Page last updated: 2024-12-05

gliclazide

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Description

Gliclazide is an oral antidiabetic drug of the sulfonylurea class, used in the treatment of type 2 diabetes. It is a second-generation sulfonylurea, meaning it is more potent and has a longer duration of action than first-generation sulfonylureas. Gliclazide works by stimulating the release of insulin from the pancreas, the organ responsible for producing insulin. It achieves this by binding to and closing ATP-sensitive potassium channels in pancreatic beta cells, which triggers the release of insulin. Gliclazide has been shown to have a variety of other effects beyond its primary action on insulin release. For example, it has been shown to improve blood lipid profiles, reduce oxidative stress, and have anti-inflammatory effects. It is also thought to have a protective effect on the cardiovascular system. Gliclazide is a commonly prescribed medication for type 2 diabetes and has been shown to be effective in lowering blood glucose levels and improving glycemic control. It is generally well-tolerated, although it can cause side effects such as hypoglycemia, weight gain, and gastrointestinal disturbances. Gliclazide is a popular subject of research due to its potential benefits in treating diabetes and its potential to improve other aspects of health beyond blood glucose control. Researchers are investigating its long-term effects, its efficacy in different populations, and its potential for use in combination with other medications.'

Gliclazide: An oral sulfonylurea hypoglycemic agent which stimulates insulin secretion. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

18alpha-glycyrrhetinic acid: a gap junction inhibitor [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID3475
CHEMBL ID427216
CHEBI ID31654
SCHEMBL ID16387
MeSH IDM0009266
PubMed CID73398
CHEMBL ID454067
SCHEMBL ID352147
MeSH IDM0009266

Synonyms (164)

Synonym
AB00053165-09
BRD-A61154809-001-04-3
DIVK1C_006966
n-(hexahydrocyclopenta[c]pyrrol-2(1h)-ylcarbamoyl)-4-methylbenzenesulfonamide
1-(3-azabicyclo(3.3.0)oct-3-yl)-3-(p-tolylsulfonyl)urea
CHEBI:31654 ,
1-(hexahydrocyclopenta(c)pyrrol-2(1h)-yl)-3-(p-tolylsulfonyl)urea
PRESTWICK3_000558
n-[(hexahydrocyclopenta[c]pyrrol-2(1h)-ylamino)carbonyl]-4-methylbenzenesulfonamide
SPECTRUM_001478
SPECTRUM5_000753
BPBIO1_000699
PRESTWICK2_000558
21187-98-4
PRESTWICK_869
gliclazide
cas-21187-98-4
NCGC00016751-01
BSPBIO_000635
BSPBIO_003304
AB00053165
gliclazide, powder, >=98%
DB01120
D01599
glimicron (tn)
gliclazide (jp17/inn)
NCGC00095107-03
NCGC00095107-01
NCGC00095107-02
KBIO1_001910
KBIO3_002806
KBIOSS_001958
KBIO2_004526
KBIO2_007094
KBIOGR_001096
KBIO2_001958
PRESTWICK0_000558
SPBIO_002556
SPECPLUS_000870
SPECTRUM3_001862
SPECTRUM4_000598
PRESTWICK1_000558
SPECTRUM1504145
SPECTRUM1505013
NCGC00095107-06
NCGC00095107-04
MLS001304077
NCGC00095107-05
smr000542971
MLS001215197
HMS2090K16
AC-12045
MLS001304118
CHEMBL427216
nsc-758673
se-1702
HMS1569P17
HMS1922D15
1-(3,3a,4,5,6,6a-hexahydro-1h-cyclopenta[c]pyrrol-2-yl)-3-(4-methylphenyl)sulfonylurea
STK803142
AKOS003237903
HMS2096P17
G0381
1-[3-azabicyclo[3.3.0]oct-3-yl]-3-p-toluenesulfonylurea
1-(3-azabicyclo[3.3.0]oct-3-yl)-3-p-tolylsulphonylurea
A815188
1-(3,3a,4,5,6,6a-hexahydro-1h-cyclopenta[c]pyrrol-2-yl)-3-(4-methylphenyl)sulfonyl-urea
BBL012275
pharmakon1600-01504145
nsc758673
dtxcid003095
tox21_110590
dtxsid9023095 ,
HMS2855P09
FT-0626712
NCGC00095107-10
AB05958
S2601 ,
AKOS016340698
CCG-213918
HY-B0753
SCHEMBL16387
tox21_110590_1
NCGC00095107-09
KS-1067
gliclazide, british pharmacopoeia (bp) reference standard
urea, 1-(hexahydrocyclopenta[c]pyrrol-2(1h)-yl)-3-(p-tolylsulfonyl)-
BOVGTQGAOIONJV-UHFFFAOYSA-N
benzenesulfonamide, n-[[(hexahydrocyclopenta[c]pyrrol-2(1h)-yl)amino]carbonyl]-4-methyl-
AB00053165_10
AB00053165_11
mfcd00409893
1-[(4-methylbenzene)sulfonyl]-3-{octahydrocyclopenta[c]pyrrol-2-yl}urea
J-522753
se1702
SR-01000816184-4
SR-01000816184-3
SR-01000816184-2
sr-01000816184
n-((hexahydrocyclopenta[c]pyrrol-2(1h)-yl)carbamoyl)-4-methylbenzenesulfonamide
gliclazide, european pharmacopoeia (ep) reference standard
HMS3656C22
bdbm50103512
J-013905
SBI-0052662.P002
HMS3713P17
SW196994-3
1-(hexahydrocyclopenta[c]pyrrol-2(1h)-yl)-3-[(4-methylphenyl)sulfonyl]urea
BCP21240
nsc-813216
nsc813216
gliclazide (diamicron)
gliclazide,(s)
Q290001
HMS3744O13
s1702;se1702
D83168
benzenesulfonamide,n-[[(hexahydrocyclopenta[c]pyrrol-2(1h)-yl)amino]carbonyl]-4-methyl-
1-(4-methylbenzenesulfonyl)-3-{octahydrocyclopenta[c]pyrrol-2-yl}urea
EN300-7359575
benzenesulfonamide, n-[[(hexahydrocyclopenta[c]pyrrol-2(1h)-yl)amino]carbonyl]-4-methyl
brn 2956366
nsc 35350
3-beta-hydroxy-11-oxo-18-alpha-olean-12-en-30-oic acid
einecs 215-907-9
ccris 3963
(3beta,18alpha,20beta)-3-hydroxy-11-oxoolean-12-en-29-oic acid
18-alpha-olean-12-en-30-oic acid, 3-beta-hydroxy-11-oxo-
18alpha-glycyrrhetinic acid; 3?-hydroxy-11-oxo-18?,20?-olean-12-en-29-oic acid
S00283
18alpha-glycyrrhetinic acid
18-alpha-glycyrrhetinic acid
18alpha-glycyrrhetinic acid, >=95%
18a-glycyrrhetinic acid
(2s,4as,6ar,6as,6br,8ar,10s,12as,14bs)-10-hydroxy-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1h-picene-2-carboxylic acid
AKOS016036161
S6456
SCHEMBL352147
LMPR0106150026
(18alpha)-3beta-hydroxy-11-oxoolean-12-en-30-oic acid
CHEMBL454067
mfcd00064897
DTXSID20872408
3ss-hydroxy-11-oxo-18a,20ss-olean-12-en-29-oic acid
18-isoglycyrrhetinic acid
b-glycyrrhetinic acid
18 alpha-glycyrrhetinic acid
18alpha-olean-12-en-30-oic acid, 3beta-hydroxy-11-oxo- (6ci,7ci,8ci)
3-hydroxy-11-oxo-(3beta,18alpha,20beta)-olean-12-en-29-oic acid
isoglycyrrhetinic acid
olean-12-en-29-oic acid, 3-hydroxy-11-oxo-, (3beta,18alpha,20beta)-
CS-8150
X6NYL2CP2E
enoxolone impurity a [ep impurity]
3beta-hydroxy-11-oxo-18alpha-olean-12-en-30-oic acid (18alpha-glycyrrhetinic acid),
18alpha-olean-12-en-30-oic acid, 3beta-hydroxy-11-oxo-
HY-N0375
18(c) paragraph sign-glycyrrhetinic acid
nsc 35350;nsc 35350;nsc 35350
BCP09996
(2s,4as,6as,6br,8ar,10s,12as,12br,14bs)-10-hydroxy-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-1,2,3,4,4a,5,6,6a,6b,7,8,8a,9,10,11,12,12a,12b,13,14b-icosahydropicene-2-carboxylic acid
AKOS037515811
EN300-7412762
Z3235068248

Research Excerpts

Overview

Gliclazide (GLZ) is a second-generation oral hypoglycemic drug used for the treatment of noninsulin-dependent diabetes mellitus. The drug is a widely used sulfonylurea hypogly diabetic drug, but its cancer risk remains controversial.

ExcerptReferenceRelevance
"Gliclazide is a second-generation oral hypoglycemic drug used for the treatment of noninsulin-dependent diabetes mellitus. "( Gliclazide.
Al-Omary, FAM,
)
3.02
"Gliclazide is a drug commonly used in type 2 diabetes mellitus. "( High-Loading Dose of Microencapsulated Gliclazide Formulation Exerted a Hypoglycaemic Effect on Type 1 Diabetic Rats and Incorporation of a Primary Deconjugated Bile Acid, Diminished the Hypoglycaemic Antidiabetic Effect.
Al-Salami, H; Calasan, J; Golocorbin-Kon, S; Lalic-Popovic, M; Mikov, M; Milijasevic, B; Vukmirovic, S, 2017
)
2.17
"Gliclazide (GLZ) is a second generation hypoglycemic drug used for the treatment of Type 2 diabetes mellitus. "( Development of a Dissolution Method for Gliclazide Modified-Release Tablets Using USP Apparatus 3 with in Vitro-in Vivo Correlation.
Bezerra, KC; Cabral, LM; de Sousa, VP; Pinto, EC, 2018
)
2.19
"Gliclazide is a widely used sulfonylurea hypoglycemic drug, but its cancer risk remains controversial."( Mutations in gliclazide-associated genes may predict poor bladder cancer prognosis.
Chen, H; Gong, J; Sun, J; Wang, M; Wen, W; Wu, P; Zhao, M, 2019
)
1.6
"Gliclazide is an oral hypoglycemic agent, indicated in non insulin dependent diabetes mellitus and in patients with diabetic retinopathy. "( Effect of two hydrophobic polymers on the release of gliclazide from their matrix tablets.
Abbas, K; Awais, A; Hussain, T; Idrees, HA; Javaid, Z; Mumtaz, AM; Saeed, T,
)
1.82
"Gliclazide (G) is an antidiabetic drug commonly used in type 2 diabetes. "( Novel artificial cell microencapsulation of a complex gliclazide-deoxycholic bile acid formulation: a characterization study.
Al-Salami, H; Al-Sallami, HS; Arfuso, F; Chen-Tan, N; Fakhoury, M; Fang, Z; Golocorbin-Kon, S; Mikov, M; Mooranian, A; Mukkur, T; Negrulj, R, 2014
)
2.09
"Gliclazide is an effective oral antidiabetic that may be suitable for the management of patients with type 2 diabetes during Ramadan."( Incidence of hypoglycemia in patients with type 2 diabetes treated with gliclazide versus DPP-4 inhibitors during Ramadan: A meta-analytical approach.
Abdel-Rahim, A; Al-Sifri, S; Mbanya, JC; Satman, I, 2015
)
1.37
"Gliclazide (G) is a commonly prescribed drug for Type 2 diabetes (T2D). "( A comprehensive study of novel microcapsules incorporating gliclazide and a permeation enhancing bile acid: hypoglycemic effect in an animal model of Type-1 diabetes.
Al-Salami, H; Arfuso, F; Chen-Tan, N; Mathavan, S, 2016
)
2.12
"Gliclazide is a second generation of hypoglycemic sulfonylurea and acts selectively on pancreatic beta cell to control diabetes mellitus. "( Applying the Taguchi design for optimized formulation of sustained release gliclazide chitosan beads: an in vitro/in vivo study.
Minayian, M; Rahdari, N; Tavakoli, N; Varshosaz, J, 2009
)
2.03
"Gliclazide is a second-generation sulfonylurea compound used in the treatment of type II diabetes mellitus."( Effect of gliclazide immobilization into layered double hydroxide on drug release.
Ambrogi, V; Ciarnelli, V; Nocchetti, M; Perioli, L; Rossi, C, 2009
)
1.48
"Gliclazide is a sulphonylurea antidiabetic drug with anti-oxidant effect due to its azabicyclo-octyl ring. "( Radical scavenging effect of gliclazide in diabetic rats fed with a high cholesterol diet.
Fujita, T; Goto, A; Onozato, ML; Tojo, A, 2004
)
2.06
"Gliclazide is a sulfonylurea compound oral hypoglycemic drug that has a unique feature of restoring the first-phase insulin secretion, which is lost in T2DM being one of the early features of disease."( NIDDM: new once-daily intervention for type 2 diabetes mellitus: Diaprel MR.
Brădescu, OM; Gavrilă, L; Guja, C; Ionescu-Tîrgovişte, C, 2004
)
1.04
"Gliclazide is a well known agent used for NIDDM. "( Synthesis and characterization of gliclazide complexes of magnesium, calcium, chromium, manganese, iron, nickel, copper, zinc and cadmium salts.
Arayne, MS; Farooq, A; Sultana, N; Zaman, MK, 2005
)
2.05
"Gliclazide is an oral hypoglycemic agent that belongs to the class of sulfonylureas: basic and clinical evidences suggest that gliclazide works as an antioxidative drug, independently from its ability to reduce hyperglycemia."( Effects of gliclazide beyond metabolic control.
Ceriello, A, 2006
)
1.45
"Gliclazide is an SU agent believed to be more protective."( 'Warm-up' phenomenon in diabetic patients with stable angina treated with diet or sulfonylureas.
Bilinska, M; Korzeniowska-Kubacka, I; Piotrowicz, R; Potocka, J, 2007
)
1.06
"Gliclazide is a potent antidiabetic agent because of its capability to decrease blood glucose level via stimulating endogenous insulin secretion from beta-pancreas cells. "( In vivo and in vitro evaluation of a solid dispersion system of gliclazide:PEG 6000.
Asyarie, S; Rachmawati, H,
)
1.81
"Gliclazide is a sulphonylurea antidiabetic drug with antioxidant effects due to its azabicyclo-octyl ring."( Antioxidant and vascular effects of gliclazide in type 2 diabetic rats fed high-fat diet.
Louro, T; Matafome, P; Monteiro, P; Nunes, E; Seiça, R; Sena, CM, 2009
)
1.35
"Gliclazide is a 'second generation' oral hypoglycaemic agent. "( Gliclazide. A preliminary review of its pharmacodynamic properties and therapeutic efficacy in diabetes mellitus.
Avery, GS; Brogden, RN; Heel, RC; Holmes, B; Speight, TM, 1984
)
3.15
"Gliclazide is a useful drug in the therapy of diabetes mellitus."( Comparison of gliclazide and glibenclamide treatment in non-insulin-dependent diabetes.
Baba, S; Fukui, I; Goto, Y; Maezawa, H; Nakagawa, S; Sakamoto, N; Takebe, K; Takeda, R, 1983
)
1.35
"Gliclazide is a second generation sulphonylurea oral hypoglycaemic agent used in the treatment of non-insulin-dependent diabetes mellitus (NIDDM). "( Gliclazide. An update of its pharmacological properties and therapeutic efficacy in non-insulin-dependent diabetes mellitus.
Brogden, RN; Palmer, KJ, 1993
)
3.17
"Gliclazide is a second-generation sulfonylures that is widely used in the treatment of non-insulin-dependent diabetes mellitus (Type 2 diabetes). "( [Gliclazide: review of metabolic and vascular action].
Alberti, KG, 1994
)
2.64
"Gliclazide is a second generation sulfonylurea that is widely used in the treatment of type II diabetes mellitus."( Hemobiological properties of gliclazide.
Drouin, P; Ziegler, O,
)
1.14
"Gliclazide is known to be a general free radical scavenger as demonstrated by inhibition of o-dianisidine photo-oxidation."( Gliclazide scavenges hydroxyl, superoxide and nitric oxide radicals: an ESR study.
Mori, A; Noda, Y; Packer, L, 1997
)
2.46
"Gliclazide is known to be a general free radical scavenger as shown by its inhibition of o-dianisidine photo-oxidation."( Gliclazide scavenges hydroxyl and superoxide radicals: an electron spin resonance study.
Cossins, E; Mori, A; Noda, Y; Packer, L, 2000
)
2.47
"Gliclazide is a high-potency sulphonylurea which shows specificity for the pancreatic beta-cell KATP channel over heart and smooth muscle. "( Gliclazide produces high-affinity block of KATP channels in mouse isolated pancreatic beta cells but not rat heart or arterial smooth muscle cells.
Ashcroft, FM; Hayabuchi, Y; Jones, P; Lawrence, CL; Proks, P; Rodrigo, GC; Standen, NB, 2001
)
3.2
"Gliclazide is an oral hypoglycaemic agent which has been shown in animal models to reduce platelet adhesiveness. "( Effect on platelet adhesiveness in diabetics after long-term treatment with a new oral hypoglycaemic agent, gliclazide.
Coce, F; Maitre, D; Mustovic, D; Rubinjoni, Z; Skrabalo, Z; Turk, Z, 1978
)
1.91
"Gliclazide is a second-generation sulfonylurea that is widely used in the treatment of non-insulin-dependent diabetes mellitus (NIDDM). "( Gliclazide: metabolic and vascular effects--a perspective.
Alberti, KG; Johnson, AB; Taylor, R, 1992
)
3.17
"Gliclazide is a sulphonylurea drug with an intermediate half-life of around 11 hours. "( The mode of action and clinical pharmacology of gliclazide: a review.
Campbell, DB; Lavielle, R; Nathan, C, 1991
)
1.98
"Gliclazide is a second-generation sulfonylurea drug whose efficacy in the treatment of NIDDM, alone or in combination with insulin, has been widely demonstrated."( Current status of non-insulin-dependent diabetes mellitus (type II): management with gliclazide.
Rifkin, H, 1991
)
1.23
"Gliclazide is an oral sulfonylurea agent that has been reported to have actions on platelet function and fibrinolysis in addition to its effects on glycemia."( Pathophysiology of vascular disease in diabetes: effects of gliclazide.
Colwell, JA, 1991
)
1.24
"Gliclazide is a suitable oral hypoglycaemic agent for use in the obese diabetic who cannot be controlled by diet alone."( A comparison of treatment with metformin and gliclazide in patients with non-insulin-dependent diabetes.
Frier, BM; Kay, JW; McAlpine, CH; McAlpine, LG; Storer, AM; Waclawski, ER, 1988
)
1.26
"Gliclazide was proven to be a reliable blood-sugar lowering agent with a generally good subjective tolerance."( [Gliclazide in the non-insulin-dependent diabetic patient in geriatrics].
Böhmer, F; Frühwald, T, 1988
)
1.91

Effects

Gliclazide has been reported to possess the properties of preventing the progression of diabetic retinopathy and of controlling blood glucose levels. It has beneficial effects on platelet behavior and function and on the endothelium, in addition to improving free radical status.

ExcerptReferenceRelevance
"Gliclazide has protective effects on high glucose and AGEs-induced damage of glomerular mesangial cells and renal tubular epithelial cells via inhibiting RAGE-NADPH oxidase-NF-kB pathway."( Protective effects of gliclazide on high glucose and AGEs-induced damage of glomerular mesangial cells and renal tubular epithelial cells via inhibiting RAGE-p22phox-NF-kB pathway.
Feng, B; Li, PC; Yang, PY, 2019
)
2.27
"Gliclazide has been suspected to be associated with a lower obesity-related cancer risk; however, current evidence is limited by important methodologic shortcomings. "( Is Gliclazide Associated with a Lower Obesity-Related Cancer Risk Compared to Other Sulfonylureas? A Long-term Prospective Cohort Study.
de Bock, GH; Du, J; Groenier, KH; Kleefstra, N; Landman, GWD; Schrijnders, D, 2020
)
2.62
"Gliclazide has variable absorption after oral administration, and thus using targeted-delivery techniques, such as microencapsulation, may optimise gliclazide absorption and potential applications in T1DM."( High-Loading Dose of Microencapsulated Gliclazide Formulation Exerted a Hypoglycaemic Effect on Type 1 Diabetic Rats and Incorporation of a Primary Deconjugated Bile Acid, Diminished the Hypoglycaemic Antidiabetic Effect.
Al-Salami, H; Calasan, J; Golocorbin-Kon, S; Lalic-Popovic, M; Mikov, M; Milijasevic, B; Vukmirovic, S, 2017
)
1.45
"Gliclazide has been associated with a low risk of hypoglycemic episodes and beneficial long-term cardiovascular safety in observational cohorts. "( Safety and efficacy of gliclazide as treatment for type 2 diabetes: a systematic review and meta-analysis of randomized trials.
Bilo, HJ; de Bock, GH; Gans, RO; Groenier, KH; Houweling, ST; Kleefstra, N; Landman, GW; van Dijk, PR; van Hateren, KJ, 2014
)
2.16
"Drug Gliclazide (Glz) has limited solubility and low bioavailability. "( Controlled release of anti-diabetic drug Gliclazide from poly(caprolactone)/poly(acrylic acid) hydrogels.
Bajpai, SK; Chand, N; Soni, S, 2015
)
1.2
"Gliclazide has been shown to possess free radical scavenging properties."( Association of gliclazide and left ventricular mass in type 2 diabetic patients.
Chang, NC; Huang, CL; Lee, TM; Lin, MS; Pan, NH, 2006
)
1.41
"Gliclazide has been reported to decrease platelet function and to inhibit the progression of diabetic retinopathy in addition to having a hypoglycemic effect. "( Comparison of gliclazide and glibenclamide treatment in non-insulin-dependent diabetes.
Baba, S; Fukui, I; Goto, Y; Maezawa, H; Nakagawa, S; Sakamoto, N; Takebe, K; Takeda, R, 1983
)
2.07
"Gliclazide also has beneficial effects on platelet behavior and function and on the endothelium, in addition to improving free radical status."( [Gliclazide: review of metabolic and vascular action].
Alberti, KG, 1994
)
1.92
"Gliclazide MR has also demonstrated antioxidant properties that are independent of glycaemic control."( Gliclazide modified release.
Goa, KL; McGavin, JK; Perry, CM, 2002
)
2.48
"Gliclazide also has beneficial effects on platelet behavior and function and on the endothelium, in addition to improving free radical status."( Gliclazide: metabolic and vascular effects--a perspective.
Alberti, KG; Johnson, AB; Taylor, R, 1992
)
2.45
"Gliclazide has been reported to possess the properties of preventing the progression of diabetic retinopathy and of controlling blood glucose levels. "( Long-term comparison of oral hypoglycemic agents in diabetic retinopathy. Gliclazide vs. other sulfonylureas.
Akanuma, Y; Aoki, S; Fukuda, M; Kanazawa, Y; Kasuga, M; Kosaka, K, 1988
)
1.95

Actions

ExcerptReferenceRelevance
"The gliclazide-induced increase in 45Ca efflux is thought to reflect a stimulation of 40Ca influx into islet cells; it is suppressed in the absence of extracellular Ca2+ or in the presence of the organic CA2/-antagonist verapamil."( Modalities of gliclazide-induced Ca2+ influx into the pancreatic B-cell.
Herchuelz, A; Lebrun, P; Malaisse, WJ, 1982
)
1.11

Treatment

Gliclazide or metformin-treated patients demonstrated lesser mortality risk than glibenclamide-treated ones in all four evaluation models. Age and duration stratification can influence this phenomenon in case of "first prescription model"

ExcerptReferenceRelevance
"Gliclazide-treated had similar kidney index, but lower glucose levels, sCr, BUN, and MAU, compared with both saline and 4-PBA-treated diabetic rats or saline-treated TM rats."( Involvement of glucose-regulated protein 78 and spliced X-box binding protein 1 in the protective effect of gliclazide in diabetic nephropathy.
Ren, X; Wang, X; Zhang, M; Zhang, YW, 2018
)
1.41
"Gliclazide treatment lessens diabetic nephropathy, probably partially by suppressing the GRP78- and sXBP1-mediated ER response."( Involvement of glucose-regulated protein 78 and spliced X-box binding protein 1 in the protective effect of gliclazide in diabetic nephropathy.
Ren, X; Wang, X; Zhang, M; Zhang, YW, 2018
)
1.41
"Gliclazide or metformin-treated patients demonstrated lesser mortality risk than glibenclamide-treated ones in all four evaluation models, but age and duration stratification can influence this phenomenon in case of "first prescription model". "( Evaluation approach can significantly influence oral glucose-lowering drugs total mortality risks in retrospective cohorts of type 2 diabetes mellitus patients.
Khalangot, M; Kovtun, V, 2014
)
1.85
"gliclazide treatment."( Glibenclamide-related excess in total and cardiovascular mortality risks: data from large Ukrainian observational cohort study.
Khalangot, M; Kovtun, V; Kravchenko, V; Tronko, M, 2009
)
1.07
"Gliclazide treatment partly restored these changes (p < 0.05)."( Remodelling of zero-stress state of small intestine in streptozotocin-induced diabetic rats. Effect of gliclazide.
Gregersen, H; Sha, H; Tong, X; Zhao, J; Zhou, S; Zhuang, FY, 2002
)
1.25
"Gliclazide treatment, but not glibenclamide, significantly reduced the oxidative products and NAD(P)H oxidase."( Radical scavenging effect of gliclazide in diabetic rats fed with a high cholesterol diet.
Fujita, T; Goto, A; Onozato, ML; Tojo, A, 2004
)
1.34
"Gliclazide MR treatment produced significant reductions in fasting plasma glucose (from 7.6 +/- 1.4 to 6.6 +/- 1.2 mmol/L, p < 0.01), HbA(1c) (from 7.6 +/- 1.1 to 6.9 +/- 0.8%, p < 0.01), and plasma IL-6 concentrations (from 2.5 +/- 1.8 to 1.8 +/- 1.2 pg/mL, p < 0.05). "( Effect of gliclazide modified release on adiponectin, interleukin-6, and tumor necrosis factor-alpha plasma levels in individuals with type 2 diabetes mellitus.
Drzewoski, J; Zurawska-Klis, M, 2006
)
2.18
"Gliclazide treatment results in increased serum C-peptide, decreased hemoglobin-A1c, decreased glucose excursion on glucose tolerance test, and 35% increased insulin-stimulated glucose disposal."( Sulfonylurea therapy improves glucose disposal without changing skeletal muscle GLUT4 levels in noninsulin-dependent diabetes mellitus subjects: a longitudinal study.
Bjørbaek, C; Hansen, L; Kahn, BB; Pedersen, O; Rosen, AS; Vestergaard, H; Weinreb, JE, 1995
)
1.01
"3. Gliclazide treatment did not modify the degree of insulinopenia and hyperglycemia, nor the myocardial energy metabolism during ischemia-reperfusion."( Chronic gliclazide treatment affects basal and post-ischemic cardiac function in diabetic rats.
Mimura, G; Murakami, K; Nagamine, F; Oshiro, K; Shimabukuro, M, 1994
)
1.24
"Gliclazide treatment was associated with significant reductions in HbA1C (p=0.001) and fasting plasma glucose (p=0.005) as well as enhanced beta-cell responses to an oral glucose load."( Unchanged gene expression of glycogen synthase in muscle from patients with NIDDM following sulphonylurea-induced improvement of glycaemic control.
Bjørbaek, C; Lund, S; Pedersen, O; Vestergaard, H, 1995
)
1.01
"2. Gliclazide treatment of diabetic rats allowed a partial recovery of the body weight decrease, but not of the hyperglycemia nor insulinopenia."( Effect of gliclazide on the functional response to calcium in diabetic rat heart.
Higa, S; Murakami, K; Nagamine, F; Shimabukuro, M; Shinzato, T; Takasu, N, 1996
)
1.21
"Gliclazide treatment did not affect the response to acetylcholine of normal rabbit aorta, and gliclazide when added in vitro had no effect on the response of diabetic rabbit aorta, suggesting that the effect of gliclazide was specific to the abnormality arising with diabetes and was not due to an acute effect of the drug."( Vascular action of the hypoglycaemic agent gliclazide in diabetic rabbits.
Cohen, RA; Griswold, MC; Pagano, PJ; Ravel, D, 1998
)
1.28
"In gliclazide-treated NIDDM patients, PDH activity in circulating lymphocytes recovered. "( Molecular effects of sulphonylurea agents in circulating lymphocytes of patients with non-insulin-dependent diabetes mellitus.
Bruno, R; Curto, M; Gamba, S; Mioletti, S; Mostert, M; Piccinini, M; Rabbone, I; Rinaudo, MT, 1998
)
0.92
"Gliclazide treatment lowered LPS-stimulated TNF-alpha production by diabetic monocytes to levels similar to those observed in control subjects."( Normalization of plasma lipid peroxides, monocyte adhesion, and tumor necrosis factor-alpha production in NIDDM patients after gliclazide treatment.
Desfaits, AC; Renier, G; Serri, O, 1998
)
1.23
"Gliclazide-treated Goto-Kakisaki rats were evaluated against Wistar and untreated Goto-Kakisaki rats."( Effect of gliclazide treatment on insulin secretion and beta-cell mass in non-insulin dependent diabetic Goto-Kakisaki rats.
Bailbé, D; Dachicourt, N; Gangnerau, MN; Portha, B; Ravel, D; Serradas, P, 1998
)
1.42
"Gliclazide treatment was associated with improved glycemic control and enhanced pancreatic beta-cell responses to meal stimulation."( Postreceptor effects of sulfonylurea on skeletal muscle glycogen synthase activity in type II diabetic patients.
Bak, JF; Pedersen, O; Schmitz, O; Sørensen, NS, 1989
)
1
"Treatment with gliclazide alone decreased serum glucose, total cholesterol, triglycerides, malondialdehyde, tumor necrosis factor-alpha and nuclear factor kappa-Beta while increased serum C-peptide, superoxide dismutase, reduced glutathione and adiponectin levels. "( New combination therapy of gliclazide and quercetin for protection against STZ-induced diabetic rats.
Abdelkader, NF; Badawi, MA; Eitah, HE; Gamaleldin, AA; Kenawy, SA; Maklad, YA, 2020
)
1.21
"Treatment with gliclazide could not restore p38 phosphorylation in insulin-resistant cells."( Gliclazide increases insulin receptor tyrosine phosphorylation but not p38 phosphorylation in insulin-resistant skeletal muscle cells.
Dey, CS; Kumar, N, 2002
)
2.1
"Treatment with gliclazide resulted in the significant reduction to about 60% of baseline in urinary 8-iso-prostaglandin F2alpha (8iPGF2alpha) excretion while no such change was detected in the glibenclamide period."( Comparison of the antioxidant and vascular effects of gliclazide and glibenclamide in Type 2 diabetic patients: a randomized crossover study.
Higa, N; Shimabukuro, M; Takasu, N,
)
0.72
"Treatment with gliclazide of patients with NIDDM has been shown to be associated with a potentiation of both insulin-mediated glucose disposal and insulin-stimulated glycogen synthase activity in skeletal muscle."( Gliclazide and insulin action in human muscle.
Bak, JF; Pedersen, O, 1991
)
2.06

Toxicity

The number of serious adverse events was higher in the gliclazide group. Unintentional sulfonylurea toxicity developed due to an adverse drug-drug interaction between glicLazide and these antifungals.

ExcerptReferenceRelevance
" Adverse effects were reported by 22 patients, including dizziness and light-headedness, diarrhea, nausea, palpitations and pruritus, but none required modification of Diamicron therapy."( Evaluation of the efficacy and safety of Diamicron in non-insulin-dependent diabetic patients.
Dudley, J; Kalb, B; Kilo, C, 1991
)
0.28
" Adverse effects were recorded in 30 (7."( Efficacy and safety of gliclazide in the treatment of non-insulin-dependent diabetes mellitus: a Canadian multicenter study.
Mailhot, J,
)
0.44
"159 patients with type 2 diabetes were parallelly assigned to a slow-released-gliclazide or gliclazide group in a randomized, open, multi-center phase III study to compare the efficacy of slow-released-gliclazide and gliclazide on overall diabetes control through HbA1c and the adverse events including hypoglycemic episodes and change of vital signs, electrocardiogram and clinical laboratory parameters after a 12-week treatment period."( [The efficacy and safety of 30 mg slow-released-gliclazide in type 2 diabetes mellitus].
Gao, Y; Guo, XH; Li, GW; Li, HB; Pan, CY; Tian, H; Xing, XY; Yang, WY; Yuan, SY, 2004
)
0.81
" No adverse event led to withdrawal of the medication."( [The efficacy and safety of 30 mg slow-released-gliclazide in type 2 diabetes mellitus].
Gao, Y; Guo, XH; Li, GW; Li, HB; Pan, CY; Tian, H; Xing, XY; Yang, WY; Yuan, SY, 2004
)
0.58
"The study objective was to determine if Ramadan fasting was safe in patients with type 2 diabetes mellitus (T2D), based upon a determination of the effect of fasting on a broad range of physiological and clinical parameters, including markers of glycemic control and blood pressure."( Is Ramadan fasting safe in type 2 diabetic patients in view of the lack of significant effect of fasting on clinical and biochemical parameters, blood pressure, and glycemic control?
Chabraoui, L; Chebraoui, L; Chraibi, A; El Guessabi, L; Fellat, S; Israili, ZH; Lyoussi, B; M'guil, M; Ragala, MA, 2008
)
0.35
" The overall incidence of any adverse events was similar in both groups (approximately 61%), but the number of serious adverse events was higher in the gliclazide group (8."( A comparison of efficacy and safety of vildagliptin and gliclazide in combination with metformin in patients with Type 2 diabetes inadequately controlled with metformin alone: a 52-week, randomized study.
Filozof, C; Gautier, JF, 2010
)
0.81
" An understanding of structure-activity relationships (SARs) of chemicals can make a significant contribution to the identification of potential toxic effects early in the drug development process and aid in avoiding such problems."( Developing structure-activity relationships for the prediction of hepatotoxicity.
Fisk, L; Greene, N; Naven, RT; Note, RR; Patel, ML; Pelletier, DJ, 2010
)
0.36
" The reduction of prescribed sulfonylurea dose in DPP-4 patients following the safety alert coincided with a decrease of adverse event reports."( Effects of a sitagliptin safety alert on prescription behaviour for oral antihyperglycaemic drugs: a propensity score-matched cohort study of prescription receipt data in Japan.
Kimura, H; Masuda, S; Sato, D; Sato, Y, 2013
)
0.39
" We sought to estimate individual beneficial and adverse effects of intensive glucose control in patients with type 2 diabetes."( Estimation of individual beneficial and adverse effects of intensive glucose control for patients with type 2 diabetes.
Chalmers, J; Grobbee, DE; Harrap, S; Heller, S; Mancia, G; Marre, M; Poulter, N; van der Graaf, Y; van der Leeuw, J; Visseren, FL; Woodward, M; Zoungas, S, 2016
)
0.43
" The estimated individual effects can inform treatment decisions once individual weights assigned to positive and adverse effects have been specified."( Estimation of individual beneficial and adverse effects of intensive glucose control for patients with type 2 diabetes.
Chalmers, J; Grobbee, DE; Harrap, S; Heller, S; Mancia, G; Marre, M; Poulter, N; van der Graaf, Y; van der Leeuw, J; Visseren, FL; Woodward, M; Zoungas, S, 2016
)
0.43
" The incidences of adverse events (AEs) were 29."( Efficacy and safety of metformin and sitagliptin based triple antihyperglycemic therapy (STRATEGY): a multicenter, randomized, controlled, non-inferiority clinical trial.
Bi, Y; Engel, SS; Ji, L; Ji, Q; Jia, W; Lu, J; Mao, A; Mu, Y; Ran, X; Weng, J; Xu, W; Yang, W; Yao, B; Zeng, L; Zhao, B; Zhao, J; Zhou, Z; Zhu, D, 2017
)
0.46
" Unintentional sulfonylurea toxicity developed due to an adverse drug-drug interaction between gliclazide and these antifungals."( Unintentional sulfonylurea toxicity due to a drug-drug interaction: a case report.
Austin, E; Gunaratne, K; Wu, PE, 2018
)
0.7
" The radioprotective effect is new indication of GL for patient's protection against side effect induced by ionizing radiation."( Radioprotective Effect of Gliclazide as an Anti-Hyperglycemic Agent Against Genotoxicity Induced by Ionizing Radiation on Human Lymphocytes.
Ghasemi, A; Hosseinimehr, SJ; Pouri, M; Shaghaghi, Z, 2019
)
0.81
" The present study was designed to assess the toxic effect of 18beta-glycyrrhetinic acid against human cervix and uterus tumor cell line SiHa cells in relation to the mitochondria-mediated cell-death process and evaluate the combined toxic effect of 18beta-glycyrrhetinic acid and anti-cancer drugs."( 18beta-Glycyrrhetinic acid induces apoptotic cell death in SiHa cells and exhibits a synergistic effect against antibiotic anti-cancer drug toxicity.
Han, ES; Kim, YJ; Lee, CS; Lee, MS; Lee, SJ, 2008
)
0.35
"Short-term exposure of transformed cells to cisplatin reduced the clonogenic survival in low-density cultures (without gap junction formation) and in high density (with gap junction formation), but the toxic effect was greater at high density."( Tramadol and flurbiprofen depress the cytotoxicity of cisplatin via their effects on gap junctions.
Harris, AL; He, B; Hong, X; Liu, B; Tao, L; Tong, X; Wang, L; Wang, Q; Ye, H, 2009
)
0.35
"This study aims to explore the mechanisms underlying the hepato-protective effect of GA in combating retrorsine (RTS, a representative toxic PA)-induced liver injury."( Nrf2-mediated liver protection by 18β-glycyrrhetinic acid against pyrrolizidine alkaloid-induced toxicity through PI3K/Akt/GSK3β pathway.
He, Y; Lin, G; Ma, J; Miu, KK; Tang, C; Wang, Z; Yao, S; Ye, Y, 2022
)
0.72

Pharmacokinetics

Pharmacokinetic and pharmacodynamic properties of gliclazide were studied after an oral administration. The half-life 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.

ExcerptReferenceRelevance
" Several pharmacokinetic parameters for the blood gliclazide were derived from the decay curves of the blood drug levels."( Influence of blood proteins on biomedical analysis. III. Pharmacokinetics and protein binding of gliclazide.
Hata, M; Kimura, M; Kitani, Y; Kobayashi, K; Matsuoka, A; Sakoguchi, T, 1981
)
0.73
" 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
)
0.89
" Gliclazide tmax exhibited a skewed unimodal distribution and was not associated with gliclazide maximum concentration, or glucose or insulin responses."( Pharmacokinetics and pharmacodynamics of gliclazide in Caucasians and Australian Aborigines with type 2 diabetes.
Barrett, PH; Beilby, JP; Daly, F; Davis, TM; Dusci, LJ; Ilett, KF; Walsh, JP, 2000
)
1.48
" A consistent and optimal release of gliclazide from this formulation leads to a low to moderate overall variability of its pharmacokinetic parameters."( Complete bioavailability and lack of food-effect on pharmacokinetics of gliclazide 30 mg modified release in healthy volunteers.
Delrat, P; Jochemsen, R; Paraire, M, 2002
)
0.82
"Pharmacokinetic and pharmacodynamic properties of gliclazide were studied after an oral administration of gliclazide tablets in healthy volunteers."( Pharmacokinetic and pharmacodynamic characterization of gliclazide in healthy volunteers.
Kim, H; Kwon, KI; Yun, M, 2003
)
0.82
" The interaction observed appears to be pharmacodynamic at the receptor level as expected."( Influence of nicorandil on the pharmacodynamics and pharmacokinetics of gliclazide in rats and rabbits.
Kilari, EK; Satyanarayana, S, 2006
)
0.57
"In a single-dose pharmacokinetic study, 24 healthy male subjects with various CYP2C9 and CYP2C19 genotypes received an oral dose of 30 mg gliclazide MR and plasma was sampled for 72 h postdose."( Influence of CYP2C9 and CYP2C19 genetic polymorphisms on pharmacokinetics of gliclazide MR in Chinese subjects.
Chen, X; Guo, Y; Lin, N; Si, D; Zhang, Y; Zhong, D; Zhou, H, 2007
)
0.77
"In the single-dose study, no significant difference in any pharmacokinetic parameters was found in CYP2C9*1/*1, *1/*3 and *1/*13 subjects."( Influence of CYP2C9 and CYP2C19 genetic polymorphisms on pharmacokinetics of gliclazide MR in Chinese subjects.
Chen, X; Guo, Y; Lin, N; Si, D; Zhang, Y; Zhong, D; Zhou, H, 2007
)
0.57
" The aim of this study was to assess potential pharmacokinetic (PK) and pharmacodynamic (PD) interactions between St John's wort and gliclazide in healthy subjects with different cytochrome P450 2C9 (CYP2C9) genotypes."( Effects of St John's wort and CYP2C9 genotype on the pharmacokinetics and pharmacodynamics of gliclazide.
Day, RO; Liauw, WS; McLachlan, AJ; Murray, M; Williams, KM; Xu, H, 2008
)
0.77
" The area under the plasma concentration-time curve (AUC(0-infinity)), apparent clearance (CL/F) and elimination half-life (t 1/2) of gliclazide and incremental changes in glucose and insulin AUC(0-4) were compared."( Effects of St John's wort and CYP2C9 genotype on the pharmacokinetics and pharmacodynamics of gliclazide.
Day, RO; Liauw, WS; McLachlan, AJ; Murray, M; Williams, KM; Xu, H, 2008
)
0.77
" The method herein described was successfully applied for the evaluation of pharmacokinetic profiles of gliclazide sustained release tablets in 18 healthy volunteers."( Liquid chromatography--mass spectrometry method for the determination of gliclazide in human plasma and application to a pharmacokinetic study of gliclazide sustained release tablets.
Ma, PC; Wang, CY; Xiang, BR; Yu, LY; Zhang, W, 2008
)
0.79
" The pharmacokinetic parameters such as AUC0-t (the area under the curve from zero to the time), AUC0- yen (the area under the curve from zero to infinity), Cmax (maximum serum concentration), tmax (time to reach Cmax) and t1/2 (terminal half-life), were analyzed by non-compartmental analysis."( Pharmacokinetics and bioequivalence evaluation of gliclazide/metformin combination tablet and equivalent doses of gliclazide and metformin in healthy Korean subjects.
Cho, HY; Lee, YB; Lim, YC; Yoon, H, 2009
)
0.61
"There were no significant differences between the single combination tablet and the individual tablets in AUC0-t, AUC0- yen, Cmax and blood glucose concentration."( Pharmacokinetics and bioequivalence evaluation of gliclazide/metformin combination tablet and equivalent doses of gliclazide and metformin in healthy Korean subjects.
Cho, HY; Lee, YB; Lim, YC; Yoon, H, 2009
)
0.61
"There was no difference in either pharmacokinetic and or pharmacodynamic parameters of gliclazide when group A (CYP2C9*1/*1, CYP2C19 extensive metabolizers) was compared with group B (CYP2C9*1/*3, CYP2C19 *1/*1)."( Influence of CYP2C9 and CYP2C19 genetic polymorphisms on pharmacokinetics and pharmacodynamics of gliclazide in healthy Chinese Han volunteers.
Chen, GM; Li, WL; Liu, NF; Ren, XM; Shao, H; Wang, DW; Zhai, ZH, 2010
)
0.8
"To find out the pharmacokinetic (PK) and pharmacodynamic (PD) parameters for assessing the bioequivalence of three marketed products."( Pharmacokinetic-pharmacodynamic equivalence of three gliclazide formulations in healthy human male subjects.
Monif, T; Pillai, KK; Saha, N; Samad, A; Sharma, PL, 2011
)
0.62
" Pharmacokinetic parameters like t(max), C(max), AUC(0-t), AUC(0-∞), AUC(0-t) / AUC(0-∞) and t(1/2) and pharmacodynamic parameters like maximum effect (minimum glucose level in the body, C(minglu)), time to minimum glucose level in the body (T(cminglu)) and partial AUC were calculated for all the products."( Pharmacokinetic-pharmacodynamic equivalence of three gliclazide formulations in healthy human male subjects.
Monif, T; Pillai, KK; Saha, N; Samad, A; Sharma, PL, 2011
)
0.62
" The test products A & B compared to reference product R were bioequivalent on the basis of pharmacokinetic and pharmacodynamic parameters."( Pharmacokinetic-pharmacodynamic equivalence of three gliclazide formulations in healthy human male subjects.
Monif, T; Pillai, KK; Saha, N; Samad, A; Sharma, PL, 2011
)
0.62
" The method reported in this study can be implemented for pharmacokinetic interaction study in rats."( Simultaneous HPLC Assay of Gliclazide and Ciprofloxacin in Plasma and its Implementation for Pharmacokinetic Study in Rats.
Adiwidjaja, J; Leo, M; Pratiwi, GK; Sasongko, L, 2021
)
0.92
"A highly sensitive and selective LC-ESI-MS was developed, validated for the simultaneous determination of 18alpha-glycyrrhetic acid (alpha-GA) and 18beta-glycyrrhetic acid (beta-GA) for pharmacokinetic studies in healthy subjects."( Simultaneous determination of 18alpha- and 18beta-glycyrrhetic acid in human plasma by LC-ESI-MS and its application to pharmacokinetics.
Ge, ZX; Li, J; Ouyang, P; Wei, P; Zou, Q, 2009
)
0.35
"An HPLC method for the determination of 18alpha-glycyrrhetinic acid and 18beta-glycyrrhetinic acid in rat plasma was established, which was used subsequently to determine the pharmacokinetic profiles of both epimers of glycyrrhetinic acid in rats."( Pharmacokinetic analysis of alpha and beta epimers of glycyrrhetinic acid in rat plasma: differences in singly and combined administrations.
Bi, KS; Chen, W; Chen, XH; Geng, LL; Li, Q; Li, X; Sun, HY, 2012
)
0.38
"The plasma pharmacokinetic profile in CD-1 mice of a novel 18β-glycyrrhetinic acid (GA) derivative, which displays in vitro anti-cancer activity, was assessed."( Synthesis and plasma pharmacokinetics in CD-1 mice of a 18β-glycyrrhetinic acid derivative displaying anti-cancer activity.
Amighi, K; Dubois, J; Goole, J; Jabin, I; Kiss, R; Lallemand, B; Lamkami, T; Mathieu, V; Ouedraogo, M; Wauthoz, N, 2013
)
0.39
" The intravenous pharmacokinetic parameters revealed that 2 was rapidly distributed (t(1/2dist) of ∼3 min) but slowly eliminated (t(1/2elim)  = ∼77 min)."( Synthesis and plasma pharmacokinetics in CD-1 mice of a 18β-glycyrrhetinic acid derivative displaying anti-cancer activity.
Amighi, K; Dubois, J; Goole, J; Jabin, I; Kiss, R; Lallemand, B; Lamkami, T; Mathieu, V; Ouedraogo, M; Wauthoz, N, 2013
)
0.39
"The aim of this study was to elucidate the inhibition mechanism of 18β-glycyrrhetic acid (GLY) on cytochrome P450 (CYP) activity and in vivo pharmacokinetic consequences of single GLY dose in rats."( Modulation of Cytochrome P450 Activity by 18β-Glycyrrhetic Acid and its Consequence on Buspirone Pharmacokinetics in Rats.
Cho, HJ; Kim, DD; Kim, SB; Kim, YS; Yoon, IS, 2015
)
0.42
"The aim of this study was to confirm pharmacokinetic screening of multiple components in healthy Korean subjects after oral administration of Samso-eum and perform quantitation of active components in the human plasma."( LC-MS/MS analysis of puerarin and 18β-glycyrrhetinic acid in human plasma after oral administration of Samso-eum and its application to pharmacokinetic study.
Jeong, JH; Kim, BN; Lee, GY; Lee, SY; Park, SJ; Park, YC, 2020
)
0.56

Compound-Compound Interactions

In patients with T2D poorly controlled with sitagliptin, whether alone or in combination with metformin and/or gliclazide, replacing it with canagliflozin may be a simple yet effective intensification strategy.

ExcerptReferenceRelevance
" gliclazide combined with bedtime NPH insulin in patients with Type 2 diabetes inadequately controlled with oral hypoglycaemic therapy [HbA1c>7."( Comparison of repaglinide vs. gliclazide in combination with bedtime NPH insulin in patients with Type 2 diabetes inadequately controlled with oral hypoglycaemic agents.
Furlong, NJ; Hardy, KJ; Hulme, SA; O'Brien, SV, 2003
)
1.52
"Over 13 weeks, both repaglinide and gliclazide, when combined with bedtime NPH insulin produce similar significant improvements in glycaemic control (-1%) and similar weight gain."( Comparison of repaglinide vs. gliclazide in combination with bedtime NPH insulin in patients with Type 2 diabetes inadequately controlled with oral hypoglycaemic agents.
Furlong, NJ; Hardy, KJ; Hulme, SA; O'Brien, SV, 2003
)
0.88
" The decrease in MKC bioavailability, when administered with gliclazide, caused by probiotic treatment in healthy but not diabetic rats suggests that probiotic treatment induced MKC metabolism or impaired its absorption, only in healthy animals."( Probiotics decreased the bioavailability of the bile acid analog, monoketocholic acid, when coadministered with gliclazide, in healthy but not diabetic rats.
Al-Salami, H; Butt, G; Golocorbin-Kon, S; Mikov, M; Tucker, I, 2012
)
0.83
" 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
" Drug-drug interactions that inhibit sulfonylurea metabolism and thus increase systemic exposure can cause unintentional sulfonylurea toxicity."( Unintentional sulfonylurea toxicity due to a drug-drug interaction: a case report.
Austin, E; Gunaratne, K; Wu, PE, 2018
)
0.48
" Unintentional sulfonylurea toxicity developed due to an adverse drug-drug interaction between gliclazide and these antifungals."( Unintentional sulfonylurea toxicity due to a drug-drug interaction: a case report.
Austin, E; Gunaratne, K; Wu, PE, 2018
)
0.7
"Adverse drug-drug interactions continue to pose challenges to clinicians."( Unintentional sulfonylurea toxicity due to a drug-drug interaction: a case report.
Austin, E; Gunaratne, K; Wu, PE, 2018
)
0.48
"To analyze the efficacy and safety of replacing sitagliptin with canagliflozin in patients with type 2 diabetes (T2D) and poor metabolic control despite treatment with sitagliptin in combination with metformin and/or gliclazide."( Efficacy and safety of replacing sitagliptin with canagliflozin in real-world patients with type 2 diabetes uncontrolled with sitagliptin combined with metformin and/or gliclazide: The SITA-CANA Switch Study.
Garcia de Lucas, MD; Gómez Huelgas, R; Olalla Sierra, J; Pérez Belmonte, LM; Suárez Tembra, M, 2018
)
0.86
"5%) treated with sitagliptin in combination with metformin and/or gliclazide, sitagliptin (and gliclazide if appropriate) were replaced by canagliflozin."( Efficacy and safety of replacing sitagliptin with canagliflozin in real-world patients with type 2 diabetes uncontrolled with sitagliptin combined with metformin and/or gliclazide: The SITA-CANA Switch Study.
Garcia de Lucas, MD; Gómez Huelgas, R; Olalla Sierra, J; Pérez Belmonte, LM; Suárez Tembra, M, 2018
)
0.91
"In patients with T2D poorly controlled with sitagliptin, whether alone or in combination with metformin and/or gliclazide, replacing it with canagliflozin may be a simple yet effective intensification strategy."( Efficacy and safety of replacing sitagliptin with canagliflozin in real-world patients with type 2 diabetes uncontrolled with sitagliptin combined with metformin and/or gliclazide: The SITA-CANA Switch Study.
Garcia de Lucas, MD; Gómez Huelgas, R; Olalla Sierra, J; Pérez Belmonte, LM; Suárez Tembra, M, 2018
)
0.89
" Based on experimental data, the combination index of the hypoglycemic drugs like metformin and gliclazide in combination with different doses of mangiferin was determined using COMPUSYN software."( Antidiabetic effect of mangiferin in combination with oral hypoglycemic agents metformin and gliclazide.
Malarvizhi, R; Mani, S; Nithya, P; Sekar, V; Vasanthi, HR, 2019
)
0.95
"Modulation of drug transporters via herbal medicines which have been widely used in combination with conventional prescription drugs may result in herb-drug interactions in clinical practice."( Inhibitory effects of herbal constituents on P-glycoprotein in vitro and in vivo: herb-drug interactions mediated via P-gp.
Hu, J; Li, X; Li, Y; Liu, Z; Sheng, L; Wang, B; Yang, S, 2014
)
0.4

Bioavailability

The absorption rate of gliclazide is slow and variable among subjects probably due to poor dissolution from the dosage form. The solubility, dissolution rate and bioavailability of Gliclaze SGNCs were significantly improved compared to pure glicLazide.

ExcerptReferenceRelevance
" Gliclazide taken 30 minutes before breakfast increased in serum concentration before the meal-induced hyperglycemia, but that taken just before or just after breakfast was poorly absorbed and showed smaller and greatly delayed peaks."( The effect of timing on gliclazide absorption and action.
Ishibashi, F; Takashina, S, 1990
)
1.5
" When bioavailability parameters were compared following oral administration of the soft capsule and Diamicron to 16 healthy Korean male subjects, the parameters representing the amount of adsorption (i."( Accelerated oral absorption of gliclazide in human subjects from a soft gelatin capsule containing a PEG 400 suspension of gliclazide.
Chung, SJ; Hong, SS; Lee, MH; Lee, SH; Lee, YJ; Shim, CK, 1998
)
0.59
" 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 was undertaken with an objective to increase the dissolution rate and bioavailability of a poorly water soluble drug gliclazide (Gz) by complexation with beta-cyclodextrin (CD) in the presence of hydroxypropylmethylcellulose (HPMC)."( Studies on solubility and hypoglycemic activity of gliclazide beta-cyclodextrin-hydroxypropylmethylcellulose complexes.
Aggarwal, S; Mishra, B; Singh, PN, 2002
)
0.77
" An absolute bioavailability study was carried out to characterise the performance of the new formulation and the food-effect was also investigated in a separate study."( Complete bioavailability and lack of food-effect on pharmacokinetics of gliclazide 30 mg modified release in healthy volunteers.
Delrat, P; Jochemsen, R; Paraire, M, 2002
)
0.55
" The formulation shows high bioavailability and its absorption profile is unaffected by coadministration with food."( Gliclazide modified release.
Goa, KL; McGavin, JK; Perry, CM, 2002
)
1.76
" Based on these statistical inferences, the two formulations are considered bioequivalent in the extent and rate of absorption from both single- and multiple-dose studies."( Single and multiple dose bioequivalence evaluation of two brands of gliclazide modified release tablets in healthy Chinese male volunteers.
He, Z; Ling, G; Sun, J; Sun, Y; Xu, X, 2006
)
0.57
" Developed Eudragit NPs revealed a decreased t(min) (ELNP), and enhanced bioavailability and sustained activity (ELNP and ERSNP) and hence superior activity as compared to plain gliclazide in streptozotocin induced diabetic rat model and glucose-loaded diabetic rat model."( Preparation and in vitro/in vivo evaluation of gliclazide loaded Eudragit nanoparticles as a sustained release carriers.
Devarajan, PV; Sonavane, GS, 2007
)
0.79
" It was found that gliclazide bioavailability was increased in healthy rats when coadministered with MKC, but there was no difference in glucose levels."( The influence of 3alpha,7alpha-dihydroxy-12-keto-5beta-cholanate on gliclazide pharmacokinetics and glucose levels in a rat model of diabetes.
Al-Salami, H; Fawcett, JP; Golocorbin-Kon, S; Mikov, M; Raskovic, A; Skrbic, R,
)
0.7
" Relative bioavailability is 96."( Liquid chromatography--mass spectrometry method for the determination of gliclazide in human plasma and application to a pharmacokinetic study of gliclazide sustained release tablets.
Ma, PC; Wang, CY; Xiang, BR; Yu, LY; Zhang, W, 2008
)
0.58
"This was an open label, balanced, randomized, 3-treatment, 3-sequence, 3 period, single-dose, cross-over bioavailability study in which 18 healthy adults were randomized to receive gliclazide 80 mg with 7 days wash out between treatments."( Pharmacokinetic-pharmacodynamic equivalence of three gliclazide formulations in healthy human male subjects.
Monif, T; Pillai, KK; Saha, N; Samad, A; Sharma, PL, 2011
)
0.81
" When coadministered with gliclazide, the bioavailability of MKC was reduced in healthy rats treated with probiotics but remained the same in diabetic pretreated rats."( Probiotics decreased the bioavailability of the bile acid analog, monoketocholic acid, when coadministered with gliclazide, in healthy but not diabetic rats.
Al-Salami, H; Butt, G; Golocorbin-Kon, S; Mikov, M; Tucker, I, 2012
)
0.89
" In the in vivo evaluation, the mean relative oral bioavailability of Eudragit-coated PPOP compared to CA-coated ones was 106."( In vitro and in vivo evaluation of gliclazide push-pull osmotic pump coated with aqueous colloidal polymer dispersions.
Chen, F; Pan, WS; Tai, LY; Tang, X; Xu, HM; Yang, XG, 2013
)
0.67
" The prototype solubilization method combined with controlled porosity osmotic pump based technique could provide a unique way to increase dissolution rate and bioavailability of many poorly water-soluble, narrow therapeutic index drugs used in diabetes, cardiovascular diseases, etc."( Controlled porosity solubility modulated osmotic pump tablets of gliclazide.
Banerjee, A; Gore, S; Verma, PR, 2015
)
0.65
"The absorption rate of gliclazide is slow and variable among subjects probably due to poor dissolution from the dosage form."( Dissolution enhancement of gliclazide using ultrasound waves and stabilizers in liquid anti-solvent precipitation.
Al-Nimry, SS; Qandil, AM; Salem, MS, 2014
)
1.01
"95% relative bioavailability compared with the commercial tablet, suggesting the bioequivalence between the two formulations."( A novel asymmetric membrane osmotic pump capsule with in situ formed delivery orifices for controlled release of gliclazide solid dispersion system.
Liu, D; Pan, W; Wang, Y; Yang, L; Yang, X; Yang, Y; Zhao, Z, 2016
)
0.65
" In vivo studies showed a twofold rise in bioavailability through SNEDDS with a significant decline in blood glucose levels compared to plain drug suspension suggesting a lipid-based system as an alternative approach for treating diabetes."( Quality by Design Approach for Developing Lipid-Based Nanoformulations of Gliclazide to Improve Oral Bioavailability and Anti-Diabetic Activity.
Cheruvu, HS; Dodoala, S; Pailla, SR; Patel, P; Rangaraj, N; Sampathi, S, 2019
)
0.74
"The antidiabetic drug gliclazide (GLZ) has a slow absorption rate and a low bioavailability due to its poor solubility."( Investigation of the formation of drug-drug cocrystals and coamorphous systems of the antidiabetic drug gliclazide.
Aljohani, M; Erxleben, A; MacFhionnghaile, P; McArdle, P, 2019
)
1.04
"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 solubility, dissolution rate and bioavailability of gliclazide SGNCs were significantly improved compared to pure gliclazide."( Fabrication of Second Generation Smarter PLGA Based Nanocrystal Carriers for Improvement of Drug Delivery and Therapeutic Efficacy of Gliclazide in Type-2 Diabetes Rat Model.
Bhattamisra, SK; Krishnamoorthy, R; Panda, BP; Patnaik, S; Seng, LB; Shivashekaregowda, NKH, 2019
)
0.96
"Solid lipid nanoparticles (SLNs) are considered a promising system in enhancing the oral bioavailability of poorly water-soluble drugs; owing to their intrinsic ability to increase the solubility together with protecting the incorporated drugs from extensive metabolism."( Lipid-Based Gliclazide Nanoparticles for Treatment of Diabetes: Formulation, Pharmacokinetics, Pharmacodynamics and Subacute Toxicity Study.
El-Kamel, AH; Hassaan, PS; Khalifa, HM; Nazief, AM; Sokar, MS, 2020
)
0.94
"Exploiting such properties, SLNs loaded with gliclazide (GLZ) were developed in an attempt to improve the oral bioavailability and the anti-diabetic action of GLZ, together with prolonging its duration of action for better glycemic control."( Lipid-Based Gliclazide Nanoparticles for Treatment of Diabetes: Formulation, Pharmacokinetics, Pharmacodynamics and Subacute Toxicity Study.
El-Kamel, AH; Hassaan, PS; Khalifa, HM; Nazief, AM; Sokar, MS, 2020
)
1.2
" Diabetic vascular complications arise from increased vascular endothelial inflammation and oxidative stress as well as decreased nitric oxide bioavailability in the vessel walls due to poor glycemic control."( Combination of Captopril with Gliclazide Decreases Vascular and Renal Complications and Improves Glycemic Control in Rats with Streptozotocin- Induced Diabetes Mellitus.
Abo-Saif, AA; Kozman, MR; Messiha, BAS; Mizar, SMM, 2021
)
0.91
" Given that probiotic bacteria and bile acids are naturally present in the gut and that each individual has a specific bacterial fingerprint, future research should extend the explanation of their effect on the gliclazide bioavailability and therapy individualization in in vivo conditions."( PAMPA model of gliclazide permeability: The impact of probiotic bacteria and bile acids.
Al-Salami, H; Lazarević, S; Mikov, M; Pavlović, N; Stanimirov, B; Vukmirović, S; Đanić, M, 2021
)
1.16
" Clearance, volume of distribution and bioavailability of gliclazide were unaffected by disease state (healthy or insulin resistant)."( Effect of Nigella sativa oil on pharmacokinetics and pharmacodynamics of gliclazide in rats.
Adiwidjaja, J; Sasongko, L, 2021
)
1.1
" The optimized formulation based on in vitro data was selected for a bioavailability study in rabbits."( Development, in vitro Evaluation, and in vivo Study of Adhesive Buccal Films for the Treatment of Diabetic Pediatrics via Trans Mucosal Delivery of Gliclazide.
Adogim, SS; Albilaihi, HM; Alburaykan, AI; Aldohan, NS; Alharbi, RF; Aljohani, AR; Alruthea, LM; Gaber, DA, 2022
)
0.92
"Human carboxylesterase 2 (hCE2), one of the major carboxylesterases in the human intestine and various tumour tissues, plays important roles in the oral bioavailability and treatment outcomes of ester- or amide-containing drugs or prodrugs, such as anticancer agents CPT-11 (irinotecan) and LY2334737 (gemcitabine)."( Design, synthesis, and structure-activity relationship study of glycyrrhetinic acid derivatives as potent and selective inhibitors against human carboxylesterase 2.
Ge, GB; Hao, DC; Hou, J; Jin, Q; Li, YG; Wang, P; Yang, L; Zhou, K; Zou, LW, 2016
)
0.43

Dosage Studied

Serum levels of gliclazide were determined by radioimmunoassay in seven healthy controls and in 18 diabetic in-patients receiving single oral dosing and consecutive dosing over 5 days. Once-daily dosing should improve patient compliance, an important factor in long-term glycaemic control. An open-label prospective cross-over trial was performed to compare the efficacy and safety of once daily low-dose glicLazide (20 mg/day) with that of nateglinide at the usual dosage.

ExcerptRelevanceReference
" Dose-response characteristics were assessed with a modified Michaelis-Menten equation."( Effect of acute administration of gliclazide on the glucose sensitivity of pancreatic B-cells in healthy subjects.
van der Veen, EA; van Haeften, TW; Veneman, TF, 1991
)
0.56
" 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
)
0.66
" Dose-response studies of the glucose-induced release of amylin and insulin revealed that they possessed a similar dependency on glucose."( Release of amylin from perfused rat pancreas in response to glucose, arginine, beta-hydroxybutyrate, and gliclazide.
Hisatomi, A; Inoue, K; Nawata, H; Umeda, F, 1991
)
0.5
" It is unclear whether the effect of SU on insulin release is additive to the effect of glucose, or whether SU act by increasing pancreatic beta-cell sensitivity to glucose (a shift in the dose-response curve of glucose-stimulated insulin release without a change in maximum release)."( Influence of gliclazide on glucose-stimulated insulin release in man.
Gerich, JE; van der Veen, EA; van Haeften, TW; Veneman, TF, 1991
)
0.65
" In diabetic patients treated with sulphonylureas and phenformin at low dosage (glibenclamide 5 mg and phenformin 50 mg) it was possible to maintain good glycometabolic control using only the sulphonylurea gliclazide (160 mg/die)."( [Efficacy of sulfonylurea and sulfonylurea-benfluorex therapy in patients with type 2 diabetes treated with commercial sulfonylurea-biguanide combinations].
Benzi, L; Cecchetti, P; Ciccarone, AM; Di Cianni, G; Giannarelli, R; Navalesi, R; Penno, G,
)
0.32
"Serum levels of gliclazide were determined by radioimmunoassay in seven healthy controls and in 18 diabetic in-patients receiving single oral dosing and consecutive dosing over 5 days."( Serum gliclazide concentration in diabetic patients. Relationship between gliclazide dose and serum concentration.
Hagura, R; Kajinuma, H; Katagiri, H; Kawai, A; Kosaka, K; Kuzuya, N; Sando, H; Shiba, T; Shirakawa, W; Suzuki, K,
)
0.96
" Serum levels of gliclazide in healthy volunteers receiving single oral dosing (40 mg/subject) have also been determined."( Determination of a new hypoglycemic drug, gliclazide, in human serum by radioimmunoassay.
Hashimoto, M; Kagemoto, A; Maeda, T; Miki, M; Negoro, T; Sekine, Y; Suzuki, H, 1981
)
0.87
" Gradually accumulating evidence suggests that gliclazide may be useful in patients with diabetic retinopathy, due to its haemobiological actions, and that addition of gliclazide to insulin therapy enables insulin dosage to be reduced."( Gliclazide. An update of its pharmacological properties and therapeutic efficacy in non-insulin-dependent diabetes mellitus.
Brogden, RN; Palmer, KJ, 1993
)
1.99
" The insulin dose-response curve of this patient shifted to the right and down, and recovered somewhat after the administration of gliclazide."( Insulin resistance in a patient with diabetes mellitus associated with Turner's syndrome.
Hashimoto, K; Hisatake, K; Kumon, Y; Suehiro, T; Sumiyoshi, R, 1994
)
0.49
" Moreover adding a bed-time dosage to the standard administration at meal times seems to be an effective therapeutical strategy."( Meformin, plasma glucose and free fatty acids in type II diabetic out-patients: results of a clinical study.
Ambrosi, F; Filipponi, P; Gregorio, F; Manfrini, S; Santucci, A, 1997
)
0.3
" All patients were stable, with no change in dosage for at least 3 months."( Monitoring of metabolic control in patients with non-insulin-dependent diabetes mellitus on oral hypoglycaemic agents: value of evening blood glucose determination.
Guillausseau, PJ, 1997
)
0.3
" Patients were randomly assigned to sulphonylurea increased up to its maximum dosage (1st group) or to addition of metformin (2nd group)."( Poorly controlled elderly Type 2 diabetic patients: the effects of increasing sulphonylurea dosages or adding metformin.
Ambrosi, F; Carle, F; Filipponi, P; Gregorio, F; Manfrini, S; Merante, D; Testa, R; Velussi, M, 1999
)
0.3
" Employing an innovative pharmaceutical form based on a hydrophilic matrix to deliver this short-acting sulfonylurea, gliclazide modified release is associated with an unsurpassed efficacy:acceptability ratio, with the potential additional advantages inherent in reduced dosage and once-daily administration."( Gliclazide modified release: from once-daily administration to 24-hour blood glucose control.
Harrower, A, 2000
)
1.96
"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
"A new modified release (MR) formulation containing 30 mg of gliclazide was developed to obtain a better predictable release of the active principle and to allow once-daily dosing regimen."( Complete bioavailability and lack of food-effect on pharmacokinetics of gliclazide 30 mg modified release in healthy volunteers.
Delrat, P; Jochemsen, R; Paraire, M, 2002
)
0.79
" In responders, the initial dose (30 mg) of the gliclazide MR dosing regimen induced half of the maximum hypoglycaemic effect."( Population PKPD modelling of the long-term hypoglycaemic effect of gliclazide given as a once-a-day modified release (MR) formulation.
Francillard, M; Frey, N; Holford, NH; Jochemsen, R; Laveille, C; Paraire, M, 2003
)
0.81
"8%, and increase in percentage of once-daily dosing regimen from 12 to 58."( [Compliance and optimisation of oral antidiabetic therapy. A longitudinal study].
Guillausseau, PJ, 2004
)
0.32
"0005), as well as in individual therapeutic subgroups of patients (having switched from multiple-daily dosing to once-daily-dosing schedules and from gliclazide 80 to gliclazide 30 MR once-daily formulation)."( [Compliance and optimisation of oral antidiabetic therapy. A longitudinal study].
Guillausseau, PJ, 2004
)
0.52
"These findings suggest that optimization of oral antidiabetic therapy favoring the use of oral antidiabetic agents with once-daily dosing administration modalities may improve metabolic control in patients with type 2 diabetes."( [Compliance and optimisation of oral antidiabetic therapy. A longitudinal study].
Guillausseau, PJ, 2004
)
0.32
" At each visit the doctor renewed the prescription for the subsequent period according to the following protocol: the starting dose was 30 mg Diaprel MR/day, if the FPG (mg/dl) was over 140 (at the next visit) the dosage was increased with 30 mg Diaprel MR/day, if the FPG (mg/dl) was under 140 the dosage remained the same as the previous dosage."( NIDDM: new once-daily intervention for type 2 diabetes mellitus: Diaprel MR.
Brădescu, OM; Gavrilă, L; Guja, C; Ionescu-Tîrgovişte, C, 2004
)
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
)
0.53
" The dose-response effect of gliclazide and glibenclamide on ischaemic preconditioning and the action of glibenclamide on signal transduction in human myocardium were investigated using right atrial appendages from cardiac surgery patients."( The effect of gliclazide and glibenclamide on preconditioning of the human myocardium.
Fowler, A; Galiñanes, M; Loubani, M; Standen, NB, 2005
)
0.98
" This newly developed method was applied for monitoring blood levels with one healthy volunteer dosing with a GL tablet."( High-performance liquid chromatography with electrochemical detection for analysis of gliclazide in plasma.
Kuo, CY; Wu, SM, 2005
)
0.55
" The objective of the DIACOM (effect of DosIng frequency of oral Antidiabetic agents on the COMpliance and biochemical control of type 2 diabetes) study was to compare the compliance of patients treated with once-daily (od) or twice-daily (bid) sulphonylureas."( The DIACOM study (effect of DosIng frequency of oral Antidiabetic agents on the COMpliance and biochemical control of type 2 diabetes).
Kardas, P, 2005
)
0.33
" Dosage of metformin was maintained throughout the study, and the sulfonylurea was stopped."( Double-blind, randomized, multicentre study of the efficacy and safety of gliclazide-modified release in the treatment of Chinese type 2 diabetic patients.
Chang, CC; Chuang, LM; Jiang, YD; Lu, CH; Wang, CY; Wu, HP, 2006
)
0.56
" Once-daily dosing with gliclazide MR should improve patient compliance, an important factor in long-term glycaemic control."( Double-blind, randomized, multicentre study of the efficacy and safety of gliclazide-modified release in the treatment of Chinese type 2 diabetic patients.
Chang, CC; Chuang, LM; Jiang, YD; Lu, CH; Wang, CY; Wu, HP, 2006
)
0.87
" The FDA has recently issued an alert regarding the potential negative influence of alcohol on extended release dosage forms."( The influence of hydro-alcoholic media on hypromellose matrix systems.
Levina, M; Rajabi-Siahboomi, AR; Vuong, H, 2007
)
0.34
" The mean therapeutic dosage of insulin glargine in group A was 14."( Therapeutic options for elderly diabetic subjects: open label, randomized clinical trial of insulin glargine added to oral antidiabetic drugs versus increased dosage of oral antidiabetic drugs.
Alagona, C; Chiavetta, A; Fedele, V; Leotta, C; Lorenti, I; Luca, S; Papa, G; Pezzino, V; Piro, S; Purrello, F; Rabuazzo, AM; Spadaro, L, 2008
)
0.35
" The results demonstrate the feasibility of the model in the development of extended release dosage form."( Development of extended zero-order release gliclazide tablets by central composite design.
Devi, VK; Narendra, C; Srinagesh, S; Vijayalakshmi, P, 2008
)
0.61
"The rats with diabetic gastroparesis induced by injecting alloxan and giving 200% Radix Rehmanniae preparata were divided into four groups randomly: Tangweian high dosage group, Tangweian low dosage group, motilium control group and the model control group, 10 rats each group."( [Effects of Tangweian granule on 5-HT(2A)R in rat model with diabetic gastroparesis].
Liu, DW; Qian, QH; Qian, WB; Wang, ZC; Zhao, Y, 2008
)
0.35
" However, glibenclamide, regardless of the dosage schedule, tends to lower the plasma glucose values between midnight and early morning."( Daily blood glucose profiles of glibenclamide and gliclazide taken once or twice daily in elderly type 2 diabetic patients.
Futami-Suda, S; Kigawa, Y; Nakano, H; Norose, J; Oba, K; Ouchi, M; Suzuki, K; Suzuki, T; Watanabe, K; Yasuoka, H, 2008
)
0.6
" Subsequently, the effects of a 1-week chronic daily dosing of DPP-IV inhibitors and sulfonylureas were investigated."( Antidiabetic effects of dipeptidyl peptidase-IV inhibitors and sulfonylureas in streptozotocin-nicotinamide-induced mildly diabetic mice.
Hayakawa, M; Matsuyama-Yokono, A; Nakano, R; Shibasaki, M; Shiraki, K; Someya, Y; Tahara, A, 2009
)
0.35
"It was thus concluded that SD formulations of GLC can be successfully used to design a solid dosage form of the drug, which would have significant advantages over the current marketed tablets."( Physicochemical characterization of gliclazide-macrogol solid dispersion and tablets based on optimized dispersion.
Khattab, IS; Nada, A; Zaghloul, AA, 2010
)
0.64
" The increase in serum glucose level at 11 h after dosing (ΔC(glu11)) in group C was significantly higher than that of group A (-1."( Influence of CYP2C9 and CYP2C19 genetic polymorphisms on pharmacokinetics and pharmacodynamics of gliclazide in healthy Chinese Han volunteers.
Chen, GM; Li, WL; Liu, NF; Ren, XM; Shao, H; Wang, DW; Zhai, ZH, 2010
)
0.58
" This study indicates that the implementation of an 80 mg dosage regimen enabled accurate predictions of AUC0-60t by the LSS model."( Limited sampling strategy models for estimating the AUC of gliclazide in Chinese healthy volunteers.
He, YC; Huang, JH; Huang, XH; Li, LJ; Sheng, YC; Wang, K; Yang, J; Zheng, QS, 2013
)
0.63
"To evaluate the antidiabetic drug dosage differences between geriatric and nongeriatric diabetics with reference to duration of disease and creatinine clearance (Crcl)."( Do geriatrics require dose titration for antidiabetic agents?
Adhikari, P; Chowta, M; Kamath, A; Pai, MR; Shastry, R; Ullal, S,
)
0.13
"The absorption rate of gliclazide is slow and variable among subjects probably due to poor dissolution from the dosage form."( Dissolution enhancement of gliclazide using ultrasound waves and stabilizers in liquid anti-solvent precipitation.
Al-Nimry, SS; Qandil, AM; Salem, MS, 2014
)
1.01
" Dose-response profile of resveratrol remains indeterminate and additional studies may be necessary to determine effective dosing in diabetes."( Comparison of the anti-diabetic effects of resveratrol, gliclazide and losartan in streptozotocin-induced experimental diabetes.
Bilgin, HM; Deniz Obay, B; Elbey, B; Şermet, A; Taşdemir, E; Yazgan, ÜC, 2015
)
0.66
"This study aimed to design a fixed-dose combination dosage form which provides a sustained release profile for both the freely water-soluble metformin HCl and the poorly soluble gliclazide, two antidiabetic compounds used to treat diabetes mellitus."( Co-extrusion as a processing technique to manufacture a dual sustained release fixed-dose combination product.
Remon, JP; Vervaet, C; Voorspoels, J; Vynckier, AK, 2016
)
0.63
" A coat layer, containing at least 30% CAPA(®) 6506 as a hydrophobic polymer, was necessary to adequately sustain the release of the highly dosed freely soluble drug from the 70% metformin HCl-loaded CAPA(®) 6506 core of the co-extrudate."( Co-extrusion as a processing technique to manufacture a dual sustained release fixed-dose combination product.
Remon, JP; Vervaet, C; Voorspoels, J; Vynckier, AK, 2016
)
0.43
"Both active pharmaceutical ingredients (APIs), which have different physicochemical characteristics, were formulated in a single dosage form, using co-extrusion."( Co-extrusion as a processing technique to manufacture a dual sustained release fixed-dose combination product.
Remon, JP; Vervaet, C; Voorspoels, J; Vynckier, AK, 2016
)
0.43
"0%) with a stable dosage of metformin plus gliclazide for more than 3 months were randomized to receive either vildagliptin 50 mg twice daily (BID, n = 37) or saxagliptin 5 mg once daily (QD, n = 36)."( Effects of vildagliptin versus saxagliptin on daily acute glucose fluctuations in Chinese patients with T2DM inadequately controlled with a combination of metformin and sulfonylurea.
Jing, W; Shunyou, D; Xiaochun, H; Xiaoyan, C; Yingyu, F; Yuyu, T, 2016
)
0.7
"The objective of this study was to determine if there is a dose-response relationship between sulfonylureas and major adverse cardiovascular events (MACE)."( Dose-response relationship between sulfonylureas and major adverse cardiovascular events in elderly patients with type 2 diabetes.
Abdelmoneim, AS; Eurich, DT; Qiu, W; Senthilselvan, A; Simpson, SH, 2016
)
0.43
"Among new users of sulfonylureas, there appears to be a dose-response relationship between glyburide and MACE, but not for gliclazide."( Dose-response relationship between sulfonylureas and major adverse cardiovascular events in elderly patients with type 2 diabetes.
Abdelmoneim, AS; Eurich, DT; Qiu, W; Senthilselvan, A; Simpson, SH, 2016
)
0.64
"In primary care, once daily, breakable extended release gliclazide XR 60 mg, with a simple two step titration to administer maximum recommended dosage is effective in achieving short term glycemic control with a low frequency of hypoglycaemia, in monotherapy or in combination with metformin."( Treatment of Type 2 Diabetes with a Breakable Extended Release Gliclazide Formulation in Primary Care: The Xrise Study.
Chopra, V; Jain, S; Jayaprakashsai, J; Mohan, V; Sanyal, D, 2015
)
0.9
" The purpose of this research was to provide a fast dissolving oral dosage form of Gliclazide (GLZ) using the concept of mixed hydrotropy."( Formulation, Characterization and In-vitro Evaluation of Fast Dissolv ing Tablets Containing Gliclazide Hydrotropic Solid Dispersions.
Awasthi, R; Dua, K; Kamate, VJ; Madan, JR, 2017
)
0.9
"The new system shows an improved pharmaceutical behavior and could be formulated in a dosage form to obtain a rapid and complete release of the drug available for absorption."( Multicomponent crystals of gliclazide and tromethamine: preparation, physico-chemical, and pharmaceutical characterization
Berbenni, V; Bruni, G; Castagna, F; Ferrara, C; Friuli, V; Girella, A; Maggi, L; Marini, A; Milanese, C; Mustarelli, P; Pardi, F, 2018
)
0.78
" It is dosed in modified release tablets."( Determination of gliclazide minimum concentration in type 2 diabetes mellitus patients.
Czyrski, A; Hermann, T; Resztak, M, 2018
)
0.82
"Bucco adhesive films of Gliclazide is a promising dosage form for the treatment of diabetes in children."( Development, in vitro Evaluation, and in vivo Study of Adhesive Buccal Films for the Treatment of Diabetic Pediatrics via Trans Mucosal Delivery of Gliclazide.
Adogim, SS; Albilaihi, HM; Alburaykan, AI; Aldohan, NS; Alharbi, RF; Aljohani, AR; Alruthea, LM; Gaber, DA, 2022
)
1.23
" To investigate various dosing regimens of gliclazide, we used publicly available data to characterise the dose-response relationship using pharmacometric models."( Optimal dosing of gliclazide-A model-based approach.
Cotton, MF; Hussein, H; Karamchand, S; Kjellsson, MC; Leisegang, R; Mim, SR; Naidoo, P; Rambiritch, V; Vidadi, S, 2023
)
1.51
" Dose-response analysis showed that increasing heptanol concentration beyond the level associated with maximal effects on cell coupling resulted in further protection against hypoxic injury."( Protective effect of gap junction uncouplers given during hypoxia against reoxygenation injury in isolated rat hearts.
García-Dorado, D; Rodríguez-Sinovas, A; Ruiz-Meana, M; Soler-Soler, J, 2006
)
0.33
"9% were prepared to investigate the dosage effect on transdermal delivery and anti-inflammatory activity."( A novel transdermal fomulation of 18β-glycyrrhetic acid with lysine for improving bioavailability and efficacy.
Gao, YH; Li, S; Qiu, YQ; Zhang, SH, 2012
)
0.38
[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.
radical scavengerA role played by a substance that can react readily with, and thereby eliminate, radicals.
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 (1)

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.
[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]

Pathways (1)

PathwayProteinsCompounds
Gliclazide Action Pathway65

Protein Targets (22)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, MAJOR APURINIC/APYRIMIDINIC ENDONUCLEASEHomo sapiens (human)Potency7.07950.003245.467312,589.2998AID2517
Chain A, Putative fructose-1,6-bisphosphate aldolaseGiardia intestinalisPotency8.91250.140911.194039.8107AID2451
Chain A, JmjC domain-containing histone demethylation protein 3AHomo sapiens (human)Potency89.12510.631035.7641100.0000AID504339
phosphopantetheinyl transferaseBacillus subtilisPotency31.62280.141337.9142100.0000AID1490
Fumarate hydrataseHomo sapiens (human)Potency37.22120.00308.794948.0869AID1347053
GLS proteinHomo sapiens (human)Potency35.48130.35487.935539.8107AID624170
aldehyde dehydrogenase 1 family, member A1Homo sapiens (human)Potency39.81070.011212.4002100.0000AID1030
cytochrome P450 family 3 subfamily A polypeptide 4Homo sapiens (human)Potency0.12300.01237.983543.2770AID1645841
EWS/FLI fusion proteinHomo sapiens (human)Potency22.08300.001310.157742.8575AID1259252; AID1259253; AID1259255; AID1259256
retinoic acid nuclear receptor alpha variant 1Homo sapiens (human)Potency28.74660.003041.611522,387.1992AID1159552; AID1159555
estrogen nuclear receptor alphaHomo sapiens (human)Potency1.80020.000229.305416,493.5996AID743080
polyproteinZika virusPotency37.22120.00308.794948.0869AID1347053
bromodomain adjacent to zinc finger domain 2BHomo sapiens (human)Potency79.43280.707936.904389.1251AID504333
Inositol monophosphatase 1Rattus norvegicus (Norway rat)Potency5.01191.000010.475628.1838AID1457
[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 pumpRattus norvegicus (Norway rat)IC50 (µMol)1,000.00000.40002.75008.6000AID1209456
Bile salt export pumpHomo sapiens (human)IC50 (µMol)574.60000.11007.190310.0000AID1209455; AID1449628; AID1473738
Aldo-keto reductase family 1 member C3Homo sapiens (human)IC50 (µMol)19.62000.05002.207010.0000AID1674109
Aldo-keto reductase family 1 member C2 Homo sapiens (human)IC50 (µMol)1,000.00000.37004.09519.2800AID1674110
Aldo-keto reductase family 1 member C1Homo sapiens (human)IC50 (µMol)300.00000.00603.12657.9000AID1674111
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 (75)

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)
retinoid metabolic processAldo-keto reductase family 1 member C3Homo sapiens (human)
prostaglandin metabolic processAldo-keto reductase family 1 member C3Homo sapiens (human)
G protein-coupled receptor signaling pathwayAldo-keto reductase family 1 member C3Homo sapiens (human)
response to nutrientAldo-keto reductase family 1 member C3Homo sapiens (human)
steroid metabolic processAldo-keto reductase family 1 member C3Homo sapiens (human)
positive regulation of cell population proliferationAldo-keto reductase family 1 member C3Homo sapiens (human)
male gonad developmentAldo-keto reductase family 1 member C3Homo sapiens (human)
cellular response to starvationAldo-keto reductase family 1 member C3Homo sapiens (human)
farnesol catabolic processAldo-keto reductase family 1 member C3Homo sapiens (human)
cyclooxygenase pathwayAldo-keto reductase family 1 member C3Homo sapiens (human)
keratinocyte differentiationAldo-keto reductase family 1 member C3Homo sapiens (human)
progesterone metabolic processAldo-keto reductase family 1 member C3Homo sapiens (human)
retinol metabolic processAldo-keto reductase family 1 member C3Homo sapiens (human)
retinal metabolic processAldo-keto reductase family 1 member C3Homo sapiens (human)
macromolecule metabolic processAldo-keto reductase family 1 member C3Homo sapiens (human)
daunorubicin metabolic processAldo-keto reductase family 1 member C3Homo sapiens (human)
doxorubicin metabolic processAldo-keto reductase family 1 member C3Homo sapiens (human)
regulation of retinoic acid receptor signaling pathwayAldo-keto reductase family 1 member C3Homo sapiens (human)
positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transductionAldo-keto reductase family 1 member C3Homo sapiens (human)
testosterone biosynthetic processAldo-keto reductase family 1 member C3Homo sapiens (human)
renal absorptionAldo-keto reductase family 1 member C3Homo sapiens (human)
cellular response to calcium ionAldo-keto reductase family 1 member C3Homo sapiens (human)
cellular response to prostaglandin stimulusAldo-keto reductase family 1 member C3Homo sapiens (human)
cellular response to corticosteroid stimulusAldo-keto reductase family 1 member C3Homo sapiens (human)
cellular response to jasmonic acid stimulusAldo-keto reductase family 1 member C3Homo sapiens (human)
cellular response to prostaglandin D stimulusAldo-keto reductase family 1 member C3Homo sapiens (human)
negative regulation of retinoic acid biosynthetic processAldo-keto reductase family 1 member C3Homo sapiens (human)
regulation of testosterone biosynthetic processAldo-keto reductase family 1 member C3Homo sapiens (human)
positive regulation of endothelial cell apoptotic processAldo-keto reductase family 1 member C3Homo sapiens (human)
positive regulation of reactive oxygen species metabolic processAldo-keto reductase family 1 member C3Homo sapiens (human)
prostaglandin metabolic processAldo-keto reductase family 1 member C2 Homo sapiens (human)
G protein-coupled receptor signaling pathwayAldo-keto reductase family 1 member C2 Homo sapiens (human)
digestionAldo-keto reductase family 1 member C2 Homo sapiens (human)
steroid metabolic processAldo-keto reductase family 1 member C2 Homo sapiens (human)
positive regulation of cell population proliferationAldo-keto reductase family 1 member C2 Homo sapiens (human)
epithelial cell differentiationAldo-keto reductase family 1 member C2 Homo sapiens (human)
progesterone metabolic processAldo-keto reductase family 1 member C2 Homo sapiens (human)
daunorubicin metabolic processAldo-keto reductase family 1 member C2 Homo sapiens (human)
doxorubicin metabolic processAldo-keto reductase family 1 member C2 Homo sapiens (human)
positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transductionAldo-keto reductase family 1 member C2 Homo sapiens (human)
cellular response to jasmonic acid stimulusAldo-keto reductase family 1 member C2 Homo sapiens (human)
cellular response to prostaglandin D stimulusAldo-keto reductase family 1 member C2 Homo sapiens (human)
retinoid metabolic processAldo-keto reductase family 1 member C1Homo sapiens (human)
xenobiotic metabolic processAldo-keto reductase family 1 member C1Homo sapiens (human)
digestionAldo-keto reductase family 1 member C1Homo sapiens (human)
bile acid metabolic processAldo-keto reductase family 1 member C1Homo sapiens (human)
bile acid and bile salt transportAldo-keto reductase family 1 member C1Homo sapiens (human)
intestinal cholesterol absorptionAldo-keto reductase family 1 member C1Homo sapiens (human)
epithelial cell differentiationAldo-keto reductase family 1 member C1Homo sapiens (human)
progesterone metabolic processAldo-keto reductase family 1 member C1Homo sapiens (human)
retinal metabolic processAldo-keto reductase family 1 member C1Homo sapiens (human)
cholesterol homeostasisAldo-keto reductase family 1 member C1Homo sapiens (human)
daunorubicin metabolic processAldo-keto reductase family 1 member C1Homo sapiens (human)
doxorubicin metabolic processAldo-keto reductase family 1 member C1Homo sapiens (human)
response to organophosphorusAldo-keto reductase family 1 member C1Homo sapiens (human)
cellular response to jasmonic acid stimulusAldo-keto reductase family 1 member C1Homo sapiens (human)
positive regulation of reactive oxygen species metabolic processAldo-keto reductase family 1 member C1Homo sapiens (human)
prostaglandin metabolic processAldo-keto reductase family 1 member C1Homo 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 (55)

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)
retinal dehydrogenase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
aldose reductase (NADPH) activityAldo-keto reductase family 1 member C3Homo sapiens (human)
aldo-keto reductase (NADPH) activityAldo-keto reductase family 1 member C3Homo sapiens (human)
estradiol 17-beta-dehydrogenase [NAD(P)] activityAldo-keto reductase family 1 member C3Homo sapiens (human)
all-trans-retinol dehydrogenase (NAD+) activityAldo-keto reductase family 1 member C3Homo sapiens (human)
oxidoreductase activity, acting on NAD(P)H, quinone or similar compound as acceptorAldo-keto reductase family 1 member C3Homo sapiens (human)
phenanthrene 9,10-monooxygenase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
dihydrotestosterone 17-beta-dehydrogenase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
prostaglandin H2 endoperoxidase reductase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
prostaglandin D2 11-ketoreductase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
geranylgeranyl reductase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
ketoreductase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
prostaglandin-F synthase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
15-hydroxyprostaglandin-D dehydrogenase (NADP+) activityAldo-keto reductase family 1 member C3Homo sapiens (human)
androsterone dehydrogenase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
5alpha-androstane-3beta,17beta-diol dehydrogenase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
testosterone dehydrogenase (NAD+) activityAldo-keto reductase family 1 member C3Homo sapiens (human)
androstan-3-alpha,17-beta-diol dehydrogenase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
testosterone 17-beta-dehydrogenase (NADP+) activityAldo-keto reductase family 1 member C3Homo sapiens (human)
ketosteroid monooxygenase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
Delta4-3-oxosteroid 5beta-reductase activityAldo-keto reductase family 1 member C3Homo sapiens (human)
all-trans-retinol dehydrogenase (NADP+) activityAldo-keto reductase family 1 member C3Homo sapiens (human)
bile acid bindingAldo-keto reductase family 1 member C3Homo sapiens (human)
aldose reductase (NADPH) activityAldo-keto reductase family 1 member C2 Homo sapiens (human)
estradiol 17-beta-dehydrogenase [NAD(P)] activityAldo-keto reductase family 1 member C2 Homo sapiens (human)
oxidoreductase activity, acting on NAD(P)H, quinone or similar compound as acceptorAldo-keto reductase family 1 member C2 Homo sapiens (human)
phenanthrene 9,10-monooxygenase activityAldo-keto reductase family 1 member C2 Homo sapiens (human)
carboxylic acid bindingAldo-keto reductase family 1 member C2 Homo sapiens (human)
bile acid bindingAldo-keto reductase family 1 member C2 Homo sapiens (human)
androstan-3-alpha,17-beta-diol dehydrogenase activityAldo-keto reductase family 1 member C2 Homo sapiens (human)
ketosteroid monooxygenase activityAldo-keto reductase family 1 member C2 Homo sapiens (human)
trans-1,2-dihydrobenzene-1,2-diol dehydrogenase activityAldo-keto reductase family 1 member C2 Homo sapiens (human)
indanol dehydrogenase activityAldo-keto reductase family 1 member C2 Homo sapiens (human)
androsterone dehydrogenase activityAldo-keto reductase family 1 member C2 Homo sapiens (human)
aldose reductase (NADPH) activityAldo-keto reductase family 1 member C1Homo sapiens (human)
aldo-keto reductase (NADPH) activityAldo-keto reductase family 1 member C1Homo sapiens (human)
estradiol 17-beta-dehydrogenase [NAD(P)] activityAldo-keto reductase family 1 member C1Homo sapiens (human)
protein bindingAldo-keto reductase family 1 member C1Homo sapiens (human)
oxidoreductase activity, acting on NAD(P)H, quinone or similar compound as acceptorAldo-keto reductase family 1 member C1Homo sapiens (human)
phenanthrene 9,10-monooxygenase activityAldo-keto reductase family 1 member C1Homo sapiens (human)
testosterone dehydrogenase [NAD(P)] activityAldo-keto reductase family 1 member C1Homo sapiens (human)
carboxylic acid bindingAldo-keto reductase family 1 member C1Homo sapiens (human)
bile acid bindingAldo-keto reductase family 1 member C1Homo sapiens (human)
3beta-hydroxy-5beta-steroid dehydrogenase activityAldo-keto reductase family 1 member C1Homo sapiens (human)
steroid dehydrogenase activity, acting on the CH-OH group of donors, NAD or NADP as acceptorAldo-keto reductase family 1 member C1Homo sapiens (human)
dihydrotestosterone 17-beta-dehydrogenase activityAldo-keto reductase family 1 member C1Homo sapiens (human)
17-alpha,20-alpha-dihydroxypregn-4-en-3-one dehydrogenase activityAldo-keto reductase family 1 member C1Homo sapiens (human)
5alpha-androstane-3beta,17beta-diol dehydrogenase activityAldo-keto reductase family 1 member C1Homo sapiens (human)
androsterone dehydrogenase (B-specific) activityAldo-keto reductase family 1 member C1Homo sapiens (human)
androstan-3-alpha,17-beta-diol dehydrogenase activityAldo-keto reductase family 1 member C1Homo sapiens (human)
testosterone 17-beta-dehydrogenase (NADP+) activityAldo-keto reductase family 1 member C1Homo sapiens (human)
ketosteroid monooxygenase activityAldo-keto reductase family 1 member C1Homo sapiens (human)
trans-1,2-dihydrobenzene-1,2-diol dehydrogenase activityAldo-keto reductase family 1 member C1Homo sapiens (human)
indanol dehydrogenase activityAldo-keto reductase family 1 member C1Homo sapiens (human)
androsterone dehydrogenase activityAldo-keto reductase family 1 member C1Homo 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 (20)

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)
nucleusAldo-keto reductase family 1 member C3Homo sapiens (human)
cytoplasmAldo-keto reductase family 1 member C3Homo sapiens (human)
cytosolAldo-keto reductase family 1 member C3Homo sapiens (human)
extracellular exosomeAldo-keto reductase family 1 member C3Homo sapiens (human)
cytosolAldo-keto reductase family 1 member C3Homo sapiens (human)
cytosolAldo-keto reductase family 1 member C2 Homo sapiens (human)
cytosolAldo-keto reductase family 1 member C1Homo sapiens (human)
extracellular exosomeAldo-keto reductase family 1 member C1Homo sapiens (human)
cytosolAldo-keto reductase family 1 member C1Homo 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 (153)

Assay IDTitleYearJournalArticle
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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
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.
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.
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.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
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.
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.
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.
AID599100Antihyperglycemic activity in Charles Foster/Wistar albino rat assessed as reduction in blood glucose level at 100 mg/kg, po administered 30 mins before sucrose challenge2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Design and synthesis of 3,5-diarylisoxazole derivatives as novel class of anti-hyperglycemic and lipid lowering agents.
AID1209456Inhibition of Sprague-Dawley rat Bsep expressed in plasma membrane vesicles of Sf21 cells assessed as inhibition of ATP-dependent [3H]taurocholate uptake2012Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 40, Issue:1
In vitro inhibition of the bile salt export pump correlates with risk of cholestatic drug-induced liver injury in humans.
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).
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]
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).
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.
AID1776773Stimulation of glucose stimulated insulin secretion in rat INS1 cells assessed as glucose stimulation index at 2.5 uM in presence of glucose measured after 1 hr2021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Identification of bioactive compounds from mulberry enhancing glucose-stimulated insulin secretion.
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).
AID396648Antihyperglycemic activity against sucrose-loaded Charles-Foster Wistar albino rat assessed as reduction in blood glucose at 100 mg/kg, po administered 30 mins before sucrose challenge relative to control2009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Novel 2-aryl-naphtho[1,2-d]oxazole derivatives as potential PTP-1B inhibitors showing antihyperglycemic activities.
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID599103Antihyperglycemic activity in C57BL/Ks db/db mouse assessed as reduction in blood glucose level measured after 3 days relative to control2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Design and synthesis of 3,5-diarylisoxazole derivatives as novel class of anti-hyperglycemic and lipid lowering agents.
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).
AID977599Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID1209455Inhibition of human BSEP expressed in plasma membrane vesicles of Sf21 cells assessed as inhibition of ATP-dependent [3H]taurocholate uptake2012Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 40, Issue:1
In vitro inhibition of the bile salt export pump correlates with risk of cholestatic drug-induced liver injury in humans.
AID476929Human intestinal absorption in po dosed human2010European journal of medicinal chemistry, Mar, Volume: 45, Issue:3
Neural computational prediction of oral drug absorption based on CODES 2D descriptors.
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).
AID396649Antihyperglycemic activity against sucrose-challenged streptozotocin-induced fasted Sprague-Dawley rat assessed as reduction in blood glucose at 100 mg/kg, po administered 30 mins before sucrose challenge measured after 5 hrs post sucrose dose relative to2009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Novel 2-aryl-naphtho[1,2-d]oxazole derivatives as potential PTP-1B inhibitors showing antihyperglycemic activities.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' 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).
AID1758891Induction of insulin secretion in rat INS-1 cells assessed as glucose stimulation index at 5 uM followed by stimulated with 16.7 mM glucose measured after 1 hrs by ELISA relative to basal insulin level2021European journal of medicinal chemistry, May-05, Volume: 217Discovery and optimization of novel 3-benzyl-N-phenyl-1H-pyrazole-5-carboxamides as bifunctional antidiabetic agents stimulating both insulin secretion and glucose uptake.
AID1758887Cytotoxicity against rat INS1 cells assessed as cell viability at 10 uM incubated for 24 hrs by MTT assay relative to untreated control2021European journal of medicinal chemistry, May-05, Volume: 217Discovery and optimization of novel 3-benzyl-N-phenyl-1H-pyrazole-5-carboxamides as bifunctional antidiabetic agents stimulating both insulin secretion and glucose uptake.
AID264868Antihyperglycemic activity in sucrose charged streptozotocin-induced beta cell damaged diabetic Sprague-Dawley rat at 100 mg/kg2006Bioorganic & medicinal chemistry letters, May-15, Volume: 16, Issue:10
Novel substituted naphthalen-1-yl-methanone derivatives as anti-hyperglycemic agents.
AID588209Literature-mined public compounds from Greene et al multi-species hepatotoxicity modelling dataset2010Chemical research in toxicology, Jul-19, Volume: 23, Issue:7
Developing structure-activity relationships for the prediction of hepatotoxicity.
AID1674109Inhibition of N-terminal His-tagged human AKR1C3 expressed in Escherichia coli BL21(Condon Plus) competent cells using 9,10-phenanthrenequinone as substrate in presence of NADPH2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Overview of AKR1C3: Inhibitor Achievements and Disease Insights.
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]
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
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).
AID416451Inhibition of CYP2C9 assessed as decrease in catalytic reaction velocity at 200 uM by substrate-inhibition assay2009European journal of medicinal chemistry, Feb, Volume: 44, Issue:2
The metabolism of CYP2C9 and CYP2C19 for gliclazide by homology modeling and docking study.
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).
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.
AID1142508Antihyperglycemic activity in glucose-fed hyperglycaemic Wistar albino rat assessed as inhibition of postprandial hyperglycemia at 0.05 mM/kg, po administered via gavage 30 mins prior to glucose challenge measured 60 mins after glucose load2014European journal of medicinal chemistry, Jun-10, Volume: 80Synthesis and biological evaluation of some new pyrazoline substituted benzenesulfonylurea/thiourea derivatives as anti-hyperglycaemic agents and aldose reductase inhibitors.
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.
AID1209457Unbound Cmax in human plasma2012Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 40, Issue:1
In vitro inhibition of the bile salt export pump correlates with risk of cholestatic drug-induced liver injury in humans.
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.
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).
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
AID317690Antidiabetic activity in sucrose loaded albino Sprague-Dawley rat model assessed as decrease in blood glucose level at 100 mg/kg, po2008Bioorganic & medicinal chemistry, Mar-01, Volume: 16, Issue:5
Omega-(2-Naphthyloxy) amino alkanes as a novel class of anti-hyperglycemic and lipid lowering agents.
AID588220Literature-mined public compounds from Kruhlak et al phospholipidosis modelling dataset2008Toxicology mechanisms and methods, , Volume: 18, Issue:2-3
Development of a phospholipidosis database and predictive quantitative structure-activity relationship (QSAR) models.
AID588210Human drug-induced liver injury (DILI) modelling dataset from Ekins et al2010Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 38, Issue:12
A predictive ligand-based Bayesian model for human drug-induced liver injury.
AID416452Inhibition of CYP2C19 assessed as decrease in catalytic reaction velocity at 100 uM by substrate-inhibition assay2009European journal of medicinal chemistry, Feb, Volume: 44, Issue:2
The metabolism of CYP2C9 and CYP2C19 for gliclazide by homology modeling and docking study.
AID1449628Inhibition of human BSEP expressed in baculovirus transfected fall armyworm Sf21 cell membranes vesicles assessed as reduction in ATP-dependent [3H]-taurocholate transport into vesicles incubated for 5 mins by Topcount based rapid filtration method2012Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 40, Issue:12
Mitigating the inhibition of human bile salt export pump by drugs: opportunities provided by physicochemical property modulation, in silico modeling, and structural modification.
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID317692Antidiabetic activity in sucrose challenged streptozotocin-induced diabetic albino Sprague-Dawley rat model assessed as decrease in blood glucose level at 100 mg/kg, po2008Bioorganic & medicinal chemistry, Mar-01, Volume: 16, Issue:5
Omega-(2-Naphthyloxy) amino alkanes as a novel class of anti-hyperglycemic and lipid lowering agents.
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).
AID1776772Cytotoxicity against rat INS1 cells assessed as cell viability at 10 uM measured after 24 hrs by MTT assay2021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Identification of bioactive compounds from mulberry enhancing glucose-stimulated insulin secretion.
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).
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID317691Antidiabetic activity in streptozotocin-induced diabetic albino Sprague-Dawley rat model assessed as decrease in blood glucose level at 100 mg/kg, po2008Bioorganic & medicinal chemistry, Mar-01, Volume: 16, Issue:5
Omega-(2-Naphthyloxy) amino alkanes as a novel class of anti-hyperglycemic and lipid lowering agents.
AID1674110Inhibition of N-terminal His-tagged human AKR1C2 expressed in Escherichia coli BL21 (Condon Plus) competent cells using 9,10-phenanthrenequinone as substrate in presence of NADPH2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Overview of AKR1C3: Inhibitor Achievements and Disease Insights.
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).
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]
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID396651Antihyperglycemic activity against C57BL/KsBom db/db type 2 diabetic mouse model assessed as decrease in postprandial blood glucose level on day 3 by OGTT relative to control2009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Novel 2-aryl-naphtho[1,2-d]oxazole derivatives as potential PTP-1B inhibitors showing antihyperglycemic activities.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
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.
AID1674111Inhibition of N-terminal His-tagged human AKR1C1 expressed in Escherichia coli BL21 (Condon Plus) competent cells using 9,10-phenanthrenequinone as substrate in presence of NADPH2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Overview of AKR1C3: Inhibitor Achievements and Disease Insights.
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.
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
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]
AID1776774Stimulation of glucose stimulated insulin secretion in rat INS1 cells assessed as glucose stimulation index at 5 uM in presence of glucose measured after 1 hr2021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Identification of bioactive compounds from mulberry enhancing glucose-stimulated insulin secretion.
AID977602Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
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]
AID420793Antidiabetic activity in streptozotocin-induced NIDDM Wistar albino rat model assessed as inhibition of rise of blood glucose level at 20 mg/kg, po administered 15 mins prior to glucose challenge measured after 90 mins of glucose loading by glucose oxidas2009European journal of medicinal chemistry, Jun, Volume: 44, Issue:6
Synthesis and blood glucose lowering effect of novel pyridazinone substituted benzenesulfonylurea derivatives.
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.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
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).
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID420792Antidiabetic activity in normal Wistar albino rat assessed as inhibition of rise of blood glucose level at 20 mg/kg, po administered 15 mins prior to glucose challenge measured after 90 mins of glucose loading by glucose oxidase-peroxidase colorimetric me2009European journal of medicinal chemistry, Jun, Volume: 44, Issue:6
Synthesis and blood glucose lowering effect of novel pyridazinone substituted benzenesulfonylurea derivatives.
AID599101Antihyperglycemic activity against sucrose challenged streptozotocin-induced diabetic Sprague-Dawley albino rat assessed as reduction in blood glucose level at 100 mg/kg, po administered 30 mins before sucrose challenge measured after 5 hrs2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Design and synthesis of 3,5-diarylisoxazole derivatives as novel class of anti-hyperglycemic and lipid lowering agents.
AID1758890Induction of insulin secretion in rat INS-1 cells assessed as glucose stimulation index at 10 uM followed by stimulated with 16.7 mM glucose measured after 1 hrs by ELISA relative to basal insulin level2021European journal of medicinal chemistry, May-05, Volume: 217Discovery and optimization of novel 3-benzyl-N-phenyl-1H-pyrazole-5-carboxamides as bifunctional antidiabetic agents stimulating both insulin secretion and glucose uptake.
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).
AID264867Antihyperglycemic activity in sucrose-loaded Sprague-Dawley rat at 100 mg/kg2006Bioorganic & medicinal chemistry letters, May-15, Volume: 16, Issue:10
Novel substituted naphthalen-1-yl-methanone derivatives as anti-hyperglycemic agents.
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]
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).
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.
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.
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.
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.
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.
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.
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.
AID1159550Human Phosphogluconate dehydrogenase (6PGD) Inhibitor Screening2015Nature cell biology, Nov, Volume: 17, Issue:11
6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling.
AID1301447Antiviral activity against Influenza A virus A/WSN/33(H1N1) infected in MDCK cells at 100 uM preincubated with virus for 15 mins followed by cells addition measured at 36 hrs post infection2016Journal of natural products, Feb-26, Volume: 79, Issue:2
Bioactive Constituents of Glycyrrhiza uralensis (Licorice): Discovery of the Effective Components of a Traditional Herbal Medicine.
AID1424305Cytotoxicity in human DU145 cells assessed as reduction in cell viability incubated for 96 hrs by SRB assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1424278Cytotoxicity in human MDA-MB-231 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1301467Inhibition of recombinant human PTP1B assessed as hydrolysis of p-nitrophenyl phosphate at 25 uM after 30 mins relative to control2016Journal of natural products, Feb-26, Volume: 79, Issue:2
Bioactive Constituents of Glycyrrhiza uralensis (Licorice): Discovery of the Effective Components of a Traditional Herbal Medicine.
AID1424300Cytotoxicity in human HCT116 cells assessed as reduction in cell viability incubated for 96 hrs by SRB assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1424296Cytotoxicity in human hTERT-RPE1 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1416423Anti-inflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced IL-6 production at 10 to 40 uM preincubated for 2 hrs followed by LPS addition measured after 20 hrs by ELISA2017MedChemComm, Jul-01, Volume: 8, Issue:7
18α-Glycyrrhetinic acid monoglucuronide as an anti-inflammatory agent through suppression of the NF-κB and MAPK signaling pathway.
AID1416421Anti-inflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced NO production at 40 uM preincubated for 2 hrs followed by LPS addition measured after 20 hrs by Griess assay relative to control2017MedChemComm, Jul-01, Volume: 8, Issue:7
18α-Glycyrrhetinic acid monoglucuronide as an anti-inflammatory agent through suppression of the NF-κB and MAPK signaling pathway.
AID1424299Cytotoxicity in rat H9c2 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1424306Cytotoxicity in human MDA-MB-231 cells assessed as reduction in cell viability incubated for 96 hrs by SRB assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1416422Cytotoxicity against mouse RAW264.7 cells assessed as cell viability at 40 uM after 24 hrs by MTT assay relative to control2017MedChemComm, Jul-01, Volume: 8, Issue:7
18α-Glycyrrhetinic acid monoglucuronide as an anti-inflammatory agent through suppression of the NF-κB and MAPK signaling pathway.
AID1424292Cytotoxicity in human HeLa cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1424303Cytotoxicity in mouse CT26 cells assessed as reduction in cell viability incubated for 96 hrs by SRB assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1424279Cytotoxicity in human MCF7 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID977599Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID1424293Cytotoxicity in human HT-29 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1424304Cytotoxicity in human PC3 cells assessed as reduction in cell viability incubated for 96 hrs by SRB assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1424297Cytotoxicity in human MDCK cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1424302Cytotoxicity in human HT-29 cells assessed as reduction in cell viability incubated for 96 hrs by SRB assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1424298Cytotoxicity in human EAhy926 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID977602Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID1424307Cytotoxicity in mouse 4T1 cells assessed as reduction in cell viability incubated for 96 hrs by SRB assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1424301Cytotoxicity in human HCT8 cells assessed as reduction in cell viability incubated for 96 hrs by SRB assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1424294Cytotoxicity in human HepG2 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay2017European journal of medicinal chemistry, Dec-15, Volume: 142Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment.
AID1159550Human Phosphogluconate dehydrogenase (6PGD) Inhibitor Screening2015Nature cell biology, Nov, Volume: 17, Issue:11
6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (1,215)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990142 (11.69)18.7374
1990's168 (13.83)18.2507
2000's336 (27.65)29.6817
2010's436 (35.88)24.3611
2020's133 (10.95)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 100.06

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 Index100.06 (24.57)
Research Supply Index7.10 (2.92)
Research Growth Index4.68 (4.65)
Search Engine Demand Index184.05 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (100.06)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials214 (21.46%)5.53%
Trials2 (0.66%)5.53%
Reviews73 (7.32%)6.00%
Reviews8 (2.63%)6.00%
Case Studies57 (5.72%)4.05%
Case Studies0 (0.00%)4.05%
Observational8 (0.80%)0.25%
Observational0 (0.00%)0.25%
Other645 (64.69%)84.16%
Other294 (96.71%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (50)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Comparison of the Action of the Rosiglitazone-metformin Fixed-dose Combination and of a Metformin-sulfonylurea Free Combination on the B-cell Function in Type 2 Diabetic Patients Not Controlled With Metformin Alone. [NCT00367055]Phase 484 participants (Actual)Interventional2004-10-31Completed
JanUmet Before Insulin Lantus In Eastern Population Evaluation Program (JUBILEE) In Type 2 Diabetic Patients [NCT01269996]Phase 471 participants (Actual)Interventional2011-05-31Completed
Incretin-based Drugs and the Risk of Heart Failure: A Multi-center Network Observational Study [NCT02456428]1,499,650 participants (Actual)Observational2014-03-31Completed
RACELINES: Renal Actions of Combined Empagliflozin and LINagliptin in Type 2 diabetES [NCT03433248]Phase 466 participants (Actual)Interventional2017-11-09Active, not recruiting
Does Glycated Hemoglobin Variability in Type 2 Diabetes Differ Depending on the Diabetes Treatment Threshold Used in the Qatari Population: Implication on Diabetes Complication Risk? [NCT02879409]150 participants (Anticipated)Interventional2016-11-30Active, not recruiting
Randomized, Open Label, Single Dose, 4 Treatment, 4 Period, Crossover Design (4 x 4) Trial to Evaluate the Bioequivalence and Secondarily Drug - Drug Interaction of Fixed Combination of Metformin Tablets 1000 mg/Gliclazide 30 mg MR, Compared With the Co-a [NCT03467945]Phase 140 participants (Actual)Interventional2018-02-16Completed
Study of Sulphonylurea Synergy With Incretins [NCT03705195]20 participants (Actual)Interventional2018-08-03Completed
Variability of Glucose Assessed in a Randomized Trial Comparing the Initiation of A Treatment Approach With Biosimilar Basal Insulin Analog Or a Titratable iGlarLixi combinatioN in Type 2 Diabetes Among South Asian Subjects (VARIATION 2 SA Trial) [NCT03819790]Phase 4119 participants (Actual)Interventional2018-10-02Completed
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
Vildagliptin Compared to Gliclazide in Combination With Metformin in Patients With Type 2 Diabetes [NCT00102466]Phase 31,007 participants (Actual)Interventional2005-01-31Completed
Sulphonylurea Receptor Mutation and Responsiveness to Gliclazide - a Pilot Proof of Concept, Randomised Cross-over Study [NCT02201602]Phase 48 participants (Actual)Interventional2014-08-31Completed
A Randomized, Open-label, Single Dose, 2x2 Crossover Trial to Evaluate the Food Effect on the Bioavailability of a Metformin/Gliclazide Fixed Combination Tablet (1000 mg /30 mg MR) Given in Fasting and Fed Conditions to Healthy Volunteers [NCT03467971]Phase 121 participants (Actual)Interventional2018-03-06Completed
[NCT02092597]Phase 442 participants (Actual)Interventional2013-10-31Completed
A Phase III Study to Assess the Efficacy, Safety and Tolerability of ASP1941 in Combination With Sulfonylurea in Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Sulfonylurea Alone [NCT01242215]Phase 3243 participants (Actual)Interventional2010-09-17Completed
Clinical Bioequivalence Study on Two Gliclazide 80mg Tablet Formulations [NCT02643329]Phase 117 participants (Actual)Interventional2016-01-31Completed
Phase 4 Study of Comparison of Combination Therapy of Gliclazide MR and Basal Insulin With Pre-mix Insulin Monotherapy for the Patients With Type 2 Diabetes Mellitus [NCT00736515]Phase 4160 participants (Actual)Interventional2008-10-31Completed
A 16-week, Multicentre, Randomised, Open-label, Parallel Group Study to Investigate the Efficacy and Safety Profiles of Repaglinide Monotherapy Compared to Gliclazide Monotherapy in Chinese Antidiabetic-naïve Subjects With Type 2 Diabetes [NCT01022762]Phase 4440 participants (Actual)Interventional2009-11-30Completed
Effect of Dapagliflozin, a Sodium Glucose Co-transporter 2 Inhibitor, on Vascular Functions in Patients With Type 2 Diabetes Compared to Gliclazide [NCT02610088]Phase 432 participants (Actual)Interventional2015-11-30Completed
Comparison of Diabetes Retinopathy Among Type 2 Diabetic Patients Treated With Different Regimens: a Multicentre Randomized Parallel-group Clinical Trial [NCT02587741]Early Phase 1600 participants (Anticipated)Interventional2015-07-31Recruiting
ADVANCE - Action in Diabetes and Vascular Disease: Preterax and Diamicron - MR Controlled Evaluation [NCT00145925]Phase 311,140 participants (Actual)Interventional2001-06-30Completed
Evaluation of the Effects of Oral Anti-Hyperglycemic Agents, Multiple Daily Injections or Continuous Subcutaneous Insulin Infusion on Glycemic Control, B-Cell Function and the Remission Rate in Newly-Diagnosed Type 2 Diabetic Patients [NCT00147836]436 participants (Actual)Interventional2004-09-30Completed
Effect of Anti-diabetic Drugs on Glycemic Variability. A Comparison Between Gliclazide MR (Modified Release) and Dapagliflozin on Glycemic Variability Measured by Continuous Glucose Monitoring (CGM) in Patients With Uncontrolled Type 2 Diabetes [NCT02925559]Phase 4135 participants (Actual)Interventional2016-10-31Completed
Effects of Rosiglitazone and Sulphonylureas on Ischaemic Burden, Blood Pressure and Novel Risk Markers Inclusive of Vascular Function in Patients With Chronic Stable Angina and Type 2 Diabetes Mellitus: A Randomised, Double-Blinded Study. [NCT00225342]Phase 460 participants InterventionalWithdrawn
A Randomised Controlled Trial for People With Established Type 2 Diabetes During Ramadan: Canagliflozin (Invokana™) vs. Standard Dual Therapy Regimen: The 'Can Do Ramadan' Study [NCT02694263]Phase 425 participants (Actual)Interventional2016-07-31Completed
The Use of Glycaemic Response to Sulphonylureas as a Tool to Investigate Type 2 Diabetes Pathophysiology [NCT00738088]Phase 414 participants (Actual)Interventional2007-06-30Terminated(stopped due to Following Regulator inspection in 2009, study terminated as inadequate approvals were in place)
A Phase III, Randomized, Clinical Trial to Evaluate the Safety and Efficacy of the Addition of Sitagliptin in Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on a Sulfonylurea in Combination With Metformin [NCT01076075]Phase 3427 participants (Actual)Interventional2010-06-03Completed
Effect of Eslicarbazepine Acetate on the Pharmacokinetics of Gliclazide in Healthy Volunteers [NCT02777671]Phase 120 participants (Actual)Interventional2007-10-31Completed
The Effects of Insulin Detemir and Gliclazide-MR Treatments in Addition to Life-style Modification and Metformin Therapy on Endothelial Functions in Patients With Type 2 Diabetes : An Open-labelled Randomized Prospective Study [NCT01420692]64 participants (Actual)Interventional2010-06-30Completed
A Prospective, Randomized, Open Label, Parallel, 6-month Study to Explore and Evaluate the Therapeutic Effects of Henagliflozin on the Cognitive Function, Olfactory Function, and Odor-induced Brain Activation in T2DM Patients With Mild Cognitive Impairmen [NCT06085703]60 participants (Anticipated)Interventional2023-09-01Recruiting
MASTERMIND - Understanding Individual Variation in Treatment Response in Type 2 [NCT01847144]Phase 4143 participants (Actual)Interventional2013-04-30Completed
Comparative Randomized, Single Dose, Three-period Crossover Open-label Study to Determine the Bioequivalence of Gliclazide 120 mg Modified Release Tablets Formula A and Gliclazide 120 mg Modified Release Tablets Formula B Manufactured by Indeus Life Scien [NCT02980757]Phase 10 participants (Actual)Interventional2014-06-30Withdrawn
Short-Term Intensive Insulin Therapy Induction of Long-term Glycemic Control Is Associated With Improvement of ß-Cell Function in Newly Diagnosed Type 2 Diabetic Patients [NCT00506194]60 participants (Anticipated)Interventional2005-10-31Completed
A Randomized Comparative Clinical Study on Suppression of Progression From Early Diabetes, Diet/Exercise Standard Intervention vs. Concurrent Pharmacological Standard Intervention [NCT00464594]2,560 participants Interventional2007-04-30Recruiting
Efficacy and Safety of Vildagliptin Compared to Gliclazide in Drug Naive Patients With Type 2 Diabetes [NCT00102388]Phase 31,092 participants (Actual)Interventional2005-01-31Completed
The DIAMET Study: Peripheral and Coronary Endothelial Dysfunction in Type 2diabetic Patients- Evaluation of Reversibility Following 3 Months of Metformin Treatment [NCT00169624]Phase 330 participants Interventional2005-10-31Terminated
Study of Sulphonylurea Synergy With DPP4 Inhibitors [NCT04192292]30 participants (Actual)Interventional2019-10-08Completed
Response To Oral Agents in Diabetes (ROAD)- Pilot Study [NCT00780715]Phase 429 participants (Actual)Interventional2008-12-31Completed
A Double Blind, Double Dummy, Randomised, Multi-centre Study to Assess the Tolerability and Efficacy Profile of Vildagliptin Compared to Gliclazide as Dual Therapy With Metformin in Muslim Patients With Type 2 Diabetes Fasting During Ramadan [NCT01758380]Phase 4557 participants (Actual)Interventional2013-01-31Completed
Metabolic Effects of Duodenal-jejunal Bypass Surgery in Non Morbidly Obese Subjects With Type 2 Diabetes [NCT01771185]24 participants (Anticipated)Interventional2012-10-31Active, not recruiting
Interaction Between Omeprazole and Gliclazide in CYP2C19 Normal/ Ultrarapid Metabolisers [NCT04198948]Phase 115 participants (Actual)Interventional2019-03-04Completed
Investigating Glucagon Secretion in HNF1-alpha and HNF4-alpha MODY [NCT03246828]10 participants (Actual)Interventional2017-07-03Completed
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
A Randomized, Double-blind, Comparator-controlled Trial to Assess the Effect of 12-week Treatment With Dapagliflozin Versus Gliclazide on Renal Physiology and Biomarkers in Metformin-treated Patients With Type 2 Diabetes Mellitus [NCT02682563]Phase 444 participants (Actual)Interventional2016-02-29Completed
Co-administration of Cabergoline and Gliclazide Improve Glycemic Parameters and Lipid Profile in T2DM Patients [NCT03313661]Phase 360 participants (Anticipated)Interventional2017-10-14Recruiting
A Phase III, Multicenter, Randomized, Double-Blind, Placebo-Controlled Clinical Trial in China to Study the Safety and Efficacy of the Addition of Sitagliptin in Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Sulfonylurea T [NCT01590771]Phase 3498 participants (Actual)Interventional2012-07-09Completed
A Multicenter, Randomized, Active-Controlled, Open-label Clinical Trial to Evaluate the Safety and Efficacy of Glimepiride, Gliclazide, Repaglinide or Acarbose as a Third OAHA on Top of Sitagliptin+Metformin Combination Therapy in Chinese Patients With Ty [NCT01709305]Phase 45,570 participants (Actual)Interventional2012-11-08Completed
Comparison of Efficacy of Liraglutide, Metformin and Gliclazide MR on Hepatic Lipid Content in Patients With Type 2 Diabetes (T2DM) and Non-alcoholic Fatty Liver (NAFLD) [NCT03068065]Phase 487 participants (Actual)Interventional2014-05-31Completed
Effect of Anti-diabetic Drugs on Bone Metabolism and Glycemic Variability.A Comparison Between Vildagliptin and Gliclazide MR [NCT01679899]Phase 456 participants (Actual)Interventional2012-12-31Completed
Dipeptidyl Peptidase-4 Inhibition in Psoriasis Patients With Diabetes (DIP): A Randomized Clinical Trial. [NCT01991197]Phase 220 participants (Actual)Interventional2014-04-30Completed
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
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00367055 (5) [back to overview]Mean Change From Baseline in FBG at Month 36
NCT00367055 (5) [back to overview]Mean Change From Baseline in HbA1c at Month 36
NCT00367055 (5) [back to overview]Mean Change From Baseline in Insulin Sensitivity Index at Months 18 and 36
NCT00367055 (5) [back to overview]Median Change From Baseline in the Insulin Secretion Capacity After an 18-month Treatment
NCT00367055 (5) [back to overview]Median Change From Baseline in the Insulin Secretory Capacity After a 36-month Treatment
NCT00780715 (1) [back to overview]HbA1c Change
NCT01022762 (11) [back to overview]Change in Fasting Serum Free Fatty Acid (FFA) From Baseline
NCT01022762 (11) [back to overview]Change in Fasting Plasma Glucose
NCT01022762 (11) [back to overview]Change in Glycosylated Haemoglobin (HbA1c)
NCT01022762 (11) [back to overview]Change in Body Weight
NCT01022762 (11) [back to overview]Change in AUC0-180 of Serum Insulin Concentration of IVGTT (Intravenous Glucose Tolerance Test)
NCT01022762 (11) [back to overview]Change in 2-hour Postprandial Serum Free Fatty Acid (FFA) Over a Standard Meal
NCT01022762 (11) [back to overview]Change in AUC0-180 of Plasma Glucose Concentration of IVGTT
NCT01022762 (11) [back to overview]Change in 2-hour Postprandial Plasma Glucose (PPG) Over a Standard Meal
NCT01022762 (11) [back to overview]Cholesterol
NCT01022762 (11) [back to overview]Number of All Treatment Emergent Hypoglycaemic Episodes
NCT01022762 (11) [back to overview]Percentage of Participants Achieving the Treatment Target of HbA1c Below or Equal to 6.5%
NCT01076075 (5) [back to overview]Change From Baseline in 2-hour Post-Meal Glucose at Week 24
NCT01076075 (5) [back to overview]Change From Baseline in Fasting Plasma Glucose at Week 24
NCT01076075 (5) [back to overview]Change From Baseline in Hemoglobin A1C (%) at Week 24
NCT01076075 (5) [back to overview]Number of Participants Discontinuing Study Drug Due to An Adverse Event
NCT01076075 (5) [back to overview]Number of Participants With One or More Adverse Events (AEs) - Week 0 to Week 54
NCT01590771 (11) [back to overview]Change From Baseline in FPG Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea Alone or in Combination With Metformin
NCT01590771 (11) [back to overview]Change From Baseline in A1C Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea in Combination With Metformin
NCT01590771 (11) [back to overview]Change From Baseline in A1C Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea Alone or in Combination With Metformin
NCT01590771 (11) [back to overview]Change From Baseline in A1C Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea Alone
NCT01590771 (11) [back to overview]Change From Baseline in 2-hr PMG Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea Alone or in Combination With Metformin
NCT01590771 (11) [back to overview]Change From Baseline in 2-hr PMG Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea Alone
NCT01590771 (11) [back to overview]Number of Participants Who Experienced an Adverse Event
NCT01590771 (11) [back to overview]Number of Participants Who Discontinued Study Drug Due to an Adverse Event
NCT01590771 (11) [back to overview]Change From Baseline in FPG Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea in Combination With Metformin
NCT01590771 (11) [back to overview]Change From Baseline in FPG Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea Alone
NCT01590771 (11) [back to overview]Change From Baseline in 2-hr PMG Levels at Week 24 in Participants Receiving Sitagliptin and a Sulfonylurea in Combination With Metformin
NCT01709305 (7) [back to overview]Change From Phase 2 Baseline to Week 44 in Participant Body Weight (Phase 2)
NCT01709305 (7) [back to overview]Change From Phase 2 Baseline to Week 44 in Hemoglobin A1c (HbA1c) Levels (Phase 2)
NCT01709305 (7) [back to overview]Percentage of Participants With a GI AE of Abdominal Pain (Phase 2)
NCT01709305 (7) [back to overview]Percentage of Participants With Hypoglycemia Events (Phase 2)
NCT01709305 (7) [back to overview]Percentage of Participants With a GI AE of Vomiting (Phase 2)
NCT01709305 (7) [back to overview]Percentage of Participants With a GI AE of Diarrhea (Phase 2)
NCT01709305 (7) [back to overview]Percentage of Participants With a Gastrointestinal (GI) AE of Nausea (Phase 2)
NCT01991197 (16) [back to overview]The Change in the Psoriasis Area and Severity Index (PASI) From Baseline to 16 Weeks in Psoriasis Patients With Type 2 Diabetes Treated With Sitagliptin Compared to Patients Treated With Gliclazide.
NCT01991197 (16) [back to overview]The Change in Levels of Systolic Blood Pressure From Baseline to 16 Weeks in the Sitagliptin and Gliclazide Arms.
NCT01991197 (16) [back to overview]The Change in PASI From Baseline to 32 Weeks in Psoriasis Patients With Type 2 Diabetes Treated With Sitagliptin Compared to Patients Treated With Gliclazide.
NCT01991197 (16) [back to overview]The Change in Levels of High Sensitivity C-reactive Protein From Baseline to 16 Weeks in the Sitagliptin and Gliclazide Arms.
NCT01991197 (16) [back to overview]The Change in Levels of Serum Glucose From Baseline to 16 Weeks in the Sitagliptin and Gliclazide Arms.
NCT01991197 (16) [back to overview]The Change in Levels of Total Cholesterol From Baseline to 16 Weeks in the Sitagliptin and Gliclazide Arms.
NCT01991197 (16) [back to overview]The Change in Weight From Baseline to 16 Weeks in the Sitagliptin and Gliclazide Arms.
NCT01991197 (16) [back to overview]The Effect of Treatment With Sitagliptin and With Gliclazide From Baseline to 16 Weeks on the Change in Dipeptidyl Peptidase-4 Levels in the Skin (in a Sub-group of Participants Willing to Undergo Skin Biopsies).
NCT01991197 (16) [back to overview]The Effect of Treatment With Sitagliptin and With Gliclazide From Baseline to 16 Weeks on the Change in Interleukin-17 Levels in the Skin (in a Sub-group of Participants Willing to Undergo Skin Biopsies).
NCT01991197 (16) [back to overview]The Effects of Treatment With Sitagliptin and Treatment With Gliclazide From Baseline to 16 Weeks on Serum Levels Interleukin-17.
NCT01991197 (16) [back to overview]The Effects of Treatment With Sitagliptin and Treatment With Gliclazide From Baseline to 16 Weeks on Serum Levels Interleukin-23.
NCT01991197 (16) [back to overview]The Effects of Treatment With Sitagliptin and Treatment With Gliclazide on the Change in Serum Leptin From Baseline to 16 Weeks.
NCT01991197 (16) [back to overview]The Effects of Treatment With Sitagliptin and Treatment With Gliclazide on the Serum Cytokine Tumour Necrosis Factor Alpha.
NCT01991197 (16) [back to overview]The Number of Patricipants in the Sitagliptin and Gliclazide Arms With Adverse Events at 32 Weeks.
NCT01991197 (16) [back to overview]The Change in Quality of Life Scores From Baseline to 16 Weeks in the Sitagliptin and Gliclazide Arms.
NCT01991197 (16) [back to overview]The Effects of Treatment With Sitagliptin and Treatment With Gliclazide on Other Efficacy Endpoints.
NCT02682563 (10) [back to overview]Urinary Albumin-Creatinine Ratio in mg/mmol
NCT02682563 (10) [back to overview]Body Weight
NCT02682563 (10) [back to overview]Effective Renal Plasma Flow (ERPF) in ml/Min
NCT02682563 (10) [back to overview]Fractional Excretion of Glucose in % of Filtered Glucose
NCT02682563 (10) [back to overview]Fractional Excretion of Potassium in % of Filtered Potassium
NCT02682563 (10) [back to overview]Fractional Excretion of Sodium in % of Filtered Sodium
NCT02682563 (10) [back to overview]Glomerular Filtration Rate (GFR) in ml/Min
NCT02682563 (10) [back to overview]Kidney Injury Molecule-1 (KIM-1) in ng/mmol
NCT02682563 (10) [back to overview]Neutrophil Gelatinase-associated Lipocalin (NGAL)
NCT02682563 (10) [back to overview]Systolic Blood Pressure
NCT03467945 (15) [back to overview]Number of Participants With Treatment-Emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)
NCT03467945 (15) [back to overview]Median Residence Time (MRT) for Metformin
NCT03467945 (15) [back to overview]Median Residence Time (MRT) for Gliclazide
NCT03467945 (15) [back to overview]Maximum Observed Plasma Concentration (Cmax) of Metformin
NCT03467945 (15) [back to overview]Maximum Observed Plasma Concentration (Cmax) of Gliclazide
NCT03467945 (15) [back to overview]Elimination Half Life (t1/2) of Metformin
NCT03467945 (15) [back to overview]Elimination Half Life (t1/2) of Gliclazide
NCT03467945 (15) [back to overview]Area Under the Plasma Concentration-Time Curve From Time Zero to Last Measurable Concentration (AUC0-t) of Metformin
NCT03467945 (15) [back to overview]Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of Metformin
NCT03467945 (15) [back to overview]Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of Gliclazide
NCT03467945 (15) [back to overview]Apparent Volume of Distribution (Vz/f) of Metformin
NCT03467945 (15) [back to overview]Apparent Volume of Distribution (Vz/f) of Gliclazide
NCT03467945 (15) [back to overview]Apparent Total Body Clearance (CL/f) of Metformin
NCT03467945 (15) [back to overview]Area Under the Plasma Concentration-Time Curve From Time Zero to Last Measurable Concentration (AUC0-t) of Gliclazide
NCT03467945 (15) [back to overview]Apparent Total Body Clearance (CL/f) of Gliclazide
NCT03467971 (8) [back to overview]Apparent Total Body Clearance (CL/f) of Metformin and Gliclazide From Plasma
NCT03467971 (8) [back to overview]Time to Reach Maximum Plasma Concentration (Tmax) of Metformin and Gliclazide
NCT03467971 (8) [back to overview]Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)
NCT03467971 (8) [back to overview]Maximum Observed Plasma Concentration (Cmax) of Metformin and Gliclazide
NCT03467971 (8) [back to overview]Elimination Half Life (t1/2) of Metformin and Gliclazide
NCT03467971 (8) [back to overview]Area Under the Plasma Concentration-Time Curve From Time Zero to Last Measurable Concentration (AUC0-t) of Metformin and Gliclazide
NCT03467971 (8) [back to overview]Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of Metformin and Gliclazide
NCT03467971 (8) [back to overview]Apparent Volume of Distribution (Vz/f) of Metformin and Gliclazide
NCT04198948 (3) [back to overview]Insulin
NCT04198948 (3) [back to overview]Glucose
NCT04198948 (3) [back to overview]Gliclazide AUC

Mean Change From Baseline in FBG at Month 36

Change from baseline was calculated as the Month 36 value minus the baseline value. FBG levels were measured by blood draw. (NCT00367055)
Timeframe: Baseline and Month 36

Interventionmillimoles per Liter (mmol/L) (Mean)
Rosiglitazone + Metformin 4 mg/2 g/Day-1.6
Gliclazide + Metformin 80 mg/2 g/Day-0.2

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Mean Change From Baseline in HbA1c at Month 36

Change from baseline was calculated as the Month 36 value minus the baseline value. HbA1c levels were measured by blood draw. (NCT00367055)
Timeframe: Baseline and Month 36

Interventionpercent change (Mean)
Rosiglitazone + Metformin 4 mg/2 g/Day-0.22
Gliclazide + Metformin 80 mg/2 g/Day0.3

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Mean Change From Baseline in Insulin Sensitivity Index at Months 18 and 36

Change from baseline was calculated as the Month 18 and 36 values minus the baseline value. Insulin sensitivity is measured as the quantity of glucose metabolized per unit of plasma insulin concentration. (NCT00367055)
Timeframe: Baseline and Months 18 and 36

,
Interventionmicromoles (umol)/kilogram/min/pmol/L (Mean)
Month 18Month 36
Gliclazide + Metformin 80 mg/2 g/Day-0.02045-0.01702
Rosiglitazone + Metformin 4 mg/2 g/Day-0.005110.00040

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Median Change From Baseline in the Insulin Secretion Capacity After an 18-month Treatment

Change from baseline was calculated as the Month 18 value minus the baseline value. Insulin secretion capacity is measured in blood (blood level of insulin) and is a response of the pancreatic beta-cells to hyperglycemia induced by a glucose IV bolus, then infusion. Hyperglycemic clamp (HC) is a reference technique to evaluate the initial and the secondary phases of insulin secretion. (NCT00367055)
Timeframe: Baseline and Month 18

,
Interventionpmol/L*min (Median)
HC, Total AUC(0-10min), n=30, 31HC, Incremental AUC(0-10min), n=27, 26HC, Total AUC(10-180min), n=26, 30HC, Incremental AUC(10-180min), n=26, 29Arginine (Arg) test, Total AUC(0-30min), n=25, 25Arg test, Incremental AUC(0-30min), n=25, 25Arg test, Incremental Conc. peak(0-30 min),n=26,29
Gliclazide + Metformin 80 mg/2 g/Day-32.360.7-7.614.610.9-8.0-111.1
Rosiglitazone + Metformin 4 mg/2 g/Day18.322.355.972.938.415.123.3

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Median Change From Baseline in the Insulin Secretory Capacity After a 36-month Treatment

Change from baseline in the insulin secretory capacity was measured by the assesment of blood insulin concentrations (conc.) using the hyperglycaemic clamp (HC) technique, per intravenous glucose perfusion by a catheter. Change from baseline for insulin conc peaks (highest conc level) was calculated as the Month 36 value minus the baseline value. Insulin secretion was assessed by calculating AUC during the first 10 minutes of HC (incremental and total AUC0-10 min) and the AUC after the first 10 minutes of the HC (10-180min). (NCT00367055)
Timeframe: Baseline and Month 36

,
Interventionpicomoles/L per minute (pmol/L*min) (Median)
Total AUC(0-10 min), n=24, 26Incremental AUC(0-10 min), n=22, 23Total concentration peak(0-10 min), n=25, 26Incremental concentration peak(0-10 min), n=24, 26Total AUC(10-180 min), n=20, 24Incremental AUC(10-180 min), n=19, 24Total concentration peak(10-180 min), n=27, 29Incremental concentation peak(10-180 min), n=25,29
Gliclazide + Metformin 80 mg/2 g/Day-75.374.63.610.8-21.213.6-9.311.5
Rosiglitazone + Metformin 4 mg/2 g/Day-3.97.0-8.6-1.840.667.07.910.8

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HbA1c Change

Units are absolute difference in %HbA1c (HbA1c being the percentage of glycated Haemoglobin, reflecting glucose exposure over the last 3 months) (NCT00780715)
Timeframe: 6 months

Interventionabsolute change in %HbA1c (Mean)
Gliclazide MR-0.42
Sitagliptin-0.58
Pioglitazone-1.04
Metformin-1.59

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Change in Fasting Serum Free Fatty Acid (FFA) From Baseline

(NCT01022762)
Timeframe: Week 0, week 16

Interventionmmol/L (Least Squares Mean)
Repaglinide-0.012
Gliclazide-0.02

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Change in Fasting Plasma Glucose

(NCT01022762)
Timeframe: Week 0, week 16

Interventionmmol/L (Least Squares Mean)
Repaglinide-1.409
Gliclazide-1.667

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Change in Glycosylated Haemoglobin (HbA1c)

(NCT01022762)
Timeframe: Week 0, week 16

Interventionpercentage (%) of total haemoglobin (Least Squares Mean)
Repaglinide-0.857
Gliclazide-0.871

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Change in Body Weight

(NCT01022762)
Timeframe: Week 0, week 16

Interventionkg (Least Squares Mean)
Repaglinide-0.750
Gliclazide-0.511

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Change in AUC0-180 of Serum Insulin Concentration of IVGTT (Intravenous Glucose Tolerance Test)

(NCT01022762)
Timeframe: Over the course of three hours at Week 0 and Week 16

Interventionmin*pmol/L (Mean)
Repaglinide5139.55
Gliclazide1426.21

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Change in 2-hour Postprandial Serum Free Fatty Acid (FFA) Over a Standard Meal

(NCT01022762)
Timeframe: Week 0, week 16

Interventionmmol/L (Least Squares Mean)
Repaglinide-0.003
Gliclazide-0.004

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Change in AUC0-180 of Plasma Glucose Concentration of IVGTT

(NCT01022762)
Timeframe: Over the course of three hours at Week 0 and Week 16

Interventionmin*mmol/L (Mean)
Repaglinide-272.30
Gliclazide-348.03

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Change in 2-hour Postprandial Plasma Glucose (PPG) Over a Standard Meal

A standard meal contains 100g carbohydrate (NCT01022762)
Timeframe: Week 0, week 16

Interventionmmol/L (Least Squares Mean)
Repaglinide-0.596
Gliclazide-0.699

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Cholesterol

"The number of participants having a change in cholesterol from normal to abnormal. Abnormal means a value of blood cholesterol is out of the normal range." (NCT01022762)
Timeframe: Week 0, week 16

Interventionparticipants (Number)
Repaglinide18
Gliclazide11

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Number of All Treatment Emergent Hypoglycaemic Episodes

A hypoglycaemic episode was defined as treatment emergent if the onset of the episode was on or after the first day of trial product and no later than the last day of the trial product. (NCT01022762)
Timeframe: Weeks 0-16

Interventionepisodes (Number)
Repaglinide165
Gliclazide147

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Percentage of Participants Achieving the Treatment Target of HbA1c Below or Equal to 6.5%

(NCT01022762)
Timeframe: Week 16

Interventionpercentage of participants (Number)
Repaglinide62
Gliclazide59

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Change From Baseline in 2-hour Post-Meal Glucose at Week 24

Change from baseline reflects the Week 24 value minus the baseline value. Two-hour post-meal glucose was measured following a standard meal. (NCT01076075)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Sitagliptin-36.8
Placebo/Pioglitazone-3.3

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Change From Baseline in Fasting Plasma Glucose at Week 24

Change from baseline reflects the Week 24 value minus the baseline value. (NCT01076075)
Timeframe: Baseline to Week 24

Interventionmg/dL (Least Squares Mean)
Sitagliptin-13.2
Placebo/Pioglitazone5.3

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

Change from baseline reflects the Week 24 value minus the baseline value. A1C represents the percentage of glycosylated hemoglobin. (NCT01076075)
Timeframe: Baseline and Week 24

InterventionPercentage of glycosylated hemoglobin (Least Squares Mean)
Sitagliptin-0.84
Placebo/Pioglitazone-0.16

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Number of Participants Discontinuing Study Drug Due to An Adverse Event

(NCT01076075)
Timeframe: Week 0 to Week 54

Interventionparticipants (Number)
Sitagliptin3
Placebo/Pioglitazone9

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Number of Participants With One or More Adverse Events (AEs) - Week 0 to Week 54

(NCT01076075)
Timeframe: Week 0 to Week 54

Interventionparticipants (Number)
Sitagliptin120
Placebo/Pioglitazone122

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Change From Baseline in FPG Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea Alone or in Combination With Metformin

This change from baseline reflects the FPG level at Week 24 minus the FPG level at Week 0. (NCT01590771)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Sitagliptin-24.4
Placebo-7.7

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Change From Baseline in A1C Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea in Combination With Metformin

A1C was measured as a percent. This change from baseline reflects the A1C percent at Week 24 minus the A1C percent at Week 0. (NCT01590771)
Timeframe: Baseline and Week 24

InterventionPercent of glycosylated hemoglobin (A1C) (Least Squares Mean)
Sitagliptin-0.86
Placebo-0.45

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Change From Baseline in A1C Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea Alone or in Combination With Metformin

A1C was measured as a percent. This change from baseline reflects the A1C percent at Week 24 minus the A1C percent at Week 0. (NCT01590771)
Timeframe: Baseline and Week 24

InterventionPercent of glycosylated hemoglobin (A1C) (Least Squares Mean)
Sitagliptin-0.88
Placebo-0.27

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Change From Baseline in A1C Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea Alone

A1C was measured as a percent. This change from baseline reflects the A1C percent at Week 24 minus the A1C percent at Week 0. (NCT01590771)
Timeframe: Baseline and Week 24

InterventionPercent of glycosylated hemoglobin (A1C) (Least Squares Mean)
Sitagliptin-0.85
Placebo-0.05

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Change From Baseline in 2-hr PMG Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea Alone or in Combination With Metformin

This change from baseline reflects the 2-hr PMG level at Week 24 minus the 2-hr PMG level at Week 0. (NCT01590771)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Sitagliptin-40.7
Placebo-7.7

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Change From Baseline in 2-hr PMG Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea Alone

This change from baseline reflects the 2-hr PMG level at Week 24 minus the 2-hr PMG level at Week 0. (NCT01590771)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Sitagliptin-49.5
Placebo-11.9

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Number of Participants Who Experienced an Adverse Event

An adverse event is any untoward medical occurrence in a participant administered study drug which does not necessarily have a causal relationship with the treatment. Adverse events may include the onset of new illness and the exacerbation of pre-existing conditions. (NCT01590771)
Timeframe: Up to 26 weeks

InterventionParticipants (Number)
Sitagliptin106
Placebo98

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Number of Participants Who Discontinued Study Drug Due to an Adverse Event

An adverse event is any untoward medical occurrence in a participant administered study drug which does not necessarily have a causal relationship with the treatment. Adverse events may include the onset of new illness and the exacerbation of pre-existing conditions. (NCT01590771)
Timeframe: Up to 24 weeks

InterventionParticipants (Number)
Sitagliptin3
Placebo7

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Change From Baseline in FPG Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea in Combination With Metformin

This change from baseline reflects the FPG level at Week 24 minus the FPG level at Week 0. (NCT01590771)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Sitagliptin-22.2
Placebo-5.7

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Change From Baseline in FPG Levels at Week 24 in Participants Receiving Sitagliptin and Sulfonylurea Alone

This change from baseline reflects the FPG level at Week 24 minus the FPG level at Week 0. (NCT01590771)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Sitagliptin-26.3
Placebo-9.3

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Change From Baseline in 2-hr PMG Levels at Week 24 in Participants Receiving Sitagliptin and a Sulfonylurea in Combination With Metformin

This change from baseline reflects the 2-hr PMG level at Week 24 minus the 2-hr PMG level at Week 0. (NCT01590771)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Sitagliptin-33.4
Placebo-6.2

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Change From Phase 2 Baseline to Week 44 in Participant Body Weight (Phase 2)

Change from baseline in body weight in Phase 2 was reported. Change from baseline reflects the Week 44 body weight minus baseline body weight. Baseline is defined as Visit 6/Week 20. If this measurement was unavailable, the Week 16 value was used. (NCT01709305)
Timeframe: Phase 2 Baseline (Week 20), Week 44

Interventionkg (Mean)
Phase 2: Metformin + Sitagliptin + Glimepiride0.4
Phase 2: Metformin + Sitagliptin + Repaglinide0.2
Phase 2: Metformin + Sitagliptin + Acarbose-0.9
Phase 2: Metformin + Sitagliptin + Gliclazide0.2

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Change From Phase 2 Baseline to Week 44 in Hemoglobin A1c (HbA1c) Levels (Phase 2)

HbA1c is blood marker used to report average blood glucose levels over prolonged periods of time and is reported as a percentage (%). Change from baseline reflects the Week 44 A1C minus baseline A1C. Baseline is defined as Visit 6/Week 20. If this measurement was unavailable, the Week 16 value was used. Change from baseline was based on the constrained longitudinal data analysis (cLDA) model including all available measurements from baseline through the last visit. The terms in the cLDA model include treatment, time in weeks (categorical), regions, and treatment-by-time interaction. (NCT01709305)
Timeframe: Phase 2 Baseline (Week 20) and Week 44

InterventionPercent (Least Squares Mean)
Phase 2: Metformin + Sitagliptin + Glimepiride-0.65
Phase 2: Metformin + Sitagliptin + Repaglinide-0.62
Phase 2: Metformin + Sitagliptin + Acarbose-0.46
Phase 2: Metformin + Sitagliptin + Gliclazide-0.69

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Percentage of Participants With a GI AE of Abdominal Pain (Phase 2)

"The percentage of participants with a GI AE of abdominal pain was reported." (NCT01709305)
Timeframe: From Week 20 through Week 44

InterventionPercentage of Participants (Number)
Phase 2: Metformin + Sitagliptin + Glimepiride0
Phase 2: Metformin + Sitagliptin + Repaglinide0
Phase 2: Metformin + Sitagliptin + Acarbose0.4
Phase 2: Metformin + Sitagliptin + Gliclazide0.2

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Percentage of Participants With Hypoglycemia Events (Phase 2)

Hypoglycemia events represent epidsodes symptomatic of hypoglycemia (e.g., weakness, dizziness, shakiness, increased sweating, palpitations, or confusion) and/or finger stick glucose values of ≤70 mg/dL (3.9 mmol/L). The percentage of participants with hypoglycemia events was reported. (NCT01709305)
Timeframe: From Week 20 through Week 44

InterventionPercentage of Participants (Number)
Phase 2: Metformin + Sitagliptin + Glimepiride8.9
Phase 2: Metformin + Sitagliptin + Repaglinide6.1
Phase 2: Metformin + Sitagliptin + Acarbose0.5
Phase 2: Metformin + Sitagliptin + Gliclazide3.6

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Percentage of Participants With a GI AE of Vomiting (Phase 2)

"The percentage of participants with a GI AE of vomiting was reported." (NCT01709305)
Timeframe: From Week 20 through Week 44

InterventionPercentage of Participants (Number)
Phase 2: Metformin + Sitagliptin + Glimepiride0.2
Phase 2: Metformin + Sitagliptin + Repaglinide0
Phase 2: Metformin + Sitagliptin + Acarbose0.2
Phase 2: Metformin + Sitagliptin + Gliclazide0.2

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Percentage of Participants With a GI AE of Diarrhea (Phase 2)

"The percentage of participants with a GI AE of diarrhea was reported." (NCT01709305)
Timeframe: From Week 20 through Week 44

InterventionPercentage of Participants (Number)
Phase 2: Metformin + Sitagliptin + Glimepiride0.5
Phase 2: Metformin + Sitagliptin + Repaglinide0.4
Phase 2: Metformin + Sitagliptin + Acarbose0.4
Phase 2: Metformin + Sitagliptin + Gliclazide0.9

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Percentage of Participants With a Gastrointestinal (GI) AE of Nausea (Phase 2)

"The percentage of participants with a GI AE of nausea was reported." (NCT01709305)
Timeframe: From Week 20 through Week 44

InterventionPercentage of Participants (Number)
Phase 2: Metformin + Sitagliptin + Glimepiride0
Phase 2: Metformin + Sitagliptin + Repaglinide0
Phase 2: Metformin + Sitagliptin + Acarbose0.4
Phase 2: Metformin + Sitagliptin + Gliclazide0.2

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The Change in the Psoriasis Area and Severity Index (PASI) From Baseline to 16 Weeks in Psoriasis Patients With Type 2 Diabetes Treated With Sitagliptin Compared to Patients Treated With Gliclazide.

Psoriasis area and severity index (0-72), higher scores worse outcome (NCT01991197)
Timeframe: 16 weeks

Interventionscore on a scale (Median)
Sitagliptin9.5
Gliclazide9.4

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The Change in Levels of Systolic Blood Pressure From Baseline to 16 Weeks in the Sitagliptin and Gliclazide Arms.

The change in systolic blood pressure from baseline to 16 weeks measured in kg (NCT01991197)
Timeframe: 16 weeks

InterventionmmHg (Median)
Sitagliptin4
Gliclazide-9

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The Change in PASI From Baseline to 32 Weeks in Psoriasis Patients With Type 2 Diabetes Treated With Sitagliptin Compared to Patients Treated With Gliclazide.

Psoriasis area and severity index 0-72, higher score worse outcome (NCT01991197)
Timeframe: baseline and 32 weeks

Interventionscore on a scale (Median)
Sitagliptin3
Gliclazide1.8

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The Change in Levels of High Sensitivity C-reactive Protein From Baseline to 16 Weeks in the Sitagliptin and Gliclazide Arms.

High sensitivity C-reactive protein (range 0 - no maximum) (NCT01991197)
Timeframe: 16 weeks

Interventionµg/ml (Median)
Sitagliptin0
Gliclazide8.4

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The Change in Levels of Serum Glucose From Baseline to 16 Weeks in the Sitagliptin and Gliclazide Arms.

The change in glucose from baseline to 16 weeks (NCT01991197)
Timeframe: 16 weeks

Interventionmmol/L (Median)
Sitagliptin-0.2
Gliclazide-0.1

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The Change in Levels of Total Cholesterol From Baseline to 16 Weeks in the Sitagliptin and Gliclazide Arms.

The change in total cholesterol from baseline to 16 weeks (NCT01991197)
Timeframe: 16 weeks

Interventionmmol/L (Median)
Sitagliptin0.1
Gliclazide-0.1

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The Change in Weight From Baseline to 16 Weeks in the Sitagliptin and Gliclazide Arms.

The change in weight from baseline to 16 weeks measured in kg (NCT01991197)
Timeframe: 16 weeks

Interventionkg (Median)
Sitagliptin-0.5
Gliclazide-0.6

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The Effect of Treatment With Sitagliptin and With Gliclazide From Baseline to 16 Weeks on the Change in Dipeptidyl Peptidase-4 Levels in the Skin (in a Sub-group of Participants Willing to Undergo Skin Biopsies).

Dipeptidyl peptidase-4 levels levels in skin (0-no maximum) (NCT01991197)
Timeframe: 16 weeks

InterventiondCt (Median)
Gliclazide-1.12
Sitagliptin0

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The Effect of Treatment With Sitagliptin and With Gliclazide From Baseline to 16 Weeks on the Change in Interleukin-17 Levels in the Skin (in a Sub-group of Participants Willing to Undergo Skin Biopsies).

Interleukin 17 levels in skin (0-no maximum) (NCT01991197)
Timeframe: 16 weeks

InterventiondCt (Median)
Sitagliptin3.41
Gliclazide2.09

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The Effects of Treatment With Sitagliptin and Treatment With Gliclazide From Baseline to 16 Weeks on Serum Levels Interleukin-17.

"Secondary outcomes:~The change in serum concentrations of the cytokine interleukin-17 (IL-17) Range: 0-no maximum" (NCT01991197)
Timeframe: 16 weeks

Interventionpg/ml (Median)
Sitagliptin0
Gliclazide0

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The Effects of Treatment With Sitagliptin and Treatment With Gliclazide From Baseline to 16 Weeks on Serum Levels Interleukin-23.

"Secondary outcomes:~The change in serum concentrations of the cytokine interleukin-23 (IL-23) Range: 0-no maximum" (NCT01991197)
Timeframe: 16 weeks

Interventionpg/ml (Median)
Sitagliptin0
Gliclazide0

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The Effects of Treatment With Sitagliptin and Treatment With Gliclazide on the Change in Serum Leptin From Baseline to 16 Weeks.

"Secondary outcomes:~The change in serum concentrations of the adipokine leptin Range: 0-no maximum" (NCT01991197)
Timeframe: 16 weeks

Interventionpg/ml (Median)
Sitagliptin-0.07
Gliclazide0.43

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The Effects of Treatment With Sitagliptin and Treatment With Gliclazide on the Serum Cytokine Tumour Necrosis Factor Alpha.

"Secondary outcomes:~The change in serum concentrations of the cytokines tumour necrosis factor alpha (TNFα) Range: 0-no maximum" (NCT01991197)
Timeframe: 16 weeks

Interventionpg/ml (Median)
Sitagliptin0
Gliclazide0

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The Number of Patricipants in the Sitagliptin and Gliclazide Arms With Adverse Events at 32 Weeks.

"Dosage: Sitagliptin: 100mg daily, or 50mg daily for participants with moderate kidney disease Gliclazide: 80-320 mg daily.~Secondary outcomes: the number participants with adverse events." (NCT01991197)
Timeframe: 32 weeks

InterventionParticipants (Count of Participants)
Sitagliptin6
Gliclazide10

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The Change in Quality of Life Scores From Baseline to 16 Weeks in the Sitagliptin and Gliclazide Arms.

"Dermatology life quality index (a skin related quality of life measure) (0-10), higher score worse outcome EQ-5D Euroqol 5 item quality of life index comprising 5 dimensions mobility, self-care, usual activities, pain, anxiety. An index can be derived from these 5 dimensions by conversion with a table of scores. The maximum score of 1 indicates the best health state and minimum score indicating the worst health outcome -0.594.~HADS Hospital anxiety and depression scale 0-16 for anxiety and 0-16 for depression, higher score worse outcome HAQ-8 Stanford 8 item disability scale. Scoring is from 0 (without any difficulty) to 3 (unable to do). The 8 scores from the 8 sections are summed and divided by 8. The result is the disability index (range 0-3 with 25 possible values). A" (NCT01991197)
Timeframe: 16 weeks

,
Interventionscore on a scale (Median)
DLQIHAQ-8HADS AnxietyHADS DepressionEQ-5D
Gliclazide-1.00.000-0.2
Sitagliptin0.00.0-100

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The Effects of Treatment With Sitagliptin and Treatment With Gliclazide on Other Efficacy Endpoints.

"Secondary outcomes:~d. number or participants who acheived a greater than 50% reduction in PASI from baseline (PASI-50); e. number of participants who achieved PASI-75 and PASI-90." (NCT01991197)
Timeframe: 16 weeks

,
InterventionParticipants (Count of Participants)
PASI 50PASI 75PASI 90
Gliclazide100
Sitagliptin100

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Urinary Albumin-Creatinine Ratio in mg/mmol

Calculated from measured urinary albumin and creatinin concentrations, in mg/mmol (NCT02682563)
Timeframe: 12 weeks

Interventionmg/mmol (Median)
Dapagliflozin 10mg Once Daily0.88
Gliclazide Modified Release 30mg Once Daily0.54

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Body Weight

Measured in kilograms (NCT02682563)
Timeframe: 12 weeks

Interventionkilograms (Mean)
Dapagliflozin 10mg Once Daily93.7
Gliclazide Modified Release 30mg Once Daily99.6

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Effective Renal Plasma Flow (ERPF) in ml/Min

Calculated from urinary and plasma para-aminohippurate concentrations, ERPF in ml/min (NCT02682563)
Timeframe: 12 weeks

Interventionml/min (Mean)
Dapagliflozin 10mg Once Daily639
Gliclazide Modified Release 30mg Once Daily678

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Fractional Excretion of Glucose in % of Filtered Glucose

Calculated fractional excretions with measured GFR (see above) and urinary and plasma concentrations of glucose. Fractional excretion in % of filtered glucose (NCT02682563)
Timeframe: 12 weeks

Intervention% of filtered glucose (Mean)
Dapagliflozin 10mg Once Daily31.1
Gliclazide Modified Release 30mg Once Daily0.6

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Fractional Excretion of Potassium in % of Filtered Potassium

Calculated fractional excretions with measured GFR (see above) and urinary and plasma concentrations of potassium. Fractional excretion in % of filtered potassium (NCT02682563)
Timeframe: 12 weeks

Intervention% of filtered potassium (Mean)
Dapagliflozin 10mg Once Daily13.6
Gliclazide Modified Release 30mg Once Daily11.8

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Fractional Excretion of Sodium in % of Filtered Sodium

Calculated fractional excretions with measured GFR (see above) and urinary and plasma concentrations of sodium. Fractional excretion in % of filtered sodium (NCT02682563)
Timeframe: 12 weeks

Intervention% of filtered sodium (Mean)
Dapagliflozin 10mg Once Daily0.74
Gliclazide Modified Release 30mg Once Daily0.66

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Glomerular Filtration Rate (GFR) in ml/Min

Calculated from urinary and plasma inulin concentrations, GFR in ml/min (NCT02682563)
Timeframe: 12 weeks

Interventionml/min (Mean)
Dapagliflozin 10mg Once Daily104
Gliclazide Modified Release 30mg Once Daily109

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Kidney Injury Molecule-1 (KIM-1) in ng/mmol

KIM-1 (ng/mmol) measured in urine as a marker of renal damage (NCT02682563)
Timeframe: 12 weeks

Interventionng/mmol (Median)
Dapagliflozin 10mg Once Daily0.25
Gliclazide Modified Release 30mg Once Daily0.265

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Neutrophil Gelatinase-associated Lipocalin (NGAL)

NGAL (ng/mmoll) measured in urine as a marker of renal damage (NCT02682563)
Timeframe: 12 weeks

Interventionng/mmol (Median)
Dapagliflozin 10mg Once Daily3.76
Gliclazide Modified Release 30mg Once Daily3.79

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Systolic Blood Pressure

Blood pressure will be measured using an automated oscillometric blood pressure device (Dinamap®) in mmHg (NCT02682563)
Timeframe: 12 weeks

InterventionmmHg (Mean)
Dapagliflozin 10mg Once Daily129.2
Gliclazide Modified Release 30mg Once Daily131.1

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Number of Participants With Treatment-Emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)

An Adverse event (AE) was defined as any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with the use of study drug, whether or not considered related to the study drug or worsening of pre-existing medical condition, whether or not related to study drug. A serious adverse event (SAE) was an AE that resulted in any of the following outcomes: death; life threatening; persistent/significant disability/incapacity; initial or prolonged inpatient hospitalization; congenital anomaly/birth defect or was otherwise considered medically important. Treatment-emergent are events between first dose of study drug that were absent before treatment or that worsened relative to pre-treatment state. TEAEs included both Serious TEAEs and non-serious TEAEs. (NCT03467945)
Timeframe: Baseline up to Day 72

,,,
InterventionParticipants (Count of Participants)
TEAEsSAEs
Gliclazide80
Metformin70
Metformin and Gliclazide Separately60
Metformin-Gliclazide Combination90

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Median Residence Time (MRT) for Metformin

MRT is the average time that the molecules introduced into the body stays in the body. (NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

InterventionHours (Mean)
Metformin-Gliclazide Combination8.3952
Metformin and Gliclazide Separately7.5836
Metformin7.7636

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Median Residence Time (MRT) for Gliclazide

MRT is the average time that the molecules introduced into the body stays in the body. (NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

InterventionHours (Mean)
Metformin-Gliclazide Combination23.0593
Metformin and Gliclazide Separately24.4927
Gliclazide25.8590

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Maximum Observed Plasma Concentration (Cmax) of Metformin

(NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

Interventionnanogram per milliliter (ng/ml) (Mean)
Metformin-Gliclazide Combination806.3895
Metformin and Gliclazide Separately1011.3941
Metformin977.2693

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Maximum Observed Plasma Concentration (Cmax) of Gliclazide

(NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

Interventionng/ml (Mean)
Metformin-Gliclazide Combination972.168
Metformin and Gliclazide Separately892.6201
Gliclazide836.7239

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Elimination Half Life (t1/2) of Metformin

Elimination Half Life (t1/2) was defined as the time required for the concentration or amount of drug in the body to be reduced by one-half. (NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

InterventionHours (Mean)
Metformin-Gliclazide Combination6.7151
Metformin and Gliclazide Separately5.9796
Metformin6.3048

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Elimination Half Life (t1/2) of Gliclazide

Elimination Half Life (t1/2) was defined as the time required for the concentration or amount of drug in the body to be reduced by one-half. (NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

InterventionHours (Mean)
Metformin-Gliclazide Combination15.3086
Metformin and Gliclazide Separately15.4587
Gliclazide15.6222

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Area Under the Plasma Concentration-Time Curve From Time Zero to Last Measurable Concentration (AUC0-t) of Metformin

(NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

Interventionnanogram*hour per milliliter (ng*h/ml) (Mean)
Metformin-Gliclazide Combination5033.8718
Metformin and Gliclazide Separately6142.2821
Metformin6090.7932

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Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of Metformin

AUC (0-inf) is defined as the area under the plasma concentration versus time curve (AUC) from time zero (pre-dose) to extrapolated infinite time (0-inf). (NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

Interventionng*h/ml (Mean)
Metformin-Gliclazide Combination5313.3897
Metformin and Gliclazide Separately6388.9849
Metformin6341.5658

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Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of Gliclazide

AUC (0-inf) is defined as the area under the plasma concentration versus time curve (AUC) from time zero (pre-dose) to extrapolated infinite time (0-inf). (NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

Interventionng*h/ml (Mean)
Metformin-Gliclazide Combination21495.2343
Metformin and Gliclazide Separately21120.6761
Gliclazide22136.9988

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Apparent Volume of Distribution (Vz/f) of Metformin

Vz/f was defined as apparent volume of distribution during terminal phase after non-intravenous administration. (NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

InterventionMilliliter (Mean)
Metformin-Gliclazide Combination1893618.4672
Metformin and Gliclazide Separately1414424.1926
Metformin1489164.0229

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Apparent Volume of Distribution (Vz/f) of Gliclazide

Vz/f was defined as apparent volume of distribution during terminal phase after non-intravenous administration. (NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

InterventionMilliliter (Mean)
Metformin-Gliclazide Combination31636.8920
Metformin and Gliclazide Separately32601.0115
Gliclazide31413.9679

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Apparent Total Body Clearance (CL/f) of Metformin

CL/f was defined as apparent total clearance of the drug from plasma after oral administration. (NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

InterventionMilliliter per Hour (mL/ h) (Mean)
Metformin-Gliclazide Combination207132.8293
Metformin and Gliclazide Separately170273.4024
Metformin167260.5841

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Area Under the Plasma Concentration-Time Curve From Time Zero to Last Measurable Concentration (AUC0-t) of Gliclazide

(NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

Interventionng.h/ml (Mean)
Metformin-Gliclazide Combination20707.7394
Metformin and Gliclazide Separately20280.3103
Gliclazide21205.2514

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Apparent Total Body Clearance (CL/f) of Gliclazide

CL/f was defined as apparent total clearance of the drug from plasma after oral administration. (NCT03467945)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 28, 32, 48, 72, 96, 120, 144 and 168 hours post-dose

InterventionmL/h (Mean)
Metformin-Gliclazide Combination1572.5246
Metformin and Gliclazide Separately1606.8952
Gliclazide1498.9932

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Apparent Total Body Clearance (CL/f) of Metformin and Gliclazide From Plasma

CL/f is defined as apparent total clearance of the drug from plasma after oral administration. (NCT03467971)
Timeframe: Pre-dose, 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 6.0, 7.0, 8.0, 10.0, 12.0, 16.0, 24.0, 28.0, 32.0, 48.0, 72.0, 96.0, 120.0, 144.0 and 168.0 hour post-dose

,
InterventionLiters (Mean)
MetforminGlilclazide
Metformin-Gliclazide (Fasted)226.791.63
Metformin-Gliclazide (Fed)125.931.55

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Time to Reach Maximum Plasma Concentration (Tmax) of Metformin and Gliclazide

Tmax is defined as the time to reach maximum plasma concentration. (NCT03467971)
Timeframe: Pre-dose, 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 6.0, 7.0, 8.0, 10.0, 12.0, 16.0, 24.0, 28.0, 32.0, 48.0, 72.0, 96.0, 120.0, 144.0 and 168.0 hour post-dose

,
InterventionHours (Mean)
MetforminGliclazide
Metformin-Gliclazide (Fasted)3.66986.5254
Metformin-Gliclazide (Fed)7.23898.5238

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Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)

Adverse event(AE) was defined as any untoward medical occurrence in participants which does not necessarily have causal relationship with treatment. AE was any unfavorable and unintended sign(including abnormal laboratory finding), symptom/disease temporally associated with use of medicinal product, whether/not considered related to medicinal product. A serious adverse event(SAE) was AE that resulted in any of the following outcomes: death; life threatening; persistent/significant disability/incapacity; initial/prolonged inpatient hospitalization; congenital anomaly/birth defect or was otherwise considered medically important. Term TEAE is defined as AEs starting/worsening after first intake of the study drug. TEAEs included both Serious TEAEs and non-serious TEAEs. (NCT03467971)
Timeframe: Baseline up to Day 39

,
InterventionParticipants (Count of Participants)
Adverse EventsSerious Adverse Events (SAEs)
Metformin-Gliclazide (Fasted)80
Metformin-Gliclazide (Fed)70

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Maximum Observed Plasma Concentration (Cmax) of Metformin and Gliclazide

Cmax is defined as the maximum observed plasma concentration. (NCT03467971)
Timeframe: Pre-dose, 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 6.0, 7.0, 8.0, 10.0, 12.0, 16.0, 24.0, 28.0, 32.0, 48.0, 72.0, 96.0, 120.0, 144.0 and 168.0 hour post-dose

,
Interventionng/mL (Mean)
MetforminGliclazide
Metformin-Gliclazide (Fasted)717.5017968.0305
Metformin-Gliclazide (Fed)870.72881013.9753

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Elimination Half Life (t1/2) of Metformin and Gliclazide

Elimination Half Life (t1/2) is defined as the time required for the concentration or amount of drug in the body to be reduced by one-half. (NCT03467971)
Timeframe: Pre-dose, 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 6.0, 7.0, 8.0, 10.0, 12.0, 16.0, 24.0, 28.0, 32.0, 48.0, 72.0, 96.0, 120.0, 144.0 and 168.0 hour post-dose

,
InterventionHours (Mean)
MetforminGliclazide
Metformin-Gliclazide (Fasted)6.254716.6222
Metformin-Gliclazide (Fed)7.489217.1044

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Area Under the Plasma Concentration-Time Curve From Time Zero to Last Measurable Concentration (AUC0-t) of Metformin and Gliclazide

AUC (0-t) is defined as the area under the plasma concentration versus time curve from time zero (pre-dose) to time of last quantifiable concentration (0-t) (NCT03467971)
Timeframe: Pre-dose, 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 6.0, 7.0, 8.0, 10.0, 12.0, 16.0, 24.0, 28.0, 32.0, 48.0, 72.0, 96.0, 120.0, 144.0 and 168.0 hour post-dose

,
Interventionng*h/mL (Mean)
MetforminGliclazide
Metformin-Gliclazide (Fasted)4722.454620348.8381
Metformin-Gliclazide (Fed)8298.562820997.1704

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Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of Metformin and Gliclazide

AUC (0-inf) is defined as the area under the plasma concentration versus time curve (AUC) from time zero (pre-dose) to extrapolated infinite time (0-inf). (NCT03467971)
Timeframe: Pre-dose, 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 6.0, 7.0, 8.0, 10.0, 12.0, 16.0, 24.0, 28.0, 32.0, 48.0, 72.0, 96.0, 120.0, 144.0 and 168.0 hour post-dose

,
InterventionNanogram*hour per milliliter (ng*h/mL) (Mean)
MetforminGliclazide
Metformin-Gliclazide (Fasted)4974.250721192.1682
Metformin-Gliclazide (Fed)8556.775221815.4021

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Apparent Volume of Distribution (Vz/f) of Metformin and Gliclazide

Vz/f is defined as apparent volume of distribution during terminal phase after non-intravenous administration (NCT03467971)
Timeframe: Pre-dose, 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 6.0, 7.0, 8.0, 10.0, 12.0, 16.0, 24.0, 28.0, 32.0, 48.0, 72.0, 96.0, 120.0, 144.0 and 168.0 hour post-dose

,
InterventionMilliliter (mL) (Mean)
MetforminGliclazide
Metformin-Gliclazide (Fasted)2003389.947435189.3864
Metformin-Gliclazide (Fed)1200933.264733813.7843

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Insulin

Change in insulin concentration - incremental area under the insulin concentration-time curve from 0 to 12 h (NCT04198948)
Timeframe: 12 hours

InterventionmIU x h/L (Mean)
Gliclazide + Omeprazole231.6
Gliclazide + Placebo265.9

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Glucose

Change in glucose concentration - incremental area under the glucose concentration-time curve from 0 to 12 h (NCT04198948)
Timeframe: 12 hours

Interventionmmol x h/L (Mean)
Gliclazide + Omeprazole4.6
Gliclazide + Placebo4.0

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Gliclazide AUC

Area under the concentration-time curve (AUC) up to the last concentration measured (NCT04198948)
Timeframe: 24 hours

Interventionμgh/mL (Geometric Mean)
Gliclazide + Omeprazole3.73
Gliclazide + Placebo3.29

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