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alloxan

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Description

Alloxan: Acidic compound formed by oxidation of URIC ACID. It is isolated as an efflorescent crystalline hydrate. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

alloxan : A member of the class of pyrimidones, the structure of which is that of perhydropyrimidine substituted at C-2, -4, -5 and -6 by oxo groups. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID5781
CHEMBL ID1096009
CHEBI ID76451
SCHEMBL ID64547
SCHEMBL ID9652639
MeSH IDM0000748

Synonyms (88)

Synonym
2,4,5,6-tetraoxohexahydropyrimidine
2,4,5,6-pyrimidintetron [czech]
nsc 7169
ai3-15282
einecs 200-062-0
AKOS005448465
urea, mesoxalyl-
wln: t6mvmvvvj
nsc-7169
2,5,6-pyrimidintetron
2,5,6(1h,3h)-pyrimidinetetrone
50-71-5
alloxan 7169
alloxane
mesoxalylurea
alloxan
nsc7169
2,5,6-tetraoxohexahydropyrimidine
mesoxalylcarbamide
barbituric acid, 5-oxo-
DIVK1C_006961
SPECTRUM_001080
BSPBIO_002150
2,4,5,6(1h,3h) pyrimidinetetrone
hexahydropyrimidine-2,4,5,6-tetrone
SPECTRUM5_001490
pyrimidine-2,4,5,6(1h,3h)-tetrone
2,4,5,6(1h,3h)-pyrimidinetetrone
inchi=1/c4h2n2o4/c7-1-2(8)5-4(10)6-3(1)9/h(h2,5,6,8,9,10
NCGC00095912-01
KBIO2_004128
KBIO1_001905
KBIO2_006696
KBIOSS_001560
KBIOGR_001132
KBIO3_001650
KBIO2_001560
SPECTRUM3_000615
SPECTRUM2_000531
SPECPLUS_000865
SPBIO_000541
SPECTRUM4_000606
SPECTRUM1500802
NCGC00095912-02
STK378289
5,6-dioxouracil
A0216
LXN ,
CHEMBL1096009
chebi:76451 ,
1,3-diazinane-2,4,5,6-tetrone
BBL002915
A828261
CCG-39561
ccris 9509
2,4,5,6-pyrimidintetron
6sw5yha5ng ,
hsdb 7493
unii-6sw5yha5ng
FT-0621991
AE-562/40299936
AB00052179-03
5-oxobarbituric acid
alloxanum [hpus]
alloxanum
alloxan [mi]
alloxan [hsdb]
SCHEMBL64547
pyrimidinetetrone
2XGM
pyrimidine-2,4,5,6(1h,3h)-tetraone
DTXSID5044946 ,
SCHEMBL9652639
2,4,5,6-pyrimidintetrone
2,4,5,6-pyrimidinetetrone
F8881-2259
5-oxo-barbiturate
mesoxalyl-urea
5-oxo-barbituric acid
alloxan tetrahydrat
5,5-dihydroxy-hexahydro-pyrimidine-2,4,6-trione
6-hydroxy-2,4,5-triketopyrimidine
Q417701
VS-01259
SB55621
EN300-21254
dtxcid3024946
Z104494840

Research Excerpts

Overview

Alloxan is an environmental food contaminant that causes DNA damage in living cells and induces hyperglycemia. It is a classical diabetogen which is used to achieve beta-cell destruction and type 1 diabetes due to its selective cytotoxic effect on pancreatic beta-cells. Alloxan apparently acts through formation of superoxide radicals formed by redox cycling.

ExcerptReferenceRelevance
"Alloxan is an environmental food contaminant that causes DNA damage in living cells and induces hyperglycemia. "( Nanopharmaceutical approach using pelargonidin towards enhancement of efficacy for prevention of alloxan-induced DNA damage in L6 cells via activation of PARP and p53.
Abraham, SK; Khuda-Bukhsh, AR; Samadder, A, 2016
)
2.09
"Alloxan is a compound widely used in models of diabetes mellitus due to its ability for damage insulin-producing β-cells. "( Inhibition of δ-aminolevulinate dehydratase is not closely related to the development of hyperglycemia in alloxan-induced diabetic mice.
Barbosa, NB; Brito, VB; da Luz, SC; da Rocha, JB; de Carvalho, NR; Folmer, V; Puntel, GO, 2011
)
2.03
"Alloxan is a classical diabetogen which is used to achieve beta-cell destruction and type 1 diabetes due to its selective cytotoxic effect on pancreatic beta-cells. "( Hepatic glucokinase activity is the primary defect in alloxan-induced diabetes of mice.
Li, H; Liang, W; Mao, Y; Tan, H; Yang, Y; Zhang, X, 2009
)
2.04
"Alloxan is a well-known and universally used agent for evoking experimental diabetes through its toxic effect on the B cells of the Langerhans islets. "( Blood levels of alloxan in children with insulin-dependent diabetes mellitus.
Chmara, E; Kiełczewska-Mrozikiewicz, D; Korzeniowska, K; Lowicki, Z; Mrozikiewicz, A; Mrozikiewicz, PM, 1994
)
2.08
"Alloxan is a diabetogenic agent which apparently acts through formation of superoxide radicals formed by redox cycling. "( Enhanced alloxan-induced beta-cell damage and delayed recovery from hyperglycemia in mice lacking extracellular-superoxide dismutase.
Jonsson, LM; Marklund, SL; Sentman, ML, 1999
)
2.16
"Alloxan is an inhibitor of the enzyme xanthine: NAD+ oxido reductase (E.C.1.2.1.37). "( Kinetic studies of the blood serum xanthine dehydrogenase inhibition by alloxan (2,4,5,6-tetraoxypyrimidine 5,6-dioxyuracil).
Affonso, OR; Mitidieri, E, 1979
)
1.93
"Alloxan is a pancreatic B-cell cytotoxic agent, which has been widely used as a tool for the elucidation of the mechanisms of insulin secretion, because its inhibitory action on insulin secretion has been presumed to be intimately related to the mechanism of glucose-induced insulin secretion."( Glucokinase in pancreatic B-cells and its inhibition by alloxan.
Lenzen, S; Panten, U; Tiedge, M, 1987
)
1.24

Effects

Alloxan has been widely used to provoke diabetes mellitus. Alloxan is a diabetogenic agent.

ExcerptReferenceRelevance
"Alloxan has been used as a diabetogenic agent to induce diabetes. "( Diabetogenic agent alloxan is a proteasome inhibitor.
Deng, S; Lai, C; Luo, X; Peng, M; Wei, L; Xiao, T; Xu, L; Zhang, F; Zhou, W, 2017
)
2.23
"Alloxan has been widely used to provoke diabetes mellitus. "( Alloxan decreases intracellular potassium content of the isolated frog skin epithelium.
Del Razo, LM; Neri, L; Soto, C, 2001
)
3.2

Actions

Alloxan was found to inhibit a Ca2+- and calmodulin-dependent protein kinase. The alloxan-induced increase in plasma FA was supported by an enhanced rate of lipolysis in the kidney. Alloxan did not inhibit glucose-induced insulin secretion by grossly altering glycolysis.

ExcerptReferenceRelevance
"Alloxan can generate diabetes in experimental animals and its action can be associated with the production of free radicals. "( Free radical scavengers can modulate the DNA-damaging action of alloxan.
Blasiak, J; Czechowska, A; Drzewoski, J; Sikora, A, 2003
)
2
"Alloxan was found to inhibit a Ca2+- and calmodulin-dependent protein kinase recently identified in pancreatic islets. "( Alloxan inhibition of a Ca2+- and calmodulin-dependent protein kinase activity in pancreatic islets.
Brooks, CL; Colca, JR; Kotagal, N; Lacy, PE; Landt, M; McDaniel, ML, 1983
)
3.15
"The alloxan-induced increase in plasma FA was supported by an enhanced rate of lipolysis in the kidney, a relatively lower rate of fatty acid synthesis in kidney, liver, and muscle, and a relatively lower renal rate of TG synthesis."( Effects of insulin on lipid metabolism of larvae and metamorphosing landlocked sea lamprey, Petromyzon marinus.
Al-Mahrouki, A; Holmes, JA; Kao, Yh; Sheridan, MA; Youson, JH, 1999
)
0.78
"Alloxan did not inhibit glucose-induced insulin secretion by grossly altering glycolysis."( Effects of alloxan on glucose-stimulated insulin secretion, glucose metabolism, and cyclic adenosine 3', 5'-monophosphate levels in rat isolated islets of langerhans.
Karl, RC; Matschinsky, FM; Zawalich, WS, 1979
)
1.37
"Alloxan did not inhibit glutathione reductase activity and no alloxan-glutathione complex was produced."( [Antimalarial action of alloxan and 5,6-diamino-2,4-dihydroxy-pyrimidine in Plasmodium berghei].
Chang, HL; Huang, ZY; Wang, JJ; Wu, KY, 1989
)
1.31
"Alloxan does not inhibit the uptake of Ca2+ but stimulates the release of Ca2+ from liver mitochondria, which is accompanied by oxidation and hydrolysis of pyridine nucleotides."( Mechanism of alloxan-induced calcium release from rat liver mitochondria.
Frei, B; Richter, C; Winterhalter, KH, 1985
)
1.36
"Alloxan is known to inhibit pancreatic B cell and liver glucokinase and glucose protects the enzyme against inhibition. "( Inhibition of glucokinase by alloxan through interaction with SH groups in the sugar-binding site of the enzyme.
Freytag, S; Lenzen, S; Panten, U, 1988
)
2.01

Treatment

Alloxan treatment of pancreatic monolayer cultures may allow for a comparison of those actions of alloxan that are directly on and specific for islet B cells. Alloxan-treated rats showed an important reduction in body and bone mass, with a greater impact on soft tissues.

ExcerptReferenceRelevance
"Alloxan treatment increased the levels of FBG, total cholesterol, LDL-cholesterol, VLDL-cholesterol, urine ketone and cardiac function indices and reduced the levels of globulin, albumin, HDL-cholesterol, globulin, liver glycogen, hexokinase and glucose-6-phosphate dehydrogenase activities. "( Identification and characterization of anti-diabetic principle in Senna alata (Linn.) flower using alloxan-induced diabetic male Wistar rats.
Ajiboye, TO; Ashafa, AOT; Uwazie, JN; Yakubu, MT, 2020
)
2.22
"Alloxan treatment also provides a method for obtaining large chromosomes for the analysis of chromosome bands, FISH and sister-chromatid exchanges."( Prometaphase accumulation in murine bone marrow cells following in vivo treatment with alloxan.
Morales-Ramírez, P; Rodríguez-Reyes, R, 2008
)
1.29
"In alloxan-treated mice (a model of type 1 diabetes), drugs were administered orally once daily for 6 days post-alloxan treatment. "( Hypoglycemic and beta cell protective effects of andrographolide analogue for diabetes treatment.
Jiang, J; Larrick, JW; Wang, Y; Yu, P; Zeng, X; Zhang, Z, 2009
)
0.97
"Alloxan treatment to the rats could induce diabetes as the fasting blood glucose (FBG) levels were > 280 mg/dl."( Anti-hyperglycemic and anti-oxidative effect of aqueous extract of Momordica charantia pulp and Trigonella foenum graecum seed in alloxan-induced diabetic rats.
Chandra, D; Tripathi, UN, 2010
)
1.29
"Alloxan treatment reduced HSP90 levels and promoted proteasomal degradation of tau, c-Jun N-amino terminal kinase, and histone deacetylase (HDAC) 6."( Adaptive responses to alloxan-induced mild oxidative stress ameliorate certain tauopathy phenotypes.
Kimura, T; Maeda, S; Mizoroki, T; Murayama, M; Sahara, N; Soeda, Y; Takashima, A; Yamashita, S; Yoshiike, Y, 2012
)
1.41
"Alloxan treatment (10 mM) increased cellular reactive oxygen species (ROS) levels in the INS-1 cells, which were inversely related to cell viabilities."( Antidiabetic effects of rice hull smoke extract in alloxan-induced diabetic mice.
Friedman, M; Kang, MY; Nam, SH; Yang, JY, 2012
)
1.35
"Alloxan-treated dogs (D; n=7) were maintained normoglycemic using 24-h/d IV insulin replacement."( Chronic intrarenal insulin replacement reverses diabetes mellitus-induced natriuresis and diuresis.
Brands, MW; Duggan, AD; Manhiani, MM; Wilson, H, 2012
)
1.1
"Alloxan treatment alone resulted in a persisting hyperglycaemic state. "( Combined gastrin and epidermal growth factor treatment induces islet regeneration and restores normoglycaemia in C57Bl6/J mice treated with alloxan.
Bouwens, L; Rooman, I, 2004
)
1.97
"In alloxan-treated rats, HSE at the dose of 200 mg/kg significantly attenuated the elevated blood glucose concentration by 57%."( Hypolipidemic and antioxidant effects of ethanolic extract from dried calyx of Hibiscus sabdariffa in alloxan-induced diabetic rats.
Farombi, EO; Ige, OO, 2007
)
1.07
"Alloxan-treated, Obese and non-obese/SHR manifested gross and microscopic degenerative changes suggesting acceleration of the normal aging process."( Resistance of obese and non-obese, spontaneously hypertensive rats to alloxan-induced diabetes.
Mc Murtry, JP; Wexler, BC, 1983
)
1.22
"Alloxan treatment of pancreatic monolayer cultures may allow for a comparison of those actions of alloxan that are directly on and specific for islet B cells."( Cytotoxic effects of alloxan treatment in vitro on monolayer cultures of neonatal rat pancreas.
Baskin, DG; Fujimoto, WY; Gorray, KC, 1983
)
1.31
"Alloxan-treated nondiabetic rats displayed marked interstitial nephritis in unprotected kidneys, while protected kidneys were normal."( The effect of alloxan, and alloxan-induced diabetes on the kidney.
Aronoff, GR; Connors, BA; Evan, AP; Luft, FC; Mong, SA, 1984
)
1.35
"In alloxan-treated animals, beta cell granules were absent."( Reduction in the diabetogenic effect of alloxan in mice by treatment with the antineoplastic agent ICRF-187.
El-Hage, AN; Ferrans, VJ; Herman, EH, 1981
)
1.04
"Alloxan treatment caused hyperglycemia and reduced boy growth."( Diabetic neuropathy in the rat: 1. Alcar augments the reduced levels and axoplasmic transport of substance P.
Di Giulio, AM; Gorio, A; Lesma, E, 1995
)
1.01
"In alloxan-treated hyperglycemic mice, PYY immunoreactive cells were increased in number and distributed throughout the islets, in parallel with the glucagon, PP, and somatostatin cells."( Pancreatic peptide YY in alloxan diabetic mice.
Ahrén, B; Böttcher, G; Ekman, R; Lundqvist, G; Sundler, F, 1994
)
1.11
"Alloxan-treated rats showed an important reduction in body and bone mass, with a greater impact on soft tissues."( Growth and development of bone mass in untreated alloxan diabetic rats. Effects of collagen glycosylation and parathyroid activity on bone turnover.
Abranzon, H; Alloatti, R; Caferra, D; Fernandez, MC; Locatto, ME; Puche, RC, 1993
)
1.26
"Alloxan pretreatment enhanced the ability of erythrocytes to reduce extracellular ferricyanide while protecting alpha-tocopherol in the cell membrane from oxidation by ferricyanide."( Similarities in the metabolism of alloxan and dehydroascorbate in human erythrocytes.
Davis, JL; May, JM; Mendiratta, S, 1998
)
1.3
"Alloxan treatment reduced nitric oxide generation, whereas L-arginine and sodium nitroprusside, when given along with alloxan, enhanced nitric oxide production to control values."( Effect of L-arginine-nitric oxide system on chemical-induced diabetes mellitus.
Das, UN; Mohan, IK, 1998
)
1.02
"Alloxan treatment, however, does not alter lymph insulin kinetics, indicating that insulin resistance of Type 1 (insulin-dependent) diabetes mellitus reflects direct impairment at the cellular level."( Evidence for direct action of alloxan to induce insulin resistance at the cellular level.
Ader, M; Bergman, RN; Richey, JM, 1998
)
1.31
"Alloxan-treated controls had similar results to age-matched controls."( Upregulation of endothelin A receptor sites in the rabbit diabetic kidney: potential relevance to the early pathogenesis of diabetic nephropathy.
Dashwood, MR; Khan, MA; Mikhailidis, DP; Morgan, RJ; Mumtaz, FH; Thompson, CS, 1999
)
1.02
"Alloxan treatment reduced the glucose oxidation in islets from LP rats to a lesser extent than in NP islets (23% vs."( Protein deficiency attenuates the effects of alloxan on insulin secretion and glucose homeostasis in rats.
Boschero, AC; Carneiro, EM; Luciano, E; Mello, MA; Prada, FJ, 2001
)
1.29
"Alloxan treatment is associated with a significant increase of thiobarbituric acid reactive substances and the activity of antioxidant enzymes superoxide dismutase and catalase."( Alloxan induced cataract in a rat.
Balog, Z; Jukić-Lesina, T; Klepac, R; Rosić, S, 2001
)
2.47
"Alloxan-treated islets showed only a marginal decrease in ATP and no change in glucose 6-phosphate concentration."( Alloxan cytotoxicity in vitro. Inhibition of rubidium ion pumping in pancreatic beta-cells.
Idahl, LA; Lernmark, A; Sehlin, J; Täljedal, IB, 1977
)
2.42
"Alloxan treatment induces a decrease of orotic acid content in various organs of carp, frog, pigeon and rat, parallel to a decrease of liver and muscle glycogen content. "( Effects of alloxan on orotic acid and glycogen content in various vertebrate species.
Fekete, I, 1978
)
2.09
"Non-alloxan-treated cultured islets decarboxylated 2-2.5 times as much pyruvate as did alloxan-treated islets cultured for 15-18h."( Stimulation of proinsulin biosynthesis and insulin release by pyruvate and lactate.
Asina, S; Jain, K; Logothetopoulos, J, 1978
)
0.74
"In alloxan-treated diabetic rats, plasma renin activity (PRA) is decreased. "( Renin-angiotensin system in phlorhizin compared with alloxan diabetes in the rat.
Christlieb, AR; Long, R, 1979
)
1.13
"In alloxan-treated dogs glucagon output was not suppressed nor did somatostatin output increase."( Intra-islet insulin permits glucose to directly suppress pancreatic A cell function.
Greenbaum, CJ; Havel, PJ; Klaff, LJ; Taborsky, GJ, 1991
)
0.8
"Alloxan-treated rats showed rather increased levels of PTH which was at variance with respect to control animals and unrelated to the calcium content of the diet."( Calcium metabolism of rats with varying degrees of insulinopenia.
Abranzón, H; Caferra, D; Fernández, MC; Locatto, ME; Puche, RC, 1990
)
1
"The alloxan-treated guinea pig may represent a unique model for studying the restoration of insulinogenic capacity in insulinopenic diabetes."( Physiological and morphological changes in islet B cells following treatment of the guinea pig with alloxan.
Baskin, DG; Fujimoto, WY; Gorray, KC, 1986
)
0.97
"Alloxan/L-glucose treated rats ate 11% and 14% of control intake, respectively, after systemic administration of 2-deoxy-D-glucose (2DG, 250 mg/kg) and fourth ventricular 5-thioglucose (5TG, 120 micrograms/5 microliter)."( Alloxan-induced glucoprivic feeding deficits are blocked by D-glucose and amygdalin.
Murnane, JM; Ritter, S, 1985
)
2.43
"Treatment of alloxan-diabetic rats with insulin, vanadate, TSP and vanadate in combination with TSP revived normoglycemia and restored the disturbances in the distribution of GLUT4 in skeletal muscle."( Modulation of glucose transporter (GLUT4) by vanadate and Trigonella in alloxan-diabetic rats.
Bamezai, RN; Baquer, NZ; Mohammad, S; Taha, A, 2006
)
0.92
"Rats treated with alloxan plus glucose did not become diabetic or show elevated vitreous fluorescein levels."( Vitreous fluorophotometry in the alloxan- and streptozocin-treated rat.
Cunha-Vaz, JG; Jones, CW; Rusin, MM, 1982
)
0.87
"Treatment of alloxan-diabetic rats with the antilipolytic agents or insulin (60 U/kg i.p.) lowered these increased concentrations of metabolites in the heart."( The effect of 5-methylpyrazole-3-carboxylate and nicotinic acid on abnormalities of carbohydrate metabolism in alloxan-diabetic rat muscle.
Haddy, JP; McAllister, A; Sennitt, MV; Thorne, DE, 1982
)
0.83
"Treatment with alloxan increased serum gamma-GT and ALAT activities."( Hepatic and pancreatic effects of polyenoylphosphatidylcholine in rats with alloxan-induced diabetes.
Borodinsky, A; Buko, V; Gorenshtein, B; Gundermann, KJ; Janz, B; Lukivskaya, O; Nikitin, V; Schumacher, R; Tarasov, Y; Zavodnik, L, 1996
)
0.86
"The treatment of alloxan-induced diabetic rats brought down the raised glucose levels, while the extract was devoid of hypoglycemic effect in normal rats."( Antihyperglycemic activity of Euphrasia officinale leaves.
Ansari, SH; Porchezhian, E; Shreedharan, NK, 2000
)
0.64
"Pretreatment with alloxan attenuated both the stimulatory effect of glucose on insulin secretion and the inhibitory effect of glucose on glucagon secretion."( Modulation by alloxan of glucagon and insulin secretion in the isolated perfused rat pancreas.
Goto, Y; Imura, H; Inoue, Y; Kadowaki, S; Mori, K; Seino, Y; Taminato, T, 1978
)
0.94
"Treatment of alloxan-diabetic mice with insulin in vivo completely reversed all immune defects, while insulin treatment of streptozotocin-diabetic mice restored immune function to only 70-80% of normal levels."( Assessment of the diabetogenic drugs alloxan and streptozotocin as models for the study of immune defects in diabetic mice.
Eardley, DD; Gaulton, GN; Schwartz, JL, 1985
)
0.9
"Pretreatment with alloxan, butylated hydroxyanisole or desferrioxamine did not alter the severity of microcystin-LR intoxication in fed mice."( No effect of modulators of reactive oxygen-induced pathology on microcystin-LR intoxication.
Bunner, DL; Franz, DR; Lawrence, WB; Leclaire, RD, 1988
)
0.6

Toxicity

Alloxan and its derivatives were selectively toxic to pancreatic beta cells. Mannoheptulose not only removes the protection provided by exogenous glucose but sensitizes the beta cell to the toxic effects of alloxan.

ExcerptReferenceRelevance
" Mannoheptulose not only removes the protection provided by exogenous glucose but sensitizes the beta cell to the toxic effects of alloxan in the fasting state, probably by inhibiting the protection provided by endogenous glucose."( Studies of alloxan toxicity on the beta cell.
Arcangeli, MA; Cahill, GF; Rossini, AA, 1975
)
0.85
" For the four B-cell toxic agents tested, an increase in medium glucose following any of these treatments reduced the percent of dead cells."( Pancreatic B cells possess defense mechanisms against cell-specific toxicity.
Pipeleers, D; Van de Winkel, M, 1986
)
0.27
" Thus, the mechanisms by which nicotinamide and thymidine protect against the toxic effects of STZ or ALX appear different."( Mechanisms of nicotinamide and thymidine protection from alloxan and streptozocin toxicity.
Forbes, PM; Hall, CR; LeDoux, SP; Patton, NJ; Wilson, GL, 1988
)
0.52
"In view of the well known species differences in the sensitivity of pancreatic B-cells to the toxic glucose analogue alloxan, it was tested whether spermatozoa from two species with a different diabetogenic effect of alloxan displayed a similar difference in their sensitivity to this drug."( Alloxan toxicity in human and canine spermatozoa. Possible biochemical basis for a species difference in sensitivity.
Finsy, R; Gorus, FK; Pipeleers, DG, 1986
)
1.92
" These results indicate that alloxan is not selectively toxic to the pancreatic beta-cell and that sugars can protect against alloxan-induced cytotoxicity in hepatocytes."( Alloxan toxicity in isolated rat hepatocytes and protection by sugars.
Fischer, LJ; Harman, AW, 1982
)
2
" Alloxan and its derivatives were selectively toxic to pancreatic beta cells, with other endocrine cells and exocrine parenchymal cells being well preserved, even at high concentration."( Comparative toxicity of alloxan, N-alkylalloxans and ninhydrin to isolated pancreatic islets in vitro.
Jörns, A; Lenzen, S; Munday, R; Tiedge, M, 1997
)
1.51
" RINm5F cells were also susceptible to butylalloxan, a lipophilic alloxan derivative that is selectively toxic to pancreatic beta-cells."( Complementary action of antioxidant enzymes in the protection of bioengineered insulin-producing RINm5F cells against the toxicity of reactive oxygen species.
Lenzen, S; Lortz, S; Munday, R; Tiedge, M, 1998
)
0.56
"We have previously shown that human beta-cells are resistant to the toxic effects of alloxan."( Human islets in mixed islet grafts protect mouse pancreatic beta-cells from alloxan toxicity.
Andersson, A; Eizirik, DL; Madsen, OD; Marklund, SL; Olejnicka, B; Tyrberg, B, 1999
)
0.76
" The lipophilic alloxan derivative, butylalloxan, was toxic also to non-transfected control cells."( Importance of the GLUT2 glucose transporter for pancreatic beta cell toxicity of alloxan.
Elsner, M; Guldbakke, B; Lenzen, S; Munday, R; Tiedge, M, 2002
)
0.89
" Both ninhydrin and uramil could not redox cycle with glutathione (GSH) and were not selectively toxic to beta cells; their structure does not allow selective cellular uptake via the GLUT2 glucose transporter."( Relation between triketone structure, generation of reactive oxygen species, and selective toxicity of the diabetogenic agent alloxan.
Elsner, M; Gurgul-Convey, E; Lenzen, S, 2008
)
0.55
" comatus is less toxic to mice than vanadium (V)."( Comparison of hypoglycemic activity and toxicity of vanadium (IV) and vanadium (V) absorbed in fermented mushroom of Coprinus comatus.
Fu, Q; Ma, Z, 2009
)
0.35
" The aim of the present study was to determine the role of reactive oxygen species (ROS) in the in vitro toxic effects of HC on insulin secretion and function of BRIN-BD11 insulin-secreting cells."( Enhancement of homocysteine toxicity to insulin-secreting BRIN-BD11 cells in combination with alloxan.
Elsner, M; Flatt, PR; Gurgul-Convey, E; Lenzen, S; McClenaghan, NH; Scullion, SM, 2012
)
0.6
" However, an adverse effect induced by nano-TiO2 in many diseased conditions, typically characterized by oxidative stress (OS), remains unknown."( Oxidative stress increased hepatotoxicity induced by nano-titanium dioxide in BRL-3A cells and Sprague-Dawley rats.
Gao, W; Gou, X; Li, W; Liang, X; Lu, TJ; Qu, Z; Sha, B; Wang, S; Xu, F, 2014
)
0.4
" reticulata extract did not cause mortality or produce any remarkable haematological, biochemical and histopathological adverse effects in rats."( Antioxidant, α-glucosidase inhibitory activity and sub-chronic toxicity of Derris reticulata extract: its antidiabetic potential.
Chudapongse, N; Kumkrai, P; Weeranantanapan, O, 2015
)
0.42
" Inhibition of OGT by OPFRs might be involved in the subsequent toxic effects, including intracellular reactive oxygen species (ROS), calcium level, as well as cell proliferation and autophagy."( Inhibition of O-linked N-acetylglucosamine transferase activity in PC12 cells - A molecular mechanism of organophosphate flame retardants developmental neurotoxicity.
Gu, Y; Guo, LH; Li, M; Wan, B; Yang, Y, 2018
)
0.48
" Here, the toxic effects of dialuric acid targeting MAPT through in silico computational predictions have been investigated."( A system-level approach to investigate alloxan-induced toxicity in microtubule-binding protein to lead type 2 diabetes mellitus.
Kannan, ND; Sathish Kumar, P, 2021
)
0.89

Pharmacokinetics

The pharmacokinetic and pharmacodynamic parameters of torasemide were compared after intravenous administration at a dose of 2 mg/kg to diabetic rats induced by alloxan (DMIA) or streptozotocin (DMIS), and their respective control rats. Possible pharmacodynamic and pharmacokinetics interactions were observed for, following single-dose as well as multiple-dose treatment protocols.

ExcerptReferenceRelevance
" After both intravenous and oral administration some pharmacokinetic and pharmacodynamic parameters of azosemide were significantly different in AIDRs."( Pharmacokinetics and pharmacodynamics of azosemide after intravenous and oral administration to rats with alloxan-induced diabetes mellitus.
Lee, MG; Park, KJ; Shin, WG; Yoon, WH, 1996
)
0.51
" However, other pharmacokinetic parameters of DAD were not significantly different among three groups of rabbits."( Pharmacokinetic changes of diltiazem and desacetyldiltiazem after oral administration of diltiazem in rabbits with diabetes mellitus induced by alloxan.
Choi, JS; Kim, YG, 2002
)
0.52
"The pharmacokinetic and pharmacodynamic parameters of torasemide were compared after intravenous administration at a dose of 2 mg/kg to diabetic rats induced by alloxan (DMIA) or streptozotocin (DMIS), and their respective control rats."( Pharmacokinetics and pharmacodynamics of intravenous torasemide in diabetic rats induced by alloxan or streptozotocin.
Kim, SH; Kim, YC; Lee, MG; Oh, EY, 2005
)
0.74
" Pharmacokinetic investigation was performed using non-diabetic rats."( The anti-diabetic effects and pharmacokinetic profiles of bis(maltolato)oxovanadium in non-diabetic and diabetic rats.
Chen, GH; Lu, WL; Zhang, Q; Zhang, SQ; Zhong, XY, 2008
)
0.35
" The altered pharmacokinetic indices observed following intravenous and oral administration of metformin to DMIA rats returned to the control values in the DMIA rats with insulin."( Effects of diabetes mellitus induced by alloxan on the pharmacokinetics of metformin in rats: restoration of pharmacokinetic parameters to the control state by insulin treatment.
Choi, YH; Lee, I; Lee, MG, 2008
)
0.61
" Thus, the pharmacokinetic changes of telithromycin in both models of diabetes mellitus compared with those in the control rats were evaluated."( Telithromycin pharmacokinetics in rat model of diabetes mellitus induced by alloxan or streptozotocin.
Lee, JH; Lee, MG, 2008
)
0.58
" This work examined the effect of hyperglycemia on the pharmacokinetic properties of cyclosporine in a diabetic dog model."( Influence of overt diabetes mellitus on cyclosporine pharmacokinetics in a canine model.
Alkharfy, KM, 2009
)
0.35
"0019) and a decrease in its biological half-life (9."( Influence of overt diabetes mellitus on cyclosporine pharmacokinetics in a canine model.
Alkharfy, KM, 2009
)
0.35
"The present study was undertaken to compare the bioavailability and pharmacokinetic parameters of diclofenac sodium and diclofenac potassium in normal and experimentally induced diabetic state in 24 rabbits using a validated reversed phase HPLC method with a washout period of one week."( Comparison of bioavailability and pharmacokinetics of diclofenac sodium and diclofenac potassium in normal and alloxan-diabetic rabbits.
Ahmad, M; Iqbal, M; Murtaza, G, 2012
)
0.59
" Both DMIS and DMIA models have served as key experimental tools to evaluate and understand the pharmacokinetic disposition of scores of drugs and therefore some key questions with respect to absorption, metabolism or elimination of drugs can be answered during the development of full-blown diabetes in the animal models."( Strategies for preclinical pharmacokinetic investigation in streptozotocin-induced diabetes mellitus (DMIS) and alloxan-induced diabetes mellitus (DMIA) rat models: case studies and perspectives.
Srinivas, NR, 2015
)
0.63
"The pharmacokinetic parameters like peak plasma concentration (Cmax), area under the plasma concentration time profile (AUC) and elimination half life of repaglinide were significantly (p<0."( Altered pharmacokinetics and pharmacodynamics of repaglinide by ritonavir in rats with healthy, diabetic and impaired hepatic function.
Goud, T; Maddi, S; Nayakanti, D; Thatipamula, RP, 2016
)
0.43
" (MS) bark juice in diabetic gastroparesis and its effect on pharmacokinetic of metformin (MET)."( Influence of Musa sapientum L. on pharmacokinetic of metformin in diabetic gastroparesis.
Darvhekar, V; Jyotishi, SG; Mazumder, PM; Shelke, PG; Tripathi, AS, 2016
)
0.43
" The effect of MS bark juice on the pharmacokinetic of orally administered single dose of MET (350 mg/kg) was evaluated on the 57th day of protocol."( Influence of Musa sapientum L. on pharmacokinetic of metformin in diabetic gastroparesis.
Darvhekar, V; Jyotishi, SG; Mazumder, PM; Shelke, PG; Tripathi, AS, 2016
)
0.43
"Diabetes mellitus (DM)-induced morphological and/or functional complications may alter the pharmacokinetic profiles of mangiferin."( Comparative Pharmacokinetic Study of Mangiferin in Normal and Alloxan-Induced Diabetic Rats after Oral and Intravenous Administration by UPLC-MS/MS.
Gu, PC; Han, MN; Han, WL; Pan, YQ; Peng, J; Shang, JC; Wang, L, 2019
)
0.75
"90% decreases in Cmax and AUC0-t, respectively, for mangiferin after oral administration, and 63."( Comparative Pharmacokinetic Study of Mangiferin in Normal and Alloxan-Induced Diabetic Rats after Oral and Intravenous Administration by UPLC-MS/MS.
Gu, PC; Han, MN; Han, WL; Pan, YQ; Peng, J; Shang, JC; Wang, L, 2019
)
0.75
"Compared to normal rats, pharmacokinetic parameters of mangiferin were altered in diabetic condition induced by alloxan."( Comparative Pharmacokinetic Study of Mangiferin in Normal and Alloxan-Induced Diabetic Rats after Oral and Intravenous Administration by UPLC-MS/MS.
Gu, PC; Han, MN; Han, WL; Pan, YQ; Peng, J; Shang, JC; Wang, L, 2019
)
0.97
" Possible pharmacodynamic and pharmacokinetic interactions were observed for, following single-dose as well as multiple-dose treatment protocols in normal and alloxan-induced diabetes in albino Wistar rats and rabbits."( Pharmacodynamic and pharmacokinetic interaction of losartan with glimepiride-metformin combination in rats and rabbits.
Anilkumar, KV; Nagaraju, B,
)
0.33

Compound-Compound Interactions

ExcerptReferenceRelevance
"We studied the effect of heparin combined with aspirin on the development and course of experimental alloxan-induced diabetes mellitus."( [Effect of heparin combined with aspirin upon intragastric administration on the state of the insulin system in animals with alloxan diabetes].
Liapina, LA; Tarasov, IuA; Ul'ianov, AM,
)
0.55
" HC in combination with Alx resulted in a more pronounced decline in insulin secretion, including that induced by 20  mM alanine, by 43% (P<0."( Enhancement of homocysteine toxicity to insulin-secreting BRIN-BD11 cells in combination with alloxan.
Elsner, M; Flatt, PR; Gurgul-Convey, E; Lenzen, S; McClenaghan, NH; Scullion, SM, 2012
)
0.6

Bioavailability

T-CA was effective in attenuating the effects of alloxan treatment. T-CA SNEDDS with a more favorable absorption and enhanced bioavailability is more effective than t-CA.

ExcerptReferenceRelevance
" Compared with subcutaneous administration of insulin solution, the relative pharmacological bioavailability and the relative bioavailability of vaginal administration of insulin vesicles were determined."( Niosomes with sorbitan monoester as a carrier for vaginal delivery of insulin: studies in rats.
Gu, Z; Guo, Y; Ning, M; Pan, H; Yu, H,
)
0.13
" The average absolute bioavailability for intragastric administration at a single dose of 3, 6 and 12 mgV/kg was 28."( The anti-diabetic effects and pharmacokinetic profiles of bis(maltolato)oxovanadium in non-diabetic and diabetic rats.
Chen, GH; Lu, WL; Zhang, Q; Zhang, SQ; Zhong, XY, 2008
)
0.35
"To verify if an experimental model of alloxan-diabetic rats promotes oxidative stress, reduces nitric oxide bioavailability and causes vascular dysfunction, and to evaluate the effect of N-acetylcysteine (NAC) on these parameters."( Oxidative stress is not associated with vascular dysfunction in a model of alloxan-induced diabetic rats.
Baldo, CF; Batalhão, ME; Capellini, VK; Cárnio, EC; Celotto, AC; Evora, PR; Rodrigues, AJ, 2010
)
0.86
"The present study was undertaken to compare the bioavailability and pharmacokinetic parameters of diclofenac sodium and diclofenac potassium in normal and experimentally induced diabetic state in 24 rabbits using a validated reversed phase HPLC method with a washout period of one week."( Comparison of bioavailability and pharmacokinetics of diclofenac sodium and diclofenac potassium in normal and alloxan-diabetic rabbits.
Ahmad, M; Iqbal, M; Murtaza, G, 2012
)
0.59
"The purpose of this study is to investigate the bioavailability and glycaemic metabolism of cinnamon oil (CIO) carried by liquid-loadable tablets (CIO-LLTs), the carrier of a CIO self-emulsifying formulation (CIO-LS)."( Improvement of the bioavailability and glycaemic metabolism of cinnamon oil in rats by liquid loadable tablets.
Cui, B; Han, C, 2012
)
0.38
" By inhibiting the metabolism of drugs, piperine improves the bioavailability of drugs."( Effect of piperine on antihyperglycemic activity and pharmacokinetic profile of nateglinide.
Bommineni, MR; Mullangi, R; Nadipelli, M; Sama, V; Yenumula, P, 2012
)
0.38
" The present study demonstrated that t-CA was effective in attenuating the effects of alloxan treatment and that t-CA SNEDDS with a more favorable absorption and enhanced bioavailability is more effective than t-CA."( Self-nanoemulsifying drug delivery system of trans-cinnamic acid: formulation development and pharmacodynamic evaluation in alloxan-induced type 2 diabetic rat model.
Cao, X; Deng, W; Li, Q; Omari-Siaw, E; Wang, H; Wang, Q; Wang, S; Xu, X; Yu, J, 2015
)
0.85
"80% of oral bioavailability respectively."( Comparative Pharmacokinetic Study of Mangiferin in Normal and Alloxan-Induced Diabetic Rats after Oral and Intravenous Administration by UPLC-MS/MS.
Gu, PC; Han, MN; Han, WL; Pan, YQ; Peng, J; Shang, JC; Wang, L, 2019
)
0.75
" The oral pharmacological bioavailability of the nanoparticles in type I diabetic mice was 12."( Insulin- and cholic acid-loaded zein/casein-dextran nanoparticles enhance the oral absorption and hypoglycemic effect of insulin.
Bao, X; Qian, K; Yao, P, 2021
)
0.62

Dosage Studied

Alloxan-streptozotocin combination administration reduced the dosage of each drug, and decreased the toxic and side effect. Alloxan made the blood sugar's increase up to the 7th d post injectionem.

ExcerptRelevanceReference
" This depended on the dosage of the drug as well as the timing."( Regeneration of the islets of Langerhans in the Guinea pig.
Jacob, S, 1977
)
0.26
" Endotoxin treatment was associated with increased activity of the protectant antioxidant enzyme systems of the lung in an apparent dose-response manner."( Endotoxin protection against oxygen-induced acute and chronic lung injury.
Frank, L; Roberts, RJ, 1979
)
0.26
" Alloxan-zinc-chelate protractedly and significantly made the blood sugar's increase up to the 7th d post injectionem, without being able to maintain a permanent hyperglycemia with half-normal dosage in comparison with alloxan."( [Effect of alloxans on pancreatic B-cells with special regard to the alloxan-metal-complex theory. I. Effects of alloxan, alloxan-zinc chelates, dilauric acid and colchicine on blood sugar and rate of mitosis of B-cell Langerhans islets].
Glass, P; Müller, H; Schmidt, R; Schneider, S; Unger, E, 1990
)
1.58
" A dose-response of a single injection of the agents with respect to pancreatic insulin content 48 hr post-injection as well as to circulating insulin and glucose, weight, and lymphocyte counts was established."( Sensitivity of BB rat beta cells as determined by dose-responses to the cytotoxic effects of streptozotocin and alloxan.
Grose, M; Marliss, EB; Videtic, GM; Yale, JF, 1986
)
0.48
" Our study was designed to explore dosage schedules which might improve rabbit responsiveness to and survival after alloxan treatment."( Variations of susceptibility to alloxan induced diabetes in the rabbit.
Beyer, MM; Brown, CD; Friedman, EA; Watschinger, B; Zhao, ZH, 1987
)
0.77
"5 times increased molar dosage required to produce islet NAD depression comparable to that of streptozotocin, 150 mg/kg."( Streptozotocin diabetes. Correlation with extent of depression of pancreatic islet nicotinamide adenine dinucleotide.
Anderson, T; Cooney, DA; McMenamin, MG; Schein, PS, 1974
)
0.25
"Comparisons were made of the dose-response and time-course characteristics of nicotinamide (NIC) and its metabolite, N1-methylnicotinamide (MNIC), protection from alloxan-induced diabetes in mice."( Characteristics of nicotinamide and N1-methylnicotinamide protection from alloxan diabetes in mice.
Falany, J; Fischer, LJ; Fisher, R, 1983
)
0.69
" In the presence of alloxan, reactions occurred within seconds and islet cells were significantly more reactive to alloxan than either red cells or hepatocytes as defined by alloxan dose-response curves with fixed cell numbers or fixed surface areas."( Alloxan-induced free radical production in isolated cells. Selective effect on islet cells.
Asayama, K; Burr, IM; English, D; Nyfeler, F; Pilkis, SJ, 1984
)
2.03
" Production of PA is increased up to 15-fold by culture in the presence of high concentrations of glucose, and the dose-response curves for the effect of glucose on secretion of PA and on insulin are superimposable."( Plasminogen activator of islets of Langerhans: modulation by glucose and correlation with insulin production.
Estensen, RD; Reich, E; Vassalli, JD; Virji, MA, 1980
)
0.26
"The diabetogenic action of the beta-cell toxin, alloxan, is transient when administered to mice at a dosage of 50 mg/kg."( Blockade of muscarinic transmission increases the frequency of diabetes after low-dose alloxan challenge in the mouse.
Ahrén, B; Mulder, H; Sundkvist, G; Sundler, F, 1996
)
0.77
" The best known diabetogenic substances, Streptozotocin and Alloxan are described, including their usage, dosage dosing intervals, and mechanism of action."( [Experimental models in research of the pathomechanism of diabetes mellitus].
Fehér, J; Prechl, J; Pusztai, P; Somogyi, A; Szaleczky, E, 1996
)
0.54
" After the vasoconstriction reached steady state conditions, a dose-response study was performed with acetylcholine (Ach) and bradykinin (Bk)."( Decreased endothelium dependent relaxation (nitric oxide) in diabetic kidneys.
Costa e Forti, A; Fonteles, MC, 1998
)
0.3
" Normal and diabetic rats were provided with a diet supplemented with fenugreek seed powder for 30 days at a dosage of 2 g/kg body weight."( Restoration on tissue antioxidants by fenugreek seeds (Trigonella Foenum Graecum) in alloxan-diabetic rats.
Anuradha, CV; Ravikumar, P, 2001
)
0.53
" Alloxan-streptozotocin combination administration reduced the dosage of each drug, and decreased the toxic and side effect of each drug."( [Chemically induced (streptozotocin-alloxan) diabetes mellitus in dogs].
Liu, S; Luo, XM; Wang, W; Ye, B, 2000
)
1.49
"We have previously shown that dose-response studies performed in streptozotocin (STZ)-diabetic nude mouse recipients bearing established, functioning islet xenografts can be used to directly compare in vivo STZ-sensitivity between donor species and that tilapia (fish) islet grafts are exceedingly STZ-resistant."( Tilapia islet grafts are highly alloxan-resistant.
Morrison, CM; Wright, JR; Xu, BY; Yang, H, 2004
)
0.61
" Conversely, each rats group was further subdivided: no further treatment or acute sildenafil dosing (25 mg/kg, 1 hour before "in vivo" electrical stimulation [ES])."( Testosterone restores diabetes-induced erectile dysfunction and sildenafil responsiveness in two distinct animal models of chemical diabetes.
Donati, S; Filippi, S; Forti, G; Luconi, M; Maggi, M; Morelli, A; Vignozzi, L; Zhang, XH, 2006
)
0.33
" Alloxan inhibited islet O-GlcNAcase with a dose-response much like that of STZ."( Alloxan is an inhibitor of O-GlcNAc-selective N-acetyl-beta-D-glucosaminidase.
Alborn, WE; Knierman, MD; Konrad, RJ; Lee, TN, 2006
)
2.69
" The tests of maximum dosage and acute toxicity showed that EJA-1 was safe (MD = 360 g/kg, LD(50) = 400."( Pharmacological studies on anti-hyperglycemic effect of folium eriobotryae.
Chen, J; Li, WL; Lu, CG; Ren, BR; Wu, JL, 2007
)
0.34
" In conclusion, at the present dosing levels and administration routes, BMOV was effective in lowering plasma glucose levels in diabetic rats."( The anti-diabetic effects and pharmacokinetic profiles of bis(maltolato)oxovanadium in non-diabetic and diabetic rats.
Chen, GH; Lu, WL; Zhang, Q; Zhang, SQ; Zhong, XY, 2008
)
0.35
" The variation in bioavailability and disposition of diclofenac sodium and diclofenac potassium in diabetic state will require adjustment of the dosage regimen prescribed for diabetics in clinical setting."( Comparison of bioavailability and pharmacokinetics of diclofenac sodium and diclofenac potassium in normal and alloxan-diabetic rabbits.
Ahmad, M; Iqbal, M; Murtaza, G, 2012
)
0.59
" The dosage of 300mg/kg body weight exhibited the best effects."( Anti-diabetic properties of Momordica charantia L. polysaccharide in alloxan-induced diabetic mice.
Liao, CH; Shan, B; Shi, JY; Wen, PW; Xie, JH; Xu, X, 2015
)
0.65
" comatus; it can remarkably reduce the blood glucose concentration in 120 min at a dosage of 1000 mg/kg administered orally."( Hypoglycemic Activity of Polysaccharide from Fruiting Bodies of the Shaggy Ink Cap Medicinal Mushroom, Coprinus comatus (Higher Basidiomycetes), on Mice Induced by Alloxan and Its Potential Mechanism.
Liu, Y; Tang, Q; Yang, Y; Zhang, J; Zhou, S, 2015
)
0.61
"This study investigates the fabrication, characterization and optimization of Linum usitatissimum mucilage (LSM) with sodium alginate mucoadhesive microspheres loaded metformin HCl, a sustained release dosage form prepared by ionic gelation technique."( Linum usitatissimum seed mucilage-alginate mucoadhesive microspheres of metformin HCl: Fabrication, characterization and evaluation.
Ghumman, SA; Noreen, S; Tul Muntaha, S, 2020
)
0.56
" Hypoglycemic activity of a combination of glimepiride + metformin was enhanced when losartan was co-administered as a single dosage schedule as well as a multiple dose schedule as indicated by a reduced blood glucose level and enhanced levels of insulin in rats as well as in rabbits."( Pharmacodynamic and pharmacokinetic interaction of losartan with glimepiride-metformin combination in rats and rabbits.
Anilkumar, KV; Nagaraju, B,
)
0.13
"It can therefore be concluded, that in diabetics with hypertension as a comorbidity condition, co-administration of losartan with glimepiride + metformin should be avoided or the dosage of a combination of glimepiride + metformin needs to be tittered to avoid recurrence of hypoglycemic episodes."( Pharmacodynamic and pharmacokinetic interaction of losartan with glimepiride-metformin combination in rats and rabbits.
Anilkumar, KV; Nagaraju, B,
)
0.13
" Group I acted as the control, whereas groups II, III, IV, and V were considered experimental groups which received a single dosage (150 mg/kg body weight) of alloxan (ALX) intraperitoneally (i."( Co-administration of
Kar, A; Panda, S; Sharma, N; Yadav, D, 2022
)
0.92
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (2)

RoleDescription
hyperglycemic agentA drug which increases the blood glucose level.
metaboliteAny intermediate or product resulting from metabolism. The term 'metabolite' subsumes the classes commonly known as primary and secondary metabolites.
[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
pyrimidoneA pyrimidine carrying one or more oxo substituents.
[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
uracil degradation II (oxidative)112

Protein Targets (14)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, Putative fructose-1,6-bisphosphate aldolaseGiardia intestinalisPotency15.81140.140911.194039.8107AID2451
Chain A, 2-oxoglutarate OxygenaseHomo sapiens (human)Potency2.81840.177814.390939.8107AID2147
Chain A, ATP-DEPENDENT DNA HELICASE Q1Homo sapiens (human)Potency39.81070.125919.1169125.8920AID2549
phosphopantetheinyl transferaseBacillus subtilisPotency14.12540.141337.9142100.0000AID1490
USP1 protein, partialHomo sapiens (human)Potency89.12510.031637.5844354.8130AID504865
TDP1 proteinHomo sapiens (human)Potency1.63600.000811.382244.6684AID686979
Microtubule-associated protein tauHomo sapiens (human)Potency2.66510.180013.557439.8107AID1460; AID1468
Bloom syndrome protein isoform 1Homo sapiens (human)Potency39.81070.540617.639296.1227AID2528
vitamin D3 receptor isoform VDRAHomo sapiens (human)Potency3.16230.354828.065989.1251AID504847
ubiquitin carboxyl-terminal hydrolase 2 isoform aHomo sapiens (human)Potency10.00000.65619.452025.1189AID927
Disintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)Potency10.00001.584913.004325.1189AID927
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, XcogtXanthomonas campestrisKd1,000.00001,000.00001,000.00001,000.0000AID977611
Chain A, XcogtXanthomonas campestrisKd1,000.00001,000.00001,000.00001,000.0000AID977611
Chain A, XcogtXanthomonas campestrisKd1,000.00001,000.00001,000.00001,000.0000AID977611
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (39)

Processvia Protein(s)Taxonomy
positive regulation of epidermal growth factor receptor signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
response to hypoxiaDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
neutrophil mediated immunityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
germinal center formationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of leukocyte chemotaxisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
proteolysisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
membrane protein ectodomain proteolysisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell adhesionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Notch receptor processingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cell population proliferationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
response to xenobiotic stimulusDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of T cell chemotaxisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
protein processingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
signal releaseDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
B cell differentiationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cell growthDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cell migrationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
response to lipopolysaccharideDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of chemokine productionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of tumor necrosis factor productionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
regulation of mast cell apoptotic processDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
T cell differentiation in thymusDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell adhesion mediated by integrinDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
wound healing, spreading of epidermal cellsDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
amyloid precursor protein catabolic processDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of blood vessel endothelial cell migrationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cyclin-dependent protein serine/threonine kinase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of epidermal growth factor-activated receptor activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of epidermal growth factor receptor signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
spleen developmentDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell motilityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
defense response to Gram-positive bacteriumDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cellular response to high density lipoprotein particle stimulusDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
commissural neuron axon guidanceDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
negative regulation of cold-induced thermogenesisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of G1/S transition of mitotic cell cycleDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of tumor necrosis factor-mediated signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of vascular endothelial cell proliferationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Notch signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (14)

Processvia Protein(s)Taxonomy
endopeptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metalloendopeptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Notch bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
interleukin-6 receptor bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
integrin bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
protein bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
peptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metallopeptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
SH3 domain bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytokine bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
PDZ domain bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
tumor necrosis factor bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metal ion bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metalloendopeptidase activity involved in amyloid precursor protein catabolic processDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (13)

Processvia Protein(s)Taxonomy
cell-cell junctionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
focal adhesionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
ruffle membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Golgi membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytoplasmDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
endoplasmic reticulum lumenDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytosolDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
plasma membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell surfaceDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
actin cytoskeletonDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
apical plasma membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
membrane raftDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
plasma membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (8)

Assay IDTitleYearJournalArticle
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.
AID1594144Inhibition of Escherichia coli GroEL expressed in Escherichia coliDH5alpha/Escherichia coli GroES expressed in Escherichia coli BL21 (DE3) assessed as reduction in GroEL/GroES-mediated denatured soluble pig heart MDH refolding by measuring MDH enzyme acti2019Bioorganic & medicinal chemistry letters, 05-01, Volume: 29, Issue:9
HSP60/10 chaperonin systems are inhibited by a variety of approved drugs, natural products, and known bioactive molecules.
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.
AID1594145Inhibition of Escherichia coli GroEL expressed in Escherichia coli DH5alpha/Escherichia coli GroES expressed in Escherichia coli BL21 (DE3) assessed as reduction in GroEL/GroES-mediated denatured rhodanese refolding by measuring rhodanese enzyme activity 2019Bioorganic & medicinal chemistry letters, 05-01, Volume: 29, Issue:9
HSP60/10 chaperonin systems are inhibited by a variety of approved drugs, natural products, and known bioactive molecules.
AID478233Antidiabetic activity in Wistar albino rat assessed as reduction of blood glucose level administered qd for 9 days by glucose oxidation method (RVb = 79.17 +/- 0.48 mg/dl)2010European journal of medicinal chemistry, May, Volume: 45, Issue:5
Derivatives of benzimidazole pharmacophore: synthesis, anticonvulsant, antidiabetic and DNA cleavage studies.
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.
AID977611Experimentally measured binding affinity data (Kd) for protein-ligand complexes derived from PDB2011Amino acids, Mar, Volume: 40, Issue:3
Substrate and product analogues as human O-GlcNAc transferase inhibitors.
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.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (2,982)

TimeframeStudies, This Drug (%)All Drugs %
pre-19901648 (55.26)18.7374
1990's316 (10.60)18.2507
2000's407 (13.65)29.6817
2010's489 (16.40)24.3611
2020's122 (4.09)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 57.38

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 Index57.38 (24.57)
Research Supply Index8.09 (2.92)
Research Growth Index4.50 (4.65)
Search Engine Demand Index99.04 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (57.38)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials6 (0.18%)5.53%
Reviews52 (1.60%)6.00%
Case Studies2 (0.06%)4.05%
Observational0 (0.00%)0.25%
Other3,199 (98.16%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]