imidazole profile

imidazole: RN given refers to parent cpd [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

1H-imidazole : An imidazole tautomer which has the migrating hydrogen at position 1. [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 (5)

imidazole is involved in 5 pathway(s), involving a total of 34 unique proteins and 105 unique compounds

ID Source	ID
PubMed CID	795
CHEMBL ID	540
CHEBI ID	16069
CHEBI ID	14434
MeSH ID	M0095023

Synonym
him
CHEBI:16069 ,
brn 0103853
nsc 60522
einecs 206-019-2
glioksal [polish]
nsc 51860
nsc-60522
wln: t5m cnj
imutex
glyoxalin
iminazole
1,4-cyclopentadiene
imidazol
nsc60522
formamidine,n'-vinylene-
usaf ek-4733
methanimidamide,n'-1,2-ethenediyl-
miazole
bdbm7882
chembl540 ,
IMD ,
nsc51860
1,3-diaza-2,4-cyclopentadiene-
MLS001055465
smr000057825
inchi=1/c3h4n2/c1-2-5-3-4-1/h1-3h,(h,4,5
1h-imidazole (9ci)
ccris 3345
imidazole (8ci)
ai3-24703
methanimidamide, n,n'-1,2-ethenediyl-
pyrro(b)monazole
formamidine, n,n'-vinylene-
NCGC00090984-01
STK362967
n,n'-vinyleneformamidine
imidazole
C01589
1,3-diazole
1,3-diaza-2,4-cyclopentadiene
pyrro[b]monazole
288-32-4
1h-imidazole
glyoxaline
n,n'-1,2-ethenediylmethanimidamide
imidazole, acs reagent, >=99% (titration)
imidazole, for molecular biology, >=99% (titration)
imidazole, >=99% (titration), crystalline
DB03366
NCISTRUC2_000693
NCISTRUC1_001975
imidazole, bioultra, for molecular biology, >=99.5% (gc)
imidazole, puriss. p.a., >=99.5% (gc)
imidazole, bioultra, >=99.5% (gc)
4286D518-643C-4C69-BCE7-519D073F4992
BMSE000096
I0001
I0014
I0288
I0290
AKOS000120177
NCGC00090984-02
BMSE000790
cas-288-32-4
tox21_303345
NCGC00257344-01
dtxcid809616
dtxsid2029616 ,
tox21_201504
NCGC00259055-01
FT-0670295
5-23-04-00191 (beilstein handbook reference)
unii-7gbn705nh1
ec 206-019-2
7gbn705nh1 ,
hsdb 8449
glioksal
BP-11451
FT-0627179
imidazole [who-dd]
ondansetron hydrochloride dihydrate impurity e [ep impurity]
clotrimazole impurity d [ep impurity]
enalapril maleate impurity i [ep impurity]
sildenafil citrate impurity e [ep impurity]
imidazole [inci]
ondansetron hydrochloride impurity, imidazole- [usp impurity]
enalapril impurity i
flutrimazole impurity a [ep impurity]
imidazole [mi]
imidazole [usp-rs]
S6006
AM82000
HY-D0837
CS-5135
1-h-imidazole
immidazole
1h-imidazol
mfcd00005183
J-200340
F2190-0638
imidazole, anhydrous, free-flowing, redi-dri(tm), acs reagent, >=99%
imidazole, pharmaceutical impurity standard, >=95.0% (hplc)
imidazole, saj special grade, >=99.0%
imidazole, united states pharmacopeia (usp) reference standard
imidazole, reagentplus(r), 99%
imidazole, european pharmacopoeia (ep) reference standard
{pyrro[b]monazole}
imidazole, acs grade
P17516
ondansetron impurity e, european pharmacopoeia (ep) reference standard
imidazole, for synthesis, 99.5%
imidazole, lr, >=99%
imidazole, pharmaceutical secondary standard; certified reference material
imidazole, vetec(tm) reagent grade, 98%
6745-43-3
Q328692
imidazole, reagent
imidazole zone refined (number of passes:30)
BCP26547
imidazole;1,3-diazole; glyoxaline; 1,3-diazacyclopenta-2,4-diene
imidazole-
227760-40-9
EN300-19083
imidazole-13c,15n2(major)
glyoxaline solution
imidazole buffer solution
imidazole (usp-rs)
enalapril maleate impurity i (ep impurity)
chebi:14434
clotrimazole impurity d (ep impurity)
sildenafil citrate impurity e (ep impurity)
Z104472692

Excerpt	Reference
"Imidazole is a biologically and pharmaceutically important nitrogen-containing heterocyclic ring."	( Kumar, P; Rani, N; Singh, R, 2023)
"The imidazole group is an ubiquitous chemical motif present in several key types of biomolecules. "	( Becerra, A; Lazcano, A; Vázquez-Salazar, A, 2018)
"Imidazole ring is an important five-membered aromatic heterocycle widely present in natural products and synthetic molecules. "	( Damu, GL; Geng, RX; Peng, XM; Zhang, L; Zhou, CH, 2014)
"Imidazole (C3H4N2) is an important biomaterial for material research and applications. "	( Murli, C; Sharma, BB; Sharma, SM; Thomas, S; Verma, AK, 2015)
"Imidazole is a small but important molecule occurring as a structure fragment in systems from amino acids, over ionic liquids, to synthetic polymers. "	( Liem, SY; Popelier, PL; Shaik, MS, 2011)
"Imidazole acts as a subunit in the DNA base adenine and the amino acid histidine-both important biomolecules which display low fluorescence quantum yields following UV excitation. "	( Evans, NL; Stavros, VG; Ullrich, S; Yu, H, 2012)
"Imidazole is a reagent widely used in protein purifying processes. "	( Guan, Y; Hua, Z; Huang, Y; Li, Y; Pan, Q; Shi, R; Zhao, M, 2007)
"Imidazole acts as a heme-site inhibitor of nitric oxide synthase (NOS). "	( Klatt, P; Mayer, B; Schmidt, K; Werner, ER, 1994)
"Thus imidazole is a stronger denaturant than urea, at least at dilute concentration."	( Ariyama, T; Eli, P; Husimi, Y; Nishigaki, K, 1999)

Excerpt	Reference
"Al-imidazole has a larger bond dissociation energy than Cu-imidazole, although the opposite order was previously found for the corresponding ions."	( Lee, JS; Wang, X; Yang, DS, 2006)
"Al-imidazole has a larger bond dissociation energy than Cu-imidazole, although the opposite order was previously found for the corresponding ions."	( Lee, JS; Wang, X; Yang, DS, 2006)
"Imidazole has been proposed to reverse renal vasoconstriction following unilateral obstruction, presumably through blockade of thromboxane A2 (TXA2) synthesis. "	( Anderson, ME; Edwards, BS; Knox, FG; Romero, JC; Strand, JC, 1981)
"Imidazole antifungals have been used with success in scalp psoriasis."	( Franssen, ME; van de Kerkhof, PC, 2001)

Excerpt	Reference
"The imidazole-induced increase in contracture appears to be mediated through increased influx of calcium."	( Sharma, PL; Singh, M, 1985)
"Imidazole was used because it is a potent inducer of cytochrome P-450 isozyme 3a which is also induced by ethanol."	( Gruenke, LD; Konopka, K; Koop, DR; Waskell, LA, 1988)

Excerpt	Reference
"In imidazole treated cells, the G1/G0 phase cell proportion increased, whereas in the S and G2/M phases the cell proportion decreased."	( Long, Y; Wang, D, 2019)
"Imidazole-treated cells showed a reduction in the level of Tcf/Lef target genes involved in the β-catenin signaling network, including ubiquitous genes such as Axin2, Lef1, and Wisp1 as well as cell lineage-restricted genes such as microphthalmia-associated transcription factor and dopachrome tautomerase."	( Bellei, B; Izzo, E; Picardo, M; Pitisci, A, 2012)
"Imidazole pretreatment prevented a rise of TxB(2), but not 6-keto-PGF(1alpha); indomethacin blocked both."	( Hechtman, HB; Krausz, MM; Levine, L; Shepro, D; Utsonomiya, T, 1982)
"Imidazole treatment (i) causes moderate inhibition of 125I-labeled transferrin binding to both control and Me2SO-treated MEL cells; (ii) markedly suppresses Me2SO-induced activation of iron uptake into MEL cells; (iii) markedly decreases the incorporation of iron into ferritin; and (iv) abolishes heme biosynthesis from [2-14C]glycine and hemoglobin accumulation in Me2SO-treated cells."	( Nunez, MT; Robinson, SH; Tsiftsoglou, AS; Wong, W, 1983)
"When imidazole as pretreated with alpha-N-tosyl-L-lysine chloromethyl ketone, the ability of this imidazole solution to restore amidolytic activity to MrhPm was eliminated, suggesting that N alpha-(p-tosyl)lysine chloromethyl ketone directs into the binding pocket a derivatized form of imidazole, which is ineffective as an His-603 substitute."	( Castellino, FJ; Chibber, BA; Mhashilkar, AM; Viswanatha, T, 1993)
"Imidazole treatment (10 mg/100 g b.m., intraperitoneally, twice a day for two days) failed to influence the arterial blood pressure, the cardiac output and its distribution in organs investigated (heart, muscle, lung [bronchial fraction], skin, liver, spleen, small intestine, adrenal gland and kidneys)."	( Bartha, J; Hably, C; Menz, V, 1991)
"Imidazole treatment significantly reduced the decrement in SV."	( Durante, W; Sunahara, FA, 1987)
"Imidazole pretreatment (50 mg/kg i.p.) significantly inhibited thromboxane production, but augmented production of prostacyclin and PGE2."	( Cowen, DE; Dempsey, RJ; Donaldson, DL; Roy, MW; Young, AB, 1988)
"Imidazole pretreatment also enhanced rates of the microsomal metabolism of 7-ethoxycoumarin and aminopyrine, but did not affect rates of aniline or p-nitrophenol hydroxylation."	( Reinke, LA; Rikans, LE; Sexter, SH, 1985)
"Treatment with imidazole led to chromatin material condensation, detaching of cells, and apoptotic nuclei."	( Long, Y; Wang, D, 2019)
"Pretreatment with imidazole, which attenuated the lipid-induced increase in thromboxane B2 concentration, completely blocked the pulmonary hemodynamic response to lipid.(ABSTRACT TRUNCATED AT 250 WORDS)"	( Berner, ME; Bland, RD; Braun, D; Clyman, RI; Raj, JU; Teague, WG, 1987)

Class	Description
imidazole
[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]

Pathway	Proteins	Compounds
histamine biosynthesis	4	21
starch degradation III	1	15
nitroethane degradation	1	15
UDP-u03B1-D-glucose biosynthesis I	14	24
L-isoleucine biosynthesis II	14	30

Protein	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Chain A, MAJOR APURINIC/APYRIMIDINIC ENDONUCLEASE	Homo sapiens (human)	Potency	0.3981	0.0032	45.4673	12,589.2998	AID2517
aldehyde dehydrogenase 1 family, member A1	Homo sapiens (human)	Potency	35.4813	0.0112	12.4002	100.0000	AID1030
retinoic acid nuclear receptor alpha variant 1	Homo sapiens (human)	Potency	52.0361	0.0030	41.6115	22,387.1992	AID1159552; AID1159555
retinoid X nuclear receptor alpha	Homo sapiens (human)	Potency	5.1868	0.0008	17.5051	59.3239	AID1159531
estrogen-related nuclear receptor alpha	Homo sapiens (human)	Potency	18.2501	0.0015	30.6073	15,848.9004	AID1224841
Nuclear receptor ROR-gamma	Homo sapiens (human)	Potency	33.4915	0.0266	22.4482	66.8242	AID651802
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Thromboxane-A synthase	Homo sapiens (human)	IC50 (µMol)	670.0000	0.0009	1.2304	10.0000	AID212779
Nitric oxide synthase, brain	Homo sapiens (human)	Ki	175.0000	0.0150	1.1811	7.3000	AID404423
Nitric oxide synthase, inducible	Mus musculus (house mouse)	IC50 (µMol)	40.0000	0.0010	3.3911	9.6000	AID147271
Glutaminyl-peptide cyclotransferase	Homo sapiens (human)	IC50 (µMol)	352.0000	5.0000	5.0000	5.0000	AID1893771
Glutaminyl-peptide cyclotransferase	Homo sapiens (human)	Ki	100.0000	0.2620	2.9358	7.0000	AID1796106
Glutaminyl-peptide cyclotransferase	Mus musculus (house mouse)	Ki	160.0000	6.4000	6.4000	6.4000	AID1796111
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Epoxide hydrolase 1	Rattus norvegicus (Norway rat)	E100	8,800.0000	6.2000	6.2000	6.2000	AID208343
Cytochrome P450 1B1	Homo sapiens (human)	Ks	1,255.0000	0.7000	0.7000	0.7000	AID1515301
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
prostaglandin biosynthetic process	Thromboxane-A synthase	Homo sapiens (human)
icosanoid metabolic process	Thromboxane-A synthase	Homo sapiens (human)
cyclooxygenase pathway	Thromboxane-A synthase	Homo sapiens (human)
intracellular chloride ion homeostasis	Thromboxane-A synthase	Homo sapiens (human)
response to ethanol	Thromboxane-A synthase	Homo sapiens (human)
positive regulation of vasoconstriction	Thromboxane-A synthase	Homo sapiens (human)
response to fatty acid	Thromboxane-A synthase	Homo sapiens (human)
response to hypoxia	Nitric oxide synthase, brain	Homo sapiens (human)
regulation of sodium ion transport	Nitric oxide synthase, brain	Homo sapiens (human)
arginine catabolic process	Nitric oxide synthase, brain	Homo sapiens (human)
nitric oxide biosynthetic process	Nitric oxide synthase, brain	Homo sapiens (human)
striated muscle contraction	Nitric oxide synthase, brain	Homo sapiens (human)
myoblast fusion	Nitric oxide synthase, brain	Homo sapiens (human)
response to heat	Nitric oxide synthase, brain	Homo sapiens (human)
negative regulation of calcium ion transport into cytosol	Nitric oxide synthase, brain	Homo sapiens (human)
regulation of cardiac muscle contraction by calcium ion signaling	Nitric oxide synthase, brain	Homo sapiens (human)
peptidyl-cysteine S-nitrosylation	Nitric oxide synthase, brain	Homo sapiens (human)
positive regulation of peptidyl-serine phosphorylation	Nitric oxide synthase, brain	Homo sapiens (human)
multicellular organismal response to stress	Nitric oxide synthase, brain	Homo sapiens (human)
xenobiotic catabolic process	Nitric oxide synthase, brain	Homo sapiens (human)
vasodilation	Nitric oxide synthase, brain	Homo sapiens (human)
negative regulation of potassium ion transport	Nitric oxide synthase, brain	Homo sapiens (human)
cell redox homeostasis	Nitric oxide synthase, brain	Homo sapiens (human)
positive regulation of DNA-templated transcription	Nitric oxide synthase, brain	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Nitric oxide synthase, brain	Homo sapiens (human)
negative regulation of hydrolase activity	Nitric oxide synthase, brain	Homo sapiens (human)
negative regulation of serotonin uptake	Nitric oxide synthase, brain	Homo sapiens (human)
negative regulation of calcium ion transport	Nitric oxide synthase, brain	Homo sapiens (human)
regulation of cardiac muscle contraction	Nitric oxide synthase, brain	Homo sapiens (human)
regulation of ryanodine-sensitive calcium-release channel activity	Nitric oxide synthase, brain	Homo sapiens (human)
cellular response to growth factor stimulus	Nitric oxide synthase, brain	Homo sapiens (human)
positive regulation of the force of heart contraction	Nitric oxide synthase, brain	Homo sapiens (human)
positive regulation of adenylate cyclase-activating G protein-coupled receptor signaling pathway	Nitric oxide synthase, brain	Homo sapiens (human)
positive regulation of sodium ion transmembrane transport	Nitric oxide synthase, brain	Homo sapiens (human)
regulation of calcium ion transmembrane transport via high voltage-gated calcium channel	Nitric oxide synthase, brain	Homo sapiens (human)
positive regulation of membrane repolarization during ventricular cardiac muscle cell action potential	Nitric oxide synthase, brain	Homo sapiens (human)
positive regulation of guanylate cyclase activity	Nitric oxide synthase, brain	Homo sapiens (human)
nitric oxide mediated signal transduction	Nitric oxide synthase, brain	Homo sapiens (human)
response to hormone	Nitric oxide synthase, brain	Homo sapiens (human)
negative regulation of blood pressure	Nitric oxide synthase, brain	Homo sapiens (human)
response to lipopolysaccharide	Nitric oxide synthase, brain	Homo sapiens (human)
negative regulation of transcription by RNA polymerase II	Nuclear receptor ROR-gamma	Homo sapiens (human)
xenobiotic metabolic process	Nuclear receptor ROR-gamma	Homo sapiens (human)
regulation of glucose metabolic process	Nuclear receptor ROR-gamma	Homo sapiens (human)
regulation of steroid metabolic process	Nuclear receptor ROR-gamma	Homo sapiens (human)
intracellular receptor signaling pathway	Nuclear receptor ROR-gamma	Homo sapiens (human)
circadian regulation of gene expression	Nuclear receptor ROR-gamma	Homo sapiens (human)
cellular response to sterol	Nuclear receptor ROR-gamma	Homo sapiens (human)
positive regulation of circadian rhythm	Nuclear receptor ROR-gamma	Homo sapiens (human)
regulation of fat cell differentiation	Nuclear receptor ROR-gamma	Homo sapiens (human)
positive regulation of DNA-templated transcription	Nuclear receptor ROR-gamma	Homo sapiens (human)
adipose tissue development	Nuclear receptor ROR-gamma	Homo sapiens (human)
T-helper 17 cell differentiation	Nuclear receptor ROR-gamma	Homo sapiens (human)
regulation of transcription by RNA polymerase II	Nuclear receptor ROR-gamma	Homo sapiens (human)
protein folding	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
response to bacterium	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
chaperone-mediated protein folding	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
protein peptidyl-prolyl isomerization	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
cellular response to organic cyclic compound	Cytochrome P450 1B1	Homo sapiens (human)
angiogenesis	Cytochrome P450 1B1	Homo sapiens (human)
trabecular meshwork development	Cytochrome P450 1B1	Homo sapiens (human)
DNA modification	Cytochrome P450 1B1	Homo sapiens (human)
xenobiotic metabolic process	Cytochrome P450 1B1	Homo sapiens (human)
nitric oxide biosynthetic process	Cytochrome P450 1B1	Homo sapiens (human)
cell adhesion	Cytochrome P450 1B1	Homo sapiens (human)
response to nutrient	Cytochrome P450 1B1	Homo sapiens (human)
steroid metabolic process	Cytochrome P450 1B1	Homo sapiens (human)
estrogen metabolic process	Cytochrome P450 1B1	Homo sapiens (human)
negative regulation of cell population proliferation	Cytochrome P450 1B1	Homo sapiens (human)
male gonad development	Cytochrome P450 1B1	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to oxidative stress	Cytochrome P450 1B1	Homo sapiens (human)
toxin metabolic process	Cytochrome P450 1B1	Homo sapiens (human)
positive regulation of vascular endothelial growth factor production	Cytochrome P450 1B1	Homo sapiens (human)
positive regulation of smooth muscle cell migration	Cytochrome P450 1B1	Homo sapiens (human)
sterol metabolic process	Cytochrome P450 1B1	Homo sapiens (human)
arachidonic acid metabolic process	Cytochrome P450 1B1	Homo sapiens (human)
epoxygenase P450 pathway	Cytochrome P450 1B1	Homo sapiens (human)
collagen fibril organization	Cytochrome P450 1B1	Homo sapiens (human)
adrenal gland development	Cytochrome P450 1B1	Homo sapiens (human)
negative regulation of cell migration	Cytochrome P450 1B1	Homo sapiens (human)
negative regulation of NF-kappaB transcription factor activity	Cytochrome P450 1B1	Homo sapiens (human)
response to follicle-stimulating hormone	Cytochrome P450 1B1	Homo sapiens (human)
response to estradiol	Cytochrome P450 1B1	Homo sapiens (human)
negative regulation of cell adhesion mediated by integrin	Cytochrome P450 1B1	Homo sapiens (human)
benzene-containing compound metabolic process	Cytochrome P450 1B1	Homo sapiens (human)
retinol metabolic process	Cytochrome P450 1B1	Homo sapiens (human)
retinal metabolic process	Cytochrome P450 1B1	Homo sapiens (human)
positive regulation of apoptotic process	Cytochrome P450 1B1	Homo sapiens (human)
blood vessel endothelial cell migration	Cytochrome P450 1B1	Homo sapiens (human)
endothelial cell migration	Cytochrome P450 1B1	Homo sapiens (human)
estrous cycle	Cytochrome P450 1B1	Homo sapiens (human)
positive regulation of translation	Cytochrome P450 1B1	Homo sapiens (human)
positive regulation of angiogenesis	Cytochrome P450 1B1	Homo sapiens (human)
positive regulation of receptor signaling pathway via JAK-STAT	Cytochrome P450 1B1	Homo sapiens (human)
membrane lipid catabolic process	Cytochrome P450 1B1	Homo sapiens (human)
response to arsenic-containing substance	Cytochrome P450 1B1	Homo sapiens (human)
blood vessel morphogenesis	Cytochrome P450 1B1	Homo sapiens (human)
retinal blood vessel morphogenesis	Cytochrome P450 1B1	Homo sapiens (human)
ganglion development	Cytochrome P450 1B1	Homo sapiens (human)
cellular response to hydrogen peroxide	Cytochrome P450 1B1	Homo sapiens (human)
cellular response to cAMP	Cytochrome P450 1B1	Homo sapiens (human)
cellular response to tumor necrosis factor	Cytochrome P450 1B1	Homo sapiens (human)
cellular response to luteinizing hormone stimulus	Cytochrome P450 1B1	Homo sapiens (human)
cellular response to cortisol stimulus	Cytochrome P450 1B1	Homo sapiens (human)
cellular response to progesterone stimulus	Cytochrome P450 1B1	Homo sapiens (human)
response to dexamethasone	Cytochrome P450 1B1	Homo sapiens (human)
endothelial cell-cell adhesion	Cytochrome P450 1B1	Homo sapiens (human)
response to indole-3-methanol	Cytochrome P450 1B1	Homo sapiens (human)
cellular response to toxic substance	Cytochrome P450 1B1	Homo sapiens (human)
omega-hydroxylase P450 pathway	Cytochrome P450 1B1	Homo sapiens (human)
response to 3-methylcholanthrene	Cytochrome P450 1B1	Homo sapiens (human)
regulation of reactive oxygen species metabolic process	Cytochrome P450 1B1	Homo sapiens (human)
positive regulation of reactive oxygen species metabolic process	Cytochrome P450 1B1	Homo sapiens (human)
positive regulation of DNA biosynthetic process	Cytochrome P450 1B1	Homo sapiens (human)
peptidyl-pyroglutamic acid biosynthetic process, using glutaminyl-peptide cyclotransferase	Glutaminyl-peptide cyclotransferase	Homo sapiens (human)
protein modification process	Glutaminyl-peptide cyclotransferase	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
monooxygenase activity	Thromboxane-A synthase	Homo sapiens (human)
thromboxane-A synthase activity	Thromboxane-A synthase	Homo sapiens (human)
iron ion binding	Thromboxane-A synthase	Homo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen	Thromboxane-A synthase	Homo sapiens (human)
heme binding	Thromboxane-A synthase	Homo sapiens (human)
12-hydroxyheptadecatrienoic acid synthase activity	Thromboxane-A synthase	Homo sapiens (human)
hydroperoxy icosatetraenoate dehydratase activity	Thromboxane-A synthase	Homo sapiens (human)
nitric-oxide synthase activity	Nitric oxide synthase, brain	Homo sapiens (human)
calcium channel regulator activity	Nitric oxide synthase, brain	Homo sapiens (human)
protein binding	Nitric oxide synthase, brain	Homo sapiens (human)
calmodulin binding	Nitric oxide synthase, brain	Homo sapiens (human)
FMN binding	Nitric oxide synthase, brain	Homo sapiens (human)
sodium channel regulator activity	Nitric oxide synthase, brain	Homo sapiens (human)
heme binding	Nitric oxide synthase, brain	Homo sapiens (human)
tetrahydrobiopterin binding	Nitric oxide synthase, brain	Homo sapiens (human)
arginine binding	Nitric oxide synthase, brain	Homo sapiens (human)
transmembrane transporter binding	Nitric oxide synthase, brain	Homo sapiens (human)
cadmium ion binding	Nitric oxide synthase, brain	Homo sapiens (human)
calcium-dependent protein binding	Nitric oxide synthase, brain	Homo sapiens (human)
flavin adenine dinucleotide binding	Nitric oxide synthase, brain	Homo sapiens (human)
NADP binding	Nitric oxide synthase, brain	Homo sapiens (human)
scaffold protein binding	Nitric oxide synthase, brain	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	Nuclear receptor ROR-gamma	Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specific	Nuclear receptor ROR-gamma	Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specific	Nuclear receptor ROR-gamma	Homo sapiens (human)
DNA-binding transcription factor activity	Nuclear receptor ROR-gamma	Homo sapiens (human)
protein binding	Nuclear receptor ROR-gamma	Homo sapiens (human)
oxysterol binding	Nuclear receptor ROR-gamma	Homo sapiens (human)
zinc ion binding	Nuclear receptor ROR-gamma	Homo sapiens (human)
ligand-activated transcription factor activity	Nuclear receptor ROR-gamma	Homo sapiens (human)
sequence-specific double-stranded DNA binding	Nuclear receptor ROR-gamma	Homo sapiens (human)
nuclear receptor activity	Nuclear receptor ROR-gamma	Homo sapiens (human)
peptidyl-prolyl cis-trans isomerase activity	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
protein binding	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
FK506 binding	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
protein-macromolecule adaptor activity	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
heat shock protein binding	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
monooxygenase activity	Cytochrome P450 1B1	Homo sapiens (human)
iron ion binding	Cytochrome P450 1B1	Homo sapiens (human)
protein binding	Cytochrome P450 1B1	Homo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygen	Cytochrome P450 1B1	Homo sapiens (human)
heme binding	Cytochrome P450 1B1	Homo sapiens (human)
aromatase activity	Cytochrome P450 1B1	Homo sapiens (human)
estrogen 16-alpha-hydroxylase activity	Cytochrome P450 1B1	Homo sapiens (human)
hydroperoxy icosatetraenoate dehydratase activity	Cytochrome P450 1B1	Homo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, NAD(P)H as one donor, and incorporation of one atom of oxygen	Cytochrome P450 1B1	Homo sapiens (human)
protein binding	Glutaminyl-peptide cyclotransferase	Homo sapiens (human)
zinc ion binding	Glutaminyl-peptide cyclotransferase	Homo sapiens (human)
glutaminyl-peptide cyclotransferase activity	Glutaminyl-peptide cyclotransferase	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
endoplasmic reticulum	Thromboxane-A synthase	Homo sapiens (human)
endoplasmic reticulum membrane	Thromboxane-A synthase	Homo sapiens (human)
cytosol	Thromboxane-A synthase	Homo sapiens (human)
photoreceptor inner segment	Nitric oxide synthase, brain	Homo sapiens (human)
nucleoplasm	Nitric oxide synthase, brain	Homo sapiens (human)
cytoplasm	Nitric oxide synthase, brain	Homo sapiens (human)
mitochondrion	Nitric oxide synthase, brain	Homo sapiens (human)
cytosol	Nitric oxide synthase, brain	Homo sapiens (human)
cytoskeleton	Nitric oxide synthase, brain	Homo sapiens (human)
plasma membrane	Nitric oxide synthase, brain	Homo sapiens (human)
sarcoplasmic reticulum	Nitric oxide synthase, brain	Homo sapiens (human)
sarcolemma	Nitric oxide synthase, brain	Homo sapiens (human)
dendritic spine	Nitric oxide synthase, brain	Homo sapiens (human)
membrane raft	Nitric oxide synthase, brain	Homo sapiens (human)
synapse	Nitric oxide synthase, brain	Homo sapiens (human)
perinuclear region of cytoplasm	Nitric oxide synthase, brain	Homo sapiens (human)
cell periphery	Nitric oxide synthase, brain	Homo sapiens (human)
protein-containing complex	Nitric oxide synthase, brain	Homo sapiens (human)
plasma membrane	Nitric oxide synthase, brain	Homo sapiens (human)
postsynaptic density	Nitric oxide synthase, brain	Homo sapiens (human)
cytosol	Nitric oxide synthase, brain	Homo sapiens (human)
nucleus	Nitric oxide synthase, brain	Homo sapiens (human)
nucleus	Nuclear receptor ROR-gamma	Homo sapiens (human)
nucleoplasm	Nuclear receptor ROR-gamma	Homo sapiens (human)
nuclear body	Nuclear receptor ROR-gamma	Homo sapiens (human)
chromatin	Nuclear receptor ROR-gamma	Homo sapiens (human)
nucleus	Nuclear receptor ROR-gamma	Homo sapiens (human)
cytoplasm	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
nucleoplasm	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
cytosol	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
membrane	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
extracellular exosome	Peptidyl-prolyl cis-trans isomerase FKBP5	Homo sapiens (human)
mitochondrion	Cytochrome P450 1B1	Homo sapiens (human)
endoplasmic reticulum membrane	Cytochrome P450 1B1	Homo sapiens (human)
intracellular membrane-bounded organelle	Cytochrome P450 1B1	Homo sapiens (human)
extracellular region	Glutaminyl-peptide cyclotransferase	Homo sapiens (human)
specific granule lumen	Glutaminyl-peptide cyclotransferase	Homo sapiens (human)
extracellular exosome	Glutaminyl-peptide cyclotransferase	Homo sapiens (human)
tertiary granule lumen	Glutaminyl-peptide cyclotransferase	Homo sapiens (human)
ficolin-1-rich granule lumen	Glutaminyl-peptide cyclotransferase	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Assay ID	Title	Year	Journal	Article
AID1515301	Binding affinity to human C-terminal 4His-tagged CYP1B1 expressed in Escherichia coli DH5alpha assessed as spectral dissociation constant by spectrophotometric analysis	2019	Bioorganic & medicinal chemistry, 01-15, Volume: 27, Issue:2	Design and synthesis of selective CYP1B1 inhibitor via dearomatization of α-naphthoflavone.
AID1893771	Inhibition of recombinant human QC using H-Gln-AMC hydrobromide as fluorogenic substrate incubated for 6 hrs by fluorometric microplate reader analysis	2022	ACS medicinal chemistry letters, Sep-08, Volume: 13, Issue:9	2-Amino-1,3,4-thiadiazoles as Glutaminyl Cyclases Inhibitors Increase Phagocytosis through Modification of CD47-SIRPα Checkpoint.
AID1543820	Antiproliferative activity against human MCF7 cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay	2019	European journal of medicinal chemistry, Apr-15, Volume: 168	Synthesis and antitumor activity of novel steroidal imidazolium salt derivatives.
AID161184	Inhibition of ram seminal vesicle Cyclooxygenase	1985	Journal of medicinal chemistry, Oct, Volume: 28, Issue:10	Selective thromboxane synthetase inhibitors. 1. 1-[(Aryloxy)alkyl]-1H-imidazoles.
AID1268846	Cytotoxicity against human HL60 cells by MTT assay	2016	Bioorganic & medicinal chemistry letters, Jan-15, Volume: 26, Issue:2	Synthesis and cytotoxic activity of novel hexahydropyrrolo[2,3-b]indole imidazolium salts.
AID26810	Partition coefficient (logP)	1985	Journal of medicinal chemistry, Aug, Volume: 28, Issue:8	Structural features of imidazole derivatives that enhance styrene oxide hydrolase activity in rat hepatic microsomes.
AID208343	Enhanced styrene oxide hydrolase activity pH 8.7	1985	Journal of medicinal chemistry, Aug, Volume: 28, Issue:8	Structural features of imidazole derivatives that enhance styrene oxide hydrolase activity in rat hepatic microsomes.
AID1543819	Antiproliferative activity against human SMMC7721 cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay	2019	European journal of medicinal chemistry, Apr-15, Volume: 168	Synthesis and antitumor activity of novel steroidal imidazolium salt derivatives.
AID1543822	Antiproliferative activity against human SW480 cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay	2019	European journal of medicinal chemistry, Apr-15, Volume: 168	Synthesis and antitumor activity of novel steroidal imidazolium salt derivatives.
AID155525	Inhibition of porcine aorta prostacyclin PGI-2 synthase	1985	Journal of medicinal chemistry, Oct, Volume: 28, Issue:10	Selective thromboxane synthetase inhibitors. 1. 1-[(Aryloxy)alkyl]-1H-imidazoles.
AID404423	Inhibition of nNOS assessed as conversion of L-[3H]arginine to L-[3H]citrulline	2008	Bioorganic & medicinal chemistry, Jun-01, Volume: 16, Issue:11	Design, synthesis, and evaluation of potential inhibitors of nitric oxide synthase.
AID1543821	Antiproliferative activity against human A549 cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay	2019	European journal of medicinal chemistry, Apr-15, Volume: 168	Synthesis and antitumor activity of novel steroidal imidazolium salt derivatives.
AID1649764	Binding affinity to 15N-labeled FKBP51 (1 to 140 residues) (unknown origin) expressed in Escherichia coli OD2N assessed as induction of chemical shift perturbations at Ile87 residues by two-dimensional 1H/15N HSQC NMR spectroscopy	2020	Journal of medicinal chemistry, 06-11, Volume: 63, Issue:11	Hybrid Screening Approach for Very Small Fragments: X-ray and Computational Screening on FKBP51.
AID147271	Inhibition of purified mouse inducible nitric oxide synthase catalyzed [14C]L-citrulline production at a compound concentration of 1 mM in presence of 50 uM L-arginine	1999	Bioorganic & medicinal chemistry letters, Oct-18, Volume: 9, Issue:20	Guanidine-substituted imidazoles as inhibitors of nitric oxide synthase.
AID25595	Dissociation constant was evaluated	1996	Journal of medicinal chemistry, May-24, Volume: 39, Issue:11	Comparative molecular moment analysis (CoMMA): 3D-QSAR without molecular superposition.
AID1268850	Cytotoxicity against human SW480 cells by MTT assay	2016	Bioorganic & medicinal chemistry letters, Jan-15, Volume: 26, Issue:2	Synthesis and cytotoxic activity of novel hexahydropyrrolo[2,3-b]indole imidazolium salts.
AID537734	Antifungal activity against yeast AD1-8u expressing Candida albicans CaMdr1p by agar disk diffusion assay	2010	European journal of medicinal chemistry, Nov, Volume: 45, Issue:11	Analysis of physico-chemical properties of substrates of ABC and MFS multidrug transporters of pathogenic Candida albicans.
AID1649766	Binding affinity to 15N-labeled FKBP51 (1 to 140 residues) (unknown origin) expressed in Escherichia coli OD2N by two-dimensional 1H/15N HSQC NMR spectroscopy	2020	Journal of medicinal chemistry, 06-11, Volume: 63, Issue:11	Hybrid Screening Approach for Very Small Fragments: X-ray and Computational Screening on FKBP51.
AID497162	Selectivity ratio of IC50 for Plasmodium falciparum to IC50 for CHO cells	2010	Bioorganic & medicinal chemistry, Aug-15, Volume: 18, Issue:16	Anti-Plasmodium activity of imidazolium and triazolium salts.
AID1195896	Inhibition of calmodulin-dependent bovine neuronal NOS using [3H]-arginine as substrate assessed as citrulline formation after 30 mins	2015	Journal of medicinal chemistry, Feb-12, Volume: 58, Issue:3	Novel 2,4-disubstituted pyrimidines as potent, selective, and cell-permeable inhibitors of neuronal nitric oxide synthase.
AID1268847	Cytotoxicity against human SMMC7721 cells by MTT assay	2016	Bioorganic & medicinal chemistry letters, Jan-15, Volume: 26, Issue:2	Synthesis and cytotoxic activity of novel hexahydropyrrolo[2,3-b]indole imidazolium salts.
AID537736	Antifungal activity against yeast AD1-8u expressing Candida albicans CaCdr1p by agar disk diffusion assay	2010	European journal of medicinal chemistry, Nov, Volume: 45, Issue:11	Analysis of physico-chemical properties of substrates of ABC and MFS multidrug transporters of pathogenic Candida albicans.
AID760059	Inhibition of [15N]-labeled humanized-Xenopus MDM2 (13-119 amino acids) interaction with p53 at 1 mM by NMR method	2013	ACS medicinal chemistry letters, Jul-11, Volume: 4, Issue:7	Deconstruction of a nutlin: dissecting the binding determinants of a potent protein-protein interaction inhibitor.
AID760057	Inhibition of Humanized-Xenopus MDM2 (13-119 amino acids) interaction with p53 at 1 to 2.5 mM by SPR analysis	2013	ACS medicinal chemistry letters, Jul-11, Volume: 4, Issue:7	Deconstruction of a nutlin: dissecting the binding determinants of a potent protein-protein interaction inhibitor.
AID213129	Inhibition of Thromboxane synthetase at 100 uM	1981	Journal of medicinal chemistry, Oct, Volume: 24, Issue:10	Highly selective inhibitors of thromboxane synthetase. 2. Pyridine derivatives.
AID537735	Binding affinity to Candida albicans CaMdr1p expressed in yeast AD1-8u	2010	European journal of medicinal chemistry, Nov, Volume: 45, Issue:11	Analysis of physico-chemical properties of substrates of ABC and MFS multidrug transporters of pathogenic Candida albicans.
AID497160	Antiplasmodial activity against Plasmodium falciparum 3D7 after 72 by LDH assay	2010	Bioorganic & medicinal chemistry, Aug-15, Volume: 18, Issue:16	Anti-Plasmodium activity of imidazolium and triazolium salts.
AID687184	Dissociation constant, pKa of the compound at pH 2 to 3 by spectrophotometric analysis	2012	Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11	Rational design of 4-aryl-1,2,3-triazoles for indoleamine 2,3-dioxygenase 1 inhibition.
AID208350	Maximum enhancement of styrene oxide hydrolase activity was reported at compound concentration of 1e-1M	1985	Journal of medicinal chemistry, Aug, Volume: 28, Issue:8	Structural features of imidazole derivatives that enhance styrene oxide hydrolase activity in rat hepatic microsomes.
AID537733	Binding affinity to Candida albicans CaCdr1p expressed in yeast AD1-8u	2010	European journal of medicinal chemistry, Nov, Volume: 45, Issue:11	Analysis of physico-chemical properties of substrates of ABC and MFS multidrug transporters of pathogenic Candida albicans.
AID1719955	Dissociation constant, pKa of the compound	2020	Journal of medicinal chemistry, 08-13, Volume: 63, Issue:15	Thiazoles, Their Benzofused Systems, and Thiazolidinone Derivatives: Versatile and Promising Tools to Combat Antibiotic Resistance.
AID1268848	Cytotoxicity against human A549 cells by MTT assay	2016	Bioorganic & medicinal chemistry letters, Jan-15, Volume: 26, Issue:2	Synthesis and cytotoxic activity of novel hexahydropyrrolo[2,3-b]indole imidazolium salts.
AID70214	Enhancement of epoxide hydrolase activity	1985	Journal of medicinal chemistry, Aug, Volume: 28, Issue:8	Structural features of imidazole derivatives that enhance styrene oxide hydrolase activity in rat hepatic microsomes.
AID1268849	Cytotoxicity against human MCF7 cells by MTT assay	2016	Bioorganic & medicinal chemistry letters, Jan-15, Volume: 26, Issue:2	Synthesis and cytotoxic activity of novel hexahydropyrrolo[2,3-b]indole imidazolium salts.
AID701844	Dissociation constant, pKa of the compound	2012	Journal of medicinal chemistry, Jul-12, Volume: 55, Issue:13	Mitigating heterocycle metabolism in drug discovery.
AID212779	Inhibitory activity against thromboxane A2 synthetase	1985	Journal of medicinal chemistry, Oct, Volume: 28, Issue:10	Selective thromboxane synthetase inhibitors. 1. 1-[(Aryloxy)alkyl]-1H-imidazoles.
AID233501	The pKa value was measured at N15 chemical shift changes due to protonation	1993	Journal of medicinal chemistry, Nov-12, Volume: 36, Issue:23	Protonation of phosphoramide mustard and other phosphoramides.
AID1266401	Binding affinity to cytochrome c peroxidase His175Gly mutant (unknown origin) assessed as equillibrium dissociation constant by Electron paramagnetic resonance spectra method	2015	Journal of medicinal chemistry, Dec-10, Volume: 58, Issue:23	New Frontiers in Druggability.
AID687185	Dissociation constant, pKa of the compound at pH 11 to 12 by spectrophotometric analysis	2012	Journal of medicinal chemistry, Jun-14, Volume: 55, Issue:11	Rational design of 4-aryl-1,2,3-triazoles for indoleamine 2,3-dioxygenase 1 inhibition.
AID25092	Ionization constant (pKa)	1991	Journal of medicinal chemistry, Jul, Volume: 34, Issue:7	Direct prediction of dissociation constants (pKa's) of clonidine-like imidazolines, 2-substituted imidazoles, and 1-methyl-2-substituted-imidazoles from 3D structures using a comparative molecular field analysis (CoMFA) approach.
AID26397	Dissociation constant (pKa, calculated using GNN method)	1997	Journal of medicinal chemistry, Dec-19, Volume: 40, Issue:26	Three-dimensional quantitative structure-activity relationships from molecular similarity matrices and genetic neural networks. 2. Applications.
AID1543818	Antiproliferative activity against human HL60 cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay	2019	European journal of medicinal chemistry, Apr-15, Volume: 168	Synthesis and antitumor activity of novel steroidal imidazolium salt derivatives.
AID497161	Cytotoxicity against CHO cells after 48 hrs by MTT assay	2010	Bioorganic & medicinal chemistry, Aug-15, Volume: 18, Issue:16	Anti-Plasmodium activity of imidazolium and triazolium salts.
AID1802737	Resonance Raman Assay from Article 10.1021/acs.biochem.7b00041: \\Interaction of Azole-Based Environmental Pollutants with the Coelomic Hemoglobin from Amphitrite ornata: A Molecular Basis for Toxicity.\\	2017	Biochemistry, 05-02, Volume: 56, Issue:17	Interaction of Azole-Based Environmental Pollutants with the Coelomic Hemoglobin from Amphitrite ornata: A Molecular Basis for Toxicity.
AID1796111	QC Inhibition Testing from Article 10.1021/bi051142e: \\Isolation, catalytic properties, and competitive inhibitors of the zinc-dependent murine glutaminyl cyclase.\\	2005	Biochemistry, Oct-11, Volume: 44, Issue:40	Isolation, catalytic properties, and competitive inhibitors of the zinc-dependent murine glutaminyl cyclase.
AID1796106	QC Inhibition Testing from Article 10.1021/jm050756e: \\The first potent inhibitors for human glutaminyl cyclase: synthesis and structure-activity relationship.\\	2006	Journal of medicinal chemistry, Jan-26, Volume: 49, Issue:2	The first potent inhibitors for human glutaminyl cyclase: synthesis and structure-activity relationship.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	421 (17.88)	18.7374
1990's	198 (8.41)	18.2507
2000's	539 (22.89)	29.6817
2010's	1000 (42.46)	24.3611
2020's	197 (8.37)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	6 (0.25%)	5.53%
Reviews	71 (2.91%)	6.00%
Case Studies	9 (0.37%)	4.05%
Observational	1 (0.04%)	0.25%
Other	2,353 (96.43%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (37)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
A Safety, Pharmacokinetic and Efficacy Study of a y-Secretase Inhibitor, Nirogacestat (PF-03084014), in Children and Adolescents With Progressive, Surgically Unresectable Desmoid Tumors[NCT04195399]	Phase 2	35 participants (Anticipated)	Interventional	2020-10-07	Active, not recruiting
Adcetris (Brentuximab Vedotin), Substituting Vincristine in the OEPA/COPDac Regimen [Treatment Group 3 (TG3) of Euro-Net C1] With Involved Node Radiation Therapy for High Risk Pediatric Hodgkin Lymphoma (HL)[NCT01920932]	Phase 2	77 participants (Actual)	Interventional	2013-08-12	Active, not recruiting
A Pilot Trial of AVD and Brentuximab Vedotin (SGN-35) in the Treatment of Stage II-IV HIV-Associated Hodgkin Lymphoma[NCT01771107]	Phase 1/Phase 2	41 participants (Actual)	Interventional	2013-03-07	Active, not recruiting
Feasibility and Dose Discovery Analysis of Zoledronic Acid With Concurrent Chemotherapy in the Treatment of Newly Diagnosed Metastatic Osteosarcoma[NCT00742924]	Phase 1	24 participants (Actual)	Interventional	2008-08-31	Completed
Non Invasive Imaging of [18F]HX4 With Positron-Emission-Tomography (PET) in Cervix Cancer.[NCT02233387]	Phase 2	4 participants (Actual)	Interventional	2014-11-30	Terminated(stopped due to patients did not want to participate)
Effects of Dexmedetomidine vs Propofol on the Recordings of Deep Brain Activity (Local Field Potentials) Measured Through Implanted Stimulators[NCT02256319]	Phase 4	12 participants (Actual)	Interventional	2014-09-30	Completed
Phase II Randomized, Open-Label Study of IMC-1121B With or Without Dacarbazine in Patients With Metastatic Malignant Melanoma[NCT00533702]	Phase 2	106 participants (Actual)	Interventional	2007-11-30	Completed
Tinidazole Versus Cefazolin Antibiotic Prophylaxis of Vaginal and Abdominal Hysterectomy[NCT00787553]		75 participants (Actual)	Interventional	2006-07-31	Active, 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 3	1,875 participants (Anticipated)	Interventional	2023-05-11	Recruiting
Study of GSK2132231A Antigen-Specific Cancer Immunotherapeutic in Association With Chemotherapy in Patients With Unresectable and Progressive Metastatic Cutaneous Melanoma[NCT00849875]	Phase 2	48 participants (Actual)	Interventional	2009-05-26	Terminated(stopped due to Early end of trial notification after termination of long term follow up due to lack of scientific justification to continue collect information.)
Non-invasive Imaging of Tumor Hypoxia With [18F]HX4 Positron-Emission-Tomography (PET): A Phase II Trial[NCT02584400]	Phase 2	1 participants (Actual)	Interventional	2016-05-31	Terminated(stopped due to patients did not want to participate)
A Phase II Randomized, Open-label, Multi-center Study of the Safety and Efficacy of IMCgp100 Compared With Investigator Choice in HLA-A*0201 Positive Patients With Previously Untreated Advanced Uveal Melanoma[NCT03070392]	Phase 2	378 participants (Actual)	Interventional	2017-10-16	Active, not recruiting
Randomized Phase II Trial of Temozolomide Versus Hyd-Sulfate AZD6244 [NSC 748727] in Patients With Metastatic Uveal Melanoma[NCT01143402]	Phase 2	120 participants (Actual)	Interventional	2010-06-30	Completed
A Randomized Phase II Study of Rituximab With ABVD Versus Standard ABVD for Patients With Advanced-Stage Classical Hodgkin Lymphoma With Poor Risk Features (IPS Score > 2)[NCT00654732]	Phase 2	58 participants (Actual)	Interventional	2008-03-19	Completed
A Phase II Randomized Study of the Effect of Zoledronic Acid Versus Observation on Bone Mineral Density of the Lumbar Spine in Women Who Elect to Undergo Surgery That Results in Removal of Both Ovaries[NCT00305695]	Phase 2	160 participants (Actual)	Interventional	2005-11-28	Completed
A Pilot Trial of Adriamycin, Pembrolizumab, Vinblastine, and Dacarbazine (APVD) for Patients With Untreated Classical Hodgkin Lymphoma[NCT03331341]	Phase 2	50 participants (Actual)	Interventional	2019-01-09	Active, not recruiting
A Phase III, Randomized Study of Nivolumab (Opdivo) Plus AVD or Brentuximab Vedotin (Adcetris) Plus AVD in Patients (Age >/= 12 Years) With Newly Diagnosed Advanced Stage Classical Hodgkin Lymphoma[NCT03907488]	Phase 3	995 participants (Actual)	Interventional	2019-08-29	Active, not recruiting
Understanding GRID Radiation Therapy Effects on Human Tumor Oxygenation and Interstitial Pressure to Increase Translation of Solid Tumor Therapy[NCT01967927]	Early Phase 1	0 participants (Actual)	Interventional	2013-12-31	Withdrawn(stopped due to Study has been open for 8 years with no enrollment. Procedures in 2013 protocol are outdated. Cannot make the radiopharmaceutical on campus anymore.)
The Role of the Tumor Microenvironment of Pancreatic Cancer to Predict Treatment Outcome[NCT01989000]		47 participants (Actual)	Interventional	2013-11-30	Completed
In Vivo Assessment of Hypoxia in Gastro-intestinal Cancer Using 18F-HX4-PET: an Optimization and Reproducibility Study[NCT01995084]		32 participants (Actual)	Interventional	2012-05-31	Completed
Phase I Trial to Determine Optimal Phase II Dose of the Oral Dual CAIX Inhibitor/ Radiosensitizer[NCT02216669]	Phase 1	0 participants (Actual)	Interventional	2017-03-31	Withdrawn(stopped due to No financial agreement)
A Randomized Phase II Study of the Efficacy and Safety of Hypofractionated Stereotactic Radiotherapy and 5FU or Capecitabine With and Without Zometa in Patients With Locally Advanced Pancreatic Adenocarcinoma[NCT03073785]	Phase 2	44 participants (Anticipated)	Interventional	2016-09-16	Recruiting
A Double Blind, Randomized, Single Dose, Placebo Controlled Study of the Pharmacokinetics and Side Effects of the mGlu5 Antagonist Fenobam in Adult Healthy Volunteers[NCT01806415]	Phase 1	32 participants (Actual)	Interventional	2013-05-31	Completed
Assessment of Hypoxia in Malignant Gliomas Using EF5[NCT00430079]		48 participants (Actual)	Interventional	2001-07-31	Terminated(stopped due to Administratively complete.)
The Detection of Tumor Hypoxia and Vascularity in Patients Undergoing Intraperitoneal Photodynamic Therapy[NCT00028782]		80 participants (Actual)	Interventional	2001-10-31	Terminated(stopped due to Administratively complete.)
A Pilot, Phase II , Open Label, Nonrandomized, Multi- Center Study of [F 18]HX4 Positron Emission Tomography (PET) to Detect Hypoxia in Tumors[NCT01075399]	Phase 2	50 participants (Actual)	Interventional	2010-02-28	Completed
A Phase II Multi-Center Open-Label Trial of Six Doses of Pembrolizumab Monotherapy Prior to Limited Chemotherapy as Front-Line Therapy for Patients With Classical Hodgkin Lymphoma, Including Elderly Patients.[NCT06164275]	Phase 2	30 participants (Anticipated)	Interventional	2023-12-31	Not yet recruiting
A Phase II Trial of PET-Directed Therapy Using AVD (Doxorubicin, Vinblastine, and Dacarbazine) Plus Brentuximab Vedotin Induction Chemotherapy, With or Without Brentuximab Vedotin Plus Nivolumab, Followed by Nivolumab Consolidation for Patients With Previ[NCT03233347]	Phase 2	82 participants (Anticipated)	Interventional	2017-10-13	Active, not recruiting
Assessment of Primary and Metastatic Brain Tumor Hypoxia With 18F-Fluoromisonidazole, [18F]Fluoro-2-deoxy-D-glucose (FDG) and [15O]Water (H215O)[NCT01246869]	Phase 1	2 participants (Actual)	Interventional	2013-03-27	Terminated(stopped due to PI retired, study closed)
Brentuximab Vedotin Plus AD in Non-bulky Limited Stage Hodgkin Lymphoma[NCT02505269]	Phase 2	34 participants (Actual)	Interventional	2015-08-07	Completed
Phase II Trial of Response-Adapted Therapy Based on Positron Emission Tomography (PET) for Bulky Stage I and II Classical Hodgkin Lymphoma (HL)[NCT01390584]	Phase 2	6 participants (Actual)	Interventional	2013-05-24	Terminated(stopped due to slow accrual)
A Randomized Phase III Trial of ABVD Versus Stanford V (+/-) Radiation Therapy in Locally Extensive and Advanced Stage Hodgkin's Disease[NCT00003389]	Phase 3	854 participants (Actual)	Interventional	1999-06-17	Completed
Pediatric Classical Hodgkin Lymphoma Consortium Study: cHOD17[NCT03755804]	Phase 2	250 participants (Anticipated)	Interventional	2018-12-12	Recruiting
A Pilot Phase II Study of Pre-Operative Radiation Therapy and Thalidomide (IND 48832; NSC 66847) for Low Grade Primary Soft Tissue Sarcoma or Pre-Operative MAID/Thalidomide/Radiation Therapy for High/Intermediate Grade Primary Soft Tissue Sarcoma of the E[NCT00089544]	Phase 2	23 participants (Actual)	Interventional	2004-06-17	Terminated
A Phase 2 Front-Line PET/CT-2 Response-Adapted Brentuximab Vedotin and Nivolumab Incorporated and Radiation-Free Management of Early Stage Classical Hodgkin Lymphoma (cHL)[NCT03712202]	Phase 2	155 participants (Actual)	Interventional	2018-11-28	Active, not recruiting
Randomized Phase II Study Comparing the MET Inhibitor Cabozantinib to Temozolomide/Dacarbazine in Ocular Melanoma[NCT01835145]	Phase 2	47 participants (Actual)	Interventional	2013-07-31	Completed
Phase II Study of PET-Directed Frontline Therapy With Pembrolizumab and AVD for Patients With Classical Hodgkin Lymphoma[NCT03226249]	Phase 2	30 participants (Actual)	Interventional	2017-11-09	Active, not recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Comparison of the Event-free (EFS) Survival in High Risk HL Patients Treated With AEPA/CAPDac to the Historical Control HOD99 Unfavorable Risk 2 Arm (UR2).

Event-free survival (EFS) is defined as the probability of survival between the date of study enrollment to the date of first event (relapsed or progressive disease, second malignancy, or death from any cause) or to last follow-up for patients without events. Under the proportional hazard model assumption, the two-sample log-rank test used to compare the EFS between HLHR13 and historical control of HOD99 unfavorable risk 2 arm (UR2). (NCT01920932)
Timeframe: From start of therapy to 2 years after completion of therapy (up to 3 years after study enrollment)

Intervention	probability (Number)
AEPA/CAPDac	0.974

Complete Response Rate Estimate for All Evaluable Participants

To evaluate the safety of AEPA/CAPDac, as well as the efficacy (early complete response) after 2 cycles of AEPA chemotherapy in high-risk patients with Hodgkin Lymphoma (HL). (NCT01920932)
Timeframe: After the first 2 cycles of chemotherapy (at 2 months from enrollment for each participant)

Intervention	percentage of participants (Number)
AEPA/CAPDac	35

Local Failure Rate in High Risk HL Patients Treated With AEPA/CAPDac.

The local failure rate within the high-risk HL participants treated with AEPA/CAPDac will be estimated with a 95% confidence interval using appropriate methods (e.g., estimate cumulative incidence in the presence of competing risks). (NCT01920932)
Timeframe: From start of therapy to 2 years after completion of therapy (up to 3 years after study enrollment)

Intervention	Probability (Number)
AEPA/CAPDac	0.013

Percentage of Initially Enrolled Patients That Have a Complete Response at Early Response Assessment Compared to Historical Control

To determine the efficacy of 2 cycles of AEPA chemotherapy, the response rate for the first 32 evaluable participants enrolled was evaluated. If it shown efficacy (detect 20% increase complete rate with 80% power and 5% type I error compared with the proportion of historical control of HOD99 (NCT00145600) unfavorable risk patients had complete rate at week 8 of 17% (24/141), the response results will be reported in a national/international meeting and the study will continue to enroll for a total of 77 patients. (NCT01920932)
Timeframe: After the first 2 cycles of chemotherapy (at approximately 2 months after enrollment)

Intervention	percentage of participants (Number)
AEPA Chemotherapy	31.25

Percentage of Initially Enrolled Patients That Have a Complete Response at Early Response Assessment Compared to Historical Control

To determine the efficacy of 2 cycles of AEPA chemotherapy, the response rate for the first 32 evaluable participants enrolled was evaluated. If it shown efficacy (detect 20% increase complete rate with 80% power and 5% type I error compared with the proportion of historical control of HOD99 unfavorable risk patients had complete rate at week 8 of 17% (24/141), the response results will be reported in a national/international meeting and the study will continue to enroll for a total of 77 patients. (NCT01920932)
Timeframe: After the first 2 cycles of chemotherapy (at approximately 2 months after enrollment)

Intervention	percentage of participants (Number)
AEPA Chemotherapy	31.25

Descriptive of Hematological Adverse Events

To describe acute hematologic, neuropathic, and infectious toxicities as they relate to transfusion requirements, growth factor support, episodes of febrile neutropenia and hospitalizations, according to the NCI Common Terminology Criteria for Adverse Events (CTCAE), version 4.0. (NCT01920932)
Timeframe: From enrollment to end of therapy (approximately 8 months)

,,,,,,,,,,,

Intervention	Participants (Count of Participants)
	Leukopenia	Neutropenia	Lymphopenia	Anemia	Thrombocytopenia
Cycle 1 - Grade 2	15	5	15	23	3
Cycle 1 - Grade 3-4	49	62	36	12	3
Cycle 2 - Grade 2	28	13	18	28	2
Cycle 2 - Grade 3-4	23	51	15	5	1
Cycle 3 - Grade 2	8	7	9	6	0
Cycle 3 - Grade 3-4	4	10	7	1	2
Cycle 4 - Grade 2	5	5	16	6	0
Cycle 4 - Grade 3-4	5	3	15	0	1
Cycle 5 - Grade 2	7	4	13	4	0
Cycle 5 - Grade 3-4	2	3	22	1	1
Cycle 6 - Grade 2	14	8	20	2	1
Cycle 6 - Grade 3-4	5	6	31	1	2

Descriptive of Infectious Adverse Events

,,,,,,,,,,,

Intervention	Participants (Count of Participants)
	Febrile neutropenia	Mucositis	Upper respiratory infection	Genitourinary infection
Cycle 1 - Grade 2	0	10	5	1
Cycle 1 - Grade 3-4	6	2	2	0
Cycle 2 - Grade 2	0	6	3	1
Cycle 2 - Grade 3-4	3	4	0	0
Cycle 3 - Grade 2	0	0	0	2
Cycle 3 - Grade 3-4	0	0	0	0
Cycle 4 - Grade 2	0	1	0	1
Cycle 4 - Grade 3-4	2	0	2	0
Cycle 5 - Grade 2	0	1	0	2
Cycle 5 - Grade 3-4	1	0	0	0
Cycle 6 - Grade 2	0	1	0	0
Cycle 6 - Grade 3-4	0	0	0	0

Descriptive of Neuropathic Adverse Events

,,,,,,,,,,,

Intervention	Participants (Count of Participants)
	Peripheral sensory neuropathy	Pain in extremity	Neuralgia	Pain NOS
Cycle 1 - Grade 2	0	3	1	1
Cycle 1 - Grade 3-4	0	1	0	0
Cycle 2 - Grade 2	1	4	0	1
Cycle 2 - Grade 3-4	0	0	0	0
Cycle 3 - Grade 2	2	1	0	0
Cycle 3 - Grade 3-4	0	0	0	0
Cycle 4 - Grade 2	3	1	0	0
Cycle 4 - Grade 3-4	0	0	0	0
Cycle 5 - Grade 2	1	2	1	0
Cycle 5 - Grade 3-4	0	0	0	0
Cycle 6 - Grade 2	1	0	0	1
Cycle 6 - Grade 3-4	0	0	0	1

To Assess the Patient Reported Symptoms and Health-related Quality of Life in Children With High Risk HL Compared to Those Treated on the Unfavorable HOD99 Treatment Arm (UR2) at Multiple Time Points. (PedsQL v.3.0)

Assess and compare the patient reported quality of life and symptom distress to that of patients treated on the HOD99 unfavorable risk 2 arm (UR2) using the Peds Quality of Life version 3. The QL scoring is a 5-point Likert scale from 0 (never) to 4 (almost always). Scores are transformed on a scale from 0 to 100. Items are reverse scored and linearly transformed to a 0-100 scale as follows: 0=100, 1=75, 2=50, 3=25, and 4=0. Total score is the sum of all items over the number of items answered on all scales. For both the total score and subscales the range is 0-100. The total score is the sum of all items from each subscale, over the number of items answered on the scale. The total score is the sum of all items on the scale over the number of items answer. If >50% of the items are missing the score should not be computed. If >50% are completed, impute the mean of the completed items in a scale. The Higher the score the better quality of life. (NCT01920932)
Timeframe: At Diagnosis (baseline) (T1), completion of 2 cycles of chemotherapy (approximately 2 months) (T2), completion of 4 cycles of chemotherapy (approximately 4 months) (T3), completion of radiation (approximately 8 months) (T4)

Intervention	score on a scale (Mean)
	PedsQL v.3.0 Total Score-T2	PedsQL v.3.0 Total Score-T3	PedsQL v.3.0 Total Score-T4	PedsQL v.3.0 Pain and Hurt-T2	PedsQL v.3.0 Pain and Hurt-T3	PedsQL v.3.0 Pain and Hurt-T4	PedsQL v.3.0 Nausea-T2	PedsQL v.3.0 Nausea-T3	PedsQL v.3.0 Nausea-T4	PedsQL v.3.0 Procedural Anxiety-T2	PedsQL v.3.0 Procedural Anxiety-T3	PedsQL v.3.0 Procedural Anxiety-T4	PedsQL v.3.0 Treatment Anxiety-T2	PedsQL v.3.0 Treatment Anxiety-T3	PedsQL v.3.0 Treatment Anxiety-T4	PedsQL v.3.0 Worry-T2	PedsQL v.3.0 Worry-T3	PedsQL v.3.0 Worry-T4	PedsQL v.3.0 Cognitive Problems-T2	PedsQL v.3.0 Cognitive Problems-T3	PedsQL v.3.0 Cognitive Problems-T4	PedsQL v.3.0 Perceived Physical Appearance-T2	PedsQL v.3.0 Perceived Physical Appearance-T3	PedsQL v.3.0 Perceived Physical Appearance-T4	PedsQL v.3.0 Communication-T2	PedsQL v.3.0 Communication-T3	PedsQL v.3.0 Communication-T4
HOD99 Unfavorable Risk 2 Arm (UR2)	71.92	73.78	79.92	66.09	69.81	82.2	60.5	60.26	78.13	71.17	73.46	77.65	85.92	85.06	83.71	64.63	66.45	69.57	75.72	78.38	81.69	78.07	79.87	79.95	79.02	81.93	84.24

To Assess the Patient Reported Symptoms and Health-related Quality of Life in Children With High Risk HL Compared to Those Treated on the Unfavorable HOD99 Treatment Arm (UR2) at Multiple Time Points. (PedsQL v.3.0)

Intervention	score on a scale (Mean)
	PedsQL v.3.0 Total Score-T1	PedsQL v.3.0 Total Score-T2	PedsQL v.3.0 Total Score-T3	PedsQL v.3.0 Total Score-T4	PedsQL v.3.0 Pain and Hurt-T1	PedsQL v.3.0 Pain and Hurt-T2	PedsQL v.3.0 Pain and Hurt-T3	PedsQL v.3.0 Pain and Hurt-T4	PedsQL v.3.0 Nausea-T1	PedsQL v.3.0 Nausea-T2	PedsQL v.3.0 Nausea-T3	PedsQL v.3.0 Nausea-T4	PedsQL v.3.0 Procedural Anxiety-T1	PedsQL v.3.0 Procedural Anxiety-T2	PedsQL v.3.0 Procedural Anxiety-T3	PedsQL v.3.0 Procedural Anxiety-T4	PedsQL v.3.0 Treatment Anxiety-T1	PedsQL v.3.0 Treatment Anxiety-T2	PedsQL v.3.0 Treatment Anxiety-T3	PedsQL v.3.0 Treatment Anxiety-T4	PedsQL v.3.0 Worry-T1	PedsQL v.3.0 Worry-T2	PedsQL v.3.0 Worry-T3	PedsQL v.3.0 Worry-T4	PedsQL v.3.0 Cognitive Problems-T1	PedsQL v.3.0 Cognitive Problems-T2	PedsQL v.3.0 Cognitive Problems-T3	PedsQL v.3.0 Cognitive Problems-T4	PedsQL v.3.0 Perceived Physical Appearance-T1	PedsQL v.3.0 Perceived Physical Appearance-T2	PedsQL v.3.0 Perceived Physical Appearance-T3	PedsQL v.3.0 Perceived Physical Appearance-T4	PedsQL v.3.0 Communication-T1	PedsQL v.3.0 Communication-T2	PedsQL v.3.0 Communication-T3	PedsQL v.3.0 Communication-T4
AEPA/CAPDac	73.38	80.41	83.33	85.33	73.41	71.77	72.63	77.5	73.97	75.52	79.66	88.1	58.6	77.55	81.61	76.83	84.52	91.39	93.97	93.17	69.22	77.55	84.2	82.17	72.34	81.25	84.38	87.04	79.64	83.53	82.69	85.17	74.6	85.38	85.34	87.33

To Assess the Patient Reported Symptoms and Health-related Quality of Life in Children With High Risk HL Compared to Those Treated on the Unfavorable HOD99 Treatment Arm (UR2) at Multiple Time Points. (PedsQL v.4.0)

Assess and compare the patient reported quality of life and symptom distress to that of patients treated on the HOD99 unfavorable risk 2 arm (UR2) using the Peds Quality of Life version 4. The QL scoring is a 5-point Likert scale from 0 (never) to 4 (almost always). Scores are transformed on a scale from 0 to 100. Items are reverse scored and linearly transformed to a 0-100 scale as follows: 0=100, 1=75, 2=50, 3=25, and 4=0. Total score is the sum of all items over the number of items answered on all scales. For both the total score and subscales the range is 0-100. The total score is the sum of all items from each subscale, over the number of items answered on the scale. The total score is the sum of all items on the scale over the number of items answer. If >50% of the items are missing the score should not be computed. If >50% are completed, impute the mean of the completed items in a scale. The Higher the score the better quality of life. (NCT01920932)
Timeframe: At Diagnosis (baseline) (T1), completion of 2 cycles of chemotherapy (approximately 2 months) (T2), completion of 4 cycles of chemotherapy (approximately 4 months) (T3), completion of radiation (approximately 8 months) (T4)

Intervention	score on a scale (Mean)
	PedsQL v.4.0 Total Score-T1	PedsQL v.4.0 Total Score-T2	PedsQL v.4.0 Total Score-T3	PedsQL v.4.0 Total Score-T4	PedsQL v.4.0 Physical Functioning-T1	PedsQL v.4.0 Physical Functioning-T2	PedsQL v.4.0 Physical Functioning-T3	PedsQL v.4.0 Physical Functioning-T4	PedsQL v.4.0 Emotional Functioning-T1	PedsQL v.4.0 Emotional Functioning-T2	PedsQL v.4.0 Emotional Functioning-T3	PedsQL v.4.0 Emotional Functioning-T4	PedsQL v.4.0 Social Functioning-T1	PedsQL v.4.0 Social Functioning-T2	PedsQL v.4.0 Social Functioning-T3	PedsQL v.4.0 Social Functioning-T4	PedsQL v.4.0 School Functioning-T1	PedsQL v.4.0 School Functioning-T2	PedsQL v.4.0 School Functioning-T3	PedsQL v.4.0 School Functioning-T4
AEPA/CAPDac	72.94	79.38	80.39	86.06	69.54	73.86	74.02	82.45	71.75	83.06	82.07	84.81	86.21	88.47	90.22	92.31	65.49	75.66	79.2	86.9
HOD99 Unfavorable Risk 2 Arm (UR2)	72.48	73.54	77.68	84.58	70.41	70.06	72.94	83.57	67.18	71.31	75.06	80.87	86.22	86.82	88.86	91.44	67.82	66.91	69.1	79.32

2-year Overall Survival

Proportion of study participants who are alive at 2 years estimated using the Kaplan-Meier survival function (NCT01771107)
Timeframe: 2 years

Intervention	proportion of participants (Number)
Phase I - Brentuximab 1.2 mg/kg	1.0
Phase II - Brentuximab 1.2 mg/kg	0.91

2-year Progression-free Survival (PFS)

2-year PFS is determined based on the Kaplan-Meier estimates and corresponding 95% confidence intervals based on standard errors using Greenwood's formula. (NCT01771107)
Timeframe: 2 years

Intervention	proportion of participants (Number)
Phase I - Brentuximab 1.2 mg/kg	1.0
Phase II - Brentuximab 1.2 mg/kg	0.84

CD4 Counts

CD4 counts (absolute) at visit 4 (cycle 5) (NCT01771107)
Timeframe: 5 months

Intervention	cells/µL (Median)
Phase I - Brentuximab 1.2 mg/kg	378
Phase II - Brentuximab 1.2 mg/kg	401

CD8 Counts

Absolute CD8 counts at cycle 5 (NCT01771107)
Timeframe: 5 months

Intervention	cells/µL (Median)
Phase I - Brentuximab 1.2 mg/kg	719.5
Phase II - Brentuximab 1.2 mg/kg	666.5

Characterization of Histologic Subtypes in HIV-HL in the HAART Era

Participants with mixed cellularity histologic subtype (NCT01771107)
Timeframe: Baseline

Intervention	Participants (Count of Participants)
Phase I - Brentuximab 1.2 mg/kg	2
Phase II - Brentuximab 1.2 mg/kg	13

Complete Response Rate

Number of participants who experienced a complete response per RECIST v1.0 criteria (NCT01771107)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Phase I - Brentuximab 1.2 mg/kg	6
Phase II - Brentuximab 1.2 mg/kg	32

Event-free Survival

Proportion of participants who are alive and progression-free at 2 years (NCT01771107)
Timeframe: 2 years

Intervention	proportion of participants (Number)
Phase I - Brentuximab 1.2 mg/kg	1.0
Phase II Brentuximab 1.2 mg/kg	0.84

Frequency of Adverse Events

Number of Participants who had one or more adverse events (NCT01771107)
Timeframe: Up to 5 years

Intervention	Participants (Count of Participants)
Phase I - Brentuximab 1.2 mg/kg	6
Phase II - Brentuximab 1.2 mg/kg	35

Incidence of Neurotoxicity

Number of participants who experience neurotoxicity at cycle 5 (visit 4) (NCT01771107)
Timeframe: 5 months

Intervention	Participants (Count of Participants)
Phase I - Brentuximab 1.2 mg/kg	4
Phase II - Brentuximab 1.2 mg/kg	23

Maximal Tolerated Dose of Brentuximab Vedotin (Phase I)

Defined as the dose level at which =< 1 of 6 subjects experience dose limiting toxicity. (NCT01771107)
Timeframe: 28 days

Intervention	mg/kg (Number)
Treatment (Brentuximab and Combination Chemotherapy)	1.2

Partial Response Rate

Number of participants who achieved a partial response per RECIST v1.0 criteria (NCT01771107)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Phase I - Brentuximab 1.2 mg/kg	1
Phase II - Brentuximab 1.2 mg/kg	4

Viral Load

HIV viral load (detectable) (NCT01771107)
Timeframe: 5 months

Intervention	Participants (Count of Participants)
Phase I - Brentuximab 1.2 mg/kg	1
Phase II - Brentuximab 1.2 mg/kg	7

Limiting Toxicity

"The occurrence of Limiting Toxicity defined as Any CTC AE version 4 Grade 3 and 4 non-hematologic toxicity thought to be possibly, probably or definitely related to zoledronic acid with the specific exclusion of:~Grade 3 nausea and vomiting controlled with adequate antiemetic prophylaxis.~Grade 3 transaminase (AST/ALT) that occurs during the evaluation period but resolves to ≤ Grade 2, before the planned dose of therapy after definitive surgery.~Grade 3 fever or infection.~Grade 3 or 4 hypocalcemia (see Section 5.1.1)~Grade 3 mucositis.~Grade 3 fatigue that returns to ≤ Grade 2, before the planned dose of therapy after definitive surgery.~Grade 3 joint range of motion, decreased or joint effusion that is related to the primary tumor." (NCT00742924)
Timeframe: Enrollment through the first 12 weeks of therapy.

Intervention	participants (Number)
Arm 1- Chemotherapy and 1.2 mg/m2 Zoledronic Acid	1
Arm 2 - Chemotherapy and 2.3 mg/m2 Zoledronic Acid	1
Arm 3 - Chemotherapy and 3.5 mg/m2 Zoledronic Acid	3
Chemotherapy and 2.3 mg/m2 Zoledronic Acid After MTD	2

Duration of Response

The duration of overall response was defined as the time from first assessment of complete response (CR) or partial response (PR) to the first date of progressive disease (PD) using Response Evaluation Criteria in Solid Tumors (RECIST v1.0), initiation of other or additional antitumor therapy, or death from any cause. CR was defined as the disappearance of all target lesions. PR was defined as having at least a 30% decrease in sum of longest diameter of target lesions. CR and PR had to be confirmed by repeat assessments and performed no fewer than 4 weeks after the criteria for response were first met. PD was defined as at least 20% increase in sum of longest diameter of target lesions. Participants who did not relapse were censored at the day of their last objective tumor assessment. (NCT00533702)
Timeframe: Cycle 1 Day 1 (of 21-day cycle) up to 17.1 months

Intervention	months (Median)
IMC-1121B (Ramucirumab) + Dacarbazine	11.0
IMC-1121B (Ramucirumab)	NA

Percentage of Participants With Complete Response (CR) or Partial Response (PR) (Response Rate) at 12 Weeks

Response rate was defined as a CR or a PR using Response Evaluation Criteria in Solid Tumors (RECIST v1.0). CR was defined as the disappearance of all target and non-target lesions and the normalization of non-target lesion tumor marker levels. PR was defined as at least a 30% decrease from baseline in sum of longest diameter of target lesions. CR and PR had to be confirmed by repeat assessments and performed no fewer than 4 weeks after the criteria for response were first met. (NCT00533702)
Timeframe: 12 weeks (4 cycles of treatment)

Intervention	percentage of participants (Number)
IMC-1121B (Ramucirumab) + Dacarbazine	13.5
IMC-1121B (Ramucirumab)	4.0

Percentage of Participants With Complete Response (CR) or Partial Response (PR) [Overall Response Rate (ORR)]

The ORR was defined as the percentage of all randomized participants with the best overall response of PR or CR using Response Evaluation Criteria in Solid Tumors (RECIST v1.0). CR was defined as the disappearance of all target and non-target lesions. PR was defined as at least a 30% decrease in sum of longest diameter of target lesions. CR and PR had to be confirmed by repeat assessments and performed no fewer than 4 weeks after the criteria for response were first met. (NCT00533702)
Timeframe: Cycle 1 Day 1 (of 21-day cycle) up to 17.1 months

Intervention	percentage of participants (Number)
IMC-1121B (Ramucirumab) + Dacarbazine	17.3
IMC-1121B (Ramucirumab)	4.0

Percentage of Participants With Stable Disease (SD) or Better (Disease Control Rate) at 12 Weeks

Disease Control Rate (DCR) was defined as complete response (CR) plus partial response (PR) plus SD using Response Evaluation Criteria in Solid Tumors (RECIST v1.0). CR was defined as the disappearance of all target and non-target lesions and the normalization of non-target lesion tumor marker levels. PR was defined as at least a 30% decrease from baseline in sum of longest diameter of target lesions. CR and PR had to be confirmed by repeat assessments and performed no fewer than 4 weeks after the criteria for response were first met. Stable Disease (SD) was defined as: neither sufficient increase to qualify for progressive disease (PD) nor sufficient shrinkage to qualify for PR, taking as reference the smallest sum of the longest diameters recorded since treatment began. PD was defined as at least 20% increase in sum of longest diameter of target lesions. (NCT00533702)
Timeframe: 12 weeks (4 cycles of treatment)

Intervention	percentage of participants (Number)
IMC-1121B (Ramucirumab) + Dacarbazine	40
IMC-1121B (Ramucirumab)	24

Percentage of Participants With Stable Disease (SD) or Better (Disease Control Rate) at 6 Weeks

Disease Control Rate (DCR) was defined as complete response (CR) plus partial response (PR) plus SD using Response Evaluation Criteria in Solid Tumors (RECIST v1.0). CR was defined as the disappearance of all target and non-target lesions and the normalization of non-target lesion tumor marker levels. PR was defined as at least a 30% decrease from baseline in sum of longest diameter of target lesions. CR and PR had to be confirmed by repeat assessments and performed no fewer than 4 weeks after the criteria for response were first met. SD was defined as: neither sufficient increase to qualify for progressive disease (PD) nor sufficient shrinkage to qualify for PR, taking as reference the smallest sum of the longest diameters recorded since treatment began. PD was defined as at least 20% increase in sum of longest diameter of target lesions. (NCT00533702)
Timeframe: 6 weeks (2 cycles of treatment)

Intervention	percentage of participants (Number)
IMC-1121B (Ramucirumab) + Dacarbazine	54
IMC-1121B (Ramucirumab)	44

Progression Free Survival (PFS)

PFS was defined as the time from the first day of therapy to the first evidence of disease progression as defined by Response Evaluation Criteria in Solid Tumors (RECIST v1.0) or death from any cause. Progressive disease (PD) was defined as at least a 20% increase in the sum of the longest diameter (LD) of the target lesions, taking as reference the smallest sum LD recorded since the treatment started in comparison with the measurement of the nadir or the appearance of 1 or more new lesions. In addition, unequivocal progression of existing non-target lesions was considered PD. New or existing pleural effusion/ascites required cytological confirmation for PD according to the protocol. Participants who did not progress and who were alive or did not have documented progression or missed ≥2 visits, or had no post baseline assessment were censored at the day of their last tumor assessment. (NCT00533702)
Timeframe: Baseline up to 36 months

Intervention	months (Median)
IMC-1121B (Ramucirumab) + Dacarbazine	2.6
IMC-1121B (Ramucirumab)	1.7

Number of Participants With Adverse Events (AE)

The number of participants who experienced any IMC-1121B (ramucirumab [RAM]) treatment-related and treatment emergent AE (TEAE), treatment-related TEAE of Grade ≥3, treatment-related TE serious AEs (SAEs), treatment-related TEAE resulting in death (Grade 5 AE) and any TEAEs resulting in death. A summary of SAEs and all other non-serious AEs, regardless of causality, is located in the Reported Adverse Events module. (NCT00533702)
Timeframe: Baseline up to 40 months

Intervention	participants (Number)
	Any RAM related TEAE	RAM related SAE	RAM related ≥ Grade 3 AE	RAM related death	RAM related TEAE leading to discontinuation of RAM	Any AE with outcome of death
IMC-1121B (Ramucirumab)	40	5	13	1	4	2
IMC-1121B (Ramucirumab) + Dacarbazine	43	9	20	1	3	2

Anti-MAGE-A3 Antibody Concentrations

Anti-MAGE-A3 antibody concentrations were presented as geometric mean concentrations (GMTs) and expressed in ELISA units per millilitre (EL.U/mL) (NCT00849875)
Timeframe: Post Dose 4 at Week 13 (W13).

Intervention	EL.U/mL (Geometric Mean)
GSK2132231A GROUP	2778.7
GSK2132231A GS+ Group	2650.8
GSK2132231A GS- Group	4046.9
GSK2132231A GS Unknown Group	336.0

Concentrations of Antibodies Against Protein D (Anti-PD)

Anti-PD antibody concentrations were presented ad geometric mean concentrations (GMTs) and expressed in ELISA units per millilitre (EL.U/mL). (NCT00849875)
Timeframe: Post Dose 4 at Week 13 (W13).

Intervention	EL.U/mL (Geometric Mean)
GSK2132231A GROUP	9979.6
GSK2132231A GS+ Group	10437
GSK2132231A GS- Group	10853.6
GSK2132231A GS Unknown Group	2176

Duration of Stable Disease (SD) Response to MAGE-A3 ASCI Study Treatment

Assessment was done based on a set of MLs identified at baseline as TLs and NTLs followed up until disease progression. Stable disease was defined as follows: 1) In case of target lesions (TL) greater than or equal to (≥) 20 mm: neither sufficient shrinkage to qualify for Partial Response nor sufficient increase to qualify for Progressive Disease, taking as references the sum of Longest Diameter (LD) of TL recorded previously but not necessarily at baseline; 2) In case of TL both less than 20 mm and ≥ 20 mm: Neither sufficient shrinkage to qualify as a PR nor sufficient increase to qualify as PD, taking as references the smallest sum LD since the start of the treatment. The minimal time interval required between 2 measurements for determination of SD was at least 12 weeks. (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Months (Median)
GSK2132231A GS+ Group	5.6
GSK2132231A GS- Group	7.7
GSK2132231A GS Unknown Group	5.1

Number of Patients Reported With Serious Adverse Events (SAEs)

Serious adverse events (SAEs) assessed include medical occurrences that result in death, are life threatening, require hospitalization or prolongation of hospitalization or result in disability/incapacity. Events which were part of the natural course of the disease under study (i.e., disease progression, recurrence) were captured as part of the clinical activity outcome variables in this study; therefore these did not need to be reported as SAEs. Progression/recurrence of the tumor in a patient was recorded as part of the clinical assessment data collection, and deaths due to progressive disease was recorded on a specific form, but not as an SAE. However, if the investigator considered that there was a causal relationship between treatment or protocol design/procedures and the disease progression/recurrence, then the event was reported as an SAE. Any new primary cancer (non-related to the cancer under study) was reported as an SAE. (NCT00849875)
Timeframe: During the entire study period, up to 5 years

Intervention	Patients (Number)
GSK2132231A GROUP	10

Number of Patients With Treatment Response for Anti-MAGE-A3 Antibodies

Treatment response defined as: For initially seronegative patients: post-administration antibody concentration ≥ 27 EL.U/mL For initially seropositive patients: post-administration antibody concentration ≥ 2 fold the pre-vaccination antibody concentration (NCT00849875)
Timeframe: Post Dose 4 at Week 13 (W13).

Intervention	Patients (Number)
GSK2132231A GROUP	28
GSK2132231A GS+ Group	19
GSK2132231A GS- Group	8
GSK2132231A GS Unknown Group	1

Number of Patients With Treatment Response for Anti-PD

Treatment response defined as: For initially seronegative patients: post-administration antibody concentration ≥ 100 EL.U/mL For initially seropositive patients: post-administration antibody concentration ≥ 2 fold the pre-vaccination antibody concentration (NCT00849875)
Timeframe: Post Dose 4 at Week 13 (W13).

Intervention	Patients (Number)
GSK2132231A GROUP	28
GSK2132231A GS+ Group	19
GSK2132231A GS- Group	8
GSK2132231A GS Unknown Group	1

Number of Seroconverted Patients for Melanoma Antigen (Anti-MAGE-A3)

Seroconversion was defined as a concentration of antibodies assessed that was greater than the cut-off value for a patient whose concentration of such antibodies was below the cut-off level before the initiation of treatment. Seroconverted patients were those patients with anti-MAGE-A3 antibody concentrations ≥ 27. (NCT00849875)
Timeframe: Post Dose 4 at Week 13 (W13).

Intervention	Patients (Number)
GSK2132231A GROUP	28
GSK2132231A GS+ Group	19
GSK2132231A GS- Group	8
GSK2132231A GS Unknown Group	1

Overall Survival (OS) by Gene Signature

OS was defined as the time from first treatment to the date of death. OS analysis was performed using the non-parametric Kaplan-Meier method. Each patient was censored out at the time of death. (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Months (Median)
GSK2132231A GROUP	9.4
GSK2132231A GS+ Group	11.4
GSK2132231A GS- Group	5.3
GSK2132231A GS Unknown Group	0

Progression-free Survival (PFS) After Slow Progressive Disease (SPD) by Gene Signature

PFS after initial SPD was defined and calculated as the time from the time point at which the disease was the most advanced during the treatment to either a new progression of the disease or the date to death, whichever occurred first as another secondary outcome of this study. In that case, the largest diameter during the course of treatment was to be used as reference measurement. This outcome was defined to take into account the delay to induce an active immune response and the strict rules set up in this study to allow pursuing investigational treatment in case of SPD. PFS after SPD analysis was performed using the non-parametric Kaplan-Meier method. (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Months (Median)
GSK2132231A GS+ Group	2.8
GSK2132231A GS- Group	2.8
GSK2132231A GS Unknown Group	5.1

Progression-free Survival (PFS) by Gene Signature

PFS was defined and calculated as the time from first treatment to either the first progression of the disease or the date of death, whichever occurred first. In case a patient went off protocol treatment, the date of first documented progression (if applicable) was to be used as date of progression. Patients still alive with no evidence of disease progression at the time of their last visit or for whom date of first documented progression was not applicable, were censored at the time of the last examination. PFS analysis was performed using the non-parametric Kaplan-Meier method. (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Months (Median)
GSK2132231A GROUP	2.8
GSK2132231A GS+ Group	2.8
GSK2132231A GS- Group	2.8
GSK2132231A GS Unknown Group	5.1

Progression-free Survival (PFS) for the Overall Population

Intervention	Months (Median)
GSK2132231A GROUP	2.8

Time to Treatment Failure (TTF), by Gene Signature

TTF was defined as withdrawal from treatment with the MAGE-A3 ASCI study product due to disease progression or death. TTF analysis was performed using the non-parametric Kaplan-Meier method. (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Months (Median)
GSK2132231A GS+ Group	2.8
GSK2132231A GS- Group	2.3
GSK2132231A GS Unknown Group	4.3

Number of Patients Reported With Unsolicited Adverse Events (AEs) That Were Causally Related to Treatment Administration by Maximum Grade.

The assessed AEs were ASCI-related grade 3/4 adverse events according to the Common Terminology Criteria for Adverse Events (CTCAE) version 3.0. An unsolicited AE covers any untoward medical occurrence in a clinical investigation patient temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product and reported in addition to those solicited during the clinical study and any solicited symptom with onset outside the specified period of follow-up for solicited symptoms. Related = AE assessed by the investigator as related to the treatment. (NCT00849875)
Timeframe: Within the 31-day (Days 0-30) post-administration period.

Intervention	Patients (Number)
	Any event, Grade 3	Any event, Grade 4	Any Blood and lymphatic system disorders, Grade 3	Any Blood and lymphatic system disorders, Grade 4	Anaemia, Grade 3	Anaemia, Grade 4	Lymphopenia, Grade 3	Lymphopenia, Grade 4	Neutropenia, Grade 3	Neutropenia, Grade 4	Thrombocytopenia, Grade 3	Thrombocytopenia, Grade 4	Any Cardiac disorders, Grade 3	Any Cardiac disorders, Grade 4	Tachycardia, Grade 3	Tachycardia, Grade 4	Any Gastrointestinal disorders, Grade 3	Any Gastrointestinal disorders, Grade 4	Constipation, Grade 3	Constipation, Grade 4	Diarrhoea, Grade 3	Diarrhoea, Grade 4	Dyspepsia, Grade 3	Dyspepsia, Grade 4	Nausea, Grade 3	Nausea, Grade 4	Paraesthesia oral, Grade 3	Paraesthesia oral, Grade 4	Vomiting, Grade 3	Vomiting, Grade 4	Any Gen. disord. and adm. site conditions, Grade 3	Any Gen. disord. and adm. site conditions, Grade 4	Asthenia, Grade 3	Asthenia, Grade 4	Chills, Grade 3	Chills, Grade 4	Fatigue, Grade 3	Fatigue, Grade 4	Influenza like illness, Grade 3	Influenza like illness, Grade 4	Injection site erythema, Grade 3	Injection site erythema, Grade 4	Injection site inflammation, Grade 3	Injection site inflammation, Grade 4	Injection site oedema, Grade 3	Injection site oedema, Grade 4	Injection site pain, Grade 3	Injection site pain, Grade 4	Injection site reaction, Grade 3	Injection site reaction, Grade 4	Mucosal dryness, Grade 3	Mucosal dryness, Grade 4	Oedema peripheral, Grade 3	Oedema peripheral, Grade 4	Pyrexia, Grade 3	Pyrexia, Grade 4	Any Investigations, Grade 3	Any Investigations, Grade 4	Haemoglobin decreased, Grade 3	Haemoglobin decreased, Grade 4	Any Metabolism and nutrition disorders, Grade 3	Any Metabolism and nutrition disorders, Grade 4	Decreased appetite, Grade 3	Decreased appetite, Grade 4	Any Musculoskeletal and conn. Tiss. Diso., Grade 3	Any Musculoskeletal and conn. Tiss. Diso., Grade 4	Arthralgia, Grade 3	Arthralgia, Grade 4	Myalgia, Grade 3	Myalgia, Grade 4	Pain in extremity, Grade 3	Pain in extremity, Grade 4	Any Nervous system disorders, Grade 3	Any Nervous system disorders, Grade 4	Burning sensation, Grade 3	Burning sensation, Grade 4	Headache, Grade 3	Headache, Grade 4	Paraesthesia, Grade 3	Paraesthesia, Grade 4	Presyncope, Grade 3	Presyncope, Grade 4	Any Psychiatric disorders, Grade 3	Any Psychiatric disorders, Grade 4	Insomnia, Grade 3	Insomnia, Grade 4	Any Resp., thoracic and mediastinal. dis., Grade 3	Any Resp., thoracic and mediastinal. dis., Grade 4	Rhinitis allergic, Grade 3	Rhinitis allergic, Grade 4	Any Skin and subcutaneous tissue disorder, Grade 3	Any Skin and subcutaneous tissue disorder, Grade 4	Alopecia, Grade 3	Alopecia, Grade 4	Eczema, Grade 3	Eczema, Grade 4	Photosensitivity reaction, Grade 3	Photosensitivity reaction, Grade 4	Pruritus, Grade 3	Pruritus, Grade 4	Any Vascular disorders, Grade 3	Any Vascular disorders, Grade 4	Hypotension, Grade 3	Hypotension, Grade 4
GSK2132231A GROUP	3	1	1	1	0	0	0	0	1	1	0	1	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	1	0	0	0	0	0	0	0	0	0	0	0	1	0	0	0	0	0	0	0	0	0	0	0	0	0	1	0	1	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0

Number of Patients With Abnormal Alanine Aminotransferase (ALT) Values by Maximum Grade

The status of each patient as regards ALT laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0), G1 and G2. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	ALT - SCR G0; SE G0	ALT - SCR G0; SE G1	ALT - SCR G0; SE G2	ALT - SCR G0; SE G3	ALT - SCR G0; SE G4	ALT - SCR G0; SE UNK	ALT - SCR G1; SE G0	ALT - SCR G1; SE G1	ALT - SCR G1; SE G2	ALT - SCR G1; SE G3	ALT - SCR G1; SE G4	ALT - SCR G1; SE UNK	ALT - SCR G2; SE G0	ALT - SCR G2; SE G1	ALT - SCR G2; SE G2	ALT - SCR G2; SE G3	ALT - SCR G2; SE G4	ALT - SCR G2; SE UNK
GSK2132231A GROUP	34	3	1	1	0	1	3	2	1	0	0	1	0	1	0	0	0	0

Number of Patients With Abnormal Alkaline Phosphatase (ALK) Values by Maximum Grade

The status of each patient as regards ALK laboratory values at baseline (SCR) up to study end(SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	ALK - SCR G0; SE G0	ALK - SCR G0; SE G1	ALK - SCR G0; SE G2	ALK - SCR G0; SE G3	ALK - SCR G0; SE G4	ALK - SCR G0; SE UNK	ALK - SCR G1; SE G0	ALK - SCR G1; SE G1	ALK - SCR G1; SE G2	ALK - SCR G1; SE G3	ALK - SCR G1; SE G4	ALK - SCR G1; SE UNK
GSK2132231A GROUP	31	11	0	0	0	1	1	3	0	0	0	1

Number of Patients With Abnormal Aspartate Aminotransferase (AST) Values by Maximum Grade

The status of each patient as regards AST laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	AST - SCR G0; SE G0	AST - SCR G0; SE G1	AST - SCR G0; SE G2	AST - SCR G0; SE G3	AST - SCR G0; SE G4	AST - SCR G0; SE UNK	AST - SCR G1; SE G0	AST - SCR G1; SE G1	AST - SCR G1; SE G2	AST - SCR G1; SE G3	AST - SCR G1; SE G4	AST - SCR G1; SE UNK
GSK2132231A GROUP	36	2	1	0	1	1	2	3	1	0	0	1

Number of Patients With Abnormal Bilirubine (BIL) Values by Maximum Grade.

The status of each patient as regards BIL laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Unknown (UNK) and Grade 0 (G0). CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	BIL - SCR UNK; SE G0	BIL - SCR UNK; SE G1	BIL - SCR UNK; SE G2	BIL - SCR UNK; SE G3	BIL - SCR UNK; SE G4	BIL - SCR UNK; SE UNK	BIL - SCR G0; SE G0	BIL - SCR G0; SE G1	BIL - SCR G0; SE G2	BIL - SCR G0; SE G3	BIL - SCR G0; SE G4	BIL - SCR G0; SE UNK
GSK2132231A GROUP	1	0	0	0	0	0	39	3	0	0	0	5

Number of Patients With Abnormal Creatinine (CREA) Values by Maximum Grade

The status of each patient as regards CREA laboratory values at baseline (SCR) up to study end(SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0). CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	CREA - SCR G0; SE G0	CREA - SCR G0; SE G1	CREA - SCR G0; SE G2	CREA - SCR G0; SE G3	CREA - SCR G0; SE G4	CREA - SCR G0; SE UNK
GSK2132231A GROUP	40	4	1	0	1	2

Number of Patients With Abnormal Gamma-glutamyl Transpeptidase (GGT) Values by Maximum Grade

The status of each patient as regards GGT laboratory values at baseline (SCR) up to study end(SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0), G1 and G3. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	GGT - SCR G0; SE G0	GGT - SCR G0; SE G1	GGT - SCR G0; SE G2	GGT - SCR G0; SE G3	GGT - SCR G0; SE G4	GGT - SCR G0; SE UNK	GGT - SCR G1; SE G0	GGT - SCR G1; SE G1	GGT - SCR G1; SE G2	GGT - SCR G1; SE G3	GGT - SCR G1; SE G4	GGT - SCR G1; SE UNK	GGT - SCR G3; SE G0	GGT - SCR G3; SE G1	GGT - SCR G3; SE G2	GGT - SCR G3; SE G3	GGT - SCR G3; SE G4	GGT - SCR G3; SE UNK
GSK2132231A GROUP	20	11	4	0	0	2	2	2	0	0	0	0	0	0	0	1	0	0

Number of Patients With Abnormal Hemoglobin (HGB) Values by Maximum Grade

The status of each patient as regards HGB laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	HGB - SCR G0; SE G0	HGB - SCR G0; SE G1	HGB - SCR G0; SE G2	HGB - SCR G0; SE G3	HGB - SCR G0; SE G4	HGB - SCR G0; SE UNK	HGB - SCR G1; SE G0	HGB - SCR G1; SE G1	HGB - SCR G1; SE G2	HGB - SCR G1; SE G3	HGB - SCR G1; SE G4	HGB - SCR G1; SE UNK
GSK2132231A GROUP	22	14	5	1	0	2	2	2	0	0	0	0

Number of Patients With Abnormal Hypercalcemia (HCA) Values by Maximum Grade

The status of each patient as regards HCA laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Unknown (UNK), Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	HCA - SCR UNK; SE G0	HCA - SCR UNK; SE G1	HCA - SCR UNK; SE G2	HCA - SCR UNK; SE G3	HCA - SCR UNK; SE G4	HCA - SCR UNK; SE UNK	HCA - SCR G0; SE G0	HCA - SCR G0; SE G1	HCA - SCR G0; SE G2	HCA - SCR G0; SE G3	HCA - SCR G0; SE G4	HCA - SCR G0; SE UNK	HCA - SCR G1; SE G1	HCA - SCR G1; SE G2	HCA - SCR G1; SE G3	HCA - SCR G1; SE G4	HCA - SCR G1; SE UNK
GSK2132231A GROUP	2	1	0	0	0	0	37	0	0	0	0	6	1	1	0	0	0

Number of Patients With Abnormal Hyperkalemia (HKA) Values by Maximum Grade

The status of each patient as regards HKA laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0), G1 and G2. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	HKA - SCR G0; SE G0	HKA - SCR G0; SE G1	HKA - SCR G0; SE G2	HKA - SCR G0; SE G3	HKA - SCR G0; SE G4	HKA - SCR G0; SE UNK	HKA - SCR G1; SE G0	HKA - SCR G1; SE G1	HKA - SCR G1; SE G2	HKA - SCR G1; SE G3	HKA - SCR G1; SE G4	HKA - SCR G1; SE UNK	HKA - SCR G2; SE G0	HKA - SCR G2; SE G1	HKA - SCR G2; SE G2	HKA - SCR G2; SE G3	HKA - SCR G2; SE G4	HKA - SCR G2; SE UNK
GSK2132231A GROUP	42	2	0	0	0	1	1	0	0	0	0	1	1	0	0	0	0	0

Number of Patients With Abnormal Hypernatremia (HNA) Values by Maximum Grade

The status of each patient as regards HNA laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	HNA - SCR G0; SE G0	HNA - SCR G0; SE G1	HNA - SCR G0; SE G2	HNA - SCR G0; SE G3	HNA - SCR G0; SE G4	HNA - SCR G0; SE UNK	HNA - SCR G1; SE G0	HNA - SCR G1; SE G1	HNA - SCR G1; SE G2	HNA - SCR G1; SE G3	HNA - SCR G1; SE G4	HNA - SCR G1; SE UNK
GSK2132231A GROUP	44	0	0	0	0	2	2	0	0	0	0	0

Number of Patients With Abnormal Hypoalbuminemia(hAL) Values by Maximum Grade

The status of each patient as regards hAL laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Unknown (UNK), Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	hAL - SCR UNK; SE G0	hAL - SCR UNK; SE G1	hAL - SCR UNK; SE G2	hAL - SCR UNK; SE G3	hAL - SCR UNK; SE G4	hAL - SCR UNK; SE UNK	hAL - SCR G0; SE G0	hAL - SCR G0; SE G1	hAL - SCR G0; SE G2	hAL - SCR G0; SE G3	hAL - SCR G0; SE G4	hAL - SCR G0; SE UNK	hAL - SCR G1; SE G1	hAL - SCR G1; SE G2	hAL - SCR G1; SE G3	hAL - SCR G1; SE G4	hAL - SCR G1; SE UNK
GSK2132231A GROUP	1	0	1	0	0	1	26	4	2	0	0	4	4	3	0	0	2

Number of Patients With Abnormal Hypocalcemia(hCA) Values by Maximum Grade

The status of each patient as regards hCA laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Unknown (UNK), Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	hCA - SCR UNK; SE G0	hCA - SCR UNK; SE G1	hCA - SCR UNK; SE G2	hCA - SCR UNK; SE G3	hCA - SCR UNK; SE G4	hCA - SCR UNK; SE UNK	hCA - SCR G0; SE G0	hCA - SCR G0; SE G1	hCA - SCR G0; SE G2	hCA - SCR G0; SE G3	hCA - SCR G0; SE G4	hCA - SCR G0; SE UNK	hCA - SCR G1; SE G0	hCA - SCR G1; SE G1	hCA - SCR G1; SE G2	hCA - SCR G1; SE G3	hCA - SCR G1; SE G4	hCA - SCR G1; SE UNK
GSK2132231A GROUP	1	1	0	0	1	0	27	7	0	0	0	5	0	5	0	0	0	1

Number of Patients With Abnormal Hypokalemia (hKA) Values by Maximum Grade

The status of each patient as regards hKA laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	hKA - SCR G0; SE G0	hKA - SCR G0; SE G1	hKA - SCR G0; SE G2	hKA - SCR G0; SE G3	hKA - SCR G0; SE G4	hKA - SCR G0; SE UNK	hKA - SCR G1; SE G0	hKA - SCR G1; SE G1	hKA - SCR G1; SE G2	hKA - SCR G1; SE G3	hKA - SCR G1; SE G4	hKA - SCR G1; SE UNK
GSK2132231A GROUP	42	1	0	0	0	1	3	0	0	0	0	1

Number of Patients With Abnormal Hyponatremia (hNA) Values by Maximum Grade

The status of each patient as regards hNA laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	hNA - SCR G0; SE G0	hNA - SCR G0; SE G1	hNA - SCR G0; SE G2	hNA - SCR G0; SE G3	hNA - SCR G0; SE G4	hNA - SCR G0; SE UNK	hNA - SCR G1; SE G0	hNA - SCR G1; SE G1	hNA - SCR G1; SE G2	hNA - SCR G1; SE G3	hNA - SCR G1; SE G4	hNA - SCR G1; SE UNK
GSK2132231A GROUP	33	10	0	1	0	2	1	1	0	0	0	0

Number of Patients With Abnormal Leukocytes (LEU) Values by Maximum Grade

The status of each patient as regards LEU laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	LEU - SCR G0; SE G0	LEU - SCR G0; SE G1	LEU - SCR G0; SE G2	LEU - SCR G0; SE G3	LEU - SCR G0; SE G4	LEU - SCR G0; SE UNK	LEU - SCR G1; SE G0	LEU - SCR G1; SE G1	LEU - SCR G1; SE G2	LEU - SCR G1; SE G3	LEU - SCR G1; SE G4	LEU - SCR G1; SE UNK
GSK2132231A GROUP	37	6	0	1	0	2	0	1	1	0	0	0

Number of Patients With Abnormal Lymphopenia (LYM) Values by Maximum Grade

The status of each patient as regards LYM laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	LYM - SCR G0; SE G0	LYM - SCR G0; SE G1	LYM - SCR G0; SE G2	LYM - SCR G0; SE G3	LYM - SCR G0; SE G4	LYM - SCR G0; SE UNK	LYM - SCR G1; SE G0	LYM - SCR G1; SE G1	LYM - SCR G1; SE G2	LYM - SCR G1; SE G3	LYM - SCR G1; SE G4	LYM - SCR G1; SE UNK
GSK2132231A GROUP	18	13	6	0	0	2	2	4	3	0	0	0

Number of Patients With Abnormal Neutrophils (NEU) Values by Maximum Grade

The status of each patient as regards NEU laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0). CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	NEU - SCR G0; SE G0	NEU - SCR G0; SE G1	NEU - SCR G0; SE G2	NEU - SCR G0; SE G3	NEU - SCR G0; SE G4	NEU - SCR G0; SE UNK
GSK2132231A GROUP	39	4	1	2	0	2

Number of Patients With Abnormal Partial Thromboplastin Time (PTT) Values by Maximum Grade

The status of each patient as regards PTT laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	PTT - SCR G0; SE G0	PTT - SCR G0; SE G1	PTT - SCR G0; SE G2	PTT - SCR G0; SE G3	PTT - SCR G0; SE G4	PTT - SCR G0; SE UNK	PTT - SCR G1; SE G0	PTT - SCR G1; SE G1	PTT - SCR G1; SE G2	PTT - SCR G1; SE G3	PTT - SCR G1; SE G4	PTT - SCR G1; SE UNK
GSK2132231A GROUP	35	3	0	1	0	7	0	1	0	1	0	0

Number of Patients With Abnormal Platelets(PLT) Values by Maximum Grade

The status of each patient as regards PLT laboratory values at baseline (SCR) up to study end (SE) was collected and graded according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. The post-treatment values were presented by worst grade versus baseline grade. SCR CTC grade statuses reported were Grade 0 (G0) and G1. CTC grade statuses reported at SE were G0, G1, G2, G3, G4, and Unknown (UNK). (NCT00849875)
Timeframe: During the entire study, up to 5 years

Intervention	Subjects (Number)
	PLT - SCR G0; SE G0	PLT - SCR G0; SE G1	PLT - SCR G0; SE G2	PLT - SCR G0; SE G3	PLT - SCR G0; SE G4	PLT - SCR G0; SE UNK	PLT - SCR G1; SE G0	PLT - SCR G1; SE G1	PLT - SCR G1; SE G2	PLT - SCR G1; SE G3	PLT - SCR G1; SE G4	PLT - SCR G1; SE UNK
GSK2132231A GROUP	39	5	1	0	0	2	1	0	0	0	0	0

Number of Patients With Any Adverse Events (AEs) and With AEs by Maximum Grade

An AE was any untoward medical occurrence in a patient or clinical investigation subject, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. AEs reported are here below tabulated irrespective of grade (any), as well as graded by maximum grade reported according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. Maximum grade reported and tabulated were Grade 1 (G1), G2, G3, G4 and G5. (NCT00849875)
Timeframe: Within the 31-day follow-up period post treatment administration.

Intervention	Subjects (Number)
	Patients with any AEs	Patients with G1 AEs	Patients with G2 AEs	Patients with G3 AEs	Patients with G4 AEs	Patients with G5 AEs
GSK2132231A GROUP	48	14	19	12	3	0

Number of Patients With Any Serious Adverse Events (SAEs) and With AEs by Maximum Grade

SAEs include medical occurrences that result in death, are life threatening, require hospitalization or prolongation of hospitalization or result in disability/incapacity, is a congenital anomaly/birth defect in the offspring of a patient, is a Grade 4 AE according to the CTCAE, version3.0. Events which were part of the natural course of the disease under study were captured as part of the clinical activity outcome variables in this study; therefore did not need to be reported as SAEs. Progression/recurrence of the tumor was recorded as part of the clinical assessment data collection, and deaths due to progressive disease was recorded on a specific form, but not as an SAE. SAEs reported are here below tabulated irrespective of grade (any), as well as graded by maximum grade reported according to the Common Terminology Criteria (CTC) Adverse event terminology, version 3.0. Maximum grade reported and tabulated were Grade 1 (G1), G2, G3, G4 and G5. (NCT00849875)
Timeframe: Within the 31-day follow-up period post treatment administration.

Intervention	Subjects (Number)
	Patients with any SAEs	Patients with G1 SAEs	Patients with G2 SAEs	Patients with G3 SAEs	Patients with G4 SAEs	Patients with G5 SAEs
GSK2132231A GROUP	10	1	2	5	2	0

Number of Patients With Mixed Response (MxR) to MAGE-A3 ASCI Study Treatment

Assessment was done based on a set of MLs identified at baseline as TLs and NTLs followed up until disease progression. MLs were assessed as regards matching below MxR definitions. In case of evaluability per RECIST: a) MxR Type 1= at least (a.l.) 30% decrease in LD in a.l. one TL measured at baseline. Such response occurring in SD/PD status of LD of TL and without appearance of one or more new lesions = SD/PD with TL regression; b) MxR Type 2: appearance of one or more new lesions occurring in SD/PR status of LD of TL, and = SD/PR with new lesion. In case of non-evaluability per RECIST: a) MxR Type 1 = a clear decrease in diameters occurring in a.l. one TL measured at baseline. Such response occurring in SD/PD status of LD of (baseline) TL and without appearance of one or more new lesions = SD/PD with TL regression; b) MxR Type 2 = appearance of one or more new lesions occurring in SD/PR status of LD of TL = SD/PR with new lesion. (NCT00849875)
Timeframe: During the entire study, up to 5 years

,,,

Intervention	Patients (Number)
	MxR: SD/PR with new lesion	MxR: SD/PD with target lesion regression
GSK2132231A GROUP	10	1
GSK2132231A GS Unknown Group	0	0
GSK2132231A GS- Group	4	1
GSK2132231A GS+ Group	6	0

Number of Patients With Objective Tumor Response (OR) to MAGE-A3 ASCI Study Treatment

Response assessment was done based on a set of measurable lesions (MLs) identified at baseline as target lesions (TLs), and followed up until disease progression. Up to 5 MLs per organ & 10 in total were identified as TLs and measured at baseline, selected based on size (those with the longest diameter [LD]) and measurability; a sum of LDs for all TLs was calculated and reported as baseline sum LD, which was used to characterize objective tumor response (OR), OR being defined as either complete response (CR) and/or partial response (PR) post MAGE-A3 ASCI treatment. After identification, MLs and TLs were assessed as regards CR and PR definitions per Response Evaluation Criteria in Solid Tumors (RECIST) criteria: CR = Disappearance of all extranodal target lesions. All pathological lymph nodes must have decreased to <10 mm in short axis; PR = At least a 30% decrease in the SLD of target lesions, taking as reference the baseline sum diameters. (NCT00849875)
Timeframe: During the entire study, up to 5 years

,,,

Intervention	patients (Number)
	OR	CR	PR
GSK2132231A GROUP	4	1	3
GSK2132231A GS Unknown Group	0	0	0
GSK2132231A GS- Group	0	0	0
GSK2132231A GS+ Group	4	1	3

Number of Patients With Stable Disease (SD) Response to MAGE-A3 ASCI Study Treatment

Assessment was done based on a set of MLs identified at baseline as TLs and NTLs followed up until disease progression. TLs and NTLs were assessed as regards matching or not SD-related definitions, 1) SD definitions per Response Evaluation Criteria in Solid Tumors (RECIST) criteria for TLs >= 20 mm and TLs both >= and < 20 mm: a) for TLs: SD = Neither sufficient shrinkage to qualify as a PR nor sufficient increase to qualify as PD, taking as references the smallest sum LD since treatment start. and b) for NTLs: SD = Persistence of one or more NTL; 2) following below criteria for TLs < 20mm e. a. a) for TLs: PR/SD = Neither sufficient shrinkage to qualify for CR nor sufficient increase, to qualify for PD taking as references the smallest sum LD since treatment start, and b) for NTLs: PR/SD = Persistence of one or more NTL. (NCT00849875)
Timeframe: During the entire study, up to 5 years

,,,

Intervention	patients (Number)
	SD	SD/PR
GSK2132231A GROUP	5	0
GSK2132231A GS Unknown Group	1	0
GSK2132231A GS- Group	0	0
GSK2132231A GS+ Group	4	0

Efficacy: Overall Survival

Overall survival is defined as the time from randomization to date of death due to any cause. (NCT03070392)
Timeframe: From randomization to the data cut off date of 13-Oct-2020; median follow-up duration was 14.1 months.

Intervention	Months (Median)
Tebentafusp	21.7
Investigator's Choice	16.0

Efficacy: Progression Free Survival (PFS)

Progression free survival (PFS) is defined as the time from randomization to the date of progression (RECIST v1.1) or death due to any cause. (NCT03070392)
Timeframe: PFS was assessed every 3 months from randomization until disease progression or death, up to 36 months.

Intervention	Months (Median)
Tebentafusp	3.3
Investigator's Choice	2.9

Safety: Number of Participants With Treatment Emergent Adverse Events

Safety was defined as the number of participants with treatment emergent adverse events, including laboratory abnormalities, ECG changes, and/or physical examination findings. (NCT03070392)
Timeframe: Safety was assessed from informed consent through 90 days after end of treatment, up to 36 months.

Intervention	Participants (Count of Participants)
Tebentafusp	245
Investigator's Choice	105

Pharmacokinetics (PK): Tebentafusp Concentration

Serum PK concentrations of tebentafusp were collected over time. (NCT03070392)
Timeframe: PK concentrations were assessed at pre-dose, end of infusion and anytime in the 12 to 24 hour window after completion of the infusion in Cycle 1 on Days 1, 8 and 15.

Intervention	pg/mL (Geometric Mean)
	Cycle 1 Day 1 - End of Infusion	Cycle 1 Day 1 - 12 to 24 hours post-infusion	Cycle 1 Day 8 - End of Infusion	Cycle 1 Day 8 - 12 to 24 hours post-infusion	Cycle 1 Day 15 - End of Infusion	Cycle 1 Day 15 - 12 to 24 hours post-infusion
Tebentafusp	4201.929	505.100	5787.139	738.602	13715.914	1685.354

Quality-of-Life: Change From Baseline in EORTC QLQ-C30 Global Health Status

Global health status and quality of life was assessed using the EORTC QLQ-C30 questionnaire. The score range for the EORTC QLQ-C30 is from 0 to 100, with higher scores indicating better functioning and better global health status and health-related quality of life. A positive change indicates improvement. (NCT03070392)
Timeframe: EORTC QLQ-C30 was assessed at baseline (Cycle 1 Day 1) and on Day 1 of every other cycle to Cycle 5 Day 1, every fourth cycle thereafter, beginning with Cycle 9 Day 1 and End of Treatment (EOT), up to 36 months. Each cycle is 21 days.

Intervention	Units on a scale (Mean)
	Baseline Cycle 1	Change at Cycle 3	Change at Cycle 5	Change at Cycle 9	Change at Cycle 13	Change at Cycle 17	Change at Cycle 21	Change at Cycle 25	Change at Cycle 29	Change at EOT
Investigator's Choice	74.872	-0.238	-10.227	-8.333	-10.185	-4.167	-4.167	0.00	0.00	-10.539
Tebentafusp	76.108	0.952	-1.152	-2.193	-5.625	-10.185	0.758	-2.381	-8.333	-10.417

Quality-of-life: Change From Baseline in EQ-5D Visual Analogue Score (VAS)

The EQ-5D VAS score records the participant's self-rated health on a vertical visual analogue scale, with 0 being the worst imaginable health state and 100 being the best imaginable health state. A positive change indicates improvement. (NCT03070392)
Timeframe: EQ-5D,5L VAS was assessed at baseline (Cycle 1 Day 1) and on Day 1 of every other cycle to Cycle 5 Day 1, every fourth cycle thereafter, beginning with Cycle 9 Day 1 and End of Treatment (EOT), up to 36 months. Each cycle is 21 days.

Intervention	Units on a scale (Mean)
	Baseline Cycle 1	Change at Cycle 3	Change at Cycle 5	Change at Cycle 9	Change at Cycle 13	Change at Cycle 17	Change at Cycle 21	Change at Cycle 25	Change at Cycle 29	Change at EOT
Investigator's Choice	80.4	-0.8	-0.7	-3.3	-2.6	-8.5	-1.0	-4.0	-2.0	-11.7
Tebentafusp	81.0	0.4	0.6	-0.9	-2.0	-10.2	-1.8	-13.6	0.0	-10.1

Quality-of-Life: Change From Baseline in EQ-5D,5L Domain Scores

General health status was assessed using the EQ-5D,5L questionnaire, which includes five dimensions (5D): mobility, self-care, usual activities, pain/discomfort, and anxiety/depression. Each dimension has 3 scoring levels, where 1 indicates a better health state (no problems) and 3 indicates a worse health state. A positive change indicates improvement. (NCT03070392)
Timeframe: EQ-5D,5L was assessed at baseline (Cycle 1 Day 1) and on Day 1 of every other cycle to Cycle 5 Day 1, every fourth cycle thereafter, beginning with Cycle 9 Day 1 and End of Treatment (EOT), up to 36 months. Each cycle is 21 days.

Intervention	Units on a scale (Mean)
	Mobility - Baseline Cycle 1	Mobility - Change at Cycle 3	Mobility - Change at Cycle 5	Mobility - Change at Cycle 9	Mobility - Change at Cycle 13	Mobility - Change at Cycle 17	Mobility - Change at Cycle 21	Mobility - Change at Cycle 25	Mobility - Change at Cycle 29	Mobility - Change at EOT	Self-care - Baseline Cycle 1	Self-care - Change at Cycle 3	Self-care - Change at Cycle 5	Self-care - Change at Cycle 9	Self-care - Change at Cycle 13	Self-care - Change at Cycle 17	Self-care - Change at Cycle 21	Self-care - Change at Cycle 25	Self-care - Change at Cycle 29	Self-care - Change at EOT	Usual activities - Baseline Cycle 1	Usual activities - Change at Cycle 3	Usual activities - Change at Cycle 5	Usual activities - Change at Cycle 9	Usual activities - Change at Cycle 13	Usual activities - Change at Cycle 17	Usual activities - Change at Cycle 21	Usual activities - Change at Cycle 25	Usual activities - Change at Cycle 29	Usual activities - Change at EOT	Pain/Discomfort - Baseline Cycle 1	Pain/Discomfort - Change at Cycle 3	Pain/Discomfort - Change at Cycle 5	Pain/Discomfort - Change at Cycle 9	Pain/Discomfort - Change at Cycle 13	Pain/Discomfort - Change at Cycle 17	Pain/Discomfort - Change at Cycle 21	Pain/Discomfort - Change at Cycle 25	Pain/Discomfort - Change at Cycle 29	Pain/Discomfort - Change at EOT	Anxiety/Depression - Baseline Cycle 1	Anxiety/Depression - Change at Cycle 3	Anxiety/Depression - Change at Cycle 5	Anxiety/Depression - Change at Cycle 9	Anxiety/Depression - Change at Cycle 13	Anxiety/Depression - Change at Cycle 17	Anxiety/Depression - Change at Cycle 21	Anxiety/Depression - Change at Cycle 25	Anxiety/Depression - Change at Cycle 29	Anxiety/Depression - Change at EOT
Investigator's Choice	1.3	0.1	0.3	0.0	0.3	0.2	0.5	0.0	0.0	0.4	1.1	0.0	0.0	0.0	0.1	0.0	0.0	0.0	0.0	0.1	1.3	0.1	0.2	0.1	0.1	0.2	0.0	0.0	0.0	0.5	1.5	0.1	0.2	-0.1	0.1	0.3	0.0	1.0	0.5	0.4	1.7	-0.3	0.0	0.1	-0.1	0.0	0.0	0.0	0.5	0.2
Tebentafusp	1.2	-0.1	0.0	0.0	-0.1	0.3	0.0	0.1	0.0	0.3	1.1	0.0	0.0	0.0	0.1	0.1	0.0	0.0	0.0	0.1	1.2	0.2	0.1	0.2	0.3	0.5	0.3	0.3	0.2	0.4	1.5	0.0	0.0	0.1	0.1	0.4	0.2	0.0	0.1	0.2	1.8	-0.2	-0.2	-0.3	-0.4	-0.4	-0.5	-0.4	-0.6	0.3

Median Overall Survival (Evaluable Randomized Patients)

The primary analysis will be performed among the Gnaq/Gna11 mutant patients. A stratified logrank test will be performed stratified by mutation status, M stage, and number of prior systemic therapies for metastatic disease. Due to the potential for a large number of strata and small strata sizes, the standard asymptotic stratified logrank test will be verified for robustness utilizing a permutation reference distribution. (NCT01143402)
Timeframe: The time from randomization to death due to any cause, assessed up to 5 years

Intervention	Months (Median)
Arm I (Temozolomide)	9.1
Arm II (Selumetinib)	11.8

Progression-free Survival (PFS) (Evaluable Randomized Patients)

Intervention	weeks (Median)
Arm I (Temozolomide)	7
Arm II (Selumetinib)	15.9

Event-free Survival (EFS) Rate

EFS will be estimated using the Kaplan-Meier method. The log-rank test will be performed to test the difference in time-to-event distributions between patient groups. Cox proportional hazards model will be utilized to include multiple covariates in the time-to-event analysis. Logistic regression will be utilized to assess the effect of patient prognostic factors on the response rate. (NCT00654732)
Timeframe: From the start of study treatment up to 3 years

Intervention	Participants (Count of Participants)
RABVD	17
ABVD	20

Bone Mineral Density of the Lumbar Spine as Measured by Dual-energy X-ray Absorptiometry (DEXA) Scan at 18 Months

To compare the effect of zoledronic acid administered every 6 months on bone loss associated with surgery (at a minimum, any surgical procedure that results in removal of both ovaries), as compared with observation alone. This is to be evaluated by measuring the change from baseline to 18 months in bone mineral density (BMD) of the lumbar spine, specifically L1-L4 dual energy X-ray absorptiometry (DEXA). (NCT00305695)
Timeframe: 18 months

Intervention	g/cm2 (Mean)
Arm I (Zoledroic Acid)	-0.001
Arm II (Clinical Observation)	-0.094

Bone Mineral Density of the Lumbar Spine as Measured by Dual-energy X-ray Absorptiometry (DEXA) Scan at 9 Months

To compare the effect of zoledronic acid administered every 6 months on bone loss associated with surgery (at a minimum, any surgical procedure that results in removal of both ovaries), as compared with observation alone. This is to be evaluated by measuring the change from baseline to 9 months in bone mineral density (BMD) of the lumbar spine, specifically L1-L4 dual energy X-ray absorptiometry (DEXA). (NCT00305695)
Timeframe: 9 Months

Intervention	g/cm2 (Mean)
Arm I (Zoledroic Acid)	-0.025
Arm II (Clinical Observation)	-0.086

Bone Mineral Density of the Total Hip as Measured by DEXA Scan on Left Hip

To compare the effect of zoledronic acid on the change in BMD of the left hip following treatment, evaluated by measuring the change from baseline to 18 months (NCT00305695)
Timeframe: 18 months

Intervention	g/cm2 (Mean)
Arm I (Zoledroic Acid)	-0.003
Arm II (Clinical Observation)	-0.058

Bone Mineral Density of the Total Hip as Measured by DEXA Scan on Right Hip

To compare the effect of zoledronic acid on the change in BMD of the right hip following treatment, evaluated by measuring the change from baseline to 18 months (NCT00305695)
Timeframe: 18 months

Intervention	g/cm2 (Mean)
Arm I (Zoledroic Acid)	0.101
Arm II (Clinical Observation)	-0.052

Reproducibility of [F18]HX4 PET Imaging in Measuring Hypoxia in Tumors

Primary tumor uptake of [F 18]HX4 was measured on PET images by onsite radiologist or nuclear medicine physician for 1st and 2nd PET scans. Values measured were: SUV (Standard Uptake Value), SUV Max (Maximum standard uptake value), SUV Mean (Mean standard uptake value), and T/B ratio (Tumor to background ratio). Pearson's correlation coefficient was calculated for each of the parameter. (NCT01075399)
Timeframe: Time between 1st and 2nd scan was 1 to 6 days

Intervention	participants (Number)
Subjects That Received 1st and 2nd [F18] HX4 Scans	39

Complete Response Rate

"The number of patients that achieved a complete response (CR) to therapy as assessed by the revised International Working Group Criteria.~Complete response:~Lymph nodes and extralymphatic sites: Score 1, 2, or 3 with or without a residual mass on 5-point (Daeuville) scale~Bone Marrow: No evidence of FDG-avi disease~No new lesions~Deauville Criteria for PET scan Interpretation in Lymphoma~Five-point scale:~No Uptake~Uptake ≤ mediastinum~Uptake >mediastinum but ≤ liver~Uptake moderately increased compared to liver at any site~Uptake markedly increased compared to the liver at any site or/and new sites of disease" (NCT02505269)
Timeframe: 4-6 months

Intervention	Participants (Count of Participants)
Brentuximab Vedotin	34

Overall Response Rate

"The number of patients that achieved a complete Metabolic Response (CR) or Partial Metabolic Response (PR) to therapy as assessed by the revised International Working Group Criteria.~Complete Metabolic Response:~Lymph nodes and extralymphatic sites: Score 1, 2, or 3 with or without a residual mass on 5-point (Daeuville) scale Bone Marrow: No evidence of FDG-avi disease No new lesions~Partial Metabolic Response:~>Lymph nodes and extralymphatic sites: Score 4, 5 with reduced uptake compared with baseline and residual mass(es) of any size.~Deauville Criteria for PET scan Interpretation in Lymphoma~Five-point scale:~No Uptake~Uptake ≤ mediastinum~Uptake >mediastinum but ≤ liver~Uptake moderately increased compared to liver at any site~Uptake markedly increased compared to the liver at any site or/and new sites of disease" (NCT02505269)
Timeframe: 4-6 months

Intervention	Participants (Count of Participants)
Brentuximab Vedotin	34

Number of Patients With Grade III and IV Adverse Events

The number of patients that experienced grade III and grade IV adverse events that were deemed to be possibly, probably, or definitely related to study treatment. Adverse events were assessed using Common Toxicology Criteria for Adverse Events (CTCAE v4.0) criteria. (NCT02505269)
Timeframe: 4-6 months

Intervention	Participants (Count of Participants)
	Grade III Adverse Events	Grade IV Adverse Events
Brentuximab Vedotin	4	0

Complete Response (CR) Rate After Induction Treatment

Complete response (CR) is defined as complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present prior to therapy. (NCT01390584)
Timeframe: Assessed at end of Cycle 2

Intervention	proportion of participants (Number)
Step 1: Induction Tx	1.0

Overall Survival

Overall survival is defined as the time from study entry to death or date last known alive. (NCT01390584)
Timeframe: Assessed at 36 months

Intervention	months (Median)
ABVD + INRT	NA
ABVD + BEACOPP + INRT	NA

Progression-free Survival at 36 Months Among Patients Who Are PET Positive After Induction Treatment

Progression-free survival is defined as the time from study entry to lymphoma progression or death from any cause. Proportion of patients who are progression-free and alive at 36 months will be reported. Progression is defined as appearance of any new lesions more than 1.5 cm in any axis, at least a 50% increase from nadir in sum of the product of the diameters (SPD) of any previously involved nodes or extranodal masses or the size of other lesions, or at least 50% increase in the longest diameter of any single previously identified node or extranodal mass more than 1 cm in its short axis. (NCT01390584)
Timeframe: Assessed at 36 months

Intervention	proportion of participants (Number)
ABVD + BEACOPP + INRT	NA

Progression-free Survival Rate

Intervention	proportion of participants (Number)
ABVD + INRT	NA
ABVD + BEACOPP + INRT	NA

Proportion of Patients Who Are PET Negative After Induction Treatment

(NCT01390584)
Timeframe: Assessed at end of Cycle 2

Intervention	proportion of participants (Number)
Step 1: Induction Tx	0.8

5-year Overall Survival

Overall survival is defined as the time from randomization to death or last known alive. The 5-year survival rate is the probability a patient survives 5 years. (NCT00003389)
Timeframe: Assessed every 2 months if patient is < 1 year from study entry, every 3 months for the second year, every 4 months for the third year, every 6 months for years 4 and 5, and yearly for 5 years

Intervention	Proportion of patients (Number)
Arm A (ABVD)	0.88
Arm B (Stanford V)	0.88

Failure-free Survival at 5 Years

"Failure-free survival is defined as the time from randomization to the earlier of progression/relapse or death. The 5-year failure-free survival is the probability a patient is failure-free and survives 5 years.~Progression is defined as an increase in size of 25% of the sum of the products of the pretreatment measurements or appearance of new lesions. Significant enlargement of the liver or spleen is evidence of progression. A significant increase in size is defined as > 2.0 cm in distance between costal margin and the inferior margin of either organ.~Relapse is defined as the re-appearance of any clinical evidence of Hodgkin's disease in a patient who has had a complete response. Relapse for partial responders is defined as progressive disease relative to disease status during the partial remission." (NCT00003389)
Timeframe: Assessed every 2 months if patient is < 1 year from study entry, every 3 months for the second year, every 4 months for the third year, every 6 months for years 4 and 5

Intervention	Proportion of patients (Number)
Arm A (ABVD)	0.74
Arm B (Stanford V)	0.71

Incidence of Second Cancers

Number of patients who developed second primary cancers (NCT00003389)
Timeframe: Assessed every 2 months if patient is < 1 year from study entry, every 3 months for the second year, every 4 months for the third year, every 6 months for years 4 and 5, and yearly for 5 years

Intervention	participants (Number)
Arm A (ABVD)	15
Arm B (Stanford V)	19

Treatment Delivery With Compliance Defined as Receiving at Least 95% of the Pre-operative Protocol Dose of RT, All 3 Cycles of MAID (if Applicable), and Receive Thalidomide on 75% of the Days During Radiation

Was to be estimated using a binomial distribution and accompanied by the associated 95% confidence interval. Due to early study closure, this endpoint could not be fully evaluated per the protocol plan. (NCT00089544)
Timeframe: Duration of treatment (which can continue up to approximately 15 months).

Intervention	participants (Number)
	Not Compliant	Compliant
Cohort A (Chemotherapy, Radiation, Thalidomide, Surgery)	5	10
Cohort B (Thalidomide, Radiation, Surgery)	2	5

Confirmed Response Rate as Determined by the RECIST Criteria (Version 1.1)

The confirmed response rates will be estimated by dividing the number of confirmed responders by the number of evaluable patients. 95% confidence intervals will be calculated. (NCT01835145)
Timeframe: Up to 2 years

Intervention	Participants (Count of Participants)
Arm I (Cabozantinib-s-malate)	0
Arm II (Temozolomide or Dacarbazine)	0

Overall Survival (OS)

The distribution of OS time will be estimated using the method of Kaplan Meier. (NCT01835145)
Timeframe: Number of days from registration until death, assessed up to 2 years

Intervention	months (Median)
Arm I (Cabozantinib-s-malate)	6.3
Arm II (Temozolomide or Dacarbazine)	7.2

Percentage of Patients Who Experienced Grade 3+ Adverse Events Regardless of Attribution

percentage of patients who experienced grade 3+ adverse events regardless of attribution, graded according to the National Cancer Institute CTCAE version 4.0 (NCT01835145)
Timeframe: Up to 2 years

Intervention	percentage of patients (Number)
Arm I (Cabozantinib-s-malate)	51.6
Arm II (Temozolomide or Dacarbazine)	20

PFS

The distribution of PFS time will be estimated using the method of Kaplan Meier and is defined as the number of days from registration until disease progression (or death). Progression is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study, with an absolute increase of at least 5 mm. The appearance of one or more new lesions is also considered progression. (NCT01835145)
Timeframe: Number of days from registration until disease progression (or death), assessed up to 2 years

Intervention	months (Median)
Arm I (Cabozantinib-s-malate)	2.0
Arm II (Temozolomide or Dacarbazine)	1.9

Proportion of Patients Without a Progression Free Survival Event at 4 Months (PFS4)

A patient will be declared a PFS4 success if they are on study and progression free for at least 4 months. Progression is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study, with an absolute increase of at least 5 mm. The appearance of one or more new lesions is also considered progression. The success for each arm will be calculated independently as the number of successes divided by the total number of evaluable patients. A one-sided chi-squared test for a difference in PFS4 proportions will be used to test for a difference between arms. (NCT01835145)
Timeframe: At 4 months

Intervention	proportion of participants (Number)
Arm I (Cabozantinib-s-malate)	.323
Arm II (Temozolomide or Dacarbazine)	.267

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)

Intervention	percentage of participants (Number)
Treatment: Pembrolizumab and AVD Chemotherapy Guided by PET-CT	37

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)

Intervention	Participants (Count of Participants)
Treatment: Pembrolizumab and AVD Chemotherapy Guided by PET-CT	30

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)

Intervention	Participants (Count of Participants)
Treatment: Pembrolizumab and AVD Chemotherapy Guided by PET-CT	30

Article	Year
First-in-Human Study to Assess the Safety, Pharmacokinetics, and Pharmacodynamics of an Oral Formulation of DS-1040, an Inhibitor of the Activated Form of Thrombin-Activatable Fibrinolysis Inhibitor, in Healthy Subjects. Journal of clinical pharmacology, Volume: 59, Issue: 12	2019
New pre-clinical evidence of anti-inflammatory effect and safety of a substituted fluorophenyl imidazole. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, Volume: 111	2019
Safety and efficacy of sofosbuvir-based direct-acting antiviral regimens for hepatitis C virus genotype 6 in Southwest China: Real-world experience of a retrospective study. Journal of viral hepatitis, Volume: 26, Issue: 3	2019
Choline- versus imidazole-based ionic liquids as functional ingredients in topical delivery systems: cytotoxicity, solubility, and skin permeation studies. Drug development and industrial pharmacy, Volume: 43, Issue: 11	2017
Acute Toxicity of Imidazole Nitrate Ionic Liquids with Varying Chain Lengths to Earthworms (Eisenia foetida). Bulletin of environmental contamination and toxicology, Volume: 99, Issue: 2	2017
Interaction of Azole-Based Environmental Pollutants with the Coelomic Hemoglobin from Amphitrite ornata: A Molecular Basis for Toxicity. Biochemistry, 05-02, Volume: 56, Issue: 17	2017
4-Alkylated Silver-N-Heterocyclic Carbene (NHC) Complexes with Cytotoxic Effects in Leukemia Cells. ChemMedChem, Volume: 10, Issue: 9	2015
Effects of imidazolium chloride ionic liquids and their toxicity to Scenedesmus obliquus. Ecotoxicology and environmental safety, Volume: 122	2015
A novel role of transient receptor potential mucolipin1 (TRPML1) in protecting against imidazole-induced cytotoxicity. Biochemistry and cell biology = Biochimie et biologie cellulaire, Volume: 92, Issue: 4	2014
Animal toxicity of hairpin pyrrole-imidazole polyamides varies with the turn unit. Journal of medicinal chemistry, Sep-26, Volume: 56, Issue: 18	2013
DNA binding and cytotoxicity of copper (II) imidazole terpyridine complexes: role of oxyanion, hydrogen bonding and π-π interaction. European journal of medicinal chemistry, Volume: 68	2013
[Effects of imidazolium chloride ionic liquids on the acute toxicity and weight of earthworm]. Huan jing ke xue= Huanjing kexue, Volume: 34, Issue: 4	2013
Cytotoxicity and DNA binding property of phenanthrene imidazole with polyglycol side chains. Bioorganic & medicinal chemistry letters, Oct-15, Volume: 22, Issue: 20	2012
Toxicity assessment of various ionic liquid families towards Vibrio fischeri marine bacteria. Ecotoxicology and environmental safety, Volume: 76, Issue: 2	2012
Evaluation of the genotoxicity of the imidazole antifungal climbazole: comparison to published results for other azole compounds. Mutation research, Volume: 672, Issue: 1	2009
Importance of sulfonylimidazolidinone motif of 4-phenyl-1-arylsulfonylimidazolidinones for their cytotoxicity: synthesis of 2-benzoyl-4-phenyl[1,2,5]thiazolidine-1,1-dioxides and their cytotoxcity. Archives of pharmacal research, Volume: 26, Issue: 1	2003
Protection by imidazol(ine) drugs and agmatine of glutamate-induced neurotoxicity in cultured cerebellar granule cells through blockade of NMDA receptor. British journal of pharmacology, Volume: 127, Issue: 6	1999
Captopril enhances aminoglycoside nephrotoxicity in potassium-depleted rats. Kidney international, Volume: 28, Issue: 2	1985
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Article	Year
New Candidate Preservative in Ophthalmic Solution Instead of Benzalkonium Chloride: 1,3-Didecyl-2-methyl Imidazolium Chloride. Chemical & pharmaceutical bulletin, Volume: 71, Issue: 7	2023
Copper is toxic to PrP-ablated mice and exacerbates disease in a mouse model of E200K genetic prion disease. Neurobiology of disease, Volume: 45, Issue: 3	2012
[Clinical use of the interaction between cyclosporine A and its inhibitors]. Przeglad lekarski, Volume: 61, Issue: 12	2004
Psoriasis of the scalp. Diagnosis and management. American journal of clinical dermatology, Volume: 2, Issue: 3	2001
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Article	Year
First-in-Human Study to Assess the Safety, Pharmacokinetics, and Pharmacodynamics of an Oral Formulation of DS-1040, an Inhibitor of the Activated Form of Thrombin-Activatable Fibrinolysis Inhibitor, in Healthy Subjects. Journal of clinical pharmacology, Volume: 59, Issue: 12	2019
Eigenmobilities in background electrolytes for CZE. V. Intensity (amplitudes) of system peaks. Electrophoresis, Volume: 27, Issue: 23	2006
Single cell volume measurement by quantitative phase microscopy (QPM): a case study of erythrocyte morphology. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, Volume: 17, Issue: 5-6	2006
[Effect of imidazole on the trabecular bone volume of rats with calcium deficiency]. Comptes rendus des seances de la Societe de biologie et de ses filiales, Volume: 178, Issue: 3	1984
Pharmacokinetic study of [14C]flutrimazole after oral and intravenous administration in dogs. Comparison with clotrimazole. Arzneimittel-Forschung, Volume: 42, Issue: 6	1992
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Article	Year
Continuous-Flow Synthesis of N-Methylated Peptides via Generation of an Acyl N-Methylimidazolium Cation. Methods in molecular biology (Clifton, N.J.), Volume: 2530	2022
The Effects of pH on the Structure and Bioavailability of Imidazobenzodiazepine-3-Carboxylate MIDD0301. Molecular pharmaceutics, 04-06, Volume: 17, Issue: 4	2020
Structure-based design and discovery of potent and selective lysine-specific demethylase 1 (LSD1) inhibitors. Bioorganic & medicinal chemistry letters, 01-01, Volume: 29, Issue: 1	2019
Tanshinone-IIA-Based Analogues of Imidazole Alkaloid Act as Potent Inhibitors To Block Breast Cancer Invasion and Metastasis in Vivo. Journal of medicinal chemistry, 12-13, Volume: 61, Issue: 23	2018
Novel 2,4-disubstituted pyrimidines as potent, selective, and cell-permeable inhibitors of neuronal nitric oxide synthase. Journal of medicinal chemistry, Feb-12, Volume: 58, Issue: 3	2015
Potent bisimidazole-based HCV NS5A inhibitors bearing annulated tricyclic motifs. Bioorganic & medicinal chemistry letters, Dec-15, Volume: 24, Issue: 24	2014
The role of imidazole in peptide cyclization by transesterification: parallels to the catalytic triads of serine proteases. Organic & biomolecular chemistry, May-14, Volume: 11, Issue: 18	2013
Design, synthesis, and structure-activity-relationship of phenyl imidazoles as potent Smoothened antagonists. Bioorganic & medicinal chemistry letters, Nov-01, Volume: 22, Issue: 21	2012
Design of inhibitors of Helicobacter pylori glutamate racemase as selective antibacterial agents: incorporation of imidazoles onto a core pyrazolopyrimidinedione scaffold to improve bioavailabilty. Bioorganic & medicinal chemistry letters, Sep-01, Volume: 22, Issue: 17	2012
Potent and selective cyclohexyl-derived imidazopyrazine insulin-like growth factor 1 receptor inhibitors with in vivo efficacy. Bioorganic & medicinal chemistry letters, Feb-15, Volume: 21, Issue: 4	2011
Designation of imidazole-containing dipeptides as pharmacological chaperones. Human & experimental toxicology, Volume: 30, Issue: 7	2011
In vivo imaging of pyrrole-imidazole polyamides with positron emission tomography. Proceedings of the National Academy of Sciences of the United States of America, Sep-02, Volume: 105, Issue: 35	2008
Pharmacokinetic study of [14C]flutrimazole after oral and intravenous administration in dogs. Comparison with clotrimazole. Arzneimittel-Forschung, Volume: 42, Issue: 6	1992
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Article	Year
Antiviral activity of pyrrole-imidazole polyamides against SV40 and BK polyomaviruses. Antiviral research, Volume: 152	2018
Imidazolium salts with antifungal potential for the control of head blight of wheat caused by Fusarium graminearum. Journal of applied microbiology, Volume: 121, Issue: 2	2016
Heterogeneous Mechanisms of Secondary Resistance and Clonal Selection in Sarcoma during Treatment with Nutlin. PloS one, Volume: 10, Issue: 10	2015
Design and synthesis of imidazole N-H substituted amide prodrugs as inhibitors of hepatitis C virus replication. Bioorganic & medicinal chemistry letters, Aug-15, Volume: 25, Issue: 16	2015
Mixture effects of imidazole fungicides on cortisol and aldosterone secretion in human adrenocortical H295R cells. Toxicology, Sep-10, Volume: 275, Issue: 1-3	2010
5-(2-Pyrimidinyl)-imidazo[1,2-a]pyridines are antibacterial agents targeting the ATPase domains of DNA gyrase and topoisomerase IV. Bioorganic & medicinal chemistry letters, Sep-15, Volume: 19, Issue: 18	2009
Evaluation of the genotoxicity of the imidazole antifungal climbazole: comparison to published results for other azole compounds. Mutation research, Volume: 672, Issue: 1	2009
Ineffectiveness of a four week treatment with the thromboxane synthetase inhibitor, imidazole salycilate, in reducing airway hyperresponsiveness to methacholine in asthmatics. Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace, Volume: 52, Issue: 2	1997
Imidazole-induced potentiation of the contractile response to various agonists in vascular smooth muscle. European journal of pharmacology, Sep-24, Volume: 83, Issue: 3-4	1982
Early processing of prothrombin and factor X by the vitamin K-dependent carboxylase. The Journal of biological chemistry, Jul-15, Volume: 263, Issue: 20	1988
Modeling the reactivity of acrylic acid and acrylate anion with biological nucleophiles. Toxicology letters, Volume: 47, Issue: 3	1989
Vulvovaginitis: the role of patient compliance in treatment success. American journal of obstetrics and gynecology, Volume: 165, Issue: 4 Pt 2	1991
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Article	Year
Evaluation of novel TGR5 agonist in combination with Sitagliptin for possible treatment of type 2 diabetes. Bioorganic & medicinal chemistry letters, 06-01, Volume: 28, Issue: 10	2018
Imidazole Nitrogens of Two Histidine Residues Participating in N-H···N Hydrogen Bonds in Protein Structures: Structural Bioinformatics Approach Combined with Quantum Chemical Calculations. The journal of physical chemistry. B, 01-25, Volume: 122, Issue: 3	2018
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Article	Year
An imidazole-based organocatalyst designed for bulk polymerization of lactide isomers: inspiration from Nature. Chemical communications (Cambridge, England), Dec-11, Volume: 48, Issue: 95	2012
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

imidazole

Description

Cross-References

Synonyms (133)

Research Excerpts

Overview

Effects

Actions

Treatment

Drug Classes (1)

Pathways (5)

Protein Targets (14)

Potency Measurements

Inhibition Measurements

Activation Measurements

Other Measurements

Biological Processes (113)

Molecular Functions (39)

Ceullar Components (28)

Bioassays (46)

Research

Studies (2,355)

Study Types

Clinical Trials (37)

Trial Overview

Trial Outcomes

Comparison of the Event-free (EFS) Survival in High Risk HL Patients Treated With AEPA/CAPDac to the Historical Control HOD99 Unfavorable Risk 2 Arm (UR2).

Complete Response Rate Estimate for All Evaluable Participants

Local Failure Rate in High Risk HL Patients Treated With AEPA/CAPDac.

Percentage of Initially Enrolled Patients That Have a Complete Response at Early Response Assessment Compared to Historical Control

Percentage of Initially Enrolled Patients That Have a Complete Response at Early Response Assessment Compared to Historical Control

Descriptive of Hematological Adverse Events

Descriptive of Infectious Adverse Events

Descriptive of Neuropathic Adverse Events

To Assess the Patient Reported Symptoms and Health-related Quality of Life in Children With High Risk HL Compared to Those Treated on the Unfavorable HOD99 Treatment Arm (UR2) at Multiple Time Points. (PedsQL v.3.0)

To Assess the Patient Reported Symptoms and Health-related Quality of Life in Children With High Risk HL Compared to Those Treated on the Unfavorable HOD99 Treatment Arm (UR2) at Multiple Time Points. (PedsQL v.3.0)

To Assess the Patient Reported Symptoms and Health-related Quality of Life in Children With High Risk HL Compared to Those Treated on the Unfavorable HOD99 Treatment Arm (UR2) at Multiple Time Points. (PedsQL v.4.0)

2-year Overall Survival

2-year Progression-free Survival (PFS)

CD4 Counts

CD8 Counts

Characterization of Histologic Subtypes in HIV-HL in the HAART Era

Complete Response Rate

Event-free Survival

Frequency of Adverse Events

Incidence of Neurotoxicity

Maximal Tolerated Dose of Brentuximab Vedotin (Phase I)

Partial Response Rate

Viral Load

Limiting Toxicity

Duration of Response

Percentage of Participants With Complete Response (CR) or Partial Response (PR) (Response Rate) at 12 Weeks

Percentage of Participants With Complete Response (CR) or Partial Response (PR) [Overall Response Rate (ORR)]

Percentage of Participants With Stable Disease (SD) or Better (Disease Control Rate) at 12 Weeks

Percentage of Participants With Stable Disease (SD) or Better (Disease Control Rate) at 6 Weeks

Progression Free Survival (PFS)

Number of Participants With Adverse Events (AE)

Anti-MAGE-A3 Antibody Concentrations

Concentrations of Antibodies Against Protein D (Anti-PD)

Duration of Stable Disease (SD) Response to MAGE-A3 ASCI Study Treatment

Number of Patients Reported With Serious Adverse Events (SAEs)

Number of Patients With Treatment Response for Anti-MAGE-A3 Antibodies

Number of Patients With Treatment Response for Anti-PD

Number of Seroconverted Patients for Melanoma Antigen (Anti-MAGE-A3)

Overall Survival (OS) by Gene Signature

Progression-free Survival (PFS) After Slow Progressive Disease (SPD) by Gene Signature

Progression-free Survival (PFS) by Gene Signature

Progression-free Survival (PFS) for the Overall Population

Time to Treatment Failure (TTF), by Gene Signature

Number of Patients Reported With Unsolicited Adverse Events (AEs) That Were Causally Related to Treatment Administration by Maximum Grade.

Number of Patients With Abnormal Alanine Aminotransferase (ALT) Values by Maximum Grade

Number of Patients With Abnormal Alkaline Phosphatase (ALK) Values by Maximum Grade

Number of Patients With Abnormal Aspartate Aminotransferase (AST) Values by Maximum Grade

Number of Patients With Abnormal Bilirubine (BIL) Values by Maximum Grade.

Number of Patients With Abnormal Creatinine (CREA) Values by Maximum Grade

Number of Patients With Abnormal Gamma-glutamyl Transpeptidase (GGT) Values by Maximum Grade

Number of Patients With Abnormal Hemoglobin (HGB) Values by Maximum Grade

Number of Patients With Abnormal Hypercalcemia (HCA) Values by Maximum Grade

Number of Patients With Abnormal Hyperkalemia (HKA) Values by Maximum Grade

Number of Patients With Abnormal Hypernatremia (HNA) Values by Maximum Grade