Page last updated: 2024-12-07

deoxyglucose

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Description

2-deoxy-D-glucose, or 2-DG, is a glucose analog that is structurally similar to glucose but lacks a hydroxyl group at the 2-position. This structural difference prevents 2-DG from being further metabolized by glycolysis, effectively blocking the breakdown of glucose. 2-DG has been studied extensively for its potential therapeutic applications, particularly in cancer treatment. It is known to inhibit tumor growth by interfering with glucose metabolism, a vital process for cancer cells. 2-DG also exhibits anti-inflammatory and antiviral properties. Additionally, it is being investigated as a potential treatment for neurodegenerative diseases such as Alzheimer's disease. 2-DG is synthesized through a multi-step chemical process involving the conversion of glucose to 2-deoxyglucose.'

Deoxyglucose: 2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

deoxyglucose : A deoxyhexose comprising glucose having at least one hydroxy group replaced by hydrogen. [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]

2-deoxy-D-glucopyranose : A 2-deoxy-D-glucose that is D-glucopyranose in which the hydroxy group at position 2 has been replaced by a hydrogen. [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 CID108223
CHEMBL ID2074932
SCHEMBL ID7670
MeSH IDM0006004
PubMed CID439268
CHEMBL ID1377788
CHEBI ID84755
SCHEMBL ID7669
MeSH IDM0006004

Synonyms (86)

Synonym
ccris 9094
brn 1723331
deoxyglucose
2-desoxy-d-glucose [french]
einecs 205-823-0
2 deoxyglucose
2 deoxy d glucose
2 desoxy d glucose
2-deoxy-d-mannose
2-deoxy-d-arabinohexose
2-desoxy-d-glucose
2-dg
d-arabino-hexose, 2-deoxy- (6ci,8ci,9ci)
d-2-deoxyglucose
hsdb 5484
2-deoxy-d-glucose, >=98% (gc), crystalline
2-deoxy-d-glucose, bioxtra, >=98%
2-deoxy-d-glucose, >=99% (gc), crystalline
5CFA0332-FB70-485D-A064-6C4C39E7CBA1
D0051
61-58-5
(3r,4s,5r)-3,4,5,6-tetrahydroxyhexanal
A26275
4-01-00-04282 (beilstein handbook reference)
unii-9g2mp84a8w
9g2mp84a8w ,
AKOS015924825
AKOS015919409
d-arabino-2-desoxyhexose
2-deoxy-d-glucose [mi]
2-deoxy-d-glucose [who-dd]
2-deoxy-d-glucose [mart.]
2-deoxy-d-glucose [hsdb]
CHEMBL2074932
DB08831
SCHEMBL7670
VRYALKFFQXWPIH-PBXRRBTRSA-N
arabino-hexose, 2-deoxy-
DTXSID1037648
d-2dglc
2-deoxy-d-glucose, united states pharmacopeia (usp) reference standard
Q3266534
AS-12502
2-deoxylglucose
AMY10934
AC-2616
nsc 15193
BIO1_001463
BIO1_000485
BIO1_000974
2-deoxy-glucose
MLS001332442
2-dglc
(4r,5s,6r)-6-(hydroxymethyl)tetrahydropyran-2,4,5-triol
2-deoxyhexose
d-arabino-2-deoxyhexose
C00586
(4r,5s,6r)-6-(hydroxymethyl)oxane-2,4,5-triol
MLS001332441
smr000857164
NCGC00247029-01
2-deoxymannopyranose
2-deoxyglucopyranose
2-deoxy-d-glucopyranose
2-deoxy-d-mannopyranose
HMS2234M06
S4701
2-deoxy-d-arabino-hexopyranose
(4r,5s,6r)-6-(hydroxymethyl)tetrahydro-2h-pyran-2,4,5-triol
[3h]-2-deoxyglucose
gtpl4643
[3h]2-deoxyglucose
CS-1718
HY-13966
SCHEMBL7669
chebi:84755 ,
CHEMBL1377788
AKOS024458197
(4r,5s,6r)-6-methyloltetrahydropyran-2,4,5-triol
2-deoxy-d-glucose, min. 98%
DTXSID501019205
CCG-266307
NCGC00247029-04
BS-1031
STARBLD0016184
mfcd00007013

Research Excerpts

Overview

2-Deoxyglucose (2DG) is a non-metabolizable glucose analog currently in clinical trials to determine its efficacy in enhancing the therapeutic effects of radiotherapy and chemotherapy of several types of cancers. progranulin is a neurotrophic factor produced mainly by microglia and has an inflammation modulator effect.

ExcerptReferenceRelevance
"2-deoxyglucose is a glucose analog that impacts many aspects of cellular physiology. "( 2-deoxyglucose transiently inhibits yeast AMPK signaling and triggers glucose transporter endocytosis, potentiating the drug toxicity.
Albanèse, V; Ballin, A; Defenouillère, Q; García-Rodríguez, FJ; Laussel, C; Léon, S, 2022
)
2.16
"2-Deoxyglucose(2-DG) is a widely used glycolysis inhibitor."( Co-delivery of 2-Deoxyglucose and a glutamine metabolism inhibitor V9302 via a prodrug micellar formulation for synergistic targeting of metabolism in cancer.
Huang, H; Li, S; Liu, Y; Luo, Z; Ma, W; Pardeshi, A; Sun, J; Wan, Z; Xu, J; Zhang, Z, 2020
)
1.46
"2-Deoxyglucose (2DG) is a non-metabolizable glucose analog currently in clinical trials to determine its efficacy in enhancing the therapeutic effects of radiotherapy and chemotherapy of several types of cancers. "( Aldo-keto reductases-mediated cytotoxicity of 2-deoxyglucose: A novel anticancer mechanism.
Chung, SK; Chung, SS; Yung, KK; Zhang, SQ, 2018
)
1.46
"2-deoxyglucose (2DG) is an analog of glucose capable of protecting the brain, and progranulin is a neurotrophic factor produced mainly by microglia and has an inflammation modulator effect."( 2-Deoxyglucose protects hippocampal neurons against kainate-induced temporal lobe epilepsy by modulating monocyte-derived macrophages (mo-MΦ) and progranulin production in the hippocampus.
Belali, R; Mohammad Khanizadeh, A; Nikbakht, F; Rasoolijazi, H, 2019
)
1.79
"2-Deoxyglucose (2DG) is an anticancer drug with excellent safety profile. "( 2-Deoxyglucose induces cell cycle arrest and apoptosisin colorectal cancer cells independent of its glycolysis inhibition.
Muley, P; Olinger, A; Tummala, H, 2015
)
1.86
"2-deoxyglucose (2-DG) is a non-metabolizable glucose analog tested in clinical trials and is frequently used in experimental settings to mimic glucose starvation."( ATF4 mediates necrosis induced by glucose deprivation and apoptosis induced by 2-deoxyglucose in the same cells.
Domínguez-Villanueva, D; Gonsberg, A; Lampidis, TJ; León-Annicchiarico, CL; Muñoz-Pinedo, C; Ramírez-Peinado, S, 2015
)
1.2
"2-Deoxyglucose (2-DG) is a glucose analogue and has been shown to inhibit angiogenesis in human umbilical vascular endothelial cells (HUVECs) through interference with N-linked glycosylation. "( The anti-angiogenic action of 2-deoxyglucose involves attenuation of VEGFR2 signaling and MMP-2 expression in HUVECs.
Chuang, IC; Hu, ML; Song, TY; Yang, CM; Yang, NC, 2015
)
1.42
"2-Deoxyglucose (2-DG) is a toxic glucose analog. "( Identification of nuclear genes affecting 2-Deoxyglucose resistance in Schizosaccharomyces pombe.
Bähler, J; Bevkal Subramanyaswamy, S; D'Souza, CJ; Rallis, C; Schweingruber, ME; Vishwanatha, A, 2016
)
1.42
"2-Deoxyglucose was found to be a substrate for the regeneration of GSH from GSSG in the red blood cells of humans, sheep, goats and cattle. "( 2-Deoxyglucose as a substrate for glutathione regeneration in human and ruminant red blood cells.
Agar, NS; O'Dea, JD; Suzuki, M; Suzuki, T, 1983
)
1.71
"2-Deoxyglucose (2-DG) uptake is an index of regional glucose utilization which reflects predominantly activity in the axonal terminal of neuronal pathways. "( Facilitation of 2-deoxyglucose uptake in rat cortex and hippocampus slices by somatostatin is independent of cholinergic activity.
Hamada, T; Koga, Y; Shibata, S; Watanabe, S, 1993
)
1.34
"2-Deoxyglucose was found to be an excellent non-metabolized analogue of D-glucose in oxidation experiments."( Extracellular oxidation of D-glucose by some members of the Enterobacteriaceae.
Bouvet, OM; Grimont, PA,
)
0.69

Effects

2-Deoxyglucose (2DG) has been shown to inhibit mammary carcinogenesis. 2DG studies have been most useful in mapping activated regions of the nervous system.

ExcerptReferenceRelevance
"2-Deoxyglucose (2-DG), which has been shown to inhibit mammary carcinogenesis, was used as a metabolic probe to investigate effects of limiting energy availability (reduced cellular ATP) on patterns of proteins' phosphorylation that play a role in the development of cancer. "( Modulation of the activities of AMP-activated protein kinase, protein kinase B, and mammalian target of rapamycin by limiting energy availability with 2-deoxyglucose.
Jiang, W; Thompson, HJ; Zhu, Z, 2008
)
1.27
"2-Deoxyglucose (2DG) studies have been most useful in mapping activated regions of the nervous system. "( Metabolic mapping with cellular resolution: c-fos vs. 2-deoxyglucose.
Sagar, SM; Sharp, FR; Swanson, RA, 1993
)
1.25
"2-deoxyglucose has been widely used to quantitate tissue glucose uptake in vivo, assuming that 2-deoxyglucose is transported and phosphorylated but not further metabolized. "( Incorporation of [3-3H]glucose and 2-[1-14C]deoxyglucose into glycogen in heart and skeletal muscle in vivo: implications for the quantitation of tissue glucose uptake.
Hämäläinen, S; Rissanen, E; Utriainen, T; Virkamäki, A; Yki-Järvinen, H, 1997
)
1.28

Actions

18F-deoxyglucose PET does not allow for metabolic labeling in the majority of untreated primary prostate cancers. 2-Deoxy glucose elicited an increase in glucose 6-phosphate (G-6-P) and a decrease in ATP levels.

ExcerptReferenceRelevance
"18F-deoxyglucose PET does not allow for metabolic labeling in the majority of untreated primary prostate cancers. "( Metabolic imaging of untreated prostate cancer by positron emission tomography with 18fluorine-labeled deoxyglucose.
Bares, R; Büll, U; Effert, PJ; Handt, S; Jakse, G; Wolff, JM, 1996
)
1.07
"2-Deoxyglucose elicited an increase in glucose 6-phosphate (G-6-P) and a decrease in ATP levels and diminished hexokinase binding to mitochondria in single cells."( Metabolic modulation of hexokinase association with mitochondria in living smooth muscle cells.
Carrington, W; Fay, FS; Fogarty, KE; Lynch, RM, 1996
)
0.85

Treatment

2-Deoxyglucose treatment did not lead to complete inhibition of glycolysis. Treatment reduced the concentrations of phosphocreatinine and adenosine triphosphate.

ExcerptReferenceRelevance
"2-deoxyglucose treatment also completely prevented the increase of ATP by BEPH treatment of L1210 cells."( Anti-mitochondrial effects of bisethyl polyamines in mammalian cells.
Beach, DC; Loudy, DE; Snyder, RD,
)
0.69
"2-Deoxyglucose/Na azide treatment also retarded decoupling."( Synergism of energy starvation and dextran-conjugated doxorubicin in the killing of multidrug-resistant KB carcinoma cells.
Chan, H; Cheng, S; Fong, W; Lam, W; Yang, M, 1999
)
0.86
"2-Deoxyglucose treatment did not lead to complete inhibition of glycolysis, was not reversible, and reduced the concentrations of phosphocreatinine and adenosine triphosphate in the heart."( Assessment of techniques for preventing glycolysis in cardiac muscle.
Allen, DG; Pirolo, JS, 1986
)
0.83

Toxicity

ExcerptReferenceRelevance
"psittaci cells had to be ingested by L cells before they were immediately toxic but, once they were phagocytosed, they did not need to multiply or to synthesize macromolecules in order to cause immediate injury to their hosts."( Immediate toxicity of high multiplicities of Chlamydia psittaci for mouse fibroblasts (L cells).
Byrne, GI; Hatch, TP; Kellogg, KR; Moulder, JW, 1976
)
0.26
"In studying the effects of 2-deoxy-D-glucose (2-DG) on the vagus nerve in preoperative patients with duodenal ulcer we have concluded that (1) in initiating gastric acid secretion 2-DG produces a response that is reproducible after 30 days; (2) 2-DG when given in a dose of 40 mg/kg intravenously produces a glucopenic state that appears safe in an otherwise healthy patient."( An assessment of the reproducibility and safety of 2-deoxy-D-glucose as a gastric acid stimulant in duodenal ulcer patients.
Gough, AL; Keddie, NC, 1975
)
0.25
" We now describe a specific toxic effect of 2-DG on the ADR cells, which is more than 15-fold greater than for WT cells."( Effects of 2-deoxyglucose on drug-sensitive and drug-resistant human breast cancer cells: toxicity and magnetic resonance spectroscopy studies of metabolism.
Cohen, JS; Faustino, PJ; Kaplan, O; Lyon, RC; Navon, G; Straka, EJ, 1990
)
0.65
" Thymidine (dThd) protected against the toxic effect of MTX on the cells."( Prevention by thymidine against toxicity and glucose uptake inhibition of methotrexate on cultured Ehrlich ascites tumour cells.
Choy, YM; Fung, KP; Lam, WP; Ng, SW, 1986
)
0.27
" Similarly synthesized nonradioactive FDG and Na 18F were not toxic under comparable experimental conditions."( Transient toxicity of 2-deoxy-2-[18F]fluoro-D-glucose in mammalian cells: concise communication.
Adelstein, SJ; Fowler, JG; Kassis, AI; Shiue, CY; Wolf, AP, 1983
)
0.27
" These results indicate that a toxic regimen of METH selectively causes striatal energy impairment and raise the possibility that perturbations of energy metabolism play a role in METH-induced dopaminergic neurotoxicity."( Rapid ATP loss caused by methamphetamine in the mouse striatum: relationship between energy impairment and dopaminergic neurotoxicity.
Chan, P; DeLanney, LE; Di Monte, DA; Irwin, I; Langston, JW; Luo, JJ, 1994
)
0.29
" METH's toxic effects on brain 5-HT neurons were either unaffected or exacerbated by 2-DG, depending on species, brain region, and dose of METH tested."( Effects of 2-deoxy-D-glucose on methamphetamine-induced dopamine and serotonin neurotoxicity.
Callahan, B; Hatzidimitriou, G; Ricaurte, G; Stover, G; Yuan, J, 1998
)
0.3
" In this study, the changes in the cellular and extracellular concentrations of these alpha-oxoaldehydes were investigated in murine P388D1 macrophages during necrotic cell death induced by median toxic concentrations of hydrogen peroxide and 1-chloro-2,4-dinitrobenzene (CDNB)."( Accumulation of alpha-oxoaldehydes during oxidative stress: a role in cytotoxicity.
Abordo, EA; Minhas, HS; Thornalley, PJ, 1999
)
0.3
" We report that, at high concentrations (300 microM-30 mM), a folic acid hexaglutamate analog is dose-dependently toxic to dissociated rat cortical cultures and that this toxicity is reversed by 2-PMPA, a potent and selective NAALADase inhibitor."( Toxicity induced by a polyglutamated folate analog is attenuated by NAALADase inhibition.
Olkowski, JL; Slusher, BS; Thomas, AG; Vornov, JJ, 1999
)
0.3
" LD50 of 2DG was found to be >8000 mg/kg in mice and rats, and at this dose no death was observed."( Acute toxicity and cardio-respiratory effects of 2-deoxy-D-glucose: a promising radio sensitiser.
Bag, BC; Dube, SN; Dwarakanath, BS; Kaushik, MP; Kumar, D; Pandey, KS; Ravindranath, T; Sekhar, K; Singh, R; Vijayaraghavan, R, 2006
)
0.33
"2DG is a safe compound but can cause a fall in the blood pressure and a decrease in respiratory frequency at high doses."( Acute toxicity and cardio-respiratory effects of 2-deoxy-D-glucose: a promising radio sensitiser.
Bag, BC; Dube, SN; Dwarakanath, BS; Kaushik, MP; Kumar, D; Pandey, KS; Ravindranath, T; Sekhar, K; Singh, R; Vijayaraghavan, R, 2006
)
0.33
" In PD-fluids GDPs have been shown in many different in vitro assays to be responsible for adverse effects such as growth inhibition, and impaired leukocyte function and impaired wound healing of peritoneal mesothelial cells."( 3,4-DGE is important for side effects in peritoneal dialysis what about its role in diabetes.
Benito, A; Justo, P; Kjellstrand, P; Linden, T; Ortiz, A; Sanchez-Niño, MD; Santamaria, B; Sanz, A; Wieslander, A, 2006
)
0.33
" There were no toxic effects of 2DG at doses of 500mg/kg/day on body weight or general health."( Behavioral, cognitive, and safety profile of 2-deoxy-2-glucose (2DG) in adult rats.
Gielissen, JM; Groble, K; Levenick, CV; Munsey, K; Ockuly, JC; Stafstrom, CE; Sutula, TP; Zeal, C, 2012
)
0.38
" Safety endpoints included hypoglycemia and any adverse events."( Efficacy and safety of sitagliptin as add-on therapy on glycemic control and blood glucose fluctuation in Japanese type 2 diabetes subjects ongoing with multiple daily insulin injections therapy.
Araki, E; Furukawa, N; Goto, R; Ichimori, S; Iwashita, S; Kawashima, J; Kondo, T; Maeda, T; Matsumura, T; Matsuo, T; Matsuo, Y; Motoshima, H; Nishida, K; Sekigami, T; Shimoda, S, 2013
)
0.39
"The collection of adverse effects (AEs) and medical supervision of vital parameters and biological variables allowed the safety evaluation."( Safety, Biodistribution, and Dosimetry of 123I-6-Deoxy-6-Iodo-D-Glucose, a Tracer of Glucose Transport, in Healthy and Diabetic Volunteers.
Ahmadi, M; Barone-Rochette, G; Calizzano, A; Desruet, MD; Djaileb, L; Fagret, D; Ghezzi, C; Perret, P; Reboulet, G; Vanzetto, G, 2019
)
0.51
"No major adverse events were observed."( Safety, Biodistribution, and Dosimetry of 123I-6-Deoxy-6-Iodo-D-Glucose, a Tracer of Glucose Transport, in Healthy and Diabetic Volunteers.
Ahmadi, M; Barone-Rochette, G; Calizzano, A; Desruet, MD; Djaileb, L; Fagret, D; Ghezzi, C; Perret, P; Reboulet, G; Vanzetto, G, 2019
)
0.51
" Considering glycolysis inhibitors as therapeutic agents, their specific delivery to cancer cells is critical not to induce adverse effects."( Nanoparticle-Mediated Delivery of 2-Deoxy-D-Glucose Induces Antitumor Immunity and Cytotoxicity in Liver Tumors in Mice.
Egashira, K; Fukuda, K; Hara, Y; Hino, K; Nishina, S; Sasaki, K; Yamamura, M; Yamauchi, A, 2021
)
0.62
" Combining 2-DG with buforin IIb had a synergistic toxic effect on DU145 cells and mouse xenograft tumors."( 2-Deoxy-d-glucose Promotes Buforin IIb-Induced Cytotoxicity in Prostate Cancer DU145 Cells and Xenograft Tumors.
Chen, Y; Liu, K; Liu, P; Wanyan, Y; Wen, J; Xu, X; Zhang, H; Zhang, R; Zhen, J, 2020
)
0.56

Pharmacokinetics

ExcerptReferenceRelevance
" In pharmacokinetic studies, HL-60/AR cells exposed to different extracellular concentrations of [14C]DNR consistently accumulated less radioactive drug than the parent HL-60 cells."( Intracellular distribution and pharmacokinetics of daunorubicin in anthracycline-sensitive and -resistant HL-60 cells.
Baker, MA; Bhalla, K; Gervasoni, JE; Hindenburg, AA; Krishna, S; Lutzky, J; Rosado, M; Stewart, VJ; Taub, RN, 1989
)
0.28
" The pharmacokinetic implications of these physiological measurements with respect to drug delivery to tumor tissue are discussed."( Regional blood flow, capillary permeability, and glucose utilization in two brain tumor models: preliminary observations and pharmacokinetic implications.
Blasberg, RG; Kobayashi, T; Miyoaka, M; Patlak, CS; Rice, JM; Shapiro, WR; Shinohara, M, 1981
)
0.26
" Pharmacological and pharmacokinetic studies of DN-108 were done."( Pharmacological and pharmacokinetic studies of the newly synthesized thiazolidinedione derivative 5-(4-(1-phenyl-1-cyclopropanecarbonylamino)benzyl)-thiazolidine-2 ,4-dio ne.
Hayashibe, M; Ino, Y; Kurumi, M; Matsuzaki, Y; Muta, Y; Nomura, Y; Suzuki, S; Ueda, N, 1998
)
0.3
" We then assessed the bio-distribution and pharmacokinetic properties of 6-FDG-GNPs in vivo using a murine model."( Pharmacokinetic and toxicological evaluation of multi-functional thiol-6-fluoro-6-deoxy-D-glucose gold nanoparticles in vivo.
Chen, J; Kong, B; Roa, W; Song, K; Wilson, J; Xing, JZ; Xiong, Y; Yang, X, 2012
)
0.38

Compound-Compound Interactions

The present study examined the anti-herpetic effect of the glycoprotein inhibitors, hydroxynorvaline and 2-deoxyglucose, alone and in combination with trifluridine on murine ocular herpes.

ExcerptReferenceRelevance
"The present study examined the anti-herpetic effect of the glycoprotein inhibitors, hydroxynorvaline and 2-deoxyglucose, alone and in combination with trifluridine on murine ocular herpes."( Efficacy of glycoprotein inhibitors alone and in combination with trifluridine in the treatment of murine herpetic keratitis.
Araullo-Cruz, T; Blough, HA; Cheng, KP; Gordon, YJ; Johnson, BJ; Romanowski, E, 1986
)
0.48
" Prenatal mortality was increased by Rh 123 in combination with 2-DOG, with values of 40%, 43%, or 41% dead or resorbed at Rh 123 doses of 8, 12, or 15 mg/kg/day, respectively."( Teratogenic effects of a lipophilic cationic dye rhodamine 123, alone and in combination with 2-deoxyglucose.
Hood, RD; Jones, CL; Ranganathan, PN; Ranganathan, S, 1988
)
0.49
" The current work tests the hypothesis that 2-deoxy-d-glucose (2DG) combined with cisplatin [cis-diamminedichloroplatinum(II)] can enhance cytotoxicity in human head and neck cancer cells (FaDu) by mechanisms involving oxidative stress."( 2-Deoxy-D-glucose combined with cisplatin enhances cytotoxicity via metabolic oxidative stress in human head and neck cancer cells.
Ahmad, IM; Dornfeld, KJ; Mattson, DM; Simons, AL; Spitz, DR, 2007
)
0.34
" These results show that treatment of human prostate cancer cells with the combination of 2DG (a nutrient stress) and overexpression of the tumor suppressor gene, wtp53, enhances clonogenic cell killing by a mechanism that involves oxidative stress as well as allowing for the speculation that inhibitors of glucose and hydroperoxide metabolism can be used in combination with Adp53 gene therapy to enhance therapeutic responses."( 2-Deoxyglucose combined with wild-type p53 overexpression enhances cytotoxicity in human prostate cancer cells via oxidative stress.
Abdalla, MY; Ahmad, IM; Aykin-Burns, N; Domann, FE; Oberley, LW; Simons, AL; Spitz, DR, 2008
)
1.07
"The present study analyses the effect of two plant phenolic compounds, namely chlorogenic acid and ferulic acid, and a plant alkaloid, berberine, alone and also in combination with two commercial oral hypoglycemic drugs (OHD), namely metformin and 2,4-thiazolodinedione (THZ), on the uptake of 2-deoxyglucose (2DG) by L6 myotubes."( Synergistic effect of phytochemicals in combination with hypoglycemic drugs on glucose uptake in myotubes.
Doble, M; Prabhakar, PK, 2009
)
0.53
", l-buthionine-S,R-sulfoximine, BSO) metabolism were utilized in combination with a chemotherapeutic agent, paclitaxel (PTX), thought to induce oxidative stress, to treat breast cancer cells."( Paclitaxel combined with inhibitors of glucose and hydroperoxide metabolism enhances breast cancer cell killing via H2O2-mediated oxidative stress.
Aykin-Burns, N; Coleman, MC; Hadzic, T; Jacobson, GM; Leick, K; Spitz, DR; Zhu, Y, 2010
)
0.36
"This phase I trial was initiated to evaluate the safety, pharmacokinetics (PK) and maximum tolerated dose (MTD) of the glycolytic inhibitor, 2-deoxy-D-glucose (2DG) in combination with docetaxel, in patients with advanced solid tumors."( A phase I dose-escalation trial of 2-deoxy-D-glucose alone or combined with docetaxel in patients with advanced solid tumors.
Chiorean, EG; Dipaola, RS; Jung, DT; Kroll, S; Kurtoglu, M; Lampidis, TJ; Langmuir, VK; Papadopoulos, K; Raez, LE; Ricart, AD; Rocha Lima, CM; Rosenblatt, J; Schlesselman, JJ; Stein, MN; Tolba, K, 2013
)
0.39
"The recommended dose of 2DG in combination with weekly docetaxel is 63 mg/kg/day with tolerable adverse effects."( A phase I dose-escalation trial of 2-deoxy-D-glucose alone or combined with docetaxel in patients with advanced solid tumors.
Chiorean, EG; Dipaola, RS; Jung, DT; Kroll, S; Kurtoglu, M; Lampidis, TJ; Langmuir, VK; Papadopoulos, K; Raez, LE; Ricart, AD; Rocha Lima, CM; Rosenblatt, J; Schlesselman, JJ; Stein, MN; Tolba, K, 2013
)
0.39
"To examine the antagonistic effects of anti-extracellular matrix metalloprotease inducer (anti-EMMPRIN) antibody when combined with chemotherapy using a hypovascular pancreatic tumor model."( Antagonistic effects of anti-EMMPRIN antibody when combined with chemotherapy against hypovascular pancreatic cancers.
Beasley, TM; Boothman, DA; Buchsbaum, DJ; Kim, H; Lee, SK; Li, LS; Martin, A; Rigell, CJ; Samuel, SL; Stockard, CR; Umphrey, HR; Zhai, G; Zinn, KR, 2014
)
0.4
" Similarly, tumor growth was significantly suppressed by β-lapachone alone, and additive effects were noted when combined with gemcitabine, but the therapeutic efficacy was reduced when anti-EMMPRIN antibody was added."( Antagonistic effects of anti-EMMPRIN antibody when combined with chemotherapy against hypovascular pancreatic cancers.
Beasley, TM; Boothman, DA; Buchsbaum, DJ; Kim, H; Lee, SK; Li, LS; Martin, A; Rigell, CJ; Samuel, SL; Stockard, CR; Umphrey, HR; Zhai, G; Zinn, KR, 2014
)
0.4
" We hypothesized that BBR in combination with 2-DG would be more efficient than either agent alone against cancer cell growth."( Berberine combined with 2-deoxy-d-glucose synergistically enhances cancer cell proliferation inhibition via energy depletion and unfolded protein response disruption.
Fan, LX; Gao, AH; Li, J; Liu, CM; Zhou, YB, 2013
)
0.39
"BBR combined with 2-DG synergistically enhanced the growth inhibition of cancer cells in vitro."( Berberine combined with 2-deoxy-d-glucose synergistically enhances cancer cell proliferation inhibition via energy depletion and unfolded protein response disruption.
Fan, LX; Gao, AH; Li, J; Liu, CM; Zhou, YB, 2013
)
0.39
"To investigate the antineoplastic effects of 2-Deoxy-D-glucose (2-DG) combined with Taxol on orthotopically transplanted breast cancer in C3H mice and explore the mechanism."( [2-Deoxy-D-glucose combined with Taxol inhibits VEGF expression and induces apoptosis in orthotopically transplanted breast cancer in C3H mice].
Chen, C; Cheng, Z; Gan, H; Jiang, C; Jiang, Z; Liu, H; Zhang, Q; Zhao, S, 2014
)
0.4
"2-DG combined with Taxol obviously suppressed the tumor growth with a tumor inhibition rate of 66."( [2-Deoxy-D-glucose combined with Taxol inhibits VEGF expression and induces apoptosis in orthotopically transplanted breast cancer in C3H mice].
Chen, C; Cheng, Z; Gan, H; Jiang, C; Jiang, Z; Liu, H; Zhang, Q; Zhao, S, 2014
)
0.4
" Additive effects were seen when these molecules were combined with 3PO."( Inhibition of Growth of Bladder Cancer Cells by 3-(3-Pyridinyl)-1-(4-pyridinyl)-2-propen-1-one in Combination with Other Compounds Affecting Glucose Metabolism.
Altayyar, M; desBordes, C; Lea, MA, 2015
)
0.42
" Of interest are results indicating that rapamycin, which similarly to BRB, suppresses mTOR signaling, when combined with 2-dG shows no synergistic properties."( Synergy of 2-deoxy-D-glucose combined with berberine in inducing the lysosome/autophagy and transglutaminase activation-facilitated apoptosis.
Darzynkiewicz, Z; Garcia, J; Halicka, HD; Li, J; Zhao, H, 2017
)
0.46
"To investigate the effect of 2-deoxy-d-glucose (2-DG) combined with hydroxycamptothecin (HCPT) on anti-tumor activity of breast cancer cells and its mechanism."( [Synergistic Effect of 2-deoxy-D-glucose Combined with Hydroxycamptothecin on Apoptosis of Breast Cancer Cells].
Ge, XM; Li, JH; Liu, H; Liu, YM; Sun, XJ; Zhang, P; Zhen, YN, 2019
)
0.51
"5, 5, 10, 20 mmol/L), HCPT(0, 5, 10, 20, 40 μmol/L) and 2-DG (5 mmol/L) combined with HCPT."( [Synergistic Effect of 2-deoxy-D-glucose Combined with Hydroxycamptothecin on Apoptosis of Breast Cancer Cells].
Ge, XM; Li, JH; Liu, H; Liu, YM; Sun, XJ; Zhang, P; Zhen, YN, 2019
)
0.51

Bioavailability

ExcerptReferenceRelevance
" In vitro radioiron uptake by isolated cells occurs by passive diffusion, is not regulated by the animal's iron status, and is primarily a function of bioavailability of iron in the incubating medium."( Iron transport by isolated rat intestinal mucosal cells.
Cook, JD; Savin, MA, 1978
)
0.26
" Thus the fundamental kinetics of AG were recognized as follows: 1) AG in the body originates mainly from foods and is well absorbed in the intestine, 2) AG is little degraded and metabolized in the body, and 3) an equilibrium exists between oral supplement plus a small but steady amount of de novo synthesis and excretion in urine."( Origin and disposal of 1,5-anhydroglucitol, a major polyol in the human body.
Akanuma, H; Akaoka, I; Minoda, S; Miyashita, H; Moromizato, H; Shinohara, T; Tachibana, Y; Yamanouchi, T, 1992
)
0.28
" The absorption rate of 3DG was obviously lower in comparison with that of glucose."( Metabolism of 3-deoxyglucosone, an intermediate compound in the Maillard reaction, administered orally or intravenously to rats.
Hayase, F; Kato, H; Sekiya, F; Shinoda, T; van Chuyen, N, 1990
)
0.28
" This substance is derived mainly from food, is well absorbed in the intestine, and is distributed to all organs and tissues."( Serum 1,5-anhydroglucitol (1,5 AG): new clinical marker for glycemic control.
Akanuma, Y; Yamanouchi, T, 1994
)
0.29
" Impairment of glucose bioavailability reduced Rh 123 fluorescence."( Mitochondrial membrane potential measurement in rat cerebellar neurons by flow cytometry.
Camarasa, J; Camins, A; Comas, J; Escubedo, E; Gabriel, C; Sureda, FX, 1997
)
0.3
"The present study demonstrates the potential of hematoporphyrin derivative pretreatment in increasing the bioavailability of 2-DG in a mice Ehrlich ascites tumor model."( Optimization of tumor radiotherapy. Part VI: Modification of tumor glucose metabolism for increasing the bioavailability of 2-deoxy-D-glucose (2-DG) in a murine tumor model.
Degaonkar, M; Jain, V; Maitra, A; Raghunathan, P; Sharma, RK; Singh, S, 2000
)
0.31
" Since typical substrates for intestinal carriers are hydrophilic and charged, the involvement of putative absorptive carriers in the transport of CPT is a novel finding that may give insight into the erratic oral bioavailability of CPTs observed in the clinic."( The intestinal absorption of camptothecin, a highly lipophilic drug, across Caco-2 cells is mediated by active transporter(s).
Gupta, E; Lallo, A; Luo, F; Ramanathan, S; Rubin, E; Sinko, P; Vyas, V,
)
0.13
" Although the core structure of these inhibitors is charged, good oral bioavailability has been observed in rat for some compounds."( Discovery and SAR of a novel selective and orally bioavailable nonpeptide classical competitive inhibitor class of protein-tyrosine phosphatase 1B.
Andersen, HS; Bakir, F; Branner, S; Christensen, MS; Collins, T; Hansen, TK; Iversen, LF; Jeppesen, L; Judge, L; Lau, JF; Moran, EJ; Mortensen, SB; Møller, NP; Newman, MJ; Olsen, OH; Ripka, WC; Shahbaz, M; Su, J; Sørensen, AL; Vo, T, 2002
)
0.31
" There is no information on the mechanism of vitamin C transport across the intestinal barrier, a step that determines the bioavailability of vitamin C in humans."( Up-regulation and polarized expression of the sodium-ascorbic acid transporter SVCT1 in post-confluent differentiated CaCo-2 cells.
Bachem, M; Bustamante, ME; Cárcamo, JG; Grünert, A; Henríquez, EA; Kempe, S; Maulén, NP; Nualart, F; Schmid-Kotsas, A; Vera, JC, 2003
)
0.32
" These findings suggest that α-DC bioavailability could actually depend not on food content but rather on reactions occurring during digestion."( Free α-dicarbonyl compounds in coffee, barley coffee and soy sauce and effects of in vitro digestion.
Gazzani, G; Mascherpa, D; Papetti, A, 2014
)
0.4

Dosage Studied

In four dogs with chronic pancreatic and gastric fistulas, dose-response studies of pancreatic bicarbonate and protein secretion were done with intravenous infusions of secretin, octapeptide of cholecystokinin (OP-CCK), and 2-deoxyglucose. On a high-fat diet, Rad tg mice develop more severe glucose intolerance than the wild-type mice.

ExcerptRelevanceReference
" This resulted in a two- to fourfold leftward shift in the insulin dose-response curves in muscles from both groups compared with control."( Effect of fasting and streptozotocin diabetes on insulin binding and action in the isolated mouse soleus muscle.
Freychet, P; Le Marchand-Brustel, Y, 1979
)
0.26
" Dose-response curves of 3-day uterotrophic assays indicate that biological potency follows the order EE3CPE greater than EE3 or estradiol greater than E3CPE greater than E3."( Temporal relationships between hormone receptor binding and biological responses in the uterus: studies with short- and long-acting derivatives of estriol.
Katzenellenbogen, BS; Lan, NC, 1976
)
0.26
" These findings represent a rightward shift in the insulin dose-response curve in the cells from the older, fatter animals, and this is the predicted functional sequelae of the observed decrease in insulin receptors."( The effects of spontaneous obesity on insulin binding, glucose transport, and glucose oxidation of isolated rat adipocytes.
Olefsky, JM, 1976
)
0.26
", a rightward shift in the insulin dose-response curve for 2-deoxy glucose uptake, was observed, and (d) since the decreased rates of insulin-mediated glucose oxidation can not be attributed to changes in insulin receptors or to changes in glucose transport, an intracellular defect in glucose metabolism is suggested."( The effects of spontaneous obesity on insulin binding, glucose transport, and glucose oxidation of isolated rat adipocytes.
Olefsky, JM, 1976
)
0.26
" When similar studies were applied to muscles of gold thioglucose obese or genetically obese (ob/ob) mice, and compared to lean controls: a) insulin binding was decreased; b) the insulin dose-response curve of 2-deoxyglucose uptake was shifted to the right; c) maximally insulin-stimulated 2-deoxyglucose uptake, glycolysis, and glycogen synthesis were markedly decreased."( Insulin binding and effects in isolated soleus muscle of lean and obese mice.
Freychet, P; Jeanrenaud, B; Le Marchand-Brustel, Y, 1978
)
0.44
" The dose-response relationships and kinetics of histamine and BK-A release from antigen-challenged peripheral leukocytes are similar."( Anaphylactic relase of a basophil kallikrein-like activity. II. A mediator of immediate hypersensitivity reactions.
Lichtenstein, LM; Newball, HH; Talamo, RC, 1979
)
0.26
" Analysis of dose-response curves shows that for pepsin secretion the Vmax values were raised by this procedure."( The secretion of pepsin.
Kondo, T; Magee, DF, 1977
)
0.26
" After PCV, the response to 200 mg/kg 2DG was reduced by about 70% for acid and 80% for pepsin; the slopes of the dose-response curves were significantly reduced after PCV."( Parietal cell vagotomy in dogs. A comparative study of the effects on gastric secretion and antral muscle contraction.
Boiselle, JC; Rozé, C; Vatier, J, 1978
)
0.26
" If a depression of brain metabolism is responsible for the previously reported protection of the brain from ischemic damage, these data suggest a substantial reduction of brain metabolic rate is achieved in the rat at a barbiturate dosage which may be therapeutically relevant in the human after acute brain ischemia."( Dose dependent reduction of glucose utilization by pentobarbital in rat brain.
Braun, LD; Cornford, EM; Crane, PD; Cremer, JE; Glass, JM; Oldendorf, WH,
)
0.13
" The rise in free fatty acids and glycerol in response to norepinephrine had the same time-course and dose-response characteristics in the sham-operated and lesioned animals, indicating comparable degrees of peripheral responsiveness to this hormone."( Ventromedial hypothalamic lesions and the mobilization of fatty acids.
Bray, GA; Nishizawa, Y, 1978
)
0.26
"A dose-response relationship for the effects of 2-deoxy-D-glucose (2-DG) (0-400 mg/kg) on food intake was established in normal and obese ventromedial hypothalamic lesioned rats."( Delayed response to 2-deoxy-D-glucose in hypothalamic obese rats.
Grossman, SP; King, BM; Stamoutsos, BA, 1978
)
0.26
" Rats subjected to daily injections at this dosage did not develop more intense seizures, and afterdischarges essentially stopped after the first injection."( Kindling of neuroanatomic pathways during recurrent focal penicillin seizures.
Collins, RC, 1978
)
0.26
" This rightward shift in the dose-response relationship was also observed when deoxyglucose uptake was monitored in soleus muscles from obese rats."( Insulin response in skeletal muscle and fat cells of the genetically obese Zucker rat.
Becker, SG; Czech, MP; Gitomer, W; Heinrich, J; Richardson, DK; Walters, CG, 1978
)
0.49
" The diminished uterine response is not due to a shift in the dose-response curve for E2, but results from a decrease in the magnitude of the maximum uterine response."( Regulation of the uterine response to estrogen by thyroid hormone.
Gardner, RM; Ireland, JS; Kirkland, JL; Stancel, GM, 1978
)
0.26
" Desalivate rats showed a marked attenuation of feeding (and prandial drinking) at low doses, but when wet mash was given instead of pellets and water a normal dose-response relationship was obtained."( Feeding and drinking interactions after acute butyrophenone administration.
Engle, DJ; Rowland, N, 1977
)
0.26
"In four dogs with chronic pancreatic and gastric fistulas, dose-response studies of pancreatic bicarbonate and protein secretion were done with intravenous infusions of secretin, octapeptide of cholecystokinin (OP-CCK), and 2-deoxyglucose (2-DG)."( Effect of extragastric and truncal vagotomy on pancreatic secretion in the dog.
Debas, HT; Grossman, MI; Konturek, SJ, 1975
)
0.44
" These results may be accounted for by the low dosage used."( Sensitivity of central chemoreceptors controlling blood glucose and body temperature during glucose deprivation.
Fiorentini, A; Müller, EE, 1975
)
0.25
" Combinations of ZOL and 2DG produced supraadditive antinociception, even though ZOL failed to significantly shift the 2DG dose-response curve to the left."( Potentiation of 2-deoxy-D-glucose antinociception, but not hyperphagia by zolantidine, a histamine (H2) receptor antagonist.
Bodnar, RJ; Hough, LB; Koch, JE, 1992
)
0.28
"The metabolic potency of recombinant human insulin-like growth factor II was studied in anaesthetized adult rats by obtaining dose-response curves for the hypoglycaemic action and for the stimulation of glucose metabolism during euglycaemic clamping."( Acute actions of insulin-like growth factor II on glucose metabolism in adult rats.
Hartmann, H; Stümpel, F, 1992
)
0.28
" Both phenotypic classes of PC12 cells respond to aurintricarboxylic acid with similar dose-response characteristics."( Nerve growth factor withdrawal-induced cell death in neuronal PC12 cells resembles that in sympathetic neurons.
Green, SH; Mesner, PW; Winters, TR, 1992
)
0.28
" In contrast, 2-DG antinociception on the jump test was significantly potentiated across the 120-min time course and across the 2-DG dose-response curve (100-650 mg/kg) by methysergide, ritanserin, and ICS-205,930 pretreatment."( 2-Deoxy-D-glucose antinociception and serotonin receptor subtype antagonists: test-specific effects in rats.
Bodnar, RJ; Fisher, MC, 1992
)
0.28
" However, the dose-response curve of insulin-stimulated thymidine incorporation in CHO-F/Y CT2 was shifted to the left (approximately 5-7-fold) compared with that in CHO-HIR."( Enhanced insulin-induced mitogenesis and mitogen-activated protein kinase activities in mutant insulin receptors with substitution of two COOH-terminal tyrosine autophosphorylation sites by phenylalanine.
Akanuma, Y; Ando, A; Kaburagi, Y; Koshio, O; Momomura, K; Sakura, H; Tamori, Y; Tobe, K; Yamamoto-Honda, R; Yazaki, Y, 1992
)
0.28
" Since all patients were scanned while on their current medication regimen, the duration and dosage of the medication of the two patient groups were compared."( Regional metabolism in microsmic patients with schizophrenia.
Clark, C; Hurwitz, T; Kopala, L; Li, D, 1991
)
0.28
" Insulin dose-response curves indicated maximal stimulation of hexose uptake at 1-2 nM insulin for both control and diabetic subjects and demonstrated a significant decrease in maximal insulin response in the latter."( Insulin-stimulated glucose transport in circulating mononuclear cells from nondiabetic and IDDM subjects.
Bilan, PJ; Daneman, D; Elliott, ME; Klip, A; Zinman, B, 1992
)
0.28
"The cognitive-enhancing effects of pramiracetam in animal models of learning and memory are characterized by an inverted U-shaped dose-response curve."( Nootropic drugs in Alzheimer's disease: symptomatic treatment with pramiracetam.
Blin, J; Chase, TN; Claus, JJ; Giuffra, M; Ludwig, C; Mohr, E, 1991
)
0.28
" Dose-response curves for both insulin-stimulated thymidine uptake and 5-bromo-2-deoxyuridine incorporation in the Y/F2 cell lines were shifted to the left (4-10-fold) compared with those observed in the cells expressing similar numbers of wild type receptors."( Mutation of the two carboxyl-terminal tyrosines results in an insulin receptor with normal metabolic signaling but enhanced mitogenic signaling properties.
Olefsky, JM; Takata, Y; Webster, NJ, 1991
)
0.28
" The inhibition of EGF stimulation by FGF is across the EGF dose-response curve, present at high and low culture densities, and stable for at least 3 days."( Fibroblast growth factor inhibits epidermal growth factor-induced responses in rat astrocytes.
Huff, KR; Schreier, W, 1990
)
0.28
" Reversibility of cirrhosis was dosage dependent; complete recovery occurred in the low- but not the high-dose group by Day 15."( Assessment of hepatic indicators of subchronic carbon tetrachloride injury and recovery in rats.
Allis, JW; Seely, JC; Simmons, JE; Ward, TR, 1990
)
0.28
" The dose-response curves for lactate production and DG uptake were similar."( Interleukin 1 stimulates hexose transport in fibroblasts by increasing the expression of glucose transporters.
Baldwin, SA; Bird, TA; Davies, A; Saklatvala, J, 1990
)
0.28
" In mice pre-transplanted with EL-4 cells, T-2-mAb increased the mean survival time (MST) with a direct dosage dependence."( Antitumor activity of T-2 toxin-conjugated monoclonal antibody to murine thymoma.
Chiba, J; Kawamura, O; Murakami, H; Ohi, K; Ohtani, K; Otokawa, M; Shibuya, O; Ueno, Y, 1990
)
0.28
" Dose-response experiments revealed that insulin stimulated D-glucose transport and 2-deoxyglucose uptake between 10(-11) and 10(-7) M with a maximal four- to sixfold stimulation."( Stimulation of glucose transport by insulin and norepinephrine in isolated rat brown adipocytes.
Bukowiecki, LJ; Marette, A, 1989
)
0.5
" The dose-response curve for insulin stimulation of glucose transport was strongly shifted to the right by pertussis-toxin treatment [EC50 (half-maximally effective insulin concn."( Role of guanine nucleotide regulatory proteins in insulin stimulation of glucose transport in rat adipocytes. Influence of bacterial toxins.
Ciaraldi, TP; Maisel, A, 1989
)
0.28
" Insulin (8 h) increased the quantity of glucose transporters, with a maximal twofold increase at 10(-7) M and a dose-response curve similar to that for insulin stimulation of glucose uptake."( Coordinate regulation of glucose transporter function, number, and gene expression by insulin and sulfonylureas in L6 rat skeletal muscle cells.
Flier, JS; Moller, D; Nayak, RC; Smith, RJ; Wang, PH, 1989
)
0.28
" The overall pattern of decreased glucose use seen with progabide was different from that noted with previously studied GABA-mimetic drugs, such as muscimol, except for those changes observed in the extrapyramidal and sensory-motor areas for which similar dose-response relationships occurred."( Effects of the GABA receptor agonist, progabide, upon local cerebral glucose utilization.
Cudennec, A; Duverger, D; Lloyd, KG; MacKenzie, ET; McCulloch, J; Motohashi, N; Nishikawa, T; Scatton, B, 1987
)
0.27
" The appearance of eating and pica at the same dosage suggested that rats may eat food as well as a nonnutritive substance as a species-specific reaction to illness and that postdrug feeding, including that observed after 2DG, is an insufficient condition for concluding that a treatment produces no internal distress."( Patterns of increased and decreased ingestive behavior after injections of lithium chloride and 2-deoxy-D-glucose.
Leitner, C; Watson, PJ, 1988
)
0.27
" In 5F, the dose-response relationships for cAMP and insulin secretion were superimposable."( Characteristics of the interaction of the glucagon receptor, cAMP, and insulin secretion in parent cells and clone 5F of a cultured rat insulinoma.
Bhathena, SJ; Korman, LY; Oie, HK; Recant, L; Voyles, NR, 1985
)
0.27
" The dose-response curve for insulin-stimulated 2-[3H]deoxyglucose transport is shifted to the right (ED50 greater than 100 nM) immediately after insulin washout but is normal by 1 h after insulin washout."( (Thr-59)-insulin-like growth factor I stimulates 2-deoxyglucose transport in BC3H1 myocytes through the insulin-like growth factor receptor, not the insulin receptor.
Cascieri, MA; Chicchi, GG; Hayes, NS; Strader, CD, 1986
)
0.77
" This change occurs in parallel with a moderate rightward shift in the insulin dose-response curve."( Isoproterenol reduces insulin stimulation of hexose uptake by rat adipocytes via a postinsulin binding alteration.
Arsenis, G; Livingston, JN, 1986
)
0.27
" Acute administration of an additional 10 IU ACTH to hypophysectomized rats on maintenance dosage of ACTH resulted in decreased SAM-DC activity in both adrenal medulla and cortex."( Decreased activity of adrenal S-adenosylmethionine decarboxylase in rats subjected to dopamine agonists, metabolic stress, or bodily immobilization.
Ekker, M; Sourkes, TL, 1987
)
0.27
" When insulin binding was first inhibited by Ab 47-9, dose-response curves for insulin were markedly shifted to the right for glucose uptake, AIB uptake, and thymidine incorporation into DNA."( Actions of insulin and insulinlike growth factors I and II in cultured microvessel endothelial cells from bovine adipose tissue.
Bar, RS; Boes, M; Dake, B; Dolash, S; Siddle, K, 1988
)
0.27
" Furthermore, 2-deoxyglucose uptake in CS-045-treated adipocytes was increased and the insulin dose-response curve was shifted to the left."( Characterization of new oral antidiabetic agent CS-045. Studies in KK and ob/ob mice and Zucker fatty rats.
Fujiwara, T; Horikoshi, H; Ushiyama, I; Yoshioka, S; Yoshioka, T, 1988
)
0.62
"The dose-response characteristics of several glucose-utilizing tissues (brain, heart, white adipose tissue, brown adipose tissue, and quadriceps muscle) to a single injection of insulin have been compared in control mice and mice made obese with a single injection of gold thioglucose (GTG)."( Insulin response in individual tissues of control and gold thioglucose-obese mice in vivo with [1-14C]2-deoxyglucose.
Astbury, LD; Caterson, ID; Cooney, GJ; Williams, PF, 1987
)
0.49
" Furthermore, we have shown that insulin-generated diacylglycerol satisfies several criteria for a mediator of insulin action, including the demonstration that insulin-stimulated endogenous diacylglycerol generation is antecedent to glucose transport and has an identical insulin dose-response curve and moreover that the magnitude and time course of subsequent stimulation of glucose transport is reproduced by the addition of the simple exogenous diacylglyerol, dioctanoylglycerol, in the complete absence of the hormone."( Insulin-induced glycerolipid mediators and the stimulation of glucose transport in BC3H-1 myocytes.
Cooper, DR; Farese, RV; Pollet, RJ; Standaert, ML, 1988
)
0.27
"Aspects of the mechanism by which insulin stimulates the membrane glucose transport system were examined by assessing the influence of the bilayer lipid structure on transport stimulation characteristics, and considering the form of the insulin dose-response curve."( Insulin stimulation of adipocyte membrane glucose transport. A graded biologic response insensitive to bilayer lipid disordering.
Hyslop, PA; Kuhn, CE; Sauerheber, RD, 1987
)
0.27
" In both age-groups, hypothyroidism increased cellular responsiveness to T3, shifting the dose-response curve to the left."( Effect of hypothyroidism on the in-vivo and in-vitro uptake of sugar by rat thymocytes and on the stimulatory response to 3,5,3'-tri-L-iodothyronine.
Segal, J, 1988
)
0.27
" In a second experiment, the effects of different melatonin doses were studied at the time of day at which melatonin had its maximal effect to determine the dose-response relationship of melatonin-induced inhibition of SCN 2-DG uptake."( Effects of melatonin on 2-deoxy-[1-14C]glucose uptake within rat suprachiasmatic nucleus.
Cassone, VM; Moore, RY; Roberts, MH, 1988
)
0.27
" The tendency of a 750 mg/kg dosage to produce a longer-term hypophagic reaction was more evident in animals given pellets instead of the liquid diet."( Intake of a liquid diet after 2-deoxy-D-glucose injections in rats.
Bartles, RR; Hawkins, C; McKinney, J; Rhea, K; Rhodes, DH; Watson, PJ, 1986
)
0.27
", increased insulin sensitivity) manifested by a leftward shift in the 2-deoxyglucose dose-response curve."( Insulin induces progressive insulin resistance in cultured rat adipocytes. Sequential effects at receptor and multiple postreceptor sites.
Garvey, WT; Marshall, S; Olefsky, JM, 1986
)
0.5
" The potentiation of insulin action follows a dose-response relationship with kallikrein and bradykinin concentrations consistent with a physiological role for the latter in the modulation of insulin action."( Potentiation of insulin stimulation of hexose transport by kallikrein and bradykinin in isolated rat adipocytes.
Goldman, J; Pfister, D; Vukmirovich, R, 1987
)
0.27
" In general, these data indicated that malaise may be an important influence of 2DG; but dosage and time course parameters associated with post-drug reductions in drinking suggested that a separable consummatory inhibition effect may also occur."( Inhibited drinking and pica in rats following 2-deoxy-D-glucose.
Bartles, RR; Beatey, S; Hawkins, C; McKinney, J; Rhea, K; Watson, PJ, 1987
)
0.27
" Dose-response relationships were calculated for the effects of gastrin on pancreatic secretion."( Pancreatic responses to endogenous and exogenous gastrin in the dog.
Devaux, MA; Johnson, CD; Sarles, H; Treffot, MJ, 1987
)
0.27
" The dose-effect curve for the adult rats was similar in shape to that for the aged rats, but the peak was much lower and occurred at the lowest dosage (0."( Effects of prolonged co-dergocrine mesylate (Hydergine) treatment on local cerebral glucose uptake in aged Fischer 344 rats.
Meier-Ruge, W, 1986
)
0.27
" One-week dosing of Indeloxazine at 2 mg/kg showed slight increases in ATP and total adenine nucleotides levels."( [Effects of indeloxazine hydrochloride on brain energy and glucose metabolism in the four-vessel occlusion rat model].
Kogure, K; Ohtomo, H; Sakamoto, N, 1986
)
0.27
" A rigorous system of analysis was devised making use of the dose-response profiles in each of the 61 brain areas to construct a regional hierarchy of responsiveness to the three drugs and allowing comparison of their effects on the brain as a whole."( The effect of diazepam upon local cerebral glucose use in the conscious rat.
Ford, I; Kelly, PA; McCulloch, J, 1986
)
0.27
" As seen with anti-R from a previous patient, desensitization consisted of both a dramatic decrease in the maximal responsiveness of the cells to insulin and a shift in the dose-response curve for insulin-stimulated glucose oxidation."( Autoantibodies against the insulin receptor. Dissociation of the acute effects of the antibodies from the desensitization seen with prolonged exposure.
Grunfeld, C; Jones, DS; Shigenaga, JK, 1985
)
0.27
" Dose-response curves for insulin action during the euglycemic clamp vary considerably among different target tissues in the rat."( Dose-response curves for in vivo insulin sensitivity in individual tissues in rats.
Chisholm, DJ; James, DE; Jenkins, AB; Kraegen, EW, 1985
)
0.27
" Insulin dose-response curves showed a threshold (approximately 50 microunits/ml) and saturation-type (approximately 1 mU/ml) kinetics, whereas isometric contraction activated glucose transport and metabolism in a linear fashion with no evidence of a threshold."( Dissociation of effects of insulin and contraction on glucose transport in rat epitrochlearis muscle.
Karl, IE; Kipnis, DM; Nesher, R, 1985
)
0.27
" A dose-response study of 14CO2 production from [14C]glucose revealed that the maximum insulin stimulation of glucose utilization occurred with 5 mU/ml."( Effects of insulin on glucose metabolism in isolated heart myocytes from adult rats.
Chen, V; McDonough, KH; Spitzer, JJ, 1985
)
0.27
" An intermediate dosage decreased cerebral glucose utilization in the inferior olivary nuclei, but increased it in the fastigial, interpositus, red, dentate, vestibular, posterior mamillary, and habenular nuclei."( Oxidative metabolism and acetylcholine synthesis during acetylpyridine treatment.
Blass, JP; Gibson, GE, 1985
)
0.27
" Dose-response curves of pGRP for amylase release and AIB uptake were found to be biphasic."( Effects of porcine gastrin-releasing peptide on amylase release, 2-deoxyglucose uptake, and alpha-aminoisobutyric acid uptake in mouse pancreatic acini.
Akanuma, Y; Iwamoto, Y; Nakamura, R, 1983
)
0.5
" However, La3+ potentiated the response of the cell to T3 in respect to calcium accumulation, cAMP concentration, and 2-DG uptake, shifting the dose-response curve of the latter two effects to the left."( An immediate increase in calcium accumulation by rat thymocytes induced by triiodothyronine: its role in the subsequent metabolic responses.
Ingbar, SH; Segal, J, 1984
)
0.27
" At the same time there was a progressive shift of the insulin dose-response curve to the right, indicating diminished insulin sensitivity and a marked decrease in maximum insulin responsiveness."( Glucose uptake and insulin sensitivity in rat muscle: changes during 3-96 weeks of age.
Belur, E; Dluz, SM; Goodman, MN; McElaney, MA; Ruderman, NB, 1983
)
0.27
" (1) Adenosine deaminase (10 micrograms/ml) caused a rightward shift in the dose-response curve for the stimulation by insulin of 2-deoxyglucose uptake, but the enzyme did not alter either the basal or the maximally insulin-stimulated uptake rate."( Glucagon inhibition of insulin-stimulated 2-deoxyglucose uptake by rat adipocytes in the presence of adenosine deaminase.
Green, A, 1983
)
0.73
" The effect was characterized by a leftward shift in the insulin dose-response curve."( Rapid increase in the insulin sensitivity of rat adipocytes after intravenous glucose administration.
Finocchiaro, L; Kingston, WJ; Livingston, JN; Moxley, RT, 1984
)
0.27
", it resulted in a leftward shift in the dose-response curve."( beta-Hydroxybutyrate increases the insulin sensitivity of adipocyte glucose transport at a postreceptor level.
Bustillos, DP; Green, A; Misbin, RI, 1984
)
0.27
" Dose-response curves to 5-TG were shifted to the left with respect to 2-DG."( [Effect of 5-thioglucose on external pancreatic secretion in rats. Comparison with 2-deoxyglucose].
Appia, F; Chariot, J; de La Tour, J; Rozé, C, 1984
)
0.49
" Subcutaneous fat cells were also somewhat less sensitive to submaximal doses of insulin and this was reflected in rightward shift in the dose-response curves for 2-deoxyglucose uptake and fatty acid synthesis."( Variations of glucose metabolism by fat cells from three adipose depots of the rat.
Fried, SK; Lavau, M; Pi-Sunyer, FX, 1982
)
0.46
"05); (c) under conditions of maximal electrical stimulation of the vagus, pancreatic response was unsignificantly increased; (d) dose-response curves to secretin and CCK-PZ were unsignificantly changed."( [Responses of exocrine pancreas to a six month oral treatment by methadone in rats (author's transl)].
Chariot, J; Lehy, T; Potet, F; Rozé, C; Souchard, M; Vaille, C,
)
0.13
" A dose-response study for histamine stimulation is presented."( Vagally innervated and denervated gastric pouch in one and the same dog--a new model.
Guldvog, I, 1980
)
0.26
" The dose-response curves were similar to those observed for the inhibition of insulin stimulation of 2-deoxyglucose transport activity."( Effects of ML-9 on insulin stimulation of glucose transport in 3T3-L1 adipocytes.
Hayashi, T; Inoue, G; Kono, S; Kosaki, A; Kubota, M; Kuzuya, H; Maeda, I; Okamoto, M; Yoshimasa, Y, 1993
)
0.5
" ATP dose-response experiments, taken together with the effect of cAMP with and without ATP, suggest that phosphorylation is necessary, but not sufficient, for activation."( Regulation of CFTR Cl- conductance in secretion by cellular energy levels.
Bell, CL; Quinton, PM, 1993
)
0.29
" This effect was greatest when oxamate was dosed after Dox, suggesting that oxamate inhibited repair of Dox-induced damage."( Modification of tumour glucose metabolism for therapeutic benefit.
Fennell, M; Hamilton, E; Stafford, DM, 1995
)
0.29
" After 6 h exposure, the dose-response curve of 2-DOG uptake to T3-MAAB was shifted to the left by at least one order of magnitude when compared to the dose-response curve obtained with T3."( The production of a monoclonal T3-antiidiotypic antibody (T3-MAAB) that mimics the effects of T3 on 2-deoxy-D-glucose uptake in chick embryo heart cells.
Gafny, M; Gordon, A; Gross, J; Mizrachi, M; Schwartz, H; Swartz, H, 1994
)
0.29
" Dosages of 2-DG in excess of 1,500 mg/kg body mass reliably induced torpor with latencies of approximately 50 min from time of injection to a decrease in Tb below 30 degrees C; 79% of females displayed torpor at a dosage of 2,500 mg/kg."( Reduced glucose availability induces torpor in Siberian hamsters.
Dark, J; Miller, DR; Zucker, I, 1994
)
0.29
" In contrast, L-687,414 did not increase limbic CMRglc, nor evoke vacuolation when given in the neuroprotective dose-regime or at the higher dosage rate."( Lack of effect of L-687,414 ((+)-cis-4-methyl-HA-966), an NMDA receptor antagonist acting at the glycine site, on cerebral glucose metabolism and cortical neuronal morphology.
Hargreaves, RJ; Hill, RG; Rigby, M; Smith, D, 1993
)
0.29
" Dose-response curves demonstrate that these cisplatin-resistant C13* cells show cross-resistance to Photofrin-mediated PDT."( Mitochondrial alterations in photodynamic therapy-resistant cells.
Moorehead, R; Sharkey, SM; Singh, G; Wilson, BC, 1993
)
0.29
" Miconazole at high dosage (60 mg/kg) suppressed mitogen-induced lymphocyte proliferation, otherwise a single dose of any of the drugs had no effect on neutrophil or lymphocyte function irrespective of concentration used."( The effects of amphotericin B, fluconazole and miconazole on neutrophil and lymphocyte function in a guinea pig model.
Drummond, DC; McCormack, JG; Whitman, LM; Wong, CW, 1995
)
0.29
" Pairing Delt II (5 microg) with low (100-200 mg/kg) 2DG doses significantly enhanced intake, producing a leftward (3-fold) shift in 2DG's hyperphagic dose-response curve."( Delta and kappa opioid receptor subtypes and ingestion: antagonist and glucoprivic effects.
Bodnar, RJ; Ruegg, H; Yu, WZ, 1997
)
0.3
" At low leptin concentrations (<1 nM), the insulin sensitivity was reduced leading to a shift to the right in the dose-response curve."( Leptin impairs metabolic actions of insulin in isolated rat adipocytes.
Ertl, J; Gerl, M; Müller, G; Preibisch, G, 1997
)
0.3
"In the beta-cells of the pancreas, glucose phosphorylation carried out by glucokinase is the rate-controlling step in glycolysis, and the kinetic characteristics of glucokinase govern to a high degree the dose-response relationship between glucose and insulin release."( Measurement and modeling of glucose-6-phosphatase in pancreatic islets.
Grodberg, J; Li, G; Matschinsky, FM; Najafi, H; Sweet, IR, 1997
)
0.3
"03), whereas insulin stimulation of glycogen synthase was reduced, exhibiting a right shift in the insulin dose-response curve."( Oxidant stress reduces insulin responsiveness in 3T3-L1 adipocytes.
Bashan, N; Kozlovsky, N; Potashnik, R; Rudich, A, 1997
)
0.3
" The median effective concentration (EC50) from the dose-response curves of glucose uptake was the same on both groups of animals."( Chronic salt overload increases blood pressure and improves glucose metabolism without changing insulin sensitivity.
da Costa Lima, NK; dos Santos, EA; Heimann, JC; Hell, NS; Lima, FB; Matsushita, DH; Okamoto, MM, 1997
)
0.3
" Only cytochalasin A and 2-deoxy-D-glucose (2dG) affected bacterial internalisation, whereas intracellular multiplication was inhibited by cytochalasins A, B, C, D and J (D being the most active) and by 2dG with a dose-response effect."( Multiplication of Legionella pneumophila in HeLa cells in the presence of cytoskeleton and metabolic inhibitors.
Carrara, S; Cattani, L; Goldoni, P; Orsi, N; Pastoris, MC; Sinibaldi, L, 1998
)
0.3
" The effect of insulin sensitizer treatment on muscle insulin action was studied using ob/ob mice after 4 days dosing with a potent (6 nM PPARgamma Kd) TZD (10 mg/kg x day)."( Role of skeletal muscle in thiazolidinedione insulin sensitizer (PPARgamma agonist) action.
Berger, J; Doebber, T; Li, Z; McCrary, C; Moller, DE; Ryder, JW; Ventre, J; Woods, J; Wu, M; Zhang, B; Zierath, JR, 1998
)
0.3
" Subsequent removal of wortmannin from the media shifted this dose-response curve to one resembling that for GLUT4 translocation and pp70 S6-kinase."( Identification of wortmannin-sensitive targets in 3T3-L1 adipocytes. DissociationoOf insulin-stimulated glucose uptake and glut4 translocation.
Birnbaum, MJ; Fingar, DC; Garza, LA; Hausdorff, SF; Morioka, K; Summers, SA; Whiteman, EL, 1999
)
0.3
"Transgenic or tumoral pancreatic islet beta cells with enhanced expression of low K(m) hexokinases (HK) exhibit a leftward shift of the normal dose-response curve for glucose-induced insulin release."( Cellular origin of hexokinase in pancreatic islets.
Heimberg, H; Moens, K; Pipeleers, D; Schuit, F, 1999
)
0.3
" To evaluate the potential interference of 1, 5-AG measurements by traditional Chinese medicines (Kampo), we examined the 1,5-AG content in 32 types of concentrated dosage forms of Kampo using high performance liquid chromatography (HPLC)."( The influence of traditional Chinese herbal drugs on serum 1, 5-anhydroglucitol levels.
Aiso, Y; Fujimori, S; Inoue, T; Kashiwabara, A; Kawasaki, T; Tanabe, T; Yamanouchi, T; Yoshimura, T, 2000
)
0.31
" Incubation with ANGII (10(-9) and 10(-8) M) had no significant effect on the dose-response curve for insulin-stimulated [(3)H]2-deoxyglucose uptake."( Possible interactions between angiotensin II and insulin: effects on glucose and lipid metabolism in vivo and in vitro.
Donnelly, R; Gray, S; Idris, I; Patiag, D; Qu, X; Seale, JP; Wilkes, M, 2000
)
0.51
" A dose-response test for 2-DG further confirmed these results."( Zinc-deficient rats are insensitive to glucoprivation caused by 2-deoxy-D-glucose.
Beverly, JL; Cole, AC; O'Brien, S; Shay, NF, 2002
)
0.31
"6 g/100 ml) was administered to control fish, whereas the experimental group received 2-DG, dissolved in saline, in the dosage of 80 mg/kg (0."( Metabolic responses to glucoprivation induced by 2-deoxy-D-glucose in Brycon cephalus (Teleostei, Characidae).
Capilla, E; Figueiredo-Garutti, ML; Gutiérrez, J; Moraes, G; Navarro, I; Souza, RH; Vicentini-Paulino, ML, 2004
)
0.32
" We also performed a dose-response study using graded doses of OxA (0, 31."( Orexin A-induced feeding is augmented by caloric challenge.
Kotz, CM; Teske, JA; Thorpe, AJ, 2005
)
0.33
" On a high-fat diet, Rad tg mice develop more severe glucose intolerance than the wild-type mice; this is due to increased insulin resistance in muscle, as exemplified by a rightward shift in the dose-response curve for insulin stimulated 2-deoxyglucose uptake."( Overexpression of Rad in muscle worsens diet-induced insulin resistance and glucose intolerance and lowers plasma triglyceride level.
Bilan, PJ; Caldwell, JS; Ilany, J; Kahn, CR; Kapur, S; Marette, A; Patti, ME, 2006
)
0.52
" The dose-response curve of insulin is similar in shape to that of T(3), and its peak stimulation can even reach 600% over the control."( 3,5,3' Triiodo-L-thyronine stimulates 2-deoxy-D-glucose transport into L6 muscle cells through the phosphorylation of insulin receptor beta and the activation of PI-3k.
Gordon, A; Shwartz, H; Swartz, H, 2006
)
0.33
" This was manifested as decrease in maximally stimulated glucose transport and a rightward shift in the dose-response curve."( Transferrin and iron induce insulin resistance of glucose transport in adipocytes.
Basile, R; Green, A; Rumberger, JM, 2006
)
0.33
" We performed 13C nuclear magnetic resonance spectroscopy on brain extracts from soman-poisoned mice (160 microg/kg; 1 LD50) that had been dosed with 13C-labeled glucose or pyruvate intravenously."( Cerebral metabolism of glucose and pyruvate in soman poisoning. A 13C nuclear magnetic resonance spectroscopic study.
Gonzalez, SV; Hassel, B; Nguyen, N; Rise, F, 2007
)
0.34
" It was hypothesized that despite the administration of AA at similar doses, the discrepancy in the observed effects was most likely due to varying AA concentrations in the administered dosing solution."( Effect of dose volume on the toxicokinetics of acrylamide and its metabolites and 2-deoxy-D-glucose.
Bai, R; Burka, LT; Ghanayem, BI, 2009
)
0.35
" Single oral dosing studies were performed in rats, mice and dogs to assess the abilities of TS-071 to increase urinary glucose excretion and to lower plasma glucose levels."( TS-071 is a novel, potent and selective renal sodium-glucose cotransporter 2 (SGLT2) inhibitor with anti-hyperglycaemic activity.
Arai, M; Asami, J; Fukuhara, N; Gunji, E; Kitano, K; Kojima, N; Kozakai, A; Okumura-Kitajima, L; Takahashi, K; Takahashi, T; Tomoike, H; Toyoda, H; Uchida, S; Yamamoto, K, 2011
)
0.37
" Analysis of the dose-response curves resulting from challenge with all possible binary and ternary mixtures revealed that the appropriate model was not clear."( Exploring the boundaries of additivity: mixtures of NADH: quinone oxidoreductase inhibitors.
Boggs, N; Boyd, J; Le, H; Patrone, JB; Saksena, A; Theodore, M; Williams, HN, 2011
)
0.37
"Thirty-four patients were enrolled: 21 on every other week, 6 on a 21 of 28-day cycle and 7 on the continuous 2DG dosing schedule."( A phase I dose-escalation trial of 2-deoxy-D-glucose alone or combined with docetaxel in patients with advanced solid tumors.
Chiorean, EG; Dipaola, RS; Jung, DT; Kroll, S; Kurtoglu, M; Lampidis, TJ; Langmuir, VK; Papadopoulos, K; Raez, LE; Ricart, AD; Rocha Lima, CM; Rosenblatt, J; Schlesselman, JJ; Stein, MN; Tolba, K, 2013
)
0.39
"Response surface methodology (RSM) was utilized to investigate the dose-response relationships of a phenolic mixture (catechin, genistein and daidzein) as a pre-thermal processing technique to reduce reactive carbonyl species (RCSs; glyoxal, methylglyoxal and 3-deoxyglucosone) in ultra-high temperature (UHT) bovine milk."( Response surface methodology as optimization strategy for reduction of reactive carbonyl species in foods by means of phenolic chemistry.
Kokkinidou, S; Peterson, DG, 2013
)
0.39
" Dose-response experiments demonstrated that curcumin (0-100 μM) inhibited basal and insulin-stimulated glucose transport, but even at the highest concentration tested did not affect lipolysis."( Curcumin is a direct inhibitor of glucose transport in adipocytes.
Green, A; Krause, J; Rumberger, JM, 2014
)
0.4
" This study's primary objective examined the relationship between GSK2141795, an oral, pan-AKT inhibitor, and (18)F-FDG PET markers of glucose metabolism in tumor tissue to determine whether (18)F-FDG PET could be used to guide personalized dosing of GSK2141795."( Dose-Finding Quantitative 18F-FDG PET Imaging Study with the Oral Pan-AKT Inhibitor GSK2141795 in Patients with Gynecologic Malignancies.
Agarwal, R; Babar, S; Blagden, S; Carme, S; Chen, M; Curry, E; Dina, R; El-Bahrawy, MA; Gabra, H; Gungor, H; Krachey, E; Madison, S; Morris, SR; Pickford, E; Rama, N; Saleem, A; Salinas, C; Santiago-Walker, A; Smith, DA; Stronach, EA, 2015
)
0.42
" No dose-response relationship was observed between GSK2141795 pharmacokinetics and (18)F-FDG PET pharmacodynamic measures; however, an exposure-response relationship was seen between maximum drug concentrations and maximal decrease in (18)F-FDG uptake in the best-responding tumor."( Dose-Finding Quantitative 18F-FDG PET Imaging Study with the Oral Pan-AKT Inhibitor GSK2141795 in Patients with Gynecologic Malignancies.
Agarwal, R; Babar, S; Blagden, S; Carme, S; Chen, M; Curry, E; Dina, R; El-Bahrawy, MA; Gabra, H; Gungor, H; Krachey, E; Madison, S; Morris, SR; Pickford, E; Rama, N; Saleem, A; Salinas, C; Santiago-Walker, A; Smith, DA; Stronach, EA, 2015
)
0.42
" The goal of current medical management for T2D is to transiently ameliorate hyperglycemia through daily dosing of one or more antidiabetic drugs."( Central injection of fibroblast growth factor 1 induces sustained remission of diabetic hyperglycemia in rodents.
Bergman, RN; Dorfman, MD; Kaiyala, KJ; Lantier, L; Matsen, ME; Mirzadeh, Z; Morton, GJ; Nguyen, HT; Rojas, JM; Scarlett, JM; Schwartz, MW; Stefanovski, D; Unterman, TG; Wasserman, DH, 2016
)
0.43
"We demonstrated a dose-response linear association between 1,5-anhydroglucitol and ACPR."( Association between 1,5-Anhydroglucitol and Acute C Peptide Response to Arginine among Patients with Type 2 Diabetes.
Bao, Y; Hu, G; Lu, J; Lu, W; Ma, X; Mo, Y; Shen, Y; Si, Y; Zhang, L; Zhou, J; Zhu, W, 2020
)
0.56
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (1)

RoleDescription
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
2-deoxy-D-glucoseA deoxyglucose that is D-glucose in which the hydroxy group at position 2 has been replaced by a hydrogen. It is an antimetabolite of glucose with antiviral activity, which acts by inhibiting the glycosylation of glycoproteins and glycolipids. Used as an antiherpes agent.
[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
Inner Membrane Transport7862

Protein Targets (4)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, Beta-lactamaseEscherichia coli K-12Potency3.98110.044717.8581100.0000AID485294
IDH1Homo sapiens (human)Potency14.58100.005210.865235.4813AID686970
DNA polymerase iota isoform a (long)Homo sapiens (human)Potency89.12510.050127.073689.1251AID588590
TAR DNA-binding protein 43Homo sapiens (human)Potency35.48131.778316.208135.4813AID652104
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (18)

Processvia Protein(s)Taxonomy
negative regulation of protein phosphorylationTAR DNA-binding protein 43Homo sapiens (human)
mRNA processingTAR DNA-binding protein 43Homo sapiens (human)
RNA splicingTAR DNA-binding protein 43Homo sapiens (human)
negative regulation of gene expressionTAR DNA-binding protein 43Homo sapiens (human)
regulation of protein stabilityTAR DNA-binding protein 43Homo sapiens (human)
positive regulation of insulin secretionTAR DNA-binding protein 43Homo sapiens (human)
response to endoplasmic reticulum stressTAR DNA-binding protein 43Homo sapiens (human)
positive regulation of protein import into nucleusTAR DNA-binding protein 43Homo sapiens (human)
regulation of circadian rhythmTAR DNA-binding protein 43Homo sapiens (human)
regulation of apoptotic processTAR DNA-binding protein 43Homo sapiens (human)
negative regulation by host of viral transcriptionTAR DNA-binding protein 43Homo sapiens (human)
rhythmic processTAR DNA-binding protein 43Homo sapiens (human)
regulation of cell cycleTAR DNA-binding protein 43Homo sapiens (human)
3'-UTR-mediated mRNA destabilizationTAR DNA-binding protein 43Homo sapiens (human)
3'-UTR-mediated mRNA stabilizationTAR DNA-binding protein 43Homo sapiens (human)
nuclear inner membrane organizationTAR DNA-binding protein 43Homo sapiens (human)
amyloid fibril formationTAR DNA-binding protein 43Homo sapiens (human)
regulation of gene expressionTAR DNA-binding protein 43Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (10)

Processvia Protein(s)Taxonomy
RNA polymerase II cis-regulatory region sequence-specific DNA bindingTAR DNA-binding protein 43Homo sapiens (human)
DNA bindingTAR DNA-binding protein 43Homo sapiens (human)
double-stranded DNA bindingTAR DNA-binding protein 43Homo sapiens (human)
RNA bindingTAR DNA-binding protein 43Homo sapiens (human)
mRNA 3'-UTR bindingTAR DNA-binding protein 43Homo sapiens (human)
protein bindingTAR DNA-binding protein 43Homo sapiens (human)
lipid bindingTAR DNA-binding protein 43Homo sapiens (human)
identical protein bindingTAR DNA-binding protein 43Homo sapiens (human)
pre-mRNA intronic bindingTAR DNA-binding protein 43Homo sapiens (human)
molecular condensate scaffold activityTAR DNA-binding protein 43Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (9)

Processvia Protein(s)Taxonomy
intracellular non-membrane-bounded organelleTAR DNA-binding protein 43Homo sapiens (human)
nucleusTAR DNA-binding protein 43Homo sapiens (human)
nucleoplasmTAR DNA-binding protein 43Homo sapiens (human)
perichromatin fibrilsTAR DNA-binding protein 43Homo sapiens (human)
mitochondrionTAR DNA-binding protein 43Homo sapiens (human)
cytoplasmic stress granuleTAR DNA-binding protein 43Homo sapiens (human)
nuclear speckTAR DNA-binding protein 43Homo sapiens (human)
interchromatin granuleTAR DNA-binding protein 43Homo sapiens (human)
nucleoplasmTAR DNA-binding protein 43Homo sapiens (human)
chromatinTAR DNA-binding protein 43Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (46)

Assay IDTitleYearJournalArticle
AID682143TP_TRANSPORTER: inhibition of pyruvate uptake in Xenopus laevis oocytes1998The Journal of biological chemistry, Oct-30, Volume: 273, Issue:44
Human monocarboxylate transporter 2 (MCT2) is a high affinity pyruvate transporter.
AID681374TP_TRANSPORTER: inhibition of pyruvate uptake in Xenopus laevis oocytes1998The Journal of biological chemistry, Oct-30, Volume: 273, Issue:44
Human monocarboxylate transporter 2 (MCT2) is a high affinity pyruvate transporter.
AID1745845Primary qHTS for Inhibitors of ATXN expression
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.
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.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
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.
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.
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.
AID1475798Cytotoxicity against human HeLa cells at 10000 cells per well assessed as decrease in cell viability up to 1 uM after 48 hrs by MTT assay2017Journal of medicinal chemistry, 09-28, Volume: 60, Issue:18
New Mandelalides Expand a Macrolide Series of Mitochondrial Inhibitors.
AID1278467Cytotoxicity against human NCI-H1299 cells assessed as viability at 500 uM after 48 hrs by MTT assay2016Bioorganic & medicinal chemistry letters, Mar-01, Volume: 26, Issue:5
Carbohydrate-based inducers of cellular stress for targeting cancer cells.
AID1882573Antiviral activity against SARS-CoV-2 B.1.1.7 in African green monkey Vero E6 cells assessed as inhibition of virus multiplication2022Journal of medicinal chemistry, 03-10, Volume: 65, Issue:5
A Comprehensive Biological and Synthetic Perspective on 2-Deoxy-d-Glucose (2-DG), A Sweet Molecule with Therapeutic and Diagnostic Potentials.
AID1436540Cytotoxicity against undifferentiated mouse P19 cells assessed as cell mass at 1 to 100 uM after 24 hrs by SRB assay relative to control2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1882572Antiviral activity against SARS-CoV-2 B.6 in African green monkey Vero E6 cells assessed as inhibition of virus multiplication2022Journal of medicinal chemistry, 03-10, Volume: 65, Issue:5
A Comprehensive Biological and Synthetic Perspective on 2-Deoxy-d-Glucose (2-DG), A Sweet Molecule with Therapeutic and Diagnostic Potentials.
AID1436545Cytotoxicity against differentiated mouse P19 cells assessed as cell mass at 1 to 100 uM after 72 hrs by SRB assay relative to control2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1436547Cytotoxicity against undifferentiated mouse P19 cells assessed as metabolic activity at 1 to 100 uM after 48 hrs by resazurin assay relative to control2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1436551Cytotoxicity against differentiated mouse P19 cells assessed as metabolic activity at 1 to 100 uM after 72 hrs by resazurin assay relative to control2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1436542Cytotoxicity against undifferentiated mouse P19 cells assessed as cell mass at 1 to 100 uM after 72 hrs by SRB assay relative to control2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1893802Induction of apoptosis in human A2780 cells assessed as early apoptosis level at 20 uM incubated for 48 hrs by PI and FITC-Annexin V staining based flow cytometry2022ACS medicinal chemistry letters, Sep-08, Volume: 13, Issue:9
Aroylhydrazone Glycoconjugate Prochelators Exploit Glucose Transporter 1 (GLUT1) to Target Iron in Cancer Cells.
AID1528313Inhibition of glucose metabolism in human LS174T cells assessed as reduction in ATP level at 10 mM by luminescence assay2019Journal of medicinal chemistry, 12-26, Volume: 62, Issue:24
An Underlying Mechanism of Dual Wnt Inhibition and AMPK Activation: Mitochondrial Uncouplers Masquerading as Wnt Inhibitors.
AID1475796Cytotoxicity against human HeLa cells at 6000 cells per well assessed as decrease in cell viability up to 1 uM after 48 hrs by MTT assay2017Journal of medicinal chemistry, 09-28, Volume: 60, Issue:18
New Mandelalides Expand a Macrolide Series of Mitochondrial Inhibitors.
AID1436543Cytotoxicity against differentiated mouse P19 cells assessed as cell mass at 1 to 100 uM after 24 hrs by SRB assay relative to control2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1436546Cytotoxicity against undifferentiated mouse P19 cells assessed as metabolic activity at 1 to 100 uM after 24 hrs by resazurin assay relative to control2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1882574Antiviral activity against SARS-CoV-2 in African green monkey Vero E6 cells assessed as inhibition of virus multiplication at 1 mM2022Journal of medicinal chemistry, 03-10, Volume: 65, Issue:5
A Comprehensive Biological and Synthetic Perspective on 2-Deoxy-d-Glucose (2-DG), A Sweet Molecule with Therapeutic and Diagnostic Potentials.
AID1528309Activation of AMPK (unknown origin) assessed as reduction in ACC phosphorylation at S79 residue by Western blot analysis2019Journal of medicinal chemistry, 12-26, Volume: 62, Issue:24
An Underlying Mechanism of Dual Wnt Inhibition and AMPK Activation: Mitochondrial Uncouplers Masquerading as Wnt Inhibitors.
AID1475812Cytotoxicity against human HeLa cells assessed as reduction in cell viability at 250 to 500 uM after 72 hrs by MTT assay2017Journal of medicinal chemistry, 09-28, Volume: 60, Issue:18
New Mandelalides Expand a Macrolide Series of Mitochondrial Inhibitors.
AID1436550Cytotoxicity against differentiated mouse P19 cells assessed as metabolic activity at 1 to 100 uM after 48 hrs by resazurin assay relative to control2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1882575Antiviral activity against SARS-CoV-2 in African green monkey Vero cells assessed as inhibition of virus multiplication in presence of extracellular glucose2022Journal of medicinal chemistry, 03-10, Volume: 65, Issue:5
A Comprehensive Biological and Synthetic Perspective on 2-Deoxy-d-Glucose (2-DG), A Sweet Molecule with Therapeutic and Diagnostic Potentials.
AID1475793Cytotoxicity against human HeLa cells at 2000 cells per well assessed as decrease in cell viability at 0.25 to 1 uM after 48 hrs by MTT assay relative to control2017Journal of medicinal chemistry, 09-28, Volume: 60, Issue:18
New Mandelalides Expand a Macrolide Series of Mitochondrial Inhibitors.
AID1436544Cytotoxicity against differentiated mouse P19 cells assessed as cell mass at 1 to 100 uM after 48 hrs by SRB assay relative to control2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1528312Inhibition of LiCl-activated Wnt signaling in HEK293 cells at 2 to 10 mM by TOPFlash reporter gene assay2019Journal of medicinal chemistry, 12-26, Volume: 62, Issue:24
An Underlying Mechanism of Dual Wnt Inhibition and AMPK Activation: Mitochondrial Uncouplers Masquerading as Wnt Inhibitors.
AID1278470Activation of AMPK in HEK293 cells assessed as AMPK phosphorylation after 16 hrs by Western blotting method2016Bioorganic & medicinal chemistry letters, Mar-01, Volume: 26, Issue:5
Carbohydrate-based inducers of cellular stress for targeting cancer cells.
AID1436548Cytotoxicity against undifferentiated mouse P19 cells assessed as metabolic activity at 1 to 100 uM after 72 hrs by resazurin assay relative to control2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1278468Induction of ROS generation in human NCI-H1299 cells at 10 mM after 3 hrs by DCF-DA staining-based assay2016Bioorganic & medicinal chemistry letters, Mar-01, Volume: 26, Issue:5
Carbohydrate-based inducers of cellular stress for targeting cancer cells.
AID1436541Cytotoxicity against undifferentiated mouse P19 cells assessed as cell mass at 1 to 100 uM after 48 hrs by SRB assay relative to control2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1436549Cytotoxicity against differentiated mouse P19 cells assessed as metabolic activity at 1 to 100 uM after 24 hrs by resazurin assay relative to control2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1528308Activation of AMPK (unknown origin) assessed as increase in AMPK phosphorylation at T172 residue by Western blot analysis2019Journal of medicinal chemistry, 12-26, Volume: 62, Issue:24
An Underlying Mechanism of Dual Wnt Inhibition and AMPK Activation: Mitochondrial Uncouplers Masquerading as Wnt Inhibitors.
AID1436571Inhibition of HK2 isolated from mouse undifferentiated P19 cell lysates at 50 mM using [U-14C]-labeled glucose as substrate in presence of ATP and NADP by G6PD enzyme coupled spectrophotometric assay2017Bioorganic & medicinal chemistry letters, 02-01, Volume: 27, Issue:3
Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity.
AID1893803Induction of apoptosis in human A2780 cells assessed as late apoptosis level at 20 uM incubated for 48 hrs by PI and FITC-Annexin V staining based flow cytometry2022ACS medicinal chemistry letters, Sep-08, Volume: 13, Issue:9
Aroylhydrazone Glycoconjugate Prochelators Exploit Glucose Transporter 1 (GLUT1) to Target Iron in Cancer Cells.
AID1711521Growth inhibition of Caenorhabditis elegans N2 L1 larvae under monoxenic condition assessed as reduction in body size at 42 mM incubated for 72 hrs by microscopic method relative to control2016Bioorganic & medicinal chemistry letters, Feb-01, Volume: 26, Issue:3
Growth inhibitory effect of D-arabinose against the nematode Caenorhabditis elegans: Discovery of a novel bioactive monosaccharide.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (11,048)

TimeframeStudies, This Drug (%)All Drugs %
pre-19904064 (36.78)18.7374
1990's3828 (34.65)18.2507
2000's1647 (14.91)29.6817
2010's1251 (11.32)24.3611
2020's258 (2.34)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 52.52

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 Index52.52 (24.57)
Research Supply Index9.36 (2.92)
Research Growth Index4.38 (4.65)
Search Engine Demand Index92.29 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (52.52)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials171 (1.50%)5.53%
Trials0 (0.00%)5.53%
Reviews358 (3.13%)6.00%
Reviews0 (0.00%)6.00%
Case Studies266 (2.33%)4.05%
Case Studies0 (0.00%)4.05%
Observational9 (0.08%)0.25%
Observational0 (0.00%)0.25%
Other10,622 (92.96%)84.16%
Other12 (100.00%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (89)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
PET fUnCtionaL Imaging to Evaluate Cardiac Radiation Damage (EUCLID) [NCT05775939]20 participants (Anticipated)Interventional2023-01-20Recruiting
A Phase 1/2 Study of Tiragolumab (NSC# 827799) and Atezolizumab (NSC# 783608) in Patients With Relapsed or Refractory SMARCB1 or SMARCA4 Deficient Tumors [NCT05286801]Phase 1/Phase 286 participants (Anticipated)Interventional2022-11-17Recruiting
Phase I Dose-Escalation Bioavailability Study of Oral Triapine in Combination With Concurrent Chemoradiation for Locally Advanced Cervical Cancer (LACC) and Vaginal Cancer [NCT02595879]Phase 122 participants (Actual)Interventional2019-09-18Active, not recruiting
A Pilot Prospective Study of the RefleXion [18F]- FDG PET-CT Subsystem Imaging Performance in Patients With Various Malignancies [NCT05844306]20 participants (Anticipated)Interventional2023-03-15Recruiting
Phase I/II Study of High Dose Interleukin 2, Aldesleukin, in Combination With the Histone Deacetylase Inhibitor Entinostat in Patients With Metastatic Renal Cell Carcinoma [NCT01038778]Phase 1/Phase 247 participants (Actual)Interventional2009-10-29Active, not recruiting
Phase I Dose-Escalation Study of BCMA/CS1 Bispecific Chimeric Antigen Receptor (CAR)-T Cells for Relapsed/Refractory Multiple Myeloma [NCT05950113]Phase 130 participants (Anticipated)Interventional2024-03-28Not yet recruiting
18F-FSPG PET/CT and Integrated Biomarkers for Early Lung Cancer Detection in Patients With Indeterminate Pulmonary Nodules [NCT03824535]Phase 250 participants (Anticipated)Interventional2019-02-04Recruiting
Clinical Feasibility Study of Hypoxia Imaging -Guided IMRT on the Individualized Radiotherapy of Nasopharyngeal Carcinoma [NCT02089204]300 participants (Anticipated)Observational2010-06-30Enrolling by invitation
Phase II Study of Bevacizumab Plus Irinotecan (Camptosar™) in Children With Recurrent, Progressive, or Refractory Malignant Gliomas, Diffuse/Intrinsic Brain Stem Gliomas, Medulloblastomas, Ependymomas and Low Grade Gliomas [NCT00381797]Phase 297 participants (Actual)Interventional2006-08-31Completed
A Pilot Study to Evaluate the Utility of Interim Digital PET/CT in Predicting Outcomes for Locally Advanced Oropharyngeal Cancer [NCT04140513]25 participants (Anticipated)Interventional2020-10-09Suspended(stopped due to PI decision)
Pilot Safety and Feasibility Study of an In Vivo Sensitivity Screen Using a Direct Tumor Microinjection Technique and FDG-PET [NCT03432741]Phase 139 participants (Anticipated)Interventional2018-03-27Suspended(stopped due to funding - sponsor filing of Chapter 11 bankruptcy)
A Phase 3 Randomized Trial for Patients With De Novo AML Comparing Standard Therapy Including Gemtuzumab Ozogamicin (GO) to CPX-351 With GO, and the Addition of the FLT3 Inhibitor Gilteritinib for Patients With FLT3 Mutations [NCT04293562]Phase 31,400 participants (Anticipated)Interventional2020-07-21Recruiting
"Combined One Stop Shop NaF/FDG PET/MRI Evaluation of Response to Xofigo® in mCRPC Patients: A Pilot Study" [NCT02429804]Phase 14 participants (Actual)Interventional2015-04-30Terminated(stopped due to Accrual factor)
Evaluation of Resectable Cervical Carcinoma With PET/MRI [NCT04219904]Early Phase 125 participants (Anticipated)Interventional2018-09-07Active, not recruiting
Pilot Study of Gene Expression and FDG-PET/MR Biomarkers for Evaluation of Response to Neoadjuvant Therapy for Locally Advanced Rectal Cancer [NCT02112162]Phase 12 participants (Actual)Interventional2014-06-30Terminated(stopped due to Loss of funding)
[18F]-Fluoro-2-Deoxy-D-Glucose and -[18F] Dihydro-Testosterone Pet Imaging in Patients With Progressive Prostate Cancer [NCT00588185]300 participants (Anticipated)Interventional2003-02-28Recruiting
A Phase Ib/II Study of AZD2171 in Combination With Daily Temozolomide and Radiation in Patients With Newly Diagnosed Glioblastoma Not Taking Enzyme-Inducing Anti-epileptic Drugs [NCT00662506]Phase 1/Phase 246 participants (Actual)Interventional2008-04-30Completed
Development of Activity MRI (aMRI): Direct Comparison to PET in Human Subjects [NCT05937776]20 participants (Anticipated)Observational2023-12-11Not yet recruiting
Ideal Imaging Time Point Assessment for Spinal Cord Lesions of Unknown Etiology With FDG PET-MRI [NCT04219969]20 participants (Anticipated)Interventional2018-09-21Active, not recruiting
A Randomized Phase 3 Interim Response Adapted Trial Comparing Standard Therapy With Immuno-oncology Therapy for Children and Adults With Newly Diagnosed Stage I and II Classic Hodgkin Lymphoma [NCT05675410]Phase 31,875 participants (Anticipated)Interventional2023-05-11Recruiting
A Pilot Study of FDG-PET Variability to Establish Biology-Guided Treatment Planning Feasibility for Stereotactic Body Radiation Therapy [NCT03493789]Phase 119 participants (Actual)Interventional2018-04-13Completed
Combined 18F-NaF/18F-FDG PET/MRI for Detection of Skeletal Metastases [NCT00375830]Phase 2114 participants (Actual)Interventional2006-01-31Completed
Diffusion-weighted MRI for Individualized Radiation Therapy Planning of Lung Cancer [NCT02059889]0 participants (Actual)Interventional2014-07-31Withdrawn(stopped due to slow accrual)
PET/MR, PET/CT and Whole Body MR in Newly Diagnosed Acute Myeloid Leukemia (AML) [NCT02390635]Phase 155 participants (Anticipated)Interventional2016-05-02Recruiting
MRI- and PET-Predictive-Assay of Treatment Outcome in Cancer of the Cervix [NCT01992861]51 participants (Actual)Observational2014-02-14Terminated
Amyloid Plaque Deposition in Chemotherapy-Induced Cognitive Impairment [NCT02317783]Phase 210 participants (Actual)Interventional2018-01-31Active, not recruiting
A Multicenter Phase 2 Study Comparing 99m Tc EC-DG SPECT/CT With 18F FDG PET/CT in the Evaluation of Patients With Non-small Cell Lung Cancer (NSCLC) [NCT00865319]Phase 222 participants (Actual)Interventional2009-06-30Completed
A Phase III Randomized Study of Maintenance Nivolumab Versus Observation in Patients With Locally Advanced, Intermediate Risk HPV Positive OPSCC [NCT03811015]Phase 3636 participants (Anticipated)Interventional2019-08-16Recruiting
A Phase I/II Trial of 2-Deoxyglucose (2DG) for the Treatment of Advanced Cancer and Hormone Refractory Prostate Cancer [NCT00633087]Phase 1/Phase 212 participants (Actual)Interventional2006-11-30Terminated(stopped due to Slow accrual)
Creating Metabolic Vulnerabilities in Patients With EGFR Activated Recurrent Glioblastoma by Inhibiting EGFR With Osimertinib [NCT03732352]Phase 212 participants (Actual)Interventional2018-11-28Active, not recruiting
Assessing Hypoxia by 18F-EF5 PET Scanning and Glycolysis by 18FFDG PET Scanning in Subjects With Non-Small Cell Lung Cancer [NCT01017133]Phase 156 participants (Anticipated)Interventional2009-05-31Completed
Treatment of Opioid-refractory Pain (WHO Level III) by Pituitary Radiosurgery: A Multicenter, Prospective, Randomized Study [NCT02637479]40 participants (Anticipated)Interventional2015-12-31Recruiting
Phase II Single-Arm Trial Comparing the Use of FLT PET to Standard Computed Tomography to Assess the Treatment Response of Neoadjuvant Docetaxel and Cisplatin in Stage IB-IIIA Resectable Non-small Cell Lung Cancer [NCT00963807]Phase 226 participants (Actual)Interventional2009-09-30Completed
[18F]-Fluoro-2-Deoxy-D-Glucose and -[18F] Dihydro-Testosterone PET Imaging In Patients Advanced Breast Cancer [NCT06145399]Early Phase 110 participants (Anticipated)Interventional2023-10-24Recruiting
A Randomized Phase II Trial of Ofatumumab and Bendamustine vs. Ofatumumab, Bortezomib (NSC # 681239) and Bendamustine in Patients With Untreated Follicular Lymphoma [NCT01286272]Phase 2135 participants (Actual)Interventional2011-04-08Active, not recruiting
A Multicenter Phase 3 Study Comparing the Diagnostic Accuracy of 99mTc EC DG SPECT/CT Versus 18F FDG PET/CT for Diagnosing and Staging Patients Who Have Clinical and Radiological (CT) Evidence Consistent With a Diagnosis of Lung Cancer [NCT01394679]Phase 3154 participants (Anticipated)Interventional2020-12-01Active, not recruiting
Improved Visualization of Glioblastoma Using Delayed 18F-FDG PET/CT. [NCT02919332]0 participants (Actual)Observational2016-06-08Withdrawn(stopped due to No participants were enrolled)
A Multi-Center Phase 1b Pharmacokinetic and Radiation Dosimetry Study Evaluating 99mTc-EC-DG SPECT/CT in Patients With Non-small Cell Lung Cancer (NSCLC) [NCT00864110]Phase 14 participants (Actual)Interventional2010-04-30Completed
A Phase II Study of Single Agent Intravenous (IV) VEGF Trap in Patients With Poor Prognostic Recurrent and/or Metastatic Thyroid Cancer After RAI Therapy [NCT00729157]Phase 241 participants (Actual)Interventional2008-08-31Completed
An Evaluation of Preoperative Chemotherapy With Irinotecan and Cisplatin for Advanced, But Resectable Gastric Cancer: A Coordinated Multidisciplinary, Multicenter Study Linking Functional Imaging, Genomic Expression Profiles and Histopathology [NCT00062374]Phase 255 participants (Actual)Interventional2003-06-30Completed
A Pilot Study of Dual Time Point FDG PET MR Imaging Optimization for the Evaluation of Brain Metastasis [NCT05054998]Phase 420 participants (Anticipated)Interventional2018-08-03Recruiting
Role of Early 18F-FDG-PET/CT Scan in Predicting Mediastinal Downstaging With Neoadjuvant Chemotherapy in Resectable Stage III A NSCLC [NCT02607423]Phase 20 participants (Actual)Interventional2015-11-19Withdrawn(stopped due to The study failed to meet its accrual targets.)
A Randomized Phase III Trial of Induction/Consolidation Atezolizumab (NSC #783608) + SBRT Versus SBRT Alone in High Risk, Early Stage NSCLC [NCT04214262]Phase 3480 participants (Anticipated)Interventional2020-08-13Recruiting
A Phase II Trial to Evaluate Functional Imaging in Prediction of Response to Abemaciclib for Advanced Hormone Receptor-Positive, HER2-Negative Breast Cancer [NCT06179303]Phase 260 participants (Anticipated)Interventional2024-06-01Not yet recruiting
Evaluation of 18F-2-fluoro-2-deoxy-D-glucose Produced by a New Manufacturer, for Safety, Through the Identification of Adverse Events, and Efficacy, Through the Evaluation of Its Ability, When Utilized in Performance of a Positron Emission Tomography Comp [NCT04615156]Phase 310,000 participants (Anticipated)Interventional2020-11-01Not yet recruiting
A Single/Multiple Ascending Dose Phase 1 Study Of The Safety, Tolerability, And Pharmacokinetics Of Intranasal 2-Deoxy-D-Glucose In Normal Healthy Volunteers [NCT05314933]Phase 145 participants (Actual)Interventional2022-03-03Completed
Vorinostat to Augment Response to Lutetium-PSMA-617 in the Treatment of Patients With PSMA-Low Metastatic Castration-Resistant Prostate Cancer [NCT06145633]Phase 215 participants (Anticipated)Interventional2024-04-01Not yet recruiting
FDG and FDOPA PET Demonstration of Functional Brain Abnormalities [NCT04315584]Early Phase 15 participants (Anticipated)Interventional2020-03-15Recruiting
Dual Time Point FDG PET Imaging Optimization for the Evaluation of Glioblastoma [NCT02885272]Early Phase 121 participants (Actual)Interventional2016-10-28Completed
Interim FDG-PET/CT for PreDIcting REsponse of HER2+ Breast Cancer to Neoadjuvant Therapy: DIRECT Trial [NCT05710328]Phase 2235 participants (Anticipated)Interventional2023-05-10Recruiting
Imaging Cell Proliferation With FLT PET: A Pilot Study in Paediatric Lymphoma Patients With Equivocal FDG PET Findings [NCT04028804]8 participants (Actual)Observational2011-07-31Completed
Studies of Activity of Brown Adipose Tissue With Positron Emission Tomography Using the Tracer 18F-deoxy Glucose in Patients With Type 1 Diabetes [NCT02984514]11 participants (Actual)Interventional2015-10-31Completed
Very Early Response Monitoring in Patients With Glioblastoma Undergoing Therapy Using FDG PET/CT [NCT02902757]50 participants (Anticipated)Interventional2015-08-25Recruiting
Determination of the Predictive Value of FDG-PET-CT Scans, Blood Proteins and Blood Cells for the Prognosis for Patients With Lung Cancer Receiving Concurrent Chemo-Radiation [NCT00522639]Phase 3120 participants (Anticipated)Interventional2008-10-31Terminated(stopped due to Poor accrual)
Serial [F-18] Fluoroestradiol (FES) PET Imaging to Evaluate Endocrine-Targeted Therapy [NCT02149173]29 participants (Actual)Interventional2010-09-15Terminated(stopped due to Terminated due to low accrual)
Evaluation of 18 Fluoro-deoxy-glucose Positrons Emission Tomography Combined With Computed Tomography (18-FDG TEP-CT ) in the Diagnosis of the Degeneration of Intraductal Papillary Mucinous Tumor of the Pancreas [NCT01485679]126 participants (Actual)Interventional2011-01-31Completed
Phase I Dose Escalation Trial of 2-Deoxy-D-Glucose (2DG) Alone and in Combination With Docetaxel in Subjects With Advanced Solid Malignancies [NCT00096707]Phase 150 participants (Anticipated)Interventional2004-02-29Completed
Multi-Tracer PET Assessment of Primary Brain Tumors [NCT00813566]Phase 111 participants (Actual)Interventional2010-11-12Completed
NORM: Nodular Lymphocyte-Predominant Hodgkin Lymphoma Patients Treated in a Randomized Phase II Trial With Either Rituximab or Mosunetuzumab [NCT05886036]Phase 270 participants (Anticipated)Interventional2024-07-27Recruiting
A Pilot Study on the Efficacy of Advanced 18F-FDG PET-MRI in Spine Stereotactic Radiosurgery [NCT05174026]10 participants (Actual)Interventional2018-11-30Active, not recruiting
FDG PET to Assess Therapeutic Response in Patients With Bone-Dominant Metastatic Breast Cancer, FEATURE [NCT04316117]Phase 2138 participants (Actual)Interventional2020-09-15Active, not recruiting
A Randomized Phase II/III Trial of De-Intensified Radiation Therapy for Patients With Early-Stage, P16-Positive, Non-Smoking Associated Oropharyngeal Cancer [NCT03952585]Phase 2/Phase 3590 participants (Anticipated)Interventional2019-10-09Suspended(stopped due to End of Initial Phase of Multi-phase protocol)
Serial Imaging of the Novel Radiotracer [^18F] FLuorthanatrace ([^18F] FTT) by PET/CT [NCT03604315]Phase 1120 participants (Anticipated)Interventional2018-12-18Recruiting
A Pilot Study to Assess the Feasibility of Detection and Quantification of Differences in Hodgkin Lymphoma and Diffuse Large B-cell Lymphoma Using FDG-PET/CT Imaging [NCT01004718]10 participants (Actual)Interventional2009-05-31Completed
Phase II Study of Pralatrexate and Docetaxel in Patients With Advanced Esophageal and Gastroesophageal Carcinoma Who Have Failed Prior Platinum-based Therapy. [NCT01129206]Phase 26 participants (Actual)Interventional2010-07-31Completed
Phase 2 Study.Tailored Therapy for Hodgkin Lymphoma Based on Predefined Risk Factors and Early Interim PET/CT for Response Assessment and Further Therapy Decisions. [NCT00392314]Phase 2365 participants (Actual)Interventional2006-10-31Completed
Phase II Study of the Role of Anti-CEA Antibody Immunoscintigraphy & Positron Emission Tomography in the Localization of Recurrent Colorectal Carcinoma in Patients With Rising Serum CEA Levels in the Absence of Imageable Disease by Conventional Modalities [NCT00001568]Phase 2200 participants Interventional1997-02-28Completed
Spatio-temporal Response of Non-Hodgkin's Lymphoma to External Beam Radiation Therapy Measuring 18F-Fluorodeoxyglucose (FDG) Uptake Using a Combined PET/CT Scanner: A Pilot Study [NCT00188929]Phase 210 participants (Anticipated)Interventional2005-08-31Completed
Pilot Project for Creation of the DLBCL Response Prediction Model: Combining Early Interim Functional Imaging, Detection of a Tumor-Specific Clonotype and Metabolic Profiling of Blood of in Patients With Relapsed/Refractory Diffuse Large B-Cell Lymphoma t [NCT02405078]Early Phase 135 participants (Actual)Interventional2015-10-13Completed
Phase I Clinical Trial: 2DG + Stereotactic Radiosurgery (SRS) Protocol for Treatment of Intracranial Metastases [NCT00247403]Phase 10 participants (Actual)Interventional2005-10-31Withdrawn(stopped due to Pharmaceutical company no longer manufactures drug)
Multi-tracer PET Assessment of Response in Various Malignancies in Investigational and Recently Approved Therapeutic Agents [NCT01243333]26 participants (Actual)Interventional2011-02-02Terminated
Randomized Phase II Trial of Individualized Adaptive Radiotherapy Using During-Treatment FDG-PET/CT and Modern Technology in Locally Advanced Non-Small Cell Lung Cancer (NSCLC) [NCT01507428]Phase 2138 participants (Actual)Interventional2012-02-22Active, not recruiting
Evaluation of 18F-FDG PET/CT in Diagnosis and Response Assessment of Patients With IgG4-Related Disease [NCT01665196]Early Phase 1100 participants (Anticipated)Interventional2012-09-30Recruiting
Dual-Time Point (DTP) FDG PET CT for the Post-Treatment Assessment of Head and Neck Tumors Following Definitive Chemoradiation Therapy [NCT03575949]50 participants (Anticipated)Interventional2018-06-15Recruiting
SiCARIO (Split Course Adaptive Radioimmunotherapy) for the Treatment of Oligometastatic Non-Small Cell Lung Cancer (NSCLC) Using Biologically-Adaptive Radiotherapy - A Phase I/II Study [NCT05501665]Phase 1/Phase 225 participants (Anticipated)Interventional2023-05-09Recruiting
A Single Center Pilot Study to Establish the 99mTc-EC-DG Imaging Protocol to Evaluate the Presence and Severity of Coronary Artery Disease [NCT01778218]Phase 22 participants (Actual)Interventional2013-01-31Completed
A Multi-modality Imaging Assessment of Chemobrain [NCT00708045]Phase 134 participants (Actual)Interventional2007-05-09Completed
FDG-PET/CT In the Evaluation of Persistent Febrile Neutropenia in Cancer Patients [NCT00707213]Phase 119 participants (Actual)Interventional2007-08-21Terminated(stopped due to Funding from the NIH ended and not all patients had been accrued)
Personalized Radiation Therapy Through Functional Lung Avoidance and Response-Adaptive Dose Escalation: Utilizing Multimodal Molecular Imaging to Improve the Therapeutic Ratio (FLARE RT) [NCT02773238]Phase 256 participants (Actual)Interventional2016-05-20Completed
Positron Emission Tomography for the Diagnosis of Immune Checkpoint Inhibitor-Related Myocarditis [NCT05062395]13 participants (Actual)Observational2021-03-30Completed
FDG-PET/CT as a Biomarker for Treatment Response in Advanced Melanoma [NCT02236546]3 participants (Actual)Interventional2012-05-31Terminated(stopped due to loss of funding)
Phase II Study of PET-Directed Frontline Therapy With Pembrolizumab and AVD for Patients With Classical Hodgkin Lymphoma [NCT03226249]Phase 230 participants (Actual)Interventional2017-11-09Active, not recruiting
Pharmacokinetics Study of Oral 2-Deoxy-D-Glucose (2DG) in Subjects With a Confirmed Diagnosis of Epilepsy [NCT05605301]Phase 29 participants (Anticipated)Interventional2022-09-02Recruiting
Assessment of Primary and Metastatic Brain Tumor Hypoxia With 18F-Fluoromisonidazole, [18F]Fluoro-2-deoxy-D-glucose (FDG) and [15O]Water (H215O) [NCT01246869]Phase 12 participants (Actual)Interventional2013-03-27Terminated(stopped due to PI retired, study closed)
Monocentric, Prospective, Uncontrolled Pilot Study of Extra Cardiomyocytary Fixation Profile in 18F-fluorodeoxyglucose (FDG) Positron Emission Tomography in Patients With Dilated Cardiomyopathy. [NCT02078141]30 participants (Actual)Interventional2014-06-24Completed
PET Imaging of Lung Cancer and Indeterminate Pulmonary Nodules With 18F-FSPG [NCT02448225]Phase 246 participants (Actual)Interventional2015-06-16Completed
Evaluation of Positron Emission Tomography in Extrapulmonary Tuberculosis [NCT01613196]55 participants (Actual)Interventional2012-05-31Completed
PET Imaging of Breast Cancer Using Oncogene Expression [NCT02810873]19 participants (Actual)Interventional2008-09-30Terminated(stopped due to Study terminated by PI)
Contribution of PET Scans for the Preoperative Assessment of Symptomatic Endometriosis Lesions: TEP-ENDORUN [NCT04831619]Phase 310 participants (Anticipated)Interventional2022-05-31Not yet recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00062374 (2) [back to overview]Histological Response Determined by FDG Uptake Correlates
NCT00062374 (2) [back to overview]Disease Free Survival (DFS)
NCT00375830 (9) [back to overview]Cohort 1 - NaF PET/CT vs 99mTc-MDP Bone Scintigraphy
NCT00375830 (9) [back to overview]Cohort 2 - 18F-NaF/18F-FDG vs 99mTc-MDP Bone Scintigraphy for Detection of Skeletal Lesions
NCT00375830 (9) [back to overview]Cohort 2 - 18F-NaF/18F-FDG PET/CT vs Whole-body MRI for Detection of Extraskeletal Lesions
NCT00375830 (9) [back to overview]Cohort 2 - Overall Sensitivity and Accuracy for 18F-NaF/18F-FDG vs Whole-body MRI/99mTc-MDP Bone Scintigraphy
NCT00375830 (9) [back to overview]Cohort 2 - Overall Sensitivity and Accuracy for 18F-NaF/18F-FDG vs Whole-body MRI
NCT00375830 (9) [back to overview]Cohort 2 - 18F-NaF/18F-FDG vs Whole-body MRI for Detection of Skeletal Lesions
NCT00375830 (9) [back to overview]Cohort 3 - Skeletal Lesions Identified by 99mTc MDP WBBS vs 18F-NaF / 18F-FDG PET/MRI
NCT00375830 (9) [back to overview]Cohort 3 - Total Skeletal Lesions Identified, Tc-99m MDP WBBS vs 18F-NaF / 18F-FDG PET/MRI
NCT00375830 (9) [back to overview]Cohort 1 - 18F-NaF PET/CT vs 18F-FDG PET/CT
NCT00381797 (26) [back to overview]Association of Log-transformed Tumor Enhancing Volume With Progression-free Survival (PFS) Using Hazard Ratio Estimates
NCT00381797 (26) [back to overview]Volume of Distribution
NCT00381797 (26) [back to overview]Progression-free Survival Hazard Ratio by VEGF-R2 Expression
NCT00381797 (26) [back to overview]Association of Log-transformed Tumor Diffusion Ratio With Progression-free Survival (PFS) Using Hazard Ratio Estimates
NCT00381797 (26) [back to overview]Descriptive Statistics for the Changes in Vascular Endothelial Growth Factor Receptor-2 (VEGF-R2) Expression in Peripheral Blood Mononuclear Cells (PBMC) Concurrently Measured With the Changes in Perfusion From Magnetic Resonance Imaging
NCT00381797 (26) [back to overview]Association of Log-transformed Tumor Volume Based on FLAIR With Progression-free Survival (PFS) Using Hazard Ratio Estimates
NCT00381797 (26) [back to overview]Association of Log-transformed Volume of Cystic Necrosis With Progression-free Survival (PFS) Using Hazard Ratio Estimates
NCT00381797 (26) [back to overview]Change in Diffusion Ratio Between the Baseline and Day 15 Brain Image
NCT00381797 (26) [back to overview]Change in Perfusion Ratio Between the Baseline and Day 15 Brain Imaging
NCT00381797 (26) [back to overview]Change in Vascular Endothelial Growth Factor Receptor-2 (VEGF-R2) Expression in Peripheral Blood Mononuclear Cells (PBMC) From Baseline to Day-15
NCT00381797 (26) [back to overview]Correlation of the Change in Vascular Endothelial Growth Factor Receptor-2 (VEGF-R2) Expression in Peripheral Blood Mononuclear Cells (PBMC) From Baseline With the Change in Perfusion From Magnetic Resonance Imaging
NCT00381797 (26) [back to overview]Cumulative Incidence of Sustained Objective Responses
NCT00381797 (26) [back to overview]Descriptive Statistics for the Change of Perfusion in Magnetic Resonance Imaging Concurrently Measured With the Change in Vascular Endothelial Growth Factor Receptor-2 (VEGF-R2) Expression in Peripheral Blood Mononuclear Cells (PBMC)
NCT00381797 (26) [back to overview]Number of Patients With High Carbonic Anhydrase 9 Expression at Baseline
NCT00381797 (26) [back to overview]Number of Patients With High Hypoxia Inducible Factor-2alpha Expression at Baseline
NCT00381797 (26) [back to overview]Number of Patients With High VEGF-A Expression at Baseline
NCT00381797 (26) [back to overview]Number of Patients With High VEGF-R2 Expression at Baseline
NCT00381797 (26) [back to overview]Number of Study Participants With Grade 3 or 4 Treatment-related Toxicity
NCT00381797 (26) [back to overview]Objective Response Rate Sustained for ≥ 8 Weeks
NCT00381797 (26) [back to overview]Progression-free Survival
NCT00381797 (26) [back to overview]Progression-free Survival Hazard Ratio by Carbonic Anhydrase 9 (CA9) Expression
NCT00381797 (26) [back to overview]Progression-free Survival Hazard Ratio by Hypoxia Inducible Factor-2alpha Expression
NCT00381797 (26) [back to overview]Progression-free Survival Hazard Ratio by VEGF-A Expression
NCT00381797 (26) [back to overview]Sustained Disease Stabilization Rate Associated With Bevacizumab and Irinotecan in Patients With Recurrent or Progressive Low-grade Glioma (Stratum E)
NCT00381797 (26) [back to overview]Systemic Clearance
NCT00381797 (26) [back to overview]Terminal Half-life
NCT00633087 (2) [back to overview]Overall Survival
NCT00633087 (2) [back to overview]Progression-free Survival
NCT00729157 (5) [back to overview]Radiographic Response Rate of Aflibercept in Patients With Recurrent and/or Metastatic Thyroid Cancer That Did Not Respond to Radioactive Iodine Therapy
NCT00729157 (5) [back to overview]The Safety and Toxicity Profile of IV VEGF Trap in Patients With Recurrent and/or Metastatic TC-FCO
NCT00729157 (5) [back to overview]To Determine the Biologic Effect of IV VEGF Trap on FDG Avidity After Four Cycles (Approximately 8 Weeks) of Therapy Through Pre- and Post-treatment FDG-PET Scans in Patients With Recurrent and/or Metastatic D-TC-FCO.
NCT00729157 (5) [back to overview]Effect of Thyroglobulin Concentration on Progression-free Survival
NCT00729157 (5) [back to overview]Progression-free Survival to Determine the 6-month Progression-free-survival (PFS) Rate
NCT00963807 (5) [back to overview]Change in 18F-Fluorodeoxyglucose (FDG) Uptake
NCT00963807 (5) [back to overview]Change in 18F-Fluorothymidine (FLT) Uptake
NCT00963807 (5) [back to overview]Change in FLT Uptake
NCT00963807 (5) [back to overview]Change in FLT Uptake in Responders and Non-responders
NCT00963807 (5) [back to overview]Overall Response Rate Reported as a Proportion of the Total Number of Patients Who Received at Least One Cycle of Therapy Assessed Using Response Evaluation Criteria in Solid Tumors (RECIST)
NCT01004718 (1) [back to overview]Percentage Change in Maximum Lesional FDG Uptake From 60 to 180 Minutes After FDG Administration
NCT01038778 (8) [back to overview]Incidence of Toxicities
NCT01038778 (8) [back to overview]Changes in the Level of Specific T Lymphocytes
NCT01038778 (8) [back to overview]Time-to-tumor Progression
NCT01038778 (8) [back to overview]Progression-free Survival
NCT01038778 (8) [back to overview]Overall Survival
NCT01038778 (8) [back to overview]Overall Response Rate (Complete Plus Partial) (Phase II)
NCT01038778 (8) [back to overview]Incidence of Toxicity (Phase I)
NCT01038778 (8) [back to overview]Dose-limiting Toxicities of Entinostat When Combined With Aldesleukin Within the Phase I
NCT01129206 (4) [back to overview]Overall Survival (OS)
NCT01129206 (4) [back to overview]Progression-free Survival (PFS)
NCT01129206 (4) [back to overview]Correlation of FDG PET Response With Response Rate
NCT01129206 (4) [back to overview]Overall Response
NCT01286272 (3) [back to overview]Complete Response Rate
NCT01286272 (3) [back to overview]Progression-free Survival (PFS)
NCT01286272 (3) [back to overview]The Number of Patients Who Experienced Grade 3+ Hematologic and Non-hematologic Adverse Events at Least Possibly Related to Treatment
NCT02149173 (4) [back to overview]Change in F-18 16 Alpha-fluoroestradiol (FES) Standardized Uptake Value (SUV), Assessed by a One-sample Test of the Percent Change in FES SUV
NCT02149173 (4) [back to overview]F-18 16 Alpha-fluoroestradiol (FES) Uptake
NCT02149173 (4) [back to overview]Proportion of Patients Experienced a Threshold in Percentage Change, or Surpassed a Targeted Follow-up F-18 16 Alpha-fluoroestradiol (FES) Standardized Uptake Value (SUV)
NCT02149173 (4) [back to overview]Time to Disease Progression
NCT02448225 (4) [back to overview]Uptake of 18F-FSPG (Expressed in Maximal Standardized Uptake Value [SUV] Within the Tumor)
NCT02448225 (4) [back to overview]Ability of 18F-FSPG PET/CT to Discriminate Benign From Malignant Nodules
NCT02448225 (4) [back to overview]Ability of 18F-FSPG PET/CT to Stage of Lung Cancer (Metastatic or Not)
NCT02448225 (4) [back to overview]CD44 and xC- Expression Levels in Tissue Samples(0-3)
NCT02810873 (1) [back to overview]Number of F-18-FDG Positive Lesions That Are Detected by the Copper Cu 64 TP3805 Analog
NCT03226249 (3) [back to overview]Complete Response (CR) With Pembrolizumab Treatment Alone
NCT03226249 (3) [back to overview]Overall Survival at Treatment Completion
NCT03226249 (3) [back to overview]Progression Free Survival (PFS) at Treatment Completion

Histological Response Determined by FDG Uptake Correlates

"The primary objective was to demonstrate that a decrease in FDG-SUV discriminates treatment response. Response was defined pathologically based on microscopic inspection for residual cancer cells and fibrosis.~Using a two sample t-test, we would be able to adequately test that the decrease in SUV early in the treatment plan is significantly different between responders and non responders. Data adjudication was invalid, and needs to be re-adjudicated~Non-Responder= Tumor Regression Grade 3 or higher Responder=Tumor Regression Grade 1 (CR) or Grade 2 (PR)" (NCT00062374)
Timeframe: Day 15

Interventionparticipants (Number)
Progression of DiseaseRespondersNon-Responders
Arm I2338

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Disease Free Survival (DFS)

Overall Survival (OS) and Disease Free Survival (DFS) are the secondary endpoints. Technical problems with measurement of OS leading to unreliable or uniterpretable data. Data adjudication was invalid, and needs to be re-adjudicated. Therefore, only DFS data is being reported. (NCT00062374)
Timeframe: Every 3 mos for the first 2 yrs, then every 6 mos for 2 years and once a year afterwards, up to 5 years

Interventionmonths (Median)
Arm I23.8

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Cohort 1 - NaF PET/CT vs 99mTc-MDP Bone Scintigraphy

"The medical value of 18F-sodium fluoride (NaF) positron emission tomography / computed tomography (PET/CT) vs 99mTc-methylene diphosphonate (MDP) bone scintigraphy was assessed on the basis of the radiation oncologist's medical assessment of image quality and detected extent of disease, for each participant. Per protocol, the data were collected and the outcome is reported for Cohort 1 only. The outcome is reported as the number of participants for whom the medical value of the image was superior for 18F-NaF vs 99mTc-MDP bone scintigraphy (18F-NaF > 99mTc-MDP), the same between both scans (18F-NaF = 99mTc-MDP), or inferior for 18F-NaF vs 99mTc-MDP bone scintigraphy (18F-NaF < 99mTc-MDP)." (NCT00375830)
Timeframe: 30 days

InterventionParticipants (Count of Participants)
18F-NaF > 99mTc-MDP18F-NaF = 99mTc-MDP18F-NaF < 99mTc-MDP
Cohort 1 Pilot-WB-MRI & Combined 18F-NaF-CT/18F-FDG-PET Scans1000

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Cohort 2 - 18F-NaF/18F-FDG vs 99mTc-MDP Bone Scintigraphy for Detection of Skeletal Lesions

Sensitivity and accuracy for the detection of skeletal lesions was assessed for 18F-sodium fluoride (NaF) / 18F-fluorodeoxyglucose (FDG) positron emission tomography / computed tomography (PET/CT) and for 99mTc-methylene diphosphonate (MDP) bone scintigraphy. Per protocol, the data were collected and the outcome is reported for Cohort 2 only. Sensitivity and accuracy are reported as a percentage, a number without dispersion. Higher numbers represent better detection. (NCT00375830)
Timeframe: 30 days

,
Interventionpercentage of participants (Number)
SensitivityAccuracy
Cohort 2 - 99mTc-MDP Bone Scintigraphy Scan64.665.9
Cohort 2 Combined 18F-NaF-CT/18F-FDG-PET Scan96.289.8

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Cohort 2 - 18F-NaF/18F-FDG PET/CT vs Whole-body MRI for Detection of Extraskeletal Lesions

"Sensitivity; positive predictive value (PPV); and accuracy for the detection of extraskeletal lesions was assessed for 18F-sodium fluoride (NaF) / 18F-fluorodeoxyglucose (FDG) positron emission tomography / computed tomography (PET/CT) and for whole body magnetic imaging resonance (WB-MRI).~Sensitivity is a percentage that defines the proportion of true positive participants with the disease in a total group of participants.~PPV is the probability that participants with a positive screening test truly have the disease.~Accuracy is the proportion of true results (both true positives and true negatives) among the total number of cases examined.~Per protocol, the data were collected and the outcome is reported for Cohort 2 only. Sensitivity, PPV, and accuracy are reported as a percentage, a number without dispersion. Higher numbers represent better detection." (NCT00375830)
Timeframe: 30 days

,
Interventionpercentage of particpants (Number)
SensitivityPositive predictive valueAccuracy
Cohort 2 - Combined 18F-NaF-CT/18F-FDG-PET Scan92.981.376.5
Cohort 2 - Whole Body-MRI Scan92.986.782.4

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Cohort 2 - Overall Sensitivity and Accuracy for 18F-NaF/18F-FDG vs Whole-body MRI/99mTc-MDP Bone Scintigraphy

Overall sensitivity and accuracy for the detection of tumor lesions was assessed for 18F-sodium fluoride (NaF) / 18F-fluorodeoxyglucose (FDG) positron emission tomography / computed tomography (PET/CT) and for 99mTc-methylene diphosphonate (MDP) bone scintigraphy. Per protocol, the data were collected and the outcome is reported for Cohort 2 only. Sensitivity and accuracy are reported as a percentage, a number without dispersion. Higher numbers represent better detection. (NCT00375830)
Timeframe: 30 days

,
Interventionpercentage of participants (Number)
SensitivityAccuracy
Cohort 2 Combined 18F-NaF-CT/18F-FDG-PET Scan95.787.6
Cohort 2 WB-MRI & 99mTc-MDP Bone Scintigraphy91.683.0

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Cohort 2 - Overall Sensitivity and Accuracy for 18F-NaF/18F-FDG vs Whole-body MRI

Overall sensitivity and accuracy for the detection of tumor lesions was assessed for 18F-sodium fluoride (NaF) / 18F-fluorodeoxyglucose (FDG) positron emission tomography / computed tomography (PET/CT) and for whole body magnetic imaging resonance (WB-MRI). Per protocol, the data were collected and the outcome is reported for Cohort 2 only. Sensitivity and accuracy are reported as a percentage, a number without dispersion. Higher numbers represent better detection. (NCT00375830)
Timeframe: 30 days

,
Interventionpercentage of participants (Number)
SensitivityAccuracy
Cohort 2 - Combined 18F-NaF-CT/18F-FDG-PET Scan95.787.6
Cohort 2 - Whole Body Magnetic Resonance Imaging (WB-MRI) Scan83.376.0

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Cohort 2 - 18F-NaF/18F-FDG vs Whole-body MRI for Detection of Skeletal Lesions

Sensitivity and accuracy for the detection of skeletal lesions was assessed for 18F-sodium fluoride (NaF) / 18F-fluorodeoxyglucose (FDG) positron emission tomography / computed tomography (PET/CT) and for whole body magnetic imaging resonance (WB-MRI). Per protocol, the data were collected and the outcome is reported for Cohort 2 only. Sensitivity and accuracy are reported as a percentage, a number without dispersion. Higher numbers represent better detection. (NCT00375830)
Timeframe: 30 days

,
Interventionpercentage of particpants (Number)
SensitivityAccuracy
Cohort 2 - Combined 18F-NaF-CT/18F-FDG-PET Scan96.289.8
Cohort 2 - WB-MRI Scan81.474.7

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Cohort 3 - Skeletal Lesions Identified by 99mTc MDP WBBS vs 18F-NaF / 18F-FDG PET/MRI

Participants in Cohort 3 received 99mTc-methylene diphosphonate (MDP) whole-body bone scintigraphy (WBBS) and 18F-sodium fluoride (NaF) / 18F-fluorodeoxyglucose (FDG) positron emission tomography / magnetic imaging resonance (PET/MRI) scans. On the basis of the scans, participants with skeletal lesions were identified. The outcome is reported as the number of Cohort 3 participants for whom skeletal lesions were identified by each scan methodology, a number without dispersion. (NCT00375830)
Timeframe: 30 days

InterventionParticipants (Count of Participants)
Cohort 3 - 99mTc-methyl Diphosphonate (MDP) Bone Scan37
Cohort 3 - 18F-NaF / 18F-FDG PET/MRI45

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Cohort 3 - Total Skeletal Lesions Identified, Tc-99m MDP WBBS vs 18F-NaF / 18F-FDG PET/MRI

Participants in Cohort 3 received 99mTc-methylene diphosphonate (MDP) whole-body bone scintigraphy (WBBS) and 18F-sodium fluoride (NaF) / 18F-fluorodeoxyglucose (FDG) positron emission tomography / magnetic imaging resonance (PET/MRI) scans. On the basis of the scans, the total number skeletal lesions identified in the participants was determined. The outcome is reported as the total number skeletal lesions identified by each scan methodology, a number without dispersion. (NCT00375830)
Timeframe: 30 days

Interventionlesions (Number)
Cohort 3 - 99mTc-methyl Diphosphonate (MDP) Bone Scan81
Cohort 3 - 18F-NaF / 18F-FDG PET/MRI140

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Cohort 1 - 18F-NaF PET/CT vs 18F-FDG PET/CT

The medical value of 18F-sodium fluoride (NaF) positron emission tomography / computed tomography (PET/CT) vs 18F-fluorodeoxyglucose (FDG) positron emission tomography / computed tomography (PET/CT) was assessed on the basis of the radiation oncologist's medical assessment of image quality and detected extent of disease, for each participant diagnosed with osseous (skeletal) metastases. Per protocol, the data were collected and the outcome is reported for Cohort 1 only. The outcome is reported as the number of participants for whom the medical value of the image was superior for 18-NaF PET/CT compared to 18F-FDG PET/CT, the same between both scans, or inferior for 18-NaF PET/CT compared to 18F-FDG PET/CT. The outcome result is represented as a number without dispersion. (NCT00375830)
Timeframe: 30 days

InterventionParticipants (Count of Participants)
18F-NaF > 18F-FDG18F-NaF = 18F-FDG18F-NaF < 18F-FDG
Cohort 1 Pilot-WB-MRI & Combined 18F-NaF-CT/18F-FDG-PET Scans300

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Association of Log-transformed Tumor Enhancing Volume With Progression-free Survival (PFS) Using Hazard Ratio Estimates

Using Cox Proportional hazards Models, the association of Log-transformed tumor enhancing volume with progression-free survival will be investigated. Volumetric magnetic resonance (MR) imaging is performed to investigate surrogate markers of tumor growth. Tumor enhancing volumes were longitudinal. As we are not comparing the strata or study arms, analyses will be done in each stratum separately, and thus we cannot report the Cox model results in the Statistical Analysis section and we consider these estimates 'descriptive' within each stratum. In this analysis, the hazard ratio is a relative measure of likelihood that a study participant experiences the event of interest compared to another participant who has a one-unit lower Log-transformed tumor enhancing volume. The Cox survival model provides the mean hazard ratio along with its 95% confidence interval, which we report below. (NCT00381797)
Timeframe: From start of treatment until the earliest of progressive disease, death, second malignancy or off study, OR up to 2 years

InterventionHazard Ratio (Mean)
High-grade Gliomas1.65
Brain Stem Tumors1.16

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Volume of Distribution

"Blood specimens were collected on the days listed for pharmacokinetic studies for Bevacizumab. These specimens were analyzed to produce steady-state plasma Bevacizumab concentration-time data in study participants. The concentration-time data were analyzed to provide an estimate of the volume of distribution. The data were collected but the analyses of the PK data were conducted by Genentech using a broader cohort of pediatric patients from multiple trials in the paper Bevacizumab dosing strategy in paediatric cancer patients based on population pharmacokinetic analysis with external validation published by British Journal of Clinical Pharmacology ,2016 volume 81(1):148-160. The estimates of the volume of distribution were calculated by the model described in the paper." (NCT00381797)
Timeframe: Baseline, Course 1 Day 1, Course 1 Day 15, Course 2 Day 1, Course 3 Day 1, Course 4 Day 1, and Course 5 Day 1

Interventionml (Mean)
Combined All Strata1729

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Progression-free Survival Hazard Ratio by VEGF-R2 Expression

The association of VEGF-R2 expression with progression-free survival will be investigated for those strata that have a sufficient number of participants with VEGF-R2 measurements. (NCT00381797)
Timeframe: From start of treatment until the earliest of progressive disease, death, second malignancy or off study

InterventionHazard Ratio (Number)
Low Grade Glioma0.632

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Association of Log-transformed Tumor Diffusion Ratio With Progression-free Survival (PFS) Using Hazard Ratio Estimates

Using Cox Proportional Hazards Models, the association of tumor diffusion ratios with progression-free survival will be investigated. Magnetic resonance (MR) diffusion imaging is performed to investigate surrogate markers of tumor growth. Tumor diffusion ratios were longitudinal. As we are not comparing the strata or study arms, analyses will be done in each stratum separately, and thus we cannot report the Cox model results in the Statistical Analysis section. And we consider these estimates 'descriptive' within each stratum. In this analysis, the hazard ratio is a relative measure of likelihood that a study participant experiences the event of interest compared to another participant who has a one-unit lower Log-transformed tumor diffusion ratio. The Cox survival model provides the mean hazard ratio along with its 95% confidence interval, which we report below. (NCT00381797)
Timeframe: From start of treatment until the earliest of progressive disease, death, second malignancy or off study

InterventionHazard Ratio (Mean)
High-grade Gliomas4.41
Brain Stem Tumors1.82

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Descriptive Statistics for the Changes in Vascular Endothelial Growth Factor Receptor-2 (VEGF-R2) Expression in Peripheral Blood Mononuclear Cells (PBMC) Concurrently Measured With the Changes in Perfusion From Magnetic Resonance Imaging

The changes in VEGF-R2 are calculated by values at Day 15 minus values at baseline for the patients who had the changes in perfusion from magnetic resonance perfusion imaging. The purpose of reporting descriptive statistics of changes of VEGF-R2 is to provide the information for the correlation coefficients in Section 19. (NCT00381797)
Timeframe: Baseline and Day 15 (after 2 doses of Bevacizumab) of course 1

InterventionRatio (Mean)
High-grade Gliomas-1.12
Brain Stem Tumors-1.20

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Association of Log-transformed Tumor Volume Based on FLAIR With Progression-free Survival (PFS) Using Hazard Ratio Estimates

Using Cox proportional hazards models, the association of tumor volume based on FLAIR images with PFS will be investigated for those strata that have a sufficient number of participants with volume FLAIR measurements. Volumetric magnetic resonance imaging is performed to investigate surrogate markers of tumor growth. Volume FLAIR measurements were longitudinal. As we are not comparing the strata, analyses will be done in each stratum separately, and thus we cannot report the Cox model results in the Statistical Analysis section. We consider these estimates 'descriptive' within each stratum. In this analysis, the hazard ratio is a relative measure of likelihood that a study participant experiences the event of interest compared to another participant who has a one-unit lower Log-transformed tumor volume based on FLAIR. The Cox survival model provides the mean hazard ratio along with its 95% confidence interval, which we report below. (NCT00381797)
Timeframe: From start of treatment until the earliest of progressive disease, death, second malignancy or off study OR up to 2 years

InterventionHazard Ratio (Mean)
High-grade Gliomas1.47
Brain Stem Tumors1.76

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Association of Log-transformed Volume of Cystic Necrosis With Progression-free Survival (PFS) Using Hazard Ratio Estimates

Using Cox Proportional Hazards Models, the association of cystic necrosis with progression-free survival will be investigated. Volumetric magnetic resonance (MR) imaging is performed to investigate surrogate markers of tumor growth. Volumes of cystic necrosis were longitudinal. As we are not comparing the strata or study arms, analyses will be done in each stratum separately, and thus we cannot report the Cox model results in the Statistical Analysis section and we consider these estimates 'descriptive' within each stratum. In this analysis, the hazard ratio is a relative measure of likelihood that a study participant experiences the event of interest compared to another participant who has a one-unit lower Log-transformed tumor volume based on cystic necrosis. The Cox survival model provides the mean hazard ratio along with its 95% confidence interval, which we report below. (NCT00381797)
Timeframe: From start of treatment until the earliest of progressive disease, death, second malignancy or off study, OR up to 2 years

InterventionHazard Ratio (Mean)
High-grade Gliomas2.56
Brain Stem Tumors1.09

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Change in Diffusion Ratio Between the Baseline and Day 15 Brain Image

Diffusion ratio obtained from magnetic resonance (MR) diffusion imaging may explain changes in the tumor after therapy. Changes in the diffusion ratio will be reported for those strata that have a sufficient number of participants with MR diffusion imaging. The change was calculated from diffusion ratio at Baseline to diffusion ratio at Day 15 (values of diffusion ratio at Day 15 -values of diffusion ration at baseline). The higher of diffusion ratio is better. MR diffusion ratio is the diffusion solid part of tumor divided by the diffusion frontal white matter. There is no a unit available. (NCT00381797)
Timeframe: Baseline and day 15

InterventionRatio (Median)
High-grade Gliomas-0.34
Brain Stem Tumors-0.17
Ependymoma0.11
Low Grade Glioma-0.11

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Change in Perfusion Ratio Between the Baseline and Day 15 Brain Imaging

"Perfusion ratio obtained from magnetic resonance(MR) diffusion imaging may explain changes in the tumor after therapy. Changes in the perfusion ratio will be reported for those strata that have a sufficient number of participants with MR diffusion imaging. The change was calculated from perfusion ratio at Baseline to perfusion ratio at Day 15(values of perfusion ratio at Day 15 - values of perfusion ratio at baseline). The higher of perfusion ratio is worse.~MR perfusion ratio is perfusion solid part of tumor from CBV divided by perfusion frontal while matter. There is no a unit available." (NCT00381797)
Timeframe: Baseline and day 15

InterventionRatio (Median)
High-grade Gliomas-0.14
Brain Stem Tumors-1.98
Low Grade Glioma-0.42

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Change in Vascular Endothelial Growth Factor Receptor-2 (VEGF-R2) Expression in Peripheral Blood Mononuclear Cells (PBMC) From Baseline to Day-15

The change in VEGF-R2 was calculated from baseline to the time of the 2nd dose (values of 24-48 hours after the 2nd dose at Day 15 - values of pre-dose 1 Day1, i.e., baseline). VEGF-R2 is measured in the relative phosphorylation score which is generated as a ratio of normalized phosphorylated VEGF-R2 versus normalized total VEGF-R2 protein. (NCT00381797)
Timeframe: Baseline and 24-48 hours after the 2nd dose of Bevacizumab in course 1

InterventionRatio (Median)
High-grade Gliomas-0.37
Brain Stem Tumors-0.21
Medulloblastoma-0.003
Ependymoma0.24
Low Grade Glioma1.70

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Correlation of the Change in Vascular Endothelial Growth Factor Receptor-2 (VEGF-R2) Expression in Peripheral Blood Mononuclear Cells (PBMC) From Baseline With the Change in Perfusion From Magnetic Resonance Imaging

Spearman correlation coefficient is used to measure the correlation of the changes in VEGF-R2 with the changes in perfusion ratios. The changes are calculated by values at Day 15 minus values at baseline for VEGF-2 in Section 17 above and perfusion in Section 18 above, respectively. The correlation coefficients are reported in each stratum separately. (NCT00381797)
Timeframe: Baseline and Day 15 (after 2 doses of Bevacizumab) of course 1

InterventionCorrelation Coefficient (Number)
High-grade Gliomas0.5
Brain Stem Tumors-0.50

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Cumulative Incidence of Sustained Objective Responses

Cumulative incidence of sustained objective response provides a percentage of participants experiencing the event of interest at a given follow-up time point (for example, 6-months, 1-year, etc.) in the presence of competing events such as progressive disease or death, and it is estimated using the event data for both the event of interest and the competing events experienced by the study participants. In this sense, it is different than the incidence rates estimated in epidemiological studies in terms of 'incidences per 1000 person years. 6-month Cumulative incidence of sustained objective responses will be reported separately for each stratum. (NCT00381797)
Timeframe: From the first imaging after treatment up to 2 years

InterventionPercentage of Participants (Number)
High-grade Gliomas0
Brain Stem Tumors0
Medulloblastoma0
Ependymoma0
Low Grade Glioma0.058

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Descriptive Statistics for the Change of Perfusion in Magnetic Resonance Imaging Concurrently Measured With the Change in Vascular Endothelial Growth Factor Receptor-2 (VEGF-R2) Expression in Peripheral Blood Mononuclear Cells (PBMC)

The change of perfusion in magnetic resonance imaging is calculated by taking the difference between the Day-15 measurements and the Baseline measurements for patients who had the changes of VEGF-R2. The purpose of reporting the descriptive statistics is to provide the information for the correlation coefficients reported in the next section, Section 19. MR perfusion ratio is the ratio of the perfusion measurements in the tumor and the perfusion measurerement in comparative frontal while matter, which is the comparative healthy part of the brain. (NCT00381797)
Timeframe: Baseline and Day 15 (after 2 doses of Bevacizumab) of course 1

InterventionRatio (Mean)
High-grade Gliomas-1.60
Brain Stem Tumors-1.54

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Number of Patients With High Carbonic Anhydrase 9 Expression at Baseline

The expression of Hypoxia inducible factor-2α, carbonic anhydrase IX (CA9), VEGF-A, and VEGF-R2 will be estimated by immunohistochemistry of paraffin sections in the medulloblastoma,ependymoma and low grade glioma strata. Reported separately for each stratum. (NCT00381797)
Timeframe: Baseline

Interventionparticipants (Number)
Medulloblastoma0
Ependymoma4
Low Grade Glioma2

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Number of Patients With High Hypoxia Inducible Factor-2alpha Expression at Baseline

The expression of Hypoxia inducible factor-2α, carbonic anhydrase IX (CA9), VEGF-A, and VEGF-R2 will be estimated by immunohistochemistry of paraffin sections in the medulloblastoma,ependymoma and low grade glioma strata. Reported separately for each stratum. (NCT00381797)
Timeframe: Baseline

Interventionparticipants (Number)
Medulloblastoma0
Ependymoma3
Low Grade Glioma7

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Number of Patients With High VEGF-A Expression at Baseline

The expression of Hypoxia inducible factor-2α, carbonic anhydrase IX (CA9), VEGF-A, and VEGF-R2 will be estimated by immunohistochemistry of paraffin sections in the medulloblastoma,ependymoma and low grade glioma strata. Reported separately for each stratum. (NCT00381797)
Timeframe: Baseline

Interventionparticipants (Number)
Medulloblastoma2
Ependymoma5
Low Grade Glioma16

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Number of Patients With High VEGF-R2 Expression at Baseline

The expression of Hypoxia inducible factor-2α, carbonic anhydrase IX (CA9), VEGF-A, and VEGF-R2 will be estimated by immunohistochemistry of paraffin sections in the medulloblastoma,ependymoma and low grade glioma strata. Reported separately for each stratum. (NCT00381797)
Timeframe: Baseline

Interventionparticipants (Number)
Medulloblastoma4
Ependymoma4
Low Grade Glioma13

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Objective Response Rate Sustained for ≥ 8 Weeks

Objective response is either a complete response or a partial response observed during the first four courses of treatment and sustained for 8 weeks. The objective response rate will be reported separately for patients with recurrent/progressive malignant glioma(Stratum A), recurrent/progressive instrinsic brain stem tumors(Stratum B), recurrent/progressive medulloblastoma(Stratum C), and recurrent/progressive ependymoma(Stratum D). CR is complete disappearance of all enhancing tumor. PR is >= 50% reduction in tumor size. This outcome measures is not defined for the Stratum E in the protocol. (NCT00381797)
Timeframe: From day 1 of treatment up to 24 weeks

Interventionparticipants (Number)
High-grade Gliomas0
Brain Stem Tumors0
Medulloblastoma0
Ependymoma0

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Progression-free Survival

Progression-Free survival is the interval of time between of protocol treatment and minimum date of documentation of progressive Disease,second malignancy,death due to any cause, or date of last follow-up. Progressive neurologic abnormalities or worsening neurologic status not explained by causes unrelated to tumor progression,OR the appearance of new tumor OR a > 25% increase in the sum of the products of two longest perpendicular diameters of all measurable tumors. K-M method was used to estimate progression-free survival. (NCT00381797)
Timeframe: From start of treatment up to 2 years

InterventionMonths (Median)
High-grade Gliomas4.20
Brain Stem Tumors2.35
Medulloblastoma2.48
Ependymoma2.15

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Progression-free Survival Hazard Ratio by Carbonic Anhydrase 9 (CA9) Expression

The association of CA9 expression with progression-free survival will be investigated for those strata that have a sufficient number of participants with CA9 measurements. (NCT00381797)
Timeframe: From start of treatment until the earliest of progressive disease, death, second malignancy or off study

InterventionHazard Ratio (Number)
Low Grade Glioma0.705

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Progression-free Survival Hazard Ratio by Hypoxia Inducible Factor-2alpha Expression

The association of hypoxia inducible factor-2alpha expression with progression-free survival will be investigated for those strata that have a sufficient number of participants with hypoxia inducible factor-2alpha measurements. The hazard ratio was reported for patients who had hypoxia inducible factor-2alpha expression. (NCT00381797)
Timeframe: From start of treatment until the earliest of progressive disease, death, second malignancy or off study

InterventionHazard Ratio (Number)
Low Grade Glioma1.36

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Progression-free Survival Hazard Ratio by VEGF-A Expression

The association of VEGF-A expression with progression-free survival will be investigated for those strata that have a sufficient number of participants with VEGF-A measurements. (NCT00381797)
Timeframe: From start of treatment until the earliest of progressive disease, death, second malignancy or off study

InterventionHazard Ratio (Number)
Low Grade Glioma0.091

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Sustained Disease Stabilization Rate Associated With Bevacizumab and Irinotecan in Patients With Recurrent or Progressive Low-grade Glioma (Stratum E)

Disease stabilization is defined as a complete response(CR) or partial response(PR) observed during the first four courses and sustained for 8 weeks; or stable disease (SD) sustained for 6 courses characterized by SD at the end of course 2, at the end of course 4 and at the end of course 6. CR is complete disappearance of all enhancing tumor. PR is >= 50% reduction in tumor size. SD is at least stable and maintenance corticosteroid dose not increased in neurologic examination. (NCT00381797)
Timeframe: From day 1 of treatment up to 24 weeks

Interventionparticipants (Number)
Low Grade Glioma23

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Systemic Clearance

"Blood specimens were collected on the days listed for pharmacokinetic studies for Bevacizumab. These specimens were analyzed to produce steady-state plasma Bevacizumab concentration-time data in study participants. The concentration-time data were analyzed to provide an estimate of the systemic clearance. The data were collected but the analyses of the PK data were conducted by Genentech using a broader cohort of pediatric patients from multiple trials in the paper Bevacizumab dosing strategy in paediatric cancer patients based on population pharmacokinetic analysis with external validation published by British Journal of Clinical Pharmacology, 2016 volume 81(1):148-160. The estimates of the systemic clearance were calculated by the model described in the paper." (NCT00381797)
Timeframe: Baseline, Course 1 Day 1, Course 1 Day 15, Course 2 Day 1, Course 3 Day 1, Course 4 Day 1, and Course 5 Day 1

Interventionml/h (Mean)
Combined All Strata9.43

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Terminal Half-life

"Blood specimens were collected on the days listed for pharmacokinetic studies for Bevacizumab. These specimens were analyzed to produce steady-state plasma Bevacizumab concentration-time data in study participants. The concentration-time data were analyzed to provide an estimate of the PK parameters. The data were collected but the analyses of the PK data were conducted by Genentech using a broader cohort of pediatric patients from multiple trials in the paper Bevacizumab dosing strategy in paediatric cancer patients based on population pharmacokinetic analysis with external validation published by British Journal of Clinical Pharmacology,2016 volume 81(1):148-160. The estimates of the terminal half-life were calculated by the method described in the paper." (NCT00381797)
Timeframe: Baseline, Course 1 Day 1, Course 1 Day 15, Course 2 Day 1, Course 3 Day 1, Course 4 Day 1, and Course 5 Day 1

Interventionhours (Mean)
Combined All Strata125.2

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Overall Survival

(NCT00633087)
Timeframe: 5 years

InterventionParticipants (Count of Participants)
2-deoxyglucose7

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Progression-free Survival

(NCT00633087)
Timeframe: 5 years

InterventionParticipants (Count of Participants)
2-deoxyglucose9

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Radiographic Response Rate of Aflibercept in Patients With Recurrent and/or Metastatic Thyroid Cancer That Did Not Respond to Radioactive Iodine Therapy

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions & assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + P RMeasurable lesions are defined as those that can be accurately measured in at least one dimension (longest diameter to be recorded) as ≥ 20 mm with conventional techniques (CT, MRI, x-ray) or as ≥ 10 mm with spiral CT scan. All tumor measurements must be recorded in millimeters (or decimal fractions of centimeters). All other lesions (or sites of disease), including small lesions (longest diameter < 20 mm with conventional techniques or < 10 mm using spiral CT scan), are considered non-measurable disease. Bone lesions, leptomeningeal disease, ascites, pleural/pericardial effusions, lymphangitis cutis/pulmonis, inflammatory breast disease, abdominal masses (not followed by CT or MRI), & cystic (NCT00729157)
Timeframe: After 8 weeks of study therapy

Interventionparticipants (Number)
Progression of DiseaseStable Disease
Treatment (Ziv-aflibercept and Fludeoxyglucose F 18)733

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The Safety and Toxicity Profile of IV VEGF Trap in Patients With Recurrent and/or Metastatic TC-FCO

The number of participants, with recurrent and/or metastatic TC-FCO, who experienced adverse events. Please see the adverse event table for the specifics for this protocol. (NCT00729157)
Timeframe: From the beginning of treatment through 30 days until participant comes off study

Interventionparticipants (Number)
Treatment (Ziv-aflibercept and Fludeoxyglucose F 18)36

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To Determine the Biologic Effect of IV VEGF Trap on FDG Avidity After Four Cycles (Approximately 8 Weeks) of Therapy Through Pre- and Post-treatment FDG-PET Scans in Patients With Recurrent and/or Metastatic D-TC-FCO.

To determine the biologic effect of IV VEGF Trap on FDG avidity after four cycles (approximately 8 weeks) of therapy through pre- and post-treatment FDG-PET scans in patients with recurrent and/or metastatic D-TC-FCO. (NCT00729157)
Timeframe: 8 weeks

Interventionpercent of SUVm change (Median)
Treatment (Ziv-aflibercept and Fludeoxyglucose F 18).64

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Effect of Thyroglobulin Concentration on Progression-free Survival

The change is serum thyroglobulin was measured by the percent change between the baseline value and the lowest value obtained while on treatment. (NCT00729157)
Timeframe: 6 months

Interventionpercent change serum thyroglobulin (Median)
Treatment (Ziv-aflibercept and Fludeoxyglucose F 18)0.4

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Progression-free Survival to Determine the 6-month Progression-free-survival (PFS) Rate

Progression-free survival to determine the 6-month progression-free-survival (PFS) rate (NCT00729157)
Timeframe: 6 months

Interventionmonths (Median)
Treatment (Ziv-aflibercept and Fludeoxyglucose F 18)5.4

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Change in 18F-Fluorodeoxyglucose (FDG) Uptake

Will be calculated by subtracting the baseline FDG uptake from the post-cycle 2 uptake (as measured by SULmax). (NCT00963807)
Timeframe: Baseline and 6 weeks

InterventionSULmax (Mean)
Treatment (Docetaxel, Cisplatin, Dexamethasone, and Surgery)-3.8

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Change in 18F-Fluorothymidine (FLT) Uptake

Will be calculated by subtracting the uptake of the scan after the first cycle of chemotherapy from the uptake of the pre-treatment scan.. Change in FLT uptake will be measured using the maximum standard uptake value adjusted for lean body mass (SULmax), which is a measure of how much radiotracer (in this case FLT) is being consumed by cells. (NCT00963807)
Timeframe: Baseline and 3 weeks

InterventionSULmax (Mean)
Treatment (Docetaxel, Cisplatin, Dexamethasone, and Surgery)-0.4

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Change in FLT Uptake

Will be calculated by subtracting the uptake of the scan after the second cycle of chemotherapy from the uptake of the pre-treatment scan. (NCT00963807)
Timeframe: Baseline and 6 weeks

InterventionSULmax (Mean)
Treatment (Docetaxel, Cisplatin, Dexamethasone, and Surgery)0.2

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Change in FLT Uptake in Responders and Non-responders

Unadjusted analysis will be performed utilizing students t-tests. If the data appears non-normal, the Wilcox on rank-sum test will be used rather than the t-test. Adjusted analysis will be performed utilizing logistic regression. (NCT00963807)
Timeframe: Baseline and 6 weeks

InterventionSULmax (Mean)
Responders-1.8
Non-Responders1.2

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Overall Response Rate Reported as a Proportion of the Total Number of Patients Who Received at Least One Cycle of Therapy Assessed Using Response Evaluation Criteria in Solid Tumors (RECIST)

RECIST version 1.1 was utilized for this outcome measure. A detailed description of RECIST 1.1 can be found here: Nishino M, Jackman DM, Hatabu H, Yeap BY, Cioffredi LA, Yap JT, et al. New Response Evaluation Criteria in Solid Tumors (RECIST) guidelines for advanced non-small cell lung cancer: comparison with original RECIST and impact on assessment of tumor response to targeted therapy. AJR Am J Roentgenol 2010;195:W221-8. (NCT00963807)
Timeframe: Up to 6 weeks

Interventionpercentage of participants (Number)
Treatment (Docetaxel, Cisplatin, Dexamethasone, and Surgery)33

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Percentage Change in Maximum Lesional FDG Uptake From 60 to 180 Minutes After FDG Administration

Lesional fluorodeoxyglucose (FDG) uptake is measured by standardized uptake value (SUV). The study compared the percentage of change in maximum SUV over 2 hours (first measure was 60 minutes post-administration and second timepoint was 180 minutes post-administration). (NCT01004718)
Timeframe: 2 hours (between 60 minutes post-administration and 180 minutes post-administration)

Interventionpercentage of change in maximum SUV (Mean)
Diffuse Large B-cell Lymphoma36.2
Hodgkin's Lymphoma32

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Incidence of Toxicities

The number of participants with serious adverse events. (NCT01038778)
Timeframe: Up to 30 days

InterventionParticipants (Count of Participants)
Treatment (Entinostat, Aldesleukin)9

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Changes in the Level of Specific T Lymphocytes

Mean percent change from baseline of T lymphocytes. (NCT01038778)
Timeframe: Baseline to approximately 4 weeks post-treatment, up to 1 year

Interventionpercentage of cells count (Mean)
Dose Level 126.3
Dose Level 210.5

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Time-to-tumor Progression

The median time to tumor progression (TTP) was estimated using standard Kaplan-Meier methods, where estimates of the median were obtained with 95% confidence intervals (CIs). TTP was defined as the time from the start of treatment to progression or last follow-up. Patients that did not progress were censored. (NCT01038778)
Timeframe: up to 12-months after the last subject enrolls

Interventionmonths (Median)
Treatment (Entinostat, Aldesleukin)14

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Progression-free Survival

"The median progression-free survival (PFS) was estimated using standard Kaplan-Meier methods, where estimates of the median were obtained with 95% confidence intervals (CIs). PFS was defined as the time from the start of treatment to progression or death due to any cause or last follow-up, patients who did not progress or die were censored.~MEASUREMENT OF EFFECT Patients underwent CT scans at week 11 (+/- 7 days) of each cycle during aldesleukin administration and then every 8-12 weeks (+/- 2 weeks). Response Evaluation Criteria in Solid Tumors (RECIST V.1.0)" (NCT01038778)
Timeframe: up to 12-months after the last subject enrolls

Interventionmonths (Median)
Treatment (Entinostat, Aldesleukin)14.0

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Overall Survival

The 3-year overall survival (OS) rate was estimated using standard Kaplan-Meier methods, where estimates of the median were obtained with 95% confidence intervals (CIs). OS was defined as the time from the start of treatment to death due to any cause or last follow-up, patients who did not die were censored. (NCT01038778)
Timeframe: up to 12-months after the last subject enrolls

Interventionpercentage of participants (Number)
Treatment (Entinostat, Aldesleukin)82.1

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Overall Response Rate (Complete Plus Partial) (Phase II)

"The proportion of patients who have a partial or complete response to treatment evaluated by RECIST V.1.0 criteria.~MEASUREMENT OF EFFECT Patients underwent CT scans at week 11 (+/- 7 days) of each cycle during aldesleukin administration and then every 8-12 weeks (+/- 2 weeks). Response Evaluation Criteria in Solid Tumors (RECIST V.1.0)" (NCT01038778)
Timeframe: Up to 12 months

InterventionProportion of participants (Number)
Treatment (Entinostat, Aldesleukin).39

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Incidence of Toxicity (Phase I)

Count of participants with grade 4 toxicity. The frequency and grade of toxicities will be tabulated for each dose level. (NCT01038778)
Timeframe: 84 days

InterventionParticipants (Count of Participants)
Dose Level 11
Dose Level 20

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Dose-limiting Toxicities of Entinostat When Combined With Aldesleukin Within the Phase I

Number of dose-limiting toxicities of entinostat when combined with aldesleukin within the Phase I MEASUREMENT OF EFFECT Patients underwent CT scans at week 11 (+/- 7 days) of each cycle during aldesleukin administration and then every 8-12 weeks (+/- 2 weeks). Response Evaluation Criteria in Solid Tumors (RECIST V.1.0) (NCT01038778)
Timeframe: 84 days

InterventionParticipants (Count of Participants)
Dose Level 10
Dose Level 20

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Overall Survival (OS)

OS was determined from the date of start of therapy to death frm any cause. (NCT01129206)
Timeframe: Approximately five years

Interventionmonths (Median)
Arm I5.5

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Progression-free Survival (PFS)

Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT01129206)
Timeframe: Approximately three years

Interventionmonths (Median)
Arm I: Pralatrexate and Docetaxel1.9

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Correlation of FDG PET Response With Response Rate

Radiological assessment of tumor response was performed by computed tomography (CT) and positron emission tomography (PET) every four cycles of therapy and responses were measured according to RECIST and PERCIST criteria. (NCT01129206)
Timeframe: Approximately three years

,
Interventionpatients (Number)
Progressive DiseaseStable DiseasePartial Response
PERCIST Criteria Per PET022
RECIST Criteria Per CT420

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Overall Response

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT01129206)
Timeframe: Approximately three years

Interventionpatients (Number)
Stable diseaseProgressive disease
Arm I: Pralatrexate and Docetaxel24

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Complete Response Rate

"A complete response was defined using International Harmonization Project Response Criteria as the complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present before therapy. If the bone marrow was involved by lymphoma before treatment, the infiltrate must have cleared on repeat bone marrow biopsy.~The complete response (CR) rate was calculated in newly diagnosed untreated follicular lymphoma patients receiving 6 cycles of ofatumumab-bendamustine (ARM A) and 6 cycles of ofatumumab, bortezomib, and bendamustine (ARM B).~The complete response rate was calculated as the number of patients with a complete response divided by the number of patients eligible for evaluation." (NCT01286272)
Timeframe: From date of randomization until patient stops treatment for any reason, up to 484 days post-randomization

Interventionproportion of patients (Number)
Arm A (Ofatumumab, Bendamustine Hydrochloride).621
Arm B (Ofatumumab, Bendamustine Hydrochloride, Bortezomib).597

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Progression-free Survival (PFS)

Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. PFS rates (percentages) at 1, 2, ,3 and 4 years are defined as the percentage of patients who are alive and progression-free at the respective time points. The p-values of the log-rank test will be calculated to compare PFS between the two arms. (NCT01286272)
Timeframe: Up to 4 years

,
Interventionpercentage of patients (Number)
PFS at 1 yearPFS at 2 yearsPFS at 3 yearsPFS at 4 years
Arm A (Ofatumumab, Bendamustine Hydrochloride)93.880.365.957.3
Arm B (Ofatumumab, Bendamustine Hydrochloride, Bortezomib)84.875.667.164.7

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Change in F-18 16 Alpha-fluoroestradiol (FES) Standardized Uptake Value (SUV), Assessed by a One-sample Test of the Percent Change in FES SUV

Uptake was quantified using lean body mass adjusted SUV (SULmean). The geometric mean was calculated for up to 3 lesions per patient. Systematic change in FES SULgmean between baseline and a second FES scan at approximately 2 or 8 weeks and a third FES scan was at approximately 8 weeks measured using a sign test where the median change is zero. (NCT02149173)
Timeframe: from time of first F-18 FES-PET/CT scan to time of second or third F-18 FES-PET/CT scan (approximately 2-8 weeks)

Interventionpercentage of change in SULgmean (Median)
FES-imaging After 2 Wks of ER Modulating (Vorinostat) Therapy8.7
FES-imaging After 8 Wks of ER Modulating (Vorinostat) Therapy1.9
FES-imaging After 2-8 Weeks of ER Blocking Therapy-60.3

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F-18 16 Alpha-fluoroestradiol (FES) Uptake

Quantitative and qualitative measures of FES uptake for each disease site, a set of 1.5 cm diameter regions on three adjacent planes with the highest lesion FES uptake will be drawn to determine maximal FES uptake. Up to 10 sites seen on the static torso survey will be quantified. Lesions will qualitatively determined to be visible or not visible. (NCT02149173)
Timeframe: from time of first F-18 FES-PET/CT scan to time of second or third F-18 FES-PET/CT scan (approximately 2-8 weeks)

Interventionnumber of ER+ lesions (Count of Units)
Quantitative Uptake281
Qualitative Uptake243

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Proportion of Patients Experienced a Threshold in Percentage Change, or Surpassed a Targeted Follow-up F-18 16 Alpha-fluoroestradiol (FES) Standardized Uptake Value (SUV)

The number of patients showing a 20% increase in FES SULgmean compared to baseline at either 2 or 8 weeks using a 90% Wilson score binomial confidence interval. (NCT02149173)
Timeframe: from time of first F-18 FES-PET/CT scan to time of second or third F-18 FES-PET/CT scan (approximately 2-8 weeks)

InterventionProportion of participants (Number)
FES With Potential ER Modulating Therapy (Vorinostat)0
FES With Potential ER Blocking Therapy0

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Time to Disease Progression

Months from the start of endocrine therapy to the time the patient is first recorded as having disease progression, (NCT02149173)
Timeframe: from start of therapy up to 20 years

Interventionmonths (Median)
FES With Potential ER Modulating Therapy (Vorinostat)2
FES With Potential ER Blocking Therapy5.6

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Uptake of 18F-FSPG (Expressed in Maximal Standardized Uptake Value [SUV] Within the Tumor)

Maximum standardized uptake values (SUVmax) were normalized to lean body mass and measured with a 1 cm diameter round region of interest over the area of greatest uptake in the lesion being measured. (NCT02448225)
Timeframe: Up to 2 years

InterventionMaximum standardized uptake values (SUVm (Mean)
Benign Patients0.8
Cancer Patients3.9

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Ability of 18F-FSPG PET/CT to Discriminate Benign From Malignant Nodules

"Sensitivity, specificity, overall accuracy and receiver operating characteristic (ROC) curves will be generated and compared for both 18F-FDG and 18F-FSPG tests.~Sensitivity is the proportion of High(positive) among cancer patients. Specificity is the proportion of low(negative) among benign tumors. Accuracy is the proportion of correctly diagnosed among analyzed patients. Area under the curve(AUC) is the area under the ROC curve, which is the plot of sensitivity by 1-specificity." (NCT02448225)
Timeframe: Up to 2 years

Interventionproportion, range 0 to 1, higher better (Number)
FDG sensitivity(low and high)FDG specificityFDG accuracyFDG AUC(area under curve)ESPG sensitivity(low and high)ESPG specificity(low and high)ESPG accuracyESPG AUC
Diagnostic (18F-FDG PET/CT, 18F-FSPG PET/CT)0.7060.7780.7310.8170.8240.6670.7690.843

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Ability of 18F-FSPG PET/CT to Stage of Lung Cancer (Metastatic or Not)

"Sensitivity, specificity, overall accuracy and ROC curves will be generated and compared for both 18F-FDG and 18F-FSPG tests. Wilcoxon rank-sum or Kruskal-Wallis tests will be applied for the group comparisons of the biodistribution characteristics of 18F-FDG and 18F-FSPG tests.~Sensitivity is the proportion of High(positive) among cancer patients. Specificity is the proportion of low(negative) among benign tumors. Accuracy is the proportion of correctly diagnosed among all patients. Area under the curve(AUC) is the area under the ROC curve." (NCT02448225)
Timeframe: Up to 2 years

Interventionproportion, range 0-1, higher better (Number)
FDG sensitivityFDG specificityFDG accuracyFDG AUCFSPG sensitivityFSPG specificityFSPG accuracyFSPG AUC
Diagnostic (18F-FDG PET/CT, 18F-FSPG PET/CT)0.80.8570.8240.8710.20.2860.2350.8

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CD44 and xC- Expression Levels in Tissue Samples(0-3)

The level of expression of xCT and CD44 proteins in the cytoplasmic membrane of tumor cells were examined by an experienced pathologist who was blinded to any patient and imaging information. The percentage of tumor cells positive for the marker and the intensity of staining were evaluated, the latter using a scale of 0 (none), 1+ (weak), 2+ (intermediate), and 3+ (strong) with a sample being reported as positive if greater than 10% of the tumor cells in the sample were positively stained with any intensity. (NCT02448225)
Timeframe: Up to 2 years

InterventionIHC score, range 0 and above (Mean)
CD44xCT
Some Cancer Patients2.61

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Number of F-18-FDG Positive Lesions That Are Detected by the Copper Cu 64 TP3805 Analog

Cu-64 results will be compared with those of F-18-FDG for: The unit of analysis will be the lesion (with potentially multiple lesions available per patient). (NCT02810873)
Timeframe: 4 hours after Cu 64 TP3805 administered

InterventionNumber of Lesions (Number)
F-18-FDG Whole-body Scan10
No F-18-FDG Scan14

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Complete Response (CR) With Pembrolizumab Treatment Alone

"To assess the primary objective of response rate following PET #2 performed after 3 doses of pembrolizumab. PET response will be assessed using the Lugano Criteria (2014) which recommends the 5 point Deauville score for assessing response. The Deauville five-point scale is an internationally-recommended scale for routine clinical reporting and clinical trials using FDG PET-CT in the initial staging and assessment of treatment response in Hodgkin lymphoma (HL). Patients with a Deauville score of 1-3 will be considered a complete response.~Deauville criteria is defined as follows:~No residual uptake~Slight uptake, but below blood pool (mediastinum)~Uptake above mediastinum, but below or equal to uptake in the liver~Uptake slightly to moderately higher than liver~Markedly increased uptake or any new lesions~Patients will be evaluable for response assessment if they have received at least one dose of pembrolizumab." (NCT03226249)
Timeframe: After 3 cycles of pembrolizumab (1 cycle = 21 days)

Interventionpercentage of participants (Number)
Treatment: Pembrolizumab and AVD Chemotherapy Guided by PET-CT37

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Overall Survival at Treatment Completion

Overall survival will be defined as the number of patients that are alive at the time of treatment completion (3 cycles of pembrolizumab and 2-6 cycles of AVD) (NCT03226249)
Timeframe: At completion of treatment with 3 cycles of pembrolizumab (21 day cycles) and up to 6 cycles of AVD (28 days cycles)

InterventionParticipants (Count of Participants)
Treatment: Pembrolizumab and AVD Chemotherapy Guided by PET-CT30

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Progression Free Survival (PFS) at Treatment Completion

"PFS is defined as the number of patients that are progression/relapse free at the time of treatment completion (3 cycles of pembrolizumab and up to 6 cycles of AVD).~Progressive or relapse disease is defined as of the following:~Appearance of any new lesion more than 1.5 cm in any axis during treatment, even if other lesions are decreasing in size.~At least a 50% increased from nadir in the sum of the product of the diameter (SPD) of any previously involved nodes, or in a single involved node, or the size of other lesions (e.g., splenic or hepatic nodules). To be considered progressive disease, a lymph node with a diameter of the short axis of less than 1.0 cm must increase by at least 50% and to a size of more than 1.5 x 1.5 cm or more than 1.5 cm in the long axis.~At least a 50% increase in the longest diameter of any single previously identified node more than 1.0 cm in its short axis.~Lymphoma confirmed by repeat biopsy." (NCT03226249)
Timeframe: At completion of treatment with 3 cycles of pembrolizumab (21 day cycles) and up to 6 cycles of AVD (28 days cycles)

InterventionParticipants (Count of Participants)
Treatment: Pembrolizumab and AVD Chemotherapy Guided by PET-CT30

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