Page last updated: 2024-12-06

streptozocin

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Cross-References

ID SourceID
PubMed CID2733335
CHEMBL ID1651906
SCHEMBL ID444088
MeSH IDM0020600
PubMed CID29327
CHEBI ID9288
SCHEMBL ID4748
MeSH IDM0020600

Synonyms (125)

Synonym
2-deoxy-2-(3-methyl-3-nitrosoureido)-d-glucopyranose
STZ ,
2-deoxy-2-[[(methylnitrosoamino)carbonyl]amino]-d-glucose
CHEMBL1651906
SCHEMBL444088
ZSJLQEPLLKMAKR-YDEIVXIUSA-N
AKOS024456708
HMS3676N09
HMS3412N09
streptozotocin-stereo
DTXSID90369855
AB00052092-03
u 9889
DIVK1C_000531
KBIO1_000531
2-deoxy-2-{[methyl(nitroso)carbamoyl]amino}-alpha-d-glucopyranose
CHEBI:9288 ,
n-d-glucosyl-(2)-n'-nitrosomethylharnstoff
n-d-glucosyl-(2)-n'-nitrosomethylurea
2-deoxy-2-(((methylnitrosoamino)carbonyl)amino)-d-glucopyranose
streptozocinium
streptozocinum
estreptozocina
streptozocine
2-deoxy-2-({[methyl(nitroso)amino]carbonyl}amino)-alpha-d-glucopyranose
SPECTRUM_000960
BSPBIO_000684
IDI1_000531
streptozosin
binds to dna
SPECTRUM5_001047
BCBCMAP01_000142
NCGC00178500-02
NCGC00178500-01
D05932
streptozocin (jan/usan/inn)
zanosar (tn)
BSPBIO_002734
SMP1_000282
PRESTWICK3_000732
BPBIO1_000754
1-methyl-1-nitroso-3-[(2s,3r,4r,5s,6r)-2,4,5-trihydroxy-6-(hydroxymethyl)tetrahydropyran-3-yl]urea
2-deoxy-2[[(methylnitrosoamino)-carbonyl]amino]-d-glucopyranose
AB00513906
streptozotocine
c8h15n3o7
C07313
DB00428
KBIO2_006576
KBIOSS_001440
KBIO2_001440
KBIOGR_001768
KBIO3_001954
KBIO2_004008
SPECTRUM4_001244
SPBIO_000243
SPECTRUM3_001087
SPECTRUM2_000062
NINDS_000531
SPECTRUM1500543
2-deoxy-2-((methylnitrosoamino)carbonyl)amino-d-glucose
streptozocin, >=75% alpha-anomer basis, >=98% (hplc), powder
HMS2092I09
HMS501K13
HMS1921A07
NCGC00178500-03
NCGC00178500-04
HMS2097C06
STREPTOZOTOCIN - ZANOSAR
dtxcid701282
dtxsid2021282 ,
NCGC00256594-01
tox21_302974
tox21_201859
NCGC00259408-01
nsc-757321
nsc757321
pharmakon1600-01500543
tox21_110585
MLS004774123
smr001233317
66395-18-4
2-desoxy-2-(3-methyl-3-nitrosoureido)-d-glucopyranose
CCG-39870
EPITOPE ID:134282
S1312
AKOS025310730
SCHEMBL4748
NCGC00178500-07
tox21_110585_1
1-methyl-1-nitroso-3-((2s,3r,4r,5s,6r)-2,4,5-trihydroxy-6-(hydroxymethyl)-tetrahydro-2h-pyran-3-yl)urea
W-201687
HB4097
1-methyl-1-nitroso-3-((2s,3r,4r,5s,6r)-2,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2h-pyran-3-yl)urea
AB00052092_04
AB00052092_05
.alpha.-streptozocin
.alpha.-d-glucopyranose, 2-deoxy-2-(((methylnitrosoamino)carbonyl)amino)-
mfcd00006607
alpha-d-glucopyranose, 2-deoxy-2-(((methylnitrosoamino)carbonyl)amino)-
unii-8h27gur065
alpha-streptozocin
8H27GUR065 ,
3-methyl-3-nitroso-1-[(2s,3r,4r,5s,6r)-2,4,5-trihydroxy-6-(hydroxymethyl)oxan-3-yl]urea
streptozocin, >=98.0% (hplc)
SR-01000939745-3
sr-01000939745
SR-05000001720-2
SR-05000001720-1
sr-05000001720
streptozocin, vetec(tm) reagent grade, 98%, powder
SBI-0051517.P003
HMS3714C06
SW199198-2
streptozotocin (stz)
Q257331
streptozotocin;u 9889
streptozocin; streptozotocin
A937380
n-(methylnitrosocarbamoyl)-a-d-glucosamine
2-deoxy-2-((methyl(nitroso)carbamoyl)amino)-alpha-d-glucopyranose
n-d-glucosyl(2)-n'-nitrosomethylharnstoff
2-deoxy-2-(((methylnitrosamino)-carbonyl)amino)-d-glucopyranose
l01ad04
EN300-7480749

Research Excerpts

Toxicity

ExcerptReferenceRelevance
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004
)
0.32
" An understanding of structure-activity relationships (SARs) of chemicals can make a significant contribution to the identification of potential toxic effects early in the drug development process and aid in avoiding such problems."( Developing structure-activity relationships for the prediction of hepatotoxicity.
Fisk, L; Greene, N; Naven, RT; Note, RR; Patel, ML; Pelletier, DJ, 2010
)
0.36

Bioavailability

ExcerptReferenceRelevance
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51

Dosage Studied

ExcerptRelevanceReference
" We proposed a systematic classification scheme using FDA-approved drug labeling to assess the DILI potential of drugs, which yielded a benchmark dataset with 287 drugs representing a wide range of therapeutic categories and daily dosage amounts."( FDA-approved drug labeling for the study of drug-induced liver injury.
Chen, M; Fang, H; Liu, Z; Shi, Q; Tong, W; Vijay, V, 2011
)
0.37
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (4)

RoleDescription
antineoplastic agentA substance that inhibits or prevents the proliferation of neoplasms.
antimicrobial agentA substance that kills or slows the growth of microorganisms, including bacteria, viruses, fungi and protozoans.
DNA synthesis inhibitorAny substance that inhibits the synthesis of DNA.
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 (2)

ClassDescription
N-acylglucosamine
N-nitrosoureasA nitroso compound that is any urea in which one of the nitrogens is substituted by a nitroso group
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (9)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
acetylcholinesteraseHomo sapiens (human)Potency43.64860.002541.796015,848.9004AID1347398
RAR-related orphan receptor gammaMus musculus (house mouse)Potency11.88320.006038.004119,952.5996AID1159521
GLI family zinc finger 3Homo sapiens (human)Potency0.29850.000714.592883.7951AID1259369
AR proteinHomo sapiens (human)Potency0.19490.000221.22318,912.5098AID743036
progesterone receptorHomo sapiens (human)Potency33.49150.000417.946075.1148AID1346795
estrogen-related nuclear receptor alphaHomo sapiens (human)Potency68.03200.001530.607315,848.9004AID1224841
estrogen nuclear receptor alphaHomo sapiens (human)Potency34.66540.000229.305416,493.5996AID743069
aryl hydrocarbon receptorHomo sapiens (human)Potency54.03970.000723.06741,258.9301AID743085
Cellular tumor antigen p53Homo sapiens (human)Potency76.95880.002319.595674.0614AID651631
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (124)

Processvia Protein(s)Taxonomy
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycle G2/M phase transitionCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
ER overload responseCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
mitophagyCellular tumor antigen p53Homo sapiens (human)
in utero embryonic developmentCellular tumor antigen p53Homo sapiens (human)
somitogenesisCellular tumor antigen p53Homo sapiens (human)
release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
hematopoietic progenitor cell differentiationCellular tumor antigen p53Homo sapiens (human)
T cell proliferation involved in immune responseCellular tumor antigen p53Homo sapiens (human)
B cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
T cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
response to ischemiaCellular tumor antigen p53Homo sapiens (human)
nucleotide-excision repairCellular tumor antigen p53Homo sapiens (human)
double-strand break repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
protein import into nucleusCellular tumor antigen p53Homo sapiens (human)
autophagyCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrestCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediatorCellular tumor antigen p53Homo sapiens (human)
transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
Ras protein signal transductionCellular tumor antigen p53Homo sapiens (human)
gastrulationCellular tumor antigen p53Homo sapiens (human)
neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
protein localizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA replicationCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
determination of adult lifespanCellular tumor antigen p53Homo sapiens (human)
mRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
rRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
response to salt stressCellular tumor antigen p53Homo sapiens (human)
response to inorganic substanceCellular tumor antigen p53Homo sapiens (human)
response to X-rayCellular tumor antigen p53Homo sapiens (human)
response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
positive regulation of gene expressionCellular tumor antigen p53Homo sapiens (human)
cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
viral processCellular tumor antigen p53Homo sapiens (human)
glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
cerebellum developmentCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell growthCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
mitotic G1 DNA damage checkpoint signalingCellular tumor antigen p53Homo sapiens (human)
negative regulation of telomere maintenance via telomeraseCellular tumor antigen p53Homo sapiens (human)
T cell differentiation in thymusCellular tumor antigen p53Homo sapiens (human)
tumor necrosis factor-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
regulation of tissue remodelingCellular tumor antigen p53Homo sapiens (human)
cellular response to UVCellular tumor antigen p53Homo sapiens (human)
multicellular organism growthCellular tumor antigen p53Homo sapiens (human)
positive regulation of mitochondrial membrane permeabilityCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
entrainment of circadian clock by photoperiodCellular tumor antigen p53Homo sapiens (human)
mitochondrial DNA repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
transcription initiation-coupled chromatin remodelingCellular tumor antigen p53Homo sapiens (human)
negative regulation of proteolysisCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of RNA polymerase II transcription preinitiation complex assemblyCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
response to antibioticCellular tumor antigen p53Homo sapiens (human)
fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
circadian behaviorCellular tumor antigen p53Homo sapiens (human)
bone marrow developmentCellular tumor antigen p53Homo sapiens (human)
embryonic organ developmentCellular tumor antigen p53Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationCellular tumor antigen p53Homo sapiens (human)
protein stabilizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of helicase activityCellular tumor antigen p53Homo sapiens (human)
protein tetramerizationCellular tumor antigen p53Homo sapiens (human)
chromosome organizationCellular tumor antigen p53Homo sapiens (human)
neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
hematopoietic stem cell differentiationCellular tumor antigen p53Homo sapiens (human)
negative regulation of glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
type II interferon-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
cardiac septum morphogenesisCellular tumor antigen p53Homo sapiens (human)
positive regulation of programmed necrotic cell deathCellular tumor antigen p53Homo sapiens (human)
protein-containing complex assemblyCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stressCellular tumor antigen p53Homo sapiens (human)
thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
necroptotic processCellular tumor antigen p53Homo sapiens (human)
cellular response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
cellular response to xenobiotic stimulusCellular tumor antigen p53Homo sapiens (human)
cellular response to ionizing radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to UV-CCellular tumor antigen p53Homo sapiens (human)
stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
cellular response to actinomycin DCellular tumor antigen p53Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
cellular senescenceCellular tumor antigen p53Homo sapiens (human)
replicative senescenceCellular tumor antigen p53Homo sapiens (human)
oxidative stress-induced premature senescenceCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
oligodendrocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of execution phase of apoptosisCellular tumor antigen p53Homo sapiens (human)
negative regulation of mitophagyCellular tumor antigen p53Homo sapiens (human)
regulation of mitochondrial membrane permeability involved in apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of G1 to G0 transitionCellular tumor antigen p53Homo sapiens (human)
negative regulation of miRNA processingCellular tumor antigen p53Homo sapiens (human)
negative regulation of glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
negative regulation of pentose-phosphate shuntCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
regulation of fibroblast apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
positive regulation of cellular senescenceCellular tumor antigen p53Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (34)

Processvia Protein(s)Taxonomy
transcription cis-regulatory region bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
core promoter sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
TFIID-class transcription factor complex bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
protease bindingCellular tumor antigen p53Homo sapiens (human)
p53 bindingCellular tumor antigen p53Homo sapiens (human)
DNA bindingCellular tumor antigen p53Homo sapiens (human)
chromatin bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activityCellular tumor antigen p53Homo sapiens (human)
mRNA 3'-UTR bindingCellular tumor antigen p53Homo sapiens (human)
copper ion bindingCellular tumor antigen p53Homo sapiens (human)
protein bindingCellular tumor antigen p53Homo sapiens (human)
zinc ion bindingCellular tumor antigen p53Homo sapiens (human)
enzyme bindingCellular tumor antigen p53Homo sapiens (human)
receptor tyrosine kinase bindingCellular tumor antigen p53Homo sapiens (human)
ubiquitin protein ligase bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase regulator activityCellular tumor antigen p53Homo sapiens (human)
ATP-dependent DNA/DNA annealing activityCellular tumor antigen p53Homo sapiens (human)
identical protein bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase bindingCellular tumor antigen p53Homo sapiens (human)
protein heterodimerization activityCellular tumor antigen p53Homo sapiens (human)
protein-folding chaperone bindingCellular tumor antigen p53Homo sapiens (human)
protein phosphatase 2A bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingCellular tumor antigen p53Homo sapiens (human)
14-3-3 protein bindingCellular tumor antigen p53Homo sapiens (human)
MDM2/MDM4 family protein bindingCellular tumor antigen p53Homo sapiens (human)
disordered domain specific bindingCellular tumor antigen p53Homo sapiens (human)
general transcription initiation factor bindingCellular tumor antigen p53Homo sapiens (human)
molecular function activator activityCellular tumor antigen p53Homo sapiens (human)
promoter-specific chromatin bindingCellular tumor antigen p53Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (19)

Processvia Protein(s)Taxonomy
nuclear bodyCellular tumor antigen p53Homo sapiens (human)
nucleusCellular tumor antigen p53Homo sapiens (human)
nucleoplasmCellular tumor antigen p53Homo sapiens (human)
replication forkCellular tumor antigen p53Homo sapiens (human)
nucleolusCellular tumor antigen p53Homo sapiens (human)
cytoplasmCellular tumor antigen p53Homo sapiens (human)
mitochondrionCellular tumor antigen p53Homo sapiens (human)
mitochondrial matrixCellular tumor antigen p53Homo sapiens (human)
endoplasmic reticulumCellular tumor antigen p53Homo sapiens (human)
centrosomeCellular tumor antigen p53Homo sapiens (human)
cytosolCellular tumor antigen p53Homo sapiens (human)
nuclear matrixCellular tumor antigen p53Homo sapiens (human)
PML bodyCellular tumor antigen p53Homo sapiens (human)
transcription repressor complexCellular tumor antigen p53Homo sapiens (human)
site of double-strand breakCellular tumor antigen p53Homo sapiens (human)
germ cell nucleusCellular tumor antigen p53Homo sapiens (human)
chromatinCellular tumor antigen p53Homo sapiens (human)
transcription regulator complexCellular tumor antigen p53Homo sapiens (human)
protein-containing complexCellular tumor antigen p53Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (135)

Assay IDTitleYearJournalArticle
AID588218FDA HLAED, lactate dehydrogenase (LDH) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1145665Acute toxicity in iv dosed dog1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1145642Toxicity in BDF1 mouse allografted with mouse L1210 cells assessed as mortality at 100 mg/kg, ip qd for 5 days1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID588215FDA HLAED, alkaline phosphatase increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID588219FDA HLAED, gamma-glutamyl transferase (GGT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID176555Diabetogenic activity in Lewis strain of albino rats after iv administration1983Journal of medicinal chemistry, Jun, Volume: 26, Issue:6
Oxidation of uric acid. 4. Synthesis, structure, and diabetogenic action of 5-imino-2,4,6(1H,3H,5H)-pyrimidinetrione salts and their alloxan-like covalent adducts.
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID588210Human drug-induced liver injury (DILI) modelling dataset from Ekins et al2010Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 38, Issue:12
A predictive ligand-based Bayesian model for human drug-induced liver injury.
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID977599Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID1145631Toxicity in ICR mouse allografted with mouse S180A assessed as mortality at 50 mg/kg, ip qd for 5 days1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1145667Toxicity in ip dosed BDF1 mouse allografted with mouse L1210 cells assessed as optimal dose required for mortality administered qd for 5 days1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID678992TP_TRANSPORTER: Branched DNA assay in vivo SD rat, kidney2002The Journal of pharmacology and experimental therapeutics, Jan, Volume: 300, Issue:1
Organ distribution of multidrug resistance proteins 1, 2, and 3 (Mrp1, 2, and 3) mRNA and hepatic induction of Mrp3 by constitutive androstane receptor activators in rats.
AID354543Cytotoxicity against rat C6 cells assessed as cell release at 50 ug/mL to 2.5 mg/mL after 5 hrs by MTT assay in absence of db-cAMP1996Journal of natural products, Dec, Volume: 59, Issue:12
Cell-based screen for identification of inhibitors of tubulin polymerization.
AID977602Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID588214FDA HLAED, liver enzyme composite activity2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID679334TP_TRANSPORTER: Branched DNA assay in vivo SD rat, liver2002Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 30, Issue:7
Tissue distribution and chemical induction of multiple drug resistance genes in rats.
AID1145661Acute toxicity in ip dosed JCL-ICR mouse assessed as animal death1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID588216FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1145651Antibacterial activity against Bacillus subtilis ATCC 6633 assessed as growth inhibition after 18 hrs by broth dilution method1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID1149773Antitumor activity against mouse L1210 cells allografted in CDF1 mouse at 66 mg/kg, ip administered from day 1 to day 9 relative to control1977Journal of medicinal chemistry, Oct, Volume: 20, Issue:10
Synthesis of nitrosourea derivatives of sucrose as central nervous system anticancer agents.
AID134112Mean life extension in mice bearing Trypanosoma rhodesiense, after ip administration at a dose of 0.2 mmol/kg1990Journal of medicinal chemistry, Feb, Volume: 33, Issue:2
Methylating agents as trypanocides.
AID1149772Antitumor activity against mouse L1210 cells allografted in CDF1 mouse at 44 mg/kg, ip administered from day 1 to day 9 relative to control1977Journal of medicinal chemistry, Oct, Volume: 20, Issue:10
Synthesis of nitrosourea derivatives of sucrose as central nervous system anticancer agents.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1145657Antibacterial activity against Sarcina lutea ATCC 9341 assessed as growth inhibition after 18 hrs by broth dilution method1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1145655Antibacterial activity against Pseudomonas fluorescens NIHJ B-254 assessed as growth inhibition after 18 hrs by broth dilution method1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1145625Antitumor activity against mouse S180A allografted in ICR mouse assessed as tumor growth at 25 mg/kg, ip qd for 5 days measured on day 7 relative to control1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1145637Antitumor activity against mouse L1210 cells allografted in BDF1 mouse assessed as increase in host lifespan at 50 mg/kg, ip qd for 5 days relative to control1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1145652Antibacterial activity against Escherichia coli NIHJ JC-2 assessed as growth inhibition after 18 hrs by broth dilution method1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1145638Antitumor activity against mouse L1210 cells allografted in BDF1 mouse assessed as increase in host lifespan at 100 mg/kg, ip qd for 5 days relative to control1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1149778Antitumor activity against mouse ependymoblastoma cells allografted in C57BL/6 mouse at 100 mg/kg, ip administered from day 1 to day 5 relative to control1977Journal of medicinal chemistry, Oct, Volume: 20, Issue:10
Synthesis of nitrosourea derivatives of sucrose as central nervous system anticancer agents.
AID409954Inhibition of mouse brain MAOA2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Quantitative structure-activity relationship and complex network approach to monoamine oxidase A and B inhibitors.
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID234895Relative potency compared to that of streptozotocin in albino rats.1983Journal of medicinal chemistry, Jun, Volume: 26, Issue:6
Oxidation of uric acid. 4. Synthesis, structure, and diabetogenic action of 5-imino-2,4,6(1H,3H,5H)-pyrimidinetrione salts and their alloxan-like covalent adducts.
AID588217FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1145645Diabetogenic activity in Wistar rat assessed as increase in blood sugar level at 65 mg/kg, iv administered as single dose by glucose oxidase method1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID354538Cytotoxicity against rat C6 cells at 50 ug/mL to 2.5 mg/mL after 3 days treated 4 hrs before db-cAMP challenge by MTT assay1996Journal of natural products, Dec, Volume: 59, Issue:12
Cell-based screen for identification of inhibitors of tubulin polymerization.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID1149771Antitumor activity against mouse L1210 cells allografted in CDF1 mouse at 29 mg/kg, ip administered from day 1 to day 9 relative to control1977Journal of medicinal chemistry, Oct, Volume: 20, Issue:10
Synthesis of nitrosourea derivatives of sucrose as central nervous system anticancer agents.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1145640Antitumor activity against mouse L1210 cells allografted in BDF1 mouse assessed as increase in host lifespan at 200 mg/kg, ip qd for 5 days relative to control1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1145666Therapeutic index, ratio of LD10 for JCL-ICR mouse to ED90 for mouse S180A cells allografted in ICR mouse1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID588209Literature-mined public compounds from Greene et al multi-species hepatotoxicity modelling dataset2010Chemical research in toxicology, Jul-19, Volume: 23, Issue:7
Developing structure-activity relationships for the prediction of hepatotoxicity.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID681065TP_TRANSPORTER: Branched DNA assay in vivo SD rat, kidney2002Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 30, Issue:7
Tissue distribution and chemical induction of multiple drug resistance genes in rats.
AID1145653Antibacterial activity against Klebsiella pneumoniae ATCC 10031 assessed as growth inhibition after 18 hrs by broth dilution method1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1145670Antitumor activity against mouse L1210 cells allografted in ip dosed BDF1 mouse assessed as 30% increase in host lifespan administered for qd for 5 days1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1145644Toxicity in BDF1 mouse allografted with mouse L1210 cells assessed as mortality at 200 mg/kg, ip qd for 5 days1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID477295Octanol-water partition coefficient, log P of the compound2010European journal of medicinal chemistry, Apr, Volume: 45, Issue:4
QSPR modeling of octanol/water partition coefficient of antineoplastic agents by balance of correlations.
AID1145658Antibacterial activity against Shigella sonnei assessed as growth inhibition after 18 hrs by broth dilution method1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID234893Relative potency compared to that of Alloxan in albino rats.1983Journal of medicinal chemistry, Jun, Volume: 26, Issue:6
Oxidation of uric acid. 4. Synthesis, structure, and diabetogenic action of 5-imino-2,4,6(1H,3H,5H)-pyrimidinetrione salts and their alloxan-like covalent adducts.
AID567091Drug absorption in human assessed as human intestinal absorption rate2011European journal of medicinal chemistry, Jan, Volume: 46, Issue:1
Prediction of drug intestinal absorption by new linear and non-linear QSPR.
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1145654Antibacterial activity against Proteus vulgaris AHU 1469 assessed as growth inhibition after 18 hrs by broth dilution method1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID1145656Antibacterial activity against Salmonella typhi IFM 3020 assessed as growth inhibition after 18 hrs by broth dilution method1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1145627Antitumor activity against mouse S180A allografted in ICR mouse assessed as tumor growth at 50 mg/kg, ip qd for 5 days measured on day 7 relative to control1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1145659Antibacterial activity against Staphylococcus aureus FDA 209P JC-1 assessed as growth inhibition after 18 hrs by broth dilution method1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID625276FDA Liver Toxicity Knowledge Base Benchmark Dataset (LTKB-BD) drugs of most concern for DILI2011Drug discovery today, Aug, Volume: 16, Issue:15-16
FDA-approved drug labeling for the study of drug-induced liver injury.
AID640725Induction of weight loss in C3H/HeN mouse at 1130 umol/kg, ip after 18 days (Rvb = 12.8 +/- 1.5 %)2012Bioorganic & medicinal chemistry, Jan-15, Volume: 20, Issue:2
Weight loss effects of quaternary salts of 5-amino-1-(chloromethyl)-1,2-dihydro-3H-benz[e]indoles; structure-activity relationships.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1145669Antitumor activity against mouse S180A cells allografted in ip dosed ICR mouse administered qd for 5 days1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1149777Antitumor activity against mouse ependymoblastoma cells allografted in C57BL/6 mouse at 130 mg/kg, ip administered from day 1 to day 5 relative to control1977Journal of medicinal chemistry, Oct, Volume: 20, Issue:10
Synthesis of nitrosourea derivatives of sucrose as central nervous system anticancer agents.
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID640724Induction of weight loss in C3H/HeN mouse at 377 umol/kg, ip after 60 days (Rvb = 24.5 +/- 3.5 %)2012Bioorganic & medicinal chemistry, Jan-15, Volume: 20, Issue:2
Weight loss effects of quaternary salts of 5-amino-1-(chloromethyl)-1,2-dihydro-3H-benz[e]indoles; structure-activity relationships.
AID1145664Acute toxicity in iv dosed mouse1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1145649Diabetogenic activity in Wistar rat assessed as increase in blood sugar level at 20 mg/kg, ip qd for 1 month measured 24 hrs last drug dosage by glucose oxidase method1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1145629Toxicity in ICR mouse allografted with mouse S180A assessed as mortality at 25 mg/kg, ip qd for 5 days1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID354542Inhibition of tubulin polymerization in rat C6 cells at 50 ug/mL to 2.5 mg/mL after 4 hrs1996Journal of natural products, Dec, Volume: 59, Issue:12
Cell-based screen for identification of inhibitors of tubulin polymerization.
AID1145641Toxicity in BDF1 mouse allografted with mouse L1210 cells assessed as mortality at 50 mg/kg, ip qd for 5 days1976Journal of medicinal chemistry, Jul, Volume: 19, Issue:7
Alkyl streptozotocin analogues with improved biological activities.
AID1149769Antitumor activity against mouse L1210 cells allografted in CDF1 mouse at 100 mg/kg, ip administered from day 1 to day 9 relative to control1977Journal of medicinal chemistry, Oct, Volume: 20, Issue:10
Synthesis of nitrosourea derivatives of sucrose as central nervous system anticancer agents.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID540299A screen for compounds that inhibit the MenB enzyme of Mycobacterium tuberculosis2010Bioorganic & medicinal chemistry letters, Nov-01, Volume: 20, Issue:21
Synthesis and SAR studies of 1,4-benzoxazine MenB inhibitors: novel antibacterial agents against Mycobacterium tuberculosis.
AID588519A screen for compounds that inhibit viral RNA polymerase binding and polymerization activities2011Antiviral research, Sep, Volume: 91, Issue:3
High-throughput screening identification of poliovirus RNA-dependent RNA polymerase inhibitors.
AID1347411qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (31)

TimeframeStudies, This Drug (%)All Drugs %
pre-19903 (9.68)18.7374
1990's2 (6.45)18.2507
2000's4 (12.90)29.6817
2010's16 (51.61)24.3611
2020's6 (19.35)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 64.02

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 Index64.02 (24.57)
Research Supply Index2.56 (2.92)
Research Growth Index5.63 (4.65)
Search Engine Demand Index99.02 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (64.02)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials0 (0.00%)5.53%
Trials0 (0.00%)5.53%
Reviews1 (5.00%)6.00%
Reviews0 (0.00%)6.00%
Case Studies0 (0.00%)4.05%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Observational0 (0.00%)0.25%
Other19 (95.00%)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 (8)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Randomized Phase 2 Trial Of Two Chemotherapy Regimens Plus Or Minus Bevacizumab In Patients With Well Differentiated Pancreatic Neuroendocrine Tumors [NCT03351296]Phase 2140 participants (Anticipated)Interventional2018-06-26Recruiting
Phase II Study of Avastin, Fluorouracil, Doxorubicin and Streptozocin in Locally Advanced and Metastatic Pancreatic Endocrine Tumors [NCT00609765]Phase 21 participants (Actual)Interventional2007-08-31Terminated(stopped due to Development of new chemotherapy standard of care for treatment rendered the trial obsolete.)
An Open Label Study to Evaluate the Effect of Avastin in Association With Chemotherapy on Progression-free Survival in Patients With Progressive Advanced/Metastatic Well-differentiated Digestive Endocrine Tumors of the Gastrointestinal Tract [NCT00448136]Phase 283 participants (Actual)Interventional2007-07-31Completed
Evaluation of Chemotherapy With Streptozotocin Combined With 5-Fluorouracil and Adriamycin in Patients With Zollinger-Ellison Syndrome and Metastatic Non-Beta-Islet Cell Neoplasm [NCT00001165]Phase 2999 participants Interventional1978-09-30Completed
A Randomised Phase II Study Comparing Capecitabine Plus Streptozocin With or Without Cisplatin Chemotherapy as Treatment for Unresectable or Metastatic Neuroendocrine Tumors [NCT00602082]Phase 284 participants (Anticipated)Interventional2005-08-31Completed
[NCT00004688]Phase 235 participants Interventional1996-08-31Completed
Phase I Study of Combination Immunochemotherapy in Patients With Advanced Colorectal Carcinoma [NCT00003543]Phase 118 participants (Anticipated)Interventional1998-06-30Completed
First International Randomized Trial in Locally Advanced and Metastatic Adrenocortical Carcinoma Treatment [NCT00094497]Phase 3304 participants (Actual)Interventional2004-06-30Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00094497 (5) [back to overview]Change in Quality of Life as Measured by QLQ-C30
NCT00094497 (5) [back to overview]Number of Disease-free Patients
NCT00094497 (5) [back to overview]Overall Survival
NCT00094497 (5) [back to overview]Progression-free Survival
NCT00094497 (5) [back to overview]Best Overall Response Rate
NCT00448136 (16) [back to overview]Duration of ODC - Time to Event
NCT00448136 (16) [back to overview]Duration of OR - Time to Event
NCT00448136 (16) [back to overview]Duration of Overall Disease Control (ODC) - Percentage of Participants With an Event
NCT00448136 (16) [back to overview]Duration of Overall Response (OR) - Percentage of Participants With an Event
NCT00448136 (16) [back to overview]OS - Time to Event
NCT00448136 (16) [back to overview]Overall Survival (OS) - Percentage of Participants With an Event
NCT00448136 (16) [back to overview]PFS - Time to Event
NCT00448136 (16) [back to overview]Progression-Free Survival (PFS) - Percentage of Participants With an Event
NCT00448136 (16) [back to overview]Duration of ODC - Percentage of Participants Maintaining Disease Control at 12 and 24 Months
NCT00448136 (16) [back to overview]Duration of OR - Percentage of Participants With Sustained Response at 12 and 24 Months
NCT00448136 (16) [back to overview]EORTC QLQ-C30 Functional and Symptom Scale Scores
NCT00448136 (16) [back to overview]Global Health Status as Assessed by the European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire - C30 (EORTC QLQ-C30)
NCT00448136 (16) [back to overview]OS - Percentage of Participants Surviving at 12 and 24 Months
NCT00448136 (16) [back to overview]Percentage of Participants With a Response by Best Overall Response
NCT00448136 (16) [back to overview]Percentage of Participants With Change From Baseline in Global Health Status by EORTC QLQ-C30 Improvement Category
NCT00448136 (16) [back to overview]PFS - Percentage of Participants Estimated to be Progression Free at 12 and 24 Months

Change in Quality of Life as Measured by QLQ-C30

scale ranged from 0 to 100 with higher score meaning greater quality of life (NCT00094497)
Timeframe: baseline and 8 weeks

Interventionunits on a scale (Mean)
EDP-M-6.0
Sz-M-7.7

[back to top]

Number of Disease-free Patients

complete response or disease-free by time of surgery (NCT00094497)
Timeframe: every 8 weeks until progression (up to 5 years)

Interventionparticipants (Number)
EDP-M6
Sz-M3

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Overall Survival

participants who died among those randomized to first-line therapy (NCT00094497)
Timeframe: every 8 weeks until death up to 5 years

Interventionparticipants (Number)
EDP-M108
Sz-M124

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Progression-free Survival

(NCT00094497)
Timeframe: every 8 weeks until progression or death up to 5 years

Interventionmonths (Median)
EDP-M5.0
Sz-M2.1

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Best Overall Response Rate

RECIST 1.0 was used to evaluate response (NCT00094497)
Timeframe: every 8 weeks up to 5 years

,
Interventionparticipants (Number)
complete responsedisease-free by time of surgerypartial responsestable diseaseprogressive diseasedid not receive treatmentcould not be evaluated
EDP-M24295343317
Sz-M12113488413

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Duration of ODC - Time to Event

Determined only for those participants with overall control disease (CR, PR, or SD per RECIST) and was defined as the time interval between the first occurrence of disease control (CR, PR or SD) and the date of progression or death from any cause. Data for participants who were lost to follow-up were censored at the date of last evaluation without progression. Data for participants who completed the study without an event of progression or death were censored at the data of last visit or follow-up without progression. Median time to event was estimated using the Kaplan-Meier method. (NCT00448136)
Timeframe: Screening, every 3 months during treatment, every 6 months during follow-up to 2 years

Interventionmonths (Median)
Bevacizumab + 5-FU + Streptozocin22.3
Bevacizumab + Capecitabine23.4

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Duration of OR - Time to Event

Determined only for those participants with an overall response (CR or PR) and was defined as the time interval between the response (CR or PR) and the date of progression or death from any cause. Data for participants who were lost to follow-up were censored at the date of last evaluation without progression. Data for participants who completed the study without an event of progression or death were censored at the data of last visit or follow-up without progression. Median duration of OR was estimated using the Kaplan-Meier method. (NCT00448136)
Timeframe: Screening, every 3 months during treatment, every 6 months during follow-up to 2 years

Interventionmonths (Median)
Bevacizumab + 5-FU + StreptozocinNA
Bevacizumab + CapecitabineNA

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Duration of Overall Disease Control (ODC) - Percentage of Participants With an Event

Determined only for those participants with overall disease control (CR, PR or SD per RECIST) and was defined as the time interval between the first occurrence of disease control (CR, PR or SD) and the date of progression or death from any cause. Data for participants who were lost to follow-up were censored at the date of last evaluation without progression. Data for participants who completed the study without an event of progression or death were censored at the data of last visit or follow-up without progression. (NCT00448136)
Timeframe: Screening, every 3 months during treatment, every 6 months during follow-up to 2 years

Interventionpercentage of participants (Number)
Bevacizumab + 5-FU + Streptozocin52.9
Bevacizumab + Capecitabine46.5

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Duration of Overall Response (OR) - Percentage of Participants With an Event

Determined only for those participants with an overall response (CR or PR) and was defined as the time interval between the response (CR or PR) and the date of progression or death from any cause. Data for participants who were lost to follow-up were censored at the date of last evaluation without progression. Data for participants who completed the study without an event of progression or death were censored at the data of last visit or follow-up without progression. (NCT00448136)
Timeframe: Screening, every 3 months during treatment, every 6 months during follow-up to 2 years

Interventionpercentage of participants (Number)
Bevacizumab + 5-FU + Streptozocin42.1
Bevacizumab + Capecitabine22.2

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OS - Time to Event

OS was defined as the time from the first treatment administration to death from any cause. Data for participants who were lost to follow-up were censored at the date of last evaluation. Data for participants who were alive at the end of the study were censored at the date of last visit. Median OS was estimated using the Kaplan-Meier method. (NCT00448136)
Timeframe: Screening, Day 1 of every cycle during treatment, every 6 months during follow-up to 2 years

Interventionmonths (Median)
Bevacizumab + 5-FU + StreptozocinNA
Bevacizumab + CapecitabineNA

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Overall Survival (OS) - Percentage of Participants With an Event

OS was defined as the time from the first treatment administration to death from any cause. Data for participants who were lost to follow-up were censored at the date of last evaluation. Data for participants who were alive at the end of the study were censored at the date of last visit. (NCT00448136)
Timeframe: Screening, Day 1 of every cycle during treatment, every 6 months during follow-up to 2 years

Interventionpercentage of participants (Number)
Bevacizumab + 5-FU + Streptozocin14.7
Bevacizumab + Capecitabine16.3

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PFS - Time to Event

PFS is defined as the interval between the date of start of treatment and the date of evaluation by the investigator of progressive disease or death from any cause. The progression was assessed according to RECIST using medical imaging during the treatment period and by the investigators (confirmed by medical imaging) during the follow-up period. Data for participants who were lost to follow-up were censored at the date of last evaluation without progression. Data for participants who completed the study without an event of disease progression or death were censored at the date of the last visit or follow-up without progression. Median PFS was estimated using the Kaplan-Meier method. (NCT00448136)
Timeframe: Screening, every 3 months during treatment, every 6 months during follow-up to 2 years

Interventionmonths (Median)
Bevacizumab + 5-FU + Streptozocin23.7
Bevacizumab + Capecitabine23.4

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Progression-Free Survival (PFS) - Percentage of Participants With an Event

PFS is defined as the interval between the date of start of treatment and the date of evaluation by the investigator of progressive disease or death from any cause. The progression was assessed according to Response Evaluation Criteria In Solid Tumors (RECIST) using medical imaging during the treatment period and by the investigators (confirmed by medical imaging) during the follow-up period. Data for participants who were lost to follow-up were censored at the date of last evaluation without progression. Data for participants who completed the study without an event of disease progression or death were censored at the date of the last visit or follow-up without progression. (NCT00448136)
Timeframe: Screening, every 3 months during treatment, every 6 months during follow-up to 2 years

Interventionpercentage of participants (Number)
Bevacizumab + 5-FU + Streptozocin52.9
Bevacizumab + Capecitabine53.1

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Duration of ODC - Percentage of Participants Maintaining Disease Control at 12 and 24 Months

Duration of ODC was determined only for those participants with overall control disease (CR, PR, or SD per RECIST) and was defined as the time interval between the first occurrence of disease control (CR, PR, or SD) and the date of progression or death from any cause. Data for participants who were lost to follow-up were censored at the date of last evaluation without progression. Data for participants who completed the study without an event of progression or death were censored at the data of last visit or follow-up without progression. (NCT00448136)
Timeframe: Screening, every 3 months during treatment, every 6 months during follow-up to 2 years

,
Interventionpercentage of participants (Number)
12 months24 months
Bevacizumab + 5-FU + Streptozocin6842
Bevacizumab + Capecitabine72NA

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Duration of OR - Percentage of Participants With Sustained Response at 12 and 24 Months

Duration of OR was determined only for those participants with an overall response of CR or PR and was defined as the time interval between the response (CR or PR) and the date of progression or death from any cause. Data for participants who were lost to follow-up were censored at the date of last evaluation without progression. Data for participants who completed the study without an event of progression or death were censored at the data of last visit or follow-up without progression. (NCT00448136)
Timeframe: Screening, every 3 months during treatment, every 6 months during follow-up to 2 years

,
Interventionpercentage of participants (Number)
12 months24 months
Bevacizumab + 5-FU + Streptozocin7455
Bevacizumab + Capecitabine70NA

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EORTC QLQ-C30 Functional and Symptom Scale Scores

EORTC QLQ-C30: included functional scales (physical, role, cognitive, emotional, and social), global health status, symptom scales (fatigue, pain, nausea/vomiting) and single items (dyspnoea, appetite loss, insomnia, constipation/diarrhea and financial difficulties). Most questions used 4-point scale (1 'Not at all' to 4 'Very much'; 2 questions used 7-point scale [1 'very poor' to 7 'Excellent']). Scores averaged, transformed to 0-100 scale; for functional scores, a higher score represents a better level of functioning. For symptom scale scores a higher level represents a more severe level of symptoms. (NCT00448136)
Timeframe: Screening, every 3 months during treatment

,
Interventionunits on a scale (Mean)
Physical functioning, Baseline (n=30,43)Physical functioning, 3 months (n=22,33)Physical functioning, 6 months (n=21,24)Physical functioning, End of Treatment (n=13,24)Role functioning, Baseline (n=30,43)Role functioning, 3 months (n=22,33)Role functioning, 6 months (n=21,24)Role functioning, End of Treatment (n=13,24)Emotional functioning, Baseline (n=30,42)Emotional functioning, 3 months (n=21,33)Emotional functioning, 6 months (n=21,24)Emotional functioning, End of Treatment (n=13,24)Cognitive functioning, Baseline (n=30,42)Cognitive functioning, 3 months (n=22,33)Cognitive functioning, 6 months (n=21,24)Cognitive functioning, End of Treatment (n=13,24)Social functioning, Baseline (n=30,41)Social functioning, 3 months (n=22,33)Social functioning, 6 months (n=21,24)Social functioning, End of Treatment (n=13,24)Fatigue, Baseline (n=30,42)Fatigue, 3 months (n=21,33)Fatigue, 6 months (n=20,24)Fatigue, End of Treatment (n=13,24)Nausea and vomiting, Baseline (n=30,42)Nausea and vomiting, 3 months (n=22,33)Nausea and vomiting, 6 months (n=21,24)Nausea and vomiting, End of Treatment (n=13,24)Pain, Baseline (n=30,43)Pain, 3 months (n=22,33)Pain, 6 months (n=21,24)Pain, End of Treatment (n=13,24)Dyspnea, Baseline (n=30,43)Dyspnea, 3 months (n=21,33)Dyspnea, 6 months (n=21,23)Dyspnea, End of Treatment (n=13,24)Insomnia, Baseline (n=30,43)Insomnia, 3 months (n=21,33)Insomnia, 6 months (n=21,24)Insomnia, End of Treatment (n=13,24)Appetite loss, Baseline (n=29,42)Appetite loss, 3 months (n=22,33)Appetite loss, 6 months (n=21,24)Appetite loss, End of Treatment (n=13,24)Constipation, Baseline (n=27,40)Constipation, 3 months (n=21,33)Constipation, 6 months (n=21,23)Constipation, End of Treatment (n=13,24)Diarrhea, Baseline (n=30,41)Diarrhea, 3 months (n=22,32)Diarrhea, 6 months (n=21,23)Diarrhea, End of Treatment (n=12,22)Financial difficulties, Baseline (n=30,413)Financial difficulties, 3 months (n=22,33)Financial difficulties, 6 months (n=21,23)Financial difficulties, End of treatment (n=13,24)
Bevacizumab + 5-FU + Streptozocin90.4489.3281.9882.8282.2285.6175.4078.2171.9481.4872.6277.5686.6789.3983.3383.3386.1189.3981.7584.6226.3027.7836.6734.196.6710.618.7310.2614.4412.8823.0220.5116.6712.7019.0520.5124.4420.6333.3323.0812.647.5815.8712.824.9415.8717.4612.8213.339.096.352.7814.449.0915.8717.95
Bevacizumab + Capecitabine87.7175.3582.5079.4483.3362.1270.8372.9271.8976.0176.0473.6187.3083.8482.6481.9487.4075.7683.3381.9427.2543.1037.9634.492.789.607.646.2521.7118.1817.3626.3916.2830.3023.1923.6124.0327.2729.1730.568.7320.2025.0025.0010.007.0711.5913.8937.4045.8343.4828.798.136.062.904.17

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Global Health Status as Assessed by the European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire - C30 (EORTC QLQ-C30)

EORTC QLQ-C30: included functional scales (physical, role, cognitive, emotional, and social), global health status, symptom scales (fatigue, pain, nausea/vomiting) and single items (dyspnoea, appetite loss, insomnia, constipation/diarrhea and financial difficulties). Most questions used 4-point scale (1 'Not at all' to 4 'Very much'; 2 questions used 7-point scale [1 'very poor' to 7 'Excellent']). Scores were averaged and transformed to 0-100 scale; higher score=better level of functioning or greater degree of symptoms. (NCT00448136)
Timeframe: Screening, every 3 months during treatment

,
Interventionunits on a scale (Mean)
Baseline (n=29,40)3 months (n=20,32)6 months (n=20,24)12 months (n=13,14)End of treatment (n=13,23)
Bevacizumab + 5-FU + Streptozocin65.2365.8360.0066.0364.74
Bevacizumab + Capecitabine65.4257.0366.3272.6257.97

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OS - Percentage of Participants Surviving at 12 and 24 Months

OS was defined as the time from the first treatment administration to death from any cause. Data for participants who were lost to follow-up were censored at the date of last evaluation. Data for participants who were alive at the end of the study were censored at the date of last visit. (NCT00448136)
Timeframe: Screening, Day 1 of every cycle during treatment, every 6 months during follow-up to 2 years

,
Interventionpercentage of participants (Number)
12 months24 months
Bevacizumab + 5-FU + Streptozocin9488
Bevacizumab + Capecitabine8885

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Percentage of Participants With a Response by Best Overall Response

Best overall response defined as best response recorded during the study as defined according to RECIST; performed by the investigator and by centralized review. Complete response (CR): complete disappearance of all target lesions and non-target disease. All lesions, both target and non-target, must have decreased to normal (short axis, less than [<]10 millimeters [mm]). No new lesions. Partial response (PR): greater than or equal to (≥)30 percent (%) decrease under baseline of the sum of diameters of all target lesions. The short axis was used in the sum for target nodes, while the longest diameter (LD) was used in the sum for all other target lesions. No unequivocal progression of non-target disease. No new lesions. Stable disease (SD): not qualifying for CR, PR, or Progressive Disease (PD). PD: at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of 1 or more new lesions. (NCT00448136)
Timeframe: Screening, every 3 months during treatment, every 6 months during follow-up to 2 years

,
Interventionpercentage of participants (Number)
PR (Investigator)PR (Centralized review)SD (Investigator)SD (Centralized review)PD (Investigator)PD (Centralized review)Not evaluable (Investigator)Not evaluable (Centralized review)
Bevacizumab + 5-FU + Streptozocin55.951.544.148.50000
Bevacizumab + Capecitabine18.412.569.481.38.204.16.3

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Percentage of Participants With Change From Baseline in Global Health Status by EORTC QLQ-C30 Improvement Category

EORTC QLQ-C30: included functional scales (physical, role, cognitive, emotional, and social), global health status, symptom scales (fatigue, pain, nausea/vomiting) and single items (dyspnoea, appetite loss, insomnia, constipation/diarrhea and financial difficulties). Most questions used 4-point scale (1 'Not at all' to 4 'Very much'; 2 questions used 7-point scale [1 'very poor' to 7 'Excellent']). Scores averaged, transformed to 0-100 scale; higher score=better level of functioning or greater degree of symptoms. Changes from baseline were categorized as follows: Very much worsening (less than [<]-20); Moderate worsening (greater than or equal to [≥]-20 to <-10); Little worsening (≥-10 to <-5); No change (≥-5 to less than or equal to [≤]5); Little improvement (>5 to ≤10); Moderate improvement (>10 to ≤20); and Very much improved (>20). (NCT00448136)
Timeframe: Screening, every 3 months during treatment

,
Interventionpercentage of participants (Number)
3 months, Very much worsening (n=20,29)3 months, Moderate worsening (n=20,29)3 months, Little worsening (n=20,29)3 months, No change (n=20,29)3 months, Little improving (n=20,29)3 months, Moderate Improving (n=20,29)3 months, Very much improving (n=20,29)6 months, Very much worsening (n=20,22)6 months, Moderate worsening (n=20,22)6 months, Little worsening (n=20,22)6 months, No change (n=20,22)6 months, Little improving (n=20,22)6 months, Moderate Improving (n=20,22)6 months, Very much improving (n=20,22)12 months, Very much worsening (n=12,13)12 months, Moderate worsening (n=12,13)12 months - Little worsening (n=12,13)12 months, No change (n=12,13)12 months, Little improving (n=12,13)12 months, Moderate Improving (n=12,13)12 months, Very much improving (n=12,13)End of treatment, Very much worsening (n=13,20)End of treatment, Moderate worsening (n=13,20)End of treatment, Little worsening (n=13,20)End of treatment, No change (n=13,20)End of treatment, Little improving (n=13,20)End of treatment, Moderate Improving (n=13,20)End of treatment, Very much improving (n=13,20)
Bevacizumab + 5-FU + Streptozocin10.010.010.040.05.015.010.015.010.05.035.010.015.010.08.38.333.325.08.316.7015.430.8015.415.415.47.7
Bevacizumab + Capecitabine17.224.117.224.13.43.410.322.718.2031.813.6013.6015.415.438.57.715.47.715.05.010.045.010.05.010.0

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PFS - Percentage of Participants Estimated to be Progression Free at 12 and 24 Months

PFS is defined as the interval between the date of start of treatment and the date of evaluation by the investigator of progressive disease or death from any cause. The progression was assessed according to RECIST using medical imaging during the treatment period and by the investigators (confirmed by medical imaging) during the follow-up period. Data for participants who were lost to follow-up were censored at the date of last evaluation without progression. Data for participants who completed the study without an event of disease progression or death were censored at the date of the last visit or follow-up without progression. (NCT00448136)
Timeframe: Screening, every 3 months during treatment, every 6 months during follow-up to 2 years

,
Interventionpercentage of participants (Number)
12 months24 months
Bevacizumab + 5-FU + Streptozocin7650
Bevacizumab + Capecitabine6548

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