexahydronaphthalenes;
polyketide;
statin (naturally occurring)		anticholesteremic drug;
antineoplastic agent;
Aspergillus metabolite;
prodrug
simvastatin
Simvastatin: A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.. simvastatin : A member of the class of hexahydronaphthalenes that is lovastatin in which the 2-methylbutyrate ester moiety has been replaced by a 2,2-dimethylbutyrate ester group. It is used as a cholesterol-lowering and anti-cardiovascular disease drug.		2.3110delta-lactone;
fatty acid ester;
hexahydronaphthalenes;
statin (semi-synthetic)		EC 1.1.1.34/EC 1.1.1.88 (hydroxymethylglutaryl-CoA reductase) inhibitor;
EC 3.4.24.83 (anthrax lethal factor endopeptidase) inhibitor;
ferroptosis inducer;
geroprotector;
prodrug
mifepristone
Mifepristone: A progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua. As a glucocorticoid receptor antagonist, the drug has been used to treat hypercortisolism in patients with nonpituitary CUSHING SYNDROME.		2.03103-oxo-Delta(4) steroid;
acetylenic compound;
tertiary amino compound		abortifacient;
contraceptive drug;
hormone antagonist;
synthetic oral contraceptive
fura-2
Fura-2: A fluorescent calcium chelating agent which is used to study intracellular calcium in tissues.		2.3110
aripiprazole
Aripiprazole: A piperazine and quinolone derivative that is used primarily as an antipsychotic agent. It is a partial agonist of SEROTONIN RECEPTOR, 5-HT1A and DOPAMINE D2 RECEPTORS, where it also functions as a post-synaptic antagonist, and an antagonist of SEROTONIN RECEPTOR, 5-HT2A. It is used for the treatment of SCHIZOPHRENIA and BIPOLAR DISORDER, and as an adjunct therapy for the treatment of depression.. aripiprazole : An N-arylpiperazine that is piperazine substituted by a 4-[(2-oxo-1,2,3,4-tetrahydroquinolin-7-yl)oxy]butyl group at position 1 and by a 2,3-dichlorophenyl group at position 4. It is an antipsychotic drug used for the treatment of Schizophrenia, and other mood disorders.		2.1110aromatic ether;
delta-lactam;
dichlorobenzene;
N-alkylpiperazine;
N-arylpiperazine;
quinolone		drug metabolite;
H1-receptor antagonist;
second generation antipsychotic;
serotonergic agonist
atorvastatin
[no description available]		2.7730aromatic amide;
dihydroxy monocarboxylic acid;
monofluorobenzenes;
pyrroles;
statin (synthetic)		environmental contaminant;
xenobiotic
adenosine
quinquefolan B: isolated from roots of Panax quinquefolium L.; RN not in Chemline 10/87; RN from Toxlit		3.6420adenosines;
purines D-ribonucleoside		analgesic;
anti-arrhythmia drug;
fundamental metabolite;
human metabolite;
vasodilator agent
glucose, (beta-d)-isomer
beta-D-glucose : D-Glucopyranose with beta configuration at the anomeric centre.. (1->4)-beta-D-glucan : A beta-D-glucan in which the glucose units are connected by (1->4) linkages.. (1->3)-beta-D-glucan : A beta-D-glucan in which the glucose units are connected by (1->3) linkages.		13.212515D-glucopyranoseepitope;
mouse metabolite
thiazolyl blue
thiazolyl blue: RN & II refers to bromide. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide : The bromide salt of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium.		2.4420organic bromide saltcolorimetric reagent;
dye
plerixafor
plerixafor: a bicyclam derivate, highly potent & selective inhibitor of HIV-1 & HIV-2. plerixafor : An azamacrocycle consisting of two cyclam rings connected by a 1,4-phenylenebis(methylene) linker. It is a CXCR4 chemokine receptor antagonist and a hematopoietic stem cell mobilizer. It is used in combination with grulocyte-colony stimulating factor (G-CSF) to mobilize hematopoietic stem cells to the perpheral blood for collection and subsequent autologous transplantation in patients with non-Hodgkin's lymphoma and multiple myeloma.		2.1310azacycloalkane;
azamacrocycle;
benzenes;
crown amine;
secondary amino compound;
tertiary amino compound		anti-HIV agent;
antineoplastic agent;
C-X-C chemokine receptor type 4 antagonist;
immunological adjuvant
epigallocatechin gallate
epigallocatechin gallate: a steroid 5alpha-reductase inhibitor and antimutagen in green tea (Camellia sinensis). (-)-epigallocatechin 3-gallate : A gallate ester obtained by the formal condensation of gallic acid with the (3R)-hydroxy group of (-)-epigallocatechin.		2.1710flavans;
gallate ester;
polyphenol		antineoplastic agent;
antioxidant;
apoptosis inducer;
geroprotector;
Hsp90 inhibitor;
neuroprotective agent;
plant metabolite
aica ribonucleotide
AICA ribonucleotide: purine precursor that has antineoplastic activity. AICA ribonucleotide : A 1-(phosphoribosyl)imidazolecarboxamide that is acadesine in which the hydroxy group at the 5' position has been converted to its monophosphate derivative.		2.51201-(phosphoribosyl)imidazolecarboxamide;
aminoimidazole		cardiovascular drug;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
plant metabolite;
Saccharomyces cerevisiae metabolite
2',5'-dideoxyadenosine
[no description available]		2.1710deoxyribonucleoside
lissamine rhodamine b
lissamine rhodamine B: RN given refers to parent cpd; Lissamine Rhodamine B refers to Na salt		2.0810
repaglinide
[no description available]		4.7930piperidines
triazoles
Triazoles: Heterocyclic compounds containing a five-membered ring with two carbon atoms and three nitrogen atoms with the molecular formula C2H3N3.. triazoles : An azole in which the five-membered heterocyclic aromatic skeleton contains three N atoms and two C atoms.		18.78132221,2,3-triazole
fluorodeoxyglucose f18
Fluorodeoxyglucose F18: The compound is given by intravenous injection to do POSITRON-EMISSION TOMOGRAPHY for the assessment of cerebral and myocardial glucose metabolism in various physiological or pathological states including stroke and myocardial ischemia. It is also employed for the detection of malignant tumors including those of the brain, liver, and thyroid gland. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1162)		5.99222-deoxy-2-((18)F)fluoro-D-glucose;
2-deoxy-2-fluoro-aldehydo-D-glucose
glycyl-glycyl-glycyl-glycine
[no description available]		2.2510
acamprosate
Acamprosate: Structural analog of taurine that is used for the prevention of relapse in individuals with ALCOHOLISM.. acamprosate : An organosulfonic acid that is propane-1-sulfonic acid substituted by an acetylamino group at position 3.		2.0310acetamides;
organosulfonic acid		environmental contaminant;
neurotransmitter agent;
xenobiotic
erythromycin propionate-n-acetylcysteinate
[no description available]		2.110
rosiglitazone
[no description available]		14.5122aminopyridine;
thiazolidinediones		EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
insulin-sensitizing drug
n-hydroxysuccinimide
N-hydroxysuccinimide: structure		2.4820
loganin
[no description available]		2.110beta-D-glucoside;
cyclopentapyran;
enoate ester;
iridoid monoterpenoid;
methyl ester;
monosaccharide derivative;
secondary alcohol		anti-inflammatory agent;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
EC 3.2.1.20 (alpha-glucosidase) inhibitor;
EC 3.4.23.46 (memapsin 2) inhibitor;
neuroprotective agent;
plant metabolite
nicotine
(S)-nicotine : A 3-(1-methylpyrrolidin-2-yl)pyridine in which the chiral centre has S-configuration. The naturally occurring and most active enantiomer of nicotine, isolated from Nicotiana tabacum.		10.42413-(1-methylpyrrolidin-2-yl)pyridineanxiolytic drug;
biomarker;
immunomodulator;
mitogen;
neurotoxin;
nicotinic acetylcholine receptor agonist;
peripheral nervous system drug;
phytogenic insecticide;
plant metabolite;
psychotropic drug;
teratogenic agent;
xenobiotic
homocysteine
Homocysteine: A thiol-containing amino acid formed by a demethylation of METHIONINE.. homocysteine : A sulfur-containing amino acid consisting of a glycine core with a 2-mercaptoethyl side-chain.. L-homocysteine : A homocysteine that has L configuration.		2.5820amino acid zwitterion;
homocysteine;
serine family amino acid		fundamental metabolite;
mouse metabolite
alanyltyrosine
alanyltyrosine: tyrosine source; RN given refers to (L)-isomer. Ala-Tyr : A dipeptide composed of L-alanine and L-tyrosine joined by a peptide linkage.		2.110dipeptidemetabolite
glucuronic acid
Glucuronic Acid: A sugar acid formed by the oxidation of the C-6 carbon of GLUCOSE. In addition to being a key intermediate metabolite of the uronic acid pathway, glucuronic acid also plays a role in the detoxification of certain drugs and toxins by conjugating with them to form GLUCURONIDES.. D-glucuronic acid : The D-enantiomer of glucuronic acid.. D-glucopyranuronic acid : A D-glucuronic acid in cyclic pyranose form.		2.830D-glucuronic acidalgal metabolite
cobalt
Cobalt: A trace element that is a component of vitamin B12. It has the atomic symbol Co, atomic number 27, and atomic weight 58.93. It is used in nuclear weapons, alloys, and pigments. Deficiency in animals leads to anemia; its excess in humans can lead to erythrocytosis.. cobalt(1+) : A monovalent inorganic cation obtained from cobalt.. cobalt atom : A cobalt group element atom that has atomic number 27.		2.0710cobalt group element atom;
metal allergen		micronutrient
sr141716
[no description available]		5.8270amidopiperidine;
carbohydrazide;
dichlorobenzene;
monochlorobenzenes;
pyrazoles		anti-obesity agent;
appetite depressant;
CB1 receptor antagonist
deoxypyridinoline
deoxypyridinoline: structure given in first source		2.0810
1,4,7-tris(carboxymethyl)-1,4,7,10-tetraazacyclododecane
1,4,7-tris(carboxymethyl)-1,4,7,10-tetraazacyclododecane: structure in first source		2.0810
geniposide
[no description available]		2.110terpene glycoside
phorbol-12-myristate
[no description available]		2.1110
deoxyglucose
Deoxyglucose: 2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.. deoxyglucose : A deoxyhexose comprising glucose having at least one hydroxy group replaced by hydrogen.		3.1550
dodecyl-beta-d-maltoside
dodecyl beta-D-maltoside : A glycoside resulting from attachment of a dodecyl group to the reducing-end anomeric centre of a beta-maltose molecule.		2.0710disaccharide derivative;
glycoside		detergent
clofarabine
[no description available]		2.0310adenosines;
organofluorine compound		antimetabolite;
antineoplastic agent
caprylates
Caprylates: Derivatives of caprylic acid. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain a carboxy terminated eight carbon aliphatic structure.. octanoate : A straight-chain saturated fatty acid anion that is the conjugate base of octanoic acid (caprylic acid); believed to block adipogenesis.		2.7220fatty acid anion 8:0;
straight-chain saturated fatty acid anion		human metabolite;
Saccharomyces cerevisiae metabolite
parecoxib
parecoxib: structure in first source. parecoxib : An N-acylsulfonamide resulting from the formal condensation of valdecoxib with propionic acid. It is a prodrug for valdecoxib.		2.0310isoxazoles;
N-sulfonylcarboxamide		cyclooxygenase 2 inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
prodrug
1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetraacetic acid
1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetraacetic acid: structure given in first source. DOTA : An azamacrocyle in which four nitrogen atoms at positions 1, 4, 7 and 10 of a twelve-membered ring are each substituted with a carboxymethyl group.		4.1831azamacrocyclechelator;
copper chelator
angiotensin ii, des-phe(8)-
Ile(5)-angiotensin II (1-7) : An angiotensin compound consisting of the linear heptapeptide sequence L-Asp-L-Arg-L-Val-L-Tyr-L-Ile-L-His-L-Pro.		2.1310amino acid zwitterion;
angiotensin		vasodilator agent
n,n-dimethylarginine
N,N-dimethylarginine: asymmetric dimethylarginine; do not confuse with N,N'-dimethylarginine. N(omega),N(omega)-dimethyl-L-arginine : A L-arginine derivative having two methyl groups both attached to the primary amino moiety of the guanidino group.		2.5820dimethylarginine;
guanidines;
L-arginine derivative;
non-proteinogenic L-alpha-amino acid		EC 1.14.13.39 (nitric oxide synthase) inhibitor
rmi 12330a
RMI 12330A: adenyl cyclase inhibitor in rat liver; RN given refers to (cis)-isomer; NM refers to HCl, (cis)-isomer; structure		2.4820
1,4,7-triazacyclononane-n,n',n''-triacetic acid
1,4,7-triazacyclononane-N,N',N''-triacetic acid: structure given in first source		5.0381
glicentin
Glicentin: A 69-amino acid peptide derived from the N-terminal of PROGLUCAGON. It is mainly produced by the INTESTINAL L CELLS. Further processing of glicentin yield a 30-amino acid N-terminal peptide (glicentin-related polypeptide) and a 37-amino acid peptide OXYNTOMODULIN. Both glicentin and oxyntomodulin can reduce digestive secretions and delay gastric emptying.		2.610
s-(bismaleimidoethyl ether)cysteine
[no description available]		2.5420
omega-n-methylarginine
omega-N-Methylarginine: A competitive inhibitor of nitric oxide synthetase.. N(omega)-methyl-L-arginine : A L-arginine derivative with a N(omega)-methyl substituent.		3.9121amino acid zwitterion;
arginine derivative;
guanidines;
L-arginine derivative;
non-proteinogenic L-alpha-amino acid
succinimidyl carbonate
succinimidyl carbonate: activates polyethylene glycol which is coupled to proteins; structure in first source		2.0710
levofloxacin
Levofloxacin: The L-isomer of Ofloxacin.. levofloxacin : An optically active form of ofloxacin having (S)-configuration; an inhibitor of bacterial topoisomerase IV and DNA gyrase.		2.07109-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid;
fluoroquinolone antibiotic;
quinolone antibiotic		antibacterial drug;
DNA synthesis inhibitor;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
topoisomerase IV inhibitor
moxifloxacin
Moxifloxacin: A fluoroquinolone that acts as an inhibitor of DNA TOPOISOMERASE II and is used as a broad-spectrum antibacterial agent.. moxifloxacin : A quinolone that consists of 4-oxo-1,4-dihydroquinoline-3-carboxylic acid bearing a cyclopropyl substituent at position 1, a fluoro substitiuent at position 6, a (4aS,7aS)-octahydro-6H-pyrrolo[3,4-b]pyridin-6-yl group at position 7 and a methoxy substituent at position 8. A member of the fluoroquinolone class of antibacterial agents.		3.4711aromatic ether;
cyclopropanes;
fluoroquinolone antibiotic;
pyrrolidinopiperidine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antibacterial drug
ruboxistaurin
ruboxistaurin: inhibits protein kinase C beta; structure in first source		3.1310
birb 796
[no description available]		2.1110aromatic ether;
morpholines;
naphthalenes;
pyrazoles;
ureas		EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
immunomodulator
nps-568
N-(2-chlorophenylpropyl)-1-(3-methoxyphenyl)ethylamine: NPS-568 is the ((R), HCl salt)-isomer; calcimimetic compound and calcium-sensing receptor agonist		2.0810
cyc 202
seliciclib : 2,6-Diaminopurine carrying benzylamino, (2R)-1-hydroxybutan-2-yl and isopropyl substituents at C-6, C-2-N and N-9 respectively. It is an experimental drug candidate in the family of pharmacological cyclin-dependent kinase (CDK) inhibitors.		2.03102,6-diaminopurinesantiviral drug;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
varenicline
Varenicline: A benzazepine derivative that functions as an ALPHA4-BETA2 NICOTINIC RECEPTOR partial agonist. It is used for SMOKING CESSATION.. varenicline : An organic heterotetracyclic compound that acts as a partial agonist for nicotinic cholinergic receptors and is used (in the form of its tartate salt) as an aid to giving up smoking.		2.1110
biotin
vitamin B7 : Any member of a group of vitamers that belong to the chemical structural class called biotins that exhibit biological activity against vitamin B7 deficiency. Vitamin B7 deficiency is very rare in individuals who take a normal balanced diet. Foods rich in biotin are egg yolk, liver, cereals, vegetables (spinach, mushrooms) and rice. Symptoms associated with vitamin B7 deficiency include thinning hair, scaly skin rashes around eyes, nose and mouth, and brittle nails. The vitamers include biotin and its ionized and salt forms.		7.4420biotins;
vitamin B7		coenzyme;
cofactor;
Escherichia coli metabolite;
fundamental metabolite;
human metabolite;
mouse metabolite;
nutraceutical;
prosthetic group;
Saccharomyces cerevisiae metabolite
angiotensin ii
Giapreza: injectable form of angiotensin II used to increase blood pressure in adult patients with septic or other distributive shock. Ile(5)-angiotensin II : An angiotensin II that acts on the central nervous system (PDB entry: 1N9V).		3.680amino acid zwitterion;
angiotensin II		human metabolite
atropine
tropan-3alpha-yl 3-hydroxy-2-phenylpropanoate : A tropane alkaloid that is (1R,5)-8-methyl-8-azabicyclo[3.2.1]octane substituted by a (3-hydroxy-2-phenylpropanoyl)oxy group at position 3.		2.520
sb 203580
[no description available]		2.1110imidazoles;
monofluorobenzenes;
pyridines;
sulfoxide		EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
geroprotector;
Hsp90 inhibitor;
neuroprotective agent
muraglitazar
muraglitazar: has glucose- and lipid-lowering activities; structure in first source; molecule composed of benzyloxazole-phenoxy-oxybenzylglycine-phenoxyl having structural analogy to PHENOXYBENZAMINE		3.13101,3-oxazoles
tesaglitazar
tesaglitazar: structure in first source		3.1310
ramelteon
ramelteon: melatonin MT1/MT2 receptor agonist		2.4320indanes
solifenacin succinate
Solifenacin Succinate: A quinuclidine and tetrahydroisoquinoline derivative and selective M3 MUSCARINIC ANTAGONIST. It is used as a UROLOGIC AGENT in the treatment of URINARY INCONTINENCE.		2.0310isoquinolines
cholic acid
Cholic Acid: A major primary bile acid produced in the liver and usually conjugated with glycine or taurine. It facilitates fat absorption and cholesterol excretion.. cholic acid : A bile acid that is 5beta-cholan-24-oic acid bearing three alpha-hydroxy substituents at position 3, 7 and 12.		2.251012alpha-hydroxy steroid;
3alpha-hydroxy steroid;
7alpha-hydroxy steroid;
bile acid;
C24-steroid;
trihydroxy-5beta-cholanic acid		human metabolite;
mouse metabolite
deoxycholic acid
Deoxycholic Acid: A bile acid formed by bacterial action from cholate. It is usually conjugated with glycine or taurine. Deoxycholic acid acts as a detergent to solubilize fats for intestinal absorption, is reabsorbed itself, and is used as a choleretic and detergent.. deoxycholic acid : A bile acid that is 5beta-cholan-24-oic acid substituted by hydroxy groups at positions 3 and 12 respectively.		2.8330bile acid;
C24-steroid;
dihydroxy-5beta-cholanic acid		human blood serum metabolite
benzofurans
Benzofurans: Compounds that contain a BENZENE ring fused to a furan ring.		2.0310
wortmannin
[no description available]		2.7330acetate ester;
cyclic ketone;
delta-lactone;
organic heteropentacyclic compound		anticoronaviral agent;
antineoplastic agent;
autophagy inhibitor;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor;
geroprotector;
Penicillium metabolite;
radiosensitizing agent
taurochenodeoxycholic acid
Taurochenodeoxycholic Acid: A bile salt formed in the liver by conjugation of chenodeoxycholate with taurine, usually as the sodium salt. It acts as detergent to solubilize fats in the small intestine and is itself absorbed. It is used as a cholagogue and choleretic.. taurochenodeoxycholate : An organosulfonate oxoanion that is the conjugate base of taurochenodeoxycholic acid arising from deprotonation of the sulfonate OH group; major species at pH 7.3.. taurochenodeoxycholic acid : A bile acid taurine conjugate of chenodeoxycholic acid.		2.1710bile acid taurine conjugatehuman metabolite;
mouse metabolite
dihydropyridines
Dihydropyridines: Pyridine moieties which are partially saturated by the addition of two hydrogen atoms in any position.		2.0510
leupeptins
Leupeptins: A group of acylated oligopeptides produced by Actinomycetes that function as protease inhibitors. They have been known to inhibit to varying degrees trypsin, plasmin, KALLIKREINS, papain and the cathepsins.		2.0710
lithium chloride
Lithium Chloride: A salt of lithium that has been used experimentally as an immunomodulator.. lithium chloride : A metal chloride salt with a Li(+) counterion.		340inorganic chloride;
lithium salt		antimanic drug;
geroprotector
biotinyl n-hydroxysuccinimide ester
biotinyl N-hydroxysuccinimide ester: used to prepare biotinylated erythrocytes		2.0510
glycogen
glycogen : A polydisperse, highly branched glucan composed of chains of D-glucopyranose residues in alpha(1->4) glycosidic linkage, joined together by alpha(1->6) glycosidic linkages. A small number of alpha(1->3) glycosidic linkages and some cumulative alpha(1->6) links also may occur. The branches in glycogen typically contain 8 to 12 glucose residues.		3.1350
elastin
[no description available]		7.5720oligopeptide
oxytocin
Oxytocin: A nonapeptide hormone released from the neurohypophysis (PITUITARY GLAND, POSTERIOR). It differs from VASOPRESSIN by two amino acids at residues 3 and 8. Oxytocin acts on SMOOTH MUSCLE CELLS, such as causing UTERINE CONTRACTIONS and MILK EJECTION.. oxytocin : A cyclic nonapeptide hormone with amino acid sequence CYIQNCPLG that also acts as a neurotransmitter in the brain; the principal uterine-contracting and milk-ejecting hormone of the posterior pituitary. Together with the neuropeptide vasopressin, it is believed to influence social cognition and behaviour.		2.2510heterodetic cyclic peptide;
peptide hormone		oxytocic;
vasodilator agent
geniposidic acid
[no description available]		2.110terpene glycoside
ao 128
AO 128: alpha-glucosidase inhibitor; structure given in first source		2.110organic molecular entity
darifenacin
darifenacin : 2-[(3S)-1-Ethylpyrrolidin-3-yl]-2,2-diphenylacetamide in which one of the hydrogens at the 2-position of the ethyl group is substituted by a 2,3-dihydro-1-benzofuran-5-yl group. It is a selective antagonist for the M3 muscarinic acetylcholine receptor, which is primarily responsible for bladder muscle contractions, and is used as the hydrobromide salt in the management of urinary incontinence.		2.03101-benzofurans;
monocarboxylic acid amide;
pyrrolidines		antispasmodic drug;
muscarinic antagonist
tretinoin
Tretinoin: An important regulator of GENE EXPRESSION during growth and development, and in NEOPLASMS. Tretinoin, also known as retinoic acid and derived from maternal VITAMIN A, is essential for normal GROWTH; and EMBRYONIC DEVELOPMENT. An excess of tretinoin can be teratogenic. It is used in the treatment of PSORIASIS; ACNE VULGARIS; and several other SKIN DISEASES. It has also been approved for use in promyelocytic leukemia (LEUKEMIA, PROMYELOCYTIC, ACUTE).. retinoic acid : A retinoid consisting of 3,7-dimethylnona-2,4,6,8-tetraenoic acid substituted at position 9 by a 2,6,6-trimethylcyclohex-1-en-1-yl group (geometry of the four exocyclic double bonds is not specified).. all-trans-retinoic acid : A retinoic acid in which all four exocyclic double bonds have E- (trans-) geometry.		3.0240retinoic acid;
vitamin A		anti-inflammatory agent;
antineoplastic agent;
antioxidant;
AP-1 antagonist;
human metabolite;
keratolytic drug;
retinoic acid receptor agonist;
retinoid X receptor agonist;
signalling molecule
arachidonic acid
icosa-5,8,11,14-tetraenoic acid : Any icosatetraenoic acid with the double bonds at positions 5, 8, 11 and 14.. arachidonate : A long-chain fatty acid anion resulting from the removal of a proton from the carboxy group of arachidonic acid.		2.1310icosa-5,8,11,14-tetraenoic acid;
long-chain fatty acid;
omega-6 fatty acid		Daphnia galeata metabolite;
EC 3.1.1.1 (carboxylesterase) inhibitor;
human metabolite;
mouse metabolite
resveratrol
trans-resveratrol : A resveratrol in which the double bond has E configuration.		4.4230resveratrolantioxidant;
phytoalexin;
plant metabolite;
quorum sensing inhibitor;
radical scavenger
oleic acid
Oleic Acid: An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed). oleic acid : An octadec-9-enoic acid in which the double bond at C-9 has Z (cis) stereochemistry.		3.0440octadec-9-enoic acidantioxidant;
Daphnia galeata metabolite;
EC 3.1.1.1 (carboxylesterase) inhibitor;
Escherichia coli metabolite;
mouse metabolite;
plant metabolite;
solvent
tacrolimus
Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro.. tacrolimus (anhydrous) : A macrolide lactam containing a 23-membered lactone ring, originally isolated from the fermentation broth of a Japanese soil sample that contained the bacteria Streptomyces tsukubaensis.		4.4260macrolide lactambacterial metabolite;
immunosuppressive agent
cocaine
Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake.. cocaine : A tropane alkaloid obtained from leaves of the South American shrub Erythroxylon coca.		10.1691benzoate ester;
methyl ester;
tertiary amino compound;
tropane alkaloid		adrenergic uptake inhibitor;
central nervous system stimulant;
dopamine uptake inhibitor;
environmental contaminant;
local anaesthetic;
mouse metabolite;
plant metabolite;
serotonin uptake inhibitor;
sodium channel blocker;
sympathomimetic agent;
vasoconstrictor agent;
xenobiotic
thapsigargin
Thapsigargin: A sesquiterpene lactone found in roots of THAPSIA. It inhibits SARCOPLASMIC RETICULUM CALCIUM-TRANSPORTING ATPASES.. thapsigargin : An organic heterotricyclic compound that is a hexa-oxygenated 6,7-guaianolide isolated fron the roots of Thapsia garganica L., Apiaceae. A potent skin irritant, it is used in traditional medicine as a counter-irritant. Thapsigargin inhibits Ca(2+)-transporting ATPase mediated uptake of calcium ions into sarcoplasmic reticulum and is used in experimentation examining the impacts of increasing cytosolic calcium concentrations.		2.7730butyrate ester;
organic heterotricyclic compound;
sesquiterpene lactone		calcium channel blocker;
EC 3.6.3.8 (Ca(2+)-transporting ATPase) inhibitor
mycophenolic acid
Mycophenolic Acid: Compound derived from Penicillium stoloniferum and related species. It blocks de novo biosynthesis of purine nucleotides by inhibition of the enzyme inosine monophosphate dehydrogenase (IMP DEHYDROGENASE). Mycophenolic acid exerts selective effects on the immune system in which it prevents the proliferation of T-CELLS, LYMPHOCYTES, and the formation of antibodies from B-CELLS. It may also inhibit recruitment of LEUKOCYTES to sites of INFLAMMATION.. mycophenolate : A monocarboxylic acid anion resulting from the removal of a proton from the carboxy group of mycophenolic acid.. mycophenolic acid : A member of the class of 2-benzofurans that is 2-benzofuran-1(3H)-one which is substituted at positions 4, 5, 6, and 7 by methyl, methoxy, (2E)-5-carboxy-3-methylpent-2-en-1-yl, and hydroxy groups, respectively. It is an antibiotic produced by Penicillium brevi-compactum, P. stoloniferum, P. echinulatum and related species. An immunosuppressant, it is widely used (partiularly as its sodium salt and as the 2-(morpholin-4-yl)ethyl ester prodrug, mycophenolate mofetil) to prevent tissue rejection following organ transplants and for the treatment of certain autoimmune diseases.		3.21102-benzofurans;
gamma-lactone;
monocarboxylic acid;
phenols		anticoronaviral agent;
antimicrobial agent;
antineoplastic agent;
EC 1.1.1.205 (IMP dehydrogenase) inhibitor;
environmental contaminant;
immunosuppressive agent;
mycotoxin;
Penicillium metabolite;
xenobiotic
valine-pyrrolidide
valine-pyrrolidide: structure given in first source		2.0210
t0901317
T0901317: an LXRalpha and LXRbeta agonist		2.0810
adenosine-5'-(n-ethylcarboxamide)
Adenosine-5'-(N-ethylcarboxamide): A stable adenosine A1 and A2 receptor agonist. Experimentally, it inhibits cAMP and cGMP phosphodiesterase activity.. N-ethyl-5'-carboxamidoadenosine : A derivative of adenosine in which the 5'-hydroxymethyl group is replaced by an N-ethylcarboxamido group.		2.1310adenosines;
monocarboxylic acid amide		adenosine A1 receptor agonist;
adenosine A2A receptor agonist;
antineoplastic agent;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
vasodilator agent
h 89
N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide: structure given in first source. N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide : A member of the class of isoquinolines that is the sulfonamide obtained by formal condensation of the sulfo group of isoquinoline-5-sulfonic acid with the primary amino group of N(1)-[3-(4-bromophenyl)prop-2-en-1-yl]ethane-1,2-diamine. It is a protein kinase A inhibitor.. (E)-N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide : A N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide in which the double bond adopts a trans-configuration.		3.6790N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide
n-succinimidyl-4-fluorobenzoate
N-succinimidyl-4-fluorobenzoate: used to label proteins with F(18); structure in first source; RN refers to 18F-labeled isomer		2.0810
iridoids
Iridoids: A type of MONOTERPENES, derived from geraniol. They have the general form of cyclopentanopyran, but in some cases, one of the rings is broken as in the case of secoiridoid. They are different from the similarly named iridals (TRITERPENES).		2.110
dactinomycin
Dactinomycin: A compound composed of a two CYCLIC PEPTIDES attached to a phenoxazine that is derived from STREPTOMYCES parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015)		2.0810actinomycinmutagen
benzyloxycarbonylleucyl-leucyl-leucine aldehyde
benzyloxycarbonylleucyl-leucyl-leucine aldehyde: proteasome inhibitor. N-benzyloxycarbonyl-L-leucyl-L-leucyl-L-leucinal : A tripeptide that is L-leucyl-L-leucyl-L-leucine in which the C-terminal carboxy group has been reduced to the corresponding aldehyde and the N-terminal amino group is protected as its benzyloxycarbonyl derivative.		2.0710amino aldehyde;
carbamate ester;
tripeptide		proteasome inhibitor
micafungin
Micafungin: A cyclic lipo-hexapeptide echinocandin antifungal agent that is used for the treatment and prevention of CANDIDIASIS.. micafungin : A cyclic hexapeptide echinocandin antibiotic which exerts its effect by inhibiting the synthesis of 1,3-beta-D-glucan, an integral component of the fungal cell wall. It is used as the sodium salt for the treatment of invasive candidiasis, and of aspergillosis in patients who are intolerant of other therapy.		2.0310antibiotic antifungal drug;
echinocandin		antiinfective agent
lisofylline
lisofylline: metabolite of pentoxifylline; structure given in first source. (R)-lisofylline : A 1-(5-hydroxyhexyl)-3,7-dimethyl-3,7-dihydro-1H-purine-2,6-dione that has (R)-configuration. A synthetic small molecule which was under development for the treatment of type 1 diabetes mellitus.		2.03101-(5-hydroxyhexyl)-3,7-dimethyl-3,7-dihydro-1H-purine-2,6-dioneanti-inflammatory agent;
immunomodulator
bromochloroacetic acid
Keratins: A class of fibrous proteins or scleroproteins that represents the principal constituent of EPIDERMIS; HAIR; NAILS; horny tissues, and the organic matrix of tooth ENAMEL. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms a coiled-coil alpha helical structure consisting of TYPE I KERATIN and a TYPE II KERATIN, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. alpha-Keratins have been classified into at least 20 subtypes. In addition multiple isoforms of subtypes have been found which may be due to GENE DUPLICATION.. bromochloroacetic acid : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is replaced by bromine while a second is replaced by chlorine. A low-melting (27.5-31.5degreeC), hygroscopic crystalline solid, it can be formed during the disinfection (by chlorination) of water that contains bromide ions and organic matter, so can occur in drinking water as a byproduct of the disinfection process.		2.02102-bromocarboxylic acid;
monocarboxylic acid;
organochlorine compound
isomethyleugenol
Methylation: Addition of methyl groups. In histo-chemistry methylation is used to esterify carboxyl groups and remove sulfate groups by treating tissue sections with hot methanol in the presence of hydrochloric acid. (From Stedman, 25th ed)		2.5920isomethyleugenol
squalene
Addavax: an oil-water nanoemulsion and adjuvant containing squalene, Tween 80, and sorbitane trioleate		2.1710triterpenehuman metabolite;
mouse metabolite;
plant metabolite;
Saccharomyces cerevisiae metabolite
stilbenes
Stilbenes: Organic compounds that contain 1,2-diphenylethylene as a functional group.. trans-stilbene : The trans-isomer of stilbene.		5.8131stilbene
arginine vasopressin
Arginine Vasopressin: The predominant form of mammalian antidiuretic hormone. It is a nonapeptide containing an ARGININE at residue 8 and two disulfide-linked cysteines at residues of 1 and 6. Arg-vasopressin is used to treat DIABETES INSIPIDUS or to improve vasomotor tone and BLOOD PRESSURE.. argipressin : The predominant form of mammalian vasopressin (antidiuretic hormone). It is a nonapeptide containing an arginine at residue 8 and two disulfide-linked cysteines at residues of 1 and 6.		2.4520vasopressincardiovascular drug;
hematologic agent;
mitogen
gw9662
2-chloro-5-nitrobenzanilide: pretreatment of peroxisome proliferator activated receptors with GW9662 results in the irreversible loss of ligand binding		2.110benzamides
dodecylphosphocholine
dodecylphosphocholine: phospholipase A2 inhibitor; RN refers to chloride. dodecylphosphocholine : A phosphocholine that is the monododecyl ester of phosphocholine		2.0610phosphocholinesdetergent
dithizone
Dithizone: Chelating agent used for heavy metal poisoning and assay. It causes diabetes.		2.1310
D-fructopyranose
[no description available]		5.05140cyclic hemiketal;
D-fructose;
fructopyranose		sweetening agent
thioacetamide
Thioacetamide: A crystalline compound used as a laboratory reagent in place of HYDROGEN SULFIDE. It is a potent hepatocarcinogen.. thioacetamide : A thiocarboxamide consiting of acetamide having the oxygen replaced by sulfur.		2.0310thiocarboxamidehepatotoxic agent
ferric ferrocyanide
ferric ferrocyanide: antidote to thallium poisoning; RN given refers to Fe(+3)[3:4] salt; structure		2.0810
digoxin
Digoxin: A cardiotonic glycoside obtained mainly from Digitalis lanata; it consists of three sugars and the aglycone DIGOXIGENIN. Digoxin has positive inotropic and negative chronotropic activity. It is used to control ventricular rate in ATRIAL FIBRILLATION and in the management of congestive heart failure with atrial fibrillation. Its use in congestive heart failure and sinus rhythm is less certain. The margin between toxic and therapeutic doses is small. (From Martindale, The Extra Pharmacopoeia, 30th ed, p666). digoxin : A cardenolide glycoside that is digitoxin beta-hydroxylated at C-12. A cardiac glycoside extracted from the foxglove plant, Digitalis lanata, it is used to control ventricular rate in atrial fibrillation and in the management of congestive heart failure with atrial fibrillation, but the margin between toxic and therapeutic doses is small.		8.4111cardenolide glycoside;
steroid saponin		anti-arrhythmia drug;
cardiotonic drug;
EC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor;
epitope
ccg 1423
CCG 1423: inhibits RhoA signaling; structure in first source		2.1310
tamoxifen
[no description available]		2.1110stilbenoid;
tertiary amino compound		angiogenesis inhibitor;
antineoplastic agent;
bone density conservation agent;
EC 1.2.3.1 (aldehyde oxidase) inhibitor;
EC 2.7.11.13 (protein kinase C) inhibitor;
estrogen antagonist;
estrogen receptor antagonist;
estrogen receptor modulator
u 0126
U 0126: protein kinase kinase inhibitor; structure in first source		2.4620aryl sulfide;
dinitrile;
enamine;
substituted aniline		antineoplastic agent;
antioxidant;
apoptosis inducer;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
osteogenesis regulator;
vasoconstrictor agent
l 783281
L 783281: structure in first source		3.1610
pica
Pica: The persistent eating of non-nutritive substances for a period of at least one month.		2.1310
cobaltous chloride
cobaltous chloride: RN given refers to unlabeled cpd; RN in Chemline for cobalt trichloride: 10241-04-0; RN for 60-labeled cpd: 14543-09-0; RN for 57-labeled cpd: 164113-89-1; RN for 58-labeled cpd: 29377-09-1; structure. cobalt dichloride : A cobalt salt in which the cobalt metal is in the +2 oxidation state and the counter-anion is chloride. It is used as an indicator for water in desiccants.		2.0710cobalt salt;
inorganic chloride		allergen;
calcium channel blocker;
sensitiser;
two-colour indicator
monooctanoin
monooctanoin: dissolution agent for retained cholesterol bile duct stones; RN in Chemline for octanoic acid, ester with 1,2,3-propanetriol, MF unknown: 11140-04-8; RN for octanoic acid, 2,3-dihydroxypropyl ester (1-monooctanoin): 502-54-5; RN in 9th CI Form Index for (+-)-1-monooctanoin: 19670-49-6. rac-1-monooctanoylglycerol : A rac-1-monoacylglycerol comprising equal amounts of 1-octanoyl-sn-glycerol and 3-octanoyl-sn-glycerol.. 1-monooctanoylglycerol : A 1-monoglyceride that has octanoyl as the acyl group.		2.25101-monoglyceride;
octanoate ester;
rac-1-monoacylglycerol
orlistat
Orlistat: A lactone derivative of LEUCINE that acts as a pancreatic lipase inhibitor to limit the absorption of dietary fat; it is used in the management of obesity.. orlistat : A carboxylic ester resulting from the formal condensation of the carboxy group of N-formyl-L-leucine with the hydroxy group of (3S,4S)-3-hexyl-4-[(2S)-2-hydroxytridecyl]oxetan-2-one. A pancreatic lipase inhibitor, it is used as an anti-obesity drug.		5.3750beta-lactone;
carboxylic ester;
formamides;
L-leucine derivative		anti-obesity agent;
bacterial metabolite;
EC 2.3.1.85 (fatty acid synthase) inhibitor;
EC 3.1.1.3 (triacylglycerol lipase) inhibitor
quinine
[no description available]		2.1110cinchona alkaloidantimalarial;
muscle relaxant;
non-narcotic analgesic
rtki cpd
RTKI cpd: preferentially inhibits human glioma cells expressing truncated rather than wild-type epidermal growth factor receptors		2.0110
4-azidophenylalanine
4-azidophenylalanine: RN given refers to (L)-isomer. 4-azido-L-phenylalanine : A 4-azidophenylalanine that has L-configuration. It is used as a bioorthogonal click-chemistry reagent.. 4-azidophenylalanine : A phenylalanine derivative that is phenylalanine substituted by an azido group at position 4.		2.1510
ovalbumin
Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily.		2.0810
sodium dodecyl sulfate
Sodium Dodecyl Sulfate: An anionic surfactant, usually a mixture of sodium alkyl sulfates, mainly the lauryl; lowers surface tension of aqueous solutions; used as fat emulsifier, wetting agent, detergent in cosmetics, pharmaceuticals and toothpastes; also as research tool in protein biochemistry.. sodium dodecyl sulfate : An organic sodium salt that is the sodium salt of dodecyl hydrogen sulfate.		2.1310organic sodium saltdetergent;
protein denaturant
crocin
crocin: a free radical scavenger		2.610
sb 242084
6-chloro-5-methyl-1-((2-(2-methylpyrid-3-yloxy)pyrid-5-yl)carbamoyl)indoline: 5-HT(2C) receptor inverse agonist (antagonist); structure in first source		2.1510
6-hydrazinopyridine-3-carboxylic acid
6-hydrazinonicotinic acid: structure in first source		2.0810
alpha-chymotrypsin
Chymotrypsin: A serine endopeptidase secreted by the pancreas as its zymogen, CHYMOTRYPSINOGEN and carried in the pancreatic juice to the duodenum where it is activated by TRYPSIN. It selectively cleaves aromatic amino acids on the carboxyl side.		2.1110
jhw 015
[no description available]		2.0810indolecarboxamide
osteoprotegerin
Osteoprotegerin: A secreted member of the TNF receptor superfamily that negatively regulates osteoclastogenesis. It is a soluble decoy receptor of RANK LIGAND that inhibits both CELL DIFFERENTIATION and function of OSTEOCLASTS by inhibiting the interaction between RANK LIGAND and RECEPTOR ACTIVATOR OF NUCLEAR FACTOR-KAPPA B.		4.3931long-chain fatty acid
dinoprostone
prostaglandin E2 : Prostaglandin F2alpha in which the hydroxy group at position 9 has been oxidised to the corresponding ketone. Prostaglandin E2 is the most common and most biologically potent of mammalian prostaglandins.		2.0810prostaglandins Ehuman metabolite;
mouse metabolite;
oxytocic
dinoprost
Dinoprost: A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.. prostaglandin F2alpha : A prostaglandins Falpha that is prosta-5,13-dien-1-oic acid substituted by hydroxy groups at positions 9, 11 and 15. It is a naturally occurring prostaglandin used to induce labor.		4.3711monocarboxylic acid;
prostaglandins Falpha		human metabolite;
mouse metabolite
linoleic acid
Linoleic Acid: A doubly unsaturated fatty acid, occurring widely in plant glycosides. It is an essential fatty acid in mammalian nutrition and is used in the biosynthesis of prostaglandins and cell membranes. (From Stedman, 26th ed). linoleic acid : An octadecadienoic acid in which the two double bonds are at positions 9 and 12 and have Z (cis) stereochemistry.		2.1510octadecadienoic acid;
omega-6 fatty acid		algal metabolite;
Daphnia galeata metabolite;
plant metabolite
thromboxane a2
Thromboxane A2: An unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).. thromboxane A2 : A thromboxane which is produced by activated platelets and has prothrombotic properties: it stimulates activation of new platelets as well as increases platelet aggregation.		2.110epoxy monocarboxylic acid;
thromboxanes A		mouse metabolite
alprostadil
[no description available]		2.4110prostaglandins Eanticoagulant;
human metabolite;
platelet aggregation inhibitor;
vasodilator agent
lipoxin a4
lipoxin A4: an antifibrolytic agent; structure given in first source; a role in ASPIRIN antiinflammatory activity. lipoxin A4 : A C20 hydroxy fatty acid having (5S)-, (6R)- and (15S)-hydroxy groups as well as (7E)- (9E)-, (11Z)- and (13E)-double bonds.		2.0810hydroxy polyunsaturated fatty acid;
lipoxin;
long-chain fatty acid		human metabolite;
metabolite
harmine
Harmine: Alkaloid isolated from seeds of PEGANUM HARMALA; ZYGOPHYLLACEAE. It is identical to banisterine, or telepathine, from Banisteria caapi and is one of the active ingredients of hallucinogenic drinks made in the western Amazon region from related plants. It has no therapeutic use, but (as banisterine) was hailed as a cure for postencephalitic PARKINSON DISEASE in the 1920's.. harmine : A harmala alkaloid in which the harman skeleton is methoxy-substituted at C-7.		2.1310harmala alkaloidanti-HIV agent;
EC 1.4.3.4 (monoamine oxidase) inhibitor;
metabolite
tranilast
tranilast: antiallergic drug; potent inhibitor of homologous passive cutaneous anaphylaxis. tranilast : An amidobenzoic acid that is anthranilic acid in which one of the anilino hydrogens is replaced by a 3,4-dimethoxycinnamoyl group.		3.2110amidobenzoic acid;
cinnamamides;
dimethoxybenzene;
secondary carboxamide		anti-allergic agent;
anti-asthmatic drug;
antineoplastic agent;
aryl hydrocarbon receptor agonist;
calcium channel blocker;
hepatoprotective agent;
nephroprotective agent
8-epi-prostaglandin f2alpha
8-epi-prostaglandin F2alpha: a potent preglomerular vasoconstrictor acting principally through thromboxane A2 receptor activation. 8-epi-prostaglandin F2alpha : An isoprostane that is prostaglandin F2alpha having inverted stereochemistry at the 8-position.		4.3711F2-isoprostanebiomarker;
bronchoconstrictor agent;
vasoconstrictor agent
glyceryl 2-arachidonate
glyceryl 2-arachidonate: binds to cannabinoid receptors; structure in first source. 2-arachidonoylglycerol : An endocannabinoid and an endogenous agonist of the cannabinoid receptors (CB1 and CB2). It is an ester formed from omega-6-arachidonic acid and glycerol.		2.13102-acylglycerol 20:4;
endocannabinoid		human metabolite
n-oleoylethanolamine
N-oleoylethanolamine: ceramidase inhibitor. oleoyl ethanolamide : An N-(long-chain-acyl)ethanolamine that is the ethanolamide of oleic acid. The monounsaturated analogue of the endocannabinoid anandamide.		2.1710endocannabinoid;
N-(long-chain-acyl)ethanolamine;
N-acylethanolamine 18:1		EC 3.5.1.23 (ceramidase) inhibitor;
geroprotector;
PPARalpha agonist
sirolimus
Sirolimus: A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to IMMUNOPHILINS. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties.. sirolimus : A macrolide lactam isolated from Streptomyces hygroscopicus consisting of a 29-membered ring containing 4 trans double bonds, three of which are conjugated. It is an antibiotic, immunosupressive and antineoplastic agent.		2.7530antibiotic antifungal drug;
cyclic acetal;
cyclic ketone;
ether;
macrolide lactam;
organic heterotricyclic compound;
secondary alcohol		antibacterial drug;
anticoronaviral agent;
antineoplastic agent;
bacterial metabolite;
geroprotector;
immunosuppressive agent;
mTOR inhibitor
topiramate
Topiramate: A sulfamate-substituted fructose analog that was originally identified as a hypoglycemic agent. It is used for the treatment of EPILEPSY and MIGRAINE DISORDERS, and may also promote weight loss.. topiramate : A hexose derivative that is 2,3:4,5-di-O-isopropylidene-beta-D-fructopyranose in which the hydroxy group has been converted to the corresponding sulfamate ester. It blocks voltage-dependent sodium channels and is used as an antiepileptic and for the prevention of migraine.		11.2731cyclic ketal;
ketohexose derivative;
sulfamate ester		anticonvulsant;
sodium channel blocker
cp 99994
3-(2-methoxybenzylamino)-2-phenylpiperidine: selective NK(1) receptor antagonist; CP-100263 is the inactive enantiomer		2.110
deamino arginine vasopressin
Deamino Arginine Vasopressin: A synthetic analog of the pituitary hormone, ARGININE VASOPRESSIN. Its action is mediated by the VASOPRESSIN receptor V2. It has prolonged antidiuretic activity, but little pressor effects. It also modulates levels of circulating FACTOR VIII and VON WILLEBRAND FACTOR.		2.0810heterodetic cyclic peptidediagnostic agent;
renal agent;
vasopressin receptor agonist
nateglinide
Nateglinide: A phenylalanine and cyclohexane derivative that acts as a hypoglycemic agent by stimulating the release of insulin from the pancreas. It is used in the treatment of TYPE 2 DIABETES.. nateglinide : An N-acyl-D-phenylalanine resulting from the formal condensation of the amino group of D-phenylalanine with the carboxy group of trans-4-isopropylcyclohexanecarboxylic acid. An orally-administered, rapidly-absorbed, short-acting insulinotropic agent, it is used for the treatment of type 2 diabetes mellitus.		2.0810phenylalanine derivative
fosbretabulin
fosbretabulin: a microtubule destabilizing agent isolated from Combretum caffrum; structure in first source		3.711
indium
Indium: A metallic element, atomic number 49, atomic weight 114.818, symbol In. It is named from its blue line in the spectrum.. indium atom : A metallic element first identified and named from the brilliant indigo (Latin indicum) blue line in its flame spectrum.		2.4110boron group element atom
naltrexone
Naltrexone: Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of NALOXONE. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence.. naltrexone : An organic heteropentacyclic compound that is naloxone substituted in which the allyl group attached to the nitrogen is replaced by a cyclopropylmethyl group. A mu-opioid receptor antagonist, it is used to treat alcohol dependence.		2.7730cyclopropanes;
morphinane-like compound;
organic heteropentacyclic compound		antidote to opioid poisoning;
central nervous system depressant;
environmental contaminant;
mu-opioid receptor antagonist;
xenobiotic
dextromethorphan
Dextromethorphan: Methyl analog of DEXTRORPHAN that shows high affinity binding to several regions of the brain, including the medullary cough center. This compound is an NMDA receptor antagonist (RECEPTORS, N-METHYL-D-ASPARTATE) and acts as a non-competitive channel blocker. It is one of the widely used ANTITUSSIVES, and is also used to study the involvement of glutamate receptors in neurotoxicity.. dextromethorphan : A 6-methoxy-11-methyl-1,3,4,9,10,10a-hexahydro-2H-10,4a-(epiminoethano)phenanthrene in which the sterocenters at positions 4a, 10 and 10a have S-configuration. It is a prodrug of dextrorphan and used as an antitussive drug for suppressing cough.		2.11106-methoxy-11-methyl-1,3,4,9,10,10a-hexahydro-2H-10,4a-(epiminoethano)phenanthreneantitussive;
environmental contaminant;
neurotoxin;
NMDA receptor antagonist;
oneirogen;
prodrug;
xenobiotic
lisinopril
Lisinopril: One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.		8.4311dipeptideEC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
enalapril
Enalapril: An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.. enalapril : A dicarboxylic acid monoester that is ethyl 4-phenylbutanoate in which a hydrogen alpha to the carboxy group is substituted by the amino group of L-alanyl-L-proline (S-configuration).		7.110dicarboxylic acid monoester;
dipeptide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
geroprotector;
prodrug
fumarates
Fumarates: Compounds based on fumaric acid.. fumarate(2-) : A C4-dicarboxylate that is the E-isomer of but-2-enedioate(2-)		2.4820butenedioate;
C4-dicarboxylate		human metabolite;
metabolite;
Saccharomyces cerevisiae metabolite
cysteine
Cysteine: A thiol-containing non-essential amino acid that is oxidized to form CYSTINE.. L-cysteinium : The L-enantiomer of cysteinium.. cysteine : A sulfur-containing amino acid that is propanoic acid with an amino group at position 2 and a sulfanyl group at position 3.		6.0291cysteiniumfundamental metabolite
thyronines
Thyronines: A group of metabolites derived from THYROXINE and TRIIODOTHYRONINE via the peripheral enzymatic removal of iodines from the thyroxine nucleus. Thyronine is the thyroxine nucleus devoid of its four iodine atoms.. thyronine : A tyrosine derivative where the phenolic hydrogen of tyrosine is substituted by 4-hydroxyphenyl.		2.0710thyronine
indium
[no description available]		2.2110
heroin
Heroin: A narcotic analgesic that may be habit-forming. It is a controlled substance (opium derivative) listed in the U.S. Code of Federal Regulations, Title 21 Parts 329.1, 1308.11 (1987). Sale is forbidden in the United States by Federal statute. (Merck Index, 11th ed). heroin : A morphinane alkaloid that is morphine bearing two acetyl substituents on the O-3 and O-6 positions. As with other opioids, heroin is used as both an analgesic and a recreational drug. Frequent and regular administration is associated with tolerance and physical dependence, which may develop into addiction. Its use includes treatment for acute pain, such as in severe physical trauma, myocardial infarction, post-surgical pain, and chronic pain, including end-stage cancer and other terminal illnesses.		2.3110morphinane alkaloidmu-opioid receptor agonist;
opioid analgesic;
prodrug
enkephalin, ala(2)-mephe(4)-gly(5)-
Enkephalin, Ala(2)-MePhe(4)-Gly(5)-: An enkephalin analog that selectively binds to the MU OPIOID RECEPTOR. It is used as a model for drug permeability experiments.		2.6920
pregabalin
Pregabalin: A gamma-aminobutyric acid (GABA) derivative that functions as a CALCIUM CHANNEL BLOCKER and is used as an ANTICONVULSANT as well as an ANTI-ANXIETY AGENT. It is also used as an ANALGESIC in the treatment of NEUROPATHIC PAIN and FIBROMYALGIA.. pregabalin : A gamma-amino acid that is gamma-aminobutyric acid (GABA) carrying an isobutyl substitutent at the beta-position (the S-enantiomer). Binds with high affinity to the alpha2-delta site (an auxiliary subunit of voltage-gated calcium channels) in central nervous system tissues.		2.4320gamma-amino acidanticonvulsant;
calcium channel blocker
aliskiren
aliskiren: orally active nonpeptidic renin inhibitor. aliskiren : A monomethoxybenzene compound having a 3-methoxypropoxy group at the 2-position and a multi-substituted branched alkyl substituent at the 4-position.		2.4820monocarboxylic acid amide;
monomethoxybenzene		antihypertensive agent
tetrodotoxin
Tetrodotoxin: An aminoperhydroquinazoline poison found mainly in the liver and ovaries of fishes in the order TETRAODONTIFORMES, which are eaten. The toxin causes paresthesia and paralysis through interference with neuromuscular conduction.. tetrodotoxin : A quinazoline alkaloid that is a marine toxin isolated from fish such as puffer fish. It has been shown to exhibit potential neutotoxicity due to its ability to block voltage-gated sodium channels.		2.7430azatetracycloalkane;
oxatetracycloalkane;
quinazoline alkaloid		animal metabolite;
bacterial metabolite;
marine metabolite;
neurotoxin;
voltage-gated sodium channel blocker
selenium
Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.97. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of GLUTATHIONE PEROXIDASE.		2.830chalcogen;
nonmetal atom		micronutrient
bafilomycin a1
bafilomycin A1: from Streptomyces griseus; structure given in first source. bafilomycin A1 : The most used of the bafilomycins, a family of toxic macrolide antibiotics derived from Streptomyces griseus.		2.8230cyclic hemiketal;
macrolide antibiotic;
oxanes		apoptosis inducer;
autophagy inhibitor;
bacterial metabolite;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor;
EC 3.6.3.14 (H(+)-transporting two-sector ATPase) inhibitor;
ferroptosis inhibitor;
fungicide;
potassium ionophore;
toxin
corrin
corrin : A tetrapyrrole fundamental parent that is the core macrocycle of vitamin B12.		2.3110
everolimus
[no description available]		7.1310cyclic acetal;
cyclic ketone;
ether;
macrolide lactam;
primary alcohol;
secondary alcohol		anticoronaviral agent;
antineoplastic agent;
geroprotector;
immunosuppressive agent;
mTOR inhibitor
rosiglitazone-metformin combination
rosiglitazone-metformin combination: a combination of metformin and rosiglitazone used for treating type 2 diabetes		2.0810
l-165041
4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid: a PPAR-delta agonist has regulatory effects on a variety of adipokines, and these effects might explain some of their metabolic function.		2.1510aromatic ketone
sq-23377
Ionomycin: A divalent calcium ionophore that is widely used as a tool to investigate the role of intracellular calcium in cellular processes.. ionomycin : A very long-chain fatty acid that is docosa-10,16-dienoic acid which is substituted by methyl groups at positions 4, 6, 8, 12, 14, 18 and 20, by hydroxy groups at positions 11, 19 and 21, and by a (2',5-dimethyloctahydro-2,2'-bifuran-5-yl)ethanol group at position 21. An ionophore produced by Streptomyces conglobatus, it is used in research to raise the intracellular level of Ca(2+) and as a research tool to understand Ca(2+) transport across biological membranes.		2.0710cyclic ether;
enol;
polyunsaturated fatty acid;
very long-chain fatty acid		calcium ionophore;
metabolite
vildagliptin
[no description available]		18.21461amino acid amide
staurosporine
staurosporinium : Conjugate acid of staurosporine.		2.0710ammonium ion derivative
sincalide
Sincalide: An octapeptide hormone present in the intestine and brain. When secreted from the gastric mucosa, it stimulates the release of bile from the gallbladder and digestive enzymes from the pancreas.		2.7630oligopeptide
vasopressin, 1-(1-mercaptocyclohexaneacetic acid)-2-(o- methyl-l-tyrosine)-8-l-arginine-
vasopressin, 1-(1-mercaptocyclohexaneacetic acid)-2-(O- methyl-L-tyrosine)-8-L-arginine-: highly potent antagonist of vasopressor response to arginine-vasopressin; structure in first source		2.4520
uk-432097
UK-432097: a highly potent and selective agonist and drug candidate for chronic obstructive pulmonary disease (COPD) treatment; structure in first source		2.1310
ursodoxicoltaurine
tauroursodeoxycholate : An organosulfonate oxoanion that is the conjugate base of tauroursodeoxycholic acid arising from deprotonation of the sulfonate OH group; major species at pH 7.3.. tauroursodeoxycholic acid : A bile acid taurine conjugate derived from ursoodeoxycholic acid.		2.1710bile acid taurine conjugateanti-inflammatory agent;
apoptosis inhibitor;
bone density conservation agent;
cardioprotective agent;
human metabolite;
neuroprotective agent
mocetinostat
mocetinostat: undergoing phase II clinical trials for treatment of cancer. mocetinostat : A benzamide obtained by formal condensation of the carboxy group of 4-({[4-(pyridin-3-yl)pyrimidin-2-yl]amino}methyl)benzoic acid with one of the amino groups of benzene-1,2-diamine. It is an orally active and isotype-selective HDAC inhibitor which exhibits antitumour activity (IC50 = 0.15, 0.29, 1.66 and 0.59 muM for HDAC1, HDAC2, HDAC3 and HDAC11).		2.4720aminopyrimidine;
benzamides;
pyridines;
secondary amino compound;
secondary carboxamide;
substituted aniline		antineoplastic agent;
apoptosis inducer;
autophagy inducer;
cardioprotective agent;
EC 3.5.1.98 (histone deacetylase) inhibitor;
hepatotoxic agent
lipid a
Lipid A: Lipid A is the biologically active component of lipopolysaccharides. It shows strong endotoxic activity and exhibits immunogenic properties.. lipid A : The glycolipid moiety of bacterial lipopolysaccharide (R can be either hydrogen or a fatty acyl group).		6.7533dodecanoate ester;
lipid A;
tetradecanoate ester		Escherichia coli metabolite
a 134974
A 134974: structure in first source		2.1310
dapagliflozin
[no description available]		13.262416aromatic ether;
C-glycosyl compound;
monochlorobenzenes		hypoglycemic agent;
sodium-glucose transport protein subtype 2 inhibitor
gw 4064
[no description available]		2.2510stilbenoid
3-iodothyronamine
3-iodothyronamine: a thyroid hormone derivative that may be involved in a fast response signaling pathway; structure in first source		2.0710aromatic ether
linagliptin
Linagliptin: A purine and quinazoline derivative that functions as an INCRETIN and DIPEPTIDYL-PEPTIDASE IV INHIBTOR. It is used as a HYPOGLYCEMIC AGENT in the treatment of TYPE II DIABETES MELLITUS.. linagliptin : A xanthine that is 7H-xanthine bearing (4-methylquinazolin-2-yl)methyl, methyl, but-2-yn-1-yl and 3-aminopiperidin-1-yl substituents at positions 1, 3, 7 and 8 respectively (the R-enantiomer). Used for treatment of type II diabetes.		5.9290aminopiperidine;
quinazolines		EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
hypoglycemic agent
alpha-synuclein
alpha-Synuclein: A synuclein that is a major component of LEWY BODIES and plays a role in SYNUCLEINOPATHIES, neurodegeneration and neuroprotection.		3.5320
piragliatin
piragliatin: glucokinase activator		7.7730
oxadiazoles
Oxadiazoles: Compounds containing five-membered heteroaromatic rings containing two carbons, two nitrogens, and one oxygen atom which exist in various regioisomeric forms.		2.2110
alogliptin
alogliptin: structure in first source. alogliptin : A piperidine that is 3-methyl-2,4-dioxo-3,4-dihydropyrimidine carrying additional 2-cyanobenzyl and 3-aminopiperidin-1-yl groups at positions 1 and 2 respectively (the R-enantiomer). Used in the form of its benzoate salt for treatment of type 2 diabetes.		6.5590nitrile;
piperidines;
primary amino compound;
pyrimidines		EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
hypoglycemic agent
sitagliptin phosphate
Sitagliptin Phosphate: A pyrazine-derived DIPEPTIDYL-PEPTIDASE IV INHIBITOR and HYPOGLYCEMIC AGENT that increases the levels of the INCRETIN hormones GLUCAGON-LIKE PEPTIDE-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). It is used in the treatment of TYPE 2 DIABETES.		19.9717035
ru 66647
telithromycin: a ketolide; semisynthetic derivative of erythromycin with cycling of the C11-12 positions to form a carbamate ring to avoid acquired resistance to macrolides; binds 70S bacterial rRNA, specifically to the 23S part (23S RIBOSOMAL RNA), preventing protein synthesis;		2.1110
losartan potassium
Erythropoietin: Glycoprotein hormone, secreted chiefly by the KIDNEY in the adult and the LIVER in the FETUS, that acts on erythroid stem cells of the BONE MARROW to stimulate proliferation and differentiation.		2.520
empagliflozin
[no description available]		3.2710aromatic ether;
C-glycosyl compound;
monochlorobenzenes;
tetrahydrofuryl ether		hypoglycemic agent;
sodium-glucose transport protein subtype 2 inhibitor
lc15-0444
LC15-0444: Dipeptidyl Peptidase IV Inhibitors; orally active small molecule for the treatment of type II diabetes		2.1310organonitrogen compound;
organooxygen compound
pituitrin
Pituitrin: A substance or extract from the neurohypophysis (PITUITARY GLAND, POSTERIOR).		2.1310
mdv 3100
[no description available]		2.2510(trifluoromethyl)benzenes;
benzamides;
imidazolidinone;
monofluorobenzenes;
nitrile;
thiocarbonyl compound		androgen antagonist;
antineoplastic agent
cytochrome c-t
Cytochromes c: Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.		3.0240
calcitonin
[no description available]		2.7730
cholecystokinin
Cholecystokinin: A peptide, of about 33 amino acids, secreted by the upper INTESTINAL MUCOSA and also found in the central nervous system. It causes gallbladder contraction, release of pancreatic exocrine (or digestive) enzymes, and affects other gastrointestinal functions. Cholecystokinin may be the mediator of satiety.		9.8571
ceruletide
Ceruletide: A specific decapeptide obtained from the skin of Hila caerulea, an Australian amphibian. Caerulein is similar in action and composition to CHOLECYSTOKININ. It stimulates gastric, biliary, and pancreatic secretion; and certain smooth muscle. It is used in paralytic ileus and as diagnostic aid in pancreatic malfunction.. ceruletide : A decapeptide comprising 5-oxoprolyl, glutamyl, aspartyl, O-sulfotyrosyl, threonyl, glycyl, tryptopyl, methionyl, aspartyl and phenylalaninamide residues in sequence. Found in the skins of certain Australian amphibians, it is an analogue of the gastrointestinal peptide hormone cholecystokinin and stimulates gastric, biliary, and pancreatic secretion. It is used in cases of paralysis of the intestine (paralytic ileus) and as a diagnostic aid in pancreatic malfunction.		2.0510oligopeptidediagnostic agent;
gastrointestinal drug
bivalirudin
bivalirudin: designed to bind to the alpha-thrombin catalytic site and anion-binding exosite for fibrin(ogen) recognition. bivalirudin : A synthetic peptide of 20 amino acids, comprising D-Phe, Pro, Arg, Pro, Gly, Gly, Gly, Gly, Asn, Gly, Asp, Phe, Glu, Glu, Ile, Pro, Glu, Glu, Tyr, and Leu in sequence. A congener of hirudin (a naturally occurring drug found in the saliva of the medicinal leech), it a specific and reversible inhibitor of thrombin, and is used as an anticoagulant.		2.5120polypeptideanticoagulant;
EC 3.4.21.5 (thrombin) inhibitor
atrial natriuretic factor
Atrial Natriuretic Factor: A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight PEPTIDES derived from a common precursor and secreted mainly by the HEART ATRIUM. All these peptides share a sequence of about 20 AMINO ACIDS.		5.0421polypeptide
enfuvirtide
Enfuvirtide: A synthetic 36-amino acid peptide that corresponds to the heptad repeat sequence of HIV-1 gp41. It blocks HIV cell fusion and viral entry and is used with other anti-retrovirals for combination therapy of HIV INFECTIONS and AIDS.. enfuvirtide : A synthetic 36-amino acid peptide consisting of N-acetyltyrosyl, threonyl, seryl, leucyl, isoleucyl, histidyl, seryl, leucyl, isoleucyl, alpha-glutamyl, alpha-glutamyl, seryl, glutaminyl, asparaginyl, glutaminyl, glutaminyl, alpha-glutamyl, lysyl, asparaginyl, alpha-glutamyl, alpha-glutamyl, alpha-glutamyl, leucyl, leucyl, alpha-glutamyl, leucyl, alpha-aspartyl, lysyl, tryptophyl, alanyl, seryl, leucyl, tryptophyl, asparaginyl, tryptophyl, and phenylalaninamide residues joined in sequence. An HIV fusion inhibitor, it was the first of a novel class of antiretroviral drugs used in combination therapy for the treatment of HIV-1 infection. It interferes with entry of HIV into cells by binding to the gp41 sub-unit of the viral envelope glycoprotein, so inhibiting fusion of viral and cellular membranes.		2.4820
glucagon-like peptide 1 (7-36)amide
glucagon-like peptide 1 (7-36)amide: potent stimulator of insulin released in perfused mammalian pancreas		8.24200
gastrins
Gastrins: A family of gastrointestinal peptide hormones that excite the secretion of GASTRIC JUICE. They may also occur in the central nervous system where they are presumed to be neurotransmitters.		4.5470
glucagon
Glucagon: A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511). glucagon : A 29-amino acid peptide hormone consisting of His, Ser, Gln, Gly, Thr, Phe, Thr, Ser, Asp, Tyr, Ser, Lys, Tyr, Leu, Asp, Ser, Arg, Arg, Ala, Gln, Asp, Phe, Val, Gln, Trp, Leu, Met, Asn and Thr residues joined in sequence.		18.9319723peptide hormone
beta-endorphin
beta-Endorphin: A 31-amino acid peptide that is the C-terminal fragment of BETA-LIPOTROPIN. It acts on OPIOID RECEPTORS and is an analgesic. Its first four amino acids at the N-terminal are identical to the tetrapeptide sequence of METHIONINE ENKEPHALIN and LEUCINE ENKEPHALIN.. beta-endorphin : A polypeptide consisting of 31 amino acid residues in the sequence Tyr-Gly-Gly-Phe-Met-Thr-Ser-Glu-Lys-Ser-Gln-Thr-Pro-Leu-Val-Thr-Leu-Phe-Lys-Asn-Ala-Ile-Ile-Lys-Asn-Ala-Tyr-Lys-Lys-Gly-Glu. It is an endogenous opioid peptide neurotransmitter found in the neurons of both the central and peripheral nervous system and results from processing of the precursor protein proopiomelanocortin (POMC).		2.8330
neuropeptide y
Neuropeptide Y: A 36-amino acid peptide present in many organs and in many sympathetic noradrenergic neurons. It has vasoconstrictor and natriuretic activity and regulates local blood flow, glandular secretion, and smooth muscle activity. The peptide also stimulates feeding and drinking behavior and influences secretion of pituitary hormones.		3.9840
heliodermin
heliodermin: MW 5,900 peptide with secretin-like properties		4.5340
helospectin i
helospectin I: 38 residue peptide from Gila monster (Heloderma suspectum) venom; amino acid sequence given in first source		3.5320
helospectin ii
helospectin II: 37 amino acid residue peptide from Gila monster (Heloderma suspectum) venom; identical to helospectin I except for serine 38		1.9910
peptide phi
Peptide PHI: A 27-amino acid peptide with histidine at the N-terminal and isoleucine amide at the C-terminal. The exact amino acid composition of the peptide is species dependent. The peptide is secreted in the intestine, but is found in the nervous system, many organs, and in the majority of peripheral tissues. It has a wide range of biological actions, affecting the cardiovascular, gastrointestinal, respiratory, and central nervous systems.		1.9910
angiotensinogen
Angiotensinogen: An alpha-globulin of about 453 amino acids, depending on the species. It is produced by the liver in response to lowered blood pressure and secreted into blood circulation. Angiotensinogen is the inactive precursor of the ANGIOTENSINS produced in the body by successive enzyme cleavages. Cleavage of angiotensinogen by RENIN yields the decapeptide ANGIOTENSIN I. Further cleavage of angiotensin I (by ANGIOTENSIN CONVERTING ENZYME) yields the potent vasoconstrictor octapeptide ANGIOTENSIN II; and then, via other enzymes, other angiotensins also involved in the hemodynamic-regulating RENIN-ANGIOTENSIN SYSTEM.		3.5311
vasoactive intestinal peptide
vasoactive intestinal peptide (6-28): vasoactive intestinal peptide fragment		2.0610
astressin
astressin : A 30-membered homodetic cyclic peptide comprising the sequence D-Phe-His-Leu-Leu-Arg-Glu-Val-Leu-Glu-Nle-Ala-Arg-Ala-Glu-Gln-Leu-Ala-Gln-Glu-Ala-His-Lys-Asn-Arg-Lys-Leu-Nle-Glu-Ile-Ile-NH2 cyclised by an amide bridge, formed by condensation of the side-chain carboxy group of the Glu residue at position 19 and the side-chain amino group of the Lys residue at position 22.		2.110homodetic cyclic peptide;
polypeptide		corticotropin-releasing factor receptor antagonist;
neuroprotective agent
glucagon-like peptide 1 (7-36)
[no description available]		2.9440
oligonucleotides
[no description available]		2.110
liraglutide
[no description available]		22.638137lipopeptide;
polypeptide		glucagon-like peptide-1 receptor agonist;
neuroprotective agent
ziconotide
ziconotide: amino acid sequence in first source; from venom of South Pacific sea cone snail, Conus magus; calcium channel blocker; administered by injection into Cerebrospinal Fluid; Prialt is synthetic form. omega-conotoxin MVIIA : A heterodetic cyclic polypeptide consisting of the linear sequence Cys-Lys-Gly-Lys-Gly-Ala-Lys-Cys-Ser-Arg-Leu-Met-Tyr-Asp-Cys-Cys-Thr-Gly-Ser-Cys-Arg-Ser-Gly-Lys-Cys-NH2 with three disulfide bridges between cysteine residues 1-16, 8-20 and 15-25. A neuronal N-type Ca(2+) channel blocker in mammalian and amphibian brain, it blocks release of GABA and glutamate at neuronal synapses. Used as a probe for calcium channel receptors, it is selective for different receptor subtypes. A synthetic form, named ziconotide, is an atypical analgesic agent for the amelioration of severe and chronic pain.		2.4320
glucagon-like peptide 1
Glucagon-Like Peptide 1: A peptide of 36 or 37 amino acids that is derived from PROGLUCAGON and mainly produced by the INTESTINAL L CELLS. GLP-1(1-37 or 1-36) is further N-terminally truncated resulting in GLP-1(7-37) or GLP-1-(7-36) which can be amidated. These GLP-1 peptides are known to enhance glucose-dependent INSULIN release, suppress GLUCAGON release and gastric emptying, lower BLOOD GLUCOSE, and reduce food intake.		30.0293472
insulin detemir
Insulin Detemir: A recombinant long-acting insulin and hypoglycemic agent in which a MYRISTIC ACID is conjugated to a LYSINE at position B29. It is used to manage BLOOD GLUCOSE levels in patients with DIABETES MELLITUS.		13.1671
diapep 277
DiaPep 277: a 24-mer laboratory-made peptide derived from Hsp60(437-460)		3.1710
alx-0600
ALX-0600: glucagon-like peptide 2 (GLP-2) analog. teduglutide : A 33-membered polypeptide consisting of His, Gly, Asp, Gly, Ser, Phe, Ser, Asp, Glu, Met, Asn, Thr, Ile, Leu, Asp, Asn, Leu, Ala, Ala, Arg, Asp, Phe, Ile, Asn, Trp, Leu, Ile, Gln, Thr, Lys, Ile, Thr and Asp residues joined in sequence. A glucagon-like peptide-2 receptor agonist used for the treatment of short-bowel syndrome.		2.5220polypeptideantioxidant;
glucagon-like peptide-2 receptor agonist;
metabolite;
protective agent
incretins
Incretins: Peptides which stimulate INSULIN release from the PANCREATIC BETA CELLS following oral nutrient ingestion, or postprandially.		20.2423628
c-peptide
C-Peptide: The middle segment of proinsulin that is between the N-terminal B-chain and the C-terminal A-chain. It is a pancreatic peptide of about 31 residues, depending on the species. Upon proteolytic cleavage of proinsulin, equimolar INSULIN and C-peptide are released. C-peptide immunoassay has been used to assess pancreatic beta cell function in diabetic patients with circulating insulin antibodies or exogenous insulin. Half-life of C-peptide is 30 min, almost 8 times that of insulin.		17.222913
exendin (9-39)
exendin (9-39): a peptide from the venom of the lizard Heloderma suspectum; inhibits glucagon-like peptide-1 (GLP-1) induced cAMP production; its structure is related to exendin-4		10.85575
endothelin-1
Endothelin-1: A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)		5.6332
phosphatidylcholines
Phosphatidylcholines: Derivatives of PHOSPHATIDIC ACIDS in which the phosphoric acid is bound in ester linkage to a CHOLINE moiety.		2.78301,2-diacyl-sn-glycero-3-phosphocholine
vendex
Torque: The rotational force about an axis that is equal to the product of a force times the distance from the axis where the force is applied.		2.1110organotin acaricide
florbenazine f 18
florbenazine F 18: a PET tracer; structure in first source		3.3510
chitosan
[no description available]		4.13140
yil 781
YIL 781: an appetite suppressant and weight loss promoter; structure in first source		2.110
bucladesine
Bucladesine: A cyclic nucleotide derivative that mimics the action of endogenous CYCLIC AMP and is capable of permeating the cell membrane. It has vasodilator properties and is used as a cardiac stimulant. (From Merck Index, 11th ed). bucladesine : A 3',5'-cyclic purine nucleotide that is the 2'-butanoate ester and 6-N-butanoyl derivative of 3',5'-cyclic AMP.		2.13103',5'-cyclic purine nucleotide
gelsemine
gelsemine: from Gelsemium sempervirens; structure given in first source		2.1710indole alkaloid
canagliflozin
canagliflozin hydrate : A hydrate that is the hemihydrate form of canagliflozin. Used for treatment of type II diabetes via inhibition of sodium-glucose transport protein subtype 2.		2.2510C-glycosyl compound;
organofluorine compound;
thiophenes		hypoglycemic agent;
sodium-glucose transport protein subtype 2 inhibitor
insulin, isophane
Insulin, Isophane: An intermediate-acting INSULIN preparation with onset time of 2 hours and duration of 24 hours. It is produced by crystallizing ZINC-insulin-PROTAMINES at neutral pH 7. Thus it is called neutral protamine Hagedorn for inventor Hans Christian Hagedorn.		8.8274
intrinsic factor
Intrinsic Factor: A glycoprotein secreted by the cells of the GASTRIC GLANDS that is required for the absorption of VITAMIN B 12 (cyanocobalamin). Deficiency of intrinsic factor leads to VITAMIN B 12 DEFICIENCY and ANEMIA, PERNICIOUS.		2.1110
quetiapine fumarate
Quetiapine Fumarate: A dibenzothiazepine and ANTIPSYCHOTIC AGENT that targets the SEROTONIN 5-HT2 RECEPTOR; HISTAMINE H1 RECEPTOR, adrenergic alpha1 and alpha2 receptors, as well as the DOPAMINE D1 RECEPTOR and DOPAMINE D2 RECEPTOR. It is used in the treatment of SCHIZOPHRENIA; BIPOLAR DISORDER and DEPRESSIVE DISORDER.		2.0510fumarate salt
cardiovascular agents
Cardiovascular Agents: Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume.		2.4820
neurotensin
neurotensin, Tyr(11)-: RN given refers to parent cpd & (D)-isomer; RN for cpd without isomeric designation not avail 5/91		2.0710peptide hormonehuman metabolite;
mitogen;
neurotransmitter;
vulnerary
substance p, phe(5)-trp(7,9)-leu(11)-
substance P, Phe(5)-Trp(7,9)-Leu(11)-: substance P antagonist; bombesin antagonist		2.110
apelin-13 peptide
apelin-13 peptide: amino acid sequence in first source. apelin-13 : A 13 amino acid oligopeptide which is the ligand for the apelin receptor (also known as the APJ receptor). It exhibits hypotensive and neuroprotective effects, and may be a potential prognostic biomarker for acute ischemic stroke and multiple sclerosis.		2.1710oligopeptideantihypertensive agent;
autophagy inhibitor;
biomarker;
human metabolite;
neuroprotective agent
triiodothyronine, reverse
Triiodothyronine, Reverse: A metabolite of THYROXINE, formed by the peripheral enzymatic monodeiodination of T4 at the 5 position of the inner ring of the iodothyronine nucleus.. 3,3',5'-triiodo-L-thyronine zwitterion : Zwitterionic form of 3,3',5'-triiodo-L-thyronine.		2.1103,3',5'-triiodothyronine;
amino acid zwitterion
piperidines
Piperidines: A family of hexahydropyridines.		8.88230
interleukin-8
Interleukin-8: A member of the CXC chemokine family that plays a role in the regulation of the acute inflammatory response. It is secreted by variety of cell types and induces CHEMOTAXIS of NEUTROPHILS and other inflammatory cells.		2.5720
anagliptin
anagliptin: anagliptin hydrochloride salt is the active compound		2.1110amino acid amide
4-(3-(benzyloxy)phenyl)-2-(ethylsulfinyl)-6-(trifluoromethyl)pyrimidine
[no description available]		2.0710
methylcellulose
Methylcellulose: Methylester of cellulose. Methylcellulose is used as an emulsifying and suspending agent in cosmetics, pharmaceutics and the chemical industry. It is used therapeutically as a bulk laxative.		7.5820
vasoactive intestinal peptide
Vasoactive Intestinal Peptide: A highly basic, 28 amino acid neuropeptide released from intestinal mucosa. It has a wide range of biological actions affecting the cardiovascular, gastrointestinal, and respiratory systems and is neuroprotective. It binds special receptors (RECEPTORS, VASOACTIVE INTESTINAL PEPTIDE).		4.370
ac3174
AC3174: exenatide analog with antihypertensive, cardioprotective, insulin-sensitizing, and renoprotective effects		7.4820
ascorbic acid
Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant.. L-ascorbic acid : The L-enantiomer of ascorbic acid and conjugate acid of L-ascorbate.. L-ascorbate : The L-enantiomer of ascorbate and conjugate base of L-ascorbic acid, arising from selective deprotonation of the 3-hydroxy group. Required for a range of essential metabolic reactions in all animals and plants.. vitamin C : Any member of a group of vitamers that belong to the chemical structural class called butenolides that exhibit biological activity against vitamin C deficiency in animals. The vitamers include L-ascorbic acid and its salt, ionized and oxidized forms.		3.1710ascorbic acid;
vitamin C		coenzyme;
cofactor;
flour treatment agent;
food antioxidant;
food colour retention agent;
geroprotector;
plant metabolite;
skin lightening agent
minocycline
Minocycline: A TETRACYCLINE analog, having a 7-dimethylamino and lacking the 5 methyl and hydroxyl groups, which is effective against tetracycline-resistant STAPHYLOCOCCUS infections.. minocycline : A tetracycline analogue having a dimethylamino group at position 7 and lacking the methyl and hydroxy groups at position 5.		2.0310
warfarin
Warfarin: An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide.. warfarin : A racemate comprising equal amounts of (R)- and (S)-warfarin. Extensively used as both an anticoagulant drug and as a pesticide against rats and mice.. 4-hydroxy-3-(3-oxo-1-phenylbutyl)-1-benzopyran-2-one : A member of the class of coumarins that is 4-hydroxycoumarin which is substituted at position 3 by a 1-phenyl-3-oxo-1-butyl group.		9.3841benzenes;
hydroxycoumarin;
methyl ketone
tigecycline
[no description available]		2.0310
almagate
pegaptanib: a 28-base ribonucleic acid aptamer covalently linked to two branched 20-kD polyethylene glycol moieties to block the activity of extracellular VEGF, specifically the 165-amino-acid isoform (VEGF165); for treatment of neovascular age-related macular degeneration		2.0310
epidermal growth factor
Epidermal Growth Factor: A 6-kDa polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. Epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and EPITHELIAL CELLS. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form.		4.140
kaolinite
Kaolin: The most common mineral of a group of hydrated aluminum silicates, approximately H2Al2Si2O8-H2O. It is prepared for pharmaceutical and medicinal purposes by levigating with water to remove sand, etc. (From Merck Index, 11th ed) The name is derived from Kao-ling (Chinese: high ridge), the original site. (From Grant & Hackh's Chemical Dictionary, 5th ed). kaolin : An aluminosilicate soft white mineral named after the hill in China (Kao-ling) from which it was mined for centuries. In its natural state kaolin is a white, soft powder consisting principally of the mineral kaolinite, and varying amounts of other minerals such as muscovite, quartz, feldspar, and anatase. It is used in the manufacture of china and porcelain and also widely used in the production of paper, rubber, paint, drying agents, and many other products.		2.0310aluminosilicate mineral;
mixture		antidiarrhoeal drug;
excipient
transforming growth factor beta
Transforming Growth Factor beta: A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.		4.761
semaglutide
[no description available]		15.133511lipopeptide;
polypeptide		anti-obesity agent;
appetite depressant;
glucagon-like peptide-1 receptor agonist;
hypoglycemic agent;
neuroprotective agent
sybr green i
SYBR Green I: binds to double stranded DNA of less than 20 pg following agarose or polyacrylamide gel electrophoresis; excited at 497 nm and emits at 520 nm. SYBR Green I : A benzothiazolium ion resulting from the methylation of the nitrogen of the benzothiazole group of N-[4-(1,3-benzothiazol-2-ylmethylene)-1-phenyl-1,4-dihydroquinolin-2-yl]-N',N'-dimethyl-N-propylpropane-1,3-diamine. A cationic unsymmetrical cyanine dye that binds to double-stranded DNA and is used as a nucleic acid stain in molecular biology.		2.0210benzothiazolium ion;
cyanine dye;
quinolines;
tertiary amine		fluorescent dye
pyrethrins
[no description available]		2.0310
kiss1 protein, human
Kisspeptins: Intercellular signaling peptides that were originally characterized by their ability to suppress NEOPLASM METASTASIS. Kisspeptins have since been found to play an important role in the neuroendocrine regulation of REPRODUCTION.		2.7730
davalintide
davalintide: a synthetic amylin-mimetic peptide with appetitie suppresant activity		2.0810
hirudin
Hirudin: A 65-residue polypeptide from LEECHES.		2.5120
glutaminase
[no description available]		3.1410
cyclin d1
Cyclin D1: Protein encoded by the bcl-1 gene which plays a critical role in regulating the cell cycle. Overexpression of cyclin D1 is the result of bcl-1 rearrangement, a t(11;14) translocation, and is implicated in various neoplasms.		2.4420
ap20187
AP20187: a nontoxic, cell-permeable analog, a wholly synthesized, cell-permeable dimeric FK506 derivative. AP20187 : A tertiary amino compound that is 2-(aminomethyl)-N,N-dimethylpropane-1,3-diamine in which the primary ammino groups have each been acylated by condensation with the carboxy group of 2-{3-[(1R)-3-(3,4-dimethoxyphenyl)-1-hydroxypropyl]phenoxy}acetic acid, the hydroxy groups of which have been esterified by condensation with the carboxy group of L-pipecolic acid, the nitrogen of which has been acylated by condensation with (2S)-2-(3,4,5-trimethoxyphenyl)butyric acid. It is a synthetic, cell-permeable ligand that can be used to induce homodimerization of fusion proteins containing the DmrB domain.		2.0410aromatic ether;
carboxylic ester;
N-acylpiperidine;
tertiary amino compound		ligand
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone: an interleukin-1beta converting enzyme (ICE)-like protease inhibitor		2.1710
peptide yy
peptide YY (3-36): amino acid sequence given in first source		2.9940
glucagon-like peptide 2
Glucagon-Like Peptide 2: A 33-amino acid peptide derived from the C-terminal of PROGLUCAGON and mainly produced by the INTESTINAL L CELLS. It stimulates intestinal mucosal growth and decreased apoptosis of ENTEROCYTES. GLP-2 enhances gastrointestinal function and plays an important role in nutrient homeostasis.		5.1780
angiotensin i
Angiotensin I: A decapeptide that is cleaved from precursor angiotensinogen by RENIN. Angiotensin I has limited biological activity. It is converted to angiotensin II, a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME.. angiotensin I : A ten amino acid peptide formed by renin cleavage of angiotensinogen. Angiotensin I has no direct biological function except that high levels can stimulate catecholamine production. It is metabolized to its biologically active byproduct angiotensin II, a potent vasoconstrictor, by angiotensin converting enzyme (ACE) through cleavage of the two terminal amino acids.. angiotensin I dizwitterion : A peptide zwitterion that is the dizwitterionic form of angiotensin I having both carboxy groups deprotonated and the aspartyl amino group and arginine side-chain protonated. It is the major species at pH 7.3.		2.1310angiotensin;
peptide zwitterion		human metabolite;
neurotransmitter agent
vitamin b 12
Vitamin B 12: A cobalt-containing coordination compound produced by intestinal micro-organisms and found also in soil and water. Higher plants do not concentrate vitamin B 12 from the soil and so are a poor source of the substance as compared with animal tissues. INTRINSIC FACTOR is important for the assimilation of vitamin B 12.		2.5420
aconitine
Aconitine: A C19 norditerpenoid alkaloid (DITERPENES) from the root of ACONITUM; DELPHINIUM and larkspurs. It activates VOLTAGE-GATED SODIUM CHANNELS. It has been used to induce ARRHYTHMIAS in experimental animals and it has anti-inflammatory and anti-neuralgic properties.. aconitine : A diterpenoid that is 20-ethyl-3alpha,13,15alpha-trihydroxy-1alpha,6alpha,16beta-trimethoxy-4-(methoxymethyl)aconitane-8,14alpha-diol having acetate and benzoate groups at the 8- and 14-positions respectively.		2.1710
insulin glargine
Insulin Glargine: A recombinant LONG ACTING INSULIN and HYPOGLYCEMIC AGENT that is used to manage BLOOD GLUCOSE in patients with DIABETES MELLITUS.		19.1612060
insulin degludec
[no description available]		5.6530
oxyntomodulin
Glucagon-Like Peptides: Peptides derived from proglucagon which is also the precursor of pancreatic GLUCAGON. Despite expression of proglucagon in multiple tissues, the major production site of glucagon-like peptides (GLPs) is the INTESTINAL L CELLS. GLPs include glucagon-like peptide 1, glucagon-like peptide 2, and the various truncated forms.		17.8610516
cyclosporine
Cyclosporine: A cyclic undecapeptide from an extract of soil fungi. It is a powerful immunosupressant with a specific action on T-lymphocytes. It is used for the prophylaxis of graft rejection in organ and tissue transplantation. (From Martindale, The Extra Pharmacopoeia, 30th ed).		9.4230
bulleyaconitine a
bulleyaconitine A: isolated from Aconitum bulleyanum Diel; structure given in first source		2.1710
peptide yy
Peptide YY: A 36-amino acid peptide produced by the L cells of the distal small intestine and colon. Peptide YY inhibits gastric and pancreatic secretion.. peptide YY : A 36-membered human gut polypeptide consisting of Tyr, Pro, Ile, Lys, Pro, Glu, Ala, Pro, Gly, Glu, Asp, Ala, Ser, Pro, Glu, Glu, Leu, Asn, Arg, Tyr, Tyr, Ala, Ser, Leu, Arg, His, Tyr, Leu, Asn, Leu, Val, Thr, Arg, Gln, Arg and Tyr-NH2 residues joined in sequence.		3.3260
catalpol
catalpol: component of dihuang; RN given refers to (1aS-(1aalpha,1bbeta,2beta,5abeta,6beta,6aalpha))-isomer; RN for cpd without isomeric designation not avail 12/92		7.5120
gallium ga 68 dotatate
gallium Ga 68 dotatate: A radioactive diagnostic agent used for POSITRON EMISSION TOMOGRAPHY (PET) imaging of SOMATOSTATIN RECEPTOR positive neuroendocrine tumors and malignant abdominal paraganglioma.		3.4110
muramidase
Muramidase: A basic enzyme that is present in saliva, tears, egg white, and many animal fluids. It functions as an antibacterial agent. The enzyme catalyzes the hydrolysis of 1,4-beta-linkages between N-acetylmuramic acid and N-acetyl-D-glucosamine residues in peptidoglycan and between N-acetyl-D-glucosamine residues in chitodextrin. EC 3.2.1.17.		2.4820
amyloid beta-peptides
amyloid beta-protein (1-40): although acutely neurotoxic in both rat & monkey cerebral cortex, neuronal degeneration in primates resembles more closely to that found in Alzheimer's disease; amino acid sequence has been determined		2.0110
exendin 3
exendin 3: from the gila monster lizard (Heloderma horridum); amino acid sequence given in first source		5.77110
entecavir
entecavir (anhydrous) : Guanine substituted at the 9 position by a 4-hydroxy-3-(hydroxymethyl)-2-methylidenecyclopentyl group. A synthetic analogue of 2'-deoxyguanosine, it is a nucleoside reverse transcriptase inhibitor with selective antiviral activity against hepatitis B virus. Entecavir is phosphorylated intracellularly to the active triphosphate form, which competes with deoxyguanosine triphosphate, the natural substrate of hepatitis B virus reverse transcriptase, inhibiting every stage of the enzyme's activity, although it has no activity against HIV. It is used for the treatment of chronic hepatitis B.		2.03102-aminopurines;
oxopurine;
primary alcohol;
secondary alcohol		antiviral drug;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
levoleucovorin
Levoleucovorin: A folate analog consisting of the pharmacologically active isomer of LEUCOVORIN.. (6S)-5-formyltetrahydrofolic acid : The pharmacologically active (6S)-stereoisomer of 5-formyltetrahydrofolic acid.		3.17105-formyltetrahydrofolic acidantineoplastic agent;
metabolite
cyclic gmp
Cyclic GMP: Guanosine cyclic 3',5'-(hydrogen phosphate). A guanine nucleotide containing one phosphate group which is esterified to the sugar moiety in both the 3'- and 5'-positions. It is a cellular regulatory agent and has been described as a second messenger. Its levels increase in response to a variety of hormones, including acetylcholine, insulin, and oxytocin and it has been found to activate specific protein kinases. (From Merck Index, 11th ed). 3',5'-cyclic GMP : A 3',5'-cyclic purine nucleotide in which the purine nucleobase is specified as guanidine.		3.9213',5'-cyclic purine nucleotide;
guanyl ribonucleotide		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
plant metabolite;
Saccharomyces cerevisiae metabolite
deoxyguanosine
[no description available]		2.9510purine 2'-deoxyribonucleoside;
purines 2'-deoxy-D-ribonucleoside		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
guanine
[no description available]		2.03102-aminopurines;
oxopurine;
purine nucleobase		algal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
inosinic acid
Inosine Monophosphate: Inosine 5'-Monophosphate. A purine nucleotide which has hypoxanthine as the base and one phosphate group esterified to the sugar moiety.		2.0610inosine phosphate;
purine ribonucleoside 5'-monophosphate		Escherichia coli metabolite;
human metabolite;
mouse metabolite
sapropterin
sapropterin: RN given refers to parent cpd; co-factor required for catalytic activity of nitric oxide synthases. (6R)-5,6,7,8-tetrahydrobiopterin : A 5,6,7,8-tetrahydrobiopterin in which the stereocentre at position 6 has R-configuration.. sapropterin : A tetrahydropterin that is 2-amino-5,6,7,8-tetrahydropteridin-4(3H)-one in which a hydrogen at position 6 is substituted by a 1,2-dihydroxypropyl group (6R,1'R,2'S-enantiomer).		2.17105,6,7,8-tetrahydrobiopterincoenzyme;
cofactor;
diagnostic agent;
human metabolite
folic acid
folcysteine: used to promote fertility in chickens. vitamin B9 : Any B-vitamin that exhibits biological activity against vitamin B9 deficiency. Vitamin B9 refers to the many forms of folic acid and its derivatives, including tetrahydrofolic acid (the active form), methyltetrahydrofolate (the primary form found in blood), methenyltetrahydrofolate, folinic acid amongst others. They are present in abundance in green leafy vegetables, citrus fruits, and animal products. Lack of vitamin B9 leads to anemia, a condition in which the body cannot produce sufficient number of red blood cells. Symptoms of vitamin B9 deficiency include fatigue, muscle weakness, and pale skin.		3.6620folic acids;
N-acyl-amino acid		human metabolite;
mouse metabolite;
nutrient
3-methyladenine
N3-methyladenine: structure in first source		3.0740
clozapine
Clozapine: A tricylic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent.. clozapine : A benzodiazepine that is 5H-dibenzo[b,e][1,4]diazepine substituted by a chloro group at position 8 and a 4-methylpiperazin-1-yl group at position 11. It is a second generation antipsychotic used in the treatment of psychiatric disorders like schizophrenia.		4.9942benzodiazepine;
N-arylpiperazine;
N-methylpiperazine;
organochlorine compound		adrenergic antagonist;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
environmental contaminant;
GABA antagonist;
histamine antagonist;
muscarinic antagonist;
second generation antipsychotic;
serotonergic antagonist;
xenobiotic
olanzapine
Olanzapine: A benzodiazepine derivative that binds SEROTONIN RECEPTORS; MUSCARINIC RECEPTORS; HISTAMINE H1 RECEPTORS; ADRENERGIC ALPHA-1 RECEPTORS; and DOPAMINE RECEPTORS. It is an antipsychotic agent used in the treatment of SCHIZOPHRENIA; BIPOLAR DISORDER; and MAJOR DEPRESSIVE DISORDER; it may also reduce nausea and vomiting in patients undergoing chemotherapy.. olanzapine : A benzodiazepine that is 10H-thieno[2,3-b][1,5]benzodiazepine substituted by a methyl group at position 2 and a 4-methylpiperazin-1-yl group at position 4.		2.2510benzodiazepine;
N-arylpiperazine;
N-methylpiperazine		antiemetic;
dopaminergic antagonist;
histamine antagonist;
muscarinic antagonist;
second generation antipsychotic;
serotonergic antagonist;
serotonin uptake inhibitor
8-hydroxy-2'-deoxyguanosine
8-Hydroxy-2'-Deoxyguanosine: Common oxidized form of deoxyguanosine in which C-8 position of guanine base has a carbonyl group.. 8-hydroxy-2'-deoxyguanosine : Guanosine substituted at the purine 8-position by a hydroxy group. It is used as a biomarker of oxidative DNA damage.		3.4120guanosinesbiomarker
concanavalin a
Concanavalin A: A MANNOSE/GLUCOSE binding lectin isolated from the jack bean (Canavalia ensiformis). It is a potent mitogen used to stimulate cell proliferation in lymphocytes, primarily T-lymphocyte, cultures.		2.4110
metallothionein
Metallothionein: A low-molecular-weight (approx. 10 kD) protein occurring in the cytoplasm of kidney cortex and liver. It is rich in cysteinyl residues and contains no aromatic amino acids. Metallothionein shows high affinity for bivalent heavy metals.		2.4220
dinitrobenzenes
Dinitrobenzenes: Benzene derivatives which are substituted with two nitro groups in the ortho, meta or para positions.		2.3110
octaarginine
octaarginine: structure in first source		2.6120
leptin
Leptin: A 16-kDa peptide hormone secreted from WHITE ADIPOCYTES. Leptin serves as a feedback signal from fat cells to the CENTRAL NERVOUS SYSTEM in regulation of food intake, energy balance, and fat storage.		5.42180
betaine
glycine betaine : The amino acid betaine derived from glycine.		3.2310amino-acid betaine;
glycine derivative		fundamental metabolite
bupropion
Bupropion: A propiophenone-derived antidepressant and antismoking agent that inhibits the uptake of DOPAMINE.. bupropion : An aromatic ketone that is propiophenone carrying a tert-butylamino group at position 2 and a chloro substituent at position 3 on the phenyl ring.		3.2310aromatic ketone;
monochlorobenzenes;
secondary amino compound		antidepressant;
environmental contaminant;
xenobiotic
aminocaproic acid
Aminocaproic Acid: An antifibrinolytic agent that acts by inhibiting plasminogen activators which have fibrinolytic properties.. 6-aminohexanoic acid : An epsilon-amino acid comprising hexanoic acid carrying an amino substituent at position C-6. Used to control postoperative bleeding, and to treat overdose effects of the thrombolytic agents streptokinase and tissue plasminogen activator.		3.2310amino acid zwitterion;
epsilon-amino acid;
omega-amino fatty acid		antifibrinolytic drug;
hematologic agent;
metabolite
niacin
Niacin: A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.. vitamin B3 : Any member of a group of vitamers that belong to the chemical structural class called pyridines that exhibit biological activity against vitamin B3 deficiency. Vitamin B3 deficiency causes a condition known as pellagra whose symptoms include depression, dermatitis and diarrhea. The vitamers include nicotinic acid and nicotinamide (and their ionized and salt forms).. nicotinic acid : A pyridinemonocarboxylic acid that is pyridine in which the hydrogen at position 3 is replaced by a carboxy group.		3.2310pyridine alkaloid;
pyridinemonocarboxylic acid;
vitamin B3		antidote;
antilipemic drug;
EC 3.5.1.19 (nicotinamidase) inhibitor;
Escherichia coli metabolite;
human urinary metabolite;
metabolite;
mouse metabolite;
plant metabolite;
vasodilator agent
pyrazinamide
pyrazinecarboxamide : A monocarboxylic acid amide resulting from the formal condensation of the carboxy group of pyrazinoic acid (pyrazine-2-carboxylic acid) with ammonia. A prodrug for pyrazinoic acid, pyrazinecarboxamide is used as part of multidrug regimens for the treatment of tuberculosis.		3.2310monocarboxylic acid amide;
N-acylammonia;
pyrazines		antitubercular agent;
prodrug
pyridoxine
4,5-bis(hydroxymethyl)-2-methylpyridin-3-ol: structure in first source. vitamin B6 : Any member of the group of pyridines that exhibit biological activity against vitamin B6 deficiency. Vitamin B6 deficiency is associated with microcytic anemia, electroencephalographic abnormalities, dermatitis with cheilosis (scaling on the lips and cracks at the corners of the mouth) and glossitis (swollen tongue), depression and confusion, and weakened immune function. Vitamin B6 consists of the vitamers pyridoxine, pyridoxal, and pyridoxamine and their respective 5'-phosphate esters (and includes their corresponding ionized and salt forms).		3.2310hydroxymethylpyridine;
methylpyridines;
monohydroxypyridine;
vitamin B6		cofactor;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
thiamine
thiamine(1+) : A primary alcohol that is 1,3-thiazol-3-ium substituted by (4-amino-2-methylpyrimidin-5-yl)methyl, methyl and 2-hydroxyethyl groups at positions 3, 4 and 5, respectively.		3.2310primary alcohol;
vitamin B1		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
phenytoin
[no description available]		3.2310imidazolidine-2,4-dioneanticonvulsant;
drug allergen;
sodium channel blocker;
teratogenic agent
acebutolol
Acebutolol: A cardioselective beta-1 adrenergic antagonist with little effect on the bronchial receptors. The drug has stabilizing and quinidine-like effects on cardiac rhythm, as well as weak inherent sympathomimetic action.. acebutolol : An ether that is the 2-acetyl-4-(butanoylamino)phenyl ether of the primary hydroxy group of 3-(propan-2-ylamino)propane-1,2-diol.		3.2310aromatic amide;
ethanolamines;
ether;
monocarboxylic acid amide;
propanolamine;
secondary amino compound		anti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
sympathomimetic agent
acetaminophen
Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.. paracetamol : A member of the class of phenols that is 4-aminophenol in which one of the hydrogens attached to the amino group has been replaced by an acetyl group.		3.2310acetamides;
phenols		antipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
cyclooxygenase 3 inhibitor;
environmental contaminant;
ferroptosis inducer;
geroprotector;
hepatotoxic agent;
human blood serum metabolite;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
acetazolamide
Acetazolamide: One of the CARBONIC ANHYDRASE INHIBITORS that is sometimes effective against absence seizures. It is sometimes useful also as an adjunct in the treatment of tonic-clonic, myoclonic, and atonic seizures, particularly in women whose seizures occur or are exacerbated at specific times in the menstrual cycle. However, its usefulness is transient often because of rapid development of tolerance. Its antiepileptic effect may be due to its inhibitory effect on brain carbonic anhydrase, which leads to an increased transneuronal chloride gradient, increased chloride current, and increased inhibition. (From Smith and Reynard, Textbook of Pharmacology, 1991, p337)		3.2310monocarboxylic acid amide;
sulfonamide;
thiadiazoles		anticonvulsant;
diuretic;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
acetohydroxamic acid
acetohydroxamic acid: urease inhibitor. oxime : Compounds of structure R2C=NOH derived from condensation of aldehydes or ketones with hydroxylamine. Oximes from aldehydes may be called aldoximes; those from ketones may be called ketoximes.. N-hydroxyacetimidic acid : A carbohydroximic acid consisting of acetimidic acid having a hydroxy group attached to the imide nitrogen.. acetohydroxamic acid : A member of the class of acetohydroxamic acids that is acetamide in which one of the amino hydrogens has been replaced by a hydroxy group.		3.2310acetohydroxamic acids;
carbohydroximic acid		algal metabolite;
EC 3.5.1.5 (urease) inhibitor
alaproclate
alaproclate: specific 5-hydroxytryptamine uptake inhibitors; RN given refers to (DL)-isomer		3.2310alpha-amino acid ester
albendazole
[no description available]		3.2310aryl sulfide;
benzimidazoles;
benzimidazolylcarbamate fungicide;
carbamate ester		anthelminthic drug;
microtubule-destabilising agent;
tubulin modulator
albuterol
Albuterol: A short-acting beta-2 adrenergic agonist that is primarily used as a bronchodilator agent to treat ASTHMA. Albuterol is prepared as a racemic mixture of R(-) and S(+) stereoisomers. The stereospecific preparation of R(-) isomer of albuterol is referred to as levalbuterol.. albuterol : A member of the class of phenylethanolamines that is 4-(2-amino-1-hydroxyethyl)-2-(hydroxymethyl)phenol having a tert-butyl group attached to the nirogen atom. It acts as a beta-adrenergic agonist used in the treatment of asthma and chronic obstructive pulmonary disease (COPD).		3.2310phenols;
phenylethanolamines;
secondary amino compound		beta-adrenergic agonist;
bronchodilator agent;
environmental contaminant;
xenobiotic
alendronate
alendronic acid : A 1,1-bis(phosphonic acid) that is methanebis(phosphonic acid) in which the two methylene hydrogens are replaced by hydroxy and 3-aminopropyl groups.		3.23101,1-bis(phosphonic acid);
primary amino compound		bone density conservation agent;
EC 2.5.1.1 (dimethylallyltranstransferase) inhibitor
alfuzosin
alfuzosin: structure given in first source		3.2310monocarboxylic acid amide;
quinazolines;
tetrahydrofuranol		alpha-adrenergic antagonist;
antihypertensive agent;
antineoplastic agent
alosetron
alosetron : A pyrido[4,3-b]indole compound having a 5-methyl-1H-imidazol-4-ylmethyl group at the 2-position.		3.2310imidazoles;
pyridoindole		antiemetic;
gastrointestinal drug;
serotonergic antagonist
alprazolam
Alprazolam: A triazolobenzodiazepine compound with antianxiety and sedative-hypnotic actions, that is efficacious in the treatment of PANIC DISORDERS, with or without AGORAPHOBIA, and in generalized ANXIETY DISORDERS. (From AMA Drug Evaluations Annual, 1994, p238). alprazolam : A member of the class of triazolobenzodiazepines that is 4H-[1,2,4]triazolo[4,3-a][1,4]benzodiazepine carrying methyl, phenyl and chloro substituents at positions 1, 6 and 8 respectively. Alprazolam is only found in individuals that have taken this drug.		3.2310organochlorine compound;
triazolobenzodiazepine		anticonvulsant;
anxiolytic drug;
GABA agonist;
muscle relaxant;
sedative;
xenobiotic
altretamine
Altretamine: A hexamethyl-2,4,6-triamine derivative of 1,3,5-triazine.		3.2310triamino-1,3,5-triazine
amantadine
amant: an antiviral compound consisting of an adamantane derivative chemically linked to a water-solube polyanioic matrix; structure in first source		3.2310adamantanes;
primary aliphatic amine		analgesic;
antiparkinson drug;
antiviral drug;
dopaminergic agent;
NMDA receptor antagonist;
non-narcotic analgesic
ambenonium
ambenonium : A symmetrical oxalamide-based bis-quaternary ammonium ion having ethyl and 2-chlorobenzyl groups attached to the nitrogens.		3.2310quaternary ammonium ionEC 3.1.1.8 (cholinesterase) inhibitor
diatrizoic acid
Diatrizoate: A commonly used x-ray contrast medium. As DIATRIZOATE MEGLUMINE and as Diatrizoate sodium, it is used for gastrointestinal studies, angiography, and urography.. amidotrizoic acid : A member of the class of benzoic acids that is benzoic acid having iodo substituents at the 2-, 4- and 6-positions and acetamido substituents at the 3- and 5-positions. It is used, mainly as its N-methylglucamine and sodium salts, as an X-ray contrast medium in gastrointestinal studies, angiography, and urography.		3.2310acetamides;
benzoic acids;
organoiodine compound		environmental contaminant;
radioopaque medium;
xenobiotic
amifostine anhydrous
Amifostine: A phosphorothioate proposed as a radiation-protective agent. It causes splenic vasodilation and may block autonomic ganglia.. amifostine : An organic thiophosphate that is the S-phospho derivative of 2-[(3-aminopropyl)amino]ethanethiol. A prodrug for the free thiol, WR-1065, which is used as a cytoprotectant in cancer chemotherapy and radiotherapy.		3.2310diamine;
organic thiophosphate		antioxidant;
prodrug;
radiation protective agent
p-aminohippuric acid
p-Aminohippuric Acid: The glycine amide of 4-aminobenzoic acid. Its sodium salt is used as a diagnostic aid to measure effective renal plasma flow (ERPF) and excretory capacity.. p-aminohippurate : A hippurate that is the conjugate base of p-aminohippuric acid, arising from deprotonation of the carboxy group.. p-aminohippuric acid : An N-acylglycine that is the 4-amino derivative of hippuric acid; used as a diagnostic agent in the measurement of renal plasma flow.		3.2310N-acylglycineDaphnia magna metabolite
theophylline
[no description available]		3.2310dimethylxanthineadenosine receptor antagonist;
anti-asthmatic drug;
anti-inflammatory agent;
bronchodilator agent;
drug metabolite;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
fungal metabolite;
human blood serum metabolite;
immunomodulator;
muscle relaxant;
vasodilator agent
amiodarone
Amiodarone: An antianginal and class III antiarrhythmic drug. It increases the duration of ventricular and atrial muscle action by inhibiting POTASSIUM CHANNELS and VOLTAGE-GATED SODIUM CHANNELS. There is a resulting decrease in heart rate and in vascular resistance.. amiodarone : A member of the class of 1-benzofurans that is 1-benzofuran substituted by a butyl group at position 2 and a 4-[2-(diethylamino)ethoxy]-3,5-diiodobenzoyl group at position 3. It is a cardiovascular drug used for the treatment of cardiac dysrhythmias.		3.23101-benzofurans;
aromatic ketone;
organoiodine compound;
tertiary amino compound		cardiovascular drug
amitriptyline
Amitriptyline: Tricyclic antidepressant with anticholinergic and sedative properties. It appears to prevent the re-uptake of norepinephrine and serotonin at nerve terminals, thus potentiating the action of these neurotransmitters. Amitriptyline also appears to antagonize cholinergic and alpha-1 adrenergic responses to bioactive amines.. amitriptyline : An organic tricyclic compound that is 10,11-dihydro-5H-dibenzo[a,d][7]annulene substituted by a 3-(dimethylamino)propylidene group at position 5.		3.2310carbotricyclic compound;
tertiary amine		adrenergic uptake inhibitor;
antidepressant;
environmental contaminant;
tropomyosin-related kinase B receptor agonist;
xenobiotic
amlodipine
Amlodipine: A long-acting dihydropyridine calcium channel blocker. It is effective in the treatment of ANGINA PECTORIS and HYPERTENSION.. amlodipine : A fully substituted dialkyl 1,4-dihydropyridine-3,5-dicarboxylate derivative, which is used for the treatment of hypertension, chronic stable angina and confirmed or suspected vasospastic angina.		3.2310dihydropyridine;
ethyl ester;
methyl ester;
monochlorobenzenes;
primary amino compound		antihypertensive agent;
calcium channel blocker;
vasodilator agent
amoxapine
Amoxapine: The N-demethylated derivative of the antipsychotic agent LOXAPINE that works by blocking the reuptake of norepinephrine, serotonin, or both; it also blocks dopamine receptors. Amoxapine is used for the treatment of depression.. amoxapine : A dibenzooxazepine compound having a chloro substituent at the 2-position and a piperazin-1-yl group at the 11-position.		3.2310dibenzooxazepineadrenergic uptake inhibitor;
antidepressant;
dopaminergic antagonist;
geroprotector;
serotonin uptake inhibitor
anastrozole
[no description available]		3.2310nitrile;
triazoles		antineoplastic agent;
EC 1.14.14.14 (aromatase) inhibitor
aspirin
Aspirin: The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5). acetylsalicylate : A benzoate that is the conjugate base of acetylsalicylic acid, arising from deprotonation of the carboxy group.. acetylsalicylic acid : A member of the class of benzoic acids that is salicylic acid in which the hydrogen that is attached to the phenolic hydroxy group has been replaced by an acetoxy group. A non-steroidal anti-inflammatory drug with cyclooxygenase inhibitor activity.		3.2310benzoic acids;
phenyl acetates;
salicylates		anticoagulant;
antipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
EC 1.1.1.188 (prostaglandin-F synthase) inhibitor;
geroprotector;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
plant activator;
platelet aggregation inhibitor;
prostaglandin antagonist;
teratogenic agent
atenolol
Atenolol: A cardioselective beta-1 adrenergic blocker possessing properties and potency similar to PROPRANOLOL, but without a negative inotropic effect.. atenolol : An ethanolamine compound having a (4-carbamoylmethylphenoxy)methyl group at the 1-position and an N-isopropyl substituent.		3.2310ethanolamines;
monocarboxylic acid amide;
propanolamine		anti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
environmental contaminant;
sympatholytic agent;
xenobiotic
azathioprine
Azathioprine: An immunosuppressive agent used in combination with cyclophosphamide and hydroxychloroquine in the treatment of rheumatoid arthritis. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance has been listed as a known carcinogen. (Merck Index, 11th ed). azathioprine : A thiopurine that is 6-mercaptopurine in which the mercapto hydrogen is replaced by a 1-methyl-4-nitroimidazol-5-yl group. It is a prodrug for mercaptopurine and is used as an immunosuppressant, prescribed for the treatment of inflammatory conditions and after organ transplantation and also for treatment of Crohn's didease and MS.		3.2310aryl sulfide;
C-nitro compound;
imidazoles;
thiopurine		antimetabolite;
antineoplastic agent;
carcinogenic agent;
DNA synthesis inhibitor;
hepatotoxic agent;
immunosuppressive agent;
prodrug
baclofen
[no description available]		3.2310amino acid zwitterion;
gamma-amino acid;
monocarboxylic acid;
monochlorobenzenes;
primary amino compound		central nervous system depressant;
GABA agonist;
muscle relaxant
bendazac
bendazac : A monocarboxylic acid that is glycolic acid in which the hydrogen attached to the 2-hydroxy group is replaced by a 1-benzyl-1H-indazol-3-yl group. Although it has anti-inflammatory, antinecrotic, choleretic and antilipidaemic properties and has been used for the treatment of various inflammatory skin disorders, its principal effect is to inhibit the denaturation of proteins. Its lysine salt is used in the management of cataracts.		3.2310indazoles;
monocarboxylic acid		non-steroidal anti-inflammatory drug;
radical scavenger
bendroflumethiazide
Bendroflumethiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. It has been used in the treatment of familial hyperkalemia, hypertension, edema, and urinary tract disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p810). bendroflumethiazide : A sulfonamide consisting of 7-sulfamoyl-3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide in which the hydrogen at position 6 is substituted by a trifluoromethyl group and that at position 3 is substituted by a benzyl group.		3.2310benzothiadiazine;
sulfonamide		antihypertensive agent;
diuretic
benzbromarone
Benzbromarone: Uricosuric that acts by increasing uric acid clearance. It is used in the treatment of gout.. benzbromarone : 1-Benzofuran substituted at C-2 and C-3 by an ethyl group and a 3,5-dibromo-4-hydroxybenzoyl group respectively. An inhibitor of CYP2C9, it is used as an anti-gout medication.		3.23101-benzofurans;
aromatic ketone		uricosuric drug
betaxolol
[no description available]		3.2310propanolamineantihypertensive agent;
beta-adrenergic antagonist;
sympatholytic agent
bethanechol
Bethanechol: A slowly hydrolyzing muscarinic agonist with no nicotinic effects. Bethanechol is generally used to increase smooth muscle tone, as in the GI tract following abdominal surgery or in urinary retention in the absence of obstruction. It may cause hypotension, HEART RATE changes, and BRONCHIAL SPASM.. bethanechol : The carbamic acid ester of 2-methylcholine. A slowly hydrolysed muscarinic agonist with no nicotinic effects, it is used as its chloride salt to increase smooth muscle tone, as in the gastrointestinal tract following abdominal surgery, treatment of gastro-oesophageal reflux disease, and as an alternative to catheterisation in the treatment of non-obstructive urinary retention.		3.2310carbamate ester;
quaternary ammonium ion		muscarinic agonist
bicalutamide
bicalutamide: approved for treatment of advanced prostate cancer. N-[4-cyano-3-(trifluoromethyl)phenyl]-3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanamide : A member of the class of (trifluoromethyl)benzenes that is 4-amino-2-(trifluoromethyl)benzonitrile in which one of the amino hydrogens is substituted by a 3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanoyl group.. bicalutamide : A racemate comprising of equal amounts of (R)-bicalutamide and (S)-bicalutamide. It is an oral non-steroidal antiandrogen used in the treatment of prostate cancer and hirsutism.		3.2310(trifluoromethyl)benzenes;
monocarboxylic acid amide;
monofluorobenzenes;
nitrile;
sulfone;
tertiary alcohol
biperiden
Biperiden: A muscarinic antagonist that has effects in both the central and peripheral nervous systems. It has been used in the treatment of arteriosclerotic, idiopathic, and postencephalitic parkinsonism. It has also been used to alleviate extrapyramidal symptoms induced by phenothiazine derivatives and reserpine.. biperiden : A member of the class of piperidines that is N-propylpiperidine in which the methyl hydrogens have been replaced by hydroxy, phenyl, and 5-norbornen-2-yl groups. A muscarinic antagonist affecting both the central and peripheral nervous systems, it is used in the treatment of all forms of Parkinson's disease.		3.2310piperidines;
tertiary alcohol;
tertiary amino compound		antidote to sarin poisoning;
antidyskinesia agent;
antiparkinson drug;
muscarinic antagonist;
parasympatholytic
bisacodyl
Bisacodyl: A diphenylmethane stimulant laxative used for the treatment of CONSTIPATION and for bowel evacuation. (From Martindale, The Extra Pharmacopoeia, 30th ed, p871)		3.2310diarylmethane
bisoprolol
Bisoprolol: A cardioselective beta-1 adrenergic blocker. It is effective in the management of HYPERTENSION and ANGINA PECTORIS.		3.2310secondary alcohol;
secondary amine		anti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
sympatholytic agent
bumetanide
[no description available]		3.2310amino acid;
benzoic acids;
sulfonamide		diuretic;
EC 3.6.3.49 (channel-conductance-controlling ATPase) inhibitor
buspirone
Buspirone: An anxiolytic agent and serotonin receptor agonist belonging to the azaspirodecanedione class of compounds. Its structure is unrelated to those of the BENZODIAZAPINES, but it has an efficacy comparable to DIAZEPAM.. buspirone : An azaspiro compound that is 8-azaspiro[4.5]decane-7,9-dione substituted at the nitrogen atom by a 4-(piperazin-1-yl)butyl group which in turn is substituted by a pyrimidin-2-yl group at the N(4) position.		3.2310azaspiro compound;
N-alkylpiperazine;
N-arylpiperazine;
organic heteropolycyclic compound;
piperidones;
pyrimidines		anxiolytic drug;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
sedative;
serotonergic agonist
busulfan
[no description available]		3.2310methanesulfonate esteralkylating agent;
antineoplastic agent;
carcinogenic agent;
insect sterilant;
teratogenic agent
secbutabarbital
secbutabarbital: Butabarbital (a synonym for Secbutabarbital) should be distinguished from Butobarbital		3.2310barbiturates
caffeine
[no description available]		3.2310purine alkaloid;
trimethylxanthine		adenosine A2A receptor antagonist;
adenosine receptor antagonist;
adjuvant;
central nervous system stimulant;
diuretic;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
environmental contaminant;
food additive;
fungal metabolite;
geroprotector;
human blood serum metabolite;
mouse metabolite;
mutagen;
plant metabolite;
psychotropic drug;
ryanodine receptor agonist;
xenobiotic
verapamil
Verapamil: A calcium channel blocker that is a class IV anti-arrhythmia agent.. verapamil : A racemate comprising equimolar amounts of dexverapamil and (S)-verapamil. An L-type calcium channel blocker of the phenylalkylamine class, it is used (particularly as the hydrochloride salt) in the treatment of hypertension, angina pectoris and cardiac arrhythmia, and as a preventive medication for migraine.. 2-(3,4-dimethoxyphenyl)-5-{[2-(3,4-dimethoxyphenyl)ethyl](methyl)amino}-2-(propan-2-yl)pentanenitrile : A tertiary amino compound that is 3,4-dimethoxyphenylethylamine in which the hydrogens attached to the nitrogen are replaced by a methyl group and a 4-cyano-4-(3,4-dimethoxyphenyl)-5-methylhexyl group.		3.2310aromatic ether;
nitrile;
polyether;
tertiary amino compound
candesartan
candesartan: a nonpeptide angiotensin II receptor antagonist. candesartan : A benzimidazolecarboxylic acid that is 1H-benzimidazole-7-carboxylic acid substituted by an ethoxy group at position 2 and a ({2'-(1H-tetrazol-5-yl)[1,1'-biphenyl]-4-yl}methyl) group at position 1. It is a angiotensin receptor antagonist used for the treatment of hypertension.		3.2310benzimidazolecarboxylic acid;
biphenylyltetrazole		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
carbamazepine
Carbamazepine: A dibenzazepine that acts as a sodium channel blocker. It is used as an anticonvulsant for the treatment of grand mal and psychomotor or focal SEIZURES. It may also be used in the management of BIPOLAR DISORDER, and has analgesic properties.. carbamazepine : A dibenzoazepine that is 5H-dibenzo[b,f]azepine carrying a carbamoyl substituent at the azepine nitrogen, used as an anticonvulsant.		3.2310dibenzoazepine;
ureas		analgesic;
anticonvulsant;
antimanic drug;
drug allergen;
EC 3.5.1.98 (histone deacetylase) inhibitor;
environmental contaminant;
glutamate transporter activator;
mitogen;
non-narcotic analgesic;
sodium channel blocker;
xenobiotic
carbinoxamine
carbinoxamine: Note: tradenames that start with Histex refer to more than one drug. carbinoxamine : An organochlorine compound that is 2-(4-chlorobenzyl)pyridine in which one of the benzylic hydrogens is substituted by 2-(dimethylamino)ethoxy group. It is an ethanolamine-type antihistamine, used as its maleate salt for treating hay fever, as well as mild cases of Parkinson's disease.		3.2310monochlorobenzenes;
pyridines;
tertiary amino compound		anti-allergic agent;
antiparkinson drug;
H1-receptor antagonist;
muscarinic antagonist
carisoprodol
Carisoprodol: A centrally acting skeletal muscle relaxant whose mechanism of action is not completely understood but may be related to its sedative actions. It is used as an adjunct in the symptomatic treatment of musculoskeletal conditions associated with painful muscle spasm. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1202). carisoprodol : A carbamate ester that is the mono-N-isopropyl derivative of meprobamate (which is a significant metabolite). Carisoprodol interrupts neuronal communication within the reticular formation and spinal cord, resulting in sedation and alteration in pain perception. It is used as a muscle relaxant in the symptomatic treatment of musculoskeletal conditions associated with painful muscle spasm.		3.2310carbamate estermuscle relaxant
carvedilol
[no description available]		3.2310carbazoles;
secondary alcohol;
secondary amino compound		alpha-adrenergic antagonist;
antihypertensive agent;
beta-adrenergic antagonist;
cardiovascular drug;
vasodilator agent
celecoxib
[no description available]		3.2310organofluorine compound;
pyrazoles;
sulfonamide;
toluenes		cyclooxygenase 2 inhibitor;
geroprotector;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
cetirizine
Cetirizine: A potent second-generation histamine H1 antagonist that is effective in the treatment of allergic rhinitis, chronic urticaria, and pollen-induced asthma. Unlike many traditional antihistamines, it does not cause drowsiness or anticholinergic side effects.. cetirizine : A member of the class of piperazines that is piperazine in which the hydrogens attached to nitrogen are replaced by a (4-chlorophenyl)(phenyl)methyl and a 2-(carboxymethoxy)ethyl group respectively.		3.2310ether;
monocarboxylic acid;
monochlorobenzenes;
piperazines		anti-allergic agent;
environmental contaminant;
H1-receptor antagonist;
xenobiotic
chlorambucil
Chlorambucil: A nitrogen mustard alkylating agent used as antineoplastic for chronic lymphocytic leukemia, Hodgkin's disease, and others. Although it is less toxic than most other nitrogen mustards, it has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (Merck Index, 11th ed). chlorambucil : A monocarboxylic acid that is butanoic acid substituted at position 4 by a 4-[bis(2-chloroethyl)amino]phenyl group. A chemotherapy drug that can be used in combination with the antibody obinutuzumab for the treatment of chronic lymphocytic leukemia.		3.2310aromatic amine;
monocarboxylic acid;
nitrogen mustard;
organochlorine compound;
tertiary amino compound		alkylating agent;
antineoplastic agent;
carcinogenic agent;
drug allergen;
immunosuppressive agent
chlorcyclizine
chlorcyclizine: was heading 1964-94 (Prov 1964-73); CHLOROCYCLIZINE & HISTACHLORAZINE were see CHLORCYCLIZINE 1977-94; use PIPERAZINES to search CHLORCYCLIZINE 1966-94; histamine H1-blocker used both orally and topically in allergies and also for the prevention of motion sickness		3.2310diarylmethane
chlordiazepoxide
Chlordiazepoxide: An anxiolytic benzodiazepine derivative with anticonvulsant, sedative, and amnesic properties. It has also been used in the symptomatic treatment of alcohol withdrawal.. chlordiazepoxide : A benzodiazepine that is 3H-1,4-benzodiazepine 4-oxide substituted by a chloro group at position 7, a phenyl group at position 5 and a methylamino group at position 2.		3.2310benzodiazepine
chlormezanone
Chlormezanone: A non-benzodiazepine that is used in the management of anxiety. It has been suggested for use in the treatment of muscle spasm.. chlormezanone : A 1,3-thiazine that is 1,3-thiazinan-4-one S,S-dioxide in which a hydrogen at position 2 is substituted by a 4-chlorophenyl group and the hydrogen attached to the nitrogen is substituted by methyl. A non-benzodiazepine muscle relaxant, it was used in the management of anxiety and in the treatment of muscle spasms until being discontinued worldwide by its manufacturer in 1996, due to rare but serious cutaneous reactions.		3.23101,3-thiazine;
lactam;
monochlorobenzenes;
sulfone		antipsychotic agent;
anxiolytic drug;
muscle relaxant
chloroquine
Chloroquine: The prototypical antimalarial agent with a mechanism that is not well understood. It has also been used to treat rheumatoid arthritis, systemic lupus erythematosus, and in the systemic therapy of amebic liver abscesses.. chloroquine : An aminoquinoline that is quinoline which is substituted at position 4 by a [5-(diethylamino)pentan-2-yl]amino group at at position 7 by chlorine. It is used for the treatment of malaria, hepatic amoebiasis, lupus erythematosus, light-sensitive skin eruptions, and rheumatoid arthritis.		3.2310aminoquinoline;
organochlorine compound;
secondary amino compound;
tertiary amino compound		anticoronaviral agent;
antimalarial;
antirheumatic drug;
autophagy inhibitor;
dermatologic drug
chlorothiazide
Chlorothiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p812). thiazide : Heterocyclic compound with sulfur and nitrogen in the ring.. chlorothiazide : 4H-1,2,4-benzothiadiazine 1,1-dioxide in which the hydrogen at position is substituted by chlorine and that at position 7 is substituted by a sulfonamide group. A diuretic, it is used for treatment of oedema and hypertension.		3.2310benzothiadiazineantihypertensive agent;
diuretic
chlorpheniramine
Chlorpheniramine: A histamine H1 antagonist used in allergic reactions, hay fever, rhinitis, urticaria, and asthma. It has also been used in veterinary applications. One of the most widely used of the classical antihistaminics, it generally causes less drowsiness and sedation than PROMETHAZINE.. chlorphenamine : A tertiary amino compound that is propylamine which is substituted at position 3 by a pyridin-2-yl group and a p-chlorophenyl group and in which the hydrogens attached to the nitrogen are replaced by methyl groups. A histamine H1 antagonist, it is used to relieve the symptoms of hay fever, rhinitis, urticaria, and asthma.		3.2310monochlorobenzenes;
pyridines;
tertiary amino compound		anti-allergic agent;
antidepressant;
antipruritic drug;
H1-receptor antagonist;
histamine antagonist;
serotonin uptake inhibitor
chlorpromazine
Chlorpromazine: The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking DOPAMINE RECEPTORS. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup.. chlorpromazine : A substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropanamine moiety.		3.2310organochlorine compound;
phenothiazines;
tertiary amine		anticoronaviral agent;
antiemetic;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
phenothiazine antipsychotic drug
chlorpropamide
Chlorpropamide: A sulfonylurea hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. (From Martindale, The Extra Pharmacopoeia, 30th ed, p277). chlorpropamide : An N-sulfonylurea that is urea in which a hydrogen attached to one of the nitrogens is substituted by 4-chlorobenzenesulfonyl group and a hydrogen attached to the other nitrogen is substituted by propyl group. Chlorpropamide is a hypoglycaemic agent used in the treatment of type 2 (non-insulin-dependent) diabetes mellitus not responding to dietary modification.		3.2310monochlorobenzenes;
N-sulfonylurea		hypoglycemic agent;
insulin secretagogue
chlorthalidone
Chlorthalidone: A benzenesulfonamide-phthalimidine that tautomerizes to a BENZOPHENONES form. It is considered a thiazide-like diuretic.		3.2310isoindoles;
monochlorobenzenes;
sulfonamide
chlorzoxazone
Chlorzoxazone: A centrally acting central muscle relaxant with sedative properties. It is claimed to inhibit muscle spasm by exerting an effect primarily at the level of the spinal cord and subcortical areas of the brain. (From Martindale, The Extra Pharmacopoea, 30th ed, p1202). chlorzoxazone : A member of the class of 1,3-benzoxazoles that is 1,3-benzoxazol-2-ol in which the hydrogen atom at position 5 is substituted by chlorine. A centrally acting muscle relaxant with sedative properties, it is used for the symptomatic treatment of painful muscle spasm.		3.23101,3-benzoxazoles;
heteroaryl hydroxy compound;
organochlorine compound		muscle relaxant;
sedative
cilostazol
[no description available]		3.2310lactam;
tetrazoles		anticoagulant;
bronchodilator agent;
EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor;
fibrin modulating drug;
neuroprotective agent;
platelet aggregation inhibitor;
vasodilator agent
cimetidine
Cimetidine: A histamine congener, it competitively inhibits HISTAMINE binding to HISTAMINE H2 RECEPTORS. Cimetidine has a range of pharmacological actions. It inhibits GASTRIC ACID secretion, as well as PEPSIN and GASTRIN output.. cimetidine : A member of the class of guanidines that consists of guanidine carrying a methyl substituent at position 1, a cyano group at position 2 and a 2-{[(5-methyl-1H-imidazol-4-yl)methyl]sulfanyl}ethyl group at position 3. It is a H2-receptor antagonist that inhibits the production of acid in stomach.		3.2310aliphatic sulfide;
guanidines;
imidazoles;
nitrile		adjuvant;
analgesic;
anti-ulcer drug;
H2-receptor antagonist;
P450 inhibitor
ciprofloxacin
Ciprofloxacin: A broad-spectrum antimicrobial carboxyfluoroquinoline.. ciprofloxacin : A quinolone that is quinolin-4(1H)-one bearing cyclopropyl, carboxylic acid, fluoro and piperazin-1-yl substituents at positions 1, 3, 6 and 7, respectively.		3.2310aminoquinoline;
cyclopropanes;
fluoroquinolone antibiotic;
N-arylpiperazine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone;
zwitterion		antibacterial drug;
antiinfective agent;
antimicrobial agent;
DNA synthesis inhibitor;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
environmental contaminant;
topoisomerase IV inhibitor;
xenobiotic
citalopram
Citalopram: A furancarbonitrile that is one of the serotonin uptake inhibitors used as an antidepressant. The drug is also effective in reducing ethanol uptake in alcoholics and is used in depressed patients who also suffer from TARDIVE DYSKINESIA in preference to tricyclic antidepressants, which aggravate dyskinesia.. citalopram : A racemate comprising equimolar amounts of (R)-citalopram and its enantiomer, escitalopram. It is used as an antidepressant, although only escitalopram is active.. 1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrile : A nitrile that is 1,3-dihydro-2-benzofuran-5-carbonitrile in which one of the hydrogens at position 1 is replaced by a p-fluorophenyl group, while the other is replaced by a 3-(dimethylamino)propyl group.		3.23102-benzofurans;
cyclic ether;
nitrile;
organofluorine compound;
tertiary amino compound
clofibrate
angiokapsul: contains clofibrate & insoitolnicotinate		3.2310aromatic ether;
ethyl ester;
monochlorobenzenes		anticholesteremic drug;
antilipemic drug;
geroprotector;
PPARalpha agonist
clomiphene
[no description available]		3.2310tertiary amineestrogen antagonist;
estrogen receptor modulator
clomipramine
Clomipramine: A tricyclic antidepressant similar to IMIPRAMINE that selectively inhibits the uptake of serotonin in the brain. It is readily absorbed from the gastrointestinal tract and demethylated in the liver to form its primary active metabolite, desmethylclomipramine.. clomipramine : A dibenzoazepine that is 10,11-dihydro-5H-dibenzo[b,f]azepine which is substituted by chlorine at position 3 and in which the hydrogen attached to the nitrogen is replaced by a 3-(dimethylamino)propyl group. One of the more sedating tricyclic antidepressants, it is used as the hydrochloride salt for the treatment of depression as well as obsessive-compulsive disorder and phobias.		3.2310dibenzoazepineanticoronaviral agent;
antidepressant;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor;
serotonergic antagonist;
serotonergic drug;
serotonin uptake inhibitor
clonazepam
Clonazepam: An anticonvulsant used for several types of seizures, including myotonic or atonic seizures, photosensitive epilepsy, and absence seizures, although tolerance may develop. It is seldom effective in generalized tonic-clonic or partial seizures. The mechanism of action appears to involve the enhancement of GAMMA-AMINOBUTYRIC ACID receptor responses.. clonazepam : 1,3-Dihydro-2H-1,4-benzodiazepin-2-one in which the hydrogens at positions 5 and 7 are substituted by 2-chlorophenyl and nitro groups, respectively. It is used in the treatment of all types of epilepsy and seizures, as well as myoclonus and associated abnormal movements, and panic disorders. However, its use can be limited by the development of tolerance and by sedation.		3.23101,4-benzodiazepinone;
monochlorobenzenes		anticonvulsant;
anxiolytic drug;
GABA modulator
clonidine
Clonidine: An imidazoline sympatholytic agent that stimulates ALPHA-2 ADRENERGIC RECEPTORS and central IMIDAZOLINE RECEPTORS. It is commonly used in the management of HYPERTENSION.. clonidine (amino form) : A clonidine that is 4,5-dihydro-1H-imidazol-2-amine in which one of the amino hydrogens is replaced by a 2,6-dichlorophenyl group.		3.2310clonidine;
imidazoline
chlorazepate
clorazepic acid : A 1,4-benzodiazepinone in which the oxo group is at position 2, and which is substituted at positions 3, 5, and 7 by carboxy, phenyl and chloro groups, respectively.		3.23101,4-benzodiazepinoneanticonvulsant;
anxiolytic drug;
GABA modulator;
prodrug
clotrimazole
[no description available]		3.2310conazole antifungal drug;
imidazole antifungal drug;
imidazoles;
monochlorobenzenes		antiinfective agent;
environmental contaminant;
xenobiotic
cyclobenzaprine
cyclobenzaprine: RN given refers to parent cpd; Lisseril is synonymous for HCl; structure. cyclobenzaprine : 5-Methylidene-5H-dibenzo[a,d]cycloheptene in which one of the hydrogens of the methylidene group is substituted by a 2-(dimethylamino)ethyl group. A centrally acting skeletal muscle relaxant, it is used as its hydrochloride salt in the symptomatic treatment of painful muscle spasm.		3.2310carbotricyclic compoundantidepressant;
muscle relaxant;
tranquilizing drug
cyclofenil
Cyclofenil: A gonadal stimulant and inducer of ovulation. It is used in the treatment of infertility and amenorrhea, but is thought to be less effective than CLOMIPHENE.		3.2310organic molecular entity
cyproheptadine
Cyproheptadine: A serotonin antagonist and a histamine H1 blocker used as antipruritic, appetite stimulant, antiallergic, and for the post-gastrectomy dumping syndrome, etc.. cyproheptadine : The product resulting from the formal oxidative coupling of position 5 of 5H-dibenzo[a,d]cycloheptene with position 4 of 1-methylpiperidine resulting in the formation of a double bond between the two fragments. It is a sedating antihistamine with antimuscarinic and calcium-channel blocking actions. It is used (particularly as the hydrochloride sesquihydrate) for the relief of allergic conditions including rhinitis, conjunctivitis due to inhalant allergens and foods, urticaria and angioedema, and in pruritic skin disorders. Unlike other antihistamines, it is also a seratonin receptor antagonist, making it useful in conditions such as vascular headache and anorexia.		3.2310piperidines;
tertiary amine		anti-allergic agent;
antipruritic drug;
gastrointestinal drug;
H1-receptor antagonist;
serotonergic antagonist
dapsone
[no description available]		3.2310substituted aniline;
sulfone		anti-inflammatory drug;
antiinfective agent;
antimalarial;
leprostatic drug
deferoxamine
Deferoxamine: Natural product isolated from Streptomyces pilosus. It forms iron complexes and is used as a chelating agent, particularly in the mesylate form.. desferrioxamine B : An acyclic desferrioxamine that is butanedioic acid in which one of the carboxy groups undergoes formal condensation with the primary amino group of N-(5-aminopentyl)-N-hydroxyacetamide and the second carboxy group undergoes formal condensation with the hydroxyamino group of N(1)-(5-aminopentyl)-N(1)-hydroxy-N(4)-[5-(hydroxyamino)pentyl]butanediamide. It is a siderophore native to Streptomyces pilosus biosynthesised by the DesABCD enzyme cluster as a high affinity Fe(III) chelator.		3.2310acyclic desferrioxaminebacterial metabolite;
ferroptosis inhibitor;
iron chelator;
siderophore
desipramine
Desipramine: A tricyclic dibenzazepine compound that potentiates neurotransmission. Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. This compound also possesses minor anticholinergic activity, through its affinity to muscarinic receptors.. desipramine : A dibenzoazepine consisting of 10,11-dihydro-5H-dibenzo[b,f]azepine substituted on nitrogen with a 3-(methylamino)propyl group.		3.2310dibenzoazepine;
secondary amino compound		adrenergic uptake inhibitor;
alpha-adrenergic antagonist;
antidepressant;
cholinergic antagonist;
drug allergen;
EC 3.1.4.12 (sphingomyelin phosphodiesterase) inhibitor;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
H1-receptor antagonist;
serotonin uptake inhibitor
amphetamine
Amphetamine: A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is DEXTROAMPHETAMINE.. 1-phenylpropan-2-amine : A primary amine that is isopropylamine in which a hydrogen attached to one of the methyl groups has been replaced by a phenyl group.. amphetamine : A racemate comprising equimolar amounts of (R)-amphetamine (also known as levamphetamine or levoamphetamine) and (S)-amphetamine (also known as dexamfetamine or dextroamphetamine.		3.2310primary amine
diazepam
Diazepam: A benzodiazepine with anticonvulsant, anxiolytic, sedative, muscle relaxant, and amnesic properties and a long duration of action. Its actions are mediated by enhancement of GAMMA-AMINOBUTYRIC ACID activity.. diazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a chloro group at position 7, a methyl group at position 1 and a phenyl group at position 5.		3.23101,4-benzodiazepinone;
organochlorine compound		anticonvulsant;
anxiolytic drug;
environmental contaminant;
sedative;
xenobiotic
diazoxide
Diazoxide: A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group.. diazoxide : A benzothiadiazine that is the S,S-dioxide of 2H-1,2,4-benzothiadiazine which is substituted at position 3 by a methyl group and at position 7 by chlorine. A peripheral vasodilator, it increases the concentration of glucose in the plasma and inhibits the secretion of insulin by the beta- cells of the pancreas. It is used orally in the management of intractable hypoglycaemia and intravenously in the management of hypertensive emergencies.		3.2310benzothiadiazine;
organochlorine compound;
sulfone		antihypertensive agent;
beta-adrenergic agonist;
bronchodilator agent;
cardiotonic drug;
diuretic;
K-ATP channel agonist;
sodium channel blocker;
sympathomimetic agent;
vasodilator agent
diclofenac
Diclofenac: A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt.. diclofenac : A monocarboxylic acid consisting of phenylacetic acid having a (2,6-dichlorophenyl)amino group at the 2-position.		3.2310amino acid;
aromatic amine;
dichlorobenzene;
monocarboxylic acid;
secondary amino compound		antipyretic;
drug allergen;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
environmental contaminant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
dichlorphenamide
Dichlorphenamide: A carbonic anhydrase inhibitor that is used in the treatment of glaucoma.. diclofenamide : A sulfonamide that is benzene-1,3-disulfonamide in which the hydrogens at positions 4 and 5 are substituted by chlorine. An oral carbonic anhydrase inhibitor, it partially suppresses the secretion (inflow) of aqueous humor in the eye and so reduces intraocular pressure. It is used for the treatment of glaucoma.		3.2310dichlorobenzene;
sulfonamide		antiglaucoma drug;
EC 4.2.1.1 (carbonic anhydrase) inhibitor;
ophthalmology drug
dicyclomine
Dicyclomine: A muscarinic antagonist used as an antispasmodic and in urinary incontinence. It has little effect on glandular secretion or the cardiovascular system. It does have some local anesthetic properties and is used in gastrointestinal, biliary, and urinary tract spasms.. dicyclomine : The ester resulting from the formal condensation of 1-cyclohexylcyclohexanecarboxylic acid with 2-(diethylamino)ethanol. An anticholinergic, it is used as the hydrochloride to treat or prevent spasm in the muscles of the gastrointestinal tract, particularly that associated with irritable bowel syndrome.		3.2310carboxylic ester;
tertiary amine		antispasmodic drug;
muscarinic antagonist;
parasympatholytic
pentetic acid
Pentetic Acid: An iron chelating agent with properties like EDETIC ACID. DTPA has also been used as a chelator for other metals, such as plutonium.		3.2310pentacarboxylic acidcopper chelator
diflunisal
Diflunisal: A salicylate derivative and anti-inflammatory analgesic with actions and side effects similar to those of ASPIRIN.. diflunisal : An organofluorine compound comprising salicylic acid having a 2,4-difluorophenyl group at the 5-position.		3.2310monohydroxybenzoic acid;
organofluorine compound		non-narcotic analgesic;
non-steroidal anti-inflammatory drug
dimercaprol
Dimercaprol: An anti-gas warfare agent that is effective against Lewisite (dichloro(2-chlorovinyl)arsine) and formerly known as British Anti-Lewisite or BAL. It acts as a chelating agent and is used in the treatment of arsenic, gold, and other heavy metal poisoning.. dimercaprol : A dithiol that is propane-1,2-dithiol in which one of the methyl hydrogens is replaced by a hydroxy group. a chelating agent originally developed during World War II as an experimental antidote against the arsenic-based poison gas Lewisite, it has been used clinically since 1949 for the treatment of poisoning by arsenic, mercury and gold. It can also be used for treatment of poisoning by antimony, bismuth and possibly thallium, and (with sodium calcium edetate) in cases of acute leaad poisoning. Administration is by (painful) intramuscular injection of a suspension of dimercaprol in peanut oil, typically every 4 hours for 2-10 days depending on the toxicity. In the past, dimercaprol was also used for the treatment of Wilson's disease, a severely debilitating genetic disorder in which the body tends to retain copper, with resultant liver and brain injury.		3.2310dithiol;
primary alcohol		chelator
diphenhydramine
Diphenhydramine: A histamine H1 antagonist used as an antiemetic, antitussive, for dermatoses and pruritus, for hypersensitivity reactions, as a hypnotic, an antiparkinson, and as an ingredient in common cold preparations. It has some undesired antimuscarinic and sedative effects.. diphenhydramine : An ether that is the benzhydryl ether of 2-(dimethylamino)ethanol. It is a H1-receptor antagonist used as a antipruritic and antitussive drug.. antitussive : An agent that suppresses cough. Antitussives have a central or a peripheral action on the cough reflex, or a combination of both. Compare with expectorants, which are considered to increase the volume of secretions in the respiratory tract, so facilitating their removal by ciliary action and coughing, and mucolytics, which decrease the viscosity of mucus, facilitating its removal by ciliary action and expectoration.		3.2310ether;
tertiary amino compound		anti-allergic agent;
antidyskinesia agent;
antiemetic;
antiparkinson drug;
antipruritic drug;
antitussive;
H1-receptor antagonist;
local anaesthetic;
muscarinic antagonist;
oneirogen;
sedative
dipyridamole
Dipyridamole: A phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells. Dipyridamole also potentiates the antiaggregating action of prostacyclin. (From AMA Drug Evaluations Annual, 1994, p752). dipyridamole : A pyrimidopyrimidine that is 2,2',2'',2'''-(pyrimido[5,4-d]pyrimidine-2,6-diyldinitrilo)tetraethanol substituted by piperidin-1-yl groups at positions 4 and 8 respectively. A vasodilator agent, it inhibits the formation of blood clots.		3.2310piperidines;
pyrimidopyrimidine;
tertiary amino compound;
tetrol		adenosine phosphodiesterase inhibitor;
EC 3.5.4.4 (adenosine deaminase) inhibitor;
platelet aggregation inhibitor;
vasodilator agent
disopyramide
Disopyramide: A class I anti-arrhythmic agent (one that interferes directly with the depolarization of the cardiac membrane and thus serves as a membrane-stabilizing agent) with a depressant action on the heart similar to that of guanidine. It also possesses some anticholinergic and local anesthetic properties.. disopyramide : A monocarboxylic acid amide that is butanamide substituted by a diisopropylamino group at position 4, a phenyl group at position 2 and a pyridin-2-yl group at position 2. It is used as a anti-arrhythmia drug.		3.2310monocarboxylic acid amide;
pyridines;
tertiary amino compound		anti-arrhythmia drug
disulfiram
[no description available]		3.2310organic disulfide;
organosulfur acaricide		angiogenesis inhibitor;
antineoplastic agent;
apoptosis inducer;
EC 1.2.1.3 [aldehyde dehydrogenase (NAD(+))] inhibitor;
EC 3.1.1.1 (carboxylesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
ferroptosis inducer;
fungicide;
NF-kappaB inhibitor
valproic acid
Valproic Acid: A fatty acid with anticonvulsant and anti-manic properties that is used in the treatment of EPILEPSY and BIPOLAR DISORDER. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of VOLTAGE-GATED SODIUM CHANNELS.. valproic acid : A branched-chain saturated fatty acid that comprises of a propyl substituent on a pentanoic acid stem.		3.2310branched-chain fatty acid;
branched-chain saturated fatty acid		anticonvulsant;
antimanic drug;
EC 3.5.1.98 (histone deacetylase) inhibitor;
GABA agent;
neuroprotective agent;
psychotropic drug;
teratogenic agent
donepezil
Donepezil: An indan and piperidine derivative that acts as a selective and reversible inhibitor of ACETYLCHOLINESTERASE. Donepezil is highly selective for the central nervous system and is used in the management of mild to moderate DEMENTIA in ALZHEIMER DISEASE.. donepezil : A racemate comprising equimolar amounts of (R)- and (S)-donepezil. A centrally acting reversible acetylcholinesterase inhibitor, its main therapeutic use is in the treatment of Alzheimer's disease where it is used to increase cortical acetylcholine.. 2-[(1-benzylpiperidin-4-yl)methyl]-5,6-dimethoxyindan-1-one : A member of the class of indanones that is 5,6-dimethoxyindan-1-one which is substituted at position 2 by an (N-benzylpiperidin-4-yl)methyl group.		3.2310aromatic ether;
indanones;
piperidines;
racemate		EC 3.1.1.7 (acetylcholinesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
nootropic agent
doxapram
Doxapram: A central respiratory stimulant with a brief duration of action. (From Martindale, The Extra Pharmocopoeia, 30th ed, p1225). doxapram : A member of the class of pyrrolidin-2-ones that is N-ethylpyrrolidin-2-one in which both of the hydrogens at the 3 position (adjacent to the carbonyl group) are substituted by phenyl groups, and one of the hydrogens at the 4 position is substituted by a 2-(morpholin-4-yl)ethyl group. A central and respiratory stimulant with a brief duration of action, it is used (generally as the hydrochloride or the hydrochloride hydrate) as a temporary treatment of acute respiratory failure, particularly when superimposed on chronic obstructive pulmonary disease, and of postoperative respiratory depression. It has also been used for treatment of postoperative shivering.		3.2310morpholines;
pyrrolidin-2-ones		central nervous system stimulant
doxazosin
Doxazosin: A prazosin-related compound that is a selective alpha-1-adrenergic blocker.. doxazosin : A member of the class of quinazolines that is quinazoline substituted by an amino group at position 4, methoxy groups at positions 6 and 7 and a piperazin-1-yl group at position 2 which in turn is substituted by a 2,3-dihydro-1,4-benzodioxin-2-ylcarbonyl group at position 4. An antihypertensive agent, it is used in the treatment of high blood pressure.		3.2310aromatic amine;
benzodioxine;
monocarboxylic acid amide;
N-acylpiperazine;
N-arylpiperazine;
quinazolines		alpha-adrenergic antagonist;
antihyperplasia drug;
antihypertensive agent;
antineoplastic agent;
vasodilator agent
doxepin
Doxepin: A dibenzoxepin tricyclic compound. It displays a range of pharmacological actions including maintaining adrenergic innervation. Its mechanism of action is not fully understood, but it appears to block reuptake of monoaminergic neurotransmitters into presynaptic terminals. It also possesses anticholinergic activity and modulates antagonism of histamine H(1)- and H(2)-receptors.. doxepin : A dibenzooxepine that is 6,11-dihydrodibenzo[b,e]oxepine substituted by a 3-(dimethylamino)propylidene group at position 11. It is used as an antidepressant drug.		3.2310dibenzooxepine;
tertiary amino compound		antidepressant
doxylamine
Doxylamine: Histamine H1 antagonist with pronounced sedative properties. It is used in allergies and as an antitussive, antiemetic, and hypnotic. Doxylamine has also been administered in veterinary applications and was formerly used in PARKINSONISM.		3.2310pyridines;
tertiary amine		anti-allergic agent;
antiemetic;
antitussive;
cholinergic antagonist;
H1-receptor antagonist;
histamine antagonist;
sedative
droperidol
Droperidol: A butyrophenone with general properties similar to those of HALOPERIDOL. It is used in conjunction with an opioid analgesic such as FENTANYL to maintain the patient in a calm state of neuroleptanalgesia with indifference to surroundings but still able to cooperate with the surgeon. It is also used as a premedicant, as an antiemetic, and for the control of agitation in acute psychoses. (From Martindale, The Extra Pharmacopoeia, 29th ed, p593). droperidol : An organofluorine compound that is haloperidol in which the hydroxy group has been eliminated with the introduction of a double bond in the piperidine ring, and the 4-chlorophenyl group has been replaced by a benzimidazol-2-on-1-yl group. It is used in the management of chemotherapy-induced nausea and vomiting, and in conjunction with an opioid analgesic such as fentanyl to maintain the patient in a calm state of neuroleptanalgesia with indifference to surroundings but still able to cooperate with the surgeon.		3.2310aromatic ketone;
benzimidazoles;
organofluorine compound		anaesthesia adjuvant;
antiemetic;
dopaminergic antagonist;
first generation antipsychotic
dyphylline
Dyphylline: A THEOPHYLLINE derivative with broncho- and vasodilator properties. It is used in the treatment of asthma, cardiac dyspnea, and bronchitis.. dyphylline : An oxopurine that is theophylline bearing a 2,3-dihydroxypropyl group at the 7 position. It has broncho- and vasodilator properties, and is used in the treatment of asthma, cardiac dyspnea, and bronchitis. It is also an ingredient in preparations that have been promoted for coughs.		3.2310oxopurine;
propane-1,2-diols		bronchodilator agent;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
muscle relaxant;
vasodilator agent
edrophonium
Edrophonium: A rapid-onset, short-acting cholinesterase inhibitor used in cardiac arrhythmias and in the diagnosis of myasthenia gravis. It has also been used as an antidote to curare principles.. edrophonium : A quaternary ammonium ion that is N-ethyl-N,N-dimethylanilinium in which one of the meta positions is substituted by a hydroxy group. It is a reversible inhibitor of cholinesterase, with a rapid onset (30-60 seconds after injection) but a short duration of action (5-15 minutes). The chloride salt is used in myasthenia gravis both diagnostically and to distinguish between under- or over-treatment with other anticholinesterases. It has also been used for the reversal of neuromuscular blockade in anaesthesia, and for the management of poisoning due to tetrodotoxin, a neuromuscular blocking toxin found in puffer fish and other marine animals.		3.2310phenols;
quaternary ammonium ion		antidote;
diagnostic agent;
EC 3.1.1.8 (cholinesterase) inhibitor
estazolam
Estazolam: A benzodiazepine with anticonvulsant, hypnotic, and muscle relaxant properties. It has been shown in some cases to be more potent than DIAZEPAM or NITRAZEPAM.. estazolam : A triazolo[4,3-a][1,4]benzodiazepine having a phenyl group at position 6 and a chloro substituent at position 8. A short-acting benzodiazepine with general properties similar to diazepam, it is given by mouth as a hypnotic in the short-term management of insomnia.		3.2310triazoles;
triazolobenzodiazepine		anticonvulsant;
anxiolytic drug;
GABA modulator
ethacrynic acid
Ethacrynic Acid: A compound that inhibits symport of sodium, potassium, and chloride primarily in the ascending limb of Henle, but also in the proximal and distal tubules. This pharmacological action results in excretion of these ions, increased urinary output, and reduction in extracellular fluid. This compound has been classified as a loop or high ceiling diuretic.. etacrynic acid : An aromatic ether that is phenoxyacetic acid in which the phenyl ring is substituted by chlorines at positions 2 and 3, and by a 2-methylidenebutanoyl group at position 4. It is a loop diuretic used to treat high blood pressure resulting from diseases such as congestive heart failure, liver failure, and kidney failure. It is also a glutathione S-transferase (EC 2.5.1.18) inhibitor.		3.2310aromatic ether;
aromatic ketone;
dichlorobenzene;
monocarboxylic acid		EC 2.5.1.18 (glutathione transferase) inhibitor;
ion transport inhibitor;
loop diuretic
ethosuximide
Ethosuximide: An anticonvulsant especially useful in the treatment of absence seizures unaccompanied by other types of seizures.. ethosuximide : A dicarboximide that is pyrrolidine-2,5-dione in which the hydrogens at position 3 are substituted by one methyl and one ethyl group. An antiepileptic, it is used in the treatment of absence seizures and may be used for myoclonic seizures, but is ineffective against tonic-clonic seizures.		3.2310dicarboximide;
pyrrolidinone		anticonvulsant;
geroprotector;
T-type calcium channel blocker
ethotoin
ethotoin: was heading 1966-94 (see under HYDANTOINS 1966-90); use HYDANTOINS to search ETHOTOIN 1966-94. ethotoin : An imidazolidine-2,4-dione that is hydantoin substituted by ethyl and phenyl at positions 3 and 5, respectively. An antiepileptic, it is less toxic than phenytoin but also less effective.		3.2310imidazolidine-2,4-dioneanticonvulsant
etidronate
Etidronic Acid: A diphosphonate which affects calcium metabolism. It inhibits ectopic calcification and slows down bone resorption and bone turnover.. etidronic acid : A 1,1-bis(phosphonic acid) that is (ethane-1,1-diyl)bis(phosphonic acid) having a hydroxy substituent at the 1-position. It inhibits the formation, growth, and dissolution of hydroxyapatite crystals by chemisorption to calcium phosphate surfaces.		3.23101,1-bis(phosphonic acid)antineoplastic agent;
bone density conservation agent;
chelator
etodolac
Etodolac: A non-steroidal anti-inflammatory agent and cyclooxygenase-2 (COX-2) inhibitor with potent analgesic and anti-arthritic properties. It has been shown to be effective in the treatment of OSTEOARTHRITIS; RHEUMATOID ARTHRITIS; ANKYLOSING SPONDYLITIS; and in the alleviation of postoperative pain (PAIN, POSTOPERATIVE).. etodolac : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is substituted by a 1,8-diethyl-1,3,4,9-tetrahydropyrano[3,4-b]indol-1-yl moiety. A preferential inhibitor of cyclo-oxygenase 2 and non-steroidal anti-inflammatory, it is used for the treatment of rheumatoid arthritis and osteoarthritis, and for the alleviation of postoperative pain. Administered as the racemate, only the (S)-enantiomer is active.		3.2310monocarboxylic acid;
organic heterotricyclic compound		antipyretic;
cyclooxygenase 2 inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
brl 42810
[no description available]		3.23102-aminopurines;
acetate ester		antiviral drug;
prodrug
felbamate
Felbamate: A PEGylated phenylcarbamate derivative that acts as an antagonist of NMDA RECEPTORS. It is used as an anticonvulsant, primarily for the treatment of SEIZURES in severe refractory EPILEPSY.. felbamate : The bis(carbamate ester) of 2-phenylpropane-1,3-diol. An anticonvulsant, it is used in the treatment of epilepsy.		3.2310carbamate esteranticonvulsant;
neuroprotective agent
felodipine
Felodipine: A dihydropyridine calcium antagonist with positive inotropic effects. It lowers blood pressure by reducing peripheral vascular resistance through a highly selective action on smooth muscle in arteriolar resistance vessels.. felodipine : The mixed (methyl, ethyl) diester of 4-(2,3-dichlorophenyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylic acid. A calcium-channel blocker, it lowers blood pressure by reducing peripheral vascular resistance through a highly selective action on smooth muscle in arteriolar resistance vessels. It is used in the management of hypertension and angina pectoris.		3.2310dichlorobenzene;
dihydropyridine;
ethyl ester;
methyl ester		anti-arrhythmia drug;
antihypertensive agent;
calcium channel blocker;
vasodilator agent
fenofibrate
Pharmavit: a polyvitamin product, comprising vitamins A, D2, B1, B2, B6, C, E, nicotinamide, & calcium pantothene; may be a promising agent for application to human populations exposed to carcinogenic and genetic hazards of ionizing radiation; RN from CHEMLINE		3.2310aromatic ether;
chlorobenzophenone;
isopropyl ester;
monochlorobenzenes		antilipemic drug;
environmental contaminant;
geroprotector;
xenobiotic
fenoldopam
Fenoldopam: A dopamine D1 receptor agonist that is used as an antihypertensive agent. It lowers blood pressure through arteriolar vasodilation.		3.2310benzazepinealpha-adrenergic agonist;
antihypertensive agent;
dopamine agonist;
dopaminergic antagonist;
vasodilator agent
fenoprofen
Fenoprofen: A propionic acid derivative that is used as a non-steroidal anti-inflammatory agent.. fenoprofen : A monocarboxylic acid that is propanoic acid in which one of the hydrogens at position 2 is substituted by a 3-phenoxyphenyl group. A non-steroidal anti-inflammatory drug, the dihydrate form of the calcium salt is used for the management of mild to moderate pain and for the relief of pain and inflammation associated with disorders such as arthritis. It is pharmacologically similar to aspirin, but causes less gastrointestinal bleeding.		3.2310monocarboxylic acidantipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
fexofenadine
fexofenadine: a second generation antihistamine; metabolite of the antihistaminic drug terfenadine; structure in first source; RN refers to HCl. fexofenadine : A piperidine-based anti-histamine compound.		3.2310piperidines;
tertiary amine		anti-allergic agent;
H1-receptor antagonist
fipexide
fipexide: regulates dopaminergic systems at macromolecular level		3.2310benzodioxoles
flavoxate
Flavoxate: A drug that has been used in various urinary syndromes and as an antispasmodic. Its therapeutic usefulness and its mechanism of action are not clear. It may have local anesthetic activity and direct relaxing effects on smooth muscle as well as some activity as a muscarinic antagonist.. flavoxate : A carboxylic ester resulting from the formal condensation of 3-methylflavone-8-carboxylic acid with 2-(1-piperidinyl)ethanol.		3.2310carboxylic ester;
flavones;
piperidines;
tertiary amino compound		antispasmodic drug;
muscarinic antagonist;
parasympatholytic
flecainide
Flecainide: A potent anti-arrhythmia agent, effective in a wide range of ventricular and atrial ARRHYTHMIAS and TACHYCARDIAS.. flecainide : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 2,5-bis(2,2,2-trifluoroethoxy)benzoic acid with the primary amino group of piperidin-2-ylmethylamine. An antiarrhythmic agent used (in the form of its acetate salt) to prevent and treat tachyarrhythmia (abnormal fast rhythm of the heart).		3.2310aromatic ether;
monocarboxylic acid amide;
organofluorine compound;
piperidines		anti-arrhythmia drug
fluconazole
Fluconazole: Triazole antifungal agent that is used to treat oropharyngeal CANDIDIASIS and cryptococcal MENINGITIS in AIDS.. fluconazole : A member of the class of triazoles that is propan-2-ol substituted at position 1 and 3 by 1H-1,2,4-triazol-1-yl groups and at position 2 by a 2,4-difluorophenyl group. It is an antifungal drug used for the treatment of mucosal candidiasis and for systemic infections including systemic candidiasis, coccidioidomycosis, and cryptococcosis.		3.2310conazole antifungal drug;
difluorobenzene;
tertiary alcohol;
triazole antifungal drug		environmental contaminant;
P450 inhibitor;
xenobiotic
flucytosine
Flucytosine: A fluorinated cytosine analog that is used as an antifungal agent.. flucytosine : An organofluorine compound that is cytosine that is substituted at position 5 by a fluorine. A prodrug for the antifungal 5-fluorouracil, it is used for the treatment of systemic fungal infections.		3.2310aminopyrimidine;
nucleoside analogue;
organofluorine compound;
pyrimidine antifungal drug;
pyrimidone		prodrug
fluphenazine
[no description available]		3.2310N-alkylpiperazine;
organofluorine compound;
phenothiazines		anticoronaviral agent;
dopaminergic antagonist;
phenothiazine antipsychotic drug
flumazenil
Flumazenil: A potent benzodiazepine receptor antagonist. Since it reverses the sedative and other actions of benzodiazepines, it has been suggested as an antidote to benzodiazepine overdoses.. flumazenil : An organic heterotricyclic compound that is 5,6-dihydro-4H-imidazo[1,5-a][1,4]benzodiazepine which is substituted at positions 3, 5, 6, and 8 by ethoxycarbonyl, methyl, oxo, and fluoro groups, respectively. It is used as an antidote to benzodiazepine overdose.		3.2310ethyl ester;
imidazobenzodiazepine;
organofluorine compound		antidote to benzodiazepine poisoning;
GABA antagonist
fluorescite
fluorescein (acid form) : A xanthene dye that is highly fluorescent and commonly used as a fluorescent tracer.		3.2310benzoic acids;
cyclic ketone;
hydroxy monocarboxylic acid;
organic heterotricyclic compound;
phenols;
xanthene dye		fluorescent dye;
radioopaque medium
fluorouracil
Fluorouracil: A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.. 5-fluorouracil : A nucleobase analogue that is uracil in which the hydrogen at position 5 is replaced by fluorine. It is an antineoplastic agent which acts as an antimetabolite - following conversion to the active deoxynucleotide, it inhibits DNA synthesis (by blocking the conversion of deoxyuridylic acid to thymidylic acid by the cellular enzyme thymidylate synthetase) and so slows tumour growth.		3.2310nucleobase analogue;
organofluorine compound		antimetabolite;
antineoplastic agent;
environmental contaminant;
immunosuppressive agent;
radiosensitizing agent;
xenobiotic
fluoxetine
Fluoxetine: The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants.. fluoxetine : A racemate comprising equimolar amounts of (R)- and (S)-fluoxetine. A selective serotonin reuptake inhibitor (SSRI), it is used (generally as the hydrochloride salt) for the treatment of depression (and the depressive phase of bipolar disorder), bullimia nervosa, and obsessive-compulsive disorder.. N-methyl-3-phenyl-3-[4-(trifluoromethyl)phenoxy]propan-1-amine : An aromatic ether consisting of 4-trifluoromethylphenol in which the hydrogen of the phenolic hydroxy group is replaced by a 3-(methylamino)-1-phenylpropyl group.		3.2310(trifluoromethyl)benzenes;
aromatic ether;
secondary amino compound
flurazepam
Flurazepam: A benzodiazepine derivative used mainly as a hypnotic.. flurazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a 2-(diethylamino)ethyl group, 2-fluorophenyl group and chloro group at positions 1, 5 and 7, respectively. It is a partial agonist of GABAA receptors and used for the treatment of insomnia.		3.23101,4-benzodiazepinone;
monofluorobenzenes;
organochlorine compound;
tertiary amino compound		anticonvulsant;
anxiolytic drug;
GABAA receptor agonist;
sedative
flurbiprofen
Flurbiprofen: An anti-inflammatory analgesic and antipyretic of the phenylalkynoic acid series. It has been shown to reduce bone resorption in periodontal disease by inhibiting CARBONIC ANHYDRASE.. flurbiprofen : A monocarboxylic acid that is a 2-fluoro-[1,1'-biphenyl-4-yl] moiety linked to C-2 of propionic acid. A non-steroidal anti-inflammatory, analgesic and antipyretic, it is used as a pre-operative anti-miotic as well as orally for arthritis or dental pain.		3.2310fluorobiphenyl;
monocarboxylic acid		antipyretic;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
flutamide
Flutamide: An antiandrogen with about the same potency as cyproterone in rodent and canine species.		3.2310(trifluoromethyl)benzenes;
monocarboxylic acid amide		androgen antagonist;
antineoplastic agent
fomepizole
Fomepizole: A pyrazole and competitive inhibitor of ALCOHOL DEHYDROGENASE that is used for the treatment of poisoning by ETHYLENE GLYCOL or METHANOL.. fomepizole : A member of the class of pyrazoles that is 1H-pyrazole substituted by a methyl group at position 4.		3.2310pyrazolesantidote;
EC 1.1.1.1 (alcohol dehydrogenase) inhibitor;
protective agent
foscarnet
Foscarnet: An antiviral agent used in the treatment of cytomegalovirus retinitis. Foscarnet also shows activity against human herpesviruses and HIV.. phosphonoformic acid : Phosphoric acid in which one of the hydroxy groups is replaced by a carboxylic acid group. It is used as the trisodium salt as an antiviral agent in the treatment of cytomegalovirus retinitis (CMV retinitis, an inflamation of the retina that can lead to blindness) and as an alternative to ganciclovir for AIDS patients who require concurrent antiretroviral therapy but are unable to tolerate ganciclovir due to haematological toxicity.		3.2310carboxylic acid;
one-carbon compound;
phosphonic acids		antiviral drug;
geroprotector;
HIV-1 reverse transcriptase inhibitor;
sodium-dependent Pi-transporter inhibitor
furosemide
Furosemide: A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.. furosemide : A chlorobenzoic acid that is 4-chlorobenzoic acid substituted by a (furan-2-ylmethyl)amino and a sulfamoyl group at position 2 and 5 respectively. It is a diuretic used in the treatment of congestive heart failure.		3.2310chlorobenzoic acid;
furans;
sulfonamide		environmental contaminant;
loop diuretic;
xenobiotic
gabapentin
Gabapentin: A cyclohexane-gamma-aminobutyric acid derivative that is used for the treatment of PARTIAL SEIZURES; NEURALGIA; and RESTLESS LEGS SYNDROME.. gabapentin : A gamma-amino acid that is cyclohexane substituted at position 1 by aminomethyl and carboxymethyl groups. Used for treatment of neuropathic pain and restless legs syndrome.		3.2310gamma-amino acidanticonvulsant;
calcium channel blocker;
environmental contaminant;
xenobiotic
gemfibrozil
[no description available]		3.2310aromatic etherantilipemic drug
glafenine
Glafenine: An anthranilic acid derivative with analgesic properties used for the relief of all types of pain.. glafenine : A carboxylic ester that is 2,3-dihydroxypropyl anthranilate in which the amino group is substituted by a 7-chloroquinolin-4-yl group. A non-steroidal anti-inflammatory drug, glafenine and its hydrochloride salt were used for the relief of all types of pain, but high incidence of anaphylactic reactions resulted in their withdrawal from the market.		3.2310aminoquinoline;
carboxylic ester;
glycol;
organochlorine compound;
secondary amino compound		inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
glimepiride
glimepiride: structure given in first source		4.0920sulfonamide
glipizide
Glipizide: An oral hypoglycemic agent which is rapidly absorbed and completely metabolized.. glipizide : An N-sulfonylurea that is glyburide in which the (5-chloro-2-methoxybenzoyl group is replaced by a (5-methylpyrazin-2-yl)carbonyl group. An oral hypoglycemic agent, it is used in the treatment of type 2 diabetes mellitus.		3.2310aromatic amide;
monocarboxylic acid amide;
N-sulfonylurea;
pyrazines		EC 2.7.1.33 (pantothenate kinase) inhibitor;
hypoglycemic agent;
insulin secretagogue
glyburide
Glyburide: An antidiabetic sulfonylurea derivative with actions like those of chlorpropamide. glyburide : An N-sulfonylurea that is acetohexamide in which the acetyl group is replaced by a 2-(5-chloro-2-methoxybenzamido)ethyl group.		3.2310monochlorobenzenes;
N-sulfonylurea		anti-arrhythmia drug;
EC 2.7.1.33 (pantothenate kinase) inhibitor;
EC 3.6.3.49 (channel-conductance-controlling ATPase) inhibitor;
hypoglycemic agent
2-cyclopentyl-2-hydroxy-2-phenylacetic acid (1,1-dimethyl-3-pyrrolidin-1-iumyl) ester
[no description available]		3.2310benzenes
granisetron
[no description available]		3.2310aromatic amide;
indazoles
guaifenesin
Guaifenesin: An expectorant that also has some muscle relaxing action. It is used in many cough preparations.		3.2310methoxybenzenes
guanethidine
Guanethidine: An antihypertensive agent that acts by inhibiting selectively transmission in post-ganglionic adrenergic nerves. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues.. guanethidine : A member of the class of guanidines in which one of the hydrogens of the amino group has been replaced by a 2-azocan-1-ylethyl group.. guanethidine sulfate : A organic sulfate salt composed of two molecules of guanethidine and one of sulfuric acid.		3.2310azocanes;
guanidines		adrenergic antagonist;
antihypertensive agent;
sympatholytic agent
guanfacine
Guanfacine: A centrally acting antihypertensive agent with specificity towards ADRENERGIC ALPHA-2 RECEPTORS.		3.2310acetamides
guanidine
Guanidine: A strong organic base existing primarily as guanidium ions at physiological pH. It is found in the urine as a normal product of protein metabolism. It is also used in laboratory research as a protein denaturant. (From Martindale, the Extra Pharmacopoeia, 30th ed and Merck Index, 12th ed) It is also used in the treatment of myasthenia and as a fluorescent probe in HPLC.. guanidine : An aminocarboxamidine, the parent compound of the guanidines.		3.2310carboxamidine;
guanidines;
one-carbon compound
haloperidol
Haloperidol: A phenyl-piperidinyl-butyrophenone that is used primarily to treat SCHIZOPHRENIA and other PSYCHOSES. It is also used in schizoaffective disorder, DELUSIONAL DISORDERS, ballism, and TOURETTE SYNDROME (a drug of choice) and occasionally as adjunctive therapy in INTELLECTUAL DISABILITY and the chorea of HUNTINGTON DISEASE. It is a potent antiemetic and is used in the treatment of intractable HICCUPS. (From AMA Drug Evaluations Annual, 1994, p279). haloperidol : A compound composed of a central piperidine structure with hydroxy and p-chlorophenyl substituents at position 4 and an N-linked p-fluorobutyrophenone moiety.		3.2310aromatic ketone;
hydroxypiperidine;
monochlorobenzenes;
organofluorine compound;
tertiary alcohol		antidyskinesia agent;
antiemetic;
dopaminergic antagonist;
first generation antipsychotic;
serotonergic antagonist
hydralazine
Hydralazine: A direct-acting vasodilator that is used as an antihypertensive agent.. hydralazine : The 1-hydrazino derivative of phthalazine; a direct-acting vasodilator that is used as an antihypertensive agent.		3.2310azaarene;
hydrazines;
ortho-fused heteroarene;
phthalazines		antihypertensive agent;
vasodilator agent
hydrochlorothiazide
Hydrochlorothiazide: A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It is used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism.. hydrochlorothiazide : A benzothiadiazine that is 3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide substituted by a chloro group at position 6 and a sulfonamide at 7. It is diuretic used for the treatment of hypertension and congestive heart failure.		3.2310benzothiadiazine;
organochlorine compound;
sulfonamide		antihypertensive agent;
diuretic;
environmental contaminant;
xenobiotic
hydroflumethiazide
Hydroflumethiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p822). hydroflumethiazide : A benzothiadiazine consisting of a 3,4-dihydro-HH-1,2,4-benzothiadiazine bicyclic system dioxygenated on sulfur and carrying trifluoromethyl and aminosulfonyl groups at positions 6 and 7 respectively. A diuretic with actions and uses similar to those of hydrochlorothiazide.		3.2310benzothiadiazine;
thiazide		antihypertensive agent;
diuretic
hydroxychloroquine
Hydroxychloroquine: A chemotherapeutic agent that acts against erythrocytic forms of malarial parasites. Hydroxychloroquine appears to concentrate in food vacuoles of affected protozoa. It inhibits plasmodial heme polymerase. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p970). hydroxychloroquine : An aminoquinoline that is chloroquine in which one of the N-ethyl groups is hydroxylated at position 2. An antimalarial with properties similar to chloroquine that acts against erythrocytic forms of malarial parasites, it is mainly used as the sulfate salt for the treatment of lupus erythematosus, rheumatoid arthritis, and light-sensitive skin eruptions.		3.2310aminoquinoline;
organochlorine compound;
primary alcohol;
secondary amino compound;
tertiary amino compound		anticoronaviral agent;
antimalarial;
antirheumatic drug;
dermatologic drug
hydroxyurea
[no description available]		3.2310one-carbon compound;
ureas		antimetabolite;
antimitotic;
antineoplastic agent;
DNA synthesis inhibitor;
EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor;
genotoxin;
immunomodulator;
radical scavenger;
teratogenic agent
hydroxyzine
Hydroxyzine: A histamine H1 receptor antagonist that is effective in the treatment of chronic urticaria, dermatitis, and histamine-mediated pruritus. Unlike its major metabolite CETIRIZINE, it does cause drowsiness. It is also effective as an antiemetic, for relief of anxiety and tension, and as a sedative.. hydroxyzine : A N-alkylpiperazine that is piperzine in which the nitrogens atoms are substituted by 2-(2-hydroxyethoxy)ethyl and (4-chlorophenyl)(phenyl)methyl groups respectively.		3.2310hydroxyether;
monochlorobenzenes;
N-alkylpiperazine		anticoronaviral agent;
antipruritic drug;
anxiolytic drug;
dermatologic drug;
H1-receptor antagonist
ibuprofen
Midol: combination of cinnamedrine, phenacetin, aspirin & caffeine		3.2310monocarboxylic acidantipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
environmental contaminant;
geroprotector;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
radical scavenger;
xenobiotic
phenelzine
Phenelzine: One of the MONOAMINE OXIDASE INHIBITORS used to treat DEPRESSION; PHOBIC DISORDERS; and PANIC.		3.2310primary amine
lidocaine
Lidocaine: A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE.. lidocaine : The monocarboxylic acid amide resulting from the formal condensation of N,N-diethylglycine with 2,6-dimethylaniline.		3.2310benzenes;
monocarboxylic acid amide;
tertiary amino compound		anti-arrhythmia drug;
drug allergen;
environmental contaminant;
local anaesthetic;
xenobiotic
ifosfamide
[no description available]		3.2310ifosfamidesalkylating agent;
antineoplastic agent;
environmental contaminant;
immunosuppressive agent;
xenobiotic
imipramine
Imipramine: The prototypical tricyclic antidepressant. It has been used in major depression, dysthymia, bipolar depression, attention-deficit disorders, agoraphobia, and panic disorders. It has less sedative effect than some other members of this therapeutic group.. imipramine : A dibenzoazepine that is 5H-dibenzo[b,f]azepine substituted by a 3-(dimethylamino)propyl group at the nitrogen atom.		3.2310dibenzoazepineadrenergic uptake inhibitor;
antidepressant;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
amrinone
Amrinone: A positive inotropic cardiotonic (CARDIOTONIC AGENTS) with vasodilator properties, phosphodiesterase 3 inhibitory activity, and the ability to stimulate calcium ion influx into the cardiac cell.. amrinone : A 3,4'-bipyridine substituted at positions 5 and 6 by an amino group and a keto function respectively. A pyridine phosphodiesterase 3 inhibitor, it is a drug that may improve the prognosis in patients with congestive heart failure.		3.2310bipyridinesEC 3.1.4.* (phosphoric diester hydrolase) inhibitor
indapamide
Indapamide: A benzamide-sulfonamide-indole derived DIURETIC that functions by inhibiting SODIUM CHLORIDE SYMPORTERS.. indapamide : A sulfonamide formed by condensation of the carboxylic group of 4-chloro-3-sulfamoylbenzoic acid with the amino group of 2-methyl-2,3-dihydro-1H-indol-1-amine.		3.2310indoles;
organochlorine compound;
sulfonamide		antihypertensive agent;
diuretic
indomethacin
Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits CYCLOOXYGENASE, which is necessary for the formation of PROSTAGLANDINS and other AUTACOIDS. It also inhibits the motility of POLYMORPHONUCLEAR LEUKOCYTES.. indometacin : A member of the class of indole-3-acetic acids that is indole-3-acetic acid in which the indole ring is substituted at positions 1, 2 and 5 by p-chlorobenzoyl, methyl, and methoxy groups, respectively. A non-steroidal anti-inflammatory drug, it is used in the treatment of musculoskeletal and joint disorders including osteoarthritis, rheumatoid arthritis, gout, bursitis and tendinitis.		3.2310aromatic ether;
indole-3-acetic acids;
monochlorobenzenes;
N-acylindole		analgesic;
drug metabolite;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
environmental contaminant;
gout suppressant;
non-steroidal anti-inflammatory drug;
xenobiotic metabolite;
xenobiotic
ioversol
[no description available]		3.2310amidobenzoic acid
iproniazid
[no description available]		3.2310carbohydrazide;
pyridines
avapro
Irbesartan: A spiro compound, biphenyl and tetrazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION, and in the treatment of kidney disease.. irbesartan : A biphenylyltetrazole that is an angiotensin II receptor antagonist used mainly for the treatment of hypertension.		3.2310azaspiro compound;
biphenylyltetrazole		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
isocarboxazid
Isocarboxazid: An MAO inhibitor that is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in the treatment of panic disorder and the phobic disorders. (From AMA, Drug Evaluations Annual, 1994, p311)		3.2310benzenes
isoniazid
Hydra: A genus of freshwater polyps in the family Hydridae, order Hydroida, class HYDROZOA. They are of special interest because of their complex organization and because their adult organization corresponds roughly to the gastrula of higher animals.. hydrazide : Compounds derived from oxoacids RkE(=O)l(OH)m (l =/= 0) by replacing -OH by -NRNR2 (R groups are commonly H). (IUPAC).		3.2310carbohydrazideantitubercular agent;
drug allergen
isoproterenol
Isoproterenol: Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.. isoprenaline : A secondary amino compound that is noradrenaline in which one of the hydrogens attached to the nitrogen is replaced by an isopropyl group. A sympathomimetic acting almost exclusively on beta-adrenergic receptors, it is used (mainly as the hydrochloride salt) as a bronghodilator and heart stimulant for the management of a variety of cardiac disorders.		3.2310catechols;
secondary alcohol;
secondary amino compound		beta-adrenergic agonist;
bronchodilator agent;
cardiotonic drug;
sympathomimetic agent
isoxsuprine
Isoxsuprine: A beta-adrenergic agonist that causes direct relaxation of uterine and vascular smooth muscle. Its vasodilating actions are greater on the arteries supplying skeletal muscle than on those supplying skin. It is used in the treatment of peripheral vascular disease and in premature labor.		3.2310alkylbenzene
isradipine
Isradipine: A potent antagonist of CALCIUM CHANNELS that is highly selective for VASCULAR SMOOTH MUSCLE. It is effective in the treatment of chronic stable angina pectoris, hypertension, and congestive cardiac failure.		3.2310benzoxadiazole;
dihydropyridine;
isopropyl ester;
methyl ester
itraconazole
[no description available]		3.2310piperazines
ketamine
Ketamine: A cyclohexanone derivative used for induction of anesthesia. Its mechanism of action is not well understood, but ketamine can block NMDA receptors (RECEPTORS, N-METHYL-D-ASPARTATE) and may interact with sigma receptors.. ketamine : A member of the class of cyclohexanones in which one of the hydrogens at position 2 is substituted by a 2-chlorophenyl group, while the other is substituted by a methylamino group.		3.2310cyclohexanones;
monochlorobenzenes;
secondary amino compound		analgesic;
environmental contaminant;
intravenous anaesthetic;
neurotoxin;
NMDA receptor antagonist;
xenobiotic
ketoconazole
1-acetyl-4-(4-{[2-(2,4-dichlorophenyl)-2-(1H-imidazol-1-ylmethyl)-1,3-dioxolan-4-yl]methoxy}phenyl)piperazine : A dioxolane that is 1,3-dioxolane which is substituted at positions 2, 2, and 4 by imidazol-1-ylmethyl, 2,4-dichlorophenyl, and [para-(4-acetylpiperazin-1-yl)phenoxy]methyl groups, respectively.		3.2310dichlorobenzene;
dioxolane;
ether;
imidazoles;
N-acylpiperazine;
N-arylpiperazine
ketoprofen
Ketoprofen: An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis.. ketoprofen : An oxo monocarboxylic acid that consists of propionic acid substituted by a 3-benzoylphenyl group at position 2.		3.2310benzophenones;
oxo monocarboxylic acid		antipyretic;
drug allergen;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
environmental contaminant;
non-steroidal anti-inflammatory drug;
xenobiotic
ketorolac
Ketorolac: A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed). ketorolac : A racemate comprising equimolar amounts of (R)-(+)- and (S)-(-)-5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid. While only the (S)-(-) enantiomer is a COX1 and COX2 inhibitor, the (R)-(+) enantiomer exhibits potent analgesic activity. A non-steroidal anti-inflammatory drug, ketorolac is mainly used (generally as the tromethamine salt) for its potent analgesic properties in the short-term management of post-operative pain, and in eye drops to relieve the ocular itching associated with seasonal allergic conjunctivitis. It was withdrawn from the market in many countries in 1993 following association with haemorrhage and renal failure.. 5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid : A member of the class of pyrrolizines that is 2,3-dihydro-1H-pyrrolizine which is substituted at positions 1 and 5 by carboxy and benzoyl groups, respectively.		3.2310amino acid;
aromatic ketone;
monocarboxylic acid;
pyrrolizines;
racemate		analgesic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
labetalol
Labetalol: A salicylamide derivative that is a non-cardioselective blocker of BETA-ADRENERGIC RECEPTORS and ALPHA-1 ADRENERGIC RECEPTORS.. labetalol : A diastereoisomeric mixture of approximately equal amounts of all four possible stereoisomers ((R,S)-labetolol, (S,R)-labetolol, (S,S)-labetalol and (R,R)-labetalol). It is an adrenergic antagonist used to treat high blood pressure.. 2-hydroxy-5-{1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl}benzamide : A member of the class of benzamides that is benzamide substituted by a hydroxy group at position 2 and by a 1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl group at position 5.		3.2310benzamides;
benzenes;
phenols;
primary carboxamide;
salicylamides;
secondary alcohol;
secondary amino compound
lamotrigine
[no description available]		3.23101,2,4-triazines;
dichlorobenzene;
primary arylamine		anticonvulsant;
antidepressant;
antimanic drug;
calcium channel blocker;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
environmental contaminant;
excitatory amino acid antagonist;
geroprotector;
non-narcotic analgesic;
xenobiotic
lansoprazole
Lansoprazole: A 2,2,2-trifluoroethoxypyridyl derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS. Lansoprazole is a racemic mixture of (R)- and (S)-isomers.		3.2310benzimidazoles;
pyridines;
sulfoxide		anti-ulcer drug;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor
leflunomide
Leflunomide: An isoxazole derivative that inhibits dihydroorotate dehydrogenase, the fourth enzyme in the pyrimidine biosynthetic pathway. It is used an immunosuppressive agent in the treatment of RHEUMATOID ARTHRITIS and PSORIATIC ARTHRITIS.. leflunomide : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 5-methyl-1,2-oxazole-4-carboxylic acid with the anilino group of 4-(trifluoromethyl)aniline. The prodrug of teriflunomide.		3.2310(trifluoromethyl)benzenes;
isoxazoles;
monocarboxylic acid amide		antineoplastic agent;
antiparasitic agent;
EC 1.3.98.1 [dihydroorotate oxidase (fumarate)] inhibitor;
EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor;
hepatotoxic agent;
immunosuppressive agent;
non-steroidal anti-inflammatory drug;
prodrug;
pyrimidine synthesis inhibitor;
tyrosine kinase inhibitor
letrozole
[no description available]		3.2310nitrile;
triazoles		antineoplastic agent;
EC 1.14.14.14 (aromatase) inhibitor
lomefloxacin
lomefloxacin: structure given in first source. lomefloxacin : A fluoroquinolone antibiotic, used (generally as the hydrochloride salt) to treat bacterial infections including bronchitis and urinary tract infections. It is also used to prevent urinary tract infections prior to surgery.		3.2310fluoroquinolone antibiotic;
N-arylpiperazine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antimicrobial agent;
antitubercular agent;
photosensitizing agent
lomustine
[no description available]		3.2310N-nitrosoureas;
organochlorine compound		alkylating agent;
antineoplastic agent
loperamide
Loperamide: One of the long-acting synthetic ANTIDIARRHEALS; it is not significantly absorbed from the gut, and has no effect on the adrenergic system or central nervous system, but may antagonize histamine and interfere with acetylcholine release locally.. loperamide : A synthetic piperidine derivative, effective against diarrhoea resulting from gastroenteritis or inflammatory bowel disease.		3.2310monocarboxylic acid amide;
monochlorobenzenes;
piperidines;
tertiary alcohol		anticoronaviral agent;
antidiarrhoeal drug;
mu-opioid receptor agonist
loratadine
Loratadine: A second-generation histamine H1 receptor antagonist used in the treatment of allergic rhinitis and urticaria. Unlike most classical antihistamines (HISTAMINE H1 ANTAGONISTS) it lacks central nervous system depressing effects such as drowsiness.. loratadine : A benzocycloheptapyridine that is 6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridine substituted by a chloro group at position 8 and a 1-(ethoxycarbonyl)piperidin-4-ylidene group at position 11. It is a H1-receptor antagonist commonly employed in the treatment of allergic disorders.		3.2310benzocycloheptapyridine;
ethyl ester;
N-acylpiperidine;
organochlorine compound;
tertiary carboxamide		anti-allergic agent;
cholinergic antagonist;
geroprotector;
H1-receptor antagonist
lorazepam
Lorazepam: A benzodiazepine used as an anti-anxiety agent with few side effects. It also has hypnotic, anticonvulsant, and considerable sedative properties and has been proposed as a preanesthetic agent.		3.2310benzodiazepine
losartan
Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.. losartan : A biphenylyltetrazole where a 1,1'-biphenyl group is attached at the 5-position and has an additional trisubstituted imidazol-1-ylmethyl group at the 4'-position		3.2310biphenylyltetrazole;
imidazoles		angiotensin receptor antagonist;
anti-arrhythmia drug;
antihypertensive agent;
endothelin receptor antagonist
loxapine
Loxapine: An antipsychotic agent used in SCHIZOPHRENIA.		3.2310dibenzooxazepineantipsychotic agent;
dopaminergic antagonist
maprotiline
Maprotiline: A bridged-ring tetracyclic antidepressant that is both mechanistically and functionally similar to the tricyclic antidepressants, including side effects associated with its use.		3.2310anthracenes
mebendazole
Mebendazole: A benzimidazole that acts by interfering with CARBOHYDRATE METABOLISM and inhibiting polymerization of MICROTUBULES.. mebendazole : A carbamate ester that is methyl 1H-benzimidazol-2-ylcarbamate substituted by a benzoyl group at position 5.		3.2310aromatic ketone;
benzimidazoles;
carbamate ester		antinematodal drug;
microtubule-destabilising agent;
tubulin modulator
mecamylamine
Mecamylamine: A nicotinic antagonist that is well absorbed from the gastrointestinal tract and crosses the blood-brain barrier. Mecamylamine has been used as a ganglionic blocker in treating hypertension, but, like most ganglionic blockers, is more often used now as a research tool.		3.2310primary aliphatic amine
mechlorethamine
nitrogen mustard : Compounds having two beta-haloalkyl groups bound to a nitrogen atom, as in (X-CH2-CH2)2NR.		3.2310nitrogen mustard;
organochlorine compound		alkylating agent
meclizine
Meclizine: A histamine H1 antagonist used in the treatment of motion sickness, vertigo, and nausea during pregnancy and radiation sickness.		3.2310diarylmethane
meclofenamic acid
Meclofenamic Acid: A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis.. meclofenamic acid : An aminobenzoic acid that is anthranilic acid in which one of the hydrogens attached to the nitrogen is replaced by a 2,6-dichloro-3-methylphenyl group. A non-steroidal anti-inflammatory drug, it is used as the sodium salt for the treatment of dysmenorrhoea (painful periods), osteoarthritis and rheumatoid arthritis.		3.2310aminobenzoic acid;
organochlorine compound;
secondary amino compound		analgesic;
anticonvulsant;
antineoplastic agent;
antipyretic;
antirheumatic drug;
EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-steroidal anti-inflammatory drug
mefenamic acid
Mefenamic Acid: A non-steroidal anti-inflammatory agent with analgesic, anti-inflammatory, and antipyretic properties. It is an inhibitor of cyclooxygenase.. mefenamic acid : An aminobenzoic acid that is anthranilic acid in which one of the hydrogens attached to the nitrogen is replaced by a 2,3-dimethylphenyl group. Although classed as a non-steroidal anti-inflammatory drug, its anti-inflammatory properties are considered to be minor. It is used to relieve mild to moderate pain, including headaches, dental pain, osteoarthritis and rheumatoid arthritis.		3.2310aminobenzoic acid;
secondary amino compound		analgesic;
antipyretic;
antirheumatic drug;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
environmental contaminant;
non-steroidal anti-inflammatory drug;
xenobiotic
memantine
[no description available]		3.2310adamantanes;
primary aliphatic amine		antidepressant;
antiparkinson drug;
dopaminergic agent;
neuroprotective agent;
NMDA receptor antagonist
mepenzolate
mepenzolic acid: anticholinergic, antispasmodic agent; RN given refers to parent cpd; structure		3.2310diarylmethane
meperidine
Meperidine: A narcotic analgesic that can be used for the relief of most types of moderate to severe pain, including postoperative pain and the pain of labor. Prolonged use may lead to dependence of the morphine type; withdrawal symptoms appear more rapidly than with morphine and are of shorter duration.. pethidine : A piperidinecarboxylate ester that is piperidine which is substituted by a methyl group at position 1 and by phenyl and ethoxycarbonyl groups at position 4. It is an analgesic which is used for the treatment of moderate to severe pain, including postoperative pain and labour pain.		3.2310ethyl ester;
piperidinecarboxylate ester;
tertiary amino compound		antispasmodic drug;
kappa-opioid receptor agonist;
mu-opioid receptor agonist;
opioid analgesic
mephenytoin
Mephenytoin: An anticonvulsant effective in tonic-clonic epilepsy (EPILEPSY, TONIC-CLONIC). It may cause blood dyscrasias.. mephenytoin : An imidazolidine-2,4-dione (hydantoin) in which the imidazolidine nucleus carries a methyl group at N-3 and has ethyl and phenyl substituents at C-5. An anticonvulsant, it is no longer available in the USA or the UK but is still studied largely because of its interesting hydroxylation polymorphism.		3.2310imidazolidine-2,4-dioneanticonvulsant
mepivacaine
Mepivacaine: A local anesthetic that is chemically related to BUPIVACAINE but pharmacologically related to LIDOCAINE. It is indicated for infiltration, nerve block, and epidural anesthesia. Mepivacaine is effective topically only in large doses and therefore should not be used by this route. (From AMA Drug Evaluations, 1994, p168). mepivacaine : A piperidinecarboxamide in which N-methylpipecolic acid and 2,6-dimethylaniline have combined to form the amide bond. It is used as a local amide-type anaesthetic.		3.2310piperidinecarboxamidedrug allergen;
local anaesthetic
meprobamate
Meprobamate: A carbamate with hypnotic, sedative, and some muscle relaxant properties, although in therapeutic doses reduction of anxiety rather than a direct effect may be responsible for muscle relaxation. Meprobamate has been reported to have anticonvulsant actions against petit mal seizures, but not against grand mal seizures (which may be exacerbated). It is used in the treatment of ANXIETY DISORDERS, and also for the short-term management of INSOMNIA but has largely been superseded by the BENZODIAZEPINES. (From Martindale, The Extra Pharmacopoeia, 30th ed, p603)		3.2310organic molecular entity
mesalamine
Mesalamine: An anti-inflammatory agent, structurally related to the SALICYLATES, which is active in INFLAMMATORY BOWEL DISEASE. It is considered to be the active moiety of SULPHASALAZINE. (From Martindale, The Extra Pharmacopoeia, 30th ed). mesalamine : A monohydroxybenzoic acid that is salicylic acid substituted by an amino group at the 5-position.		3.2310amino acid;
aromatic amine;
monocarboxylic acid;
monohydroxybenzoic acid;
phenols		non-steroidal anti-inflammatory drug
mesoridazine
Mesoridazine: A phenothiazine antipsychotic with effects similar to CHLORPROMAZINE.. mesoridazine : A phenothiazine substituted at position 2 (para to the S atom) by a methylsulfinyl group, and on the nitrogen by a 2-(1-methylpiperidin-2-yl)ethyl group.		3.2310phenothiazines;
sulfoxide;
tertiary amino compound		dopaminergic antagonist;
first generation antipsychotic
metaproterenol
Metaproterenol: A beta-2 adrenergic agonist used in the treatment of ASTHMA and BRONCHIAL SPASM.. orciprenaline : A racemate composed of equimolar amounts of (R)- and (S)-orciprenaline. Used (as its sulfate salt) to relax the airway muscles and improve breathing for patients suffering from asthma or bronchitis.. 5-[1-hydroxy-2-(isopropanylamino)ethyl]benzene-1,3-diol : A member of the class of resorcinols bearing an additional 1-hydroxy-2-(isopropanylamino)ethyl substituent at position 5 of resorcinol itself.		3.2310aralkylamino compound;
phenylethanolamines;
resorcinols;
secondary alcohol;
secondary amino compound
metformin
Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289). metformin : A member of the class of guanidines that is biguanide the carrying two methyl substituents at position 1.		4.0920guanidinesenvironmental contaminant;
geroprotector;
hypoglycemic agent;
xenobiotic
methadone
Methadone: A synthetic opioid that is used as the hydrochloride. It is an opioid analgesic that is primarily a mu-opioid agonist. It has actions and uses similar to those of MORPHINE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1082-3). methadone : A racemate comprising equimolar amounts of dextromethadone and levomethadone. It is a opioid analgesic which is used as a painkiller and as a substitute for heroin in the treatment of heroin addiction.. 6-(dimethylamino)-4,4-diphenylheptan-3-one : A ketone that is heptan-3-one substituted by a dimethylamino group at position 6 and two phenyl groups at position 4.		3.2310benzenes;
diarylmethane;
ketone;
tertiary amino compound
methazolamide
Methazolamide: A carbonic anhydrase inhibitor that is used as a diuretic and in the treatment of glaucoma.		3.2310sulfonamide;
thiadiazoles
methocarbamol
Methocarbamol: A centrally acting muscle relaxant whose mode of action has not been established. It is used as an adjunct in the symptomatic treatment of musculoskeletal conditions associated with painful muscle spasm. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1206). methocarbamol : A racemate comprising equimolar amounts of (R)- and (S)-methocarbamol. A centrally acting skeletal muscle relaxant, it is used as an adjunct in the short-term symptomatic treatment of painful muscle spasm. The (R)-enantiomer is more active than the (S)-enantiomer.. 2-hydroxy-3-(2-methoxyphenoxy)propyl carbamate : A carbamate ester that is glycerol in which one of the primary alcohol groups has been converted to its 2-methoxyphenyl ether while the other has been converted to the corresponding carbamate ester.		3.2310aromatic ether;
carbamate ester;
secondary alcohol
methoxsalen
Methoxsalen: A naturally occurring furocoumarin compound found in several species of plants, including Psoralea corylifolia. It is a photoactive substance that forms DNA ADDUCTS in the presence of ultraviolet A irradiation.. methoxsalen : A member of the class of psoralens that is 7H-furo[3,2-g]chromen-7-one in which the 9 position is substituted by a methoxy group. It is a constituent of the fruits of Ammi majus. Like other psoralens, trioxsalen causes photosensitization of the skin. It is administered topically or orally in conjunction with UV-A for phototherapy treatment of vitiligo and severe psoriasis.		3.2310aromatic ether;
psoralens		antineoplastic agent;
cross-linking reagent;
dermatologic drug;
photosensitizing agent;
plant metabolite
methyclothiazide
Methyclothiazide: A thiazide diuretic with properties similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p825)		3.2310benzothiadiazine
methylphenidate
Methylphenidate: A central nervous system stimulant used most commonly in the treatment of ATTENTION DEFICIT DISORDER in children and for NARCOLEPSY. Its mechanisms appear to be similar to those of DEXTROAMPHETAMINE. The d-isomer of this drug is referred to as DEXMETHYLPHENIDATE HYDROCHLORIDE.. methylphenidate : A racemate comprising equimolar amounts of the two threo isomers of methyl phenyl(piperidin-2-yl)acetate. A central stimulant and indirect-acting sympathomimetic, is used (generally as the hydrochloride salt) in the treatment of hyperactivity disorders in children and for the treatment of narcolepsy.. methyl phenyl(piperidin-2-yl)acetate : A amino acid ester that is methyl phenylacetate in which one of the hydrogens alpha to the carbonyl group is replaced by a piperidin-2-yl group.		3.2310beta-amino acid ester;
methyl ester;
piperidines
metoclopramide
Metoclopramide: A dopamine D2 antagonist that is used as an antiemetic.. metoclopramide : A member of the class of benzamides resulting from the formal condensation of 4-amino-5-chloro-2-methoxybenzoic acid with the primary amino group of N,N-diethylethane-1,2-diamine.		3.2310benzamides;
monochlorobenzenes;
substituted aniline;
tertiary amino compound		antiemetic;
dopaminergic antagonist;
environmental contaminant;
gastrointestinal drug;
xenobiotic
metolazone
Metolazone: A quinazoline-sulfonamide derived DIURETIC that functions by inhibiting SODIUM CHLORIDE SYMPORTERS.. metolazone : A quinazoline that consists of 1,2,3,4-tetrahydroquinazolin-4-one bearing additional methyl, 2-tolyl, sulfamyl and chloro substituents at positions 2, 3, 6 and 7 respectively. A quinazoline diuretic, with properties similar to thiazide diuretics.		3.2310organochlorine compound;
quinazolines;
sulfonamide		antihypertensive agent;
diuretic;
ion transport inhibitor
metoprolol
Metoprolol: A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.. metoprolol : A propanolamine that is 1-(propan-2-ylamino)propan-2-ol substituted by a 4-(2-methoxyethyl)phenoxy group at position 1.		3.2310aromatic ether;
propanolamine;
secondary alcohol;
secondary amino compound		antihypertensive agent;
beta-adrenergic antagonist;
environmental contaminant;
geroprotector;
xenobiotic
metronidazole
Metronidazole: A nitroimidazole used to treat AMEBIASIS; VAGINITIS; TRICHOMONAS INFECTIONS; GIARDIASIS; ANAEROBIC BACTERIA; and TREPONEMAL INFECTIONS.. metronidazole : A member of the class of imidazoles substituted at C-1, -2 and -5 with 2-hydroxyethyl, nitro and methyl groups respectively. It has activity against anaerobic bacteria and protozoa, and has a radiosensitising effect on hypoxic tumour cells. It may be given by mouth in tablets, or as the benzoate in an oral suspension. The hydrochloride salt can be used in intravenous infusions. Metronidazole is a prodrug and is selective for anaerobic bacteria due to their ability to intracellularly reduce the nitro group of metronidazole to give nitroso-containing intermediates. These can covalently bind to DNA, disrupting its helical structure, inducing DNA strand breaks and inhibiting bacterial nucleic acid synthesis, ultimately resulting in bacterial cell death.		3.2310C-nitro compound;
imidazoles;
primary alcohol		antiamoebic agent;
antibacterial drug;
antimicrobial agent;
antiparasitic agent;
antitrichomonal drug;
environmental contaminant;
prodrug;
radiosensitizing agent;
xenobiotic
metyrapone
Metyrapone: An inhibitor of the enzyme STEROID 11-BETA-MONOOXYGENASE. It is used as a test of the feedback hypothalamic-pituitary mechanism in the diagnosis of CUSHING SYNDROME.. metyrapone : An aromatic ketone that is 3,3-dimethylbutan-2-one in which the methyl groups at positions 1 and 4 are replaced by pyridin-3-yl groups. A steroid 11beta-monooxygenase (EC 1.14.15.4) inhibitor, it is used in the diagnosis of adrenal insufficiency.		3.2310aromatic ketoneantimetabolite;
diagnostic agent;
EC 1.14.15.4 (steroid 11beta-monooxygenase) inhibitor
mexiletine
Mexiletine: Antiarrhythmic agent pharmacologically similar to LIDOCAINE. It may have some anticonvulsant properties.. mexiletine : An aromatic ether which is 2,6-dimethylphenyl ether of 2-aminopropan-1-ol.		3.2310aromatic ether;
primary amino compound		anti-arrhythmia drug
midazolam
Midazolam: A short-acting hypnotic-sedative drug with anxiolytic and amnestic properties. It is used in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. The short duration and cardiorespiratory stability makes it useful in poor-risk, elderly, and cardiac patients. It is water-soluble at pH less than 4 and lipid-soluble at physiological pH.. midazolam : An imidazobenzodiazepine that is 4H-imidazo[1,5-a][1,4]benzodiazepine which is substituted by a methyl, 2-fluorophenyl and chloro groups at positions 1, 6 and 8, respectively.		3.2310imidazobenzodiazepine;
monofluorobenzenes;
organochlorine compound		anticonvulsant;
antineoplastic agent;
anxiolytic drug;
apoptosis inducer;
central nervous system depressant;
GABAA receptor agonist;
general anaesthetic;
muscle relaxant;
sedative
midodrine
Midodrine: An ethanolamine derivative that is an adrenergic alpha-1 agonist. It is used as a vasoconstrictor agent in the treatment of HYPOTENSION.. midodrine : An aromatic ether that is 1,4-dimethoxybenzene which is substituted at position 2 by a 2-(glycylamino)-1-hydroxyethyl group. A direct-acting sympathomimetic with selective alpha-adrenergic agonist activity, it is used (generally as its hydrochloride salt) as a peripheral vasoconstrictor in the treatment of certain hypotensive states. The main active moiety is its major metabolite, deglymidodrine.		3.2310amino acid amide;
aromatic ether;
secondary alcohol		alpha-adrenergic agonist;
prodrug;
sympathomimetic agent;
vasoconstrictor agent
milrinone
[no description available]		3.2310bipyridines;
nitrile;
pyridone		cardiotonic drug;
EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor;
platelet aggregation inhibitor;
vasodilator agent
minoxidil
Minoxidil: A potent direct-acting peripheral vasodilator (VASODILATOR AGENTS) that reduces peripheral resistance and produces a fall in BLOOD PRESSURE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p371). minoxidil : A pyrimidine N-oxide that is pyrimidine-2,4-diamine 3-oxide substituted by a piperidin-1-yl group at position 6.		3.2310dialkylarylamine;
tertiary amino compound
mirtazapine
Mirtazapine: A piperazinoazepine tetracyclic compound that enhances the release of NOREPINEPHRINE and SEROTONIN through blockage of presynaptic ALPHA-2 ADRENERGIC RECEPTORS. It also blocks both 5-HT2 and 5-HT3 serotonin receptors and is a potent HISTAMINE H1 RECEPTOR antagonist. It is used for the treatment of depression, and may also be useful for the treatment of anxiety disorders.		3.2310benzazepine;
tetracyclic antidepressant		alpha-adrenergic antagonist;
anxiolytic drug;
H1-receptor antagonist;
histamine antagonist;
oneirogen;
serotonergic antagonist
mitotane
Mitotane: A derivative of the insecticide DICHLORODIPHENYLDICHLOROETHANE that specifically inhibits cells of the adrenal cortex and their production of hormones. It is used to treat adrenocortical tumors and causes CNS damage, but no bone marrow depression.		3.2310diarylmethane
mitoxantrone
Mitoxantrone: An anthracenedione-derived antineoplastic agent.. mitoxantrone : A dihydroxyanthraquinone that is 1,4-dihydroxy-9,10-anthraquinone which is substituted by 6-hydroxy-1,4-diazahexyl groups at positions 5 and 8.		3.2310dihydroxyanthraquinoneanalgesic;
antineoplastic agent
modafinil
Modafinil: A benzhydryl acetamide compound, central nervous system stimulant, and CYP3A4 inducing agent that is used in the treatment of NARCOLEPSY and SLEEP WAKE DISORDERS.. modafinil : A racemate comprising equimolar amounts of armodafinil and (S)-modafinil. A central nervous system stimulant, it is used for the treatment of sleeping disorders such as narcolepsy, obstructive sleep apnoea, and shift-work sleep disorder. The optical enantiomers of modafinil have similar pharmacological actions in animals.. 2-[(diphenylmethyl)sulfinyl]acetamide : A sulfoxide that is dimethylsulfoxide in which two hydrogens attached to one of the methyl groups are replaced by phenyl groups, while one hydrogen attached to the other methyl group is replaced by a carbamoyl (aminocarbonyl) group.		3.2310monocarboxylic acid amide;
sulfoxide
moxisylyte
Moxisylyte: An alpha-adrenergic blocking agent that is used in Raynaud's disease. It is also used locally in the eye to reverse the mydriasis caused by phenylephrine and other sympathomimetic agents. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1312)		3.2310monoterpenoid
nabumetone
Nabumetone: A butanone non-steroidal anti-inflammatory drug and cyclooxygenase-2 (COX2) inhibitor that is used in the management of pain associated with OSTEOARTHRITIS and RHEUMATOID ARTHRITIS.. nabumetone : A methyl ketone that is 2-butanone in which one of the methyl hydrogens at position 4 is replaced by a 6-methoxy-2-naphthyl group. A prodrug that is converted to the active metabolite, 6-methoxy-2-naphthylacetic acid, following oral administration. It is shown to have a slightly lower risk of gastrointestinal side effects than most other non-steroidal anti-inflammatory drugs.		3.2310methoxynaphthalene;
methyl ketone		cyclooxygenase 2 inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
prodrug
nadolol
[no description available]		3.2310tetralins
nalidixic acid
[no description available]		3.23101,8-naphthyridine derivative;
monocarboxylic acid;
quinolone antibiotic		antibacterial drug;
antimicrobial agent;
DNA synthesis inhibitor
naratriptan
naratriptan: structure given in first source		3.2310heteroarylpiperidine;
sulfonamide;
tryptamines		serotonergic agonist;
vasoconstrictor agent
nefazodone
nefazodone: may be useful as an opiate adjunct		3.2310aromatic ether;
monochlorobenzenes;
N-alkylpiperazine;
N-arylpiperazine;
triazoles		alpha-adrenergic antagonist;
analgesic;
antidepressant;
serotonergic antagonist;
serotonin uptake inhibitor
nevirapine
Nevirapine: A potent, non-nucleoside reverse transcriptase inhibitor used in combination with nucleoside analogues for treatment of HIV INFECTIONS and AIDS.. nevirapine : A dipyridodiazepine that is 5,11-dihydro-6H-dipyrido[3,2-b:2',3'-e][1,4]diazepine which is substituted by methyl, oxo, and cyclopropyl groups at positions 4, 6, and 11, respectively. A non-nucleoside reverse transcriptase inhibitor with activity against HIV-1, it is used in combination with other antiretrovirals for the treatment of HIV infection.		3.2310cyclopropanes;
dipyridodiazepine		antiviral drug;
HIV-1 reverse transcriptase inhibitor
nialamide
Nialamide: An MAO inhibitor that is used as an antidepressive agent.		3.2310organonitrogen compound;
organooxygen compound
nicardipine
Nicardipine: A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents.. nicardipine : A racemate comprising equimolar amounts of (R)- and (S)-nicardipine. It is a calcium channel blocker which is used to treat hypertension.. 2-[benzyl(methyl)amino]ethyl methyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate : A dihydropyridine that is 1,4-dihydropyridine substituted by a methyl, {2-[benzyl(methyl)amino]ethoxy}carbonyl, 3-nitrophenyl, methoxycarbonyl and methyl groups at positions 2, 3, 4, 5 and 6, respectively.		3.2310benzenes;
C-nitro compound;
diester;
dihydropyridine;
methyl ester;
tertiary amino compound
nifedipine
Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.		3.2310C-nitro compound;
dihydropyridine;
methyl ester		calcium channel blocker;
human metabolite;
tocolytic agent;
vasodilator agent
nilutamide
[no description available]		3.2310(trifluoromethyl)benzenes;
C-nitro compound;
imidazolidinone		androgen antagonist;
antineoplastic agent
nimesulide
nimesulide: structure. nimesulide : An aromatic ether having phenyl and 2-methylsulfonamido-5-nitrophenyl as the two aryl groups.		3.2310aromatic ether;
C-nitro compound;
sulfonamide		cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
nimodipine
Nimodipine: A calcium channel blockader with preferential cerebrovascular activity. It has marked cerebrovascular dilating effects and lowers blood pressure.. nimodipine : A dihydropyridine that is 1,4-dihydropyridine which is substituted by methyl groups at positions 2 and 6, a (2-methoxyethoxy)carbonyl group at position 3, a m-nitrophenyl group at position 4, and an isopropoxycarbonyl group at position 5. An L-type calcium channel blocker, it acts particularly on cerebral circulation, and is used both orally and intravenously for the prevention and treatment of subarachnoid hemorrhage from ruptured intracranial aneurysm.		3.23102-methoxyethyl ester;
C-nitro compound;
dicarboxylic acids and O-substituted derivatives;
diester;
dihydropyridine;
isopropyl ester		antihypertensive agent;
calcium channel blocker;
cardiovascular drug;
vasodilator agent
nisoldipine
Nisoldipine: A dihydropyridine calcium channel antagonist that acts as a potent arterial vasodilator and antihypertensive agent. It is also effective in patients with cardiac failure and angina.. nisoldipine : A racemate consisting of equimolar amounts of (R)- and (S)-nisoldipine. A calcium channel blocker, it is used in the treatment of hypertension and angina pectoris.. methyl 2-methylpropyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate : A dihydropyridine that is 1,4-dihydropyridine which is substituted by methyl groups at positions 2 and 6, a methoxycarbonyl group at position 3, an o-nitrophenyl group at position 4, and an isobutoxycarbonyl group at position 5. The racemate, a calcium channel blocker, is used in the treatment of hypertension and angina pectoris.		3.2310C-nitro compound;
dicarboxylic acids and O-substituted derivatives;
diester;
dihydropyridine;
methyl ester
nitroglycerin
Nitroglycerin: A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.. nitroglycerol : A nitrate ester that is glycerol in which nitro group(s) replace the hydrogen(s) attached to one or more of the hydroxy groups.. nitroglycerin : A nitroglycerol that is glycerol in which the hydrogen atoms of all three hydroxy groups are replaced by nitro groups. It acts as a prodrug, releasing nitric oxide to open blood vessels and so alleviate heart pain.		3.2310nitroglycerolexplosive;
muscle relaxant;
nitric oxide donor;
prodrug;
tocolytic agent;
vasodilator agent;
xenobiotic
nizatidine
[no description available]		3.23101,3-thiazoles;
C-nitro compound;
carboxamidine;
organic sulfide;
tertiary amino compound		anti-ulcer drug;
cholinergic drug;
H2-receptor antagonist
nomifensine
Nomifensine: An isoquinoline derivative that prevents dopamine reuptake into synaptosomes. The maleate was formerly used in the treatment of depression. It was withdrawn worldwide in 1986 due to the risk of acute hemolytic anemia with intravascular hemolysis resulting from its use. In some cases, renal failure also developed. (From Martindale, The Extra Pharmacopoeia, 30th ed, p266). nomifensine : An N-methylated tetrahydroisoquinoline carrying phenyl and amino substituents at positions C-4 and C-8, respectively.		3.2310isoquinolinesdopamine uptake inhibitor
norfloxacin
Norfloxacin: A synthetic fluoroquinolone (FLUOROQUINOLONES) with broad-spectrum antibacterial activity against most gram-negative and gram-positive bacteria. Norfloxacin inhibits bacterial DNA GYRASE.. norfloxacin : A quinolinemonocarboxylic acid with broad-spectrum antibacterial activity against most gram-negative and gram-positive bacteria. Norfloxacin is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase.		3.2310fluoroquinolone antibiotic;
N-arylpiperazine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antibacterial drug;
DNA synthesis inhibitor;
environmental contaminant;
xenobiotic
nortriptyline
Nortriptyline: A metabolite of AMITRIPTYLINE that is also used as an antidepressive agent. Nortriptyline is used in major depression, dysthymia, and atypical depressions.. nortriptyline : An organic tricyclic compound that is 10,11-dihydro-5H-dibenzo[a,d][7]annulene substituted by a 3-(methylamino)propylidene group at position 5. It is an active metabolite of amitriptyline.		3.2310organic tricyclic compound;
secondary amine		adrenergic uptake inhibitor;
analgesic;
antidepressant;
antineoplastic agent;
apoptosis inducer;
drug metabolite
ofloxacin
Ofloxacin: A synthetic fluoroquinolone antibacterial agent that inhibits the supercoiling activity of bacterial DNA GYRASE, halting DNA REPLICATION.. 9-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid : An oxazinoquinoline that is 2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinolin-7-one substituted by methyl, carboxy, fluoro, and 4-methylpiperazin-1-yl groups at positions 3, 6, 9, and 10, respectively.. ofloxacin : A racemate comprising equimolar amounts of levofloxacin and dextrofloxacin. It is a synthetic fluoroquinolone antibacterial agent which inhibits the supercoiling activity of bacterial DNA gyrase, halting DNA replication.		3.23103-oxo monocarboxylic acid;
N-arylpiperazine;
N-methylpiperazine;
organofluorine compound;
oxazinoquinoline
omeprazole
Omeprazole: A 4-methoxy-3,5-dimethylpyridyl, 5-methoxybenzimidazole derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits an H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.. omeprazole : A racemate comprising equimolar amounts of (R)- and (S)-omeprazole.. 5-methoxy-2-{[(4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl}-1H-benzimidazole : A member of the class of benzimidazoles that is 1H-benzimidazole which is substituted by a [4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl group at position 2 and a methoxy group at position 5.		3.2310aromatic ether;
benzimidazoles;
pyridines;
sulfoxide
ondansetron
Ondansetron: A competitive serotonin type 3 receptor antagonist. It is effective in the treatment of nausea and vomiting caused by cytotoxic chemotherapy drugs, including cisplatin, and has reported anxiolytic and neuroleptic properties.		3.2310carbazoles
orphenadrine
Orphenadrine: A muscarinic antagonist used to treat drug-induced parkinsonism and to relieve pain from muscle spasm.. orphenadrine : A tertiary amino compound which is the phenyl-o-tolylmethyl ether of 2-(dimethylamino)ethanol.		3.2310ether;
tertiary amino compound		antidyskinesia agent;
antiparkinson drug;
H1-receptor antagonist;
muscarinic antagonist;
muscle relaxant;
NMDA receptor antagonist;
parasympatholytic
oxaprozin
Oxaprozin: An oxazole-propionic acid derivative, cyclooxygenase inhibitor, and non-steroidal anti-inflammatory drug that is used in the treatment of pain and inflammation associated with of OSTEOARTHRITIS; RHEUMATOID ARTHRITIS; and ARTHRITIS, JUVENILE.. oxaprozin : A monocarboxylic acid that is a propionic acid derivative having a 4,5-diphenyl-1,3-oxazol-2-yl substituent at position 3. It is non-steroidal anti-inflammatory drug commonly used to relieve the pain and inflammatory responses associated with osteoarthritis and rheumatoid arthritis.		3.23101,3-oxazoles;
monocarboxylic acid		analgesic;
non-steroidal anti-inflammatory drug
oxazepam
Oxazepam: A benzodiazepine used in the treatment of anxiety, alcohol withdrawal, and insomnia.. oxazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a chloro group at position 7, a hydroxy group at position 3 and phenyl group at position 5.		3.23101,4-benzodiazepinone;
organochlorine compound		anxiolytic drug;
environmental contaminant;
xenobiotic
oxybutynin
oxybutynin: RN given refers to parent cpd. oxybutynin : A racemate comprising equimolar amounts of (R)-oxybutynin and esoxybutynin. An antispasmodic used for the treatment of overactive bladder.		3.2310acetylenic compound;
carboxylic ester;
racemate;
tertiary alcohol;
tertiary amino compound		antispasmodic drug;
calcium channel blocker;
local anaesthetic;
muscarinic antagonist;
muscle relaxant;
parasympatholytic
aminosalicylic acid
Aminosalicylic Acid: An antitubercular agent often administered in association with ISONIAZID. The sodium salt of the drug is better tolerated than the free acid.. 4-aminosalicylic acid : An aminobenzoic acid that is salicylic acid substituted by an amino group at position 4.		3.2310aminobenzoic acid;
phenols		antitubercular agent
pamidronate
[no description available]		3.2310phosphonoacetic acid
pantoprazole
Pantoprazole: 2-pyridinylmethylsulfinylbenzimidazole proton pump inhibitor that is used in the treatment of GASTROESOPHAGEAL REFLUX and PEPTIC ULCER.. pantoprazole : A member of the class of benzimidazoles that is 1H-benzimidazole substituted by a difluoromethoxy group at position 5 and a [(3,4-dimethoxypyridin-2-yl)methyl]sulfinyl group at position 2.		3.2310aromatic ether;
benzimidazoles;
organofluorine compound;
pyridines;
sulfoxide		anti-ulcer drug;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor;
environmental contaminant;
xenobiotic
papaverine
Papaverine: An alkaloid found in opium but not closely related to the other opium alkaloids in its structure or pharmacological actions. It is a direct-acting smooth muscle relaxant used in the treatment of impotence and as a vasodilator, especially for cerebral vasodilation. The mechanism of its pharmacological actions is not clear, but it apparently can inhibit phosphodiesterases and it may have direct actions on calcium channels.. papaverine : A benzylisoquinoline alkaloid that is isoquinoline substituted by methoxy groups at positions 6 and 7 and a 3,4-dimethoxybenzyl group at position 1. It has been isolated from Papaver somniferum.		3.2310benzylisoquinoline alkaloid;
dimethoxybenzene;
isoquinolines		antispasmodic drug;
vasodilator agent
pemoline
Pemoline: A central nervous system stimulant used in fatigue and depressive states and to treat hyperkinetic disorders in children.. pemoline : A member of the class of 1,3-oxazoles that is 1,3-oxazol-4(5H)-one which is substituted by an amino group at position 2 and by a phenyl group at position 5. A central nervous system stimulant, it was used to treat hyperactivity disorders in children, but withdrawn from use following reports of serious hepatotoxicity.		3.23101,3-oxazolescentral nervous system stimulant
pentamidine
Pentamidine: Antiprotozoal agent effective in trypanosomiasis, leishmaniasis, and some fungal infections; used in treatment of PNEUMOCYSTIS pneumonia in HIV-infected patients. It may cause diabetes mellitus, central nervous system damage, and other toxic effects.. pentamidine : A diether consisting of pentane-1,5-diol in which both hydroxyl hydrogens have been replaced by 4-amidinophenyl groups. A trypanocidal drug that is used for treatment of cutaneous leishmaniasis and Chagas disease.		3.2310aromatic ether;
carboxamidine;
diether		anti-inflammatory agent;
antifungal agent;
calmodulin antagonist;
chemokine receptor 5 antagonist;
EC 2.3.1.48 (histone acetyltransferase) inhibitor;
NMDA receptor antagonist;
S100 calcium-binding protein B inhibitor;
trypanocidal drug;
xenobiotic
pentobarbital
Pentobarbital: A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236). pentobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by ethyl and sec-pentyl groups.		3.2310barbituratesGABAA receptor agonist
pentoxifylline
[no description available]		3.2310oxopurine
perhexiline
Perhexiline: 2-(2,2-Dicyclohexylethyl)piperidine. Coronary vasodilator used especially for angina of effort. It may cause neuropathy and hepatitis.		3.2310piperidinescardiovascular drug
perphenazine
Perphenazine: An antipsychotic phenothiazine derivative with actions and uses similar to those of CHLORPROMAZINE.. perphenazine : A phenothiazine derivative in which the phenothiazine tricycle carries a chloro substituent at the 2-position and a 3-[4-(2-hydroxyethyl)piperazin-1-yl]propyl group at N-10.		3.2310N-(2-hydroxyethyl)piperazine;
N-alkylpiperazine;
organochlorine compound;
phenothiazines		antiemetic;
dopaminergic antagonist;
phenothiazine antipsychotic drug
phenobarbital
Phenobarbital: A barbituric acid derivative that acts as a nonselective central nervous system depressant. It potentiates GAMMA-AMINOBUTYRIC ACID action on GABA-A RECEPTORS, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations.. phenobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by ethyl and phenyl groups.		3.2310barbituratesanticonvulsant;
drug allergen;
excitatory amino acid antagonist;
sedative
phenoxybenzamine
Phenoxybenzamine: An alpha-adrenergic antagonist with long duration of action. It has been used to treat hypertension and as a peripheral vasodilator.		3.2310aromatic amine
phentermine
Phentermine: A central nervous system stimulant and sympathomimetic with actions and uses similar to those of DEXTROAMPHETAMINE. It has been used most frequently in the treatment of obesity.		3.2310primary amineadrenergic agent;
appetite depressant;
central nervous system drug;
central nervous system stimulant;
dopaminergic agent;
sympathomimetic agent
4-phenylbutyric acid
4-phenylbutyric acid: RN refers to the parent cpd. 4-phenylbutyric acid : A monocarboxylic acid the structure of which is that of butyric acid substituted with a phenyl group at C-4. It is a histone deacetylase inhibitor that displays anticancer activity. It inhibits cell proliferation, invasion and migration and induces apoptosis in glioma cells. It also inhibits protein isoprenylation, depletes plasma glutamine, increases production of foetal haemoglobin through transcriptional activation of the gamma-globin gene and affects hPPARgamma activation.		3.2310monocarboxylic acidantineoplastic agent;
apoptosis inducer;
EC 3.5.1.98 (histone deacetylase) inhibitor;
prodrug
pindolol
Pindolol: A moderately lipophilic beta blocker (ADRENERGIC BETA-ANTAGONISTS). It is non-cardioselective and has intrinsic sympathomimetic actions, but little membrane-stabilizing activity. (From Martindale, The Extra Pharmocopoeia, 30th ed, p638). pindolol : A member of the class of indols which is the 2-hydroxy-3-(isopropylamino)propyl ether derivative of 1H-indol-4-ol.		3.2310indoles;
secondary amine		antiglaucoma drug;
antihypertensive agent;
beta-adrenergic antagonist;
serotonergic antagonist;
vasodilator agent
pioglitazone
Pioglitazone: A thiazolidinedione and PPAR GAMMA agonist that is used in the treatment of TYPE 2 DIABETES MELLITUS.. pioglitazone : A member of the class of thiazolidenediones that is 1,3-thiazolidine-2,4-dione substituted by a benzyl group at position 5 which in turn is substituted by a 2-(5-ethylpyridin-2-yl)ethoxy group at position 4 of the phenyl ring. It exhibits hypoglycemic activity.		3.2310aromatic ether;
pyridines;
thiazolidinediones		antidepressant;
cardioprotective agent;
EC 2.7.1.33 (pantothenate kinase) inhibitor;
EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
geroprotector;
hypoglycemic agent;
insulin-sensitizing drug;
PPARgamma agonist;
xenobiotic
polythiazide
[no description available]		3.2310benzothiadiazine
duodote
duodote: consists of atropine and pralidoxime chloride; for treating those exposed to organophosphorus-containing nerve agents		3.2310pyridinium ionantidote to organophosphate poisoning;
antidote to sarin poisoning;
cholinergic drug;
cholinesterase reactivator
praziquantel
azinox: Russian drug		3.2310isoquinolines
prazosin
Prazosin: A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.. prazosin : A member of the class of piperazines that is piperazine substituted by a furan-2-ylcarbonyl group and a 4-amino-6,7-dimethoxyquinazolin-2-yl group at positions 1 and 4 respectively.		3.2310aromatic ether;
furans;
monocarboxylic acid amide;
piperazines;
quinazolines		alpha-adrenergic antagonist;
antihypertensive agent;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
primaquine
Primaquine: An aminoquinoline that is given by mouth to produce a radical cure and prevent relapse of vivax and ovale malarias following treatment with a blood schizontocide. It has also been used to prevent transmission of falciparum malaria by those returning to areas where there is a potential for re-introduction of malaria. Adverse effects include anemias and GI disturbances. (From Martindale, The Extra Pharmacopeia, 30th ed, p404). primaquine : An N-substituted diamine that is pentane-1,4-diamine substituted by a 6-methoxyquinolin-8-yl group at the N(4) position. It is a drug used in the treatment of malaria and Pneumocystis pneumonia.		3.2310aminoquinoline;
aromatic ether;
N-substituted diamine		antimalarial
primidone
Primidone: A barbiturate derivative that acts as a GABA modulator and anti-epileptic agent. It is partly metabolized to PHENOBARBITAL in the body and owes some of its actions to this metabolite.. primidone : A pyrimidone that is dihydropyrimidine-4,6(1H,5H)-dione substituted by an ethyl and a phenyl group at position 5. It is used as an anticonvulsant for treatment of various types of seizures.		3.2310pyrimidoneanticonvulsant;
environmental contaminant;
xenobiotic
probenecid
Probenecid: The prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy.. probenecid : A sulfonamide in which the nitrogen of 4-sulfamoylbenzoic acid is substituted with two propyl groups.		3.2310benzoic acids;
sulfonamide		uricosuric drug
procainamide
Procainamide: A class Ia antiarrhythmic drug that is structurally-related to PROCAINE.. procainamide : A benzamide that is 4-aminobenzamide substituted on the amide N by a 2-(diethylamino)ethyl group. It is a pharmaceutical antiarrhythmic agent used for the medical treatment of cardiac arrhythmias.		3.2310benzamidesanti-arrhythmia drug;
platelet aggregation inhibitor;
sodium channel blocker
procarbazine
Procarbazine: An antineoplastic agent used primarily in combination with mechlorethamine, vincristine, and prednisone (the MOPP protocol) in the treatment of Hodgkin's disease.. procarbazine : A benzamide obtained by formal condensation of the carboxy group of 4-[(2-methylhydrazino)methyl]benzoic acid with the amino group of isopropylamine. An antineoplastic chemotherapy drug used for treatment of Hodgkin's lymphoma. Metabolism yields azo-procarbazine and hydrogen peroxide, which results in the breaking of DNA strands.		3.2310benzamides;
hydrazines		antineoplastic agent
prochlorperazine
Prochlorperazine: A phenothiazine antipsychotic used principally in the treatment of NAUSEA; VOMITING; and VERTIGO. It is more likely than CHLORPROMAZINE to cause EXTRAPYRAMIDAL DISORDERS. (From Martindale, The Extra Pharmacopoeia, 30th ed, p612). prochlorperazine : A member of the class of phenothiazines that is 10H-phenothiazine having a chloro substituent at the 2-position and a 3-(4-methylpiperazin-1-yl)propyl group at the N-10 position.		3.2310N-alkylpiperazine;
N-methylpiperazine;
organochlorine compound;
phenothiazines		alpha-adrenergic antagonist;
antiemetic;
cholinergic antagonist;
dopamine receptor D2 antagonist;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
first generation antipsychotic
procyclidine
Procyclidine: A muscarinic antagonist that crosses the blood-brain barrier and is used in the treatment of drug-induced extrapyramidal disorders and in parkinsonism.. procyclidine : A tertiary alcohol that consists of propan-1-ol substituted by a cyclohexyl and a phenyl group at position 1 and a pyrrolidin-1-yl group at position 3.		3.2310pyrrolidines;
tertiary alcohol		antidyskinesia agent;
antiparkinson drug;
muscarinic antagonist
promethazine
Promethazine: A phenothiazine derivative with histamine H1-blocking, antimuscarinic, and sedative properties. It is used as an antiallergic, in pruritus, for motion sickness and sedation, and also in animals.. promethazine : A tertiary amine that is a substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropan-2-amine moiety.		3.2310phenothiazines;
tertiary amine		anti-allergic agent;
anticoronaviral agent;
antiemetic;
antipruritic drug;
H1-receptor antagonist;
local anaesthetic;
sedative
propafenone
Propafenone: An antiarrhythmia agent that is particularly effective in ventricular arrhythmias. It also has weak beta-blocking activity.. propafenone : An aromatic ketone that is 3-(propylamino)propane-1,2-diol in which the hydrogen of the primary hydroxy group is replaced by a 2-(3-phenylpropanoyl)phenyl group. It is a class 1C antiarrhythmic drug with local anesthetic effects, and is used as the hydrochloride salt in the management of supraventricular and ventricular arrhythmias.		3.2310aromatic ketone;
secondary alcohol;
secondary amino compound		anti-arrhythmia drug
propantheline
Propantheline: A muscarinic antagonist used as an antispasmodic, in rhinitis, in urinary incontinence, and in the treatment of ulcers. At high doses it has nicotinic effects resulting in neuromuscular blocking.		3.2310xanthenes
propofol
Propofol: An intravenous anesthetic agent which has the advantage of a very rapid onset after infusion or bolus injection plus a very short recovery period of a couple of minutes. (From Smith and Reynard, Textbook of Pharmacology, 1992, 1st ed, p206). Propofol has been used as ANTICONVULSANTS and ANTIEMETICS.. propofol : A phenol resulting from the formal substitution of the hydrogen at the 2 position of 1,3-diisopropylbenzene by a hydroxy group.		3.2310phenolsanticonvulsant;
antiemetic;
intravenous anaesthetic;
radical scavenger;
sedative
propranolol
Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.. propranolol : A propanolamine that is propan-2-ol substituted by a propan-2-ylamino group at position 1 and a naphthalen-1-yloxy group at position 3.		3.2310naphthalenes;
propanolamine;
secondary amine		anti-arrhythmia drug;
antihypertensive agent;
anxiolytic drug;
beta-adrenergic antagonist;
environmental contaminant;
human blood serum metabolite;
vasodilator agent;
xenobiotic
protriptyline
Protriptyline: Tricyclic antidepressant similar in action and side effects to IMIPRAMINE. It may produce excitation.		3.2310carbotricyclic compoundantidepressant
pyridostigmine
[no description available]		3.2310pyridinium ion
pyrimethamine
Maloprim: contains above 2 cpds		3.2310aminopyrimidine;
monochlorobenzenes		antimalarial;
antiprotozoal drug;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor
sch 16134
quazepam: structure given in first source		3.2310benzodiazepine
quetiapine
[no description available]		3.2310dibenzothiazepine;
N-alkylpiperazine;
N-arylpiperazine		adrenergic antagonist;
dopaminergic antagonist;
histamine antagonist;
second generation antipsychotic;
serotonergic antagonist
rabeprazole
Rabeprazole: A 4-(3-methoxypropoxy)-3-methylpyridinyl derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.		3.2310benzimidazoles;
pyridines;
sulfoxide		anti-ulcer drug;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor
raloxifene
raloxifene : A member of the class of 1-benzothiophenes that is 1-benzothiophene in which the hydrogens at positions 2, 3, and 6 have been replaced by p-hydroxyphenyl, p-[2-(piperidin-1-yl)ethoxy]benzoyl, and hydroxy groups, respectively.		3.23101-benzothiophenes;
aromatic ketone;
N-oxyethylpiperidine;
phenols		bone density conservation agent;
estrogen antagonist;
estrogen receptor modulator
riluzole
Riluzole: A glutamate antagonist (RECEPTORS, GLUTAMATE) used as an anticonvulsant (ANTICONVULSANTS) and to prolong the survival of patients with AMYOTROPHIC LATERAL SCLEROSIS.		3.2310benzothiazoles
rimantadine
Rimantadine: An RNA synthesis inhibitor that is used as an antiviral agent in the prophylaxis and treatment of influenza.		3.2310alkylamine
risperidone
Risperidone: A selective blocker of DOPAMINE D2 RECEPTORS and SEROTONIN 5-HT2 RECEPTORS that acts as an atypical antipsychotic agent. It has been shown to improve both positive and negative symptoms in the treatment of SCHIZOPHRENIA.. risperidone : A member of the class of pyridopyrimidines that is 2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one carrying an additional 2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl group at position 2.		3.23101,2-benzoxazoles;
heteroarylpiperidine;
organofluorine compound;
pyridopyrimidine		alpha-adrenergic antagonist;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
H1-receptor antagonist;
psychotropic drug;
second generation antipsychotic;
serotonergic antagonist
rizatriptan
rizatriptan: structure given in first source; RN given refers to benzoate		3.2310tryptaminesanti-inflammatory drug;
serotonergic agonist;
vasoconstrictor agent
ropinirole
[no description available]		3.2310indolones;
tertiary amine		antidyskinesia agent;
antiparkinson drug;
central nervous system drug;
dopamine agonist
salicylsalicylic acid
salicylsalicylic acid: structure. salsalate : A dimeric benzoate ester obtained by intermolecular condensation between the carboxy of one molecule of salicylic acid with the phenol group of a second. It is a prodrug for salycylic acid that is used for treatment of rheumatoid arthritis and osteoarthritis and also shows activity against type II diabetes.		3.2310benzoate ester;
benzoic acids;
phenols;
salicylates		antineoplastic agent;
antirheumatic drug;
EC 3.5.2.6 (beta-lactamase) inhibitor;
hypoglycemic agent;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
prodrug
secobarbital
Secobarbital: A barbiturate that is used as a sedative. Secobarbital is reported to have no anti-anxiety activity.. secobarbital : A member of the class of barbiturates that is barbituric acid in which the hydrogens at position 5 are substituted by prop-2-en-1-yl and pentan-2-yl groups.		3.2310barbituratesanaesthesia adjuvant;
GABA modulator;
sedative
sibutramine
sibutramine: serotonin and norepinephrine transporter inhibitor; Meridia is tradename for sibutramine hydrochloride		3.2310organochlorine compound;
tertiary amino compound		anti-obesity agent;
serotonin uptake inhibitor
sulfadiazine
Sulfadiazine: One of the short-acting SULFONAMIDES used in combination with PYRIMETHAMINE to treat toxoplasmosis in patients with acquired immunodeficiency syndrome and in newborns with congenital infections.. sulfadiazine : A sulfonamide consisting of pyrimidine with a 4-aminobenzenesulfonamido group at the 2-position.. diazine : The parent structure of the diazines.		3.2310pyrimidines;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
antimicrobial agent;
antiprotozoal drug;
coccidiostat;
drug allergen;
EC 1.1.1.153 [sepiapterin reductase (L-erythro-7,8-dihydrobiopterin forming)] inhibitor;
EC 2.5.1.15 (dihydropteroate synthase) inhibitor;
environmental contaminant;
xenobiotic
risedronic acid
Risedronic Acid: A pyridine and diphosphonic acid derivative that acts as a CALCIUM CHANNEL BLOCKER and inhibits BONE RESORPTION.		3.2310pyridines
sotalol
Sotalol: An adrenergic beta-antagonist that is used in the treatment of life-threatening arrhythmias.. sotalol : A sulfonamide that is N-phenylmethanesulfonamide in which the phenyl group is substituted at position 4 by a 1-hydroxy-2-(isopropylamino)ethyl group. It has both beta-adrenoreceptor blocking (Vaughan Williams Class II) and cardiac action potential duration prolongation (Vaughan Williams Class III) antiarrhythmic properties. It is used (usually as the hydrochloride salt) for the management of ventricular and supraventricular arrhythmias.		3.2310ethanolamines;
secondary alcohol;
secondary amino compound;
sulfonamide		anti-arrhythmia drug;
beta-adrenergic antagonist;
environmental contaminant;
xenobiotic
imatinib
[no description available]		3.2310aromatic amine;
benzamides;
N-methylpiperazine;
pyridines;
pyrimidines		antineoplastic agent;
apoptosis inducer;
tyrosine kinase inhibitor
vorinostat
Vorinostat: A hydroxamic acid and anilide derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used in the treatment of CUTANEOUS T-CELL LYMPHOMA and SEZARY SYNDROME.. vorinostat : A dicarboxylic acid diamide comprising suberic (octanedioic) acid coupled to aniline and hydroxylamine. A histone deacetylase inhibitor, it is marketed under the name Zolinza for the treatment of cutaneous T cell lymphoma (CTCL).		3.2310dicarboxylic acid diamide;
hydroxamic acid		antineoplastic agent;
apoptosis inducer;
EC 3.5.1.98 (histone deacetylase) inhibitor
succinylcholine
Succinylcholine: A quaternary skeletal muscle relaxant usually used in the form of its bromide, chloride, or iodide. It is a depolarizing relaxant, acting in about 30 seconds and with a duration of effect averaging three to five minutes. Succinylcholine is used in surgical, anesthetic, and other procedures in which a brief period of muscle relaxation is called for.. succinylcholine : A quaternary ammonium ion that is the bis-choline ester of succinic acid.		3.2310quaternary ammonium ion;
succinate ester		drug allergen;
muscle relaxant;
neuromuscular agent
sulfamethizole
Sulfamethizole: A sulfathiazole antibacterial agent.. sulfamethizole : A sulfonamide consisting of a 1,3,4-thiadiazole nucleus with a methyl substituent at C-5 and a 4-aminobenzenesulfonamido group at C-2.		3.2310sulfonamide antibiotic;
sulfonamide;
thiadiazoles		antiinfective agent;
antimicrobial agent;
drug allergen;
EC 2.5.1.15 (dihydropteroate synthase) inhibitor
sulfasalazine
Sulfasalazine: A drug that is used in the management of inflammatory bowel diseases. Its activity is generally considered to lie in its metabolic breakdown product, 5-aminosalicylic acid (see MESALAMINE) released in the colon. (From Martindale, The Extra Pharmacopoeia, 30th ed, p907). sulfasalazine : An azobenzene consisting of diphenyldiazene having a carboxy substituent at the 4-position, a hydroxy substituent at the 3-position and a 2-pyridylaminosulphonyl substituent at the 4'-position.		3.2310
sulfathiazole
Sulfathiazole: A sulfathiazole compound that is used as a short-acting anti-infective agent. It is no longer commonly used systemically due to its toxicity, but may still be applied topically in combination with other drugs for the treatment of vaginal and skin infections, and is still used in veterinary medicine.. sulfathiazole : A 1,3-thiazole compound having a 4-aminobenzenesulfonamido group at the 2-position.		3.23101,3-thiazoles;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
drug allergen;
EC 2.5.1.15 (dihydropteroate synthase) inhibitor;
environmental contaminant;
xenobiotic
2-(octylamino)-1-[4-(propan-2-ylthio)phenyl]-1-propanol
[no description available]		3.2310alkylbenzene
sumatriptan
Sumatriptan: A serotonin agonist that acts selectively at 5HT1 receptors. It is used in the treatment of MIGRAINE DISORDERS.. sumatriptan : A sulfonamide that consists of N,N-dimethyltryptamine bearing an additional (N-methylsulfamoyl)methyl substituent at position 5. Selective agonist for a vascular 5-HT1 receptor subtype (probably a member of the 5-HT1D family). Used (in the form of its succinate salt) for the acute treatment of migraine with or without aura in adults.		3.2310sulfonamide;
tryptamines		serotonergic agonist;
vasoconstrictor agent
temazepam
Temazepam: A benzodiazepine that acts as a GAMMA-AMINOBUTYRIC ACID modulator and anti-anxiety agent.		3.2310benzodiazepine
temozolomide
[no description available]		3.2310imidazotetrazine;
monocarboxylic acid amide;
triazene derivative		alkylating agent;
antineoplastic agent;
prodrug
terazosin
Terazosin: induces decreased blood pressure; used in the treatment of benign prostatic hyperplasia		3.2310furans;
piperazines;
primary amino compound;
quinazolines		alpha-adrenergic antagonist;
antihypertensive agent;
antineoplastic agent
terbutaline
Terbutaline: A selective beta-2 adrenergic agonist used as a bronchodilator and tocolytic.. terbutaline : A member of the class of phenylethanolamines that is catechol substituted at position 5 by a 2-(tert-butylamino)-1-hydroxyethyl group.		3.2310phenylethanolamines;
resorcinols		anti-asthmatic drug;
beta-adrenergic agonist;
bronchodilator agent;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
hypoglycemic agent;
sympathomimetic agent;
tocolytic agent
thalidomide
Thalidomide: A piperidinyl isoindole originally introduced as a non-barbiturate hypnotic, but withdrawn from the market due to teratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppressive and anti-angiogenic activity. It inhibits release of TUMOR NECROSIS FACTOR-ALPHA from monocytes, and modulates other cytokine action.. thalidomide : A racemate comprising equimolar amounts of R- and S-thalidomide.. 2-(2,6-dioxopiperidin-3-yl)-1H-isoindole-1,3(2H)-dione : A dicarboximide that is isoindole-1,3(2H)-dione in which the hydrogen attached to the nitrogen is substituted by a 2,6-dioxopiperidin-3-yl group.		3.2310phthalimides;
piperidones
thiabendazole
Tresaderm: dermatologic soln containing dexamethasone, thiabendazole & neomycin sulfate		3.23101,3-thiazoles;
benzimidazole fungicide;
benzimidazoles		antifungal agrochemical;
antinematodal drug
thioridazine
Thioridazine: A phenothiazine antipsychotic used in the management of PHYCOSES, including SCHIZOPHRENIA.. thioridazine : A phenothiazine derivative having a methylsulfanyl subsitituent at the 2-position and a (1-methylpiperidin-2-yl)ethyl] group at the N-10 position.		3.2310phenothiazines;
piperidines		alpha-adrenergic antagonist;
dopaminergic antagonist;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
first generation antipsychotic;
H1-receptor antagonist;
serotonergic antagonist
thiotepa
Thiotepa: A very toxic alkylating antineoplastic agent also used as an insect sterilant. It causes skin, gastrointestinal, CNS, and bone marrow damage. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), thiotepa may reasonably be anticipated to be a carcinogen (Merck Index, 11th ed).		3.2310aziridines
ticlopidine
Ticlopidine: An effective inhibitor of platelet aggregation commonly used in the placement of STENTS in CORONARY ARTERIES.. ticlopidine : A thienopyridine that is 4,5,6,7-tetrahydrothieno[3,2-c]pyridine in which the hydrogen attached to the nitrogen is replaced by an o-chlorobenzyl group.		3.2310monochlorobenzenes;
thienopyridine		anticoagulant;
fibrin modulating drug;
hematologic agent;
P2Y12 receptor antagonist;
platelet aggregation inhibitor
tinidazole
Tinidazole: A nitroimidazole alkylating agent that is used as an antitrichomonal agent against TRICHOMONAS VAGINALIS; ENTAMOEBA HISTOLYTICA; and GIARDIA LAMBLIA infections. It also acts as an antibacterial agent for the treatment of BACTERIAL VAGINOSIS and anaerobic bacterial infections.. tinidazole : 1H-imidazole substituted at C-1 by a (2-ethylsulfonyl)ethyl group, at C-2 by a methyl group and at C-5 by a nitro group. It is used as an antiprotozoal, antibacterial agent.		3.2310imidazolesantiamoebic agent;
antibacterial drug;
antiparasitic agent;
antiprotozoal drug
tiopronin
Tiopronin: Sulfhydryl acylated derivative of GLYCINE.		3.2310N-acyl-amino acid
tizanidine
tizanidine: RN given refers to parent cpd; structure. tizanidine : 2,1,3-Benzothiadiazole substituted at C-4 by a Delta(1)-imidazolin-2-ylamino group and at C-4 by a chloro group. It is an agonist at alpha2-adrenergic receptor sites.		3.2310benzothiadiazole;
imidazoles		alpha-adrenergic agonist;
muscle relaxant
tolazamide
Tolazamide: A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE.. tolazamide : An N-sulfonylurea that is 1-tosylurea in which a hydrogen attached to the nitrogen at position 3 is replaced by an azepan-1-yl group. A hypoglycemic agent, it is used for the treatment of type 2 diabetes mellitus.		3.2310N-sulfonylureahypoglycemic agent;
potassium channel blocker
tolbutamide
Tolbutamide: A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290). tolbutamide : An N-sulfonylurea that consists of 1-butylurea having a tosyl group attached at the 3-position.		3.5720N-sulfonylureahuman metabolite;
hypoglycemic agent;
insulin secretagogue;
potassium channel blocker
tolmetin
Tolmetin: A non-steroidal anti-inflammatory agent (ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL) similar in mode of action to INDOMETHACIN.. tolmetin : A monocarboxylic acid that is (1-methylpyrrol-2-yl)acetic acid substituted at position 5 on the pyrrole ring by a 4-methylbenzoyl group. Used in the form of its sodium salt dihydrate as a nonselective nonsteroidal anti-inflammatory drug.		3.2310aromatic ketone;
monocarboxylic acid;
pyrroles		EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-steroidal anti-inflammatory drug
ultram
2-[(dimethylamino)methyl]-1-(3-methoxyphenyl)cyclohexanol : A tertiary alcohol that is cyclohexanol substituted at positions 1 and 2 by 3-methoxyphenyl and dimethylaminomethyl groups respectively.		3.2310aromatic ether;
tertiary alcohol;
tertiary amino compound
tranexamic acid
Tranexamic Acid: Antifibrinolytic hemostatic used in severe hemorrhage.		3.2310amino acid
trazodone
Trazodone: A serotonin uptake inhibitor that is used as an antidepressive agent. It has been shown to be effective in patients with major depressive disorders and other subsets of depressive disorders. It is generally more useful in depressive disorders associated with insomnia and anxiety. This drug does not aggravate psychotic symptoms in patients with schizophrenia or schizoaffective disorders. (From AMA Drug Evaluations Annual, 1994, p309). trazodone : An N-arylpiperazine in which one nitrogen is substituted by a 3-chlorophenyl group, while the other is substituted by a 3-(3-oxo[1,2,4]triazolo[4,3-a]pyridin-2(3H)-yl)propyl group.		3.2310monochlorobenzenes;
N-alkylpiperazine;
N-arylpiperazine;
triazolopyridine		adrenergic antagonist;
antidepressant;
anxiolytic drug;
H1-receptor antagonist;
sedative;
serotonin uptake inhibitor
triamterene
Triamterene: A pteridinetriamine compound that inhibits SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS.. triamterene : Pteridine substituted at positions 2, 4 and 7 with amino groups and at position 6 with a phenyl group. A sodium channel blocker, it is used as a diuretic in the treatment of hypertension and oedema.		3.2310pteridinesdiuretic;
sodium channel blocker
triazolam
Triazolam: A short-acting benzodiazepine used in the treatment of insomnia. Some countries temporarily withdrew triazolam from the market because of concerns about adverse reactions, mostly psychological, associated with higher dose ranges. Its use at lower doses with appropriate care and labeling has been reaffirmed by the FDA and most other countries.		3.2310triazolobenzodiazepinesedative
trifluoperazine
[no description available]		3.2310N-alkylpiperazine;
N-methylpiperazine;
organofluorine compound;
phenothiazines		antiemetic;
calmodulin antagonist;
dopaminergic antagonist;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor;
EC 5.3.3.5 (cholestenol Delta-isomerase) inhibitor;
phenothiazine antipsychotic drug
trihexyphenidyl
Trihexyphenidyl: One of the centrally acting MUSCARINIC ANTAGONISTS used for treatment of PARKINSONIAN DISORDERS and drug-induced extrapyramidal movement disorders and as an antispasmodic.		3.2310amine
trimethadione
Trimethadione: An anticonvulsant effective in absence seizures, but generally reserved for refractory cases because of its toxicity. (From AMA Drug Evaluations Annual, 1994, p378). trimethadione : An oxazolidinone that is 1,3-oxazolidine-2,4-dione substituted by methyl groups at positions 3, 5 and 5. It is an antiepileptic agent.		3.2310oxazolidinoneanticonvulsant;
geroprotector
trimethobenzamide
trimethobenzamide: major descriptor (64-84); on-line search BENZAMIDES (64-84); Index Medicus search TRIMETHOBENZAMIDE (64-84); RN given refers to parent cpd. trimethobenzamide : The amide obtained by formal condensation of 3,4,5-trihydroxybenzoic acid with 4-[2-(N,N-dimethylamino)ethoxy]benzylamine. It is used to prevent nausea and vomitting in humans.		3.2310benzamides;
tertiary amino compound		antiemetic
trimethoprim
Trimethoprim: A pyrimidine inhibitor of dihydrofolate reductase, it is an antibacterial related to PYRIMETHAMINE. It is potentiated by SULFONAMIDES and the TRIMETHOPRIM, SULFAMETHOXAZOLE DRUG COMBINATION is the form most often used. It is sometimes used alone as an antimalarial. TRIMETHOPRIM RESISTANCE has been reported.. trimethoprim : An aminopyrimidine antibiotic whose structure consists of pyrimidine 2,4-diamine and 1,2,3-trimethoxybenzene moieties linked by a methylene bridge.		3.2310aminopyrimidine;
methoxybenzenes		antibacterial drug;
diuretic;
drug allergen;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
environmental contaminant;
xenobiotic
trimetrexate
Trimetrexate: A nonclassical folic acid inhibitor through its inhibition of the enzyme dihydrofolate reductase. It is being tested for efficacy as an antineoplastic agent and as an antiparasitic agent against PNEUMOCYSTIS PNEUMONIA in AIDS patients. Myelosuppression is its dose-limiting toxic effect.		3.2310
trimipramine
Trimipramine: Tricyclic antidepressant similar to IMIPRAMINE, but with more antihistaminic and sedative properties.. trimipramine : A dibenzoazepine that is 10,11-dihydro-5H-dibenzo[b,f]azepine substituted by a 3-(dimethylamino)-2-methylpropyl group at the nitrogen atom. It is used as an antidepressant.		3.2310dibenzoazepine;
tertiary amino compound		antidepressant;
environmental contaminant;
xenobiotic
troglitazone
Troglitazone: A chroman and thiazolidinedione derivative that acts as a PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS (PPAR) agonist. It was formerly used in the treatment of TYPE 2 DIABETES MELLITUS, but has been withdrawn due to hepatotoxicity.		3.2310chromanes;
thiazolidinone		anticoagulant;
anticonvulsant;
antineoplastic agent;
antioxidant;
EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
hypoglycemic agent;
platelet aggregation inhibitor;
vasodilator agent
tyramine
[no description available]		3.2310monoamine molecular messenger;
primary amino compound;
tyramines		EC 3.1.1.8 (cholinesterase) inhibitor;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
neurotransmitter
delavirdine
Delavirdine: A potent, non-nucleoside reverse transcriptase inhibitor with activity specific for HIV-1.. delavirdine : The amide resulting from the formal condensation of 5-[(methylsulfonyl)amino]-1H-indole-2-carboxylic acid and 4-amino group of 1-[3-(isopropylamino)pyridin-2-yl]piperazine, delavirdine is a non-nucleoside reverse transcriptase inhibitor with activity specific for HIV-1. Viral resistance emerges rapidly when delavirdine is used alone, so it is therefore used (as the methanesulfonic acid salt) with other antiretrovirals for combination therapy of HIV infection.		3.2310aminopyridine;
indolecarboxamide;
N-acylpiperazine;
sulfonamide		antiviral drug;
HIV-1 reverse transcriptase inhibitor
venlafaxine
venlafaxine : A tertiary amino compound that is N,N-dimethylethanamine substituted at position 1 by a 1-hydroxycyclohexyl and 4-methoxyphenyl group.		3.2310cyclohexanols;
monomethoxybenzene;
tertiary alcohol;
tertiary amino compound		adrenergic uptake inhibitor;
analgesic;
antidepressant;
dopamine uptake inhibitor;
environmental contaminant;
serotonin uptake inhibitor;
xenobiotic
vigabatrin
[no description available]		3.2310gamma-amino acidanticonvulsant;
EC 2.6.1.19 (4-aminobutyrate--2-oxoglutarate transaminase) inhibitor
ici 204,219
zafirlukast: a leukotriene D4 receptor antagonist		3.2310carbamate ester;
indoles;
N-sulfonylcarboxamide		anti-asthmatic agent;
leukotriene antagonist
zaleplon
zaleplon: an azabicyclo(4.3.0)nonane; a nonbenzodiazepine; one of the so-called of Z drugs (zopiclone, eszopiclone, zolpidem, and zaleplon) for which there is some correlation with tumors; a hypnotic with less marked effect on psychomotor functions compared to lorazepam. zaleplon : A pyrazolo[1,5-a]pyrimidine having a nitrile group at position 3 and a 3-(N-ethylacetamido)phenyl substituent at the 7-position.		3.2310nitrile;
pyrazolopyrimidine		anticonvulsant;
anxiolytic drug;
central nervous system depressant;
sedative
zolpidem
Zolpidem: An imidazopyridine derivative and short-acting GABA-A receptor agonist that is used for the treatment of INSOMNIA.. zolpidem : An imidazo[1,2-a]pyridine compound having a 4-tolyl group at the 2-position, an N,N-dimethylcarbamoylmethyl group at the 3-position and a methyl substituent at the 6-position.		3.2310imidazopyridinecentral nervous system depressant;
GABA agonist;
sedative
zonisamide
Zonisamide: A benzisoxazole and sulfonamide derivative that acts as a CALCIUM CHANNEL blocker. It is used primarily as an adjunctive antiepileptic agent for the treatment of PARTIAL SEIZURES, with or without secondary generalization.. zonisamide : A 1,2-benzoxazole compound having a sulfamoylmethyl substituent at the 3-position.		3.23101,2-benzoxazoles;
sulfonamide		anticonvulsant;
antioxidant;
central nervous system drug;
protective agent;
T-type calcium channel blocker
cortisone acetate
Cortisone Acetate: The acetate ester of cortisone that is used mainly for replacement therapy in adrenocortical insufficiency and in the treatment of many allergic and inflammatory disorders.		3.2310corticosteroid hormone
mitomycin
Mitomycin: An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.. mitomycin : A family of aziridine-containing natural products isolated from Streptomyces caespitosus or Streptomyces lavendulae.		3.2310mitomycinalkylating agent;
antineoplastic agent
prednisolone
Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.. prednisolone : A glucocorticoid that is prednisone in which the oxo group at position 11 has been reduced to the corresponding beta-hydroxy group. It is a drug metabolite of prednisone.		3.231011beta-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
C21-steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		adrenergic agent;
anti-inflammatory drug;
antineoplastic agent;
drug metabolite;
environmental contaminant;
immunosuppressive agent;
xenobiotic
reserpine
Reserpine: An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria. Reserpine inhibits the uptake of norepinephrine into storage vesicles resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals. It has been used as an antihypertensive and an antipsychotic as well as a research tool, but its adverse effects limit its clinical use.. reserpine : An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria.		3.2310alkaloid ester;
methyl ester;
yohimban alkaloid		adrenergic uptake inhibitor;
antihypertensive agent;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
environmental contaminant;
first generation antipsychotic;
plant metabolite;
xenobiotic
phentolamine
Phentolamine: A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of RAYNAUD DISEASE and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease.. phentolamine : A substituted aniline that is 3-aminophenol in which the hydrogens of the amino group are replaced by 4-methylphenyl and 4,5-dihydro-1H-imidazol-2-ylmethyl groups respectively. An alpha-adrenergic antagonist, it is used for the treatment of hypertension.		3.2310imidazoles;
phenols;
substituted aniline;
tertiary amino compound		alpha-adrenergic antagonist;
vasodilator agent
sorbitol
D-glucitol : The D-enantiomer of glucitol (also known as D-sorbitol).		3.2310glucitolcathartic;
Escherichia coli metabolite;
food humectant;
human metabolite;
laxative;
metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite;
sweetening agent
thyroxine
Thyroxine: The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (MONOIODOTYROSINE) and the coupling of iodotyrosines (DIIODOTYROSINE) in the THYROGLOBULIN. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form TRIIODOTHYRONINE which exerts a broad spectrum of stimulatory effects on cell metabolism.. thyroxine : An iodothyronine compound having iodo substituents at the 3-, 3'-, 5- and 5'-positions.		3.23102-halophenol;
iodophenol;
L-phenylalanine derivative;
non-proteinogenic L-alpha-amino acid;
thyroxine zwitterion;
thyroxine		antithyroid drug;
human metabolite;
mouse metabolite;
thyroid hormone
dextroamphetamine
Dextroamphetamine: The d-form of AMPHETAMINE. It is a central nervous system stimulant and a sympathomimetic. It has also been used in the treatment of narcolepsy and of attention deficit disorders and hyperactivity in children. Dextroamphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulating release of monamines, and inhibiting monoamine oxidase. It is also a drug of abuse and a psychotomimetic.. (S)-amphetamine : A 1-phenylpropan-2-amine that has S configuration.		3.23101-phenylpropan-2-amineadrenergic agent;
adrenergic uptake inhibitor;
dopamine uptake inhibitor;
dopaminergic agent;
neurotoxin;
sympathomimetic agent
carbachol
Carbachol: A slowly hydrolyzed CHOLINERGIC AGONIST that acts at both MUSCARINIC RECEPTORS and NICOTINIC RECEPTORS.		2.2510ammonium salt;
carbamate ester		cardiotonic drug;
miotic;
muscarinic agonist;
nicotinic acetylcholine receptor agonist;
non-narcotic analgesic
spironolactone
Spironolactone: A potassium sparing diuretic that acts by antagonism of aldosterone in the distal renal tubules. It is used mainly in the treatment of refractory edema in patients with congestive heart failure, nephrotic syndrome, or hepatic cirrhosis. Its effects on the endocrine system are utilized in the treatments of hirsutism and acne but they can lead to adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p827). spironolactone : A steroid lactone that is 17alpha-pregn-4-ene-21,17-carbolactone substituted by an oxo group at position 3 and an alpha-acetylsulfanyl group at position 7.		3.23103-oxo-Delta(4) steroid;
oxaspiro compound;
steroid lactone;
thioester		aldosterone antagonist;
antihypertensive agent;
diuretic;
environmental contaminant;
xenobiotic
penicillamine
Penicillamine: 3-Mercapto-D-valine. The most characteristic degradation product of the penicillin antibiotics. It is used as an antirheumatic and as a chelating agent in Wilson's disease.. penicillamine : An alpha-amino acid having the structure of valine substituted at the beta position with a sulfanyl group.		3.2310non-proteinogenic alpha-amino acid;
penicillamine		antirheumatic drug;
chelator;
copper chelator;
drug allergen
cysteine
[no description available]		3.2310cysteine zwitterion;
cysteine;
L-alpha-amino acid;
proteinogenic amino acid;
serine family amino acid		EC 4.3.1.3 (histidine ammonia-lyase) inhibitor;
flour treatment agent;
human metabolite
prednisone
Prednisone: A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.. prednisone : A synthetic glucocorticoid drug that is particularly effective as an immunosuppressant, and affects virtually all of the immune system. Prednisone is a prodrug that is converted by the liver into prednisolone (a beta-hydroxy group instead of the oxo group at position 11), which is the active drug and also a steroid.		3.231011-oxo steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
C21-steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		adrenergic agent;
anti-inflammatory drug;
antineoplastic agent;
immunosuppressive agent;
prodrug
estrone
Hydroxyestrones: Estrone derivatives substituted with one or more hydroxyl groups in any position. They are important metabolites of estrone and other estrogens.		3.231017-oxo steroid;
3-hydroxy steroid;
phenolic steroid;
phenols		antineoplastic agent;
bone density conservation agent;
estrogen;
human metabolite;
mouse metabolite
oxandrolone
Oxandrolone: A synthetic hormone with anabolic and androgenic properties.		3.231017beta-hydroxy steroid;
3-oxo steroid;
anabolic androgenic steroid;
oxa-steroid		anabolic agent;
androgen
penicillin g
Penicillin G: A penicillin derivative commonly used in the form of its sodium or potassium salts in the treatment of a variety of infections. It is effective against most gram-positive bacteria and against gram-negative cocci. It has also been used as an experimental convulsant because of its actions on GAMMA-AMINOBUTYRIC ACID mediated synaptic transmission.. benzylpenicillin : A penicillin in which the substituent at position 6 of the penam ring is a phenylacetamido group.		3.2310penicillin allergen;
penicillin		antibacterial drug;
drug allergen;
epitope
pilocarpine
Pilocarpine: A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma.. (+)-pilocarpine : The (+)-enantiomer of pilocarpine.		3.2310pilocarpineantiglaucoma drug
triiodothyronine
Triiodothyronine: A T3 thyroid hormone normally synthesized and secreted by the thyroid gland in much smaller quantities than thyroxine (T4). Most T3 is derived from peripheral monodeiodination of T4 at the 5' position of the outer ring of the iodothyronine nucleus. The hormone finally delivered and used by the tissues is mainly T3.. 3,3',5-triiodo-L-thyronine : An iodothyronine compound having iodo substituents at the 3-, 3'- and 5-positions. Although some is produced in the thyroid, most of the 3,3',5-triiodo-L-thyronine in the body is generated by mono-deiodination of L-thyroxine in the peripheral tissues. Its metabolic activity is about 3 to 5 times that of L-thyroxine. The sodium salt is used in the treatment of hypothyroidism.		3.23102-halophenol;
amino acid zwitterion;
iodophenol;
iodothyronine		human metabolite;
mouse metabolite;
thyroid hormone
chloramphenicol
Amphenicol: Chloramphenicol and its derivatives.		3.2310C-nitro compound;
carboxamide;
diol;
organochlorine compound		antibacterial drug;
antimicrobial agent;
Escherichia coli metabolite;
geroprotector;
Mycoplasma genitalium metabolite;
protein synthesis inhibitor
glutamine
Glutamine: A non-essential amino acid present abundantly throughout the body and is involved in many metabolic processes. It is synthesized from GLUTAMIC ACID and AMMONIA. It is the principal carrier of NITROGEN in the body and is an important energy source for many cells.. L-glutamine : An optically active form of glutamine having L-configuration.. glutamine : An alpha-amino acid that consists of butyric acid bearing an amino substituent at position 2 and a carbamoyl substituent at position 4.		3.2310amino acid zwitterion;
glutamine family amino acid;
glutamine;
L-alpha-amino acid;
polar amino acid zwitterion;
proteinogenic amino acid		EC 1.14.13.39 (nitric oxide synthase) inhibitor;
Escherichia coli metabolite;
human metabolite;
metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
Saccharomyces cerevisiae metabolite
vincristine
[no description available]		3.2310acetate ester;
formamides;
methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
tertiary alcohol;
tertiary amino compound;
vinca alkaloid		antineoplastic agent;
drug;
microtubule-destabilising agent;
plant metabolite;
tubulin modulator
physostigmine
Physostigmine: A cholinesterase inhibitor that is rapidly absorbed through membranes. It can be applied topically to the conjunctiva. It also can cross the blood-brain barrier and is used when central nervous system effects are desired, as in the treatment of severe anticholinergic toxicity.		3.2310carbamate ester;
indole alkaloid		antidote to curare poisoning;
EC 3.1.1.8 (cholinesterase) inhibitor;
miotic
apomorphine
Apomorphine: A derivative of morphine that is a dopamine D2 agonist. It is a powerful emetic and has been used for that effect in acute poisoning. It has also been used in the diagnosis and treatment of parkinsonism, but its adverse effects limit its use.		3.2310aporphine alkaloidalpha-adrenergic drug;
antidyskinesia agent;
antiparkinson drug;
dopamine agonist;
emetic;
serotonergic drug
methyltestosterone
Methyltestosterone: A synthetic hormone used for androgen replacement therapy and as an hormonal antineoplastic agent (ANTINEOPLASTIC AGENTS, HORMONAL).. methyltestosterone : A 17beta-hydroxy steroid that is testosterone bearing a methyl group at the 17alpha position.		3.231017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
enone		anabolic agent;
androgen;
antineoplastic agent
tetrabenazine
9,10-dimethoxy-3-isobutyl-1,3,4,6,7,11b-hexahydro-2H-pyrido[2,1-a]isoquinolin-2-one : A benzoquinolizine that is 1,2,3,4,4a,9,10,10a-octahydrophenanthrene in which the carbon at position 10a is replaced by a nitrogen and which is substituted by an isobutyl group at position 2, an oxo group at position 3, and methoxy groups at positions 6 and 7.		3.2310benzoquinolizine;
cyclic ketone;
tertiary amino compound
kanamycin a
Kanamycin: Antibiotic complex produced by Streptomyces kanamyceticus from Japanese soil. Comprises 3 components: kanamycin A, the major component, and kanamycins B and C, the minor components.. kanamycin : Kanamycin is a naturally occurring antibiotic complex from Streptomyces kanamyceticus that consists of several components: kanamycin A, the major component (also usually designated as kanamycin), and kanamycins B, C, D and X the minor components.		3.2310kanamycinsbacterial metabolite
edetic acid
Edetic Acid: A chelating agent that sequesters a variety of polyvalent cations such as CALCIUM. It is used in pharmaceutical manufacturing and as a food additive.		3.2310ethylenediamine derivative;
polyamino carboxylic acid;
tetracarboxylic acid		anticoagulant;
antidote;
chelator;
copper chelator;
geroprotector
cysteamine
Cysteamine: A mercaptoethylamine compound that is endogenously derived from the COENZYME A degradative pathway. The fact that cysteamine is readily transported into LYSOSOMES where it reacts with CYSTINE to form cysteine-cysteamine disulfide and CYSTEINE has led to its use in CYSTINE DEPLETING AGENTS for the treatment of CYSTINOSIS.. cysteamine : An amine that consists of an ethane skeleton substituted with a thiol group at C-1 and an amino group at C-2.		3.2310amine;
thiol		geroprotector;
human metabolite;
mouse metabolite;
radiation protective agent
acetylcholine chloride
acetylcholine chloride : The chloride salt of acetylcholine, and a parasympatomimetic drug.		3.2310quaternary ammonium salt
phlorhizin
[no description available]		3.1410aryl beta-D-glucoside;
dihydrochalcones;
monosaccharide derivative		antioxidant;
plant metabolite
mepazine
mepazine: major descriptor (66-85); on-line search PHENOTHIAZINES (66-85); Index Medicus search MEPAZINE (66-85); RN given refers to parent cpd. pacatal : A phenothiazine derivative in which 10H-phenothiazine has an N-methylpiperidin-4-ylmethyl substituent at the N-10 position.		3.2310phenothiazines
cloxacillin
Cloxacillin: A semi-synthetic antibiotic that is a chlorinated derivative of OXACILLIN.. cloxacillin : A semisynthetic penicillin antibiotic carrying a 3-(2-chlorophenyl)-5-methylisoxazole-4-carboxamido group at position 6.		3.2310penicillin allergen;
penicillin;
semisynthetic derivative		antibacterial agent;
antibacterial drug
calcium acetate
calcium acetate: a principal compound used as phosphate binders in patients with chronic renal failure; used like sevelamer. calcium acetate : The calcium salt of acetic acid. It is used, commonly as a hydrate, to treat hyperphosphataemia (excess phosphate in the blood) in patients with kidney disease: the calcium ion combines with dietary phosphate to form (insoluble) calcium phosphate, which is excreted in the faeces.		3.2310calcium saltchelator
methionine
Methionine: A sulfur-containing essential L-amino acid that is important in many body functions.. methionine : A sulfur-containing amino acid that is butyric acid bearing an amino substituent at position 2 and a methylthio substituent at position 4.		3.2310aspartate family amino acid;
L-alpha-amino acid;
methionine zwitterion;
methionine;
proteinogenic amino acid		antidote to paracetamol poisoning;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical
colchicine
(S)-colchicine : A colchicine that has (S)-configuration. It is a secondary metabolite, has anti-inflammatory properties and is used to treat gout, crystal-induced joint inflammation, familial Mediterranean fever, and many other conditions.		3.2310alkaloid;
colchicine		anti-inflammatory agent;
gout suppressant;
mutagen
mebanazine
mebanazine: RN given refers to parent cpd without isomeric designation; structure		3.2310benzenes
oxacillin
Oxacillin: An antibiotic similar to FLUCLOXACILLIN used in resistant staphylococci infections.. oxacillin : A penicillin antibiotic carrying a 5-methyl-3-phenylisoxazole-4-carboxamide group at position 6beta.		3.2310penicillinantibacterial agent;
antibacterial drug
cycloserine
Cycloserine: Antibiotic substance produced by Streptomyces garyphalus.. D-cycloserine : A 4-amino-1,2-oxazolidin-3-one that has R configuration. It is an antibiotic produced by Streptomyces garyphalus or S. orchidaceus and is used as part of a multi-drug regimen for the treatment of tuberculosis when resistance to, or toxicity from, primary drugs has developed. An analogue of D-alanine, it interferes with bacterial cell wall synthesis in the cytoplasm by competitive inhibition of L-alanine racemase (which forms D-alanine from L-alanine) and D-alanine--D-alanine ligase (which incorporates D-alanine into the pentapeptide required for peptidoglycan formation and bacterial cell wall synthesis).		3.23104-amino-1,2-oxazolidin-3-one;
organonitrogen heterocyclic antibiotic;
organooxygen heterocyclic antibiotic;
zwitterion		antiinfective agent;
antimetabolite;
antitubercular agent;
metabolite;
NMDA receptor agonist
benziodarone
benziodarone: minor descriptor (75-89); on-line & INDEX MEDICUS search BENZOFURANS (68-89) & IODOBENZOATES (74)		3.2310aromatic ketone
ampicillin
Ampicillin: Semi-synthetic derivative of penicillin that functions as an orally active broad-spectrum antibiotic.. ampicillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-amino-2-phenylacetamido group.		3.2310beta-lactam antibiotic;
penicillin allergen;
penicillin		antibacterial drug
mannitol
[no description available]		3.2310mannitolallergen;
antiglaucoma drug;
compatible osmolytes;
Escherichia coli metabolite;
food anticaking agent;
food bulking agent;
food humectant;
food stabiliser;
food thickening agent;
hapten;
metabolite;
osmotic diuretic;
sweetening agent
cytarabine
[no description available]		3.2310beta-D-arabinoside;
monosaccharide derivative;
pyrimidine nucleoside		antimetabolite;
antineoplastic agent;
antiviral agent;
immunosuppressive agent
arginine
Arginine: An essential amino acid that is physiologically active in the L-form.. arginine : An alpha-amino acid that is glycine in which the alpha-is substituted by a 3-guanidinopropyl group.		3.2310arginine;
glutamine family amino acid;
L-alpha-amino acid;
proteinogenic amino acid		biomarker;
Escherichia coli metabolite;
micronutrient;
mouse metabolite;
nutraceutical
perflutren
Definity: a fluorocarbon-filled ultrasonic contrast agent; Definity is tradename. octafluoropropane : A fluorocarbon that is propane in which all of the hydrogens have been replaced by fluorines.		3.2310fluoroalkane;
fluorocarbon
fluoxymesterone
Fluoxymesterone: An anabolic steroid that has been used in the treatment of male HYPOGONADISM, delayed puberty in males, and in the treatment of breast neoplasms in women.		3.231011beta-hydroxy steroid;
17beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
anabolic androgenic steroid;
fluorinated steroid		anabolic agent;
antineoplastic agent
methsuximide
methsuximide: anticonvulsant effective in petit mal & psychomotor epilepsy; has a number of unpleasant & toxic side effects; minor descriptor (75-86); on-line & INDEX MEDICUS search SUCCINIMIDES (75-86); RN given refers to parent cpd without isomeric designation		3.2310organic molecular entity
tromethamine
Tromethamine: An organic amine proton acceptor. It is used in the synthesis of surface-active agents and pharmaceuticals; as an emulsifying agent for cosmetic creams and lotions, mineral oil and paraffin wax emulsions, as a biological buffer, and used as an alkalizer. (From Merck, 11th ed; Martindale, The Extra Pharmacopoeia, 30th ed, p1424)		3.2310primary amino compound;
triol		buffer
methylprednisolone
Methylprednisolone: A PREDNISOLONE derivative with similar anti-inflammatory action.. 6alpha-methylprednisolone : The 6alpha-stereoisomer of 6-methylprednisolone.		3.23106-methylprednisolone;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		adrenergic agent;
anti-inflammatory drug;
antiemetic;
environmental contaminant;
neuroprotective agent;
xenobiotic
brompheniramine
Brompheniramine: Histamine H1 antagonist used in treatment of allergies, rhinitis, and urticaria.. brompheniramine : Pheniramine in which the hydrogen at position 4 of the phenyl substituent is substituted by bromine. A histamine H1 receptor antagonist, brompheniramine is used (commonly as its maleate salt) for the symptomatic relief of allergic conditions, including rhinitis and conjunctivitis.		3.2310organobromine compound;
pyridines		anti-allergic agent;
H1-receptor antagonist
penicillin v
Penicillin V: A broad-spectrum penicillin antibiotic used orally in the treatment of mild to moderate infections by susceptible gram-positive organisms.. phenoxymethylpenicillin : A penicillin compound having a 6beta-(phenoxyacetyl)amino side-chain.		3.2310penicillin allergen;
penicillin
isosorbide dinitrate
Isosorbide Dinitrate: A vasodilator used in the treatment of ANGINA PECTORIS. Its actions are similar to NITROGLYCERIN but with a slower onset of action.		3.2310glucitol derivative;
nitrate ester		nitric oxide donor;
vasodilator agent
pseudoephedrine
Pseudoephedrine: A phenethylamine that is an isomer of EPHEDRINE which has less central nervous system effects and usage is mainly for respiratory tract decongestion.. pseudoephedrine : A member of the class of the class of phenylethanolamines that is (1S)-2-(methylamino)-1-phenylethan-1-ol in which the pro-S hydrogen at position 2 is replaced by a methyl group.		3.2310phenylethanolamines;
secondary alcohol;
secondary amino compound		anti-asthmatic drug;
bronchodilator agent;
central nervous system drug;
nasal decongestant;
plant metabolite;
sympathomimetic agent;
vasoconstrictor agent;
xenobiotic
diethylpropion
Diethylpropion: A appetite depressant considered to produce less central nervous system disturbance than most drugs in this therapeutic category. It is also considered to be among the safest for patients with hypertension. (From AMA Drug Evaluations Annual, 1994, p2290). diethylpropion : An aromatic ketone that is propiophenone in which one of the hydrogens alpha- to the carbonyl is substituted by a diethylamino group. A central stimulant and indirect-acting sympathomimetic, it is an appetite depressant and is used as the hydrochloride as an anoretic in the short term management of obesity.		3.2310aromatic ketone;
tertiary amine		appetite depressant
benzonatate
benzonatate: structure in Merck Index, 9th ed, #1107. benzonatate : The ester obtained by formal condensation of 4-butylaminobenzoic acid with nonaethylene glycol monomethyl ether. Structurally related to procaine and benzocaine, it has an anaesthetic effect on the stretch sensors in the lungs, and is used as a non-narcotic cough suppressant.		3.2310benzoate ester;
secondary amino compound;
substituted aniline		anaesthetic;
antitussive
methylergonovine
Methylergonovine: A homolog of ERGONOVINE containing one more CH2 group. (Merck Index, 11th ed)		3.2310ergoline alkaloid
cinchophen
cinchophen: was heading 1963-94; ACIPHENOCHINOLIUM was see CHINOPHEN 1978-94; use QUINOLINES to search CINCHOPHEN 1966-94		3.2310quinolines
nafcillin
Nafcillin: A semi-synthetic antibiotic related to penicillin.. nafcillin : A penicillin in which the substituent at position 6 of the penam ring is a (2-ethoxy-1-naphthoyl)amino group.		3.2310penicillin allergen;
penicillin		antibacterial drug
methohexital
Methohexital: An intravenous anesthetic with a short duration of action that may be used for induction of anesthesia.. methohexital : A barbiturate, the structure of which is that of barbituric acid substituted at N-1 by a methyl group and at C-5 by allyl and 1-methylpent-2-ynyl groups.		3.2310acetylenic compound;
barbiturates		drug allergen;
intravenous anaesthetic
ephedrine
Ephedrine: A phenethylamine found in EPHEDRA SINICA. PSEUDOEPHEDRINE is an isomer. It is an alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. It has been used for asthma, heart failure, rhinitis, and urinary incontinence, and for its central nervous system stimulatory effects in the treatment of narcolepsy and depression. It has become less extensively used with the advent of more selective agonists.. (-)-ephedrine : A phenethylamine alkaloid that is 2-phenylethanamine substituted by a methyl group at the amino nitrogen and a methyl and a hydroxy group at position 2 and 1 respectively.		3.2310phenethylamine alkaloid;
phenylethanolamines		bacterial metabolite;
environmental contaminant;
nasal decongestant;
plant metabolite;
sympathomimetic agent;
vasoconstrictor agent;
xenobiotic
aminophylline
Aminophylline: A drug combination that contains THEOPHYLLINE and ethylenediamine. It is more soluble in water than theophylline but has similar pharmacologic actions. It's most common use is in bronchial asthma, but it has been investigated for several other applications.. aminophylline : A mixture comprising of theophylline and ethylenediamine in a 2:1 ratio.		3.2310mixturebronchodilator agent;
cardiotonic drug
azacitidine
Azacitidine: A pyrimidine analogue that inhibits DNA methyltransferase, impairing DNA methylation. It is also an antimetabolite of cytidine, incorporated primarily into RNA. Azacytidine has been used as an antineoplastic agent.. 5-azacytidine : An N-glycosyl-1,3,5-triazine that is 4-amino-1,3,5-triazin-2(1H)-one substituted by a beta-D-ribofuranosyl residue via an N-glycosidic linkage. An antineoplastic agent, it is used in the treatment of myeloid leukaemia.		3.2310N-glycosyl-1,3,5-triazine;
nucleoside analogue		antineoplastic agent
galantamine
Galantamine: A benzazepine derived from norbelladine. It is found in GALANTHUS and other AMARYLLIDACEAE. It is a cholinesterase inhibitor that has been used to reverse the muscular effects of GALLAMINE TRIETHIODIDE and TUBOCURARINE and has been studied as a treatment for ALZHEIMER DISEASE and other central nervous system disorders.. galanthamine : A benzazepine alkaloid isolated from certain species of daffodils.		3.2310benzazepine alkaloid fundamental parent;
benzazepine alkaloid;
organic heterotetracyclic compound;
tertiary amino compound		antidote to curare poisoning;
cholinergic drug;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
plant metabolite
nandrolone decanoate
Nandrolone Decanoate: Decanoic acid ester of nandrolone that is used as an anabolic agent to prevent or treat WASTING SYNDROME associated with severe chronic illness or HIV infection (HIV WASTING SYNDROME). It may also be used in the treatment of POSTMENOPAUSAL OSTEOPOROSIS.		3.2310steroid ester
dextropropoxyphene
Dextropropoxyphene: A narcotic analgesic structurally related to METHADONE. Only the dextro-isomer has an analgesic effect; the levo-isomer appears to exert an antitussive effect.. propoxyphene : A racemate of the (1R,2R)- and (1S,2R)- diastereoisomers.. dextropropoxyphene : The (1S,2R)-(+)-diastereoisomer of propoxyphene.		3.23101-benzyl-3-(dimethylamino)-2-methyl-1-phenylpropyl propanoatemu-opioid receptor agonist;
opioid analgesic
chenodeoxycholic acid
Chenodeoxycholic Acid: A bile acid, usually conjugated with either glycine or taurine. It acts as a detergent to solubilize fats for intestinal absorption and is reabsorbed by the small intestine. It is used as cholagogue, a choleretic laxative, and to prevent or dissolve gallstones.. chenodeoxycholic acid : A dihydroxy-5beta-cholanic acid that is (5beta)-cholan-24-oic acid substituted by hydroxy groups at positions 3 and 7 respectively.. chenodeoxycholate : Conjugate base of chenodeoxycholic acid; major species at pH 7.3.		3.2310bile acid;
C24-steroid;
dihydroxy-5beta-cholanic acid		human metabolite;
mouse metabolite
4-hydroxybutyric acid
4-hydroxybutyric acid: was an entry term to Sodium Oxybate (74-98). 4-hydroxybutyric acid : A 4-hydroxy monocarboxylic acid that is butyric acid in which one of the hydrogens at position 4 is replaced by a hydroxy group.		3.23104-hydroxy monocarboxylic acid;
hydroxybutyric acid		general anaesthetic;
GHB receptor agonist;
neurotoxin;
sedative
dihydroergotamine
Dihydroergotamine: A 9,10alpha-dihydro derivative of ERGOTAMINE. It is used as a vasoconstrictor, specifically for the therapy of MIGRAINE DISORDERS.. dihydroergotamine : Ergotamine in which a single bond replaces the double bond between positions 9 and 10. A semisynthetic ergot alkaloid with weaker oxytocic and vasoconstrictor properties than ergotamine, it is used (as the methanesulfonic or tartaric acid salts) for the treatment of migraine and orthostatic hypotension.		3.2310ergot alkaloid;
semisynthetic derivative		dopamine agonist;
non-narcotic analgesic;
serotonergic agonist;
sympatholytic agent;
vasoconstrictor agent
medroxyprogesterone
[no description available]		3.231017alpha-hydroxy steroid;
20-oxo steroid;
3-oxo-Delta(4) steroid;
tertiary alpha-hydroxy ketone		contraceptive drug;
progestin;
synthetic oral contraceptive
dimenhydrinate
gravinol: has antioxidant and ant-inflammatory activities; structure in first source		3.2310diarylmethane
methamphetamine
Methamphetamine: A central nervous system stimulant and sympathomimetic with actions and uses similar to DEXTROAMPHETAMINE. The smokable form is a drug of abuse and is referred to as crank, crystal, crystal meth, ice, and speed.. methamphetamine : A member of the class of amphetamines in which the amino group of (S)-amphetamine carries a methyl substituent.		3.2310amphetamines;
secondary amine		central nervous system stimulant;
environmental contaminant;
neurotoxin;
psychotropic drug;
xenobiotic
levocarnitine
(R)-carnitine : The (R)-enantiomer of carnitine.		3.2310carnitineantilipemic drug;
nootropic agent;
nutraceutical;
Saccharomyces cerevisiae metabolite;
water-soluble vitamin (role)
sulfanilylurea
sulfanilylurea: antimicrobial agent; structure		3.2310benzenes;
sulfonamide
lactulose
[no description available]		3.2310glycosylfructosegastrointestinal drug;
laxative
pamabrom
[no description available]		3.2310
acetylcysteine
N-acetyl-L-cysteine : An N-acetyl-L-amino acid that is the N-acetylated derivative of the natural amino acid L-cysteine.		3.2310acetylcysteine;
L-cysteine derivative;
N-acetyl-L-amino acid		antidote to paracetamol poisoning;
antiinfective agent;
antioxidant;
antiviral drug;
ferroptosis inhibitor;
geroprotector;
human metabolite;
mucolytic;
radical scavenger;
vulnerary
erythromycin
Erythromycin: A bacteriostatic antibiotic macrolide produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.. erythromycin : Any of several wide-spectrum macrolide antibiotics obtained from actinomycete Saccharopolyspora erythraea (formerly known as Streptomyces erythraeus).. erythromycin A : An erythromycin that consists of erythronolide A having 2,6-dideoxy-3-C-methyl-3-O-methyl-alpha-L-ribo-hexopyranosyl and 3,4,6-trideoxy-3-(dimethylamino)-beta-D-xylo-hexopyranosyl residues attahced at positions 4 and 6 respectively.		3.2310cyclic ketone;
erythromycin
levonorgestrel
Levonorgestrel: A synthetic progestational hormone with actions similar to those of PROGESTERONE and about twice as potent as its racemic or (+-)-isomer (NORGESTREL). It is used for contraception, control of menstrual disorders, and treatment of endometriosis.		3.231017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
terminal acetylenic compound		contraceptive drug;
female contraceptive drug;
progestin;
synthetic oral contraceptive
diphenoxylate
Diphenoxylate: A MEPERIDINE congener used as an antidiarrheal, usually in combination with ATROPINE. At high doses, it acts like morphine. Its unesterified metabolite difenoxin has similar properties and is used similarly. It has little or no analgesic activity.. diphenoxylate : A piperidinecarboxylate ester that is the ethyl ester of difenoxin.		3.2310ethyl ester;
nitrile;
piperidinecarboxylate ester;
tertiary amine		antidiarrhoeal drug
ethambutol
Ethambutol: An antitubercular agent that inhibits the transfer of mycolic acids into the cell wall of the tubercle bacillus. It may also inhibit the synthesis of spermidine in mycobacteria. The action is usually bactericidal, and the drug can penetrate human cell membranes to exert its lethal effect. (From Smith and Reynard, Textbook of Pharmacology, 1992, p863). ethambutol : An ethylenediamine derivative that is ethane-1,2-diamine in which one hydrogen attached to each of the nitrogens is sutstituted by a 1-hydroxybutan-2-yl group (S,S-configuration). It is a bacteriostatic antimycobacterial drug, effective against Mycobacterium tuberculosis and some other mycobacteria. It is used (as the dihydrochloride salt) in combination with other antituberculous drugs in the treatment of pulmonary and extrapulmonary tuberculosis; resistant strains of M. tuberculosis are readily produced if ethambutol is used alone.		3.2310ethanolamines;
ethylenediamine derivative		antitubercular agent;
environmental contaminant;
xenobiotic
vancomycin
Vancomycin: Antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to RISTOCETIN that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear.. vancomycin : A complex glycopeptide from Streptomyces orientalis. It inhibits a specific step in the synthesis of the peptidoglycan layer in the Gram-positive bacteria Staphylococcus aureus and Clostridium difficile.		3.2310glycopeptideantibacterial drug;
antimicrobial agent;
bacterial metabolite
d-alpha tocopherol
Vitamin E: A generic descriptor for all TOCOPHEROLS and TOCOTRIENOLS that exhibit ALPHA-TOCOPHEROL activity. By virtue of the phenolic hydrogen on the 2H-1-benzopyran-6-ol nucleus, these compounds exhibit varying degree of antioxidant activity, depending on the site and number of methyl groups and the type of ISOPRENOIDS.. tocopherol : A collective name for a group of closely related lipids that contain a chroman-6-ol nucleus substituted at position 2 by a methyl group and by a saturated hydrocarbon chain consisting of three isoprenoid units. They are designated as alpha-, beta-, gamma-, and delta-tocopherol depending on the number and position of additional methyl substituents on the aromatic ring. Tocopherols occur in vegetable oils and vegetable oil products, almost exclusively with R,R,R configuration. Tocotrienols differ from tocopherols only in having three double bonds in the hydrocarbon chain.. vitamin E : Any member of a group of fat-soluble chromanols that exhibit biological activity against vitamin E deficiency. The vitamers in this class consists of a chroman-6-ol core which is substituted at position 2 by a methyl group and (also at position 2) either a saturated or a triply-unsaturated hydrocarbon chain consisting of three isoprenoid units. The major function of vitamin E is to act as a natural antioxidant by scavenging free radicals and molecular oxygen.. (R,R,R)-alpha-tocopherol : An alpha-tocopherol that has R,R,R configuration. The naturally occurring stereoisomer of alpha-tocopherol, it is found particularly in sunflower and olive oils.		3.2310alpha-tocopherolalgal metabolite;
antiatherogenic agent;
anticoagulant;
antioxidant;
antiviral agent;
EC 2.7.11.13 (protein kinase C) inhibitor;
immunomodulator;
micronutrient;
nutraceutical;
plant metabolite
ibufenac
ibufenac: used in the treatment of rheumatism; also possesses antipyretic properties; minor descriptor (75-84); on-line & Index Medicus search PHENYLACETATES (75-84); RN given refers to parent cpd. ibufenac : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is replaced by a 4-isobutylphenyl group. Although it was shown to be effective in treatment of rheumatoid arthritis, the clinical use of ibufenac was discontinued due to hepatotoxic side-effects.		3.2310monocarboxylic acidEC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
hepatotoxic agent;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
metaxalone
[no description available]		3.2310aromatic ether
spectinomycin
Spectinomycin: An antibiotic produced by Streptomyces spectabilis. It is active against gram-negative bacteria and used for the treatment of GONORRHEA.. spectinomycin dihydrochloride : A hydrochloride obtained by combining spectinomycin with two molar equivalents of hydrochloric acid. An antibiotic that is active against gram-negative bacteria and used (as its pentahydrate) to treat gonorrhea.. spectinomycin : A pyranobenzodioxin and antibiotic that is active against gram-negative bacteria and used (as its dihydrochloride pentahydrate) to treat gonorrhea. It is produced by the bacterium Streptomyces spectabilis.		3.2310cyclic acetal;
cyclic hemiketal;
cyclic ketone;
pyranobenzodioxin;
secondary alcohol;
secondary amino compound		antibacterial drug;
antimicrobial agent;
bacterial metabolite
dronabinol
Dronabinol: A psychoactive compound extracted from the resin of Cannabis sativa (marihuana, hashish). The isomer delta-9-tetrahydrocannabinol (THC) is considered the most active form, producing characteristic mood and perceptual changes associated with this compound.. Delta(9)-tetrahydrocannabinol : A diterpenoid that is 6a,7,8,10a-tetrahydro-6H-benzo[c]chromene substituted at position 1 by a hydroxy group, positions 6, 6 and 9 by methyl groups and at position 3 by a pentyl group. The principal psychoactive constituent of the cannabis plant, it is used for treatment of anorexia associated with AIDS as well as nausea and vomiting associated with cancer chemotherapy.		3.2310benzochromene;
diterpenoid;
phytocannabinoid;
polyketide		cannabinoid receptor agonist;
epitope;
hallucinogen;
metabolite;
non-narcotic analgesic
amiloride
Amiloride: A pyrazine compound inhibiting SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS. This inhibition creates a negative potential in the luminal membranes of principal cells, located in the distal convoluted tubule and collecting duct. Negative potential reduces secretion of potassium and hydrogen ions. Amiloride is used in conjunction with DIURETICS to spare POTASSIUM loss. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p705). amiloride : A member of the class of pyrazines resulting from the formal monoacylation of guanidine with the carboxy group of 3,5-diamino-6-chloropyrazine-2-carboxylic acid.		3.2310aromatic amine;
guanidines;
organochlorine compound;
pyrazines		diuretic;
sodium channel blocker
pimozide
Pimozide: A diphenylbutylpiperidine that is effective as an antipsychotic agent and as an alternative to HALOPERIDOL for the suppression of vocal and motor tics in patients with Tourette syndrome. Although the precise mechanism of action is unknown, blockade of postsynaptic dopamine receptors has been postulated. (From AMA Drug Evaluations Annual, 1994, p403). pimozide : A member of the class of benzimidazoles that is 1,3-dihydro-2H-benzimidazol-2-one in which one of the nitrogens is substituted by a piperidin-4-yl group, which in turn is substituted on the nitrogen by a 4,4-bis(p-fluorophenyl)butyl group.		3.2310benzimidazoles;
heteroarylpiperidine;
organofluorine compound		antidyskinesia agent;
dopaminergic antagonist;
first generation antipsychotic;
H1-receptor antagonist;
serotonergic antagonist
dexbrompheniramine
dexbrompheniramine : The (pharmacologically active) (S)-(+)-enantiomer of brompheniramine. A histamine H1 receptor antagonist, it is used (commonly as its maleate salt) for the symptomatic relief of allergic conditions, including rhinitis and conjunctivitis.		3.2310brompheniramineanti-allergic agent;
H1-receptor antagonist
stavudine
Stavudine: A dideoxynucleoside analog that inhibits reverse transcriptase and has in vitro activity against HIV.. stavudine : A nucleoside analogue obtained by formal dehydration across positions 2 and 3 of thymidine. An inhibitor of HIV-1 reverse transcriptase		3.2310dihydrofuran;
nucleoside analogue;
organic molecular entity		antimetabolite;
antiviral agent;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
dicloxacillin
Dicloxacillin: One of the PENICILLINS which is resistant to PENICILLINASE.. dicloxacillin : A penicillin that is 6-aminopenicillanic acid in which one of the amino hydrogens is replaced by a 3-(2,6-dichlorophenyl)-5-methyl-1,2-oxazol-4-yl]formyl group.		3.2310dichlorobenzene;
penicillin		antibacterial drug
megestrol
Megestrol: A progestational hormone used most commonly as the acetate ester. As the acetate, it is more potent than progesterone both as a progestagen and as an ovulation inhibitor. It has also been used in the palliative treatment of breast cancer.. megestrol : A 3-oxo Delta(4)-steroid that is pregna-4,6-diene-3,20-dione substituted by a methyl group at position 6 and a hydroxy group at position 17.		3.231017alpha-hydroxy steroid;
20-oxo steroid;
3-oxo-Delta(4) steroid;
tertiary alpha-hydroxy ketone		antineoplastic agent;
appetite enhancer;
contraceptive drug;
progestin;
synthetic oral contraceptive
streptomycin
[no description available]		3.2310antibiotic antifungal drug;
antibiotic fungicide;
streptomycins		antibacterial drug;
antifungal agrochemical;
antimicrobial agent;
antimicrobial drug;
bacterial metabolite;
protein synthesis inhibitor
cladribine
[no description available]		3.2310organochlorine compound;
purine 2'-deoxyribonucleoside		antineoplastic agent;
immunosuppressive agent
carbenicillin
Carbenicillin: Broad-spectrum semisynthetic penicillin derivative used parenterally. It is susceptible to gastric juice and penicillinase and may damage platelet function.. carbenicillin : A penicillin antibiotic having a 6beta-2-carboxy-2-phenylacetamido side-chain.		3.2310penicillin allergen;
penicillin		antibacterial drug
clomacran
clomacran: RN given refers to parent cpd; structure		3.2310acridines
methenamine hippurate
methenamine hippurate: both parts of molecule contribute to its antibacterial action		3.2310N-acylglycine
olsalazine
olsalazine: cpd with 2 salicylate molecules linked together by an azo bond. olsalazine : An azobenzene that consists of two molecules of 4-aminosalicylic acid joined by an azo linkage. A prodrug for mesalazine, an anti-inflammatory drug, it is used (as the disodium salt) in the treatment of inflammatory bowel disease.		3.2310azobenzenes;
dicarboxylic acid		non-steroidal anti-inflammatory drug;
prodrug
sodium thiosulfate
sodium thiosulfate: do not confuse synonym sodium hyposulfite with sodium hyposulfite, synonym for di-Na salt of dithionous acid. sodium thiosulfate : An inorganic sodium salt composed of sodium and thiosulfate ions in a 2:1 ratio.		3.2310inorganic sodium saltantidote to cyanide poisoning;
antifungal drug;
nephroprotective agent
selegiline
Selegiline: A selective, irreversible inhibitor of Type B monoamine oxidase that is used for the treatment of newly diagnosed patients with PARKINSON DISEASE, and for the treatment of depressive disorders. The compound without isomeric designation is Deprenyl.		3.2310selegiline;
terminal acetylenic compound		geroprotector
clemastine
Clemastine: A histamine H1 antagonist used as the hydrogen fumarate in hay fever, rhinitis, allergic skin conditions, and pruritus. It causes drowsiness.. clemastine : 2-[(2R)-1-Methylpyrrolidin-2-yl]ethanol in which the hydrogen of the hydroxy group is substituted by a 1-(4-chlorophenyl)-1-phenylethyl group (R configuration). An antihistamine with antimuscarinic and moderate sedative properties, it is used as its fumarate salt for the symptomatic relief of allergic conditions such as rhinitis, urticaria, conjunctivitis and in pruritic (severe itching) skin conditions.		3.2310monochlorobenzenes;
N-alkylpyrrolidine		anti-allergic agent;
antipruritic drug;
H1-receptor antagonist;
muscarinic antagonist
cephalexin
Cephalexin: A semisynthetic cephalosporin antibiotic with antimicrobial activity similar to that of CEPHALORIDINE or CEPHALOTHIN, but somewhat less potent. It is effective against both gram-positive and gram-negative organisms.. cephalexin : A semisynthetic first-generation cephalosporin antibiotic having methyl and beta-(2R)-2-amino-2-phenylacetamido groups at the 3- and 7- of the cephem skeleton, respectively. It is effective against both Gram-negative and Gram-positive organisms, and is used for treatment of infections of the skin, respiratory tract and urinary tract.		3.2310beta-lactam antibiotic allergen;
cephalosporin;
semisynthetic derivative		antibacterial drug
danazol
Danazol: A synthetic steroid with antigonadotropic and anti-estrogenic activities that acts as an anterior pituitary suppressant by inhibiting the pituitary output of gonadotropins. It possesses some androgenic properties. Danazol has been used in the treatment of endometriosis and some benign breast disorders.		3.231017beta-hydroxy steroid;
terminal acetylenic compound		anti-estrogen;
estrogen antagonist;
geroprotector
fenclozic acid
fenclozic acid: an analgesic & antipyretic with anti-inflammatory properties; minor descriptor (75-86); on-line & INDEX MEDICUS search THIAZOLES (75-86); RN given refers to parent cpd		3.2310
laxagetten 4,4'-diacetoxydiphenylpyridylemethane
[no description available]		3.2310
daunorubicin
Daunorubicin: A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.. anthracycline : Anthracyclines are polyketides that have a tetrahydronaphthacenedione ring structure attached by a glycosidic linkage to the amino sugar daunosamine.. daunorubicin : A natural product found in Actinomadura roseola.		3.2310aminoglycoside antibiotic;
anthracycline;
p-quinones;
tetracenequinones		antineoplastic agent;
bacterial metabolite
fludarabine phosphate
fludarabine phosphate: structure given in first source. fludarabine phosphate : A purine arabinonucleoside monophosphate having 2-fluoroadenine as the nucleobase. A prodrug, it is rapidly dephosphorylated to 2-fluoro-ara-A and then phosphorylated intracellularly by deoxycytidine kinase to the active triphosphate, 2-fluoro-ara-ATP. Once incorporated into DNA, 2-fluoro-ara-ATP functions as a DNA chain terminator. It is used for the treatment of adult patients with B-cell chronic lymphocytic leukemia (CLL) who have not responded to, or whose disease has progressed during, treatment with at least one standard alkylating-agent containing regimenas.		3.2310nucleoside analogue;
organofluorine compound;
purine arabinonucleoside monophosphate		antimetabolite;
antineoplastic agent;
antiviral agent;
DNA synthesis inhibitor;
immunosuppressive agent;
prodrug
alclofenac
alclofenac: was heading 1975-94 (was see under PHENYLACETATES 1975-90); use PHENYLACETATES to search ALCLOFENAC 1975-94; an anti-inflammatory agent used in the treatment of rheumatoid arthritis; acts also as an analgesic and an antipyretic. alclofenac : An aromatic ether in which the ether oxygen links an allyl group to the 4-position of (3-chlorophenyl)acetic acid.A non-steroidal anti-inflammatory drug, it was withdrawn from the UK market in 1979 due to concerns with its association with vasculitis and rash.		3.2310aromatic ether;
monocarboxylic acid;
monochlorobenzenes		drug allergen;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
bromocriptine
Bromocriptine: A semisynthetic ergotamine alkaloid that is a dopamine D2 agonist. It suppresses prolactin secretion.		3.2310indole alkaloidantidyskinesia agent;
antiparkinson drug;
dopamine agonist;
hormone antagonist
oxyphenisatin
[no description available]		3.2310indoles
fludrocortisone
Fludrocortisone: A synthetic mineralocorticoid with anti-inflammatory activity.		3.231011beta-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
C21-steroid;
fluorinated steroid;
mineralocorticoid		adrenergic agent;
anti-inflammatory drug
ursodeoxycholic acid
Ursodeoxycholic Acid: An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic.. ursodeoxycholic acid : A bile acid found in the bile of bears (Ursidae) as a conjugate with taurine. Used therapeutically, it prevents the synthesis and absorption of cholesterol and can lead to the dissolution of gallstones.. ursodeoxycholate : A bile acid anion that is the conjugate base of ursodeoxycholic acid, obtained by deprotonation of the carboxy group; major species at pH 7.3.		3.2310bile acid;
C24-steroid;
dihydroxy-5beta-cholanic acid		human metabolite;
mouse metabolite
dexchlorpheniramine
dexchlorpheniramine: RN given refers to parent cpd(S)-isomer		3.2310chlorphenamine
clometacin
clometacin: structure		3.2310N-acylindole
cefazolin
Cefazolin: A semisynthetic cephalosporin analog with broad-spectrum antibiotic action due to inhibition of bacterial cell wall synthesis. It attains high serum levels and is excreted quickly via the urine.. cefazolin : A first-generation cephalosporin compound having [(5-methyl-1,3,4-thiadiazol-2-yl)sulfanyl]methyl and (1H-tetrazol-1-ylacetyl)amino side-groups at positions 3 and 7 respectively.		3.2310beta-lactam antibiotic allergen;
cephalosporin;
tetrazoles;
thiadiazoles		antibacterial drug
amoxicillin
Amoxicillin: A broad-spectrum semisynthetic antibiotic similar to AMPICILLIN except that its resistance to gastric acid permits higher serum levels with oral administration.. amoxicillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-amino-2-(4-hydroxyphenyl)acetamido group.		3.2310penicillin allergen;
penicillin		antibacterial drug
timolol
(S)-timolol (anhydrous) : The (S)-(-) (more active) enantiomer of timolol. A beta-adrenergic antagonist, both the hemihydrate and the maleate salt are used in the mangement of glaucoma, hypertension, angina pectoris and myocardial infarction, and for the prevention of migraine.		3.2310timololanti-arrhythmia drug;
antiglaucoma drug;
antihypertensive agent;
beta-adrenergic antagonist
oxcarbazepine
Oxcarbazepine: A carbamazepine derivative that acts as a voltage-gated sodium channel blocker. It is used for the treatment of PARTIAL SEIZURES with or without secondary generalization. It is also an inducer of CYTOCHROME P-450 CYP3A4.. oxcarbazepine : A dibenzoazepine derivative, having a carbamoyl group at the ring nitrogen, substituted with an oxo group at C-4 of the azepeine ring which is also hydrogenated at C-4 and C-5. It is a anticholinergic anticonvulsant and mood stabilizing drug, used primarily in the treatment of epilepsy.		3.2310cyclic ketone;
dibenzoazepine		anticonvulsant;
drug allergen
carbidopa
carbidopa (anhydrous) : 3-(3,4-Dihydroxyphenyl)propanoic acid in which the hydrogens alpha- to the carboxyl group are substituted by hydrazinyl and methyl groups (S-configuration). Carbidopa is a dopa decarboxylase inhibitor, so prevents conversion of levodopa to dopamine. It has no antiparkinson activity by itself, but is used (commonly as its hydrate) in the management of Parkinson's disease to reduce peripheral adverse effects of levodopa.		3.2310catechols;
hydrazines;
monocarboxylic acid		antiparkinson drug;
dopaminergic agent;
EC 4.1.1.28 (aromatic-L-amino-acid decarboxylase) inhibitor
moricizine
Moricizine: An antiarrhythmia agent used primarily for ventricular rhythm disturbances.. moricizine : A phenothiazine substituted on the nitrogen by a 3-(morpholin-4-yl)propanoyl group, and at position 2 by an (ethoxycarbonyl)amino group.		3.2310carbamate ester;
morpholines;
phenothiazines		anti-arrhythmia drug
amineptin
amineptin: used in treatment of neuroses with psychoasthenic, anxio-phobic & depressive manifestations; synonym S 1694 refers to HCl; structure. amineptine : A carbocyclic fatty acid that is 5-aminoheptanoic acid in which one of the hydrogens attached to the nitrogen is replaced by a 10,11-dihydro-5H-dibenzo[a,d][7]annulen-5-yl group. A tricyclic antidepressant, it was never approved in the US and was withdrawn from the French market in 1999 due to concerns over abuse, dependence and severe acne.		3.2310amino acid;
carbocyclic fatty acid;
carbotricyclic compound;
secondary amino compound		antidepressant;
dopamine uptake inhibitor
zidovudine
Zidovudine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIV-induced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia.. zidovudine : A pyrimidine 2',3'-dideoxyribonucleoside compound having a 3'-azido substituent and thymine as the nucleobase.		3.2310azide;
pyrimidine 2',3'-dideoxyribonucleoside		antimetabolite;
antiviral drug;
HIV-1 reverse transcriptase inhibitor
pirprofen
pirprofen: anti-inflammatory agent used in therapy of rheumatoid arthritis; prostaglandin synthetase inhibitor; more potent than indomethacin; structure		3.2310pyrroline
paclitaxel
Taxus: Genus of coniferous yew trees or shrubs, several species of which have medicinal uses. Notable is the Pacific yew, Taxus brevifolia, which is used to make the anti-neoplastic drug taxol (PACLITAXEL).		3.2310taxane diterpenoid;
tetracyclic diterpenoid		antineoplastic agent;
human metabolite;
metabolite;
microtubule-stabilising agent
etoposide
[no description available]		3.2310beta-D-glucoside;
furonaphthodioxole;
organic heterotetracyclic compound		antineoplastic agent;
DNA synthesis inhibitor
dobutamine
Dobutamine: A catecholamine derivative with specificity for BETA-1 ADRENERGIC RECEPTORS. It is commonly used as a cardiotonic agent after CARDIAC SURGERY and during DOBUTAMINE STRESS ECHOCARDIOGRAPHY.. dobutamine : A catecholamine that is 4-(3-aminobutyl)phenol in which one of the hydrogens attached to the nitrogen is substituted by a 2-(3,4-dihydroxyphenyl)ethyl group. A beta1-adrenergic receptor agonist that has cardiac stimulant action without evoking vasoconstriction or tachycardia, it is used as the hydrochloride to increase the contractility of the heart in the management of acute heart failure.		3.2310catecholamine;
secondary amine		beta-adrenergic agonist;
cardiotonic drug;
sympathomimetic agent
penbutolol
Penbutolol: A nonselective beta-blocker used as an antihypertensive and an antianginal agent.		3.2310ethanolamines
ribavirin
Rebetron: Rebetron is tradename		3.23101-ribosyltriazole;
aromatic amide;
monocarboxylic acid amide;
primary carboxamide		anticoronaviral agent;
antiinfective agent;
antimetabolite;
antiviral agent;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
amikacin
Amikacin: A broad-spectrum antibiotic derived from KANAMYCIN. It is reno- and oto-toxic like the other aminoglycoside antibiotics.. amikacin : An amino cyclitol glycoside that is kanamycin A acylated at the N-1 position by a 4-amino-2-hydroxybutyryl group.		3.2310alpha-D-glucoside;
amino cyclitol glycoside;
aminoglycoside;
carboxamide		antibacterial drug;
antimicrobial agent;
nephrotoxin
cephradine
Cephradine: A semi-synthetic cephalosporin antibiotic.. cephradine : A first-generation cephalosporin antibiotic with a methyl substituent at position 3, and a (2R)-2-amino-2-cyclohexa-1,4-dien-1-ylacetamido substituent at position 7, of the cephem skeleton.		3.2310beta-lactam antibiotic allergen;
cephalosporin		antibacterial drug
ticrynafen
Ticrynafen: A novel diuretic with uricosuric action. It has been proposed as an antihypertensive agent.. tienilic acid : An aromatic ketone that is 2,3-dichlorophenoxyacetic acid in which the hydrogen at position 4 on the benzene ring is replaced by a thiophenecarbonyl group. A loop diuretic used to treat hypertension, it was withdrawn from the market in 1982 due to links with hepatitis.		3.2310aromatic ether;
aromatic ketone;
dichlorobenzene;
monocarboxylic acid;
thiophenes		antihypertensive agent;
hepatotoxic agent;
loop diuretic
methyldopa
Methyldopa: An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.. alpha-methyl-L-dopa : A derivative of L-tyrosine having a methyl group at the alpha-position and an additional hydroxy group at the 3-position on the phenyl ring.		3.2310L-tyrosine derivative;
non-proteinogenic L-alpha-amino acid		alpha-adrenergic agonist;
antihypertensive agent;
hapten;
peripheral nervous system drug;
sympatholytic agent
diltiazem
Diltiazem: A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of CALCIUM ion on membrane functions.. diltiazem : A 5-[2-(dimethylamino)ethyl]-2-(4-methoxyphenyl)-4-oxo-2,3,4,5-tetrahydro-1,5-benzothiazepin-3-yl acetate in which both stereocentres have S configuration. A calcium-channel blocker and vasodilator, it is used as the hydrochloride in the management of angina pectoris and hypertension.		3.23105-[2-(dimethylamino)ethyl]-2-(4-methoxyphenyl)-4-oxo-2,3,4,5-tetrahydro-1,5-benzothiazepin-3-yl acetateantihypertensive agent;
calcium channel blocker;
vasodilator agent
vecuronium
vecuronium : A 5alpha-androstane compound having 3alpha-acetoxy-, 17beta-acetoxy-, 2beta-piperidino- and 16beta-N-methylpiperidinium substituents.		3.2310acetate ester;
androstane;
quaternary ammonium ion		drug allergen;
muscle relaxant;
neuromuscular agent;
nicotinic antagonist
benoxaprofen
benoxaprofen: RN given refers to parent cpd; structure. benoxaprofen : A monocarboxylic acid that is propionic acid substituted at position 2 by a 2-(4-chlorophenyl)-1,3-benzoxazol-5-yl group. It was used as a non-steroidal anti-inflammatory drug until 1982 when it was withdrawn from the market due to adverse side-effects including liver necrosis, photosensitivity, and carcinogenicity in animals.		3.23101,3-benzoxazoles;
monocarboxylic acid;
monochlorobenzenes		antipsoriatic;
antipyretic;
EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor;
hepatotoxic agent;
nephrotoxin;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
protein kinase C agonist
exifone
[no description available]		3.2310benzophenones
mefloquine
(-)-(11S,2'R)-erythro-mefloquine : An optically active form of [2,8-bis(trifluoromethyl)quinolin-4-yl]-(2-piperidyl)methanol having (-)-(11S,2'R)-erythro-configuration. An antimalarial agent, used in racemic form, which acts as a blood schizonticide; its mechanism of action is unknown.		3.2310[2,8-bis(trifluoromethyl)quinolin-4-yl]-(2-piperidyl)methanolantimalarial
nitazoxanide
nitazoxanide: a 5-nitrothiazolyl derivative used for a broad range of intestinal parasitic infections including CRYPTOSPORIDIUM and GIARDIA; it is a redox-active nitrothiazolyl-salicylamide prodrug		3.2310benzamides;
carboxylic ester
sufentanil
Sufentanil: An opioid analgesic that is used as an adjunct in anesthesia, in balanced anesthesia, and as a primary anesthetic agent.. sufentanil : An anilide resulting from the formal condensation of the aryl amino group of 4-(methoxymethyl)-N-phenyl-1-[2-(2-thienyl)ethyl]piperidin-4-amine with propanoic acid.		3.2310anilide;
ether;
piperidines;
thiophenes		anaesthesia adjuvant;
intravenous anaesthetic;
mu-opioid receptor agonist;
opioid analgesic
acarbose
[no description available]		3.2310tetrasaccharide derivativeEC 3.2.1.1 (alpha-amylase) inhibitor;
EC 3.2.1.20 (alpha-glucosidase) inhibitor;
geroprotector;
hypoglycemic agent
torsemide
Torsemide: A pyridine and sulfonamide derivative that acts as a sodium-potassium chloride symporter inhibitor (loop diuretic). It is used for the treatment of EDEMA associated with CONGESTIVE HEART FAILURE; CHRONIC RENAL INSUFFICIENCY; and LIVER DISEASES. It is also used for the management of HYPERTENSION.. torasemide : An N-sulfonylurea obtained by formal condensation of [(3-methylphenyl)amino]pyridine-3-sulfonic acid with the free amino group of N-isopropylurea. It is a potent loop diuretic used for the treatment of hypertension and edema in patients with congestive heart failure.		3.2310aminopyridine;
N-sulfonylurea;
secondary amino compound		antihypertensive agent;
loop diuretic
epirubicin
Epirubicin: An anthracycline which is the 4'-epi-isomer of doxorubicin. The compound exerts its antitumor effects by interference with the synthesis and function of DNA.		3.2310aminoglycoside;
anthracycline antibiotic;
anthracycline;
deoxy hexoside;
monosaccharide derivative;
p-quinones;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		antimicrobial agent;
antineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
idarubicin
Idarubicin: An orally administered anthracycline antineoplastic. The compound has shown activity against BREAST NEOPLASMS; LYMPHOMA; and LEUKEMIA.		3.2310anthracycline antibiotic;
deoxy hexoside;
monosaccharide derivative
piperacillin
Piperacillin: Semisynthetic, broad-spectrum, AMPICILLIN derived ureidopenicillin antibiotic proposed for PSEUDOMONAS infections. It is also used in combination with other antibiotics.. piperacillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-[(4-ethyl-2,3-dioxopiperazin-1-yl)carboxamido]-2-phenylacetamido group.		3.2310penicillin allergen;
penicillin		antibacterial drug
paroxetine
Paroxetine: A serotonin uptake inhibitor that is effective in the treatment of depression.. paroxetine : A benzodioxole that consists of piperidine bearing 1,3-benzodioxol-5-yloxy)methyl and 4-fluorophenyl substituents at positions 3 and 4 respectively; the (3S,4R)-diastereomer. Highly potent and selective 5-HT uptake inhibitor that binds with high affinity to the serotonin transporter (Ki = 0.05 nM). Ki values are 1.1, 350 and 1100 nM for inhibition of [3H]-5-HT, [3H]-l-NA and [3H]-DA uptake respectively. Displays minimal affinity for alpha1-, alpha2- or beta-adrenoceptors, 5-HT2A, 5-HT1A, D2 or H1 receptors at concentrations below 1000 nM, however displays weak affinity for muscarinic ACh receptors (Ki = 42 nM). Antidepressant and anxiolytic in vivo.		3.2310aromatic ether;
benzodioxoles;
organofluorine compound;
piperidines		antidepressant;
anxiolytic drug;
hepatotoxic agent;
P450 inhibitor;
serotonin uptake inhibitor
captopril
Captopril: A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.. captopril : A L-proline derivative in which L-proline is substituted on nitrogen with a (2S)-2-methyl-3-sulfanylpropanoyl group. It is used as an anti-hypertensive ACE inhibitor drug.		3.2310alkanethiol;
L-proline derivative;
N-acylpyrrolidine;
pyrrolidinemonocarboxylic acid		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
cefoperazone
Cefoperazone: Semisynthetic broad-spectrum cephalosporin with a tetrazolyl moiety that is resistant to beta-lactamase. It may be used to treat Pseudomonas infections.. cefoperazone : A semi-synthetic parenteral cephalosporin with a tetrazolyl moiety that confers beta-lactamase resistance.		3.2310cephalosporinantibacterial drug
atracurium
Atracurium: A non-depolarizing neuromuscular blocking agent with short duration of action. Its lack of significant cardiovascular effects and its lack of dependence on good kidney function for elimination provide clinical advantage over alternate non-depolarizing neuromuscular blocking agents.. atracurium : A diester compound consisting of pentane-1,5-diol with both hydroxyls bearing 3-[1-(3,4-dimethoxybenzyl)-6,7-dimethoxy-2-methyl-3,4-dihydroisoquinolinium-2(1H)-yl]propanoyl groups.		3.2310diester;
quaternary ammonium ion		muscle relaxant;
nicotinic antagonist
pergolide
Pergolide: A long-acting dopamine agonist which has been used to treat PARKINSON DISEASE and HYPERPROLACTINEMIA but withdrawn from some markets due to potential for HEART VALVE DISEASES.. pergolide : A diamine that is ergoline in which the beta-hydrogen at position 8 is replaced by a (methylthio)methyl group and the hydrogen attached to the piperidine nitrogen (position 6) is replaced by a propyl group. A dopamine D2 receptor agonist which also has D1 and D2 agonist properties, it is used as the mesylate salt in the management of Parkinson's disease, although it was withdrawn from the U.S. and Canadian markets in 2007 due to an increased risk of cardiac valve dysfunction.		3.2310diamine;
methyl sulfide;
organic heterotetracyclic compound		antiparkinson drug;
dopamine agonist
cefadroxil anhydrous
Cefadroxil: Long-acting, broad-spectrum, water-soluble, CEPHALEXIN derivative.. cefadroxil : A cephalosporin bearing methyl and (2R)-2-amino-2-(4-hydroxyphenyl)acetamido groups at positions 3 and 7, respectively, of the cephem skeleton.		3.2310cephalosporinantibacterial drug
fialuridine
[no description available]		3.2310
cefaclor anhydrous
Cefaclor: Semisynthetic, broad-spectrum antibiotic derivative of CEPHALEXIN.. cefaclor : A cephalosporin bearing chloro and (R)-2-amino-2-phenylacetamido groups at positions 3 and 7, respectively, of the cephem skeleton.		3.2310cephalosporinantibacterial drug;
drug allergen
alfentanil
Alfentanil: A short-acting opioid anesthetic and analgesic derivative of FENTANYL. It produces an early peak analgesic effect and fast recovery of consciousness. Alfentanil is effective as an anesthetic during surgery, for supplementation of analgesia during surgical procedures, and as an analgesic for critically ill patients.. alfentanil : A member of the class of piperidines that is piperidine having a 2-(4-ethyl-5-oxo-4,5-dihydro-1H-tetrazol-1-yl)ethyl group at the 1-position as well as N-phenylpropanamido- and methoxymethyl groups at the 4-position.		3.2310monocarboxylic acid amide;
piperidines		central nervous system depressant;
intravenous anaesthetic;
mu-opioid receptor agonist;
opioid analgesic;
peripheral nervous system drug
miglustat
miglustat: a glucosylceramide synthase inhibitor. miglustat : A hydroxypiperidine that is deoxynojirimycin in which the amino hydrogen is replaced by a butyl group.		3.2310piperidines;
tertiary amino compound		anti-HIV agent;
EC 2.4.1.80 (ceramide glucosyltransferase) inhibitor
haloperidol decanoate
[no description available]		3.2310organic molecular entity
cefotetan
Cefotetan: A semisynthetic cephamycin antibiotic that is administered intravenously or intramuscularly. The drug is highly resistant to a broad spectrum of beta-lactamases and is active against a wide range of both aerobic and anaerobic gram-positive and gram-negative microorganisms.. cefotetan : A semi-synthetic second-generation cephamycin antibiotic with [(1-methyl-1H-tetrazol-5-yl)sulfanyl]methyl, methoxy and {[4-(2-amino-1-carboxy-2-oxoethylidene)-1,3-dithietan-2-yl]carbonyl}amino groups at the 3, 7alpha, and 7beta positions, respectively, of the cephem skeleton. It is resistant to a wide range of beta-lactamases and is active against a broad spectrum of aerobic and anaerobic Gram-positive and Gram-negative microorganisms.		3.2310
lovastatin
Lovastatin: A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.. lovastatin : A fatty acid ester that is mevastatin carrying an additional methyl group on the carbobicyclic skeleton. It is used in as an anticholesteremic drug and has been found in fungal species such as Aspergillus terreus and Pleurotus ostreatus (oyster mushroom).		3.2310delta-lactone;
fatty acid ester;
hexahydronaphthalenes;
polyketide;
statin (naturally occurring)		anticholesteremic drug;
antineoplastic agent;
Aspergillus metabolite;
prodrug
tolrestat
tolrestat: RN & structure given in first source		3.2310naphthalenesEC 1.1.1.21 (aldehyde reductase) inhibitor
simvastatin
Simvastatin: A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.. simvastatin : A member of the class of hexahydronaphthalenes that is lovastatin in which the 2-methylbutyrate ester moiety has been replaced by a 2,2-dimethylbutyrate ester group. It is used as a cholesterol-lowering and anti-cardiovascular disease drug.		3.2310delta-lactone;
fatty acid ester;
hexahydronaphthalenes;
statin (semi-synthetic)		EC 1.1.1.34/EC 1.1.1.88 (hydroxymethylglutaryl-CoA reductase) inhibitor;
EC 3.4.24.83 (anthrax lethal factor endopeptidase) inhibitor;
ferroptosis inducer;
geroprotector;
prodrug
balsalazide
balsalazide: a mesalamine 5-aminosalicylate prodrug; 99% of ingested drug remains intact through the stomach and is delivered to and activated in the colon; used for inflammatory bowel disease, ulcerative colitis and radiation-induced proctosigmoiditis but avoided in patients with known hypersensitivity reaction to salicylates or mesalamine; structure in first source. balsalazide : A monohydroxybenzoic acid consisting of 5-aminosalicylic acid (mesalazine) linked to 4-aminobenzoyl-beta-alanine via an azo bond.		3.2310
pravastatin
Pravastatin: An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).. pravastatin : A carboxylic ester resulting from the formal condensation of (S)-2-methylbutyric acid with the hydroxy group adjacent to the ring junction of (3R,5R)-7-[(1S,2S,6S,8S,8aR)-6,8-dihydroxy-2-methyl-1,2,6,7,8,8a-hexahydronaphthalen-1-yl]-3,5-dihydroxyheptanoic acid. Derived from microbial transformation of mevastatin, pravastatin is a reversible inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA). The sodium salt is used for lowering cholesterol and preventing cardiovascular disease. It is one of the lower potency statins, but has the advantage of fewer side effects compared with lovastatin and simvastatin.		3.23103-hydroxy carboxylic acid;
carbobicyclic compound;
carboxylic ester;
hydroxy monocarboxylic acid;
secondary alcohol;
statin (semi-synthetic)		anticholesteremic drug;
environmental contaminant;
metabolite;
xenobiotic
cabergoline
Cabergoline: An ergoline derivative and dopamine D2-agonist that inhibits PROLACTIN secretion. It is used in the management of HYPERPROLACTINEMIA, and to suppress lactation following childbirth for medical reasons. Cabergoline is also used in the management of PARKINSON DISEASE.. cabergoline : An N-acylurea that is (8R)-ergoline-8-carboxamide in which the hydrogen attached to the piperidine nitrogen (position 6) is substituted by an allyl group and the hydrogens attached to the carboxamide nitrogen are substituted by a 3-(dimethylamino)propyl group and an N-ethylcarbamoyl group. A dopamine D2 receptor agonist, cabergoline is used in the management of Parkinson's disease and of disorders associated with hyperprolactinaemia.		3.2310N-acylureaantineoplastic agent;
antiparkinson drug;
dopamine agonist
atomoxetine
atomoxetine : A secondary amino compound having methyl and 3-(2-methylphenoxy)-3-phenylpropan-1-yl substituents.		3.2310aromatic ether;
secondary amino compound;
toluenes		adrenergic uptake inhibitor;
antidepressant;
environmental contaminant;
xenobiotic
quinapril
Quinapril: A tetrahydroisoquinoline derivative and ANGIOTENSIN CONVERTING ENZYME inhibitor that is used in the treatment of HYPERTENSION and HEART FAILURE.. quinapril : A member of the class of isoquinolines that is (3S)-2-L-alanyl-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid in which the alpha-amino group of the alanyl residue has been substituted by a 1-ethoxycarbonyl-4-phenylbutan-2-yl group (the all-S isomer). A prodrug for quinaprilat (by hydrolysis of the ethyl ester to the corresponding carboxylic acid), it is used as an angiotensin-converting enzyme inhibitor (ACE inhibitor) used (generally as the hydrochloride salt) for the treatment of hypertension and congestive heart failure.		3.2310dicarboxylic acid monoester;
ethyl ester;
isoquinolines;
tertiary carboxamide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
alpidem
[no description available]		3.2310imidazoles
mifepristone
Mifepristone: A progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua. As a glucocorticoid receptor antagonist, the drug has been used to treat hypercortisolism in patients with nonpituitary CUSHING SYNDROME.		3.23103-oxo-Delta(4) steroid;
acetylenic compound;
tertiary amino compound		abortifacient;
contraceptive drug;
hormone antagonist;
synthetic oral contraceptive
fosphenytoin
fosphenytoin: structure given in first & second source		3.2310imidazolidine-2,4-dione
ranolazine
Ranolazine: An acetanilide and piperazine derivative that functions as a SODIUM CHANNEL BLOCKER and prevents the release of enzymes during MYOCARDIAL ISCHEMIA. It is used in the treatment of ANGINA PECTORIS.. N-(2,6-dimethylphenyl)-2-{4-[2-hydroxy-3-(2-methoxyphenoxy)propyl]piperazin-1-yl}acetamide : An aromatic amide obtained by formal condensation of the carboxy group of 2-{4-[2-hydroxy-3-(2-methoxyphenoxy)propyl]piperazin-1-yl}acetic acid with the amino group of 2,6-dimethylaniline.. ranolazine : A racemate comprising equal amounts of (R)- and (S)-ranolazine. Used for treatment of chronic angina.		3.2310aromatic amide;
monocarboxylic acid amide;
monomethoxybenzene;
N-alkylpiperazine;
secondary alcohol
finasteride
Finasteride: An orally active 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE inhibitor. It is used as a surgical alternative for treatment of benign PROSTATIC HYPERPLASIA.. finasteride : An aza-steroid that is a synthetic drug for the treatment of benign prostatic hyperplasia.		3.23103-oxo steroid;
aza-steroid;
delta-lactam		androgen antagonist;
antihyperplasia drug;
EC 1.3.1.22 [3-oxo-5alpha-steroid 4-dehydrogenase (NADP(+))] inhibitor
esmolol
methyl 3-{4-[2-hydroxy-3-(propan-2-ylamino)propoxy]phenyl}propanoate : A methyl ester that is methyl 3-(4-hydroxyphenyl)propanoate in which the hydrogen attached to the phenolic hydroxy group is substituted by a 2-hydroxy-3-(isopropylamino)propyl group.. esmolol : A racemate comprising equimolar amounts of (R)- and (S)-esmolol. A cardioselective and short-acting beta1 receptor blocker with rapid onset but lacking intrinsic sympathomimetic and membrane-stabilising properties, it is used as the hydrochloride salt in the management of supraventricular arrhythmias, and for the control of hypertension and tachycardia during surgery. While the S enantiomer possesses all of the heart rate control, both enantiomers contribute to lowering blood pressure.		3.2310aromatic ether;
ethanolamines;
methyl ester;
secondary alcohol;
secondary amino compound
adefovir
adefovir: inhibitor of African swine fever virus. adefovir(1-) : A organophosphonate oxoanion obtained by removal of a proton from the phosphonate group of adefovir, a nucleoside reverse transcriptase inhibitor. It is the major microspecies at pH 7.3 (according to Marvin v 6.2.0.).. adefovir : A member of the class of phosphonic acids that is methylphosphonic acid in which one of the methyl hydrogens has been replaced by a 2-(6-amino-9H-purin-9-yl)ethoxy group. An inhibitor of HIV-1 reverse transcriptase, the bis(t-butoxycarbonyloxymethyl) ester (dipivoxil ester) prodrug is used to treat chronic hepatitis B viral infection.		3.23106-aminopurines;
ether;
phosphonic acids		antiviral drug;
DNA synthesis inhibitor;
drug metabolite;
HIV-1 reverse transcriptase inhibitor;
nephrotoxic agent
aromasil
[no description available]		3.231017-oxo steroid;
3-oxo-Delta(1),Delta(4)-steroid		antineoplastic agent;
EC 1.14.14.14 (aromatase) inhibitor;
environmental contaminant;
xenobiotic
zileuton
[no description available]		3.23101-benzothiophenes;
ureas		anti-asthmatic drug;
EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor;
ferroptosis inhibitor;
leukotriene antagonist;
non-steroidal anti-inflammatory drug
clopidogrel
Clopidogrel: A ticlopidine analog and platelet purinergic P2Y receptor antagonist that inhibits adenosine diphosphate-mediated PLATELET AGGREGATION. It is used to prevent THROMBOEMBOLISM in patients with ARTERIAL OCCLUSIVE DISEASES; MYOCARDIAL INFARCTION; STROKE; or ATRIAL FIBRILLATION.. clopidogrel : A thienopyridine that is 4,5,6,7-tetrahydrothieno[3,2-c]pyridine in which the hydrogen attached to the nitrogen is replaced by an o-chlorobenzyl group, the methylene hydrogen of which is replaced by a methoxycarbonyl group (the S enantiomer). A P2Y12 receptor antagonist, it is used to inhibit blood clots and prevent heart attacks.		3.2310methyl ester;
monochlorobenzenes;
thienopyridine		anticoagulant;
P2Y12 receptor antagonist;
platelet aggregation inhibitor
cidofovir anhydrous
Cidofovir: An acyclic nucleoside phosphonate that acts as a competitive inhibitor of viral DNA polymerases. It is used in the treatment of RETINITIS caused by CYTOMEGALOVIRUS INFECTIONS and may also be useful for treating HERPESVIRUS INFECTIONS.. cidofovir anhydrous : Cytosine substituted at the 1 position by a 3-hydroxy-2-(phosphonomethoxy)propyl group (S configuration). A nucleoside analogue, it is an injectable antiviral used for the treatment of cytomegalovirus (CMV) retinitis in AIDS patients.		3.2310phosphonic acids;
pyrimidone		anti-HIV agent;
antineoplastic agent;
antiviral drug;
photosensitizing agent
tiagabine
Tiagabine: A nipecotic acid derivative that acts as a GABA uptake inhibitor and anticonvulsant agent. It is used in the treatment of EPILEPSY, for refractory PARTIAL SEIZURES.. tiagabine : A piperidinemonocarboxylic acid that is (R)-nipecotic acid in which the hydrogen attached to the nitrogen has been replaced by a 1,1-bis(3-methyl-2-thienyl)but-1-en-4-yl group. A GABA reuptake inhibitor, it is used (generally as the hydrochloride salt) for the treatment of epilepsy.		3.2310beta-amino acid;
piperidinemonocarboxylic acid;
tertiary amino compound;
thiophenes		anticonvulsant;
GABA reuptake inhibitor
topotecan
Topotecan: An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA TOPOISOMERASES, TYPE I.. topotecan : A pyranoindolizinoquinoline used as an antineoplastic agent. It is a derivative of camptothecin and works by binding to the topoisomerase I-DNA complex and preventing religation of these 328 single strand breaks.		3.2310pyranoindolizinoquinolineantineoplastic agent;
EC 5.99.1.2 (DNA topoisomerase) inhibitor
bromfenac
bromfenac: bromfenac sodium is the active cpd; structure in first source. bromfenac : Amfenac in which the the hydrogen at the 4 position of the benzoyl group is substituted by bromine. It is used for the management of ocular pain and treatment of postoperative inflammation in patients who have undergone cataract extraction. It was withdrawn from the US market in 1998, following concerns over off-label abuse and hepatic failure.		3.2310aromatic amino acid;
benzophenones;
organobromine compound;
substituted aniline		non-narcotic analgesic;
non-steroidal anti-inflammatory drug
gemcitabine
gemcitabine : A 2'-deoxycytidine having geminal fluoro substituents in the 2'-position. An inhibitor of ribonucleotide reductase, gemcitabine is used in the treatment of various carcinomas, particularly non-small cell lung cancer, pancreatic cancer, bladder cancer and breast cancer.		3.2310organofluorine compound;
pyrimidine 2'-deoxyribonucleoside		antimetabolite;
antineoplastic agent;
antiviral drug;
DNA synthesis inhibitor;
EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor;
environmental contaminant;
immunosuppressive agent;
photosensitizing agent;
prodrug;
radiosensitizing agent;
xenobiotic
ibutilide
ibutilide: RN & structure in first source; RN refers to the fumarate salt		3.2310benzenes;
organic amino compound
aripiprazole
Aripiprazole: A piperazine and quinolone derivative that is used primarily as an antipsychotic agent. It is a partial agonist of SEROTONIN RECEPTOR, 5-HT1A and DOPAMINE D2 RECEPTORS, where it also functions as a post-synaptic antagonist, and an antagonist of SEROTONIN RECEPTOR, 5-HT2A. It is used for the treatment of SCHIZOPHRENIA and BIPOLAR DISORDER, and as an adjunct therapy for the treatment of depression.. aripiprazole : An N-arylpiperazine that is piperazine substituted by a 4-[(2-oxo-1,2,3,4-tetrahydroquinolin-7-yl)oxy]butyl group at position 1 and by a 2,3-dichlorophenyl group at position 4. It is an antipsychotic drug used for the treatment of Schizophrenia, and other mood disorders.		3.2310aromatic ether;
delta-lactam;
dichlorobenzene;
N-alkylpiperazine;
N-arylpiperazine;
quinolone		drug metabolite;
H1-receptor antagonist;
second generation antipsychotic;
serotonergic agonist
remifentanil
Remifentanil: A piperidine-propionate derivative and opioid analgesic structurally related to FENTANYL. It functions as a short-acting MU OPIOID RECEPTOR agonist, and is used as an analgesic during induction or maintenance of general anesthesia, following surgery, during childbirth, and in mechanically ventilated patients under intensive care.. remifentanil : A piperidinecarboxylate ester that is methyl piperidine-4-carboxylate in which the hydrogen attached to the nitrogen is substituted by a 3-methoxy-3-oxopropyl group and the hydrogen at position 4 is substituted the nitrogen of N-propanoylaniline.		3.2310alpha-amino acid ester;
anilide;
monocarboxylic acid amide;
piperidinecarboxylate ester		intravenous anaesthetic;
mu-opioid receptor agonist;
opioid analgesic;
sedative
atorvastatin
[no description available]		3.2310aromatic amide;
dihydroxy monocarboxylic acid;
monofluorobenzenes;
pyrroles;
statin (synthetic)		environmental contaminant;
xenobiotic
lamivudine
[no description available]		3.2310monothioacetal;
nucleoside analogue;
oxacycle;
primary alcohol		allergen;
anti-HBV agent;
antiviral drug;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor;
HIV-1 reverse transcriptase inhibitor;
prodrug
duloxetine
[no description available]		3.2310duloxetine
irinotecan
[no description available]		3.2310carbamate ester;
delta-lactone;
N-acylpiperidine;
pyranoindolizinoquinoline;
ring assembly;
tertiary alcohol;
tertiary amino compound		antineoplastic agent;
apoptosis inducer;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
prodrug
valsartan
Valsartan: A tetrazole derivative and ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to treat HYPERTENSION.. valsartan : A monocarboxylic acid amide consisting of L-valine in which the amino hydrogens have been replaced by a pentanoyl and a [2'-(1H-tetrazol-5-yl)biphenyl]-4-yl]methyl group. It exhibits antihypertensive activity.		3.2310biphenylyltetrazole;
monocarboxylic acid amide;
monocarboxylic acid		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
ibandronic acid
Ibandronic Acid: Aminobisphosphonate that is a potent inhibitor of BONE RESORPTION. It is used in the treatment of HYPERCALCEMIA associated with malignancy, for the prevention of fracture and bone complications in patients with breast cancer and bone metastases, and for the treatment and prevention of POSTMENOPAUSAL OSTEOPOROSIS.		3.2310
ziprasidone
ziprasidone: a benzisothiazoylpiperazine derivative; has combined dopamine and serotonin receptor antagonist activity; structurally related to tiospirone. ziprasidone : A piperazine compound having 1,2-benzothiazol-3-yl- and 2-(6-chloro-1,3-dihydro-2-oxindol-5-yl)ethyl substituents attached to the nitrogen atoms.		3.23101,2-benzisothiazole;
indolones;
organochlorine compound;
piperazines		antipsychotic agent;
dopaminergic antagonist;
histamine antagonist;
muscarinic antagonist;
psychotropic drug;
serotonergic antagonist
zolmitriptan
zolmitriptan: an antimigraine compound; a serotonin (5HT)-1D receptor agonist. zolmitriptan : A member of the class of tryptamines that is N,N-dimethyltryptamine in which the hydrogen at position 5 of the indole ring has been replaced by a [(4S)-2-oxo-1,3-oxazolidin-4-yl]methyl group. A serotonin 5-HT1 B and D receptor agonist, it is used for the treatment of migraine.		3.2310oxazolidinone;
tryptamines		anti-inflammatory drug;
serotonergic agonist;
vasoconstrictor agent
emtricitabine
Emtricitabine: A deoxycytidine analog and REVERSE TRANSCRIPTASE INHIBITOR with antiviral activity against HIV-1 and HEPATITIS B viruses. It is used to treat HIV INFECTIONS.. emtricitabine : An organofluorine compound that is 5-fluorocytosine substituted at the 1 position by a 2-(hydroxymethyl)-1,3-oxathiolan-5-yl group (2R,5S configuration). It is used in combination therapy for the treatment of HIV-1 infection.		3.2310monothioacetal;
nucleoside analogue;
organofluorine compound;
pyrimidone		antiviral drug;
HIV-1 reverse transcriptase inhibitor
tasosartan
tasosartan: angiotensin II antagonist; structure given in first source		3.2310biphenyls
tiludronic acid
tiludronic acid: a bone resorption inhibitor; an antihypercalcemic agent; used in the tratment of Paget's disease; used in the treatment and prevention of osteoporosis; structure given in first source		3.2310organochlorine compound
tirofiban
Tirofiban: Tyrosine analog and PLATELET GLYCOPROTEIN GPIIB-IIIA COMPLEX antagonist that inhibits PLATELET AGGREGATION and is used in the treatment of ACUTE CORONARY SYNDROME.. tirofiban : A member of the class of piperidines that is L-tyrosine in which a hydrogen attached to the amino group is replaced by a butylsulfonyl group and in which the hydrogen attached to the phenolic hydroxy group is replaced by a 4-(piperidin-4-yl)butyl group.		3.2310L-tyrosine derivative;
piperidines;
sulfonamide		anticoagulant;
fibrin modulating drug;
platelet glycoprotein-IIb/IIIa receptor antagonist
capecitabine
Capecitabine: A deoxycytidine derivative and fluorouracil PRODRUG that is used as an ANTINEOPLASTIC ANTIMETABOLITE in the treatment of COLON CANCER; BREAST CANCER and GASTRIC CANCER.. capecitabine : A carbamate ester that is cytidine in which the hydrogen at position 5 is replaced by fluorine and in which the amino group attached to position 4 is converted into its N-(penyloxy)carbonyl derivative. Capecitabine is a antineoplastic agent used in the treatment of cancers.		3.2310carbamate ester;
cytidines;
organofluorine compound		antimetabolite;
antineoplastic agent;
prodrug
adenosine
quinquefolan B: isolated from roots of Panax quinquefolium L.; RN not in Chemline 10/87; RN from Toxlit		3.2310adenosines;
purines D-ribonucleoside		analgesic;
anti-arrhythmia drug;
fundamental metabolite;
human metabolite;
vasodilator agent
trovafloxacin
trovafloxacin: a trifluoronaphthyridone derivative of 7-(3-azabicyclo(3.1.0)hexyl)naphthyridone; has antineoplastic activity. trovafloxacin : A 1,8-naphthyridine derivative that is 4-oxo-1,4-dihydro-1,8-naphthyridine-3-carboxylic acid bearing additional 2,4-difluorophenyl, fluoro and 6-amino-3-azabicyclo[3.1.0]hex-3-yl substituents at positions 1, 6 and 7 respectively. A broad-spectrum antibiotic that was withdrawn from the market due to risk of liver failure.		3.2310
cefprozil
[no description available]		3.2310cephalosporin;
semisynthetic derivative		antibacterial drug
efavirenz
efavirenz: HIV-1 reverse transcriptase inhibitor. efavirenz : 1,4-Dihydro-2H-3,1-benzoxazin-2-one substituted at the 4 position by cyclopropylethynyl and trifluoromethyl groups (S configuration) and at the 6 position by chlorine. A non-nucleoside reverse transcriptase inhibitor with activity against HIV, it is used with other antiretrovirals for combination therapy of HIV infection.		3.2310acetylenic compound;
benzoxazine;
cyclopropanes;
organochlorine compound;
organofluorine compound		antiviral drug;
HIV-1 reverse transcriptase inhibitor
nelfinavir
Nelfinavir: A potent HIV protease inhibitor. It is used in combination with other antiviral drugs in the treatment of HIV in both adults and children.. nelfinavir : An aryl sulfide that is used (as its mesylate salt) for treatment of HIV and also exhibits some anticancer properties.		3.2310aryl sulfide;
benzamides;
organic heterobicyclic compound;
phenols;
secondary alcohol;
tertiary amino compound		antineoplastic agent;
HIV protease inhibitor
fenofibric acid
fenofibric acid: RN given refers to parent cpd without isomeric designation; structure. fenofibric acid : A monocarboxylic acid that is 2-methylpropanoic acid substituted by a 4-(4-chlorobenzoyl)phenoxy group at position 2. It is a metabolite of the drug fenofibrate.		3.2310aromatic ketone;
chlorobenzophenone;
monocarboxylic acid		drug metabolite;
marine xenobiotic metabolite
plerixafor
plerixafor: a bicyclam derivate, highly potent & selective inhibitor of HIV-1 & HIV-2. plerixafor : An azamacrocycle consisting of two cyclam rings connected by a 1,4-phenylenebis(methylene) linker. It is a CXCR4 chemokine receptor antagonist and a hematopoietic stem cell mobilizer. It is used in combination with grulocyte-colony stimulating factor (G-CSF) to mobilize hematopoietic stem cells to the perpheral blood for collection and subsequent autologous transplantation in patients with non-Hodgkin's lymphoma and multiple myeloma.		3.2310azacycloalkane;
azamacrocycle;
benzenes;
crown amine;
secondary amino compound;
tertiary amino compound		anti-HIV agent;
antineoplastic agent;
C-X-C chemokine receptor type 4 antagonist;
immunological adjuvant
amprenavir
[no description available]		3.2310carbamate ester;
sulfonamide;
tetrahydrofuryl ester		antiviral drug;
HIV protease inhibitor
oseltamivir
Oseltamivir: An acetamido cyclohexene that is a structural homolog of SIALIC ACID and inhibits NEURAMINIDASE.. oseltamivir : A cyclohexenecarboxylate ester that is the ethyl ester of oseltamivir acid. An antiviral prodrug (it is hydrolysed to the active free carboxylic acid in the liver), it is used to slow the spread of influenza.		3.2310acetamides;
amino acid ester;
cyclohexenecarboxylate ester;
primary amino compound		antiviral drug;
EC 3.2.1.18 (exo-alpha-sialidase) inhibitor;
environmental contaminant;
prodrug;
xenobiotic
histamine phosphate
histamine phosphate : A phosphate salt that is the diphosphate salt of histamine.		3.2310phosphate salthistamine agonist
tilbroquinol
[no description available]		3.2310organohalogen compound;
quinolines
bendamustine
[no description available]		3.2310benzimidazoles
droxicam
droxicam: structure given in first source. droxicam : An organic heterotricyclic compound that is 2H,5H-[1,3]oxazino[5,6-c][1,2]benzothiazine-2,4(3H)-dione 6,6-dioxide substituted at positions 3 and 5 by pyridin-2-yl and methyl groups respectively. A prodrug of piroxicam, it is used for the relief of pain and inflammation in musculoskeletal disorders such as rheumatoid arthritis and osteoarthritis.		3.2310organic heterotricyclic compound;
pyridines		cyclooxygenase 1 inhibitor;
hepatotoxic agent;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
platelet aggregation inhibitor;
prodrug
ebrotidine
ebrotidine: an H2-receptor antagonist and gastric mucosa protector		3.2310sulfonamide
repaglinide
[no description available]		4.0920piperidines
telmisartan
Telmisartan: A biphenyl compound and benzimidazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION.. telmisartan : A member of the class of benzimidazoles used widely in the treatment of hypertension.		3.2310benzimidazoles;
biphenyls;
carboxybiphenyl		angiotensin receptor antagonist;
antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
environmental contaminant;
xenobiotic
sertraline
Sertraline: A selective serotonin uptake inhibitor that is used in the treatment of depression.. sertraline : A member of the class of tetralins that is tetralin which is substituted at positions 1 and 4 by a methylamino and a 3,4-dichlorophenyl group, respectively (the S,S diastereoisomer). A selective serotonin-reuptake inhibitor (SSRI), it is administered orally as the hydrochloride salt as an antidepressant for the treatment of depression, obsessive-compulsive disorder, panic disorder and post-traumatic stress disorder.		3.2310dichlorobenzene;
secondary amino compound;
tetralins		antidepressant;
serotonin uptake inhibitor
zoledronic acid
Zoledronic Acid: An imidobisphosphonate inhibitor of BONE RESORPTION that is used for the treatment of malignancy-related HYPERCALCEMIA; OSTEITIS DEFORMANS; and OSTEOPOROSIS.. zoledronic acid : An imidazole compound having a 2,2-bis(phosphono)-2-hydroxyethane-1-yl substituent at the 1-position.		3.23101,1-bis(phosphonic acid);
imidazoles		bone density conservation agent
acamprosate
Acamprosate: Structural analog of taurine that is used for the prevention of relapse in individuals with ALCOHOLISM.. acamprosate : An organosulfonic acid that is propane-1-sulfonic acid substituted by an acetylamino group at position 3.		3.2310acetamides;
organosulfonic acid		environmental contaminant;
neurotransmitter agent;
xenobiotic
isaxonine
isaxonine: promotes nerve growth		3.2310aminopyrimidine
nebivolol
2,2'-iminobis[1-(6-fluoro-3,4-dihydro-2H-chromen-2-yl)ethanol] : A member of the class of chromanes that is 2,2'-iminodiethanol in which one hydrogen attached to each hydroxy-bearing carbon is replaced by a 6-fluorochroman-2-yl group.		3.2310chromanes;
diol;
organofluorine compound;
secondary alcohol;
secondary amino compound
uk 68798
[no description available]		3.2310aromatic ether;
sulfonamide;
tertiary amino compound		anti-arrhythmia drug;
potassium channel blocker
hp 873
iloperidone: an atypical, negative symptom antipsychotic agent. iloperidone : A member of the class of piperidines that is the 4-acetyl-2-methoxyphenyl ether of 3-(piperidin-1-yl)propan-1-ol which is substituted at position 4 of the piperidine ring by a 6-fluoro-1,2-benzoxazol-3-yl group. A member of the group of second generation antipsychotics (also known as an atypical antipsychotics), it is used for the treatment of schizophrenia.		3.23101,2-benzoxazoles;
aromatic ether;
aromatic ketone;
methyl ketone;
monoamine;
organofluorine compound;
piperidines;
tertiary amino compound		dopaminergic antagonist;
second generation antipsychotic;
serotonergic antagonist
dexrazoxane
Dexrazoxane: The (+)-enantiomorph of razoxane.		3.2310razoxaneantineoplastic agent;
cardiovascular drug;
chelator;
immunosuppressive agent
fenoxypropazine
[no description available]		3.2310aromatic ether
voriconazole
Voriconazole: A triazole antifungal agent that specifically inhibits STEROL 14-ALPHA-DEMETHYLASE and CYTOCHROME P-450 CYP3A.. voriconazole : A triazole-based antifungal agent used for the treatment of esophageal candidiasis, invasive pulmonary aspergillosis, and serious fungal infections caused by Scedosporium apiospermum and Fusarium spp. It is an inhibitor of cytochrome P450 2C9 (CYP2C9) and CYP3A4.		3.2310conazole antifungal drug;
difluorobenzene;
pyrimidines;
tertiary alcohol;
triazole antifungal drug		P450 inhibitor
aceclofenac
[no description available]		3.2310amino acid;
carboxylic ester;
dichlorobenzene;
monocarboxylic acid;
secondary amino compound		EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
nitrefazole
[no description available]		3.2310imidazoles
doripenem
Doripenem: A carbapenem derivative antibacterial agent that is more stable to renal dehydropeptidase I than IMIPENEM, but does not need to be given with an enzyme inhibitor such as CILASTATIN. It is used in the treatment of infections such as HOSPITAL-ACQUIRED PNEUMONIA, and complicated intra-abdominal or urinary-tract infections, including PYELONEPHRITIS.		3.2310carbapenems
atovaquone
Atovaquone: A hydroxynaphthoquinone that has antimicrobial activity and is being used in antimalarial protocols.. atovaquone : A naphthoquinone compound having a 4-(4-chlorophenyl)cyclohexyl group at the 2-position and a hydroxy substituent at the 3-position.		3.2310hydroxy-1,2-naphthoquinone
rivastigmine
[no description available]		3.2310carbamate ester;
tertiary amino compound		cholinergic drug;
EC 3.1.1.8 (cholinesterase) inhibitor;
neuroprotective agent
frovatriptan
[no description available]		3.2310carbazoles
eletriptan
eletriptan: 5-HT(1B/1D) receptor agonist; structure in first source. eletriptan : An N-alkylpyrrolidine, that is N-methylpyrrolidine in which the pro-R hydrogen at position 2 is replaced by a {5-[2-(phenylsulfonyl)ethyl]-1H-indol-3-yl}methyl group.		3.2310indoles;
N-alkylpyrrolidine;
sulfone		non-steroidal anti-inflammatory drug;
serotonergic agonist;
vasoconstrictor agent
rosiglitazone
[no description available]		4.0920aminopyridine;
thiazolidinediones		EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
insulin-sensitizing drug
bexarotene
[no description available]		3.2310benzoic acids;
naphthalenes;
retinoid		antineoplastic agent
clarithromycin
Clarithromycin: A semisynthetic macrolide antibiotic derived from ERYTHROMYCIN that is active against a variety of microorganisms. It can inhibit PROTEIN SYNTHESIS in BACTERIA by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation.. clarithromycin : The 6-O-methyl ether of erythromycin A, clarithromycin is a macrolide antibiotic used in the treatment of respiratory-tract, skin and soft-tissue infections. It is also used to eradicate Helicobacter pylori in the treatment of peptic ulcer disease. It prevents bacteria from growing by interfering with their protein synthesis.		3.2310macrolide antibioticantibacterial drug;
environmental contaminant;
protein synthesis inhibitor;
xenobiotic
moexipril
[no description available]		3.2310peptide
mci 9038
[no description available]		3.2310peptide
fulvestrant
Fulvestrant: An estradiol derivative and estrogen receptor antagonist that is used for the treatment of estrogen receptor-positive, locally advanced or metastatic breast cancer.. fulvestrant : A 3-hydroxy steroid that is 17beta-estradiol in which the 7alpha hydrogen has been replaced by a nonyl group in which one of the hydrogens of the terminal methyl has been replaced by a (4,4,5,5,5-pentafluoropentyl)sulfinyl group. An estrogen receptor antagonist, it is used in the treatment of breast cancer.		3.231017beta-hydroxy steroid;
3-hydroxy steroid;
organofluorine compound;
sulfoxide		antineoplastic agent;
estrogen antagonist;
estrogen receptor antagonist
bosentan anhydrous
Bosentan: A sulfonamide and pyrimidine derivative that acts as a dual endothelin receptor antagonist used to manage PULMONARY HYPERTENSION and SYSTEMIC SCLEROSIS.		3.2310primary alcohol;
pyrimidines;
sulfonamide		antihypertensive agent;
endothelin receptor antagonist
perindopril
Perindopril: An angiotensin-converting enzyme inhibitor. It is used in patients with hypertension and heart failure.. perindopril : An alpha-amino acid ester that is the ethyl ester of N-{(2S)-1-[(2S,3aS,7aS)-2-carboxyoctahydro-1H-indol-1-yl]-1-oxopropan-2-yl}-L-norvaline		3.2310alpha-amino acid ester;
dicarboxylic acid monoester;
ethyl ester;
organic heterobicyclic compound		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
tadalafil
[no description available]		3.2310benzodioxoles;
pyrazinopyridoindole		EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor;
vasodilator agent
paliperidone
3-{2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl}-9-hydroxy-2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one : A member of the class of pyridopyrimidines that is 9-hydroxy-2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one carrying an additional 2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl group at position 2.. paliperidone : A racemate comprising equimolar amounts of (R)- and (S)-paliperidone. Paliperidone is the primary active metabolite of the older antipsychotic risperidone and is used for treatment of schizophrenia.		3.23101,2-benzoxazoles;
heteroarylpiperidine;
organofluorine compound;
pyridopyrimidine;
secondary alcohol
nitisinone
[no description available]		3.2310(trifluoromethyl)benzenes;
C-nitro compound;
cyclohexanones;
mesotrione		EC 1.13.11.27 (4-hydroxyphenylpyruvate dioxygenase) inhibitor
clofarabine
[no description available]		3.2310adenosines;
organofluorine compound		antimetabolite;
antineoplastic agent
pramipexole
Pramipexole: A benzothiazole derivative and dopamine agonist with antioxidant properties that is used in the treatment of PARKINSON DISEASE and RESTLESS LEGS SYNDROME.. pramipexole : A member of the class of benzothiazoles that is 4,5,6,7-tetrahydro-1,3-benzothiazole in which the hydrogens at the 2 and 6-pro-S-positions are substituted by amino and propylamino groups, respectively.		3.2310benzothiazoles;
diamine		antidyskinesia agent;
antiparkinson drug;
dopamine agonist;
radical scavenger
valdecoxib
[no description available]		3.2310isoxazoles;
sulfonamide		antipyretic;
antirheumatic drug;
cyclooxygenase 2 inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
almotriptan
almotriptan : An indole compound having a 2-(dimethylamino)ethyl group at the 3-position and a (pyrrolidin-1-ylsulfonyl)methyl group at the 5-position.		3.2310indoles;
sulfonamide;
tertiary amine		non-steroidal anti-inflammatory drug;
serotonergic agonist;
vasoconstrictor agent
gefitinib
[no description available]		3.2310aromatic ether;
monochlorobenzenes;
monofluorobenzenes;
morpholines;
quinazolines;
secondary amino compound;
tertiary amino compound		antineoplastic agent;
epidermal growth factor receptor antagonist
desloratadine
desloratadine: major metabolite of loratadine. desloratadine : Loratadine in which the ethoxycarbonyl group attached to the piperidine ring is replaced by hydrogen. The major metabolite of loratidine, desloratadine is an antihistamine which is used for the symptomatic relief of allergic conditions including rhinitis and chronic urticaria. It does not readily enter the central nervous system, so does not cause drowsiness.		3.2310benzocycloheptapyridineanti-allergic agent;
cholinergic antagonist;
drug metabolite;
H1-receptor antagonist
desvenlafaxine
O-desmethylvenlafaxine : A tertiary amino compound that is N,N-dimethylethanamine substituted at position 1 by a 1-hydroxycyclohexyl and 4-hydroxyphenyl group. It is a metabolite of the drug venlafaxine.		3.2310cyclohexanols;
phenols;
tertiary amino compound		antidepressant;
drug metabolite;
marine xenobiotic metabolite
methotrexate
[no description available]		3.2310dicarboxylic acid;
monocarboxylic acid amide;
pteridines		abortifacient;
antimetabolite;
antineoplastic agent;
antirheumatic drug;
dermatologic drug;
DNA synthesis inhibitor;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
immunosuppressive agent
tamsulosin
[no description available]		3.23105-(2-{[2-(2-ethoxyphenoxy)ethyl]amino}propyl)-2-methoxybenzenesulfonamidealpha-adrenergic antagonist;
antineoplastic agent
rufinamide
rufinamide: for treatment of Lennox-Gastaut syndrome; structure in first source		3.2310aromatic amide;
heteroarene
olmesartan medoxomil
Olmesartan Medoxomil: An ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to manage HYPERTENSION.		3.2310biphenyls
dexpanthenol
dexpanthenol: The alcohol of pantothenic acid		3.2310amino alcohol;
monocarboxylic acid amide		cholinergic drug;
provitamin
fosamprenavir
fosamprenavir: a prodrug of the protease inhibitor amprenavir. fosamprenavir : A sulfonamide with a structure based on that of sulfanilamide substituted on the sulfonamide nitrogen by a (2R,3S)-4-phenyl-2-(phosphonooxy)-3-({[(3S)-tetrahydrofuran-3-yloxy]carbonyl}amino)butyl group. It is a pro-drug of the HIV protease inhibitor and antiretroviral drug amprenavir.		3.2310sulfonamideprodrug
febuxostat
Febuxostat: A thiazole derivative and inhibitor of XANTHINE OXIDASE that is used for the treatment of HYPERURICEMIA in patients with chronic GOUT.. febuxostat : A 1,3-thiazolemonocarboxylic acid that is 4-methyl-1,3-thiazole-5-carboxylic acid which is substituted by a 3-cyano-4-(2-methylpropoxy)phenyl group at position 2. It is an orally-active, potent, and selective xanthine oxidase inhibitor used for the treatment of chronic hyperuricaemia in patients with gout.		3.23101,3-thiazolemonocarboxylic acid;
aromatic ether;
nitrile		EC 1.17.3.2 (xanthine oxidase) inhibitor
escitalopram
Escitalopram: S-enantiomer of CITALOPRAM. Belongs to a class of drugs known as SELECTIVE SEROTONIN REUPTAKE INHIBITORS, used to treat depression and generalized anxiety disorder.. escitalopram : A 1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrile that has S-configuration at the chiral centre. It is the active enantiomer of citalopram.		3.23101-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrileantidepressant;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
10-propargyl-10-deazaaminopterin
10-propargyl-10-deazaaminopterin: structure in first source. pralatrexate : A pteridine that is the N-4-[1-(2,4-diaminopteridin-6-yl)pent-4-yn-2-yl]benzoyl derivative of L-glutamic acid. Used for treatment of Peripheral T-Cell Lymphoma, an aggressive form of non-Hodgkins lymphoma.		3.2310N-acyl-L-glutamic acid;
pteridines;
terminal acetylenic compound		antimetabolite;
antineoplastic agent;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor
docetaxel anhydrous
Docetaxel: A semisynthetic analog of PACLITAXEL used in the treatment of locally advanced or metastatic BREAST NEOPLASMS and NON-SMALL CELL LUNG CANCER.. docetaxel anhydrous : A tetracyclic diterpenoid that is paclitaxel with the N-benzyloxycarbonyl group replaced by N-tert-butoxycarbonyl, and the acetoxy group at position 10 replaced by a hydroxy group.		3.2310secondary alpha-hydroxy ketone;
tetracyclic diterpenoid		antimalarial;
antineoplastic agent;
photosensitizing agent
atazanavir
atazanavir : A heavily substituted carbohydrazide that is an antiretroviral drug of the protease inhibitor (PI) class used to treat infection of human immunodeficiency virus (HIV).		3.2310carbohydrazideantiviral drug;
HIV protease inhibitor
levofloxacin
Levofloxacin: The L-isomer of Ofloxacin.. levofloxacin : An optically active form of ofloxacin having (S)-configuration; an inhibitor of bacterial topoisomerase IV and DNA gyrase.		3.23109-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid;
fluoroquinolone antibiotic;
quinolone antibiotic		antibacterial drug;
DNA synthesis inhibitor;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
topoisomerase IV inhibitor
ezetimibe
Ezetimibe: An azetidine derivative and ANTICHOLESTEREMIC AGENT that inhibits intestinal STEROL absorption. It is used to reduce total CHOLESTEROL; LDL CHOLESTEROL, and APOLIPOPROTEINS B in the treatment of HYPERLIPIDEMIAS.. ezetimibe : A beta-lactam that is azetidin-2-one which is substituted at 1, 3, and 4 by p-fluorophenyl, 3-(p-fluorophenyl)-3-hydroxypropyl, and 4-hydroxyphenyl groups, respectively (the 3R,3'S,4S enantiomer).		3.2310azetidines;
beta-lactam;
organofluorine compound		anticholesteremic drug;
antilipemic drug;
antimetabolite
ertapenem
Ertapenem: A carbapenem derivative antibacterial agent that is more stable to renal dehydropeptidase I than IMIPENEM, but does not need to be given with an enzyme inhibitor such as CILASTATIN. It is used in the treatment of Gram-positive and Gram-negative bacterial infections including intra-abdominal infections, acute gynecological infections, complicated urinary tract infections, skin infections, and respiratory tract infections. It is also used to prevent infection in colorectal surgery.. ertapenem : Meropenem in which the one of the two methyl groups attached to the amide nitrogen is replaced by hydrogen while the other is replaced by a 3-carboxyphenyl group. The sodium salt is used for the treatment of moderate to severe susceptible infections including intra-abdominal and acute gynaecological infections, pneumonia, and infections of the skin and of the urinary tract.		3.2310carbapenemcarboxylic acid;
pyrrolidinecarboxamide		antibacterial drug
cox 189
lumiracoxib: a COX-2 inhibitor. lumiracoxib : An amino acid that is phenylacetic acid which is substituted at position 2 by the nitrogen of 2-chloro-6-fluoroaniline and at position 5 by a methyl group. A highly selective cyclooxygenase 2 inhibitor, it was briefly used for the treatment of osteoarthritis, but was withdrawn due to concersns of hepatotoxicity.		3.2310amino acid;
monocarboxylic acid;
organochlorine compound;
organofluorine compound;
secondary amino compound		cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
conivaptan
conivaptan : The amide resulting from the formal condensation of 4-[(biphenyl-2-ylcarbonyl)amino]benzoic acid with the benzazepine nitrogen of 2-methyl-1,4,5,6-tetrahydroimidazo[4,5-d][1]benzazepine. It is an antagonist for two of the three types of arginine vasopressin (AVP) receptors, V1a and V2. It is used as its hydrochloride salt for the treatment of hyponatraemia (low blood sodium levels) caused by syndrome of inappropriate antidiuretic hormone (SIADH).		3.2310benzazepineaquaretic;
vasopressin receptor antagonist
moxifloxacin
Moxifloxacin: A fluoroquinolone that acts as an inhibitor of DNA TOPOISOMERASE II and is used as a broad-spectrum antibacterial agent.. moxifloxacin : A quinolone that consists of 4-oxo-1,4-dihydroquinoline-3-carboxylic acid bearing a cyclopropyl substituent at position 1, a fluoro substitiuent at position 6, a (4aS,7aS)-octahydro-6H-pyrrolo[3,4-b]pyridin-6-yl group at position 7 and a methoxy substituent at position 8. A member of the fluoroquinolone class of antibacterial agents.		3.2310aromatic ether;
cyclopropanes;
fluoroquinolone antibiotic;
pyrrolidinopiperidine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antibacterial drug
pralnacasan
pralnacasan: NSAID, ICE inhibitor & metastasis inhibitor; RN & structure in first source		3.2310
clevidipine
clevidipine: a calcium channel blocker and antihypertensive agent; structure in first source		3.2310dihydropyridine
solifenacin
[no description available]		3.2310isoquinolines
dexmethylphenidate
dexmethylphenidate : A methyl phenyl(piperidin-2-yl)acetate in which both stereocentres have R configuration. It is the active enantiomer in the racemic drug methylphenidate.		3.2310methyl phenyl(piperidin-2-yl)acetateadrenergic agent
naproxen
Naproxen: An anti-inflammatory agent with analgesic and antipyretic properties. Both the acid and its sodium salt are used in the treatment of rheumatoid arthritis and other rheumatic or musculoskeletal disorders, dysmenorrhea, and acute gout.. naproxen : A methoxynaphthalene that is 2-methoxynaphthalene substituted by a carboxy ethyl group at position 6. Naproxen is a non-steroidal anti-inflammatory drug commonly used for the reduction of pain, fever, inflammation and stiffness caused by conditions such as osteoarthritis, kidney stones, rheumatoid arthritis, psoriatic arthritis, gout, ankylosing spondylitis, menstrual cramps, tendinitis, bursitis, and for the treatment of primary dysmenorrhea. It works by inhibiting both the COX-1 and COX-2 enzymes.		3.2310methoxynaphthalene;
monocarboxylic acid		antipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
environmental contaminant;
gout suppressant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
cinacalcet
cinacalcet : A secondary amino compound that is (1R)-1-(naphthalen-1-yl)ethanamine in which one of the hydrogens attached to the nitrogen is substituted by a 3-[3-(trifluoromethyl)phenyl]propyl group.		3.2310(trifluoromethyl)benzenes;
naphthalenes;
secondary amino compound		calcimimetic;
P450 inhibitor
lubiprostone
[no description available]		3.2310
telbivudine
[no description available]		3.2310pyrimidine 2'-deoxyribonucleosideantiviral drug;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
paromomycin
Paromomycin: An aminoglycoside antibacterial and antiprotozoal agent produced by species of STREPTOMYCES.. paromomycin : An amino cyclitol glycoside that is the 1-O-(2-amino-2-deoxy-alpha-D-glucopyranoside) and the 3-O-(2,6-diamino-2,6-dideoxy-beta-L-idopyranosyl)-beta-D-ribofuranoside of 4,6-diamino-2,3-dihydroxycyclohexane (the 1R,2R,3S,4R,6S diastereoisomer). It is obtained from various Streptomyces species. A broad-spectrum antibiotic, it is used (generally as the sulfate salt) for the treatment of acute and chronic intestinal protozoal infections, but is not effective for extraintestinal protozoal infections. It is also used as a therapeutic against visceral leishmaniasis.		3.2310amino cyclitol glycoside;
aminoglycoside antibiotic		anthelminthic drug;
antibacterial drug;
antiparasitic agent;
antiprotozoal drug
anidulafungin
Anidulafungin: Echinocandin antifungal agent that is used in the treatment of CANDIDEMIA and CANDIDIASIS.. anidulafungin : A semisynthetic echinocandin anti-fungal drug. It is active against Aspergillus and Candida species and is used for the treatment of invasive candidiasis.		3.2310antibiotic antifungal drug;
azamacrocycle;
echinocandin;
heterodetic cyclic peptide;
semisynthetic derivative
17 alpha-hydroxyprogesterone caproate
17 alpha-Hydroxyprogesterone Caproate: Hydroxyprogesterone derivative that acts as a PROGESTIN and is used to reduce the risk of recurrent MISCARRIAGE and of PREMATURE BIRTH. It is also used in combination with ESTROGEN in the management of MENSTRUATION DISORDERS.		3.2310corticosteroid hormone
varenicline
Varenicline: A benzazepine derivative that functions as an ALPHA4-BETA2 NICOTINIC RECEPTOR partial agonist. It is used for SMOKING CESSATION.. varenicline : An organic heterotetracyclic compound that acts as a partial agonist for nicotinic cholinergic receptors and is used (in the form of its tartate salt) as an aid to giving up smoking.		3.2310
fiduxosin
fiduxosin: fiduxosin (ABT-980) is the (3aR,9bR)-isomer; structure in first source		3.2310
atropine
tropan-3alpha-yl 3-hydroxy-2-phenylpropanoate : A tropane alkaloid that is (1R,5)-8-methyl-8-azabicyclo[3.2.1]octane substituted by a (3-hydroxy-2-phenylpropanoyl)oxy group at position 3.		3.2310
erlotinib
[no description available]		3.2310aromatic ether;
quinazolines;
secondary amino compound;
terminal acetylenic compound		antineoplastic agent;
epidermal growth factor receptor antagonist;
protein kinase inhibitor
etravirine
[no description available]		3.2310aminopyrimidine;
aromatic ether;
dinitrile;
organobromine compound		antiviral agent;
HIV-1 reverse transcriptase inhibitor
dronedarone
Dronedarone: A non-iodinated derivative of amiodarone that is used for the treatment of ARRHYTHMIA.. dronedarone : A member of the class of 1-benzofurans used for the treatment of cardiac arrhythmias.		3.23101-benzofurans;
aromatic ether;
aromatic ketone;
sulfonamide;
tertiary amino compound		anti-arrhythmia drug;
environmental contaminant;
xenobiotic
ramelteon
ramelteon: melatonin MT1/MT2 receptor agonist		3.2310indanes
lapatinib
[no description available]		3.2310furans;
organochlorine compound;
organofluorine compound;
quinazolines		antineoplastic agent;
tyrosine kinase inhibitor
darunavir
Darunavir: An HIV PROTEASE INHIBITOR that is used in the treatment of AIDS and HIV INFECTIONS. Due to the emergence of ANTIVIRAL DRUG RESISTANCE when used alone, it is administered in combination with other ANTI-HIV AGENTS.. darunavir : An N,N-disubstituted benzenesulfonamide bearing an unsubstituted amino group at the 4-position, used for the treatment of HIV infection. A second-generation HIV protease inhibitor, darunavir was designed to form robust interactions with the protease enzyme from many strains of HIV, including those from treatment-experienced patients with multiple resistance mutations to other protease inhibitors.		3.2310carbamate ester;
furofuran;
sulfonamide		antiviral drug;
HIV protease inhibitor
deferasirox
Deferasirox: A triazole and benzoate derivative that acts as a selective iron chelator. It is used in the management of chronic IRON OVERLOAD due to blood transfusion or non-transfusion dependent THALASSEMIA.. deferasirox : A member of the class of triazoles, deferasirox is 1,2,4-triazole substituted by a 4-carboxyphenyl group at position 1 and by 2-hydroxyphenyl groups at positions 3 and 5. An orally active iron chelator, it is used to manage chronic iron overload in patients receiving long-term blood transfusions.		3.2310benzoic acids;
monocarboxylic acid;
phenols;
triazoles		iron chelator
tbc-11251
sitaxsentan: endothelin A receptor antagonist; structure in first source		3.2310benzodioxoles
tolvaptan
[no description available]		3.2310benzazepine;
benzenedicarboxamide		aquaretic;
vasopressin receptor antagonist
sorafenib
[no description available]		3.2310(trifluoromethyl)benzenes;
aromatic ether;
monochlorobenzenes;
phenylureas;
pyridinecarboxamide		angiogenesis inhibitor;
anticoronaviral agent;
antineoplastic agent;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
ferroptosis inducer;
tyrosine kinase inhibitor
lenalidomide
[no description available]		3.2310aromatic amine;
dicarboximide;
isoindoles;
piperidones		angiogenesis inhibitor;
antineoplastic agent;
immunomodulator
regadenoson
[no description available]		3.2310purine nucleoside
lacosamide
Lacosamide: An acetamide derivative that acts as a blocker of VOLTAGE-GATED SODIUM CHANNELS. It is used as an anticonvulsant, for adjunctive or monotherapy, in the treatment of PARTIAL SEIZURES.		3.2310N-acyl-amino acid
vincaleukoblastine
[no description available]		3.2310acetate ester;
indole alkaloid fundamental parent;
methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
tertiary alcohol;
tertiary amino compound;
vinca alkaloid		antineoplastic agent;
immunosuppressive agent;
microtubule-destabilising agent;
plant metabolite
benzarone
benzarone: antihemorrhagic agent; structure		3.23101-benzofurans
estramustine
Estramustine: A nitrogen mustard linked to estradiol, usually as phosphate; used to treat prostatic neoplasms; also has radiation protective properties.. estramustine : A carbamate ester obtained by the formal condensation of the hydroxy group of 17beta-estradiol with the carboxy group of bis(2-chloroethyl)carbamic acid.		3.231017beta-hydroxy steroid;
carbamate ester;
organochlorine compound		alkylating agent;
antineoplastic agent;
radiation protective agent
bortezomib
[no description available]		3.2310amino acid amide;
L-phenylalanine derivative;
pyrazines		antineoplastic agent;
antiprotozoal drug;
protease inhibitor;
proteasome inhibitor
ritonavir
Ritonavir: An HIV protease inhibitor that works by interfering with the reproductive cycle of HIV. It also inhibits CYTOCHROME P-450 CYP3A.. ritonavir : An L-valine derivative that is L-valinamide in which alpha-amino group has been acylated by a [(2-isopropyl-1,3-thiazol-4-yl)methyl]methylcarbamoyl group and in which a hydrogen of the carboxamide amino group has been replaced by a (2R,4S,5S)-4-hydroxy-1,6-diphenyl-5-{[(1,3-thiazol-5-ylmethoxy)carbonyl]amino}hexan-2-yl group. A CYP3A inhibitor and antiretroviral drug from the protease inhibitor class used to treat HIV infection and AIDS, it is often used as a fixed-dose combination with another protease inhibitor, lopinavir. Also used in combination with dasabuvir sodium hydrate, ombitasvir and paritaprevir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.		3.23101,3-thiazoles;
carbamate ester;
carboxamide;
L-valine derivative;
ureas		antiviral drug;
environmental contaminant;
HIV protease inhibitor;
xenobiotic
oxytocin
Oxytocin: A nonapeptide hormone released from the neurohypophysis (PITUITARY GLAND, POSTERIOR). It differs from VASOPRESSIN by two amino acids at residues 3 and 8. Oxytocin acts on SMOOTH MUSCLE CELLS, such as causing UTERINE CONTRACTIONS and MILK EJECTION.. oxytocin : A cyclic nonapeptide hormone with amino acid sequence CYIQNCPLG that also acts as a neurotransmitter in the brain; the principal uterine-contracting and milk-ejecting hormone of the posterior pituitary. Together with the neuropeptide vasopressin, it is believed to influence social cognition and behaviour.		3.2310heterodetic cyclic peptide;
peptide hormone		oxytocic;
vasodilator agent
pentostatin
Pentostatin: A potent inhibitor of ADENOSINE DEAMINASE. The drug induces APOPTOSIS of LYMPHOCYTES, and is used in the treatment of many lymphoproliferative malignancies, particularly HAIRY CELL LEUKEMIA. It is also synergistic with some other antineoplastic agents and has immunosuppressive activity.. pentostatin : A member of the class of coformycins that is coformycin in which the hydroxy group at position 2' is replaced with a hydrogen. It is a drug used for the treatment of hairy cell leukaemia.		3.2310coformycinsantimetabolite;
antineoplastic agent;
Aspergillus metabolite;
bacterial metabolite;
EC 3.5.4.4 (adenosine deaminase) inhibitor
quinidine
Quinidine: An optical isomer of quinine, extracted from the bark of the CHINCHONA tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular ACTION POTENTIALS, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission.. quinidine : A cinchona alkaloid consisting of cinchonine with the hydrogen at the 6-position of the quinoline ring substituted by methoxy.		3.2310cinchona alkaloidalpha-adrenergic antagonist;
anti-arrhythmia drug;
antimalarial;
drug allergen;
EC 1.14.13.181 (13-deoxydaunorubicin hydroxylase) inhibitor;
EC 3.6.3.44 (xenobiotic-transporting ATPase) inhibitor;
muscarinic antagonist;
P450 inhibitor;
potassium channel blocker;
sodium channel blocker
meropenem
Meropenem: A thienamycin derivative antibacterial agent that is more stable to renal dehydropeptidase I than IMIPENEM, but does not need to be given with an enzyme inhibitor such as CILASTATIN. It is used in the treatment of bacterial infections, including infections in immunocompromised patients.. meropenem : A carbapenemcarboxylic acid in which the azetidine and pyrroline rings carry 1-hydroxymethyl and in which the azetidine and pyrroline rings carry 1-hydroxymethyl and 5-(dimethylcarbamoyl)pyrrolidin-3-ylthio substituents respectively.		3.2310alpha,beta-unsaturated monocarboxylic acid;
carbapenemcarboxylic acid;
organic sulfide;
pyrrolidinecarboxamide		antibacterial agent;
antibacterial drug;
drug allergen
griseofulvin
Griseofulvin: An antifungal agent used in the treatment of TINEA infections.. griseofulvin : An oxaspiro compound produced by Penicillium griseofulvum. It is used by mouth as an antifungal drug for infections involving the scalp, hair, nails and skin that do not respond to topical treatment.		3.23101-benzofurans;
antibiotic antifungal drug;
benzofuran antifungal drug;
organochlorine compound;
oxaspiro compound		antibacterial agent;
Penicillium metabolite
cefoxitin
Cefoxitin: A semisynthetic cephamycin antibiotic resistant to beta-lactamase.. cefoxitin : A semisynthetic cephamycin antibiotic which, in addition to the methoxy group at the 7alpha position, has 2-thienylacetamido and carbamoyloxymethyl side-groups. It is resistant to beta-lactamase.		3.2310beta-lactam antibiotic allergen;
cephalosporin;
cephamycin;
semisynthetic derivative		antibacterial drug
saquinavir
Saquinavir: An HIV protease inhibitor which acts as an analog of an HIV protease cleavage site. It is a highly specific inhibitor of HIV-1 and HIV-2 proteases, and also inhibits CYTOCHROME P-450 CYP3A.. saquinavir : An aspartic acid derivative obtained by formal condensation of the primary amino group of (2S,3R)-4-[(3S,4aS,8aS)-3-(tert-butylcarbamoyl)octahydroisoquinolin-2(1H)-yl]-3-hydroxy-1-phenylbutan-2-ylamine with the carboxy group of N(2)(-quinolin-2-ylcarbonyl)-L-asparagine. An inhibitor of HIV-1 protease.		3.2310L-asparagine derivative;
quinolines		antiviral drug;
HIV protease inhibitor
pancuronium
Pancuronium: A bis-quaternary steroid that is a competitive nicotinic antagonist. As a neuromuscular blocking agent it is more potent than CURARE but has less effect on the circulatory system and on histamine release.. pancuronium : A steroid ester in which a 5alpha-androstane skeleton is C-3alpha- and C-17beta-disubstituted with acetoxy groups and 2beta- and 16beta-disubstituted with 1-methylpiperidinium-1-yl groups. It is a non-depolarizing curare-mimetic muscle relaxant.		3.2310acetate ester;
steroid ester		cholinergic antagonist;
muscle relaxant;
nicotinic antagonist
abacavir
abacavir: a carbocyclic nucleoside with potent selective anti-HIV activity. abacavir : A 2,6-diaminopurine that is (1S)-cyclopent-2-en-1-ylmethanol in which the pro-R hydrogen at the 4-position is substituted by a 2-amino-6-(cyclopropylamino)-9H-purin-9-yl group. A nucleoside analogue reverse transcriptase inhibitor (NRTI) with antiretroviral activity against HIV, it is used (particularly as the sulfate) with other antiretrovirals in combination therapy of HIV infection.		3.23102,6-diaminopurinesantiviral drug;
drug allergen;
HIV-1 reverse transcriptase inhibitor
miglitol
[no description available]		3.2310piperidines
metyrosine
alpha-methyl-L-tyrosine : An L-tyrosine derivative that consists of L-tyrosine bearing an additional methyl substituent at position 2. An inhibitor of the enzyme tyrosine 3-monooxygenase, and consequently of the synthesis of catecholamines. It is used to control the symptoms of excessive sympathetic stimulation in patients with pheochromocytoma.		3.2310L-tyrosine derivative;
non-proteinogenic L-alpha-amino acid		antihypertensive agent;
EC 1.14.16.2 (tyrosine 3-monooxygenase) inhibitor
linezolid
[no description available]		3.2310acetamides;
morpholines;
organofluorine compound;
oxazolidinone		antibacterial drug;
protein synthesis inhibitor
clindamycin phosphate
[no description available]		3.2310
eplerenone
Eplerenone: A spironolactone derivative and selective ALDOSTERONE RECEPTOR antagonist that is used in the management of HYPERTENSION and CONGESTIVE HEART FAILURE, post-MYOCARDIAL INFARCTION.		3.23103-oxo-Delta(4) steroid;
epoxy steroid;
gamma-lactone;
methyl ester;
organic heteropentacyclic compound;
oxaspiro compound;
steroid acid ester		aldosterone antagonist;
antihypertensive agent
tolterodine
[no description available]		3.2310tertiary amineantispasmodic drug;
muscarinic antagonist;
muscle relaxant
darifenacin
darifenacin : 2-[(3S)-1-Ethylpyrrolidin-3-yl]-2,2-diphenylacetamide in which one of the hydrogens at the 2-position of the ethyl group is substituted by a 2,3-dihydro-1-benzofuran-5-yl group. It is a selective antagonist for the M3 muscarinic acetylcholine receptor, which is primarily responsible for bladder muscle contractions, and is used as the hydrobromide salt in the management of urinary incontinence.		3.23101-benzofurans;
monocarboxylic acid amide;
pyrrolidines		antispasmodic drug;
muscarinic antagonist
acarbose
[no description available]		3.1410amino cyclitol;
glycoside
tretinoin
Tretinoin: An important regulator of GENE EXPRESSION during growth and development, and in NEOPLASMS. Tretinoin, also known as retinoic acid and derived from maternal VITAMIN A, is essential for normal GROWTH; and EMBRYONIC DEVELOPMENT. An excess of tretinoin can be teratogenic. It is used in the treatment of PSORIASIS; ACNE VULGARIS; and several other SKIN DISEASES. It has also been approved for use in promyelocytic leukemia (LEUKEMIA, PROMYELOCYTIC, ACUTE).. retinoic acid : A retinoid consisting of 3,7-dimethylnona-2,4,6,8-tetraenoic acid substituted at position 9 by a 2,6,6-trimethylcyclohex-1-en-1-yl group (geometry of the four exocyclic double bonds is not specified).. all-trans-retinoic acid : A retinoic acid in which all four exocyclic double bonds have E- (trans-) geometry.		3.2310retinoic acid;
vitamin A		anti-inflammatory agent;
antineoplastic agent;
antioxidant;
AP-1 antagonist;
human metabolite;
keratolytic drug;
retinoic acid receptor agonist;
retinoid X receptor agonist;
signalling molecule
retinol
Vitamin A: Retinol and derivatives of retinol that play an essential role in metabolic functioning of the retina, the growth of and differentiation of epithelial tissue, the growth of bone, reproduction, and the immune response. Dietary vitamin A is derived from a variety of CAROTENOIDS found in plants. It is enriched in the liver, egg yolks, and the fat component of dairy products.. vitamin A : Any member of a group of fat-soluble retinoids produced via metabolism of provitamin A carotenoids that exhibit biological activity against vitamin A deficiency. Vitamin A is involved in immune function, vision, reproduction, and cellular communication.. all-trans-retinol : A retinol in which all four exocyclic double bonds have E- (trans-) geometry.. retinol : A retinoid consisting of 3,7-dimethylnona-2,4,6,8-tetraen-1-ol substituted at position 9 by a 2,6,6-trimethylcyclohex-1-en-1-yl group (geometry of the four exocyclic double bonds is not specified).		3.2310retinol;
vitamin A		human metabolite;
mouse metabolite;
plant metabolite
tacrolimus
Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro.. tacrolimus (anhydrous) : A macrolide lactam containing a 23-membered lactone ring, originally isolated from the fermentation broth of a Japanese soil sample that contained the bacteria Streptomyces tsukubaensis.		3.2310macrolide lactambacterial metabolite;
immunosuppressive agent
rosuvastatin
rosuvastatin : A dihydroxy monocarboxylic acid that is (6E)-7-{4-(4-fluorophenyl)-2-[methyl(methylsulfonyl)amino]-6-(propan-2-yl)pyrimidin-5-yl} hept-6-enoic acid carrying two hydroxy substituents at positions 3 and 5 (the 3R,5S-diastereomer).		3.2310dihydroxy monocarboxylic acid;
monofluorobenzenes;
pyrimidines;
statin (synthetic);
sulfonamide		anti-inflammatory agent;
antilipemic drug;
cardioprotective agent;
CETP inhibitor;
environmental contaminant;
xenobiotic
mycophenolic acid
Mycophenolic Acid: Compound derived from Penicillium stoloniferum and related species. It blocks de novo biosynthesis of purine nucleotides by inhibition of the enzyme inosine monophosphate dehydrogenase (IMP DEHYDROGENASE). Mycophenolic acid exerts selective effects on the immune system in which it prevents the proliferation of T-CELLS, LYMPHOCYTES, and the formation of antibodies from B-CELLS. It may also inhibit recruitment of LEUKOCYTES to sites of INFLAMMATION.. mycophenolate : A monocarboxylic acid anion resulting from the removal of a proton from the carboxy group of mycophenolic acid.. mycophenolic acid : A member of the class of 2-benzofurans that is 2-benzofuran-1(3H)-one which is substituted at positions 4, 5, 6, and 7 by methyl, methoxy, (2E)-5-carboxy-3-methylpent-2-en-1-yl, and hydroxy groups, respectively. It is an antibiotic produced by Penicillium brevi-compactum, P. stoloniferum, P. echinulatum and related species. An immunosuppressant, it is widely used (partiularly as its sodium salt and as the 2-(morpholin-4-yl)ethyl ester prodrug, mycophenolate mofetil) to prevent tissue rejection following organ transplants and for the treatment of certain autoimmune diseases.		3.23102-benzofurans;
gamma-lactone;
monocarboxylic acid;
phenols		anticoronaviral agent;
antimicrobial agent;
antineoplastic agent;
EC 1.1.1.205 (IMP dehydrogenase) inhibitor;
environmental contaminant;
immunosuppressive agent;
mycotoxin;
Penicillium metabolite;
xenobiotic
clindamycin
Clindamycin: An antibacterial agent that is a semisynthetic analog of LINCOMYCIN.. clindamycin : A carbohydrate-containing antibiotic that is the semisynthetic derivative of lincomycin, a natural antibiotic.		3.2310
fosfomycin
Fosfomycin: An antibiotic produced by Streptomyces fradiae.. fosfomycin : A phosphonic acid having an (R,S)-1,2-epoxypropyl group attached to phosphorus.		3.2310epoxide;
phosphonic acids		antimicrobial agent;
EC 2.5.1.7 (UDP-N-acetylglucosamine 1-carboxyvinyltransferase) inhibitor
zithromax
Azithromycin: A semi-synthetic macrolide antibiotic structurally related to ERYTHROMYCIN. It has been used in the treatment of Mycobacterium avium intracellulare infections, toxoplasmosis, and cryptosporidiosis.. azithromycin : A macrolide antibiotic useful for the treatment of bacterial infections.		3.2310macrolide antibioticantibacterial drug;
environmental contaminant;
xenobiotic
octreotide
[no description available]		3.2310
eptifibatide
[no description available]		3.2310homodetic cyclic peptide;
macrocycle;
organic disulfide		anticoagulant;
platelet aggregation inhibitor
decitabine
[no description available]		3.23102'-deoxyribonucleoside
teniposide
[no description available]		3.2310aromatic ether;
beta-D-glucoside;
cyclic acetal;
furonaphthodioxole;
gamma-lactone;
monosaccharide derivative;
phenols;
thiophenes		antineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
dactinomycin
Dactinomycin: A compound composed of a two CYCLIC PEPTIDES attached to a phenoxazine that is derived from STREPTOMYCES parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015)		3.2310actinomycinmutagen
melphalan
Melphalan: An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - MELPHALAN, the racemic mixture - MERPHALAN, and the dextro isomer - MEDPHALAN; toxic to bone marrow, but little vesicant action; potential carcinogen.. melphalan : A phenylalanine derivative comprising L-phenylalanine having [bis(2-chloroethyl)amino group at the 4-position on the phenyl ring.		3.2310L-phenylalanine derivative;
nitrogen mustard;
non-proteinogenic L-alpha-amino acid;
organochlorine compound		alkylating agent;
antineoplastic agent;
carcinogenic agent;
drug allergen;
immunosuppressive agent
tenofovir
tenofovir (anhydrous) : A member of the class of phosphonic acids that is methylphosphonic acid in which one of the methyl hydrogens is replaced by a [(2R)-1-(6-amino-9H-purin-9-yl)propan-2-yl]oxy group. An inhibitor of HIV-1 reverse transcriptase, the bis(isopropyloxycarbonyloxymethyl) ester (disoproxil ester) prodrug is used as the fumaric acid salt in combination therapy for the treatment of HIV infection.		3.2310nucleoside analogue;
phosphonic acids		antiviral drug;
drug metabolite;
HIV-1 reverse transcriptase inhibitor
posaconazole
[no description available]		3.2310aromatic ether;
conazole antifungal drug;
N-arylpiperazine;
organofluorine compound;
oxolanes;
triazole antifungal drug;
triazoles		trypanocidal drug
micafungin
Micafungin: A cyclic lipo-hexapeptide echinocandin antifungal agent that is used for the treatment and prevention of CANDIDIASIS.. micafungin : A cyclic hexapeptide echinocandin antibiotic which exerts its effect by inhibiting the synthesis of 1,3-beta-D-glucan, an integral component of the fungal cell wall. It is used as the sodium salt for the treatment of invasive candidiasis, and of aspergillosis in patients who are intolerant of other therapy.		3.2310antibiotic antifungal drug;
echinocandin		antiinfective agent
riboflavin
vitamin B2 : Any member of a group of vitamers that belong to the chemical structural class called flavins that exhibit biological activity against vitamin B2 deficiency. Symptoms associated with vitamin B2 deficiency include glossitis, seborrhea, angular stomaitis, cheilosis and photophobia. The vitamers include riboflavin and its phosphate derivatives (and includes their salt, ionised and hydrate forms).		3.2310flavin;
vitamin B2		anti-inflammatory agent;
antioxidant;
cofactor;
Escherichia coli metabolite;
food colouring;
fundamental metabolite;
human urinary metabolite;
mouse metabolite;
photosensitizing agent;
plant metabolite
sodium bicarbonate
Sodium Bicarbonate: A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions.		3.2310one-carbon compound;
organic sodium salt		antacid;
food anticaking agent
arsenic trioxide
Tetraarsenic Oxide: A form of As2O3 that exists as As4O6 in the solid state. It dissociates to As2O3 upon heating to the vapor phase above 800 degrees Celsius.		3.2310arsenic oxideantineoplastic agent;
insecticide
sr 90107
fondaparinux sodium : An organic sodium salt, being the decasodium salt of fondaparinux.		3.2310
meglumine iodipamide
[no description available]		3.2310organoammonium saltradioopaque medium
thyrotropin-releasing hormone
PR 546: no other info available 9/89. protirelin : A tripeptide composed of L-pyroglutamyl, L-histidyl and L-prolinamide residues joined in sequence.		3.2310peptide hormone;
tripeptide		human metabolite
arginine vasopressin
Arginine Vasopressin: The predominant form of mammalian antidiuretic hormone. It is a nonapeptide containing an ARGININE at residue 8 and two disulfide-linked cysteines at residues of 1 and 6. Arg-vasopressin is used to treat DIABETES INSIPIDUS or to improve vasomotor tone and BLOOD PRESSURE.. argipressin : The predominant form of mammalian vasopressin (antidiuretic hormone). It is a nonapeptide containing an arginine at residue 8 and two disulfide-linked cysteines at residues of 1 and 6.		3.2310vasopressincardiovascular drug;
hematologic agent;
mitogen
s 1033
[no description available]		3.2310(trifluoromethyl)benzenes;
imidazoles;
pyridines;
pyrimidines;
secondary amino compound;
secondary carboxamide		anticoronaviral agent;
antineoplastic agent;
tyrosine kinase inhibitor
propylthiouracil
Propylthiouracil: A thiourea antithyroid agent. Propythiouracil inhibits the synthesis of thyroxine and inhibits the peripheral conversion of throxine to tri-iodothyronine. It is used in the treatment of hyperthyroidism. (From Martindale, The Extra Pharmacopeoia, 30th ed, p534). 6-propyl-2-thiouracil : A pyrimidinethione consisting of uracil in which the 2-oxo group is substituted by a thio group and the hydrogen at position 6 is substituted by a propyl group.		3.2310pyrimidinethioneantidote to paracetamol poisoning;
antimetabolite;
antioxidant;
antithyroid drug;
carcinogenic agent;
EC 1.14.13.39 (nitric oxide synthase) inhibitor;
hormone antagonist
etomidate
Etomidate: Imidazole derivative anesthetic and hypnotic with little effect on blood gases, ventilation, or the cardiovascular system. It has been proposed as an induction anesthetic.. etomidate : The ethyl ester of 1-[(1R)-1-phenylethyl]-1H-imidazole-5-carboxylic acid. It is an intravenous general anaesthetic with no analgesic activity.		3.2310ethyl ester;
imidazoles		intravenous anaesthetic;
sedative
mercaptopurine
Mercaptopurine: An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by inhibiting purine metabolism and is used, usually in combination with other drugs, in the treatment of or in remission maintenance programs for leukemia.. purine-6-thiol : A thiol that is the tautomer of mercaptopurine.. mercaptopurine : A member of the class of purines that is 6,7-dihydro-1H-purine carrying a thione group at position 6. An adenine analogue, it is used in the treatment of acute lymphocytic leukemia (ALL), chronic myeloid leukemia (CML), Crohn's disease, and ulcerative colitis.		3.2310aryl thiol;
purines;
thiocarbonyl compound		anticoronaviral agent;
antimetabolite;
antineoplastic agent
pyrantel
Pyrantel: A depolarizing neuromuscular-blocking agent, that causes persistent nicotinic activation resulting in spastic paralysis of susceptible nematodes. It is a drug of second-choice after benzimidazoles for treatment of ascariasis, hookworm, and pinworm infections, being effective after a single dose. (From Smith and Reynard, Textbook of Pharmacology, 1992, p920). pyrantel : A carboxamidine that is 1,4,5,6-tetrahydropyrimidine that is substituted at position 1 by a methyl group and at position 2 by an (E)-2-(2-thienyl)vinyl group. It is used, particularly as the embonate [4,4'-methylenebis(3-hydroxy-2-naphthoate)] salt, as an anthelmintic that is effective against intestinal nematodes including threadworms, roundworms and hookworms, and is included in the WHO 'Model List of Essential Medicines'.		3.23101,4,5,6-tetrahydropyrimidines;
carboxamidine;
thiophenes		antinematodal drug
thiothixene
[no description available]		3.2310N-methylpiperazineanticoronaviral agent
eszopiclone
Eszopiclone: A pyridine, pyrazine, and piperazine derivative that is used as a HYPNOTIC AND SEDATIVE in the treatment of INSOMNIA.. eszopiclone : The (5S)- (active) enantiomer of zopiclone. Unlike almost all other hypnotic sedatives, which are approved only for the relief of short-term (6-8 weeks) insomnia, eszopiclone is approved by the U.S. Food and Drug Administration for long-term use.		3.2310zopiclonecentral nervous system depressant;
sedative
benztropine
Benztropine: A centrally active muscarinic antagonist that has been used in the symptomatic treatment of PARKINSON DISEASE. Benztropine also inhibits the uptake of dopamine.. benzatropine : Tropane in which a hydrogen at position 3 is substituted by a diphenylmethoxy group (endo-isomer). An acetylcholine receptor antagonist, it is used (particularly as its methanesulphonate salt) in the treatment of Parkinson's disease, and to reduce parkinsonism and akathisia side effects of antipsychotic treatments.		3.2310diarylmethane
methimazole
Methimazole: A thioureylene antithyroid agent that inhibits the formation of thyroid hormones by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin. This is done by interfering with the oxidation of iodide ion and iodotyrosyl groups through inhibition of the peroxidase enzyme.. methimazole : A member of the class of imidazoles that it imidazole-2-thione in which a methyl group replaces the hydrogen which is attached to a nitrogen.		3.23101,3-dihydroimidazole-2-thionesantithyroid drug
sulindac
Sulindac: A sulfinylindene derivative prodrug whose sulfinyl moiety is converted in vivo to an active NSAID analgesic. Specifically, the prodrug is converted by liver enzymes to a sulfide which is excreted in the bile and then reabsorbed from the intestine. This helps to maintain constant blood levels with reduced gastrointestinal side effects.. sulindac : A monocarboxylic acid that is 1-benzylidene-1H-indene which is substituted at positions 2, 3, and 5 by methyl, carboxymethyl, and fluorine respectively, and in which the phenyl group of the benzylidene moiety is substituted at the para position by a methylsulfinyl group. It is a prodrug for the corresponding sulfide, a non-steroidal anti-inflammatory drug, used particularly in the treatment of acute and chronic inflammatory conditions.		3.2310monocarboxylic acid;
organofluorine compound;
sulfoxide		analgesic;
antineoplastic agent;
antipyretic;
apoptosis inducer;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
prodrug;
tocolytic agent
terbinafine
[no description available]		3.2310acetylenic compound;
allylamine antifungal drug;
enyne;
naphthalenes;
tertiary amine		EC 1.14.13.132 (squalene monooxygenase) inhibitor;
P450 inhibitor;
sterol biosynthesis inhibitor
thioguanine anhydrous
Thioguanine: An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia.. tioguanine : A 2-aminopurine that is the 6-thiono derivative of 2-amino-1,9-dihydro-6H-purine. Incorporates into DNA and inhibits synthesis. Used in the treatment of leukaemia.		3.23102-aminopurinesanticoronaviral agent;
antimetabolite;
antineoplastic agent
succimer
Succimer: A mercaptodicarboxylic acid used as an antidote to heavy metal poisoning because it forms strong chelates with them.. succimer : A sulfur-containing carboxylic acid that is succinic acid bearing two mercapto substituents at positions 2 and 3. A lead chelator used as an antedote to lead poisoning.		3.2310dicarboxylic acid;
dithiol;
sulfur-containing carboxylic acid		chelator
digoxin
Digoxin: A cardiotonic glycoside obtained mainly from Digitalis lanata; it consists of three sugars and the aglycone DIGOXIGENIN. Digoxin has positive inotropic and negative chronotropic activity. It is used to control ventricular rate in ATRIAL FIBRILLATION and in the management of congestive heart failure with atrial fibrillation. Its use in congestive heart failure and sinus rhythm is less certain. The margin between toxic and therapeutic doses is small. (From Martindale, The Extra Pharmacopoeia, 30th ed, p666). digoxin : A cardenolide glycoside that is digitoxin beta-hydroxylated at C-12. A cardiac glycoside extracted from the foxglove plant, Digitalis lanata, it is used to control ventricular rate in atrial fibrillation and in the management of congestive heart failure with atrial fibrillation, but the margin between toxic and therapeutic doses is small.		3.2310cardenolide glycoside;
steroid saponin		anti-arrhythmia drug;
cardiotonic drug;
EC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor;
epitope
streptozocin
[no description available]		3.2310
tamoxifen
[no description available]		3.2310stilbenoid;
tertiary amino compound		angiogenesis inhibitor;
antineoplastic agent;
bone density conservation agent;
EC 1.2.3.1 (aldehyde oxidase) inhibitor;
EC 2.7.11.13 (protein kinase C) inhibitor;
estrogen antagonist;
estrogen receptor antagonist;
estrogen receptor modulator
ethionamide
Ethionamide: A second-line antitubercular agent that inhibits mycolic acid synthesis.. ethionamide : A thiocarboxamide that is pyridine-4-carbothioamide substituted by an ethyl group at position 2. A prodrug that undergoes metabolic activation by conversion to the corresponding S-oxide.		3.2310pyridines;
thiocarboxamide		antilipemic drug;
antitubercular agent;
fatty acid synthesis inhibitor;
leprostatic drug;
prodrug
cancidas
[no description available]		3.2310
lincomycin
Lincomycin: An antibiotic produced by Streptomyces lincolnensis var. lincolnensis. It has been used in the treatment of staphylococcal, streptococcal, and Bacteroides fragilis infections.. lincomycin : A carbohydrate-containing antibiotic produced by the actinomyces Streptomyces lincolnensis.		3.2310carbohydrate-containing antibiotic;
L-proline derivative;
monocarboxylic acid amide;
pyrrolidinecarboxamide;
S-glycosyl compound		antimicrobial agent;
bacterial metabolite
ranitidine
Ranitidine: A non-imidazole blocker of those histamine receptors that mediate gastric secretion (H2 receptors). It is used to treat gastrointestinal ulcers.. ranitidine : A member of the class of furans used to treat peptic ulcer disease (PUD) and gastroesophageal reflux disease.		3.2310C-nitro compound;
furans;
organic sulfide;
tertiary amino compound		anti-ulcer drug;
drug allergen;
environmental contaminant;
H2-receptor antagonist;
xenobiotic
aplaviroc
aplaviroc: a spiro-diketo-piperazine; a potent noncompetitive allosteric antagonist of the CCR5 receptor with concomitantly potent antiviral effects for HIV-1; structure in first source		3.2310
hmr 3647
[no description available]		3.2310
maraviroc
[no description available]		3.2310tropane alkaloid
toremifene
Toremifene: A first generation selective estrogen receptor modulator (SERM). Like TAMOXIFEN, it is an estrogen agonist for bone tissue and cholesterol metabolism but is antagonistic on mammary and uterine tissue.		3.2310aromatic ether;
organochlorine compound;
tertiary amine		antineoplastic agent;
bone density conservation agent;
estrogen antagonist;
estrogen receptor modulator
nelarabine
nelarabine: prodrug of ara-G. nelarabine : A purine nucleoside in which O-methylguanine is attached to arabinofuranose via a beta-N(9)-glycosidic bond. Inhibits DNA synthesis and causes cell death; a prodrug of 9-beta-D-arabinofuranosylguanine (ara-G).		3.2310beta-D-arabinoside;
monosaccharide derivative;
purine nucleoside		antineoplastic agent;
DNA synthesis inhibitor;
prodrug
dermatan sulfate
Dermatan Sulfate: A naturally occurring glycosaminoglycan found mostly in the skin and in connective tissue. It differs from CHONDROITIN SULFATE A (see CHONDROITIN SULFATES) by containing IDURONIC ACID in place of glucuronic acid, its epimer, at carbon atom 5. (from Merck, 12th ed). alpha-L-IdopA-(1->3)-beta-D-GalpNAc4S : An oligosaccharide sulfate that is 2-acetamido-2-deoxy-4-O-sulfo-beta-D-galactopyranose in which the hydroxy group at position 3 has been converted to the corresponding alpha-L-idopyranuronoside.. dermatan sulfate : Any of a group of glycosaminoglycans with repeating units consisting of variously sulfated beta1->4-linked L-iduronyl-(alpha1->3)-N-acetyl-D-galactosamine units.		3.2310amino disaccharide;
glycosylgalactose derivative;
iduronic acids;
oligosaccharide sulfate
dolasetron
[no description available]		3.2310indolyl carboxylic acid
orlistat
Orlistat: A lactone derivative of LEUCINE that acts as a pancreatic lipase inhibitor to limit the absorption of dietary fat; it is used in the management of obesity.. orlistat : A carboxylic ester resulting from the formal condensation of the carboxy group of N-formyl-L-leucine with the hydroxy group of (3S,4S)-3-hexyl-4-[(2S)-2-hydroxytridecyl]oxetan-2-one. A pancreatic lipase inhibitor, it is used as an anti-obesity drug.		3.2310beta-lactone;
carboxylic ester;
formamides;
L-leucine derivative		anti-obesity agent;
bacterial metabolite;
EC 2.3.1.85 (fatty acid synthase) inhibitor;
EC 3.1.1.3 (triacylglycerol lipase) inhibitor
quinine
[no description available]		3.2310cinchona alkaloidantimalarial;
muscle relaxant;
non-narcotic analgesic
fospropofol
[no description available]		3.2310alkylbenzene
rasagiline
[no description available]		3.2310indanes;
secondary amine;
terminal acetylenic compound		EC 1.4.3.4 (monoamine oxidase) inhibitor;
neuroprotective agent
dasatinib
N-(2-chloro-6-methylphenyl)-2-((6-(4-(2-hydroxyethyl)piperazin-1-yl)-2-methylpyrimidin-4-yl)amino)-1,3-thiazole-5-carboxamide: a dasatinib prodrug; structure in first source. dasatinib (anhydrous) : An aminopyrimidine that is 2-methylpyrimidine which is substituted at position 4 by the primary amino group of 2-amino-1,3-thiazole-5-carboxylic acid and at position 6 by a 4-(2-hydroxyethyl)piperazin-1-yl group, and in which the carboxylic acid group has been formally condensed with 2-chloro-6-methylaniline to afford the corresponding amide. A multi-targeted kinase inhibitor, it is used, particularly as the monohydrate, for the treatment of chronic, accelerated, or myeloid or lymphoid blast phase chronic myeloid leukemia. Note that the name 'dasatinib' is used to refer to the monohydrate (USAN) as well as to anhydrous dasatinib (INN).		3.23101,3-thiazoles;
aminopyrimidine;
monocarboxylic acid amide;
N-(2-hydroxyethyl)piperazine;
N-arylpiperazine;
organochlorine compound;
secondary amino compound;
tertiary amino compound		anticoronaviral agent;
antineoplastic agent;
tyrosine kinase inhibitor
sitagliptin
sitagliptin : A triazolopyrazine that exhibits hypoglycemic activity.		4.0920triazolopyrazine;
trifluorobenzene		EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
environmental contaminant;
hypoglycemic agent;
serine proteinase inhibitor;
xenobiotic
tolcapone
Tolcapone: A benzophenone and nitrophenol compound that acts as an inhibitor of CATECHOL O-METHYLTRANSFERASE, an enzyme involved in the metabolism of DOPAMINE and LEVODOPA. It is used in the treatment of PARKINSON DISEASE in patients for whom levodopa is ineffective or contraindicated.. tolcapone : Benzophenone substituted on one of the phenyl rings at C-3 and C-4 by hydroxy groups and at C-5 by a nitro group, and on the other phenyl ring by a methyl group at C-4. It is an inhibitor of catechol O-methyltransferase.		3.23102-nitrophenols;
benzophenones;
catechols		antiparkinson drug;
EC 2.1.1.6 (catechol O-methyltransferase) inhibitor
calcitriol
dihydroxy-vitamin D3: as a major in vitro metabolite of 1alpha,25-dihydroxyvitamin D3, produced in primary cultures of neonatal human keratinocytes		3.2310D3 vitamins;
hydroxycalciol;
triol		antineoplastic agent;
antipsoriatic;
bone density conservation agent;
calcium channel agonist;
calcium channel modulator;
hormone;
human metabolite;
immunomodulator;
metabolite;
mouse metabolite;
nutraceutical
vitamin d 2
Ergocalciferols: Derivatives of ERGOSTEROL formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. They differ from CHOLECALCIFEROL in having a double bond between C22 and C23 and a methyl group at C24.. vitamin D2 : A vitamin D supplement and has been isolated from alfalfa.		3.2310hydroxy seco-steroid;
seco-ergostane;
vitamin D		bone density conservation agent;
nutraceutical;
plant metabolite;
rodenticide
amphotericin b
Amphotericin B: Macrolide antifungal antibiotic produced by Streptomyces nodosus obtained from soil of the Orinoco river region of Venezuela.. amphotericin B : A macrolide antibiotic used to treat potentially life-threatening fungal infections.		3.2310antibiotic antifungal drug;
macrolide antibiotic;
polyene antibiotic		antiamoebic agent;
antiprotozoal drug;
bacterial metabolite
pulmicort
Budesonide: A glucocorticoid used in the management of ASTHMA, the treatment of various skin disorders, and allergic RHINITIS.. budesonide : A glucocorticoid steroid having a highly oxygenated pregna-1,4-diene structure. It is used mainly in the treatment of asthma and non-infectious rhinitis and for treatment and prevention of nasal polyposis.		3.231011beta-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
cyclic acetal;
glucocorticoid;
primary alpha-hydroxy ketone		anti-inflammatory drug;
bronchodilator agent;
drug allergen
oxymetholone
Oxymetholone: A synthetic hormone with anabolic and androgenic properties. It is used mainly in the treatment of anemias. According to the Fourth Annual Report on Carcinogens (NTP 85-002), this compound may reasonably be anticipated to be a carcinogen. (From Merck Index, 11th ed). oxymetholone : A 3-oxo-5alpha- steroid that is 4,5alpha-dihydrotestosterone which is substituted by a hydroxymethylidene group at position 2 and by a methyl group at the 17alpha position. A synthetic androgen, it was mainly used for the treatment of anaemias until being replaced by treatments with fewer side effects.		3.2310
eprosartan
eprosartan: angiotensin II receptor antagonist. eprosartan : A member of the class of imidazoles and thiophenes that is an angiotensin II receptor antagonist used for the treatment of high blood pressure.		3.2310dicarboxylic acid;
imidazoles;
thiophenes		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
montelukast
montelukast: a leukotriene D4 receptor antagonist		3.2310aliphatic sulfide;
monocarboxylic acid;
quinolines		anti-arrhythmia drug;
anti-asthmatic drug;
leukotriene antagonist
mivacurium
Mivacurium: An isoquinoline derivative that is used as a short-acting non-depolarizing agent.		3.2310isoquinolines
hemabate
carboprost tromethamine : The tromethamine salt of carboprost. It is used as an abortifacient agent that is effective in both the first and second trimesters of pregnancy.		3.2310
mycophenolate mofetil
mycophenolate mofetil : A carboxylic ester resulting from the formal condensation between the carboxylic acid group of mycophenolic acid and the hydroxy group of 2-(morpholin-4-yl)ethanol. In the liver, it is metabolised to mycophenolic acid, an immunosuppressant for which it is a prodrug. It is widely used to prevent tissue rejection following organ transplants as well as for the treatment of certain autoimmune diseases.		3.2310carboxylic ester;
ether;
gamma-lactone;
phenols;
tertiary amino compound		anticoronaviral agent;
EC 1.1.1.205 (IMP dehydrogenase) inhibitor;
immunosuppressive agent;
prodrug
entacapone
entacapone: structure given in first source. entacapone : A monocarboxylic acid amide that is N,N-diethylprop-2-enamide in which the hydrogen at position 2 is substituted by a cyano group and the hydrogen at the 3E position is substituted by a 3,4-dihydroxy-5-nitrophenyl group.		3.23102-nitrophenols;
catechols;
monocarboxylic acid amide;
nitrile		antidyskinesia agent;
antiparkinson drug;
central nervous system drug;
EC 2.1.1.6 (catechol O-methyltransferase) inhibitor
paricalcitol
[no description available]		3.2310hydroxy seco-steroid;
seco-cholestane		antiparathyroid drug
7432 s
Ceftibuten: A cephalosporin antibacterial agent that is used in the treatment of infections, including urinary-tract and respiratory-tract infections.. ceftibuten : A third-generation cephalosporin antibiotic with a [(2Z)-2-(2-amino-1,3-thiazol-4-yl)-4-carboxybut-2-enoyl]amino substituent at the 7 position of the cephem skeleton. An orally-administered agent, ceftibuten is used as the dihydrate to treat urinary-tract and respiratory-tract infections.		3.2310cephalosporin;
dicarboxylic acid		antibacterial drug
isotretinoin
Isotretinoin: A topical dermatologic agent that is used in the treatment of ACNE VULGARIS and several other skin diseases. The drug has teratogenic and other adverse effects.. isotretinoin : A retinoic acid that is all-trans-retinoic acid in which the double bond which is alpha,beta- to the carboxy group is isomerised to Z configuration. A synthetic retinoid, it is used for the treatment of severe cases of acne and other skin diseases.		3.2310retinoic acidantineoplastic agent;
keratolytic drug;
teratogenic agent
epoprostenol
[no description available]		3.2310prostaglandins Imouse metabolite
indocyanine green
[no description available]		3.23101,1-diunsubstituted alkanesulfonate;
benzoindole;
cyanine dye
triprolidine
Triprolidine: Histamine H1 antagonist used in allergic rhinitis; ASTHMA; and URTICARIA. It is a component of COUGH and COLD medicines. It may cause drowsiness.. triprolidine : An N-alkylpyrrolidine that is acrivastine in which the pyridine ring is lacking the propenoic acid substituent. It is a sedating antihistamine that is used (generally as the monohydrochloride monohydrate) for the relief of the symptoms of uticaria, rhinitis, and various pruritic skin disorders.		3.2310N-alkylpyrrolidine;
olefinic compound;
pyridines		H1-receptor antagonist
pitavastatin
pitavastatin : A dihydroxy monocarboxylic acid that is (6E)-7-[2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl]hept-6-enoic acid in which the two hydroxy groups are located at positions 3 and 5 (the 3R,5S-stereoisomer). Used as its calcium salt for treatment of hypercholesterolemia (elevated levels of cholesterol in the blood) on patients unable to sufficiently lower their cholesterol levels by diet and exercise.		3.2310cyclopropanes;
dihydroxy monocarboxylic acid;
monofluorobenzenes;
quinolines;
statin (synthetic)		antioxidant
ethamolin
monoethanolamine oleate: used for treatment of pyogenic granuloma		3.2310long-chain fatty acid
alatrofloxacin mesylate
[no description available]		3.2310
codeine
[no description available]		3.2310morphinane alkaloid;
organic heteropentacyclic compound		antitussive;
drug allergen;
environmental contaminant;
opioid analgesic;
opioid receptor agonist;
prodrug;
xenobiotic
cyclosporine
ramihyphin A: one of the metabolites produced by Fusarium sp. S-435; RN given refers to cpd with unknown MF		3.2310homodetic cyclic peptideanti-asthmatic drug;
anticoronaviral agent;
antifungal agent;
antirheumatic drug;
carcinogenic agent;
dermatologic drug;
EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor;
geroprotector;
immunosuppressive agent;
metabolite
acitretin
Acitretin: An oral retinoid effective in the treatment of psoriasis. It is the major metabolite of ETRETINATE with the advantage of a much shorter half-life when compared with etretinate.. acitretin : A retinoid that consists of 3,7-dimethylnona-2,4,6,8-tetraenoic acid having a 4-methoxy-2,3,6-trimethylphenyl group attached at position 9.		3.2310acitretin;
alpha,beta-unsaturated monocarboxylic acid;
retinoid		keratolytic drug
estropipate
estropipate: used therapeutically in menopausal patients		3.2310piperazinium salt;
steroid sulfate
hydromorphone
Hydromorphone: An opioid analgesic made from MORPHINE and used mainly as an analgesic. It has a shorter duration of action than morphine.. hydromorphone : A morphinane alkaloid that is a hydrogenated ketone derivative of morphine. A semi-synthetic drug, it is a centrally acting pain medication of the opioid class.		3.2310morphinane alkaloid;
organic heteropentacyclic compound		mu-opioid receptor agonist;
opioid analgesic
levetiracetam
Levetiracetam: A pyrrolidinone and acetamide derivative that is used primarily for the treatment of SEIZURES and some movement disorders, and as a nootropic agent.. levetiracetam : A pyrrolidinone and carboxamide that is N-methylpyrrolidin-2-one in which one of the methyl hydrogens is replaced by an aminocarbonyl group, while another is replaced by an ethyl group (the S enantiomer). An anticonvulsant, it is used for the treatment of epilepsy in both human and veterinary medicine.		3.2310pyrrolidin-2-onesanticonvulsant;
environmental contaminant;
xenobiotic
ly 163892
loracarbef: 1-carbacephem antibiotic; has a broad spectrum of antimicrobial activity; structure given in first source; carbacephems differ from cephalosporins in the substitution of a sulfur atom in the dihydrothiazine ring with a methylene group to form a tetrahydropyridine ring. loracarbef : A synthetic "carba" analogue of cefaclor, with carbon replacing sulfur at position 1. Used to treat a wide range of infections caused by both gram-positive and gram-negative bacteria.		3.2310carbacephem;
zwitterion		antibacterial drug;
antimicrobial agent
nabilone
nabilone: cannabinol deriv; RN given refers to cpd without isomeric designation; structure		3.2310
naloxone
Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.. naloxone : A synthetic morphinane alkaloid that is morphinone in which the enone double bond has been reduced to a single bond, the hydrogen at position 14 has been replaced by a hydroxy group, and the methyl group attached to the nitrogen has been replaced by an allyl group. A specific opioid antagonist, it is used (commonly as its hydrochloride salt) to reverse the effects of opioids, both following their use of opioids during surgery and in cases of known or suspected opioid overdose.		3.2310morphinane alkaloid;
organic heteropentacyclic compound;
tertiary alcohol		antidote to opioid poisoning;
central nervous system depressant;
mu-opioid receptor antagonist
oxycodone
Oxycodone: A semisynthetic derivative of CODEINE.. oxycodone : A semisynthetic opioid of formula C18H21NO4 that is derived from thebaine. It is a moderately potent opioid analgesic, generally used for relief of moderate to severe pain.		3.2310organic heteropentacyclic compound;
semisynthetic derivative		antitussive;
mu-opioid receptor agonist;
opioid analgesic
oxymorphone
Oxymorphone: An opioid analgesic with actions and uses similar to those of MORPHINE, apart from an absence of cough suppressant activity. It is used in the treatment of moderate to severe pain, including pain in obstetrics. It may also be used as an adjunct to anesthesia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1092)		3.2310morphinane alkaloid
vitamin k 1
Vitamin K 1: A family of phylloquinones that contains a ring of 2-methyl-1,4-naphthoquinone and an isoprenoid side chain. Members of this group of vitamin K 1 have only one double bond on the proximal isoprene unit. Rich sources of vitamin K 1 include green plants, algae, and photosynthetic bacteria. Vitamin K1 has antihemorrhagic and prothrombogenic activity.. phylloquinone : A member of the class of phylloquinones that consists of 1,4-naphthoquinone having methyl and phytyl groups at positions 2 and 3 respectively. The parent of the class of phylloquinones.		3.2310phylloquinones;
vitamin K		cofactor;
human metabolite;
plant metabolite
sirolimus
Sirolimus: A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to IMMUNOPHILINS. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties.. sirolimus : A macrolide lactam isolated from Streptomyces hygroscopicus consisting of a 29-membered ring containing 4 trans double bonds, three of which are conjugated. It is an antibiotic, immunosupressive and antineoplastic agent.		3.2310antibiotic antifungal drug;
cyclic acetal;
cyclic ketone;
ether;
macrolide lactam;
organic heterotricyclic compound;
secondary alcohol		antibacterial drug;
anticoronaviral agent;
antineoplastic agent;
bacterial metabolite;
geroprotector;
immunosuppressive agent;
mTOR inhibitor
topiramate
Topiramate: A sulfamate-substituted fructose analog that was originally identified as a hypoglycemic agent. It is used for the treatment of EPILEPSY and MIGRAINE DISORDERS, and may also promote weight loss.. topiramate : A hexose derivative that is 2,3:4,5-di-O-isopropylidene-beta-D-fructopyranose in which the hydroxy group has been converted to the corresponding sulfamate ester. It blocks voltage-dependent sodium channels and is used as an antiepileptic and for the prevention of migraine.		3.2310cyclic ketal;
ketohexose derivative;
sulfamate ester		anticonvulsant;
sodium channel blocker
trospium chloride
trospium chloride : An organic chloride salt of trospium. It is an antispasmodic drug used for the treatment of overactive bladder.		3.2310
morphine
Meconium: The thick green-to-black mucilaginous material found in the intestines of a full-term fetus. It consists of secretions of the INTESTINAL GLANDS; BILE PIGMENTS; FATTY ACIDS; AMNIOTIC FLUID; and intrauterine debris. It constitutes the first stools passed by a newborn.		3.2310morphinane alkaloid;
organic heteropentacyclic compound;
tertiary amino compound		anaesthetic;
drug allergen;
environmental contaminant;
geroprotector;
mu-opioid receptor agonist;
opioid analgesic;
plant metabolite;
vasodilator agent;
xenobiotic
benzphetamine
Benzphetamine: A sympathomimetic agent with properties similar to DEXTROAMPHETAMINE. It is used in the treatment of obesity. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1222). benzphetamine : Dextroamphetamine in which the the hydrogens attached to the amino group are substituted by a methyl and a benzyl group. A sympathomimetic agent with properties similar to dextroamphetamine, it is used as its hydrochloride salt in the treatment of obesity.		3.2310amphetamines;
tertiary amine		adrenergic uptake inhibitor;
appetite depressant;
dopamine uptake inhibitor;
sympathomimetic agent
deamino arginine vasopressin
Deamino Arginine Vasopressin: A synthetic analog of the pituitary hormone, ARGININE VASOPRESSIN. Its action is mediated by the VASOPRESSIN receptor V2. It has prolonged antidiuretic activity, but little pressor effects. It also modulates levels of circulating FACTOR VIII and VON WILLEBRAND FACTOR.		3.2310heterodetic cyclic peptidediagnostic agent;
renal agent;
vasopressin receptor agonist
dexmedetomidine
[no description available]		3.2310medetomidinealpha-adrenergic agonist;
analgesic;
non-narcotic analgesic;
sedative
goserelin
Goserelin: A synthetic long-acting agonist of GONADOTROPIN-RELEASING HORMONE. Goserelin is used in treatments of malignant NEOPLASMS of the prostate, uterine fibromas, and metastatic breast cancer.		3.2310organic molecular entity
nalbuphine
Nalbuphine: A narcotic used as a pain medication. It appears to be an agonist at KAPPA RECEPTORS and an antagonist or partial agonist at MU RECEPTORS.		3.2310organic heteropentacyclic compoundmu-opioid receptor antagonist;
opioid analgesic
nateglinide
Nateglinide: A phenylalanine and cyclohexane derivative that acts as a hypoglycemic agent by stimulating the release of insulin from the pancreas. It is used in the treatment of TYPE 2 DIABETES.. nateglinide : An N-acyl-D-phenylalanine resulting from the formal condensation of the amino group of D-phenylalanine with the carboxy group of trans-4-isopropylcyclohexanecarboxylic acid. An orally-administered, rapidly-absorbed, short-acting insulinotropic agent, it is used for the treatment of type 2 diabetes mellitus.		3.2310phenylalanine derivative
vinorelbine
[no description available]		3.2310acetate ester;
methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
ring assembly;
vinca alkaloid		antineoplastic agent;
photosensitizing agent
silodosin
silodosin: an alpha(1a)-adrenoceptor-selective antagonist; structure given in first source		3.2310indolecarboxamide
fluvoxamine
Fluvoxamine: A selective serotonin reuptake inhibitor that is used in the treatment of DEPRESSION and a variety of ANXIETY DISORDERS.. fluvoxamine : An oxime O-ether that is benzene substituted by a (1E)-N-(2-aminoethoxy)-5-methoxypentanimidoyl group at position 1 and a trifluoromethyl group at position 4. It is a selective serotonin reuptake inhibitor that is used for the treatment of obsessive-compulsive disorder.		3.2310(trifluoromethyl)benzenes;
5-methoxyvalerophenone O-(2-aminoethyl)oxime		antidepressant;
anxiolytic drug;
serotonin uptake inhibitor
su 11248
[no description available]		3.2310monocarboxylic acid amide;
pyrroles		angiogenesis inhibitor;
antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
immunomodulator;
neuroprotective agent;
vascular endothelial growth factor receptor antagonist
(6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid
(6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid : A dihydroxy monocarboxylic acid that is N-isopropylindole which is substituted at position 3 by a p-fluorophenyl group and at position 2 by a 6-carboxy-3,5-dihydroxyhex-1-en-1-yl group. It has four possible diastereoisomers.		3.2310dihydroxy monocarboxylic acid;
indoles;
organofluorine compound
levorphanol
Levorphanol: A narcotic analgesic that may be habit-forming. It is nearly as effective orally as by injection.		3.2310morphinane alkaloid
naltrexone
Naltrexone: Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of NALOXONE. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence.. naltrexone : An organic heteropentacyclic compound that is naloxone substituted in which the allyl group attached to the nitrogen is replaced by a cyclopropylmethyl group. A mu-opioid receptor antagonist, it is used to treat alcohol dependence.		3.2310cyclopropanes;
morphinane-like compound;
organic heteropentacyclic compound		antidote to opioid poisoning;
central nervous system depressant;
environmental contaminant;
mu-opioid receptor antagonist;
xenobiotic
dextromethorphan
Dextromethorphan: Methyl analog of DEXTRORPHAN that shows high affinity binding to several regions of the brain, including the medullary cough center. This compound is an NMDA receptor antagonist (RECEPTORS, N-METHYL-D-ASPARTATE) and acts as a non-competitive channel blocker. It is one of the widely used ANTITUSSIVES, and is also used to study the involvement of glutamate receptors in neurotoxicity.. dextromethorphan : A 6-methoxy-11-methyl-1,3,4,9,10,10a-hexahydro-2H-10,4a-(epiminoethano)phenanthrene in which the sterocenters at positions 4a, 10 and 10a have S-configuration. It is a prodrug of dextrorphan and used as an antitussive drug for suppressing cough.		3.23106-methoxy-11-methyl-1,3,4,9,10,10a-hexahydro-2H-10,4a-(epiminoethano)phenanthreneantitussive;
environmental contaminant;
neurotoxin;
NMDA receptor antagonist;
oneirogen;
prodrug;
xenobiotic
butorphanol
Butorphanol: A synthetic morphinan analgesic with narcotic antagonist action. It is used in the management of severe pain.. butorphanol : Levorphanol in which a hydrogen at position 14 of the morphinan skeleton is substituted by hydroxy and one of the hydrogens of the N-methyl group is substituted by cyclopropyl. A semi-synthetic opioid agonist-antagonist analgesic, it is used as its (S,S)-tartaric acid salt for relief or moderate to severe pain.		3.2310morphinane alkaloidantitussive;
kappa-opioid receptor agonist;
mu-opioid receptor agonist;
opioid analgesic
cefixime
[no description available]		3.2310cephalosporinantibacterial drug;
drug allergen
lisinopril
Lisinopril: One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.		3.2310dipeptideEC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
benazepril
benazepril: structure given in first source. benazepril : A benzazepine that is benazeprilat in which the carboxy group of the 2-amino-4-phenylbutanoic acid moiety has been converted to the corresponding ethyl ester. It is used (generally as its hydrochloride salt) as a prodrug for the angiotensin-converting enzyme inhibitor benazeprilat in the treatment of hypertension and heart failure.		3.2310benzazepine;
dicarboxylic acid monoester;
ethyl ester;
lactam		EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
ramipril
Ramipril: A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.. ramipril : A dipeptide that is the prodrug for ramiprilat, the active metabolite obtained by hydrolysis of the ethyl ester group. An angiotensin-converting enzyme (ACE) inhibitor, used to treat high blood pressure and congestive heart failure.. quark : Quarks comprise one of two classes of the fundamental particles. Quarks possess fractional electric charges and are not observed in free state. The word "quark" first appears in James Joyce's Finnegans Wake and has been chosen by Murray Gell-Mann as a name for fundamental building blocks of particles.		3.2310azabicycloalkane;
cyclopentapyrrole;
dicarboxylic acid monoester;
dipeptide;
ethyl ester		bradykinin receptor B2 agonist;
cardioprotective agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
matrix metalloproteinase inhibitor;
prodrug
verteporfin
(2R,2(1)S)-8-ethenyl-2(1),2(2)-bis(methoxycarbonyl)-17-(3-methoxy-3-oxopropyl)-2,7,12,18-tetramethyl-2,2(1)-dihydrobenzo[b]porphyrin-13-propanoic acid : The 2(1),2(2),17-trimethyl ester of (2R,2(1)S)-2(1),2(2)-dicarboxy-8-ethenyl-2,7,12,18-tetramethyl-2,2(1)-dihydrobenzo[b]porphyrin-13,17-dipropanoic acid.		3.2310
indinavir sulfate
Indinavir: A potent and specific HIV protease inhibitor that appears to have good oral bioavailability.		3.2310dicarboxylic acid diamide;
N-(2-hydroxyethyl)piperazine;
piperazinecarboxamide		HIV protease inhibitor
zimeldine
Zimeldine: One of the SEROTONIN UPTAKE INHIBITORS formerly used for depression but was withdrawn worldwide in September 1983 because of the risk of GUILLAIN-BARRE SYNDROME associated with its use. (From Martindale, The Extra Pharmacopoeia, 29th ed, p385)		3.2310styrenes
enalapril
Enalapril: An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.. enalapril : A dicarboxylic acid monoester that is ethyl 4-phenylbutanoate in which a hydrogen alpha to the carboxy group is substituted by the amino group of L-alanyl-L-proline (S-configuration).		3.2310dicarboxylic acid monoester;
dipeptide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
geroprotector;
prodrug
trientine hydrochloride
[no description available]		3.2310
n-methylscopolamine bromide
scopolamine methobromide : A quaternary ammonium salt resulting from the reaction of the amino group of scopolamine with methyl bromide.		3.2310
bleomycin
[no description available]		3.2310bleomycinantineoplastic agent;
metabolite
enalaprilat anhydrous
Enalaprilat: The active metabolite of ENALAPRIL and one of the potent, intravenously administered, ANGIOTENSIN-CONVERTING ENZYME INHIBITORS. It is an effective agent for the treatment of essential hypertension and has beneficial hemodynamic effects in heart failure. The drug produces renal vasodilation with an increase in sodium excretion.. enalaprilat dihydrate : The dihydrate form of enalaprilat, an angiotensin-converting enzyme (ACE) inhibitor that is used (often in the form of its prodrug, enalapril) in the treatment of hypertension and heart failure, for reduction of proteinuria and renal disease in patients with nephropathies, and for the prevention of stroke, myocardial infarction, and cardiac death in high-risk patients. Unlike enalapril, enalaprilat is not absorbed by mouth but is administered by intravenous injection.. enalaprilat (anhydrous) : Enalapril in which the ethyl ester group has been hydrolysed to the corresponding carboxylic acid. Enalaprilat is an angiotensin-converting enzyme (ACE) inhibitor and is used (often in the form of its prodrug, enalapril) in the treatment of hypertension and heart failure, for reduction of proteinuria and renal disease in patients with nephropathies, and for the prevention of stroke, myocardial infarction, and cardiac death in high-risk patients. Unlike enalapril, enalaprilat is not absorbed by mouth but is given by intravenous injection, usually as the dihydrate.		3.2310dicarboxylic acid;
dipeptide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
ximelagatran
ximelagatran: prodrug (via hydroxylation) of melagatran & a direct thrombin inhibitor; liver toxicity concerns so AZD0837 being developed to replace this. ximelagatran : A member of the class of azetidines that is melagatran in which the carboxylic acid group has been converted to the corresponding ethyl ester and in which the amidine group has been converted into the corresponding amidoxime. A prodrug for melagatran, ximelagatran was the first orally available direct thrombin inhibitor to be brought to market as an anticoagulant, but was withdrawn in 2006 following reports of it causing liver damage.		3.2310amidoxime;
azetidines;
carboxamide;
ethyl ester;
hydroxylamines;
secondary amino compound;
secondary carboxamide;
tertiary carboxamide		anticoagulant;
EC 3.4.21.5 (thrombin) inhibitor;
prodrug;
serine protease inhibitor
cefuroxime
[no description available]		3.23103-(carbamoyloxymethyl)cephalosporin;
furans;
oxime O-ether		drug allergen
ceftriaxone
[no description available]		3.23101,2,4-triazines;
1,3-thiazoles;
cephalosporin;
oxime O-ether		antibacterial drug;
drug allergen;
EC 3.5.2.6 (beta-lactamase) inhibitor
cefepime
Cefepime: A fourth-generation cephalosporin antibacterial agent that is used in the treatment of infections, including those of the abdomen, urinary tract, respiratory tract, and skin. It is effective against PSEUDOMONAS AERUGINOSA and may also be used in the empiric treatment of FEBRILE NEUTROPENIA.. cefepime : A cephalosporin bearing (1-methylpyrrolidinium-1-yl)methyl and (2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetamido groups at positions 3 and 7, respectively, of the cephem skeleton.		3.2310cephalosporin;
oxime O-ether		antibacterial drug
pafuramidine
pafuramidine: a prodrug of furamidine		3.2310
ceftazidime
[no description available]		3.2310cephalosporin;
oxime O-ether		antibacterial drug;
drug allergen;
EC 2.4.1.129 (peptidoglycan glycosyltransferase) inhibitor
trandolapril
trandolapril : A heterobicylic compound that is (2S,3aR,7aS)-1-[(2S)-2-aminopropanoyl]octahydro-1H-indole-2-carboxylic acid in which the hydrogen of the amino group is substituted by a (2R)-1-ethoxy-1-oxo-4-phenylbutan-2-yl group. It is a angiotensin-converting enzyme inhibitor and a prodrug used for the treatment of hypertension.		3.2310dicarboxylic acid monoester;
dipeptide;
ethyl ester;
organic heterobicyclic compound;
secondary amino compound;
tertiary carboxamide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
pregabalin
Pregabalin: A gamma-aminobutyric acid (GABA) derivative that functions as a CALCIUM CHANNEL BLOCKER and is used as an ANTICONVULSANT as well as an ANTI-ANXIETY AGENT. It is also used as an ANALGESIC in the treatment of NEUROPATHIC PAIN and FIBROMYALGIA.. pregabalin : A gamma-amino acid that is gamma-aminobutyric acid (GABA) carrying an isobutyl substitutent at the beta-position (the S-enantiomer). Binds with high affinity to the alpha2-delta site (an auxiliary subunit of voltage-gated calcium channels) in central nervous system tissues.		3.2310gamma-amino acidanticonvulsant;
calcium channel blocker
alvimopan anhydrous
alvimopan: mu opioid receptor antagonist; intended to treat constipation in patients taking opiates for pain		3.2310peptide
aliskiren
aliskiren: orally active nonpeptidic renin inhibitor. aliskiren : A monomethoxybenzene compound having a 3-methoxypropoxy group at the 2-position and a multi-substituted branched alkyl substituent at the 4-position.		3.2310monocarboxylic acid amide;
monomethoxybenzene		antihypertensive agent
famotidine
[no description available]		3.23101,3-thiazoles;
guanidines;
sulfonamide		anti-ulcer drug;
H2-receptor antagonist;
P450 inhibitor
cefotaxime
Cefotaxime: Semisynthetic broad-spectrum cephalosporin.. cefotaxime : A cephalosporin compound having acetoxymethyl and [2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetyl]amino side groups.		3.23101,3-thiazoles;
cephalosporin;
oxime O-ether		antibacterial drug;
drug allergen
aztreonam
[no description available]		3.2310beta-lactam antibiotic allergen;
monobactam		antibacterial drug;
drug allergen;
EC 2.4.1.129 (peptidoglycan glycosyltransferase) inhibitor
cefpodoxime
[no description available]		3.2310carboxylic acid;
cephalosporin		antibacterial drug
palonosetron
Palonosetron: Isoquinoline and quinuclidine derivative that acts as a 5-HT3 RECEPTOR antagonist. It is used in the prevention of nausea and vomiting induced by cytotoxic chemotherapy, and for the prevention of post-operative nausea and vomiting.. palonosetron : An organic heterotricyclic compound that is an antiemetic used (as its hydrochloride salt) in combination with netupitant (under the trade name Akynzeo) to treat nausea and vomiting in patients undergoing cancer chemotherapy.		3.2310azabicycloalkane;
delta-lactam;
organic heterotricyclic compound		antiemetic;
serotonergic antagonist
rifaximin
[no description available]		3.2310acetate ester;
cyclic ketal;
lactam;
macrocycle;
organic heterohexacyclic compound;
rifamycins;
semisynthetic derivative		antimicrobial agent;
gastrointestinal drug;
orphan drug
everolimus
[no description available]		3.2310cyclic acetal;
cyclic ketone;
ether;
macrolide lactam;
primary alcohol;
secondary alcohol		anticoronaviral agent;
antineoplastic agent;
geroprotector;
immunosuppressive agent;
mTOR inhibitor
ixabepilone
[no description available]		3.23101,3-thiazoles;
beta-hydroxy ketone;
epoxide;
lactam;
macrocycle		antineoplastic agent;
microtubule-destabilising agent
ceftizoxime
[no description available]		3.2310cephalosporinantibacterial drug
1-methyl-d-lysergic acid butanolamide
[no description available]		3.2310ergot alkaloid;
monocarboxylic acid amide		serotonergic antagonist;
sympatholytic agent;
vasoconstrictor agent
nitrofurantoin
Nitrofurantoin: A urinary anti-infective agent effective against most gram-positive and gram-negative organisms. Although sulfonamides and antibiotics are usually the agents of choice for urinary tract infections, nitrofurantoin is widely used for prophylaxis and long-term suppression.. nitrofurantoin : An imidazolidine-2,4-dione that is hydantoin substituted at position 1 by a [(5-nitro-2-furyl)methylene]amino group. An antibiotic that damages bacterial DNA.		3.2310imidazolidine-2,4-dione;
nitrofuran antibiotic;
organonitrogen heterocyclic antibiotic;
organooxygen heterocyclic antibiotic		antibacterial drug;
antiinfective agent;
hepatotoxic agent
dantrolene
[no description available]		3.2310
cefdinir
[no description available]		3.2310cephalosporin;
ketoxime		antibacterial drug
etonogestrel
[no description available]		3.231017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
terminal acetylenic compound		contraceptive drug;
female contraceptive drug;
progestin
temsirolimus
[no description available]		3.2310macrolide lactam
dutasteride
Dutasteride: A 5-ALPHA-REDUCTASE INHIBITOR that is reported to inhibit both type-1 and type2 isoforms of the enzyme and is used to treat BENIGN PROSTATIC HYPERPLASIA.. dutasteride : An aza-steroid that is inasteride in which the tert-butyl group is replaced by a 2,5-bis(trifluoromethyl)phenyl group. A synthetic 4-azasteroid, dutasteride is a selective inhibitor of both the type 1 and type 2 isoforms of steroid 5alpha-reductase, an intracellular enzyme that converts testosterone to 5alpha-dihydrotestosterone. Dutasteride is used for the treatment of symptomatic benign prostatic hyperplasia in men with an enlarged prostate gland.		3.2310(trifluoromethyl)benzenes;
aza-steroid;
delta-lactam		antihyperplasia drug;
EC 1.3.1.22 [3-oxo-5alpha-steroid 4-dehydrogenase (NADP(+))] inhibitor
lu 208075
ambrisentan: an ET(A) receptor antagonist and antihypertensive agent; studied for use in pulmonary arterial hypertension		3.2310diarylmethane
bibx 1382bs
BIBX 1382BS: an ErbB receptor kinase inhibitor; no further information available 4/2001		3.2310substituted aniline
fesoterodine
fesoterodine: a muscarinic antagonist for treatment of overactive bladder		3.2310diarylmethane
gemifloxacin
Gemifloxacin: A naphthyridine and fluoroquinolone derivative antibacterial agent and DNA TOPOISOMERASE II inhibitor that is used for the treatment of community-acquired pneumonia and acute bacterial infections associated with chronic bronchitis.. gemifloxacin : A 1,4-dihydro-1,8-naphthyridine with a carboxy group at the 3-position, an oxo sustituent at the 4-position, a fluoro substituent at the 5-position and a substituted pyrrolin-1-yl group at the 7-position.		3.23101,8-naphthyridine derivative;
fluoroquinolone antibiotic;
monocarboxylic acid;
quinolone antibiotic		antibacterial drug;
antimicrobial agent;
topoisomerase IV inhibitor
dexlansoprazole
Dexlansoprazole: The R-isomer of lansoprazole that is used to treat severe GASTROESOPHAGEAL REFLUX DISEASE.		3.2310benzimidazoles;
sulfoxide
fosinopril
[no description available]		3.2310
armodafinil
armodafinil : A 2-[(diphenylmethyl)sulfinyl]acetamide that has R configuration at the sulfur atom. Like its racemate, modafinil, it is used for the treatment of sleeping disorders such as narcolepsy, obstructive sleep apnoea, and shift-work sleep disorder. Peak concentration in the blood later occurs later following administration than with modafinil, so it is thought that armodafinil may be more effective than modafinil in treating people with excessive daytime sleepiness.		3.23102-[(diphenylmethyl)sulfinyl]acetamidecentral nervous system stimulant;
eugeroic
sergliflozin etabonate
sergliflozin: a hypoglycemic agent that inhibits SGLT2 sodium-glucose transporter; structure in first source		3.1410glycoside
sincalide
Sincalide: An octapeptide hormone present in the intestine and brain. When secreted from the gastric mucosa, it stimulates the release of bile from the gallbladder and digestive enzymes from the pancreas.		3.2310oligopeptide
tapentadol
Tapentadol: An opioid analgesic, MU OPIOID RECEPTOR agonist, and noradrenaline reuptake inhibitor that is used in the treatment of moderate to severe pain, and of pain associated with DIABETIC NEUROPATHIES.		3.2310alkylbenzene
pentagastrin
Pentagastrin: A synthetic pentapeptide that has effects like gastrin when given parenterally. It stimulates the secretion of gastric acid, pepsin, and intrinsic factor, and has been used as a diagnostic aid.		3.2310organic molecular entity
cefditoren
cefditoren: structure given in first source; RN given refers to the (6R-(3(Z),6alpha,7beta(Z)))-isomer. cefditoren : A broad spectrum, third-generation cephalosporin antibiotic with (Z)-2-(4-methyl-1,3-thiazol-5-yl)ethenyl and (2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetamido groups at positions 3 and 7, respectively, of the cephem skeleton. Generally administered as its orally absorbed pivaloyloxymethyl ester prodrug, it is used for the treatment of mild to moderate infections caused by susceptible strains of microorganisms in acute bacterial exacerbation of chronic bronchitis, community-acquired pneumonia, pharyngitis/tonsillitis, and uncomplicated skin and skin-structure infections.		3.2310carboxylic acid;
cephalosporin		antibacterial drug
remogliflozin etabonate
remogliflozin etabonate: orally administered hypoglycemic agent; structure in first source		3.1410glycoside
dapagliflozin
[no description available]		3.1410aromatic ether;
C-glycosyl compound;
monochlorobenzenes		hypoglycemic agent;
sodium-glucose transport protein subtype 2 inhibitor
pazopanib
pazopanib: a protein kinase inhibitor. pazopanib : A pyrimidine that is 5-(pyrimidin-2-yl}amino-2-methylbenzenesulfonamide substituted at position 4 by a (2,3-dimethylindazol-6-yl)(methyl)amino group. Used as its hydrochloride salt for treatment of kidney cancer.		3.2310aminopyrimidine;
indazoles;
sulfonamide		angiogenesis modulating agent;
antineoplastic agent;
tyrosine kinase inhibitor;
vascular endothelial growth factor receptor antagonist
prasugrel hydrochloride
Prasugrel Hydrochloride: A piperazine derivative and PLATELET AGGREGATION INHIBITOR that is used to prevent THROMBOSIS in patients with ACUTE CORONARY SYNDROME; UNSTABLE ANGINA and MYOCARDIAL INFARCTION, as well as in those undergoing PERCUTANEOUS CORONARY INTERVENTIONS.. prasugrel hydrochloride : A racemate comprising equal amounts of (R)- and (S)-prasugrel hydrochloride. Used to prevent blood clots in people with acute coronary syndrome who are undergoing a procedure after a recent heart attack or stroke, and in people with certain disorders of the heart or blood vessels.		3.2310
baci-im
[no description available]		3.2310homodetic cyclic peptide;
polypeptide;
zwitterion		antibacterial agent;
antimicrobial agent
bms 477118
[no description available]		3.2310adamantanes;
azabicycloalkane;
monocarboxylic acid amide;
nitrile;
tertiary alcohol		EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
hypoglycemic agent
nystatin a1
Nystatin: Macrolide antifungal antibiotic complex produced by Streptomyces noursei, S. aureus, and other Streptomyces species. The biologically active components of the complex are nystatin A1, A2, and A3.. nystatin : A heterogeneous mixture of polyene compounds produced by cultures of Streptomyces noursei. It mainly consists of three biologically active components designated nystatin A1, nystatin A2, and nystatin A3. It is used to treat oral and dermal fungal infections.. nystatin A1 : A polyene macrolide antibiotic; part of the nystatin complex produced by several Streptomyces species. It is an antifungal antibiotic used for the treatment of topical fungal infections caused by a broad spectrum of fungal pathogens comprising yeast-like and filamentous species.		3.2310nystatins
milnacipran
[no description available]		3.2310acetamides
scopolamine hydrobromide
[no description available]		3.2310
bivalirudin
bivalirudin: designed to bind to the alpha-thrombin catalytic site and anion-binding exosite for fibrin(ogen) recognition. bivalirudin : A synthetic peptide of 20 amino acids, comprising D-Phe, Pro, Arg, Pro, Gly, Gly, Gly, Gly, Asn, Gly, Asp, Phe, Glu, Glu, Ile, Pro, Glu, Glu, Tyr, and Leu in sequence. A congener of hirudin (a naturally occurring drug found in the saliva of the medicinal leech), it a specific and reversible inhibitor of thrombin, and is used as an anticoagulant.		3.2310polypeptideanticoagulant;
EC 3.4.21.5 (thrombin) inhibitor
enfuvirtide
Enfuvirtide: A synthetic 36-amino acid peptide that corresponds to the heptad repeat sequence of HIV-1 gp41. It blocks HIV cell fusion and viral entry and is used with other anti-retrovirals for combination therapy of HIV INFECTIONS and AIDS.. enfuvirtide : A synthetic 36-amino acid peptide consisting of N-acetyltyrosyl, threonyl, seryl, leucyl, isoleucyl, histidyl, seryl, leucyl, isoleucyl, alpha-glutamyl, alpha-glutamyl, seryl, glutaminyl, asparaginyl, glutaminyl, glutaminyl, alpha-glutamyl, lysyl, asparaginyl, alpha-glutamyl, alpha-glutamyl, alpha-glutamyl, leucyl, leucyl, alpha-glutamyl, leucyl, alpha-aspartyl, lysyl, tryptophyl, alanyl, seryl, leucyl, tryptophyl, asparaginyl, tryptophyl, and phenylalaninamide residues joined in sequence. An HIV fusion inhibitor, it was the first of a novel class of antiretroviral drugs used in combination therapy for the treatment of HIV-1 infection. It interferes with entry of HIV into cells by binding to the gp41 sub-unit of the viral envelope glycoprotein, so inhibiting fusion of viral and cellular membranes.		3.2310
ganirelix
[no description available]		3.2310polypeptide
teriparatide
[no description available]		3.2310polypeptide
salmon calcitonin
[no description available]		3.2310heterodetic cyclic peptide;
peptide hormone;
polypeptide		bone density conservation agent;
metabolite
ly-146032
[no description available]		3.2310heterodetic cyclic peptide;
lipopeptide antibiotic;
lipopeptide;
macrocycle;
macrolide		antibacterial drug;
bacterial metabolite;
calcium-dependent antibiotics
liraglutide
[no description available]		4.1640lipopeptide;
polypeptide		glucagon-like peptide-1 receptor agonist;
neuroprotective agent
glucagon-like peptide 1
Glucagon-Like Peptide 1: A peptide of 36 or 37 amino acids that is derived from PROGLUCAGON and mainly produced by the INTESTINAL L CELLS. GLP-1(1-37 or 1-36) is further N-terminally truncated resulting in GLP-1(7-37) or GLP-1-(7-36) which can be amidated. These GLP-1 peptides are known to enhance glucose-dependent INSULIN release, suppress GLUCAGON release and gastric emptying, lower BLOOD GLUCOSE, and reduce food intake.		2.8530
acetyl-2-naphthylalanyl-3-chlorophenylalanyl-1-oxohexadecyl-seryl-4-aminophenylalanyl(hydroorotyl)-4-aminophenylalanyl(carbamoyl)-leucyl-ilys-prolyl-alaninamide
acetyl-2-naphthylalanyl-3-chlorophenylalanyl-1-oxohexadecyl-seryl-4-aminophenylalanyl(hydroorotyl)-4-aminophenylalanyl(carbamoyl)-leucyl-ILys-prolyl-alaninamide: FE-200486 is the acetate salt		3.2310polypeptide
c-peptide
C-Peptide: The middle segment of proinsulin that is between the N-terminal B-chain and the C-terminal A-chain. It is a pancreatic peptide of about 31 residues, depending on the species. Upon proteolytic cleavage of proinsulin, equimolar INSULIN and C-peptide are released. C-peptide immunoassay has been used to assess pancreatic beta cell function in diabetic patients with circulating insulin antibodies or exogenous insulin. Half-life of C-peptide is 30 min, almost 8 times that of insulin.		2.2510
mesna
Mesna: A sulfhydryl compound used to prevent urothelial toxicity by inactivating metabolites from ANTINEOPLASTIC AGENTS, such as IFOSFAMIDE or CYCLOPHOSPHAMIDE.		3.2310organosulfonic acid
sodium lactate
Sodium Lactate: The sodium salt of racemic or inactive lactic acid. It is a hygroscopic agent used intravenously as a systemic and urinary alkalizer.. sodium lactate : An organic sodium salt having lactate as the counterion.		3.2310lactate salt;
organic sodium salt		food acidity regulator;
food preservative
sodium iothalamate
[no description available]		3.2310
cetrorelix
cetrorelix: LHRH antagonist. cetrorelix : A synthetic ten-membered oligopeptide comprising N-acetyl-3-(naphthalen-2-yl)-D-alanyl, 4-chloro-D-phenylalanyl, 3-(pyridin-3-yl)-D-alanyl, L-seryl, L-tyrosyl, N(5)-carbamoyl-D-ornithyl, L-leucyl, L-arginyl, L-prolyl, and D-alaninamide residues coupled in sequence. A gonadotrophin-releasing hormone (GnRH) antagonist, it is used for treatment of infertility and of hormone-sensitive cancers of the prostate and breast.		3.2310oligopeptideantineoplastic agent;
GnRH antagonist
amg-837
AMG-837: GPR40 agonist		2.0810
4-(3-(benzyloxy)phenyl)-2-(ethylsulfinyl)-6-(trifluoromethyl)pyrimidine
[no description available]		2.4110
ascorbic acid
Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant.. L-ascorbic acid : The L-enantiomer of ascorbic acid and conjugate acid of L-ascorbate.. L-ascorbate : The L-enantiomer of ascorbate and conjugate base of L-ascorbic acid, arising from selective deprotonation of the 3-hydroxy group. Required for a range of essential metabolic reactions in all animals and plants.. vitamin C : Any member of a group of vitamers that belong to the chemical structural class called butenolides that exhibit biological activity against vitamin C deficiency in animals. The vitamers include L-ascorbic acid and its salt, ionized and oxidized forms.		3.2310ascorbic acid;
vitamin C		coenzyme;
cofactor;
flour treatment agent;
food antioxidant;
food colour retention agent;
geroprotector;
plant metabolite;
skin lightening agent
raltegravir
[no description available]		3.23101,2,4-oxadiazole;
dicarboxylic acid amide;
hydroxypyrimidine;
monofluorobenzenes;
pyrimidone;
secondary carboxamide		antiviral drug;
HIV-1 integrase inhibitor
tetracycline
Tetracycline: A naphthacene antibiotic that inhibits AMINO ACYL TRNA binding during protein synthesis.. tetracycline : A broad-spectrum polyketide antibiotic produced by the Streptomyces genus of actinobacteria.		3.2310
oxytetracycline, anhydrous
Oxytetracycline: A TETRACYCLINE analog isolated from the actinomycete STREPTOMYCES RIMOSUS and used in a wide variety of clinical conditions.. oxytetracycline : A tetracycline used for treatment of infections caused by a variety of Gram positive and Gram negative microorganisms including Mycoplasma pneumoniae, Pasteurella pestis, Escherichia coli, Haemophilus influenzae (respiratory infections), and Diplococcus pneumoniae.		3.2310
minocycline
Minocycline: A TETRACYCLINE analog, having a 7-dimethylamino and lacking the 5 methyl and hydroxyl groups, which is effective against tetracycline-resistant STAPHYLOCOCCUS infections.. minocycline : A tetracycline analogue having a dimethylamino group at position 7 and lacking the methyl and hydroxy groups at position 5.		3.2310
dicumarol
Dicumarol: An oral anticoagulant that interferes with the metabolism of vitamin K. It is also used in biochemical experiments as an inhibitor of reductases.		2.0810hydroxycoumarinanticoagulant;
EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor;
Hsp90 inhibitor;
vitamin K antagonist
piroxicam
[no description available]		3.2310benzothiazine;
monocarboxylic acid amide;
pyridines		analgesic;
antirheumatic drug;
cyclooxygenase 1 inhibitor;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-steroidal anti-inflammatory drug
mobic
Meloxicam: A benzothiazine and thiazole derivative that acts as a NSAID and cyclooxygenase-2 (COX-2) inhibitor. It is used in the treatment of RHEUMATOID ARTHRITIS; OSTEOARTHRITIS; and ANKYLOSING SPONDYLITIS.. meloxicam : A benzothiazine that is piroxicam in which the pyridin-2-yl group is replaced by a 5-methyl-1,3-thiazol-2-yl group. A non-steroidal anti-inflammatory drug and selective inhibitor of COX-2, it is used particularly for the management of rheumatoid arthritis.		3.23101,3-thiazoles;
benzothiazine;
monocarboxylic acid amide		analgesic;
antirheumatic drug;
cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
warfarin
Warfarin: An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide.. warfarin : A racemate comprising equal amounts of (R)- and (S)-warfarin. Extensively used as both an anticoagulant drug and as a pesticide against rats and mice.. 4-hydroxy-3-(3-oxo-1-phenylbutyl)-1-benzopyran-2-one : A member of the class of coumarins that is 4-hydroxycoumarin which is substituted at position 3 by a 1-phenyl-3-oxo-1-butyl group.		3.2310benzenes;
hydroxycoumarin;
methyl ketone
demeclocycline
Demeclocycline: A TETRACYCLINE analog having a 7-chloro and a 6-methyl. Because it is excreted more slowly than tetracycline, it maintains effective blood levels for longer periods of time.. demeclocycline : Tetracycline which lacks the methyl substituent at position 7 and in which the hydrogen para- to the phenolic hydroxy group is substituted by chlorine. Like tetracycline, it is an antibiotic, but being excreted more slowly, effective blood levels are maintained for longer. It is used (mainly as the hydrochloride) for the treatment of Lyme disease, acne and bronchitis, as well as for hyponatraemia (low blood sodium concentration) due to the syndrome of inappropriate antidiuretic hormone (SIADH) where fluid restriction alone has been ineffective.		3.2310
tipranavir
tipranavir: inhibits HIV-1 protease. tipranavir : A pyridine-2-sulfonamide substituted at C-5 by a trifluoromethyl group and at the sulfonamide nitrogen by a dihydropyrone-containing m-tolyl substituent. It is an HIV-1 protease inhibitor.		3.2310sulfonamideantiviral drug;
HIV protease inhibitor
tigecycline
[no description available]		3.2310
am 1638
[no description available]		2.0810
fertinex
[no description available]		3.2310
entecavir
entecavir (anhydrous) : Guanine substituted at the 9 position by a 4-hydroxy-3-(hydroxymethyl)-2-methylidenecyclopentyl group. A synthetic analogue of 2'-deoxyguanosine, it is a nucleoside reverse transcriptase inhibitor with selective antiviral activity against hepatitis B virus. Entecavir is phosphorylated intracellularly to the active triphosphate form, which competes with deoxyguanosine triphosphate, the natural substrate of hepatitis B virus reverse transcriptase, inhibiting every stage of the enzyme's activity, although it has no activity against HIV. It is used for the treatment of chronic hepatitis B.		3.23102-aminopurines;
oxopurine;
primary alcohol;
secondary alcohol		antiviral drug;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
acyclovir
Acyclovir: A GUANOSINE analog that acts as an antimetabolite. Viruses are especially susceptible. Used especially against herpes.. acyclovir : An oxopurine that is guanine substituted by a (2-hydroxyethoxy)methyl substituent at position 9. Used in the treatment of viral infections.		3.23102-aminopurines;
oxopurine		antimetabolite;
antiviral drug
folic acid
folcysteine: used to promote fertility in chickens. vitamin B9 : Any B-vitamin that exhibits biological activity against vitamin B9 deficiency. Vitamin B9 refers to the many forms of folic acid and its derivatives, including tetrahydrofolic acid (the active form), methyltetrahydrofolate (the primary form found in blood), methenyltetrahydrofolate, folinic acid amongst others. They are present in abundance in green leafy vegetables, citrus fruits, and animal products. Lack of vitamin B9 leads to anemia, a condition in which the body cannot produce sufficient number of red blood cells. Symptoms of vitamin B9 deficiency include fatigue, muscle weakness, and pale skin.		3.2310folic acids;
N-acyl-amino acid		human metabolite;
mouse metabolite;
nutrient
rifampin
Rifampin: A semisynthetic antibiotic produced from Streptomyces mediterranei. It has a broad antibacterial spectrum, including activity against several forms of Mycobacterium. In susceptible organisms it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis. Rifampin is bactericidal, and acts on both intracellular and extracellular organisms. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1160)		3.2310cyclic ketal;
hydrazone;
N-iminopiperazine;
N-methylpiperazine;
rifamycins;
semisynthetic derivative;
zwitterion		angiogenesis inhibitor;
antiamoebic agent;
antineoplastic agent;
antitubercular agent;
DNA synthesis inhibitor;
EC 2.7.7.6 (RNA polymerase) inhibitor;
Escherichia coli metabolite;
geroprotector;
leprostatic drug;
neuroprotective agent;
pregnane X receptor agonist;
protein synthesis inhibitor
clozapine
Clozapine: A tricylic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent.. clozapine : A benzodiazepine that is 5H-dibenzo[b,e][1,4]diazepine substituted by a chloro group at position 8 and a 4-methylpiperazin-1-yl group at position 11. It is a second generation antipsychotic used in the treatment of psychiatric disorders like schizophrenia.		3.2310benzodiazepine;
N-arylpiperazine;
N-methylpiperazine;
organochlorine compound		adrenergic antagonist;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
environmental contaminant;
GABA antagonist;
histamine antagonist;
muscarinic antagonist;
second generation antipsychotic;
serotonergic antagonist;
xenobiotic
dacarbazine
(E)-dacarbazine : A dacarbazine in which the N=N double bond adopts a trans-configuration.		3.2310dacarbazine
didanosine
Didanosine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. Didanosine is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase; ddI is then metabolized to dideoxyadenosine triphosphate, its putative active metabolite.. didanosine : A purine 2',3'-dideoxyribonucleoside that is inosine in which the hydroxy groups at both the 2' and the 3' positions on the sugar moiety have been replaced by hydrogen. An antiviral drug, it is used as a medication to treat HIV/AIDS.		3.2310purine 2',3'-dideoxyribonucleosideantimetabolite;
antiviral drug;
EC 2.4.2.1 (purine-nucleoside phosphorylase) inhibitor;
geroprotector;
HIV-1 reverse transcriptase inhibitor
ganciclovir
[no description available]		3.23102-aminopurines;
oxopurine		antiinfective agent;
antiviral drug
valacyclovir
Valacyclovir: A prodrug of acyclovir that is used in the treatment of HERPES ZOSTER and HERPES SIMPLEX VIRUS INFECTION of the skin and mucous membranes, including GENITAL HERPES.		3.2310L-valyl esterantiviral drug
sildenafil
sildenafil : A pyrazolo[4,3-d]pyrimidin-7-one having a methyl substituent at the 1-position, a propyl substituent at the 3-position and a 2-ethoxy-5-[(4-methylpiperazin-1-yl)sulfonyl]phenyl group at the 5-position.		3.2310piperazines;
pyrazolopyrimidine;
sulfonamide		EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor;
vasodilator agent
olanzapine
Olanzapine: A benzodiazepine derivative that binds SEROTONIN RECEPTORS; MUSCARINIC RECEPTORS; HISTAMINE H1 RECEPTORS; ADRENERGIC ALPHA-1 RECEPTORS; and DOPAMINE RECEPTORS. It is an antipsychotic agent used in the treatment of SCHIZOPHRENIA; BIPOLAR DISORDER; and MAJOR DEPRESSIVE DISORDER; it may also reduce nausea and vomiting in patients undergoing chemotherapy.. olanzapine : A benzodiazepine that is 10H-thieno[2,3-b][1,5]benzodiazepine substituted by a methyl group at position 2 and a 4-methylpiperazin-1-yl group at position 4.		3.2310benzodiazepine;
N-arylpiperazine;
N-methylpiperazine		antiemetic;
dopaminergic antagonist;
histamine antagonist;
muscarinic antagonist;
second generation antipsychotic;
serotonergic antagonist;
serotonin uptake inhibitor
vardenafil
vardenafil : The sulfonamide resulting from formal condensation of the sulfo group of 4-ethoxy-3-(5-methyl-7-propylimidazo[5,1-f][1,2,4]triazin-4(1H)-one-2-yl)benzenesulfonic acid and the secondary amino group of 4-ethylpiperazine.		3.2310imidazotriazine;
N-alkylpiperazine;
N-sulfonylpiperazine		EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
vasodilator agent
allopurinol
Allopurinol: A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.. allopurinol : A bicyclic structure comprising a pyrazole ring fused to a hydroxy-substituted pyrimidine ring.		3.2310nucleobase analogue;
organic heterobicyclic compound		antimetabolite;
EC 1.17.3.2 (xanthine oxidase) inhibitor;
gout suppressant;
radical scavenger
citrovorum factor
[no description available]		3.2310tetrahydrofolic acid
leucovorin
5-formyltetrahydrofolic acid : A formyltetrahydrofolic acid in which the formyl group is located at position 5.		3.2310formyltetrahydrofolic acidEscherichia coli metabolite;
mouse metabolite
rifapentine
rifapentine: cyclopentyl derivative of rifampicin		3.2310N-alkylpiperazine;
N-iminopiperazine;
rifamycins		antitubercular agent;
leprostatic drug
bl 4162a
anagrelide: imidazoquinazoline derivative which lowers platelet count probably by inhibiting thrombopoiesis and reduces platelet aggregation; used for thrombocythemia; structure in first source. anagrelide : A 1,5-dihydroimidazo[2,1-]quinazoline having an oxo substituent at the 2-position and chloro substituents at the 6- and 7-positions.		3.2310imidazoquinazolineanticoagulant;
antifibrinolytic drug;
cardiovascular drug;
platelet aggregation inhibitor
tegaserod
tegaserod: a nonbenzamide 5-hydroxytryptamine(4) agonist; used in treatment of irritable bowel syndrome; marketing suspended 2007 in US due to higher incidence of MI, stroke, and unstable angina; structure given in first source		3.2310carboxamidine;
guanidines;
hydrazines;
indoles		gastrointestinal drug;
serotonergic agonist
pemetrexed
pemetrexed disodium : An organic sodium salt that is the disodium salt of N-{4-[2-(2-amino-4-oxo-4,7-dihydro-1H-pyrrolo[2,3-d]pyrimidin-5-yl)ethyl]benzoyl}-L-glutamic acid. Inhibits thymidylate synthase (TS), 421 dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT).		3.2310N-acyl-L-glutamic acid;
pyrrolopyrimidine		antimetabolite;
antineoplastic agent;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
EC 2.1.1.45 (thymidylate synthase) inhibitor;
EC 2.1.2.2 (phosphoribosylglycinamide formyltransferase) inhibitor
valganciclovir
Valganciclovir: A ganciclovir prodrug and antiviral agent that is used to treat CYTOMEGALOVIRUS RETINITIS in patients with AIDS, and for the prevention of CYTOMEGALOVIRUS INFECTIONS in organ transplant recipients who have received an organ from a CMV-positive donor.. valganciclovir : The L-valinyl ester of ganciclovir, into which it is rapidly converted by intestinal and hepatic esterases. It is a synthetic analogue of 2'-deoxyguanosine.		3.2310L-valyl ester;
purines		antiviral drug;
prodrug
aprepitant
Aprepitant: A morpholine neurokinin-1 (NK1) receptor antagonist that is used in the management of nausea and vomiting caused by DRUG THERAPY, and for the prevention of POSTOPERATIVE NAUSEA AND VOMITING.. aprepitant : A morpholine-based antiemetic, which is or the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of highly emetogenic cancer chemotherapy. Aprepitant is a selective high-affinity antagonist of human substance P/neurokinin 1 (NK1) receptors.		3.2310(trifluoromethyl)benzenes;
cyclic acetal;
morpholines;
triazoles		antidepressant;
antiemetic;
neurokinin-1 receptor antagonist;
peripheral nervous system drug;
substance P receptor antagonist
fosaprepitant
fosaprepitant: a pro-drug form of aprepitant. fosaprepitant : A morpholine derivative that is the (1R)-1-[3,5-bis(trifluoromethyl)phenyl]ethyl ether of (3-{[(2R,3S)-3-(4-fluorophenyl)-2-hydroxymorpholin-4-yl]methyl}-5-oxo-4,5-dihydro-1H-1,2,4-triazol-1-yl)phosphonic acid.		3.2310(trifluoromethyl)benzenes;
cyclic acetal;
morpholines;
phosphoramide;
triazoles		antiemetic;
neurokinin-1 receptor antagonist;
prodrug
rifabutin
[no description available]		3.2310
levomefolate calcium
levomefolate calcium: an ingredient in Contraceptives, Oral, Combined. levomefolate calcium : An organic calcium salt of (6S)-5-methyltetrahydrofolic acid.		3.2310organic calcium saltantidepressant
ConditionIndicatedRelationship StrengthStudiesTrials
Body Weight
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.		023.44388177
Insulin Sensitivity
[description not available]		017.7214032
Polycystic Ovarian Syndrome
[description not available]		014.533218
Insulin Resistance
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.		017.7214032
Polycystic Ovary Syndrome
A complex disorder characterized by infertility, HIRSUTISM; OBESITY; and various menstrual disturbances such as OLIGOMENORRHEA; AMENORRHEA; ANOVULATION. Polycystic ovary syndrome is usually associated with bilateral enlarged ovaries studded with atretic follicles, not with cysts. The term, polycystic ovary, is misleading.		116.533218
Diabetes Mellitus, Adult-Onset
[description not available]		030.392,007600
Diabetes Mellitus, Type 2
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.		132.392,007600
Adenoma, beta-Cell
[description not available]		010.47483
Cancer of Pancreas
[description not available]		010.45472
Insulinoma
A benign tumor of the PANCREATIC BETA CELLS. Insulinoma secretes excess INSULIN resulting in HYPOGLYCEMIA.		015.47483
Pancreatic Neoplasms
Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).		010.45472
Nerve Pain
[description not available]		03.3150
Neuralgia
Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve.		03.3150
Alloxan Diabetes
[description not available]		010.152210
Autoimmune Diabetes
[description not available]		017.9211022
Diabetes Mellitus, Type 1
A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.		119.9211022
Overweight
A status with BODY WEIGHT that is above certain standards. In the scale of BODY MASS INDEX, overweight is defined as having a BMI of 25.0-29.9 kg/m2. Overweight may or may not be due to increases in body fat (ADIPOSE TISSUE), hence overweight does not equal over fat.		015.714631
Obesity
A status with BODY WEIGHT that is grossly above the recommended standards, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).		123.91279106
Disease Models, Animal
Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases.		014.311991
Complications of Diabetes Mellitus
[description not available]		09.65213
Hyperglycemia, Postprandial
Abnormally high BLOOD GLUCOSE level after a meal.		018.4612846
Hyperglycemia
Abnormally high BLOOD GLUCOSE level.		120.4612846
Cardiac Failure
[description not available]		08.71111
Cardiovascular Diseases
Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.		019.2510248
Heart Failure
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.		08.71111
Diseases, Metabolic
[description not available]		04.1250
Metabolic Diseases
Generic term for diseases caused by an abnormal metabolic process. It can be congenital due to inherited enzyme abnormality (METABOLISM, INBORN ERRORS) or acquired due to disease of an endocrine organ or failure of a metabolically important organ such as the liver. (Stedman, 26th ed)		04.1250
Atherosclerotic Parkinsonism
[description not available]		02.8430
Parkinson Disease, Secondary
Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)		02.8430
Weight Reduction
[description not available]		028.29299193
Weight Loss
Decrease in existing BODY WEIGHT.		125.29299193
Alcohol Drinking
Behaviors associated with the ingesting of ALCOHOLIC BEVERAGES, including social drinking.		07.41122
Drug Withdrawal Symptoms
[description not available]		04.9621
Substance Withdrawal Syndrome
Physiological and psychological symptoms associated with withdrawal from the use of a drug after prolonged administration or habituation. The concept includes withdrawal from smoking or drinking, as well as withdrawal from an administered drug.		04.9621
Weight Gain
Increase in BODY WEIGHT over existing weight.		014.424114
Cold Panniculitis
[description not available]		03.0640
Anoxemia
[description not available]		03.680
Hypoxia
Sub-optimal OXYGEN levels in the ambient air of living organisms.		08.680
Optic Atrophy
Atrophy of the optic disk which may be congenital or acquired. This condition indicates a deficiency in the number of nerve fibers which arise in the RETINA and converge to form the OPTIC DISK; OPTIC NERVE; OPTIC CHIASM; and optic tracts. GLAUCOMA; ISCHEMIA; inflammation, a chronic elevation of intracranial pressure, toxins, optic nerve compression, and inherited conditions (see OPTIC ATROPHIES, HEREDITARY) are relatively common causes of this condition.		03.8830
Fatty Liver, Nonalcoholic
[description not available]		011.98476
Cirrhosis, Liver
[description not available]		03.5970
Liver Cirrhosis
Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules.		08.5970
Non-alcoholic Fatty Liver Disease
Fatty liver finding without excessive ALCOHOL CONSUMPTION.		113.98476
Hyperlipemia
[description not available]		08.6393
Hyperlipidemias
Conditions with excess LIPIDS in the blood.		08.6393
Cognitive Decline
[description not available]		012.222818
Cognitive Dysfunction
Diminished or impaired mental and/or intellectual function.		012.222818
Liver Steatosis
[description not available]		010.97393
Fatty Liver
Lipid infiltration of the hepatic parenchymal cells resulting in a yellow-colored liver. The abnormal lipid accumulation is usually in the form of TRIGLYCERIDES, either as a single large droplet or multiple small droplets. Fatty liver is caused by an imbalance in the metabolism of FATTY ACIDS.		010.97393
Allodynia
[description not available]		03.460
Familial Hyperinsulinemic Hypoglycemia 1
[description not available]		02.8330
Congenital Hyperinsulinism
A familial, nontransient HYPOGLYCEMIA with defects in negative feedback of GLUCOSE-regulated INSULIN release. Clinical phenotypes include HYPOGLYCEMIA; HYPERINSULINEMIA; SEIZURES; COMA; and often large BIRTH WEIGHT. Several sub-types exist with the most common, type 1, associated with mutations on an ATP-BINDING CASSETTE TRANSPORTERS (subfamily C, member 8).		02.8330
Cicatrization
The formation of fibrous tissue in the place of normal tissue during the process of WOUND HEALING. It includes scar tissue formation occurring in healing internal organs as well as in the skin after surface injuries.		02.8220
Injuries, Spinal Cord
[description not available]		03.0840
Cicatrix
The fibrous tissue that replaces normal tissue during the process of WOUND HEALING.		02.8220
Spinal Cord Injuries
Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).		03.0840
Apoplexy
[description not available]		09.16158
Acute Ischemic Stroke
[description not available]		04.2821
Bleeding
[description not available]		07.8930
Ischemic Stroke
Stroke due to BRAIN ISCHEMIA resulting in interruption or reduction of blood flow to a part of the brain. When obstruction is due to a BLOOD CLOT formed within in a cerebral blood vessel it is a thrombotic stroke. When obstruction is formed elsewhere and moved to block a cerebral blood vessel (see CEREBRAL EMBOLISM) it is referred to as embolic stroke. Wake-up stroke refers to ischemic stroke occurring during sleep while cryptogenic stroke refers to ischemic stroke of unknown origin.		16.2821
Hemorrhage
Bleeding or escape of blood from a vessel.		02.8930
Stroke
A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)		111.16158
Morbid Obesity
[description not available]		07.8795
Obesity, Morbid
The condition of weighing two, three, or more times the ideal weight, so called because it is associated with many serious and life-threatening disorders. In the BODY MASS INDEX, morbid obesity is defined as having a BMI greater than 40.0 kg/m2.		19.8795
Diabetes Mellitus
A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.		120.542306
Chronic Kidney Failure
[description not available]		05.5731
Kidney Failure, Chronic
The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.		05.5731
Sterility, Female
[description not available]		05.8321
Infertility, Female
Diminished or absent ability of a female to achieve conception.		05.8321
Pregnancy
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.		010.45252
Right Ventricular Dysfunction
[description not available]		03.811
Idiopathic Parkinson Disease
[description not available]		016.074829
Parkinson Disease
A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)		118.074829
Burns
Injuries to tissues caused by contact with heat, steam, chemicals (BURNS, CHEMICAL), electricity (BURNS, ELECTRIC), or the like.		09.23104
Alcohol Abuse
[description not available]		06.0642
Alcoholism
A primary, chronic disease with genetic, psychosocial, and environmental factors influencing its development and manifestations. The disease is often progressive and fatal. It is characterized by impaired control over drinking, preoccupation with the drug alcohol, use of alcohol despite adverse consequences, and distortions in thinking, most notably denial. Each of these symptoms may be continuous or periodic. (Morse & Flavin for the Joint Commission of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to Study the Definition and Criteria for the Diagnosis of Alcoholism: in JAMA 1992;268:1012-4)		18.0642
Anoxia-Ischemia, Brain
[description not available]		03.7830
Acute Brain Injuries
[description not available]		04.4270
Brain Injuries
Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.		04.4270
Hypoxia-Ischemia, Brain
A disorder characterized by a reduction of oxygen in the blood combined with reduced blood flow (ISCHEMIA) to the brain from a localized obstruction of a cerebral artery or from systemic hypoperfusion. Prolonged hypoxia-ischemia is associated with ISCHEMIC ATTACK, TRANSIENT; BRAIN INFARCTION; BRAIN EDEMA; COMA; and other conditions.		03.7830
Anaphylactic Reaction
[description not available]		02.9430
Anaphylaxis
An acute hypersensitivity reaction due to exposure to a previously encountered ANTIGEN. The reaction may include rapidly progressing URTICARIA, respiratory distress, vascular collapse, systemic SHOCK, and death.		07.9430
Aggression
Behavior which may be manifested by destructive and attacking action which is verbal or physical, by covert attitudes of hostility or by obstructionism.		02.4110
Degenerative Diseases, Central Nervous System
[description not available]		08.87140
Neurodegenerative Diseases
Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures.		08.87140
Innate Inflammatory Response
[description not available]		09.39392
Inflammation
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.		09.39392
Astrocytosis
[description not available]		03.0540
Anxiety
Feelings or emotions of dread, apprehension, and impending disaster but not disabling as with ANXIETY DISORDERS.		03.5770
Injury, Myocardial Reperfusion
[description not available]		017.159938
Cardiovascular Stroke
[description not available]		017.4411553
Myocardial Infarction
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).		122.07230106
Albuminuria
The presence of albumin in the urine, an indicator of KIDNEY DISEASES.		08.0186
Atherogenesis
[description not available]		06.99140
Elevated Cholesterol
[description not available]		02.9130
Hypercholesterolemia
A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.		02.9130
Atherosclerosis
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.		06.99140
Benign Intracranial Hypertension
[description not available]		05.3121
Pseudotumor Cerebri
A condition marked by raised intracranial pressure and characterized clinically by HEADACHES; NAUSEA; PAPILLEDEMA, peripheral constriction of the visual fields, transient visual obscurations, and pulsatile TINNITUS. OBESITY is frequently associated with this condition, which primarily affects women between 20 and 44 years of age. Chronic PAPILLEDEMA may lead to optic nerve injury (see OPTIC NERVE DISEASES) and visual loss (see BLINDNESS).		05.3121
Ischemia
A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.		03.3760
Diabetes Insipidus and Mellitus with Optic Atrophy and Deafness
[description not available]		02.930
Wolfram Syndrome
A hereditary condition characterized by multiple symptoms including those of DIABETES INSIPIDUS; DIABETES MELLITUS; OPTIC ATROPHY; and DEAFNESS. This syndrome is also known as DIDMOAD (first letter of each word) and is usually associated with VASOPRESSIN deficiency. It is caused by mutations in gene WFS1 encoding wolframin, a 100-kDa transmembrane protein.		07.930
Alcoholic Fatty Liver
[description not available]		02.610
Hypergonadotropic Hypogonadism
[description not available]		02.610
Hypogonadism
Condition resulting from deficient gonadal functions, such as GAMETOGENESIS and the production of GONADAL STEROID HORMONES. It is characterized by delay in GROWTH, germ cell maturation, and development of secondary sex characteristics. Hypogonadism can be due to a deficiency of GONADOTROPINS (hypogonadotropic hypogonadism) or due to primary gonadal failure (hypergonadotropic hypogonadism).		07.610
Cardiometabolic Syndrome
A cluster of symptoms that are risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components not only include metabolic dysfunctions of METABOLIC SYNDROME but also HYPERTENSION, and ABDOMINAL OBESITY.		07.27122
Cirrhosis
[description not available]		05.27101
Fibrosis
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.		05.27101
Metabolic Syndrome
A cluster of symptoms that are risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components of metabolic syndrome include ABDOMINAL OBESITY; atherogenic DYSLIPIDEMIA; HYPERTENSION; HYPERGLYCEMIA; INSULIN RESISTANCE; a proinflammatory state; and a prothrombotic (THROMBOSIS) state.		07.27122
Recrudescence
[description not available]		04.3260
Prediabetes
[description not available]		013.312319
Prediabetic State
The time period before the development of symptomatic diabetes. For example, certain risk factors can be observed in subjects who subsequently develop INSULIN RESISTANCE as in type 2 diabetes (DIABETES MELLITUS, TYPE 2).		115.312319
Smoking Cessation
Discontinuing the habit of SMOKING.		18.6733
Asymmetric Diabetic Proximal Motor Neuropathy
[description not available]		08.18112
Diabetic Neuropathies
Peripheral, autonomic, and cranial nerve disorders that are associated with DIABETES MELLITUS. These conditions usually result from diabetic microvascular injury involving small blood vessels that supply nerves (VASA NERVORUM). Relatively common conditions which may be associated with diabetic neuropathy include third nerve palsy (see OCULOMOTOR NERVE DISEASES); MONONEUROPATHY; mononeuropathy multiplex; diabetic amyotrophy; a painful POLYNEUROPATHY; autonomic neuropathy; and thoracoabdominal neuropathy. (From Adams et al., Principles of Neurology, 6th ed, p1325)		08.18112
Neuroblastoma
A common neoplasm of early childhood arising from neural crest cells in the sympathetic nervous system, and characterized by diverse clinical behavior, ranging from spontaneous remission to rapid metastatic progression and death. This tumor is the most common intraabdominal malignancy of childhood, but it may also arise from thorax, neck, or rarely occur in the central nervous system. Histologic features include uniform round cells with hyperchromatic nuclei arranged in nests and separated by fibrovascular septa. Neuroblastomas may be associated with the opsoclonus-myoclonus syndrome. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2099-2101; Curr Opin Oncol 1998 Jan;10(1):43-51)		03.2450
Arteriosclerosis, Coronary
[description not available]		05.2331
Coronary Artery Disease
Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.		010.2331
Acute Confusional Senile Dementia
[description not available]		09.76261
Alzheimer Disease
A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)		09.76261
Choked Disk
[description not available]		03.5210
Papilledema
Swelling of the OPTIC DISK, usually in association with increased intracranial pressure, characterized by hyperemia, blurring of the disk margins, microhemorrhages, blind spot enlargement, and engorgement of retinal veins. Chronic papilledema may cause OPTIC ATROPHY and visual loss. (Miller et al., Clinical Neuro-Ophthalmology, 4th ed, p175)		03.5210
Fasting Hypoglycemia
HYPOGLYCEMIA expressed in the postabsorptive state, after prolonged FASTING, or an overnight fast.		020.6214480
Hypoglycemia
A syndrome of abnormally low BLOOD GLUCOSE level. Clinical hypoglycemia has diverse etiologies. Severe hypoglycemia eventually lead to glucose deprivation of the CENTRAL NERVOUS SYSTEM resulting in HUNGER; SWEATING; PARESTHESIA; impaired mental function; SEIZURES; COMA; and even DEATH.		020.6214480
Adolescent Obesity
[description not available]		03.5520
Benign Neoplasms
[description not available]		018.021241
Neoplasms
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.		018.021241
Disease Exacerbation
[description not available]		014.433419
Angiogenesis, Pathologic
[description not available]		07.8254
Diabetic Retinopathy
Disease of the RETINA as a complication of DIABETES MELLITUS. It is characterized by the progressive microvascular complications, such as ANEURYSM, interretinal EDEMA, and intraocular PATHOLOGIC NEOVASCULARIZATION.		013.64144
Colitis, Mucous
[description not available]		02.8530
Irritable Bowel Syndrome
A disorder with chronic or recurrent colonic symptoms without a clearcut etiology. This condition is characterized by chronic or recurrent ABDOMINAL PAIN, bloating, MUCUS in FECES, and an erratic disturbance of DEFECATION.		02.8530
Anochlesia
[description not available]		02.8230
Peripheral Arterial Diseases
[description not available]		04.9621
Peripheral Arterial Disease
Lack of perfusion in the EXTREMITIES resulting from atherosclerosis. It is characterized by INTERMITTENT CLAUDICATION, and an ANKLE BRACHIAL INDEX of 0.9 or less.		04.9621
Cerebral Infarction, Middle Cerebral Artery
[description not available]		03.6680
Infarction, Middle Cerebral Artery
NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.		03.6680
Diabetic Angiopathies
VASCULAR DISEASES that are associated with DIABETES MELLITUS.		014.363411
Friedreich Disease
[description not available]		02.2510
Friedreich Ataxia
An autosomal recessive disease, usually of childhood onset, characterized pathologically by degeneration of the spinocerebellar tracts, posterior columns, and to a lesser extent the corticospinal tracts. Clinical manifestations include GAIT ATAXIA, pes cavus, speech impairment, lateral curvature of spine, rhythmic head tremor, kyphoscoliosis, congestive heart failure (secondary to a cardiomyopathy), and lower extremity weakness. Most forms of this condition are associated with a mutation in a gene on chromosome 9, at band q13, which codes for the mitochondrial protein frataxin. (From Adams et al., Principles of Neurology, 6th ed, p1081; N Engl J Med 1996 Oct 17;335(16):1169-75) The severity of Friedreich ataxia associated with expansion of GAA repeats in the first intron of the frataxin gene correlates with the number of trinucleotide repeats. (From Durr et al, N Engl J Med 1996 Oct 17;335(16):1169-75)		07.2510
Acute Coronary Syndrome
An episode of MYOCARDIAL ISCHEMIA that generally lasts longer than a transient anginal episode that ultimately may lead to MYOCARDIAL INFARCTION.		010.5522
Diabetic Cardiomyopathies
Diabetes complications in which VENTRICULAR REMODELING in the absence of CORONARY ATHEROSCLEROSIS and hypertension results in cardiac dysfunctions, typically LEFT VENTRICULAR DYSFUNCTION. The changes also result in myocardial hypertrophy, myocardial necrosis and fibrosis, and collagen deposition due to impaired glucose tolerance.		09.41154
Kidney Diseases
Pathological processes of the KIDNEY or its component tissues.		04.4141
Arrhythmia
[description not available]		013.0474
Arrhythmias, Cardiac
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.		08.0474
Autosomal Dominant Juvenile Parkinson Disease
[description not available]		04.5180
Parkinsonian Disorders
A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.		04.5180
Cancer of Prostate
[description not available]		03.2550
Invasiveness, Neoplasm
[description not available]		03.2650
Prostatic Neoplasms
Tumors or cancer of the PROSTATE.		03.2550
Obstructive Lung Diseases
[description not available]		02.5420
Lung Diseases, Obstructive
Any disorder marked by obstruction of conducting airways of the lung. AIRWAY OBSTRUCTION may be acute, chronic, intermittent, or persistent.		02.5420
Diathesis
[description not available]		02.2510
Airflow Obstruction, Chronic
[description not available]		02.6620
Pulmonary Disease, Chronic Obstructive
A disease of chronic diffuse irreversible airflow obstruction. Subcategories of COPD include CHRONIC BRONCHITIS and PULMONARY EMPHYSEMA.		02.6620
Cancer of Ovary
[description not available]		02.8930
Ovarian Neoplasms
Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.		02.8930
Diabetic Glomerulosclerosis
[description not available]		09.99262
Diabetic Nephropathies
KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.		09.99262
Cancer of Lung
[description not available]		02.2510
Lung Neoplasms
Tumors or cancer of the LUNG.		02.2510
Cardiac Remodeling, Ventricular
[description not available]		03.6280
Injury, Ischemia-Reperfusion
[description not available]		09.45225
Reperfusion Injury
Adverse functional, metabolic, or structural changes in tissues that result from the restoration of blood flow to the tissue (REPERFUSION) following ISCHEMIA.		09.45225
Peripheral Nerve Injury
[description not available]		02.6920
Peripheral Nerve Injuries
Injuries to the PERIPHERAL NERVES.		02.6920
Arterial Diseases, Carotid
[description not available]		03.6411
Carotid Artery Diseases
Pathological conditions involving the CAROTID ARTERIES, including the common, internal, and external carotid arteries. ATHEROSCLEROSIS and TRAUMA are relatively frequent causes of carotid artery pathology.		03.6411
Varices
[description not available]		02.2510
Varicose Veins
Enlarged and tortuous VEINS.		02.2510
Tachyarrhythmia
[description not available]		02.8130
Tachycardia
Abnormally rapid heartbeat, usually with a HEART RATE above 100 beats per minute for adults. Tachycardia accompanied by disturbance in the cardiac depolarization (cardiac arrhythmia) is called tachyarrhythmia.		07.8130
Eosinophilia, Tropical
[description not available]		02.5520
Eosinophilia
Abnormal increase of EOSINOPHILS in the blood, tissues or organs.		07.5520
Abdominal Obesity
[description not available]		06.343
Encephalopathy, Traumatic
[description not available]		02.8830
Brain Injuries, Traumatic
A form of acquired brain injury which occurs when a sudden trauma causes damage to the brain.		02.8830
Cognition Disorders
Disorders characterized by disturbances in mental processes related to learning, thinking, reasoning, and judgment.		03.7190
Autism
[description not available]		07.2510
Delayed Effects, Prenatal Exposure
[description not available]		03.7630
Autistic Disorder
A disorder beginning in childhood. It is marked by the presence of markedly abnormal or impaired development in social interaction and communication and a markedly restricted repertoire of activity and interest. Manifestations of the disorder vary greatly depending on the developmental level and chronological age of the individual. (DSM-V)		02.2510
Froehlich's Syndrome
[description not available]		05.0550
Vascular Calcification
Deposition of calcium into the blood vessel structures. Excessive calcification of the vessels are associated with ATHEROSCLEROTIC PLAQUES formation particularly after MYOCARDIAL INFARCTION (see MONCKEBERG MEDIAL CALCIFIC SCLEROSIS) and chronic kidney diseases which in turn increase VASCULAR STIFFNESS.		02.5520
Genetic Predisposition
[description not available]		03.2150
Aging
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.		04.6290
Impaired Glucose Tolerance
[description not available]		012.583015
Glucose Intolerance
A pathological state in which BLOOD GLUCOSE level is less than approximately 140 mg/100 ml of PLASMA at fasting, and above approximately 200 mg/100 ml plasma at 30-, 60-, or 90-minute during a GLUCOSE TOLERANCE TEST. This condition is seen frequently in DIABETES MELLITUS, but also occurs with other diseases and MALNUTRITION.		012.583015
Cat Diseases
Diseases of the domestic cat (Felis catus or F. domesticus). This term does not include diseases of the so-called big cats such as CHEETAHS; LIONS; tigers, cougars, panthers, leopards, and other Felidae for which the heading CARNIVORA is used.		04.832
Breast Cancer
[description not available]		05.761
Germinoblastoma
[description not available]		03.711
Breast Neoplasms
Tumors or cancer of the human BREAST.		05.761
Lymphoma
A general term for various neoplastic diseases of the lymphoid tissue.		03.711
Anasarca
[description not available]		04.8421
Edema
Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.		04.8421
Palmoplantaris Pustulosis
[description not available]		08.490
Psoriasis
A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis.		013.490
Cell Transformation, Neoplastic
Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.		02.8130
Binge Eating
[description not available]		02.2510
Bulimia
Eating an excess amount of food in a short period of time, as seen in the disorder of BULIMIA NERVOSA. It is caused by an abnormal craving for food, or insatiable hunger also known as ox hunger.		02.2510
Necrosis
The death of cells in an organ or tissue due to disease, injury or failure of the blood supply.		0840
Depression, Involutional
Form of depression in those MIDDLE AGE with feelings of ANXIETY.		02.5120
Depressive Disorder, Major
Disorder in which five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure. Symptoms include: depressed mood most of the day, nearly every daily; markedly diminished interest or pleasure in activities most of the day, nearly every day; significant weight loss when not dieting or weight gain; Insomnia or hypersomnia nearly every day; psychomotor agitation or retardation nearly every day; fatigue or loss of energy nearly every day; feelings of worthlessness or excessive or inappropriate guilt; diminished ability to think or concentrate, or indecisiveness, nearly every day; or recurrent thoughts of death, recurrent suicidal ideation without a specific plan, or a suicide attempt. (DSM-5)		02.5120
Cocaine Abuse
[description not available]		04.4841
Cocaine-Related Disorders
Disorders related or resulting from use of cocaine.		16.4841
Root Resorption
Resorption in which cementum or dentin is lost from the root of a tooth owing to cementoclastic or osteoclastic activity in conditions such as trauma of occlusion or neoplasms. (Dorland, 27th ed)		02.3110
Hyperinsulinism, Familial, with Pancreatic Nesidioblastosis
[description not available]		03.420
Nesidioblastosis
An inherited autosomal recessive syndrome characterized by the disorganized formation of new islets in the PANCREAS and CONGENITAL HYPERINSULINISM. It is due to focal hyperplasia of pancreatic ISLET CELLS budding off from the ductal structures and forming new islets of Langerhans. Mutations in the islet cells involve the potassium channel gene KCNJ11 or the ATP-binding cassette transporter gene ABCC8, both on CHROMOSOME 11.		15.420
Emesis
[description not available]		016.264933
Nausea
An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses.		022.47145
Vomiting
The forcible expulsion of the contents of the STOMACH through the MOUTH.		021.264933
Adhesions, Tissue
[description not available]		02.3110
Angioneurotic Edema
[description not available]		02.3110
Angioedema
Swelling involving the deep DERMIS, subcutaneous, or submucosal tissues, representing localized EDEMA. Angioedema often occurs in the face, lips, tongue, and larynx.		02.3110
Hepatocellular Carcinoma
[description not available]		04.9221
Cancer of Liver
[description not available]		05.5451
Carcinoma, Hepatocellular
A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.		04.9221
Liver Neoplasms
Tumors or cancer of the LIVER.		05.5451
Bone Diseases
Diseases of BONES.		03.5520
ST Elevated Myocardial Infarction
[description not available]		04.9621
ST Elevation Myocardial Infarction
A clinical syndrome defined by MYOCARDIAL ISCHEMIA symptoms; persistent elevation in the ST segments of the ELECTROCARDIOGRAM; and release of BIOMARKERS of myocardial NECROSIS (e.g., elevated TROPONIN levels). ST segment elevation in the ECG is often used in determining the treatment protocol (see also NON-ST ELEVATION MYOCARDIAL INFARCTION).		04.9621
Cancer of Cervix
[description not available]		02.7220
Uterine Cervical Neoplasms
Tumors or cancer of the UTERINE CERVIX.		02.7220
Diabetic Feet
[description not available]		03.4220
Gangrene
Death and putrefaction of tissue usually due to a loss of blood supply.		02.3110
Diabetic Foot
Common foot problems in persons with DIABETES MELLITUS, caused by any combination of factors such as DIABETIC NEUROPATHIES; PERIPHERAL VASCULAR DISEASES; and INFECTION. With the loss of sensation and poor circulation, injuries and infections often lead to severe foot ulceration, GANGRENE and AMPUTATION.		03.4220
a-Synucleinopathies
[description not available]		02.3110
Hyperphagia
Ingestion of a greater than optimal quantity of food.		06.4451
Aberrant Tissue
[description not available]		03.2310
Cancer of Stomach
[description not available]		03.2310
Stomach Neoplasms
Tumors or cancer of the STOMACH.		03.2310
Pulmonary Arterial Remodeling
[description not available]		02.6620
Atrophy
Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes.		02.5820
Pain, Chronic
[description not available]		02.3110
Age-Related Memory Disorders
[description not available]		04.4570
Memory Disorders
Disturbances in registering an impression, in the retention of an acquired impression, or in the recall of an impression. Memory impairments are associated with DEMENTIA; CRANIOCEREBRAL TRAUMA; ENCEPHALITIS; ALCOHOLISM (see also ALCOHOL AMNESTIC DISORDER); SCHIZOPHRENIA; and other conditions.		04.4570
Chronic Pain
Aching sensation that persists for more than a few months. It may or may not be associated with trauma or disease, and may persist after the initial injury has healed. Its localization, character, and timing are more vague than with acute pain.		02.3110
Alstrom Syndrome
Rare autosomal recessive disease characterized by multiple organ dysfunction. The key clinical features include retinal degeneration (NYSTAGMUS, PATHOLOGIC; RETINITIS PIGMENTOSA; and eventual blindness), childhood obesity, sensorineural hearing loss, and normal mental development. Endocrinologic complications include TYPE 2 DIABETES MELLITUS; HYPERINSULINEMIA; ACANTHOSIS NIGRICANS; HYPOTHYROIDISM; and progressive renal and hepatic failures. The disease is caused by mutations in the ALMS1 gene.		02.3110
Inadequate Sleep
[description not available]		02.3110
Depression
Depressive states usually of moderate intensity in contrast with MAJOR DEPRESSIVE DISORDER present in neurotic and psychotic disorders.		09.6651
Foreign-Body Reaction
Chronic inflammation and granuloma formation around irritating foreign bodies.		02.3110
Granulomas
[description not available]		02.5720
Granuloma
A relatively small nodular inflammatory lesion containing grouped mononuclear phagocytes, caused by infectious and noninfectious agents.		07.5720
Absence Seizure Disorder
[description not available]		02.3110
Absence Seizure
[description not available]		02.3110
Epilepsy, Absence
A seizure disorder usually occurring in childhood characterized by rhythmic electrical brain discharges of generalized onset. Clinical features include a sudden cessation of ongoing activity usually without loss of postural tone. Rhythmic blinking of the eyelids or lip smacking frequently accompanies the SEIZURES. The usual duration is 5-10 seconds, and multiple episodes may occur daily. Juvenile absence epilepsy is characterized by the juvenile onset of absence seizures and an increased incidence of myoclonus and tonic-clonic seizures. (Menkes, Textbook of Child Neurology, 5th ed, p736)		02.3110
Seizures
Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or seizure disorder.		02.3110
Dermatitis, Eczematous
[description not available]		02.4110
Dermatitis
Any inflammation of the skin.		07.4110
Eczema
A pruritic papulovesicular dermatitis occurring as a reaction to many endogenous and exogenous agents (Dorland, 27th ed).		02.4110
Cancer of Colon
[description not available]		03.0340
Colonic Neoplasms
Tumors or cancer of the COLON.		03.0340
Experimental Hepatoma
[description not available]		02.1510
Multiple System Atrophy Syndrome
[description not available]		03.4720
Protein Aggregation, Pathological
A biochemical phenomenon in which misfolded proteins aggregate either intra- or extracellularly. Triggered by factors such as MUTATION; POST-TRANSLATIONAL MODIFICATIONS, and environmental stress, it is generally associated with ALZHEIMER DISEASE; PARKINSON DISEASE; HUNTINGTON DISEASE; and TYPE 2 DIABETES MELLITUS.		03.0610
Multiple System Atrophy
A syndrome complex composed of three conditions which represent clinical variants of the same disease process: STRIATONIGRAL DEGENERATION; SHY-DRAGER SYNDROME; and the sporadic form of OLIVOPONTOCEREBELLAR ATROPHIES. Clinical features include autonomic, cerebellar, and basal ganglia dysfunction. Pathologic examination reveals atrophy of the basal ganglia, cerebellum, pons, and medulla, with prominent loss of autonomic neurons in the brain stem and spinal cord. (From Adams et al., Principles of Neurology, 6th ed, p1076; Baillieres Clin Neurol 1997 Apr;6(1):187-204; Med Clin North Am 1999 Mar;83(2):381-92)		15.4720
Atheroma
[description not available]		02.5520
Aortic Diseases
Pathological processes involving any part of the AORTA.		02.5520
Brain Inflammation
[description not available]		02.1510
Encephalitis
Inflammation of the BRAIN due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see ENCEPHALITIS, VIRAL) are a relatively frequent cause of this condition.		02.1510
Sensitivity and Specificity
Binary classification measures to assess test results. Sensitivity or recall rate is the proportion of true positives. Specificity is the probability of correctly determining the absence of a condition. (From Last, Dictionary of Epidemiology, 2d ed)		06.1962
Electron Transport Chain Deficiencies, Mitochondrial
[description not available]		03.4720
Mitochondrial Diseases
Diseases caused by abnormal function of the MITOCHONDRIA. They may be caused by mutations, acquired or inherited, in mitochondrial DNA or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondria dysfunction due to adverse effects of drugs, infections, or other environmental causes.		03.4720
Allergic Encephalomyelitis
[description not available]		03.0910
Out-of-Hospital Cardiac Arrest
Occurrence of heart arrest in an individual when there is no immediate access to medical personnel or equipment.		08.8986
Left Ventricular Dysfunction
[description not available]		06.9153
Ventricular Dysfunction, Left
A condition in which the LEFT VENTRICLE of the heart was functionally impaired. This condition usually leads to HEART FAILURE; MYOCARDIAL INFARCTION; and other cardiovascular complications. Diagnosis is made by measuring the diminished ejection fraction and a depressed level of motility of the left ventricular wall.		06.9153
Complication, Intraoperative
[description not available]		04.4511
Complication, Postoperative
[description not available]		05.2421
Postoperative Complications
Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery.		05.2421
Blast Injuries
Injuries resulting when a person is struck by particles impelled with violent force from an explosion. Blast causes pulmonary concussion and hemorrhage, laceration of other thoracic and abdominal viscera, ruptured ear drums, and minor effects in the central nervous system. (From Dorland, 27th ed)		02.5420
Dermatitis Medicamentosa
[description not available]		02.1710
Chronic Illness
[description not available]		04.7360
Chronic Disease
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care (Dictionary of Health Services Management, 2d ed). For epidemiological studies chronic disease often includes HEART DISEASES; STROKE; CANCER; and diabetes (DIABETES MELLITUS, TYPE 2).		04.7360
Lung Injury, Acute
[description not available]		02.5220
Hemorrhagic Shock
[description not available]		02.1510
Acute Lung Injury
A condition of lung damage that is characterized by bilateral pulmonary infiltrates (PULMONARY EDEMA) rich in NEUTROPHILS, and in the absence of clinical HEART FAILURE. This can represent a spectrum of pulmonary lesions, endothelial and epithelial, due to numerous factors (physical, chemical, or biological).		02.5220
Adipocere
[description not available]		02.1510
Aqueductal Stenosis
[description not available]		02.1510
Hemorrhage, Subarachnoid
[description not available]		02.1710
Subarachnoid Hemorrhage
Bleeding into the intracranial or spinal SUBARACHNOID SPACE, most resulting from INTRACRANIAL ANEURYSM rupture. It can occur after traumatic injuries (SUBARACHNOID HEMORRHAGE, TRAUMATIC). Clinical features include HEADACHE; NAUSEA; VOMITING, nuchal rigidity, variable neurological deficits and reduced mental status.		02.1710
Gastric Ulcer
[description not available]		02.1510
Stomach Ulcer
Ulceration of the GASTRIC MUCOSA due to contact with GASTRIC JUICE. It is often associated with HELICOBACTER PYLORI infection or consumption of nonsteroidal anti-inflammatory drugs (NSAIDS).		02.1510
Coma
A profound state of unconsciousness associated with depressed cerebral activity from which the individual cannot be aroused. Coma generally occurs when there is dysfunction or injury involving both cerebral hemispheres or the brain stem RETICULAR FORMATION.		09.4811
Kidney Failure
A severe irreversible decline in the ability of kidneys to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism.		03.940
Renal Insufficiency
Conditions in which the KIDNEYS perform below the normal level in the ability to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism. Renal insufficiency can be classified by the degree of kidney damage (as measured by the level of PROTEINURIA) and reduction in GLOMERULAR FILTRATION RATE.		15.940
Dementia Praecox
[description not available]		08.5864
Schizophrenia
A severe emotional disorder of psychotic depth characteristically marked by a retreat from reality with delusion formation, HALLUCINATIONS, emotional disharmony, and regressive behavior.		013.5864
Chronic Lung Injury
[description not available]		02.1710
Pulmonary Hypertension
[description not available]		02.5820
Hypertension, Pulmonary
Increased VASCULAR RESISTANCE in the PULMONARY CIRCULATION, usually secondary to HEART DISEASES or LUNG DISEASES.		02.5820
Acute Kidney Failure
[description not available]		04.2760
Acute Kidney Injury
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.		04.2760
Infusion Site Adverse Event
[description not available]		02.1710
Precordial Catch
[description not available]		02.1710
Chest Pain
Pressure, burning, or numbness in the chest.		02.1710
Diarrhea
An increased liquidity or decreased consistency of FECES, such as running stool. Fecal consistency is related to the ratio of water-holding capacity of insoluble solids to total water, rather than the amount of water present. Diarrhea is not hyperdefecation or increased fecal weight.		05.4470
Pericementitis
[description not available]		02.5420
Periodontitis
Inflammation and loss of connective tissues supporting or surrounding the teeth. This may involve any part of the PERIODONTIUM. Periodontitis is currently classified by disease progression (CHRONIC PERIODONTITIS; AGGRESSIVE PERIODONTITIS) instead of age of onset. (From 1999 International Workshop for a Classification of Periodontal Diseases and Conditions, American Academy of Periodontology)		07.5420
Bone Loss, Perimenopausal
[description not available]		02.1710
Osteoporosis, Postmenopausal
Metabolic disorder associated with fractures of the femoral neck, vertebrae, and distal forearm. It occurs commonly in women within 15-20 years after menopause, and is caused by factors associated with menopause including estrogen deficiency.		02.1710
Bone Loss, Osteoclastic
[description not available]		03.730
Sex Disorders
[description not available]		02.1710
Sexual Dysfunction, Physiological
Physiological disturbances in normal sexual performance in either the male or the female.		02.1710
Impotence
[description not available]		02.1710
Erectile Dysfunction
The inability in the male to have a PENILE ERECTION due to psychological or organ dysfunction.		02.1710
Mucositis
An INFLAMMATION of the MUCOSA with burning or tingling sensation. It is characterized by atrophy of the squamous EPITHELIUM, vascular damage, inflammatory infiltration, and ulceration. It usually occurs at the mucous lining of the MOUTH, the GASTROINTESTINAL TRACT or the airway due to chemical irritations, CHEMOTHERAPY, or radiation therapy (RADIOTHERAPY).		02.1710
Neointima
The new and thickened layer of scar tissue that forms on a PROSTHESIS, or as a result of vessel injury especially following ANGIOPLASTY or stent placement.		03.0340
Preterm Birth
[description not available]		02.1710
Complications, Pregnancy
[description not available]		02.5420
Premature Birth
CHILDBIRTH before 37 weeks of PREGNANCY (259 days from the first day of the mother's last menstrual period, or 245 days after FERTILIZATION).		02.1710
Cerebral Ischemia
[description not available]		05.19101
Brain Ischemia
Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.		05.19101
Carotid Arteriopathies, Traumatic
[description not available]		04.1450
Brain Contusion
A bruise of the brain from an impact of the skull.		02.1710
Osteoporotic Fractures
Breaks in bones resulting from low bone mass and microarchitectural deterioration characteristic of OSTEOPOROSIS.		03.0910
Benign Neoplasms, Brain
[description not available]		02.5220
Glial Cell Tumors
[description not available]		02.1710
Brain Neoplasms
Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.		02.5220
Glioma
Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)		02.1710
Acidosis, Diabetic
[description not available]		03.921
Diabetic Ketoacidosis
A life-threatening complication of diabetes mellitus, primarily of TYPE 1 DIABETES MELLITUS with severe INSULIN deficiency and extreme HYPERGLYCEMIA. It is characterized by KETOSIS; DEHYDRATION; and depressed consciousness leading to COMA.		08.921
Cystic Fibrosis of Pancreas
[description not available]		03.5911
Cystic Fibrosis
An autosomal recessive genetic disease of the EXOCRINE GLANDS. It is caused by mutations in the gene encoding the CYSTIC FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR expressed in several organs including the LUNG, the PANCREAS, the BILIARY SYSTEM, and the SWEAT GLANDS. Cystic fibrosis is characterized by epithelial secretory dysfunction associated with ductal obstruction resulting in AIRWAY OBSTRUCTION; chronic RESPIRATORY INFECTIONS; PANCREATIC INSUFFICIENCY; maldigestion; salt depletion; and HEAT PROSTRATION.		08.5911
Muscle Contraction
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.		03.3560
Postoperative Cognitive Complications
COGNITIVE IMPAIRMENT or functional decline after a surgical procedure.		02.2110
Cerebral Concussion
[description not available]		02.8330
Brain Concussion
A nonspecific term used to describe transient alterations or loss of consciousness following closed head injuries. The duration of UNCONSCIOUSNESS generally lasts a few seconds, but may persist for several hours. Concussions may be classified as mild, intermediate, and severe. Prolonged periods of unconsciousness (often defined as greater than 6 hours in duration) may be referred to as post-traumatic coma (COMA, POST-HEAD INJURY). (From Rowland, Merritt's Textbook of Neurology, 9th ed, p418)		02.8330
Cancer of the Thyroid
[description not available]		08.1891
Thyroid Neoplasms
Tumors or cancer of the THYROID GLAND.		08.1891
Thrombopenia
[description not available]		03.5320
Thrombocytopenia
A subnormal level of BLOOD PLATELETS.		08.5320
Gastric Stasis
[description not available]		02.7630
Gastroparesis
Chronic delayed gastric emptying. Gastroparesis may be caused by motor dysfunction or paralysis of STOMACH muscles or may be associated with other systemic diseases such as DIABETES MELLITUS.		02.7630
Brain Dead
[description not available]		02.8330
Rheumatoid Arthritis
[description not available]		07.2110
Arthritis, Rheumatoid
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.		02.2110
Chemical Dependence
[description not available]		03.1210
Substance-Related Disorders
Disorders related to substance use or abuse.		03.1210
Leanness
[description not available]		02.7730
Pancreatic Diseases
Pathological processes of the PANCREAS.		03.4520
Carcinoma, Neuroendocrine
A group of carcinomas which share a characteristic morphology, often being composed of clusters and trabecular sheets of round blue cells, granular chromatin, and an attenuated rim of poorly demarcated cytoplasm. Neuroendocrine tumors include carcinoids, small (oat) cell carcinomas, medullary carcinoma of the thyroid, Merkel cell tumor, cutaneous neuroendocrine carcinoma, pancreatic islet cell tumors, and pheochromocytoma. Neurosecretory granules are found within the tumor cells. (Segen, Dictionary of Modern Medicine, 1992)		04.5111
Amyloid Deposits
[description not available]		02.2110
Cardiomyopathies, Primary
[description not available]		02.2110
Cardiomyopathies
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).		02.2110
Acute Disease
Disease having a short and relatively severe course.		07.99162
Cacosmia
[description not available]		011.461616
Colonic Inertia
Symptom characterized by the passage of stool once a week or less.		011.451816
Constipation
Infrequent or difficult evacuation of FECES. These symptoms are associated with a variety of causes, including low DIETARY FIBER intake, emotional or nervous disturbances, systemic and structural disorders, drug-induced aggravation, and infections.		011.451816
Acute Edematous Pancreatitis
[description not available]		016.941620
Pancreatitis
INFLAMMATION of the PANCREAS. Pancreatitis is classified as acute unless there are computed tomographic or endoscopic retrograde cholangiopancreatographic findings of CHRONIC PANCREATITIS (International Symposium on Acute Pancreatitis, Atlanta, 1992). The two most common forms of acute pancreatitis are ALCOHOLIC PANCREATITIS and gallstone pancreatitis.		016.941620
Fetal Growth Restriction
[description not available]		04.9480
Fetal Growth Retardation
Failure of a FETUS to attain expected GROWTH.		04.9480
Age-Related Osteoporosis
[description not available]		04.1150
Osteoporosis
Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis (OSTEOPOROSIS, POSTMENOPAUSAL) and age-related or senile osteoporosis.		04.1150
Blood Pressure, High
[description not available]		010.16182
Hypertension
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.		010.16182
Hyperplasia
An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.		04.150
Atrioventricular Nodal Re-Entrant Tachycardia
[description not available]		02.5120
Heart Disease, Ischemic
[description not available]		03.730
Ventricular Fibrillation
A potentially lethal cardiac arrhythmia that is characterized by uncoordinated extremely rapid firing of electrical impulses (400-600/min) in HEART VENTRICLES. Such asynchronous ventricular quivering or fibrillation prevents any effective cardiac output and results in unconsciousness (SYNCOPE). It is one of the major electrocardiographic patterns seen with CARDIAC ARREST.		07.8864
Tachycardia, Ventricular
An abnormally rapid ventricular rhythm usually in excess of 150 beats per minute. It is generated within the ventricle below the BUNDLE OF HIS, either as autonomic impulse formation or reentrant impulse conduction. Depending on the etiology, onset of ventricular tachycardia can be paroxysmal (sudden) or nonparoxysmal, its wide QRS complexes can be uniform or polymorphic, and the ventricular beating may be independent of the atrial beating (AV dissociation).		02.5120
Myocardial Ischemia
A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).		03.730
Malnourishment
[description not available]		03.420
Malnutrition
An imbalanced nutritional status resulting from insufficient intake of nutrients to meet normal physiological requirement.		03.420
Left Ventricular Hypertrophy
[description not available]		03.0240
Dyslipidemia
[description not available]		04.7260
Hypertrophy, Left Ventricular
Enlargement of the LEFT VENTRICLE of the heart. This increase in ventricular mass is attributed to sustained abnormal pressure or volume loads and is a contributor to cardiovascular morbidity and mortality.		03.0240
Dyslipidemias
Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.		04.7260
Central Retinal Edema, Cystoid
[description not available]		02.110
Macular Edema
Fluid accumulation in the outer layer of the MACULA LUTEA that results from intraocular or systemic insults. It may develop in a diffuse pattern where the macula appears thickened or it may acquire the characteristic petaloid appearance referred to as cystoid macular edema. Although macular edema may be associated with various underlying conditions, it is most commonly seen following intraocular surgery, venous occlusive disease, DIABETIC RETINOPATHY, and posterior segment inflammatory disease. (From Survey of Ophthalmology 2004; 49(5) 470-90)		07.110
Carcinogenesis
The origin, production or development of cancer through genotypic and phenotypic changes which upset the normal balance between cell proliferation and cell death. Carcinogenesis generally requires a constellation of steps, which may occur quickly or over a period of many years.		02.5120
Reticulum Cell-Like Sarcoma, Yoshida
[description not available]		02.110
Cachexia
General ill health, malnutrition, and weight loss, usually associated with chronic disease.		02.110
Adverse Drug Event
[description not available]		04.8370
Drug-Related Side Effects and Adverse Reactions
Disorders that result from the intended use of PHARMACEUTICAL PREPARATIONS. Included in this heading are a broad variety of chemically-induced adverse conditions due to toxicity, DRUG INTERACTIONS, and metabolic effects of pharmaceuticals.		04.8370
B16 Melanoma
[description not available]		02.110
Cardiac Hypertrophy
Enlargement of the HEART due to chamber HYPERTROPHY, an increase in wall thickness without an increase in the number of cells (MYOCYTES, CARDIAC). It is the result of increase in myocyte size, mitochondrial and myofibrillar mass, as well as changes in extracellular matrix.		02.5120
Cardiomegaly
Enlargement of the HEART, usually indicated by a cardiothoracic ratio above 0.50. Heart enlargement may involve the right, the left, or both HEART VENTRICLES or HEART ATRIA. Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (HEART FAILURE) or several forms of CARDIOMYOPATHIES.		02.5120
Proteinuria
The presence of proteins in the urine, an indicator of KIDNEY DISEASES.		03.0340
Bone Fractures
[description not available]		04.8120
Fractures, Bone
Breaks in bones.		04.8120
ANS (Autonomic Nervous System) Diseases
[description not available]		03.9210
Bilateral Headache
[description not available]		04.422
Headache
The symptom of PAIN in the cranial region. It may be an isolated benign occurrence or manifestation of a wide variety of HEADACHE DISORDERS.		04.422
Nicotine Addiction
[description not available]		0310
Tobacco Use Disorder
Tobacco used to the detriment of a person's health or social functioning. Tobacco dependence is included.		0310
Hypernutrition
[description not available]		02.110
Cholangiocellular Carcinoma
[description not available]		02.0810
Bile Duct Cancer
[description not available]		02.0810
Bile Duct Neoplasms
Tumors or cancer of the BILE DUCTS.		02.0810
Cholangiocarcinoma
A malignant tumor arising from the epithelium of the BILE DUCTS.		02.0810
Dermatoses
[description not available]		02.110
Skin Diseases
Diseases involving the DERMIS or EPIDERMIS.		02.110
Abnormalities, Cardiovascular
[description not available]		02.0810
Cardiovascular Abnormalities
Congenital, inherited, or acquired anomalies of the CARDIOVASCULAR SYSTEM, including the HEART and BLOOD VESSELS.		02.0810
Cholera Infantum
[description not available]		07.2781
Psychoses
[description not available]		04.411
Psychotic Disorders
Disorders in which there is a loss of ego boundaries or a gross impairment in reality testing with delusions or prominent hallucinations. (From DSM-IV, 1994)		04.411
Low Bone Density
[description not available]		04.3220
Bone Diseases, Metabolic
Diseases that affect the METABOLIC PROCESSES of BONE TISSUE.		04.3220
Adenoma, Prostatic
[description not available]		02.1110
Prostatic Hyperplasia
Increase in constituent cells in the PROSTATE, leading to enlargement of the organ (hypertrophy) and adverse impact on the lower urinary tract function. This can be caused by increased rate of cell proliferation, reduced rate of cell death, or both.		02.1110
Labhart-Willi Syndrome
[description not available]		07.0652
Anorexia
The lack or loss of APPETITE accompanied by an aversion to food and the inability to eat. It is the defining characteristic of the disorder ANOREXIA NERVOSA.		03.5880
Prader-Willi Syndrome
An autosomal dominant disorder caused by deletion of the proximal long arm of the paternal chromosome 15 (15q11-q13) or by inheritance of both of the pair of chromosomes 15 from the mother (UNIPARENTAL DISOMY) which are imprinted (GENETIC IMPRINTING) and hence silenced. Clinical manifestations include MENTAL RETARDATION; MUSCULAR HYPOTONIA; HYPERPHAGIA; OBESITY; short stature; HYPOGONADISM; STRABISMUS; and HYPERSOMNOLENCE. (Menkes, Textbook of Child Neurology, 5th ed, p229)		07.0652
Hepatic Insufficiency
Conditions in which the LIVER functions fall below the normal ranges. Severe hepatic insufficiency may cause LIVER FAILURE or DEATH. Treatment may include LIVER TRANSPLANTATION.		04.411
Blood Poisoning
[description not available]		02.5220
Co-infection
[description not available]		02.110
Sepsis
Systemic inflammatory response syndrome with a proven or suspected infectious etiology. When sepsis is associated with organ dysfunction distant from the site of infection, it is called severe sepsis. When sepsis is accompanied by HYPOTENSION despite adequate fluid infusion, it is called SEPTIC SHOCK.		02.5220
Island Cell Tumor
[description not available]		02.110
Adenoma, Islet Cell
A benign tumor of the pancreatic ISLET CELLS. Usually it involves the INSULIN-producing PANCREATIC BETA CELLS, as in INSULINOMA, resulting in HYPERINSULINISM.		02.110
Bile Duct Obstruction
[description not available]		02.4720
Cholestasis
Impairment of bile flow due to obstruction in small bile ducts (INTRAHEPATIC CHOLESTASIS) or obstruction in large bile ducts (EXTRAHEPATIC CHOLESTASIS).		02.4720
Deep Vein Thrombosis
[description not available]		02.110
Chronic Kidney Diseases
[description not available]		02.110
Venous Thrombosis
The formation or presence of a blood clot (THROMBUS) within a vein.		02.110
Renal Insufficiency, Chronic
Conditions in which the KIDNEYS perform below the normal level for more than three months. Chronic kidney insufficiency is classified by five stages according to the decline in GLOMERULAR FILTRATION RATE and the degree of kidney damage (as measured by the level of PROTEINURIA). The most severe form is the end-stage renal disease (CHRONIC KIDNEY FAILURE). (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002)		02.110
Compensatory Hyperinsulinemia
A GLUCOSE-induced HYPERINSULINEMIA, a marker of insulin-resistant state. It is a mechanism to compensate for reduced sensitivity to insulin.		06.0861
Hyperinsulinism
A syndrome with excessively high INSULIN levels in the BLOOD. It may cause HYPOGLYCEMIA. Etiology of hyperinsulinism varies, including hypersecretion of a beta cell tumor (INSULINOMA); autoantibodies against insulin (INSULIN ANTIBODIES); defective insulin receptor (INSULIN RESISTANCE); or overuse of exogenous insulin or HYPOGLYCEMIC AGENTS.		06.0861
Ventricular Dysfunction
A condition in which HEART VENTRICLES exhibit impaired function.		02.110
Acute Necrotizing Pancreatitis
[description not available]		02.110
Pancreatic Insufficiency
[description not available]		02.110
Exocrine Pancreatic Insufficiency
A malabsorption condition resulting from greater than 10% reduction in the secretion of pancreatic digestive enzymes (LIPASE; PROTEASES; and AMYLASE) by the EXOCRINE PANCREAS into the DUODENUM. This condition is often associated with CYSTIC FIBROSIS and with chronic PANCREATITIS.		02.110
Amentia
[description not available]		02.110
Dementia
An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness.		07.110
Glycosuria
The appearance of an abnormally large amount of GLUCOSE in the urine, such as more than 500 mg/day in adults. It can be due to HYPERGLYCEMIA or genetic defects in renal reabsorption (RENAL GLYCOSURIA).		03.4420
Neoplasm Metastasis, Unknown Primary
[description not available]		02.1110
Allergy, Drug
[description not available]		04.1531
Drug Hypersensitivity
Immunologically mediated adverse reactions to medicinal substances used legally or illegally.		04.1531
Bright Disease
A historical classification which is no longer used. It described acute glomerulonephritis, acute nephritic syndrome, or acute nephritis. Named for Richard Bright.		02.1110
Glomerulonephritis
Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.		02.1110
Muscle Relaxation
That phase of a muscle twitch during which a muscle returns to a resting position.		02.4620
Appetite Disorders
[description not available]		02.1110
Feeding and Eating Disorders
A group of disorders characterized by physiological and psychological disturbances in appetite or food intake.		02.1110
Carotid Artery Narrowing
[description not available]		02.1110
Carotid Stenosis
Narrowing or stricture of any part of the CAROTID ARTERIES, most often due to atherosclerotic plaque formation. Ulcerations may form in atherosclerotic plaques and induce THROMBUS formation. Platelet or cholesterol emboli may arise from stenotic carotid lesions and induce a TRANSIENT ISCHEMIC ATTACK; CEREBROVASCULAR ACCIDENT; or temporary blindness (AMAUROSIS FUGAX). (From Adams et al., Principles of Neurology, 6th ed, pp 822-3)		02.1110
Hyperactivity, Motor
[description not available]		02.1110
Injuries
Used with anatomic headings, animals, and sports for wounds and injuries. Excludes cell damage, for which pathology is used.		02.1110
Wounds and Injuries
Damage inflicted on the body as the direct or indirect result of an external force, with or without disruption of structural continuity.		02.1110
Alveolar Bone Atrophy
[description not available]		02.1110
Liver Dysfunction
[description not available]		02.4920
Liver Diseases
Pathological processes of the LIVER.		02.4920
Adenocarcinoma, Basal Cell
[description not available]		03.7130
Peripheral Nerve Diseases
[description not available]		03.3820
Adenocarcinoma
A malignant epithelial tumor with a glandular organization.		03.7130
Peripheral Nervous System Diseases
Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves.		03.3820
Cardiac Diseases
[description not available]		02.4720
Heart Diseases
Pathological conditions involving the HEART including its structural and functional abnormalities.		02.4720
Acute Liver Injury, Drug-Induced
[description not available]		03.6930
Milk-Alkali Syndrome
[description not available]		02.1110
Hypercalcemia
Abnormally high level of calcium in the blood.		02.1110
Rhabdomyolysis
Necrosis or disintegration of skeletal muscle often followed by myoglobinuria.		02.1110
Chemical and Drug Induced Liver Injury
A spectrum of clinical liver diseases ranging from mild biochemical abnormalities to ACUTE LIVER FAILURE, caused by drugs, drug metabolites, herbal and dietary supplements and chemicals from the environment.		03.6930
Carcinoma, Anaplastic
[description not available]		02.1310
Cancer of Esophagus
[description not available]		02.1310
Carcinoma
A malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm and not a synonym for cancer.		02.1310
Esophageal Neoplasms
Tumors or cancer of the ESOPHAGUS.		02.1310
Cancer of Endometrium
[description not available]		02.1310
Endometrial Neoplasms
Tumors or cancer of ENDOMETRIUM, the mucous lining of the UTERUS. These neoplasms can be benign or malignant. Their classification and grading are based on the various cell types and the percent of undifferentiated cells.		02.1310
Viral Diseases
[description not available]		02.1110
Virus Diseases
A general term for diseases caused by viruses.		02.1110
Malignant Melanoma
[description not available]		02.1310
Melanoma
A malignant neoplasm derived from cells that are capable of forming melanin, which may occur in the skin of any part of the body, in the eye, or, rarely, in the mucous membranes of the genitalia, anus, oral cavity, or other sites. It occurs mostly in adults and may originate de novo or from a pigmented nevus or malignant lentigo. Melanomas frequently metastasize widely, and the regional lymph nodes, liver, lungs, and brain are likely to be involved. The incidence of malignant skin melanomas is rising rapidly in all parts of the world. (Stedman, 25th ed; from Rook et al., Textbook of Dermatology, 4th ed, p2445)		02.1310
Blood Clot
[description not available]		02.1310
Thrombosis
Formation and development of a thrombus or blood clot in the blood vessel.		02.1310
Intestinal Obstruction
Any impairment, arrest, or reversal of the normal flow of INTESTINAL CONTENTS toward the ANAL CANAL.		07.1310
Retinal Diseases
Diseases involving the RETINA.		02.1310
Allotriophagy
An unusual desire or craving for abnormal foods.		02.1310
Neutropenia
A decrease in the number of NEUTROPHILS found in the blood.		04.4311
Dyskinesia Syndromes
[description not available]		02.1310
Urination Disorders
Abnormalities in the process of URINE voiding, including bladder control, frequency of URINATION, as well as the volume and composition of URINE.		02.1310
Movement Disorders
Syndromes which feature DYSKINESIAS as a cardinal manifestation of the disease process. Included in this category are degenerative, hereditary, post-infectious, medication-induced, post-inflammatory, and post-traumatic conditions.		02.1310
Nasopharyngitis
Inflammation of the NASOPHARYNX, usually including its mucosa, related lymphoid structure, and glands.		03.8920
Infections, Respiratory
[description not available]		03.0410
Respiratory Tract Infections
Invasion of the host RESPIRATORY SYSTEM by microorganisms, usually leading to pathological processes or diseases.		03.0410
Brain Vascular Disorders
[description not available]		04.4311
Cerebrovascular Disorders
A spectrum of pathological conditions of impaired blood flow in the brain. They can involve vessels (ARTERIES or VEINS) in the CEREBRUM, the CEREBELLUM, and the BRAIN STEM. Major categories include INTRACRANIAL ARTERIOVENOUS MALFORMATIONS; BRAIN ISCHEMIA; CEREBRAL HEMORRHAGE; and others.		04.4311
Bronchial Hyperreactivity
Tendency of the smooth muscle of the tracheobronchial tree to contract more intensely in response to a given stimulus than it does in the response seen in normal individuals. This condition is present in virtually all symptomatic patients with asthma. The most prominent manifestation of this smooth muscle contraction is a decrease in airway caliber that can be readily measured in the pulmonary function laboratory.		02.1310
Aging, Premature
Changes in the organism associated with senescence, occurring at an accelerated rate.		03.0410
Cochlear Hearing Loss
[description not available]		03.0410
Hearing Loss, Sensorineural
Hearing loss resulting from damage to the COCHLEA and the sensorineural elements which lie internally beyond the oval and round windows. These elements include the AUDITORY NERVE and its connections in the BRAINSTEM.		03.0410
Chronic Pancreatitis
[description not available]		02.520
Carcinoma, Intraepithelial
[description not available]		02.1310
Cystadenoma
A benign neoplasm derived from glandular epithelium, in which cystic accumulations of retained secretions are formed. In some instances, considerable portions of the neoplasm, or even the entire mass, may be cystic. (Stedman, 25th ed)		02.1310
Carcinoma in Situ
A lesion with cytological characteristics associated with invasive carcinoma but the tumor cells are confined to the epithelium of origin, without invasion of the basement membrane.		02.1310
Neuroendocrine Tumors
Tumors whose cells possess secretory granules and originate from the neuroectoderm, i.e., the cells of the ectoblast or epiblast that program the neuroendocrine system. Common properties across most neuroendocrine tumors include ectopic hormone production (often via APUD CELLS), the presence of tumor-associated antigens, and isozyme composition.		02.1310
Pancreatitis, Chronic
INFLAMMATION of the PANCREAS that is characterized by recurring or persistent ABDOMINAL PAIN with or without STEATORRHEA or DIABETES MELLITUS. It is characterized by the irregular destruction of the pancreatic parenchyma which may be focal, segmental, or diffuse.		02.520
Anterior Cerebral Circulation Infarction
[description not available]		02.9940
Nervous System Disorders
[description not available]		02.1310
Nervous System Diseases
Diseases of the central and peripheral nervous system. This includes disorders of the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscle.		02.1310
Brain Infarction
Tissue NECROSIS in any area of the brain, including the CEREBRAL HEMISPHERES, the CEREBELLUM, and the BRAIN STEM. Brain infarction is the result of a cascade of events initiated by inadequate blood flow through the brain that is followed by HYPOXIA and HYPOGLYCEMIA in brain tissue. Damage may be temporary, permanent, selective or pan-necrosis.		02.9940
Monkey Diseases
Diseases of Old World and New World monkeys. This term includes diseases of baboons but not of chimpanzees or gorillas (= APE DISEASES).		02.1310
Coronary Artery Stenosis
[description not available]		02.1510
Coronary Stenosis
Narrowing or constriction of a coronary artery.		02.1510
Ureteral Obstruction
Blockage in any part of the URETER causing obstruction of urine flow from the kidney to the URINARY BLADDER. The obstruction may be congenital, acquired, unilateral, bilateral, complete, partial, acute, or chronic. Depending on the degree and duration of the obstruction, clinical features vary greatly such as HYDRONEPHROSIS and obstructive nephropathy.		02.1310
Menopause
The last menstrual period. Permanent cessation of menses (MENSTRUATION) is usually defined after 6 to 12 months of AMENORRHEA in a woman over 45 years of age. In the United States, menopause generally occurs in women between 48 and 55 years of age.		02.9610
Akinetic-Rigid Variant of Huntington Disease
[description not available]		02.4620
Huntington Disease
A familial disorder inherited as an autosomal dominant trait and characterized by the onset of progressive CHOREA and DEMENTIA in the fourth or fifth decade of life. Common initial manifestations include paranoia; poor impulse control; DEPRESSION; HALLUCINATIONS; and DELUSIONS. Eventually intellectual impairment; loss of fine motor control; ATHETOSIS; and diffuse chorea involving axial and limb musculature develops, leading to a vegetative state within 10-15 years of disease onset. The juvenile variant has a more fulminant course including SEIZURES; ATAXIA; dementia; and chorea. (From Adams et al., Principles of Neurology, 6th ed, pp1060-4)		02.4620
Diabetes Mellitus, Gestational
[description not available]		02.0510
Diabetes, Gestational
Diabetes mellitus induced by PREGNANCY but resolved at the end of pregnancy. It does not include previously diagnosed diabetics who become pregnant (PREGNANCY IN DIABETICS). Gestational diabetes usually develops in late pregnancy when insulin antagonistic hormones peaks leading to INSULIN RESISTANCE; GLUCOSE INTOLERANCE; and HYPERGLYCEMIA.		02.0510
Bile Duct Diseases
Diseases in any part of the ductal system of the BILIARY TRACT from the smallest BILE CANALICULI to the largest COMMON BILE DUCT.		02.0510
Chronic Hepatitis C
[description not available]		02.0510
Hepatitis C, Chronic
INFLAMMATION of the LIVER in humans that is caused by HEPATITIS C VIRUS lasting six months or more. Chronic hepatitis C can lead to LIVER CIRRHOSIS.		02.0510
Primary Graft Dysfunction
A form of ischemia-reperfusion injury occurring in the early period following transplantation. Significant pathophysiological changes in MITOCHONDRIA are the main cause of the dysfunction. It is most often seen in the transplanted lung, liver, or kidney and can lead to GRAFT REJECTION.		07.4744
Dysphagia
[description not available]		02.0510
Deglutition Disorders
Difficulty in SWALLOWING which may result from neuromuscular disorder or mechanical obstruction. Dysphagia is classified into two distinct types: oropharyngeal dysphagia due to malfunction of the PHARYNX and UPPER ESOPHAGEAL SPHINCTER; and esophageal dysphagia due to malfunction of the ESOPHAGUS.		02.0510
Hyperhomocysteinemia
Condition in which the plasma levels of homocysteine and related metabolites are elevated (		02.0510
Hypertension, Renal
Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.		02.0510
MODS
[description not available]		02.0510
Multiple Organ Failure
A progressive condition usually characterized by combined failure of several organs such as the lungs, liver, kidney, along with some clotting mechanisms, usually postinjury or postoperative.		02.0510
Endotoxemia
A condition characterized by the presence of ENDOTOXINS in the blood. On lysis, the outer cell wall of gram-negative bacteria enters the systemic circulation and initiates a pathophysiologic cascade of pro-inflammatory mediators.		02.0510
Cardiomyopathy, Congestive
[description not available]		03.3820
Cardiomyopathy, Dilated
A form of CARDIAC MUSCLE disease that is characterized by ventricular dilation, VENTRICULAR DYSFUNCTION, and HEART FAILURE. Risk factors include SMOKING; ALCOHOL DRINKING; HYPERTENSION; INFECTION; PREGNANCY; and mutations in the LMNA gene encoding LAMIN TYPE A, a NUCLEAR LAMINA protein.		03.3820
Cardiovirus Infections
Infections caused by viruses of the genus CARDIOVIRUS, family PICORNAVIRIDAE.		02.0610
Vascular Injuries
[description not available]		02.4820
Hypertrophy
General increase in bulk of a part or organ due to CELL ENLARGEMENT and accumulation of FLUIDS AND SECRETIONS, not due to tumor formation, nor to an increase in the number of cells (HYPERPLASIA).		02.4820
Anterior Circulation Transient Ischemic Attack
[description not available]		02.0610
Ischemic Attack, Transient
Brief reversible episodes of focal, nonconvulsive ischemic dysfunction of the brain having a duration of less than 24 hours, and usually less than one hour, caused by transient thrombotic or embolic blood vessel occlusion or stenosis. Events may be classified by arterial distribution, temporal pattern, or etiology (e.g., embolic vs. thrombotic). (From Adams et al., Principles of Neurology, 6th ed, pp814-6)		02.0610
Short Bowel Syndrome
A malabsorption syndrome resulting from extensive operative resection of the SMALL INTESTINE, the absorptive region of the GASTROINTESTINAL TRACT.		07.0610
HIV Coinfection
[description not available]		02.4520
HIV Infections
Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).		02.4520
Nerve Degeneration
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.		04.1130
Adrenal Cancer
[description not available]		02.0610
Cushing's Syndrome
[description not available]		02.0610
Pheochromocytoma, Extra-Adrenal
[description not available]		02.0610
Cushing Syndrome
A condition caused by prolonged exposure to excess levels of cortisol (HYDROCORTISONE) or other GLUCOCORTICOIDS from endogenous or exogenous sources. It is characterized by upper body OBESITY; OSTEOPOROSIS; HYPERTENSION; DIABETES MELLITUS; HIRSUTISM; AMENORRHEA; and excess body fluid. Endogenous Cushing syndrome or spontaneous hypercortisolism is divided into two groups, those due to an excess of ADRENOCORTICOTROPIN and those that are ACTH-independent.		02.0610
Pheochromocytoma
A usually benign, well-encapsulated, lobular, vascular tumor of chromaffin tissue of the ADRENAL MEDULLA or sympathetic paraganglia. The cardinal symptom, reflecting the increased secretion of EPINEPHRINE and NOREPINEPHRINE, is HYPERTENSION, which may be persistent or intermittent. During severe attacks, there may be HEADACHE; SWEATING, palpitation, apprehension, TREMOR; PALLOR or FLUSHING of the face, NAUSEA and VOMITING, pain in the CHEST and ABDOMEN, and paresthesias of the extremities. The incidence of malignancy is as low as 5% but the pathologic distinction between benign and malignant pheochromocytomas is not clear. (Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1298)		02.0610
ALS - Amyotrophic Lateral Sclerosis
[description not available]		02.0710
Amyotrophic Lateral Sclerosis
A degenerative disorder affecting upper MOTOR NEURONS in the brain and lower motor neurons in the brain stem and SPINAL CORD. Disease onset is usually after the age of 50 and the process is usually fatal within 3 to 6 years. Clinical manifestations include progressive weakness, atrophy, FASCICULATION, hyperreflexia, DYSARTHRIA, dysphagia, and eventual paralysis of respiratory function. Pathologic features include the replacement of motor neurons with fibrous ASTROCYTES and atrophy of anterior SPINAL NERVE ROOTS and corticospinal tracts. (From Adams et al., Principles of Neurology, 6th ed, pp1089-94)		02.0710
Abnormal Movements
[description not available]		02.0710
Active Hyperemia
[description not available]		04.3711
Hyperemia
The presence of an increased amount of blood in a body part or an organ leading to congestion or engorgement of blood vessels. Hyperemia can be due to increase of blood flow into the area (active or arterial), or due to obstruction of outflow of blood from the area (passive or venous).		04.3711
Daytime Sleepiness
[description not available]		08.4711
Disorders of Excessive Somnolence
Disorders characterized by hypersomnolence during normal waking hours that may impair cognitive functioning. Subtypes include primary hypersomnia disorders (e.g., IDIOPATHIC HYPERSOMNOLENCE; NARCOLEPSY; and KLEINE-LEVIN SYNDROME) and secondary hypersomnia disorders where excessive somnolence can be attributed to a known cause (e.g., drug affect, MENTAL DISORDERS, and SLEEP APNEA SYNDROME). (From J Neurol Sci 1998 Jan 8;153(2):192-202; Thorpy, Principles and Practice of Sleep Medicine, 2nd ed, p320)		03.4711
Interstitial Nephritis
[description not available]		07.0810
Nephritis, Interstitial
Inflammation of the interstitial tissue of the kidney. This term is generally used for primary inflammation of KIDNEY TUBULES and/or surrounding interstitium. For primary inflammation of glomerular interstitium, see GLOMERULONEPHRITIS. Infiltration of the inflammatory cells into the interstitial compartment results in EDEMA, increased spaces between the tubules, and tubular renal dysfunction.		02.0810
Hyperpotassemia
[description not available]		02.0610
Hyperkalemia
Abnormally high potassium concentration in the blood, most often due to defective renal excretion. It is characterized clinically by electrocardiographic abnormalities (elevated T waves and depressed P waves, and eventually by atrial asystole). In severe cases, weakness and flaccid paralysis may occur. (Dorland, 27th ed)		07.0610
Cancer, Embryonal
[description not available]		02.0710
Benign Hypothalamic Neoplasms
[description not available]		02.0710
Neoplasms, Germ Cell and Embryonal
Neoplasms composed of primordial GERM CELLS of embryonic GONADS or of elements of the germ layers of the EMBRYO, MAMMALIAN. The concept does not refer to neoplasms located in the gonads or present in an embryo or FETUS.		02.0710
Electrocardiogram QT Prolonged
[description not available]		03.4711
Long QT Syndrome
A condition that is characterized by episodes of fainting (SYNCOPE) and varying degree of ventricular arrhythmia as indicated by the prolonged QT interval. The inherited forms are caused by mutation of genes encoding cardiac ion channel proteins. The two major forms are ROMANO-WARD SYNDROME and JERVELL-LANGE NIELSEN SYNDROME.		03.4711
Coma, Hyperglycemic Hyperosmolar Nonketotic
[description not available]		02.9910
Aberrant Crypt Foci
Clusters of colonic crypts that appear different from the surrounding mucosa when visualized after staining. They are of interest as putative precursors to colorectal adenomas and potential biomarkers for colorectal carcinoma.		02.0710
Adenoma, Basal Cell
[description not available]		02.0710
Adenoma
A benign epithelial tumor with a glandular organization.		02.0710
Infections, Listeria
[description not available]		02.0710
Coronary Occlusion
Complete blockage of blood flow through one of the CORONARY ARTERIES, usually from CORONARY ATHEROSCLEROSIS.		03.4611
Bovine Diseases
[description not available]		03.4711
Affective Psychosis, Bipolar
[description not available]		02.0810
Disorder, Borderline Personality
[description not available]		02.0810
Bipolar Disorder
A major affective disorder marked by severe mood swings (manic or major depressive episodes) and a tendency to remission and recurrence.		02.0810
Borderline Personality Disorder
A personality disorder marked by a pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity beginning by early adulthood and present in a variety of contexts. (DSM-IV)		02.0810
Drug Overdose
Accidental or deliberate use of a medication or street drug in excess of normal dosage.		02.4620
Adrenal Gland Hypofunction
[description not available]		02.0810
Adenohypophyseal Hyposecretion
[description not available]		02.0810
Adrenal Insufficiency
Conditions in which the production of adrenal CORTICOSTEROIDS falls below the requirement of the body. Adrenal insufficiency can be caused by defects in the ADRENAL GLANDS, the PITUITARY GLAND, or the HYPOTHALAMUS.		07.0810
Hypopituitarism
Diminution or cessation of secretion of one or more hormones from the anterior pituitary gland (including LH; FOLLICLE STIMULATING HORMONE; SOMATOTROPIN; and CORTICOTROPIN). This may result from surgical or radiation ablation, non-secretory PITUITARY NEOPLASMS, metastatic tumors, infarction, PITUITARY APOPLEXY, infiltrative or granulomatous processes, and other conditions.		07.0810
Anesthesia
A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures.		02.7230
Cadaver
A dead body, usually a human body.		02.4620
Binge-Eating Disorder
A disorder associated with three or more of the following: eating until feeling uncomfortably full; eating large amounts of food when not physically hungry; eating much more rapidly than normal; eating alone due to embarrassment; feeling of disgust, DEPRESSION, or guilt after overeating. Criteria includes occurrence on average, at least 2 days a week for 6 months. The binge eating is not associated with the regular use of inappropriate compensatory behavior (i.e. purging, excessive exercise, etc.) and does not co-occur exclusively with BULIMIA NERVOSA or ANOREXIA NERVOSA. (From DSM-IV, 1994)		02.0810
Cancer of Pituitary
[description not available]		02.0810
Craniopharyngioma, Adamantinous
[description not available]		02.0810
Craniopharyngioma
A benign pituitary-region neoplasm that originates from Rathke's pouch. The two major histologic and clinical subtypes are adamantinous (or classical) craniopharyngioma and papillary craniopharyngioma. The adamantinous form presents in children and adolescents as an expanding cystic lesion in the pituitary region. The cystic cavity is filled with a black viscous substance and histologically the tumor is composed of adamantinomatous epithelium and areas of calcification and necrosis. Papillary craniopharyngiomas occur in adults, and histologically feature a squamous epithelium with papillations. (From Joynt, Clinical Neurology, 1998, Ch14, p50)		02.0810
Pituitary Neoplasms
Neoplasms which arise from or metastasize to the PITUITARY GLAND. The majority of pituitary neoplasms are adenomas, which are divided into non-secreting and secreting forms. Hormone producing forms are further classified by the type of hormone they secrete. Pituitary adenomas may also be characterized by their staining properties (see ADENOMA, BASOPHIL; ADENOMA, ACIDOPHIL; and ADENOMA, CHROMOPHOBE). Pituitary tumors may compress adjacent structures, including the HYPOTHALAMUS, several CRANIAL NERVES, and the OPTIC CHIASM. Chiasmal compression may result in bitemporal HEMIANOPSIA.		02.0810
Placental Insufficiency
Failure of the PLACENTA to deliver an adequate supply of nutrients and OXYGEN to the FETUS.		02.0110
Anxiety Neuroses
[description not available]		02.0210
Anxiety Disorders
Persistent and disabling ANXIETY.		02.0210
Colicky Pain
[description not available]		02.4420
Abdominal Pain
Sensation of discomfort, distress, or agony in the abdominal region.		02.4420
Long Sleeper Syndrome
[description not available]		02.0310
Sleep Wake Disorders
Abnormal sleep-wake schedule or pattern associated with the CIRCADIAN RHYTHM which affect the length, timing, and/or rigidity of the sleep-wake cycle relative to the day-night cycle.		02.0310
Age-Related Macular Degeneration
[description not available]		02.0310
Mucositis, Oral
[description not available]		02.0310
Macular Degeneration
Degenerative changes in the RETINA usually of older adults which results in a loss of vision in the center of the visual field (the MACULA LUTEA) because of damage to the retina. It occurs in dry and wet forms.		02.0310
Stomatitis
INFLAMMATION of the soft tissues of the MOUTH, such as MUCOSA; PALATE; GINGIVA; and LIP.		02.0310
Urinary Incontinence
Involuntary loss of URINE, such as leaking of urine. It is a symptom of various underlying pathological processes. Major types of incontinence include URINARY URGE INCONTINENCE and URINARY STRESS INCONTINENCE.		02.0310
Bile Duct Obstruction, Extrahepatic
[description not available]		02.0310
Decerebrate Posturing
[description not available]		02.0410
Bezoars
Concretions of swallowed hair, fruit or vegetable fibers, or similar substances found in the alimentary canal.		02.0410
Pyrexia
[description not available]		0210
Fever
An abnormal elevation of body temperature, usually as a result of a pathologic process.		0210