Page last updated: 2024-12-05

glipizide

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Description

Glipizide is an oral sulfonylurea drug used to treat type 2 diabetes. It works by stimulating the pancreas to release more insulin. The synthesis of glipizide involves a multi-step process starting with a sulfonylurea derivative and a substituted aromatic compound. Glipizide is well absorbed after oral administration and has a long duration of action. It is effective in lowering blood glucose levels and improving glycemic control in patients with type 2 diabetes. It has been shown to reduce the risk of cardiovascular events in some studies. Glipizide is studied extensively to understand its mechanisms of action, its long-term effects, and its potential for combination therapies with other diabetes medications.'

Glipizide: An oral hypoglycemic agent which is rapidly absorbed and completely metabolized. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

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. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID3478
CHEMBL ID1073
CHEBI ID5384
SCHEMBL ID17094
MeSH IDM0009278

Synonyms (226)

Synonym
BIDD:GT0476
AC-15789
CBIOL_001788
chebi:5384 ,
cp-28720
nsc-759120
glipizide slow release
cp-28,720
CHEMBL1073 ,
MLS001148176
AKOS005564405
BRD-K12219985-001-04-8
MLS000069386 ,
EU-0100621
glipizide, solid
PRESTWICK_242
glipizide
29094-61-9
BIO1_000074
BIO2_000069
cas-29094-61-9
BIO1_000563
lopac-g-117
NCGC00016802-01
NCGC00015462-01
BIO2_000549
BIO1_001052
IDI1_033819
PRESTWICK2_000131
BSPBIO_001349
LOPAC0_000621
PRESTWICK3_000131
BSPBIO_000202
BPBIO1_000224
n-{4-[beta-(5-methylpyrazine-2-carboxamido)ethyl]benzenesulphonyl}-n'-cyclohexylurea
1-cyclohexyl-3-({p-[2-(5-methylpyrazinecarboxamido)ethyl]phenyl}sulfonyl)urea
DB01067
glucotrol (tn)
D00335
glipizide (usp/inn)
NCGC00023748-05
NCGC00023748-06
glipizida [inn-spanish]
cp 28,720
napizide
glypidizine
glucolip
glibenese
glucotrol
glupizide
pyrazinecarboxamide, n-(2-(4-((((cyclohexylamino)carbonyl)amino)sulfonyl)phenyl)ethyl)-5-methyl-
gluco-rite
glipizidum [inn-latin]
glydiazinamide
dipazide
tk 1320
n-(4-(beta-(5-methylpyrazine-2-carboxamido)ethyl)benzenesulphonyl)-n'-cyclohexylurea
urea, 1-cyclohexyl-3-((p-(2-(5-methylpyrazinecarboxamido)ethyl)phenyl)sulfonyl)-
sucrazide
glupitel
minodiab
aldiab
minidab
mindiab
glide
glidiab
glibetin
ozidia
cp 28720
k 4024
glucozide
1-cyclohexyl-3-((p-(2-(5-methylpyrazinecarboxamido)ethyl)phenyl)sulfonyl)urea
glipid
k-4024 ,
glican
glidiazinamide
melizide
brn 0903495
minidiab
digrin
glyde
einecs 249-427-6
glucotrol xl
smr000058455
KBIO3_000137
KBIO3_000138
KBIO2_005205
KBIOSS_000069
KBIOGR_000069
KBIO2_000069
KBIO2_002637
PRESTWICK0_000131
PRESTWICK1_000131
SPBIO_002141
NCGC00023748-04
NCGC00015462-02
NCGC00023748-03
NCGC00023748-07
n-(2-{4-[(cyclohexylcarbamoyl)sulfamoyl]phenyl}ethyl)-5-methylpyrazine-2-carboxamide
NCGC00015462-05
HMS2093J09
G-117 ,
HMS2089C21
HMS1989D11
NCGC00015462-11
HMS1791D11
HMS1361D11
FT-0659737
HMS1568K04
n-[2-[4-(cyclohexylcarbamoylsulfamoyl)phenyl]ethyl]-5-methylpyrazine-2-carboxamide
bdbm50012956
1-cyclohexyl-3-(4-(2-(2-methylpyrazine-5-carboxamido)ethyl)phenylsulfonyl)urea
1-cyclohexyl-3-[[p-[2-(5-methylpyrazinecarboxamido)ethyl]phenyl]sulfonyl]urea
NCGC00015462-07
HMS3259K12
HMS3261N04
HMS2095K04
n-[2-(4-{[(cyclohexylcarbamoyl)amino]sulfonyl}phenyl)ethyl]-5-methylpyrazine-2-carboxamide
NCGC00255522-01
dtxcid8020676
tox21_301834
dtxsid0040676 ,
29094-66-4
G0369
n-[4-(3-cyclohexylureidosulfonyl)phenethyl]-5-methyl-2-pyrazinecarboxamide
1-cyclohexyl-3-{4-[2-(5-methylpyrazine-2-carboxamido)ethyl]phenylsulfonyl}urea
pharmakon1600-01505433
nsc759120
tox21_110156
CCG-204710
HMS2233N11
STK631952
NCGC00015462-03
NCGC00015462-06
NCGC00015462-09
NCGC00015462-04
NCGC00015462-10
NCGC00015462-12
NCGC00015462-08
unii-x7wdt95n5c
glipizide [usan:usp:inn:ban]
x7wdt95n5c ,
glipizida
nsc 759120
glipizidum
FT-0626714
LP00621
glipizide [inn]
glipizide [jan]
glipizide [vandf]
glipizide [ep monograph]
metaglip component glipizide
glipizide [usan]
glipizide [who-dd]
glipizide component of metaglip
glipizide [orange book]
glipizide [mi]
glipizide [usp-rs]
glipizide [usp monograph]
glipizide [mart.]
S1715
gtpl6821
HMS3369L12
HY-B0254
NC00564
BBL028143
SCHEMBL17094
tox21_110156_1
NCGC00015462-14
KS-1068 ,
tox21_500621
NCGC00261306-01
ZJJXGWJIGJFDTL-UHFFFAOYSA-N
pyrazinecarboxamide, n-[2-[4-[[[(cyclohexylamino)carbonyl]amino]sulfonyl]phenyl]ethyl]-5-methyl-
n-(4-(.beta.-(5-methylpyrazine-2-carboxamido)ethyl)benzenesulphonyl)-n'-cyclohexylurea
n-(2-[4-(([(cyclohexylamino)carbonyl]amino)sulfonyl)phenyl]ethyl)-5-methyl-2-pyrazinecarboxamide
metaglip (salt/mix)
n-(4-[n-(cyclohexylcarbamoyl)sulfamoyl]phenethyl)-5-methylpyrazine-2-carboxamide
W-107005
n-(4-(n-(cyclohexylcarbamoyl)sulfamoyl)phenethyl)-5-methylpyrazine-2-carboxamide
HMS3402D11
OPERA_ID_1908
mfcd00072159
SR-01000000010-2
sr-01000000010
glipizide, united states pharmacopeia (usp) reference standard
glipizide, european pharmacopoeia (ep) reference standard
HMS3655G04
SR-01000000010-5
glipizide, pharmaceutical secondary standard; certified reference material
SBI-0050603.P002
HMS3712K04
SW196549-3
cp 28720;k 4024
Q3108899
nsc813218
nsc-813218
glipizide (glucotrol)
glipizide,(s)
172964-66-8
BCP09195
BRD-K12219985-001-15-4
SDCCGSBI-0050603.P003
NCGC00015462-23
glipizide/glucotrol
1-cyclohexyl-3-{{p=[2-[5-methylpyrazine-carboxamido)-ethyl]phenyl}sulphonyl}urea
glipizide 100 microg/ml in acetonitrile
n-[2-[4[[[(cyclohexylamino)carbonyl]amino]sulfonyl]phenyl]ethyl]-5-methylpyrazinecarboxamide; 1-cyclohexyl-3-[[p-[2-(5-methylpyrazinecarboxamido)
2-pyrazinecarboxamide, n-[2-[4-[[[(cyclohexylamino)carbonyl]amino]sulfonyl]phenyl]ethyl]-5-methyl-
SY009252
n-[4-[n-(cyclohexylcarbamoyl)sulfamoyl]phenethyl]-5-methylpyrazine-2-carboxamide
Z1575081877
glipizide xl
glipizide er
glipizideerer
glipizide (usp monograph)
glipizide (ep monograph)
glipizidum (inn-latin)
glipizidexl
glipizide (usan:usp:inn:ban)
glipizide (usp-rs)
n-(2-(4-((cyclohexylcarbamoyl)sulfamoyl)phenyl)ethyl)-5-methylpyrazine-2-carboxamide
glipizide (mart.)
glipizideer
glipizida (inn-spanish)
glucotrolxl

Research Excerpts

Overview

Glipizide is a second-generation sulfonylurea commonly used to treat patients with noninsulin-dependent diabetes mellitus. It has been reported to inhibit tumor growth and metastasis by upregulating the expression of natriuretic peptide receptor A.

ExcerptReferenceRelevance
"Glipizide, which is a widely used drug for type 2 diabetes mellitus, has been reported to inhibit tumor growth and metastasis by upregulating the expression of natriuretic peptide receptor A (NPRA)."( Glipizide Combined with ANP Suppresses Breast Cancer Growth and Metastasis by Inhibiting Angiogenesis through VEGF/VEGFR2 Signaling.
Cao, J; Li, J; Liu, X; Mao, G; Qi, C; Wang, L; Zhang, Q; Zheng, L; Zheng, S; Zhou, Q, 2022
)
2.89
"Glipizide was found to be a low-solubility compound."( The biopharmaceutics of successful controlled release drug product: Segmental-dependent permeability of glipizide vs. metoprolol throughout the intestinal tract.
Agbaria, R; Cohen, N; Dahan, A; Zur, M, 2015
)
1.35
"Glipizide is a second-generation sulfonylurea commonly used to treat patients with noninsulin-dependent diabetes mellitus."( Stevens-Johnson syndrome associated with glipizide therapy.
Anderson, RC; Cheng, JB; Cruz, PD, 2006
)
1.32
"Glipizide is a "second generation" sulfonylurea compound, and in this study the effects of several months of glipizide treatment on various aspects of glucose, insulin, and lipid metabolism were documented in 23 patients with noninsulin-dependent diabetes mellitus. "( Effect of glipizide treatment on various aspects of glucose, insulin, and lipid metabolism in patients with noninsulin-dependent diabetes mellitus.
Reaven, GM, 1983
)
2.11
"Glipizide seemed to be a more potent and more rapid insulin releaser than glibenclamide, but this may be secondary to biopharmaceutic differences between the two preparations."( Comparative single-dose kinetics and effects of four sulfonylureas in healthy volunteers.
Melander, A; Sartor, G; Scherstén, B; Wåhlin-Boll, E, 1980
)
0.98
"Glipizide is a second generation of sulphonylurea compound, effective in lowering of blood glucose, well-tolerated as well as safe during long-term treatment. "( [Glipizide--a short-acting sulphonylurea derivative].
Ogonowski, J, 1996
)
2.65
"Glipizide is an oral antidiabetic drug that has been used in the treatment of post-transplant diabetes mellitus (PTDM). "( Glipizide treatment of post-transplant diabetes does not interfere with cyclosporine pharmacokinetics in renal allograft recipients.
Asberg, A; Berg, KJ; Bergan, S; Hartmann, A; Sagedal, S, 1998
)
3.19
"Glipizide is a second generation sulphonylurea agent that is available in a Gastrointestinal Therapeutic System (GITS) extended-release formulation. "( Glipizide. A review of the pharmacoeconomic implications of the extended-release formulation in type 2 diabetes mellitus.
Foster, RH; Plosker, GL, 2000
)
3.19
"Glipizide is a 'second generation' oral hypoglycaemic agent similar in potency to glibenclamide. "( Glipizide: a review of its pharmacological properties and therapeutic use.
Avery, GS; Brogden, RN; Heel, RC; Pakes, GE; Speight, TM, 1979
)
3.15
"Glipizide is a relatively new sulphonylurea- antidiabetic agent. "( A clinical trial with glipizide - a relative new sulphonylurea.
Singarayar, J; Sunderam, S,
)
1.89
"Glipizide is a new hypoglycaemic sulphonylurea. "( [Experimental study of glipizide. A comparison with other hypoglycemic sulfonamides (author's transl)].
Alric, R; Loubatières, AL; Loubatieres-Mariani, MM; Ribes, G; Sorial, G; Tarasco, A, 1975
)
2.01
"Glipizide is a second-generation sulfonylurea in which the substitutions on the arylsulfonylurea nucleus are large, relatively nonpolar groups. "( Glipizide: a second-generation sulfonylurea hypoglycemic agent. Pharmacology, pharmacokinetics and clinical use.
Lebovitz, HE,
)
3.02

Effects

Glipizide was found to has an interfacial adsorptive character onto the mercury electrode surface. It has a terminal elimination half-life of 2-7 hours.

Glipizide (GPZ) has been widely used in the treatment of type-2 diabetics as insulin secretogague. It has the most rapid absorption and onset of action, as well as the shortest half-life and effect-duration.

ExcerptReferenceRelevance
"Glipizide was found to has an interfacial adsorptive character onto the mercury electrode surface."( Stripping voltammetric quantification of the anti-diabetic drug glipizide in bulk form and pharmaceutical formulation.
El-Attar, MA; Ghoneim, EM; Hammam, E; Khashaba, PY, 2007
)
1.3
"Glipizide has a terminal elimination half-life of 2-7 hours."( Glyburide and glipizide, second-generation oral sulfonylurea hypoglycemic agents.
Prendergast, BD,
)
1.21
"Glipizide (GPZ) has been widely used in the treatment of type-2 diabetics as insulin secretogague. "( Development and validation of RP-HPLC method for quantification of glipizide in biological macromolecules.
Acharya, S; Pani, NR; Patra, S, 2014
)
2.08
"Glipizide was found to has an interfacial adsorptive character onto the mercury electrode surface."( Stripping voltammetric quantification of the anti-diabetic drug glipizide in bulk form and pharmaceutical formulation.
El-Attar, MA; Ghoneim, EM; Hammam, E; Khashaba, PY, 2007
)
1.3
"Glipizide has the most rapid absorption and onset of action, as well as the shortest half-life and effect-duration; hence the risk of long-lasting hypoglycemia is minute."( Clinical pharmacology of glipizide.
Melander, A; Wåhlin-Boll, E, 1983
)
1.29
"Glipizide has a terminal elimination half-life of 2-7 hours."( Glyburide and glipizide, second-generation oral sulfonylurea hypoglycemic agents.
Prendergast, BD,
)
1.21
"Glipizide has been shown to increase glucose metabolism by both pancreatic and extrapancreatic actions."( Effects of glipizide on beta-endorphin secretions in response to hyperglycaemia in obese cafeteria rats.
Belon, JP; Henry, JC; Jacquot, C; Orosco, M,
)
1.24

Actions

Glipizide did not inhibit alpha-ketoisocaproate-induced insulin secretion. It did, however, increase cytoplasmic retention of the acidic dopamine metabolites, 3, 4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), indicating blockade of their outward transport.

ExcerptReferenceRelevance
"That glipizide did not inhibit alpha-ketoisocaproate-induced insulin secretion was not the result of elevated [Ca2+]c, as glucose caused a more marked [Ca2+]c increase."( Fuel-induced amplification of insulin secretion in mouse pancreatic islets exposed to a high sulfonylurea concentration: role of the NADPH/NADP+ ratio.
Panten, U; Rustenbeck, I, 2008
)
0.8
"Glipizide provoked an increase in serum insulin and C-peptide concentrations (AUC0-4.insulin: baseline 698 +/- 327, single dose 954 +/- 461, long-term dosing 945 +/- 600 pmol/L/hr)."( The influence of multiple dosing and age on the pharmacokinetics and pharmacodynamics of glipizide in patients with type II diabetes mellitus.
Ducharme, MP; Edwards, DJ; Grunberger, G; Jaber, LA; Slaughter, RL,
)
1.07
"Glipizide did, however, increase cytoplasmic retention of the acidic dopamine metabolites, 3, 4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), indicating blockade of their outward transport."( Effect of glipizide on dopamine synthesis, release and metabolism in PC12 cells.
Eisenhofer, G; Harvey-White, J; He, L; Kopin, IJ; Lamensdorf, I; Milan, R; Nechushtan, A; Rojas, E, 2000
)
1.43
"Glipizide did not produce glucose variations in either test but did result in a significant decrease, in the first test only, in mean plasma baseline levels of lactate, which were higher than normal in these patients."( Plasma levels of glucose and lactate after intravenous glipizide administration in some insulin-dependent diabetics. Therapeutic effects of an associated glipizide-insulin treatment.
Boni, C; Buzzigoli, G; Giampietro, O; Navalesi, R, 1979
)
1.23

Treatment

Glipizide used in the treatment of diabetes was selected as model drug. It was successfully loaded into commercial polyvinyl alcohol (PVA) filaments by HME method. Glipzide treatment decreased dilated renal tubule number, improved glomerulus integrity, and reduced inflammatory infiltration.

ExcerptReferenceRelevance
"Glipizide-treated periodontitis mice showed reduced micro-vessel density and leukocyte/macrophage infiltration in PAPT."( Glipizide Alleviates Periodontitis Pathogenicity via Inhibition of Angiogenesis, Osteoclastogenesis and M1/M2 Macrophage Ratio in Periodontal Tissue.
Ge, L; Ge, Q; Guo, X; Huang, Y; Huang, Z; Jiang, Y; Liang, D; Pathak, JL; Wang, L; Yang, L, 2023
)
3.07
"Glipizide used in the treatment of diabetes was selected as model drug, and was successfully loaded into commercial polyvinyl alcohol (PVA) filaments by HME method."( Preparation and investigation of controlled-release glipizide novel oral device with three-dimensional printing.
Guan, X; Jia, D; Li, Q; Pan, H; Pan, W; Wen, H; Xiang, R; Yang, Y; Yu, S; Zhu, Z, 2017
)
1.43
"Glipizide treatment decreased dilated renal tubule number, improved glomerulus integrity, and reduced inflammatory infiltration."( Glipizide blocks renal interstitial fibrosis by inhibiting AKT signaling pathway.
Huang, JJ; Huang, SJ; Jiang, O; Wu, DQ; Wu, JP; Yang, G; Zeng, G; Zeng, YB, 2017
)
2.62
"Glipizide treatment was initiated at 2.5 or 5 mg/day and uptitrated to a maximum of 20 mg/day."( Safety and efficacy of sitagliptin in patients with type 2 diabetes and chronic renal insufficiency.
Amatruda, JM; Arjona Ferreira, JC; Chan, JC; Davies, MJ; Gonzalez, E; Kaufman, KD; Scott, R; Sheng, D; Stein, PP; Williams-Herman, D, 2008
)
1.07
"Glipizide treatment also led to enhanced in vivo insulin action, whether measured by the insulin clamp technique (P < 0.001) or the insulin suppression test (P< 0.02)."( Effect of sulfonylurea treatment on in vivo insulin secretion and action in patients with non-insulin-dependent diabetes mellitus.
Doberne, L; Greenfield, MS; Reaven, GM; Rosenthal, M; Schulz, B; Widstrom, A, 1982
)
0.99
"Glipizide treatment did not significantly alter basal glucose turnover, Ra, mean glucose values, or mean insulin levels as determined by radioimmunoassay."( Selective potentiation of insulin-mediated glucose disposal in normal dogs by the sulfonylurea glipizide.
Andersen, DK; Jones, RS; Lebovitz, HE; Putnam, WS, 1981
)
1.2
"In glipizide-treated BB rats at 240 days, only 44% of rats had islet inflammation compared to 86% in the control group (P < 0.01)."( Glipizide-induced prevention of diabetes and autoimmune events in the BB rat.
Chan, E; Charles, MA; Hosszufalusi, N; Reinherz, L; Takei, S, 1994
)
2.25
"With glipizide treatment, there was a decrease in FPG level at T3 (9.4 +/- 0.5 mmol/L in previously treated, 6.9 +/- 0.4 mmol/L in previously untreated), which persisted at T4."( Verbal learning and/or memory improves with glycemic control in older subjects with non-insulin-dependent diabetes mellitus.
Gradman, TJ; Laws, A; Reaven, GM; Thompson, LW, 1993
)
0.74
"Glipizide GITS treatment resulted in a significant reduction in hyperglycemia and increases in insulin and C-peptide secretion. "( The effect of glipizide gastrointestinal therapeutic system on islet cell hormonal responses to a test meal in NIDDM.
Albert, SG; Bernbaum, M; Mooradian, AD; Plummer, S, 1996
)
2.1
"Glipizide GITS treatment failed to ameliorate the hyperglucagonemia of NIDDM and did not alter amylin secretion even though it increased insulin secretion and significantly ameliorated the hyperglycemia. "( The effect of glipizide gastrointestinal therapeutic system on islet cell hormonal responses to a test meal in NIDDM.
Albert, SG; Bernbaum, M; Mooradian, AD; Plummer, S, 1996
)
2.1
"Glipizide treatment appears to affect fasting sensitivity to insulin, but results in a decrement of insulin response to oral or intravenous glucose challenge."( Glipizide treatment of pancreas autotransplantation: effects on alterations in glucose-insulin relationships.
Barr, JD; Cornett, G; Flanagan, TL; Freedlender, AE; Hanks, JB; Kaiser, DL; Parish, ES, 1991
)
2.45
"Glipizide-treated mice improved their OGTT."( Diabetic microangiopathy in KK mice. VI. Effect of glycemic control on renal glycoprotein metabolism and established glomerulosclerosis.
Camerini-Davalos, RA; Khan, MY; Reddi, AS; Reddy, PR; Velasco, CA, 1990
)
1
"Glipizide treatment did not result in an increase in glucose uptake by the various tissues studied."( The effect of sulphonylurea on the in vivo tissue uptake of glucose in normal rats.
Mooradian, AD, 1987
)
0.99
"Treatment with Glipizide went on in 95% of previously untreated patients and in 90% of patients with previous oral hypoglycemias, with a mean daily dose of 10 mg (2 tablets)."( [Glipizide in the treatment of non-insulin-dependent diabetes mellitus].
Luis Iriarte, J, 1989
)
1.53

Toxicity

The once-daily glipizide GITS lowered HbA1c, FPG, and PPG over a dose range of 5-60 mg. There was a lower incidence of symptomatic hypoglycemia adverse events (AEs) with sitagliptin versus glipzide.

ExcerptReferenceRelevance
"The once-daily glipizide GITS 1) lowered HbA1c, FPG, and PPG over a dose range of 5-60 mg, 2) was maximally effective at 5 mg (using HbA1c) or 20 mg (using FPG) based on pharmacokinetic and pharmacodynamic relationships, 3) maintained its effectiveness in poorly controlled patients (those with entry FPG > or = 250 mg/dl), 4) was safe and well tolerated in a wide variety of patients with NIDDM, and 5) did not produce weight gain or adversely affect lipids."( Efficacy, safety, and dose-response characteristics of glipizide gastrointestinal therapeutic system on glycemic control and insulin secretion in NIDDM. Results of two multicenter, randomized, placebo-controlled clinical trials. The Glipizide Gastrointest
Feinglos, M; Fischette, CT; Kourides, IA; Shamoon, H; Simonson, DC, 1997
)
0.9
"A retrospective analysis was conducted to determine the effects of metformin on glycosylated hemoglobin (HbA1c), body weight, and adverse events in an African-American population."( A retrospective analysis of the efficacy and safety of metformin in the African-American patient.
Anderson, D; Briscoe, TA; Cooper, GS; Usifo, OS, 1997
)
0.3
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004
)
0.32
" The overall incidence of adverse experiences was generally similar between groups."( Safety and efficacy of sitagliptin in patients with type 2 diabetes and chronic renal insufficiency.
Amatruda, JM; Arjona Ferreira, JC; Chan, JC; Davies, MJ; Gonzalez, E; Kaufman, KD; Scott, R; Sheng, D; Stein, PP; Williams-Herman, D, 2008
)
0.35
" The primary outcome was to maintain safe fasting glucose and random glucose levels of <350 and <500 mg/dL up to 4 weeks and <300 and <400 mg/dL, respectively, thereafter and to have no return ED visits (responders)."( Safe and simple emergency department discharge therapy for patients with type 2 diabetes mellitus and severe hyperglycemia.
Babu, A; Chen, Z; Fogelfeld, L; Guerrero, P; Koh, CK; Mehta, A; Meyer, PM; Roberts, R; Schaider, J,
)
0.13
" Use of sulfonylurea alone once daily can be considered a safe discharge regimen for such patients and an effective bridge between ED intervention and subsequent follow-up."( Safe and simple emergency department discharge therapy for patients with type 2 diabetes mellitus and severe hyperglycemia.
Babu, A; Chen, Z; Fogelfeld, L; Guerrero, P; Koh, CK; Mehta, A; Meyer, PM; Roberts, R; Schaider, J,
)
0.13
" The main objective of this study is to assess the safety of Glipizide (GZ) loaded polymeric nanoparticle systematically and to observe the toxic effects of nanoparticles on the functions of various tissues and organs in rats."( Sub acute toxicity assessment of glipizide engineered polymeric nanoparticles.
Kishore, N; Lekshmi, UM; Reddy, PN, 2011
)
0.89
" There was a lower incidence of symptomatic hypoglycemia adverse events (AEs) with sitagliptin versus glipizide (6."( Efficacy and safety of sitagliptin versus glipizide in patients with type 2 diabetes and moderate-to-severe chronic renal insufficiency.
Arjona Ferreira, JC; Barzilai, N; Goldstein, BJ; Golm, GT; Guo, H; Kaufman, KD; Marre, M; Sisk, CM, 2013
)
0.87
" Adverse events (AE) and hypoglycemia were monitored."( Saxagliptin efficacy and safety in patients with type 2 diabetes mellitus stratified by cardiovascular disease history and cardiovascular risk factors: analysis of 3 clinical trials.
Bryzinski, B; Cook, W; Hirshberg, B; Minervini, G, 2014
)
0.4
" We compared the effects of three SU medications and initial SU doses on adverse glycemic and cardiovascular events among NH residents."( Comparative safety of sulfonylureas among U.S. nursing home residents.
Berry, SD; Hayes, KN; Munshi, MN; Riester, MR; Zullo, AR, 2023
)
0.91

Pharmacokinetics

The timing of a glipizide dose in relation to a meal and simulated delayed or prolonged absorption appear to have little influence on the drug's pharmacodynamic effects. Long-term dosing and aging have little effect on the pharmacokinetic profile of glipzide.

ExcerptReferenceRelevance
"Complex pharmacokinetic perturbations follow kidney failure."( [Pharmacokinetic perturbations in kidney failure. Anomalies of metabolites and tissue diffusion (author's transl)].
Balant, L; Blanchard, P; Fabre, J; Rudhardt, M,
)
0.13
" Both pharmacokinetic and pharmacodynamic factors may contribute to these differences."( Comparison of pharmacokinetics, metabolic effects and mechanisms of action of glyburide and glipizide during long-term treatment.
Fyhrquist, F; Groop, L; Groop, PH; Melander, A; Saloranta, C; Stenman, S; Tötterman, KJ,
)
0.35
" Clearance, volume of distribution at steady state, and half-life were estimated from the serum concentration-time curve data."( Glipizide pharmacokinetics in young and elderly volunteers.
Bauer, LA; Horn, JR; Kobayashi, KA; Kradjan, WA; Opheim, K; Wood, F, 1988
)
1.72
" In addition, the pharmacokinetic properties, spectrum and severity of side effects and metabolism of this agent are somewhat different from those of first-generation sulfonylureas."( Glipizide: a second-generation sulfonylurea hypoglycemic agent. Pharmacology, pharmacokinetics and clinical use.
Lebovitz, HE,
)
1.57
" The biologic half-life of glyburide is not significantly correlated with renal function in subjects with creatinine clearances of 30 ml/minute/1."( Pharmacokinetics of glyburide.
Pearson, JG, 1985
)
0.27
" The distribution volume at assumed distribution equilibrium was small (10L), and the elimination half-life was short (2 to 4 hours)."( Bioavailability, pharmacokinetics and effects of glipizide in type 2 diabetics.
Almér, LO; Melander, A; Wåhlin-Boll, E,
)
0.39
"kg-1), and half-life (4."( Pharmacokinetics and pharmacodynamics of glipizide after once-daily and divided doses.
Kradjan, WA; Opheim, KE; Takeuchi, KY; Wood, FC,
)
0.4
"The timing of a glipizide dose in relation to a meal and simulated delayed or prolonged absorption appear to have little influence on the drug's pharmacodynamic effects."( Pharmacokinetics and pharmacodynamics of glipizide after once-daily and divided doses.
Kradjan, WA; Opheim, KE; Takeuchi, KY; Wood, FC,
)
0.74
" Glipizide pharmacokinetics were assessed by serum concentrations obtained during a 24-h pharmacokinetic evaluation performed after the first 5-mg dose (SD) and after 12 weeks of chronic therapy (CD)."( The effects of obesity on the pharmacokinetics and pharmacodynamics of glipizide in patients with non-insulin-dependent diabetes mellitus.
Ducharme, MP; Halapy, H; Jaber, LA, 1996
)
1.44
"A 24-hour pharmacokinetic evaluation of glipizide was assessed after a 5-mg dose at the start of therapy and after 12 weeks of therapy."( The influence of multiple dosing and age on the pharmacokinetics and pharmacodynamics of glipizide in patients with type II diabetes mellitus.
Ducharme, MP; Edwards, DJ; Grunberger, G; Jaber, LA; Slaughter, RL,
)
0.62
"No significant differences in time to peak concentration, apparent volumes of distribution for the central and peripheral compartments, apparent oral clearance from the central compartment, distributional clearance between the central and peripheral compartments, or terminal elimination half-life were observed with a single dose and long-term dosing."( The influence of multiple dosing and age on the pharmacokinetics and pharmacodynamics of glipizide in patients with type II diabetes mellitus.
Ducharme, MP; Edwards, DJ; Grunberger, G; Jaber, LA; Slaughter, RL,
)
0.35
"Long-term dosing and aging have little effect on the pharmacokinetic profile of glipizide."( The influence of multiple dosing and age on the pharmacokinetics and pharmacodynamics of glipizide in patients with type II diabetes mellitus.
Ducharme, MP; Edwards, DJ; Grunberger, G; Jaber, LA; Slaughter, RL,
)
0.58
" The half-life is a far more important property."( [Pharmacokinetics of hypoglycemic sulfonamides: Ozidia, a new concept].
Selam, JL, 1997
)
0.3
" The half-life of gliclazide was higher than that of the other three hypoglycemic agents in middle-aged subjects and was the sole to be significantly increased in aged subjects."( Pharmacokinetics of gliquidone, glibenclamide, gliclazide and glipizide in middle-aged and aged subjects.
Courtois, P; Herbaut, C; Malaisse, WJ; Sener, A; Turc, A, 1999
)
0.54
"This study was designed to compare the pharmacokinetic and short-term pharmacodynamic profile of extended-release glipizide GITS (Glucotrol XL) given in a dosage of 20 mg once daily with that of immediate-release glipizide (Glucotrol) 10mg twice daily in patients with type II diabetes mellitus."( Pharmacokinetics and pharmacodynamics of extended-release glipizide GITS compared with immediate-release glipizide in patients with type II diabetes mellitus.
Canovatchel, W; Chaiken, RL; Chung, M; Kourides, I; Messig, M; Sutfin, T, 2002
)
0.77
"In vitro ultrafiltration human plasma protein binding displacement studies and a phase I clinical study were used to characterise the potential for pharmacokinetic interaction of ISIS 113715 and three marketed oral antidiabetic agents."( Lack of pharmacokinetic interaction for ISIS 113715, a 2'-0-methoxyethyl modified antisense oligonucleotide targeting protein tyrosine phosphatase 1B messenger RNA, with oral antidiabetic compounds metformin, glipizide or rosiglitazone.
Bradley, JD; Geary, RS; Kwon, Y; van Lier, JJ; VanVliet, AA; Watanabe, T; Wedel, M, 2006
)
0.52
" The results of the phase I clinical study further indicate that there were no measurable changes in glipizide (5 mg), metformin (500 mg) or rosiglitazone (2 mg) exposure parameters, maximum plasma concentration and the area under the concentration-time curve, or pharmacokinetic parameter, elimination half-life when coadministered with ISIS 113715."( Lack of pharmacokinetic interaction for ISIS 113715, a 2'-0-methoxyethyl modified antisense oligonucleotide targeting protein tyrosine phosphatase 1B messenger RNA, with oral antidiabetic compounds metformin, glipizide or rosiglitazone.
Bradley, JD; Geary, RS; Kwon, Y; van Lier, JJ; VanVliet, AA; Watanabe, T; Wedel, M, 2006
)
0.74
"These data provide evidence that ISIS 113715 exhibits no clinically relevant pharmacokinetic interactions on the disposition and clearance of the oral antidiabetic drugs."( Lack of pharmacokinetic interaction for ISIS 113715, a 2'-0-methoxyethyl modified antisense oligonucleotide targeting protein tyrosine phosphatase 1B messenger RNA, with oral antidiabetic compounds metformin, glipizide or rosiglitazone.
Bradley, JD; Geary, RS; Kwon, Y; van Lier, JJ; VanVliet, AA; Watanabe, T; Wedel, M, 2006
)
0.52
"The evaluation of drug disposition properties of chemical entities in drug discovery research typically involves the conduct of pharmacokinetic studies in rodents that requires blood sampling over several time points, preferably without disrupting the physiological status of the animals."( Pharmacokinetic comparisons of tail-bleeding with cannula- or retro-orbital bleeding techniques in rats using six marketed drugs.
Bina, H; Chiang, A; Ebbert, L; Huang, NH; Hui, YH; Kern, T; Maples, C; Patel, N; Pritt, M,
)
0.13
" pharmacokinetic data on 670 drugs representing, to our knowledge, the largest publicly available set of human clinical pharmacokinetic data."( Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
Lombardo, F; Obach, RS; Waters, NJ, 2008
)
0.35
" The presented HPLC-MS/MS method was proved to be suitable for the pharmacokinetic study of metformin hydrochloride and glipizide tablets in healthy volunteers after oral administration."( Simultaneous quantification of metformin and glipizide in human plasma by high-performance liquid chromatography-tandem mass spectrometry and its application to a pharmacokinetic study.
Deng, Y; Li, F; Li, N; Qin, F; Yu, J, 2013
)
0.86
" The quantitation method was successfully applied for simultaneous estimation of glipizide, cilostazol and 3, 4-dehydro-cilostazol in a pharmacokinetic drug-drug interaction study in wistar rats."( Liquid chromatography - tandem mass spectrometry for the simultaneous quantitation of glipizide, cilostazol and its active metabolite 3, 4-dehydro-cilostazol in rat plasma: application for a pharmacokinetic study.
Kanthikiran, VV; Mukkanti, K; Satheeshmanikandan, TR; Sridhar, V; Swaroopkumar, VV, 2012
)
0.83
" For the colesevelam coadministration periods, 3,750 mg once daily was dosed throughout the pharmacokinetic sampling period."( The effects of colesevelam HCl on the single-dose pharmacokinetics of glimepiride, extended-release glipizide, and olmesartan medoxomil.
He, L; Lee, J; Mendell-Harary, J; Tao, B; Walker, J; Wickremasingha, P; Wight, D, 2014
)
0.62
"Serial sampling methods have been used for rat pharmacokinetic (PK) studies for over 20 years."( Utility of capillary microsampling for rat pharmacokinetic studies: Comparison of tail-vein bleed to jugular vein cannula sampling.
Guo, Y; Ho, S; Korfmacher, W; Luo, Y; O'Shea, T; Shen, L; Snow, G; Sun, W; Wang, J; Wu, Z,
)
0.13
"The present study was carried out to investigate the pharmacokinetic and pharmacodynamic drug interaction of irbesartan with glipizide after single and multi dose treatment in normal and hypertensive rat models to evaluate the safety and effectiveness of the combination."( Influence of Single and Multi Dose Treatment of Glipizide on Pharmacokinetics and Pharmacodynamics of Irbesartan in Normal and Hypertensive Rats.
Anusha, A; Goverdhan, P; Krishna Murthy, B; Narendar, D, 2017
)
0.92
" The blood samples were analyzed for various pharmacokinetic and pharmacodynamic parameters."( Influence of Single and Multi Dose Treatment of Glipizide on Pharmacokinetics and Pharmacodynamics of Irbesartan in Normal and Hypertensive Rats.
Anusha, A; Goverdhan, P; Krishna Murthy, B; Narendar, D, 2017
)
0.71
" The combination of irbesartan and glipizide in hypertensive rats produce significant change in blood pressure (pharmacodynamic) and also significance in pharmacokinetic parameters of irbesartan with glipizide in single dose and multiple doses."( Influence of Single and Multi Dose Treatment of Glipizide on Pharmacokinetics and Pharmacodynamics of Irbesartan in Normal and Hypertensive Rats.
Anusha, A; Goverdhan, P; Krishna Murthy, B; Narendar, D, 2017
)
0.99
" TCE was co- administered in three different groups (0, 100 and 400 mg/kg) with Glibenclamide at 1 mg/kg dose to observe the alteration in pharmacokinetic parameters of Glibenclamide."( Effect of Tinospora cordifolia aqua-alcoholic extract on pharmacokinetic of Glibenclamide in rat: An herb-drug interaction study.
Ahmed, T; Punde, R; Sahu, R; Sangana, R; Subudhi, BB, 2018
)
0.48
") ethanolic extract (APE) and andrographolide (AND) (a potent CYP2C9 inducer/inhibitor) can alter the pharmacokinetic parameters of glipizide (GLZ)."( Pharmacokinetic Herb-Drug Interactions of Glipizide with
Amalia Prihati, D; Lukitaningsih, E; Nugroho, AE; Nurrochmad, A; Puspitasari, I; Sundhani, E, 2022
)
1.19

Compound-Compound Interactions

This case suggests that, when TMP/SMX is combined with glipizide, patients should be closely monitored, especially those at high risk for hypoglycemia.

ExcerptReferenceRelevance
" This case suggests that, when TMP/SMX is combined with glipizide, patients should be closely monitored, especially those at high risk for hypoglycemia."( Symptomatic hypoglycemia secondary to a glipizide-trimethoprim/sulfamethoxazole drug interaction.
Dobmeier, ME; Johnson, JF, 1990
)
0.79
" The glycemic response to each of the progressive, sequential phases of insulin treatment was assessed, along with the incidence of hypoglycemic reactions and the relative efficacy of different doses of glipizide in combination with fixed doses of insulin."( Response to intensive therapy steps and to glipizide dose in combination with insulin in type 2 diabetes. VA feasibility study on glycemic control and complications (VA CSDM).
Abraira, C; Colwell, JA; Comstock, JP; Emanuele, NV; Henderson, WG; Levin, SR; Nuttall, FQ; Sawin, CT; Silbert, CK, 1998
)
0.75
" Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor."( Potential CYP2C9-mediated drug-drug interactions in hospitalized type 2 diabetes mellitus patients treated with the sulphonylureas glibenclamide, glimepiride or glipizide.
Heikkilä, P; Huupponen, R; Laine, K; Tirkkonen, T, 2010
)
0.75
"Almost 20% of patients were exposed to a potential drug-drug interaction with a CYP2C9 inhibitor during sulphonylurea treatment."( Potential CYP2C9-mediated drug-drug interactions in hospitalized type 2 diabetes mellitus patients treated with the sulphonylureas glibenclamide, glimepiride or glipizide.
Heikkilä, P; Huupponen, R; Laine, K; Tirkkonen, T, 2010
)
0.56
"The hepatic organic anion transporting polypeptides (OATPs) influence the pharmacokinetics of several drug classes and are involved in many clinical drug-drug interactions."( Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
Artursson, P; Haglund, U; Karlgren, M; Kimoto, E; Lai, Y; Norinder, U; Vildhede, A; Wisniewski, JR, 2012
)
0.38
" Aqueous extract of Annona squamosa was administered orally at 350 mg/kg body weight alone and in combination with reduced and reducing dose combinations of Glipizide."( Polypharmacy (herbal and synthetic drug combination): a novel approach in the treatment of type-2 diabetes and its complications in rats.
Afzal, M; Ahamd, I; Ahmad, S; Ahmed, Z; Ali, B; Anwar, F; Kaur, R; Kazmi, I, 2013
)
0.59
" We aimed to compare mortality and cardiovascular risk among users of metformin in combination with pharmacologically different ISs."( Metformin in combination with various insulin secretagogues in type 2 diabetes and associated risk of cardiovascular morbidity and mortality--a retrospective nationwide study.
Andersson, C; Fosbøl, EL; Gislason, G; Køber, L; Mogensen, UM; Scheller, NM; Schramm, TK; Torp-Pedersen, C; Vaag, A, 2015
)
0.42
"Most ISs in combination with metformin were associated with similar mortality and cardiovascular risk."( Metformin in combination with various insulin secretagogues in type 2 diabetes and associated risk of cardiovascular morbidity and mortality--a retrospective nationwide study.
Andersson, C; Fosbøl, EL; Gislason, G; Køber, L; Mogensen, UM; Scheller, NM; Schramm, TK; Torp-Pedersen, C; Vaag, A, 2015
)
0.42
" We aimed to systematically screen for drugs that interact with the five most commonly used secretagogues-glipizide, glyburide, glimepiride, repaglinide, and nateglinide-to cause serious hypoglycemia."( Biomedical Informatics Approaches to Identifying Drug-Drug Interactions: Application to Insulin Secretagogues.
Bilker, WB; Brensinger, CM; Chiang, C; Han, X; Hennessy, S; Leonard, CE; Li, L, 2017
)
0.67
" We first predicted the drug-drug interaction potential based on the pharmacokinetics of each secretagogue-precipitant pair."( Biomedical Informatics Approaches to Identifying Drug-Drug Interactions: Application to Insulin Secretagogues.
Bilker, WB; Brensinger, CM; Chiang, C; Han, X; Hennessy, S; Leonard, CE; Li, L, 2017
)
0.46
"We predicted 34 pharmacokinetic drug-drug interactions with the secretagogues, nine moderate and 25 weak."( Biomedical Informatics Approaches to Identifying Drug-Drug Interactions: Application to Insulin Secretagogues.
Bilker, WB; Brensinger, CM; Chiang, C; Han, X; Hennessy, S; Leonard, CE; Li, L, 2017
)
0.46
"The self-controlled case series design has the potential to be widely applicable to screening for drug-drug interactions that lead to adverse outcomes identifiable in healthcare databases."( Biomedical Informatics Approaches to Identifying Drug-Drug Interactions: Application to Insulin Secretagogues.
Bilker, WB; Brensinger, CM; Chiang, C; Han, X; Hennessy, S; Leonard, CE; Li, L, 2017
)
0.46
"d for 14 days and on the 14th day all three groups were administered with 1 mg/kg Glibenclamide."( Effect of Tinospora cordifolia aqua-alcoholic extract on pharmacokinetic of Glibenclamide in rat: An herb-drug interaction study.
Ahmed, T; Punde, R; Sahu, R; Sangana, R; Subudhi, BB, 2018
)
0.48
" The purpose of this study was to explore the effect of glipizide combined with ANP on breast cancer growth and metastasis."( Glipizide Combined with ANP Suppresses Breast Cancer Growth and Metastasis by Inhibiting Angiogenesis through VEGF/VEGFR2 Signaling.
Cao, J; Li, J; Liu, X; Mao, G; Qi, C; Wang, L; Zhang, Q; Zheng, L; Zheng, S; Zhou, Q, 2022
)
2.41
"This study aimed at investigating the effect of glipizide combined with ANP on breast cancer."( Glipizide Combined with ANP Suppresses Breast Cancer Growth and Metastasis by Inhibiting Angiogenesis through VEGF/VEGFR2 Signaling.
Cao, J; Li, J; Liu, X; Mao, G; Qi, C; Wang, L; Zhang, Q; Zheng, L; Zheng, S; Zhou, Q, 2022
)
2.42
"Glipizide combined with ANP was found to inhibit breast cancer growth and metastasis in MMTV-PyMT mice, which spontaneously develop breast cancer."( Glipizide Combined with ANP Suppresses Breast Cancer Growth and Metastasis by Inhibiting Angiogenesis through VEGF/VEGFR2 Signaling.
Cao, J; Li, J; Liu, X; Mao, G; Qi, C; Wang, L; Zhang, Q; Zheng, L; Zheng, S; Zhou, Q, 2022
)
3.61
"These results demonstrate that glipizide combined with ANP has a greater potential than glipizide alone to be repurposed as an effective agent for the treatment of breast cancer by targeting tumor-induced angiogenesis."( Glipizide Combined with ANP Suppresses Breast Cancer Growth and Metastasis by Inhibiting Angiogenesis through VEGF/VEGFR2 Signaling.
Cao, J; Li, J; Liu, X; Mao, G; Qi, C; Wang, L; Zhang, Q; Zheng, L; Zheng, S; Zhou, Q, 2022
)
2.45
" GLZ was administered alone and in combination with APE or AND to normal and diabetic rats."( Pharmacokinetic Herb-Drug Interactions of Glipizide with
Amalia Prihati, D; Lukitaningsih, E; Nugroho, AE; Nurrochmad, A; Puspitasari, I; Sundhani, E, 2022
)
0.99

Bioavailability

The bioavailability of glipizide, plasma glucose, and insulin levels were measured in seven patients with non-insulin-dependent diabetes mellitus. A male Caucasian who participated in six bioavailability studies in our laboratory over a period of several years showed extremely low clearance of two drugs.

ExcerptReferenceRelevance
" This delay of absorption may be clinically relevant, since the efficacy of short-acting sulphonylureas is dependent upon the absorption rate of the drug."( Hyperglycaemia and absorption of sulphonylurea drugs.
DeFronzo, RA; Groop, LC; Luzi, L; Melander, A, 1989
)
0.28
" Post-dose glipizide concentrations were three times higher than those of glibenclamide, due to the incomplete bioavailability of the latter."( Pharmacokinetics and metabolic effects of glibenclamide and glipizide in type 2 diabetics.
Fyhrqvist, F; Groop, L; Groop, PH; Melander, A; Tolppanen, EM; Tötterman, KJ; Wåhlin-Boll, E, 1985
)
0.9
" Glyburide and glipizide are well absorbed after oral administration."( Glyburide and glipizide, second-generation oral sulfonylurea hypoglycemic agents.
Prendergast, BD,
)
0.84
"The bioavailability of glipizide, plasma glucose, and insulin levels were measured in seven patients with non-insulin-dependent diabetes mellitus."( Bioavailability of glipizide and its effect on blood glucose and insulin levels in patients with non-insulin-dependent diabetes.
Jones, RL; Peterson, CM; Rieders, F; Sims, RV,
)
0.77
" Food did not affect the bioavailability of any of the four drugs, but delayed Gz absorption."( Kinetics-effect relations of glipizide and other sulfonylureas.
Melander, A; Sartor, G; Scherstén, B; Wåhlin-Boll, E, 1980
)
0.55
" The bioavailability of glipizide was apparently greater than that of glibenclamide."( Comparative single-dose kinetics and effects of four sulfonylureas in healthy volunteers.
Melander, A; Sartor, G; Scherstén, B; Wåhlin-Boll, E, 1980
)
0.57
" Food intake did not influence the peak concentration, the elimination half-life or the bioavailability of the drug."( Influence of food intake on the absorption and effect of glipizide in diabetics and in healthy subjects.
Melander, A; Sartor, G; Scherstén, B; Wåhlin-Boll, E, 1980
)
0.51
" Gastrointestinal bioavailability was 100%."( Bioavailability, pharmacokinetics and effects of glipizide in type 2 diabetics.
Almér, LO; Melander, A; Wåhlin-Boll, E,
)
0.39
"The pharmacokinetics and bioavailability of glipizide were studied in 8 healthy male volunteers after a single oral dose of 5 mg in capsule or in tablet."( [Pharmacokinetics and bioavailability of glipizide capsules].
Chao, CH; Chen, QC; Chen, WL; Li, XN; Ma, YG; Yang, CQ, 1995
)
0.82
" A male Caucasian who participated in six bioavailability studies in our laboratory over a period of several years showed extremely low clearance of two drugs: phenytoin and glipizide (both substrates of CYP2C9), but not for nifedipine (a CYP3A4 substrate) and chlorpheniramine (a CYP2D6 substrate)."( Pharmacokinetics of chlorpheniramine, phenytoin, glipizide and nifedipine in an individual homozygous for the CYP2C9*3 allele.
Blaisdell, J; Dalton, JT; Goldstein, JA; Kidd, RS; Meyer, MC; Straughn, AB, 1999
)
0.75
"The quantitative structure-bioavailability relationship of 232 structurally diverse drugs was studied to evaluate the feasibility of constructing a predictive model for the human oral bioavailability of prospective new medicinal agents."( QSAR model for drug human oral bioavailability.
Topliss, JG; Yoshida, F, 2000
)
0.31
" The absorption rate of glibenclamide and tolbutamide was not affected by food."( [Timing of administration of sulfonyl urea derivatives].
de Smet, PA; Fischer, HR, 2000
)
0.31
" This study demonstrated that factors such as high pH and high ionic strength can alter drug-protein binding and consequently increase free drug in plasma and increase bioavailability of slightly water insoluble drug such as antidiabetic drugs."( Protein binding of glipizide using equilibrium dialysis technique: effects of hydrogen ion concentration, drug concentration and ionic strength.
Garcia, JJ; Ghaly, ES, 2001
)
0.64
" Developed bioadhesive spheres and tablets increase the solubility of glipizide which may increase its bioavailability and also increased the adherence of the bioadhesive systems to the mucous membrane so that once daily dose can be administered."( Evaluation of bioadhesive glipizide spheres and compacts from spheres prepared by extruder/marumerizer technique.
Garcia, J; Ghaly, ES, 2001
)
0.84
"In a single-dose, four-period, four-treatment, Latin-square crossover study, the bioavailability of immediate-release glipizide 5mg (Glynase) [GL], extended-release glipizide 5mg (Glynase) XL [GLXL], Glucotrol XL [GTXL], and the new formulation developed in our laboratory [GLPF]) was compared."( Bioavailability of immediate- and extended-release formulations of glipizide in healthy male volunteers.
Dash, RJ; Dhawan, S; Garg, SK; Hota, D; Singh, B; Singla, AK; Sinha, VR, 2006
)
0.78
" Oral therapy with glipizide comprises problems of bioavailability fluctuations and may be associated with severe hypoglycaemia and gastric disturbances."( A transdermal delivery system for glipizide.
Ammar, HO; El-Nahhas, SA; Elmotasem, H; Ghorab, M; Salama, HA, 2006
)
0.94
" Cannula-bleeding, especially coupled with automated blood-collection techniques, has become the most efficient way for pharmaceutical industry to perform rat bioavailability studies."( Pharmacokinetic comparisons of tail-bleeding with cannula- or retro-orbital bleeding techniques in rats using six marketed drugs.
Bina, H; Chiang, A; Ebbert, L; Huang, NH; Hui, YH; Kern, T; Maples, C; Patel, N; Pritt, M,
)
0.13
" Human oral bioavailability is an important pharmacokinetic property, which is directly related to the amount of drug available in the systemic circulation to exert pharmacological and therapeutic effects."( Hologram QSAR model for the prediction of human oral bioavailability.
Andricopulo, AD; Moda, TL; Montanari, CA, 2007
)
0.34
"Oral bioavailability (F) is a product of fraction absorbed (Fa), fraction escaping gut-wall elimination (Fg), and fraction escaping hepatic elimination (Fh)."( Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
Chang, G; El-Kattan, A; Miller, HR; Obach, RS; Rotter, C; Steyn, SJ; Troutman, MD; Varma, MV, 2010
)
0.36
"The purpose of this study was to evaluate the potential of a newly modified cyclodextrin derivative, water-soluble β-cyclodextrin-epichlorohydrin polymer (β-CDP), as an effective drug carrier to enhance the dissolution rate and oral bioavailability of glipizide as a poorly water-soluble model drug."( In vitro and in vivo studies on the complexes of glipizide with water-soluble β-cyclodextrin-epichlorohydrin polymers.
Liu, Y; Nie, S; Pan, W; Zhang, S, 2011
)
0.8
" The relative bioavailability (BA) was approximately 92% at 10 mg and 79% at 30 mg dose."( Comparative pharmacokinetics studies of immediate- and modified-release formulations of glipizide in pigs and dogs.
Cox, A; Knipp, GT; Kulkarni, R; McCain, R; Ruterbories, K; Tang, CC; Wang, Z; Yumibe, N; Zhang, X, 2012
)
0.6
" In this work, enhancement of the solubility and dissolution of the practically insoluble drug glipizide was achieved by formation of bionanocomposites (BNCs) using microwave-induced diffusion (MIND), which ultimately leads to bioavailability enhancement."( Microwave-generated bionanocomposites for solubility and dissolution enhancement of poorly water-soluble drug glipizide: in-vitro and in-vivo studies.
Gattani, SG; Kushare, SS, 2013
)
0.82
" In-vivo pharmacokinetic study in rabbits revealed that the relative bioavailability of GPZ from MW-SD tablets improved greatly (153."( Microwave-induced solid dispersion technology to improve bioavailability of glipizide.
Ganguly, S; Ghosh, A; Isaac, J; Kaity, S, 2013
)
0.62
"MW-induced SD technology could be a better alternative to CH-SD for the enhanced solubility and bioavailability of GPZ."( Microwave-induced solid dispersion technology to improve bioavailability of glipizide.
Ganguly, S; Ghosh, A; Isaac, J; Kaity, S, 2013
)
0.62
" Bioavailability in vivo was determined by administering the compression-coated tablets to rabbits in contrast with Glucotrol XL(®)."( Compression-coated tablets of glipizide using hydroxypropylcellulose for zero-order release: in vitro and in vivo evaluation.
Chen, H; Chen, Q; Huang, H; Qi, X; Rui, Y; Wu, Z; Xing, J; Zhang, H, 2013
)
0.68
" In-vitro buoyancy and dissolution studies showed that non-effervescent floating drug delivery systems provide a promising method of achieving prolonged gastric retention time and improved bioavailability of glipizide."( Preparation and in vitro characterization of a non-effervescent floating drug delivery system for poorly soluble drug, glipizide.
Dharmalingham, SR; Gorajana, A; Meka, VS; Pillai, S; Sheshala, R,
)
0.53
" Compared with conventional tablets, the EOP tablet demonstrates a controlled release behavior with relative bioavailability of 99."( Synchronized and controlled release of metformin hydrochloride/glipizide from elementary osmotic delivery.
Chen, T; Jing, H; Pan, H; Pan, W; Yang, X, 2017
)
0.69
" Hence, it was concluded that glipizide-stearic acid co-crystals could offer an improved drug design strategy to overcome dissolution and bioavailability related challenges associated with lipophilic glipizide."( Stable Co-crystals of Glipizide with Enhanced Dissolution Profiles: Preparation and Characterization.
Bawa, P; Garg, V; Gaur, T; Gowthamarajan, K; Gulati, M; Kumar, B; Narang, R; Pandey, NK; Rajesh, SY; Sehal, HR; Sharma, P; Singh, SK, 2017
)
1.06
" In conclusion, AZI can decrease the bioavailability of GZ, and hence, it should be cautiously used."( Effect of Aqueous Extract of Azadirachta indica Leaves on Pharmacokineics and Pharmacodynamics of Glipizide.
Ali, M; Chaudhari, S; Zambad, S, 2019
)
0.73
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51
" The oral bioavailability of the glipizide-phospholipid nanocomplex was measured by using HPLC in Wistar rats' plasma."( Formulation, Characterization, and Pharmacokinetic Evaluation of Novel Glipizide-phospholipid Nano-complexes with Improved Solubility and Bio-availability.
Bhatt, DC; Rathor, S, 2022
)
1.24

Dosage Studied

Glipizide is well tolerated, but careful adjustment of dosage and attention to diet may be needed to avoid hypoglycaemic symptoms a few hours after a single daily dose.

ExcerptRelevanceReference
" Glipizide is well tolerated, but careful adjustment of dosage and attention to diet may be needed to avoid hypoglycaemic symptoms a few hours after a single daily dose."( Glipizide: a review of its pharmacological properties and therapeutic use.
Avery, GS; Brogden, RN; Heel, RC; Pakes, GE; Speight, TM, 1979
)
2.61
" It is concluded that, in the dosage used, intravenous glipizide probably has no hypoglycaemic effects in insulin-dependent diabetics."( Plasma levels of glucose and lactate after intravenous glipizide administration in some insulin-dependent diabetics. Therapeutic effects of an associated glipizide-insulin treatment.
Boni, C; Buzzigoli, G; Giampietro, O; Navalesi, R, 1979
)
0.75
" 24 maturity-onset diabetics were studied to determine the dosage required to produce adequate control and the safety and tolerance of the drug."( A clinical trial with glipizide - a relative new sulphonylurea.
Singarayar, J; Sunderam, S,
)
0.45
"The clinically effective duration of blood glucose lowering action of a new hypoglycaemic sulphonylurea, glipizide, given in single before breakfast dosage (up to 20 mg) has been studied in 20 apparently insulin-independent diabetics."( [Duration of effective hypoglycaemic action of glipizide given once daily (author's transl)].
Azzopardi, J; Campbell, IW; Clarke, BF; Duncan, LJ, 1975
)
0.73
" The most frecuently used dosage was 5 mg daily, with a minimum of 2,5 mg and a maximum of 30 mg."( [Clinical evaluation of glipizide. Results of a multicentric study in Spain].
Calvet, J; Cerdeño, VM; Passigli, AG; Soler, J,
)
0.44
" Seventy-five percent of patients receiving glyburide were controlled with once-daily dosing compared with 29."( Glyburide versus glipizide in the treatment of patients with non-insulin-dependent diabetes mellitus.
Bloomgarden, Z; Kilo, C; Meenan, A,
)
0.47
"Randomized (between agents and in order of dosing regimens), prospective, open, crossover study among 14 NIDDM patients to compare glucose, insulin, and C-peptide responses to a standard diet and to 10 mg of oral GP or GB taken without food 1) after 2 wk without therapy, 2) after 4 wk of either GP (n = 7) or GB (n = 7) treatment OD, and 3) after 4 wk of TD therapy with the same agent."( Chronic sulfonylurea therapy augments basal and meal-stimulated insulin secretion while attenuating insulin responses to sulfonylurea per se.
Bird, DM; Cameron, DP; Ma, A; McIntyre, HD; Patterson, CA, 1992
)
0.28
"Therapeutic equivalence of OD and TD dosing with GP and GB during chronic therapy."( Chronic sulfonylurea therapy augments basal and meal-stimulated insulin secretion while attenuating insulin responses to sulfonylurea per se.
Bird, DM; Cameron, DP; Ma, A; McIntyre, HD; Patterson, CA, 1992
)
0.28
" Gluburide, as adjunctive therapy, may reduce the daily dosage needed by those who require insulin."( Glyburide in non-insulin-dependent diabetes: an update.
Kolterman, OG,
)
0.13
"Despite extensive clinical experience with second-generation oral hypoglycemic agents, the relative dosing equivalence of glyburide and glipizide remains controversial."( Conversion from glipizide to glyburide: a prospective cost-impact survey.
Alexis, G; Henault, R; Sparr, HB,
)
0.68
"The effect of a rapid-acting sulphonylurea, glipizide, on the dose-response relationship between the beta-cell response (insulin and C-peptide secretion) and the ambient plasma glucose concentration was examined in 12 healthy and 6 non-insulin-dependent diabetic subjects."( Effect of sulphonylurea on glucose-stimulated insulin secretion in healthy and non-insulin dependent diabetic subjects: a dose-response study.
Bonadonna, RC; DeFronzo, RA; Groop, LC; Luzi, L; Melander, A; Petrides, A; Ratheiser, K; Simonson, DC; Widén, E, 1991
)
0.54
" The dosage was adjusted to obtain adequate control or up to the maximum recommended dosage."( Efficacy of gliclazide in comparison with other sulphonylureas in the treatment of NIDDM.
Harrower, AD, 1991
)
0.28
" Insulin dosage fell in the glipizide group from 36 to 26 U day-1, as 4 patients experienced hypoglycaemic symptoms."( Combination of insulin with glipizide increases peripheral glucose disposal in secondary failure type 2 diabetic patients.
Reckless, JP; Simpson, HC; Stirling, CA; Sturley, R, 1990
)
0.87
" The purpose of this study was to determine the effects of aging, the presence of NIDDM, and multiple dosing on the pharmacokinetics of glipizide, an oral hypoglycemic drug."( Glipizide pharmacokinetics: effects of age, diabetes, and multiple dosing.
Bauer, LA; Horn, JR; Kobayashi, KA; Kradjan, WA; Opheim, KE; Wood, FJ, 1989
)
1.92
" Further study is required to determine whether significant pharmacokinetic differences between young and elderly subjects appear with multiple dosing of glipizide."( Glipizide pharmacokinetics in young and elderly volunteers.
Bauer, LA; Horn, JR; Kobayashi, KA; Kradjan, WA; Opheim, K; Wood, F, 1988
)
1.92
"The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of glyburide and glipizide, two second-generation oral sulfonylurea hypoglycemic agents, are reviewed."( Glyburide and glipizide, second-generation oral sulfonylurea hypoglycemic agents.
Prendergast, BD,
)
0.7
" Indobufen was first given as a single 200 mg dose and then for a 5 day period in a dosage of 200 mg twice daily, to six healthy volunteers."( Indobufen interacts with the sulphonylurea, glipizide, but not with the beta-adrenergic receptor antagonists, propranolol and atenolol.
Elvander-Ståhl, E; Melander, A; Wåhlin-Boll, E, 1984
)
0.53
" The AUCs did not differ between the two dosage regimens."( Glipizide pharmacokinetics and response in diabetics.
Huupponen, R; Iisalo, E; Seppälä, P, 1982
)
1.71
" For each of the four drugs, the steady state concentrations showed very large between-patient variations, not attributable to dosage or weight differences but to individual differences in drug kinetics and to insufficient compliance."( Kinetics-effect relations of glipizide and other sulfonylureas.
Melander, A; Sartor, G; Scherstén, B; Wåhlin-Boll, E, 1980
)
0.55
" In accordance with the augmented physiologic insulin release in the morning, a single morning dose of sulfonylureas may be the preferable dosage regimen in the treatment of elderly insulin-independent diabetics of moderate degree."( Diurnal pattern of plasma insulin and blood glucose during glibenclamide and glipizide therapy in elderly diabetics.
Groop, L; Harno, K, 1980
)
0.49
"05) increased by glipizide treatment at both insulin dosage levels (paired analysis)."( Selective potentiation of insulin-mediated glucose disposal in normal dogs by the sulfonylurea glipizide.
Andersen, DK; Jones, RS; Lebovitz, HE; Putnam, WS, 1981
)
0.82
"Randomized (in order of dosing regimens), open-label, crossover study."( Pharmacokinetics and pharmacodynamics of glipizide after once-daily and divided doses.
Kradjan, WA; Opheim, KE; Takeuchi, KY; Wood, FC,
)
0.4
"Glipizide peak concentrations and time to peak differed significantly with the dosage schedule; when smaller doses were administered more often, peak concentrations were lower and more delayed."( Pharmacokinetics and pharmacodynamics of glipizide after once-daily and divided doses.
Kradjan, WA; Opheim, KE; Takeuchi, KY; Wood, FC,
)
1.84
"The appropriate use of second-generation oral hypoglycemic agents is limited by the lack of definitive guidelines for their use in elderly diabetic patients and controversy over relative dosing equivalence."( Conversion from glipizide to glyburide: long-term follow-up of a cost-impact survey focusing on the elderly.
Alexis, G; Henault, R; Sparr, HB,
)
0.48
"To determine the pharmacokinetics and pharmacodynamics of glipizide after a single dose and 12 weeks of dosing in patients with type II diabetes mellitus, and evaluate the influence of aging."( The influence of multiple dosing and age on the pharmacokinetics and pharmacodynamics of glipizide in patients with type II diabetes mellitus.
Ducharme, MP; Edwards, DJ; Grunberger, G; Jaber, LA; Slaughter, RL,
)
0.6
"insulin: baseline 698 +/- 327, single dose 954 +/- 461, long-term dosing 945 +/- 600 pmol/L/hr)."( The influence of multiple dosing and age on the pharmacokinetics and pharmacodynamics of glipizide in patients with type II diabetes mellitus.
Ducharme, MP; Edwards, DJ; Grunberger, G; Jaber, LA; Slaughter, RL,
)
0.35
"Long-term dosing and aging have little effect on the pharmacokinetic profile of glipizide."( The influence of multiple dosing and age on the pharmacokinetics and pharmacodynamics of glipizide in patients with type II diabetes mellitus.
Ducharme, MP; Edwards, DJ; Grunberger, G; Jaber, LA; Slaughter, RL,
)
0.58
"To investigate the efficacy, safety, and dose-response characteristics of an extended-release preparation of glipizide using the gastrointestinal therapeutic system (GITS) on plasma glucose, glycosylated hemoglobin (HbA1c), and insulin secretion to a liquid-mixed meal in NIDDM patients."( Efficacy, safety, and dose-response characteristics of glipizide gastrointestinal therapeutic system on glycemic control and insulin secretion in NIDDM. Results of two multicenter, randomized, placebo-controlled clinical trials. The Glipizide Gastrointest
Feinglos, M; Fischette, CT; Kourides, IA; Shamoon, H; Simonson, DC, 1997
)
0.76
" It appears that the same dosage principles could be used for Caucasian and Chinese patients with type-2 diabetes when Gb or Gz are prescribed."( Effects and pharmacokinetics of oral glibenclamide and glipizide in Caucasian and Chinese patients with type-2 diabetes.
Chan, JC; Cockram, CS; Critchley, JA; Hallengren, B; Jönsson, A; Melander, A; Rydberg, T; Vaaler, S, 2000
)
0.55
"A simple, precise and accurate high performance liquid chromatography (HPLC) method was developed for the simultaneous estimation of metformin with gliclazide and glipizide present in multicomponent dosage forms."( ION-pair liquid chromatography technique for the estimation of metformin in its multicomponent dosage forms.
Ravi, J; Ravisankar, S; Suresh, B; Vasudevan, M, 2001
)
0.51
"To compare prescribing, dosage and blood glucose levels in patients with type 2 diabetes in two communities with differences in anti-hyperglycaemic drug utilization."( Differences in pharmacotherapy and in glucose control of type 2 diabetes patients in two neighbouring towns: a longitudinal population-based study.
Gottsäter, M; Lindberg, G; Lindwall, K; Melander, A; Olsson, J; Tisell, A, 2001
)
0.31
" However, there were pronounced between-town differences in dosage and glucose control."( Differences in pharmacotherapy and in glucose control of type 2 diabetes patients in two neighbouring towns: a longitudinal population-based study.
Gottsäter, M; Lindberg, G; Lindwall, K; Melander, A; Olsson, J; Tisell, A, 2001
)
0.31
"We evaluated differences in adherence and persistence with prescribed therapy of once-daily (OD) dosing compared with twice-daily (BID) dosing of glipizide in patients with type 2 diabetes."( Effects of once-daily and twice-daily dosing on adherence with prescribed glipizide oral therapy for type 2 diabetes.
Dezii, CM; Kawabata, H; Tran, M, 2002
)
0.75
" These data suggest that dosing frequency exerts a greater impact on patient adherence and persistence than number of tablets per dose."( Effects of once-daily and twice-daily dosing on adherence with prescribed glipizide oral therapy for type 2 diabetes.
Dezii, CM; Kawabata, H; Tran, M, 2002
)
0.55
"This study was designed to compare the pharmacokinetic and short-term pharmacodynamic profile of extended-release glipizide GITS (Glucotrol XL) given in a dosage of 20 mg once daily with that of immediate-release glipizide (Glucotrol) 10mg twice daily in patients with type II diabetes mellitus."( Pharmacokinetics and pharmacodynamics of extended-release glipizide GITS compared with immediate-release glipizide in patients with type II diabetes mellitus.
Canovatchel, W; Chaiken, RL; Chung, M; Kourides, I; Messig, M; Sutfin, T, 2002
)
0.77
" Awareness and application of this knowledge will improve drug use in clinical practice and provide the physician with further appreciation that standard drug dosing may not be appropriate in all patients."( Pharmacogenetics affects dosing, efficacy, and toxicity of cytochrome P450-metabolized drugs.
Bertino, JS; Nafziger, AN; Rogers, JF, 2002
)
0.31
"This paper describes the validation of a sensitive, accurate, and reproducible method for the determination of a release profile of glipizide from controlled-release dosage forms."( Performance liquid chromatographic analysis of glipizide: application to in vitro and in vivo studies.
Dhawan, S; Singla, AK, 2003
)
0.78
" The decision to prescribe one of these three insulinotropic agents should be based on factors such as the patient's ability to comply with complex dosing regimens, the need to control fasting hyperglycemia, the risk of interprandial hypoglycemia, and pharmacoeconomic considerations, rather than postprandial glucose-lowering efficacy."( Targeting postprandial hyperglycemia: a comparative study of insulinotropic agents in type 2 diabetes.
Carroll, MF; Castro, M; Gutierrez, A; Schade, DS; Tsewang, D, 2003
)
0.32
" The simultaneous determination of these analytes is important for the routine monitoring of diabetic patients who take combination medications and for studying the pharmacokinetics of the combined dosage forms."( The development and validation of liquid chromatography method for the simultaneous determination of metformin and glipizide, gliclazide, glibenclamide or glimperide in plasma.
Aburuz, S; McElnay, J; Millership, J, 2005
)
0.54
" In a separate study, five women were given a daily dosage (5 mg/day) of glyburide or glipizide, starting on the first postpartum day."( Transfer of glyburide and glipizide into breast milk.
Ambrose, PJ; Briggs, GG; Donat, DJ; Feig, DS; Klein, J; Koren, G; Kraemer, JM; Moskovitz, DN; Nageotte, M; Padilla, G; Wan, S, 2005
)
0.85
"We describe a patient with Stevens-Johnson syndrome (erythema multiforme major) associated with an increase in glipizide dosage administration."( Stevens-Johnson syndrome associated with glipizide therapy.
Anderson, RC; Cheng, JB; Cruz, PD, 2006
)
0.81
" We report such an experience where a patient in a long-term care facility received multi-day, excessive dosing of glipizide rather than her anti-spasticity medication, baclofen."( Look-alike medications: a formula for possible morbidity and mortality in the long-term care facility.
Grossberg, R; Reed, MD; Walliser, G, 2007
)
0.55
"Defining a quantitative and reliable relationship between in vitro drug release and in vivo absorption is highly desired for rational development, optimization, and evaluation of controlled-release dosage forms and manufacturing process."( Extended release dosage form of glipizide: development and validation of a level A in vitro-in vivo correlation.
Bhaumik, UK; Bose, A; Chakrabarty, US; Chatterjee, B; Ghosh, A; Gowda, V; Mandal, U; Pal, TK, 2008
)
0.63
" Three dosage groups were examined: glyburide 5 mg twice daily increased to 10 mg twice daily (GLYB), glipizide 5 mg twice daily increased to 10 mg twice daily (GLIPA), and glipizide 10 mg twice daily increased to 20 mg twice daily (GLIPB)."( Effect of sulfonylurea dose escalation on hemoglobin A1c in Veterans Affairs patients with type 2 diabetes.
Bartley, EP; Hurren, KM; O'Neill, JL; Ronis, DL, 2013
)
0.61
"To (a) identify whether hemoglobin A1c remained equivalent in patients converted from glyburide to glipizide, (b) evaluate the prevalence of hypoglycemia during treatment with glyburide or glipizide, (c) compare change in glycemic control for renally impaired versus nonimpaired patients, and (d) analyze dosage conversion ratios selected by providers and measures of patient follow-up after conversion including time until A1c measurement and number of glipizide dose titrations."( Glycemic control and hypoglycemia in Veterans Health Administration patients converted from glyburide to glipizide.
Cantrell, M; Egge, JA; Shaw, RF; Skoff, RA; Waterbury, NV, 2011
)
0.8
" 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
)
0.89
" Drug release was nearly independent of paddle speeds of 50 and 100 rpm releasing 80% over 14 h similar to the commercial glipizide osmotic pump tablet during dissolution testing while keeping the benefits of multiparticular dosage forms."( Compression of coated drug beads for sustained release tablet of glipizide: formulation, and dissolution.
Ayres, JW; Christensen, JM; Nguyen, C, 2014
)
0.85
" The mechanism for zero-order release of these compression-coated tablets was solvent penetration into the dosage form and drug dissolution from the erosion of the gelled HPC matrix."( Compression-coated tablets of glipizide using hydroxypropylcellulose for zero-order release: in vitro and in vivo evaluation.
Chen, H; Chen, Q; Huang, H; Qi, X; Rui, Y; Wu, Z; Xing, J; Zhang, H, 2013
)
0.68
"Multiparticulate dosage forms are pharmaceutical formulations in which the active substance is present as number of small independent subunits."( Formulation and optimisation of sustained release spray-dried microspheres of glipizide using natural polysaccharide.
Bagal, A; Bhalekar, M; Gunjal, S; Madgulkar, A,
)
0.36
"52) and lower missed dosing (Peto odds ratio 11."( Effects and patient compliance of sustained-release versus immediate-release glipizides in patients with type 2 diabetes mellitus: a systematic review and meta-analysis.
Du, L; Li, H; Li, Y; Sun, X; Tian, H; Wang, L; Yuan, Q, 2011
)
0.6
" For the colesevelam coadministration periods, 3,750 mg once daily was dosed throughout the pharmacokinetic sampling period."( The effects of colesevelam HCl on the single-dose pharmacokinetics of glimepiride, extended-release glipizide, and olmesartan medoxomil.
He, L; Lee, J; Mendell-Harary, J; Tao, B; Walker, J; Wickremasingha, P; Wight, D, 2014
)
0.62
"The present work aims at the development of a low-cost controlled release system of glipizide beads embedded in pectin to overcome the problem of frequent dosing of drug."( Design and evaluation of mucoadhesive beads of glipizide as a controlled release drug delivery system.
Bera, K; Khanam, J; Mazumder, B; Mohanraj, KP, 2014
)
0.88
" We present an analysis that identifies metoprolol's jejunal permeability as the low/high permeability class benchmark anywhere throughout the intestinal tract; we show that the permeability of both glipizide and metoprolol matches/exceeds this threshold throughout the entire intestinal tract, accounting for their success as controlled-release dosage form."( The biopharmaceutics of successful controlled release drug product: Segmental-dependent permeability of glipizide vs. metoprolol throughout the intestinal tract.
Agbaria, R; Cohen, N; Dahan, A; Zur, M, 2015
)
0.82
"In this report, five compounds were dosed orally into rats."( Utility of capillary microsampling for rat pharmacokinetic studies: Comparison of tail-vein bleed to jugular vein cannula sampling.
Guo, Y; Ho, S; Korfmacher, W; Luo, Y; O'Shea, T; Shen, L; Snow, G; Sun, W; Wang, J; Wu, Z,
)
0.13
" These two mixtures were, therefore, subjected to studies for the evaluation of precompression parameters in order to find their amenability to satisfactory compression into tablet dosage form."( Stable amorphous binary systems of glipizide and atorvastatin powders with enhanced dissolution profiles: formulation and characterization.
Gulati, M; Narang, R; Singh, SK, 2017
)
0.73
"  Methotrexate, gemfibrozil and glipizide were used as test compounds and were dosed either orally or intravenously, followed by DBS collection and LC-MS/MS analysis to compare PK with various bleeding methods."( Evaluation and Optimization of Blood Micro-Sampling Methods: Serial Sampling in a Cross-Over Design from an Individual Mouse.
Barr, A; Hanes, J; Hui, YH; Kern, T; Masterson, N; Patel, NJ; Perkins, E; Ruterbories, K; Weller, J; Wickremsinhe, E,
)
0.41
" CoE combines oral medications with the IS without altering the quality of the native formulation, generating "digitized" medications for remote capture of dosing histories."( Digitizing Medicines for Remote Capture of Oral Medication Adherence Using Co-encapsulation.
Benson, CA; Blaschke, TF; Browne, SH; Haubrich, R; Moser, K; Muttera, L; Peloquin, C; Santillo, F; Savage, GM, 2018
)
0.48
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (3)

RoleDescription
hypoglycemic agentA drug which lowers the blood glucose level.
EC 2.7.1.33 (pantothenate kinase) inhibitorAn EC 2.7.1.* (phosphotransferases with an alcohol group as acceptor) inhibitor that interferes with the action of pantothenate kinase (EC 2.7.1.33).
insulin secretagogueA secretagogue that causes the secretion of insulin.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (4)

ClassDescription
N-sulfonylureaA urea in which one of the hydrogens attached to a nitrogen of the urea group is replaced by a sulfonyl group. The N-sulfonylurea moiety is a key group in various herbicides, as well as in a number of antidiabetic drugs used in the management of type 2 diabetis mellitus.
pyrazines
aromatic amideAn amide in which the amide linkage is bonded directly to an aromatic system.
monocarboxylic acid amideA carboxamide derived from a monocarboxylic acid.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (58)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, Beta-lactamaseEscherichia coli K-12Potency14.12540.044717.8581100.0000AID485294
acetylcholinesteraseHomo sapiens (human)Potency43.64860.002541.796015,848.9004AID1347398
hypoxia-inducible factor 1 alpha subunitHomo sapiens (human)Potency1.06823.189029.884159.4836AID1224846
RAR-related orphan receptor gammaMus musculus (house mouse)Potency14.96010.006038.004119,952.5996AID1159521
SMAD family member 2Homo sapiens (human)Potency54.94100.173734.304761.8120AID1346859
ATAD5 protein, partialHomo sapiens (human)Potency32.62940.004110.890331.5287AID493107
NFKB1 protein, partialHomo sapiens (human)Potency0.01120.02827.055915.8489AID895; AID928
SMAD family member 3Homo sapiens (human)Potency54.94100.173734.304761.8120AID1346859
GLI family zinc finger 3Homo sapiens (human)Potency32.89900.000714.592883.7951AID1259369; AID1259392
Microtubule-associated protein tauHomo sapiens (human)Potency44.66840.180013.557439.8107AID1468
AR proteinHomo sapiens (human)Potency31.32580.000221.22318,912.5098AID1259243; AID743036
thyroid stimulating hormone receptorHomo sapiens (human)Potency3.98110.001318.074339.8107AID926
EWS/FLI fusion proteinHomo sapiens (human)Potency21.06990.001310.157742.8575AID1259252; AID1259253; AID1259255; AID1259256
retinoic acid nuclear receptor alpha variant 1Homo sapiens (human)Potency68.58960.003041.611522,387.1992AID1159555
pregnane X nuclear receptorHomo sapiens (human)Potency21.68990.005428.02631,258.9301AID1346982
estrogen nuclear receptor alphaHomo sapiens (human)Potency61.64480.000229.305416,493.5996AID743069; AID743075
GVesicular stomatitis virusPotency13.80290.01238.964839.8107AID1645842
glucocerebrosidaseHomo sapiens (human)Potency35.48130.01268.156944.6684AID2101
peroxisome proliferator activated receptor gammaHomo sapiens (human)Potency27.53570.001019.414170.9645AID743191
vitamin D (1,25- dihydroxyvitamin D3) receptorHomo sapiens (human)Potency58.19650.023723.228263.5986AID743241
euchromatic histone-lysine N-methyltransferase 2Homo sapiens (human)Potency10.61010.035520.977089.1251AID504332
Bloom syndrome protein isoform 1Homo sapiens (human)Potency50.11870.540617.639296.1227AID2364; AID2528
cytochrome P450 2C19 precursorHomo sapiens (human)Potency0.50120.00255.840031.6228AID899
cytochrome P450 2C9 precursorHomo sapiens (human)Potency19.78310.00636.904339.8107AID883
chromobox protein homolog 1Homo sapiens (human)Potency23.77810.006026.168889.1251AID488953
potassium voltage-gated channel subfamily H member 2 isoform dHomo sapiens (human)Potency35.48130.01789.637444.6684AID588834
nuclear factor erythroid 2-related factor 2 isoform 1Homo sapiens (human)Potency59.52350.000627.21521,122.0200AID743202; AID743219
DNA polymerase iota isoform a (long)Homo sapiens (human)Potency100.00000.050127.073689.1251AID588590
gemininHomo sapiens (human)Potency0.00520.004611.374133.4983AID624296
survival motor neuron protein isoform dHomo sapiens (human)Potency1.25890.125912.234435.4813AID1458
cytochrome P450 3A4 isoform 1Homo sapiens (human)Potency12.58930.031610.279239.8107AID884; AID885
lamin isoform A-delta10Homo sapiens (human)Potency0.08910.891312.067628.1838AID1487
Gamma-aminobutyric acid receptor subunit piRattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Interferon betaHomo sapiens (human)Potency13.80290.00339.158239.8107AID1645842
HLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)Potency13.80290.01238.964839.8107AID1645842
Gamma-aminobutyric acid receptor subunit beta-1Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit deltaRattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-2Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-5Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-3Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-1Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-2Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-4Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-3Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-6Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Histamine H2 receptorCavia porcellus (domestic guinea pig)Potency19.78310.00638.235039.8107AID883
Gamma-aminobutyric acid receptor subunit alpha-1Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit beta-3Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit beta-2Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
GABA theta subunitRattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Inositol hexakisphosphate kinase 1Homo sapiens (human)Potency13.80290.01238.964839.8107AID1645842
Gamma-aminobutyric acid receptor subunit epsilonRattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
cytochrome P450 2C9, partialHomo sapiens (human)Potency13.80290.01238.964839.8107AID1645842
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
ATP-binding cassette sub-family C member 3Homo sapiens (human)IC50 (µMol)133.00000.63154.45319.3000AID1473740
Multidrug resistance-associated protein 4Homo sapiens (human)IC50 (µMol)133.00000.20005.677410.0000AID1473741
Bile salt export pumpHomo sapiens (human)IC50 (µMol)134.00000.11007.190310.0000AID1443980; AID1473738
Cytochrome P450 3A4Homo sapiens (human)IC50 (µMol)7.44730.00011.753610.0000AID428564
Canalicular multispecific organic anion transporter 1Homo sapiens (human)IC50 (µMol)133.00002.41006.343310.0000AID1473739
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (104)

Processvia Protein(s)Taxonomy
xenobiotic metabolic processATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
bile acid and bile salt transportATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transportATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
leukotriene transportATP-binding cassette sub-family C member 3Homo sapiens (human)
monoatomic anion transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transport across blood-brain barrierATP-binding cassette sub-family C member 3Homo sapiens (human)
prostaglandin secretionMultidrug resistance-associated protein 4Homo sapiens (human)
cilium assemblyMultidrug resistance-associated protein 4Homo sapiens (human)
platelet degranulationMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic metabolic processMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
bile acid and bile salt transportMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transportMultidrug resistance-associated protein 4Homo sapiens (human)
urate transportMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
cAMP transportMultidrug resistance-associated protein 4Homo sapiens (human)
leukotriene transportMultidrug resistance-associated protein 4Homo sapiens (human)
monoatomic anion transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
export across plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
transport across blood-brain barrierMultidrug resistance-associated protein 4Homo sapiens (human)
guanine nucleotide transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell activation involved in immune responseInterferon betaHomo sapiens (human)
cell surface receptor signaling pathwayInterferon betaHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to virusInterferon betaHomo sapiens (human)
positive regulation of autophagyInterferon betaHomo sapiens (human)
cytokine-mediated signaling pathwayInterferon betaHomo sapiens (human)
natural killer cell activationInterferon betaHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT proteinInterferon betaHomo sapiens (human)
cellular response to interferon-betaInterferon betaHomo sapiens (human)
B cell proliferationInterferon betaHomo sapiens (human)
negative regulation of viral genome replicationInterferon betaHomo sapiens (human)
innate immune responseInterferon betaHomo sapiens (human)
positive regulation of innate immune responseInterferon betaHomo sapiens (human)
regulation of MHC class I biosynthetic processInterferon betaHomo sapiens (human)
negative regulation of T cell differentiationInterferon betaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIInterferon betaHomo sapiens (human)
defense response to virusInterferon betaHomo sapiens (human)
type I interferon-mediated signaling pathwayInterferon betaHomo sapiens (human)
neuron cellular homeostasisInterferon betaHomo sapiens (human)
cellular response to exogenous dsRNAInterferon betaHomo sapiens (human)
cellular response to virusInterferon betaHomo sapiens (human)
negative regulation of Lewy body formationInterferon betaHomo sapiens (human)
negative regulation of T-helper 2 cell cytokine productionInterferon betaHomo sapiens (human)
positive regulation of apoptotic signaling pathwayInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell differentiationInterferon betaHomo sapiens (human)
natural killer cell activation involved in immune responseInterferon betaHomo sapiens (human)
adaptive immune responseInterferon betaHomo sapiens (human)
T cell activation involved in immune responseInterferon betaHomo sapiens (human)
humoral immune responseInterferon betaHomo sapiens (human)
positive regulation of T cell mediated cytotoxicityHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
adaptive immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, TAP-independentHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of T cell anergyHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
defense responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
detection of bacteriumHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of interleukin-12 productionHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of interleukin-6 productionHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protection from natural killer cell mediated cytotoxicityHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
innate immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of dendritic cell differentiationHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class IbHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
lipid hydroxylationCytochrome P450 3A4Homo sapiens (human)
lipid metabolic processCytochrome P450 3A4Homo sapiens (human)
steroid catabolic processCytochrome P450 3A4Homo sapiens (human)
xenobiotic metabolic processCytochrome P450 3A4Homo sapiens (human)
steroid metabolic processCytochrome P450 3A4Homo sapiens (human)
cholesterol metabolic processCytochrome P450 3A4Homo sapiens (human)
androgen metabolic processCytochrome P450 3A4Homo sapiens (human)
estrogen metabolic processCytochrome P450 3A4Homo sapiens (human)
alkaloid catabolic processCytochrome P450 3A4Homo sapiens (human)
monoterpenoid metabolic processCytochrome P450 3A4Homo sapiens (human)
calcitriol biosynthetic process from calciolCytochrome P450 3A4Homo sapiens (human)
xenobiotic catabolic processCytochrome P450 3A4Homo sapiens (human)
vitamin D metabolic processCytochrome P450 3A4Homo sapiens (human)
vitamin D catabolic processCytochrome P450 3A4Homo sapiens (human)
retinol metabolic processCytochrome P450 3A4Homo sapiens (human)
retinoic acid metabolic processCytochrome P450 3A4Homo sapiens (human)
long-chain fatty acid biosynthetic processCytochrome P450 3A4Homo sapiens (human)
aflatoxin metabolic processCytochrome P450 3A4Homo sapiens (human)
oxidative demethylationCytochrome P450 3A4Homo sapiens (human)
inositol phosphate metabolic processInositol hexakisphosphate kinase 1Homo sapiens (human)
phosphatidylinositol phosphate biosynthetic processInositol hexakisphosphate kinase 1Homo sapiens (human)
negative regulation of cold-induced thermogenesisInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol phosphate biosynthetic processInositol hexakisphosphate kinase 1Homo sapiens (human)
xenobiotic metabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
negative regulation of gene expressionCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bile acid and bile salt transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
heme catabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic export from cellCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transepithelial transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
leukotriene transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
monoatomic anion transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (62)

Processvia Protein(s)Taxonomy
ATP bindingATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type bile acid transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATP hydrolysis activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
icosanoid transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
guanine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
protein bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ATP bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type xenobiotic transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
urate transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
purine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type bile acid transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
efflux transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
15-hydroxyprostaglandin dehydrogenase (NAD+) activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATP hydrolysis activityMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
cytokine activityInterferon betaHomo sapiens (human)
cytokine receptor bindingInterferon betaHomo sapiens (human)
type I interferon receptor bindingInterferon betaHomo sapiens (human)
protein bindingInterferon betaHomo sapiens (human)
chloramphenicol O-acetyltransferase activityInterferon betaHomo sapiens (human)
TAP bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
signaling receptor bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protein bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
peptide antigen bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
TAP bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protein-folding chaperone bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
monooxygenase activityCytochrome P450 3A4Homo sapiens (human)
steroid bindingCytochrome P450 3A4Homo sapiens (human)
iron ion bindingCytochrome P450 3A4Homo sapiens (human)
protein bindingCytochrome P450 3A4Homo sapiens (human)
steroid hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
retinoic acid 4-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
oxidoreductase activityCytochrome P450 3A4Homo sapiens (human)
oxygen bindingCytochrome P450 3A4Homo sapiens (human)
enzyme bindingCytochrome P450 3A4Homo sapiens (human)
heme bindingCytochrome P450 3A4Homo sapiens (human)
vitamin D3 25-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
caffeine oxidase activityCytochrome P450 3A4Homo sapiens (human)
quinine 3-monooxygenase activityCytochrome P450 3A4Homo sapiens (human)
testosterone 6-beta-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
1-alpha,25-dihydroxyvitamin D3 23-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
anandamide 8,9 epoxidase activityCytochrome P450 3A4Homo sapiens (human)
anandamide 11,12 epoxidase activityCytochrome P450 3A4Homo sapiens (human)
anandamide 14,15 epoxidase activityCytochrome P450 3A4Homo sapiens (human)
aromatase activityCytochrome P450 3A4Homo sapiens (human)
vitamin D 24-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
estrogen 16-alpha-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
estrogen 2-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
1,8-cineole 2-exo-monooxygenase activityCytochrome P450 3A4Homo sapiens (human)
inositol-1,3,4,5,6-pentakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol heptakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 5-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
protein bindingInositol hexakisphosphate kinase 1Homo sapiens (human)
ATP bindingInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 1-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 3-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol 5-diphosphate pentakisphosphate 5-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol diphosphate tetrakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
protein bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
organic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type xenobiotic transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP hydrolysis activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (34)

Processvia Protein(s)Taxonomy
plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basal plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basolateral plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
nucleolusMultidrug resistance-associated protein 4Homo sapiens (human)
Golgi apparatusMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
membraneMultidrug resistance-associated protein 4Homo sapiens (human)
basolateral plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
platelet dense granule membraneMultidrug resistance-associated protein 4Homo sapiens (human)
external side of apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
extracellular spaceInterferon betaHomo sapiens (human)
extracellular regionInterferon betaHomo sapiens (human)
Golgi membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
endoplasmic reticulumHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
Golgi apparatusHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
plasma membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
cell surfaceHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
ER to Golgi transport vesicle membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
secretory granule membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
phagocytic vesicle membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
early endosome membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
recycling endosome membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular exosomeHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
lumenal side of endoplasmic reticulum membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
MHC class I protein complexHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular spaceHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
external side of plasma membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
cytoplasmCytochrome P450 3A4Homo sapiens (human)
endoplasmic reticulum membraneCytochrome P450 3A4Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 3A4Homo sapiens (human)
plasma membraneGamma-aminobutyric acid receptor subunit gamma-2Rattus norvegicus (Norway rat)
plasma membraneGamma-aminobutyric acid receptor subunit alpha-1Rattus norvegicus (Norway rat)
plasma membraneGamma-aminobutyric acid receptor subunit beta-2Rattus norvegicus (Norway rat)
fibrillar centerInositol hexakisphosphate kinase 1Homo sapiens (human)
nucleoplasmInositol hexakisphosphate kinase 1Homo sapiens (human)
cytosolInositol hexakisphosphate kinase 1Homo sapiens (human)
nucleusInositol hexakisphosphate kinase 1Homo sapiens (human)
cytoplasmInositol hexakisphosphate kinase 1Homo sapiens (human)
plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
cell surfaceCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
intercellular canaliculusCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (184)

Assay IDTitleYearJournalArticle
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID1347059CD47-SIRPalpha protein protein interaction - Alpha assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID588349qHTS for Inhibitors of ATXN expression: Validation of Cytotoxic Assay
AID1347405qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS LOPAC collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID504810Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347045Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot counterscreen GloSensor control cell line2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347057CD47-SIRPalpha protein protein interaction - LANCE assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347049Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot screen2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347151Optimization of GU AMC qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID504836Inducers of the Endoplasmic Reticulum Stress Response (ERSR) in human glioma: Validation2002The Journal of biological chemistry, Apr-19, Volume: 277, Issue:16
Sustained ER Ca2+ depletion suppresses protein synthesis and induces activation-enhanced cell death in mast cells.
AID1347058CD47-SIRPalpha protein protein interaction - HTRF assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347050Natriuretic polypeptide receptor (hNpr2) antagonism - Pilot subtype selectivity assay2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID588378qHTS for Inhibitors of ATXN expression: Validation
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347410qHTS for inhibitors of adenylyl cyclases using a fission yeast platform: a pilot screen against the NCATS LOPAC library2019Cellular signalling, 08, Volume: 60A fission yeast platform for heterologous expression of mammalian adenylyl cyclases and high throughput screening.
AID540299A screen for compounds that inhibit the MenB enzyme of Mycobacterium tuberculosis2010Bioorganic & medicinal chemistry letters, Nov-01, Volume: 20, Issue:21
Synthesis and SAR studies of 1,4-benzoxazine MenB inhibitors: novel antibacterial agents against Mycobacterium tuberculosis.
AID588519A screen for compounds that inhibit viral RNA polymerase binding and polymerization activities2011Antiviral research, Sep, Volume: 91, Issue:3
High-throughput screening identification of poliovirus RNA-dependent RNA polymerase inhibitors.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347153Confirmatory screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347152Confirmatory screen NINDS AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347168HepG2 cells viability qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347169Tertiary RLuc qRT-PCR qHTS assay for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347167Vero cells viability qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347149Furin counterscreen qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347161Confirmatory screen NINDS Rhodamine qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID599064Plasma protein binding in human2011Bioorganic & medicinal chemistry letters, Jun-15, Volume: 21, Issue:12
Lipophilicity of acidic compounds: impact of ion pair partitioning on drug design.
AID481442Transcellular permeability at pH 6.5 calculated from in vitro P app values in Caco-2 and/or MDCK cells2010Journal of medicinal chemistry, May-13, Volume: 53, Issue:9
How well can the Caco-2/Madin-Darby canine kidney models predict effective human jejunal permeability?
AID1698011Fraction unbound in human plasma
AID449417Antidiabetic activity against glucose loaded Wistar rat assessed as serum glucose level at 10 mg/kg, po by oral glucose tolerance test2009European journal of medicinal chemistry, Nov, Volume: 44, Issue:11
Stimulatory effect of apigenin-6-C-beta-L-fucopyranoside on insulin secretion and glycogen synthesis.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID5985271-Octanol-sodium citrate buffer distribution coefficient, log D of the compound at pH 5.5 by shake-flask method2011Bioorganic & medicinal chemistry letters, Jun-15, Volume: 21, Issue:12
Lipophilicity of acidic compounds: impact of ion pair partitioning on drug design.
AID1698004Fraction unbound in cynomolgus monkey plasma
AID1698007Ratio of drug level in human blood to plasma administered through iv dosing by LC-MS/MS analysis
AID699539Inhibition of human liver OATP1B1 expressed in HEK293 Flp-In cells assessed as reduction in E17-betaG uptake at 20 uM by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID428564Inhibition of CYP3A42009European journal of medicinal chemistry, Jul, Volume: 44, Issue:7
Comparative chemometric modeling of cytochrome 3A4 inhibitory activity of structurally diverse compounds using stepwise MLR, FA-MLR, PLS, GFA, G/PLS and ANN techniques.
AID540210Clearance in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1473739Inhibition of human MRP2 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID444055Fraction absorbed in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID311524Oral bioavailability in human2007Bioorganic & medicinal chemistry, Dec-15, Volume: 15, Issue:24
Hologram QSAR model for the prediction of human oral bioavailability.
AID540213Half life in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588216FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
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.
AID588215FDA HLAED, alkaline phosphatase increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID588219FDA HLAED, gamma-glutamyl transferase (GGT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID468443Inhibition of human FAAH at 1 uM2009Bioorganic & medicinal chemistry letters, Dec-01, Volume: 19, Issue:23
Mining biologically-active molecules for inhibitors of fatty acid amide hydrolase (FAAH): identification of phenmedipham and amperozide as FAAH inhibitors.
AID1473740Inhibition of human MRP3 overexpressed in Sf9 insect cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 10 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID444053Renal clearance in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID515780Intrinsic solubility of the compound in water2010Bioorganic & medicinal chemistry, Oct-01, Volume: 18, Issue:19
QSAR-based solubility model for drug-like compounds.
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID28681Partition coefficient (logD6.5)2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID386623Inhibition of 4-(4-(dimethylamino)styryl)-N-methylpyridinium uptake at human OCT1 expressed in HEK293 cells at 100 uM by confocal microscopy2008Journal of medicinal chemistry, Oct-09, Volume: 51, Issue:19
Structural requirements for drug inhibition of the liver specific human organic cation transport protein 1.
AID467613Volume of distribution at steady state in human2009European journal of medicinal chemistry, Nov, Volume: 44, Issue:11
Prediction of volume of distribution values in human using immobilized artificial membrane partitioning coefficients, the fraction of compound ionized and plasma protein binding data.
AID699541Inhibition of human liver OATP2B1 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E3S uptake at 20 uM incubated for 5 mins by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID1423682Induction of hypoglycemia in C57BL/6N mouse assessed as decrease in basal blood glucose levels at 10 mg/kg, po measured at 60 mins
AID588214FDA HLAED, liver enzyme composite activity2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1473738Inhibition of human BSEP overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-taurocholate in presence of ATP measured after 15 to 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID444052Hepatic clearance in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1698002Intrinsic clearance in cryopreserved human hepatocytes at 1 uM measured up to 120 mins by LC-MS/MS analysis
AID1698000Apparent permeability in dog MDCKII-LE cells at pH 7.4
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588218FDA HLAED, lactate dehydrogenase (LDH) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1697999Dissociation constant, acidic pKa of compound measured up to 18 mins by capillary electrophoresis
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1698001Lipophilicity, log D of the compound at pH 7.4 by by shake flask method
AID1698009Hepatic clearance in cynomolgus monkey at < 1 mg/kg, iv administered as cassette dosing
AID161273Inhibition of [125I]-I binding to ATP-inhibited Potassium channel receptor of Rat brain homogenate1990Journal of medicinal chemistry, Dec, Volume: 33, Issue:12
Expedient synthesis and biochemical properties of an [125I]-labeled analogue of glyburide, a radioligand for ATP-inhibited potassium channels.
AID1473741Inhibition of human MRP4 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588217FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1698010Hepatic clearance in human administered through iv dosing
AID711937Antidiabetic activity in C57BL/6N mouse assessed as reduction of blood glucose level at 10 mg/kg, po measured after 60 mins post administration2012ACS medicinal chemistry letters, Jun-14, Volume: 3, Issue:6
The Discovery of MK-4256, a Potent SSTR3 Antagonist as a Potential Treatment of Type 2 Diabetes.
AID699540Inhibition of human liver OATP1B3 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E17-betaG uptake at 20 uM incubated for 5 mins by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID449419Antidiabetic activity against glucose loaded Wistar rat assessed as serum glucose level at 10 mg/kg, po after 30 mins by oral glucose tolerance test2009European journal of medicinal chemistry, Nov, Volume: 44, Issue:11
Stimulatory effect of apigenin-6-C-beta-L-fucopyranoside on insulin secretion and glycogen synthesis.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID373867Hepatic clearance in human hepatocytes in absence of fetal calf serum2009European journal of medicinal chemistry, Apr, Volume: 44, Issue:4
First-principle, structure-based prediction of hepatic metabolic clearance values in human.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID467611Dissociation constant, pKa of the compound2009European journal of medicinal chemistry, Nov, Volume: 44, Issue:11
Prediction of volume of distribution values in human using immobilized artificial membrane partitioning coefficients, the fraction of compound ionized and plasma protein binding data.
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID444050Fraction unbound in human plasma2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID540209Volume of distribution at steady state in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID404304Effect on human MRP2-mediated estradiol-17-beta-glucuronide transport in Sf9 cells inverted membrane vesicles relative to control2008Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11
Prediction and identification of drug interactions with the human ATP-binding cassette transporter multidrug-resistance associated protein 2 (MRP2; ABCC2).
AID521220Inhibition of neurosphere proliferation of mouse neural precursor cells by MTT assay2007Nature chemical biology, May, Volume: 3, Issue:5
Chemical genetics reveals a complex functional ground state of neural stem cells.
AID1443980Inhibition of human BSEP expressed in fall armyworm sf9 cell plasma membrane vesicles assessed as reduction in vesicle-associated [3H]-taurocholate transport preincubated for 10 mins prior to ATP addition measured after 15 mins in presence of [3H]-tauroch2010Toxicological sciences : an official journal of the Society of Toxicology, Dec, Volume: 118, Issue:2
Interference with bile salt export pump function is a susceptibility factor for human liver injury in drug development.
AID444056Fraction escaping gut-wall elimination in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID27167Delta logD (logD6.5 - logD7.4)2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID444058Volume of distribution at steady state in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID425652Total body clearance in human2009Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15
Physicochemical determinants of human renal clearance.
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID29359Ionization constant (pKa)2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID444054Oral bioavailability in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID449420Antidiabetic activity against glucose loaded Wistar rat assessed as serum glucose level at 10 mg/kg, po after 60 mins by oral glucose tolerance test2009European journal of medicinal chemistry, Nov, Volume: 44, Issue:11
Stimulatory effect of apigenin-6-C-beta-L-fucopyranoside on insulin secretion and glycogen synthesis.
AID444051Total clearance in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID29811Oral bioavailability in human2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID444057Fraction escaping hepatic elimination in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
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.
AID598525Lipophilicity, log P of the compound2011Bioorganic & medicinal chemistry letters, Jun-15, Volume: 21, Issue:12
Lipophilicity of acidic compounds: impact of ion pair partitioning on drug design.
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID540211Fraction unbound in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID540212Mean residence time in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID425653Renal clearance in human2009Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15
Physicochemical determinants of human renal clearance.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID5985261-Octanol-water distribution coefficient, log D of the compound at pH 7.4 by shake-flask method2011Bioorganic & medicinal chemistry letters, Jun-15, Volume: 21, Issue:12
Lipophilicity of acidic compounds: impact of ion pair partitioning on drug design.
AID481439Absolute bioavailability in human2010Journal of medicinal chemistry, May-13, Volume: 53, Issue:9
How well can the Caco-2/Madin-Darby canine kidney models predict effective human jejunal permeability?
AID384955Intrinsic aqueous solubility at pH 10 by shake-flask method2008Journal of medicinal chemistry, May-22, Volume: 51, Issue:10
Molecular characteristics for solid-state limited solubility.
AID1698006Ratio of drug level in cynomolgus monkey blood to plasma administered through iv dosing by LC-MS/MS analysis
AID449418Antidiabetic activity against glucose loaded Wistar rat assessed as serum glucose level at 10 mg/kg, po after 15 mins by oral glucose tolerance test2009European journal of medicinal chemistry, Nov, Volume: 44, Issue:11
Stimulatory effect of apigenin-6-C-beta-L-fucopyranoside on insulin secretion and glycogen synthesis.
AID467612Fraction unbound in human plasma2009European journal of medicinal chemistry, Nov, Volume: 44, Issue:11
Prediction of volume of distribution values in human using immobilized artificial membrane partitioning coefficients, the fraction of compound ionized and plasma protein binding data.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID1347411qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).2014Journal of biomolecular screening, Jul, Volume: 19, Issue:6
A High-Throughput Assay to Identify Inhibitors of the Apicoplast DNA Polymerase from Plasmodium falciparum.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1224864HCS microscopy assay (F508del-CFTR)2016PloS one, , Volume: 11, Issue:10
Increasing the Endoplasmic Reticulum Pool of the F508del Allele of the Cystic Fibrosis Transmembrane Conductance Regulator Leads to Greater Folding Correction by Small Molecule Therapeutics.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (740)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990168 (22.70)18.7374
1990's164 (22.16)18.2507
2000's175 (23.65)29.6817
2010's190 (25.68)24.3611
2020's43 (5.81)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 103.90

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index103.90 (24.57)
Research Supply Index6.90 (2.92)
Research Growth Index4.57 (4.65)
Search Engine Demand Index192.40 (26.88)
Search Engine Supply Index2.01 (0.95)

This Compound (103.90)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials176 (21.52%)5.53%
Reviews37 (4.52%)6.00%
Case Studies49 (5.99%)4.05%
Observational0 (0.00%)0.25%
Other556 (67.97%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (40)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Incretin-based Drugs and the Risk of Heart Failure: A Multi-center Network Observational Study [NCT02456428]1,499,650 participants (Actual)Observational2014-03-31Completed
Sulfonylurea Safety and Effectiveness (SUSS) for Patients With Hyperglycemia and Pancreatic Ductal Adenocarcinoma: A Pragmatic Clinical Trial and Accompanying Retrospective Revie [NCT06168812]Phase 240 participants (Anticipated)Interventional2023-12-05Recruiting
A Multi-center, Double-blind, Placebo-controlled, Randomized Study to Compare the Effect of a Subcutaneous Canakinumab Administration to Placebo in Patients With Impaired Glucose Tolerance or Patients With Type 2 Diabetes Treated With Differing Baseline D [NCT01068860]Phase 2246 participants (Actual)Interventional2010-02-28Completed
Investigate the Relationship Between CYP2C19 Genetic Polymorphisms and Pharmacokinetics of Glipizide in Healthy Chinese Subjects [NCT01082796]14 participants (Actual)Interventional2009-11-30Completed
A Multicenter, Double-Blind, Randomized Study to Evaluate the Safety and Efficacy of the Addition of MK0431 Compared With Sulfonylurea Therapy in Patients With Type 2 Diabetes With Inadequate Glycemic Control on Metformin Monotherapy [NCT00094770]Phase 31,172 participants (Actual)Interventional2004-09-30Completed
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 Relative Bioavailability Study of 5 mg Glipizide/500 mg Metformin Hydrochloride Tablets Under Fasting Conditions. [NCT00835497]Phase 140 participants (Actual)Interventional2004-06-30Completed
Combination of Sulfonylureas and Insulin Glargine as Safety Net Outpatient Therapy for Unstable Diabetes and Impending Diabetic Ketoacidosis (DKA) [NCT00732524]Phase 480 participants (Actual)Interventional2004-09-30Completed
A 52-Week International, Multi-centre, Randomised, Parallel-group, Double-blind, Active-controlled, Phase III Study With a 156-Week Extension Period to Evaluate the Efficacy and Safety of Dapagliflozin in Combination With Metformin Compared With Sulphonyl [NCT00660907]Phase 31,217 participants (Actual)Interventional2008-03-31Completed
Open-Label, Randomized, Pharmacokinetic Study of Single-Dose Modified Release Glipizide in Healthy Volunteers [NCT05159427]Phase 140 participants (Anticipated)Interventional2022-03-15Recruiting
The Effect of Food on the Bioavailability of Glipizide [NCT00947024]Phase 118 participants (Actual)Interventional1993-11-30Completed
A Pilot Study of Outpatient Discharge Therapy With Saxagliptin + Metformin XR or Sulphonylurea for Recently Diagnosed Type 2 Diabetes Presenting With Severe Hyperglycemia [NCT01267448]Phase 4100 participants (Anticipated)Interventional2014-09-09Completed
A Multicenter, Randomized, Double-Blind Study to Evaluate the Safety and Efficacy of the Addition of MK0431 to Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Metformin Therapy [NCT00086515]Phase 3701 participants (Actual)Interventional2004-06-30Completed
Single-Dose Fasting In Vivo Bioequivalence Study of Glipizide and Metformin HCl Tablets (5 mg/500 mg; Mylan) to Metaglip® Tablets (5 mg/500 mg; Bristol-Myers Squibb) in Healthy Volunteers [NCT00649454]Phase 136 participants (Actual)Interventional2005-06-30Completed
An Open-Label, Randomized, Single-Dose, Two-Way Crossover Bioequivalence Study Of Glucotrol XL 2.5 Mg Tablets Manufactured At Brooklyn, New York Versus At Barceloneta, Puerto Rico In Healthy Subjects [NCT00550329]32 participants Observational2007-10-31Completed
A Multicenter, Randomized, Double-Blind Study to Evaluate the Efficacy and Safety of Sitagliptin Versus Glipizide in Patients With Type 2 Diabetes Mellitus and Chronic Renal Insufficiency Who Have Inadequate Glycemic Control [NCT00509262]Phase 3426 participants (Actual)Interventional2007-10-09Completed
A Phase III, 18 Month, Multicenter, Randomized, Double-Blind, Active-Controlled Clinical Trial to Compare Rosiglitazone Versus Glipizide on the Progression of Atherosclerosis in Subjects With Type 2 Diabetes Mellitus and Cardiovascular Disease (APPROACH) [NCT00116831]Phase 3672 participants (Actual)Interventional2005-01-31Completed
Single-Dose Food In Vivo Bioequivalence Study of Glipizide and Metformin HCl Tablets (5 mg/500 mg; Mylan) to Metaglip® Tablets (5 mg/500 mg; Bristol-Myers Squibb) in Healthy Volunteers [NCT00648505]Phase 136 participants (Actual)Interventional2005-06-30Completed
Comparison of Type 2 Diabetes Pharmacotherapy Regimens Using Targeted Learning [NCT05073692]270,000 participants (Anticipated)Observational2021-07-01Recruiting
Switching From Insulin to Sulfonylurea in Childhood and Adult Diabetes Due to Variants in the HNF1A, HNF4A, or HNF1B Genes [NCT04239586]Phase 430 participants (Anticipated)Interventional2017-04-18Enrolling by invitation
A Two-Way Crossover Bioequivalence Study Comparing Single 10 mg Doses of Geneva's 10 mg Glipizide Tablets To Roerig's 10 mg Glucotrol Tablets [NCT00946504]Phase 128 participants (Actual)Interventional1992-10-31Completed
A Phase III Randomized, Placebo-Controlled Clinical Trial to Study the Safety and Efficacy of the Addition of Sitagliptin (MK0431) in Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Combination Therapy With Metformin and a P [NCT00350779]Phase 3262 participants (Actual)Interventional2006-06-12Completed
Sitagliptin Study in Patients With Type 2 Diabetes Mellitus and Chronic Renal Insufficiency [NCT00095056]Phase 391 participants (Actual)Interventional2004-10-31Completed
A 4-month, Randomized, Double-blind, Placebo- and Active-Controlled, Multi-centre, Parallel-Group Study, With an Optional 2-month Extension, to Evaluate Efficacy, Safety and Tolerability of AZD1656 as Add-on Treatment to Metformin in Type 2 Diabetes Melli [NCT01020123]Phase 2530 participants (Actual)Interventional2009-10-31Completed
A Multicenter, Randomized, Double-Blind, Active-Controlled Study to Evaluate the Durability of the Efficacy and Safety of Alogliptin Compared to Glipizide When Used in Combination With Metformin in Subjects With Type 2 Diabetes [NCT00856284]Phase 32,639 participants (Actual)Interventional2009-03-31Completed
A Phase III Randomized, Placebo-Controlled Clinical Trial to Study the Safety and Efficacy of the Addition of Sitagliptin (MK-0431) in Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Combination Therapy With Metformin and Pi [NCT00885352]Phase 3313 participants (Actual)Interventional2009-04-15Completed
A Multicenter, Randomized Double-Blind Study to Evaluate the Efficacy and Safety of Sitagliptin Versus Glipizide in Participants With Type 2 Diabetes Mellitus and End-Stage Renal Disease Who Are on Dialysis and Who Have Inadequate Glycemic Control [NCT00509236]Phase 3129 participants (Actual)Interventional2007-10-19Completed
Phase 4 Study on the Prognosis and Effect of Anti-diabetic Drugs on Type-2 Diabetes Mellitus With Coronary Artery Disease [NCT00513630]Phase 4304 participants (Actual)Interventional2004-06-30Completed
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
An Open-label, Randomized , Phase 4 Study to Compare the Different Efficacies of α-glucosidase Inhibitor and Sulfonylurea on Improvement of Intestinal Microbiome and Serum Incretins in Patients With Type 2 Diabetes [NCT01758471]Phase 4160 participants (Anticipated)Interventional2012-12-31Recruiting
Study to Understand the Genetics of the Acute Response to Metformin and Glipizide in Humans [NCT01762046]Phase 11,000 participants (Anticipated)Interventional2008-01-31Active, not recruiting
Treatment of Early Insulinization With Glargine in Type 2 Diabetes Patients Uncontrolled on Sulfonylurea or Metformin Monotherapy [NCT00347100]Phase 4387 participants (Actual)Interventional2006-06-30Completed
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
Continuous Glucose Monitoring to Assess Glycemia in Chronic Kidney Disease - Changing Glucose Management [NCT02608177]3 participants (Actual)Interventional2015-11-30Completed
A Phase III, Multicenter, Randomized, Double-blind Study to Evaluate the Efficacy and Safety of MK-3102 Versus Placebo in Subjects With Type 2 Diabetes Mellitus With Moderate or Severe Chronic Kidney Disease or Kidney Failure on Dialysis Who Have Inadequa [NCT01698775]Phase 3213 participants (Actual)Interventional2012-10-02Completed
A Relative Bioavailability Study of 5 mg Glipizide/500 mg Metformin Hydrochloride Tablets Under Non-Fasting Conditions. [NCT00834587]Phase 140 participants (Actual)Interventional2004-06-30Completed
Ertugliflozin: Cardioprotective Effects on Epicardial Fat [NCT04167761]Early Phase 120 participants (Actual)Interventional2020-07-01Active, not recruiting
Effect of Farxiga on Renal Function and Size in Type 2 Diabetic Patients With Hyperfiltration [NCT02911792]Phase 472 participants (Actual)Interventional2016-12-20Completed
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
A Multicenter, Randomized, Double-Blind Study to Evaluate the Efficacy and Safety of Alogliptin Compared to Glipizide in Elderly Subjects With Type 2 Diabetes [NCT00707993]Phase 3441 participants (Actual)Interventional2008-06-30Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00086515 (3) [back to overview]Change From Baseline in Hemoglobin A1C (A1C) at Week 24
NCT00086515 (3) [back to overview]Change From Baseline in 2-hour Post-meal Glucose (PMG) at Week 24
NCT00086515 (3) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG) at Week 24
NCT00094770 (12) [back to overview]Hypoglycemic Events at Week 52
NCT00094770 (12) [back to overview]Number of Participants With Drug-related CAEs at Week 104
NCT00094770 (12) [back to overview]Number of Participants With Clinical Adverse Experiences (CAEs) at Week 104
NCT00094770 (12) [back to overview]Number of Participants With Laboratory Adverse Experiences (LAEs) at Week 104
NCT00094770 (12) [back to overview]Number of Participants With Serious CAEs at Week 104
NCT00094770 (12) [back to overview]Number of Participants With Serious LAEs at Week 104
NCT00094770 (12) [back to overview]Change From Baseline in Body Weight at Week 52
NCT00094770 (12) [back to overview]Change From Baseline in HbA1c at Week 104
NCT00094770 (12) [back to overview]Change From Baseline in Body Weight at Week 104
NCT00094770 (12) [back to overview]Change From Baseline in HbA1c at Week 52
NCT00094770 (12) [back to overview]Number of Participants With Drug-related LAEs at Week 104
NCT00094770 (12) [back to overview]Hypoglycemic Events at Week 104
NCT00095056 (2) [back to overview]Safety and Tolerability of Sitagliptin Over 54 Weeks
NCT00095056 (2) [back to overview]Safety and Tolerability of Sitagliptin After 12 Weeks of Treatment
NCT00116831 (36) [back to overview]Change From Baseline in Normalized Atheroma Volume
NCT00116831 (36) [back to overview]Change From Baseline in Percent Atheroma Volume (PAV) to Month 18
NCT00116831 (36) [back to overview]Change in Atheroma Volume Within the 10 mm of the Non-intervened Vessel Segment With the Greatest Atheroma Volume at Baseline
NCT00116831 (36) [back to overview]Model Adjusted Percent Change in Brain Natriuretic Peptide (BNP) From Baseline to Month 18
NCT00116831 (36) [back to overview]Number of Other Cardiovascular Events
NCT00116831 (36) [back to overview]Percent Change From Baseline to Month 18 in Apoprotein B (apoB)
NCT00116831 (36) [back to overview]Percent Change From Baseline to Month 18 in HDL-2
NCT00116831 (36) [back to overview]Percent Change From Baseline to Month 18 in HDL-3
NCT00116831 (36) [back to overview]Percent Change From Baseline to Month 18 in High Density Lipoprotein Cholesterol (HDL-c)
NCT00116831 (36) [back to overview]Percent Change From Baseline to Month 18 in Low Density Lipoprotein Cholesterol (LDL-c)
NCT00116831 (36) [back to overview]Percent Change From Baseline to Month 18 in Total Cholesterol (TC)
NCT00116831 (36) [back to overview]Percent Change From Baseline to Month 18 in Triglycerides (TG)
NCT00116831 (36) [back to overview]Percent Change in Brain Natriuretic Peptide (BNP) From Baseline to Month 18
NCT00116831 (36) [back to overview]Percent Change From Baseline to Month 18 in Free Fatty Acids (FFA)
NCT00116831 (36) [back to overview]Change in Atheroma Area Within the 10 mm of the Non-intervened Vessel Segment With the Greatest Atheroma Volume at Baseline
NCT00116831 (36) [back to overview]Repeated Measures Analysis of Percent Change in hsCRP From Baseline to Month 18
NCT00116831 (36) [back to overview]Repeated Measures Analysis of Percent Change in MMP 9 From Baseline to Month 18
NCT00116831 (36) [back to overview]Change From Baseline to Month 18 in LDL-c Peak Particle Density Measured by LDL Relative Flotation
NCT00116831 (36) [back to overview]Number of Participants With the Indicated Treatment Emergent Major Cardiovascular Events (MACE) for All-cause Death, Non-fatal MI, Non-fatal Stroke, Coronary Revascularization, or Hospitalization for Recurrent Myocardial Ischemia (MACE Composite 1)
NCT00116831 (36) [back to overview]Number of Participants With the Indicated Treatment Emergent Major Cardiovascular Events (MACE) for Cardiovascular Death, Nonfatal MI, or Nonfatal Stroke (MACE Composite 2)
NCT00116831 (36) [back to overview]Change From Baseline in Atheroma, Vessel, and Lumen Area to Month 18
NCT00116831 (36) [back to overview]Change From Baseline in Atheroma, Vessel, and Lumen Volume to Month 18
NCT00116831 (36) [back to overview]Model Adjusted Change in Atheroma Volume Within the 10 mm of the Non-intervened Vessel Segment With the Greatest Atheroma Volume at Baseline
NCT00116831 (36) [back to overview]Change From Baseline to Month 18 in LDL-c/HDL-c Ratio
NCT00116831 (36) [back to overview]Change From Baseline to Month 18 in Total Cholesterol/HDL-c Ratio
NCT00116831 (36) [back to overview]Model Adjusted Change From Baseline in Atheroma Area to Month 18
NCT00116831 (36) [back to overview]Model Adjusted Change From Baseline in Atheroma Volume to Month 18
NCT00116831 (36) [back to overview]Model Adjusted Change From Baseline in Lumen Area to Month 18
NCT00116831 (36) [back to overview]Model Adjusted Change From Baseline in Lumen Volume to Month 18
NCT00116831 (36) [back to overview]Model Adjusted Change From Baseline in Normalized Atheroma Volume
NCT00116831 (36) [back to overview]Model Adjusted Change From Baseline in Percent Atheroma Volume (PAV) to Month 18
NCT00116831 (36) [back to overview]Model Adjusted Change From Baseline in Vessel Area to Month 18
NCT00116831 (36) [back to overview]Model Adjusted Change From Baseline in Vessel Volume to Month 18
NCT00116831 (36) [back to overview]Model Adjusted Change in Atheroma Area Within the 10 mm of the Non-intervened Vessel Segment With the Greatest Atheroma Volume at Baseline
NCT00116831 (36) [back to overview]Model Adjusted Change in Fasting Plasma Glucose (FPG) From Baseline to Month 18
NCT00116831 (36) [back to overview]Model Adjusted Change in Glycated Hemoglobin (HbA1c) From Baseline to Month 18
NCT00350779 (6) [back to overview]Change From Baseline in FPG (Fasting Plasma Glucose) at Week 54
NCT00350779 (6) [back to overview]Change From Baseline in 2-hour PMG (Post-meal Glucose) at Week 18
NCT00350779 (6) [back to overview]Change From Baseline in FPG (Fasting Plasma Glucose) at Week 18
NCT00350779 (6) [back to overview]Change From Baseline in HbA1c (Hemoglobin A1C) at Week 18
NCT00350779 (6) [back to overview]Change From Baseline in HbA1c (Hemoglobin A1C) at Week 54
NCT00350779 (6) [back to overview]Change From Baseline in 2-hour PMG (Post-meal Glucose) at Week 54
NCT00509236 (5) [back to overview]Change From Baseline in Hemoglobin A1c After Sitagliptin Treatment
NCT00509236 (5) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG)
NCT00509236 (5) [back to overview]Number of Participants With Symptomatic Hypoglycemic Adverse Events
NCT00509236 (5) [back to overview]Number of Participants With Clinical Adverse Events
NCT00509236 (5) [back to overview]Change From Baseline in Hemoglobin A1c for Sitagliptin Versus Glipizide Treatment
NCT00509262 (4) [back to overview]Change From Baseline in Hemoglobin A1c (A1C) Levels at Week 54
NCT00509262 (4) [back to overview]Change From Baseline in Body Weight at Week 54
NCT00509262 (4) [back to overview]Percentage of Participants With Hypoglycemic Events
NCT00509262 (4) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG) at Week 54
NCT00660907 (4) [back to overview]Adjusted Mean Change in Body Weight
NCT00660907 (4) [back to overview]Adjusted Mean Change in HbA1c Levels
NCT00660907 (4) [back to overview]Proportion of Participants With at Least One Episode of Hypoglycemia
NCT00660907 (4) [back to overview]Proportion of Participants With Body Weight Reduction of at Least 5%
NCT00707993 (19) [back to overview]Change From Baseline in Fasting Proinsulin
NCT00707993 (19) [back to overview]Change From Baseline in Serum Lipids (Total Cholesterol)
NCT00707993 (19) [back to overview]Change From Baseline in Body Weight
NCT00707993 (19) [back to overview]Change From Baseline in 2-hour Postprandial Glucose
NCT00707993 (19) [back to overview]Incidence of Hypoglycemia
NCT00707993 (19) [back to overview]Change From Baseline in Glycosylated Hemoglobin at Week 52.
NCT00707993 (19) [back to overview]Incidence of Subjects Achieving Glycosylated Hemoglobin <=7%
NCT00707993 (19) [back to overview]Change From Baseline in Fasting Plasma Glucose
NCT00707993 (19) [back to overview]Change From Baseline in Glycosylated Hemoglobin
NCT00707993 (19) [back to overview]Change From Baseline in High Sensitivity C-reactive Protein
NCT00707993 (19) [back to overview]Change From Baseline in Insulin
NCT00707993 (19) [back to overview]Change From Baseline in Proinsulin/Insulin Ratio
NCT00707993 (19) [back to overview]Change From Baseline in Serum Lipids (High-Density Lipoprotein Cholesterol)
NCT00707993 (19) [back to overview]Change From Baseline in Serum Lipids (Low-Density Lipoprotein Cholesterol)
NCT00707993 (19) [back to overview]Change From Baseline in Serum Lipids (Triglycerides)
NCT00707993 (19) [back to overview]Homeostasis Model Assessment of Beta Cell Function
NCT00707993 (19) [back to overview]Incidence of Glycosylated Hemoglobin Decrease From Baseline.
NCT00707993 (19) [back to overview]Incidence of Hyperglycemic Rescue
NCT00707993 (19) [back to overview]Incidence of Marked Hyperglycemia (Fasting Plasma Glucose ≥200 mg Per dL).
NCT00834587 (6) [back to overview]AUC0-t [Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant) - Metformin
NCT00834587 (6) [back to overview]AUC0-inf [Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)] - Metformin
NCT00834587 (6) [back to overview]AUC0-inf [Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)] - Glipizide
NCT00834587 (6) [back to overview]AUC0-t [Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)] - Glipizide
NCT00834587 (6) [back to overview]Cmax (Maximum Observed Concentration) - Glipizide in Plasma
NCT00834587 (6) [back to overview]Cmax (Maximum Observed Concentration) - Metformin in Plasma
NCT00835497 (6) [back to overview]AUC0-inf [Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)] - Metformin
NCT00835497 (6) [back to overview]AUC0-inf [Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)]- Glipizide
NCT00835497 (6) [back to overview]AUC0-t [Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)]- Metformin
NCT00835497 (6) [back to overview]Cmax (Maximum Observed Concentration) - Glipizide in Plasma
NCT00835497 (6) [back to overview]Cmax (Maximum Observed Concentration) - Metformin in Plasma
NCT00835497 (6) [back to overview]AUC0-t [Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)] - Glipizide
NCT00856284 (7) [back to overview]Percentage of Participants With Glycosylated Hemoglobin Less Than or Equal to 6.5%
NCT00856284 (7) [back to overview]Change From Baseline in Glycosylated Hemoglobin (HbA1c) at Week 52
NCT00856284 (7) [back to overview]Percentage of Participants With Glycosylated Hemoglobin Less Than or Equal to 7.0%
NCT00856284 (7) [back to overview]Change From Baseline in Glycosylated Hemoglobin (HbA1c) at Week 104
NCT00856284 (7) [back to overview]Change From Baseline in Body Weight Over Time
NCT00856284 (7) [back to overview]Change From Baseline in Fasting Plasma Glucose Over Time
NCT00856284 (7) [back to overview]Change From Baseline in Glycosylated Hemoglobin at Other Time Points
NCT00885352 (3) [back to overview]Change From Baseline in 2-Hour Post-Meal Glucose (PMG) at Week 26
NCT00885352 (3) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG) at Week 26
NCT00885352 (3) [back to overview]Change From Baseline in Hemoglobin A1c (A1C) at Week 26
NCT01020123 (30) [back to overview]Potassium; Change From Baseline
NCT01020123 (30) [back to overview]Pulse, Change From Baseline
NCT01020123 (30) [back to overview]QTcF; Electorcardiagram Change From Baseline
NCT01020123 (30) [back to overview]SMPG: Change From Baseline to 4 Month, Compared With Placebo, FAS Prior to Rescue.
NCT01020123 (30) [back to overview]Sodium; Change From Baseline
NCT01020123 (30) [back to overview]Systolic Blood Pressure, Change From Baseline
NCT01020123 (30) [back to overview]Total Cholesterol: Change From Baseline
NCT01020123 (30) [back to overview]Triglycerides: Change From Baseline
NCT01020123 (30) [back to overview]Weight, Change From Baseline
NCT01020123 (30) [back to overview]OGTT/Pro-insulin/Insulin
NCT01020123 (30) [back to overview]CL/F to Characterise the PK Properties of AZD1656.
NCT01020123 (30) [back to overview]Alkaline Phosphatase; Change From Baseline
NCT01020123 (30) [back to overview]ALT; Change From Baseline
NCT01020123 (30) [back to overview]AST; Change From Baseline
NCT01020123 (30) [back to overview]Bilirubin; Change From Baseline
NCT01020123 (30) [back to overview]C-reactive Protein: Change From Baseline
NCT01020123 (30) [back to overview]Creatinine; Change From Baseline
NCT01020123 (30) [back to overview]Diastolic Blood Pressure, Change From Baseline
NCT01020123 (30) [back to overview]EC50 to Characterise the PD Properties of AZD1656.
NCT01020123 (30) [back to overview]FPG: to Evaluate Change From Baseline to 4 Month, Compared With Placebo, FAS Prior to Rescue.
NCT01020123 (30) [back to overview]Haemoglobin; Change From Baseline
NCT01020123 (30) [back to overview]HbA1c ≤ 6.5
NCT01020123 (30) [back to overview]HbA1c ≤ 7
NCT01020123 (30) [back to overview]HbA1c: Change From Baseline to 4 Month
NCT01020123 (30) [back to overview]HDL-C: Change From Baseline
NCT01020123 (30) [back to overview]LDL-C: Mean Ratio
NCT01020123 (30) [back to overview]Leukocytes; Change From Baseline
NCT01020123 (30) [back to overview]OGTT/C-peptide
NCT01020123 (30) [back to overview]OGTT/Insulin
NCT01020123 (30) [back to overview]OGTT/Plasma Glucose
NCT01068860 (16) [back to overview]Mean Change in Peak Plasma Glucose, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in Fasting Glucose Disposition Index(GDI)1 and Index 2, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Number of Participants Reporting Death, Serious Adverse Events (SAEs) and Adverse Events (AEs) Above 5% Frequency, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in Quantitative Insulin Sensitivity Check Index (QUICKI) Score, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in Absolute Glucose Level at 2 Hours, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in Post-prandial Glucose Area Under the Curve (AUC)0-4 Hours, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in Peak Plasma Insulin, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in Insulin Area Under the Curve (AUC) 0-4 Hours, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in Fructosamine, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in Fasting Plasma Insulin, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in Fasting Plasma Glucose, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in Peak Plasma C-peptide Level, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in C-peptide Area Under the Curve (AUC), 0-4 Hours, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in Meal Stimulated Insulin Secretion Rate (ISR) Relative to Glucose 2-4 Hours, From Baseline to 4 Weeks
NCT01068860 (16) [back to overview]Mean Change in Meal Stimulated Insulin Secretion Rate (ISR) Relative to Glucose 0-4 Hours, From Baseline to 4 Weeks.
NCT01068860 (16) [back to overview]Mean Change in Meal Stimulated Insulin Secretion Rate (ISR) Relative to Glucose 0-2 Hours, From Baseline to 4 Weeks.
NCT01698775 (10) [back to overview]Percentage of Participants Who Experienced at Least One Adverse Event (Phase A: 24-week Placebo Controlled Period + Phase B: 30-week Active Controlled Period)
NCT01698775 (10) [back to overview]Change From Baseline in Estimated Glomerular Filtration Rate (eGFR) at Week 24
NCT01698775 (10) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG) at Week 24
NCT01698775 (10) [back to overview]Change From Baseline in FPG at Week 54
NCT01698775 (10) [back to overview]Change From Baseline in Glycosylated Hemoglobin (A1C) at Week 24
NCT01698775 (10) [back to overview]Percentage of Participants Who Discontinued Study Drug Due to an Adverse Event (Phase A: 24-week Placebo Controlled Period + Phase B: 30-week Active Controlled Period)
NCT01698775 (10) [back to overview]Percentage of Participants Who Discontinued Study Drug Due to an Adverse Event (Phase A: 24-week Placebo Controlled Period)
NCT01698775 (10) [back to overview]Change From Baseline in A1C at Week 54
NCT01698775 (10) [back to overview]Change From Baseline in eGFR at Week 54
NCT01698775 (10) [back to overview]Percentage of Participants Who Experienced at Least One Adverse Event (Phase A: 24-week Placebo Controlled Period)
NCT01951651 (4) [back to overview]Monocyte Inflammatory Protein Nuclear Factor Kappa-B (NFkappaB) (%)
NCT01951651 (4) [back to overview]Myocardial Fat Content
NCT01951651 (4) [back to overview]Hepatic Fat Content
NCT01951651 (4) [back to overview]Left Ventricular Ejection Fraction (LVEF)(%).
NCT02608177 (3) [back to overview]Glucose Time in Range
NCT02608177 (3) [back to overview]Glycemic Variability
NCT02608177 (3) [back to overview]Hypoglycemia
NCT02911792 (1) [back to overview]GFR (Glomerular Filtration Rate) Change After Treatment

Change From Baseline in Hemoglobin A1C (A1C) at Week 24

"A1C is measured as a percent. Thus, this change from~baseline reflects the Week 24 A1C percent minus the Week 0 A1C percent." (NCT00086515)
Timeframe: Baseline and Week 24

InterventionPercent (Least Squares Mean)
Sitagliptin 100 mg-0.67
Placebo / Glipizide 5 mg-0.02

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Change From Baseline in 2-hour Post-meal Glucose (PMG) at Week 24

Change from baseline at Week 24 is defined as PMG at Week 24 minus PMG at Week 0. (NCT00086515)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Sitagliptin 100 mg-62.0
Placebo / Glipizide 5 mg-11.4

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Change From Baseline in Fasting Plasma Glucose (FPG) at Week 24

"Change from baseline at Week 24 is defined as FPG at~Week 24 minus FPG at Week 0." (NCT00086515)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Sitagliptin 100 mg-16.9
Placebo / Glipizide 5 mg8.5

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Hypoglycemic Events at Week 52

Number of participants who reported 1 or more episodes of the adverse experience (AEs) of hypoglycemia. (NCT00094770)
Timeframe: Baseline to Week 52

,
InterventionParticipants (Number)
Participants with one or more Hypoglycemic AEsTotal number of Hypoglycemic episodesParticipants with no Hypoglycemic AEs
Glipizide187657397
Sitagliptin 100 mg2950559

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Number of Participants With Clinical Adverse Experiences (CAEs) at Week 104

An adverse experience (AE) is defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the SPONSOR'S product, whether or not considered related to the use of the product. (NCT00094770)
Timeframe: Baseline to Week 104

,
InterventionParticipants (Number)
With CAESWithout CAES
Glipizide480104
Sitagliptin 100 mg452136

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Number of Participants With Laboratory Adverse Experiences (LAEs) at Week 104

A laboratory adverse experience (LAE) is defined as any unfavorable and unintended change in the chemistry of the body temporally associated with the use of the SPONSOR'S product, whether or not considered related to the use of the product. (NCT00094770)
Timeframe: Baseline to Week 104

,
InterventionParticipants (Number)
With LAEsWithout LAEs
Glipizide74510
Sitagliptin 100 mg85503

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Number of Participants With Serious CAEs at Week 104

Serious CAEs are any AEs occurring at any dose that; Results in death; or Is life threatening; or Results in a persistent or significant disability/incapacity; or Results in or prolongs an existing inpatient hospitalization; or Is a congenital anomaly/birth defect; or Is a cancer; or Is an overdose. (NCT00094770)
Timeframe: Baseline to Week 104

,
InterventionParticipants (Number)
With serious CAEsWithout serious CAEs
Glipizide73511
Sitagliptin 100 mg64524

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Number of Participants With Serious LAEs at Week 104

Serious LAEs are any LAEs occurring at any dose that: results in death; or is life threatening; or results in a persistent or significant disability/incapacity; or results in or prolongs an existing inpatient hospitalization; or is a congenital anomaly/birth defect; or is a cancer; or is an overdose. (NCT00094770)
Timeframe: Baseline to Week 104

,
InterventionParticipants (Number)
With serious LAEsWithout serious LAEs
Glipizide0584
Sitagliptin 100 mg0588

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Change From Baseline in Body Weight at Week 52

Change from baseline at Week 52 is defined as Week 52 minus Week 0. (NCT00094770)
Timeframe: Baseline and Week 52

InterventionKilograms (Least Squares Mean)
Sitagliptin 100 mg-1.5
Glipizide1.1

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Change From Baseline in HbA1c at Week 104

HbA1c is measured as percent. Thus, this change from baseline reflects the Week 104 HbA1c percent minus the Week 0 HbA1c percent. (NCT00094770)
Timeframe: Baseline and Week 104

InterventionPercent (Least Squares Mean)
Sitagliptin 100 mg-0.54
Glipizide-0.51

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Change From Baseline in Body Weight at Week 104

Change from baseline at Week 104 is defined as Week 104 minus Week 0. (NCT00094770)
Timeframe: Baseline and Week 104

InterventionKilograms (Least Squares Mean)
Sitagliptin 100 mg-1.6
Glipizide0.7

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Change From Baseline in HbA1c at Week 52

HbA1c is measured as percent. Thus, this change from baseline reflects the Week 52 HbA1c percent minus the Week 0 HbA1c percent. (NCT00094770)
Timeframe: Baseline and Week 52

InterventionPercent (Least Squares Mean)
Sitagliptin 100 mg-0.67
Glipizide-0.67

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Hypoglycemic Events at Week 104

Number of participants who reported 1 or more episodes of the adverse experience of hypoglycemia. (NCT00094770)
Timeframe: Baseline to Week 104

,
InterventionParticipants (Number)
Participants with one or more Hypoglycemic AEsTotal number of Hypoglycemic episodesParticipants with no Hypoglycemic AEs
Glipizide199805385
Sitagliptin 100 mg3157557

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Safety and Tolerability of Sitagliptin Over 54 Weeks

Safety and tolerability were measured in terms of the number of patients with clinical adverse experiences (CAEs), serious CAEs, drug-related CAEs, laboratory adverse experiences (LAEs), serious LAEs, and drug-related LAEs. Drug-relationship was assessed by the study investigator according to his/her best clinical judgment. (NCT00095056)
Timeframe: Week 0 through Week 54

,
InterventionParticipants (Number)
With CAEsWith drug-related CAEsWith serious CAEsWith LAEsWith drug-related LAEsWith serious LAEs
Placebo22510800
Sitagliptin508201520

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Safety and Tolerability of Sitagliptin After 12 Weeks of Treatment

Safety and tolerability were measured in terms of the number of patients with clinical adverse experiences (CAEs), serious CAEs, drug-related CAEs, laboratory adverse experiences (LAEs), serious LAEs, and drug-related LAEs. Drug-relationship was assessed by the study investigator according to his/her best clinical judgment. (NCT00095056)
Timeframe: Week 0 through Week 12

,
InterventionParticipants (Number)
With CAEsWith drug-related CAEsWith serious CAEsWith LAEsWith drug-related LAEsWith serious LAEs
Placebo1611500
Sitagliptin4189910

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Change From Baseline in Normalized Atheroma Volume

IVUS-derived endpoints measured within the same segment (in non-intervened coronary arteries) from Baseline to Month 18. Normalized atheroma volume is defined as mean atheroma area x median segment length in cohort. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionmillimeters cubed (mm3) (Mean)
BaselineMonth 18Change from Baseline
Glipizide (GLP) 5 mg232.772233.1530.381
Rosiglitazone (RSG) 4 mg226.075221.599-4.476

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Change From Baseline in Percent Atheroma Volume (PAV) to Month 18

The primary efficacy endpoint was change in PAV (defined as total atheroma volume divided by total vessel volume x 100) within a 40 mm segment in non-intervened coronary arteries from Baseline to Month 18, based upon Intravascular Ultrasound (IVUS) assessment. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent (absolute change) (Mean)
BaselineMonth 18Change from Baseline
Glipizide (GLP) 5 mg40.59341.0130.420
Rosiglitazone (RSG) 4 mg40.42240.182-0.240

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Change in Atheroma Volume Within the 10 mm of the Non-intervened Vessel Segment With the Greatest Atheroma Volume at Baseline

IVUS-derived endpoints measured within the same 10 mm segment of non-intervened coronary arteries with the greatest degree of atheroma volume at Baseline, from Baseline to Month 18, including the nominal change in atheroma volume and atheroma area (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionmillimeters cubed (mm3) (Mean)
BaselineMonth 18Change from Baseline
Glipizide (GLP) 5 mg75.64972.225-3.424
Rosiglitazone (RSG) 4 mg70.96166.020-4.941

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Model Adjusted Percent Change in Brain Natriuretic Peptide (BNP) From Baseline to Month 18

It was measured as ratio to baseline as percentage change based on log-transformed data : 100 x (exp(Mean change on log scale) - 1). Model Adjusted change based on ANCOVA: Log(value) - log(Baseline) = log(Baseline) + sex + region + treatment + prior OAD + cardiac procedure. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent change (Number)
Adjusted Geometric Mean + Standard ErrorAdjusted Geometric MeanAdjusted Geometric Mean - Standard Error
Glipizide (GLP) 5 mg-4.865-11.388-17.465
Rosiglitazone (RSG) 4 mg24.57615.7207.499

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Number of Other Cardiovascular Events

This was one of the secondary endpoints of the study. (NCT00116831)
Timeframe: Baseline to Month 21

,
InterventionNumber of events (Number)
All-cause deathCardiovascular deathNon-fatal myocardial infarctionNon-fatal strokeCoronary revascularizationHospitalization for recurrent myocardial ischemiaNon-MACE congestive heart failure
Glipizide (GLP) 5 mg73612773
Rosiglitazone (RSG) 4 mg847526118

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Percent Change From Baseline to Month 18 in Apoprotein B (apoB)

Repeated measures analysis model: Log(value) - log (Baseline) = log(Baseline) + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent change (Number)
Adjusted Geometric Mean + Standard ErrorAdjusted Geometric MeanAdjusted Geometric Mean - Standard Error
Glipizide (GLP) 5 mg-6.588-8.320-10.021
Rosiglitazone (RSG) 4 mg-6.967-8.744-10.488

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Percent Change From Baseline to Month 18 in HDL-2

Repeated measures analysis model: Log(value) - log (Baseline) = log(Baseline) + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent change (Number)
Adjusted Geometric Mean + Standard ErrorAdjusted Geometric MeanAdjusted Geometric Mean - Standard Error
Glipizide (GLP) 5 mg2.065-0.783-3.550
Rosiglitazone (RSG) 4 mg18.24114.82111.507

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Percent Change From Baseline to Month 18 in HDL-3

Repeated measures analysis model: Log(value) - log (Baseline) = log(Baseline) + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent change (Number)
Adjusted Geometric Mean + Standard ErrorAdjusted Geometric MeanAdjusted Geometric Mean - Standard Error
Glipizide (GLP) 5 mg10.6839.0747.490
Rosiglitazone (RSG) 4 mg15.16513.44011.732

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Percent Change From Baseline to Month 18 in High Density Lipoprotein Cholesterol (HDL-c)

Repeated measures analysis model: Log(value) - log (Baseline) = log(Baseline) + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent change (Number)
Adjusted Geometric Mean + Standard ErrorAdjusted Geometric MeanAdjusted Geometric Mean - Standard Error
Glipizide (GLP) 5 mg7.2085.7104.233
Rosiglitazone (RSG) 4 mg15.10413.44011.808

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Percent Change From Baseline to Month 18 in Low Density Lipoprotein Cholesterol (LDL-c)

Repeated measures analysis model: Log(value) - log (Baseline) = log(Baseline) + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent change (Number)
Adjusted Geometric Mean + Standard ErrorAdjusted Geometric MeanAdjusted Geometric Mean - Standard Error
Glipizide (GLP) 5 mg-8.955-11.600-14.172
Rosiglitazone (RSG) 4 mg1.795-1.237-4.180

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Percent Change From Baseline to Month 18 in Total Cholesterol (TC)

Repeated measures analysis model: Log(value) - log (Baseline) = log(Baseline) + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent change (Number)
Adjusted Geometric Mean + Standard ErrorAdjusted Geometric MeanAdjusted Geometric Mean - Standard Error
Glipizide (GLP) 5 mg-4.205-5.644-7.062
Rosiglitazone (RSG) 4 mg3.1511.5670.007

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Percent Change From Baseline to Month 18 in Triglycerides (TG)

Repeated measures analysis model: Log(value) - log (Baseline) = log(Baseline) + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent change (Number)
Adjusted Geometric Mean + Standard ErrorAdjusted Geometric MeanAdjusted Geometric Mean - Standard Error
Glipizide (GLP) 5 mg-7.415-10.309-13.110
Rosiglitazone (RSG) 4 mg-13.601-16.381-19.067

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Percent Change in Brain Natriuretic Peptide (BNP) From Baseline to Month 18

It was measured as ratio to baseline as percentage change based on log-transformed data : 100 x (exp(Mean change on log scale) - 1)It was measured as ratio to baseline as percentage change based on log-transformed data : 100 x (exp(Mean change on log scale) - 1). Ratio to baseline as %change mean (%) was used as the estimation parameter for both groups. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent change (Number)
Mean + Standard ErrorMeanMean - Standard Error
Glipizide (GLP) 5 mg1.141-6.608-13.764
Rosiglitazone (RSG) 4 mg30.18920.58211.683

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Percent Change From Baseline to Month 18 in Free Fatty Acids (FFA)

Repeated measures analysis model: Log(value) - log (Baseline) = log(Baseline) + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent change (Number)
Adjusted Geometric Mean + Standard ErrorAdjusted Geometric MeanAdjusted Geometric Mean - Standard Error
Glipizide (GLP) 5 mg32.90927.30321.943
Rosiglitazone (RSG) 4 mg13.8358.8804.142

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Change in Atheroma Area Within the 10 mm of the Non-intervened Vessel Segment With the Greatest Atheroma Volume at Baseline

IVUS-derived endpoints measured within the same 10 mm segment of non-intervened coronary arteries with the greatest degree of atheroma volume at Baseline, from Baseline to Month 18, including the nominal change in atheroma volume and atheroma area (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionmillimeters squared (mm2) (Mean)
BaselineMonth 18Change from Baseline
Glipizide (GLP) 5 mg7.5697.185-0.384
Rosiglitazone (RSG) 4 mg7.0936.625-0.468

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Repeated Measures Analysis of Percent Change in hsCRP From Baseline to Month 18

Changes in cardiovascular biomarkers from Baseline to Month 18, such as high sensitivity C-reactive protein (hsCRP) . Repeated measures analysis model: Log(value) - log(baseline) = log(baseline) + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent change (Number)
Adjusted Geometric Mean + Standard ErrorAdjusted Geometric MeanAdjusted Geometric Mean - Standard Error
Glipizide (GLP) 5 mg-62.82-65.18-67.40
Rosiglitazone (RSG) 4 mg-80.33-81.63-82.84

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Repeated Measures Analysis of Percent Change in MMP 9 From Baseline to Month 18

Changes in cardiovascular biomarkers from Baseline to Month 18, such as matrix metalloproteinase-9 (MMP-9). Repeated measures analysis model: Log(value) - log(baseline) = log(baseline) + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionpercent change (Number)
Adjusted Geometric Mean + Standard ErrorAdjusted Geometric MeanAdjusted Geometric Mean - Standard Error
Glipizide (GLP) 5 mg-26.5-30.5-34.3
Rosiglitazone (RSG) 4 mg-38.8-42.2-45.5

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Change From Baseline to Month 18 in LDL-c Peak Particle Density Measured by LDL Relative Flotation

From repeated measures analysis model: Change = baseline + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

InterventionRatio (Mean)
Glipizide (GLP) 5 mg0.0040
Rosiglitazone (RSG) 4 mg0.0204

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Number of Participants With the Indicated Treatment Emergent Major Cardiovascular Events (MACE) for All-cause Death, Non-fatal MI, Non-fatal Stroke, Coronary Revascularization, or Hospitalization for Recurrent Myocardial Ischemia (MACE Composite 1)

This was 1 of 2 MACE composite endpoints and was a secondary efficacy endpoint. (NCT00116831)
Timeframe: Baseline to Month 21

InterventionParticipants (Number)
Glipizide (GLP) 5 mg38
Rosiglitazone (RSG) 4 mg39

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Number of Participants With the Indicated Treatment Emergent Major Cardiovascular Events (MACE) for Cardiovascular Death, Nonfatal MI, or Nonfatal Stroke (MACE Composite 2)

This was 1 of 2 MACE composite endpoints and was a secondary efficacy endpoint. (NCT00116831)
Timeframe: Baseline to Month 21

InterventionParticipants (Number)
Glipizide (GLP) 5 mg10
Rosiglitazone (RSG) 4 mg14

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Change From Baseline in Atheroma, Vessel, and Lumen Area to Month 18

IVUS-derived endpoints measured within the same segment (in non-intervened coronary arteries) from Baseline to Month 18 (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionmillimeters squared (mm2) (Mean)
Atheroma Area, BaselineAtheroma Area, Month 18Change from Baseline in Atheroma AreaVessel Area, BaselineVessel Area, Month 18Change from Baseline in Vessel AreaLumen Area, BaselineLumen Area, Month 18Change from Baseline in Lumen Area
Glipizide (GLP) 5 mg5.9185.9280.01014.36414.261-0.1028.4478.335-0.113
Rosiglitazone (RSG) 4 mg5.7485.634-0.11414.16613.977-0.1898.4198.344-0.075

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Change From Baseline in Atheroma, Vessel, and Lumen Volume to Month 18

IVUS-derived endpoints measured within the same segment (in non-intervened coronary arteries) from Baseline to Month 18 (NCT00116831)
Timeframe: Baseline to Month 18

,
Interventionmillimeters cubed (mm3) (Mean)
Atheroma Volume, BaselineAtheroma Volume, Month 18Change from Baseline in Atheroma VolumeVessel Volume, BaselineVessel Volume, Month 18Change from Baseline in Vessel VolumeLumen Volume, BaselineLumen Volume, Month 18Change from Baseline in Lumen Volume
Glipizide (GLP) 5 mg249.747249.625-0.123609.378603.088-6.290359.726353.513-6.213
Rosiglitazone (RSG) 4 mg222.431218.576-3.854555.062547.186-7.876332.688328.676-4.012

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Model Adjusted Change in Atheroma Volume Within the 10 mm of the Non-intervened Vessel Segment With the Greatest Atheroma Volume at Baseline

IVUS-derived endpoints measured within the same 10 mm segment of non-intervened coronary arteries with the greatest degree of atheroma volume at Baseline, from Baseline to Month 18, including the nominal change in atheroma volume and atheroma area. Model Adjusted Change = Baseline + Region + Sex + Treatment + Cardiac Procedure + Prior OAD Medication. (NCT00116831)
Timeframe: Baseline to Month 18

Interventionmillimeters cubed (mm3) (Mean)
Glipizide (GLP) 5 mg-3.56
Rosiglitazone (RSG) 4 mg-5.28

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Change From Baseline to Month 18 in LDL-c/HDL-c Ratio

From repeated measures analysis model: Change = baseline + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

Interventionratio (Mean)
Glipizide (GLP) 5 mg-0.365
Rosiglitazone (RSG) 4 mg-0.226

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Change From Baseline to Month 18 in Total Cholesterol/HDL-c Ratio

From repeated measures analysis model: Change = baseline + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

Interventionratio (Mean)
Glipizide (GLP) 5 mg-0.495
Rosiglitazone (RSG) 4 mg-0.377

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Model Adjusted Change From Baseline in Atheroma Area to Month 18

IVUS-derived endpoints measured within the same segment (in non-intervened coronary arteries) from Baseline to Month 18. Model Adjusted Change (MAC) = Baseline + Region + Sex + Treatment + Cardiac Procedure + Prior OAD Medication. (NCT00116831)
Timeframe: Baseline to Month 18

Interventionmillimeters square (mm2) (Mean)
Glipizide (GLP) 5 mg0.03
Rosiglitazone (RSG) 4 mg-0.10

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Model Adjusted Change From Baseline in Atheroma Volume to Month 18

IVUS-derived endpoints measured within the same segment (in non-intervened coronary arteries) from Baseline to Month 18. Model Adjusted Change (MAC) = Baseline + Region + Sex + Treatment + Cardiac Procedure + Prior OAD Medication. (NCT00116831)
Timeframe: Baseline to Month 18

Interventionmillimeters cubed (mm3) (Mean)
Glipizide (GLP) 5 mg0.98
Rosiglitazone (RSG) 4 mg-3.60

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Model Adjusted Change From Baseline in Lumen Area to Month 18

IVUS-derived endpoints measured within the same segment (in non-intervened coronary arteries) from Baseline to Month 18. Model Adjusted Change (MAC) = Baseline + Region + Sex + Treatment + Cardiac Procedure + Prior OAD Medication. (NCT00116831)
Timeframe: Baseline to Month 18

Interventionmillimeters square (mm2) (Mean)
Glipizide (GLP) 5 mg-0.14
Rosiglitazone (RSG) 4 mg-0.11

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Model Adjusted Change From Baseline in Lumen Volume to Month 18

IVUS-derived endpoints measured within the same segment (in non-intervened coronary arteries) from Baseline to Month 18. Model Adjusted Change (MAC) = Baseline + Region + Sex + Treatment + Cardiac Procedure + Prior OAD Medication. (NCT00116831)
Timeframe: Baseline to Month 18

Interventionmillimeters cubed (mm3) (Mean)
Glipizide (GLP) 5 mg-4.91
Rosiglitazone (RSG) 4 mg-4.59

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Model Adjusted Change From Baseline in Normalized Atheroma Volume

IVUS-derived endpoints measured within the same segment (in non-intervened coronary arteries) from Baseline to Month 18. Normalized atheroma volume is defined as mean atheroma area x median segment length in cohort. Model Adjusted Change = Baseline + Region + Sex + Treatment + Cardiac Procedure + Prior OAD Medication. (NCT00116831)
Timeframe: Baseline to Month 18

Interventionmillimeters cubed (mm3) (Mean)
Glipizide (GLP) 5 mg1.20
Rosiglitazone (RSG) 4 mg-3.92

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Model Adjusted Change From Baseline in Percent Atheroma Volume (PAV) to Month 18

Model Adjusted Change (MAC) = Baseline + Region + Sex + Treatment + Cardiac Procedure + Prior Oral Anti-Hyperglycemic Diabetic Medications(s) (OAD). (NCT00116831)
Timeframe: Baseline to Month 18

Interventionpercent (absolute change) (Mean)
Glipizide (GLP) 5 mg0.43
Rosiglitazone (RSG) 4 mg-0.21

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Model Adjusted Change From Baseline in Vessel Area to Month 18

IVUS-derived endpoints measured within the same segment (in non-intervened coronary arteries) from Baseline to Month 18. Model Adjusted Change (MAC) = Baseline + Region + Sex + Treatment + Cardiac Procedure + Prior OAD Medication. (NCT00116831)
Timeframe: Baseline to Month 18

Interventionmillimeters square (mm2) (Mean)
Glipizide (GLP) 5 mg-0.10
Rosiglitazone (RSG) 4 mg-0.21

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Model Adjusted Change From Baseline in Vessel Volume to Month 18

IVUS-derived endpoints measured within the same segment (in non-intervened coronary arteries) from Baseline to Month 18. Model Adjusted Change (MAC) = Baseline + Region + Sex + Treatment + Cardiac Procedure + Prior OAD Medication. (NCT00116831)
Timeframe: Baseline to Month 18

Interventionmillimeters cubed (mm3) (Mean)
Glipizide (GLP) 5 mg-4.56
Rosiglitazone (RSG) 4 mg-8.13

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Model Adjusted Change in Atheroma Area Within the 10 mm of the Non-intervened Vessel Segment With the Greatest Atheroma Volume at Baseline

IVUS-derived endpoints measured within the same 10 mm segment of non-intervened coronary arteries with the greatest degree of atheroma volume at Baseline, from Baseline to Month 18, including the nominal change in atheroma volume and atheroma area. Model Adjusted Change = Baseline + Region + Sex + Treatment + Cardiac Procedure + Prior OAD Medication. (NCT00116831)
Timeframe: Baseline to Month 18

Interventionmillimeters squared (mm2) (Mean)
Glipizide (GLP) 5 mg-0.39
Rosiglitazone (RSG) 4 mg-0.50

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Model Adjusted Change in Fasting Plasma Glucose (FPG) From Baseline to Month 18

From repeated measures analysis model: Change = Baseline + visit + sex + region + treatment + prior OAD + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

Interventionmillimole/Liter (mmol/L) (Mean)
Glipizide (GLP) 5 mg-0.46
Rosiglitazone (RSG) 4 mg-1.34

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Model Adjusted Change in Glycated Hemoglobin (HbA1c) From Baseline to Month 18

From repeated measures analysis model: Change = Baseline + visit + sex + region + treatment + prior Oral Anti-Hyperglycemic Diabetic Medications(s) (OAD) + cardiac procedure + treatment x visit. (NCT00116831)
Timeframe: Baseline to Month 18

InterventionPercentage (Mean)
Glipizide (GLP) 5 mg-0.20
Rosiglitazone (RSG) 4 mg-0.30

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Change From Baseline in FPG (Fasting Plasma Glucose) at Week 54

Change from baseline at Week 54 is defined as Week 54 minus Week 0 (NCT00350779)
Timeframe: Baseline and Week 54

Interventionmg/dL (Least Squares Mean)
Sitagliptin 100 mg-28.0
Placebo-10.7

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Change From Baseline in 2-hour PMG (Post-meal Glucose) at Week 18

Change from baseline at Week 18 is defined as Week 18 minus Week 0 (NCT00350779)
Timeframe: Baseline and Week 18

Interventionmg/dL (Least Squares Mean)
Sitagliptin 100 mg-59.9
Placebo-22.0

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Change From Baseline in FPG (Fasting Plasma Glucose) at Week 18

Change from baseline at Week 18 is defined as Week 18 minus Week 0 (NCT00350779)
Timeframe: Baseline and 18 Weeks

Interventionmg/dL (Least Squares Mean)
Sitagliptin 100 mg-30.7
Placebo-11.7

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Change From Baseline in HbA1c (Hemoglobin A1C) at Week 18

HbA1c is measured as a percent. Thus, this change from baseline reflects the Week 18 HbA1c percent minus the Week 0 HbA1c percent. (NCT00350779)
Timeframe: Baseline and 18 Weeks

InterventionPercent (Least Squares Mean)
Sitagliptin 100 mg-1.03
Placebo-0.31

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Change From Baseline in HbA1c (Hemoglobin A1C) at Week 54

HbA1c is measured as a percent. Thus, this change from baseline reflects the Week 54 HbA1c percent minus the Week 0 HbA1c percent. (NCT00350779)
Timeframe: Baseline and Week 54

InterventionPercent (Least Squares Mean)
Sitagliptin 100 mg-1.05
Placebo-0.28

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Change From Baseline in 2-hour PMG (Post-meal Glucose) at Week 54

Change from baseline at Week 54 is defined as Week 54 minus Week 0. (NCT00350779)
Timeframe: Baseline and Week 54

Interventionmg/dL (Least Squares Mean)
Sitagliptin 100 mg-50.7
Placebo-16.6

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Change From Baseline in Hemoglobin A1c After Sitagliptin Treatment

Change from baseline in mean hemoglobin A1c after treatment with sitagliptin for 54 weeks. Hemoglobin A1c is the percent of hemoglobin that is glycated. Results for the glipizide arm are not reported in this table because the primary outcome measure is for the sitagliptin arm only. (NCT00509236)
Timeframe: Baseline / Week 54

InterventionPercent hemoglobin A1c (Mean)
BaselineWeek 54Change from Baseline at Week 54
Sitagliptin 25 mg7.897.15-0.74

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Change From Baseline in Fasting Plasma Glucose (FPG)

Change from baseline in mean Fasting Plasma Glucose after treatment with sitagliptin versus glipizide for 54 weeks. (NCT00509236)
Timeframe: Baseline / Week 54

,
Interventionmg/dL (Mean)
BaselineWeek 54Change from Baseline to Week 54
Glipizide 2.5 mg - 20 mg167.0134.0-33.0
Sitagliptin 25 mg160.3135.8-24.5

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Number of Participants With Symptomatic Hypoglycemic Adverse Events

A symptomatic hypoglycemic adverse event is an episode with clinical symptoms attributed to hypoglycemia, without regard to fingerstick glucose level. (NCT00509236)
Timeframe: 54 Week Treatment Period + 28 days

InterventionParticipants (Number)
Sitagliptin 25 mg4
Glipizide 2.5 mg - 20 mg7

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Number of Participants With Clinical Adverse Events

Reported experiences assessed by investigators as adverse events, excluding data after initiation of glycemic rescue therapy. (NCT00509236)
Timeframe: 54 Week Treatment Period + 28 days

InterventionParticipants (Number)
Sitagliptin 25 mg53
Glipizide 2.5 mg - 20 mg52

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Change From Baseline in Hemoglobin A1c for Sitagliptin Versus Glipizide Treatment

Change from baseline in least square means hemoglobin A1c after treatment with sitagliptin versus glipizide for 54 weeks. Hemoglobin A1c is the percent of hemoglobin that is glycated. (NCT00509236)
Timeframe: Baseline / Week 54

InterventionPercent hemoglobin A1c (Least Squares Mean)
Sitagliptin 25 mg-0.72
Glipizide 2.5 mg - 20 mg-0.87

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Change From Baseline in Hemoglobin A1c (A1C) Levels at Week 54

A1C represents percentage of glycosylated hemoglobin. (NCT00509262)
Timeframe: Baseline to Week 54

,
InterventionPercent of glycosylated hemoglobin (Mean)
BaselineChange from Baseline at Week 54
Glipizide7.79-0.62
Sitagliptin7.76-0.70

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Change From Baseline in Body Weight at Week 54

(NCT00509262)
Timeframe: Baseline to Week 54

Interventionkg (Least Squares Mean)
Sitagliptin-0.6
Glipizide1.2

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Percentage of Participants With Hypoglycemic Events

Percentage of participants with at least one symptomatic hypoglycemic adverse event, excluding data after initiation of glycemic rescue therapy. (NCT00509262)
Timeframe: Baseline up to 28 days following the last dose of study therapy

Interventionpercentage of participants (Number)
Sitagliptin6.2
Glipizide17.0

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Change From Baseline in Fasting Plasma Glucose (FPG) at Week 54

(NCT00509262)
Timeframe: Baseline to Week 54

,
Interventionmg/dL (Mean)
BaselineChange from Baseline at Week 54
Glipizide143.9-20.2
Sitagliptin148.6-16.7

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Adjusted Mean Change in Body Weight

To assess the effect of dapagliflozin plus metformin compared to glipizide plus metformin on body weight after 52 weeks double-blind treatment. (NCT00660907)
Timeframe: Baseline to Week 52

Interventionkg (Least Squares Mean)
Dapagliflozin Plus Metformin-3.22
Glipizide Plus Metformin1.44

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Adjusted Mean Change in HbA1c Levels

To assess the effect of dapagliflozin plus metformin compared to glipizide plus metformin on the absolute change from baseline in HbA1c level after 52 weeks double-blind treatment in patients with type 2 diabetes who have inadequate glycaemic control on 1500 mg/day or higher doses of metformin therapy alone. (NCT00660907)
Timeframe: Baseline to Week 52

Interventionpercent (Least Squares Mean)
Dapagliflozin Plus Metformin-0.52
Glipizide Plus Metformin-0.52

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Proportion of Participants With at Least One Episode of Hypoglycemia

To assess the effect of dapagliflozin plus metformin treatment compared to glipizide plus metformin on the occurrence of hypoglycemic events. Least Squares Mean represents the percent of participants adjusted for HbA1c baseline value. (NCT00660907)
Timeframe: Baseline to Week 52

InterventionPercentage of participants (Least Squares Mean)
Dapagliflozin Plus Metformin3.5
Glipizide Plus Metformin40.8

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Proportion of Participants With Body Weight Reduction of at Least 5%

To evaluate the effect of dapagliflozin plus metformin compared to glipizide plus metformin on body weight assessed by a reduction after 52 weeks of at least 5% compared to baseline. Least Squares Mean represents the percent of participants adjusted for baseline value. (NCT00660907)
Timeframe: Baseline to Week 52

InterventionPercentage of participants (Least Squares Mean)
Dapagliflozin Plus Metformin33.3
Glipizide Plus Metformin2.5

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Change From Baseline in Fasting Proinsulin

The change between the value of fasting proinsulin collected at each week indicated including final visit relative to baseline. (NCT00707993)
Timeframe: Baseline, Week 12, Week 26, Week 42 and Week 52.

,
Interventionpmol/L (Least Squares Mean)
Week 12 (n=207; n=186)Week 26 (n=211; n=194)Week 42 (n=211; n=194)Week 52 (n=211; n=194)
Alogliptin 25 mg QD-6.0-4.6-4.6-4.9
Glipizide 5 mg QD1.03.03.13.0

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Change From Baseline in Serum Lipids (Total Cholesterol)

The change in total cholesterol measured at each week indicated including final visit from baseline. (NCT00707993)
Timeframe: Baseline, Week 8, Week 12, Week 26, Week 42 and Week 52.

,
Interventionmg/dL (Least Squares Mean)
Week 8 (n=208; n=195)Week 12 (n=213; n=201)Week 26 (n=213; n=201)Week 42 (n=213; n=201)Week 52 (n=213; n=201)
Alogliptin 25 mg QD-5.6-4.21.60.2-0.8
Glipizide 5 mg QD-1.6-0.70.10.1-0.5

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Change From Baseline in Body Weight

The change in body weight measured at each week indicated including final visit from baseline. (NCT00707993)
Timeframe: Baseline, Week 8, Week 12, Week 26, Week 42 and Week 52.

,
Interventionkg (Least Squares Mean)
Week 8 (n=213; n=200)Week 12 (n=215; n=203)Week 26 (n=215; n=204)Week 42 (n=215; n=204)Week 52 (n=215; n=204)
Alogliptin 25 mg QD-0.42-0.52-0.68-0.72-0.62
Glipizide 5 mg QD0.550.420.660.570.60

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Change From Baseline in 2-hour Postprandial Glucose

The change in postprandial (after eating a meal) glucose levels at week 52 relative to baseline. Standard 2-hour postprandial glucose (PPG) tests performed following an overnight fast and evaluated right before and after a 120-minute (2-hour) timeframe relative to ingestion of a standard oral glucose drink. (NCT00707993)
Timeframe: Baseline and Week 52.

,
Interventionmg/dL (Least Squares Mean)
Week 52 PPG level (n=109; n=93)Week 52 PPG excursion (n=109; n=93)
Alogliptin 25 mg QD-5.801.82
Glipizide 5 mg QD6.307.17

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Incidence of Hypoglycemia

Percentage of participants with at least one hypoglycemic episode during 52 week study. (NCT00707993)
Timeframe: On occurrence (up to 52 weeks).

Interventionpercentage of participants (Number)
Alogliptin 25 mg QD5.4
Glipizide 5 mg QD26.0

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Change From Baseline in Glycosylated Hemoglobin at Week 52.

The change in the percentage of glycosylated hemoglobin (the concentration of glucose bound to hemoglobin as a percent of the absolute maximum that can be bound) collected at week 52 or final visit and glycosylated hemoglobin collected at baseline. (NCT00707993)
Timeframe: Baseline and Week 52.

Interventionpercentage of Glycosylated Hemoglobin (Least Squares Mean)
Alogliptin 25 mg QD-0.14
Glipizide 5 mg QD-0.09

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Incidence of Subjects Achieving Glycosylated Hemoglobin <=7%

The percentage of participants with a value for the percentage of glycosylated hemoglobin (HbA1c; the percentage of hemoglobin that is bound to glucose) less than or equal to 6.5 and 7.0% during the 52 week study. (NCT00707993)
Timeframe: Baseline and Week 52.

,
Interventionpercentage of participants (Number)
HbA1c ≤6.5%HbA1c ≤7.0%
Alogliptin 25 mg QD22.348.8
Glipizide 5 mg QD18.245.3

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Change From Baseline in Fasting Plasma Glucose

The change in the value of fasting plasma glucose collected at each week indicated including final visit relative to baseline. (NCT00707993)
Timeframe: Baseline, Week 2, Week 4, Week 8, Week 12, Week 16, Week 20, Week 26, Week 34, Week 42 and Week 52.

,
Interventionmg/dL (Least Squares Mean)
Week 2 (n=196; n=199)Week 4 (n=217; n=213)Week 8 (n=217; n=214)Week 12 (n=217; n=214)Week 16 (n=217; n=214)Week 20 (n=217; n=214)Week 26 (n=217; n=214)Week 34 (n=217; n=214)Week 42 (n=217; n=214)Week 52 (n=217; n=214)
Alogliptin 25 mg QD-3.8-7.7-8.9-10.2-7.9-9.8-7.9-5.4-3.6-2.4
Glipizide 5 mg QD-5.0-7.6-8.7-9.9-11.4-8.7-6.2-5.7-7.4-4.2

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Change From Baseline in Glycosylated Hemoglobin

The change in the value of glycosylated hemoglobin (the concentration of glucose bound to hemoglobin as a percent of the absolute maximum that can be bound) collected at each week indicated including final visit relative to baseline. (NCT00707993)
Timeframe: Baseline, Week 4, Week 8, Week 12, Week 16, Week 20, Week 26, Week 34 and Week 42.

,
Interventionpercentage of Glycosylated Hemoglobin (Least Squares Mean)
Week 4 (n=175; n=148)Week 8 (n=180; n=161)Week 12 (n=180; n=162)Week 16 (n=180; n=162)Week 20 (n=180; n=162)Week 26 (n=180; n=162)Week 34 (n=180; n=162)Week 42 (n=180; n=162)
Alogliptin 25 mg QD-0.14-0.27-0.34-0.31-0.31-0.28-0.21-0.17
Glipizide 5 mg QD-0.11-0.23-0.25-0.32-0.27-0.25-0.21-0.17

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Change From Baseline in High Sensitivity C-reactive Protein

The change between the high sensitivity C-reactive protein value collected at each week indicated including final visit from baseline. (NCT00707993)
Timeframe: Baseline, Week 12, Week 26, Week 42 and Week 52.

,
Interventionmg/L (Least Squares Mean)
Week 12 (n=209; n=192)Week 26 (n=212; n=198)Week 42 (n=212; n=198)Week 52 (n=212; n=198)
Alogliptin 25 mg QD0.45-0.020.330.01
Glipizide 5 mg QD0.100.470.530.21

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Change From Baseline in Insulin

The change between the value of insulin collected at each week indicated including final visit relative to baseline. (NCT00707993)
Timeframe: Baseline, Week 12, Week 26, Week 42 and Week 52.

,
InterventionmcIU/mL (Least Squares Mean)
Week 12 (n=207; n=188)Week 26 (n=210; n=194)Week 42 (n=210; n=194)Week 52 (n=210; n=194)
Alogliptin 25 mg QD-2.36-0.41-0.58-1.72
Glipizide 5 mg QD0.843.031.533.15

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Change From Baseline in Proinsulin/Insulin Ratio

The change between the ratio value of proinsulin and insulin collected at each week indicated including final visit relative to baseline. (NCT00707993)
Timeframe: Baseline, Week 12, Week 26, Week 42 and Week 52.

,
Interventionratio (Least Squares Mean)
Week 12 (n=206; n=185)Week 26 (n=210; n=193)Week 42 (n=210; n=193)Week 52 (n=210; n=193)
Alogliptin 25 mg QD-0.288-0.253-0.289-0.155
Glipizide 5 mg QD0.0530.5620.183-0.057

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Change From Baseline in Serum Lipids (High-Density Lipoprotein Cholesterol)

The change in high-density lipoprotein cholesterol measured at each week indicated including final visit from baseline. (NCT00707993)
Timeframe: Baseline, Week 8, Week 12, Week 26, Week 42 and Week 52.

,
Interventionmg/dL (Least Squares Mean)
Week 8 (n=206; n=193)Week 12 (n=212; n=201)Week 26 (n=212; n=201)Week 42 (n=212; n=201)Week 52 (n=212; n=201)
Alogliptin 25 mg QD-0.10.41.71.40.8
Glipizide 5 mg QD1.20.50.20.10.3

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Change From Baseline in Serum Lipids (Low-Density Lipoprotein Cholesterol)

The change in low-density lipoprotein cholesterol measured at each week indicated including final visit from baseline. (NCT00707993)
Timeframe: Baseline, Week 8, Week 12, Week 26, Week 42 and Week 52.

,
Interventionmg/dL (Least Squares Mean)
Week 8 (n=200; n=185)Week 12 (n=208; n=195)Week 26 (n=208; n=196)Week 42 (n=208; n=197)Week 52 (n=209; n=197)
Alogliptin 25 mg QD-3.2-2.03.11.20.9
Glipizide 5 mg QD-2.8-2.4-1.1-0.8-1.4

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Change From Baseline in Serum Lipids (Triglycerides)

The change in triglycerides measured at each week indicated including final visit from baseline. (NCT00707993)
Timeframe: Baseline, Week 8, Week 12, Week 26, Week 42 and Week 52.

,
Interventionmg/dL (Least Squares Mean)
Week 8 (n=208; n=195)Week 12 (n=213; n=201)Week 26 (n=213; n=201)Week 42 (n=213; n=201)Week 52 (n=213; n=201)
Alogliptin 25 mg QD-12.8-15.5-16.3-12.6-13.2
Glipizide 5 mg QD2.77.53.95.51.9

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Homeostasis Model Assessment of Beta Cell Function

The change between homeostasis model assessment of beta cell function collected at each week indicated including final visit relative to baseline. Homeostasis model assessment of beta cell function measures beta cell function, calculated by a constant (20) times insulin, divided by fasting plasma glucose minus a constant (3.5). (NCT00707993)
Timeframe: Baseline, Week 12, Week 26, Week 42 and Week 52.

,
Interventionpercent score of beta cell function (Least Squares Mean)
Week 12 (n=203; n=184)Week 26 (n=207; n=193)Week 42 (n=207; n=193)Week 52 (n=207; n=193)
Alogliptin 25 mg QD-6.104-0.136-5.571-9.755
Glipizide 5 mg QD30.08131.66916.00435.281

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Incidence of Glycosylated Hemoglobin Decrease From Baseline.

The percentage of participants with a decrease from baseline in the percentage of glycosylated hemoglobin (the percentage of hemoglobin that is bound to glucose) greater than or equal to 0.5, 1.0, 1.5 and 2.0% during the 52 week study. (NCT00707993)
Timeframe: Baseline and Week 52.

,
Interventionpercentage of participants (Number)
Decrease from Baseline in HbA1c ≥0.5%Decrease from Baseline in HbA1c ≥1.0%Decrease from Baseline in HbA1c ≥1.5%Decrease from Baseline in HbA1c ≥2.0%
Alogliptin 25 mg QD32.112.65.12.8
Glipizide 5 mg QD29.010.32.31.4

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Incidence of Hyperglycemic Rescue

The number of participants requiring rescue for failing to achieve pre-specified glycemic targets during the 52 week study. (NCT00707993)
Timeframe: On Occurrence (up to 52 weeks).

,
Interventionparticipants (Number)
Week 2 to Week 4 to Week 8 to Week 12 to Week 16 to Week 20 to Week 26 to Week 34 to Week 42 to Week 52Overall
Alogliptin 25 mg QD12114651061050
Glipizide 5 mg QD010149827637

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Incidence of Marked Hyperglycemia (Fasting Plasma Glucose ≥200 mg Per dL).

The number of participants with a fasting plasma glucose value ≥ to 200 mg per dL during the 52 week study. (NCT00707993)
Timeframe: On Occurrence (up to 52 weeks).

,
Interventionparticipants (Number)
Baseline to Week 4 to Week 8 to Week 12 to Week 16 to Week 20 to Week 26 to Week 34 to Week 42 to Week 52Overall
Alogliptin 25 mg QD301112115232950
Glipizide 5 mg QD175884384637

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AUC0-t [Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant) - Metformin

Bioequivalence based on AUC0-t (NCT00834587)
Timeframe: Blood samples collected over 36 hour period

Interventionng*h/mL (Mean)
Glipizide Metformin4220.7
Metaglip™4233.5

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AUC0-inf [Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)] - Metformin

Bioequivalence based on AUC0-inf (NCT00834587)
Timeframe: Blood samples collected over 36 hour period

Interventionng*h/mL (Mean)
Glipizide Metformin4397.8
Metaglip™4423.2

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AUC0-inf [Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)] - Glipizide

Bioequivalence based on AUC0-inf (NCT00834587)
Timeframe: Blood samples collected over 36 hour period

Interventionng*h/mL (Mean)
Glipizide Metformin2214.7
Metaglip™2204.7

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AUC0-t [Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)] - Glipizide

Bioequivalence based on AUC0-t (NCT00834587)
Timeframe: Blood samples collected over 36 hour period

Interventionng*h/mL (Mean)
Glipizide Metformin2197.6
Metaglip™2188.2

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Cmax (Maximum Observed Concentration) - Glipizide in Plasma

Bioequivalence based on Cmax (NCT00834587)
Timeframe: Blood samples collected over 36 hour period

Interventionng/mL (Mean)
Glipizide Metformin377.949
Metaglip™381.282

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Cmax (Maximum Observed Concentration) - Metformin in Plasma

Bioequivalence based on Cmax (NCT00834587)
Timeframe: Blood samples collected over 36 hour period

Interventionng/mL (Mean)
Glipizide Metformin661.03
Metaglip™644.64

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AUC0-inf [Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)] - Metformin

Bioequivalence based on AUC0-inf (NCT00835497)
Timeframe: Blood samples collected over 36 hour period

Interventionng*h/mL (Mean)
Glipizide Metformin3912.0
Metaglip®4212.7

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AUC0-inf [Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)]- Glipizide

Bioequivalence based on AUC0-inf (NCT00835497)
Timeframe: Blood samples collected over 36 hour period

Interventionng*h/mL (Mean)
Glipizide Metformin2032.8
Metaglip®2092.9

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AUC0-t [Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)]- Metformin

Bioequivalence based on AUC0-t (NCT00835497)
Timeframe: Blood samples collected over 36 hour period

Interventionng*h/mL (Mean)
Glipizide Metformin3701.3
Metaglip®3979.2

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Cmax (Maximum Observed Concentration) - Glipizide in Plasma

Bioequivalence based on Cmax (NCT00835497)
Timeframe: Blood samples collected over 36 hour period

Interventionng/mL (Mean)
Glipizide Metformin337.100
Metaglip®392.150

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Cmax (Maximum Observed Concentration) - Metformin in Plasma

Bioequivalence based on Cmax (NCT00835497)
Timeframe: Blood samples collected over 36 hour period

Interventionng/mL (Mean)
Glipizide Metformin640.00
Metaglip®724.98

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AUC0-t [Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)] - Glipizide

Bioequivalence based on AUC0-t (NCT00835497)
Timeframe: Blood samples collected over 36 hour period

Interventionng*h/mL (Mean)
Glipizide Metformin2005.8
Metaglip®2065.1

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Percentage of Participants With Glycosylated Hemoglobin Less Than or Equal to 6.5%

The percentage of participants with HbA1c less than or equal to 6.5% at Weeks 26, 52, 78, and 104. Participants who did not complete the scheduled Week 104 visit were assessed based on their response at the time of discontinuation. (NCT00856284)
Timeframe: Weeks 26, 52, 78, and 104.

,,
Interventionpercentage of participants (Number)
Week 26Week 52Week 78Week 104
Metformin + Alogliptin 12.5 mg25.624.524.223.5
Metformin + Alogliptin 25 mg26.224.826.424.1
Metformin + Glipizide24.820.821.819.0

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Change From Baseline in Glycosylated Hemoglobin (HbA1c) at Week 52

The change from Baseline to Week 52 in HbA1c (the concentration of glucose bound to hemoglobin as a percent of the absolute maximum that can be bound). The least squares (LS) means are from an analysis of covariance (ANCOVA) model with treatment, study schedule, and geographic region as class variables, and Baseline metformin dose and Baseline HbA1c as covariates. (NCT00856284)
Timeframe: Baseline and Week 52

Interventionpercentage glycosylated hemoglobin (Least Squares Mean)
Metformin + Alogliptin 12.5 mg-0.81
Metformin + Alogliptin 25 mg-0.76
Metformin + Glipizide-0.73

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Percentage of Participants With Glycosylated Hemoglobin Less Than or Equal to 7.0%

Percentage of participants with HbA1c ≤ 7.0% at Weeks 26, 52, 78, and 104. Participants who did not complete the scheduled Week 104 visit were assessed based on their response at the time of discontinuation. (NCT00856284)
Timeframe: Weeks 26, 52, 78, and 104.

,,
Interventionpercentage of participants (Number)
Week 26Week 52Week 78Week 104
Metformin + Alogliptin 12.5 mg56.451.748.845.6
Metformin + Alogliptin 25 mg59.255.552.448.5
Metformin + Glipizide56.147.446.642.8

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Change From Baseline in Glycosylated Hemoglobin (HbA1c) at Week 104

The change from Baseline to Week 104 in HbA1c (the concentration of glucose bound to hemoglobin as a percent of the absolute maximum that can be bound). The least squares (LS) means are from an analysis of covariance (ANCOVA) model with treatment, study schedule, and geographic region as class variables, and Baseline metformin dose and Baseline HbA1c as covariates. (NCT00856284)
Timeframe: Baseline and Week 104

Interventionpercentage glycosylated hemoglobin (Least Squares Mean)
Metformin + Alogliptin 12.5 mg-0.68
Metformin + Alogliptin 25 mg-0.72
Metformin + Glipizide-0.59

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Change From Baseline in Body Weight Over Time

LS Means are from an ANCOVA model with treatment, study schedule and geographic region as class variables, and Baseline weight and Baseline metformin dose as covariates. (NCT00856284)
Timeframe: Baseline and Weeks 12, 26, 39, 52, 65, 78, 91, and 104.

,,
Interventionkg (Least Squares Mean)
Week 12Week 26Week 39Week 52Week 65Week 78Week 91Week 104
Metformin + Alogliptin 12.5 mg-0.51-0.65-0.60-0.63-0.70-0.78-0.67-0.68
Metformin + Alogliptin 25 mg-0.53-0.71-0.86-0.90-0.92-0.94-0.88-0.89
Metformin + Glipizide0.710.860.970.890.870.880.890.95

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Change From Baseline in Fasting Plasma Glucose Over Time

The change from Baseline in fasting plasma glucose (FPG) was assessed at Weeks 2, 4, 8, 12, 16, 20, 26, 39, 52, 65, 78, 91, and 104. LS means are from an ANCOVA model with treatment, study schedule, and geographic region as class variables, and Baseline FPG and Baseline metformin dose as covariates. (NCT00856284)
Timeframe: Baseline and Weeks 2, 4, 8, 12, 16, 20, 26, 39, 52, 65, 78, 91, and 104.

,,
Interventionmg/dL (Least Squares Mean)
Week 2 (n=781, 803, 777)Week 4 (n=863, 865, 855)Week 8 (n=867, 867, 859)Week 12 (n=867, 867, 859)Week 16 (n=867, 867, 859)Week 20 (n=867, 867, 859)Week 26 (n=867, 867, 859)Week 39 (n=867, 867, 859)Week 52 (n=867, 867, 859)Week 65 (n=867, 867, 859)Week 78 (n=867, 867, 859)Week 91 (n=867, 867, 859)Week 104 (n=867, 867, 859)
Metformin + Alogliptin 12.5 mg-10.2-10.6-9.2-10.7-8.6-7.6-7.5-6.9-5.0-3.4-2.8-0.9-0.9
Metformin + Alogliptin 25 mg-11.4-11.6-11.6-11.2-9.9-10.1-10.1-8.4-7.0-5.9-5.1-3.4-3.2
Metformin + Glipizide-7.7-10.2-9.3-9.4-7.1-5.5-4.3-0.60.91.45.14.95.4

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Change From Baseline in Glycosylated Hemoglobin at Other Time Points

The change from Baseline over time in HbA1c (the concentration of glucose bound to hemoglobin as a percent of the absolute maximum that can be bound). LS means are from an ANCOVA model with treatment, study schedule, and geographic region as class variables, and Baseline metformin dose and Baseline HbA1c as covariates. (NCT00856284)
Timeframe: Baseline and Weeks 4, 8, 12, 16, 20, 26, 39, 65, 78, and 91.

,,
Interventionpercentage of glycosylated hemoglobin (Least Squares Mean)
Week 4 (n=341, 354, 318)Week 8 (n=370, 382, 336)Week 12 (n=371, 382, 336)Week 16 (n=371, 382, 336)Week 20 (n=371, 382, 336)Week 26 (n=371, 382, 336)Week 39 (n=371, 382, 336)Week 65 (n=371, 382, 336)Week 78 (n=371, 382, 336)Week 91 (n=371, 382, 336)
Metformin + Alogliptin 12.5 mg-0.37-0.56-0.69-0.74-0.76-0.80-0.81-0.81-0.82-0.76
Metformin + Alogliptin 25 mg-0.40-0.60-0.71-0.76-0.78-0.79-0.81-0.83-0.80-0.77
Metformin + Glipizide-0.41-0.66-0.78-0.78-0.79-0.80-0.74-0.76-0.73-0.68

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Change From Baseline in 2-Hour Post-Meal Glucose (PMG) at Week 26

Change from baseline reflects the Week 26 value minus the baseline value. (NCT00885352)
Timeframe: Baseline and Week 26

Interventionmg/dL (Least Squares Mean)
Sitagliptin-54.4
Placebo-14.7

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Change From Baseline in Fasting Plasma Glucose (FPG) at Week 26

Change from baseline reflects the Week 26 value minus the baseline value. (NCT00885352)
Timeframe: Baseline and Week 26

Interventionmg/dL (Least Squares Mean)
Sitagliptin-20.3
Placebo-2.8

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Change From Baseline in Hemoglobin A1c (A1C) at Week 26

Change from baseline reflects the Week 26 value minus the baseline value. A1C represents the percentage of glycosylated hemoglobin. (NCT00885352)
Timeframe: Baseline and Week 26

InterventionPercent of glycosylated hemoglobin (Least Squares Mean)
Sitagliptin-1.15
Placebo-0.40

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Potassium; Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

InterventionmEq/L (Mean)
Higher Dose0.02
Lower Dose-0.02
40 mg Fixed Dose0.00
20 mg Fixed Dose-0.01
Placebo-0.02
Glipizide0.07
Open Label0.05

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Pulse, Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

InterventionBeats/min (Mean)
Higher Dose0.4
Lower Dose1.6
40 mg Fixed Dose1.3
20 mg Fixed Dose0.3
Placebo-1.1
Glipizide-0.4
Open Label1.3

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QTcF; Electorcardiagram Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

Interventionmsec (Mean)
Higher Dose4.4
Lower Dose4.0
40 mg Fixed Dose-2.6
20 mg Fixed Dose3.8
Placebo2.2
Glipizide2.7
Open Label1.6

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SMPG: Change From Baseline to 4 Month, Compared With Placebo, FAS Prior to Rescue.

AZD1656 is analyzed in a ANCOVA model (Glipized and Open Label is Not Included in the model), FAS Prior to Rescue. (NCT01020123)
Timeframe: baseline to 4 month

Interventionmmol/L (Mean)
Higher Dose-1.596
Lower Dose-1.557
40 mg Fixed Dose-0.874
20 mg Fixed Dose-0.604
Placebo-0.213

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Sodium; Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

InterventionmEq/L (Mean)
Higher Dose-0.6
Lower Dose-0.7
40 mg Fixed Dose-0.4
20 mg Fixed Dose-0.1
Placebo0.0
Glipizide-0.6
Open Label0.5

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Systolic Blood Pressure, Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

InterventionmmHg (Mean)
Higher Dose-0.4
Lower Dose0.4
40 mg Fixed Dose5.7
20 mg Fixed Dose0.1
Placebo-0.2
Glipizide-1.1
Open Label-0.3

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Total Cholesterol: Change From Baseline

Geometric mean ratio (safety analysis set, regardless of rescue) and a 95 % CI. (NCT01020123)
Timeframe: baseline to 4 month

Interventionratio (Geometric Mean)
Higher Dose1.09
Lower Dose1.08
40 mg Fixed Dose1.07
20 mg Fixed Dose1.04
Placebo1.03

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Triglycerides: Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

Interventionmg/dL (Mean)
Higher Dose40.9
Lower Dose38.7
40 mg Fixed Dose19.8
20 mg Fixed Dose4.4
Placebo13.7
Glipizide18.7
Open Label29.8

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Weight, Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

Interventionkg (Mean)
Higher Dose-0.3
Lower Dose-0.6
40 mg Fixed Dose-1.2
20 mg Fixed Dose-1.4
Placebo-1.0
Glipizide1.0
Open Label-0.4

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OGTT/Pro-insulin/Insulin

The relative change, FAS prior to rescue (NCT01020123)
Timeframe: baseline to 4 month

InterventionRatio (Geometric Mean)
Higher Dose1.496
Lower Dose1.199
40 mg Fixed Dose1.248
20 mg Fixed Dose1.431
Placebo1.185

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CL/F to Characterise the PK Properties of AZD1656.

The value is calculated using an allometric model (of a patient weighting 75 kg). The value is independent treatment given. (NCT01020123)
Timeframe: at 4 month

InterventionL/h (Mean)
Higher Dose9.29
Lower Dose9.29
40 mg Fixed Dose9.29
20 mg Fixed Dose9.29
Open Label9.29

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Alkaline Phosphatase; Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

InterventionIU/L (Mean)
Higher Dose3.8
Lower Dose-1.3
40 mg Fixed Dose0.0
20 mg Fixed Dose-1.8
Placebo-3.4
Glipizide-4.2
Open Label-11.7

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ALT; Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

InterventionIU/L (Mean)
Higher Dose2.0
Lower Dose1.7
40 mg Fixed Dose3.2
20 mg Fixed Dose-1.8
Placebo-0.4
Glipizide2.0
Open Label-0.4

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AST; Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

InterventionIU/L (Mean)
Higher Dose2.4
Lower Dose2.0
40 mg Fixed Dose2.8
20 mg Fixed Dose-0.6
Placebo-0.1
Glipizide2.1
Open Label2.7

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Bilirubin; Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

Interventionmg/dL (Mean)
Higher Dose-0.02
Lower Dose-0.06
40 mg Fixed Dose0.02
20 mg Fixed Dose-0.05
Placebo-0.01
Glipizide-0.07
Open Label-11.7

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C-reactive Protein: Change From Baseline

Geometric mean ratio (safety analysis set, regardless of rescue) and a 95 % CI (NCT01020123)
Timeframe: baseline to 4 month

Interventionratio (Geometric Mean)
Higher Dose0.30
Lower Dose0.08
40 mg Fixed Dose0.09
20 mg Fixed Dose0.06
Placebo-0.02

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Creatinine; Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

InterventionIU/L (Mean)
Higher Dose0.4
Lower Dose-9.9
40 mg Fixed Dose8.5
20 mg Fixed Dose-8.3
Placebo-0.1
Glipizide15.9
Open Label-7.3

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Diastolic Blood Pressure, Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

InterventionmmHg (Mean)
Higher Dose1.1
Lower Dose1.4
40 mg Fixed Dose1.3
20 mg Fixed Dose-0.9
Placebo-0.3
Glipizide-0.1
Open Label0.5

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EC50 to Characterise the PD Properties of AZD1656.

The value is model based. The value is independent treatment given. (NCT01020123)
Timeframe: at 4 month

Interventionnmol/L (Mean)
Higher Dose60.2
Lower Dose60.2
40 mg Fixed Dose60.1
20 mg Fixed Dose60.2
Open Label60.2

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FPG: to Evaluate Change From Baseline to 4 Month, Compared With Placebo, FAS Prior to Rescue.

AZD1656 is analyzed in a ANCOVA model (Glipized and Open Label is Not Included in the model), FAS Prior to Rescue. (NCT01020123)
Timeframe: baseline to 4 month

Interventionmmol/L (Mean)
Higher Dose-0.818
Lower Dose-1.08
40 mg Fixed Dose0.041
20 mg Fixed Dose0.024
Placebo-0.182

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Haemoglobin; Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

Interventiong/dL (Mean)
Higher Dose-0.20
Lower Dose-0.18
40 mg Fixed Dose0.00
20 mg Fixed Dose-0.11
Placebo-0.20
Glipizide0.02
Open Label-0.25

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HbA1c ≤ 6.5

Number of Responders ≤ 6.5, FAS Prior to Rescue (NCT01020123)
Timeframe: baseline to 4 month

InterventionParticipants (Number)
Higher Dose35
Lower Dose27
40 mg Fixed Dose9
20 mg Fixed Dose4
Placebo9
Glipizide30
Open Label16

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HbA1c ≤ 7

Number of responders ≤ 7, FAS prior to rescue. (NCT01020123)
Timeframe: baseline to 4 month

InterventionParticipants (Number)
Higher Dose43
Lower Dose43
40 mg Fixed Dose14
20 mg Fixed Dose11
Placebo16
Glipizide50
Open Label24

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HbA1c: Change From Baseline to 4 Month

AZD1656 is analyzed in a ANCOVA model (Glipized and Open Label is Not Included in the model), FAS Prior to Rescue (NCT01020123)
Timeframe: Baseline to 4th Month

InterventionPercentage (Mean)
Higher Dose-1.25
Lower Dose-1.26
40 mg Fixed Dose-0.67
20 mg Fixed Dose-0.61
Placebo-0.45

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HDL-C: Change From Baseline

Geometric mean ratio (safety analysis set, regardless of rescue) and a 95 % CI. (NCT01020123)
Timeframe: baseline to 4 month

Interventionratio (Geometric Mean)
Higher Dose1.06
Lower Dose1.06
40 mg Fixed Dose1.05
20 mg Fixed Dose1.03
Placebo1.03

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LDL-C: Mean Ratio

Geometric mean ratio (safety analysis set, regardless of rescue) and a 95 % CI. (NCT01020123)
Timeframe: baseline to 4 month

Interventionratio (Geometric Mean)
Higher Dose1.07
Lower Dose1.02
40 mg Fixed Dose1.07
20 mg Fixed Dose1.04
Placebo1.02

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Leukocytes; Change From Baseline

Summary statistic of change from baseline (NCT01020123)
Timeframe: baseline to 4 month

Intervention*10^3 cells/µL (Mean)
Higher Dose0.39
Lower Dose0.34
40 mg Fixed Dose0.35
20 mg Fixed Dose-0.15
Placebo-0.8
Glipizide0.27
Open Label-40

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OGTT/C-peptide

The relative change, FAS prior to rescue (NCT01020123)
Timeframe: baseline to 4 month

Interventionratio (Geometric Mean)
Higher Dose0.97
Lower Dose1.11
40 mg Fixed Dose0.90
20 mg Fixed Dose0.95
Placebo1.00

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OGTT/Insulin

The Relative Change in AUC FAS Prior to Rescue (NCT01020123)
Timeframe: baseline to 4 month

Interventionratio (Geometric Mean)
Higher Dose0.81
Lower Dose1.08
40 mg Fixed Dose0.97
20 mg Fixed Dose0.90
Placebo0.91

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OGTT/Plasma Glucose

The relative change in AUC (NCT01020123)
Timeframe: baseline to 4 month

Interventionratio (Geometric Mean)
Higher Dose0.92
Lower Dose0.84
40 mg Fixed Dose1.02
20 mg Fixed Dose0.99
Placebo0.99

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Mean Change in Peak Plasma Glucose, From Baseline to 4 Weeks

"Change in peak plasma glucose level as measured from Baseline to 4 weeks of treatment.~A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab versus placebo within each T2DM population. The mixed model did not include participants from the IGT population." (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionmmol/L (Least Squares Mean)
Canakinumab 150 mg + Metformin-0.41
Placebo + Metformin0.21
Canakinumab 150 mg + Metformin + Sulfonylurea-0.43
Placebo + Metformin + Sulfonylurea-0.03
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia-0.82
Placebo + Met + Sulfonyl + Thiaz-0.77
Canakinumab 150 mg + Insulin-0.15
Placebo + Insulin-0.60
Canakinumab 150 mg in Participants With IGT-0.34
Placebo in Participants With IGT-0.04

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Mean Change in Fasting Glucose Disposition Index(GDI)1 and Index 2, From Baseline to 4 Weeks

GDI 1 is the product of insulin sensitivity index (Si)during the 1st phase of insulin secretion and β-cell function as measured by the acute insulin response (AIR).GDI 2 is the product of (Si)during the 2nd phase of insulin secretion and β-cell function as measured by the acute insulin response (AIR). A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab versus placebo within each T2DM population. The mixed model did not include participants from the IGT group. (NCT01068860)
Timeframe: Baseline, 4 weeks

,,,,,,,,,
Interventionnumber (Least Squares Mean)
Index 1Index 2 (n= 32,15, 29,15, 30,13, 25, 15, 20, 26)
Canakinumab 150 mg + Insulin0.25-0.21
Canakinumab 150 mg + Metformin0.060.14
Canakinumab 150 mg + Metformin + Sulfonylurea0.06-0.94
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia0.240.62
Canakinumab 150 mg in Participants With IGT-0.51-0.16
Placebo + Insulin-0.27-0.25
Placebo + Met + Sulfonyl + Thiaz0.330.49
Placebo + Metformin-0.29-0.81
Placebo + Metformin + Sulfonylurea0.370.81
Placebo in Participants With IGT-0.64-0.31

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Number of Participants Reporting Death, Serious Adverse Events (SAEs) and Adverse Events (AEs) Above 5% Frequency, From Baseline to 4 Weeks

An adverse event is any unwanted event, whether related to study drug or not occuring during the study period. A Serious Adverse Event (SAE) is an event resulting in death, requiring or prolonging hospitalization, a congenital anomaly or other important medical event. AEs and SAEs were recorded at each visit. (NCT01068860)
Timeframe: Baseline, 4 weeks

,,,,,,,,,
Interventionparticipants (Number)
Number of Participants with Serious Adverse EventsNumber of Participants with Non-serious AEs > 5%
Canakinumab 150 mg + Insulin06
Canakinumab 150 mg + Metformin00
Canakinumab 150 mg + Metformin + Sulfonylurea06
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia04
Canakinumab 150 mg in Participants With IGT00
Placebo + Insulin03
Placebo + Met + Sulfonyl + Thiaz03
Placebo + Metformin04
Placebo + Metformin + Sulfonylurea03
Placebo in Participants With IGT00

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Mean Change in Quantitative Insulin Sensitivity Check Index (QUICKI) Score, From Baseline to 4 Weeks

"The Quantitative Insulin Sensitivity Check Index (QUICKI) score, measures insulin sensitivity which is the inverse of insulin resistance. The score is calculated by the equation: 1 /(log(fasting insulin µU/mL) + log(fasting glucose mg/dL)). In normal subjects the mean score ± SE is 0.366 ± 0.029.~A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab versus placebo within each T2DM population. The mixed model did not include participants from the IGT population." (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionnumber (Least Squares Mean)
Canakinumab 150 mg + Metformin0.004
Placebo + Metformin-0.000
Canakinumab 150 mg + Metformin + Sulfonylurea0.002
Placebo + Metformin + Sulfonylurea0.009
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia0.018
Placebo + Met + Sulfonyl + Thiaz-0.001
Canakinumab 150 mg + Insulin-0.003
Placebo + Insulin0.005
Canakinumab 150 mg in Participants With IGT-0.001
Placebo in Participants With IGT0.001

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Mean Change in Absolute Glucose Level at 2 Hours, From Baseline to 4 Weeks

"Change in glucose level measured after 2 hours of fasting. Blood sample was drawn at 0 minutes and at 240 minutes.~A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab versus placebo within each T2DM population. The mixed model did not include participants from the IGT population." (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionmmol/L (Least Squares Mean)
Canakinumab 150 mg + Metformin-0.53
Placebo + Metformin0.13
Canakinumab 150 mg + Metformin + Sulfonylurea-0.60
Placebo + Metformin + Sulfonylurea0.18
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia-1.08
Placebo + Met + Sulfonyl + Thiaz-0.56
Canakinumab 150 mg + Insulin-0.56
Placebo + Insulin-0.16
Canakinumab 150 mg in Participants With IGT-0.26
Placebo in Participants With IGT-0.25

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Mean Change in Post-prandial Glucose Area Under the Curve (AUC)0-4 Hours, From Baseline to 4 Weeks

Blood samples were drawn after a test meal at 0, 15, 30, 45, 60, 90, 120, 180 and 240 min. Insulin levels over 4 hrs were shown as Area Under the Curve,(AUC). AUC was calculated as: x=1 AUC ΣAx n Where Ax = AUC for the 240 min.interval, and X = 1 for the 1st interval. A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab vs placebo within each T2DM group. The mixed model didn't include the IGT group. (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionmmol*hr/L (Least Squares Mean)
Canakinumab 150 mg + Metformin-0.59
Placebo + Metformin0.46
Canakinumab 150 mg + Metformin + Sulfonylurea-1.37
Placebo + Metformin + Sulfonylurea-1.24
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia-3.58
Placebo + Met + Sulfonyl + Thiaz-2.88
Canakinumab 150 mg + Insulin-1.49
Placebo + Insulin-1.76
Canakinumab 150 mg in Participants With IGT-0.71
Placebo in Participants With IGT-0.10

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Mean Change in Peak Plasma Insulin, From Baseline to 4 Weeks

Change in mean peak plasma Insulin level as measured from Baseline to 4 weeks of treatment. A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab versus placebo within each T2DM population. The mixed model did not include participants from the IGT population. (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionpmol/L (Least Squares Mean)
Canakinumab 150 mg + Metformin8.09
Placebo + Metformin44.56
Canakinumab 150 mg + Metformin + Sulfonylurea-55.07
Placebo + Metformin + Sulfonylurea11.33
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia5.13
Placebo + Met + Sulfonyl + Thiaz-5.15
Canakinumab 150 mg + Insulin91.74
Placebo + Insulin36.87
Canakinumab 150 mg in Participants With IGT56.21
Placebo in Participants With IGT-26.43

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Mean Change in Insulin Area Under the Curve (AUC) 0-4 Hours, From Baseline to 4 Weeks

Blood samples were drawn after a test meal at 0, 15, 30, 45, 60, 90, 120, 180 and 240 min. Insulin levels over 4 hrs were shown as Area Under the Curve,(AUC). AUC was calculated as: x=1 AUC ΣAx n Where Ax = AUC for the 240 min.interval, and X = 1 for the 1st interval. A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab vs placebo within each T2DM group. The mixed model didn't include the IGT group. (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionpmol*hour/L (Least Squares Mean)
Canakinumab 150 mg + Metformin-9.37
Placebo + Metformin1.21
Canakinumab 150 mg + Metformin + Sulfonylurea-73.25
Placebo + Metformin + Sulfonylurea-38.32
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia-36.96
Placebo + Met + Sulfonyl + Thiaz8.46
Canakinumab 150 mg + Insulin163.87
Placebo + Insulin139.24
Canakinumab 150 mg in Participants With IGT44.27
Placebo in Participants With IGT-106.68

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Mean Change in Fructosamine, From Baseline to 4 Weeks

"Change in Fructosamine Level taken from plasma, measured at Baseline and after 4 weeks of treatment.~A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab versus placebo within each T2DM population. The mixed model did not include participants from the IGT population" (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionmmol/L (Least Squares Mean)
Canakinumab 150 mg + Metformin-5.30
Placebo + Metformin-0.75
Canakinumab 150 mg + Metformin + Sulfonylurea-3.45
Placebo + Metformin + Sulfonylurea-7.50
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia-1.81
Placebo + Met + Sulfonyl + Thiaz-3.07
Canakinumab 150 mg + Insulin-3.00
Placebo + Insulin-19.73
Canakinumab 150 mg in Participants With IGT-6.36
Placebo in Participants With IGT1.39

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Mean Change in Fasting Plasma Insulin, From Baseline to 4 Weeks

"Change in Fasting Insulin level taken from plasma, measured at Baseline and after 4 weeks of treatment.~A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab versus placebo within each T2DM population. The mixed model did not include participants from the IGT population" (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionpmol/L (Least Squares Mean)
Canakinumab 150 mg + Metformin-3.58
Placebo + Metformin10.73
Canakinumab 150 mg + Metformin + Sulfonylurea-16.07
Placebo + Metformin + Sulfonylurea-9.40
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia-0.77
Placebo + Met + Sulfonyl + Thiaz2.31
Canakinumab 150 mg + Insulin21.27
Placebo + Insulin25.67
Canakinumab 150 mg in Participants With IGT-.021
Placebo in Participants With IGT-3.43

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Mean Change in Fasting Plasma Glucose, From Baseline to 4 Weeks

"Change in Fasting Glucose Level measured from plasma taken at Baseline and after 4 weeks of treatment.~A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab versus placebo within each T2DM population. The mixed model did not include participants from the IGT population" (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionmmol/L (Least Squares Mean)
Canakinumab 150 mg + Metformin-0.32
Placebo + Metformin0.33
Canakinumab 150 mg + Metformin + Sulfonylurea-0.20
Placebo + Metformin + Sulfonylurea-0.23
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia-0.33
Placebo + Met + Sulfonyl + Thiaz-0.36
Canakinumab 150 mg + Insulin-0.26
Placebo + Insulin-0.80
Canakinumab 150 mg in Participants With IGT-0.06
Placebo in Participants With IGT0.10

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Mean Change in Peak Plasma C-peptide Level, From Baseline to 4 Weeks

"Change in mean peak plasma C-peptide level measured from Baseline to 4 weeks of treatment.~A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab versus placebo within each T2DM population. The mixed model did not include participants from the IGT population." (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionnmol/L (Least Squares Mean)
Canakinumab 150 mg + Metformin-0.04
Placebo + Metformin-0.04
Canakinumab 150 mg + Metformin + Sulfonylurea-0.10
Placebo + Metformin + Sulfonylurea0.16
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia-0.21
Placebo + Met + Sulfonyl + Thiaz0.05
Canakinumab 150 mg + Insulin0.07
Placebo + Insulin-0.14
Canakinumab 150 mg in Participants With IGT-0.18
Placebo in Participants With IGT-0.18

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Mean Change in C-peptide Area Under the Curve (AUC), 0-4 Hours, From Baseline to 4 Weeks

Blood samples were drawn after a test meal at 0, 15, 30, 45, 60, 90, 120, 180 and 240 min. Insulin levels over 4 hrs were shown as Area Under the Curve,(AUC). AUC was calculated as: x=1 AUC ΣAx n Where Ax = AUC for the 240 min.interval, and X = 1 for the 1st interval. A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab vs placebo within each T2DM group. The mixed model didn't include the IGT group. (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionnmol*hour/L (Least Squares Mean)
Canakinumab 150 mg + Metformin-0.18
Placebo + Metformin-0.18
Canakinumab 150 mg + Metformin + Sulfonylurea-0.21
Placebo + Metformin + Sulfonylurea0.12
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia-0.61
Placebo + Met + Sulfonyl + Thiaz0.02
Canakinumab 150 mg + Insulin0.16
Placebo + Insulin-0.29
Canakinumab 150 mg in Participants With IGT-0.43
Placebo in Participants With IGT-0.40

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Mean Change in Meal Stimulated Insulin Secretion Rate (ISR) Relative to Glucose 2-4 Hours, From Baseline to 4 Weeks

Change in Insulin Secretion Rate stimulated by Liquid mixed-meal challenge Blood samples were taken prior to and after meal for glucose and insulin at sample times: -20, -10, -1 and 10, 20, 30, 60, 90, 120, 180, and 240 minutes relative to the start of the meal. A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab versus placebo within each T2DM population. The mixed model did not include participants from the IGT population (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionpmol/min/m^2/mmol/L (Least Squares Mean)
Canakinumab 150 mg + Metformin0.21
Placebo + Metformin-2.15
Canakinumab 150 mg + Metformin + Sulfonylurea-2.98
Placebo + Metformin + Sulfonylurea2.02
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia0.15
Placebo + Met + Sulfonyl + Thiaz1.19
Canakinumab 150 mg + Insulin-0.43
Placebo + Insulin-0.51
Canakinumab 150 mg in Participants With IGT-0.71
Placebo in Participants With IGT-1.00

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Mean Change in Meal Stimulated Insulin Secretion Rate (ISR) Relative to Glucose 0-4 Hours, From Baseline to 4 Weeks.

Change in Insulin Secretion Rate stimulated by Liquid mixed-meal challenge. Blood samples were taken prior to and after meal for glucose, insulin and C-peptide at sample times: -20, -10, -1 and 10, 20, 30, 60, 90, 120, 180, and 240 minutes relative to the start of the meal. A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab versus placebo within each T2DM population. The mixed model did not include participants from the IGT population. (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionpmol/min/m^2/mmol/L (Least Squares Mean)
Canakinumab 150 mg + Metformin0.44
Placebo + Metformin-0.99
Canakinumab 150 mg + Metformin + Sulfonylurea-0.32
Placebo + Metformin + Sulfonylurea1.22
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia-0.63
Placebo + Met + Sulfonyl + Thiaz1.24
Canakinumab 150 mg + Insulin0.53
Placebo + Insulin-0.49
Canakinumab 150 mg in Participants With IGT-1.38
Placebo in Participants With IGT-1.35

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Mean Change in Meal Stimulated Insulin Secretion Rate (ISR) Relative to Glucose 0-2 Hours, From Baseline to 4 Weeks.

Change in Insulin Secretion Rate stimulated by Liquid mixed-meal challenge. Blood samples were taken prior to and after meal for glucose and insulin at sample times: -20, -10, -1 and 10, 20, 30, 60, 90, 120, 180, and 240 minutes relative to the start of the meal.A mixed model with treatment fitted as fixed effect, and population and the interaction of population and treatment fitted as random effects were used for the comparison of Canakinumab versus placebo within each T2DM population. The mixed model did not include patients from the IGT population (NCT01068860)
Timeframe: Baseline, 4 weeks

Interventionpmol/min/m^2/mmol/L (Least Squares Mean)
Canakinumab 150 mg + Metformin-0.06
Placebo + Metformin-0.23
Canakinumab 150 mg + Metformin + Sulfonylurea0.04
Placebo + Metformin + Sulfonylurea0.45
Canakinumab 150 mg Canakinumab 150 mg + Met + Sulfonyl + Thia-0.79
Placebo + Met + Sulfonyl + Thiaz1.16
Canakinumab 150 mg + Insulin1.23
Placebo + Insulin-0.49
Canakinumab 150 mg in Participants With IGT-1.50
Placebo in Participants With IGT-1.93

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Percentage of Participants Who Experienced at Least One Adverse Event (Phase A: 24-week Placebo Controlled Period + Phase B: 30-week Active Controlled Period)

An adverse event is defined as any untoward medical occurrence in a participant administered a pharmaceutical product and which does not necessarily have to have a causal relationship with this treatment. Presented data exclude data after glycemic rescue. (NCT01698775)
Timeframe: Up to 58 weeks (including 28 days following the last dose of study therapy)

InterventionPercentage of participants (Number)
Omarigliptin (Phase A) → Omarigliptin (Phase B)77.4
Placebo to Omarigliptin (Phase A) → Glipizide (Phase B)78.3

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Change From Baseline in Estimated Glomerular Filtration Rate (eGFR) at Week 24

Based on an cLDA model including terms for treatment, renal status stratum, treatment on insulin at screening stratum, time, the interaction of time by treatment, the interaction of time by renal status stratum, and the interaction of time by treatment on insulin at screening stratum, with the constraint that the mean baseline is the same for all treatment groups. Excluding data after glycemic rescue or initiation of dialysis as well as participants classified with end stage renal disease (ESRD) on dialysis. (NCT01698775)
Timeframe: Baseline and Week 24

InterventionmL/min/1.73 m^2 (Least Squares Mean)
Omarigliptin (Phase A)-0.5
Placebo to Omarigliptin (Phase A)-0.0

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Change From Baseline in Fasting Plasma Glucose (FPG) at Week 24

Change from baseline in FPG at Week 24 was analyzed using cLDA method with a restriction of the same baseline mean across treatment groups. The cLDA model included terms for treatment, renal insufficiency stratum, baseline treatment with insulin stratum, time, the interaction of time by treatment, the interaction of time by renal insufficiency stratum, and the interaction of time by baseline treatment with insulin stratum. (NCT01698775)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Omarigliptin (Phase A)-24.6
Placebo to Omarigliptin (Phase A)-20.7

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Change From Baseline in FPG at Week 54

Change from baseline in FPG at Week 54 was analyzed using cLDA method with a restriction of the same baseline mean across treatment groups. The cLDA model included terms for treatment, renal insufficiency stratum, baseline treatment with insulin stratum, time, the interaction of time by treatment, the interaction of time by renal insufficiency stratum, and the interaction of time by baseline treatment with insulin stratum. (NCT01698775)
Timeframe: Baseline and Week 54

Interventionmg/dL (Least Squares Mean)
Omarigliptin (Phase A) → Omarigliptin (Phase B)-19.3
Placebo to Omarigliptin (Phase A) → Glipizide (Phase B)-16.4

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Change From Baseline in Glycosylated Hemoglobin (A1C) at Week 24

A1C is measured as a percent. Change from baseline in A1C at Week 24 was analyzed using constrained longitudinal data analysis (cLDA) method with a restriction of the same baseline mean across treatment groups. The cLDA model included terms for treatment, renal insufficiency stratum, baseline treatment with insulin stratum, time, the interaction of time by treatment, the interaction of time by renal insufficiency stratum, and the interaction of time by baseline treatment with insulin stratum. (NCT01698775)
Timeframe: Baseline and Week 24

InterventionPercent (Least Squares Mean)
Omarigliptin (Phase A)-0.77
Placebo to Omarigliptin (Phase A)-0.44

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Percentage of Participants Who Discontinued Study Drug Due to an Adverse Event (Phase A: 24-week Placebo Controlled Period + Phase B: 30-week Active Controlled Period)

An adverse event is defined as any untoward medical occurrence in a participant administered a pharmaceutical product and which does not necessarily have to have a causal relationship with this treatment. Presented data exclude data after glycemic rescue. (NCT01698775)
Timeframe: Up to 54 weeks

InterventionPercentage of participants (Number)
Omarigliptin (Phase A) → Omarigliptin (Phase B)6.6
Placebo to Omarigliptin (Phase A) → Glipizide (Phase B)3.8

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Percentage of Participants Who Discontinued Study Drug Due to an Adverse Event (Phase A: 24-week Placebo Controlled Period)

An adverse event is defined as any untoward medical occurrence in a participant administered a pharmaceutical product and which does not necessarily have to have a causal relationship with this treatment. Presented data exclude data after glycemic rescue. (NCT01698775)
Timeframe: Up to 24 weeks

InterventionPercentage of participants (Number)
Omarigliptin (Phase A)2.8
Placebo to Omarigliptin (Phase A)0.9

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Change From Baseline in A1C at Week 54

A1C is measured as a percent. Change from baseline in A1C at Week 54 was analyzed using cLDA method with a restriction of the same baseline mean across treatment groups. The cLDA model included terms for treatment, renal insufficiency stratum, baseline treatment with insulin stratum, time, the interaction of time by treatment, the interaction of time by renal insufficiency stratum, and the interaction of time by baseline treatment with insulin stratum. (NCT01698775)
Timeframe: Baseline and Week 54

InterventionPercent (Least Squares Mean)
Omarigliptin (Phase A) → Omarigliptin (Phase B)-0.79
Placebo to Omarigliptin (Phase A) → Glipizide (Phase B)-0.83

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Change From Baseline in eGFR at Week 54

Based on an cLDA model including terms for treatment, renal status stratum, treatment on insulin at screening stratum, time, the interaction of time by treatment, the interaction of time by renal status stratum, and the interaction of time by treatment on insulin at screening stratum, with the constraint that the mean baseline is the same for all treatment groups. Excluding data after glycemic rescue or initiation of dialysis as well as participants classified with ESRD on dialysis. (NCT01698775)
Timeframe: Baseline and Week 54

InterventionmL/min/1.73 m^2 (Least Squares Mean)
Omarigliptin (Phase A) → Omarigliptin (Phase B)-2.0
Placebo to Omarigliptin (Phase A) → Glipizide (Phase B)-2.3

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Percentage of Participants Who Experienced at Least One Adverse Event (Phase A: 24-week Placebo Controlled Period)

An adverse event is defined as any untoward medical occurrence in a participant administered a pharmaceutical product and which does not necessarily have to have a causal relationship with this treatment. Presented data exclude data after glycemic rescue. (NCT01698775)
Timeframe: Up to 28 weeks (including 28 days following the last dose of study therapy for participants who discontinued study drug)

InterventionPercentage of participants (Number)
Omarigliptin (Phase A)66.0
Placebo to Omarigliptin (Phase A)69.8

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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

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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

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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

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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

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Glucose Time in Range

Time with glucose 70-140 mg/dL (NCT02608177)
Timeframe: last 6 days of each 28-day treatment period

Interventionminutes per day (Mean)
Glipizide495.2
Linagliptin573.3

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Glycemic Variability

SD of glucose readings (NCT02608177)
Timeframe: last 6 days of each 28-day treatment period

Interventionmg/dL (Mean)
Glipizide40.9
Linagliptin41.5

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Hypoglycemia

Glucose <70 mg/dL for at least 10 minutes (NCT02608177)
Timeframe: last 6 days of each 28-day treatment period

Interventionevents (Number)
Glipizide4
Linagliptin2

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GFR (Glomerular Filtration Rate) Change After Treatment

Change from baseline in GFR after treatment from baseline to 4 months (NCT02911792)
Timeframe: 4 months

Interventionml/min/1.73m^2 (Mean)
Dapagliflozin/Hyperfiltration22
Metformin/Hyperfiltration1
Dapagliflozin/Normofiltration8
Metformin/Normofiltration0

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