Page last updated: 2024-11-08

cortisone

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Cross-References

ID SourceID
PubMed CID222786
CHEMBL ID1499
CHEBI ID16962
SCHEMBL ID4888
MeSH IDM0005219

Synonyms (160)

Synonym
MLS001076142
BRD-K43736954-001-03-3
AKOS015840096
pregn-4-en-17alpha,21-diol-3,11,20-trione
delta(4)-pregnene-17alpha,21-diol-3,11,20-trione
kortison
cortison
4-pregnene-17alpha,21-diol-3,11,20-trione
CHEBI:16962 ,
17,21-dihydroxypregn-4-ene-3,11,20-trione
pregn-4-ene-3,11,20-trione, 17,21-dihydroxy-
delta(sup4)-pregnene-17alpha,21-diol-3,11,20-trione
(8s,9s,10r,13s,14s,17r)-17-hydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-1,2,6,7,8,9,12,14,15,16-decahydrocyclopenta[a]phenanthrene-3,11-dione
NCI60_042165
PRESTWICK3_000273
cortisone [inn:ban]
cortisonum [inn-latin]
nsc 9703
einecs 200-162-4
17alpha-hydroxy-11-dehydrocorticosterone
cortisona [inn-spanish]
ai3-52938
[3h]cortisone
17alpha,21-dihydroxypregn-4-ene-3,11,20-trione
LMST02030090
EU-0100240
cortisone, >=98%
4-pregnene-17.alpha.,11,20-trione
17.alpha.,11,20-trione
cortisal
pregn-4-ene-3,20-trione, 17,21-dihydroxy-
11-dehydro-17-hydroxycorticosterone
.delta.(sup4)-pregnene-17.alpha.,11,20-trione
cortisate
wintersteiner's compound f
cortandren
cortivite
adrenalex
wln: l e5 b666 cv ov mutj a1 e1 fv1q fq
nsc-9703
pregn-4-en-17.alpha.,11,20-trione
kendall's compound
17-hydroxy-11-dehydrocorticosterone
nsc9703
reichstein fa
andreson
17.alpha.-hydroxy-11-dehydrocorticosterone
cortogen
cortistal
PRESTWICK_132 ,
cas-53-06-5
BPBIO1_000162
PRESTWICK2_000273
BSPBIO_000146
cortisone (inn)
cortisone (tn)
D07749
LOPAC0_000240
SPECTRUM5_002051
[3h]-cortisone
C00762
reichstein's substance fa
kendall's compound e
CORTISONE ,
53-06-5
17alpha,21-dihydroxy-4-pregnene-3,11,20-trione
NCGC00023939-06
NCGC00023939-05
NCGC00095935-01
smr000058334
MLS000028540 ,
PRESTWICK1_000273
PRESTWICK0_000273
SPBIO_002365
NCGC00023939-03
NCGC00023939-07
NCGC00023939-04
kendall's compound e; 4-pregnene-17alpha,21-diol-3,11,20-trione; reichstein's substance fa
C 2755
HMS2052A21
NCGC00023939-09
MLS002207137
CHEMBL1499
BMSE000663
(10r,13s,17r)-17-hydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-1,2,6,7,8,9,12,14,15,16-decahydrocyclopenta[a]phenanthrene-3,11-dione
HMS1568H08
NCGC00023939-08
HMS2095H08
HMS3260P21
dtxsid5022857 ,
NCGC00255108-01
dtxcid102857
tox21_301440
tox21_111539
MLS001424269
HMS2235P19
CCG-101143
unii-v27w9254fz
cortisona
v27w9254fz ,
cortisonum
LP00240
cortisone [usp-rs]
prednisone impurity a [ep impurity]
cortisone [inn]
hydrocortisone impurity b [ep impurity]
cortisone [who-dd]
cortisone [vandf]
cortisone [mi]
AKOS015894868
S5869
gtpl5171
NC00393
bdbm13739
(1s,2r,10s,11s,14r,15s)-14-hydroxy-14-(2-hydroxyacetyl)-2,15-dimethyltetracyclo[8.7.0.0^{2,7}.0^{11,15}]heptadec-6-ene-5,17-dione
SCHEMBL4888
tox21_111539_1
NCGC00023939-11
NCGC00260925-01
CS-5097
tox21_500240
W-105776
ricortex (salt/mix)
cortelan (salt/mix)
17.alpha.,21-dihydroxy-4-pregnene-3,11,20-trione
cortadren (salt/mix)
scheroson (salt/mix)
4-pregnene-17.alpha.,21-diol-3,11,20-trione
corlin (salt/mix)
17.alpha.,21.beta.-dihydroxypregn-4-ene-3,11,20-trione
.delta.4-pregnene-17.alpha.,21-diol-3,11,20-trione
pregn-4-en-17.alpha.,21-diol-3,11,20-trione
HY-17461
AC-33118
OPERA_ID_541
mfcd00003610
cortisone, certified reference material, tracecert(r)
cortisone 0.1 mg/ml in methanol
sr-01000000094
SR-01000000094-3
HMS3712H08
Q423185
DB14681
AS-11686
SDCCGSBI-0050228.P002
NCGC00023939-15
D96089
pregn-4-ene-3,11,20-trione, 17,21-dihydroxy
17,21-dihydroxy-pregn-4-ene-3,11,20-trione
UQC ,
therapeutic cortisone
cortisone (usp-rs)
hydrocortisone impurity b (ep impurity)
h02ab10
cortisona (inn-spanish)
cortisonum 30 special order
s01ba03
prednisone impurity a (ep impurity)
cortisonum (inn-latin)
cortisone, 1mg/ml in methanol

Research Excerpts

Overview

Cortisone (CRT) is a corticosteroid clinically used for the management of inflammatory diseases like colitis and other inflammatory bowel diseases. Cortisone is an injected anti-inflammatory drug that can cause painful side effects known as "steroid flares" which are caused by cortisone crystallizing at the injection site.

ExcerptReferenceRelevance
"Cortisone is a metabolite belonging to the corticosteroid class that is used pharmaceutically directly as a drug or prodrug. "( Biological activity of new bioactive steroids deriving from biotransformation of cortisone.
Beggiato, S; Buzzi, R; Costa, S; Ferraro, L; Grandini, A; Manfredini, S; Sacchetti, G; Tedeschi, P; Valacchi, G, 2022
)
2.39
"Cortisone (CRT) is a corticosteroid clinically used for the management of inflammatory diseases like colitis and other inflammatory bowel diseases."( Cortisone-loaded stearoyl ascorbic acid based nanostructured lipid carriers alleviate inflammatory changes in DSS-induced colitis.
Ahmad, A; Ali, A; Almashjary, MN; Jori, C; Khan, R; Kumar, A; Mishra, RK; Raza, SS; Tabrez, S; Zughaibi, TA, 2023
)
3.07
"Cortisone is a steroid widely used as an anti-inflammatory drug able to suppress the immune system, thus reducing inflammation and attendant pain and swelling at the site of an injury. "( Biotransformation of Cortisone with
Bertolasi, V; Buzzi, R; Costa, S; Pedrini, P; Semeraro, B; Summa, D; Vertuani, S; Zappaterra, F, 2021
)
2.38
"Cortisone is an injected anti-inflammatory drug that can cause painful side effects known as "steroid flares" which are caused by cortisone crystallizing at the injection site. "( The Lipid Bilayer Provides a Site for Cortisone Crystallization at High Cortisone Concentrations.
Alsop, RJ; Hub, JS; Khondker, A; Rheinstädter, MC, 2016
)
2.15
"Cortisone is a highly potent inhibitor of influenza virus synthesis in the chick embryo, inducing manifest inhibition in doses of 0.1 to 1.0 microg/egg. "( The influence of cortisone on experimental viral infection. V. Inhibition of influenza virus synthesis.
KILBOURNE, ED, 1957
)
2.02
"Cortisone is an endogenous corticosteroid that has negligible intrinsic glucocorticoid activity but can be converted to the active corticosteroid cortisol by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1). "( Circulating cortisone levels are associated with biochemical markers of bone formation and lumbar spine BMD: the Hertfordshire Cohort Study.
Cooper, C; Cooper, MS; Dennison, EM; Fall, CH; Stewart, PM; Syddall, HE; Wood, PJ, 2005
)
2.15
"Cortisone was found to be a valuable aid to the therapy arsenal."( Treatment and prognosis of diffuse sclerosing osteomyelitis (DSO) of the mandible.
Hollender, L; Jacobsson, S, 1980
)
0.98

Effects

Cortisone has a large content in rivers because of its wide range of medical applications and elimination by organisms that naturally secrete it. It has been proposed as a useful additional biomarker for stress research.

ExcerptReferenceRelevance
"Cortisone has a large content in rivers because of its wide range of medical applications and elimination by organisms that naturally secrete it. "( Chronic exposure to cortisone induces thyroid endocrine disruption and retinal dysfunction in adult female zebrafish (Danio rerio).
Geng, Y; Guo, Y; Hou, L; Huang, M; Wu, Y; Zou, H, 2023
)
2.68
"Cortisone has a large content in rivers because of its wide range of medical applications and elimination by organisms that naturally secrete it. "( Chronic exposure to cortisone induces thyroid endocrine disruption and retinal dysfunction in adult female zebrafish (Danio rerio).
Geng, Y; Guo, Y; Hou, L; Huang, M; Wu, Y; Zou, H, 2023
)
2.68
"Cortisone has been proposed as a useful additional biomarker for stress research. "( Hair cortisone level is associated with PTSD׳s dysphoric arousal symptoms in highly traumatized Chinese females.
Cao, C; Deng, H; Wang, L; Wang, W; Xu, H; Zhang, J, 2015
)
2.37
"Cortisone has been shown to induce the de novo synthesis of protein alpha."( [Specific acid-soluble chromatin protein synthesized in the rat liver after cortisone administration].
Iakovleva, MF; Konstantinova, IM; Turoverova, LV; Vorob'ev, VI,
)
1.08

Actions

The cortisone caused an increase in the serum cholesterol, fatty metamorphosis of the liver, and fat emboli visible in sections of the femur and humerus. Free cort isone was slightly lower in the pill group.

ExcerptReferenceRelevance
"of cortisone may cause depression of resistance and may decrease the survival time for 3 to 6 days afterward."( The effect of adrenal steroids, corticotropin, and growth hormone on resistance to experimental infections.
FINLAND, M; KASS, EH; LUNDGREN, MM, 1954
)
0.75
"The cortisone caused an increase in the serum cholesterol, fatty metamorphosis of the liver, and fat emboli visible in sections of the femur and humerus."( Fat-cell changes as a mechanism of avascular necrosis of the femoral head in cortisone-treated rabbits.
Reger, SI; Sweet, DE; Thompson, RC; Wang, GJ, 1977
)
0.97
"Free cortisone was slightly lower in the pill group (I: 10.8 +/- 2.55 nmol/l; II 8.5 +/- 1.86 nmol/l) whereas salivary cortisone was 2.3 (I) and 4.4 (II) times higher than plasma free cortisone and tended to follow the plasma free and salivary cortisol pattern, both within and between the study groups.(ABSTRACT TRUNCATED AT 250 WORDS)"( The effect of oral contraceptives on plasma-free and salivary cortisol and cortisone.
Benraad, TJ; Meulenberg, PM; Ross, HA; Swinkels, LM, 1987
)
0.96
"The cortisone-mediated increase in intestinal sucrase activity which normally occurs by 20 days is not effected by prolonged suckling."( Intestinal glucose metabolism during development. II. The role of glucocorticoids and weaning.
Kimura, RE; Reinersman, GT, 1985
)
0.75

Treatment

Cortisone treatment in cholesterol-fed rabbits did not significantly affect the levels of serum lipoproteins, cholesterol concentration, or atherosclerosis. Cortisone acetate treatment which was sufficient for eggs inoculated to mature (a total of 75 or even 200 mg, from Day 5 of egg inoculation) had no effects of immunosuppression.

ExcerptReferenceRelevance
"Cortisone treatment also reduced basal and insulin-stimulated glucose oxidation in adipose tissue, increased plasma glucose levels after administration of the pyruvate, the substrate of gluconeogenesis, and increased liver glycogen content."( An 11-Beta Hydroxysteroid Dehydrogenase Type 1 Inhibitor, JTT-654 Ameliorates Insulin Resistance and Non-obese Type 2 Diabetes.
Fukuda, S; Goto, H; Heitaku, S; Katsumi, S; Maki, M; Nishiu, J; Sasase, T; Sotani, T; Yamamoto, H, 2023
)
1.63
"Cortisone acetate treatment at 20-wk posttransplantation accelerated the ontogeny of lactase but did not alter sucrase and trehalase activities."( Normal and glucocorticoid-induced development of the human small intestinal xenograft.
Fernandez, I; Klopcic, CE; Nanthakumar, NN; Walker, WA, 2003
)
1.04
"Non-cortisone-treated asthmatic patients displayed higher levels of both R- and S-salbutamol in plasma than did healthy volunteers after one single ingestion of racemic salbutamol (CMAX both comparisons P<0.05)."( Metabolism of salbutamol differs between asthmatic patients and healthy volunteers.
Ahlner, J; Andersson, RG; Josefsson, M; Naidu Sjöswärd, K; Schmekel, B, 2003
)
0.8
"(3) Cortisone treatment caused a moderate hypercholesterolemia in normal rabbits."( The effect of cortisone on the serum lipids and on the development of experimental cholesterol atherosclerosis in the rabbit.
DUFF, GL; GORDON, D; KOBERNICK, SD; McMILLAN, GC, 1954
)
1.08
"The cortisone treatment had thus completely suppressed immunity."( The effect of cortisone on the multiplication of M. tuberculosis in normal and immune mice.
ROBSON, JM; SULLIVAN, FM, 1957
)
1.08
"Cortisone-treated mice were inoculated with vaccinia virus, and then five paintings of methylcholanthrene were applied over the site of inoculation. "( Vaccinia dermal infection and methylcholanthrene in cortisone-treated mice.
DURAN-REYNALS, ML; STANLEY, B, 1961
)
1.93
"Cortisone treatment reversed these changes noted in the ileum."( Rat transcobalamin: cloning and regulation of mRNA expression.
Kalra, S; Seetharam, B; Seetharam, S; Yammani, RR, 2004
)
1.04
"In cortisone-treated rabbits, a single intradermal injection of toxin produced a primary reaction of hemorrhage and necrosis in the skin at the injected site."( The effect of cortisone on the Shwartzman reaction; the production of lesions resembling the dermal and generalized Shwartzman reactions by a single injection of bacterial toxin in cortisone-treated rabbits.
GOOD, RA; THOMAS, L, 1952
)
1.11
"Cortisone treatment in cholesterol-fed rabbits did not significantly affect the levels of serum lipoproteins, cholesterol concentration, or atherosclerosis produced by a 1.0 per cent cholesterol diet alone."( The effects of cholesterol dosage, cortisone, and DCA on total serum cholesterol, lipoproteins, and atherosclerosis in the rabbit.
CALVIN, LD; COOK, DL; DAVISSON, E; FELDSTEIN, LM; GREEN, DM; RAY, G, 1952
)
1.23
"Cortisone treatment had no effect on time of peak response to Con A stimulation but significantly depressed (P less than or equal to 0.05) the magnitude of the response."( Delayed T-cell maturation and suppression of mitogen-induced blastogenesis in turkey poults fed cortisone acetate and furazolidone.
Czarnecki, CM; Dunnette, JL; Redig, PT,
)
1.07
"Cortisone acetate treatment which was sufficient for eggs inoculated to mature (a total of 75 or even 200 mg, from Day 5 of egg inoculation) had no effects of immunosuppression, whereas cortisone acetate treatment which was sufficient for immunosuppression (a total of 150 mg from Day -2, two days prior to the initial egg inoculation) induced some adult formation as well."( Hymenolepis nana: maturation in an immunosuppressed unnatural rat host.
Ito, A, 1983
)
0.99
"Cortisone-treated subcutaneously injected animals did not develop a leukocytosis."( Experimental pythiosis in rabbits.
Campbell, RS; Miller, RI, 1983
)
0.99
"Cortisone treatment thus accelerates development of adult permeability characteristics in the pulmonary epithelium."( Effect of cortisone on permeability of the neonatal rat lung to drugs.
Hemberger, JA; Schanker, LS, 1981
)
1.39
"Cortisone treatment affected the ability of peritoneal exudate cells to respond to migratory inhibition after exposure to purified whole organisms of C."( Reactivation of Chlamydia trachomatis lung infection in mice by cortisone.
Chen, WJ; Kuo, CC; Yang, YS, 1983
)
1.23
"Cortisone treatment of mice was found to lower their resistance to infection at a given spore dosage as measured by ET50 values."( The comparative virulence of thermotolerant Mucorales species in mice.
Cazin, J; Embree, RW; Kitz, DJ, 1983
)
0.99
"Cortisone treatment resulted in a decrease in corticosterone output by quartered adrenals and an earlier and more marked drop in corticosterone production by whole adrenal homogenates."( Effects of long-term steroid suppression on rat adrenal 5 alpha-reductase and 11 beta-hydroxylase activities and corticosterone production in vitro.
Malendowicz, LK, 1982
)
0.99
"Cortisone-treated rabbits provide a new and expedient laboratory model for cryptococcal disease."( Chronic cryptococcal meningitis: a new experimental model in rabbits.
Durack, DT; Lang, SD; Perfect, JR, 1980
)
0.98
"Cortisone and T4 treatment was associated with increased rough endoplasmic reticulum and nucleolar enlargement, while GH treatment was associated with marked dilatation of the endoplasmic reticulum."( Hormone responsiveness of a transplantable rat chondrosarcoma: III. ultrastructural evidence of in vivo hormone dependence.
Lebovitz, HE; McCarty, KS; McCumbee, WD, 1981
)
0.98
"Cortisone treatment produced a profound leukocytosis, lymphocytopenia, and monocytopenia in the peripheral blood while decreasing by greater than 40% the number of AM obtainable by lung washings."( The effects of cortisone therapy on lung macrophage host defense function and glucose metabolism.
Gudewicz, PW, 1981
)
1.34
"In cortisone-treated mice, on the other hand, the yeasts caused mortalities, the extent of which varied according to the infecting species and the challenge dose."( Pathogenicity of some ordinarily harmless yeasts for cortisone-treated mice.
Damodaran, VN; Khan, ZU; Misra, VC; Randhawa, HS, 1980
)
1.02
"Cortisone treatment attenuated these effects."( Immune-modulatory drugs alter Candida albicans-induced sleep patterns in rabbits.
Toth, LA, 1995
)
1.01
"Cortisone treatment of rats resulted in both hyperglycemia and hyperinsulinemia."( Glucocorticoid regulation of insulin receptor and substrate IRS-1 tyrosine phosphorylation in rat skeletal muscle in vivo.
Almahfouz, A; Giorgino, F; Goodyear, LJ; Smith, RJ, 1993
)
1.01
"In cortisone treated and diabetic groups, mild cellular reaction was observed."( Effect of immunomodulation on experimental hymenolepiasis nana in mice.
el Kadery, AA; Makled, MK; Mohamed, NH; Otifa, NM; Sabry, NM; Soffar, SA, 1994
)
0.8
"Cortisone treatment of patients suffering from systemic lupus erythematosus and rheumatoid arthritis impressively normalized elevated XOD concentrations in rheumatic sera to those of healthy controls."( Elevated levels of xanthine oxidase in serum of patients with inflammatory and autoimmune rheumatic diseases.
Miesel, R; Zuber, M, 1993
)
1.01
"Cortisone treatment of patients with rheumatoid arthritis, systemic lupus erythematosus, and polymyalgia rheumatica replenished impressively the serum concentration of Cu-thionein."( Copper-dependent antioxidase defenses in inflammatory and autoimmune rheumatic diseases.
Miesel, R; Zuber, M, 1993
)
1.01
"Cortisone treatment provoked a decline in the number of microglial cells but did not modify GFAP levels in control rats which were not exposed to HI."( Microglia-astrocyte interactions after cortisone treatment in a neonatal hypoxia-ischemia model.
Bona, E; Hagberg, H; McRae, A, 1996
)
1.28
"Cortisone treatment on day 12 induced a precocious increase of H and decrease of L mRNA expression on day 15."( Glucocorticoids and dietary iron regulate postnatal intestinal heavy and light ferritin expression in rats.
Glass, J; Yeh, KY; Yeh, M, 2000
)
1.03
"Cortisone pretreatment considerably enhances the mortality of young, male, streptozotocin-injected Holtzman rats. "( Modification of streptozotocin-induced diabetes in rats by pretreatment with cortisone.
Volk, BW; Wellmann, KF, 1977
)
1.93
"Cortisone treatment rendered mice susceptible to killing by 22114."( Comparison of the growth of virulent and attenuated strains of Candida albicans in the kidneys of normal and cortison-treated mice by chitin assay.
Gibb, E; Newham, HC; Richardson, MD; Warren, RC; White, LO, 1979
)
0.98
"Cortisone or T3 treatment to mothers increased sucrase and maltase activity in jejunum and ileum of the offspring."( Effect of cortisone or L-triiodothyronine administration to pregnant rats on the activity of fetal intestinal disaccharidases and lysosomal acid beta-galactosidase.
Celano, P; Horowitz, C; Jumawan, J; Koldovsky, O; Lau, H, 1977
)
1.38
"Cortisone pretreatment for four days to intact mice (10 mg/kg/day/4 days) had a significant protective effect in both males and females against arachidonate toxicity, eliminating the sex difference previously observed."( Effect of corticosteroids on arachidonate induced mortality in male and female mice.
Montalbert-Smith, M; Penhos, JC; Rabbani, F; Ramey, E; Ramwell, PW, 1979
)
0.98
"Cortisone-treated Buffalo rats have been parabiosed with untreated controls of the same age. "( Cortisone induced alterations of costal cartilage in single and in parabiosed rats.
Dearden, LC; Espinosa, T; Mosier, HD, 1978
)
3.14
"Cortisone-treated animals expelled primary worm burdens without complication about 2 wk after steroid treatment."( Strongyloides ratti infections in rats. II. Effects of cortisone treatment.
Olson, CE; Schiller, EL, 1978
)
1.23
"Cortisone treatment prevented or markedly decreased this phenomenon indicating that cortisone exerts a definite inhibitory effect upon vascular permeability to antibody molecules."( Effect of cortisone upon vascular permeability to antibody.
Germuth, FG; Valdes, AJ, 1978
)
1.38
"Cortisone treatment of the donors of effector cells revealed that the cortisone resistant subpopulation of thymocytes, 2 days after cortisone injection, exhibited an increased cytotoxicity against target cells treated with unfractionated antiserum and its IgM fraction."( Antibody-dependent cell-mediated cytotoxicity in the Moloney sarcoma virus system: differential activity of IgG and IgM with different subpopulations of lymphocytes.
Fuson, EW; Goodson, S; Lamon, EW; Lidin, B; Shaw, MW; Walia, AS, 1977
)
0.98
"Only cortisone acetate treatment caused a true delay in ovo-implantation."( Studies on the effects of pharmacologic doses of cortisone acetate and several nonsteroidal anti-inflammatory compounds on ovo-implantation, early pregnancy, and the deciduomal response in the rat.
Bennett, DR; Cochrane, RL; Powell, JG; Rathmacher, RP; Shaar, CJ; Smalstig, EB, 1977
)
0.97
"Cortisone pretreatment rendered mice more susceptible to infection by A."( Chitin assay used to demonstrate renal localization and cortisone-enhanced growth of Aspergillus fumigatus mycelium in mice.
Lehmann, PF; White, LO, 1975
)
1.22
"Cortisone treatment of the neonate results in near-adult levels of alpha 1 mRNA expression."( Expression and developmental regulation of Na+,K+ adenosine triphosphatase in the rat small intestine.
Chu, SH; Walker, WA; Zemelman, BV, 1992
)
1
"Cortisone treatment attenuated these effects in S."( Modulation of sleep by cortisone in normal and bacterially infected rabbits.
Gardiner, TW; Krueger, JM; Toth, LA, 1992
)
1.32
"In cortisone-treated rats recovering for 1-3 weeks, the FCFU census and EsMR normalized during the first posttreatment week, remained at control levels after 2-3 weeks, and exhibited a relapse in the third week which signified only partial recovery."( Effect of cortisone on cells at the bone-marrow interface.
Kidder, L; Simmons, DJ; Thomas, M, 1990
)
1.2
"Cortisone and insulin treatments reduced WGA and enhanced UEA bindings to UN membranes."( Effect of malnutrition and hormone treatments on intestinal microvillus membrane glycosylation in suckling rats.
Babbar, HS; Jaswal, VM; Mahmood, A, 1990
)
1
"Cortisone acetate treatment, which produced impaired cell-mediated immune function, was followed by nasal inoculation of 5 x 10(4) CFU of N."( Therapy of pulmonary nocardiosis in immunocompromised mice.
Aulicino, TM; Berkowitz, LB; duBouchet, L; Gombert, ME, 1990
)
1
"Cortisone treatment was used to study non-malignant proliferation."( Comparative analysis and anatomic distribution of ras p21, IL-2R, and MEL-14 in malignant and hyperplastic murine thymus.
Cordon, C; Newcomb, EW; Pellicer, A, 1990
)
1
"Only cortisone-MTP treatment led to an absence of capillary extension from surrounding blood vessels into the scant tumor stroma."( Evaluation of cortisone-heparin and cortisone-maltose tetrapalmitate therapies against rodent tumors. II. Pathological studies.
Benrezzak, O; Elhilali, M; Madarnas, P; Nigam, VN; Pageau, R,
)
0.95
"Cortisone treatment (5 days) resulting in weight loss, hyperglycemia, and hyperinsulinemia did not affect the number, insulin binding affinity, or kinase activity of solubilized receptors activated with insulin in vitro or in vivo."( Effects of hypercortisolemia and diabetes on skeletal muscle insulin receptor function in vitro and in vivo.
Block, NE; Buse, MG, 1989
)
1
"Cortisone treatment significantly stunted body wt, tail length, and tibia length."( Rats stunted by high-dose glucocorticoid treatment are capable of undergoing catch-up growth after fasting.
Jansons, RA; Mosier, HD, 1989
)
1
"Cortisone-treated animals had a diffuse, progressive pneumonitis, but the influx of neutrophils to the lung, the serum antibody response, and the sensitization of splenocytes to L."( Impaired clearance of aerosolized Legionella pneumophila in corticosteroid-treated rats: a model of Legionnaires' disease in the compromised host.
Martin, TR; Schmidt, RA; Skerrett, SJ, 1989
)
1
"Cortisone treatment (10 mg X 100 g body wt-1 X day-1 for 2-5 days) resulted in an approximate doubling of the percentage of active enzyme."( Glucocorticoid-mediated activation of muscle branched-chain alpha-keto acid dehydrogenase in vivo.
Block, KP; Buse, MG; Mehard, WB; Richmond, WB, 1987
)
0.99
"Cortisone treatment was started 24 h after testicular torsion and continued for 4 weeks."( The effect of testicular torsion on the contralateral testis and the value of various types of treatment.
Amato, S; Buyuksu, C; Canda, MS; Kaplanoglu, N; Mertan, S; Sade, M, 1988
)
1
"Cortisone treatment also resulted in the worms being located more anteriorly in the small intestine."( Immunological aspects in the rejection process of Hymenolepis muris-sylvaticae from CFLP and NMRI mice.
De Rycke, PH; Van Haeren, C, 1986
)
0.99
"Cortisone-treated animals had a normal periodicity of GH plasma concentration, but they showed a reduction in values in the range of 50 to 99 ng/ml (P less than 0.01) and an increase of values in the range of 200 to 499 ng/ml (P less than 0.025) and above 1000 ng/ml (P less than 0.05)."( Increase in pulsatile secretion of growth hormone during failure of catch-up growth following glucocorticoid-induced growth inhibition.
Jansons, RA; Mosier, HD, 1985
)
0.99
"Cortisone-treated mice regularly developed infections after inoculation by any of the routes tested."( Pathogenicity of Allescheria boydii for mice.
Cazin, J; Lupan, DM, 1973
)
0.97
"Cortisone-treated human liver tissue, obtained by needle biopsy, also shows an increase in acid alpha-glucosidase activity."( Studies on type II glycogenosis. Effects of cortisone derivatives on acid -glucosidase.
Bourne, EJ; Clarke, K; Pridham, JB; Rowe, JJ, 1971
)
1.23
"Cortisone-treated animals tolerated their allografts for at least 3 weeks."( Effect of synthetic progestational agents on allograft rejection and circulating antibody production.
Hulka, JF; Lieberman, MW; Mohr, K, 1965
)
0.86
"Cortisone treatment results in an increase in average parenchymal cell cytoplasmic volume from 5100 to 5800 micro(3) and a decrease in average nuclear diameter from 7.1 to 6.5 micro."( A quantitative description of cortisone-induced alterations in the ultrastructure of rat liver parenchmal cells.
Kimberg, DV; Loud, AV; Spiro, D; Wiener, J, 1968
)
1.26
"Cortisone treatment is responsible for a 14-40% decrease in the amount of oxygen consumed per mg of mitochondrial protein when succinate, alpha-ketoglutarate, or beta-hydroxybutyrate are used as substrates, or with ascorbate and N,N,N(1),N(1)-tetramethyl p-phenylenediamine as electron donors."( Cortisone-induced alterations in mitochondrial function and structure.
Kimberg, DV; Loud, AV; Wiener, J, 1968
)
2.41
"Mice treated with cortisone yielded both the avirulent bacteria and virulent C."( CORYNEBACTERIAL PSEUDOTUBERCULOSIS IN MICE. II. ACTIVATION OF NATURAL AND EXPERIMENTAL LATENT INFECTIONS.
DUBOS, R; FAUVE, RM; PIERCE-CHASE, CH, 1964
)
0.57
"Treatment with cortisone did not alter the antibody titres."( Attempts to infect experimentally immunosuppressed iris monkeys (Macaca iris) with Brugia malayi.
Aiyar, S, 1983
)
0.61
"Pretreatment with cortisone (40 mg/kg) reduced the permeability changes induced by trypsinated serum but had no significant effect on trypsin-induced leakages."( Anti-inflammatory agents inhibit leukocyte accumulation and vascular leakage induced by trypsin and trypsin-digested serum in hamster cheek pouch.
Heideman, M; Roxvall, L; Sennerby, L, 1993
)
0.61
"Mice treated with cortisone acetate and with cyclosporin A, respectively, as well as athymic nice were injected intravenously, intranasally, perorally and subcutaneously with spores of Nosema algerae, a microsporidian species of culicine mosquitoes."( Opportunistic properties of Nosema algerae (Microspora), a mosquito parasite, in immunocompromised mice.
Doehring, M; Dombrowski, F; Maier, WA; Seitz, HM; Trammer, T,
)
0.45
"Treatment with cortisone up to 18 months later reactivated virus latent in the ganglia, and virus returned to the skin where it produced small but typical herpes lesions which shed virus."( Hazards from simian herpes viruses: reactivation of skin lesions with virus shedding.
McCarthy, K; Tosolini, FA, 1975
)
0.59
"2. Treatment with cortisone between 3 and 5 weeks of age markedly suppressed growth but did not inhibit GH secretion."( Plasma growth hormone concentrations in growth-retarded, cortisone treated chickens.
Harvey, S; Scanes, CG, 1979
)
0.83
"Treatment with cortisone acetate, however, markedly retarded spontaneous tumor development."( Enhancement and retardation of spontaneous reticulum cell neoplasm development in SJL/J mice.
Ben-Yaakov, M; Haran-Ghera, N; Meshorer, A, 1975
)
0.59
"Treatment with cortisone significantly reduced the CSF chemotactic activity for both cell types; this reduction may contribute to the severe CSF leukopenia observed in cortisone-treated animals, which are unable to eradicate this yeast infection."( Chemotactic activity of cerebrospinal fluid in experimental cryptococcal meningitis.
Durack, DT; Perfect, JR, 1985
)
0.61

Toxicity

ExcerptReferenceRelevance
"Striking mortality in mice receiving amphotericin B and cortisone acetate concomitantly prompted studies to characterize the toxic interaction of these two drugs further."( Synergistic nephrotoxicity of amphotericin B and cortisone acetate in mice.
Evan, AP; Kisch, AL; Maydew, RP, 1978
)
0.76
" To determine if both groups of substances act through similar biologic mechanisms, their capacity to protect macrophages from the direct toxic effects of LPS was examined in vitro."( Inhibition of LPS toxicity for macrophages by metallothionein-inducing agents.
Costa, M; Lewis, VM; Patierno, SR; Peavy, DL, 1983
)
0.27
"To emphasize an underestimated side effect following long-term use of steroids."( Subacute steroid-induced paraparesis: surgical treatment of a devastating "invisible" side effect.
Goessling, T; Huefner, T; Javad Mirzayan, M; Krauss, JK; Mirzayan, MJ, 2012
)
0.38

Pharmacokinetics

A trace amount (5 mg) of stable isotopically labelled cortisol was administered orally to a healthy human subject. The pharmacokinetic and biopharmaceutic profiles of a single dose of oral cortisone acetate were developed for 23 healthy normal adult volunteers.

ExcerptReferenceRelevance
"The pharmacokinetic and biopharmaceutic profiles of a single dose of oral cortisone acetate were developed for 23 healthy normal adult volunteers using cortisone and cortisol plasma concentration data."( Pharmacokinetic interpretation of plasma cortisol and cortisone concentrations following a signle oral administration of cortisone acetate to human subjects.
Colburn, WA; DeSante, KA; DiSanto, AR; Monovich, RE; Stubbs, SS, 1980
)
0.74
"Stable isotopically labeled steroids can, without radiation hazards, be safely used as biological internal standards to perform pharmacokinetic studies of steroids in man."( [Stable isotope methodology in the pharmacokinetic study of steroids].
Kasuya, Y, 1994
)
0.29
"A trace amount (5 mg) of stable isotopically labelled cortisol ([1,1,19,19,19-2H5]cortisol, cortisol-d5) was administered orally to a healthy human subject to examine the pharmacokinetic behaviour of exogenous cortisol and study the interconversion of cortisol to cortisone catalysed by 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD)."( Pharmacokinetic studies of cortisol after oral administration of deuterium-labelled cortisol to a normal human subject.
Furuta, T; Iwano, M; Kasuya, Y; Shibasaki, H, 1995
)
0.47
" Using data from a previously performed single-dose study and present multiple-dose treatment, a physiologically based pharmacokinetic model for glycyrrhetic acid was developed."( A population physiologically based pharmacokinetic/pharmacodynamic model for the inhibition of 11-beta-hydroxysteroid dehydrogenase activity by glycyrrhetic acid.
Deerenberg, C; DeJongh, J; Mensinga, T; Meulenbelt, J; Ploeger, B; Sips, A, 2001
)
0.31
" The area under the DXM plasma concentration curve (AUC) was 113."( Pharmacokinetics of dexamethasone with pharmacokinetic/pharmacodynamic model of the effect of dexamethasone on endogenous hydrocortisone and cortisone in the horse.
Boston, RC; Guan, F; Luo, Y; Moate, PJ; Soma, LR; Uboh, CE, 2005
)
0.53
"PK parameters were studied for total serum cortisol (SerF), free serum cortisol (FreeF) and cortisone (FreeE), and salivary cortisol (SalF) and cortisone (SalE): area under the curve (AUC), clearance (CL), half-life and volume of distribution (V(d))."( Corticosteroid-binding globulin regulates cortisol pharmacokinetics.
Aarons, L; Miller, AG; Perogamvros, I; Ray, DW; Trainer, PJ, 2011
)
0.59
"Following IV hydrocortisone, AUC and half-life of SerF were significantly higher in the OCP group and lower in the CBG null."( Corticosteroid-binding globulin regulates cortisol pharmacokinetics.
Aarons, L; Miller, AG; Perogamvros, I; Ray, DW; Trainer, PJ, 2011
)
0.7
" Pharmacokinetic studies performed on these groups indicated that urinary free cortisol and cortisol-to-cortisone ratios can be treated as biomarkers of stress and depressive disorders."( Simultaneous determination of urinary cortisol, cortisone and corticosterone in parachutists, depressed patients and healthy controls in view of biomedical and pharmacokinetic studies.
Bączek, T; Konieczna, L; Kowalski, P; Olędzka, I; Plenis, A, 2011
)
0.84
" The serum concentrations of E and F were determined by HLPC and pharmacokinetic parameters were calculated using DASver2."( The effect of glycyrrhetinic acid on pharmacokinetics of cortisone and its metabolite cortisol in rats.
Chen, LG; Chen, XL; Ge, RS; Hu, GX; Li, WS; Lin, D; Sun, W; Wang, SH; Wang, Z, 2012
)
0.62
" Multicompartmental modeling was used to characterize the lung bioreactor data, and pharmacokinetic parameters, including elimination clearance and elimination half-life, were estimated."( Glucocorticoid Clearance and Metabolite Profiling in an In Vitro Human Airway Epithelium Lung Model.
Avram, MJ; Borenstein, JT; Coppeta, JR; Lever, AR; Rivera-Burgos, D; Sarkar, U; Tannenbaum, SR; Wishnok, JS, 2016
)
0.43
" The aim of the present study was to evaluate the pharmacokinetic (PK) and pharmacodynamic (PD) characteristics of evogliptin in participants with renal impairment (RI)."( Effects of renal impairment on the pharmacokinetics and pharmacodynamics of a novel dipeptidyl peptidase-4 inhibitor, evogliptin (DA-1229).
Bahng, MY; Cho, H; Cho, JY; Jang, IJ; Kim, AH; Kim, YS; Lee, S; Oh, J; Yoon, SH; Yu, KS, 2017
)
0.46

Compound-Compound Interactions

ExcerptReferenceRelevance
"Subcutaneous injection of cortisone acetate administered with or without oral heparin retarded the growth of two HSV-2 induced hamster fibrosarcomas."( Therapy of spontaneously metastatic HSV-2 induced hamster tumours with cortisone acetate administered with or without heparin.
Potter, CW; Rees, RC; Teale, DM; Underwood, JC, 1987
)
0.81
"To test the effect of a drug combination therapy on ocular perfusion in human eyes affected by idiopathic intermediate uveitis."( Effect of a drug combination treatment on ocular perfusion in recurrent idiopathic intermediate uveitis.
Cimino, L; Finzi, G; Gandolfi, SA; Mora, P; Orsoni, JG; Zavota, L, 2003
)
0.32
"In eyes affected by idiopathic intermediate uveitis, treated with a systemic drug combination therapy, the improvement of the visual acuity seems to correlate with a proportional improvement of the retrobulbar circulation."( Effect of a drug combination treatment on ocular perfusion in recurrent idiopathic intermediate uveitis.
Cimino, L; Finzi, G; Gandolfi, SA; Mora, P; Orsoni, JG; Zavota, L, 2003
)
0.32
" It is also suitable for future drug-drug interaction studies to continue evaluating the potential of these steroids as biomarkers for CYP3A inhibition and induction."( UHPLC-MS/MS bioanalysis of urinary DHEA, cortisone and their hydroxylated metabolites as potential biomarkers for CYP3A-mediated drug-drug interactions.
Arnold, ME; Aubry, AF; Buzescu, A; Christopher, LJ; Garonzik, SM; Ji, QC; Kandoussi, H; LaCreta, F; Ma, X; Zeng, J; Zheng, N, 2016
)
0.7

Bioavailability

GH replacement may lower bioavailability of hydrocortisone tablets. The relativeBioavailability of oral cortisol and cortisone acetate varied widely (cortisol 26-91%, mean 54 +/- 6%)

ExcerptReferenceRelevance
"Gastrointestinal absorption of cefazolin, which is poorly absorbed in adults, and of cephradine, which is well absorbed in adults, was studied in rats during their development."( Effect of gastrointestinal maturation on absorption of beta-lactam antibiotics.
Mizuno, N; Morita, E; Nishikata, M; Takahashi, K, 1992
)
0.28
"Cortisol bioavailability (total urine cortisol metabolites, urine free cortisol and cortisol binding globulin) was similar in both sexes."( Sexual dimorphism in 11 beta hydroxysteroid dehydrogenase activity and its relation to fat distribution and insulin sensitivity; a study in hypopituitary subjects.
Kelly, WF; Monson, JP; Taylor, NF; Weaver, JU; Wood, PJ, 1998
)
0.3
" The reduction in total cortisol metabolite excretion suggests that GH also affects bioavailability of hydrocortisone tablets."( Growth hormone replacement inhibits renal and hepatic 11 beta-hydroxysteroid dehydrogenases in ACTH-deficient patients.
Andrew, R; MacLeod, KM; Padfield, PL; Walker, BR, 1998
)
0.51
" Moreover, GH replacement may lower bioavailability of hydrocortisone tablets."( Effects of growth hormone replacement on cortisol metabolism in hypopituitary patients treated with cortisone acetate.
Beentjes, JA; Dullaart, RP; Kerstens, MN, 2001
)
0.77
" Enhancement of GC bioavailability is maintained or increased upon terminal differentiation induced by signals associated with innate immune activation."( Expression of 11beta-hydroxysteroid dehydrogenase type 1 permits regulation of glucocorticoid bioavailability by human dendritic cells.
Chakraverty, R; Evans, KN; Freeman, L; Hardie, D; Hewison, M; Hughes, SV; Means, TK, 2005
)
0.33
" Proinflammatory cytokines regulate 11beta-HSD1 expression in various cell types and thereby modulate the bioavailability of cortisol to the glucocorticoid receptor (GR)."( Th2 cytokine-induced upregulation of 11beta-hydroxysteroid dehydrogenase-1 facilitates glucocorticoid suppression of proasthmatic airway smooth muscle function.
Cao, J; Fatma, S; Grumbach, Y; Grunstein, JS; Grunstein, MM; Hu, A; Nino, G, 2009
)
0.35
" The aim of this study was to determine whether in major depression changes in the activity patterns of local modulators of glucocorticoid action might contribute to an increase in cortisol bioavailability and if they change during antidepressant treatment and clinical response."( Cortisol metabolism in depressed patients and healthy controls.
Deuschle, M; Frankhauser, P; Gilles, M; Hamann, B; Kopf, D; Lederbogen, F; Lewicka, S; Onken, V; Römer, B; Schilling, C, 2009
)
0.35
" These changes suggest an increase in cortisol bioavailability within tissues."( Cortisol metabolism in depressed patients and healthy controls.
Deuschle, M; Frankhauser, P; Gilles, M; Hamann, B; Kopf, D; Lederbogen, F; Lewicka, S; Onken, V; Römer, B; Schilling, C, 2009
)
0.35
" In addition, 25f has 94% oral bioavailability in rat and >1000× selectivity over 11β-HSD2."( Structure-based design and synthesis of 1,3-oxazinan-2-one inhibitors of 11β-hydroxysteroid dehydrogenase type 1.
Berbaum, J; Bruno, JG; Bukhtiyarov, Y; Cacatian, S; Carroll, PJ; Claremon, DA; Guo, J; Guo, R; Harrison, RK; He, W; Johnson, JA; Krosky, PM; Kruk, BA; Lindblom, P; McGeehan, GM; McKeever, BM; Panemangalore, R; Scott, BB; Singh, SB; Tice, CM; Togias, J; Xu, Z; Ye, YJ; Zhao, W; Zhao, Y; Zhuang, L, 2011
)
0.37
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51
"Our findings suggest that altered nocturnal cortisol metabolism and morning HPA axis hyperactivity in children with T1DM leads to greater cortisol bioavailability and lower cortisol production as a compensatory effect."( Altered Cortisol Metabolism Increases Nocturnal Cortisol Bioavailability in Prepubertal Children With Type 1 Diabetes Mellitus.
Barat, P; Bergeron, A; Brossaud, J; Corcuff, JB; Lienhardt, A; Moisan, MP; Valade, A; Vautier, V, 2021
)
0.62
" A satisfactory IVIVR was generated for cortisone, whereas testosterone and desoxycorticosterone showed higher bioavailability in vitro compared to in vivo."( Percutaneous absorption of steroids from finite doses: Predicting urinary excretion from in vitro skin permeation testing.
Anissimov, YG; Cheruvu, HS; Ghosh, P; Grice, JE; Liu, X; Ni, Z; Roberts, MS; Tsakalozou, E; van der Hoek, J, 2022
)
0.99

Dosage Studied

Hydrocortisone (free alcohol) is more than 50 per cent greater than that of either the free or acetated forms of cortisone. Cortisone in the dosage employed had no effect on the elimination of antigen following its intravenous administration.

ExcerptRelevanceReference
" Potencies of estrogens varied greatly, but all compounds tested prevented DIC at adequate dosage levels."( Disseminated intravascular coagulation induced by progesterone in the pregnant rat. Prevention by estogens.
Stamler, FW, 1977
)
0.26
" Potencies of estrogens varied greatly, but all compounds tested prevented DIC at adequate dosage levels."( Disseminated intravascular coagulation induced by progesterone in the pregnant rat. Prevention by estogens.
Stamler, FW, 1977
)
0.26
" Doubtless because of the effect of cortisone by itself the slope of the dose-response relationship for haptoglobin was greatly reduced."( Effects of bacterial endotoxin and corticosteroids on plasma concentrations of alpha 2 macroglobulin, haptoglobin and fibrinogen in rats.
Gordon, AH; Limaos, EA, 1979
)
0.53
" The mean height velocity attained at the optimal dosage (0."( Medical Research Council of Canada therapeutic trial of human growth hormone: first 5 years of therapy.
Bailey, JD; Beck, JC; Friesen, H; Guyda, H; Leboeuf, G, 1975
)
0.25
" Both values could not be correlated with the clinically individualised and satisfactory long-term substitution dosage and cannot be used, therefore, in the customary manner to assess a normal hormonal state."( [On the question of cortisol administration in adrenocortical insufficiency (author's transl)].
August, S; Hesch, RD; LeBlanc, S; von zur Mühlen, A, 1979
)
0.26
" The dosage of corticosteroids ingested during the initial period of therapy in patients with AN was tabulated and compared with that of 25 SLE control patients."( Aseptic necrosis of bone in systemic lupus erythematosus. Relationship to corticosteroid therapy.
Abeles, M; Rothfield, NF; Urman, JD, 1978
)
0.26
"5 mg/kg intraperitoneally) in a checkerboard combination dosage pattern for 30 days."( Synergistic nephrotoxicity of amphotericin B and cortisone acetate in mice.
Evan, AP; Kisch, AL; Maydew, RP, 1978
)
0.51
"The examples of 6-AN- and cortisone-induced cleft palate in the mouse suggest that dose-response studies can be used to discriminate whether mechanisms of action are different for different teratogens."( Use of dose-response relationships to discriminate between the mechanisms of cleft-palate induction by different teratogens: an argument for discussion.
Biddle, FG, 1978
)
0.56
" Although the log dose-response relationships had a similar form, the BFU-E were much more sensitive than the CFU-C to either glucocorticoid."( Differential response of early erythropoietic and granulopoietic progenitors to dexamethasone and cortisone.
Maloney, MA; Patt, HM; Zalman, F, 1979
)
0.48
" From these results it seems logical to continue to follow up the acute treatment of cerebral insult with cortisone and search for an optimal dosage and better confirmation."( [Cortisone in non-hemorrhagic stroke. An anterospective comparative study (author's transl)].
Barolin, GS; Hemmer, W; Scholz, H; Widhalm, K, 1976
)
1.38
" The dose-response curves were parallel during treatment and early recovery; but the slopes of the dose-response curves of the cartilage of cortisone-treated rats were greater than those of the controls during late recovery."( Cartilage sulfation and serum somatomedin in rats during and after cortisone-induced growth arrest.
Dearden, LC; Hill, RR; Jansons, RA; Mosier, HD, 1976
)
0.69
" Probit analysis demonstrated a family of linear and parallel dose-response curves for different inbred and hybrid embryos."( Genetics of cortisone-induced cleft palate in the mouse-embryonic and maternal effects.
Biddle, FG; Fraser, FC, 1976
)
0.63
" The radiation treatment consisted of a single intense dosing of microwave energy (38 mW/g for 600 sec."( Teratology, survival, and reversal learning after fetal irradiation of mice by 2450-MHz microwave energy.
Chernovetz, ME; Justesen, DR; King, NW; Wagner, JE, 1975
)
0.25
" High dosage immunosuppressive chemotherapy caused a marked reduction in serum IgM."( Patterned relationships between IgM and blast cells in peripheral blood in a child with acute leukemia.
Parker, JE; Rockerbie, RA, 1976
)
0.26
" Comparing to a control-group a distinctly less accentuated reaction and scarring of the connected tissues as well as calcified reactionless necrosises can be found in the histology depending of the dosage of the postoperative cortison-treatment."( [Hormonal tendolysis in animal experiment].
Küsswetter, W; Kuzmany, J; Lüdinghausen, Mv; Matzen, K; Walcher, K, 1975
)
0.25
"Various factors that might influence the dose-response effect of growth hormone on the longitudinal bone growth were investigated with tetracycline as intravital marker of the bone growth in hypophysectomized rats."( Conditions influencing the dose-response effect of growth hormone on longitudinal bone growth in the hypophysectomized rat.
Hansson, LI; Thorngren, KG, 1975
)
0.25
"Infection of human foreskin cells (D-550) by the Snyder-Theilen strain of feline sarcoma virus produced small but countable foci and demonstrated "single-hit" dose-response kinetics."( Influence of glucocorticoid, estrogen, and androgen hormones on transformation of human cells in vitro by feline sarcoma virus.
Blakeslee, JR; Milo, GE; Olsen, RG; Schaller, JP; Yohn, DS, 1976
)
0.26
" Low dosage dexamethasone improved the hypokalemia within several days and hypertension was corrected after 3 weeks of treatment."( Evidence for cortisol as the mineralocorticoid in the syndrome of apparent mineralocorticoid excess.
Melis, A; Pala, A; Tedde, R; Ulick, S, 1992
)
0.28
" Clinical symptoms worsened despite corticosteroids in a daily dosage of 1 mg/kg with three pulses of 800 mg methylprednisolone."( [Lupus chorea revealing. Study in magnetic resonance imaging. Success of plasma exchanges after resistance to pulsed cortisone].
Duplay, H; Euller-Ziegler, L; Grisot, C; Nectoux, F; Quaranta, JF; Ziegler, G, 1992
)
0.49
" The latency period between the steroid therapy and the occurrence of AON ranged from 12 to 60 months; steroid therapy lasted for 12 to 16 days with a total dosage equivalent to 2370-7180 mg prednisolone."( [Craniocerebral trauma and aseptic osteonecrosis. Steroid-induced sequelae after therapy of brain edema].
Griss, P; Pfeiffer, M, 1992
)
0.28
"Two hundred dogs with pituitary dependent hyperadrenocorticism (PDH) were treated with mitotane at an initial daily dosage of 21 to 69 mg/kg (mean = 45."( Mitotane (o,p'-DDD) treatment of 200 dogs with pituitary-dependent hyperadrenocorticism.
Kintzer, PP; Peterson, ME,
)
0.13
" This study suggests: 1) oral absorption of l-T4 is variable, but clinical response occurs quickly even in myxoedema ileus; 2) the intravenous route involves high peaks of plasma T4 and T3; 3) peripheral conversion of T4 to T3 allows gradually T3 delivery to organ systems, even if only l-T4 is used and 4) initial and daily dosage determinations need further studies."( Myxoedema coma: response of thyroid hormones with oral and intravenous high-dose L-thyroxine treatment.
Arlot, S; Debussche, X; Fournier, A; Lalau, JD; Mesmacque, A; Quichaud, J; Tolani, M, 1991
)
0.28
" We conclude that a physiologic replacement dosage of cortisone acetate given once daily is not effective in controlling excessive adrenal androgen secretion in congenital adrenal hyperplasia."( Inappropriate adrenal androgen secretion with once-a-day corticosteroid therapy for congenital adrenal hyperplasia.
Clayton, GW; Eberle, AE; Keenan, BS; Lin, TH, 1990
)
0.53
" Corticosteroid dosage plays a role in the occurrence of aseptic bone necrosis at an early stage of treatment."( [Bone and osteo-articular complications of corticotherapy].
Meunier, PJ; Terreaux, F, 1990
)
0.28
" Insulin dose-dependently reversed the suppressed angiogenesis of 20 micrograms corticosterone-treated mice and the dose-response curve approximated the curve of alloxan-treated mice."( Involvement of glucocorticoid in insulin-induced angiogenesis of adjuvant pouch granuloma in diabetic mice.
Amemiya, K; Kimura, M; Suzuki, J; Yamada, T, 1987
)
0.27
"To assess the influence of immaturity on the responsiveness of enterocytes to specific pathogens, a dose-response curve for cholera toxin (CT)-induced fluid secretion was determined in the proximal small intestine of rats at 2 and 4 wk of age."( Age and cortisone alter host responsiveness to cholera toxin in the developing gut.
Chu, SH; Ely, IG; Walker, WA, 1989
)
0.71
" Mice were untreated or injected with cortisone acetate (CA) or cyclophosphamide (CY) in various dosage regimens."( Fungus dose-dependent primary pulmonary aspergillosis in immunosuppressed mice.
Dixon, DM; Polak, A; Walsh, TJ, 1989
)
0.55
" Either suboptimal dosage of corticosteroid replacement therapy or omission of such therapy in adrenal insufficiency must be considered in the differential diagnosis of enigmatic postoperative fever."( Secondary adrenal insufficiency manifested as an acute febrile illness.
Cole, CP; Cupp, HB; Hall, BD; Soto-Hernandez, JL; Verghese, A, 1989
)
0.28
" A steep dose-response curve was observed with no measurable effect seen below 2 units/ml and maximal IL-2 receptor expression with greater than 5 units/ml."( Interleukin-2 differentially regulates IL-2 receptors on murine cloned cytolytic and helper T cells.
Fitch, FW; Havran, WL; Kim, DK; Lancki, DW; Moldwin, RL, 1986
)
0.27
" Contrary to the majority of similar reported cases, no decompression operation was performed, because the neurological signs had not progressed and the clinical findings in fact quickly regressed once the steroid dosage had been reduced and they showed a clear dependence on the amount of steroid administered."( [Epidural lipomatosis as a complication of a long-term glucocorticoid therapy].
Bischoff, C, 1988
)
0.27
" Neither dosage nor duration of treatment influenced severity, onset or duration of this mental disorders."( [Cortisone-induced psychoses].
Bleistein, J; Bräunig, P, 1988
)
1.19
" Bulk drug or dosage form is dissolved in an acetonitrile-buffer mixture and analyzed by an external standard method."( Reverse-phase liquid chromatographic determination of dexamethasone acetate and cortisone acetate in bulk drug substance and dosage forms: collaborative study.
Ng, LL,
)
0.36
" The present work explored the effect of a modified dosage regimen of the drug in five patients."( Chronopharmacology of hydrocortisone and 9 alpha-fluorhydrocortisone in the treatment for congenital adrenal hyperplasia.
Moeller, H, 1985
)
0.57
"A patient with Addison's disease required increased corticosteroid dosage whilst receiving rifampicin."( Changes in cortisol metabolism following rifampicin therapy.
Courtenay-Evans, RJ; Edwards, OM; Galley, JM; Hunter, J; Tait, AD, 1974
)
0.25
" This property of endotoxin can serve as a sensitive bioassay, although the dose-response curve is steep."( Inhibition of hepatic enzyme induction as a sensitive assay for endotoxin.
Berry, LJ; Colwell, LS; Smythe, DS, 1968
)
0.25
" Regression lines of the dose-response curves for ACTH, crude CRH and different volumes of medium from electrically stimulated hypothalami were parallel."( Stimulation electrically and by acetylcholine of the rat hypothalamus in vitro.
Bradbury, MW; Burden, J; Hillhouse, EW; Jones, MT, 1974
)
0.25
" The reduction of oestradiol-17 beta dosage from 60 mg to 30-40 mg day-1 with progesterone at 150 or 200 mg day-1 for the initial 7 days increased both milk yield and the success rate of the hormonal induction of lactation and eliminated pelvic fractures and excessive oestrous activity in treated cows."( Artificial induction of lactation in dry cows.
Bílek, J; Pícha, J; Skarda, J; Tersch, P; Urbanová, E, 1982
)
0.26
"Too often neglected, dosage of phosphatemia should yet be kept on mind."( [Hypophysphatemia (author's transl)].
Vinceneux, P,
)
0.13
" So far, all strains of mice that have been treated with cortisone do react with induced cleft palate and, from their dose-response behaviors, they appear to react in the same way."( Genetics of palate development.
Biddle, FG; Vekemans, MJ, 1984
)
0.51
" Cortisone treatment of mice was found to lower their resistance to infection at a given spore dosage as measured by ET50 values."( The comparative virulence of thermotolerant Mucorales species in mice.
Cazin, J; Embree, RW; Kitz, DJ, 1983
)
1.18
" A dose-response curve constructed by counting the number of cells on day 16, or at regular intervals, showed that glucocorticoids (hydrocortisone and cortisone) and mineralocorticoids (aldosterone and deoxycorticosterone) caused an increase in cell density when added at physiological concentrations or higher."( Effects of various steroids on in vitro lifespan and cell growth of human fetal lung fibroblasts (WI-38).
Kasuga, H; Kondo, H; Noumura, T,
)
0.33
" corymbifera, when administered in an intranasal dosage of 10(6) spores, produced death in some cortisone-treated mice."( Comparative virulence of Absidia corymbifera strains in mice.
Cazin, J; Embree, RW; Kitz, DJ, 1981
)
0.48
" Oral treatment was continued at the same dosage for 20-30 days and the patient was then discharged."( Treatment of benign intracranial hypertension.
d'Avella, D; Mingrino, S; Scanarini, M, 1980
)
0.26
" Height SD score for age (HtSDS(ca)), HtSDS for bone age (HtSDS(ba)), BMI and steroid dosage in early childhood (3."( Adult height in women with early-treated congenital adrenal hyperplasia (21-hydroxylase type): relation to body mass index in earlier childhood.
Grant, DB; Yu, AC, 1995
)
0.29
" Multiple replicate assays were conducted under identical conditions to assess the reproducibility of the dose-response curve for cleft palate."( Reproducibility of the dose-response curve of steroid-induced cleft palate in mice.
Freni, SC; Moore, GE; Razzaghi, M, 1994
)
0.29
" Postoperative administration of cortisone and hydrocortisone as a steroid replacement has been reduced in duration and dosage in recent 10 years."( [A survey of postoperative steroid replacement in 40 patients with Cushing's syndrome].
Aso, Y; Higashihara, E; Homma, Y; Minowada, S; Nutahara, K; Saiko, Y; Shinohara, M, 1993
)
0.57
" No differences between males and females were noted throughout this time with regard to: (a) A or 17-OHP levels (neither of which were suppressed to 'control values'); (b) the dosage of cortisone received (13."( Growth pattern during the first 36 months of life in congenital adrenal hyperplasia (21-hydroxylase deficiency).
Argenziano, A; Di Maio, S; Franzese, A; Gasparini, N; Salerno, M; Tenore, A, 1997
)
0.49
"43) and (2) dosing with only 5 mg of the deuterium-labeled steroids suppressed the plasma concentrations of endogenous cortisol and cortisone."( Stable isotope methodology for kinetic studies of interconversion of cortisol and cortisone in a human subject.
Furuta, T; Ishimaru, H; Kasuya, Y; Shibasaki, H, 1998
)
0.73
" Significant lowering of the substitutional hormonal therapy (steroid preparations) dosage was permitted due to the noted improvement of hypocorticism clinical course and an organism hormonal security indexes."( [Transplantation of organic culture of adrenal grand cortical substance in the treatment of post-adrenalectomy hypocorticoidism].
Komissarenko, IV; Rybakov, SI; Sichinava, RM; Turchin, IS, 1997
)
0.3
" The dose-response curve was bell shaped."( Nongenomic mechanisms of glucocorticoid inhibition of nicotine-induced calcium influx in PC12 cells: involvement of protein kinase C.
Chen, YZ; Huang, XY; Lou, LG; Lou, SJ; Pei, G; Qiu, J, 1998
)
0.3
"The clinical observation revealed that the asthmatic symptoms in most of the patients began to be improved after several acupuncture treatments with the dosage of the drug gradually reduced."( Clinical observation on 25 cases of hormone dependent bronchial asthma treated by acupuncture.
Hu, J, 1998
)
0.3
"Randomised trials comparing different routes of administration and dosage schemes of corticosteroid or adrenocorticotrophic hormone therapy versus a control group where no therapy considered effective for this condition was administered, unless it was also given in a similar way to the experimental group."( Corticosteroids for Bell's palsy (idiopathic facial paralysis).
Alvarez, G; Alvarez, MI; Ferreira, J; Salinas, RA, 2002
)
0.31
" Our results suggest that furosemide does not play a significant role in 11 beta-OHSD modulation in humans, at least at the dosage used in clinical practice."( Furosemide and 11beta-hydroxysteroid dehydrogenase activity, in man.
Armanini, D; Cossu, M; Delitala, G; Palermo, M; Roitman, E; Scaroni, C; Shackleton, CH; Sorba, G, 2002
)
0.31
" As for the dose regimen, one should start with an initial dose which suffices to treat the acute state, and subsequently reduce the dosage after the first positive results are obtained."( [Cortisone therapy today].
Kaiser, H, 2003
)
1.23
" Comparisons of potency made by determining maintenance dosage requirements for equivalent degrees of clinical control in the same patients indicated that the effectiveness of hydrocortisone (free alcohol) is more than 50 per cent greater than that of either the free or acetated forms of cortisone and approximately twice as great as that of hydrocortisone acetate."( Rheumatoid arthritis; experiences with hydrocortisone (free alcohol) and hydrocortisone acetate.
BOLAND, EW, 1952
)
0.69
" Cortisone in the dosage employed had no effect on the elimination of antigen following its intravenous administration or on the appearance of circulating antibody."( The mechanism of action of cortisone in experimental hypersensitivity. II. Hypersensitivity of the serum sickness type.
GERMUTH, FG, 1953
)
1.44
" The number of coughs is shown to be linearly related to log dose of antibody within a limited range and a dose-response curve is presented."( The effects of drugs upon a graded cough response obtained in sensitized guinea pigs exposed to aerosol of specific antigen.
FLATAKER, L; WINTER, CA, 1955
)
0.23
" Under stable conditions, established dosage schedules required surprisingly little adjustment over long periods of time."( Long-term management of patients after adrenalectomy.
SIMKIN, B, 1957
)
0.24
" The newest addition to available male hormone preparations is fluoxymesterone which is anabolic in smaller dosage than the older forms."( Newer hormonal preparations.
ESCAMILLA, RF, 1960
)
0.24
" The decrease was more pronounced when the same dosage of OPB was administered 24 hours before formal-dehyde injection."( Effects of oxyphenbutazone (Tandearil) on plasma seromucoids. I. In experimental inflammation.
BARCELO, R; LEGRESLEY, LP; RIOPEL, P, 1963
)
0.24
"Twenty patients with intractable asthma were treated with cortisone on various dosage schedules."( Cortisone in treatment of bronchial asthma.
HARRIS, MS, 1951
)
1.92
"The concurrent administration of compound E at a daily dosage of 2 mg."( The mechanism of action of 17-hydroxy-11-dehydrocorticosterone (compound E) and of the adrenocorticotropic hormone in experimental hypersensitivity in rabbits.
GERMUTH, FG; OTTINGER, B; OYAMA, J, 1951
)
0.23
"The systemic use of ACTH and cortisone in dermatology at present should be confined to patients with known fatal or hopelessly incapacitating diseases and to patients with extreme hypersensitivity reactions which may be protracted or life-endangering, and which can be controlled or cured with a relatively small total dosage of the agents in a short time."( The topical and systemic use of cortisone in dermatology.
FELDMAN, FF; NEWMAN, BA, 1951
)
0.81
" This suggests that the present dosing schemes have to be improved and that cortisone substitution should be individualized."( Non-physiological levels of circulating cortisol in growth hormone-treated hypopituitary adults after conventional cortisone substitution.
Andersson, PO; Arnqvist, HJ; Blomgren, J; Ekman, B, 2004
)
0.76
"Randomised trials comparing different routes of administration and dosage schemes of corticosteroid or adrenocorticotrophic hormone therapy versus a control group where no therapy considered effective for this condition was administered, unless it was also given in a similar way to the experimental group."( Corticosteroids for Bell's palsy (idiopathic facial paralysis).
Alvarez, G; Ferreira, J; Salinas, RA, 2004
)
0.32
"Randomised trials comparing different routes of administration and dosage schemes of corticosteroid or adrenocorticotrophic hormone therapy versus a control group where no therapy considered effective for this condition was administered, unless it was also given in a similar way to the experimental group."( WITHDRAWN: Corticosteroids for Bell's palsy (idiopathic facial paralysis).
Alvarez, G; Ferreira, J; Salinas, RA, 2009
)
0.35
" The reduction of cortisone conversion was time- and dose-dependent as well as dependent on dosing volume (suggestive of increased spillover and washout with greater dosing volume)."( In vivo evaluation of 11beta-hydroxysteroid dehydrogenase activity in the rabbit eye.
Anderson, S; Carreiro, S; Cheng, H; Gale, D; Gukasyan, H; Krauss, A; Lafontaine, J; Prasanna, G; Quenzer, T; Xiang, C, 2009
)
0.69
" Dosing concentration and volume play an important role in the pharmacokinetic and pharmacodynamic effects of topically delivering an 11beta-HSD1 inhibitor."( In vivo evaluation of 11beta-hydroxysteroid dehydrogenase activity in the rabbit eye.
Anderson, S; Carreiro, S; Cheng, H; Gale, D; Gukasyan, H; Krauss, A; Lafontaine, J; Prasanna, G; Quenzer, T; Xiang, C, 2009
)
0.35
"Randomised trials comparing different routes of administration and dosage schemes of corticosteroid or adrenocorticotrophic hormone therapy versus a control group where no therapy considered effective for this condition was administered, unless it was also given in a similar way to the experimental group."( Corticosteroids for Bell's palsy (idiopathic facial paralysis).
Alvarez, G; Daly, F; Ferreira, J; Salinas, RA, 2010
)
0.36
" In conclusion, the large interindividual variation in ACTH levels most likely indicates varying sensitivity to cortisol with a need for individualized dosing schemes."( Variable sensitivity to the glucocorticoid activity of cortisol in patients with primary adrenal insufficiency: assessment with ACTH profiles.
Andersson, PO; Arnqvist, HJ; Blomgren, J; Carlsson, M; Ekman, B, 2010
)
0.36
" The aim of this work is to investigate the effect of a low dosage and long term dexamethasone treatment on the levels of endogenous corticosteroids in cattle and to evaluate the possible presence of prednisolone residues in bovines bred under strictly controlled conditions."( Studies on the presence of natural and synthetic corticosteroids in bovine urine.
Bozzetta, E; Caramelli, M; Draisci, R; Ferranti, C; Marchiafava, C; Palleschi, L; Pezzolato, M; Quadri, FD, 2011
)
0.37
" The experimental results demonstrated that repetitive dosing of noradrenalin, phentolamine, and propranolol during chronic stress might region-dependently attenuate stress-induced microstructural and biochemical changes in the hippocampus, although propranolol intensified stress-induced behavioral changes."( Effects of adrenergic agents on stress-induced brain microstructural and immunochemical changes in adult male Wistar rats.
Fan, SJ; Jiang, H; Liu, X; Pan, F; Song, J; Yang, LJ, 2011
)
0.37
" Optimization of the dose and dosing frequency of ABIP dose may help to further enhance the anti-Aspergillus activity of this novel amphotericin B formulation."( Prophylactic efficacy of single dose pulmonary administration of amphotericin B inhalation powder in a guinea pig model of invasive pulmonary aspergillosis.
Bocanegra, R; Kirkpatrick, WR; Kugler, AR; Najvar, LK; Patterson, TF; Perkins, K; Pfeiffer, J; Sweeney, TD; Vallor, AC; Wiederhold, NP, 2012
)
0.38
" Base on desired target range of tacrolimus trough concentrations, individual daily dosage regimen was calculated, and all the observed daily doses were within the predicted range."( Prediction of tacrolimus metabolism and dosage requirements based on CYP3A4 phenotype and CYP3A5(*)3 genotype in Chinese renal transplant recipients.
Cai, NF; Cheng, ZN; Luo, X; Zheng, LY; Zhu, LJ, 2016
)
0.43
"This study provides the equations to predict tacrolimus metabolism and dosage requirements based on the endogenous CYP3A4 phenotype, CYP3A5(*)3 genotype and other non-genetic variables."( Prediction of tacrolimus metabolism and dosage requirements based on CYP3A4 phenotype and CYP3A5(*)3 genotype in Chinese renal transplant recipients.
Cai, NF; Cheng, ZN; Luo, X; Zheng, LY; Zhu, LJ, 2016
)
0.43
"Randomised trials and quasi-randomised trials comparing different routes of administration and dosage schemes of corticosteroid or adrenocorticotrophic hormone therapy versus a control group receiving no therapy considered effective for this condition, unless the same therapy was given in a similar way to the experimental group."( Corticosteroids for Bell's palsy (idiopathic facial paralysis).
Daly, F; Gagyor, I; Gammie, F; Madhok, VB; Somasundara, D; Sullivan, F; Sullivan, M, 2016
)
0.43
" Information on the use and dosage of calcium supplements was collected."( Calcium supplementation and risk of dementia in women with cerebrovascular disease.
Blennow, K; Börjesson-Hanson, A; Guo, X; Kern, J; Kern, S; Östling, S; Skoog, I; Waern, M; Zetterberg, H, 2016
)
0.43
" Fatigue is a common adverse event during treatment with these and other TKIs and a common cause of drug discontinuation or dosage reduction."( Primary Adrenal Insufficiency During Lenvatinib or Vandetanib and Improvement of Fatigue After Cortisone Acetate Therapy.
Colombo, C; De Leo, S; Di Stefano, M; Fugazzola, L; Persani, L; Vannucchi, G, 2019
)
0.73
"We show that the occurrence of PAI may be a common cause of fatigue during lenvatinib and vandetanib treatment, and we therefore recommend testing adrenal function for a prompt start of replacement therapy to avoid treatment discontinuation, dosage reduction, and potentially severe PAI complications."( Primary Adrenal Insufficiency During Lenvatinib or Vandetanib and Improvement of Fatigue After Cortisone Acetate Therapy.
Colombo, C; De Leo, S; Di Stefano, M; Fugazzola, L; Persani, L; Vannucchi, G, 2019
)
0.73
" Aims of this study were to assess the influence of sex and body weight on GC dosing and to describe the choice of GC in AI of different etiologies."( What factors have impact on glucocorticoid replacement in adrenal insufficiency: a real-life study.
Borretta, G; Cannavò, S; Dughera, F; Ferrau', F; Latina, A; Parisi, A; Pellegrino, M; Pia, A; Puglisi, S; Ragonese, M; Reimondo, G; Rossini, A; Tabaro, I; Terzolo, M, 2021
)
0.62
" In vivo models were derived by convolution of a skin absorption input function for finite dosing with that for in vivo disposition PK."( Percutaneous absorption of steroids from finite doses: Predicting urinary excretion from in vitro skin permeation testing.
Anissimov, YG; Cheruvu, HS; Ghosh, P; Grice, JE; Liu, X; Ni, Z; Roberts, MS; Tsakalozou, E; van der Hoek, J, 2022
)
0.72
"This multicenter prospective study included 3 groups of female patients: CushMed = 16 treated with a stable cortisol-lowering drug dosage and normal urinary free cortisol (UFC); CushSurg = 13 cured by pituitary surgery; CushBla = 15 receiving stable recommended doses of hydrocortisone following bilateral adrenalectomy."( Evidence of Persistent Mild Hypercortisolism in Patients Medically Treated for Cushing Disease: the Haircush Study.
Bertherat, J; Brossaud, J; Castinetti, F; Chanson, P; Drui, D; Fafin, M; Mohammedi, K; Raverot, G; Reznik, Y; Tabarin, A, 2023
)
1.09
" Six of 15 CushMed patients exhibited increased HE concentrations and had increased antihypertensive drug dosage compared to CushMed patients with normal HE (P = ."( Evidence of Persistent Mild Hypercortisolism in Patients Medically Treated for Cushing Disease: the Haircush Study.
Bertherat, J; Brossaud, J; Castinetti, F; Chanson, P; Drui, D; Fafin, M; Mohammedi, K; Raverot, G; Reznik, Y; Tabarin, A, 2023
)
0.91
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (2)

RoleDescription
human metaboliteAny mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
mouse metaboliteAny mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (9)

ClassDescription
glucocorticoidGlucocorticoids are a class of steroid hormones that regulate a variety of physiological processes, in particular control of the concentration of glucose in blood.
17alpha-hydroxy steroidThe alpha-stereoisomer of 17-hydroxy steroid.
21-hydroxy steroid
11-oxo steroidAny oxo steroid that has an oxo substituent at position 11.
20-oxo steroidAn oxo steroid carrying an oxo group at position 20.
C21-steroidA steroid that has a structure based on a 21-carbon (pregnane) skeleton. Note that individual examples may have ring substituents at other positions and/or contain double bonds, aromatic A-rings, expanded/contracted rings etc., so the formula and mass may vary from that given for the generic structure.
3-oxo-Delta(4) steroidA 3-oxo steroid conjugated to a C=C double bond at the alpha,beta position.
primary alpha-hydroxy ketoneAn alpha-hydroxy ketone in which the carbonyl group and the hydroxy group are linked by a -CH2 (methylene) group.
tertiary alpha-hydroxy ketoneAn alpha-hydroxy ketone in which the carbonyl group and the hydroxy group are linked by a carbon bearing two organyl groups.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Pathways (21)

PathwayProteinsCompounds
Metabolism14961108
Metabolism of lipids500463
Metabolism of steroids111135
Metabolism of steroid hormones2537
Glucocorticoid biosynthesis616
Steroidogenesis1142
Adrenal Hyperplasia Type 3 or Congenital Adrenal Hyperplasia Due to 21-Hydroxylase Deficiency1142
Congenital Lipoid Adrenal Hyperplasia (CLAH) or Lipoid CAH1142
Adrenal Hyperplasia Type 5 or Congenital Adrenal Hyperplasia Due to 17 alpha-Hydroxylase Deficiency1142
17-alpha-Hydroxylase Deficiency (CYP17)1142
11-beta-Hydroxylase Deficiency (CYP11B1)1142
21-Hydroxylase Deficiency (CYP21)1142
Corticosterone Methyl Oxidase I Deficiency (CMO I)1142
Corticosterone Methyl Oxidase II Deficiency (CMO II)1142
Apparent Mineralocorticoid Excess Syndrome1142
3-beta-Hydroxysteroid Dehydrogenase Deficiency1142
Glucocorticoid biosynthesis1411
Glucocorticoid & Mineralcorticoid Metabolism013
Glucocorticoid and Mineralcorticoid Metabolism04
Biochemical pathways: part I0466
Classical pathway of steroidogenesis with glucocorticoid and mineralocorticoid metabolism325
Prostaglandin synthesis and regulation08

Protein Targets (63)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, HADH2 proteinHomo sapiens (human)Potency7.94330.025120.237639.8107AID893
Chain B, HADH2 proteinHomo sapiens (human)Potency7.94330.025120.237639.8107AID893
endonuclease IVEscherichia coliPotency0.63100.707912.432431.6228AID1708
dopamine D1 receptorHomo sapiens (human)Potency0.02590.00521.30228.1995AID624455
thioredoxin reductaseRattus norvegicus (Norway rat)Potency32.81770.100020.879379.4328AID488773; AID588453
pregnane X receptorRattus norvegicus (Norway rat)Potency35.48130.025127.9203501.1870AID651751
RAR-related orphan receptor gammaMus musculus (house mouse)Potency68.58960.006038.004119,952.5996AID1159523
GLS proteinHomo sapiens (human)Potency31.62280.35487.935539.8107AID624146
TDP1 proteinHomo sapiens (human)Potency33.49830.000811.382244.6684AID686979
GLI family zinc finger 3Homo sapiens (human)Potency35.85580.000714.592883.7951AID1259369; AID1259392
AR proteinHomo sapiens (human)Potency9.41730.000221.22318,912.5098AID1259243; AID1259247; AID1259381; AID588515; AID743035; AID743036; AID743040; AID743053; AID743063
aldehyde dehydrogenase 1 family, member A1Homo sapiens (human)Potency39.81070.011212.4002100.0000AID1030
progesterone receptorHomo sapiens (human)Potency11.37690.000417.946075.1148AID1346795
regulator of G-protein signaling 4Homo sapiens (human)Potency89.12510.531815.435837.6858AID504845
glucocorticoid receptor [Homo sapiens]Homo sapiens (human)Potency14.87370.000214.376460.0339AID588533; AID720692
retinoic acid nuclear receptor alpha variant 1Homo sapiens (human)Potency33.64580.003041.611522,387.1992AID1159552; AID1159553; AID1159555
retinoid X nuclear receptor alphaHomo sapiens (human)Potency48.96620.000817.505159.3239AID1159531
pregnane X nuclear receptorHomo sapiens (human)Potency50.71630.005428.02631,258.9301AID1346982; AID720659
estrogen nuclear receptor alphaHomo sapiens (human)Potency7.76060.000229.305416,493.5996AID743069
peroxisome proliferator-activated receptor deltaHomo sapiens (human)Potency54.94100.001024.504861.6448AID743215
peroxisome proliferator activated receptor gammaHomo sapiens (human)Potency61.64480.001019.414170.9645AID743094
vitamin D (1,25- dihydroxyvitamin D3) receptorHomo sapiens (human)Potency24.54120.023723.228263.5986AID743222
euchromatic histone-lysine N-methyltransferase 2Homo sapiens (human)Potency37.18850.035520.977089.1251AID504332
nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105), isoform CRA_aHomo sapiens (human)Potency54.941019.739145.978464.9432AID1159509
v-jun sarcoma virus 17 oncogene homolog (avian)Homo sapiens (human)Potency15.48450.057821.109761.2679AID1159528
peripheral myelin protein 22 isoform 1Homo sapiens (human)Potency30.131323.934123.934123.9341AID1967
atrial natriuretic peptide receptor 1 precursorHomo sapiens (human)Potency0.75690.134610.395030.1313AID1347049
chromobox protein homolog 1Homo sapiens (human)Potency44.56550.006026.168889.1251AID488953; AID540317
heat shock protein beta-1Homo sapiens (human)Potency61.64480.042027.378961.6448AID743210
flap endonuclease 1Homo sapiens (human)Potency0.00190.133725.412989.1251AID588795
nuclear factor erythroid 2-related factor 2 isoform 1Homo sapiens (human)Potency61.13060.000627.21521,122.0200AID743202
gemininHomo sapiens (human)Potency23.72460.004611.374133.4983AID624296; AID624297
survival motor neuron protein isoform dHomo sapiens (human)Potency1.25890.125912.234435.4813AID1458
cytochrome P450 3A4 isoform 1Homo sapiens (human)Potency10.00000.031610.279239.8107AID884; AID885
M-phase phosphoprotein 8Homo sapiens (human)Potency100.00000.177824.735279.4328AID488949
muscarinic acetylcholine receptor M1Rattus norvegicus (Norway rat)Potency16.27100.00106.000935.4813AID943; AID944
Gamma-aminobutyric acid receptor subunit piRattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit beta-1Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit deltaRattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-2Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-5Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-3Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-1Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-2Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-4Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-3Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-6Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-1Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit beta-3Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit beta-2Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
TAR DNA-binding protein 43Homo sapiens (human)Potency8.91251.778316.208135.4813AID652104
GABA theta subunitRattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit epsilonRattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Bile salt export pumpHomo sapiens (human)IC50 (µMol)108.10000.11007.190310.0000AID1449628
Glucocorticoid receptorHomo sapiens (human)IC50 (µMol)2.37800.00000.495310.0000AID625263
Glucocorticoid receptorHomo sapiens (human)Ki1.08100.00010.38637.0010AID625263
Glycine receptor subunit alpha-1Rattus norvegicus (Norway rat)IC50 (µMol)2.37800.00150.76005.0740AID625263
Glycine receptor subunit alpha-1Rattus norvegicus (Norway rat)Ki1.08100.00070.76537.0010AID625263
Corticosteroid-binding globulinHomo sapiens (human)Ki0.12880.01323.248110.0000AID51055
Glycine receptor subunit betaRattus norvegicus (Norway rat)IC50 (µMol)2.37800.00150.76005.0740AID625263
Glycine receptor subunit betaRattus norvegicus (Norway rat)Ki1.08100.00070.78467.0010AID625263
Glycine receptor subunit alpha-2Rattus norvegicus (Norway rat)IC50 (µMol)2.37800.00150.80445.0740AID625263
Glycine receptor subunit alpha-2Rattus norvegicus (Norway rat)Ki1.08100.00070.78467.0010AID625263
Glycine receptor subunit alpha-3Rattus norvegicus (Norway rat)IC50 (µMol)2.37800.00150.76005.0740AID625263
Glycine receptor subunit alpha-3Rattus norvegicus (Norway rat)Ki1.08100.00070.78467.0010AID625263
Multidrug and toxin extrusion protein 1Homo sapiens (human)IC50 (µMol)21.40000.01002.765610.0000AID721754
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Sex hormone-binding globulinHomo sapiens (human)Kd0.37150.00020.34964.7863AID318680
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (106)

Processvia Protein(s)Taxonomy
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
negative regulation of transcription by RNA polymerase IIGlucocorticoid receptorHomo sapiens (human)
regulation of gluconeogenesisGlucocorticoid receptorHomo sapiens (human)
chromatin organizationGlucocorticoid receptorHomo sapiens (human)
regulation of DNA-templated transcriptionGlucocorticoid receptorHomo sapiens (human)
apoptotic processGlucocorticoid receptorHomo sapiens (human)
chromosome segregationGlucocorticoid receptorHomo sapiens (human)
signal transductionGlucocorticoid receptorHomo sapiens (human)
glucocorticoid metabolic processGlucocorticoid receptorHomo sapiens (human)
gene expressionGlucocorticoid receptorHomo sapiens (human)
microglia differentiationGlucocorticoid receptorHomo sapiens (human)
adrenal gland developmentGlucocorticoid receptorHomo sapiens (human)
regulation of glucocorticoid biosynthetic processGlucocorticoid receptorHomo sapiens (human)
synaptic transmission, glutamatergicGlucocorticoid receptorHomo sapiens (human)
maternal behaviorGlucocorticoid receptorHomo sapiens (human)
intracellular glucocorticoid receptor signaling pathwayGlucocorticoid receptorHomo sapiens (human)
glucocorticoid mediated signaling pathwayGlucocorticoid receptorHomo sapiens (human)
positive regulation of neuron apoptotic processGlucocorticoid receptorHomo sapiens (human)
negative regulation of DNA-templated transcriptionGlucocorticoid receptorHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIGlucocorticoid receptorHomo sapiens (human)
astrocyte differentiationGlucocorticoid receptorHomo sapiens (human)
cell divisionGlucocorticoid receptorHomo sapiens (human)
mammary gland duct morphogenesisGlucocorticoid receptorHomo sapiens (human)
motor behaviorGlucocorticoid receptorHomo sapiens (human)
cellular response to steroid hormone stimulusGlucocorticoid receptorHomo sapiens (human)
cellular response to glucocorticoid stimulusGlucocorticoid receptorHomo sapiens (human)
cellular response to dexamethasone stimulusGlucocorticoid receptorHomo sapiens (human)
cellular response to transforming growth factor beta stimulusGlucocorticoid receptorHomo sapiens (human)
neuroinflammatory responseGlucocorticoid receptorHomo sapiens (human)
positive regulation of miRNA transcriptionGlucocorticoid receptorHomo sapiens (human)
intracellular steroid hormone receptor signaling pathwayGlucocorticoid receptorHomo sapiens (human)
regulation of transcription by RNA polymerase IIGlucocorticoid receptorHomo sapiens (human)
glucocorticoid metabolic processCorticosteroid-binding globulinHomo sapiens (human)
negative regulation of endopeptidase activityCorticosteroid-binding globulinHomo sapiens (human)
startle responsePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
regulation of muscle contractionPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
neuroblast proliferationPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
protein localizationPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
cell communication by electrical couplingPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
magnesium ion homeostasisPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
neuronal action potentialPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
optic nerve developmentPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
hippocampus developmentPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
cerebral cortex developmentPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
corpus callosum developmentPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
neuronal signal transductionPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
regulation of membrane potentialPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
neuromuscular processPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
detection of mechanical stimulus involved in sensory perception of painPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
detection of mechanical stimulus involved in sensory perception of touchPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
protein homooligomerizationPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
regulation of postsynaptic membrane potentialPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
axon developmentPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
cellular response to magnesium ionPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
potassium ion transmembrane transportPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
membrane repolarization during action potentialPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
regulation of presynaptic membrane potentialPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
action potentialPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
negative regulation of protein phosphorylationTAR DNA-binding protein 43Homo sapiens (human)
mRNA processingTAR DNA-binding protein 43Homo sapiens (human)
RNA splicingTAR DNA-binding protein 43Homo sapiens (human)
negative regulation of gene expressionTAR DNA-binding protein 43Homo sapiens (human)
regulation of protein stabilityTAR DNA-binding protein 43Homo sapiens (human)
positive regulation of insulin secretionTAR DNA-binding protein 43Homo sapiens (human)
response to endoplasmic reticulum stressTAR DNA-binding protein 43Homo sapiens (human)
positive regulation of protein import into nucleusTAR DNA-binding protein 43Homo sapiens (human)
regulation of circadian rhythmTAR DNA-binding protein 43Homo sapiens (human)
regulation of apoptotic processTAR DNA-binding protein 43Homo sapiens (human)
negative regulation by host of viral transcriptionTAR DNA-binding protein 43Homo sapiens (human)
rhythmic processTAR DNA-binding protein 43Homo sapiens (human)
regulation of cell cycleTAR DNA-binding protein 43Homo sapiens (human)
3'-UTR-mediated mRNA destabilizationTAR DNA-binding protein 43Homo sapiens (human)
3'-UTR-mediated mRNA stabilizationTAR DNA-binding protein 43Homo sapiens (human)
nuclear inner membrane organizationTAR DNA-binding protein 43Homo sapiens (human)
amyloid fibril formationTAR DNA-binding protein 43Homo sapiens (human)
regulation of gene expressionTAR DNA-binding protein 43Homo sapiens (human)
xenobiotic transmembrane transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
organic cation transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
putrescine transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
xenobiotic transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
transmembrane transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
thiamine transmembrane transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
amino acid import across plasma membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
L-arginine import across plasma membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
L-alpha-amino acid transmembrane transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
proton transmembrane transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
L-arginine transmembrane transportMultidrug and toxin extrusion protein 1Homo sapiens (human)
xenobiotic detoxification by transmembrane export across the plasma membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (49)

Processvia Protein(s)Taxonomy
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
RNA polymerase II transcription regulatory region sequence-specific DNA bindingGlucocorticoid receptorHomo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingGlucocorticoid receptorHomo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificGlucocorticoid receptorHomo sapiens (human)
core promoter sequence-specific DNA bindingGlucocorticoid receptorHomo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificGlucocorticoid receptorHomo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specificGlucocorticoid receptorHomo sapiens (human)
DNA-binding transcription factor activityGlucocorticoid receptorHomo sapiens (human)
RNA bindingGlucocorticoid receptorHomo sapiens (human)
nuclear receptor activityGlucocorticoid receptorHomo sapiens (human)
nuclear glucocorticoid receptor activityGlucocorticoid receptorHomo sapiens (human)
steroid bindingGlucocorticoid receptorHomo sapiens (human)
protein bindingGlucocorticoid receptorHomo sapiens (human)
zinc ion bindingGlucocorticoid receptorHomo sapiens (human)
TBP-class protein bindingGlucocorticoid receptorHomo sapiens (human)
protein kinase bindingGlucocorticoid receptorHomo sapiens (human)
identical protein bindingGlucocorticoid receptorHomo sapiens (human)
Hsp90 protein bindingGlucocorticoid receptorHomo sapiens (human)
steroid hormone bindingGlucocorticoid receptorHomo sapiens (human)
sequence-specific double-stranded DNA bindingGlucocorticoid receptorHomo sapiens (human)
estrogen response element bindingGlucocorticoid receptorHomo sapiens (human)
androgen bindingSex hormone-binding globulinHomo sapiens (human)
protein bindingSex hormone-binding globulinHomo sapiens (human)
steroid bindingSex hormone-binding globulinHomo sapiens (human)
steroid bindingCorticosteroid-binding globulinHomo sapiens (human)
serine-type endopeptidase inhibitor activityCorticosteroid-binding globulinHomo sapiens (human)
voltage-gated potassium channel activityPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
delayed rectifier potassium channel activityPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
protein bindingPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
disordered domain specific bindingPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
voltage-gated monoatomic ion channel activity involved in regulation of presynaptic membrane potentialPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
voltage-gated monoatomic ion channel activity involved in regulation of postsynaptic membrane potentialPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingTAR DNA-binding protein 43Homo sapiens (human)
DNA bindingTAR DNA-binding protein 43Homo sapiens (human)
double-stranded DNA bindingTAR DNA-binding protein 43Homo sapiens (human)
RNA bindingTAR DNA-binding protein 43Homo sapiens (human)
mRNA 3'-UTR bindingTAR DNA-binding protein 43Homo sapiens (human)
protein bindingTAR DNA-binding protein 43Homo sapiens (human)
lipid bindingTAR DNA-binding protein 43Homo sapiens (human)
identical protein bindingTAR DNA-binding protein 43Homo sapiens (human)
pre-mRNA intronic bindingTAR DNA-binding protein 43Homo sapiens (human)
molecular condensate scaffold activityTAR DNA-binding protein 43Homo sapiens (human)
protein bindingMultidrug and toxin extrusion protein 1Homo sapiens (human)
organic cation transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
L-amino acid transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
thiamine transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
antiporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
putrescine transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
L-arginine transmembrane transporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
polyspecific organic cation:proton antiporter activityMultidrug and toxin extrusion protein 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (46)

Processvia Protein(s)Taxonomy
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
nucleusGlucocorticoid receptorHomo sapiens (human)
nucleusGlucocorticoid receptorHomo sapiens (human)
nucleoplasmGlucocorticoid receptorHomo sapiens (human)
cytoplasmGlucocorticoid receptorHomo sapiens (human)
mitochondrial matrixGlucocorticoid receptorHomo sapiens (human)
centrosomeGlucocorticoid receptorHomo sapiens (human)
spindleGlucocorticoid receptorHomo sapiens (human)
cytosolGlucocorticoid receptorHomo sapiens (human)
membraneGlucocorticoid receptorHomo sapiens (human)
nuclear speckGlucocorticoid receptorHomo sapiens (human)
synapseGlucocorticoid receptorHomo sapiens (human)
chromatinGlucocorticoid receptorHomo sapiens (human)
protein-containing complexGlucocorticoid receptorHomo sapiens (human)
extracellular regionSex hormone-binding globulinHomo sapiens (human)
extracellular exosomeSex hormone-binding globulinHomo sapiens (human)
extracellular regionCorticosteroid-binding globulinHomo sapiens (human)
extracellular spaceCorticosteroid-binding globulinHomo sapiens (human)
extracellular exosomeCorticosteroid-binding globulinHomo sapiens (human)
extracellular spaceCorticosteroid-binding globulinHomo sapiens (human)
plasma membraneGamma-aminobutyric acid receptor subunit gamma-2Rattus norvegicus (Norway rat)
plasma membraneGlycine receptor subunit betaRattus norvegicus (Norway rat)
plasma membraneGamma-aminobutyric acid receptor subunit alpha-1Rattus norvegicus (Norway rat)
plasma membraneGamma-aminobutyric acid receptor subunit beta-2Rattus norvegicus (Norway rat)
endoplasmic reticulumPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
cytosolPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
plasma membranePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
cell surfacePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
apical plasma membranePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
cell junctionPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
dendritePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
cytoplasmic vesiclePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
paranode region of axonPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
presynaptic membranePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
neuronal cell bodyPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
axon initial segmentPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
perikaryonPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
axon terminusPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
juxtaparanode region of axonPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
calyx of HeldPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
synapsePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
postsynaptic membranePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
anchoring junctionPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
glutamatergic synapsePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
voltage-gated potassium channel complexPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
dendritePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
paranode region of axonPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
membranePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
synapsePotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
juxtaparanode region of axonPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
neuronal cell bodyPotassium voltage-gated channel subfamily A member 1Homo sapiens (human)
intracellular non-membrane-bounded organelleTAR DNA-binding protein 43Homo sapiens (human)
nucleusTAR DNA-binding protein 43Homo sapiens (human)
nucleoplasmTAR DNA-binding protein 43Homo sapiens (human)
perichromatin fibrilsTAR DNA-binding protein 43Homo sapiens (human)
mitochondrionTAR DNA-binding protein 43Homo sapiens (human)
cytoplasmic stress granuleTAR DNA-binding protein 43Homo sapiens (human)
nuclear speckTAR DNA-binding protein 43Homo sapiens (human)
interchromatin granuleTAR DNA-binding protein 43Homo sapiens (human)
nucleoplasmTAR DNA-binding protein 43Homo sapiens (human)
chromatinTAR DNA-binding protein 43Homo sapiens (human)
plasma membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
basolateral plasma membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
apical plasma membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
membraneMultidrug and toxin extrusion protein 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (167)

Assay IDTitleYearJournalArticle
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).2014Journal of biomolecular screening, Jul, Volume: 19, Issue:6
A High-Throughput Assay to Identify Inhibitors of the Apicoplast DNA Polymerase from Plasmodium falciparum.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504810Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1224864HCS microscopy assay (F508del-CFTR)2016PloS one, , Volume: 11, Issue:10
Increasing the Endoplasmic Reticulum Pool of the F508del Allele of the Cystic Fibrosis Transmembrane Conductance Regulator Leads to Greater Folding Correction by Small Molecule Therapeutics.
AID521220Inhibition of neurosphere proliferation of mouse neural precursor cells by MTT assay2007Nature chemical biology, May, Volume: 3, Issue:5
Chemical genetics reveals a complex functional ground state of neural stem cells.
AID188016Anti-inflammatory effect in rat granuloma assay, activity relative to hydrocortisone and hydrocortisone 21-acetate1983Journal of medicinal chemistry, Mar, Volume: 26, Issue:3
Structure-activity relationships in the antiinflammatory steroids: a pattern-recognition approach.
AID500681Activation of KV1.1 expressed in Xenopus laevis oocytes coexpressing Kvbeta1 assessed as increase in steady state current normalized to initial inactivating current at 500 uM by electrophysiology method2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID51052In silico binding affinity to corticosteroid binding globulin (CBG)1997Journal of medicinal chemistry, Dec-19, Volume: 40, Issue:26
Three-dimensional quantitative structure-activity relationships from molecular similarity matrices and genetic neural networks. 1. Method and validations.
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID500690Induction of dissociation of KV1.1 T1 domain/rat Kvbeta2 I211R mutant complex at 2 mM by solid phase binding assay2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID74377Relative binding affinity to glucocorticoid receptor on cytosol from thymus at 24 hr1988Journal of medicinal chemistry, Jun, Volume: 31, Issue:6
Binding of steroids to the progestin and glucocorticoid receptors analyzed by correspondence analysis.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID126435Relative binding affinity for mineralocorticoid receptor of rat kidney at 24 hr1988Journal of medicinal chemistry, Jun, Volume: 31, Issue:6
Binding of steroids to the progestin and glucocorticoid receptors analyzed by correspondence analysis.
AID500680Activation of KV1.1 expressed in Xenopus laevis oocytes coexpressing Kvbeta1 assessed as increase in channel current at 500 uM by electrophysiology method2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID228061Binding affinity towards human testosterone binding globulin.1993Journal of medicinal chemistry, Oct-01, Volume: 36, Issue:20
QSAR's from similarity matrices. Technique validation and application in the comparison of different similarity evaluation methods.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID212931Binding affinity towards human testosterone binding globulin.1997Journal of medicinal chemistry, Sep-26, Volume: 40, Issue:20
Validation of EGSITE2, a mixed integer program for deducing objective site models for experimental binding data.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID977599Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID51059Binding affinity to corticosteroid binding globulin1998Journal of medicinal chemistry, Jul-02, Volume: 41, Issue:14
Three-dimensional quantitative similarity-activity relationships (3D QSiAR) from SEAL similarity matrices.
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID500682Activation of KV1.1 expressed in Xenopus laevis oocytes coexpressing Kvbeta1 assessed as increase in steady state current normalized to initial inactivating current by electrophysiology method2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID74378Relative binding affinity to glucocorticoid receptor on cytosol from thymus at 4 hr1988Journal of medicinal chemistry, Jun, Volume: 31, Issue:6
Binding of steroids to the progestin and glucocorticoid receptors analyzed by correspondence analysis.
AID977602Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID74375Relative binding affinity to glucocorticoid receptor on cytosol from liver at 24 hr1988Journal of medicinal chemistry, Jun, Volume: 31, Issue:6
Binding of steroids to the progestin and glucocorticoid receptors analyzed by correspondence analysis.
AID681354TP_TRANSPORTER: transepithelial transport in MDR1-expressing LLC-PK1 cells2003Pharmaceutical research, Nov, Volume: 20, Issue:11
Structural determinants of P-glycoprotein-mediated transport of glucocorticoids.
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID311367Permeability coefficient in human skin2007Bioorganic & medicinal chemistry, Nov-15, Volume: 15, Issue:22
Transdermal penetration behaviour of drugs: CART-clustering, QSPR and selection of model compounds.
AID50906Inhibition of mouse constitutive androstane receptor (mCAR) activity at 10 uM was determined as percent remaining activity2003Journal of medicinal chemistry, Oct-23, Volume: 46, Issue:22
Molecular determinants of steroid inhibition for the mouse constitutive androstane receptor.
AID1449628Inhibition of human BSEP expressed in baculovirus transfected fall armyworm Sf21 cell membranes vesicles assessed as reduction in ATP-dependent [3H]-taurocholate transport into vesicles incubated for 5 mins by Topcount based rapid filtration method2012Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 40, Issue:12
Mitigating the inhibition of human bile salt export pump by drugs: opportunities provided by physicochemical property modulation, in silico modeling, and structural modification.
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1132664Glucocorticoid activity in sc dosed bilaterally adrenalectomized rat assessed as glycogen deposition in liver administered for 5 days relative to cortisol1978Journal of medicinal chemistry, May, Volume: 21, Issue:5
A Fujita--Ban structure--activity analysis of 44 steroids.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID266004Inhibition of MR-mediated transactivation of galactosidase reporter gene in HEK293 cells expressing 11betaHSD12006Journal of medicinal chemistry, Jun-15, Volume: 49, Issue:12
The discovery of new 11beta-hydroxysteroid dehydrogenase type 1 inhibitors by common feature pharmacophore modeling and virtual screening.
AID220020Binding affinity towards human corticosteroid binding globulin.1993Journal of medicinal chemistry, Oct-01, Volume: 36, Issue:20
QSAR's from similarity matrices. Technique validation and application in the comparison of different similarity evaluation methods.
AID162613Relative binding affinity for progestin receptor of uterus of rabbit at 24 hr1988Journal of medicinal chemistry, Jun, Volume: 31, Issue:6
Binding of steroids to the progestin and glucocorticoid receptors analyzed by correspondence analysis.
AID356333Antiedemic activity against DMSO-induced paw edema in sc dosed Albino rat2003Journal of natural products, Aug, Volume: 66, Issue:8
Acinospesigenin-A, -B, and -C: three new triterpenoids from Phytolacca acinosa.
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID51056Binding affinity to the corticosteroid-binding globulin (CBG) receptor.2000Journal of medicinal chemistry, Aug-24, Volume: 43, Issue:17
GRid-INdependent descriptors (GRIND): a novel class of alignment-independent three-dimensional molecular descriptors.
AID39320Relative binding affinity for androgen receptor of prostate of rat at 2 hr1988Journal of medicinal chemistry, Jun, Volume: 31, Issue:6
Binding of steroids to the progestin and glucocorticoid receptors analyzed by correspondence analysis.
AID500691Activation of KV1.1/Kvbeta1 complex expressed in Xenopus laevis oocytes assessed as increase in steady state current normalized to initial inactivating current at 500 uM by electrophysiology method2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID1351943Effective permeability of compound at 100 uM at pH 7.4 by PAMPA2018European journal of medicinal chemistry, Feb-10, Volume: 145Novel donepezil-like N-benzylpyridinium salt derivatives as AChE inhibitors and their corresponding dihydropyridine "bio-oxidizable" prodrugs: Synthesis, biological evaluation and structure-activity relationship.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID127351Binding affinity against human monoclonal antibody (mAb)-5C22002Journal of medicinal chemistry, Jul-18, Volume: 45, Issue:15
Three-dimensional quantitative structure-activity relationship analysis of ligand binding to human sequence antidigoxin monoclonal antibodies using comparative molecular field analysis.
AID500684Activation of KV1.1 expressed in Xenopus laevis oocytes assessed as increase in steady state current normalized to initial inactivating current by electrophysiology method2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID127349Binding affinity against human monoclonal antibody (mAb)-11E62002Journal of medicinal chemistry, Jul-18, Volume: 45, Issue:15
Three-dimensional quantitative structure-activity relationship analysis of ligand binding to human sequence antidigoxin monoclonal antibodies using comparative molecular field analysis.
AID318680Displacement of [3H]5alpha dihydrotestosterone from human sex hormone binding globulin2008Journal of medicinal chemistry, Apr-10, Volume: 51, Issue:7
An updated steroid benchmark set and its application in the discovery of novel nanomolar ligands of sex hormone-binding globulin.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID213396Glucocorticoid induced Tyrosine Aminotransferase activity relative to Dexamethasone1988Journal of medicinal chemistry, Jun, Volume: 31, Issue:6
Binding of steroids to the progestin and glucocorticoid receptors analyzed by correspondence analysis.
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID212920Binding affinity against transport protein testosterone binding globulin.1994Journal of medicinal chemistry, Jul-22, Volume: 37, Issue:15
Compass: predicting biological activities from molecular surface properties. Performance comparisons on a steroid benchmark.
AID500679Binding affinity to KVbeta1 assessed as reduction of fluorescence by NADPH fluorescence spectrum based assay2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID212919Binding affinity towards testosterone binding globulin is expressed as log(1/k).1996Journal of medicinal chemistry, May-24, Volume: 39, Issue:11
Comparative molecular moment analysis (CoMMA): 3D-QSAR without molecular superposition.
AID51062In silico steroid binding affinity to transport protein corticosteroid binding globulin1994Journal of medicinal chemistry, Jul-22, Volume: 37, Issue:15
Compass: predicting biological activities from molecular surface properties. Performance comparisons on a steroid benchmark.
AID51058Binding affinity towards corticosteroid-binding globulin (CBG)2003Journal of medicinal chemistry, Apr-10, Volume: 46, Issue:8
Mapping property distributions of molecular surfaces: algorithm and evaluation of a novel 3D quantitative structure-activity relationship technique.
AID51049Binding affinity against corticosteroid-binding globulin1993Journal of medicinal chemistry, Feb-19, Volume: 36, Issue:4
Structure-activity relationships from molecular similarity matrices.
AID74374Relative binding affinity to glucocorticoid receptor on cytosol from hepatoma tissue cells at 4 hr1988Journal of medicinal chemistry, Jun, Volume: 31, Issue:6
Binding of steroids to the progestin and glucocorticoid receptors analyzed by correspondence analysis.
AID346025Binding affinity to beta cyclodextrin2009Bioorganic & medicinal chemistry, Jan-15, Volume: 17, Issue:2
Convenient QSAR model for predicting the complexation of structurally diverse compounds with beta-cyclodextrins.
AID721753Inhibition of human MATE1-mediated ASP+ uptake expressed in HEK293 cells at 20 uM after 1.5 mins by fluorescence assay2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID74376Relative binding affinity to glucocorticoid receptor on cytosol from liver at 4 hr1988Journal of medicinal chemistry, Jun, Volume: 31, Issue:6
Binding of steroids to the progestin and glucocorticoid receptors analyzed by correspondence analysis.
AID23943Diffusion constant for permeability of stratum corneum1987Journal of medicinal chemistry, Jul, Volume: 30, Issue:7
The role of solvent-accessible surface area in determining partition coefficients.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID127352Binding affinity against human monoclonal antibody (mAb)-7F22002Journal of medicinal chemistry, Jul-18, Volume: 45, Issue:15
Three-dimensional quantitative structure-activity relationship analysis of ligand binding to human sequence antidigoxin monoclonal antibodies using comparative molecular field analysis.
AID500683Activation of KV1.1/Kvbeta1 chimera deficient in conserved AKR core domain and containing N-type inactivation gate from Kvbeta1 expressed in Xenopus laevis oocytes assessed as increase in steady state current normalized to initial inactivating current at 2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID500685Activation of Kvbeta1 containing inactivation gate spliced into conserved core expressed in Xenopus laevis oocytes coexpressing KV1.1 assessed as increase in steady state current normalized to initial inactivating current at 500 uM by electrophysiology me2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID721754Inhibition of human MATE1-mediated ASP+ uptake expressed in HEK293 cells after 1.5 mins by fluorescence assay2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Discovery of potent, selective multidrug and toxin extrusion transporter 1 (MATE1, SLC47A1) inhibitors through prescription drug profiling and computational modeling.
AID51055Binding affinity to human CBG receptor (corticosteroid-binding globulins)2004Journal of medicinal chemistry, May-20, Volume: 47, Issue:11
Comparative molecular active site analysis (CoMASA). 1. An approach to rapid evaluation of 3D QSAR.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID500686Activation of KV1.1 expressed in Xenopus laevis oocytes coexpressing Kvbeta1 W155A mutant assessed as increase in steady state current normalized to initial inactivating current at 500 uM by electrophysiology method2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID237685Lipophilicity determined as logarithm of the partition coefficient in the alkane/water system2005Journal of medicinal chemistry, May-05, Volume: 48, Issue:9
Calculating virtual log P in the alkane/water system (log P(N)(alk)) and its derived parameters deltalog P(N)(oct-alk) and log D(pH)(alk).
AID74373Relative binding affinity to glucocorticoid receptor on cytosol from hepatoma tissue cells at 24 hr1988Journal of medicinal chemistry, Jun, Volume: 31, Issue:6
Binding of steroids to the progestin and glucocorticoid receptors analyzed by correspondence analysis.
AID127350Binding affinity against human monoclonal antibody (mAb)-1B32002Journal of medicinal chemistry, Jul-18, Volume: 45, Issue:15
Three-dimensional quantitative structure-activity relationship analysis of ligand binding to human sequence antidigoxin monoclonal antibodies using comparative molecular field analysis.
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID455986Permeability across human Caco-2 cells2009Bioorganic & medicinal chemistry, Oct-01, Volume: 17, Issue:19
Computational modeling of novel inhibitors targeting the Akt pleckstrin homology domain.
AID51048In silico binding affinity to human corticosteriod binding globulin1997Journal of medicinal chemistry, Sep-26, Volume: 40, Issue:20
Validation of EGSITE2, a mixed integer program for deducing objective site models for experimental binding data.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID500688Activation of KV1.1 expressed in Xenopus laevis oocytes coexpressing Kvbeta1 V245R mutant assessed as increase in steady state current normalized to initial inactivating current at 500 uM by electrophysiology method2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID500689Induction of dissociation of KV1.1 T1 domain/rat Kvbeta2 complex by solid phase binding assay2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID500687Activation of KV1.1 expressed in Xenopus laevis oocytes coexpressing Kvbeta1 W155A mutant assessed as increase in steady state current normalized to initial inactivating current by electrophysiology method2008Nature chemical biology, Nov, Volume: 4, Issue:11
Cortisone dissociates the Shaker family K+ channels from their beta subunits.
AID51054Binding affinity for corticosteroid binding globulin is expressed as log(1/k)1996Journal of medicinal chemistry, May-24, Volume: 39, Issue:11
Comparative molecular moment analysis (CoMMA): 3D-QSAR without molecular superposition.
AID592681Apparent permeability across human Caco2 cell membrane after 2 hrs by LC-MS/MS analysis2011Bioorganic & medicinal chemistry, Apr-15, Volume: 19, Issue:8
QSAR-based permeability model for drug-like compounds.
AID212737Binding affinity against testosterone-binding globulin (TeBG)1993Journal of medicinal chemistry, Feb-19, Volume: 36, Issue:4
Structure-activity relationships from molecular similarity matrices.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347059CD47-SIRPalpha protein protein interaction - Alpha assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID588349qHTS for Inhibitors of ATXN expression: Validation of Cytotoxic Assay
AID1347045Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot counterscreen GloSensor control cell line2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347405qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS LOPAC collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347050Natriuretic polypeptide receptor (hNpr2) antagonism - Pilot subtype selectivity assay2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID504836Inducers of the Endoplasmic Reticulum Stress Response (ERSR) in human glioma: Validation2002The Journal of biological chemistry, Apr-19, Volume: 277, Issue:16
Sustained ER Ca2+ depletion suppresses protein synthesis and induces activation-enhanced cell death in mast cells.
AID588378qHTS for Inhibitors of ATXN expression: Validation
AID1347058CD47-SIRPalpha protein protein interaction - HTRF assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347057CD47-SIRPalpha protein protein interaction - LANCE assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347049Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot screen2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347151Optimization of GU AMC qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347410qHTS for inhibitors of adenylyl cyclases using a fission yeast platform: a pilot screen against the NCATS LOPAC library2019Cellular signalling, 08, Volume: 60A fission yeast platform for heterologous expression of mammalian adenylyl cyclases and high throughput screening.
AID588519A screen for compounds that inhibit viral RNA polymerase binding and polymerization activities2011Antiviral research, Sep, Volume: 91, Issue:3
High-throughput screening identification of poliovirus RNA-dependent RNA polymerase inhibitors.
AID540299A screen for compounds that inhibit the MenB enzyme of Mycobacterium tuberculosis2010Bioorganic & medicinal chemistry letters, Nov-01, Volume: 20, Issue:21
Synthesis and SAR studies of 1,4-benzoxazine MenB inhibitors: novel antibacterial agents against Mycobacterium tuberculosis.
AID1159550Human Phosphogluconate dehydrogenase (6PGD) Inhibitor Screening2015Nature cell biology, Nov, Volume: 17, Issue:11
6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (17,594)

TimeframeStudies, This Drug (%)All Drugs %
pre-199015695 (89.21)18.7374
1990's591 (3.36)18.2507
2000's620 (3.52)29.6817
2010's499 (2.84)24.3611
2020's189 (1.07)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 87.61

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index87.61 (24.57)
Research Supply Index9.89 (2.92)
Research Growth Index4.37 (4.65)
Search Engine Demand Index226.08 (26.88)
Search Engine Supply Index2.73 (0.95)

This Compound (87.61)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials171 (0.87%)5.53%
Reviews500 (2.55%)6.00%
Case Studies606 (3.09%)4.05%
Observational9 (0.05%)0.25%
Other18,299 (93.43%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (145)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
An Open-label, 2-part Study Designed to Assess the Absolute Bioavailability of CORT118335 and Determine the Mass Balance Recovery, Absorption, Metabolism and Elimination, and Metabolite Profile and Identification of Metabolite Structures of [14C]-CORT1183 [NCT03878264]Phase 112 participants (Actual)Interventional2018-08-06Completed
A Multicenter Study, Randomized, Double-blind With 2 Groups as Prove of Concept for the Treatment of ACEI Induced Angioedema With Subcutaneous Icatibant [NCT01154361]Phase 20 participants InterventionalCompleted
Lipografting Versus Steroid Injections for Treatment of Primary Mild to Moderate Carpal Tunnel Syndrome [NCT03722303]Early Phase 1100 participants (Anticipated)Interventional2016-12-19Recruiting
A Phase II Study of Dose-Adjusted Etoposide, Prednisone, Vincristine, Cyclophosphamide, and Doxorubicin (DA-EPOCH) as Front-Line Therapy for Adults With Acute Lymphoblastic Leukemia/Lymphoma [NCT03023046]Phase 254 participants (Actual)Interventional2017-02-23Completed
Immune Checkpoint Blockade for Kidney Transplant Recipients With Selected Unresectable or Metastatic Cancers [NCT03816332]Phase 112 participants (Actual)Interventional2019-11-08Active, not recruiting
Randomized Phase II Open Label Study of Lenalidomide R-CHOP (R2CHOP) vs. RCHOP (Rituximab, Cyclophosphamide, Doxorubicin, Vincristine and Prednisone) in Patients With Newly Diagnosed Diffuse Large B Cell Lymphoma [NCT01856192]Phase 2349 participants (Actual)Interventional2013-08-27Active, not recruiting
Non-surgical Treatment of Knee Osteoarthritis - a Comparison of Effects in 2200 Patients [NCT02091830]2,262 participants (Actual)Observational2013-01-31Completed
A Phase 1 Adaptive Dose, Double-Blind, Placebo-Controlled, Single and Multiple Ascending Dose Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of Orally Administered CORT113176 in Healthy Subjects, With an Optional Pharmacological Effects [NCT04249323]Phase 1110 participants (Actual)Interventional2020-01-27Completed
A Phase III Randomized Trial of Intravenous Gammaglobulin Therapy for Patients With Neuroblastoma Associated Opsoclonus-Myoclonus-Ataxia Syndrome Treated With Chemotherapy and Prednisone [NCT00033293]Phase 353 participants (Actual)Interventional2004-03-15Completed
A Phase 1, Randomized, Open-label, Crossover Study to Determine the Relative Bioavailability of Relacorilant Administered as 3×100-mg Softgel Capsules, 3×100 mg Hard Shell Capsules, and 6×50-mg Hard-shell Capsules in Healthy Adult Subjects [NCT03540836]Phase 130 participants (Actual)Interventional2018-05-24Completed
A Phase I Study of Dose-Adjusted Etoposide, Prednisone, Vincristine, Cyclophosphamide, and Doxorubicin Plus Escalating Doses of Inotuzumab Ozogamicin (DA-EPOCH-InO) in Relapsed or Refractory B-Cell Acute Lymphoblastic Leukemia [NCT03991884]Phase 124 participants (Actual)Interventional2019-09-24Completed
A Phase I Adaptive Dose, Double-blind, Placebo-controlled, Single and Multiple Ascending Dose Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Pharmacological Effects of Orally Administered CORT118335 in Healthy Subjects [NCT03315338]Phase 1143 participants (Actual)Interventional2017-09-15Completed
Phase II Study of Combination of Hyper-CVAD and Dasatinib (NSC-732517) With or Without Allogeneic Stem Cell Transplant in Patients With Philadelphia (Ph) Chromosome Positive and/or BCR-ABL Positive Acute Lymphoblastic Leukemia (ALL) (A BMT Study) [NCT00792948]Phase 297 participants (Actual)Interventional2009-09-01Active, not recruiting
A Phase I Adaptive Dose, Double-Blind, Placebo-Controlled, SAD and MAD Study to Measure the Safety, Tolerability, Pharmacokinetics and Pharmacological Effects of Orally Administered CORT125134 in Healthy Subjects [NCT03508635]Phase 1130 participants (Actual)Interventional2014-09-30Completed
A Phase I-II Trial of DA-EPOCH-R Plus Ixazomib as Frontline Therapy for Patients With MYC-aberrant Lymphoid Malignancies: The DACIPHOR Regimen [NCT02481310]Phase 1/Phase 238 participants (Actual)Interventional2015-10-28Active, not recruiting
A Pilot Study of Intravenous EZN-2285 (SC-PEG E. Coli L-asparaginase) or Intravenous Oncaspar® in the Treatment of Patients With High-Risk Acute Lymphoblastic Leukemia (ALL) [NCT00671034]Phase 3166 participants (Actual)Interventional2008-07-21Completed
A Pilot Study to Estimate the Safety and Tolerability of the Combination of Polatuzumab Vedotin With Dose Adjusted Rituximab, Etoposide, Cyclophosphamide, and Doxorubicin (DA-EPCH-PR) for Upfront Treatment of Aggressive B-Cell Non-Hodgkin Lymphomas [NCT04231877]Phase 150 participants (Anticipated)Interventional2020-10-27Recruiting
A Phase II Study to Determine the Response Kinetics, Safety, and Efficacy of Brentuximab Vedotin and Nivolumab Alone and Then Combined With Rituximab, Cyclophosphamide, Doxorubicin, and Prednisone for Patients With Untreated Primary Mediastinal Large B-Ce [NCT04745949]Phase 240 participants (Anticipated)Interventional2021-05-10Recruiting
Stop LCNP: High Dose Steroid Therapy for Late Radiation-Associated Lower Cranial Neuropathy: A Phase I/II Dose Finding Trial and Data Registry [NCT04151082]Phase 1/Phase 215 participants (Actual)Interventional2019-10-31Active, not recruiting
A Phase III Randomized Trial of Blinatumomab for Newly Diagnosed BCR-ABL-Negative B Lineage Acute Lymphoblastic Leukemia in Adults [NCT02003222]Phase 3488 participants (Actual)Interventional2014-05-19Active, not recruiting
Phase II Study of Combination of Hyper-CVAD and Dasatinib in Patients With Philadelphia (Ph) Chromosome Positive and/or BCR-ABL Positive Acute Lymphoblastic Leukemia (ALL) [NCT00390793]Phase 2107 participants (Actual)Interventional2006-09-28Active, not recruiting
A Phase II Study With a Lead-in Safety Phase of Abiraterone in Combination With PDMX1001/Niclosamide in Castration-Resistant Prostate Cancer (CRPC) [NCT02807805]Phase 237 participants (Actual)Interventional2016-10-31Active, not recruiting
Phase II Study of Combination of Hyper-CVAD and Ponatinib in Patients With Philadelphia (PH) Chromosome Positive and/or BCR-ABL Positive Acute Lymphoblastic Leukemia (ALL) [NCT01424982]Phase 288 participants (Actual)Interventional2011-10-05Active, not recruiting
A Phase I/II Trial of Vorinostat (SAHA) (NSC-701852) in Combination With Rituximab-CHOP in Patients With Newly Diagnosed Advanced Stage Diffuse Large B-Cell Lymphoma (DLBCL) [NCT00972478]Phase 1/Phase 283 participants (Actual)Interventional2010-11-15Active, not recruiting
Phase I and Dose-Expansion Study of Ibrutinib and R-da-EPOCH for Front Line Treatment of AIDS-Related Lymphomas [NCT03220022]Phase 154 participants (Anticipated)Interventional2018-03-16Recruiting
A Sequential Phase I/Randomized Phase II Trial of Vorinostat and Risk-Adapted Chemotherapy With Rituximab in HIV-Related B-Cell Non-Hodgkin's Lymphoma [NCT01193842]Phase 1/Phase 2107 participants (Actual)Interventional2010-10-06Completed
An Intergroup Phase III Randomized Controlled Trial Comparing Melphalan, Prednisone and Thalidomide (MPT) Versus Melphalan, Prednisone and Lenalidomide (Revlimid(TM))(MPR) in Newly Diagnosed Multiple Myeloma Patients Who Are Not Candidates for High-Dose T [NCT00602641]Phase 3306 participants (Actual)Interventional2008-02-29Active, not recruiting
Intensified Methotrexate, Nelarabine (Compound 506U78) and Augmented BFM Therapy for Children and Young Adults With Newly Diagnosed T-cell Acute Lymphoblastic Leukemia (ALL) or T-cell Lymphoblastic Lymphoma [NCT00408005]Phase 31,895 participants (Actual)Interventional2007-01-22Active, not recruiting
A Phase II Neoadjuvant Study of Apalutamide, Abiraterone Acetate, Prednisone, Degarelix and Indomethacin in Men With Localized Prostate Cancer Pre-Prostatectomy [NCT02849990]Phase 222 participants (Actual)Interventional2017-03-09Completed
High Risk B-Precursor Acute Lymphoblastic Leukemia (ALL) [NCT00075725]Phase 33,154 participants (Actual)Interventional2003-12-29Completed
A Phase III Groupwide Study of Dose-Intensive Response-Based Chemotherapy and Radiation Therapy for Children and Adolescents With Newly Diagnosed Intermediate Risk Hodgkin Disease [NCT00025259]Phase 31,734 participants (Actual)Interventional2002-09-30Completed
Phase I/Ib Study of Parsaclisib (INCB50465), Rituximab, Cyclophosphamide, Doxorubicin, Vincristine, and Prednisone (PaR-CHOP) Immunochemotherapy for Patients With Newly Diagnosed High Risk Diffuse Large B-Cell Lymphoma [NCT04323956]Phase 150 participants (Actual)Interventional2020-06-15Active, not recruiting
A Double-blind, Randomised, Placebo-controlled Study of the Safety, Tolerability, Pharmacokinetics (PK), and Pharmacodynamics (PD) of SAD and MAD of CORT125281 in Healthy Subjects [NCT03335956]Phase 148 participants (Actual)Interventional2017-09-21Completed
A Phase II Study Evaluating Safety and Efficacy of Polatuzumab Vedotin in Combination With Rituximab, Cyclophosphamide, Doxorubicin, and Prednisone in Patients With Previously Untreated Double and Triple Hit Lymphoma, Double Expressor Lymphoma and High-Gr [NCT04479267]Phase 249 participants (Anticipated)Interventional2020-08-21Recruiting
Randomized Three-Arm Trial to Evaluate the Effect of Neoadjuvant Apalutamide Alone or in Combination With Abiraterone Acetate and GnRH Agonist on Enhancing Surgical Outcome of Nerve-Sparing Radical Prostatectomy in Men With High-Risk Prostate Cancer [NCT02949284]Phase 290 participants (Anticipated)Interventional2017-06-20Recruiting
A Phase 1 Study of Lenalidomide in Combination With EPOCH Chemotherapy for HTLV-Associated Adult T-Cell Leukemia-Lymphoma (ATLL) [NCT04301076]Phase 130 participants (Anticipated)Interventional2021-08-31Recruiting
Advanced ChemoHormonal Therapy for Treatment Naïve Metastatic Prostate Cancer: Apalutamide and Abiraterone Acetate With Prednisone and Androgen Deprivation Therapy After Treatment With Docetaxel and Androgen Deprivation Therapy [NCT04267887]Phase 27 participants (Actual)Interventional2020-05-11Active, not recruiting
The Efficacy of Botulinum Toxin to the Flexor Digitorum Brevis Versus Corticosteroid to the Plantar Fascia for the Treatment of Refractory Plantar Fasciitis: A Randomized-Controlled Trial [NCT05367271]Phase 2/Phase 365 participants (Anticipated)Interventional2022-08-23Recruiting
A Randomized Study of Finite Androgen Ablation vs. Finite Androgen Ablation in Combination With Abiraterone Acetate and Prednisone in Patients With Prostate Cancer Who Have PSA Progression After Prostatectomy and/or Radiotherapy [NCT01786265]Phase 2310 participants (Anticipated)Interventional2013-02-05Active, not recruiting
A Pragmatic Phase II Study Evaluating Tolerability in Prostate Cancer Patients Treated With Abiraterone + Prednisone or Darolutamide [NCT06173362]Phase 275 participants (Anticipated)Interventional2023-11-09Recruiting
A Phase 1/2 Study of Nivolumab and Ipilimumab in Combination With Sirolimus and Prednisone in Kidney Transplant Recipients With Selected Unresectable or Metastatic Cutaneous Cancers [NCT05896839]Phase 1/Phase 216 participants (Anticipated)Interventional2024-08-11Recruiting
A Phase II Study of Nivolumab in Combination With DA-REPOCH Followed by Short Course Nivolumab Consolidation in Patients With Aggressive B-Cell Non-Hodgkin's Lymphoma [NCT03749018]Phase 230 participants (Anticipated)Interventional2019-01-02Active, not recruiting
A Phase 1 Study Combining Venetoclax With a Pediatric-Inspired Regimen for Newly Diagnosed Adults With B Cell Ph-Like Acute Lymphoblastic Leukemia [NCT05157971]Phase 16 participants (Anticipated)Interventional2022-03-17Recruiting
A Phase II Study of Blinatumomab and POMP (Prednisone, Vincristine, Methotrexate, 6-Mercaptopurine) for Patients ≥ 65 Years of Age With Newly Diagnosed Philadelphia-Chromosome Negative (Ph-) Acute Lymphoblastic Leukemia (ALL) and of Dasatinib, Prednisone [NCT02143414]Phase 253 participants (Actual)Interventional2015-06-30Active, not recruiting
A Phase II Study of Dose-Adjusted Etoposide, Prednisone, Vincristine, Cyclophosphamide, and Doxorubicin Plus Asparaginase (DA-EPOCH-A) for Adults With Acute Lymphoblastic Leukemia/Lymphoma [NCT02538926]Phase 20 participants (Actual)Interventional2018-07-01Withdrawn(stopped due to Drugs unavailable)
Phase II Study of the Hyper-CVAD Regimen in Sequential Combination With Blinatumomab With or Without Inotuzumab Ozogamicin as Frontline Therapy for Adults With B-Cell Lineage Acute Lymphocytic Leukemia [NCT02877303]Phase 280 participants (Anticipated)Interventional2016-11-01Recruiting
A Prospective, Randomized Study Comparing One vs. Two Cortisone Injections for Trigger Finger [NCT00951236]392 participants (Anticipated)Interventional2009-05-31Recruiting
Impact of Obesity on the Pharmacokinetics of Anticancer Therapy in Children With High Risk Acute Lymphoblastic Leukemia (ALL) [NCT00900445]0 participants (Actual)Observational2008-03-24Withdrawn
A Randomized Phase 3 Study of Brentuximab Vedotin (SGN-35) for Newly Diagnosed High-Risk Classical Hodgkin Lymphoma (cHL) in Children and Young Adults [NCT02166463]Phase 3600 participants (Actual)Interventional2015-03-19Active, not recruiting
An Open-Label, Repeat-Dose Study to Evaluate the Pharmacokinetics of Orally Administered CORT125134 Using the Current Capsule Formulation in Healthy Subjects [NCT06094790]Phase 132 participants (Actual)Interventional2017-05-18Completed
A Phase 1, Randomized, Open-Label, Single-Dose, Three-Way Crossover Study to Evaluate The Effect of Food on the Oral Bioavailability of Relacorilant in Healthy Subjects [NCT06094738]Phase 130 participants (Actual)Interventional2020-09-19Completed
A Randomized Phase 3 Interim Response Adapted Trial Comparing Standard Therapy With Immuno-oncology Therapy for Children and Adults With Newly Diagnosed Stage I and II Classic Hodgkin Lymphoma [NCT05675410]Phase 31,875 participants (Anticipated)Interventional2023-05-11Recruiting
A Phase II/III Randomized Study of R-MiniCHOP With or Without CC-486 (Oral Azacitidine) in Participants Age 75 Years or Older With Newly Diagnosed Diffuse Large B Cell Lymphoma, Grade IIIB Follicular Lymphoma, Transformed Lymphoma, and High-Grade B-Cell L [NCT04799275]Phase 2/Phase 3422 participants (Anticipated)Interventional2021-05-20Recruiting
A Phase 3 Trial Investigating Blinatumomab (NSC# 765986) in Combination With Chemotherapy in Patients With Newly Diagnosed Standard Risk or Down Syndrome B-Lymphoblastic Leukemia (B-ALL) and the Treatment of Patients With Localized B-Lymphoblastic Lymphom [NCT03914625]Phase 36,720 participants (Anticipated)Interventional2019-07-03Recruiting
Comparative, Randomized Study on the Anti-inflammatory and Regenerative Efficacy of a New Medical Device (DM) Based on Hydrolyzed Collagen Peptides in Patients With Femoro-acetabular Impingement Undergoing Hip Arthroscopy [NCT06082271]25 participants (Actual)Interventional2021-05-28Active, not recruiting
A Phase II Study of Modified VR-CAP and Acalabrutinib as First Line Therapy for Transplant-Eligible Patients With Mantle Cell Lymphoma [NCT04626791]Phase 245 participants (Anticipated)Interventional2021-08-03Recruiting
A Phase 1 Study of R-CHOP Plus SYK Inhibitor TAK-659 for the Front-Line Treatment of High-Risk Diffuse Large B Cell Lymphoma (DLBCL) [NCT03742258]Phase 112 participants (Actual)Interventional2019-03-13Active, not recruiting
Phase 2 Clinical Trial for Comprehensive Treatment Program for Patients With Blastic Plasmacytoid Dendritic Cell Neoplasm (BPDCN): Tagraxofusp (SL-401) in Combination With HCVAD/Mini-CVD and VENETOCLAX [NCT04216524]Phase 240 participants (Anticipated)Interventional2020-05-29Recruiting
Correlation of Auditory Evoked Brainstem Response Characteristics and Salivary Cortisone Concentration in Noise-exposed Workers [NCT04183361]100 participants (Anticipated)Observational2019-11-01Enrolling by invitation
Cortisone Injection vs Trigger Point Dry Needling Fin the Treatment of Greater Trochanter Pain Syndrome: A Pilot Study [NCT02639039]Phase 450 participants (Actual)Interventional2013-02-28Completed
Randomized Phase II Trial of Docetaxel With or Without PSA-TRICOM Vaccine in Patients With Castrate-Resistant Metastatic Prostate Cancer [NCT01145508]Phase 210 participants (Actual)Interventional2010-08-31Terminated(stopped due to Poor accrual)
A Phase 1b, Open-Label Study Evaluating the Safety, Efficacy, and Pharmacokinetics of Miricorilant in Adult Patients With Presumed Nonalcoholic Steatohepatitis (NASH) [NCT05117489]Phase 170 participants (Anticipated)Interventional2021-11-23Recruiting
Smart Stop: A Phase II Trial of Rituximab, Lenalidomide, Acalabrutinib, Tafasitamab Prior to and With Standard Chemotherapy for Patients With Newly Diagnosed DLBCL [NCT04978584]Phase 260 participants (Anticipated)Interventional2022-03-03Recruiting
A Phase I Study Evaluating the Safety, Tolerability and Biological Activity of EZN-3042, a Survivin mRNA Antagonist, Administered With Re-induction Chemotherapy in Children With Relapsed Acute Lymphoblastic Leukemia (ALL) [NCT01186328]Phase 16 participants (Actual)Interventional2010-08-24Terminated(stopped due to Enzon Pharmaceuticals decided to end its development of EZN-3042.)
The Use of Bone Marrow Aspirate Concentrate in the Context of Hip Osteoarthritis: A Randomized Controlled Trial [NCT03410355]6 participants (Actual)Interventional2018-02-01Terminated(stopped due to Health Canada no longer allowed use of BMAC)
A Randomized Clinical Study Comparing Topical 0.05% Clobetasol Propianate in Vaseline With UVA-1 Phototherapy in the Treatment of Vulvar Lichen Sclerosus [NCT01400022]30 participants (Actual)Interventional2010-08-31Completed
ACADEMIC: A Randomized Phase II Clinical Trial of ADT Combined With Abiraterone or Docetaxel in Metastatic Hormone Sensitive Prostate Cancer [NCT03827473]Phase 21 participants (Actual)Interventional2019-02-08Terminated(stopped due to The trial was closed because the changing standard of care landscape, making this trial not impactful anymore.)
Phase III Randomised Study on Liposomal Cytarabine (DepoCyte®) vs. Intrathecal Triple for CNS-Treatment During Maintenance Therapy in High-Risk Acute Lymphoblastic Leukemia Patients in NOPHO ALL 2008 Treatment Protocol [NCT00991744]Phase 3100 participants (Anticipated)Interventional2009-01-31Suspended(stopped due to Sterility problems in DepoCyte production)
Intensified Tyrosine Kinase Inhibitor Therapy (Dasatinib NSC# 732517) in Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia (ALL) [NCT00720109]Phase 2/Phase 363 participants (Actual)Interventional2008-07-14Completed
Influence of Cortisone on QTc-interval [NCT03082339]105 participants (Actual)Observational [Patient Registry]2017-04-01Completed
A Phase I/II Trial of CHOEP Chemotherapy Plus Lenalidomide as Front Line Therapy for Patients With Stage II, III and IV Peripheral T-Cell Non-Hodgkin's Lymphoma [NCT02561273]Phase 1/Phase 254 participants (Actual)Interventional2015-09-28Completed
A Prospective, Open, Randomized Controlled Stage II Trial Investigating the Efficacy and Safety of Thymosin Alpha-1 in Treating Moderate to Severe Immune-related Adverse Events [NCT06178146]Phase 440 participants (Anticipated)Interventional2023-09-01Recruiting
A Phase III Randomized Trial of Steroids + Tyrosine Kinase Inhibitor (TKI) Induction With Chemotherapy or Blinatumomab for Newly Diagnosed BCR-ABL-Positive Acute Lymphoblastic Leukemia (ALL) in Adults [NCT04530565]Phase 3348 participants (Anticipated)Interventional2021-01-25Recruiting
Phase II Study of Talazoparib With Androgen Deprivation Therapy and Abiraterone in Castration Sensitive Prostate Cancer [NCT04734730]Phase 270 participants (Anticipated)Interventional2021-05-04Recruiting
A Randomized Single-blinded Clinical Trial of the Efficacy of Intra-articular Infiltration of Cingal (Sodium Hyaluronate/Triamcinolone) Versus Cortisone (Triamcinolone) in Patients With Osteoarthritis of the Shoulder. [NCT05408065]84 participants (Anticipated)Interventional2023-09-30Not yet recruiting
Optimizing Immunosuppression for Steroid-Refractory Anti-PD-1/PD-L1 Pneumonitis [NCT04438382]Phase 21 participants (Actual)Interventional2021-01-07Active, not recruiting
Randomized Phase II Trial in Early Relapsing or Refractory Follicular Lymphoma [NCT03269669]Phase 295 participants (Anticipated)Interventional2018-01-23Recruiting
A Phase 1 Study to Assess the Safety, Tolerability, and Pharmacokinetics of Miricorilant Tablet Formulations Following Single and Multiple Oral Doses in Healthy Participants [NCT04672499]Phase 136 participants (Actual)Interventional2020-04-27Completed
A Dynamic Allocation Modular Sequential Trial of Approved and Promising Therapies in Men With Metastatic Castrate Resistant Prostate Cancer [NCT02703623]Phase 2196 participants (Actual)Interventional2016-05-18Active, not recruiting
Phase II Study of the Dose Adjusted EPOCH Regimen in Combination With Ofatumumab/Rituximab as Therapy for Patients With Newly Diagnosed or Relapsed/Refractory Burkitt Leukemia or Relapsed/Refractory Acute Lymphoblastic Leukemia [NCT02199184]Phase 26 participants (Actual)Interventional2015-01-14Completed
Treatment of Children With Newly-Diagnosed Low Stage Lymphocyte Predominant Hodgkin Disease (LPHD) [NCT00107198]Phase 2188 participants (Actual)Interventional2006-01-02Active, not recruiting
Randomized, Double-blind, Two Arms, Multicenter, Phase III Study of Berinert for Treatment of ACE Induced Angioedema [NCT01843530]Phase 331 participants (Actual)Interventional2013-11-30Completed
Intensified PEG-Asparaginase in High Risk Acute Lymphoblastic Leukemia (ALL): A Pilot Study [NCT00866307]Phase 1104 participants (Actual)Interventional2009-02-23Completed
A Phase 2 Study of SNDX-5613 in Combination With Chemotherapy for Patients With Relapsed or Refractory KMT2A-Rearranged Infant Leukemia [NCT05761171]Phase 278 participants (Anticipated)Interventional2023-11-20Recruiting
A Phase I Study of Venetoclax in Combination With Cytotoxic Chemotherapy, Including Calaspargase Pegol, for Children, Adolescents and Young Adults With High-Risk Hematologic Malignancies [NCT05292664]Phase 192 participants (Anticipated)Interventional2023-03-29Recruiting
Interest of Cryotherapy or Cortisone Aerosol Therapy in Early Post-operative Swallowing Disorders Following Total Thyroidectomy [NCT02855866]240 participants (Actual)Interventional2013-09-03Completed
A Phase II Study of Rituximab, Lenalidomide, and Ibrutinib Combined With Chemotherapy for Patients With High Risk Diffuse Large B-Cell Lymphoma [NCT02636322]Phase 260 participants (Actual)Interventional2016-03-29Completed
A Phase I Adaptive Dose, Double-Blind, Placebo-Controlled, Single and Multiple Ascending Dose Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of Orally Administered CORT125236 in Healthy Subjects, With an Optional Pharmacological Effects [NCT05003713]Phase 182 participants (Actual)Interventional2021-08-03Completed
A Randomized Trial of Cortisone Injection Versus Bone Marrow Aspirate Injection Therapy for Glenohumeral Osteoarthritis [NCT03580148]Phase 2/Phase 334 participants (Actual)Interventional2015-10-08Completed
Phase II Study of the Hyper-CVAD Regimen in Sequential Combination With Inotuzumab Ozogamicin as Frontline Therapy for Adults With B-Cell Lineage Acute Lymphocytic Leukemia [NCT03488225]Phase 24 participants (Actual)Interventional2018-03-28Terminated(stopped due to the study was closed early due to competing trials)
A Selective Frontline Cabazitaxel Therapeutic Pathway for Castration-Resistant Prostate Cancer With Integrated Biomarkers [NCT02844582]Phase 22 participants (Actual)Interventional2017-12-20Terminated(stopped due to Poor accrual of subjects onto study)
A Groupwide Pilot Study to Test the Tolerability and Biologic Activity of the Addition of Azacitidine (NSC# 102816) to Chemotherapy in Infants With Acute Lymphoblastic Leukemia (ALL) and KMT2A (MLL) Gene Rearrangement [NCT02828358]Phase 278 participants (Actual)Interventional2017-04-01Active, not recruiting
A Phase III Study of Risk Directed Therapy for Infants With Acute Lymphoblastic Leukemia (ALL): Randomization of Highest Risk Infants to Intensive Chemotherapy +/- FLT3 Inhibition (CEP-701, Lestaurtinib; NSC#617807) [NCT00557193]Phase 3218 participants (Actual)Interventional2008-01-15Active, not recruiting
Safety and Efficacy of Adult Adipose-Derived Stem Cell Injections Into Partial Thickness Rotator Cuff Tears [NCT02918136]18 participants (Actual)Interventional2016-12-31Completed
Phase II Study to Determine the Effects of Neoadjuvant Docetaxel on Newly Diagnosed Intermediate and High Grade Cancer of the Prostate in Patients Who Are Scheduled for Radical Prostatectomy With Genomic Correlates of Pathological Response [NCT00598858]Phase 20 participants (Actual)Interventional2009-01-31Withdrawn(stopped due to Halted due to zero accrual and lack of funding)
A PedAL/EuPAL Phase 1/2 Trial of IMGN632 in Pediatric Patients With Relapsed or Refractory Leukemia [NCT05320380]Phase 1/Phase 20 participants (Actual)Interventional2023-08-01Withdrawn(stopped due to Withdrawn per CS0150757)
A Phase 2, Study of Apalutamide and Abiraterone Acetate in Castration-Resistant Metastatic Prostate Cancer Patients Evaluating a Predetermined Biomarker Signature [NCT03360721]Phase 27 participants (Actual)Interventional2018-03-06Active, not recruiting
A Dose-Finding Phase Ib Study of the Oral BCL-2 Inhibitor Venetoclax (ABT-199) in Combination With Standard Induction Therapy, Dasatinib, Prednisone, (and Rituximab in CD20+ Patients) in Adult Patients With Newly Diagnosed and Relapsed Philadelphia Chromo [NCT04872790]Phase 120 participants (Anticipated)Interventional2022-09-02Recruiting
A Phase 2 Course Determining Study for Men With Hormone-Naïve Metastatic Prostate Cancer (HNMPCa) [NCT03821792]Phase 260 participants (Anticipated)Interventional2019-07-22Active, not recruiting
A Randomized Phase 3 Trial of Nivolumab (NSC# 748726) in Combination With Chemo-Immunotherapy for the Treatment of Newly Diagnosed Primary Mediastinal B-Cell Lymphoma [NCT04759586]Phase 3244 participants (Anticipated)Interventional2021-10-05Recruiting
Randomized Phase II/III Study of Venetoclax (ABT199) Plus Chemoimmunotherapy for MYC/BCL2 Double-Hit and Double Expressing Lymphomas [NCT03984448]Phase 2/Phase 3363 participants (Anticipated)Interventional2019-10-22Active, not recruiting
Phase II Study of Hyper-CVAD Plus Nelarabine in Previously Untreated T-ALL and Lymphoblastic Lymphoma [NCT00501826]Phase 2160 participants (Anticipated)Interventional2007-07-11Recruiting
A Phase I-II Study of the Combination of Ruxolitinib or Dasatinib With Chemotherapy in Patients With Philadelphia Chromosome (Ph)-Like Acute Lymphoblastic Leukemia (ALL) [NCT02420717]Phase 211 participants (Actual)Interventional2015-07-15Terminated(stopped due to Study was closed early due to low accrual and lack of response.)
Gene Transfer for Patients With Fanconi Anemia Complementation Group A (FANCA) [NCT01331018]Phase 13 participants (Actual)Interventional2012-02-22Active, not recruiting
Open Label Pharmacodynamic Study of Abiraterone Acetate in the Treatment of Metastatic, Castration Resistant Prostate Cancer [NCT01503229]Phase 232 participants (Actual)Interventional2012-12-31Completed
Role of Microbiome in the Realm of Immune-Checkpoint Inhibitor Induced GI Complications In Cancer Population [NCT03819296]Phase 1/Phase 2800 participants (Anticipated)Interventional2021-02-21Recruiting
A Randomized Gene Fusion Stratified Phase 2 Trial of Abiraterone With or Without ABT-888 for Patients With Metastatic Castration-Resistant Prostate Cancer [NCT01576172]Phase 2159 participants (Actual)Interventional2012-03-30Completed
Phase I/II Study to Evaluate the Safety and Efficacy of Nivolumab in Combination With R-CHOP in a Cohort of Patients With DLBCL/tFL/ High Grade B-NHL [NCT03704714]Phase 1/Phase 230 participants (Anticipated)Interventional2018-11-20Suspended(stopped due to Protocol being amended for stats/accrual changes as per PI)
Phase Ib/II Study of the Combination of Low-Intensity Chemotherapy and Tagraxofusp in Patients With Acute Lymphoblastic Leukemia (ALL) [NCT05032183]Phase 1/Phase 240 participants (Anticipated)Interventional2022-02-17Recruiting
Intra-articular Botulinum Toxin Type-A in Knee Osteoarthritis - a Randomized, Cortisone Controlled, Double Blind Study. [NCT00279903]Phase 162 participants (Actual)Interventional2005-11-30Completed
Conservative Treatment of Trigger Finger: Outcomes of a Randomized Controlled Trial [NCT05837286]146 participants (Anticipated)Interventional2023-05-01Not yet recruiting
Congenital Adrenal Hyperplasia: Innovative Once Daily Dual Release Hydrocortisone Treatment [NCT03760835]Phase 4150 participants (Anticipated)Interventional2016-08-11Recruiting
Continuous Subcutaneous Hydrocortisone Infusion in Congenital Adrenal Hyperplasia [NCT01771328]Phase 220 participants (Anticipated)Interventional2013-02-28Recruiting
Botulinum Toxin A Versus Steroids for the Treatment of Chronic Plantar Fasciitis: a Randomized Controlled Study [NCT02196155]54 participants (Anticipated)Interventional2016-07-31Recruiting
Effectiveness of Facet Joint Infiltration in Low Back Pain [NCT01447160]Phase 360 participants (Anticipated)Interventional2011-10-31Not yet recruiting
High-Dose Immunosuppressive Therapy Using Carmustine, Etoposide, Cytarabine, and Melphalan (BEAM) + Thymoglobulin Followed by Syngeneic or Autologous Hematopoietic Cell Transplantation for Patients With Autoimmune Neurologic Diseases [NCT00716066]Phase 280 participants (Anticipated)Interventional2008-06-30Recruiting
The Effect of Low-dose Corticosteroids and Theophylline on the Risk of Acute Exacerbations of COPD: the TASCS Randomised Clinical Trial [NCT02261727]Phase 41,670 participants (Actual)Interventional2014-06-30Completed
Comparison of IntraArticular Platelet-Rich-Plasma to Corticosteroid Injections for Patients With Zygapophyseal Joint (Z-Joint) Low Back Pain Confirmed by Dual Intra-Articular Local Anesthetic Injections: A Triple Blinded Randomized Controlled Trial [NCT05188820]50 participants (Anticipated)Interventional2022-04-01Recruiting
Calcific Tendonitis Treatment: Barbotage vs. Barbotage With Cortisone Injection: A Randomized Controlled Double-Blind Study [NCT04126278]Phase 4150 participants (Anticipated)Interventional2020-12-01Recruiting
A Pilot Phase I/II Study to Evaluate the Effects of Taxotere/Prednisone Plus Sunitinib in Chemotherapy-Naïve, Hormone Refractory Prostate Cancer Patients With Biochemical Relapse [NCT00879619]Phase 1/Phase 24 participants (Actual)Interventional2009-07-31Terminated(stopped due to Terminated due to slow accrual.)
A Multicenter, Open-Label Feasibility Study of Daratumumab With Dose-Adjusted EPOCH in Newly Diagnosed Plasmablastic Lymphoma With or Without HIV [NCT04139304]Early Phase 115 participants (Anticipated)Interventional2021-05-24Recruiting
A Phase I/II Trial of Concurrent Chemohormonal Therapy Using Enzalutamide (MDV-3100) and Cabazitaxel in Patients With Metastatic Castration Resistant Prostate Cancer [NCT02522715]Phase 1/Phase 237 participants (Actual)Interventional2015-10-13Active, not recruiting
MK-3475 in Combination With Standard RCHOP Therapy for Previously Untreated Diffuse Large B-Cell Lymphoma [NCT02541565]Phase 130 participants (Actual)Interventional2015-11-24Completed
Radiation Enhancement of Local and Systemic Anti-Prostate Cancer Immune Responses [NCT03649841]Phase 210 participants (Actual)Interventional2020-06-29Terminated(stopped due to Terminated due to low accrual.)
Phase III Randomized Trial of Standard Systemic Therapy (SST) Versus Standard Systemic Therapy Plus Definitive Treatment (Surgery or Radiation) of the Primary Tumor in Metastatic Prostate Cancer [NCT03678025]Phase 31,273 participants (Anticipated)Interventional2018-09-24Recruiting
Cabazitaxel With Abiraterone Versus Abiraterone Alone Randomized Trial for Extensive Disease Following Docetaxel: The CHAARTED2 Trial [NCT03419234]Phase 2223 participants (Actual)Interventional2018-04-26Active, not recruiting
A Phase 2 Study of Brentuximab Vedotin Plus Cyclophosphamide, Doxorubicin, Etoposide, and Prednisone (CHEP-BV) Followed by BV Consolidation in Patients With CD30-Positive Peripheral T-Cell Lymphomas [NCT03113500]Phase 248 participants (Actual)Interventional2017-05-25Active, not recruiting
A Pre-Operative Study to Assess the Effects of Apalutamide Plus LHRH Agonist or Apalutamide Plus Abiraterone Acetate Plus LHRH Agonist for Six Months for Prostate Cancer Patients at High Risk for Recurrence [NCT03279250]Phase 286 participants (Actual)Interventional2017-10-13Completed
An Open-Label Phase 1/2 Multi-Arm Study of DS-1594b as a Single-Agent and in Combination With Azacitidine and Venetoclax or Mini-HCVD for the Treatment of Patients With Acute Myeloid Leukemia (AML) and Acute Lymphoblastic Leukemia (ALL) [NCT04752163]Phase 1/Phase 217 participants (Actual)Interventional2021-03-25Completed
A Phase III Randomized Trial for Newly Diagnosed High Risk B-Lymphoblastic Leukemia (B-ALL) Including a Stratum Evaluating Dasatinib (NSC#732517) in Patients With Ph-like Tyrosine Kinase Inhibitor (TKI) Sensitive Mutations [NCT02883049]Phase 35,937 participants (Actual)Interventional2012-02-29Active, not recruiting
A Study to Assess 11 Beta-hydroxysteroid Dehydrogenase Type 1 Inhibition in Adipose Tissue by SPI-62 [NCT05409027]Phase 112 participants (Actual)Interventional2021-08-05Active, not recruiting
A Randomized International Phase 3 Trial of Imatinib and Chemotherapy With or Without Blinatumomab in Patients With Newly-Diagnosed Philadelphia Chromosome-Positive or Philadelphia Chromosome-Like ABL-Class B-Cell Acute Lymphoblastic Leukemia [NCT06124157]Phase 3680 participants (Anticipated)Interventional2024-01-22Not yet recruiting
Multiple Dose Safety, Tolerability, Plasma and Cerebrospinal-Fluid Pharmacokinetic Study of Oral Doses of CORT113176 [NCT04994743]Phase 116 participants (Actual)Interventional2021-07-13Completed
A Phase Ib Trial of Zanubrutinib in Combination With R-CHOP (ZaR-CHOP) for Patients With Newly Diagnosed Diffuse Large B-Cell Lymphoma [NCT04850495]Phase 124 participants (Anticipated)Interventional2021-11-16Suspended(stopped due to Pending amendment)
A Pilot Study: Association of Beta-2 Adrenergic Agonist and Corticosteroid Injection in the Treatment of Lipomas [NCT00624416]Phase 1/Phase 210 participants (Actual)Interventional2007-10-31Completed
A Phase 2 Study of Loncastuximab Tesirine and Rituximab (Lonca-R) Followed by DA-EPOCH-R in Previously Untreated High-Risk Diffuse Large B-Cell Lymphoma [NCT05600686]Phase 224 participants (Anticipated)Interventional2023-05-24Recruiting
Phase I/II Study of the Combination of Low-Intensity Chemotherapy and Venetoclax (ABT-199) in Patients With Relapsed/Refractory Acute Lymphoblastic Leukemia (ALL) [NCT03808610]Phase 1/Phase 250 participants (Anticipated)Interventional2019-04-03Recruiting
A Multicenter, Randomized, Double-blind, Parallel Controlled Clinical Study on the Efficacy and Safety of Compound E Jiao Jiang(cEJJ)in the Treatment of Postpartum Anemia [NCT06175117]Phase 4360 participants (Anticipated)Interventional2023-12-31Not yet recruiting
A Randomized, Controlled, Multi-Centre Trial on the Effects of Dual-release Hydrocortisone Preparations Versus Conventional Glucocorticoid Replacement Therapy in Patients Affected by Primary and Secondary Adrenal Insufficiency. DREAM Trial. [NCT02277587]Phase 489 participants (Actual)Interventional2014-03-31Completed
A Phase 1, Open-label, Single-dose, Randomized, Crossover Study in Healthy Subjects of the Effects of Co-administration With Food on Exposure, and to Determine the Within-subject Variability in Exposure, to Relacorilant and Its Metabolites [NCT03442621]Phase 130 participants (Actual)Interventional2018-01-16Completed
Phase 2 Study of CJNJ-67652000 (Niraparib/Abiraterone Acetate Fixed-Dose Combination) and Prednisone for Metastatic Castration-Resistant Prostate Cancer Associated With SPOP Mutation With or Without Homologous Recombination Deficiency [NCT05689021]Phase 230 participants (Anticipated)Interventional2023-07-07Recruiting
Phase II Trial of Primary Radiotherapy With Androgen Ablation With or Without Adjuvant Niraparib for Selected High-Risk Locoregional Prostate Cancer [NCT04947254]Phase 2200 participants (Anticipated)Interventional2021-08-05Recruiting
A Randomized Phase II Pilot of Tailored Prednisone Reduction Versus Usual Care for the Treatment of Hyperglycemia During R-CHOP Chemotherapy [NCT03505762]Phase 280 participants (Anticipated)Interventional2018-07-19Recruiting
Extension Study of Protocol RC-001b- Safety and Efficacy of Adult Adipose-Derived Stem Cell Injection Into Partial Thickness Rotator Cuff Tears [NCT04077190]15 participants (Actual)Interventional2019-08-01Completed
Dose-Adjusted Etoposide, Prednisone, Vincristine, Cyclophosphamide, and Doxorubicin (DA-EPOCH) +/- Rituximab (R) + Tafasitamab-cxix for the Treatment of Newly-Diagnosed Adults With Philadelphia Chromosome-Negative (Ph-) B-cell Lymphoblastic Lymphoma/Leuke [NCT05453500]Phase 230 participants (Anticipated)Interventional2023-03-27Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00025259 (4) [back to overview]Grade 3 or 4 Non-hematologic Toxicity
NCT00025259 (4) [back to overview]Event-free Survival
NCT00025259 (4) [back to overview]Disease Response Assessed by Modified RECIST Criteria
NCT00025259 (4) [back to overview]Overall Survival
NCT00033293 (5) [back to overview]Motor Coordination as Assessed by Neurological Examination and Vineland Adaptive Behavior Scale (VABS)
NCT00033293 (5) [back to overview]Tumor Outcome in Terms of Event-free Survival (EFS) Rate Defined as a Relapse or Progression of Neuroblastoma, a Second Malignancy, or Death
NCT00033293 (5) [back to overview]Tumor Outcome in Terms of Overall Survival (OS) Rate
NCT00033293 (5) [back to overview]Functional Outcome as Assessed by Age-appropriate Neuropsychological Testing
NCT00033293 (5) [back to overview]Number of Responders
NCT00075725 (7) [back to overview]Comparison of the Increase in Cure Rate of High Risk ALL Without Causing More Serious Side Effects Between Interventions
NCT00075725 (7) [back to overview]Correlation of Minimal Residual Disease (MRD) Positive With Overall Survival (OS)
NCT00075725 (7) [back to overview]Correlation of Minimal Residual Disease (MRD) Positive With Event Free Survival (EFS)
NCT00075725 (7) [back to overview]Correlation of Minimal Residual Disease (MRD) Negative With Event Free Survival (EFS).
NCT00075725 (7) [back to overview]Correlation of Minimal Residual Disease (MRD) Negative With Overall Survival (OS).
NCT00075725 (7) [back to overview]Correlation of Early Marrow Response Status With MRD Positive.
NCT00075725 (7) [back to overview]Correlation of Early Marrow Response Status With MRD Negative.
NCT00107198 (5) [back to overview]Cure by AV-PC x 3 or AV-PC x 3 + IFRT for Stage I Unresected, Stage I Resected Whose Disease Recurred, and Stage II Patients
NCT00107198 (5) [back to overview]Grade 3 or 4 Toxicity
NCT00107198 (5) [back to overview]Failure-free Survival (FFS)
NCT00107198 (5) [back to overview]Cure by Surgery Alone in Stage I Resected Patients
NCT00107198 (5) [back to overview]Event-free Survival
NCT00408005 (8) [back to overview]Disease-free Survival (DFS) for Randomized Nelarabine T-ALL Cohort (Arm I + Arm III vs. Arm II + Arm IV)
NCT00408005 (8) [back to overview]Disease-free Survival (DFS) for Randomized Nelarabine T-ALL Cohort (Arm I vs. Arm II vs. Arm III vs. Arm IV)
NCT00408005 (8) [back to overview]Cumulative Incidence of CNS Relapse for T-ALL by Risk Group
NCT00408005 (8) [back to overview]Disease-free Survival (DFS) for Randomized Methotrexate T-ALL Cohort (Arm I vs. Arm II vs. Arm III vs. Arm IV)
NCT00408005 (8) [back to overview]Disease-free Survival (DFS) for Randomized Methotrexate T-ALL Cohort (Arm I + Arm II vs. Arm III + Arm IV)
NCT00408005 (8) [back to overview]Disease-free Survival (DFS) for T-cell Lymphoblastic Lymphoma (T-LLy) Cohort
NCT00408005 (8) [back to overview]Cumulative Incidence of CNS Relapse for T-ALL by Risk Group
NCT00408005 (8) [back to overview]Disease-free Survival (DFS) for T-cell Lymphoblastic Lymphoma (T-LLy) Cohort
NCT00557193 (10) [back to overview]Pharmacodynamics PIA Levels in Infants Given Lestaurtinib at DL2 in Combination With Chemotherapy
NCT00557193 (10) [back to overview]Percent Probability of Event Free Survival (EFS) by MRD Status and Treatment Arm
NCT00557193 (10) [back to overview]Percent Probability for Event-free Survival (EFS) of MLL-R Infants Treated With Combination Chemotherapy With or Without Lestaurtinib at DL2
NCT00557193 (10) [back to overview]Percent Probability for Event-free Survival (EFS) for Patients on Arm C at Dose Level 2 (DL2)
NCT00557193 (10) [back to overview]Describe in Vitro Sensitivity as a Molecular Mechanism of Primary Resistance to Lestaurtinib in Leukemic Blasts
NCT00557193 (10) [back to overview]Percent Probability for Event-free Survival (EFS) for Patients on Arm A
NCT00557193 (10) [back to overview]Describe FLT3 Protein Expression as a Molecular Mechanism of Primary Resistance to Lestaurtinib in Leukemic Blasts
NCT00557193 (10) [back to overview]Describe in Vitro Sensitivity as a Molecular Mechanism of Acquired Resistance to Lestaurtinib in Leukemic Blasts
NCT00557193 (10) [back to overview]Describe FLT3 Protein Expression as a Molecular Mechanism of Acquired Resistance to Lestaurtinib in Leukemic Blasts
NCT00557193 (10) [back to overview]Number of Patients Who Experienced Lestaurtinib-related Dose Limiting Toxicity (DLT)
NCT00602641 (4) [back to overview]Progression-Free Survival (PFS)
NCT00602641 (4) [back to overview]Very Good Partial Response (VGPR) Rate
NCT00602641 (4) [back to overview]Change in Functional Assessment of Cancer Therapy-Neurotoxicity Trial Outcome Index (FACT-Ntx TOI) Score From Baseline to Cycle 12
NCT00602641 (4) [back to overview]Overall Survival
NCT00624416 (3) [back to overview]The Number of Subjects Elected to Have the Lipoma Removed.
NCT00624416 (3) [back to overview]The Number of Lipoma Increased in Volume.
NCT00624416 (3) [back to overview]The Average Percent Volume Reduction in the Lipoma.
NCT00671034 (9) [back to overview]Percentage of Participants With Event-free Survival (EFS)
NCT00671034 (9) [back to overview]Plasma and CSF Concentrations of Asparagine in ug/ml
NCT00671034 (9) [back to overview]Percentage of Participants With Complete Remission at the End of Induction
NCT00671034 (9) [back to overview]Toxicities During Post Induction Intensification Therapy (All Grades)
NCT00671034 (9) [back to overview]Pharmacokinetics (PK) (Half-life of SC-PEG E. Coli L-asparaginase (EZN-2285) Compared to Pegaspargase During Induction and Consolidation Therapy)
NCT00671034 (9) [back to overview]Immunogenicity
NCT00671034 (9) [back to overview]Pharmacodynamics (PD)
NCT00671034 (9) [back to overview]Asparaginase Level
NCT00671034 (9) [back to overview]Percentage of Participants With Minimal Residual Disease (MRD)<0.01% at the End of Induction
NCT00720109 (5) [back to overview]Event-Free Survival (EFS) of Patients With Standard-risk Disease Treated With Dasatinib in Combination With Intensified Chemotherapy
NCT00720109 (5) [back to overview]Percent of Patients MRD Positive (MRD > 0.01%) at End of Consolidation
NCT00720109 (5) [back to overview]Overall EFS Rate for the Combined Cohort of Standard- and High-Risk Patients (Who Receive the Final Chosen Dose of Dasatinib)
NCT00720109 (5) [back to overview]Contribution of Dasatinib on Minimal Residual Disease (MRD) After Induction Therapy
NCT00720109 (5) [back to overview]Feasibility and Toxicity of an Intensified Chemotherapeutic Regimen Incorporating Dasatinib for Treatment of Children and Adolescents With Ph+ ALL Assessed by Examining Adverse Events
NCT00792948 (3) [back to overview]Overall Survival (OS)
NCT00792948 (3) [back to overview]Relapse-free Survival (RFS) After Allogeneic Stem Cell Transplantation
NCT00792948 (3) [back to overview]Continuous Complete Remission (CCR) Rate
NCT00866307 (2) [back to overview]AALL08P1 Safety Outcome
NCT00866307 (2) [back to overview]AALL08P1 Feasibility Outcome
NCT00972478 (5) [back to overview]Progression-free Survival (Phase II)
NCT00972478 (5) [back to overview]Toxicity of Vorinostat-R-CHOP in Patients With Newly Diagnosed DLBCL
NCT00972478 (5) [back to overview]Safe Dose of Vorinostat to be Used in Combination With R-CHOP Assessed by CTCAE Version 4.0 (Phase I)
NCT00972478 (5) [back to overview]Response Rate (Complete Response [CR]+Partial Response [PR]) (Phase II)
NCT00972478 (5) [back to overview]Overall Survival (Phase II)
NCT01145508 (1) [back to overview]Overall Survival
NCT01193842 (14) [back to overview]Changes in Epstein-Barr Virus (EBV) Viral Load
NCT01193842 (14) [back to overview]Changes in Human Herpes Virus (HHV)-8 Viral Load
NCT01193842 (14) [back to overview]Changes in Human Herpes Virus (HHV)-8 Viral Load
NCT01193842 (14) [back to overview]Changes in Human Immunodeficiency Virus (HIV) Viral Load
NCT01193842 (14) [back to overview]Percentage of Participant Experiencing Adverse Events (AEs) for Each Treatment Arm as Assessed by Common Terminology Criteria for Adverse Events Version 4.0 (CTCAE v4.0) (Phase II)
NCT01193842 (14) [back to overview]Pharmacokinetic Clearance (Phase I)
NCT01193842 (14) [back to overview]Tumor Response (Phase I)
NCT01193842 (14) [back to overview]Change in Plasma Associated Human Immunodeficiency Virus (HIV)-1 Ribonucleic Acid (RNA) (Phase I)
NCT01193842 (14) [back to overview]Change in CD8 Cell Counts (Phase I)
NCT01193842 (14) [back to overview]Changes in Absolute CD4 Cell Counts (Phase I)
NCT01193842 (14) [back to overview]Percentage of Participants With Complete Response (CR) as Assessed by Response Evaluation Criteria in Solid Tumors (Phase II)
NCT01193842 (14) [back to overview]Overall Survival (OS) (Phase II)
NCT01193842 (14) [back to overview]Event-free Survival (EFS) (Phase II)
NCT01193842 (14) [back to overview]Recommended Phase II Dose of Vorinostat Determined According to Dose-limiting Toxicities Graded Using Common Terminology Criteria for Adverse Events Version 4.0 (CTCAE v4.0) (Phase I)
NCT01503229 (1) [back to overview]Change in Tissue Testosterone and Dihydrotestosterone
NCT01576172 (5) [back to overview]Grade 4 or 5 Adverse Events
NCT01576172 (5) [back to overview]Objective Response Rates in Patients With Measurable Disease.
NCT01576172 (5) [back to overview]Progression-free Survival (PFS)
NCT01576172 (5) [back to overview]Rates of PSA Decline
NCT01576172 (5) [back to overview]Confirmed Prostate-specific Antigen (PSA) Response Rate
NCT01856192 (4) [back to overview]Proportion of Patients With Response
NCT01856192 (4) [back to overview]3-year Progression-free Survival Rate
NCT01856192 (4) [back to overview]Overall Survival Rate at 3 Years
NCT01856192 (4) [back to overview]Proportion of Patients With Complete Response
NCT02143414 (6) [back to overview]Disease-free Survival (Cohort II)
NCT02143414 (6) [back to overview]Number of Participants With Grade 3 Through 5 Adverse Events That Are Related to Study Drugs
NCT02143414 (6) [back to overview]Complete Response Rate (Cohort I)
NCT02143414 (6) [back to overview]Minimal Residual Disease Negativity
NCT02143414 (6) [back to overview]Overall Survival Rate (Cohort I)
NCT02143414 (6) [back to overview]Incidence of Dose-limiting Toxicity (Cohort II)
NCT02166463 (3) [back to overview]Percentages of Patients Experiencing Grade 3+ Peripheral Neuropathy Assessed by Modified Balis Scale
NCT02166463 (3) [back to overview]Event Free Survival (EFS), Where Events Include Disease Progression or Relapse, Second Malignancy, or Death
NCT02166463 (3) [back to overview]Percentages of Patients With Early Response Defined as no Slow Responding Lesions (SRL) and no Progressive Disease (PD) at Any Disease Sites Determined by Positron Emission Tomography (PET) Per Deauville Criteria Through Central Review
NCT02261727 (6) [back to overview]Total COPD Exacerbation Rate
NCT02261727 (6) [back to overview]Time to First COPD Exacerbation
NCT02261727 (6) [back to overview]Quality of Life Measured by St. George's Respiratory Questionnaire (SGRQ)
NCT02261727 (6) [back to overview]Post Bronchodilator FEV1
NCT02261727 (6) [back to overview]Hospitalisations
NCT02261727 (6) [back to overview]Change in COPD Assessment Test (CAT) Score
NCT02420717 (4) [back to overview]Overall Survival
NCT02420717 (4) [back to overview]Maximal Tolerated Dose (MTD) of Ruxolitinib in Combination With Chemotherapy Defined as the Highest Dose Level at Which no More Than 1 Out of 6 Patients Experience a Dose Limiting Toxicity (Phase I)
NCT02420717 (4) [back to overview]Participants With Complete Response (Complete Response [CR]/CR With Incomplete Marrow Recovery [CRi]) (Phase II)
NCT02420717 (4) [back to overview]Progression-free Survival
NCT02481310 (2) [back to overview]To Determine the Recommended Phase II Dose (RP2D) of Ixazomib in Combination With DA-EPOCH-R.
NCT02481310 (2) [back to overview]12-month PFS (Progression Free Survival) of Treatment With Ixazomib in Combination With DA-EPOCH-R (Phase II)
NCT02522715 (4) [back to overview]PSA Response 2, Defined as >= 50% PSA Decline From Baseline
NCT02522715 (4) [back to overview]PSA Response 3, Defined as >= 30% PSA Decline From Baseline
NCT02522715 (4) [back to overview]PSA Response 1, Defined as >= 90% PSA Decline From Baseline
NCT02522715 (4) [back to overview]Percentage of Participants With Dose Limiting ToxicitiesGgraded by National Cancer Institute Common Terminology Criteria for Adverse Events, Version 4.0 (Phase I)
NCT02541565 (1) [back to overview]Number of Participants With a Grade 3 or Higher Toxicity Graded According to National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.0
NCT02561273 (7) [back to overview]Number of Participants With Adverse Events Graded According to Common Toxicity Criteria (CTC) (Phase I)
NCT02561273 (7) [back to overview]Progression-free Survival
NCT02561273 (7) [back to overview]Overall Survival
NCT02561273 (7) [back to overview]Overall Response Rate
NCT02561273 (7) [back to overview]Number of Participants With Adverse Events Graded According to CTC (Phase II)
NCT02561273 (7) [back to overview]Maximum Tolerated Dose (MTD) of Lenalidomide and CHOEP
NCT02561273 (7) [back to overview]Complete Response Rate (Phase II)
NCT02828358 (5) [back to overview]Biologic Activity, Defined as Global Deoxyribonucleic Acid (DNA) Methylation Change in Peripheral Blood Mononuclear Cells (PBMC)s; Day 1 Prior to Second Course of Azacitidine
NCT02828358 (5) [back to overview]Biologic Activity, Defined as Global Deoxyribonucleic Acid (DNA) Methylation Change in Peripheral Blood Mononuclear Cells (PBMC)s; Day 5 of First Course of Azacitidine
NCT02828358 (5) [back to overview]Biologic Activity, Defined as Global Deoxyribonucleic Acid (DNA) Methylation Change in Peripheral Blood Mononuclear Cells (PBMC)s; Day 5 of Second Course of Azacitidine
NCT02828358 (5) [back to overview]Biologic Activity, Defined as Global Deoxyribonucleic Acid (DNA) Methylation Change in Peripheral Blood Mononuclear Cells (PBMC)s; Day 1 Prior to First Course of Azacitidine
NCT02828358 (5) [back to overview]Tolerability of Azacitidine in Combination With Interfant-06 Standard Chemotherapy in Evaluable Infant Patients With Newly Diagnosed ALL With KMT2A Gene Rearrangement (KMT2A-R). KMT2A Gene Rearrangement (KMT2A-R)
NCT02844582 (2) [back to overview]PSA Response Rate, Defined as >= 50% Decline in PSA From Baseline Maintained for at Least 3 Weeks and Measured by the Same Laboratory, and Without Evidence of Other Disease Progression Documented at Time of Confirmatory Values
NCT02844582 (2) [back to overview]Incidence of Adverse Events, Serious Adverse Events, and Discontinuations, Described and Graded According to the National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.03
NCT02849990 (7) [back to overview]Number of Patients With Pathologic T3 Disease After 3 Months of Treatment.
NCT02849990 (7) [back to overview]Number of Participants Without Biochemical Failure at 2 Years
NCT02849990 (7) [back to overview]Pathologic Complete Response Rate as Assessed From Prostatectomy Specimens Following Neoadjuvant Treatment
NCT02849990 (7) [back to overview]The Proportion of Men Who Receive Adjuvant Radiation Therapy
NCT02849990 (7) [back to overview]Number of Patients With no Nodal Metastases After 3 Months of Treatment.
NCT02849990 (7) [back to overview]Overall Survival (OS)
NCT02849990 (7) [back to overview]Number of Patients With a Near Pathologic Complete Response After 3 Months of Treatment
NCT03023046 (5) [back to overview]Number of Participants With Morphological Complete Response Rate
NCT03023046 (5) [back to overview]Number of Participants With Adverse Events
NCT03023046 (5) [back to overview]Event-free Survival
NCT03023046 (5) [back to overview]Number of Participants With Complete Measurable Residual Disease (MRD) Response Rate
NCT03023046 (5) [back to overview]Overall Survival
NCT03113500 (2) [back to overview]Complete Response (CR) Rate After Cyclophosphamide, Doxorubicin, Etoposide, Prednisone, and Brentuximab Vedotin (CHEP-BV) Induction Therapy
NCT03113500 (2) [back to overview]Overall Survival at 1 Year
NCT03279250 (2) [back to overview]The Number of Participants With Rate of Pathologic Stage =< pT2N0 at Prostatectomy
NCT03279250 (2) [back to overview]Number of Participants With Incidence of Adverse Events
NCT03488225 (5) [back to overview]Number of Participants With Adverse Events
NCT03488225 (5) [back to overview]Participants to Achieve Complete Remission (CR):
NCT03488225 (5) [back to overview]Overall Survival
NCT03488225 (5) [back to overview]Number of Participants With Minimal Residual Disease (MRD) Negativity
NCT03488225 (5) [back to overview]Event-Free Survival
NCT03649841 (2) [back to overview]Incidence of Adverse Events
NCT03649841 (2) [back to overview]Rate of Undetectable Prostate Specific Antigen (PSA) (< 0.2)
NCT03816332 (4) [back to overview]Rate of Allograft Loss After Receiving Ipilimumab, Nivolumab, Tacrolimus, and Prednisone
NCT03816332 (4) [back to overview]Number (and Percentage) of Outcome Responses After Receiving Nivolumab, Tacrolimus, and Prednisone
NCT03816332 (4) [back to overview]Duration of Progression-free Survival After Receiving Nivolumab, Tacrolimus, and Prednisone
NCT03816332 (4) [back to overview]Duration of Overall Survival After Receiving Nivolumab, Tacrolimus, and Prednisone
NCT03827473 (5) [back to overview]Prostate Specific Antigen Progression Free Survival (PSA-PFS)
NCT03827473 (5) [back to overview]Change in Quality of Life - PROMIS Fatigue
NCT03827473 (5) [back to overview]Change in Quality of Life - FACT/GOG-NTX
NCT03827473 (5) [back to overview]Change in Quality of Life - FACT-P
NCT03827473 (5) [back to overview]Prostate-specific Antigen (PSA) Response

Grade 3 or 4 Non-hematologic Toxicity

Occurrence of any grade 4 non-hematologic toxicity or grade 3 non-hematologic toxicity which doesn't respond to treatment within 7 days despite recommended therapy modification, or toxic death, which is any death primarily attributable to treatment. Grade 3 is defined to be severe or medically significant but not immediate life-threatening; hospitalization or prolongation of hospitalization indicated; disabling; limiting self-care ADL. Grade 4 refers to toxicities with life-threatening consequences; urgent intervention indicated. (NCT00025259)
Timeframe: Protocol therapy: the overall duration of which is: (n=1684) an average of 137.3 days, median 133.0 days, interquartile range: 101.0, 164.0 days.

InterventionNumber of participants (Number)
Arm I (Patients Off-therapy Before Callback-Induction Only)10
Arm II (RER With CR [ABVE-PC, IFRT])153
Arm III (RER With CR [ABVE-PC])130
Arm IV (RER With Less Than CR [ABVE-PC, IFRT])216
Arm V (RER With PD)11
Arm VI (SER [DECA, ABVE-PC, IFRT])62
Arm VII (SER [ABVE-PC, IFRT])45

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Event-free Survival

Probability of event-Free survival which is defined as the time from study entry to treatment failure (disease progression, disease recurrence, biopsy positive residual after completion of all protocol therapy), occurrence of a second malignant neoplasm, or death from any cause. Patients without report of such events where censored at last contact. (NCT00025259)
Timeframe: 5 years

InterventionProbability of survival (Number)
Arm I (Patients Off-therapy Before Callback-Induction Only)0.89
Arm II (RER With CR [ABVE-PC, IFRT])0.87
Arm III (RER With CR [ABVE-PC])0.84
Arm IV (RER With Less Than CR [ABVE-PC, IFRT])0.87
Arm V (RER With PD)0.70
Arm VI (SER [DECA, ABVE-PC, IFRT])0.79
Arm VII (SER [ABVE-PC, IFRT])0.74

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Disease Response Assessed by Modified RECIST Criteria

Number of participants with complete response and very good partial response at the end of protocol therapy. (NCT00025259)
Timeframe: Protocol therapy: the overall duration of which is: (n=1527) an average of 137.1 days, median 133.0 days, interquartile range: 101.0, 164.0 days.

InterventionNumber of participants (Number)
Arm I (Patients Off-therapy Before Callback-Induction Only)5
Arm II (RER With CR [ABVE-PC, IFRT])370
Arm III (RER With CR [ABVE-PC])380
Arm IV (RER With Less Than CR [ABVE-PC, IFRT])538
Arm V (RER With PD)29
Arm VI (SER [DECA, ABVE-PC, IFRT])105
Arm VII (SER [ABVE-PC, IFRT])100

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Overall Survival

Probability of overall survival which is defined as the time from study entry to death from any cause. Patients alive where censored at last contact. (NCT00025259)
Timeframe: 5 years

InterventionProbability of survival (Number)
Arm I (Patients Off-therapy Before Callback-Induction Only)0.93
Arm II (RER With CR [ABVE-PC, IFRT])0.98
Arm III (RER With CR [ABVE-PC])0.98
Arm IV (RER With Less Than CR [ABVE-PC, IFRT])0.98
Arm VI (SER [DECA, ABVE-PC, IFRT])0.96
Arm VII (SER [ABVE-PC, IFRT])0.93

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Motor Coordination as Assessed by Neurological Examination and Vineland Adaptive Behavior Scale (VABS)

"The best score at the two time points will be used in this analysis. For a given patient, this best score will be used to calculate the change from baseline. The mean change from baseline for each treatment group will be calculated." (NCT00033293)
Timeframe: Changes from baseline to the better of 6 months or 1 year

InterventionChange in VABS score (Mean)
Arm I (Chemotherapy, Immunoglobulin Therapy)84.53
Arm II (Chemotherapy, Observation)144.73

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Tumor Outcome in Terms of Event-free Survival (EFS) Rate Defined as a Relapse or Progression of Neuroblastoma, a Second Malignancy, or Death

EFS rate for neuroblastoma event from time of study enrollment. (NCT00033293)
Timeframe: Up to 3 years

Intervention3 year EFS (Number)
Arm I (Chemotherapy, Immunoglobulin Therapy)92.3
Arm II (Chemotherapy, Observation)96.0

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Tumor Outcome in Terms of Overall Survival (OS) Rate

OS rate from time of study enrollment. (NCT00033293)
Timeframe: Up to 3 years

Intervention3 year OS (Number)
Arm I (Chemotherapy, Immunoglobulin Therapy)100
Arm II (Chemotherapy, Observation)96.0

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Functional Outcome as Assessed by Age-appropriate Neuropsychological Testing

"The Bayley Scales of infant development mental scale best score of two time points will be used in the analysis. For a given patient, this score will be used to calculate the change from baseline." (NCT00033293)
Timeframe: Changes from baseline to the better of 6 months or 1 year

InterventionChange in Bayley's score (Mean)
Arm I (Chemotherapy, Immunoglobulin Therapy)117.5
Arm II (Chemotherapy, Observation)100.75

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Number of Responders

A multi-stage design followed by a test of proportions between the treatment arms (chemo vs. chemo + therapeutic immune globulin (IVIG)) will be performed. The first stage of the multi-stage design will also function as an early stopping rule for insufficient activity of chemotherapy in OMA. (NCT00033293)
Timeframe: Changes from baseline to 2 months, 6 months, and 1 year

Interventionparticipants (Number)
Arm I (Chemotherapy, Immunoglobulin Therapy)21
Arm II (Chemotherapy, Observation)11

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Comparison of the Increase in Cure Rate of High Risk ALL Without Causing More Serious Side Effects Between Interventions

Event Free Probability. (NCT00075725)
Timeframe: 5 years

Interventionpercentage of participants (Number)
Dexamethasone and Capizzi Methotrexate Patients < 10 Years83.2
Dexamethasone, High Dose Methotrexate (Non Randomly Assigned)81.6
Dexamethasone & Capizzi Methotrexate Patients => 10 Years Old69.1
Dexamethasone, High Dose Methotrexate (IM) < 10 Years91.2
Prednisone, Capizzi Methotrexate <10 Years82.1
Prednisone, Capezzi Methotrexate >= 10 Years73.5
Predisone and High Dose Methotrexate < 10 Yrs Old80.8
Prenisone and High Dose Methotrexate >=10 Years75.8
Dexamethasone, High Dose Methotrexate (IM) >= 10 Years77.0
Prenisone, Capezzi Methotrexate (Down's Syndrome)61.8
Dexamethasone, Capizzi Methotrexate Down Syndrome (Non Random)44.4

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Correlation of Minimal Residual Disease (MRD) Positive With Overall Survival (OS)

Bone marrow MRD status is defined as positive with >= 0.1 detectable leukemia cells, and negative with < 0.1 detectable leukemia cells. (NCT00075725)
Timeframe: 5 Years

Interventionpercentage of participants (Number)
Dexamethasone and Capizzi Methotrexate Patients < 10 Years79.2
Dexamethasone, High Dose Methotrexate (Non Randomly Assigned)69.9
Dexamethasone & Capizzi Methotrexate Patients => 10 Years Old65.6
Dexamethasone, High Dose Methotrexate (IM) < 10 Years86.2
Prednisone, Capizzi Methotrexate <10 Years93.8
Prednisone, Capizzi Methotrexate >= 10 Years63.1
Predisone and High Dose Methotrexate < 10 Yrs Old84.2
Prednisone and High Dose Methotrexate >=10 Years73.6
Dexamethasone, High Dose Methotrexate (IM) >= 10 Years74.6

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Correlation of Minimal Residual Disease (MRD) Positive With Event Free Survival (EFS)

Bone marrow MRD status is defined as positive with >= 0.1 detectable leukemia cells. (NCT00075725)
Timeframe: 5 years

Interventionpercentage of participants (Number)
Dexamethasone and Capizzi Methotrexate Patients < 10 Years66.5
Dexamethasone, High Dose Methotrexate (Non Randomly Assigned)43.3
Dexamethasone & Capizzi Methotrexate Patients => 10 Years Old35.4
Dexamethasone, High Dose Methotrexate (IM) < 10 Years80
Prednisone, Capizzi Methotrexate <10 Years34.7
Prednisone, Capizzi Methotrexate >= 10 Years39
Prednisone and High Dose Methotrexate < 10 Yrs Old55
Prednisone and High Dose Methotrexate >=10 Years47.8
Dexamethasone, High Dose Methotrexate (IM) >= 10 Years49.4

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Correlation of Minimal Residual Disease (MRD) Negative With Event Free Survival (EFS).

Bone marrow MRD status is defined as negative with < 0.1 detectable leukemia cells. (NCT00075725)
Timeframe: 5 years

Interventionpercentage of participants (Number)
Dexamethasone and Capizzi Methotrexate Patients < 10 Years86.4
Dexamethasone, High Dose Methotrexate (Non Randomly Assigned)93.6
Dexamethasone & Capizzi Methotrexate Patients => 10 Years Old80.5
Dexamethasone, High Dose Methotrexate (IM) < 10 Years93.1
Prednisone, Capizzi Methotrexate <10 Years86.5
Prednisone, Capezzi Methotrexate >= 10 Years83.4
Prednisone and High Dose Methotrexate < 10 Yrs Old84.2
Prednisone and High Dose Methotrexate >=10 Years83.9
Dexamethasone, High Dose Methotrexate (IM) >= 10 Years85.3
Prednisone, Capezzi Methotrexate (Down's Syndrome)74.4
Dexamethasone, Capizzi Methotrexate Down Syndrome (Non Random)25

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Correlation of Minimal Residual Disease (MRD) Negative With Overall Survival (OS).

Bone marrow MRD status is defined as negative with < .01 detectable leukemia cells. (NCT00075725)
Timeframe: 5 years

Interventionpercentage of participants (Number)
Dexamethasone and Capizzi Methotrexate Patients < 10 Years95.4
Dexamethasone, High Dose Methotrexate (Non Randomly Assigned)92.9
Dexamethasone & Capizzi Methotrexate Patients => 10 Years Old87.4
Dexamethasone, High Dose Methotrexate (IM) < 10 Years98.1
Prednisone, Capizzi Methotrexate <10 Years93.3
Prednisone, Capizzi Methotrexate >= 10 Years90.2
Prednisone and High Dose Methotrexate < 10 Yrs Old94.5
Prednisone and High Dose Methotrexate >=10 Years90.5
Dexamethasone, High Dose Methotrexate (IM) >= 10 Years91.6
Prednisone, Capizzi Methotrexate (Down's Syndrome)78.3
Dexamethasone, Capizzi Methotrexate Down Syndrome (Non Random)25.0

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Correlation of Early Marrow Response Status With MRD Positive.

Bone marrow status is defined as: M1: < 5% lymphoblasts; M2: 5-25% lymphoblasts; M3: > 25% lymphoblasts. Bone marrow MRD status is defined as positive with >= 0.1 detectable leukemia cells, and negative with < 0.1 detectable leukemia cells. (NCT00075725)
Timeframe: Day 29

Interventionparticipants (Number)
Dexamethasone and Capizzi Methotrexate Patients < 10 Years26
Dexamethasone, High Dose Methotrexate (Non Randomly Assigned)12
Dexamethasone & Capizzi Methotrexate Patients => 10 Years Old43
Dexamethasone, High Dose Methotrexate (IM) < 10 Years14
Prednisone, Capizzi Methotrexate <10 Years16
Prednisone, Capezzi Methotrexate >= 10 Years95
Prednisone and High Dose Methotrexate < 10 Yrs Old17
Prednisone and High Dose Methotrexate >=10 Years98
Dexamethasone, High Dose Methotrexate (IM) >= 10 Years39
Prednisone, Capezzi Methotrexate (Down's Syndrome)3
Dexamethasone, Capizzi Methotrexate Down Syndrome (Non Random)3
Prednisone and High Dose Methotrexate (Non Randomly Assigned)3

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Correlation of Early Marrow Response Status With MRD Negative.

Bone marrow status is defined as: M1: < 5% lymphoblasts; M2: 5-25% lymphoblasts; M3: > 25% lymphoblasts. Bone marrow MRD status is defined as positive with >= 0.1 detectable leukemia cells, and negative with < 0.1 detectable leukemia cells. (NCT00075725)
Timeframe: Day 29

Interventionparticipants (Number)
Dexamethasone and Capizzi Methotrexate Patients < 10 Years182
Dexamethasone, High Dose Methotrexate (Non Randomly Assigned)72
Dexamethasone & Capizzi Methotrexate Patients => 10 Years Old198
Dexamethasone, High Dose Methotrexate (IM) < 10 Years188
Prednisone, Capizzi Methotrexate <10 Years195
Prednisone, Capezzi Methotrexate >= 10 Years471
Prednisone and High Dose Methotrexate < 10 Yrs Old190
Prednisone and High Dose Methotrexate >=10 Years479
Dexamethasone, High Dose Methotrexate (IM) >= 10 Years208
Prednisone, Capezzi Methotrexate (Down's Syndrome)25
Dexamethasone, Capizzi Methotrexate Down Syndrome (Non Random)3
Prednisone and High Dose Methotrexate (Non Randomly Assigned)18

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Cure by AV-PC x 3 or AV-PC x 3 + IFRT for Stage I Unresected, Stage I Resected Whose Disease Recurred, and Stage II Patients

To estimate the proportions of Stage I unresected, Stage I resected (whose disease has recurred after observation), and Stage II LPHD patients who can be cured with AV-PC x 3, with IFRT for those who are not in a CR after chemotherapy. (NCT00107198)
Timeframe: At 5 years

InterventionProbability participants (Number)
Surgery or Combination Chemotherapy, With/Without Radiotherapy0.89

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Grade 3 or 4 Toxicity

(NCT00107198)
Timeframe: Any time during chemoradiotherapy, up to the end of 3-cycles of AV-PC induction. Each cycle is 21 days.

InterventionParticipants (Number)
Surgery or Combination Chemotherapy, With/Without Radiotherapy26

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Failure-free Survival (FFS)

The time to a treatment (strategy) failure, where failure includes one of the following occurrences as a first event: disseminated disease (> Stage I/II) progression or recurrence at any time, local disease progression or recurrence anytime during or after treatment with AV-PC +/- IFRT, occurrence of a second malignant neoplasm, death from any cause. (NCT00107198)
Timeframe: At 5 years

InterventionProbability participants (Number)
Surgery or Combination Chemotherapy, With/Without Radiotherapy0.91

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Cure by Surgery Alone in Stage I Resected Patients

To estimate the proportion of Stage I patients (with a single involved lymph node that is totally resected) who can be cured with surgery alone. (NCT00107198)
Timeframe: At 2 years

InterventionProbability participants (Number)
Surgery or Combination Chemotherapy, With/Without Radiotherapy0.82

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Event-free Survival

Failure includes one of the following occurrences as a first event: relapse/progression or second malignancy from enrollment. (NCT00107198)
Timeframe: At 5 years

InterventionProbability participants (Number)
Surgery or Combination Chemotherapy, With/Without Radiotherapy0.85

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Disease-free Survival (DFS) for Randomized Nelarabine T-ALL Cohort (Arm I + Arm III vs. Arm II + Arm IV)

Disease Free Probability where DFS time is defined as time from randomization end of induction to first event (relapse, second malignant neoplasm, death) or date of last contact for patients who are event (NCT00408005)
Timeframe: 4 years from randomization at the end of induction

Interventionpercent probability (Number)
ARM I and ARM III (Combination Chemotherapy)82.96
ARM II and ARM IV (Combination Chemotherapy)88.30

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Disease-free Survival (DFS) for Randomized Nelarabine T-ALL Cohort (Arm I vs. Arm II vs. Arm III vs. Arm IV)

Disease Free Probability where DFS time is defined as time from randomization end of induction to first event (relapse, second malignant neoplasm, death) or date of last contact for patients who are event-free. (NCT00408005)
Timeframe: 4 years from randomization at the end of induction

Interventionpercent probability (Number)
ARM I (Combination Chemotherapy)89.01
ARM II (Combination Chemotherapy)90.53
ARM III (Combination Chemotherapy)78.07
ARM IV (Combination Chemotherapy)86.46

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Cumulative Incidence of CNS Relapse for T-ALL by Risk Group

Cumulative incidence of CNS relapse adjusting for DFS events, was calculated using the method Gray et. al. High risk patients receive cranial radiation and low risk patients receive no cranial radiation. (NCT00408005)
Timeframe: 4 years from randomization at the end of induction

,
Interventionpercent probability (Number)
Intermediate RiskHigh Risk
ARM II (Combination Chemotherapy)1.080
ARM IV (Combination Chemotherapy)0.853.45

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Disease-free Survival (DFS) for Randomized Methotrexate T-ALL Cohort (Arm I vs. Arm II vs. Arm III vs. Arm IV)

Disease-free survival defined as time from randomization end of induction to first event (relapse, second malignant neoplasm, remission death) or date of last contact for those who are event-free. (NCT00408005)
Timeframe: 4 years from randomization at the end of induction

Interventionpercent probability (Number)
ARM I (Combination Chemotherapy)91.76
ARM II (Combination Chemotherapy)90.53
ARM III (Combination Chemotherapy)86.06
ARM IV (Combination Chemotherapy)84.89

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Disease-free Survival (DFS) for Randomized Methotrexate T-ALL Cohort (Arm I + Arm II vs. Arm III + Arm IV)

Disease Free Probability where DFS time is defined as time from randomization end of induction to first event (relapse, second malignant neoplasm, death) or date of last contact for patients who are event-free. (NCT00408005)
Timeframe: 4 years from randomization at the end of induction

Interventionpercent probability (Number)
ARM I and ARM II (Combination Chemotherapy)91.45
ARM III and ARM IV (Combination Chemotherapy)85.78

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Disease-free Survival (DFS) for T-cell Lymphoblastic Lymphoma (T-LLy) Cohort

Disease Free Probability where DFS time is defined as time from randomization end of induction to first event (relapse, second malignant neoplasm, death) or date of last contact for patients who are event-free. (NCT00408005)
Timeframe: 4 years from end of induction

Interventionpercent probability (Number)
Standard RiskHigh Risk
ARM I (Combination Chemotherapy)87.485.1

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Cumulative Incidence of CNS Relapse for T-ALL by Risk Group

Cumulative incidence of CNS relapse adjusting for DFS events, was calculated using the method Gray et. al. High risk patients receive cranial radiation and low risk patients receive no cranial radiation. (NCT00408005)
Timeframe: 4 years from randomization at the end of induction

,
Interventionpercent probability (Number)
Low RiskIntermediate RiskHigh Risk
ARM I (Combination Chemotherapy)1.851.163.64
ARM III (Combination Chemotherapy)1.929.16.52

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Disease-free Survival (DFS) for T-cell Lymphoblastic Lymphoma (T-LLy) Cohort

Disease Free Probability where DFS time is defined as time from randomization end of induction to first event (relapse, second malignant neoplasm, death) or date of last contact for patients who are event-free. (NCT00408005)
Timeframe: 4 years from end of induction

Interventionpercent probability (Number)
High RiskInduction Failure
ARM II (Combination Chemotherapy)85.0100

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Pharmacodynamics PIA Levels in Infants Given Lestaurtinib at DL2 in Combination With Chemotherapy

Summarized with mean and standard deviation for those with available data in Arm C (NCT00557193)
Timeframe: Sampled between weeks 6-12 from start of induction

InterventionActivity percentage (Mean)
Arm C (Safety/Efficacy Dose Level 2)69.00

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Percent Probability of Event Free Survival (EFS) by MRD Status and Treatment Arm

Three-year EFS estimates and 90% CI will be reported by treatment arm and end-induction MRD status. (NCT00557193)
Timeframe: 3 Years from end of Induction)

Interventionpercent probability (Number)
Arm A (MRD Negative)86.05
Arm A (MRD Positive)87.5
Arm B (MRD Negative)47.37
Arm B (MRD Positive)22.73
Arm C (MRD Negative)51.85
Arm C (MRD Positive)27.03

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Percent Probability for Event-free Survival (EFS) of MLL-R Infants Treated With Combination Chemotherapy With or Without Lestaurtinib at DL2

Event Free Probability where EFS time is defined as time from randomization to first event (relapse, second malignant neoplasm, death) or date of last contact for patients who are event-free. EFS is constructed using the Kaplan-Meier life table method with confidence interval based on standard errors computed using the method of Peto and Peto. EFS will be compared between patients on treatment Arm C at DL2 to those on Arm B. (NCT00557193)
Timeframe: From start of post-induction therapy for up to 10 years.

Interventionpercent probability (Number)
Arm B (IR/HR MLL-R Chemotherapy)38.89
Arm C (IR/HR MLL-R Chemotherapy and Lestaurtinib)35.82

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Percent Probability for Event-free Survival (EFS) for Patients on Arm C at Dose Level 2 (DL2)

EFS time is defined as time from randomization to first event (relapse, second malignant neoplasm, death) or date of last contact for patients who are event-free. EFS is constructed using the Kaplan-Meier life table method with confidence interval based on standard errors computed using the method of Peto and Peto. (NCT00557193)
Timeframe: From start of post-induction therapy for up to 10 years

Interventionpercentage probability (Number)
Arm C (Safety/Efficacy Dose Level 2)35.82

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Describe in Vitro Sensitivity as a Molecular Mechanism of Primary Resistance to Lestaurtinib in Leukemic Blasts

Described via means and standard deviations in samples which have primary resistance to lestaurtinib (NCT00557193)
Timeframe: Sampled at the start of induction

InterventionProportion of cells that are viable (Median)
Arm A (Standard Risk MLL-G)0.75
Arm B (IR/HR MLL-R Chemotherapy)0.48
Arm C (IR/HR MLL-R Chemotherapy and Lestaurtinib)0.47

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Percent Probability for Event-free Survival (EFS) for Patients on Arm A

EFS time is defined as time from treatment assignment to first event (relapse, second malignant neoplasm, death) or date of last contact for patients who are event-free. EFS is constructed using the Kaplan-Meier life table method with confidence interval based on standard errors computed using the method of Peto and Peto. (NCT00557193)
Timeframe: From start of post-induction therapy for up to 10 years

Interventionpercentage probability (Number)
Arm A (Standard Risk MLL-G)86.67

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Describe FLT3 Protein Expression as a Molecular Mechanism of Primary Resistance to Lestaurtinib in Leukemic Blasts

Described via mean and standard deviation by group. (NCT00557193)
Timeframe: Sampled at the start of induction

InterventionqPCR fold expression ratio (Mean)
Arm A (Standard Risk MLL-G)1.25
Arm B (IR/HR MLL-R Chemotherapy)7.85
Arm C (IR/HR MLL-R Chemotherapy and Lestaurtinib)5.83

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Describe in Vitro Sensitivity as a Molecular Mechanism of Acquired Resistance to Lestaurtinib in Leukemic Blasts

Described via means and standard deviations in samples which have acquired resistance to lestaurtinib (NCT00557193)
Timeframe: At relapse (up to 3 years)

InterventionProportion of cells that are viable (Mean)
Arm C (IR/HR MLL-R Chemotherapy and Lestaurtinib)0.69

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Describe FLT3 Protein Expression as a Molecular Mechanism of Acquired Resistance to Lestaurtinib in Leukemic Blasts

Described via means and standard deviations in available Arm C relapse samples (NCT00557193)
Timeframe: At relapse (up to 3 years)

InterventionqPCR fold expression ratio (Mean)
Arm C (Safety/Efficacy Dose Level 2)5.73

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Progression-Free Survival (PFS)

PFS is defined as the time from randomization to the earlier of progression or death of any cause. (NCT00602641)
Timeframe: Assessed every 3 months for 2 years, then every 6 months for 3 years, then annually for 10 years from the date of randomization.

Interventionmonths (Median)
Arm I (MPT-T)21.0
Arm II (mPR-R)18.7

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Very Good Partial Response (VGPR) Rate

Response evaluation was based on the International Myeloma Working Group (IMWG) response criteria. VGPR rate was defined as patients achieving at least VGPR which include patients who achieving complete response (CR) and VGPR. CR refers to patients who have complete disappearance of an M-protein and no evidence of myeloma in the bone marrow. VGPR refers to patients who meet the following criteria: Serum and urine M-component detectable by immunofixation but not on electrophoresis; Or 90% or greater reduction in serum M-component plus urine M-component <100 mg per 24 hours; If the serum and urine M protein are unmeasurable and the immunoglobulin free light chain parameter is being used to measure response, a ≥ 90% decrease in the difference between involved and uninvolved free light chain (FLC) levels is required in place of the M protein criteria. (NCT00602641)
Timeframe: Assessed every cycle (1 cycle=28 days) for the first 12 cycles, and then every 2 cycles while on treatment. Post treatment assessed every 3 months < 2 years from study entry, every 6 months if 2-5 years, every 12 months if 6-10 years from study entry.

Interventionproportion of participants (Number)
Arm I (MPT-T)0.247
Arm II (mPR-R)0.316

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Change in Functional Assessment of Cancer Therapy-Neurotoxicity Trial Outcome Index (FACT-Ntx TOI) Score From Baseline to Cycle 12

A combined scale was used to assess the quality of life (QOL) comprising of the well established and validated functional well-being (FWB) and physical well-being (PWB) components of FACT-G version 4 (14 questions), which will address the physical and functional well-being of multiple myeloma patients plus the FACT-neurotoxicity (NTX, 11 questions), which will evaluate symptoms of neurotoxicity. This pooled scale is referred to as the FACT Ntx TOI. The FACT-Ntx TOI has 25 items and the score ranges from 0 (worst possible outcome) to 100 (best possible outcome). (NCT00602641)
Timeframe: Administered at registration, the beginning of cycle 7 d1, the end of cycle 12 d28, then at the end of cycle 18, 24, and 38 d28. For patients who discontinue treatment early, assessed at time of discontinuation and at the next quarterly follow-up visit.

Interventionunits on a scale (Mean)
Arm I (MPT-T)-2.8
Arm II (mPR-R)3.3

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Overall Survival

Overall survival was defined as time from randomization to death from any cause. (NCT00602641)
Timeframe: Assessed every 3 months for 2 years, then every 6 months for 3 years, then annually for 10 years from the date of randomization.

Interventionmonths (Median)
Arm I (MPT-T)52.6
Arm II (mPR-R)47.7

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The Number of Subjects Elected to Have the Lipoma Removed.

(NCT00624416)
Timeframe: After four weeks up to one year.

Interventionparticipants (Number)
Prednisolone and Isoproteronol8

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The Number of Lipoma Increased in Volume.

(NCT00624416)
Timeframe: After four weeks of treatment up to one year.

InterventionLipomas (Number)
Prednisolone and Isoproteronol9

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The Average Percent Volume Reduction in the Lipoma.

(NCT00624416)
Timeframe: Baseline and 4 weeks

InterventionPercent Volume reduction (cc^3) (Mean)
Prednisolone and Isoproteronol50

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Percentage of Participants With Event-free Survival (EFS)

Percentage of participants who were event free. Event Free Probability defined as time from randomization at study entry to first event (induction failure, induction death, relapse, second malignant neoplasm, remission death) or date of last contact for subjects who are event-free. (NCT00671034)
Timeframe: 5 Years

InterventionPercentage of participants (Number)
Arm I (Calaspargase Pegol 2100)72.35
Arm II (Calaspargase Pegol 2500)80.8
Arm III (Pegaspargase 2500)79.34

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Plasma and CSF Concentrations of Asparagine in ug/ml

The plasma and CSF concentrations of asparagine in ug/ml after administration of EZN-2285 compared to Oncaspar. (NCT00671034)
Timeframe: 25 Days Post-dose (Day 29)

,,
Interventionug/mL (Mean)
CSF asparagine concentration (ug/mL)Plasma asparagine concentration (ug/mL)
Arm I (Calaspargase Pegol 2100)0.20.2
Arm II (Calaspargase Pegol 2500)0.190.25
Arm III (Pegaspargase 2500)0.260.83

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Percentage of Participants With Complete Remission at the End of Induction

Complete Remission (CR) rate; where CR is defined as M1 marrow (< 5% lymphoblasts in the bone marrow) (NCT00671034)
Timeframe: End of induction (Day 29)

InterventionPercentage of participants (Number)
Arm I (Calaspargase Pegol 2100)92.4
Arm II (Calaspargase Pegol 2500)97.6
Arm III (Pegaspargase 2500)94.1

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Toxicities During Post Induction Intensification Therapy (All Grades)

The calculation of AE incidence will be based on the number of patients per AE category. For each patient who has multiple AEs classified to the same category, that patient will be tabulated under the worst toxicity grade for that AE category. The incidence of AEs will be tabulated by treatment arm and by organ class. Special attention will be paid to hypersensitivity, pancreatitis, coagulopathy, infection, neurologic dysfunction and thromboembolic events. (NCT00671034)
Timeframe: Up to 5 years

,,
InterventionPercentage of participants (Number)
Alergic Reaction - ConsolidationAlergic Reaction - Delayed Intensification IAlergic Reaction - Interim Maintenance ICNS - ConsolidationCNS - Delayed Intensification ICNS - Interim Maintenance IHyperbilirubinemia - ConsolidationHyperbilirubinemia - Delayed Intensification IHyperbilirubinemia - Interim Maintenance IHyperglycemia - ConsolidationHyperglycemia - Delayed Intensification IHyperglycemia - Interim Maintenance IHyperlipidemia - ConsolidationHyperlipidemia - Delayed Intensification IHyperlipidemia - Interim Maintenance I% patients w/INR increase - Consolidation% pts w/INR increase - Delayed Intensification I% patients w/INR increase - Interim Maintenance IPancreatitis - ConsolidationPancreatitis -Delayed Intensification IPancreatitis - Interim Maintenance I% pts w/prolongation of APT time - Consolidation% pts w/prolongation APT time -Delayed Intension I%pts w/prolongation APT time-Interim maintenance IThrombosis - ConsolidationThrombosis - Delayed Intensification IThrombosis - Interim Maintenance I
Arm I (Calaspargase Pegol 2100)20.44.40.00.00.00.053.128.941.344.944.434.82.02.22.26.16.72.210.22.22.28.28.96.50.02.20.0
Arm II (Calaspargase Pegol 2500)27.30.00.00.03.80.045.538.527.642.461.544.83.00.03.43.03.80.06.17.73.49.126.96.90.00.00.0
Arm III (Pegaspargase 2500)23.30.02.10.02.60.030.210.533.346.536.833.37.00.02.67.00.02.67.00.02.67.018.47.72.30.00.0

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Pharmacokinetics (PK) (Half-life of SC-PEG E. Coli L-asparaginase (EZN-2285) Compared to Pegaspargase During Induction and Consolidation Therapy)

Mean half-life of plasma asparaginase during consolidation and Induction; half-life is defined as the time taken for drug concentration to decrease by half. (NCT00671034)
Timeframe: Post Day 29 of Induction and Post Day 22 of Consolidation

,,
Interventionhours (Mean)
Asparaginase half-life during ConsolidationAsparaginase half-life during Induction
Arm I (Calaspargase Pegol 2100)415.8305.1
Arm II ( Calaspargase Pegol 2500)355.9321.5
Arm III (Pegaspargase 2500)117.2126.9

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Immunogenicity

Number of Patients with Positive Immunogenicity tests (NCT00671034)
Timeframe: 25 Days Post-dose (Day 29)

InterventionParticipants (Count of Participants)
Arm I (Calaspargase Pegol 2100)2
Arm II (Calaspargase Pegol 2500)2
Arm III (Pegaspargase 2500)4

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Pharmacodynamics (PD)

Plasma Asparaginase Concentration During consolidation and induction. (NCT00671034)
Timeframe: Day 29 of consolidation and induction

,,
InterventionmIU/mL (Median)
Plasma Asparaginase Concentration- ConsolidationPlasma Asparaginase Concentration- Induction
Arm I (Calaspargase Pegol 2100)575.9271.6
Arm II (Calaspargase Pegol 2500)617.2339.6
Arm III (Pegaspargase 2500)562.172.8

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Asparaginase Level

The proportion of patients with an asparaginase level of at least 0.1 IU/mL and the proportion with at least 0.4 IU/mL on Days 4, 15, 22 and 29 of Induction compared to Oncaspar (NCT00671034)
Timeframe: Days 4, 15, 22 and 29 of Induction

,,
Interventionpercentage of patients (Number)
Level at least 0.1 IU/mL day 4Level at least 0.1 IU/mL day 15Level at least 0.1 IU/mL day 22Level at least 0.1 IU/mL day 29Level at least 0.4 IU/mL day 4Level at least 0.4 IU/mL day 15Level at least 0.4 IU/mL day 22Level at least 0.4 IU/mL day 29
Arm I (Calaspargase Pegol 2100)098.498.294.9075.837.513.6
Arm II (Calaspargase Pegol 2500)010010095.0095.062.527.5
Arm III (Pegaspargase 2500)010095.128.6093.014.60

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Percentage of Participants With Minimal Residual Disease (MRD)<0.01% at the End of Induction

Percentage of participants with Negative MRD (MRD<0.01%). (NCT00671034)
Timeframe: End of induction (Day 29)

InterventionPercentage of participants (Number)
Arm I (Calaspargase Pegol 2100)65.2
Arm II (Calaspargase Pegol 2500)81
Arm III (Pegaspargase 2500)72.5

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Event-Free Survival (EFS) of Patients With Standard-risk Disease Treated With Dasatinib in Combination With Intensified Chemotherapy

Event-Free Survival (EFS) curves will be constructed using the Kaplan-Meier life table method with standard errors computed using the method of Peto and Peto. A 1-sided 95% confidence interval for EFS will be constructed. (NCT00720109)
Timeframe: At 3 years

InterventionPercent probability (Number)
Treatment Induction (Enzyme Inhibitor Therapy & Chemotherapy)79.8
Standard-risk83.2
High-risk66.7

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Percent of Patients MRD Positive (MRD > 0.01%) at End of Consolidation

A 1-sample Z-test of proportions (alpha=5%, 1-sided test) will be used. (NCT00720109)
Timeframe: At end of consolidation (at 11 weeks)

InterventionPercentage of participants (Number)
Treatment Induction (Enzyme Inhibitor Therapy & Chemotherapy)10.5
Standard-risk0
High-risk66.7

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Overall EFS Rate for the Combined Cohort of Standard- and High-Risk Patients (Who Receive the Final Chosen Dose of Dasatinib)

An event is defined as: Induction failure, relapse at any site, secondary malignancy, or death. (NCT00720109)
Timeframe: From the time entry on study to first event or date of last follow-up, assessed up to 7 years

Interventionpercentage of patients (Number)
Treatment Induction (Enzyme Inhibitor Therapy & Chemotherapy)79.8
Standard-risk83.2
High-risk66.7

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Contribution of Dasatinib on Minimal Residual Disease (MRD) After Induction Therapy

Percent of patients MRD Positive (MRD > 0.01%) at End of Induction. (NCT00720109)
Timeframe: At the end of induction therapy (at 5 weeks)

InterventionPercentage of participants (Number)
Treatment Induction (Enzyme Inhibitor Therapy & Chemotherapy)40.7
Standard-risk29.2
High-risk100.0

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Feasibility and Toxicity of an Intensified Chemotherapeutic Regimen Incorporating Dasatinib for Treatment of Children and Adolescents With Ph+ ALL Assessed by Examining Adverse Events

Number of patients in safety cohort with dose limiting toxicity (DLT)(including treatment delay) (NCT00720109)
Timeframe: Weeks 3 through 23 of treatment (From week 3 Induction through Intensification Block 1)

InterventionPts with DLTs (Number)
Treatment Induction (Enzyme Inhibitor Therapy & Chemotherapy)1

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Overall Survival (OS)

OS will be estimated using the method of Kaplan-Meier. (NCT00792948)
Timeframe: From the date of initial registration on the study until death from any cause, assessed up to 5 years

InterventionProbability of surviving 12 months (Number)
Treatment0.88

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Relapse-free Survival (RFS) After Allogeneic Stem Cell Transplantation

Will be estimated using the method of Kaplan-Meier. (NCT00792948)
Timeframe: 12 months

InterventionProbability of 12-month RFS (Number)
Treatment0.83

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Continuous Complete Remission (CCR) Rate

Will be testing using an exact binomial test (NCT00792948)
Timeframe: 18 months

Interventionpercentage of participants (Number)
Treatment57

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AALL08P1 Safety Outcome

Percentage of Group B (High Risk-High) patients taking less than 49 weeks from day 1 of consolidation to day 1 of maintenance therapy. Only Group B analyzed since this is prespecified in protocol. (NCT00866307)
Timeframe: Consolidation through Delayed Intensification

Interventionpercentage of participants (Number)
Group B (High Risk-High)50.0

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AALL08P1 Feasibility Outcome

Percentage of Group B (High Risk-High) patients that tolerate at least 8 of the 12-14 total doses of pegaspargase during Consolidation, Interim Maintenance, and Delayed Intensification periods. Only Grp B analyzed since this is prespecified in protocol. (NCT00866307)
Timeframe: Consolidation through Delayed Intensification

Interventionpercentage of participants (Number)
Group B (High Risk-High)53.3

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Progression-free Survival (Phase II)

From date of registration to date of first documentation of progressive disease, or death due to any cause. Patients last known to be alive and progression free are censored at date of last contact. (NCT00972478)
Timeframe: Up to 2 years

Interventionpercentage of participants (Number)
Ph II: R-CHOP+Vorinostat73

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Toxicity of Vorinostat-R-CHOP in Patients With Newly Diagnosed DLBCL

Incidence of toxicity as assessed by the Common Terminology Criteria for Adverse Events (CTCAE) version 4.0. For each patient, worst grade of each event type is reported. Grade 3 = Severe, Grade 4 = Life-threatening, Grade 5 = Fatal. (NCT00972478)
Timeframe: Up to week 26

,
InterventionParticipants (Number)
Abdominal painAcute kidney injuryAlanine aminotransferase increasedAnemiaAnorexiaAspartate aminotransferase increasedAtrial fibrillationBladder spasmBronchial infectionCD4 lymphocytes decreasedCPK increasedCarbon monoxide diffusing capacity decreasedColitisCreatinine increasedCystitis noninfectiveDehydrationDepressionDiarrheaDisseminated intravascular coagulationDizzinessDuodenal perforationDysphagiaDyspneaElectrocardiogram QT corrected interval prolongedFatigueFebrile neutropeniaFecal incontinenceGastrointestinal disorders - Other, specifyGeneralized muscle weaknessHematuriaHiccupsHyperglycemiaHypoalbuminemiaHypocalcemiaHypokalemiaHyponatremiaHypophosphatemiaHypotensionInfections and infestations - Other, specifyJejunal perforationLeft ventricular systolic dysfunctionLeukocytosisLung infectionLymphocyte count decreasedMucosal infectionMucositis oralMulti-organ failureMyalgiaMyocardial infarctionNauseaNeutrophil count decreasedObstruction gastricPainParonychiaPeripheral motor neuropathyPlatelet count decreasedPneumonitisRecurrent laryngeal nerve palsyRespiratory failureSepsisSinus tachycardiaSinusitisSmall intestinal obstructionStoma site infectionSyncopeUrinary tract infectionUrinary tract painUrine output decreasedVasovagal reactionVisceral arterial ischemiaVomitingWeight lossWhite blood cell decreased
Ph I: R-CHOP+Vorinostat (400mg D1-9)1004100000001102121100013300210011201010000401110180001400030000000101007
Ph II: R-CHOP+Vorinostat31122211111110014020011119241120143086233111420130223371110221111111114320102332

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Safe Dose of Vorinostat to be Used in Combination With R-CHOP Assessed by CTCAE Version 4.0 (Phase I)

Safe dose of Vorinostat (in combination with R-CHOP) at which 3/10 or fewer patients have doselimiting toxicities (DLT). Toxicities graded according to the NCI Common Terminology Criteria for Adverse Events Version 4.0 (CTCAE 4.0). DLT apply only during cycle 1 and should be drug-related (possible, probable, or definite). (NCT00972478)
Timeframe: 21 days

Interventionmg PO Once daily Days 1-9 (Number)
Ph I: R-CHOP+Vorinostat (400mg D1-9)400

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Response Rate (Complete Response [CR]+Partial Response [PR]) (Phase II)

Objective disease status is evaluated according to the 2007 revised Cheson et al. criteria. Complete Response(CR) is a complete disappearance of all disease with the exception of nodes. No new lesions. previously enlarged organs must have regressed and not be palpable. Bone marrow (BM) must be negative if positive at baseline. Normalization of markers. Partial Response (PR) is a 50% decrease in the sum of products of greatest diameters (SPD) for up to 6 identified dominant lesions, including spleenic and hepatic nodules from baseline. No new lesions and no increase in the size of liver, spleen or other nodes. (NCT00972478)
Timeframe: Up to week 26

Interventionpercentage of participants (Number)
Ph II: R-CHOP+Vorinostat81

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Overall Survival (Phase II)

From date of registration to date of death due to any cause. Patients last known to be alive are censored at date of last contact. (NCT00972478)
Timeframe: Up to 2 years

Interventionpercentage of participants (Number)
Ph II: R-CHOP+Vorinostat86

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Overall Survival

Overall survival is defined as the time from randomization to death or the date of last known alive. (NCT01145508)
Timeframe: Assessed every 3 months for 2 years, and then every 6 months for 3 years

InterventionMonths (Median)
Arm A (Vaccine and Chemotherapy)20.8
Arm B (Chemotherapy)NA

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Changes in Epstein-Barr Virus (EBV) Viral Load

Differences from baseline (specified follow-up assessment minus baseline) in EBV viral load. (NCT01193842)
Timeframe: Baseline up to 12 months

,,,
InterventionIU/mL (Median)
End of Cycle 2At treatment discontinuation6-month follow-up12-month follow-up
Phase I: VR-DA-EPOCH, Dose Level 10000
Phase I: VR-DA-EPOCH, Dose Level 2-2436.1-1.92-1.92-1.15
Phase II, DA-R-EPOCH0-0.280-2.7
Phase II, VR-DA-EPOCH-0.61-2.9-1.55-0.56

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Changes in Human Herpes Virus (HHV)-8 Viral Load

Differences from baseline (specified follow-up assessment minus baseline) in (HHV)-8 viral load. (NCT01193842)
Timeframe: Baseline up to 12 months

Interventioncopies per 100uL (Median)
12-month follow-up
Phase II: VR-DA-EPOCH0

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Changes in Human Herpes Virus (HHV)-8 Viral Load

Differences from baseline (specified follow-up assessment minus baseline) in (HHV)-8 viral load. (NCT01193842)
Timeframe: Baseline up to 12 months

Interventioncopies per 100uL (Median)
At treatment discontinuation6-month follow-up12-month follow-up
Phase II: DA-R-EPOCH000

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Changes in Human Immunodeficiency Virus (HIV) Viral Load

Differences from baseline (specified follow-up assessment minus baseline) in HIV viral load. Undetectable viral load results were treated as 0 values. (NCT01193842)
Timeframe: Baseline up to 12 months

,
Interventionmedian change in copies per mL (Median)
End of Cycle 2At treatment discontinuation6-month follow-up12-month follow-up
Phase II: DA-R-EPOCH-25-22.5-18-20
Phase II: VR-DA-EPOCH-20-87-200

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Percentage of Participant Experiencing Adverse Events (AEs) for Each Treatment Arm as Assessed by Common Terminology Criteria for Adverse Events Version 4.0 (CTCAE v4.0) (Phase II)

The percentage of participants with AEs and their worst severity will be tabulated for each treatment arm. If a participant has more than one AE, the most severe AE is analyzed. All adverse events will be assessed by the investigator from the first dose of protocol therapy through the post-treatment discontinuation visit. Participants are planned to be treated for a total of 6 cycles (21 day cycle length), or roughly 4 months. After this evaluation, assessment and reporting of AEs will only be required for all grade 5 AEs and any serious AE (SAE) that the investigator considers related to protocol therapy. (NCT01193842)
Timeframe: Up to 5 years

,
Interventionpercentage of participants (Number)
DeathLife-threateningSevereModerateMild
Phase II: DA-R-EPOCH20.028.931.117.80
Phase II: VR-DA-EPOCH28.937.820.08.92.2

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Pharmacokinetic Clearance (Phase I)

Serial plasma samples for pharmacokinetic analysis were collected at 24-48, 48-72, and 72-96 hours after the start of the first chemotherapy infusion. Doxorubicin, etoposide, and vincristine concentrations were determined using a validated liquid chromatography-tandem mass spectrometry method. The clearance was determined by dividing the drug-infusion rate by the steady-state concentrations, which was the average of the three time points. (NCT01193842)
Timeframe: 24-48, 48-72, and 72-96 hours after the start of the first chemotherapy infusion

,
InterventionLiter/hour (Mean)
DoxorubicinEtoposideVincristine
Phase I: VR-DA-EPOCH, Dose Level 178.63.022.4
Phase I: VR-DA-EPOCH, Dose Level 276.02.416.8

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Tumor Response (Phase I)

The percentage of participants whose best tumor response is complete response (CR) or partial response (PR). Based on clinical, radiologic (CT), and pathologic criteria, CR requires 1) complete disappearance of all detectable disease and disease-related symptoms if present before therapy, 2) bone marrow aspirate and biopsy to confirm a CR if initially positive or if clinically indicated by new abnormalities in the peripheral blood counts or blood smear, 3) negative PET results, depending on typically, variably, or unknown pre-treatment FDG status, and 4) spleen and/or liver, if considered to be enlarged before therapy on physical examination or CT scan, not being palpable on physical examination and considered normal size by imaging studies, and nodules related to lymphoma disappeared. PR includes 1) ≥50% decrease in sum of product of diameters (SPD), 2) no increase in size of nodes, liver, or spleen, 3) splenic/hepatic nodules regressed by ≥ 50% SPD, 4) no new sites of disease (NCT01193842)
Timeframe: Up to 2 years post treatment

,,
Interventionpercentage of participants (Number)
Complete responsePartial Response
Phase I: Arm C (VR-CHOP) Dose Level 11000
Phase I: VR-DA-EPOCH, Dose Level 183.316.7
Phase I: VR-DA-EPOCH, Dose Level 283.316.7

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Change in Plasma Associated Human Immunodeficiency Virus (HIV)-1 Ribonucleic Acid (RNA) (Phase I)

Differences from baseline (specified follow-up assessment minus baseline) in HIV viral load. Undetectable viral load results were treated as 0 values. (NCT01193842)
Timeframe: Baseline up to 12 months

,,
Interventioncopies per milliliter (Median)
End of cycle 2Treatment discontinuation6-month follow-up12-month follow-up
Phase I: VR-CHOP, Dose Level 128000
Phase I: VR-DA-EPOCH, Dose Level 1-14518-4517-551160
Phase I: VR-DA-EPOCH, Dose Level 2-12.5000

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Change in CD8 Cell Counts (Phase I)

Differences from baseline (specified follow-up assessment minus baseline) in absolute CD8 counts. (NCT01193842)
Timeframe: Baseline up to 12 months

,,
Interventioncells/mm^3 (Median)
End of cycle 2Treatment discontinuation6-month follow-up12-month follow-up
Phase I: VR-CHOP, Dose Level 1-172-81-16128
Phase I: VR-DA-EPOCH, Dose Level 135.5-164.5-56604
Phase I: VR-DA-EPOCH, Dose Level 2-115211275154

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Changes in Absolute CD4 Cell Counts (Phase I)

Differences from baseline (specified follow-up assessment minus baseline) in absolute CD4 counts. (NCT01193842)
Timeframe: Baseline up to 12 months

,,
Interventioncell/mm^3 (Median)
End of cycle 2Treatment discontinuation6-month follow-up12-month follow-up
Phase I: VR-CHOP, Dose Level 1-218-190-175-84
Phase I: VR-DA-EPOCH, Dose Level 192-3976169
Phase I: VR-DA-EPOCH, Dose Level 2-9-293131

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Percentage of Participants With Complete Response (CR) as Assessed by Response Evaluation Criteria in Solid Tumors (Phase II)

"Percentage of participants with complete response as assessed by Response Evaluation Criteria in Solid Tumors (Phase II) according to treatment arm. Participants are planned to be treated for a total of 6 cycles (21 day cycle length). Participants with CR after Cycle 4 will receive two additional cycles of chemotherapy and complete 6 cycles of chemotherapy. Participants who achieve a partial response (PR) only after Cycle 4 may continue on protocol therapy or they may be removed from the study at the AMC discretion of the physician (local Principal Investigator). Participants with stable disease after 4 cycles (i.e., who did not achieve at least a PR) or progressive disease at any time will be removed from study.~In phase II, there are two arms: Vorinostat RPTD+rituximab-DA-EPOCH arm (VR-DA-EPOCH) and Rituximab-DA-EPOCH arm (DA-R-EPOCH)." (NCT01193842)
Timeframe: Up to 6 months

Interventionpercentage of participants (Number)
Phase II: VR-DA-EPOCH67.5
Phase II: DA-R-EPOCH76.2

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Overall Survival (OS) (Phase II)

The percentage of participants surviving one year after starting treatment. (NCT01193842)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Phase II: VR-DA-EPOCH77.6
Phase II: DA-R-EPOCH86.7

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Event-free Survival (EFS) (Phase II)

The percentage of participants surviving without events (relapse or death) one year after starting treatment. (NCT01193842)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Phase II: VR-DA-EPOCH75.6
Phase II: DA-R-EPOCH82.2

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Change in Tissue Testosterone and Dihydrotestosterone

Tissue testosterone will be measured in biopsy tissues (NCT01503229)
Timeframe: From baseline to week 4

Interventionpg/mg (Median)
Treatment (Abiraterone Acetate and Prednisone)0.156

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Grade 4 or 5 Adverse Events

Grade 4 or greater toxicity graded by the National Cancer Institute Common Terminology Criteria for Adverse Events version 4.0 at least possibly related to treatment. (NCT01576172)
Timeframe: 30 days after completion of study treatment

InterventionParticipants (Count of Participants)
Arm I (Abiraterone Acetate and Prednisone)1
Arm II (Abiraterone Acetate, Prednisone, and Veliparib)3

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Objective Response Rates in Patients With Measurable Disease.

Overall response per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by CT or MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT01576172)
Timeframe: Up to 3 years

InterventionParticipants (Count of Participants)
Arm I (Abiraterone Acetate and Prednisone)18
Arm II (Abiraterone Acetate, Prednisone, and Veliparib)24

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Progression-free Survival (PFS)

Time from randomization to disease progression or death. (NCT01576172)
Timeframe: Up to 42 months

Interventionmonths (Median)
Arm I (Abiraterone Acetate and Prednisone)10.1
Arm II (Abiraterone Acetate, Prednisone, and Veliparib)11.0

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Rates of PSA Decline

Change in PSA from baseline to 12 weeks (NCT01576172)
Timeframe: 12 weeks

Interventionng/ml (Mean)
Arm I (Abiraterone Acetate and Prednisone)-41.1
Arm II (Abiraterone Acetate, Prednisone, and Veliparib)-52.9

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Confirmed Prostate-specific Antigen (PSA) Response Rate

50% or greater decline in PSA from baseline. (NCT01576172)
Timeframe: Up to 3 years

InterventionParticipants (Count of Participants)
Arm I (Abiraterone Acetate and Prednisone)46
Arm II (Abiraterone Acetate, Prednisone, and Veliparib)55

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Proportion of Patients With Response

"Response is defined as complete response (CR) or partial response (PR) CR: Complete disappearance of all detectable clinical evidence of disease and disease-related symptoms~PR:~>=50% decrease in sum of the product of the diameters (SPD) of up to 6 of the largest dominant nodes or extranodal masses~No increase in the size of other nodes, liver or spleen~Bone marrow assessment is irrelevant for determination of a PR if the sample was positive prior to treatment. However, if positive, the cell type should be specified~No new sites of disease~The post-treatment PET should be positive at any previously involved sites~For variably FDG-avid lymphomas/FDG-avidity unknown, without a pretreatment PET scan, or if a pretreatment PET scan was negative, CT scan criteria should be used~Patients with a CR and persistent morphologic bone marrow involvement~Patients with bone marrow involved before therapy and a clinical CR but no bone marrow assessment after treatment" (NCT01856192)
Timeframe: Assessed every 3 months for 2 years, every 6 months for year 3, and then annually for years 4-10

Interventionproportion of participants (Number)
Arm A (R2CHOP)0.97
Arm B (RCHOP)0.92

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3-year Progression-free Survival Rate

"Progression-free survival is defined as the time from randomization to disease progression, new primary of the same type or death, whichever occurs first. Progressive disease is defined as:~Appearance of any new lesion more than 1.5 cm in any axis during or at the end of therapy, even if other lesions are decreasing in size.~>= 50% increase from nadir in the sum of the product of the diameters of any previously involved nodes or extranodal masses, or in a single involved node or extranodal mass, or the size of other lesions.~>= 50% increase in the longest diameter of any single previously identified node or extranodal mass > 1 cm in its short axis.~Lesions should be PET positive unless the lesion is too small to be detected with current PET systems.~Measurable extranodal disease should be assessed in a manner similar to that for nodal disease.~3-year progression-free survival rate was calculated using Kaplan-Meier method." (NCT01856192)
Timeframe: Assessed every 3 months for 2 years, every 6 months for year 3, and then annually for years 4-10, 3-year PFS rate reported

Interventionproportion of participants (Number)
Arm A (R2CHOP)0.727
Arm B (RCHOP)0.615

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Overall Survival Rate at 3 Years

Overall survival is defined as time from randomization to death or date last known alive. Overall survival rate at 3 years was calculated using the method of Kaplan Meier. (NCT01856192)
Timeframe: Assessed every 3 months for 2 years, every 6 months for year 3, and then annually for years 4-10

Interventionproportion of participants (Number)
Arm A (R2CHOP)0.826
Arm B (RCHOP)0.751

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Proportion of Patients With Complete Response

Complete response is defined as complete disappearance of all detectable clinical evidence of disease, and disease-related symptoms if present prior to therapy. (NCT01856192)
Timeframe: Assessed every 3 months for 2 years, every 6 months for year 3, and then annually for years 4-10

Interventionproportion of participants (Number)
Arm A (R2CHOP)0.73
Arm B (RCHOP)0.68

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Disease-free Survival (Cohort II)

An estimate of disease free survival in Ph-positive ALL and Ph-like DSMKF ALL (Cohort II). Disease free survival is measured by the number of years between the date the patient first achieves complete remission (CR) or complete remission with incomplete platelet recovery (CRi) until relapse from CR/CRi or death from any cause. CR is defined as having <5% marrow aspirate blasts, ANC >1,000/mcL, platelets > 100,000/mcL, no blasts in peripheral blood, and C1 extramedullary disease status. CRi is the same as CR but platelet count may be <= 100,000/mcL and/or ANC <=1,000/mcL. (NCT02143414)
Timeframe: Duration of treatment and follow up until death or date of primary analysis (about 7.5 years)

Interventionyears (Median)
Cohort II (Ph+/Ph-like)5.3

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Complete Response Rate (Cohort I)

Complete response rate is measured by the number of participants achieving complete remission (CR) or complete remission with incomplete platelet recovery (CRi) rate. CR is defined as having <5% marrow aspirate blasts, ANC >1,000/mcL, platelets > 100,000/mcL, no blasts in peripheral blood, and C1 extramedullary disease status. CRi is the same as CR but platelet count may be <= 100,000/mcL and/or ANC <=1,000/mcL. (NCT02143414)
Timeframe: Participants are assessed after induction treatment and again after re-induction treatment, if re-induction treatment is received (i.e. up to 85 days after registration)

InterventionParticipants (Count of Participants)
CR or CRiNo CR or CRi
Cohort I (Ph-)1910

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Minimal Residual Disease Negativity

To estimate in each cohort the rate of minimal residual disease (MRD) negativity. (NCT02143414)
Timeframe: Participants are assessed after induction treatment and again after re-induction treatment, if re-induction treatment is received (i.e. up to 85 days after registration)

,
InterventionParticipants (Count of Participants)
MRD-MRD+
Cohort I (Ph-)121
Cohort II (Ph+/Ph-like)79

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Overall Survival Rate (Cohort I)

To evaluate the 3-year overall survival rate in elderly participants with newly diagnosed Ph-negative ALL treated with blinatumomab followed by POMP maintenance. Overall (NCT02143414)
Timeframe: From the day of registration on study until death from any cause, assessed at 3 years

Interventionpercentage of participants (Number)
Cohort I (Ph-)34

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Incidence of Dose-limiting Toxicity (Cohort II)

Defined as any grade 4 or higher treatment-related, non-hematologic toxicity in the first cycle of post-remission therapy (blinatumomab/dasatinib) graded by National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 4.0. Only participants with Ph-positive ALL or Ph-like DSMKF ALL were evaluated. (NCT02143414)
Timeframe: Up to day 42 of post-remission therapy

InterventionParticipants (Count of Participants)
Cohort II (Ph+/Ph-like)0

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Percentages of Patients Experiencing Grade 3+ Peripheral Neuropathy Assessed by Modified Balis Scale

"The percentages of patients experiencing grade 3+ peripheral neuropathy assessed by the treating clinician using the modified Balis scale. The Modified Balis scale of Pediatric Neuropathy allows clinicians to assign a score for sensory or motor neuropathy symptoms separately. Scores range from 1 to 4 with 1 being the least symptomatic state and 4 indicating a severe debility. The percentages of patients (with a score >/=3) will be compared between the 2 arms by two-sample Z test at 1-sided alpha level of 0.05." (NCT02166463)
Timeframe: From the enrollment of the patient to the time of analysis or the last follow-up; an average of 3.6 years.

InterventionPercentage of patients (Number)
Arm I (ABVE-PC)5.5
ARM II (Bv-AVEPC)6.7

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Event Free Survival (EFS), Where Events Include Disease Progression or Relapse, Second Malignancy, or Death

Primary analysis will be based 1-sided log rank test comparison of EFS curves between the 2 randomized arms per intention-to-treat principle. Progression is defined as an ≥50% increase of in the product of the perpendicular diameters of any of the involved nodes or nodal masses or focal organ lesions in sites that were persistently PET positive; or recurrent PET positive lesions (Deauville 4, 5) in sites that had previously been PET negative regardless of change of size, as was the development of new PET avid measurable lesion(s) >1.5cm in any axis, or new sites of assessable disease. Relapse is defined in patients who achieved a prior CR but subsequently has an increase of ≥50% of the PPD in prior nodal or extranodal sites in a recurrently PET positive lesion(s), or the development of new measurable lesion(s) >1.5cm in any axis, or new sites of assessable disease. Second malignancy is defined based on report of a cancer that is not considered to be classic Hodgkin Lymphoma. (NCT02166463)
Timeframe: Up to 48 months after the last enrollment

Interventionpercentage of participants (Number)
Arm I (ABVE-PC)82.5
ARM II (Bv-AVEPC)92.1

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Percentages of Patients With Early Response Defined as no Slow Responding Lesions (SRL) and no Progressive Disease (PD) at Any Disease Sites Determined by Positron Emission Tomography (PET) Per Deauville Criteria Through Central Review

The percentages of patients (with available PET scan) with no SRL and no PD will be compared between the two randomized arms to see if brentuximab vedotin in the chemotherapy backbone of doxorubicin hydrochloride, vincristine sulfate, etoposide, prednisone and cyclophosphamide (Bv-AVEPC) arm has a higher rate of early response compared to doxorubicin hydrochloride, bleomycin sulfate, vincristine sulfate, etoposide, prednisone, and cyclophosphamide (ABVE-PC) arm. Two-sample Z test of proportions at 1-sided alpha level of 0.05 will be used for these comparisons. (NCT02166463)
Timeframe: After 42 days of chemotherapy

InterventionPercentage of patients (Number)
Arm I (ABVE-PC)80.7
ARM II (Bv-AVEPC)81.2

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Total COPD Exacerbation Rate

The total number of COPD exacerbations reported within 48 weeks (NCT02261727)
Timeframe: 48 weeks observation; rate annualised

InterventionExacerbations per participant year (Number)
Placebo1.00
Low-dose Theophylline Arm0.86
Theophylline and Prednisone Arm0.89

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Time to First COPD Exacerbation

The median time (days) from randomisation to first exacerbation per participant (NCT02261727)
Timeframe: Median time (days) from randomisation to first exacerbation over a 48 week period per participant

InterventionDays (Median)
Placebo137
Low-dose Theophylline Arm150
Theophylline and Prednisone Arm151

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Quality of Life Measured by St. George's Respiratory Questionnaire (SGRQ)

THe St. George's Respiratory Questionnaire (SGRQ) is a disease-specific instrument designed to measure impact on overall health, daily life, and perceived well-being in patients with obstructive airways disease. Scores range from 0 to 100, with higher scores indicating more limitations. (NCT02261727)
Timeframe: Change over 48 week study duration

InterventionScores on a scale (Mean)
Placebo-4.95
Low-dose Theophylline Arm-6.85
Theophylline and Prednisone Arm-6.48

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Post Bronchodilator FEV1

The change in post bronchodilator FEV1 from baseline to 48 weeks (NCT02261727)
Timeframe: Change at 48 weeks

InterventionL/sec (Mean)
Placebo-0.02
Low-dose Theophylline Arm-0.01
Theophylline and Prednisone Arm-0.02

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Hospitalisations

The total number of hospitalisation events within 48 weeks (NCT02261727)
Timeframe: 48 weeks

InterventionNumber of hospitalisation events (Number)
Placebo120
Low-dose Theophylline Arm101
Theophylline and Prednisone Arm122

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Change in COPD Assessment Test (CAT) Score

The COPD Assessment Test (CAT) is a patient-completed questionnaire assessing globally the impact of COPD (cough, sputum, dysnea, chest tighteness) on health status. The range of CAT scores from 0-40. Higher scores denote a more severe impact of COPD on a patient's life. The outcome measure is assessing the change in score from baseline to 48 weeks. A negative change denotes an improvement in health status. (NCT02261727)
Timeframe: 48 weeks

InterventionScore on a scale (Mean)
Placebo-2.29
Low-dose Theophylline Arm-2.77
Theophylline and Prednisone Arm-2.57

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Overall Survival

Time from date of treatment start until date of death due to any cause or last Follow-up. (NCT02420717)
Timeframe: Up to 4 years 7 months

InterventionMonths (Median)
Phase I Ruxolitinib 15mg4.8
Phase I Ruxolitinib 20mg5.4
Phase I Ruxolitinib 25mg38.5

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Maximal Tolerated Dose (MTD) of Ruxolitinib in Combination With Chemotherapy Defined as the Highest Dose Level at Which no More Than 1 Out of 6 Patients Experience a Dose Limiting Toxicity (Phase I)

The method of Thall, Simon and Estey will be used for toxicity monitoring for this study. The severity of the toxicities will be graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events version 4.0 whenever possible. Safety data will be summarized by category, severity and frequency. (NCT02420717)
Timeframe: 42 days

InterventionMilligrams (mg) (Number)
Phase I Ruxolitinib 15mg25

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Participants With Complete Response (Complete Response [CR]/CR With Incomplete Marrow Recovery [CRi]) (Phase II)

Complete Response (CR) is disappearance of all clinical and/or radiologic evidence of disease, Neutrophil count ≥ 1.0 x 10^9/L, Platelet count ≥ 100 x 10^9/L, Normal bone marrow differential (≤ 5% blasts), No extra-medullary leukemia. Complete Remission with Incomplete Blood Count Recovery (CRi) is CR except for ANC < 1.0 x 10^9/L and/or platelets < 100 x 10^9/L. (NCT02420717)
Timeframe: 42 days

InterventionParticipants (Count of Participants)
Phase I Ruxolitinib 15mg0
Phase I Ruxolitinib 20mg1
Phase I Ruxolitinib 25mg0

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Progression-free Survival

Time from date of treatment start until the date of first objective documentation of disease-relapse. (NCT02420717)
Timeframe: Up to 4 years 7 months

InterventionMonths (Median)
Phase I Ruxolitinib 15mg2.3
Phase I Ruxolitinib 20mg1.8
Phase I Ruxolitinib 25mg1.9

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12-month PFS (Progression Free Survival) of Treatment With Ixazomib in Combination With DA-EPOCH-R (Phase II)

12-month PFS will be defined as the percentage of patients alive and progression free 12 months from start of therapy. Patients lost to follow up will be censored from last point of contact. PFS was calculated using a Kplan-meier estimation with the probability of patients being progression free at 12 months, presented as the percentage based on this probability. (NCT02481310)
Timeframe: Up to 12 months from initiation of treatment

Interventionprobability (%) of patients alive (Number)
Treatment (Combination Chemotherapy, Rituximab, Ixazomib)75.84

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PSA Response 2, Defined as >= 50% PSA Decline From Baseline

The percentage of participants with a >= 50% PSA decline from baseline will be reported with 95% confidence interval using exact method. 'PSA response' is based on Prostate Cancer Working Group 2's (PCWG2) recommendations, which do not offer a specific definition as no single degree of decline has been established. (NCT02522715)
Timeframe: Baseline to time of >= 50% PSA decline, assessed up to 68 weeks

Interventionpercentage of subjects (Number)
Phase I and Phase II - Treatment (Cabazitaxel, Enzalutamide)77.8

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PSA Response 3, Defined as >= 30% PSA Decline From Baseline

The percentage of participants with a >= 30% PSA decline from baseline will be reported with 95% confidence interval using exact method. 'PSA response' is based on Prostate Cancer Working Group 2's (PCWG2) recommendations, which do not offer a specific definition as no single degree of decline has been established. (NCT02522715)
Timeframe: Baseline to time of >= 30% PSA decline, assessed up to 68 weeks

Interventionpercentage of subjects (Number)
Phase I and Phase II - Treatment (Cabazitaxel, Enzalutamide)80.6

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PSA Response 1, Defined as >= 90% PSA Decline From Baseline

The percentage of participants with a >= 90% PSA decline from baseline will be reported with 95% confidence interval using exact method. 'PSA response' is based on Prostate Cancer Working Group 2's (PCWG2) recommendations, which do not offer a specific definition as no single degree of decline has been established. (NCT02522715)
Timeframe: Baseline to time of >= 90% PSA decline, assessed up to 68 weeks

Interventionpercentage of subjects (Number)
Phase I and Phase II - Treatment (Cabazitaxel, Enzalutamide)55.6

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Percentage of Participants With Dose Limiting ToxicitiesGgraded by National Cancer Institute Common Terminology Criteria for Adverse Events, Version 4.0 (Phase I)

The percentage of participants will be reported with 95% confidence interval using exact method. (NCT02522715)
Timeframe: Up to 42 days

Interventionpercentage of participants (Number)
Phase I - Treatment (Cabazitaxel, Enzalutamide)0.0

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Number of Participants With a Grade 3 or Higher Toxicity Graded According to National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.0

The Primary Outcome measures toxicity, with particular attention to Events of Clinical Interest when adding MK-3475 to standard RCHOP therapy. The sample size of 30 patients will permit the estimation of a 40% incidence of grade 3-5 clinically relevant toxicity. (NCT02541565)
Timeframe: Up to 90 days after completion of study treatment

InterventionParticipants (Count of Participants)
Treatment (Pembrolizumab, Combination Chemotherapy)13

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Number of Participants With Adverse Events Graded According to Common Toxicity Criteria (CTC) (Phase I)

Non-hematologic toxicities will be evaluated via the ordinal CTC standard toxicity grading. Hematologic toxicity measures of thrombocytopenia, neutropenia, and leukopenia will be assessed using continuous variables as the outcome measures (primarily nadir) as well as categorization via CTC standard toxicity grading. Overall toxicity incidence as well as toxicity profiles by dose level and patient will be explored and summarized. (NCT02561273)
Timeframe: Up to 6 cycles of treatment (approximately 5 months)

,
InterventionParticipants (Count of Participants)
grade 3,4 neutropeniagrade 3, 4 anemiagrade 3, 4 thrombocytopeniagrade 3,4 neutropenia fevergrade 3, 4 diarrheagrade 3, 4 hyperglycemiagrade 3, 4 hypokalemiagrade 3, 4 hypotensiongrade 3, 4 hyperbilirubinemiagrade 3, 4 mucositisgrade 3,4 nauseagrade 3,4 vomiting
10 mg Lenalidomide Participants532400000000
15 mg Lenalidomide Participants433022111221

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Progression-free Survival

The distribution of PFS will be estimated using the method of Kaplan-Meier. The PFS rate at 2 years will be estimated. A 2-year PFS rate of 60% will be considered of interest. (NCT02561273)
Timeframe: Time from registration to progression or death due to any cause, assessed up to 2 years

Interventionpercentage of participants (Number)
Treatment (Combination Chemotherapy, Lenalidomide)55

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Overall Survival

The distribution of overall survival will be estimated using the method of Kaplan-Meier. (NCT02561273)
Timeframe: Time from registration to death due to any cause, assessed up to 1 year

Interventionpercentage of participants (Number)
Treatment (Combination Chemotherapy, Lenalidomide)89

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Overall Response Rate

The ORR will be estimated by the total number of patients who achieve a PR or CR at the end of six cycles of treatment divided by the total number of evaluable patients. Exact binomial 95% confidence intervals for the true ORR will be calculated. (NCT02561273)
Timeframe: Up to the completion of course 6 (18 weeks)

Interventionpercentage of participants (Number)
Treatment (Combination Chemotherapy, Lenalidomide)69

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Number of Participants With Adverse Events Graded According to CTC (Phase II)

"The toxicity profile will be further assessed based on phase II patients. Overall toxicity incidence of maximum tolerated dose level of the Intent to treat (ITT) group of subjects is summarized.~39 subjects were dosed with 10 mg dose of Lenalidamide as the ITT group." (NCT02561273)
Timeframe: Up to 1 year

InterventionParticipants (Count of Participants)
grade 3,4 neutropeniagrade 3, 4 leukopeniagrade 3, 4 anemiagrade 3, 4 thrombocytopeniagrade 3, 4 lymphopeniagrade 3, 4 febrile neutropeniagrade 3, 4 diarrheagrade 3, 4 Peripheral sensory neuropathygrade 3, 4 fatiguegrade 3, 4 nauseagrade 3, 4 anorexiagrade 3, 4 vomitinggrade 3, 4 mucositis oralgrade 3, 4 Rash maculo-papulargrade 3, 4 hypotensiongrade 3, 4 back pain
Treatment (Combination Chemotherapy, Lenalidomide)2725171718153211111111

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Maximum Tolerated Dose (MTD) of Lenalidomide and CHOEP

MTD is defined as the dose level below the lowest dose that induces dose-limiting toxicity in at least one-third of patients (at least 2 of a maximum of 6 new patients) (Phase I) within the first cycle of study treatment. (NCT02561273)
Timeframe: 21 days

Interventionmilligrams (Number)
Treatment (Combination Chemotherapy, Lenalidomide)10

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Complete Response Rate (Phase II)

A success is defined to be an objective status of CR after completion of 6 cycles of treatment. The proportion of successes will be estimated by the number of successes divided by the total number of evaluable patients. A 95% confidence interval for the true overall CR rate will be calculated according to the method of Duffy and Santner. (NCT02561273)
Timeframe: Up to the completion of course 6 (18 weeks)

Interventionpercentage of participants (Number)
Treatment (Combination Chemotherapy, Lenalidomide)49

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Biologic Activity, Defined as Global Deoxyribonucleic Acid (DNA) Methylation Change in Peripheral Blood Mononuclear Cells (PBMC)s; Day 1 Prior to Second Course of Azacitidine

Will calculate the percentage of CpG site methylation for all patients before the second course of azacitidine. Mean and standard deviation will be reported. (NCT02828358)
Timeframe: Week 13, Day 1 (Following induction phase (5 weeks), the first course of Azacitidine (1 week), and consolidation (6 weeks), the second course of Azacitidine began around Week 13 of therapy)

InterventionPercentage of CpG methylation (Mean)
KMT2A-Rearranged76.5

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Biologic Activity, Defined as Global Deoxyribonucleic Acid (DNA) Methylation Change in Peripheral Blood Mononuclear Cells (PBMC)s; Day 5 of First Course of Azacitidine

Will calculate the percentage of CpG site methylation for all patients after the first course of azacitidine. Mean and standard deviation will be reported. (NCT02828358)
Timeframe: Week 6, Day 5 (Following the induction phase (35 days), the first course of Azacitidine began around Week 6 of therapy)

InterventionPercentage of CpG methylation (Mean)
KMT2A-Rearranged75.54

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Biologic Activity, Defined as Global Deoxyribonucleic Acid (DNA) Methylation Change in Peripheral Blood Mononuclear Cells (PBMC)s; Day 5 of Second Course of Azacitidine

Will calculate the percentage of CpG site methylation for all patients after the second course of azacitidine. Mean and standard deviation will be reported. (NCT02828358)
Timeframe: Week 13, Day 5 (Following induction phase (5 weeks), the first course of Azacitidine (1 week), and consolidation (6 weeks), the second course of Azacitidine began around Week 13 of therapy)

InterventionPercentage of CpG methylation (Mean)
KMT2A-Rearranged74.52

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Biologic Activity, Defined as Global Deoxyribonucleic Acid (DNA) Methylation Change in Peripheral Blood Mononuclear Cells (PBMC)s; Day 1 Prior to First Course of Azacitidine

Will calculate the percentage of CpG site methylation for all patients before the first course of azacitidine. Mean and standard deviation will be reported. (NCT02828358)
Timeframe: Week 6, Day 1 (Following the induction phase (35 days), the first course of Azacitidine began around Week 6 of therapy)

InterventionPercentage of CpG methylation (Mean)
KMT2A-Rearranged78.17

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Tolerability of Azacitidine in Combination With Interfant-06 Standard Chemotherapy in Evaluable Infant Patients With Newly Diagnosed ALL With KMT2A Gene Rearrangement (KMT2A-R). KMT2A Gene Rearrangement (KMT2A-R)

Proportion of KMT2A-Rearranged patients treated with azacitidine with Dose Limiting Toxicities (DLTs) from the first course of azacitidine administration up to fourth course of azacitidine administration. (NCT02828358)
Timeframe: 6 months

Interventionpercentage of participants (Number)
KMT2A-Rearranged6.45

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PSA Response Rate, Defined as >= 50% Decline in PSA From Baseline Maintained for at Least 3 Weeks and Measured by the Same Laboratory, and Without Evidence of Other Disease Progression Documented at Time of Confirmatory Values

The response rate will be compared to a historical response rate of 20% using the exact binomial test for a single proportion. Confidence intervals for the response rate will be calculated using Wilson's method. (NCT02844582)
Timeframe: Up to 18 months.

InterventionParticipants (Count of Participants)
Treatment (Cabazitaxel, Prednisone)0

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Incidence of Adverse Events, Serious Adverse Events, and Discontinuations, Described and Graded According to the National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.03

Incidence of adverse events, serious adverse events, and discontinuations, described and graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events version 4.03 (NCT02844582)
Timeframe: Up to 28 days after discontinuation of study drug

Interventionparticipants (Number)
Back painDiarrheaFatigueHot flashesNeutrophil count decreasedNon-cardiac chest painPainRenal and urinary disorders - Other, specifyWhite blood cell decreased
Treatment (Cabazitaxel, Prednisone)112121112

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Number of Patients With Pathologic T3 Disease After 3 Months of Treatment.

The presence of T3 disease (e.g. extraprostatic tumor not invading adjacent structures) will be determine from the prostatectomy specimen after 3 months of treament. (NCT02849990)
Timeframe: At 3 months

InterventionParticipants (Count of Participants)
Treatment (Neoadjuvant Chemotherapy)18

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Number of Participants Without Biochemical Failure at 2 Years

Prostate-specific antigen progression (i.e. biochemical failure) will be defined per the American Urological Association guidelines (i.e. confirmed prostate-specific antigen post-radical prostatectomy >= 0.2 ng/mL). We will report the number of patients without biochemical failure at 2 years. (NCT02849990)
Timeframe: At 2 years

Interventionparticipants (Number)
Treatment (Neoadjuvant Chemotherapy)18

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Pathologic Complete Response Rate as Assessed From Prostatectomy Specimens Following Neoadjuvant Treatment

Pathologic complete response is defined as no evidence of cancer on fully submitted prostatectomy specimens using standard surgical pathology assessments (i.e. H&E assessment will be used for the purpose of defining pathologic complete response per protocol) at 3 months. (NCT02849990)
Timeframe: At 3 months

InterventionParticipants (Count of Participants)
Treatment (Neoadjuvant Chemotherapy)1

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The Proportion of Men Who Receive Adjuvant Radiation Therapy

Patients that received radiation following prostatetomy (NCT02849990)
Timeframe: Up to 1 year post prostatectomy

InterventionParticipants (Count of Participants)
Treatment (Neoadjuvant Chemotherapy)7

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Number of Patients With no Nodal Metastases After 3 Months of Treatment.

The presence of tumor cells within surgically excised lymph nodes will be assessed after 3 months of treament. (NCT02849990)
Timeframe: At 3 months

InterventionParticipants (Count of Participants)
No nodal metastasesNodal metastases
Treatment (Neoadjuvant Chemotherapy)137

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Overall Survival (OS)

Will will report the number of participants alive at 2-years following enrollment. (NCT02849990)
Timeframe: At 2 years

InterventionParticipants (Count of Participants)
Treatment (Neoadjuvant Chemotherapy)20

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Number of Patients With a Near Pathologic Complete Response After 3 Months of Treatment

The near pathologic complete response will be defined as =< 5 mm of residual tumor as assessed on prostatectomy specimens after 3 months of treatment. (NCT02849990)
Timeframe: At 3 months

InterventionParticipants (Count of Participants)
Treatment (Neoadjuvant Chemotherapy)6

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Number of Participants With Morphological Complete Response Rate

Morphological complete remission (CR) was determined by bone marrow aspirate morphology and defined as <5% blasts by morphology, absolute neutrophil count >1000/uL, and platelet count >100,000/uL. (NCT03023046)
Timeframe: Within 4 cycles of study therapy

InterventionParticipants (Count of Participants)
Ph+ Subjects27
Ph- Subjects20

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Number of Participants With Adverse Events

Grade 1 or higher non-hematologic adverse events will be assessed by Common Terminology Criteria for Adverse Events version 5.0. (NCT03023046)
Timeframe: Within 28 days of the last dose of the study drugs

InterventionParticipants (Count of Participants)
Treatment (Chemotherapy)44

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Event-free Survival

Events were defined as any of the following: (1) unable to achieve either morphologic complete remission (CR) or MRD- by MFC, (2) relapse after CR, (3) MRD recurrence after achieving MRD-, or (4) death from any cause. (NCT03023046)
Timeframe: Up to 2 years

InterventionPercentage of Participants (Number)
Treatment (Chemotherapy)32

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Number of Participants With Complete Measurable Residual Disease (MRD) Response Rate

"Response was determined by having no detectable disease by multiparameter flow cytometry (MFC-). For Ph+ subjects, complete molecular response (CMR) by BCR-ABL RT-PCR was assigned when MFC was undetectable.~When no measurable residual disease was detected by MFC (MFC-) per EuroFlow criteria, high-throughput sequencing-based MRD testing (HTS; ClonoSEQ) was performed." (NCT03023046)
Timeframe: Within 4 cycles of study therapy

InterventionParticipants (Count of Participants)Participants (Count of Participants)
MFC-72545885MFC-72545886CMR72545885HTS-72545885HTS-72545886
Achieve within 4 cyclesNot achieved within 4 cycles
Ph+ Subjects20
Ph- Subjects9
Ph+ Subjects11
Ph+ Subjects17
Ph+ Subjects8
Ph- Subjects6
Ph+ Subjects16
Ph- Subjects16

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Overall Survival

Alive at 2 years after enrollment (NCT03023046)
Timeframe: Up to 2 years

InterventionPercentage of Participants (Number)
Treatment (Chemotherapy)70

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Complete Response (CR) Rate After Cyclophosphamide, Doxorubicin, Etoposide, Prednisone, and Brentuximab Vedotin (CHEP-BV) Induction Therapy

CR rate was estimated by the proportion of evaluable patients achieving CR after CHEP-BV induction therapy, along with the 95% exact binomial confidence interval. (NCT03113500)
Timeframe: Up to the end of the CHEP-BV treatment

Interventionpercentage of response rate (Number)
Treatment (CHEP-BV)79

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Overall Survival at 1 Year

Overall survival (OS) was measured from enrollment to death from any cause. OS was estimated using the product-limit method of Kaplan and Meier along with the Greenwood estimator of standard error. (NCT03113500)
Timeframe: The time from enrollment to death from any cause assessed up to 1 year.

Interventionpercentage of survival probability (Number)
Treatment (CHEP-BV)91

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The Number of Participants With Rate of Pathologic Stage =< pT2N0 at Prostatectomy

The study will provide a point estimate and 95% confidence interval of the proportion of patients with pathologic stage =< pT2N0 at prostatectomy for each arm. Patient characteristics will be summarized using descriptive statistics for each arm. (NCT03279250)
Timeframe: At the time of radical prostatectomy

InterventionParticipants (Count of Participants)
Arm A (LHRHa, Apalutamide)13
Arm B (LHRHa, Apalutamide, Abiraterone Acetate)12

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Number of Participants With Incidence of Adverse Events

Will be graded according to Common Terminology Criteria for Adverse Events (CTCAE) version 4.03. Incidence of serious adverse events and 95% confidence interval will be provided overall as well as for each major affected organ category. (NCT03279250)
Timeframe: From screening up to 4 weeks post-surgery, an average of 7 months

,
InterventionParticipants (Count of Participants)
SeriousNon Serious
Arm A (LHRHa, Apalutamide)134
Arm B (LHRHa, Apalutamide, Abiraterone Acetate)234

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Number of Participants With Adverse Events

For the purpose of toxicity monitoring, toxicities are defined as any treatment -related grade 3 or 4 non-hematologic AEs occurred any time during the trial.NCI Common Terminology Criteria for Adverse Events (CTCAE) version 4.03 utilized for adverse event reporting. (NCT03488225)
Timeframe: Start of treatment up to 30 days after last dose received.

InterventionParticipants (Count of Participants)
Neutropenic FeverPeripheral Sensory NeuropathyAllergic ReactionMuscle Weakness
Treatment (Hyper-CVAD, Inotuzumab Ozogamicin)2111

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Participants to Achieve Complete Remission (CR):

Complete Remission (CR) is defined as - Normalization of the peripheral blood and bone marrow blasts /= 100X10^9/L and complete resolution of all sites of extramedullary disease. (NCT03488225)
Timeframe: Start of treatment up to 2 years

InterventionParticipants (Count of Participants)
Treatment (Hyper-CVAD, Inotuzumab Ozogamicin)4

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Overall Survival

Time from date of treatment start until date of death due to any cause or last Follow-up. (NCT03488225)
Timeframe: Start of treatment up to 2 years

InterventionMonths (Median)
Treatment (Hyper-CVAD, Inotuzumab Ozogamicin)24

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Number of Participants With Minimal Residual Disease (MRD) Negativity

MRD levels continuously assessed during induction and consolidation therapy by 6-color multiparameter flow. MRD negativity defined by a value of at least 10-4 and confirmed on a second bone marrow aspiration/biopsy performed after a subsequent cycle. (NCT03488225)
Timeframe: Start of treatment up to 2 years

InterventionParticipants (Count of Participants)
Treatment (Hyper-CVAD, Inotuzumab Ozogamicin)4

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Event-Free Survival

Event-free survival defined as the time interval from date of treatment start until the date of death, disease progression or relapse. (NCT03488225)
Timeframe: Start of treatment up to 2 years

InterventionMonths (Median)
Treatment (Hyper-CVAD, Inotuzumab Ozogamicin)24

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Incidence of Adverse Events

Will be assessed per Common Terminology Criteria for Adverse Events (CTCAE) version 4.0. Safety and tolerability as evaluated by the incidence, severity, duration, causality, seriousness of adverse events. Toxicities will be summarized as the number of patients with grade 3 or higher toxicities per CTCAE v4.0, in addition to total number of toxicities (allowing for multiple toxicities within a patient) among all patients, and per treatment arm. (NCT03649841)
Timeframe: Up to 6 months

InterventionParticipants (Count of Participants)
Arm I (ADT, Abiraterone, Prednisone)2
Arm II (ADT, Abiraterone, Prednisone, Radiation Therapy)0

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Rate of Undetectable Prostate Specific Antigen (PSA) (< 0.2)

The number of patients with undetectable PSA at 6-months will be summarized by each arm and all combined. (NCT03649841)
Timeframe: At 6 months after start of abiraterone acetate

InterventionParticipants (Count of Participants)
Arm I (ADT, Abiraterone, Prednisone)1
Arm II (ADT, Abiraterone, Prednisone, Radiation Therapy)1

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Rate of Allograft Loss After Receiving Ipilimumab, Nivolumab, Tacrolimus, and Prednisone

Number of patients who experienced allograft loss after receiving nivolumab, ipilimumab, tacrolimus, and prednisone. (NCT03816332)
Timeframe: Up to 3 years

InterventionParticipants (Count of Participants)
Experienced allograft lossDid not experience allograft loss
Ipilimumab, Nivolumab, Tacrolimus, and Prednisone33

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Number (and Percentage) of Outcome Responses After Receiving Nivolumab, Tacrolimus, and Prednisone

Percentage of kidney transplant recipients who experienced complete response (CR), partial response (PR) or stable disease (SD) without allograft loss. (NCT03816332)
Timeframe: At 16 weeks

InterventionParticipants (Count of Participants)
Complete response (CR), partial response (PR) or stable disease (SD) without allograft lossProgressive Disease (PD) without allograft loss
Nivolumab, Tacrolimus, and Prednisone08

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Duration of Progression-free Survival After Receiving Nivolumab, Tacrolimus, and Prednisone

From the first dose of nivolumab to the date of the first documented tumor progression or death due to any cause, whichever occurs first. (NCT03816332)
Timeframe: Up to 4 months

Interventiondays (Mean)
Nivolumab, Tacrolimus, and Prednisone59

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Duration of Overall Survival After Receiving Nivolumab, Tacrolimus, and Prednisone

The time from the participant's first dose of nivolumab to the date of death from any cause. (NCT03816332)
Timeframe: Up to 3 years

Interventionmonths (Median)
Nivolumab, Tacrolimus, and Prednisone9.1

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Prostate Specific Antigen Progression Free Survival (PSA-PFS)

Prostate Specific Antigen (PSA) will be measured every three months while on study. PSA Progression Free Survival (PSA-PSF) will be reported as the number of participants who have not demonstrated PSA progression by the end of the follow-up period. PSA progression is defined by meeting the following criteria: 1) an increase in PSA of greater than or equal to 25% from baseline or nadir, AND 2) an increase in PSA of at least 2 ng/dL, AND 3) the increase is confirmed at least 3 weeks later. This analysis was planned for up to 18 months following study enrollment, but the only participant enrolled on the study was only followed for 3 months. (NCT03827473)
Timeframe: Planned up to 18 months, but actual was 3 months

InterventionParticipants (Count of Participants)
Arm A (ADT, Docetaxel)1

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Change in Quality of Life - PROMIS Fatigue

Quality of Life questionnaires will be done every 3 months while participants are on treatment. The scale used will be the Patient-Reported Outcomes Measurement Information System (PROMIS) Fatigue scale. Total raw scores range from 7 to 35, with higher scores indicating a higher level of fatigue. (NCT03827473)
Timeframe: Planned for up to 18 months, but actual was 3 months

Interventionscore on a scale (Number)
Baseline ScoreMonth 3 Score
Arm A (ADT, Docetaxel)1016

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Change in Quality of Life - FACT/GOG-NTX

Quality of Life questionnaires will be done every 3 months while participants are on treatment. The scale used will be the Functional Assessment of Cancer Therapy (FACT)/Gynecologic Oncology Group (GOG)-Neurotoxicity (NTX) (FACT/GOG-NTX) scale (version 4). FACT/GOG-NTX total score ranges from 0 to 152, with higher scores indicating a higher quality of life. (NCT03827473)
Timeframe: Planned for up to 18 months, but actual was 3 months

Interventionscore on a scale (Number)
Baseline ScoreMonth 3 Score
Arm A (ADT, Docetaxel)131.83126

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Change in Quality of Life - FACT-P

The impact of abiraterone acetate and docetaxel on health related quality of life will be assessed every 3 months from screening to month 12 of treatment or follow-up. The scale used will be the Functional Assessment of Cancer Therapy-Prostate (FACT-P) scale. The total score ranges from 0 to 156, with higher scores indicating a higher quality of life. The primary endpoint was intended to be quality of life at 12 months, but since no participants completed 12 months of treatment/follow-up, scores at baseline and 3 months are reported instead. (NCT03827473)
Timeframe: Planned for up to one year, but actual was 3 months

Interventionscore on a scale (Number)
Baseline ScoreMonth 3 Score
Arm A (ADT, Docetaxel)139.83127

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Prostate-specific Antigen (PSA) Response

PSA evaluations will occur every 3 months while on study. PSA response is defined as a reduction in PSA value of greater than or equal to 90% from baseline, reported as a count of participants who had a PSA response on the study. (NCT03827473)
Timeframe: Planned for up to 18 months, but actual was 3 months

InterventionParticipants (Count of Participants)
Arm A (ADT, Docetaxel)1

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